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MBBS IV - Teaching Clinics, Data Interpretation, Interactive Tutorials > Block A - Medicine - GI Data interpretation > Flashcards

Block A - Medicine - GI Data interpretation Flashcards

1
Q

Parameters of liver function test

A

Cellular integrity:
- ALT and AST

Protein synthesis:
- Albumin and PT

Excretory function:
- Bilirubin, ALP and GGT

Other parameters:

  • Arterial ammonia for Hepatic encephalopathy
  • LDH
  • AFP (HCC)
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2
Q

Markers of hepatocellular injuries
Intrinsic functions of these markers
Sources of these markers

A

ALT and AST

Gluconeogenesis function
transfer of amino acid from alanine acid (ALT) or aspartic acid (AST) to Ketoglutaric acid to produce Oxaloacetic acid and pyruvic acid respectively

Sources:
ALT: Cytosolic enzyme, specific to liver*****
AST: Cytosolic and mitochondrial enzyme, found in liver, cardiomyocytes, skeletal muscles, kidneys, pancreases, blood cells

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3
Q

ALP

  • sources
  • confounding conditions that change ALP level
  • Confirmation of source of ALP
A

Sources: Liver, bone, intestines, placenta

Conditions: Fracture, growth spurt, age, sex…etc

Confirm liver origin of ALP:

  • ALP isoenzyme test
  • Check GGT level (concomitant increase)
  • 5’ nucleotidase
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4
Q

GGT

Intrinsic function
Causes of isolated GGT increase w/ normal ALP

A

Function: Microsomal enzyme which transfers gamma-glutamyl groups from gamma-glutamyl peptides to other proteins

Causes of isolated GGT increase

  • Drug: Phenytoin, carbamazepine, barbituates
  • Alcohol
  • Fatty liver disease: a/w metabolic syndrome
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5
Q

Causes of increased unconjugated bilirubin

A
  • Increase bilirubin production: Hemolysis, ineffective erythropoiesis, resorption of hematoma
  • Decrease hepatic uptake: e.g. Rifampicin reaction
  • Decrease conjugation (isolated hyperbilirubinemia) - Gilbert’s syndrome, Criggler-Najjar syndrome
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6
Q

Infective, autoimmune and metabolic markers of liver function

A

Infective:
- Viral hepatitis markers

Autoimmune: e.g. PBC, PBS
- ANF, AMA, Anti-Smooth muscle Ab

Metabolic:

  • Iron: Total Fe, Ferritin, TIBC
  • Copper: Total Cu, Ceruloplasmin
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7
Q

Define the units of alcohol and recommended consumption

A

1 unit = 10g of alcohol
e.g. 1 beer = 5% alcohol at 200mL = 10g of alcohol

Male: average 2-3 unit per day maximum
Female: average 1-2 unit per day maximum

Alcoholic cirrhosis: 9-10 units per day

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8
Q

40-year-old male with one week history of non-specific symptoms, with development of jaundice 2 days ago, and a relatively unremarkable P/E apart from jaundice

Ddx

A

o Pre-hepatic: hemolysis (CBC)
o Intrahepatic: viral hepatitis, drugs, cirrhosis, tumors (LFT)
o Post-hepatic: gallstones, cancers of the bile duct…

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9
Q

Investigations for viral hepatitis

A

Acute HAV:
- Anti-HAV IgM
Chronic HAV:
- Anti-HAV IgG

Acute HBV:
- Anti-HBc IgM
- HBsAg 
Recovered HBV: 
- Anti-HBs 
- Anti-HBc IgG

Acute HEV:
- Anti-HEV IgM

Acute HCV (no marker)
Recovered HCV:
- Anti-HCV
- HCV RNA

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10
Q

How to differentiate acute Hep. B vs Chronic Hep B with flare

A

Acute Hepatitis B or Chronic Hep B with flare BOTH give high Anti-HBc IgM
IgM does not distinguish between acute flare and acute infection

Differentiation by HBV DNA level and waiting 6 months for remeasurement of IgM and HBsAg clearance

HBV DNA > 640 million copies/ mL is acute Hep B

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11
Q

Describe the serological course of Acute Hep B infection with recovery

A
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12
Q

Immediate investigations for acute, markedly elevated ALT and AST

A

Flare or new onset of autoimmune hepatitis
- Check autoimmune antibodies e.g. ANA, anti-smooth muscle antibody, anti-LKM1

