Physiology

TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY MAIN DIGITAL HANDOUT BY ENRICO PAOLO C.
BANZUELA, MD
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This handout is only valid for the September 2021 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.
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This handout is only valid for the September 2021 PLE batch.
This will be rendered obsolete for the next batch
DISCLOSURE
The handouts/review materials must be treated with utmost confidentiality. It shall be the since we update our handouts regularly.
responsibility of the person, whose name appears therein, that the handouts/review
materials are not photocopied or in any way reproduced, shared or lent to any person or
disposed in any manner. Any handout/review material found in the possession of another 1. CELL & MUSCLE PHYSIOLOGY
person whose name does not appear therein shall be prima facie evidence of violation of RA
8293. Topnotch review materials are updated every six (6) months based on the current 1. Cell Membranes
trends and feedback. Please buy all recommended review books and other materials listed 2. Transport Across Cell Membranes
below.
THIS HANDOUT IS NOT FOR SALE!
3. Osmosis
4. Diffusion Potential, Resting Membrane Potential, Action Potential
5. Neuromuscular and Synaptic Transmission
INSTRUCTIONS
To scan QR codes on iPhone and iPad 6. Skeletal Muscles
1. Launch the Camera app on your IOS device 7. Cardiac Muscles
2. Point it at the QR code you want to scan 8. Smooth Muscles
3. Look for the notification banner at the top
9. Comparison of Skeletal Muscles, Smooth Muscles and Cardiac
of the screen and tap
To scan QR codes on Android Muscles
1. Install QR code reader from Play Store
2. Launch QR code app on your device
3. Point it at the QR code you want to scan 1.1 CELL MEMBRANES
4. Tap browse website CELL NUMBER
• Approximate number of human cells + bacterial
68 trillion
cells inside the human body
A PRAYER FOR EXAMS • Approximate number of human cells (80% are
30 trillion
TO ST. JOSEPH OF RBCs – most abundant type of cell in the body)
CUPERTINO (optional) 1 trillion • Approximate number of glial (supporting) cells
https://qrs.ly/gtcmq3t • Approximate number of neurons (actual value
100 billion
closer to 86B)
CELL MEMBRANE
Approach to Topnotch Physiology
• The Guardian of the Cell: divides the body into extracellular fluid
• Please buy the following: Physio BRS 6th ed and Ganong
(ECF) and intracellular fluid (ICF) compartments
Physiology 23rd ed or 25th ed, and Pre-Test Physiology 14th Ed
o To be used as major reference books • Contains many protein, little carbohydrates, no water
o they’re very good books that will help you in this subject • Semipermeable
o Lecture utilizes mainly Physio BRS supplemented by other • Has variable composition throughout the life of the cell
sources (e.g. Guyton, Berne and Levy, Ganong); those that you • Made up of a Lipid Bilayer (Fluid-Mosaic Model)
don’t understand or need further discussion, refer to Physio BRS o 55%: Proteins
and Ganong o 25%: Phospholipids
• We won’t try to cover all of physio; we’ll try to cover: § Outer Leaflet: Phosphatidylcholine, Sphingomyelin,
o What you need as a General Physician (must-knows) § Inner Leaflet: Phosphatidylethanolamine,
o Less important topics that has been asked in the past (nice-to- Phosphatidylserine, Phosphatidylinositol
knows) o 13%: Cholesterol: confers membrane fluidity and permeability
• Guided highlighting system: highlight only those that are bold to water-soluble substances
and italicized → we’ve identified them for you § major lipoprotein source of cholesterol: LDL
• This handout is only for the one whose name appears as a o 4%: Other lipids: glycolipids confer antigenicity
watermark. Videos are only for enrolled students. Handouts will o 3% Carbohydrates
expire September 2021. Remember: cell membrane lets hydrophobic/fat-soluble substances to
move in or out of the cell membrane with ease according to concentration
gradient. Imagine oxygen, carbon dioxide and steroid hormones directly
PHYSIOLOGY penetrating the cell membrane. The lipid bilayer basically allows fat-
soluble substances to move across it.
By Enrico Paolo C. Banzuela, MD, Dr. Banzuela
• Studded with the following proteins:

MSEd, MHPEd, FPSP o Integral Proteins
University of the Philippines College of Medicine Class 2005
§ Has tight attachment (needs detergent to remove) using
Master in Educational Entrepreneurship (MSEd), University of Pennsylvania Graduate
School of Education hydrophobic interactions
Master in Health Professions Education (MHPEd), University of the Philippines Manila, § spans the entire cell membrane
National Teacher Training Center for the Health Professions § e.g. Aquaporins, Ion Channels, Solute Carriers (GLUT,
Master of Health Professions Education (MHPE), University of Maastricht (current
student) Symport, Antiport), ATP-dependent Transporters
Management Development Program, Asian Institute of Management o Peripheral Proteins
Postgraduate Certificate in Teaching Evidence-Based Healthcare, University of Oxford § Has loose attachment using electrostatic interactions
Program for Leading Innovations in Health Care and Education, Harvard Macy Institute
(incoming student 2021)
§ Found in the inner leaflet or outer leaflet
Course Coordinator (Chairman) for Physiology, San Beda University College of Medicine
Associate Professor II, San Beda College of Medicine
Guest Lecturer, Ateneo School of Medicine & Public Health
Physiology Teacher, Topnotch Medical Board Prep
Co-Author, IM Platinum, Surgery Platinum and Pedia Platinum
Vice-President, Philippine Society of Physiologists (PSP)
Fellow, Philippine Society of Physiologists (PSP)
TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY MAIN DIGITAL HANDOUT BY ENRICO PAOLO C. BANZUELA, MD Page 1 of 97
For inquiries visit www.topnotchboardprep.com.phor https://www.facebook.com/topnotchmedicalboardprep/
TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY MAIN DIGITAL HANDOUT BY ENRICO PAOLO C. BANZUELA, MD
© Topnotch Medical Board Prep
Look at the picture above. The integral proteins are TIGHTLY-attached and
do not move. The peripheral proteins are loosely-attached and tend to
“float” in the lipid bilayer – like leaves or flowers floating in a pond. Viewed © Topnotch Medical Board Prep
externally – those peripheral proteins floating around gives the cell a

“mosaic” appearance, giving rise to the term “fluid-mosaic model”
Dr. Banzuela
• Movement of different substances across the cell membrane:

o Water
§ Undergoes Osmosis via Aquaporins
o Lipid-Soluble (Non-polar, Hydrophobic) Substances
§ Substances undergo Simple Diffusion
o Water-Soluble (Polar, Hydrophilic) Substances © Topnotch Medical Board Prep
§ Substances undergo Carrier-mediated Transport
INTERCELLULAR STRUCTURES BETWEEN CELL MEMBRANES
TYPE DESCRIPTION LOCATION NOTES
Macula Adherens • Disk-shaped;
• Epithelium • Like intercellular stapler wires
(Desmosomes) • For tight intercellular adhesion
• Epithelial & endothelial cells • Equivalent in cardiomyocytes is Fascia
• Ring-shaped
Zonula Adherens • Intercalated disks of cardiac Adherens (ribbon-like patterns;
• increases surface area for contact
muscles doesn’t completely enclose cell)
• Transcellular Transport: movement
• Barrier to movement of proteins
Zonula Occludens • Leaky: PCT, Jejunum across apical and basolateral sides
across membranes; divides cell
(Tight Junctions) • Tight: CD, terminal Colon, BBB • Paracellular Transport: movement
into apical and basolateral side
through TJ
• bridge for sharing of small
molecules between cells; For • Cardiac and unitary smooth • Functional Unit: ConneXON (its
Gap Junctions
rapid intercellular muscles Subunit: ConneXIN)
communication
When you hear desmosomes, think STAPLER wires – they hold cells • H conc →
together in tight attachment. They make cells ADHERE to each other – Facilitated • GLUT transporters,
L conc
kaya tinatawag din siyang Macula ADHEREns. Gap Junctions – they enable Diffusion • AA transporters
• (Passive; Downhill)
the cells to contract together as one. When you hear gap junctions, think
SYNCYTIUM – the ability of muscle cells to contract together as one. • Na+-K+-ATPase
Dr. Banzuela pump,
✔GUIDE QUESTION • H+-K+ ATPase pump
The low-resistance pathways between myocardial cells that allow for the of the parietal cells
spread of action potentials are the (stomach),
(A) gap junctions • H+-ATPase pump in
(B) T tubules Primary • L conc →
intercalated cells
(C) sarcoplasmic reticulum (SR) Active H conc)
(kidneys)
(D) intercalated disks Transport • (Active; Uphill)
(E) mitochondria Costanzo LS. BRS Physiology. 6 ed. 2014. th
• Ca2+-ATPase pump
in the cell membrane
& SR,
1.2 TRANSPORT ACROSS CELL MEMBRANES • multi-drug
resistance
transporters
CELL TRANSPORT
• SGLT-1 in the S.I.
https://qrs.ly/3ocmq41
• SGLT-2 in the PCT
• Na2+-K+-2Cl- in TAL
Secondary • L conc →
Refer to this audio file while reading this very important table. of LH
Active H conc)
Dr. Banzuela • Na-Ca2+ exchange in
Transport • (Active; Uphill)
TYPE MOVEMENT EXAMPLES almost all cells
I. NON- CARRIER MEDIATED TRANSPORT • Na+-H+ exchange in
the PCT (kidneys)
• Oxygen, Nitrogen,
Simple H conc → L conc CO2, alcohol, lipid
Diffusion (Passive; Downhill) hormones, SPECIAL NOTES: SIMPLE DIFFUSION
anesthetic drugs • Measured using the formula:
• Divided in Pino- and 𝑱 = 𝑷𝑨 × (𝑪𝟏 − 𝑪𝟐 )
Phagocytosis; J = flux (flow (mmol/sec)
Endocytosis - P = permeability (cm/sec)
• e.g. Neutrophils and
Bacteria A = area (cm2)
C1 = higher concentration 1 (mmol/L)
Exocytosis - • Hormones and NTs C2 = lower concentration 2 (mmol/L)
II. CARRIER-MEDIATED TRANSPORT
• L conc →
Osmosis • Water
H conc
SPECIAL NOTES: FACILITATED DIFFUSION
• At low-solute concentrations: Facilitated Diffusion is faster than
Simple diffusion (because FD involves carrier proteins, which
makes it go faster, analogous to a person riding a fast car)
• At high-solute concentrations: Facilitated Diffusion is slower
than Simple Diffusion (because FD exhibits saturation and
transport maximum (basically a speed limit), unlike SD)
GLUT 1 • Blood-brain barrier, RBCs, Cornea, Placenta
• Liver, Pancreas (β islet cells), Basement Membrane
GLUT 2
of Small Intestine, Kidney
GLUT 3 • Neurons, Placenta
• Muscles, Adipose (only insulin-dependent glucose
GLUT 4
transporter)
• For fructose transport from SI lumen to SI cell,
GLUT 5 Spermatocytes (fructose is the energy source for
sperm motility)
When we place formulas in the handout, it means they are important. Look
at the formula above. Memorize these formulas.
Dr. Banzuela
• P (permeability) in the formula J= PA (C1-C2) is increased by the
following:
o Increased Oil / water partition coefficient of solute (increases
solubility in the lipid of the membrane)
o Decreased Radius of solute
o Decreased Membrane Thickness
• Small Hydrophobic Solutes (O2, CO2): high permeability
• Hydrophilic Solutes (Na, K): uses aquaporins or transporters to
cross cell membrane
• Most important characteristic of hydrophobic hormones that
GLUT TRANSPORTERS
governs diffusion across cell membrane: Lipid Solubility
MNEMONIC
Take note of the formula for simple diffusion (J=PA(C1-C2), and the factors https://qrs.ly/4ycmq9h
that will increase permeability – increased oil/water partition coefficient
of the solute, small size, thin membrane. You need that to answer the guide
question below: SPECIAL NOTES: PRIMARY ACTIVE TRANSPORT
Dr. Banzuela
• Exhibits co-transport (“symport”) and Countertransport (“anti-
✔GUIDE QUESTIONS port” or “exchange”)
Which of the following will double the permeability of a solute in a lipid • Source of energy: ATP hydrolysis
bilayer? • Na+-K+ ATPase Pump
(A) Doubling the molecular radius of the solute o 3 Sodium Out, 2 Potassium In (Mnemonic: “TRI-NA TO-K-EN”)
(B) Doubling the oil/water partition coefficient of the solute
o Keeps Na+ in the ECF and K+ in the ICF
(C) Doubling the thickness of the bilayer
(D) Doubling the concentration difference of the solute across the
o Contributes to RMP (-4mv out of the -70mv)
bilayer 1-19 Costanzo LS. BRS Physiology. 7 ed. 2019. th
o Contributes to Basal Metabolic Rate (BMR)
Solutions A and B are separated by a membrane that is permeable to o Some cardiac Na+-K+-ATPase pump inhibited by Digoxin
urea. Solution A is 10 mM urea, and solution B is 5 mM urea. If the o Found in the basement membrane side except for Choroid
concentration of urea in solution A is doubled, the flux of urea across Plexus
the membrane will • Ca2+-ATPase pump in the sarcoplasmic reticulum: SERCA
(A) double • H+-K+-ATPase pump in the lumen of the parietal cells of the
(B) triple
stomach: Proton Pump
(C) be unchanged
(D) decrease to one-half
(E) decrease to one-third 1-11 Costanzo LS. BRS Physiology. 7 ed. 2019.th
For the guide question above:

J1 = PA (C1-C2) =PA (10-5) = 5
J2 = PA (C1-C2) = PA (20-5) = 15
J2 is 3x more than J1. Kaya “triple” yung sagot.
Remember: flux of urea is from high concentration to low concentration
since urea undergoes simple diffusion.
Dr. Banzuela
SPECIAL NOTES: CARRIER-MEDIATED TRANSPORT
• Important Characteristics:
o Stereospecificity: Two substances may have the same chemical
composition, but different “shape”. Carriers accommodate a
specific “shape” (e.g. D-glucose vs. L-glucose) © Topnotch Medical Board Prep
Remember:” basta may ATP sa name, Primary yan.”
o Saturation: number of carriers are finite. Once all carriers are Dr. Banzuela
filled up or saturated, rate of transport becomes constant SPECIAL NOTES: SECONDARY ACTIVE TRANSPORT
(Transport Maximum) • Exhibits co-transport (“symport”) and Countertransport (“anti-
o Competition: different solutes may compete for same carrier port” or “exchange”)
(e.g. Gal vs. Glu in the SGLT-1 of small intestine) • Source of Energy: downhill transport of Na+ (indirectly relies on
o SGLT-1 Deficiency in newborns lead to glu/gal malabsorption Na+-K+-ATPase pump)
leading to severe diarrhea Remember:” basta may sodium sa name, Secondary yan.”
Dr. Banzuela
Remember the properties of Carrier-Mediated Transport: S-S-C –
• Co-Transport (Symport): solutes move in same direction
stereospecificity, saturation and competition. May shape lang na
• Countertransport (Antiport, Exchange): solutes move in
pwedeng gumamit ng carrier protein (stereospecificity), limited and
number ng carrier protein (saturation), at pwedeng magkaroon ngopposite directions
competition for the carrier proteins (competition: parang “Trip to
• Sodium-Glucose Cotransport (SGLT)
Jerusalem”). o Na+ moves downhill, Glu moves uphill, both move in the same
Dr. Banzuela
direction (Cotransport)
o SGLT-1: SI, SGLT-2: Kidneys
Adenosine triphosphate (ATP) is used indirectly for which of the
following processes?
(A) Accumulation of Ca2+ by the sarcoplasmic reticulum (SR)
(B) Transport of Na+ from intracellular to extracellular fluid
(C) Transport of K+ from extracellular to intracellular fluid
(D) Transport of H+ from parietal cells into the lumen of the stomach
(E) Absorption of glucose by intestinal epithelial cells
1-28 Costanzo LS. BRS Physiology. 7th ed. 2019
Because all secondary active transports (e.g. SGLT-1), relies on the

Na+-gradient created by the Na+-K+-ATPase pump.
Dr. Banzuela
A new drug is developed that blocks the transporter for H+ secretion in
gastric parietal cells. Which of the following transport processes is
being inhibited?
(A) Simple diffusion
(B) Facilitated diffusion
© Topnotch Medical Board Prep (C) Primary active transport
(D) Cotransport
Mnemonic: SGLT-1 is in the small intestines, SGLT-2 is in the kidneys. Think
(E) Countertransport 1-32 Costanzo LS. BRS Physiology. 7 ed. 2019 th
of it this way: you have 1 Intestine, but you have 2 kidneys: SGLT-1 and
SGLT-2. H+-K+-ATPase pump is the proper term for the proton pump of the
Dr. Banzuela parietal cells of the stomach. It is a Primary Active Transport,
• Sodium-Calcium Countertransport (Na+-Ca2+ Exchange) countertransport.
o Na+ moves downhill, Ca2+ moves uphill, they move in opposite Dr. Banzuela
directions
o Na+-Ca2+ exchange in the cardiac membrane: decreases 1.3 OSMOSIS
intracellular Ca2+ OSMOLARITY
o MOA of Digoxin: inhibits cardiac Na+-K+-ATPase Pump → • Concentration of osmotically active particles in a solution
inhibits Na+-Ca2+ pump → greater intracellular calcium → • Measured in Osmoles/Liter
greater cardiac contractility • “Pogi” points of water
§ Hypokalemia increases the risk and severity of digitalis o The higher the osmolarity of a solution, the more it attracts
toxicity because: hyperpolarized cardiac membrane → water from an opposite compartment
further increased inhibition of the Na-K-ATPase pump 𝑂𝑠𝑚𝑜𝑙𝑎𝑟𝑖𝑡𝑦 = 𝐶𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 × # 𝑜𝑓 𝐷𝑖𝑠𝑠𝑜𝑐𝑖𝑎𝑏𝑙𝑒 𝑃𝑎𝑟𝑡𝑖𝑐𝑙𝑒𝑠
✔ GUIDE QUESTIONS 𝑚𝑂𝑠𝑚/𝐿 = 𝑚𝑚𝑜𝑙/𝐿 × 𝑁𝑢𝑚𝑏𝑒𝑟 𝑜𝑓𝑝𝑎𝑟𝑡𝑖𝑐𝑙𝑒𝑠/𝑚𝑜𝑙
Which of the following characteristics is shared by simple and facilitated • Normal ECF Osmolarity: 300 mOsm/L
diffusion of glucose? • Normal ICF Osmolarity: 300 mOsm/L
(A) Occurs down an electrochemical gradient
(B) Is saturable Normal values differ depending on the textbook that you are going to use
(C) Requires metabolic energy – so do not obsess about it, at alam din yan ng examiners – they rarely ask
(D) Is inhibited by the presence of galactose you what is the normal value of this or that. In some books, ECF and ICF
(E) Requires a Na+ gradient 1-1 Costanzo LS. BRS Physiology. 7 ed. 2019. th
osmolarity is 285, in other books it’s 310. The values here reflect commonly
accepted normal values by physiology teachers in the Philippines.
Movement is from high-concentration to low-concentration. Dr. Banzuela
Dr. Banzuela
• *ECF and ICF are Isoosmotic relative to each other!
Transport of D- and L-glucose proceeds at the same rate down an
electrochemical gradient by which of the following processes?
• Substance with an osmolarity/osmolality of zero: Water
(A) Simple diffusion • Movement of water across a semipermeable membrane from a
(B) Facilitated diffusion solution with low solute concentration to a solution with high
(C) Primary active transport solute concentration
(D) Cotransport
Remember: water utilizes OSMOSIS and not simple diffusion. Water will
(E) Countertransport 1-18 Costanzo LS. BRS Physiology. 7 ed. 2019. th
move according to CONCENTRATION GRADIENT (concentration
Glucose is supposed to be transported via carrier-mediated differences between two compartments) and not according to volume
means. Dapat may stereospecificity, so normally hindi same rate differences between two compartments. Water will move from LOW
and transport ng D-glucose at L-glucose. Pag same lang rate of CONCENTRATION (“dilute” compartment) to HIGH-CONCENTRATION
transport ng D-glucose and L-glucose, ibig sabihin hindi siya (“concentrated” compartment). Do not confuse water movement (osmosis)
carrier-mediated – simple diffusion na siya. Ingat, this is a tricky with solute movement using simple diffusion.
question since the transport of D-glucose and L-glucose is not Dr. Banzuela
through simple diffusion in real life. • Driving Force: Osmotic Pressure

Dr. Banzuela o Osmotic Pressure computed using van’t Hoff’s Law
Which of the following would occur as a result of the inhibition of Na+,K+-
ATPase?
(A) Decreased intracellular Na+ concentration
(B) Increased intracellular K+ concentration
(C) Increased intracellular Ca2+ concentration
(D) Increased Na+–glucose cotransport
(E) Increased Na+–Ca2+ exchange 1-23 Costanzo LS. BRS Physiology. 7 ed. 2019.th
If you inhibit the primary transport Na-K-ATPase pump, you will

prevent Na+-gradient in the ECF from occurring. This would then
prevent all secondary active transport processes including the
Na+-Ca2+ pump (a pump that causes Na+ influx and Ca2+ efflux).
Less calcium then goes out, leading to increased intracellular
calcium concentration. A drug that inhibits Na+-K+-ATPase
pump: think DIGOXIN.
Dr. Banzuela
Which of the following transport processes is involved if transport of
glucose from the intestinal lumen into a small intestinal cell is © Topnotch Medical Board Prep
inhibited by abolishing the usual Na+ gradient across the cell 𝝅 = 𝒈 × 𝑪 × 𝑹𝑻

membrane? where:
(A) Simple diffusion π = Osmotic pressure (atm or mm Hg)
(B) Facilitated diffusion g = Number of particles per mole in solution (Osm/mol)
(C) Primary active transport
C = Concentration (mmol/L)
(D) Cotransport
(E) Countertransport 1-25 Costanzo LS. BRS Physiology. 7 ed. 2019. th
R = Gas constant (0.082 L − atm/mol − K)
T = Absolute temperature (K)
SGLT-1 is used to transport glucose from S.I. lumen to S.I. cells. It
is a secondary active transport utilizing co-transport-symport.
Walang Secondary active transport sa choices, so best answer is
co-transport.
Dr. Banzuela
EFFECTIVE OSMOTIC PRESSURE ✔ GUIDE QUESTIONS
• Effective Osmotic Pressure = Osmotic Pressure x Reflection In a hospital error, a 60-year-old woman is infused with large volumes of
Coefficient a solution that causes lysis of her red blood cells (RBCs). The solution
• Same effective osmotic pressure: Isotonic was most likely:
• Higher effective osmotic pressure: Hypertonic (A) 150 mM NaCl
• Lower effective osmotic pressure: Hypotonic (B) 300 mM mannitol
(C) 350 mM mannitol
• Rule: water undergoes osmosis from hypotonic solution to (D) 300 mM urea
hypertonic solution (E) 150 mM CaCl2 1-9 Costanzo LS. BRS Physiology. 7 ed. 2019 th
• Osmotic pressure exerted by proteins: Oncotic Pressure or

A and B are isotonic compared to the RBC ICF (yung A, kaya
Colloid Osmotic Pressure 5hypoosmotic isotonic, remember na magseseparate yung Na and
Remember that proteins can exert osmotic pressure, it can attract water. Cl, kaya and actual effective osmotic pressure nyan ay 150 x 2 =
This is the basis for ONCOTIC pressure – something that you will read again 300. C and E are hypertonic (C is hypertonic dahil 150 x 3 naman).
and again in this handout. D is hypotonic – not because of the concentration na 300, but
Dr. Banzuela because ang RC niya is less than 1 (ineffective osmole siya, so ang
effective osmotic pressure niya is actually less than 300). Because
D is hypotonic, water will move from ECF to ICF causing cellular
RBC AND OSMOSIS swelling, and eventually, cellular rupture.
https://qrs.ly/8lcmq9k Dr. Banzuela
Solutions A and B are separated by a semi-permeable membrane.
Solution A contains 1 mM sucrose and 1 mM urea. Solution B contains
Refer to this audio file as you look at the picture below. 1 mM sucrose. The reflection coefficient for sucrose is one and the
Dr. Banzuela reflection coefficient for urea is zero. Which of the following
statements about these solutions is correct?
(A) Solution A has a higher effective osmotic pressure than solution B
(B) Solution A has a lower effective osmotic pressure than solution B
(C) Solutions A and B are isosmotic
(D) Solution A is hyperosmotic with respect to solution B, and the
solutions are isotonic
(E) Solution A is hypoosmotic with respect to solution B, and the
solutions are isotonic
Iba ang osmotic pressure sa effective osmotic pressure (see these

formulas in the previous discussion). Urea osmotic pressure is
1mM. Pero yung effective osmotic pressure niya is zero. So,
solution A is hyperosmotic but same lang ang tonicity sa solution
REFLECTION COEFFICIENT (OSMOTIC COEFFICIENT) B (since ang terms na “isotonic”, “hypertonic” and “hypotonic”
refer to effective osmotic pressure and not just osmotic pressure)
• Number between zero and one Dr. Banzuela
• Describes ease by which solute permeates a membrane Assuming complete dissociation of all solutes, which of the following
RC DESCRIPTION EXAMPLE NOTES solutions would be hyperosmotic to 1 mM NaCl?
• Effective (A) 1 mM glucose
(B) 1.5 mM glucose
• No solute Osmole
One • Albumin (C) 1 mM CaCl2
penetration (creates (D) 1 mM sucrose
Osm P) (E) 1 mM KCl From Physiology BRS, 6th Ed
Between
• Some solute • Most 1mM x 3 kasi ang C.
Zero and - Dr. Banzuela
penetration substances
One
• Ineffective 1.4 DIFFUSION POTENTIAL, RESTING MEMBRANE
• Complete
Osmole (No
Zero solute • Urea
osmotic
POTENTIAL, ACTION POTENTIAL
penetration ION CHANNELS
effect)
• Cell membrane integral proteins that permit passage of certain
ions
o Selective for specific ions
o Maybe open or closed
VOLTAGE-GATED LIGAND-GATED
CHANNELS CHANNELS
• Opened or closed
• Opened or closed by
by changes in
Mechanism hormones, 2nd
membrane
messengers, NTs
potential
• Activation vs. • Skeletal Muscle AChR
Inactivation gate (NM Receptor) that
Examples
of nerve Na+ opens gate for Na+ and
channel K+ when Ach binds
Don’t be afraid of the term “ligand”. Ligand means “messenger.” That
messenger can either be hormones or neurotransmitters.
Dr. Banzuela
DIFFUSION POTENTIAL AND EQUILIBRIUM POTENTIAL

REFLECTION COEFFICIENT (σ) • Diffusion Potential
© Topnotch Medical Board Prep o Potential difference generated across a membrane because of
Look at the pic above. Wag matakot sa RC. Think of RC as a formula: a concentration difference of an ion
RC = amount “returned”/amount “sent” • Equilibrium Potential (Nernst Potential)
Albumin has an RC of one – meaning if 8 molecules of Albumin try to o Diffusion potential that exactly balances (opposes) the tendency
penetrate the membrane, none will be able to do so. 8 “sent”, 8 “returned”.
RC = 8/8 = 1. Albumin has an RC of 1. It’s an effective osmole and attracts
for diffusion caused by concentration difference
water to where it is concentrated. o At electrochemical equilibrium, chemical and electrical driving
Urea has an RC of 0. If 8 molecules of urea try to penetrate the membrane, forces that act on an ion are equal and opposite; no net diffusion
8 molecules (all molecules) will penetrate. RC = 0/8 = 0. Urea has RC of occurs
zero. It’s an ineffective osmole and cannot easily attract water.
Dr. Banzuela
o Calculated by Nernst Equation: – remember the 3 characteristics – Stereotypical size and shape (meaning
if I graph it, I will get the same thing again and again), propagation
(kumakalat – pag nag AP ang isang cell, magkakaroon ng AP yung next
cell) and all-or-none (“on” or “off” state. It will be in the “on” state once
threshold is reached.
Dr. Banzuela
NERVE ACTION POTENTIAL
• Depolarization
o Opening of Na-Activation Gate (m gate) → Na inward current
• Repolarization
o Closure of Na-Inactivation Gate (h gate) → stop Na inward
current
o Equilibrium Potentials in Nerve and Muscle:
o Opening of K gates → K outward current
o ENa+ = +65mV, ECa2+ = +120mV, EK+ = -85mV, ECl- = -85mV
Depolarization – you make the cell more positive (you turn it “on”).
Repolarization – you make the cell more negative (you turn it “off”). Look
at the Na+-Channels and the K+-channels of an excitable cell like neurons
above. The Na channels has two gates similar to an anteroom/waiting
room. These two gates are the Na-activation and Na-inactivation gates.
At rest, the Na-activation gates (m gate) is closed, while the Na-
inactivation gates (h gate) is open. K-channels have just one gate.
When you have depolarization, the Na-activation gates open. And since Na
concentration is greater in the ECF compared to the ICF, Na influx will
occur, causing the cell to become more positive.
In repolarization, Na+-inactivation gates close (preventing Na+-influx) and
K gates open (causing positive charges to leave the cell, making the cell
more negative).
Dr. Banzuela

✔GUIDE QUESTION
Solutions A and B are separated by a semipermeable membrane that is
permeable to K+, but not to Cl–. Solution A is 100 mM KCl, and solution
B is 1 mM KCl. Which of the following statements about solution A and
solution B is true?
(A) K+ ions will diffuse from solution A to solution B until the [K+] of both
solutions is 50.5 mM
(B) K+ ions will diffuse from solution B to solution A until the [K+] of both
(C) KCl will diffuse from solution A to solution B until the [KCl] of both
(D) K+ will diffuse from solution A to solution B until a membrane
potential develops with solution A negative with respect to solution
B
(E) K+ will diffuse from solution A to solution B until a membrane
potential develops with solution A positive with respect to solution B
K+ is positively charged. It will move from Solution A to B (high

concentration to low concentration). Solution A will now become
negative compared to Solution B.
Dr. Banzuela
RESTING MEMBRANE POTENTIAL

• Exhibited by all cells
• By convention, refers to intracellular charge
• Established by diffusion potentials resulting from concentration
differences of various ions as each attempt to drive the
membrane potential towards its equilibrium potential
• Normal Nerve RMP: -70mV
o Caused by:
§ Nernst Potential for Na+ and K+
§ K+ Leak Channels
§ Na+-K+-ATPase Pump
o Closer to EK+ −85mV ENa+ +65mV
§ Nerve membrane more permeable to K+ than Na+ (high
resting conductance to K)
• Causes reduction of potassium leak out of the cells:
Hyperpolarizing the membrane potential
ACTION POTENTIAL
• Exhibited only by excitable cells (neurons, all muscle types)
• Consists of rapid depolarization/upstroke (“on”) followed by
repolarization (“off”)
• Characteristics of a True Action Potential:
1. Stereotypical size and shape: each normal AP for a given cell
type looks identical, depolarizes to the same potential and
repolarizes to the same RMP
2. Propagating: AP at one cell causes depolarization of adjacent
cells in a nondecremental manner
3. All-or-none: if threshold is reached, a full-sized AP will be
produced, otherwise, none at all
Remember: all cells have a Resting Membrane Potential. But only excitable
cells have an Action Potential. These excitable cells are neurons, skeletal
muscle, cardiac muscles, and smooth muscles. In terms of action potential
SPECIAL NOTES: ACTION POTENTIAL Remember: the thicker the nerve, the faster it is. The more myelinated the
TERM DESCRIPTION nerve, the faster it is. Myelin is an insulator, not a conductor, produced by
Schwann Cells (in the peripheral nervous system or PNS) and
Depolarization • Make the MP more positive Oligodendrocytes (in the central nervous system or CNS). AP is
Hyperpolarization • Make the MP more negative REGENERATED in each Node of Ranvier – this ensures that no matter how
• Positive charges flow into the cell far you are from the initial segment/axon hillock (where AP is first
Inward Current generated), the strength of the signal is maintained, since regenerated
causing depolarization
yung AP in each Node of Ranvier.
• Positive charges flow out of the cell
Outward Current Dr. Banzuela
causing hyperpolarization
• MP where AP is inevitable ✔GUIDE QUESTION
o net inward current > net The velocity of conduction of action potentials along a nerve will be
Threshold outward current increased by __________.
o Na+ inward current > K+ outward (A) stimulating the Na+–K+ pump
current from K leak channels (B) inhibiting the Na+–K+ pump
(C) decreasing the diameter of the nerve
• Occurs during an AP when
Overshoot (D) myelinating the nerve
MP > 0mV (E) lengthening the nerve fiber 1-16 Costanzo LS. BRS Physiology. 7 ed. 2019
th
Undershoot • Occurs during an AP when

(After-hyperpolarization) MP < RMP
1.5 NEUROMUSCULAR AND SYNAPTIC
• Occurs during an AP when no new
Absolute Refractory AP can be elicited no matter how TRANSMISSION
Period (ARP) large the stimulus SUPPORTING CELLS OF THE NERVOUS SYSTEM
• Basis: closed Na+-inactivation gates (NON-NEURONS)
• Occurs during an AP after ARP when CHARACTERISTICS CELL
a new AP can be elicited by required • A tissue macrophage that act as
Relative Refractory greater than usual Na+ inward scavenger cells, removing debris
Period (RRP) current resulting from injury, infection,
• Basis: prolonged opening of K+ and disease (e.g. multiple MICROGLIA
channels sclerosis, AIDS-related dementia,
• Occurs when cell membrane is Parkinson disease, & Alzheimer
depolarized but not rapidly enough, disease)
Accommodation thus causing Na-inactivation gates • Macroglia that forms myelin in OLIGODENDROCYTES
to eventually close → no AP the CNS and PNS respectively & SCHWANN CELLS
• e.g. Hyperkalemia • Macroglia that send processes
• non-propagated local potential that envelop synapses and the
ASTROCYTES
Electrotonic potential due to local change in ionic surface of nerve cells, and helps
conductance form the BBB
• local electrical charge in the • Astrocytes in the white matter FIBROUS ASTROCYTES
Generator potential / generator/sensitive region of the • Astrocytes in gray matter, with
Synaptic Potential receptor cell granular cytoplasm and produce
• graded potential substances that are tropic to
PROTOPLASMIC
• principal inputs signals to which a neurons to help maintain
ASTROCYTES
appropriate concentration of
neuron responds
Synaptic potentials ions and NTs by taking up K and
+
• conductance changes are triggered
the NTs Glutamate and GABA
by neurotransmitters
✔GUIDE QUESTIONS PARTS OF THE NEURON
During the upstroke of the nerve action potential
(A) there is net outward current and the cell interior becomes more
negative
(B) there is net outward current and the cell interior becomes less
negative
(C) there is net inward current and the cell interior becomes more
negative
(D) there is net inward current and the cell interior becomes less
negative 1-2 Costanzo LS. BRS Physiology. 7 ed. 2019 th
A newly developed local anesthetic blocks Na+ channels in nerves.

Which of the following effects on the action potential would it be
expected to produce?
(A) Decrease the rate of rise of the upstroke of the action
potential
(B) Shorten the absolute refractory period
(C) Abolish the hyperpolarizing afterpotential
(D) Increase the Na+ equilibrium potential
(E) Decrease the Na+ equilibrium potential
Lidocaine blocks neuronal voltage-gated sodium channels responsible for

PARTS OF A
action potential generation and propagation. It can also act on cardiac NEURON
muscles and cause arrhythmias. https://qrs.ly/59cmq9s
Dr. Banzuela
Refer to this audio file as
you look at this picture.
PROPAGATION OF ACTION POTENTIAL Dr. Banzuela
• Done through local currents to adjacent areas of the membrane

• Conduction velocity is increased by:
o Fiber Size: the larger the nerve fiber, the smaller the internal
resistance, and the faster the conduction velocity
o Conduction velocity is most dependent on: nerve diameter
o Myelination: myelin acts as insulator. AP is regenerated in
Nodes of Ranvier (unmyelinated portions of the axon) that
contains the highest concentration of Na+ channels per
square micrometer of cell membrane
• Conduction Velocity = Distance/Latent Period
• Dendrites: where NT receptors are found SYNAPTIC TRANSMISSION
• Cell Body (Soma): where organelles, nucleus is seen PHENOMENON CAUSED BY
Speaking of nucleus – the nucleus of the cell is the one that controls and • Endplate Potential (in
• Increase in Na+ Conductance
regulates cellular activities since it is the one that carries the genes that is skeletal muscle motor
(Na+ Influx)
used in the production of cellular proteins like enzymes. endplate)
Dr. Banzuela
• Can be caused by opening of Cl-
• Initial Segment: where AP starts • Fast Inhibitory Post-
Channels (Cl- Influx), opening of K+
• Axon: transmitting portion Synaptic Potential
channels (K+ efflux), or closure of
• Nodes of Ranvier: unmyelinated portion of the axon (IPSP)
Na+ or Ca2+ channels
• Neural Fibril: branches of the axon • Fast Excitatory Post- • Increase in Na+ Conductance
Synaptic Potential (Na+ Influx) or Ca2+ Conductance
(Fast EPSP) (Ca2+ influx)
• Slow Excitatory Post-
• Decrease in K+ Conductance
Synaptic Potential
(Slow K+ efflux)
(Slow EPSP)
• Presynaptic • Opening of voltage-gated K+
Inhibition channels (K+ Efflux)
Adapted from 6-1, 6-7, 6-8. Barrett et al. Ganong’s Review of Medical Physiology. 26th ed. 2019
✔GUIDE QUESTION
An inhibitory postsynaptic potential:
(A) depolarizes the postsynaptic membrane by opening Na+ channels
(B) depolarizes the postsynaptic membrane by opening K+ channels
(C) hyperpolarizes the postsynaptic membrane by opening Ca2+
channels
(D) hyperpolarizes the postsynaptic membrane by opening
Cl- channels 1-22 Costanzo LS. BRS Physiology. 7 ed. 2019 th
Remember – you can inhibit an AP several ways – cause influx, Cl-

or cause K+ efflux or inhibit Na+ influx/Ca2+ influx. All of these will
© Topnotch Medical Board Prep make the cell more negative/less positive.
Dr. Banzuela
• Terminal Boutons (End-Feet): distal tips of the axon
• Voltage-Gated Calcium Channels (VGCC): stimulated by AP; NEUROTRANSMITTERS (NTS)
triggers release of NT into the synapse • For communication between neurons
o LAMBERT-EATON MYASTHENIC SYNDROME: autoimmune • Maybe excitatory or inhibitory or both
disease marked by auto-antibodies against these voltage-gated • Categories:
calcium channels → prevents Acetylcholine from being released o Small-Molecule NTs
to the neuromuscular junction § Monoamines: e.g. Ach, Serotonin, Histamine
• Synapse: space between neurons § Catecholamines: Dopamine, NE, Epi
• NTs: either excitatory (depolarizes) or inhibitory § Amino Acids: Glutamate, GABA, Glycine
(hyperpolarizes); binds to post-synaptic receptors o Large-Molecule NTs
§ Neuropeptides including substance P, enkephalin,
CLINICAL CORRELATES MULTIPLE SCLEROSIS vasopressin, and a host of others
• Multiple Sclerosis: autoimmune disease directed against the
NEUROTRANSMITTERS
components of the myelin sheath
o Brain MRI and CSF analysis (presence of oligoclonal CHARACTERISTICS NEUROTRANSMITTER
bands): used to diagnose MS • Maybe excitatory or inhibitory
• Associated with HLA-DR2 • Found in the NMJ, Sympa and Para
• Clinical Presentation: Distinct episodes of neurologic Preganglionic neurons, Para and
deficits that are separated in time, and are attributable to some Sympa Post-ganglionic
patchy white matter lesions that are separate in space neurons, basal ganglia, large
pyramidal cells of the motor cortex,
• Paraparesis (weakness in LE), paresthesia, optic neuritis
gigantocellular neurons of the REA
(blurred vision, change in color perception, central scotoma,
pain in eye movements) • Created by: Choline Acetyl-
ACETYLCHOLINE
• Relapsing-Remitting MS: transient episodes lasting weeks or transferase from Acetyl CoA and
Choline
months that recur
• Degraded by: Acetylcholinesterase
• Primary-Progressive MS: no periods of remission
4-8. Barrett et al. Ganong’s Review of Medical Physiology. 26th ed. 2019 into Acetate and Choline (½ of which
will undergo reuptake)
SYNAPTIC TRANSMISSION • Triggers REM sleep;
• Synaptic Transmission is Orthodromic (Synapse to Axon) rather • decreased levels in Huntington’s
than Antidromic (Axon to Synapse) dementia and Alzheimer’s dementia
• One-to-one synapses: one neuron, one post-synaptic element • Found in the locus coeruleus of pons,
(e.g. NMJ) • NeuroMODULATOR in the CNS and
• Many-to-one synapses: Many neurons, one post-synaptic NeuroTRANSMITTER in the PNS
element (e.g. spinal motor neurons) • synthesized INSIDE synaptic vesicles
• Excitatory Post-Synaptic Potentials (EPSPs): depolarizes • HALF-LIFE: 2 MINUTES (short
NOREPINEPHRINE
postsynaptic cell, brings it closer to threshold compared to renin, aldosterone,
o e.g. due to Na+ influx corticosterone, and DHEA)
• Inhibitory Post-Synaptic Potentials (IPSPs): hyperpolarizes • Primary NT from post-ganglionic
postsynaptic cells sympa neurons;
o e.g. due to Cl- influx • For arousal/ wakefulness
• Spatial Summation: 2 or more excitatory inputs at the same time • Secreted mainly by the adrenal
(A + B + C) medulla
• Temporal summation: 2 or more excitatory inputs at rapid • greater Beta-2 action than NE
EPINEPHRINE
succession (A…A…A…) • Relieve effects of bee sting by
• Facilitation / Augmentation / Postetanic Stimulation: brings decreasing contraction of airway
cell closer to threshold smooth muscles
CHARACTERISTICS NEUROTRANSMITTER ✔GUIDE QUESTION
• Secreted in the substantia nigra Degeneration of dopaminergic neurons has been implicated in:
(fine-tunes movement) (A) Schizophrenia (C) Myasthenia gravis
(B) Parkinson disease (D) Curare poisoning
• Also secreted by the hypothalamus
(PIF or PIH) to inhibit prolactin;
• D1 Receptor: activates adenylate CHARACTERISTICS NEUROTRANSMITTER
cyclase using Gs protein; D2: inhibits Spinal cord main inhibitory NT;
GLYCINE
adenylate cyclase using Gi protein; DOPAMINE • increases Cl influx
• ↓ in Parkinson Disease, ↑ D2 in • Brain main inhibitory NT (e.g.
Schizophrenia spiny neurons of the striatum,
o Schizophrenia: can be due to Purkinje Cells of the cerebellum);
abnormalities in the prefrontal • increases Cl- influx (GABAA) or K+
lobes, frontal lobes and limbic Efflux (GABAB)
system (hippocampus) • decreases anxiety: GABAA
GABA
• Found in the median raphe of the • GABA Receptors in the Retina
brain stem, from tryptophan, o GABA A: ionotropic; ubiquitous
converted to melatonin; SEROTONIN o GABA B: metabotropic
• low levels association with o GABA C: ionotropic; enriched in
depression the retina compared to other
• NO synthase converts Arginine to parts of the CNS
citrulline and NO; Brain main excitatory NT;
NITRIC OXIDE • formed from reactive amination of
• Permeant gas, inhibitory NT,
vasodilator Alpha-ketoglutarate
• 3 Receptor subtypes Ionotropic
Let me reiterate important points about the neurotransmitter table above: GLUTAMATE
Ach is found in a variety of areas. It is unique among neurotransmitters in (ligand-gated) including NMDA
that it is degraded before “reuptake” (process of recovering the receptors;
neurotransmitter by the releasing neuron) takes place. Usually, reuptake • 1 subtype metabotropic
muna before degradation nangyayari. • Activates NMDA receptors
For NE – remember that is the main secretion of post-ganglionic • Inhibits neurons in the brain
sympathetic neurons (compared to the adrenal medulla which secretes
involved in pain perception (e.g.
mainly EPI and not NE).
Epi has greater Beta-2 effect than NE, kaya siya ginagamit for asthma at enkephalin, endorphins, OPIOID PEPTIDE
hindi NE. dynorphins; does NOT include
Dopamine – remember na iba yung substantia nigra dopamine morphine which is exogenous)
(modulates movement) at yung hypothalamic dopamine (inhibits • Involved in Fast Pain and Slow GLUTAMATE &
prolactin). Pain SUBSTANCE P
Serotonin is the “happy hormone” – pag mababa siya, it’s associated with
depression (serotonin rich food: chocolate! J).
Nitric Oxide – remember its formula is NO and not N2O. N2O is nitrous
oxide or laughing gas. NO is an INHIBITORY NT and a VASODILATOR. NEUROTRANSMITTERS
Again, NO is an INHIBITORY NT and a VASODILATOR – do not forget these https://qrs.ly/86cmqas
please.
Dr. Banzuela
Refer to this audio file for a summary of the table above along with some
mnemonics
Dr. Banzuela
MNEMONICS: NEUROTRANSMITTERS
“Ilocus Norte” ”Pare True Love Does Not Exist To Me” “Trip Mo Sya Noh?”
locus coeruleus, NE Phenylalanine Derivatives Tryptophan Derivatives: melatonin, serotonin, niacin
✔GUIDE QUESTION NEUROTRANSMITTER RECEPTORS

Metabotropic Receptors
Which of the following is an inhibitory neurotransmitter in the central
nervous system (CNS)? o G-protein Coupled Receptors (GPCR) that utilizes second
(A) Norepinephrine messengers like IP3/DAG or cAMP
(B) Glutamate o e.g. GABAB receptor, Neurokinin receptor, Opioid Receptors
(C) g -Aminobutyric acid (GABA)
(D) Serotonin
Ionotropic Receptors
(E) Histamine o Ion-channel linked-receptors that utilizes ligand-gated ion
From BRS Physiology, 6th Ed
channels
o e.g. GABAA Receptor (Cl-), Nicotinic Receptor (Na+, K+), NMDA
Receptor (Ca2+), Glycine Receptor (Cl-), ANP receptor, 5HT3
receptor
OPIOID PEPTIDE RECEPTORS TYPES OF MUSCLES
• Come in 3 types: Skeletal Muscles
o Kappa: analgesia, diuresis, sedation, meiosis, dysphoria o Intrafusal: detects changes in Muscle Length (innervation:
o Mu: site of action of morphine, causes analgesia, respiratory gamma-motorneurons)
depression, constipation, euphoria, sedation, meiosis, increased o Extrafusal: for voluntary muscle contraction (innervation:
GH and prolactin alpha-motorneurons), has 2 types:
o Delta: analgesia PARAMETER TYPE I TYPE II
• Affinity of opioid peptides shown below: Contraction
o Mu: Endorphins > Enkephalins > Dynorphin Slow Fast
velocity
o Kappa: Enk > End and Dy Fiber color Red White
o Delta: Dyn > End and Enk Oxidative
This is based on Ganong 25th ed → iba yung nakasulat sa Ganong 23rd ed. Predominant phosphorylation → Anaerobic
Iba rin nakasulat sa Katzung Pharma. metabolism sustained glycolysis
Dr. Banzuela
contraction
FUNCTION OF MUSCLES Mitochondria,
↑ ↓
1. Mobility, Stability & Posture myoglobin
2. Circulation (e.g., pumping action of blood by cardiac muscles, Type of Weight/resistance
maintenance of BP by smooth muscles in the vessels) Endurance training
training training, Sprinting
3. Respiration (e.g., via diaphragm)
Think of “1 slow, red ox with a perfect posture.” Type I fibers are slow,
4. Digestion red fibers using oxidative phosphorylation to allow sustained contraction
5. Urination in endurance training. Postural muscles of the back have greater
6. Childbirth percentage of Type I fiber since they require endurance more than power.
7. Vision (e.g. intraocular and extraocular muscles) Dr. Rubio & Dr. Banzuela
8. Organ protection (e.g. anterior abdominal wall muscles) Cardiac Muscles

9. Temperature regulation (85% of body heat comes from o Atrial muscle: (+) gap junctions, (+) syncytium
contracting muscles) o Ventricular muscle: (+) gap junctions, (+) syncytium
o Pacemakers (e.g., SA Node): (+) autorhythmicity
Largest Muscle: Gluteus Maximus. Strongest muscle by weight: Smooth Muscle
masseter in the jaw. o Unitary smooth muscle: (+) gap junctions, (+) syncytium, for
Dr. Banzuela
gross motor movements
o Multi-unit smooth muscle: (-) gap junctions, for fine motor
1.6 SKELETAL MUSCLES movements
MUSCLE TYPES SARCOMERE

• Functional and structural unit of a muscle of skeletal and cardiac
https://qrs.ly/n5cmr18
muscles
• Area between two Z lines
Watch this video on the various muscle types as you read the next portion. “Nooks and crannies.” Remember that sarcomere is the contractile unit of
Dr. Banzuela BOTH skeletal and cardiac muscle.
Dr. Banzuela
THICK FILAMENTS THIN FILAMENTS

• Thin Filament: contains actin, tropomyosin, troponin
• Thick Filament: contains myosin that act as cross-bridges of the • Tropomyosin: “relaxing protein” that covers actin binding sites at
sarcomeres rest
o 1 pair of heavy chains, two pairs of light chains • Troponin has 3 subunits: Troponin T, Troponin I, Troponin C
o 2 heads, 1 tail • Troponin T: attaches troponin complex to tropomyosin
• Troponin I: inhibits actin-myosin binding
• Troponin C: calcium binding protein
Troponin T-I-C.
T for tropomyosin (Troponin T is found in tropomyosin)
I for inhibition (Troponin I inhibits actin-myosin interaction)
C for calcium (Troponin C is the one that binds with calcium)
Dr. Banzuela
• Z lines (“Zwischenscheibe”): borders

• M line (“Mittelscheibe”): midline
• A Band (” Anisotropic”): entire length of
myosin
• H Band (”Heller”): inside A band; purely
myosin, no actin interspersed
• Bare Zone: inside H band; no myosin
heads
• I band (“Isotropic): purely actin, no
myosin interspersed
The H-band is the area inside the A-band without
actin filaments. The area in the H-band
containing pure myosin (no myosin heads) is the
© Topnotch Medical Board Prep bare zone.
Dr. Banzuela
• T-Tubules: invaginations of the
sarcolemma; spreads the action potential
to all parts of the muscles; contains DHPR
• DHPR: voltage-sensitive, activates
Ryanodine Receptors
• Sarcoplasmic Reticulum (SR): contains
Ca2+ needed for muscle contraction
• Ryanodine: Ca2+-release channel in the SR
activated by DHPR
• Calsequestrin: protein that stores Ca2+ in
the SR
• SERCA: pumps Ca2+ from ICF to the SR
• Titin: binds myosin to Z lines, binds Z lines
to M line (determines normal stiffness of
© Topnotch Medical Board Prep the ventricular muscle)
Titin mutations are associated with tibial muscular dystrophy, hypertrophic cardiomyopathy, familial dilated cardiomyopathy, limb-girdle muscular dystrophy
type 2J, centronuclear myopathy, core myopathy with heart disease and fatal cardiomyopathy.
These mutations can cause premature stop codons and other defects.
In scleroderma, autoantibodies to titin are also produced.
Dr. Banzuela
• Dystrophin: stabilizes sarcolemma and prevents contraction-

induced rupture (binds actin to beta-dystroglycan in the
sarcolemma)
• Actinin, CapZ Protein: binds Actin to Z lines
• Desmin: binds Z lines to sarcolemma
• Nebulin: acts as molecular rulers that sets the length of actin
MUSCLE CONTRACTION
https://qrs.ly/3lcmr19
Watch this video on skeletal muscle contraction first, then read the
complete steps listed below.
Dr. Banzuela
STEPS IN MUSCLE CONTRACTION
1. Action Potential starts at the initial segment of the motor
neuron, spreads through the axon, neural fibril and then the
terminal boutons.
2. At the terminal boutons, voltage-gated Ca2+ channels are
activated. Vesicles containing Ach fuses with the nerve © Topnotch Medical Board Prep
membrane and release Ach in the NMJ.
3. Ach binds with the Ach Receptors (NM Receptors) at the Muscle
End Plate (MEP). This NM Receptors are ligand-gated ion
channels. Once they’re activated, they will open Na+ and K+
channels.
4. The open Na+ channels causes Na+ influx and produces a
Miniature End Plate Potential (MEPP). MEPP summate to
produce EPP. This depolarizes the sarcolemma.
5. Depolarization spreads from sarcolemma to T-Tubules. At the
T-Tubules, DHPR is activated.
6. Once DHPR is activated, Ryanodine Receptors in the SR are also
activated.
7. Ryanodine Receptors then release Ca2+ from the SR to the ICF.
Ca2+ binds with Troponin C.
8. Binding of Trop C with Ca2+ displaces Tropomyosin. This
tropomyosin displacement causes exposure of binding sites in
actin for myosin. © Topnotch Medical Board Prep
9. Myosin heads binds to First Binding Site in Actin. ✔GUIDE QUESTIONS

10. ATP binds to myosin head. This causes myosin to unbind with The correct temporal sequence for events at the neuromuscular junction
the First Binding Site in actin. is:
11. ATP bound to myosin head undergoes partial hydrolysis, (A) action potential in the motor nerve; depolarization of the muscle
end plate; uptake of Ca2+ into the presynaptic nerve terminal
producing ADP. This causes “recocking” of the myosin heads. (B) uptake of Ca2+ into the presynaptic terminal; release of
Myosin moves such that it now points to the Second Binding Site acetylcholine (ACh); depolarization of the muscle end plate
in Actin and it moves closer to the (+) pole. (C) release of ACh; action potential in the motor nerve; action potential
12. Myosin binds to Second Binding Site in actin. in the muscle
13. ADP bound to myosin undergoes complete hydrolysis. This (D) uptake of Ca2+ into the motor end plate; action potential in the
causes the “power / force-generating stroke” to occur. Myosin motor end plate; action potential in the muscle
heads pull actin towards the M line or the (-) pole. A cross- (E) release of ACh; action potential in the muscle end plate; action
bridge cycle happens. This shortens the sarcomere by 10Nm. potential in the muscle 1-4 Costanzo LS. BRS Physiology. 7 ed. 2019
th
At the muscle end plate, acetylcholine (ACh) causes the opening of:
14. Do this again and again to have significant muscle contraction.
(A) Na+ channels and depolarization toward the Na+ equilibrium
potential
STEPS IN MUSCLE RELAXATION (B) K+ channels and depolarization toward the K+ equilibrium
1. Remove the Ca2+ from Troponin C. potential
2. Tropomyosin the goes back to its original location, covering the (C) Ca2+ channels and depolarization toward the Ca2+ equilibrium
binding site of actin for myosin. potential
3. Place the Ca2+ back to the SR using SERCA. (D) Na+ and K+ channels and depolarization to a value halfway
4. Use Acetylcholinesterase to degrade ACh to Acetate and Choline. between the Na+ and K+ equilibrium potentials
(E) Na+ and K+ channels and hyperpolarization to a value halfway
5. Choline may undergo reuptake.
between the Na+ and K+ equilibrium potentials
Which of the following temporal sequences is correct for excitation– • Preload: muscle length
contraction coupling in skeletal muscle? • Afterload: load against which the muscle contracts
(A)Increased intracellular [Ca2+]; action potential in the muscle o Velocity of muscle shortening decreases as afterload increases
membrane; cross-bridge formation
(B) Action potential in the muscle membrane; depolarization of the
• Passive Tension: tension due to muscle stretch
T tubules; release of Ca2+ from the sarcoplasmic reticulum (SR) • Active Tension: tension due to muscle contraction; proportional
(C)Action potential in the muscle membrane; splitting of adenosine to number of cross-bridge cycles formed
triphosphate (ATP); binding of Ca2+ to troponin C • Rigor Mortis: usually occurs 3-6 hours after death due to lack of
(D)Release of Ca2+ from the sarcoplasmic reticulum (SR); ATP
depolarization of the T tubules; Action potential in the muscle • Tetanus / Tetanic Spasm: happens when all Ca2+ from the SR has
membrane 1-24 Costanzo LS. BRS Physiology. 7 ed. 2019
been released; no further increase in muscle strength
th
In skeletal muscle, which of the following events occurs before

depolarization of the T Tubules in the mechanism of excitation– ✔GUIDE QUESTIONS
contraction coupling? Which of the following causes rigor in skeletal muscle?
(A) Depolarization of the sarcolemmal membrane. (A) No action potentials in motoneurons
(B) Opening of Ca2+ release channels on the sarcoplasmic reticulum (B) An increase in intracellular Ca2+ level
(SR) (C) A decrease in intracellular Ca2+ level
(C) Uptake of Ca2+ into the SR by Ca2+-adenosine triphosphatase (D) An increase in adenosine triphosphate (ATP) level
(ATPase) (E) A decrease in ATP level 1-29 Costanzo LS. BRS Physiology. 7th ed. 2019
(D) Binding of Ca2+ to troponin C
“Rigor” here refers to rigor mortis. When you die → calcium
(E) Binding of actin and myosin 1-26 Costanzo LS. BRS Physiology. 7 ed. 2019 th
enters cells → calcium binds to trop C → binding of myosin head
The steps in muscle contraction and relaxation are not just important to actin occurs. Since there is no more ATP produced when you
medically, they are also board-relevant. Review them again, and if you have die, no more unbinding of myosin from actin. This will cause
problems understanding or memorizing them, message me on Viber. muscle rigidity – this will cause rigor mortis. Rigor mortis
Dr. Banzuela happens around 3-6 hours after death. It will eventually end when
DRUGS THAT AFFECT THE NMJ proteolysis (another one of the changes in death) occurs.
DESCRIPTION ANSWER Dr. Banzuela
Blocks release of Ach from Repeated stimulation of a skeletal muscle fiber causes a sustained
BOTULINUM TOXIN contraction (tetanus). Accumulation of which solute in intracellular fluid
pre-synaptic terminals
is responsible for the tetanus?
Competes with Ach for (A) Na+ (D) Mg2+
CURARE
receptors on Motor End Plate (B) K+ (E) Ca2+
Inhibits Acetylcholinesterase NEOSTIGMINE (C) Cl– 1-6 Costanzo LS. BRS Physiology. 7 ed. 2019
th
Blocks reuptake of Choline

HEMICHOLINIUM
into presynaptic Terminal 1.7 CARDIAC MUSCLES
• Mechanism behind botulinum type A (Botox) smoothing out CARDIAC MUSCLE
glabellar lines: Block the release of synaptic transmitter from • Skeletal Muscle: relies purely on intracellular Ca2+ (SR Ca2+)
alpha motoneurons (specifically acetylcholine) • Smooth Muscle: relies mainly on extracellular Ca2+ (ECF Ca2+)
✔GUIDE QUESTION • Cardiac Muscle: relies on both intracellular and extracellular Ca2+
A 42-year-old man with myasthenia gravis notes increased muscle • “Calcium-Induced Calcium-Release” system
strength when he is treated with an acetylcholinesterase (AChE) o seen in smooth and cardiac muscles
inhibitor. The basis for his improvement is increased
(A) amount of acetylcholine (ACh) released from motor nerves
(B) levels of ACh at the muscle end plates
CARDIAC
(C) number of ACh receptors on the muscle end plates ACTION POTENTIAL
(D) amount of norepinephrine released from motor nerves https://qrs.ly/rhcmr1l
(E) synthesis of norepinephrine in motor nerves
Neostigmine is part of the treatment for MG. By inhibiting AChase, Watch this video and refer to the graphs on Cardiac and SA Node Action
ACh levels will increase, decreasing muscle weakness. Potential on the next page,
Dr. Banzuela
Dr. Banzuela
CARDIAC ACTION POTENTIAL
ISOTONIC VS ISOMETRIC CONTRACTION • Phase 0: Due to Na+ influx
• Isometric Contraction • Phase 1: Brief period of repolarization
o Length is held constant while muscle contracts Due to K+ efflux and decrease in Na+ influx
§ Force generated is not enough to move or lift an object • Phase 2: Plateau of AP
o No muscle shortening/lengthening Due to Ca2+ influx
o e.g. pushing against the wall • Phase 3: Repolarization
• Isotonic Contraction Decrease Ca2+ influx and increased K+ efflux
o Load is held constant while muscle contracts • Phase 4: Resting membrane potential
o With muscle shortening: concentric contraction
(e.g. pulling a weight up)
o With muscle lengthening: eccentric contraction
(e.g. lowering a weight down)
Iso means “same.” iso-METRIC (length) means “same length”. Iso-TONIC
(tone of muscle) means “same tone”. Isometric contraction is muscle
contraction with same muscle length – no shortening/lengthening.
Isotonic contraction means same muscle tone – there is change in muscle
length, but due to a constant load on the muscle, same muscle tone.
Isometric contraction – think of pushing against an immovable wall –
there’s muscle contraction but no change in muscle length. Isotonic
contraction – think of holding objects in midair – there’s a constant load on
the muscle causing a constant tone.
Dr. Banzuela
SPECIAL NOTES ON MUSCLE CONTRACTION
• In Skeletal Muscle Contraction:
o More tension produced in isometric contractions than isotonic © Topnotch Medical Board Prep
contractions CALCIUM REGULATION OF CARDIAC MUSCLES

o More work (force x distance) produced in isotonic • Increases Intracellular Calcium
contractions than isometric contractions o L-Type or Slow-Calcium channel: major & voltage-gated
o Muscle Fiber has no refractory period: repeated stimulation o T-Type or Fast-Calcium channel
before relaxation can result in incomplete or complete tetany • Decreases Intracellular Calcium
o Muscle contraction starts BEFORE action potential is over and o 3Na+-1Ca2+ Countertransport
last LONGER than the action potential o Ca2+-ATPase pump
1.8 SMOOTH MUSCLES

SMOOTH MUSCLE
• No Troponin
• Contains
o Myosin-Light Chain Kinase (MLCK): phosphorylates and
activates myosin heads
o Myosin-Light Chain Phosphatase (MLCP): dephosphorylates
and inactivates myosin heads
o Calmodulin: binds with Ca
o Caldesmon and Calponin: inhibits muscle contraction
o Dense Bodies: analogous to Z lines
o Rudimentary SR
o Rudimentary T-Tubules (Caveoli)
• Main difference in contraction of smooth muscles vs. skeletal
muscles: role of Ca2+ in initiating contraction
To emphasize: MLCK causes smooth muscle CONTRACTION. MLCP causes
REFRACTORY
DESCRIPTION smooth muscle RELAXATION. Calmodulin is analogous to Troponin C – it
PERIODS binds with calcium. Caldesmon is analogous to Troponin I – it inhibits
• Begins at the upstroke of the action actin-myosin interaction.
Absolute Refractory
potential and ends after the plateau Dr. Banzuela
Period (ARP)
No action potential can be INITIATED
• Longer than ARP TYPES OF SMOOTH MUSCLES
SINGLE-UNIT /
• Conducted action potential cannot
Effective Refractory MULTI-UNIT SMOOTH MUSCLE
UNITARY SMOOTH MUSCLE /
be elicited SYNCYTIAL SMOOTH MUSCLE /
Period (ERP)
• No action potential can be VISCERAL SMOOTH MUSCLE
PROPAGATED • One nerve, multiple muscle • One nerve, multiple muscle
• Occurs after ARP fibers that may act on fibers that are act together as
Relative Refractory • Action potential is possible but will their own one
Period (RRP) require more than usual inward • Mainly controlled by nerve
current • Controlled mainly by nerve signals (ACh, NE) & non-
signals (ACh, NE) nerve signals (hormones,
SA NODE ACTION POTENTIAL stretch, local factors)
• SA Node and AV node have prominent pacemaker or • (-) Gap junctions • (+) Gap junctions
prepotentials • No true AP (no
o SA Node has a slowly depolarizing prepotential due to slow Na • Slow waves, spike potentials
propagation!);
influx and plateau potentials
• Junctional potential only
• Phase 4: slow Na+ Influx towards threshold • (-) Spontaneous • May exhibit spontaneous
• Phase 0: Ca++ Influx (depolarization) contractions contractions
• Phase 3: K+ Efflux (repolarization) • E.g., Ciliary eye muscle,
• E.g., Intestines, bile ducts,
iris, piloerector muscle,
ureters, uterus
vas deferens
Multi-Unit Smooth muscle is for FINE MOTOR CONTROL. Unitary Smooth
muscle is for GROSS/COARSE MOTOR CONTROL. Ang uterus, unitary
smooth muscles yan → gross motor control ang kailangan kasi. Ang
smooth muscles naman controlling pupillary size, multi-unit smooth
muscles yan → fine motor control ang kailangan kasi.
Dr. Banzuela
✔ GUIDE QUESTIONS
Which of the following is the result of an inward Na+ current?
(A) Upstroke of the action potential in the sinoatrial (SA) node
(B) Upstroke of the action potential in Purkinje fibers
(C) Plateau of the action potential in ventricular muscle
(D) Repolarization of the action potential in ventricular muscle
(E) Repolarization of the action potential in the SA node
3-29. Costanzo LS. BRS Physiology. 7th ed. 2019.
In the sinoatrial (SA) node, phase 4 depolarization (pacemaker

potential) is attributable to
(A) an increase in K+ conductance
(B) an increase in Na+ conductance STEPS IN SMOOTH MUSCLE CONTRACTION & RELAXATION
(C) a decrease in Cl− conductance 1. Hormones, NTs, stretch triggers increased ICF Ca
(D) a decrease in Ca2+ conductance 2. ICF Ca binds with Calmodulin
(E) simultaneous increases in K+ and Cl− conductance 3. Calcium-Calmodulin Complex activates MLCK
4. MLCK phosphorylates (and activates) Myosin Heads
Remember: the slope of phase 4 in the SA Node Action Potential is the one 5. Activated Myosin Heads: causes smooth muscle contraction
that determines heart rate. Sympathetic and Parasympathetic NS may
6. MLCP dephosphorylates (and inactivates) Myosin Heads
affect this slope.
Dr. Banzuela 7. Inactivated Myosin Heads: causes smooth muscle relaxation
• Responsible for relaxation of contracted smooth muscles and
formation of latch bridges: Dephosphorylation of actomyosin
1.9 COMPARISON OF SKELETAL MUSCLES, SMOOTH MUSCLES AND CARDIAC MUSCLES

SKELETAL CARDIAC SMOOTH MUSCLE
Sarcomeres,
(+) (+) (-)
striations, troponin
Mitochondria 3-8% of skeletal muscle volume 35% of cardiac muscle volume 3-5% of smooth muscle cell volume
• Ca2+ Influx (SA Node);
Upstroke of AP Na+ Influx • Na+ Influx (atria, ventricles, Ca2+ Influx
Purkinje Fibers)
• No (SA Node)
Plateau No • Yes (atria, ventricles, Purkinje No
Fibers)
• 150 msec (SA Node, Atria)
AP Duration 1 msec • 250-300 sec (ventricles, Purkinje 10 msec
Fibers)
• AP opens cell membrane voltage-
Excitation-
gated Ca2+ channels;
Contraction Use of SR Calcium Ca2+-induced Ca2+-Release
• Hormones & NTs open IP3-gated
Coupling
SR Ca2+ Channels
Gap Junctions (-) (+) (+) only for unitary smooth muscles
SR Greatest --- Least
Regulation Actin-Based using Tropomyosin Actin-Based using Tropomyosin Myosin-Based using MLCK
Among the types of muscles, cardiac muscles have the greatest number of mitochondria due to the heart’s energy requirements. Take note that 90% of the heart’s
ATP requirements is met by cardiac mitochondria through beta-oxidation of fats at rest.
Dr. Banzuela
✔GUIDE QUESTIONS NERVOUS SYSTEM

Which characteristic or component is shared by skeletal muscle and • Somatic Nervous System: voluntary, 1-motor neuron system
smooth muscle? • Autonomic Nervous System (ANS): involuntary, 2-motor neuron
(A) Thick and thin filaments arranged in sarcomeres system
(B) Troponin
(C) Elevation of intracellular [Ca2+] for excitation–contraction
o Sympathetic Nervous System:” Fight or Flight”; capable of
coupling mass discharge
(D) Spontaneous depolarization of the membrane potential o Parasympathetic Nervous System:” Rest and Digest”
(E) High degree of electrical coupling between cells • Enteric Nervous System: involuntary, subject to ANS control BUT
can function independently of the ANS
Remember this personal mnemonic of mine: Calcium is to muscle o Also called the “second brain” since it utilizes neurons and
what spinach is to Popeye. It provides you with power, the neurotransmitters similar to the central nervous system
stimulus for contraction. o Submucosal Plexus: for secretions
Dr. Banzuela
In contraction of gastrointestinal smooth muscle, which of the following o Myenteric Plexus: for motility
events occurs after binding of Ca2+ to calmodulin?
(A) Depolarization of the sarcolemmal membrane AUTONOMIC NERVOUS SYSTEM (ANS)
(B) Ca2+-induced Ca2+ release • Two-Motor Neuron System:
(C) Increased myosin-light chain kinase o Preganglionic Neuron synapses with Postganglionic neuron.
(D) Increased intracellular Ca2+ concentration
o Postganglionic neuron synapses with effector organ receptors
(E) Opening of ligand-gated Ca2+ channels
1-34. Costanzo LS. BRS Physiology. 7th ed. 2019. • Preganglionic Neuron
o Sympa: Cell Body is in the Thoracic and Lumbar segment of the
2. NEUROPHYSIOLOGY Spinal Cord (thoracolumbar distribution)
o Para: Cell Body is in the Brainstem, Sacral Segment of the Spinal
1. Autonomic Nervous System (ANS) Cord (craniosacral distribution)
2. Sensory Systems • Postganglionic Neuron
3. Motor Systems o Sympa: Cell Body is in the Paravertebral or Prevertebral Ganglia
4. Higher Functions of the Cerebral Cortex
o Para: Cell Body is in the Ganglia at the walls of Effector Organs
5. Blood-Brain Barrier and Cerebrospinal Fluid (CSF)
6. Temperature Regulation ANS NEUROTRANSMITTERS
• Adrenergic Neurons: release NE (sympa)
2.1 AUTONOMIC NERVOUS SYSTEM (ANS) • Cholinergic Neurons: release Ach (sympa or para)
• Nonadrenergic, noncholinergic Neurons: release Substance P,
VIP or NO (some postganglionic parasympathetic neurons of the
ANS GIT)
https://qrs.ly/h6cmr1z
Watch this video on ANS first, then read and highlight the portions below.
Dr. Banzuela
ANS RECEPTORS: ADRENORECEPTORS (SYMPA) For the discussion on G proteins, and 2nd messengers like cAMP, go to the
ADRENO- Endocrine Physiology Module.
MOA EFFECT Dr. Banzuela
RECEPTOR ANS RECEPTORS: CHOLINOCEPTORS (BOTH SYMPA & PARA)
Alpha-1 RECEPTOR LOCATION MOA
• Gq protein • Causes smooth muscle
Receptors
• ↑ IP3/Ca2+ contraction NICOTINIC RECEPTORS
(𝛂1)
• Skeletal Muscle • binds with ACh,
• Seen in sympathetic NM (N1)
MEP • opens Na-K Channel
postganglionic presynaptic
• Autonomic
nerve terminals. Also seen in
Ganglia
platelet, fat cells, walls of the • binds with Ach
Alpha-2 NN (N2) (dendrites of
• Gi protein GIT • opens Na-K Channel
Receptors Postganglionic
• ↓ cAMP • Inhibits release of NE for
(𝛂 2) Neurons)
presynaptic nerve terminals
MUSCARINIC RECEPTORS
→ inhibits sympathetic
effects, promotes • binds with Ach, Gq,
M1 • CNS
parasympathetic effects • ↑ IP3/Ca2+
Beta-1 • Seen in the heart (SA Node, AV • binds with Ach, Gi,
• Gs protein M2 • Heart
Receptors Node, ventricles) and kidneys • ↓ cAMP
• ↑ cAMP • Glands
(𝛃1) • Causes excitation • binds with Ach,
Beta-2 M3 • smooth
• Gs protein • Causes smooth muscle • Gq, ↑ IP3/Ca2+
Receptors muscles
• ↑ cAMP relaxation for the other subjects, be careful of the terms: “nicotinic,
(𝛃 2)
cholinergic” or “muscarinic cholinergic” or “adrenergic”
© Topnotch Medical Board Prep.

