Physiology Study Materials

APPOLO ACADEMYA 1
PHYSIOLOGY & BIOCHEMISTRY
APPOLO ACADEMYA
for UPSC, PSC, RO, SRF, JRF, AIIMS, AIAPGET
Study material
CONTENTS
GENERAL PHYSIOLOGY
• General Physiology
• Concepts in physiology
• Cell membrane & Transport proteins
• Transport process
NERVE MUSCLE PHYSIOLOGY
• Membrane potential
• Action potential
• Nerve
• Muscle
GASTRO INTESTINAL TRACT
BLOOD PHYSIOLOGY
CARDIO VASCULAR SYSTEM
• Conducting system of Heart

• ECG
• Cardiac cycle
• Cardiac output
• Circulation
RESPIRATORY SYSTEM
EXCRETORY SYSTEM
ENDOCRINE SYSTEM
REPRODUCTIVE SYSTEM
• Female Reproductive System

• Male Reproductive System
THE NERVOUS SYSTEM
• Introductions to CNS
• Sensory System
• Motor System
• Higher functions
• ANS
• Special senses
BIOCHEMISTRY
APPOLO ACADEMYA 2
GENERAL PHYSIOLOGY
BODY FLUID COMPARTMENTS
• Total Body water = F 0.6 x Body weight = 42L (70 Kg)

• ICF = 0.4 * Body Weight = 28L
• ECF = 0.2 * Body weight = 14L
• Interstitial Fluid = 0.75 x ECF = 11L
• Plasma = 0.25 x ECF = 3L
• Blood = 8% of Body weight
• Plasma = 5% of Body weight
MEASUREMENT OF BODY FLUIDS
INDICATOR DILUTION METHOD / DYE DILUTLON METHOD = STEWART-HAMILTON DYE

DILUTION METHOD
PREREQUISITES
1. Dye Should be evenly distributed

2. Dye Should not leave the compartment
• V = I/C where, V = Volume of ECF, I = Initial volume of dye injected, C = Concentration of dye
• V = (I-A)/C, where A = Amount of dye that left the compartment
DEHYDRATION
1. ISOTONIC DEHYDRATION
Water & Na ion lost in equal proportions
NO Shift OF H2O due to isotonicity of ECF
CONDITIONS: GI Fluid Loss, Burns, Haemorrhage
2. HYPERTONIC DEHYDRATION
H2O lost from ECF
ECF becomes hypertonic
H2O moves From ICF to ECF
ICV volume shrunken secondarily
CONDITIONS: DM, DI, Chronic Alcoholism
3. HYPOTONIC DEHYDRATION
H2O & Na ion lost [ Na ion loss is much higher]
ECF becomes hypotonic
ECF H2O Shifts Into ICF
ICF Volume increased secondarily
CONDITIONS: Primary hypoaldnosteronism, Primary hypoadrenocorticolism
OVER HYDRATLON / VOLUME EXPANSION STATES
• ISOTONIC OVERHYDRATION: administration of Oral/ IV isotonic Saline

• HYPERTONIC OVERHYDRATION: administration of Oral / IV hypertonic saline
• HYPOTONIC OVER HYDRATION:
CONDITION: SIADH [Syndrome of Inappropriate & ADH secretion], occurs in Surgery
& Stress - Increased Volume causes increased Atrial Filling pressure causes increased
ANP causes Natriuresis & Diuresis [Euvolemic Hyponatremia]
If The Osmolarity of consumed Fluid is <1200 Mosm/L = Hypertonic Overhydration
If the Osmolarity of Consumed Fluid is >1200 Mosm/L = Hypertonic Dehydration.
ANP, BNP & CNP Synthesized by HEART
APPOLO ACADEMYA 3
CONCEPTS IN PHYSIOLOGY
ENDOLYMPH: ECF which resembles ICF in body, has increased concentration of K+
DIFFUSION occurs due to electric gradient [along with concentration gradient]
ELECTRIC GRADIENT: ECF K+ concentration = 4mEq/L, ICF K+ concentration = 145mEq/L
MILIEU INTERIOR [ECF] = internal Environment of body.
HOMEOSTASLS: maintaining the constancy / Stability in milieu Interior
MILIEU INTERIOR coined by CLAUDE BERNARD & WALTER F CANNON
HOMEOSTATIC REGULATORY MECHANLGMS
• FEED FORWARD REGULATION — No time lag

• FEED BACK REGULATION – Time lag present
FEED FORWARD MECHANISMS
• Controller Anticipates Changes & takes a desired action

• No time lag present
• Ex: 1. Cephalic phase of gastric acid secretion 2. Ventilatory drive increased in exercise
FEED BACK MECHANISMS
• Change occur in Controlled variable & that Change is fed back to controller & then the Controller takes
action
• Time lag present
• TYPES:
o NEGATIVE FEED BACK
o POSITIVE FEED BACK
1. NEGATIVE FEED BACK
a. Controller does the opposite
b. Change is negated OR error is minimised
c. Measure of efficiency is GAIN
d. Ex. Kidney Body Fluid mechanism (has infinite gain), Temperature Regulation, Baroreceptor
mechanism
2. POSITIVE FEED BACK MECHANISM / Vicious Cycle
a. Controller does the game in direction of error & Error is amplified
b. Ex. Circulatory shock (2nd stage), Oxytocin In parturition, Platelet Plug / clot formation, Action
potential from RMP to threshold, LH Surge leading to Ovulation, Bladder Filling =
MICTURITION, HEAD's PARADOXICAL REFLEX (distension leads to more distension, occurs
at birth), Vomiting
c. All these positive Feedback will end with negative feedback
d. Positive Feedback is part of Larger Scheme of negative Feedback process Ex. Oxytocin in
parturition, Platelet plug & clot formation.
CELL MEMBRANE & TRANSPORT PROTEINS
CELL MEMBRANE
FLULD MOSATC MODEL
• Most accepted model [SINGER NICOLSEN MODEL]

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• Lipid bilayer with Protein embedded in it

• Micro needle injury healed by - HYDROPHOBIC INTERACTIONS [Self Sealing]
• Membrane fluidity is determined by
Cholesterol
• Asymmetry of the Membrane due to
CARBOHYDRATES
COMPOSITION
• Lipid layer: Occupy 42% of surface area

o Phospholipid:
Maximum Concentration & main constituent of Lipids
Contains
ontains Aminophospholipids, sphingomyelins, phosphatidylcholine,
phosphatidyletholamine, phosphatidylglycerol, phosphatidylserine and
phosphatidyletholamine,
phosphatidylinositol
Consists
onsists of 2 layers:
• Head / Polar end is hydrophilic which is outer part
• Tail / Non-polar
polar end is hydrophobic which is inner part
o Cholesterol
Fluidity Buffer of membrane ~ responsible forr Membrane Fluidity
Arranged in between the phospholipid molecules.
Helps to maintain structural integrity of phospholipid layer
• Protein layer
o Concentration varies from cell to cell, from time to time even in the same membrane.
o Types:
o Integral or transmembrane
transmem proteins
Pass through entire thickness of cell membrane from one side to the other side.
Examples of integral protein: Cell adhesion proteins, Cell junction proteins, Some
carrier (transport) proteins, Channel proteins, Some hormone receptors, Antigens,
Antig
Some enzymes.
o Peripheral proteins or peripheral membrane proteins
Partially embedded in the outer and inner surfaces of the cell membrane and do not
penetrate the cell membrane.
Examples of peripheral proteins: Proteins of cytoskeleton, Some carrier (transport)
proteins, Some enzymes
• CARBOHYDRATES - Occupy 3% Surface area, provide symmetry, responsible for immune reactions
• By weight, Lipid : Protein – 1:1
FUNCTION
UNCTION OF CELLULAR ORGANELLES:
ORGANELLES
• Rough endoplasmic reticulum
1. Synthesis of proteins
2. Degradation
tion of worn out
• Smooth endoplasmic reticulum
1. Synthesis of lipids and steroids
2. Role in cellular metabolism
3. Storage and metabolism of calcium
4. Catabolism and detoxification of toxic substances
• Golgi apparatus
1. Processing, packaging, labelling and delivery of proteins and lipids
• Lysosomes
1. Degradation of macromolecules
2. Degradation of worn out organelles
3. Removal of excess of secretory products
4. Secretion of perforin, granzymes, melanin and serotonin
• Peroxisomes
1. Breakdown of excess fatty acids
2. Detoxification of hydrogen peroxide and other metabolic products
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3. Oxygen utilization
4. Acceleration of gluconeogenesis
5. Degradation of purine to uric acid
6. Role in the formation of myelin
7. Role in the formation of bile acids
• Centrosome
1. Movement of chromosomes during cell division
• Mitochondria
1. Production of energy
2. Synthesis of ATP
3. Initiation of apoptosis
• Ribosomes
1. Synthesis of proteins
• Cytoskeleton
1. Determination of shape of the cell
2. Stability of cell shape
3. Cellular movements
• Nucleus
1. Control of all activities of the cell
2. Synthesis of RNA
3. Sending genetic instruction to cytoplasm for protein synthesis
4. Formation of subunits of ribosomes
5. Control of cell division
6. Storage of hereditary information
informati in genes (DNA)
CELL JUNCTIONS
TIGHT JUNCTIONS [ZONULA

OCCLUDENS]
• Selectively permeable
• Found at - Blood Brain Barrier,
Barri
Lining of Gut
• dins,
Proteins involved – Claudin
Occludins, JAMS
AMS [Junctional
Adhesive molecules]
ADHERING JUNCTIONS
• Responsible for coherent

epithelium formation
• Responsible for identification
ion of
apical & basolateral sides
es of a
Cell
TRANSPORT PROTEINS IN THE

MEMBRANE
• PORES - always Open,, responsible for H2O Movement

• CHANNELS - intermittently
intermittent Open, carry out simple diffusion
o Types:
LEAKY CHANNELS – Na+ Leaky channel present on all cells)
GATED CHANNELS
• VOLTAGE GATED ION CHANNELS - Na channel in nerve membranes
• LIGAND GATED ION CHANNELS – GABAA, Nicotinic Acetyl choline
Receptor
APPOLO ACADEMYA 6
• CYCLIC NUCLEOTIDE GATED CHANNEL (cAMP, cGMP) - G Protein

coupled Receptor involved, Ex. GABAB, Muscarinic ACh Receptor
• TIME GATED CHANNELS – Ex. Slow Ca++ channels in heart, K+
channels in Nerve Membrane
• MECHANICALLY GATED CHANNELS – Ex. Touch Receptors In the
Skin
• CHEMICAL GATED CHANNELS – Ex. Hypoxia Causes vasodilation
everywhere, but vasoconstriction in lungs.
• CARRIERS - Never Open, involved in
o Facilitated diffusions (Uniport) – Ex. Glucose transport in all cells by GLUT except GIT &
Kidney occurs by Symport by SGLT.
o 20 active transport (Symport / antiport) – Ex. Glucose transport in GIT & Kidney.
• Pumps - directly uses ATPs, carries 10 active transport. Ex. Na+K+ ATP pump in all membranes.
TRANSPORT PROCESSES
TYPES
• ACROSS MEMBRANE:
o Endocytosis: occur for large molecules, particles, foreign substances
Types:
• Phagocytosis: Cell eating Ex. Bacteria entry Into neutrophil
• Pinocytosis Cell drinking Ex. Soluble proteins enters the cell
o Exocytosis: Cell vomiting - Reversed pinocytosis of liquid
Types:
• Constitutive exocytosis: Ex: Mucus Secretion, Ig Secretion by plasma Cell
• Regulated exocytosis: Ex: Neurotransmitter Secretion at Synapse, Hormone
Secretion
All types OF Exocytosis need increased intracytoplasmic Ca++ Except PTH Secretion
& Renin Secretion by JG cell
• THROUGH MEMBRANE: Osmosis, Diffusion, Active Transport
o Types:
Osmosis: H2O moves from low Solute to high Solute Concentration
• Occurs in CSF absorption, Capillary filtration, Descending limb of Loop of
Henle.
• OSMOLARITY = No. of Solute / Solution in it
• OSMOLALITY = Mass of Solute / Kg of water
Diffusion: Passive transport (no ATP needed)
• Types:
o Simple diffusion: Lipid soluble substances diffuses by lipid bilayer
& water soluble substances through channel.
FICK’s law of simple diffusion: J = DA * C/d where, J =
flux, D = Diffusion coefficient, A = Surface area, C =
Concentration gradient, d = Thickness of membrane or
distance
o Facilitated diffusion: Carrier mediated,
Active transport: Needs ATP.
• Types:
o 1° Active transport: carried by pumps, ATP used directly, Ex. Na+
K+ Pump, SERCA Pump
o 2° Active transport: achieved by carrier, ATP used indirectly
Types:
APPOLO ACADEMYA 7
Symport / Co-transport: Ex. SGLT for Glucose entry to

GIT & Kidney cells, Transport of Amino acids
Antiport / Countertransport / Exchange: Ex. Sodium-
Calcium exchanger, Cl-HCO3- exchanger in RBC
membrane
o All 2° Active transport is dependent on 1° Active transport.
• ACROSS MEMBRANE: vesicular transport also called CYTOPEMPSIS
REGULATION OF ACID-BASE BALANCE
REGULATION OF ACID-BASE BALANCE BY ACID-BASE BUFFER SYSTEM
Body fluids have three types of buffer systems, which act under different conditions:
1. Bicarbonate buffer system – acts in ECF
2. Phosphate buffer system – acts in ICF & tubular fluid as it is rich in phosphates
3. Protein buffer system – acts in blood both erythrocytes & plasma
REGULATION OF ACID-BASE BALANCE BY RESPIRATORY SYSTEM

Lungs play an important role in the maintenance of acid-base balance by removing CO2. This CO2
combines with water to form carbonic acid. Since carbonic acid is unstable, it splits into H+ and HCO3-
. Increased H+ concentration increases the pulmonary ventilation (hyperventilation) by acting through
the chemoreceptors.
Respiratory acidosis –
o Caused by alveolar hypoventilation e.g. in:
Bronchitis
Emphysema
Pneumonia
Lung fibrosis
Flail chest, kyphosis & scoliosis or mix
Poliomyelitis & respiratory paralysis
o Normal partial pressure of CO2 in arterial blood is about 40 mm Hg. When it increases above
60 mm Hg acidosis occurs.
Respiratory alkalosis –
o Caused by alveolar hyperventilation e.g. in:
High altitude
Severe anemia
Pulmonary diseases from oedema & embolism
Voluntary hyperventilation from emotional trauma
Cerebral disturbances causing increased respiratory drive
o When partial pressure of CO2 in arterial blood falls below 20 mm Hg alkalosis occurs.
REGULATION OF ACID-BASE BALANCE BY RENAL SYSTEM

Kidney maintains the acid-base balance of the body by the secretion of H+ and by the retention &
reabsorbing of HCO3-.
METABOLIC ACIDOSIS: acid-base imbalance characterized by excess accumulation of organic acids which
naturally occurs (lactic acid, ketoacids and uric acid) in the body, caused by abnormal metabolic processes.
Caused by:
Lactic acidosis from Circulatory shock
Ketoacidosis in DM
Uric acidosis in renal failure
Renal tubular acidosis
Loss of HCO3- due to diarrhoea, pancreatic, intestinal & biliary fistula.
METABOLIC ALKALOSIS: acid-base imbalance caused by loss of excess H+ resulting in increased HCO3
concentration. Caused by vomiting, congenital diarrhoea, Cushing syndrome, Conn’s syndrome, Diuretic
therapy.
APPOLO ACADEMYA 8
NERVE MUSCLE PHYSIOLOGY
MEMBRANE POTENTIAL
RMP (Resting membrane potential)
MEMBRANE POTENTIAL: due to excess negative charges which create negative potential
Red cells, Epithelial Cells = — 6 to — 2mv

Smooth muscle cells = — 35 to — 45mv
Pacemaker cells — SA Node = — 55 to — 65mv
Nerve = — 70mv
Skeletal Muscle & purkinjee fibres — 90mv
All these cells are surrounded by Same ECF (potential is ‘0’) Except HAIR CELLS IN COCHLEA surrounded
by Endolymph (ECF) which resembles ICF because it has high ECF Concentration. ENDOCOCHLERR
POTENTIAL is 80 mv. Transmembrane voltage difference is highest in body = 150mv)
RMP (RESTING MEMBRANE POTENTIAL) applied only for nerve & muscle (excitable tissues)
RMP for nerve is —70mv.

