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Gastrointestinal and Liver > Lectures 5-7: Small Intestine > Flashcards

Lectures 5-7: Small Intestine Flashcards

1
Q

Where are new cells born in the small intestine? What is there pathway?

A

Born near crypt, differentiate and mature as they migrate up the villus

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2
Q

How much fluid is presented to the SI? How much is drank? How much of this gets to the colon? How much excreted fecally?

A

8000 mL, 2000 mL, 1500 mL, 150 mL

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3
Q

Max abs capacity of SI and colon

A

12 L, 5 L

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4
Q

What solute drives absorption through the mucosa?

A

Na+

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5
Q

What are the sodium channels in the intestine? (4, 1 basolateral)

A
  1. Apical Na+ channel; 2. Basolateral Na-K ATPase (balances Na+ in); 3. Solute-coupled Na+ transport; 4. Na/H exchanger (w/ HCO3/Cl exchanger as well)
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6
Q

What does aldosterone do?

A

Increases function of apical Na+ channel

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7
Q

What is the mechanism of oral rehydration therapy?

A

Requires glucose and Na+ to bring water into cell via solute-coupled Na+ transport, meaning that Na+ can be absorbed in the lumen (hence, ORAL rehydration)

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8
Q

Describe the Na/H Exchanger (what in, what out)

A

Na+ AND Cl- in, H+ AND HCO3- out

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9
Q

What enhances sodium absorption?

A

Mineralcorticoids (aldosterone), glucocorticoids, somatostatin, adrenergic agonists (epinephrine)

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10
Q

What slows the intestinal transit? How does this affect Na+ absorption?

A

Opiates and somatostatin; increases sodium absorption

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11
Q

What is the key ion that drives secretion?

A

Cl-

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12
Q

How does Cl- get into the body?

A

Via the Na/H exchanger

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13
Q

How does Cl- enter the cell to drive secretion? How is it secreted?

A

Basolaterally (Na/K/2Cl transporter); apically (Cl channel = CFTR)

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14
Q

Cl- secretion becomes increased by any factor that activates what?

A

cAMP, cGMP, intracellular calcium

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15
Q

What four hormones/NTs increase cAMP leading to diarrhea?

A

VIP, secretin, PGE1, bradykinin

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16
Q

What three hormones/NTs increase calcium leading to diarrhea?

A

ACh, 5-HT, histamine

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17
Q

What four bacteria increase cAMP leading to diarrhea?

A

V. cholera, E. coli (heat labile), campylobacter, salmoneella

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18
Q

What two bacteria increase cGMP leading to diarrhea?

A

Yersinia enterocolitica, E. coli (heat stable)

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19
Q

What are some laxatives that act on the cAMP/calcium pathways?

A

Bile acids, long chain fatty acids, castor oil, senokot

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20
Q

What factors increase colonic transport?

A

Cholinergics, anxiety, feeding, laxatives/hormones, distention

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21
Q

What factors slow colonic transit?

A

Anti-cholinergics, depression, colonic wall inflammation, opiates, electrolyte disturbances

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22
Q

Which will cause more water in the stool: small intestinal or colonic dysfunction?

A

Small intestinal (does the majority of the water absorption, about 7 L)

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23
Q

Sx of small bowel/colonic diarrhea

A

Large amount of stool, moderate increase in number, minimal urgency, no tenesmus, little mucus

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24
Q

Sx of recto-sigmoid diarrhea

A

Small amount of stool, frequency, urgency, tenesmus, mucus, blood

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25
Q

Bile acid-induced diarrhea results from _______ dysfunction. Why?

A

Ileal; ileum is the ONLY site of active bile acid absorption

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26
Q

Mechanisms of osmotic diarrhea. What is intact?

A

Nonabsorbable solute in bowel lumen –> water enters lumen –> solute/water load exceeds colonic absorptive capacity; mucosal transport processes intact

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27
Q

What are some examples of osmols that will not be absorbed and will increase secretion?

A

Carbohydrates: lactose (if lactase deficiency), sorbital; Minerals: Na Sulfate lavage, Mg Citrate

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28
Q

Osmotic diarrhea: what is depleted? What is not depleted?

