Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PSA > Top 100 Drugs > Flashcards

Top 100 Drugs Flashcards

1
Q

Give 1 example of a 5-alpha-reductase inhibitor

A

Finasteride

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Give 1 common indication for a 5-alpha-reductase inhibitor

A

Benign Prostatic Hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Give the mechanism of action for a 5-alpha-reductase inhibitor

A

Inhibit 5-alpha-reductase, which prevents the conversion of testosterone to it’s more active form - dihydrotestosterone which normally stimulates prostatic growth. Inhibiting this enzyme causes the prostate to shrink, reducing bulk of the gland and reducing obstruction to the outflow of urine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the common side effects of 5-alpha-reductase inhibitors?

A

Relate to anti-androgen action: gynaecomastia, impotence, reduced libido.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Give 1 caution for 5-alpha-reductase use

A

Exposure to the male fetus can cause malformation of the external genitalia. The drug may not be prepared or handled by anyone who could be pregnant. The drug is also passed via semen, so caution should be used in those having unprotected sex with those who could be pregnant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Give 2 examples of alpha blockers

A
  1. Doxazosin
  2. Tamsulosin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Give 2 common indications for alpha blockers

A
  1. BPH
  2. Resistant hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Give the mechanism of action for alpha blockers

A

Antagonise alpha-1-adrenoreceptors, which are found in smooth muscle (including blood vessels and the urinary tract), causing relaxation. They therefore cause vasodilation and a subsequent fall in blood pressure, and reduced resistance to bladder outflow.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the common side effects of alpha blockers?

A

Relate to their effect on vascular tone: postural hypotension, dizziness, syncope.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Give 1 caution for alpha blocker use

A

Existing postural hypotension.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Give 1 interaction for alpha blocker use

A

Beta blockers - they prevent the reflex tachycardia that forms part of the compensatory response to the vasodilation caused by alpha blockers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What time of day should alpha blockers be administered?

A

Bedtime - due to pronounced BP lowering effect and the associated risk of dizziness, syncope and falls.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Give 2 examples of acetylcholinesterase inhibitors

A
  1. Donepezil
  2. Rivastigmine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Give 2 common indications for acetylcholinesterase inhibitors

A
  1. Alzheimer’s disease
  2. Dementia in Parkinson’s disease.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Give the mechanism of action for acetylcholinesterase inhibitors

A

ACh is an important neurotransmitter for cognition and memory, a decrease in which is seen in Alzheimer’s disease and dementia associated with Parkinson’s disease. These drugs inhibit the acetylcholinesterase enzyme, preventing the breakdown of ACh and increasing it’s availability for neurotransmission. They therefore decrease the rate of cognitive decline.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the common side effects of acetylcholinesterase inhibitors?

A

Relating to increased peripheral cholinergic activity: nausea, vomiting, diarrhoea.

Relating to increased central cholinergic activity: hallucinations, altered behaviour, extra-pyramidal side effects, neuroleptic malignant syndrome.

Exacerbation of asthma and COPD.

Peptic ulcers, bradycardia, heart block.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Give 4 cautions for acetylcholinesterase inhibitors

A
  1. Asthma and COPD
  2. Peptic ulcer disease
  3. Heart block
  4. Parkinson’s disease - rivastigmine may worsen tremor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Give 2 indications for n-acetylcysteine

A
  1. Paracetamol overdose
  2. To reduce the viscosity of respiratory secretions (as a mucolytic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Give the mechanism of action of n-acetylcysteine

A

Paracetamol metabolism normally produces a small amount of the hepatotoxic substance NAPQI, which is detoxified by conjugation with glutathione. In paracetamol overdose the body’s supply of glutathione is overwhelmed, and so n-acetylcysteine aims to replenish the body’s supply of glutathione and prevent hepatic damage.

Breaks disulphide bonds in mucus, reducing it’s viscosity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the common side effects of n-acetylcysteine?

A

Anaphylactoid reaction - similar to anaphylaxis but involves histamine release independent of IgE, so once symptoms have settled (with help of antihistamine and bronchodilator) acetylcysteine therapy may be recommenced at a lower rate of infusion.

May cause bronchospasm when given nebulised (as a mucolytic).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Give 1 indication for activated charcoal

A

To reduce absorption of certain poisons (including some drugs in overdose) from the gut.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Give the mechanism of action of activated charcoal

A

Molecules are adsorbed onto the surface of the charcoal by Van der Waals forces, reducing their absorption into the circulation. Weakly ionic and hydrophobic substances are generally well adsorbed to activated charcoal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Give 2 drugs which are well adsorbed by activated charcoal, and 4 which are not

A

Well adsorbed:
1. Benzodiazepines
2. Methotrexate

Poorly adsorbed:
1. Strong acids/bases
2. Alcohol
3. Iron
4. Lithium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the common side effects of activated charcoal?

A

Intestinal obstruction, black stools, vomiting.