✔GUIDE QUESTIONS A 42-year-old woman with elevated blood pressure, visual disturbances,
Which autonomic receptor is blocked by hexamethonium at the ganglia, and vomiting has increased urinary excretion of 3-methoxy-4-
but not at the neuromuscular junction? hydroxymandelic acid (VMA). A computerized tomographic scan shows
(A) Adrenergic α1 receptors an adrenal mass that is consistent with a diagnosis of
(B) Adrenergic β1 receptors pheochromocytoma. While awaiting surgery to remove the tumor, she is
(C) Adrenergic β2 receptors treated with phenoxybenzamine to lower her blood pressure. What is the
(D) Cholinergic muscarinic receptors mechanism of this action of the drug?
(E) Cholinergic nicotinic receptors 2-1. Costanzo LS. BRS Physiology. 7 ed. 2019. th (A) Increasing cyclic adenosine monophosphate (cAMP)
Hexamethonium is a non-depolarizing ganglionic blocker (B) Decreasing cAMP
Dr. Banzuela (C) Increasing inositol 1,4,5-triphosphate (IP3)/Ca2+
Which autonomic receptor mediates secretion of epinephrine by the (D) Decreasing IP3/Ca2+
adrenal medulla? (E) Opening Na+/K+ channels
(A) Adrenergic α1 receptors (F) Closing Na+/K+ channels 2-35. Costanzo LS. BRS Physiology. 7 ed. 2019
th
(B) Adrenergic β1 receptors Phenoxybenzamine is an alpha-1 antagonist. Alpha-1 MOA involves

(C) Adrenergic β2 receptors increased IP3/Ca2+. Phenoxybenzamine will decrease that. Take
(D) Cholinergic muscarinic receptors note that Phenoxybenzamine will actually block both alpha-1 and
(E) Cholinergic nicotinic receptors 2-16. Costanzo LS. BRS Physiology. 7 ed. 2019. th
alpha-2 but it has some selectivity (more potent) for alpha-1.
Which autonomic receptor is activated by low concentrations of Dr. Banzuela
epinephrine released from the adrenal medulla and causes vasodilation? • Best initial treatment for pheochromocytoma: alpha-adrenergic
(A) Adrenergic α1 receptors antagonist like Phentolamine, Propranolol (beta-blocker), also
(B) Adrenergic β1 receptors given.
(C) Adrenergic β2 receptors • Hallmark of pheochromocytoma: HPN
(D) Cholinergic muscarinic receptors
(E) Cholinergic nicotinic receptors 2-27. Costanzo LS. BRS Physiology. 7 ed. 2019. th
Remember: Beta-2 will always cause smooth muscle RELAXATION

while Alpha-1 will always cause smooth muscle CONTRACTION.
Dr. Banzuela
MNEMONICS AUTONOMIC NERVOUS SYSTEM MNEMONICS AUTONOMIC NERVOUS SYSTEM
“QISS AND QIQ (KISS AND KICK)” PLASMA OPPOSITE
G-proteins from 𝛼1- β2 and M1-M3 P arasympathetic S ympa
How to Memorize Muscarinic Receptor Locations L ong Pre-Ganglionic Tract S hort Pre-Ganglionic Tract
Parang pagmamahal lang yan. Remember M = Mahal. A ch used A ch used pa rin
Ano ba ang dapat sundin pag nagmamahal? S hort Post-Ganglionic Tract L ong Post-Ganglionic Tract
1st: you listen to your Brain (M1=CNS) M uscaric Receptors A drenergic Receptors
2nd: you listen to your Heart (M2= Heart)
A ch used E pi, NE used
3rd: you listen to your, ahem, “Other Organs"
(M3 = other organs)
SYMPATHETIC PARASYMPATHETIC PARASYMPATHETIC
ORGAN SYMPATHETIC ACTION
RECEPTOR ACTION RECEPTOR
↑ heart rate β1 ↓ heart rate M2
Heart ↑ contractility β1 ↓ contractility (atria) M2
↑ AV node conduction β1 ↓ AV node conduction M2
Constricts blood vessels in α1 ⏤
Vascular smooth skin; splanchnic
muscle Dilates blood vessels in β2 ⏤
skeletal muscle
↓ motility α2’ β2 ↑ motility M3
Gastrointestinal tract
Constrict sphincters α1 Relaxes sphincters M3
Dilates bronchiolar smooth β2 Constricts bronchiolar M3
Bronchioles
muscle smooth muscle
Male sex organs Ejaculation α Erection M
Relaxes bladder wall β2 Contracts bladder wall M3
Bladder
Constricts sphincter α1 Relaxes sphincter M3
M (sympathetic
Sweat glands ↑ sweating ⏤
cholinergic)
Eye
Radial muscle, iris Dilates pupil (mydriasis) α1 ⏤
Circular sphincter
⏤ Constricts pupil (miosis) M
muscle, iris
Ciliary muscle Dilates (far vision) β Contracts (near vision) M
Kidney ↑ renin secretion β1 ⏤
Fat cells ↑ lipolysis β1 ⏤
Table 2.4. Costanzo LS. BRS Physiology. 7th ed. 2019.
✔GUIDE QUESTIONS Administration of which of the following drugs is contraindicated in a
Which of the following is a feature of the sympathetic, but not the 10-year-old child with a history of asthma?
parasympathetic, nervous system? (A) Albuterol (D) Norepinephrine
(A) Ganglia located in the effector organs (B) Epinephrine (E) Propranolol
(B) Long preganglionic neurons (C) Isoproterenol 2-12. Costanzo LS. BRS Physiology. 6 ed. 2014
th
(C) Preganglionic neurons release norepinephrine Because propranolol is non-selective beta-blocker. It will also block
(D) Preganglionic neurons release acetylcholine (ACh) beta-2 receptors – the ones responsible for bronchodilation. You don’t
(E) Preganglionic neurons originate in the thoracolumbar spinal want that in a patient with asthma
cord 2-7. Costanzo LS. BRS Physiology. 7 ed. 2019. th Dr. Banzuela
Sympa will use thoracic nerves and lumbar nerves (thoracolumbar). Patients are enrolled in trials of a new atropine analog. Which of the
Para will use cranial nerves and sacral nerves (craniosacral). following would be expected?
Remember this mnemonic for the cranial nerves utilized by the (A) Increased AV node conduction velocity
parasympathetic nervous system: 1973 (CN X, IX, VII, III). Hindi 1972 (B) Increased gastric acidity (D) Sustained erection
(Vit-K dependent clotting factors yun). Hindi rin 1975 (mixed motor- (C) Pupillary constriction (E) Increased sweating
2-12. Costanzo LS. BRS Physiology. 6th ed. 2014
sensory CN yun) Wag malillito sa 1972, 1973, 1975 J
Dr. Banzuela
Atropine is anti-muscarinic. It will therefore promote mainly
Which autonomic receptor mediates an increase in heart rate? sympathetic effects – in this case, choice A. Choice E is not the correct
(A) Adrenergic α1 receptors answer since sweating, even if it is sympathetic, utilizes muscarinic
(B) Adrenergic β1 receptors receptors as final receptors.
(C) Adrenergic β2 receptors Dr. Banzuela
(D) Cholinergic muscarinic receptors
(E) Cholinergic nicotinic receptors 2-8. Costanzo LS. BRS Physiology. 7 th ed. 2019. SPECIAL NOTES ON THE ANS
Remember: puso at bato, Beta-1. • Singly-Innervated Areas
Dr. Banzuela
A 66-year old man with chronic hypertension is treated with prazosin by SYMPATHETIC ONLY PARASYMPATHETIC ONLY
his physician. The treatment successfully decreases his blood pressure to • Sweat glands • Lacrimal muscle (tear
within the normal range. What is the mechanism of the drug’s action? • Adrenal glands glands)
(A) Inhibition of β1 receptors in the sinoatrial (SA) node • Most blood vessels • Ciliary muscle (for
(B) Inhibition of β2 receptors in the SA node • Pilomotor muscle accommodation)
(C) Stimulation of muscarinic receptors in the SA node
(D) Stimulation of nicotinic receptors in the SA node
• Cardiac Ventricles
(E) Inhibition of α1 receptors on vascular smooth muscle • Pregnant Uterus
• Adrenal Medulla:
Alpha-1 in the blood vessels causes vasoconstriction. Inhibiting alpha- o Not essential for life; supplements sympathetic effects
1 can therefore lower BP.
Dr. Banzuela especially during exercise
Which of the following responses is mediated by parasympathetic o Chromaffin cells in the adrenal medulla are migrated neural
muscarinic receptors? cells that secretes Epi (80%) and NE (20%)
(A) Dilation of bronchiolar smooth muscle • Sympathetic distribution, but final NT is Ach and final receptor
(B) Erection is Muscarinic:
(C) Ejaculation
o Sweat glands (some, not all)
(D) Constriction of gastrointestinal (GI) sphincters
(E) Increased cardiac contractility 2-3. Costanzo LS. BRS Physiology. 6 ed. 2014. th
o Piloerector muscles (controversial, utilizes 𝛼1 according to
some sources)
There’s an old mnemonic for this: “Point and Shoot.” Point (Para) is
o 𝜷3 Receptors: seen in Brown Adipose Tissue of babies
erection. Shoot (Sympa) is ejaculation.
Dr. Banzuela
Refer to the audio guide as you read the table below: To emphasize: A Receptor Potential/Generator potential is NOT a true
action potential – it merely brings you closer to threshold. “Slow waves”
(to be discussed in the GI module), are also not true action potentials.
AUTONOMIC CENTERS Dr. Banzuela
AND CEREBRAL CORTEX ✔GUIDE QUESTION

https://qrs.ly/9scmr3z Sensory receptor potentials
(A) are action potentials
Dr. Banzuela (B) always bring the membrane potential of a receptor cell toward
AUTONOMIC CENTERS AND CEREBRAL CORTEX threshold
CHARACTERISTICS AREA (C) always bring the membrane potential of a receptor cell away from
• Vasomotor Center, Respiratory threshold
(D) are graded in size, depending on stimulus intensity
Center (DRG, VRG), Swallowing, MEDULLA
(E) are all-or-none 2-29. Costanzo LS. BRS Physiology. 7 ed. 2019
th
Coughing & Vomiting Centers

• Exhibits adaptation: change in a way a receptor responds to
• Micturition Center, Pneumotaxic, sequential or prolonged stimulation
PONS
Apneustic Centers o “adapt” = “manhid” = non-responsive to stimuli
• Temperature Regulation • Slowly-adapting Receptors (Tonic Receptors)
HYPOTHALAMUS
• Thirst, Food Intake o for continuous stimulus strength (detects steady stimulus)
• Relay Center for almost all o e.g. Muscle Spindle, Golgi Tendon, Slow Pain Receptor,
THALAMUS
sensations, Memory Recall Baroreceptor, Chemoreceptor, Pressure
• Motor, Personality, Calculation, • Rapidly-adapting Receptors (Phasic Receptors)
FRONTAL LOBE
Judgment o for detecting change in stimulus strength (detects onset and
• Somatosensory Cortex PARIETAL LOBE offset of stimulus)
• Vision OCCIPITAL LOBE o Has a Predictive function
• Hearing, vestibular processing, o e.g. Pacinian Corpuscle, Light Touch
recognition of faces, TEMPORAL LOBE When sensory receptors “adapt”, they become non-responsive. So you
• optic pathway (Meyer’s Loop) have two types of receptors – “martyrs” and “players”. Slowly-adapting
receptors are “martyrs” – as long as you love them, kahit kaunti lang, they
• Behavior, Emotions, Motivation LIMBIC LOBE
will love you back. As long as may stimulus, may response pa rin yung
Just for fun. Student asked me this question - which part of the brain is then sensory receptor. Matagal sila mag “adapt”; matagal sila maging manhid.
most needed in catching a fly? Answer: the cerebral cortex – since judgment Rapidly-adapting receptors are “players” – ang dali nila magsawa, ang
and integration of various parts of the brain occurs here. dali nila maging “manhid.” Kahit mahal mo pa sila, hindi ka na nila mahal.
Dr. Banzuela Kahit may stimulus pa, wala nang response yung sensory receptors. They
only enjoy the start and end of relationships – they only detect the onset
2.2 SENSORY SYSTEMS and offset of stimulus. See the pictures below:
Dr. Banzuela
SENSATION
• Sends info to the Brain about the state of the body and/or the
immediate environment
• Sensory Systems encode for Modality, Location, Intensity,
Duration
• Divided into:
o Somatic Sensation (Somatosensory)
o Special Senses
SENSORY RECEPTORS
• Specialized epithelial cells or neurons that converts
environmental signals into neural signals
• Types:
o Mechanoreceptors: Pacinian corpuscles, joint receptors, muscle
stretch receptors, auditory hair cells, baroreceptors
o Thermoreceptors: Temperature Receptors
§ unmyelinated/lightly myelinated, innervated by Type A Delta
Fibers and Type C Fibers, found in both hairy and glabrous
skin and deep tissues, warmth threshold: 30°C, cold
threshold: 24°C, cold receptors inactive again at <10°C
o Nociceptors: Pain
§ activated by strong pressure, severe cold/heat, chemicals,
• Has a Receptive Field: skin region controlled by each sensory
organ distention in the viscera
neuron
§ Unmyelinated, innervated by Type A Delta Fibers and Type
o Maybe excitatory or inhibitory receptive field
C Fibers
o Types:
o Electromagnetic Receptors: rods and cones
§ Type 1 Receptive Field: smaller with well-defined borders
o Chemoreceptors: olfactory receptors, taste receptors, receptors
§ Type 2 Receptive Field: wider but with poorly-defined
to detect O2 and CO2
borders
• MOA: Ion channels open, causing current to flow, producing
depolarization (or rarely, in the case of photoreceptors,
hyperpolarization)
• Depolarization causes receptor potential / generator potential
o Change in membrane potential produced by stimulus
o Not a True AP: Merely brings you closer to threshold
o increases in amplitude as more intense stimulus is applied

Importante yang Receptive Field Types. Don’t ignore these. A receptive
IMPORTANT POINTS SENSORY NERVE FIBERS
field is a region controlled by a single sensory neuron. Pag type 1, small
area but with well-defined borders. Pag type 2, large areas, pero poorly TYPE A (Type I): Thicker, More Myelinated, Faster
defined ang borders. Which is therefore best for 2-point discrimination For temporal and spatial fidelity
(ability to detect two separate touch stimuli as two discrete points)? Type TYPE C (Type IV): Thinner, Unmyelinated, Slower
1 is the answer – kasi smaller areas with well-defined borders ang
Less Energy-requiring
kontrolado ng bawat sensory neuron na may Type 1 receptive field.
Dr. Banzuela
Most Least
SENSORY NERVE FIBER Agent Intermediate
Susceptible Susceptible
• Bundles of axons joined together that vary in thickness, Hypoxia B A C
myelination, conduction velocity, fidelity
Pressure A B C
Listen to this audio guide as you look at the table below about nerve fibers:
Local
C B A
Anesthetics
Adapted from Table 4-3. Barrett et al. Ganong’s Review of Medical Physiology. 26th ed. 2019
NERVE FIBERS
https://qrs.ly/4rcmr72
Conduction
General Fiber Type and Example Sensory Fiber Type and Example Diameter
Velocity
Ia
Largest Fastest
A-alpha Muscle spindle afferents
Large α-motoneurons Ib
Largest Fastest
Golgi tendon organs
II
A-beta
Secondary afferents of muscle spindles; touch and Medium Medium
Touch, pressure
pressure
A-gamma
y- Motoneurons to muscle spindles (intrafusal ⏤ Medium Medium
fibers)
A-delta III
Small Medium
Touch, pressure, temperature, and pain Touch, pressure, fast pain, and temperature
B
⏤ Small Medium
Preganglionic autonomic fibers
C IV
Smallest Slowest
Slow pain; postganglionic autonomic fibers Pain and temperature (unmyelinated)
Table 2.5. Costanzo LS. BRS Physiology. 7th ed. 2019.
✔GUIDE QUESTION Dorsal Column – for speed, accuracy and precision. Utilizes faster nerve
Which of the following is a property of C fibers? fibers. Antero-lateral System (spinothalamic tract) – slower, less accurate
(A) Have the slowest conduction velocity of any nerve fiber type and precise. Utilizes slower nerve fibers. Look at the examples in the table
(B) Have the largest diameter of any nerve fiber type above.
(C) Are afferent nerves from muscle spindles Dr. Banzuela
(D) Are afferent nerves from Golgi tendon organs MNEMONIC ANTEROLATERAL SYSTEM
(E) Are preganglionic autonomic fibers
2-4. Costanzo LS. BRS Physiology. 7th ed. 2019 SLAP SOMEONE IN THE FACE REALLY FAST
His head will move in an anterolateral direction.
SENSORY PATHWAY: There will be quick decussation of his head.
SENSORY RECEPTOR TO THE SENSORY CORTEX He’ll feel pain and temperature.
• Sensory Receptors Watch the video as you read and highlight the table below on tactile
o Transduces stimulus to electrical signal receptors:
• First-order Neurons
o Cell Body: Dorsal Root or Cranial Nerve Ganglia
• Second-order Neurons
TACTILE RECEPTORS
https://qrs.ly/w5cmr7h
o Cell Body: Spinal Cord or Brainstem
o Axons may decussate
Dr. Banzuela
• Third-order Neurons
o Cell Body: Relay Nucleus of the Thalamus TACTILE
DESCRIPTION SENSORY ENCODED
• Fourth-order Neurons RECEPTOR
o Cell Body: Sensory Cortex • Crude touch,
Free Nerve
o Results in conscious perception of stimulus • In the skin temperature and
Endings
pressure
SOMATOSENSORY PATHWAYS: • Dendrites • Movement of
TOUCH, MOVEMENT, TEMPERATURE, PAIN Meissner encapsulated in CT objects
ANTERO-LATERAL Corpuscles and found in non- • low-frequency
DORSAL COLUMN-MEDIAL
SYSTEM (FA1) hairy skin (fingertips (slow) vibration
LEMNISCUS PATHWAY
(SPINOTHALAMIC TRACT) & lips) • determines texture
• Uses large myelinated fibers • Uses smaller myelinated • Gives steady-state
(Type II), conduction velocity fibers (Type III, IV), 8-40 • Expanded tip tactile
signals for
30-110 m/s m/s receptor/dendritic
Merkel continuous touch
endings
• With temporal and spatial Disc (SA1) • Localizes touch
• Less fidelity • Combine to form Iggo
fidelity sensation and to
Dome Receptors
• Decussates near the medulla • Decussates immediately determine texture
• Touch sensations requiring Hair-end • Movement of
• In hair base
high degree of localization & organ object on the skin
• Pain;
fine gradation of intensity • Enlarged dendritic • Heavy and
• Temperature Sensation
• Vibration endings with prolonged touch
• Light Touch and Pressure
• Sensations that signal Ruffini elongated capsules in (detects sustained
Sensation
movement against the skin Corpuscles deep skin, internal or STEADY
• Tickle and Itch Sensation
• Position Sense and Fine (SA2) tissues and joint PRESSURE) and to
• Sexual Sensation
Pressure capsules; signal degree of
• Two –Point Discrimination • encapsulated joint rotation
• Unmyelinated • Detects deep Look at the picture of the dermatomes above. In med school, when we were
Pacinian dendritic endings, pressure shown a standing man with dermatomes labeled all over, I used to wonder
why there doesn’t seem to be a regular pattern when it comes to those
Corpuscles onion-shaped, found • high-frequency
dermatomes – they seemed haphazardly arranged. Later on, I realized that
(FA2) in subcutaneous skin (fast) vibration the problem was in the presentation of those dermatomes in the books
and deep fascia • tapping themselves – in the picture above of a man assuming his original animal-
Merkel and • 2-point like “four-legged” stance, you will notice that the dermatomes are actually
--
Meissner discrimination regularly arranged in a regular manner from front to back.
Dr. Banzuela
Chemicals and NTs involved in Pain Modulation
SOMATOSENSORY CORTEX
• Nucleus Raphe Magnum and Spinal Dorsal Horn: Serotonin
• Primary Somatosensory Area (S1) and Secondary Somatosensory
• Locus Coeruleus: NE
Area (S2) has somatotopic organization (Sensory Homunculus)
• Periaqueductal gray matter: Morphine
o Largest areas are for the fingers, hands and face
• Spinal Dorsal Horn: Enkephalin
§ For precise localization
• Dorsal Root Ganglion: Opioids
TYPES OF PAIN
FAST / FIRST PAIN SLOW / SECOND PAIN VISION
• after 0.1 sec of stimulus • After 1 sec of stimulus • Refractive Power
• Associated with tissue o ability to bend light
destruction; o measured in Diopters (Reciprocal of focal distance in meters)
• Poorly-localized • Eye: 59 diopters of refractive power
• Superficial; o 2/3 by the Cornea
• if VISCERAL PAIN: poorly-
• rapid onset and offset; § Fixed refractive power
localized, (+) nearby skeletal
• localized o 1/3 by the Lens
muscle spasm, slow
adaptation, uses Type C § Variable refractive power
Fibers § Held by suspensory ligaments (zonula fibers)
• Stimulated by mechanical, • Stimulated by mechanical,

thermal stimuli thermal, chemical stimuli
• Type A-delta fibers or Type
• Type C fibers or Type IV
III (nerve velocity 6-30
(0.5-2m/sec)
m/sec)
• NT: Substance P (relieved
• NT: Glutamate by opioids)
• Mediates synaptic
Remember the mnemonic? J
pronounce it really, really transmission between pain
fast… glutamate!) fibers from pelvis and spinal
Dr. Banzuela cord in a patient with
gonorrhea: Substance P
SPECIAL NOTES ON PAIN

• Receptors: free-nerve endings that exhibits little or no adaptation © Topnotch Medical Board Prep
• Triggered by Temp < 15°C or > 43°C • When Ciliary Muscles are relaxed
• Referred Pain: o Increased tension from Suspensory Ligaments
o Due to sharing of 2nd order neurons in the spinal cord of visceral o Lens becomes Flat
pain fibers and skin pain fibers • When Ciliary Muscles are contracted
o Follows the Dermatome rule o Decreased tension from Suspensory Ligaments
• Endogenous Analgesia System: o Lens becomes Spherical
o NTs include Serotonin, Epi, NE
§ Blocks pain signal at entry point in the spinal cord

Watch this video to emphasize what you have just read regarding lens,
suspensory ligaments and the circular muscles:
LENS OF THE EYE

https://qrs.ly/sscmr7x
Dr. Banzuela
IMPORTANT POINTS VISION • Synapses with
• Not present in fovea,
FAR OBJECTS FOCUS: NEAR OBJECTS FOCUS: bipolar cells
Receptors but has high
Flat Lens Not flat (Spherical) Lens • Sensitive to low-
Cells: Rods concentration in
intensity light
REFRACTIVE ERRORS Parafoveal region
(night vision)
CORRECTIVE
DISORDER DESCRIPTION • Synapses with
LENSES
• “Long Eyeball”: light rays bipolar cells • Present in Fovea
Myopia (Near- • Biconcave Receptors
converge IN FRONT of the • Sensitive to high- centralis (area of
Sightedness) Lenses Cells: Cones
retina intensity light most acute vision)
Hyperopia • “Short Eyeball”: light rays (day, color vision)
(Far- converge BEHIND the • Convex Lenses • Few Cones synapse
Sightedness) retina on single bipolar
• Interneuron
• Irregular/Non-uniform cells: causes high
• Cylindrical
between Receptor
Curvature of the Cornea: acuity, low
Astigmatism Bipolar Cells (Rods, Cones)
multiple convergences of Lenses sensitivity of cones
light in the retina Cells and Ganglion cells
• Many Rods synapse
• Age-Related Loss of • Contrast
on single bipolar
Accommodation (>35y/o) Detectors
• Convex Lenses cells: less acuity,
• Presbyopia presents with greater sensitivity
Presbyopia if initially with
inability to read
20/20 vision Amacrine, • Interneurons;
newspaper due to inability
to contract: ciliary body Horizontal • form local circuits
Cells with bipolar cells
RETINAL
FUNCTION NOTES • Maintains internal
CELL
• Absorb stray light Müller Cells geometry of the • Retinal glial cell
(prevents light • Involved in macular retina
Pigment
scattering) degeneration, • P Cells: Color, Form,
Epithelial
• Converts 11-cis retinal detachment • Output cells of the Fine Details
Cells
retinal to all- and albinism Ganglion Retina • M Cells: Illumination,
trans retinal Cells • Axons form optic Movement
nerve • W Cells: Unknown
function
Tandaan ang favorite sa med school at sa med boards: optic chiasm… bitemporal hemianopsia =) Actually, they can ask any disorder and corresponding sites
above. Go through them and memorize.
Dr. Banzuela
✔GUIDE QUESTIONS PHYSIOLOGIC BLIND SPOT/BLIND SPOT

Cutting which structure on the left side causes total blindness in the left • Corresponds to the OPTIC DISC
eye? o Are in the retina with no light sensitive rods or cones
(A) Optic nerve § No image detection
(B) Optic chiasm
o This is also where ganglion cells axons exit the eye to form the
(C) Optic tract
(D) Geniculocalcarine tract 2-9. Costanzo LS. BRS Physiology. 7 ed. 2019
th
optic nerve
Cutting which structure causes blindness in the temporal fields of the
left and right eyes? STEPS IN PHOTORECEPTION OF RODS
(A) Optic nerve 1. Vitamin A regenerates 11-cis rhodopsin/retinal.
(B) Optic chiasm 2. Photons (light particles) converts 11-cis rhodopsin/retinal to
(C) Optic tract all-trans rhodopsin/retinal.
(D) Geniculocalcarine tract 3. Several intermediates from all-trans rhodopsin are formed. The
2-30. Costanzo LS. BRS Physiology. 7 ed. 2019
th
Cutting which structure on the right-side causes blindness in the

most important: Metarhodopsin II.
temporal field of the left eye and the nasal field of the right eye?
(A) Optic nerve
4. Metarhodopsin II activates a Gt or Transducin. Transducin
(B) Optic chiasm activates Phosphodiesterase.
(C) Optic tract 5. Phosphodiesterase converts cGMP to 5’GMP decrease cGMP
(D) Geniculocalcarine tract levels.
th
6. Decreased cGMP causes closure of Na+ channels. This EAR
decreases Na influx leading to hyperpolarization. The brighter • Outer Ear
the light, the greater the hyperpolarization. o Pinna and external auditory canal
7. Hyperpolarized photoreceptors lead to decreased glutamate o For sound localization and sound collection
8. Decreased glutamate → Excitatory ionotropic glutamate
receptors in bipolar and horizontal cells are inhibited.
9. Decreased glutamate → Inhibitory metabotropic glutamate
receptors in bipolar and horizontal cells are excited and
depolarized.
• Increases when light strikes the eye: activity of transducin
• Middle Ear
o Tympanic membrane, auditory ossicles (malleus, incus,
stapes) that inserts into oval window (membrane between
middle ear and inner ear)
o Auditory ossicles amplify sound from large tympanic membrane
going into smaller oval window
§ For Impedance matching: sound in air from outer ear is
matched with sound in fluid in inner ear
Memorize all the steps above since it’s a favorite in any physio exam.
Unique ang vision because hyperpolarization causes the action potential.
Somethings to help you: remember, ang Vitamin A, CIS muna bago maging
TRANS. Metarhodopsin II activates transducin that activates
phosphodiesterase. From here on, negative statements na lahat –
DECREASED cGMP, CLOSED Na+ channels, HYPERPOLARIZATION,
DECREASED glutamate.
Dr. Banzuela
✔GUIDE QUESTION
Which of the following is a step-in photoreception in the rods? © Topnotch Medical Board Prep
(A) Light converts all-trans rhodopsin to 11-cis rhodopsin Watch this video explaining attenuation reflex:
(B) Metarhodopsin II activates transducin
(C) Cyclic guanosine monophosphate (cGMP) levels increase
(D) Rods depolarize ATTENUATION REFLEX
(E) Release of neurotransmitter increases
https://qrs.ly/dmcmrje
RECEPTIVE FIELDS OF THE GANGLION CELLS, LATERAL
GENICULATE CELLS, VISUAL CORTEX Dr. Banzuela
• Receptor Cells Connected to Ganglion cells via Bipolar Cells: • Inner Ear
forms Center of Receptive Field of the Ganglion Cells o Bony labyrinth (semicircular canals, cochlea, vestibule)
• Receptor Cells connected to Horizontal Cells: forms Surround of o Membranous labyrinth (series of ducts)
Receptive Field of the Ganglion Cells o Endolymph is seen in the scala media/cochlear duct
• On-Center, Off-Surround is one pattern (center depolarizes, § high in potassium
surround hyperpolarizes); opposite pattern can occur; Lateral o Perilymph is seen in the scala vestibuli and scala tympani
Geniculate Cells of the thalamus retains pattern § high in sodium
• In the Visual Cortex, 3 Cell Types detect shape and orientation of
figures:
o Simple Cells: have center surround and on-off patterns,
elongated rods. Respond to Bars of Light with correct position
and orientation
o Complex Cells: respond to Moving Bars or Edges of Light
o Hypercomplex: respond to Lines with particular Length and
to curves/angles
✔GUIDE QUESTION
Which type of cell in the visual cortex responds best to a moving bar of
light?
(A) Simple
(B) Complex
(C) Hypercomplex
(D) Bipolar
(E) Ganglion 2-11. Costanzo LS. BRS Physiology. 7 ed. 2019 th
A mnemonic to help you: Simple Cells: Bars of light Lang. Complex:

gumagalaw na yung bar (Moving Bars). Hypercomplex: yung shape ng bar
naging Curved na.
Dr. Banzuela
HEARING
• Sound Frequency: measured in Hertz (Hz)
o Directly correlated with PITCH
o Human ear: 20-20,000 Hz
• Sound Intensity/Pressure: measured in Decibels (dB)
o Directly correlated with sound AMPLITUDE (loudness/clarity)
o 60dB: conversational Speech
o 85 dB: limit to prevent Occupational Hearing Loss
o >120 dB: causes pain, triggers attenuation reflex (stapedius
and tensor tympani contract reflexively) © Topnotch Medical Board Prep
HEARING
• Sound waves causes cochlea to vibrate → cilia on inner hair cells
bend by shearing force since basilar membrane is stiffer than
tectorial membrane
o Depolarization of inner hair cells is caused by: K+ going into
the cells (since endolymph is rich in K+ compared to ICF)

• Bended cilia on one direction causes depolarization, the opposite
hyperpolarization as it changes K+ conductance → causes
oscillating potential called cochlear microphonic potential
• Outer hair cells characteristics
o Respond to sound like inner hair cells
o Motor protein: Prestin
o Depolarization: shortens outer hair cells
o Hyperpolarization: lengthens outer hair cells
o Damage leads to reduced sound clarity (due to reduced
amplitude)
• Place Theory of Hearing:
o Inner hair Cells near BASE (oval and round windows):
respond to high-frequency sounds
o Inner hair Cells near Apex (helicotrema): respond to low-
frequency sounds
• If a patient is unable to hear high-frequency sound, damage is
closest to: oval window
Here’s a video discussing the Place Theory of Hearing. Refer to the pictures
and readings above:
✔GUIDE QUESTION
Which of the following would produce maximum excitation of the hair
PLACE THEORY cells in the right horizontal semicircular canal?
OF HEARING (A) Hyperpolarization of the hair cells
https://qrs.ly/gdcmrki (B) Bending the stereocilia away from the kinocilia
(C) Rapid ascent in an elevator
Dr. Banzuela (D) Rotating the head to the right 2-25. Costanzo LS. BRS Physiology. 7 ed. 2019
th
✔GUIDE QUESTION Mnemonic: where you head turns, is where depolarization

Which of the following statements best describes the basilar membrane happens. In the opposite direction, hyperpolarization happens.
of the organ of Corti? You turn your head to the right, and the stereocilia bends towards
(A) The apex responds better to low frequencies than the base the kinocilium, and depolarization happens on the right ear.
Dr. Banzuela
does
(B) The base is wider than the apex
(C) The base is more compliant than the apex NYSTAGMUS
(D) High frequencies produce maximal displacement of the basilar • Direction is frequently horizontal (i.e. the eyes move in the
membrane near the helicotrema horizontal plane), but it can also be vertical (when the head is
(E) The apex is relatively stiff compared to the base tipped sidewise during rotation) or rotatory (when the head is
“Apex” is in the helicotrema. “Base” is near the oval and round
tipped forward)
windows. • Direction of Nystagmus: same direction as head rotation
Dr. Banzuela • Postrotatory Nystagmus: occurs in opposite direction of the
Central Auditory Pathways head rotation
o Fibers ascend through lateral lemniscus to inferior colliculus to o Due to continued movement of endolymph in the
medial geniculate nucleus of thalamus to auditory cortex semicircular canals, with consequent bending of the cupula
o Fibers maybe crossed or uncrossed and stimulation of hair cells
§ Lesions of cochlea of one ear: unilateral deafness
§ Central unilateral lesions: may not present with unilateral ✔GUIDE QUESTION
deafness due to mixture of ascending auditory fibers from A ballet dancer spins to the left. During the spin, her eyes snap quickly to
both ears the left. This fast eye movement is
(A) nystagmus
o (+) tonotropic representation of all frequencies at all levels of
(B) Postrotatory nystagmus
central auditory pathway (C) ataxia
(D) aphasia 2-18. Costanzo LS. BRS Physiology. 7 ed. 2019
th
VESTIBULAR SYSTEM
Again, nystagmus – same direction as head rotation. Postrotatory
• Allows reflex adjustments of the head, eyes and postural muscles nystagmus, opposite direction.
to provide stable visual image and steady posture Dr. Banzuela
• Consists of:
o 3 Perpendicular Semicircular Canals: detect angular OLFACTION
acceleration • Olfactory Neurons
o Detects position of head in space: Otolith organs: o Only Neurons capable of reproduction (non-permanent cells)
§ Utricle: detect horizontal (linear) acceleration
Some board-relevant facts about olfaction (and favorite questions in quiz
§ Saccule: detect vertical (linear) acceleration bee competitions): it uses Type C nerve fibers (the slowest, least precise and
• Happens when head rotated to the right: both L and R eyes accurate nerve fiber), it is the only sensory modality that does NOT send
deviate towards Left fibers to the thalamus (hindi marunong magmano sa thalamus!), and
• Receptors: Hair Cells olfactory neurons are the only neurons capable of reproduction.
• Cupula: gelatinous structure Dr. Banzuela
• Olfactory Epithelium innervated by:

• Kinocilium: single long cilium of hair cell
o CN I (Olfactory Nerve): detects scent
• Stereocilia: smaller cilia of hair cell
o CN V (Trigeminal Nerve): detects noxious / painful stimuli
• Rule: (e.g., ammonia)
o Stereocilia bends towards kinocilium: depolarization
• Odorant Receptors
o Stereocilia bends away from kinocilium: hyperpolarization
o Located on neurons in the olfactory epithelium that project
to mitral cells and from there directly to the olfactory cortex
• Olfactory memories: found in entorhinal cortex
• Cribriform Plate Fracture: damages CN I but not CN V:
o (+) anosmia but (+) response to ammonia
• MOA: • Group Ib
Golgi • Muscle Tension
o Odorant molecules bind to receptors in the cilia of olfactory afferents (in
Tendon (Mnemonic: “Tendon:
receptor cells series with
Organs Tension”)
o Golf are used as transducers to activate cAMP second extrafusal fibers)
messenger system • Group II afferents
o ↑ cAMP opens Na+ channels causing depolarizing receptor Pacinian
(distributed • Vibration
potential Corpuscles
throughout)
o Action potentials are then generated and propagated once
threshold is reached Free Nerve
• Group III and IV • Noxious Stimuli
Endings
✔GUIDE QUESTION
Which of the following statements about the olfactory system is true? Muscle spindles and Golgi tendon are proprioceptors – they are for position
(A) The receptor cells are neurons sense. Muscle spindles are INTRAFUSAL fibers. Proprioceptors use Type
(B) The receptor cells are sloughed off and are not replaced A-alpha fibers – the best, fastest, most myelinated, most precise and
(C) Axons of cranial nerve (CN) I are A-delta fibers accurate nerve fibers. They use this type of nerve fiber because position
(D) Axons from receptor cells synapse in the prepiriform cortex sense requires speed, accuracy and precision.
(E) Fractures of the cribriform plate can cause inability to detect Muscles involved in fine movements use MORE muscle spindles compared
ammonia 2-23. Costanzo LS. BRS Physiology. 7 ed. 2019 th
to muscles that are used for coarse movements/posture.
Dr. Banzuela
TASTE MOA OF MUSCLE SPINDLE (INTRAFUSAL FIBERS)

1. When muscle is stretched, muscle spindle also stretched
• Taste Receptors: not true neurons, not synonymous with taste 2. This stimulates Group I and Group II afferent Fibers of the
buds Muscle Spindle
o Taste receptor is a type of chemoreceptor, Innervated by 3. This stimulates Alpha Motoneurons that innervates extrafusal
afferents of CN VII, IX, X muscle fibers → causes appropriate muscle contraction and
• Anterior 2/3 of tongue: CN VII (chorda tympani Facial Nerve) shortening
• Posterior 1/3 of tongue: CN IX (Glossopharyngeal Nerve) 4. Gamma Motoneurons that innervate muscle spindles are also
• Back of throat and epiglottis: CN X (Vagus Nerve) co-activated to adjust sensitivity of muscle spindle during
muscle contraction
PART OF THE TONGUE WHERE 5. When dynamic Gamma Motoneurons are activated at the
TASTE RESPOND TO
IT IS BEST DETECTED same time as Alpha Motoneurons, the number of spindle 1a
Sweet • Sugar • Tip afferents impulses is greater than when alpha discharge
Umami • Glutamate • Tip alone is increased.
Salty • Na • Sides MNEMONICS: MUSCLE SPINDLE
Sour • Acids • Sides AEGIS:
Bitter • Alkaloids • Back Alpha-Extrafusal,
All 5 tastes can be detected all throughout the borders of the tongue (the Gamma-Intrafusal,
center of the tongue is relatively “tasteless” due to decreased taste S-basta may “S” para macomplete yung mnemonic =)
receptors in there). But particular sites are more sensitive to particular
Again, with feelings, AEGIS. J
tastes (e.g., tip of the tongue for sweet). Trivia: What is the 6th taste? Dr. Banzuela
Answer: Fat. We’re all chubby-chasers. =) I’ll explain during the Phase
I/II/III videos.
• Most important role of Gamma Motoneurons: maintain 1a
Dr. Banzuela afferent activity during muscle contraction
✔GUIDE QUESTION
A lesion of the chorda tympani nerve would most likely result in
TYPES MUSCLE SPINDLE (INTRAFUSAL FIBERS)
(A) impaired olfactory function NUCLEAR BAG NUCLEAR CHAIN
(B) impaired vestibular function FIBERS FIBERS
(C) impaired auditory function • Detect Dynamic • Detect Static
(D) impaired taste function Function
changes changes
(E) nerve deafness 2-24. Costanzo LS. BRS Physiology. 7 th ed. 2019
• Group Ia • Group II
Sensory Fiber
TASTE PATHWAY Afferents Afferents
• CN VII, CN IX, and CN X → enter medulla → ascend in the solitary Arrangement of • Central “Bag”
• In rows
tract → terminate on second-order taste neurons in the solitary Nuclei region
nucleus → ascend ipsilaterally to the ventral posteromedial
nucleus of the thalamus → end at the taste cortex
• Cause of dysgeusia (altered taste) following tooth extraction:
damage to the gustatory afferent nerves
2.3 MOTOR SYSTEMS

MOTOR UNIT
• Single motoneuron + all the muscle fibers that it innervates
o Small MU (Small Motoneurons): innervate few muscle fibers
o Large MU (Large Motoneurons): innervate many muscle fibers
• Size Principle: Small MU are “recruited first” (fire first) before Big
MU to gradually increase muscle tension
The definition of motor units, and the “size principle” are important. Small © Topnotch Medical Board Prep
MU active first before large MU to make sure that you have muscle
✔GUIDE QUESTION
contraction that starts as weak, and gradually becomes strong (you don’t
Which of the following is a characteristic of nuclear bag fibers?
want the opposite to happen – if the opposite occurs, it will mess up your
(A) They are one type of extrafusal muscle fiber
movements).
Dr. Banzuela (B) They detect dynamic changes in muscle length
MUSCLE SENSORS (C) They give rise to group Ib afferents
(D) They are innervated by α-motoneurons
MUSCLE
NERVE FIBER FUNCTION 2-24. Costanzo LS. BRS Physiology. 7th ed. 2019
SENSOR Nuclear BAG – dynamic. Nuclear CHAIN – static. Mnemonic:
• Static and dynamic imagine a girl holding a very expensive bag that a thief tries to
• Group Ia and II
changes in muscle steal in broad daylight. Hinampas ni girl si thief using the bag.
Muscle afferents (in
length (Mnemonic: Yung act ng paghampas – DYNAMIC. Afterwards, dumating yung
Spindle parallel with
“SpindLLLLLLe, police, ang they tied up the thief using CHAINS. Hindi makagalaw
extrafusal fibers) yung thief – STATIC.
Length”)
Dr. Banzuela
STRETCH REFLEX
• Muscle that was stretched will contract along with Synergistic
muscles; Antagonistic Muscles will relax
• Patellar Knee Jerk Reflex: tapping patellar tendon → quadriceps
stretch → Muscle Spindles activated → Group Ia afferent
activated → Alpha motoneurons activated → quadriceps contract
✔GUIDE QUESTION
Muscle stretch leads to a direct increase in firing rate of which type of
nerve?
(A) α-Motoneurons
(B) γ-Motoneurons
(C) Group Ia fibers
(D) Group Ib fibers From Physiology BRS, 6th Ed

MUSCLE REFLEXES
REFLEX # OF SYNAPSES STIMULUS AFFERENT FIBERS RESPONSE
Contraction of the
Stretch Reflex (Knee-Jerk) Monosynaptic Muscle is stretched Ia
muscle
Golgi-Tendon Reflex (Clasp
Knife) also called INVERSE Disynaptic Muscle contracts Ib Relaxation of the muscle
STRETCH REFLEX
Flexor-Withdrawal Reflex Ipsilateral flexion;
Polysynaptic Pain II, III, IV
(after touching a hot stove) contralateral extension
In flexor-withdrawal reflex, stronger stimuli will produce greater flexion and shorter reaction times that may lead to AFTER-DISCHARGE (prolonged, repeated
firing of the motor neurons producing series of movements)
Dr. Banzuela
✔GUIDE QUESTIONS DISTRIBUTION ACTIONS

Which reflex is responsible for monosynaptic excitation of ipsilateral • Stimulates
• From Red Nucleus
homonymous muscle? Rubrospinal flexors
to interneurons of
(A) Stretch reflex (myotatic) Tract • Inhibits
(B) Golgi tendon reflex (inverse myotatic) lateral SC
extensors
(C) Flexor withdrawal reflex
• Stimulates both
(D) Subliminal occlusion reflex 2-10. Costanzo LS. BRS Physiology. 7 ed. 2019 th
Pontine flexors and

Which reflex is responsible for polysynaptic excitation of contralateral • From Pons to
extensors? Reticulospinal extensors
ventromedial SC
(A) Stretch reflex (myotatic) Tract (mainly
(B) Golgi tendon reflex (inverse myotatic) extensors)
(C) Flexor withdrawal reflex • From Medullary
(D) Subliminal occlusion reflex • Inhibits both
2-24. Costanzo LS. BRS Physiology. 7 ed. 2019 th
Reticular
Medullary flexors and
Formation to SC
VOLUNTARY MOTOR MOVEMENTS Reticulospinal extensors
interneurons in the
Tract (mainly
• Originate in the Cerebral Cortical Association Areas intermediate gray
extensors)
area
• From Deiters
Lateral nucleus to • Inhibits Flexors,
Vestibulospinal ipsilateral • Stimulates
Tract motoneurons and extensors
interneurons
• From Superior
Tectospinal • Controls neck
Colliculus to
Tract muscles
cervical SC
CORTICOSPINAL (PYRAMIDAL) TRACT

Motor cortex
• downward the brain stem, forming the pyramids of the medulla
• fibers cross in the lower medulla to the opposite side and
descend into the lateral corticospinal tracts (80%)
o cortical control of the movement of an entire limb
• Few fibers do not cross to the opposite side in the medulla but
pass ipsilaterally down the cord in the ventral/anterior
corticospinal tracts (20%)
MOTOR CENTERS AND PATHWAYS o concerned with control of bilateral postural movements by
• Pyramidal Tracts: corticospinal and cortical bulbar tracts that the supplementary motor cortex
passes through medullary pyramids
o Essential for voluntary movement: precentral gyrus,
corticospinal, corticobulbar tracts
• Extrapyramidal Tracts: motor pathways that originate in
following brainstem structures:

CORTICOBULBAR TRACT
• tract arises primarily from areas of the motor cortex related to
the head and face
• Descending motor pathway that terminates in the pons and
medulla
Cranial equivalent of the corticospinal tract
• Responsible for voluntary movement of cranial muscles
Oh I Olfactory SEnsory
Oh II Optic SEnsory
Oh III Oculomotor MOtor
To IV Trochlear MOtor
Touch V Trigeminal MIxed
And VI Abducens MOtor
© Topnotch Medical Board Prep Feel VII Facial MIxed
Very VIII Vestibulocochlear Sensory
Good IX Glossopharyngeal MIxed
Velvet X Vagus MIxed
A… XI Accessory MOtor
(Spinal)
H… XII Hypoglossal MOtor

RUBROSPINAL TRACT VESTIBULOSPINAL TRACT (MEDIAL)
• Originates in the red nucleus in the midbrain • arises in the medial vestibular nucleus
• projects to the spinal cord interneurons and alpha motor neurons • terminates on LMN circuit neurons of cervical and upper thoracic
Stimulate flexor muscles levels
inhibits the activity of extensor muscles o controlling the neck muscles (tandem with corticobulbar
tract)
RETICULOSPINAL TRACT o stabilizing the head
Pontine Reticulospinal Tract o coordinating head movements with eye movements
o Arises from nuclei in the medial pontine reticular formation VESTIBULOSPINAL TRACT (LATERAL)
o projects to the ventromedial motor neurons of the spinal cord • arises in the lateral vestibular nucleus
o Stimulate flexors and (primarily) extensor muscles Stimulate extensor muscles
Predominates the medullary counterpart Inhibits flexor
Medullary Reticulospinal Tract
• serves to mediate postural adjustments
o Arises from the medullary reticular formation,
o projects to motor neurons in the lateral spinal cord TECTOSPINAL TRACT
o Counterbalances the pontine reticular system and inhibits • originates in the superior colliculus of the midbrain
the extensors of the body • project to the cervical spinal cord
• innervate motor neurons responsible for neck movements
• responsible for orienting the head and neck during eye movement

DECORTICATION VS. DECEREBRATION CEREBELLUM
• Functions:
o Vestibulocerebellum: for control of balance and eye movements
o Pontocerebellum: for planning and initiation of movement
o Spinocerebellum: for synergy (controls rate, force, range,
direction of movement)
• Clinical Conditions associated with cerebellar dysfunction:
o Ataxia: lack of muscle coordination that includes delay in
initiation, poor execution of movement sequence and failure to
perform rapid alternating movements (dysdiadochokinesia)
o Intention Tremor: low frequency tremor (<5 Hz) whose
amplitude of increases as an extremity approaches the endpoint
of deliberate and visually guided movement
o Absent Rebound Phenomenon: failure of antagonistic muscle
to contract after removal of resistance to limb movement
When you hear the word “cerebellum”, I want you to think of two things:
Ataxia and Dysdiadochokinesia.
Dr. Banzuela
✔GUIDE QUESTIONS
© Topnotch Medical Board Prep Which of the following structures has a primary function to coordinate
EFFECT OF TRANSECTIONS: AT THE SC rate, range, force, and direction of movement?
(A) Primary motor cortex
• Paraplegia: loss of voluntary movements below level of lesion
(B) Premotor cortex and supplementary motor cortex
• Loss of conscious sensation below level of lesion (C) Prefrontal cortex
• Spinal Shock (Absent reflexes) (D) Basal ganglia
o Limbs flaccid, reflexes absent immediately after (E) Cerebellum 2-31. Costanzo LS. BRS Physiology. 7 ed. 2019
th
transection. Partial recovery may occur after sometime (e.g. The inability to perform rapidly alternating movements
after several hours to a few weeks) (dysdiadochokinesia) is associated with lesions of the:
§ reflexes are NOT chronically suppressed after spinal cord (A) premotor cortex
transection (B) motor cortex
(C) Cerebellum
o C7 transection: HR and BP decreases
(D) substantia nigra
o C3 transection: breathing stops (E) medulla 2-26. Costanzo LS. BRS Physiology. 7 ed. 2019
th
o C1 transection: death • Layers of the Cerebellar Cortex (from innermost to outermost)

EFFECT OF TRANSECTIONS: ABOVE SC 1. Granular Layer: contains granule cells, Golgi Type II cells,
• Lesions above Lateral Vestibular Nucleus: decerebrate rigidity glomeruli
• Lesions between Pontine Reticular Formation and Midbrain: 2. Purkinje Cell Layer: contains Purkinje Cells
decerebrate rigidity § Only output of the cerebellar cortex
o Decerebrate rigidity is spasticity due to facilitation of § Output are always inhibitory, using GABA
myotactic stretch reflex § Output projects to deep cerebellar nuclei and to the
• Lesions above Red Nucleus: decorticate posturing and intact vestibular nucleus
tonic neck reflexes § Modulates output of cerebellum and regulates rate, range and
✔GUIDE QUESTIONS direction of movement (synergy)
The excessive muscle tone produced in decerebrate rigidity can be 3. Molecular Layer: contains stellate and basket cells, dendrites of
reversed by Purkinje and Golgi Type II cells, parallel fibers (axons of granule
(A) stimulation of group Ia afferents cells)
(B) cutting the dorsal roots
(C) transection of cerebellar connections to the lateral vestibular
NEURAL CONNECTIONS IN THE CEREBELLUM
nucleus
(D) stimulation of α-motoneurons • Granule Cell (GC): releases Glutamate → excite basket cells and
(E) stimulation of γ-motoneurons 2-14. Costanzo LS. BRS Physiology. 7 ed. 2019 th stellate cells
Complete transection of the spinal cord at the level of T1 would most • Basket Cells (BC): releases GABA → inhibit Purkinje Cells
likely result in • Climbing and mossy fiber inputs → exert strong excitatory effect
(A) temporary loss of stretch reflexes below the lesion on Purkinje Cells
(B) temporary loss of conscious proprioception below the lesion • Purkinje Cells: releases GABA → inhibit deep cerebellar nuclei
(C) permanent loss of voluntary control of movement above the lesion
(D) permanent loss of consciousness above the lesion
• Golgi Cells à excited by mossy fiber collaterals
• Primary Motor Cortex (BA 4)
o Executes movement that is then transferred to brainstem and
spinal cord where lower motoneurons causes voluntary
movements
o Epileptic event here causes Jacksonian seizures (focal partial
seizure)
✔GUIDE QUESTION
Which of the following parts of the body has cortical motoneurons with
the largest representation on the primary motor cortex (area 4)?
(A) Shoulder
(B) Ankle
(C) Fingers
(D) Elbow
(E) Knee 2-15. Costanzo LS. BRS Physiology. 7 ed. 2019
th
CLINICAL CORRELATES
• Brown-Sequard Syndrome
o Caused by functional hemisection of the spinal cord
o (+) contralateral loss of pain and temperature sensation
beginning 1-2 segments below the lesion
BC – Basket Cell; GC – Golgi Cell; GR – Granule Cell; NG – Cell in deep nucleus; o (+) ipsilateral weakness and spasticity in certain muscles
(+) – excitatory; (-) – inhibitory groups
BASAL GANGLIA • Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrig Disease
• Consists of striatum, globus pallidus, subthalamic nuclei and o (+) Degeneration & loss of motor neurons in the motor
substantia nigra cortex, spinal cord, brain stem & corticospinal tract
• Modulates thalamic outflow to motor cortex to plan and execute o Does NOT usually affect sensation
smooth movements o May present with UMN or LMN SSx depending on location
• Primary function of basal ganglia is the planning and • Patients with Transected Spinal Cords
programming of movement o Have negative nitrogen balance as they catabolize large
• Main NT: GABA amounts of body protein because they are paralyzed below
the level of transection
• NT between striatum and substantia nigra: Dopamine
• Trinucleotide Repeat Diseases
o Inhibits the inhibitory indirect pathway using D2 receptors
o Include Fragile X, Spinocerebellar ataxia type 3, Huntington
o Stimulates the excitatory direct pathway using D1 receptors
Disease, Friedreich Ataxia
• Subthalamic Nucleus: releases Glutamate → excites globus
pallidus, internal segment
• Substantia Nigra Parts Reticulata → releases GABA → inhibits 2.4 HIGHER FUNCTIONS OF THE CEREBRAL
thalamus CORTEX
• Substantia Nigra Pars Compacta → releases Dopamine → EEG WAVES
inhibit the striatum • Made up of alternating excitatory and inhibitory synaptic
• Striatum → releases ACh → inhibit substantia nigra pars potentials in the pyramidal cells of the cerebral cortex
reticulata • Cortical Evoked Potential: changes in the ECG that reflect synaptic
• Globus Pallidus External Segment → releases GABA → inhibit potentials evoked in large number of neurons
subthalamic nucleus • Gamma Rhythm (30-80Hz) in the EEG maybe a mechanism to
• Lesions: “bind” together diverse sensory information into a single
o Globus Pallidus: inability to maintain posture percept and action
o Subthalamic Nucleus: wild, flailing movements • Absence seizures are generalized nonconvulsive seizures with
(hemiballismus) spike-and-wave discharge in the EEG
o Striatum: quick, continuous, uncontrollable movements (e.g. • Disappears when a patient’s eye is open: Alpha rhythm/waves
in Huntington disease)
o Substantia nigra: Tremors, cogwheel Rigidity, reduced
voluntary movement (Akinesia), Postural problems
(Mnemonic: “T-R-A-P” of Parkinson Disease)
§ in Parkinson’s there is continued degeneration of the
dopaminergic neurons of the Substantia Nigra

SLEEP
• Due to an active inhibitory process and not merely due to fatigue
of reticular activating systems
© Topnotch Medical Board Prep o Possible cause: secretion of Muramyl Peptide
MOTOR CORTEX Here’s an audio recording discussing brain waves and Sleep Types:
• Pre-Motor Cortex and Supplementary Motor Cortex (BA 6)
o Generates movement plan that is then transferred to primary
SLEEP AND
motor cortex for execution
o Supplementary motor cortex: rehearses complex motor BRAIN WAVES
sequences https://qrs.ly/wwcmrl5
Dr. Banzuela
SLOW-WAVE SLEEP REM SLEEP
(NREM SLEEP) (PARADOXICAL SLEEP)
• With Active Dreaming;
• Usually dreamless or
• occurs every 90 minutes of
unremembered dreams
slow-wave sleep
• ↑ brain metabolism,
• ↓ muscle tone,
• (+) 10-30% ↓ BP, HR and • Pupillary constriction,
BMR; • Active body movements,
• ↑ in GI motility • Irregular BP, HR, RR;
• Penile erection
• Rapid eye movements
• More difficult to arouse by
sensory stimuli
• Difficult to arouse by
• (REM sleep presents with:
sensory stimuli
periods of loss of skeletal
muscle tone or atonia)
• Stages:
1 – Alpha waves interspersed
with Theta waves
2 – Theta waves interrupted
by Sleep Spindles (12-14 Hz)
• Beta waves
and K+ complexes (large,
slow potentials)
3 – Delta waves interrupted by
Sleep Spindles
4 – Delta waves alone
SPECIAL NOTES: SLEEP
• Young Adults: 25% REM Sleep
• Newborns: 50% REM Sleep
• Decreases duration of REM sleep © Topnotch Medical Board Prep
o Age, Alcohol, Benzodiazepines, Amphetamine

• From NREM to Awake state: MEMORY
o Increase in: Norepinephrine, Serotonin, Histamine • Explicit / Declarative Memory: “Knowing what”
o Decrease in: Acetylcholine, GABA • Implicit Memory: “Knowing How”
• Narcolepsy characteristics • Short-Term Memory: lasts minutes, involve mere chemical
o Starts with REM rather than NREM sleep change
o Associated with Class II antigen of MHC on Chromosome 6 o Working Memory: keeps info available while individual plans
o Fewer hypocretin (orexin)-producing neurons actions based on it
• Long-Term Memory: resistant to disruption, lasts for a lifetime
LANGUAGE
• Corpus Callosum: for interhemispheric communication
• R Cerebral hemisphere:
o NON-DOMINANT or REPRESENTATIONAL hemisphere in most
R-handed people
o dominant in facial expression, intonation, body language, spatial
task
• L Cerebral hemisphere: usually dominant in language; lesions
here causes aphasia
o DOMINANT or CATEGORICAL hemisphere in most R-handed
people
o usually dominant in language; lesions here causes aphasia
§ Wernicke Aphasia: receptive aphasia – “can say, but can’t
understand” (Mnemonic: “Wordy Wernicke”)
§ Broca Aphasia: expressive aphasia – “can understand, but
cannot say” (Mnemonic: “Broken <speech> Broca”)
A very important message regarding Wernicke Aphasia =):
WERNICKE APHASIA
https://qrs.ly/b2cmrmo
Dr. Banzuela
CLINICAL CORRELATES
Damage to:
• Angular Gyrus in the categorical hemisphere: Anomic
Aphasia
• Inferior parietal lobule (a region in the posterior part of the
parietal lobe that is close to the occipital lobe): unilateral
attention and neglect
• Parietal Lobe of the representational hemisphere:
Astereognosis (inability to recognize objects by feeling them)
and Agnosia
• Mamillary bodies: loss of recent memory
• Cholinergic neurons in the nucleus basalis of Meynert and
related areas of the forebrain: loss of recent memory © Topnotch Medical Board Prep
SPECIAL NOTES ON MEMORY 2.6 TEMPERATURE REGULATION
• Consolidation: conversion of short-term to long-term memory REGULATION OF BODY TEMPERATURE
o Rehearsal, Sleep, Adequate Nutrition (especially Vit B) • Mediated by the Hypothalamus
promotes consolidation o Sensors: Temperature sensors in skin and hypothalamus
• Temporal Lobe: where memory is mainly stored o Detected Temperature compared with Set-point
• Hippocampus: Temperature
o helps ENCODE events of the recent past into long-term § Detected Temp < Set-Point Temp: Initiate Heat Generating
memory Mechanisms
o promotes memory formation when reward and punishment § Detected Temp > Set-Point Temperature: Initiate Heat Loss
centers are stimulated Mechanisms
§ Reward Center: Medial Forebrain Bundle (Mnemonic • Heat-Generating Mechanisms
“MEDIAL as Reward”) o Shivering (most potent), Thyroid Hormone production,
§ Punishment Center: Central Gray Area surrounding the decreased sweating, piloerection, skin (cutaneous)
Aqueduct of Sylvius (Mnemonic: “Mr. Grey punishment! vasoconstriction (𝛼1), brown fat in babies (𝜷3)
Hwapishhh!!! J) • Heat Loss Mechanisms
• Thalamus: helps RECALL memory o Radiation (most potent), convection, Sweating, Skin
Remember: hippocampus is NOT for memory storage (memory is stored (cutaneous) Vasodilatation, Decreased Heat Production
throughout the brain but mainly in the temporal lobe). Hippocampus helps
ENCODE or form new memory. Thalamus meanwhile helps you RECALL SPECIAL NOTES ON TEMPERATURE REGULATION
previously-formed memories. Destroying your hippocampus would cause
ANTEROGRADE amnesia (cannot form new memories). Destroying your • Anterior Hypothalamus: for heat loss
thalamus would cause RETROGRADE amnesia (cannot recall old • Posterior Hypothalamus: for heat gain
memories). Some mnemonics. think of yourself fanning the anterior part of the body.
Dr. Banzuela
ANTERIOR hypothalamus: heat loss. Think of yourself placing on a jacket
SPECIAL NOTES ON MEMORY to keep yourself warm. You first place that jacket on the posterior part of
• Neocortical Areas: for remote memories the body. POSTERIOR hypothalamus: heat gain/preservation.
• Prefrontal Cortex: for working memory Dr. Banzuela
• Inferior Temporal Lobe: for ability to recall faces and forms • Fever
• Amygdala: for production of inappropriate emotional o MOA: Pyrogens → ↑ IL-1 (alpha and beta), IL-6 → ↑ PGE2 →
responses when recalling events of the recent past ↑set-point temperature in hypothalamus → causes heat-
generating mechanisms
o ASA: inhibits COX → ↓ PGE2 → ↓ set-point temp
2.5 BLOOD-BRAIN BARRIER (BBB) AND o Steroids: inhibits release of arachidonic acid from brain
CEREBROSPINAL FLUID (CSF) phospholipids → ↓ PGE2 → ↓ set-point temp
BLOOD-BRAIN BARRIER • * PGE1: keeps ductus arteriosus open.
• Consists of: • PGE2: increases set-point temp.
o Endothelial cells of cerebral capillaries (and the tight • Mnemonic: PGE1 – “PGE1: E1 mong bukas ang ductus arteriosus.
junctions between them) PGE2: E2 ang para sa fever!” (fine print: technically, PGE2 can also
o Astrocyte foot processes keep the ductus arteriosus open. Use the mnemonic as a rough
o Choroid plexus epithelium guide)
• Functions:
o Maintain constant environment for neurons ✔GUIDE QUESTION
Pathogens that produce fever cause _________.
o Prevents escape of neurotransmitters
(A) decreased production of interleukin-1 (IL-1)
o Drugs penetrate BBB to various degrees (easier if lipid-soluble (B) decreased set-point temperature in the hypothalamus
and nonionized) (C) shivering
• Exists in all areas of the brain EXCEPT in Circumventricular (D) vasodilation of blood vessels in the skin
Organs (CVOs) 2-22. Costanzo LS. BRS Physiology. 7th ed. 2019
o Some areas of the Hypothalamus (including neurohypophysis) Main mechanism for heat conservation/heat gain: SHIVERING (behavioral
o Pineal gland change). Main mechanism for heat loss: RADIATION (60%).
o Area Postrema Other mechanisms for heat loss: evaporation (22%), conduction to air
(15%), conduction to objects (3%).
Dr. Banzuela
CSF
• CSF in brain: 150 mL • Heat Exhaustion: excessive sweating that decreases BP and
• CSF produced per day: 500 mL causes syncope
o 70% by Choroid Plexus • Heat Stroke: high body temperature that causes tissue damage;
o 30% by Brain Parenchyma sweating is impaired which further increases temperature;
• Functions: Cushioning, buoyancy, maintain normal CNS volume maybe lethal
• Composition approximately the same as interstitial fluid but • Hypothermia: when ambient temperature is so low, that core
differs from blood temperature cannot be maintained at set-point
o CSF < BLOOD • Malignant hyperthermia (MH): overexcitation of skeletal
§ Glucose, Protein (negligible in CSF), Cholesterol (negligible muscles due to defective ryanodine receptors (that results in
in CSF) excess Ca2+ release from SR). Triggers of MH:
o CSF > BLOOD o Halothane (also: inhaled general anesthesia, desflurane,
§ Na+ enflurane, ether, isoflurane, sevoflurane)
o CSF = BLOOD o succinylcholine
§ Osmolarity o Heat stress
CSF is isotonic to blood because even if CSF has higher Na+ concentration, o Vigorous exercise
blood has higher protein concentration. This is based on Berne and Levy. • Treatment of MH: Dantrolene, a Ca2+-channel (ryanodine
Iba nakasulat sa Physio BRS. We follow Berne and Levy regarding this one. receptor) blocker and muscle relaxant
Dr. Banzuela
✔GUIDE QUESTION
Which of the following has a much lower concentration in the
cerebrospinal fluid (CSF) than in cerebral capillary blood?
(A) Na+ (D) Protein
(B) K+ (E) Mg2+
(C) Osmolarity th
3. CARDIOVASCULAR PHYSIOLOGY DESCRIPTION VESSEL

• Control Conduits;
1. Circuitry of the Cardiovascular System
2. Hemodynamics • may rapidly dilate and constrict;
ARTERIOLES
3. Cardiac Electrophysiology • (+) site of greatest resistance, 𝛂1-
4. Cardiac Output Vasoconstricts; 𝜷2-Vasodilates
5. Cardiac Cycle • Contains stressed volume;
ARTERIES
6. Regulation of BP • high pressure
7. Microcirculation and Lymph • Largest total cross-sectional area;
8. Special Circulation • has endothelial cells only;
9. Gravity, Exercise, Hemorrhage • slowest blood flow velocity; CAPILLARIES
• metarterioles and pre-capillary sphincters
3.1 CIRCUITRY OF THE CARDIOVASCULAR SYSTEM control blood flow
Listen to this audio recording about CO and VR while reading the next • a.k.a. Capacitance Vessels;
passages: • 64% of blood found here, with one-way VEINS
valves
CARDIAC OUTPUT • Drains proteins and fluids from the
LYMPHATIC
AND VENOUS RETURN interstitium, carries chylomicrons and
VESSELS
https://qrs.ly/qkcmrn6 involved in immunity and cancer
Look at the illustration at the next page. Let’s tackle the basics. “Blood and
Dr. Banzuela air will always flow from high pressure to low”. Remember that dictum. So,
if you want blood to flow from arteries to capillaries to veins, saan
IMPORTANT PRINCIPLES pinakamababa ang pressure? Answer: sa veins. All veins will eventually
• Cardiac Output (CO) drain into the vena cava and then to the right atrium. That’s why pressure
o = HR x SV = VR is lowest sa Right Atrium – around 0-4mmHg. Since all veins will drain into
the Right Atrium, we call right atrial pressure by another name, we call it
o CO L Heart = CO R Heart
Central Venous Pressure (you can think of the right atrium as the “central
§ CO L Heart: Systemic Blood Flow vein” since all veins drain through it eventually). From the R atrium, blood
§ CO R Heart: Pulmonary Blood Flow will flow to the R ventricle (after passing through tricuspid). From R
o At rest: 5L/min ventricle it will go to the pulmonary artery → pulmonary arterioles →
o Max CO (Non-Athlete): 20L/min pulmonary capillaries → pulmonary veins → L atrium (passing through
o Max CO (Athlete): 30L/min mitral valve) → L ventricle (passing through aortic valve) → aorta →
• Pulmonic Circulation, compared to Systemic Circulation, has: systemic arteries → systemic arterioles → systemic capillaries → veins.
o Lower resistance, afterload, stroke work Remember: site of highest oxygenation: pulmonary vein (100%
oxygenated). Only arteries that contain deoxygenated blood: pulmonary
o Same preload, heart rate, stroke volume, cardiac output
artery and umbilical artery. Only veins that contain oxygenated blood:
• Blood flow per 100g of tissue is greatest in the KIDNEYS pulmonary vein and umbilical vein.
Dr. Banzuela
✔GUIDE QUESTIONS
Cardiac output of the right side of the heart is what percentage of the ✔GUIDE QUESTION
cardiac output of the left side of the heart? The greatest pressure decrease in the circulation occurs across the
(A) 25% (D) 100% arterioles because
(B) 50% (E) 125% (A) they have the greatest surface area
3-40. Costanzo LS. BRS Physiology. 7 ed. 2019.
(C) 75% th
(B) they have the greatest cross-sectional area
(C) the velocity of blood flow through them is the highest
And what is the reason for the answer? =) Because once again: CO (D) the velocity of blood flow through them is the lowest
of the L heart should be equal to the CO of the R heart. (E) they have the greatest resistance
Dr. Banzuela
In which of the following situations is pulmonary blood flow greater than At which site is systolic blood pressure the highest?
aortic blood flow? (A) Aorta (D) Right atrium
(A) Normal adult (B) Central vein (E) Renal artery
(B) Fetus (C) Pulmonary artery 3-3. Costanzo LS. BRS Physiology. 7 ed. 2019. th
(C) Left-to-right ventricular shunt Bakit hindi aorta eh aorta pinakamalapit sa L ventricle? The
(D) Right-to-left ventricular shunt reason for this → when blood moves from aorta to a branch of that
(E) Right ventricular failure 3-18. Costanzo LS. BRS Physiology. 7 ed. 2019. th
aorta, the change in direction of blood will hit the branching
points and increase the pressure slightly. Kaya yung branch point
ng aorta (among the choices above, only renal artery is a branch
COMPONENTS OF THE CIRCULATION
of the aorta) sa renal artery mas mataas ang pressure nyan
Listen to the audio recording while reading the next table on various
compared sa aorta itself. Analogy: imagine driving a very fast car
vessels:
along EDSA. Then you made a sudden left turn in one of the side
streets and hit the gutter. Mataas ang pressure ngayon dun sa
branch points ng EDSA papunta sa side street. Message me on
BLOOD VESSELS Viber if you have a hard time with this so I can explain better.
https://qrs.ly/4pcmrn9 Dr. Banzuela
Dr. Banzuela

Atria Must-know yung Ohm’s law ha. Blood flow (Q) is directly proportional to
• Primer pumps of the ventricles. pressure, inversely proportional to resistance. Blood flow to the entire body
• 80% of the blood flows from atria to the ventricles before the is CO. Resistance to this CO is TPR. Ergo, CO=BP/TPR or rearranged, BP
= CO x TPR (the classic cardio physio formula that you encountered in
atria contracts. Atrial contraction is responsible for 20% medical school). That formula is based on Ohm’s law (Ohm’s law btw, if
ventricular filling you remember your high school physics, is more commonly expressed as I =
• Not necessary in the resting state since heart pumps 300-400% V/R, where I is current, V is voltage and R is resistance)
more blood than is required at rest Dr. Banzuela
• Becomes an issue only during exercise – atrial damage may lead ✔GUIDE QUESTION
to shortness of breath An increase in arteriolar resistance, without a change in any other
component of the cardiovascular system, will produce
(A) a decrease in total peripheral resistance (TPR)
3.2 HEMODYNAMICS (B) an increase in capillary filtration
BLOOD FLOW VELOCITY (C) an increase in arterial pressure
• Fastest: aorta (D) a decrease in afterload 3-27. Costanzo LS. BRS Physiology. 7 ed. 2019.
th
• Slowest: capillaries (because of Listen to this audio recording while reading Poiseuille Law and the
large total cross-sectional area) subsequent guide question that follows:
• Blood Flow Velocity is
INVERSELY PROPORTIONAL to
total cross-sectional area POISEUILLE LAW
https://qrs.ly/4jcmrnn
Dr. Banzuela
RESISTANCE TO BLOOD FLOW
• Based on Poiseuille Law (pronounced as “Pwa-zweeh”)
• Remember: blood viscosity = hematocrit

© Topnotch Medical Board Prep o Polycythemia: increased resistance
BLOOD FLOW • If a vessel radius decreases: highly increases resistance
• Directly proportional to Pressure Difference o Important when it comes to the control conduits arterioles
• Inversely proportional to resistance
✔GUIDE QUESTION
• Based on Ohm’s Law:
A 53-year-old woman is found, by arteriography, to have 50% narrowing
of her left renal artery. What is the expected change in blood flow
through the stenotic artery?
(A) Decrease to 1⁄2 (D) Decrease to 1⁄16
(B) Decrease to 1⁄4 (E) No change
3-1. Costanzo LS. BRS Physiology. 7 ed. 2019.
(C) Decrease to 1⁄8 th
Radius = ½ its original value

Resistance = 8ηl/π ½)4
= 16x its original value
new Q =ΔP/16R
* this is where we derive the formula BP = CO x TPR The new Q will be 1/16 its original value
Dr. Banzuela
LAMINAR VS. TURBULENT BLOOD FLOW Pressure differential
• Laminar Blood flow: Streamline blood flow, with blood velocity Pressure (mmHg) in (mmHg) between
fastest in the center and slowest near the vessel walls Aorta and
• Turbulent Blood Flow: irregular, disorderly blood flow Left Right Right
Aorta Left Vent
associated with high Reynold’s Number (>2000) & bruits Vent Vent Vent
(audible vibrations) Systole 120 121 25 -1 95
Diastole 80 0 0 80 80
ARTERIAL PRESSURES
DESCRIPTION ANSWER
Highest Arterial Blood Pressure SYSTOLIC PRESSURE
Lowest Arterial Blood Pressure
DIASTOLIC PRESSURE
• Anemia: ↓ blood viscosity → Turbulent BF = Systolic Pressure – Diastolic
• Atherosclerotic blood vessel → ↑ blood velocity → Turbulent BF PULSE PRESSURE
Pressure
Laminar blood flow is normal, turbulent blood flow is abnormal. = Stroke Volume / Arterial
PULSE PRESSURE
Turbulence is predicted by Reynold’s number. The higher the Reynold’s Compliance
number, the greater the probability of turbulence. Reynold’s number – take Most important determinant of
a look at its formula. Yung viscosity (n) is inversely proportional to your STROKE VOLUME
Pulse Pressure
Reynold’s number. So saan ka nakakita ng turbulent blood flow – anemia
= 2/3 (Diastole) + 1/3 (Systole) = MEAN ARTERIAL
or polycythemia? Answer: anemia. Mababa ang n, mataas ang Reynold’s.
Saan ka naman makakakita ng higher resistance to blood flow, and lower Diastole + 1/3 PP PRESSURE
blood flow – anemia or polycythemia? Answer: polycythemia. Kasi n is CENTRAL VENOUS
Synonym: Right Atrial Pressure
directly proportional to R based on law of Poiseuille. Be careful with this PRESSURE
anemia vs. polycythemia issue. Anemia: turbulent blood flow. Measured using Swan-Ganz
Polycythemia: higher resistance to blood flow. PULMONARY CAPILLARY
Catheter. Estimates Left Atrial
Dr. Banzuela WEDGE PRESSURE
Pressure.
✔GUIDE QUESTION * PP increases with age due to âarterial compliance (âcapacitance)
The tendency for blood flow to be turbulent is increased by
MEAN ARTERIAL PRESSURE is also called MEAN PRESSURE; the average
(A) increased viscosity
pressure throughout the cardiac cycle.
(B) increased hematocrit
(C) partial occlusion of a blood vessel Take note – the formula of pulse pressure is not just systolic pressure –
(D) decreased velocity of blood flow 3-15. Costanzo LS. BRS Physiology. 7 th ed. 2019. diastolic pressure. Pulse pressure = stroke volume/arterial compliance.
Wag niyo kakalimutan itong alternative formula na ito. So, what happens
Because partial occlusion of a blood vessel will decrease the cross-
to pulse pressure as you grow older? As you grow older, arterial
sectional area, increasing blood flow velocity (remember that
compliance decreases (arteries become stiffer) due to arteriolosclerosis.
blood flow velocity is inversely proportional to cross-sectional
Because arterial compliance decreases as you grow older, Stroke Volume
area of the vessel).
Dr. Banzuela
INCREASES as you grow older. These are the kinds of questions that you
may encounter in your med boards – it’s a favorite din kasi in med school.
Dr. Banzuela
CAPACITANCE/ COMPLIANCE • in exercise among cardiac transplant patients, cardiac output
• Distensibility of blood vessel increases mainly due to increase in: Stroke Volume
• Inversely proportional to elastance (stiffness) • increases when CVP increases: ANP
INCREASED (WIDENED) DECREASED (NARROW)
PULSE PRESSURE PULSE PRESSURE
• Well-conditioned
endurance runner
• Old age • Heart Failure (decreased
• Aortic regurgitation pumping)
• Capacitance of Veins > Arteries • Aortic sclerosis • Blood loss (decreased blood
o ratio of arterial compliance to venous compliance: 1:20 • Severe iron deficiency volume)
• Capacitance of Arteries decreases with age anemia (reduced blood • Aortic stenosis (reduced
Remember that easy-to-forget formula: C=V/P. Formulas like this, in the
viscosity) stroke volume)
“nooks and crannies” of this handout, has been asked before in the med
boards. • Arteriosclerosis (less • Cardiac tamponade
Dr. Banzuela compliant artery) (decreased filling time)
BLOOD PRESSURE AT DIFFERENT POINTS • Hyperthyroidism
(increased systolic pressure
✔GUIDE QUESTION
Pulse pressure is
(A) the highest pressure measured in the arteries
(B) the lowest pressure measured in the arteries
(C) measured only during diastole
(D) determined by stroke volume
(E) decreased when the capacitance of the arteries decreases
3.3 CARDIAC ELECTROPHYSIOLOGY

ECG
• P wave: Atrial Depolarization
• QRS Complex: Vent Depolarization
Remember the normal values of the various blood vessels above. Observe • T Wave: Vent Repolarization
also that the systolic pressure in the branches of the aorta (the one labeled • PR Interval: depends on Conduction Velocity through AV Node
“large arteries” here), is higher than the aorta itself – again, as previously o During PR Interval, cardiac AP passes through the AV Node
mentioned, this is based dun sa pagtama ng dugo sa mga branching points • QT Interval: Period of Vent Depolarization + Repolarization
ng aorta. • PR Segment: AV Node Conduction
Dr. Banzuela
o During PR Interval, cardiac AP passes through the AV Node
• ST Segment: isoelectric; correlates with plateau of Vent AP
Refer to the ECG picture while you listen to this audio

recording:
ECG
https://qrs.ly/fjcmro0
Dr. Banzuela
SPECIAL NOTES ON THE ECG ✔GUIDE QUESTIONS

ECG CHANGES ANSWER The ventricles are completely depolarized during which isoelectric
• Stimulates AV Node → ↑ Conduction portion of the electrocardiogram (ECG)?
SYMPATHETIC NS (A) PR interval (D) ST segment
Velocity → ↓ PR Interval
(B) QRS complex (E) T wave
• Can decrease AV Node Conduction → ↓ (C) QT interval 3-17. Costanzo LS. BRS Physiology. 7 ed. 2019 th
Conduction Velocity → ↑ PR Interval A person’s electrocardiogram (ECG) has no P wave, but has a normal QRS
• 1st degree AV Block: all atrial impulses complex and a normal T wave. Therefore, his pacemaker is located in the
reach the ventricles, but PR interval is (A) sinoatrial (SA) node (D) Purkinje system
long (B) atrioventricular (AV) node (E) ventricular muscle
• 2nd degree AV Block: no all impulses (C) bundle of His th
conducted to ventricles, ventricular A 30-year-old female patient’s electrocardiogram (ECG) shows two P
waves preceding each QRS complex. The interpretation of this pattern is
rate < atrial rate. P Wave NOT always (A) decreased firing rate of the pacemaker in the sinoatrial (SA) node
followed by QRS (B) decreased firing rate of the pacemaker in the atrioventricular (AV)
o Mobitz Type I: (+) Wenckebach node
phenomenon (gradual exhaustion of (C) increased firing rate of the pacemaker in the SA node
impulse conduction: ECG shows HEART BLOCK (D) decreased conduction through the AV node
gradual increase of PR interval before (E) increased conduction through the His-Purkinje system
a block occurs)
o Mobitz Type II: sporadically Kindly review the videos on the cardiac AP and SA Node AP found in Cell
Physiology Module
occurring blocks, (-) Wenckebach Dr. Banzuela
phenomenon. Constant PR intervals CARDIAC ACTION POTENTIAL
before block occurs • Stable RMP: -90mV (almost similar to K equilibrium potential)
o 3rd degree (Complete) AV Block: • Cardiac AP: Phase 0,1,2,3,4
Atrioventricular dissociation may
cause fainting, syncope, worsening CARDIAC PACEMAKERS
exercise intolerance from cerebral • Sequence: SA node à AV Node à Bundle of His à Purkinje
ischemia Fibers
• Flat/inverted T waves • SA Node: Master Pacemaker (exerts overdrive suppression of
• prominent U waves (increased other pacemakers)
susceptibility to Torsades de Pointes) HYPOKALEMIA • AV Node, Bundle of His, Purkinje: Latent Pacemakers
• ↑ amplitude and width of P waves • When latent pacemakers assume pacemaking activity: Ectopic
• ST depression, QT Prolongation Pacemaker
• Intrinsic rate of Phase 4 Depolarization (and Heart Rate):
• Low P waves, Tall T waves HYPERKALEMIA SA Node > AV Node > His-Purkinje
• Prolonged QT Interval: associated o SA Node: 70-80 beats/min
with long QT syndrome (can cause o AV Node: 40-60 beats/min
sudden fainting and sudden death), (slowest conduction velocity at 0.01-0.05 m/sec)
HYPOCALCEMIA
torsades de pointes (can cause o Bundle of His: 40 beats/min
ventricular arrhythmias/ o Purkinje Fibers: 15-20 beats/min
ventricular fibrillation) (fastest conduction velocity at 2-4 m/sec)
• Shortened QT Interval HYPERCALCEMIA SA Node has the shortest duration among the pacemakers – this is the
reason why it’s the master pacemaker (nag-aattempt pa lang mag self-
Q-WAVE INFARCT
excite yung ibang pacemakers, na-stimulate na sila ng prior pacemakers
• ST Segment Elevation / TRANSMURAL like the SA Node).
INFARCT So, what will happen when the SA Node dies (e.g. due to MI)? Answer: HR
NON-Q-WAVE will decrease, since the duration of the action potential of the other
INFARCT / pacemakers are longer, leading to less cycles per minute, leading to
• ST Segment Depression decrease in heart rate.
SUBENDOCARDIAL
Dr. Banzuela
INFARCT
SA NODE AP
1st degree AV block: prolonged PR interval. 2nd degree: dropped QRS • Has unstable RMP (Phase 4)
complex. 3rd degree: atrioventricular dissociation (meaning may sariling • No sustained Plateau, no Phase 1, no Phase 2
rhythms na ang atrium vs. ventricles). 3rd degree is the one associated
with SYNCOPE. Analogy: Parang stages sa break-up yan. 1st degree AV
• Contains Phase 4, 0, 3 <see discussion on cardiac muscles>
block – para kayong bf-gf na nagkakalaboan na; nagiging malayo na • If channels or “slow, funny sodium channels”: responsible for
feelings nyo sa isa’t isa (prolonged PR interval). 2nd degree: you drop dates slow Na influx during Phase 4
and meetings na for one another (dropped QRS complex). 3rd degree:
hiwalayan na talaga – kanya-kanyang buhay na (AV dissociation).
Dr. Banzuela
o Triggered by K+ efflux of Phase 3 which causes automaticity - predisposes athletes to PVCs: Bradycardia
and pacemaking activity of the SA Node (Phase 3 will always - may compromise stroke volume post-M.I.: increased heart
cause Phase 4) rate (due to decreased filling time)
CONDUCTION VELOCITY • Sympathetic NS stimulation
• Time required for excitation to spread throughout the cardiac o Increases Ca2+ influx in Phase 2 of Cardiac AP
muscle o Increases SR Ca2+-ATPase pump (through phosphorylation of
• Depends on size of the inward current during the upstroke of phospholamban) → more Ca2+ accumulated by SR → more Ca2+
the cardiac AP available for release to the sarcomere
• Fastest: Purkinje fibers § increased by increasing phospholamban: concentration of
• Slowest: AV node (allows time for ventricular filling) Ca2+ within the SR
✔GUIDE QUESTION • Cardiac Glycosides (digitalis)
The physiologic function of the relatively slow conduction through the o Inhibition of some cardiac Na-K-ATPase pump → ↓ activity of
atrioventricular (AV) node is to allow sufficient time for Na+-Ca2+ pump → ↑ intracellular Ca2+
(A) runoff of blood from the aorta to the arteries There are 3 factors that increases stroke volume (positive inotropes):
(B) venous return to the atria digitalis, beta-1 stimulation and INCREASED HEART RATE. The faster the
(C) filling of the ventricles heart beats, the stronger the heart beats → this is the staircase effect and
(D) contraction of the ventricles has something to do with increased amount of calcium being released from
(E) repolarization of the ventricles 3-41. Costanzo LS. BRS Physiology. 7 ed. 2019
th
the sarcoplasmic reticulum with each round of heart contraction. PVC
Between the atria and ventricles is an area of fibrous tissue with (Extrasystole) is a form of arrhythmia where the heart prematurely
little gap junctions. This causes the AV nodal delay contracts. During PVC, stroke volume decreases. But during the first
(pinakamabagal ang conduction velocity sa AV Node). normal contraction after PVC, stroke volume will actually increase (due to
Importante yang AV nodal delay na yan – it ensures that the increased ventricular filling time caused by shifting from abnormal rhythm
atrium will contract first before the ventricles, and it allows for to normal rhythm). This increase in SV during the first normal contraction
ventricular filling. after PCV is called POSTEXTRASYSTOLIC POTENTIATION. Staircase effect
Dr. Banzuela and Postextrasystolic potentiation are the mechanisms for increased heart
Listen to the audio recording while you study and highlight the table on the rate causing an increase in stroke volume.
Dr. Banzuela
autonomic effects on HR and SV below:
✔GUIDE QUESTIONS
Which of the following agents or changes has a negative inotropic effect
AUTONOMIC EFFECTS on the heart?
ON HR AND SV (A) Increased heart rate (D) Acetylcholine (ACh)
https://qrs.ly/zvcmrob (B) Sympathetic stimulation (E) Cardiac glycosides
(C) Norepinephrine th
Dr. Banzuela
ACh kasi is the final neurotransmitter for the PARASYMPATHETIC
AUTONOMIC EFFECTS ON HR AND CV nervous system. And while para does not have a direct negative
DESCRIPTION ANSWER inotropic effect on the heart (remember para has no direct effect
Produces changes in on the cardiac ventricles), para can affect heart rate – it decreases
INOTROPIC EFFECT
Contractility your heart rate. Decreased heart rate will cause a negative
Produces changes in Rate of inotropic effect. So, ACh has an indirect negative inotropic effect.
LUSITROPIC EFFECT Dr. Banzuela
Relaxation An electrocardiogram (ECG) on a person shows ventricular extrasystoles.
Produces changes in Heart The extrasystolic beat would produce
CHRONOTROPIC EFFECT
Rate (A) increased pulse pressure because contractility is increased
Produces changes in (B) increased pulse pressure because heart rate is increased
DROMOTROPIC EFFECT (C) decreased pulse pressure because ventricular filling time is
Conduction Velocity
VENTRICULAR increased
(D) decreased pulse pressure because stroke volume is decreased
Inotropes affect: CONTRACTION
(E) decreased pulse pressure because the PR interval is increased
(STROKE VOLUME) 3-6. Costanzo LS. BRS Physiology. 7th ed. 2019
Remember the formula for Pulse Pressure is not just systolic
Chronotropes affect: SA NODE (HEART RATE) pressure – diastolic pressure. The other formula is SV/arterial
AV NODE compliance. During extrasystolic beat (PVC), SV decreases due to
Dromotropes affect: premature contraction that lead to decreased ventricular filling
(CONDUCTION VELOCITY)
time. Decreased SV means decreased pulse pressure (PP =
Dromotropes are affected by: INWARD CALCIUM CURRENT SV/arterial compliance again).
STRONGER Dr. Banzuela
(positive inotrope), An electrocardiogram (ECG) on a person shows ventricular extrasystoles.