A

Water (NOT Na+ depletion) = not life threatening

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29
Q

Osmotic diarrhea: stool volume __________ with fasting

A

Decreases

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30
Q

Osmotic diarrhea: what can you detect in fecal fluid (osmolality and pH)

A

Osmotic gap = unmeasured osmolality due to nonabsorbed solute; acidic stool pH due to bacterial fermentation of solute

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31
Q

Mechanism of secretory diarrhea. What is intact?

A

Stimulation of normal secretory processes; absorptive processes intact but overwhelmed

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32
Q

What 2nd transporters cause secretory diarrhea?

A

cAMP, cGMP, Ca2+

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33
Q

What is the mechanism of cholera toxin?

A

Increases intracellular cAMP via AC, driving Cl- out of cell and decreasing Cl- reabsorption (via Na/H transporter), keeping water out of the cell. NOTE the Na/Glucose transporter is spared, hence oral rehydration

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34
Q

Secretory diarrhea: what is depleted?

A

Salt and water (life-threatening)

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35
Q

Secretory diarrhea: stool volume while fasting

A

Persists despite fasting

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36
Q

Secretory diarrhea: osmotic gap? pH?

A

NOPE: all osmolality accounted for by electrolytes; neutral pH

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37
Q

Describe two types of motility diarrhea

A

Hypermotility: insufficient contact time for absorption (laxatives, anxiety); Hypomotility: altered peristalsis –> stasis (water can flow aound stool and cause both diarrhea and constipation)

38
Q

What is preferentially absorbed in the duodenum?

A

Iron and other minerals

39
Q

What is preferentially absorbed in the ileum?

A

Cobalamin and bile acids

40
Q

Secretin

A

Released by duodenum in response to low pH, increase pancreatic bicarbonate secretion

41
Q

CCK (cholecystokinin)

A

Released by duodenum in response to FAs and AAs, causes gallbladder emptying (bile acids) and increases pancreatic enzyme secretion

42
Q

Starch digestion

A

Amylase (saliva, pancreas) –> maltose, maltase (BBM) –> glucose

43
Q

Sucrose digestion

A

Sucrase-isomaltase (BBM) –> glucose, fructose

44
Q

Lactose digestion

A

Lactase (BBM) –> glucose, galactose

45
Q

How are monosaccharides absorbed?

A

Actively transported into cell –> portal vein

46
Q

What happens to unabsorbed CHO?

A

Converted to short chain fatty acids in colon

47
Q

Stomach’s role in protein digestion

A

HCl denatures, pepsin hydrolyzes into polypeptides

48
Q

Duodenum and pancreas role in protein digestion

A

Pancreas releases pro-proteases, enterokinase in duodenal BBM activates trypsin which then activates other pro-enzymes

49
Q

Small intestine’s role in protein digestion

A

BBM oligopeptidases hydrolyze oligopeptides into smaller peptides

50
Q

How are AAs and oligopeptides absorbed?

A

They are transported into the cell –> portal vein

51
Q

Stomach’s role in lipid digestion

A

Churns fat (mostly TGs) into unstable emulsion

52
Q

Duodenum and small intestine’s role in lipid digestion

A

Emulsion stabilized by phospholipids (diet) and bile salts (liver), dietary fat –> CCK –> lipase (pancrease) and bile salts, micelles form

53
Q

What does lipase do?

A

Lipase + co-lipase break down TGs into MGs and FFAs

54
Q

Describe a micelle

A

MGs and FFAs inside with bile salts outside

55
Q

How are MGs and FFAs absorbed?

A

Micelles bring them to the BBM and then they are released and passively diffuse into cell, then they are resynthesized into chylomicrons and VLDL, exported into lymphatics (lacteal)

56
Q

What is different about medium chain TGs?

A

Bypass lymphatics and are absorbed into portal vein

57
Q

What are the four stages of chylomicron formation?

A

Esterification, surface stabilization, addition of lipoprotein, and secretion via intracellular spaces into lacteals

58
Q

How is B12 absorbed?

A

Ingested in food –> binds to R factor in saliva –> intrinsic factor (IF) made by parietal cells –> pancreatic proteases breaks up B12*R –> B12 binds with IF –> absorbed in ileum

59
Q

What could go wrong with B12 levels?

