Alcoholic liver disease Flashcards

(41 cards)

1
Q

What is alcoholic liver disease

A

liver damage caused by excess alcohol intake

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Epedemiology of alcoholic liver diease

A
  • M>F prevalence
  • ArLD is the foremost health risk in developing countries and ranks third in developed countries.
  • The mortality related to liver cirrhosis increases with age.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

stepwise progression of alcoholic liver disease

A

1 alcohol related fatty liver ( steatosis)
2 alcoholic hepatitis
3 cirrhosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

2 main pathways of alcohol metabolisation

A

alcohol dehydrogenase and cytochrome P450 2E1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Alcohol dehydrogenase pathway

A

alcohol dehydrogenase (hepatic enzyme) > converts alochol to acetaldehyde > metabolised to acetate by acetaldehyde dehydrogenase

Both enzymes reduce NAD to NADH > inhibits gluconeogenesis and increase fatty acid oxidation which promotes fatty infiltration liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

cytochrome P450 2E1 pathway

A

generates free radicals through the oxidation of NADPH to NADP. Chronic alcohol use upregulates cytochrome P450 2E1 and produces more free radicals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does chronic alcohol exposure also do

A

activate hepatic macrophages> produce (TNF)-alpha and induce the production of reactive oxygen species in the mitochondria.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Alcoholic hepatitis pathophysiology

A

acetaldehyde formed from metabolism of alcohol can react with molecules in the liver, forming acetaldehyde adducts

Recognised as foreign > attacked by immune system > inflammation + hepatitis

Leads to activation of stellate cells which causes deposition of extracellular matrix proteins, generation of portal hypertension and fibrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Risk factors of ALD

A

hep c
chronic alcohol
obesity
age
female

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

uk recommended alcohol consumption

A

14 units a week
spread evenly over 3 or more days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

describe the CAGE questionnare

A

C – CUT DOWN? Ever thought you should?
A – ANNOYED? Do you get annoyed at others commenting on your drinking?
G – GUILTY? Ever feel guilty about drinking?
E – EYE OPENER? Ever drink in the morning to help your hangover/nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

1st line investigations for ALD

A
  • serum AST ; ALT
  • serum alkaline phosphotase
  • serum bilirubin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Other investigations for ALD

A
  • Full blood count
  • Urea & electrolytes
  • Liver function tests
  • C-reactive protein
  • Liver ultrasound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

complications 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

signs of liver disease

A

Jaundice
Hepatomegaly
hand signs
ascites
spider naevi
confusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What hand signs may occur in ALLD

A

-palmar erythema
- dupuytrens contracture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What symptoms may be present in alcoholic liver disease

A
  • malaise
  • weakness
  • weight loss
  • abdo pain
  • pruritus
18
Q

What would LFT’s SHOW IN ALD

A
  • raised bilirubin
  • AST> ALT ratio
  • low albumin
19
Q

what would bloods show for ALD

A

elevated bilirubin
decrease in albumin
increase PT
increase ggt

20
Q

what would fbc show for ALD

A

-Macrocytic non megaloblastic anaemia
- thrombocytopenia

21
Q

general management of ALD

A
  • Stop drinking alcohol permanently
  • Consider a detoxication regime
  • Nutritional support with vitamins
  • Steroids improve short term outcomes
  • Treat complications of cirrhosis
  • Referral for liver transplant in severe disease however they must abstain from alcohol for 3 months prior to referral
  • IV Thiamine to prevent Wernicke-Korsakoff encephalopathy
22
Q

timeline of alcohol withdrawal symptoms

A

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

23
Q

how is thiamine deficiency linked to alcohol

A

-thiamine is poorly absorbed in the presence of alcohol
-alcoholics tend to have poor diets and rely on the alcohol for their calories

24
Q

what can thiamine deficiency cause

A

wernickes encephalopathy
korsakoffs syndrome

25
Features of Wernicke’s encephalopathy
- Confusion - Oculomotor disturbances (disturbances of eye movements) - Ataxia (difficulties with coordinated movements
26
Features of Korsakoffs syndrome
Memory impairment (retrograde and anterograde) Behavioural changes
27
what is non alcoholic fatty liver disease
It is characterised by fat deposited in liver cells. These fat deposits can interfere with the functioning of the liver cells
28
stage of NAFLD
1-Non-alcoholic Fatty Liver Disease 2-Non-Alcoholic Steatohepatitis (NASH) 3-Fibrosis 4-Cirrhosis
29
Epidemiology of NAFLD
- Commonest liver disorder in industrialised western countries - Affects around 3/4's of all obese individuals
30
Aetiology of NAFL
- Obesity - Hypertension - Diabetes - Hypertriglyceridemia - Hyperlipidemia
31
How does insulin play a role in NAFLD
- insulin receptors are less responsive to insulin so - excess fat is deposited in liver- less secretion of FA in blood stream - steatosis occurs (increased synthesis of FFA from blood)
32
What happens as fat droplets form within hepatocytes
- hepatocytes to swell up with fat and push nuclei to edge of cell. - Liver appears large, soft, yellow and greasy. - Unsat FA vulnerable to ROS > form FA radicals which can react with non-radicals like O2
33
What does the reaction of radicals and non radicals cause?
This ultimately damages lipid membrane, leading to mitochondrial dysfunction and cell death. This generates inflammation. Inflammation + steatosis = steatohepatitis.
34
S + S of NAFLD
Sometimes symptoms are vague: - Fatigue - Malaise Sufficient damage presents with: - Hepatomegaly - Pain in RUQ - Jaundice - Ascites
35
RISK FACTORS FOR nafld
Obesity Poor diet and low activity levels Type 2 diabetes High cholesterol Middle age onwards Smoking High blood pressure
36
Investigation in Non-Alcoholic Fatty Liver Disease
**Serum AST and ALT:** Increase in ALT and sometimes AST. (Different to alcoholic liver disease where AST>ALT) **LFT:** raised bilirubin, ALP, GGT, prothrombin time, low serum albumin **FBC:** anemia and thrombocytopenia due to hypersplenism **Imaging:** US, CT, MRI to look for fatty infiltrates **Biopsy:** used to diagnose and assess severity - Differential diagnosis
37
what would liver US show for NAFLD
WILL show the diagnosis of hepatic steatosis
38
DDs of NAFLD
- Alcoholic liver disease - Autoimmune hepatitis - Hepatitis B and C - Hemochromatosis - PSC - PBC
39
conservative management of NAFLD
- Weight loss , approx 0.5- 1.0 kg a week through diet and exercise - limit alcohol intake - optimise blood pressure
40
medical management of NAFLD
- orlisat - enteric lipase inhibitor which prevents absorption of fat - metformin - to improve insulin sensitivity - antihyperlipidaemics - for patients with hyperlipidaemia
41
Complications of NAFLD
- Ascites - Varices and variceal haemorrhage - Encephalopathy - Hepatocellular carcinoma