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Met3 > Hepatology: Chronic Liver Failure > Flashcards

Hepatology: Chronic Liver Failure Flashcards

1
Q

Describe the disease trajectory of CLD [2]

A

Asymptomatic phase
- 20 to 40 yrs

Symptomatic phase
- 1 to 5 yrs
}

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2
Q

Describe the pathophysiology of chronic liver disease [4]

A
  • Chronic liver disease may result from repeated insults that cause inflammation (i.e. chronic hepatitis) or cholestasis (i.e. impairment of bile flow)
  • Excess deposition of fat in the liver (i.e. steatosis) can also promote an inflammatory response (e.g. NAFLD)
  • Leads to scarring known as fibrosis: the normal liver architecture is replaced by fibrotic tissue and regenerative nodules
  • If fibrogenesis continues then the end result is cirrhosis, which describes irreversible liver remodeling
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3
Q

Chronic liver disease can arise due to a wide range of pathologies.

Name 8 overall causes of CLD [8]

A
  • Alcohol
  • Viral (Hep A-E)
  • Autoimmine (autoimmune hepatitis)
  • Metabolic (NAFLD)
  • Drug induced
  • Biliary
  • Vascular (Budd-Chiari syndrome)
  • Inherited (alpha-1 antitrypsan deficiency; wilsons disease; hereditary haemochromatosis)
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4
Q

The severity of cirrhosis can be graded using the []

A

The severity of cirrhosis can be graded using the Child-Pugh score.

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5
Q

Describe the natural history of alcohol-induced liver injury [4]

A
  1. normal liver
  2. fatty liver
    3 steatohepatitis
  3. fibrosis/ cirrhosis
  4. (increases risk of hepatocellular cancer)
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6
Q

What LFT results would indicate alcoholic hepatitis? [2]

A

AST: ALT >2.5
Associated with Alcoholic hepatitis

Raised GGT (sensitive to alcohol ingestion, but non-specific to hepatocellular damage)

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7
Q

What are the arrows pointing to? [1]
What pathology does this indicate? [1]

A

Mallory bodies are highly eosinophilic and thus appear pink on H&E stain. The bodies themselves are made up of intermediate keratin filament proteins that have been UBIQUINATED, or bound by other proteins such as heat shock protein

Found in ALCOHOLIC HEPATITIS

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8
Q

What are signs & symptoms of alcoholism associated with:

  • CNS [6]
A

CNS:
- Reduced memory
- cortical atropy
- fits & falls
- wide based gait (cerebellar dysfunction)
- Korsakoffs (memory disorder that results from vitamin B1 deficiency and is associated with alcoholism)
- W.Enceph.

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9
Q

What are signs & symptoms of alcoholism associated with the gut [5]

A
  • Obesity
  • D&V
  • Gastric erosions
  • varices
  • oesoph. rupture
  • Boerrhave syndrome (transmural tear of oesophagus due to vomiting)
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10
Q

What are signs & symptoms of alcoholism associated with the blood [3]

A
  • Increased MCV: non-megaloblastic macrocytic anaemia
  • anaemia from marrow depression
  • Folate deficiency: decreased intake; inhibits folate absorption
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11
Q

What are signs & symptoms of alcoholism associated with the heart [4]

A
  • increased BP:decreasing the vasodilators such as NO in the vascular endothelium either due to inhibition of endothelial nitric oxide synthase (eNOS) or inflammatory/oxidative injury to the endothelium.
  • arrythmias: can trigger atrial fibrillation
  • cardiomyopathy
  • sudden death in binge drinkers
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12
Q

What are signs & symptoms of alcoholism associated with reproduction [4]

A
  • testicular atrophy
  • decreased testosterone and progesterone
  • increased oestrogen
  • fetal alcohol withdrawal
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13
Q

Describe the three HIT hypothesis for the pathogenesis of alcohol related liver injury:

A

Metabolic:
- alcohol
- obesity
- insulin resistance

Inflammatory:
- translation of lipid signal in inflammation (chemokines / cytokines / kupffer ells / endothelial cells & gut microbiota all contribute to inflammatory cascade)

Genetic disturbance of lipid metabolism:
- PNPLA3
- TM6SF2
- MBOAT7

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14
Q

Give a basic overview of the metabolism of alcohol [2]

Describe why this is clinically significant [1]

A

Metabolism:
- Alcohol is metabolised to acetaldehyde via alcohol dehydrogenase
- Cytochrome P450 2E1 (CYP2E1) also converts alcohol to acetaldehyde (and this enzyme tends to be up-regulated in heavy alcohol consumers). This reaction results in oxidative damage to hepatic tissue

Significance:
- Acetaldehyde is a highly reactive, toxic metabolite: carcinogenic so increases risk of hepatocellular carcinoma

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15
Q

Which score is used to calculate risk of alcohol dependence? [1]

A

AUDIT

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16
Q

Explain why it is importance to determine a patient’s level of alcohol dependence? [1]

A

Work out the impact / level of alcohol withdrawal syndromes:
- Seizures
- Hallucinosis
- GI upset
- HTN
- Fever

There is a risk of mortality

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17
Q

Describe the treatment plan for alcohol withdrawal [2]

A

Benzodiazapenes:
- Chlordizepoxide: give for 1st 3D 10-50mg/6hrs, then plan on weaning
- Lorazepan (for patients with underlying cirrhosis)

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18
Q

What are the two key symptomatic phases of alcoholic related liver disease (ArLD) [2]

A
  • Alcoholic hepatitis
  • Alcholic related liver cirrhosis
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19
Q

Describe the clinical presentation of AH (alcoholic hepatitis): [6]

A
  • jaundice
  • ascites
  • malaise
  • D&V
  • tender hepatomegaly
  • ongoing alcohol abuse
  • fever
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20
Q

Describe diagnosis of AH [7]

A
  • MCV raised
  • Raised GGT
  • WCC increased
  • AST:ALT >1
  • Serum bilirubin raised (Elevated bilirubin reflects impaired metabolic function of the liver in the absence of biliary obstruction)
  • Raised INR
  • Biopsy (gold standard but not always done in practise): steotosis; hepatic ballooing, inflammatory infiltrate
  • Negative liver screen: rules out other causes of liver disease
  • Raised ALP (later in disease)
  • USS
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21
Q

What type of diet should be provided to patients of alcoholic hepatitis? [3]

A

A high protein diet should be instituted: use NG feed if need

Vitamins:
* Vitamin K
* Thiamine (can give Pabrinex

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22
Q

Describe the different symptoms for alcohol withdrawal symptoms for the following time periods:
6-12 hours: [1]
12-24 hours [1]
24-48 hours: [1]
24-72 hours: [1]

A

6-12 hours: tremor, sweating, headache, craving and anxiety
12-24 hours: hallucinations
24-48 hours: seizures
24-72 hours: delirium tremens

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23
Q

Explain why alcohol withdrawal syndrome can lead to mortality [2]

A

Chronic alcohol use results in the GABA system becoming down-regulated and the glutamate system becoming up-regulated to balance the effects of alcohol

When alcohol is removed, the GABA system under-functions and the glutamate system over-functions, causing extreme excitability of the brain and excessive adrenergic (adrenalin-related) activity

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24
Q

How does NAFLD present? [4]

A

Most are asymptomatic and the condition is often discovered incidentally during routine blood tests or imaging studies.

Patients may present with non-specific symptoms such as:
* fatigue
* malaise
* right upper quadrant discomfort (~50%)

  • Hepatomegaly
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25
Q

NAFLD is associated with which syndrome? [1]

A

Metabolic syndrome, which is a combination of hypertension, obesity and diabetes.

Metabolic syndrome is common and dramatically increases the risk of cardiovascular disease and other health problems.

