GI Flashcards by ANC V.

Harbinger of more severe disease in acute pancreatitis

Hemoconcentration (Hct >44%)

vs azotemia - significant risk factor for mortality

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Risk factors for severity in acute pancreatitis

Agre >60
BMI >30
Comorbid disease

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Most important clinical finding regarding severity of the acute pancreatitis episode

Persistent organ failure (>48h)

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IV fluid resuscitation in Acute pancreatitis

PLR or normal saline initially bolused at 15-20mL/kg (1050-1400mL) followed by 2-3mL/kg/hr (200-250mL/h) to maintian UO >0.5mL/kg/hr

*Repeat volume challange with 2L crystalloid bolus and increase rate to 1.5mg/kg/hr if (+) rise in Hct or BUN during serial measurement

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Components of BISAP score

BUN >25
Impaired mental status (GCS<15)
SIRS
Age > 60
Pleural effusion

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2 most common etiologic factors for recurrent acute pancreatitis

Alcohol and cholelithiasis

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Treatment of steatorrhea in chronic panccreatitis

Enzyme therapy
Lipase 25,000-50,000 units during each male (up to 100,000 units depending on response, nutritional parameters, and /or panreas function results)

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2 types of gallstones

Cholesterol and pigment stones

Cholsteerol - more common in West (90%)
Pigment - brown/black (*brown forms secondary to chronic liary infection)

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Most important mechanism in the formation of lithogenic bile

Increased biliary secretion of cholesterol

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Conditions that are associated with cholesterol-stone or biliary sludge formation

Pregnancy and rapid weight reduction through very low calorie diet

*UDCA 600mg/day proved highly effective in preventing gallstone formation

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3 factors to consider to recommend cholecystectomy

(1) the presence of symptoms that are frequent enough or severe enough to interfere with the patient’s general routine;

(2) the presence of a prior complication of gallstone disease, that is, history of acute cholecystitis, pancreatitis, gallstone fistula, etc.; or

(3) the presence of an underlying condition predisposing the patient to increased risk of gallstone complications (e.g., a previous attack of acute cholecystitis regardless of current symptomatic status)

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Patient profile who will benefit frmo UDCA

Radiolucent <5mm in diameter (stones >10mm rarely dissolve)
Functioning galbladder
CHOLESTEROL STONES ONLY (pigment not responsive

Give UDCA 10-15mg/kg/day

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Bacteria most frequently cultures in emphysematous cholecystitis

Anarobes, C. welchii or C. perfringes
and aerobes - E coli

*most frequent in DM px and men
*Prompt surgical intervention & antibiotics needed
*diagnosed on plain abdominal film (+) gas within the gallbladder

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Jaundice without dark urine is typical of…

Hemolytic anemia

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Toxin that causes watery diarrhea by acting directly on secretory mechanisms in intestinal mucosa

Enterotoxin .. watery diarrhea

*Cholera-increases cAMP to increase Cl secretion and decrease Na absorption
*Enterotoxigenic strains of E. coli (heat labile, similar to cholera
and heat stable guanlyate cyclase and elevation of cGMP)

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Toxin that causes destruction of mucosal cells and associated inflammatory diarrhea

Cytotoxins .. produce dysentery

*Shigella dystenteriae type 1
*Vibrio parahaemolyticus
*C. difficile

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Toxin that act directly on CNS or PNS to cause diarrhea

Neurotoxins … causes symptoms SOON after ingestion

*Staphylococcal
*Bacillus cereus toxins - CNS –> vomiting

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Bacterial food poisoning: Agents that have 8-16h incubation period

Clostridium perfringens (beef, poultry, legumes, gravies)

B. cereus diarrheal form (meats vegetables, dried beans, cereals)

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Antibacterial drugs for dysentery

If the level of suspicion is low for fluoroquinolone-resistant Campylobacter: Adults:
(1) A fluoroquinolone such as ciprofloxacin, 750 mg as a single dose or 500 mg bid for 3 days; levofloxacin, 500 mg as a single dose or 500 mg qd for 3 days; or norfloxacin, 800 mg as a single dose or 400 mg bid for 3 days

(2) Azithromycin, 1000 mg as a single dose or 500 mg qd for 3 days

(3) Rifaximin, 200 mg tid or 400 mg bid for 3 days (not recommended for use in dysentery).

*If with travel to Southeast asia, Azithromycin

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Type of ascites presenting with SAAG >1.1 g/dL

Cirrhosis
Late Budd-Chiara syndrome
Massive liver metastases
————
Heart failure/constrictive pericarditis
Early Budd-Chiari syndrome
IVC obstruction
Sinusoidal obstruction syndrome

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Type of ascites presenting with SAAG < 1.1 g/dL (5)

Biliary leak
Nephrotic syndrome
Pancreatitis
Peritoneal carcinomatosis
Tuberculosis

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SAAG >1.1g/dL, ascitic protein > 2.5

Heart failure/constrictive pericarditis
Early Budd-Chiari syndrome
IVC obstruction
Sinusoidal obstruction syndrome

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SAAG >1.1g/dL, ascitic protein < 2.5

Cirrhosis, Late Budd-Chiari syndrome,
Massive liver mets

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Diagnostic criteria for IBS

Study These Flashcards

Rome IV: recurrent abdominal pain at least once a week for 3 months, associated with 2 or more:
Related to defacation
Associated with change in frequency of stool
Associated with change in form/appearance of stool

