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FBS1 > PPP - digestive system > Flashcards

PPP - digestive system Flashcards

1
Q

Where does the digestion of carbohydrates start?

A

in the mouth by amylase in saliva

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2
Q

What are lymphatics important for in the GI tract?

A

intestinal absorption of fat

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3
Q

What are the major salivary glands?

A

sublingual, submandibular and parotid

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4
Q

What are the layers of the GI tract?

A

Mucosa
Submucosa
Muscularis externa
Adventitia/serosa

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5
Q

What are the stages of gastric acid secretion?

A 
basal/fasting phase
stimulated phases:
- cephalic
- gastric
- intestinal
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6
Q

What are the secretions of the gastric pit cells?

A

neck cells - mucus
parietal cells - HCl
chief cells - pepsinogen
endocrine cells - gastrin

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7
Q

What happens when parietal cells are activated?

A

tubulovescicles fuse at the membrane to form the H+/K+ pump

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8
Q

What 3 factors regulated parietal cell secretion of HCl?

A

Ach, histamine, gastrin

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9
Q

What are the main components of pancreatic juice?

A

proteases, amylase, lipase and bicarbonate

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10
Q

What does CCK stimulate in the biliary system?

A

gallbladder contraction and relaxation of sphincter of Oddi

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11
Q

What does secretin do in the biliary system?

A

stimulates liver duct secretion

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12
Q

What is the relationship of bile with blood flow and pressure?

A
  • bile flow has a linear relationship with blood flow to liver
  • independent of pressure
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13
Q

What is the composition of bile?

A

bile acids, bilirubin, ions, cholesterol, phospholipids, fatty acids

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14
Q

How are bile acids concentrated?

A
  • NaCl and HCO3- are taken up via Na-H and Cl-HCO3- exchanges
  • Na+ moves to interstitial space via Na/K+ pump
  • Cl- leaves via channels
  • H20 follows ion movement, concentrated bile acids
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15
Q

How does bilirubin travel in blood?

A

bound to albumin

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16
Q

What is conjugated bilirubin?

A

when it is conjugated with glucaronic acid

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17
Q

How does obstructive jaundice occur?

A

blockage of bile ducts means conjugated bilirubin can’t be excreted

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18
Q

What happens to bilirubin when it is taken up by the liver?

A

conjugated with glucaronic acid and secreted into bile canaliculi

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19
Q

What is bilirubin broken down to for excretion?

A

urobilinogen

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20
Q

What is the total pool of bile acids?

A

around 3g

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21
Q

What happens to bile acids in the intestine?

A

95% are reabsorbed and brought back to the liver

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22
Q

How can liver clearance be measured?

A

BSP

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23
Q

How are medium and short chain fatty acids absorbed?

A

can pass through fenestrations directly into blood in stomach

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24
Q

When does the duodenum release CCK and GIP?

A

when fatty acids, low pH etc are sensed in the duodenum

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25
Q

How are lipids transported from the small intestine?

A

packaged into chylomicrons and exported into lacteals

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26
Q

What factors control bile secretion?

A

Vagus - increases
VIP and serotonin - decreases
Secretin - increases watery secretion (not bile salts)

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27
Q

What are the causes of gallstones?

A
  • excess water in bile
  • excess bile acid absorption
  • excess cholesterol in bile
  • epithelium inflammation
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28
Q

What is the purpose of saliva?

A

to lubricate food for swallowing and initiate starch digestion

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29
Q

What is the maximum rate of saliva flow?

A

1ml/min.g

30
Q

What is the order of salivary ducts?

A
  • acinar cells surrounding central lumen
  • intercalated duct
  • large ducts
  • main excretory duct
31
Q

What stimulates saliva secretion?

A

taste, smell, touch of food, chewing etc

32
Q

What is the 2 stage process of saliva secretion?

A
  1. primary isotonic fluid produced by acinar cells

2. duct cells reabsorb Na+/Cl- and secrete K+/HCO3- to make hypotonic saliva

33
Q

What stimuatles secretion in salivary acinar cells?

A

SNS -> noradrenaline on a/b receptors

PNS -> VIP and AcH (muscarinic)

34
Q

What is the result of saliva acinar cell stimulation?

A
  • intracellular rise in Ca2+
  • activates basolateral K+ channel and Cl- luminal channel
  • H20 and Na+ move into lumen paracellularly
35
Q

What can cause hyposalivation?

