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Year 3 - Met3a > Diseases of the liver > Flashcards

Diseases of the liver Flashcards

1
Q

there is an increase in

A
  • the prevalence of liver disease mortality
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2
Q

what are the two types of liver disease presentation

A
  • acute liver failure - rare

- chronic liver disease/cirrhosis - common

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3
Q

What can cause acute liver failure

A
  • Drugs - paracetamol
  • infections - hepatitis A or B
  • toxins
  • ischaemic
  • metabolic
  • vascular
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4
Q

What can cause chronic liver disease/cirrhosis

A
  • alcohol
  • viral hepatitis B or C
  • non alcoholic fatty liver disease
  • autoimmune hepatitis
  • primary biliary cirrhosis
  • primary sclerosing cholangitis
  • haemochromatosis and wilsons disease
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5
Q

How long can liver disease be asymptomatic for

A

20-40 years

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6
Q

How long can the symptomatic phase of liver disease be for

A

1-5 years

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7
Q

what can be done in the asymptomatic phase of liver disease

A

Can do prevention and treatment

assess risk of liver disease

  • life-stage approach
  • genetic
  • environmental
  • behaviour risks

Early identification of liver disease

  • role of tests
  • find treatable disease

monitoring and management

  • review for progression
  • agree and use the pathways for intervention repetition
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8
Q

what can you do in terms of treatment for the symptomatic phase of liver failure

A
  • transplant

- if that person is not suitable for a transplant than you treat the symptoms or do palliation

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9
Q

What are the complications in the symptomatic phase of liver failure

A
  • Ascites
  • haemorrhage
  • encephalopathy
  • HCC
  • jaundice
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10
Q

name the types of acute liver failure

A

Acute liver failure = occurs suddenly in the previously healthy liver

  • hyperacute - 7 days or less
  • acute - 8-12 days
  • subacute - 2-26 weeks
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11
Q

Name the diseases that alcohol can cause

A
  • hypertension
  • coronary heart disease
  • ischaemic stroke
  • haemorrhagic stroke
  • oral pharyngeal cancer
  • pancreatitis
  • liver disease
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12
Q

describe the natural history of alcohol induce liver injury

A
  • starts with fatty liver
  • progresses to steatohepatitis - fat and inflammation
  • the progresses to fibrosis and cirrhosis
  • then can progress to hepatoceullar cancer
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13
Q

What does the extent of liver damage by alcohol depend on

A
  • volume of alcohol

- duration of alcohol liver consumption

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14
Q

What do you have to have regularly when you get cirrhosis

A

regular 6 months ultrasound scans when you have cirrhosis

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15
Q

What is the three HIT hypothesis for alcohol related liver disease

A

Idea that alcohol mediated injury

  1. can trigger a metabolic insult
    - you are more at risk of a metabolic insult from alcohol if you have obesity and insulin resistance (diabetes)
  2. there is an inflammatory cascade
    - translation of lipid signal in inflammation - chemokines, cytokines, hepatic stellate ceiss, kupffer cells, endothelial cells and gut microbiota; DAMPS and PAMPs
  3. there is also an increased risk if you have a genetic predisposition
    - genetic disturbance of lipid metabolism
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16
Q

What genes lead to a genetic disturbance of lipid metabolism and are genes that are associated with steatosis (increased risk for alcohol related liver disease)

A
  • PNPLA3
  • TM6SF2
  • MBOAT7
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17
Q

How do you manage alcohol related liver disease

A
  • Avoidance of alcohol - address alcohol addiction
  • Glucocorticoids often used during acute episodes of alcoholic hepatitis - Maddrey’s criteria is used during acute episodes to determine who would benefit
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18
Q

Name the types of alcohol withdrawal syndromes and the time frame in which they happen in

A
  • Minor withdrawal = 6 to 36 hours
  • Seizures = 6-48 hours
  • alcoholic hallucinosis = 12-48 hours
  • delirium tremens = 48-96 hours
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19
Q 
Describe what happens in 
- minor withdrawal 
- seizures 
- alcohol hallucinosis 
- delirium tremens 
for alcohol withdrawal symptoms
A

minor withdrawal
- tremulousness, mild anxiety, headache, diaphoresis, palpitations, anorexia, GI upset, normal mental status

seizures
- single or brief flurry of generalised, tonic-clonic seizures, short post-ictal period, status epilepticus is rare

alcohol hallucinosis
- visual, auditory, and or tactile hallucinations with intact orientation and normal vital signs

delirium tremens
- delirium, agitation, tachycardia, hypertension, fever, diaphoresis

