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CC2 > Therapuetics > Flashcards

Therapuetics Flashcards

1
Q

Which drugs are included in the BNF?

A

All licensed drugs used in UK

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2
Q

If a person prescribes a different dose of a drug that indicated what is this called?

A

Off-label

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3
Q

What are late effects of chemotherapy?

A

Impact brain, spinal cord and nerves (also endocrine and reproductive) so can cause hearing loss, peripheral neuropathy, lung fibrosis, cardiomyopathy and myelodysplasia

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4
Q

Which chemotherapy drug can cause long-term hearing loss?

A

Cisplatin

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5
Q

What can TCAs do to the pupils?

A

Dilate

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6
Q

What will happen to pupils on drug overdose?

A

Constrict

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7
Q

What pupil effects do opioids have?

A

Pinpoint pupils

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8
Q

How can you directly assess drug compliance?

A

Measure levels in blood or urine

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9
Q

How does compliance change with increasing the number of drugs?

A

Decreases

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10
Q

Which drug can be used for hypertension, migraine prophylaxis and angina?

A

Beta-blockers

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11
Q

Which drug can be used for generalised seizures, trigeminal neuralgia and manic depression?

A

Carbamazepine

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12
Q

What is pharmacokinetics?

A

How the body works on the drug

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13
Q

What is pharmacodynamics?

A

How the drug works on the body

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14
Q

What type of receptor is a beta-adrenoceptor? How does it work?

A

G protein coupled: receptor binding leads to interaction with G protein coupled with intracellular activation (cAMP/cGMP or ion channel)

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15
Q

What type of receptors are kinase-linked?

A

Insulin receptors

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16
Q

Give examples of DNA-linked receptors and what/how do they work?

A

Located in cell nucleus (nuclear receptors) and promotes/inhibits protein synthesis - e.g. glucocorticoid receptors, thyroid receptors, vitamin D receptors

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17
Q

Which drugs block Na voltage dependent channels?

A

Anaesthetics e.g. lidocaine

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18
Q

What type of channels are L-type calcium channels?

A

Voltage gated

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19
Q

Which enzyme does aspirin inhibit?

A

Cyclo-oxygenase

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20
Q

What type of medication targets HMGCoA reductase?

A

Statins

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21
Q

What type of medication is paroxetine?

A

SSRI

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22
Q

What drug class does omeprazole belong to?

A

PPIs

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23
Q

Do antacids have specific or non-specific function?

A

Non-specific

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24
Q

What 3 things do drug-receptor interactions depend on?

A
  1. chemical composition of the drug
  2. stereochemical composition of the drug
  3. ability of drug to reach receptor
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25
Q

What 3 things can impact the affinity of a drug?

A
  1. other drugs
  2. aging
  3. genetic mutations
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26
Q

What is efficacy?

A

The relative ability of a drug to impart a functional change on the receptor.

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27
Q

How do partial and full agonists vary in terms of efficacy?

A

A partial agonist binds and activates the receptor with only partial efficacy.

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28
Q

What is the potency of a drug? What does it depend on?

A

The amount of the drug required for a given intensity of effect. This is proportional to affinity and efficacy.

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29
Q

What is plotted on the axes of a dose-response curve?

A

Concentration (x) vs drug effect (y)

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30
Q

What are the 3 possible mechanisms for increased tolerance?

A
  1. Down regulation of receptors
  2. Decreased receptor binding affinity
  3. Modulation of downstream response to initial signal
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31
Q

What can increased tolerance make a patient experience?

A

Withdrawal reactions

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32
Q

How long does tolerance to a medication take to increase?

A

Days to weeks

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33
Q

What off-target effect can opioids cause?

A

EConstipation

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34
Q

Which 2 effects need to be considered to find the therapeutic index?

A

Toxic and therapeutic effect

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35
Q

Which drugs have a particularly narrow therapeutic index?

A

Gentamycin, vancomycin, lithium, digoxin, warfarin

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36
Q

How can you monitor drugs with a narrow therapeutic index?

A

Measure concentration of drug in the blood

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37
Q

How does a “dose” differ from a “dosage”?

A

Dose: total quantity of active agent taken in/absorbed at one time
dosage: includes characteristics of the organism e.g. body weight, surface area

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38
Q

What are the 4 processes that occur when drugs are taken?

A
  1. Uptake
  2. Distribution
  3. Metabolism
  4. Elimination
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39
Q

What are the 3 types of routes of administration?

A
  1. Topical: local effect
  2. Enteral: systemic effect via digestive tract
  3. Parenteral: systemic effect via other routes - IV, transdermal (nicotine patches), transmucosal, inhalational
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40
Q

What does affinity mean?

A

The probability of the drug occupying a receptir at any given time

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41
Q

What is meant by the efficacy of a drug?

A

The ability of a drug-receptor complex to produce a maximum functional response

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42
Q

What drug class does buprenorphine belong to and how does it act?

A

Opioid which acts as a partial agonist

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43
Q

Drug activity in terms of amount required to produce an effect of given intensity - what word is this?

A

Potency

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44
Q

What word describes the relative ability of a drug-receptor complex to produce a maximum functional response?

A

Efficacy

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45
Q

What is therapeutic efficacy?

A

The effectiveness of a drug to produce an effect

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46
Q

What do you use to determine the dose of a step up painkiller if someone is already on one?

A

Conversion tables

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47
Q

Do IM or subcut injections have a faster onset?

A

IM

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48
Q

Which drugs are given intrathecally?

A

Anaesthesia and chemotherapy

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49
Q

What type of drugs are given by transdermal route?

A

Lipophillic - nicotine patches, oestradiol (menopause), fentanyl (severe pain)

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50
Q

Are modified release and normal release formulas interchangeable?

A

No

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51
Q

Which drugs could exacerbate/trigger asthma?

A

Beta blockers and aspirin

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52
Q

How can you manage asthma non-pharmacologically?

A

Avoid triggers, personalised asthma plan, secondary prevention (smoking cessation, weight loss intervention, breathing exercises)

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53
Q

Which inhalers are given first to someone with asthma?

A

SABA (selective beta-2 agonist) and low dose inhaled corticosteroid

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54
Q

What type of inhaler is terbutaline?

A

SABA

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55
Q

Apart from inhalers, how else can SABAs be given?

A

Nebuliser, IV infusion, oral tablets

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56
Q

What inhalers are beclomethasone, fluticasone and budesonide all examples of?

