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Cheat sheet exams

Human Anatomy and Physiology (University of Technology Sydney)

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Digestion:
5 stages of digestion
Ingestion: Intake
Digestion: Breakdown (chemical and
mechanical, acid` and teeth: small particles
for absorp
Absorption: Nutrients
Compaction: Water
Defecation:
Esophagus tube from pharynx to orifice
(opening). Lower sphincter stops food
entering stomach until brain sends signal to
bolus.
Short reflex: Mechanical distension
(stretching) or chemical change (pH)
Detected by ENS and triggers effector
organs e.g. secretory cells, smooth muscles
in walls releasing enzymes alerting gastric
motility
Long reflexes: External input detecting
stimuli (sight/smell of food) sent to
parasympathetic which prepares body for
eating, altering enzyme release and gastric
motility
Peristaltic rate is 3/min. Contractile rhythm
set by pacemaker cells in longitudinal
smooth muscle layer. Contraction mix and
churn food. Frequency differs at each
location: 3/min stomach, 12/min
duodenum, 9/min ileum
Gastric motility: Absorption occurs after
chyme enters SI, Peristaltic wave send
chyme down to duodenum, antrum adds
3mL of at time to digest and neutralise HCl
If duodenum overfilled inhibits motility
Liver: carb metabolism, releases glucose
into blood, storage of hormones
Pancreatic juice is alkaline, neutralises
gastric juice, stops action of pepsin for
homeostasis (pH too low = denature)
Pancreatic amylase -> carb and starch
breakdown
Trypsin and chymotrypsin -> protein
breakdown
Pancreatic lipase -> Fat (triglyceride)
breakdown
Deoxyribonuclease and ribonuclease ->
digest RNA and RNA respectively
Digestion of nutrients
Carbs: Mouth and duodenum break down
starch (amylase) Brush border uses lactase
and maltase to digest disaccharides into
mono
Nucleic: Duodenum uses pancreatic
ribonuclease for RNA
Protein: HCL to denature and pepsin to
break to peptides
Lipids: Lingual lipase released in mouth,
degrades lipids. Duodenum emulsification
(break down of fat to tiny droplets)
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Hormones:
Gastrin stimulates secretion of HCl by
partiel cells in stomach, aids gastric
motility.
Secretin controls environment in
duodenum, regulates pH by inhibiting
gastric acid the stimulates bicarbonate in
pancreas
Paracrine secretions:
Chemical messengers diffuse through
tissue fluids to stimulate target
Histamine stimulates HCl
Prostaglanid inhibit gastric secretion
Stomach: Breaks down food with HCl,
starts digestion of protein (with pepsin)
and fat (gastric lipase)
Chyme = semi ingested food in stomach
4 regions: Cardiac (opening)
Fundic: (dome shaped portion)
Body: Main bulk
Pyloric: Gateway to duodenum, regulates
passage of chyme to duodenum
Mucus and Submucosa sit flat when full to
allow more and increase consumption,
when empty is wrinkles
Stomach is protected by mucous coat, tight
junctions (prevent juice seeping between
destroying connective tissue) and epithelial
cell replacement.
DIGESTION 2
Nervous + endocrine collab so gastric
secretion and motility increases when food
eaten. Suppresses when empty
Split into 3 phases: Cephalic (Brain, vagus)
Gastric (controlled by itself)
Intestinal (controlled by SI)
Stimuli for pancreatic juice release
Acetylcholine: Vagus; stimulates acini to
secrete enzymes during cephalic phase
Cholecystokinin: Mucosa of duodenum in
response to fats in SI, stimulates
Gallbladder
Secretin: Duodenum when chyme arrives in
stomach. Stimulates ducts in liver and
pancreas to secrete sodium bicarbonate
All chemical digestion and nutrient
absorption occurs in SI
Bile: Bile used to emulsify dietary lipids,
allows them to be water soluble. Increases
SA to enzymatic attack
80% of bile is reabsorbed,
Bile is yellow-green fluid containing
minerals, fats, cholesterol, phospholipids
and bile acids
- Bacteria in large intestine allow
bilirubin to metabolize to
urobilinogen which gives poo its
brown colour.
Bellybrain (Enteric nervous system)
Nervous network that regulates digestion,
secretion + blood flow. Sensory neurons
minor gut wall tension, condition in lumen.