Beta-1 stimulation of the BRIEFER (positive lusitrope) After an extrasystole, the next “normal” ventricular contraction produces
(A) increased pulse pressure because the contractility of the
heart would cause: & MORE FREQUENT
ventricle is increased
(positive chronotrope) (B) increased pulse pressure because total peripheral resistance (TPR)
CONTRACTIONS is decreased
Caffeine is an example of a positive chronotropic agent. It acts by inhibiting (C) increased pulse pressure because compliance of the veins is
phosphodiesterase (PDE). decreased
Dr. Banzuela (D) decreased pulse pressure because the contractility of the ventricle
✔GUIDE QUESTION is increased
(E) decreased pulse pressure because TPR is decreased
Myocardial contractility is best correlated with the intracellular 3-7. Costanzo LS. BRS Physiology. 7th ed. 2019
concentration of After PVC, there is increased ventricular filling time, increasing SV.
(A) Na+ (D) Cl− This will increase Pulse pressure (PP = SV/arterial compliance
(B) K+ (E) Mg2+ once again)
(C) Ca2+ th
Dr. Banzuela
An increase in contractility is demonstrated on a Frank–Starling diagram:
Remember – Calcium is to Muscle what Spinach is to Popeye.
Dr. Banzuela (A) by increased cardiac output for a given end-diastolic volume
FACTORS THAT CAUSES POSITIVE INOTROPISM (B) by increased cardiac output for a given end-systolic volume
(C) by decreased cardiac output for a given end-diastolic volume
• Increased Heart Rate
(D) by decreased cardiac output for a given end-systolic volume
o The greater the number of AP, the greater the intracellular Ca2+
AUTONOMIC EFFECTS ON HEART AND BLOOD VESSELS
released from SR, the greater the cardiac contractility, e.g.
§ Positive Staircase / Bowditch Staircase / Treppe • Sympathetic NS
- the faster the heart beats, the stronger the heart beatso HR, Conduction Velocity (AV Node) and Cardiac Contractility: ↑
§ Postextrasystolic Potentiation (in Premature Ventricular via β1
Contraction (PVC) or Extrasystole) o Skin and splanchnic arterioles, veins: vasoconstrict via 𝛼1
- The next normal beat immediately after PVC will have o Skeletal muscle arterioles: vasodilate via 𝜷2
o Ephedrine effects: tachycardia, palpitations, arteriolar
greater force of contraction due to greater Ca influx due to
increased ventricular filling time smooth muscle contraction leading to vasoconstriction
• Parasympathetic NS
o HR, Conduction Velocity (AV Node) and Atrial Contractility: for computing for CO → the Fick Equation. Wag kalimutan yang Fick
↓ via M2 Equation na yan.
Dr. Banzuela
o Little to no effect on blood vessels
✔GUIDE QUESTION ✔GUIDE QUESTIONS
Which receptor mediates constriction of arteriolar smooth muscle? A hospitalized patient has an ejection fraction of 0.4, a heart rate of 95
(A) α1 Receptors (C) β2 Receptors beats/min, and a cardiac output of 3.5 L/min. What is the patient’s end-
(B) β1 Receptors (D) Muscarinic receptors diastolic volume?
(A) 14 mL (D) 92 mL
Remember our discussion in the Neuro module. Alpha-1 causes (B) 37 mL (E) 140 mL
smooth muscle contraction. Beta-2 causes smooth muscle (C) 55 mL 3-59. Costanzo LS. BRS Physiology. 7 ed. 2019 th
relaxation. Alpha-1 causes vasoconstriction. Beta-2 causes

vasodilation. EF = SV/EDV
Dr. Banzuela EDV = SV/EF
CO = HR x SV
SV = CO/HR = 3500/95 = 36.8mL
3.4 CARDIAC OUTPUT EDV = 36.8/0.4 = 92mL
Listen to this audio guide while reading the section below on preload, Dr. Banzuela
afterload, FSM and BR: The following measurements were obtained in a male patient:
Central venous pressure: 10 mm Hg
Heart rate: 70 beats/min
PRELOAD, AFTERLOAD, Pulmonary vein [O2] = 0.24 mL O2/mL
FSM AND BR Pulmonary artery [O2] = 0.16 mL O2/mL
https://qrs.ly/e3cmrpg Whole body O2 consumption: 500 mL/min
What is this patient’s cardiac output?
Dr. Banzuela
(A) 1.65 L/min (D) 6.25 L/min
(B) 4.55 L/min (E) 8.00 L/min
LENGTH-TENSION RELATION IN THE VENTRICLES (C) 5.00 L/min 3-28. Costanzo LS. BRS Physiology. 7 th ed. 2019
• Cardiac Preload:
o Equivalent to End-Diastolic Volume (EDV), which in turn is
influenced by R Atrial Pressure
§ ↑ Preload → ↑ Cardiac Output (by increasing SV) Fick Equation – don’t forget it. =)
• Cardiac Afterload: Dr. Banzuela
If the ejection fraction increases, there will be a decrease in
o Equivalent to Aortic Pressure for the L ventricle, and (A) cardiac output (D) pulse pressure
Pulmonary Artery Pressure for the R ventricle (B) end-systolic volume (E) stroke volume
§ Inversely proportional to velocity of contraction at fixed (C) heart rate 3-5. Costanzo LS. BRS Physiology. 7 th ed. 2019
muscle length
EF = SV/EDV. An increase in SV will cause an increase in EF. When
§ ↑ Afterload → ↓ Cardiac Output (by increasing resistance to SV increases, there will be less blood in the ventricles after
ventricular outflow) contraction → decreased ESV. That’s why B is the answer here.
• Frank-Starling Mechanism Dr. Banzuela
o ↑ Venous Return (VR) → ↑ R Atrial Pressure → ↑ EDV (Preload)

→ ↑ Stretch of cardiac sarcomeres (↑ ventricular fiber length) → • Stroke work
greater force of contraction (due to greater tension) → ↑ SV → o Work heart performs on each beat
↑CO o Main Energy for Stroke Work: Fatty Acids
• Bainbridge Reflex • Cardiac O2 consumption
o ↑ Venous Return (VR) → ↑ R Atrial Pressure → stimulates o Directly related to amount of tension developed by ventricles
cardiopulmonary baroreceptors (low-pressure receptors) → o Increased by an increase in the following: afterload, size of the
↑HR → ↑CO heart, contractility, heart rate
FRANK-STARLING MECHANISM VS. ✔GUIDE QUESTION

MNEMONICS
BAINBRIDGE REFLEX Which of the following changes will cause an increase in myocardial O2
consumption?
Frank-Starling Mechanism Bainbridge Reflex (A) Decreased aortic pressure
↑ VR → ↑ SV → ↑ CO ↑ VR → ↑ HR → ↑ CO (B) Decreased heart rate
(C) Decreased contractility
IMPORTANT CARDIO CONCEPTS (D) Increased size of the heart
(E) Increased influx of Na+ during the upstroke of the action potential
• Stroke Volume 3-46. Costanzo LS. BRS Physiology. 7th ed. 2019
o Blood ejected by the ventricle per heart beat
o Equal to EDV - ESV
o Normal Value: 70mL
3.5 CARDIAC CYCLE
Watch these 2 videos on the cardiac cycle while reading the corresponding
• Ejection Fraction
portions of the handout below:
o Percentage of EDV that is actually ejected by the ventricle
o Equal to SV/EDV
o Normal value: 55%
• Cardiac Output
o Total blood volume ejected per unit of time
o Equal to HR x SV
o Normal value: 5L/min (resting) CARDIAC CYCLE PART 1/2 CARDIAC CYCLE PART 2/2
https://qrs.ly/umcmrph https://qrs.ly/fqcmrpx
Dr. Banzuela
FICK EQUATION
• Alternative way of computing for cardiac output
• Cardiac events that occur in a single heartbeat illustrated in the
Wigger Diagram
• CO = Cardiac Output • Wigger Diagram has the following components:
• VO2 = steady state Oxygen Consumption by the body o Heart Sounds (Phonocardiogram)
• AVO2 = difference in arterial O2 content and mixed venous O2 o ECG
content o Ventricular Volume Curve
Remember the formulas above. SV = EDV-ESV. EF = SV/EDV. Do NOT o Ventricular Pressure Curve
confuse the formula for EF with Pulse Pressure (PP). PP = SV/arterial o Atrial Pressure Curve
compliance. Finally, please remember that there is an alternative formula o Aortic Pressure Curve
7 PHASES OF THE CARDIAC

CYCLE
1. Atrial Contraction/ Systole
(occurs during distal third of
diastole)
2. Isovolumic Contraction
3. Rapid Ventricular Ejection
4. Slow/Reduced Ventricular
Ejection
5. Isovolumic Relaxation
6. Rapid Ventricular Filling
(occurs during early third of
diastole)
7. Slow/Reduced Ventricular
Filling (occurs during middle
third of diastole)
1. ATRIAL CONTRACTION 4. REDUCED VENTRICULAR EJECTION

• Occurs during the distal third of diastole • ECG: T-wave occurs
• NOT essential for ventricular filling • Ventricular Pressure: Decreases
• ECG: preceded by p-wave • Ventricular Volume: Decreases
• Atrial Pressure: Increases slightly • Aortic pressure: decreases because of runoff of blood from large
• Ventricular Pressure: Increases slightly arteries to smaller arteries
• Ventricular Volume: Increases slightly 5. ISOVOLUMIC RELAXATION
• Atrial Pressure curve: a-wave seen • ECG: preceded by t-wave
• Heart Sounds: 4th heart sound maybe heard due to atria o aortic valve closes during this portion of the ECG: T-wave
contracting against stiff ventricles (e.g. in LV hypertrophy) o Atrial Pressure Curve: v wave seen
• Atrial Fibrillation is most likely accompanied by increase in: Left • Ventricular Pressure: rapidly decreases but Ventricular
Atrial Pressure. Ventricular fibrillation in comparison leads to Pressure > Atrial Pressure
fatal arrhythmia o AV valves are still closed
o No blood flow from Atria to Ventricles
2. ISOVOLUMIC CONTRACTION • Ventricular Volume: remains the same
• ECG: preceded by QRS complex • Ventricular Pressure < Aortic Pressure
• Atrial Pressure Curve: c wave is seen o Semilunar valves will close
• Ventricular Pressure: Increases but Ventricular Pressure is still • Heart Sounds: S2 is heard (physiologic split S2: occurs during
< Aortic Pressure inspiration)
o Semilunar valves are still closed • Aortic Pressure Curve: Incisura / Dicrotic Notch seen
§ Blood will NOT flow from LV to Aorta
6. RAPID VENTRICULAR FILLING
• Ventricular Volume: remains the same
• Ventricular Pressure > Atrial Pressure • Ventricular Pressure: rapidly decreases to a point that it is now
o AV valves will close less than Atrial Pressure
• Heart Sounds: S1 will be heard o Opening of the AV valves
§ Blood rapidly flows from Atrium to Ventricles
Remember: if Aortic Pressure > Ventricular Pressure, there is no • Heart Sounds: 3rd Heart sound may be heard (due to rapid
ventricular ejection (no outflow of blood from the ventricle. Ventricular
Pressure > Aortic Pressure if you want ejection of blood from the
ventricular filling)
ventricles. • Ventricular Volume: rapidly increases
Dr. Banzuela
7. REDUCED VENTRICULAR FILLING (DIASTASIS)
3. RAPID VENTRICULAR EJECTION
• Longest phase of the cardiac cycle
• Atrial filling begins
o Dependent on heart rate
• Ventricular Pressure: rapidly increases to a point that it is now
• Ventricular Volume: Reduced increase
greater than Aortic Pressure
o Semilunar valves open MNEMONICS CARDIAC CYCLE
§ Blood will flow from LV to aorta 3 Instances when Atrial Pressure Increases
• Ventricular Volume: rapidly decreases a wave: atrial contraction
c wave: contraction of ventricles, carotid pulsation; closed TV
• during ventricular ejection, pressure difference is smallest in
magnitude between: L Ventricle and Aorta bulging into right atrium
v wave: venous blood going to atria
Vp Vv
DIASTOLE
late (3/3)
1. Atrial Non-compliant P wave a

S4 ↑ ↑
Contraction ventricular (atrial depolarization) wave
2. Isovolumic Closure of AV VP < AoP QRS complex (ventricular c

S1 ↑↑ Ø
Contraction valves VP > AP depolarization) wave
3. Rapid VP > AoP
Ventricular Opening of ↑ ↓↓
SYSTOLE
Ejection SL valves
4. Slow T wave
Ventricular (ventricular ↓ ↓
Ejection repolarization)
5. Isovolumic Closure of SL VP < AoP v INCISURA
S2 ↓↓ Ø
Relaxation valves VP > AP wave (dicrotic notch)
early (1/3)
DIASTOLE
6. Rapid VP < AP
Rapid ventricular
Ventricular S3 Opening of ↑ ↑↑
filling
Filling AV valves
DIASTOLE
mid (2/3)
7. Slow
Ventricular Ø ↑
Filling
NOTES: VP = Ventricular pressure; VV = Ventricular volume; AP = Atrial pressure; AoP = Aortic pressure; ECG = electrical → mechanical
Contributed by Jake Bryan Cortez, MD
✔GUIDE QUESTIONS PHYSIOLOGICALLY SPLIT S2

During which phase of the cardiac cycle does the mitral valve open?
(A) Atrial systole
(B) Isovolumetric ventricular contraction
(C) Rapid ventricular ejection
(D) Reduced ventricular ejection
(E) Isovolumetric ventricular relaxation
The correct answer is actually at the END of isovolumic

ventricular relaxation (or the start of rapid ventricular filling)
Dr. Banzuela
During which phase of the cardiac cycle is aortic pressure highest?
(A) Atrial systole
(B) Isovolumetric ventricular contraction
(C) Rapid ventricular ejection
(D) Reduced ventricular ejection
(E) Isovolumetric ventricular relaxation
The correct answer is actually BETWEEN rapid ventricular
ejection and reduced ventricular ejection. • Common ECG finding in Paradoxical Splitting of the 2nd heart
Dr. Banzuela sound (P2 comes before A2): Left Bundle Branch Block
During which phase of the cardiac cycle is ventricular volume lowest?
(A) Atrial systole Whenever you inhale, there is a decrease in intrathoracic pressure. This
(B) Isovolumetric ventricular contraction decreased intrathoracic pressure has an effect not just on the lungs but also
(C) Rapid ventricular ejection on the blood vessels going to the left and right atrium. It increases the
(D) Reduced ventricular ejection venous return of the Right, decreases the venous return on the Left.
(E) Isovolumetric ventricular relaxation Increased blood in the R atrium and consequently R ventricle will delay
3-45. Costanzo LS. BRS Physiology. 7th ed. 2019 closure of pulmonic valve. Decreased blood in the L atrium and
consequently the L ventricle will result in earlier closure of the aortic valve.
HEART SOUNDS The earlier closure of the aortic valve coupled with the delayed closure of
the pulmonic valve will result in the splitting of the second heart sound
HEART
CAUSE PHASE (remember – the second heart sound is caused by the closure of the
SOUND semilunar valves – the aortic and pulmonic valves).
• Isovolumic Dr. Banzuela
S1 • Closure of AV Valves
Contraction ✔GUIDE QUESTION
S2 Inspiration “splits” the second heart sound because
(split • Isovolumic (A) the aortic valve closes before the pulmonic valve
• Closure of Semilunar Valves
during Relaxation (B) the pulmonic valve closes before the aortic valve
inspiration) (C) the mitral valve closes before the tricuspid valve
(D) the tricuspid valve closes before the mitral valve
• Rapid Ventricular Filling
(E) filling of the ventricles has fast and slow components
• (Normal in children, young 3-23. Costanzo LS. BRS Physiology. 7th ed. 2019
• Rapid
adults, pregnant patients;
S3 Ventricular
• L-Sided S3 in patients with MURMURS AND LOCATIONS
Filling
CHF indicative of CV MURMUR LOCATION BEST HEARD
morbidity, mortality) Aortic Valve 2nd ICS R Parasternal
• Stiff Ventricles / Vibration • Atrial Pulmonary Valve 2nd ICS L Parasternal
S4 in the ventricular wall Contraction/ Tricuspid Valve 4th-5th ICS L Parasternal
during systole Systole Mitral Valve 5th ICS L MCL
ANS EFFECT ON THE HEART AND BLOOD VESSELS
SYMPATHETIC PARASYMPATHETIC
Effect Receptor Effect Receptor
Heart Rate ↑ 𝛽1 ↓ M2
Conduction
Velocity (AV ↑ 𝛽1 ↓ M2
Node)
↓ (atria
Contractility ↑ 𝛽1 M2
only)
VASCULAR SMOOTH MUSCLE
Skin, Dilation
Constriction 𝛼1 M3
splanchnic (EDRF)
Skeletal Dilation
Muscle (EDRF)
Dilation 𝛽2 - -
Veins Constriction 𝛼1 - -
Regarding the location of heart murmurs – we have a classic mnemonic for ✔GUIDE QUESTIONS
this when we were first year medical students: “Always Pray To Mary” Which receptor mediates slowing of the heart?
(with your hand going in a “z” direction. See pic above). Eventually my (A) α1 Receptors (C) β2 Receptors
classmates changed this to “Ayos Pare, Tagay Muna” =) (B) β1 Receptors (D) Muscarinic receptors
Dr. Banzuela
VALVULAR LESIONS Which muscarinic receptor? M1, M2 or M3? Answer: M2. Ginawa nyo
CASE DESCRIPTION VALVULAR LESION yung mnemonic natin in your head sa neuro module, right? J
Dr. Banzuela
66/M has diastolic murmur over L
AORTIC Propranolol has which of the following effects?
sternal border, decreased diastolic (A) Decreases heart rate
REGURGITATION
pressure, increased pulse pressure: (B) Increases left ventricular ejection fraction
41/M IV drug user has early systolic (C) Increases stroke volume
murmur. Distance between the height TRICUSPID (D) Decreases splanchnic vascular resistance
of the blood in the R IJV and sternal REGURGITATION (E) Decreases cutaneous vascular resistance
angle is 7cm (normal is 3cm): When propranolol is administered, blockade of which receptor is
67/M with RHD presents with difficulty responsible for the decrease in cardiac output that occurs?
breathing while exercising. (+) (A) α1 Receptors (D) Muscarinic receptors
MITRAL
holosystolic murmur at the L 5th ICS (B) β1 Receptors (E) Nicotinic receptors
REGURGITATION (C) β2 Receptors 3-44. Costanzo LS. BRS Physiology. 7 th ed. 2019
MCL. Murmur loudest at the apex,
(WITH INCREASED
radiates to axilla, enhanced during Listen to this audio recording while reading about the Baroreceptor Reflex
V WAVE)
expiration, and when patient is part:
instructed to make a fist:
75/F with exertional dyspnea, and
episode of syncope while dancing with BARORECEPTOR REFLEX
her husband. (+) prominent systolic AORTIC STENOSIS https://qrs.ly/zwcmrq3
ejection click and crescendo- (WITH DECREASED
decrescendo murmur over the R sternal PULSE PRESSURE) Dr. Banzuela
border that radiates to the carotid
✔GUIDE QUESTIONS
arteries: Following a sympathectomy, a 66-year-old man experiences orthostatic
The table above contains classic descriptions for valvular lesions. hypotension. The explanation for this occurrence is
Understand and remember them. Pinakaimportante yung sa aortic (A) an exaggerated response of the renin–angiotensin–aldosterone
regurgitation/insufficiency. If you see murmur with “wide pulse pressure” system
(or a BP reading na sobrang taas ng systolic pressure and sobrang baba ng (B) a suppressed response of the renin–angiotensin–aldosterone
diastolic pressure, e.g. BP=150/20), think Aortic Regurgitation. system
Dr. Banzuela (C) an exaggerated response of the baroreceptor mechanism
(D) a suppressed response of the baroreceptor mechanism
3.6 REGULATION OF BLOOD PRESSURE An acute decrease in arterial blood pressure elicits which of the following
BP CONTROL compensatory changes?
Vasomotor Area of the Medulla (A) Decreased firing rate of the carotid sinus nerve
o Center responsible for regulation of HR and BP (B) Increased parasympathetic outflow to the heart
o Found in the Medulla (C) Decreased heart rate
(D) Decreased contractility
§ Lateral Portion: Excitatory Area (↑ HR & BP)
(E) Decreased mean systemic pressure
§ Medial Portion: Inhibitory Area (↓ HR & BP) 3-21. Costanzo LS. BRS Physiology. 7th ed. 2019
o Controlled by the Hypothalamus and other higher nervous
centers BP CONTROL
Acute Control • Baroreceptors
o ANS Control, Baroreceptors, Chemoreceptors, Low-Pressure o Act fast; Buffers minute-to-minute changes in BP
Receptors, CNS Ischemic Response o Stretch Receptors on the Carotid Sinus and Aortic Arch
• Long-term Control § ↑ BP → ↑ Stretch → ↑ Firing of CN IX to NTS → trigger
o Renin-Angiotensin-Aldosterone-System (RAAS) parasympathetic response
• ANS § ↓ BP → ↓ Stretch → ↓ Firing of CN IX to NTS → trigger
o Sympathetic > Parasympathetic sympathetic response
o To increase BP via ANS: o Hering nerve: branch of CN IX that carries signals from carotid
§ Arteriolar Vasoconstriction → ↑ TPR → ↑ BP sinus to NTS
§ Venous Vasoconstriction → ↑ VR → ↑ CO → ↑BP o Carotid Baroreceptors: respond increase/decrease in
§ ↑ HR & SV via 𝜷1 Receptors of the Heart → ↑ CO → ↑ BP pressures from 50mmHg-180 mmHg
Medulla contains the vasomotor center. This is the center that controls BP o Aortic Baroreceptors: respond to increase in pressure
and HR. if you shoot someone between the eyes and it destroys the medulla, >80mmHg
the person will surely die because of the destruction of the vasomotor o Set Point for MAP in Vasomotor Center: 100mmHg
center – wala nang BP at HR yan. o Post-op patient suddenly stands up after being supine. This will
Dr. Banzuela
increase: heart rate
RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM (RAAS)

• Activated first before RAAS: Baroreceptor Reflex
• Senses decrease in NaCl delivery in the DCT: Macula Densa
• Macula Densa: stimulates Juxtaglomerular (JG) Cells (also called
Granular Cells) to release Renin
o also increases renin secretion: sympathetic nerve activity (via
𝛽1 receptors)
• Renin → converts Liver Angiotensinogen to Angiotensin I
• Lung ACE: converts Angiotensin I to Angiotensin II
• Angiotensin II Effects:
o Maintains (PRESERVES) normal GFR (vasoconstricts Efferent >
Afferent)
o Vasoconstricts systemic arterioles → ↑TPR
o Stimulates Aldosterone secretion by zona glomerulosa of the
adrenal cortex
o ↑ Na+-H+ exchange in the PCT → contraction alkalosis
o ↑ thirst and ADH secretion → ↑ intravascular volume
o ↑ Epi, NE, Cortisol secretion → vasoconstricts arterioles
• Aldosterone Effects on the KIDNEYS:
o Na+ reabsorption
o K+ secretion
o H+ secretion
✔GUIDE QUESTIONS
• Valsalva Maneuver
Which agent is released or secreted after a hemorrhage and causes an
o Expiring against closed Glottis → ↑ Intrathoracic Pressure →
increase in renal Na reabsorption?
↓VR → ↓ CO and BP → sensed by BR → ↑HR (A) Aldosterone (D) Antidiuretic hormone (ADH)
o Once you stop Valsalva Maneuver → sudden rebound ↑ in VR, (B) Angiotensin I (E) Atrial natriuretic peptide
CO and BP → sensed by BR → âHR (C) Angiotensinogen 3-57. Costanzo LS. BRS Physiology. 7 ed. 2019 th
• Chemoreceptors A 60-year-old businessman is evaluated by his physician, who

o could also induce changes in BP determines that his blood pressure is significantly elevated at 185/130
o Responds to low O2, high CO2 concentration whenever mm Hg. Laboratory tests reveal an increase in plasma renin activity,
BP<80mmHg plasma aldosterone level, and left renal vein renin level. His right renal
vein renin level is decreased. What is the most likely cause of the patient’s
§ when chemoreceptors are stimulated, they activate
hypertension?
vasomotor centers for systemic vasoconstriction → ↑ TPR → (A) Aldosterone-secreting tumor
↑BP (B) Adrenal adenoma secreting aldosterone and cortisol
• Low-pressure Receptors (Cardiopulmonary Baroreceptors) (C) Pheochromocytoma
o In the atria and pulmonary arteries (D) Left renal artery stenosis
o Detects “fullness” of vascular system (↑ intravascular volume) (E) Right renal artery stenosis 3-49. Costanzo LS. BRS Physiology. 7 ed. 2019 th
o In response to increased intravascular volume: The L renal artery stenosis means less blood in the left kidney,
§ ↑ Atrial Natriuretic Peptide (ANP): ↑ Na+ & H2O excretion which means less blood pressure in the L kidney. This will
- in dehydration, there is ↑ ADH, ↑ Angiotensin II, stimulate the macula densa in the L kidney, triggering R-A-A-S.
↑Aldosterone, ↑ NE and ↓ ANP This would result in increased BP. The increased aldosterone
would cause negative feedback on renin production on the R
- ANP is released in response to increased atrial pressure
kidney (the normal kidney) but not on the L kidney (the abnormal
from increased blood volume kidney) resulting in decreased renin on the R and increased renin
§ ↓ Anti-Diuretic Hormone (ADH): ↑ urine output on the L.
§ Renal Vasodilation: ↑ urine output Dr. Banzuela
§ ↑ Heart Rate (Bainbridge Reflex): helps match VR w/ CO

• CNS Ischemic Response 3.7 MICROCIRCULATION AND LYMPH
o The vasomotor center itself responds directly to the ischemia EXCHANGE OF SUBSTANCES ACROSS CAPILLARIES
during low BP • Lipid-Soluble Substances
o Starts at BP<60mmHg and optimal at a BP=15-20mmHg o Simple diffusion across capillary endothelial cells
o The “last-ditch” stand: o e.g. O2 and CO2
§ All systemic arterioles vasoconstrict severely EXCEPT for
• Small Water-Soluble Substances
Coronary Vessels, Cerebral Vessels
o Uses clefts (pores) between endothelial cells
• Cushing Reaction or Cushing Reflex o e.g. water, glucose, amino acids
o Occurs in response to increased Intracranial Pressure (e.g. o Tight clefts: BBB; Wide clefts: Liver Sinusoids
following head trauma) • Large Water-Soluble Substances
o Triad: HPN, Bradycardia, Irregular Respirations
o Uses pinocytosis
o Occurs in response to increase in intracranial pressure: BP
o e.g. Proteins
increases while heart rate decreases (Cushing Reaction)
• Long-term Control Wag niyo deadmahin yung nakasulat sa taas. Lipid-soluble substances –
simple diffusion across capillaries. Small water-soluble substances –
o Renin-Angiotensin-Aldosterone-System (R-A-A-S)
clefts/pores across capillaries. Large water-soluble substances –
o Slow: Takes 20 minutes to take effect; takes several hours for pinocytosis (cellular drinking).
optimal effects Dr. Banzuela
o Activated when faster mechanisms (e.g. baroreceptors) fail to ✔GUIDE QUESTION

regulate BP Which of the following substances crosses capillary walls primarily
o Also responsible for maintaining normal BP despite wide through water-filled clefts between the endothelial cells?
variation in salt intake (A) O2 (C) CO
(B) CO2 (D) Glucose
Listen to the audio recording on RAAS as you read the next section: 3-47. Costanzo LS. BRS Physiology. 7th ed. 2019
Listed to the audio recording while reading the next section on Starling
RAAS Forces:
https://qrs.ly/qecmrqi
STARLING FORCES
Dr. Banzuela https://qrs.ly/vbcmrqo
Dr. Banzuela
STARLING FORCES • Lymph Flow is increased by
• Describes fluid movement into (absorption) or out of (filtration) o Massage secondary to extremity muscle contractions
the capillary o Negative intrathoracic pressure during inspiration
o Suction effect of high velocity flow of blood in the veins
o Increased capillary permeability
• Lymph Flow will be decreased if there is an increase in: Capillary
Oncotic Pressure (remember lymph flow is proportional to
capillary filtration)
EDEMA
• Excess fluid in the interstitial spaces beyond the capability of the
lymphatic system to return in to the blood vessels
CAUSES OF EDEMA EXAMPLES
• Arteriolar dilatation
• Venous constriction
STARLING EQUATION ↑ Capillary
• ↑ venous pressure
• Fluid Movement (Jv) Hydrostatic
• Heart failure
o if Positive, promotes filtration (fluid moves out of the capillary) Pressure
• ECF volume expansion
o If Negative, promotes absorption (fluid moves into the
capillary) • Standing
• âplasma protein concentration
↓ Capillary Oncotic • Severe liver disease
Pressure • Protein malnutrition
• Nephrotic syndrome
• Burns
↑ Filtration
• Inflammation (due to release of
Coefficient
histamine, cytokines)
Focus on the causes of edema above. Importante lahat yan. Some key
STARLING FORCES points: Right-Sided heart failure btw will cause PERIPHERAL edema, while
Left-Sided heart failure will cause PULMONARY edema. Kwashiorkor
STARLING NORMAL
DESCRIPTION syndrome (a form of protein malnutrition) can cause edema because of
FORCES VALUE decreased albumin synthesis resulting in decreased capillary oncotic
Capillary • Favors filtration; pressure.
Hydrostatic • determined by pressure & • 25mmHg Dr. Banzuela
Pressure resistance in arteries & veins ✔GUIDE QUESTION

• Opposes filtration (favors The tendency for edema to occur will be increased by
Capillary (A) arteriolar constriction
absorption);
Oncotic • 28mmHg (B) increased venous pressure
• increased by increases in
Pressure (C) increased plasma protein concentration
plasma protein concentration (D) muscular activity 3-22. Costanzo LS. BRS Physiology. 7th ed. 2019
• Opposes filtration (favors
Interstitial
absorption); 3.8 SPECIAL CIRCULATIONS
Hydrostatic • -3mmHg
• slightly negative due to CONTROL OF BLOOD FLOW
Pressure
lymphatic pump • Maybe Intrinsic (Local) or Extrinsic (Hormonal/Humoral)
Interstitial • Favors filtration; REASONS FOR LOCAL CONTROL OF BLOOD FLOW
Oncotic • determined by interstitial • 8mmHg • For the tissues to get their proper amounts of oxygen and
Pressure protein concentration nutrients and to remove wastes
• Hydraulic conductance of • For thermoregulation (e.g. in the skin)
Filtration capillary wall (capillary • For homeostasis (e.g. kidneys)
-
Coefficient permeability;
• promotes filtration) Blood Flow to Different Organs
Normal Net and Tissues under Basal Conditions
- • 2mL/ min mL/min
Filtration Percent mL/min
100g
✔GUIDE QUESTIONS Brain 14 700 50
In a capillary, Pc is 30mmHg, Pi is –2mmHg, πc is 25mmHg, and πi is
Heart 4 200 70
2mmHg. What is the direction of fluid movement and the net driving
force? Bronchi 2 100 25
(A) Absorption; 6 mm Hg Kidneys 22 1100 360
(B) Absorption; 9 mm Hg Liver 27 1350 95
(C) Filtration; 6 mm Hg Portal (21) 1050
(D) Filtration; 9 mm Hg Arterial (6) 300
(E) There is no net fluid movement
3-13. Costanzo LS. BRS Physiology. 7th ed. 2019 Muscle (inactive state) 15 750
In a capillary, Pc is 30mmHg, Pi is –2mmHg, πc is 25mmHg, and πi is Bone 5 250 3
2mmHg. If Kf is 0.5 mL/min/mm Hg, what is the rate of water flow across Skin (cool weather) 6 300 3
the capillary wall? Thyroid gland 1 50 160
(A) 0.06 mL/min (D) 9.00 mL/min
(B) 0.45 mL/min (E) 18.00 mL/min
Adrenal glands 0.5 25 300
(C) 4.50 mL/min 3-14. Costanzo LS. BRS Physiology. 7 ed. 2019 th
Other tissues 3.5 175 1.3
TOTAL 100.0 5000
Water flow = K f × Net pressure
= 0.5 mL/min/mm Hg × 9 mm Hg MECHANISMS FOR LOCAL BLOOD FLOW CONTROL
= 4.5 mL/min • Acute Control
Dr. Banzuela
o Decreased tissue oxygenation will increase blood flow
LYMPHATIC SYSTEM o Mechanisms for Acute Control of Local Blood Flow
• 2-3 L of lymph produced per day § Myogenic Theory: when vascular smooth muscle are
• Has one-way valves, flow is unidirectional stretched, there’s a reflex contraction and vice versa
• Functions: - May explain autoregulation, but not active or reactive
o Reabsorbs proteins and excess fluid back to the circulatory hyperemia
system § Metabolic Theory: vasodilator metabolites (Adenosine, CO2,
o Absorbs fat (using lacteals) H+, K+, lactate) are produced as a result of metabolic activity
o Contains lymph nodes increasing blood flow during hypoxia
• Acute Control: Examples of Metabolic Theory HORMONAL / HUMORAL MECHANISMS
o Reactive Hyperemia FOR BLOOD FLOW CONTROL
§ ↑ in blood flow in response to brief period of ↓ blood flow VASOCONSTRICTORS VASODILATORS
§ e.g. if vessels blocked for a few seconds to an hour → blood • Vasopressin: most potent • Prostacyclin (PGI2):
flow increases 4-7x the normal vasoconstrictor counteracts TXA2
o Active Hyperemia • Nitric Oxide (NO): vasodilates
§ Blow flow increases to meet increased metabolic demand upstream blood vessels
§ e.g. In exercising muscle, G.I. glands during hypersecretory o MOA: guanylate cyclase and
period, brain during rapid mental activity cGMP
• Acute Control: Autoregulation of Blood Flow o Acetylcholine causes
o Brain: CO2 and H+ • Serotonin: released as a
vasodilation by increasing
§ an increase will cause vasodilation to wash out excess CO2 result of blood vessel
production of NO in vascular
o Heart: Perfusion Pressure damage; causes arteriolar
smooth muscle
§ If perfusion pressure to the heart is suddenly decreased, vasoconstriction;
o Acetylcholine causes
compensatory vasodilation of arterioles would occur to implicated in migraine
VASOCONSTRICTION
maintain constant flow instead of vasodilation
§ Highest coronary blood flow per gram of L ventricular whenever the endothelium
myocardium occurs during: beginning of diastole is damaged due to
o Kidneys: Tubuloglomerular Feedback decreased NO
§ Macula densa in the distal tubule detects fluid levels • Endothelin: released by
§ Afferent arteriole constriction/dilation occurs to maintain • PGE: vasodilators
damaged endothelium
appropriate renal blood flow and GFR • Lactate, Adenosine: found in
• PGF and TXA2
Refer to the text above about Autoregulation of blood flow as you listed to muscles
this audio recording: • Bradykinin & Histamine:
causes arteriolar dilation &
AUTOREGULATION • NE, Epi venous constriction leading to
OF BLOOD FLOW increased filtration (local
https://qrs.ly/4bcmrqs edema)
• Angiotensin II • H+, CO2, K, ANP
Dr. Banzuela
Memorize the vasoconstrictors and vasodilators listed above. Key points:
• Long-term Control ADH is the most powerful vasoconstrictor of them all – it’s also called
o Via Angiogenesis VASOPRESSIN to remind you it’s a vasoconstrictor. Thromboxane A2 has
§ Due to VEGF, FGF, Angiogenin 2 effects: vasoconstriction and platelet aggregation. Its natural inhibitor is
- a drug that can stimulate production of VEGF receptors is of PROSTACYCLIN. Lactic Acid is a vasodilator released by muscles lacking
value in the treatment of Coronary Artery Disease as it oxygen (it makes sense that it’s a vasodilator – to give more blood, oxygen
would help bypass blocked arteries and glucose to the starving muscles). Lactic Acid can stimulate pain nerve
§ Occurs in response to hypoxia endings – lactic acid is the cause of chest pain in M.I. and muscle pain in
muscle fatigue. Lactic Acid is a product of ANAEROBIC glycolysis.
o Vascularity is determined by Maximum Blood Flow Need, not Dr. Banzuela
by average need
✔GUIDE QUESTION
§ A lot of capillary beds are closed most of the time, and only
Which of the following is an effect of histamine?
open needed (A) Decreased capillary filtration
(B) Vasodilation of the arterioles
EXTRINSIC CONTROL OF BLOOD FLOW (C) Vasodilation of the veins
• Through (D) Decreased Pc
o Sympathetic NS (E) Interaction with the muscarinic receptors on the blood vessels
o Vasoactive Hormones
SUMMARY OF CONTROL OF SPECIAL CIRCULATIONS
Circulation* (% of
Local Metabolic Vasoactive
Resting Cardiac Sympathetic Control Mechanical Effects
Control Metabolites
Output)
Most important Hypoxia Mechanical compression
Coronary (5%) Least important mechanism
mechanism Adenosine during systole
Increases in intracranial
Most important CO2
Cerebral (15%) Least important mechanism pressure decrease cerebral
mechanism H+
blood flow
Most important mechanism at rest
Most important Lactate Muscular activity causes
(α1 receptor causes
Muscle (20%) mechanism during K+ temporary decrease in blood
vasoconstriction;
exercise Adenosine flow
β2 receptor causes vasodilation)
Least important Most important mechanism
Skin (5%)
mechanism (temperature regulation)
Most important Hypoxia
Pulmonary+ (100%) Least important mechanism Lung inflation
mechanism vasoconstricts
Adapted from Costanzo LS. BRS Physiology. 7th ed. 2019.
Take note of the various vasoactive metabolites involved in various organs above (e.g., hypoxia and adenosine for the heart, CO2 and H+ for brain, etc.)
Dr. Banzuela
✔GUIDE QUESTIONS 3.9 GRAVITY, EXERCISE AND HEMORRHAGE

Carbon dioxide (CO2) regulates blood flow to which one of the following
organs? STANDING
(A) Heart (D) Skeletal muscle at rest • Blood pools in the veins → ↓ VR → ↓ CO → ↓BP
(B) Skin (E) Skeletal muscle during exercise • ↓ Baroreceptor stretch → ↓ firing rate of CN IX → ↑ Sympathetic
(C) Brain 3-39. Costanzo LS. BRS Physiology. 7 ed. 2019 th
Outflow
Blood flow to which organ is controlled primarily by the sympathetic • ↑ HR, ↑ SV → ↑ CO → ↑ BP
nervous system rather than by local metabolites? • Vasoconstriction of systemic arterioles → ↑ TPR → ↑BP
(A) Skin (C) Brain
(B) Heart (D) Skeletal muscle during exercise
• Vasoconstriction of Veins → ↑VR → ↑CO → ↑BP
✔GUIDE QUESTIONS The nostrils cause conditioning of air during inspiration (unlike breathing
When a person moves from a supine position to a standing position, through the mouth) – it will warm the air (cold air can damage respiratory
which of the following compensatory changes occurs? lining), humidify the air (dry air can damage the respiratory lining, the
(A) Decreased heart rate water vapor can act as lubricant) via the capillaries of the nose, filter the
(B) Increased contractility air (preventing large particles from obstructing/damaging the respiratory
(C) Decreased total peripheral resistance (TPR) lining), and is involve in the special sense of smell (which also has an impact
(D) Decreased cardiac output in terms of taste)
Dr. Banzuela
(E) Increased PR intervals
3-2. Costanzo LS. BRS Physiology. 7th ed. 2019 SINUSES
A 24-year-old woman presents to the emergency department with severe • Frontal sinuses, Maxillary sinus, Sphenoid sinus, Ethmoid sinus
diarrhea. When she is supine (lying down), her blood pressure is 90/60
o Surround nasal passageways
mm Hg (decreased) and her heart rate is 100 beats/min (increased).
When she is moved to a standing position, her heart rate further • FUNCTIONS: Lighten the skull & offer resonance to voice
increases to 120 beats/min. Which of the following accounts for the
further increase in heart rate upon standing?
(A) Decreased total peripheral resistance
(B) Increased venoconstriction
(C) Increased contractility
(D) Increased afterload
(E) Decreased venous return
EXERCISE
• ↑ Sympathetic outflow → ↑ HR, ↑ SV → ↑ CO → ↑ blood flow to
skeletal muscles
o during exercise, blood flow to:
§ Brain (cerebral blood flow): remains constant
§ Heart (coronary blood flow), skin: increased
§ Gut, kidneys, non-exercising muscles: decreased
• Increase in cardiac output during exercise is due to a LARGE
increase in heart rate and a SMALL increase in stroke volume
• Vasoconstriction of splanchnic and renal arterioles → ↑ blood
flow to skeletal muscles
• Vasoconstriction of veins → ↑ VR → ↑ CO → ↑ blood flow to skeletal
muscles © Topnotch Medical Board Prep
• ↑vasodilator metabolites → vasodilation of skeletal muscle LARYNX

arterioles → ↓ TPR → ↑blood flow to skeletal muscle • MAJOR STRUCTURES
✔GUIDE QUESTION o Vocal Cords: Protects the airway form choking, Produces sounds
During exercise, total peripheral resistance (TPR) decreases because of used for speech
the effect of o Epiglottis, Arytenoids: Covers vocal cords during swallowing
(A) the sympathetic nervous system on splanchnic arterioles
(B) the parasympathetic nervous system on skeletal muscle arterioles
(C) local metabolites on skeletal muscle arterioles
(D) local metabolites on cerebral arterioles
(E) histamine on skeletal muscle arterioles
Which of the following parameters is decreased during moderate
exercise?
(A) Arteriovenous O2 difference
(B) Heart rate
(C) Cardiac output
(D) Pulse pressure
(E) Total peripheral resistance (TPR)
HEMORRHAGE
• ↑ BRR → ↑ HR, ↑ SV, ↑ TPR, ↑ vasoconstriction of veins (↑ VR) →
↑BP
• ↑ RAAS activation → ↑ Na+ reabsorption → ↑ intravascular volume
→ ↑ BP
• ↓ Systemic Capillary Hydrostatic Pressure → ↑ fluid absorption →
↑ intravascular volume → ↑ BP
TRACHEA
4. RESPIRATORY PHYSIOLOGY • In the trachea, C-shaped cartilages are found anteriorly
1. Functional Anatomy of the Respiratory System
2. Lung Volumes and Capacities
3. Mechanics of Breathing
4. Gas Exchange
5. Oxygen Transport
6. CO2 Transport
7. Pulmonary Circulation
8. V/Q Defects
9. Control of Breathing
10. Integrated Responses to the Respiratory System
4.1 FUNCTIONAL ANATOMY OF THE RESPIRATORY

SYSTEM
RESPIRATORY SYSTEM
UPPER AIRWAYS: Nose, Sinuses, Larynx
LOWER AIRWAYS: Trachea, Airways, Alveoli © Topnotch Medical Board Prep
Why C-shaped and not “O-shaped”? So that when you swallow, the bolus
NOSE
will cause “dilations” in the esophagus that will compress on the trachea
FUNCTIONS: Warms, humidifies, & filters air, smell, defense (the part without the cartilage) – this helps prevent aspiration).
Dr. Banzuela

TRACHEA, BRONCHI, BRONCHIOLES

• Trachea → Main Stem Bronchi → Lobar Bronchi → Segmental GOBLET CELLS, • Produces Mucus
Bronchi →→→ Terminal bronchioles → Respiratory bronchiole SUBMUCOSAL • Hyperplasia, Hypertrophy seen in
→ Alveoli GLANDS chronic smokers
o Right vs Left: Right bronchi is wider, shorter and more vertical • Non—ciliated cells of the respiratory
(hence it is more prone to aspiration of material) CLARA CELLS epithelium
(CLUB CELLS) • Produces protective GAGs and
metabolize air-borne toxins
DUST CELLS
• Engulfs respiratory pathogens &
(ALVEOLAR
foreign material (dust)
MACROPHAGES)
COUGH REFLEX (STEPS):

1. 2.5 L of air rapidly inspired
2. Epiglottis closes
3. Abdominal muscles contract
4. Epiglottis opens
• SNEEZE REFLEX
o Similar to cough reflex but applied to nasal passageways (upper
respiratory passageways)
o With depression of the uvula
LUNGS
• Weighs 1kg
o 60% lung tissue
o 40% blood
Alveolar Spaces
o Responsible for most of lung’s volume
o Divided by lung interstitium
• Gas Exchange Area: 70-85 m2
RIGHT LUNG
o 3 Lobes (Upper, Middle, Lower)
o Oblique Fissure, Horizontal Fissure
LEFT LUNG
o 2 Lobes (Upper, Lower)
o Oblique Fissure
BRONCHIOLE
o Terminal Bronchiole vs Respiratory Bronchiole: Respiratory
Bronchiole is capable of Gas Exchange
• (+) presence of Respiratory Epithelium
o Maintains periciliary fluid so that cilia may function
• Respiratory bronchiole, alveolar ducts,
alveolar sacs
These are the only 3 areas in the
respiratory system capable of gas RESPIRATORY
exchange. Be careful with terminal UNIT OF THE
bronchiole vs. respiratory bronchiole – LUNG
respiratory bronchiole is the first part of
the respiratory unit of the lung capable of
gas exchange. Not terminal bronchiole.
Dr. Banzuela
• For gas exchange; TYPE I

• Larger than Type II PNEUMOCYTE
• For surfactant production; TYPE II
• Smaller than Type I PNEUMOCYTE
• Produces mucus for lubrication in the
GOBLET CELLS
respiratory system
• Produces protective GAGs and metabolize CLARA CELLS /
air-borne toxins CLUB CELLS
• Alveolar Macrophages DUST CELLS
© Topnotch Medical Board Prep When you see the term “dead space” in physio, it means an area with no gas
• VISCERAL PLEURA exchange. Normal Anatomic dead space is 150mL – physiologically, there
• PARIETAL PLEURA is no gas exchange from the nose to the trachea to the terminal bronchioles.
Normal Alveolar Dead Space meanwhile is 0mL – physiologically, all alveoli
• PLEURAL FLUID should be capable of gas exchange, therefore alveolar dead space should
o Found in potential space between the two pleura ideally be zero. Physiologic dead space is just the sum of anatomic dead
o Keeps the 2 pleura together (allows them to slide) space and alveolar dead space.
o Has negative pressure Dr. Banzuela
• Physiologic Dead Space: (calculated using BOHR EQUATION):
ALVEOLI
• TYPE I PNEUMOCYTE
o 96-98% of surface area
o For Gas Exchange
• TYPE II PNEUMOCYTE
o 2-4% of surface area
o Small, cuboidal, found at corners of alveoli
o May turn into Type I if needed
o For Surfactant production • Minute Ventilation:
§ Decreases surface tension (preventing alveolar collapse)
• Alveolar Ventilation:
Alveolar Ventilation is also called CORRECTED MINUTE VENTILATION. Its

formula is basically minute ventilation minus physiologic dead space.
Dr. Banzuela
✔GUIDE QUESTION
A healthy 65-year-old man with a tidal volume (TV) of 0.45 L has a
breathing frequency of 16 breaths/min. His arterial PCO2 is 41 mm Hg,
and the PCO2 of his expired air is 35 mm Hg. What is his alveolar
ventilation?
(A) 0.066 L/min (D) 6.14 L/min
© Topnotch Medical Board Prep (B) 0.38 L/min (E) 8.25 L/min
(C) 5.0 L/min th
4.2 LUNG VOLUMES AND CAPACITIES Computation:

VA = (VT-VD) x RR
SPECIAL NOTES ON RESPIRATORY PHYSIOLOGY VD = VT x (PaCO2 x PeCO2)/PaCO2
DESCRIPTION ANSWER = (0.45) x (41-35)/41
• Air from the Nose to Terminal =0.066L
Bronchioles (conducting zone) that does ANATOMIC VA = (0.45 – 0.066L) x 16 = 6.14L/min
NOT undergo gas exchange DEAD SPACE
• (Normal Value: 150 mL) LUNG VOLUMES AND CAPACITIES
• Air in the respiratory unit of the lung • Air in lungs is divided into:
o Lung Volumes: IRV, TV, ERV, RV
(respiratory zone) that does NOT
ALVEOLAR o Lung Capacities: Sum of 2 or more lung volumes:
undergo gas exchange due to V/Q
DEAD SPACE § IC, FRC, VC, TLC
mismatch
• Lung volumes and Capacities: 20-25% lower in females
• (Normal Value: 0 mL)
• Anatomic + Alveolar Dead Space.
PHYSIOLOGIC
Normally EQUAL to Anatomic Dead
DEAD SPACE
Space Value
FUNCTIONAL
• Bronchopulmonary Segments (segmental ANATOMIC
bronchi to alveoli) UNIT OF THE
LUNG
While you look at this figure, watch

this video on lung volumes and
capacities:
LUNG VOLUMES
AND CAPACITIES
https://qrs.ly/ixcmrrg
Dr. Banzuela
TERM DESCRIPTION Which volume remains in the lungs after a maximal expiration?
• Air inspired over and above the tidal volume; (A) Tidal volume (TV)
IRV (B) Vital capacity (VC)
• Utilized during exercise
(C) Expiratory reserve volume (ERV)
• Amount of air inhaled or exhaled during the (D) Residual volume (RV)
relaxed state. (E) Functional residual capacity (FRC) From Physiology BRS, 6 Ed th
TV • Normal Value: 500mL divided into: In a maximal expiration, the total volume expired is
o anatomic dead space (150mL) (A) tidal volume (TV)
o respiratory unit of the lung (350mL) (B) vital capacity (VC)
(C) expiratory reserve volume (ERV)
• Amount of air exhaled after expiration of tidal
ERV (D) residual volume (RV)
volume (E) functional residual capacity (FRC) From Physiology BRS, 6 Ed th
• Remaining air in the lungs after maximal

exhalation;
RV FEV1 AND FVC
• Maintains oxygenation in between breaths;
• Cannot be measured by spirometry • FEV1: volume of air expired after one second of forced maximal
exhalation
IC • TV + IRV
• FVC: total volume of air expired of forced maximal exhalation
• ERV + RV;
• FEV1/FVC: normal value: 80%
• Equilibrium/resting volume of the lung;
• Marker for lung function;
FRC OBSTRUCTIVE LD RESTRICTIVE LD
• During this time, alveolar pressure =
(e.g. COPD) (e.g. Fibrosis)
atmospheric pressure;
FEV1 ↓↓ ↓
• Cannot be measured by spirometry
FVC ↓ ↓↓
• IRV + TV + ERV;
VC or FEV1/FVC ↓ Normal or ↑
• Maximum volume of air that can be inhaled or
FVC
exhaled FRC ↑ ↓
• IRV + TV + ERV + RV; The table above is very important. Obstructive Lung Diseases (OLD) have
TLC
• Cannot be measured by spirometry problems with EXPIRATION, typical examples are asthma and COPD.
Restrictive Lung Diseases (RLD) have problems with INSPIRATION, typical
✔GUIDE QUESTIONS example is lung fibrosis. In both OLD and RLD, FEV1 and FVC would
Which of the following lung volumes or capacities can be measured by decrease, but at different rates. In OLD, there is a greater decrease in FEV1
spirometry? than FVC, while for RLD, there is a greater decrease in FVC rather than
(A) Functional residual capacity (FRC) FEV1. These would result in a decrease in FEV1/FVC ratio in OLD (since
(B) Physiologic dead space mathematically, pag mas mataas yung pagbagsak ng numerator kaysa sa
(C) Residual volume (RV) denominator, bababa yung quotient) and normal or increase FEV1/FVC
(D) Total lung capacity (TLC) ratio in RLD (since mathematically, pag mas mataas yung pagbagsak ng
(E) Vital capacity (VC) From Physiology BRS, 6 Ed th
denominator kaysa sa numerator, tataas yung quotient). Wag
A spirometer is a device that can measure exhaled air. RV and lung makakalimutan: decreased FEV1/FVC ratio in OLD and increased
capacities that have RV in its formula (namely FRC and TLC), FEV1/FVC ratio in RLD.
Dr. Banzuela
cannot be measured by a spirometer. Physiologic dead space
(made up of anatomic and alveolar dead spaces) cannot also be • Primary drive to breath in COPD patients: Hypoxic Drive (low
measured using a spirometer, we use Bohr Equation for PaO2 stimulating peripheral chemoreceptors. Hypercapneic
physiologic dead space computation. drive is blunted due to compensated respiratory acidosis)
Dr. Banzuela
• PFT result in person with pulmonary fibrosis (restrictive lung
Which volume remains in the lungs after a tidal volume (TV) is expired?
(A) Tidal volume (TV)
disease): Decreasing diffusing capacity of the lung
(B) Vital capacity (VC)
(C) Expiratory reserve volume (ER) 4.3 MECHANICS OF BREATHING
(D) Residual volume (RV)
MUSCLES INVOLVED IN PULMONARY VENTILATION
(E) Functional residual capacity (FRC)
(F) Inspiratory capacity • Inspiration
(G) Total lung capacity From Physiology BRS, 6 Ed th o Normal Inspiration: Active (main muscle: Diaphragm)
If I change the question to the volume in the lungs after maximal § diaphragm descends, ribs move upward and outward,
expiration, the answer would be residual volume. Be careful and lungs become wider and taller
read the question thoroughly. I recommend you underline key o Forced Inspiration (occurs during exercise): External
words in the questions in the medical board exams. Intercostals, Accessory Muscles: SCM, Anterior Serrati,
Dr. Banzuela
Scalene, Alae Nasi, Genioglossus, Arytenoid
A 35-year old man has a vital capacity (VC) of 5 L, a tidal volume (TV) of
0.5 L, an inspiratory capacity of 3.5 L, and a functional residual capacity o Ribs move upward and outward; abdominal contents move
(FRC) of 2.5 L. What is his expiratory reserve volume (ERV)? downward
(A) 4.5 L (D) 3.0 L
(B) 3.9 L (E) 1.5 L
From Physiology BRS, 6 Ed
(C) 3.6 L th
• Expiration
o Normal Expiration: Passive
o Forced Expiration (occurs during exercise): Internal
Intercostals, Abdominal muscles (Rectus Abdominis, Internal
and External Oblique, Transversus Abdominis)
o Ribs move downward and inward; abdominal contents move
upward
Again, with feelings. Main muscle for normal inspiration: diaphragm. Main
muscle for normal expiration: none. EXTERNAL intercostals are for forced
INSPIRATION. INTERNAL intercostals are for forced EXPIRATION. Wag
mapagbaligtad ha. ACCESSORY Muscles are used also for forced
inspiration, while ABDOMINAL Muscles are used also for forced expiration.
Dr. Banzuela
COMPLIANCE OF THE LUNGS © Topnotch Medical Board Prep

• Pre-Term Babies have high collapsing pressure due to:
• Distensibility of the lungs and chest wall
o Smaller alveolar radius (50 micrometers) compared to adults
• Change in volume for a given change in pressure (analogous to o Lack mature surfactant
capacitance of vessels)
• In comparison to term infant, Pre-term infant has:
• Inversely related to elastance o INCREASED pulmonary vascular resistance, pulmonary
• Slope of the press-volume curve artery pressure (PAP), pulmonary capillary hydrostatic
o Inspiration has a different curve than expiration due to need to pressure, pressure gradient from pulmonary artery to the
overcome surface tension forces during inspiration (hysteresis) aorta
o Highest compliance: at middle range of pressures o DECREASED Pulmonary Blood Flow
o Lowest compliance: at high pressures (curve flattens here)
Remember the Law of Laplace. Collapsing pressure (P) is directly
proportional to surface tension (T) and inversely proportional to radius of
the alveoli (r). In pre-term babies, perfect storm – walang mature
surfactant kaya mataas ang surface tension; at the same time pre-term nga
kaya maliit yung mga alveoli. High T and Low r = very high P. That very
high collapsing pressure causes neonatal respiratory distress syndrome
Surfactant decreases surface tension which PREVENTS alveolar collapse
(decreased collapsing pressure)
Dr. Banzuela
LUNG SURFACTANT
DESCRIPTION ANSWER
Cells that produces
TYPE II PNEUMOCYTES
surfactant
Main component of
WATER
Surfactant
Active component of DIPALMITOYL-
Surfactant PHOSPHATIDYLCHOLINE (DPPC)
Mechanism for DPPC AMPHIPATHIC NATURE
• Lungs: has natural tendency to collapse reducing surface (HYDROPHOBIC AND
• Chest wall: has a natural tendency to expand tension HYDROPHILIC)
• At FRC: lungs and chest wall are at equilibrium Effect of Surfactant on
o Intrapleural pressure is negative INCREASE
Lung Compliance
• Pneumothorax (presence of gas in pleural space) Start of Surfactant
o Intrapleural pressure = atmospheric pressure 24TH WEEK AOG
production
§ Lungs on affected side collapses, chest wall expands Maturation of
§ V/Q ratio decreases 35TH WEEK AOG
Surfactant
§ Trachea shifts AWAY FROM THE AFFECTED LUNG Deficiency in NEONATAL RESPIRATORY
• Atelectasis (collapse of lung parenchyma) surfactant causes DISTRESS SYNDROME (RDS)
o Trachea shifts TOWARD THE AFFECTED LUNG AMNIOTIC
LECITHIN:SPHINGOMYELIN RATIO
CLINICAL CONDITIONS Test for Surfactant
(RATIO OF 2:1 OR GREATER =
• Emphysema MATURE FETAL LUNGS)
o Lung compliance is increased → new, higher FRC will be seen Treatment for
to balance tendency of chest wall to expand vs tendency of lungs STEROIDS, SURFACTANT
newborn RDS
to collapse → patient becomes barrel-chested
• Fibrosis LUNG SURFACTANT
o Lung compliance is decreased → new, lower FRC will be seen
• Helps prevent alveolar collapse
to maintain balance
• Produced by Type II Alveolar Cells
o Remember: Lung Compliance is inversely related to the elastic
recoil properties of the lung • Mixture of DPPC, other lipids and proteins
• Decreased in the lungs of chronic smokers
SURFACE TENSION ✔GUIDE QUESTION
• Force caused by water molecules at the air-liquid interface that An infant born prematurely in gestational week 25 has neonatal
tends to minimize surface area respiratory distress syndrome. Which of the following would be expected
• Law of Laplace in this infant?
(A) Arterial PO2 of 100 mm Hg
(B) Collapse of the small alveoli
(C) Increased lung compliance
(D) Normal breathing rate
(E) Lecithin:sphingomyelin ratio of greater than 2:1 in amniotic fluid
From Physiology BRS, 6th Ed
AIRWAY RESISTANCE Remember the factors that causes bronchodilation and

• Described by Poiseuille Law bronchoconstriction above.
Dr. Banzuela
BREATHING CYCLE
• Remember: lung pressures are expressed relative to atmospheric
pressure
o At FRC, alveolar pressure = 0
• Before inspiration:
o Intrapleural pressure is negative, alveolar pressure = 0
• During inspiration:
• Major site of airway resistance: medium-sized bronchi
o Intrapleural pressure becomes more negative, alveolar
(controversial: largest bronchi in Guyton and Hall)
pressure becomes more negative
• Airway resistance is increased by bronchial smooth muscle
• During expiration:
contraction, decreased if lungs are removed and inflated by saline
o Alveolar pressure increases and becomes greater than
and affected by work of breathing
atmospheric pressure
• The 3 Factors affecting Airway Resistance:
o Intrapleural pressure increases back to its resting value
o Bronchial Smooth Muscle Contraction/Relaxation due to ANS:
§ alters radius of airways (see image below) When you inhale, the contraction of the diaphragm will
cause a decrease in intrapleural pressure which will cause a decrease in
o Lung Volume
alveolar pressure. That drop in alveolar pressure will cause the alveolar
§ due to radial traction exerted on airways by surrounding lung pressure to be less than atmospheric pressure → this will lead to air moving
tissue from the atmosphere and into the alveoli. During expiration, intrapleural
§ High lung volumes → greater traction, decreased airway pressure will increase which will cause an increase in alveolar pressure.
resistance The alveolar pressure will now become greater than atmospheric pressure
§ asthmatic patients “learn” to breathe at higher volumes to causing air to move from alveoli to the atmosphere.
Dr. Banzuela
offset airway resistance
o Viscosity/Density of inspired gas
§ Low-density gas (e.g. helium) reduces resistance to airflow
✔GUIDE QUESTION
Which of the following is the site of highest airway resistance?
(A) Trachea (D) Smallest bronchi
(B) Largest bronchi (E) Alveoli
(C) Medium-sized bronchi th
✔GUIDE QUESTION
Which of the following is true during inspiration?
BRONCHIAL SMOOTH MUSCLES
(A) Intrapleural pressure is positive
• Causes Bronchodilation (B) The volume in the lungs is less than the functional residual
o Sympathetic Nervous system (adrenergic) capacity (FRC)
o Atropine (C) Alveolar pressure equals atmospheric pressure
o Vasointestinal Peptide (VIP) (D) Alveolar pressure is higher than atmospheric pressure
• Causes Bronchoconstriction (E) Intrapleural pressure is more negative than it is during
o Parasympathetic Nervous System (cholinergic) expiration From Physiology BRS, 6 th Ed
o Cool air, exercise

o Irritants (e.g., sulfur dioxide)
o Leukotrienes, Histamine
4.4 GAS EXCHANGE
PERTINENT LAWS OF PHYSICS FOR RESPIRATORY PHYSIOLOGY
𝑷𝟏 𝑽𝟏 = 𝑷𝟐 𝑽𝟐 • Law implying that an ↑ in Lung
Boyle’s Law
𝑷𝒙 = 𝑷𝑩 × 𝑭 Volume will ↓ Pressure
𝑃𝑎𝑟𝑡𝑖𝑎𝑙 𝑝𝑟𝑒𝑠𝑠𝑢𝑟𝑒 = 𝑇𝑜𝑡𝑎𝑙 𝑝𝑟𝑒𝑠𝑠𝑢𝑟𝑒 ×
Dalton’s Law of Partial Pressure 𝐹𝑟𝑎𝑐𝑡𝑖𝑜𝑛𝑎𝑙 𝑔𝑎𝑠 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 • Law for Mixed Gases
𝑪𝒙 = 𝑷𝒙 × 𝒔𝒐𝒍𝒖𝒃𝒊𝒍𝒊𝒕𝒚
Henry’s Law for Concentration of Where:
Cx = concentration of dissolved gas (mL gas/100mL blood) • Law for Gases dissolved in solution
Dissolved Gases Px = Partial pressure of gas (mmHg)
Solubility = Solubility of gas in blood (mL gas/100mL blood/mmHg
!" ∆%
𝑉𝑥 = • Law for transfer of gases through simple
diffusion in cell membranes or capillary
∆& walls
Fick’s Law of Diffusion Where: Vx = Volume of gas transferred per unit time • Driving force for diffusion: Partial
D = diffusion coefficient of the gas A = surface area Pressure difference (NOT
ΔP = partial pressure difference of the gas concentration of gases)
Δx = thickness of the membrane
• Gas exchange from alveoli into the blood uses PASSIVE DIFFUSION
PARTIAL PRESSURES OF O2 AND CO2 (mmHg)
Dry Humidified Tracheal
Gas Alveolar Air Systemic Arterial Blood Mixed Venous Blood
Inspired Air Air
150 100 Slightly <100 40
PO2 160 (Addition of water vapor (O2 has diffused due to equilibration & (O2 has diffused to tissues
decreases PO2) decreasing PO2) “physiologic shunt” decreasing PO2)
40 40 46
PCO2 0 0 (CO2 has been added due to equilibration with (CO2 has diffused from
increasing PCO2 alveolar air tissues increasing PCO2)
A major cause of cor pulmonale in COPD is a decrease in: Alveolar PO2
✔GUIDE QUESTION Movement of oxygen from alveoli to blood at rest (normal condition) is
If an area of the lung is not ventilated because of bronchial obstruction, PERFUSION-LIMITED – meaning mabilis naman yung pag transfer ng gas
the pulmonary capillary blood serving that area will have a PO2 that is from alveoli to blood, ang limitation is the number of capillaries and the
(A) equal to atmospheric PO2 blood inside it. See the graph of perfusion-limited exchange above – ang
(B) equal to mixed venous PO2 bilis maachieve yung peak early sa length ng capillary.
(C) equal to normal systemic arterial PO2 Movement of oxygen from alveoli to blood during exercise is DIFFUSION-
(D) higher than inspired PO2 LIMITED – the limiting factor is the diffusion characteristics of the gas
(E) lower than mixed venous PO2 itself, and not blood anymore. In exercise kasi, tumataas yung blood flow to
From Physiology BRS, 6 Ed th
the lungs, so hindi na perfusion-limited ang gas exchange during exercise.
ALVEOLAR-BLOOD GAS EXCHANGE Take a look at the graph of diffusion-limited gas exchange above – kahit
• Perfusion-limited Gas Exchange patapos na ng length ng capillary, hindi pa rin mataas yung peak, kasi nga
o Gas equilibrates with the pulmonary capillary near the start of even with increased blood flow doon, hindi naman nagbabago yung
the pulmonary capillary diffusing characteristics ng oxygen itself.
Dr. Banzuela
o Diffusion of gas increased only by increasing blood flow
o E.g. N2O, O2, CO2 under normal conditions 4.5 OXYGEN TRANSPORT
HEMOGLOBIN
• Oxygen (O2):
o 98%: transported via hemoglobin (Hgb)
§ Hgb has the greatest effect on the ability of blood to
transport oxygen
§ Contain highest proportion of stored oxygen in the body
o 2%: transported freely dissolved in plasma
• Hemoglobin can bind with oxygen (oxyhemoglobin), carbon
monoxide (carboxyhemoglobin) or carbon dioxide
(carbaminohemoglobin)
o Carbon Monoxide poisoning has the greatest reduction in O2
delivery to the tissues
o Characteristic of CO poisoning: normal PaO2, lower than
normal Arterial O2 saturation
• Oxygen normally binds with Fe2+(ferrous state) and not
Fe3+(ferric state)
• HbA: 𝝰2𝝱2
• HbF: 𝝰2𝝲2
• Hemoglobin S: 𝛼%& 𝛽%'
• 2,3 BPG binds more to HbA and binds less with HbF
Diffusion-limited Gas Exchange
o O2 affinity is higher in HbF than HbA (shift to the left of the O2-
o Gas Does NOT equilibrate even until the end of the pulmonary
HgB dissociation curve)
capillary
o Facilitates release of O2 from mother to fetus
o CO and O2 during strenuous exercise and disease states
• O2-binding capacity
(emphysema, fibrosis)
o Maximum amount of O2 that can be bound to Hgb
o Measured at 100% saturation
o Expressed in mL O2/gram of hemoglobin
o Normal value: 1.34
• O2 content of the blood
o Total amount of O2 carried in blood, including bound and
dissolved O2
𝑂% 𝑐𝑜𝑛𝑡𝑒𝑛𝑡 = (ℎ𝑒𝑚𝑜𝑔𝑙𝑜𝑏𝑖𝑛 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛 × 𝑂% 𝑏𝑖𝑛𝑑𝑖𝑛𝑔 𝑐𝑎𝑝𝑎𝑐𝑖𝑡𝑦
× %𝑠𝑎𝑡𝑢𝑟𝑎𝑡𝑖𝑜𝑛) + 𝐷𝑖𝑠𝑠𝑜𝑙𝑣𝑒𝑑 𝑂%
Remember: 2,3 BPG binds more to adult Hgb and binds less with HbF. 2,3
BPG binds to an allosteric site in Hgb and cause a shift to the right of the
O2-HgB dissociation curve – it causes O2 to unbind with Hgb. The
mechanism for transfer of O2 from mother to fetus is through 2,3 BPG.
Watch this video on the O2-HgB dissociation curve first, then read and
highlight the corresponding portions below:
O2-HGB DISSOCIATION CURVE

https://qrs.ly/xccmrri
© Topnotch Medical Board Prep Dr. Banzuela
O2-HgB DISSOCIATION CURVE A-a GRADIENT
• Sigmoidal in shape • Difference between Alveolar PO2 and Arterial PO2
o PO2 of 25 mmHg: 50% saturated (P50)
o PO2 of 40 mmHg: 75% saturated (mixed venous blood)
o PO2 of 100 mmHg: almost 100% saturated (arterial blood)
• Exhibits Positive Cooperativity
o Binding of first O2 molecule increases affinity for second O2
molecule and so forth
PAO2, PaO2, PACO2, PaCO2. Don’t get confused by the capital letter “A” and
the small letter “a.” Capital letter A is for “Alveolar”, small letter “a” is for
arterial. (mnemonic: “A” comes before “a”, “alveolar” comes before
“arterial” alphabetically) A-a gradient therefore is the difference between
Alveolar PO2 and Arterial PO2. Ideally A-a gradient should be zero, because
of Oxygen will diffuse across the alveolar membrane, it should do so until
the alveoli and the blood equilibrate (equal pressures). But the normal A-
a gradient is actually around 10mmHg – meaning mas mataaas slightly
yung alveolar PO2 sa arterial PO2. Why? Because there are areas in the
lungs that receives less/little blood flow (“bypass” areas) compared to the
rest. That’s why the normal A-a gradient is not 0mm.
Dr. Banzuela
CAUSES OF HYPOXEMIA
Cause PaO2 A-a Gradient
High altitude (↓PBàPAO2) Decreased Normal
SHIFT TO THE Hypoventilation (↓P PAO2) Decreased Normal
SHIFT TO THE LEFT Diffusion defect (e.g., fibrosis) Decreased Increased
RIGHT
• Increased • Increased V/Q defect Decreased Increased
Attachment Right-to-left shunt Decreased Increased
UNLOADING of O2 BINDING of O2
of O2 to Hgb A-a gradient = difference in PO2 between alveolar gas and arterial blood; PB =
from Hgb from Hgb
barometric pressure; PAO2 alveolar PO2; PaO2 = arterial PO2; V/Q =
P50 • Increased • Decreased ventilation/perfusion ratio
• Carbon DIOXIDE, Adapted from Costanzo LS. BRS Physiology. 7th ed. 2019.
Acidosis (Bohr CAUSES OF HYPOXIA

• Carbon CAUSE MECHANISM
Causes Effect), 2,3 BPG,
MONOXIDE, HbF
Exercise & ↓ cardiac output • ↓ blood flow
Temperature • ↓ PaO2 causes ↓ % saturation of
Hypoxemia
hemoglobin
• ↓ hemoglobin concentration causes ↓
Anemia
O2 content of blood
Carbon monoxide • ↓ O2 content of blood and left shift of
poisoning hemoglobin - O2 dissociation curve
Cyanide poisoning • ↓ O2 utilization by tissues
PaO2 = arterial PO2
Adapted from Costanzo LS. BRS Physiology. 7th ed. 2019.
The two tables above are very important. Remember the causes of
hypoxemia with increased A-a gradient (pag tumaas yung A-a gradient, it
means there’s a problem transferring O2 from alveoli to blood). Remember
also the causes of hypoxia – hypoxemia take note is just one of them.
Dr. Banzuela
✔GUIDE QUESTIONS
Which of the following causes of hypoxia is characterized by a decreased
arterial PO2 and an increased A–a gradient?
(A) Hypoventilation
(B) Right-to-left cardiac shunt
(C) Anemia
(D) Carbon monoxide poisoning
(E) Ascent to high altitude From Physiology BRS, 6 Ed th
Which person would be expected to have the largest A–a gradient?

