Cirrhosis Flashcards Preview

Internal Medicine > Cirrhosis > Flashcards

Flashcards in Cirrhosis Deck (18):
1

Definition

Irreversible liver damage
Loss of normal architecture
Fibrosis, nodular regeneration

2

Most common causes (3)

Hepatitis C
Alcohol
Non-alcoholic fatty liver
Hepatitis B

3

Other causes

Obesity
Haemachromatosis
Wilson's
Alpha 1 ATD
Glycogen storage diseases
Cholestatic
Primary biliary cirrhosis
PSC
Autoimmune hepatitis
Buddchiari, veno-occlusive, right sided heart failure
Amiodarone, methotrexate

4

Pathogenesis

Hepatocyte death
ECM deposition
Vascular reorganisation
Collagen deposition->stellate cells +++
Chronic inflammation

5

Clinical features

Leukoniychia, clubbing, palmar erythema, gynaecomastia
Abdominal distension
Jaundice and pruritus
Melaena, coffee ground vomitus
Telangiectasia
Spider naevi
Anorexia, weakness, weight loss
Endocrine: loss of hair, loss of libido, breast atrophy, irregular menses, impotence, testicular atrophy, gynaecomastia
Hepatomegaly

6

Aim of investigations

1. Detect hepatic abnormality
2. Measure severity
3. Pattern of function test abnormality
4. Identify cause
5. Possible complications

7

Investigations

LFTs
GGT
Serum albumin
EUC->low sodium
Clotting
PLT
Albumin

To find the cause:
Hepatitis C, hepatitis B serology, HIV
Ferritin, TIBC, transferrin, ferritin
ANA->AIH
anti-smooth muscle->AIH
anti-mitochondrial->PBC
Serum caeruloplasmin
alpha 1 anti-trypsin

Abdominal CT/MRI
Upper GI->varices, portal hypertensive gastropathy
Liver biopsy
Ascitic tap

8

What does low PLT and low WCC indicate

Hypersplenism

9

Management

1. Treat underlying cause
2. Good nutrition, physical activity
3. Alcohol avoidance, hepatotoxic drugs (NSAID, high dose paracetamol)
4. Weight loss
5. Monitor for complications->ascites, varices, hepatorenal, portal HTN, HCC->USS, upper GI, CT, aFP
6. Salt restriction, daily weights, bed rest + frusemide + spirinolactone for ascites
7. Cholestyramine for pruritis
8. Immunisation for hepatitis A and B
9. Monitor for SBP, variceal bleeding, renal failure
10. Consider spontaneous bacterial peritonitis if ascites and deteriorates

10

Complications

Coagulopathy + confusion/coma, hypoalbuminemia, asterixis
Sepsis
SBP
Ascites
Splenomegaly
Varices
HCC + risk

11

Prognosis

5yr survival 50%
Encephalopathy, hyponatremia, hypoalbuminemia and coagulopathy are poor prognostic factors

12

Common causes of SBP

Klebsiella, E. coli, Strep

13

Child pugh C

1. Bilirubin
3 mg/dL (>50 µmol/L)+3
2. Albumin
>3.5 g/dL (>35 g/L)+1
2.8-3.5 g/dL (28-35 g/L))+2
2.2+3
4. Ascites
No Ascites+1
Ascites, Medically Controlled+2
Ascites, Poorly Controlled+3
5. Encephalopathy
No Encephalopathy+1
Encephalopathy, Medically Controlled+2
Encephalopathy, Poorly Controlled+3

14

MELD score

Dialysis at least twice in past week
Creatinine
Bilirubin
INR

15

Interpreting CPC score

Grade A= 5-6
Grade B = 7-9
Grade C= >10

16

Cirrhosis and deteriorating renal function

1. Negative clearance of IgA-> IgA nephropathy +/= hepatic glomerulosclerosis
2. HCV can cause cryoglobulinaemia +/- membranoproliferative GN
3. HBV membranous nephropathy +/ PAN
4. Hepatorenal syndrome
5. MembranoP glomeruloN in a1 antitrypsin deficiency

17

Define hepatorenal syndrome
Management of hepatorenal syndrome

Hepatorenal syndrome (HRS) is functional renal failure->may be precipitated by infection (particularly spontaneous bacterial peritonitis), diuretics, nephrotoxic drugs, gastrointestinal bleeding or large-volume paracentesis.
a. Type 1 HRS is associated with a rapidly rising serum creatinine concentration, and has a poor prognosis.
b. Type 2 HRS is usually a slowly progressive deterioration in renal function that develops over weeks, and may be reversible with correction of precipitants and/or therapeutic intervention.

18

Management of hepatorenal

1. Monitor diuretic use and reduce in accordance to renal impairment
2. IV albumin for those at risk of SBP
3. Prophylaxtic antibiotics for those with GIT bleed
4. Avoid nephrotoxic medications

Terlipressin + albumin