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
o Referred rebound tenderness:
compressing and then release the contralateral quadrant to where the patient has pain
• Positive when elicits pain in the original site where pt first felt it (pain at site of palpation=negative test)
Alternatives:
- jar tenderness
- cough test
- valsalva
o Abdominal hyperesthesia:
hypersensitivity to light touch to abdominal areas over an inflamed viscus
not specific to localized peritonitis
seen in herpes zoster, PUD
PE manuevers appendicitis
o McBurney’s sign: maximum tenderness and rigidity by pressing one finger over Mcburney’s point)
o Rovsing’s sign: pain in the R. iliac fossa caused by pressure over left lower quadrant
o Obturator test: pt flexes hip and rotates it internally while supine,
- pain indicates inflammation around organ surrounding obtrurator (retrocecal appendix)
- for OB-GYN conditions pain usually positive on both legs
- for appendicitis, pain only w/ right leg
o Reverse Psoas: detects irritation of iliopsoas muscle; if pain when extending R. hip=positive; useful for retrocecal appendix
o Rectal tenderness: tenderness on rectal exam elicited w/ appendicitis confined to pelvis
- Most useful: right sided tender mass representing pelvic abscess
Pt presents w/ acute diarrhea w/o blood
DDx?
management
acute gastroenteritis
antibiotic induced
food poisoning
parasites
usually self-limited and doesn’t present to physician; check stool for enteric pathogens, fecal leukocytes, hx of recent antibiotic use or C. diff risk factors; maintain adequate hydration
pt presents w/ acute diarrhea w/ blood
DDX?
Managment?
o Infectious: salmonella, shigella, campylobacter, yersinia, E. coli O157 (Dx w/ stool cultures)
o Ischemic colitis: elderly pt w/ abdominal pain, resolves after few days, look for cause (hypotension, thromboembolic, atherosclerotic)
o IBD: commonly ulcerative colitis, acute presentation, dx w/ colonoscopy
o Colon cancer: blood in stool, anemia, lethargy; >50yo; family hx
o Diverticular disease: acute, painless, voluminous blood diarrhea; bleed several times; self-limited
o Meds
o Management:
• Usually present to physician
• Stool for enteric pathogen and C. diff toxin routinely
• Manage GI bleed
• Colonoscopy
pt presents with chronic diarrhea w/ blood
DDX?
management?
o Ulcerative colitis
o Colon cancer
o Colon polyps
o Management: colonoscopy
pt presents w/ chronic diarrhea w/ blood
o Celiac: can also present w/ iron deficiency anemia, tx is dietary avoidance
o IBD: crohn; systemic complaints arthritis, rash, uveitis; multiple movements per day; dx w/ colonoscopy, radiology or capsule endoscopy
o Lactose intolerance: common! Diarrhea/cramps after dairy; dx w/ lactose breath test; tx is avoidance dairy
o Infectious: acute, HIV (crypto, isospora, microsporidia)
o Diabetes (nocturnal BM, worse when elevated glucose, tx w/ glucose control or clonidine_
o IBS: unrevealing workup assoc w/ abdominal pain/cramps; diarrhea or constipation predominant; develop sx after eating; pain relieved w/ BM
o Microscopic colitis: women >50yo, ASA exposure, slow insidious onset; collagen deposition in subepithelial lining; dx w/ colonic biopsy; tx w/ removal ASA, Imodium, aminosalicylates, steroids
o Malabsorption: pancreatic insufficiency, small intestinal bacterial overgrowth; lactose intolerance; celiac sprue
o Management:
• Start easy: lactose free diet trial; thyroid function tests; stool for WBCs, O&P, enteric culture
• Colonoscopy: polyps, mild IBD, collagenous colitis, microscopic colitis
• Fasting: osmotic diarrhea will decrease; secretory will not
• Malabsorption (presents w/ steatorrhea)
• 72hr fecal fat collection: normal <7g/24hrs
• D-xylose test: abnormal=small bowel malabsorption
• Pancreatic insufficiency: pancreatic calcifications, trial pancreatic enzyme replacement, bentiramide test, secretin test
• Small bowel malaborption: biopsy—look for celiac, whipples etc; barium study
• Test bacterial overgrowth: breath test
• Schilling test: B12 absorption
• Screening tests: cholesterol, prothrombin, carotene, albumin, calcium
diverticular disease
- Common in elderly
- Pathogenesis:
- Related to intestinal motility, colonic structure, diet, genetics
- Low residue diet (reduced fiber)
- Muscular hypertrophy of colon and ability to increase intraluminal pressure
- Prolonged colonic transit, decreased fecal fiber, increased intraluminal pressure
• Clinical classification:
- Symptomatic uncomplicated
- Recurrent symptomatic
- Complicated
- Hemorrhage, abscess, phlegmon, perforation, purulent fecal peritonitis, stricture, fistula, small bowel obstruction from adhesive disease
- Sx: most asymptomatic; abdominal pain and impaired bowel function, fever
- Tx: antibiotics; low fiber followed by high fiber diet
epidemiology of gallstone formation
o 10% population
o F>M (childbearing, estrogen replacement, OCP)
o Age>60yo
o Ethnicity: high in Scandinavia, chile, native americans. Low in Africa, asia
o Family Hx
o Assoc. diseases: crohn’s, cirrhosis, hemolytic d/o
o Obesity, rapid weight loss, estrogen
black pigment gallstones
o Black Pigment: calcium bilirubinate, mucoprotein, <10% cholesterol
- 50% radioopaque (d/t calcium, see on plain X-ray)
- seen it pts w/ cirrhosis and chronic hemolytic d/o (thalassemias, sickle cell)
brown pigment gallstones
o Brown Pigment: calcium salts of unconjugated bilirubin and variable amounts of protein and cholesterol
- Primary bile duct stones
- Assoc. w/ biliary infection leading to bacterial deconjugation of bilirubin
- Asians, secretory IgA deficiency
cholesterol gallstones
- Most common in US; most radiolucent
- Cholesterol saturated bile is a prerequisite
- Cholesterol is less soluble d/t: decrease in bile salt, inc. in cholesterol, decrease in lecithin
Pathogenesis:
- cholesterol supersaturation
- nucleation
- gallbladder hypomotility
risk factors for developing gallstones
o Demographics: older age, female, obesity, wt loss, TPN
o Drugs: clofibrate, OCP, estrogens, progesterones, ceftriaxone, octreotide
o Genetics: native Americans, Scandinavians
o Ileal disease: crohns, resection
bile duct stones primary vs secondary
o Primary: calcium biliruubinate (brown); form in bile duct d/t stasis; above a stricture, foreign body or in infection
o Secondary: migrated out of gallbladder; 80% cholesterol; 20% black pigment stones
biliary colic
o Biliary colic: Most common presenting symptom of cholelithiasis!
