GI clinical Flashcards
Sx: Dysphagia to solids and liquids, regurgitation, chest pain, wt loss
manometry (gold-standard):
1) complete absence peristalsis
2) incomplete relaxation LES
Barium swallow: bird’s beak appearance
Dx?
Tx?
Dx: achalasia
Tx:
- -dilation of esophagus (risk perforation)
- -surgical myotomy
- -Botox
- -pharmacologic tx usually ineffective
ddx: exclude malignancies of esophagus and pleura; chagas disease
Sx: Dysphagia (liquids), heartburn, chest pain
- manometry: triple peaked contraction, inc. wave amplitude and duration
- barium swallow: corkscrew esophagus
- EGD: normal
Dx?
Tx?
DDx?
Dx: diffuse esophageal spasm
Tx:
- nitrates
- Calcium Channel Blockers
- Botox when LES pressure is high
Ddx:
- GERD
- cardiac chest pain
- panic attacks
50yo diabetic man presents with bloating, nausea, vomiting after meals.
gastric empyting scan shows delayed gastric emptying. EGD is normal.
Dx?
Tx?
Dx: delayed gastric emptying due to gastroparesis (common in diabetics!)
Tx: prokinetics, botox pyloric sphincter, frequent small meals
Other causes of delayed gastric emptying: outlet obstruction due to pyloric stenosis,extrinsic compression (pancreatic cancer), mass lesions of stomach
Sx: abdominal distension, vomitng, abdominal pain
Hx: diabetes or scleroderma
Dx?
Dx: chronic idiopathic intestinal pseudoobstruction
6 wk old infant fails to move bowels and has had problems since birth.
barium enema:
anal manometry: incomplete relaxation of internal anal sphincter on
rectal biopsy
Dx?
Tx?
Dx: Hirschprung’s diseae
Tx: resection aganglionic segment of colon
35 yo women presents with constipation since the birth of her last child. She has 4 children.
anorectal manometry
defogram
Dx: outlet obstruction due to pelvic floor dysfx (failure to relax of puborectalis muscle)
Tx; correct underlying etiology, find bowel regimen that works
40 yo nulliparous woman presents with change in bowel habits and constipation for the last 6months. She currently does not take any medications.
colonoscopy: normal
anorectal manometry: normal
Thyroid hormone levels: normal
Dx?
Tx?
Dx: chronic idiopathic constipation
Tx: diet, fluids, exercise
consider fiber supplement or laxatives
24yo woman presents with abdominal pain and distension and diarrhea for the past 3 months. She reports the pain decreases after a bowel movement and that she sometimes passes mucus. She has no history of lactase deficiency. she has no recent weight loss, no blood in stool. She dislcoses that she has been sexually abused in the past.
She is not taking any meds.
lactulose test is normal
Stool exam cis negative for ova and parasites, leukocytes or excessive fat
Dx: Irritable bowel syndrome
Tx: symptoms, form positive relationship, fiber, anticholinergics
35 yo male presents with pain with swallowing. Pt has AIDS.
X-ray shows cobblestone esophagus
Dx?
Odynophagia due to esophageal moniliasis
50 yo female presents with chest pain. Cardiac chest pain has been ruled out. Pt has been a smoker for 20 years and drinks 3 beers per day. 24 hour pH monitoring test shows dec. pH after meals and at night.
Dx?
Tx?
complications?
Dx: GERD
Tx: avoid exacerbating factors, acid suppression therapy, smoking cessation
• Complications GERD:
o Esophagitis
o Peptic stricture
o Esophageal hemorrhage
o Esophageal ulcer
o Pulmonary sx
o Barrett’s esophagus: intestinal metaplasia above GE junction
55yo male presents with difficulty swallowing. He feels like food gets caught in his throat. This happens with solid foods only and it has been getting worse for the past 6 months. He’s also noticed that he’s lost 10lbs in the last month.
suspected Dx?
Biopsy shows intesinal metaplasia above the GE junction, suspected etiology?
