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GI/Liver > Lec6 > Flashcards

Lec6 Flashcards

1
Q

Where are most minerals absorbed?

A

duodenum

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2
Q

Where are bile acids absorbed?

A

ileum

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3
Q

Where is cobalamin [B12] absorbed?

A

ileum

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4
Q

Where is iron absorbed?

A

duodenum

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5
Q

What are gross folds of the small bowel vs the large bowel called?

A 
small = plicae circulares
large = haustrae
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6
Q

How is digestion initiated in the small intestine?

A
  • acid in duodenum –> duodenal S cells secrete secretin –> cause pancreas to secrete bicarb
  • fatty acids and amino acids in duodenum –> duodenal I cells secrete CCK –> cause pancreas to secrete enzymes, gallbladder to empty
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7
Q

What is ratio of starch to sucrose to lactose of ingested carbs?

A

starch 50%
sucrose 30%
lactose 10%

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8
Q

How is starch digested?

A
  • amylase from pancreas/saliva converts to maltose

- maltase on intestinal BBM to glucose

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9
Q

How is sucrose digested?

A

sucrase-isomaltase on intestinal BBM to glucose and fructose

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10
Q

How is lactose digested?

A

lactase on intestinal BBM to glucose and galactose

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11
Q

How are carbs absorbed?

A

glucose/galactose active transported into cell then diffuse into portal vein

fructose facilitated diffusion

unabsorbed carbs converted to short chain fatty acids in colon

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12
Q

What are the components of starch?

A

maltoses each made of glucose

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13
Q

What are the components of sucrose?

A

glucose and fructose

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14
Q

What are the components of lactose?

A

glucose and galactose

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15
Q

How are proteins digested?

A

in stomach: denatured by acid; pepsin hydrolyzes into polypeptides

in duodenum: digested by pancreatic proteases; duodenal brush border membrane enterokinase activates trypsin which then activated the other pancreatic pro-enzymes

BBM oligopeptidases then hydrolyze into smaller oligopeptides and amino acids

final digestion inside enterocytes by intracellular peptidases that convert everything to amino acids

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16
Q

How are proteins absorbed?

A

as amino acids and oligopeptides

intracellular pepitdases in enterocytes finish digestion into AAs

AAs absorbed and transported to capillaries into portal vein

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17
Q

What is role of brush border membrane enterokinase in protein digestion?

A

activates trypsin which in turn activates other pancreatic pro-enzymes

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18
Q

How are lipids digested?

A

in stomach: churn fats into unstable emulsion

in duodenum/small intestine: emulsion stabilized by phospholipids and bile salts

CCK released in response to dietary fat in duodenum causes bile salt and lipase [panc.] release

pancreatic lipase and co-lipase convert TG–> MG + FFA

mixed micelles form with MGs and FFAs inside; bile salts outside

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19
Q

What is necessary for pancreatic lipase to work?

A
  • CCK causes its release from pancreas in response to fatty acids in duodenum
  • requires neutral pH in duodenum to work
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20
Q

How are lipids absorbed ?

A

passive diffusion across BBM into cell

intracellular resynthesized as cylomicrons and VLDL –> exported into lymphatics

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21
Q

What is exception to the rule that lipids are absorbed into the lymph system?

A

medium chain TGs are absorbed into the portal vein

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22
Q

What is role of B lipoprotein in fat absorption?

A

important role in repackaging of fats into chylomicrons inside enterocytes for absorption into lymphatics

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23
Q

How is vit B12 absorbed [steps]?

A
  • dietary B12 complexes with salivary R protein in stomach
  • in duodenum trypsin cleaves R-B12 complex
  • IF from gastric parietal cells binds B12
  • IF-B12 complex absorbed in terminal ileum
  • B12 transported into portal circulation
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24
Q

Which vitamins are fat soluble?

A

ADEK

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25
Q

What happens to B12 with bacterial overgrowth?