(A) Person with pulmonary fibrosis
(B) Person who is hypoventilating due to morphine overdose
(C) Person at 12,000 feet above sea level
(D) Person with normal lungs breathing 50% O2
• *CO: binds 250x better to Hgb than O2, decreases O2 content of (E) Person with normal lungs breathing 100% O2
blood and causes shift to the left of O2-Hgb dissociation curve
Again, hypoxemia with high A-a gradient: diffusion defect like
HYPOXEMIA VS. HYPOXIA lung fibrosis, V/Q defect, and R-to-L shunting of the blood.
HYPOXEMIA HYPOXIA Dr. Banzuela
• Decreased arterial PO2 • Decreased tissue PO2 4.6 CO2 TRANSPORT

• Not always caused by• Transported in 3 Forms:
• Will lead to hypoxia
hypoxemia o 70%: HCO3-
• A-a gradient used to • Triggers: EPO production
o 23%: CarbaminoHgb
differentiate between (through increased o 7%: freely-dissolved in plasma
causes of hypoxemia production of hypoxia-
• Deoxyhemoglobin buffers H+ inside RBCs
inducible factor 1𝝰)• Note that reaction 1 in the equation shown primarily occurs in
Hypoxemia can lead to hypoxia but not all cases of hypoxia are caused by PLASMA (although it can also occur inside RBCs)
hypoxemia. Hypoxemia – low ARTERIAL PO2. Hypoxia – low TISSUE PO2. • Carbonic Acid (via carbonic acid-bicarbonate system) is the
Dr. Banzuela
principal buffer in the interstitial fluid
Oxygen in the blood is transported two ways: mainly (98%) via Hgb (as Oxyhemoglobin) and partly as a freely-dissolved substance (2%). CO2 is transported in
the blood three ways: mainly (70%) as chemically converted substance HCO3-, partly as a substance bound to Hgb or CarbaminoHgb (23%), and partly (7%) as
a freely-dissolved substance in blood.
Dr. Banzuela
This is the immortal bicarbonate buffer system! =)

the reaction facilitated by carbonic anhydrase on
CO2 and H2O inside the RBC is also seen inside the
parietal cells (refer to the GI module).
Dr. Banzuela
Refer to the audio recording below while looking

at the picture above about Haldane and Bohr
Effect:
HALDANE AND BOHR EFFECT

https://qrs.ly/9ucmrsr
Dr. Banzuela
✔GUIDE QUESTIONS Effect of Hypoxia (low PAO2)

VASOCONSTRICTION
In the transport of CO2 from the tissues to the lungs, which of the on Pulmonary Arterioles
following occurs in venous blood? Causes of Pulmonary Global HIGH ALTITUDE, FETAL
(A) Conversion of CO2 and H2O to H+ and HCO3– in the red blood Hypoxic Vasoconstriction CIRCULATION
cells (RBCs) Other Lung Vasoactive
(B) Buffering of H+ by oxyhemoglobin TXA2, PGI2
Substances
(C) Shifting of HCO3– into the RBCs from plasma in exchange for Cl–
(D) Binding of HCO3– to hemoglobin Causes Bronchoconstriction LEUKOTRIENES
(E) Alkalinization of the RBCs From Physiology BRS, 6 Ed th
Hypoxia causes VASOCONSTRICTION in the pulmonary arterioles (to shunt
The pH of venous blood is only slightly more acidic than the pH of arterial blood towards better ventilated areas of the lungs) and VASODILATION in
blood because the systemic arterioles (to give more oxygen to hypoxic tissues). Pulmonary
(A) CO2 is a weak base arterioles kasi PICK-UP oxygen while systemic arterioles GIVE UP oxygen.
(B) there is no carbonic anhydrase in venous blood Be careful about this. Also – the leukotrienes that cause
(C) the H+ generated from CO2 and H2O is buffered by HCO3– in venous bronchoconstriction in ASTHMA are your LTC4, D4, E4 – these are
blood collectively called the Slow-Reactive Substance of Anaphylaxis (SRS-A).
(D) the H+ generated from CO2 and H2O is buffered by That’s why we use steroids to decrease asthma attacks – to decrease these
deoxyhemoglobin in venous blood leukotrienes. Asthma bronchoconstriction is due to SRS-A and not due to
(E) oxyhemoglobin is a better buffer for H+ than is deoxyhemoglobin histamine.
From Physiology BRS, 6th Ed Dr. Banzuela
✔GUIDE QUESTION
4.7 PULMONARY CIRCULATION In which vascular bed does hypoxia cause vasoconstriction?
PULMONARY CIRCULATION (A) Coronary (D) Muscle
(B) Pulmonary (E) Skin
DESCRIPTION ANSWER (C) Cerebral From Physiology BRS, 6 Ed th
Pulmonary Circulation: Compared with the systemic circulation, the pulmonary circulation has a
< SYSTEMIC CIRCULATION
PRESSURE (A) higher blood flow (D) higher capillary pressure
Pulmonary Circulation: (B) lower resistance (E) higher cardiac output
< SYSTEMIC CIRCULATION (C) higher arterial pressure From Physiology BRS, 6 Ed
RESISTANCE
th
Pulmonary Circulation: Watch the video as you refer to the discussion below about Lung Zones:
= SYSTEMIC CIRCULATION
CARDIAC OUTPUT
Pulmonary Blood Flow: SAME THROUGH THE
SUPINE ENTIRE LUNG LUNG ZONES
Pulmonary BLOOD FLOW: LOWEST AT THE APEX, https://qrs.ly/1qcmrv6
STANDING HIGHEST AT THE BASE
Dr. Banzuela
3 POSSIBLE LUNG ZONES

✔GUIDE QUESTIONS
When a person is standing, blood flow in the lungs is
(A) equal at the apex and the base
(B) highest at the apex owing to the effects of gravity on arterial
pressure
© Topnotch Medical Board Prep (C) highest at the base because that is where the difference
• Zone 1 between arterial and venous pressure is greatest
o Local Alveolar Capillary Pressure < Alveolar Air Pressure (D) lowest at the base because that is where alveolar pressure is
greater than arterial pressure
throughout the cycle From Physiology BRS, 6th Ed
• Zone 2 A 49-year-old man has a pulmonary embolism that completely blocks
o Local Alveolar Capillary Systolic Pressure > Alveolar Air blood flow to his left lung. As a result, which of the following will occur?
Pressure during systole but less than that during diastole (A) Ventilation/perfusion (V/Q) ratio in the left lung will be zero
• Zone 3 (B) Systemic arterial PO2 will be elevated
(C) V/Q ratio in the left lung will be lower than in the right lung
o Local Alveolar Capillary Pressure > Alveolar Air Pressure
(D) Alveolar PO2 in the left lung will be approximately equal to the
throughout the cycle PO2 in inspired air
(E) Alveolar PO2 in the right lung will be approximately equal to the
LUNG ZONES PO2 in venous blood From Physiology BRS, 6 Ed th
DESCRIPTION ANSWER Because no blood flow → no gas exchange. Alveolar PO2 with
Apex of the Lungs (standing) ZONE 2, ZONE 3 therefore be the same as inspired air (hindi pumupunta oxygen
Base of the Lungs (standing) ZONE 3 from alveoli to blood)
Dr. Banzuela
Entire lungs In a Supine
ZONE 3 Compared with the apex of the lung, the base of the lung has
Position
(A) a higher pulmonary capillary PO2
Entire lungs During exercise ZONE 3 (B) a higher pulmonary capillary PCO2
Pulmonary Hemorrhage and (C) a higher ventilation/perfusion (V/Q) ratio
ZONE 1
Positive Pressure Ventilation (D) the same V/Q ratio From Physiology BRS, 6 Ed th
A person with a ventilation/perfusion (V/Q) defect has hypoxemia and

SHUNTS is treated with supplemental O2. The supplemental O2 will be most
• Right-to-Left Shunts helpful if the person’s predominant V/Q defect is
o Normal to a small extent since 2% of cardiac output bypasses (A) dead space (D) low V/Q
(B) shunt (E) V/Q=0
lungs
(C) high V/Q (F) V/Q=×
o Abnormal conditions (e.g. TOF) results in hypoxemia From Physiology BRS, 6th Ed
• Left-to-Right Shunts Low V/Q here means mababa yung ventilation, or mataas yung
o More common than right-to-left shunts (e.g. PDA) perfusion or both. So, if you give O2, naimprove mo yung
o Does not cause hypoxemia; PO2 will be elevated on the R side of oxygenation ng blood (at dahil pwedeng mataas yung perfusion,
the heart mas appreciated yung supplemental O2). Hindi pwedeng E yung
sagot dito – no ventilation means no effect at all with
supplemental O2.
4.8 V/Q DEFECTS Dr. Banzuela
V/Q RATIO
• V: Ventilation (Alveolar Ventilation) 4.9 CONTROL OF BREATHING
• Q: Perfusion (Pulmonary Blood Flow) COMPONENTS FOR CONTROL OF BREATHING
• Normal V/Q Ratio: 0.8 • Cerebral Cortex
o Results in: PO2 = 100mmHg, PCO2 = 40mmHg • Control Centers in the Midbrain and Pons
• High V/Q: high PO2, low PCO2 (e.g. lung apex) • Central and Peripheral Chemoreceptors
• Low V/Q: low PO2, high PCO2 (e.g. lung base) • Mechanoreceptors
• V/Q = Zero • Respiratory Muscles
o Shunt (e.g., R-L shunt, airway obstructions)
• V/Q = infinite CEREBRAL CORTEX
o Dead Space (e.g., pulmonary embolism) • Can override the autonomic brainstem centers
• In an upright position, which area of the lung will have a HIGHER
• Voluntary Hyperventilation
compliance: Base of the Lungs
o ↓ PaCO2 → ↑ pH → LOC
Refer to the next picture as we discuss V and Q: • Voluntary Hypoventilation (breath-holding)
o ↓ PaO2, ↑ PaCO2 → ↓ pH → LOC
V AND Q
https://qrs.ly/mncmszv
Dr. Banzuela
CONTROL CENTERS IN THE MIDBRAIN, PONS
MEDULLA PONS
• Creates the Basic Respiratory • Modifies the Basic
Rhythm Respiratory Rhythm
• Reticular formation of medulla • contains the
contains the Dorsal Respiratory Apneustic and
Group (DRG), Ventral Respiratory Pneumotaxic
Group (VRG) and Central centers
Chemoreceptors
• main respiratory centers send out
regular busts of impulses to © Topnotch Medical Board Prep
inspiratory muscles during quiet • Peripheral Chemoreceptors

respiration and are affected by o Location: Carotid and Aortic Bodies
impulses from pain receptors and § drug that stimulates the carotid bodies would cause ↓ PCO2 in
the cerebral cortex arterial blood due to peripheral chemoreceptors
o Responds MAINLY to PaO2 <60mmHg
• Medulla
§ Possibly due to excitable Glomus Cells (also seen in central
o Creates the Basic Respiratory Rhythm
chemoreceptors)
o Reticular formation of medulla contains the Dorsal
- Glomus Cell Action Potential: ↑ PCO2/↓ PO2 → ↓ potassium
Respiratory Group (DRG), Ventral Respiratory Group (VRG)
efflux → opening of voltage-gated calcium channels →
and Central Chemoreceptors
Calcium Influx → Secretion of NTs (e.g. Ach, NE, dopamine,
o main respiratory centers send out regular busts of impulses to
Substance P, met-enkephalin)
inspiratory muscles during quiet respiration and are
o Causes ↑ RR
affected by impulses from pain receptors and the cerebral
o Also respond to high PaCO2, high arterial H+ (low plasma pH)
cortex
§ Intravenous lactic acid increases ventilation by stimulating
• Pons
the peripheral chemoreceptors
o Modifies the Basic Respiratory Rhythm
o contains the Apneustic and Pneumotaxic centers MNEMONICS CHEMORECEPTORS
Central Chemoreceptors = CSF H+ (stated another way, low pH
in the CSF. This is caused by high PaCO2)
Peripheral Chemoreceptors = Pang Low Oxygen (O2)
Remember the LOCATIONS, TRIGGERS and ACTIONS of Central and
Peripheral chemoreceptors. We will discuss this again during the Phase
1,2,3 videos.
Dr. Banzuela
✔GUIDE QUESTION
A 42-year-old woman with severe pulmonary fibrosis is evaluated by her
physician and has the following arterial blood gases: pH = 7.48, PaO2 = 55
mm Hg, and PaCO2 = 32 mm Hg. Which statement best explains the
observed value of PaCO2?
(A) The increased pH stimulates breathing via peripheral
chemoreceptors
© Topnotch Medical Board Prep (B) The increased pH stimulates breathing via central chemoreceptors
CONTROL (C) The decreased PaO2 inhibits breathing via peripheral
DESCRIPTION chemoreceptors
CENTER
(D) The decreased PaO2 stimulates breathing via peripheral
• Main Respiratory Center; chemoreceptors
• generates basic rhythm for breathing; (E) The decreased PaO2 stimulates breathing via central
• for Normal/Resting Inspiration chemoreceptors From Physiology BRS, 6 Ed th
• Input: CN IX (peripheral DRG Remember: hypoxemia is the main trigger for peripheral chemoreceptors.
chemoreceptors) and CN X (peripheral The hypoxemia here (PaO2=55mmHg) stimulated the peripheral
chemoreceptors and lung chemoreceptors. Peripheral chemoreceptors in turn increased the
mechanoreceptors) respiratory rate (RR). The increased RR is then responsible for the decrease
• Output: phrenic nerve → diaphragm in PaCO2 (PaCO2=32mmHg).
Dr. Banzuela
• Supplements effect of DRG during
exercise; MECHANORECEPTORS
• for forced inspiration and expiration DESCRIPTION MECHANORECEPTORS
(overdrive mechanism) VRG • Stimulated by Lung Distension
• Pacemaker Neurons responsible for • Initiates Hering-Breuer Reflex LUNG STRETCH
respiratory rhythmogenesis: VRG Pre- that decreases Respiratory Rate RECEPTORS
Botzinger Complex by prolonging expiratory time
• Location: Upper Pons PNEUMOTAXIC
• Stimulated by Limb Movement
• Shortens time for inspiration → ↑ RR CENTER JOINT & MUSCLE
• Causes anticipatory increase in
• Location: Lower Pons RECEPTORS
Respiratory Rate during Exercise
• Prolongs time for inspiration → ↓ RR APNEUSTIC
• Causes deep and prolonged inspiratory CENTER • Stimulated by Noxious chemicals
gasp (apneusis) • Causes bronchoconstriction and IRRITANT RECEPTORS
increases the Respiratory Rate
The respiratory centers (DRG, VRG) are found in the MEDULLA. The one
that modifies the output of the respiratory centers (Pneumotaxic, • Found in “juxtacapillary” areas
Apneustic Centers) are found in the PONS. DRG is the MAIN respiratory • Stimulated by pulmonary
center, VRG merely supplements during exercise. Pneumotaxic Center – capillary engorgement
think “pneumonia” – pampabilis ng paghinga – it increases respiratory • Causes rapid shallow breathing
rate. Apneustic center – think “apnea” – pampabagal ng paghinga – it and responsible for the feeling of J RECEPTORS
decreases respiratory rate. dyspnea (e.g. in L-sided heart
Dr. Banzuela
CENTRAL AND PERIPHERAL CHEMORECEPTORS failure)
• Central Chemoreceptors • Responsible for the feelings of
o Location: ventral medulla dyspnea
o Respond directly to CSF H+ Here’s a mnemonic – J receptors detect what? Jyspnea! =)
o Causes ↑ RR Dr. Banzuela
✔GUIDE QUESTION The table above is very important. If you go to a place of high altitude (e.g.,
Hypoxemia produces hyperventilation by a direct effect on the Baguio, the following may happen):
(A) phrenic nerve The decreased alveolar PO2 is due to decreased barometric pressure. This
(B) J receptors leads to decreased arterial PO2 (hypoxemia).
(C) lung stretch receptors
(D) medullary chemoreceptors The increased ventilation rate (increased RR) is secondary to hypoxemia
(E) carotid and aortic body chemoreceptors (decreased arterial PO2), That hyperventilation will result in an increase
From Physiology BRS, 6th Ed in arterial pH (Respiratory Alkalosis). During this time there is also an
increased in Hgb concentration due to increased EPO secretion (stimulated
by hypoxia). The increase in RBCs will cause an increase in 2,3 BPG. The
increased 2,3 BPG in turn will cause a shift to the RIGHT of the O2-HgB
dissociation curve (decreasing affinity of Hgb to O2 and increasing the P50).
Finally, Pulmonary vascular resistance is expected to INCREASE due to
HYPOXIC VASOCONSTRICTION – remember that lung hypoxia causes
pulmonary arteriolar VASOCONSTRICTION.
Dr. Banzuela
✔GUIDE QUESTIONS
A 38-year-old woman moves with her family from New York City (sea
level) to Leadville Colorado (10,200 feet above sea level). Which of the
following will occur as a result of residing at high altitude?
(A) Hypoventilation
(B) Arterial PO2 greater than 100 mm Hg
(C) Decreased 2,3-diphosphoglycerate (DPG) concentration
(D) Shift to the right of the hemoglobin–O2 dissociation curve
(E) Pulmonary vasodilation From Physiology BRS, 6 Ed th
Living in high altitude results in higher production of 2,3 BPG due

to reaction of the body to the low O2 pressure in the atmosphere.
This would cause a shift to the R of the O2-HgB dissociation curve.
Dr. Banzuela
A 12-year-old boy has a severe asthmatic attack with wheezing. He
experiences rapid breathing and becomes cyanotic. His arterial PO2 is 60
mm Hg and his PCO2 is 30 mm Hg. Which of the following statements
about this patient is most likely to be true?
(A) Forced expiratory volume/forced vital capacity (FEV1/FVC) is
increased
(B) Ventilation/perfusion (V/Q) ratio is increased in the affected
areas of his lungs
(C) His arterial PCO2 is higher than normal because of inadequate gas
exchange
(D) His arterial PCO2 is lower than normal because hypoxemia is
causing him to hyperventilate
(E) His residual volume (RV) is decreased
To treat this patient, the physician should administer
(A) an α1-adrenergic antagonist
(B) a β1-adrenergic antagonist
© Topnotch Medical Board Prep (C) a β2-adrenergic agonist
(D) a muscarinic agonist
4.10 INTEGRATED RESPONSES OF THE (E) a nicotinic agonist From Physiology BRS, 6th Ed
RESPIRATORY SYSTEM
PRETEST EQUATIONS
RESPIRATORY RESPONSES TO EXERCISE
INCREASES (↑) DECREASES (↓) NO CHANGE ALVEOLAR GAS EQUATION
• O2 Consumption • Arterial pH • Arterial PO2 and
• CO2 Production (strenuous PCO2
• Respiratory Rate exercise due to • Arterial pH
• Venous PCO2 lactic acidosis) (moderate
• Pulmonary exercise)
Blood Flow
• Type of reached at workloads that is >60% of maximal workload
marked by increased muscle lactic acid production, decreased
arterial pH, increased alveolar ventilation: Anaerobic Exercise © Topnotch Medical Board Prep
• Question:
PO2 and PCO2 do NOT change during moderate exercise due to
o 36/M placed on ventilator with rate of 16, TV=600mL, FiO2 = 1.0
compensatory mechanisms like tachypnea. They might change during
STRENUOUS exercise.
o ABG reveals PO2=350mmHg, PCO2 = 36mmHg, pH = 7.32 At
Dr. Banzuela barometric pressure = 757mmHg, with normal respiratory
✔GUIDE QUESTION exchange ratio (R) of 0.8,
Which of the following changes occurs during strenuous exercise? o What is the patient’s alveolar oxygen tension?
(A) Ventilation rate and O2 consumption increase to the same • Answer:
extent o 665mmHg (PAO2=PIO2-(PaCO2/R) = (1.0) (757-47) - (36/0.8) =
(B) Systemic arterial PO2 decreases to about 70 mm Hg 710-45 = 665mmHg
(C) Systemic arterial PCO2 increases to about 60 mm Hg
(D) Systemic venous PCO2 decreases to about 20 mm Hg
• Pulmonary Vascular Resistance (PVR) Equation
(E) Pulmonary blood flow decreases at the expense of systemic blood
flow From Physiology BRS, 6 Ed th
RESPIRATORY RESPONSES TO HIGH ALTITUDE

INCREASES (↑) DECREASES (↓) o Note: Left Atrial Pressure (LAP) above could be replaced by
• Respiratory Rate • Alveolar PO2 Pulmonary Capillary Wedge Pressure (PCWP); CO of R heart =
• Arterial pH • Arterial PO2 Pulmonary Blood Flow
• Hgb Concentration o Question
• 2,3 BPG § 67/M cardiac transplant candidate has the following labs:
• Pulmonary Vascular Resistance Pulmonary Artery Pressure (PAP) = 35mmHg, Cardiac Output
(Hypoxic vasoconstriction) = 4L/min, Left Atrial Pressure(LAP) = 15mmHg, Right Atrial
Pressure = 10mmHg
§ What is his PVR? % OF
MAJOR MAJOR
COMPARTMENT BODY MARKERS
o Answer WEIGHT
CATIONS ANIONS
§ PVR = Mean PAP – mean LAP/pulmonary blood flow Titrated
§ = 35 – 15mmHg/4L/min Total Body
60% water, D2O,
§ = 5mmHg/L/min Water (TBW)
antipyrine
SHUNT FRACTION Extracellular
(RATIO OF SHUNTED TO TOTAL PULMONARY BLOOD FLOW) Sulfate,
Fluid
20% Inulin, Na Cl, HCO3-
Compartment
Mannitol
(ECF)
Radioactive
Iodinated
5%
Serum
Plasma (25% Na Cl- HCO3-
Albumin
of ECF)
(RISA),
Evans Blue
ECF-
15%
Interstitial plasma
(75% Na Cl, HCO3-
Fluid (IF) volume
of ECF)
(indirect)
Organic
Intracellular TBW-ECF
40% K phosphate,
Fluid (ICF) (indirect)
© Topnotch Medical Board Prep Protein
• Question: Memorize the various “indicator molecules” or “markers” – they help
o 32/M severe respiratory disease after aspiration pneumonia. calculate the volume of the various body compartments. See guide question
Inhaled NO given, and patient placed in prone position. Mean below on how to compute for these volumes. Mannitol for example is a
pulmonary capillary oxygen content = 19mL/dL, Arterial O2 marker for ECF, Evans Blue is marker for Plasma, Tritiated water is
content = 18 mL/dL, Mixed Venous O2 content = 14 mL/dL, marker for TBW.
Dr. Banzuela
Cardiac Output = 6L/min. What is the patient’s shunt fraction
✔GUIDE QUESTIONS
(ratio of shunted to total pulmonary blood flow)?
One gram of mannitol was injected into a woman. After equilibration, a
• Answer: plasma sample had a mannitol concentration of 0.08 g/L. During the
o Shunt Fraction = (CCO2 – Ca2)/(CCO2-CvO2) equilibration period, 20% of the injected mannitol was excreted in the
o =(19mL/dL-18mL/dL)/(19mL/dL-14mL/dL) urine. The subject’s
o = 0.2 (A) extracellular fluid (ECF) volume is 1 L
(B) intracellular fluid (ICF) volume is 1 L
OXYGEN CONSUMPTION VO2 (C) ECF volume is 10 L
(CAN BE COMPUTED USING FICK EQUATION; SEE) (D) ICF volume is 10 L
(E) interstitial volume is 12.5 L
𝑽𝑶𝟐 = 𝑪𝑶 × (𝑪𝒂𝑶𝟐 − 𝑪𝒗𝑶𝟐 ) ECF volume = amount of mannitol/concentration of mannitol
Please remember the formulas above – they’ve been utilized before in the = 1 g – 0.2 g/0.08 g/L = 10 L.
med boards. Which of the following substances or combinations of substances could
Dr. Banzuela
be used to measure interstitial fluid volume?
Types of Hypoxia
(A) Mannitol (D) Inulin and D2O
TYPE OF (B) D2O alone (E) Inulin and radioactive albumin
CHARACTERISTICS
HYPOXIA (C) Evans blue From Physiology BRS, 6 Ed th
Hypoxic • (+) Alveolar hypoventilation (high PaCO2) and Dietary reference value for Na+ and Cl- per day – 3,100mg for adults
Hypoxia hypoxemia (low PaO2) including pregnant and lactating women. Adequate intake of K+ per day
• ↓ Hb (anemia) or ↓ saturation of hemoglobin (no RDA) – 3,400mg for adult males, 2,600 for adult females, 2,900mg for
Anemic
with oxygen (SaO2) expected for a given PaO2 pregnant patients and 2,800mg for lactating women.
Hypoxia
(e.g., CO poisoning or methemoglobinemia) Dr. Banzuela
Stagnant ✔GUIDE QUESTIONS

• ↓ cardiac output
hypoxia Subjects A and B are 70-kg men. Subject A drinks 2 L of distilled water,
Histotoxic • impaired O2 extraction → ↓ CaO2-CvO2 and ↑ and subject B drinks 2 L of isotonic NaCl. As a result of these ingestions,
subject B will have a
Hypoxia SVO2
(A) greater change in intracellular fluid (ICF) volume
(B) higher positive free-water clearance (CH2O)
5. RENAL & ACID-BASE PHYSIOLOGY (C) greater change in plasma osmolarity
(D) higher urine osmolarity
1. Body Fluids (E) higher urine flow rate From Physiology BRS, 6 Ed th
2. The Nephron, Reabsorption and Secretion, Renal Clearance,

Renal Blood Flow (RBF) and Glomerular Filtration Rate (GFR) Subject A drinks water alone, subject B drinks water + salt.
Therefore, subject B will excrete more salt compared to subject A,
3. K Regulation
resulting in higher urine osmolarity.
4. Renal Regulation of Urea, Phosphate, Calcium & Magnesium Dr. Banzuela
5. Concentration and Dilution of Urine A woman runs a marathon in 32°C weather and replaces all volume lost
6. Acid-Base Balance in sweat by drinking distilled water. After the marathon, she will have
7. Integrative Examples (A) decreased total body water (TBW)
(B) decreased hematocrit
5.1 BODY FLUIDS (C) decreased intracellular fluid (ICF) volume
(D) decreased plasma osmolarity
MNEMONIC “60-40-20” RULE (E) increased intracellular osmolarity From Physiology BRS, 6 Ed th
60% of BW: Water

Woman lost water + salt from sweating during the marathon. She
40% of BW: ICF
was able to replace the water lost from sweating, but she was not
20% of BW: ECF able to replace the salt lost from sweating because she drank only
Actually, ang tawag ko dito “60-40-20-15-5” rule. Kasi ECF can be distilled water. Her plasma osmolarity would therefore decrease
subdivided into Interstitial Fluid (IF) and Plasma. IF makes up 75% of ECF, since it might have the same volume of water, but the is decreased
while plasma makes up 25% of ECF. So mathematically, 15% of your body Na concentration.
Dr. Banzuela
weight is IF, 5% of your body weight is plasma.
Dr. Banzuela
Watch these 3 videos as while analyzing the next diagram: 5.2 NEPHRON, RENAL CLEARANCE,
VOLUME AND CONCENTRATION CHANGES ACROSS
COMPARTMENTS RENAL BLOOD FLOW (RBF),
GLOMERULAR FILTRATION RATE (GFR)
Refer to the following videos as you go through the readings below
PART 1 OF 3 PART 2 OF 3 PART 3 OF 3

https://qrs.ly/rpcmszz https://qrs.ly/yxcmt0c https://qrs.ly/rncmt0h
Dr. Banzuela
TYPES OF RENAL RENAL TUBULAR
NEPHRONS CORPUSCLE SYSTEM
https://qrs.ly/kncmt0o https://qrs.ly/dccmt12 https://qrs.ly/qpcmt1a
Dr. Banzuela
NEPHRON
• Structural and Functional Unit of the Kidneys
• There are two major types of nephrons:
• 75% of nephrons
Cortical • Located in the renal cortex
Nephron • With shorter Loops of Henle
• Has peritubular capillaries
• 25% of nephrons
• Located in the corticomedullary junction
Juxtamedullary
• With longer Loops of Henle
• Has vasa recta
• A nephron has two major parts:
Renal or • Afferent arterioles, glomerular capillaries,
Malpighian efferent arterioles, podocytes, mesangial
Corpuscle cells, JG cells, Bowman’s capsule & space
Renal Tubules • PCT, LH, DT, CD
ENDOCRINE FUNCTION OF THE KIDNEYS

• From interstitial cells in peritubular
capillary bed
• Released in response to hypoxia →
Erythropoietin
stimulates RBC proliferation in bone
(EPO)
marrow
• Chronic kidney disease (CKD) causes ↓
EPO → chronic anemia
• PCT converts 25-OH vitamin D3 → 1,25-
(OH)2 vitamin D3 (calcitriol, active form)
Calciferol
• Conversion is mediated by 1α-
(Vitamin D)
hydroxylase (which is upregulated by
PTH)
• Paracrine secretion vasodilates the
afferent arterioles → ↑RBF
• NSAIDs block the renal protective
Prostaglandins prostaglandin synthesis → afferent
arteriole constriction → ↓GFR → Acute
Kidney Injury (in low renal blood flow
states)
• From PCT cells
Daily Intake or Prolonged Heavy • Promotes natriuresis
Normal
Output Exercise (in mL)
• At low doses: dilates interlobular
Intake Dopamine
arteries, afferent arterioles, efferent
Water ingested 2,100 ? arterioles → ↑ RBF
Water from • At high does: acts as vasoconstrictor
200 200
metabolism
Total Water Intake 2,300 ? RENAL CORPUSCLE – 3 CHARGE AND FILTRATION BARRIERS
Output OF THE GLOMERULUS
Insensible: skin 350 350
• Capillary Endothelium
Insensible: lungs 350 650 o Highly-fenestrated with pores 8 nm in diameter
Sweat 100 5,000 o Secrete NO and endothelin-1 (ET-1)
Feces 100 100 • Basement Membrane
Urine 1,400 500 o With type IV Collagen
Total Water Output 2,300 6,600 o Main charge barrier
ESTIMATE FOR PLASMA OSMOLARITY § Destroyed in glomerular diseases
• Podocytes
o Also called Bowman’s epithelial cells or visceral epithelium
o Contains foot processes and filtration slits
True plasma osmolarity is difficult to determine since there are a lot of

solutes in plasma. A reasonable estimate, however, can be determined from
the 3 main solutes in there – sodium, glucose and BUN. See the formula
above.
Dr. Banzuela
The basement membrane of the renal corpuscle is clinically significant. It © Topnotch Medical Board Prep
is an anionic barrier (negatively-charged proteins are found here). It TUBULAR SYSTEM
therefore prevents filtration of negatively-charged plasma proteins like
albumin. Destruction of the basement membrane would lead to • Proximal Convoluted Tubule (PCT)
proteinuria (e.g., in nephrotic syndrome) since albumin is actually small • Loop of Henle (LH)
enough to pass through the pores of the capillary endothelium. o Descending Limb of the Loop of Henle
Speaking of proteinuria: Orthostatic proteinuria is a benign condition o Thin Ascending Limb of the Loop of Henle
marked by normal urinary protein excretion during the night but with o Thick Ascending Limb of the Loop of Henle
increased excretion during the day, that is associated with activity and • Distal Tubule (DT)
upright posture (proteinuria <1g/24 hours).
Dr. Banzuela
o First Part: Early Distal Tubule
RENAL CORPUSCLE – OTHER CELLS o Second Part: Late Distal Tubule/Connecting Tubule, Cortical
• Mesangial Cells Collecting Tubule
o Intraglomerular: modified smooth muscles capable of • Collecting Duct (CD)
phagocytosis o Medullary Collecting Tubule
§ Keeps the basement membrane free of debris by removing o Collecting Duct
trapped residues and aggregated protein
§ Causes mesangial cell CONTRACTION: angiotensin II,
Arginine Vasopressin (AVP), Endothelin-1 (ET-1), Platelet-
derived growth factor (PDGF) and Platelet-Activating Factor
(PAF)
§ Causes mesangial cell RELAXATION: Atrial Natriuretic
Peptide (ANP), Nitric Oxide (NO)
o Extraglomerular (Lacis Cells): may play role in renal
autoregulation, and RAAS
• Juxtaglomerular (JG) Cells
o At the walls of afferent arterioles
o Secrete renin
• Macula Densa
o In DT
o Monitor Na+ concentration in the lumen of DT (and
consequently, Blood Pressure)
PCT
• “workhorse” of the nephron
o Reabsorption
§ 66% of filtered Na+, K+, H2O
§ 100% of filtered glucose, amino acids
o Secretion
§ Excess acids
• (+) microvilli, convolutions
• Isosmotic fluid reabsorption: occurs in the PCT from lumen to
the PCT cell to peritubular capillaries
o Isosmotic since at the PCT, there is same ratio of Na and water
reabsorbed – 66%.
• Most susceptible to hypoxia, toxins
LOOP OF HENLE
• Descending Limb
o Permeable to: water
o Impermeable to: solutes
© Topnotch Medical Board Prep • Ascending Limb
o Permeable to: solutes
o Impermeable to water
o Thick Ascending Limb of LH (TAL of LH)
o Na-K-2Cl symport seen here
§ One of the basis for countercurrent multiplier
o Also called the “diluting segment”
DISTAL TUBULE IMPORTANT FORMULAS
• Early Distal Tubule (EDT)
o Also called “cortical diluting segment”
o site of Macula Densa
• Late Distal Tubule (LDT)
o Principal Cells • Where V = urine flow rate of substance (in mL/min)
§ Reabsorb: Na+ (and consequently water) o Plasma = Plasma concentration of substance (in mg/dL)
§ Secrete: K+ o Urine = urine concentration of substance (in mg/dL)
o Intercalated Cells • If filtered load > excretion rate: net reabsorption
§ Reabsorb: K+
• If filtered load < excretion rate: net secretion
§ Secrete: H+
o Site of action of Aldosterone
o Dietary K+ has effect on K+ secretion/reabsorption
COLLECTING DUCT
• Site of ADH action
o ↑ ADH → ↑ aquaporin-2 channels → ↑water reabsorption
§ Results in ↑ intravascular volume → ↑VR, CO, BP
§ Results in ↓ urine volume, ↑ urine concentration
Watch the video on countercurrent mechanism as you read the section
below:
COUNTERCURRENT
MECHANISM
https://qrs.ly/6wcmt1f
Dr. Banzuela
COUNTERCURRENT MECHANISM
• Countercurrent Multiplier: Loop of Henle
o Creates “graded osmolarity” in renal medulla
• Countercurrent Exchanger: Vasa Recta
o Preserves “graded osmolarity” in the renal medulla
Watch the video below while reading the section on the basic movements
involved in urine formation:
THE BASIC MOVEMENTS

INVOLVED IN URINE FORMATION
https://qrs.ly/ducmt20
Dr. Banzuela Most solutes (e.g. glucose) actively reabsorbed or secreted exhibit:
o Renal Threshold
BASIC MOVEMENTS INVOLVED IN URINE FORMATION § Substance start to appear in the urine
• (Glomerular) Filtration § Some nephrons exhibit saturation
o Movement from Glomerular Capillaries to Bowman’s Space o Renal Transport Maximum
• (Tubular) Reabsorption § All excess substance appear in the urine
o Movement from Tubules to Interstitium to Peritubular § All nephrons exhibit saturation
Capillaries
• (Tubular) Secretion SPECIAL NOTES ON TM CURVE
o Movement from Peritubular Capillaries to Interstitium to • Tm Curve of Glucose
Tubules o Normal: Filtered, 100% reabsorbed
• Excretion o Filtration: proportional to plasma glucose concentration
o Excretion = (Amount Filtered) – (Amount Reabsorbed) + o Reabsorption: occurs using SGLT-2 in PCT
(Amount Secreted) o Renal Threshold: plasma glucose 200mg/dL (some nephrons
saturated)
o Renal Transport Maximum: plasma glucose > 375mg/dL (all
nephrons saturated)
o Splay: between 200mg/dL – 375mg/dL (glucose excretion
before complete saturation of all nephrons)
• Tm Curve of PAH CLEARANCE
o Normal: Filtered, Secreted, Not reabsorbed • Volume of plasma cleared of a substance per unit of time (in
o Secretion of PAH occurs using carriers in the PCT mL/min or mL/24 hour)
o Filtration load proportional to plasma PAH secretion o Remember: You “clear” the blood to make it go to the urine
o Secretion: also exhibits saturation
Remember: the renal threshold for glucose: 200mg/dL – at this point, one
nephron is already saturated (nephrons are not saturated all at the same
time) The transport maximum for glucose: 375mg/dL (at this point, all
nephrons are already saturated).
Dr. Banzuela
✔GUIDE QUESTIONS
At plasma concentrations of glucose higher than occur at transport
maximum (Tm), the • If substance has high clearance: most will be found in the urine
(A) clearance of glucose is zero • If substance has low clearance: most will be found in the blood
(B) excretion rate of glucose equals the filtration rate of glucose • Relative Clearances:
(C) reabsorption rate of glucose equals the filtration rate of glucose o PAH > K > inulin > urea > Na > glucose, amino acids and HCO3-
(D) excretion rate of glucose increases with increasing plasma • Highest Clearance: PAH
glucose concentrations o Reason: Filtered and Secreted, not reabsorbed
(E) renal vein glucose concentration equals the renal artery glucose
concentration From Physiology BRS, 6 Ed th
o Used to estimate for Renal Blood Flow (RBF) and Renal Plasma
Flow (RPF)
There’s no saturation for filtration and excretion of glucose. The • Lowest Clearance: Protein, Na, Glucose, amino Acids, HCO3- and
higher the plasma concentration, the higher the glucose filtered
and excreted
Cl-
Dr. Banzuela o Reason: Not filtered (protein), or filtered but mostly reabsorbed
At plasma para-aminohippuric acid (PAH) concentrations below the (everything else listed above)
transport maximum (Tm), PAH o Normally not found or found in small amounts in the urine
(A) reabsorption is not saturated • Clearance equal to GFR: inulin, creatinine
(B) clearance equals inulin clearance
o Reason: filtered but not secreted not reabsorbed
(C) secretion rate equals PAH excretion rate
(D) concentration in the renal vein is close to zero § more concentrated at the end of PCT that at the start of PCT:
(E) concentration in the renal vein equals PAH concentration in the Creatinine
renal artery From Physiology BRS, 6 Ed th o Marker for Kidney function (glomerular marker)
PAH is supposed to be highly excreted since it is filtered, secreted
o Crea Clearance = Crea excreted/plasma crea concentration
and not reabsorbed. Since PAH concentration is still below Tm, it ✔GUIDE QUESTIONS
means we have not fully saturated the nephrons – PAH is still being Which of the following substances has the highest renal clearance?
excreted. Since it is still being excreted, little PAH can be found in (A) Para-aminohippuric acid(PAH) (D) Na+
the renal vein – almost all PAH goes to the urine. Message me if (B) Inulin (E) Cl–
you’re having a hard time with this one. (C) Glucose From Physiology BRS, 6 Ed th
Dr. Banzuela
The following information was obtained in a 20-year-old college student
NONIONIC DIFFUSION who was participating in a research study in the Clinical Research Unit:
WEAK ACIDS WEAK BASES Plasma: [Inulin] = 1 mg/mL [X] = 2 mg/mL
• HA Form (lipid- • BH+ Form (water- Urine: [Inulin] = 150 mg/mL [X] = 100 mg/mL
Urine flow rate = 1 mL/min
Forms soluble) and A- Form soluble) and B Form Assuming that X is freely filtered, which of the following statements is
(water-soluble) (lipid-soluble) most correct?
• BH+ Form (A) There is net secretion of X
predominates, less (B) There is net reabsorption of X
• HA Form (C) There is both reabsorption and secretion of X
“back diffusion”,
predominates: more (D) The clearance of X could be used to measure the glomerular
In Acidic • increased excretion
“back-diffusion”, filtration rate (GFR)
Urine pH of weak base (e.g.,
• decreased excretion (E) The clearance of X is greater than the clearance of inulin
• Morphine excretion From Physiology BRS, 6th Ed
of weak acids
increased by Cinulin = UinulinV/Pinulin
acidifying urine) Cinulin = (150mg/dL)(1mL/min)/(1mg/mL)
Cinulin = 150mL/min
• A- Form
predominates: less • B form Cx = UxV/Px
In back-diffusion, predominates, more Cx = (100mg/mL) (1mL/min)/(2mg/ml)
Cx = 50mL/min
Alkaline • increased excretion of “back-diffusion”,
Urine pH weak acids (e.g., ASA • decreased excretion Cx < Cinulin
excretion increased of weak bases Cx < GFR since Cinulin is used to estimate GFR
X is therefore a substance that undergoes net reabsorption.
by alkalinizing urine)
Side Note: if X here is greater than GFR, there is net secretion. If X
Here’s a mnemonic – “do the opposite” rule: if you overdose with an ACIDIC = GFR, then X is either inulin or creatinine.
drug (e.g. ASA), ALKALINIZE the urine so that the weak acid will be in its Dr. Banzuela
water-soluble (charged) form. If you overdose with an ALKALINE/BASIC
drug (e.g., morphine), ACIDIFY the urine so that the weak base will once RENAL BLOOD FLOW (RBF)
again be in its water-soluble (charged) form). • Right vs. Left Renal Artery:
Dr. Banzuela
Right Renal • Longer than left renal artery
✔GUIDE QUESTION
Artery • Runs an inferior course posterior to the IVC
A person who takes an aspirin (salicylic acid) overdose is treated in the
emergency room. The treatment produces a change in urine pH that • Slightly higher origin compared to right
increases the excretion of salicylic acid. What was the change in urine pH, Left Renal renal artery
and what is the mechanism of increased salicylic acid excretion? Artery • Runs more horizontally, posterior to the left
(A) Acidification, which converts salicylic acid to its HA form renal vein
(B) Alkalinization, which converts salicylic acid to its A– form • Renal Blood flow: 25% of Cardiac Output
(C) Acidification, which converts salicylic acid to its A– form o RBF is directly proportional to pressure difference between
(D) Alkalinization, which converts salicylic acid to its HA form
From Physiology BRS, 6 Ed renal artery and renal vein; inversely proportional to resistance
th
Listen to this audio recording while reading the section on clearance:

of renal vasculature
o Vasodilation of Renal Arterioles: Increases RBF
§ e.g. PGE2, PGI2, bradykinin, NO, dopamine
CLEARANCE o Vasoconstriction of Renal Arterioles: Decreases RBF
https://qrs.ly/s3cmt29 § e.g. Sympathetic NS and Angiotensin II (preferentially
constricts efferent arterioles)
§ ANP: vasodilates Afferent Arterioles and to a lesser extent
Dr. Banzuela
vasoconstricts Efferent Arterioles. Net effect: increases RBF
• Renal Plasma Flow (RPF) • “Proteins attracting water” at the GC.
o Estimated by PAH Clearance GC Oncotic
• Opposes GFR.
o Take note: PAH Clearance underestimates true RPF by 10% Pressure
• Increased by plasma protein concentration.
due to RPF to kidney regions that do not filter and secrete • “Usually ignored”.
PAH BS Oncotic
• Normal value: 0 (no protein is normally filtered
• Renal Blood Flow Pressure
to BS)
• Not a Starling Force.
• Hydraulic conductance/filtration coefficient
Kf describes capillary permeability.
Remember the formula above. RPF is the numerator.(1-Hct) is the • Promotes GFR. Increased by histamine
denominator.
Dr. Banzuela
• (e.g. in burns)
✔GUIDE QUESTIONS ✔GUIDE QUESTION
A patient is infused with para-aminohippuric acid (PAH) to measure Glomerular capillary hydrostatic pressure = 47mmHg
renal blood flow (RBF). She has a urine flow rate of 1 mL/min, a plasma Bowman’s space hydrostatic pressure = 10mmHg
[PAH] of 1 mg/mL, a urine [PAH] of 600 mg/mL, and a hematocrit of Bowman’s space oncotic pressure = 0 mm Hg
45%. What is her “effective” RBF? At what value of glomerular capillary oncotic pressure would
(A) 600 mL/min (C) 1091 mL/min glomerular filtration stop?
(B) 660 mL/min (D) 1333 mL/min (A) 57 mm Hg (D) 10 mm Hg
From Physiology BRS, 6th Ed (B) 47 mm Hg (E) 0 mm Hg
CPAH = UPAH × V/PPAH = 600 mL/min (C) 37 mm Hg th
CPAH = RPF since clearance of PAH is used to estimate RPF Listen to the audio recording below while reading the following section
about GFR, RPF and FF:
RBF = RPF/ (1 – hematocrit)
RBF = (6000mL/min)/ (1-0.45)
RBF = 600mL/min/0.55
RBF = 1091 mL/min
GFR, RPF and FF
Dr. Banzuela https://qrs.ly/9fcmt2w
GFR Dr. Banzuela
• Amount filtered in the glomerular capillaries per unit time

o Normal Value: 125mL/min or 180L/day FILTRATION FRACTION (FF)
o Determined by Starling Forces at the level of the glomerular • Fraction of renal plasma flow that is filtered
capillary (glomerulus) • Normal Filtration Fraction: 20%
• BUN and Creatinine increase when GFR decreases o ↑ Filtration Fraction → ↑ peritubular capillary protein
o In pre-renal azotemia (e.g. Hypovolemia), BUN increases concentration → ↑ reabsorption in the tubules
more than creatinine and BUN/Crea ratio > 20:1
o GFR decreases with age, but Creatinine remains constant due to
decreased muscle mass
Watch the video on Starling Forces and GFR while reading the relevant
GFR, RPF, FF
portions below:
EFFECT EFFECT EFFECT
ON GFR OF RPF ON FF
STARLING FORCES AND GFR Vasoconstriction of No
↓ ↓
https://qrs.ly/s4cmt2p Afferent Arteriole Change
Vasoconstriction of
↑ ↓ ↑
Dr. Banzuela
Efferent Arteriole
STARLING FORCES No
↑ Plasma Protein ↓ ↓
• Describes fluid movement into (absorption) or out of Change
(filtration) the capillary No
Ureteral Stone ↓ ↓
Change
• GFR and RBF would increase if we vasodilate: afferent and
efferent arterioles
• Compression of the renal capsule will cause: decreased GFR
✔GUIDE QUESTIONS
Which of the following would produce an increase in the reabsorption of
isosmotic fluid in the proximal tubule?
(A) Increased filtration fraction
(B) Extracellular fluid (ECF) volume expansion
(C) Decreased peritubular capillary protein concentration
GLOMERULAR FILTRATION RATE (D) Increased peritubular capillary hydrostatic pressure
• GFR = Kf [(PGC-PBS) – (OGC- OBS)] (E) Oxygen deprivation From Physiology BRS, 6 Ed
th
o Kf = Filtration coefficient of the Glomerular Capillaries Which of the following would cause an increase in both glomerular
o PGC= Glomerular Capillary Hydrostatic Pressure filtration rate (GFR) and renal plasma flow (RPF)?
o PBS = Bowman’s Space Hydrostatic Pressure (A) Hyperproteinemia (D) Dilation of the efferent arteriole
(B) A ureteral stone (E) Constriction of the efferent arteriole
o OGC= Glomerular Capillary Oncotic Pressure (mmHg) (C) Dilation of the afferent arteriole From Physiology BRS, 6 Ed
th
o OBS = Bowman’s Space Oncotic Pressure (mmHg)

AUTOREGULATION OF RENAL BLOOD FLOW
NOTES ON GLOMERULAR CAPILLARY STARLING FORCES
• helps maintain constant GFR
STARLING o Occurs at BP 80-200mmHg (in other textbooks: at BP 75-
DESCRIPTION
FORCE 160mmHg), renal blood flow remains constant via
• ” Water pressure” at the GC. § Myogenic mechanism
GC • Promotes GFR. - renal afferent arterioles reflexively responds to stretch
Hydrostatic • Increased by vasodilation of afferent arteriole by contracting in order to maintain constant renal blood
Pressure or moderate vasoconstriction of efferent flow and subsequently, GFR
arteriole § Tubuloglomerular Feedback / Macula Densa Feedback
BS • “Water pressure” at the BS that opposes GC - Remember: this is not the same as glomerulotubular balance
Hydrostatic hydrostatic Pressure and GFR.
Pressure • Increased by ureteral obstruction
Scenario 1: if BP is low (e.g. 80mmHg)
• ↓ BP → ↓ GC Hydrostatic Pressure → ↓ GFR (<125ml/min) →
Detected by Macula Densa
• Macula Densa increases secretion of:
o Angiotensin II (via RAAS stimulation)
§ Vasoconstricts EFFERENT Arteriole → ↑ GFR back to normal
(125ml/min)
o Nitric Oxide
§ Vasodilates AFFERENT Arteriole → ↑ GFR back to normal
(125ml/min)
Scenario 2: if BP is high (e.g. 200mmHg)

• ↑ BP → ↑ GC Hydrostatic Pressure → ↑ GFR (>125ml/min) →
Detected by Macula Densa
o Adenosine: Vasoconstricts AFFERENT arteriole → ↓ GFR back to
normal (125ml/min)
§ Adenosine is normally a vasodilator, but in the kidney, it
acts as a vasoconstrictor of the AFFERENT arteriole!
Remember that there are 3 organs that have autoregulation of blood flow
as discussed in the cardio module: brain, heart and kidney. For the kidney, K+ SECRETION IN THE DT USING PRINCIPAL CELLS
the reason why they are given the power to regulate the diameter of their • K+ secretion by the Principals Cells in the LDT can be increased
arterioles (and therefore regulate their own blood flow) is to maintain a or decreased by several factors.
CONSTANT GFR. The number one suspected mechanism for renal • This can lead to changes in plasma K+
autoregulation of blood flow is Tubuloglomerular feedback/macula densa CAUSES OF INCREASED CAUSES OF DECREASED
feedback. Take note of the substances produced to dilate/constrict the
DISTAL K SECRETION DISTAL K SECRETION
afferent/efferent arterioles whenever BP is low or high (see section above).
Dr. Banzuela • High K+ diet • Low K+ Diet
REMEMBER! AUTOREGULATION OF RENAL BLOOD FLOW • Hyperaldosteronism • Hypoaldosteronism
TUBULOGLOMERULAR FEEDBACK • Alkalosis • Acidosis
Macula Densa Feedback; For Autoregulation of GFR • Thiazide Diuretics • K+-Sparing Diuretics
• Loop Diuretics
GLOMERULOTUBULAR BALANCE
• Luminal Anions
Percentage of solute reabsorbed is held constant; Buffers effect
of drastic GFR changes on urine output Memorize also the table above.
Dr. Banzuela
✔GUIDE QUESTION
5.3 K+ REGULATION Secretion of K+ by the distal tubule will be decreased by
REGULATION OF POTASSIUM (A) metabolic alkalosis (D) spironolactone
• Plasma K+ = 4.2 mEq/L and tightly-regulated (B) a high-K+ diet administration
(C) hyperaldosteronism (E) thiazide diuretic administration
• 1st Line of defense From Physiology BRS, 6th Ed
o Movement of K+ across ECF and ICF Remember the spironolactone is an aldosterone antagonist, it will
decrease K+ secretion to the urine, and may in fact cause
CAUSES OF K+ EFFLUX → CAUSES OF K+ INFLUX → hyperkalemia. Spironolactone has another adverse effect btw:
HYPERKALEMIA HYPOKALEMIA gynecomastia.
Dr. Banzuela
• Insulin deficiency • Insulin
• Beta-adrenergic antagonist • Beta-adrenergic agonists
• Acidosis • Alkalosis 5.4 RENAL REGULATION OF UREA, PHOSPHATE,
• Hyperosmolarity • Hypoosmolarity CALCIUM AND MAGNESIUM
• Inhibitors of Na+-K+-ATPase REGULATION OF UREA
pump like digitalis • PCT: reabsorbs 50% of filtered Urea via simple diffusion
• Exercise • Thin Descending Limb of LH: secretes urea via simple diffusion
• Cell Lysis • DT, Cortical Collecting Ducts and Outer Medullary Collecting
Memorize the table above. Some key points: insulin causes K+ influx that’s Ducts: Impermeable to Urea
why it’s used in the treatment of hyperkalemia. Mechanism is unknown but • Inner Medullary Collecting Ducts: ADH increases permeability
number one suspected mechanism is to increase activity of the Na+-K+- of these ducts to via facilitated diffusion transporter for urea
ATPase pump. Acidosis causes K+ efflux, predisposing you to hyperkalemia. (UT1)
Why? Our body prioritizes acid-base balance in plasma more than anything o Contributes to urea recycling and development of
else since acids/bases can kill you very fast through denaturation of
corticopapillary osmotic gradient
proteins. So, if you have acidosis, our body compensates by moving H+ from
ECF to ICF in exchange for K+ (the number one intracellular cation) moving
o ↑ ADH secretion → ↑ Water AND Urea reabsorption → Low Urine
from ICF to ECF. Cell lysis (e.g., in tumor lysis syndrome) can cause rupture Flow Rate
of cells, which will release their contents – including the intracellular K+. Urea is important. Without urea and UT-1 transporters, maximum
Dr. Banzuela
osmolarity at the renal interstitium near the tip of the LH would only be
600 instead of 1200mOsm/L. Urea is a solute that increases maximum
✔GUIDE QUESTION urine osmolality (it doubles it).
Which of the following causes hyperkalemia? Dr. Banzuela
(A) Exercise (D) Decreased serum osmolarity

(B) Alkalosis (E) Treatment with β-agonists REGULATION OF CALCIUM
(C) Insulin injection th
• Plasma Ca2+ = 2.4mEq/L
• Hypercalcemia: can cause arrhythmias
RENAL REGULATION OF K+ BALANCE • Hypocalcemia: can cause tetany
• K+ Balance achieved when: • Calbindin: Stimulated by vit D; binds with calcium in the
o Urinary excretion of K+ = K+ dietary intake intestines
• K excretion varies from 1-110% of filtered load depending of • 60% of plasma Ca2+ is filtered
dietary K, aldosterone levels and acid-base status • PCT and LH reabsorbs 90% of filtered Calcium
• Principal Cells: secrete K • DT and CD reabsorbs 8% of filtered Calcium
• Intercalated Cells: reabsorbed K (active in low K diet) • PTH, Thiazides increases Ca Reabsorption
• Loop Diuretics decreases Ca Reabsorption
• Mechanisms:
o Corticopapillary Osmotic Gradient / Graded Osmolarity in
the Renal Interstitium
§ Created by Countercurrent Multiplier: Loop of Henle
§ Supplemented by Urea Recycling: increases maximum
osmolarity from 600mOsm/L to 1200mOsm/L
§ Maintained by Countercurrent Exchanger: Vasa Recta
o High ADH secretion
§ inserts AQP-2 (water channels) in the LDT and CD to ↑ water
reabsorption → ↑ urine osmolarity and ↓ urine volume
§ Inserts UT1 to ↑ Urea recycling and ↑ NaK2Cl activity in TAL
LH to ↑ osmolarity of the corticopapillary osmotic gradient
PRODUCTION OF DILUTE URINE
• Dilute urine / Hypoosmotic Urine:
o Urine osmolarity < blood osmolarity
• ADH levels are low or ineffective
o Less countercurrent multiplication, urea recycling and insertion
of AQP-2
• Urine: high volume, low concentration
FREE WATER CLEARANCE (CH2O)
• Free Water (Solute Free Water)
© Topnotch Medical Board Prep o Produced by diluting segments of the kidney (TAL LH and EDT)
REGULATION OF PHOSPHATE where NaCl is reabsorbed but not water
• Transport Maximum = 0.1mM/min • Free Water Clearance (CH20)
• Often exceeded in diets with milk and meat o Estimates ability to concentrate or dilute the urine
• PCT: reabsorbs 85% of filtered Phosphate via Na-PO4 § If (-) ADH: Free Water excreted and CH2O is positive
cotransport; other parts to do not reabsorb PO4 § If (+) ADH: Free Water is NOT excreted (water is
o remaining 15% is excreted in the urine reabsorbed) and CH20 is negative
o Reabsorption inhibited by PTH (adenylate cyclase and cAMP
inhibition of the Na-PO4 cotransport)
§ Causes Phosphaturia (increased urinary PO4) and
increased urinary cAMP
o Unreabsorbed PO4 serve as urinary buffer for H+
This is board-relevant: PCT reabsorption occurs only in the PCT and
nowhere else. 85% of filtered phosphate is reabsorbed in the PCT, the
remaining 15% is not reabsorbed anywhere else, and becomes part of the Again: Free water clearance → if positive (or high), free water is going to
urinary buffer for excess acids. your urine (it is excreted); this happens when there is no ADH. If you have
Dr. Banzuela ADH, free water is reabsorbed and free water clearance is negative (or
low). Wag mapagbabaligtad ang positive and negative free water
REGULATION OF MAGNESIUM clearance.
Dr. Banzuela
• Plasma Mg2+ = 1.8mEq/L
Refer to the next table as you listen to the audio recording:
• 50% stored in the bones
• Only 10% of plasma Mg excreted daily
o PCT -25% reabsorption CONDITIONS INVOLVING ADH
o TAL of LH – 65% reabsorption https://qrs.ly/4wcmt33
§ In the TAL of LH, Ca2+ and Mg2+ compete for reabsorption
- Hypercalcemia causes hypomagnesemia
Dr. Banzuela
- Hypocalcemia causes hypermagnesemia
CONDITIONS INVOLVING ADH
This is a favorite in quiz bee competitions: Magnesium is the only solute not Urine
Serum
mainly reabsorbed in the PCT. It is mainly reabsorbed in the TAL of LH. Flow
Serum Osm/
Dr. Banzuela Urine Osm Rate / CH2O
ADH Serum
Urine
Na
Volume
5.5 CONCENTRATION & DILUTION OF URINE
Primary
WATER DEPRIVATION VS. WATER INTAKE ↓ ↓ Hypoosmotic ↑ (+)
Polydipsia
WATER WATER Central DI ↓ ↑ Hypoosmotic ↑ (+)
DEPRIVATION INTAKE Peripheral
↑ ↑ Hypoosmotic ↑ (+)
Immediate effect on DI
↑ ↓ Water ↑ TO
Plasma Osmolarity ↑ Hyperosmotic ↓ (-)
Effect on Osmoreceptors Deprivation NORMAL
SIADH ↑↑ ↓ Hyperosmotic ↓ (-)
in Anterior Stimulates Inhibits
Hypothalamus • Cause of Hyponatremia in patient with Small Cell Lung CA:
ADH Secretion from Arginine Vasopressin (SIADH)
↑ ↓
Posterior Pituitary • increased free water clearance is a hallmark of: Diabetes
Effect on water Insipidus
↑ ↓
permeability in DT & CD ✔GUIDE QUESTIONS
Effect on Urine Which of the following would best distinguish an otherwise healthy
↑ ↓
Osmolarity person with severe water deprivation from a person with the syndrome
Effect on Urine Volume ↓ ↑ of inappropriate antidiuretic hormone (SIADH)?
↓ Plasma ↑ Plasma (A) Free-water clearance (CH2O)
Final Result on Plasma (B) Urine osmolarity
osmolarity osmolarity back
Osmolarity (C) Plasma osmolarity
back to normal to normal
(D) Circulating levels of antidiuretic hormone (ADH)
(E) Corticopapillary osmotic gradient From Physiology BRS, 6 Ed th
PRODUCTION OF CONCENTRATED URINE

Person with severe water deprivation will have HIGH plasma
• In the presence of ADH, filtrate will be isotonic to plasma in the: osmolarity due to water loss from sweating not replaced by water
cortical collecting tubule intake. Person with SIADH will have LOW plasma osmolarity due
• Concentrated urine / Hyperosmotic Urine: to increased water reabsorption from the kidneys that goes to
o Urine osmolarity > blood osmolarity plasma.
Dr. Banzuela
A negative free-water clearance (–CH2O) will occur in a person who 5.6 ACID-BASE BALANCE
(A) drinks 2 L of distilled water in 30 minutes
(B) begins excreting large volumes of urine with an osmolarity of 100 BASIC ACID-BASE PHYSIOLOGY
mOsm/L after a severe head injury • Almost all enzyme systems are influenced by H+ levels and must
(C) is receiving lithium treatment for depression, and has polyuria be regulated
that is unresponsive to the administration of antidiuretic o Normal Plasma H+ = 0.00004 mEq/L
hormone (ADH) § Cumbersome!
(D) has an oat cell carcinoma of the lung, and excretes urine with § Reason for using pH system
an osmolarity of 1000 mOsm/L From Physiology BRS, 6 Ed th
o Normal Plasma pH = -log [H+] = 7.4
Since D is associated with SIADH which will cause a negative free- • pH = 6.8 – 8.0
water clearance due to the high levels of ADH. o Compatible with life
Dr. Banzuela
Compared with a person who ingests 2 L of distilled water, a person with H+ Concentration (mEq/L) pH
water deprivation will have a Extracellular fluid
(A) higher free-water clearance (CH2O) Arterial blood 4.0 x 10-5 7.40
(B) lower plasma osmolarity Venous blood 4.5 x 10-5 7.35
(C) lower circulating level of antidiuretic hormone (ADH)
Interstitial fluid 4.5 x 10-5 7.35
(D) higher tubular fluid/plasma (TF/P) osmolarity in the proximal
tubule Intracellular fluid 1 x 10-3 to 4 x 10-5 6.0-7.4
(E) higher rate of H2O reabsorption in the collecting ducts Urine 3 x 10-2 to 1 x 10-5 4.5-8.0
Gastric HCI 160 0.8
A person with water deprivation will have a higher plasma .
Adapted from Table 31-1. Hall JE. Guyton and Hall Textbook of Medical Physiology. 13th ed. 2016
osmolarity due to sweating not replaced with water intake. ADH Look at the table above from Guyton. Gastric HCl has a pH of 0.8 (in review
secretion will ensue due to increased plasma osmolarity. ADH will books, they round this off to 1-3.5). pH can indeed be less than 1 (it can even
then cause increase water reabsorption in the CD. be a negative number) or be more than 14; it’s just difficult to measure
Dr. Banzuela those values that’s why pH scale is written usually as 0-14 or 1-14.
A woman has a plasma osmolarity of 300 mOsm/L and a urine osmolarity Dr. Banzuela
of 1200 mOsm/L. The correct diagnosis is ✔GUIDE QUESTION
(A) syndrome of inappropriate antidiuretic hormone (SIADH)
To maintain normal H+ balance, total daily excretion of H+ should equal
(B) water deprivation
the daily
(C) central diabetes insipidus
(A) fixed acid production plus fixed acid ingestion
(D) nephrogenic diabetes insipidus
(B) HCO3– excretion
(E) drinking large volumes of distilled water
From Physiology BRS, 6th Ed (C) HCO3– filtered load
(D) titratable acid excretion
Patient here has normal plasma osmolarity but high normal urine (E) filtered load of H+ From Physiology BRS, 6th Ed
osmolarity. If you are deprived of water (while sweating is still
going on), you would lose water more than salt via sweating. This BASIC ACID-BASE PHYSIOLOGY
would increase the plasma osmolarity. ADH will be secreted as a • Systems that regulate H+ Concentrations
response to normalize plasma osmolarity. However, that ADH o Body Fluid Buffer Systems
would cause increased urine osmolarity and decreased urine § CO2 + H2O ↔ H2CO3 ↔ H+ + HCO3-
volume due to increased water reabsorption from the kidneys.
§ Phosphate Buffer System (H2PO4- and HPO4-)
This is NOT SIADH – SIADH would cause an increase in urine § Intracellular Proteins
osmolarity, but it would also cause a DECREASE in plasma o Respiratory Center
osmolarity (plasma osmolarity < 300mOsm/L)
§ Controls PCO2 (Respiratory Acidosis/Alkalosis)
Condition that presents with hypernatremia, polyuria, low urine o Kidneys
Na, hypoosmolar urine: Diabetes Insipidus § Controls HCO3- (Metabolic Acidosis/Alkalosis)
• Most of the volatile acid entering the blood is buffered by:
RENAL HORMONES Hemoglobin
HORMONE SITE OF ACTION EFFECTS
↑ Na+ and H2O RESPIRATORY REGULATION OF ACID-BASE BALANCE
reabsorption • Responds to H+ levels
Aldosterone DT
↑ K+ secretion o ↑ H+ → ↑ RR → ↓ plasma PCO2
↑ H+ Secretion o ↓ H+ → ↓ RR → ↑plasma PCO2
↑ Na+ reabsorption • 50-75% effective in returning pH back to normal within 3-12
↑ H2O reabsorption minutes
Angiotensin II PCT, TAL, LH, DT ↑ Na+-H+ antiport and
HCO3- reabsorption in RENAL REGULATION OF ACID-BASE BALANCE
the PCT • Mechanisms:
PCT, TAL LH, DT, ↑ Water, Na+ o Secretion of excess H+
Catecholamines
CD reabsorption § Na+-H+ Countertransport in the PCT , LH, DT
DT, CD (MOA: § H+ATPase pump in the Distal Tubules and CD
ANP, BNP guanylate cyclase, ↓ Na+ reabsorption o Reabsorption of filtered HCO3- if warranted
cGMP) § Coupled to H+ Secretion
Uroguanylin, ↓ Water, Na+ o Production of New HCO3- if warranted
PCT, CD
Guanylin reabsorption § Use of Ammonia (NH3) and Phosphate (NaHPO4-) buffers
↓ Water, Na+ - These buffers also help excrete titratable acids
Dopamine PCT
reabsorption
↓ phosphate
reabsorption
PCT, TAL LH
↑ Ca2+ reabsorption
PTH (MOA: Adenylate
Stimulates 1-alpha
cyclase, cAMP)
hydroxylase for Vit D
final activation
TAL LH, LDT, CD
(MOA: V2 ↑ water permeability,
ADH receptor, ↑reabsorption and
adenylate cyclase, Na-K-2Cl activity
cAMP)
• Formula for Net Acid Excretion:
o NAE: Net acid excretion

o V: Volume of urine produced per unit time
o UNH4: Urine concentration of ammonium
o UTA: Urine concentration of titratable acid
o UHCO3: Urine concentration of bicarbonate
✔GUIDE QUESTION • High-anion gap metabolic acidosis (HAGMA)
The reabsorption of filtered HCO3– o Decreased HCO3-
(A) results in reabsorption of less than 50% of the filtered load when o ↑ Organic Anions (e.g. ketoacids, salicylate) to maintain
the plasma concentration of HCO3– is 24 mEq/L electroneutrality
(B) acidifies tubular fluid to a pH of 4.4 • Normal-anion gap metabolic acidosis (NAGMA)
(C) is directly linked to excretion of H+ as NH4+ o Decreased HCO3-
(D) is inhibited by decreases in arterial PCO2
o ↑ Chloride to maintain electroneutrality
(E) can proceed normally in the presence of a renal carbonic
anhydrase inhibitor From Physiology BRS, 6 Ed th
o Also called Hyperchloremic Metabolic Acidosis with Normal
Anion Gap
Listen to this audio recording while reading the section below on acid-
based abnormalities:
MNEMONICS METABOLIC ACIDOSIS
MUDPILES: HAGMA
ACID-BASE ABNORMALITIES Methanol, Uremia, DKA, Paraldehyde, Propylene Glycol, Iron
https://qrs.ly/encmt3e Isoniazid, Idiopathic Acidosis, Lactic Acidosis (in Sepsis, Shock),
Ethylene Glycol, Ethanol, Salicylic Acid
Dr. Banzuela HARD-UP: NAGMA
Hyperalimentation, Acetazolamide, RTA, Diarrhea,
ACID-BASE ABNORMALITIES Ureteroenteric fistula, Pancreaticoduodenal Fistula
pH H+ PCO2 HCO3- COMPENSATION
40 40 24 Memorize MUDPILES and HARD-UP mnemonic. Very useful shortcuts
Normal 7.4 -- whenever you have cases in the exams dealing with ABG interpretation.
mEq/L mmHg mEq/L
• ↑ H+ Excretion Acetazolamide: drug used in the treatment of acute mountain sickness. It
Respiratory is a Carbonic Anhydrase Inhibitor (CAI) and the one associated with
↓ ↑ ↑↑ ↑ • ↑HCO3-
Acidosis metabolic ACIDOSIS (mnemonic: ACIDazolamide)
Reabsorption
Dr. Banzuela
• ↓ H+ Excretion
Respiratory
↑ ↓ ↓↓ ↓ • ↓ HCO3-
Alkalosis METABOLIC ALKALOSIS
Reabsorption
Metabolic • Due to conditions resulting in loss of acid or gain of base
↓ ↑ ↓ ↓↓ • Hyperventilation
Acidosis • e.g. Loop Diuretics, Thiazide Diuretics, Vomiting,
Metabolic Hyperaldosteronism, Ingestion of Alkaline Drugs (Sodium
↑ ↓ ↑ ↑↑ • Hypoventilation Bicarbonate)
Alkalosis
REMEMBER TRIO OF ELECTROLYTES
✔GUIDE QUESTIONS
H+, Ca++, K+ Which of the following is a cause of metabolic alkalosis?
áH+ levels à HyperCalcemia (A) Diarrhea (D) Treatment with acetazolamide
HyperKalemia (B) Chronic renal failure (E) Hyperaldosteronism
(C) Ethylene glycol ingestion th
RESPIRATORY ACIDOSIS
• Due to conditions resulting in Decreased Ventilation (RR) Since aldosterone cause H+ secretion to the urine,
hyperaldosteronism (e.g., Conn syndrome) will cause metabolic
• e.g. Opiates, Sedatives, Anesthetics, Guillain-Barré Syndrome,
alkalosis.
Polio, Amyotrophic Lateral Sclerosis, Multiple Sclerosis, Airway Dr. Banzuela
Obstruction, ARDS, COPD A 45-year-old woman develops severe diarrhea while on vacation. She
• MOA of motor paralysis in GBS: demyelination of Type A-Beta has the following arterial blood values:
Fibers pH = 7.25
PcO2 = 24 mm Hg
RESPIRATORY ALKALOSIS [HCO3–] = 10 mEq/L
• Due to conditions resulting in Increased Ventilation (RR) Venous blood samples show decreased blood [K+] and a normal anion
• e.g. Pneumonia, Pulmonary embolus, High Altitude, Psychogenic, gap. The correct diagnosis for this patient is
Salicylate Intoxication (A) metabolic acidosis (D) respiratory alkalosis
(B) metabolic alkalosis (E) normal acid–base status
METABOLIC ACIDOSIS (C) respiratory acidosis From Physiology BRS, 6 Ed th
• Due to conditions resulting in excess acid or loss of base A 45-year-old woman develops severe diarrhea while on vacation. She
• e.g. Ketoacidosis, Lactic Acidosis, Salicylate Intoxication, has the following arterial blood values:
pH = 7.25
Methanol/ Formaldehyde Intoxication, Ethylene glycol
PcO2 = 24 mm Hg
intoxication, Diarrhea [HCO3–] = 10 mEq/L
• Anion Gap (AG) used to help diagnose cause of metabolic acidosis Venous blood samples show decreased blood [K+] and a normal anion
gap. Which of the following statements about this patient is correct?
(A) She is hypoventilating
(B) The decreased arterial [HCO3–] is a result of buffering of excess H+
by HCO3–
(C) The decreased blood [K+] is a result of exchange of intracellular H+
for extracellular K+
(D) The decreased blood [K+] is a result of increased circulating
Remember:
levels of aldosterone
ECF: major cation: Na+. major
(E) The decreased blood [K+] is a result of decreased circulating levels
anions: Cl- and HCO3-.
of antidiuretic hormone (ADH)
ICF: major cation: K+. major From Physiology BRS, 6th Ed
anions: proteins, ATP, ADP
Dr. Banzuela
A patient has the following arterial blood values: PRE-TEST EQUATIONS
pH = 7.52
PCO2 = 20 mm Hg FRACTIONAL EXCRETION OF NA
[HCO3–] = 16 mEq/L
Which of the following statements about this patient is most likely to be
correct? • Question
(A) He is hypoventilating
(B) He has decreased ionized [Ca2+] in blood
o 38/F decreased urine output. (+) ibuprofen use.
(C) He has almost complete respiratory compensation o Labs:
(D) He has an acid–base disorder caused by overproduction of fixed § BUN: 49mg/dL
acid § Serum Na = 135 mmol/L
(E) Appropriate renal compensation would cause his arterial § Serum creatinine: 7.5mg/dL
[HCO3–] to increase From Physiology BRS, 6 Ed th
§ Urine Na = 33 mmol/L
Remember trio of electrolytes mnemonic? Alkalosis will cause § Urine creatinine = 90mg/dL
decreased plasma Ca2+ What is her fractional Na excretion?
Dr. Banzuela
• Answer
A patient arrives at the emergency room with low arterial pressure, o Fractional Excretion (FE)
reduced tissue turgor, and the following arterial blood values: ( ×*
pH = 7.69 o FE = amount excreted/amount filtered = + !"×,-.
!"
[HCO3–] = 57 mEq/L (#$%" ×*
o 𝐺𝐹𝑅 =
PCO2 = 48 mm Hg +#$%"
(!" ×* (!" ×+#$%"
Which of the following responses would also be expected to occur in this o 𝐹𝐸 = &#$%" ×( =
+!" × +!" ×(#$%"
patient? )#$%"
(A) Hyperventilation //01×2.405/78
o = 9/401×:;05/78 = 0.02
(B) Decreased K+ secretion by the distal tubules
(C) Increased ratio of H2PO4– to HPO4–2 in urine § FE<1%: volume depletion
(D) Exchange of intracellular H+ for extra-cellular K+ § FE>2%: acute renal failure
From Physiology BRS, 6 Ed th
6. GASTROINTESTINAL PHYSIOLOGY
5.7 INTEGRATIVE EXAMPLES
1. Structure and Innervation of the GIT
ADDISON DISEASE 2. Regulatory Substances in the GIT
• ↓ adrenocortical hormones – aldosterone, cortisol and weak 3. GI Motility
androgens 4. GI Secretion
• ↓ aldosterone results in: 5. Digestion and Absorption
o ↓ Na and H2O reabsorption: 6. Liver Physiology
§ ↓ IVV → ↓ VR → ↓ CO → ↓ BP → stimulates BRR → ↑HR The GI tract is just one long tube from mouth to anus. For an intro to the
§ ECF Volume Contraction → ↑ inappropriate ADH GIT, watch this video:
secretion → hypoNa
o ↓ K secretion: Hyperkalemia
o ↓ H secretion: Metabolic acidosis INTRO TO THE GIT
✔GUIDE QUESTION
https://qrs.ly/wlcmt3n
A man presents with hypertension and hypokalemia. Measurement of his
arterial blood gases reveals a pH of 7.5 and a calculated HCO3– of 32 Dr. Banzuela
mEq/L. His serum cortisol and urinary vanillylmandelic acid (VMA) are
normal, his serum aldosterone is increased, and his plasma renin activity
is decreased. Which of the following is the most likely cause of his 6.1 STRUCTURE & INNERVATION OF THE GIT
hypertension? LAYERS OF THE GIT
(A) Cushing syndrome (D) Renal artery stenosis • Mucosa
(B) Cushing disease (E) Pheochromocytoma
From Physiology BRS, 6 Ed o Epithelium: for secretion and absorption
(C) Conn syndrome th
o Lamina Propria: contains connective tissue, blood vessels and

HPN can have the following lethal effects: heart attack, heart failure, stroke lymphoid structures (Peyer’s patches)
(cerebral blood vessels rupture or clog more easily), kidney failure, vision o Muscularis Mucosa: smooth muscle controlling epithelium
loss, sexual dysfunction, angina, peripheral artery disease. .
Dr. Banzuela • Submucosa
VOMITING o Collagen, elastin, glands, blood vessels
• Loss of HCl from stomach: • Muscularis externa
o Metabolic alkalosis, hypochloremia and ECF Volume o Inner Circular: decreases diameter of lumen
Contraction o Outer Longitudinal: shortens segment of GIT
• ECF Volume Contraction: • Serosa
o ↓ Renal Perfusion Pressure → ↑ Angiotensin II and Aldosterone o a.k.a. adventitia / mesothelium
• ↑ Angiotensin II:
o ↑ Na+-H+ exchange, ↑ HCO3- reabsorption → Metabolic Alkalosis
• ↑ Aldosterone:
o ↑ H+ secretion → Metabolic Alkalosis
o ↑ K+ secretion → Hypokalemia
DIARRHEA
• Loss of HCO3-
o Metabolic Acidosis
• Respiratory Compensation: Hyperventilation
• ECF Volume Contraction:
o Stimulates BRR → ↑ HR
o Stimulates RAAS → hypokalemia
• most likely seen in osmotic diarrhea: increase in the stool
osmotic gap (>50mOsm)