Dx: carcinoma
adenocarcinoma: GERD, barret’s esophagus
squamous cell carcinoma: smoking, alcohol
50yo female presents with difficulty swallowing. She has trouble with solids only. Her symptoms have been getting worse for the past 6 months. She has a 10 year history of GERD.
barium swallow shows fixed narrowing
Dx?
peptic stricture
40yo female presents with difficulty swallowing solids only. For the last year she has had brief episodes of trouble swallowing but now it’s difficult all the time.
barium swallow is unremarkable
dx?
Lower esophageal ring (schatzkis)
must include marshmallow bolus to see on barium swallow
30yo male presents with trouble swallowing both solids and liquids. His symptoms come and go and are not present all the time. He has a history of asthma.
endoscopy shows ribbed or feline esophagus
eosinophilic esophagitis
treat with steroids, dietary restriction, dilatation
60yo male presents with chest pain relieved by nitroglycerin. Cardiac cause is excluded. He also notes occasional difficulty swallowing both solids and liquids.
manometry reveals non-peristaltic contractions intermixed with peristaltic contractions
Dx?
Dx: diffuse esophageal spasm
50yo female presents with trouble swallowing to both solids and liquids. Her symptoms have been worsening in the past 3 months. she also notes that she wakes up at night and has trouble breathing.
barium swallow: birds beak, distal esophagus
endoscopy is normal
dx?
tx?
DX: achalasia
Tx; botox, pneumatic dilatation, surgical myotomy
30 yo male presents with heartburn and acid taste in mouth, worse when lying down. He also has trouble swallowing both solids and liquids which has gotten worse in the past 3 wks.
PE: hardened and thickend skin on face, telangiectasia, sclerodactylyl, calinosis cutis
Dx?
scleroderma
assoc. w/ raynauds syndrome
gastric mucosal defenses
o Pre-epithelial: mucus-bicarbonate barrier (mucus neck cells; “mechanical barrier”); surface phospholipids; mucoid cap (micorenvironment for mucosal repair)
o Epithelial: tight junctions; rapid turnover damaged cells; reconstitution (migration of cells along pit to repair small defects); regeneration (cell proliferation to repair larger defects); surface cells maintain neutral pH
o Subepithelial: mucosal blood flow (nutrients to support cell turnover, supply HCO3-, buffer H+)
o Duodenum: bicarb from pancreas
Diagnostic tests for H. pylori
o Serum H. pylori IgG antibody: past but not current infection, pt w/ documented ulcer that is treatment naïve, don’t use to confirm eradication
o Urease breath test: pt ingests radiolabeled urea, H. pylori will hydrolyze yielding labeled bicarb which is exhaled in lungs as CO2; *Positive test=active infection!; False negs due to PPI, bismuth, antibiotics
o Biopsy gastric mucosa: H&E, Urease test; PCR
o Stool antigen test: detects active infection!; can be used to confirm eradication
pathogenesis of NSAID ulcers
o Direct: high intracellular conc are toxic to epithelial cells
o Indirect: reduced prostaglandins—decreased mucus and bicarb, reduce epithelial cell repair and regeneration, reduce mucosal flow
complications of peptic ulcer disease
o Bleeding (risk factors: inc. age, cormorbid disease, antiplatelet and anti-coag meds)
o Perforation
o Penetration
o Obstruction
reasons for ulcer peptic ulcer recurrence
failure to eradicate H. pylori, surreptitious use NSAID, tobacco use, malignance, ZE syndrome (hyergastrinemia, hyperchlorhydia)
Peptic ulcer disease therapy
o Meds:
• Acid suppression: H2 receptor antagonists, PPI (acute bleeding, maintenance pts high risk NSAID ulcer)
• Sucralfate: mechanical barrier, promotes ulcer healing
• Bismuth: protects and promotes ulcer healing
• Prostaglandin analogs (Misoprostol PGE1 analog): enhances mucus/bicarb layer, improves mucosal blood flow, side effect: diarrhea, utermine muscle contraction
**• H. pylori: **
• PPI+2 antibiotics (amoxicillin + clarithryomycin)
• PPI or H2RA + bismuth + metronidazole +tetracycline
o Endoscopy:
o Surgery:
• Indications: persistent bleeding, failure endoscopic therapy, perforation, obstruction
pt has bright red blood coming from rectum
• Hematochezia
colonic bleeding or brisk bleeding from proximal sites
pt has black tarry malodorous stool
melena
upper GI bleed (esophagus, stomach, duodenum)
comes from bacterial metabolism of RBC
pt is vomiting red blood (or coffee grounds)
hemetemesis
due to upper GI bleed (esophagus, stomach, duodenum)
Pt has fatigue, light-headedness, dyspnea on exertion
anemia possibly due to occult GI bleed
positive stool hemoccult test
suspect pt has GI bleeding. How can you quickly classify the amount of blood lost?