- pain is steady, severe aching or pressure type sensation in epigastrum or RUQ; radiates to infrascapular area or R. scapula; pain occurs suddenly and lasts 1-3hrs
- visceral type pain (d/t transient obstruction of cystic duct by stone)
- attacks may be precipitated by fatty meals, or can occur anytime day or night
- N/V common
- Lab tests normal
- Recurrent pain attacks in 50% of pts
acute cholecystitis
- Acute inflammation of gallbladder due to Persistent obstruction of cystic duct (contrast to transient w/ biliary colic)
- Bacterial infection
- Parietal type epigastric or RUQ pain
- Positive Murphy’s sign; tenderness in scapular area (Boas’ sign)
- N/V common
- Low grade fever and leukocyte ccount of 10,000-15,000/mm3 with a shift to the left. Liver enzymes may be elevated
- 75% resolve spontaneously
- 25% inflammation progresses to necrosis, perforation, or empyema of gallbladder
- Indications of progression: persistent signs/sx or peritonitis or inc. temp, pulse rate, and WBC. Elderly or diabetic pts may only have mild sx despite severe disease
- Complications: empyema, intraluminal gallbladder abscess, perforation
complications of gallstones
o Common bile duct obstruction (choledocholithiasis)
o Cholangitis (triad fever, pain, jaundice)
o Acute pancreatitis (gallstone causes obstruction ampulla)
o Gallstone ileus (small bowel obstruction)
o Papillary stensosis
o Choledocho-enteric fistula (stone erodes thru wall of bowel)
o Mirizzi’s syndrome: gallstone in cystic duct obstructs common bile duct by extrinsic compression
o Gallbladder cancer (esp porcelain gallbladder)
o Surgical complications: biliary strictures, bile leaks, transection of bile ducts
Tools for diagnosing gallstones
o Abdominal X-ray (see 20%)
o Ultrasound: initial test; signs acute cholecystitis
o Hepatobiliary scan (HIDA)—confirmatory, see obstruction, see gallbladder muscular function
o Endoscopic ultrasound: gallbladder and common bile duct stones
o MRI/MRCP
treatment of gallstones
o Surgical removal: pts w/ recurrent biliary colic, acute cholecystitis, complications
• Stabilize pts w/ IV fluids, antibiotics, and kept NPO
• Complications: biliary strictures, bile leaks, choledocholithiasis (still have stone in bile duct)
• Transection of bile duct (catastrophic)
o Non-surgical management for pts unfit for surgery:
• Dissolution therapy:
• Ursodeoxycholic acid (ursodiol) reduces biliary output cholestrol (dec. cholesterol saturation);
• MTBE: dissolve in 24hrs; requires direct instillation into gallbladder either endoscopically or percutaneously
• Lithotripsy
o Endoscopic retrograde cholangiograpy w/ sphincterotomy is used for new bile duct stones after cholecystectomy
local effects of pancreatic enzymes
o Inflammation
o 3rd space losses
o fat necrosis
o pancreatic and peripancreatic necrosis
acute pancreatitis def
Reversible; Normal pancreas becomes acutely inflamed
chronic pancreatitis def
Persistent and progressive process; changes in pancreatic structure/function precede sx and persist after cause of pancreatitis corrected.
acute pancreatitis pathophysiology
Pathophysiology:
- Cellular: altered acinar cell protective mechanisms leading to intracellular activation of digestive enzymes
- dissolution organelles and cell membranes
- release cell components (phospholipase, elastase etc)
- release cytokines (PAF, TNFa, Interluekins, ICAM-1) - Glandular: increased vascular permeability
- influx and activation of inflammatory cells, formation reactive metabolites
- dissolution blood vessels and ECM
- Thrombosis, hemorrhage, tissue necrosis - Systemic:
- Respiratory failure (phospholipase A2, subdiaphragmatic inflammation, pain w/ inspiration, hemorrhage dec. oxygen carrying capacity)
- renal failure
- DIC
- Shock
acute pancreatitis etiology
Etiology:
-Triggers: ductal obstruction, ductal hypertension damages apical surface of acinar and duct cells, altered acinar cell/duct cell permeability, direct cytotoxic effect on acinar/duct cell
- Common duct stones
- Alcohol
- Idiopathic
- Other: partial duct obstruction (tumors, sphincter dysfunction/stenosis, cysts/stones/strictures, helminthic infection, congential anamolie, choledochochocele); meds; hypertriglyceridemia, hypercalcemia, iatrogenic (surgery, ERCP), toxins, trauma, vascular (hypoperfusion, vasculitis), autoimmune, infectious (MUMPS, coxsackie), Genetic (PRSS1, SPINK1, CFTR
acute pancreatitis clinical presentation
Clinical presentation
- Sx: abdominal pain, N/V, low-grade fever, dehydration
- PE: tenderness, mild distension, decreased or absent bowel sounds
acute pancreatitis diagnosis
Diagnosis:
-H&P, PE, elevated pancreatic enzymes most imp!