Definition of portal hypertension (in mmHg)

Elevation of hepatic venous gradient to >5mmHg *Clinically significant portal hypertension is >10mmHg

Most common cause of portal hypertension

Cirrhosis

3 primary complications of portal hypertension

Gastroesophageal varices with hemorrhage Ascites Hypersplenism

Usually the first indication of portal hypertension

Congestive splenomegaly and hypersplenismDI

Diuretics used in ascites management

Spironolactone 100mg/day single dose up to max 400mg/day Furosemide 40mg/day then up to 160mg/day

Management of hepatorenal syndrome

Diuretics should be stopped Infusion of albumin 1g/kg is recommended Tx with vasoconstrictors (terlipressin, low dose NE, midodrine) Best therapy: liver transplant

Duration of refractory GU

Failure to heal after 12 weeks

Duration of refractory DU

Failure to heal after 8 weeks

Major types of chemical hepatotoxicity

Direct toxic & idiosyncratic

Characteristics of idiosyncratic drug reaction

Liver injury is infrequent Response not as clearly dose dependent,unpredictable May occur anytime after exposure (Typically 5-90 days following initiation)

Four agents that have phenotype of autoimmune hepatitis, with high likelyhood of positive ANA

Nitrofurantoin Minocycline Hydralazine Methyldopa

R value (ratio of ALT to alkaline phosphatase values) cut offs to determine hepatocellular or cholestatic injury

R>5 Hepatocellular 2-5 Mixed <2 Cholestatic

Prototype drugs that cause idiosyncratic drug reaction

Co-amoxiclav Isoniazid Ciprofloxacin *Direct toxic: Acetaminophen, carbon tetrachloride

Most common agent implicated as causing DILI in US and EU

Co-amoxiclav

Type of reaction caused by Amiodarone hepatotoxicity

Toxic AND idiosyncratic *Can present with modest serum aminotransferase elevations, detectable hepatomegaly

Type of reaction caused by Statin hepatotoxicity

Idiosyncratic mixed hepatocellular and cholestatic reaction

Signs to suspect CBD stone in px with cholecystitis

Serum bili >5mg/dL (if >15, suspect concomitant hepatic or renal disease or other actor lreading to marked hyperbilirubinemia) Elevated ALP (often precedes clinical jaundice) 2-10 fold elevation of ALT

Preferred initial procedure for cholangitis

ERCP with sphincterotomy

4 serologic tests to request for px with acute hepatitis

HbsAg Anti HBc IgM Anti HAV IgM Anti HCV

Initial testing in chronic hepatitis

HbsAg and anti HCV If established Hep B, test for HbeAg and anti-Hbe to evaluate relative infectivity

Sine qua non for determining on treatment and durable responsiveness when treating for hepatitis C

HCV RNA *Not a reliable marker of disease severity or prognosis but helpful in predicting relative RESPONSIVENESS to antiviral therapy

Features suggesting progression of acute to chronic hepatitis

1) lack of complete resolution of symptoms, persistence of hepatomegaly 2) presence of bridging/interface or multilobular hepatic necrosis on liver biopsy during protracted, severe acute viral hepatitis 3)failure of serum aminotransferase, bilirubin, and globulin levels return to normal within 6-12 months after acute illness 4) persistence of HbeAg > 3 months or HbsAg > 6 months

Tx duration for acute viral hepatitis

should continue until 3 months after HBsAg seroconversion or 6 months after HBeAg seroconversion

Adjuncts in mgt of acute viral hepatitis

Severe pruritus - cholestyramine Glucocorticoids - no value Blood precautions for hep B and C

Conventional serum marker for HBV replication

HbeAg

Most important risk factor for the ultimate development of cirrhosis and HCC

Level of HBV replication

Antiviral recommended for chronic hep B with reduced renal function (CrCl <50)

Tenofovir alafenamide (TAF)

Treatment pearls in chronic Hep B

Treat only if HBV DNA >2x10^3 IU/mL and ALT >ULN (*except in compensated cirrhosis - treat as long as HBV DNA is detectable at >2x10^3, if decompensated-treat) PEG IFN not used for immunocompromised or IFN-intolerant/refffractory Oral agents are administered daily for at least a year and 6 months after HbeAg seroconversion

2 major histologic features suggesting chronicity of UC

-Crypt architecture of the colon is distorted -Basal plasma cells and multiple basal lymphoid aggregates

IBD complications more common in UC

Pyoderma gangrenosum Primary sclerosing cholangitis *More common in CD- peripheral arthritis, erythema nodosum, AS, nephrolithiasis, reactive amyloidosis *Equal = sacroiliitis

Extraintestinal manifestations of IBD that correlate with bowel activity

Erythema nodosum Peripheral arthritis - worsens with exacerbation *Does not correlate: Psoriasis, ankylosing spondylitis, sacroiilitis

UC patients who are more likely to require biologics

Moderate to severe disease Steroid dependent Steroid refractory (+) Refractory pouchitis

CD patients who are more likely to require biologics

<30 years old, extensive disease Perianal or severe rectal disease and/or deep ulcerations in the colon Structuring and penetrating disease behavior

Most common cause of acute gastritis

Infectious

2 types of chronic gastritis

Type A: body predominant (autoimmune), associated with pernicious anemia, gastrin levels markedly elevated >500pg/mL Type B: antral predominant, H. pylori related more common Histology improves after H pylori eradication

GI Flashcards

(59 cards)