Liver disease Flashcards

1
Q

Blood borne hepatitis

A

HBV (+HDV) ,HCV (these are also the chronic ones)

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2
Q

Enteric transmission hepatitis

A

HAV,HEV ( these are also acute)

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3
Q

Surface antigen HBsAg

A

active infection (either acute or chronic)

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4
Q

HBeAg

A

a marker of viral replication and infectivity, therefore is positive in acute hepatitis B infection.

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5
Q

Surface antibody (HBsAb) Anti-HBs

A

implies vaccination or past or current infection

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6
Q

Core antibodies HBcAb

A

Anti-HBc implies previous (or current) infection.
IgM implies an active infection and is present for about 6 months.
IgG persists and indicates a past infection

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7
Q

Clinical presentation of acute liver failure

A

Malaise, anorexia and fever
Jaundice
Bleeding
Confusion
Abnormal liver function tests
Abdominal pain
Bruising
oliguria/anuria
Acutely may be asymptomatic and anicteric

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8
Q

Clinical signs of acute liver failure

A

Jaundice
hepatomegaly
Spider naevi
Palmar erythema
Severe RUQ pain
Hepatic encephalopathy
Bruising
Ascites
GI bleeding
Hypotension
Tachycardia
Raised ICP
AKI

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9
Q

Causes of acute liver failure

A

Viruses eg hepatitis
Toxins
Metabolic eg Acute fatty liver of pregnancy
Vascular Events
Wilson disease
Autoimmune hepatitis
Malignancy infiltration

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10
Q

Causes of hepatitis

A

Alcoholic hepatitis
Non alcoholic fatty liver disease
Viral hepatitis
Autoimmune hepatitis
Drug induced hepatitis (e.g. paracetamol overdose)

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11
Q

Drug causes of induced liver injury

A

Paracetamol
Anti-TB medications (Isoniazid)
Ecstasy, cocaine
Chemotherapy (cyclophosphamide, 6MP)
Carbamazepine
Macrolide
Statin
Roziglitazone
flucloxacillin

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12
Q

Hepatitis A

A

most common viral hepatitis worldwide but it is relatively rare in the UK
RNA virus, faecal-oral route
Mx: resolves without treatment in around 1-3 months, analgesia, vaccination available
notifiable disease

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13
Q

Hepatitis B

A

transmitted by direct contact with blood or bodily fluids
DNA virus
Chronic HBV is linked to liver cancer
Vaccination available

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14
Q

Hepatitis C

A

It is spread by blood and body fluids.
RNA virus
the most common blood-borne infection and the leading cause of chronic viral infection
Cx: liver cirrhosis and associated complications and hepatocellular carcinoma

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15
Q

Hepatitis E

A

faecal oral route eg seafood/contaminated pork/sausages/ transmitted by water in endemic areas
RNA virus

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16
Q

Mx Hepatitis B

A

Screen for other blood borne viruses (hepatitis A and B and HIV) and other sexually transmitted diseases
Refer to gastroenterology, hepatology or infectious diseases for specialist management
Notify Public Health (it is a notifiable disease)
Stop smoking and alcohol
Education about reducing transmission and informing potential at risk contacts
Testing for complications: FibroScan for cirrhosis and ultrasound for hepatocellular carcinoma
Antiviral medication can be used to slow the progression of the disease
Liver transplantation for end-stage liver disease

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17
Q

Type 1 Autoimmune hepatitis

A

affects women in their late forties or fifties
most common
fatigue and features of liver disease
30% have concurrent immune diseases,especially autoimmune thyroiditis, synovitis, or ulcerative colitis

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18
Q

Type 2 Autoimmune hepatitis

A

teenage or early twenties present with acute hepatitis with high transaminases and jaundice
commonly have other concurrent autoimmune disorders such as type 1 diabetes, vitiligo

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19
Q

Type 1 Autoimmune hepatitis Autoantibodies

A

Anti-nuclear antibodies (ANA)
Anti-smooth muscle antibodies (anti-actin)

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20
Q

Type 2 Autoimmune hepatitis Autoantibodies

A

Anti-liver kidney microsomes-1 (anti-LKM1)
Anti-liver cytosol antigen type 1 (anti-LC1)

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21
Q

Tx autoimmune hepatits

A

high dose steroids (prednisolone) that are tapered over time as other immunosuppressants, particularly azathioprine, are introduced.