- Class 1: pulse <100bpm
- Class 2: pulse>100bpm
- Class 3: blood pressure decreased
- Class 4: confused, lethargic
What diagnostic tests are availble for evaluating GI bleed? Upper, small bowel, colon
**o Upper GI: **
• Endoscopy (esophagus, stomach, duodenum, proximal jejunum)
o Small bowel evaluation
• Capsule enteroscopy (ID obscure cause)
• Meckel scan
• Small bowel barium x-ray
• Enteroscopy
o Colon:
• Colonoscopy: not helpful for active GI bleed, ID structural abnormalities, therapy at bleeding source
• Nuclear medicine:
• Red Cell scintigraphy: bleeding at 0.5-.1mL/min
• Sulfur colloid scan (bleeding at .1ml/min)
• Angiography: generally use after positive nuclear medicine scan; therapy
Therapies for Upper GI bleeding
o Pharmacotherapy:
• PPI
• Somatostatin analog (octreotide) given IV for bleeding esophageal varices
• IV erythromycin to enhance gastric motility (endoscopy)
• Vasopressin/telipressin: dec. portal venous flow via splanchnic vasoconstriction, give w/ nitrates to prevent organ ischemia
**o Endoscopic: **
• Injection: dilute epinephrine, saline, sclerosant, alcohol
• Electrothermal: ablate bleeding vessels
• Band ligation for varices
• Argon plasma coagulation: ablate sites of blood loss
• Endoclips to tamponade bleeding vessel
o Interventional radiology:
• Embolization
• Transjugular intrahepatic portosystemic shunt (TIPS): variceal bleeding, refractory esophageal varices, gastric varices
o Surgery: failure of other therapy
Therapies for lower GI bleeding
o Colonoscopy:
• Diagnostic, directs other therapies
• Can’t visualize active bleeding
• Not much therapeutic value
o Nuclear medicine: Red cell scintigraphy, sulfur colloid scan
o Angiography:
• Usually after positive nuclear scan
• Detect low rates of bleeding
• Embolization therapy
o Surgery: failure other therapy, massive, recurrent bleeding
Pt presents with a massive amount of bright red blood from the rectum. Pulse is 115 (class?). You give IV fluid support. Upper GI bleed is excluded by endoscopy. next tests?
Class 2
Next: nuclear medicine scan
(vs if it had been small amount of blood, exclude anorectal source, and evaluate w/ colonoscopy)
Pt presents with vomiting bright red blood. He has a history of cirrhosis and portal hypertension. You suspect bleeding esophageal varices. How would you evalulate and manage this patient?
