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302 SBM: Metabolic & Renal > Introduction to hepatology > Flashcards

Introduction to hepatology Flashcards

1
Q

Why might a patient have acute abnormal liver tests?

What does acute mean?

A

<6 weeks

Causes

  • Drugs
  • VIral Hepatitis (A,B,C,E)
  • Autoimmune hepatitis
  • Wilsons disease
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2
Q

Why might a patient have subacute abnormal liver tests?

What does acute mean?

A

6-26 weeks (6 months)

Causes

  • Drugs
  • VIral Hepatitis (A,B,C)
  • Autoimmune hepatitis
  • Wilsons disease
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3
Q

Why might a patient have chronic abnormal liver tests?

What does acute mean?

A

> 6 months

Causes

  • Viral hepatitis (B,C)
  • Alcohol
  • NAFLD
  • Autoimmune hepatitis
  • Wilsons disease
  • Haemochromatosis
  • A1 antitrypsin deficiency
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4
Q

What does a liver panel investigate?

A

Bilirubin- which has prognostic value
Liver enzymes- ALT, AST, ALP, GGT
Albumin
PT and INR- which have prognostic value

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5
Q

What does the PT measure?

A

The extrinsic coagulation pathway

- factor II, V, VII, and fibrinogen

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6
Q

How do we screen for viral hepatitis?

A

Hep A- Hep A IgM
Hep B- Hep B surface antigen
Hep C- Hep C antibody
Hep E- Hep E IgG and IgM

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7
Q

How do we screen for autoimmune hepaititis and primary biliary cholangitis ?

A

Autonimmune Hep- ANA, SMA, LKM

Primary biliary cholangitis- AMA

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8
Q

How do we screen for the following disorders?

  • Alpha-1-antitrypsin deficiency
  • Wilsons disease
  • Genetic haemochromatosis
A
  • Alpha 1 antitrypsin
  • Copper and caeruloplasmin
  • Ferritin
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9
Q

You review a patients liver panel and notice that the ALT and AST are significantly raised compared to the bilirubin and ALP.

What kind of picture is this?
What may be the cause?

A

Hepatitic picture

  • Drugs
  • Viral hepatitis: A,B,C,E
  • Autoimmune hepatitis
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10
Q

You review a patients liver panel and notice that the Bilirubin and ALP are significantly raised compared to the AST and ALT

What kind of picture is this?
What may be the cause?

A

Cholestatic picture

Biliary obstruction
Viral Hep A, B, E
Drug-induced liver injury (DILI)
Primary biliary cholangitis
Primary sclerosing cholangitis

(remember things that cause hepatitis can cause cholestatic dysfunction)

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11
Q

Outline the routes of transmission of Hep A, B, C, E

A

Hep A and E
- orofaecal matter (in the developing world)

Hep B and C
- bodily fluids so high-risk sex, IV drug use, recipients of blood products before screening

Hep E
- in the UK it is mainly a zoonotic disease acquired through eating uncooked pork or shellfish

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12
Q

What is cirrhosis?

A

Generally irreversible scarring of the liver causing chronic liver disease
The main feature is damage to the portal vein (which is formed by the superior mesenteric and splenic vein) causing increased pressure in portal circulation (portal hypertension)

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13
Q

What are the features of decompensated cirrhosis?

A
  • Variceal bleeding
  • Ascites
  • Hepatic encephalopathy
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14
Q

What are the signs of chronic liver disease you would look for on examination?

A

Hands
- Liver flap, palmar erythema, dupuytrens contracture

Jaundice

Spider naevi, caput medusae

Splenomegaly

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15
Q

How does the survival of those compensated and decompensated cirrhosis differ?

A

Compensated
- have a median survival of 9 years

Decompensated

  • median survival of 1.5 years
  • development of complications: ascites, variceal bleeding, hepatic encephalopathy, jaundice
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16
Q

How do you manage ascites in cirrhosis?

A
  • Salt restiriction
  • Fluid restriction if low Na
  • Diuretics (spironolactone and furosemide)
  • Large volume paracentesis (LVP) with albumin cover

If refractory

  • recurrent LVP
  • TIPS procedure
  • Liver transplant
  • Long term drains (in palliative care)
17
Q

In the haemodynamically stable patient how do you manage variceal bleeding in the acute scenario?

A
  • Correct coagulopathy (INR)
  • Correct thrombocytopenia
  • IV Terlipressin (a vasopressin analogue which will reduce portal HTN and bleeding)
  • IV antibiotics (GI bleed increases risk of SBP due to increased bacteria translocation)
  • If you suspect variceal bleeding endoscope in theatre with patient intubated and anaesthetist present (even if out of hours)
18
Q

On endoscopy, a patient has stigmata of variceal bleeding

How can you manage this to stop the bleeding?