Subdivision of PNS, functions independently
but reports to CNS
Submucosal: Controls glandular secretion of
mucus and muscularis mucosae (dislodged
good particles that slipped from mucus
Myenteric: Parasympathetic ganglia
(Increases intestinal activity, relaxes sphincter
in GI, controls peristalsis) Peristalsis is the
wave like motion of muscles to push the bolus
Cells of gastric:
Mucous: secrete mucous, neck of gland and
predominate pyloric and cardiac glands
Regenerative: Stem cells that divide and
produce new cells to replace dead
Parietal: Secrete HCl, absorb VB12
Chief cells: most abundant, secrete gastric
lipase, lower half of gastric glands
G Cells: release gastrin (stimulates gastric
glands to secrete HCl and enzymes. Stimulates
intestinal motility and relaxes ileocecal valve
(separates small from large intestine)
Cephalic: Excite parasympathetic prepares
body for food, releases histamine and gastrin
Gastric: Distension stimulates and chief +
parietal cells produce more
gastrin/histamine. Controls gastric emptying.
Duodenum can only do so much so sphincter
controls
Intestinal: chyme in duodenum with a pH less
than 2 inhibits so motility, waits for
bicarbonate to raise pH and decreases gastric
secretion
SI receives chyme from stomach. Function to
produce copious amounts of chyme,
neutralise acids before damaging inner
linings, regulates rate of emptying stomach
via sphincter control
Ileum: final segment which controls SI to LI
Brushborder: Fuzzy border of apical surface,
increase absorptive SA, when in contact it
moistens chyme to increase motility and
carries out final stages of enzymatic digestion
LI: reabsorption of water, storage of faeces
Hydrophobic quality of lipids make digestion
and absorption more difficult.
Lipases are fat digesting enzymes. Lingual
lipase is in saliva and secreted by the intrinsic
salivary glands of the tongue
Pancreatic lipase in the small intestine digests
most of the fats, they enter the duodenum as
large globules but get emulsified by bile so
that the lipases and reach all components
Micelles are produced in the liber and are
used to absorb fat in the duodenum. They
transport lipids to intestinal absorptive cells.

Renal1:
Kidneys function to regulate Extracellular
fluid, volume, osmosis, homeostasis
Kidney: The kidney is used for filtration and
reabsorption via nephrons.
Glomerular filtration: Occurs from
glomerulus to bowman’s capsule.
Reabsorption: Tubules to peritubular
capillaries
Secretion: From peritubular capillaries to
tubules
Excretion: From tubules out of body
3 cells involved:
Macula densa cells: slender, closely spaced
epithelial cells and end of nephron loop.
Senses variation in flow or fluid
composition and secretes a paracrine that
stimulates JG cells Juxtaglomerular cells:
Used to dilate and constrict arteriole, they
also contain granules of renin which
secrete in response to drop in blood
pressure Mesangial cells: Build supportive
matrix for glomerulus by constricting and
relaxing capillaries to regulate flow.
Controls blood flow via glomerulus.
Renal 2:
GF makes a plasma fluid, travels down
tubules, reabsorption occurs, filtrating
useful solutes, adds them to blood, waste is
added to fluid (creates urine)
Water conservation depends on thirst,
reabsorption. Proximal convoluted tubule
(PCT) responsible for reabsorption,
reabsorbs 60-70%
Transcellular: Pass through cytoplasm of
PCT epithelial and out base
Paracellular: Through gap junctions, taken
up by peritubular capillarires.
Cortical – Juxtamedullary –
80% of N 20% of Nephrons
Short loops Long loops of
of Henle Henle
Produce Used for
dilute urine concentrating
urine
Glomerulus Large glomerulus
in outer (High GFR)
cortex
Counter current:
The Nephron loop acts as a counter-current
multiplier as it continually recaptures salt
and returns it to the extracellular fluid of
the medulla which multiples the salinity if
the adrenal medulla
H2O is reabsorbed from urine via collecting
ducts and salts are left behind in the
Extracellular fluid and are not removed
from renal medulla as they establish
osmotic gradient.
