Retired__LSS2__Alimentary Flashcards
1
Q
Describe the normal relationship of the epiglottis and upper oesophageal sphincter
A
Epiglottis: usually upright, but upon swalling covers the trachea
UO Sphincter: usually closed because tonically active, but relaxes to allow passage of boluses of food
2
Q
Describe the structure of the upper oesophageal sphincter
A
Structure: skeletal muscle control
Constrictor pharyngis medius: commonality with circular muscle layer of GI tract
Constrictor pharyngis inferior: commonality with longitudinal muscle layer
3
Q
Describe the structure of the lower oesophageal sphincter
A
Structure: only smooth muscle
Internal component: built into circular smooth muscle
External component: formed by right crus of diaphragm (voluntary control)
4
Q
Describe the muscles of the middle oesophagus and pressures generated
A
Muscles:Composed of both skeletal and smooth muscle (neither voluntarily controlled)
Pressures: oesophagus -ve pressure and stomach is +ve pressure
5
Q
Describe the lining of the epithelium, and where any changes occur
A
Non-keratinised stratified squamous cells to form robust wear and tear lining to protect from ingested foods (e.g. Abrasive, hot, and acidic)At lower sphincter become simple columnar epithelia as need to resist stomach acid (change occurs within sphincter along jagged Z-line)
6
Q
Describe the process of swallowing
A
“0) Oral phase: chewing and saliva prepare bolus
1) Pharyngeal phase: food bolus moves to back of pharynx; pharyngeal musculature guides to oesophagus - both sphincters open
2) Upper oesophageal phase: upper sphincter closes and superior rings of circular muscle contract as inferior dilate - sequential contractions help guide food down gullet
3) Lower oesophageal phase: as food passes down sphincter it closes and peristaltic waves push to stomach
”
7
Q
Summarise the location and function of the gastro-oesophageal junction
A
Region where the oesophagus meets the stomach, just inferior of the diaphragm (at lower sphincter)Lining changes from stratified squamous to simple columnar in order to resist stomach acid - function is to separate acidic contents from vulnerable oesophageal tissue
8
Q
List the main functions of the stomach
A
- chemical digestion [acid/enzymes]- mechanical digestion [mixing/churning]- food storage reservoir- immunological protection
9
Q
Describe the structure of the stomach wall
A
Similar to rest of tract with extra oblique layer of smooth muscle in the circular layer to aid performance of grinding motions
Empty: contracts and submucosa fold to form rugae that are stretched by food
10
Q
List the regions of the stomach that secrete hydrochloric acid in the stomach and its functions
A
Secreted by fundus and body
Functions:- Kills ingested pathogens- Activates protein zymogens- Alters protein structures
11
Q
Draw and lable a diagram of the stomach, identifying what is produced by each region
A
”
Fundus: Mucous, hydrochloric acid and pepsinogen
Body: Mucous, hydrochloric acid and pepsinogen
Pyloric Antrum: Gastrin
Pyloric Canal: Mucous
Cardia: Mucous
“
12
Q
Describe the movements of the stomach
A
Peristalsis: 20% - moves chyme towards colon, getting increasingly powerful (ANS essential) - centrally driven
Segmentation: 80% - weaker and fluid chyme moves toward pyloric sphincter while solid food moved away from sphincter to allow for greater breakdown - local contraction (NOT centrally)
13
Q
Describe the role of mucous cells in the stomach
A
Secrete bicarb rich mucous to protect lining from acid (neutralises to ~7) and from active lipases/proteases that would interfere with bilayer/protein transporters (tend to be closest to lumen)
14
Q
Describe the role of parietal cells in the stomach
A
Acid-secreting cells which are quiescent until activatedTubovesicles fuse with small invaginations on surface of canalicular surface to produce large s/area for secretion by creating a large reservoirRich in mitochondria to provide energy for transport
15
Q
Describe the role of chief cells in the stomach
A
Produce pepsinogen (protease zymogen - activated by stomach acid) and gastric lipase (digests fats by removing a fatty acid)Have abundant RER and Golgi for packaging and many apical secretion granules
16
Q
Describe the role of G cells in the stomach
A
Enteroendocrine cells found at bottom of gastric pits to release gastrin hormone to bloodstream when Vagus (X) nerve stimulation/peptides in stomach/stomach distension
17
Q
Describe the role of gastric stem cells in the stomach
A
Can differentiate to all different cell types
18
Q
Describe the role of gastrin in the enteroendocrine system
A
Gastrin binds to chromaffin cells in stomach to stimulate gastric secretion and motility (via histamine release) to cause stronger contractions of stomach and opening of pyloric sphincter
19
Q
Describe the mechanism of parietal cells
A
1) CO2 diffuses into parietal cells and combines with water to form carbonic acid2) Carbonic acid dissociates to proton and bicarbonate3) Chloride ion outside cell exchange for bicarbonate4) Chloride ion enters lumen using chloride channel down concentration gradient5) Na+/K+-ATPase on basal cell membrane exchanges intracellular Na+ for K+6) K+ enters lumen down concentration gradient7) H+/K+-ATPase on apical cell membrane exchanges K+ for H+ which enters lumen (yielding H+Cl-)
20
Q
Summarise the cephalic response, stating the afferents, efferents and effects
A
Afferents: sight/smell/taste/thought of food
Efferents: Vagus = mucous/parietal/chief/G cell secretion via submucosal plexus; Gastrin and histamine stimulate parietal cell secretion
Effects: small secretion for a few minutes
21
Q
Summarise the gastric response, stating the afferents, efferents and effects
A
Afferents: stomach distention
Efferents: Vagus nerve stimulates mucous/chief/parietal/G cells using submucosal plexus and increase motility via myenteric plexus; Gastrin and histamine stimulate parietal cell secretion
Effects: 3-4 hours of gastric activity and mechanical digestion
22
Q
Summarise the intestinal response, stating the afferents, efferents and effects
A
Afferents: duodenal stretch and acid detection
Efferents: I-cells secrete cholecystokinin and S-cells secretin which both decrease parietal cell secrteion and inhibit gastric motility
Effects: gastric emptying slows to allow dowsntream processing time
23
Q
State the innervation that can affect mucous/chief/parietal/G cells and that which affects motility in the stomach
A
Cells: submucosal plexus
Motility: myenteric plexus
24
Q
Describe the effect of the concentrations of lipids and proteins in chyme
A
25
Describe the action of omeprazole
inhibits K+/H+-ATPase of parietal cells to prevent acid formation (proton pump inhibitors)
26
Describe the action of ranitidine
