Top 100 drugs Flashcards
N-acetylcysteine; what is it used for? (common indications)
As the antidote for paracetamol poisoning.
To help prevent renal injury due to radiographic contrast material (contrast nephropathy).
To reduce the viscosity of respiratory secretions (acting as a mucolytic).
MoA: N-acetylcysteine
Paracetamol is metabolised by conjugation with glucuronic acid and sulphate.
Small amount converted to N-acetyl-p-benzoquinone (hepatotoxic)
In paracetamol poisoning stops glutathione in body (normally) detoxifying it.
Acetylcysteine replenishes body’s glutathione.
= antioxidant effects prevents contrast nephropathy
liquifies mucous (for bronchiectasis)
How long do you administer N-Acetylcysteine for after paracetamol overdose?
21 hour drip
Common indications: Activated charcoal
- 1 dose may reduce absorption of poisons (e.g. drug overdose from gut)
- multiple doses of activated charcoal= increase elimination of certain poisons
MoA: Activated charcoal?
VDW forces: molecules are adsorbed onto the surface of charcoal as they travel through the gut (reduces absorption into circulation).
Activated charcoal only useful when poison ingested is likely to be adsorbed on it.
Weakly ionic, hydrophobic substances (e.g. benzodiazepines, methotrexate) are well adsorbed to activated charcoal.
By contrast, strongly ionic and hydrophilic substances (e.g. strong acids/bases, alcohols, lithium and iron) are not.
Activated charcoal can also increase the elimination of certain poisons.
Common indications: Adenosine
First-line diagnostic and therapeutic agent in supra-ventricular tachycardia (SVT).
“restarts the heart”- may be uncomfortable for 30 seconds
MoA: Adenosine
Adenosine= agonist of adenosine receptors on cell surface
In the heart, activation of adenosine GPCRs= reduces frequency of spontaneous depolarisations, increases resistance to depolarisation
^ = slower sinus rate, conduction velocity and increases AV node refractoriness (breaks circuit reentry)
Important adverse effects: adenosine
Bradycardia Asystole "sinking feeling in the chest" Breathlessness "impending doom"
When should you not administer adenosine?
Hypotension
Coronary ischeamia
Decompensated heart failure
Sometimes in
Asthma, COPD, heart transplant
Important interactions: adenosine
Dipyridamole blocks cellular uptake of adenosine.
How is adenosine prescribed?
Always IV
One-dose only
Common indications: adrenaline
In cardiac arrest - Advanced Life Support (ALS) treatment algorithm.
Anaphylaxis
injected directly into tissues to induce local vasoconstriction e.g. in endoscopy to control mucosal bleeding
Sometimes mixed with local anaesthetic drugs (e.g. lidocaine) to prolong local anaesthesia.
MoA: adrenaline
Adrenaline is a potent agonist of the α1, α2, β1 and β2 adrenoceptors
sympathetic (fight or flight’) effects.
These include: vasoconstriction of vessels supplying skin, mucosa and abdominal viscera (mainly α1-mediated); increases in heart rate, force of contraction and myocardial excitability (β1); and vasodilatation of vessels supplying the heart and muscles (β2).
cardiac arrest- redistribution of blood flow in favour of the heart- improve the chances of restoring an organised rhythm.
Additional effects of adrenaline, mediated by β2 receptors, are bronchodilatation and suppression of in ammatory mediator release from mast cells.
