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GI Exam 2 > Physiology > Flashcards

Physiology Flashcards

1
Q

Exocrine pancreas

A

secretion of essential digestive enzymes and bicarbonate into duodenum –> neutralize acidic chyme

  • secretes approximately 1 L/day
  • Acinar cells –> secrete digestive enzymes (zymogen granules)
  • Centroacinar/duct cells –> dilute enzymes and render HCO3
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2
Q

Primary ionic components of pancreatic juice

A

Na and HCO3

- HCO3 is dependent on Cl- exchanger

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3
Q

Cephalic/Gastric Phase

A

pancreatic exocrine secretion is 30%, mostly enzyme and low volume
Acinar cells activated by parasympathetic efferents from vagal centers

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4
Q

Intestinal Phase

A

pancreatic exocrine secretion is 70%, increased enzyme and high volume

  1. Acinar cells are activated by vago-vagal reflex and by fat/AA in duodenum (CCK from I-cells)
  2. H+ ions cause S cells to release secretin activating ductal cell secretion of HCO3
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5
Q

Secretagogues

A

promote compound exocytosis in acinar cells

  • CCK and vagal stimulation
  • Ca2+ signaling –> most important with cAMP signaling playing a modifying role
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6
Q

Regulation of CCK

A

regulated by CCK-RP and Monitor Peptide

  1. During cephalic/gastric –> vagal stimulation causes release of pancreatic enzymes including MP
  2. Intestinal phase –> AA and FAs cause CCK-RP release
  3. CCK-RP and MP cause release of CCK from I-cells
  4. CCK increases release of MP and pancreatic enzymes
  5. Pancreatic enzymes digest luminal nutrients, CCK-RP, MP –> turn off CCK secretion
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7
Q

CCK

A

master regulator of duodenal cluster unit

  • cause contraction of gallbladder and relaxation of sphincter of oddi –> need bile salts for fat digestion
  • increase acinar secretion in pancreas
  • reduces gastric emptying –> takes time to digest fats
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8
Q

Enteropeptidase

A
  • duodenal brush border membranes cleaves trypsinogen into trypsin –> activates lipases and endopeptidases
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9
Q

Hereditary pancreatitis

A

occurs to mutation in trypsinogen gene preventing trypsin elimination –> causes activation of digestive enzymes in pancreas

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10
Q

Release of secretin

A

pH < 4.5 –> S-cells release secretin –> raises pH with HCO3 (neutralization)

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11
Q

Secretin

A

initiates secretion of HCO3 by pancreas

  • CFTR supplies Cl for HCO/Cl exchanger and is regulated by secretin activation of cAMP
  • patient with CF won’t have exchanger gradient –> less neutralization of acid –> poorly functioning enzymes –> malabsorption of fats and fat soluble vitamins
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12
Q

Intestinal L cells

A

secrete incretin GLP-1 –> increases insulin and decreases glucagon

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13
Q

Stimulation of insulin secretion of pancreatic beta-cells?

A

GLP-1, gastrin, CCK, ACh

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14
Q

Satiety signals

A

GLP-1, CCK, insulin, leptin (adipose tissue)

  • act at hypothalamus to decrease food intake and increase energy expenditure
  • lack of sleep can lower leptin levels
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15
Q

Ghrelin

A

produced in fundus of stomach during fasting –> stimulates appetite and decreases energy expenditure at hypothalamus

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16
Q

Liver

A
  1. Processing of all ingested nutrients and substances
  2. Metabolism of carbs, fats, proteins
  3. Buffering of glucose within normal limits
  4. Synthesis of factors important for circulatory system
  5. Bile formation –> lipid uptake
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17
Q

Hepatocytes

A

80% of total liver cells –> metabolic factories that regenerate and produce bile

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18
Q

What happens in liver cell after meal?

A
  1. Increased blood enters the sinusoids –> maximizing exposure of hepatocytes to blood
  2. Blood leaves liver and enters central vein (IVC)
  3. Bile is secreted continously into R and L hepatic ducts
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19
Q

Cirrhosis

A

hardening of liver due to irreversible deposition of collagen
- causes increased resistance to flow –> portal HTN

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20
Q

Bile salts

A

facilitate excretion of hydrophobic molecules (cholesterol) and uptake of fatty acids and fat soluble vitamins
- act as emulsifiers (polar side interacts with water, non-polar side interacts with lipids)

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21
Q

Enterohepatic circulation

A

bile is secreted into bile duct –> into duodenum –> reabsorbed in ileum –> portal vein
- recirculates 4-5 times during fatty meal

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22
Q

Primary bile acids

A

synthesized from cholesterol
- Chenodoxycholic acid, cholic acid
Bile acids are conjugated to bile salts –> increased aqueous solubility and decreased pKa
- bacteria can deconjugate the bile salts back to bile acids to be reabsorbed.