A

Inhaled corticosteroids

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57
Q

What would cause you to step up someone’s asthma treatment?

A
  1. Exacerbation in last 2 years
  2. Symptoms need SABA 3x a week
  3. Symptoms at least 1 night a week
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58
Q

What are adverse effects of SABAs?

A

Tremor, tachycardia, hypokalaemia

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59
Q

What are adverse effects of ICS?

A

Sore throat/oral candidiasis, osteoporosis in adults, growth suppression in children

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60
Q

How could you reduce risk of oral candidiasis using an inhaler?

A

Use a spacer or rinse mouth after inhalation

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61
Q

What type of inhalers are salmeterol and formoterol?

A

LABA

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62
Q

Which 2 types of inhalers are included in combination inhalers?

A

ICS and LABA

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63
Q

What would you do if a patient was on a LABA and ICS combined inhaler and were not responding to treatment at all?

A

Stop LABA and increase dose of ICS

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64
Q

What would you do if a patient was on a LABA and ICS combined inhaler and were responding to LABA but of asthma control was not sufficient?

A

Continue this therapy and either increase dose of ICS to medium or introduce LTRA, LAMA or theophylline

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65
Q

What are examples of high dose asthma therapies? How would you manage the patient if it got to this stage?

A

High dose ICS, or adding a fourth drug (LRTA, SR theophylline, LABA tablet or LAMA). Refer to specialist!

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66
Q

What is the final step of pharmacological asthma management?

A

Lowest dose of daily steroid tablets, high dose ICS. Refer to specialist.

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67
Q

What should you assess and do in an asthma review?

A

Symptoms, lung function, inhaler technique and adherence, adjust dose, update self-management plan, move up and down as appropriate

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68
Q

What is the highest dose of ICS possible?

A

800mg beclomethasone

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69
Q

How long is the duration of action for LABAs?

A

12 hours

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70
Q

What type of inhalers are salmeterol and formoterol?

A

LABAs

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71
Q

What drug is montelukast?

A

leukotriene receptor antagonist

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72
Q

What side effects can leukotriene receptor antagonists cause?

A

Hypersensitivity reaction and GI upset

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73
Q

What is theophylline derived from?

A

Xanthine

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74
Q

What are adverse effects of xanthine derivatives?

A

Cardiac arrhythmias and seizures

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75
Q

What class of inhaler is tiotropium?

A

LAMA

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76
Q

Why might someone be responding poorly to their asthma treatment?

A
  1. Poor compliance: understanding, polypharmacy, complicated, stress/psychological
  2. Trigger presence
  3. Poor inhaler technique
  4. Wrong diagnosis - GORD, COPD, bronchiectasis
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77
Q

What is clinically classified as acute severe asthma?

A
  1. Cannot complete sentences, HR>=110bpm, RR>=25

4. PEFR <33% predicted

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78
Q

How is acute severe asthma treated?

A
  1. Admit to hospital
  2. Oxygen
  3. Nebulised salbutamol or terbutaline (SABA)
  4. Prednisolone 40-50mg PO or hydrocortisone 100mg IV (if cannot swallow)
  5. If response poor… inhaled ipratropium bromide 500mg every 4-6 hours via O2 driven nebuliser OR IV beta-agonist (magnesium sulphate or aminophylline)
  6. Over next few days - education and support: nebs, steroids, find reason, anxiety expected, compliance, technique
  7. Asthma follow-up at GP and nurse specialists
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79
Q

What is meant by “difficult” asthma?

A

Persistent symptoms/frequent exacerbations despite high-dose therapy

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80
Q

What can be used under strict adherence for difficult asthma?

A

Monoclonal antibodies

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81
Q

What 4 thing are assessed in a COPD assesment?

A
  1. Amount of bronchospasm
  2. Infections - do they need antibiotics?
  3. Right-sided HF?
  4. How much emphysema? - more has more limitations to treating
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82
Q

Which 3 factors contribute to asthma airway narrowing?

A

Bronchial muscle contraction, mucosal swelling/inflammation (mast cell and basophil degranulation –> inflammatory mediators) and increased mucus production

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83
Q

What is the pathophysiology of COPD?

A
  1. Emphysema: alveolar destruction due to protease-antiprotease imbalance (proteases from noxious particles overwhelm).
  2. Bronchitis: Hyperplasia and hypertrophy of mucus-secreting glands in submucosa of bronchi
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84
Q

What is the steps in management of COPD?

A
  1. SABA or SAMA as needed
  2. If no asthmatic features = LABA + LAMA
  3. LABA + LAMA + ICS
  4. Oral bronchodilators - theophylline
    - Always use antibiotics if indicated, vaccinations (flu, pneumococcal), mucolytic (carbocisteine tablets for chronic productive cough), treat HF with diuretics, oxygen therapy for respiratory failure, smoking cessation
    - Manage exacerbations: controlled O2, corticosteroids, antibiotics, nebulised bronchodilators, physiotherapy
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85
Q

If you get to the stage in COPD management to add tiotropium, what else should you do?

A

Tiotropium is a LAMA so stop SAMA (ipratropium). Add SABA and then LABA and inhaled corticosteroids if still needed.

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86
Q

What venturi mask should you start on for type 2 respiratory failure?

A

Blue (24%; 2L/min)

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87
Q

Order of venturi masks, percentage oxygen and rate?

A
  1. Blue - 24% - 2L/min
  2. White - 28% - 4L/min
  3. Orange - 31% - 6L/min
  4. Yellow - 35% - 8L/min
  5. Red - 40% - 10L/min
  6. Green - 60% - 15L/min
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88
Q

What are bupropion (Zyban) and varenicline (champix) tablets used for? What drug class are each of them?

A

Smoking cessation

  • Bupropion is an SSRI and mechanism is not understood - contraindicated in <18yo, pregnant, breastfeeding or history of seizures
  • Varenicline is a selective nicotine receptor partial agonist - contraindicated in <18yo, pregnant, breastfeeding and caution with psychiatric history
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89
Q

Why is particle size important for inhaled drugs?

A

It is proportional to area of deposition

  • > 10micrometers deposited in mouth to large airway
  • <5micrometers in small airways
  • around 2 micrometres in alveoli
  • > 1micrometers may be exhaled again
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90
Q

What are the 3 methods to deliver drugs by inhalation?