Descending = Salt in, water out, permeable
to water not salt
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Nephron
- 80% of Nephrons in the cortical
o Short nephron loops
produce dilute urine
o ability for muscles to respond to pressure
- 20% in the juxta-medullary
o Long loops produce
concentrated urine
(conserves water in the
medulla)
Endothelial cells block all cells platelets
from coming through and being filtrated
Glomerular filtration:
Autoregulation of the GFR
Reduced blood flow or low glomerular
blood pressure triggers. Dilation of afferent
arterioles. Dilation of glomerular capillaries
Constriction of efferent arterioles
Rise in renal blood pressure results in:
o Stretching of walls of
afferent arterioles
o Causes smooth muscles
to contract arterioles
o Decreased GBF
Animals living in moist conditions have
short loops of Henle that don’t descend
quickly into the medulla (cortical nephrons)
BEAVER
Animals living in arid conditions have long
loops that descend quickly into the medulla
(juxtamedullary nephrons) KANGAROO
ADH: Due to dehydration, increases water
reabsorption. Stored is pituitary gland,
conservation of body wayer
Aldosterone: Controls ion pumps and
channels, reduces sodium loss in urine,
reabsorption of Na+
Glomerular filtration rate (GFR) tests how
well kidneys are functioning: Estimates how
much blood passes through glomeruli each
minute. Myogenic response – is the internal
changes
GFR regulation: Through tubuloglomerular
feedback (a paracrine signalling mechanism
which changes in fluid flow or fluid
composition through loop of Henle influences
GFR). The glomerulus receives feedback on
the status from downstream tubular and
adjusts filtration accordingly to stabilise GFR.
The renin-angiotensin system:
Stimuli cause the juxtaglomerular cells in
afferent arteriole to release renin
This causes a decrease in blood pressure at
glomerulus due to decrease in blood volume
Renin is secreted by juxtaglomerular cells if BP
drops dramatically. An enzyme then converts
angiotensinogen 2 which is an active hormone
which works to restore fluid volume and BP
Fluid flowing downward in descending limb;
most of the descending limb is very
permeable to water but impermeable to salt
meaning that salt is left behind.
Fluid flowing upward in ascending limb is
impermeable to water but absorbs sodium,
potassium and chlorine by active transport
and is pumped into the extra cellular fluid.
Vasa recta – Capillary provides blood supply
to medulla and does not remove
NaCl and Urea from medullary CG

Respiration 1:
Conducting division: Those passages that
serve for only airflow and no gas exchange
Respiratory division: Consists of alveoli and
other gas exchange regions
Trachea (windpipe): rings of collagen to
stop collapsing
Bronchial tree: Branching system of air
tubules in lung. Terminal bronchioles are
final conducting, Epithelium contains Clara,
stop collapsing, no mucus. Respiratory
have alveoli budding their walls exchange
Lung pressures: Interpulmonary pressure:
the pressure within the lungs which varies
with respiration and expiration.
Intrapleural pressure: Pressure in the
intrapleural space, it is negative due to lack
of air in this space. Transpulmonary
pressure: Pressure difference across wall of
lung. Intrapulmonary-intrapleural pressure
keeps the lungs against the chest wall and
stops them from collapsing. Pleural
pressure: Lungs are very elastic so they
have a natural tendency to collapse/recoil
and the chest expands so pleural function
holds pressure with a vacuum between the
parietal and visceral pleural layers of the
lungs
Air that doesn’t reach the alveoli remain
anatomical dead space
In pulmonary diseases, some alveoli will
not be able to exchange gas because they
lack blood flow or have been blocked by
thickened membrane.
Physiologic dead space is the sum of
anatomic dead space and any pathological
alveolar dead space
Membrane thickness: This can create
blockages for the alveoli. Pneumonia
causes thickening of respiratory membrane
Membrane surface area: Emphysema, lung
cancer decrease the surface area in which
gaseous exchange can occur
Ventilation-perfusion coupling: The ability
to match ventilation and perfusion to each
other. Gas exchange requires both good
ventilation of the alveoli and good
perfusion from capillaries so an imbalance
in one leads to inefficiency in the other
As pCO2 increase the saturation curve Haldane vs Bohr
shifts to the right (higher levels of
uptake)
- pH decrease means the curve
shifts to the right (higher
levels)
- Increase in temperature
means Hb releases oxygen
and curve shifts to the right
- Increase in BPG leads to Hb
releasing more O2 and shifts
curve to the right
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Bronchoconstriction: Constrict bronchi,
caused by allergies
Bronchodilation: Reduces resistance,
dilation of airways
Alveoli: 150 million each lung, for gaseous
exchange. Squamosa: Rapid diffusion
between alveoli and blood stream (95%)
Great: (5%) repairs the squamous and
secretes pulmonary surfactant to coat and
prevent from collapse when exhale
Many lung diseases come from the
deterioration of the alveoli such as
Emphysema
Respiration 2:
Respiratory airflow: flow, pressure and
resistance. F α P / R equal to I = V/R
Boyles law – At a constant temperature,
the pressure of a given quantity of gas is
inversely proportional to its volume
Inspiratory effect causes a fall in
intrapleural pressure, alveolar pressure,
pressure gradient from mouth to alveoli
Expiration causes relaxed breathing.
