GI Flashcards
Harbinger of more severe disease in acute pancreatitis
Hemoconcentration (Hct >44%)
vs azotemia - significant risk factor for mortality
Risk factors for severity in acute pancreatitis
Agre >60
BMI >30
Comorbid disease
Most important clinical finding regarding severity of the acute pancreatitis episode
Persistent organ failure (>48h)
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
Components of BISAP score
BUN >25
Impaired mental status (GCS<15)
SIRS
Age > 60
Pleural effusion
2 most common etiologic factors for recurrent acute pancreatitis
Alcohol and cholelithiasis
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)
2 types of gallstones
Cholesterol and pigment stones
Cholsteerol - more common in West (90%)
Pigment - brown/black (*brown forms secondary to chronic liary infection)
Most important mechanism in the formation of lithogenic bile
Increased biliary secretion of cholesterol
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
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)
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
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
Jaundice without dark urine is typical of…
Hemolytic anemia
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)
Toxin that causes destruction of mucosal cells and associated inflammatory diarrhea
Cytotoxins .. produce dysentery
*Shigella dystenteriae type 1
*Vibrio parahaemolyticus
*C. difficile
Toxin that act directly on CNS or PNS to cause diarrhea
Neurotoxins … causes symptoms SOON after ingestion
*Staphylococcal
*Bacillus cereus toxins - CNS –> vomiting
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)
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
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
Type of ascites presenting with SAAG < 1.1 g/dL (5)
Biliary leak
Nephrotic syndrome
Pancreatitis
Peritoneal carcinomatosis
Tuberculosis
SAAG >1.1g/dL, ascitic protein > 2.5
Heart failure/constrictive pericarditis
Early Budd-Chiari syndrome
IVC obstruction
Sinusoidal obstruction syndrome
SAAG >1.1g/dL, ascitic protein < 2.5
Cirrhosis, Late Budd-Chiari syndrome,
Massive liver mets
Diagnostic criteria for IBS
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
