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Physiology > Exam3Lec9GI:SI/PancreaticFxn > Flashcards

Exam3Lec9GI:SI/PancreaticFxn Flashcards

1
Q

What is the intestinal phase of digestion?

A

Initiated by entry of chyme from the stomach into the duodenum.** Influenced by size of bolus, particle size, and macronutrient composition**. 🌟

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2
Q

Reflex response to 4 things: 🌟

A

distention, low pH, osmolarity, and digestive products.

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3
Q

What are the responses of the intestinal phase of digestion?

A
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4
Q

How does a meal digest in the stomach? (think entry and departure)

A
  • Bolus: small particles, emulsion
  • Triglycerides: trigs, monoglycerides, FFA
  • Proteins: protein, peptides, some amino
  • Starch: Starch, oligosaccharides
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5
Q

What increases gastric emptying?

A

Gastric distention->empty rate is proportional to size of meal

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6
Q

What is gastric emptying inhibited/slowed by ⭐️

A
  • Entry of chyme into duodenum (duodenal
    distention)
  • Fat, protein, cations (electrolytes)
  • Acidity (pH < 3.5) in duodenum
  • Hypo/hyper-osmotic chyme in duodenum
  • Solid food more inhibitory than liquids.
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7
Q

What are some hormones/enterogastrones that might inhibit or slow gastric emptying ⭐️

A

cholecystokinin (CCK), vasoactive intestinal polypeptide (VIP), Gastric Inhibitory Peptide (GIP), somatostatin, secretin

Inhibits the caudal (or “forward) motion of the contents of chyme

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8
Q

How does gastric emptying from teh stomach to duodenum trigger feedback?

A
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9
Q

Gastric emptying rate depends on what?

A

macronutrient composition, osmolality, and caloric

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10
Q

What are some implications of gastric emptying?

A

considerations for diabetics, foods effects on drug absorption, metabolism, restoring hydration status (with isotonic solution)

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11
Q

What is the osmolality of meal with hypertonic meal and hypo? where does this occur mostly?

A
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12
Q

Intestinal motility is coordinated by what? What is is modified by?

A
  • Intestinal motility is coordinated by the enteric nervous system (ENS)
  • modified by long and short reflexes, neurotransmitters and hormones
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13
Q

What happens during and shortly after meal with intestinal motility? ⭐️

A

hyme is mixed by segmenting movements of intestinal wall (both directions; circular muscles)

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14
Q

After food is digested and absorbed, segmentation is replaced by what? ⭐️

A

by peristalsis moving undigested material from small intestine into large intestine (one way; longitudinal muscles).

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15
Q

Circular and longitudinal contractions
Regulated by what?

A

Myenteric plexus (part of ENS) (aka Auerbach plexus)

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16
Q

Peristalsis vs segmentation

A
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17
Q

Circular sm vs longitudinal sm

A
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18
Q

slide 13

A
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19
Q

Interstitial Cells of Cajal (ICC) generate what?

A

generate GI slow waves (aka: BER; basal electrical rhythm)

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20
Q

Pacemaker ICC links what?

A

nervous system to smooth muscle

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21
Q

What is happening in fed state with small intestine?

A

Segmental Contractions
* slows food propulsion, mixes to expose chyme to enzymes and GI surface

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22
Q

Peristaltic activity (propels food) replaces
segmentation when? ⭐️

A

completeion of absorption

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23
Q

What is the motilin candidate hormone?

A
  • secreted from M cells
  • MMCs appear when in fasted state.
  • Motilin receptor agonists stimulate intestinal peristalsi
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24
Q

_ alter amplitude and duration of MMCs

A

Cathartics (laxatives) alter amplitude and duration of MMCs

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25
Q

Motilin is assoicated with _

A
  • MMCs
  • Plasma motilin peaks in fasting (interdigestive period). Note motilin is released cyclically every 80–120 min to induce contraction of the MMCs from the stomach to the ileum
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26
Q
A
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27
Q

vili and microvili?

A
  • By projecting into the lumen, the Villi increases the surface area for absorption of nutrients.
  • Microvilli (aka brush Border, 100nm) fringe the villi to further increase surface area
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28
Q

What is in the villus that is part of our lympathic system and imp for fats?

A

lacteal

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29
Q

What are the barriers within the paracellular pathway between intestinal epithelial cells

A

tight jxns

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30
Q

What happens when barrier function is messed up?

A

Disruption -> hyper-permeability (“leaky gut”) and potentially autoimmune or neurological disorders

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31
Q

What are the different anatomical features that are increases SA in small intestine

A
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32
Q

What are the 3 sub phases of intestinal digestion? + what they are doing in each

A
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33
Q

How is proteins digested in gut? ⭐️

A

All 3 phases, luminal, brush border and cytosolic digestion may be involved

34
Q

How are carbs digested in gut ⭐️

A

Only luminal and brush border digestion – no intracellular digestion by the enterocyte

35
Q

How are lipids digested in gut?

A

All digestion is luminal (micelle);** triglyceride is re- formed in the enterocyte (chylomicron) **and transferred to lacteal (not capillary).

36
Q

How does proteins get absorped?