Labs:
-elevated **Lipase (and amylase but lipase better)
-magnitude of elevations are of no prognostic sig
Imaging:
-CT: Method of choice! Can determine severity and detects complications
MRI is not better but used in pregnant pts
acute pancreatitis prognosis
Prognosis:
- 80% mild, 20% severe, 9% mortality (d/t organ failure/infection)
- bedside assessment (underestimates severity of disease esp. in younger pts)
- bedside indicators of severe disease: tachycardia >120, hypotension, hemoconcentration Hct>50%, oliguria, tachypnea, hypoxemia, encephalopathy
- CT criteria
- Scoring Systems: Ranson, Glasgow, Apache II
- Serum markers: CRP, Trypsinogen activation peptide (TAP), Monocyte chemotactic protein (MCP-1)
acute pancreatitis treatment
-no therapy interrupts acute autodigestion/inflammation
-Assess severity/assign level of care
-prevent and treat complications
-seek etiology
Supportive care:
-aggressive fliud and electrolyte replacement
-NPO (d/t gut inflammation)
-Monitor: PE, vitals, urine output, O2 saturation, intravascular volumes
-Analgesia, anti-emetics
-antibiotics if indication of infection
-nutritional support
chronic pancreatitis pathophysiology
Pathophysiology:
- acinar and duct cell damage→inc. membrane permeability
- inc. intraductal calcium and protein precipitate to from plugs/stones→partial duct obstruction - inflammation, fibrosis, atrophy, and disruption of ducts and exocrine/endocrine tissue
- hard fibrotic (cirrhotic-like) organ (dec. number and size of acini and islets)
chronic pancreatitis etiology
Etiology:
- Alcohol:
- direct acinar cell toxicity
- alters membrane infrastructure (inc. permeability)
- inc. basal protein secretion
- dec. trypsin inhibitor
- althers lithostatin (ppt of calcium) - Hereditary:
- abnormal trypsinogen or trypsin inhibitor
- cystic fibrosis (CFTR mutations) - chronic partial duct obstruction
- autoimmune
- idiopathic
- tropical
chronic pancreatitis presentation
Presentation:
- recurrent: 50%
- insidious: 35% abdominal pain; 15% w/ malabsorption (lose digestive enzymes), diabetes, jaundice (obstruction bile duct)
- Sx:
- acute pancreatitis
- chronic pain/nausea (constant, dull, radiates to back, worse w/ food)
- malabsorption (diarrhea, steatorrhea—bulky, fatty, foul smelling stool)
- diabetes
- Wt loss
chronic pancreatitis diagnosis
Diagnosis:
-PE and labs not helpful
-Hx: recurrent episodes, chronic disease, ETOH
Imaging:
-plain film: calcifications
-CT: irregular contour, calcifications, dilated duct, cysts
-MRI/MRCP: Gold standadrd! Parenchymal fibrosis and ductal abnormalities
-EUS (endoscopic ultrasound)
chronic pancreatitis complications
Complications:
- pain, malabsorption, wt loss, diabetes
- narcotic addiction
- pseudocyst formation
- common bile duct obstruction, duodenal obstruction
- splenic vein thrombosis (gastric varices)
chronic pancreatitis treatment
Treatment:
- alcohol abstinence
- low fat diet
- pancreatic enzymes +/- acid suppression
- analgesics
- insulin
- ductal decompression (surgical, endoscopic)
- celiac plexus neurolysis
- pancreatectomy
general PE signs of liver disease
o General: muscle wasting, paucity of body hair, parotid enlargement, testicular atrophy, gynecomastia
o Skin: excoriations, ecchymoses, petechiae, spider angiomata, palmar erythema, pallor, abnormal pigmentation, needle tracks, scarring from skin abscesses or popping, dupuytren’s contractions, abdominal collateral vessels
o HEENT: scleral icterus, Kayser-Fleisher rings
o Abdomen: liver tenderness, enlargement, firmness; ascites; splenomegaly; prominent abdominal collateral vessels
o Neuropsychiatric: confusion, depression, memory loss, unusual behavior, asterixis, fetor hepaticus
unconjugated hyperbilirubinemia
o Unconjugated hyperbilirubinemia: >80% of elevated total bilirubin is indirect
Inc. bilirubin production
• Hemolytic anemia
• Hematoma
• Ineffective erythropoeisis (thalassemia, pernicious anemia)
• Neonatal (physiological) jaundice
Dec. hepatic ability to conjugate bilirubin (reduced glucoronosyltransferase activity)
• Gilbert syndrome (young men, hereditary)
• Crigler-Najjar syndrome
• Neonatal physiological jaundice
conjugated hyperbilirubinemia
o Conjugated hyperbilirubinemia: >50% elevated bilirubin is direct
Impaired hepatic secretion:
• Extrahepatic obstruction (stones, tumors, stricture)
• Intrahepatic hepatocellular, canalicular, or ductular damage
• Rotor’s syndrome (rare)
Dec hepatic uptake of conjugated bilirubin
ALT>1000
- Acute viral hepatitis (HAV, HBV)
- Drug toxicity (acetominophen)
- Shock liver (hypotensive episode)
- Autoimmune hepatitis
AST/ALT>2
alcoholic hepatitis
ALT predominance
- Chronic viral hepatitis
- Nonalcoholic fatty liver disease
- Metabolic disease (Wilsons, AAT deficiency)
- Meds
- Autoimmune hepatitis
elevated AP and GGT
o Extrahepatic biliary obstruction: synthesis of AP by biliary epithelial cells is increased, leading to serum elevation. Imaging by ultrasound, CT, MRI will show biliary dilation
• Gallstones
• Tumor (pancreas, ampulla of vater, bile duct, lymph nodes)
• Stricture (PSC)
• Iatrogenic—surgical ligation
o Intrahepatic cholestasis: dysfx of bile transport d/t acute or chronic injury
• PBC
• Medication induced
• Congential ductopenic syndromes
o Infiltrative d/o
• Granulomatous hepatitis (sarcoidosis, mycobacterial
• Malignant infiltration (lymphoma)
• Amyloidosis
decreased albumin
severe liver disease w/ dysfx (other causes nephritic syndrome, protein losing enteropathy, malnutrition)
elevated INR
• INR: measures prothrombin (marker of liver synthetic dysfx)
o Acute liver injury: elevated INR=worse prognosis
o Chronic liver disease: early sign of liver dysfx→advanced disease
o Cholestatic liver disease: malabsorption fat soluble vitamin K
o Vit K deficiency d/t extensive antibiotic use and malnutrition
pt management abnomral LFTs