Evaluate w/ endoscopy]
Therapies:
- Pharm: octreotide
- endoscopic: band ligation, ablation, endoclips
- radiology: TIPS
- surgery: failure of other therapies
features of ulcerative colitis
Ulcerative Colitis
Anatomic location: Colon
Distribution: Continuous from rectum proximally
Granulomas: Absent
Inflammation: Mucosal
Fistula, Abscess, Stricture: Absent
Serologies: pANCA
Smoking: May be protective
Appendectomy: May be protective
Clinical presentation: Small volume bloody diarrhea, tenesmus, urgency
Surgery: Curative (total proctocolectomy)
Monozygotic Twin concordance: 15-20%
features of crohn’s disease
Crohn’s Disease
Anatomic location: Entire GI tract (ileum/colon), perianal disease
Distribution: Skip areas, patchy
Granulomas: May be present
Inflammation: Transmural
Fistula, Abscess, Stricture: May be present
Serologies: ASCA, OmpC, CBir1
Smoking: Increases risk, worsens disease
Appendectomy: May increase risk
Clinical presentation: Variable: abdominal pain, diarrhea, weight loss, fever
Surgery: Not curative
Monozygotic Twin concordance: 20-50%
epidemiology of IBD
o Northern > southern hemispheres
o Industrialized > developing countries
o CD: female predominance
o UC: male predominance
o Caucasians > non-whites
o Inc. rates: AA, Hispanics, Asians
Sx: Hematochezia, diarrhea, constipation, tenesmus, urgency, incontinence, nocturnal awakening, abdominal cramps
PE: Pallor, abdominal tenderness, red blood on rectal exam.
Toxic Megacolon: abd distention, hypoactive bs, tympany
Perforation: hypoactive bs, rebound, guarding
EMI: conjunctival erythema, skin lesions (tender nodules, ulcers), joint tenderness
Dx?
ulcerative colitis
Sx: RLQ pain, diarrhea, fever
PE: Fever, orthostatic hypotension, tachycardia, pallor, cachexia, Abdominal tenderness (esp RLQ)
Dx?
Crohns disease
Iron deficiency anemia (low Hgb/Hct, low MCV, low ferritin, high platelets), elevated CRP/ESR/WBC, low K+/albumin; +pANCA
disease?
ulcerative colitis
Iron and/or B12 deficiency anemia, elevated CRP/ESR, low K+; low fat soluble vitamins (A, D, E, K), elevated PT, low albumin; + ASCA, OmpC, CBir1
disease?
Crohns
endoscopic findings UC
*Continuous from rectum proximally*
Distribution: Rectosigmoid 46%
Left colon 37%
Pancolitis 17%
Mild: erythema, edema, abnormal vascular pattern
Moderate: granularity, erosions, ulcers, friability
Severe: coalescence of ulcers, mucopurulent exudate, spontaneous bleeding, pseudopolyps
Chronic: featureless → mucosal atrophy, muscular hypertrophy, loss of haustra, shortened/narrowed
endoscopic findings crohns
*Patchy, “skip” lesions, rectal sparing
Distribution: Ileum + colon: 35%
Ileum: 28%
Colon: 32%
Perianal: ≤ 30%
Esophageal: <1%
Gastroduodenal: 1-4%
(Peds: 30-40%)
Mild: aphthoid ulcers, edema, hyperemic spots, loss of vascular pattern
Moderate/Severe: deep, linear, stellate, coalescing “bear-claw” ulcers, pseudopolyps; cobblestoning
histologic findings UC
Early: mucosal infiltration by neutrophils, lymphocytes, plasma cells, macs→cryptitis, crypt abscesses
Chronic: key to distinguish from acute colitides → Paneth cell metaplasia, crypt distortion/branching, basal lymphoid aggreg, chr. inflamm. infilt.
