Gastrointestinal system

• severe blood loss causes change in arteriole blood pressure 
• loss of blood pressure due to loss of blood 
• blood pressure rises back after a few hours 

• reabsorption of tissue fluids into plasma 
• baroreceptor reflexes - high/low pressure 
• sympathetic surge 
• release of other vasoconstriction substances 
• renal conservation of salt/water 

• transcapillary refill/ autoinfusion 
• fluid movement from interstitium(fluid between skin and organs) to vasculative 
• fluid movement driven by hydrostatic pressure(difference between capillary and extravascular pressure) AND oncotic pressure(differences across capillary wall)
• hypotension during haemorrhage causes a drop in hydrostatic pressure of the capillaries = higher hydrostatic pressure in the interstitial fluid = water movement into the capillaries due to osmotic gradient 
• albumin secreted by the liver re establishes osmolarity 

• baroreceptors detect stretch in arteries 
• barorecptors at the aortic arch and carotid sinus (type of mechanoreceptors detecting inc in stretch)

• located in the right atria
• respond to dec in stretch 
• dec in blood pressure = +afferent pathways = medulla = increased sympathetic output = increased vassopressin secretion and synthesis 

• baroreceptors activate sympathetic postganglionic neurons to release adrenaline/noradrenaline, triggered by the adrenal medulla 
• sympathetic post granglionic neurons are differientiated by forming neurosecretory chromaffin cells which release adrenaline upon sympathetic stimulation 
• nurotransmitter release proportional to haemorrhage severity 
• sympotoms of sympathetic release: tachycardia,inotropy,arteriole constriction 

• symathetic stimulation = stronger depolarization = more APs= ncreased HR 
• adrenoceptor on heart muscle detects any adrenaline/noradrenaline causes increased contractile force 
• ligand:adrenaline, receptor: B1 adrenoceptor 
• APs cause Ca channels to open= Ca influx =  higher release of Ca from sarcoplasmic reticulum = positive inotropy 

• noradrenaline release onto a1/B2 receptors causes increased sympathetic tone and vasoconstriction 
• vasoconstriction- inc blood pressure and arteriole pressure 
• sympathetic surge however DOES NOT cause vasoconstriction in supply to the heart/brain 

• no vasoconstriction 
• cerebral/ coronary vascular beds regulate blood flow through local mediatiors not neuronal influences 

• renin release from juxtaglomerular apparatus 
• reduction in blood flow= reduction in renin circulating = detected by baroreceptor in the afferent renal arterioles= renin release stimulated = renin cleaves to angiotensinogen which converts it to angiotensin 1 = angiotensin 1 converted to angiotensin 2 by ACE enzyme
• angiotensin 2 is a vasoconstricter, stimulates aldesterone release from adrenal glands
• aldosterone is a lipid soluble hormone regulating the expression of epithelial sodium channels 

• aldosterone release promotes sodium reabsorption in kidney collecting ducts 
• controlling sodium amount in extracellular space 
• sodium control is important as is the primary osmotically active particle, during hypovelmic shock you want to preserve fluid 

• afferent atrial receptors synapse the medulla and paraentricular nucleus of the hypothalamus 
• medulla then increases sympathetic output 
• vassopressin is a vasoconstricter and increases water rebasorption 
• vassopressin also increases the number of water channels in the collecting duct 

• rapid and weak pulse caused by tachycardia due to sympathetic heart stimulation 
• feeling cold - due to vasoconstriction and sympathetic stimulation of sweat glands 
• low urine output - due to vassopressin secretion 
• sodium retention - due to aldosterone affect causing thirst 

• made up of 3 layers:
• 1) epithelium 
• 2)lamina propria (loose connective tissue layer containing capillaries,lymph and immune mast cells) - underlying connective tissue layer 
• 3) muscalaris mucosae (smooth outer layer)
• inner layer of the GI tract

• loose collagenous connective tissue which contains the larger blood vessels, lymphs, nerves and glands 

•  contains longitudinal smooth muscle 
• and contains circular smooth muscle on the inside 

• outermost layer 
• eneveloping tough layer of connective tissue keeping everything within the GI tract 
• serosa forms the outer wall of the GI tract

• mucosa layer of the stomach forms gastric pits (gastric mucosa cells)
• structure of the gastric pits are:
• 1) superficial epithelial cells - HCO3- secretion 
• 2) mucous neck cell - mucous secretion 
• 3) stem/regenerative cell - for repair 
• 4) parietal cell - for Hcl secretion 
• 5) chief cell - for pepsinogen secretion 
• 6) endocrine cell - for hormone secretion

• 1) digestion 
• 2) secretion 
• 3) defence 
• 4) motility 

• happens in the chief cells 
• chef cells secrete pepsionogens 
• pepsinogens hydrolyzed by acid stomach activating them into pepsins 
• protein digestion by pepsin

• tubolovesicular parietel cells change conformational shape into canalicular shape when stimulated, then secrete acid to kill bacteria/denautre proteins
• change in shape as it increses the SA of the cells therefore increasing the SA for insertion of proton pumps for increased acid secretion 

• contain lots of mitochondria 
• contain various transporters, channels and enzymes for hcl secretion 
• Na/H exchanger and Na pump control pH of the cytoplasm 
• K+ channel/ HCO3 CL exchanger allows HCO3 to leave the cell

DIRECTLY:

• Ach,histamine stimulate parietal cell to secrete protons into the lumen

INDIRECTLY 

• Ach, gastrin stimulate ECL cell which secretes histamine
• histamine acts on parietal cell to secrete acid

• 1) vagus nerve stimulates parietel cell directly 
• 2) vagal stimulation of ECL cells increases histamine release 
• 3) histamine stimulates acid secretion 
• 4)vagal stimulation of G cells triggers gastrin release 
• 5)gastrin directly stimulates acid secretion from the parietal cell 
• 6) gastrin indirectly stimulates acid secretion by increasing histamine release from ECL cells 
• 7)luminal acid stimulates D cells to release somatostatin 
• 8) somatostatin inhibits acid secretion directly at the parietal cell
• 9)somatostatin inhibits gastrin release at the G cell 
• 10)somatostatin inhibits histamine release at the ECL cell

• histamine, gastrin, ach stimulate secretion directly through binding to receptors on parietal cells 

• gastrin and ach stimulate histamine secretion from ECL cells 
• histamine release stimulates acid secretion from parietal cells 
• somatostatin from D cells inhbits acid secretion 

•  mucus secreted by mucous neck cells traps HCO3_  forming a protective mucus gel layer 
• HCO3 secreted by surface epithelium cells 
• mucus creates a diffusion barrier for H+ and pepsins = creates a neutralization zone which protects gastric epithelia from H+/inactive pepsins 
• this maintains pH of surface epithelium at pH 7 

• stomach is the first line of defence as its the first hollow organ to recieve external food in the chyme 
• acid pH of stomach kills most bacteria 

• movement of food by propulsive movements along the GI tract 
• mechanically mix food to maximise exposure of particles to digestive enzymes by churning movements