- abnormal AST/ALT
- abnormal AP/GGT
o Abnormal AST/ALT→Hepatocellular injury→H&P/INR/Albumin→1. Acute or 2. Chronic
o Abnormal AP/GGT→cholestatic disease→Ultrasound! (or MRI or CT)→1. Intrahepatic or 2. Extrahepatic cholestasis
Acute viral hepatitis HAV
o Virus shed in stool
o Anti-HAV IgM present at onset of illness
o Anti-HAV IgG is persistent and protective against future infection
o Prognosis: all pts recover, no chronicity
o Prophylaxis: household contacts→immune globulin; highly effective vaccine
acute viral hepatitis HBV
o HBsAg is first marker of infection then
o HBeAg and HBV DNA shortly after (disappearance later=good prognosis)
o Anti-HBc IgM is marker of acute infection
o Anti-HBc IgG is persistent but is not protective
o Anti-HBs appears after clearance of HBsAg, this is protective antibody
o Prognosis: 95% recover w/o sequalae; 1% get fulminant hepatitis; 1-10% get chronic hepatitis
o Prophylaxis:
• preexposure: vaccine to high risk individuals;
• postexposure: HBIG (immune globulin) + vaccine
acute viral hepatitis HCV
o HCV RNA is earliest marker of infection
o Anti-HCV appears at 6-8wks but is not neutralizing
o Majority of infections are subclinical and asymptomatic
o Prognosis: 85% become chronic
o Screen blood donors
acute viral hepatitis HDV
o Requires HBV
o Coinfection; clearance of HbsAg accompanied by clearance HDV
o Superinfection: HDV infection usually becomes chronic
o Prognosis: coinfection sim. To HBV, superinfection=inc. mortality
o Prevent w/ HBV immunization
acute viral hepatitis HEV
o Enteric; contaminated water; India, Asia, Africa, Central America
o Recovery is rule except in pregnancy (20% fulminant hep)
o Prognosis: good except pregnancy
hepatitis G
• Hepatitis G: liver transplant pts
signs/sx of acute viral hepatitis
o Prodrome: anorexia, N/V, fatigue, malaise, fever
o Icteric: jaundice, RUQ pain
o Recovery: constituitional sx disappear, lab abnormalities improve
o Hospitalization indicated: inability to take oral fluids, synthetic dysfx (coagulopathy), encephalopathy
lab abnormalitis in acute viral hepatitis
o AST, ALT>1000
o Elevated serum bilirubin
o Elevated INR=poor prognosis
chronic HBV epidemiology and phases
o ***persistent HbsAg
o 1-10% of adults get chronic HBV (high in children)
o Phases of chronic Hep B
• Immune tolerant phase: perinatal, normal AST/ALT, HBV DNA high, mild histology
• Immune active (clearance): elevated ALT, HBV DNA>20,000 w/ HBeAg+, HBV DNA>2000 w/ anti-HBeAg, active histo
• Inactive: anti-HBe+, ALT levels normal, HBV DNA low <2000
• Recovery: clearance of HBsAg, screen for HCC
o Pts have inc. risk HCC
chronic HBV infection clinical
- Sx: fatigue, jaundice, anorexia, pruritis, cachexia
- Signs of liver disease: ascites, edema, GI bleed, coagulopathy, encephalopathy, hypersplenism
- Exacerbations of acute hepatitis-like sx represent reactivation
- Extrahepatic d/t immune complex deposition: arthralgia, arthritis, leukocytoclastic vasculitis, glomerulonephritis, polyarteritis nodosa
chronic HBV infection treatment
- Interferon (immune active HBV infection)
- Side effects: flu-like Sx, bone marrow suppression, irritability, thyroiditis, suicide
- Nucleoside/Nucleotide analogues: lamivudine, adefovir, entecavir, telbivudine, tenofovir
- Re-infection common after liver transplant
- Reactivation in pts undergoing immunosuppresion/chemo
chronic HCV epidemiology
o 85% of infections, progression to cirrhosis in 20-30%
o even w/ sig. pathology, can be asymptomatic
o pts who develop cirrhosis at inc. risk HCC (vs HBV where all pts at inc. risk)
chronic HCV clinical
o Clinical: severe histologic activity and cirrhosis can be present in asymptomatic individuals
- Sx: fatigue is common, jaundice is unusual
- Extrahepatic: cyroglobulinemia, glomerulonephritis, porphyria cutanea tarda
chronic HCV infection treatment
- Peginterferon + oral ribavirin + oral protease inhibitor for 6-12months
- Don’t’ use interferon in pts w/ decompensated liver disease
- Re-infection common after liver transplant
fulminant hepatitis
- Onset of encephalopathy within 6wks of onset of liver disease (see jaundice)
- Most common etiology=acetominophen toxicity
- Next most frequent is infectious d/t HBV (only 1% of HBV cases present as fulminant); also HEV in pregnancy, HBV+HDV
• Clinical:
o Encephalopathy within 6 wks of presentation
o Labs: high AST and ALT, synthetic dysfx (elevated INR, impaired gluconeogenesis), hypotension, renal failure, hypoxemia
o Cerebral edema (leading cause mortality), bacterial infection (2nd)
• Treatment: supportive (protect airway, treat infection, support BP, dec. intracranial pressure); liver transplant
non-alcoholic fatty liver disease
- Steatosis (no hepatocellular necrosis) and steatohepatitis
- Assoc. w/ type 2 DM, obesity, hyperlipidemia
- Most common cause of abnormal serum aminotransferases in blood donors;
- “cryptogenic cirrhosis”
• Clinical:
o Present w/ asymptomatic elevated in serum aminotransferases
o Can progress to cirrhosis/liver disease
• Diagnosis
o Hepatomegaly
o US, CT MRI detect fat in liver
o Biopsy (can’t distinguish from alcoholic liver disease): see steatosis or steatohepatitis
**• Treatment: ** control underlying diseases
autoimmune hepatitis
- Chronic inflammation of liver w/ hepatocellular inflammation, necrosis, fibrosis
- Type 1 is most common
- Young—middle aged women
- Liver injury d/t cell mediated attack of hepatocytes
• Clinical:
o Similar to viral hepatitis
o Fatigue, myalgia, RUQ pain, jaudice
o Can progress to cirrhosis very quickly
• Diagnosis:
o ALT>1000, can also have elvated bilirubin and alk-phos
o ANA+, AMSA+
o Hypergammaglobulinemia
o Liver biopsy: portal inflammation, lobular inflammation, plasma cell infiltration, hepatocyte apoptosis (If severe: bridging necrosis, periportal collapse, fibrosis)
• Treatment:
o Corticosteroids!
