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Cheat sheet exams

Human Anatomy and Physiology (University of Technology Sydney)

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Digestion: Hormones: Bellybrain (Enteric nervous system)

5 stages of digestion Gastrin stimulates secretion of HCl by Nervous network that regulates digestion,
Ingestion: Intake partiel cells in stomach, aids gastric secretion + blood flow. Sensory neurons
Digestion: Breakdown (chemical and motility. minor gut wall tension, condition in lumen.
mechanical, acid` and teeth: small particles Secretin controls environment in Subdivision of PNS, functions independently
for absorp duodenum, regulates pH by inhibiting but reports to CNS
Absorption: Nutrients gastric acid the stimulates bicarbonate in Submucosal: Controls glandular secretion of
Compaction: Water pancreas mucus and muscularis mucosae (dislodged
Defecation: Paracrine secretions: good particles that slipped from mucus
Esophagus tube from pharynx to orifice Chemical messengers diffuse through Myenteric: Parasympathetic ganglia
(opening). Lower sphincter stops food tissue fluids to stimulate target (Increases intestinal activity, relaxes sphincter
entering stomach until brain sends signal to Histamine stimulates HCl in GI, controls peristalsis) Peristalsis is the
bolus. Prostaglanid inhibit gastric secretion wave like motion of muscles to push the bolus
Short reflex: Mechanical distension Stomach: Breaks down food with HCl, Cells of gastric:
(stretching) or chemical change (pH) starts digestion of protein (with pepsin) Mucous: secrete mucous, neck of gland and
Detected by ENS and triggers effector and fat (gastric lipase) predominate pyloric and cardiac glands
organs e.g. secretory cells, smooth muscles Chyme = semi ingested food in stomach Regenerative: Stem cells that divide and
in walls releasing enzymes alerting gastric 4 regions: Cardiac (opening) produce new cells to replace dead
motility Fundic: (dome shaped portion) Parietal: Secrete HCl, absorb VB12
Long reflexes: External input detecting Body: Main bulk Chief cells: most abundant, secrete gastric
stimuli (sight/smell of food) sent to Pyloric: Gateway to duodenum, regulates lipase, lower half of gastric glands
parasympathetic which prepares body for passage of chyme to duodenum G Cells: release gastrin (stimulates gastric
eating, altering enzyme release and gastric Mucus and Submucosa sit flat when full to glands to secrete HCl and enzymes. Stimulates
motility allow more and increase consumption, intestinal motility and relaxes ileocecal valve
when empty is wrinkles (separates small from large intestine)

Peristaltic rate is 3/min. Contractile rhythm Stomach is protected by mucous coat, tight Cephalic: Excite parasympathetic prepares
set by pacemaker cells in longitudinal junctions (prevent juice seeping between body for food, releases histamine and gastrin
smooth muscle layer. Contraction mix and destroying connective tissue) and epithelial Gastric: Distension stimulates and chief +
churn food. Frequency differs at each cell replacement. parietal cells produce more
location: 3/min stomach, 12/min DIGESTION 2 gastrin/histamine. Controls gastric emptying.
duodenum, 9/min ileum Nervous + endocrine collab so gastric Duodenum can only do so much so sphincter
Gastric motility: Absorption occurs after secretion and motility increases when food controls
chyme enters SI, Peristaltic wave send eaten. Suppresses when empty Intestinal: chyme in duodenum with a pH less
chyme down to duodenum, antrum adds Split into 3 phases: Cephalic (Brain, vagus) than 2 inhibits so motility, waits for
3mL of at time to digest and neutralise HCl Gastric (controlled by itself) bicarbonate to raise pH and decreases gastric
If duodenum overfilled inhibits motility Intestinal (controlled by SI) secretion

