Diverticulitis Flashcards
what is diverticulosis? what layers? most commonly occurs where? RFs? sxs? see on what procedure?
sac-like out-pouching of colon MUCOS & SUBMUSCOSA most commonly in sigmoid
dt factors that chronically increase intraluminal P: low fiber diet, high refined carbs
usu asx
may have chronic or intermittent LLQ abd pain, often constipation
may cause rectal bleeding if erosion of mucosa
often observed on barium studies
Where is diverticular dz common? What are its 3 parts?
common in industrialized western society
diverticulosis, diverticulitis & Meckel’s diverticulum
what is diverticulitis? usun from what? can potentially lead to what? prognosis? etiology?
inflammation of 1 or more diverticular, potentially leads to obstruction, perforation & to abscess & fistula formation
may heal spontaneously or may enlarge & adhere to adjacent organs, fistulas can form
repeated inflam may lead to obstruction & potentially dangerous perforation!
etiology of diverticulitis?
low-fiber diet is highest RF= low bulk stool= increased intraluminal P & formation of diverticula
diet: high fat & grain-fed beef
genetic: asians have R sided diverticular, westerners mostly L
aging= change in collagen structure
colonic motility d/os
corticosteroids increase risk (not NSAIDs)
colonic segmentation: non-propulsive contractions
defects in colonic wall strength
ssxs of diverticulosis vs diverticulitis?
diverticulosis: often asx, mb recurrent LLQ tenderness, flatulence, mb hx of painless rectal bleeding
diverticulitis: abd pain, LLQ, stead, severe & deep, fever/chills, previous episodes of dull, colicky & diffuse abd pain accompanied w/flatulence, distention & change in bowel habits
altered bowel habits: diarrhea, constipation, tenesmus
N/V, rectal bleeding, onset of bleeding is typically sudden, painless & accompanied by urge to defecate, bleeding may stop spontaneously
Complications of diverticulitis or diverticulosis?
perforation or fistula development pnematuria or recurrent UTIs feculent vaginal d/c severe & generalized abd pain,absent bowel sounds, fever back or lower extremity pain
PE for diverticular dz?
localized abd tenderness, rebound tenderness, may palpate mass
assess vial signs to determine hemodynamic stability
DRE
proctoscopic exam may reveal a mass in the cul-de-sac
DDDx of diverticular dz?
hemorrhoids an/or anal fissures, UTI, nephrolithiasis, obstruction, colon CA, hx of wt loss & mucus in stools indicates IBD
Imaging for diverticlar dz?
sigmoidoscopy shows narrowing & inflam
barium xray is hazardaous in acute phase & may cause a perforation
What is Meckle’s diverticulum? more common in what gender? sxs? may look like what other dz?
congenital bulge in distal ileum, remnant of omphalomesenteric duct
2% of pop, more common in males
most asx
can produce bleeding, obstruction, volvulus, intussusception
acute presentation may look like appendicitis
General SSXS of malabsorption?
chronic diarrhea, steatorrhea, abd bloating, wt loss, amenorrhea, macrocytic anemia, microcytic anemia, easy bruising, edema, glossitis, night blindness, bone pain/fractures, muscle spasm, peripheral neuropathy
What are 6 causes of malabsorption?
insufficient digestive elements, carbohydrate intolerance/lactose intolerance, tropical sprue, celiac dz, whipple’s dz, short bowel syndrome
What does having insufficient digestive elements include and lead to?
decreased pancreatic ezymes, liver enz, bile salts, HCl
post-surgical syndromes, biliary obstruction, CF, etc.
What is carb/lactose intolerance? lack of what? what are the disaccharidases?
disaccharidases: lactase, maltase, isomaltase, sucrase
lack of splitting of molecules leads to increased osmotic load, then watery diarrhea
fermentation leads to gas, flatulence, distention, abd pain
enzyme deficiencies may be congenital (rare), primary or secondary
Most common form of lactase deficiency? prevalence in different ethnicities? worldwide? very common among what populations?
acquired lactase deficient is most common form
in US 80% prevalence in blacks & hispanics, ~100% in Asian american pop, 25% in whites of NW european descent
worldwide >75% pop estimated, very common among Asian, South American & African pops
what is congenital lactose intolerance? primary lactose intolerance? secondary lactase deficiency? what can cause secondary lactase deficiency?
congenital: inherited as autosomal recessive trait
primary: dt low levels of lactase, develop after childhood
secondary: develop w/small bowel mucosal damage dt: acute gastroenteritis, carcinoid syndrome, chemo, diabetic gastropathy, Kwashiorkor, tropical sprue, celiac sprue, Crohn’s dz, gastrinoma, HIV enteropathy, whipple syndrome
Lab test of choice for carb/lactose intolerance?
hydrogen breath test
dietary elimination
Who is tropical sprue common in ? etiology? what does it lead to?
