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phase 1 > GI > Flashcards

GI Flashcards

1
Q

what are the derivatives of the foregut?

A
  • oesophagus
  • stomach
  • first half of duodenum (parts 1 + 2)
  • pancreas
  • liver & biliary system
  • dorsal & ventral mesentery (omentum)
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2
Q

what are the three developmental parts to the gut?

A
  • foregut: starting at lower end of hypopharnyx
  • midgut: starting at third part of duodenum
  • hindgut: starting 2/3 of way along transverse colon & finishing at anal canal
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3
Q

what is the arterial & nerve supply of the foregut?

A

-coeliac trunk & greater splanchnic nerve (T6-T9)

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4
Q

what is the arterial & nerve supply of the midgut?

A

-superior mesenteric artery & lesser splanchnic nerve (T10-T11)

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5
Q

what is the arterial & nerve supply of the hind-gut?

A

-inferior mesenteric artery & least splanchnic nerve (T12, sometimes L1)

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6
Q

what does the endoderm give rise to in the gut?

A

-bowel epithelium, liver hepatocytes and end/exocrine cells of the pancreas

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7
Q

what does the visceral mesoderm give rise to in the gut?

A

-muscle wall, connective tissues for wall, liver, pancreas and visceral peritoneum

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8
Q

what are the parts of the pancreas?

A
  • head: the part which sits right next to the duodenum
  • neck: the part directly anterior to the hepatic portal vein and superior mesenteric vein
  • body:main part of pancreas extending to the left side
  • tail: most lateral part of the pancreas
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9
Q

what are the five stages for development of gut tube?

A

1) elongation
2) physiological herniation
3) rotation
4) retraction
5) fixation

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10
Q

what are the fixed/mobile parts of the gut?

A 
fixed:
-duodenum (except 1st cm)
-ascending colon
-descending colon
-rectum 
mobile:
-stomach 
-jejunum & ileum 
-appendix (caecum)
-transverse colon
-sigmoid colon
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11
Q

what are the functions of the stomach?

A
  • store & mix food
  • dissolve & continue digestion
  • regulate emptying into duodenum
  • kill microbes
  • secrete proteases
  • secrete intrinsic factor
  • activate proteases
  • lubrication
  • mucosal protection
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12
Q

what are the key cell types in the stomach & their functions?

A
  • mucous cells - bicarb rich mucus to protect against attack by HCl
  • parietal cells - secrete HCl & intrinsic factor
  • chief cells - pepsinogen
  • enteroendocrine - hormones
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13
Q

summarise how H+ and Cl- ions are secreted into stomach lumen

A
  • H+ ions exchanged against conc. gradient - H+/K+ ATPase pump on luminal surface (neutral charge must be maintained)
  • K+ & Cl- can be lost passively via ion channels
  • H+ & Cl- combine in stomach to form HCl
  • bicarb pumped out at capillary end, Cl- pumped in replenishing those lost at luminal end
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14
Q

summarise turning gastric acid secretion on during cephalic phase

A
  • parasympathetic nervous system (CNX)
  • sight, smell, taste, chewing
  • Ach release from nerve fibres
  • Ach acts directly on parietal cells, turns gastric cells on
  • Ach triggers release of gastrin & histamine
  • net effect- increased HCl production
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15
Q

summarise turning gastric acid secretion on during gastric phase

A
  • gastric distension, presence of peptides & amino acids
  • gastrin release
  • gastrin (by g cells) directly acts on parietal cells
  • gastrin triggers histamine release
  • histamine acts directly on parietal cells
  • net effect - increased acid production
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16
Q

summarise turning gastric acid secretion off during gastric phase

A
  • low luminal pH
  • directly inhibits gastrin secretion
  • indirectly inhibits histamine release
  • stimulates somatostatin release, inhibiting parietal cell activity
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17
Q

summarise turning gastric acid secretion off during intestinal phase

A
  • in duodenum:
  • -duodenal distension
  • -low luminal pH
  • -hypertonic luminal contents
  • -presence of amino acids & fatty acids
  • trigger release of enterogastrones:
  • secretin (inhibits gastrin, promotes somatostatin)
  • cholecystokinin (CCK)
18
Q

summarise factors affecting digestion

A
  • controlled by brain, stomach & duodenum
  • 1 (parasympathetic) neurotransmitter (ACh +)
  • 1 hormone (gastrin +)
  • 2 paracrine factors (histamine +, somatostatin -)
  • 2 key enterogastrones (secretin -, CCK -)
19
Q

what are the main causes of peptic ulcers?

A
  • helicobacter pylori (majority)
  • drugs (NSAIDs)
  • chemical irritants (alcohol, bile salts, diet)
  • gastrinoma
  • increased acid production
  • reduced mucosal defence
20
Q

how does gastric mucosa defend itself?

A
  • alkaline mucus
  • tight junctions b/t epithelial cells in gastric epithelium
  • rapid replacement of damaged cells
  • feedback loops (-ve)
21
Q

how does helicobacter pylori cause peptic ulcers?

