GI Flashcards

1
Q

layers of the gut wall, from inner to outer

A

lumen

  • mucosa
  • submucosa
  • musclaris externa (circular then longitudinal)
  • serosa
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2
Q

layers of the mucosa, from inner to outer

A

epithelium (specialized)
lamina propria
muscularis mucosae

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3
Q

2 nerve plexuses in GI mucosa (enteric nervous system) and where they are located

A

submucosal plexus- in submucosa

myenteric plexus- between two muscle layers

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4
Q

unit of absorption

A

villus

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5
Q

how is the salivary system regulated? what about the rest of the GI tract?

A
  • saliva: only neural

- all others: neural, paracrine, endocrine

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6
Q

5 motility patterns

A
  • segmentation (mixing, breaking down)- SI
  • peristalsis (movement of food)- SI
  • reverse peristalsis- vomiting - SI?
  • MMC- between meals, stimulated by motilin between meals
  • mass movement (moving fecal matter)- colon
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7
Q

functions of saliva & key enzymes

A

lubrication
protection
initial digestion - not major

  • alpha amylase- starches
  • lingual lipase- lipids
  • lysozyme- maintains oral hygiene
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8
Q

final saliva is hypo/iso/hypertonic to plasma; it was initially hypo/iso/hypertonic ; at what flow rate is it most similar to plasma

A

final= hypotonic (ALWAYS); initially= isotonic

most similar to plasma at high flow rates

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9
Q

what are the net processes involved in saliva creation? which one is abnormal?

A

secrete K+, HCO3-
absorb Na+, Cl-

  • HCO3- stimulated by parasympathetics, increases with flow rate
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10
Q

describe regulation of saliva secretion - stimulating and inhibiting factors

A

both result in saliva secretion!

1) parasympathetic (dominant)- releases Ach via CN 7&9 onto muscarininc receptors, Ip3/Ca2+ blocked by atropine

stimulating: conditioning, food, nausea, smell
inhibiting: dehydration, fear, sleep

2) sympathetic- T1-T3, Ne on beta-adrenergics, cAMP

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11
Q

3 phases of swallowing reflex, which is voluntary

A

1) oral - voluntary

2) pharyngeal

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12
Q

what is receptive relaxation?

A

LES and orad stomach relax at the same time

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13
Q

roles of the UES and LES, and which one is important for GERD

A

1) UES- protects airway- keeps food/acid out of airway, keeps air out of esophagus
2) LES- keeps acid out of esophagus - GERD

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14
Q

what does chronic gastric reflux cause?

A

change in esophageal mucosa from stratified squamous epithelium

1) to simple columnar (like in stomach) - just metaplasia
2) to simple columnar with goblet cells- barretts esophagus/intestinal metaplasia

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15
Q

what is the essential factor the the stomach secretes?

A

intrinsic factor, required for vitamin B12 absorption, don’t produce anywhere else

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16
Q

6 secretory cells of stomach

A

1) parietal/oxyntic- HCl, Intrinsic factor
2) mucous neck cells- mucus
3) peptic/chief cells- pepsinogens
4) enterochromaffin-like cells (ECLs)- histamine
5) D cells- somatostatin
6) G cells- gastrin

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17
Q

where are goblet cells located? where are cholangiocytes located?

A

goblet: intestinal, mostly large intestine
cholangiocytes: lining the bile duct

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18
Q

where does a proton pump inhibitor such as omeprazole work? what is lacking when you give this drug?

A

H+/K+ ATPase on luminal side

see no somatostatin b/c it only responds to low pH, have high levels of gastrin in their blood

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19
Q

what is the net result of gastric acid secretion?

A

net secretion: HCl

net absorption: bicarb

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20
Q

what protects the stomach from ulcers (what causes damage)?

A
  • damage caused by H+/pepsins
  • pepsin only works in low pH
  • thick layer of mucus with bicarb trapped inside
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21
Q

stimulating agents for gastric acid secretion and drugs that block them

A

1) Vagus releasing Ach on M3 receptors (blocked by atropine) - neurocrine- directly working on parietal cells & potentiates
2) G-cells releasing gastrin on CCKb receptors - endocrine
3) ECL cells releasing histamine on H2 receptors (blocked by cimetidine) - paracrine

22
Q

inhibition of gastric acid secretion

A

1) somatostatin - inhibits histamine
* direct by blocking cAMP
* indirect by inhibiting histamine and gastrin release
2) prostaglandins- inhibit cAMP

23
Q

difference between gastric and duodenal ulcer

A
  • gastric- defect in mucosa barrier (not hypersecretion)
  • duodenal- more common- excess H+ (and pepsin) in duodenum overpowers bicarb buffering (if pancreatic secretion isn’t enough)
24
Q

what major factors contribute to the slowing of gastric emptying? what hormone is this effect mediated by?

A
  • fat & AA in duodenum
  • H+ in duodenum
    mediated by CCK released from I cells
25
Q

what does CCK regulate?

