Chapter 17 (Part 2): Small Intestine and Colon Flashcards
What are the 4 most common obstructions of the Small Intestine and Colon? (H/A/I/V)
Hernias
Adhesions
Intussusceptions
Volvulus
What are hernias?
What is Incarceration and what problem can hernias cause if not treated?
- serosa-lined peritoneal protrusion that traps bowel segments externally (MOST COMMON OBSTRUCTION, 3rd MC in U.S.)
I: permanent entrapment due to stasis and edema (cannot be reduced back down)
- causes bowel infarction due to strangulation at neck
Adhesions vs Volvulus
What are they and what problem can arise because of them?
A: MOST COMMON cause of obstruction in the U.S.
- localized inflammation causes fibrous bridges (heal)
- viscera can slide through = INTERNAL HERNIAS
V: complete twisting of bowel loop about mesenteric vascular base (usually seen in SIGMOID COLON)
- can lead to TOXIC MEGACOLON/gangrenous necro.
Intussusception
What is it, who is it most commonly seen in, and what is the difference between causes in children vs adults?
- intestinal segment telescopes into immediate distal segment (peristalsis propels with attached mesentery)
- MOST COMMON in children < 2 yrs old
C: spontaneous or rotavirus vaccine (enemas)
- reactive Peyers Patches as leading edge
A: intraluminal mass/tumor (surgery)
What are two vascular problems of the Small Intestine and Colon?
Ischemic Bowel Disease and Angiodysplasia
Ischemic Bowel Disease
What is it, what two areas does it most commonly affect, and what does it look like?
- abrupt compromise of vessel leading to infarct of several meters of intestine (mucosa hemorrhage/ulcers and thick edematous bowel wall)
Affects: splenic flexure (Marginal Artery of Drummond) and sigmoid colon/rectum (WATERSHED ZONES)
M: LLQ pain with patchy lesions, coagulative necrosis, crypt hyperproliferation, and epithelium slough off
Ischemic Bowel Disease
What causes it and what is the prognosis?
- pts > 70 yo; cocaine, CMV/E. coli (vasoconstriction or epithelial damage)
- embolism, AAA, atherosclerosis (mesenteric vessel)
Acute: sudden onset of cramps, LLQ pain, desire to defecate, passage of blood/bloody diarrhea (SHOCK)
P: 10% of transmural die in 30 days and is doubled in pts with right-sided colonic disease (worse with COPD)
Radiation Enterocolitis vs Necrotizing Enterocolitis
RE: epithelial damage + vascular injury
- radiation fibroblasts in stroma
- anorexia, cramps, malabsorption diarrhea
NE: most common acquired GI emergency (neonates)
- presents when oral feeding initiated
- acute disorder –> transmural necrosis
Angiodysplasia
What is it, where does it most commonly occur, and how is it diagnosed?
- malformed tortuous, ectatic dilations of veins, venules, capillaries in mucosa and submucosa (60 yo)
- most common in CECUM and ASCENDING COLON (20% of major GI bleeds) –> significant bleeding
Diagnosis of exclusion
How does malabsorption commonly present as and what are 4 common causes of it? (P/C/C/G)
usually presents as chronic diarrhea with STEATORRHEA (hallmark - fatty, clay-colored, oil stool)
MCC: pancreatic insufficiency, Celiacs Disease, Crohn’s Disease, and intestinal GVHD (allogenic HSC trans)
What is the difference between:
Secretory Diarrhea
Osmotic Diarrhea
Malabsorptive Diarrhea
Exudative Diarrhea
How is each affected by FASTING?
S: isotonic stool (to plasma)
- PERSISTS during fasting
O: fluid > 50 mOsm more concentrated than plasma
- lactase deficiency, ABATES during fasting
M: failure of nutrient absorption (STEATORRHEA)
- RELIEVED by fasting
E: inflammatory disease; PURULENT, bloody stool
- PERSISTS during fasting
What disease(s) ONLY have issues with:
Intraluminal Digestion
Terminal Digestion
Lymphatic Transport
Transepithelial Transport
I: Chronic Pancreatitis or Cystic Fibrosis
TD: Disaccharidase Deficiency (Lactose Intolerance)
L: Whipple Disease
TT: Abetalipoproteinemia
What is Cystic Fibrosis?