A
  1. Metered dose inhalers
  2. Breath actuated device
  3. Nebuliser
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91
Q

Why might you add a spacer device to a metered dose inhaler (MDI)?

A

Reduces need for coordination and risk of oral thrush

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92
Q

What are negatives of using spacers?

A

Reduce amount of medication absorbed in system and less convenient to carry

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93
Q

How much of the prescribed dose in a nebuliser reaches the lungs?

A

10%

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94
Q

What are ADRs?

A

Adverse drug reactions - a response to a drug which is noxious and unintended at normal doses

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95
Q

What type of drugs can cause impaired renal function if not monitored in the lab?

A

ACEi

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96
Q

Which common drug can cause haemorrhage or elevated INR if not therapeutically monitored?

A

Warfarin

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97
Q

What is Stevens-Johnson syndrome?

A

Rare, serious disorder of skin usually as a result of a reaction to medication. Starts as flu-like symptoms, then a red/purple rash that spreads to form blisters which eventually die and peel off. MEDICAL EMERGENCY.

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98
Q

What is a less severe ADR similar to Stevens-Johnson syndrome?

A

Erythema multiforme

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99
Q

What is type of arrhythmia is Torasades de Pointes and what is it a complication of?

A

Polymorphic ventricular tachycardia which occurs in long-QT syndrome

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100
Q

Which drugs can influence the development of Torsades de Pointes?

A

Antiarrhythmic drugs (quinidine, procainamide, disopyramide)
Antipsychotics
TCAs
Methadone, erythromycin and ketoconazole

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101
Q

Which drugs can cause a butterfly rash? What is this condition called?

A

Drug-induced Lupus

- Hydralazine (vasodilator) and procainamide (antiarrhythmic can cause)

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102
Q

Which drugs can induce gingival hyperplasia?

A

Phenytoin (anti-epileptic) and amlodipine (Ca2+ channel blocker)

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103
Q

How can ARDs be classified?

A
  1. Type A Reactions/Augmented Reactions: dose-dependent and predictable on basis of pharmacology of the drug
  2. Type B Reactions/Bizarre Reactions: idiosyncratic and not predictable
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104
Q

What type of ARDs are drowsiness and respiratory depression to codeine?

A

Type A

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105
Q

What 3 things do DoTS use to classify ARDs?

A
  1. Dose of drug
  2. Time course of reaction
  3. Relevant susceptibility factors
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106
Q

What patient characteristic can make them more susceptible to haemolysis (ARD) with chloroquine?

A

G6PD deficiency

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107
Q

What patient characteristic can make them more susceptible to parkinsonism (ARD) with prochlorperazine?

A

Elderly

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108
Q

What patient characteristic can make them more susceptible to cough (ARD) with ACEi?

A

Female

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109
Q

What patient characteristic can make them more susceptible to ARD with phenytoin?

A

Pregnancy

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110
Q

How does cranberry juice contribute to increased risk of ARDs?

A

Cytochrome P450 enzyme inhibition

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111
Q

What patient characteristic can make them more susceptible to deafness (ARD) with gentamycin?

A

Renal failure as these drugs are eliminated by the kidneys

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112
Q

What ADR is icatibant used for?

A

ACEi induced life-threatening angioedema affecting airway, head and neck as it is a selective bradykinin B2 receptor antagonist

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113
Q

What ARD is idarucizumab used for? What type of drug is it?

A

A monoclonal antibody for dabigatran-prolonged coagulation

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114
Q

What ARDs are intravenous lipid emulsions used for?

A

Local anaesthetic toxicity (e.g. severe cardiotoxic effects of lidocaine), intravascular infection or rapid absorption effects from injections in highly vascular sites.

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115
Q

Name a pharmovigilance tool

A

Yellow card scheme

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116
Q

What symbol is used to indicate a new drug and vaccine in order to encourage reporting of ARDs?

A

Black upside down triangle

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117
Q

What are the 3 stages of hypertension?

A
  1. Clinic BP 140/90mmHg or higher/ABPM 135/85mmHg or higher
  2. 160/100mmHg or 150/95mmHg
  3. 180/110mmHg
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118
Q

What are the 4 steps of treatment of HTN?

A
  1. ACEi/ARB or CCB if over 55/Black
  2. ACEi/ARB + CCB
  3. ACEi/ARB + CCB + thiazide-like diuretic
  4. Resistant HTN (seek expert advice): ACEi/ARB + CCB + thiazide-like diuretic + diuretic/alpha-blocker/beta-blocker
119
Q

Why do you start on a CCB for older age/African/Carribean?

A

Decreased renin levels

120
Q

What is the RAAS?

A
  1. Angiotensinogen is produced in the liver
  2. Renin is produced from JG cells of kidney in response to decreased blood pressure. It converts angiotensinogen to angiotensin I.
  3. Angiotensin I converted to angiotensin II by ACE from lungs
  4. Angiotensin II acts directly to vasoconstrict and stimulate release of aldosterone from adrenal gland
  5. Aldosterone acts of kidneys to stimulate reabsorption of NaCl and H2O.
121
Q

What are the 2 ways antihypertensives could work?

A
  1. Reduce vasoconstriction

2. Reduce Na+ and H2O retention

122
Q

What drug class do ramapril, perindopril, lisinopril and enalapril belong to?

A

ACEi

123
Q

Adverse effects of ACEi

A

Dry cough, first-dose hypotension, reversible AKI (creatinine levels rise), hyperkalaemia (be careful in CKD), rarely angioedema

124
Q

What are ACEi used for?

A

HTN, CKD, HF, post-MI

125
Q

What are contraindications to using ACEi? Therefore, what do you need to check before and after starting?

A

Pregnancy (do test), breastfeeding and bilateral renal artery stenosis (measure kidney function prior and monitor U&Es for 1 week after commencing)

126
Q

What are losartan, candesartan, valsartan and irbesartan examples of?

A

Angiotensin II AT1 receptor antagonists

127
Q

What do you need to do when starting someone on ARBs?

A

Monitor U&Es for 1 week as can cause reversible AKI and hyperkalaemia

128
Q

How do CCBs help in HTN?

A

Cause vasodilation by blocking entry of Ca2+ through L-type channels

129
Q

What are amlodipine, felodipine, nifedipine all examples of? What do they act preferentially on?

A

Non-rate limiting (dihydropyridines) calcium channel blockers which act on vascular smooth muscle

130
Q

What are verapamil and diltiazem examples of?