Wag deadmahin ang muscularis mucosa. This muscularis mucosa is the
smooth muscle responsible for GI secretions. It is innervated by the
Meissner plexus. The circular and longitudinal muscles are the ones
innervated by the Auerbach plexus for motility.
Dr. Banzuela
INNERVATION OF THE GI TRACT • TRIGGER: All Types of Food (main
• Extrinsic trigger: Fatty Acids)
o Parasympathetic (Excitatory) • SOURCE: I cells in the DUODENUM
• From pharynx to proximal 2/3 of transverse • ACTIONS: Bile Secretion (GB CCK
colon contraction, SOO relaxation), Increases
Vagus GET (Decreases GE), Increases
• Vagovagal reflexes: Reflexes in which both
Nerve pancreatic enzyme secretion
afferent & efferent pathways are contained in
Vagus nerve • TRIGGER: H+ in the duodenum, FA in
Pelvic • Innervates from distal 1/3 of transverse colon to duodenum
Nerve upper portion of anal canal • SOURCE: S cells in the duodenum
o Sympathetic (Inhibitory) • ACTIONS: Inhibits HCl secretion,
SECRETIN
• Intrinsic (Enteric Nervous System): Coordinates and relays increases biliary and pancreatic
info from ANS to GI tract HCO3-
• *this hormone does NOT affect
MEISSNER PLEXUS AUERBACH PLEXUS pancreatic ENZYME secretion!
• Submucosal • TRIGGER: Oral Glucose GLUCOSE-
SYNONYM • Myenteric Plexus
Plexus • SOURCE: K cells in the duodenum DEPENDENT
• between • between inner • ACTIONS: Stimulates insulin secretion; INSULINOTROPIC
submucosa and circular and outer inhibits gastric emptying (above PEPTIDE
LOCATION
inner circular longitudinal normal physiologic levels) (GIP)
muscle layer muscle layer • TRIGGER: Fasting
• inner circular and • SOURCE: M cells in the duodenum and
MUSCLE(S)
• Muscularis Mucosa outer longitudinal Jejunum
INNERVATED
muscles • ACTIONS: activates interdigestive /
MOTILIN
ACTION • SECRETION • MOTILITY migrating myoelectric complex
The differences between Meissner Plexus and Auerbach Plexus are favorites (MMC). Acts only on the stomach and
in any physiology exam. Know them by heart – their synonyms, location and small intestines (has no effect on the
actions. Remember the most basic: Meissner for Secretions, Auerbach for large intestines)
Motility.
Dr. Banzuela
Another favorite in the med boards. Remember the characteristics of the 5
official GI hormones listed above. Remember everything listed in the table
above. To help you – when you see gastrin, think of HCl. When you see
SPECIAL NOTES ON THE LAYERS OF THE GIT
secretin, think of anti-HCl actions. When you see CCK, think of fat, bile
• Layer not seen in Esophagus: Serosa secretion and decreased gastric emptying. When you see GIP, think
• Strongest Layer of the esophagus: Submucosa increased insulin as a result of oral (not IV) glucose. And when you see
• 3 Muscle Layers of the Stomach: Inner Oblique, Middle Circular, motilin, think of fasting and increased GI motility to remove remnant food
Outer Longitudinal in the GI tract.
Dr. Banzuela
• Myenteric Plexus is mainly excitatory EXCEPT for: Pyloric
✔GUIDE QUESTIONS
Sphincter (PS), Ileocecal Valve (ICV)
Cholecystokinin (CCK) has some gastrin-like properties because both
CCK and gastrin
6.2 REGULATORY SUBSTANCES IN THE GIT (A) are released from G cells in the stomach
Hormones are chemical messengers released into the blood and acts on (B) are released from I cells in the duodenum
distant sites. There are 5 OFFICIAL GI hormones and several CANDIDATE (C) are members of the secretin-homologous family
GI hormones (not officially accepted). Paracrines are substances released (D) have five identical C-terminal amino acids
to act on NEARBY cells (“para” means “near”). Neurocrines are substances (E) have 90% homology of their amino acids
that induce action potentials. Take note of the definitions of hormones,
Cholecystokinin (CCK) inhibits
paracrines and neurocrines.
Dr. Banzuela
(A) gastric emptying
(B) pancreatic HCO3– secretion
(C) pancreatic enzyme secretion
(D) contraction of the gallbladder
(E) relaxation of the sphincter of Oddi From Physiology BRS, 6 Ed th
Which of the following substances is secreted in response to an oral

glucose load?
(A) Secretin
(B) Gastrin
(C) Cholecystokinin (CCK)
(D) Vasoactive intestinal peptide (VIP)
(E) Glucose-dependent insulinotropic peptide (GIP)
Which of the following substances inhibits gastric emptying?
(A) Secretin
(B) Gastrin
(C) Cholecystokinin (CCK)
(E) Gastric inhibitory peptide (GIP) From Physiology BRS, 6 th Ed
© Topnotch Medical Board Prep CANDIDATE GI HORMONES

(NOT OFFICIALLY ACCEPTED AS GI HORMONES)
THE 5 OFFICIAL GI HORMONES • Pancreatic Polypeptide
DESCRIPTION HORMONE o Secreted by pancreas in response to CHO, CHON, lipids
• TRIGGER: CHON and AA (especially the o Inhibits pancreatic HCO3- and enzyme secretion
amino acids phenylalanine (F), • Enteroglucagon
tryptophan (W) and methionine (M), o Secreted by intestinal cells in response to hypoglycemia
Gastric Distention o Stimulates glycogenolysis and gluconeogenesis
• SOURCE: G cells of the GASTRIC • Glucagon-Like Peptide 1 (GLP-1)
GASTRIN o Secreted by L-cells of small intestines
ANTRUM (not in the cardia-fundus
area!) o Stimulates insulin secretion
• ACTIONS: Stimulates Parietal cells in o Maybe helpful in the treatment of DM Type 2
FUNDUS for HCl Secretion, growth of o Insulin secretion following a CHO-rich meal is stimulated by:
gastric mucosa GLP-1
GIP, GLP-1 are INCRETIN HORMONES. INCRETIN EFFECT occurs when 6.3. GI MOTILITY
ingested glucose has a greater effect on insulin secretion than injected
glucose. GIP, GLP-1 mediate this phenomenon. • Contractile Tissue in the GI tract is made up of Unitary
Dr. Banzuela Smooth Muscles EXCEPT:
GI PARACRINES o Pharynx
o Upper 1/3 of Esophagus
• Somatostatin
o External Anal Sphincter
o Secreted by cells throughout the GI tract in response to H+
§ Depolarization of Circular Muscle: decreases diameter of
o Inhibits release of ALL GI hormones
that segment
o Inhibits gastric H+ secretion
§ Depolarization of Longitudinal Muscle: decreases length of
• Histamine that segment
o Secreted by mast cells of gastric mucosa
o Increases H+ secretion; potentiates gastrin and Ach action GI SMOOTH MUSCLE CONTRACTIONS
TONIC CONTRACTIONS PHASIC CONTRACTIONS
Pronounce it this way: somatoSTOPin. Somatostatin is the ultimate
inhibitory hormone. Hypothalamic somatostatin inhibits Growth Hormone • Constant level of contraction • Periodic contractions
(GH), Pancreatic somatostatin inhibits insulin and glucagon, and GIT or tone without regular followed by relaxation
somatostatin inhibits all GI hormones. periods of relaxation • For mixing and propulsion
Dr. Banzuela
• Orad (upper) region of the • Seen in the esophagus,
NEUROCRINES stomach and in the lower gastric antrum, small
• VIP esophageal, ileocecal and intestines
o Relaxes Lower Esophageal Sphincter (LES), Orad Stomach, internal anal sphincters • Due to spike potentials
Pyloric Sphincter, Ileocecal Valve • Due to subthreshold slow
o Stimulates HCO3- secretion and Inhibits gastric H secretion waves
o Secreted by pancreatic islet cell tumors and involved in Tonic contractions are TONICALLY (continuously) contracted. Think
pancreatic cholera Sphincters. Tonic Contractions are caused by SLOW WAVES. Phasic
contraction are contractions in PHASES (alternate contraction and
VIP is the ultimate smooth muscle relaxant – it relaxes the LES, Orad
relaxation). Phasic contractions are caused by SPIKE POTENTIALS.
Stomach, PS and ICV. Mnemonic: kapag VIP ang bisita, dapat chillax siya Dr. Banzuela
pagdating sa bahay nyo. VIP is a chillax substance – it provides smooth ELECTRICAL ACTIVITY OF GI SMOOTH MUSCLE
muscle relaxation.
Dr. Banzuela • Slow Waves
• Enkephalins (met-enkephalin and leu-enkephalin) o Not true action potentials
o Contracts LES, Pyloric Sphincter, Ileocecal Valve o Determine pattern of contraction
o Inhibits intestinal secretion of fluids and electrolytes (basis for o Slow, oscillating membrane potentials
use of opiates in diarrhea) § Cyclic opening of Ca2+ channels (depolarization) followed by
• GRP (Bombesin) opening of K+ channels (repolarization)
o Stimulates gastrin release from G cells o Due to GI Pacemaker: Interstitial Cells of Cajal
o Slowest Frequency: Stomach (3/min)
✔GUIDE QUESTION
o Fastest Frequency: Duodenum (12/min)
Which of the following substances is released from neurons in the GI tract
and produces smooth muscle relaxation? • Spike Potentials
(A) Secretin (D) Vasoactive intestinal peptide o True Action Potentials
(B) Gastrin (VIP) o Depolarization: due to Calcium Influx
(C) Cholecystokinin (CCK) (E) Gastric inhibitory peptide (GIP) o Threshold: -40Mv
DESCRIPTION ANSWER
Inhibits appetite; found at the
SATIETY CENTER
Ventromedial Hypothalamus
Stimulates appetite; found at the APPETITE/HUNGER
Lateral Hypothalamic Area CENTER
Sends signals to Satiety & Hunger
ARCUATE NUCLEUS
Centers
ANOREXIGENIC
Releases POMC to decrease appetite
NEURONS
Releases Neuropeptide Y to increase OREXIGENIC © Topnotch Medical Board Prep
appetite NEURONS Remember: slow waves are NOT true action potentials. They only bring you
closer to threshold. Spike potentials are true action potentials. Slow waves
Stimulates Anorexigenic Neurons, are produced by the interstitial cells of Cajal (the GI Pacemaker), slowest
LEPTIN, INSULIN,
inhibits orexigenic Neurons; frequency in the stomach, fastest in the duodenum.
GLP-1
secreted by fat cells Dr. Banzuela
Inhibits Anorexigenic Neurons; ✔GUIDE QUESTION

GHRELIN
secreted by gastric cells Slow waves in small intestinal smooth muscle cells are
Inhibits Ghrelin PEPTIDE YY (A) action potentials
(B) phasic contractions
If you damage the ventromedial hypothalamic area will the patient have
(C) tonic contractions
weight gain or weight loss? Answer: weight Gain. Ventromedial
(D) oscillating resting membrane potentials
hypothalamus is the satiety center. If that is destroyed, patient would be
(E) oscillating release of cholecystokinin (CCK)
less satiated (less busog), so patient would eat more, and then gain weight.
Leptin (from the Greek word “leptos” meaning thin) decreases food intake SPECIAL NOTES ON PERISTALSIS
(through its anorexigenic effect) and may also increase energy • Most common stimulus for GI peristalsis: Distention
expenditure. • Composition of Myenteric Reflex: Muscles Upstream (nearer the
Dr. Banzuela
mouth) will contract, Muscles Downstream (nearer the anus) will
MNEMONICS APPETITE exhibit receptive relation
VENTROMEDIAL: “VUCHOG” • Time to transfer material from pylorus to ileocecal valve: 3-5 hours
Satiety Center • Time to transfer material from ileocecal valve to colon: 8-15 hours
LATERAL: “LAMON”
Hunger Center CHEWING
• Maybe voluntary or involuntary
• Functions:
o Lubricates food with saliva
o Decreases size of food particles
o Amylase begins CHO digestion
SWALLOWING INCREASES GASTRIC DECREASES GASTRIC

• Swallowing Center: Medulla (utilizing CN IX and X) EMPTYING EMPTYING
1. Oral Phase: triggers reflex when food is at the pharynx Increased GASTRIC volume Increased DUODENAL volume
2. Pharyngeal Phase: soft palate pulled upward (closes Isotonic content Hypertonic & Hypotonic
nasopharynx), glottis covered (prevents aspiration), Upper content
Esophageal Sphincter (UES) relaxes Chyme Formation Fat in the duodenum
3. Esophageal Phase: UES closes, Primary and Secondary HCl in the duodenum (acids)
Esophageal Peristalsis occurs ✔GUIDE QUESTION
Which of the following abolishes “receptive relaxation” of the stomach?
(A) Parasympathetic stimulation
(B) Sympathetic stimulation
(C) Vagotomy
(D) Administration of gastrin
(E) Administration of vasoactive intestinal peptide (VIP)
Receptive relaxation of the orad stomach occurs using a

vagovagal reflex. Vagotomy would prevent that.
Dr. Banzuela
SMALL INTESTINAL MOTILITY

• Segmentation Contraction
o Back-and-forth movement with no net forward motion
o Mixes chyme with pancreatic enzymes
• Peristaltic Contraction
o Propels chyme towards large intestines
§ rhythmic phasic contraction propels chyme in a unilateral
direction
o (+) contraction behind bolus and (+) relaxation in front of bolus
ESOPHAGEAL PERISTALSIS
• Primary Peristaltic Contraction
o Creates high pressure behind bolus of food propelling it towards
the stomach
o Accelerated by Gravity (you don’t need gravity to swallow, since
the pressure is high enough to put bolus into the stomach;
gravity assists though)
• Relaxation of the Lower Esophageal Sphincter (LES)
o Utilizes VIP and NO from inhibitory ganglionic neurons
• Receptive Relaxation of the Orad Stomach
o Food enters the stomach
• Secondary Peristaltic Contraction
o Clears esophagus of remaining food
o Gastric acid reflux into the esophagus triggers: secondary © Topnotch Medical Board Prep
esophageal peristalsis
• In Achalasia, esophageal myenteric plexus is deficient, NO and
VIP is deficient (due to decreased expression of neuronal NO
synthase) à no anterograde/receptive relaxation ahead of the
stimulus
• 49/F vomiting shortly after eating has normal rate of liquid
emptying but prolonged time for emptying of solids. Diagnosis:
Pyloric Stenosis
REMEMBER! ESOPHAGEAL PRESSURES

Intraesophageal Pressure = Intrathoracic Pressure.
Intraesophageal Pressure < Atmospheric Pressure.
You can swallow food upside down (against gravity)
Gravity assists, but is not a necessity, in swallowing
Dr. Banzuela
GASTRIC MOTILITY © Topnotch Medical Board Prep

• VIP, CCK: facilitates Receptive Relaxation of Orad Stomach ✔GUIDE QUESTION
o Fundus and upper portion of the stomach body relaxes A 24-year-old male graduate student participates in a clinical research
o Receptive Relaxation of the stomach is the reason why gastric study on intestinal motility. Peristalsis of the small intestine
pressure seldom rise above the levels that breach the LES even (A) mixes the food bolus
if stomach is filled with meal (B) is coordinated by the central nervous system (CNS)
(C) involves contraction of smooth muscle behind and in front of the
• Parasympathetic NS (via VN X): stimulates gastric contractions food bolus
• Capacity of Stomach: 1.5L (D) involves contraction of smooth muscle behind the food bolus
• Motilin: stimulates gastric contractions (MMC) every 90 and relaxation of smooth muscle in front of the bolus
minutes to help clear stomach of residual food (E) involves relaxation of smooth muscle simultaneously throughout
• Retropulsion: food in the caudad stomach going back to orad the small intestine From Physiology BRS, 6 Ed th
stomach for further mixing and digestion

Gastric emptying: movement of material from stomach to
duodenum; takes approximately 3 hours
LARGE INTESTINAL MOTILITY ✔GUIDE QUESTION

Which of the following changes occurs during defecation?
• Ileocecal valve: prevents reflux into the ileum (A) Internal anal sphincter is relaxed
• Proximal Colon: for absorption of water (B) External anal sphincter is contracted
• Distal Colon: for storage of feces (C) Rectal smooth muscle is relaxed
• Segmentation Contractions (Haustrations): responsible for the (D) Intra-abdominal pressure is lower than when at rest
appearance of Haustra (sac-like structures in the colon) (E) Segmentation contractions predominate
• Mass movements: occur 1-3x a day to move colonic contents over
long distances GASTROILEAL & GASTROCOLIC REFLEX
• Emotions: influences large intestinal motility via extrinsic ANS • Gastroileal Reflex
o May cause diarrhea or constipation o Food in the stomach increases peristalsis in the ileum and
relaxation of the ileocecal sphincter
• Gastrocolic Reflex
o Food in the stomach increases peristalsis in the colon and
frequency of mass movements
§ Mediated by the Parasympathetic NS, CCK, Gastrin
o Gastrocolic reflex is the reason why in infants, defecation
often follows a meal
o Cause of normal bowel movements in newborns: gastrocolic
reflex
VOMITING
• Wave of reverse peristalsis (orad direction) that begins from the
Small Intestines
• Preceded usually by Nausea
• Vomiting Center: Medulla
o Receives info from the vestibular system, back of the throat,
GI tract and the Chemoreceptor Trigger Zone
o Location of the chemoreceptor Trigger Zone: Area Postrema
§ Triggers
1. Emetics
DEFECATION 2. Radiation
3. Vestibular stimulation
• Urge to defecate occurs once rectum is 25% filled
• Retching: incomplete vomiting due to Closed UES
• Gas from colon is primarily derived from: Fermentation of
undigested oligosaccharides 6.4 GI SECRETION
• Internal Anal Sphincter GASTRO-INTESTINAL JUICES
o Involuntary TYPE DAILY VOLUME (ML) PH
o Relaxed by rectal contents (rectosphincteric reflex) Saliva 1000 6.0-7.0
• External Anal Sphincter Gastric Secretion 1500 1.0-3.5
o Voluntary Pancreatic Secretion 1000 8.0-8.3
o Must be relaxed by the person for defecation to occur Bile 1000 7.8
• Valsalva Maneuver S.I. Secretion 1800 7.5-8.0
o Expiring against a closed glottis (increasing intra-abdominal
Brunner’s Gland Secretion 200 8.0-8.9
pressure)
L.I Secretion 200 7.5-8.0
o Assists in defecation
TOTAL 6700
Urge to defecate once rectum is 25% filled. Urge to urinate occurs once
In Ganong 25-3, Pancreatic Juice is the most basic (alkaline) simply
urinary bladder is 25% filled. External anal sphincter is voluntary, internal
because there is no Brunner Gland Secretion in the choices. If there is,
anal sphincter is involuntary. External urethral sphincter is voluntary,
Brunner Gland secretion is the correct answer.
internal urethral sphincter is involuntary. Both external and internal anal
Remember the magic number 1.5L: you produce 1.5L of HCl per day, 1.5L
sphincters must relax for defecation to occur. Both external and internal
of water is absorbed in the large intestines to dry up the feces, and 1.5L is
urethral sphincters must relax for urination to occur.
Dr. Banzuela the capacity of the stomach.
Dr. Banzuela
SUMMARY OF GASTROINTESTINAL (GI) SECRETIONS

GI SECRETION MAJOR CHARACTERISTICS STIMULATED BY INHIBITED BY
• High HCO3-
• High K+ • Sleep
• Parasympathetic nervous system
Saliva • Hypotonic • Dehydration
• Sympathetic nervous system
• ⍺-Amylase • Atropine
• Lingual lipase
• ↓ Stomach pH
• Gastrin • Chyme in duodenum (via secretin and GIP)
• HCl • Parasympathetic nervous system • Somatostatin
Gastric
• Histamine • Atropine
secretion
• Cimetidine, Omeprazole
• Pepsinogen • Parasympathetic nervous system -
• Intrinsic Factor - -
• Secretin
• High HCO3-
• CCK (potentiates secretin) -
Pancreatic • Isotonic
secretion
• Pancreatic lipase, • CCK
-
amylase, proteases • Parasympathetic nervous system
• CCK (causes contraction of
• Bile salts
gallbladder and relaxation of
• Bilirubin
Bile sphincter of Oddi) • Ileal resection
• Phospholipids
• Cholesterol
(causes contraction of gallbladder)
CCK = Cholecystokinin; GIP = glucose-dependent insulinotropic peptide
SALIVA Which of the following is the site of secretion of gastrin?
• Formed mainly by parotid, submandibular and sublingual (A) Gastric antrum (D) Ileum
(B) Gastric fundus (E) Colon
glands From Physiology BRS, 6 Ed
(C) Duodenum th
• Composition: When parietal cells are stimulated, they secrete

o High volume relative to salivary gland size (A) HCl and intrinsic factor (D) HCO3– and intrinsic factor
o High K and HCO3- (B) HCl and pepsinogen (E) mucus and pepsinogen
o Low Na and Cl (C) HCl and HCO3– From Physiology BRS, 6 th Ed
o Hypotonic
o (+) amylase, lingual lipase and kallikrein HCL SECRETION
• Increased by:
o Food in the mouth, smells, conditioned reflexes, nausea
• Inhibited by:
o Sleep, dehydration, fear, anticholinergic drugs
Refer to the next picture and table as you listen to this audio recording
regarding salivation:
SALIVATION
https://qrs.ly/uscmt3x
Dr. Banzuela

Refer to the picture above as we discuss HCl secretion in the stomach using
the audio recording below:
HCl SECRETION
IN THE STOMACH
https://qrs.ly/7vcmt4q
DESCRIPTION ANSWER
Effect of Parasympathetic NS INCREASES SALIVATION Dr. Banzuela
Effect of Sympathetic NS INCREASES SALIVATION • Stimulates HCl Secretion

Initial Saliva is high in: Na+, Cl- o Histamine on H2 receptors, Ach on M3 receptors and Gastrin
on CCKB receptors
Final Saliva is high in: HCO3-, K+
o Note: above 3 can potentiate
Hormone involved in absorbing
ALDOSTERONE o Basal acid output is increased by: alkalinization of antrum
Na+ at the ductal cells
(releases gastrin-releasing cells from inhibitory influence of
HIGH Na+, Cl-, LOW K+ & somatostatin)
At High Flow Rates, Saliva has
HIGH HCO3
• Inhibits HCl Secretion
LOW Na+, Cl -, HIGH K+ &
At Low Flow Rates, Saliva has o Low pH (<3.0) of the stomach, somatostatin, prostaglandins
LOW HCO3-
• Phases:
o Cephalic Phase (30%), Gastric Phase (60%) and Intestinal Phase
✔GUIDE QUESTION
(10%)
Which of the following is characteristic of saliva?
(A) Hypotonicity relative to plasma Sight, smell, taste of food (cephalic phase) contributes to INCREASED
(B) A lower HCO3– concentration than plasma gastric/HCl secretion.
(C) The presence of proteases Low gastric pH (e.g., gastric pH<3.0) contributes to DECREASED
(D) Secretion rate that is increased by vagotomy gastric/HCl secretion
(E) Modification by the salivary ductal cells involves reabsorption of Dr. Banzuela
K+ and HCO3– From Physiology BRS, 6 Ed th • Drugs that block HCl secretion
It’s hypotonic because of the low Na concentration. o Atropine on M3, Cimetidine on H2 and PPI (Omeprazole) on H+-
Dr. Banzuela K+-ATPase exchange pump
o Best describes H2 blockers: inhibits both gastrin- and
GASTRIC CELLS & SECRETIONS acetylcholine-mediated secretion of acid
DESCRIPTION ANSWER
✔GUIDE QUESTIONS
Contains Mucus Neck Cells, Secretion of which of the following substances is inhibited by low pH?
OXYNTIC GLANDS (BODY)
Parietal Cells and Chief Cells (A) Secretin
Contains G Cells, Mucus Cells PYLORIC GLANDS (ANTRUM) (B) Gastrin
MUCUS CELLS, MUCUS NECK (C) Cholecystokinin (CCK)
Secretes Mucus and HCO3 -
CELLS
PARIETAL CELLS/OXYNTIC (E) Gastric inhibitory peptide (GIP) From Physiology BRS, 6 Ed th
Secretes HCl and IF A patient with a duodenal ulcer is treated successfully with the drug
CELLS
cimetidine. The basis for cimetidine’s inhibition of gastric H+ secretion is
Secretes Gastrin G CELLS that it
Secretes Serotonin ENTEROCHROMAFFIN CELLS (A) blocks muscarinic receptors on parietal cells
ENTEROCHROMAFFIN-LIKE (B) blocks H2 receptors on parietal cells
Secretes Histamine
(ECL) CELLS (C) increases intracellular cyclic adenosine monophosphate (cAMP)
CHIEF/PEPTIC/ZYMOGENIC levels
Secretes Pepsinogen (D) blocks H+, K+-adenosine triphosphatase (ATPase)
CELLS
(E) enhances the action of acetylcholine (ACh) on parietal cells
✔GUIDE QUESTIONS From Physiology BRS, 6th Ed
Which of the following is the site of secretion of intrinsic factor? A patient with Zollinger–Ellison syndrome would be expected to have
(A) Gastric antrum (D) Ileum which of the following changes?
(B) Gastric fundus (E) Colon (A) Decreased serum gastrin levels
(C) Duodenum From Physiology BRS, 6 th Ed (B) Increased serum insulin levels
(C) Increased absorption of dietary lipids
IF is the only essential secretion of the stomach. It is essential (D) Decreased parietal cell mass
because we need it to absorb Vitamin B12 (this vitamin is needed (E) Peptic ulcer disease From Physiology BRS, 6 Ed th
for proper DNA synthesis)

Dr. Banzuela
CLINICAL CORRELATES ZOLLINGER-ELLISON SYNDROME • CCK causes Sphincter of Oddi Relaxation
Gastrinoma → High levels of Gastrin → (+) hypersecretion of HCl • Bile is release in “pulsatile spurts” due to intermittent
→ severe ulcers formed contraction of the duodenum
• 94% Bile salts are recirculated back to the liver using Na-Bile salt
EXOCRINE PANCREATIC SECRETION
cotransporter in the terminal ileum (enterohepatic circulation)
• Characteristics o Removal of terminal ileum results in: steatorrhea (Increased
o High Volume excretion of fatty acids)
o Much higher HCO3- than plasma (counteracts acids in o Best describes bile acid function: The amount lost in the stool
duodenum) each day represents the daily loss of cholesterol
o Isotonic o Surgical resection of Ileum would cause: Increase in water
o Same Na and K as plasma content of feces
o Lower Cl than plasma o Protects duodenal mucosa from gastric acid: Bicarbonate
o Contains pancreatic amylase, lipase (also called carboxylic contained in bile
esterase), protease, trypsin inhibitor • Gallbladder has:
§ Steatorrhea in patients with pancreatitis is secondary to o ↑ Na+, Ca2+, Bile Salts, Cholesterol, Lecithin concentration
decrease in luminal levels of: pancreatic lipase o ↓ Cl- and HCO3- concentration
o Also has cephalic, gastric and intestinal phase
• Stimulated by
o Secretin
§ Secreted by S Cells
§ Acts on ductal cells
§ Increases HCO3- secretion
§ 2nd messenger: cAMP
o CCK
§ Secreted by I Cells
§ Acts on CCKA receptors in acinar cells and ductal cells to
increase enzyme secretion
§ Potentiates effect of secretin in increasing HCO3- secretion
§ 2nd messenger: IP3-DAG
o Ach
§ Via vagovagal reflexes
§ Acts on muscarinic receptors in acinar cells and ductal cells to
stimulate enzyme secretion
§ Also potentiates effect of secretin in increasing HCO3-
secretion
✔GUIDE QUESTION © Topnotch Medical Board Prep
Which of the following is true about the secretion from the exocrine
pancreas?
(A) It has a higher Cl– concentration than does plasma
(B) It is stimulated by the presence of HCO3– in the duodenum
(C) Pancreatic HCO3– secretion is increased by gastrin
(D) Pancreatic enzyme secretion is increased by cholecystokinin
(CCK)
(E) It is hypotonic From Physiology BRS, 6 Ed th
CLINICAL CORRELATES PANCREATECTOMY

Pancreatectomy is associated with:
• Loss of exocrine pancreatic secretions → steatorrhea and
protein malabsorption
• Loss of insulin secretion:
o High glucagon/insulin ratio → hyperglycemia
o ↓ intracellular uptake of glucose, ↑ protein and fat catabolism
→ weight loss (instead of weight gain)
§ ↑ ketone production and use → metabolic acidosis
BILE
• Most common component: Water
• Active Component: Bile Salts
• Bile Salts: Amphipathic
o Emulsify Fats © Topnotch Medical Board Prep
o Forms Micelles for fat absorption ✔GUIDE QUESTION
o Removes cholesterol from the body Which of the following is the site of Na+–bile acid cotransport?
• Other Components: (A) Gastric antrum (D) Ileum
o Bilirubin, Cholesterol, Phospholipids, Electrolytes (B) Gastric fundus (E) Colon
(C) Duodenum th
Like surfactant, bile salts are AMPHIPATHIC – they have a lipid-soluble side
and a water-soluble side. They are basically both DETERGENTS –
substances that can help dissolve lipids in water. The process of 6.5 DIGESTION AND ABSORPTION
emulsification basically means you make large lipid droplets into smaller DIGESTION OF CARBOHYDRATES
lipid droplets. This would happen when bile salts surround the large lipid
droplets → when you dissolve the large lipid droplets in water, you make
• Salivary and Pancreatic Amylase: hydrolyzes 𝛼1,4-glycosidic
smaller lipid droplets. Smaller lipid droplets mean they are easier to bonds in starch yielding maltose, maltotriose and 𝛼-limit dextrins
absorb and be acted upon by pancreatic lipase. Think of Bile Salts as • Intestinal brush border Maltase, 𝛼-dextrinase and sucrase:
something similar to Joy dishwashing fluid (“isang patak, tanggal sebong degrade oligosaccharides to glucose
sangkatutak”) – emulsification is about breaking down fat into smaller • Lactase, trehalase and sucrase: degrades disaccharides to
lipid droplets using detergent action. monosaccharides
Dr. Banzuela
• Bile is stored AND concentrated in the Gallbladder

• CCK and Ach causes GB contraction

CLINICAL CORRELATES DUMPING SYNDROME
• Gastric Bypass → loss of “reservoir function” of stomach → if
patient eats large meals → rapid absorption of glucose in the
intestines → hyperglycemia → insulin secretion →
HYPOGLYCEMIA 2 hours after meals presenting as weakness
dizziness and sweating (DUMPING SYNDROME)
• After gastric bypass surgery, patients presents with crampy
abdominal discomfort 15-30 mins after meals, with nausea,
diarrhea, belching, tachycardia, palpitations, diaphoresis,
light-headedness. These symptoms most likely arise from:
Release of VIP and motilin
© Topnotch Medical Board Prep DIGESTION OF PROTEINS

ABSORPTION OF CARBOHYDRATES • Brush border enzyme Enterokinase (also called
• Only Monosaccharides are absorbed ENTEROPEPTIDASE) is required for PROTEIN ASSIMILATION
• Luminal Side: • Endopeptidases: degrade proteins from interior peptide bonds
o SGLT-1 (secondary active transport): for glucose and • Exopeptidases: degrade proteins from the” edge” of the protein
galactose (C terminus)
o GLUT-5 (facilitated diffusion): for fructose • Pepsin:
• Basolateral Side: o inessential protease initially (pepsinogen)
o GLUT-2 (facilitated diffusion): all types of monosaccharides o secreted by Chief Cells of stomach, activated by gastric H+
Again, with feelings: only monosaccharides (glucose, galactose, fructose) o ACTIVE (optimum pH) at pH 1-3
can be absorbed in the small intestines. We cannot absorb disaccharides o INACTIVE (denatured) at pH of 5
or polysaccharides. SGLT-1 is used to absorb glu/gal from lumen to • Pancreatic Proteases (essential): trypsin, chymotrypsin,
intestinal cell, GLUT-5 for fru from lumen to intestinal cell. GLUT-2 is used elastase, carboxypeptidase A and B
to absorb glu/gal/fru from intestinal cell to the blood.
Dr. Banzuela Pepsin and HCl are considered “inessential” – you can live without them –
they merely supplement pancreatic proteases. The pancreatic protease
✔GUIDE QUESTION Trypsin is the one considered “essential” – this is the one that does most of
Which of the following substances must be further digested before it can the work in terms of proteolysis. Once you have Trypsin, it can activate the
be absorbed by specific carriers in intestinal cells? other zymogens (inactive proteases) including other trypsinogen
(A) Fructose (D) Dipeptides molecules, chymotrypsinogen, proelastase, procarboxypeptidase.
(B) Sucrose (E) Tripeptides Dr. Banzuela
(C) Alanine th
ABSORPTION OF PROTEINS
• Free Amino Acids
o Luminal Membrane: Na-AA (amino acid) symport
o Basolateral Membrane: facilitated diffusion
o 4 separate carriers for neutral, acidic, basic and imino acids
• Dipeptides and Tripeptides
o Absorbed faster than free AA
o Luminal Membrane: H+-dipeptide/tripeptide symport
o Intestinal Cells: Cytoplasmic peptidases degrade them into
free AA
o Basolateral Membrane: Facilitated diffusion of free AA
✔GUIDE QUESTION
Which of the following is transported in intestinal epithelial cells by a
Na+-dependent cotransport process?
(A) Fatty acids (D) Alanine
(B) Triglycerides (E) Oligopeptides
(C) Fructose th

DIGESTION OF LIPIDS
• Triglyceride, Cholesterol Esters and Phospholipids are broken
down as they enter the intestinal cells and then recreated as they
exit
• Enter intestinal cells via: Micelles
• Leave intestinal cells via: Chylomicrons
• Steatorrhea is seen in:
o Pancreatic Disease (e.g., pancreatitis, cystic fibrosis):
insufficient pancreatic lipase
§ Describes pancreatic function in patients with acute
pancreatitis: Phospholipase A2 maybe prematurely
activated by trypsin
o Gastrinoma: resulting low duodenal pH inactivates pancreatic
lipase
o Ileal resection: insufficient bile acid pool
o Bacterial overgrowth: deconjugation of bile acids
o Tropical Sprue: decrease surface area for lipid absorption
o Inability to synthesize apoprotein B: inability to form
chylomicrons
✔GUIDE QUESTION
A 49-year-old male patient with severe Crohn’s disease has been
unresponsive to drug therapy and undergoes ileal resection. After the
surgery, he will have steatorrhea because
(A) the liver bile acid pool increases
(B) chylomicrons do not form in the intestinal lumen
(C) micelles do not form in the intestinal lumen
(D) dietary triglycerides cannot be digested
(E) the pancreas does not secrete lipase From Physiology BRS, 6 Ed th
• Will be seen in Crohn disease with ileal inflammation:

Decreased bile acid pool size
Refer to the two pictures below as we discuss absorption of lipids using this
audio recording:
ABSORPTION OF LIPIDS
https://qrs.ly/g5cmt4y
Dr. Banzuela
WATER AND ELECTROLYTES
DESCRIPTION
• S.I.: SGLT-1, Na-aa, NaCl symport, Na+-H+
Na+ antiport
absorption • L.I: passive diffusion (paracellular route,
stimulated by aldosterone)
• Accompanies Na+ via Passive diffusion
Cl-
(paracellular route), Na-Cl symport, Cl-HCO3-
absorption
antiport
• S.I.: passive diffusion (paracellular route)
K+
• L.I.: active secretion (stimulated by
absorption
aldosterone)
• Secondary to solute absorption
H2O
• S.I. and Gallbladder: isosmotic
absorption
• L.I.: lower water permeability compared to S.I.
• Primary ion secreted
• Utilizes Cl- channels in the luminal membrane
Cl-
regulated by cAMP
secretion
• Na is secreted into lumen passively follows Cl.
Water then follows NaCl
• Best describes water and electrolyte absorption: majority
happens in the jejunum
OTHER SUBSTANCES • Kupffer Cells
NUTRIENT DESCRIPTION o Found in the liver sinusoids and act as antigen-presenting cells
• Produced by bacteria o Kupffer cells protects against sepsis secondary to translocation
Short-Chain Fatty of intestinal bacteria
Acids • Absorption almost exclusively happens
in the: colon CLINICAL CORRELATES UROBILINOGEN
Fat-Soluble • Incorporated into micelles and • Colectomy → antibowel preparation + resection of entire colon
Vitamins (ADEK) absorbed with lipids → ↓ colonic bacteria → ↓ deconjugation of bacteria →
Water-Soluble ↓absorption of urobilinogen → ↓ urobilinogen excretion in the
• Na+-dependent symport
Vitamins urine
• Absorbed in Ileum using Intrinsic • Found in patients with infectious hepatitis: increase in both
Factor (IF) direct and indirect bilirubin
• *Vit B12 deficiency + pernicious anemia
Vitamin B12 is caused by: Lack of IF
• *MOA of neurologic deficits in Vit B12
deficiency: Decreased myelin
synthesis
• 1,25 dihydroxycholecalciferol → ↑
Calcium
calbindin D-28K → ↑calcium absorption
• Heme Iron broken down in intestinal
cells → Free Fe2+ binds to apoferritin
Iron
and transported in blood → Free Fe2+
binds to transferrin in blood
Remember: Sites of absorption: duodenum – iron and Vitamin C. Jejunum
– fat, proteins, carbohydrates, water. Ileum – Vitamin ADEK, IF-B12
complex, Bile Salts.
Dr. Banzuela
Daily Water Turnover in the GI Tract

Ingested 2000
Endogenous
7000
secretions
Salivary glands 1500
Stomach 2500
Bile 500
Pancreas 1500
Intestine +1000
7000
Total Input 9000
Reabsorbed 8800
Jejunum 5500
Ileum 2000
Colon +1300
8800
Balance in tool 200
Adapted from Figure 25-5. Barrett et al. Ganong’s Review of Medical Physiology. 26th ed. 2019
CLINICAL CORRELATES CHOLERA

Cholera toxin → increase cAMP → opens chloride channels →
chloride ions secretion → activate a sodium pump → secretion of
sodium ions → NaCl formed in the crypts → extreme osmosis of
water from the blood into the intestinal lumen.
✔GUIDE QUESTIONS
Vibrio cholerae causes diarrhea because it
(A) increases HCO3– secretory channels in intestinal epithelial cells
(B) increases Cl– secretory channels in crypt cells
(C) prevents the absorption of glucose and causes water to be Do not confuse bilirubin with bile salts. Bilirubin is a breakdown product of
retained in the intestinal lumen isosmotically heme and RBCs and give the urine and feces its yellow color. Bile Salts come
(D) inhibits cyclic adenosine monophosphate (cAMP) production in from cholesterol, and is used for emulsification of fats.
intestinal epithelial cells Dr. Banzuela
(E) inhibits inositol 1,4,5-triphosphate (IP3) production in intestinal

epithelial cells From Physiology BRS, 6 Ed th
7. ENDOCRINE AND REPRODUCTIVE
Micelle formation is necessary for the intestinal absorption of PHYSIOLOGY
(A) glycerol (C) bile acids 1. Overview of Hormones
(B) galactose (D) vitamin B12
(E) vitamin D
2. Cell Mechanisms and Second Messengers
From Physiology BRS, 6th Ed 3. Pituitary Gland
4. Thyroid Gland
6.6 LIVER PHYSIOLOGY 5. Adrenal Cortex and Adrenal Medulla
LIVER 6. Endocrine Pancreas-Glucagon and Insulin
• Central Organ of Biochemistry 7. Calcium Metabolism
• Cytochrome P450 Enzymes 8. Sexual Differentiation
o Superfamily of enzymes that inactivates/activates xenobiotics 9. Male Reproduction
o Important role in the following 10. Female Reproduction
§ Bile acid formation Listen to this audio recording while reading the next section on the types of
§ Carcinogenesis hormones and hormone regulation:
§ Steroid hormone formation
§ Detoxification of drugs TYPES OF HORMONES
• Stellate cells of Ito (found in perisinusoidal space of Disse) AND HORMONE REGULATION
o Responsible for vitamin A storage https://qrs.ly/jhcmt5w
o Responsible for liver fibrosis (when regeneration potential of
liver has reached its limit) Dr. Banzuela
7.1 OVERVIEW OF HORMONES

HORMONES
• Chemical messengers released into the blood
PROTEIN HORMONE LIPID HORMONE
(WATER-SOLUBLE) (LIPID-SOLUBLE)
• Nuclear /
Location of • Cell Membrane
Cytoplasmic
receptors Receptors
Receptors
• Causes
Mechanism • Utilizes G Proteins
transcription of
of action and 2nd messengers
Genes
• Activates existing
• Synthesizes new
intracellular
Final Effect intracellular
enzymes via
enzymes
phosphorylation
• Aldosterone,
• Insulin, © Topnotch Medical Board Prep
• Cortisol,
Examples • Glucagon,
• Sex Hormones,
• Growth Hormone
• Vitamin D
7.2 CELL MECHANISMS AND SECOND MESSENGERS
Listen to this audio recording while reading the section on G proteins and
HORMONE REGULATION 2nd messenger systems below:
• Hormone Secretion Regulation
o Negative-Feedback: limits final products (e.g., Insulin and
G PROTEINS AND
Blood Glucose)
2ND MESSENGER SYSTEMS
o Positive-Feedback: increases final products (e.g., Oxytocin
https://qrs.ly/dicmt5y
during breastfeeding and delivery, estrogen-induced LH and
FSH surge during ovulation)
• Hormone Receptor Regulation Dr. Banzuela
G-PROTEINS
o Upregulation: increase in receptor number or sensitivity (e.g.,
uterus: estrogen upregulating estrogen receptor (its own • ” Guanosine Triphosphate (GTP)-activated” proteins
receptor) and LH receptor) • “Transducers” (bridges): couple 1st messenger (hormone or NT
o Downregulation: decrease in receptor number or sensitivity binding to cell membrane receptor) with the 2nd messenger (2nd
(e.g., uterus: progesterone downregulating progesterone messenger systems like cAMP and IP3/DAG)
receptors (its own receptors) and estrogen receptor) • 3 subunits: α, β, and γ
o Most important: α subunit – binds with GDP (inactivates G
protein) or GTP (activates G protein)
o GTP: stimulated by GEFs and inhibited by GAPS and RGS
proteins
• Gs or Gi: depends on presence of αs or αi
2ND MESSENGERS
• Mediate the intracellular responses to many different hormones
and neurotransmitters
• Remember the sequence:
o 1st messenger (hormone/NT) → G-protein coupled receptors
(cell membrane receptors!) for hormones/NTs → G Proteins →
2nd Messengers →→→ kinases → activated enzyme →
intracellular response
cAMP 2nd MESSENGER SYSTEM

• Most common 2nd messenger system
• Mnemonic: Alpha subunit of G proteins activates Adenylate cyclase
converts ATP to cAMP → activates Protein Kinase A (PKA)

IP3/DAG 2nd MESSENGER SYSTEM
• Use by all hypothalamic hormones except CRH
• Mnemonic: “Phospholipase Ceeeee, PIPeeeeee, IPthreeee,
DAGeeee, Protein Kinase Ceeee”

Tyrosine-Kinase Associated Receptor
o e.g. GH, EPO
o Hormone binds to cell membrane receptor → noncovalent
association with Tyrosine Kinase (e.g., Janus family of receptor-
associated TK or JAK) → targets activators of transcription
CATALYTIC RECEPTOR MECHANISM (STAT) → new protein synthesis
• Hormone cell membrane receptors are associated with enzymatic
activity on the intracellular side of the cell membrane
• Guanylyl Cyclase
o e.g. in ANP, BNP, EDRF and NO
o Hormone binds to cell membrane receptor → Guanylyl cyclase
activated → coverts GTP to cGMP (acts as second messenger)
• Receptor Tyrosine Kinase

o E.g., in NGF (monomer receptor) and Insulin, IGF (dimeric
receptor)
o Hormone binds to cell membrane receptor → intracellular
tyrosine kinase activated → phosphorylation of tyrosine
moieties on proteins → leads to physiologic action

STEROIDS HORMONE AND THYROID HORMONE MECHANISM
• (+) penetration of cell membrane and synthesis of new proteins

STEROID HORMONES Lipid soluble →
CYTOPLASMIC receptor Cortisol
Cholesterol derivative Act on INTRACELLULAR receptors →
THYROID HORMONES Initiate gene transcription → Aldosterone, testosterone, Progesterone,
NUCLEAR receptor
Tyrosine derivative CREATE new proteins Estrogen, Vitamin D, T3 / T4
ADH (V2), angiotensin II
Activates PKA à (epithelial cells), catecholamines
ɑs (Gs) Activates AC ↑cAMP phosphorylation of (ß1 and ß2), ACTH, LH, FSH, TSH,
enzymes HCG, MSH, CRH, calcitonin, PTH,
secretin, somatostatin, glucagon
G protein Inhibits PKA à
coupled decreased
receptors
ɑi (Gi) Inhibits AC ↓cAMP
phosphorylation of
catecholamines (ɑ2)
water soluble à (GPCR) enzymes
Activates cGMP closes GTP-dependent
act on CELL ɑt (transducin) PDE
↓cGMP
ion channels
retinal transducin
PROTEIN MEMBRANE
ADH (V1), angiotensin II (vascular
HORMONES receptors à PIP2 à IP3 à Ca release
ɑq (Gq) Activates PLC
IP3 + DAG DAG à activates PKC
smooth muscles), catecholamines
(ɑ1), GnRH, TRH, GHRH, oxytocin
MODIFY existing
Activates PKG à
proteins
Cell surface GC Activates GC ↑cGMP phosphorylation of ANP, NO, EDRF
enzymes
Enzyme- Serine/Threonine Phosphorylates Initiates gene
Smad signaling TGF-ß
linked kinase (RS/TK) RS/TK transcription
receptors Tyrosine kinase Phosphorylates Initiates gene NGF, EGF, PDGF, IGF-1, prolactin,
MAPK cascade
(RTK) RTK transcription leptin, insulin
Tyrosine- No intrinsic Src and JAK/STAT Initiates gene
EPO, interferons, cytokines, GH
associated kinase catalytic activity proteins transcription
✔GUIDE QUESTION SPECIAL NOTES ON ANTERIOR PITUITARY HORMONES
Which of the following hormones acts on its target tissues by a steroid • If the pituitary stalk is damaged, all anterior pituitary hormones
hormone mechanism of action? will be decreased EXCEPT: Prolactin
(A) Thyroid hormone
(B) Parathyroid hormone (PTH)
• Top 2 cells of the Anterior Pituitary: Somatotropes (40%) and
(C) Antidiuretic hormone (ADH) on the collecting duct Corticotropes (20%)
(D) β1 adrenergic agonists • 3 Families of Hormones of the Anterior Pituitary
(E) Glucagon From Physiology BRS, 6 Ed th o TSH, LH, FSH (same alpha unit, unique beta unit)
Again, even if thyroid hormone is made from the amino acid o MSH, ACTH, Beta-Lipotropin, Beta-Endorphin (derived from
tyrosine, it is lipid-soluble and will have a MOA similar to steroid POMC)
hormones. o GH, Prolactin, HPL (homologous)
Dr. Banzuela
Which of the following hormones acts by an inositol 1,4,5-triphosphate
✔GUIDE QUESTION
(IP3)–Ca2+ mechanism of action?
Which of the following substances is derived from proopiomelanocortin
(A) 1,25-Dihydroxycholecalciferol
(POMC)?
(B) Progesterone
(A) Adrenocorticotropic hormone (ACTH)
(C) Insulin
(B) Follicle-stimulating hormone (FSH)
(D) Parathyroid hormone (PTH)
(C) Melatonin
(E) Gonadotropin-releasing hormone (GnRH)
From Physiology BRS, 6th Ed (D) Cortisol
Again, all hypothalamic hormones except CRH utilize IP3-DAG. (E) Dehydroepiandrosterone From Physiology BRS, 6 Ed
th
Dr. Banzuela
GROWTH HORMONE (GH)

7.3 PITUITARY GLAND • Has both catabolic and anabolic effects
PITUITARY GLAND • Released in pulsatile fashion every 2 hours
• Anterior Pituitary • Nocturnal peak: 1 hour after Stage 3 or 4 Sleep
o Derived from oral ectoderm (Rathke Pouch) • Growth is due to interplay of GH, Thyroid Hormone, Androgens,
o Basophilic Cells: Estrogens, Glucocorticoid, Insulin
§ FSH, LH, ACTH, TSH, MSH o Inactive anterior pituitary (hypopituitarism) will decrease
§ Mnemonic: BFLAT Major GH which can lead to stunted growth
o Acidophilic Cells: • GH receptor requires dimerization to exert its effect
§ GH, Prolactin • GH activates: JAK2-STAT Pathway
• Posterior Pituitary
o Derived from neural ectoderm (neural outgrowth of INDIRECT ACTIONS
DIRECT ACTIONS
Hypothalamus) (VIA IGF-1)
o Pituicytes store and secrete: • ↑ Plasma Glucose • ↑ Bone Length and
§ Vasopressin (ADH), Oxytocin (diabetogenic) Thickness (pubertal growth
Take note however that vasopressin and oxytocin are synthesized by the
• ↑ protein deposition and spurt)
nerve cell bodies in the supraoptic and paraventricular nuclei, respectively. lean body mass • ↑ protein synthesis in
Dr. Banzuela • ↑ Lipolysis muscles and other organs
• ↑ IGF-1 and ↑ lean body mass
• Anti-aging effects • ↑ organ size
The indirect effects of GH (via IGF-1) is more powerful. IGF-1 is the one that
actually makes you grow and not GH – via an increase in both bone length
and thickness. Remember the 2nd messenger of IGF-1: tyrosine kinase.
Dr. Banzuela
Regulation of GH Secretion
FACTORS INCREASING GH FACTORS DECREASING GH
SECRETION SECRETION
• Starvation • Hyperglycemia
• Hypoglycemia • High fatty acid levels
• Low fatty acid levels • Aging
• Exercise • Obesity
• Excitement • Somatostatin
Be careful with Prolactin vs. Oxytocin. Prolactin increases milk
PRODUCTION. It comes from the anterior pituitary. Oxytocin increases • Trauma • Exogenous GH
milk SECRETION. It comes from the anterior hypothalamus (mainly the • Testosterone • Somatomedins (IGF)
paraventricular nuclei) and only stored and secreted in the posterior • Estrogen
pituitary. Vasopressin is also synthesized in the anterior hypothalamus • GHRH
(mainly the supraoptic nuclei) and only stored and secreted in the posterior • Deep sleep
pituitary.
Dr. Banzuela • Secretion requires normal plasma levels of Thyroid Hormones
ANTERIOR PITUITARY HORMONES
ANTERIOR ✔GUIDE QUESTION
HYPOTHALAMIC TARGET ORGAN TARGET
PITUITARY Which of the following inhibits the secretion of growth hormone by the
HORMONE HORMONE ORGAN
HORMONE anterior pituitary?
Liver, (A) Sleep (D) Somatomedins
muscle, (B) Stress (E) Starvation
GHRH (+) GH IGF-1 (C) Puberty From Physiology BRS, 6 Ed
th
bone,
Somatostatin (-) (Somatotropin) (Somatomedin)
kidney, GH Pathophysiology
etc. • GH Deficiency:
Thyroid o Growth retardation, short stature, mild obesity, delayed
TRH (+) TSH T3, T4
gland
puberty → dwarfism (in children)
GC (main),
o Causes: lack of anterior pituitary GH, hypothalamic dysfunction
along with MC Adrenal
CRH (+) ACTH (↓ GHRH), failure to generate IGF in liver, growth hormone
and weak Cortex
androgens
receptor deficiency
Estrogen, • GH Excess:
GnRH (+) FSH, LH Progesterone, Gonads o Gigantism: symmetrical bone growth, occurs before closure of
Testosterone epiphyses
PIH/ Dopamine o Acromegaly: asymmetrical bone growth, occurs after closure
Prolactin --- Breast of epiphyses
(-)
Gigantism, acromegaly and Cushing Syndrome can all lead to glucose OXYTOCIN
intolerance and diabetes because both GH and Cortisol can increase
plasma glucose (they are diabetogenic hormones along with Epi and • Secreted by Hypothalamic Paraventricular Nuclei
Glucagon) • Actions:
Dr. Banzuela o Milk ejection (contraction of myoepithelial cells)
o Uterine contraction
PROLACTIN § basis for Nipple Stimulation
• Stimulates milk production (lactogenesis) • Stimuli:
o Synthesis of lactose, casein, lipids o Suckling of the breast
• Inhibits ovulation (females) or spermatogenesis (males) by o Cervical dilation
INHIBITING GnRH o Orgasm
• together with estrogen and progesterone, stimulates breast o Sight, sound, smell of infant
development during puberty and pregnancy ✔GUIDE QUESTION
Lactation amenorrhea in the first 6 months after delivery with regular Secretion of oxytocin is increased by
breastfeeding is caused by prolactin inhibiting GnRH, preventing the LH (A) milk ejection
surge from occurring. (B) dilation of the cervix
Dr. Banzuela
(C) increased prolactin levels
(D) increased extracellular fluid (ECF) volume
Regulation of Prolactin Secretion (E) increased serum osmolarity From Physiology BRS, 6 Ed th
FACTORS INCREASING FACTORS DECREASING Which of the following hormones originates in the anterior pituitary?
PROLACTIN SECRETION PROLACTIN SECRETION (A) Dopamine
• Estrogen (pregnancy) • Dopamine (B) Growth hormone–releasing hormone (GHRH)
• Breast feeding • Bromocriptine (dopamine (C) Somatostatin
(D) Gonadotropin-releasing hormone (GnRH)
• Sleep agonist)
(E) Thyroid-stimulating hormone (TSH)
• Stress • Somatostatin From Physiology BRS, 6th Ed
• TRH • Prolactin (via negative

• Dopamine antagonists feedback) 7.4 THYROID GLAND
• Thyroid Follicular Epithelial Cells
✔GUIDE QUESTION o Synthesize thyroglobulin and thyroid hormone
A 38-year-old man who has galactorrhea is found to have a prolactinoma.
§ Remember: Thyroglobulin is NOT the same as Thyroxine-
His physician treats him with bromocriptine, which eliminates the
galactorrhea. The basis for the therapeutic action of bromocriptine is that Binding Globulin (TBG)
it - High or Low Levels of TBG is associated with
(A) antagonizes the action of prolactin on the breast EUTHYROIDISM; it has no effect on thyroid hormone
(B) enhances the action of prolactin on the breast function
(C) inhibits prolactin release from the anterior pituitary
Therefore, high TBG does not affect the metabolic rate as much as TRH,
(D) inhibits prolactin release from the hypothalamus
TSH and Thyroid hormone
(E) enhances the action of dopamine on the anterior pituitary Dr. Banzuela
o Thyroid hormone can be stored for 3 months in the thyroid
follicular lumen
POSTERIOR PITUITARY HORMONE: VASOPRESSIN o Thyroid hormone receptor is a heterodimer with retinoid X
• a.k.a. Anti-Diuretic Hormone (ADH) or Arginine Vasopressin receptor
(AVP) • Thyroid Parafollicular Cells (C Cells)
• Synthesized by Hypothalamic Supraoptic Nuclei o Secrete calcitonin
• Responds to ECF changes detected by osmoreceptors in the
organum vasculosum (anteroventral wall 3rd ventricle)
• Stimulus: ↑ plasma osmolarity (most potent), ↓ blood pressure,
↓ blood volume
• Acts on:
ADH 2ND
EFFECT
RECEPTOR MESSENGER
V1 • vasoconstriction of
• IP3/DAG
Receptors arterioles
• insertion of AQP-2 in the late
V2
• cAMP distal tubule and collecting
Receptors
ducts
Mnemonic: V1 – think of 1 blood vessel. V2 – think of your 2 kidneys.
Dr. Banzuela
Regulation of ADH Secretion © Topnotch Medical Board Prep
FACTORS INCREASING ADH FACTORS DECREASING ADH Don’t get confused ha – Chief Cells of the Parathyroid Gland: produces PTH.
SECRETION SECRETION C cells of the Thyroid Gland: produces Calcitonin.
• ↑ serum osmolarity • ↓ serum osmolarity Dr. Banzuela
• Volume contraction • Ethanol Listen to the audio recording as you read the next section on thyroid
• Pain • α-agonists hormone synthesis and secretion:
• Nausea • ANP
• Hypoglycemia THYROID HORMONE SYNTHESIS
• Nicotine, opiates, AND SECRETION
antineoplastic agents https://qrs.ly/5vcmt6d
Dr. Banzuela
STEPS IN THYROID HORMONE SYNTHESIS AND SECRETION

• Each step in thyroid hormone synthesis is stimulated by TSH
STEP EVENT SITE ENZYME
1 • Synthesis of Thyroglobulin (TG) and extrusion into follicular lumen • RER, Golgi Apparatus -
• Na+-I- symporter (NIS), a form of secondary active transport, causes Iodide
2 • Basal Membrane -
(I-) uptake
• Apical / Luminal
3 • Transport of I- to follicular lumen. (using Pendrin) Oxidation of I- to I2 • Peroxidase
Membrane
4 • Organification of I2 and Tyrosine to MIT and DIT • Peroxidase
Membrane
5 • Coupling: MIT + DIT → T3 and DIT + DIT → T4 • Peroxidase
Membrane
6 • Endocytosis of iodinated TG due to TSH -
Membrane
7 • Hydrolysis of T3 and T4 → T4 and T4 enter circulation • Lysosomes • Proteases
8 • Deiodination of residual MIT, DIT & recycling of I- & tyrosine • Intracellular • Deiodinase
Please memorize also the sites inside the cell where each step
occurs (seen in the table above)
Dr. Banzuela
THYROID HORMONE PATHOPHYSIOLOGY OF THYROID HORMONE

T4 T3 CONDITION DESCRIPTION
• 3,5,3',5'- • 3,5,3'- • ↑ BMR, ↑ cardiac output, weight loss,
Other name
tetraiodothyronine triiodothyronine tremors, heat intolerance, pre-tibial
Percentage myxedema, exophthalmos (in Graves
• 93% • 7% Disease)
synthesized
Half-life • More (6 days) • Less (1 day) Hyperthyroidism • Hyperthyroidism presents with 2-3x
larger thyroid, hyperplasia and
Affinity for
binding infolding of the follicular cell lining into
• More • Less the follicles decreasing the cross-
plasma
protein sectional area occupied by the colloid
Binding to • ↓ BMR, weight gain, cold intolerance,
• Less (10% of the • More (90% of the lethargy, whole-body myxedema,
nuclear
receptors) receptors) mental and grown retardation (in
receptor Hypothyroidism
congenital hypothyroidism)
• 4x faster (12
Onset of action • 4x slower (2 days) • Hypothyroidism causes cholesterol
hours)
levels to INCREASE
EFFECTS OF THYROID HORMONES • Ingestion of large amount of iodine
Wolff-Chaikoff
• ↑ O2 consumption and Basal Metabolic Rate (BMR) reduces T3 and T4.
Effect
o ↑ mitochondria and Na-K-ATPase pump activity • Used as treatment of hyperthyroidism.
• Hyperthyroidism following small
• Stimulates carbohydrate, fat and protein metabolism increased ingestion of iodine typically
Jod-Basedow
o ↑ glucose uptake, gluconeogenesis, glycogenolysis in patients with endemic goiter (due to
Phenomenon
o ↓ cholesterol, phospholipids and triglycerides but ↑ fatty acids iodine deficiency) who relocate to
§ ↑ cholesterol secretion to bile & number of liver LDL iodine-rich areas.
receptors
Exophthalmos is the protrusion of the eyeball caused by fat and
o ↑ protein synthesis needed for Growth glycosaminoglycans (GAGS) behind the eyeball. It is seen in Graves disease.
• Works together with GH and IGF-1 for bone formation and bone Exophthalmos is specific to Graves disease and not to hyperthyroidism –
maturation remember that not all cases of hyperthyroidism is Graves, therefore not all
• ↑ requirements for vitamins cases of hyperthyroidism will have exophthalmos.
• ↑ blood flow, Cardiac Output, Heart Rate, Heart Strength (Normal Dr. Banzuela
/ ↑ BP, wide pulse pressure due to ↓TPR) ✔GUIDE QUESTIONS

o (+) chronotropic, inotropic and lusitropic effect Which of the following would be expected in a patient with Graves’
o ↑ B1 receptors, myosin, SR Ca-ATPase in the heart disease?
• ↑ respiration (A) Cold sensitivity
(B) Weight gain
• ↑ gastrointestinal motility (C) Decreased O2 consumption
• ↑ cerebration in adults (D) Decreased cardiac output
• For CNS maturation in the perinatal period (E) Increased triiodothyronine (T3) levels
• ↑ muscle vigor = fine Muscle Tremors From Physiology BRS, 6th Ed
Blood levels of which of the following substances is decreased in Graves
• ↑ risk for somnolence disease?
• Needed for proper sexual function (A) Triiodothyronine (T3)
o Loss may cause loss of libido, impotence, menstrual changes (B) Thyroxine (T4)
(C) Diiodotyrosine (DIT)
(D) Thyroid-stimulating hormone (TSH)
(E) Iodide (I–) From Physiology BRS, 6 Ed th
Propylthiouracil can be used to reduce the synthesis of thyroid hormones Hormone Half-Life
in hyperthyroidism because it inhibits oxidation of Aldosterone 20 minutes
(A) Triiodothyronine (T3)
Corticosterone 60-90 minutes
(B) Thyroxine (T4)
(C) Diiodotyrosine (DIT) DHEA 7-22 hours
(D) Thyroid-stimulating hormone (TSH) Epinephrine 2 minutes
(E) Iodide (I–) From Physiology BRS, 6 Ed th Norepinephrine 2 minutes
Renin 15 minutes
7.5 ADRENAL CORTEX AND MEDULLA MNEMONICS ADRENAL CORTEX
Listen to this audio recording while reading the next section on adrenal G-F-R
hormones:
Glomerulosa, Fasciculata, Reticularis
“The deeper you go, the sweeter it gets.”
ADRENAL HORMONES “Salt, Sweet, Sex”
https://qrs.ly/t4cmt9l Aldosterone, Cortisol, Weak Sex Hormones
✔GUIDE QUESTION
Dr. Banzuela Selective destruction of the zona glomerulosa of the adrenal cortex
ADRENAL HORMONES would produce a deficiency of which hormone?
• Adrenal Cortex (A) Aldosterone (D) Dehydroepiandrosterone
(B) Androstenedione (E) Testosterone
LAYER HORMONE(S) SECRETED (C) Cortisol From Physiology BRS, 6th Ed
Zona Glomerulosa • Aldosterone (mineralocorticoid) Which step in steroid hormone biosynthesis is stimulated by
• Cortisol, Corticosterone adrenocorticotropic hormone (ACTH)?
Zona Fasciculata (A) Cholesterol → pregnenolone
(glucocorticoids)
• De-hydro-epi-androsterone (DHEA) (B) Progesterone → 11-deoxycorticosterone
Zona Reticularis (C) 17-Hydroxypregnenolone → dehydroepiandrosterone
• Androstenedione (weak androgens)
(D) Testosterone → estradiol
• Adrenal Medulla (E) Testosterone → dihydrotestosterone
o Epinephrine: 80% From Physiology BRS, 6th Ed
o Norepinephrine: 20% Which step in steroid hormone biosynthesis, if inhibited, blocks the
production of all androgenic compounds but does not block the
production of glucocorticoids?
(A) Cholesterol → pregnenolone
(B) Progesterone → 11-deoxycorticosterone
(C) 17-Hydroxypregnenolone → dehydroepiandrosterone
(E) Testosterone → dihydrotestosterone
Look at ACTH and Angiotensin II at the image below. Remember: ACTH

stimulates desmolase. It will therefore increase all adrenocortical
hormones. Remember also this: Angiotensin II stimulates aldosterone
synthase. It will therefore increase aldosterone.
Dr. Banzuela
ALDOSTERONE Adrenal Disorders

• Under tonic control by ACTH but separately regulated by RAAS CONDITION CLINICAL FEATURES
and Serum Potassium (hyperkalemia increases aldosterone • Low Aldosterone causes: hypotension,
secretion to restore K levels to normal) hyperkalemia, metabolic acidosis
• Effects • Low Cortisol causes: hypoglycemia,
o ↑ Na+ Reabsorption in the kidneys, sweat glands, salivary anorexia, weight loss, nausea, vomiting,
glands and colon weakness
§ Best describes colonic function: Absorption of Na+ in the Addison • Low weak androgen causes: decreased
colon is under hormonal control by aldosterone Disease pubic and axillary hair in women
o ↑ K+ Secretion in the kidneys and colon • Hyperpigmentation (due to increased
o ↑H+ Secretion in the kidneys (maybe triggered by POMC secretion as response to low levels of
hyperkalemia) adrenal hormones; recall that POMC has
• Aldosterone increases transport of Epithelial Na Channels MSH – which causes stimulation of
(ENaCs) from cytoplasm to cell membrane melanocytes to secrete melanin)
• Mole for mole, Aldosterone has the greatest effect on Na+ • Hyperglycemia, muscle wasting, central
excretion Cushing obesity, round face, supraclavicular fat,
o Mole for mole, ADH has the greatest effect on plasma Syndrome / buffalo hump, osteoporosis, striae,
osmolality (BE CAREFUL NOT TO CONFUSE ALDOSTERONE VS. Disease virilization and menstrual disorders in
ADH!!!) women, hypertension
Conn • Hypertension, hypokalemia, metabolic
✔GUIDE QUESTION
Syndrome alkalosis, decreased renin
Which of the following causes increased aldosterone secretion?
(A) Decreased blood volume • Virilization in women, pseudo-precocious
21-Beta
(B) Administration of an inhibitor of angiotensin-converting enzyme puberty in men, early acceleration of linear
Hydroxylase
(ACE) growth, SSx of glucocorticoid and
(C) Hyperosmolarity
deficiency
mineralocorticoid deficiency
(D) Hypokalemia From Physiology BRS, 6 Ed th
17-Alpha • Lack of pubic and axillary hair in women,
Hydroxylase SSx of glucocorticoid deficiency and
CORTISOL deficiency mineralocorticoid excess
• Essential for response to stress
• Oscillates with circadian rhythm ✔GUIDE QUESTIONS
o Highest levels: before waking up (approx. 8am) A 46-year-old woman has hirsutism, hyperglycemia, obesity, muscle
o Lowest levels: in the evening (approx. midnight) wasting, and increased circulating levels of adrenocorticotropic hormone
(ACTH). The most likely cause of her symptoms is
o Rise sharply during sleep, peak soon after awakening, sink to a
(A) primary adrenocortical insufficiency (Addison’s disease)
low level 12 hours later: Cortisol (B) pheochromocytoma
• Carbohydrate Effects (C) primary overproduction of ACTH (Cushing disease)
o Stimulates gluconeogenesis (D) treatment with exogenous glucocorticoids
o ↑ protein catabolism in muscles (E) hypophysectomy From Physiology BRS, 6 Ed
th
o ↓ glucose utilization and insulin sensitivity of adipose tissue Increased adrenocorticotropic hormone (ACTH) secretion would be
• Protein Effects expected in patients
o ↓ cellular proteins (except liver) (A) with chronic adrenocortical insufficiency (Addison disease)
(B) with primary adrenocortical hyperplasia
o ↑ blood amino acids
(C) who are receiving glucocorticoid for immunosuppression after a
o ↑ liver and plasma proteins renal transplant
• Fat Effects (D) with elevated levels of angiotensin II From Physiology BRS, 6 Ed
th
o ↑ lipolysis
§ Moon Face and Buffalo hump: due to increase appetite, and
fat being generated in some tissues faster than it is being
7.6 ENDOCRINE PANCREAS
metabolized ISLETS OF LANGERHANS: ENDOCRINE PANCREAS
• Anti-inflammatory Effects CELL TYPE PERCENTAGE AREA SECRETION
o induces synthesis of lipocortin which inhibits Phospholipase A2 • 60% (in Central
Beta Cells • Insulin and Amylin
needed for PG and LT synthesis Islet)
o Stabilizes lysosomal membranes Alpha Cells • 25% (in Outer Rim) • Glucagon
o Decreases migration and phagocytosis of WBCs Delta Cells • 10% (Intermixed) • Somatostatin
o Suppression of T-lymphocytes F Cell / PP • Pancreatic
o ↓ IL-1, IL-2 • 5%
Cell Polypeptide
o ↑ resolution of inflammation
Insulin – utilizes tyrosine kinase as second messenger. Comes from Beta
o Blocks inflammatory response to allergies
Cells. Glucagon – utilizes cAMP as second messenger. Comes from Alpha
o ↓ eosinophils and lymphocytes Cells.
o Inhibits histamine and serotonin release Dr. Banzuela
o ↑ RBCs (unknown MOA)
• Anti-inflammatory effects require HIGH LEVELS of circulating
GLUCAGON
glucocorticoids • Main Stimulus: Low Blood Glucose
• Basis for anti-inflammatory effect of exogenous glucocorticoids: • 2nd Messenger: cAMP
inhibition of activation factor-KB (NF-KB) • Actions
• Maintenance of Vascular Responsiveness to Catecholamines o ↑ Blood Glucose
o Upregulates 𝛼1 receptors on arterioles, increasing § ↑ glycogenolysis
Epinephrine’s vasoconstrictor effects →→ Increases BP § ↑ gluconeogenesis
• Inhibits Bone Formation o ↑ Blood Fatty acid and Ketoacids
o ↓ synthesis of Type I collagen, decreasing formation of new bone o ↑ Urea production (due to ↑ amino acids)
by osteoclast, and decreasing calcium absorption o ↑ Insulin
• Increases GFR
o Vasodilation of afferent arterioles
• CNS Effects
o ↓ REM sleep, ↑ slow-wave sleep, ↑ waking time
✔GUIDE QUESTION
A 39-year-old man with untreated diabetes mellitus type I is brought to
the emergency room. An injection of insulin would be expected to cause
an increase in his
(A) urine glucose concentration (D) blood pH
(B) blood glucose concentration (E) breathing rate
(C) blood K+ concentration
Patient here is having diabetic ketoacidosis (plasma pH<7.35).