Aspiration, leading to:
1. Bronchospasm
2. Pneumonitis
3. Airway obstruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Give 3 cautions for activated charcoal use

A
  1. Reduced consciousness (unless ET tube in place as may result in aspiration)
  2. Persistent vomiting (due to risk of aspiration)
  3. Reduced gut motility (due to risk of intestinal obstruction)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Give 1 indication for adenosine

A

First-line diagnostic and therapeutic agent for rapid reversion to sinus rhythm in paroxysmal supra-ventricular tachycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Give the mechanism of action of adenosine

A

Activates adenosine receptors on cell surfaces in the heart, resulting in reduced frequency of spontaneous depolarisation (automaticity) and increasing resistance to depolarisation (refractoriness). This slows sinus rate and conduction velocity, and increases AV node refractoriness.

Many forms of SVT result from a self-perpetuating re-entry circuit in the AV node. Increased refractoriness in the AV node breaks the re-entry circuit, allowing the normal depolarisations of the SA node to re-take control over heart rate.

Has a half-life of roughly 10 seconds.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the common side effects of adenosine?

A

Interferes with function of SA and AV nodes, and so can induce bradycardia and asystole.

Breathlessness and bronchospasm.

Can cause deeply unpleasant feeling in the chest, described as a ‘sinking feeling’ or ‘sense of impending doom’.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Give 5 cautions for adenosine use

A

Those who could not tolerate it’s transient bradycardic effects:
1. Hypotension
2. Coronary ischaemia
3. Decompensated heart failure

Those who could not tolerate bronchospasm:
4. Asthma
5. COPD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Give 3 indications for adrenaline

A
  1. Cardiac arrest
  2. Anaphylaxis
  3. Local vasoconstriction, e.g. to control mucosal bleeding in endoscopy and prolong local anaesthesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Give the mechanism of action for adrenaline

A

Potent a1, a2, B1 and B2 adrenoreceptor agonist, therefore having multiple sympathetic effects:
1. Vasoconstriction of vessels supplying the skin, mucosa and abdominal viscera (mainly a1 mediated)
2. Increased force of contraction, myocardial excitability and heart rate (mainly B1 mediated)
3. Vasodilation of vessels supplying the heart and muscles (mainly B2 mediated)

These therefore cause redistribution of blood flow in favour of the heart, bronchodilation and suppression of inflammatory mediator release.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are the common side effects of adrenaline?

A
  1. Adrenaline-induced hypertension
  2. Anxiety
  3. Tremor
  4. Headache
  5. Palpitations
  6. MI/angina/arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Give 1 caution for adrenaline use

A
  1. Do not use in areas with poor vascularisation (e.g. fingers and toes) due to risk of tissue necrosis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Give 2 examples of aldosterone antagonists

A
  1. Spironolactone
  2. Eplerenone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Give 3 common indications for aldosterone antagonist use

A
  1. Ascites and oedema due to liver cirrhosis
  2. Chronic heart failure
  3. Primary hyperaldosteronism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Give the mechanism of action for aldosterone antagonists

A

Aldosterone is a mineralocorticoid which normally acts on the distal tubules of the nephron to increase the activity of luminal epithelial sodium channels (ENaC) - subsequently increasing sodium and water retention and elevating blood pressure, with associated increased potassium excretion.

Aldosterone antagonists competitively inhibit the aldosterone receptors to increase sodium and water excretion, as well as potassium retention.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the common side effects of aldosterone antagonists?

A
  1. Hyperkalaemia (weakness, arrhythmia, cardiac arrest)
  2. Gynaecomastia (spironolactone)
  3. Liver impairment and jaundice
  4. Stevens-Johnson syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Give 4 cautions to aldosterone antagonist use

A
  1. Hyperkalaemia
  2. Severe renal impairment
  3. Addison’s disease (those who are aldosterone deficient)
  4. Pregnant or lactating women (can cross placenta and are expressed in breast milk)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Name 3 important drug interactions for aldosterone antagonists

A
  1. ACE-inhibitors
  2. ARBs
  3. Potassium supplements

All of these drugs can also elevate potassium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Give 2 examples of alginates and antacids

A
  1. Gaviscon
  2. Peptac
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Give 2 common indications of alginate and antacid use

A
  1. GORD (for symptomatic relief)
  2. Dyspepsia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Give the mechanism of action for alginates and antacids

A

Antacids: buffer stomach acids

Alginates: increase the viscosity of stomach contents, reducing reflux into the oesophagus. Form a floating ‘raft’ to separate the gastric contents from the gastro-oesophageal junction to prevent mucosal damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Give 2 side effects of alginate and antacids

A
  1. Constipation (aluminium salts)
  2. Diarrhoea (magnesium salts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Give 2 cautions to alginate and antacid use

A
  1. Thickened milk preparations in infants - can lead to excessively thick stomach contents.
  2. Renal failure - sodium and potassium containing compounds should be used with caution
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Give 6 drug interactions for alginates and antacids

A

Can bind to other drugs and reduce serum concentrations, so doses should be separated by 2 hours.

  1. PPIs
  2. Digoxin
  3. ACE inhibitors
  4. Antibiotics (ciprofloxacin, cephalosporins, tetracycline)
  5. Bisphosphonates
  6. Levothyroxine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Give 3 indications for allopurinol use

A
  1. Gout
  2. Prevention of uric acid and calcium oxalate renal stones
  3. Prevention of hyperuricaemia and tumour lysis syndrome in chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Give the mechanism of action for allopurinol

A

Xanthine oxidase inhibitor.

