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GIR Test 4 > B5.072 Malabsorption Syndrome > Flashcards

B5.072 Malabsorption Syndrome Flashcards

1
Q

malabsorption syndrome

A

diminished intestinal absorption of one or more nutrients

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2
Q

steatorrhea

A

an increase in stool fat excretion to >6% of dietary fat intake

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3
Q

osmotic diarrhea

A

diarrhea secondary to diminished absorption of one or more dietary nutrients
ceases during fasting

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4
Q

secretory diarrhea

A

diarrhea due to small and/or large intestinal fluid and electrolyte secretion
associated with enterotoxins
unaffected by fasting

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5
Q

how can bile acid defects contribute to steatorrhea

A

defects in any of the steps in enterohepatic circulation of bile acids can result in a decrease in the duodenal concentration of the conjugated bile acids and consequently in the development of steatorrhea

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6
Q

steps in enterohepatic circulation of bile acids that can go awry

A
  1. decreased synthesis
  2. decreased biliary secretion
  3. maintenance of conjugated bile acids
  4. decrease in reabsorption
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7
Q

defect causing decreased bile acid synthesis

A

decreased hepatic function

ex: cirrhosis

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8
Q

defect causing decreased biliary secretion of bile acids

A

defective canalicular excretion of organic anions, including bile acids
ex: PBC

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9
Q

defect causing impaired maintenance of conjugated bile acids

A

bacterial overgrowth in the small intestine results in decrease in conjugated bile acids below the critical micellar concentration (CMC)
ex: jejunal diverticulosis

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10
Q

why cant unconjugated bile acids form micelles?

A

quickly absorbed

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11
Q

defect causing decrease in reabsorption of bile acids

A

increase in delivery of bile acids to the large intestines

ex: ileal dysfunction caused by Crohns or surgical resection

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12
Q

what is choleretic enteropathy

A

bile acid diarrhea

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13
Q

discuss bile acid diarrhea (choleretic enteropathy)

A

limited ileal disease causing reduced bile acid absorption
fecal bile acid secretion COMPENSATED by extra hepatic synthesis
mild to no steatorrhea bc extra hepatic synthesis is compensating

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14
Q

treatment for bile acid diarrhea

A

cholestyramine

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15
Q

discuss the pathophys of fatty acid diarrhea

A

extensive ileal disease leading to reduced bile acid absorption
fecal bile acid loss NOT COMPENSATED by hepatic synthesis
reduced bile acid pool size; intraduodenal concentration of bile acids is reduced to less than the CMC
>20 g steatorrhea

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16
Q

treatment of fatty acid diarrhea

A

low fat diet

cholestyramine many not be effective and may further exacerbate the problem

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17
Q

3 types of fatty acids in fats

A

LCFAs
MCFAs
SCFAs

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18
Q

dietary fat compositions

A

long chain triglycerides (LCTs)

glycerol bound via ester linkages to 3 LCFAs

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19
Q

3 integrated processes that assimilate dietary lipids

A
  1. an intraluminal/digestive phase
  2. mucosal/absorptive phase
  3. delivery/post-absorptive phase
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20
Q

pathophysiological defects in lipolysis

A
  1. decreased pancreatic lipase secretion down to 5% or lower
  2. reduction in intraduodenal pH (pancreatic lipase inactivated below 7)
  3. decrease in pancreatic bicarb secretion for same reason as above
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21
Q

disease that can lead to defects in lipolysis

A

chronic pancreatitis

CF

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22
Q

pathophysiological defect in mucosal uptake

A

steatorrhea can result from impaired movement of mixed micelles across the unstirred aqueous fluid layer if the relative thickness of the unstirred water layer increases
ex: celiac, bacterial overgrowth syndrome

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23
Q

what is abetalipoproteinemia

A

impaired synthesis of B lipoproteins
deficiency in chylomicron formation leads to lipid laden small intestinal epithelial cells that before normal in appearance after fasting
disorder associated with abnormal erythrocytes, neuro problems, and steatorrhea

