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Prescribing safety assessment > Common drugs > Flashcards

Common drugs Flashcards

1
Q

ACE-inhibitors: indications (5)

A
  1. HTN
  2. IHD
  3. Chronic HF
  4. Diabetic nephropathy
  5. CKD + proteinuria
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2
Q

ACE-inhibitors: mechanism of action

A

Prevent conversion of angiotensin I to angiotensin II

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3
Q

What does angiotensin II do?

A
  • Vasoconstrictor

- Stimulates aldosterone secretion

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4
Q

What are the effects of blocking angiotensin II (i.e. using an ACE-inhibitor)?

A
  • ↓ PVR (afterload) ∴ ↓BP
  • Dilates efferent glomerular arteriole ⇒ ↓ intraglomerular pressure ⇒ slows progression of CKD
  • ↓ aldosterone ⇒ promotes Na+ and H20 excretion ⇒ ↓ preload (good for HF)
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5
Q

ACE-inhibitors: adverse effects

A
  • Hypotension (esp. after first dose)
  • Persistent dry cough (ACE usually clears bradykinin, ∴ inhibition ⇒ ↑ bradykinin ⇒ cough)
  • Hyperkalaemia (↓ aldosterone ⇒ ↑ K+ retention)
  • Worsen renal failure
  • Angioedema (R)
  • Anaphylaxis (R)
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6
Q

ACE-inhibitors: contraindications

A

Absolute:

  • Renal artery stenosis
  • AKI

Relative:

  • WOCP (caution - teratogenic)
  • Breastfeeding (caution)
  • CKD (use lower doses + monitor kidney function)
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7
Q

ACE-inhibitors: interactions

A
  • Potassium-elevating drugs

- NSAIDs (↑ risk of nephrotoxicity)

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8
Q

Ramipril: prescription

A
  • PO
  • 1.25mg OD for HF or CKD
  • 2.5mg OD for other indications
  • Titrate up to 10mg OD
  • First dose before bed (↓ hypotension symptoms)
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9
Q

5α-reductase inhibitor: common indications (2) (e.g. finasteride)

A
  • Second-line intervention for BPH
  • Improve LUTS ∴ ↓ need for surgery
  • Androgenetic alopecia (MPB)
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10
Q

5α-reductase inhibitors: mechanism of action

A

↓ size of prostate

  • Inhibits conversion of testosterone → active dihydrotestosterone
  • Dihydrotestosterone stimulates prostatic growth
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11
Q

Why is an α-blocker first line for BPH instead of 5α-reductase inhibitors?

A

5α-reductase inhibitors take months to have an effect

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12
Q

5α-reductase inhibitors: adverse effects

A

Adverse effects related to anti-androgen action;

  • Impotence (transient)
  • ↓ libido (transient)
  • Gynaecomastia
  • ↑ hair growth
  • Breast cancer
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13
Q

5α-reductase inhibitors: contraindications

A

Pregnancy
- Exposure (either by handling tablets or through semen of man using these drugs) can cause abnormal genitalia development of a male foetus

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14
Q

Finasteride: prescription

A
  • Usually 5mg PO OD for BPH Tx

- Follow-up 3-6m after first prescription, then review every 6-12m after

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15
Q

α-blockers: common indications (2)

A
  1. First-line for BPH

2. Add-on Tx in resistant HTN

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16
Q

α-blockers: mechanism of action

A
  • Highly selective for α1-adrenoreceptors, which are found in smooth muscles (particularly blood vessels, bladder neck and prostate)
  • Stimulation ⇒ contraction
  • Blockade ⇒ relaxation ∴ vasodilation (⇒ ↓BP) and ↓ resistance of bladder outflow
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17
Q

α-blockers: examples

A
  • Doxazosin
  • Tamsulosin
  • Alfuzosin
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18
Q

α-blockers: adverse effects

A
  • Postural hypotension
  • Dizziness
  • Syncope
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19
Q

α-blockers: contraindications

A

Existing postural hypotension

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20
Q

α-blockers: interactions

A

Other antihypertensive drugs (⇒ extra BP-lowering effects, but this might be the desired effect)

