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Year 2 > Alcoholic Liver Disease > Flashcards

Alcoholic Liver Disease Flashcards

1
Q

How does Ethanol metabolism effect NADH/NAD ratio

A

Increases it

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2
Q

How does increased ethanol metabolism effect fatty acid synthesis in the liver

A

Increases it

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3
Q

How does ethanol effect fatty acid oxidation in the liver

A

Decreases it

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4
Q

What is the consequence of increased fatty acid synthesis and decreased oxidation

A

Hepatic accumulation of fatty acids which are esterified to glyceries

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5
Q

How does changed in oxidation-reduction effect carbs and protein metabolism

A

Impairs them - causes centrilobular necrosis od the hepatic acinus (typical of alcohol damage)

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6
Q

What do kupffer cells release in reaction to ethanol accumulation

A

TNF-alpha

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7
Q

Result of TNF-alpha release

A

Release of ROS leading to tissue injury and fibrosis

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8
Q

How is acetaldehyde formed

A

By the oxidation of ethanol and its effect on hepatic proteins could be a factor in producing liver cell damage

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9
Q

How does alcohol effect drugs

A

Enhance the effects of their toxic metabolites

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10
Q

Main causes of alcoholic liver disease

A
  1. Abuse
  2. Genetic predisposition
  3. Immunological mechanisms
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11
Q

How does fatty liver occur

A
  1. Metabolism of alcohol produces fat in liver
  2. No liver cell DAMAGE
  3. Sometimes, collagen lays down around central hepatic veins + this can progress to cirrhosis without a preceding hepatitis
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12
Q

How does alcohol effect stellate cells

A

Transforms them to myofibroblastic cells

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13
Q

Can fat disspear on stopping alcohol

A

Yes

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14
Q

How does alcoholic hepatitis occur

A

Infiltration of polymorphonuclear leucocytes and hepatocyte necrosis

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15
Q

Features of alcoholic hepatitis

A

Dense cytoplasmic inclusions - Mallory bodies

Giant mitochondria

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16
Q

Characteristics of alcoholic cirrhosis

A
  1. Micronodular Types
  2. Fatty change seen
  3. Evidence of pre-existing alcoholic hepatitis
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17
Q

Clinical presentation of Fatty Liver

A
  1. Asymptomatic
  2. Vague abdominal symptoms of nausea, vomiting, diarrhoea
  3. Hepatomegaly
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18
Q

Clinical presentation of alcoholic hepatitis

A
  1. Mild jaundice
  2. Signs of chronic liver disease (ascites, bruising, clubbing)
  3. Abdominal pain with high fever
  4. Deep jaundice
  5. ankle oedema
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19
Q

Diagnosis of fatty liver

A
  1. ELEVATED MCV
  2. RAISED Alt and AST
  3. Ultrasound demonstrates fatty infiltration as well as liver histology
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20
Q

Diagnosis of alcoholic hepatitis

A
  1. Leucocytosis
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21
Q

What would blood tests show in alcoholic hepatitis

A

Serum bilirubin
Serum AST and Alt
Serum alkalin phosphate

PTT

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22
Q

How to treat alcoholic liver disease

A
  1. STOP DRINKING
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23
Q

How to treat withdrawal symptoms from not taking alcohol

A

Diazepam

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24
Q

How do we prevent Wernicke-Korsakoff encephalopathy associated with alcoholic liver disease

A

IV THIAMINE

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25
Q

What is Wernicke-Korsakoff encephalopathy

A

Presents with ataxia
Confusion
Nystagmus

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26
Q

When do people suffer from Wernicke-Korsakoff

A

During withdrawal

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27
Q

When does Wernicke-Korsakoff occur

A

6-24 hours after last drink (lasts up to a week)

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28
Q

How do we alter diet for those with alcoholic liver disease

A

High in vitamins and proteins

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29
Q

Ho wis fatty liver disease treated

A

Stopping alcohol

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30
Q

How is alcoholic hepatitis treated

A
  1. Nutrition maintained by enteral feeding + supplements
  2. Steroids
  3. Infections should be treated
  4. Stop drinking alcohol for life
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31
Q