RMP for muscle is —90mv.
NERNST EQUATION calculates individual equilibrium potential of an ion.
EMF (mv) = +-61 * Log C1/C2
GOLDMAN’S CONSTANT FIELD EQUATTON (GHK EQUATION): When all 3 ions, Na+, K+, Cl- move
and reach equilibrium, charge will be calculated by GHK Equation. It is dependent on -
Concentration gradient of 3 ions

Membrane permeability
Polarity of Charge
EXCITATION & ACTION POTENTIAL
ACTION POTENTLAL
STIMULUS — PROPERTIES
INTENSITY:
o Should be rapidly rising
o Slowly rising Stimulus intensity result in Membrane Accommodation.
DURATION:
o Should be OPTIMUM enough
RHEOBASE = minimum Strength of stimulus that can excite the tissue.
CHRONAXIE = Time taken by tissue to excite, when the Stimulus Strength is double the Rheobase. It is the
measure of excitability.
Increasing order of Chronaxie / Order of excitability
a. Myelinated nerve (least chronaxie, most excitable)

b. Unmyelinated nerve
c. Skeletal muscle
d. Cardiac muscle
APPOLO ACADEMYA 9
e. Smooth muscle
MEMBRANE EXCITATION & IMPULSE TRANSMISSION
MEMBRANE EXCITATION occurs in 2 Forms
Electronic Conduction
Action Potential Propagation
ELECTROTONIC CONDUCTION / GRADED CONDUCTION: Direct & passive charge Spread from point of
entry, charges leak because of Membrane capacitance, such transmission is called as DECREMENTAL
CONDITION, Carry impulse only for 10 mm Length, from dendrites to axon hillock, node to node charges
travel by electronic conduction. NODE to NODE conduction is less decremental as the overlying myelin sheath
decreases the capacitance & increases the resistance. It also occurs in Retinal cells.
SALTATORY CONDUCTION — ADVANTAGES
1. Faster (Slower in unmyelinated Nerve Fibres)

2. Less energy consumed (Which is required for recharging, Recharging occur only at Nodes of
Ranvier by Na+ K+ ATP Pump).
MULTIPLE SCLEROSIS
Demyelinating disease of neuron

After demyelination CONDUCTION BLOCK Occurs.
Internodal distance > 1-3 mm
Electronic conduction occur only for 10mm
MS involves >3 nodes, resulting in Conduction Block.
Hot bath increases Conduction Block
ACTION POTENTIAL
• Self regenerative process

• Self propagated process
• Non decremental Conduction
• Obeys all or None law
• Not graded
PHASES OF AP
• Recorded by cathode ray Oscilloscope

• Depolarisation is due to Na+ Entry
o Other ways of depolarisation:
Ca++ entry into heart muscle cell
K+ entry into hair cell
Accumulation of K+ inside membrane, ex. Pancreatic beta cell
• Repolarisation is due to K+ Exit
BASIS FOR REFRACTORY PERIOD
ABSOLUTE REFRACTORY PERIOD: The time period after stimulus, during which another stimulus can't
stimulate for another time
RELATIVE REFRACTORY PERIOD: A normal stimulus can’t excite tissue, stronger than normal stimulus can
generate another action potential.
APPOLO ACADEMYA 10
SIGNIFICANCE: It determines the FREQUENCY OF Stimulation, highest frequency time = 60/ min, longer
the refractory period, Frequency of Stimulation will not be higher.
EFFECTS OF IONS
(Changes in ECF Concentration)
1. Na+
HYPONATREMIA: amplitude of AP will decrease, In Severe condition, Conduction may
stop Completely
HYPERNBTREMIA: more conduction = More action potential
2. K+
RMP will be affected more
HYPOKALEMIA: membrane will be hyperpolarised
HYPERKALEMIA: concentration gradient will narrow -> membrane will be depolarized
3. Ca+
ECF Ca+ is necessary for stability of Na+ channel
HYPOCALCEMIA (TETANY): Na+ channel gating unstable, open & remain activated =
Sustained contractions = TETANUS (TROUSSEAU’S & CHOVSTEK'S SIGN)
NERVE
DEPOLARISATION
• It is a travelling impulse, resulting in muscle contraction.

• Relaxation occurs if One more depolarisation does not come in.
REPOLARISATION
• Do not travel, occurs by point by point

• Recovery from excitation
CLASSIFICATION OF NEURON
1. MULTI POLAR: Brain & cerebral Cortex

2. BIPOLAR: Retina , olfactory neuron
3. PSEUDO UNIPOLAR: Nerve cell in dorsal root ganglion
4. ANAXONAL NEURON: Post ganglionic Parasympathetic neuron. Ex: Anacrine cell in Retina
NO new Neurons formed after birth EXCEPT for OLFACTORY NEURONS
CLASSIFICATION OF NERVE FIBRES (Diameter decreasing order = Conduction velocity decreasing order)
1. Aα (Ia) = Myelinated
2. Aβ (Ib) = Myelinated
3. Aγ (II) = Myelinated
4. Aδ (III) = Myelinated
5. β/B = Myelinated
6. C (IV) = Non-Myelinated
In myelinated nerve fiber conduction velocity is proportional to 6 times the diameter.
In myelinated nerve fiber conduction velocity is proportional to √diameter.

APPOLO ACADEMYA 11
MYELINATION IS BY
1. In PNS (20:1) →Schwan

Schwan cells
2. In CNS (1:20) → Oligodendroctes
ERLANGER
LANGER & GASTER CLASSIFICATION
Aα = proprioception & α motor Neurons;

Neurons Fastest conduction for voluntary movements
Aβ = touch & pressure
Aγ = Maintains excitability of Muscle Spindle,

Spindle Ex. JENDRASSIK’S MANEUVER
Aδ = Fast pain & temperature
B = Preganglionic Autonomic Nerve Fibres
C = Somatic → Slow pain; Autonomic

omic → Post ganglionic Sympathetic. (Opioids acts onn type C fibres relieve
SLOW pain).
INJURY TO NERVE FIBRES
• Most susceptible to Pressure

sure → A
• Most susceptible to Hypoxia
poxia → B
• Most susceptible to Local anaesthesia
an →C
SUNDERLAND’S Classification
• 1° Mild pressure, hypoxia

• 2° Severe & Sustained pressure
• 3° Single axonal transaction
saction
• 4° Nerve Fascicles are disrupted
• 5° Nerve trunk transaction
SEDAN’S Classification
• 1° & 2° → in NEUROPRAXIA
• 3° → AXONOTMESIS
APPOLO ACADEMYA 12
• 4° & 5° → NEUROTMESIS
WALLERIAN DEGENERATION::
• Repair of Nerve fibres after

ter Injury
• Seen after 5° degree injury when entire nerve trunk damaged
• Changes seen in distal Stump
ump or proximal stump
s near the nodes of Ranvier
MUSCLE
NEUROMUSCULAR JUNCTION
EPP (END PLATE POTENTIAL)
Amplitude is 40mV,
Depolarisation reaches threshold → AP → Contraction
Graded potential, forerunner of Actio

tion Potential (AP)
EPSP (EXCITATORY POST SYNAPTIC

NAPTIC POTENTIAL)
• Developed
eveloped in CNS Synapses
• Amplitude is 2, 3, 4 orr 5 mV.
m
• Multi EPSP will summate
mmate to create Action potential
MEPP (MINIATURE
MINIATURE END PLATE POTENTIAL)
• Even in resting conditions, Small

Sma pockets of ACh released,
creating MEPP
• The amplitude of this
is potential is only up to 0.5 mV
NEUROMUSCULAR BLOCKERS
• Curare: blocks by combining with Ach receptors

• Bungarotoxin: snake venom that blocks by combining
with Ach receptors
• Botulinum toxin:: prevent release of Ach
AUTONOMIC DISEASES RELATED TO NM JUNCTION
• Antibodies against Caa channels in axon terminal →

LAMBERT EATON DISEASE
• Antibodies against Cholinergic
Cholinerg Receptor channel →
MYAESTHENIA A GRAVIS
ACTION POTENTIAL CURVE
1. Latent period:
a. duration: 0.5-1ms,
1ms,
b. Stimulus effect is seen
2. Depolarisation A = Opening of few Na+ channels
a. Initial slow depolarisation: upto -75mV B = Opening of many Na+ channels
b. Overshoot: upto +55mV C = Closure of Na+ channels and
3. Repolarisation opening of K+ channels
D = Closure of K+ channels
a. Spike potential: lasts 0.4ms
APPOLO ACADEMYA 13
b. After depolarization or negative after potential

i. Duration: 2-4ms
ii. Rapid fall follows slow repolarisation
c. After hyperpolarization or positive after potential
i. Duration: >50ms
ii. Becomes more –ve
GRADED POTENTIAL:
• Mild local change in the membrane potential
• Non-propagative
• Short distance signal
• Does not obey all or none law
• No refractory period
• Summation is possible
SARCOMERE
• The distance between the two Z- Lines

• Normal resting length = 2µ.
• STARLING LAW: Greater the Initial length of Muscle, stronger is the contraction.
DURING MUSCLE CONTRACTION
• Sarcomere shortened
• I band shortened
• A band unchanged
• H zone disappears
• M line prominent
ISOMETRIC CONTRACTION
• Only tension developed in Muscle

• No shortening, length remains same
• No work done
• More heat liberated
ISOTONIC CONTRACTION
• Tension remains same

• Muscle shortening occurs
• Work is done only during Isotonic Contraction
TYPES OF MUSCLE FIBRES
RED (Aerobic) WHITE (Pale)

Slow oxidative Fast glycolytic
High myoglobin content Low myoglobin content
High mitochondria Low mitochondria
High vascularity Low vascularity
Slow, Sustained Lesser duration
SMOOTH MUSCLE
APPOLO ACADEMYA 14
Involuntory muscle that lines hollow internal viscera like GIT, respiratory tract, genital tract, ureter, bladder,
urethra, blood vessels, arrector pili of skin, iris & ciliary body of eye
TYPES
1. le of fibers work together as Single unit.

SINGLE unit → Bundle u Ex: Viscera
2. MULTI unit → Individual fibres, behave
beh independently as separate units. Ex. Iris, Arrector pili muscle
of skin.
ACTION POTENTIAL OF SMOOTH MUSCLE:

MUSCLE 3 types
• Spike potential:
o Similar to skeletal muscles
o Duration of spike potential: 30-50ms
30
o Sometimes rises above isoelectric point / overshoot
• Slow wave rhythm
o One ne or two spikes at the peak of each slow wave.
o Self-excitatory
excitatory without any external stimuli
o Spike potential initiated by slow wave rhythm called Pacemaker waves
• Action potential with plateau
o Muscle remains depolarized for long periods of about 100 to 1,000ms
o Responsible for sustained contraction
MOLECULAR BASIS OF SMOOTH
MUSCLE CONTRACTION
1. Calcium-Calmodulin
Calmodulin complex: In
smooth muscle, the myosin has to be
phosphorylated for the activation
activat of
myosin ATPase.
2. Length-tension
tension relationship: Starling law
is not applicable (applicable in skeletal
& cardiac muscle). It adapts with wide
range of lengths. It is important for GIT
which undergo wide change in volumes.
Molecular basis of smooth muscle contraction
Hormones and neurotransmitters, which act on smooth muscles, are:

1. Acetylcholine
2. Antidiuretic hormone (ADH)
3. Adrenaline
4. Angiotensin II, III and IV
5. Endothelin
6. Histamine
7. Noradrenaline
8. Oxytocin
9. Serotonin.
Humoral factors other than the hormones cause relaxation of smooth muscle
mus fibres:
1. Lack of oxygen
2. Excess of carbon dioxide
3. Increase in hydrogen ion concentration
4. Adenosine
5. Lactic acid
6. Excess of potassium ion
APPOLO ACADEMYA 15
7. Decrease in calcium ion

8. Nitric oxide (NO), the endothelium-derived
endothelium relaxing factor (EDRF).
MYOPATHY
• Disorder of skeletal muscles lead to weakness

• Causes
o Muscular dystrophy
Duchenne Muscular dystrophy: Absence of Dystrophin d/t X-chromosome
X chromosome linked
recessive defect
Becker Muscular dystrophy:
dystrophy: Reduction in quantity or qualitative defect of
Dystrophin d/t
d X-chromosome linked recessive defect
o Diseases involving muscle tone
Hypertonia
Hypotonia
Myotonia: Congenital defect of continuous contraction & slow relaxation;
Myotonia: relaxation non
progressive
o Fibrillation and denervation hypersensitivity
o Myasthenia gravis
o Lambert Eaton syndrome
o McArdle disease
o Mitochondrial myopathy
o Nemaline myopathy
GASTROINTESTINAL TRACT
INTRODUCTION
LAYERS
1. Mucosa
2. Sub mucosa
3. Muscularis Mucosa
4. Serous layer
APPOLO ACADEMYA 16
ENTERIC NERVOUS SYSTEM
• Branch of ANS
• aka Peripheral / mini brain
• Sub mucous / meissner’s plexus (Sensory)
• Myenteric plexus / Auerbach's plexus (motor)
NEUROTRANSMITTERS
• EXCITATORY NTs = Ach, Substance P

• INHIBITORY NTs = VIP (inhibits motility), NO
ELECTRICRL ACTIVITY
• Pacemaker Cell Interstitial cell of CAJAL

• Electric activity occurs at a frequency
• Frequency differs at different parts of GIT.
ANTI PERTSTALSTS
• Naturally occurs in colon (From hepatic Flexure of Colon to Caecum)

• Significance: to reabsorb Water
MAXIMUM ABSORPTLON Of WATER TAKES PLACE AT JEJUNUM (6.6L/day)
REFLEXES
TYPES OF REFLEXES
o LOCAL REFLEXES
• Entirely confined to digestive wall (ENS). Ex. Peristaltic reflex
o SHORT LOOP REFLEXES
• ENS ↔ Spinal cord. Ex: orthocolic reflex
o LONG LOOP REFLEXES
• ENS → Spinal Cord → higher centres. Ex Defecation Reflex
MOTILITY IN DIGESTIVE TRACT
• 3 PHASES
a. Oral phase: voluntary
b. Pharyngeal phase: Involuntary
c. Oesophageal: Involuntary
o Swallowing centre is in medulla.
Oral phase: Tongue is pressed upward & backward, bolus of Food pushed into post-pharynx
Pharyngeal phase: Sensitive part - Tonsillar pillar, Food touches tonsillar pillars & Swallowing centre in
medulla activated cause Deglutition Apnoea & Sends Signals for Co-ordinated contraction are seen in pharynx
& oesophagus. IX & X CN involved
EVENTS AFTER UPPER OESOPHAGEAL SPHINCTER RELAXATION
1. Soft palate moves upwards, so that posterior nares are closed

2. Epiglottis falls & closes the respiratory Passage
3. Palato pharyngeal folds approximate in mid line & Leaves a narrow slit for the passage of bolus.
4. Opening of oesophagus widened & Wave of peristalsis sent downwards.
APPOLO ACADEMYA 17
OESOPHAGEAL PHASE
LOWER GASTRO OESOPHAGEAL SPHINCTER: Physiological Sphincter / Functional Sphincter, no

anatomical entity,
MOTOR FUNCTIONS OF THE STOMACH
1. STORAGE: Receptive relaxation of stomach wall, 1-1.5L Food can be accumulated without rising
Intragastric pressure. Pacemaker of stomach located in middle of body.
2. MIXING: Retropulsion, Chyme empties from pyloric sphincter, some goes back to stomach & process
repeats.
3. SLOW EMPTYING: Normally after 4-6hrs, after fat food upto 8hrs.
FACTORS INFLUENCING EMPTYING
1. WEAK FACTOR (Gastric factor): Gastrin, promotes emptying