Recoil compresses the lungs, volume of
thoracic cavity decreases
Forced happens with exercise
The rate of respiration obviously changes
to oxygen demands
The number of breaths per minute =
Respiratory rate
The volume of air moved per breath = Tidal
volume
The respiratory minute volume =
Respiratory rate x Tidal volume
Alveolar ventilation: The amount of air
reaching the alveoli each minute
Respiratory rate x (Tidal volume –
Anatomical dead space)
Respiration 3:
Oxygen transport:
- 95% to the haemoglobin, 1.5%
dissolved in plasma
- One haemoglobin binds to 4 O2
Carbon dioxide transport:
- 75% as bicarbonate ions
- 20% bound to haemoglobin
- 5% to dissolve in plamsa
Partial pressure = levels of oxygen and
carbon dioxide dissolved in blood and how
well it moves space of the lungs into blood
(Oxygen) and the body (CO2)
- Haldane effect describes how
oxygen concentrations
determine haemoglobins affinity
for Carbon dioxide, high levels
of oxygen will lead to unloading
of CO2
- Bohr effect describes how CO2
and Hydrogen affect the affinity
of haemoglobin for oxygen. High
levels of CO2 and H+ will lead to
Oxygen unloading (low affinity)
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Respiratory distress syndrome:
Lack of surfactant; infants are not strong
enough to inhale enough air to inflate their
alveoli . Protein rich fluid leaks into the alveoli
forming a membrane which blocks alveoli
from oxygen uptake
Pleurae is a double folded membrane in the
chest cavity which holds serious fluid to
reduce friction and acts as a protective layer
of the lungs. It also creates a pressure
gradient. It also stops the spread of infection
from organ in the midsection to others.
Compliance is indicator of expandability
Low compliance requires greater force cant
breathe in, high requires less force (poor
recoil so exhale is hard)
Resistance restricts airflow
Sympathetic stimulation leads to
bronchodilation and parasympathetic
stimulation leads to bronchoconstriction
Pulmonary compliance: Reduced by
degenerative lung disease in which the lungs
are stiffened by scar tissue and increased in
emphysema due to poor elastic recoil
Air in the alveolus is in contact with a film of
water covering the alveolar epithelium, for
oxygen to get into the blood it must dissolve
in this water. For CO2 to leave the blood it
must diffuse out of the water and into the
alveolar air. Henrys law: The amount of gas
dissolved I the water is determined by its
solubility in water The solubility of a gas over
a liquid is proportional to the pressure of that
gas So the greater the pressure in the alveolar
air, the more oxygen the blood picks up
Alvelous, the blood unloads CO2 and load O2
Haemoglobin and O2 transport:
- High levels of PO2 favours loading, if
populated it will pick up passengers
- Low PO2 will favour unloading
- Oxygen – Hb affinity (Mood)
o High affinity favours loading
o Low affinity favours
unloading
Factors that affect affinity are pH,
temperature and pCO2 (patrial pressure of
Carbon dioxide)
Brainstem respiratory centres
Dorsal respiratory group (DRG) Innervate external
intercostal muscles and diaphragm. This centre
functions in every cycle
VRG (Ventral respiration group): both inspiratory +
expiratory centres. function when ventilation
demands increase and accessory muscles become
involved (exercise)
Pons: 2 centres: The Apneustic centre which
promotes inhalation by stimulating the DRG. The
pneumotaxic centre which inhibits the apneustic
centre and promotes passive or active exhalation.