Insulin would address this ketoacidosis and increase his plasma
pH
Dr. Banzuela
DIABETES MELLITUS
FEATURE TYPE 1 TYPE 2
• Usually < 30
Age of onset • Usually > 40 y/o
y/o
Body mass • Low to normal • Obese
PANCREATIC SOMATOSTATIN • Coxsackie • Insulin resistance
• Inhibits both glucagon and insulin to modulate their effects virus, (this can be
Pathophysiology
• Inhibits all GI hormones • Anti-islet cell decreased using
• Stimulated by all types of nutrients autoantibodies weight reduction)
• Decreases motility of stomach, duodenum and gallbladder • Normal to high
Plasma insulin • Low or absent
• Decreases both absorption and secretion in the GI tract initially
• * take note: there’s also GI somatostatin and hypothalamic Plasma • High; can be • High; resistant to
somatostatin glucagon suppressed suppression
Plasma glucose •↑ •↑
INSULIN Insulin
• Main Stimulus: High Blood Glucose • Normal • Reduced
sensitivity
• 2nd messenger: Tyrosine Kinase Receptor Crisis • DKA • HHS
• Half-Life: 6 minutes (degraded by liver insulinase) • Weight loss,
• Connecting Peptide (C Peptide): packaged and secreted with • thiazolidinediones,
endogenous insulin Therapy • Insulin • metformin,
• sulfonylureas,
• insulin
• Causes high LDL, high VLDL, high TG, low HDL in DM Type 2:
decreased lipoprotein lipase activity due to insufficient insulin
action in adipose
Hypoglycemia
• Counter-regulatory hormones (Diabetogenic Hormones)
o Epinephrine (main)
o Glucagon (main)
© Topnotch Medical Board Prep o Cortisol (supplemental)
✔GUIDE QUESTION o Growth Hormone (Supplemental)
Which of the following pancreatic secretions has a receptor with four • Combined medullary insufficiency (decreased Epinephrine)
subunits, two of which have tyrosine kinase activity? and Glucagon deficiency will cause delay in response to
(A) Insulin (C) Somatostatin hypoglycemia
(B) Glucagon (D) Pancreatic lipase • Meal rich in proteins containing amino acids that causes insulin
secretion → also increases glucagon secretion to prevent
INSULIN VS. GLUCAGON hypoglycemia
HORMONE STIMULI EFFECTS • Physiologic secretion of growth hormone is increased by:
• ↑ Plasma hypoglycemia
• ↑ Cellular Glucose uptake
Glucose
• ↓ Glycogenolysis,
• ↑ Plasma AA
gluconeogenesis
7.7 CALCIUM METABOLISM
• ↑ Plasma FA • ↑ Protein synthesis BONE
Insulin • Organic Matrix (30%)
• Glucagon • ↑ Lipogenesis
o Ground Substances
• GIP (via oral § ECF + Chondroitin Sulfate + Hyaluronic Acid
• ↑ K+ uptake
glucose) § Gelatinous medium
• GH - o Collagen Fibers
• Cortisol - § 95% of Organic Matrix
• ↓ Plasma • ↑ Glycogenolysis and § for Tensile Strength
Glucose gluconeogenesis • Bone Salts (70%)
• ↑ lipolysis and ketone body o Ca10(PO4)6(OH)2
Glucagon • ↑ Plasma AA
formation § for Compressional Strength
• CCK - Why shouldn’t the bone be made up of 100% bone salts? Because if the
• NE, Epinephrine, ACh bone is made up entirely of bone salts, it would be hard but breakable
similar to marble. You need the collagen for tensile strength so it won’t be
Insulin for well-fed state pathways. Glucagon for fasting state pathways. easy to break.
Dr. Banzuela
Dr. Banzuela
DIABETIC KETOACIDOSIS BONE REMODELING
• Hyperglycemia: Due to insulin deficiency BONE DEPOSITION BONE RESORPTION
• Hypotension: due to high filtered load of glucose acting as • Osteoblast • Osteoclasts
osmotic diuretic decreasing intravascular volume • Secrete Collagen & Ground • Secrete Lysosomal
• High Anion Gap Metabolic Acidosis: due to overproduction of Substance where calcium enzymes, Citric Acid and
ketone bodies. (+) Kussmaul respiration seen precipitates Lactic Acid
• Hyperkalemia: due to insulin deficiency
PTH
• Secreted by: Chief Cells of the Parathyroid Gland
• Stimulus: low plasma Ca2+
o ↑ number and activity of osteoclasts
o ↑ plasma Ca2+
• Also stimulated by hypomagnesemia
o Except hypomagnesemia caused by alcoholism
• 2nd Messenger: cAMP
• In hypoparathyroidism (e.g., secondary to parathyroidectomy):
o Low plasma Ca2+, High Plasma PO4-
o (+) neuromuscular excitability
o (+) Hypocalcemic tetany (Chvostek and Trousseau Sign)
BONE REMODELING PROCESS
BODY CALCIUM CALCITONIN
• 99% as hydroxyapatite in Bone • Secreted by: Parafollicular cells (C Cells) of the Thyroid Gland
• 0.1% in the interstitium • Stimulus: high plasma Ca2+
• <0.5% in plasma o Inhibits bone resorption
o 41% as protein-bound calcium o ↓ number and activity of osteoclast
o 9% as anion-bound calcium o ↓ plasma Ca2+
o 50% as Free and ionized calcium (5mg/dL): biologically Listen to this audio recording while reading the table of PTH vs. Vitamin D
active below:
CALCIUM METABOLISM
• To maintain Ca2+ balance, net intestinal absorption (calcium PTH VS. VITAMIN D
intake) must be balanced by urinary excretion (calcium https://qrs.ly/zdcmt9v
excretion)
• Positive Calcium Balance Dr. Banzuela
o Calcium Intake > Calcium Excretion
o e.g. in growing children ORGAN PTH VITAMIN D
• Negative Calcium Balance • ↑ calcium &
o Calcium Intake < Calcium Excretion Intestines • None phosphate
o e.g. in pregnant or lactating women absorption
• ↑ calcium
VITAMIN D reabsorption (DT)
• ↑ calcium &
• Vitamin D is primarily absorbed by: simple diffusion • ↓ phosphate
phosphate
Kidney reabsorption (PCT)
• ACTIVE Vitamin D: 1,25 dihydroxy-cholecalciferol (calcitriol) reabsorption
o Increases intestinal Ca2+ absorption via alteration in activity of • ↑ Active Vit D (by
• ↑ urinary calcium
genes involved in calcium transport (Ca2+ ATPase) and increasing 1 alpha
Calbindin hydroxylase)
• INACTIVE Vitamin D: 24, 25 dihydroxy-cholecalciferol • At normal levels:
o Produced instead when there is Hypercalcemia calcium and
• Increases both plasma Ca++ and PO4- phosphate
• Calcium and
deposition
Bone phosphate
• At high toxic levels:
resorption
calcium and
phosphate
resorption
Net effect on • ↑ serum calcium • ↑ serum calcium
serum levels • ↓ serum phosphate • ↑ serum phosphate
✔GUIDE QUESTIONS
Which of the following results from the action of parathyroid hormone
(PTH) on the renal tubule?
(A) Inhibition of 1-alpha-hydroxylase
(B) Stimulation of Ca2+- reabsorption in the distal tubule
© Topnotch Medical Board Prep (C) Stimulation of phosphate reabsorption in the proximal tubule
• Delayed dentation, short stature, painful walking, bowing of legs (D) Interaction with receptors on the luminal membrane of the
is caused by: decreased calcification of bone matrix (rickets) proximal tubular cells
(E) Decreased urinary excretion of cyclic adenosine monophosphate
Wag dedeadmahin ang inactive (storage) form of Vitamin D – (cAMP) From Physiology BRS, 6 Ed th
24,25(OH)2CC. Importante yan. If you have hypercalcemia, siya ang A 41-year-old woman has hypocalcemia, hyperphosphatemia, and
madami. Pag may hypocalcemia naman, dadami ang active form of decreased urinary phosphate excretion. Injection of parathyroid
Vitamin D – 1,25(OH)2CC. hormone (PTH) causes an increase in urinary cyclic adenosine
Dr. Banzuela
monophosphate (cAMP). The most likely diagnosis is
✔GUIDE QUESTION (A) primary hyperparathyroidism
Which of the following decreases the conversion of 25- (B) vitamin D intoxication
hydroxycholecalciferol to 1,25-dihydroxycholecalciferol? (C) vitamin D deficiency
(A) A diet low in Ca2+ (D) Hypophosphatemia (D) hypoparathyroidism after thyroid surgery
(B) Hypocalcemia (E) Chronic renal failure (E) pseudohypoparathyroidism From Physiology BRS, 6 Ed th

(C) Hyperparathyroidism th
7.8 SEXUAL DIFFERENTIATION

SEXUAL DIFFERENTIATION
• Genetic Sex: determined by sex chromosomes
• Gonadal Sex: determined by presence of testes in males and
ovaries in females
• Phenotypic Sex: determine by characteristics of internal genital
tract and external genitalia

Key points: remember SRY gene and TDF. SRY gene is seen in the Y BIPOTENTIAL
chromosome. SRY gene encodes for TDF. TDF is the protein that causes MALE FEMALE
STRUCTURE
creation of testes. Mullerian inhibiting factor (MIF) causes degeneration GONADS
of the Mullerian ducts (female structures). Testosterone stimulate growth REGRESSES OVARIES
(cortex)
of the Wolffian ducts (the one that develops into male genital tract).
Dr. Banzuela GONADS
TESTIS REGRESSES
(medulla)
Epididymis, Vas
WOLFFIAN
Deferens, Seminal REGRESSES
DUCT
Vesicle
Fallopian tubes,
MÜLLERIAN
REGRESSES Uterus, Cervix,
DUCT
Vagina (Upper 1/3)
Glans Penis,
Corpus GENITAL Glans Clitoris,
cavernosum & TUBERCLE Vestibular Bulb
spongiosum
Penis (Ventral
GENITAL FOLDS Labia minora
shaft)
GENITAL
Scrotum, Labia majora
SWELLING
Female urethra,
Male urethra
lower vagina
Urethral &
UROGENITAL
Prostate gland Paraurethral
SINUS
glands of Skene
Bulbourethral Greater vestibular
glands of Cowper glands of Bartholin
There’s really no good mnemonic for the table above. You have to do hard
core memorization for it – importante ‘yan
Dr. Banzuela
© Topnotch Medical Board Prep 7.9 MALE REPRODUCTION

PHYSIOLOGIC ANATOMY OF MALE SEX ORGANS
STRUCTURE FUNCTION
• Sperm production
Seminiferous • Full development and function of
Tubules seminiferous tubules require
androgens and FSH Ganong 25 23-1 th
Epididymis • Sperm maturation, motility

Vas Deferens • Sperm storage
• Sperm nutrition (contains fructose,
Seminal Vesicle
prostaglandins)
• For semen alkalinity (using
spermine); contains 5-alpha
Prostate Gland
reductase that converts testosterone
to DHT
Ejaculatory Duct -
Urethra -
Urethral Glands,
Bulbourethral • Supplies mucus for lubrication
Glands
Sperm is produced in the seminiferous tubules, mature in the epididymis,
stored in the vas deferens, gets its nutrition (fructose) from seminal vesicle
and becomes alkaline in the prostate gland. Don’t forget these.
Dr. Banzuela
REMEMBER PATH OF SEMEN

S eminiferous tubules (N othing) © Topnotch Medical Board Prep
E pididymis U rethra Take note that the Sertoli Cells can release both Androgen-Binding Protein
and Inhibin. But FSH will only stimulate the Sertoli Cells to secrete
V as deferens P enis Androgen-Binding Protein (ABP) and not inhibin (inhibin decreases FSH
E jaculatory ducts levels). This ABP ensures a high testosterone supply for spermatogenesis.
LH meanwhile stimulates testosterone secretion from the Leydig Cells
SPECIAL NOTES ON MALE REPRODUCTIVE PHYSIOLOGY Dr. Banzuela
• Testes temperature: 1-2°C cooler than core body ✔GUIDE QUESTIONS

o requires temperature lower than body temp: Spermatogenesis Which step in steroid hormone biosynthesis occurs in the accessory sex
• Activation of sperm in the female genital tract: capacitation target tissues of the male and is catalyzed by 5α-reductase?
• NTs used in erection: NO and Ach (A) Cholesterol → pregnenolone
o Nitric Oxide synthase → ↑ NO → activates guanylyl cyclase → (B) Progesterone → 11-deoxycorticosterone
(C) 17-Hydroxypregnenolone → dehydroepiandrosterone
↑cGMP → potent vasodilator → Erection
• Definition of Low Sperm Count: <20 million sperms/mL (E) Testosterone → dihydrotestosterone
• Vestigial remnant of 3rd eye; secretes melatonin involved in From Physiology BRS, 6th Ed
reproduction and sex drive: pineal gland Which of the following functions of the Sertoli cells mediates negative
feedback control of follicle-stimulating hormone (FSH) secretion?
o Circadian rhythm is controlled by: Suprachiasmatic Nuclei
(A) Synthesis of inhibin
(SCN) of the Hypothalamus (in turn regulated by Pineal (B) Synthesis of testosterone
Gland thru melatonin) (C) Aromatization of testosterone
• Sperm: viable for 1-5 days in the female genital tract (average of (D) Maintenance of the blood–testes barrier
3 days or 72 hours) • function of Sertoli Cells in the seminiferous tubules: Maintenance of
• Childhood: FSH and LH are at their lowest, FSH > LH blood-testis barrier (Sertoli cells intimately associated with
• Puberty: FSH and LH increase, FSH < LH developing spermatozoa)
• Senescence: FSH and LH at their highest, FSH > LH
• Weakest to strongest androgens: androstenedione, MNEMONICS MALE SEX HORMONES
testosterone, dihydrotestosterone (DHT) S-S-S
FSH, Sertoli Cell, Sperm
L-L-L
LH, Leydig Cell, Libido Hormone (Testosterone)
TESTOSTERONE DIHYDROTESTOSTERONE
• Differentiation of epididymis, • Differentiation of penis,
vas deferens, & seminal vesicles scrotum, and prostate
• Descent of testes • Male hair pattern
• ↑ bone and muscle mass (e.g., • Male pattern baldness
broad shoulders) • Sebaceous gland activity
• ↑ BMR • Growth of prostate
• Pubertal growth spurt
• Epiphyseal closure
• Growth of penis & seminal
vesicles
• Deepening of voice
(enlargement of larynx)
© Topnotch Medical Board Prep • Spermatogenesis
Sperm has 72 hours (3 days) to meet its reproductive destiny, the egg cell. • Negative feedback on anterior
The egg cell has 24 hours to meet its reproductive destiny, the sperm cell. pituitary
Dr. Banzuela • Libido
✔GUIDE QUESTION
A 16-year-old, seemingly normal female is diagnosed with androgen
insensitivity disorder. She has never had a menstrual cycle and is found
to have a blind- ending vagina; no uterus, cervix, or ovaries; a 46 XY
genotype; and intra- abdominal testes. Her serum testosterone is
elevated. Which of the following characteristics is caused by lack of
androgen receptors?
(A) 46 XY genotype (D) Lack of uterus and cervix STEPS:
(B) Testes (E) Lack of menstrual cycles 1. Mitotic division of germ cell (Spermatogonia Type A) into
(C) Elevated serum
spermatogonia Type A and B
testosterone
2. Enlargement of spermatogonia type B or undergo mitosis to
SPERMATOGENESIS form spermatocytes.
3. 1st meiotic division: primary spermatocytes become
secondary spermatocytes (haploid).
4. 2nd meiotic division: secondary spermatocytes becomes two
spermatids.
5. Spermiogenesis: Spermatids change shape to become
spermatozoon.
7.10 FEMALE REPRODUCTION

ESTROGEN
• Forms of Estrogen
o Estrone: secreted by adrenal cortex and thecal cell
o Estradiol: secreted by ovaries
o Estriol: secreted by placenta
• Aromatase
o Enzyme that catalyzes conversion of Androstenedione →
Estrone & Testosterone → Estradiol
o Needed for development of female (not male) secondary sex
characteristics
MNEMONICS FORMS OF ESTROGEN PROGESTERONE EFFECTS

• Maintenance of secretory activity of uterus during luteal phase
EstraDIOL 2 pa lang kayo (wifey, hubby)
Main form of estrogen during the reproductive years • Breast development
• Negative feedback effects on FSH and LH secretion
EsTRIOL: 3 na kayo (wifey, hubby, baby) • Maintenance of pregnancy
Main form of estrogen during pregnancy • Raising uterine threshold to contractile stimuli during pregnancy
EstrONE: 1 ka na lang (wifey na lang, deds na si hubby) • Effect of HRT: Reduces the incidence of hot flashes (but may
Main form of estrogen during post-menopausal years increase risk of coronary artery disease, endometrial CA, breast
PROGESTERONE CA, venous thromboembolism, gallbladder disease)
• Secreted by the corpus luteum, placenta, adrenal cortex, testes Listen to the audio recording below while looking at the diagram for the
menstrual cycle:
ESTROGEN EFFECTS
• Produce cyclic changes in the vagina and endometrium MENSTRUAL CYCLE
• cervical mucus becomes thinner, more alkaline and exhibit https://qrs.ly/uscmtab
fernlike pattern upon drying
• Inhibits osteoclasts (protective against osteoporosis)
• Decreases serum cholesterol Dr. Banzuela
• Increases libido MENSTRUAL CYCLE

• stimulates growth of ovarian follicle, glandular epithelium of • Proper term: female monthly sexual cycle
endometrium, smooth muscle of uterus and uterine vascular • Normal length: 28 +/- 7 days
system • In a lifetime: occurs approximately 400x
• stimulates ductal elements of the breast (progesterone stimulates • Has 2 Phases
growth of glandular elements of the breasts) o Follicular Phase (Proliferative Phase)
• Maturation of uterus, fallopian tubes, cervix, and vagina § Estrogen predominates
• Breast development o Luteal Phase (Secretory Phase)
• Development of granulosa cells § Progesterone predominates
• Up-regulation of estrogen, progesterone, and LH receptors
• Negative and positive feedback effects on FSH and LH secretion FOLLICULAR PHASE (DAY 0-14)
• Maintenance of pregnancy • Primordial follicle develops to Graafian stage, with atresia of
• Lowering of uterine threshold to contractile stimuli neighboring follicles
• Stimulates prolactin secretion • LH and FSH receptors: upregulated
• Blocks action of prolactin on breast • Estrogen: increases
• Slightly increases BMR but causes fat deposition o Causes proliferation of uterus
• Creates soft skin o Causes selective negative feedback: ↑ FSH, ↓ LH
OVULATION (DAY 14) FERTILIZATION
• Occurs 14 days before menses regardless of cycle length • Usually occurs in the Ampulla of the Uterine Tubes
• At the peak of estrogen secretion one day before ovulation, • If fertilization occurs, corpus luteum will be maintained by HCG
estrogen will cause positive feedback on FSH and LH secretion, produced by the placenta
causing their levels to surge • Implants into the uterine wall: blastocyst
• Estrogen-induced LH surge triggers ovulation • Implantation: occurs 6-7 days after fertilization
o Indication that ovulation has taken place: increased • First trimester: HCG-stimulated corpus luteum is responsible
progesterone levels for production of estradiol and progesterone. Peak HCG levels at
• Cervical mucus increases, becomes less viscous and more week 9.
penetrable by sperm o Start-Peak-Decline of B-HCG in pregnancy: 6-8 days ovulation
• Granulosa cells undergo luteinization to luteal cells – 7-9 weeks – 20 weeks
• Egg cell: has 24 hours to be fertilized • Second and Third Trimester: Placenta produces progesterone
o If fertilized: corpus luteum becomes corpus luteum of and fetal adrenal gland-fetal liver-placenta produces estrogen.
pregnancy Major estrogen: estriol. Human Chorionic Somatomammotropin
o If unfertilized: corpus luteum will regress to corpus albicans or HCS (formerly called HPL) produced through pregnancy
What do you measure in the urine as sign that ovulation has happened? o GnRH levels during pregnancy: Decreased
Answer: LH. ✔GUIDE QUESTION
Dr. Banzuela
The source of estrogen during the second and third trimesters of
LUTEAL PHASE (DAY 14-28) pregnancy is the
• Corpus luteum synthesizes both estrogen and progesterone (A) corpus luteum
• Progesterone causes non-selective negative feedback of both LH (B) maternal ovaries
and FSH (C) maternal ovaries and fetal adrenal gland
(D) maternal adrenal gland and fetal liver
• ↑ Vascularity and secretory activity of endometrium (preparation
(E) fetal adrenal gland, fetal liver, and placenta
for possible implantation)
• Principal steroid secreted by the fetal adrenal cortex: DHEA
• ↑ basal body temperature due to progesterone From Physiology BRS, 6th Ed
RELAXIN
MENSES (DAY 0 TO 4)
• Protein hormone (NOT A STEROID)
• Sloughing of endometrium due to abrupt cessation of estradiol • produced by corpus luteum, uterus, placenta and mammary
and progesterone gland
• Spiral arterioles will break • Also produced by the prostate gland in males
• Menstrual Cycle • Effects:
o During pregnancy: relaxes pubic symphysis, softens and
dilates the cervix
o In males: found in semen, maintains sperm motility and aid in
sperm penetration
PARTURITION
• Umbilical Artery: PO2: 60% (very low compared to maternal
artery’s 98% and umbilical vein’s 80%)
• At week 24 to birth: terminal sacs in the lungs develop, thus
survival of premature babies is possible
• Progesterone increases threshold for uterine contraction
throughout pregnancy
• Near term: estrogen/progesterone ratio increases → uterus more
sensitive to contractile stimuli
• Initiating event in parturition: unknown
o Trigger for onset of labor is fetal ACTH
o Final event required for conversion of the transitional
circulation in the newborn to the adult circulatory pattern:
functional closure of the ductus arteriosus
o Baby’s first breath causes: ↑ PaO2 → ↓ pulmonary vascular
resistance, increased systemic vascular resistance
• Oxytocin: powerful stimulant of uterine contraction
LACTATION
© Topnotch Medical Board Prep • Prolactin increases during pregnancy
o Actions block by estrogen and progesterone
Estrogen Progesterone FSH LH • After parturition, drop in estrogen and progesterone causes
Menstruation ↓ ↓* ↓ ↓ actions of prolactin to manifest
Follicular phase ↑* ↓ ↑ ↓ • Prolactin may inhibit ovulation for the next 6 months due to
Ovulation ↑ ↓ ↑ ↑* inhibition of GnRH (preventing LH surge from ultimately
Luteal phase ↓ ↑* ↓ ↓ happening)
• causes amenorrhea in anorexia nervosa: decreased GnRH (due to
Look at the table above. Key points: drop in progesterone levels trigger
menstruation. Estrogen is the predominant hormone during the
decreased leptin associated with decreased mass of adipose
proliferative/follicular phase; it causes selective negative feedback. tissue)
Progesterone is the predominant hormone during the secretory/luteal ✔GUIDE QUESTION
phase; it causes non-selective negative feedback. LH surge is the trigger Which of the following explains the suppression of lactation during
for Ovulation. LH levels are highest during ovulation. pregnancy?
LH triggers both ovulation and luteinization of the granulosa cells into LH (A) Blood prolactin levels are too low for milk production to occur
receptive cells (enabling the granulosa cells to respond to LH levels and (B) Human placental lactogen levels are too low for milk production
produce progesterone). FSH as the name implies trigger follicular to occur
development. (C) The fetal adrenal gland does not produce sufficient estriol
(D) Blood levels of estrogen and progesterone are high
Follicular phase is the determinant of menstrual cycle length since the
(E) The maternal anterior pituitary is suppressed
luteal phase is relatively constant in duration. From Physiology BRS, 6th Ed
Dr. Banzuela
8. HEMATOLOGY AND SPECIAL

ENVIRONMENTS PHYSIOLOGY
1. Overview of Blood Cells
2. Red Blood Cells
3. White Blood Cells, Immunity and Infection
4. Antigenicity of Blood and Tissues
5. Hemostasis
6. Inflammation and Wound Healing
7. Physiology in Special Environments
8.1 OVERVIEW OF BLOOD CELLS

COMPOSITION OF WHOLE BLOOD
• Plasma
o Fluid medium of the blood/non-cellular part of the blood
o It is where the cells are suspended
o Composition: 90% water, 9% plasma protein, 1% inorganic
salts, 0.5% lipids, 0.1% sugar
• Serum
o Plasma minus clotting proteins (fibrinogen and clotting
factors II, V, and VIII) and with higher serotonin content
COMPOSITION OF PLASMA
PLASMA PROTEIN
Blood
coagulation • Essential component of clotting system
proteins
• Major contributors to osmotic pressure
Albumin © Topnotch Medical Board Prep
of plasma
• Alpha globulins: proteases,
antiproteases, transport proteins
Globulin • Beta globulins: transferrin & other
transport proteins
• Gamma globulins: immunoglobulins
OTHERS
Electrolytes • Major ECF cation: Na+
Organic • Lipids (fatty acids, cholesterol),
nutrients carbohydrates (glucose) & amino acids
• Carried to sites of breakdown or
Organic wastes excretion (urea, uric acid, bilirubin &
ammonium ions)
SERUM OR PLASMA
NAME PRINCIPAL FUNCTION BINDING CHARACTERISTICS
CONCENTRATION
Binding and carrier protein; osmotic Hormones, amino acids, steroids,
Albumin 4500-5000mg/dL
regulator vitamins, fatty acids
Orosomucoid Uncertain; may have a role in inflammation Trace; rises in inflammation
Proteases in serum and tissue
α1-Antiprotease Trypsin and general protease inhibitor 1.3-1.4 mg/dL
secretions
Osmotic regulation; binding and carrier
α-Fetoprotein Hormones, amino acids Found normally in fetal blood
proteina
α2-Macroglobulin Inhibitor of serum endoproteases Proteases 150-420 mg/dL
Protease inhibitor of intrinsic coagulation
Antithrombin-III 1:1 binding to proteases 17-30 mg/dL
system
Ceruloplasmin Transport of copper Six atoms copper/molecule 15-60 mg/dL
<1 mg/dL; rises in
C-reactive protein Uncertain; has role in tissue inflammation Complement C1 q
inflammation
Fibrinogen Precursor to fibrin in hemostasis 200-450 mg/dL
Haptoglobin Binding, transport of cell-free hemoglobin Hemoglobin 1:1 binding 40-180 mg/dL
Binds to porphyrins, particularly heme for
Hemopexin 1:1 with heme 50- 100 mg/dL
heme recycling
Transferrin Transport of iron Two atoms iron/molecule 3.0-6.5 mg/dL
Apolipoprotein B Assembly of lipoprotein particles Lipid carrier
Angiotensinogen Precursor to pressor peptide angiotensin II
Proteins coagulation factors II,
Blood clotting 20 mg/dL
VII, IX, X
Antithrombin C, protein C Inhibition of blood clotting
Mediator of anabolic effects of growth
Insulin-like growth factor I IGF-I receptor
hormone
Steroid hormone- binding
Carrier protein for steroids in bloodstream Steroid hormones 3.3 mg/dL
globulin
Carrier protein for thyroid hormone in
Thyroxine-binding globulin Thyroid hormones 1.5 mg/dL
bloodstream
Transthyretin (thyroid-binding Carrier protein for thyroid hormone in
Thyroid hormones 25 mg/dL
prealbumin) bloodstream
αThe function of α⎻fetoprotein is uncertain, but because of its structural homology to albumin it is often assigned these functions.
No need to memorize the table above. Just familiarize and appreciate the various plasma proteins and their functions.
Dr. Banzuela
MNEMONICS BLOOD CELL FORMATION

YOUNG LIVER SYNTHESIZES BLOOD.
Yolk Sac à Liver, Spleen à Bone Marrow
BLOOD CELL FORMATION Reticulocytes are nicknamed “baby RBCs.” Remember their synonym:
• 1st Trimester: Yolk Sac / Aortic Gonad Mesonephros polychromatic erythrocyte. This is the form released into the blood. It will
• 2nd and 3rd Trimester: Liver (with minor contribution from take around 2 days for these reticulocytes to change into mature RBCs.
spleen, LN) Dr. Banzuela
• After birth to puberty: Bone Marrow of all Bones

• Age 20 and above: Bone Marrow of “Centrally-located” Bones
• Extramedullary hematopoiesis in full-term infant: always
abnormal
8.2 RED BLOOD CELLS
• Biconcave (due to spectrin) which allows pliability to squeeze
through capillaries
• Size: 2x8 micrometer
• Protein inside RBC that binds with O2: Hemoglobin
o Males: 14-18 g/dl
o Females: 12-18 g/dl
• Percentage of Cells in whole blood: Hematocrit
o Males: 46 (40-54)
o Females: 42 (37-47)
o Sign of hemorrhagic shock: Low Hematocrit
RBCs are LARGER than the capillaries that they pass through. So, RBCs
would have to bend/flex (like man kneeling) for them to be able to pass
through these narrow capillaries. “Bag pliability” brought by spectrin
enables RBCs to do that. They will have this bag pliability for 120 days, after
which, they will die in very narrow capillaries because they cannot
bend/flex properly anymore. Where do old RBCs die? What is the
“graveyard” of RBCs? Answer: the spleen. What if the spleen is removed,
where do RBCs come to die then? Answer: the liver.
Dr. Banzuela
MNEMONICS RBC Stages

“PB PORE”
CELL DESCRIPTION
P roerythroblast (or • Synthesis of hemoglobin
Pronormoblast or starts (Source: William’s
Rubriblast) Hematology 9th Ed)
• Nucleoli disappear
B asophilic erythroblast (Take note: According to
(Macroblast or Early Junqueira's Basic Histology (15th
normoblast or rubricyte) ed) , hemoglobin synthesis starts
in basophilic erythroblast stage)
P olychromatic
erythroblast • Hemoglobin appears
(intermediate normoblast)
O rthochromatic © Topnotch Medical Board Prep
erythroblast HEMOGLOBIN
(Normoblast or Late • Nucleus disappears HEMOGLOBIN COMPONENTS
normoblast or IN THE EMBRYO
metarubricyte) Gower I hemoglobin • ζ2 - ε2
R eticulocytes • Formed reticulum
Gower II hemoglobin • α2 - ε2
(Polychromatic Hemoglobin Portland I • ζ2 - γ2
• Stage that enters blood
erythrocyte) Hemoglobin Portland II • ζ2 - β2
• Final Product IN THE FETUS
E rythrocyte • Reticulum disappears Hemoglobin F (HbF)
• α2 - γ 2
• Achieves biconcave shape • binds less with 2,3-BPG
AFTER BIRTH FORMATION OF HEMOGLOBIN
• α2 - β 2
Hemoglobin A (HbA) • binds more with 2,3-BPG
• 95% of hemoglobin after birth
• α2 -δ2
Hemoglobin A2 (HbA2) • 1.5-3.5% of hemoglobin after
birth
• α2 - γ 2
• can be elevated in persons with
Hemoglobin F (HbF)
sickle cell disease & beta-
thalassemia
Contributed by Frinz Moey C. Rubio, MD
• Primary mechanism for change in RBC shape during a sickle cell

crisis: Polymerization of HbS as it deoxygenated
IRON METABOLISM
Listen to this audio recording while

looking at the figure for iron
metabolism:
IRON METABOLISM
https://qrs.ly/89cmvhe
Dr. Banzuela
8.3 WHITE BLOOD CELLS, IMMUNITY AND ADAPTIVE

INNATE IMMUNITY
IMMUNITY
INFECTION
• Not sufficient;
Immunity
• Those with severe
• “Ability of the human body to resist almost all types of combined
organisms/toxins that tend to damage the tissues and organs” Sufficiency immunodeficiency • Yes
(body’s ability to fight against infection) disease suffer from
• Divided into Innate Immunity and Adaptive Immunity life threatening
infections
BRANCHES OF IMMUNE SYSTEM
• Phagocytes • Lymphocytes (T, B
ADAPTIVE
INNATE IMMUNITY • Monocytes and plasma cells)
IMMUNITY Components
• Macrophages • Antigen presenting
Specificity • Non-specific • Extremely specific Cells
• Neutrophils cells (macrophages,
• Structures shared • Special antigens of • Natural killer cells B & dendritic cells)
Triggered by by a group of microbial and non- Blood
microbes microbial agents • Complement • Antibodies
proteins
• Long term memory Anatomic • Lymph nodes
Memory • No memory • Skin
(memory cells) and • Spleen
• Same intensity of • Mucous
physiological • Mucosal Associated
action from • Improves after each membranes
Adaptation barriers Lymphoid Tissue
subsequent repeated exposure
exposure Innate immunity is first-line, non-specific, does not require prior exposure
and less powerful. Adaptive immunity is second-line, specific, requires
• No – requires prior exposure and is more powerful. Innate immunity – basta walang
• Yes – acts within
Effectivity several days before lymphocytes na involved. Adaptive immunity – basta lymphocytes ang
minutes
becoming effective involved. Analogy: innate immunity – done by security guards (first line,
Potency • Less • More non-specific (pwede sa magnanakaw, troublemaker, etc), does not require
prior exposure, less powerful (compared sa SWAT team). Adaptive
• 1st
line as immunity – done by SWAT team (second-line (tinatawag pag di kaya ng
Line of • Develops after
intrinsically guards), specific (e.g., hostage-takers), requires prior exposure (may
defense exposure training), more powerful) =)
present
Dr. Banzuela
Speed • Faster response • Slower response
• Least common type,
similar to mast cells,
produce histamine,
heparin, bradykinin,
• Bilobed/trilobed
serotonin
nucleus, largely
Basophils • Mast Cells:
densely basophilic
degranulation
(blue) granules
produces clinical
manifestations of
Allergy to
Anaphylaxis
• Large, kidney-
• Phagocytes, largest of
shaped nucleus
Monocytes WBC, mature to
• “frosted glass”
macrophages in tissues
cytoplasm
• Small, biconvex, • Not a WBC;
non-nucleated • involved in
Platelets
© Topnotch Medical Board Prep cells from hemostasis;
TYPES OF ADAPTIVE IMMUNITY megakaryocytes • lifespan 7-10 days
HUMORAL CELL MEDIATED
IMMUNITY IMMUNITY Remember the table above. When you hear neutrophils, think bacteria and
acute inflammation. When you hear eosinophils, think parasites and
Main cells • B-lymphocytes • T-lymphocytes
allergies. When you hear basophils, think histamine and allergies. When
• Originated in bone you hear monocytes, think of immature cells found in the blood.
• Originated and marrow and Macrophages are the mature forms found in the tissues. And finally, when
Maturation matured in bone completed you hear platelets, think “7-10 days.”
marrow development in Dr. Banzuela
thymus MECHANISM OF INNATE IMMUNITY

• Extracellular • Intracellular
microbes and their microbes
toxins o Viruses
• Toxin induced o Parasites
Protect
diseases (Leishmania)
against
• Infections o Bacteria
(virulence related (Mycobacterium,
to polysaccharide Listeria)
capsule) • Kills tumor cells
Location in
lymph • Superficial cortex • Paracortical areas
nodes
• Periarteriolar
Location in
• White pulp lymphoid sheaths
spleen
(PALS)
• Differentiation of B
• Secrete locally
End result cells into antibody
acting proteins
of activation secreting cells
called cytokines
called plasma cells
Hyper-
I, II, III are antibody
sensitivity • IV is cell mediated
mediated
reactions
• Delayed type
Onset • Rapid
hypersensitivity © Topnotch Medical Board Prep
• Splinter in your finger → Break in the skin → pathogen will enter

Antibodies • Formed • Not formed
the break → Tissue injury occurs
• Skin test for
• Mast Cells: will release histamine causing vasodilation and
• From plasma level development of
Evaluation increased vascular permeability
of antibodies delayed type of
• Tissue Macrophages
hypersensitivity
o 1st line of defense
• Ab synthesis • Macrophage o Present within minutes
requires 3 cells:
Cells • Helper T cells o identifies the pathogen → phagocytosis
o T lymphocytes
involved • Natural killer T cells • Neutrophils Invasion
o B lymphocytes
• Cytotoxic T cells o 2nd line of defense
o Macrophage
o Will start migrating in response to inflammatory cytokines
o Cause Phagocytosis
CELLS OF INNATE IMMUNITY (WBCs, Platelet)
• Monocytes → Macrophage Invasion
WBC APPEARANCE DESCRIPTION
o 3rd line of defense
• Most common type, o Blood monocytes (inactive) are converted to tissues:
• Involved in bacterial macrophage (active)
• Multilobed infection (neutrophils o This response takes time (at least 8 hours)
Neutrophils
nucleus utilize oxidants/ROS • ↑ Monocytes & Granulocyte production by Bone marrow
to kill bacteria) and o 4th line of defense
acute inflammation o Takes 3-4 days
• Weak phagocytes o Mediated by TNF, IL-1, GM-CSF, M-CSF
involved in parasitic • Pus formation = battlefield of dead cells and pathogens
• Bilobed nucleus, infections and
Eosinophils stain bright red allergies
with eosin dye • Highly phagocytic for
antigen-antibody
(immune) complexes
INNATE IMMUNITY • Effect:
• Cells of innate immunity (Neutrophils, Macrophages, NK cells) o Direct: agglutination, precipitation, neutralization, lysis
respond to lipid and carbohydrate sequences in bacterial cells o Indirect: activation of complement system
walls and other substances characteristic of tumor and
transplant cells
ADAPTIVE IMMUNITY
• is caused by a special immune system that forms Antibodies
and/or activated lymphocytes that attack and destroy the specific
invading organism or toxin
• Lymphocytes:
o Main cells of Adaptive Immunity
o Part of body’s defense against cancer
ANTIBODIES / IMMUNOGLOBULINS
• 1015 possible different immunoglobulins; 1015 possible different
T cell receptors
• Variable Portion: determines specificity to antigen © Topnotch Medical Board Prep
• Constant Portion: determines other properties of antibodies

TYPE FUNCTION HEAVY CHAIN STRUCTURE NOTES
• Most abundant type in serum (IgG > IgA >
• Fixed complement IgM > IgD > IgE)
• Opsonizes bacteria • Smallest, responsible for secondary immune
IgG γ1, γ2, γ3, γ4 • Monomer
• Neutralized bacterial toxins and response
viruses • Only isotype capable of crossing the placenta
(IgG Greets the Growing fetus)
• Most produced antibody overall (in
mucous membranes) but has lower serum
concentrations
• Localized protection in human • Protects mucosa via “immune exclusion”
body secretions (milk, saliva, • Monomer (in (binds to pathogen and prevents it from
tears, respiratory, intestinal, circulation) making contact with epithelial cells or
IgA genital tract α1, α2 • Dimer (w/ J mucus membranes)
• Prevents attachment of bacteria chain when • At least in the gut, unusually cross-reactive
and viruses to mucous secreted) (coping with antigenic drift)
membranes • Does not efficiently activate/fix
complement proteins (which prevents
initiating inflammation that can be
damaging)
• Monomer (on B
cells) • Largest; responsible in primary immune
IgM • Complement activation μ • Pentamer (w/ J response
chain when • Found on the surface of naïve B cells
secreted)
• Binds mast cells, basophils →
cross-links when exposed to
allergen → mediates type I
IgE hypersensitivity (via histamine ε • Monomer • Associated with allergies
release)
• Activates eosinophils → immunity
to parasites
IgD • Has unclear function δ • Monomer • Found on the surface of naïve B cells
Listen to the audio recording below while looking at the table above: COMPLEMENT SYSTEM
ANTIBODIES
https://qrs.ly/mfcmvig
Listen to the audio recording below while reading the section on

complement proteins:
COMPLEMENT PROTEINS
https://qrs.ly/4dcmvjc
Dr. Banzuela
Complement Proteins: targets Ag-Ab complexes CYTOKINES
• “Complement” the effects of antibodies • Hormone-like molecules that act on nearby cells (paracrine) to
o Opsonization: serve as marker that makes it easier to regulate immune responses
phagocytize foreign bodies • Secreted by lymphocytes, macrophages, endothelial cells,
o Stimulate Inflammation neurons, glial cells, other types of cells
o Membrane Attack Complex: perforate foreign organisms → • Chemokines: superfamily of >40 cytokines that attract
bacterial cell lysis neutrophils and other WBCs to areas of inflammation or immune
• Pathways: response
o Classic pathway: triggered by immune complex o Also has role in cell growth and angiogenesis
o Mannose-binding lectin pathway: triggered by lectin binding
with mannose groups in bacteria HEMATOPOIETIC GROWTH FACTORS
o Alternative / properdin pathway: triggered by contact with • Stem Cell Factors (SCF): for proliferation of Hematopoietic Stem
various viruses, bacteria, fungi and tumor cells Cells
• Causes Opsonization: C3b • CSF (G-, GM- and M-Colony Stimulating Factors - CSF): causes
• Induces inflammation (anaphylatoxin): C3a, C4a, C5a colonies to proliferate in soft agar
• Causes WBC chemotaxis: C5a • IL-1, IL-6, IL-3: convert pluripotent uncommitted stem cells to
• Members of the Membrane Attack Complex (MAC): C5b-C9 committed progenitor cells
MNEMONICS COMPLEMENT SYSTEM • IL-3: also called multi-CSF (promotes proliferation of all types of
C3b-O (the robot in Star Wars) blood cell)
• C3b – Opsonization • Chromosome 5: encode for most hematopoietic GF
C5a – chemoTAXIs
• Think of a Taxi travelling along the C5 Highway HEMATOPOIETIC GROWTH FACTORS
CELL TYPES
CYTOKINE SOURCE
CELLS OF ADAPTIVE IMMUNITY (LYMPHOCYTES) STIMULATED
CYTOKINE Erythrocyte
CELL FUNCTION Granulocyte
SECRETED IL-1 Multiple cell types
Megakaryocyte
• IL-2 • Stimulates cellular immunity
TH1 Monocyte
• γ-interferon (activated T-Cells)
Erythrocyte
• IL-4 • Interact with B cells in relation Granulocyte
TH2 IL-3 T lymphocytes
• IL-5 to humoral immunity Megakaryocyte
• Induced in response to Monocyte
bacterial infections, IL-4 Basophil T lymphocytes
• Help recruit neutrophils & IL-5 Eosinophil T lymphocytes
• IL-6
TH17 monocytes; Erythrocyte
• IL-17 Endothelial cells,
• Generate harmful Granulocyte
inflammatory responses in IL-6 fibroblasts,
Megakaryocyte
autoimmune diseases macrophages
Monocyte
• Dampen T-Cell-driven Erythrocyte
Treg • IL-10 Fibroblasts,
responses IL-11 Granulocyte
• Recognize and bind to MHC osteoblasts
αβ T Megakaryocyte
--- proteins and antigen Kidney
cells
fragments Erythropoietin Erythrocyte Kupffer cells of
• Seen in GIT mucosa; liver
γδ T
--- • Form link between innate and Erythrocyte
cells
acquired immune system Granulocyte
SCF Multiple cell types
• Cytotoxic lymphocyte of innate Megakaryocyte
NK Cell --- Monocyte
immune system
• Cytotoxic lymphocyte that has Endothelial,
NKT Cell --- features of T-lymphocyte and G-CSF Granulocyte fibroblast,
NK cell monocytes
Plasma • Activated Naïve B-Cells; Endothelial cells,
--- Erythrocyte
Cell • Secretes antibodies fibroblasts,
GM-CSF Granulocyte
monocytes, T
Megakaryocyte
lymphocytes
Endothelial cells,
M-CSF Monocyte fibroblasts,
monocytes
Thrombopoietin Megakaryocyte Liver, kidney
Barrett et al. Ganong’s Review of Medical Physiology. 26th ed. 2019
EXAMPLES OF CYTOKINES AND THEIR CLINICAL RELEVANCE
CYTOKINE CELLULAR SOURCES MAJOR ACTIVITIES CLINICAL RELEVANCE
• Activation of T cells and • Implicated in the pathogenesis of septic
IL-1 • Macrophages macrophages; promotion of shock, rheumatoid arthritis, and
inflammation atherosclerosis
• Used to induce lymphokine-activated killer
• Type 1 (Th1) helper • Activation of lymphocytes, natural cells; used in the treatment of metastatic
IL-2
T cells killer cells, and macrophages renal cell carcinoma, melanoma, and various
other tumors
• Type 2 (Th2) helper • As a result of its ability to stimulate IgE
T cells, mast cells, • Activation of lymphocytes, monocytes production, plays a part in mast-cell
IL-4
basophils, and and IgE class switching sensitization and thus in allergy and in
eosinophils defense against nematode infections
• Type 2 (Th2) helper • Monoclonal antibody against interleukin-5
IL-5 T cells, mast cells, • Differentiation of eosinophils used to inhibit the antigen-induces late-phase
and eosinophils eosinophilia in animal models of allergy
• Activation of lymphocytes;
• Type 2 (Th2) helper • Overproduces in Castleman disease acts as
differentiation of B cells, stimulation
IL-6 T cells and an autocrine growth factor in myeloma and in
of the production of acute-phase
macrophages mesangial proliferative glomerulonephritis
proteins
• Levels are increased in diseases.
• T cells and • Chemotaxis of neutrophils,
IL-8 Accompanied by neutrophilia, making it a
macrophages basophils, and T cells
potentially useful marker of disease activity
• Bone marrow • Stimulation of the production of • Used to reduce chemotherapy-induced
IL-11
stromal cells acute-phase proteins thrombocytopenia
• Stimulation of the production of
interferon γ by type 1 (Th1) helper T
• Macrophages and B
IL-12 cells and by natural killer cells; • May be useful as an adjuvant for vaccines
cells
induction of type 1 (Th1) helper T
cells
• Implicated in many immune/autoimmune
• Promotion of inflammatory cell
IL-17 • T cells diseases such as rheumatoid arthritis,
chemotaxis and inflammation
asthma, and psoriasis
• Macrophages,
• Treatment with antibodies against tumor
Tumor necrosis natural killer cells, T
• Promotion of inflammation necrosis factor-⍺ beneficial in rheumatoid
factor-⍺ cells, B cells, and
arthritis and Chron disease
mast cells
Lymphotoxin • Implicated in the pathogenesis of multiple
• Type 1 (Th1) helper
(tumor necrosis • Promotion of inflammation sclerosis and insulin-dependent diabetes
T cells and B cells
factor-β) mellitus
• T cells,
Transforming • May be useful therapeutic agent in multiple
macrophages, B • Immunosuppression
growth factor-β sclerosis and myasthenia gravis
cells, and mast cells
• Used to reduce neutropenia after
• T cells,
chemotherapy for tumors and in ganciclovir-
macrophages, • Promotion of the growth of
GM CSF treated patients with AIDS; used to stimulate
natural killer cells, granulocytes and monocytes
cell production after hematopoietic stem cell
and B cells
transplantation
• Used to treat AIDS-related Kaposi sarcoma,
• Induction of resistance of cells to viral
Interferon-⍺ • Virally infected cells melanoma, chronic Hepatitis B infection, and
infections
chronic Hepatitis C infection
• Induction of resistance of cells to viral • Used to reduce the frequency and severity of
Interferon-β • Virally infected cells
infections relapses in multiple sclerosis
• Activation of macrophages; inhibition • Used enhance the killing of phagocytosed
Interferon-γ T cells and natural
of type 2 (Th2) helper T cells bacteria in chronic granulomatous disease
killer cells
Should you memorize the table on cytokines above? Unfortunately, yes. DEVELOPMENT OF B-CELL AND T-CELL
They’ve been asked before. We recommend that you don’t memorize them
now. Makakalimutan niyo kaagad yan. Memorize them on the day of your
physiology exam, just a few minutes before it starts. The adrenaline
running through your veins during that time, will help you memorize the
table (or at least facilitate familiarity that will give you a fighting chance).
Dr. Banzuela
✔GUIDE QUESTION
The ability of the blood to phagocytose pathogens and mount a
respiratory burst is increased by
A. interleukin-2 (IL-2)
B. granulocyte colony-stimulating factor (G-CSF)
C. erythropoietin
D. interleukin-4 (IL-4)
E. interleukin-5 (IL-5) From Ganong Physiology 25th Ed
IMMUNITY ANTIGEN RECOGNITION AND PRESENTATION
• MHC-I proteins:” ID” of all host nucleated cells
• MHC-II proteins: “ID” of all host professional APCs
• CD8: in cytotoxic T cells that bind with MHC-I proteins
o MHC-1: coupled to mutant or viral proteins (digested in
proteosomes)
• CD4: in T-helper cells that bind with MHC-II proteins
o MHC-2: concerned with extracellular antigens like bacteria
that are endocytosed (digested in late endosomes)
Mnemonic: remember the number “8”. CD4 is matched to MHC-2. CD8 is
matched to MHC-1. 4x2=8, 8:1=8.
HIV attacks CD4 (T-Helper cells).
Dr. Banzuela
8.4 ANTIGENICITY OF BLOOD AND TISSUES

ANTIGENICITY OF BLOOD
• Antigen groups most likely to cause blood transfusion reactions
o O-A-B Blood Groups
§ Type A: N-Acetyl-Galactosamine
§ Type B: Galactose
§ Type AB: Both
§ Type O: None
o Rh System
§ Rh (+): has D Antigen
© Topnotch Medical Board Prep § Rh (-): no D Antigen
When a Rh(-) mom has a Rh(+) baby, fetal RBCs will stimulate maternal
antibody production during feto-maternal hemorrhage (anti-D IgM
initially, then Anti-D IgG). Reexposure to D antigen in subsequent
pregnancies will produce anti-D IgG in sufficient concentration. This Anti-
D IgG can cross the placenta and cause erythroblastosis fetalis or
Hemolytic Disease of the fetus and newborn (HDFN).
Dr. Banzuela

RED BLOOD CELL SERA
TYPES ANTI-A ANTI-B
O (–) (–)
A (+) (–)
B (–) (+)
AB (+) (+)

Prothrombin Time (PT) measures the integrity of the Extrinsic Pathway
along with factors common to both intrinsic and extrinsic pathway. Partial
Thromboplastin Time (PTT) measures the integrity of the Intrinsic
Pathway and factors common to both intrinsic and extrinsic pathway.
Dr. Banzuela
ANTIGENICITY OF TISSUES BLOOD COAGULATION

• Types of organ transplantation CLOTTING
SYNONYMS
o Autograft: Self FACTOR
o Isograft/Syngeneic Graft: Twin Factor I • Fibrinogen
o Allograft: same species Factor II • Prothrombin
o Xenograft: other species Factor III • Tissue factor; tissue thromboplastin
Factor IV • Calcium
8.5 HEMOSTASIS Factor V • Proaccelerin; labile factor; Ac-globulin
Watch the video recording on Steps of Hemostasis while referring to the • Serum Prothrombin Conversion
next table: Factor VII Accelerator;
• proconvertin; stable factor
HEMOSTASIS • Antihemophilic Factor
https://qrs.ly/jscmvjd Factor VIII • antihemophilic globulin,
• antihemophilic factor A
• Plasma thromboplastin component;
Dr. Banzuela
STEPS OF HEMOSTASIS Factor IX • Christmas factor;
STEP DESCRIPTION • antihemophilic Factor B
• Due to local myogenic spasm, • Stuart Factor;
1. Vascular Factor X
endothelin 1 (ET-1) • Stuart-Prower Factor
Constriction
• Prevents further blood loss • Plasma Thromboplastin antecedent;
Factor XI
• Platelet Adhesion: mediated by vWF of • antihemophilic Factor C
ruptured blood vessels walls and Gp1b Factor XII • Hageman Factor
2. Primary
of platelets Factor XIII • Fibrin-stabilizing factor
Hemostasis /
• Platelet Activation: platelets change Prekallikrein • Fletcher Factor
Formation of
shape • Fitzgerald factor;
Loose Platelet HMW Kininogen
Plug • Platelet Aggregation: mediated by • High-molecular-weight kininogen
fibrinogen and Gp2b-3a of platelets
(also by PAF) ANTICLOTTING MECHANISM
• Extrinsic Pathway (initiated by Factor • Antithrombin III
III or Tissue Factor) and Intrinsic o Binds to serine proteases in the coagulation system
Pathway (initiated by Factor XII or § Binding facilitated by heparin
3. Secondary o Inhibits active forms of Factors IX, X, XI and XII
Hagemann Factor) lead to formation of
Hemostasis / • Thrombomodulin
Thrombin that then converts
Blood Coagulation o Expressed in all endothelial cells except in cerebral
fibrinogen to fibrin
• Fibrin: meshwork that strengthens the microcirculation
loose platelet plug o Binds to thrombin and turns it into an anticoagulant
• Due to Fibrinolysin or Plasmin: lyses • Plasmin
4. Resolution o Lyse fibrin and fibrinogen
blood clot
o Produce Fibrinogen Degradation Products (FDP) that inhibit
thrombin
o Plasminogen receptors: plenty in endothelial cells; discourages
clot formation
↑ ESR ↓ ESR
• Most anemias • Sickle cell anemia (altered
• Infections shape → inability to form
• Inflammations dense RBC aggregates)
• Cancer (metastases, • Polycythemia (↑ RBCs
multiple myeloma) “dilute” aggregation factors)
• Renal disease (ESRD, • Heart failure
nephrotic syndrome) • Microcytosis
• Pregnancy • Hypofibrinogenemia
• Major Prototypical APR: CRP (activates monocytes and other

cytokines)
APR FUNCTION
POSITIVE APRs (UPREGULATED IN INFLAMMATION)
• Binds and sequesters iron (nutrient
Ferritin needed for bacterial growth) to inhibit
microbial iron scavenging
• Coagulation factor
8.6 INFLAMMATION AND WOUND HEALING Fibrinogen • Promotes endothelial repair
INFLAMMATION • Correlates with ESR
Serum amyloid A • Prolonged elevation → amyloidosis
• Complex localized response to foreign substances (e.g. bacteria)
o Acute inflammation: think neutrophils • ↓ iron intestinal absorption (degrades
o Chronic inflammation: think macrophages ferroportin) and ↓ iron release (from
Hepcidin
• Protective response to prevent further spread of injury macrophages) → anemia of chronic
• Arterioles dilate, capillary permeability increase disease
• nuclear factor-κ B: plays key role in inflammatory response • Opsonin; fixes complement and
(e.g., rheumatoid arthritis) C-reactive facilitates phagocytosis
protein • Measured clinically as a nonspecific
WOUND HEALING sign of ongoing inflammation
• Wounds: gain 20% of ultimate strength in 3 weeks, maximum • Binds free plasma hemoglobin →
Haptoglobin prevents loss of iron via the kidneys &
tensile strength in 12 weeks but never 70% of the strength of
normal skin protects kidney damage by hemoglobin
• Main transporter of copper in blood
Remember this: “Wounds never fully heal, you could only stop the bleeding. Ceruloplasmin
plasma
J
Dr. Banzuela NEGATIVE APRs (DOWNREGULATED IN INFLAMMATION)
PHASES CELLS FUNCTION • Reduction conserves amino acids for
Albumin
positive reactants
• Thrombin formation to • Internalized by macrophages to allow
Hemostasis • Platelet Transferrin
stop the bleeding iron sequestration
• Release of bactericidal • Transports thyroxine and retinol
• Neutrophils Transthyretin • Carries T4 and retinol-binding protein
substances
(RBP) bound to retinol
Inflammation • Release of angiogenic
substance to promote Retinol-binding • Transports vitamin A from liver to
• Macrophage protein (RBP) other peripheral tissues
capillary growth and
granulation process. Adiponectin • Serves as the “fat-burning” molecule
Contributed by Frinz Moey C. Rubio, MD
• Secretes glycoproteins and
• Fibroblast
collagen
• Epidermal • Responsible for 8.7 PHYSIOLOGY IN SPECIAL ENVIRONMENTS
cells reepithelialization MEN VS WOMEN
Proliferation
• **Granulation tissue is MEN WOMEN
formed from Overall strength • More • Less
-
macrophages, fibroblasts, Strength per
and new capillaries. square cm of x-sec • 3-4 kg/cm2 • 3-4 kg/cm2
• Remodeling of collagen area
from type III to type I • Long-distance
Remodeling • Fibroblast World records • Marathon
• Myofibroblast: wound swimming
contraction. • Testosterone → • Estrogen →
Effect of hormones
more muscle more fat
ACUTE PHASE REACTANTS (APR)
• Increases size (girth) of skeletal
• Proteins whose concentration increase/decrease by >25% during Effect of Exercise
muscles
inflammatory states
• Major Inducer: IL-6 Men are stronger overall than women simply because they have larger
• Other Inducers: IL-1 beta, (TNF)-alpha, and interferon gamma body sizes brought by testosterone. But on a per unit area basis, women are
o TNF (cachectin): involved in cachexia in cancer (thus the name just as strong as men – 3-4kg/cm2.
“cachectin”) and septic shock Dr. Banzuela
• Indirect measure of APRs: ESR

o Characterizes Polymyalgia Rheumatic: Increased ESR
o RBCs normally remain separated via (-) charges
o Products of inflammation (fibrinogen) coat the RBCs → ↓ (-)
charge → ↑ RBC aggregation (rouleaux formation – “stack of
coins”)
o Denser RBC aggregates → fall at a faster rate within a pipette
tube → ↑ESR
ENERGY SYSTEMS
NOTES ONSET & DURATION EXAMPLE
Phosphagen energy • Cell ATP, cell phospho- • 100m dash,
• First 8-10 seconds
system creatine jumping, diving
• Anaerobic;
Glycogen-lactic acid
• reconstitute ATP & • For 1.3 to 1.6 minutes after phosphagen system used up • Tennis, soccer
system
phosphocreatine
• Aerobic; • For unlimited time as long as with energy supply
• reconstitute ATP, (glycogen, FA, ketones, amino acids) • Long-distance
Aerobic system
phosphocreatine, • Fats supply 50% energy requirements after 3-4 hours) jogging
• Glycogen-lactic acid cycle after glycogen-lactic acid system used up
• Sometimes used by athletes to increase muscle strength: creatine • High Altitude predisposes to Hypocalcemic Tetany (e.g., calf
(converted to phosphorylcreatine that increases ATP) muscles cramping) because: Plasma proteins are more ionized
The energy system used in the first 10 seconds of athletic competitions is under alkalotic conditions, which provide more protein anion
the phosphagen energy system (the existing ATP and creatine phosphate in to bind with Calcium causing hypocalcemia
the cell). After 10 seconds, for the next almost 2 minutes, anaerobic system • Returns to normal after acclimatization: Cardiac Output
(glycogen-lactic acid system) is utilized. Only after approximately 2
minutes will you use the aerobic system. All of these are based on the ADAPTATIONS TO FLIGHT
premise that there is continuous use of the muscles. If you stop to rest at
any time, precursors are replenished, and you will go back to the
• Positive G
phosphagen energy system. That’s why specific sports will utilize specific o Pilot pushed against his seat
energy systems. 100m dash for example will utilize the phosphagen energy o More dangerous
system exclusively – dahil kung competent athlete ka dapat tapos yang o Blood shunted to the Lower Extremities
100m dash in around 10 seconds at hindi 2 minutes. =) Tennis and soccer o +6 to +10G → blackouts, LOC, death
will utilize exclusively the glycogen-lactic acid system naman – because you o +20G → Vertebral Fracture
have frequent breaks in muscle use (e.g., in tennis: palo…pak! Rest… • Negative G
palo…pak! Rest… Yosi muna… palo…pak! Rest… Tambay muna… =)
o Pilot pushed against his seatbelt
Marathon will exclusively use the aerobic system because you don’t stop
every 2 minutes while running a marathon. o Less dangerous
Dr. Banzuela o Blood shunted to the Head
ADAPTATION TO HIGH ALTITUDE § May result in “red-out” of the eyes and transient psychotic
DESCRIPTION ANSWER disturbances
Unacclimatized o -20G → death
person, Acute • 12,000 feet
Effects are felt at: ADAPTATION TO SPACE
Unacclimatized • Acute Effects
• 18,000 feet o Motion sickness
person, Seizures at:
Unacclimatized o Translocation of fluids
• 23,000 feet o Diminished physical activity
person, Death at
Natural • Chronic Effects
• Larger heart, lungs, shorter height o Decreased blood volume
Acclimatization
• ↑ RR → respiratory alkalosis → renal o Decreased RBC
compensation → normal pH o Decreased muscle strength
• Polycythemia via EPO → ↑ 2,3 BPG → o Decreased maximum cardiac output
shift to R of O2-HgB Dissociation o Loss of calcium and phosphate from bones → decrease in bone
Mechanisms for mass
Curve
Acclimatization
• ↑ Diffusing Capacity for O2
• Angiogenesis via VEGF DIVING PHYSIOLOGY
• ↑ ability of cells to use O2 → ↑ • Maximum” safe” depth: 200 feet below sea-level
mitochondria • Rapid ascent causes: nitrogen bubble formation in the blood
(decompression sickness)
Natanong na dati yang 12,000 feet, 18,000 feet at 23,000 feet na yan (these
o Bends: pain in the extremities
are the numbers written in Guyton). But the options given at that time are
in centimeters and not in feet. =) Life gets crazy sometimes. So, remember o Chokes: difficulty breathing
2.54cm=1 inch, 12 inches = 1 foot.
Dr. Banzuela
END OF PHYSIOLOGY
SOURCES:
Important Legal Information 1. BRS Physiology 6th Edition by Linda Costanzo, 2015, Published: Lippincott and Williams &
The handouts, videos and other review materials, provided by Topnotch Medical Board Wilkins
2. BRS Physiology 7th Edition by Linda Costanzo, 2019, Published: Lippincott and Williams &
Preparation Incorporated are duly protected by RA 8293 otherwise known as the Intellectual
Wilkins
Property Code of the Philippines, and shall only be for the sole use of the person: a) whose
3. Ganong Review of Medical Physiology, 23rd Edition, by Barrett, Kim , Barrett, Kim E., Barman,
name appear on the handout or review material, b) person subscribed to Topnotch Medical Susan, Boitano, Scott, Brooks, Heddwen, Published: New York : McGraw-Hill Medical, 2010
Board Preparation Incorporated Program or c) is the recipient of this electronic 4. Ganong Review of Medical Physiology, 25th Edition, by Barrett, Kim , Barrett, Kim E., Barman,
communication. No part of the handout, video or other review material may be reproduced, Susan, Boitano, Scott, Brooks, Heddwen, Published: New York : McGraw-Hill Medical, 2016
shared, sold and distributed through any printed form, audio or video recording, electronic 5. Ganong Review of Medical Physiology, 26th Edition, by Barrett, Kim , Barrett, Kim E., Barman,
medium or machine-readable form, in whole or in part without the written consent of Susan, Boitano, Scott, Brooks, Heddwen, Published: New York : McGraw-Hill Medical, 2019
Topnotch Medical Board Preparation Incorporated. Any violation and or infringement, 6. Costanzo Physiology 6th Edition by Linda Costanzo Published in Philadelphia, Pennsylvania:
whether intended or otherwise shall be subject to legal action and prosecution to the full Saunders/Elsevier, 2018
extent guaranteed by law. 7. Pre-Test Physiology, 14th Edition by Patricia Mettin, published: McGraw-Hill Medical, 2014
8. Guyton & Hall Textbook of Medical Physiology 12th Edition by Hall, John &, Guyton, Arthur C. , ,
Published in Philadelphia, Pennsylvania: Saunders/Elsevier, 2011
DISCLOSURE 9. Berne & Levy Physiology 6th Edition by Berne, Robert M., 1918-2001., Koeppen, Bruce M.,
Published: Philadelphia : Mosby/Elsevier, 2008
The handouts/review materials must be treated with utmost confidentiality. It shall be the 10. Kaplan Medical Step 1 Lecture Notes (Physiology) 2010
responsibility of the person, whose name appears therein, that the handouts/review 11. Medical Physiology: Big Picture by (author) Jonathan Kibble, Colby Halsey, Published: Lange
materials are not photocopied or in any way reproduced, shared or lent to any person or 12. Harper’s Illustrated Biochemistry 27th Edition by Murray, Robert K. by Lange
disposed in any manner. Any handout/review material found in the possession of another 13. Basic and Clinical Pharmacology 11th Edition by Katzung, Bertram G., Published: New York :
person whose name does not appear therein shall be prima facie evidence of violation of RA McGraw-Hill Medical, 2009
8293. Topnotch review materials are updated every six (6) months based on the current 14. Harrison’s Principles of Internal Medicine, 18Th Edition
trends and feedback. Please buy all recommended review books and other materials listed 15. SBCM Physiology Lectures
below. 16. Various Internet Websites including https://ods.od.nih.gov/factsheets/Potassium-
THIS HANDOUT IS NOT FOR SALE! HealthProfessional/, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7009052/
Of course, he knew that my mom's case was a true emergency, but he's
DANCING IN THE MOONLIGHT counting on the fact that i may not. When I told him I was a doctor, he got
Enrico Paolo C. Banzuela, MD rattled. Because both of us knew that doctors are required by law to render
(Facebook Post after The Med Boards) emergency care.
And that was the exact moment that I finally cried.
"Sir, 30 minutes to 1-hour po yung duration - "How to Establish your
Practice Ethically and Effectively" - 1.) How to choose area of practice, I cried more than anything else, because of the irony of it all. We train
hospitals, 2. How to set-up your clinic - room size, secretary, materials, medical graduates in the best way possible for them to pass the med boards
accounting, 3. How to "market" your practice ethically 4. How to deal with and practice immediately… only to have them practice unethically and
your competition ethically 5. Tips on how to work effectively with your incompetently such that they may ultimately be the cause of our own
superiors, residents, nurses, admin staff 6. Tips in managing common death. Teach them for months, only for them to practice with personal
problems - how to charge, dealing with med reps, referring to other convenience in mind rather than the patient's well-being.
specialists, dealing with hospital politics, etc.”.
And then the "What Ifs" came. What if I wasn't there, what if it was just my
… and so I texted the consultant. But he begged off citing his busy schedule. dad who brought her to moonlighting physician?
I asked another one. He also said that he's too busy, despite initial
interest. Texted another consultant, and this time, was totally ignored. =) What if what happened to my mom happened to me? What if this happened
And so, a day before the start of our moonlighting seminar, we're frantically to other people, especially those without any medical background?
searching for someone who can deliver this lecture. I got angry again. We've had lecture on Ethics, and Legal Medicine and Juris…
This moonlighting seminar is very close to my heart, because my mom was but it never really strikes home until you experienced it.
almost killed by a moonlighting physician/moonlighter. And then at last, sleep came. We were awakened by the nurse, and was told
4 years ago, at around 3am, she had severe, unremitting asthma attack that my mom was awake. Since she was intubated, she was given this
(status asthmaticus) at home that eventually lead to cardiac arrest. Still "keyboard" thing for her to type her responses to questions. At that point, I
wearing our night clothes, and while applying CPR, we rushed her to the was already resigned to the fact that her mind might be gone now. I was just
nearest hospital just in front of our village. In the car, I can feel her ribs break hoping that she'll at least be able to recognize us. Kahit yung man lang.
while applying emergency chest compressions, her body limped, her skin So, she "typed": "P"… "A"… "P"… "A…" "BAYARAN MO UTANG MO" =)
changing from pale to ashen-gray. There was only one thing in my mind: 4 And everybody burst into laughter. Ok, memory intact, calculation probably
minutes. In 4 minutes, without oxygen, she'll be brain-dead. Her body may intact, communication intact… I was grinning from ear-to-ear.
still be here, but her mind won't be. I told my dad to drive faster. She stayed in the ICU for two more weeks, in the hospital for a
Finally, we reached the hospital. Upon seeing the ashen-gray body of my month. Friends, relatives, former students visited. With each doctor, I
mom, brought in our old family car, with us dressed in "pambahay" clothes, discussed our experience with the moonlighter.
the moonlighting physician at the ER of this secondary hospital stopped us
and said: "Wag nyo na po siyang ibaba at dalhin dito, i-rush nyo na po sya sa I later learned that the nurses on duty in that hospital made an incident
FEU" report to the hospital director regarding the moonlighter's actions. He was
ultimately relieved of his duties.
I flared up immediately and told the doctor that my mom arrested, and had
status asthmaticus. He insisted that they cannot handle her case. So i said After a year, we started giving this moonlighting and pre-residency seminar
the magic words: "Doctor po ako. Bigyan nyo ng epi at i-intubate natin yung here in Topnotch. General physicians, the backbone of the medical
mommy ko." It finally dawned on the moonlighting physician that a lawsuit profession, have oftentimes been "mistrained" by their own experiences
is just around the corner, so he finally admitted her. after passing the med boards. Natuto sa nakasanayan, natuto rin ng maling
pamamaraan.
The first thing he did? He got an ECG. I think my BP went from HPN Stage 1
to HPN Stage 2 at this point. I know that the reason he got did that was to We gave them practical lectures on Internal Medicine, Pediatrics, Ob-Gyne,
document that I brought my mom arrested. So, I shouted at him to stop, and and Surgery that moonlighters need. We conducted workshops on
to give my mom some epi. Well, I think he went from "Scared of Lawsuit intubation, suturing, and basic casting/splinting. We gave lectures on
Stage 1" to "Scared of being Killed on the Spot by a Very Big Guy Stage 2" =) Medical Jurisprudence (practical ones like "how to avoid a lawsuit", "how to
So, he went to the pushcart in the ER… and there was no epi! He immediately transfer patients from one hospital to another", "how to fill up
rushed to the pharmacy. Epi found. A few minutes after it was given, I heard medical/death certificates properly") and Ethics. We did life planning -
my mom breathe again, felt her heart beating again. I looked hard at the setting goals for your family, career, etc. We even had talks about savings
moonlighting physician, and saw, in his eyes, inexperience. And so, I told my plan and how to invest in stocks and other financial instruments. And
dad not to have my mom intubated here. We rushed her to FEU. Literally in finally, we presented them with career options - doctors from the Doctors to
a few seconds, she was admitted, intubated, and immediately referred to the Barrios Program, from politics, from residency, from moonlighting…
specialists. they each have their moment to share their story and inspire these general
physicians. Hindi lang moonlighting, residency, at USMLE ang choices ng
It's one thing to learn BLS and ACLS and apply it yourself to other mga batang doktor. Maraming, marami pa.
patients. It's a different thing altogether seeing someone else apply it to
your mom. My mom was awake, but incoherent, and flailing her arms wildly. We kept the price low so that more GPs can be trained. We added
I wanted to cry, but I can't. The shock is still there. Fleeting images of nurses improvements gradually - we're currently conducting our first ever BLS-
and long-term care entered my mind. It's probably been more than 4 ACLS activity immediately after the moonlighting seminar, and in the future,
minutes. I talked to my dad and sister and told them to prepare for the we hope to add BEST (Basic Emergency Skills in Trauma), a job fair, CME
worst. accreditation, and perhaps PMA registration onsite.
I was angry at the moonlighter. Because I've heard it enough from the The way I see it, if we can have just one more doctor who will value patient
horror stories of other physicians and patients why he acted the way he well-being above anything else, one more doctor who's happy with the
did. Seeing the patient arrested and in need of intubation, with the patient's career path he's chosen, one more doctor who can afford to send his son or
family looking destitute (hey, no time naman kasi to change from our daughter to the school of his choice because he's a little more financially-
pambahay clothes), he didn't want the hassle of managing a toxic patient at secure thanks to the moonlighting seminar… then we would have done our
3am in the morning, with the extended hardship of trying to transfer an part.
intubated charity patient to another hospital. It might prolong his duty, get ...and my mom's experience, our experience, with the moonlighter, won't be
him in trouble legally if the patient dies, get him a scolding from the hospital for naught. =)
director on why he admitted such a toxic charity patient.
By the way, we did find someone to lecture on "How to Establish your
Practice Ethically and Effectively" =)
To all our participants and teachers, thank you very much! =)
TOPNOTCH MOONLIGHTING AND PRE-RESIDENCY SEMINAR

After you pass your med boards, we would like to invite you to join the Topnotch Moonlight and Pre-Residency Seminar. It will teach you the
knowledge, attitudes and skills needed as a General Physician (especially as a moonlighter and resident), provide you with information on various career
choices, and teach you things important in life but may not have been taught during med school.
By tradition, this seminar will start 10 days after the last day of the Med Boards. (this would be tentatively on March 25-April 8, 2021)
tentatively for P4,500. Here’s the schedule for LAST BATCH (November 2020) to give you an idea what’s in store during this seminar:
TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY MAIN DIGITAL HANDOUT BY ENRICO PAOLO C. BANZUELA, MD Appendix
TOPNOTCH ONLINE MOONLIGHTING AND PRE-RESIDENCY SEMINAR DAY 4 – MARCH 29 – PEDIATRICS FOR MOONLIGHTERS
SCHEDULE 8:00am- 8:15am – Introduction to the Day’s Activities
MARCH 2021 8:15am- 3:00pm – Diagnosis and Management of Pediatric Cases (by
Pediatrician)
LEARNING OUTCOMES FOR THE TOPNOTCH MOONLIGHTING AND 1. Fluid Management (Computation of Fluids, when to fast drip, etc.)
PRE-RESIDENCY SEMINAR OUTCOMES 2. Approach to Fever
At the end of the two-week training seminar, the licensed Topnotch MD must 3. Approach to Pediatric Rashes
be able to: 4. Approach to Diarrhea, Vomiting
1. Create appropriate management plans of common emergent, out- 5. Approach to Abdominal Pain (how to differentiate appendicitis vs
patient, ward and surgical cases seen by a General Practitioner in the colic vs cholecystitis vs PUD, etc.)
moonlighting setting. (CHED Program Outcomes 1, 2, 3, 6, 7) 6. Dengue
2. Correctly perform procedures expected of a General Practitioner 7. Typhoid
(intubations, casting/splinting, suturing) with confidence. (CHED Program 8. Allergies
Outcome 1) 9. Ascariasis and other Helminthic Infections
3. Correctly interpret ECG, Chest-Xray, CT-Scan, MRI, and common 10. Acute Otitis Media/Externa
laboratory findings in the moonlighting setting. (CHED Program Outcome 11. Conjunctivitis
1) 12. Drug computation of common Pediatric Drugs ( especially
4. Discuss basic leadership strategies and principles applicable to the diphenhydramine, paracetamol, diazepam, common antibiotics)
health care setting. (CHED Program Outcome 3) 12:00pm-1:00pm LUNCH
5. Apply principles in synergizing their work with other members of the
health care team (e.g. nurse, med tech). (CHED Program Outcome 5) MARCH 30 – NO CLASSES – OATH TAKING
6. Discuss guidelines on how to practice in the moonlighting and residency
setting ethically and in accordance with Philippine laws. (CHED Program DAY 5 – MARCH 31, WEDNESDAY – MANAGEMENT OF EMERGENCY AND
Outcomes 8,9) TRAUMA CASES; RESEARCH IDEAS; ETHICS FOR MOONLIGHTER;
7. Discuss strategies in applying to local and international residency RESEARCH IDEAS; ETHICS FOR MOONLIGHTER
programs, and other career opportunities offered for general physicians 8:00am-8:15am – Introduction to the Day’s Activities
here and abroad. (CHED Program Outcome 7, 10) 8:15am-12:00nn – Diagnosis and Management of ER Cases (By ER MED)
8. Design a research proposal in collaboration with their participants. 1. How to Man an Emergency Room
(CHED Program Outcome 4) 2. Application/Sources needed
9. Write career, family and personal plans taking into consideration their 3. ER Equipment
niche in the systems-based approach to healthcare, their own social 4. Approach to Influenza Like Illness Symptoms
accountability, interests and dreams in life. (CHED Program Outcome 6, 5. Code Blue
10) 6. How to give inotropes
10. Write their own Resume in the correct format and style. (CHED Program 7. Approach to Anaphylaxis
Outcome 2, 7) 8. Approach to Hypotension and Shock
9. Approach to Syncope
DAY 1 – MARCH 25, THURSDAY – INTRODUCTION TO MOONLIGHTING 10. Approach to Cardiac Dysrhythmia
SEMINAR 11. Approach to Chest Pain
8:00-10:00am – Opening Remarks and Orientation 12. Approach to Difficulty of Breathing
10:00am-11:00am – Awarding of the Top 10 13. Approach to Alcohol Intoxication
11:00am-11:30am – Career Planning 14. Approach to Seizures
15. Common First aid on snakebites, jellyfish, poisoning, etc.
DAY 2 – MARCH 26, FRIDAY – COVID 19 MUST KNOWS; INTRODUCTION 12:00pm-1:00pm LUNCH
TO AFP MEDICAL CORPS; INTRODUCTION TO THE DOCTORS TO THE 1:00PM-2:00PM – How to create research idea, conduct optimal literature
BARRIOS; TIPS FOR TAKING THE AUSTRALIAN, UK PLAB AND US review, and write a research proposal
MEDICAL LICENSURE EXAMS
8:00am-8:15am – Introduction to the Day’s Activities APRIL 1, THURSDAY- NO CLASSES
8:15-9:30am – Latest updates on diagnosis and management of Covid-19 and APRIL 2, FRIDAY- NO CLASSES
info on vaccination (by Pulmonologist) APRIL 3, SATURDAY- NO CLASSES
9:30am-11:00am – Introduction to the Doctors to the Barrios Experience
11:00am-12:30pm – Tips on Taking the Australian Medical DAY 6 – APRIL 4, SUNDAY – TECHNIQUES OF ENDOTRACHEAL
12:30pm-1:30pm LUNCH INTUBATION; TRENDS IN AESTHETIC MEDICINE; PREPARING FOR AN
1:30pm-3:00pm – Tips on Taking the USMLE INTERVIEW AND RESUME BUILDING
3:00pm-4:30pm – Tips on Taking the UK Professional and Linguistic 8:00am-8:15am – Introduction to the Day’s Activities
Assessments Board 8:15am-10:00am – Endotracheal Intubation Workshop (including indications,
1. Basic information about Foreign Exams– how it’s conducted, cost, techniques, post-intubation orders) (by Anesthesiologist)
where and how to apply 10:00am-11:30am – Trends in Aesthetic
2. How to Study for the Exam; Tips on how to be matched 11:30am-12:30pm LUNCH
12:30pm-1:00pm – Entering the Military Life (AFP Doctor )
MARCH 27, SATURDAY – NO CLASSES 1:00pm-2:30pm – How to Write Proper Resume and Preparing for your
Interview
DAY 3 – MARCH 28, SUNDAY – SURGERY FOR MOONLIGHTERS AND
SUTURING WORKSHOP; DONNING AND DOFFING OF PERSONAL DAY 7 – APRIL 5, MONDAY – BASIC HEMODIALYSIS FOR THE
PROTECTIVE EQUIPMENT MOONLIGHTER; LEGAL ASPECT OF MOONLIGHTING; OB-GYN FOR
8:00am-8:15am – Introduction to the Day’s Activities THE MOONLIGHTER
8:15am-11:00am – Basic Surgery (By Surgeon) 8:00am- 8:15am – Introduction to the Day’s Activities
1. How to give ATS, TeANA properly and appropriately 8:15am-9:00am – How to handle patients for hemodialysis (By Nephrologist)
2. Managing V-A Injuries 9:00am-11:30am – Legal and Ethical side of Moonlighting (by doctor-lawyer)
3. Managing Gunshot and Stab Wound Injuries 1. Legal Basis for Moonlighting
4. Managing Burn Patients 2. Written and Unwritten Rules of Moonlighting
5. Tips in mass excision, I and D, ungiectomy 3. How to Avoid Lawsuits based on Actual Cases in the Philippines for
6. Proper techniques in Circumcision the level of moonlighter and hospital resident
7. Proper techniques in the suturing of Scalp, Face, Extremities 4. How to Write a Proper Medical Certificate and Death Certificate
8. Chest Tube Insertion – Video Only; along with tips from Dr. Antonio 5. How to Properly Charge Patients for Services Rendered
9. Lumbar Tap Insertion – Video Only; along with tips from Dr. 6. How to Transfer a Patient to Another Hospital Properly
Antonio 7. How to Deal with Various Health Cards (Practical Tips)
11:00am-11:30am – Basic Suturing Technique Workshop (KURT ASPERAS, MD) 8. How to Legally Deal with your co-workers – Nurses, Fellow
Materials: Moonlighters, Consultants, Hospital Staff
*suturing set including scalpel, needle holder, scissors, expired sutures (with 11:30-12:30pm – LUNCH
needle)
11:30am-12nn – Aseptic Technique, Donning and Doffing of PPEs
12:30-4:00pm – OB-GYN for Moonlighters (BY OB-GYN) APRIL 10, SATURDAY – NO CLASSES
1. Basic Principles in Prenatal Care
2. Delivering babies in the Hospital Setting DAY 12 – APRIL 11, SUNDAY – MOONLIGHTERS AND RESIDENCY
3. Delivering babies in the Emergency, Non-Hospital Setting (e.g. at PANEL TALK; FINDING YOUR NICHE IN THE MEDICAL FIELD
home) 8:15am-9:00am – Panel Discussion – Residents talk about their residency
4. Management of STDs experiences
5. Contraception 9:00am-10:00am – Panel Discussion – Different Moonlighting Experiences of
6. Techniques for Pap smear and Internal Examination 3 Moonlighting Physicians
7. Basic Principles in Prenatal Care 10:00am-11:30am – Career Options after the Med Boards
8. Delivering babies in the Hospital Setting 11:30am-12:00nn – Leadership for MDs
9. Delivering babies in the Emergency, Non-Hospital Setting (e.g. at 12:00nn – Awarding of Certificates
home)
10. Management of STDs
11. Contraception
DAY 8 – APRIL 6, TUESDAY – I.M. FOR MOONLIGHTERS; ESSENTIAL

MOONLIGHTING SKILLS; LABORATORY AND ECG INTERPRETATION
8:00am-8:15am – Introduction to the Day’s Activities
8:15am-11:30am – Diagnosis and Management of Adult Cases (By IM)
1. Pneumonia, URTIs, Asthma, COPD
2. UTIs
3. DM
4. HPN
5. Approach to the Jaundiced Patient
6. Approach to Poisons and Snakebites
7. Approach to Electrolyte Abnormalities (Hypo- and Hyper-kalemia,
Hypo- and Hypercalcemia, etc.)
8. Pain Medications (indications, dosage, contraindications, side
effects)
9. Management of Neuro Emergencies
11:30-12:30pm – LUNCH
12:30pm-1:30pm – Dealing with Abnormal CBC
1:30pm-2:30pm – Management of electrolyte abnormalities
2:30pm-3:00pm – ABG Interpretation
3:00pm-5:00pm – Basic 12L ECG Interpretation
Topnotch Moonlighting and Pre-Residency Seminar Onsite 2019
DAY 9 – APRIL 7, WEDNESDAY – ORTHOPEDIC EMERGENCIES,
SPLINTING WORKSHOP; SYNERGIZING THE PHYSICIAN-NURSE
RELATIONSHIP FROM THE POINT OF VIEW OF A NURSE; PRACTICAL
IMAGING PEARLS; PATIENT ROUNDS AND PROGRESS NOTES; LIFE OF
A PNP MEDICOLEGAL OFFICER
8:00am- 8:15am – Introduction to the Day’s Activities
8:15am-10:00am – How to Handle Common Ortho Emergencies and Casting
workshop (By Orthopedic Surgeon)
10:00am-11:00am – Synergizing the Physician-Nurse Relationship (by Nurse)
11:00am-12:00nn – LUNCH
12:00-1:30pm – CXR and Fracture Interpretation, Basic CT Scan
Interpretation (by Radiologist)
1:30pm-2:30pm – Daily Rounds and Progress Notes
2:30-3:30pm – Life of a PNP Medicolegal Officer
DAY 10 – APRIL 8, THURSDAY – FINANCIAL WEALTH AND HEALTH FOR

THE MOONLIGHTER AND THE RESIDENT; ALL ABOUT BANKING
8:00am-8:15am – Introduction to the Day’s Activities
8:15am-12:00nn – Stocks and Investments for the Busy Resident and
Moonlighter
12:00-1:00pm – LUNCH
1:00pm-2:00pm – All about Banking by BPI representative
1. How to open savings and current account
2. How to Apply for a credit card
3. How to properly issue checks
4. Different types of loans and how to avail of these loans
DAY 11 – APRIL 9, FRIDAY – ROAD TO ALTERNATIVE MEDICINE;

SETTING-UP YOUR OWN CLINIC FROM AN MD-MBA STANDPOINT;
HEALTH AND LIFE INSURANCE; ADULTING 101
8:00am- 8:15am – Introduction to the Day’s Activities
8:15am-9:00am – Road to Alternative Medicine
9:00am-10:00am – Setting Up a Clinic from an MD-MBA standpoint
10:00am-11:00am – The must-knows of health and life insurance
10:00am-12:00nn – Adulting 101: Your guide to getting your PTR license,
SSS, Philhealth and paying your taxes
TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY PHASE 0 CORRECTION HANDOUT BY DR. ENRICO PAOLO BANZUELA
For inquiries visit www.topnotchboardprep.com.ph or https://www.facebook.com/topnotchmedicalboardprep/
This handout is only valid for September 2021 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.
INSTRUCTIONS
For those who have printed the initial handout: This handout is only valid for the September 2021 PLE batch.
Please use this handout as a guide to correct the initial handout. This will be rendered obsolete for the next batch
Page guides are available to assist you in doing so. since we update our handouts regularly.
The corrected handout is now also available in the Resources Tab
of the Topnotch Online Portal.
PHYSIOLOGY – PHASE 0 CORRECTIONS