o Can relapse
o Azathioprine inc. chance of successful withdrawal of steroids
Hemochromatosis
- Defect in iron absorption
- Males in 40s-50s; females in 60s
- Hepcidin inhibits iron uptake; mutation in HFE allows unregulated iron absorption
• Clinical:
o Skin bronzing
o Dec. gonadotropins (impotence)
o Heart deposition (cardiomyopathy, arrhythmias)
o DM
o Arthropathy (fingers)
o Liver: insidious onset w/ progression to cirrhosis and HCC
• Diagnosis:
o Labs: high serum iron, low total iron binding capacity (TIBC), high transferring saturation, high ferritin
o Radiology:
• Radiograph: arthropathy in hands and hips
• CT: high attenuation in liver, normal spleen
• MIR: reduced liver signal intensity on T2 wted image (shows black)
_o Genetics: _ C282Y in HLA-H gene
o Biospy:
• Qualitative and quantitative (hepatic iron index) hepatic staining for iron
o Response to phlebotomy
• Prognosis:
o Liver disease is reversible prior to onset of cirrhosis
o At high risk HCC
• Sceening family: serum Iron, TIBC, and ferritin then confirmatory genetic testing
Alpha1-antitrypsin deficiency:
• Genetics: normal phenotype is PiMM; PiMZ and PiZZ assoc. w/ disease (Europeans and Scandinavians)
o Neonatal jaundice in 10% PiZZ
o Pi Null=no liver disease but emphysema
• Alpha1-antitrypsin is protease inhibitor, esp. elastase
o Deficiency=precocious emphysema (male smokers)
• Liver disease;
o 15% PiZZ
o d/t inability to excrete abnormal protein
o adolescents: chronic active hepatitis or cirrhosis
o adults: cyptogenic cirrhosis w/ portal hypertension
o HCC inc. in pts w/ cirrhosis
o Biopsy: PAS+ globules in periportal hepatocytes
o No Tx; liver transplant is curative
Wilson’s Disease
• Genetics: AR; decreased hepatic excretion of copper
• Clinical:
o Kayser-Fleischer rings (ocular copper deposits)
o Cardiomyopathy
o Renal tubular deposition→aminoaciduria and glycosuria→fanconi syndrome
o Hemolysis
o Liver: abnormal LFTs, acute hepatitis, fulminant hepatitis, chronic active hepatitis, cirrhosis
• Diagnosis:
o Labs: low ceruloplasmin, high urinary copper
o Biopsy: quantiate copper
• Tx:
o First line is Trientine (chelates copper)
o D-penicillamine (chelator; side effects: rash, lupus-like sx)
o Interruption of chelation can lead to fulminant hepatic failure
o Liver transplant is curative
Primary Biliary Cirrhosis
• Cholestatic liver disease caused by autoimmune destruction of small interlobular and septal bile ducts
• Clinical:
o Commonly asymptomatic elevation in Alk-Phos
o Women 35-60
o Early findings: pruritis, fatigue, malabsorption lipid-soluble vitamins, hypercholesterolemia
o Later findings: xanthelasmas, skin hyperpigmentation, osteoporosis, jaundice, ascites, portal HTN
• Diagnosis:
o Inc serum Alk-Phos
o AMA+ (antimitochondrial antibody)
o Biopsy: chronic non-suppurative destructive cholangitis
• Therapy:
o Ursodeoxycholic acid (ursodiol)
o Cholestyramine (relieves pruritis)
o Liver transplant curative
Primary Sclerosing Cholangitis
• Progressive cholestatic d/o w/ inflammation, obliteration, and fibrosis or medium and large sized intra-and extra-hepatic bile ducts
• Clinical:
o Underlying ulcerative colitis
o 70% male; age 40
o asymptomatic elevated Alk-Phos
o Symptomatic: jaundice, pruritis, fever w/ abdominal pain due to ascending cholangitis
o Late presentation: end-stage liver disease and portal HTN; cholangiocarcinoma (inc. risk)
• Diagnosis:
o Labs: elevated Alk-Phos; mildly elevated transaminases
o Cholangiography: strictures, outpouching (beading)
o Biopsy: periductal inflammation/fibrosis
• Tx: none
o Manage biliary complications strictures, cholangitis
o Liver transplant curative
steatosis (fatty liver)
o Most frequent; even brief periods of alcohol indigestion can result
o Binge drinking interspersed w/ periods sobriety
o Usually asymptomatic
o 1/3 have abnormal LFTs
o fatty liver w/o hepatocellular injury is reversible and does not progress
o Tx: alcohol withdrawal and adequate diet
Alcoholic hepatitis
o Sx: wt loss, anorexia, abdominal pain, nausea
o PE: fever, jaundice, ascites, fluid retention, bleeding neurologic dysfx
o Labs: AST/ALT>2; elevated bilirubin and phosphatase; leukocytosis
o Biopsy: hepatocyte necrosis, Mallory bodies, inflammatory infiltrate w/ PMNs, fibrosis, fatty change
o Prognosis: depends on severity and presence of cirrhosis
o Therapy: alcohol cessation, adequate nutrition, general medical support
• Severe cases corticosteroids help
Alcoholic Cirrhosis
o 15-20% chronic alcoholics
o Sx: fatigue, wt loss, GI bleed, hepatic encephalopathy, jaundice inc. abdominal girth
o PE: dupuyten’s contracture, parotid gland enlargement, hepatomegaly, splenomegaly, ascites
o Labs: hypoalbuminuria, hypergammaglobulinemia, hyperbilirubinemia, hypoprothrombinemia
o Biopsy:
• Regenerative nodules
• Fibrous bands linking central and portal zones
• Fatty change
o Prognosis: depends on cessation of alcohol; better before onset ascites, jaundice hematemesis
classification of portal HTN
o Pre-hepatic: splenic and portal vein thrombosis,
o Intra-hepatic: sinusoidal (schistosomiasis), sinusoidal (cirrhosis), post-sinusoidal (veno-occlusive)
o Post-hepatic: budd Chiari (hepatic vein thrombosis) and right sided heart failure
esophageal varices
• Portal hypertensive gastropathy – “snakeskin”
o Predictors of variceal rupture: size of varix, presence of decompensated liver disease, “red wale” sign (stretching epithelium)
**• Diagnosis: **
o Signs of portal HTN: splenomegaly, ascites, caput medusae, gastroesophageal varices
