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Focused 1 > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Drugs causing lung fibrosis?

A
  1. Amiodarone
  2. Anti-rheumatoid = Methotrexate, sulfasalazine
  3. Cytotoxic = busulphan, bleomycin
  4. Ergot-derived dopamine receptor agonists = bromocriptine, cabergoline, pergolide
  5. Nitrofurantoin
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2
Q

Most common feature of CO poisoning?

A

Headache

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3
Q

Features of CO toxicity?

A
  1. Headache
  2. N&V
  3. Vertigo
  4. Confusion
  5. Subjective weakness
  6. Severe toxicity = pink skin and toxicity, hyperpyrexia, arrhythmias, extrapyramidal features, coma, death
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4
Q

Typical carboxyhaemoglobin level?

A
  1. <3% non-smokers
  2. <10% smokers
  3. 10-30% symptomatic = headache, vomiting
  4. > 30% severe toxicity
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5
Q

CO poisoning Rx?

A
  1. 100% high flow O2 via non-rebreather mask (min 6h, target SpO2 100%, Rx until all symptoms resolved)
  2. Hyperbaric oxygen (if LOC at any point, neurological signs, myocardial ischaemia/arrhythmia, pregnancy)
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6
Q

TB drugs?

A

Rifampicin
Isoniazid
Pyrazinamide
Ethambutol

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7
Q

Rifampicin mushkies?

A
  1. MOA = inhibits bacterial DNA dependent RNA polymerase, preventing transcription of DNA into mRNA
  2. Potent liver enzyme inducer
  3. Hepatitis, orange secretions
  4. Flu-like symptoms
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8
Q

Isoniazid mushkies?

A
  1. MOA = inhibits mycolic acid synthesis
  2. Peripheral neuropathy = prevent with pyridoxine (Vitamin B6)
  3. Hepatitis, agranulocytosis
  4. Liver enzyme inducer
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9
Q

Pyrazinamide mushkies?

A
  1. MOA = converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I
  2. Hyperuricaemia causing gout
  3. Arthralgia, myalgia
  4. Hepatitis
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10
Q

Ethambutol mushkies?

A
  1. MOA = inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan
  2. Optic neuritis = check visual acuity before and during treatment
  3. Dose needs adjusting in patients with renal impairment
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11
Q

Metformin MOA?

A
  1. Activation of AMP-activated protein kinase
  2. Increases insulin sensitivity
  3. Decreases hepatic gluconeogenesis
  4. May reduce gastrointestinal absorption of carbohydrates
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12
Q

Metformin s/e?

A
  1. GI upset intolerable in 20% (nausea, anorexia, diarrhoea)
  2. Reduced Vitamin B12 absorption (rarely a clinical problem)
  3. Lactic acidosis with severe liver disease or renal failure
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13
Q

Metformin contraindications?

A
  1. CKD eGFR <30 or Cr > 150
  2. Lactic acidosis during period where there is tissue hypoxia
  3. Iodine-containing X-ray contrast media (discontinue metformin on day of procedure and 48h after)
  4. Alcohol abuse is a relative contraindication
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14
Q

Starting metformin mushkies?

A
  1. Titrated up slowly to reduce incidence of GI side effects
  2. If pts develop unacceptable s/e then modified-release metformin should be considered
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15
Q

Verapamil mushkies?

A
  1. Angina, hypertension, arrhythmias
  2. Highly negatively inotropic
  3. Should not be given with beta blocker as may cause heart block
  4. S/e = HF, constipation, hypotension, bradycardia, flushing
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16
Q

Diltiazem mushkies?

A
  1. Angina, hypertension
  2. Less negatively inotropic than verapamil but caution should still be exercised when patients have heart failure or are taking beta-blockers
  3. S/e = hypotension, bradycardia, HF, ankle swelling
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17
Q

Nifedipine, amlodipine, felodipine mushkies

A
  1. Dihydropyridines
  2. Hypertension, angina, Raynaud’s
  3. Affects the peripheral vascular smooth muscle more than the myocardium and therefore do not result in worsening of HF but may therefore may cause ankle swelling
  4. Flushing, headache, ankle swelling
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18
Q

Amiodarone s/e?