- pancreatic intraductal concentrations = duct obstruct. (CFTR absence)
- ion transport disorder that affects the GI, respiratory, and reproductive tracts
- causes thick secretions that block organ passages (Meconium Ileus) and pancreas autodigestion
Celiac Disease
What 2 genetics are associated with it, what product of gluten breakdown causes it and how, and where does it most commonly occur in the GI tract?
G: Class II HLADQ2 (more common) and HLADQ8
- a-gliadin (breakdown product of gluten at brush border); deaminated by transglutaminase = T-Cell activation = destruction of epithelium (MIMICRY)
- IL-15 activates CD8+ expressing NKGD2 which attack MIC-A on enterocytes (apoptosis); also inc. in IgA to endomysial cells (EMA) and tissue transglutaminase
MC: 2nd part of duodenum to proximal jejunum
- villous atrophy (FLATTENED), inc. mitosis in crypts
Celiac Disease
What is the difference between Adult and Pediatric forms? What is a common skin lesion that occurs in the adult form?
A: 30-60 yo females; chronic diarrhea, bloating, anemia
- DERMATITIS HERPETIFORMIS (itchy, blistering - 10%)
- papillae abscesses, sub-epi blister, IgA BM proteins
C: onset 6-24 months; irritable, failure to thrive, weight loss, muscle wasting, anorexia
- Non-classic: later onset
- short statures, arthritis, delayed puberty
- iron deficiency anemia, aphthous stomatitis
What are two considerations if symptoms return in a Celiac patient?
- no longer adherent to diet
- ENTEROPATHY-ASSOCIATED T-Cell LYMPHOMA (EATL) or small intestinal adenocarcinoma
What is Environmental Enteropathy?
Who is it most commonly seen in and what symptoms does it cause?
- tropical enteropathy or tropical sprue (seen in areas/populations with poor sanitation/hygiene)
- seen in young patient who travel or are from endemic areas (DISTAL BOWEL MOST AFFECTED)
Sx: malabsorption/malnutrition, stunted growth, defective intestinal mucosal immune function
- NOT corrected with oral antibiotics or supplements
Autoimmune Enteropathy
What is it and who is it seen in, what mutation is associated with it, and how is it differentiated from Celiac Disease?
- severe, persistent diarrhea/autoimmune disease in children (IPEX)
- X-linked FOXP3 mutation = defective Treg cells
- generate auto-Abs to enterocytes/Goblet cells
- see intraepithelial lymphocytes and NEUTROPHILS in intestinal mucosa (Neutrophils NOT in Celiacs)
Lactase (Disaccharidase) Deficiency
What is it and what is the difference between Congenital and Acquired forms?
- enzyme is located in BRUSH BORDER of villi
C: explosive diarrhea, water/frothy stools and abdominal distension after dairy
- AR LOF mutation of Lactase gene
A: abdominal fullness, diarrhea, flatulance
- downregulation of Lactase gene (post-infection)
- Native Americans, African Americans, Chinese
Abetalipoproteinemia
What is it and what mutation is it caused by, what can it be stained with, and what is a common clinical finding on blood smear?
- Auto Recessive mutation of MTP (present in infancy)
- inability to secrete triglyceride-rich lipoproteins
- intracellular lipid accumulation (oil-red O stain)
- especially after fatty-meals
- causes failure to thrive, diarrhea (steatorrhea) and ACANTHOCYTIC red cells (BURR CELLS) in smears
- deficiency of fat-soluble (ADEK) vitamins
Vibrio cholera
What is it and where is it acquired, what diarrhea does it cause, and how can it be treated?
- comma-shaped Gram (-) endemic in INDIA and BANGLADESH (fecal-oral; drinking dirty water)
- produces toxin; also from raw oysters (seafood)
- causes “rice-water diarrhea” with fishy odor
Treatment: oral rehydration (99% success rate)
Campylobacter enterocolitis
What is it and where is it acquired, how does it present clinically, and what are 3 sequelae of infection? (RA/EN/GBS)
- FLAGELLATED comma-shaped Gram (-) from raw chicken, milk, water causing TRAVELER’S DIARRHEA (most common enteric pathogen in developed areas)
- causes acute watery diarrhea (food-poisoning or flows flu prodrome); can somtimes have blood (get a stool culture)
S: reactive arthritis (HLA-B27), erythema nodosum, and GUILLAIN-BARRE syndrome (ascending flaccid paralysis; mimicry due to LPS cross-reactivity)