o *endoscopy
o varices less likely to bleed if portal pressure <12mmHg
• Treatment:
- Transfuse to hemoglobin ~ 8 gm/dL
- Short term antibiotics
- Expedient endoscopic therapy
- Pharmacotherapy for 5 days (Octreotide)
- Tamponade and TIPS for uncontrolled bleeding
Ascites causes
• Accumulation of excessive fluid within the peritoneal cavity
• Most commonly caused by cirrhosis and portal hypertension
o Ascites in cirrhosis → 50% 2-year survival
o Pathophysiology: physiologic response to decreased EABV→upregulated renin-angiotensin→renovascular constriction and sodium and water retention
• Other causes of ascites
o Neoplasm
o Congestive heart failure
o Infection
ascites dianosis
• Diagnosis:
o Abdominal distension in a pt w/ portal HTN
o Flank dullness by percussion
o Shifting dullness
SAAG
o Use serum-ascites alubumin gradient (SAAG)
• SAAG = (serum albumin) – (ascites albumin)
• SAAG ≥ 1.1 → ascites likely from portal hypertension
• SAAG<1.1: infection or malignancy
Treatment of ascites
o Determine underlying cause
o Sodium restriction (2.0 g/day)
o Fluid restriction not necessary unless serum Na+ <120 mmol/L
o Diuretics
• K+ sparing - Spironolactone, Amiloride, Triamterene
• Loop diuretics - Furosemide, Bumetanide, Torsemide
• Don’t use thiazides
o Tx of refractory Ascites:
• Ascites not responsive to maximal conventional therapy
• Only 5-10% of patients with ascites meet these criteria
• High volume paracentesis
• TIPS
• Surgical mesocaval shunt
o Liver transplant
spontaneous bacterial peritonitis
Spontaneous Bacterial Peritonitis (complication of ascites)
- Intra-abdominal infection in cirrhosis without apparent underlying cause
- Suspect when any decompensation in a patient with stable cirrhosis
- Sx: fever, abdominal pain, worsening ascites
- Monomicrobial infection: E. Coli, Klebsiella, S. pneumoniae
- Diagnosis: paracentesis of ascites with > 250 PMN/mm3
- Therapy: 3rd generation cephalosporin
- 50% 6-month survival
hepatorenal syndrome
Hepatorenal syndrome (complication of ascites)
- Rapidly progressive renal failure in the setting of cirrhosis without significant morphological abnormalities of kidneys
- Vasoconstriction of the renal circulation
- Worsening renal function, Low urinary sodium despite adequate intravascular volume
- Type 1: anuria, rapid, high mortality
- Type 2: slowly progressive
- Pts will die w/o liver transplant
• Therapy:
o reversal of peripheral vasodilation→vasoconstrictors (midodrine)
o inhibit vasodilation→octreotide
o aggressive volume replacement
o Only real tx is liver transplant
portosystemic encephelopathy diagnosis
o Changes in state of arousal in patient with chronic liver disease
o Investigate other causes of Δ in mentation
• Drugs, trauma, infection, stroke, intracranial bleed, metabolic causes
o Venous ammonia
o Presence of asterixis (“liver flap”)
o Neuropsychiatric testing
o EEG (seldom used)
portosystemic encephelopathy treatment
o Correct underlying precipitating factors
o Decrease dietary animal protein
o Increased dietary vegetable protein
o Lactulose
• Hydrolyzed by colonic bacteria, reduces colonic pH, “trapping” nitrogenous waste
• Goal of therapy: 2-3 semi-solid BM/day
o Rifaximin, Neomycin (now rarely used)
• Poorly absorbed antibiotics
• Eradicate colonic bacteria responsible for making ammonia and toxic amines
prognostic indices of cirrhosis
- Child Pugh Score: A is best C is worst
- MELD score: predict survival in pts undergoing surgery
abdominal plain films
o Adv: cheap easy, portable
o Disadv: superimposition of structures, lack contrast resolution
o Free air (upright of left lateral decubitus)
o Intestinal obstruction series
Upper GI imaging
o Single contrast: uses thin barium; evaluate anatomy, detect large mass, assess organ caliber, obstruction, motility response to maneuvers (GERD)
o Air contrast (double contrast): uses thick barium; mucosal disease (gastritis), ulcers, tumors, biphasic exam
o If perforation suspected use water soluble contrast (gastrogafin)—contraind: small bowel obstruction, pt likely to aspirate, tracheoesophageal fistula
o Do endoscopy or CT first, the barium
o Barium swallow: esophagus and GE junction
o Small bowel follow through: adds jejunum and ileum
• Enterocolysis
dilute contrast solution pumped into small bowel via oral or nasal tube; time-consuming; uncomfortable
• Cine-esophagram:
: evaluates swallowing function; recurrent aspiration, cervical spine surgery, laryngectomy, stroke, myasthenia gravis, pts intubated for long time
barium enema
o Single contrast: poylpys, diverticula, preferred over double contrast in emergency situation, assess patency of appendix
o Air contrast (double contrast): detect mucosal colonic disease (IBD); greater sensitivity than single contrast for colonic polyps; requires great pt cooperation
o If concerns for perforation, use single contrast w/ water soluble contrast
o Contraind: free air or extreme dilation, peritoneal signs
o Do CT first, then BE
o Prep: 24hrs, dietary restriction, hydration, osmotic laxatives, contact laxatives **imp b/c adherent stool cannot be distinguished from a polyp
CT colonography
o No contrast and less pt cooperation compared to BE
o No sedation and fewer complications than colonoscopy
o Expensive, used only in pts who failed colonoscopy
CT scan
o Eliminates problem of superimposition of structures
o IV contrast media can be used to evaluate blood flow
o Disadv: expensive, not portable, can’t use in pregnancy
• Oral contrast to see bowel loops
