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Stage 4 CSIM > Abnormal Liver Function > Flashcards

Abnormal Liver Function Flashcards

1
Q

What is the most common cause of liver disease in the UK?

A

NAFLD (20-30% of the population)

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2
Q

What is the most common cause of liver death?

A

Alcoholic Liver Disease (84% of deaths from liver disease)

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3
Q

Describe the 4 stages of alcoholic liver disease

A

Normal –> Steatosis –> Steatohepatitis –> Fibrosis/Cirrhosis

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4
Q

Describe Charcots Triad of Cholangits

A

Fever (with rigors) + RUQ pain + Jaundice

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5
Q

What type of liver disease is pruritis associated with?

A

Cholestatic diseases

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6
Q

What LFTs would indicate a cholestatic picture?

A

Raised Alk Phos, Bilirubin and Gamma GT

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7
Q

What LFTs would indicate hepatocellular injury?

A

Raised “transaminases”

ALT and AST

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8
Q

Does how much the transaminases are raised indicate a certain diagnosis?

A 
Mildly raised (1.5-3x normal) = ALD/NAFLD
Significantly raised (>3) = viral, drug and autoimmune hepatitis
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9
Q

What level does the bilirubin have to be to be a clinical jaundice AND to see a visible jaundice?

A

> 30 micromol/L = Clinical Jaundice

> 50 micromol/L = Visible Jaundice

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10
Q

What are the causes of unconjugated jaundice?

A

Gilberts or Haemolysis

all others have a mixed or conjugated picture

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11
Q

Describe what happens to coagulation studies and why in liver disease.

A 
Increased prothrombin (PT) time due to reduced synthesis of vitamin K dependent clotting factors by the liver. 
Should be excluded from Vit K deficiency which can commonly occur in biliary obstruction as reduced bile salts in the intestine cause reduced absorption of Vitamin K.
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12
Q

What is the tumour marker tested for in hepatocellular carcinoma?

A

alpha - fetoprotein

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13
Q

What is the tumour marker tested for in cholangiocarcinoma?

A

Ca 19.9

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14
Q

List some of the common indications for liver biopsy

A

Diagnosis and Staging of Fibrosis
Focal Liver Lesions (guided)
Post Transplant - rejection

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15
Q

List some of the other non-invasive methods of staging fibrosis?

A

NAFLD Fibrosis Score
Transient Elastography (Fibroscan)
Blood Tests ?ALT role

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16
Q

In Liver disease, what does a large spleen indicate?

A

Portal Hypertension

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17
Q

Describe the diagnostic criteria for Metabolic Syndrome

A 
Any 3 of the following: 
Increased weight circumference (or BMI >30)
Raised Triglycerides
Reduced HDL-cholesterol
Raised Blood Pressure
Raised Fasting Plasma Glucose
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18
Q

What does a serum lipid profile test include?

A

Total Cholesterol
HDL
LDL
Triglycerides

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19
Q

What sign on Liver US would indicate NAFLD

A

Bright Liver

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20
Q

Why are beta blockers used in patients at risk of variceal haemorrhage or as secondary prevention following a variceal haemorrhage?

A

They reduce portal pressures by decreasing cardiac output
They also cause splanchnic vasocontriction (increase in splachnic blood blow in portal hypertension contributes to the hyper-dynamic state and worsens the effects of cirrhosis and portal hypertension)

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21
Q

In patients with cirrhosis, describe the surveillance for hepatocellular carcinoma

A

6 monthly alpha feta protein measurements and liver ultrasound

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22
Q

Describe hepatopulmonary syndrome

A

Triad of Liver Disease, hypoxaemia and evidence of pulmonary vessel dilatation.

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23
Q

Describe hepatorenal syndrome

A

A complication of end-stage liver disease which occurs in patients who have chronic liver dysfunction with cirrhosis and ascites and also in acute liver failure. In hepatorenal syndrome (HRS) there is impaired renal function which is often precipitated by events lowering blood pressure.

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24
Q

Briefly summarise the management for NAFLD

A 
Diet (calorie restrict)
Increase Exercise
Orlistat
Bariatric Surgery
Pioglitazone
Vitamin E
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25
Q

Describe the role of Hepatic Stellate cells in development of cirrhosis

A

In quiescent state - act as a store for Vitamin A in the liver
They are activated in response to injury and lay down collagen - the fibrous tissue which forms the bands which make up cirrhosis.

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26
Q

What are the 4 important sings of decompensation in chronic liver disease?