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22
Q

Blood results in alcoholic hepatitis

A

Ratio of AST to ALT >2:1
raised gamma-GT
raised MCV
Low albumin
elevated prothrombin time
U+Es may be deranged in hepatorenal syndrome.
Elevated INR- decline in hepatic function/ dietary vitamin K deficiency.
Thrombocytopenia
Hypoglycaemia

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23
Q

Ix alcoholic hepatitis

A

US/fibroscan- fatty changes , degree of cirrhosis
Endoscopy- asses varices hen portal hypertension is suspected
CT and MRI- fatty infiltration of the liver, hepatocellular carcinoma, hepatosplenomegaly, abnormal blood vessel changes and ascites
Liver biopsy - confirm the diagnosis of alcohol-related hepatitis or cirrhosis

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24
Q

Mx alcoholic liver disease

A

Stop drinking alcohol permanently
Consider a detoxication regime
Nutritional support
Steroids improve short term outcomes (over 1 month) in severe alcoholic hepatitis
Treat complications of cirrhosis
Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral

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25
Q

Cx of alcohol

A

Alcoholic Liver Disease
Cirrhosis and the complications of cirrhosis including hepatocellular carcinoma
Alcohol Dependence and Withdrawal
Wernicke-Korsakoff Syndrome (WKS)
Pancreatitis
Alcoholic Cardiomyopathy

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26
Q

Delirium Tremens

A

medical emergency associated with alcohol withdrawal 24-72 hours after last alcohol consumption

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27
Q

Clinical presentation Delirium tremens

A

Acute confusion
Severe agitation
Delusions and hallucinations
Tremor
Tachycardia
Hypertension
Hyperthermia
Ataxia (difficulties with coordinated movements)
Arrhythmias

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28
Q

Wernicke-Korsakoff Syndrome (WKS)

A

due to thiamine vitamin B1 deficiency
can be caused by chronic alcohol abuse, malnutrition, bariatric surgery, or hyperemesis gravidarum.
treatment is with high-dose intravenous thiamine

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29
Q

Clinical features of Wernicke-Korsakoff Syndrome (WKS)

A

Confusion
Oculomotor disturbances (disturbances of eye movements-nystagmus/horizontal or vertical opthalmoplegia)
Ataxia

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30
Q

Korsakoffs syndrome

A

follows an episode of Wernicke’s Encephalopathy
Memory impairment (retrograde and anterograde)
Behavioural changes
destruction of the mammillary bodies
often irreversible

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31
Q

Ix Non alcoholic fatty liver disease

A

ALT increases more than AST
Liver Ultrasound
can confirm the diagnosis of hepatic steatosis
CT with contrast
Liver biopsy
ELF/NAFLD fibrosis score / Fibrosis scan

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32
Q

Mx Non alcoholic fatty liver disease

A

Goal is to reverse the factors that contribute to insulin resistance
Weight loss
Exercise
Stop smoking
Control of diabetes, blood pressure and cholesterol
Avoid alcohol

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33
Q

four most common causes of liver cirrhosis.

A

Alcoholic liver disease
Non Alcoholic Fatty Liver Disease
Hepatitis B
Hepatitis C

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34
Q

Features of decompensated liver cirrhosis

A

Ascites and oedema
Jaundice
Pruritus
Palmar erythema
Gynaecomastia and testicular atrophy
Easy bruising

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35
Q

hepatocellular carcinoma screening

A

Alpha-fetoprotein can be checked every 6 months as a screening test in patients with cirrhosis along with ultrasound.

