week 7- lower GI Flashcards

1
Q

• What is acute intestinal perforation? Causes?

A

o emergency!
o Any part of GI, spill gastric, intestinal contents into abd cavity
o General causes: blunt or penetrating trauma, foreign bodies
o in SI: duodenal ulcer, corrosives, strangulation of bowel, acute appendicitis
o colon: obstruction, diverticulitis, IBD, toxic megacolon

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2
Q

• what are ssx of acute intestinal perforation? PE? Work-up?

A

o Ssx: sudden, severe general abd pn, tender, signs shock, N/V, anorexia
o PE: quiet to absent BS; peritoneal (guarding, rigidity)
o ***Note: in pts w underlying GI do, looks like “worsening” (more gradual, localized pn)
o Work-up: free air seen (usu SI) on abd xray or CT

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3
Q

• What is gastroenteritis? Hx?

A

o inflam lining of stomach, SI, LI (mc dt infx)
o usu self-limiting, mb serious in young, elderly, immunocompromised
o hx: ingest potentially contaminated food, water, travel, contact w similarly ill person, meds (eg abx)

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4
Q

• what are normal intestinal microflora?

A

o GI has 500 bacteria spp
o Stomach and proximal SI: few bacteria dt acidity
o Jejunum: lactobacilli, enterococci, gram (+) aerobes, facultative anaerobes
o Terminal ileum: enterobacteria, coliforms
o Colon: anaerobes: bacteriodes, lactobacillus, clostridium, bifidobacterium

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5
Q

• What are general ssx of gastroenteritis? PE? Work-up?

A

o Vary. Sudden N/V, anorexia, abd cramps, diarrhea. mb malaise, myalgia
o PE: distension, tender, borborymi
o Wu: Stool test (hemoccult, fecal WBCs, O&P, culture), Rapid enzyme assays (viral ags, Shiga toxin), CBC, CMP (hypokalemia; vomiting → metabolic alkalosis, diarrhea → acidosis)

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6
Q

• What is viral gastroenteritis?

A

o 30-40% infx diarrhea in US
o Viruses infect enterocytes in SI villi → transudate of fluid/salt into lumen
o →watery diarrhea, rare blood or mucus

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7
Q

• What is rotavirus GE?

A

o Mc infx diarrhea worldwide. 33% hospitalizations, 20% of GE
o Highly contagious: fecal-oral, peaks in winter
o Severe, dehydrating diarrhea in kids (peaks 3-15 mos). Mild in adults
o Ssx: vomit, fever >102°F. sxs can last 5-7 d

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8
Q

• What is norovirus GE? Astrovirus?

A

o N: older children and adults, year-round incidence, mb epidemic w water and food-borne outbreaks, highly contagious; acute onset vomit, abd cramps, diarrhea, fever, HA; lasts 1-2 d
o A: infants and young kids, winter months, fecal-oral, ssx similar to rotavirus

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9
Q

• What is enteric adenovirus GE? Other?

A

o E: kids <2, year-round/summer, fecal-oral. Diarrhea 1-2 wks → mild
o In immunocompromised, CMV and enterovirus can cause gastroenteritis

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10
Q

• How does exotoxin cause GE?

A

o Bacterial toxin → environment, pre-formed toxin ingested in contaminated food → N/V, watery diarrhea in 12hr of ingestion, minimal systemic sx (except botulinum), relief in 36 hrs; Stools have no blood or WBCs

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11
Q

• Describe GE caused byStaphylococcus aureus:

A

o MC food poisoning, dt food-handlers; Custard, milk products, potato salad, salad dressing, coleslaw, processed meat/fish at room temp
o Ssx: sudden severe vomit 2-6 hr after ingesting, explosive diarrhea, abd. cramps, rare fever; last 3-6 hours, usu complete recovery

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12
Q

• Describe GE dt Bacillus cereus:

A

o spore-forming, in soil, survive high heat of cooking; usu contaminated rice or meat
o 2 distinct syndromes:
o Emesis: 2-6 hrs after ingestion, severe vomit, abd. pain w or wo diarrhea; no fever, no systemic sxs
o Diarrhea: 8-16 hrs; foul smelling, profuse w nausea, abd pain, tenesmus
o resolves in 12-24 hours

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13
Q

• describe GE dt Clostridium perfringens:

A

o spore-forming anaerobe, in feces, soil, air, water; most toxin synthesized before ingestion, additional produced in GI; beef, beef products, poultry; food inadequately pre-cooked, reheated before served
o ssx: watery diarrhea, foul-smelling w severe, crampy abd. pn, 8-16 hr after ingestion
o self-limited, resolves in 24-36 hrs

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14
Q

• describe GE dt Clostridium botulinum?

