Top 100 drugs

Question 1

N-acetylcysteine; what is it used for? (common indications)

Answer 1

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).

Question 2

MoA: N-acetylcysteine

Answer 2

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)

Question 3

How long do you administer N-Acetylcysteine for after paracetamol overdose?

Answer 3

21 hour drip

Question 4

Common indications: Activated charcoal

Answer 4

• 1 dose may reduce absorption of poisons (e.g. drug overdose from gut)
• multiple doses of activated charcoal= increase elimination of certain poisons

Question 5

MoA: Activated charcoal?

Answer 5

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.

Question 6

Common indications: Adenosine

Answer 6

First-line diagnostic and therapeutic agent in supra-ventricular tachycardia (SVT).

“restarts the heart”- may be uncomfortable for 30 seconds

Question 7

MoA: Adenosine

Answer 7

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)

Question 8

Important adverse effects: adenosine

Answer 8

Bradycardia
Asystole 
"sinking feeling in the chest"
Breathlessness
"impending doom"

Question 9

When should you not administer adenosine?

Answer 9

Hypotension
Coronary ischeamia
Decompensated heart failure

Sometimes in
Asthma, COPD, heart transplant

Question 10

Important interactions: adenosine

Answer 10

Dipyridamole blocks cellular uptake of adenosine.

Question 11

How is adenosine prescribed?

Answer 11

Always IV

One-dose only

Question 12

Common indications: adrenaline

Answer 12

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.

Question 13

MoA: adrenaline

Answer 13

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.

Question 14

Adverse effects: adrenaline

Answer 14

Adrenaline-induced hypertension
Anxiety
Tremor
Headache
Palpitations
Angina
Myocardial Infarction
Arrhythmias

Question 15

Common indications: aldosterone antagonists

Answer 15

• Ascites and oedema due to liver cirrhosis
• Chronic heart failure (with beta blocker and ACE inhibitor)
• Primary hyperaldosteronism
  e. g. spironolactone

Question 16

MoA: aldosterone antagonists

Answer 16

• 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)

Question 17

Important adverse effects: aldosterone antagonists

Answer 17

• Hyperkalaemia –> muscle weakness, arrhythmias, cardiac stress
• Gynaecomastia (caused by sprionolactone)
• Liver impairment, jaundice
• Stevens-Johnson syndrome (T-cell mediated hypersensitivity reaction)= bulious skin eruption

Question 18

Contraindications: Aldosterone antagonists

Answer 18

• Renal impairment
• Hyperkalaemia
• Addison’s disease (low aldosterone)
• Pregnancy/breast feeding

Question 19

Interactions: aldosterone antagonists

Answer 19

• K+ elevating drugs
• ACE Inhibitors
• Angiotensin receptor blockers

Question 20

Common indications: Alginates and antacids

Answer 20

• GORD (heart burn relief)

- Dyspepsia (short-term indigestion relief)

Question 21

MoA: Alginates and antacids

Answer 21

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

Question 22

Important adverse effects: Alginates and antacids

Answer 22

• Magnesium salts cause diarrhoea

- Aluminium salts cause constipation

Question 23

Name some alginates and antacids

Answer 23

Gaviscon and peptac

Question 24

Common indications: allopurinol

Answer 24

• prevent acute attacks of gout
• prevent uric acid and calcium oxalate renal stones
• prevent hyperuricaemia and tumour lysis syndrome associated with chemotherapy

Question 25

MoA: allopurinol

Answer 25

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.

Question 26

Common indications: alpha-blockers

Answer 26

• 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

Question 27

MoA: alpha-blocker

Answer 27

• 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

Question 28

Common indications: Aminoglycosides

Answer 28

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

Question 29

MoA: aminoglycosides

Answer 29

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.

Question 30

Common indications: aminosalicylates

Answer 30

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.

Question 31

MoA: aminosalicylates

Answer 31

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.