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24
Q

what is intestinal lymphangiectasia

A

abnormal intestinal lymphatics

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25
Q

MCT digestion

A

do not require lipolysis and can be absorbed intact by intestinal epithelial cells
no micelle formation necessary

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26
Q

SCFAs

A

not dietary lipids
synthesized by colonic bacterial enzymes from nonabsorbed carbohydrates
rapidly absorbed and stimulate colonic NaCl and fluid absorption

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27
Q

cause of antibiotic associated diarrhea

A

antibiotic suppression of the colonic microbiota with a resulting decrease in SCFA production

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28
Q

forms of carbohydrates in diet

A

starch
disaccharides (sucrose + lactose)
glucose

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29
Q

big picture absorption of carbohydrates

A

only absorbed in small intestine and only in the form of monosaccharides

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30
Q

clinically important disorder of carbohydrate absorption

A

lactose malabsorbtion

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31
Q

how is lactose digested

A

brush border lactase

broken down into glucose and galactose which can be transported into cells via SGLT

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32
Q

primary lactase deficiency

A

genetically determined decrease or absence of lactase
all other aspects of both intestinal absorption and brush border enzymes are normal
common in adulthood

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33
Q

secondary lactase deficiency

A

caused by diseases that destroy the lining of the small intestine along with lactase
seen in celiac, crohns, UC, chemo, and long courses of antibiotics

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34
Q

symptoms of lactose malabsorption

A

diarrhea
abdominal pain
cramps
flatus

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35
Q

pathology often confused with lactase deficiency

A

IBS

persistence of symptoms in an individual who exhibits lactose intolerance while on a lactose free diet suggests IBS

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36
Q

factors that may play into severity of symptoms related to lactose intolerance

A
  1. amount of lactose in diet
  2. rate of gastric emptying (faster=worse)
  3. small intestine transit time (faster=worse)
  4. colonic compensation by production of SCFAs from nonabsorbable lactose (reduced microflora=increased symptoms)
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37
Q

glucose and galactose malabsorption

A

congenital absence of SGLT1

diarrhea with glucose and galactose but not with fructose

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38
Q

protein digestion and absorption

A

present in food as polypeptides and broken down into di- and tri-peptides
absorbed by separate transport systems for di and tripeptides and for different types of AAs (nonpolar and dibasic)

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39
Q

enterokinase deficiency

A

absence of enterokinase which converts trypsinogen to trypsin
associated with diarrhea, growth retardation, and hypoproteinemia

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40
Q

Hartnup’s syndrome

A

defect in transport of nonpolar AAs

pellagra like rash and neuropsychiatric symptoms

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41
Q

cystinuria

A

defect in dibasic AA transport

associated with renal calculi and chronic pancreatitis

42
Q

clinical picture of short bowel syndrome

A

symptoms of malabsorption

recent small intestinal resection for mesenteric ischemia

43
Q

gold standard for establishing diagnosis of steatorrhea

A

quantitative stool fat determination

44
Q

Sudan II staining

A

qualitative stool fat test

rapid and inexpensive but not as good as qualitative test

45
Q

vitamins that may be deficient in cases of steatorrhea

A

A, D, E, K

46
Q

vitamin D malabsorption symptoms

A

metabolic bone disease
elevated alk phos
reduced serum calcium

47
Q

vitamin K deficiency findings

A

elevated PT without liver disease or anticoagulants

48
Q

macrocytic anemia

A

evaluate for cobalamin or folic acid malabsorption

49
Q

iron deficiency anemia without occult bleeding

A

evaluate for iron malabsorption

exclude celiacs

50
Q

where is iron absorbed

A

proximal small intestine

51
Q

the schilling test

A

test to determine the cause of cobalamin malabsorption

52
Q

urinary d-xylose test

A

test for carbohydrate absorption
provides assessment of proximal small intestine mucosal function
administer 25 g or d-xylose and collect urine for 5 h, excreting < 4.5 g reflects duodenal/ jejunal disease