Xanthine oxidase metabolises xanthine (produced from purines) to uric acid, so inhibiting this enzyme reduces plasma uric acid concentrations and subsequent deposition in joints and kidneys.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Give 5 side effects of allopurinol use

A
  1. Triggering/worsening of acute attack of gout (risk of triggering acute attack may be reduced by co-prescription of NSAID or colchicine)
  2. Skin rash
  3. Stevens-Johnson Syndrome
  4. Toxic epidermal necrolysis
  5. Allopurinol hypersensitivity syndrome (rare, life-threatening reaction to allopurinol characterised by fever, eosinophilia, lymphadenopathy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Give 4 cautions to allopurinol use

A
  1. Acute attacks of gout
  2. Severe hypersensitivity
  3. Hepatic impairment (metabolised by liver)
  4. Renal impairment (excreted by kidney)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Give 2 drug interactions for allopurinol

A
  1. Azathioprine - it’s active metabolite is metabolised by xanthine oxidase
  2. ACE inhibitors - co-prescription increases the risk of hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Give 3 examples of aminoglycosides

A
  1. Gentamicin
  2. Neomycin
  3. Amikacin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Give 5 indications for aminoglycoside use

A
  1. Severe sepsis
  2. Pyelonephritis and complicated UTIs
  3. Biliary and intra-abdominal sepsis
  4. Endocarditis
  5. Bacterial skin/eye/external ear infections (topical preparations)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Give the spectrum of activity of aminoglycosides

A

Gram-negative aerobic bacteria

Inactive against streptococci and anaerobes, so should be co-prescribed with penicillin or metronidazole when the causative organism is unknown.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Give the mechanism of action of aminoglycosides

A

Bind irreversibly to bacterial ribosomes to inhibit protein synthesis - bactericidal.

Enter cells via an oxygen-dependent mechanism, and so are ineffective against anaerobes and streptococci (which do not have this mechanism).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Give 2 side effects of aminoglycoside use

A
  1. Nephrotoxicity - accumulate in renal tubular epithelial cells
  2. Ototoxicity - accumulate in cochlear and vestibular hair cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Give 4 cautions to aminoglycoside use

A
  1. Renal impairment - as renally excreted
  2. Neonates
  3. Elderly
  4. Myasthenia gravis - can impair neuromuscular transmission
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Give 3 important drug interactions of aminoglycosides

A
  1. Loop diuretics (increased risk of ototoxicity)
  2. Vancomycin (increased risk of ototoxicity and nephrotoxicity)
  3. Cephalosporins (increased risk of nephrotoxicity)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Give 2 examples of aminosalicylates

A
  1. Mesalazine
  2. Sulfasalazine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Give 2 indications of aminosalicylate use

A
  1. Ulcerative colitis (mesalazine)
  2. Rheumatoid arthritis (sulfasalazine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Give the mechanism of action of aminosalicylates

A

Release 5-aminosalicylic acid (5-ASA), which has anti-inflammatory and immunosuppressive effects. Acts topically in the gut rather than systemically.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Give 6 side effects of aminosalicylate use

A
  1. GI upset
  2. Headache
  3. Blood abnormalities (leucopenia, thrombocytopenia)
  4. Renal impairment
  5. Oligospermia
  6. Hypersensitivity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Give 1 caution to aminosalicylate use

A
  1. Aspirin sensitivity - aspirin is also a salicylate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Give 2 drug interactions for aminosalicylates

A
  1. PPIs - mesalazine has a pH sensitive coating, and so drugs which alter gastric pH may cause the coating to breakdown prematurely.
  2. Lactulose - alters stool pH and may prevent 5-ASA release in the colon.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Give 1 indication for amiodarone use

A
  1. Tachyarrhythmias (e.g. AF, atrial flutter, SVT, VT and VF) - where other therapeutic options (drugs or electrical cardioversion) are ineffective or inappropriate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Give the mechanism of action of amiodarone

A

Blockade of sodium, potassium and calcium channels in myocardial cells.

Antagonism of alpha and beta adrenergic receptors.

These effects reduce spontaneous depolarisation (automaticity), slow conduction velocity and increase resistance to depolarisation (refractoriness).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Give 5 side effects of amiodarone use

A
  1. Hypotension
  2. Pneumonitis
  3. Bradycardia and AV block
  4. Hepatitis
  5. Thyroid abnormality
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Give 3 cautions for amiodarone use

A
  1. Hypotension
  2. Heart block
  3. Active thyroid disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Give 3 drug interactions for amiodarone

A

Increases plasma concentrations of:

  1. Digoxin
  2. Diltiazem
  3. Verapamil
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Give 3 examples of ACE inhibitor

A
  1. Ramipril
  2. Lisinopril
  3. Perindopril
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Give 4 indications for ACE inhibitor use

A
  1. Hypertension - 1st/2nd line
  2. CHF - 1st line
  3. IHD
  4. Diabetic nephropathy and CKD with proteinuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Give the mechanism of action of ACE inhibitors

A

Block angiotensin converting enzyme to prevent the conversion of angiotensin I to angiotensin II.

Angiotensin II is a vasoconstrictor and stimulates aldosterone secretion. Blocking it’s action reduces peripheral vascular resistance to lower BP.

Dilates the efferent glomerular arteriole to reduce intraglomerular pressure and reduce progression of CKD.