A

Rate limiting (non-dihydropyridines) calcium channel blockers that act on both heart and blood vessels.
Verapamil - heart only.
Diltiazem - heart and blood vessels.

131
Q

When would you use rate limiting (non-dihydropyridines) calcium channel blockers?

A

HTN, tachyarrhythmias, angina, migraine and cluster headaches.

132
Q

What are potential adverse effects of rate limiting (non-dihydropyridines) calcium channel blockers?

A

Worsening HF, bradycardia, heart block and constipation.

133
Q

What are non-rate limiting (dihydropyridines) calcium channel blockers used for?

A

1st line for HTN over 55 or African/Caribbean, Raynaud’s, angina

134
Q

Adverse effects of non-rate limiting (dihydropyridines) calcium channel blockers?

A

Ankle oedema, acid reflux, flushing, gingival hyperplasia

135
Q

What is mannitol and where does it act?

A

Osmotic diuretic which acts at PCT and descending loop of Henle

136
Q

What is furosemide and where and how does it act?

A

Loop diuretic - acts at thick ascending limb of Loop of Henle by blocking Na+/K+/Cl- pump

137
Q

What is hydrochlorothiazide (HCTZ) and where and how does it act?

A

Thiazide diuretic acts by blocking Na/Cl channels at DCT leading to Na+ and water loss

138
Q

What is spironolactone and where does it act?

A

Potassium-sparing diuretic acting at the collecting duct

139
Q

Which type of diuretics are less effective with increasing renal impairment and can cause gout?

A

Thiazide: Bendroflumethiazide, hydrochlorothiazide

& Thiazide-Like: indapamide, chlortalidone

140
Q

When are loop diuretics used?

A

Pulmonary oedema (due to HF), nephrotic syndrome and ascites - less commonly in HTN

141
Q

How are K+-sparing diuretics classified and how do they work? When are the different types used?

A
  1. Aldosterone antagonists: prevents aldosterone from stimulating Na+ and H2O reabsorption and K+ secretion in the collecting duct. Used in low doses for HTN, in hyperaldosteronism and Conn’s syndrome, HF and ascites (portal HTN).
  2. Non-aldosterone antagonists (amiloride, triamterene): block Na+ channels and inhibit K+ excretion in CD so only weak diuretic activity.
142
Q

How do alpha blockers work?

A

Block alpha mediated vasoconstriction so cause vasodilation

143
Q

What are the different types of beta-blockers and their indications?

A
  1. Cardioselective (target beta-1 adrenoreceptors): decrease HR and force of contraction - bisoprolol, metoprolol, atenolol
  2. Non-selective (target beta-1 and beta-2) - propranolol: HR and contraction effects but also reduce renin release
    Beta-2 activation causes smooth muscle relaxation and bronchodilation –> beta blockers contraindicated in asthma, peripheral arterial disease and acute HF.

Indications: HF, IHD, arrhythmias, anxiety, migraine prophylaxis, oesophageal varices, glaucoma, thyrotoxicosis, essential tremor

144
Q

How is orthostatic HTN defined?

A

> =20mmHg SBP drop + >=10mmHg DBP drop on standing (up to 5 minutes)

145
Q

How is oedema caused in HF?

A

Kidneys are under perfused so RAAS stimulated leading to Na+ and H2O retention and oedema.

146
Q

Which medications can be used for HFrEF and what do they all do?

A
  1. ACEi/ARBs: reduce preload and afterload - decrease symptoms, disease progression and prolong life.
  2. Beta-blockers: reduce sympathetic overactivity - improve survival, can worsen in acute settings.
  3. Aldosterone antagonists: reduce mortality
  4. Diuretics: reduce preload and circulating volume - symptom management
  5. Digoxin: increase force of contraction so useful with AF
147
Q

What is sacubitril, how does it work and what can it be used for?

A

A neprilysin inhibitor for chronic HFrEF. Neprilysin usually breaks down BNP so sacubitril prevents this and leads to decreased sympathetic tone, vasodilation, decreased BP, decreased ventricular hypertrophy, decreased fibrosis, decreased aldosterone and diuresis.

148
Q

What are the 4 classes of drugs used as anti-arrhythmics?

A
  1. Drugs blocking voltage-gated Na+ channels: classified with speed they dissociate from receptor (intermediate, fast and slow).
  2. Beta-blockers: block sympathetic AVN conduction
  3. Drugs that substantially prolong cardiac AP: amiodarone
  4. CCBs: verapamil, diltiazem
  5. Not classified: digoxin, adenosine
149
Q

What 3 types of pharmacological management need to be given for AF?

A
  1. Anticoagulation to prevent stroke: warfarin, DOACS (rivaroxaban, apixaban, dabigatran)
  2. Rate control (older patients) or rhythm control (younger)
    - Rate: beta-blocker, diltiazem, verapamil, digoxin (only if also have LV dysfunction or CCF)
    - Rhythm: amiodarone (not if have COPD), flecainide
150
Q

What does digoxin do and how does it work?

A

Cardiac Glycoside: Positive inotropic effect (increases force of myocardial contraction) and reduces conductivity within the AVN by enhancing vagal inhibition.

  1. Inhibits Na+/K+ ATPase in cardiac myocytes
  2. Increases intracellular Na+
  3. Inhibits Na+/Ca2+ exchange so increases intracellular Ca2+
151
Q

What is digoxin used for?

A

AF, atrial flutter, heart failure

152
Q

What can over treatment with digoxin cause?

A

Hyperkalaemia –> cardiac arrhythmias, N&V, diarrhoea, fatigue, confusion, xanthopsia

153
Q

What will happen if overdose on digoxin? What should you give?

A

Atropine (speed up HR) and digoxin-specific antibody fragments

154
Q

What does the CHADVASC score assess and which factors are included?

A

Stroke risk for patients with AF /9
Congestive heart failure, HTN, Age >75, Diabetes mellitus, Stroke/TIA/TE, Vascular disease (prior MI, PAD, aortic plaque), Aged 65-75, Sex Category (+1 if female)

155
Q

What does the HASBLED score assess and which factors are included?

A

Risk of bleeding in AF /9
Hypertension >160mmHg, Abnormal renal and liver function, Stroke, Bleeding tendency/predisposition, Labile INRs (if on warfarin), Elderly (>65), Drugs & alcohol

156
Q

What are the 2 types of DOACs?

