Pharmacology Flashcards

1
Q

Which antibiotics act on the 30s Ribosome?

A

Aminoglycosides, tetracyclines, tigecycline

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2
Q

Which antibiotics act on the 50s ribosome?

A

Chloramphenicol, clindamycin, linezolid, macrolides, streptogramins

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3
Q

Which antibiotics act on the metabolic pathways (aka folate synthesis)?

A

Sulphonamides, trimethoprim

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4
Q

Which antibiotics act on nucleic acid synthesis?

A

Fluoroquinolones, metronidazole, rifamycins

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5
Q

Which antibiotics act on membrane stability?

A

Polymyxin, daptomycin

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6
Q

Which antibiotics act on cell wall synthesis?

A

Beta-lactams (penicillin’s, cephalosporins, carbapenems, monobactams), bacitracin, glycopeptides

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7
Q

What are the SEs of drinking alcohol whilst taking metronidazole? How long should you wait after finishing a course before drinking?

A

N+V, skin flushing, headaches, abdo pain, tachycardia.
48 hours.

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8
Q

Ciprofloxacin and levofloxacin are what class of antibiotic?

A

Fluoroquinolones: act on nucleic acid synthesis.

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9
Q

Why is nitrofurantoin CI in G6PD pts?

A

Can trigger a haemolytic crisis

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10
Q

Why do pts on long term nitrofurantoin require lung function monitoring?

A

Can cause pulmonary fibrosis with long-term use.

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11
Q

Under what eGFR is nitrofurantoin CI? What should you give instead?

A

<45: give them trimethoprim

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12
Q

Why does trimethoprim cause a false rise in creatinine? What electrolyte may rise?

A

It competes with creatinine for excretion in the kidney causing it to rise in the absence of AKI.
K+ can also go up: this is true do not ignore.

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13
Q

What is co-trimoxazole a combination of? What are the possibly drug reactions?

A

Trimethoprim and sulfamethoxazole.
ADRs: pancreatitis, nephrotoxicity, haemolysis in G6PD pts.

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14
Q

Gentamicin is what type of antibiotic? What should be measured between 18-24 hours after dose? How does this affect management?

A

Aminoglycosides: measure trough levels.
If trough is high increase time between doses, if peak is high decrease dose.

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15
Q

What is a key SE of gentamicin?

A

Ototoxicity

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16
Q

How does demeclocycline (tetracycline) affect the collecting duct?

A

Decreases responsiveness to ADH (nephrogenic DI)

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17
Q

What is 1st line for cholera?

A

Doxycycline

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18
Q

What macrolide is associated with dyspepsia?

A

Clarithromycin.

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19
Q

In the case of ESBL producing bacteria, which antibiotic should be used?

A

Carbepenems such as meropenem

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20
Q

How might co-amoxiclav affect LFTS?

A

ALP, bilirubin and transaminases may be raised

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21
Q

What is 1st line for septic arthritis?

A

Flucloxacillin IV: good penetration of joints and treats staph.A which is the most common cause

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22
Q

At what point do you measure the trough levels of vancomycin? How does this affect doasage?

A

From the 3rd dose: if too low increase dose, if too high increase time between doses

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23
Q

What route is vancomycin given by?

A

IV unless treating C.Diff

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24
Q

When do you measure teicoplanin trough levels?

A

6-8 days after starting so less relevant to those on short courses.

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25
Q

What are the side effects of isoniazid?

A

peripheral neuropathy, liver toxicity

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26
Q

Why would someone who has been treated with chloramphenicol present with bleeding/bruising and recurrent illness?

A

Chloramphenicol can cause aplastic anaemia and other blood dyscrasias.

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27
Q

What are the side effects of rifampicin?

A

Orange secretions, haemolysis, p450 inducer, liver toxicity

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28
Q

What are the side effects of ethambutol?

A

loss of visual acuity, colour blindness (especially red and green), kidney toxicity,

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29
Q

What are the side effects of pyrazinamide?

A

Most likely (out of TB drugs) to cause liver toxicity, hyperuricaemia (>7), arthralgia, can trigger gout

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30
Q

What is first line for athlete’s foot?

A

Terbinafine

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31
Q

What is the MOA of oseltamivir? When is it used?

A

Neuraminidase inhibitor used to help the sx of flu in pts with significant comorbidities.