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21
Q

Doxazosin: prescription

A
  • Licensed for BPH and HTN
  • Start at 1mg PO OD, and increase at 1-2w intervals until clinically effective
  • Take at bedtime (to avoid BP lowering symptoms)
  • Monitor from pt’s LUTS
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22
Q

Tamsulosin: prescription

A
  • Licensed for BPH only
  • 400mcg PO OD
  • Monitor by pt’s LUTS
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23
Q

Acetylcholinesterase inhibitors: examples

A
  • Donepezil

- Rivastigmine

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24
Q

Acetylcholinesterase inhibitors: common indications

A
  1. Mild-moderate Alzheimer’s

2. Mild-moderate dementia in Parkinson’s (rivastigmine)

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25
Q

Acetylcholinesterase inhibitors: mechanism of action

A
  • ACh is an essential neurotransmitter involved in learning and memory
  • Alzheimer’s and Parkinson’s results in ↓ cholinergic activity in the brain
  • Inhibitors prevent the breakdown of ACh, making it more available for cognitive function
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26
Q

Acetylcholinesterase inhibitors: adverse effects

A
  • N,V&D (caused by ↑ cholinergic activity in PNS)
  • Exacerbation of asthma/COPD Sx
  • Worsening of tremor in pts with Parkinson’s (rivastigmine)

Less common, but serious;

  • Peptic ulcers
  • Bleeding
  • Bradycardia
  • Heart block
  • Hallucinations
  • Altered/aggressive behaviour
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27
Q

Acetylcholinesterase inhibitors: contraindications

A

Use with caution;

  • Asthma/COPD
  • People at risk of peptic ulcer development

Absolute;

  • Heart block
  • Sick sinus syndrome
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28
Q

Acetylcholinesterase inhibitors: interactions

A
  • NSAIDs and corticosteroids ⇒ ↑ risk of peptic ulcers
  • Antipsychotics ⇒ ↑ risk of neuroleptic malignant syndrome
  • Rate-limiting medications ⇒ bradycardia and/or heart block
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29
Q

Donepezil: prescription

A
  • Start at 5mg
  • Titrate up after 2-4w
  • Reassess for treatment efficacy at 3m
  • Take before bed
  • Available as tablet, capsule, or liquid
  • Explain to pt/caregivers that it is not a cure for dementia
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30
Q

Rivastigmine: prescription

A
  • Start at 1.5mg 12-hrly
  • Titrate up after 2-4w
  • Reassess for treatment efficacy at 3m
  • Available as tablet, capsule, or liquid OR
  • Available as a patch for pts with swallowing difficulties
  • Explain to pt/caregivers that it is not a cure for dementia
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31
Q

Acetylcysteine: indications (2)

A
  1. Antidote to paracetamol poisoning

2. ↓ viscosity of respiratory secretions (mucolytic) for inpatients

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32
Q

Acetylcysteine: mechanism of action

A
  • Paracetamol OD overwhelms glutathione protein responsible for ‘mopping up’ hepatotoxic metabolite, NAPQI
  • Excess NAPQI is ∴ free to cause liver damage
  • Acetylcysteine replenishes body’s supply of glutathione
  • Breaks disulphide bonds in mucus ⇒ mucolytic activity
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33
Q

Acetylcysteine: adverse effects

A

Anaphylactoid rx (if administered IV)

  • Different to anaphylaxis as there is no IgE involvement
  • ∴ once rx has settled (by stopping infusion + giving antihistamine ± bronchodilator) it is safe to restart at a lower rate of infusion

Bronchospasm (if nebulised)
- Manage by giving a bronchodilator (e.g. salbutamol) immediately beforehand

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34
Q

Acetylcysteine: prescription for paracetamol poisoning

A

Weight-adjusted dose as IV infusion with 3 components over 21hrs

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35
Q

Acetylcysteine: prescription for respiratory secretions

A

2.5-5mL of acetylcysteine 10% solution by nebuliser every 6hrs

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36
Q

Activated charcoal: indications (2)

A
  1. Single dose to ↓ absorption of certain poisons in gut
  2. Multiple dose to ↑ elimination of certain poisons

Certain poisons include (weakly ionic, hydrophobic);