2. STRONG (Duodenal Factors): Inhibits emptying
a. Acidic Chyme: Secretin from S cells cause constriction of pyloric sphincter.
b. Irritation of duodenal mucosa→ Initiation of enterogastric reflex
c. Hypertonic contents reaching duodenum (Dumping syndrome)
d. Fat breakdown products in duodenum→ CCK released→ Decreased Gastric motility→
Feeling of fullness
REGULATORY PEPTIDE SECRETIONS IN DIGESTIVE TRACT
STOMACH CELL SECRETION FUNCTIONS

ECL cells Secretes HISTAMINE ↑Gastric acid Secretion, potentiates Ach, Gastrin
G cells Secretes GASTRIN ↑Gastric acid Secretion, ↑Gastric motility
SOMATOSTATIN [Proinsulin as well as antiinsulin] ↓ Gastric acid Secretion, ↓Insulin & Glucagon
synthesized by D cells in Pylorus & Duodenum, δ Secretion
cells in Pancreas, Hypothalamus
SMALL INTESTINAL CELL SECRETION FUNCTIONS
S cells in duodenum Secretes Secretin Maintains alkaline pH in Duodenum,
Constrict pyloric sphincter,
↑Secretion of HCO3 rich pancreatic juice
I cells in duodenum Secretes CCK ↑Gastric motility, ↑Intestinal motility, ↑Secretion of
enzyme rich pancreatic juice,
↑Bile flow from GB (Cholagogue)
Mo cells in duodenum Secretes Motilin ↑MMC contraction
GLANDS IN GIT
• Parotid
o Wt: 20-30g in adult
o Duct: Stenson duct (35-40mm length)
• Submaxilary
o Wt: 8-10g in adult
o Duct: Wharton duct (40mm length)
• Submandibular
o Wt: 2-3g in adult
o Ducts: Ducts of Rivinus (15-20 in number); the larger duct is called Bartholin duct
• Fundic glands of stomach
o Cells of fundic glands
Chief cells or pepsinogen cells
Parietal cells or oxyntic cells
APPOLO ACADEMYA 18
Mucus neck cells

Enterochromaffin (EC) cells or Kulchitsky cells
Enterochromaffin like (ECL) cells.
• Pyloric glands of stomach
o Cells of pyloric glands
G cell
Mucus cells
• Cardiac glands of stomach
o Cells of cardiac glands
Chief cells or pepsinogen cells
Mucus neck cells
• Exocrine pancreatic glands: secrete digestive enzymes
• Endocrine pancreatic glands: secrete hormones
• Crypts of Lieberkühn or intestinal glands
o Argentaffin cells or enterochromaffin cells, secrete intrinsic factor of Castle
o Goblet cells, secrete mucus
o Paneth cells, secrete the cytokines called defensins
• Brunner gland: secrete mucus
SECRETIONS IN GIT
• SALIVA
o Secretes highest Volume of K+
o It have no endocrine control, only neural control
o pH: 6 – 6.5 4, hypotonic to isotonic
o 2 ions: K+, HCO3-
o 2 enzymes: Ptyalin (α- amylase), Lingual Lipase (for Lipid digestion)
o Have Thiocyanate ions, IgA, Lysozyme
• GASTRIC SECRETION
o GASTRIC GLANDS
MUCUS NECK CELLS: Secretes Mucus
PEPTIC or CHLEF CELLS: Secretes Pepsinogen, Rennin, Gelatinase, Lipase,
Urease
PARIETAL or OXYNTIC CELLS: Secretes HCl & Intrinsic Factor of Castle
G CELLS: Gastrin
EC CELLS: Serotonin
ECL CELLS: Histamin
o PEPSIN
aids in 10 -20% of Protein digestion
Needed for further gastric acid Secretion & digestion of Meat protein (collagen)
o RENNIN
Secreted in Stomach
Helps in digestion of milk protein
o GASTRIC LIPASE
α-Tributyrase
Digest tributiric acid / Butter Fat
• PANCREATIC JULCE
o pH: 8.0 (isotonic)
o Vol: 500-800ml/day
o HCO3- rich (for chyme)
o Enzyme rich (for nutrients)
APPOLO ACADEMYA 19
o Heighest protein content

o Proteolytic enzymes:
Trypsin, Chymotrypsin are called endopeptidases
Carboxypeptidase, Aminopeptidase are called exopeptidese.
Elastase & Collagenase
o Lipolytic enzymes:
Lipase, Phospholipase-A & B, Co-lipase, Cholesterol ester hydrolase, Bile salt
activated lipase
o Amylolytic enzymes: Amylase
o Nuclease
o Disaccharidases → Di & tripeptidases , Trehalase
• BILE
o Secreted by LIVER
o Gall Bladder:
Stores & Concentrates bile
Acidifies bile
Add mucous to bile
o Function of Bile salts:
Digestion of Lipids→ emulsification
Absorption of Lipids
Micelle formation for Fat absorption
• DUODENUM
o Absorbs Divalent cations Fe++, Ca++
• JEJUNUM
o All major nutrients
o Max. H2O Absorption (6.6L/day) (1.5L/day from colon)
o Long chain fatty acids absorbed into lymphatic circulation
Appears milky called LACTEALS
Lymphatics in form of chylomicrons
• ILEUM
o Mg++, Vit B12, Bile salts absorbed from Ileum
o Enterohepatic cycling occurs 7-8 times a day (of bile)
o Maternal Antibodies are absorbed from Ileum
• SMALL INTESTINE ENZYMES
o Proteolytic: Peptidase
o Amyolytic: Lactase, Sucrase, Maltase, Dextrinase, Trehalase
o Lypolytic: Lipase
• GUT or COLONIC MICROFLORA
o Synthesized & absorb Vit B12, folic acids, Vit K & Short chain fatty acids
GASTRIC HORMONES
APPOLO ACADEMYA 20
BLOOD PHYSIOLOGY
BLOOD COMPOSITION
1. PLASMA (55%)
APPOLO ACADEMYA 21
2. CELLS (45%) [RBCs, WBCs, Platelets]
PLASMA PROTEINS
Total: 7-8 gm%

o Alburmin: 4-4.5 gm%
o Globulin 2-2.5 gm%
o Fibrinogen 0.2-0.4 gm%
o Prothrombin 0.02-0.04 gm%
All are Synthesised by Liver Except γ-Globulin
Normal Albumin : Globulin Ratio: 1.7-2:1
ALBUMIN exerts plasma colloid osmotic pressure
GLOBULIN α & β: transport protein, Ceruloplasmin for Cu++, Transferrin for Fe++
HEMOGLOBIN
Age wise normal haemoglobin:

• At birth : 25 g/dL
• After 3rd month : 20 g/dL
• After 1 year : 17 g/dL
• From puberty onwards : 14 to 16 g/dL
Types:
• Adult: HbA (α2β2)

• Fetal: HbF (α2γ2)
Replacement of fetal hemoglobin by adult haemoglobin starts immediately after birth. It is completed at about
10th -12th wk after birth.
Abnormal hemoglobins:
• Carboxy Hb: formed by CO combined with Hb. Normally found 1-3%.
• Methemoglobin: formed when Fe of Hb turn into Fe+++ instead of Fe++.
• Sulphhemoglobin: formed when Hb is combined with hydrogen sulphide.
Hemoglobinopathies: genetic disorders causing abnormal chains of Hb.

• Hemoglobin S:
o Found in sickle cell anemia.
o α-chains are normal and β-chains are abnormal.
• Hemoglobin C:
o β-chains are abnormal.
o characterized by mild hemolytic anemia and splenomegaly.
• Hemoglobin E:
o β-chains are abnormal.
o characterized by mild haemolytic anemia and splenomegaly.
• Hemoglobin M:
o Abnormal haemoglobin present in the form of methemoglobin.
o mutation of genes of both in α and β chains.
RBCs
8µ diameter, biconcave, non-motile, non-nucleated

STAGES OF ERYTHROPOIESIS
1. 1st TRIMESTER = Mesoderm of Yolksac
2. 3-6 months of PREGNANCY = Hepatic stage: Liver cells form RBC
3. 3rd TRIMESTER = Bone marrow: Myeloid stage
RED BONE MARROW
o At birth, all bones have RBC
APPOLO ACADEMYA 22
o After Fat infiltration, Few have RBM (Long bones, flat bones, Sternum, Ant. Sup Iliac Spine)
o In Bone marrow, Myeloid : Erythroid ratio = 3:1
o Precursors are nucleated, matured RBC non-nucleated
o Normal Reticulocyte count 0.2-2%; High in Infants, children & hypoxia
o Erythropoiesis takes about 7-9 Days
PLEURIPOTENT
HAEMATOPOLETEC STEM CELL
(24µ diameter)
CFU ERYTHROCYTE CFU GRANULOCYTE

↓ CFU MEGAKARYOCYrE
MONOCYTE
Proerythroblast ↓
↓
↓ Platelet
Monocyte
Normoblast
↓
Reticulocyte
↓
RBC
NUTRLTLONAL FACTORS
o IRON: For heme Synthesis
o Vit B12 & FOLIC ACID: For maturation OF DNA, deficiency leads to MEGALOBLASTIC
ANEMIA
o Other factors: Cu, Zn etc.
OTHER FACTORS
o HYPOXIA: Interstitial cells of Kidney Stimulated →ERYTHROPOIESIS (in about 5-6 days)
HORMONAL FACTORS
o ESTROGEN: Inhibit Erythropoiesis
o TESTOSTERONE: Stimulates Erythropoiesis
WBC
GRANULOCYTES AGRANULOCYTES
1. Neutrophils (50- 70%) 1. Monocytes (2-8%)
2. Eosinophils (1-4%) 2. Lymphocytes (20-30%)
3. Basophils (0-1%)
• ABSOLUTE COUNTS
o Total Leucocyte Count
o Differential Leucocyte Count
• NEUTROPHILS (50-70%)
• ARNETH COUNT
• STAGE I (Single lobe) → 5% in peripheral Circulation
• STAGE II (Double lobes) → 15% in peripheral Circulation
• STAGE III (3 lobes) → 35-45% in peripheral Circulation
• STAGE IV (4 lobes) → 10-15% in peripheral Circulation
• STAGE V (5 lobes) → 5-10% in peripheral Circulation
o SHIFT TO LEFT: Younger neutrophils↑ - In case of infection
o SHIFT TO RIGHT: Older neutrophils in bone marrow↑
LIFE SPAN (SCHILLING’S INDEX]
APPOLO ACADEMYA 23
• Neutrophils: 4-6bhre
• Lymphocytes: 300 days | mocrophaqes
• Monocytes: Few hrs to Few days (Converts into macrophages in tissue)
• RBC: 120 days
• Stored RBC: 60 days
• t1/2 of Stored RBC: 28-32 days
• Neutrophils: 4-8 hrs to few days
• Platelets: 8-12 days
• t1/2 of platelets: 4 days
• t1/2 of Stored platelets: < 1 day
MONOCYTES
• 2nd line of defence
• largest WBC (18-20µ)
• Monocyte count increased in Malaria
LYMPHOCYTES
o 3rd Line of defence
o Basis for Immunity
o T - Lymphocytes involved in cell-mediated Immunity
o B – Lymphocytes
Involved in Humoral cell Immunity
Plasma cell: Antibodies Secretion
Antibodies in humoral immunity: IgG, IgA, IgM, IgD, IgE
EOSINOPHILS (1-4%)
o COUNT INCREASES IN
Parasitic / Worm Infection: due to Major Basic protein
Allergic Conditions
BASOPHILS (0- 1%)
o Synthesize & Secrete Heparin & Histamine
o BASOPHILIA = Basophilic count↑, Seen in Allergy
o PUNCTATE BASOPHILLA:
Seen in Lead poisoning
maturarion arrested in early Stages
Known as Basophilic Stippling of RBC.
PLATELETS / THROMBOCYTES
o formed from Megakaryocytes
o Normal Size: 2-4µ diameter
o Non motile; Non nucleated
o Lifespan: 10days
o Normal Count: 1.5-3 lacs/ mm3
o CRITICAL PLATELET COUNT
<40000/mm3
Arrest of bleeding is very difficult
o OPEN CANALICULI for entry of Ca++ present
o Granules release ADP & TxA2
o Ca++ cause exocytosis of granules
o Ca++ also required for contractile Filaments (actin, myosin, Thrombosthenin) helps in retraction of
Clot.
o Platelets stops bleeding about 1-3 min (by platelet plug)
o Deficiency leads to Thrombocytopenia. Thrombocytopenia occurs in the following conditions:
i. Acute infections
ii. Acute leukemia
iii. Aplastic and pernicious anemia
APPOLO ACADEMYA 24
iv. Chickenpox
v. Smallpox
vi. Splenomegaly
vii. Scarlet fever
viii. Typhoid
ix. Tuberculosis
x. Purpura
xi. Gaucher’s disease.
o Increase leads to Thrombocytosis. Thrombocytosis occurs in the following conditions:

i. Allergic conditions
ii. Asphyxia
iii. Hemorrhage
iv. Bone fractures
v. Surgical operations
vi. Splenectomy
vii. Rheumatic fever
viii. Trauma (wound or injury or damage caused by external force).
o Thrombocythemia - persistent and abnormal increase in platelet count. Thrombocythemia
occurs in the following conditions:
i. Carcinoma
ii. Chronic leukemia
iii. Hodgkin’s disease.
o Glanzmann’s thrombasthenia - inherited hemorrhagic disorder, caused by structural or functional
abnormality of platelets characterised by normal clotting time, normal or prolonged bleeding time
& abnormal clot retraction.
ACTIVATORS OF PLATELETS
o Collagen, which is exposed during damage of blood vessels

o von Willebrand factor
o Thromboxane A2
o Platelet-activating factor
o Thrombin
o ADP
o Calcium ions
o P-selectin: Cell adhesion molecule secreted from endothelial cells
o Convulxin: Purified protein from snake venom.
INHIBITORS OF PLATELETS
o Nitric oxide
o Clotting factors: II, IX, X, XI and XII
o Prostacyclin
o Nucleotidases which breakdown the ADP.
CLOT FORMATION
Occurs in 4-9 min

Small injuries are addressed by platelet plugs
Clot formation occurs in larger Injuries
Platelet plug is temporary
Clot Stabilizes the platelet plug & aids in healing
STEPS:
• PROTHROMBIN → THROMBIN (Prothrombin activator)
• FIBRINOGEN → FIBRIN (by Polymerisation)
• PROTHROMBIN ACTIVATOR FORMED BY
EXTRINSIC PATHWAY: Tissue injury releases Tissue Thromboplastin
APPOLO ACADEMYA 25
INTRINSIC PATHWAY: Trauma to blood vessel itself, Factor XII comes in Contact
with Subendothelial tissue.
CLOTTING FACTORS
1. Fibrinogen
2. Prothrombin
3. Tissue Thromboplastin
4. Ca++
5. Labile Factor
6. Unknown
7. Stable Factor
8. Anti Haemophilic Factor
9. Christmas Factor
10. Stuwart power Factor
11. PTA
12. Hagemen factor
13. HMWK
14. Prekallikrein
ANTI COAGULENT MECHANISMS
IN VITRO
• Dilution of blood >20 times

• Heparin
• Citrates, Oxalates, EDTA used for collection & storage
IN VIVO:
• Heparin → acts as antithrombin-III

• Smoothness of Endothelium
• Glycocalyx layer on Endothelium
• Thrombomodulin layer Endomelium
• Tissue plasminogen activator: (Streptokinase, Urokinase) converts Plasminogen → Plasmin (has
trypsin like activity to digest fibrin threads)
• Coumarin derivatives eg. Warfarin by inhibiting Vit-K.
ESR
ESR increases in diseases such as the following conditions:

• Tuberculosis
• All types of anemia except sickle cell anemia
• Malignant tumors
• Rheumatoid arthritis
• Rheumatic fever
• Liver diseases.
• Normally
o Age as increases
o Female
o Pregnancy
o Menstruation
ESR decreases in the following conditions:
• Allergic conditions
• Sickle cell anemia
APPOLO ACADEMYA 26
• Polycythemia
• Peptone shock
• Severe leukocytosis
BLOOD GROUPS
• Landsteiner law:
o If a particular agglutinogen (antigen) is present in the RBCs, corresponding agglutinin
(antibody) must be absent in the serum.
o If a particular agglutinogen is absent in the RBCs, the corresponding agglutinin must be
present in the serum.
o Second part of Landsteiner law is not applicable to Rh factor.
• Divided into 20 blood group system so far, like
o ABO
o Rh
o Kell
o Duffy
o M&N: can be used for paternity dispute
• ABO SYSTEM
o ANTIGENS: A&B
o Blood Group: 4
o A = anti B
o B = anti B
o AB = NO antibodies (universal recipient)
o O = anti A, anti B (universal donor)
• Rh BLOOD GROUP SYSTEM
o Based C,c, D,d, E,e
o 90% of times, Rh = D
o Anti Rh antibody
o Not present in any individual
o Not Naturally occurring antibody
o 85% Rh positive
o 15% Rh negative
o Present only the Rh -ve individuals who exposed to Rh +ve blood
o Erythroblastosis fetalis
Mother Rh —ve + 1st Baby Rh +ve = Sensitization → Starts forming anti Rh antibodies
(48-72hrs) → anti Rh antibodies Fully developed by 2-4 months → 2nd Baby Rh +ve →
antigen-antibody reaction occurs = Erythroblastosis fetalis (Jaundice + Anaemia)
Preventive Measure: Anti D Serum given to Mother after delivery of 1st baby
Treatment
• Exchange transfusion for anaemia
• Phototherapy For Jaundice
SPLEEN
• Splenomegali: Increase size of spleen

o Causes
Infectious diseases such as malaria, typhoid and tuberculosis
Inflammatory diseases like rheumatoid arthritis
Pernicious anemia
Liver diseases
Hematological disorders like spherocytosis
Cysts in spleen
Hodgkin’s disease
APPOLO ACADEMYA 27
Glandular fever.
• Hypersplenism: Increase activity of spleen
• Hyposplenism: Decrease activity of spleen
• Asplenia: Absence of spleen
• Autosplenectomy: Diseases (sickle cell anemia, spherocytosis) destroy spleen such an extent that it
becomes non functional
BLOOD INDICES
• PCV (Haematkocrit): 38 — 45%; In anaemia ↓, In polycythemia ↓

• MCV (Mean corpuscular volume): 78-93 µ3; < 78: Microcytic anaemia (iron def. Anemia); >93: macrocytic
/ megaloblastic anaemia
• MCH (Mean corpuscular Hb): 28 - 32 pg; ↓ in iron def. Anaemia
• MCHC (Mean corpuscular Hb concentration): 32-38%; denotes percentage of saturation of RBC by Hb. If
MCH normal & MCHC reduced →Macrocytic / megaloblastic anaemia
• COLOUR INDEX: Hb% / RBC%; Normal: 0.8-1; <0.8 = Hypochromic anaemia
CARDIOVASCULAR SYSTEM
CONDUCTING SYSTEM OF HEART
INTRODUCTION
1. Heart muscle works like SYNSITIUM.

a. All fibres contracts as Single bundle
b. Made up of 2 Synsitia, Atria contracts together, Ventricles contracts together
2. Contains INTERCALATED DISCS provides electro-mechanical tethering to fibers
INNERVATION
o Sympathetic Fibres (mainiy from T1 - T5)

o Predominanty epicardial distribution
o Mainly control Contractility
o Vagal fiber
o Predominantly endocardial distribution
o Mainly controls heart rate
o Rt vagus innervates SA Node
o Lt vagus innervates AV Node
ANATOMICAL PARTS
o SA Node
o AV Node (cause most slow down of conduction, has Smallest diameter of fibres, Least no. of gap
Junctions)
o 3 Inter Nodal Tracts connects SA Node to AV Node
Anterior: Bachman’s bundle
Middle: Wenckebach’s bundle
Posterior = Thorel’s bundle
o Br. of Anterior bundle innervates Lt Atrium
BUNDLE of KENT
Aberrent anomalous path that connects atria directly to ventricle bypassing AV Node
No AV Nodal delay
Shortened PR interval, Appears as δ wave on ECG
APPOLO ACADEMYA 28
Seen in Wolff Parkinson White Syndrome
GATE CELLS of HEART
1. AV Nodal cells & Purkinje fibres

2. Allows Impulses to reach ventricles
3. Higher the HR Longer the Refractory period
4. Provides a physiological block
LAST PARTS TO DEPOLARISE
Epicardium of Base of Left ventricle

Pulmonary Conus
Uppermost Part of inter ventricular septum
Impulse Spreads From apex to base & From endocardium to epicardium
LAST TO REPOLARISE: Apex endocardium
FUNCTIONAL ASPECTS
RATES OF DEPOLARISATION
Fastest depolarising cell is at base

Fibre at apex depolarises first, last to complete the depolarisation
Fibre at base repolarises First
ISCHEMIA
MI
Na+ K+ Pump Fails
K+ Starts accumulating in
ECF
Electric gradient created
Intracellular K+ accumulate
at inner asect of membrane
Membrane begins to
depolarise
CONDUCTION SPEED (m/Sec)
SA NODE: 0.05 – 0.3

Atrial muscles: 0.3
Internodal fibres: 1
AV NODE 0.05 – 0.1 (Slowest)
Bundle of HIS: 0.1 - 1
Purkinje fibre: 1.5 - 4 (Fastest)
APPOLO ACADEMYA 29
Ventricular muscles: 0.5
RHYTHMICITY / MIN (Rate of Repolarisation determines ITNTRINSIC RHYTHMICITY OF THAT PART)
SA Node: 80-100
AV Node: 60
Purkinje Fibres: 35-40
Ventricular muscles: 20-40
Fastest repolarising Part: SA Node (Pace maker)
ACTIONS OF HEART
• Chronotropic action: Frequency of heartbeat / heartrate.

o Types: Tachycardia (↑HR) & Bradycardia (↓HR)
• Inotropic action: Conduction of impulse through heart
o Types: Positive: ↑force of conduction, Negative: ↓force of conduction
• Dromotropic action:
o Types: Positive: ↑velocity of conduction, Negative: ↓velocity of conduction
• Bathmotropic action
o Types: Positive:↑excitability of cardiac muscle, Negative: ↓ excitability of cardiac muscle
ECG
RECORDING OF ECG
• Graphic record of electric activity of heart from body Surface

• Summated activity
• CARDIAC JELLY decreases the resistance offered by the Skin; NaCl also can be used
LEADS
• EINTHOVEN recorded 1st ECG (1905)

• KIRCHHOFF ’S LAW: I + II + III = 0
• By reversing the polarity of Lead II, we can get Upward deflections →now KIRCHHOFF’S LAW → I
+ III + (- II) = 0; so II = I + III (EINTHOVEN EQUATION)
• CHEST LEADS record cardiac activity in antero-posterior direction
• LIMB LEADS record cardiac activity in 2 dimensions (from above downwards)
• Chest leads are Anterior Leads
• II, III, avf are inferior Leads
• V2 – V4: Septal Leads
CHEST LEADS / PRE CORDIAL LEADS
• Electrocle placed On anterior wall of heart

• V1 to V6
• All are unipolar
• V1: Right sternal border
• V2: Left sternal border
• V3: between V2 & V4
• V4: 5th intercostal space, mid sternal line
• V5: anterior axillary line
• V6: mid axillary line
APPOLO ACADEMYA 30
NORMAL ECG
• P: Atrial depolarisarion
• QRS: Ventricular depolarisation
• T: Ventricular repolarisation
ion
• U: Repolarisation of Papillary
apillary muscles, not always seen
s
Waves of normal ECG
HEART RATE
• The distance between Two Successive “R”

“R waves are 1 beat
• Speed of paper 25 mm/sec,, so speed in 1 min 1500 mm
• If R to R gap = x mm, then in 1500 mm, no. of heart beats: 1500/x.
ATRIAL DEPOLARIZATION
• P Wave if the Summated potential of both the atria depolarizing

APPOLO ACADEMYA 31
• BIFID/ M SHAPED P WAVE

o Seen in Mitral stenosis
o Due to hypertrophy of Left atrium
o This ↑ in mass: ↑ depolarisation time of LA → BIFID P WAVE
o SAW TOOTHED P WAVE: Seen in ATRIAL FLUTTER
• Small or absent P wave: Hyperkalemia
• Absent P wave: SA / AV nodal block, atrial fibrillation
• Inverted P wave: Atrial paroxysmal tachycardia, sometime SA nodal block
ATRIAL REPOLARISATLON
• Not Seen Normally

• Merged with QRS complex
• Can make it visible by changing the Speed of Paper
VENTRICULAR DEPOLARIZATION
• Represented by QRS Complex

• Normal: 0.08 - 0.1 Sec
VENTRICULAR REPOLARIZATION
• represented by T Wave
• T wave variation
o Acute myocardial ischemia: Hyperacute ‘T’ wave develops. Hyperacute ‘T’ wave refers to a
tall and broad-based ‘T’ wave, with slight asymmetry.
o Old age, hyperventilation, anxiety, myocardial infarction, left ventricular hypertrophy and
pericarditis: ‘T’ wave is small, flat or inverted
o Hypokalemia: ‘T’ wave is small, flat or inverted
o Hyperkalemia: ‘T’ wave is tall and tented.
J POINT: The point where ST segment starts is known as J point.
U WAVE
• Not usually seen

• Seen in
o Hypercalcemia, thyrotoxicosis and hypokalemia. It is very prominent in hypokalemia.
o Myocardial ischemia: Inverted ‘U’ wave
PR INTERVAL
• Signifies AV nodal delay

• From the Start of P wave to Start of R Wave
• Normal: 0.12 to 0.16s (max 0.2s)
HEART BLOCK
1°
• PR interval prolongation [0.24 sec]

• All P Waves are followed by QRS Complex
2°
APPOLO ACADEMYA 32
• Not All P Waves are followed by ORS Complex (INCOMPLETE

OMPLETE HEART BLOCK)
• Mobitz Type 1
o PR interval
rval goes on increasing In successive
s beats & ultimately drops (QRS absent)
• Mobitz Type 2
o Atria to ventricular
entricular Ratio:
R 8:7 (inconsistent)
o 8th beat not reaching the ventricle
vent
o PR interval is Fixed
• Mobitz Type 3
o Consistent (3:2)
o Every 3rd beat will not reach
rea ventricle
o P wave not followed
ollowed by QRS Complex
3°: No P Wave is followed by QRS

RS complex
WOLFF PARKINSON WHITE

HITE SYNDROME
o SHORTENING
RTENING OF PR INTERVAL
o NO AV NODAL DELAY due to accessory connection from atria to ventricles, bypassing AV Node.
o Delta wave seen on ECG
J – POINT: End of S Wave; Iso-electric

electric point / reference point
QT INTERVAL
o Normal: 0.41 – 0.43s

o Includes ventricular depolarisation
epolarisation + repolarisation
CARDIAC CYCLE EVENTS (Heart Rate)
ATRIAL EVENTS (0.8 Sec)
1. Systole (0.1 Sec)

2. Diastole (0.7 Sec)
APPOLO ACADEMYA 33
VENTRICULAR EVENTS (0.8 Sec)
1. Systole (0.3 Sec)

• Isometric contraction = 0.05
• Ejection period = 0.22
2. Diastole (0.5 Sec)
• Protodiastole = 0.04
• Isometric relaxation = 0.08
• Rapid filling = 0.11
• Slow filling = 0.19
• Last rapid filling = 0.11
JVP (JUGULAR
LAR VENOUS PRESSURE)
PRESSURE
o RA pressures are recorded from Internal

Intern Jugular veins
o Normal: 0-5cm of H2O / 0--2mm of Hg
o a wave: atrial systole
Larger
er a waves / cannon ‘a’ waves Seen in
Tricuspid Stenosis
AV Dissociation
o c wave:
Isovolumic contraction of rt. Ventricle
Balloning backward OF Tricuspid valve into Rt. atrium)
o x Downslope: ventricular ejection
eje
o v Wave:
Venous blood accumulates in Rt. atrium
atri due to ISOVOLUMIC IC RELAXATION of Rt.
Ventricle
Larger in lt atrium (receives 1-2%
1 2% [of bronchial circulation] more blood & Some amount of
venous admixture
dmixture of blood)
o y Downslope: Ventricular Filling
Abnormal y slope in Cardiac tamponade, Constrictive pericarditis
peri
APPOLO ACADEMYA 34
PCWP (PULMONARY CAPILLARY

LLARY WEDGE PRESSURE)
o Left atrium pressure is recorded as PCWP

o Not a Naturally occurring pressure
o Normal valve: 5mm of Hgg or 5-8cm
5 OF H2O
CARDIAC OUTPUT
Cardiac Output = Stroke Volume * Heart Rate

CARDIAC INDEX: Cardiac Output /Body Surface Area
FACTORS DETERMININ ING CARDIAC OUTPUT
o STROKE VOLUME:
VOLUME
depends On Strength of contraction
more the Filling,
Filling More the Stroke Volume
more the venous return, more the Stroke Volume
Determined by Frank Starling law.
INDICES
NDICES
• EJECTION FRACTLON:
o Stroke Volume / End diastolic volume * 100
o Normal: 60-65%
o Decreases in LVF
• HEART RATE:
• 72-130/min
o ↑Heart rate → ↑Stroke volume
rcoplasmic Ca++ contration
o STAIRCASE EFFECT: Due to ↑ Sarcoplasmic
becomes Stronger, reach peaks at 130 bpm
• 130-160/min
o ↑ Heart rate → Stroke volume Constant
• 160-180/min
o Filling suffers
o ↑ Heart rate →↓ Stroke volume
• >180/min
o Cardiac output becomes virtually nil.
o HRmax = 220
BAINBRIDGE
REFLEX
IV Saline →
Sudden ↑Heart
Rate & Cardiac
Output i.e.
increase venous
return causes
increase HR
APPOLO ACADEMYA 35
CIRCULATION
BLOOD FLOW
• Largest fraction of blood flow goes to Liver (25-27%), next Kidney (25%)
TYPES:
1. LAMINAR/ STREAMLINE BLOOD FLOW: Follows parabolic path; Silent

2. TURBULENT BLOOD FLOW: Eddy Currents produced; Sounds heard
REYNOLD'S NUMBER determine the type of Blood Flow
• Re < 2000 → Laminar

• Re >2000 → Turbulent
• Re α VDP/ɳ where V = velocity, D = Diameter, P = density, ɳ = Viscosity
FOURTH POWER LAW
• Flow α r4 where r = radius
FUNCTIONAL TYPES OF BLOOD VESSELS
1. WINDKESSEL VESSELS
a. Aorta, large arteries
b. Shows WINDKESSEL EFFECT
c. Aorta distends & accumulates the blood during ventricular systole without rising pressure
Much.
d. During Left ventricle diastole, aorta coils back & pushes the blood forward. (Potential energy
→ kinetic energy)
2. RESISTANCE vessels
a. Arterioles
b. Offer greatest resistance to blood Flow
c. Has maximum effect on Blood Pressure (pressure head drops Maximally)
d. Greatest drop of pressure occurs at Arteriolar Segment (Resistance vessels]
e. Average Capillary pressure: 15-20 mm of Hg
f. Pressure Of circulation in a dead person 6mm of Hg due to TISSUE PRESSURE
g. CRITICAL CLOSING PRESSURE:
i. Arterial pressure of 20mm OF Hg
ii. Pressure below which blood flow Stops & vessels close down
3. CAPACITANCE VESSELS
a. Veins
b. More than half the volume Of blood (54%) is presents in Venous compartment
4. EXCHANGE VESSELS
a. Capillaries
5. THOROUGHFARE VESSELS
a. A-V anastomosis / Shunt vessels
BLOOD PRESSURE
• Stroke volume is best indicated by Pulse pressure

