B5.072 Malabsorption Syndrome Flashcards
malabsorption syndrome
diminished intestinal absorption of one or more nutrients
steatorrhea
an increase in stool fat excretion to >6% of dietary fat intake
osmotic diarrhea
diarrhea secondary to diminished absorption of one or more dietary nutrients
ceases during fasting
secretory diarrhea
diarrhea due to small and/or large intestinal fluid and electrolyte secretion
associated with enterotoxins
unaffected by fasting
how can bile acid defects contribute to steatorrhea
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
steps in enterohepatic circulation of bile acids that can go awry
- decreased synthesis
- decreased biliary secretion
- maintenance of conjugated bile acids
- decrease in reabsorption
defect causing decreased bile acid synthesis
decreased hepatic function
ex: cirrhosis
defect causing decreased biliary secretion of bile acids
defective canalicular excretion of organic anions, including bile acids
ex: PBC
defect causing impaired maintenance of conjugated bile acids
bacterial overgrowth in the small intestine results in decrease in conjugated bile acids below the critical micellar concentration (CMC)
ex: jejunal diverticulosis
why cant unconjugated bile acids form micelles?
quickly absorbed
defect causing decrease in reabsorption of bile acids
increase in delivery of bile acids to the large intestines
ex: ileal dysfunction caused by Crohns or surgical resection
what is choleretic enteropathy
bile acid diarrhea
discuss bile acid diarrhea (choleretic enteropathy)
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
treatment for bile acid diarrhea
cholestyramine
discuss the pathophys of fatty acid diarrhea
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
treatment of fatty acid diarrhea
low fat diet
cholestyramine many not be effective and may further exacerbate the problem
3 types of fatty acids in fats
LCFAs
MCFAs
SCFAs
dietary fat compositions
long chain triglycerides (LCTs)
glycerol bound via ester linkages to 3 LCFAs
3 integrated processes that assimilate dietary lipids
- an intraluminal/digestive phase
- mucosal/absorptive phase
- delivery/post-absorptive phase
pathophysiological defects in lipolysis
- decreased pancreatic lipase secretion down to 5% or lower
- reduction in intraduodenal pH (pancreatic lipase inactivated below 7)
- decrease in pancreatic bicarb secretion for same reason as above
disease that can lead to defects in lipolysis
chronic pancreatitis
CF
pathophysiological defect in mucosal uptake
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
what is abetalipoproteinemia
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
what is intestinal lymphangiectasia
abnormal intestinal lymphatics
MCT digestion
do not require lipolysis and can be absorbed intact by intestinal epithelial cells
no micelle formation necessary
SCFAs
not dietary lipids
synthesized by colonic bacterial enzymes from nonabsorbed carbohydrates
rapidly absorbed and stimulate colonic NaCl and fluid absorption
cause of antibiotic associated diarrhea
antibiotic suppression of the colonic microbiota with a resulting decrease in SCFA production
forms of carbohydrates in diet
starch
disaccharides (sucrose + lactose)
glucose
big picture absorption of carbohydrates
only absorbed in small intestine and only in the form of monosaccharides
clinically important disorder of carbohydrate absorption
lactose malabsorbtion
how is lactose digested
brush border lactase
broken down into glucose and galactose which can be transported into cells via SGLT
primary lactase deficiency
genetically determined decrease or absence of lactase
all other aspects of both intestinal absorption and brush border enzymes are normal
common in adulthood
secondary lactase deficiency
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
symptoms of lactose malabsorption
diarrhea
abdominal pain
cramps
flatus
pathology often confused with lactase deficiency
IBS
persistence of symptoms in an individual who exhibits lactose intolerance while on a lactose free diet suggests IBS
factors that may play into severity of symptoms related to lactose intolerance
- amount of lactose in diet
- rate of gastric emptying (faster=worse)
- small intestine transit time (faster=worse)
- colonic compensation by production of SCFAs from nonabsorbable lactose (reduced microflora=increased symptoms)
glucose and galactose malabsorption
congenital absence of SGLT1
