Drugs

Question 1

Gold risk in rheumatology

Answer 1

• myelosupression
• renal toxicity
• mouth ulcer
• photosensitivity

Question 2

MAO inhibitors side effects

Answer 2

Hypertensive reaction to foods high in tyramine (cheese, processed meats…)

Question 3

Drugs cause delirium

Answer 3

Question 4

Labetalol risks

Answer 4

• hypoglycaemia
• bradycardia

Question 5

Mechanism of ACE inhibitors

Answer 5

inhibits the conversion angiotensin I to angiotensin II
→ decrease in angiotensin II levels → to vasodilation and reduced blood pressure
→ decrease in angiotensin II levels → reduced stimulation for aldosterone release → decrease in sodium and water retention by the kidneys

Question 6

renoprotective mechanism ACE inhibitors

Answer 6

angiotensin II constricts the efferent glomerular arterioles
ACE inhibitors therefore lead to dilation of the efferent arterioles → reduced glomerular capillary pressure → decreased mechanical stress on the delicate filtration barriers of the glomeruli
this is particularly important in diabetic nephropathy

Question 7

How are ACE inhibitors are activated

Answer 7

phase 1 metabolism in the liver

Question 8

Side effects of ACE inhibitors

Answer 8

• cough
• angioedema
• hyperkalmeia
• first dose hypotension

Question 9

ACE inhibitors cautions and contradictions

Answer 9

pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema
specialist advice should be sought before starting ACE inhibitors in patients with a potassium >= 5.0 mmol/L

Question 10

Interactions of ACE inhibitors

Answer 10

patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)
significantly increases the risk of hypotension

Question 11

Mechanism of Adenosine

Answer 11

causes transient heart block in the AV node

agonist of the A1 receptor in the atrioventricular node, which inhibits adenylyl cyclase thus reducing cAMP and causing hyperpolarization by increasing outward potassium flux

adenosine has a very short half-life of about 8-10 seconds

Question 12

Adverse effects adenosine

Answer 12

chest pain
bronchospasm
transient flushing
can enhance conduction down accessory pathways, resulting in increased ventricular rate (e.g. WPW syndrome)

Question 13

Contradictions of Adenosine

Answer 13

Asthmatics
Causes bronchospasm

Question 14

Adenosine should ideally be infused

Answer 14

large-calibre cannula due to it’s short half-life,

Question 15

Interactions of adenosine

Answer 15

dipyridamole (antiplatelet agent) and blocked by theophyllines.

Question 16

Noticible adverse effects ADP receptor inhibitors

Answer 16

ticagrelor may cause dyspnoea
due to the impaired clearance of adenosine

Question 17

Clopidogrel contradictions

Answer 17

clopidogrel and proton pump inhibitors, particularly omeprazole and esomeprazole, leading to reducing antiplatelet effects.

Question 18

contraindications to prasugrel use.

Answer 18

prior stroke or transient ischaemic attack, high risk of bleeding, and prasugrel hypersensitivity are absolute contraindication

Question 19

Salbutamol

Answer 19

• beta receptor agonist
• short-acting bronchodilator
• Relaxes bronchial smooth muscles through beta 2 receptors

Question 20

Corticosteroids

Answer 20

• Anti-inflammatory
• used as maintenance therapy

Question 21

Ipratropium

Answer 21

• Blocks the muscarinic acetylcholine receptors
• Short-acting inhaled bronchodilator. Relaxes bronchial smooth muscle
  • Used primarily in COPD
  • Tiotropium has similar effects but is long-acting

Question 22

Methylxanthines (e.g. theophylline)

Answer 22

• Non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP
• Given orally or intravenously
  • Has a narrow therapeutic index

Question 23

Monteleukast, zafirlukast

Answer 23

• Blocks leukotriene receptors
• Usually taken orally
  • Useful in aspirin-induced asthma

Question 24

Oxygen saturation targets
acutely ill patients

Answer 24

94-98%

Question 25

Oxygen saturation targets patients at risk of hypercapnia (e.g. COPD patients)

Answer 25

88-92%

Question 26

COPD management O2

Answer 26

prior to availability of blood gases, use a 28% Venturi mask at 4 l/min and aim for an oxygen saturation of 88-92% for patients with risk factors for hypercapnia but no prior history of respiratory acidosis
adjust target range to 94-98% if the pCO2 is normal

Question 27

When not to use O2 therapy (no hypoxia present, but conditions diagnoses)

Answer 27

myocardial infarction and acute coronary syndromes
stroke
obstetric emergencies
anxiety-related hyperventilation

Question 28

Theophylline poisoning

Answer 28

acidosis, hypokalaemia
vomiting
tachycardia, arrhythmias
seizures

Question 29

Management of theophylline poisoning

Answer 29

• consider gastric lavage if <1 hour prior to ingestion
  activated charcoal
• whole-bowel irrigation can be performed if theophylline is sustained release form
  charcoal haemoperfusion is preferable to haemodialysis

Question 30

Potential mechanism of theophylline

Answer 30

theophyllines may be a non-specific inhibitor of phosphodiesterase resulting in an increase in cAMP. Other proposed mechanisms include antagonism of adenosine and prostaglandin inhibition

Question 31

canakinumab

Answer 31

• monoclonal antibody targeted at IL-1 beta
• used systemic juvenile idiopathic arthritis and adult-onset Still’s disease

Question 32

anakinra

Answer 32

• IL-1 receptor antagonist
• used in the management of rheumatoid arthritis