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GSS > The Liver Pharmacology > Flashcards

The Liver Pharmacology Flashcards

1
Q

Alcohol effects the GABA system. what does GABA stand for?

A

Gamma- Aminobutyric Acid

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2
Q

bilirubin is usually excreted via

A

excretion via bile ducts as a water-soluble conjugate

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3
Q

fibrosis and cirrhosis are characterised by

A

Inflammation + Fibrogenesis + Collagen deposition

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4
Q

high levels of ALT can be indicative of:

A

viral hepatitis, drugs, sepsis

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5
Q

How are Radicals produced in the liver?

A

When there’s higher alcohol intake, CYP450 2EI metabolises alcohol to unstable free radicals

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6
Q

list 5 signs of liver disease

A

Varices, Fatty Stools, Spider Naevi, Ascites and Jaundice

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7
Q

liver fibrosis can lead to

A

cirrhosis

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8
Q

name 3 other investigations done with LFTs

A

CT scan, liver Ultrasound, MRI

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9
Q

Name and explain an invasive treatment of Ascites

A

Paracentesis. is extracted from peritoneal cavity and colloids, albumin and terlipressin is exchanged

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10
Q

what is Steatohepatitis

A

Steatohepatitis is a type of fatty liver disease, characterized by inflammation of the liver with concurrent fat accumulation in liver. Mere deposition of fat in the liver is termed steatosis, and together these constitute fatty liver changes

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11
Q

normal albumin range?

A

35-50 g/dl

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12
Q

role of kupffer cells?

A

release macrophages to kill off bacteria and viruses in the liver

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13
Q

Treatment of SBP

A

3rd generation Cephalosporin, Co-Amoxiclav

Norfloxacin/Ciprofloxacin as prophylaxis

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14
Q

what are Ascites patients at risk of in terms of infection? where does it infect?

A

SBP - Spontaneous Bacterial Peritonitis. infects the peritoneal fluid

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15
Q

Long and short term consequences of alcohol

A

Short term:

  • Loss of consciousness
  • impotence
  • anxiety
  • acute poisoning
  • GI disturbances

Long term:

  • GI ulcer
  • Stroke
  • Increased BP
  • Obesity
  • Insomnia

(additionally generate free radicals, and affects GABA system)

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16
Q

what are the three main theories of Ascites

A
  1. underfill - reduction of circulating plasma volume
  2. overfill - increased plasma volume
  3. peripheral artery vasodilation
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17
Q

What are the two patterns of liver damage?

A

Cholestasis or Hepatocellular damage

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18
Q

what condition is Terlipressin used in? what is it?

A

Ascites and Variceal bleeding. It is a vasoactive drug used to raise blood pressure when norepinephrine doesn’t help.

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19
Q

what does ‘compensated liver disease’ mean

A

the small amount of viable liver you have left, works well.

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20
Q

what does ‘deompensated liver disease’ mean

A

the small amount of viable liver cells you have left doesn’t work well

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21
Q

normal range of bilirubin?

A

5-20 micromol/L

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22
Q

What is Varices, and what drug is used to treat it

A

Collateral vessels formed that enables blood to bypass the liver. Treat with Terlipressin

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23
Q

what is acute liver failure

A

history of onset does not exceed 6 months

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24
Q

what is cholestasis

A

Disruption of bile flow. Can be intra out extra hepatic

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25
Q

what is chronic liver failure

A

persists for more than 6 months, with permanent structural changes following standing cell damage

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26
Q

what is elevated bilirubin a clinical sign of

A

Haemolysis

Hepatocellular damage

Cholestasis

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27
Q

what is first line in alcohol withdrawal management plan and why?

How to administer?

If the patient has cirrhosis what do we give?

A

A Benzodiazepine: Chlordiazepoxide long half life sedative + anticonvulsant properties slower onset of action.

Shorter acting than Oxazepam.

Front loading - loading dose followed by repeat dose every 90 minutes

In cirrhosis, give lorazepam or oxazepam

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28
Q

what is Hepatitis

A

Inflammation of the liver. can be caused by viruses

29
Q

what is Hepatocellular disease caused by

A
  • inflammation (Hepatitis) - Fatty infiltration (steatosis) - Injury to hepatocytes - necrosis
30
Q

what is liver fibrosis.

A

in injury to liver, collagen develops haphazardly and scars replace liver cells. the hard tissue formed is non functioning

31
Q

what is Sepsis

A

the body’s own response to infection injures it’s tissues and organs

32
Q

what is Steatohepatitis

A

accumulation of fat plus hepatocellular injury

33
Q

what is Steatosis?