• BP recorded by IV Catheter & Sphygmomanometer (gives Slight higher valves)
DETERIMINANTS OF ARTERTRAL BLOOD PRESSURE

APPOLO ACADEMYA 36
• OHM’S LAW: BP = CO x TPR
PRESSURE IN CIRCULATION
• Blood Flows from high pressure to low pressure

• Hydrostatic factor: Beneath the Surface of water, pressure increases
• TRANSMURAL Pressure: Pressure across the vessel wall
TYPES OF BP
1. SYSTOLIC BP
a. Highest pressure of Systole
b. Indicates the force of Contraction
2. DIASTOLIC BP
a. Lowest pressure of diastole
b. Indicates Peripheral Resistance
c. Greatest peripheral resistance offered by skeletal muscle contraction
d. Cutaneous circulation contributes 20-30% of peripheral resistance
3. PULSE PRESSURE: SBP — DBP
a. Indicates Stroke Volume
b. DBP + Pulse pressure = SBP
4. MEAN ARTERIAL PRESSURE
a. Average pressure
b. MAP = DBP + 1/3rd of Pulse pressure
c. MAP is not the exact arithmetic Average due to longer duration of Diastole.
REGULATION OF BLOOD PRESSURE
1. Chemical
2. Neural /Short term
CHEMICAL REGULATLON
VASOCONSTRICTORS (↑BP)
• Vasopressin
• Noradrenaline
• Angiotensin [Angiotensinogen (plasma protein) formed by Liver]
• Endothelin (most potent Local vaso-constrictor)
• Urotensin (most potent Circulating vaso-constrictor)
VASODILATORS
• HYPOXIA
o causes vasodilatation everywhere EXCEPT in LUNGS
o ATP Sensitive K+ channels are present everywhere causes vasodilatation
o O2 Sensitive K+ channel in the membrane of pulmonary vessel causes vasoconstriction
• CO2
o Local vasodilator
o Systemic vasoconstrictor (if it accumulates in medulla)
• H+
• Lactic Acid
• Histamine
• Adenosine: Coronary vasodilator except in afferent arteriole of KIDNEY
APPOLO ACADEMYA 37
• Nitric Oxide: Endothelium

helium derived Relaxing factor (Strongest
( Vasodilator)
NEURAL / SHORT TERM REGULATLON
• BRARORECEPTOR
EPTOR MECHANISM
o BR impulse frequency is highest at 180 mm of Hg
o BR System is most sensitive at 100 mm of Hg. This is the NATURAL SET POINT PO for BR
o Vasomotor centres in medulla (Rostral ventro lateral medulla – vasoconstrictor area,
Cardioaccelarator area present
pr behind cardioinhibitory area in medulla)
o BARO
RO RECEPTORS are
Mechano
echano-Sensitive receptors
Stretch
ch receptors
Sprayy type endings
IX & Xth Nerves area called
lled on BUFFER NERVES (Buffer the Changes of BP)
Operational
perational Range
Carotid baroreceptors → 60 — 180 mm of Hg
Aortic baroreceptors → 90 — 210 mm of Hg
• CHEMORECEPTOR MECHANISM
MECHANI
o CAROTID BODY Y is
Present
resent in common carotid Artery
Chemosensitive cell = glomus cell
Sensitive to hypoxia
BP from
rom 60-30mm
60 Hg, causes ↓ Blood Flow (hypoxia)
• CNS ISCHEMIC RESPONSE / LAST DITCH STAND
o At Low BP (<30mm Hg), Blood flow to VMC is decreased & CO2 accumulates
accumulat around VMC
& Stimulates vasoconstrictor
soconstrictor centre & BP rises immediately.
o CUSHING’S REACTION
ICT ↑
CSF Pressure
Pres ↑
ICT > Cerebral artery pressure
pres
APPOLO ACADEMYA 38
INTERMEDIATE TERM REGULATION
• ADH & Thirst mechanism

• Capillary fluid mechanism
• RAAS (Intermediate to long term)
• ANP (Atrial Natriuretic Peptide) mechanism: ANP → Kidney → Natriuresis & diuresis
LONG TERM REGULATION
• KIDNEY BODY FLUID MECHANISM: Urine output adjusted on a Long term basis
o at 100mm of Hg, Urine Output 1 - 1,5 ltr/day (normal)
o at 60mm of Hg, urine Output Zero
o at I60mm of Hg, Urine Output 4-6 times the normal
RESPIRATORY SYSTEM
INTRODUCTION
• 23 generations of Respiratory Tree

• First 7 generations = cartilaginous, non compressible
• Last 16 generations non-cartilaginous
o Compressible
o Thin layer of smooth muscles present
o Some Neuroendocrine cells present like APUD, KULCHITSKY CELLS
• First 16 generations: CONDUCTING ZONE (DEAD SPACE)
• Last 7 generations: RESPIRATORY ZONE
o CLARA CELL
Present in middie & lower generations
Synthesizes surfactant like materials (also produced by type II pneumocytes)
Surfactant synthesis begins by 20 weeks of gestation
Surfactant begins to appear by 28-32 weeks of gestation
Surfactant reduces the surface tension in the alveoli and prevents collapsing tendency
of lungs.
In surfactant hydrophilic proteins SPA and SPD destroy the bacteria and viruses by
means of opsonization.
• Last 6 generations: ACHILLES HEEL OF RESPIRATORY SYSTEM (muco-ciliary clearance is
weakest)
MECHANICS OF BREATHING
o In normal quiet breathing

o Inspiration is Active (work done)
o Expiration is Passive
MUSCLES FOR BREATHING
o DIAPHRAGM (Major contribution in males): Abdomino thoracic breathing

o EXTERNAL INTERCOSTALS (Major Contribution in females): Thoraco abdominal breathing
o Accessory Muscles of inspiration
Ala nasi
STM [Sternocleidomastoid]
Scaleni
Serratus anterior
o Muscles for forceful Expiration / Accessory Muscles of inspiration
Abdominals
APPOLO ACADEMYA 39
Internal Intercostals: depress the rib cage
MOVEMENT OF THORACIC CAGE
• Thoracic lid
o Formed by manubrium sterni
o Movement increases AP diameter of thoracic cage
• Upper coastal series
o Pump handle movement: increases AP diameter of thoracic cage
o Bucket handle movement: increases transverse diameter of thoracic cage
• Lower coastal series
o Bucket handle movement: increases transverse diameter of thoracic cage
• Diaphragm
o Movement increase vertical diameter of thoracic cage
PRESSURES
o INTRA PLEURAL INTRA THORACIC PRESSURE

Around the lungs, between the 2 layer of pleura
Mostly negative except for forceful expiration
Keeps the lung distended
o Greatest negative intra thoracic pressure created at Muller’s Maneuver (Forced Inspiratory effort
against closed glottis)
o Greatest positive intra thoracic pressure created at Valsalva Maneuver (Forced Expiratory effort against
closed Glottis)
PLEURAL FLUID
o Keeps the pleurae together especially during inspiration
PLEURAL PRESSURE
o INTRA ALVEOLAR PRESSURE / INTRA PULMONARY PRESSURE:

At the start of Inspiration = - 1
At the start of Expiration = + 1
o INTRAPLEURAL / INTRATHORACIC / TRANS PULMONARY PRESSURE
Pressure between visceral & parietal pleura
Responsible for opening of lungs during inspiration
At the end of normal inspiration: –6 mm Hg
At the end of normal expiration: –2 mm Hg
At the end of forced inspiration: –30 mm Hg
At the end of forced inspiration with closed glottis (Müller maneuver): –70 mm Hg
At the end of forced expiration with closed glottis (Valsalva maneuver): +50 mm Hg.
o TRANS MURAL PRESSURE
Pressure across the airway wall
Pressure inside the airway — Pressure in interstitium
SURFACTANT
Surface active material that reduces the surface tension.
CONSTITUENTS
1. BPPC (DiPalmitoyl Phosphatidyl choline) (major)
2. Surface apo proteins (Sp A,B,C,D) regulate the Surfactant turnover
3. Ca++ ions helps in faster Spread of Surfactant
APPOLO ACADEMYA 40
FUNCTIONS
• ↓ Collapsibility of the lung
• ↑ Distensibility of the lung (compliance)
• ↓ Surface tension
• Keeps alveoli dry
• Absence of surfactant in infants: collapse of lungs and the condition is called respiratory
distress syndrome or hyaline membrane disease.
• Deficiencyy of surfactant in adults is called adult respiratory distress syndrome (ARDS).
PNEUMOCYTES: alveolarr epithelial cells
Type 1— covers 93% Surface

urface Area of alveoli, helps in gaseous exchange
Type 2 — covers 5% Surface Area of alveoli, Synthesize Surfactant, size very small & numerous
o During
uring development,
development entire area is covered by Type 2 cells, att the time of birth,
bir type 1 replace
type 2 cells
lveolar injury, Type 1 degenerates, Type 2 regenerates
o In alveolar
Type 3 — cover 2% Surface Area of alveoli, acts as chemoreceptor cells
COMPLIANCE
Measure of Stretchability /distensibility

distensibility of
o Lung
Compliance α 1/ST
LUNG VOLUMES & CAPACITIES
measured by HUTCHISON’SSON’S SPIROMETER

TIDAL VOLUME [TV] (500m 500ml): amount of air that we can inspire or expire with each quiet breath
INSPIRATORY RY RESERVE VOLUME [IRV] (3000 ( ml): amount of air that can maximally breath in
beyond quiet inspiration
EXPIRATORY
RATORY RESERVE VOLUME V [ERV] (1100ml): amount of air, we can forcefully breath out
beyond quiet expiration
RESIDUAL VOLUME [R RV] (1200ml): amount of air that remaining
ng in lung after forceful expiration
INSPIRATORY
RATORY CAPACITY [TV + IRV]: Total volume of air that con be inspired nspired
APPOLO ACADEMYA 41
FUNCTIONAL L RESIDUAL CAPACITY

CAPAC [ERV + RV]: amount nt of air that remaining
remain in at the end
quiet expiration
VITAL CAPACITY [TV+IR +IRV+ERV]: amount of air that maximally exhale out after
a 1st maximal
inspiration
TOTAL LUNG CAPACITY CITY [TV + IRV+ ERY +RV]
DEAD SPACE
• Normal: 1ml /pound

pound of body wt
• 150 ml
• TYPES:
natomical Dead space
1. Anatomical
1st 166 generations
measured by FOWLER’s
F METHOD
2. Physiological / total
tot Dead space
Anatomical
natomical dead Space + Alveolar dead Space
measured by BOHR’ S METHOD
with deep forceful inspiration alveolar dead space decreases, anatomical dead space
increases
RESPIRATORY
RATORY MINUTE VOLUME (RMV):
( TV * RR →6-8 L/ min
ALVEOLAR
LVEOLAR VENTILATION PER MINUTE:
MINUTE (TV - PSV) → 4 - 4.2 L/ min
MAXIMUM VOLUNTARY
RY VENTILATION / MAXIMUM BREATHING CAPACITY: 125 — 140 L/ min
BREATHING RESERVE (BR):: (MVV — RMV) → 117 L/ min
O2 DISSOCIATION CURVE
• Relation between PO2, & %

Saturation of Hb
• Sigmoid Shape
o Initial slow rise of
curve due to first O2
molecules combining
with Hb molecules in
Tense state
o Further Rapid rise of
curve (Steep Rise) due
to Relaxed State of Hb
molecule, also due to
POSITIVE CO-
OPERATIVITY
between O2 molecules.
SHIFT OF THE CURVE
• SHIFT TO RIGHTWARD & DOWNWARDS (liberation of O2)

↑ H+
↑Temperature
↑PCO2
↑2,3-DPG — Occurs in RBC
• BOHR's EFFECT: Shift of O2- Dissociation curve to right due to ↑ PCO2.
APPOLO ACADEMYA 42
• SHIFT TO LEFTWARD & UPWARD (holding of O2)

↓ H+
↓Temperature
↓PCO2
↓2,3-DPG — Occurs in RBC
CO2 TRANSPORT
• Occurs in 3 FORMS:
o HCO3- (70%)
o Carbaminomino compounds (20-25%)
(
o Free/ dissolved
ssolved in plasma (5-7%)
(
• HALDANE EFFECT/ REVERSE BOHR EFFECT
o Inspired O2 enters in RBC & Combines with Hb displacing H+
o Cl- leaves & HCO3- enters into RBC through Band 3
o CO2 reformed
o DOUBLE the volume
volum % OF CO2 is Liberated
REGULATION OF BREATHING
NEURAL REGULATION
o Automatic Regulation (Brain

Brain stem)
o Voluntary Regulation (Cortex)
ortex)
AUTOMATICC REGULATION (BRAIN

(BR
STEM RESPIRATORY CENTER)
PRE BODZINGER COMPLEX
o present in upper medulla

o ous
pace maker for Spontaneous
breathing
o Neurons of DRG / VRG Synapse
here
PNEUMOTAXIC & APNEUSTIC

CENTERS: Controls Rate & Depth of
breathing
PNEUMOTAXIC CENTER
o Causes an early switch off to

Inspiratory Ramp Signal
o Rapid & Shallow breathing occurs
APNEUSTIC CENTER
o Not allow early Switch

witch off to
Inspiratory Ramp Signal
o Slow & deep breathing occurs
VRG
o In forceful Expiration, spill over of impulses from DRG to VRG occurs

o Neurons of VRG sends signals
ignals to forceful expiration (to respiratory muscles)
APPOLO ACADEMYA 43
LESIONS EFFECTS
Vagotomy Prolonged Inspiration
Transection in Lower border of medulla (above C-3) Spontaneous breathing Stops
Transection in Upper border of medulla Irregular & Jerky Spontaneous breathing
Mid pontine transection Long inspiratory spasms, Apneustic breathing
Lower pontine transection Rapid, shallow breathing
CHEMICAL REGULATION OF BREATHING
CHEMORECERTORS
PERIPHERAL RECEPTORS
o located in Carotid & aortic bodies

o Glomus Cell = Chemosensitive cell
o has O2 Sensitive K+ channel
o Sense the hypoxia
o K+ channel closes, depolarisation occurs
o Sends signals via IXth CN from Carotid body & Xth CN From aortic body
o Responds to
1. Arterial hypoxia: most acid Production occur at AEROBIC METABOLISM
2. Fixed Acids: Lactic acids, Keto acids
o O2 does not drive the ventilation via peripheral chemoreceptors until PO2 <60 mm Hg
CENTRAL CHEMORECEPTORS
• Situated in 1/5th mm beneath the Upper aspect of Medulla

• Part of respiratory centre
• Responds to H+ in CSF or Interstitial Fluid of brain. (H+ ion reflects the CHANGES IN ARTERTAL
CO2)
• ↑CO2 / H+ → Stimulates ventilation; ↓CO2 / H+ → Depresses ventilation
• When arterial PO2 <60 mm Hg, Hypoxic Stimulation of peripheral Chemoreceptor is so strong that it
overrides the effect of CO2 & H+ acting on central chemoreceptors to depress ventilation.
CHANGES DURING ACCLIMATIZATION TO HIGH ALTITUDES (HYPOXIC HYPOXIA)
1. ↑ 2,3 — DPG
2. ↑ Sensitivity of Peripheral chemoreceptors
3. ↓ Sensitivity of Central chemoreceptors
HYPOXIA
1. HYPOXIC HYPOXIA: occurs at high altitudes, Heart & Lung diseases

2. ANEMIC HYPOXIA: occurs in anaemia, CO poisoning; Arterial PO2 is normal.
3. STAGNANT / HYPOKINETIC / ISCHEMIC HYPOXIA: seen in Shock (↓CO2, ↓BP)
4. HISTOTOXIC HYPOXIA: Seen in Cyanide poisoning
J - RECEPTOR
• Juxta alveolar receptor in pulmonary interstitium