• Dense objects (metal) obscure surrounding structures
o Good at:
• detecting masses, determining site of origin, and characterizing them
• guidance for percutaneous biopsy
• assess internal organs after trauma
• extraluminal disease (inflammation, abscess)
• pancreas, retroperitoneum
• abdominal aortic aneursym
• non-operative staging fo neoplastic disease
o Ideal pt: some intraperitoneal fat, not obese, hold breath, oral and IV contrast
o Prep: NPO for 4hrs (vomiting common w/ IV contrast, don’t want to risk aspiration)
abdominal ultrasound
o Adv: portable, multiple planes, no radiation, cheaper than CT/MRI, see “real-time”
o Dis: obese pts can’t penetrate, can’t penetrate air or bone, small field of view, operator dependent, little use in intraluminal GI disease
o Good at:
• Bile ducts
• Gallbladder,
• Renal collecting system
• Reanl mass (cystic vs solid)
• Focal liver lesions
• Renal calculi
• Guidance for biopsy/drainage
• Uterus/ovaries in women
• Pancreatic mass/peripancreatic collections
• Characterize abdominal mass, detect abscess,
• evaluate retroperitoneum for adenopathy or hemorrhage
o Pt: thin and cooperate w/ breathholding
o Prep:
• Hepatic, biliary, complete abdominal ultrasound NPO for 6hrs
• No prep for renal
• Abdominal aort or renal artery doppler NPO for 6hrs
• Pelvic: full bladder
o Doppler: evaluate portal vein flow and collaterals, occlusion hepatic veins,
abdominal MRI
o characterize abdominal masses;
o assess blood vessels in looking for aortic dissection, tumor invasion, vessel thrombosis
Mid-abdominal pain and hypotension in a 72 year old male
T= 99.2 P=116 BP=90/60 R=16
o DDX:
• Abdominal Aortic Aneurysm**
• Pyelonephritis
• Cholecystitis
• Appendicitis
• Small Bowel Obstruction
• Diverticulitis
• Mesenteric Ischemia*
• Ureterolithiasis
Right Lower Quadrant Pain in a 28-Year-Old Female
o RLQ pain for 48 hrs.
o PMH: PID
o Fam Hx: Inflammatory Bowel Disease
o ? LNMP
o T= 99.2 P= 84 BP=110/60 R=16
o DDX:
• Appendicitis*
• Crohn’s disease
• Mesenteric adenitis
• Ectopic pregnancy**
• Pelvic inflammatory disease (PID)
• Ruptured ovarian cyst
• Ovarian torsion
• Ureterolithiasis
• Pyelonephritis
• Urinary tract infection (UTI)
o Key points:
• In a 28-year-old female who presents with a hx of lower abdominal pain associated with fever, separate GI and GYN causes.
• An appropriate menstrual and sexual hx are essential, as is hx of GI and GU symptoms.
• Obtain a quantitative β-hCG pregnancy test to r/o ectopic pregnancy, a U/A and CBC
• Look for the prodrome of appendicitis.
• If tachycardia and hypotension are present, particularly in face of a missed period, seriously entertain dx of ectopic pregnancy.
• Appendicitis is usually a clinical dx, but if unclear, pelvic ultrasonography (pediatrics) or CT of the abdomen and pelvis would be helpful.
• When the dx is between appendicitis and a GYN condition, diagnostic laparoscopy may be of great benefit
Right Upper Quadrant Pain in a 44-Year-Old Female
o DDX:
• Biliary colic
• Cholangitis **
• Pancreatitis
• Peptic ulcer disease
• Acute cholecystitis
• Hepatitis
• Pyelonephritis
• Pneumonia
o Key points:
• In 44-year-old female patient with RUQ pain, initial focus is on the hepatobiliary system.
• Questions about the pain, and its duration and radiation; include hx of alcohol intake (hepatitis, pancreatitis) and urinary tract symptoms (pyelonephritis).
• Hx of intermittent RUQ postprandial pain → suspect gallbladder disease
• Hx of jaundice, pale stools, and pruritis will lead to consideration of either a primary hepatic process or posthepatic biliary obstruction.
• A CBC, U/A, liver function tests, amylase, and lipase (pancreatitis) should be routinely considered.
• Pay attention to pattern of Liver function tests:
• primarily elevated transaminases suggest hepatic dysfunction;
• elevated bilirubin and alkaline phosphatase suggest posthepatic obstruction.
• ***Ultrasonography of the RUQ is often a first choice for imaging
• **RUQ tenderness
• differentiate between biliary colic and acute cholecystitis and helps determine the appropriate timing for surgery.
• positive Murphy’s sign (mid-inspiratory arrest when palpating the RUQ)
• ?Fever and leukocytosis
Biliary colic vs acute cholecystitis
Biliary Colic
- intermittent
- no fever
- ? tenderness
- no WBC
- No Ultrasound criteria
Acute cholecystitis
- Persistent pain
- Fever
- Tenderness + guarding
- WBC
- Ultrasound criteria
Epigastric Pain in a 47-Year-Old Male
o DDX:
• Peptic ulcer disease (PUD)/gastritis
• Esophageal reflux/esophagitis
• Biliary colic/cholecystitis
• Hepatitis
• Pancreatitis
• Pneumonitis
• Myocardial ischemia**
o Key points:
• Use the hx to distinguish between GI pathologies: (esophagitis, PUD, GERD,), peri-intestinal (biliary tract, pancreatitis, hepatitis), and supra-diaphragmatic (pneumonitis, cardiac) pathologies
• Virtually all patients should have an EKG and troponin/cardiac enzymes, CXR, liver function tests, and amylase
• Ultrasonography when the hx is suggestive of biliary symptoms
• When the hx suggests esophageal or gastroduodenal disease, a diagnostic EGD may be indicated
Lower Left Quadrant Pain in a 67-Year-Old Male
T= 101.2 P= 92 BP=140/70
PMH: “prone to constipation, worse lately”
o DDx:
• Diverticulitis
• Ischemic colitis**
• Volvulus
• Colon cancer*
• Hernia (incarcerated)
• Ureterolithiasis
o KeY points:
• Separate infectious from noninfectious causes
• Ask about onset of symptoms, bowel habits, previous hx of similar episodes, GI symptoms, and hx of previous colonoscopy.