A

o 3-exotoxin types (A, B, E); 1/3 deaths from food borne dz.
o A, B: improperly prepared home-canned non-acidic food (string beans, corn, mushroom, spinach, olives, beets, asparagus)
o E: smoked freshwater fish
o Boiling in water for 15 min can inactivate exotoxin
o Ssx: incubation 4 hr- 8 d after ingesting
o phase 1: vague, short period fatigue, N/V, abd cramps, diarrhea
o 2: visual, diplopia, ↓ acuity, PERRLA, ptosis
o 3: neuro, descending weakness or paralysis, dysarthria, dysphagia, weakness of trunk and extremities, sensorium unaffected, norm or ↓ temp; blood, urine, CSF normal
o 65% mortality 2-9 d after ingestion; with tx., < 10%- supportive to prevent respiratory impairment
o Ddx: polio, encephalitis, M gravis, curare, belladonna poisoning

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15
Q

• How does enterotoxin cause GE?

A

o Bacterial cytotoxin, specific for mucous membrane of intestine (in vivo). ↓intestinal absorption, ↑secretion water, electrolytes →watery diarrhea

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16
Q

• Describe GE dt cholera and non-cholera vibrio:

A

o endemic in Asia, fecal contaminated water or food, saltwater crabs and freshwater shrimp. incubation 1-3 d after ingestion
o ssx: sudden, painless, profuse, large volume, watery diarrhea, no blood or mucus, usu no fever vomit tenesmus
o water and electrolyte loss → thirst, oliguria, muscle cramps, weakness, cold, cyanotic skin, dehydration, hypotension, tachycardia
o recover in 7-10 w rehydration; fatal in > 50% untx severe cases

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17
Q

• describe GE dt Enterotoxigenic Escherichia coli:

A

o diarrhea dt tissue invasion or enterotoxin
o fecal/oral, contaminated water or food, traveler’s pathogen
o Incubation: 1-3 days
o SSX: Profuse, watery diarrhea, lasts 3-5 days

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18
Q

• Describe GE dt Clostridium difficile ( “C diff”)

A

o overgrowth of intrinsic organisms (post antibiotic) or infx by external source (soil, water, pets) →pseudomembranous colitis; common nosocomial dz, or iatrogenic after abx
o Ssx: watery diarrhea, cramping abd pain. N/V rare.

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19
Q

• What is toxin megacolon?

A

o Complication of C diff → pseudomembranous colitis
o Other possible causes: UC, Crohn’s, Entamoeba histolytica, Yersinia infx
o Dilated colon w fever, abd pain, tachycardia
o PE: tender abdomen, absent BS
o Work-up: ↑ WBC, distended bowel on xray. Colonoscopy is contraindicated (risk of perforation, sepsis, septic shock)

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20
Q

• What is mucosal invasion by microorganisms?

A

o by ingested organism → microscopic ulceration, bleeding, exudates, secretion of electrolytes and water
o Stool has WBCs, RBCs. mb gross bloody or watery diarrhea
o watery: > 1 L/d; usu no fever, h/a, myalgia, arthralgia
o bloody: usu abd pn, tenesmus, N/V, fever, malaise
o fever and prostration common

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21
Q

• describe GE dt salmonella mucosal invasion:

A

o undercooked chicken or eggs, unpasteurized milk, contact w reptiles
o requires large inoculum to produce infx → exudative diarrhea; (also enterotoxin causes secretory diarrhea)
o ssx: watery diarrhea mc, mb bloody, h/a, malaise, N/V, abd. pain 6-48 hr after ingestion, may have fever
o usu self-limited to 7 days

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22
Q

• describe GE dt Campylobacter jejuni and fetus mucosal invasion:

A

o mc bacterial cause of bloody diarrhea in US; pork, lamb, beef, milk products, water, infx pets
o incubation period 1-7 d
o ssx: mb prodrome of h/a, myalgia, malaise for 12-24 hr, then severe abd pain, ↑ fever, profuse watery diarrhea, then bloody diarrhea
o usu self-limited to 7-10 d

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23
Q

• describe GE dt Shigella mucosal invasion:

A

o mc 6 mos - 5 yrs; food, water, milk; person to person; highly contagious with very small inoculum
o ssx: incubation 1-3 d; usu start low abd pn, diarrhea; fever in 50%; many have biphasic illness 1) fever, abd. pain, diarrhea; 3-5 days, 2) rectal burning, tenesmus, small volume bloody D
o Course: variable, kids resolves in 1-3 d; adults resolves in 1-7 d

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24
Q

• describe GE dt Enterohemorrhagic Escherichia coli mucosal invasion:

A

o E. Coli 0157:H7 strain, produces Shiga toxin; bovine reservoir → beef, unpasteurized milk; fecal-oral toddlers diapers; usu affects several people (anyone else sick?)
o Ssx: acute onset severe abd cramps, watery diarrhea >16 hr after ingestion →bloody in 24 hr. 1-8 days if uncomplicated
o Comp in 5%: hemolytic-uremic syndrome (HUS) → hemolytic anemia, thrombocytopenia, acute renal failure
o thrombotic thrombocytopenic purpura (TTP) → HUS, fever, neurological deficits

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25
Q

• describe GE dt Yersinia enterocolitica mucosal invasion:

A

o pork, unpasteurized milk, water
o ssx: watery or bloody diarrhea and fever
o May mimic appendicitis (RLQ pn, fever, vomit, leukocytosis) if infx in terminal ileum. AKA “acute ileitis”

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26
Q

• What is Traveler’s Diarrhea?

A

o Aka Turista. GE dt organism endemic to locale visited (water, food)
o Enterotoxigenic E coli mc, also norovirus
o Ssx: N/V, borborygmi, abd pain/cramps, diarrhea, onset 12-72 hr after ingestion
o Usu self-limiting, fever and bloody diarrhea suggest more serious dz

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27
Q

• What are the parasitic infxs?

A

o Giardia lamblia
o Cryptosporidium parvum
o Entamoeba histolytica
o Isospora, microsporidia, esp immunocompromised

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28
Q

• Describe Giardia lamblia infx:

A

o Fecal-oral, water, person to person (daycare), traveling (esp low IgA, hypochlorhydria, malnutrition), ingestion of cysts which break down releasing organism
o Ssx: inc 7 d, mb asx, mild watery diarrhea, abd bloating, cramps, flatulence for 1-3 wk, stools bulky, foul smelling
o Course: mb self-limiting, chronic or recurrent dz (celiac-like lesion →lactose intolerance and malabsorption), fatigue, wt loss

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29
Q

• Describe Cryptosporidium parvum infx:

A

o Common in HIV, immune-compromised, daycare; water, food, pets (esp cats)
o Ssx: immune competent: profuse, watery diarrhea, anorexia, lo fever 5 days after ingestion; usu self-limited, lasts ~2wks
o immune-compromised: mb chronic, watery diarrhea, up to 17/d, → dehydration

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30
Q

• describe Entamoeba histolytica infx:

A

o endemic, travel, fecal-oral
o institutionalized pt, HIV, AIDS, immune-compromised
o cysts ingested, released → ulcers like IBD
o ssx: mild: crampy, abd pn, intermittent diarrhea
seere: bloody diarrhea, abd pn, tenesmus, fever, toxic megacolon

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31
Q

• example of Fungal overgrowth:

A

o Basidiobolomycosis: SE US. Contaminated food or dirt

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32
Q

• What is Drug and Chemical-related Gastroenteritis?

A
o	Many agents and drugs → N/V, diarrhea 
o	Pharmaceuticals: antacids, antibiotics, antihelminthics, colchicine, digoxin
o	Heavy metal poisoning
o	Laxative abuse
o	Poisonous mushrooms or plants
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33
Q

• What is inflammatory bowel dz?

A
o	Crohn’s and UC
o	Dt loss of tolerance to normal flora 
o	Triggers: ↑intestinal permeability: tight junctions defect dt pathogens or inflammatory mediators (cytokines, chemokines, TNF, etc)
o	Imbalanced microflora	    
o	Psychological stress exacerbates
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34
Q

• What is crohn’s dz?

A

o Aka Regional enteritis
o Chronic transmural inflammation of colon, involves mesentery and regional LN. May involve entire GI tract from mouth to anus, rare: stomach, duodenum, esophagus; w “skip lesions” (normal)
o Early mucosal involvement = longitudinal and transverse aphthous ulcers (cobblestone appearance). → deep fissures, sinuses and fistulas
o Typical pattern is intermittent exacerbations and periods of remission, worse w stress

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35
Q

• What is etio and risk factors for crohn’s?

A

o Unknown, genetic (assoc NOD2/CARD15), infx, immunologic, psychological…
o Smoking
o OCP, 2x risk
o diet: diary, refined sugar, ↓ fiber, ↑ animal fat
o dysbiosis, abx
o inflamed appendectomy early in life

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36
Q

• what is incidence of crohn’s?

A

o bimodal: peak 15-25, smaller peak 55-65
o 40
o 2-4X in Jewish, also higher in Caucasians
o inc in higher socioeconomic group, Type A personality
o F slightly >M

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37
Q

• What are ssx of crohn’s? PE?

