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Pharmacology > Pharmacology P1 > Flashcards

Pharmacology P1 Flashcards

1
Q

How does adrenaline work?

A
  • sympathomimetic amine with both alpha and beta adrenergic stimulating properties
  • acts on alpha 1 and 2 and beta 1 and 2 receptors
  • beta 2 receptors in skeletal muscle caused vasodilation
  • alpha receptors: inhibits insulin secretion by pancreas, stimulates glycogenolysis in liver and muscle and glycolysis in muscle
  • beta receptors: stimulates glucagon secretion in pancreas, ACTH and lipolysis in adipose tissue
  • increases cardiac output and total peripheral resistance
  • causes vasoconstriction in skin and kidneys - narrow pulse pressure
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2
Q

What are the indications, recommended doses and management of accidental injection of adrenaline?

A
  • anaphlyaxis and cardiac arrest
  • anaphylaxis: 0.5ml 1:1000 IM
  • cardiac arrest: 10ml 1:10,000 IV or 1ml 1:1000 IV
  • local infiltration phentolamine
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3
Q

Acute withdrawal of alcohol:

A

Benzodiazepines

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4
Q

Drugs to manage chronic alcoholism:

A
  • disulfiram: promotes abstinence - severe reaction with alcohol due to inhibition of acetaldehyde dehydrogenase (CONTRA in IHD and psychosis)
  • acamprosate: reduces craving, weak NMDA antagonist
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5
Q

How does allopurinol work?

A

xanthine oxidase inhibitor

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6
Q

How should allopurinol be initiated?

A
  • initially 100mg od
  • titrated every few weeks and aim serum uric acid <300 micro mol/L
  • lower initial dose if reduced eGFR
  • colchicine cover consider
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7
Q

Indications allopurinol for gout:

A
  • offer to all after first attack
  • particularly if: more than 2 attack in a year, tophi, renal disease, uric acid renal stones, prophylaxis if on cytotoxics or diuretics, Lesch-Nyhan syndrome
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8
Q

Adverse reactions allopurinol:

A
  • severe cutaneous adverse reaction (SCAR)
  • drug reaction with eosinophilia with systemic symptoms (DRESS)
  • Steven-Johnson syndrome
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9
Q

Interactions of allopurinol:

A
  • azathioprine: xanthine oxidase converts 6-mercaptopurine to 6-thiouric acid, so high levels of mercaptopurine (reduce dose)
  • cyclophosphamide: allopurinol reduces renal clearance - marrow toxicity
  • theophylline: increased plasma concentration due to reduced breakdown
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10
Q

Indications and side effects of alpha blockers:

A
  • e.g. doxazosin, tamsulosin
  • BPH, HTN
  • ADR: postural hypotension, drowsiness, dyspnoea, cough
  • CONTRA: cataract surgery (intra-operative floppy iris syndrome)
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11
Q

Admiodarone induced thyrotoxicosis type 1:

A
  • excess iodine-induced thyroid hormone synthesis
  • goitre present
  • manage with carbimazole or potassium perchlorate
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12
Q

Amiodarone induced thyrotoxicosis type 2:

A
  • amiodarone-related destructive thyroiditis
  • absent goitre
  • corticosteroids
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13
Q

How can amiodarone cause hypothyroidism?

A

high iodine content - Wolf-Chaikoff effect (autoregulatory effect where thyroxine formation inhibited due to high levels of circulating iodide)

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14
Q

Amiodarone adverse effects:

A
  • thyroid dysfunction
  • corneal deposits
  • pulmonary fibrosis/pneumonitis
  • liver fibrosis/hepatitis
  • peripheral neuropathy/myopathy
  • photosensitivity
  • slate grey appearance
  • thrombophlebitis and injection site reactions
  • bradycardia
  • lengthens QT interval
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15
Q

Amiodarone drug interactions:

A
  • reduced metabolism warfarin - increased INR

- increased digoxin levels

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16
Q

How does aspirin work?

A
  • blocks action of both cyclooxyrgenase-1 and 2
  • cyclooxygenase responsible for PG, prostacyclin and thromboxane synthesis
  • reduces platelet aggregation
  • first line in patients with IHD
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17
Q

What does aspirin potentiate and who should not take it?

A
  • oral hypoglycaemics, warfarin, steroids

- not in children <16yo - Reye’s syndrome (with exception of Kawasaki disease)

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18
Q

Features of beta-blocker overdose and management:

A
  • bradycardia, hypotension, heart failure, syncope

- Atropine, glucagon

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19
Q

What is botulinum toxin used for:

A
  • blepharospasm
  • hemifacial spasm
  • focal spasticity including cerebral palsy, hand and wrist disability with stroke
  • spasmodic torticollis
  • severe hyperhidrosis of axillae
  • achalasia
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20
Q

Indications and ADR verapamil:

A
  • angina, HTN, arrhythmias
  • highly negatively inotropic with beta blockers (heart block)
  • HF, constipation, hypotension, bradycardia, flushing
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21
Q

Indications and ADR diltiazem:

A
  • angina, HTN
  • less negatively inotropic than verapamil but still not ideal with HF
  • hypotension, bradycardia, HF and ankle swelling
22
Q

Indications and ADR nifedipine, amlodipine (dihydropyridines):

A
  • HTN, angina, Raynaud’s
  • affects peripheral vascular smooth muscle more than the myocardium, no worsening HF
  • flushing, headache, ankle swelling
23
Q

Features of carbon monoxide toxicity:

A
  • headache: 90%
  • nausea and vomiting
  • vertigo
  • confusion
  • subjective weakness
  • severe toxicity: pink skin and mucosa, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death
24
Q

Investigations CO poisoning:

A
  • pulse oximetry may be falsely high due to similarities oxyhemoglobin
  • venous or arterial blood gas
  • <3% non smokers and <10% smokers
  • > 30% severe toxicity
  • ECG to look for cardiac ischaemia
25
Q

Management CO poisoning:

A
  • 100% high flow oxygen non-rebreather
  • target 100%
  • hyperbaric oxygen
26
Q

How does ciclosporin work?