A

1) pylorus contraction
2) gallbladder contraction- produce bile
3) relaxes sphincter of oddi- so bile/pancreatic juice can center
4) pancreatic secretion

26
Q

2 components of exocrine pancreas secretions

A

1) aqueous- high in bicarb (ductal cells)

2) enzymatic (acinar cells)

27
Q

regulation of pancreatic ductal secretion

A

1) low pH in duodenum
2) stimulates S cells to release secretin
3) secretin increases ductal bicarb secretion via CFTR chloride channel
* bicarb from NBC-1 or carbonic anhydrase
4) pH of intestinal lumen increases
5) secretin secretion is inhibited

28
Q

3 things that trigger CCK release

A

1) direct action of AAs/Fats
2) fats/AA binding to paracrine cells that release CCKRP
3) pancreatic acinar cells secreting monitor peptide (neural regulation)

29
Q

how are bile acids recycled?

A
  • enterohepatic circulation

- terminal ileum asbt recycles conjugated bile acids back to liver

30
Q

difference in Na absorption between jejunum and ileum

A

jejenum- Na+ transported with sugar/AAs on luminal side, absorbed with bicarb- on basolateral

ileum- Na+ transported with sugar/AAs on luminal side, absorbed with Cl- on basolateral side

31
Q

what is an illeal brake and what does it do?

A

EECs in terminal ileum secrete peptide YY in response to lipids in the lumen

  • decreases gastric emptying, reduces Cl (and fluid) secretion by intestinal cells
  • reduces fluidity
32
Q

final mechaism for the absorption of H20

A

ENaC - Na+ channel in distal colon, patients w/ bowel inflammation have defects here

33
Q

major contribution of colonic microflora

A

production of ammonia from urea; urease activity

34
Q

what is hepatic triad

A

hepatic artery, portal vein, bile duct

35
Q

zone 1 vs zone 2 vs zone 3 cells of liver

A
  • zone 1- periportal- most sensitive to oxidative species, toxins b/c they encounter them first
  • zone 3- pericentral- close to hepatic vein- most sensitive to ischemia, most active in bile synthesis
36
Q

what does a gallstone near the sphincter of oddi cause

A

blocks bile duct and pancreatic flow

can cause pancreatitis and cholangitis

37
Q

where does bilirubin come from and how is it excreted?

A
  • comes from heme degradation in reticuloendothelial system (macrophages)
    Hemeoglobin- biliverdin- bilirubin- bilirubin + albumin- taken up by OATP- conjugated in liver with UDPGT, is now water soluble- some secreted in bile - de-conjugated by bacteria to urobilinogen - urobilin & stercobilin excreted in feces
38
Q

major cause of hyperbilirubinemia that cause jaudice

A

1) intrahepatic/extrahepatic bile duct obstruction

2) newborns don’t have UDPGT

39
Q

pathologies of liver

A

1) hepatic encephalopathy- no urea cycle to get rid of ammonia which can cross BBB
2) liver cirrhosis- activate hepatic stellate cells which produce lots of collagen, leading to fibrosis
3) portal hypertension- increased resistance of vascular system in liver, results in spleenomegaly & fluid accumulation

40
Q

energy values of food

A

carbs- 4 kcal/g
protein- 4 kcal/g
fat- 9 kcal/g

41
Q

main enzyme for starch digestion and what bonds does it digest

A

amylase (salivary & pancreatic)

- digests alpha 1, 4 linkages (cellulose is beta 1,4)

42
Q

disaccharides in food and the monosaccharides they are made up of which we can absorb

A

trehalose- 2 glucose
sucrose- glucose + fructose
lactose- glucose + galactose

43
Q

what products does pancreatic amylase produce? what are they digested by?

A

a-limit dextrins (isomaltase), maltose (maltase), maltriose (sucrase)
digested by brush border enzymes
products are glucose

44
Q

glucose transporter on luminal side?

A

SGLT1 requires Na/K ATPase

45
Q

glucose/fructose/galactose transporter on basolateral side?

A

GLUT2

46
Q

emulsification vs micelle formation

A

emulsification- processing before fat digestion has taken place; break down into small pieces; bile acids play big role; most in duodenum

micelle formation- after fat digestion, exterior lined with amphipathic bile salts (hydrophilic ends outside)

47
Q

3 important lipolytic enzymes in pancreatic juice (most of lipid digestion in SI)

A
  • pancreatic lipase (triglycerides),
  • phospholipase A2 (lysolecthin),
  • cholesterol ester hydrolase
48
Q

where does protein digestion start and with what? what is it secreted as? what is it activated by?

A

stomach with action of pepsin, secreted as pepsinogen; activated by low pH

49
Q

where is (90% of) protein digestion completed?

A

duodenal area by pancreatic brush border proteases (endo & exopeptidases)

50
Q

proenzymes in the pancreatic juice are activated by what? what is that activated by?

A

trypsin activated from trypsinogen by enterokinase in brush border

trypsin in pancreatic juice
enterokinase in brush border

51
Q

what forms of proteins are absorbable? how?

A

AAs, di & tri peptides

- some symported with Na, H+ (PEPT1)