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32
Q

Diarrhoea is a SE of which commonly used T2DM medication?

A

Metformin

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33
Q

How do sulfonylureas work? What is a major SE?

A

Stimulate the release of insulin from beta cells. Therefore can cause hypoglycaemia.
‘zides’ e.g., glipizide

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34
Q

Pioglitazone is is associated with what SE which leads to SOB?

A

Fluid retention

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35
Q

What is 1st line for diabetic neuropathy?

A

Pregabalin, duloxetine, or gabapentin.

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36
Q

How do manage insulin dosage in pts around surgery?

A

stop short acting insulin once pt is NBM, continue long acting at a reduced rate such as 80%.

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37
Q

How do you manage a severe hypoglycaemic episode where the pt is unconscious and you have IV access?

A

100ml of 20ml glucose

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38
Q

How do you manage a severe hypoglycaemic episode where the pt is unconscious and you DO NOT have IV access?

A

IM glucagon

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39
Q

How do you manage a hypoglycaemic episode where the pt is conscious?

A

Buccal gluogel if not able to eat or any fast acting carb if they can eat

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40
Q

What is the difference between a mineralocorticoid and a glucocorticoid?

A

M: mimic aldosterone, regulate blood volume and pressure.
G: mimic cortisol, aka corticosteroids, regulate immune cells and glucose response

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41
Q

Long-term effects of steroids?

A

Osteoporosis, aseptic joint necrosis, adrenal insufficiency, gastro/hepatic/ophthalmological effects, hyperlipidaemia, growth suppression.

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42
Q

Corticosteroids can cause disfunction of what immune cells?

A

Leucocytosis: increased WCC not related to infection

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43
Q

How do you define steroid-induced diabetes? Mx?

A

Glucose >12mmol/L twice over 24 hours whilst taking steroids.
Mx- gliclazide

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44
Q

What is 1st line for absence seizures?

A

Ethosuximide

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45
Q

What is 1st line for tonic-clonic seizures?

A

Na Valproate or lamotrigine/levetiracetam if this is not appropriate.

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46
Q

What are the SEs of Na Valproate?

A

VALPROATE:
- Vomiting
- Anorexia
- Liver toxicity
- Pancytopenia and pancreatitis
- Retention of fat (weight gain)
- Oedema
- Alopecia
- Tremor
- Enzyme inhibition

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47
Q

What is 1st line for Myoclonic Seizures?

A

Na Valproate or levetiracetam if this is not appropriate.

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48
Q

Which seizure medications can worsen absence and myoclonic seizures?

A

Carbamazepine, gabapentin, lamotrigine, oxcarbazepine, phenytoin, pregabalin, tiagabine, vigabatrin.

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49
Q

What is 1st line for atonic seizures?

A

Na Valproate or lamotrigine if this is not appropriate.

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50
Q

What is the MOA for levetiracetam?

A

Binds to SV2A vesicle in protein in the brain and modulates synaptic NTM release.

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51
Q

What is the MOA for lamotrigine? What severe complication should be monitored for when first starting the drug?

A

Na channel blocker.
Stevens-Johnson Syndrome.

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52
Q

What is first line for focal seizures?

A

Levetiracetam or lamotrigine

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53
Q

What is the MOA of carbamazepine? When is it used?

A

Stabilises electric signals and reduces glutamate release.
Used for trigeminal neuralgia, bipolar I disorder, and epilepsy syndromes:
- Partial seizures
- Generalised tonic clonic (grand mal) seizures
- Some mixed seizure patterns

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54
Q

When should pharmacotherapy be commenced during seizures?

A

> 5 minutes (when status is reached)

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55
Q

What is first, second, and third line for status epilepticus?

A

1) benzodiazepine (lorazepam) which can be given twice
2) IV phenytoin infusion
3) General anaesthetic (Propofol or thiopental)

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56
Q

What medication can be used post traumatic brain injury to prevent seizures?

A

Phenytoin (often 7 days post TBI).
Measure plasma levels throughout 7 days and if it doesn’t meet therapeutic threshold then increase dose.

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57
Q

What is the MOA of Phenytoin?

A

Voltage gated sodium channel inhibitor.

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58
Q

What medications can lower the seizure threshold?