A

o RLQ pain, steady, localized, fatigue
o Occult blood, in stool if colonic involvement (less common that UC)
o Stool: formed, or loose if extensive colonic involvement or terminal ileum,
o Fat malabsorption (steatorrhea) ↑ risk of gallstones, renal oxalate stones
o 1/3 have perianal dz: fissures, fistulas, perianal abscess
o PE: RLQ tenderness w assoc fullness or mass. Abdominal distention, fever, wt loss

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38
Q

• What are the 4 sx patterns w crohn’s?

A

o inflammation: RLQ pn, tender, like appendicitis (esp in young)
o obstruction: severe colic, abd distention, constipation, vomit
o diffuse jejunoileitis: both inflam and obstruction → chronic debility
o abd fistulas and abscesses: usu late, fever, painful masses, wasting

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39
Q

• what are complications of Crohn’s?

A

o Intestinal obstruction. initial from edema and inflammation, esp ileum= reversible. → fibrosis → constipation, intractable obstruction from fixed luminal narrowing
o Fistula → indolent abscess, malabsorption, cutaneous fistula, persistent UTI or pneumaturia (Enteroenteric, enterovesical, enterovaginal, enterocutaneous, retroperitoneal)
o Perforation, hemorrhage: rare, dt thickened mucosa
o ↑ risk SCC

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40
Q

• What are labs for crohn’s? ddx?

A

o CBC: mild anemia, leukocytosis
o ↑ESR, CRP (higher than in UC)
o ↓serum iron, low vit B12
o + fecal lysozyme
o Serology: ASCA (higher in Crohn’s), ANCA (higher in UC)
o Ddx: IBS, lactose intolerance, Infx colitis, UC, appendicitis, diverticulitis, Carcinoma

41
Q

• What imaging is done for crohn’s?

A

o plain film, double-contrast barium enema exam
o single-contrast upper GI series w SI follow-though barium x-ray: irregularity, nodularity, stiffness, thickening of terminal ileum, narrowed ileum lumen. Adv: string sign=marked stricture of ileum
o CT and double-contrast SI. US and MRI as adjuncts if radiation an issue
o Colonoscopy: “skip areas”, “cobblestone appearance”, longitudinal ulcers, rectal sparing, narrowing, fistulas
o 50% have pathognomonic sarcoid-type epitheloid granulomas in intestinal wall, st involved mesenteric nodes

42
Q

• What is ulcerative colitis? Ulcerative proctitis?

A

o chronic, recurrent inflammatory, in colon or rectal mucosal layer
o superficial ulceration of colon usu involves rectum (95%)
o continuous involvement w any other portion of colon (NO skip areas)
o UP: common, limited form, localized to rectum

43
Q

• What is etio and risk factors for UC?

A

o abn humoral and cell-mediated immunity, or generalized ↑ reactivity against intestinal bacterial ags. AI serum and mucosal abs vs intestinal epithelial cells
o mb genetic (chrom 12 and 16), st pos FHx
o mb environmental factors
o diet: dairy, refined sugar, ↓ fiber, ↑ animal fat
o smoking is negatively associated with ulcerative colitis (reverse in Crohn’s)

44
Q

• what is incidence of UC?

A

o 2-4x in Jewish, also higher in Caucasians
o M slightly >F
o Bimodal: peak 15-25 and 55-65 yrs (or any age)

45
Q

• What are ssx of UC?

A

o Mild to severe
o Cramping abd pain
o Series of attacks of bloody diarrhea w asx intervals, insidious, ȑ urgency, low abd cramps, blood and mucus
o if confined to recto-sigmoid area, stool mb normal, hard, dry w rectal d/c of mucus, RBCs, WBCs
o if proximal, stools looser, 10-20/d w severe cramps, rectal tenesmus. Watery stools with pus, blood, mucus
o Systemic: malaise, fever, anemia, wt loss

46
Q

• What are complications of UC? Px?

A

o Hemorrhage mc
o Toxic megacolon: markedly distended colon (ballooning, >6 cm) w attenuated walls, severe: immediate danger of perforation
o Mb dysplasia w ↑ risk colon cancer, inc 0.5-1% per year
o Px: usu controlled w tx, lifelong exacerbations and remissions. Severe: surgery required

47
Q

• What are labs for UC?

A

o CBC: anemia, plt >350,000/mL
o ↑ ESR, CRP
o CMP: hypoalbuminemia, hypokalemia, hypomagnesemia, ↑alk phos
o Stool: organisms (clostridium, salmonella, shigella, E coli, yersinia)

48
Q

• What imaging is done for UC?