A

luminal bacteria compete for B12; with bacterial overgrowth –> have low serum B12

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26
Q

What are some causes of B12 deficiency

A
  • not enough dietary B12 [rare]
  • not enough R
  • not enough IF [autoimmune gastritis]
  • pancreatic insufficiency [can’t dissociate B12-R]
  • ileal disease [can’t absorb]
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27
Q

What happens to folate level if bacterial overgrowth?

A

high serum folate

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28
Q

How is Ca absorbed?

A

active transport in duodenum;

calbindin in cell delivers Ca to ATPase for export into circulation

vit D stimulates calbindin synthesis and helps Ca entry into enterocytes

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29
Q

What is major symptom of protein malabsorption?

A

edema

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30
Q

What major symptoms of fat malabsorption?

A

steatorrhea

weight loss

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31
Q

What major symptoms of carb malabsorption?

A
  • diarrhea
  • bloat
  • gas

from bacteria in colon

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32
Q

What major symptoms of vit A malabsorption?

A

nigh blindness (nyctalopia)
dry scaly skin (zerosis, cutis)
alopecia

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33
Q

What major symptoms of vit D/Ca malabsorption?

A 
tetany = cramping of fingers/toes
osteomalacia = thinning of bones
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34
Q

What major symptoms of Vit E malabsorption?

A

neuropathy

muscle weakness

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35
Q

What major symptoms of Vit K malabsorption?

A

ecchymoses = non raised discoloration

bruising

36
Q

What major symptoms of Vit B12 malabsorption?

A

macrocytic megaloblastic anemia
glossitis
neuropathy; parasthesias

37
Q

What major symptoms of folate malabsorption?

A

macrocytic, megaloblastic anemia

glossitis

38
Q

What major symptoms of iron malabsorption?

A

microcytic anemia
dyspnea
fatigue
glossitis

39
Q

When does lactase deficiency present?

A

lactase almost always present at birth; symptoms occur in adulthood

40
Q

What is pathogenesis of lactase deficiency?

A
  • lactose osmotically active in lumen –> get diarrhea, gas, bloating, borborygmi [stomach gurgling]
41
Q

What are symptoms of lactase deficiency?

A

diarrhea, gas, bloating, borborygmi [stomach gurgling]

42
Q

Who gets primary lactase deficiency?

A

asian, african, mediterranean descent

43
Q

What causes secondary lactase deficiency?

A

after loss of enterocytes from infection, resection, radiation

44
Q

How do you diagnose lactase deficiency?

A

hydrogen breath test

lactose intolerance test

45
Q

What is treatment for lactase deficiency?

A

avoid dairy

use exogenous lactase or lactose-free products

46
Q

What is pathogenesis of pancreatic exocrine insufficiency?

A
  • need to lose > 90-95% of pancreatic function to get this
47
Q

What are some underlying diseases associated with pancreatic exocrine insufficiency?

A

cystic fibrosis [in kids]
chronic pancreatitis
pancreatic resection

48
Q

How does pancreatic exocrine insufficiency present?

A

maldigestion of fat, protein, carbohydrates

49
Q

What is treatment for pancreatic exocrine insufficiency?

A

oral pancreatic enzyme replaement

50
Q

How does bile salt deficiency present?

A

maldigestion of fats and fat soluble vitamins

51
Q

What are some causes of bile salt deficiency?

A
  • severe cholestasis
  • distal ileal resection or disease [Crohns]
  • bacterial overgrowth
52
Q

What is treatment for bile salt deficiency?

A

treat underlying conditions and give medium chain TGs

53
Q

What is bacterial count in small intestine vs large instestine?

A

way lower in small intestine; but flourishes if stasis

54
Q

What are some underlying cause of bacterial overgrowth?

A
  • motility disorder: ileus, pseudo-obstruction

- anatomical disorder: blind loop, fistulae, diverticula

55
Q

What are consequences of bacterial overgrowth?

A
  • fat malabsorption: bacteria deconjugate bile acids

- vitamin B12 deficiency: bacteria consume vit B12

56
Q

How do you diagnose bacterial overgrowth?