• Accessed from pulmonary vessels
• Stimulated by –
o Pulmonary Congestion
o Pulmonary embolism
o Pulmonary oedema
APPOLO ACADEMYA 44
• EFFECTS –
o Apnoea
o Rapid shallow breathing
o Strong vagal Stimulation
Stim
Bradycardia
Hypotension
ypotension
BREATHING
• APNEUSTIC
PNEUSTIC BREATHING:
BREATHING Long inspiratory spasms
• CHENNE- STOKES BREATHING: Apnoea Ap followed by hyperapnoea with waxing waning type
breathing
o Physiological conditions where Cheyne-Stokes
Cheyne breathing occurs
During deep sleep
In high altitude
After prolonged voluntary hyperventilation
During hibernation in animals
In newborn babies
After severe muscular exercise.
o Pathological causes of Cheyne-Stokes
Cheyne breathing:
During increased intracranial pressure
During advanced cardiac diseases, leading to cardiac failure
During advanced renal diseases, leading to uremia
Poisoning by narcotics
In premature
ature infants.
• BIOT BREATHING: Apnoea followed by hyperapnoea without waxing waning type breathing.
• KUSSMAUL BREATHING: increased depth & Prolonged inspiration
• IRREGULARLY IRREGULAR:ULAR: seen in Meningitis
• Image from left to right: APNEUSTIC BREATHING, CHENNE-

CHEN STOKES BREATHING,
KUSSMAUL BREATHING
MOUTH TO MOUTH BREATHING → contains 16% Oxygen
EXERCISE increases TV
V & RR, so Respiratory Minute volume↑
HERING - BREUVER
VER REFLEXES
• Classic negative feedback

back reflex
• INFLATION REFLEX
o Protective reflex
o Initiate at TV > 1 Ltr
• DEFLATLON REFLEX
o Ex: Yawning — more negative intra thoracic pressure Created & Opens up terminal
termin alveoli
HEAD’S
D’S PARADOXICAL REFLEX
positive Feedback occurs at birth

Distension Distension
APPOLO ACADEMYA 45
EFFECTS OF HIGH BAROMETRIC PRESSURE
• Seen in divers & Mine workers

• Types:
1. NITROGEN NARCOSIS
2. CAISSON’S DISEASE
NITROGEN NARCOSIS
• N2 dissolves in body fluids if works at depth for long time

• N2 has high affinity for lipids, so dissolves in neuronal membranes of myelin → NITROGEN
NARCOSIS
o Similar to alcoholic intoxication
o Loss of recent memory
o Fine motor activity impaired
CAISSON’S DISEASE/ DECOMPRESSION SICKNESS
• Seen in persons working at depth for long time & comes at the surface Suddenly
• Pressure released, N2 expands suddenly forms bubbles
• N2 BUBBLES
o 1st formed in tissues (muscles & tendons)→ BENDS
o Comes to Systemic Circulation
o Then Comes to Pulmonary Circulation → CHOKES
o Order of elimination: Systemic → pulmonary circulation → Fats (last)
• Prevented by Slowly Coming to Surface
• Rx by Decompression Chambers
EXCRETORY SYSTEM
NEPHRON
Types:
1. Cortical Nephrons:
a. 85%
b. Have short loops
c. Entirely located in Cortex
d. Forms Normotonic urine
2. Juxta Glomerular Nephrons
a. 15%
b. Glomeruli situated in the cortex at the junction of cortex & medulla
c. Have long loops
d. Forms concentrated urine
BLOOD FLOW TO THE KIDNEY
• Both the kidneys receive about 1,300 mL of blood per minute, i.e. about 26% of cardiac output.
Kidneys are the second organs to receive maximum blood flow, the first organ being the liver, which
receives 1,500 mL per minute, i.e. about 30% of cardiac output.
• Renal circulation has a portal system, i.e. a double network of capillaries, the glomerular capillaries
and peritubular capillaries.
• Renal glomerular capillaries form high pressure bed with a pressure of 60 mm Hg to 70 mm Hg. It is
much greater than the capillary pressure elsewhere in the body, which is only about 25 mm Hg.
APPOLO ACADEMYA 46
• Peritubular capillaries form a low pressure bed with a pressure of 8 mm Hg to 10 mm Hg. This low
pressure helps tubular reabsorption.
• Cortex receives most of blood flow because of glomerulus.
• Medulla Consumes more O2
o O2 Consumption metabolic rate / ATP load is directly linked to tubular load for Na+
reabsorption
JUXTA GLOMERULAR APPARATUS
• Lies close in relation to GLOMERULUS

• Has 3 cells
o Cell in Wall of afferent arteriole
o Cell lining the early DCT
o Cell between the above two
CELL IN THE WALL OF AFFERENT ARTERIOLE
• JG cell / GRANULAR CELL: Synthesizes Renin enzyme which converts ANGIOTENSINOGEN from
liver to ANGIOTENSIN I.
ANGIOTENSIN II FUNCTIONS
1. Vasoconstriction
2. Salt & Water Retention
3. Aldosterone Secretion (Adrenal gland) — Na+ Reabsorption.
CELL LINING THE EARLY PCT: MACULA DENSA CELL
• Senses the Na+ & Cl- In tubular Fluids (TUBULO GLOMERULAR FEED BACK)
• Ligand → ADENOSINE
• Causes vasoconstriction of efferent arterioles
MESENGIAL / LACIS / GOORMAGHTIGH / PSEUDOMESENARIAN CELL
• alter vessel diameter

• has role in immune complex formation
ERYTHROPOETIN
• Type 1 Cortical Interstitial cell around peritubular capillaries synthesizes it

• Type 1 Cortical Interstitial cell CONTAINS O2 Sensitive K+ Channels (O2 Sensitive K+ Channels also
seen in Pulmonary vascular smooth muscle cell, Carotid body, Type 1 Cortical interstitial cell)
• 90% produced by Kidney
• 10% produced by Liver
MERSUREMENT OF GFR
• Best substance Inulin (has to be injected)

• Most common Substance: Creatinine (endogenous, need not be injected)
• Factors affecting GFR:
o Renal blood flow
o Tubuloglomerular feedback – Macula densa is sensitive to NaCl of tubular fluid
Factors increasing the sensitivity of tubuloglomerular feedback:
• Adenosine
• Thromboxane
APPOLO ACADEMYA 47
• Prostaglandin E2
• Hydroxyeicosatetranoic acid.
Factors decreasing the sensitivity of tubuloglomerular feedback:
• Atrial natriuretic peptide
• Prostaglandin I2
• Cyclic AMP (cAMP)
• Nitrous oxide.
Glomerular capillary pressure
Colloidal osmotic pressure
Hydrostatic pressure in Bowman capsule
Constriction in afferent arteriole
Constriction in efferent arteriole
Systemic arterial pressure
Sympathetic stimulation
Surface area of capillary membrane
Permeability of capillary membrane
Contraction of glomerular mesangeal cells
Hormonal & other factors
• Factors increasing GFR by vasodilatation
o Atrial natriuretic peptide
o Brain natriuretic peptide
o cAMP
o Dopamine
o Endothelial derived nitric oxide
o Prostaglandin (PGE2).
• Factors decreasing GFR by vasoconstriction
o Angiotensin II
o Endothelins
o Noradrenaline
o Platelet activating factor
o Platelet derived growth factor
o Prostaglandin (PGF2).
TUBULAR FUNCTIONS
• GLOMERULUS → Isotonic ultra filtration

• PCT Reabsorbs
o 67% Na+
o 67% H2O
o 100% Glucose
o 100% Amino Acids
o >90%. HCO3-
o 70-75% K+, Ca+, Cl-
• H2O REABSORPTION
o PCT →67% OBLIGATORY H20 REARSORPTION (irrespective OF body osmolarity)
o LH & DCT → 10-15%
o Collecting duct by ADH →10-12% FACULTATIVE REABSORPTION (Under the Influence
of Osmolarity)
• Under ADH influence, greatest fraction of H2O is reabsorbed from PCT (not collecting duct)
• In the absence of ADH, 88% of Water is reabsorbed
• In the presence OF ADH, 99% of water is reabsorbed
LOOP of HENLE
• Descending Limb
APPOLO ACADEMYA 48
o Some H2O into interstitium

o Na+ (BuIk Flow/ Solvent Drag)
• THICK Ascending Limb
• NKCC Transporter (Na+ K+ Cl- Cotransporter) [Loop diuretics Acts on it]
• Impermeable to H2O
• Fluid reaching to early DCT → hypotonic (DILUTING SEGMENT → Thick Ascending Limb)
DCT
• Containing NCC transporter (Thiazides acts on it)

• 10% of Na+, Cl- removed
• Removes some H2O
COLLECTING DUCT
• Absorbs of 10-12% of H2O under ADH

• Concentric Segment
• ‘P' cell (PRINCIPLE CELL): reabsorbs Na+, secretes K+
• I (INTERCALATED) CELL: reabsorbs K+, secretes HCO3-, Buffering cell of kidney.
TUBULAR / TRANSPORT MAXIMUM (Tmax)
• Maximum race, upto which a Substance can transported across tubule

• Glucose Tmax : 320 mg/min (373 in Males & 303 in Females)
• Only substance without transport maximum → Na+ reabsorption
• K+ Secretion in distal nephron has no transport maximum
UREA
• Urea transported via UT1 & UT2

• Urea transport is under the influence of ADH
• Contributes to 40% of interstitial osmolarity
• Recycled & excreted in a concentrated manner
COUNTERCURRENT EXCHANGE
Vasa recta (Blood vessels)
• Responsible for countercurrent exchange

• Do not actively contribute to hyperosmolarity
• Blood Flow is sluggish
• Blood collects Na+ K+ Cl- & gives out as it moves down descending limb & becomes hypotonic
MAXIMUM CONCENTRATED URINE →1200 mosm/L (4 times the normal)
Most hypotonic urine → 50 mosm/L
OBLIGATORY URINE output → 0-5 L/day)
Minimum Urine output required to excrete at least 600 mosm /day of solutes if urine concentrated maximally.
Oliguria → 400 ml/day, Anuria → 100 ml/day
Max. urine output with most hypotonic Urine → I8L/day

APPOLO ACADEMYA 49
BLADDER
• 50 ml → Residual volume
• 150 ml → First reflex
• 250 ml → First desire
• >400 ml → urgency
• >600ml → Painful urgency
rgency
• 800-900ml → Physiological
hysiological capacity
• 1000 ml → Anatomical capacity
INNERVATION OF
F MICTURATION
• Mainly under Parasympathetic

arasympathetic Control (S-2,3,4)
(S
• Forms reflex arc
• Sympathetic innervation carries Pain Sensation
• PUDENDAL NERVE
o Somatic nerve which controls external urethral sphincter
• BRAIN STEM
o BARRINGTON’S
ARRINGTON’S MICTURATION
M CENTRE
for facilitation
facilita or inhibition of reflex arc
micturition
ion reflexes → Barrington’s reflexes
• CEREBRAL CORTEX
o Paracentrall lobule of frontal lobe has Cortical Voluntary centre for mictturation
o Predominantyanty inhibitory to external Urethral sphincter
s
LESIONS
• Atonic bladder: If afferents from bladder are cut

APPOLO ACADEMYA 50
• Hypertonic bladder / Automatic bladder: Transection above S2, Reflex arc Intact (UMNL)
• Hypotonic bladder / Autonomous bladder / Overflow Incontinence: Lesion at S2, S3 or S4, flaccid
bladder (LMNL)
Subtypes:
Motor Paralytic bladder – Motor (efferent) pathway is damaged. However, patient
can sense bladder fullness, resulting in prompt diagnosis. Associated with:
• Complication of abdominal/ pelvic surgery
• Lumbar canal stenosis
• Lumbo-sacral meningo-myelocele
Sensory Paralytic bladder – Sensory (afferent) pathway is damaged and hence,
patient cannot sense bladder fullness, resulting in delayed diagnosis. Associated with:
• Diabetes mellitus
• Syringomyelia
• Urge Incontinence/ Spastic neurogenic bladder/ Uninhibited bladder/ Mid stream holding lost/
Cortical bladder: Lesion between Voluntary Centre & Brain Stem, A/w Stroke, Parkinson’s disease,
Multiple sclerosis
Types as per position of lesion:
Postcentral cortex -- Loss of awareness of bladder fullness, Incontinence
Precentral cortex -- Hesitancy = Difficulty in initiating micturition
Frontal cortex Precipitancy = micturition with ‘easy’ stimulus, eg: sound of running
water, Inappropriate micturition/ loss of social inhibition (infant-like)
ENDOCRINOLOGY
PEPTIDE / PROTEIN HORMONES
• Not bounded to plasma proteins, have short t1/2;

• Exception: (IGF [insulin Like growth Factors / Somatomedins)
• STEROTD HORMONES - Bound to plasma proteins, has longer t1/2
PLTUITARY GLAND
ADENO HYPOPHYSIS secretes
1. GH
2. Prolactin
3. FSH
4. LH
5. ACTH
6. TSH
NEUROHYPOPHYSIS Secretes ADH & OXYTOCIN
INTERMEDIATE LOBE has Basophils which Secretes PMOC (Proopiomelanocortin). PMOC → ACTH →
MSH; PMOC → beta-LPH → Endorphin
ADH & OXYTOCIN
• Synthesized in Supra optic (ADH), para ventricular (Oxytocin) nuclei of hypothalamus, bound to
NEUROPHYSINS, carried to post. Pituitary, then upon signal from hypothalamus it cleaved From
Neuophysins & free hormones are released.
HERRING BODIES: The neurosecretory bodies which are basically end of axons of hypothalamic cells where
ADH & Oxytocins are stored & released.
OXYTOCIN function:
APPOLO ACADEMYA 51
• MILK Ejection Reflex

• Contraction of Uterus during parturition
ANT. PITUITARY HORMONES
• Under the hypothalamic pituitary control

• 2 types of cells in ant pituitary, Chromophil cells & Chromophobe cells.
• CHROMOPHIL CELLS (50%)
o Acidophils – 80% - GH & Prolactin
Somatotropes – 50% - GH
Lactotropes – 10-20% - Prolactin
o Basophils (20%) - FSH, LH, ACTH, TSH
GONAPOTROPES
CORTICOTROPES
THYROTROPES
ADH / VASOPRESSIN
• Primarily regulates the OSMOLARITY (not the volume)

• Nerve cells in hypothalamus Sense osmolarity of plasma if it is HYPERTONIC
• HYPOSECRETION = DIABETES INSIPIDUS
o CENTRAL DI: ADH Synthesis & release affected
o NEPHROGENIC DI: Acts on Kidney affected due to lack of receptors
o Diuresis occurs
• HYPERSECRETION = SIADH (Syndrome of Inappropriate ADH)
• Plasma osmolarity is Normal, Still ADH Secreted
• Occurs in Stressful conditions
• Hypotonic plasma
• Plasma volume increases
GROWTH HORMONE
• Diabetogenic, anti-insulin Hormones

• ACTIONS
o METABOLIC : Carbohydrate metabolism: ↑ peripheral utilisation, hyperglycemia, pituitary
diabetes +
o NON METABOLIC (Action on growth): ↑osteoblastic activity, ↑deposition of new bone,
↑Protein deposition, ↑soft tissue mass.
DIABETES MELITUS
• PITUITARY DIABETES: Weakly Sensitive to Insulin

• ADRENAL DIABETES: Moderately Sensitive to insulin
• PANCRETIC DIABETES: Strongly Sensitive to insulin; ↑Protein Synthesis, ↓Protein degradation;
↑breakdown of triglyceride; ↑ free fatty acid levels
GH
• HYPERSECRETION
o Before puberty: GIGANTISM
o After puberty: ACROMEGALY (↑ Thickness of membranous bones, Prognathism,
Organomegaly – macroglosia)
• HYPOSECRETION
o Before puberty: DWARFISM (pituitary dwarf)
APPOLO ACADEMYA 52
o After puberty: ACROMICRIA
LEVI LORAIN DWARFISM
• Seen in african pigmes