inhibits histamine binding to receptors on parietal cells (histamine receptor antagonist)
27
Describe the gross structure of the liver
Four lobes, with the left and right joined by the falciform ligament; mainly present RUQ with some LUQ
28
Describe the structural organisation of the liver
Separated to 8 independent segments, each with own blood supply and bile drainage, labelled I-VIII clockwiseCan resect segments without affecting others; veins drain to left/middle/right hepatic veins which join the vena cava
29
Describe the blood supply of the liver
25% CO dual supply
20% arterial blood from hepatic arteries
80% venous blood from the gut via the hepatic portal vein
30
Describe the structure of hepatic lobules
"Structural units that are roughly hexagonal in shape with a portal triad at each corner to link with adjacent lobules, and a central vein in the middle which collects blood draining from hepatic sinusoids to return to venous system (contain rows of hepatocytes, each with a sinusoid-facing and caniculi-facing side)
"
31
Describe the structure of a portal triad
Three conduit vessels with blood flowing inwards and bile outwards
1) Branch of the hepatic portal vein: mixed venous blood from GI organs and spleen, rich in raw nutrients, bacteria, toxins and waste products - hepatocytes process nutrients, detoxify blood and excrete waste
2) Branch of the hepatic artery: brings some oxygen-rich blood to liver tissue to support high energy demand of hepatocytes (fuses with portal vein to form sinusoids)
3) Bile duct: bile produced by hepatocytes drains into tiny canals (bile canaliculi) which coalesce with cholangiocyte-lined bile ducts located around lobules
32
State what is meant by a hepatic acinus
Functional unit of liver tissue that is harder to define; consists of two adjacent sixths of a lobule that share two portal triads and extend as far into the lobule as the central veins
33
Explain the three-zone model of a hepatic acinus
"Blood received from vessels at A and drains to B, so those in zone one receive early exposure to toxins, but also most oxygen; Zone 1 = high toxin risk but also high oxygen supply; Zone 2 = medium toxin risk and medium oxygen supply; Zone 3 = low toxin risk but also low oxygen supply
"
34
Identify the function and location of endothelial cells in the liver
"Function: many fenestrations and discontinous arrangment allows sinusoids to be leaky and transfer lipids/carbs
Location: walls of the sinusoids
"
35
Identify the function and location of Kuppfer cells in the liver
"Function: sinusoidal macrophages that are stellate shaped and eliminate/detoxify substances arriving from portal circulation
Location: attached to endothelial cells
"
36
Identify the function and location of hepatic stellate cells in the liver
"Function: exist in quiescent state to store VitA in cytosolic droplets and are activated when liver damaged to deposit collagen in ECM
Location: perisinusoidal
"
37
Identify the function and location of hepatocytes in the liver
"Function: represent 80% liver mass and synthesise albumin, clotting products and bile salts while recieving nutrients and metabolising drugs
Location: between the space of disse and bile ducts
"
38
Identify the function and location of cholangioocytes in the liver
"Function: secrete bicarbonates and water to form bile
Location: line the bile ducts
"
39
List the organelles found in hepatocytes and explain why they are present
- Peroxisomes: key role in detoxification, waste management and cholesterol/bile synthesis - Mitochondria: produces ATP to meet high demand - Rough ER: abundant for protein synthesis e.g. Clotting factors/albumin - Golgi Apparatus: package many manufactured molecules for exocytosis - Lysosomes: acidic organelle needed for breakdown of lipids/proteins/carbs and nucleic acids
40
Describe the role of the liver in metabolism of carbohydrates
Stores glucose as glycogen (enough for 24h) which is broken down when hypoglycaemic
Performs gluconeogenesis when neededConverts lactate to pyruvate using 6 ATP and lactate dehydrogenase
41
Describe the role of hepatocytes in the metabolism of proteins
Use amino acids to produce plasma proteins, clotting factors and lipoproteins while perorming transamination reactions to produce those not found in the diet
42
State the transaminations that can be performed in the liver
AlphaKG produces: glutamate, proline and arginine
Pyruvate produces: alanine, valine and leucine
Oxaloacetate produces: aspartate, methionine and lysineAll Goddamn Politicians ArguePoliticians Aren't Valuable LeadersOnly A Madman Likes (politicians)
43
Explain the deamination process that occurs in the liver
Occurs using the glucose-alanine cycleAlanine transferred to liver and reacts with alphaKG to form glutamate and pyruvate; glutamate then converted to urea using 4ATP and pyruvate converted to glucose using 6ATP
44
Explain the role of hepatocytes in the metabolism of fats
Use NEFAs for beta oxidation for TCA/acetoacetate production for ketones
45
Describe lipoprotein synthesis in the liver
Glucose enters liver and is converted to pyruvate > A-CoA > fatty acids/cholesterol OR to glycerolglycerol is converted to triglycerides and when combined with fatty acids, cholesterol, apoproteins and phospholipids, lipoproteins are formed
46
Describe the storage of vitamins in the liver
Stores fat soluble vitamins (ADEK) with a 6-12 month supply and iron as ferritin
47
Describe the process of detoxification in the liver
P450 enzymes make compounds more hydrophilic and then phase 2 enzymes attach water soluble side chains to make less reactive
48
State the functions of bile
Cholesterol homeostasis: secretion/excretion to fine tune [serum]
Absorption/digestion: bile salts solubilise fats and Vits A/D/E/KToxin secretion
49
Describe the production of bile
500ml per day with
60% from hepatocytes (reflect serum concentrations; secrete bile acids, lipids and organic ions)
40% from cholangiocytes (alter pH, allow water to enter bile, reabsorb sugars/acids and secrete HCO3- and Cl-)
50
Describe the composition of bile, stating which components are synthesised in the liver and what they are converted to
Salts (acids), with cholic and chenodeoxycholic acid synthesised in the liver and converted to deoxycholic and lithocholic acids respectively by gut bacteriaAq solution so also contains water and solutes, and is yellow/green due to biliverdin/bilirubin
51
Explain the role of the enterohepatic circulation
Cycling of substances between gut and liver by continuous reabsorption in the gut and hepatocyte secretion allows for recycling of bile salts to be more efficientSome drugs are secreted to bile and faeces but enterohepatic circulation may lead to reabsorption and re-entering the portal circulation cyclically to increase their half-life
52