A
  1. Thyroid (hyper and hypo)
  2. Lung fibrosis
  3. Liver fibrosis
  4. Corneal deposits
  5. Peripheral neuropathy/myopathy
  6. Photosensitivity
  7. Slate-grey appearance
  8. Thrombophlebitis and injection site reactions
  9. Bradycardia
  10. Lengthens QTi
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19
Q

Important amiodarone interactions?

A
  1. Decreased metabolism of warfarin, therefore increased INR
  2. Increased Digoxin levels
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20
Q

Statin monitoring?

A

LFTS at baseline, 3m, 12m

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21
Q

ACEi monitoring?

A

U&E prior to treatment, after increasing dose, annually

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22
Q

Amiodarone monitoring?

A
  1. TFT, LFT U&E, CXR prior
  2. TFT, LFT every 6m
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23
Q

Methotrexate monitoring?

A

FBC, U&E, LFTs = before starting, weekly until therapy established, then every 2-3 months

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24
Q

Azathioprine monitoring?

A
  1. FBC and LFT before
  2. FBC weekly for first 4w
  3. FBC, LFT every 3m
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25
Q

Lithium monitoring?

A
  1. U&E, TFT prior to treatment
  2. Lithium weekly until stabilised then every 3m
  3. TFT, U&E every 6m
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26
Q

Sodium valproate monitoring?

A
  1. FBC, LFT before treatment
  2. LFT ‘periodically’ during first 6m
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27
Q

Glitazone monitoring?

A
  1. LFT before
  2. LFT ‘regularly’ during treatment
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28
Q

PDE5 inhibitor MOA?

A

Cause vasodilation through an increase in cGMP leading to smooth muscle relaxation in blood vessels supplying the corpus cavernosum

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29
Q

PDE5 inhibitor examples?

A
  1. Sildafenil - Viagra = short acting, usually taken 1 hour before sexual activity
  2. Tadalafil = Cialis = Longer acting than sildafenil, may be taken on regular basis eg. OD
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30
Q

PDE5 inhibitor indications?

A

Erectile dysfunction and Pulmonary HTN

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31
Q

PDE5i contraindications?

A
  1. Nitrates and nicorandil
  2. Hypotension
  3. Recent stroke or MI (NICE recommend waiting 6m)
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32
Q

PDE5i s/e?

A
  1. Visual disturbances = blue discolouration, non-arteritic anterior ischaemic neuropathy
  2. Nasal congestion
  3. Flushing
  4. GI side effects
  5. Headache
  6. Priapism
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33
Q

What is HRT?

A

Involves the use of a small dose of oestrogen, combined with a progestogen (in women with a uterus), to help alleviate menopausal symptoms

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34
Q

HRT indications?

A
  1. Vasomotor symptoms e.g. flushing, insomnia, headaches = most important factor in choosing whether to start, other indications such as reversal of vaginal atrophy should be treated with other agents as first line therapies
  2. Premature menopause = should be continued until age of 50 years, most important reason in giving HRT to younger women is preventing the development of osteoporosis
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35
Q

HRT choice of hormone?

A
  1. Oestrogens = ‘natural’ oestrogens such as estradiol, estrone and conjugated oestrogen are generally used rather than synthetic oestrogens such as ethinylestradiol (which is used in the combined oral contraceptive pill)
  2. Progestogens = ‘synthetic’ progestogens such as medroxyprogesterone, norethisterone, levonorgestrel, and drospirenone are usually used. a levonorgestrel-releasing intrauterine system (e.g. Mirena) may be used as the progestogen component of HRT, i.e. a woman could take an oral oestrogen and have endometrial protection using a Mirena coil
  3. Tibolone = synthetic compound with both oestrogenic, progestogenic, and androgenic activity
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36
Q

HRT route?