  • Benzodiazepines
  • Methotrexate
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37
Q

Activated charcoal: mechanism of action

A
  • Poisonous molecules are adsorbed onto the surface of the charcoal as they pass through the gut ⇒ ↓ absorption into circulation
  • If molecules are likely to diffuse back into the gut, multiple doses are used to maintain a steep concentration gradient and eliminate the poison (‘gut dialysis’)
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38
Q

Activated charcoal: adverse effects

A
  • Black stools
  • Vomiting
  • Aspiration ⇒ pneumonitis, bronchospasm, airway obstruction
  • Intestinal obstruction
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39
Q

Activated charcoal: contraindications

A
  • Pts with ↓ level of consciousness unless airway is protected with endotracheal intubation
  • Persistent vomiting (caution, ↑ risk of aspiration)
  • Reduced gut motility (caution, ↑ risk of obstruction)
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40
Q

Activated charcoal: single dose prescription

A
  • Used for patients presenting within 1hr of ingestion of poison
  • Prescribe on the ‘once-only’ section of drug chart
  • 50mg orally (or nasogastric tube if intubated)
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41
Q

Activated charcoal: multiple dose prescription

A
  • 50mg PO every 4hrs

- Consider prescribing with an antiemetic and a laxative

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42
Q

Adenosine: indication

A

First-line diagnostic and therapeutic agent for supraventricular tachycardia (SVT)

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43
Q

Adenosine: mechanism of action

A
  • Agonist of adenosine receptors on cell surfaces
  • In the heart ⇒ ↓ frequency of spontaneous depolarisations (automaticity) and ↑ resistance to depolarisation (refractoriness)
  • ∴ slows sinus rate and conduction velocity and ↑ AVN refractoriness
  • ↑ refractoriness in AVN breaks re-entry circuit (cause of SVT) ⇒ allows normal depolarisations from SAN to resume control of HR - CARDIOVERSION
  • Half-life in plasma is <10s - it is rapidly taken up by RBCs
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44
Q

Adenosine: adverse effects

A
  • Bradycardia
  • Asystole
  • ‘Sinking’ feeling in chest + breathlessness + sense of ‘impending doom’

Only lasts for <10s

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45
Q

Adenosine: contraindications

A

Absolute (any pt who will not tolerate its transient bradycardic effects);

  • Hypotension
  • Coronary ischaemia
  • Decompensated HF
  • Asthma (induces bronchospasm)

Relative;

  • COPD (induces bronchospasm)
  • Heart transplant recipients
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46
Q

Adenosine: important interactions

A

Dypyridamole

  • Antiplatelet that blocks cellular uptake of adenosine
  • Prolongs and potentiates adenosine’s effects ∴ dose of adenosine should be halved

Theophylline/aminophylline

  • Competitive antagonists ∴ ↓ effect
  • Require higher dose of adenosine
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47
Q

Adenosine: prescription

A
  • IV
  • Written in the ‘once-only’ section of drug chart
  • Start at 6mg IV
  • If 6mg ineffective ⇒ 12mg IV may be given
  • If using a central line, halve the dose (i.e. 3mg)
  • Resuscitation facilities should be on hand
  • Important that adenosine reaches heart ASAP to avoid peripheral uptake ∴ use a large-bore cannula, sited as proximally as possible (i.e. ACF)
  • Administer as rapid injection then immediately flush
  • MUST have a continuous cardiac rhythm strip recorded when administered
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48
Q

Adrenaline: indications (3)

A
  1. Cardiac arrest
  2. Anaphylaxis
  3. Local vasoconstriction (injected directly into tissue to stop bleeding, i.e. mucosal bleeding during endoscopy)
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49
Q

Adrenaline: mechanism of action

A
  • Potent agonist of α1, α2, β1, and β2 adrenoreceptors
  • Vasoconstriction of vessels to skin, mucosa, and abdominal viscera (α1)
  • ↑ HR, force of contraction, and myocardial excitability (β1)
  • Vasodilation of vessels supplying heart and muscles (β2)
  • ∴ redirects blood away from non-essential organs and towards the heart
  • Bronchodilatation and suppression of inflammatory mediator release from mast cells (β2)
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50
Q