Describe the embryogenesis of the pancreas
Foregut derivative arises at foregut-midgut junction and forms ventral (hepatobiliary) and dorsal buds; duodenum rotates to C-shape and ventral bud swings round to lie adjacent to dorsal bud, allowing for fusion and the ventral duct becomes the main pancreatic duct
53
Draw and label the pancreas
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54
Describe the location of the pancreas and its perfusion
Location of the pancreas: head sits in C-shaped part of duodenum and tail within hilum of the spleen; situated posteriorly to the stomach
Perfusion: uses branches of superior mesenteric artery and celiac trunk; drained by the hepatic portal vein
55
State the structure and function of pancreatic acini cells
Secrete digestive enzymes into ducts which coalesce to pancreatic ducts, lined with a columnar epitheliumArranged in circles around the ducts, and contain zymogen granules (usually inactive proteases - prevents tissue degradation) alongside active amylases/lipases
56
Describe the location and function of acinar cells within a pancreatic acinus
Function: many RER to produce apical zymogen granules (enzymes and inhibitors) for secretion
Location: at terminal end of duct to secrete enzyme rich, viscous, low-volume fluid into terminal end of duct
57
Describe the location and function of centroacinar cells within a pancreatic acinus
Join the acinar cells to pancreatic ducts, sharing characteristics of duct and acinar cells
58
Describe the location and function of duct cells within a pancreatic acinus
Location: line the ducts draining acini
Function: modify fluid - secreting watery, dilute, bicarb rich fluid to pancreatic duct to mobilise enzyme rich component of the juice and help decrease viscosity to move towards duodenum; also neutralises acid chyme for optimum enzyme pH
59
Describe the mechanism for duct cell secretion
1) CO2 diffuses into cell and combines with water using carbonic anhydrase to form carbonic acid that dissociates to HCO3- 2) Sodium moves paracellularly from interstitium to duct lumen 3) Water moves due to osmotic gradient (interstitium > lumen) 4) Watery secretion produced in duct lumen 5) Cl- moves into lumen using CFTR channels 6) Cl- in lumen exchanged for HCO3- (which moves into lumen) 7) Protons pumped into the interstitium in exchange for sodium using a Na+/H+ antiporter using Na+ concentration gradient (no change in membrane potential) 8) In order to maintain extracellular [Na+], Na+/K+-ATPase is used to replenish extracellular sodium for osmosis and proton exchange 9) K+ diffuses out of cell using potassium channels
60
Describe the activation and role of trypsin
Formed from trypsinogen - powerful protease, Conversion stimulated by duodenal brush border enterokinase enzymeTrypsin can then activate protease zymogens to proteases, procolipase to colipases and autocatalyses activation of trypsinogen
61
Describe the role of trypsin inhibitors in the pancreas
Also secreted by pancreas to inhibit conversion of trypsinogen to trypsin to prevent massive amplification of chemical reactions
62
Describe the role of pancreatic amylase
Converts polysaccharides to disaccharides (and then disaccharidases convert to monosaccharides for absorption)
63
Describe the role of trypsin, chymotrypsin and carboxypeptidases
Convert long peptides to shorter chains ready for membrane dipeptidases
64
State the names of long-chain and di- peptidases in the gut
Long-chain: trypsin, chymotrypsin and carboxypeptidase
| Di: dipeptidase, endopeptidase and carboxypeptidase
65
Describe the impact of a pancreatic duct obstruction on trypsin
Can stop flow of juice and the accumulation of enzymes can overpower trypsin inhibitor, allowing activation without enterokinase, leading to pancreatic autodigestion (acute pancreatitis)
66
Describe the action and side effect of orlistat
Inhibits pancreatic lipase - anti-obesity drug but does cause steatorrhoea
67
Describe the role of S-cells in control of pancreatic function
Decrease in duodenal pH detected by S cells among enterocytes which secrete secretinThis travels to the pancreas via liver and heart, binding to basolateral surface of duct cells
68
Describe the mechanism of secretin upon binding to pancreatic duct cells
1) Increases intracellular [cAMP] to activate chloride channels and cause an efflux of Cl- ions to lumen2) This creates a concentration gradient to allow increased activity of anion exchanger to swap lumen Cl- for HCO3- (efflux)3) bicarb rich fluid travels to duodenum, and reduces concentration of free acid, combing to form carbonic acid, neutralising the stomach acid for optimum pH of acid
69
Describe the role of I-Cells in control of pancreatic function
Fats and peptides in the duodenum detected by I-cells amongst enterocytes, and these secrete cholecystokinin (CCK) to bloodCCK travels to pancreas via liver and heart, binding to CCK1 receptors on acinar cells
70
Describe the mechanism of CCK upon binding to acinar CCK1 receptors
1) Triggers PLC/IP3 second messenger system to cause Ca2+ release2) This triggers exocytosis of granules (enzyme zymogens, enzyme inhibitors and active enzymes e.g. Amylases/lipases)3) The molecules are secreted to terminal ducts of pancreatic ducts, moving into duodenum (where zymogens are activated by enterokinases/trypsin
71
Describe nervous stimulation of pancreatic function
Vagus (X) secretes ACh which bind to muscarinic receptors on acinar cells, triggering increase in cytosolic calcium (and hence granule exocytosis to release zymogens/enzymes)
72
Describe the interactions of cholecystokinin and secretin on bicarbonate secretion
CCK (alone) doesn't affect rate of bicarbonate secretion
Secretin (alone) increases bicarbonate secretion
Secretin and CCK together amplifies secretin effects and massively increases rate of bicarbonate secretion
73
State the order and lengths of the parts of the small intestine
1) Duodenum: 0.25m - digestion and gut regulation
2) Jejunum: 2.5m - absorption
3) Ileum: 3.75m - absorption
74
Describe the structure of the wall of the small intestine, including the muscles and innervation
Lining: similar to rest of tube with villi projections, mucosa in folds with 1mm villi and crypts of Lieberkuehn; external wall has longitudinal and circular muscles
Villi: only occur in small intestine and are motile, with a rich blood supply and lymph drainage; innervated by the submucosal plexus with a simple epithelium and dominated by enterocytes
75
Describe the ending of the small intestines
Separated from colon by ileocaecal sphincter, and relaxation/contraction controls passage of material and stops backflow of bacteria
76
State the distinguishing features of the duodenum