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36
Q

Screening for cirrhosis

A

Fibroscan retesting every 2 years
in patients at risk of cirrhosis:
Hepatitis C
Heavy alcohol drinkers (men drinking > 50 units or women drinking > 35 units per week)
Diagnosed alcoholic liver disease
Non alcoholic fatty liver disease and evidence of fibrosis on the ELF blood test
Chronic hepatitis B (although they suggest yearly for hep B)

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37
Q

Scoring systems for cirrhosis

A

Child-Pugh Score for Cirrhosis
Model for End-stage Liver Disease (MELD) UK End-stage Liver Disease (UKELD)

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38
Q

MELD score

A

recommended by NICE to be used every 6 months in patients with compensated cirrhosis. It is a formula that takes into account the bilirubin, creatinine, INR and sodium and whether they are requiring dialysis. It gives a percentage estimated 3 month mortality and helps guide referral for liver transplant.

39
Q

Enhanced Liver Fibrosis (ELF) blood test

A

first line recommended investigation for assessing fibrosis in non-alcoholic fatty liver disease

40
Q

Mx Cirrhosis

A

Alcohol cessation
stop offending med
antiviral therapy for viral hepatitis
Colestyramine (bile acid sequestrant) can be used to manage pruritus.
Ultrasound and alpha-fetoprotein every 6 months for hepatocellular carcinoma
Endoscopy every 3 years in patients without known varices
High protein, low sodium diet ( low sodium reduces fluid retention)
MELD score every 6 months
Consideration of a liver transplant
Managing complications

41
Q

Cx cirrhosis

A

Malnutrition
Portal Hypertension, Varices and Variceal Bleeding
Ascites and Spontaneous Bacterial Peritonitis (SBP)
Hepato-renal Syndrome
Hepatic Encephalopathy
Hepatocellular Carcinoma

42
Q

Ascites

A

Ascites describes the accumulation of fluid within the peritoneal cavity.
involves portal hypertension causing increased hydrostatic pressure leading to transudation of fluid.

43
Q

Serum ascites albumin gradient (SAAG)calculation

A

is calculated by subtracting the albumin concentration of the ascitic fluid from the serum albumin concentration.

44
Q

Causes of high SAAG (>1.1g/dL)

A

suggests that the cause of the ascites is due to raised portal pressure.Raised hydrostatic pressure forces water into the peritoneal cavity whilst albumin remains within the vessels

causes include:
Cirrhosis
Heart failure
Budd Chiari syndrome
Constrictive pericarditis
Hepatic failure
alcoholic hepatitis
portal vein thrombosis
massive hepatic metastases

45
Q

Causes of a low SAAG (<1.1g/dL)

A

indicates that the patient does not have portal hypertension and indicates a peritoneal cause of ascites

Cancer of the peritoneum
Tuberculosis and other infections
Pancreatitis
Nephrotic syndrome
serositis (including lyphoma),
peritoneal carcinomatosis.

46
Q

Mx Ascites

A
  • Address the underlying cause
  • Salt restricted diet
  • Fluid restriction
  • Anti-aldosterone diuretics (spironolactone is first line , if doesnt work furosemide can be added)
  • Patients with ascites refractory to medical management may require regular therapeutic paracentesis
  • Prophylactic antibiotics against spontaneous bacterial peritonitis (ciprofloxacin or norfloxacin) in patients with less than 15g/litre of protein in the ascitic fluid
  • Daily weights
47
Q

Hepatorenal Syndrome

A

Hypertension in the portal system leads to dilation of the portal blood vessels, stretched by large amounts of blood pooling there. This leads to a loss of blood volume in other areas of the circulation, including the kidneys–> decline in function

48
Q

Mx Hepatorenal syndrome

A

vasopressin analogues, for example 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

49
Q

Transjugular Intra-hepatic Portosystemic Shunt (TIPS)

A

wire inserted under xray into the jugular vein, down the vena cava and into the liver via the hepatic vein.
They then make a connection through the liver tissue between the hepatic vein and the portal vein and put a stent in place.
This allows blood to flow directly from the portal vein to the hepatic vein and relieves the pressure in the portal system and varices.

50
Q

Hepatic Encephalopathy

A

build up of toxins/ammonia in the brain, which is produced by intestinal bacteria when they break down proteins and is absorbed in the gut.