• GH is Normal
• Deficiency of Somatomedin C
LARON’S DWARFISM
• GH is Normal / increased
• Receptor insensitivity
THYROID HORMONE
• Regulates BMR
• THYROID HORMONE SYNTHESTS (T3, T4)
o Iodides enter thyroid gland through Na+l symporter
TYROSINE + Iodine = MIT
MIT + I = DIT
DIT + DIT = T4
DIT + MIT = T3
o Enzyme involved: Peroxidase
o 90% T4, 9% T3, 1% reverse T3
o T3 is 4 times more potent than T4
• ACTIONS
o Regulates BMR
↑Carbohydrate metabolism: ↑ Glucose
↑Fat metabolism
↑Protein metabolism: Slightly more catabolic
o CVS
Stimulatory: ↑SV, ↑HR, ↑CO, ↑BP
o RS
Stimulatory: ↑TV, ↑RMV, ↑RR
o GIT: ↑motility
o CNS & Neuromuscular junction: ↑synaptic excitability
o Reproductive system:
Hyperthyroidism: oligomenormhea, Amenorrhea
Hypothyroidism: Polymenorrhea, Menorrhagia
• Hypo secretion:
o In pregnancy & infancy: Cretinism
Short Statured
Mentally retarded (not seen in Dwarfism)
Milestones delayed
Sexual immaturity
o Adults: Myxedema
Non pitting edema due to mucopolysaccharides (GAGS) accumulation in tissues
Absorbs water
Pretibial myxedema
• Goitre: Enlargement of Thyroid gland for any reason
• Hyper secretion:
o THYROTOXICOSIS (Hyperthyroidism with toxic manifestations)
TOXIC Manifestations: Tachycardia with Sleeping heart rate >90, Tremors
APPOLO ACADEMYA 53
o GRAVE'S DISEASE
Autoimmune disease
LATS (long acting thyroid stimulator) / TSI (Thyroid stimulating immunoglobulin)
Exophthalmos: due to deposition of fat & fluid in retrobulbar space & degeneration
of extra occular muscles)
ADRENAL GLAND
CORTEX
Zona glomerulosa → Mineralocorticoids (Aldosterone)

Zona fasculata → Glucocorticoids
Zona Reticularis → Sex steroids
MEDULLA
• Adrenaline (Epinephrine)
GLUCOCORTICOIDS
• Metabolic actions
o Gluconeogenesis → ↑Blood glucose (Adrenal diabetes)
• Non metabolic actions
o Antiinflamatory action
o Immuno suppressives
o Anti allergic
o Anti stress
HYPO SECRETION
ADDISON’S DISEASE
• Weak & Frail patient with low glucose & low BP

• ↑ACTH → pigmentation
HYPER SECRETION
CUSHING DISEASE
• Due to fat breakdown & centripetal redistribution of Fat

o Moon face
o Buffalo hump
o Protuberant belly
• Thin limbs
• Striations
CALCIUM HOMEOSTASIS
• PTH:
o ↓ Serum Ca = ↑PTH
o Anticipatory release
o Acts on osteoblast → ↑ Osteoclastic activity → ↑Bone resorption
o ↑Ca resorption from kidney
o Phosphate excretion
o Potentiate the action of Vit D
o ↑Ca++ absorption from intestine
APPOLO ACADEMYA 54
o TETANY (hypocalcemia) 1st manifestation) occurs at <7mg%. <6mg% death can occur
o Trousseau's sign: Carpopedal spasm
o Chvostek's sign — Facial muscle spasm
CALCITONIN
• Synthesized by Para follicular ‘C’ cells of Thyroid gland

• ↓Ca++ deposit on bone
VITAMIN D
• ↑Ca++ resorption from intestine & deposit on bone

• Deficiency in children — Rickets
• Adults — Osteomalacia
ENDOCRINE PANCREAS
• 98% exocrine
• 2% endocrine (by Islets of langerhans of tail portion)
o α cell (10%): Outer rim of Islets of langerhans – secretes Glucagon
o β cell (75-80%): Middle portion of Islets of langerhans – secretes Insulin
o δ cell (5%): Disperse - secretes Somatostatin
o F cell: Pancreatic Polypeptide
INSULIN
• Anabolic Hormone
• Receptor: Tyrosine Kinase (Catalytic receptor)
• METABOLIC ACTION
o CARROHYDRATES:
↑ peripheral uptake & utilisation (done via GLUT-4 at skeletal muscle & fat cell
Upregulates Glucagon Synthesis
↓Glycogenolysis
o FATS:
↑Uptake & lipogenesis promoted by ↑expression of lipoprotein lipase
o Skeletal muscle:
Protein Synthesis↑ & Protein degradation↓
TYPE I DM: Absolute lack of Insulin, Juvenile onset
TYPE II DM: Relative lack of Insulin (peripheral Insulin Resistance), Adult onset
LADA: Late Adulthood onset Diabetes of Autoimmune Origin, has Anti-GAM Antibodies
GLUCAGON
• ↑Blood glucose (Diabetogenic)

o Glycogenolytic
o Gluconeogenic
o Stimulates lipolysis
o Ketogenic
SOMATOSTATIN
• Inhibits Gastrin, TSH, VIP Secretion

APPOLO ACADEMYA 55
• Inhibits both Insulin & Glucagon Secretion
FEMALE REPRODUCTIVE SYSTEM
Primary aim: Survival of species (indirect way of homeostasis)
PUBERTY
• Pulsatile GnRH Secretions causes puberty
Girls Sequence
1. Thelarche
2. Pubarche
3. Menarche
4. Adrenarche
FEMALE REPRODUCTIVE SYSTEM
• Inherently cyclic function

• OVARIES: SEX STEROIDS & FUNCTIONS
o Secreted locally nourishes the Ovum
o Circulating & acts on different organs
• Fundamental reproductive Unit → Single ovarian Follicle
PRIMORDIAL FOLLICLE: Granulosa cells surrounding oocyte
SECONDARY FOLLICLES:
• Granulosa cells forms multilayered epithelium

• Granulosa cells secrete paracrine factors (Stromal cells differentiated into epiltheloid cells → THECA
CELLS) & forms MATURE FOLLICLE
MENSTRUAL CYCLE
At the Start of each cycle-
• 5-6 follicles enlarge

• Cavity formed around the Ovum → ANTRUM, filled with Antral / follicular fluid, contains GAGS,
electrolytes, FSH, LH, IGF-I, IGF-II, TGF-β etc.
• At 5-6 Day, 1 Follicle becomes dominant
• All the circulating oestrogen comes from theca interna cells, local estrogen comes from Granulosa
cells.
• At 14th day, Ovum with surrounding cumulus oophorus extruded from follicle
• Remaining part converted into Corpus Luteum
• On the 1st day, it converted into Corpus Haemorrhagicum
• MITTELSCHMERZ: Minor bleeding into Peritoneum & pain
• Granulosa & Theca cell line the corpus luteum, called granulosa lutein cells, Theca Lutein cells
• Corpus luteum dominated by progesterone
• If pregnancy, Occurs, Corpus luteum persists
• If pregnancy do not occurs, CL regressed by Luteolysis occurs 4 days prior to next cycle.
• lt replaced by Scar tissue & Converted into Corpus albicans
NORMAL MENSTRUATION
APPOLO ACADEMYA 56
• MENSTRUAL BLOOD
o predominantly arterial, 25% venous
o Contains tissue debris, PGs, Fibrinolysin
o Average loss: 30 mI
• CYCLICAL CHANGES IN CERVIX
o Before ovulation (estrogen): Cervix MUCUS thinner & More alkaline
o After ovulation (progesterone): 3 cm MUCUS thick, cellular, tenacious
o SPINNBARKEIT (Elasticity): Can be stretched into long thin thread
o Dries in a Fern like pattern
• VAGINAL CYCLE
o Under Estrogen, vaginal epithelium Cornified
o Under progesterone, vaginal epithelium proliferated, mucus becomes thick
• CYCLICAL CHANGES IN BREAST
o Under estrogen, proliferation of mammary ducts
o Under progesterone, growth of lobules, alveoli.
OVARIAN STEROIDOGENESIS
• Before ovulation, LSH & FH acts on cells of developing follicles

• Theca cells have the receptors for LH, can take up cholesterol & produce testosterone under LH but do
not have aromatase enzyme, essential for the Conversion of testosterone into estrogen.
• Granulosa cells have receptors for both LH & FSH contains aromatase & converts testosterone into
estrogen under FSH.
MID CYCLE LH SURGE
• Estrogen creates positive feedback for LH

• Just before Ovulation, estrogen creates positive Feed back to LH
MALE REPRODUCTIVE SYSTEM
TESTIS
SEMINIFEROUS TUBULES
• Fluid Composition
o Less glucose & proteins
o Rich in androgens, estrogens, K+, inositol, glutamic acid, aspartic acid
• SPERMATOGENESIS
o Phase I: Stem cell renewal & production of Spermatogonia via Primitive Germ cells. From
primitive germ cell primary spermatocytes formed by mitosis
o Phase II: Primary spermatocytes form secondary spermatocytes through meiosis, then forms
Spermatids.
o Phase III: Spermatids form Spermatozoa by the process Spermiogenesis.
o 1 Spermatogonium forms 64 Spermatozoa
o Spermatogenesis completes in 74 days
o Sperm production rate is most reliable expression of Sperm production.
SPERMATOGENESIS VS OOGENESIS
• In Female the mitotic proliferation of oogonia occurs entirely before birth, in male, mitotic
proliferation of Spermatogonia occurs only after Puberty.
• Meiotic division of by 10 oocyte forms single OVUM & 10 Spermatocyte forms 4 Spermatozoa.
APPOLO ACADEMYA 57
SPERM
• Intricate motile cell

• Rich in DNA
• ACROSOME cap with hyaluronidase enzyme essential for dilution of Hyaluronic acid for penetrating
Cervix Mucus; also contain Germinal ACE, related to Fertility
SPERMATOGENESIS REGULATED BY
• LEYDIG CELLS produce testosterone for Sperm maturation

• SERTOLI CELLS nurture Spermatozoa
• LH/ INTERSTITIAL CELL STIMULATING HORMONE acts on Interstitial cells of Leydig to form
testosterone
• FSH for Spermatogenesis
• Mature sperm acquires motility in epididymis after 48hrs, here protein involved is CATSPER
SERTOLI CELL FUNCTIONS
• Forms Blood Testis barrier

• Secretes inhibin (inhibits FSH)
• Testosterone exerts negative Feedback on pituitary gonadotropin, LH as well as hypothalamic GnRH
• Nurture Spermatozoa
• Synthesize Mullerian inhibiting substance
NERVOUS SYSTEM
NERVOUS SYSTEM
1. CNS
2. PNS
3. ANS
ANS
• Controls involuntary Functions

• Includes
o Sympathetic Nervous System
Thoraco lumbar outflow
Preganglionic fibres are short
Post ganglionic fibres are long
o Parasympathetic Nervous system
Controls day to day Functions of the body like Resting HR, Secretions & Movements
of GIT.
Craniosacral out Flow
CN 3, 4, 9, 10
Pre ganglionic fibres are long
Post ganglionic fibres are short (anaxonal type)
Ganglion is located just outside/ wall of organ
o Preganglionic nerves are cholinergic - ganglionic transmission is cholinergic
o Post ganglionic nerves:
Parasympathetic = Cholinergic
Sympathetic = adrenergic (Noradrenaline)
CNS
APPOLO ACADEMYA 58
CELLS
1. Neurons
2. Glias: 4-10 times the No. of Neurons
Neurons
• Majority in CNS → Multipolar

• No neurons formed after birth except for OLFACTORY NEURONS
• New Synapses can be formed after birth
GLIA
• Supporting cells
• Only cells formed outside the CNS & migrates to CNS → microglia
• TYPES:
1. MACROGLIA
a. Astrocytes:
i. Involved in formation of BBB (Blood Brain Barrier)
ii. Involved in NT reuptake & redistribution
iii. Involved H+ & K+ homeostasis
b. Oligodendrocytes
i. Involved in myelination of
c. Microglia
i. Scavengers of CNS → Phagocytic cells
ii. Devived From Macrocyte Monocyte Lineage
2. CEREBELLUM has highest no. of Neuron
3. Greatest dencity of Serotonergic Neurons found in NUCLEUS RAPHE MAGNUS (part of descending
analgesia System)
4. Max density of nor-adrenergic neurons found in Locus Ceruleus (part of descending analgesia System)
5. Max. density of dopaminergic neurons found in Nucleus accumbens (D3) [involved in reward &
addictive behaviour]
6. Orexigenic neurons found Only in hypothalamus
NEUROTRANSMITTER
• EXCITATORY NTs: Glutamate & Aspartate opens Na+/ Ca++ Channels in post synaptic membrane
• INHIBLTORY NTs:
o Glycine (commonest in Spinal cord) [STRYCHININE — antagonist]
o GABA (Commonest in Brain) → opens K+ / Cl- channels' in post synaptic membrane.
SENSORY SYSTEM ORGANIZATION
• Functioning governed by
o 1° Neuron — Starts from receptor & enters the Spinal cord
o 2° Neuron – Start from spinal cord, croses midline & ends on thalamus
o 3° Neuron – Starts from thalamus to the Sensory cortex
THALAMUS is the OBLIGATE RELAY STATION for all general & Special senses Except OLFACTION
SENSES
GENERAL SPECIAL
Touch Vision
Pain Hearing
APPOLO ACADEMYA 59
Pressure Taste
Proprioception Hearing
Vibrarion Equilibrium
SPECIAL SENSES
• Contains Specialized end organ

• Carried by Cranial Nerve
GENERAL SENSES (Based On Stimulus)
EXTEROCEPTIVE SENSES
• Source of Stimulus is on external aspect of body
TELERECEPTORS
• Source of Stimulus is at a certain distance from the body. Ex: Vision, Hearing, Smell
INTEROCEPTIVE SENSES
• Source of Stimulus is deep inside the body
OLFACTION
Meet other Sensations at Amygdala, Neo cortex
Gives the collaterals & potentiate other Senses. Ex: Taste — In Common cold, taste can’t be appreciated
properly
THALAMUS
• OBLIGATE RELAY STATION for all SENSES

• Encodes intensity, duration, locakion & modality etc
DALE’S PRINCLPLE
• applicable for entire Nervous System

• SAME NT IS RELEASED FROM ALL THE BRANCHES OF AN AXON
LABELLED LINE PRINCIPLE
• encodes modality , location (to Some extent)

• EACH SENSORY MODALITY IS CARRIED BY 8 SPECIFIC TRACT IN CNS LOCATED IN A
SPECIFIC PART OF CNS
• Ex: Fine touch carried by dorsal columns
MULLER'S DOCTRINE OF SPECIFIC NERVE ENERGIES
• NO MATTER WHAT FORM OF ENERGY IS APPLIED, EACH SENSORY PATHWAY

CONVEYS THE SAME FORM OF ENERGY THAT IT SUPPOSED TO CONVEY
LAW OF PROJECTION
• PHANTOM LIMB
APPOLO ACADEMYA 60
• NO MATTER WHERE YOU APPLIED A STIMULUS, CORTEX ALWAYS PROJECT THE

SENSATION ONTO THE RECEPTOR FROM WHICH THE PATHWAY STARTS.
• Phantom pain Sensation may disappear after 6 Months.
o CORTICAL PLASTICITY: Gradually impulses from amputed area diminishes.
INTENSITY DISCRIMINATION
Intensity discrimination in CNS occurs by Changing AP FREQUENCY
WEBER FECHNER LAW: S = K x Log I ; where
• S = magnitude OF Sensation Felt

• K = Proportional constant
• I = actual intensity applied
STEVEN'S POWER LAW: S = k * (I)n
BELL MEGENDIE LAW: DORSAL ROOTS ARE SENSORY & VENTRAL ROOTS ARE MOTOR
RECEPTORS CLASSIFICATION
MECHANO RECEPTORS
• Meissner's corpuscle
• Merkel disc
• Paccinian corpuscle
THERMO RECEPTORS
• belong to TRP (Transient Receptor Potential) Super Family
• Cold & mechano-sensitive receptor)
CHEMO RECEPTORS
• Smell
• Taste
• Glomus Cell
ELECTRO MAGNETIC RECEPTORS: Rods & Cones
NOCICEPTORS
• belongs to TRP Super Family
• vanilloid Receptor
• Not FREE NERVE ENDINGS
MECHANORECEPTORS
RECEPTOR LOCATION RECEPTIVE SPEED OF SENSATION

