Liver Disease Flashcards

1
Q

What is chronic hepatitis?

A

Liver inflammation persisting >6 months

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2
Q

What is acute hepatits?

A

Acute inflammation of the liver. Can progress to fulminant hepatitis or chronic hepatitis.

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3
Q

What are the signs and symptoms of acute hepatitis?

A
  • Unwell, Jaundice, RUQ pain

- Severe –> confusion (encephalopathy), bruising (coagulopathy)

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4
Q

Where do bloods test show in Acute Hep? (4)

A

Raised ALT/AST (ALT >1000), raised bilirubin, elongated coagulopathy, renal impairment

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5
Q

What are the symptoms of chronic hep? (3)

A

Often none, fatigue, possible RUQ

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6
Q

How does chronic hep present? (2)

A

Liver screening (Abnormal LFTs), cirrhosis

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7
Q

What is fulminant hepatitis?

A
  • Acute hepatitis with liver failure
  • The development of encephalopathy within 28 days of jaundice
  • Poor prognosis - often needs transplantation
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8
Q

What is cirrhosis?

A

Fibrosis of the liver and nodular formation. initially, patient can compensate but eventually, patient decompensates leading to Loss of Function and symptoms.

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9
Q

What are loss of function signs? (5)

A
  • Jaundice
  • Coagulopathy
  • Decreased drug metabolism - watch out benzodiazepines and opiates
  • Decreased hormone metabolism - increased oestrogen (signs - spider naevi, palmar erythema, gynaecomastia, loss of secondary body hair, genitalia shrink)
  • Increased sepsis risk
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10
Q

What are the variceal sites? (4)

A

oesophageal varices, rectal varices (piles), varices around umbilicus (Caput medusa), retro-peritoneal varices

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11
Q

What are the signs of portal hypertension? (4)

A

Varices, ascites, renal failure, encephalopathy

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12
Q

What is the treatment of portal hypertension?

A

Beta-blockers and shunts

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13
Q

How is Hepatitis A spread?

A

Faeco-oral

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14
Q

What is Hep A serology? (4)

A

Hep A IgM - acute infection
Hep A IgG - previous infection
HAV in stool - 1 week post-infection
ALT - acute increase with peak at weak 4

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15
Q

How is hep B spread? (3)

A

Blood (IVDU, medical), sex, vertical (mother to child)

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16
Q

What are serological markers of an acute Hep B infection? (2)

A

Anti-HBc IgM - first marker to test for as early rise. Suggests acute infection if raised.

HBsAg (surface antigen) - rises early. Disappears after 24 weeks. +ve means chronic/acute. If core IgM negative and well, then chronic

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17
Q

What is the serology in chronic Hep B? (3)

A

Persistent HbsAg (Hep B surface antigen), Anti-HBc IgG +ve

HbeAg +ve - immuno-tolerant so high viral loads –> INFECTIOUS

Anti-Hbe +ve - immunoreactive so low viral levels –> less infectious. ALT RAISED.

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18
Q

What is the treatment for chronic Hep B? (2)

A

Antiviral (entecavir/tenofovir) - life-long

Interferon - 48 week course

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19
Q

How is Hep C transmitted?

A

Blood, medical, IVDU, sex, vertical

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20
Q

What are tests for Hep c?

A

Hep C IgG antibodies - +ve means exposure

Hep C RNA -

-ve - exposed but not cleared,
+ve - chronic

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21
Q

How is Hep E transmitted?

A

Faeco-oral

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22
Q

What are the tests for Hep E?

A

IgG and IgM

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23
Q

What is delirium tremens?

A

An acute confusional state which results when someone who drinks excess alcohol daily, suddenly stops drinking. Untreated it results in seizures and even death.

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24
Q

What is the treatment for acute alcohol withdrawal?

A

Benzodiazepine/carbmazepine

25
Q

What is treatment for delirium tremens and alcohol withdrawal seizures?

A

oral lorzepam

26
Q

What is the cause of wernicke’s encephalopathy?

A

Organic brain disorder results from damage to the mamillary bodies, dorsomedial nuclei of the thalamus and adjacent areas of periventricular grey matter caused by a deficiency of thiamine (vitamin B1).

27
Q

What are symptoms of Wernicke’s Encephalopathy?

A

nystagmus, ophthalmoplegia, ataxia and confusion

28
Q

What are the symptoms of Korsakoff’s Syndrome?

A

Severe short-term memory deficits and confabulation

29
Q

What are the three presentations of Alcoholic liver disease (ALD)?