A
  1. Can be taken orally or transdermally (via a patch or gel)
  2. Transdermal is preferred if the woman is at risk of venous thromboembolism (VTE), as the rates of VTE do not appear to rise with transdermal preparations
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37
Q

Why do you need to give progesterone if still have a uterus?

A

Unopposed oestrogen can increase risk of endometrial cancer

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38
Q

Cyclical combined HRT indication?

A

If their LMP was less than 1 year ago

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39
Q

Continuous combines HRT indication?

A
  1. If taken cyclical combined for at least 1 year or
  2. It has been at least 1 year since their LMP or
  3. It has been at least 2 years since their LMP if they have had a premature menopause
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40
Q

Premature menopause age?

A

< 40 y/o

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41
Q

Vasomotor symptom control if unwilling to take HRT?

A
  1. SSRI
  2. SNRI
  3. Clonidine
  4. Gabapentin
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42
Q

Cytochrome P450 enzyme induces?

A

PC BRASSS
1. Phenytoin
2. Carbamazepine
3. Barbiturates
4. Rifampicin
5. Alcohol (chronic)
6. Sulfonylureas
7. St John’s Wort
8. Smoking

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43
Q

Cytochrome P450 enzyme inhibitors?

A

AO DEVICES GR
1. Allopurinol, antifungals, amiodarone
2. Omeprazole
3. Disulfiram
4. Erythromycin
5. Valproate
6. Isoniazid
7. Clarithromycin, ciprofloxacin
8. Ethanol (acute)
9. Sulphonamides, SSRIs
10. Grapefruit juice
11. Ritonavir

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44
Q

Yellow-green vision?

A

Digoxin

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45
Q

Gentamicin s/e?

A
  1. Ototoxocity = due to auditory or vestibular nerve damage
  2. Irreversible
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46
Q

Nephrotoxocity s/e?

A
  1. Accumulates in renal failure
  2. This toxicity is secondary to ATN
  3. Concomitant use of furosemide increases risk
  4. Lower doses and more frequent monitoring is required
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47
Q

Gentamicin C/I?

A

Myasthenia gravis (can cause clinically significant muscle weakness in myasthenia patients resulting in respiratory depression)

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48
Q

Gentamicin dosing?

A
  1. Peak (1 hour after administration) and trough levels (just before the next dose) are measured
  2. If the trough (pre-dose) level is high the interval between the doses should be increased
  3. If the peak (post-dose) level is high the dose should be decreased
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49
Q

What classically predisposed to digoxin toxicity?

A

Hypokalaemia

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50
Q

Digoxin MOA?

A
  1. Cardiac glycoside
  2. Mainly used for rate control in AF
  3. As has positive inotropic properties sometimes used for improving symptoms, but not mortality, in pts with HF
  4. Decreases conduction through AVN which slows the ventricular rate in AF and flutter
  5. Increases force of cardiac muscle contraction due to inhibition of the Na/K ATPase, also stimulates vagus nerve
  6. Has a narrow therapeutic index
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51
Q

Digoxin monitoring?

A
  1. Not monitored routinely, except in suspected toxicity
  2. If toxicity is suspected, digoxin concentrations should be measured within 8-12 hours of the last dose
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52
Q

Digoxin toxicity plasma concentration?

A

Plasma concentration alone does not determine whether a patient has developed digoxin toxicity. Toxicity may occur even when the concentration is within the therapeutic range. The BNF advises that the likelihood of toxicity increases progressively from 1.5 to 3 mcg/l.

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53
Q

Digoxin toxicity features?

A
  1. Generally unwell, lethargy, N&V, anorexia, confusion, yellow-green vision
  2. Arrhythmias (AV block, bradycardia)
  3. Gynaecomastia
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54
Q

Precipitating factor for digoxin toxicity?

A
  1. Hypokalaemia
  2. Age
  3. Renal failure
  4. MI
  5. Hypo = magnesium, albumin, thermia, thyroidism
  6. Hyper = calcium, sodium, acidosis
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55
Q

Digoxin toxicity management?