diarrhea with glucose and galactose but not with fructose
protein digestion and absorption
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)
enterokinase deficiency
absence of enterokinase which converts trypsinogen to trypsin
associated with diarrhea, growth retardation, and hypoproteinemia
Hartnup’s syndrome
defect in transport of nonpolar AAs
pellagra like rash and neuropsychiatric symptoms
cystinuria
defect in dibasic AA transport
associated with renal calculi and chronic pancreatitis
clinical picture of short bowel syndrome
symptoms of malabsorption
recent small intestinal resection for mesenteric ischemia
gold standard for establishing diagnosis of steatorrhea
quantitative stool fat determination
Sudan II staining
qualitative stool fat test
rapid and inexpensive but not as good as qualitative test
vitamins that may be deficient in cases of steatorrhea
A, D, E, K
vitamin D malabsorption symptoms
metabolic bone disease
elevated alk phos
reduced serum calcium
vitamin K deficiency findings
elevated PT without liver disease or anticoagulants
macrocytic anemia
evaluate for cobalamin or folic acid malabsorption
iron deficiency anemia without occult bleeding
evaluate for iron malabsorption
exclude celiacs
where is iron absorbed
proximal small intestine
the schilling test
test to determine the cause of cobalamin malabsorption
urinary d-xylose test
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
what findings may be illuminated on small intestine radiologic examination
intestinal dilation w extensive mucosal disease anatomic abnormalities (crohns, blind loop)
indications for a small intestine biopsy
- documented or suspected steatorrhea or chronic diarrhea
2. diffuse or focal abnormalities of the small intestine defined on a small intestinal series
categories of lesions on a small intestine biopsy
- diffuse, specific
- patchy, specific
- diffuse, nonspecific
diseases associated with diffuse, specific lesions on SI biposy
whipples disease
agammaglobulinemia
abetalipoproteinemia
diseases associated with patchy, specific lesions on SI biopsy
intestinal lymphoma intestinal lymphangiectasia eosinophilic gastroenteritis amyloidosis crohns infections mastocytosis
diseases associated with diffuse, nonspecific lesions on SI biopsy
celiac tropical sprue bacterial overgrowth folate deficiency vitamin B12 deficiency radiation enteritis Zollinger-Ellison syndrome protein calorie malnutrition drug induced enteritis
pathologic findings with whipples disease
lamina propria includes macrophages containing material positive on periodic acid Schiff staining
pathologic findings with agammaglobulinemia
absence of plasma cells
flat mucosa
often patients have a giardia infection
pathologic findings with abetalipoproteinemia
normal villi
epithelial cells vacuolated with fat postprandially
pathologic findings in intestinal lymphangiectasia
dilated lymphatics
clubbed villi
pathologic findings in celiac
short or absent villi
mononuclear infiltrate
epithelial cell damage
hypertrophy of crypts
test for pancreatic exocrine function
secretin test
measures pancreatic secretions by duodenal intubation following IV admin of secretin
test results in chronic pancreatitis
d-xylose = normal
Schilling = 50% abnormal, if abnormal use pancreatic enzyme treatment
duodenal mucosal biopsy = normal
test results in bacterial overgrowth syndromes
d-xylose = normal or modestly abnormal
Schilling = often abnormal, treat w antibiotics
duodenal mucosal biopsy = usually normal
test results in ileal disease
d-xylose = normal
Schilling = abnormal
duodenal mucosal biopsy = normal
test results in celiac
d-xylose = decreased
Schilling = normal
duodenal mucosal biopsy = flat
test results in intestinal lymphangiectasia
d-xylose = normal Schilling = normal biopsy = dilated lymphatics
what is celiac disease
autoimmune disorder affecting small intestine
caused by a reaction to gluten
common cause of malabsorption
symptomatic presentations of celiac disease
- small number have classical symptoms
- much larger number have atypical presentation (anemia, infertility neuro symptoms)
- some are symptomatic despite histo abnormalities
hallmark of celiac
abnormal small intestinal biopsy and response to the elimination of gluten from the diet
distribution of severity in celiac
proximal to distal
reflects exposure of intestine to varied amounts of dietary gluten
when might symptoms of celiac appear?