51
Q

Precipitating Factors of Hepatic Encephalopathy

A

Constipation
Electrolyte disturbance
Infection
GI bleed
High protein diet
Medications (particularly sedative medications eg zopiclone)

52
Q

Clinical presentation hepatic encephalopathy

A

Four stages of hepatic encephalopathy
Altered mood and behaviour, disturbance of sleep pattern and dyspraxia
Drowsiness, confusion, slurring of speech and personality change
Incoherency, restlessness, asterixis
Coma

53
Q

Mx Hepatic encephalopathy.

A

Septic screen
Correct electrolytes
Laxatives (i.e. lactulose) promote the excretion of ammonia.
Antibiotics (i.e. rifaximin) reduces the number of intestinal bacteria producing ammonia.
Nutritional support.
Stop diuretics

54
Q

Reye syndrome

A

An acute encephalopathy with hepatic dysfunction stemming from mitochondrial damage.

55
Q

Reye syndrome presentation

A

acute onset of profuse vomiting and altered mental status, ranging from a personality change to coma, in children recovering from a recent viral infection.

56
Q

Reye syndrome presentation

A

acute onset of profuse vomiting and altered mental status, ranging from a personality change to coma, in children recovering from a recent viral infection.

57
Q

Budd chairi syndrome

A

Hepatic venous outflow obstruction.
Classic triad of symptoms is abdominal pain (normally RUQ), ascites, and hepatomegaly.

58
Q

Budd chairi syndrome

A

Hepatic venous outflow obstruction.
Classic triad of symptoms is abdominal pain (normally RUQ), ascites, and hepatomegaly.

59
Q

HELLP syndrome in pregnancy

A

severe form of pre-eclampsia characterised by haemolysis (H), elevated liver enzymes (EL), and low platelets (LP) in a pregnant or puerperal patient (usually within 7 days of delivery).

60
Q

Complications of acute liver failure :

A

Hepatic encephalopathy ( signs: altered mental status/ confusion, asterixis)
Ascites
Sepsis
AKI
Haemorrhage
Cerebral dysfunction due to increased ICP

61
Q

Wilsons disease

A
  • autosomal recessive disease that is due to mutations in the ATP7B gene.
  • It is a copper transport protein deficiency disease, characterised by excessive copper deposition in the tissues
62
Q

Clinical presentation of Wilsons disease

A

hepatitis, cirrhosis, akinetic-rigid syndrome, speech, behavioural and psychiatric problems ,Kayser-Fleischer rings,blue nails

63
Q

Clinical signs in Wilson disease

A

Kayser-Fleischer rings- green-brown rings in the periphery of the iris
sunflower cataracts in the lens

64
Q

Wilsons disease Ix

A
  • slit lamp examination for Kayser-Fleischer rings
  • reduced serum caeruloplasmin, may be normal
  • reduced total serum copper
  • increased 24hr urinary copper excretion
  • genetic analysis of the ATP7B gene
  • liver biopsy
65
Q

Wilsons disease Mx

A

penicillamine (chelates copper)
trientine hydrochloride is an alternative

66
Q

Causes of Fanconi syndrome

A

Complication of Wilsons disease,cystinosis (most common cause in children), Sjogren’s syndrome, multiple myeloma and nephrotic syndrome

67
Q

Fanconi syndrome

A

generalised reabsorptive disorder of renal tubular transport in the proximal convoluted tubule resulting in:
type 2 (proximal) renal tubular acidosis
polyuria
aminoaciduria
glycosuria
phosphaturia
osteomalacia

68
Q

Drug-induced liver disease hepatocellular picture

A

paracetamol
sodium valproate, phenytoin
MAOIs
halothane
anti-tuberculosis: isoniazid, rifampicin, pyrazinamide
statins
alcohol
amiodarone
methyldopa
nitrofurantoin

69
Q

Drug-induced liver disease causing cholestasis (+/- hepatitis):

A

combined oral contraceptive pill
antibiotics: flucloxacillin, co-amoxiclav, erythromycin*
anabolic steroids, testosterones
phenothiazines: chlorpromazine, prochlorperazine
sulphonylureas
fibrates
rare reported causes: nifedipine

70
Q

Drug-induced liver disease causing cirrhosis

A

methotrexate
methyldopa
amiodarone

71
Q

Causes of hepatomegaly

A

Cirrhosis
Malignancy
Right heart failure
viral hepatitis
glandular fever
malaria
abscess: pyogenic, amoebic
hydatid disease
haematological malignancies
haemochromatosis
primary biliary cirrhosis
sarcoidosis, amyloidosis

72
Q

Haemochromatosis

A

multi-system disorder
There is increased intestinal iron absorption.