histo findings of crohns
mucosal infiltration by neutrophils, lymphocytes, plasma cells, macs→cryptitis, crypt + non-caseating granulomas
Gross pathology: transmural inflammation, fistulas, strictures; creeping fat
radiographic findings UC
Barium Enema: granularity, ulcers, thickened folds → loss of haustra from relaxation taeniae coli →“lead-pipe”/shortened colon, strictures/ca, dilation, widening of presacral space
CT: diffuse/symmetric thickening, dilation, perforation, EMI
MR/CT colonography
radiographic findings crohns
Small bowel series/Enteroclysis: lymphoid hyperplasia, granularity, fold/wall thickening, ulceration, cobblestoning, polyps, fistulae, stricture (“string sign”)
CT: ileal/colon thickening, fat stranding, “halo” sign, abscess, obstruction, EMI
CT/MR enterography (negative/neutral contrast): greater mucosal detail
MRI: perianal/rectovaginal fistulae
extra-intestinal manifestations of IBD
o Related to IBD Activity:
• Pauciarticular arthritis
• Erythema nodosum
• Sweet’s Syndrome
• Episcleritis
o Unrelated to IBD Activity:
• Polyarticular arthropathy
• Ankylosing spondylitis Sacroiliitis
• PSC
• Pyoderma Gangrenosum
• Uveitis
IBD treatment 5-ASA
a. Original indication: rheumatoid arthritis
b. Active moiety: 5-ASA
c. Oral, topical (rectal)
d. Multiple immune system effects
e. Therapeutic uses:
i. UC: induction, maintenance (YES!)
ii. CD: induction (weak), ? Maintenance (EH)
iii. Chemoprophylaxis (colon cancer)
f. Safety: Hypersensitivity, nephrotoxicity, reversible oligospermia (sulfasalazine)
IBD treatment antibiotics
- *a. Efficacy:**
i. Ciprofloxacin/Metronidazole: CD → colonic and perianal disease; UC → pouchitis
ii. Rifaximin: elevated CRP
b. Safety
i. Cipro: C.Diff, arthropathy, tendon rupture
ii. Metronidazole: metallic taste, peripheral neuropathy, Antabuse-like effect
IBD treatment systemic glucocorticoids
a. Binds GC receptors → inhibits inflamm. mediators, WBC migration/function
b. + induction, NOT maintenance
c. No benefit >40-60 mg prednisone
d. Intravenous, oral, rectal
e. Time Course: 5-10 days
f. Short term therapy, bridge to another med!
g. AE: moon face, wt gain, acne, hirsutism, irritability, HTN, DM, bone metabolism, cataracts, adrenal insufficiency, ecchymoses, osteonecrosis
IBD treatment budesonide
a. High 1st-pass metabolism=Few systemic side effects!
- *b. Efficacy:**
i. CD: Ileal/R colonic
ii. Ulcerative Proctitis (enema formulation)
IBD treatment azathioprine/6-mercaptopurine
a. AZA→6-MP→6-TGN → proliferation activated lymphocytes; apoptosis
b. Steroid withdrawal, maintenance
c. Maximal clinical benefit: 3-4 months
d. Early reactions: fever, pancreatitis
e. Adverse reactions: leukopenia, hepatotoxicity, infection (viral), lymphoma, non-melanoma skin ca
IBD treatment methotrexate
a. Mechanism: Folate analog, rever. comp. inhib DHFR; interferes with DNA syn, mult anti-inflamm effects
b. Indication: induction & maintenance in CD
c. Safety: pulmonitis, hepatotoxicity, BM suppression, teratogen/abortifacient
IBD treatment cyclosporine
a. Mechanism: lipophlic peptide; downregulation of IL2→inhibition of prolif/activ TH cells
b. Indications: UC induction for severe, steroid refractory pts
c. Safety: infection, HTN, neurotoxicity, renal toxicity
IBD treatment natalizumab
a. Mechanism: alpha 4 integrin antibody→dec. WBC trafficking to sites of inflammation
b. Indication: CD + induction/maintenance
c. Safety: Progressive multifocal leukoencephalopathy
IBD treatment anti-TNFa (infliximab, adalimumab, cerolizumab)
a. Inhibits TNFa
b. Used in CD and UC for induction and maintenance
c. Safety: malignany/lymphoma, serum sickness, drug-induced lupus, demyelination, heart failure, hepatotoxicity, opportunistif infections
Surgery in CD
i. Indications: stricture, perforation, abscess, fistula, refractory dz, hemorrhage, cancer