A

Antis:
- Antibiotics: imipenem, penicillin’s, cephalosporins, metronidazole, isoniazid
- Antipsychotics
- Antidepressants: bupropion, tricyclics, venlafaxine
- Antihistamines
Pain:
- Fentanyl
- Ketamine
- Lidocaine
- Tramadol
Psych:
- lithium

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59
Q

Why must a quantiferon test be completed before commencing biologics?

A

They can reactivate latent TB

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60
Q

What is the MOA of colchicine? SEs?

A

Reduced inflammation by reducing microtubule assembly.
SEs: GI (N, V, D)

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61
Q

What cytotoxic therapy is associated with haemorrhagic cystitis?

A

Cyclophosphamide

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62
Q

Which chemotherapy agent is associated with peripheral neuropathy?

A

Vinblastine

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63
Q

Which chemotherapy agent is associated with dilated cardiomyopathy and subsequent heart failure?

A

Doxorubicin

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64
Q

Which chemotherapy agent is associated with pulmonary fibrosis?

A

Bleomycin

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65
Q

Which chemotherapy agent is associated with neurotoxicity?

A

Asparaginase

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66
Q

MOA of imatinib? What is it used for?

A

TKI (tyrosine kinase inhibitor) used for CML and GI stromal tumours.

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67
Q

What is PD-1 and PDL-1 therapy?

A

Programmed cell death receptor/ligand is targets. The monoclonal antibody binds to these, initiating cell death of these cells

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68
Q

How long do patch medications take to reach the required dose?

A

24 hours

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69
Q

How long does it take for a syringe driver (SC) to reach desired systemic concentration?

A

4 hours

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70
Q

What is used for rapid tranq in Parkinson’s pts? What is CI?

A

PR/PO lorazepam.
Haloperidol is CI!!

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71
Q

What are the SEs of dopamine precursors such as levodopa?

A

N+V, orthostatic hypotension, vivid dreams, and hallucinations.

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72
Q

Which Parkinson’s drug is CI in those with pre-existing impulse control disorders?

A

Dopamine agonists such as pramipexole.

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73
Q

What is Co-careldopa composed of? Why is this beneficial?

A

Levadopa + carbidopa.
The carbidopa increases bioavailability of levadopa, reducing peripheral breakdown.

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74
Q

How do you manage Hypokalaemia? At what rate can you replace K+?

A

When K+ falls below 2.5mmol/L give 0.9% NaCL + 4 mmol KCL and check magnesium as a low K+ is associated with a low magnesium.
You can replace at 10mmol/hr

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75
Q

How do you manage Hyperkalaemia?

A
  • Calcium carbonate
  • Insulin/dextrose
  • Lokelma?
  • Salbutamol?
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76
Q

How do you manage malignant hypercalacaemia?

A
  • Fluids
  • Bisphosphonates (e.g., pamidronate)
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77
Q

How do you manage hypocalcaemia? What needs monitoring?

A

Calcium carbonate and calcitriol.
Monitor ECG as can cause prolonged QT/arrhythmias.

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78
Q

How/ when do you manage hyponatreamia?

A

<125 mmol/L: hypertonic saline (slowly)

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79
Q

How do you manage hypernatremia in the context of dehydration or excessive salt intake? What rate of correction should not be exceeded?

A

hypernatremia is >145mmol/L.
Dehydration: NaCl or Hartmann’s
Excessive salt intake: hypotonic fluid such as dextrose.
Do not exceed correction of >10mmol/L over 24 hours.

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80
Q

What are the sx of lithium toxicity? Mx?

A

Disturbance to CNS: dysarthria, seizures, impaired coordination.
IV fluid therapy.

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81
Q

What are the sx of clozapine toxicity? By what mechanism does this happen?

A

Confusion, agitation, drowsiness, ataxia, tachycardia.
It is metabolised by CYP450 so anything causing downregulation of this will lead to a build up.

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82
Q

What are the signs/sx of Tricyclic antidepressants OD? Mx?

A

Anticholinergic sx: tachycardia, hypotension, flushing, decreased urinary/bowel retention, blurred vision, respiratory depression, coma.
You also get QRS widening due to Na channel blockade.
Mx- IV Na bicarb to raise serum pH and alkalisation favours the neutral form of the drug.

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83
Q

What is 1st and 2nd line for pharmacological management of ADHD?

A

1) Methylphenidate
2) Atomoxetine

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84
Q

What are the SEs of methylphenidate?