A
  1. Digibind
  2. Correct arrhythmias
  3. Monitor potassium
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56
Q

Finasteride indications?

A
  1. BPH
  2. Male-pattern baldness
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57
Q

Finasteride s/e?

A
  1. Impotence
  2. Decreased libido
  3. Ejaculation disorders
  4. Gynaecomastia and breast tenderness
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58
Q

Finasteride effect on PSA?

A

Lowers it

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59
Q

Abx contraindicated in pregnancy?

A
  1. Tetracyclines
  2. Aminoglycosides
  3. Sulphonamides and trimethoprim
  4. Quinolones
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60
Q

Drugs contraindicated in pregnancy?

A
  1. ACEi, ARB
  2. Statins
  3. Warfarin
  4. Sulfonylureas
  5. Retinoids (including topical)
  6. Cytotoxic agents
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61
Q

ACEi teratogen?

A
  1. Renal dysgenesis
  2. Craniofacial abnormalities
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62
Q

Alcohol teratogen?

A

Craniofacial abnormality

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63
Q

Aminoglycoside teratogen?

A

Ototoxicity

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64
Q

Carbamazepine teratogen?

A
  1. Neural tube defects
  2. Craniofacial abnormalities
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65
Q

Chloramphenicol teratogen?

A

‘Grey baby’ syndrome

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66
Q

Cocaine teratogen?

A
  1. IUGR
  2. Preterm labour
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67
Q

Diethylstilbesterol teratogen?

A

Vaginal clear cell adenocarcinoma

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68
Q

Lithium teratogen?

A

Ebstein’s anomaly (atrialisation of the RV)

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69
Q

Maternal DM teratogen?

A
  1. Macrosomia
  2. NTDs
  3. Polyhydramnios
  4. Preterm labour
  5. Caudal regression syndrome
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70
Q

Smoking teratogen?

A
  1. IUGR
  2. Preterm labour
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71
Q

Tetracycline teratogen?

A

Discoloured teeth

72
Q

Thalidomide teratogen?

A

Limb reduction defects

73
Q

Valproate teratogen?

A
  1. NTD
  2. Craniofacial abnormalities
74
Q

Warfarin teratogen?

A

Craniofacial abnormalities

75
Q

P450 system Isoniazid?

A

Isoniazid inhibits

76
Q

How slowly should metformin be titrated?

A

At least 1 week before increasing dose to reduce risk of developing GI side effects

77
Q

St John’s Wort mushkies?

A
  1. Shown to be as effective as TCAs in the treatment of mild-moderate depression
  2. MOA = similar to SSRIs (although SNRI also been demonstrated)
78
Q

St John’s Wort adverse effects?

A
  1. Can cause serotonin syndrome
  2. Inducer of P450 system, therefore decreased levels of drugs such as warfarin, ciclosporin. The effectiveness of the combined oral contraceptive pill may also be reduced
79
Q

Drugs causing corneal opacities?

A

Amiodarone and Indomethacin

80
Q

Drug causing cataracts?

A

Steroids

81
Q

Drugs causing optic neuritis?

A
  1. Ethambutol
  2. Amiodarone
  3. Metronidazole
82
Q

Drugs causing retinopathy?

A
  1. Chloroquine
  2. Quinine
83
Q

Beta blocker overdose Rx?

A
  1. If bradycardic then atropine
  2. In resistant cases glucagon may be used
84
Q

Drugs causing photosensitivity?

A
  1. Thiazides
  2. Tetracyclines, sulphonamides, ciprofloxacin
  3. Amiodarone
  4. NSAIDs e.g. piroxicam
  5. Psoralens
  6. Sulphonylureas
85
Q

Aspirin OD bloods?

A

Mixed respiratory alkalosis and metabolic acidosis

86
Q

Aspirin OD features?