Liver: carb metabolism, releases glucose Stimuli for pancreatic juice release SI receives chyme from stomach. Function to
into blood, storage of hormones Acetylcholine: Vagus; stimulates acini to produce copious amounts of chyme,
Pancreatic juice is alkaline, neutralises secrete enzymes during cephalic phase neutralise acids before damaging inner
gastric juice, stops action of pepsin for Cholecystokinin: Mucosa of duodenum in linings, regulates rate of emptying stomach
homeostasis (pH too low = denature) response to fats in SI, stimulates via sphincter control
Pancreatic amylase -> carb and starch Gallbladder Ileum: final segment which controls SI to LI
breakdown Secretin: Duodenum when chyme arrives in Brushborder: Fuzzy border of apical surface,
Trypsin and chymotrypsin -> protein stomach. Stimulates ducts in liver and increase absorptive SA, when in contact it
breakdown pancreas to secrete sodium bicarbonate moistens chyme to increase motility and
Pancreatic lipase -> Fat (triglyceride) carries out final stages of enzymatic digestion
breakdown All chemical digestion and nutrient LI: reabsorption of water, storage of faeces
Deoxyribonuclease and ribonuclease -> absorption occurs in SI
digest RNA and RNA respectively
Digestion of nutrients Bile: Bile used to emulsify dietary lipids, Hydrophobic quality of lipids make digestion
Carbs: Mouth and duodenum break down allows them to be water soluble. Increases and absorption more difficult.
starch (amylase) Brush border uses lactase SA to enzymatic attack Lipases are fat digesting enzymes. Lingual
and maltase to digest disaccharides into 80% of bile is reabsorbed, lipase is in saliva and secreted by the intrinsic
mono Bile is yellow-green fluid containing salivary glands of the tongue
Nucleic: Duodenum uses pancreatic minerals, fats, cholesterol, phospholipids Pancreatic lipase in the small intestine digests
ribonuclease for RNA and bile acids most of the fats, they enter the duodenum as
Protein: HCL to denature and pepsin to - Bacteria in large intestine allow large globules but get emulsified by bile so
break to peptides bilirubin to metabolize to that the lipases and reach all components
Lipids: Lingual lipase released in mouth, urobilinogen which gives poo its Micelles are produced in the liber and are
degrades lipids. Duodenum emulsification brown colour. used to absorb fat in the duodenum. They
(break down of fat to tiny droplets) transport lipids to intestinal absorptive cells.
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Renal1: Nephron Glomerular filtration rate (GFR) tests how

