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CDM Lina > Liver > Flashcards

Liver Flashcards

1
Q

What does the liver metabolise?

A
  • carbohydrates
  • protein
  • aldosterone
  • Insulin
  • bilirubin
  • steroid hormones

DRUGS !!!!!

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2
Q

List the 6 main synthetic functions of the liver?

A
  • proteins
  • clotting factors
  • fibrinogen
  • cholesterol
  • 25-OH of vitamin D
  • glucose from fat and protein
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3
Q

What are the 5 main functions of the liver?

A
  • Immunological (Kupffer cells)
  • Storage (fat soluble vitamins)
  • Glucose homeostasis
  • Clearance of drugs/bilirubin/toxins
  • Production of bile
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4
Q

What are the classes of Liver disease?

A

Can be:

  • Cholestatic
  • hepatocellular

They can overlap and both can lead to fibrosis and cirrhosis

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5
Q

What is cholestasis liver disease?

A
  • Disruption of bile ducts

Intrahepatic: biliary ductules

Extrahepatic: mechanical obstruction

Ultimately you get impaired biliary excretion and reduced absorption of fatty substances.

Accumulation of bile salts can lead to damage of hepatocytes.

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6
Q

What is hepatocellular disease?

A
  • Injury to hepatocytes
  • Fatty infiltration (steatosis)
  • Inflammation (hepatitis)
  • Necrosis
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7
Q

what is fibrosis and Cirrhosis?

A
  • Extensive hepatocyte damage (active deposition of collagen = formation of scar tissue = fibrosis)
  • Cirrhosis = scar tissue takes over most of the liver.
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8
Q

Acute vs. Chronic liver disease

A

Acute - onset of symptoms does not exceed 6 months.

Acute liver failure - hyperacute, acute or subacute, depending on time from jaundice to encephalopathy.

Chronic - persists for more than 6 months, permanent structural changes following long standing cell damage.

Compensated vs. Decompensated

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9
Q

What are the normal bilirubin levels? What’s it function?

A
  • Bilirubin (5-20 micromol/L)
  • Product of RBC breakdown
  • Attached to albumin
  • transformed into a water-soluble conjugate which is excreted via the bile into the intestine.

Jaundice when bilirubin > 50 micromol/L

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10
Q

Liver function test

Transaminase enzymes

A

AST (0-40 iu/L)

ALT (5-30 iu/L)

— Levels increase in viral hepatitis, alcohol related liver injury, drugs, sepsis

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11
Q

Liver function tests

ALP and y-GT

A

Alkaline phosphatase (30-120 iu/L)

y-Glutamyltransferase (5-55 iu/L) = increased by enzyme inducers e.g. alcohol

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12
Q

Other tests that can tell us about liver function

A
  • Albumin (35 - 50g/dL) = long half life (20-26 days)
  • PT (10-14 secs)/ INR = short half-life (2-3 days)

PT/INR increase in acute and chronic liver disease

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13
Q

What is the Child’s Pugh scoring system ? And what does it take into account ?

A

Used to assess the prognosis of chronic liver disease.

Takes into account:

Bilirubin 
Albumin 
PT/INR
Ascites 
Encephalopathy
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14
Q

What are the other investigations needed to assess liver function?

A 
Liver ultrasound 
CT scan 
ERCP and MRCP 
MRI 
Fibroscan 
Liver biopsy 
MELD

-Never take LFTs in isolation !

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15
Q

What is Jaundice? How does it occur ?

A

Pre-hepatic jaundice - the disruption occurs before the bilirubin has been transported from the blood to the liver (sickle cell anaemia)

Intra-hepatic - disruption occurs inside the liver (Gilbert’s syndrome and cirrhosis)

Post-hepatic - disruption prevents the bile from draining out of the gallbladder (gallstones or tumours)

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16
Q

What is ascites?

A

Accumulation of fluid in the peritoneal cavity = swollen abdomen

  • underfill = reduction circulating plasma volume
  • overflow = increased plasma volume
  • peripheral artery vasodilation
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17
Q

Ascites treatment ?

A

Diuretics:

  • spironolactone
  • Amiloride
  • Furosemide

Fluid/sodium restriction

Paracentesis - drain fluids

Transjugular intrahepatuc portosystemic shuts (TIPS)

18
Q

ASCITES monitoring

A

Monitor

  • electrolytes
  • daily weight
  • fluid chart
  • avoid high Na contents preparation
19
Q

Hepatic encephalopathy

A
  • Neuropsychiatric changes including changes in mood and behaviour, confusion, poor sleep rhythm, delirium and coma.
  • due to accumulation of toxins, increased permeability of BBB, increased levels of neurotransmitters.
20
Q

Hepatic encephalopathy treatments

A

Lactulose
Rifaximin
Metronidazole
Neomycin

21
Q

Variceal bleeding and portal hypertension

A

Portal hypertension is caused by increased resistance to flow.