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20
Q

How do you treat alcohol withdrawal

A
  • Chlordiazepoxide
  • lorazepam

can be either a fixed dose or used when there are symptoms

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21
Q

what is the benefit of using symptom triggered alcohol withdrawal treatment

A
  • shorter time
  • lower dose
  • requires training to use
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22
Q

What criteria is used to judge how severe alcoholic hepatitis is

A

Maddrey’s criteria

- looks at the prothrombin time and bilirubin

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23
Q

describe alcoholic hepatitis presentation

A
  • Clinical syndrome of recent onset jaundice with or without ascites with ongoing alcohol abuse
  • can have a fever
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24
Q

What do the bloods look like in alcoholic hepatitis presentation

A

can have

  • raised white cell count
  • raised platelets
  • raised AST
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25
Q

alcoholic hepatitis on a liver screen will be

A

negative

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26
Q

What is the gold standard test for alcoholic hepatitis

A
  • Liver biopsy
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27
Q

What will alcoholic hepatitis look like on a liver biopsy

A
  • steatosis - fat infiltration
  • hepatocyte ballooning
  • inflammatory infiltrate
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28
Q

How do you manage cirrhosis

A

Cirrhosis care bundle

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29
Q

What is the downside of using a liver biopsy

A
  • 20% of liver biopsy that show cirrhosis miss the alcohol hepatitis in the liver
  • 20-40% of liver biopsy that show alcoholic hepatitis miss the cirrhosis in the liver as it might elsewhere in the liver
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30
Q

How do you treat alcoholic hepatitis

A
  • Sepsis treatment - low threshold to treat them at first sign of sepsis
  • nutrition - NG feed
  • Maddrey’s criteria - DF is greater than 32 then use steroids/pentoxyfilline
  • long term prognosis - dependent on alcohol abstinence
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31
Q

What two measurements does the maddrey’s criteria use (alcoholic hepatitis)

A
  • Prothrombin time

- bilirubin level

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32
Q

What criteria is used in alcoholic hepatitis

A

maddrey’s criteria

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33
Q

What is important in the long term prognosis of alcoholic hepatitis

A
  • alcohol abstinence
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34
Q

What is non alcoholic steatohepatitis (NASH)

A
  • features of alcoholic hepatitis on biopsy

- absence of history of alcohol excess

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35
Q

What is the difference between NASH (non alcoholic steatohepatitis) and NAFLD (non alcoholic fatty liver disease)

A

NAFLD - this is a spectrum whereas NASH is just part of the spectrum

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36
Q

What conditions does NAFLD include

A
  • fatty liver
  • NASH
  • cirrhosis
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37
Q

What is the pathogenesis of NAFLD

A
  • There is hepatic triglyceride accumulation - this causes free fatty acids to be released from lipid stores
  • this leads to oxidative stress and inflammatory mediators
  • this causes progressive fibrosis
  • this leads to cirrhosis
  • this causes liver failure and hepatocellular caner
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38
Q

What is the pathogenesis of NAFLD

A
  • There is hepatic triglyceride accumulation - this causes free fatty acids to be released from lipid stores
  • this leads to oxidative stress and inflammatory mediators
  • this causes progressive fibrosis
  • this leads to cirrhosis
  • this causes liver failure and hepatocellular cancer
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39
Q

NASH has worse prognosis than ..

A

fatty liver

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40
Q

what is NASH an important cause in

A
  • NASH has been suggested as an underlying cause in majority of patients with cryptogenic cirrhosis

Outcome of NASH related cirrhosis is worse that hepatitis C related cirrhosis

  • higher mortality
  • identical risk of primary liver cancer
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41
Q

How common is NAFLD

A

10-24% of the population

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42
Q

How does NAFLD present

A
  • Jaundice
  • Hepatomegaly
  • ALT is typically greater than AST
  • Fatigue
  • Right upper quadrant pain
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43
Q

what liver marker is elevated in alcoholic liver disease

A

AST is higher than the ALT

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44
Q

What conditions are related to NAFLD

A
  • obesity - particularly central/visceral
  • T2DM or impaired glucose tolerance
  • hypertriglyceridemia/ hyperuricaemia
  • hypertension
  • liver manifestation of insulin resistance ‘metabolic’ syndrome
  • genetic predisposition
  • rapid weight reducing surgery - jejuno ileal bypass
  • protein calorie malnutrition
  • total parenteral nutrition
  • iron overload
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45
Q

name the drugs that are associated with NAFLD

A
  • steroids
  • amiodarone
  • methotrexate
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46
Q

