eScript 3 Flashcards
What is an electrolyte abnormality caused by spironolactone?
hyperkalaemia
are ACE inhibitors contraindicated in severe liver disease?
yes
In severe liver disease, the patient relies in part on activation of the renin-angiotensin system to maintain peripheral vascular resistance. Administration of an ACE inhibitor can lead to a rapid drop in blood pressure and the development of renal failure.
signs on examination of chronic liver disease?
Spider naevi Clubbing Jaundice Loss of secondary sexual hair Gynaecomastia Ascites Splenomegaly Peripheral oedema
tests to evaluate hepatic function?
Albumin, prothrombin time, bilirubin
USS
what is child pugh score?
The Child Pugh score was developed to evaluate operative risk in patients with liver cirrhosis, but it remains one of the easiest bedside scores to calculate. It considers five variables; the severity of ascites and of encephalopathy, serum bilirubin, serum albumin and clotting time. It stages patients as Child class A, B or C, with class C patients having the most severe liver dysfunction.
what liver complications can flucloxacillin cause?
hepatitis and cholestatic jaundice
the onset may be delayed for up to 2 months
name some commonly prescribed drugs that can cause acute liver injury?
Paracetamol causes a dose-dependent acute liver injury that can lead to acute liver failure.
Co-amoxiclav and flucloxacillin can cause cholestatic hepatitis that resolves in most cases after withdrawal of the drug.
NSAIDs (e.g. ibuprofen, naproxen, diclofenac) can cause an ideosyncratic hepatitis that resolves in most cases after withdrawal of the drug. Aspirin can also cause hepatitis but it tends to be dose related.Ibuprofen classically causes a cholestatic hepatitis.
Antituberculosis drugs (e.g. rifampicin) can cause liver injury.
Methotrexate can cause severe fibrosis and cirrhosis if not adequately monitored.
Amiodarone can cause a steato hepatitis.
how does paracetamol OD cause toxicity?
Paracetamol is primarily metabolised in the liver and metabolism of paracetamol is required prior to hepatotoxicity. Liver injury does not occur until glutathione is depleted. After this, the reactive metabolites of paracetamol bind to cellular macromolecules, causing lethal damage to the hepatocyte.
when is NAC treatment commenced?
Treatment should be commenced if a patient has taken more than 150 mg/kg in any 24-hour period, unless:
The plasma-paracetamol concentration is undetectable
The patient is asymptomatic
LFTs, serum creatinine and INR are all normal
what happens if a patient presents after 8 hours who has taken potentially toxic amounts of paracetamol, even if plasma concs are not available?
given NAC
what are the 2 phases of drug metabolism?
Phase 1 - The cytochrome P450 group of enzymes is responsible for the majority of Phase 1 reactions. In cirrhosis, the activity of these enzymes can be markedly reduced.
Phase 2 - conjugation, which results in a water soluble compound that is usually inactive and more easily excreted in the urine or bile.
what is first pass metabolism?
They will pass through the liver and be partially or wholly metabolised before reaching the systemic circulation, reducing oral bioavailability.
If the blood flow through the liver is slowed, a drug may be subject to increased metabolism, as it may stay in the liver for longer.
However, patients with cirrhosis often develop collaterals, enabling the blood to bypass the liver, resulting in a decrease in first-pass metabolism
adverse effects of liver disease?
encephalopathy
clotting abnormalities
gastric and oesophageal varices, secondary to portal hypertension
ascites
what medication can be prescribed for hepatic encephalopathy?
lactulose
why are NSAIDs contraindicated in chronic liver disease?
The risk of bleeding is increased. NSAIDs can irritate the gastrointestinal tract, which may increase the risk of bleeding from GI varices. NSAIDs may also increase fluid retention in ascites. Patients with liver failure may depend on renal prostaglandins to maintain blood flow. NSAIDs inhibit prostaglandin production, reducing renal perfusion and can therefore precipitate renal impairment.
how does body composition change with age?
Decrease in lean body mass.
Decrease in body water.
Increase in body fat in relation to total body weight.
Decrease in bone mass.
what is the effect on distribution of drugs in elderly people for water-soluble and lipid-soluble drugs?
The distribution of lipid-soluble drugs (e.g. diazepam) may increase, resulting in a prolonged action or a ‘hangover effect’.
The distribution of water-soluble drugs (e.g. paracetamol, digoxin, ethanol) may decrease resulting in a higher initial plasma concentration for any dose based on body weight.
what is the clinical relevance in decrease in lean body mass?
doses may need to be reduced e.g. digoxin
what are the changes to drug metabolism as you get older?
decrease in hepatic function
decline in hepatic blood flow
name some drugs that can cause toxicity due to a decline in renal function with age?
Aminoglycosides (e.g. gentamicin) Digoxin Lithium salts Metformin Thiazide diuretics
What should be calculated to estimate a decline in renal function in elderly people with extremes of weight?
creatinine clearance- eGFR not accurate
what drugs can cause hypothermia in older people?
- sedatives- benzos, opioid analgesics, TCAs
- impair awareness of temp- chlorpromazine
- decrease motility- antipsychotics, antiparkinsonian drugs
- cause vasodilation- e.g. amlodipine
what drugs can cause peripheral oedema resistant to diuretics?
calcium channel blockers e.g. amlodipine
drugs that can cause confusion and affect cognition?
Anticholinergics Antihistamines Beta-blockers Hypnotics Opioid analgesics Tricyclic antidepressants