By Enrico Paolo Banzuela, MD
• Page 28, RUQ image
• Page 32, annotation on mean arterial pressure, RUQ
END OF <SUBJECT> PHASE <N>
TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY PHASE 0 CORRECTION HANDOUT BY DR. ENRICO PAOLO BANZUELA. Page 1 of 1
For inquiries visit www.topnotchboardprep.com.ph or email us at topnotchmedicalboardprep@gmail.com
TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY PHASE 2 HANDOUT BY DR. BANZUELA AND DR. RUBIO
After passing the med boards, Patricia, 25/F went to
Important Legal Information
The handouts, videos and other review materials, provided by Topnotch Medical Board Taste of LA café to celebrate with her family. They
Preparation Incorporated are duly protected by RA 8293 otherwise known as the ordered the ribeye salpicao. After smelling the
Intellectual Property Code of the Philippines, and shall only be for the sole use of the person: aroma of the food presented before her, Patricia
a) whose name appear on the handout or review material, b) person subscribed to Topnotch
Medical Board Preparation Incorporated Program or c) is the recipient of this electronic began secreting HCl. What phase of GI secretion is
6.
communication. No part of the handout, video or other review material may be reproduced, she in?
shared, sold and distributed through any printed form, audio or video recording, electronic
medium or machine-readable form, in whole or in part without the written consent of A. Cephalic Phase
Topnotch Medical Board Preparation Incorporated. Any violation and or infringement, B. Gastric Phase
whether intended or otherwise shall be subject to legal action and prosecution to the full C. Intestinal Phase
D. Rectal Phase
Which of the following is an effect of caffeine?
DISCLOSURE A. Stimulates adenosine receptors
The handouts/review materials must be treated with utmost confidentiality. It shall be the
responsibility of the person, whose name appears therein, that the handouts/review B. Inhibit Phosphodiesterases
materials are not photocopied or in any way reproduced, shared or lent to any person or 7. C. Inhibit calcium release from intracellular
disposed in any manner. Any handout/review material found in the possession of another
person whose name does not appear therein shall be prima facie evidence of violation of RA
stores
8293. Topnotch review materials are updated every six (6) months based on the current D. Stimulates GABAA receptors
trends and feedback. Please buy all recommended review books and other materials listed E. All of the above
below.
THIS HANDOUT IS NOT FOR SALE! Rh (-) mom has an Rh (+) first baby. Which of the
following is true?
I. Complications can arise during this first
REMINDERS pregnancy
1. Finish the Phase 0 handout and Phase 1 video before proceeding to the II. Erythroblastosis Fetalis can happen during
Phase 2 handout and video. subsequent pregnancies
2. Phase 2 handouts are based on commonly used review books and III. Rho(D) immune globulin should be given at 28
previous question feedback from students.
3. Answer the Pre-Test (Guide Questions) first prior to watching the video
weeks AOG, Within 72 hours of pregnancy
lectures. 8. termination, after any episode of vaginal
4. The guided content of the video lectures are in the 2nd part of the Phase bleeding, After amniocentesis or chorionic
2 handouts and are meant to complement the video lecture. villus sampling
This handout is only valid for the September 2021 PLE batch. Choose the best answer:
This will be rendered obsolete for the next batch A. I, II, III
since we update our handouts regularly. B. I and II
C. II and III
D. I and III
PHYSIOLOGY – PHASE 2 Renal afferent arterioles reflexively responds to
stretch by contracting in order to maintain constant
By Enrico Paolo C. Banzuela, MD renal blood flow and subsequently, GFR: ______________
Frinz Moey C. Rubio, MD 9.
A. Tubuloglomerular Feedback / Macula Densa
Feedback
B. Myogenic Mechanism
QUESTIONNAIRE C. Glomerulotubular Balance
Ampie, 25/F, was anxiously waiting for the medical D. All of the above
board exam results when she read in the PRC Measured using a Swan-Ganz catheter to estimate
website that she passed the med boards and even for Left Atrial Pressure: ____________.
placed in the Top 10. She was unbelievably happy, A. Pulse Pressure
10.
and then suddenly lost consciousness. What most B. Central Venous Pressure
1. C. Pulmonary Capillary Wedge Pressure
likely happened?
A. Myocardial infarction D. Central Venous Pressure
B. Vasovagal Syncope Which of the following can cause an increase in
C. Vagovagal Reflex pulse pressure?
D. Oculocardiac Reflex A. Well-conditioned endurance runner
The part of the enteric nervous system responsible 11. B. Old age
for contraction of the muscularis mucosa? C. Aortic regurgitation
A. Meissner plexus D. Aortic sclerosis
2. E. All of the above
B. Auerbach plexus
C. Submucosal plexus Jesce, 30/F lifts weights 3x a week for
D. Myenteric plexus approximately 2 hours each session, for the past 10
Which part of the brain do you need the most to help years. Which of the following is expected?
catch a fly? A. Her skeletal muscles will increase in size, but
A. Cerebral cortex not in number
3. 12. B. Venous Return, Cardiac Output and Blood
B. Thalamus
C. Cerebellum Pressure will all increase during the weight
D. Limbic Lobe sessions
Competes with Acetylcholine for receptors on the C. Jesce is just as strong as any other man in a per
motor end plate? unit area basis
A. Botulinus Toxin D. All of the above
4. Solutions X and Y are separated by a semi-
B. Curare
C. Neostigmine permeable membrane. Solution X has 20mM of
D. Hemicholinium Urea, while solution Y has 10 mM of urea. If we
Which of the following is rich in tyramine? triple the concentration of urea in Solution X, what
A. Salami will happen to the flux of urea across the
13.
B. Aged Cheddar membrane?
5. A. 2x
C. Corned beef
D. Kimchi B. 3x
E. All of the above C. 5x
D. None of the above
TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY PHASE 2 HANDOUT BY DR. BANZUELA AND DR. RUBIO Page 1 of 14
Male pattern baldness is an effect of: _____________. Which of the following characterizes Capacitance?
A. Testosterone I. Equal to volume/pressure
14. B. Dihydrotestosterone II. Greater in veins than in arteries
C. Both A and B III. Inversely proportional to elastance (stiffness)
D. Neither A nor B
26.
Ventricular volume are at its highest and lowest Choose the best answer:
respectively during which phases of the cardiac A. I, II and III
cycle? B. I and III
A. Isovolumic Contraction, Isovolumic Relaxation C. II and III
15. B. Isovolumic Relaxation, Isovolumic Contraction D. I and II
C. Rapid Ventricular Ejection, Reduced What will happen if a hypertensive patient was
Ventricular Ejection given NaCl solution?
D. Rapid Ventricular Filling, Reduced Ventricular A. ECF volume increases, ICF Volume Decreases if
Filling solution is hypertonic
27.
Which diuretic acts on the early distal tubule? B. ECF Volume increases, ICF Volume remains
A. Acetazolamide the same if solution is isotonic
B. Furosemide C. Blood Pressure increases
16.
C. Hydrochlorothiazide D. All of the above
D. Spironolactone Muscles of GIT are smooth except?
E. Mannitol A. Pharynx
Which skeletal muscle type has the greatest number 28. B. Upper 1/3 Esophagus
of mitochondria? C. External Anal Sphincter
A. Skeletal D. All of the above
17.
B. Cardiac True of capillaries except?
C. Smooth A. Cannot dilate/constrict since they don’t have
D. Type 1 tunica media
29.
What is the numerator in the computation for renal B. Contains most of our blood
blood flow? C. Can be “open” or ”close”
A. Renal Plasma Flow D. Blood flow is slowest
18.
B. Hematocrit What is antihemophilic factor?
C. Hemoglobin A. Factor VIII
D. Kf 30. B. Factor IX
Conduction Velocity is most dependent on: __________? C. Factor X
A. Myelination D. Factor XI
19. B. Nerve Diameter How do you compute for URINE Anion Gap?
C. Neurotransmitter A. UAG = Na+ – HCO3- + Cl-
D. Calcium channels 31. B. UAG = Na+ + K+ – Cl-
The Na-K-ATPase pump is an example of ____________. C. UAG = Na+ – HCO3- + Cl- + K+
A. Secondary Active Transport D. None of the above
20. B. Anabolic reaction What is the mechanism behind cadmium toxicity?
C. Integral protein A. Interacts with calcium to cause osteoporosis
D. 2 Na+ out, 3K+ in B. Disturbs zinc metabolism
32.
A man lost in the desert would have the following C. Decreases plasma copper and ceruloplasmin
changes: __________ D. Interacts with iron causing anemia
A. Decreased ECF and ICF volume, Increased ECF E. All of the above
and ICF Osmolarity Uses group Ia afferents, detects dynamic changes:
B. Increased ECF and ICF volume, Decreased ECF ________.
21.
and ICF Osmolarity A. Nuclear Bag Fibers
C. Increased ECF and ICF volume, Increased ECF B. Nuclear Chain Fibers
33.
and ICF Osmolarity C. Either Nuclear Bag Fibers or Nuclear Chain
D. Decreased ECF and ICF volume, Decreased ECF Fibers
and ICF Osmolarity D. Neither Nuclear Bag Fibers nor Nuclear Chain
What is the formula for Ejection Fraction? Fibers
A. SV/EDV What is the formula for clearance?
22. B. VO2 / AVO A. UV/P
C. (HR x [EDV-ESV]) X TPR 34. B. UP/V
D. None of the above C. RPF/(1-Hct)
From red nucleus to interneurons of lateral spinal D. GFR/RPF
cord. Stimulates flexors, inhibits extensors: Joy, 30/F, reads a NYT news article about Hidilyn
____________. Diaz. Which muscle in the eye helps her focus in this
23. A. Rubrospinal tract activity?
B. Pontine Reticulospinal tract 35. A. Radial Muscle
C. Medullary Reticulospinal Tract B. Circular muscle
D. Lateral Vestibulospinal Tract C. Ciliary Muscle
The following are respiratory responses to high D. All of the above
altitude EXCEPT: ________. Cytokine involved in the chemotaxis of neutrophils,
A. Increases respiratory rate basophils and T cells?
24.
B. Increased 2,3 BPG A. IL-4
36.
C. Decreased pulmonary vascular resistance B. IL-6
D. Decreased Alveolar PO2 and Arterial PO2 C. IL-8
Which of the following is FALSE? D. TNF-alpha
A. Initial saliva is high in Na
25. B. Initial saliva is produced by the ductal cells
C. Final saliva is rich in K
D. Final saliva is hypotonic
40/F on ventilator with rate of 20, TV=500mL, Function of IgD?
FIO2=1.0. ABG later shows PaO2 = 360mmHg, A. Enhance mucosal homeostasis and immune
PCO2=36mmHg, pH of 7.3. Barometric Pressure = surveillance
760mmHg, Respiratory exchange ratio = 0.8. What 49. B. Prevents attachment of bacteria and viruses to
37. is the patient’s alveolar oxygen tension? mucous membranes
A. 665 C. Neutralized bacterial toxins and viruses
B. 668 D. Complement activation
C. 720 What is hexamethonium?
D. None of the above A. NMJ blocker
Adequate intake of potassium everyday for adult 50. B. Non-selective beta agonist
male: C. Non-depolarizing ganglionic blocker
A. 2,600mg D. Depolarizing ganglionic blocker
38.
B. 2,800mg
C. 2,900mg
D. 3,400mg DISCUSSION
Increasing Ventricular Pressure, Ventricular TIPS IN STUDYING PHYSIOLOGY
Pressure < Aortic Pressure: _________. • Read thoroughly and understand deeply the Physiology Phase 0
A. Isovolumic Relaxation handout
39.
B. Isovolumic Contraction o Med board feedback for the past 3 batches: does not focus on
C. Rapid Ventricular Filling the essentials but also on the “Nooks and crannies” of the
D. Rapid Ventricular Ejection handout (small, seemingly insignificant details)
What kind of contraction happens in the small • “Namnamin” ang handout
intestines during fasting? o Original onsite lecture: 20 hours
A. Segmental Contraction o Online lecture: 6 hours
40.
B. Peristaltic Contraction § Selected content only, therefore will require intensive self-
C. Slow wave Contraction study of the remaining material
D. Skeletal muscle contraction
What delays movement of food? Ampie, 25/F, was anxiously waiting for the medical
A. Chyme board exam results when she read in the PRC
41. B. Lipase website that she passed the med boards and even
C. Secretin placed in the Top 10. She was unbelievably happy,
D. HCl in the duodenum and then suddenly lost consciousness. What most
What is the contractile units of myocardial cells? 1.
likely happened?
A. Myosin A. Myocardial infarction
42. B. Sarcomere B. Vasovagal Syncope
C. Sarcoplasm C. Vagovagal Reflex
D. Myocytes D. Oculocardiac Reflex
Corrective lens for hyperopia: _________.
A. Biconcave lenses REMEMBER
43. B. Cylindrical lenses • Vasovagal Syncope
C. Convex lenses o Emotional fainting
D. Bifocal lenses o (+) activation of muscle vasodilator system + increased vagus
What urine test to do for ovulation? nerve stimulation of the heart (decreasing heart rate) à acute
A. FSH decrease in BP à decreased blood flow to the brain à loss of
B. LH consciousness
44.
C. Estrogen • Oculocardiac Reflex/Aschner phenomenon/Ashner-Dagnini
D. Progesterone Reflex
E. B-HCG o Compression of eyeball/EOMS à decreased HR
Sperm becomes motile in the ________. o Due to nerve connection between CN V (ophthalmic branch)
A. Seminiferous tubules and CN X
B. Epididymis • Vagovagal Reflex
45.
C. Vas Deferens o Stomach à Brain à stomach
D. Seminal Vesicle o Causes HCl secretion while food is in stomach
E. Prostate Gland
Secretin actions include: The part of the enteric nervous system responsible
I. Inhibits HCl secretion for contraction of the muscularis mucosa?
II. Increases biliary and pancreatic bicarbonate A. Meissner plexus
III. Increases pancreatic enzyme secretion 2.
B. Auerbach plexus
46. Choose the best answer: C. Submucosal plexus
A. I, II, III D. Myenteric plexus
B. I and II
C. II and III LESSONS
D. I and III • Errors are inevitable in the med boards
Which band is associated with myosin? • Don’t lose your shit because of them
I. A Band INNERVATION OF THE GI TRACT
II. I Band
• Intrinsic: Coordinates and relays info from ANS to GI tract
III. H Band
47. Choose the best answer:
A. I, II, III
B. I and III
C. II and III
D. I and II
How long does the sperm live in the female
reproductive tract?
A. 1-5 days
48.
B. 3-7 days
C. 5-9 days
D. 7-12 days
Which part of the brain do you need the most to help After passing the med boards, Patricia, 25/F went to
catch a fly? Taste of LA café to celebrate with her family. They
A. Cerebral cortex ordered the ribeye salpicao. After smelling the
3.
B. Thalamus aroma of the food presented before her, Patricia
C. Cerebellum began secreting HCl. What phase of GI secretion is
6.
D. Limbic Lobe she in?
A. Cephalic Phase
BRAIN B. Gastric Phase
• Cerebral cortex: C. Intestinal Phase
o Frontal: calculation, judgment, rational thought D. Rectal Phase
o Parietal: sensory
o Occipital: vision • Stimulates HCl Secretion
o Temporal: Hearing o Histamine on H2 receptors, Ach on M3 receptors and Gastrin on
o Limbic: behavior, emotions, motivation CCKB receptors
• Thalamus o Note: above 3 can potentiate
o Sensory modalities o Basal acid output is increased by: alkalinization of antrum
o Recall of memories (releases gastrin-releasing cells from inhibitory influence of
• Cerebellum somatostatin) PreTest 14th (316)
o balance • Inhibits HCl Secretion
o Low pH (<3.0) of the stomach, somatostatin, prostaglandins
Competes with Acetylcholine for receptors on the • Phases:
motor end plate? o Cephalic Phase (30%), Gastric Phase (60%) and Intestinal
A. Botulinus Toxin Phase (10%)
4. • Drugs that block HCl secretion
B. Curare
C. Neostigmine o Atropine on M3, Cimetidine on H2 and PPI (Omeprazole) on H+-
D. Hemicholinium K+-ATPase exchange pump
o Best describes H2 blockers: inhibits both gastrin- and
DESCRIPTION ANSWER acetylcholine-mediated secretion of acid PreTest 14th (322)
Blocks release of Ach from pre- BOTULINUS
synaptic terminals TOXIN Sight, smell, taste of food (cephalic phase) contributes to
Competes with Ach for receptors on INCREASED gastric/HCl secretion.
CURARE
Motor End Plate
Inhibits Acetylcholinesterase NEOSTIGMINE Low gastric pH (e.g., gastric pH<3.0) contributes to
DECREASED gastric/HCl secretion
Blocks reuptake of Choline into
HEMICHOLINIUM
presynaptic Terminal
Which of the following is an effect of caffeine?
A. Stimulates adenosine receptors
B. Inhibit Phosphodiesterases
7. C. Inhibit calcium release from intracellular
stores
D. Stimulates GABAA receptors
E. All of the above
CAFFEINE
• Inhibits all types of adenosine receptors (ARs): A1, A2A, A3, and
A2B (affects brain functions such as sleep, cognition, learning
and memory)
• inhibit phosphodiesterases (PDEs) (e.g., PDE1, PDE4, PDE5)
• promote calcium release from intracellular stores
Which of the following is rich in tyramine?

A. Salami
B. Aged Cheddar
5.
C. Corned beef
D. Kimchi
E. All of the above
TYRAMINE AND MAOI

• MAOIs – blocks monoamine oxidase
o Blocking this enzyme relieves depression
o However, monoamine oxidase breaks down tyramine
§ MAOIs would therefore increase tyramine levels
§ Eating tyramine-rich foods will exacerbate the problem https://www.semanticscholar.org/paper/Caffeine-and-adenosine.-Ribeiro-
• Tyramine-rich foods Sebastião/88601b52a5fbf6d0d18ce47a678e099577b7dc9a/figure/1
o Strong/aged cheeses
o Cured meats/smoked meats/processed meats Rh (-) mom has an Rh (+) first baby. Which of the
o Pickled/fermented foods like kimchi following is true?
o Sauces (soy sauce, shrimp paste, etc) I. Complications can arise during this first
o Soybeans, fava beans pregnancy
o Dried fruits II. Erythroblastosis Fetalis can happen during
o Alcohol 8. subsequent pregnancies
o Spoiled food III. Rho(D) immune globulin should be given at 28
weeks AOG, Within 72 hours of pregnancy
termination, after any episode of vaginal
bleeding, After amniocentesis or chorionic
villus sampling
Choose the best answer: TUBULOGLOMERULAR FEEDBACK
A. I, II, III Macula Densa Feedback;
B. I and II For Autoregulation of GFR
C. II and III
D. I and III GLOMERULOTUBULAR BALANCE
Percentage of solute reabsorbed is held constant; Buffers
• When a Rh(-) mom has a Rh(+) baby, fetal RBCs will stimulate effect of drastic GFR changes on urine output
maternal antibody production during feto-maternal hemorrhage Measured using a Swan-Ganz catheter to estimate
(anti-D IgM initially, then Anti-D IgG). Re-exposure to D antigen for Left Atrial Pressure: ____________.
in subsequent pregnancies will produce anti-D IgG in sufficient A. Pulse Pressure
concentration. This Anti-D IgG can cross the placenta and cause 10.
B. Central Venous Pressure
erythroblastosis fetalis or Hemolytic Disease of the fetus and C. Pulmonary Capillary Wedge Pressure
newborn (HDFN). D. Central Venous Pressure
RED BLOOD CELL SERA
TYPES ANTI-A ANTI-B ARTERIAL PRESSURES
O (–) (–) DESCRIPTION ANSWER
A (+) (–) Highest Arterial Blood Pressure SYSTOLIC PRESSURE
B (–) (+) Lowest Arterial Blood Pressure DIASTOLIC PRESSURE
AB (+) (+) = Systolic Pressure – Diastolic
PULSE PRESSURE
Pressure
= Stroke Volume / Arterial
PULSE PRESSURE
Compliance
Most important determinant of
STROKE VOLUME
Pulse Pressure
= 2/3 (Diastole) + 1/3 (Systole) MEAN ARTERIAL
= Diastole + 1/3 PP PRESSURE
CENTRAL VENOUS
Synonym: Right Atrial Pressure
PRESSURE
Measured using Swan-Ganz PULMONARY
Catheter. Estimates Left Atrial CAPILLARY WEDGE
Pressure. PRESSURE
Which of the following can cause an increase in
pulse pressure?
A. Well-conditioned endurance runner
11. B. Old age
C. Aortic regurgitation
Renal afferent arterioles reflexively responds to D. Aortic sclerosis
stretch by contracting in order to maintain constant E. All of the above
renal blood flow and subsequently, GFR: ______________
A. Tubuloglomerular Feedback / Macula Densa
9. INCREASED (WIDENED) DECREASED (NARROW)
Feedback
PULSE PRESSURE PULSE PRESSURE
B. Myogenic Mechanism
C. Glomerulotubular Balance • Well-conditioned • Heart Failure (decreased
D. All of the above endurance runner pumping)
• Old age • Blood loss (decreased blood
SCENARIO 1: IF BP IS LOW (E.G. 80MMHG) • Aortic regurgitation volume)
• Aortic sclerosis • Aortic stenosis (reduced
• Low BP à Low GC Hydrostatic Pressure à Decreased GFR
• Severe iron deficiency stroke volume)
(<125ml/min) à Detected by Macula Densa
anemia (reduced blood • Cardiac tamponade
viscosity) (decreased filling time)
• Arteriosclerosis (less
compliant artery)
• Hyperthyroidism
(increased systolic pressure
Jesce, 30/F lifts weights 3x a week for

approximately 2 hours each session, for the past 10
years. Which of the following is expected?
SCENARIO 2: IF BP IS HIGH (E.G. 200MMHG) A. Her skeletal muscles will increase in size, but
• High BP à High GC Hydrostatic Pressure à Increased GFR not in number
(>125ml/min) à Detected by Macula Densa 12. B. Venous Return, Cardiac Output and Blood
• Macula Densa increases secretion of: Pressure will all increase during the weight
sessions
C. Jesce is just as strong as any other man in a per
unit area basis
D. All of the above
NOTES ONSET & DURATION EXAMPLE

Phosphagen • Cell ATP, cell phospho-creatine • First 8-10 seconds • 100m dash,
energy system jumping, diving
Glycogen-lactic • Anaerobic; • For 1.3 to 1.6 minutes after phosphagen system
• Tennis, soccer
acid system • reconstitute ATP & phosphocreatine used up
• For unlimited time as long as with energy supply
• Aerobic;
(glycogen, FA, ketones, amino acids) • Long-distance
Aerobic system • reconstitute ATP, phosphocreatine,
• Fats supply 50% energy requirements after 3-4 jogging
• Glycogen-lactic acid cycle
hours) after glycogen-lactic acid system used up
≈ MEN WOMEN MNEMONICS MALE SEX HORMONES
Overall S-S-S
• More • Less
strength FSH, Sertoli Cell, Sperm
Strength per L-L-L
square cm • 3-4 kg/cm2 • 3-4 kg/cm2 LH, Leydig Cell, Libido Hormone (Testosterone)
of x-sec area
World • Long-distance TESTOSTERONE DIHYDROTESTOSTERONE
• Marathon
records swimming • Differentiation of epididymis, • Differentiation of penis,
Effect of • Testosterone → • Estrogen → more vas deferens, & seminal vesicles scrotum, and prostate
hormones more muscle fat • Descent of testes • Male hair pattern
Effect of • ↑ bone and muscle mass (e.g., • Male pattern baldness
• Increases size (girth) of skeletal muscles
Exercise broad shoulders) • Sebaceous gland activity
• ↑ BMR • Growth of prostate
Solutions X and Y are separated by a semi- • Pubertal growth spurt
permeable membrane. Solution X has 20mM of • Epiphyseal closure
Urea, while solution Y has 10 mM of urea. If we • Growth of penis & seminal
triple the concentration of urea in Solution X, what vesicles
will happen to the flux of urea across the • Deepening of voice
13.
membrane? (enlargement of larynx)
A. 2x • Spermatogenesis
B. 3x • Negative feedback on anterior
C. 5x pituitary
D. None of the above • Libido
SPECIAL NOTES: SIMPLE DIFFUSION Ventricular volume are at its highest and lowest
• Measured using the formula: respectively during which phases of the cardiac
𝑱 = 𝑷𝑨 × (𝑪𝟏 − 𝑪𝟐 ) cycle?
J = flux (flow (mmol/sec) A. Isovolumic Contraction, Isovolumic
P = permeability (cm/sec) Relaxation
A = area (cm2) 15.
B. Isovolumic Relaxation, Isovolumic Contraction
C1 = higher concentration 1 (mmol/L) C. Rapid Ventricular Ejection, Reduced
C2 = lower concentration 2 (mmol/L) Ventricular Ejection
D. Rapid Ventricular Filling, Reduced Ventricular
Filling
• P (permeability) in the formula J= PA (C1-C2) is increased by

the following:
o Increased Oil / water partition coefficient of solute
(increases solubility in the lipid of the membrane)
o Decreased Radius of solute Which diuretic acts on the early distal tubule?
o Decreased Membrane Thickness A. Acetazolamide
B. Furosemide
16.
Male pattern baldness is an effect of: _____________. C. Hydrochlorothiazide
A. Testosterone D. Spironolactone
14. B. Dihydrotestosterone E. Mannitol
C. Both A and B
D. Neither A nor B
CLASS SITE OF ACTION EFFECTS MOA

CAI ↑ HCO3- excretion
PCT Inhibition of Carbonic Anhydrase
(e.g. Acetazolamide) Metabolic acidosis
↑ NaCl excretion
↑ K excretion
Inhibition of Na-K-2Cl pump in
Loop Diuretic TAL LH ↑ Ca excretion
TAL LH
↓ ability to concentrate or dilute urine
Metabolic alkalosis
↑ NaCl excretion
↑ K excretion
↓ Ca excretion
Thiazides EDT Inhibition of Na-Cl pump ↓ ability to concentrate or dilute urine
Metabolic alkalosis
HyperGLUC (glycemia, lipidemia,
uricemia, calcemia)
CLASS SITE OF ACTION MOA EFFECTS
↑ Na excretion
Aldosterone antagonism or Na
K-sparing diuretics LDT and CD ↓ K excretion
inhibition
↓ H excretion
Osmotic diuretic (e.g. Entire nephron except Large polysaccharides absorbing
↓ ICP
Mannitol) TAL LH water
Which skeletal muscle type has the greatest number GLOMERULAR FILTRATION RATE
of mitochondria? • GFR = Kf [(PGC-PBS) – (OGC- OBS)]
A. Skeletal o Kf = Filtration coefficient of the Glomerular Capillaries
17.
B. Cardiac o PGC= Glomerular Capillary Hydrostatic Pressure
C. Smooth o PBS = Bowman’s Space Hydrostatic Pressure
D. Type 1 o OGC= Glomerular Capillary Oncotic Pressure (mmHg)
SMOOTH
SKELETAL CARDIAC
MUSCLE
Sarcomeres,
striations, (+) (+) (-)
troponin
3-8% of 35% of 3-5% of
skeletal cardiac smooth
Mitochondria
muscle muscle muscle cell
volume volume volume
• Ca2+ Influx
(SA Node);
• Na+ Influx
Upstroke of
Na+ Influx (atria, Ca2+ Influx
AP
ventricles,
Purkinje Conduction Velocity is most dependent on: __________?
Fibers) A. Myelination
19. B. Nerve Diameter
• No (SA
C. Neurotransmitter
Node)
D. Calcium channels
• Yes (atria,
Plateau No No
ventricles,
PROPAGATION OF ACTION POTENTIAL
Purkinje
Fibers) • Done through local currents to adjacent areas of the membrane
• 150 msec • Conduction velocity is increased by:
(SA Node, o Fiber Size: the larger the nerve fiber, the smaller the internal
Atria) resistance, and the faster the conduction velocity
• 250-300 o Conduction velocity is most dependent on: nerve diameter
AP Duration 1 msec 10 msec PreTest 14th (126)
sec o Myelination: myelin acts as insulator. AP is regenerated in
(ventricles, Nodes of Ranvier (unmyelinated portions of the axon) that
Purkinje contains the highest concentration of Na+ channels per
Fibers) square micrometer of cell membrane Ganong 26th PBEQ 4-2
• AP opens • Conduction Velocity = Distance/Latent Period Ganong 26th PBEQ 4-9
cell
membrane
voltage-
gated Ca2+
Excitation-
Use of SR Ca2+-induced channels;
Contraction
Calcium Ca2+-Release • Hormones
Coupling
& NTs
open IP3-
gated SR
Ca2+
Channels
(+) only for
Gap unitary
(-) (+)
Junctions smooth
muscles
SR Greatest --- Least
Actin-Based Actin-Based Myosin-
Regulation using using Based using
Tropomyosin Tropomyosin MLCK
What is the numerator in the computation for renal

blood flow?
A. Renal Plasma Flow
18.
B. Hematocrit
C. Hemoglobin
D. Kf
The Na-K-ATPase pump is an example of ____________.
A. Secondary Active Transport
20. B. Anabolic reaction
C. Integral protein
D. 2 Na+ out, 3K+ in
© Topnotch medical Board Prep
What is the formula for Ejection Fraction?

A. SV/EDV
22. B. VO2 / AVO
C. (HR x [EDV-ESV]) X TPR

A man lost in the desert would have the following
changes: __________
A. Decreased ECF and ICF volume, Increased
ECF and ICF Osmolarity
B. Increased ECF and ICF volume, Decreased ECF
21.
and ICF Osmolarity
C. Increased ECF and ICF volume, Increased ECF
and ICF Osmolarity
D. Decreased ECF and ICF volume, Decreased ECF
and ICF Osmolarity
From red nucleus to interneurons of lateral spinal

cord. Stimulates flexors, inhibits extensors:
____________.
23. A. Rubrospinal tract
B. Pontine Reticulospinal tract
C. Medullary Reticulospinal Tract
D. Lateral Vestibulospinal Tract
DISTRIBUTION ACTIONS
• Stimulates
• From Red Nucleus
Rubrospinal flexors
to interneurons of
Tract • Inhibits
lateral SC
extensors
• Stimulates both
Pontine flexors and
• From Pons to
Reticulospinal extensors
ventromedial SC
Tract (mainly
extensors)
DISTRIBUTION ACTIONS What will happen if a hypertensive patient was
• From Medullary given NaCl solution?
• Inhibits both A. ECF volume increases, ICF Volume Decreases if
Reticular
Medullary flexors and
Formation to SC solution is hypertonic
Reticulospinal extensors 27.
interneurons in the B. ECF Volume increases, ICF Volume remains
Tract (mainly
intermediate gray the same if solution is isotonic
extensors) C. Blood Pressure increases
area
• From Deiters D. All of the above
Lateral nucleus to • Inhibits Flexors, Muscles of GIT are smooth except?
Vestibulospinal ipsilateral • Stimulates A. Pharynx
Tract motoneurons and extensors 28. B. Upper 1/3 Esophagus
interneurons C. External Anal Sphincter
• From Superior D. All of the above
Tectospinal • Controls neck
Colliculus to
Tract muscles GI SMOOTH MUSCLE CONTRACTIONS
cervical SC
TONIC CONTRACTIONS PHASIC CONTRACTIONS
The following are respiratory responses to high • Constant level of • Periodic contractions
altitude EXCEPT: ________. contraction or tone without followed by relaxation
A. Increases respiratory rate regular periods of • For mixing and propulsion
24. relaxation • Seen in the esophagus,
B. Increased 2,3 BPG
C. Decreased pulmonary vascular resistance • Orad (upper) region of the gastric antrum, small
D. Decreased Alveolar PO2 and Arterial PO2 stomach and in the lower intestines
esophageal, ileocecal and • Due to spike potentials
RESPIRATORY RESPONSES TO HIGH ALTITUDE internal anal sphincters
INCREASES (↑) DECREASES (↓) • Due to subthreshold slow
• Respiratory Rate • Alveolar PO2 waves
• Arterial pH • Arterial PO2
• Hgb Concentration True of capillaries except?
A. Cannot dilate/constrict since they don’t have
• 2,3 BPG
tunica media
• Pulmonary Vascular 29.
B. Contains most of our blood
Resistance (Hypoxic
C. Can be “open” or ”close”
vasoconstriction)
D. Blood flow is slowest
BLOOD VESSELS
INCREASES (↑) DECREASES (↓) NO CHANGE
• Arteries
• Arterioles
exercise due to • Arterial pH • Capillaries
• Respiratory Rate
lactic acidosis) (moderate • Venules
• Venous PCO2
exercise) • Veins
• Pulmonary
Blood Flow
What is antihemophilic factor?
A. Factor VIII
Which of the following is FALSE?
30. B. Factor IX
A. Initial saliva is high in Na
C. Factor X
25. B. Initial saliva is produced by the ductal cells
D. Factor XI
C. Final saliva is rich in K
D. Final saliva is hypotonic
BLOOD COAGULATION
Which of the following characterizes Capacitance?
CLOTTING
I. Equal to volume/pressure SYNONYMS
FACTOR
II. Greater in veins than in arteries
III. Inversely proportional to elastance (stiffness) Factor I • Fibrinogen
26. Choose the best answer: Factor II • Prothrombin
A. I, II and III Factor III • Tissue factor; tissue thromboplastin
B. I and III Factor IV • Calcium
C. II and III Factor V • Proaccelerin; labile factor; Ac-globulin
D. I and II • Serum Prothrombin Conversion
Factor VII Accelerator;
BLOOD PRESSURE AT DIFFERENT POINTS • proconvertin; stable factor
• Antihemophilic Factor
Factor VIII • antihemophilic globulin,
• Plasma thromboplastin component;
Factor IX • Christmas factor;
• antihemophilic Factor B
• Stuart Factor;
Factor X
• Stuart-Prower Factor
• Plasma Thromboplastin antecedent;
Factor XI
• antihemophilic Factor C
Factor XII • Hageman Factor
Factor XIII • Fibrin-stabilizing factor
© Topnotch Medical Board Prep Prekallikrein • Fletcher Factor
• Fitzgerald factor;
HMW Kininogen
• High-molecular-weight kininogen
How do you compute for URINE Anion Gap?
A. UAG = Na+ – HCO3- + Cl-
31. B. UAG = Na+ + K+ – Cl-
C. UAG = Na+ – HCO3- + Cl- + K+
https://cjasn.asnjournals.org/content/13/2/195
What is the mechanism behind cadmium toxicity?

A. Interacts with calcium to cause osteoporosis
B. Disturbs zinc metabolism
32.
C. Decreases plasma copper and ceruloplasmin
D. Interacts with iron causing anemia
E. All of the above
https://www.researchgate.net/figure/Values-of-cadmium-toxicity-Adapted-from-Flora-et-al-2008_fig5_266560390
Did you know?
Itai-itai disease was documented in case of mass Cadmium
poisoning in Toyoma Prefecture, Japan starting around 1912.
Cadmium was released into rivers by mining companies. The Cd
poisoning caused softening of bones and kidney failure. The
mining companies were successfully sued for the damage.
What is the formula for clearance?
A. UV/P
34. B. UP/V
C. RPF/(1-Hct)
D. GFR/RPF
Joy, 30/F, reads a NYT news article about Hidilyn
Diaz. Which muscle in the eye helps her focus in this
activity?
35. A. Radial Muscle
B. Circular muscle
C. Ciliary Muscle
D. All of the above
Uses group Ia afferents, detects dynamic changes:

________.
A. Nuclear Bag Fibers
B. Nuclear Chain Fibers
33.
C. Either Nuclear Bag Fibers or Nuclear Chain
Fibers
D. Neither Nuclear Bag Fibers nor Nuclear Chain
Fibers
TYPES MUSCLE SPINDLE (INTRAFUSAL FIBERS)

NUCLEAR BAG NUCLEAR CHAIN
FIBERS FIBERS
• Detect Dynamic • Detect Static
Function
changes changes
• Group Ia • Group II
Sensory Fiber
Afferents Afferents
Arrangement of • Central “Bag”
• In rows
Nuclei region
https://pmgbiology.com/tag/ciliary-muscle/
Cytokine involved in the chemotaxis of neutrophils,

basophils and T cells?
A. IL-4
36.
B. IL-6
C. IL-8
D. TNF-alpha

• Activation of T cells and • Implicated in the pathogenesis of septic
IL-1 • Macrophages macrophages; promotion of shock, rheumatoid arthritis, and
inflammation atherosclerosis
• Used to induce lymphokine-activated killer
• Type 1 (Th1) helper • Activation of lymphocytes, natural cells; used in the treatment of metastatic
IL-2
T cells killer cells, and macrophages renal cell carcinoma, melanoma, and various
other tumors
• Type 2 (Th2) helper • As a result of its ability to stimulate IgE
T cells, mast cells, • Activation of lymphocytes, monocytes production, plays a part in mast-cell
IL-4
basophils, and and IgE class switching sensitization and thus in allergy and in
eosinophils defense against nematode infections
• Type 2 (Th2) helper • Monoclonal antibody against interleukin-5
IL-5 T cells, mast cells, • Differentiation of eosinophils used to inhibit the antigen-induces late-phase
and eosinophils eosinophilia in animal models of allergy
• Activation of lymphocytes;
• Type 2 (Th2) helper • Overproduces in Castleman disease acts as
differentiation of B cells, stimulation
IL-6 T cells and an autocrine growth factor in myeloma and in
of the production of acute-phase
macrophages mesangial proliferative glomerulonephritis
proteins
• T cells and • Chemotaxis of neutrophils,
IL-8 Accompanied by neutrophilia, making it a
macrophages basophils, and T cells
potentially useful marker of disease activity
• Bone marrow • Stimulation of the production of • Used to reduce chemotherapy-induced
IL-11
stromal cells acute-phase proteins thrombocytopenia
interferon γ by type 1 (Th1) helper T
• Macrophages and B
IL-12 cells and by natural killer cells; • May be useful as an adjuvant for vaccines
cells
cells
• Implicated in many immune/autoimmune
• Promotion of inflammatory cell
IL-17 • T cells diseases such as rheumatoid arthritis,
chemotaxis and inflammation
asthma, and psoriasis
• Macrophages,
• Treatment with antibodies against tumor
Tumor necrosis natural killer cells, T
• Promotion of inflammation necrosis factor-⍺ beneficial in rheumatoid
factor-⍺ cells, B cells, and
arthritis and Chron disease
mast cells
Lymphotoxin • Implicated in the pathogenesis of multiple
(tumor necrosis • Promotion of inflammation sclerosis and insulin-dependent diabetes
T cells and B cells
factor-β) mellitus
• T cells,
Transforming • May be useful therapeutic agent in multiple
macrophages, B • Immunosuppression
growth factor-β sclerosis and myasthenia gravis
• T cells,
chemotherapy for tumors and in ganciclovir-
macrophages, • Promotion of the growth of
GM CSF treated patients with AIDS; used to stimulate
natural killer cells, granulocytes and monocytes
cell production after hematopoietic stem cell
and B cells
transplantation
• Used to treat AIDS-related Kaposi sarcoma,
• Induction of resistance of cells to viral
Interferon-⍺ • Virally infected cells melanoma, chronic Hepatitis B infection, and
infections
chronic Hepatitis C infection
• Induction of resistance of cells to viral • Used to reduce the frequency and severity of
Interferon-β • Virally infected cells
infections relapses in multiple sclerosis
• Activation of macrophages; inhibition • Used enhance the killing of phagocytosed
Interferon-γ T cells and natural
of type 2 (Th2) helper T cells bacteria in chronic granulomatous disease
killer cells
40/F on ventilator with rate of 20, TV=500mL, Adequate intake of potassium every day for adult
FIO2=1.0. ABG later shows PaO2 = 360mmHg, male:
PCO2=36mmHg, pH of 7.3. Barometric Pressure = A. 2,600mg
38.
760mmHg, Respiratory exchange ratio = 0.8. What B. 2,800mg
37. is the patient’s alveolar oxygen tension? C. 2,900mg
A. 665 D. 3,400mg
B. 668
C. 720
Increasing Ventricular Pressure, Ventricular

Pressure < Aortic Pressure: _________.
A. Isovolumic Relaxation
39.
B. Isovolumic Contraction
C. Rapid Ventricular Filling
D. Rapid Ventricular Ejection
What kind of contraction happens in the small
PAO2 = (1 x (760-47)) – (36/0.8) intestines during fasting?
A. Segmental Contraction
= 713 -45 40.
B. Peristaltic Contraction
= 668mmHg
C. Slow wave Contraction
D. Skeletal muscle contraction
• Pulmonary Vascular Resistance (PVR) Equation
SMALL INTESTINAL MOTILITY

• Segmentation Contraction
o Back-and-forth movement with no net forward motion
SHUNT FRACTION o Mixes chyme with pancreatic enzymes
(RATIO OF SHUNTED TO TOTAL PULMONARY BLOOD FLOW) • Peristaltic Contraction
o Propels chyme towards large intestines
§ rhythmic phasic contraction propels chyme in a unilateral
direction
o (+) contraction behind bolus and (+) relaxation in front of
bolus

OXYGEN CONSUMPTION VO2
(CAN BE COMPUTED USING FICK EQUATION; SEE)
𝑽𝑶𝟐 = 𝑪𝑶 × (𝑪𝒂𝑶𝟐 − 𝑪𝒗𝑶𝟐 )
Corrective lens for hyperopia: _________.
A. Biconcave lenses
43. B. Cylindrical lenses
C. Convex lenses
D. Bifocal lenses
What urine test to do for ovulation?
A. FSH
B. LH
44.
C. Estrogen
D. Progesterone
E. B-HCG
Sperm becomes motile in the ________.
A. Seminiferous tubules
B. Epididymis
45.
C. Vas Deferens
D. Seminal Vesicle
E. Prostate Gland
PHYSIOLOGIC ANATOMY OF MALE SEX ORGANS

STRUCTURE FUNCTION
• Sperm production
Seminiferous • Full development and function of
Tubules seminiferous tubules require
androgens and FSH Ganong 25 23-1 th
Epididymis • Sperm maturation, motility

Vas Deferens • Sperm storage
• Sperm nutrition (contains fructose,
Seminal Vesicle
prostaglandins)
• For semen alkalinity (using
spermine); contains 5-alpha
https://veteriankey.com/motility-patterns-of-the-gastrointestinal-tract/
Prostate Gland
• Phases of MMC reductase that converts
o Phase I: No spike potentials, no contractions testosterone to DHT
o Phase II: Irregular spike potentials and contractions Ejaculatory Duct -
o Phase III: Regular spike potentials and contractions Urethra -
• The MMCs are initiated by motilin Urethral Glands,
Bulbourethral • Supplies mucus for lubrication
What delays movement of food? Glands
A. Chyme
41. B. Lipase Secretin actions include:
C. Secretin I. Inhibits HCl secretion
D. HCl in the duodenum II. Increases biliary and pancreatic bicarbonate
III. Increases pancreatic enzyme secretion
INCREASES GASTRIC DECREASES GASTRIC 46. Choose the best answer:
EMPTYING EMPTYING A. I, II, III
Increased GASTRIC volume Increased DUODENAL B. I and II
volume C. II and III
Isotonic content Hypertonic & Hypotonic D. I and III
content Which band is associated with myosin?
Chyme Formation Fat in the duodenum I. A Band
HCl in the duodenum (acids) II. I Band
III. H Band
What is the contractile units of myocardial cells? 47. Choose the best answer:
A. Myosin A. I, II, III
42. B. Sarcomere B. I and III
C. Sarcoplasm C. II and III
D. Myocytes D. I and II
How long does the sperm live in the female

reproductive tract?
A. 1-5 days
48.
B. 3-7 days
C. 5-9 days
D. 7-12 days
Function of IgD?
A. Enhance mucosal homeostasis and immune
surveillance
49. B. Prevents attachment of bacteria and viruses to
mucous membranes
C. Neutralized bacterial toxins and viruses
D. Complement activation
HEAVY
TYPE FUNCTION STRUCTURE NOTES
CHAIN
• Most abundant type in serum (IgG > IgA > IgM >
• Fixed complement IgD > IgE)
• Opsonizes bacteria γ1, γ2, γ3, • Smallest, responsible for secondary immune
IgG • Monomer
• Neutralized bacterial toxins γ4 response
and viruses • Only isotype capable of crossing the placenta (IgG
Greets the Growing fetus)
• Most produced antibody overall (in mucous
• Localized protection in membranes) but has lower serum concentrations
human body secretions • Protects mucosa via “immune exclusion” (binds to
(milk, saliva, tears, • Monomer (in pathogen and prevents it from making contact with
respiratory, intestinal, circulation) epithelial cells or mucus membranes)
IgA α1, α2
genital tract • Dimer (w/ J chain • At least in the gut, unusually cross-reactive (coping
• Prevents attachment of when secreted) with antigenic drift)
bacteria and viruses to • Does not efficiently activate/fix complement
mucous membranes proteins (which prevents initiating inflammation
that can be damaging)
• Monomer (on B cells)
• Largest; responsible in primary immune response
IgM • Complement activation μ • Pentamer (w/ J chain
• Found on the surface of naïve B cells
when secreted)
• Binds mast cells, basophils
→ cross-links when exposed
to allergen → mediates type
IgE I hypersensitivity (via ε • Monomer • Associated with allergies
histamine release)
• Activates eosinophils →
immunity to parasites
IgD • Has unclear function δ • Monomer • Found on the surface of naïve B cells
END PHYSIOLOGY PHASE 2
What is hexamethonium?
A. NMJ blocker
50. B. Non-selective beta agonist
C. Non-depolarizing ganglionic blocker
D. Depolarizing ganglionic blocker
TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY PHASE 3 DIGITAL HANDOUT BY ENRICO PAOLO BANZUELA, MD
Important Legal Information

The handouts, videos and other review materials, provided by Topnotch Medical Board
PHYSIOLOGY – PHASE 3
Preparation Incorporated are duly protected by RA 8293 otherwise known as the by Enrico Paolo C. Banzuela, MD
Intellectual Property Code of the Philippines, and shall only be for the sole use of the person:
a) whose name appear on the handout or review material, b) person subscribed to Topnotch
Medical Board Preparation Incorporated Program or c) is the recipient of this electronic
communication. No part of the handout, video or other review material may be reproduced, MODULE 1: CELL PHYSIOLOGY
shared, sold and distributed through any printed form, audio or video recording, electronic
medium or machine-readable form, in whole or in part without the written consent of Characterizes the Cell Membrane:
Topnotch Medical Board Preparation Incorporated. Any violation and or infringement, A. Mainly made up of proteins
whether intended or otherwise shall be subject to legal action and prosecution to the full
B. Guardian of the Genome
C. Integral proteins are loosely attached
D. Hydrophilic heads are directed inward, hydrophobic
DISCLOSURE tails are directed outward
The handouts/review materials must be treated with utmost confidentiality. It shall be the
responsibility of the person, whose name appears therein, that the handouts/review
materials are not photocopied or in any way reproduced, shared or lent to any person or TRUE OR FALSE
disposed in any manner. Any handout/review material found in the possession of another
person whose name does not appear therein shall be prima facie evidence of violation of RA • Aquaporins are used in osmosis:
8293. Topnotch review materials are updated every six (6) months based on the current ___________________________
trends and feedback. Please buy all recommended review books and other materials listed
below. • Lipid-Soluble substances use Simple Diffusion
THIS HANDOUT IS NOT FOR SALE! ___________________________
• Hydrophilic substances use carrier-mediated transport
REMINDERS ___________________________
1. Phase 3 serves as the final coaching. It is expected that you have finished • ECF: major cation: Na+. major anions: Cl- and HCO3-
at least the Phase 1 videos prior to watching the Phase 3 videos ___________________________
2. The guided content of the video lectures are seen within the handout. • ICF: major cation: K+. major anions: proteins, ATP, ADP
Answers to questions / blanks will be seen in the Phase 3 video. ___________________________
This handout is only valid for the September 2021 PLE batch. MATCHING TYPE
This will be rendered obsolete for the next batch 1. For tight intercellular adhesion A. Gap Junctions
since we update our handouts regularly. between epithelial cells B. Zonula Adherens
2. Equivalent in cardiomyocytes is C. Macula Adherens
fascia adherens D. Zonula Occludens
3. Has two types: leaky (e.g., PCT) (Tight Junctions)
and tight (e.g., BBB)
4. Functional unit is the Connexon
(subunit: connexin)
INTERCELLULLAR STRUCTURES BETWEEN CELL MEMBRANES
TYPE DESCRIPTION LOCATION NOTES
Macula Adherens • Disk-shaped;
• Epithelium • Like intercellular stapler wires
(Desmosomes) • For tight intercellular adhesion
• Epithelial &
• Equivalent in cardiomyocytes is Fascia
• Ring-shaped endothelial cells
Zonula Adherens Adherens (ribbon-like patterns; doesn’t
• increases surface area for contact • Intercalated disks of
completely enclose cell)
cardiac muscles
• Barrier to movement of proteins • Leaky: PCT, Jejunum • Transcellular Transport: movement across
Zonula Occludens
across membranes; divides cell into • Tight: CD, terminal apical and basolateral sides
(Tight Junctions)
apical and basolateral side Colon, BBB • Paracellular Transport: movement through TJ
• bridge for sharing of small
• Cardiac and unitary • Functional Unit: ConneXON (its Subunit:
Gap Junctions molecules between cells; For rapid
smooth muscles ConneXIN)
intercellular communication
CELL MEMBRANE TRANSPORTERS CHARACTERISTICS OF CARRIER-MEDIATED TRANSPORT

A. Simple Diffusion C. Primary Active Transport DESCRIPTION ANSWER
B. Facilitated Diffusion D. Secondary Active Transport • Due to finite number of carriers, a
transport maximum maybe
1. Passive, Downhill, Non-Carrier-Mediated reached
2. Passive, Downhill, Carrier-Mediated • Two substances may have the
3. Active, Uphill, Carrier-Mediated, Uses ATP same chemical composition, but
4. Active, Uphill, Carrier-Mediated, uses Na+ Gradient different “shape”. (e.g., D-glucose
5. Gases, Alcohol, Steroid Hormones vs. L-Glucose)
6. Na+-K+-ATPase Pump, Proton Pump • different solutes may compete for
7. SGLT-1, SGLT-2, Na+-K+-2Cl- same carrier (e.g. Gal vs. Glu in
8. GLUT-1,2,3,4,5 the SGLT-1 of SI)
SPECIAL NOTES
DESCRIPTION ANSWER
• Co-transport and Countertransport
as seen in which form of active
transport?
The formula for simple diffusion has permeability as a factor. • Which substance has an osmolarity
State if the following will increase permeability (True or False) of zero?
• Higher effective osmotic pressure:
• Decreased oil/water partition coefficient of solute hypertonic or hyperosmotic?
________________________
• Increased radius of solute
________________________
• Increased membrane thickness
________________________
TOPNOTCH MEDICAL BOARD PREP PHYSIO PHASE 3 DIGITAL HANDOUT BY ENRICO PAOLO C. BANZUELA, MD Page 1 of 27
Osmotic Pressure vs. Effective Osmotic Pressure
Solutions A and B are separated by a semi-permeable
membrane. Solution A contains 1 mM sucrose and 1 mM urea.
Solution B contains 1 mM sucrose. The reflection coefficient for
sucrose is one and the reflection coefficient for urea is zero.
Which of the following statements about these solutions is
correct?
(A) Solution A has a higher effective osmotic pressure than
solution B
(B) Solution A has a lower effective osmotic pressure than
solution B
(C) Solutions A and B are isosmotic
(D) Solution A is hyperosmotic with respect to solution B,
and the solutions are isotonic
(E) Solution A is hypoosmotic with respect to solution B, and
the solutions are isotonic
TRUE OR FALSE
• All cells have RMP. Only muscles and Neurons have AP
________________________
• Characteristics of AP: stereotypical size and shape,
propagation, all-or-none response if less than threshold
_______________________
• Opening of the m gate causes nerve AP, closure of h gate and
opening of K+ gates caused repolarization
_______________________
SPECIAL NOTES: ACTION POTENTIAL
TERM DESCRIPTION
Depolarization • Make the MP more positive
Hyperpolarization • Make the MP more negative
• Positive charges flow into the cell
Inward Current
causing depolarization
• Positive charges flow out of the cell
Outward Current
causing hyperpolarization
• MP where AP is inevitable
o net inward current > net outward
Threshold current
o Na+ inward current > K+ outward
current from K leak channels
Overshoot • Occurs during an AP when MP > 0mV
Undershoot (After-
• Occurs during an AP when MP < RMP
hyperpolarization)
• Occurs during an AP when no new
Absolute
AP can be elicited no matter how
Refractory Period MATCHING TYPE
large the stimulus
(ARP) 1. Decreased Levels in Huntington A. Glycine
• Basis: closed Na+-inactivation gates
dementia and Alzheimer dementia; B. Glutamate
• Occurs during an AP after ARP when
triggers REM sleep C. Nitric Oxide
a new AP can be elicited by required
2. Has greater β2 effect than NE; D. Nitrous oxide
Relative Refractory greater than usual Na+ inward
produced mainly by adrenal medulla E. Acetylcholine
Period (RRP) current
3. Receptor subtypes Ionotropic F. Epinephrine
• Basis: prolonged opening of K+
(ligand-gated) including NMDA G. Serotonin
channels
receptors; 1 subtype metabotropic H. Dopamine
• Occurs when cell membrane is 4. Permeant gas, inhibitory NT,
depolarized but not rapidly enough, vasodilator
Accommodation thus causing Na+-inactivation gates to
5. low levels are associated with
eventually close → no AP
depression
• e.g. Hyperkalemia 6. Decreased in Parkinson Disease,
Increased D2 in schizophrenia
THE NEURON (Schizophrenia: can be due to
abnormalities in the prefrontal lobes,
frontal lobes and limbic system
(hippocampus)
TYPES OF MUSCLES
• Skeletal Muscles
o Intrafusal: detects changes in Muscle Length (innervation:
gamma-motorneurons)
o Extrafusal: for voluntary muscle contraction (innervation:
alpha-motorneurons)
§ Type I/Slow-Twitch Muscle Fiber/Red Muscle
Fiber/Oxidative Muscle Fiber: provides Endurance
- Smaller diameter, less fatigability, decreased force of
contraction, decreased speed of reaction but GREATER
OXIDATIVE CAPACITY
§ Type 2/Fast-Twitch Muscle Fiber/White Muscle Fiber:
provides Power
- further divided into Type IIa and Type IIb/x
• Cardiac Muscles 12. Myosin binds to Second Binding Site in actin.
o Atrial muscle: (+) gap junctions, (+) syncytium 13. ADP bound to myosin undergoes complete hydrolysis. This
o Ventricular muscle: (+) gap junctions, (+) syncytium causes the “power / force-generating stroke” to occur.
o Pacemakers (e.g., SA Node): (+) autorhythmiticity Myosin heads pull actin towards the M line or the (-) pole. A
• Smooth Muscle cross-bridge cycle happens. This shortens the sarcomere by
o Unitary smooth muscle: (+) gap junctions, (+) syncytium, for 10Nm.
gross motor movements 14. Do this again and again to have significant muscle contraction.
o Multi-unit smooth muscle: (-) gap junctions, for fine motor
movements STEPS IN MUSCLE RELAXATION
1. Remove the Ca2+ from Troponin C.
MATCHING TYPE 2. Tropomyosin the goes back to its original location, covering
1. Ach binds to _______ in the A. NN receptor the binding site of actin for myosin.
Motor End Plate B. NM Receptor / Ligand - 3. Place the Ca2+ back to the SR using SERCA.
2. Activated at the T-Tubules gated Ion Channel 4. Use Acetylcholinesterase to degrade ACh to Acetate and
3. Calcium Channels in the C. DHPR Choline. Choline may undergo reuptake.
SR activated by DHPR D. Ryanodine Receptors
4. Binds to Trop C E. Calcium STEPS IN SMOOTH MUSCLE CONTRACTION & RELAXATION
5. Happens when Ca2+ binds F. Displaced Tropomyosin 1. Hormones, NTs, stretch triggers increased ICF Ca2+
with Trop C → exposure of binding sites 2. ICF Ca2+ binds with Calmodulin
6. Happens when ATP binds in actin 3. Calcium-Calmodulin Complex activates MLCK
4. MLCK phosphorylates (and activates) Myosin Heads
with Myosin G. Myosin detaches from
5. Activated Myosin Heads: causes smooth muscle contraction
7. Partial ATP Hydrolysis Actin
6. MLCP dephosphorylates (and inactivates) Myosin Heads
8. Complete ATP Hydrolysis H. Recocking of Myosin
7. Inactivated Myosin Heads: causes smooth muscle relaxation
Heads
I. Powerstroke
DESCRIPTION ANSWER
Blocks release of Ach from pre-synaptic
MUSCLE CONTRACTION AND RELAXATION BOTULINUS TOXIN
terminals
STEPS IN MUSCLE CONTRACTION Competes with Ach for receptors on
CURARE
1. Action Potential starts at the initial segment of the motor Motor End Plate
neuron, spreads through the axon, neural fibril and then the Inhibits Acetylcholinesterase NEOSTIGMINE
terminal boutons. Blocks reuptake of Choline into
2. At the terminal boutons, voltage-gated Ca2+ channels are HEMICHOLINIUM
presynaptic Terminal
activated. Vesicles containing Ach fuses with the nerve
membrane and release Ach in the NMJ.
3. Ach binds with the Ach Receptors (NM Receptors) at the
Muscle End Plate (MEP). This NM Receptors are ligand-gated
ion channels. Once they’re activated, they will open Na+ and K+
channels.
4. The open Na+ channels causes Na+ influx and produces a
Miniature End Plate Potential (MEPP). MEPP summate to
produce EPP. This depolarizes the sarcolemma.
5. Depolarization spreads from sarcolemma to T-Tubules. At the
T-Tubules, DHPR is activated.
6. Once DHPR is activated, Ryanodine Receptors in the SR are
also activated.
7. Ryanodine Receptors then release Ca2+ from the SR to the ICF.
Ca2+ binds with Troponin C.
8. Binding of Trop C with Ca2+ displaces Tropomyosin. This
tropomyosin displacement causes exposure of binding sites in
actin for myosin.
9. Myosin heads binds to First Binding Site in Actin.
10. ATP binds to myosin head. This causes myosin to unbind with
the First Binding Site in actin.
11. ATP bound to myosin head undergoes partial hydrolysis,
producing ADP. This causes “recocking” of the myosin heads.
Myosin moves such that it now points to the Second Binding
Site in Actin and it moves closer to the (+) pole.
SKELETAL CARDIAC SMOOTH MUSCLE

Sarcomeres,
(+) (+) (-)
striations, troponin
Ca2+ Influx (SA Node); Na+ Influx
Upstroke of AP Na+ Influx Ca2+ Influx
(atria, ventricles, Purkinje Fibers)
No (SA Node)
Plateau No No
Yes (atria, ventricles, Purkinje Fibers)
150 msec (SA Node, Atria)
AP Duration 1 msec 250-300 sec (ventricles, Purkinje 10 msec
Fibers)
Ca2+-induced Ca2+-Release; AP opens
Excitation-
cell membrane voltage-gated Ca2+
Contraction Use of SR Calcium Ca2+-induced Ca2+-Release
channels; Hormones and NTs open
Coupling
IP3-gated SR Ca2+ Channels
Gap Junctions (-) (+) (+) only for unitary smooth muscles
SR Greatest Least
Actin-Based using
Regulation Actin-Based using Tropomyosin Myosin-Based using MLCK
Tropomyosin
MODULE 2: NEUROPHYSIOLOGY • MOA of Alpha-2 receptors involves Gi protein and decreased

cAMP
TRUE OR FALSE
__________________
• Cell body of sympathetic preganglionic neuron is in the T-L
• 3 areas have little parasympathetic innervation: cardiac
segment of the spinal cord; while cell body of sympathetic atrium, pregnant uterus, blood vessels
postganglionic neuron is in the paravertebral or prevertebral
__________________
ganglia
__________________
PARASYMPATHETIC VS. SYMPATHETIC
SYMPATHETIC NS PARASYMPATHETIC NS
Responses • Fight-or-flight (capable of mass discharge) • Rest-or-digest (not capable of mass discharge)
Distribution • Thoraco-Lumbar • Cranio-Sacral
Pre-Ganglioninc Tract • Short • Long
Post-Ganglionic Tract • Long • Short
Pre-Ganglionic to Post • Ach using NN/N1 receptors (nicotinic,
• Ach using NN/N1 receptors (nicotinic, cholinergic)
Ganglionic Communication cholinergic)
Post-Ganglionic to Target • Ach using Muscarinic Receptors (M1-M5)
• NE using Adrenergic Receptors (𝛼1-𝛽3)
Organ Communication (muscarinic, cholinergic)
• Sweat Glands and Piloerector Muscles
• No/Little Para Innervation: Blood vessels,
Special Notes (controversial, maybe 𝛼1): Final NT is Ach, Final
cardiac ventricles, pregnant uterus
Receptor is Muscarinic
ANS RECEPTORS: ADRENORECEPTORS (SYMPA)

ADRENO-
MOA EFFECT
RECEPTOR
• Gq
Alpha-1
protein • Causes smooth muscle
Receptors SPECIAL NOTES
•↑ contraction
(𝛂1)
IP3/Ca2+
• Seen in sympathetic DESCRIPTION ANSWER
postganglionic presynaptic
nerve terminals. Also seen in • Type of Sensory Receptor that
Alpha-2 • Gi platelet, fat cells, walls of the GIT detects onset and offset of
stimulus
Receptors protein • Inhibits release of NE for
(𝛂2) • ↓ cAMP presynaptic nerve terminals → • Type of Receptive Field with
inhibits sympathetic effects, smaller area, and well-defined
promotes parasympathetic borders used by Meissner and
effects Merkel (the “Germans”)
Beta-1 • Gs • Seen in the heart (SA Node, AV • Type of nerve Fiber used by
Receptors protein Node, ventricles) and kidneys Preganglionic autonomic fibers
(𝛃1) • ↑ cAMP • Causes excitation
Beta-2 • Gs NERVE FIBERS
• Causes smooth muscle
Receptors protein • Type A (alpha, beta, gamma, delta)
relaxation
(𝛃2) • ↑ cAMP o Thickest, most myelinated, fastest conduction velocity, has
temporal and spatial fidelity
ANS RECEPTORS: CHOLINORECEPTORS (BOTH SYMPA & o Proprioceptors will use Type A-Alpha
PARA) o Fast pain will use Type A-Delta
RECEPTOR LOCATION MOA • Type B
Nicotinic Receptors o Think preganglionic nerve fiber
• binds with ACh • Type C
NM (N1) • Skeletal Muscle MEP • opens Na+-K+ o Slowest, least myelinated, slowest conduction velocity, least
Channel precise and accurate
• Autonomic Ganglia o Think Slow pain, temperature, tickle, itch, smell,
• binds with Ach
(dendrites of postganglionic autonomic fibers
NN (N2) • opens Na+-K+
Postganglionic
Channel
Neurons) Characterizes Pain receptors:
Muscarinic Receptors A. Referred pain is secondary to sharing of 3rd order
• binds with Ach, neurons in the spinal cord of visceral pain fibers and
M1 • CNS skin pain fibers
• Gq, ↑ IP3/Ca2+
• binds with Ach B. Slowly-adapting/non-adapting
M2 • Heart C. Endogenous analgesia system includes serotonin,
• Gi, ↓ cAMP
• Glands • binds with Ach epinephrine, NE, Ach as neurotransmitters
M3 D. Extremes in temperature cannot trigger pain
• smooth muscles • Gq, ↑ IP3/Ca2+
receptors
DORSAL COLUMNS VS ANTEROLATERAL COLUMNS
TACTILE RECEPTORS
MEISSNER CORPUSCLE MERKEL DISC PACINIAN CORPUSCLE RUFFINI CORPUSCLE

Adaptation • Fast-Adapting • Slowly-Adapting • Fast-Adapting • Slowly-Adapting
Receptive
• Type 1 • Type 1 • Type 2 • Type 2
Field
• Glabrous Skin (lips, • Expanded tip tactile • Subcutaneous skin and • Deep skin, internal tissues,
Location
fingertips) receptor deep fascia joint capsules
• Low-frequency • Texture;
vibration; • continuous/ sustained • High-frequency vibration; • Sustained pressure;
Function
• Movement of objects; touch; • tapping/deep pressure • degree of joint rotation
• 2PD • 2PD
Important • Form Iggo Dome
- • Onion-shaped -
Notes Receptors
RETINA REFRACTIVE ERRORS
• Prevents light from scattering (the dark room of the eyes); • Light rays converge in FRONT of the eyeball; biconcave lenses to
converts 11-cis retinal to all-trans retinal; associated with correct: Myopia (nearsightedness)
albinism, macular degeneration, retinal detachment: Pigment • Light rays converge BEHIND the eyeball; convex lens to correct:
Epithelial Cells Hyperopia (Farsightedness)
• Interneuron, detects contrast: Bipolar Cells • Irregularly curved cornea; cylindrical lens to correct:
• Maintains internal geometry of the Eyes: Mueller Cells Astigmatism
• Axons form the Optic Nerve: Ganglion Cells • Age-related loss of accommodation due to stiffening lens; convex
lens to correct: Presbyopia
HEARING
• Outer Ear (Pinna, Auditory Canal): for sound collection and
localization
• Middle Ear (Malleus, Incus, Stapes): for impedance matching
and attenuation reflex
• Inner Ear (Cochlea): contains inner and outer hair cells for
hearing (Place Theory of Hearing)
o Base (near round window): 20,000Hz, Apex (near
helicotrema): 20Hz
o Endolymph: Scala Media, Perilymph: Scala Vestibuli and
Scala Tympani
o Basilar Membrane: Frequency Analyzer
• Semicircular Canals: Angular Acceleration (head rotation)
• Utricle: Horizontal Acceleration (heat tilt)
• Saccule: Vertical Acceleration (heat tilt)
Lifted from When-What-Now. http://what-when-how.com/neuroscience/visual-system-sensory-system-part-5/
.HEARING
• Outer Ear (Pinna, Auditory Canal): for sound collection and
localization
• Middle Ear (Malleus, Incus, Stapes): for impedance matching
and attenuation reflex
• Inner Ear (Cochlea): contains inner and outer hair cells for
hearing (Place Theory of Hearing)
o Base (near round window): 20,000Hz, Apex (near
helicotrema): 20Hz
o Endolymph: Scala Media, Perilymph: Scala Vestibuli and
Scala Tympani
o Basilar Membrane: Frequency Analyzer
• Semicircular Canals: Angular Acceleration (head rotation)
• Utricle: Horizontal Acceleration (heat tilt)
• Saccule: Vertical Acceleration (heat tilt)
TASTE RECEPTORS
REFLEX ARCS
# OF AFFERENT
REFLEX STIMULUS RESPONSE
SYNAPSES FIBERS
Stretch Reflex
Monosynaptic Muscle is stretched Ia Contraction of the muscle
(Knee-Jerk)
Golgi-Tendon Reflex
Disynaptic Muscle contracts Ib Relaxation of the muscle
(Clasp Knife)
Flexor-Withdrawal Reflex
(after touching a hot Polysynaptic Pain II, III, IV Ipsilateral flexion; contralateral extension
stove)
MUSCLE SENSORS DESCRIPTION ANSWER
MUSCLE • Brain wave seen in those who awake with
NERVE FIBER FUNCTION
SENSOR eyes closed (”relaxed”)
• Static and dynamic • Type of Sleep associated with active
• Group Ia and II
changes in muscle dreaming, penile erection, rapid eye
Muscle afferents (in
length (Mnemonic: movements and Beta waves
Spindle parallel with
“SpindLLLLLLe, • Structure used for Interhemispheric
extrafusal fibers)
Length”) communication
• Group Ib
Golgi • Muscle Tension • Promotes memory formation when reward
afferents (in
Tendon (Mnemonic: “Tendon: and punishment centers are stimulated
series with
Organs Tension”)
extrafusal fibers) • Osmolarity between CSF and Plasma
• Group II • Main Heat Loss (anterior hypothalamus)
Pacinian afferents and Heat Gain Mechanisms (post
• Vibration
Corpuscles (distributed hypothalamus) respectively
throughout)
Free Nerve
• Group III and IV • Noxious Stimuli MODULE 3: CARDIAC PHYSIOLOGY
Endings
Cardiac Output has which characteristic?
A. CO Left heart = CO Right heart
MEISSNER VS AUERBACH PLEXUS B. CO at rest is 5L/min, 20-30L/min during exercise
C. Equal to venous return
D. Equal to HR x SV
E. All of the above
VESSELS
• “Stressed volume”, less compliant/distensible than veins;
Arteries
• “Control conduits”, site of greatest resistance: Arterioles
o Vasoconstriction (via Alpha-1) : ↓ Blood Flow, ↑ TPR and BP
o Vasodilation (via Beta-2): ↑ Blood Flow, ↓ TPR and BP
• Largest cross-sectional area, slowest blood flow velocity, does
not dilate/constrict: Capillaries
THE BRAIN
• Higher compliance/distensibility than arteries, one-way valves
MATCHING TYPE prevent backflow: Veins
1. Hearing and Balance A. Frontal Lobe
2. Vision B. Occipital Lobe
3. Judgement, Calculation, Personality C. Parietal Lobe BASIC CV TERMS
4. Motor D. Temporal Lobe DESCRIPTION TERM
5. Somatosensory E. Hypothalamus • Force exerted by the blood
6. Sex, Thirst, Appetite, body Clock, F. Midbrain against the blood vessel wall
Temperature G. Pons • Amount of blood pumped by the
7. Coughing, Vomiting, Swallowing, H. Medulla heart per unit of time
Respiratory, and Vasomotor I. Limbic System • Amount of blood pumped per
8. Apneustic, Pneumotaxic Center heart beat
9. Micturition Center • Pressure at the level of arteries
10. Behavior, Emotions, Motivation and arterioles that opposes
11. Catching a Fly blood coming out of the heart;
decreased during moderate
HYPOTHALAMUS AND OTHER AREAS exercise
MATCHING TYPE • Formula for Ejection Fraction
1. Synthesizes Vasopressin A. Paraventricular Nuclei • Ohm Law
2. Synthesizes Oxytocin B. Supraoptic Nuclei • Amount of blood in the ventricle
3. Responsible for Appetite C. Ventromedial Nuclei immediately before systole
4. Responsible for Satiety D. Lateral Nuclei • Amount of blood in the ventricle
5. Dissipation of Heat E. Anterior nuclei immediately before diastole
6. Conservation of Heat F. Posterior nuclei • LVEDV
7. Reward Center G. Medial Forebrain Bundle • Aortic pressure
8. Punishment Center H. Central Gray Area near • Systole – Diastole (Alternative:
9. Social inhibition Aqueduct of Sylvius Stroke Volume / Arterial
I. Amygdala Compliance
SLEEP INCREASED (WIDENED) DECREASED (NARROW)

• Young Adults: 25% REM Sleep PULSE PRESSURE PULSE PRESSURE
• Newborns: 50% REM Sleep • Well-conditioned
• Decreases duration of REM sleep endurance runner
o Age, Alcohol, Benzodiazepines, Amphetamine • Old age
• Heart Failure (decreased
• From NREM to Awake state: Ganong 25 14-2 • Aortic regurgitation
th
pumping)
o Increase in: Norepinephrine, Serotonin, Histamine • Aortic sclerosis
• Blood loss (decreased
o Decrease in: Acetylcholine, GABA • Severe iron deficiency
blood volume)
• Narcolepsy characteristics Ganong 25 14-6 anemia (reduced blood
• Aortic stenosis (reduced
th
o Starts with REM rather than NREM sleep viscosity)

stroke volume)
o Associated with Class II antigen of MHC on Chromosome 6 • Arteriosclerosis (less
• Cardiac tamponade
o Fewer hypocretin (orexin)-producing neurons compliant artery)
(decreased filling time)
o Fewer hypocretin (orexin)-producing neurons PreTest 14th (103) • Hyperthyroidism
(increased systolic
pressure
DESCRIPTION TERM SPECIAL NOTES ON THE ECG
• Synonym: Right Atrial ECG CHANGES ANSWER
Pressure (Normal: 0-4mmHg) • Stimulates AV Node → ↑ Conduction Velocity SYMPATHETIC
→ ↓ PR Interval NS
• 2/3 Diastole + 1/3 Systole
• Can decrease AV Node Conduction → ↓
(Alternative: Diastolic
Conduction Velocity → ↑ PR Interval
Pressure + 1/3 Pulse • 1st degree AV Block: all atrial impulses reach
Pressure) the ventricles, but PR interval is long
• Used to estimate L Arterial • 2nd degree AV Block: no all impulses
pressure conducted to ventricles, ventricular rate <
• Changes in HR atrial rate. P Wave NOT always followed by
QRS
• Changes in Cardiac
o Mobitz Type I: (+) Wenckebach
Contractility phenomenon (gradual exhaustion of
• Changes in Conduction HEART BLOCK
impulse conduction: ECG shows gradual
Velocity increase of PR interval before a block
• Changes in Rate of Relaxation occurs)
• Predominant contributor of o Mobitz Type II: sporadically occurring
blocks, (-) Wenckebach phenomenon.
Diastolic BP Constant PR intervals before block occurs
o 3rd degree (Complete) AV Block:
ECG Atrioventricular dissociation may cause
fainting, syncope, worsening exercise
• P wave: Atrial Depolarization intolerance from cerebral ischemia
• QRS Complex: Ventricular Depolarization • Flat/inverted T waves
• T Wave: Ventricular Repolarization • prominent U waves (increased susceptibility
• PR Interval: atrial depol to conduction through AV Node to Torsades de Pointes) HYPOKALEMIA
• QT Interval: Period of Vent Depolarization + Repolarization • ↑ amplitude and width of P waves
• PR Segment: AV Node Conduction • ST depression, QT Prolongation
• ST Segment: isoelectric; correlates with plateau of Vent AP • Low P waves, Tall T waves HYPERKALEMIA
• Height of T wave → directly proportional with plasma K+ • Prolonged QT Interval: associated with long
• Duration of QT Interval → inversely proportional with plasma QT syndrome (can cause sudden fainting
Ca2+ and sudden death), torsades de pointes (can HYPOCALCEMIA
cause ventricular arrhythmias/ ventricular
• U wave: hypokalemia
fibrillation)
• Shortened QT Interval HYPERCALCEMIA
CARDIAC CYCLE
EVENTS
•
Preceded by P-wave
Atrial •
a wave seen
Contraction •
S4 is heard
•
Vent P and Vent V increase slightly
•
Preceded by QRS complex
•
c wave seen
•
S1 heard due to closure of AV valves
Isovolumic
•
Vent P is increasing but Vent Volume
Contraction
remains the same
• highest ventricular volume (EDV)
• SL valves open at the end of this phase
• At the start, Ventricular Pressure > Aortic
Rapid
Pressure causing SL valves to open
Ventricular
• Highest ventricular pressure and aortic
Ejection
pressure seen at the end of this phase
Reduced Ventricular Ejection
• Preceded by T wave
• v wave seen
• S2 heard due to closure of SL valves
• Vent P is decreasing but Vent Volume
Isovolumic
remains the same
Relaxation
• incisura/dicrotic notch seen in the aortic
pressure curve
• lowest ventricular volume (EDV)
• AV valves open at the end of this phase
Rapid
• At the start, Atrial P > Ventricular Pressure
Ventricular
causing AV valves to open, S3 is heard
Filling
Reduced
Ventricular • Longest phase of the cardiac cycle
Filling
mm/mV 1 square = 0.04 sec/0.1mV
Contributed by Michael Like Magussad, MD
Which pacemaker has the is responsible for overdrive

suppression?
A. SA Node
B. AV Node
C. Bundle of His
D. Purkinje Fibers
STARLING EQUATION
• in which:
Fluid movement = k [(Pc – Pi) – (πc – πi)] o R is resistance,
• where o DP is the pressure difference
o k = capillary filtration coefficient o r is the radius of the vessel
o Pc = capillary hydrostatic pressure 35-14= 11mmHg o l is length of the vessel
o Pi = interstitial hydrostatic pressure 0 o h is viscosity of the blood.
o πc = capillary colloid osmotic pressure 25mmHg
o πi = interstitial colloid osmotic pressure 1mmHg • ↑ hematocrit → ↑ viscosity → ↑ resistance → ↑ mean BP
CAUSES OF EDEMA EXAMPLES BP CONTROL

• Arteriolar dilatation BARORECEPTORS
• venous constriction • Act fast; Buffers minute-to-minute changes in BP
↑ Capillary • ↑ venous pressure • Stretch Receptors on the Carotid Sinus and Aortic Arch
Hydrostatic Pressure • heart failure o ↑ BP → ↑ Stretch → ↑ Firing of CN IX to NTS → trigger
• ECF volume expansion parasympathetic response
• standing o ↓ BP → ↓ Stretch → ↓ Firing of CN IX to NTS → trigger
• ↓ plasma protein concentration sympathetic response
↓ Capillary Oncotic • severe liver disease • Hering nerve: branch of CN IX that carries signals from carotid
Pressure • protein malnutrition sinus to NTS
• nephrotic syndrome • Carotid Baroreceptors: respond increase/decrease in
• Burns pressures from 50mmHg-180 mmHg
↑ Filtration • Aortic Baroreceptors: respond to increase in pressure
• inflammation (due to release of
Coefficient >80mmHg
histamine, cytokines)
• Set Point for MAP in Vasomotor Center: 100mmHg
CHEMORECEPTORS 6. Differences among sexes lower in females

7. Factors that increase VC J. Lung volumes and
PERIPHERAL CENTRAL
CHEMORECEPTORS CHEMORECEPTORS capacities 20-25%
lower in males
• Aortic Bodies, Carotid
Location • Medulla K. Body size, male
Bodies
gender,
• Hypoxemia of PaO2 conditioning, youth,
<60mmHg (main),
• CSF H+ from plasma
Stimulus • High plasma H+,
CO2 PHYSIOLOGIC DEAD SPACE
Hypercarbia (High
PaCO2)
Response • ↑ RR, ↑ BP • ↑ RR
ANS EFFECT ON THE HEART AND BLOOD VESSELS

PARA-
SYMPATHETIC
SYMPATHETIC
Effect Receptor Effect Receptor
Heart Rate ↑ 𝛽1 ↓ M2
Conduction VENTILATION
Velocity (AV ↑ 𝛽1 ↓ M2 MINUTE VENTILATION
Node)
↓ (atria
Contractility ↑ 𝛽1 M2
only)
Vascular Smooth Muscle ALVEOLAR VENTOLATION
Skin, Dilation
splanchnic (EDRF)
Dilation
Skeletal Constriction 𝛼1 M3
(EDRF)
Muscle
Dilation 𝛽2 - -
Veins Constriction 𝛼1 - -
TRUE OR FALSE INSPIRATION VS. EXPIRATION

• Water, glucose and amino acids travels across capillaries MUSCLES INVOLVED
using clefts/pores between endothelial cells: Normal
• Diaphragm
__________________ Inspiration
• Adenosine is a vasodilator suspected to be involved in the • External Intercostals, Accessory Muscles:
Forced
Metabolic Theory. SCM, Anterior Serrati, Scalene, Alae Nasi,
Inspiration
__________________ Genioglossus, Arytenoid
• Lactic Acid is the cause of chest pain in M.I. and muscle fatigue Normal
• Passive
__________________ Expiration
• Cerebral blood flow increases while coronary blood flow • Internal Intercostals, Abdominal muscles
Forced
remains the same during exercise (Rectus Abdominis, Internal and External
Expiration
__________________ Oblique, Transversus Abdominis)
VASOCONSTRICTORS AND VASODILATORS SURFACTANT

MATCHING TYPE • Gas Exchange: Type I Pneumocyte
1. Substance involved in Vasodilator A. ADH • Surfactant Production: Type II Pneumocyte
Theory (Metabolic Theory) B. Adenosine • Law of Laplace: Collapsing pressure = 2T/r
2. Responsible for Angiogenesis C. Serotonin • Surfactant: active component: DPPC
3. Most potent vasoconstrictor D. VEGF • Amphipathic molecule that decreases surface tension and
4. Vasoconstrictor, involved in migraine E. Endothelin subsequently, collapsing pressure
5. Vasoconstrictor, release by damaged F. Bradykinin, • Pre-term infant compared to term infant:
endothelium Histamine o Increased: pulmonary vascular resistance, pulmonary artery
6. Counteracts TXA2 G. PGI2 pressure (PAP), pulmonary capillary hydrostatic pressure,
7. Arteriorlar Dilation, Venous pressure gradient from pulmonary artery to the aorta
Constriction o Decreased: Pulmonary Blood flow
Which of the following causes bronchoconstriction?