A

o Plain abd film: colonic dilatation in severe suggests toxic megacolon. Mb perforation, obstruction, ileus
o Barium enemas in mild case only. narrow, tubular, shortened colon w loss of haustral folds, pseudopolyps, small ulcers; “lead pipe” appearance (caution, barium enemas may precipitate toxic megacolon in severe cases)
o flexible sigmoidoscopy: to dx
o colonoscopy w bx: confirms Dx. see extent of dz, monitoring dz activity, watch for dysplasia, CA. risk perforation w severe dz

49
Q

• what are extra-intestinal manifestations of IBD (Crohn’s and UC)?

A

o Jts: Peripheral arthritis, Sacroiliitis, Ankylosing spondylitis
o Skin: Erythema nodosum, Pyoderma gangrenosum
o Eyes: Conjunctivitis, Iritis, Episcleritis
o Liver: Fatty liver, Chronic active hepatitis, Pericholangitis, Sclerosing angitis, Bile duct carcinoma
o Kidneys: Pyelonephritis, Urolithiasis
o General: amyloidosis

50
Q

• What are extra-intestinal manifestations of Crohn’s?

A
o	Cholelithiasis
o	Renal oxalate stones
o	Vitamin B12 def
o	Obstructive hydronephrosis
o	Aphthous ulcers
51
Q

• What is IBS?

A

o aka: Functional Dyspepsia, Spastic Colitis, Mucous Colitis
o Dx of exclusion: over-dx, too hastily
o Mc of all GI dos, up to 50% of pt to gastroenterologist
o Counseling is helpful dt pt frustration w problem

52
Q

• What are (postulated) etio of IBS?

A

o Changes in GI motility (↑ luminal contractions, motor activity)
o Hypersensitive visceral afferent nerves of gut
o ↑ mast cell in gut, release local histamine
o Colonic mm hyper-reactivity, neural, immune changes in S/L I may persist after gastroenteritis
o abn glutamate activation of N-methyl-D-aspartate (NMDA) receptors, activate NOS, neurokinin receptors, induce calcitonin gene-related peptide
o limbic system, emotion, autonomic response ↑ bowel motility, ↓gastric motility, more in ppl w IBS than normal
o HPA. ↑ hypothalamic corticotropin-releasing factor (CRF) → alter motility, dt stress. CRF antagonists eliminate these changes.
o SIBO in >50%, →bloating, gaseous distention.
o Diet: ↓fiber, intolerance to lactose (diarrhea) and other sugars, (glucose intolerant, milk intolerant (casein) → congestion, bronchitis, asthma, mucus; gluten
dd

53
Q

• What is AGA (2004) dx criteria or IBS?

A

o w/o red flag/alarm features or positive screening studies, additional dx test usu not necessary. RF:
o sx onset > 50
o severe, unrelenting diarrhea
o nocturnal sxs
o unintentional weight loss
o hematochezia
o FHx organic GI dzs (IBD, celiac sprue, CA)

54
Q

• What are Rome III (2006) dx criteria for IBS?

A

o recurrent abd pn or discomfort at least 3 days/month in past 3 mos, assoc w 2+ of following:
o relieved by defecation
o onset assoc w change in stool frequency
o onset assoc w change in stool form or appearance

55
Q

• what is clinical picture of IBS (chronicity of these sxs)?

A

o crampy abd pain
o constipation, diarrhea, both, or alternating
o ↑ colonic mucus production
o flatulence, bloating/distention, nausea, anorexia
o anxiety or depression
o sxs related to stress
o appearance of health

56
Q

• what is PE for IBS? Imaging?

A

o PE: Diffuse abd tenderness over colon, some areas worse, or fullness
o x-ray: altered GI motility (spasm)
o sigmoidoscopy: ↑mucus & spasm (or often nothing)

57
Q

• What labs are done for IBS?

A

o only to confirm other possible dx
o CBC: anemia, inflammation, and infection
o CMP: metabolic dos, r/o dehydration, electrolyte abn w diarrhea
o hemoccult test
o stool: complete GI health panel, lysozyme test normal
o hydrogen breath tests for lactose intolerance
o celiac testing

58
Q

• How can you confidently dx IBS?

A

o identify typical sxs, complete PE, and exclude alarm features.
o if alarm features → more detailed work-up by predominant sxs
o If tx not success → more extensive work-up
o Celiac mb more prevalent in pts w suspected IBS
o > 50 w IBS sxs → colonoscopy for CA screen

59
Q

• What is SIBO?

A

o ↑ # (>105/ml) or type of bacteria in SI → fermentation, inflammation, malabsorption. Ferm gas: hydrogen, methane
o Enteric toxins produced: ammonia, D-lactic acidosis, bacterial endotoxin stimulating cytokine release
o Mb Carb, protein, fat, B12 malabsorption
o Organisms: Streptococci, Bacteriodes, Escherichia, Lactobacillus, Clostridium, Klebsiella

60
Q

• What can prevent SIBO?