Reducing aldosterone secretion promotes sodium and water excretion, reducing venous return (preload) and having a beneficial effect on BP and in HF.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Give 6 side effects of ACE inhibitor use

A
  1. Persistent dry cough
  2. Hypotension
  3. Renal failure
  4. Hyperkalaemia
  5. Angioedema
  6. Anaphylactoid reaction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Give 3 cautions to ACE inhibitor use

A
  1. Renal artery stenosis
  2. AKI
  3. Pregnancy and breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Give 2 drug interactions for ACE inhibitors

A
  1. Potassium elevating drugs (including potassium supplements)
  2. NSAIDs - when co-prescribed there is an increased risk of nephrotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Give 2 examples of ARBs

A
  1. Candesartan
  2. Losartan
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Give 4 indications for ARB use

A
  1. Hypertension - 1st/2nd line
  2. CHF - 1st line
  3. IHD
  4. Diabetic nephropathy and CKD with proteinuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Give the mechanism of action of ARBs

A

Angiotensin receptor blockers.

Block the action of angiotensin II on the angiotensin receptors, resulting in vasodilation and reduced aldosterone secretion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Give 3 side effects of ARB use

A
  1. Hypotension
  2. Renal failure
  3. Hyperkalaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Give 3 cautions to ARB use

A
  1. Renal artery stenosis
  2. AKI
  3. Pregnancy and breastfeeding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Give 2 drug interactions of ARBs

A
  1. Potassium elevating drugs (including potassium supplements)
  2. NSAIDs - when co-prescribed there is an increased risk of nephrotoxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Give 4 examples of SSRI

A
  1. Fluoxetine
  2. Citalopram
  3. Sertraline
  4. Escitalopram
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Give 3 indications for SSRI use

A
  1. Moderate to severe depression
  2. Panic disorder
  3. OCD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Give the mechanism of action for SSRIs

A

Selective serotonin reuptake inhibitors.

Inhibit neuronal reuptake of serotonin from the synaptic cleft to increase availability for neurotransmission.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Give 7 side effects of SSRIs

A
  1. GI upset
  2. Changes in appetite and weight loss
  3. Suicidal ideation
  4. Serotonin syndrome
  5. Hyponatraemia
  6. Lowered seizure threshold
  7. Prolonged QT interval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Give 4 cautions for SSRI use

A
  1. Epilepsy
  2. Peptic ulcer disease
  3. Young people - have poor efficacy and have associated increased risk of self harm and suicidal thoughts
  4. Hepatic impairment - SSRIs are metabolised by the liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Give 3 drug interactions for SSRIs

A
  1. Monoamine oxidase inhibitors - seretonergic
  2. Tramadol - seretonergic
  3. Antipsychotics - prolong the QT interval
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Give 1 example of a tricyclic antidepressant

A
  1. Amitriptyline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Give 2 indications for tricyclic antidepressants

A
  1. Moderate to severe depression
  2. Neuropathic pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Give the mechanism of action for tricyclic antidepressants

A

Inhibit neuronal reuptake of serotonin and noradrenaline from the synaptic cleft, making more available for neurotransmission.

Also have effect on many receptors (e.g. muscarinic, H1, D2 and a1/a2) which accounts for large array of side effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Give 8 side effects of tricyclic antidepressant use

A
  1. Dry mouth/constipation/urinary retention/blurred vision - due to antimuscarinic effects
  2. Sedation and hypotension - due to blockade oh H1 and a1 receptors
  3. Arrhythmias
  4. Convulsions
  5. Hallucinations
  6. Mania
  7. Sexual dysfunction
  8. Extrapyramidal side effects - tremor and dyskinesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Give 6 cautions to tricyclic antidepressant use

A
  1. Epilepsy
  2. Elderly
  3. CVD
  4. Prostatic hypertrophy (due to antimuscarinic effect)
  5. Glaucoma
  6. Constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Give 1 drug interaction for tricyclic antidepressants

A
  1. Monoamine oxidase inhibitors - both drugs increase serotonin and noradrenaline levels at the synapse
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Give 2 indications for venlafaxine and mirtazapine use

A
  1. Major depression - 2nd line where SSRIs are ineffective
  2. Generalised anxiety disorder (venlafaxine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Give the mechanism of action of venlafaxine

A

Serotonin and noradrenaline reuptake inhibitor (SNRI), increasing availability for neurotransmission.

Weaker antagonist of muscarinic and H1 receptors than tricyclic antidepressants, so cause fewer antimuscarinic side effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Give the mechanism of action of mirtazapine

A

Antagonist of inhibitory pre-synaptic a2-adrenoreceptors, increasing availability of monoamines for neurotransmission.

Potent H1 antagonist, but weaker antagonist of muscarinic receptors - have fewer antimuscarinic side effects than tricyclic antidepressants but frequently cause sedation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Give 5 side effects of venlafaxine and mirtazapine use

A
  1. GI upset
  2. Serotonin syndrome
  3. Hyponatraemia
  4. Suicidal thoughts
  5. Neurological effects (e.g. headache, abnormal dreams, insomnia, confusion, convulsions)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Give 4 cautions for venlafaxine and mirtazapine use

A
  1. Elderly
  2. Arrhythmias
  3. Hepatic impairment
  4. Renal impairment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Give 2 examples of D2-receptor antagonists

A
  1. Metoclopramide
  2. Domperidone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Give 1 indication for D2-receptor antagonist use

A
  1. Nausea and vomiting - particularly in reduced gut motility
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

Give the mechanism of action of D2-receptor antagonists

A

D2-receptor is the main chemoreceptor in the chemoreceptor-trigger zole (CTZ) - the area responsible for sensing emetogenic substances in the blood and transmitting it to the vomiting centre in the medulla.