What is the diagnosis of NAFLD based on

A
  • based on exclusion of other liver diseases: liver screen
  • screen for metabolic syndrome to confirm

Liver biopsy

  • to make diagnosis
  • provide prognostic iformation
  • invasive
  • Fibroscan
  • non invasive
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47
Q

What factors make up the metabolic syndrome

A
  • impaired glucose tolerance
  • central obesity
  • elevated triglyceride and low HDL
  • hypertension
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48
Q

What does a fibroscan measure

A
  • Measures liver stiffness (steatosis and fibrosis)

- non invasive

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49
Q

What is the treatment of non alcoholic fatty liver disease

A
  • Weight loss - bariatric surgery

Treat metabolic factors

  • hypertension
  • diabetes
  • lipid lowering drugs
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50
Q

What are the acute hepatitis virus

A

A and E

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51
Q

describe hepatitis A

  • virus class
  • genome
  • route of transmission
  • incubation
  • chronicity
A
  • virus class = Picornavirus
  • genome = RNA
  • route of transmission= Faecal-oral
  • incubation = 15-50 days
  • chronicity = No
52
Q

describe hepatitis E

  • virus class
  • genome
  • route of transmission
  • incubation
  • chronicity
A
  • virus class = Calcivirus
  • genome = RNA
  • route of transmission = faecal oral
  • incubation = 15-45 days
  • chronicity = No
53
Q

describe hepatitis B

  • virus class
  • genome
  • route of transmission
  • incubation
  • chronicity
A
  • virus class = hepadnavirus
  • genome = DNA
  • route of transmission = Bodily fluids
  • incubation = 28-160 days
  • chronicity = yes
54
Q

describe hepatitis C

  • virus class
  • genome
  • route of transmission
  • incubation
  • chronicity
A
  • virus class = flavivirus
  • genome = RNA
  • route of transmission = bodily fluids
  • incubation = 15-150 days
  • chronicity = yes
55
Q

describe hepatitis D

  • virus class
  • genome
  • route of transmission
  • incubation
  • chronicity
A
  • virus class = deltavirus
  • genome = RNA
  • route of transmission = Bodily fluids
  • incubation = variable
  • chronicity = yes
56
Q

What type of hepatitis is more dangerous in pregnant women

A

Hepatitis E is more dangerous in pregnant women

57
Q

What is the antibody that is positive in a test for hepatitis A and E

A
  • Hepatitis A = HAV IgM

- Hepatits E = HEV IgM

58
Q

What hepatitis virus is the only one that has a DNA genome

A

Hepatitis B is the only DNA virus

59
Q

Which two hepatitis viruses are associated with liver disease

A

B and C are important in chronic liver disease

60
Q

describe the difference between hepatitis B and C presentation

A
  • B usually acute and self limited

- C presents chronically

61
Q

What cancer is hepatitis B associated with

A

hepatocellular cancer

62
Q

How is hepatitis B transmitted

A
  • Maternal transmission (vertical) - children and neonates are more likely to remain chronically infected
  • blood contact
  • sexual contact - acute infection usually with jaundice illness and clearance
63
Q

when is hepatitis D only seen

A

Hepatitis D is only seen in hepatitis B

64
Q

describe what the different pathways are with hepatitis B

A

Acute HBV infection

  • 65% are asymptomatic - create antibodies and there is resolution and recovery
  • 25% have a strong Th1 and CTL response - develop acute hepatitis and there is resolution and recovery
  • 10% have a weak Th1 and CTL response - get chronic infection, 70-90% become an asymptomatic chronic carrier, 10-30% develop chronic hepatitis, either regress or go to cirrhosis which then either regresses or goes to hepatocellular carcinoma
65
Q

How do you diagnose HBV

A

Check serology

  • HbsAg - marker of active infection - if this progresses more than 6 months then this shows it is a chronic infection
  • HbsAb - this is a marker of active immunisation (vacccine)
  • HbcAb - IgG past exposure, IgM - acute infection
  • HbeAg/Ab - in early phase E antigen is positive and in the chronic stages there is an E antibody that is positive
  • HBV DNA - confirms presence of virus - can be used to monitor the treatment
  • HDV IgG - also screened
  • HDV RNA confirms hepatitis D
66
Q

