GI clinical Flashcards

Question

pt has bright red blood coming from rectum

Answer 1

• Hematochezia colonic bleeding or brisk bleeding from proximal sites

Answer 2

melena upper GI bleed (esophagus, stomach, duodenum) comes from bacterial metabolism of RBC

Answer 3

hemetemesis due to upper GI bleed (esophagus, stomach, duodenum)

Answer 4

anemia possibly due to occult GI bleed positive stool hemoccult test

Answer 5

* Class 1: pulse \<100bpm * Class 2: pulse\>100bpm * Class 3: blood pressure decreased * Class 4: confused, lethargic

Answer 6

**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

Answer 7

**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

Answer 8

**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

Answer 9

**Class 2** **Next:** nuclear medicine scan (vs if it had been small amount of blood, exclude anorectal source, and evaluate w/ colonoscopy)

Answer 10

Evaluate w/ endoscopy] Therapies: - Pharm: octreotide - endoscopic: band ligation, ablation, endoclips - radiology: TIPS - surgery: failure of other therapies

Answer 11

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%

Answer 12

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%

Answer 13

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

Answer 14

ulcerative colitis

Answer 15

Crohns disease

Answer 16

ulcerative colitis

Answer 17

\*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

Answer 18

\*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

Answer 19

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.

Answer 20

mucosal infiltration by neutrophils, lymphocytes, plasma cells, macs→cryptitis, crypt + **non-caseating granulomas** ## Footnote Gross pathology: transmural inflammation, fistulas, strictures; creeping fat

Answer 21

**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

Answer 22

**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

Answer 23

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

Answer 24

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)

Answer 25

* *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

Answer 26

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

Answer 27

a. High 1st-pass metabolism=Few systemic side effects! * *b. Efficacy:** i. CD: Ileal/R colonic ii. Ulcerative Proctitis (enema formulation)

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

a. Mechanism: alpha 4 integrin antibody→dec. WBC trafficking to sites of inflammation b. Indication: CD + induction/maintenance c. Safety: Progressive multifocal leukoencephalopathy

Answer 32

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

Answer 33

i. Indications: stricture, perforation, abscess, fistula, refractory dz, hemorrhage, cancer ii. Types: ileocecectomy, stricturoplasty, fisulotomy/setons iii. Lifetime incidence 60-70%

Answer 34

i. Indications: refractory dz, neoplasia, fulminant colitis, toxic megacolon, hemorrhage ii. Types: TPC +/- IPAA iii. Lifetime incidence 30%

Answer 35

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

Answer 36

painful arrest in inspiratoinn triggered by palpation of inflamed gallbladder pt is lying supine, examiner places fingers over R. costal margin in MCL

Answer 37

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)

Answer 38

* Fat * Fertile * Female * Forty/Fifty

Answer 39

* Symptoms: N/V, RUQ pain * Positive Murphy’s sign * Boas’ sign (low sensitivity): area of hypersensitivity at costophrenic angle * Audible rub over gallbladder

Answer 40

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)

Answer 41

likely have ultrasound, no ultrasound needed

Answer 42

Pt is unlikely to have ascites no ultrasound

Answer 43

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

Answer 44

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

Answer 45

* 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

Answer 46

* 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

Answer 47

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

Answer 48

hypersensitivity to light touch to abdominal areas over an inflamed viscus not specific to localized peritonitis seen in herpes zoster, PUD

Answer 49

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

Answer 50

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

Answer 51

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

Answer 52

o Ulcerative colitis o Colon cancer o Colon polyps o Management: colonoscopy

Answer 53

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

Answer 54

* 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

Answer 55

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

Answer 56

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)

Answer 57

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

Answer 58

* 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

Answer 59

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

Answer 60

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

Answer 61

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

Answer 62

* 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

Answer 63

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

Answer 64

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

Answer 65

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

Answer 66

o Inflammation o 3rd space losses o fat necrosis o pancreatic and peripancreatic necrosis

Answer 67

Reversible; Normal pancreas becomes acutely inflamed

Answer 68

Persistent and progressive process; changes in pancreatic structure/function precede sx and persist after cause of pancreatitis corrected.

