Mucosal Absorption II - GI Blood Flow Flashcards

1
Q

where is the primary site for Na+ absorption?

A

SI
*similar to kidney PT

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2
Q

what are the mechanisms of Na+ absorption in the SI?

A

co-transporters
Na/H exchange
paracellular Cl absorption
net absorb of bicarb
water follows solutes

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3
Q

Na/H exchange ___ lumen and therefore neutralizes luminal bicarb

A

acidifies

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4
Q

how is Ca absorbed in GI tract?

A

facilitated diffusion
via concentration gradient (lumen&raquo_space; intracellular)

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5
Q

high Ca concentration causes ___ diffusion

A

paracellular

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6
Q

low Ca concentration stimulates ___ transport

A

transcellular

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7
Q

what does transcellular transport adjust for regarding Ca absorption?

A

variations in diet Ca levels

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8
Q

describe the three steps of Ca transport in the duodenum

A
  1. apical uptake via Ca channel
  2. calbindin carries Ca within cell
  3. basolateral Ca pump and Na/Ca exchanger extrudes Ca into lateral space
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9
Q

what is calbindin?

A

Ca carrier protein within cell to maintain low free Ca concentration

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10
Q

how does Mg get absorbed at high vs normal concentrations?

A

HIGH - paracellular uptake
NORMAL - intracellular transport, uses TRP transporters on apical side

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11
Q

what’s present on the basolateral side in regards to Mg absorption?

A

Mg/Na exchanger
secondary active

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12
Q

the amount of iron ingested ___ amount absorbed

A

GREATER THAN

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13
Q

describe the process of iron nonheme absorption

A

nonheme absorbed as Fe2+, which crosses duodenal apical membrane through DMT1, driven by H+ gradient (maintained by Na/H exchange)

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14
Q

describe the process of iron heme absorption

A

heme enters enterocyte and inside cell, heme oxygenase releases Fe3+, which then reduces to Fe2+
goes through basolateral membrane in mobilferrin

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15
Q

transferrin is required for…

A

iron plasma transport

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16
Q

what is ferritin?

A

intracellular storage depot
releases iron in controlled fashion

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17
Q

iron bound to ferritin is ___ when enterocyte it sloughed off

A

lost

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18
Q

what are fat soluble vitamins processed in the same fashion as?

A

dietary lipids
(micelles, enter circulation in chylomicrons, etc)

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19
Q

how are water soluble vitamins typically absorbed?

A

via Na dependent co-transport

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20
Q

how is vitamin B12 protected from digestion?

A

binds to gastric intrinsic factor (parietal cells)

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21
Q

where is B12 absorbed?

A

absorbed in ileum

22
Q

the celiac artery supplies…

A

stomach, first part duodenum, pancreas head, liver

23
Q

cranial mesenteric artery supplies…

A

pancreas, gut (through first 2/3 of transverse colon)

24
Q

caudal mesenteric artery supplies…

A

distal colon, proximal rectum

25
Q

the splanchnic area gets __% of CO, but only makes up __% of body weight

A

25% CO
5% body weight

26
Q

the fraction of CO ___ after meal ingestion

A

increases

27
Q

the liver regulates ___ concentration

A

nutrient

28
Q

where does the hepatic portal vein collect blood from?

A

stomach, SI, LI

29
Q

which two capillary beds does splanchnic blood run through before it reaches the heart?

A

mesenteric and portal

30
Q

what drives blood through the mesenteric and portal capillary beds?

A
  1. P in portal vein is slightly higher than in hepatic sinusoids. resistance in portal vein is very low
  2. sinusoids of liver are large, so resistance is also very low
  3. venous outflow of liver goes into vena cava
    *hepatic hemodynamic!!!
31
Q

small changes in P can have ___ effect on fluid exchange of splanchnic blood at capillary beds

A

MAJOR

32
Q

blood flow in each GI segment corresponds with local ___ and ___ activity

A

digestive and absorptive

33
Q

what does the magnitude of postprandial hyperemia depend on?

A
  1. cephalic phase parasympathetic stim motility and secretion
  2. rate of active transport across epithelium
  3. hyperosmolarity in villus stim blood flow
  4. vasoactive hormones (CCK, neurotensin)
  5. intestinal epithelium releases bradykinin (vasodilate)
34
Q

bile acids and fats promote…

A

hyperemia

35
Q

what is postprandial hyperemia?

A

increased blood flow due to digestion and absorption

36
Q

what three things cause large flow rate variation in micro-circulation of GI?

A
  1. increased resistance in liver which reduces blood flow from intestine (portal hypertension)
  2. R heart insufficiency increases vena cava P, leading to reduced blood flow from intestine
  3. increased resistance in intestinal circulation due to sympathetic stim
37
Q

how is ischemia caused in GI relating to blood flow?

A

low blood flow and long transit time
causes necrosis at villus

38
Q

explain how the vessels in intestinal villus have antiparallel blood flow

A

arterial vessels and venules are parallel
oxygen concentration flows from artery to venule

39
Q

describe how the countercurrent exchange of the villus may be susceptible to damage/issues

A

oxygen begins to diffuse before reaching the tip of the villus
this means an oxygen gradient is created from the tip (low O2) to the base (high O2)
may cause anoxic damage at tip of villus due to premature O2 exchange

40
Q

when is the countercurrent exchange in the villus particularly strong?

A

when blood flow is low

41
Q

what can become trapped in the interstitial space of the villus tip, when blood flow is low and transit time is prolonged?

A

SOLUTES
increases interstitial osmolarity near the tip with issues of nutrient absorption and water movement as a result

42
Q

how does exercise induced heat stress affect the GI tract?

A

blood flow becomes shunted from GI in effort to increase heat dissipation
if core temperature continues to rise, then intestinal ischemia may occur due to complete shunt of GI
release of endotoxin occurs, causing systemic inflammatory response and coagulation cascade
multi-organ failure or death may occur

43
Q

what are some short term adaptations of the GI tract?

A
  1. modulation of membranous enzymatic setup
  2. modulate blood supply - adjust metabolic demands and postprandial hyperemia
  3. increase absorptive surface area (villi hypertrophy)
44
Q

mesenteric blood flow rates ___ in response to metabolic demands (milk production)

A

increase

45
Q

what are the postprandial responses of a PYTHON?

A

metabolic rates rise
SI grows
blood flow to intestines triples
HCl production drops luminal pH from 7 to 2 within 24hrs

46
Q

what does the image represent in a python?

A

rapid postprandial lengthening of intestinal microvilli

47
Q

how does the python rapidly modulate gut form and function with each meal?

A

rapid postprandial increase in SA and in plasma concentration of…cholecystokinin, neurotensin, glucagon, insulin

48
Q

what happens to GI tract organs of animals that go through hibernation?

A

selective reduction of tissue mass of GI organs to reduce energy consumption

49
Q

what symptoms occur during malabsorption syndrome after SI resection?

A

V, D, malabsorption, weight loss, fluid/electrolyte imbalance, steatorrhea, malnutrition
DIGESTIVE/ABSORPTIVE CAPACITY MAJORLY COMPROMISED

50
Q

what happens as a result of the ileum being resected?

A

overall fat absorption decreases because main site of bile salt absorption and vitamin B12 absorption is impaired

51
Q

what happens as a result of the colon being resected?

A

reduced VFA absorption, fluid/electrolyte absorption impaired

52
Q

what’s the response to undamaged mucosa when a part of the GI is resected?

A

villous hyperplasia - limited to doubling SA, requires intact crypt epithelium
absorptive capacity will greatly increase