A

“Liver Enlargement”.

There’s a disruption of metabolic pathways (redox imbalance) in liver which cause accumulation large droplets lipid within hepatocyte.

34
Q

what is the most important metabolite leading to liver disease?

A

Accumulation of Acetylaldehyde which is produced by oxidising ethanol (with alcohol dehydrogenase)

35
Q

what unfortunate condition can occur several weeks after quitting alcohol? what can we give as first line?

A

Acute Alcoholic Hepatitis. Prednisone 40m OD to switch off the inflammatory process

36
Q

what vitamin supplement do you recommend for alcohol management, and why do we need vitamins?

A

Panrinex. Patient is vitamin deficient due to poor diet.

Pabinex contains a mixture of vitamins for supplementation e.g Thiamine and Ascorbic acid

37
Q

What is this and what is the treatment for it?

A

Asterexis (a sign of liver diease)

Lactulose, Phosphate enema - Metronidazole, Neomycin, Sodium benzoate - Rifaximin

38
Q

what is jaundice? and what causes it?

A

Yellowing of the skin and whites of eyes.

  • It’s caused by a build-up of bilirubin in the blood and tissues of the body.
  • Common signs of jaundice are: -yellowing of the skin, eyes and mucus membrane (the lining of the body’s passageways and cavities, such as the mouth and nose
  • pale-coloured stools (faeces) -dark-coloured urine
39
Q
A
40
Q

What is Ascites?

A

Accumulation of fluid in the peritoneal cavity leading to swollen abdomen

41
Q

Main theory of Ascites?

A

Most common cause overflow which begins from cirrhosis of the liver. There is a decreased effective intravascular volume which leads to renal sodium retention. This now causes increased blood volume resulting in acites as water moves out into peritonieal cavity

42
Q

Treatment of Ascites

A

Diuretics: • Spironolactone • Amiloride • Furosemide •

*Fluid/Sodium restriction*

• Paracentesis for large volume. Need to maintain adequate circulating volume – colloids, albumin, Terlipressin • TIPS for more refractory ascites (along with paracentesis)

43
Q

what does TIPS stand for?

A

Transjugular intrahepatic portosystemic shunting

44
Q

Monitoring points in Ascites

A

Monitor: Daily U&Es – esp Na, K, Cr

  • Daily wt – aim for 0.5-1kg/day wt loss
  • Fluid chart – note fluid restriction, urine output
  • Avoid high Na contents preparation
  • Complications – dilutional hypoNa, HE, HRS, gynaecomastia, hyperK, muscle cramps, SBP
45
Q
A
46
Q

Terlipressin Indication, action and monitoring points. How to administer dose.

A

Indicated for vasiceal bleed.

Has a Biphasic action: • Intact molecule has an immediate vasoconstricting effect

  • Followed by delayed effect caused by slow transformation of terlipressin in-vivo to lysine vasopressin
  • Administer in bolus doses 1-2mg every 4-6hours (continue until haemostasis achieved)

Monitor - Blood pressure, sodium, potassium, fluid balance

Side-effects include headaches, abdominal cramps, ischaemia

47
Q

Secondary prophylaxis in variceal bleeds

A
  • Non-selective beta-blocker e.g Propranolol
  • Splanchnic vasoconstriction (beta2 blockade)
  • reduced Cardiac output results in reduced portal pressures (beta1 blockade)
  • Beta-blockers: Prevent re-bleeding and Increase survival
48
Q

What is this and what causes it?

A

Spider Naevi. Caused by raised oestrogen level imbalance

  • pregnant women. Hormone replacement therapy, Oral Contraceptive Pill. (raised oestrogen)
  • Hepatic Disease – failure to metabolise oestrogen
49
Q
A
50
Q

What do Albumin and INR tell us about Drug Handling?

