GI Flashcards

1
Q

Harbinger of more severe disease in acute pancreatitis

A

Hemoconcentration (Hct >44%)

vs azotemia - significant risk factor for mortality

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Risk factors for severity in acute pancreatitis

A

Agre >60
BMI >30
Comorbid disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Most important clinical finding regarding severity of the acute pancreatitis episode

A

Persistent organ failure (>48h)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

IV fluid resuscitation in Acute pancreatitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Components of BISAP score

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

2 most common etiologic factors for recurrent acute pancreatitis

A

Alcohol and cholelithiasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Treatment of steatorrhea in chronic panccreatitis

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

2 types of gallstones

A

Cholesterol and pigment stones

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Most important mechanism in the formation of lithogenic bile

A

Increased biliary secretion of cholesterol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A

Pregnancy and rapid weight reduction through very low calorie diet

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

3 factors to consider to recommend cholecystectomy

A

(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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Patient profile who will benefit frmo UDCA

A

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

Give UDCA 10-15mg/kg/day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bacteria most frequently cultures in emphysematous cholecystitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Jaundice without dark urine is typical of…

A

Hemolytic anemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

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

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Toxin that causes destruction of mucosal cells and associated inflammatory diarrhea

A

Cytotoxins .. produce dysentery

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Toxin that act directly on CNS or PNS to cause diarrhea

A

Neurotoxins … causes symptoms SOON after ingestion

*Staphylococcal
*Bacillus cereus toxins - CNS –> vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Clostridium perfringens (beef, poultry, legumes, gravies)

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Antibacterial drugs for dysentery

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Type of ascites presenting with SAAG >1.1 g/dL

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

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

A

Biliary leak
Nephrotic syndrome
Pancreatitis
Peritoneal carcinomatosis
Tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

SAAG >1.1g/dL, ascitic protein > 2.5

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

SAAG >1.1g/dL, ascitic protein < 2.5

A

Cirrhosis, Late Budd-Chiari syndrome,
Massive liver mets

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diagnostic criteria for IBS

A

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

25
Q

Definition of portal hypertension (in mmHg)

A

Elevation of hepatic venous gradient to >5mmHg

*Clinically significant portal hypertension is >10mmHg

26
Q

Most common cause of portal hypertension

A

Cirrhosis

27
Q

3 primary complications of portal hypertension

A

Gastroesophageal varices with hemorrhage
Ascites
Hypersplenism

28
Q

Usually the first indication of portal hypertension

A

Congestive splenomegaly and hypersplenismDI

29
Q

Diuretics used in ascites management

A

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

30
Q

Management of hepatorenal syndrome

A

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

Best therapy: liver transplant

31
Q

Duration of refractory GU

A

Failure to heal after 12 weeks

32
Q

Duration of refractory DU

A

Failure to heal after 8 weeks

33
Q

Major types of chemical hepatotoxicity

A

Direct toxic & idiosyncratic

34
Q

Characteristics of idiosyncratic drug reaction

A

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

35
Q

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

A

Nitrofurantoin
Minocycline
Hydralazine
Methyldopa

36
Q

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

A

R>5 Hepatocellular
2-5 Mixed
<2 Cholestatic

37
Q

Prototype drugs that cause idiosyncratic drug reaction

A

Co-amoxiclav
Isoniazid
Ciprofloxacin

*Direct toxic: Acetaminophen, carbon tetrachloride

38
Q

Most common agent implicated as causing DILI in US and EU

A

Co-amoxiclav

39
Q

Type of reaction caused by Amiodarone hepatotoxicity

A

Toxic AND idiosyncratic

*Can present with modest serum aminotransferase elevations, detectable hepatomegaly

40
Q

Type of reaction caused by Statin hepatotoxicity

A

Idiosyncratic mixed hepatocellular and cholestatic reaction

41
Q

Signs to suspect CBD stone in px with cholecystitis

A

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

42
Q

Preferred initial procedure for cholangitis

A

ERCP with sphincterotomy

43
Q

4 serologic tests to request for px with acute hepatitis

A

HbsAg
Anti HBc IgM
Anti HAV IgM
Anti HCV

44
Q

Initial testing in chronic hepatitis

A

HbsAg and anti HCV

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

45
Q

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

A

HCV RNA

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

46
Q

Features suggesting progression of acute to chronic hepatitis

A

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

47
Q

Tx duration for acute viral hepatitis

A

should continue until 3 months after HBsAg seroconversion

or

6 months after HBeAg seroconversion

48
Q

Adjuncts in mgt of acute viral hepatitis

A

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

49
Q

Conventional serum marker for HBV replication

A

HbeAg

50
Q

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

A

Level of HBV replication

51
Q

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

A

Tenofovir alafenamide (TAF)

52
Q

Treatment pearls in chronic Hep B

A

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

53
Q

2 major histologic features suggesting chronicity of UC

A

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

54
Q

IBD complications more common in UC

A

Pyoderma gangrenosum
Primary sclerosing cholangitis

*More common in CD- peripheral arthritis, erythema nodosum, AS, nephrolithiasis, reactive amyloidosis
*Equal = sacroiliitis

55
Q

Extraintestinal manifestations of IBD that correlate with bowel activity

A

Erythema nodosum
Peripheral arthritis - worsens with exacerbation

*Does not correlate: Psoriasis, ankylosing spondylitis, sacroiilitis

56
Q

UC patients who are more likely to require biologics

A

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

57
Q

CD patients who are more likely to require biologics

A

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

58
Q

Most common cause of acute gastritis

A

Infectious

59
Q

2 types of chronic gastritis

A

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