ii. Types: ileocecectomy, stricturoplasty, fisulotomy/setons
iii. Lifetime incidence 60-70%
Surgery in UC
i. Indications: refractory dz, neoplasia, fulminant colitis, toxic megacolon, hemorrhage
ii. Types: TPC +/- IPAA
iii. Lifetime incidence 30%
risk colon cancer in IBD
o Inc risk duration, extent, PSC, inflammation severity, psudopolyps, family hx, smoking
o 5-ASA dec. risk
o surveillance: >8-10yrs, q1-2 years, 4 quadrant biopsies every 10cm
murphy’s sign
painful arrest in inspiratoinn triggered by palpation of inflamed gallbladder
pt is lying supine, examiner places fingers over R. costal margin in MCL
courvoisier’s law
painless jaundice an enlarged, palpable and non-tender gallbladder is not due to cholelithiasis but to cancer of biliary tract of pancreatic head (extrahepatic obstruction)
gallbladder disease 4 F’s
- Fat
- Fertile
- Female
- Forty/Fifty
Signs of cholecystitis
- Symptoms: N/V, RUQ pain
- Positive Murphy’s sign
- Boas’ sign (low sensitivity): area of hypersensitivity at costophrenic angle
- Audible rub over gallbladder
PE ascites
o Due to:
• Increased hydrostatic pressure (Right sided heart failure or biventricular failure)
• Decreased oncotic pressure (malnutrition, protein loss from cirrhosis, nephrosis, enteropathy)
• Peritoneal inflammation (neoplastic of infectious)
o Ankle swelling is important finding; also look for history of liver disease or increasing abdominal girth
o Small volumes of fluid 50-100ml must be detected by ultrasound
o 4 classic PE maneuvers: note must have at least 500-1000ml of fluid to visualize these findings
• inspection for bulging flanks (sensitive but not specific)
• percussion for flank dullness (sensitive but not specific)–+ is periumbilical tympany, flanked by dullness.
• *shifting-dullness maneuver (sensitive but not specific)
• *fluid-wave test (specific but not sensitive)**only specific test for ascites
• *=best sensitivity and specificity
o most useful sign to r/o gross ascites is the absence of shifting dullness
o most useful sign to rule in ascites are a positive fluid-wave maneuver and a history of ankle edema (or liver disease or prolonged PT)
• Pts w/ a hx of liver disease, prolonged PT, and a positive fluid-wave test
ascites?
ultrasound?
likely have ultrasound, no ultrasound needed
• Pts w/ normal PT and no shifting dullness
ascites?
ultrasound?
Pt is unlikely to have ascites
no ultrasound
signs of liver disease
o Spider nevi
o Palmar erythema
o Asterixis
o Dilated abdominal veins (caput medusae)
o Palpable spleen: d/t portal hypertension
o Foetor hepaticus: portal systemic shunting from severe liver disease
Guarding (localized/induced):
diffuse or localized tension of the abdominal wall
- Involuntary=rigidity
- Voluntary=elicited one exam
- Localized rigidity: specific indicator of a focal area of peritonitis (overlying inflamed viscus)
- Induced guarding: tenses abdominal muscles and protects inflamed intra-abdominal organs; used to elicit carnett’s sign
o Carnett’s sign and AWT:
- Use induced guarding to differentiate b/t inflamed intra-abdominal viscus and abdominal tenderness caused by inflamed abdominal wall. Pt tenses ab muscles while examiner presses on belly
- If pain increases (positive test)→pain from abdominal wall
- If pain decreases (negative test)→pain from intra-abdominal viscus
- Positive Carnett’s or AWT indicates good liklihood of absence of intra-abdominal or peritoneal pathology
- When not to use”
- Children/elderly—can be misinterpreted
- Useless/inhumane in pts with diffuse abdominal pain and rigidity
- Dangerous in pts w / intra-abdominal abscess
o Rebound tenderness (Blumberg’s sign)
- Sudden pain of abdominal wall indirectly elicited by release of hand pressure
- Localized pain in pts w/ localized peritonitis
- Less painful alternative=light percussion
- Unnecessary in pts who have guarding/rigidity