Answer 69

Pathophysiology: 1. 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) 2. Glandular: increased vascular permeability - influx and activation of inflammatory cells, formation reactive metabolites - dissolution blood vessels and ECM - Thrombosis, hemorrhage, tissue necrosis 3. Systemic: - Respiratory failure (phospholipase A2, subdiaphragmatic inflammation, pain w/ inspiration, hemorrhage dec. oxygen carrying capacity) - renal failure - DIC - Shock

Answer 70

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 - 1. Common duct stones - 2. Alcohol - 3. Idiopathic - 4. 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

Answer 71

Clinical presentation - Sx: abdominal pain, N/V, low-grade fever, dehydration - PE: tenderness, mild distension, decreased or absent bowel sounds

Answer 72

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

Answer 73

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)

Answer 74

-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

Answer 75

Pathophysiology: 1. acinar and duct cell damage→inc. membrane permeability - inc. intraductal calcium and protein precipitate to from plugs/stones→partial duct obstruction 2. inflammation, fibrosis, atrophy, and disruption of ducts and exocrine/endocrine tissue 3. hard fibrotic (cirrhotic-like) organ (dec. number and size of acini and islets)

Answer 76

Etiology: 1. Alcohol: - direct acinar cell toxicity - alters membrane infrastructure (inc. permeability) - inc. basal protein secretion - dec. trypsin inhibitor - althers lithostatin (ppt of calcium) 2. Hereditary: - abnormal trypsinogen or trypsin inhibitor - cystic fibrosis (CFTR mutations) 3. chronic partial duct obstruction 4. autoimmune 5. idiopathic 6. tropical

Answer 77

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

Answer 78

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)

Answer 79

Complications: - pain, malabsorption, wt loss, diabetes - narcotic addiction - pseudocyst formation - common bile duct obstruction, duodenal obstruction - splenic vein thrombosis (gastric varices)

Answer 80

Treatment: - alcohol abstinence - low fat diet - pancreatic enzymes +/- acid suppression - analgesics - insulin - ductal decompression (surgical, endoscopic) - celiac plexus neurolysis - pancreatectomy

Answer 81

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

Answer 82

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

Answer 83

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**

Answer 84

* Acute viral hepatitis (HAV, HBV) * Drug toxicity (acetominophen) * Shock liver (hypotensive episode) * Autoimmune hepatitis

Answer 85

alcoholic hepatitis

Answer 86

* Chronic viral hepatitis * Nonalcoholic fatty liver disease * Metabolic disease (Wilsons, AAT deficiency) * Meds * Autoimmune hepatitis

Answer 87

**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

Answer 88

severe liver disease w/ dysfx (other causes nephritic syndrome, protein losing enteropathy, malnutrition)

Answer 89

• 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

Answer 90

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

Answer 91

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

Answer 92

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

Answer 93

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

Answer 94

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

Answer 95

o Enteric; contaminated water; India, Asia, Africa, Central America o Recovery is rule except in pregnancy (20% fulminant hep) o Prognosis: good except pregnancy

Answer 96

• Hepatitis G: liver transplant pts

Answer 97

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

Answer 98

o AST, ALT\>1000 o Elevated serum bilirubin o Elevated INR=poor prognosis

Answer 99

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

Answer 100

* 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

Answer 101

* 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

Answer 102

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)

Answer 103

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

Answer 104

* 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

Answer 105

* 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

Answer 106

* 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

Answer 107

* 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

Answer 108

* 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

Answer 109

• 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

Answer 110

• 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

Answer 111

• 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

Answer 112

• 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

Answer 113

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

Answer 114

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

Answer 115

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

Answer 116

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

Answer 117

• 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

Answer 118

• 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

Answer 119

• Diagnosis: o Abdominal distension in a pt w/ portal HTN o Flank dullness by percussion o Shifting dullness

Answer 120

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

Answer 121

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

Answer 122

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

Answer 123

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

Answer 124

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)

Answer 125

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

Answer 126

* Child Pugh Score: A is best C is worst * MELD score: predict survival in pts undergoing surgery

Answer 127

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

Answer 128

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

Answer 129

dilute contrast solution pumped into small bowel via oral or nasal tube; time-consuming; uncomfortable

Answer 130

: evaluates swallowing function; recurrent aspiration, cervical spine surgery, laryngectomy, stroke, myasthenia gravis, pts intubated for long time

Answer 131

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

Answer 132

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

Answer 133

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)

Answer 134

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,

Answer 135

o characterize abdominal masses; o assess blood vessels in looking for aortic dissection, tumor invasion, vessel thrombosis

Answer 136

o DDX: • Abdominal Aortic Aneurysm\*\* • Pyelonephritis • Cholecystitis • Appendicitis • Small Bowel Obstruction • Diverticulitis • Mesenteric Ischemia\* • Ureterolithiasis

Answer 137

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

Answer 138

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

Answer 139

Biliary Colic * intermittent * no fever * ? tenderness * no WBC * No Ultrasound criteria Acute cholecystitis * Persistent pain * Fever * Tenderness + guarding * WBC * + Ultrasound criteria

Answer 140

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

Answer 141

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.

Answer 142

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

Answer 143

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.

Answer 144

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

Answer 145

• 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)

Answer 146

• 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

Answer 147

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

Answer 148

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

Answer 149

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

Answer 150

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

Answer 151

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

Answer 152

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