A

Appetite suppression causing growth suppression.

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85
Q

What is more likely to cause SEs: 1st or 2nd generation antipsychotics?

A

Second (olanzapine, quetiapine, clozapine, risperidone).

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86
Q

Why do SSRIs cause a euvolaemic hyponatraemia?

A

Can cause SIADH so you get low serum osmolality, high urine osmolality, and a high urinary sodium.

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87
Q

Which SSRI is associated with priaprism?

A

Trazadone due to a-adrenergic blocking activity.

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88
Q

What changes can SSRIs make to ECGs?

A

QT prolongation

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89
Q

Why may someone on an SSRI present with maleena?

A

They carry a risk of peptic ulcer disease and therefore upper GI bleeding.

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90
Q

How often should methotrexate pts have a FBC done? Why?

A

Every 1-2 weeks until therapy is stabilised, then every 2-3 months after that.
Can cause bone marrow suppression.

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91
Q

What are the SEs of ciclosporin?

A

Hypertrophy of the gums, hypertrichosis, hypertension, hyperkalaemia, hyperglycaemia (diabetes).

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92
Q

Why are pts who carry an epipen CI to have labetalol?

A

Combined would mean unopposed alpha adrenergic effects which causes a hypertensive crisis.

93
Q

When is the dose/conc of adrenaline for anaphylaxis adult vs child?

A

IM in injection conc of 1:1000…
<6 months: 100-150 micrograms
6 months to 5 years: 150 micrograms
6-11 years: 300 micrograms ‘
>12: 500 micrograms

94
Q

How long prior to surgery should the COCP be stopped? Why?

A

4 weeks prior to reduce risk of thromboembolic disease.

95
Q

What is the absolute CI to HRT?

A

Personal hx of breast or ovarian cancer

96
Q

Why is transdermal oestrogen better than oral?

A

Oral increases risk of CVD, PVD, cholestasis/gallstones

97
Q

Why must women with uteri take progesterone with their HRT?

A

To protect their endometrium

98
Q

When would you do cyclical HRT? What does this involve?

A

Still having periods or final MP was <12months ago.
2 weeks on, 2 weeks off.

99
Q

When can a lady have continuous HRT?

A

Once she has reached the day of menopause (12 months after last MP).

100
Q

What factors does warfarin act on?

A

10, 9, 7, 2 (vitamin K dependent factors)

101
Q

How should warfarin pts be managed around surgery?

A

Stop a few days before (or reverse if emergent) and bridge with heparin if at risk of thromboembolic disease.

102
Q

How should warfarin pts who present with bleeding or suspected intracranial bleed be managed?

A

Stop warfarin and reverse (IV vitamin K and PT complex).

103
Q

How should warfarin pts who present with an INR between 5-8 but no signs of bleeding be managed?

A

Stop warfarin until INR stabilises.

104
Q

How should warfarin pts who present with INR >8 but no signs of bleeding be managed?

A

Stop warfarin and commence oral vit K.

105
Q

Where does heparin act in the coagulation cascade?

A

Inactivates thrombin and activated factor 10.

106
Q

What type of heparin is used in pts with a GFR <30?

A

Unfractionated.

107
Q

What has the longest 1/2 life: LMW heparin, unfractionated heparin, or fondaparinux?

A

Fondaparinux.

108
Q

Dabigatran acts where in the coagulation cascade? How is it reversed?

A

FIIa (thrombin) inhibitor.
Idarucizumab.

109
Q

Apixaban and Edoxaban are what type of anticoagulants? Which is better in someone with declining renal function?

A

DOACs.
Edoxaban is preferred.

110
Q

Where do apixaban and rivoroxaban work in the coagulation cascade?

A

Inhibits FXa.

111
Q

Edoxaban acts where in the coagulation cascade?

A

Inhibits prothrombinase.

112
Q

What does aspirin inhibit?

A

Cyclooxygenase 1

113
Q

What are the manifestations of an aspirin OD? Mx?

A

Hyperpnoea (deep breathing), tinnitus, N+V.
Raised anion gap metabolic acidosis with some respiratory alkalosis and raised base excess.
Mx- fluids, Na bicarb, potassium chloride to maintain kidney function, and may need dialysis.

114
Q

What are the three PY12 inhibitors?

A

Clopidogrel, prasugrel, ticagrelor

115
Q

What is the MOA of dipyridamole? What is it used for?