D2 is a neurotransmitter in the gut, promoting relaxation of the gut and lower oesophageal sphincter. Antagonising D2 receptors has a prokinetic effect - promoting gastric emptying and contributing to their effect in N+V due to reduced gut motility (e.g. due to opioids).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Give 5 side effects of D2-receptor antagonist use

A
  1. Diarrhoea
  2. Extrapyramidal syndromes - metoclopramide only, as domperidone does not cross the blood-brain barrier
  3. Acute dystonic reaction - involuntary muscle contractions (e.g. oculogyric crisis - spasmodic movements of the eyeballs into a fixed position)
  4. Prolonged QI interval
  5. Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Give 5 cautions for D2-receptor antagonist use

A
  1. Parkinson’s disease (only metoclopramide - domperidone does not cross the blood-brain barrier)
  2. Neonates
  3. Hepatic impairment (domperidone)
  4. Intestinal obstruction/perforation - due to prokinetic effects
  5. Cardiac conduction abnormalities (domperidone)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Give 4 drug interactions for D2-receptor antagonists

A
  1. Dopaminergic agents for Parkinson’s - metoclopramide as it antagonises their effects
  2. Antipsychotics - metoclopramide only due to risk of extra-pyramidal side effects
  3. Drugs which prolong the QT interval (e.g. antipsychotics, quinine, SSRIs)
  4. Cytochrome P450 inhibitors (e.g. amiodarone, diltiazem, macrolides, fluconazole, protease inhibitors)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Give 3 examples of antiemetic H1-receptor antagonists

A
  1. Cinnarizine
  2. Cyclizine
  3. Promethazine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Give 1 indication for antiemetic H1-receptor antagonist use

A
  1. Nausea and vomiting - particularly in motion sickness or vertigo
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Give the mechanism of action of antiemetic H1-receptor antagonists

A

H1 and ACh (muscarinic) receptors predominate the vomiting centre in the medulla, and in it’s communication with the vestibular system.

Blocking these receptors prevents the sensation of nausea and subsequent vomiting - particularly in motion sickness and vertigo due to the vestibular effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Give 4 side effects of antiemetic H1-receptor antagonists

A
  1. Drowsiness
  2. Dry throat and mouth - due to anticholinergic effects
  3. Tachycardia
  4. Palpitations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Give 2 cautions to antiemetic H1-receptor antagonist use

A
  1. Hepatic encephalopathy - due to sedating effect
  2. Prostatic enlargement - due to risk of urinary retention as a result of antimuscarinic effects.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Give 2 drug interactions for antiemetic H1-receptor antagonists

A
  1. Other sedative medications, e.g. benzodiazepines, opioids
  2. Antimuscarinics, e.g. ipratropium, tiotropium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Give 2 examples of 5-HT3-receptor antagonists

A
  1. Ondansetron
  2. Granisetron
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Give 1 indication for 5-HT3-receptor antagonists

A
  1. Nausea and vomiting - particularly in general anaesthesia and chemotherapy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Give the mechanism of action of 5-HT3-receptor antagonists

A

High density of 5-HT3-receptors in the chemoreceptor trigger zone (CTZ), and 5-HT3 is the key neurotransmitter released by the gut in response to emetogenic stimuli. Therefore blockade of these receptors prevents vomiting.

5-HT3 is not involved in communication with the vestibular system, and so these drugs are not useful in N+V due to motion sickness or vertigo.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Give 1 caution for 5-HT3-receptor antagonist use

A
  1. Prolonged QT interval - as these medications can also have this effect.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Give 3 drug interactions for 5-HT3-receptor antagonists

A

Drugs which prolong the QT interval:
1. Quinine
2. SSRIs
3. Antipsychotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Give 3 examples of anti-fungal drugs

A
  1. Fluconazole
  2. Clotrimazole
  3. Nystatin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Give 2 indications for anti-fungal drug use

A
  1. Local fungal infection - including oropharynx, vagina and skin
  2. Systemic fungal infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Give the mechanism of action of anti-fungal drugs

A

Fungal cell membranes contain ergosterol, which is not seen in animal or human cells.

Nystatin (polyene antifungal) binds to ergosterol to create a polar pore, allowing ions to leak from the cell and resulting in death or slowed growth of the fungus.

Fluconazole (triazole antifungal) and clotrimazole (imidazole antifungal) inhibit ergosterol synthesis, subsequently impairing cell growth and replication.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Give 3 side effects of anti-fungal drugs

A
  1. Local irritation
  2. GI upset for those taken orally
  3. Hepatitis and severe hepatic toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Give 4 examples of antihistamine H1-receptor antagonists

A
  1. Cetirizine
  2. Loratadine
  3. Fexofenadine
  4. Chlorphenamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Give 3 indications for antihistamine H1-receptor antagonist use

A
  1. Allergies (particularly hayfever - seasonal allergic rhinitis)
  2. Prutitus and urticaria
  3. Anaphylaxis (as an adjunct after administration of life-saving medications)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Give the mechanism of action of antihistamine H1-receptor antagonists

A

Histamine is released from mast cells as a result of IgE binding.