A

gland atrophy caused by aging, drugs and disease

36
Q

What type of epithelium is in the stomach?

A

simple columnar

- contains gastric pits and mucus cells

37
Q

What is the turnover of cells in the stomach?

A

2-6 days

38
Q

What are the features of cardia mucosa?

A
  • highly coiled and branched
  • mainly secretes mucus
  • no peptic or parietal cells
39
Q

What are the features of pyloric mucosa?

A

secrete alkaline mucus and electrolytes

- characterised by deep gastric pits

40
Q

What are the features of the fundus and body mucosa?

A
  • numerus gastric pits
  • key HCl secretion
  • G cells
41
Q

What are the 3 regions of gastric pits?

A
  1. isthmus - parietal and neck cells
  2. neck - parietal and neck cells
  3. base - chief and endocrine cells
42
Q

What can stimulate granule release in the stomach?

A

aspirin, food, stress, ethanol

43
Q

What are the steps of acid secretion in the stomach?

A
  1. G-cells secrete gastrin
  2. gastrin acts on CCK receptor on ECL cells
  3. Release of histamine
  4. histamine acts on H2 receptors on parietal cells
  5. parietal cells release HCl
44
Q

How is Hcl secretion in the stomach terminated?

A
  • Hcl acts on D cells

- D cells release somatostatin which inhibts gastrin release from g cells

45
Q

What is omeprazol?

A

A PPI

  • prevents HCl release from parietal cells
  • inhibits 80% of secretions
46
Q

What is an alternative method of preventing HCl secretion?

A

H2 agonists

e.g. famotidine

47
Q

What is omeprazol used to treat?

A

Peptic ulcers and reflux

48
Q

What can other factors can stimulate parietal cells along with histamine?

A
  • Gastrin on CCK2 receptors

- Ach on M3 receptors

49
Q

How is the stomach protected from low pH

A

Bicarbonate rich mucus layer

50
Q

What happens in the cephalic phase?

A

activated by smell, chewing etc

- vagus stimulation is sent to stomach in anticipation of digestion

51
Q

What happens in the gastric phase?

A
  • food enters the stomach

- stomach distention triggers acid secretion and gastrin release

52
Q

What is the intestinal phase of digestion?

A

food enters the inestine and is sensed by duodenal cells -> release of pancreatic enzymes

53
Q

What is zollinger-ellison syndroem?

A

gastrin-secreting tumours

  • increase Hcl secretion
  • cause peptic ulcers and other symptoms
54
Q

What are the components of pancreatic juice?

A

high conc of bicarbonate, trypsinogen, chymotrypsinogne, other proteases, amylase, lipase

55
Q

What is the type of fluid is secreted along with pancreatic juice?

A

NaCl-rich isotonic fluid

56
Q

How is isotonic fluid made in the pancreas?

A
  1. Na/K/Cl cotransporter brings Cl into cells from interstitial space
  2. Cl- enters lumen via Cl channels
  3. Na+ and water move paracellularly
57
Q

Where is CCK released from?

A

I-cells in the small intestine

58
Q

What stimulates peristalsis in the stomach?

A

distention

59
Q

What is the neuronal control of gut motility?

A

PNS via vagus - Ach +, VIP & ADP -

SNS: inhibitory via noradrenaline

60
Q

What are the hormonal controls of gut motility?

A

Gastrin, CCK and motilin

61
Q

What are the effects of gastrin and CCK on stomach motility?

A

increase antrum contraction and relax proximal stomach

-> reduces gastric emptying

62
Q

What is the stomach plasticity?

A

it’s ability to maintain constant pressure until it contains 1L of food

63
Q

What type of chyme moves fastest to the duodenum?

A

carb-rich > protein-rich

64
Q

What are the plexuses of the enteric nervous system?

A

myenteric/auberbach’s & submucosal/meissner’s

65
Q

What do the ENS neurones respond to?

A

mechanical and chemical stimuli and temperature

66
Q

What type of neurons are in the ENS?

A

sensory, motor and interneurons

67
Q

What are the effects of secretin?

A

increases bicarbonate secretion

inhibits stomach activity

68
Q

what are the effects of CCK?

A

stimulates gallbladder

inhibits stomach activity

69
Q

What are the effects of GIP?

A

inhibits gastric contractions

70
Q

What are the effects of motilin?

A

increases motility

FBS1 (9 decks)

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