Adrenaline: adverse effects

A
  • Adrenaline-induced hypertension (following cardiac arrest)
  • If given to conscious patients ⇒ anxiety, tremor, headache, and palpitations
  • Angina, MI, arrhythmias
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51
Q

Adrenaline: warnings

A

Absolute;
- As an anaesthetic-adrenaline preparation in areas supplied by end-artery (⇒ necrosis)

Relative;
- Caution as a vasoconstrictor in pts with heart disease

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52
Q

Adrenaline: interactions

A

Β-blockers - adrenaline may induce widespread vasoconstriction because α1 vasoconstriction is not opposed by β2 vasodilatation

53
Q

Adrenaline: prescription for cardiac arrest with shockable rhythm (e.g. VF, pulseless VT)

A
  • Administer first, prescribe later (when life-threatening situation)
  • 1mg IV after THIRD shock, and every 3-5mins thereafter
  • Pre-filled syringe containing 1:10,000 (1mg in 10mL) solution, then flush
54
Q

Adrenaline: prescription for cardiac arrest without shockable rhythm (systole, PEA)

A
  • 1mg IV as soon as IV access is available
  • Then every 3-5mins thereafter
  • Pre-filled syringe containing 1:10,000 (1mg in 10mL) solution, then flush
55
Q

Adrenaline: prescription in anaphylaxis

A
  • 500mcg IM, repeated after 5mins if necessary
  • 0.5mL of 1:1000 (1mg in 1mL) solution
  • Inject into anterolateral aspect of thigh halfway between knee and hip
56
Q

Aldosterone antagonists: examples

A
  • Spironolactone

- Eplerenone

57
Q

Aldosterone antagonists: indications (3)

A
  1. Ascites and oedema due to liver cirrhosis
  2. Chronic HF
  3. Primary hyperaldosteronism
58
Q

Aldosterone antagonists: mechanisms of action

A
  • Aldosterone causes ↑ activity of Na+ channels
  • ⇒ ↑ reabsorption of sodium + H20 ⇒ ↑BP + ↑K+ excretion
  • Antagonists inhibit aldosterone by competitively binding to receptors
  • ⇒ ↑ Na+ + H20 excretion and ↑ K+ retention
59
Q

Aldosterone antagonists: adverse effects

A
  • Hyperkalaemia ⇒ muscle weakness, arrhythmias, cardiac arrest
  • Spironolactone ⇒ gynaecomastia
  • Liver impairment and jaundice
  • Stevens-Johnsons syndrome ⇒ bullous skin eruption
60
Q

Aldosterone antagonists: contraindications

A

Absolute;

  • Severe renal impairment
  • Hyperkalaemia
  • Addison’s disease

Relative;
- Pregnant or lactating women (teratogenic)

61
Q

Aldosterone antagonists: interactions

A

Potassium-elevating drugs (e.g. ACE-inhibitors and ARBs)

- Can still use but requires monitoring

62
Q

Spironolactone: prescription

A
  • PO OD
  • Higher doses for ascites vs. HF
  • 100mg daily (ascites)
  • 25mg daily (HF)
  • Taken with food
  • Tell men about the possibility of growth and tenderness of breast tissue + impotence
  • Monitor efficacy based on clinical findings (e.g. ↓ ascites or BP)
  • Monitor safety by checking renal function and serum K+

Spironolactone is used for all indications, eplerenone is only used for HF

63
Q

Alginates and antacids: examples

A
  • Gaviscon (R)

- Peptic (R)

64
Q

Alginates and antacids: indications (2)

A
  1. GORD

2. Dyspepsia

65
Q

Alginates and antacids: mechanisms of action

A
  • Compounds of alginates + antacids (e.g. sodium bicarbonate)
  • Antacids - buffer stomach acid
  • Alginates - increase viscosity of stomach contents ⇒ ↓ reflux of acid into oesophagus
  • Drugs form a ‘raft’ which blocks contents from the gastro-oesophageal junction
66
Q

Alginates and antacids: adverse effects

A
  • Magnesium salts ⇒ diarrhoea

- Aluminium salts ⇒ constipation

67
Q

Alginates and antacids: contraindications

A

Relative:

  • Compound alginates should not be given to infants with thickened milk preparations ⇒ excessively viscous stomach contents ⇒ bloating + discomfort
  • Patients with fluid overload or hyperkalaemia (e.g. renal failure)
68
Q

Alginates and antacids: interactions

A
  • Alginates bind to other drugs to ↓ absorption
  • Antacids ↓ serum conc. of many drugs
  • Should take 2hrs after/before taking the following drugs;
  • ACE-inhibitors
  • Cephalosporins, ciprofloxacin, tetracyclines
  • Bisphosphonates
  • Digoxin
  • Levothyroxine
  • PPIs
69
Q

Gaviscon / Peptac: prescribing

A
  • Oral suspensions or chewable tablets
  • Usually PRN
  • Caution in diabetics as they can have sucrose in
70
Q

Allopurinol: indications

A
  1. Gout
  2. Renal stones
  3. Hyperuricaemia and tumour lysis syndrome
71
Q

Allopurinol: mechanism of action

A
  • Xanthine oxidase inhibitor
  • Xanthine oxidase metabolises xanthine → uric acid
  • Inhibitor ↓ plasma uric acid ⇒ ↓ precipitation in joints/kidneys
72
Q

Allopurinol: adverse effects

A
  • Trigger or worsen an acute gout attack (when starting)
  • Skin rash
  • Stevens-Johnson syndrome
  • Toxic epidermal necrolysis
  • Allopurinol hypersensitivity syndrome
73
Q

Allopurinol: contraindications

A

Absolute;

  • Current acute gout attack
  • Recurrent skin rash
  • Signs of severe hypersensitivity to allopurinol

Relative;

  • Renal impairment (lower dose)
  • Hepatic impairment (lower dose)
74
Q

Allopurinol: interactions

A
  • Azathioprine (↑ risk of toxicity, as azathioprine active metabolite is metabolised by xanthine oxidase)
  • ACE-inhibitors or thiazides (↑ risk of hypersensitivity rx)
  • Amoxicillin (↑ risk of skin rash)
75
Q

Allopurinol: prescription

A
  • PO
  • Start at low dose (e.g. 100mg OD)
  • Titrate up according to serum uric acid conc.
  • Usual maintenance = 200-600mg OD
  • Prescribe NSAID when first starting for gout to avoid triggering an attack
  • Encourage good hydration, take after meals
  • If used for cancer treatment, start before chemotherapy
76
Q

Aminoglycosides: examples

A
  • Gentamicin
  • Amikacin
  • Neomycin
77
Q

Aminoglycosides: indications (5)

A
  1. Severe sepsis
  2. Pylonephritis and complicated UTI
  3. Biliary and other intraabdominal sepsis
  4. Endocarditis
  5. Bacterial skin, eye, or external ear infections (topical)
78
Q

Aminoglycosides: spectrum of activity

A
  • Against G-ve aerobic bacteriaa

- Inactive against streptococci and anaerobes, so combine with penicillin/metronidazole when organism is unknown

79
Q

Aminoglycosides: mechanism of action

A
  • Bind irreversibly to bacterial ribosomes ⇒ inhibit protein synthesis
  • Bactericidal
  • Enter bacteria via oxygen-dependent transport system (hence ineffective with anaerobes and strep as they don’t have these)
  • Penicillins weaken cell walls, so can enhance aminoglycoside activity by ↑ bacterial intake
80
Q

Aminoglycosides: adverse effects

A
  • Nephrotoxicity (PC: ↓ urine output + ↑ serum Cr and urea) - reversible
  • Ototoxicity (PC: hearing loss, tinnitus, vertigo) - irreversible

Aminoglycosides accumulate in renal tubular epithelial cells and cochlear and vestibular hair cells ⇒ apoptosis ⇒ death

81
Q

Aminoglycosides: contraindications

A

Relative;

  • Neonates
  • Elderly patients
  • Renal impairment
  • Myasthenia gravis
82
Q

Aminoglycosides: interactions

A
  • Loop diuretics and vancomycin (⇒ ototoxicity)

- Ciclosporin, Pl chemotherapy, cephalosporins, and vancomycin (⇒ nephrotoxicity)

83
Q

Aminoglycosides: prescription

A
  • Given parenterally (IV for severe infection)
  • Dose calculated from patient’s weight and renal function
  • Dose is usually 5mg/kg (normal renal function) or 3mg/kg (renal impairment)
  • Dose interval time is determined by drug level monitoring → subsequent doses only given when plasma conc. has fallen to a safe level (usually 24hr - 48hrs)
84
Q

How do you calculate the dose of aminoglycosides in obese patients?