Histamine induces the features of type 1 (immediate) hypersensitivity (oedema, erythema, irritation, urticaria and itch).

Antagonising the H1 receptor blocks these actions of excess histamine.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Give 1 side effect of antihistamine H1-receptor antagonists

A
  1. Sedation - as H1 has a role in the brain in maintaining wakefulness. Newer ‘second-generation’ antihistamines (e.g. loratadine, cetirizine, fexofenadine) do not cross the blood-brain barrier and so do not cause sedation.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Give 1 caution to antihistamine H1-receptor antagonist use

A
  1. Severe liver disease - may precipitate hepatic encephalopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Give 1 example of an anti-motility drug

A
  1. Loperamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Give 1 indication for anti-motility drug use

A
  1. Diarrhoea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Give the mechanism of action for anti-motility drugs

A

Loperamide is an opioid which does not cross the blood-brain barrier, but still has gastrointestinal effects.

It is an agonist of the opioid receptors in the gut, reducing peristaltic contractions and slowing the passage of bowel contents. This facilitates more time for water absorption, resulting in hardening of stool.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Give 1 side effect of anti-motility drug use

A
  1. GI upset - constipation, abdominal cramping, flatulence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Give 3 cautions for anti-motility drug use

A
  1. Acute ulcerative colitis - inhibition of peristalsis may increase the risk of megacolon and perforation
  2. C. diff infection
  3. Acute bloody diarrhoea (dysentery)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Give 2 examples of antimuscarinic bronchodilators

A
  1. Tiotropium
  2. Ipratropium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Give 2 indications for antimuscarinic bronchodilator use

A
  1. COPD
  2. Asthma (short acting for fast relief alongside SABA, or long acting for maintenance alongside LABA and corticosteroid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Give the mechanism of action for antimuscarinic bronchodilators

A

Bind to the muscarinic receptor, where they act as a competitive inhibitor of ACh.

Stimulation of ACh receptors causes parasympathetic effects.

Inhibition of ACh causes sympathetic effects: increased heart rate, reduced smooth muscle tone (including respiratory tract and bladder), reduced secretions (including tears, respiratory and GI tract), pupillary dilation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Give 2 side effects of antimuscarinic bronchodilator use

A
  1. Respiratory tract irritation
  2. GI upset - dry mouth and constipation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Give 3 cautions to antimuscarinic bronchodilator use

A

Due to antimuscarinic sympathetic effects - although in practice most patients can take these drugs inhaled without any significant effects, due to the drugs being quickly hydrolysed once they enter the circulation.

  1. Angle-closure glaucoma
  2. Arrhythmias
  3. Urinary retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

Give 1 example of a cardiovascular antimuscarinic

A
  1. Atropine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Give 1 indication for cardiovascular antimuscarinic use

A
  1. Bradycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Give the mechanism of action for cardiovascular antimuscarinics

A

Competitively inhibit muscarinic (ACh) receptors, resulting in sympathetic effects - such as increased heart rate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Give 4 side effects of cardiovascular antimuscarinic use

A
  1. Tachycardia
  2. Dry mouth
  3. Constipation
  4. Urinary retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

Give 3 cautions to cardiovascular antimuscarinic use

A
  1. Angle-closure glaucoma
  2. Arrhythmias
  3. Urinary retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Give 1 example of a gastrointestinal antimuscarinic

A
  1. Hyoscine butylbromide (buscopan)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Give 1 indication for gastrointestinal antimuscarinic use

A
  1. Irritable bowel syndrome

Also used to reduce secretions in palliative care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Give the mechanism of action for gastrointestinal antimuscarinics

A

Competitively inhibit muscarinic ACh receptors, resulting in sympathetic effects such as reduced smooth muscle tone and reduced secretions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Give 4 side effects of gastrointestinal antimuscarinic use

A
  1. Tachycardia
  2. Dry mouth
  3. Constipation
  4. Urinary retention
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Give 3 cautions to gastrointestinal antimuscarinic use

A
  1. Angle-closure glaucoma
  2. Arrhythmias
  3. Urinary retention
144
Q

Give 2 examples of genitourinary antimuscarinics

A
  1. Oxybutynin
  2. Tolterodine
145
Q

Give 1 indication for genitourinary antimuscarinic use

A
  1. Overactive bladder
146
Q

Give the mechanism of action for genitourinary antimuscarinics

A

Competitively inhibit M3 muscarinic ACh receptors, having sympathetic effects - promoting smooth muscle relaxation (including the bladder). This reduces urinary urge and frequency.

