module 13 malabsorption Flashcards
malabsorption syndromes
inadequate digestion pancreatic insufficiency lactase deficiency bile salt deficiency gluten-sensitive enteropathy
pancreatic insufficiency
dec. pancreatic enzyme production
- lipase, amylase, trypsin, or chymotrypsin
- > fat maldigestion, fatty stools and wt loss.
causes of pancreatic insufficiency
pancreatitis
pancreatic carcinoma
pancreatic resection
cystic fibrosis
lactase dificiency
inability to break down lactose to monosaccharides -> no lactose digestion/monosaccharide absorption
Fermentation of lactose by bacteria -> cramps, flatulence, gas, and osmotic diarrhea
bile salt deficiency
dec. conjugated bile salts needed to emulsify and absorb fats
- synthesized from cholesterol in liver
- > poor absorption of lipids -> fatty stools, diarrhea, loss of fat-soluble vitamins (ADEK)
bile salt deficiency r/t
liver disease
bile obstructions
fat-soluble vitamin deficiencies
must have fat substance to be absorbed
vitamin A deficiency
night blindess
vit. D deficiency
dec. Ca absorption
bone pain
osteoporosis
fractures
Vit K. deficiency
prolonged PT time
purpura
petechiae
gluten sensitive enterophaty
celiac disease
gluten: structural protein component in cereal grains: wheat, rye, barley, oat, malr
Loss of villous epithelium in intestinal tract: gluten protein acts as toxin
Dietary, genetic, and immunologic factors
celiac and autoimmunity
T-cell mediated injury to small intestine epithelial cells Antibodies produced - antitissue transglutaminase (tTG) - antiendomysium (EMA) - antideamidated gliadin peptides (DGP)
celiac s/s
children fail to grow/thrive malabsorption s/s - rickets, bleeding, anemia Celiac crisis: - severe diarrhea - dehydration - malabsorption - protein loss
gluten intolerance primary effects
T-cell, antibody, and complement activator
- > villus injury
- > dec. surface area
- > dec. carb, protein, fat absorption, and inflammatory enteritis
- > osmotic diarrhea
- > secretory diarrhea
- > dec. electrolytes and proteins
- > malnutrition
gluten intolerance secondary effects
T-cell, antibody, and complement activator
- > mucosal damage
- > dec. intestinal hormones
- > dec. pancreatic function
- > dec. carb, protein, and fat absorption
- > malnutrition
inflammatory bowel diseases
chronic, relapsing disorders of unknown origin - genetics - alteration of epithelial barrier - immune reactions to intestinal flora - abnormal T-cell responses Life-altering dx usually dx in peds-early adulthood
crohn’s disease
granulomatous colitis, ileocolitis, or reginal enteritis
idiopathic inflammatory disorder
affects any part of digestive tract
affects all layers of intestinal wall
Skip lesions
Ulcerations can cause longitudinal and transverse fissures: extend into lymphatics
- become blocked
-> engorgement, inflammation and surrounding tissue, ulcers, fibrous scar tissue
fissures -> fistulas
crohn’s s/s
result of bowel incapable of absorbing contents
- perianal fissures
- fistulas
- abscesses
- strictures
ulcerative colitis
chronic inflammatory disease with ulceration of colonic mucosa
- sigmoid colon and rectum
continuous, no skip lesions
Infectious, immunologic, dietary, genetic components
UC s/s
diarrhea (10-20/day) - dec. ability to absorb H2O and Na bloody stools cramps rectal bleeding
appendicitis
inflammation of the vermiform appendix possible causes - obstruction - ischemia - inc. intraluminal pressure - infection - ulceration
appendicitis s/s
epigastric and RLQ pain (McBurney) rebound tenderness N/V fever leukocytosis < 45, peak 10-19 y/o male diarrhea
hirshsprung disease
congenital distened sigmoid colon fills up r/t - aganglionic portion (usually rectosigmoid area): no nerve innervation -> always constricted male>female
hirshsprung s/s
infants - fecal stagnation -> enterocolitis with bacterial overgrowth profuse diarrhea hypovolemic shock intestinal perforation
Cleft palate
variations in clefts of the lip and palate
- notch in vermilion border (line above lip)
- unilateral cleft lip and palate
- bilateral cleft lip and palate
- cleft palate (not visible without opening mouth)
esophageal atresia and tracheoesophageal fistulae
5 types
- simple esophageal atresia: proximal and distal esophagus enid in blind pouches, no tracheal communication (food/water goes nowhere, regurgitated)
- proximal and distal esophagus end in blind pouches, fistula connects proximal esophagus to trachea (food/water enters lungs)
- proximal esophagus with blind pouch, fistula connect trachea to distal esophagus (air enters stomach, regurgitated content -> lungs)
- fistula connects proximal and distal esophageal segments to the trachea (air, food/fluid enter the stomach and lungs)
- simple tracheoesophageal fistula between otherwise nml esophagus and trachea (air, food/fluid enters lungs and stomach)