A
  1. Direct thrombin (IIa) inhibitors - dabigatran

2. Factor Xa inhibitors - rivaroxaban, apixaban, edoxaban (ALL HAVE XA IN NAME)

157
Q

How does warfarin work?

A

Inhibits synthesis of vitamin K dependent clotting factors (II, VII, IX and X)

158
Q

What needs to be monitored when on warfarin? What is the aim?

A

INR - higher the number, the longer it takes blood to clot, aim between 2-3 or 2.5-3.5 with mechanic valve

159
Q

What increases INR when on warfarin and why?

A

Cranberry juice, ciprofloxacin, clarithromycin and metronidazole = inhibits cytochrome P450 enzymes

160
Q

What decreases INR when on warfarin and why?

A

Dietary vitamin K, rifampicin, carbamazepine, St Johns Wort = induce cytochrome P450 so increase metabolism of warfarin

161
Q

Why might DOACs be preferred over warfarin?

A
  • Don’t need to monitor INR

- Lower risk of intracranial bleeding

162
Q

Which scoring system can be used to predict a cardiovascular incident (MI or stroke)% risk over 10 years?

A

QRISK

163
Q

What should be prescribed if a patients QRISK is over 10%?

A

Statin

164
Q

What medications can be used for smoking cessation?

A
  1. Nicotine replacement therapy
  2. Varenicline (champix): nicotine receptor partial agonist - can lead to suicide ideation
  3. Buproprion: NA (and dopamine) reuptake inhibitor - lowers seizures so not used in epilepsy
165
Q

Which drugs can help obesity in diabetic patients?

A
  1. GLP1 agonists: liraglutide

2. SGLT2 inhibitors: empagliflozin - excrete more glucose in urine but risk of UTI/thrush/developing DKA

166
Q

What do statins do and how do they work?

A

HMG CoA reductase inhibitors. This is a rate-limiting enzyme in the hepatic synthesis of cholesterol so reduce LDL cholesterol by 20-55%.

167
Q

What is the most potent statin?

A

Rosuvastatin

168
Q

Adverse effects of statins?

A

Myalgia, myositis, raised LFTs, new onset diabetes, rhabdomyolysis (rare).

169
Q

What drug class do bezafibrate, fenofibrate and gemfibrozil all belong to?

A

Fibrates - markedly reduce circulating VLDL and triglyceride, modest effects on LDL and HDL.

170
Q

What are adverse effects of fibrates?

A

GI symptoms, rash, pruritic, rhabdomyolysis

171
Q

What are the main strategies for pharmacotherapy of angina pectoris?

A
  1. Slow HR and reduce metabolic demand
  2. Improve blood supply - coronary vasodilation
  3. Reduce preload - venodilation
  4. Reduce afterload - lower systemic BP
  5. Treat symptoms - GTN
172
Q

How do nitrates work? How can they vary?

A

Donate NO (vasodilator causing smooth muscle relaxation). Can be spray, sublingual/buccal tablet or patch. Immediate release or modified release (MR).

173
Q

Problems with nitrates?

A
  • Tolerance develops in long-term use

- Side effects: headache, postural hypotension

174
Q

What drug classes are used in standard ACS treatment?

A
  1. Aspirin 300mg loading dose
  2. Clopidogrel/ticagrelor (anti-platelet)
  3. LMWH e.g. enoxiparin/fondaparinux
  4. GTN (glyceryl trinitrate) spray/buccal tablet/infusion
  5. Analgesia e.g. IV morphine
  6. Anti-emetic e.g. IV metoclopramide
  7. Oxygen only to maintain 94-98%
175
Q

What is standard treatment for STEMI?

A
  1. PCI - angioplasty +/- stenting

2. Thrombolysis only if PCI not available

176
Q

How do heparins work?

A

Activate antithrombin II which inhibits thrombin

177
Q

What are the 2 possible types of heparin, how do they differ?

A

Unfractionated Heparin:

  • IV bolus/infusion (continuous)
  • immediate action and short half-life
  • monitor by APTT (prolongs it)
  • can cause heparin-induced thrombocytopenia (HIT) where platelets progressively drop

LMWH:

  • subcut injection (can be self-administered)
  • enoxaparin, tinzaparin, dalteparin
  • longer half-life
  • does not prolong APTT so monitoring not required
  • reduce dose if have renal impairment
  • use for PE, DVT, treatment and prophylaxis
  • inactivates factor Xa
178
Q

How does aspirin work? What are it’s main adverse effects?

A

Irreversibly inhibit COX1, preventing the production of thromboxane A2 (TXA2) and thereby inhibiting platelet activation and aggregation via expression of GPIIa/IIIa complex.
Main adverse effects: upper GI bleed as inhibits prostaglandins in stomach lining

179
Q

What are clopidogrel and prasugrel, how do they work and what are they used for?

A

Anti-platelet drugs which inhibit adenosine P2Y12 so irreversibly inhibit ADP-induced platelet aggregation. They are prodrugs so require conversion to activate by cytochrome P450.
Used 1 year post-coronary stent insertion and first line for prevention of stroke.

180
Q

When could clopidogrel therapy fail?

A

Patients with variant alleles of CYP2C19

181
Q

What is used as secondary prevention following IHD diagnosis?

A
  1. Dual antiplatelet therapy - aspirin and clopidogrel/prasugrel
  2. Beta-blocker
  3. ACEi
  4. Statin
  5. Smoking cessation
182
Q

What is the mechanism of action of morphine?

A

Binds to opioid receptors in CNS which suppress the release of glutamate from presynaptic terminals and inhibit neurons by hyperpolarising post-synaptic membranes. This prevents passage of nociception from the dorsal horn to higher levels of the brain where pain is perceived.

183
Q

How are most drugs absorbed?

A

Passive diffusion

184
Q

What 3 factors impact absorption of a drug?

A

pH, surface area and blood flow

185
Q

What is the AUC under a drug?

A

Area under the curve - describes the variation of drug concentration in blood plasma over time

186
Q

What is bioavailability in terms of AUC?

A

(AUC oral / AUC IV) x 100

187
Q

Which factors contribute to drug distribution?

A
  1. Lipophilicity - increased increases
  2. Blood flow - more in brain than skin
  3. Capillary permeability - increased in liver and decreased in brain
    Plasma binding and tissue binding - decreased if bind to albumin
  4. Volume of distribution (VD) = amount of drug in body / concentration of drug in blood plasma
    High molecular weight drugs have higher concentration in plasma
188
Q

What are the 3 main routes for elimination of a drug?