A

Adjusted body weight = [ideal body weight] + 0.4 x ([actual body weight] - [ideal body weight])

  • Adipose tissue contains more fat than water
  • Aminoglycosides are distributed through WATER not fat, and therefore extra weight in obesity complicates dosing
  • Calculate dose by using adjusted body weight
85
Q

Aminoglycosides: preparation and administration

A

Diluted and infused slowly to prevent exposure of ear to high conc. bolus

86
Q

Aminosalicylates: examples

A
  • Mesalazine

- Sulfasalazine

87
Q

Aminosalicylates: indications (2)

A
  • Ulcerative colitis (mesalazine)

- Rheumatoid arthritis (sulfasalazine)

88
Q

Aminosalicylates: mechanism of action

A
  • Release 5-aminosalicylic acid (5-ASA)
  • Anti-inflam and immunosuppressive effects
  • Acts topically on gut (not systemically)
  • Prepared in a way that active molecules are only released in the colon
89
Q

Aminosalicylates: adverse effects

A
  • GI upset
  • Headache
  • Blood abnormalities (R) - leucopenia, thrombocytopenia
  • Renal impairment
  • Oligospermia (reversible) - sulfasalazine
  • Serious hypersensitivity reaction - sulfasalazine

Mesalazine causes fewer SFx than sulfasalazine

90
Q

Aminosalicylates: contraindications

A

Absolute:

- Aspirin hypersensitivity (both salicylates)

91
Q

Aminosalicylates: interactions

A
  • PPIs (increase gastric pH ⇒ tablets are broken down prematurely, i.e. not the colon)
  • Lactulose (lowers stool pH ⇒ prevents 5-ASA release in colon)
92
Q

Mesalazine: prescription

A
  • For mild-moderate rectal/rectosigmoidal UC ⇒ mesalazine enema or suppository
  • In an acute attack, take once or 12hrly for 4-6w to induce remission
  • If disease is more proximal or pt doesn’t want rectal administration, use oral formulation
93
Q

Aminosalicylates: monitoring

A

Efficacy:

  • Pt’s symptoms for UC
  • Disease activity scores and measurement of acute phase reactant conc. (CRP, ESR) for RA

Safety:

  • Renal function (for oral mesalazine)
  • FBC and liver profile (for sulfasalazine)
94
Q

Amiodarone: indications

A

Tachyarrhythmias (inc. AF, atrial flutter, SVT, VT, and VF)

95
Q

Amiodarone: mechanism of action

A
  • Blockade of sodium, calcium, and potassium channels in myocardial cells
  • Antagonism of α and β adrenergic receptors in myocardial cells
  • ↓ spontaneous depolarisation (automaticity), slow conduction velocity, and ↑ refractoriness
96
Q

Amiodarone: adverse effects

A

Acute use:
- Hypotension (IV, though probably effect of solvent)

Chronic use:

  • Pneumonitis
  • Bradycardia
  • AV block
  • Hepatitis
  • Skin photosensitivity
  • Grey discolouration of skin
  • Thyroid abnormalities (amIODarone - contains iodine)
  • Phlebitis (if chronic peripheral administration)
97
Q

Amiodarone: contraindications

A

Relative:

  • Severe hypotension
  • Heart block
  • Active thyroid disease
98
Q

Amiodarone: interactions

A

LOADS, but notably…

  • Digoxin
  • Diltiazem
  • Verapamil
  • Grapefruit juice
99
Q

Amiodarone: prescribing

A
  • Always requires senior involvement

Cardiac arrest:

  • Given immediately after 3rd shock in ALS algorithm in shockable arrest
  • 300mg IV, followed by 20mL of 0.9% sodium chloride/5% glucose as a flush
  • Administer first, prescribe later
100
Q

Angiotensin receptor blockers (ARBs): examples

A
  • Losartan
  • Candesartan
  • Irbesartan
101
Q

When should you use ARBs?