residents/natives & prolonged visitors of Caribbean, South India, SE Asia, sxs may improve after moving but sxs may reappear yrs later
etiology unk but thought to be from SI chronic infxn by toxigenic coliform bac
leads to malabsorption of folate, B12, iron
Ssxs of tropical sprue? two phases
acute phase: diarrhea w/fever & malaise
chronic phase: diarrhea, nausea, anorexia, abd cramps, steatorrhea, paresthesias
PE will reveal what vitamin deficiency signs?
glossitis, stomatitis, cheilosis, cutaneous hyperpigmentation, dry rough skin, abd distention, tenderness & edema, wt loss, dehydration
labs for tropical sprue?
no definitive marker exists
CBC shows megaloblastic anemia
stool analysis shows fecal fat >6 g in 24 hrs, fatty stools
CMP shows decreased serum protein, calcium, phosphorus, cholesterol & prothrombin, hypochlorhydria
D-xylose absorption test
upper Gi endoscopy will show characteristic histology
What is celiac dz? epidemiology? peaks at what age? gender preference? all pts express what 2 possible antigens?
immune-mediated enteropathy rxn to gluten leads to mucosal damage)
AI condition: environmental trigger= gluten, autoantigen= tissue transglutaminase
elimination of environmental trigger leads to complete resolution
etiology: highest in europe & US, affects 0.5-1% of pop, high in those w/GI sxs & in those w/first-degree relative w/celiac, low in blacks, Asian & Hispanic descent
can occur at any age but peaks in 5th decade
females more than males
all pts express human leukocyte antigen (HLA-DQ2 or HLA-DQ8) which facilitates immune response against gluten proteins
pathophys of celiac dz?
gliadins & glutenins in presence of CD4+ T cells w/HLD-DQ genotypes activate cytokine production & clonal expansion of antibody producing B cells= lymphocyte mediated destruction of proximal sm intestine mucosal villi
when villi damaged, vitamins, miners, calcium, carbs, proteins & fats are not well absorbed
T cells may react w/tissue transglutaminase & set in motion inflam events that result in characteristic celiac mucosal lesion
RFs of celiac dz?
heredity, early intro of gluten in infant diet, type 1 DM, down syndrome, absent breastfeeding, Crohn’s dz, chronic fatigue syndrome, AI thyroid dz, viral exposures may trigger an immunologic response
what pts will you screen for celiac dz? they are presenting with what sxs?
unexplained iron deficiency, early onset osteopenia, unexplained epilepsy, failure to thrive, poor glucose control, chronic diarrhea, infertility, miscarriages, elevated liver enzymes
Ssxs of celiac dz?
some asx class sxs: diarrhea, steatorrhea, bloating, flatulence, vit/min deficiencies, atypical presentation may have extraintestinal sxs: anemia, dermatitis herpetiformis, DM, aphthous stomatitis, neurological sxs, osteopathy
ssxs more common in the infant with celiac dz? the older child? the adult?
infant: fulminant presentation likely but not common
diarrhea, abd distention, failure to thrive, anorexia, vomiting, psychomotor impairment, hypoproteinemia, acidosis
older child: usu ~ 4 yo, diarrhea or constipation, anemia, short stature, osteoporosis, aphthous ulcers
adult: intestinal sxs may be absent, diarrhea or constipation, anemia, aphthous ulcers, sore tongue & mouth, dyspepsia, abd pain, bloating, fatigue, infertility, neuropsychiatric sxs, bone pain, weakness, dermatitis herpetiformis
labs for celiac dz? special tests?
CBC: anemia, leukopenia
CMP: increased AST, low albumin/plasma protein, low cholesterol increased alk phos
do a bone mineral density scan which will be low
special tests: serology: serum IgA quantitation & anti-endomysial abs, IgA anti-tissue transglutaminase abs, abn >100 units is highly specific,
tTG abs recommended as single serologic test for celiac dz screening in the primary care setting; deamidated gliadin peptide IgA & IgG= high sensitivity & specificity esp in elderly
Procedure for dx of celiac?
small bowel biopsy is CONFIRMATORY
4 or more samples from 2nd & 3rd portion of SI, pt must include gluten in a diet a minimum of 2 wks, preferably 4+ weeks
characteristic villous atrophy is found
5 ddxs of celiac dz?
anorexia nervosa, crohn’s dz, IBS, lactose intolerance, tropical sprue
what can look similar in terms of ssxs to celiac dz but lacks villous atrophy? tTG levels, biopsy results, gliadin abs, total IgA levels?
non-celiac gluten intolerance!
negative IgA tTG antibody, biopsy negative, positive glidadin abs, total IgA normal
What is whipple’s dz? caused by what? ssxs?
rare, multi-system condition caused by tropheryma whipplei
ssxs: diarrhea, wt loss, arthralgia, fever, malabsorption
What is short bowel syndrome? what section esp?
malabsorption from surgical bowel resection, esp jejunum