A

Hepatic, renal and billiary

189
Q

What is special about aspirin in terms of it’s elimination?

A

Eliminated by zero order kinetics - rate of elimination is constant (amount NOT fraction same per each time period)

190
Q

What is the “steady state” concentration of a drug?

A

Rate of administration = rate of elimination

about 4-5 half lifes

191
Q

Which type of drugs can a kidney not get rid of? Why?

A

Lipid-soluble drugs as they are passively reabsorbed

192
Q

What does the liver do to help with removal of lipophillic drugs?

A

Transfers them into water soluble molecules which are then easily removed by kidneys.
PHASE 1: make drug more hydrophilic by oxidation, hydrolysis and reduction (remove polar group)
- these reactions are catalysed by cytochrome P450
PHASE 2: conjugation reaction (adding a polar group) including glucathione conjugation, acetylation, sulfation, glucoronidation

193
Q

What are CYP 3A4/3A5/2D6/2C8/2C9/1A2 all examples of?

A

Cytochrome P450 enzymes

194
Q

Which drugs induce cytochrome P450 enzymes?

A

PCRABS - phenytoin, carbamezapine, rifampin, alcohol (chronic), barbiturates, St. Johns Wort

195
Q

Which drugs inhibit cytochrome P450?

A

GPACMAN
Grapefruit, Protease inhibitors, Azole antifungals, Cimetidine, Macrolides (except azithromycin), Amiodarone, Non-DHP CCBs (diltiazem, verapamil)

196
Q

Why might you need to alter the dose of a drug in pregnancy?

A

If it has a narrow therapeutic index because the placenta is involved in the metabolism of drugs

197
Q

How does absorption of drugs change in pregnancy?

A

Decreased in oral drugs (N/V, increased gut transit time) and increased in IM injections and inhalation

198
Q

What impacts susceptibility of a foetus to a teratogen?

A

Genotype of mum and baby and developmental stage

199
Q

When is the period of highest sensitivity to teratogens?

A

3-8 weeks due to organogenesis

200
Q

What is fetotoxicity?

A

When intrauterine growth (IUGR), functional development, or toxic effects on tissues occur in 2/3rd trimester

201
Q

Why should diazepam not be given shortly before or during labour?

A

After birth, the baby may not be able to metabolise this drug as well on it’s own.

202
Q

Which type of antibiotics can cause skeletal abnormalities?

A

Quinolone

203
Q

What can sodium valproate do to a foetus?

A

neural tube defects, facial and neuropsychiatric effects

204
Q

Which way do you often need to adjust the dose of a medication in pregnancy?

A

Increase as increased plasma volume, ECF, placental metabolism

205
Q

What factors contribute to the potential for harm of taking a drug during breastfeeding?

A
  1. Amount of drug delivered in milk
  2. Efficiency of absorption, distribution and elimination of a drug by infant
  3. Effect of the drug on the infant
206
Q

Which characteristics of a drug reduces it’s passage into breast milk?

A
  1. High molecular weight (insulin, heparins)
  2. High protein binding (warfarin, NSAIDs)
  3. Low lipid solubility (loratadine)
  4. Low pH (eg amoxicillin) - as pH of breast milk lower than plasma
207
Q

Which drugs need to be avoided in breast feeding?

A

Amiodarone, antithyroid drugs, benzodiazepines, lithium salts, radioactive iodine, statins, sulphonamides

208
Q

What is recommended as initial contraception post-birth? Why?

A

Progesterone-only as oestrogen may reduce milk volume

209
Q

Which hormone changes effect lactation?

A

Dopamine

210
Q

How does absorption of a drug change in children?

A
  1. Oral: developmental changes in GI motility, epithelium and pH = slower emptying
  2. IM absorption erratic as muscle mass and blood flow varies from injection site
  3. Percutaneous: younger patients have thinner stratum corneum and increased skin hydration so increased absorption
211
Q

Why do higher doses per kg of gentamycin need to be given to children?

A

Water soluble drugs have a higher volume of distribution

212
Q

Why is the distribution of morphine, phenytoin and diazepam increased in neonates?

A

They are protein bound drugs and neonates have reduced plasma proteins so more free drug

213
Q

How does total body water and fat change as we grow up?

A

%total body water decreases, %fat increases then decreases in old adult

214
Q

How do the hepatic enzyme pathways (metabolism of drug) vary in neonates and infants?

A

Phase 1: enzymes (cytochrome P450s) appear after birth so be aware in preterm infants (can give caffeine as respiratory stimulant)
Phase 2: less well understood - appears later

215
Q

How does excretion vary in infants?

A

GFR takes up to 6 months to mature to adult values therefore drugs excreted by kidneys (gentamycin) accumulates

216
Q

What factors usually determine a paediatric dose?

A

(Childs body surface area/adult body surface area) x adult dose

217
Q

What 3 ways can you express dosing in children?

A
  1. Age: paracetamol, amoxicillin
  2. Weight: mg/kg for more worrying drugs
  3. Body surface area: mg/m^2 for drugs with narrow therapeutic window (chemo, immunosuppression)
218
Q

What can make you exceed the adult dose when dosing by weight in children?

A

Obesity

219
Q

At what age is adult dose usually recommended?

A

12

220
Q

What is Broselow tape?

A

A measure relating child’s length to age to be used when dosing in an emergency

221
Q

Why is IM route discouraged in neonates and young children?

A

Lack of muscle mass

222
Q

What are special routes of administration used in children?

A

Interosseous (highly vascularised bone marrow) and buccal

223
Q

Why should you avoid IV chloramphenicol in children?

A

Cause grey baby syndrome in neonates = cyanosis, grey skin colour, hypotension and cardiovascular collapse

224
Q

Why should you avoid aspirin in children?

A

Can cause Reye’s syndrome = mitochondrial damage leading to rash, vomiting and liver damage

225
Q

Why should you avoid tetracycline in children?

A

Affects growing teeth (discolouration) and bones

226
Q

Why should you avoid codeine in children?

A

Toxicity, could produce more morphine

227
Q

What is the most important pharmacokinetic change in the elderly?

A

Decreased renal elimination as GFR falls

228
Q

Why is the bioavailability of nifedipine, nitrates and verapamil significantly increased in the elderly?

A

First pass metabolism reduced due to reduced hepatic blood flow or cytochrome P450 reduction

229
Q

Why might pharmacodynamics change in the elderly?