A
  1. Hyperventilation (centrally stimulated respiration)
  2. Tinnitus
  3. Sweating, pyrexia
  4. N&V
  5. Hyper and hypoglycaemia
  6. Seizures
  7. Coma
87
Q

Salicylate OD Rx?

A
  1. General = ABC, charcoal
  2. Urinary alkalinisation with IV sodium bicarbonate = enhances elimination of aspirin in urine
  3. Haemodialysis
88
Q

Indications for haemodialysis in salicylate OD?

A
  1. Serum concentration >700mg/L
  2. Metabolic acidosis resistant to treatment
  3. Acute renal failure
  4. Pulmonary oedema
  5. Seizures
  6. Coma
89
Q

Cocaine MOA?

A

Blocks uptake of DA, NA, and HT

90
Q

Cocaine effect classification?

A
  1. Cardiovascular = coronary artery spasm, tachycardia and bradycardia, hypertension, QRS widening and QT prolongation, aortic dissection
  2. Neurological = seizures, mydriasis, hypertonia, hyperreflexia
  3. Psychiatric = agitation, psychosis, hallucinations
  4. Others = ischaemic colitis, hyperthermia, metabolic acidosis, rhabdomyolysis
91
Q

Cocaine toxicity Rx?

A
  1. Benzodiazepines
  2. Chest pain = Benzodiazepines + GTN, if MI develops then primary PCI
  3. HTN = Benzodiazepines + Sodium nitroprusside
92
Q

When should NAC be given for Paracetamol OD?

A
  1. If staggered overdose or there is doubt over time of the paracetamol ingestion, regardless of the plasma paracetamol concentration
  2. If the plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity
93
Q

NAC administration mushkies?

A
  1. Infused over 1 hour to reduce risk of s/e
  2. Commonly causes an anaphylactoid reaction (non-IgE mediated mast cell release) –> stop infusion and restart at a slower rate
94
Q

King’s College Hospital criteria for liver transplantation (paracetamol liver failure)?

A
  1. Arterial pH < 7.3, 24 hours after ingestion
  2. Or all of the following = PT > 100s, Cr > 300, Grade III/IV encephalopathy
95
Q

Staggered OD definition?

A

If all the tablets were not taken within 1 hour

96
Q

When should plasma paracetamol levels be taken?

A

Minimum of 4 hours after ingestion

97
Q

Aspirin MOA?

A

Aspirin works by blocking the action of both cyclooxygenase-1 and 2. Cyclooxygenase is responsible for prostaglandin, prostacyclin and thromboxane synthesis. The blocking of thromboxane A2 formation in platelets reduces the ability of platelets to aggregate which has lead to the widespread use of low-dose aspirin in cardiovascular disease.

98
Q

Aspirin indication?

A

First line for all pts with IHD

99
Q

Aspirin potentiates?

A
  1. Oral hypoglycaemics
  2. Warfarin
  3. Steroids
100
Q

First line Rx following ischaemic stroke and PAD?

A

Clopidogrel (although NICE still states aspirin + dipyridamole)

101
Q

Most common s/e of sildafenil?

A

Headache

102
Q

Drug-induced thrombocytopenia?

A
  1. Quinine
  2. Abciximab
  3. NSAIDs
  4. Furosemide
  5. Abx = penicillins, sulphonamides, rifampicin
  6. Anticonvulsants = carbamazepine, valproate
  7. Heparin
103
Q

Adrenaline indications?

A

Anaphylaxis and cardiac arrest

104
Q

Anaphylaxis adrenaline dose?

A

0.5ml 1:1000 IM

105
Q

Cardiac arrest adrenaline dose?

A
  1. 10ml 1:10,000 IV
  2. 1ml 1:1000 IV
106
Q

Management of accidental injection of adrenaline?

A

Local infiltration of phentolamine

107
Q

Adrenaline actions on alpha adrenergic receptors?

A
  1. Inhibits insulin secretion by pancreas
  2. Stimulates glycogenolysis in the liver and muscle
  3. Stimulates glycolysis in myscle
108
Q

Adrenaline action on beta adrenergic receptor?