Coiled mucous secreting submucosal (Brunner's) glands that produce bicarb rich alkaline solution into crypts to neutralise acidic chyme and protect lining (+normal enzyme pH)
77
State the distinguishing features of the jejunum
Large submucosal folds (plicae circularis) which are larger and closer than the rest of the small intestine
78
State the distinguishing features of the ileum
Up to 100 Peyer's patches (aggregates of lymphoid tissue) - initiate leukocyte/Ig responses and contain M-cells with no microvilli
79
Describe the three forms of motility in the small intestine
Segmentation: alternate contraction and relaxation of non-adjacent sections of circular muscle pushes food back and forth to mix and break down (minor effect = propulsion)
Peristalsis: sequential contraction of adjacent circular muscle (combined with longitudinal muscle) propels food distally (minor effect = mixing)
Migrating motor complex: periodic contractions from stomach to distal ileum during fasted state that restart once complete - prevent colonic flora travelling backwards and cleanse small intestine of residual food
80
Describe the digestion of carbohydrates in the small intestine
Pancreatic amylases break down polysaccharides to sucrose, maltose or lactose that are then hydrolysed by disaccharidases to release monomers
81
Describe the digestion of proteins in the small intestine
Pepsin breaks down in stomach and continues in the duodenum where protease-rich pancreatic juices breaks long peptides to di/tripeptides (including trypsin, chymotrypsin and carboxypeptidase)Final stage occurs in brush border using epithelial cell enzymes (di/tripeptidases) such as endopeptidase, dipeptidase, aminopolypeptidase and carboxypeptidase
82
Describe the digestion of lipids in the small intestine
Bile enters the duodenum to provide chemical emulsification and huge increase in surface areaPancreatic juice contains lipases to cleave two fatty acids and form monoglycerides and NEFAs in luminal digestionAt the brush border, these combine with bile salts to form micelles that can cross the unstirred layer
83
Describe the absorption of carbohydrates in the small intestine
Glucose and galactose are apically transported with Sodium Linked Glucose Transporter 1 (SGLT-1 - secondary active transport) Fructose uses GLUcose Transporter 5 (GLUT-5 - facilitated diffusion) to enter the apical membraneAt the basolateral surfaces GLUT-2 is used
84
Describe the absorption of proteins in the small intestine
Apically, amino acids use an AA/Na+ symporter whereas di/tripeptides use an AA/H+ symporterOnly amino acids enter the blood and do so using facilitate diffusion
85
Describe the absorption of lipids in the small intestine
At the brush border, lipolytic products diffuse over the apical membrane whereas bile salts remain in the lumenIn the cell monoglycerides and free fatty acids are resynthesised to triglycerides and packaged with proteins, phospholipids and cholesterols to form chylomicrons which enter lacteals
86
Describe the two pathways to produce triglycerides in enterocytes of the small intestine
Monoglyceride acylation pathway: primary - fatty acids bind to apical membrane and fatty acid binding proteins transfer fatty acids to smooth ER where esterified to di/triglycerides
Phosphatidic pathway: secondary - triglycerides synthesised form fatty acid CoA and alpha-glycerophosphate
87
Describe the action of Phospolipase A2 and pancreatic cholesterol esterase
Phospholipase A2: hydrolyses fatty acids at the 2 position
| Pancreatic cholesterol esterase: hydrolyses cholesterol esters to free cholesterol and fatty acids
88
Describe the structure and role of enterocytes in the small intestine mucosa
Columnar epithelia with microvilli/RER on apical surface, nucleus near basal surface and many mitochondria; connected by tight junctions, these cells only survive 1-6days and form a brush border with the microvilliApical membrane has rich carb network (glycocalyx) that traps water, mucous and enzymes to protect from luminal contents (unstirred layer)
89
Describe the structure and role of goblet cells in the small intestine mucosa
Apical cytoplasm packed with mucin granules which distort cell to goblet shapeMucous consists of water and glycoproteins and lubricates the gut passageWater reabsorbed along gut so number of goblet cells increases along length to replace
90
Describe the structure and role of paneth cells in the small intestine mucosa (CoL)
Immune cells at base of crypt and containing a high number of acidophilic granules (containing lysozymes, glycoproteins and zinc [cofactor])Located near stem cells to protect these - can also phagocytose
91
Describe the structure and role of stem cells in the small intestine mucosa (CoL)
Used to constantly replace enterocytes/goblet cells
92
Describe the structure and role of enteroendocrine cells in the small intestine mucosa (CoL)
Hormone secreting epithelial cells, found at the base of crypts, with a sensory apical portion, and a basolateral region containing manufactured hormones
93
State the secretory products of G, I, S and D cells in the small intestine mucosa
G: Gastrin
I: Cholecystokinin (CCK)
S: Secretin
D: Somatostatin
94
Describe the migration of newly formed gut epithelia including the energy requirement and benefits
Pluripotent stem cells proliferate in crypts and move up villus towards the tipAt top become senescent and are broken down and reabsorbed (continuous escalator) - very energy intensive and allows lesions to be short lived and the effects of gut toxins/drugs to be limited
95
Describe the lifespan of the gut epithelia
Cell proliferation, differentiation and death are continuous with enterocytes/goblet cells having a 36h lifespan
96
Describe the effect of the cholera enterotoxin
Results in prolonged opening of chloride channels in small intestine to cause uncontrolled water secretion, so body fluid moves freely to lumen and is lostLeads to rapid and massive dehydration and death so rehydrate and if survive a few days, cells are replaced and no longer affected
97
List the structures that comprise the large intestine
Colon, caecum, appendix, rectum and anal canal
98
Describe the vasculature of the large intestine
Mid colic artery (Sup Mesenteric Artery): ascending colon and 2/3 of transverse
Inf Mestenteric Artery: distal 1/3 of transverse, descending and sigmoid colon
99
Describe the role of the ileocaecal valve and caecum
Ileocaecal valce: muscular sphincter that separates distal ileum from the caecum - tonically active to prevent backflow of microbiota
Caecum: blind pouch distal to valve with appendix as a refuge for gut bacteria
100
Describe the course of the ascending, transverse and descending colon
Ascending colon: starts at valve, running superiorly to the hepatic flexure
Transverse colon: crosses from hepatic to splenic flexure