A

Increased receptor sensitivity or changes to receptor number

230
Q

Why are the elderly more at risk of extra-pyramidal side effects and hypotension with antihypertensive therapy?

A
  1. Decreased dopamine receptors

2. Reduced baroreceptor function

231
Q

What are the 4 geriatric giants that drugs will influence?

A
  1. Immobility
  2. Instability
  3. Incontinence
  4. Impaired intellect/memory
232
Q

Which drugs are known to cause falls in elderly?

A

Sedation as slow reaction times: benzos, sedatives, antidepressants, antipsychotics
Hypotension & arrythmias: cardiovascular medication

233
Q

Which drugs can mimic dementia?

A

Anticholinergics

234
Q

Which criteria is used for looking at prescribing in elderly?

A

STOPP/START

235
Q

What are the STOPP criteria?

A
  1. Drug without EBM clinical indication
  2. Duplicate drug class
  3. Verapamil or diltiazem with HF
  4. Loop diuretic for HTN if have urinary incontinence
236
Q

What are the START criteria?

A
  1. Vitamin K antagonists/NOACs if chronic AF
  2. Acetylcholinesterase inhibitor for mild/moderate Alzheimer’s
  3. Vitamin D supplements in housebound or experiencing falls or with osteopenia
237
Q

What are the STOPPfrail criteria?

A

Must fulfill all

  1. End-stage irreversible pathology
  2. Poor one year survival prognosis
  3. Severe functional/cognitive impairment
  4. Symptom control not prevention is priority
238
Q

Which drugs should be avoided with renal impairment and why?

A
  1. Aminoglycosides
  2. Metformin: increased risk of lactic acidosis
  3. Nitrofurantoin: not effective if eGFR <45
  4. Potassium supplements/sparing diuretics: hyperkalaemia
  5. Lithium: renally excreted with narrow therapeutic index
  6. NSAIDs: avoid in CKD as can exacerbate fluid overload and oedema
239
Q

Which function of the liver is measured by PT/INR?

A

Synthetic (synthesis of clotting factors) not metabolic

240
Q

Why does hepatic impairment mostly not impact drug metabolism?

A

It has great metabolic reserve and is large

241
Q

How can hepatic insufficiency impact action of drugs?

A
  1. Hypoproteinaemia - affects protein binding
  2. Reduced clotting - sensitivity to warfarin, NSAIDs
  3. Biliary obstruction - prevents excretion (rifampicin) and action (cholestyramine) of drugs
  4. Hypoalbuminaemia - complicates interpretation of plasma phenytoin concentrations
  5. Fluid overload which can be exacerbated by NSAIDs, corticosteroids
  6. Hepatic encephalopathy could be precipitated: sedatives, diuretics (hypokalaemia), constipation
242
Q

What is rhabdomyolysis?

A

Hypoxic muscle damage. Release of muscle cell contents – creatinine kinase (CK), myoglobin, potassium. Myoglobin precipitation in kidney causes renal failure –> coca cola urine and increased total CK in plasma.

243
Q

Which drug overdose can cause mydriasis?

A

Large pupils

Sympathomimetics (stimulants) and anticholinergics

244
Q

What ca cocaine, amphetamines, ecstasy and serotonergic drugs (SSRIs) do to body temperature?

A

Increase (hyperthermia)

245
Q

Which drug poisonings require specific drug blood concentrations required to guide management?

A

paracetamol, salicylate, iron, lithium, methanol/ethylene glycol, ethanol

246
Q

If someone presents with nausea, vomiting, tinnitus, deafness, sweating, hyperventilation, metabolic acidosis and hyperthermia what could they be poisoned with?

A

Salicylates (aspirin)

247
Q

If someone presents with coma, hypertonia, mydriasis, tachycardia what could they be poisoned with?
coma, convulsions, cardiac arrhythmias (broad QRS)

A

TCAs

248
Q

How can you stop a drug being absorbed into the bloodstream if indication of poison?

A
  1. Gastric lavage - not often used
  2. Single dose activated charcoal
  3. Whole bowel irrigation
249
Q

How can you increase the clearance rate of a drug thought to be causing poisoning from the bloodstream?

A
  1. Multiple dose activated charcoal: “GI dialysis” as conc gradient
  2. Urine alkalinization: administer IV sodium bicarbonate
  3. Extracorporeal elimination: haemodialysis/haemofiltration
  4. Chelating agents: chelate binds to ion and is eliminated via the kidneys
250
Q

What category of drugs do amfetamines, cocaine, piperazines, cahinones and synthetic cathinones belong to?

A

Stimulants

251
Q

How can you manage a patient on stimulants?

A
  1. ACTIVE COOLING - fluids, ice packs, dantrolene (interferes with calcium efflux in muscle cells so reduces contractions)
  2. Supportive
  3. Diazepam 10mg IV if agitated
252
Q

What class of drugs do alcohol, opiates, opioids, GHB/GBL and ketamine all belong to?

A

Sedatives/dissociatives

253
Q

What is the chemical name for heroin and how is it metabolised?

A

Diacetylmorphine –> 6-monoacetylmorphine (6-MAM) via esterase in blood
6-MAM –> morphine in liver and brain

254
Q

What agonist is heroin?

A

mu-opioid agonist

255
Q

What can occur in opiate poisoning and how would you manage it?

A

Coma, respiratory depression with low pO2 and high pCO2 = resp acidosis

  1. ABC
  2. Naloxone - opiate receptor competitive antagonist
256
Q

Which drug class do magic mushrooms, LSD, phenylethylamines and synthetic tryptamines belong to?

A

Hallucinogens/

257
Q

How do cannabinoids work?

A

CB1 and CB2 receptor agonists

258
Q

How is alcohol absorbed?

A

Over 80% in duodenum-jejunum by simple diffusion

259
Q

How is alcohol distributed in the body?

A

Rapidly distributed, especially with rich blood supply and crosses BBB and placenta easily. Higher concentration in people with more fat.

260
Q

How is alcohol metabolised?

A
  1. Ethanol to acetaldehyde by alcohol dehydrogenase (ADH) - zero order
  2. Acetaldehyde –> Acetate by ALDH (alcohol dehydrogenase) - genetic variation
  3. Acetate –> CO2 and H2O
261
Q

How is alcohol eliminated from the body?

