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Alcoholic Liver Disease Flashcards

(114 cards)

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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
What is Wernicke-Korsakoff encephalopathy
Presents with ataxia Confusion Nystagmus
26
When do people suffer from Wernicke-Korsakoff
During withdrawal
27
When does Wernicke-Korsakoff occur
6-24 hours after last drink (lasts up to a week)
28
How do we alter diet for those with alcoholic liver disease
High in vitamins and proteins
29
Ho wis fatty liver disease treated
Stopping alcohol
30
How is alcoholic hepatitis treated
1. Nutrition maintained by enteral feeding + supplements 2. Steroids 3. Infections should be treated 4. Stop drinking alcohol for life
31
How are infections in alcoholic hepatitis treated
anti-fungal prophylaxis
32
How is alcoholic cirrhosis treated
Reduce salt intake Stop drinking for life Avoid aspirin and NSAIDS Liver transplant
33
When should drugs be considered as a cause of live injury
When abnormal liver biochemical tests are found
34
What four ways can drugs cause liver damage
1. Disruption of intracellular Ca homeostasis 2. Disruption of bile canalicular transport mechanisms 3. Induction of apoptosis 4. Inhibition of mitochondrial function
35
How is inhibiting mitochondria function dangerous
Prevents fatty acid metabolism and accumulation of both lactate and reaction oxygen species
36
What is the most common cause of acute liver failure in the USA
Drug hepatotoxicity
37
When do most drug reactions occur
Within 3 months of starting the drug 'not so much what drug bu what drug you started recently'
38
When is onset of drug hepatotoxicity seen
1-12 weeks of starting
39
Main causes of drug haeptotoxicity
1. Antibiotics (Augmentin, Flucloxacillin, TB drugs and Erythromycin) 2. CNS 3. Immunosuppressants 4. Analgesics 5. GI Drugs
40
Name two CNS drugs that can induce liver damage
Chlorpromazine | Carbamazepine
41
Name an analgesic that causes liver injury
DICLOFENAC
42
What drugs do not induce liver injury
1. ASPIRIN 2. NSAIDS (except diclofenac) 3. Beta0blockers 4. ACE 5. Thiazides 6. Calcium channel blockers
43
How is drug-induced liver injury treated
Stops within 3 months of stopping the drug
44
How is paracetamol metabolised
Phase II reaction: conjugated with glucuronic acid or sulphate
45
What happens to paracetamol if glucuronic acid and sulphate stores are low
Phase I metabolism via oxidation to produce NAPQI then conjugated with glutathione and excreted
46
How does paracetamol poisoning occur
Liver GLUTATHIONE becomes depleted eventually so NAPQI can't be conjugated
47
Clinical features of paracetamol hepatotoxicity
1. ANorexia 2. Nausea 3. Vomiting 4. Upper right quadrant pain 5. Jaundice and encephalopathy due to liver damager
48
Is paracetamol-induced liver injury detectable on liver biochemistry
Not until 18 hours after ingestion
49
How long do patients initially remain asymptomatic for following overdose on paracetamol
24 hours
50
When does liver damage reach its peak
Raised ALT PTT 72-96 hours after ingestion
51
What is encephalopathy
impaired functioning of the brain
52
What happens if paracetamol induced liver injury is not treated
Hepatic failure (fulminant)
53
Why is there acute kidney injury from paracetamol-induced liver injury
Acute tubular necrosis
54
Blood tests for paracetamol-induced liver damage
1. Metabolic acidosis 2. Hypoglycaemia (overdose inhibits glucose production) 3. Prolonged PTT 4. Raised creatinine
55
How is paracetamol-induced liver damage treated
Gastric decontamination Replenish cellular glutathione stores Treat rash
56
How is gastric decontamination treated
ACTIVATED CHARCOAL
57
How do we replenish cellular glutathione stores
IV N-ACETYLCYSTEINE
58
How is rash treated
CHLORPHENAMINE
59
Where is aspirin metabolised
Liver
60
How is aspirin metabolised
To salicylic acid by esterase's -> salicylic acid and sailcyl phenolic glururonide
61
What happens in an overdose
Metabolic pathway is oversaturated so kidneys compensated by increasing renal excretion of aspirin (PATHWAY IS EXTREMELY SENSITIVE to urinary pH)
62
How does overdose of aspirin effect respiratory centre
Stimulates it, increasing depth and rate of respiration = repisratoy alkalosis as you excrete more acidic CO2
63
Compensatory mechanisms for respiratory alkalis
Renal excretion of bicarbonate and potassium = metabolic acidosis
64
What processes does aspirin interfere with
Carbs, fat and protein metabolism Disrupt oxidative phosphorylation Increased conc. of lactates, pyruvate and ketones (metabolic acidosis)
65
Clinical features of aspiring poisoning
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 1. HYPERVENTILATION and TACHYPNOEA (this causes respiratory alkalosis) 2. Sweating, vomiting, dehydration, epigastric pain, tinnitus and deafness 3. Rarely in severe poisoning there may be coma and convulsion
66
Treatment of aspirin
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
How is metabolic acidosis with apisirn poisoning treated
IV NA BICARBONATE
68