73
Q

Haemachromatosis epidemiology

A

middle-aged males
autosomal recessive

74
Q

Haemachromatosis clinical presentation

A

lethargy, fatigue
loss of libido
arthropathy/ arthralgia - 2nd and 3rd MCP joints
skin hyperpigmentation - slate/grey/Bronze
Hepatomegaly
deranged liver function
development of diabetes
erectile dysfunction
Cirrhosis
dilated cardiomyopathy
osteoporosis

75
Q

Haemachromatosis Ix

A

Serum iron (↑) and ferritin (↑)
TIBC (↓) (relates to the amount of transferrin in your blood that’s available to attach to iron)
transferrin saturation > 55% in men or > 50% in women

MRI brain /heart imaging may show evidence of iron deposition.
Liver biopsy- increased iron stores- perls stain

76
Q

Haemachromatosis Cx

A

skin pigmentation (often decreases after phlebotomy)
diabetes
Severe myocardial siderosis
hepatic cirrhosis→ cancer risk of HCC
chondrocalcinosis and arthropathy
hypogonadism and pituitary dysfunction

77
Q

Haemachromatosis Mx

A

Venesection
Another option is desferrioxamine, a iron chelating agent

78
Q

Notching of the inferior border of the ribs

A

Coarctation of the aorta

79
Q

firm, smooth, tender liver edge. May be pulsatile

A

right heart failure

80
Q

hard, irregular liver edge.

A

liver mets

81
Q

hepatomegaly if early disease, later liver decreases in size. Associated with a non-tender, firm liver

A

cirrhosis

82
Q

Amoebic liver abscess

A

Typical symptoms are malaise, anorexia and weight loss. The associated RUQ pain tends to be mild and jaundice is uncommon.

83
Q

Types of liver cancer

A

hepatocellular carcinoma (80%) and cholangiocarcinoma (bile duct cancer, 20%)

84
Q

Risk factors for hepatocellular carcinoma

A

Viral hepatitis (B and C)
Alcohol
Non alcoholic fatty liver disease
Other chronic liver disease
haemachromatosis

85
Q

Liver cancer presentation

A

Weight loss
Abdominal pain RUQ
Anorexia
Nausea and vomiting
Jaundice
Pruritus
Ascites
hepato/splenomegaly
possible presentation is decompensation in a patient with chronic liver disease

86
Q

Cholangiocarcinoma presentation

A

painless jaundice in a similar way to pancreatic cancer
periumbilical lymphadenopathy (Sister Mary Joseph nodes) and left supraclavicular adenopathy (Virchow node) may be seen

87
Q

2ww US to assess for liver cancer

A

in people with an upper abdominal mass consistent with an enlarged liver

88
Q

Liver cancer Ix

A

Alpha-fetoprotein- hepatocellular carcinoma
CA19-9 - cholangiocarcinoma
liver US
CT and MRI
ERCP - biopsies in cholangiocarcinoma

89
Q

Hepatocellular Carcinoma Tx

A

Surgery - resection, transplant
Other - radiofrequency ablation,
transarterial chemoembolisation, several kinase inhibitors eg sorafenib

generally considered resistant to chemo and radiotherapy

90
Q

Cholangiocarcinoma Tx

A

Surgery - resection, ERCP to place stent for symptom relief

generally considered resistant to chemo and radiotherapy.

91
Q

Alcoholic liver disease Ix findings

A

gamma-GT is characteristically elevated

the ratio of AST:ALT > 3

91
Q

Cancers most likely to metastasise to the liver

A

colorectal (via the portal circulation which drains the gut), breast and lung.

92
Q

Maddrey’s discriminant function

A

often used during acute alcoholic liver episodes to determine who would benefit from glucocorticoid therapy
calculated by a formula using prothrombin time and bilirubin concentration