Acute viral hepatitis (by Hep ABCE)
- Anti- HAV IgM, HBsAg, Anti-HBc IgM, Anti-HCV, Anti-HEV

Drug-induced liver damage:
- Toxicology for paracetamol (+ Others)

Ultrasound

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13
Q

Differentiate the underlying causes:

  • Only Anti-HBs Antibody
  • Only Anti-HBc antibody
  • Anti-HBc antibody and Anti-HBs antibody
  • Anti- HBc and HBsAg
A
  • Only Anti-HBs Antibody: Vaccinated against Hep B
  • Only Anti-HBc antibody: Occult Hep B infection/ recovering from acute infection, distant resolved infection
  • Anti-HBc antibody and Anti-HBs antibody: Past infection, resolved
  • Anti- HBc and HBsAg: Active HBV infection (with anti-HBc IgM)
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14
Q

Role of Hep B - e antigen?

A

Testing for HBeAg and anti-HBe is not part of the diagnostic panel for HBV

Phases of infection determines amount of E antigens

Amount of E antigens can indicate antiviral treatment and further investigations (e.g. liver biopsy)

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15
Q

Define the phases of Hep B infection and HepB- E Antigen levels

A
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16
Q

Role of liver fibroscan

Stages of fibrosis

A

noninvasive assessment of liver fibrosis (3 min) for staging fibrosis

Measures liver stiffness (kPa): correlates with underlying fibrosis
Controlled attenuation parameter (CAP): correlates with underlying steatosis

F0 = No fibrosis 
F1 = Portal fibrosis with no speta 
F2 = Portal fibrosis with infrequent septa 
F3 = Numerous septa but no cirrhosis 
F4 = Cirrhosis (asymptomatic unless decompensated)
17
Q

Wilson’s disease

Genetic defect
Inheritance
Diagnostic tests

A

Genetic defect: ATP7B - Copper-transporting ATPase defect

Inheritance: AR

Diagnostic tests:

  • Neurological S/S: Ceruloplasmin <20mg/dL + Kayser Fleischer rings
  • Asymptomatic: Hepatic Cu concentration >250mg/g of dry weight + Low serum ceruloplasmin level
18
Q

Ceruloplasmin level

  • Causes of increase
  • Causes of false negative
A

Increase: Inflammation, pregnancy, estrogen use

False positive: protein deficiency states (e.g. nephrotic syndrome, liver cirrhosis, malnutrition, malabsorption, protein-losing enteropathy…)

Overall not a very specific marker to Wilson’s disease

19
Q

Clinical scenario:
Past IVDU, chronic alcoholism
2 weeks abdominal swelling with mild fever
Umbilical hernia with shifting dullness, scattered spider naevi on P/E
Overall picture: decompensated liver cirrhosis with development of ascites

Outline next investigations

A 
Full blood tests:
CBC with diff. 
MCV and Hb
WCC 
Plt, PT, INR 
Electrolytes

LFT:

  • ALT, AST, ALT:AST ratio
  • ALP and GGT
  • Albumin
  • AFP (HCC or necro-inflammation in liver)

Viral hepatitis panel (Especially HCV for IVDU)

Ultrasound

OGD for variceal screening, Portal-hypertensive gastropathy

Diagnostic paracentesis (All ascites cases to r/o SBP)

20
Q

Outline the spectrum of tests in Diagnostic paracentesis

A

Color and turbidity

Protein

RBC

WCC count with PMN count - SBP = >250 PMN/mm3 or positive culture with <250 PMN/mm3

Serum ascites albumin gradient (SAAG): serum albumin – ascites albumin
High SAAG > 11 – non-peritoneal cause
Low SAAG <11 – peritoneal cause

21
Q

Causes of high vs low SAAG from Diagnostic paracentesis

A 
High SAAG > 11 – non-peritoneal cause:
 Cirrhosis
 Acute liver failure
 Veno-occlusive disease
 Hepatic vein obstruction
 CHF
 Nephrotic syndrome
 Protein-losing enteropathy
 Malnutrition
Low SAAG <11 – peritoneal cause:
 Primary peritoneal mesothelioma
 Secondary peritoneal carcinoma
 TB
 Peritonitis
22
Q