147
Q

Give 4 side effects of genitourinary antimuscarinic use

A
  1. Tachycardia
  2. Dry mouth
  3. Constipation
  4. Blurred vision
148
Q

Give 4 cautions for genitourinary antimuscarinic use

A
  1. Angle-closure glaucoma
  2. Arrhythmias
  3. Urinary retention
  4. UTI
149
Q

Give 1 drug interaction for all antimuscarinic drugs

A
  1. Tricyclic antidepressants - also have antimuscarinic effect
150
Q

Give 3 examples of first generation (typical) antipsychotics

A
  1. Haloperidol
  2. Prochlorperazine
  3. Chlorpromazine
151
Q

Give 4 indications for typical antipsychotic use

A
  1. Psychomotor agitation
  2. Schizophrenia
  3. Bipolar disorder
  4. Nausea and vomiting - particularly in palliative care
152
Q

Give the mechanism of action for typical antipsychotics

A

Block post-synaptic D2 receptors, affecting the main dopaminergic pathways in the brain:
1. Nigrostriatal pathway (substantia nigra to corpus striatum of the basal ganglia)
2. Mesolimbic pathway (midbrain to limbic system)
3. Tuberohypophyseal pathway (hypothalamus to pituitary)

153
Q

Give 7 side effects of typical antipsychotic use

A
  1. Drowsiness
  2. Erectile dysfunction
  3. QT interval prolongation

Extra-pyramidal side effects:

  1. Acute dystonic reactions (involuntary parkinsonian movements or muscle spasms - including oculogyric crisis)
  2. Akathisia (a state of inner restlessness)
  3. Neuroleptic malignant syndrome
  4. Tardive dyskinesia (late effect - pointless, repetitive involuntary movements such as lip smacking)
154
Q

Give 3 cautions to typical antipsychotic use

A
  1. Parkinson’s disease - due to extrapyramidal side effects
  2. Elderly
  3. Dementia - may increase risk of death and stroke
155
Q

Give 1 drug interaction for typical antipsychotics

A
  1. Drugs which prolong the QT interval - e.g. amiodarone, macrolides
156
Q

Give 4 examples of second-generation (atypical) antipsychotic

A
  1. Quetiapine
  2. Olanzapine
  3. Risperidone
  4. Clozapine
157
Q

Give 3 indications for atypical antipsychotic use

A
  1. Psychomotor agitation
  2. Schizophrenia
  3. Bipolar disorder
158
Q

Give the mechanism of action for atypical antipsychotics

A

Block post-synaptic D2 receptors, reducing transmission in the main dopaminergic pathways.

Atypical antipsychotics are better at managing treatment-resistant schizophrenia and negative symptoms, and have a lower risk of extra-pyramidal side effects - potentially due to them having a higher affinity for other receptors and looser binding to D2.

159
Q

Give 6 side effects of atypical antipsychotic use

A
  1. Sedation
  2. Extra-pyramidal side effects (less common than with typical antipsychotics)
  3. Prolonged QT interval
  4. Sexual dysfunction
  5. Arrhythmias
  6. Clozapine can cause agranulocytosis (deficiency of neutrophils) and myocarditis
160
Q

Give 3 cautions for atypical antipsychotic use

A
  1. Cardiovascular disease
  2. Severe heart disease (clozapine)
  3. Neutropenia (clozapine)
161
Q

Give 2 drug interactions for atypical antipsychotics

A
  1. D2 antagonising anti-emetics
  2. Drugs which prolong the QT interval (e.g. macrolides, amiodarone, quinine, SSRIs)
162
Q

Give 1 example of an antiviral drug

A
  1. Aciclovir
163
Q

Give 2 indications for antiviral drug use

A
  1. Acute episodes of herpesvirus infection
  2. Suppression of recurrent herpes simplex attacks
164
Q

Give the mechanism of action for antiviral drugs

A

The herpes family includes HS1, HS2 and varicella zoster.

These viruses contain double-stranded DNA, which requires herpes-specific DNA polymerase for replication.

Aciclovir enters herpes-infected cells and inhibits the herpes-simplex DNA polymerase, stopping viral DNA synthesis and therefore replication.

165
Q

Give 6 side effects of antiviral drug use

A
  1. Headache
  2. Dizziness
  3. GI disturbance
  4. Skin rash
  5. Phlebitis at injection site
  6. Acute renal failure during high dose IV infusion, due to precipitation in the renal tubules
166
Q

Give 3 cautions for antiviral drug use

A
  1. Pregnancy - crosses the placenta
  2. Breastfeeding - expressed in breast milk
  3. Renal impairment - as aciclovir excreted by the kidneys
167
Q

Give 1 example of an adenosine diphosphate (ADP) receptor antagonist

A
  1. Clopidogrel
168
Q

Give 3 indications for ADP receptor antagonist use

A
  1. Acute coronary syndromes - usually in combination with aspirin
  2. Prevention of occlusion of coronary artery stents
  3. Secondary prevention of thrombotic arterial events (e.g. MI, stroke, peripheral arterial disease)
169
Q

Give the mechanism of action of ADP receptor antagonists

A

Prevent platelet aggregation by binding irreversibly to adenosine diphosphate receptors (P2Y12 subtype) on the surface of platelets.

This process is independent of COX, and so the actions are synergistic with those of aspirin.