A

-lives in alkaline environment
-secretes urease, splitting urea -> CO2 + ammonia
-ammonia + H+ = ammonium
-ammonium, secreted proteases, phospholipase & vacuolating cytotoxin A damage gastric epithelium
-inflammatory response
reduced mucosal defence of stomach
(requires triple therapy- 1PPI, 2 antibiotics)

22
Q

how do NSAIDs cause peptic ulcers?

A

-mucus secretion stimulated by prostaglandins
-cyclo-oxygenase 1 (target of NSAIDs) needed for prostaglandin synthesis
NSAIDs inhibit cyclo-oxygenase 1
-reduced mucosal defence
(treatment: prostaglandin analogues

23
Q

how do bile salts cause peptic ulcers

A
  • duodeno-gastric reflex
  • regurgitated bile strips away mucus layer
  • reduced mucosal surface
24
Q

how is protease secreted and mediated?

A
  • chief cells produce pepsinogen
  • synthesised in inactive form (zymogen)
  • pepsinogen mediated by input from enteric nervous system (ACh)
  • secretion parallels HCl secretion
  • luminal activation
25
Q

how is protease activated?

A
  • pepsinogen->pepsin conversion is pH dependent
  • most efficient when pH<2
  • +ve feedback loop
  • irreverible inactivation in small intestine by HCO3-
  • HCl action cleaves pepsinogen to pepsin
26
Q

what is receptive relaxation & how is it mediated?

A
  • stomach can relax & distend without pressure changes
  • mediated via PS NS acting on enteric nerve plexuses
  • coordination - afferent input via CNX
  • nitric oxide & serotonin released by enteric nerves mediate relaxation of smooth muscle in gastric wall
27
Q

how is basic electrical rhythm determined in gastric wall?

A
  • interstitial cells of Cajan located throughout gastric wall are pacemaker cells, ~3 gastric contractions per minute
  • frequency determined by pacemaker cells in muscularis propria
  • pacemaker cells undergo slow depolarisation-repolarisation cycles
  • depolarisation waves transmitted through gap junctions to adjacent smooth muscle cells
28
Q

what increases strength of peristaltic contractions?

A
  • gastrin

- gastric distension

29
Q

what decreases strength of peristaltic contractions?

A
  • duodenal distension
  • inc. duodenal luminal fat
  • inc. duodenal osmolality
  • dec. duodenal luminal pH
  • inc. S NS action
  • dec. PS NS action
30
Q

what is gastric emptying?

A
  • capacity of stomach>capacity of duodenum

- overfilling of duodenum by hypertonic solution causes dumping syndrome

31
Q

what is gastroparesis and its causes?

A
  • delayed gastric emptying
  • -idiopathic
  • -autonomic neuropathies
  • -drugs
  • -abdo surgery
  • -parkinsons
  • -MS
  • -schleroderma
  • -amyloidosis
  • -female
32
Q

what is the presentation of delayed gastric emptying?

A
  • nausea
  • early satiety
  • vomiting undigested food
  • GORD
  • abdo pain/bloating
  • anorexia
33
Q

what are the functions of the liver?

A
  • carbohydrate metabolism
  • fat metabolism
  • protein metabolism
  • hormone metabolism
  • toxin/drug metabolism & secretion
  • storage
  • bilirubin metabolism & excretion
34
Q

what is ferritin & where is it found?

A
  • large spherical protein consisting of 24 non-covalently linked subunits
  • subunits form shell surrounding central core
  • core contains up to 5000 atoms of iron
  • found in cytoplasm but also in serum
  • conc. directly proportional to total iron stores in the body
35
Q

what causes low ferritin levels?

A

iron deficiency

36
Q

which vitamins are water soluble & which are fat soluble?

A
  • water soluble: B + C

- fat soluble: A, D, E & K

37
Q

what do vitamins act as?

A
  • gene activators
  • free-radical scavengers
  • coenzymes/cofactors in metabolic reactions
38
Q

how do macrophages breakdown haemoglobin?

A
  • heme: 1st converted into biliverdin via heme oxygenase, then into unconjugated bilirubin via biliverdin reductase, plus iron which re-enters circulation
  • globin: protein therefore broken down into amino acids then re-enters bloodstream
39
Q

what happens after heme is converted to unconjugated bilirubin?

A
  • attached to albumin to be transported around bloodstream, transported to liver for further metabolism
  • unconjugated bilirubin gets conjugated by glucuronic acid
  • now soluble, so secreted along with bile, eventually traveling through small intestine to colon
40
Q

what happens to the conjugated bilirubin in the colon?

A
  • converted to urobilinogen by intestinal bacteria by removing glucuronic acid (reduction reaction)
  • now lipid-soluble; 10-15% reabsorbed into bloodstream with addition of albumin
  • remainder quickly oxidised by other intestinal bacteria to form stercobilin, which is then excreted in faeces
41
Q

what happens to urobilinogen reabsorbed into bloodstream?

A
  • carried back to liver via portal system
  • 5% will travel to be re-excreted
  • remiander transported by blood to kidneys, where it is converted to urobilin + excreted in urine

phase 1 (2 decks)

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