Descending colon: starts at splenic flexure and runs inferiorly to the bend of the sigmoid colon
101
Describe the location and structure of the sigmoid colon
S-shaped region of the colon running to the rectum
102
Describe the structure of the rectum and anal canal
Rectum: dilated portion of the colon that can store faeces with extra submucosal transverse rectal folds and no taeniae coli
Anal canal: controls movement out of GI tract, surrounded by two sphincters
103
Describe the anal sphincters
Internal: smooth muscle and centrally controlled
External: striated muscle and pudendal nerve control
104
Describe the muscle of the large intestine
Longitudinal muscles: instead of a continuous muscle layer like rest of tract, colon has three bands of longitudinal muscle that are equally spaced; shorter than actual colon, causing bunching and formation of haustra
Circular muscle: segmentally thickened and bundles of taeniae coli penetrate circular muscle at regular intervals to keep together
105
Describe the reabsorption role of the large intestine
Predominantly occurs proximally where chyme most fluid-like, and as water reabsorbed, contents are dehydrated; sodium and chloride absorbed using exchange mechanism and water follows by osmosis
106
State the maximum and normal capacity of the large intestine to absorb water, and what happens if this is exceeded
Maximum: 4500ml day-1
Normal: 1500ml day-1
Exceeded? causes diarrhoea
107
State which cells are present in the large intestine, and those that are present in the small but not large intestine
ARE present: enterocytes, crypts, enteroendocrine, glycocalyx
ARE NOT present: paneth cells and villi
108
Contrast the mucosa of the small and large intestine
Large intestine has no paneth cells or villi (smaller s/area as little nutrient absorption occurs)
109
Descibe the roles of glycocalyx and enterocytes in the large intestine
Enterocytes: have short, irregular microvilli and intracellular machinery that reflects role in salt absorption
Glycocalyx: present but doesn't contain digestive brush border enzymes as not needed
110
Describe the roles of colonic crypts and enteroendocrine cells in the large intestine
Colonic crypts: dominated by goblet cells to secrete mucous to facilitate passage of increasingly dry stool, so abundance increases along length; stimulated by local acetylcholine secretion from nerves
Enteroendocrine cells: are fewer in number because regulation of bowel is simpler than small intestine
111
Describe the motility of the large intestine in the ascending and then transverse/descending regions
Ascending: antipropulsive patterns dominate to retain chyme and allow kneading
Transverse/descending: haustal contractions of circular muscle shuffle contents back and forth
112
Describe mass movement in the large intestine
1-3x day coordinated mass movement occurs to propel contents 3/4 length large intestine
113
Describe the storage of faecal matter and defecation reflex
Storage: occurs on shelves in the rectum created by membranous folds
Reflex: distension of the rectal wall detected by pressure receptors that use myenteric plexus to intitiate peristaltic waves in the sigmoid colon/rectum
114
Describe the composition of, and weight produced per day of faeces
Weight: 150g/day
Composition: 2/3 water, rest cellulose, bacteria, debris, bile and salt
115
Describe the autonomic innervation of the large intestine
PSNS Innervation: ascending colon and most of transverse innervated by Vagus nerve and descending colon and distal transverse innervated by pelvic nerves
SNS Innervation: lower thoracic and upper lumbar spinal cord (usually inhibiting blood flow/motility)
116
Describe the enteric nervous system and control of the external anal sphincter
External anal sphincter: controlled by somatic fibres of pudendal nerve
Enteric nervous system: myenteric plexus ganglia are concentrated below the taenia coli, and the presence of food in the stomach can stimulate mass movement
117
Describe the role of the microbiota and major species
Role: symbiotic relationship
| Major species: Bacteriodetes (gram neg anaerobic non-spore forming bacteria)
118
List the physiological roles of the intestinal microbiome
- Synthesise VitK- Prevent pathogen colonisation- Antagonise other bacteria- Stimulate cross-reactive antibody production- Break down fibre- Prime/maintain immunological system- Drug/lipid/bile metabolism
119
Describe possible links between pathophysiology and the gut microbiome
- Insulin resistance- Obesity- Lactose intolerance
120
Recall the name and functions of the biliary transporters
BSEP: active transport of bile acids across hepatocyte membranes
MDR1: canalicular excretion of xenobiotics
MDR3: translocates phosphatidylcholine from inner to outer canalicular membrane
121
Describe the cytotoxicity of bile
At high concentrations has detergent like actions
122
Describe the enterohepatic circulation of bile salts
95% salts reabsorbed from ileum using Na+/Bile Salt co-transport (5% converted to secondary acids)
123
Explain the effect of ileum disease on EHC of bile salts
Prevents recirculation of bile salts - cytotoxic bile salts then lead to irritation and dia/steatorrhoea
124
Recall the functions of the liver
- Protein synthesis: coagulation/complement/albumin
- Protein metabolism: amino acids -> urea
- Blood sugar: glycogenolysis/genesis
- Lipids: manufactures cholesterol, lipoproteins and TAGs
- Bilirubin/bile salts: formed from cholesterol
125
Recall the most common causes of liver disease in the developed and developing world
Developed: alcohol and non-alcoholic fatty liver disease
Developing: HepB/C
126
Recall the early signs and symptoms of liver disease
Early signs: jaundice, spider naevi, loss of body hair, gynaecomastia)
Early symptoms: lethargy, anorexia, malaise, RUQ pain
127
Recall the late signs and symptoms of liver disease
Late signs: clubbed nails, ascites, hepatomegaly, oedema and weight loss
Late symptoms: peripheral swelling, abdominal bloating, bruising and vomiting blood
128
Explain the aetiology and process of liver cirrhosis
Aetiology: alcohol in west, HepB/C globally
Process: common final pathway characterised by necrosis of liver cells followed by fibrosis, nodule formation and gross distortion of architecture
129
Define acute liver failure and differentiate between hyperacute, acute and subacute
Acute liver failure: massive loss of hepatocutes within 6 months of symptom onset
Hyperacute: encephalopathy within 7 days of jaundice onset
Acute: encephalopathy within 8-28 days of jaundice onset
Subacute: encephalopathy within 5-12 weeks of jaundice onset
130
Describe the clinical features of acute liver failure
- Sepsis
- Cardiovascular: reduction in TPR requires increased CO that leads to HF
- Renal: decreased renal blood flow leads to failure