• Determine if the patient is clinically obstructed.
• Look for focal versus diffuse abdominal tenderness, masses, hernias.
• Noncomplicated diverticulitis is often the clinical dx; if unclear, a plain abdominal x-ray and CT of the abdomen and pelvis can be helpful.
• When the CT shows thickening of the bowel wall without evidence of diverticula, dx of an enteritis versus ischemic colitis may be made by endoscopic evaluation of the colonic mucosa.
“Free Air” in a 72-Year-Old Female
T= 99.2 P=120 BP=85/60 R=16
o DDx:
• Perforated ulcer**
• Perforated diverticulitis**
• Perforated cancer**
• Perforated small bowel obstruction**
• Perforated cecum**
o Key points:
• Consider the patient most likely needs an operation, as the vast majority of conditions that cause free air require surgical correction.
• Determine how to prepare the patient for the OR.
• Most of these patients require volume resuscitation prior to the induction of anesthesia
Abdominal Pain and Distention in a 63-Year-Old male
o DDX:
• Small bowel obstruction
• Volvulus
• Mesenteric ischemia**
• Ileus
• Large bowel obstruction
• Ogilvie’s syndrome
• Ascites
• Intestinal perforation**
• Hernia with incarceration*
o Key points:
• Consider all reasons abdomen may be distended.
• Is the situation acute vs non-acute?
• Is there peritonitis on physical examination?
• Does the patient appear ill? (i.e., severe discomfort, abnormal VS: (tachycardia, increased respiratory rate, hypotension, fever )
• Resuscitation (IV fluids, O2, Foley catheter)
• Obtain an obstruction series to r/o perforation (free air) or bowel obstruction.
• Always keep in mind the dx of mesenteric ischemia, so as not to be fooled by a relatively benign physical examination, which is characteristic of mesenteric ischemia in its early phases.
kids vs adult GI managment
o Communication difficult
o More congenital anomalies
o Gastrointestinal cancer is rare
o “Allergy” more common
o Invasive procedures more difficult
o Systemic infections more likely to present as GI symptoms
DDX of chronic vomiting in infants
• Chronicity is >3wks
• DDx of vomiting in infants:
o GI infection (mostly acute vomiting, chronic=parasites, H. pylori)
o Gastroesophageal reflux (GER)
o Congenital anomalies
o Urinary tract abnormalities (kidney stones, UTI, dyplastic kidney)
o Metabolic disease (esp. acidosis)
o Systemic infections (otitis, urinary, etc)
o Increased intracranial pressure (hydrocephalus, brain tumors, intracranial bleed)
pediatric GER
• GERD: common cause of chronic vomiting
o 80% of normal full-term infants
o Sx:
• Recurrent vomiting; Recurrant vomiting and irritability; Recurrent vomiting and poor weght gain
• Dysphagia or feeding refusal, Esophagitis, Apnea or ALTE Wheezing/asthma (can exacerbate existing), Pnuemonia (aspiration, RUL), Upper airway symptoms
o Diagnosis:
• Clinical history (“regurgitation” small volume spitting up, up to 20-30x day, non-bilious, can contain blood—esophagitis)
• Upper GI series (UGI)—detects anatomic abnormalities, but cannot discriminate b/t physiologic and nonphysiologic GERD
• Nuclear medicine scintiscan (milkscan)
• 24 hour ph probe: **gold standard
• Endoscopy
• Impedance monitoring
o Treatment:
• Conservative: change composition of formula, change positioning of infant
• Pharmacotherapy (same as adults, H2 blockers more than PPI)
• Surgical therapy: only if severe documented respiratory events
• Typically resolves by age 2
pediatric eosinophilic gastroenteritis
o Enteropathy (mucosal)
o Eosinophilic esophagitis (inflammation esophagus, endoscopic diagnosis, 25 eosinophils per hpf)
o Eosinophilic gastritis (older children, food impaction, difficulty swallowing)
o Serosal eosinophilic enteritis (non-allergic diet)
o Sx: chronic vomiting, failure to thrive, feeding d/o
o Cowsmilk, soymilk protein implicated
o Atopic families
o Treatment is dietary
o Exclude congential anomalies of GI tract; more proximal anomaly is the earlier it is detected
pediatric esophageal atresia
o Assoc w/ tracheoesophageal fistula
o Presentation:50% polyhydramnios (before birth), aspiration and emesis first few hours of life
o Diagnosis: clinical and Xray
o Treatment: surgical
pediatric pyloric stenosis
o Narrowing of the pyloric outlet due to hypertrophy of the pylorus muscle
o Presents 3-6 weeks of life
o Presentation: emesis (non-bilious, can have blood, projectile), failure to thrive, dehydration (hypochloremic alkalosis); can palpate pylorus on abdominal exam “olive”
o Diagnosis: clinical, ultrasound, UGI
o Treatment: surgery
pediatric duodenal atresia, stenosis
o Presentation: emesis (bilious or not) within first 2 days of life, abdominal distension (high obstruction)
o Associated with chromosomal abnormalities (down’s)
o Diagnosis: obstruction series, UGI; double bubble sign on xray (dilated stomach and duodenal bulb)
o Treatment: surgery
pediatric intestinal malrotation
o “Non-rotation “ most common: small intestine on right, colon on left
o Presentation:volvulus (bilious emesis, abdominal obstruction, GI bleed)
o Diagnosis: obstruction series, UGI, barium enema
o Treatment: surgery
o Predisposes to volvulus (or twisted bowel)→bowel ischemia and necrosis,
o Presents in first few months of life
pediatric intestinal atresia
o Complete obstruction of lumen of bowel
o Jejunum and ileum most common
o Presentation: bilious emesis, abdominal distension, growth failure at any time in infancy
o Diagnosis: UGI/SBFT, barium enema
o Treatment: surgery
o Normal bowel pattern suggests against obstruction