A
  1. Stimulates glucagon secretion in the pancreas
  2. Stimulates ACTH
  3. Stimulates lipolysis by adipose tissue
109
Q

Drugs causing urinary retention?

A
  1. TCAs = Amitryptiline
  2. Anticholinergics = antipsychotics, antihistamines
  3. Opioids
  4. NSAIDs
  5. Disopyramide
110
Q

Opioid OD Rx?

A

Naloxone

111
Q

Benzodiazepine OD Rx?

A
  1. Majority are managed with supportive care only due to risk of seizures with flumazenil
  2. It is generally only used with severe or iatrogenic doses
112
Q

TCA OD Rx?

A
  1. IV bicarbonate may reduce risk of seizures and arrhythmias in severe toxicity
  2. Dialysis
113
Q

Lithium OD Rx?

A
  1. Mild-moderate toxicity may respond to volume resuscitation with normal saline
  2. Haemodialysis may be needed in severe toxicity
  3. Sodium bicarbonate is ometimes used but there is limited evidence to support this. By increasing the alkalinity of the urine it promotes lithium excretion
114
Q

Warfarin OD Rx?

A

Vitamin K, PCC

115
Q

Heparin OD Rx?

A

Protamine sulphate

116
Q

BB OD Rx?

A
  1. If bradycardic then atropine
  2. In resistant cases glucagon may be used
117
Q

Ethylene glycol OD Rx?

A
  1. Fomepizole first line
  2. Ethanol
  3. Haemodialysis in refractory cases
118
Q

Methanol OD Rx?

A
  1. Fomepizole or ethanol
  2. Haemodialysis
119
Q

Organophosphate poisoning Rx?

A
  1. Atropine
  2. Role of pralidoxime unclear
120
Q

Iron OD Rx?

A

Desferrioxamine

121
Q

Lead OD Rx?

A
  1. Dimercaprol
  2. Calcium edetate
122
Q

Cyanide OD Rx?

A
  1. Hydroxocobalamin
  2. Combination of amyl nitrite, sodium nitrite and sodium thiosulfate
123
Q

Sulfonylurea side effect?

A
  1. Hypoglycaemic episodes
  2. Increased appetite and weight gain
  3. SIADH
  4. Liver dysfunction (cholestatic)
124
Q

Glitazone s/e?

A
  1. Weight gain
  2. Fluid retention
  3. Liver dysfunction
  4. Fractures
125
Q

Gliptins s/e?

A

Pancreatitis

126
Q

Features of opioid misuse?

A
  1. Rhinorrhoea
  2. Needle track marks
  3. Pinpoint pupils
  4. Drowsiness
  5. Watering eyes
  6. Yawning
127
Q

Rx of opioid dependence?

A
  1. Specialist drug dependence clinics/GPSI
  2. Maintenance therapy or detoxification
  3. Methadone or buprenorphine first line in detox
  4. Compliance monitored using urinalysis
  5. Detoxification should last up to 4 weeks in an inpatient/residential setting and up to 12 weeks in the community
128
Q

When is diclofenac contraindicated?

A
  1. IHD
  2. PAD
  3. Cerebrovascular disease
  4. Congestive HF
    This advice does not apply to topical diclofenac
129
Q

Lithium toxicity precipitants?

A
  1. Dehydration
  2. Renal failure
  3. Drugs = diuretics (esp. thiazides), ACEi, ARBs, NSAIDs, Metronidazole
130
Q

Lithium toxicity features?

A
  1. Coarse tremor (fine tremor seen in therapeutic levels)
  2. Hyperreflexia
  3. Confusion
  4. Polyuria
  5. Seizure
  6. Coma
131
Q

Mefloquine use?

A

Prophylaxis and treatment of certain types of malaria

132
Q

Mefloquine mushkies?

