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Diagnosis and investigations of conditions of the: > Liver, Biliary And Pancreatic System > Flashcards

Liver, Biliary And Pancreatic System Flashcards

1
Q

Which tests indicate liver function?

A
  1. Prothrombin time (AKA INR test)
    - tests extrinsic pathway
  2. Serum albumin
  3. Serum bilirubin
  4. Serum AST and ALT (Transaminases for conjugation of products to be excreted, raised indicates hepatocellular damage raised indicates obstruction of the biliary system)
  5. Serum ALP (Alkaline phosphatase, raised indicates obstruction of the biliary system)
  6. Serum Ferritin and total iron binding capacity (TIBC)
    - Raised ferritin means general inflammation from any trauma/infection or haemachromatosis)
    - Transferrin is also synthesised by the liver, TIBC measures the ability of the blood to attach itself to iron (basically transferrin function/conc); TIBC goes up in iron deficiency to try and grab more iron, TIBC goes down in haemachromatosis since transferrin is saturated.
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2
Q

What information does a USS of the biliary tree give us?

A

Presence of cholelithiasis (stones)

Duct dilation (chronic obstruction)

State of health of liver, pancreas, GB.

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3
Q

What is a transudate?

A

A fluid that has been pushed across a membrane.

Transudate = Thrust

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4
Q

What is an exudate?

A

A fluid that has been drawn across a membrane.

Exudate = Entice

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5
Q

What is the serum albumin ascites gradient?

A

The serum albumin concentration minus the ascites pic fluid albumin concentration. (Serum - Ascitic fluid)

SAAG >1.1 = transudate

SAAG <1 = exudate

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6
Q

Causes of increased serum/ascitic albumin gradient?

A

Increased SAAG means transudate is occurring, no exudate, forcing fluid over.

Congestive cardiac failure

Nephrotic syndrome

Liver cirrhosis

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7
Q

Causes of a decreased serum/ascitic albumin gradient?

A

Decreased SAAG meaning exudate is occurring, the ascitic fluid is closer to matching serum.

Cancer within the peritoneum
TB causing peritonitis

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8
Q

What is the pathway for determining hepatitis B status?

The order that you do the tests

A 
sAg = Infected
IgM = Acute
Anti- HBs = Vaccinated or PREVIOUS
IgG = 32 weeks post infection/chronic, If sAg present  then CHRONIC, but if no sAg then PREVIOUS
HBe = Infectiousness marker

Reminder: HBs antigen is given to vaccinate, but this is cleared by the body during immunisation. There will be NO antibody to core antigen because there was never any core virus

  1. HBsAg - ACUTE/CHRONIC INFECTION: indicates infection presence
    (From four weeks post-exposure onwards, will disappear in 6months unless it’s chronic)
  2. Anti HBc IgM - ACUTE INFECTION:acute infection, M has not yet had time to change to IgG
    (32weeks max, switches to IgG)
  3. Anti HBs - BEAT IT:indicates previous acute infection, immunisation or natural infection (not chronic)
    (24 weeks post-infection it begins, then will hang around for life, proof that you beat HBV, not present in chronic infection since the body hasn’t beaten the virus)
  4. Anti HBc IgG - CHRONIC: chronic infection, had time for antibodies to change from M to G
  5. HBeAg - INFECTIOUSNESS: immuno-status marker, will be present in acute and chronic
    - immunotolerant (+ve: highly infectious and no signs)
    - immunoreactive (-ve: mildly infectious, signs present)
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9
Q

What are the steps in the investigation of suspected hepatitis A infection?

Tip: no chronic stage!

A
  1. Test stool for viral DNA (shows 1 week post-infection)
  2. Anti-HAV IgM - acute infection (week 2-week 4)
  3. ALT level - raised (peaks between week 2- week 4)
  4. Anti-HAV IgG - Previous infection
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10
Q

What is the investigation pathway for suspected hepatitis C?