How are infections in alcoholic hepatitis treated

A

anti-fungal prophylaxis

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32
Q

How is alcoholic cirrhosis treated

A

Reduce salt intake
Stop drinking for life
Avoid aspirin and NSAIDS
Liver transplant

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33
Q

When should drugs be considered as a cause of live injury

A

When abnormal liver biochemical tests are found

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34
Q

What four ways can drugs cause liver damage

A
  1. Disruption of intracellular Ca homeostasis
  2. Disruption of bile canalicular transport mechanisms
  3. Induction of apoptosis
  4. Inhibition of mitochondrial function
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35
Q

How is inhibiting mitochondria function dangerous

A

Prevents fatty acid metabolism and accumulation of both lactate and reaction oxygen species

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36
Q

What is the most common cause of acute liver failure in the USA

A

Drug hepatotoxicity

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37
Q

When do most drug reactions occur

A

Within 3 months of starting the drug

‘not so much what drug bu what drug you started recently’

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38
Q

When is onset of drug hepatotoxicity seen

A

1-12 weeks of starting

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39
Q

Main causes of drug haeptotoxicity

A
  1. Antibiotics (Augmentin, Flucloxacillin, TB drugs and Erythromycin)
  2. CNS
  3. Immunosuppressants
  4. Analgesics
  5. GI Drugs
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40
Q

Name two CNS drugs that can induce liver damage

A

Chlorpromazine

Carbamazepine

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41
Q

Name an analgesic that causes liver injury

A

DICLOFENAC

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42
Q

What drugs do not induce liver injury

A
  1. ASPIRIN
  2. NSAIDS (except diclofenac)
  3. Beta0blockers
  4. ACE
  5. Thiazides
  6. Calcium channel blockers
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43
Q

How is drug-induced liver injury treated

A

Stops within 3 months of stopping the drug

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44
Q

How is paracetamol metabolised

A

Phase II reaction: conjugated with glucuronic acid or sulphate

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45
Q

What happens to paracetamol if glucuronic acid and sulphate stores are low

A

Phase I metabolism via oxidation to produce NAPQI then conjugated with glutathione and excreted

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46
Q

How does paracetamol poisoning occur

A

Liver GLUTATHIONE becomes depleted eventually so NAPQI can’t be conjugated

47
Q

Clinical features of paracetamol hepatotoxicity

A
  1. ANorexia
  2. Nausea
  3. Vomiting
  4. Upper right quadrant pain
  5. Jaundice and encephalopathy due to liver damager
48
Q

Is paracetamol-induced liver injury detectable on liver biochemistry

A

Not until 18 hours after ingestion

49
Q

How long do patients initially remain asymptomatic for following overdose on paracetamol

A

24 hours

50
Q

When does liver damage reach its peak

A

Raised ALT
PTT

72-96 hours after ingestion

51
Q

What is encephalopathy

A

impaired functioning of the brain

52
Q

What happens if paracetamol induced liver injury is not treated

A

Hepatic failure (fulminant)

53
Q

Why is there acute kidney injury from paracetamol-induced liver injury

A

Acute tubular necrosis

54
Q

Blood tests for paracetamol-induced liver damage

A
  1. Metabolic acidosis
  2. Hypoglycaemia (overdose inhibits glucose production)
  3. Prolonged PTT
  4. Raised creatinine
55
Q

How is paracetamol-induced liver damage treated

A

Gastric decontamination
Replenish cellular glutathione stores
Treat rash

56
Q

How is gastric decontamination treated

A

ACTIVATED CHARCOAL

57
Q

How do we replenish cellular glutathione stores

A

IV N-ACETYLCYSTEINE

58
Q

How is rash treated

A

CHLORPHENAMINE

59
Q

Where is aspirin metabolised

A

Liver

60
Q

How is aspirin metabolised

A

To salicylic acid by esterase’s -> salicylic acid and sailcyl phenolic glururonide

61
Q

What happens in an overdose

A

Metabolic pathway is oversaturated so kidneys compensated by increasing renal excretion of aspirin (PATHWAY IS EXTREMELY SENSITIVE to urinary pH)