A

PDE3 enzyme inhibitor.
Secondary prevention of ischaemic stroke.

116
Q

What is the dose and conc of adrenaline sued in cardiac arrest?

A

300mg 1:10000

117
Q

What is the MOA of amiodarone?

A

Blocks Na channels which usually cause repolarisation in the 3rd phase of the cardiac AP, therefore preventing repolarisation.

118
Q

Why is amiodarone CI in breastfeeding women?

A

Toxic effects of iodine on infants.

119
Q

What is the MOA of digoxin?

A

Inhibits Na/K adenosine triphosphatase ion pump in myocardium and exhibits parasympathetic effects on the AV node. So it slows the heart and increases contractility.

120
Q

What are the signs of digoxin toxicity? Mx?

A

Palpitations, dyspnoea, GI sk, visual sx.
Mx- digibind.

121
Q

What electrolyte imbalance is associated with digoxin?

A

Hyperkalaemia.

122
Q

What is the starting doses for primary and secondary prevention with atorvastatin? When are pts advised to take them?

A

P- 200mg OD
S- 80mg OD
Take at night as this is when most cholesterol synthesis occurs.

123
Q

Propranolol, labetalol, and atenolol are what type of medications? What are the known SEs?

A

Beta blockers: antagonise B1 receptors.
SEs- bradycardia, reflex tachycardia when stopped, can worsen PVD, GI upset, sleep disturbance

124
Q

What is used to manage benign essential tremours?

A

Propranolol

125
Q

What is 1st line for Pre-eclampsia?

A

Labetalol

126
Q

What is the MOA for CCBs? What are the two types? Which is used for HeTN?

A

Block the L type Calcium channels to stop/reduce vascular contraction = decrease afterload.
Dihydropyridine: Amlodipine and Nifedipine - used for HeTN.
Non-dihydropyridine: Diltiazem and Verapamil - more cardio selective.

127
Q

What are the SEs of CCBs?

A

Bradycardia, reflex tachycardia when stopped, ankle oedema, hot flushes, headaches, constipation

128
Q

What class of medications are Ramipril and lisinopril? What is the MOA?

A

ACEis = Reduced ACE = reduced angiotensin (which vasoconstricts vessels) = decreased wall stress and decreased afterload.

129
Q

What are the SEs of ACEis? Why do they occur?

A

Dry cough, hepatotoxicity, hyperkalaemia due to increase in bradykinin (usually inactivated by ACE).

130
Q

What type of medication are candesartan and losartan? Why is there less SEs than ACEis? What SE does it still cause?

A

ARBs = block angiotensin II receptor to decrease its effect = decreased afterload. Does not impact ACE and therefore does not cause increase in bradykinin = less SEs.
Hyperkalaemia.

131
Q

In who are ARBs CI?

A

Pregnant women

132
Q

Nimodipine is a dihydropyridine CCB used for what?

A

Preventing vasospasm induced cerebral ischaemia in subarachnoid haemorrhage due to ruptures intracranial aneurysms.

133
Q

What is the MOA of Bosentan? What must be monitored when taking this medication? CIs?

A

Endothelin A receptor antagonist to reduce vasoconstriction and reduce BP.
Must monitor LFTs as can rarely cause liver injury and is therefore CI in pts with moderate-severe hepatic impairment.

134
Q

What is the MOA of Midodrine? What is it used for?

A

Alpha1 agonist used for significant orthostatic HoTN.

135
Q

What is used to manage low and high risk essential thrombocytopenia?

A

Hydroxycarbamide (type of chemo) for high, aspirin for low.

136
Q

What is used to manage Von Willebrand Disease?

A

Desmopressin (increases release of VWF)

137
Q

What type of drug is Tranexamic acid? Who is it CI in?

A

Anti-fibrinolytic.
CI in haematuria.

138
Q

How does Emicizumab work?

A

It brings together Factor X and Factor IX to replace the function of Factor XIII.
Used for Factor XIII deficiencies.

139
Q

What is given in open angle glaucoma?

A

Prostaglandin E1: Lantoprost - to improve uveoscleral outflow by increasing the sclera’s permeability to aqueous humour.

140
Q

What is used to maintain a PDA in transposition of the great vessles? What else is it used for?

A

Prostaglandin E1: alprostadil.
Also used for erectile dysfunction.