A

Alcoholic Fatty Liver Disease (AFLD), alcoholic hepatitis and alcoholic cirrhosis

30
Q

How does AFLD present?

A

Elevated transaminases in absence of hepatomegaly. Steatosis usually disappears after 3 months of abstinence.

31
Q

How does alcoholic hepatitis present?

A

jaundice and hepatomegaly; complications of portal hypertension may also be present.

32
Q

How does alcoholic cirrhosis present?

A

Variceal haemorrhage or ascites

33
Q

What are the investigations of ALD? (4)

A

Macroytosis (raised MCV), raised Gamma-GT, jaundice, liver biopsy

34
Q

What is the test for prognosis of alcoholic hepatitis?

A

Maddrey score/discriminant function - uses PT and bilirubin

35
Q

How is ALD managed?

A

cessation of alcohol consumption, nutrition (via NG tube), corticosteroids (severe hepatitis, DF >32), pentoxifylline (severe), liver transplantation

36
Q

How is cirrhosis managed?

A

Treatment of the underlying cause, maintenance of nutrition, treatment of complications

Endoscopy - every 2 years, looking for oesophageal varices

Regular surveillance for hepatocellular carcinoma

Liver transplant

37
Q

What is ascites?

A

It is accumulation of free fluid in the peritoneal cavity.

38
Q

What are the causes ascites? (5)

A

Splachnic vasodilation, activation of RAAS, portal hypertension, salt and water retention, reduced albumin

39
Q

How is ascites investigated? (3)

A

Ultrasonography, paracentesis to obtain fluid, CXR - pleural effusions!

40
Q

What is the serum serum-ascites albumin gradient (SAAG) and how is it calculated ?

A

o Measurement of the protein concentration and the serum-ascites albumin gradient (SAAG) are used to distinguish a transudate from an exudate.

Calculate the SAAG by subtracting the concentration of the ascites fluid albumin from the serum albumin.

41
Q

What is transudative ascites?

A

SAAG >11g/L (T is later in alphabet, so greater gradient)

Causes include portal hypertension, venous outflow obstruction

42
Q

What investigations can be carried out on the ascitic fluid?

A

Total albumin (+ serum) and protein, amylase, neutrophil count, cytology, microscopy and culture

43
Q

What does the colour of ascitic fluid tell you?

A
Clear, straw-coloured, light green - cirrhosis
Bloody - malignant
cloudy - infection
bile stained - biliary communication
Milky-white - lymphatic obstruction
44
Q

What is exudative ascites

A

SAAG <11g/L

Possible the possibility of infection (especially tuberculosis), malignancy, hepatic venous obstruction, pancreatic ascites or, rarely, hypothyroidism.

45
Q

What does a raised ascites amylase show?

A

pancreatic ascites

46
Q

What does low ascitic glucose concentration suggest?

A

TB or malignant disease

47
Q

What does cytological exam reveal?

A

Malignant cells

48
Q

What do raised Polymorphonuclear leucocyte counts above indicate?

A

Infection - SBP

49
Q

How is ascites managed? (4)

A

Sodium and water restriction, diuretics (spironolactone/amiloride)

Paracentesis - refractory ascites

transjugular intrahepatic portosystemic stent shunt (TIPSS)

peritonea-venous shunt

50
Q

What are poor prognostic indicators in cirrhosis (5)?

A

Encephalopathy, ascites, raised bilirubin, prolonged PT time, reduced albumin

51
Q

What is the child-pugh scoring system?

A

assess the prognosis of chronic liver disease, mainly cirrhosis.

52
Q

What is MELD scoring system?

A

model for end-stage liver disease. Renal function, INR, bilirubin. Prognostic of survival in next couple of months

53
Q

What is Madley’s scoring system?

A

A measure of alcoholic hepatitis

54
Q

What do blood tests show in auto-immune hepatitis (5)?

A

Raised ALT, raised IgG and +ve ANA (anti-nuclear antibody), anti SMA, anti LKM1.

55
Q

What is Wilson’s disease?

A

Copper overload syndrome

56
Q

How does Wilson’s present?

A

advance liver disease – cirrhosis

57
Q

What vaccinations should be offered to patients with chronic hepatitis?

A

Should be offered both the annual influenza vaccine and the pneumococcal vaccine, which is given one a one-off basis.

58
Q

What is the main risk factor for developing hepatocellular carcinoma?

A

liver cirrhosis, for example secondary to e.g. hepatitis B & C, alcohol