A
  1. Nightmares or anxiety may be prodromal of a more serious neuropsychiatric effect
  2. Suicide and DSH have been reported
  3. Adverse reactions may continue for several months
  4. Should not be used in pts with Hx of anxiety, depression, schizophrenia or other psychiatric disorders
133
Q

Which TB medication can cause gout?

A

Pyrazinamide

134
Q

Which TB medication can cause rash?

A

Ethambutol

135
Q

Is routine digoxin monitoring required?

A

No, only in suspected toxicity, which if suspected should be measured 8-12 hours since last dose

136
Q

Amoxicillin s/e?

A

Rash with infectious mononucleosis

137
Q

Co-amoxiclav s/e?

A

Cholestasis

138
Q

Flucloxacillin s/e?

A

Cholestasis (usually develops several weeks after use)

139
Q

Erythromycin s/e?

A
  1. GI upset
  2. Prolongs QTi
140
Q

Ciprofloxacin s/e?

A
  1. Lowers seizure threshold
  2. Tendonitis
141
Q

Metronidazole s/e?

A

Reaction following alcohol ingestion

142
Q

Doxycycline s/e?

A

Photosensitivity

143
Q

Trimethoprim s/e?

A
  1. Rashes, including photosensitivity
  2. Pruritis
  3. Suppression of haematopoiesis
144
Q

Allopurinol MOA?

A

Inhibits xanthine oxidase

145
Q

Initiating allopurinol prophylaxis?

A
  1. Commencement of ULT (urate lowering therapy) is best delayed until inflammation has settled as ULT is better discussed when the patient is not in pain
  2. Initial dose of 100 mg od, with the dose titrated every few weeks to aim for a serum uric acid of < 300 µmol/l. Lower initial doses should be given if the patient has a reduced eGFR
  3. Colchicine cover should be considered when starting allopurinol. NSAIDs can be used if colchicine cannot be tolerated. The BSR guidelines suggest this may need to be continued for 6 months
146
Q

Allopurinol indication?

A
  1. To all patients after first attack of gout
  2. Particularly recommended if: >=2 attacks in 12 months, tophi, renal disease, uric acid renal stones, prophylaxis if on cytotoxics or diuretics
  3. Pts with Lesch-Nyhan syndrome for life
147
Q

Allopurinol adverse effects?

A
  1. Severe cutaneous adverse reaction (SCAR)
  2. DRESS
  3. Stevens-Johnson Syndrome
148
Q

Allopurinol indications?

A
  1. Azathioprine = can lead to very high levels of 6-mercaptopurine, a 25% dose must therefore be used if the combination cannot be avoided
  2. Cyclophosphamide = reduces renal clearance, therefore may cause marrow toxicity
  3. Theophylline = increases plasma conc of theophylline by inhibiting its breakdown
149
Q

What medications can exacerbate HF?

A
  1. Thiazolidinediones e.g. pioglitazone c/i as it causes fluid retention
  2. Verapamil = -ve inotropic effect
  3. NSAIDs/glucocorticoids = can cause fluid retention
  4. Class I antiarryhthmics = fleicanide (negative inotropic and proarryhthmic effect)
150
Q

Metformin renal consideration?

A

NICE recommend that the dose of metformin should be reviewed if the creatinine is > 130 micromol/l (or eGFR < 45 ml/min) and stopped if the creatinine is > 150 micromol/l (or eGFR < 30 ml/min)

151
Q

Ecstasy (MDMA) poisoning features?

A
  1. Neurological = agitation, anxiety, confusion, ataxia
  2. CVS = tachycardia, hypertension
  3. Hyponatraemia
  4. Hyperthermia
  5. Rhabdomyolysis
152
Q

Ecstasy OD management?

A
  1. Supportive
  2. Dantrolene may be used for hyperthermia if simple measures fail
153
Q

Amiodarone thyroid dysfunction prevalence?

A

1 in 6 pts taking amiodarone

154
Q

Amiodarone induced hypothyroidism mushkies?