141
Q

What is 1st and 2nd line for urge incontinence?

A

1) Oxybutynin
2) Mirabegron: for those CI such as those with cataracts

142
Q

Pyridostigmine is an anti-cholinergic used for what?

A

Myasthenia gravis, paralytic ileus, and post-operative urinary retention.

143
Q

What can be used to manage extrapyramidal SEs associated with antipsychotics?

A

Procyclidine (anti-cholinergic).

144
Q

What is given in the case of a benzodiazepine OD?

A

Flumazenil.

145
Q

What is given to reverse the effects of an opioid OD?

A

Naloxone

146
Q

When you switch oral morphine to a SC syringe driver how do change the dose?

A

Half oral dose = SC driver dose

147
Q

Why do opioids increase the risk of an anal fistula?

A

Cause constipation which leads to straining which can cause a fistula to form.

148
Q

How much opioid do you prescribe for breakthrough pain?

A

1/6 daily dose

149
Q

Chloroquine is used for malarial prophylaxis, who is it CI in? What can be given instead?

A

Epileptics, pts with long QT syndrome, and diabetics (can cause severe hypos).
Proguanil.

150
Q

What is Artesunate used to treat?

A

Acute severe malaria

151
Q

How long after paracetamol OD should a blood sample be sent to check level? What is given in the mean time if dose is unknown?

A

4 hours.
IV NAC.

152
Q

What are the known SEs of NSAIDs?

A

kidney toxicity, gastric ulceration/perforation, bronchospasm, HeTN, interruption of coagulation, urticaria.

153
Q

On what substance does celecoxib act? Who is it useful for?

A

Cox-2 inhibitor.
Pts with have high GI bleed risk - it doesn’t target cox-1 so doesn’t affect mucosa.

154
Q

Mannitol is what type of diuretic? How does it work? How is it given?

A

Osmotic diuretic: increases osmotic pressure in the glomeruli to increase water absorption = more excreted.
Given over slow infusion to insure water is taken from the intercellular space and not intracellular.

155
Q

What type of diuretic is acetazolamide? How do these work?

A

Inhibit carbonic anhydrase….
reduces formation of H ions which means less are exchanged with Na in the PCT so less Na is reabsorbed (and water follows).

156
Q

What are the SEs of carbonic anhydrase inhibitors?

A

Dizzy/lightheaded, blurred vision, loss of appetite, stomach upset.

157
Q

What is acetazolamide used for?

A

Acute angle closure glaucoma, idiopathic intracranial HeTN, occasionally in heart failure and altitude sickness.

158
Q

How do loop diuretics such as furosemide and bumetanide work? SEs?

A

Inhibit Na/K/Cl channel in the LoH to reduce Na reabsorption and increased excretion (water follows).
SEs- hypovolaemia, hypotension, hyperkalaemia, hearing loss, raised urate.

159
Q

How do thiazide diuretics work? SEs?

A

Block Na/Cl channel on the apical side of the DCT causing reduced Na and water reabsorption.
Hypokalaemia, hypercalcaemia, hypomagnesaemia, hyponatraemia, hyperglycaemia, raised urate.

160
Q

Why are thiazide diuretics limited by aldosterone?

A

When blood volume decreases, RAAS will act and aldosterone will increase BP.

161
Q

What are the two types of K sparing diuretics?

A

Anti-aldosterone: spironolactone, eplerenone
Amiloride: block endothelial Na channels

162
Q

Why does spironolactone cause gynaecomastia?

A

interrupts testosterone production

163
Q

What are the SEs of K sparing diuretics?

A

Hyperkalaemia, rash, GI upset, menstrual disorders, testicular atrophy.

164
Q

Repeated doses of salbutamol can do what to potassium and lactate levels?

A

Hypokalaemia, raised lactate

165
Q

What type of breast cancer pts is Goserelin used in? What is it? SEs?

A

Premenopausal women.
GnRH analogue.
Can cause menopausal sx.

166
Q

Tamoxifen is used in what breast cancer pts?

A

Oestrogen receptor +ve postmenopausal women.

167
Q

Trastuzumab is used in which breast cancer pts? What needs monitoring?

A

HER2+ breast cancers.
Can be cardiotoxic so monitor cardiac function.

168
Q

What is Cholestyramine?

