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GI > Prescribing in liver disease > Flashcards

Prescribing in liver disease Flashcards

1
Q

what are the main features of cirrhosis

A

reduced metabolic capacity

portal hypertension
shunting of blood to by pass the liver

reduced liver blood flow

reduced plasma proteins

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2
Q

what is the result of portal hypertension + low albumin

A

ascites

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3
Q

why does a blood shunt affect drug dose

A

as drugs dont undergo first pass metabolism and remain in blood

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4
Q

how can you tell if a drug is highly metabolised

A

if its oral dose is much higher than its IV dose

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5
Q

what are the two orders of saturable kinetics

A

first order- plasma concentration increasing

zero order- plasma concentration remains contrast as fully saturated

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6
Q

what does a low albumin cause

A

baroreceptors think the body has low plasma volume so trigger renin to convert angiotensinogen to ATI to ATII to retain sodium and water and increase oncotic pressue=re

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7
Q

why do people with cirrhosis have very high aldosterone levels- secondary aldosteronism

A

as liver cant metabolism steroids well + produced in excess in cirrhosis

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8
Q

what hormone causes spider naevi

A

oestrogen- not being metabolised in cirrhosis

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9
Q

what do endothelin do, is it increased or decreased in cirrhosis

A

vasoconstrictor- increased as hormone not metabolised by the liver

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10
Q

what vasoconstrictors act on the kidney

A

angiotensin II and aldosterone

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11
Q

what is vasopressin

A

ADH

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12
Q

what does ADH do

A

retains water

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13
Q

what do the effects of the symp nevous system, angiotensin II, aldosterone and ADH have on the kidneys in cirrhosis

A

potassium loss, sodium and water retention

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14
Q

vasopressin is usually controlled by osmolarity but what can override this

A

low plasma volume

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15
Q

how do you treat the adverse effects (sodium and water retention) of the kidneys in cirrhosis

A

high levels or spirolactone and stop giving fluids

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16
Q

what is spirolonlactone

A

aldosterone antagonist

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17
Q

what do renal prostaglandins do

A

stimulate the kidney to vasodilate in normal people

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18
Q

what can high endothelin cause

A

hepato-renal syndrome

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19
Q

what will NSAIDs shut off in the kidney

A

renal prostaglandins

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20
Q

what are the consequences of moderate hepatic impairment

A

decreased renal clearance, renal function reduced:

-gut oedema (poor absorption
-liver and kidney congestion
reduced function
-gross oedema and ascites
-CHF

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21
Q

what is hepatorenal syndrome

A

rapid deterioration of kidney function in individuals with cirrhosis or fulminant liver disease

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22
Q

what causes gynaecomastea

A

oestrogen not broken down by liver

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23
Q

what is the result of using NSAIDs in people with cirrhosis

A

reduced renal prostaglandin synthesis:

  • worsens renal impairment
  • further sodium retention
  • risk of hepao renal syndrome
  • worsening of CHF

increase in cirrhosis peptic ulcers
-risk of GI bleed or perforation

24
Q

what are the adverse drug reactions of NSAIDs

A

UGI ulcer complications,

CV toxicity,

hypertension,

CHF,

sodium retention,

asthma (Cox 1),

diarrhoea/colitis,

renal failure

25
Q

what should NSAIDs or COX-2 inhibitors be prescribed with

A

PPI

26
Q

what metabolises drugs in phase I

A

P450

27
Q

what happens in phase II of drug metabolism

A

conjugation

28
Q

drugs that are metabolised in what phase should be prescribed in liver disease

A

phase II

29
Q

what is codeine metabolised by

A

P450

30
Q

how much of paracetamol dose in metabolised into highly reactive intermediate

A

8%

31
Q

how is the highly reactive intermediate removed by the body

A

gluthanthione stores in the body

32
Q

what metabolises paracetamol into highly reactive intermediate

A

P4502E1

33
Q

what does gluathione turn the highly reactive paracetamol intermediate into

A

cysteine and mercapturic acid conjugates

34
Q

why does alcohol reduce paracetamol toxicity

A

as prevents binding

35
Q

why is paracetamol more toxic if you havent eaten recently

A

as less glutathione in the liver

36
Q

what happens when you deplete your liver glutathione store (e.g in very large paracetamol dose)

A

will then attack liver

37
Q

why is paracetomal more dangerous in alcoholics who are not drunk

A

they have increased P4502E1

38
Q

are intentional or unintentional paracetamol overdoses more common

A

unintentional

39
Q

what does paracetamol toxicity cause

A

fulminant hepatitis

40
Q

what is the risk associated with opiates in cirrhosis

A

sedation as plasma levels high, encephalopathy and depressed respiratory drive

41
Q

how do you treat pain in cirrhosis

A

paracetamol 1g 2x daily, codeine 30mg 3x daily (watch for sedation), AVOID NSAIDs

42
Q

what antibiotics can cause induced hepatitis

A

amoxicillin and clavulanic acid

43
Q

what antigen determines induced hepatitis

A

HLA surface antigen

44
Q

what is hy’s rule

A

that a patient is at risk of developing fatal drug induced liver injury if given a medication that causes hepatocellular injury

when ALT/AST> 5x ULN
AND
bilirubin> 3mg/dl

45
Q

who is drug induced liver injury more common in

A

women

46
Q

what is the negative of a loop diuretic (frusemide)

A

damages kidney, reduced intra-vascular volume, hypokalaemia and hypomagnesaemia

47
Q

what is the diruetic of choice in liver disease

A

spironolactone

48
Q

what is the negative of a thiazide diuretic

A

hypokalaemia, hypomagnesaemia

49
Q

how much fluid should you aim to loose a day

A

1kg

50
Q

what drugs achieve sedation in cirrhosis

A

phase II metabolised benzodiazepines

51
Q

what are the negatives of the antiobiotics;

  • aminoglycosides
  • quinolones
  • metronidazole

in cirrhosis

A

aminoglycosides- nephrotoxic

quinolones- epilptogenic (causes epilepsy)

metronidazole- reduced metabolism

52
Q

what are the worst hepatic disorders

A

fulminant hepatic failure,
decompensated cirrhosis,
severe acute/ chronic hepatitis,
sever congestive heart failure

53
Q

what causes a mild/mod reduction in liver function

A

compensated cirrhosis,
cholestatic jaundice,
enzyme blockers (quinolones, grapefruit juice),
hypothyroidism, old age

54
Q

what are the general rules in prescribing in cirrhosis

A

dose reduction regardless of the route of elimination of drug or metabolite

avoid pro drugs

use drugs with renal rather than liver excretion

be wary of sedatives, CNS drugs, anticoagulants, NSAIDs, theophyllines, aminoglycosides

start low go slow

55
Q

what is a pro drug

A

drug that is metabolised into active form

GI (64 decks)

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