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26
Q

Describe which tests may pick up that somone has NAFLD [6]

A
  • Often no clinical markers until cirrhosis
  • ALT/AST > 1
  • Liver ultrasound can confirm the diagnosis of hepatic steatosis (fatty liver), seen as increased echogenicity. (Ultrasound does not indicate the severity, function of the liver or presence of fibrosis. It can be normal in NAFLD)
  • Enhanced liver fibrosis (ELF) blood test is the first-line investigation for assessing fibrosis in non-alcoholic fatty liver disease.

NAFLD Fibrosis Score (NFS) is another option for assessing liver fibrosis in NAFLD. It is based on an algorithm of age, BMI, liver enzymes (AST and ALT), platelet count, albumin and diabetes.

Fibrosis 4 (FIB-4) score is another option for assessing liver fibrosis in NAFLD. It is based on an algorithm of age, liver enzymes (AST and ALT) and platelet count.

Transient elastography (“FibroScan”) can be used to assess the stiffness of the liver using high-frequency sound waves. It helps determine the degree of fibrosis (scarring) to test for liver cirrhosis. It is used where the enhanced liver fibrosis (ELF) test indicates advanced fibrosis.

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27
Q

TOM TIP: Both the NFS and FIB-4 scores use the AST:ALT ratio to assess the severity of liver fibrosis.

The normal ratio is []/

A ratio [] in NAFLD suggests advanced fibrosis

. An AST:ALT ratio [] indicates alcohol-related liver disease rather than NAFLD.

A

TOM TIP: Both the NFS and FIB-4 scores use the AST:ALT ratio to assess the severity of liver fibrosis.

The normal ratio is less than 1.

A ratio greater than 0.8 in NAFLD suggests advanced fibrosis.

An AST:ALT ratio greater than 1.5 (meaning a disproportionately high AST) indicates alcohol-related liver disease rather than NAFLD.

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28
Q

Name 3 drugs that are associated with increasing risk factor for NAFLD [3]

Name a surgery that is associated associated as a risk factor for NAFLD [1]

Describe nutrition that is associated with increasing risk factor for NAFLD [2]

A

Drugs:
- Steroids
- Amiodarone
- Methotrexate

Weight reducing surgery:
- jejuno-ileal by pass

Nutrition
* Protein calorie malnutrition & TPN

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29
Q

Describe the treatment algorithm for NAFLD [6]

A
  • Weight loss: diet & exercise
  • Consider vitamin E
  • Consider pioglitazone (reduces peripheral insulin resistance)
  • Consider weight loss medication: orlistat
  • Consider bariatric surgery if BMI > 35 and one other obesity co-morbid / BMI > 40.
  • Liver transplant

BMJ BP

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30
Q

Diagnosis of NAFLD? [3]

A

The diagnosis requires the presence of

  • ultrasound findings of a fatty liver
  • risk factors
  • excluding other causes of liver disease with a careful alcohol history and full non-invasive liver screen.
  • Liver biopsy is the gold standard test.
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31
Q

Viral hepatitis:

  • Which viruses cause acute hepatitis [2]
  • Which viruses cause chronic hepatitis [3]
A

Acute:
- Hepatitis A
- Hepatitis E

Chronic:
- Hepatitis B
- Hepatitis C
- Hepatitis D

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32
Q

Which hepatitis viruses are transmissable via faecal-oral routes? [2]

Which hepatitis viruses are transmissable via bodily fluids ? [3]

A

Faecal-oral::
- Hepatitis A
- Hepatitis E

Bodily fluids::
- Hepatitis B
- Hepatitis C
- Hepatitis D

33
Q

Describe the transmission of Hep B [3]

A
  • Vertical
  • Blood contact / products
  • Sexual contact (presents with acute infection w/ jaundice)
34
Q

Hepatitis D requires a co-infection with []

A

Hep B: requires Hep B surface antigens

35
Q

Describe the natural history of Hep B (HBV) [3]

A
  • Majority (65%) exposed to acute HBV infection have asymptomatic recovery
  • 25% have acute hepatitis but recover
  • 10% have chronic infection (HBV antigens >6months)
    i) 90% these: asymptomatic
    ii) 10% lead to chronic hepatitis; cirrhosis; HCC
36
Q

Explain how do you diagnose HBV using serology [5]

A

Hepatitis B surface antigen (HbsAGs):
- will only be positive in current infection, whether acute or chronic.