Increase stimulation causes increase rate of
inhalation and decrease stimulation slows
respiratory rate and increases depth of respiration
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Pericardium- Is a double walled sack made Coronary circulation – supplied blood to Interatrial septum: Wall that separates atria
of collagen fibres. Encloses and stabilises the heart itself Coronary arteries – come Pectinate muscles: Ridges of cardiac muscle
the heart. allows heart to beat without off the aorta with oxygen and nutrients in which increases the strength of atrial
friction and allows expansion. order to supply these to the heart muscle. - contraction without increasing mass
Myocardium- muscle of the heart forming Angina – when the heart muscle is not Interventricular septum: Muscular wall that
the atria and ventricles. Contains cardiac receiving the oxygen it needs Coronary separates ventricles Trabecula carneae:
s
muscle tissue, blood vessels and nerves. sinus – the ‘vein’ of the heart. Cardiac veins Internal ridges in ventricles that prevent
Concentric superficial muscle layer forms a return blood to the coronary sinus. The suction which would impair hearts ability to
figure 8 shape waste products from the heart muscle are pump Direction of blood flow–Superior and
Endocardium- Covers inner surface of the dumped into the coronary sinus and then Inferior Vena Cava- Right Atrium -Tricuspid
heart, including valves. Arteries pump released back into the right atrium. Valve-Right Ventricle-Pulmonary Valve-
blood upwards, valves open allowing blood Superior vena cava– receives blood from Pulmonary Trunk-Right and Left Pulmonary
to go against the flow of gravity It is rough head, neck, upper limbs Inferior vena cava Artery -TO LUNGS -Right and Left Pulmonary
so there is no friction and surface tension. – receives blood from lower body Veins-Left Atrium-Bicuspid Valve- Left
Ventricle-Aortic Valve-Ascending/Descending
Cardiac cycle: Aorta-Periphery.
1.Atrial systole: Atrial contraction begins Right and left AV valves are open
2.Atria eject blood into ventricles Filling ventricles S1: Loud sounds,Produced by AV valves closing
3.Atrial systole ends S2: Loud sounds, Produced by semilunar
AV valves close, Ventricles contain maximum blood volume known as End-Diastolic valves closing
Volume (EDV) Cardiac output: amount of blood pumped by
4.Ventricular systole:Isovolumetric contraction – all 4 valves are shut for a very brief the each ventricle per minute.
period of time, Pressure in ventricles rises, AV valves shut Heart Rate (HR) x Stroke Volume(SV)
5.Ventricular ejection: Semilunar valves open,Blood flows into pulmonary and aortic (heart beats per minute x ml pumped by
trunks.Stroke volume (SV) = 60% of end-diastolic volume ventricle per beat)
6.Ventricular pressure falls: Semilunar valves close, Vventricles contain end-systolic
volume (ESV), about 40% of end-diastolic volume
7.Ventricular diastole: Ventricular pressure is higher than atrial pressure, All heart valves
are closed,Ventricles relax (isovolumetric relaxation) – all 4 valves are shut for a very brief SVL factors that affect SV also affect SO. SV is
period of time determined by: EDV which is affected by:
8.Atrial pressure is higher than ventricular pressure :AV valves open, Passive atrial filling Filling time – duration of ventricular diastole,
Passive ventricular filling, cardiac cycle ends Venous return: blood flow during ventricular
Cardiac cycle ends Stroke volume: the amount of blood diastole, An increase in both of these will
Cardiac plexuses: group of nerves that pumped out by the ventricle with each increase EDV
innervate the heart. Sympathetic nerves = beat – ESV is dependent on: Preload: how much
increases heart rate. Vagus nerves carry End-Diastolic Volume (EDV) – blood is coming back to heart, Force of
Parasympathetic fibres to the cardiac End-Systolic Volume (ESV) - (how much we contraction, Afterload: resistance against
plexus and slows down heart rate. Cardiac fill up with before contraction, during which heart has to pump, e.g. valve not
centres of medulla oblongata:Cardio Diastole) –(how much remains in heart opening effectively, As afterload increases,
acceleratory centre – controls sympathetic after blood contracts) stroke volume decreases
neurons (increase heart rate)  Cardio
inhibitory centre – slows heart rate.
Controls parasympathetic neurons

Conduction:
SA node: cluster of cells in wall of right
atria. Excitation spreads to AV node Fibrous
skeleton: insulates atria from ventricles AV
node: electrical gateway. Transmits signal
to bundle of His. From SA there is a small
delay because it has so many fibres that
new signal must get passed. AV bundle
(bundle of his): pathway for signals from av
node. Connection between atria and
ventricles. Purkinje fibres: located in the
inner ventricular walls of the heart and
stimulate myocytes.

SA node fires spontaneously 70 times/min

at rest. AV node fires 40-50 times/min. if
no nodes fire, the ventricles fire by
themselves 20-49 times/min. Non-SA nodal
tissues are latent pacemakers that can take
over should the SA node fail, but they keep
the rhythm at a slower pace.

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