A

Bile acid sequestrant: binds to bile acids to prevent them being reabsorbed.
Used for pruritis secondary to biliary pathology such as PBC.

169
Q

What drugs need to be stopped in AKI?

A

Diuretics + Digoxin, ACEIs metformin, NSAIDs (DAMN drugs)

170
Q

What is 1st line for ascites?

A

Spironolactone.

171
Q

What drugs should be stopped in a pt with a peptic ulcer?

A

NSAIDs, steroids, bisphosphonates, potassium supplements, SSRIs, crack cocaine

172
Q

What are the main 4 receptors targeted by antiemetics? Give an example for each.

A

H1: Cyclizine
D2: domperidone, metoclopramide
5HT3: ondansetron
Anti-muscarinic: hyoscine hydrobromide

173
Q

Where does cyclizine have an effect? Who is it CI in? SEs?

A

Vestibular system and chemoreceptor trigger zone and central anticholinergic effect.
CI in acute porphyria’s.
SEs dry mouth, dizziness.

174
Q

What is 1st line antiemetic for hyperemesis gravidum?

A

Cyclizine

175
Q

Who is metoclopramide CI in? Why?

A

Bowel obstruction, parkinson’s, pheochromocytoma as it is prokinetic.

176
Q

What is the 1st line antiemetic for Parkinson’s pts?

A

Domperidone

177
Q

What complication can be caused by D2 receptor antagonist antiemetics?

A

Acute dystonia and tardive dyskinesia with chronic use due to D2 receptor antagonism in the pyramidal circuits.

178
Q

How do you manage oculogyric crises and cervical dystonias?

A

Procyclidine

179
Q

Ondansetron antagonises which receptor?

A

5HT3 - acting on chemoreceptors in the gut.

180
Q

Which antiemetic is 1st line for a post chemotherapy patient experiencing nausea but no vomiting?

A

Ondansetron 4-8mg

181
Q

What are the SEs of ondansetron?

A

Diarrhoea, constipation, headaches, dizziness, drowsiness.

182
Q

Hyoscine hydrobromide acts on what receptor?

A

They are anti-muscarinic (block muscarinic receptors).

183
Q

SEs of hyoscine hydrobromide?

A

CNS stimulation, respiratory reaction, GI upset, hallucination, hypersensitivity, hyperthermia, hypohidrosis, mydriasis, oedema, restlessness, seizure

184
Q

What is 1st line for a pt taking an opioid struggling with constipation?

A

Stimulant laxative such as senna: up to 30mg TD

185
Q

How does lactulose work? What is it used for?

A

Reduces ammonia production by bacteria in the gut and therefore reduces absorbability of the gut.
Used for constipation and hepatic encephalopathy.

186
Q

What class of medication is doxazosin? What is it used for?

A

Alpha blocker used for acute urinary retention due to BPH

187
Q

What is first line for stress incontinence?

A

Duloxetine

188
Q

Who are alpha blockers CI in? What can be used for BPH instead?

A

Postural HoTN - use finasteride instead (5- alpha-reductase inhibitor).

189
Q

What is 1st line for urge incontinence? Who is it CI in? What can be used instead.

A

Oxybutynin.
CI in frail/elderly pts due to anticholinergic SEs,
Use Mirabegron instead in these pts.

190
Q

Chlorpheniramine antagonises which receptor? SEs?

A

Hi antagonist used as an antihistamines.
Does have anticholinergic properties so causes confusion, dry mouth, urinary retention.

191
Q

What is used to manage the pruritis associated with cholestasis of pregnancy?

A

Chlorpheniramine.

192
Q

Can chlorpheniramine cross the blood/brain barrier?

A

Yes

193
Q

What is promethazine? Who might it be avoided in?

A

Antihistamine with sedative and antiemetic effects.
Avoid in elderly due to sedative effects.

194
Q

MOA of Carbimazole? SEs?

A

Inhibits thyroid peroxidase to reduce thyroid production in Grave’s disease.
SEs- rash, pruritis, agranulocytosis, neutropenia,

195
Q

What drugs interact with levothyroxine?

A

Ferrous sulphate, calcium chloride, digoxin, HRT

196
Q

What is first line for cluster headaches?

A

Nasal sumatriptan for acute attacks, verapamil for prophylaxis.

197
Q

What is used for migraine prophylaxis in asthmatic pts?