- intro of cereals into an infant’s diet
2. any age throughout adulthood w frequent spontaneous remissions or exacerbations
celiac serologies
IgA antigliadin, anti-tTG , and antendomysial antibodies
genetics factors in celiac
HLA-DQ2,8
how to diagnose celiac
histo changes on small intestine biopsy with improvement after initiation of gluten free diet
what % of patients w celiac respond to complete gluten restriction
90%
outcomes of refractory celiac disease (does not respond to gluten free diet)
- respond to restriction of other dietary protein (soy)
- respond to glucocorticoid treatment
- temporary symptoms
- fail to respond to all measures and have a fatal outcome w complications like intestinal T cell lymphoma or autoimmune enteropathy
mechanisms of diarrhea in celiac
- steatorrhea from changes in jejunal mucosal function
- secondary lactase deficiency due to changes in jejunal brush border enzymatic function
- bile acid malabsorption (in cases with ileal involvement)
- endogenous fluid secretion from crypt hyperplasia
diseases associated w celiac
dermatitis herpetiformis (DH) DM1 IgA def down syndrome turner's syndrome
complications of celiac
most important: cancer -GI and nonGI neoplasms -intestinal lymphoma intestinal ulceration independent of lymphoma iron deficiency anemia
what is short bowel syndrome
clinical problems that follow resection of various lengths of small intestine
rarely congenital
situations that mandate intestinal resection
- mesenteric vascular disease
- primary mucosal and submucosal disease (crohns)
- traumas
how does removal of the ileum impact diarrhea
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
nonintestinal symptoms of short bowel syndrome
- increased frequency of renal calcium oxalate calculi
- increase in cholesterol gallstones related to a decrease in bile acid pool size
- gastric hypersecretion due to reduced hormonal inhibition of acid secretion or increased gastrin levels due to reduced SI catabolism of circulating gastrin
treatment of short bowel syndrome
- opiates to reduce stool output and establish effective diet (low fat, high carb)
- consider and treat bacterial overgrowth if ileocecal valve is missing
- PPI if acid hypersecretion is contributing
- vitamin and mineral therapy
- home PN if other methods fail
- SI transplant
what are bacterial overgrowth syndromes
SIBO
group of disorders with diarrhea, steatorrhea, and macrocytic anemia whose common feature is the proliferation of colonic type bacteria within the small intestine
what causes bacterial proliferation in SIBO
impaired peristalsis (functional stasis) changes in intestinal anatomy (anatomic stasis) direct communication between the small and large intestine
other names for SIBO
stagnant bowel syndrome
blind loop syndrome
bacteria commonly found in SIBO
e. coli
bacteroides
macrocytic anemia in SIBO
due to cobalamin, not folate def
bacteria need cobalamin for growth and use up the limited dietary amounts
steatorrhea in SIBO
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
what if you don’t have steatorrhea in SIBO, but there is still diarrhea present?
likely due to bacterial enterotoxins causing fluid secretion
examples of anatomic stasis
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
examples of etiologies functional stasis
scleroderma
DM
etiologies of direct communication between small and large intestines
ileocolonic resection
enterocolic anastomosis
making a diagnosis of SIBO
- low cobalamin and high folate
- jejunal aspirate w increased levels of bacteria (culture and count)
- breath hydrogen test w admin of lactulose
- schilling test
10 signs of SIBO
gas bloating diarrhea ab pain/cramps constipation IBS or IBD food intolerances chronic illnesses B12 deficiency fat malabsorption
treatment of SIBO
- surgical correction of anatomic blind loop if present
2. broad spectrum antibiotics for 3 weeks for functional causes that cannot be corrected