A

The pathophysiology of amiodarone-induced hypothyroidism (AIH) is thought to be due to the high iodine content of amiodarone causing a Wolff-Chaikoff effect. Amiodarone may be continued if this is desirable

155
Q

Amiodarone induced thyrotoxicosis types?

A
  1. AIT Type I = Excess iodine-induced thyroid hormone synthesis, goitre present, Rx with carbimazole or potassium perchlorate
  2. AIT Type II = Amiodarone-related destructive thyroiditis, goitre absent, Rx with corticosteroids
  3. Unlike in AIH, amiodarone should be stopped if possible in patients who develop AIT
156
Q

What is the Wolff-Chaikoff effect?

A

An autoregulatory phenomenon where thyroxine formation is inhibited due to high levels of circulating iodide

157
Q

Why avoid nitrofurantoin in pts with CKD Stage II or higher?

A

Significant risk of treatment failure and occurrence of side effects due to drug accumulation

158
Q

Drugs to avoid in renal failure?

A
  1. Abx = tetracyclines, nitrofurantoin
  2. NSAIDs
  3. Lithium
  4. Metformin
159
Q

Quinolone MOA?

A

Inhibit DNA synthesis (inhibit topoisomerase II (DNA gyrase) and topoisomerase IV) and are bactericidal in nature, e.g. ciprofloxacin and levofloxacin

160
Q

Quinolone adverse effects?

A
  1. Lowers seizure threshold in pts with epilepsy
  2. Tendon damage incl. rupture
  3. Cartilage damage in animal models (therefore generally avoided in children)
  4. Prolongs QTi
161
Q

Quinolone contraindications?

A
  1. Avoided in pregnant/breastfeeding women
  2. Avoid in G6PD
162
Q

Macrolide MOA?

A

Post-transcriptional methylation of the 23S bacterial ribosomal RNA. Macrolides act by inhibiting bacterial protein synthesis by blocking translocation. If pushed to give an answer they are bacteriostatic in nature, but in reality this depends on the dose and type of organism being treated.

163
Q

Macrolide examples?

A

Erythromycin, clarithromycin, azithromycin

164
Q

Macrolide adverse effects?

A
  1. QT prolongation
  2. GI s/e (nausea less common with clarithromycin than erythromycin)
  3. Cholestatic jaundice
  4. P450 inhibitor
  5. Azithromycin associated with hearing loss and tinnitus
165
Q

Macrolide common interaction?

A

Statins - should be stopped whilst taking a course of macrolides. Macrolides inhibit the cytochrome P450 isoenzyme CYP3A4 that metabolises statins. Taking macrolides concurrently with statins significantly increases the risk of myopathy and rhabdomyolysis

166
Q

Tamoxifen adverse effects?

A
  1. Menstrual disturbance = vaginal bleeding, amenorrhoea
  2. Hot flushes = 3% stop taking due to climacteric s/e
  3. VTE
  4. Endometrial cancer
167
Q

How long is tamoxifen usually used for?

A

For 5 years following removal of the tumour

168
Q

Sildafenil and stroke?

A

Contraindication = recent stroke or MI –> NICE recommend waiting 6m

169
Q

ACEi s/e?

A

Cough and hyperkalaemia

170
Q

Bendroflumethiazide s/e?

A
  1. Gout
  2. Hypokalaemia, hyponatraemia
  3. Impaired glucose tolerance
171
Q

Calcium channel blocker s/e?

A
  1. Headache
  2. Flushing
  3. Ankle oedema
172
Q

BB s/e?

A
  1. Bronchospasm (especially in asthmatics)
  2. Fatigue
  3. Cold peripheries
173
Q

Doxazosin s/e?

A

Postural hypotension

174
Q

If metformin not tolerated due to GI side effects?

A

Try a modified release formulation

175
Q

Vancomycin class?

A

Glycopeptide

176
Q

Tetracycline s/e?

A

Phototoxicity and IIH

177
Q

Carbamazepine P450 enzyme?

A

An inducer of the P450 –> increases the metabolism of itself = auto-induction

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