A
  • BAND LIGATION
  • if a complete blood bath, balloon tamponade will decompress varices and gives time to stabilise patient
  • TIPS (also decompresses pressure)
19
Q

What drug is used as secondary prophylaxis of variceal bleeding?

A
  • Non-selective B blocker e.g. propanolol, carvedilol
20
Q

What is hepatorenal syndrome?

What are the signs?

A

A type of renal fialure seen in patients with severe liver disease, caused by cirrhosis. Rapid renal impairment caused by reduced renal perfusion

Type 1 and 2

Increase in serum creatinine by 50% from baseline within 3 months

(remember that the primary problem here is with the liver, if the kidneys were removed and given to a patient with functioning liver they would work just fine)

21
Q

How do you manage hepatorenal syndrome?

A

Treat underlying cause
Terlipressin
Liver transplant

22
Q

What is liver failure?

A

Hepatic encephalopathy (confusion, reduced GCS)

Coagulopathy (iNR>1.5)

Jaundice

It is life threatening

23
Q

Describe heaptic encephalopathy

  • Why does it happen?
  • How is it diagnosed?
  • How is it treated?
A

Liver cannot adequately remove toxins from the blood so there is build up of ammonia (this is produced by gut bacteria, protein degradation)

It is a diagnosis of exclusion

Treat underlying cause: constipation, diuretics, infection, sedative, GI bleed
Lactulose (removes ammonia)
Non-absorbable antibiotics (Rifaximin- eliminates gut bacteria)

24
Q

How do we classify the development of liver failure?

A

By time
Acute development of coagulopathy encephalopathy <4 weeks
Subacute 4-12 weeks

Acute on chronic
- acute liver failure in a patient with underlying chronic liver disease (e.g. alcohol)

25
Q

Describe acute liver failure

  • context
  • pathognomonic features
  • presentation
  • prognosis
  • causes
A
  • No preexisting liver disease
  • coagulopathy, encephalopathy
  • jaundice, abnormal LFTs, cerebral edema, increased risk of infections, hepatorenal syndrome, intracranial hypertension
  • good survival without liver transplant (50-60)
  • PARACETAMOL DRUGS (50%), non-paracetamol drugs (15%), Hep A, Hep B
26
Q

Describe subacute liver failure

  • prognosis
  • causes
A
  • Poor spontaneous survival (10-15%)

- Caused by non paracetamol drug induced liver innjur

27
Q

What is the toxic dose of paracetamol?

A

Recommended dose is 4g/day

Toxic >15g

In pre-existing liver disease the toxic dose is lower

28
Q

Outline the pathogenesis of paracetamol toxicity

A

Glucuronidation and sulphation pathways are rapidly saturated which leads to increased metabolism to NAPQI

usually glutathione breaks down this toxic metabolite but in overdose glutathione stores are depleted so toxic metabolite build up

29
Q

How would a patient with paracetamol overdose present?

A
  • nausea
  • vomiting
  • RUQ pain
  • confusion
  • Jaundice and liver failure develop 3-4 days later

Highly raised liver enzymes
Raised PT

30
Q

How can you prevent acute liver failure in paracetamol overdose?

A 
Administer NAC (N-acetyl cysteine) which replenishes glutathione 
- glutathione is required to inactivate NAPQI and when levels depleted -> hepatocellular death takes place

Important to give within 16 hours

Dont withhold to confirm diagnosis

31
Q

What is severe alcoholic hepatitis?

A
  • most serious form of alcohol related injury
  • characterised by jaundice and coagulopathy
  • 40% mortality if left untreated
    Discrimant function score used to determine prognosis
  • Treat steroids (+ pentoxifylline)
32
Q

Describe non-alcoholic fatty liver disease

  • pathology
  • risk factors
A
  • A spectrum of disorders that resembles alcoholic liver disease but occur in the absence of alcohol abuse. The underying mechanism if insulin resistance
  • fatty liver –> non-alcohol steatohepatitis (NASH) –> cirrhosis
  • obesity, T2DM, HTN, hyperlipidaemia (elevated TG)
33
Q

How could you identify paracetamol induced acute liver failure on blood gas/boods?

A

Acidotic

  • pH<7.3 after resuscitation
  • arterial lactate >3.5 (after 4 hours); >3 (after 12 hours)

Coagulopathic

  • INR>6.5
  • PT> 100seconds

Serum creatinine >300mmol/L

Encephalopathic (Grade 3/4)

34
Q

How might a non-paracetamol induced acute liver failure appear?

A

Age
- <11yo; >40yo

Jaundice
- longer than 7 days before onset of confusion

PT >50s (INR>3.5)

Serum bilirubin >300

Aetiology: Non-Hep A/Hep B; halothane hepatitis; idiosyncratic drug reactions

302 SBM: Metabolic & Renal (6 decks)

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