Kidneys function to regulate Extracellular - 80% of Nephrons in the cortical well kidneys are functioning: Estimates how
fluid, volume, osmosis, homeostasis o Short nephron loops much blood passes through glomeruli each
Kidney: The kidney is used for filtration and produce dilute urine minute. Myogenic response – is the internal
reabsorption via nephrons. o ability for muscles to respond to pressure
Glomerular filtration: Occurs from - 20% in the juxta-medullary changes
glomerulus to bowman’s capsule. o Long loops produce GFR regulation: Through tubuloglomerular
Reabsorption: Tubules to peritubular concentrated urine feedback (a paracrine signalling mechanism
capillaries (conserves water in the which changes in fluid flow or fluid
Secretion: From peritubular capillaries to medulla) composition through loop of Henle influences
tubules Endothelial cells block all cells platelets GFR). The glomerulus receives feedback on
Excretion: From tubules out of body from coming through and being filtrated the status from downstream tubular and
adjusts filtration accordingly to stabilise GFR.
3 cells involved: Glomerular filtration: The renin-angiotensin system:
Macula densa cells: slender, closely spaced Autoregulation of the GFR Stimuli cause the juxtaglomerular cells in
epithelial cells and end of nephron loop. Reduced blood flow or low glomerular afferent arteriole to release renin
Senses variation in flow or fluid blood pressure triggers. Dilation of afferent This causes a decrease in blood pressure at
composition and secretes a paracrine that arterioles. Dilation of glomerular capillaries glomerulus due to decrease in blood volume
stimulates JG cells Juxtaglomerular cells: Constriction of efferent arterioles
Used to dilate and constrict arteriole, they Rise in renal blood pressure results in: Renin is secreted by juxtaglomerular cells if BP
also contain granules of renin which o Stretching of walls of drops dramatically. An enzyme then converts
secrete in response to drop in blood afferent arterioles angiotensinogen 2 which is an active hormone
pressure Mesangial cells: Build supportive o Causes smooth muscles which works to restore fluid volume and BP
matrix for glomerulus by constricting and to contract arterioles
relaxing capillaries to regulate flow. o Decreased GBF
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: Animals living in moist conditions have Fluid flowing downward in descending limb;
The Nephron loop acts as a counter-current short loops of Henle that don’t descend most of the descending limb is very
multiplier as it continually recaptures salt quickly into the medulla (cortical nephrons) permeable to water but impermeable to salt
and returns it to the extracellular fluid of BEAVER meaning that salt is left behind.
the medulla which multiples the salinity if Animals living in arid conditions have long
the adrenal medulla loops that descend quickly into the medulla Fluid flowing upward in ascending limb is
H2O is reabsorbed from urine via collecting (juxtamedullary nephrons) KANGAROO impermeable to water but absorbs sodium,
ducts and salts are left behind in the ADH: Due to dehydration, increases water potassium and chlorine by active transport
Extracellular fluid and are not removed reabsorption. Stored is pituitary gland, and is pumped into the extra cellular fluid.
from renal medulla as they establish conservation of body wayer Vasa recta – Capillary provides blood supply
osmotic gradient. Aldosterone: Controls ion pumps and to medulla and does not remove
Descending = Salt in, water out, permeable channels, reduces sodium loss in urine, NaCl and Urea from medullary CG
to water not salt reabsorption of Na+
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Respiration 1: Bronchoconstriction: Constrict bronchi, Respiratory distress syndrome:

Conducting division: Those passages that caused by allergies Lack of surfactant; infants are not strong
serve for only airflow and no gas exchange Bronchodilation: Reduces resistance, enough to inhale enough air to inflate their
Respiratory division: Consists of alveoli and dilation of airways alveoli . Protein rich fluid leaks into the alveoli
other gas exchange regions Alveoli: 150 million each lung, for gaseous forming a membrane which blocks alveoli
exchange. Squamosa: Rapid diffusion from oxygen uptake
Trachea (windpipe): rings of collagen to between alveoli and blood stream (95%) Pleurae is a double folded membrane in the
stop collapsing Great: (5%) repairs the squamous and chest cavity which holds serious fluid to
Bronchial tree: Branching system of air secretes pulmonary surfactant to coat and reduce friction and acts as a protective layer
tubules in lung. Terminal bronchioles are prevent from collapse when exhale of the lungs. It also creates a pressure
final conducting, Epithelium contains Clara, Many lung diseases come from the gradient. It also stops the spread of infection
stop collapsing, no mucus. Respiratory deterioration of the alveoli such as from organ in the midsection to others.
have alveoli budding their walls exchange Emphysema
Lung pressures: Interpulmonary pressure: Respiration 2: Compliance is indicator of expandability
the pressure within the lungs which varies Respiratory airflow: flow, pressure and Low compliance requires greater force cant
with respiration and expiration. resistance. F α P / R equal to I = V/R breathe in, high requires less force (poor
Intrapleural pressure: Pressure in the Boyles law – At a constant temperature, recoil so exhale is hard)
intrapleural space, it is negative due to lack the pressure of a given quantity of gas is Resistance restricts airflow
of air in this space. Transpulmonary inversely proportional to its volume Sympathetic stimulation leads to
pressure: Pressure difference across wall of Inspiratory effect causes a fall in bronchodilation and parasympathetic
lung. Intrapulmonary-intrapleural pressure intrapleural pressure, alveolar pressure, stimulation leads to bronchoconstriction
keeps the lungs against the chest wall and pressure gradient from mouth to alveoli Pulmonary compliance: Reduced by
stops them from collapsing. Pleural Expiration causes relaxed breathing. degenerative lung disease in which the lungs
pressure: Lungs are very elastic so they Recoil compresses the lungs, volume of are stiffened by scar tissue and increased in
have a natural tendency to collapse/recoil thoracic cavity decreases emphysema due to poor elastic recoil
and the chest expands so pleural function Forced happens with exercise
holds pressure with a vacuum between the Air in the alveolus is in contact with a film of
The rate of respiration obviously changes
parietal and visceral pleural layers of the water covering the alveolar epithelium, for
to oxygen demands
lungs oxygen to get into the blood it must dissolve
The number of breaths per minute =
in this water. For CO2 to leave the blood it
Air that doesn’t reach the alveoli remain Respiratory rate
must diffuse out of the water and into the
anatomical dead space The volume of air moved per breath = Tidal
alveolar air. Henrys law: The amount of gas
In pulmonary diseases, some alveoli will volume
dissolved I the water is determined by its
not be able to exchange gas because they The respiratory minute volume =
solubility in water The solubility of a gas over
lack blood flow or have been blocked by Respiratory rate x Tidal volume
a liquid is proportional to the pressure of that
thickened membrane. Alveolar ventilation: The amount of air
gas So the greater the pressure in the alveolar
Physiologic dead space is the sum of reaching the alveoli each minute
air, the more oxygen the blood picks up
anatomic dead space and any pathological Respiratory rate x (Tidal volume –
Alvelous, the blood unloads CO2 and load O2
alveolar dead space Anatomical dead space)