62
Q

How does overdose of aspirin effect respiratory centre

A

Stimulates it, increasing depth and rate of respiration = repisratoy alkalosis as you excrete more acidic CO2

63
Q

Compensatory mechanisms for respiratory alkalis

A

Renal excretion of bicarbonate and potassium = metabolic acidosis

64
Q

What processes does aspirin interfere with

A

Carbs, fat and protein metabolism
Disrupt oxidative phosphorylation
Increased conc. of lactates, pyruvate and ketones (metabolic acidosis)

65
Q

Clinical features of aspiring poisoning

A
  1. Patients with respiratory alkalosis due to stimulation of salicylic acid on the central respiratory centre and develop metabolic acidosis to compensate
  2. Hyper- or hypoglycaemia
  3. HYPERVENTILATION and TACHYPNOEA (this causes respiratory alkalosis)
  4. Sweating, vomiting, dehydration, epigastric pain, tinnitus and deafness
  5. Rarely in severe poisoning there may be coma and convulsion
66
Q

Treatment of aspirin

A
  1. Fluid + electrolyte replacement with special attention (mild cases)
  2. Urine alkalisation (enhance renal elimination of aspirin)
  3. Haemodialysis (treatment of choice for poisoned patients)
67
Q

How is metabolic acidosis with apisirn poisoning treated

A

IV NA BICARBONATE

68
Q

What is Hereditary HAEMOCHROMATOSIS

A

Inherited disorder of iron metabolism where there is increased intestinal iron absorption leads to iron deposition in joints, liver, heart, pancreas, adrenals and skin

69
Q

What does hereditary haemochromatosis lead to

A

Fibrosis and functional organ failure

70
Q

What people does this disorder commonly effect

A

Caucasians Male

71
Q

Why is hereditary haemochromatosis not common in females

A

Since menstrual blood loss is protective

72
Q

Main cause of hereditary haemochromatosis

A

HFE gene mutation on chromosome 6 - AUTOSOMA RECESSIVE

High intake of iron and chelating agents

Alcoholics

73
Q

Is autosomal dominant mutation common

A

No

74
Q

Risk factors for hereditary haemochromatosis

A

Family history

Alcoholic

75
Q

Pathophysiology for hereditary haemochromatosis

A
  1. HFE gene protein interacts with transferrin R1
  2. Hepcidin is increases in iron deficiency states and decreases in iron overload
  3. Expression of hepcidin is decreased in hereditary haemochromatosis and causes iron overload
  4. Excess iron is taken up by the liver
  5. Fibrosis
  6. Iron content is increased in th liver and pancreas
  7. Cirrhosis
76
Q

What age group is hereditary haemochromatosis common in

A

50s

77
Q

Early onset of hereditary haemochromatosis

A

Tiredness and arthralgia

78
Q

How does hereditary haemochromatosis effect endocrine function

A

Hypogonadism (less testosterone and oestrogen)

Pituitary dysfunction

79
Q

Late sunsets of hereditary haemochromatosis

A 
Slate-grey pigmentation 
Chronic liver disease
Hepatomegaly 
Cirrhosis
Dilates Cardiomyopathy
Osteoporosis
Cardiac Manifestations (e.g. heart failure, arrhythmias)
80
Q

Symptoms in hereditary haemochromatosis due to iron overload

A
  1. Bronze skin pigmentation
  2. Hepatomegaly
  3. Diabetes mellitus
81
Q

How is hereditary haemochromatosis diagnosed (homozygotes)

A
  1. Raised resume iron
  2. Raised scrim ferritin
  3. Normal liver biochemistry
82
Q

hereditary haemochromatosis diagnosed (heterozygotes)

A
  1. Normal biochemical tests

2. Raised serum iron transferring saturation or serum ferritin

83
Q

How is MRI good in hereditary haemochromatosis

A

Shows iron overload

84
Q

How does a liver biopsy help in hereditary haemochromatosis

A

Extent of tissue damage

85
Q

How does ECHO and ECG help in hereditary haemochromatosis

A

Cardiomyopathy suspected

86
Q

How is hereditary haemochromatosis treated

A 
Venesection
Treat Diabetes
3. Testosterone replacement 
4. Diet low in iron 
5. Avoid druit/fruit juice
6. Screening all first-degree relatives
87
Q