- Coagulopathy: normally synthesises factors and clears activated fibrin/tPA
131
Define chronic liver failure and list the causes
Chronic liver failure: deterioration in liver function superimposed on chronic disease (may be rapid)
Causes: viral hepatitis, fatty liver, genetic, drug induced and autoimmune
132
Recall the primary and minor sources of bilirubin
Primary: splenic Hb degradation
Minor: catabolism of other haem proteins and ineffective bone marrow erythropoiesis
133
Describe the solubility of bilirubin and how it is transported in blood
Solubility: not soluble
Transport: bound to albumin
134
Describe how bilirubin is modified in the liver and then the gut
Liver: glucuronyl transferase converts to bilirubin glucuronide to make water soluble
Gut: bacteria degrade bilirubin glucuronide to mix of urobilinogen and stercobilinogen (water soluble)
135
Describe how urobiliongen is processed in the GI tract
Most reabsorbed and secreted by kidneys, but some converted to stercobilinogen by gut bacteria, which is oxidised to stercobilin for faecal excretion
136
Define pancreatitis and recall the signs and symptoms
Pancreatitis: acute inflammatory process that leads to necrosis of the pancreatic parenchyma
S/S: abdo pain, nausea, D&V, fever and shock
137
Recall the aetiology of pancreatitis
GallstonesEthanolTrauma
| SteroidsMumpsAutoimmuneScorpion biteHyperlipidaemia/hypercalcaemiaERCPDrugs (azithrioprine/valproate)
138
Recall the local and systemic complications of pancreatitis
Local: pancreatic necrosis, splenic vein thrombosis and fluid collection
Systemic: hypovolaemia, hypoxia, hyperglycaemia and DIC
139
Define chronic pancreatitis and the complications it causes
Chronic pancreatitis: progressive fibroinflammatory process of the pancreas that leads to permanent structual damage
Complications: malabsorption, loss of exocrine function and fat-soluble vitamin malabsorption
140
Outline the investigations needed for suspected chronic pancreatitis
Plain x-ray: shows calcifications
CT Scan: shows duct issues
Faecal elastase: secreted by pancreas so marker for all enzymes
141
Recall the general symptoms of upper GI and hepatobiliary disease
Upper GI: chest pain, belching, nausea, haemoptysis/emesis
| Hepatobiliary: RUQ pain, dark urine, pale stool, ascites and jaundice
142
Recall the general symptoms of mid GI and lower GI disease
Mid GI: umbilical pain, steatorrhoea/diarrhoea, distension
| Lower GI: suprapubic, rectal bleeding, constipation, incontinence and flatulance
143
Explain the appearance and causes of melaena and steatorrhoea
Melaena: black tarry stool due to upper GI bleed that has been altered by gut flora, enzymes and secretions
Steatorrhoea: sloppy, oily faeces caused by excess fat in stool
144
Define dysphagia, odynophagia and ascites
Dysphagia: difficulty swallowing
Odynophagia: pain when swallowing
Ascites: fluid accumulation in abdominal cavity
145
Recall the BMI ranges for underweight, healthy, overweight and obese persons
Underweight: < 18.5
Healthy: 18.5 - 24.9
Overweight: 25 - 29.9
Obese: > 30
146
Recall the complications of obesity
CVAs, depression, hypertension, diabetes, gout, infertility, cancers, ischaemic heart disease and sleep apnoea
147
Describe the importance of the location of fat storage on the risk of disease
Visceral fat: raises CHD risk more than subcutaneous fat as has larger impact on metabolism due to vascular supply
Adipose tissue: has trapped immune cells, so when inflamed by gaining fat, these release mediators that affect liver metabolism
148
List management strategies for obesity and describe the compensatory physiological responses
Management: Diet, exercise, drug treatment and surgery
| Physiological response: body sees weight loss as starvation so increase hunger hormones
149
Define jaundice and cholestasis
Jaundice: yellowing of the eyes and sclera due to excess bilirubin in the blood
Cholestasis: slow bile flow normally resulting in jaundice
150
Explain the abnormality found in pre-hepatic jaundice and list causes
Abnormality: increased quantity of bilirubin (produced faster than downstream path can process)Causes:- Haemolysis- Massive transfusion- Haematoma resorption- Ineffective erythropoiesis
151
Explain the abnormality found in hepatic jaundice and list causes
Abnormality: hepatocytes are not workingCauses:- Defective bilirubin conjugation
- Liver failure- Viral hepatitis- Alcoholic liver disease
152
Explain the abnormality found in post-hepatic jaundice and list causes
Abnormality: obstructive disease after the liverCauses:- Sepsis- Neoplasia/stones in the biliary tree
153
Describe how to distinguish between pre-hepatic, hepatic and post-hepatic jaundice
Pre-Hepatic: BR unconjugated, LFTs normal
Hepatic: BR unconjugated, LFTs deranged
Post-Hepatic: BR conjugated, pale faeces
154
Outline gilbert's syndrome
Most common hereditary cause of increased (unconjugated) bilirubin because glucuronidation by UDPGT enzymes is reduced 70-80%
155
Outline the three pathways of alcohol metabolism
Catalase: ethanol converted to acetaldehyde in peroxisomes using hydrogen peroxide
CYP2E1: ethanol converted to acetaldehyde in microsomes using NADPH
ADH: reversibly catalyses the production of acetaldehyde in the cytosol
156
Recall the process and consequences of acetaldehyde metabolism
Process: converted to acetate in mitochondria by reducing NAD+
Consequences: increased NADH and ROS formation (limits NAD+)
157
Recall the eatwell plate guidelines
- 5 fruit + veg a day- Base meals on potatoes/bread/rice/pasta/starchy carbs- Include dairy/alternatives- Eating beans/pulses/fish/eggs/meat/proteins- Unsaturated oils/spreads- 6-8 cups water day-1
158
Recall advice on low-carb and intermittent fasting diets
Low-carb: may decrease TAGs and increase HDLs; lowest mortality at 50-55% energy from carbs
Intermittent-fasting: replacement of processed food has larger impact rather than fractionation
159
Define malnutrition and recall its determinants
Malnutrition: state of nutrition in which a deficiency or excess of energy, protein or other nutrients cause measurable adverse effects on tissue/body form
Determinants: inadequate food intake (poverty/isolation/skill) interacts with disease (N&V/immobility/increased requirement) to produce malnutrition
160
Describe the practical impact and mortality associated with undernutrition
Mortality: exponentially increases with greater body mass loss
Practical impact: increased risk of falls/#s, muscle wasting, low mood, increased admissions, reduced independence, increased infections and increased confusion
161
Describe the stages at which nutrition may be assessed in a clinical setting
1) Screening: performed on admission in hospitals and regularly in the community and then at regular intervals