A

Generally: • Decreased Albumin and/or increased INR indicate reduced synthetic function • Significance will depend on the drug and is difficult to predict • Lower doses with close monitoring may be required

Albumin

  • Decreased Albumin = decreased protein binding
  • Highly protein bound drugs - increase in “free” drug available to act and hence an increased clinical effect e.g. Phenytoin
  • Dose adjustment if PT > 130% normal
51
Q
A
52
Q

Explain the Key liver function tests

A
  1. Albumin
    • Hypoalbuminaemia = feature of advanced chronic liver disease (LD)
  2. Bilirubin
    • An increase means a blockage in bile flow
  3. Aminotransferase (AST and ALT)
    • An increase means hepatocellular damage
  4. Gamma-glutamyltransferase (γGT)
    • Sensitive to drugs and alcohol
  5. Alkaline phosphatase (ALP)
    • An increase means blockage of bile flow
  • yGT and ALP together indicate cholestatis -> Partial or full blockage of bile ducts
  • If bile duct is inflamed/damaged, yGT and ALP spill out of liver into blood stream due to pressure.
53
Q

what conditions cause a rise in yGT and ALP levels?

A

Scarring of the bile ducts

Fatty liver (steatosis)

Liver tumors

Gall stones

Alcoholic liver disease

54
Q

what causes AST and ALT to rise

A

Viral hepatitis

excess alcohol intake

liver inflammation from medicines

fatty liver

autoimmune

55
Q

normal range of:

  • AST
  • ALT
  • ALP
  • yGT
  • Albumin

And what do they stand for?

A

AST (0-40 iu/L) Aspartate aminotransferase

ALT (5-30 iu/L) Alanine aminotransferase

ALP (30-120 iu/L) Alkaline Phospatase

yGT-(5-55 iu/L) y-Glutamyltransferase

Albumin (35-50 g/dL)

56
Q

How do I interpret a LFT?

A
  • LFTs are fairly non-specific
  • Generally if 2 x ULN considered abnormal
  • If Liver dysfunction – usually at least 2 will be deranged
  • Trends not isolation
  • Check reference ranges and units
  • Child’s Pugh Scoring System takes into acount EABAI - Encephalopathy, Ascites, Bilirubin, Albumin and INR
57
Q

what is hepatic encephalopathy

A
  • Several theories including accumulation of toxins esp. ammonia, increased permeability of BBB, increased levels of neurotransmitters
  • Precipitating factors – increased protein load, reduced ammonia excretion, electrolyte disturbance, dehydration, drugs, infection
  • Occurs in 4 stages
58
Q

what are the four stages of hepatic encephalopathy

A

mental status

  1. Impaired attention, irritability, depression
  2. Drowsiness and memory impairment
  3. Confusion and amnesia
  4. Stupor and coma

corresponding neuromuscular function

​at stage 1: Tremor and incoordination

at stage 2: Asterexis and slurred speech

at stage 3: Hypoactive refleces

at stage 4: dilated pupils

59
Q

state invasive techniques to manage variceal bleeds

A
  1. sclerotherapy (glue)
  2. balloon taponade
  3. band ligation
60
Q

state 5 causes of liver disease

A
  • Alcohol
  • viral infections
  • drugs
  • toxins
  • cancer
  • autoimmune
61
Q
A
62
Q

Outline the management plan for Alcoholic hepatitis

A
  1. Manage withdrawal symptoms
  2. Manage Vitamin deficiency
  3. Treate acute alcoholic hepatits with anti-inflammatory agent
  4. Manage any complications associated with liver disease e.g cirrhosis, coagulopathy, ascites
63
Q

what are the presenting signs of alcohol withdrawal? What first line

A

delerium

fever

seizures

rapid pulse

tremor

First line is to manage the symptom. Give Chlordiazepoxide + Pabrinex

64
Q
A
65
Q

If a patient is getting additional seizures from alcohol withdrawal, what do you reccommend?

A

Lorazepam or Haloperidol in sever psychosis

66
Q

what markers are elevated in Acute Alcoholic Hepatits?

A

White Cell Count

Neutrophil count

Bilirubin

INR

Raised AST

67
Q

How to treat alcoholic cirrhosis?

How to manage Alcoholic Cirrhosis?

A

Treatments

  • anti-TNF agents - Infliximab
  • Antioxidants
  • Vitamin E

Management

  • Diuretics for Ascites
  • Propanolol for Portal Hypertension
  • Vitamin K for
  • Coagulopathy
  • Antibiotics for SBP
  • Lactulose for HE
68
Q

what causes alcohol dependence to begin with?

A

The release of β-endorphins, coupled with the release of dopamine, is thought to result in the pleasurable feelings associated with alcohol dependence.

When alcohol is withdrawn the result is CNS Hyperactivity. This explains the seizures

69
Q

what agents can we give to help abstincence of alcholol

A

Disulfiram! - inhibits acetaldehyde degydeogenase. 800mg OD then reduce by 200mg each day.

maintain at 100-200mg OD

GSS (10 decks)

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