A
  1. HCV antibody testing - exposed or not
    (or within six weeks of exposure so no antibodies produced yet)
  2. RNA PCR for the virus - tests for activity; indicating current infection

Up to 20% of people naturally clear the virus

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11
Q

What is the pathway for diagnosis of alcoholic liver disease?

A
  1. Serum LFTs: ALT, AST, ALP, INR
  2. Exclude other causes of abnormal LFTs
  3. Refer to liver specialist for diagnosis
  4. Consider liver biopsy to confirm diagnosis
    - distinct risk of morbidity/mortality
    - should only be immediately done if the condition is severe enough to require corticosteroids
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12
Q

How do you diagnose chronic pancreatitis?

A
  1. History of symptoms must show exocrine dysfunction (steatorrhoea, weight loss, malnutrition)
  2. Check LFTs (may indicate obstructive cause of chronic pancreatitis)
  3. CT-abdomen or MRICP confirms diagnosis

Also you want to check the impact of the chronic pancreatitis:

  • glucose (endocrine function: diabetes)
  • faecal elastase (tests for exocrine function: elastase enzyme should be high normally)
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13
Q

If we perform an ascitic tap on a patient with ascites and their WCC is raised, which differential is most likely?

A

Spontaneous bacterial peritonitis

WCC= >500/mm3

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14
Q

If we perform an ascitic tap on a patient with ascites and their serum ascitic albumin gradient is raised, which differentials are most likely?

A

Increased SAAG is indicative of transudate.

Differentials:
Cancer

TB

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15
Q

If we perform an ascitic tap on a patient with ascites and their serum ascitic albumin gradient is reduced, which differential is most likely?

A

Reduced SAAG is indicative of exudate. (Ascitic fluid is more like serum)

Differentials:

Peritoneal disease e.g. cancer

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16
Q

In a case of diabetes, at what R grade (in retinoscopy) is a retinopathy considered referable?

A

R2 or more

Prior to this it is ‘background retinopathy’ (R1)

R2 = pre-proliferative

  • venous beading
  • multiple boot haemorrhages

R3 = proliferative

  • fibrosis
  • retinal detachment
  • neoangiogenesis
  • vitreoushaemorrhage
17
Q

How do you diagnose type one diabetes mellitus?

A

A clinical diagnosis:

Diagnose type 1 diabetes on clinical grounds in adults presenting with hyperglycaemia

> 7mmol/L fasting glucose

or: 2–hour plasma glucose ≥ 11.1mmol/L

Typically will have one or more:

  • ketosis
  • rapid weight loss
  • age of onset below 50 years
  • BMI below 25 kg/m2
  • personal and/or family history of autoimmune disease
If atypical presentation:
C-Peptide test = C-peptide is the byproduct of proinsulin cleavage to insulin, indicates the level of insulin production 
Autoantibodies testing (islet cell/anti-GAD)

(GAD: glutamic acid decarboylase)

Impaired fasting Glucose (IFG) is diagnosed at 6.1-7mmol/L

After diagnosis will want to screen for CVD risk, and signs of microvascular damage.

18
Q

How do you diagnose type two diabetes mellitus?

A

Fasting plasma glucose ≥ 7.0mmol/L

or: 2–hour plasma glucose ≥ 11.1mmol/L

Impaired fasting Glucose (IFG) is diagnosed at 6.1-7mmol/L

19
Q

Which investigations are required to diagnose haemochromatosis?

A
  1. Serum transferrin saturation - >45%
  2. Serum ferritin - >300ng/ml Male, >200ng/ml female
    (But inflammation, alcoholism, NAFLD and others will raise this because it is an acute phase inflammatory marker)
  3. Liver biopsy (If confounding factors present for serum ferritin rise)
20
Q

What to do in delirium tremens?

A

LFTs
U+Es
ABGs

Diagnosis and investigations of conditions of the: (18 decks)

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