What molecule confirms the presence of HBV and is used to monitor HBV treatment

A

HBV DNA

67
Q

What is the aim of HBV treatment

A
  • aim to reduce viral replication
  • aim of improve immunological response
  • progression to cirrhosis can be halted/fibrosis reduced
  • reduced risk of HCC
68
Q

how do you treat HBV

A

Nucleoside/nucelotide analogues

  • Entecavir
  • tenofovir
  • PEG-IFN - increases immune response to fight the virus
69
Q

what are the risk factors for HCV infection

A

High risk

  • IV drug use
  • before 1987 - recipients of clotting factors

Moderate risk

  • haemodilaysis patients
  • recipients of blood or solid organ transplant before 1992
  • persons with undiagnosed liver problems
  • infants born to infected mothers

Low risk

  • occupational exposures
  • sexual practices
70
Q

Describe the disease progression in hepatitis C

A
  • Normal liver
  • there can be an acute infection - this spontaneously resolves in 20% of people
  • or this can lead to a chronic infection in 80% of people
  • this leads to chronic hepatitis this this could either lead to stable hepatitis in 80% of people or cirrhosis in 20% of people
  • this leads to decompensation in 20% of people or slowly progressive i n75 of people or HCC in 1-4% of people
71
Q

How do you diagnose HCV

A
  • HCV IgG+
  • HCV RNA - estimate the viral load and the genotype of HCV
  • liver function tests

HCC screen

  • liver ultrasound
  • AFP checked (if raised then HCC)

Liver biopsy or fibroscan
- stage fibrosis

72
Q

How many HCV genotypes are there

A

6

73
Q

Who is at a higher risk of progressive liver disease and reinfection in HCV

A
  • alcohol
  • BMI
  • psychiatric/mood disorder
  • lifestyl e
74
Q

How do you treat HCV

A
  • 8-12 weeks therapy
  • aim of sustained virological response
  • combination of oral directly acting antiviral agents depend on

Genotypes G1-4

  • harvoni
  • Vierkirax and Exvira
  • Zepatier
  • Epclusa
  • Maviret
75
Q

What is the presentation of haemochromatosis

A
  • excess iron absorption and deposition
  • Fatigue, erectile dysfunction, arthralgia
  • Bronze skin pigmentation
  • Diabetes
  • Liver – chronic liver disease, hepatomegaly, cirrhosis, hepatocellular deposition
  • Dilated cardiomyopathy
  • Arthritis
  • Hypogonadism
76
Q

What organs are involved in haemochromatosis

A
  • pancreas
  • pituitary
  • cardiac
  • skin and joints
77
Q

What is the treatment of haemochromatosis

A
  • venesection -use ferritin as a marker – transferrin saturation should be kept below 50% and serum ferritin concentration below 50ug/l
  • Fe chelation therapy
78
Q

How do you diagnose haemochromatosis

A
  • Ferrtin: increased
  • TF: increased in saturation
  • Low TIBC
  • HFE mutation
  • Liver biopsy
  • MRI scan
79
Q

who is affected by haemochromatosis

A
  • autosomal recessive
  • more men then females
  • 9% heterozygous
80
Q

What are you at risk of if you have haemochromatosis

A

HCC

81
Q

describe the genetics of wilsons disease

A
  • Autosomal recessive

- ATP7B

82
Q

What is wilsons disease

A
  • dysregulated copper homeostasis
83
Q

How does Wilsons disease present

A

Liver deposition

  • acute liver failure
  • cirrhosis

Basal ganglia deposition

  • movement disorders
  • psychiatric
84
Q

how do you diagnose wilsons disease

A
  • decrease in Caer
  • increase in urinary copper
  • liver biopsy
  • MRI of the brain as it can deposit on basal ganglia
85
Q

Where does copper deposition occur in wilsons disease

A

Liver and basal ganglia

86
Q

What are kayser-fleischer rings in wilsons disease

A

copper deposition in the cornea

87
Q

What is wilsons disease associated with

A

haemolytic anaemia

88
Q

How do you treat wilsons disease

A
  • Penicillamine – chelates copper - 1st line
  • Trientine hydrochloride – alternative chelating agent
  • liver transplantation
89
Q

What are the risk factors for hepatocellular carcinoma

A
  • Cirrhosis is the main risk factor

- HBV, HCV, Haemochromatosis

90
Q

How do you screen for hepatocellular carcinoma

A
  • ultrasound every 6 to 12 months

- AFP marker

91
Q

How do you diagnose hepatoceullar carcinoma

A
  • CT triple phase

- MRI

92
Q

What is the treatment for HCC

A

curative

  • surgical resection
  • liver transplantation
  • radiofrequency ablation

Palliative

  • transcatheter arterial chemoembolisation (TACE)
  • Radioembolisation (SIRT)
  • RFA
  • Sorafenib
93
Q