Hepatitis B surface antibody (Anti-HBs):
- Confers immunity (can be after infection or vaccination)

Hepatitis B core antigen (HBcAg):
- expressed by infected hepatocytes, not used in the vaccination
- anti-HBc will only be present in a previous or current infective state (never post-vaccination).
- IgG: past exposure / chronic infection
- IgM: acute infection

HBV DNA:
- used to confirm virus
- used to monitor treatment (undetectable?)

HDV IgG: in case of also Hep D infection

HbeAg/Ab: level correlates to replication level & therefore infectivity

37
Q

Which test for HBV is present in serum 1-6 months immediately after exposure? [1]

A

HBsAG

38
Q

Which test for HBV is present in serum 1-3 months after acute illness and infers high infectivity? [1]

A

HbeAg

39
Q

How would you infer that a patient has had a vaccination and no infection? [1]

A

solely having antibodies to HBsAG: HBsAB

Surface AB: Safe

40
Q

How can you tell from serum anti-bodies if a ptx is HBV chronic or acutely suffering from the virus? [2]

A

Acute HBV: IgM
Chronic HBV: IgG

41
Q

Explain how E antigen (HBeAg) is used in understanding the level of virus in patient? [4]

A

E antigen (HBeAg): marker of viral replication and implies high infectivity:

Where the HBeAg is present it implies the patient is in an acute phase of the infection where the virus is actively replicating.

The level of HBeAg correlates with their infectivity

If the HBeAg is higher, they are highly infectious to others

42
Q

What does it imply if a patient with HBV is HBeAg negative but the HBeAb is positive? [2]

A

Been through a phase where the virus WAS replicating but the virus has now stopped replicating and they are less infectious

43
Q

Describe the treatment for HBV [3]

A

Nucleoside analogues:
- Entecavir
- Tenofovir

PEG-IFN (peginterferon alfa 2a)

44
Q

Describe symptoms of acute HBV infection [6]

A

Asymptomatic (majority)
Jaundiced
RUQ pain
N&V
Arthralgia
urticaria (hives)

45
Q

Describe symptoms of chronic HBV infection [4]

A
  • most people with chronic HBV are also asymptomatic
  • symptoms of chronic liver disease: palmar erythema; spider angiomas (the number and size of spider angiomata correlate with increasing severity of liver disease); asterixis; easy bruising
  • symptoms of cirrhosis and portal hypertension: ascites; hepatomegaly; splenomegaly; caput medusae

Extra-hepatic manifestations (10-20%): serum sickness-like syndrome (fever, arthralgia, malaise, lethargy); Polyarteritis nodosa; Glomerular disease (membranous nephropathy)

46
Q

Describe the difference in chronicity in HBV v HBC [2]

Why is this clinically significant? [1]

A

HBV: low
HBC: 80% develop risk of chronicity (therefore higher risk of cirrohosis & HCC)

C = Chronic

47
Q
A
48
Q

Describe the risk factors for HCV infection (high; moderate; low)

A

High risk:
- IV drug use
- recieved clotting factors before 1987

Moderate risk:
- Haemodialysis patients
- Recieved blood transfusion prior to 1992
- Infants born to infected mothers

Low risk:
- Occupation exposure
- Sexual practices

49
Q

Describe the disease course of Hep C [2]

A
  • 1 in 4 fight off the virus and make a full recovery
  • 3 in 4 develop chronic hepatitis C: chronic hepatitis; cirrhosis; HCC
50
Q