A

o Antegrade peristalsis, gastric acid, bile, proteolytic enzymes, sIgA, intact ileocecal valve

61
Q

• What can cause SIBO?

A

o Anatomical anomalies: stricture, diverticula
o Insufficient enzymes: hypochlorhydria, PPI use, ↓ bile salts
o Abnormal motility: obstruction, DM, scleroderma, Crohn’s, radiation damage, opiates
o Abnormal communication bw S/L I: fistula, defective valve
o Other: immunocompromised, alcoholism, cirrhosis, pancreatitis

62
Q

• How may SIBO pt present? Hx. Ssx.

A

o Hx: transient improve after abx, worse w probiotic/prebiotic, worse w more fiber
o Ssx: abd pain/cramps, borborygmus, eructation, flatulence, bloating, watery diarrhea may alt w constipation, dyspepsia, vomiting, heartburn, wt loss, steatorrhea, systemic sxs (HA, joint pain, fatigue, rosacea

63
Q

• What is PE for SIBO? Work-up?

A

o PE: surgical scar? Abd distention, succussion splash
o CBC: macroscopic (B12) or microscopic anemia, ↓ ferritin
o Glucose Breath Hydrogen analysis (H2)
o C14-d-xylose breath test (Methane)
o Jejunal aspirate during endoscopy

64
Q

• What is incidence of diverticular dz?

A

o ↑ w age: 70; 66% >85

o Common in industrialized western society

65
Q

• What is diverticulosis?

A

o Sac-like outpouchings of colon sub/mucosa, mc in sigmoid
o Dt factors that chronically ↑ intraluminal P: ↓ fiber, ↑ refined carbs
o Usu asx (up to 70%)
o Mb chronic or intermittent LLQ pain; often constipation
o Mb rectal bleeding if erosion of mucosa
o often observed on barium studies
o 20% progresses to diverticulitis

66
Q

• what is diverticulitis?

A

o inflam 1+ diverticula, may → obstruction, perforation, abscess, fistula
o may heal spontaneously, or enlarge and adhere to adjacent organs (bladder, vagina)

67
Q

• what is etio of diverticulosis/itis?

A

o ↓ fiber diet is highest risk factor → low-bulk stool → ↑intra-luminal P, form diverticula
o Diet: ↑ fat and grain-fed beef
o Genetic: Asians on R side, westerners usu L side
o Aging → change in collagen structure
o Colonic motility dos
o Corticosteroids ↑ risk (not NSAIDs)
o Colonic segmentation: non-propulsive contractions → isolated segments, little chambers w ↑ P
o Defects in colonic wall strength

68
Q

• What are ssx of diverticulosis?

A

o Usu asx, mb recurrent LLQ tenderness, flatulence

o Mb hx painless rectal bleeding

69
Q

• What are ssx of diverticulitis?

A

o LLQ pn, steady, severe, deep
o fever/chills, N/V
o previous episodes dull, colicky, diffuse abd pain w flatulence, distention, change in BM (initially diverticulosis)
o altered BM: diarrhea, constipation, tenesmus
o Rectal bleeding: bright red or wine-colored stools; sudden onset, painless, w urge to defecate, usu massive, stop spontaneously

70
Q

• What are concominatnt and complication sxs of diverticulitis?

A

o Con: Dysuria, pyuria, urinary frequency if bladder or ureter irritated
o Comp: if perforation or fistula
o Pneumaturia (gas, “air” in urine), recurrent UTIs (colovesicular fistulas)
o Feculent vaginal d/c (fistulas w uterus, vagina)
o Severe, general abd pn, absent BS, fever (diffuse peritonitis)
o Back or lower extremity pain (perforation)

71
Q

• What is PE for diverticulitis?

A

o Local abd tenderness, rebound tenderness, mb mass
o Vitals, determine hemodynamic stability
o ↓ fever
o DRE: tenderness, color of stools, presence and extent of GI bleeding
o Proctoscopic exam: mass in cul-de-sac

72
Q

• What is ddx for diverticulitis? Imaging?

A

o Ddx: hemorrhoids, anal fissures (pn w defecation); UTI, nephrolithiasis, obstruction, colon CA
o Hx weight loss and mucus in stool indicates IBD
o Image: sigmoidoscopy: narrowing and inflammation
o barium x-ray hazardous in acute phase, may cause perforation

73
Q

• what is meckel’s diverticulum?