A

Jaundice
Encephalopathy
Ascites
Asterixis

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27
Q

Describe the role of Child-Pugh score in Liver Disease

A

Used to assess liver function and prognosis in cirrhotic patients. It measures
Bilirubin, ascites, albumin, INR/PTT and encephalopathy

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28
Q

Describe the Model of End Stage Liver Disease (MELD) score in Liver Disease

A

Used to prioritize patients for liver transplant. It measures
Bilirubin, creatinine and INR

29
Q

Described the three pathophysiology drivers of ascites

A

Essentially, on a background of chronic liver disease there is likely to be vasodilatation. Vasodilatation = reduced perfusion of the kidneys. Kidneys programmed though renin-angiotensin system that when they are hypoperfused they should retain salt and water
Portal hypertension - exerts local hydrostatic pressure and leads to transudation of fluid into the peritoneal cavity
Low serum albumin may further contribute by a reduction in plasma oncotic pressure

30
Q

Describe the Serum Ascites Albumin Gradient, and what different values mean

A 
High Gradient (>1.1 g/L) suggests portal hypertension as the cause
Low Gradient ( 97% accuracy)
31
Q

What condition should be suspected in any person with ascites who deteriorates suddenly?

A

Spontaneous Bacterial Peritonitis

32
Q

What investigation would you do to confirm spontaneous bacterial peritonitis?

A

Check for neutrophils in the ascitic fluid, if present = evidence enough to start treatment

33
Q

Recurrence of SBP is high, up to 70% in the first year, what can be done for prophylaxis?

A

An oral quinolone antibitoic

34
Q

Describe the difference between Type 1 and Type 2 Hepatorenal Syndrome

A

Type 1 - rapidly progressive, usually occurs with acute liver failure, clinical pattern of acute renal failure - DIE OF
Type 2 - Moderate renal failure with steady, slow progressive course, clinical pattern of refractory ascites - DIE WITH

35
Q

Describe the pathophysiology of hepatic encepaholpathy.

A

In cirrhosis the portal blood bypasses the liver via the collaterals and the “toxic” metabolites pass directly into the brain to produce the encephalopathy.
An acute onset usually has a precipitating factor e.g. high dietary protein, GI haemorrhage, SBP

36
Q

Describe the 4 grades of hepatic encephalopathy

A 
Grade 1 
Lack of awareness
Grade 2 
Lethargy or apathy
Grade 3 
Somnolence or semi-stupor
Grade 4
Coma - unresponsive to verbal or noxious stimuli
37
Q

How are cirrhotic patients monitored for oesophageal varicies at risk of bleeding?

A

OGD at diagnosis of cirrhosis and every 2 years after

Beta blocker as primary prevention for variceal haemorrhage

38
Q

Over 90% of liver tumours are secondary. What common primary tumours metastasise to liver?

A

Bowel
Lung
Breast

39
Q

Describe the main risk factors for developing HCC

A

Hep B or Hep C infection (important globally, esp where Hep B is endemic)
Alcoholic Cirrhosis
NAFLD

40
Q

Where do HCCs commonly metastasise to?

A

Regional lymph nodes, bones and lungs

41
Q

Describe how CT is used to diagnose HCC

A

4-Phase CT - in arterial phase tumour is white as highly vascularised, in venous phase, tumour looks blacker than rest of liver
Can diagnose HCC in patients with these CT findings with 99% accuracy

42
Q

Describe the pathophysiology behind low platelets in liver disease

A

Splenomegaly caused by portal hypertension, leads to pooling and sequestration of platelets in he spleen
Also decreased production of thrombopoeitin by the liver leads to decreased thrombopoeisis in the bone marrow.

43
Q

The terms Fulfilmant Hepatic Failure and Acute Hepatic failure are often used interchangeably. HOWEVER, what does the word fulfilmant specifically imply?

A

The presence of encephalopathy AND the absence of pres-existing liver disease
(makes it clinically significant from acute on chronic liver disease)

44
Q

What is the commonest cause of fulfilmant hepatic failure in the UK and what is commonest cause worldwide?

A 
UK = paracetamol poisoning (>50%)
Globally = viral hepatitis
45
Q

How common is cerebral oedema in fulfilmant hepatic failure?

A

Up to 80% of patients get it

25% of all deaths from FHF attributable to it

46
Q

Describe the pathophysiology of cerebral oedema in FHF

A

Patients with liver dysfunction have impaired urea synthesis
The brain acts as an alternative ammonia detoxification pathway. Ammonia combines with glutamate in astrocytes to from glutamine.
Glutamine attracts water into astrocytes causing them to swell.
Astrocyte swelling and increased brain water = cerebral oedema
Cerebrel oedema causes intracranial hypertension, raised ICP and brain herniation

47
Q

Describe the other effects FHF has due to loss of metabolic function in the liver.