Assessment/ scoring systems of liver cirrhosis

A 
Child Pugh score: A(5-6), B(7-9), C(>=10) or 3-15
Metrics:
 Bilirubin
 Albumin
 INR / prothrombin time
 Ascites
 Encephalopathy
 Decompensation indicates cirrhosis with a Child-Pugh score of 7 or more (class B)
MELD score
Metrics: 
 Serum Cr
 Serum bilirubin 
 INR
23
Q

Treatment of HCV infection in a previous IVDU and chronic alcoholic with ascites

A

o HCV – direct acting antivirals (now ~100% cure rate for Hep C)
o Alcoholic liver disease – abstinence
o Ascites – large vol paracentesis (7L removed), diuretics

24
Q

Clinical scenario:
62-year-old man admitted to ED with acute onset of central abdomen pain, radiating to back, with associated nausea and vomiting for 12 hours, with fever
Tender epigastrium with guarding, no rebound, Scant bowel sounds on P/E
Preliminary investigations reveal lymphocytosis, cholestatic liver enzyme pattern

Ddx and investigations

A

Ddx: post-hepatic causes of liver enzyme elevation: acute cholecystitis, cholangitis, pancreatitis

Investigations: 
Full bloods 
For Ranson's criteria: 
- Serum Amylase 
- WBC
- Glucose
- LDH, Hct
- AST 
- Ca, HCO3, BUN
- PaO2

Imaging:
AXR
US abdomen
ERCP if gallstones

25
Q

Clinical scenario:
20-year-old female presented with 3-week history of diarrhoea, with blood and mucus over the last 5 days with increasing abdominal pain and mild fever
No other significant Hx
Soft, diffuse tenderness on abdomen with fever, dehydration

Ddx and next investigations

A

Ddx:
o Infectious gastroenteritis – Campylobacter, Shigella, rotavirus
o Inflammatory bowel disease
o Less common – vasculitis, Behcets, C. difficile colitis, malabsorption

Investigations:

  • CBC
  • RFT and LFT
  • Inflammatory marker CRP and ESR
  • AXR
  • Stool: Culture, microscopy, cell counts, C.diffile toxins, Fecal calprotectin
  • Colonoscopy
26
Q

Fecal Calprotectin

Intrinsic function
Test function

A

Calprotectin = small calcium-binding protein, 60% of content of cytosol in neutrophils

Distinguishes between functional (e.g. irritable bowel syndrome) and organic diarrhea (e.g. inflammatory bowel disease):
neutrophils migrate to intestinal mucosa in active intestinal inflammation, inflammatory disturbance to mucosa leads to leakage of calprotectin

Calprotectin <50μg/g = IBS likely
Calprotectin 50-150μg/g: Exclude other possible causes of GI tract inflammation, e.g. infection, NSAIDs etc.
Calprotectin >150μg/g = organic disease likely (IBD, colorectal cancer)

27
Q 
Clinical scenario: 
58 year old man with increasing weight loss and RUQ pain
Chronic Hep B carrier with no Tx 
Slight hepatomegaly on P/E 
Slightly high AST, ALT; High GGT, ALP

Most useful investigations?

A

Hep B status: active and chronic

AFP

Triphasic CT scan if positive AFP

28
Q

High AFP is diagnostic of HCC

True or False, why?

A

False

AFP high in many conditions:
Pregnancy
HCC 
Acute hepatitis, active hepatocyte regeneration and necro-inflammation  
Germ cell tumour 
Lymphoma

Must do triphasic CT scan for supporting radiological Dx of HCC

29
Q

Ddx the following profile:

65 year old woman with Hypochromic Microcytic anaemia
CEA 12 (2x normal limit)
FOB 1/3 positive

Most useful next investigation

A

GI bleeding, likely malignant due to elevated CEA (only very advanced)
Insidious bleed causing iron deficiency anaemia

Colonoscopy and CT abdomen

30
Q

Factors of high CEA

A

Colon, lung, breast, stomach cancer

Chronic smoking

31
Q

Peutz-Jeghers Syndrome

Genetic Defect and inheritance
Manifestations

A

STK11 (LKB1) mutation
Autosomal dominant

Manifestations:

  • Benign hamartomatous polyps in GIT
  • Hyperpigmented macules on lips and oral mucosa
  • Intestinal obstruction due to intussusception (teenage)
  • High risk GI cancer (adulthood)

MBBS IV - Teaching Clinics, Data Interpretation, Interactive Tutorials (8 decks)

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