A

o Congenital bulge in distal ileum, remnant of omphalomesenteric duct
o 2% pop, M>F
o Usu asx, mb bleeding, obstruction, volvulus, intussusception, Acute mb like appendicitis

74
Q

• What are general ssx of malabsorption syndromes?

A

o Chronic diarrhea, steatorrhea, bloating, weight loss, amenorrhea
o Macrocytic anemia (B12); microcytic anema (iron); easy bruising (Vit K and C); edema (protein); glossitis (B vits, iron); night blindness (vit A); bone pain/fractures (K, Mg, Ca, Vit D); muscle spasm (Ca, Mg); peripheral neuropathy (B 1,6,12)

75
Q

• What is malabsorption dt insufficient digestive elements?

A

o ↓ pancreatic/liver enzymes, bile salts, HCl

o post-surgical syndromes, biliary obstruction, cystic fibrosis, etc

76
Q

• what is Carbohydrate intolerance?

A
o	Enzyme deficiencies mb congenital (rare), primary or secondary
o	Disaccharides (lactase, maltase, isomaltase, sucrase) normally split to monosaccharides by duodenal enterocytes’ enzymes
o	Lactose is dt Lactase deficiency
o	Def → ↑ osmotic load, watery diarrhea; fermentation → gas (H2,CO2, methane), flatulence, distention, abd pain
77
Q

• What is epidem of lactose intolerance?

A

o Acquired lactase def MC
o US: 80% blacks and Hispanics; ~100% Asians, 25% N Euro whites
o Worldwide: >75% mb lactose-deficient. Very common in Asian, South American, African

78
Q

• What is etio of lactose intolerance?

A

o Congential: AR (rare)
o Primary: ↓ lactase, develops after childhood
o Secondary (acquired): dt SI mucosal damage: acute gastroenteritis, ascariasis, carcinoid, celiac, chemo, Crohn’s, diabetic gastropathy, gastrinoma, giardiasis , HIV enteropathy, Kwashiorkor, radiation enteritis, tropical sprue, Whipple syndrome

79
Q

• What are ssx of lactase def?

A

o Varias, minor abd discomfort, bloating to severe diarrhea dt even small amounts of lactose
o watery diarrhea, abd bloating and pain, flatulence, nausea, borborygmi

80
Q

• what labs are done for lactase deficiency? Ddx?

A

o hydrogen breath test: test of choice; lactose given after 8hr fast → collect expiration every 30 mins for 3 hrs. (+) = ↑ by > 20 ppm
o dietary elimination: elim lactose foods → sxs resolve, return w reintroduction
o ddx: IBS

81
Q

• what is tropical sprue? Etio?

A

o Residents, natives, prolonged visitors (>1mo) of Caribbean, S India, SE Asia; may improve after moving from tropics, or reappear years later (all dt vit/min deficiencies)
o Etio: unknown, mb SI chronic infx by toxigenic coliform bacteria → folate, B12, iron malabsorption

82
Q

• What are ssx of tropical spru? PE? Ddx?

A

o acute phase: diarrheam fever, malaise
o chronic phase: diarrhea, nausea, anorexia, abd cramps, steatorrhea, paresthesias
o PE: vit def signs: glossitis, stomatitis, cheilosis, cutaneous hyperpigmentation, dry rough skin, abd distention, tenderness, edema (late), weight loss, dehydration
o Ddx: GI infx (giardia, E hist, etc), intestinal lymphoma, AIDS, Celiac, pancreatitis

83
Q

• What is work-up for tropical sprue?

A

o No definitive marker exists
o CBC: megaloblastic anemia (60%)
o Stool: fecal fat > 6 g in 24 hrs is (+) fat malabsorption). Fatty stools usu observed when fat content >15 g
o CMP: ↓serum protein, calcium, phosphorus, cholesterol, prothrombin, hypochlorhydria, check pancreatic function
o D-Xylose absorption test: 25 g D-xylose orally. In well-hydrated patients with normal renal function (+) for mucosal malabsorption
o 5-hr urine collection < 4 g
o 1-hr serum collection < 20 mg/dL
o Endoscopy: characteristic histology

84
Q

• What is celiac dz?

A

o Aka Celiac Sprue, Nontropical Sprue, Gluten Enteropathy
o AI reaction to gluten proteins → mucosal damage; Environmental trigger = gluten; Autoantigen = tissue transglutaminase
o Elimination of environmental trigger → complete resolution

85
Q

• What is epidemiology of celiac?

A

o ↑ in US and Europe; 0.5-1% pop.
o Higher prev in pp w GI sxs (1/56), w first-degree relative w celiac (1/22)
o ↓ in blacks, Hispanic, Asian
o any age, but peaks in 40s
o F:M, 2:1
o Genetics: Most all pts express human leukocyte antigen (HLA-DQ2 or HLA DQ8), facilitate immune response against gluten

86
Q

• What is pathophysiology of celiac?