A

Not enough B12 in diet, no IF (autoimmune gastritis), no R factor (salivary glands), no proteases (pancreatic insufficiency), no absorption (ileal disease), and bacterial overgrowth

60
Q

Malabsorbed: protein

A

Edema

61
Q

Malabsorbed: fats

A

Weight loss and steatorrhea

62
Q

Malabsorbed: carbs

A

Diarrhea, bloat, gas

63
Q

Malabsorbed: vit A

A

Hyperkeratosis, night blindness

64
Q

Malabsorbed: vit D, Ca2+

A

Tetany, osteomalacia

65
Q

Malabsorbed: vitamin E

A

Neuropathy (pins and needles); deficiency = hemolytic anemia, acanthocytosis, weakness, posterior column/spinocerebellar tract demyelination

66
Q

Malabsorbed: vit K

A

Bruising (made by intestinal bacteria)

67
Q

Malabsorbed: vit B12

A

Megaloblastic anemia, glossitis, cheilosis, neuropathy

68
Q

Malabsorbed: folate

A

Megaloblastic anemia, glossitis

69
Q

Malabsorbed: iron

A

Microcytic anemia, dyspnea, fatigue, glossitis

70
Q

Lactase deficiency can be what two types?

A

Primary (genetic) and secondary (loss of enterocytes due to infection, resection, radiation)

71
Q

How much pancreas must be lost before you have pancreatic exocrine insufficiency?

A

90-95%

72
Q

What can cause pancreatic exocrine insufficiency?

A

CF, chronic pancreatitis, pancreatic resection

73
Q

How do you treat pancreatic exocrine insufficiency?

A

Oral pancreatic enzyme replacement (enteric coated)

74
Q

How does bile salt deficiency cause maldigestion?

A

Low bile salt pool = maldigestion of fat/fat-soluble vitamins

75
Q

What can cause bile salt deficiency?

A

Severe cholestasis, distal ileal resection or disease (Crohn’s), bacterial overgrowth

76
Q

How do you treat bile salt deficiency?

A

Treat underlying condition and give medium chain triglycerides

77
Q

What prevents bacterial overgrowth?

A

Gastric acids, small bowel motility, ileocecal valve, secreted immunoglobulins

78
Q

What conditions are associated with the development of bacterial overgrowth? (2 classes)

A

Motility disorders (stasis) and anatomic disorders (fistula, diverticulitis, blind loop)

79
Q

Consequences of bacterial overgrowth

A

Deconjugate the bile salts –> fat malabsorption and B12/iron deficiency due to bacterial consumption

80
Q

How can bacterial overgrowth be dx?

A

Breath tests

81
Q

How can bacterial overgrowth be treated?

A

Correct underlying problem and give antibiotics

82
Q

What two broad categories of disease cause malabsorption?

A

Loss of absorptive surface and impaired mucosal/lymphatic transport

83
Q

Three examples of loss of absorptive surface

A

Short bowel syndrome, celiac sprue, tropical sprue

84
Q

Three examples of impaired mucosal/lymphatic transport

A

Abetalipoproteinemia, Whiple’s disease, intestinal lymphangiectasia

85
Q

How could one get short bowel syndrome?

A

Caused by resection or bypass

86
Q

Celiac disease is an inappropriate response to…where does it favor in the bowel?

A

Gliadin (in gluten); proximal > distal

87
Q

What is tropical sprue? Tx?

A

Infection seen after Central America, Caribbean, SE Asia that is histologically similar to celiac sprue but is PANenteric (not just duodenum); tx = antibiotics

88
Q

What is abetalipoproteinemia? Tx?

A

AR disease in which epithelial cells CANNOT assemble chylomicros, so lipids accumulate in cells, causes fat malabsorption; tx = fat restriction and MCT oil

89
Q

What des the D-Xylose test test? Describe.

A

Tests functioning of SI absorption; under normal conditions, 25% of ingested amount of D-Xylose should be in urine, if less, than not enough absorbed

90
Q

There is fat malabsorption. D-Xylose normal =

A

Pancreatic disease

91
Q

There is fat malabsorption. D-Xylose abnormal =

A

Small bowel disease

Gastrointestinal and Liver (19 decks)

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