How do you investigate for HCV? [5]

A

Test for:
- HCV antibody IgG
- HCV RNA (6 genotypes; can change treatment strategies)
- LFTs
- HCC screen (given higher risk): USS and AFP
- Liver biopsy (rare) or Fibroscan to investigate stage of fibrosis}

51
Q

How do you confirm an ongoing HCV infection? [1]

What would be the next mangament step if found to be positive [1]

A

HCV PCR [1]

Procede to have biospy to see extent of damage

52
Q

Describe HCV treatment:

  • Length? [1]
  • Therapies? [3]
A

8-12 weeks

Therapies:
- ARVs: aim sustained virological response (SVR; undetectable serum HCV RNA six months after the end of therapy)

  • Combination dependent on genotype and stage of fibrosis
  • currently a combination of protease inhibitors (e.g. daclatasvir + sofosbuvir or sofosbuvir + simeprevir) with or without ribavirin are used
53
Q

Define haemochromatosis [1]

A

an iron storage disorder in which iron depositions in multiple organs (such as the liver, skin, pituitary, heart and pancreas) leading to oxidative damage.

It is the most common genetic condition in the UK but may initially present with non-specific symptoms, leading to under-diagnosis.

54
Q

Which gene is associated with haemochromatosis? [1]

Describe the inheritance pattern [1]

How does this gene mutation cause the pathogenesis of the disease? [5]

A
  • human haemochromatosis protein (HFE) gene
  • autosomal recessive
  • HFE mutation causes decreased hepcidin activity (regulates iron stores); increased duodenal/jejunal iron absorption AND release of iron from bone marrow macrophages → iron deposition in cells → Fenton reaction and hydroxyl free radicals → DNA, lipid and protein damage → organ dysfunction

Fenton reaction:
Iron freely undergoes oxidation in cells from Fe2+ to Fe3+ as part of the Fenton reaction
In this process, hydroxyl free radicals are generated which then cause oxidative damage

55
Q

Why does haemochromatosis present later in women than men? [1]

A

menstruation acting to eliminate iron from the body

56
Q

Describe the early [7] and late [3] clinical presentation of haemochromatosis

A
  • Chronic tiredness
  • Joint pain
  • Pigmentation (bronze skin)
  • Testicular atrophy
  • Erectile dysfunction
  • Amenorrhoea (absence of periods in women)
  • Cognitive symptoms (memory and mood disturbance)

Later:
- Slate-grey skin pigmentation
- Hepatomegaly
- Dilated cardiomyopathy

57
Q

Describe investigations used to diagnose haemochromatosis [5]

A
  • Raised serum ferritin
  • Elevation transferrin saturation
  • Raised AST & ALT (not more than 2x)
  • Test for HFE gene
  • Liver bx / Fibroscan
  • MRI (Ferriscan)}
58
Q

Tx for haemochromatosis? [2]

A

Venesection (regularly removing blood to remove excess iron – initially weekly)

Iron chelation therapy (iron chelator) works by binding to the extra iron so that it can be removed from the body): Oral: Deferasirox and parenteral agents Desferrioxamine.

59
Q

What presentation of haemochromatosis may be highlighted via XR imaging? [1]

A

Chondrocalcinosis: causes stressed joints to deteriorate faster than resting joints

60
Q

Define Wilson’s disease [1]

A

Wilson’s disease is an autosomal recessive disorder characterised by excessive copper deposition in the tissues

61
Q

How does Wilson’s disease present? [5]

A

Liver: hepatitis, cirrhosis

neurological: basal ganglia degeneration, speech, behavioural and psychiatric problems are often the first manifestations. Also: asterixis, chorea, parkinsonism, dementia

Kayser-Fleischer rings

renal tubular acidosis (esp. Fanconi syndrome)

haemolysis

blue nails

62
Q

How is Wilson’s disease diagnosed? [4]