A

o Gliadins and glutenins → CD4 cells w HLA-DQ → cytokines, B cell clones → lymphocyte-mediated destruction of proximal SI mucosal villi.
o →vitamins, minerals, Ca+2, CHO, protein, fat malabsorption
o T cells may react w TGT (principal component of endomysium autoantigen) →inflam events →characteristic celiac mucosal lesion

87
Q

• What are risk factors for celiac?

A
o	Heredity
o	Type 1 DM
o	Early introduction of gluten in infant diet
o	Down’s
o	no breastfed
o	Chronic Fatigue Syn
o	Crohn’s
o	AI thyroid dz
o	Viral may trigger immunologic response (Adenovirus type 12 implicated)
88
Q

• What are some gluten containing foods?

A

o Wheat, wheat bran, Kamut, Spelt, triticale, bulgar, couscous, semolina
o Barley, malt, malt extract
o Rye
o Some may not tolerate oats: React to avenin, or cross-contamination w gluten

89
Q

• When should you screen for celiac?

A
o	Unexplained iron deficiency
o	early onset osteopenia
o	unexplained epilepsy
o	failure to thrive,
o	poor glucose control
o	chronic diarrhea
o	infertility
o	miscarriages
o	↑ liver enz
90
Q

• What are ssx of celiac? In infants?

A

o Mb asx
o Classic: diarrhea, steatorrhea, bloating, flatulence, vit/min def,
o Atypical: extraintestinal signs: anemia, dermatitis herpetiformis, DM, aphthous stomatitis, neuro, osteopathy
o <2: st more fulminant, chronic diarrhea (miserable, pale), abdominal distension, failure to thrive (↓weight, fat, hair thinning), anorexia, vomiting, psychomotor (muscle wasting), hypoproteinemia, acidosis

91
Q

• What are ssx of celiac in kids and adults?

A
o	Kids (avg 4): diarrhea or constipation, anemia, short stature, osteoporosis, aphthous ulcers
o	Adults: st intestinal, diarrhea or constipation, anemia, aphthous ulcers, sore tongue and mouth (mouth ulcers, glossitis, stomatitis), dyspepsia, abd pain, bloating (weight loss), fatigue, infertility, neuropsychiatric (anxiety, depression), bone pain (osteoporosis), weakness (myopathy, neuropathy), dermatitis herpetiformis
92
Q

• What is lab work-up for celiac?

A

o CBC: Anemia (microcytic, hypochromic/normocytic, normochromic w RDW), Leukopenia
o CMP: ↑ AST; ↓Albumin/plasma protein; ↓cholesterol (total, LDL, HDL), ↑ALP
o Serology: Serum IgA, serum IgA a-endomysial Abs (IgA EMA)
o IgA tTG (>100): mc sero test, cheap (ELISA)
o Deamidated gliadin peptide (DGP) IgA and IgG: ↑sn &sp, esp in elderly who have normal standard tests

93
Q

• What are sn, sp, and method for the IgA celiac tests? What if there’s IgA deficiency?

A
o	Gliadin (not used anymore): 57-100, 42-98, ELISA
o	Endomysial: 75-98, 96-100, Indirect IF
o	tGT: 98-100, 97-98, ELISA
o	def: in 8%, IgG EMA and tGT can be used
94
Q

• what procedures are done for celiac dx?

A

o ↓Bone mineral density
o Dx by SI bx: need 4+ samples from jejunum and ileum, must eat gluten past 2-4+ wks
o histo = characteristic villous atrophy

95
Q

• what is ddx of celiac?

A
o	Anorexia nervosa, AI enteropathy
o	Crohn's 
o	Giardiasis
o	HIV enteropathy, Hypogammaglobulinemia
o	Infx GE, Intestinal lymphoma, IBS, Ischemic enteritis
o	Lactose intolerance
o	Pancreatic insufficiency
o	SIBO, Soy protein intolerance
o	Tropical sprue, TB
o	Whipple's disease
o	ZES
96
Q

• What is non Non-Celiac Gluten Intolerance? Dx?

A

o mb similar sxs, WITHOUT villous atrophy
o (-) IgA tTG
o Bx (-)
o (+) Gliadin Ab (IgA or IgG) (immune rxn to gluten)
o Total IgA normal

97
Q

• What is whipple’s dz?

A

o rare, multisystem, dt bacterium Tropheryma whipplei

o diarrhea, weight loss, arthralgia, fever, malabsorption

98
Q

• what is short bowel syndrome?

A

o malabsorption from surgical bowel resection (esp jejunum)