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23
Q

Cholangiocytes

A

epithelial cells of bile duct

glucose and AA are actively reabsorbed from bile (prevents overgrowth of bacteria which could lead to deconjugation)

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24
Q

Gallbladder

A

concentrates the bile between meals

  • tight junctions preclude water movement
  • active sodium pumping into lateral spaces with chloride following produces osmotic gradient that pulls water along
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25
Q

Between meals –> gallbladder?

A

gallbladder is filled with bile by:

  1. hepatic secretion
  2. contraction of sphincter of oddi
  3. receptive relaxation of gallbladder by NO/VIP
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26
Q

Bile uptake by intestinal epithelial cells

A

Uptake of conjugated bile salts by APICAL SODIUM-DEPENDENT BILE SALT TRANSPORTER (ileum) –> coupled to sodium uptake

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27
Q

Cholestasis

A

impaired bile secretion
Effects
- bile accumulates in liver leading to metabolic dysfunction
- itching –> bile regurgitation into plasma
- hypercholesterolemia –> cholesterol aggregation
- deficiency in fat soluble vitamins
Symptoms –> RUQ pain, fever

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28
Q

General mechanism of digestion and absorption

A

95% of nutrients are absorbed by time meal reaches distal jejunum

29
Q

Features of duodenum and jejunum

A

plicae circularis –> slows transit of food
villi –> increase surface area
segmenting contractions –> mixes food

30
Q

Enzymatic hydrolysis of carbs and proteins

A
  1. In lumen by pancreatic enzymes
  2. at microvilli by brush border enzymes
  3. at enterocytes for peptides
31
Q

Lactose intolerance

A
  • lactose is breast milk major source of carbs for infants
  • there is a normal decrease in lactase in adults
    Symptoms –> bacterial fermentation of lactose –> gas accumulation and lactic acid production –> increased osmotic load –> water enters
32
Q

SGLT1

A

Sodium-glucose/galactose cotransporter 1 –> luminal side!

  • critically dependent on low intracellular Na from Na/K ATPase
  • also drive fluid uptake
33
Q

GLUT5

A

fructose transporter –> luminal side

34
Q

GLUT2

A

all monosaccharides leave basolateral membrane going to liver via this transporter

35
Q

Protein digestion

A

initiated by pepsin

- pancreatic proteases require brush border enteropeptidase for activation (trypsin)

36
Q

AA absorption

A

occurs in villi of duodenum and jejunum

AA transported across apical membrane by Na dependent symporters

37
Q

Peptide Absorption

A

PEPT1 cotransports peptides with protons

- once inside, they are digested to AA

38
Q

Digestion of lipids

A

90% are TAG, 10% cholesterol, lipids

  • gastric lipase helps, only cleaves FA at #1 position
  • pancreatic lipase cleaves at #1,3 leaving 2-MG
  • FA in duodenum trigger CCK –> lipase and procolipase
39
Q

What happens to lipase when bile acids enter?

A

Lipase is inhibited by bile acids –> procolipase recruits and activates lipase to cleave FAs when bile acids present

40
Q

Mechanism of digesting fats

A
  1. bile salts and phospholipids emulsify the globules
  2. packaged into micelles by bile salts
  3. enter enterocyte by carrier mediate transport, or nonionic diffusion or collision with membrane (2nd two not in micelle)
41
Q

Ezetimibe

A

reduces uptake of cholesterol by inhibiting Niemann Pick C1 Like 1 channel

42
Q

Once in the enterocyte with fats?