FIELD SIZE ADAPTATION ENCODED
Merkel’s disc Epidermis Smallest Slowly Location of touch
Meissner corpuscle Dermis Small Rapidly Speed of
application of touch
Paccinian corpuscle Dermis & deeper Large Very rapidly Vibration
tissue
Ruffini’s corpuscle Ligaments, muscle, Large Slowly Deep pressure
tendons
BRAILLE: mainly Meissner corpuscle, then Ruffini's corpuscle
ASCENDING TRACTS
APPOLO ACADEMYA 61
1. DORSAL COLUMN SYSTEM: Carries Fine touth (2 point discrimination), Pressure, Vibration,
Proprioception (conscious)
2. ANTERO LATERAL SYSTEM: Carries Crude touch, pain, temperature, tickle, itch, sexual sensations
[pain, temperature by Lateral white column]
SYRINGOMYELIA: Cyst Filled lesion in central canal, grows anteriorly, damage pain & temperature fibres
first.
PHYSIOLOGY OF PAIN
PAIN INSENSITIVE STRUCTURES: Brain, Cornea, Lung parenchyma, Liver parenchyma Bronchi
PAIN SENSITIVE STRUCTURES: Kidney, Heart, vessels, pleura, menninges, pericardium, Liver Capsule,
Gall-bladdar, Bile duct, Ureter, Bladder.
Intestines: not sensitive to sharp cutting pain, sensitive to torsional pain
TYPES OF PAIN
• Fast / 1st / SHARP/ ACUTE / PRICKING PAIN (Aδ): Neospinothalamic tract carries fast pain
• Slow / 2nd / DULL / CHRONIC / ACHING PAIN (C): Paleospinothalamic track carries Slow pain
Pain carried by Lateral Spinothalamic tract
MOTOR SYSTEM
ORGANIZATION
• Area 4: Primary Motor area

• Area 6: Premotor area & Supplementary motor area
• Area 8: Frontal eye fields
• Area 9, 10, 11,12: Seat of intelligence, in prefrontal Cortex
BODY REPRESENTATION
• Inverted
• Motor Homunculus - Greatest representation: Thumb, Muscles of Vocalisation & mastication
ORGANIZATION & FUNCTION
• 1st impulse of voluntary movement is recorded = Area 6, Thought / idea starts here
• 2nd impulse comes from Basal ganglia
o converts abstract thought into voluntary movement
o Selects the desired movement
o Suppress the other movement
o Provide Spontaneity & purpose of the movement
o Provide proportion to the movement
• 3rd impulse comes from CEREBELLUM, provides the sequencing of muscle contraction
• 4th impulse comes from AREA 4 & command will be formed in concerned muscles & command sent
down for execution; sending down of Command done by Cortico Spinal tract. Initiates The Voluntary
movements
PYRAMIDAL TRACT
7. Cortico spinal fibers

8. Cortico bulbar fibers
APPOLO ACADEMYA 62
9. Cortico nuclear fibers
Extra pyramidal tract:
• Vestibulospinal tract: Controls posture & equilibrium

• Reticulospinal tract: Controls trunk muscles
• Rubrospinal tract: Controls proximal muscle tract
• Tectospinal tract: Tectum: Roof of midbrain; Tegmentum: Floor of midbrain
UNCONSCIOUS PROPRIOCEPTION
• Carried by spinothalamic tract

• Comparing function done by Cerebrum & sends signal back to adjust the contractions.
CEREBELLUM
VESTIBULO/ ARCHI CEREBELLUM
• Connected with vestibular apparatus

• Oldest in evolution
• Controls the posture & equilibrium
• Controls vestibulo ocular reflex
SPINO CEREBELLUM / PALEO CEREBELLUM
• Connected to & from spinal cord

• Co-ordinates between muscle group
• Movement become smooth precise
• Damping Function
• Controls alternate rapid movements
• Maintaining muscle tone
CEREBRO / NEO CEREBELLUM
• Connects with Cortex

• Newer in evolution
• Α-δ co-linkage occurs here
• Helps the cortex in planning & programming
• Provides sequencing of muscle contraction to the cortex
DISORDERS OF CEREBELLUM
• Ataxia
• Post Pointing
• Loss of muscle tone
• Intention tremor
• Romberg sign +ve
ATAXIA
• Sensory ataxia
o With eyes open — Patient can perform the test
o With eyes close — Patient cont perform the test
• Cerebellar ataxia
APPOLO ACADEMYA 63
o With eyes open/close — Patient can’t perform the test
BASAL GANGLIA
• Subcortical masses of grey matter

1. Caudate nucleus
2. Putamen
3. Globus Pallidus
4. Substantia nigra
5. Subthalamic nuclei
In WILSON'S DISEASE, hepatolenticular degeneration due to excess Copper deposition
PARKINSONISM
• Degeneration of Nigro Striatal tracts

• Bradykinesia
SUB THALAMIC NUCLEUS
• Controls associated movements of body (swinging of arms while waking)

• Lesion leads to Hemiballismus
HUNTINGTON’S DISEASE
• Hyper kinetic
• Due to Huntington's gene
HIGHER FUNCTIONS
HYPOTHALAMUS
NUCLEUS CONNECTIONS FUNCTION LESION

SUPRA OPTIC nucleus Osmoreceptors ADH synthesis Central DI
PARAVENTRICULAR Neuroendocrine reflex Oxytocin synthesis Delayed labour
nucleus
SUPRACHIASMATIC Retina Circadian rhythm Jet lag (Disturbed
nucleus Circadian rhythm)
PREOPTIC nucleus Anterior: Androgen Sexual function in males Loss of libido, altered
sensitive; Posterior: & females sexual preferences
Estrogen sensitive
VENTROMEDIAL CART Satiety Hyperphagia, Obesity
nucleus
Lateral hypothalamic area Orexigenic neuron / Hunger Anorexia
Glucostatic neuron
Lateral superior Osmoreceptors Thirst Adypsia
hypothalamic area
HYPOTHALAMUS
• Part of Diencephalon
• Concerned with vegetative & visceral Function
• Heighest Seat for ANS Control present here
APPOLO ACADEMYA 64
BIOCHEMISTRY
All anabolic pathways occur in cytoplasm

All catabolic pathways occur in mitochondria except Glycolysis & Glycogenolysis which occur in
cytoplasm
Insulin activatess all anabolic pathway enzymes & 2 catabolic pathway reaction glycolysis & link
reaction
Glucagon activates all catabolic pathway enzymes
Fuel of body [Mn: Fuel for FED, FASTING & STARVATION]
o Carbohydrates (FED)
o Fats (FASTING) – β-oxydation of fatty acid → Gluconeogenesis, TCA cycle & ketone body
o Protein (STARVATION)
Diabetes is a fasting like state where only one anabolic process is happening – Fat synthesis in liver
40% of carbohydrates stored as endogenous fats & 10% of carbohydrates
carbohydrates stored as glycogen
Endogenous
ndogenous fats transported in blood as VLDL & Fat (exogenous / dietary) transported in blood as
chylomicrons.
ATKIN diet: Low carb low calorie diet
FRUIT JUICE diet: Most lipogenic as having fructose
Thermogenic effects of food
food / Specific Dynamic action of food: Energy require to digest, absorb,
transport & metabolize
o From high to low: Protein > Carbohydrate > Fat
PATHWAYS OCCUR BOTH IN MITOCHONDRA & CYTOPLASM
Gluconeogenesis
Urea cycle
Heme synthesis
URAE CYCLE / KREBS HANSELEIT CYCLE / ORNITHINE CYCLE
• Happens in liver
• Have
components in
both
mitochondria &
cytoplasm
• OTC (Ornithine
transcarboxylase
) which is
deficient in brain
changes
Carbamoyl P to
Citrulin
• In cytoplasm
Carbamoyl P
changes to
Orotic acid
followed by
Uridine
monophosphate.
• OTC deficiency is the main cause of Urea cycle defect
• During starvation ↑ due to protein catabolism
APPOLO ACADEMYA 65
TCA cycle / Krebs cycle / Citric acid cycle
TCA mitochondria have no hormonal control. 1st substrate is citric acid.

CA cycle occur inside mitochondria,
Fate of Acetyl CoA
• In Mitochondria
o TCA cycle
o Ketone body synthesis
o Activation of Gluconeogenesis
• In Cytoplasm
o Fatty acid synthesis
o Cholesterol synthesis
Anabolic role of TCA cycle
• TCA intermediates used to synthesis of different compounds like from Succinyl CoA to Haem
TCA is Vital Cycle as no enzyme deficiency present, no enzyme needed to activate it.
Anaplerotic reaction replenishes TCA intermediates.
TCA cycle operate in aerobic condition as ETC needed oxygen to operate.

APPOLO ACADEMYA 66
Pentose phosphate pathway /

Hexose monophosphate shunt
• HMP is minor pathway

for oxidation of glucose
• Glucose 6-P is the
starting material
• Anabolic pathway
• Activated by Insulin
• Inhibited by Glucagon
• Occurs in cytoplasm
• Called Pentose
phosphate pathway as
Ribose 5-P is
synthesized
• Sites of HMP:
o Liver
o Adipose tissue
o Lactating
mammary
gland
o Gonad
o Adrenal tissue
o Placenta
o RBC
o Low activity
seen in
Skeletal
muscle
o Never seen in skin
• Role of HMP in RBC
o HMP → NADPH → Reduced Glutathione → Maintain the shape of RBC
o So G6-PD PD deficiency,
deficiency, enzymatic deficiency in HMP & glycolysis leads to Hemolytic anemia
Glycolysis
• occurs in cytosol
APPOLO ACADEMYA 67
Cori Cycle: If the oxygen supply is insufficient, the pyruvate can continue
continue through the process of fermentation
producing lactate and ethyl alcohol plus NAD+ to replenish the necessary supply of NAD+ for continuing
glycolysis. During intense exertion, glycogen stores in the muscle stores are mobilized and used to produce
pyruvate,
vate, and if the oxygen supply is low, this contributes further to the production of lactate in the cells.
Uronic acid pathway
• Minor pathway for oxidation of glucose

APPOLO ACADEMYA 68
• No ATP formed (like HMP)

• Site: Cytoplasm
• Uses:
o Vit C synthesis
o Glucoronic acid synthesis
o Pentose synthesis
o UDP glucoronides used for:
GAG synthesis
Detoxification of phase II reaction of Xenobiotics
Conjugation of bilirubin in liver
GARROD tetrad
• Cystinuria (Defective di basic a-a transporter)

• Alkaptonuria
• Albinism (Tyrosinase deficiency)
• Essential pentosuria (d/t deficiency of Xylulose reductase)
LIPID TRANSPORT
• Lipid is nonpolar, so insoluble in blood which is water based, hence polar.

• Exogenous lipid or triglycerides converted to lipoprotein in intestinal cell to become soluble in water.
• Lipoprotein is transported via blood to peripheral tissue
• Lipids presents in lipoprotein: Tryglycerides, Phospholipid, Cholesterol, Cholesterol ester (Cholesterol
+ FA)
• Soluble lipoprotein in blood according to density: Chylomicron, Chylomicron remnant, VLDL, IDL,
LDL, HDL or Lipoprotein A.
• VLDL, IDL, LDL & HDL are synthesized in liver.
• HDL has maximum phospholipids, mainly Lecithin & has a empty core; so it can bring back extra
cholesterol in tissue or circulation; it is called Reverse Cholesterol Transport.
• HDL takes cholesterol from tissue or circulation & adds fatty acid to it to form Cholesterol ester &
send it to liver, hence called Good Cholesterol.
β-oxydation of Fatty acid
• Occurs in mitochondria
• Activated by glucagon
• Inhibited by insulin
• For each cleavage 4 enzymes are required: Dehydrogenase (FADH2), Hydratase, Dehydrogenase
(NADH), Thiolase
• Any defect in pathway leads to Non-ketotic hypoglycaemia
α-oxydation of Fatty acid
• Occurs in peroxysomes & ER

• For branched chain fatty acid
• No ATP produced
• REFSUM disease: Defect in α-oxydation of peroxysomes; restriction of dairy products & green leafy
vegetables are needed.

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APPOLO ACADEMYA 1

PHYSIOLOGY & BIOCHEMISTRY

NERVE MUSCLE PHYSIOLOGY

GASTRO INTESTINAL TRACT

CARDIO VASCULAR SYSTEM

• Conducting system of Heart

• Female Reproductive System

THE NERVOUS SYSTEM

BODY FLUID COMPARTMENTS

• Total Body water = F 0.6 x Body weight = 42L (70 Kg)

MEASUREMENT OF BODY FLUIDS

INDICATOR DILUTION METHOD / DYE DILUTLON METHOD = STEWART-HAMILTON DYE

1. Dye Should be evenly distributed

OVER HYDRATLON / VOLUME EXPANSION STATES

• ISOTONIC OVERHYDRATION: administration of Oral/ IV isotonic Saline

ENDOLYMPH: ECF which resembles ICF in body, has increased concentration of K+

DIFFUSION occurs due to electric gradient [along with concentration gradient]

ELECTRIC GRADIENT: ECF K+ concentration = 4mEq/L, ICF K+ concentration = 145mEq/L

MILIEU INTERIOR [ECF] = internal Environment of body.

HOMEOSTASLS: maintaining the constancy / Stability in milieu Interior

MILIEU INTERIOR coined by CLAUDE BERNARD & WALTER F CANNON

HOMEOSTATIC REGULATORY MECHANLGMS

• FEED FORWARD REGULATION — No time lag

FEED FORWARD MECHANISMS

• Controller Anticipates Changes & takes a desired action

FEED BACK MECHANISMS

CELL MEMBRANE & TRANSPORT PROTEINS

FLULD MOSATC MODEL

• Most accepted model [SINGER NICOLSEN MODEL]

• Lipid bilayer with Protein embedded in it

• Lipid layer: Occupy 42% of surface area

TIGHT JUNCTIONS [ZONULA

• Responsible for coherent

TRANSPORT PROTEINS IN THE

• PORES - always Open,, responsible for H2O Movement

• CYCLIC NUCLEOTIDE GATED CHANNEL (cAMP, cGMP) - G Protein

Symport / Co-transport: Ex. SGLT for Glucose entry to

REGULATION OF ACID-BASE BALANCE

REGULATION OF ACID-BASE BALANCE BY ACID-BASE BUFFER SYSTEM

REGULATION OF ACID-BASE BALANCE BY RESPIRATORY SYSTEM

REGULATION OF ACID-BASE BALANCE BY RENAL SYSTEM

NERVE MUSCLE PHYSIOLOGY

RMP (Resting membrane potential)

Red cells, Epithelial Cells = — 6 to — 2mv

RMP for nerve is —70mv.

NERNST EQUATION calculates individual equilibrium potential of an ion.

EMF (mv) = +-61 * Log C1/C2

Concentration gradient of 3 ions

EXCITATION & ACTION POTENTIAL

RHEOBASE = minimum Strength of stimulus that can excite the tissue.

Increasing order of Chronaxie / Order of excitability

a. Myelinated nerve (least chronaxie, most excitable)

MEMBRANE EXCITATION & IMPULSE TRANSMISSION

MEMBRANE EXCITATION occurs in 2 Forms

SALTATORY CONDUCTION — ADVANTAGES

1. Faster (Slower in unmyelinated Nerve Fibres)

Demyelinating disease of neuron

• Self regenerative process

• Recorded by cathode ray Oscilloscope

BASIS FOR REFRACTORY PERIOD

(Changes in ECF Concentration)

• It is a travelling impulse, resulting in muscle contraction.

• Do not travel, occurs by point by point

1. MULTI POLAR: Brain & cerebral Cortex