Benefits of venesection

A

Prolongs life and reverses tissue damage

88
Q

How often do we do venesection

A

3-4 times a year

89
Q

How is hereditary haemochromatosis managed

A

Monitor serum iron and ferritin during venesection

90
Q

What is done when patients can’t tolerate venesection

A

DESFERRIOXAMINE is given (Chelation therapy - preventing absorption of iron by forming bonds with a single metal ion)

91
Q

What is Wilson’s Disease

A

Inherited disorder where too much copper is in the liver (not enough excretion) and CNS

92
Q

What kind of genetic inheritance is wilson’s disease

A

AUTOSOMAL RECESSIVE on chromosome 13 resulting in a molecular defect within a copper-transporting ATPase

93
Q

In which population is Wilson’s disease common

A

Countries where marrying first degree relatives is common

94
Q

Where is dietary copper commonly absorbed

A

Stomach

Small upper intestines

95
Q

Where is copper transported to

A

Liver bound to albumin

96
Q

What happens to copper in liver

A

Incorporated into Caeruloplasmin and secreted into the blood

97
Q

Is Liver histology for Wilson’s disease diagnostic

A

No

98
Q

Appearance of inner body in Wilson’s disease

A

Basal ganglia are damaged and show cavitation, kidney shows tubular degeneration

Erosions seen in bone

99
Q

Clinical presentation of Wilson’s disease

A
  1. Hepatitis/Cirrhosis/Fulminant liver failure
  2. Young adults have CNS problems (dementia, tremors, dysphagia)
  3. educed memory
    4, Liver disease (acute hepatitis to chronic to cirrhosis)
  4. Kayser-Fleischer ring
100
Q

What is Kayser-Fleischer ring caused by

A

Copper deposition in corners results in greenish-brown pigments at the corneoscleral junction

101
Q

Blood tests in Wilson’s disease

A
  1. Serum copper and caeruloplasmin are reduced
102
Q

What does liver biopsy show in wilson’s disease

A

Increased hepatic copper, hepatitis and cirrhosis

Haemolysis and anaemia

103
Q

What will an MRI show for Wilson’s disease

A

Basal ganglia and cerebella degeneration

104
Q

How is Wilson’s Disease treated

A
  1. Avoid foods high in copper

2. Lifelong chelating agent (PENICILLAMINE)

105
Q

Side-effects of using lifelong chelating agents

A
  1. Skin rashes
  2. Fall in WBC
  3. Haematuria
  4. Renal Damage
106
Q

Symptoms of alcoholic hepatitis

A
  1. Fatigue
  2. Ascites
  3. Jaundice
  4. Hepatic encephalopathy (Wernicke-Korsakoff syndrome)
  5. Delirium tremens
107
Q

What is delirium tremens

A

SHAKING
Irregular heart rate
Sweating
Hallucination

108
Q

Histopathology seen in alcoholic hepatitis

A
  1. Mallory’s hyaline body
  2. Hepatocytes swell up with excess fat, water and protein
  3. Inflammation due to neutrophilic invasion (necrotic changes causes this)
  4. MEGAMITOCHONDRIA
109
Q

What causes Wernicke’s encephalopathy

A
  1. Thiamine deficiency
  2. Poor diet
  3. Poor intake of vitamins
  4. Gastritis
110
Q

How is Wernicke’s encephalopathy treated

A
  1. PABRINEX + Vit B/Thiamine
111
Q

How is alcoholic withdrawal relapse prevented

A
  1. ACAMPROSATE
  2. DISULFIRAM
  3. NALMEFINE
112
Q

Pharmacology of DISULFIRAM

A
  1. directs oxidative metabolism of alcohol:

Causes build up of acetaldehyde

113
Q

Side-Effects of DISULIFRAM

A
  1. Flushing of skin
  2. Tachycardia
  3. SOB
  4. Nausea
  5. VOmiting
114
Q

What is NALMEFINE

A
  1. Opioid receptor antagonist
  2. Modifies activity at receptor sites linked to reward centres (acts on dopamine)
  3. Reduced feeling of reward

Year 2 (155 decks)

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