53
Q

what findings may be illuminated on small intestine radiologic examination

A 
intestinal dilation w extensive mucosal disease
anatomic abnormalities (crohns, blind loop)
54
Q

indications for a small intestine biopsy

A
  1. documented or suspected steatorrhea or chronic diarrhea

2. diffuse or focal abnormalities of the small intestine defined on a small intestinal series

55
Q

categories of lesions on a small intestine biopsy

A
  1. diffuse, specific
  2. patchy, specific
  3. diffuse, nonspecific
56
Q

diseases associated with diffuse, specific lesions on SI biposy

A

whipples disease
agammaglobulinemia
abetalipoproteinemia

57
Q

diseases associated with patchy, specific lesions on SI biopsy

A 
intestinal lymphoma
intestinal lymphangiectasia
eosinophilic gastroenteritis
amyloidosis
crohns
infections
mastocytosis
58
Q

diseases associated with diffuse, nonspecific lesions on SI biopsy

A 
celiac
tropical sprue
bacterial overgrowth
folate deficiency
vitamin B12 deficiency
radiation enteritis
Zollinger-Ellison syndrome
protein calorie malnutrition
drug induced enteritis
59
Q

pathologic findings with whipples disease

A

lamina propria includes macrophages containing material positive on periodic acid Schiff staining

60
Q

pathologic findings with agammaglobulinemia

A

absence of plasma cells
flat mucosa
often patients have a giardia infection

61
Q

pathologic findings with abetalipoproteinemia

A

normal villi

epithelial cells vacuolated with fat postprandially

62
Q

pathologic findings in intestinal lymphangiectasia

A

dilated lymphatics

clubbed villi

63
Q

pathologic findings in celiac

A

short or absent villi
mononuclear infiltrate
epithelial cell damage
hypertrophy of crypts

64
Q

test for pancreatic exocrine function

A

secretin test

measures pancreatic secretions by duodenal intubation following IV admin of secretin

65
Q

test results in chronic pancreatitis

A

d-xylose = normal
Schilling = 50% abnormal, if abnormal use pancreatic enzyme treatment
duodenal mucosal biopsy = normal

66
Q

test results in bacterial overgrowth syndromes

A

d-xylose = normal or modestly abnormal
Schilling = often abnormal, treat w antibiotics
duodenal mucosal biopsy = usually normal

67
Q

test results in ileal disease

A

d-xylose = normal
Schilling = abnormal
duodenal mucosal biopsy = normal

68
Q

test results in celiac

A

d-xylose = decreased
Schilling = normal
duodenal mucosal biopsy = flat

69
Q

test results in intestinal lymphangiectasia

A 
d-xylose = normal
Schilling = normal
biopsy = dilated lymphatics
70
Q

what is celiac disease

A

autoimmune disorder affecting small intestine
caused by a reaction to gluten
common cause of malabsorption

71
Q

symptomatic presentations of celiac disease

A
  1. small number have classical symptoms
  2. much larger number have atypical presentation (anemia, infertility neuro symptoms)
  3. some are symptomatic despite histo abnormalities
72
Q

hallmark of celiac

A

abnormal small intestinal biopsy and response to the elimination of gluten from the diet

73
Q

distribution of severity in celiac

A

proximal to distal

reflects exposure of intestine to varied amounts of dietary gluten

74
Q

when might symptoms of celiac appear?

A
  1. intro of cereals into an infant’s diet

2. any age throughout adulthood w frequent spontaneous remissions or exacerbations

75
Q

celiac serologies

A

IgA antigliadin, anti-tTG , and antendomysial antibodies

76
Q

genetics factors in celiac

A

HLA-DQ2,8

77
Q

how to diagnose celiac

A

histo changes on small intestine biopsy with improvement after initiation of gluten free diet

78
Q

what % of patients w celiac respond to complete gluten restriction

A

90%

79
Q

outcomes of refractory celiac disease (does not respond to gluten free diet)