A

Decreased gluconeogenesis = hypoglycemia
Decreased lactate clearance = lactic acidosis
Decreased synthetic capacity = coagulopathy

48
Q

What investigations would you do in a patient who presented with symptoms of FHF?

A

Paracetamol levels
Hepatitis Screen
Auto-antibody screen
Screen for Wilsons - 24 hr urine copper and Caeruloplasmin levels

49
Q

Whether FHF is defined as Hyper-acute, Acute or Sub-acute is dependent on the time from jaundice to hepatic encephalopathy, what are those time parameters?

A 
Hyper-acute = 0-7 days
Acute = 8-28 days
Sub-Acute = 1-3 months
50
Q

What signs would you find on examination in a patient presenting with FHF?

A

Jaundice, small liver, signs of encephalopathy, fetor hepaticus
fever, vomitng, hypotension and hypoglycemia occur
Neurological examination shows spasticity and hyperreflexia

51
Q

Why should metformin be suspended n

in patients who are having a CT scan?

A

If the contract medium causes renal failure
Metformin is excreted primarily be the kidneys
Continued intake of metformin results in a toxic accumulation of the drug and subsequent lactic acidosis.
To avooid this complication metformin should be suspended after the administration of the contrast agent for 48 hours, during which the contrast induced renal failure will become apparent. If renal function is normal at 48 hours then metformin can be restarted.

52
Q

Describe the typical population affected by PBC

A

90% of those affected are WOMEN in the age range of 40-50

53
Q

Describe the clinical features of PBC

A

Pruritis - typically worse on palms and soles at night time
Fatigue - can be disabling
Dry eyes and mouth (sicca symptoms) - seen in 70% cases
Poor memory
Liver Sx e.g. jaundice, hepatomegaly,

54
Q

Describe the three things used to diagnose PBC

A

Abnormal LFTs (cholestatic raised ALP)
Positive AMA
Compatible Histology (rarely done now as AMA so useful)
ESSENTIALLY AMA AND RAISED ALP THINK PBC

55
Q

Describe the pathophysiology of PBC

A

Progressive destruction of small bile ducts through immune infiltration leads to biliary cirrhosis
Granulomatous

56
Q

Describe the treatment for PBC

A

DISEASE PROGRESSION
UCDA (ursodeoxycholic acid) is the only licenced therapy for PBC. 80% have a full response rate.
Transplantation if not effective or refractory
SYMPTOM RELIEF
Itch - cholestyramine
Fatigue - no Tx

57
Q

Describe the two types of autoimmune hepatitis

A

Type 1 = 74% cases, all ages, ANA/ASMA. Patients may be aymptomatic, have abnormal LFTS or signs of chronic liver disease on examination
Type 2 -

58
Q

What two test results in combination would make you consider autoimmune hepatitis?

A

ANA/ASMA and raised IgG

59
Q

Describe the pathophysiology of PSC

A

PSC occurs because of inflammation in the bile ducts , which results in hardening (sclerosis) and narrowing of the bile ducts both inside and outside of the liver. The resulting scarring of the bile ducts blocks the flow of bile, causing cholestasis

60
Q

Describe the typical population affected by PSC

A

70% are male and average age of onset is 40 years

61
Q

What condition is commonly associated with PSC?

A

IBD (60-80% of patients with PSC have IBD - everyone diagnosed with PSC should undergo colonoscopy
If they are found to have IBD - should be regularly screened for colorectal cancer)

62
Q

Describe the presentation of patients with PSC

A

With increasing screening of patients with IBD, PSC is often detected in the aymptomatic phase wiith abnormal liver biochemistry (usually increased ALP)
Symptomatic presentation is usually with fluctuating pruritis, fatigue, jaundice, RUQ pain and cholangitis

63
Q

What antibody is associated with PSC?

A

ANCA is found in 60% of cases

64
Q

Describe what you would see on imaging of a patient with PSC

A

Ultrasound - will appear normal
MRCP - see multifocal strictures and segmental dilatation of bile ducts
MRCP may fail to idenify minor (but clinically significant) intrahepatic changes, these will have to be picked up on ERCP

65
Q

How is the scar tissue of PSC classically described on histology?

A

onion skin

66
Q

What cancer are people with PSC at significantly increased risk of?

A

Cholangiocarcinoma - patients should be screened by checking Ca 19.9 tumour marker)

67
Q

Can PSC be cured with tranplantation?

A

No - it can return after transplantation and each transplantation increases mortality signifcantly

68
Q

What two investigation results in combination would make you think of PSC

A

Raised ALP and ANCA

Stage 4 CSIM (9 decks)

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