Collateral vessels form enabling the blood to bypass the liver

22
Q

Variceal bleeding treatments

A

Terlipressin (potent splanchnic vasoconstrictor)

Somatostatin and analogues (causes selective vasoconstriction and reduces portal pressure on the portal blood flow).

Endoscopic (band ligation/ sclerotherapy/ballon tamponade)

23
Q

What is spider Naevi ?

A

Central red arteriole, representing the body of the spider.

Cause: failure to metabolise oestrogen

24
Q

What is Pruritus? (Caused by liver disease)

A

Severe itching of the skin

25
Q

What are the Factors effecting drug handling in liver disease?

A
  • Patient factors (such as LFTs)
  • Drug factors (PK/PD/side effects)
  • Therapeutic effect

Child-Pugh scoring system is used to make recommendations in drug SPCs.

26
Q

Increased bilirubin effect on drugs

A
  • Reduces absorption for highly lipophilic drugs = reduced clinical effect.
  • Biliary clearance will be reduced = this may affect drugs which are cleared by biliary system e.g. digoxin.
  • Competition for protein binding sites (potential displacement of drug = enhancing clinical effect) such as warfarin and phenytoin.
27
Q

Decreased albumin effect on drugs

A

Decreased protein binding =

Highly protein bound drugs - increase in “free” drug available to act = increased clinical effect.

28
Q

INR/PT effect on drugs

A

Dose adjustment if prothrombin time > 130% normal

29
Q

Effect of liver disease on metabolism

A

High extraction ratio drugs
= drugs that are highly first-pass metabolised.

Reduced hepatic blood flow = increased bioavailability

30
Q

What are the caused of reduced hepatic blood flow?

A 
Cirrhosis
Portal vein thrombosis
Cardiac failure
Shock ( reduced BP)
Portal systemic shunting
31
Q

Pharmacodynamic

A

Patients may be at risk of:


  • Increased toxicity
  • Exaggerated response
  • Reduced response
32
Q

Route of administration for liver disease

A

Oral – generally preferred

Avoid modified release and long-acting preparations

Avoid IM if coagulopathy

Topical preparations – consider transdermal absorption

Topical preparations – may cause irritation

PR – consider presence varices/bleeding

33
Q

Risk factors which may pre-dispose drug induced liver disease

A
  • Gender (tends to be more common in females)
  • Age
  • Genetics
  • Concurrent diseases e.g. obesity, diabetes, co-infection with HIV
  • Polypharmacy
34
Q

Intrinsic drug induced liver disease

A 
Predictable
Reproducible
Dose dependent
Tend to occur rapidly e.g. within hours
Tend to cause necrosis, acute liver failure
E.g. paracetamol overdose
35
Q

Idiosyncratic drug induced liver disease

A

Not predictable
Not reproducible
Not dose dependent
Tend to take longer to occur – weeks to months
Can result from metabolic idiosyncrasy or immunoallergic reaction
Can cause any type of liver injury e.g. increased LFTs, jaundice, fever, rash, eosinophilia
E.g. NSAIDS (metabolic), carbamazepine (immunoallegic)

36
Q

Drugs that can cause liver disease

A

Cholestasis – OCP, warfarin, azathioprine

ALF – allopurinol, NSAIDS, MDMA

Steatosis – amiodarone, steroids, TPN

Fibrosis and Cirrhosis – methotrexate

Vascular disorders – OCP, azathioprine

37
Q

Symptoms of alcohol withdrawal

A 
Marked tremor
Fear and delusions
Restlessness and agitation
Fever
Rapid pulse
Dehydration
Seizures
Delirium tremens
38
Q

Alcohol withdrawal treatment

A

combination sedatives and vitamin supplementation – Chlordiazepoxide + Pabrinex

  • Benzos can be given e.g. Diazepam
  • Shorter acting, e.g. Oxazepam or lorazepam, more suitable in patients with hepatic impairment
39
Q

Acute Alcoholic Hepatitis treatments

A
  • Prednisolone 40mg OD for at least 5-7 days.
    Problem: increased risk infection and GI bleeding
  • Pentoxifylline (Oxpentifylline)
    Non-selective phosphodiesterase inhibitor which inhibits TNFα.
  • Other anti-TNF agents – Infliximab, Etanercept
40
Q

Management of Alcoholic Cirrhosis

A
  • Diuretics for ascites
  • Propanolol for portal hypertension
  • Vitamin K for coagulopathy
  • Antibiotics for spontaneous bacterial peritonitis
  • Lactulose for hepatic encephalopathy (+ avoidance precipitants)
41
Q

How to achieve abstinence?

A

Abstinence can be achieved by:
Psychological treatments
Pharmacological treatments
Combination of both

Agents available:

  • Acamprosate
  • Disulfiram (Antabuse)
  • Naltrexone
42
Q

key points

A
  • Patients may present at any stage 
– need to understand degree underlying dysfunction
  • Abstinence is key 

  • Appropriate use of benzodiazepines in management of withdrawal
  • For AAH 
– in severe cases Prednisolone treatment should be used but stopped after 7 days if no fall in bilirubin

CDM Lina (4 decks)

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