What is Hereditary HAEMOCHROMATOSIS
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
What does hereditary haemochromatosis lead to
Fibrosis and functional organ failure
70
What people does this disorder commonly effect
Caucasians Male
71
Why is hereditary haemochromatosis not common in females
Since menstrual blood loss is protective
72
Main cause of hereditary haemochromatosis
HFE gene mutation on chromosome 6 - AUTOSOMA RECESSIVE High intake of iron and chelating agents Alcoholics
73
Is autosomal dominant mutation common
No
74
Risk factors for hereditary haemochromatosis
Family history | Alcoholic
75
Pathophysiology for hereditary haemochromatosis
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
What age group is hereditary haemochromatosis common in
50s
77
Early onset of hereditary haemochromatosis
Tiredness and arthralgia
78
How does hereditary haemochromatosis effect endocrine function
Hypogonadism (less testosterone and oestrogen) Pituitary dysfunction
79
Late sunsets of hereditary haemochromatosis
``` Slate-grey pigmentation Chronic liver disease Hepatomegaly Cirrhosis Dilates Cardiomyopathy Osteoporosis Cardiac Manifestations (e.g. heart failure, arrhythmias) ```
80
Symptoms in hereditary haemochromatosis due to iron overload
1. Bronze skin pigmentation 2. Hepatomegaly 3. Diabetes mellitus
81
How is hereditary haemochromatosis diagnosed (homozygotes)
1. Raised resume iron 2. Raised scrim ferritin 3. Normal liver biochemistry
82
hereditary haemochromatosis diagnosed (heterozygotes)
1. Normal biochemical tests | 2. Raised serum iron transferring saturation or serum ferritin
83
How is MRI good in hereditary haemochromatosis
Shows iron overload
84
How does a liver biopsy help in hereditary haemochromatosis
Extent of tissue damage
85
How does ECHO and ECG help in hereditary haemochromatosis
Cardiomyopathy suspected
86
How is hereditary haemochromatosis treated
``` Venesection Treat Diabetes 3. Testosterone replacement 4. Diet low in iron 5. Avoid druit/fruit juice 6. Screening all first-degree relatives ```
87
Benefits of venesection
Prolongs life and reverses tissue damage
88
How often do we do venesection
3-4 times a year
89
How is hereditary haemochromatosis managed
Monitor serum iron and ferritin during venesection
90
What is done when patients can't tolerate venesection
DESFERRIOXAMINE is given (Chelation therapy - preventing absorption of iron by forming bonds with a single metal ion)
91
What is Wilson's Disease
Inherited disorder where too much copper is in the liver (not enough excretion) and CNS
92
What kind of genetic inheritance is wilson's disease
AUTOSOMAL RECESSIVE on chromosome 13 resulting in a molecular defect within a copper-transporting ATPase
93
In which population is Wilson's disease common
Countries where marrying first degree relatives is common
94
Where is dietary copper commonly absorbed
Stomach | Small upper intestines
95
Where is copper transported to
Liver bound to albumin
96
What happens to copper in liver
Incorporated into Caeruloplasmin and secreted into the blood
97
Is Liver histology for Wilson's disease diagnostic
No
98
Appearance of inner body in Wilson's disease
Basal ganglia are damaged and show cavitation, kidney shows tubular degeneration Erosions seen in bone
99
Clinical presentation of Wilson's disease
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) 5. Kayser-Fleischer ring
100
What is Kayser-Fleischer ring caused by
Copper deposition in corners results in greenish-brown pigments at the corneoscleral junction
101
Blood tests in Wilson's disease
1. Serum copper and caeruloplasmin are reduced
102
What does liver biopsy show in wilson's disease
Increased hepatic copper, hepatitis and cirrhosis Haemolysis and anaemia
103
What will an MRI show for Wilson's disease
Basal ganglia and cerebella degeneration
104
How is Wilson's Disease treated
1. Avoid foods high in copper | 2. Lifelong chelating agent (PENICILLAMINE)
105
Side-effects of using lifelong chelating agents
1. Skin rashes 2. Fall in WBC 3. Haematuria 4. Renal Damage
106
Symptoms of alcoholic hepatitis
1. Fatigue 2. Ascites 3. Jaundice 4. Hepatic encephalopathy (Wernicke-Korsakoff syndrome) 5. Delirium tremens
107
What is delirium tremens
SHAKING Irregular heart rate Sweating Hallucination
108
Histopathology seen in alcoholic hepatitis
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
What causes Wernicke's encephalopathy
1. Thiamine deficiency 2. Poor diet 3. Poor intake of vitamins 4. Gastritis
110
How is Wernicke's encephalopathy treated
1. PABRINEX + Vit B/Thiamine
111
How is alcoholic withdrawal relapse prevented
1. ACAMPROSATE 2. DISULFIRAM 3. NALMEFINE
112
Pharmacology of DISULFIRAM
1. directs oxidative metabolism of alcohol: Causes build up of acetaldehyde
113
Side-Effects of DISULIFRAM
1. Flushing of skin 2. Tachycardia 3. SOB 4. Nausea 5. VOmiting
114
What is NALMEFINE
1. Opioid receptor antagonist 2. Modifies activity at receptor sites linked to reward centres (acts on dopamine) 3. Reduced feeling of reward

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