A

Active transport of amino acids and small peptides (< 5 amino acids).

37
Q

How does carbs get absorped in gut

A
  • Uptake of monomers only
  • Active transport of Glucose; facilitated diffusion for Fructose
38
Q

How does lipids get absorped in gut?

A
  • Uptake of free fatty acids and glycerol.
  • Mechanism of uptake by the enterocytes is probably diffusion.
39
Q

Starches digested in duodenal lumen by what? What does that produce?

A

Starches digested in duodenal lumen by amylase to produce oligosaccharides and disaccharides

40
Q

What forms monosaccharides? +enzymes

A

Brush border digestion of polymers by specific amylases and disaccharidases forms monosaccharides. Note: Maltase, lactase and sucrase are at brush border

41
Q

Simple sugars Glucose (and Galactose) taken up by what?

A

active transport processes into enterocytes.

42
Q

Generally NO uptake of what?

A

disaccharides (trehalose) or oligosaccharides (fiber)

43
Q

What are the transporters on the brush border membrane for monosaccharide absorption?

A

Note: SGLT2 is in Kidney (glucose reabsorption function)

44
Q

meal glucose is completely absorbed where?

A

duodenum

45
Q

Meal lactose absorption is where? variations?

A
46
Q

For protein digestion, proteases stored how and where?

A

in inactive form in pancreas & secreted in response to neurohormonal stimulation

47
Q

Pancreatic trypsinogen converted to what?

A

to active form (trypsin) by duodenal brush-border enterokinase

48
Q

What does trysin do? 🌟

A

Trypsin activates all other luminal peptidases

49
Q

Digestion of oligopeptides in lumen and small peptides happens where?

A

brush border

50
Q

_ _ of free amino acids,di-andtri- peptides.

A

active transport

protein

51
Q

_ degradation of di- and tri-peptides.

A

Cytosolic degradation of di- and tri-peptides.

protein

52
Q

What is the activation of proteases in the small intestine?

A
53
Q

What are the three sites of protein digestion?

A

lumen, brush border and cytoplasm

54
Q

Short peptide uptake coupled to what?

A

to proton transport followed by cytosolic digestion

55
Q

Removal of protein by digestion and absorption occurs where?

A
56
Q

Lipid digestion in _ phase only.

A

luminal

57
Q

Digestion of lipids require what?

A

bile salts, pancreatic lipase, co-lipase and phospholipids to form micelles

58
Q

Digestion of lipids require what?

A

bile salts, pancreatic lipase, co-lipase and phospholipids to form micelles

59
Q

Lipids emulsify by what?

A

bile salts and phospholipids

60
Q

Lipids emulsify by what?

A

bile salts and phospholipids

61
Q

Triglyceride digested to what?

A

to form free fatty acids and a monoglyceride

62
Q

Digestion productions taken up by diffusion and packaged into what?

A

chylomicrons

63
Q

Bile salts and phospholipids convert large fat globules into what?

A

smaller pieces with polar surfaces that inhibit reaggregation

64
Q

Absorbed products of lipolysis are synthesized into triglycerides in the _ and exit as _

A

enterocytes
chylomicrons

65
Q

Lipid digestion process

A
66
Q

absorption of lipolytic produces occur where?

A
67
Q

Sodium absorption generally coupled to what?

A

to nutrient absorption (e.g. SGLT1, PEPT1).

68
Q

Electrogenic:

A

forces anions (mainly chloride) to passively follow the sodium transport by paracellular route

69
Q

Water transported _ , following _ _ (favoring absorption).

A

Water transported passively, following osmotic gradients (favoring absorption).

70
Q

What is the major mediator of mvt of water?

A

cl-

71
Q

What is the driving force for chorlide efflux

A

potassium efflux

72
Q

Cystic fibrosis transmembrane conductance regulator?

A

Mutations of the CFTR gene affecting chloride ion channel function lead to dysregulation of epithelial fluid transport in the lung resulting in cystic fibrosis.

73
Q

Sodium, Potassium, Chloride co-transporter is driven by what

A

na gradient

74
Q

What happens with cholerae?

A
75
Q

What is IF and what is it required for?

A

is a glycoprotein and required for vitamin B12 (cobalamin) uptake

76
Q

What is IF and what is it required for?

A

is a glycoprotein and required for vitamin B12 (cobalamin) uptake

77
Q

Where is absorption of IF? What protects it?

A
  • Absorption is in terminal ileum.
  • “R” Protein (haptocorrin) protects acid-sensitive B12 from degrading
78
Q

B12 is essential for what?

A

B12 essential for metabolism, DNA synthesis and RBC production

79
Q

What are causes of ulcers

A

ause (~90%) is mucosal breakdown from H. pylori.
* NSAIDs, gastrinoma

80
Q

Gastric (peptic) ulcer vs. Duodenal (peptic) ulcer

A
  • Gastric (Peptic) Ulcer - mucosa damage due to leakage of acid from stomach.
  • Duodenal (Peptic) Ulcer - More acid present in duodenum than normal (not clear, though) - increased parietal cell mass. Increased HCl + pepsinogen secretion.

Physiology (22 decks)

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