A
  • reduced serum caeruloplasmin
  • reduced serum copper(counter-intuitive, but 95% of plasma copper is carried by ceruloplasmin)
  • Liver bx
  • MRI brain
  • increased 24hr urinary copper excretion
  • haemolytic anaemia
63
Q

Tx of Wilson’s diease? [3]

A

Copper chelation using either:
* Penicillamine
* Trientine

Zinc salts (inhibit copper absorption in the gastrointestinal tract)

Liver transplantation

64
Q

If have high risk of HCC (have liver cirrhosis), what screening is undertaken to ID risk? [2]

A
  • USS: 6 months
  • test for AFP - tumour marker
65
Q

What imaging is used for HCC? [2]

A

CT
MRI

66
Q

The MELD Score is used to measure severity of? [1]

A

Cirrhosis

The Model of End-Stage Liver Disease (MELD)

Score measures the severity of cirrhosis based on five parameters: serum bilirubin, INR, sodium, creatinine and need for dialysis.

67
Q

What is the first line treatment for hepatic encephalopathy? [1]

What is the secondory prophylaxis of hepatic encephalopathy? [1]

A

NICE recommend lactulose first-line
rifaximin for the secondary prophylaxis of hepatic encephalopathy

68
Q

What SAAG level indicates portal HTN? [1]

A

Ascites: a high SAAG gradient (> 11g/L) indicates portal hypertension

69
Q

[] is the first line treatment for hereditary haemochromatosis.

[] may be used second-line

A

Venesection is the first line treatment for hereditary haemochromatosis.

Desferrioxamine may be used second-line (medicine that removes excess iron that builds up after having regular blood transfusions)

70
Q

[] are used in the management of severe alcoholic hepatitis

A

Corticosteroids are used in the management of severe alcoholic hepatitis

71
Q

How do you determine if a patient is acutely suffering from HBV? [1]

How you determine if a patient has immunisation from vaccination? [1]

How you determine if a patient has immunisation from previous infection? [1]

A

How do you determine if a patient is acutely suffering from HBV? [1]
- HBsAg

How you determine if a patient has immunisation from vaccination? [1]
- A vaccine would only lead to anti-HBs antibodies

How you determine if a patient has immunisation from previous infection? [1]
- immunity due to natural infection also leads to the presence of anti-HBc antibodies & anti-HBs antibodies

Anti-HBs = Safe (Have immunity so either immunised or previously exposed, -ve in chronic disease)

Anti -HBc = Caught (acquired infection at some point rather than immunised)

72
Q

What is pneumonic for remembering the factors that influence Child-Pugh score? [5]

A

ABCDE

A - albumin
B - bilirubin
C - clotting
D - distention (ascites)
E - encephalopathy

73
Q

Which LFT is NOT useful in determining severity of liver cirrhosis? [1]

A

ALT

(not included in Child-Pugh Score)

74
Q

How do you differentiate between ferritin levels from acute response to liver versus haemochromatosis? [1]

A

Both get high ferritin levels; haemochromatosis normally presents after fifth decade

75
Q

Which iron serological marker may be the earliest indictor hereditary haemochromatosis? [1]

A

Raised transferrin saturation may be the earliest indicator of hereditary haemochromatosis.

76
Q

You diagnose a patient with active AIH.
What is the two step treatment regime? [1]
How long does treatment for AIH need to occur to prevent relapse? [1]

A

1st line: prednisolone
2nd line: aziothropine

Continue treatment for 2 years

77
Q

What is the triad of hepatorenal syndrome? [3]

A

Cirrhosis
Ascites
AKI not attributable to any other cause.

78
Q

How do you treat type 1 HRS? [3]

A

terlipressin, have a growing evidence base supporting their use. They work by causing vasoconstriction of the splanchnic circulation

volume expansion with 20% albumin

transjugular intrahepatic portosystemic shunt

(still have a v poor prognosis)

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