A
  • immunosuppressant - decreases clonal proliferation of T cells by reducing IL-2 release
  • binds to cyclophilin to form complex which inhibits calcineurin - activates transcription factors in T cells
27
Q

ADR ciclosporin:

A
  • nephrotoxicity
  • hepatotoxicity
  • fluid retention
  • HTN
  • hyperkalaemia
  • hypertrichosis
  • gingival hyperplasia
  • tremor
  • impaired glucose tolerance
  • hyperlipidaemia
  • increased susceptibility severe infection
28
Q

Indications ciclosporin:

A
  • organ transplant
  • RA
  • psoriasis
  • UC
  • pure red cell aplasia
29
Q

MOA cocaine:

A

blocks dopamine, noradrenaline and serotonin uptake

30
Q

ADR cocaine:

A
  • CVS: coronary artery spasm (ischaemia and spasm), tachy and bradycardia, HTN, QRS widening, QT prolongation, aortic dissection
  • neuro: seizures, mydriasis, hypertonia, hyperreflexia
  • psychosis, agitation, hallucinations
  • other: ischaemic colitis, hyperthermia, metabolic acidosis, rhabdomyolysis
31
Q

Management cocaine toxicity:

A
  • benzodiazepines
  • chest pain: benzo + GTN
  • HTN: benzo + sodium nitroprusside
32
Q

Who should not take diclofenac:

A
  • IHD
  • peripheral arterial disease
  • cerebrovascular disease
  • congestive heart failure
33
Q

How does digoxin work and how should you monitor it?

A
  • decreases conduction through AV node which slows ventricular rate in AF and flutter
  • increases force of cardiac muscle contraction due to Na/K ATPase inhibition
  • stimulates vagus nerve
  • narrow therapeutic index
  • not monitored routinely
  • in toxicity - digoxin concentrations should be measured within 8-12 hours of the last dose
34
Q

Features of digoxin toxicity:

A
  • generally unwell, lethargy, n&v, anorexia, confusion, yellow-green vision
  • arrhythmias
  • gynaecomastia
35
Q

Precipitating factors digoxin toxicity:

A
  • hypokalaemia
  • increasing age
  • renal failure
  • myocardial ischaemia
  • hypomagnesaemia, hypercalcaemia, hypernatraemia, acidosis
  • hypoalbuminaemia
  • hypothermia
  • hypothyroidism
  • drugs: amiodarone, quinidine, verapamil, diltiazem, spironolactone, circlosporin, thiazides and loop diuretics
36
Q

Management of digoxin toxicity:

A
  • digibind
  • correct arrhythmias
  • monitor potassium
37
Q

Dopamine receptor agonist indications:

A
  • Parkinson’s
  • prolactinoma/galactorrhoea
  • cyclical breast disease
  • acromegaly
38
Q

Dopamine receptor agonist examples and ADR:

A
  • bromocriptine, ropinirole, cabergoline, apomorphine
  • ergot-derived associated with pulmonary, retroperitoneal and cardiac fibrosis
  • ADR: nausea and vomiting, postural hypotension, hallucination, daytime somnolence
39
Q

Drugs causing urticaria:

A
  • aspirin
  • penicillins
  • NSAIDs
  • opiates
40
Q

Statin monitoring:

A

LFTs at baseline, 3 months and 12 months

41
Q

ACEi monitoring:

A

U&E prior to treatment, after increasing and at least anually

42
Q

Amiodarone monitoring:

A
  • TFT, LFT , U&E prior

- TFT, LFT every 6 months

43
Q

Methotrexate monitoring:

A

FBC, LFT, U&E every 2-3 months

44
Q

Azathioprine monitoring:

A
  • FBC, LFT prior
  • FBC weekly for first 4 weeks
  • FBC, LFT every 3 months
45
Q

Lithium monitoring:

A
  • TFT, U&E prior
  • Lithium levels weekly until stable, then every 3 months
  • TFT, U&E every 6 months
46
Q

Sodium valproate monitoring:

A
  • LFT, FBC prior

- LFT during first 6 months

47
Q

Glitazone monitoring:

A
  • LFT prior to treatment

- LFT regularly during treatment

48
Q

Drugs causing impaired glucose intolerance:

A
  • thiazides, furosemide
  • steroids
  • tacrolimus, ciclosporin
  • interferon-alpha
  • nicotinic acid
  • antipsychotics
  • beta blockers slightly
49
Q

Drugs causing thrombocytopenia:

A
  • quinine
  • abciximab
  • NSAIDs
  • diuretics: furosemide
  • antibiotics: penicillins, sulphonamides, rifampicin
  • carbamazepine, valproate
  • heparin
50
Q

Drugs causing urinary retention:

A
  • TCA e.g. amitriptyline
  • anticholinergics
  • opioids
  • NSAIDs
  • disopyramide
51
Q

Should aspirin be stopped before dental procedures?

A

no - continue to take anti-platelets as normal

Pharmacology (4 decks)

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