A

FAs are reassembled into TAG and coated with apoproteins into chylmicrons –> taken up in lacteals –> venous circulation

43
Q

Intrinsic factor

A

secreted by parietal cell –> binds B12 (cobalamin) and protects it from degradation and assists in absorption in ileum

44
Q

Anismus

A

anal sphincter dyssynergia

45
Q

Haustra

A

pouch of colon produced by length of teniae coli

46
Q

Ileus

A

failure of forward movement of intestinal contents

47
Q

Purgative

A

substance that promotes bowel loosening and movement

48
Q

Tenesmus

A

feeling you need to pass stool even when bowel is empty

49
Q

Fluid movement in intestines

A

water can move transcellularly or paracellularly

- water follows osmotic gradient

50
Q

Fluid absorption and secretion can occur simultaneously

A

cells at tips of villi absorb fluid

cells in crypts secrete fluid driven by Cl gradient

51
Q

Electroneutral

A

coupled activity of sodium/hydrogen exchanger (NHE) and chloride/bicarb exhcanger in apical membrane

  • mediates fluid uptake
  • have basolateral Na/K ATPase and K/Cl channels
  • overall –> H/HCO3 into lumen, NaCl into blood (water follows)
52
Q

Electrogenic

A

no active transport of counterion –> instead anions and water follow passively through tight junctions
- SGLT on apical membrane gets Na and glu into cell –> GLUT2 transports glu into blood, and Na/K ATPase gets Na into blood –> Cl and water follow through tight junctions

53
Q

Major mechanism of fluid entry INTO lumen?

A

chloride secretion by crypts
- NKCC in basolateral side pumps chloride into cell –> chloride leaves into lumen via CFTR –> Na and water follow into lumen via tight junctions (electrogenic)

54
Q

Calcium transit?

A

transcellular or paracellular

  • enters –> interacts with calbindin –> basolateral Ca ATPase pumps it into blood
  • enhanced by vit D
55
Q

Secretory diarrhea

A

elevating cAMP in enterocyte –> promote opening of CFTR –> Cl leaves –> Na and water follow

  • can occur via prostaglandins, VIP, or CHOLERA
  • binds receptor –> A.C and Gsalpha –> increase cAMP –> PKA –> activation of CFTR
56
Q

Guanylin

A

gastrointestinal polypeptide secreted by goblet and ECL cells –> binds GC-C receptor and promotes secretion
- similar to secretory diarrhea but with cGMP

57
Q

Desiccation

A

“sucking water out of stool”

  • electrogenic = ENaC brings in Na –> N/K ATPase pumps it out and Cl and water follow (distal colon)
  • electroneutral = NHE and Cl/HCO3 exchanger pump Na and Cl into cells, pumped out by Na/K ATPase and K channel –> water follows
58
Q

Osmotic diarrhea

A

poor absorption of luminal substances –> pull water from bloodstream by osmosis

59
Q

Fluid flux depends on surface area available for transport and time in lumen

A

hypermotility –> diarrhea

hypomotility –> constipation

60
Q

Motile processes

A

Mass peristalsis –> 1-3 times a day –> promotes rapid forward propulsion
Segmental -> contractions promote mixing (dependent of Basal Electrical Rhythm) –> 12 cycles/min in jejunum –> decreases as you travel
- more action potentials = higher amplitude of BER = higher smooth muscle response

61
Q

Primary regulator of motility?

A

Enteric nervous system -> reflexes through sensory (stimulated by 5-HT) and motoneurons (ACh, substance P, NO, VIP)

62
Q

Migrating Motor Complex

A

FASTED STATE

  • depends on intact enteric nervous system –> stopped when meal ingested
  • sweeps out bacteria, cells, and undigested meal
  • doesn’t occur in large intestine
63
Q

Tonic contraction of ileocecal sphincter

A
  • limits bacteria entry into small intestine from large
  • distention of ileum due to peristalsis –> reduces tone
  • distention of cecum –> increases tone and decreases emptying to ileum
64
Q

Peristaltic reflex

A

initiated by distention of gut wall –> proximal contraction and distal relaxation

65
Q

Intestinointestinal reflex

A

over-distention or trauma to gut –> relaxation of entire gut (adynamic ileus)

66
Q

Ileal-gastric reflex

A

distention of ileum –> decreases gastric motility

67
Q

Gastro-ileal reflex

A

increased gastric activity –> ileal contractions

68
Q

Motility of large intestine

A

much slower frequency of BER than small intestine

69
Q

Defecation reflex

A
  1. Afferent nerves –> anal sampling
  2. Pelvic nerves provide extrinsic input to colon and inhibit sphincter
  3. somatic pudendal nerves stimulate sphincters
    - involves descending, sigmoid, and rectum contraction
    - relaxation of sphincters
    - contraction of diaphragm and abs
    - relaxation of pelvic floor

GI Exam 2 (7 decks)

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