A

Slow clearance rate, small amount not metabolised and excreted in urine and breath

262
Q

What are the pharmacological effects of alcohol?

A
  1. CNS depressant
  2. GABA-A potentiation
  3. NMDA antagonist: glutamate inhibition
  4. Effects on reward centres (serotonin, opioid and dopamine transmission)
263
Q

What is the common cause of death in acute alcohol intoxication?

A

Aspiration from vomiting

264
Q

What is Wernicke’s encephalopathy?

A

Central and peripheral nervous system condition caused by thiamine deficiency that could lead to Korsakoff’s syndrome if untreated.
Triad: eyes (opthalmoplegia/nystagmus), ataxia and confusion
Treatment: high dose vitamin B complex (pabrinex then oral thiamine)

265
Q

What are the CAGE questions?

A
  1. Have you ever tried to cut down how much you drink?
  2. Have you ever got annoyed by others criticising your drinking?
  3. Have you ever had guilty feelings about drinking?
  4. Do you ever need an eye-opener in the morning?
266
Q

What can bloods look like for someone with chronic alcohol use?

A 
FBC: Macrocytosis in absence of anaemia 
U&Es: low urea 
LFTs: raised transaminases 
GGT: elavated with no/small ALP raise 
INR: elavated if problems with livers synthetic function
267
Q

What is the end-stage of alcohol withdrawal called and at what time will it occur?

A

48-72 hours later - Delirium Tremens - hallucinations, disorientation, tachycardia, increased BP, mild fever, agitation, diaphoresis

268
Q

How can alcohol withdrawal symptoms be prevented?

A

Specialist advice!

Benzodiazepines e.g. chlordiazepoxide or diazepam - prevent seizures

269
Q

Which drugs can be used to maintain abstinence from alcohol?

A
  1. Acamprosate: stabilises glutamate and GABA systems - reduce alcohol cravings, anxiety and insomnia
  2. Naltrexone: opioid antagonist - reduce relapse
  3. Nalmefene: opioid receptor modulator - reduces consumption
  4. Disulfiram: inhibits intermediate metabolism of alcohol leading to flushing, nausea and sweating
270
Q

What are the 3 types of pain?

A
  1. Nociceptive: stimulation of intact primary afferent nerves responding to stimuli
  2. Neuropathic: pain signal generated ectopically often in absence of ongoing noxious event
  3. Psychogenic: no apparent organic basis but strict diagnostic criteria
271
Q

What is allodynia?

A

A non-painful stimulus causing pain

272
Q

What is paraesthesia?

A

Stimulus interpreted as something else e.g. cold as pain

273
Q

Where can pain management target?

A
  1. Source of pain
    2, Nociceptive substances - prostaglandins, cytokines
  2. Nerve transmitter substances - serotonin
  3. Modulators in brain or spinal cord
  4. Emotional reaction to pain
274
Q

How does the WHO pain ladder work?

A
  1. Non opioid - e.g. paracetamol
  2. Weak opioid + non-opioid - e.g. codeine
  3. Strong opioid + non-opioid - e.g. morphine (titrate carefully more elderly)
    + analgesia if required e.g. anticonvulsant/antidepressant
275
Q

How do NSAIDs work?

A

Inhibit prostaglandin synthase (COX enzymes). On target effects on COX1 (inflammatory process and kidneys), off-target effects on COX2 (protects gastric mucosa).

276
Q

When is diclofenac used?

A

Moderate inflammatory or post-operative pain

277
Q

What are the main risks/adverse effects of NSAIDs?

A

Risks:

  1. Bleeding
  2. Nephrotoxic

Adverse effects: cardiovascular, renal dysfunction, GI (peptic ulcers, gastritis, bleeding), hypersensitivity reactions (rases, angioedema, bronchospasm - can affect asthma)

278
Q

What can you do for patients who require an NSAID but have a history of peptic ulcer disease?

A

Prescribe PPI - e.g. 15mg lansoprazole

279
Q

Do opioids have anti-inflammatory properties?

A

No

280
Q

What are the 2 types of weak opioids?

A

Codeine phosphate and dihydrocodeine

281
Q

How do opioids work?

A

Activates mu/kappa receptors in spinal cord producing anti-nociceptive effect and opioid receptors in brain, reducing affective component of pain. Receptors suppress the release of glutamate from presynaptic terminals and inhibit neurons by hyperpolarising post-synaptic membranes. Prevent passage of nociception from dorsal horn to higher levels of the brain where perception of pain is generated.

282
Q

Why is codeine metabolised faster by some specific people meaning lots of morphine is produced?

A

They have genetic variation in cytochrome 2D6 which metabolised codeine in the liver

283
Q

Which drug strength is between codeine and morphine? Apart from working as an opioid analgesic, what other effect does it have?

A

Tramadol - enhanced 5HT and adrenergic pathways

284
Q

What are morphine, fentanyl, oxycodone and pethidine all examples of?

A

Strong opioids

285
Q

Why are strong opioids associated with dependence?

A

Rapidly cross BBB as lipid-soluble and cause euphoric effect

286
Q

When are strong opioids contraindicated?

A

Respiratory depression (as impact these centres in brain), hypotension and liver impairment = these are not important in terminal illness

287
Q

What is an ADR of pethidine?

A

Stimulate CNS and cause seizures

288
Q

What are adjuvant agents of pain?

A

Drugs intended for indications other than pain but work on CNS. Response varies between patients.
o TCAs – amitriptyline
o Antiepileptic agents – pregabalin, carbamazepine
o Anxiolytics – diazepam

289
Q

What can be used for diabetic neuropathy or trigeminal neuralgia?

A
  1. Amitriptyline (TCA)

2. Anti-epileptics: gabapentin or carbamezapine

290
Q

Which adjuvant pain medication can be given to reduce associated muscle spasm pain?

A

Diazepam 2mg

291
Q

Which pain medications do you need to be careful with with someone with liver disease?

A

NSAIDs (increased bleeding risk), paracetamol, opioids (encephalopathy as slowly metabolised)

292
Q

Which pain medications do you need to be careful with with someone with kidney disease?

A

NSAIDs (further renal impairment), elimination of some drugs

293
Q

Which pain medications do you need to be careful with children?

A

Not aspirin as risk of Reye’s syndrome (swelling of liver and brain).
Codeine phosphate with caution as metabolism varies.

294
Q

How often should patients on morphine be reviewed?

A

1x month at least to detect emerging harms and consider ongoing effectiveness

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