2) Assessment: in-depth assessment including weight, food diary and albumin/CRP/creatinine/cholesterol
162
Define refeeding syndrome and recall the pathomechanism
Refeeding syndrome: patients starved for 5 days or more can have metabolic disturbances when nutrition restarted
Pathomechanism: insulin release due to eating causes rapid uptake of phosphorus, magnesium, potassium and glucose - causes hypophosphataemia, hypokalaemia, hypomagnesaemia and sodium retension
163
Recall the consequences and managment of refeeding syndrome
Consequences: arrhythmias and respiratory distress/depression as well as weakness, paralysis and confusion
Management: daily biochemistry, vitamin supplementation and slow reintroduction of nutrition support
164
Recall the cancers found in the oesophagus and the risk factors associated with these
Squamous cell carcinoma: occurs in the squamous epithelium of the upper 2/3rd of the oesophagus
Adenocarcinoma: occurs in the columnar epithelium of the lower 1/3rd of the oesophagus
Risk factors: smoking, drinking and obesity linked to both, but acid reflux strongly linked to adenocarcinoma
165
Recall the stepwise development of adenocarcinoma and squamous cell carcinoma
1) Normal epitheliumAdenocarcinoma:2) Hyperplasia 3) Adenomatous polyps form Squamous cell:2) Metaplasia3) Dysplasia (then severe dysplasia)4) X-in-situ develops 5) Metastasis occurs
166
Describe the symptoms and pathology of pancreatic cancer
Pancreatic cancer: silent killer as diagnosed late
Symptoms: depression, abdominal pain and glucose intolerance early on, progressing to weight loss, jaundice, ascites and gall bladder
167
Recall when symptoms of oesophageal cancer present and how it may be treated
Onset: usually after >50% circumference cancerous
Treatment: surgery to remove part of wall affected
168
Outline the stepwise development of colorectal cancer, including the mutations present
1) Normal epithelium2) Hyperproliferative epithelium (APC mutation/COX 2 overexpression)3) Small adenoma4) Large adenoma (K-ras mutation)5) Colon carcinoma (p53 mutation)
169
Recall the symptoms, investigations and treatment of colorectal cancer
Symptoms: worsening constipation, blood in stool, loss of appetite and weight, anaemia, N&V
Investigations: abdo X-ray/CT, barium enema and colonoscopy
Treatment: surgery to remove tumour (colonoscopy/laparotomy) and chemo/radiotherapy
170
Explain why the GI tract epithelium is an external environment and recall its normal state of activation
External environment: as can be reached by bacteria without crossing a membrane - hosts a resident bacterial population
Restrained activation: need a level of tolerance to commensal bacteria but immunoreactivity to pathogens
171
Define symbiont, commensal and pathobiont bacteria and explain what is meant by dysbiosis
Symbiont bacteria: beneficial bacteria in symbiotic relationship
Commensal bacteria: occupy niches but exact role unknown
Pathobiont bacteria: capable of inflammation
Dysbiosis: altered microbiota composition (more pathobionts - leads to inflammation); can be caused by drugs, diet, infection or genetics
172
Describe the barriers and protection provided in mucosal defences
Physical barriers: tight epithelial wall, glycocalyx, mucous and unstirred layer
Chemical barrier: bactericidal enzymes from paneth cells and stomach acid
Bacterial protection: commensals maintain immune system priming and may attack foreign species
Immunological: MALTs (including GALTs) are rich in B/T cells
173
Describe the structure of MALT/GALT
MALT: sub-epithelially in the submucosa as lymphoid masses containing follicles
GALT: can be organised (e.g. peyer's patches) or disorganised (e.g. lymphocytes in the interstitial space)
174
Describe the structure and role of Peyer's patches
Structure: aggregated lymphoid follicles covered in follicle associated epithelium; found in small intestine (most concentrated in the distal ileum)
Role: immune sensors to monitor local bacteria (development requires exposure to bacterial flora) - rich in B/T cells, macrophages and dendritic cells
175
Describe the composition of the follicle associated epithelium of the gut
Reduced number of goblet cells and enterocytes, with a sub-epithelial dome containing the lymphocytes, macrophages and dendritic cells
176
Describe the role of M-cells in the gut
Specialised enterocytes that perform transcytosis of bacteria, antigens and proteinsExpress IgA receptors to transfer IgA-Bacteria complexes to the patches - work with dendritic cells to take up antigens for presentation to lymphocytes for assessment and potential immunological response
177
Decribe the topology of microfold cells
No microvilli, but with an invaginated basolateral membrane that has pockets to harbour lymphocytes for rapid transport of antigensLack glycocalyx and digestive enzymes on the apical surface so antigens are transported free of alteration
178
Explain the production of sIgA in the gut
Dimeric form of IgA produced by lamina propia B cells which join the immunoglobulins with a J chain; binds to pIgR (polymeric immunoglobulin receptor) on the basolateral surface of enterocytes, and is ingested with the receptor to a vesicle; this vesicle is then exocytosed from the apical surface with the secretory (pIgR) component still attached - preventing from enzymatic/acidic degradation
179
Explain the function of SIgA in the gut
binding to pathogens to prevent adherence to mucosal wall; antigen-specific SIgA production stimulated by the actions of M-Cells and dendritic cells in Peyer's patches
180
Describe lymphocyte circulation from the gut
Mucosal lymphocytes in PPs stimulated by antigens migrate to local mesenteric lymph nodes, draining to lymphatic system and then the systemic circulation (via thoracic duct)Spread throughout body and remain in blood until activated by tissue-specific endothelial adhesion molecules in the mucosa (MAdCAM-1) that permit transmigration to occur at HEVs in gut
181
Define transcellular and paracellular routes
Transcellular routes: through epithelial cells
| Paracellular routes: through tight junctions and lateral intercellular spaces
182
Define primary and secondary active transport
Primary active transport: linked directly to cellular metabolism (uses ATP to power)
Secondary active transport: derives energy from concentration of another substance that is actively transport
183
Describe the process of absorption of monosaccharides in the small intestine
Apical membrane:- Glucose/galactose: secondary active transport with SGLT-1
- Fructose: facilitated diffusion using GLUT-5 Basolateral membrane:
- Glucose: uses GLUT-2
184
Describe the reabsorption of water in the small intestine, recalling the mechanisms of the proximal bowel, jejunum, ileum and colon
Driven by sodium ions, with concentration gradients established by:
Proximal bowel: counter-transport in exchange for H+
Jejunum: Co-transport with amino acids, monosaccharides
Ileum: Co-transport with Cl-
Colon: Restricted movement through ion channels
185
Describe the absorption of chloride and potassium ions in the GI tract
Chloride ions: co-transported with sodium in the ileum and exchanged for bicarb in the colon (both secondary active transport)
Potassium: diffuses via paracellular pathways in small intestine to basement membrane, leaking between cells in colon to lumen (passive transport)
186
Recall the approximate intra- and extra-cellular cconcentrations of calcium, and the location of absorption
[Intracellular]: approx. 100nm but increases for cell functions
[Extracellular]: approx. 1-3mM, with plasma 2.2-2.6mM (higher than intracellular)
Location: small intestine
187
Recall the apical and basolateral transport of calcium in the small intestine and cytosolic binding
Apical transport: ion channels and intestinal calcium binding proteins (IMcal)
Cytosol: binds to calbindin to stop calcium acting as a signal
Basolateral transport: active processes
- Ca2+ ATPase: (PMCA) high affinity for Ca2+ but slow - maintaining very low level of calcium observed in cell
- Na+/Ca2+ exchanger: low affinity but rapid - requires larger concentrations of calcium to be effective
188
Describe the role, daily intake and absorption of iron
Role: electron donor and acceptor needed for oxygen transport/oxidative phosphorylation
Intake: 0.5-1.5mg day-1 present as inorganic ions/haem groups
Absorption: only Fe2+ absorbed as Fe3+ forms insoluble salts with hydroxides, bicarb and phosphate - VitC reduces 3+ to 2+ so more can be absorbed
189
Outline the absorption of haem and Fe3+ in the small intestine
Haem:1a) absorbed intact to enterocytes via haem carrier protein 1 (HCP-1) via receptor mediator endocytosis2a) Fe2+ liberated by haem oxygenase Fe3+ ions:1b) Duodenal cytochrome B catalyses reduction of 3+ to 2+
2b) Fe2+ transported by DMT1 - hydrogen ion coupled co-transporter3) Fe2+ binds to cytosolic factors and is carried to basolateral membrane4) Ferroportin channels move to blood
190
Describe the movement of iron within the blood
1) Hephaestin: transmembrane copper-dependent ferroxidase that converts Fe2+ to Fe3+
2) Apotransferrin: Fe3+ binds to apotransferrin, travelling in blood as transferrin
191
Describe the mechanisms to regulate iron and prevent toxicity due to excessive consumption
Iron regulation: hepcidin suppresses ferroportin production to decrease absorption
Toxicity: prevented using ferritin, because any excess binds irrevocably leading to excretion
192
Describe the role of apoferritin in the absorption of iron
Binds Fe2+ in cytosol to form ferritin micelles - golbular protein complexes that oxidise 2+ to 3+ which crystallise to lock up iron within the enterocyte (not absorbed, not affecting biochemistry)
193
Describe the normal absorption of fat soluble vitamins and that of B12
ADEK: passively diffuse to blood
B12: R-protein produced by salivary glands and parietal cells to bind to cleaved B12 in the stomach to prevent degradation by HCl
- Intrinsic factor: produced by parietal cells to protect B12, and in distal ileum B12-IF complex detected by cubulin for absorption
- Enterocytes: break down complex and B12 crosses basolateral membane with transcobalamin II - travelling to liver to release B12
194
Describe the hormonal control of water balance
Osmoreceptors: cell bodies present outside the blood-brain barrier so bathed in ECF; sensitive to environment and if ECF varies from 290mOsm/kg then proportionally grow/shrink to affect the rate of firing and hence adjust basal level of ADH secretion
Locations: hypothalamus, organum vasculosum and subfornical organ
195
Describe the structures of the hypothalamic nuclei responsible for the control of appetite stating what they produce
Arcuate nucleus: located at base of brain with incomplete blood-brain barrier to allow direct activation; produces NPY/Agrp (medially) and POMC (laterally) to stimulate and inhibit food intake
Paraventricular nucleus: axons emerging from arcuate nucleus secrete neuropeptides that bind to receptors in the paraventricular nucleus to regulate food intake
196
Describe the role of the melanocortin 4 receptor in the paraventricular nucleus
Role: regulates food intake/appetitePOMC: cleaved to alphaMSH, binding to agonise the receptor and reduce food intake
Agrp: antagonises the receptor, blocking the satiating signal from alphaMSH to increase food intake
Morbid obesity: linked to POMC deficiency and MC4R mutation
197
Recall where leptin is secreted and its function
Secretion: white adipose tissue
Function: hormone for long term appetite regulation, binding to hypothalamic receptors to stimulate anorexigenic receptors to suppress appetite
Leptin deficicency: linked to hyperphagia and obesity
198
Describe the tole of ghrelin and PYY in regulating appetite
Ghrelin: secreted from stomach cells when not fed, binding to hypothalamic receptors to increase perception of hunger and urge to eat, promoting eating behaviours in short-term regulation (stimulates NPY/Agrp and inhibits POMC)
Peptide YY3-36: satiety hormone, secreted by the ileum and colon in response to a meal to bind to hypothalamic arcuate nucleus receptors and reduces hunger, suppressing eating behaviours in short-term regulation (stimulates POMC and inhibits NPY release)
199
Describe the plexuses of the ENS
Myenteric (Auerbach's) Plexus: located between circular and longitudinal smooth muscle layers, with efferent innervation of each - careful control of muscularis externa allows for coordinated control of motor function and motility Submucosal (Meissner's) Plexus: - Afferent: senses lumen environment using mechanoreceptors, chemoreceptors and osmoreceptors
- Efferent: fine tunes local blood glow, epithelial transport and secretory/paracrine/endocrine cell function
200
Recall the functions of the enteric nervous system
SPAMSecretion: controls secretion of enzymes, paracrine signals and endocrine hormones
Perfusion: ensures high perfusion to gut that is working (enterocytes/submucosal glands)
Absorption: careful control of nutrient/vitamin/mineral/ion absorption
Motility: smooth muscle can contract and relax to cause motility
201
State the products of chief and parietal cells, as well as the body, fundus, pyloric canal and pyloric antrum
"Chief cells produce pepsinogen and gastric lipaseParietal cells produce acidBody and fundus produce HCl, mucous and pepsinogenPyloric antrum produces gastrinPyloric canal produces mucous"
202
Describe the release of acid from parietal cells
1) Canaliculi fuse to form a large reservoir continous with the cell exterior
2) Tubulovesicles fuse with the canaliculi to empty acid to the stomach