A

Used when ACE-i are not tolerated (usually because of the cough)

Also preferred in black people of African or Caribbean origin

102
Q

ARBs: prescription

A
  • PO
  • Lower starting dose in HF
  • e.g. 12.5mg OD in HF or 50mg OD for other indications
  • Titrate up over a period of weeks
103
Q

SSRIs: examples

A
  • Citalopram
  • Fluoxetine
  • Sertraline
  • Escitalopram
104
Q

SSRIs: indications (3)

A
  1. Moderate-severe depression (or mild if psychological Tx haven’t worked)
  2. Panic disorder
  3. OCD
105
Q

SSRIs: mechanisms of action

A

Inhibit neuronal reuptake of 5-HT ⇒ ↑ availability for neurotransmission

106
Q

SSRIs: adverse effects

A
  • GI upset
  • Change in appetite and weight
  • Hypersensitivity reactions
  • Hyponatraemia ⇒ confusion + ↓ consciousness
  • ↑ suicidal thoughts and behaviour
  • ↓ seizure threshold(?)
  • Prolong QT interval (citalopram particularly) ⇒ arrhythmias
  • ↑ risk of bleeding
  • Serotonin syndrome ⇒ autonomic hyperactivity + altered mental state + neuromuscular excitement
  • Sudden withdrawal ⇒ GI upset, neurological and influenza-like symptoms, sleep disturbance
107
Q

SSRIs: contraindications

A

Relative:

  • Epilepsy (↑ risk of SFx)
  • Peptic ulcer disease (↑ risk of SFx)
  • Young people (↑ risk of self-harm and suicidality)
  • Hepatic impairment (↓ dose)
108
Q

SSRIs: important interactions

A

Absolute:

  • MAOIs
  • Serotonergic drugs (e.g. tramadol)

Relative:

  • NSAIDs (use gastroprotection due to ↑ risk of bleeding)
  • Anticoagulants
  • Other drugs that prolong the QT interval (e.g. antipsychotics)
109
Q

Citalopram: prescription

A
  • PO
  • Start low and titrate up until good response
  • Start with 20mg OD
110
Q

Tricyclic antidepressants and other related drugs: examples

A
  • Amitriptyline

- Lofepramime

111
Q

TCAs: indications (2)

A
  • Second line for moderate-severe depression

- Neuropathic pain (unlicensed)

112
Q

TCAs: mechanisms of action

A
  • Inhibit neuronal reuptake of 5-HT and noradrenaline

- Block a wide array of receptors (hence why they have a lot of adverse effects)

113
Q

TCAs: adverse effects

A

Antimuscarinic receptor blockade:

  • Dry mouth
  • Constipation
  • Urinary retention
  • Blurred vision

H1 and α1 receptor blockade:

  • Sedation
  • Hypotension

Cardiac adverse effects (multiple mechanisms):

  • Arrhythmias
  • ECG changes

Cerebral adverse effects:

  • Convulsions
  • Hallucinations
  • Mania

Dopamine receptor blockade:

  • Breast changes
  • Sexual dysfunction
  • EPSEs (tremor, dyskinesia)

Overdose:

  • Hypotension
  • Arrhythmias
  • Convulsions
  • Coma
  • Respiratory failure

Sudden withdrawal:

  • GI upset
  • Neurological and influenza-like symptoms
  • Sleep disturbance
114
Q

TCAs: contraindications

A

Relative:

  • Elderly (↑ risk of SFx)
  • Epilepsy (↑ risk of SFx)
  • Cardiovascular disease (↑ risk of SFx)
  • Prostatic hypertrophy (worsening of urinary retention)
  • Constipation (worsening symptoms)
  • Glaucoma (worsening of symptoms)
115
Q

TCAs: interactions

A

Absolute:

- MAOIs

116
Q

TCAs: prescription for depression

A
  • Reserved for use only when other options have failed
  • Prescribe a small quantity for people at risk of attempting suicide by OD
  • e.g. amitriptyline 75mg OD
117
Q