A

Topiramate or amitriptyline

198
Q

What SEs is topiramate associated with?

A

Weight loss, renal stones, and cognitive/behavioural changes.

199
Q

What type of acidosis can topiramate cause?

A

Mixed type 1 and 2 renal tubular acidosis (presents with non specific sx)

200
Q

What is 1st line for peripheral neuropathy?

A

Tricyclic antidepressant such as amitriptyline.

201
Q

What is 1st line for diabetic neuropthy?

A

Pregabulin

202
Q

What two medications are used for medical abortion?

A

1) Mifepristone (induce miscarriage)
2) Misoprostol (expulsion of foetal tissue)

203
Q

What can be used for restlessness in EOL care?

A

Haloperidol

204
Q

What is used to manage secretions which cause ‘the ‘death rattle’ in EOL care?

A
  • Glycopyrronium bromide
  • Hyoscine hydrobromide
  • Hyoscine butyl bromide (buscapan)
205
Q

What is used for pain management and breathlessness in EOL care?

A

Morphine

206
Q

Which antiemetic medications are used for EOL care?

A

Cyclizine, levomepromazine

207
Q

What is sued for anxiety and dyspnoea in EOL care?

A

Benzodiazepines

208
Q

What can be used in pts taking high doses of opioids in EOL, who are facing significant constipation?

A

Bowel-specific opioid antagonists (relistor).

209
Q

What is the MOA of bisphosphonates such as Risedronate? SEs?

A

inhibit osteoclastic activity meaning less bone breakdown = reduced fracture risk.
SEs- dyspepsia/reflux so often given alongside PPI, can get necrosis of the jaw (should have dentist check before starting).

210
Q

What is the MOA of fomepizole?

A

Inhibits alcohol dehydrogenase to treat ethylene glycol (anti-freeze) or methanol poisoning.

211
Q

Acamprosate is used for what?

A

Used to reduce cravings during recovery from alcohol dependence.

212
Q

What happens when sildenafil an GTN interact?

A

Drop in BP - significant raise in cGMP levels cause vasodilation and profound HoTN.

213
Q

What happens when loop diuretics and digoxin interact?

A

Precipitates hypokalaemia leading to digoxin toxicity (visual discolouration, dizziness, palpitations, dyspnoea, syncope)

214
Q

What happens when trimethoprim and methotrexate interact?

A

Bone marrow suppression

215
Q

What are the common cytochrome P450 inhibitors?

A

O DEVICES:
- omeprazole
- disulfiram
- erythromycin and other macrolides
- valproate
- isoniazid
- ciprofloxacin
- ethanol
- sulphonamides

216
Q

What happens when statins interact with macrolides?

A

rhabdomyolysis

217
Q

What happens when allopurinol and azathioprine interact?

A

bone marrow dyscrasias and neutropenic sepsis

218
Q

What happens when methadone and ondansetron interact?

A

QT prolongation

219
Q

Why does ciprofloxacin increase INR in warfarin pts?

A

Cipro is a p450 inhibitor therefore increases warfarin levels as less in broken down/excreted.

220
Q

Which asthma medications can cause nightmares, especially in the paediatric pts?

A

Montelukast

221
Q

Short term use of levodopa can cause which of of the following:
- Morning hypokinesia
- Dyskinesia
- Abnormal Dreams

A

Abnormal dreams

222
Q

How can you manage a beta blocker OD?

A

Atropine to treat bradycardia and hypotension, if this fails give glucagon.

223
Q

Someone with G6PD presenting with a UTI is CI to what antibiotic? What would you give them instead?

A

CI to nitrofurantoin.
Give trimethoprim (unless this is CI, in which case give pivmecillinam).

224
Q

Why might someone on carbamazepine have a low sodium?

A

It can trigger SIADH which causes a euvolemic hyponatraemia with a low plasma osmolality and high urine osmolality.

225
Q

What is the MOA of allopruinol?

A

Xanthine oxidase inhibitor, by blocking this it reduces production of purines thereby reducing uric acid production.

226
Q

What level of lithium toxicity requires haemodialysis?

A

> 4 or >2.5 with kidney dysfunction

227
Q

Which antihypertensive is known to cause gum hypertrophy and pain?

A

Amlodipine

228
Q

What type of kidney disease is caused by PPIs such as omeprazole?

A

Acute interstitial nephritis.

229
Q
A