Adverse effects: adrenaline
Adrenaline-induced hypertension Anxiety Tremor Headache Palpitations Angina Myocardial Infarction Arrhythmias
Common indications: aldosterone antagonists
- Ascites and oedema due to liver cirrhosis
- Chronic heart failure (with beta blocker and ACE inhibitor)
- Primary hyperaldosteronism
e. g. spironolactone
MoA: aldosterone antagonists
- Aldosterone= mineralocorticoid produced in adrenal cortex; acts on mineralocorticoid receptors in distal tubules of kidney to increase activity of ENaCs= ^ reabsorption of Na and water= ^bp with increased K+ excretion
- Inhibits aldosterone effect by competitively binding to aldosterone receptor= increases Na and water excretion and K+ retention
- Effect greatest in primary hyperaldosteronism e.g. cirrhosis (^^^aldosterone)
Important adverse effects: aldosterone antagonists
- Hyperkalaemia –> muscle weakness, arrhythmias, cardiac stress
- Gynaecomastia (caused by sprionolactone)
- Liver impairment, jaundice
- Stevens-Johnson syndrome (T-cell mediated hypersensitivity reaction)= bulious skin eruption
Contraindications: Aldosterone antagonists
- Renal impairment
- Hyperkalaemia
- Addison’s disease (low aldosterone)
- Pregnancy/breast feeding
Interactions: aldosterone antagonists
- K+ elevating drugs
- ACE Inhibitors
- Angiotensin receptor blockers
Common indications: Alginates and antacids
- GORD (heart burn relief)
- Dyspepsia (short-term indigestion relief)
MoA: Alginates and antacids
Often contain alginate and 1 or more antacid e.g. sodium bicarbonate, calcium carbonate, magnesium or aluminium salts
- Antacids: buffer stomach acid
- Alginates increase viscosity of the stomach contents, reducing stomach contents into the oesophagus. After reacting with stomach acid, it forms a floating raft which separates the gastric contents from the GOJ to prevent mucosal damage
Important adverse effects: Alginates and antacids
- Magnesium salts cause diarrhoea
- Aluminium salts cause constipation
Name some alginates and antacids
Gaviscon and peptac
Common indications: allopurinol
- prevent acute attacks of gout
- prevent uric acid and calcium oxalate renal stones
- prevent hyperuricaemia and tumour lysis syndrome associated with chemotherapy
MoA: allopurinol
Allopurinol is a xanthine oxidase inhibitor.
Xanthine oxidase metabolises xanthine (produced from purines) to uric acid.
Inhibition of xanthine oxidase lowers plasma uric acid concentrations and reduces precipitation of uric acid in the joints or kidneys.
Common indications: alpha-blockers
- improve benign prostatic hyperplasia :) :) :) (can add 5alpha-reductase inhibitors, surgery)
- add-on treatment for resistant hypertension when other medicines are insufficient e.g. Ca+ channel blockers, ACE inhibitors, thiazide diuretics
- e.g. doxazosin, tamsulosin, alfuzosin
MoA: alpha-blocker
- highly selective for alpha- adrenoreceptor found in smooth muscle (blood vessels, urinary tract- bladder neck and prostate)
- Stimulation= contraction, therefore blockade induces relaxation
- Alpha-blocker= vasodilation and fall in blood pressure–> reduced resistance to bladder outflow
Common indications: Aminoglycosides
Severe infections, particularly those caused by Gram-negative aerobes (including Pseudomonas aeruginosa):
- Severe sepsis, including where the source is unidenti ed.
- Pyelonephritis and complicated urinary tract infection.
- Biliary and other intra-abdominal sepsis.
- Endocarditis.
Aminoglycosides lack activity against streptococci and anaerobes (see Mechanisms of action), so should be combined with penicillin and/or metronidazole when the organism is unknown.
e.g. gentamicin, amikacin
MoA: aminoglycosides
Aminoglycosides bind irreversibly to bacterial ribosomes (30S subunit) and inhibit protein synthesis.
They are bactericidal (i.e. they kill bacteria)
Their spectrum of action includes Gram-negative aerobic bacteria, staphylococci and mycobacteria (for example, streptomycin was one of the rst effective treatments for tuberculosis).
Aminoglycosides enter bacterial cells via an oxygen-dependent transport system.
Streptococci and anaerobic bacteria do not have
this transport system, so have innate aminoglycoside resistance.
Other bacteria acquire resistance through reduced cell membrane permeability to aminoglycosides or acquisition of enzymes that modify aminoglycosides to prevent them from reaching the ribosomes.
As penicillins weaken bacterial cell walls, they may enhance aminoglycoside activity by increasing bacterial uptake.
Common indications: aminosalicylates
First-line in the treatment of mild-to-moderate ulcerative colitis
Sulfasalazine is one of several options for the management of rheumatoid arthritis, in which it is used as a disease-modifying antirheumatic drug (DMARD), usually as part of combination therapy.
MoA: aminosalicylates
In ulcerative colitis (UC): release 5-aminosalicylic acid (5-ASA). The precise mechanism of action of 5-ASA is unknown, but it has both anti-inflammatory and immunosuppressive effects, and appears to act topically on the gut rather than systemically.