MODULE 4: RESPIRATORY PHYSIOLOGY A. Sympathetic nervous System
Function as Alveolar Macrophages: B. Atropine
A. Type I Pneumocyte C. VIP
B. Type 2 Pneumocyte D. Exercise
C. Goblet Cells
D. Clara Cells MATCHING TYPE
E. Dust Cells 1. Percentage of Dissolved O2 A. Deoxyhemoglobin
2. Percentage of O2 bound to B. Oxyhemoglobin
LUNG VOLUMES AND CAPACITIES HgB C. Methemoglobin
MATCHING TYPE 3. HgB with attached O2 D. Fetal Hemoglobin (HbF)
1. Cannot be measured directly by A. IRV 4. HgB without attached O2 E. Hemoglobin S (HbS)
spirometry B. TV 5. HgB with Fe3+; doesn’t F. 2%
2. Amount of air inspired / expired C. ERV bind to O2 G. 98%
during quiet breathing D. RV 6. 𝛼2𝛾2, higher affinity for O2 H. O2-binding capacity
3. Maintains Oxygenation in E. TLC I. Utilization Coefficient
between breaths/ Prevents lung F. VC
collapse after max exhalation G. IC
4. Equilibrium/Resting Volume H. FRC
of the Lung I. Lung Volumes and
5. Marker of Lung Function Capacities 20-25%
MATCHING TYPE o Dead Space (e.g., pulmonary embolism)
1. 70% of CO2 in the blood A. Carbaminohemoglobin
2. 7% of CO2 in the blood B. Dissolved CO2 CAUSES OF HYPOXEMIA
3. 23% of CO2 in the blood C. HCO3- Cause PaO2 A-a Gradient
4. Cl--HCO3- exchange in RBC D. Chloride Shift (using High altitude (↓PBàPAO2) Decreased Normal
5. O2 affecting affinity of Band 3 Protein) Hypoventilation (↓P PAO2) Decreased Normal
CO2/H+ to HgB E. Alkaline Tide Diffusion defect (e.g., Decreased Increased
6. CO2/H+ affecting affinity of F. Haldane Effect fibrosis)
O2 to HgB G. Bohr Effect V/Q defect Decreased Increased
Right-to-left shunt Decreased Increased
A-a gradient = difference in PO2 between alveolar gas and arterial blood; PB
O2-HGB DISSOCIATION CURVE = barometric pressure; PAO2 alveolar PO2; PaO2 = arterial PO2; V/Q =
ventilation/perfusion ratio
Costanzo LS. BRS Physiology. 7th ed. 2019.
RESPIRATORY RESPONSES TO HIGH ALTITUDE

INCREASES (↑) DECREASES (↓)
• Respiratory Rate • Alveolar PO2
• Arterial pH • Arterial PO2
• HgB Concentration
• 2,3 BPG
• Pulmonary Vascular Resistance
(Hypoxic vasoconstriction)

INCREASES (↑) DECREASES (↓) NO CHANGE
• Respiratory Rate exercise due to • Arterial pH
• Venous PCO2 lactic acidosis) (moderate
• Pulmonary exercise)
Blood Flow
MNEMONICS O2-HgB DISSOCIATION CURVE

“CABET, do the RIGHT thing, LET GO” CONTROL OF RESPIRATION
CO2 CHARACTERISTICS CENTER
Acidosis • For Normal Inspiration; Sends
BPG (2,3 BPG) Inspiratory Ramp Signal
Exercise • For Forced Inspiration and
Expiration; Overdrive mechanism
Temperature in exercise
• In Upper Pons; Limits duration of
MATCHING TYPE Inspiration and Increases RR
1. Most susceptible to baro- A. Apex of Lungs • In Lower Pons; Prolongs duration
trauma from overventilation B. Middle of Lungs of Inspiration and Decreases RR
2. Highest V C. Base of Lungs • In Ventral Medulla; excited by CSF
3. Highest Q D. Uniform throughout H+ from plasma CO2; adapt within
4. Highest V/Q ratio E. 60% 1-2days
5. V/Q ratio in exercise F. 80% • In Carotid Bodies (CN IX)and
6. Normal V/Q ratio G. Bronchoconstriction Aortic Bodies (CN X); activated
7. Normal FEV1/FVC H. Vasoconstriction when PO2 < 70mmHg and to a very
8. Effect of hypoxia on lungs lesser extent, CO2 AND H+
9. Effect of SRS-A on lungs
IMPORTANT EQUATIONS
V/Q RATIO ALVEOLAR GAS EQUATION
Question:
36/M placed on ventilator with rate of 16, TV = 600mL, FiO2 =
1.0. ABG reveals PO2 = 350mmHg, PCO2 = 36mmHg, pH=7.32
At barometric pressure = 757mmHg, with normal respiratory
exchange ratio (R) of 0.8, What is the patient’s alveolar oxygen
tension?
Answer:
• High V/Q: high PO2, low PCO2 (e.g. lung apex) 665mmHg (PAO2 = PIO2-(PaCO2/R) = (1.0)(757-47) - (36/0.8)
• Low V/Q: low PO2, high PCO2 (e.g. lung base) = 710-45 = 665mmHg
• V/Q = Zero Pre-Test 14th (172)
o Shunt (e.g., R-L shunt, airway obstructions)

• V/Q = infinite
PULMONARY VASCULAR RESISTANCE TRUE OR FALSE
• FEV1/FVC is decreased in emphysema
_____________
• Hypoxemia is synonymous with Hypoxia
_____________
• Apex of the lungs in a relaxed standing individual has Zone 2
Note: Left Atrial Pressure (LAP) above could be replaced by Pulmonary and 3.
Capillary Wedge Pressure (PCWP); CO of R heart = Pulmonary Blood Flow _____________
• J receptors are responsible for the feelings of Dyspnea.
Question: _____________
67/M cardiac transplant candidate has the following labs:
Pulmonary Artery Pressure (PAP) = 35mmHg, Cardiac Output = Pre-Test: Types of Hypoxia
4L/min, Left Atrial Pressure (LAP) = 15mmHg, Right Atrial TYPE OF
Pressure = 10mmHg. What is his PVR? CHARACTERISTICS
HYPOXIA
Answer:
PVR = Mean PAP – mean LAP/pulmonary blood flow Hypoxic • (+) Alveolar hypoventilation (high PaCO2)
= 35 – 15mmHg/4L/min Hypoxia and hypoxemia (low PaO2)
= 5mmHg/L/min • ↓ Hb (anemia) or ↓ saturation of hemoglobin
Pre-Test 14th (181) Anemic
with oxygen (SaO2) expected for a given PaO2
Hypoxia
SHUNT FRACTION (e.g., CO poisoning or methemoglobinemia)
Stagnant
• ↓ cardiac output
hypoxia
Histotoxic • impaired O2 extraction → ↓ CaO2-CvO2 and ↑

Hypoxia SVO2
MODULE 5:
RENAL AND ACID-BASE PHYSIOLOGY
BODY FLUIDS
% OF
MAJOR MAJOR
COMPARTMENT BODY MARKERS
CATIONS ANIOINS
WEIGHT
Titrated
Total Body
60% water, D2O,
Water (TBW)
antipyrine
Question: Extracellular
Sulfate,
32/M severe respiratory disease after aspiration pneumonia. Fluid
20% Inulin, Na Cl, HCO3-
Inhaled NO given, and patient placed in prone position. Mean Compartment
Mannitol
pulmonary capillary oxygen content = 19mL/dL, Arterial O2 (ECF)
content = 18 mL/dL, Mixed Venous O2 content = 14 mL/dL, Radioactive
Cardiac Output = 6L/min. What is the patient’s shunt fraction 5% Iodinated
(ratio of shunted to total pulmonary blood flow)? (25% Serum
Plasma Na Cl- HCO3-
Answer: of Albumin
Shunt Fraction = (CCO2 – Ca2)/(CCO2-CvO2) ECF) (RISA),
= (19mL/dL-18mL/dL) / Evans Blue
(19mL/dL-14mL/dL) 15% ECF-
= 0.2 Interstitial (75% plasma
Na Cl, HCO3-
Pre-Test 14th (211)
Fluid (IF) of volume
ECF) (indirect)
OXYGEN CONSUMPTION VO2 Organic
(can be computed using Fick Equation; see Pre-Test 212) Intracellular TBW-ECF
40% K phosphate,
Fluid (ICF) (indirect)
Protein
ECF ICF ECF ICF

CASE MECHANISM
VOLUME VOLUME OSMOLARITY OSMOLARITY
Diarrhea Loss of Isotonic fluid DECREASED NO CHANGE NO CHANGE NO CHANGE
Infusion of Isotonic NaCl Gain of isotonic fluid INCREASED NO CHANGE NO CHANGE NO CHANGE
Lost in Desert (excessive sweating with no
Loss of hypotonic fluid DECREASED DECREASED INCREASED INCREASED
access to water)
Excessive NaCl Intake Gain of hypertonic fluid INCREASED DECREASED INCREASED INCREASED
Loss of hypertonic fluid to
Adrenal Insufficiency DECREASED INCREASED DECREASED DECREASED
the urine
SIADH Gain of hypotonic fluid INCREASED INCREASED DECREASED DECREASED
Refer to next page for Tubular system
RENAL CORPUSCLE
Which of the following statements is TRUE?
A. Countercurrent multiplier: VR
B. Countercurrent exchanger: LH
C. Countercurrent multiplier preserves graded
osmolarity in renal medulla
D. Countercurrent exchanger creates graded osmolarity
in renal medulla
E. Na+-K+-2Cl- symport in the TAL of LH contributes to
countercurrent mechanism in the kidneys
TUBULAR SYSTEM
RENAL THRESHOLD • Renal Blood Flow

VS. RENAL TRANSPORT MAXIMUM
GLOMERULAR FILTRATION RATE

• GFR = Kf [(PGC-PBS) – (OGC- OBS)]
o Kf = Filtration coefficient of the Glomerular Capillaries
o PGC= Glomerular Capillary Hydrostatic Pressure
o PBS = Bowman’s Space Hydrostatic Pressure
o OGC= Glomerular Capillary Oncotic Pressure (mmHg)
AFFERENT AND EFFERENT ARTERIOLES

AFFERENT EFFERENT
AFFERENT ARTERIOLE EFFERENT ARTERIOLE
ARTERIOLE ARTERIOLE
VASOCONSTRICTION VASOCONSTRICTION
VASODILATION VASODILATION
GFR á â â á
RPF, RBF á â á â
FILTRATION
FRACTION No Change No Change ââ áá
(GFR/RPF)
ARTERIOLES AND GFR CAUSES OF INCREASED CAUSES OF DECREASED
DISTAL K+ SECRETION DISTAL K+ SECRETION
ARTERIOLE EFFECT ON GFR
• High K+ diet
Afferent Vasodilation
• Hyperaldosteronism • Low K+ Diet
Afferent Vasoconstriction
• Alkalosis • Hypoaldosteronism
Efferent Vasodilation
• Thiazide Diuretics • Acidosis
Moderate Efferent Vasoconstriction
• Loop Diuretics • K+-Sparing Diuretics
Severe Efferent Vasoconstriction
• Luminal Anions
RENAL CLEARANCE
ACID-BASE EQUILIBRIUM
• Normal Values
o pH = 7.35-7.45
• Renal Clearance = UV/P o PaCO2 = 40mmHg
• Filtered, Not Secreted, Not Reabsorbed: Inulin/Creatinine o PaO2 = 100mmHg
o Clearance of Inulin/Creatinine used to estimate GFR o Plasma HCO3- = 24
• Filtered, Secreted, Not Reabsorbed: PAH o Anion Gap (AG) = 8-16
o Clearance of PAH used to estimate RPF Respiratory ACIDOSIS Metabolic ACIDOSIS
o PAH has highest clearance • Due to condition with • Due to gain of acids
o PAH mainly secreted in the PCT Hypoventilation (e.g., (HAGMA) or loss of bases
• Filtered, Not Secreted, 100% Reabsorbed in the PCT: sedative overdose, GBS) (NAGMA)
Glucose/amino acids • Compensation: • HAGMA: MUDPILES,
o Glucose and Amino Acids have Zero Clearance o ↑H+ excretion, NAGMA: HARD-UP
o Renal Threshold for Glucose: 200mg/dL o ↑HCO3- reabsorption, • Compensation:
o Renal Transport Maximum for Glucose: 375mg/dL o ↑synthesis of new HCO3- Hyperventilation
o Used to reabsorbed glucose in the PCT: SGLT-2 Respiratory ALKALOSIS Metabolic ALKALOSIS
• Due to condition with • Due to gain of bases, loss of
RAAS Hyperventilation (e.g., panic acids (e.g., vomiting, TD, LD)
• Macula densa → JG Cells → Renin → Angiotensinogen → attacks, high altitude) • Compensation:
Angiotensin I → Angiotensin II → Aldosterone • Compensation: Hypoventilation
• Aldosterone Effects on the KIDNEYS: opposite that of respiratory
o Na+ reabsorption acidosis
o K+ secretion REMEMBER TRIO OF ELECTROLYTES
o H+ secretion H+, Ca++, K+
áH+ levels à HyperCalcemia
K+ REGULATION HyperKalemia
CAUSES OF K+ EFFLUX → CAUSES OF K+ INFLUX →
HYPERKALEMIA HYPOKALEMIA TRUE OR FALSE
• Insulin deficiency • Insulin • Phosphate is only reabsorbed in the PCT, and nowhere else in
• Beta-adrenergic antagonist • Beta-adrenergic agonists the renal tubules
• Acidosis • Alkalosis _____________
• Hyperosmolarity • Hypoosmolarity • TAL LH is the main site for magnesium reabsorption
• Inhibitors of Na+-K+-ATPase _____________
-- • Increased plasma H+ is associated with increased plasma Ca2+
pump like digitalis
• Exercise -- and K+
_____________
• Cell Lysis --
CLASS SITE OF ACTION MOA EFFECTS
↑HCO3- excretion
CAI (e.g. Acetazolamide) PCT Inhibition of Carbonic Anhydrase
Metabolic acidosis
↑NaCl excretion
↑K+ excretion
Inhibition of Na-K-2Cl pump in
Loop Diuretic TAL LH ↑Ca2+ excretion
TAL LH
↓ ability to concentrate or dilute urine
Metabolic alkalosis
↑NaCl excretion
↑K+ excretion
↓Ca2+ excretion
Thiazides EDT Inhibition of Na-Cl pump ↓ ability to concentrate or dilute urine
Metabolic alkalosis
HyperGLUC (glycemia, lipidemia,
uricemia, calcemia)
↑Na+ excretion
Aldosterone antagonism or Na+
K-sparing diuretics LDT and CD ↓K+ excretion
inhibition
↓H+ excretion
Osmotic diuretic (e.g. Entire nephron except Large polysaccharides absorbing
↓ICP
Mannitol) TAL LH water
MODULE 6: GI PHYSIOLOGY
KEY POINTS ABOUT THE GI TRACT
CONCEPT KEY POINTS
• Mucosa,
• Submucosa (strongest layer in
esophagus)
Layers of the
• Muscularis: Inner Circular (decreases
GI Tract
diameter of segment), Outer Longitudinal
(decreases length of segment)
• Serosa (not seen in esophagus) INCREASES GASTRIC DECREASES GASTRIC
• Tonic Contraction: constant level of EMPTYING EMPTYING
GI Smooth contraction without regular rest due to Increased GASTRIC volume Increased DUODENAL
Muscle subthreshold slow waves (not true AP) volume
Contractions • Phasic Contraction: periodic contractions Isotonic content Hypertonic & Hypotonic
due to spike potentials (true AP) content
• Slow waves: slow, oscillating membrane Chyme Formation Fat in the duodenum
potentials due to cyclic opening of Ca2+ HCl in the duodenum (acids)
Electrical channels followed by opening of K+
Activity of GI channels cause by GI pacemakers
Smooth (Interstitial cells of Cajal); slowest in the THE 5 OFFICIAL GI HORMONES
Muscles stomach, fastest in the duodenum DESCRIPTION HORMONE
• Spike Potentials: depolarization due to • TRIGGER: CHON and AA (especially
Calcium influx the amino acids phenylalanine (F),
• Extrinsic: Parasympathetic (excitatory) via tryptophan (W) and methionine
Vagus Nerve and Pelvic Nerve and (M), Gastric Distention
Sympathetic (inhibitory) • SOURCE: G cells of the ANTRUM
• Intrinsic: Meissner’s (Submucosal) • ACTIONS: Stimulates Parietal cells
Innervation of in FUNDUS for HCl Secretion,
Plexus for Secretion (contraction of
the GIT growth of gastric mucosa
muscularis mucosa), and Auerbach’s
(Myenteric) Plexus for Motility • TRIGGER: All Types of Food (main
(contraction of IC and OL muscles and trigger: Fatty Acids)
relaxation of PS and ICV) • SOURCE: I cells in the DUODENUM
• ACTIONS: Bile Secretion (GB
GIT ABSORPTION contraction, SOO relaxation),
MATCHING TYPE Increases GET (Decreases GE),
1. Types of CHO absorbed A. Chylomicrons Increases pancreatic enzyme
2. Activates Trypsinogen B. Micelles secretion
3. Glu, Gal absorption from lumen C. Acid-labile • TRIGGER: H+ in the duodenum, FA
to SI D. Acid-stable in duodenum
4. Fru absorption from lumen to SI E. GLUT 2 • SOURCE: S cells in the duodenum
5. Glu, Gal, Fru absorption from SI F. GLUT 5 • ACTIONS: Inhibits HCl secretion,
to blood G. SGLT 1 increases biliary and pancreatic
6. Lingual Lipase, Gastric Lipase H. Enterokinase HCO3-
7. Pancreatic Lipase I. Monosaccharides • *this hormone does NOT affect
8. Fat absorption from lumen to SI pancreatic ENZYME secretion!
9. Fat absorption from SI to Lacteals • TRIGGER: Oral Glucose
• SOURCE: K cells in the duodenum
GASTROINTESTINAL TRACT • ACTIONS: Stimulates insulin
secretion; inhibits gastric
emptying (above normal
physiologic levels)
• TRIGGER: Fasting
• SOURCE: M cells in the duodenum
and Jejunum
• ACTIONS: activates interdigestive
/ migrating myoelectric complex.
Acts only on the stomach and
small intestines (has no effect on
the large intestines)
MATCHING TYPE
1. Inhibits pancreatic HCO3- A. Pancreatic polypeptide
enzymes (candidate hormone)
• Myenteric Reflex: muscles upstream contract while muscles 2. Secreted by intestinal cells B. Enteroglucagon
downstream relax in response to hypoglycemia (candidate hormone)
• Only essential secretion of the stomach: IF 3. Secreted by L cells; C. GLP-1 (candidate
• Digestion of: stimulates insulin secretion hormone)
o CHO: monosaccharides only 4. Inhibits all GI hormones D. Somatostatin (Paracrine)
o CHON: AA, dipeptides and tripeptides (utilize brush border EK 5. Potentiates Gastrin & ACh E. Histamine (Paracrine)
to activate Trypsinogen) action on the parietal cells
o Fat: Micelles to enter, Chylomicrons to leave
MATCHING TYPE WATER AND ELECTROLYTES
1. Mucus A. Parietal / Oxyntic Cell DESCRIPTION
2 HCl B. Chief / Peptic Cell • S.I.: SGLT-1, Na-aa, NaCl symport, Na+-H+
3. Pepsinogen C. Mucous Neck Cell Na+ antiport
4. IF (secreted in fundus) D. G Cell absorption • L.I: passive diffusion (paracellular route,
5. Serotonin E. D Cell stimulated by aldosterone)
6. Bicarbonate F. Enterochromaffin Cells • Accompanies Na+ via Passive diffusion
Cl-
7. Gastrin G. ECL Cells (paracellular route), Na-Cl symport, Cl-
absorption
8. Histamine HCO3- antiport
• S.I.: passive diffusion (paracellular route)
K+
MATCHING TYPE • L.I.: active secretion (stimulated by
absorption
1. Inhibits appetite A. Hunger Center aldosterone)
2 Stimulates appetite B. Satiety Center • Secondary to solute absorption
3. Releases POMC to decrease C. Orexigenic Neurons H2O • S.I. and Gallbladder: isosmotic
appetite D. Anorexigenic Neurons absorption • L.I.: lower water permeability compared to
4. Releases Neuropeptide Y to E. Ghrelin (Gastric Cells) S.I.
increase appetite F. Leptin (Fat Cells, • Primary ion secreted
5. Stimulates Anorexigenic Insulin, GLP-1 • Utilizes Cl- channels in the luminal
neurons G. Peptide YY (PYY) Cl- secretion membrane regulated by cAMP
6. Inhibits Anorexigenic • Na is secreted into lumen passively follows
Neurons Cl. Water then follows NaCl
7. Inhibits Ghrelin
OTHER SUBSTANCES
GASTRO-INTESTINAL JUICES NUTRIENT DESCRIPTION
TYPE DAILY VOLUME (ML) PH • Produced by bacteria Ganong 25 26-1 th
Saliva 1000 6.0-7.0 Short-Chain

• Absorption almost exclusively happens in
Fatty Acids
Gastric Secretion 1500 1.0-3.5 the: colon PreTest 14 (345) th
Pancreatic Secretion 1000 8.0-8.3 Fat-Soluble

• Incorporated into micelles and absorbed
Bile 1000 7.8 Vitamins
with lipids
S.I. Secretion 1800 7.5-8.0 (ADEK)
Brunner’s Gland Water-
200 8.0-8.9
Secretion Soluble • Na+-dependent symport
L.I Secretion 200 7.5-8.0 Vitamins
TOTAL 6700 -- • Absorbed in Ileum using Intrinsic Factor
(IF)
DESCRIPTION ANSWER • *Vit B12 deficiency + pernicious anemia is
Effect of Parasympathetic NS INCREASES SALIVATION Vitamin B12 caused by: Lack of IF PreTest 14 (41) th
Effect of Sympathetic NS INCREASES SALIVATION • *MOA of neurologic deficits in Vit B12

Initial Saliva is high in: Na+, Cl- deficiency: Decreased myelin synthesis
Pre-Test 14th (132)
Final Saliva is high in: HCO3-, K+
• 1,25 dihydroxycholecalciferol → ↑ calbindin
Hormone involved in absorbing Calcium
ALDOSTERONE D-28K → ↑calcium absorption
Na+ at the ductal cells
• Heme Iron broken down in intestinal cells
HIGH Na+, Cl-, LOW K+ &
At High Flow Rates, Saliva has → Free Fe2+ binds to apoferritin and
HIGH HCO3 Iron
transported in blood → Free Fe2+ binds to
LOW Na+, Cl -, HIGH K+ & transferrin in blood
At Low Flow Rates, Saliva has
LOW HCO3-
TRUE OR FALSE
Defecation following a meal in infants is due to which • VIP relaxes the UES, LES, PS, ICV
reflex?
_____________
A. Enterogastric reflex
• Tonic contractions are due to spike potentials
B. Intestinointestinal reflex
_____________
C. Gastrocolic reflex
• 1.5L: capacity of stomach, water volume absorbed in the L.I.,
D. Pyloric reflex
volume of HCl produced per day
_____________
• Most HCl is produced once food is in the stomach
_____________
• Sight, smell, taste, of food increases HCl secretion. High
gastric pH decreases HCl secretion
_____________
SUMMARY OF GASTROINTESTINAL (GI) SECRETIONS

High HCO3-
• Sleep
High K+ • Parasympathetic nervous system
Saliva • Dehydration
Hypotonic ⍺-Amylase • Sympathetic nervous system
Lingual lipase • Atropine
• ↓ Stomach pH
• Chyme in duodenum (via
• Gastrin secretin and GIP)
HCl • Parasympathetic nervous system • Somatostatin
Gastric secretion • Histamine • Atropine
• Cimetidine
• Omeprazole
Pepsinogen • Parasympathetic nervous system -
Intrinsic Factor - -
• Secretin
High HCO3-
• CCK (potentiates secretin) -
Isotonic
Pancreatic secretion • Parasympathetic nervous system
• CCK
Pancreatic lipase, amylase, proteases -
• CCK (causes contraction of
Bile salts
gallbladder and relaxation of
Bilirubin
Bile sphincter of Oddi) • Ileal resection
Phospholipids
Cholesterol
(causes contraction of gallbladder
CCK = Cholecystokinin; GIP = glucose-dependent insulinotropic peptide
§ Utilizes G proteins and 2nd messengers
MODULE 7: ENDOCRINE PHYSIOLOGY § Activates existing intracellular enzymes via phosphorylation
o Lipid/Steroid Hormone (Lipid-Soluble)
KEY POINTS ABOUT HORMONES § Binds to nuclear / cytoplasmic receptors
• Hormones: chemical messengers released into the blood § Causes transcription of genes
o Protein Hormone (Water-Soluble) § Synthesizes new intracellular enzymes
§ Binds to Cell Membrane Receptors

PARATHYROID HORMONE
• Trigger: HypoCa
• Source: Chief Cells, Parathyroid Gland
• Counter-regulatory Hormone: Calcitonin (C Cells / Parafollicular
Cells, Thyroid Gland)
• ↑ Bone Calcium and Phosphate resorption, ↑ renal calcium
reabsorption in the DT, ↓ renal phosphate reabsorption in the
PCT, ↑ active Vit D by ↑ 1 alpha hydroxylase
ALDOSTERONE
HORMONES • Renin → Angiotensin I → Angiotensin II → Aldosterone (ZG, AC)
GROWTH HORMONE • Renal: Inc Na+ reabsorption (increases ENaCs), K+ Secretion, H+
• GHRH → GH → IGF-1 secretion
• ↑ blood glucose, has direct and indirect effects • Others: ↑ Na+ reabsorption in the sweat glands and salivary
(via IGF-1) gland, ↑ K+ influx in other cells
PROLACTIN CORTISOL
• Hypothalamic Dopamine (PIH) → inhibits Prolactin • CRH → ACTH → Cortisol (ZF [largest area in the AC], AC)
• Milk production, inhibits GnRH • Anti-inflammatory effects (e.g. inhibits phospholipase A2),
↑blood sugar, ↑lipolysis, has multiple other organ effects
OXYTOCIN
• Milk secretion, pregnant uterine contraction WEAK ANDROGENS
• DHEA, Androstenedione (ZR, AC): significant only in females
VASOPRESSIN/ADH
• Insertion of Aquaporin at the renal collecting ducts, INSULIN
vasoconstriction (↑ TPR) • Source: Beta Cells, Islets of Langerhans, Endocrine Pancreas
• Greater effect on plasma osmolarity than aldosterone • 2nd Messenger: Tyrosine Kinase
• Precursor: proinsulin (splits into insulin and C peptide)
THYROID HORMONES • Increases well-fed state pathways: glycolysis, lipid and protein
• TRH → TSH → T4 (more common), T3 (more active) synthesis
• ↑ BMR (via stimulation of Na+-K+-ATPase pump), ↑ cerebration, • Increases K+ influx in other cells
causes maturity of CNS in the perinatal period, stimulates B1 • GLUT-4: only one that is insulin-mediated
receptors in the heart, needed for GH to work properly, ↑ Glu • Counter-regulatory Hormone: Glucagon (Alpha Cells)
absorption, glycogenolysis, gluconeogenesis, lipolysis
PITUITARY HORMONES • Ingestion of large amount of iodine

Wolf-Chaikoff
reduces T3 and T4.
Effect
• Used as treatment of hyperthyroidism.
• Hyperthyroidism following small
increased ingestion of iodine typically
Jod-Basedow
in patients with endemic goiter (due to
Phenomenon
iodine deficiency) who relocate to
iodine-rich areas.
PARATHYROID HORMONES
ORGAN PTH VITAMIN D
When the anterior lobe of the pituitary gland is removed, • ↑ calcium &
what will happen? Intestines • None phosphate
A. Decreased production of thyroid hormone absorption
B. Decrease NE
• ↑ calcium
C. Increased glucagon reabsorption (DT)
D. All of the above • ↑ calcium &
• ↓ phosphate
phosphate
• Storage CHON in the thyroid gland for Kidney reabsorption (PCT)
reabsorption
thyroid hormone • ↑ Active Vit D (by
• ↑ urinary calcium
• Secondary active transporter used for increasing 1 alpha
iodide trapping hydroxylase)
• Transports iodide from follicular cell to • At normal levels:
colloid calcium and
• Produces MIT and DIT phosphate
• Calcium and
• Produced T3 and T4 deposition
Bone phosphate
• Trigger for T3 and T4 release to plasma • At high toxic levels:
resorption
calcium and
PATHOPHYSIOLOGY OF THYROID HORMONE phosphate
CONDITION DESCRIPTION resorption
• ↑ BMR, ↑ cardiac output, weight loss, Net effect on • ↑ serum calcium • ↑ serum calcium
tremors, heat intolerance, pre-tibial serum levels • ↓ serum phosphate • ↑ serum phosphate
myxedema, exophthalmos (in Graves
Disease) SUPPLEMENT VITAMIN D SYNTHESIS
Hyperthyroidism • Hyperthyroidism presents with 2-3x Vitamin D comes from Cholesterol
larger thyroid, hyperplasia and
Starts at the Skin
infolding of the follicular cell lining into
7-Dehydrocholesterol à Vit D3 or
the follicles decreasing the cross-
Calciol (Cholecalciferol)
sectional area occupied by the colloid
Ganong 25th 19-1 1st activation: Liver
• ↓ BMR, weight gain, cold intolerance, Calcidiol (25 hydroxyCholecalciferol)
lethargy, whole-body myxedema, 2nd activation: Kidney
mental and grown retardation (in Calcitriol (1,25 dihydroxyCholecalciferol)
Hypothyroidism
congenital hypothyroidism)
• Hypothyroidism causes cholesterol
levels to INCREASE Ganong 25 19-6 th
CONGENITAL ADRENAL HYPERPLASIA TRUE OR FALSE

• Testosterone has no second messenger
21-b- 11-b- 17-a-
Hydroxylase Hydroxylase Hydroxylase _____________
Aldosterone ↓ ↓ ↑ • Thyroid hormone increases risk for somnolence
_____________
Cortisol ↓ ↓ ↓
• Addison Disease is associated with low aldosterone, low
Androgens ↑ ↑ ↓
cortisol and high weak androgens
ACTH ↑ ↑ ↑
_____________
Blood
↓ ↑ ↑
Pressure
Accumulating 17-hydroxy- 11-deoxy- MODULE 8:
Pregnenolone
substrate progesterone corticosterone HEMA PHYSIOLOGY AND SPECIAL TOPICS
DESCRIPTION CELL
MALE SEX PHYSIOLOGY • Biconcave (due to spectrin), lasts
EVENTS/CHARACTERISTICS 120 days, anucleated, relies on
ANAEROBIC glycolysis, acid-base
Sperm Formation
buffer due to Carbonic Anhydrase
Sperm Motility / Sperm Maturation • Derived from megakaryocytes; last
7-10 days; forms initial thrombus
Sperm Storage • Granulocytes
• Derived from B-Cells, secrete Ig
Production of Fructose, Prostaglandin • Involved in Cell-Mediated Response
• Involved in INNATE Immunity
Contributes to semen alkalinity (first-line, non-specific, non-
lymphocyte-mediated, “security
Supplies Mucus guards”)
• Involved in ADAPTIVE Immunity
MNEMONICS MALE SEX HORMONES (second-line, specific, requires prior
S-S-S exposure lymphocyte-mediated,
FSH, Sertoli Cell, Sperm “SWAT TEAM”)
L-L-L • C3b, C3a, C5a, C5b-C9 (NOT BLOOD
LH, Leydig Cell, Libido Hormone (Testosterone) CELLS)
TESTOSTERONE DIHYDROTESTOSTERONE KEY POINTS ABOUT RBCS

• Differentiation of epididymis, • Differentiation of penis,
vas deferens, & seminal vesicles scrotum, and prostate KEY POINT DESCRIPTION
• Descent of testes • Male hair pattern
• ↑ bone and muscle mass (e.g., • Male pattern baldness
• Trigger: Hypoxia
broad shoulders) • Sebaceous gland activity
• ↑ BMR • Growth of prostate • Site of Secretion: Interstitial Cells of Renal
• Pubertal growth spurt EPO Peritubular Capillaries
• Epiphyseal closure • Effects: Causes increased bone marrow RBC
• Growth of penis & seminal vesicles production (results seen only days later)
• Deepening of voice (enlargement • Biconcave due to spectrin (provides bag
of larynx) Appearance
pliability)
• Spermatogenesis • Storage protein for O2 inside RBCs
• Negative feedback on anterior
pituitary
• Building blocks: Succinyl CoA, Glycine
• Libido • Adult HgB: 2 Alpha chains, 2 Beta chains
HgB (binds MORE with 2,3 BPG)
SPECIAL NOTES ON MALE REPRODUCTIVE PHYSIOLOGY • Fetal HgB: 2 Alpha chains, 2 Gamma chains
(binds LESS with 2,3 BPG)
• Testes temperature: 1-2°C cooler than core body
o requires temperature lower than body temp: • 1 gram of HgB carries 1.34mL of O2
Spermatogenesis PreTest 14 (436) th
• Fe2+ and NOT Fe3+ is active
• Activation of sperm in the female genital tract: capacitation • Transferrin: plasma iron transport protein
• NTs used in erection: NO and Ach • Ferritin: primary storage protein found in
Iron
o Nitric Oxide synthase → ↑ NO → activates guanylyl cyclase → the LIVER
↑cGMP → potent vasodilator → Erection Ganong 25 23-3 th
• Hemosiderin: secondary / supplemental
• Definition of Low Sperm Count: <20 million sperms/mL storage protein found outside of the liver
• Vestigial remnant of 3rd eye; secretes melatonin involved in • Where RBCs come to die (“graveyard” of
Spleen
reproduction and sex drive: pineal gland RBCs)
o Circadian rhythm is controlled by: Suprachiasmatic Nuclei
(SCN) of the Hypothalamus (in turn regulated by Pineal MNEMONIC VITAMIN B12 AND FOLIC ACID
Gland thru melatonin) PreTest 14 (101) th VITAMIN B12
• Sperm: viable for 1-5 days in the female genital tract Baboy
• Childhood: FSH and LH are at their lowest, FSH > LH FOLIC ACID
• Puberty: FSH and LH increase, FSH < LH Froccoli, cauliFlower
• Senescence: FSH and LH at their highest, FSH > LH
• Weakest to strongest androgens: androstenedione,
testosterone, dihydrotestosterone (DHT)
FEMALE SEX PHYSIOLOGY

Estrogen Progesterone FSH LH
Menstruation ↓ ↓* ↓ ↓
Follicular phase ↑* ↓ ↑ ↓
Ovulation ↑ ↓ ↑ ↑*
Luteal phase ↓ ↑* ↓ ↓
WBCS ANTIBODIES
MATCHING TYPE
• Antibodies bound to antigens serve as markers for complement
1. Most common A. Basophils
proteins
2 Least common B. Eosinophils
• can be monomeric, dimeric, trimeric: IgA
3. Highly lobulated nucleus C. Neutrophils
• Pentameric: IgM
4. Bilobulated, pink D. Monocytes
• All the other Ig: monomeric
5. Bilobulated / trilobulated, blue E. Platelets
• Primary response, largest: IgM
6. Eccentrically placed nucleus F. Lymphocytes
• Secondary response, smallest, crosses the placenta: IgG
7. Last 7-10 days
• Found in human body secretions like saliva, tears, Peyer’s
8. Round, densely staines nucleus with patches: IgA
pale basophilic, non-granular • Involved in allergies: IgE
cytoplasm
9. Largest
10. Adaptive immunity STEPS OF HEMOSTASIS
STEP DESCRIPTION
TYPES OF IMMUNITY • Due to local myogenic spasm, endothelin 1
1. Vascular
(ET-1)
ACQUIRED / ADAPTIVE Constriction
INNATE IMMUNITY • Prevents further blood loss
IMMUNITY
• Platelet Adhesion: mediated by vWF of
• Pre-existing (skin, mucous
ruptured blood vessels walls and Gp1b of
membranes, phagocytic cells, • Antibody 2. Primary
platelets
inflammatory mediators, mediated/lymphoid cells Hemostasis /
• Platelet Activation: platelets change
complement system) Formation of
shape
• Not acquired through contact • Occurs after exposure to Loose Platelet
• Platelet Aggregation: mediated by
with a non-self (antigen) an antigen Plug
fibrinogen and Gp2b-3a of platelets (also
• NON-SPECIFIC (activated by PAF)
most commonly by
• SPECIFIC • Extrinsic Pathway (initiated by Factor III
carbohydrate sequences in
bacterial cell walls) or Tissue Factor) and Intrinsic Pathway
3. Secondary
(initiated by Factor XII or Hagemann
• Quick • Delayed response Hemostasis /
Factor) lead to formation of Thrombin
• 1st line of defense • 2nd line of defense Blood
that then converts fibrinogen to fibrin
Coagulation
• Fibrin: meshwork that strengthens the
BLOOD TYPING loose platelet plug
SERA • Due to Fibrinolysin or Plasmin: lyses
RED BLOOD CELL TYPES 4. Resolution
ANTI-A ANTI-B blood clot
(-) (-)
(+) (-)
(-) (+)
(+) (+)

• Activation of T cells and • Implicated in the pathogenesis of
IL-1 • Macrophages macrophages; promotion of septic shock, rheumatoid arthritis,
inflammation and atherosclerosis
• Used to induce lymphokine-activated
• Type 1 (Th1) helper T • Activation of lymphocytes, natural killer cells; used in the treatment of
IL-2
cells killer cells, and macrophages metastatic renal cell carcinoma,
melanoma, and various other tumors
• As a result of its ability to stimulate
• Type 2 (Th2) helper T
IgE production, plays a part in mast-
cells, mast cells, • Activation of lymphocytes,
IL-4 cell sensitization and thus in allergy
basophils, and monocytes and IgE class switching
and in defense against nematode
eosinophils
infections
• Monoclonal antibody against
• Type 2 (Th2) helper T interleukin-5 used to inhibit the
IL-5 cells, mast cells, and • Differentiation of eosinophils antigen-induces late-phase
eosinophils eosinophilia in animal models of
allergy
• Activation of lymphocytes; • Overproduces in Castleman disease
• Type 2 (Th2) helper T differentiation of B cells, acts as an autocrine growth factor in
IL-6
cells and macrophages stimulation of the production of myeloma and in mesangial
acute-phase proteins proliferative glomerulonephritis
• Chemotaxis of neutrophils, Accompanied by neutrophilia,
IL-8 • T cells and macrophages
basophils, and T cells making it a potentially useful marker
of disease activity
• Bone marrow stromal • Stimulation of the production of • Used to reduce chemotherapy-
IL-11
cells acute-phase proteins induced thrombocytopenia
interferon γ by type 1 (Th1) helper
• May be useful as an adjuvant for
IL-12 • Macrophages and B cells T cells and by natural killer cells;
vaccines
cells
• Implicated in many
• Promotion of inflammatory cell immune/autoimmune diseases such
IL-17 • T cells
chemotaxis and inflammation as rheumatoid arthritis, asthma, and
psoriasis
• Treatment with antibodies against
• Macrophages, natural
Tumor necrosis factor- tumor necrosis factor-⍺ beneficial in
killer cells, T cells, B • Promotion of inflammation
rheumatoid arthritis and Chron
disease
• Implicated in the pathogenesis of
Lymphotoxin (tumor • Type 1 (Th1) helper T
• Promotion of inflammation multiple sclerosis and insulin-
necrosis factor-β) cells and B cells
dependent diabetes mellitus
• May be useful therapeutic agent in
Transforming growth • T cells, macrophages, B
• Immunosuppression multiple sclerosis and myasthenia
factor-β cells, and mast cells
gravis
chemotherapy for tumors and in
• T cells, macrophages,
• Promotion of the growth of ganciclovir-treated patients with
GM CSF natural killer cells, and B
granulocytes and monocytes AIDS; used to stimulate cell
cells
production after hematopoietic stem
cell transplantation
• Used to treat AIDS-related Kaposi
• Induction of resistance of cells to sarcoma, melanoma, chronic
Interferon- • Virally infected cells
viral infections Hepatitis B infection, and chronic
Hepatitis C infection
• Used to reduce the frequency and
• Induction of resistance of cells to
Interferon-β • Virally infected cells severity of relapses in multiple
viral infections
sclerosis
• Type 1 (Th1) helper T • Activation of macrophages; • Used enhance the killing of
Interferon-γ cells and natural killer inhibition of type 2 (Th2) helper T phagocytosed bacteria in chronic
cells cells granulomatous disease
BLOOD COAGULATION Factor XIII • Fibrin-stabilizing factor
CLOTTING
SYNONYMS Prekallikrein • Fletcher Factor
FACTOR
Factor I • Fibrinogen • Fitzgerald factor;
HMW Kininogen
Factor II • Prothrombin • HMWK
Factor III • Tissue factor; tissue thromboplastin
Factor IV • Calcium SPECIAL TOPICS
Factor V • Proaccelerin; labile factor; Ac-globulin • Start of High altitude sickness, seizures and death in
• Serum Prothrombin Conversion unacclimatized individuals: 12,000 feet, 18,000 feet, 23,000
Factor VII Accelerator; feet above sea level
• proconvertin; stable factor • Adaptation to High Altitude: Hyperventilation, Polycythemia,
• Antihemophilic Factor Increased diffusing capacity of oxygen, angiogenesis,
increased mitochondria
Factor VIII • antihemophilic globulin,
• Natural acclimatization: larger heart and lungs, smaller height
• G Forces: Positive G more dangerous because blood is shunted
• Plasma thromboplastin component; away from the brain; Max: +6-10G or -20G
Factor IX • Christmas factor; • Caused by formation of nitrogen bubbles in blood that blocks
• antihemophilic Factor B blood vessels: Decompression sickness
• Stuart Factor; • Maximum safe depth to dive: 200 feet
Factor X
• Stuart-Prower Factor • Used for deep dives: Helium
• Plasma Thromboplastin antecedent;
Factor XI
• antihemophilic Factor C
Factor XII • Hageman Factor
END OF PHYSIOLOGY PHASE 3
QUESTIONS ANSWER
BUZZ WORDS Zona Glomerulosa Adrenal
Site of aldosterone secretion
QUESTIONS ANSWER Cortex
Hyperventilation causes 2 functional classes of eye Gaze stabilization and gaze
which acid-base Respiratory alkalosis movements shifting
abnormality Irreversible sensorineural
Barr body Female chromosome Type of hearing loss if you hearing loss (usually affecting
Important eye movement blinking damage the inner hair cells first those involved in high-
Spherical lens (focus on near frequency sounds)
Ciliary muscle contraction objects; accommodation) Predominant hormone
Progesterone
during secretory phase
Most important progestin progesterone Rapid alternating
dysdiadochokinesia
Progesterone from corpus movements
Hormone involved in fetal Lateral (hunger) nuclei,
luteum (placenta after 12
life Parts of the brain involved in
weeks) ventromedial (satiety) nuclei of
hunger
Determines length of the hypothalamus
Follicular Stage
menstrual cycle
QUESTIONS ANSWER QUESTIONS ANSWER
Non-depolarizing ganglionic Part of the brain your need
MOA of hexamethonium Cerebral cortex
blocker the most to help catch a fly
Enhances mucosal homeostasis Competes with Ach for
Function of IgD
and immune surveillance receptors on the motor end Curare
Viability of sperm in the plate
1-5 days (average of 3 days)
female genital tract Strong/aged cheeses
Myosin associated bands A Band, H Band Cured meats/smoked
Inhibits HCl, increases biliary meats/processed meats
Secretin actions Pickled/fermented foods like
and pancreatic bicarbonate
Sperm motility occurs in Epididymis kimchi
Examples of tyramine-rich
Urine test for ovulation LH Sauces (soy sauce, shrimp
food
Corrective lens: myopia, paste, etc)
Biconcave, convex, cylindrical Soybeans, fava beans
hyperopia, astigmatism
Contractile units of Dried fruits
Sarcomere Alcohol
myocardial cells
Small intestinal contraction Spoiled food
Peristaltic Contraction Sight, smell, though of food
during fasting Cephalic Phase
3,400mg adult males causes HCl secretion
2,600mg adult females - Inhibits all types of adenosine
Normal daily K intake receptors (ARs): A1, A2A, A3,
2,900mg pregnant patients
2,800mg lactating women and A2B (affects brain
PAO2=(FiO2 x (Patmos-PH2O)) – functions such as sleep,
Formula for PAO2 cognition, learning and
(PaCO2/RespQ)
Cytokine involved in Actions of Caffeine memory)
chemotaxis of neutorphils, IL-8 - inhibit phosphodiesterases
basophils and T cells (PDEs) (e.g., PDE1, PDE4,
Formula for Clearance C = UV/P PDE5)
- promote calcium release from
Uses Group Ia afferents,
Nuclear Bag Fibers intracellular stores
detects dynamic changes
Renal afferent arterioles
Interacts with calcium to cause
reflexively responds to
osteoporosis
stretch by contracting in
Disturbs zinc metabolism Myogenic Mechanism
order to maintain constant
MOA of Cadmium Toxicity Decreases plasma copper and
renal blood flow and
ceruloplasmin
subsequently, GFR
Interacts with iron causing
anemia Which instrument is used to Swan-Ganz catheter (balloon-
measure Pulmonary tipped, multi-lumen catheter).
Formula for Urine Anion Gap UAG = Na + K - Cl
Capillary Wedge Pressure This estimates LEFT ATRIAL
Formula for Capacitance C = V/P
(PCWP)? PRESSURE
When hypertensive patient ECF Volume (and BP) increases,
Male pattern baldness is an
is given hypertonic solution ICF Volume Decreases DHT (not testosterone)
effect of
Contains skeletal muscles Pharynx, upper 1/3 esophagus,
Diuretic whose MOA
instead of smooth muscles external anal sphincter HCT
involves the EDT?
Approximate number of
100 billon Muscle with greatest
neurons Cardiac Muscle
number of mitochondria
Muscle fiber involved in
Type I muscle fiber, extrafusal Formula for RBF RBF = (RPF)/(1-Hct)
muscle endurance
Conduction Velocity is most Nerve Diameter (more than
Involved in
dependent on myelination)
interhemispheric Corpus callosum
Decreased ECF and ICF Volume;
communication A man lost in desert would
Increased ECF and ICF
Treatment for malignant have
Dantrolene Osmolarity
hyperthermia
Ejection Fraction Formula EF = SV/EDV. Normal: 55%
Gas that is always an
From red nucleus to
inhibitory NT, can vasodilate Nitric Oxide (NO)
interneurons of lateral
arterioles, involves cGMP? Rubrospinal Tract
spinal cord. Stimulates
Primer pumps of the heart Atria
flexors, inhibits extensors
Longest phase of the cardiac
Reduced ventricular filling Location of GABA C
cycle Retina
Receptors
Relaxes LES, PS, ICV, orad
Greatest resistance in the
stomach, bronchial smooth Vasointestinal Peptide (VIP) Arterioles
blood vessels
muscles
Phase of the cardiac cycle
When rectum is 25% filled
Urge to defecate vs urge to where ventricular volume at Isovolumic relaxation
When urinary bladder is 25%
urinate its lowest
filled
What is the sympathetic
Also called the “second Beta-1
supply of the kidney?
brain” since it utilizes Enteric Nervous System (local
What will increase in Glycolysis, Glycogenesis,
neurons and innnervation/ instrinsic
insulin? Lipogenesis, Protein Synthesis
neurotransmitters similar to innervation of the GIT)
the central nervous system Which part of the ECG
corresponds to ventricular T-Wave
Vasoconstrictor of the
Adenosine repolarization?
afferent arteriole
What is the pacemaker of the
Site of weak androgen Adrenal Cortex Zona SA Node
heart?
secretion Reticularis
Detect changes in BP and GFR
LH is highest during Ovulation What are the functions of the
through Na concentration in
Emotional fainting Vasovagal Syncope macula densa?
the DT lumen
Contracts muscularis Meissner Plexus (Submucosal
What is the action of JG cell? Secrete Renin
mucosa Plexus)
Which vaccines are live? Severe water deprivation:
§ BCG vaccine INCREASED Plasma osmolarity
§ Measles vaccine (due to increased sweating
§ MMR vaccine that causes greater water loss
Severe water deprivation vs.
§ Varicella vaccine than Na loss).
SIADH
§ Rotavirus vaccine SIADH: DECREASED plasma
§ Influenza attenuated vaccine (intranasal) osmolarity (due to increased
§ Typhoid fever (oral) vaccine water reabsorption in the
§ Oral polio vaccine kidneys)
§ Japanese Encephalitis What is reabsorbed in the Na, K, H20, glucose, amino
Which vaccines are inactivated? PCT? acids, Phosphate
• Hepatitis B vaccine What is reabsorbed in the
Na, K, Cl, H2O
• DPT vaccine LH?
• H. influenzae b vaccine What is reabsorbed in the
Na, K, H2O
• Pneumococcal vaccine CCT?
• Hepatitis A vaccine Precursor of Eicosanoids:
Arachidonic Acid
• Meningococcal vaccine ___________
• Influenza trivalent vaccine BMI of obese persons:
>30
• Human papillomavirus vaccine ____________
• Typhoid fever vaccine (IM) Implants into the uterine
Blastocyst
• Rabies vaccine wall
• Inactivated polio vaccine (IPV) What are the adrenal gland
Epi, NE, weak androgens,
Rapid Ascent causing nitrogen hormones from innermost
What is the basis for cortisol, aldosterone
bubbles that block blood to outermost?
decompression sickness? Also known as the
vessels
Increase in VR leading to craniosacral division: Parasympathetic NS
increase in SV: Frank-Starling mechanism __________________
_______________. Has four subunits and
Insulin
Thermoregulatory centers tyrosine kinase activity
for heat loss and heat Target of HIV T-helper Cells
Anterior, Posterior What facilitates the release
conservation respectively:
_________________ of Ach from the synaptic Calcium influx
Hyperaldosteronism (e.g., vesicles?
Metabolic alkalosis (due to autoimmune diseased
Conn syndrome) is
increased H+ secretion to the marked by auto-antibodies
associated with which acid-
urine) against these voltage-gated
base abnormality Lambert-Eaton Myesthenic
In which blood vessel does calcium channels →
Capillaries Syndrome
gas exchange occur? prevents Acetylcholine from
Where is iron absorbed in being released to the
Duodenum nueromuscular junction
the small intestines?
What is the purpose of Compression of Oculocardiac Reflex/Aschner
brown bag in Increase PaCO2 eyeball/EOMS leading to phenomenon/Ashner-Dagnini
hyperventilation? decreased HR Reflex
Phase 4, 0 and 3 of the SA Causes HCl secretion while
Vagovagal Reflex
Node Action potential is Slow Na influx, Ca influx, K food is in stomach
caused by the following influx Stimulation of Beta-2
respectively: ______________ receptors in the lungs will Bronchodilation
Vent Pressure increases but cause _______________.
Vent Volume remains the same 1. Mobility
since Vent P < Aortic Pressure. 2. Stability
3. Posture
What happens during 4. Circulation (e.g., pumping
(+) S1, highest Vent Volume, c
isovolumic contraction? action of blood by cardiac
wave of atrial pressure curve
muscles, maintenance of
SL valves will open at the END BP by smooth muscles in
of this phase the vessels)
Increases size (girth) of 5. Respiration (e.g., via
Exercise Functions of muscles diaphragm)
skeletal muscles
Downregulatdx 6. Digestion
progesterone receptors (its 7. Urination
Progesterone 8. Childbirth
own receptors) and
estrogen receptor 9. Vision
Putamen and anterior horn 10. Organ protection
Motor pathways 11. Temperature regulation
cells are involved in
(85% of body heat comes
Which part of the cardiac
cycle will you see closure of from contracting
Isovolumic contraction, muscles)
AV valves and semilunar
Isovolumic relaxation INACTIVATED at gastric pH
valves respectively that Pepsin
causes S1 and S2? > 5.0
Protein-energy malnutrition Cytokine involved in cancer
Kwashiorkor TNF-⍺ (also called “cachectin”)
with (+) edema: ____________ and septic shock
Needed for development of Allows the absorption of
female (not male) nutrients across the small
Enzyme aromatase intestinal epithelial brush
secondary sex Fatty Acids
characteristics borders by secondary active
transport with sodium:
_______________
Hormone secreted in Motor unit
Insulin
response to GIP
Blocking the H+ secretion of Fine motor movement –
1 motor neuron + all muscle
the gastric parietal cells “small” motor unit
Primary Active Transport (H- fiber it innervates
mean that you will block
K-ATPase exchange pump)
this type of transport: Large/Gross motor movement
_________________. – “large” motor unit
Percentage of cells in whole What percentage of blood
Hematocrit (Normal: 45%)
blood: __________. goes to the kidney from the
22-25%
Involved in regulation of heart (percentage cardiac
Melatonin output of the kidneys)?
body clock: ______________.
Site of fertilization Ampulla Normal EF 55%
Appetite and Satiety centers I + T + E? VC
are found in which part of GABA A: ionotropic; ubiquitous
Lateral, Ventromedial
the Hypothalamus GABA B: metabotropic
respectively? Types of GABA receptors GABA C: ionotropic; enriched
• Differentiation of epididymis, in the retina compared to other
• vas deferens, & seminal parts of the CNS
vesicles Gastric FUNDUS (location of
Intrinsic factor is secreted
• Descent of testes CHIEF CELLS that produces
in this part of the stomach
• ↑ bone and muscle mass HCl and IF)
• ↑ BMR Living in high altitude (e.g., Shift to the right of the O2-HgB
• Pubertal growth spurt Baguio) can cause dissociation curve
What are the actions of • Epiphyseal closure Nucleus (since it is the one that
testosterone? • Growth of penis & seminal controls and regulates carries the genes that is used in
vesicles cellular activities the production of cellular
• Deepening of voice proteins like enzymes)
• Spermatogenesis PAH Clearance 10% due to RPF to kidney
• Negative feedback on underestimates true RPF by regions that do not filter and
anterior how many percent? secrete PAH
pituitary Increased intravascular
• Libido Triggers for ANP secretion volume that leads to increased
Self-limiting mechanism to left atrial pressure
control hormonal effect: Negative Feedback Bronchiole capable of gas
Respiratory bronchiole
______________ exchange
Used for night vision: Last bronchiole not capable
Rods Terminal bronchiole
_________. of gas exchange
Which part of the Benign proteinuria Orthostatic proteinuria
glomerulus prevents Stimulates glycogenolysis Glucagon
Basement Membrane
albumin from being Stimulates potassium influx Insulin
filtered? Nystagmus (Direction of
What are your Nystagmus: same direction as
C3a, C4a, C5a After a rapid spin to the
anaphylatoxins? head rotation
right, eyes snaps quickly in
Triggers of the Postrotatory Nystagmus:
Emetics the same direction
Chemoreceptor Trigger occurs in opposite direction of
Radiation the head rotation)
Zone found in the area
Vestibular stimulation
postrema Gastrinoma associated with
Zollinger-Ellison Syndrome
Peripheral Chemoreceptors in peptic ulcer disease
Aortic Bodies, Carotid Bodies: May spark hypertensive
MAOIs and tyramine-rich food
Chemoreceptors react to hypoxemia (main), crisis
which stimulus? hypercarbia, acidosis Anemia in chronic kidney Due to Low EPO synthesis and
Central Chemoreceptors in disease secretion
medulla: CSF H+ Halothane (also: inhaled
Pulmonary Vein à L Atrium à general anesthesia, esflurare,
L Ventricle à Aorta à other enflurane, ether, isoflurane,
Triggers of malignant
arteries à arterioles à sevoflurane)
hyperthermia
Blood Pathway from capillaries à veins à SVC/IVC succinylcholine
pulmonary vein à R atrium à R ventricle à Heat stress
Pulmonary Artery à vigorous exercise
Pulmonary Arteriole à Diuretic used in the
Pulmonary Capillaries treatment of acute Acetazolamide
Which nerve when damage mountain sickness
cause Superior Gluteal nerve HALF-LIFE: 2 MINUTES
gluteal/Trendelenberg gait? (short compared to renin,
Norepinephrine
No action potential possible aldosterone, corticosterone,
even with increased Absolute Refractory Period and DHEA
stimulus: _______________. Better “air-conditioning” if
In comparison to skeletal Inhalation through nostrils through nostrils
muscle cells, cardiac muscle Sarcosomes (large specialized vs. mouth (humidification and warming
cells contain more mitochondria) occurs as air enters)
____________. Flexor-withdrawal reflex.
What is the formula for Golgi-Tendon/clasp-
HR x SV
cardiac output? POLYSYNAPTIC reflex knife/inverse stretch reflex is
Usually 7, but maybe up to 18. DISYNAPTIC. Stretch/Knee-
How many renal pyramid
It consists of tubules that jerk reflex is MONOSYMPATIC
(malphigian pyramids) are
transport urin from the renal
there in each kidney
cortex to the renal papilla.
Responsible for lactation In comparison to term INCREASED pulmonary
amenorrhea (prevents Prolactin (MOA: inhibition of infant, Pre-term infant has vascular resistance, pulmonary
pregnancy during first six GnRH prevents LH surge and artery pressure (PAP),
months of regular consequently, ovulation) pulmonary capillary
breastfeeding) hydrostatic pressure, pressure
Physiologic Blind Spot Optic Disc gradient from pulmonary
Action potential is artery to the aorta
inevitable at this membrane Threshold DECREASED Pulmonary Blood
potential Flow
binds myosin to Z lines, Functions of blood-brain Maintain constant
binds Z lines to M line, Titin (largest protein in the barrier (BBB) environment for neurons
determines normal stiffness body)
of the ventricular muscle) Prevents escape of
stabilizes sarcolemma and neurotransmitters
prevents contraction-
induced rupture (Pre-Test Drugs penetrate BBB to
Dystrophin various degrees (easier if lipid-
149: binds actin to beta-
dystroglycan in the soluble and nonionized)
sarcolemma)
Lack of ATP prevents Has the greatest percentage Beta Cells (produces INSULIN)
Basis for rigor mortis unbinding of myosin heads of cells in the Islets of
from actin binding sites Langerhans
stimulate the Sertoli Cells to Respiratory quotient High carbohydrate diet
secrete Androgen-Binding increases in
FSH Mechanism of penile Nitric Oxide à Guanylate
Protein (ABP) and not
inhibin erection cyclase à cGMP à vascular
↑ PaO2 → ↓ pulmonary smooth muscle relaxation à
Baby’s first breath causes vascular resistance, increased vasodilation à penile erection
systemic vascular resistance decreases food intake Leptin
(through its anorexigenic
effect) and may also
increase energy
expenditure.
Reason why percentage of Glomerulotubular Balance
solute (e.g., Na or Glucose)
reabsorbed in the tubules
will remain the same
despite changes in GFR
TOPNOTCH MOONLIGHTING AND PRE-RESIDENCY SEMINAR

After you pass your med boards, we would like to invite you to 3. Correctly interpret ECG, Chest-Xray, CT-Scan, MRI, and
join the Topnotch Moonlight and Pre-Residency Seminar. It will teach you common laboratory findings in the moonlighting setting.
the knowledge, attitudes and skills needed as a General Physician (CHED Program Outcome 1)
(especially as a moonlighter and resident), provide you with information
4. Discuss basic leadership strategies and principles applicable
on various career choices, and teach you things important in life but may
not have been taught during med school. to the health care setting. (CHED Program Outcome 3)
By tradition, this seminar will start 10 days after the last day of 5. Apply principles in synergizing their work with other
the Med Boards. (this would be tentatively on November 26-December members of the health care team (e.g. nurse, med tech).
14, 2020 ONLINE) for P5,500. An optional PHA-Accredited BLS-ACLS (CHED Program Outcome 5)
course (conducted by PGH Sagip Foundation – PGH cardio fellows are the 6. Discuss guidelines on how to practice in the moonlighting
teachers) – is also held for an additional P4,500. and residency setting ethically and in accordance with
For the clinical skills component of the program (e.g., suturing, Philippine laws. (CHED Program Outcomes 8,9)
splinting and intubation), we would give a demo online, but you may
7. Discuss strategies in applying to local and international
participate in the immediate onsite Topnotch moonlighting and pre-
residency seminar (e.g., if the pandemic is over, and we conduct this residency programs, and other career opportunities offered
seminar in September 2021, you can participate in the clinical skills for general physicians here and abroad. (CHED Program
component onsite also, even if you have taken the online version for Nov Outcome 7, 10)
2020. This will allow you to actually practice and be tested on the clinical 8. Design a research proposal in collaboration with their
skills under the guidance of a specialist consultant (general surgeon, participants. (CHED Program Outcome 4)
anesthesiologist, orthopedic surgeon) 9. Write career, family and personal plans taking into
consideration their niche in the systems-based approach to
Here’s the schedule for LAST BATCH (September 2019) to give
healthcare, their own social accountability, interests and
you an idea what’s in store during this seminar:
dreams in life. (CHED Program Outcome 6, 10)
TOPNOTCH ONLINE MOONLIGHTING AND PRE-RESIDENCY 10. Write their own Resume in the correct format and style.
SEMINAR (CHED Program Outcome 2, 7)
SCHEDULE
DECEMBER 2020 DAY 1 – DECEMBER 1, TUESDAY- INTRO TO MOONLIGHTING
8:00-10:00am- Opening Remarks and Orientation
LEARNING OUTCOMES FOR THE TOPNOTCH MOONLIGHTING 10:00am-11:00am- Awarding of the Top 10
AND PRE-RESIDENCY SEMINAR OUTCOMES
At the end of the two-week training seminar, the licensed
Topnotch MD must be able to:
1. Create appropriate management plans of common emergent,
out-patient, ward and surgical cases seen by a General
Practitioner in the moonlighting setting. (CHED Program
Outcomes 1, 2, 3, 6, 7)
2. Correctly perform procedures expected of a General
Practitioner (intubations, casting/splinting, suturing) with
confidence. (CHED Program Outcome 1)
DAY 2- DECEMBER 2, WEDNESDAY- MANAGEMENT OF 11:00am-12:00nn LUNCH
EMERGENCY AND TRAUMA CASES 12nn-1pm- Road to Alternative Medicine– RYAN DALMAN, MD
8:00am- 8:15am - Introduction to the Day’s Activities 1:00pm-2:00pm – Setting Up a Clinic from an MD-MBA standpoint-
8:15am-11:00am- Diagnosis and Management of ER Cases (By ER
Med Specialist DAY 7- DECEMBER 8, TUESDAY
1. How to Run a Code OB-GYN FOR THE MOONLIGHTER;; INTRODUCTION TO THE
2. How to Give Your Inotropes DOCTORS TO THE BARRIOS; TIPS FOR TAKING THE
3. Approach to Hypotension AUSTRALIAN AND US MEDICAL LICENSURE EXAMS
4. Approach to the Unconscious Patient 8:00am- 8:15am - Introduction to the Day’s Activities
5. Alcohol Intoxication 8:15am- 11:00am- OB-GYN for Moonlighters (BY OB-GYN)
6. Seizures 1. Basic Principles in Prenatal Care
7. Anaphylaxis 2. Delivering babies in the Hospital Setting
8. Electrocution 3. Delivering babies in the Emergency, Non-Hospital
9. Drowning Setting (e.g. at home)
4. Management of STDs
DAY 3- DECEMBER 3, THURSDAY- FINANCIAL WEALTH AND 5. Contraception
HEALTH FOR THE MOONLIGHTER AND THE RESIDENT; 11-12:00nn- Introduction to the Doctors to the Barrios Experience
PREPARING FOR AN INTERVIEW 12:00-1pm- LUNCH
8:00am- 8:15am - Introduction to the Day’s Activities 1:00-2:00pm- Tips on Taking the Australian Medical Exam
8:15-11:00am- Stocks and Investments for the Busy Resident and 2:00-3:00pm- Tips on Taking the USMLE
Moonlighter (by JOHN FRANCIS LEEHOK, MD) a. Basic information about the USMLE– how it’s
11:00am-12nn- How to Write Proper Resume and Preparing for conducted, cost, where and how to apply
your Interview (RAQUEL T. LIM, MD b. How to Study for the Exam; Tips on how to be matched
DAY 4- DECEMBER 4, FRIDAY- SURGERY FOR MOONLIGHTERS DAY 8- DECEMBER 9, WEDNESDAY

AND SUTURING WORKSHOP PEDIATRICS FOR MOONLIGHTERS; INTRODUCTION TO AFP
8:00am- 8:15am - Introduction to the Day’s Activities MEDICAL CORPS; TRENDS IN AESTHETIC MEDICINE
8:15am-11:00am – Basic Surgery (By Surgeon) 8:00am- 8:15am - Introduction to the Day’s Activities
1. How to give ATS, TeANA properly and appropriately 8:15am- 12:00nn- Diagnosis and Management of Pediatric Cases
2. Managing V-A Injuries (by Pediatrician)
3. Managing Gunshot and Stab Wound Injuries 1. Fluid Management (Computation of Fluids, when to fast
4. Managing Burn Patients drip, etc.)
5. Tips in mass excision, I and D, ungiectomy 2. Approach to Fever
6. Proper techniques in Circumcision 3. Approach to Pediatric Rashes
7. Proper techniques in the suturing of Scalp, Face, 4. Approach to Diarrhea, Vomiting
Extremities 5. Approach to Abdominal Pain (how to differentiate
8. Chest Tube Insertion – Video Only; along with tips from appendicitis vs colic vs cholecystitis vs PUD, etc)
Dr.Antonio 6. Dengue
9. Lumbar Tap Insertion – Video Only; along with tips 7. Typhoid
from Dr.Antonio 8. Allergies
11:00am-12nn - Basic Suturing Technique Workshop 9. Ascariasis and other Helminthic Infections
Materials: 10. Acute Otitis Media/Externa
*suturing set including scalpel, needle holder, scissors, expired 11. Conjunctivitis
sutures (with needle) 12. Drug computation of common Pediatric Drugs (
especially diphenhydramine, paracetamol, diazepam,
DECEMBER 5, SATURDAY- NO CLASSES common antibiotics)
12:00pm-1:00pm LUNCH
DAY 5- DECEMBER 6, SUNDAY 1:00pm-2:00pm- Entering the Military Life (AFP Doctor)
8:00am-12:00nn - How to Handle Common Ortho Emergencies 2:00pm-3:00pm- Trends in Aesthetic Medicine
and Casting workshop (By Orthopedic Surgeon)
Materials: DAY 9- DECEMBER 10, THURSDAY- RADIOLOGIC DIAGNOSIS;
1. Elastic bandage, 6 inches- 2 pcs RESEARCH IDEAS; ETHICS FOR MOONLIGHTERS; ADULTING
2. Elastic bandage: 3 inches 1 pc 101
3. Wadding sheet 6 inches 1 pc 8:00am- 8:15am - Introduction to the Day’s Activities
4. Plaster of Paris 6 inches: 2 pcs 8:15am-10:00am- CXR and Fracture Interpretation, Basic CT Scan
5. Plaster of Paris 4 inches: 2 pcs Interpretation (by Radiologist)
6. Leukopast 4 inches: 1 10:00am-11:00am- How to create research idea, conduct optimal
7. String 1 foot literature review, and write a research proposal
11:00am-12nn- Ethics for Moonlighters, Residents and
DAY 6- DECEMBER 7, MONDAY- LEGAL ASPECT OF Consultants
MOONLIGHTING; ROAD TO ALTERNATIVE MEDICINE; 12:00-1:00pm- LUNCH
SETTING-UP YOUR OWN CLINIC FROM AN MD-MBA 1:00-2:00pm- Adulting 101: Your guide to getting your PTR
STANDPOINT license, SSS, Philhealth and paying your taxes
8:00am- 8:15am - Introduction to the Day’s Activities
8:15am-11:00am - Legal and Ethical side of Moonlighting (by DAY 10- DECEMBER 11, FRIDAY- I.M. FOR MOONLIGHTERS;
doctor-lawyer ALBERT REBOSA, MD) ESSENTIAL MOONLIGHTING SKILLS; LABORATORY AND ECG
1. Legal Basis for Moonlighting INTERPRETATION; MANAGEMENT OF NEURO EMERGENCIES
2. Written and Unwritten Rules of Moonlighting 8:00am- 8:15am - Introduction to the Day’s Activities
3. How to Avoid Lawsuits based on Actual Cases in the 8:15am-12:00pm- Diagnosis and Management of Adult Cases (By
Philippines for the level of moonlighter and hospital Cardio-intensivist)
resident 1. Pneumonia, URTIs, Asthma, COPD
4. How to Write a Proper Medical Certificate and Death 2. UTIs
Certificate 3. DM
5. How to Properly Charge Patients for Services Rendered 4. HPN
6. How to Transfer a Patient to Another Hospital Properly 5. Approach to the Jaundiced Patient
7. How to Deal with Various Health Cards (Practical Tips) 6. Approach to Poisons and Snakebites
8. How to Legally Deal with your co-workers – Nurses, 7. Approach to Electrolyte Abnormalities (Hypo- and
Fellow Moonlighters, Consultants, Hospital Staff Hyper-kalemia, Hypo- and Hypercalcemia, etc)
8. Pain Medications (indications, dosage,
contraindications, side effects)
9. Management of Neuro Emergencies
12:00-1:00pm- LUNCH
1:00pm-2:00pm- Basic ECG interpretation
2:00-3:00pm- Basic Lab interpretation
DECEMBER 12- SATURDAY- NO CLASSES
DAY 11- DECEMBER 13- SUNDAY- TECHNIQUES OF

ENDOTRACHEAL INTUBATION
8:15am-12:00nn- Endotracheal Intubation Workshop (including
indications, techniques, post-intubation orders) (by
Anesthesiologist)
DAY 12- DECEMBER 14, MONDAY- MOONLIGHTERS AND
RESIDENCY PANEL TALK; FINDING YOUR NICHE IN THE
MEDICAL FIELD
8:15am-9:00am-Panel Discussion- Residents talk about their
residency experiences
9:00am-10:00am- Panel Discussion- Different Moonlighting
Experiences of 3 Moonlighting Physicians
10:00-12:00nn- Leadership For MDs and Finding Your Niche In
Medicine (by ENRICO PAOLO C. BANZUELA,MD)

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TOPNOTCH MEDICAL BOARD PREP PHYSIOLOGY MAIN DIGITAL HANDOUT BY ENRICO PAOLO C.

• Studded with the following proteins:

© Topnotch Medical Board Prep

externally – those peripheral proteins floating around gives the cell a

• Movement of different substances across the cell membrane:

For the guide question above:

Because all secondary active transports (e.g. SGLT-1), relies on the

through simple diffusion in real life. • Driving Force: Osmotic Pressure

If you inhibit the primary transport Na-K-ATPase pump, you will

inhibited by abolishing the usual Na+ gradient across the cell 𝝅 = 𝒈 × 𝑪 × 𝑹𝑻

• Osmotic pressure exerted by proteins: Oncotic Pressure or

Iba ang osmotic pressure sa effective osmotic pressure (see these

DIFFUSION POTENTIAL AND EQUILIBRIUM POTENTIAL

© Topnotch Medical Board Prep

K+ is positively charged. It will move from Solution A to B (high

RESTING MEMBRANE POTENTIAL

Undershoot • Occurs during an AP when

A newly developed local anesthetic blocks Na+ channels in nerves.

Lidocaine blocks neuronal voltage-gated sodium channels responsible for

• Done through local currents to adjacent areas of the membrane

Remember – you can inhibit an AP several ways – cause influx, Cl-

© Topnotch Medical Board Prep

✔GUIDE QUESTION NEUROTRANSMITTER RECEPTORS

8. Organ protection (e.g. anterior abdominal wall muscles) Cardiac Muscles

MUSCLE TYPES SARCOMERE

THICK FILAMENTS THIN FILAMENTS

© Topnotch Medical Board Prep

© Topnotch Medical Board Prep

• Z lines (“Zwischenscheibe”): borders

• Dystrophin: stabilizes sarcolemma and prevents contraction-

9. Myosin heads binds to First Binding Site in Actin. ✔GUIDE QUESTIONS

In skeletal muscle, which of the following events occurs before

Blocks reuptake of Choline

contractions CALCIUM REGULATION OF CARDIAC MUSCLES

1.8 SMOOTH MUSCLES

© Topnotch Medical Board Prep

In the sinoatrial (SA) node, phase 4 depolarization (pacemaker

© Topnotch Medical Board Prep

1.9 COMPARISON OF SKELETAL MUSCLES, SMOOTH MUSCLES AND CARDIAC MUSCLES

✔GUIDE QUESTIONS NERVOUS SYSTEM

© Topnotch Medical Board Prep.

(B) Adrenergic β1 receptors Phenoxybenzamine is an alpha-1 antagonist. Alpha-1 MOA involves

Remember: Beta-2 will always cause smooth muscle RELAXATION

AND CEREBRAL CORTEX ✔GUIDE QUESTION

Coughing & Vomiting Centers

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• Stimulated by mechanical, • Stimulated by mechanical,

SPECIAL NOTES ON PAIN

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LENS OF THE EYE

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✔GUIDE QUESTIONS PHYSIOLOGIC BLIND SPOT/BLIND SPOT

Cutting which structure on the right-side causes blindness in the

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A mnemonic to help you: Simple Cells: Bars of light Lang. Complex:

the cells (since endolymph is rich in K+ compared to ICF)

✔GUIDE QUESTION Mnemonic: where you head turns, is where depolarization

• Olfactory Epithelium innervated by:

TASTE MOA OF MUSCLE SPINDLE (INTRAFUSAL FIBERS)

2.3 MOTOR SYSTEMS

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✔GUIDE QUESTIONS DISTRIBUTION ACTIONS

Pontine flexors and

CORTICOSPINAL (PYRAMIDAL) TRACT