What is fulminant hepatic failure

A
  • A clinical syndrome resulting from massive necrosis of liver cells leading to severe impairment of liver function
94
Q

What drugs can cause liver failure

A
  • paracetamol
  • HAART
  • amiodarone
  • NSAIDs
  • chlorpromazine
  • halothane
  • oestrogen and anabolic steroids
  • statins
  • trimethoprime
  • isoniazid
  • ketoconazole
  • methotrexate
  • sodium valproate
95
Q

What are the signs of acute liver disease

A
  • may be few apart from jaundice and hepatomegaly
  • pale stools and dark urine in cholestatic phase
  • spider naevi and palmar erythema usually indicate chronic disease but can also occur in severe acute disease
96
Q

What does chronic compensated liver failure look like in the skin

A
  • Spider naevi
  • slate-grey appearance of the skin - in haemochromatosis
  • palmar erythema - due to hyper dynamic circulation
  • dupytren’s contracture - in alcoholic cirrhosis
  • Xanthomas - cholesterol deposits seen in the palmar creases or above the eyes in PBC
  • clubbing - occasionally occurs
  • leukonychia - white nails with lunula demarcated form hypoalbuminaemia
  • Terry’s nails - white proximally but distal 1/3 reddened by telangiectasis
97
Q

What does chronic compensated liver failure look like on the abdomen

A
  • hepatomegaly followed by small liver

- splenomegaly occurs with portal hypertension

98
Q

What does chronic compensated liver failure look like in terms of endocrine function in males

A
  • gynaecomastia - occasionally unilateral

- testicular atrophy

99
Q

What is spider naevi

A
  • telangiectases that consist of a central arteriole with radiating small vessels found in the distribution of the SVC, more than 5 are diagnostic (may also occur in pregnancy)
100
Q

How does hepatic encephalopathy develop

A

As the liver fails, nitrogenous waste (ammonia) builds up in the circulation and passes to the brain, where astrocytes clear it (by processes involving the conversion of glutamate to glutamine)
This excess glutamine causes an osmotic imbalance and shift of fluid into these cells – hence cerebral oedema

101
Q

describe the four stages of hepatic encephalopathy

A

I

  • altered mood/behaviour
  • sleep disturbance
  • dyspraxia
  • poor arithmetic
  • no liver failure

II

  • increasing drowsiness
  • confusion
  • slurred speech
  • inappropriate behaviour/personality change
  • +- liver flap

III

  • incoherent
  • restless
  • stupor
  • Liver flap

IV
- coma

102
Q

What is hepatorenal syndrome

A
  • cirrhosis + renal failure + ascites

- abnormal haemodynamics cause splanchnic and systemic vasodilation but renal vasoconstriction

103
Q

describe hepatorenal syndrome 1 and how you would treat it

A
  • Rapidly progressive deterioration in circulatory and renal function (median survival <2wks), often triggered by other deteriorating pathologies
  • Terlipressin resists hypovolaemia
  • Haemodialysis may be needed
104
Q

describe hepatorenal syndrome 2 and how you would treat it

A
  • more steady deterioration (survival - 6 months)

- trans jugular intraheaptic porto-systemic stent shunting may be required (TIPS)

105
Q

How do you treat hepatorenal syndrome

A
  • liver transplant may be required

- after 8-12 week of pre-transplant dialysis some may be considered for combined liver-kidney transplantation

106
Q

what should you be aware of in liver failure treatment

A
  • sepsis
  • hypoglycaemia
  • GI bleeds/varices
  • encephalopathy
107
Q

What is the management of liver failure

A
  • Nurse with a 20° head-up tilt in ITU. Protect the airway with intubation and insert NG tube to avoid aspiration and remove any blood from the stomach.
  • Insert urinary and central venous catheters to help assess fluid status.
  • Monitor T°, RR, HR, BP, pupils, urine output hourly. Daily weights.
  • Check FBC, U&E, LFT, INR.
  • 10% glucose IV 1L/12h to avoid hypoglycaemia. Blood glucose every 1-4h.
  • Treat the cause if known (eg GI bleed, sepsis, paracetamol poisoning).
  • If malnourished, get dietary help: good nutrition can decrease mortality. Give thiamine and folate supplements.
  • Treat seizures with phenytoin.
  • Haemofiltration and haemodialysis, if hepatorenal syndrome (HRS) develops.
  • Try to avoid sedatives and other drugs with hepatic metabolism.
  • Consider PPI as prophylaxis against stress ulceration, eg omeprazole 40mg/d IV/PO.
  • Liaise early with nearest transplant centre regarding appropriateness.
108
Q