Membrane thickness: This can create Respiration 3: Haemoglobin and O2 transport:

blockages for the alveoli. Pneumonia Oxygen transport: - High levels of PO2 favours loading, if
causes thickening of respiratory membrane - 95% to the haemoglobin, 1.5% populated it will pick up passengers
Membrane surface area: Emphysema, lung dissolved in plasma - Low PO2 will favour unloading
cancer decrease the surface area in which - One haemoglobin binds to 4 O2 - Oxygen – Hb affinity (Mood)
gaseous exchange can occur Carbon dioxide transport: o High affinity favours loading
Ventilation-perfusion coupling: The ability - 75% as bicarbonate ions o Low affinity favours
to match ventilation and perfusion to each - 20% bound to haemoglobin unloading
other. Gas exchange requires both good - 5% to dissolve in plamsa Factors that affect affinity are pH,
ventilation of the alveoli and good Partial pressure = levels of oxygen and temperature and pCO2 (patrial pressure of
perfusion from capillaries so an imbalance carbon dioxide dissolved in blood and how Carbon dioxide)
in one leads to inefficiency in the other well it moves space of the lungs into blood
Brainstem respiratory centres
(Oxygen) and the body (CO2) Dorsal respiratory group (DRG) Innervate external
As pCO2 increase the saturation curve Haldane vs Bohr intercostal muscles and diaphragm. This centre
shifts to the right (higher levels of - Haldane effect describes how functions in every cycle
uptake) oxygen concentrations VRG (Ventral respiration group): both inspiratory +
- pH decrease means the curve determine haemoglobins affinity expiratory centres. function when ventilation
shifts to the right (higher for Carbon dioxide, high levels demands increase and accessory muscles become
levels) of oxygen will lead to unloading involved (exercise)
- Increase in temperature of CO2 Pons: 2 centres: The Apneustic centre which
means Hb releases oxygen - Bohr effect describes how CO2 promotes inhalation by stimulating the DRG. The
and curve shifts to the right and Hydrogen affect the affinity pneumotaxic centre which inhibits the apneustic
- Increase in BPG leads to Hb of haemoglobin for oxygen. High centre and promotes passive or active exhalation.
releasing more O2 and shifts levels of CO2 and H+ will lead to Increase stimulation causes increase rate of
curve to the right Oxygen unloading (low affinity) 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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