Chronic liver disease Flashcards
What are the causes of chronic liver disease?
Infectious
- Chronic Hep B +/- Hep D: Superinfection of Hep D is more severe w/ early onset Cirrhosis in 2-3Y
- Chronic Hep C
NAFLD
AFLD
Autoimmune Hepatitis
Metabolic (rare)
- Wilson’s Disease
- Alpha 1 antitrypsin deficiency
- Haemochromatosis
Cardiac – CCF
Budd Chiari (more commonly acute)
What are the clinical features of compensated CLD?
- Jaundice, Scleral Icterus
- Clubbing
- Leukonychia (hypoalbuminaemia)
- Palmar Erythema
- Dupuytren’s Contracture (If AFLD)
- B/L Parotidomegaly (if AFLD)
- Spider Naevi
- Loss of axillary Hair (from ↑ Estrogen)
- Gynaecomastia (from ↑ Estrogen)
- Testicular Atrophy (from ↑ Estrogen)
What are the clinical features of decompensated CLD
Jaundice, Scleral Icterus (+/- Pruritis)
Ascites (from Portal HTN)
- +/- Caput Medusae
- +/- Splenomegaly
- +/- Haemorrhoids
- +/- Variceal UBGIT
Pedal Edema
Easy Bruising / Coagulopathy ↑INR
Encephalopathy, Asterixis
What are the causes of portal hypertension?
Pre-hepatic: portal v. thrombosis
Hepatic: cirrhosis, infiltrative dz
Post-hepatic: RHF, Budd-Chiari syndrome
What are the clinical features suggesting haemochromatosis as an etiology of chronic liver disease?
- Bronzing of skin
- CCF
- Diabetes
- Hypothyroidism
- Hypopituitarism
What are the clinical features suggesting wilson’s disease as an etiology of chronic liver disease?
Kleiser Fleisher Rings, Neurological FIndings
What are the clinical features suggesting alcoholic disease as an etiology of chronic liver disease?
Dupuytren’s Contracture, B/L Parotidomegaly
What are the investigations to assess impaired liver function in chronic liver disease?
LFTs
- AST > ALT in cirrhosis
- AST:ALT > 2:1 + raised GGT in AFLD
- Liver Function will be severely deranged only if late decompensated cirrhosis / CLD. To pick up early compensated cirrhosis 🡪 requiring biopsy / imaging modalities
Bilirubin
Albumin
PT / APTT / INR
FBC (for thrombocytopenia): Thrombocytopenia from ↓ Hepatic thrombopoietin production & Hypersplenism (2’ to Splenomegaly)
APRI index (AST/Plt) >1.0 suggestive of cirrhosis in hep C patients
What are the investigations to assess complications in chronic liver disease?
Renal Panel, U/E/Cr: 2’ to hypoperfusion due to hepato-renal syndrome
Na: ↑RAAS can lead to Hypervolemic Hypo-osmolal HypoNa
If ascites: SAAG (serum ascites-albumin gradient)
- ≥1.1g/L 🡪 extra-peritoneal i.e. transudate
- <1.1g/L 🡪 exudate i.e. peritoneal carcinomatosis, infection
If suspect varices: OGD
What are the investigations to monitor/ diagnose cirrhosis in chronic liver disease?
Biopsy: Gold Standard, but rarely done
- Best modality to pick up EARLY (Compensated) cirrhosis!
- Not necessary if clinical, lab, imaging strongly suggest cirrhosis and if the results would not alter the patient’s management
Imaging:
Liver USS: looking for shrunken, nodular, irregular liver
Fibroscan (i.e. Elastography via Liver USS)
What is the Child Pugh score
Child Pugh Score: the current scoring method for prognosticating 1-year survivability of liver cirrhosis
A= Albumin (Hypoalbuminaemia: Pedal Edema, Leukonychia)
- 1 point: >3.5mg/dL
- 2 points: 2.8 - 3.5 mg/dL
- 3 points <2.8mg/dL
B = Bilirubin (Hyperbilirubinaemia, Jaundice)
- 1 point: <2mg/dL
- 2 points: 2-3 mg/dL
- 3 points >3mg/dL
C = Coagulopathy (Prolonged PT &INR)
- 1 point: <4s prolonged, INR <1.7
- 2 points: 4-6s prolonged, INR 1.7- 2.3
- 3 points: >6s prolonged, INR >2.3
D = Distension / Ascites (Portal HTN)
- 1 point: none
- 2 points: mild to moderate (diuretic responsive)
- 3 points: severe (diuretic refractory)
E = Encephalopathy
- 1 point: none
- 2 points: mild to moderate (grade 1 or 2)
- 3 points: severe (grade 3 or 4)
Child A = 5 to 6 points (least severe liver disease)
Child B= 7 to 9 points (moderately severe liver disease)
Child C= 10-15 points (most severe liver disease)
Child’s A = Well Compensated Cirrhosis
Child’s B = Compensated w/ Functional Compromise Cirrhosis
C = Decompensated
What is the investigation & management of ascites?
Investigation
- Ascitic / Abdominal Tap (i.e. abdo paracentesis) 🡪 Dx & Therapeutic
- Calculation of SAAG from ascitic tap
Management
- Fluid (1.5-2L/day) & Salt (2-3g/day) Restriction
- Spironolactone +/- Lasix (if massive)
- Large volume Paracentesis w/ IV salt-free Albumin (to prevent hepatorenal syndrome)
- TIPSS: N/B: increased risk of HE
What are the differentials of high Serum Ascites Albumin Gradient ≥1.1g/dl?
Pre-Hepatic
- Portal Vein thrombosis
Hepatic
- Cirrhosis
- Liver Failure
- AFLD
- MASSIVE Mets (you require massive mets to significantly reduce hepatic function)
Post-Hepatic
- Budd Chiari
- R Heart Failure
What are the differentials of high Serum Ascites Albumin Gradient <1.1g/dl?
Hypoalbuminaemia
- Nephrotic Syndrome
- Protein Losing Enteropathy (eg: IBD)
Malignancy
- Ca that cause Peritoneal Carcinomatosis: Ovarian, Bladder, Peritoneal Mesothelioma
- Peritoneal Carcinomatosis 2’ to liver mets: Breast, Lung, Colon, Stomach
- Chylous Ascites: Lymph obstruction (by a lymphoma)
Infectious – eg: TB (Peritoneal TB)
Pancreatitis – Accumulation of pancreatic fluid in the peritoneal cavity
Serositis – AI Disease Eg: RA
What is required for the diagnosis of Spontaneous Bacterial Peritonitis?
S&S (Pain, Tense abdo wall, +/- Fever, +/- Diarrhoea +/- Paralytic Ileus). But may also be asymptomatic –> suspect in unexplained decompensation
PMN cells >250cells/mm3
+/- Culture results (We can diagnose SBP even with -ve cultures!)
SBP 🡪 must be in the absence of other intra-abdominal causes (eg: diverticulitis). Otherwise, known as Secondary Bacterial Peritonitis