What complications do you experience in liver failure

A
  • cerebral oedema
  • ascites
  • bleeding
  • increased risk of infection
  • hypoglycaemia
  • enecaphlopathy
109
Q

how do you treat cerebral oedema

A
  • 20% mannitol IV
  • hyperventilate
  • On ITU
110
Q

How do you treat ascites

A
  • restrict fluid
  • low salt diet
  • weight daily
  • diuretics
111
Q

How do you treat bleeding

A
  • vitamin K 10mg/d IV for 3 days
  • platelets
  • FFP + blood as needed +- endoscopy
112
Q

what do you do if blood glucose falls

A
  • if <2mmol/L or symptomatic give 50ml of 50% glucose IV

- check often

113
Q

How do you treat encephalopathy

A
  • Avoid sedatives
  • 20° head-up tilt in ITU
  • Correct electrolytes
  • Lactulose 30-50mL/8h (aim for 2-4 soft stools/d) – catabolised by colonic flora to short-chain fatty acids which decreased colonic pH and trap NH3 in the colon as NH4+
  • Rifaximin 550mg/12h – non-absorbable oral Abx that decreases numbers of nitrogen-forming gut bacteria
114
Q

what are the risk factors in progression for NAFLD

A
  • older age
  • obesity
  • diabetes
  • NASH
115
Q

What is the treatment for NAFLD

A
  • control risk factors
  • address CV risk
  • avoid alcohol
  • no drug is proven benefit although vitamin E may improve histology in fibrosis (e.g. 400IU/d - higher doses are associated with excess mortality)
116
Q

what is the follow up for NAFLD

A
  • monitor for complications - NASH, Cirrhosis, DM

- if cirrhotic - screen for HCC with Ultrasound and AFP twice a year

117
Q

How many tablets of paracetamol can be fatal in an adult

A

12g = 24 tablets or 150mg/kg in adults may be fatal

118
Q

What are the signs and symptoms of paracetamol toxicity

A
  • non initially
  • vomiting
  • RUQ pain
  • jaundice and encephalopathy from liver damage
  • AKI
119
Q

What is the management of paracetamol toxicity

A
  • Glucose, U&E, LFTs, INR, ABG, FBC, bicarbonate, blood paracetamol level at 4 hour post-ingestion
  • if less than 10-12 hours since the overdose and the patient is not vomitng and plasma paracetamol is above the line on the graph start acetylcysteine
  • if >8-24 hours and suspicion of large overdose (>7.5g) start acetylcystiene stopping it if the level is below the treatment line and INR/ALT is normal

ongoing management

  • next day to INR, U&E, LFT, if INR is rising continue acetylcysteine until <1.4
  • Consider referral to specialist liver unit if continued deterioration
120
Q

How is acetylcysteine given

A
  • given via IVI: 150mg/kg glucose over 15-60 minutes
  • then 50mg/kg in 500mL of 5% glucose over 4 hour
  • then 100mg/kg/16hour in 1L of 5% glucose
121
Q

What is a common side effect of acetylcysteine

A

Rash - treat with chlorphenamine

122
Q

What drugs should you avoid in liver failure

A

Drugs that cause constipation - this increases the risk of enceaphlopathy

warfarin effects are increased

Hepatoxtic drugs

  • Paracetamol
  • methotrexate
  • isoniazid
  • azathioprine
  • oestrogen
  • 6-mercaptopurine
  • salicylates
  • tetra cycles
123
Q

What is the presentation of Wilsons disease

A
  • Kayser-fleischer rings – copper deposition in the cornea
  • Speech, behavioural and psychiatric problems
  • Chorea, dementia and parkinsonism, personality change, memory loss
  • Renal tubular acidosis
  • Haemolysis
124
Q

what is the blood copper diagnosis of Wilsons disease

A
  • Reduced serum caeruloplasmin
  • Reduced total serum copper
  • Free serum copper is increased
  • Increased 24 hour urinary copper excretion
125
Q

What are the symptoms of hepatocellular carcinoma

A
  • Liver cirrhosis or failure
  • Jaundice, ascites, RUQ pain, hepatomegaly, pruritus, splenomegaly, fever
  • Raised AFP

Year 3 - Met3a (43 decks)

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