TCAs: prescription for neuropathic pain

A

Amitriptyline 10mg at night = starting dose

118
Q

Venlafaxine and mirtazapine: indications

A
  1. Major depression (where SSRIs are ineffective)

2. GAD (venlafaxine)

119
Q

Venlafaxine: mechanism of action

A
  • SNRI
  • ↑ availability of monoamines for neurotransmission
  • Weaker antagonist of muscarinic and histamine receptors than TCAs ⇒ ↓ antimuscarinic SFx than TCAs
120
Q

Mirtazapine: mechanism of action

A
  • Antagonist of inhibitory pre-synaptic α2-adrenoreceptors
  • ↑ availability of monoamines for neurotransmission
  • Potent antagonist of histamine receptors (but not muscarinic) ⇒ ↓ antimuscarinic SFx, but DOES cause sedation
121
Q

Venlafaxine and mirtazapine: adverse effects

A
  • GI upset
  • Neurological effects
  • Hyponatraemia (R)
  • Serotonin syndrome (R)
  • ↑ suicidality
  • Prolonged QT interval (venlafaxine)
  • ↑ risk of ventricular arrhythmias (venlafaxine)
  • Same withdrawal symptoms as other antidepressants, but venlafaxine causes much worse Sx
122
Q

Venlafaxine and mirtazapine: contraindications

A

Relative:

  • Elderly (↑ SFx)
  • Hepatic and renal impairment (↓ dose)
  • Arrhythmias (venlafaxine)
123
Q

Venlafaxine and mirtazapine: prescription

A
  • PO
  • Low starting dose and titrate up

Venlafaxine:

  • Start with 37.5mg PO 12-hrly
  • Maximum 375mg OD

Mirtazapine:

  • Start with 15mg PO OD
  • Maximum 45mg OD
  • Take at night to minimise/benefit from sedative effects
124
Q

Antiemetics (dopamine D2-receptor antagonists): examples

A
  • Metoclopramide

- Domperidone

125
Q

Antiemetics (dopamine D2-receptor antagonists): indications

A
  • Prophylaxis and treatment of N&V

- Particularly used with ↓ gut motility associated N&V

126
Q

Antiemetics (dopamine D2-receptor antagonists): mechanism of action

A
  • Many stimuli trigger N&V
  • Various pathways converge on ‘vomiting centre’ in medulla, which receives input from many systems (e.g. chemoreceptor trigger zone, vestibular system, solitary tract nucleus, etc.)
  • D2 receptor is the MAIN receptor in the chemoreceptor trigger zone (CTZ)
  • Receptors detect emetogenic substances in blood
  • D2-receptor antagonists ∴ are used to counteract nausea from CTZ stimulation
  • Dopamine also promotes relaxation of the stomach and LOS and inhibits gasproduodenal coordination
  • D2-receptor antagonists ∴ have prokinetic effect ⇒ ↑ gastric emptying
127
Q

Antiemetics (dopamine D2-receptor antagonists): adverse effects

A
  • Diarrhoea
  • EPSEs, usually acute dystonic reaction (e.g. oculogyric crisis) (metoclopramide only, domperidone does not cross the BBB)
  • QT-interval prolongation (domperidone)
  • Arrhythmias (domperidone)
128
Q

Antiemetics (dopamine D2-receptor antagonists): contraindications

A

Absolute:

  • Neonates
  • Cardiac conduction abnormalities (domperidone)
  • Perforation

Relative:

  • Children (at ↑ risk of SFx)
  • Young adults (at ↑ risk of SFx)
  • Severe hepatic impairment (domperidone)
  • Intestinal obstruction
  • Parkinson’s disease (metoclopramide, domperidone is fine as it doesn’t cross the BBB)
129
Q

Antiemetics (dopamine D2-receptor antagonists): interactions

A

Absolute:

  • Dopaminergic agents for Parkinson’s disease (will antagonise effects)
  • Drugs that prolong the QT interval (domperidone)
  • Drugs that inhibit CYP450

Relative:
- Antipsychotics

Prescribing safety assessment (3 decks)

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