A

schilling test

breath tests for bacterial counts

57
Q

What is short bowel syndrome? effect?

A

removal of terminal ileum due to crohns, infarct, or cancer, etc

effects: B12 and bile acid malabsorption, rapid transit, cholesterol gallstones due to bile acid depletion; oxalate kidney stones

58
Q

Why do you get oxalate kidney stones in patient with short bowel?

A

normally oxalate precipitated by Ca and excreted in stool; but if fat malabsorption –> long chain free fatty acids bind Ca leaving free oxalate to be absorbed by colon and excreted in kidney

59
Q

What is D-lactic acidosis?

A

rare syndrome of metabolic acidosis with neurologic symptoms; due to colonic bacteria

occurs in short bowel syndrome

60
Q

What is treatment for short bowel syndrome?

A

enteral feeding; total parenteral nutrition; small intestine transplant

61
Q

What is peptide YY action? from where?

A

slows gastric emptying

secreted from ileum

62
Q

What is pathogenesis of celiac?

A

inappropriate immune response to gliadin

causes malabsorption and villous atrophy

primarily duodenum/jejunum not ileum

63
Q

What do you see histologically with celiac?

A
  • villous atrophy
  • crypt hyperplasia
  • intra-epithelial lymphocytes
64
Q

What HLA types in celiac?

A

HLA-DQ2

HLA-DQ8

65
Q

What immune abnormalities associated with celiac?

A
  • selective IgA deficiency
  • diabetes
  • autoantibodies to tissue transglutaminase, endomysial, and gliadin
66
Q

What other complications with celiac?

A
  • dermatitis herpetiformis
  • T cell lymphoma
    collagenous sprue
67
Q

What are is tropical sprue?

A

acquired malabsorption syndrome in central america, caribbean, southeast asia

cause unknownl responds to antibiotics

68
Q

What is treatment for tropical sprue?

A

replace folate + vitamin B12

antibiotics

69
Q

What is distribution of tropical sprue vs celiac?

A

celiac = proximal small intestine

tropical sprue = throughout small intestine

70
Q

What is clinical picture of tropical sprue?

A

steatorrhea following diarrhea

71
Q

What is radiation enteritis?

A

loss of replicating epithelial cells –> villous atrophy but not hyperplastic crypts

heals over wks to mos

72
Q

What is abetaliporpoteinemia?

A

genetic; epithelial cells cannot assemble chylomicrons so lipid accumulates in cell

have fat malabsorption

73
Q

What is inheritence of abatalipoproteinemia?

A

autosomal recessive

74
Q

What is treatment for abetaliporpoteinemia?

A
  • dietary fat restriction
75
Q

What does CBC tells you?

A

if microcytic anemia –> iron deficiency

if macrocytic anemia –> B12 or folate deficiency

76
Q

What does prolonged thrombin time tell you?

A

vit K deficiency

77
Q

What does low albumin tell you?

A

problem absorbing protein

78
Q

What does low Ca tell you?

A

vitamin D deficient

79
Q

What does low cholesterol tell you?

A

fat malabsorption

80
Q

What is D-Xylose test of malabsorption?

A
  • drink D xylose [monosaccharide]

50% absorbed –> liver –> circ –> kidney –> at least 25% secreted in urine

81
Q

What is whipples disease?

A

rare systemic disease due to tropheryma whippelii causing malabsorption

82
Q

What do you see in histology of whipple’s?

A

macrophages with pas positive bacteria in intestinal lamina propria

lymphatic obstruction
“foamy macrophages”

83
Q

What is pseudo-whipples?

A

seen in AIDS patients –> macrophages filled with acid fast mycobacteria

84
Q

What is treatment for whipples?

A

antibiotics [sulfonamides]

watch for relapse

85
Q

What are symptoms of whipples?

A

cardiac symptoms
arthralgias/joint pain
neurologic symptoms
malabsorption symptoms

GI/Liver (36 decks)

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