A
  1. respond to restriction of other dietary protein (soy)
  2. respond to glucocorticoid treatment
  3. temporary symptoms
  4. fail to respond to all measures and have a fatal outcome w complications like intestinal T cell lymphoma or autoimmune enteropathy
80
Q

mechanisms of diarrhea in celiac

A
  1. steatorrhea from changes in jejunal mucosal function
  2. secondary lactase deficiency due to changes in jejunal brush border enzymatic function
  3. bile acid malabsorption (in cases with ileal involvement)
  4. endogenous fluid secretion from crypt hyperplasia
81
Q

diseases associated w celiac

A 
dermatitis herpetiformis (DH)
DM1
IgA def
down syndrome
turner's syndrome
82
Q

complications of celiac

A 
most important: cancer
-GI and nonGI neoplasms
-intestinal lymphoma
intestinal ulceration independent of lymphoma
iron deficiency anemia
83
Q

what is short bowel syndrome

A

clinical problems that follow resection of various lengths of small intestine
rarely congenital

84
Q

situations that mandate intestinal resection

A
  1. mesenteric vascular disease
  2. primary mucosal and submucosal disease (crohns)
  3. traumas
85
Q

how does removal of the ileum impact diarrhea

A

more severe diarrhea than jejunal resection
can cause diarrhea by an increase in bile acids entering the colon stimulating secretions
absence of ileocecal valve is associated with decrease in intestinal transit time and bacterial overgrowth from the colon

86
Q

nonintestinal symptoms of short bowel syndrome

A
  1. increased frequency of renal calcium oxalate calculi
  2. increase in cholesterol gallstones related to a decrease in bile acid pool size
  3. gastric hypersecretion due to reduced hormonal inhibition of acid secretion or increased gastrin levels due to reduced SI catabolism of circulating gastrin
87
Q

treatment of short bowel syndrome

A
  1. opiates to reduce stool output and establish effective diet (low fat, high carb)
  2. consider and treat bacterial overgrowth if ileocecal valve is missing
  3. PPI if acid hypersecretion is contributing
  4. vitamin and mineral therapy
  5. home PN if other methods fail
  6. SI transplant
88
Q

what are bacterial overgrowth syndromes

A

SIBO
group of disorders with diarrhea, steatorrhea, and macrocytic anemia whose common feature is the proliferation of colonic type bacteria within the small intestine

89
Q

what causes bacterial proliferation in SIBO

A 
impaired peristalsis (functional stasis)
changes in intestinal anatomy (anatomic stasis)
direct communication between the small and large intestine
90
Q

other names for SIBO

A

stagnant bowel syndrome

blind loop syndrome

91
Q

bacteria commonly found in SIBO

A

e. coli

bacteroides

92
Q

macrocytic anemia in SIBO

A

due to cobalamin, not folate def

bacteria need cobalamin for growth and use up the limited dietary amounts

93
Q

steatorrhea in SIBO

A

impaired micelle formation
reduced concentration of conjugated bile acids and the presence of unconjugated bile acids
bacteroides can deconjugate bile acids and the unconjugated form is more rapidly absorbed

94
Q

what if you don’t have steatorrhea in SIBO, but there is still diarrhea present?

A

likely due to bacterial enterotoxins causing fluid secretion

95
Q

examples of anatomic stasis

A

diverticula
fistulas/strictures
proximal duodenal afferent loop following subtotal gastrectomty and gastrojejunostomy
bypass of SI (jejunoileal bypass or roux en y gastric bypass)
dilation at site of previous intestinal anastomosis

96
Q

examples of etiologies functional stasis

A

scleroderma

DM

97
Q

etiologies of direct communication between small and large intestines

A

ileocolonic resection

enterocolic anastomosis

98
Q

making a diagnosis of SIBO

A
  1. low cobalamin and high folate
  2. jejunal aspirate w increased levels of bacteria (culture and count)
  3. breath hydrogen test w admin of lactulose
  4. schilling test
99
Q

10 signs of SIBO

A 
gas
bloating
diarrhea
ab pain/cramps
constipation
IBS or IBD
food intolerances
chronic illnesses
B12 deficiency
fat malabsorption
100
Q

treatment of SIBO

A
  1. surgical correction of anatomic blind loop if present

2. broad spectrum antibiotics for 3 weeks for functional causes that cannot be corrected

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