170
Q

Give 3 side effects of ADP receptor antagonist use

A
  1. Bleeding - particularly serious if GI, intracranial or following surgery
  2. GI upset
  3. Thrombocytopenia
171
Q

Give 3 cautions for ADP receptor antagonist use

A
  1. Elective surgery
  2. Active bleeding
  3. Renal and hepatic impairment
172
Q

Give 4 drug interactions for ADP receptor antagonists

A
  1. CYP inhibitors - e.g. omeprazole, ciprofloxacin, erythromycin, antifungals, SSRIs.
  2. Antiplatelet drugs
  3. Anticoagulant drugs (e.g. heparin)
  4. NSAIDs - increase risk of bleeding
173
Q

Give 2 indications for aspirin use

A
  1. Acute coronary syndromes and acute ischaemic stroke
  2. Secondary prevention of thrombotic arterial events
174
Q

Give the mechanism of action for aspirin

A

Antiplatelet.

Irreversibly inhibits cyclooxygenase (COX) to reduce production of the aggregatory factor thromboxane. This reduces platelet aggregation.

The effect last for the lifetime of the platelet.

175
Q

Give 5 side effects of aspirin use

A
  1. GI irritation
  2. Peptic ulceration
  3. Haemorrhage
  4. Bronchospasm
  5. Tinnitus
176
Q

Give 5 cautions for aspirin use

A
  1. Children under 16 years - risk of Reye’s syndrome
  2. Aspirin hypersensitivity
  3. Third trimester of pregnancy
  4. Peptic ulceration
  5. Gout
177
Q

Give 2 drug interactions for aspirin

A
  1. Antiplatelet drugs (e.g. clopidogrel)
  2. Anticoagulant drugs (e.g. heparin, warfarin)
178
Q

Give 4 indications for azathioprine use

A
  1. Crohn’s disease
  2. Ulcerative colitis
  3. DMARD in rheumatoid arthritis and other autoimmune conditions not responding to corticosteroid use
  4. Prevention of organ rejection following transplant
179
Q

Give the mechanism of action of azathioprine

A

Pro-drug which is metabolised to active substances which inhibit purine synthesis, and therefore inhibit DNA and RNA replication.

Metabolised by xanthine oxidase

180
Q

Give 1 side effect of azathioprine use

A
  1. Bone marrow suppression - resulting in leucopenia and increased risk of infection
181
Q

Give 2 drug interactions for azathioprine

A
  1. Xanthine oxidase inhibitors (e.g. allopurinol) - reduce azathioprine metabolism and increase risk of toxicity
  2. Corticosteroids - increased risk of infection
182
Q

Give 3 examples of beta blockers

A
  1. Atenolol
  2. Propranolol
  3. Bisoprolol
183
Q

Give 5 indications for beta blocker use

A
  1. IHD
  2. Chronic heart failure
  3. Atrial fibrillation
  4. Supraventricular tachycardia
  5. Hypertension
184
Q

Give the mechanism of action for beta blockers

A

Beta-1 adrenoreceptors are located mainly in the heart.

Beta-2 adrenoreceptors are found mainly in the smooth muscle of blood vessels and airways.

Beta blockers reduce contractile force and speed of conduction through the heart, reducing myocardial work and subsequently oxygen demand. Relax peripheral smooth muscle to contribute towards reducing blood pressure.

They prolong the refractory period of the AV node, accounting for their effect in AF and SVT.

Reduce renin secretion by the kidneys.

185
Q

Give 1 side effect of beta blocker use

A
  1. Impotence
186
Q

Give 3 cautions for beta blocker use

A
  1. Hepatic impairment
  2. Heart block
  3. Asthma
187
Q

Give 3 examples of beta-2 agonists

A
  1. Salbutamol
  2. Salmeterol
  3. Formeterol
188
Q

Give 3 indications for beta-2 agonist use

A
  1. Asthma
  2. COPD
  3. Hyperkalaemia
189
Q

Give the mechanism of action of beta-2 agonists

A

Stimulation of beta-2 receptors leads to smooth muscle relaxation, improving flow through obstructed airways.

Stimulate Na+/K+ ATPase pumps, resulting in a shift of K+ to the intracellular compartment, making them useful in the management of hyperkalaemia.

190
Q

Give 5 side effects of beta-2 agonist use

A
  1. Tachycardia
  2. Tremor
  3. Muscle cramps
  4. Palpitations
  5. Anxiety
191
Q

Give 5 examples of benzodiazepines

A
  1. Diazepam
  2. Temazepam
  3. Lorazepam
  4. Chlordiazepoxide
  5. Midazolam
192
Q

Give 4 indications for benzodiazepine use

A
  1. Seizures and status epilepticus
  2. Alcohol withdrawal reactions
  3. Sedation
  4. Anxiety and insomnia
193
Q

Give the mechanism of action for benzodiazepines

A

Facilitate the binding of GABA to GABAa receptors - the main inhibitory neurotransmitter.

The GABAa receptor is a chloride channel, and binding of GABA facilitates the movement of Cl- into the cell to make it more resistant to depolarisation.

194
Q

Give 3 side effects of benzodiazepine use

A
  1. Dependence
  2. Sedation/drowsiness
  3. Coma
195
Q

Give 4 cautions for benzodiazepine use

A
  1. Hepatic impairment
  2. Elderly
  3. Respiratory impairment
  4. Neuromuscular impairment (e.g. myasthenia gravis)
196
Q

Give 1 drug interaction for benzodiazepines

A
  1. CYP inhibitors (e.g. amiodarone, diltiazem, macrolides, fluconazole, SSRIs) - as many benzodiazepines rely on CYP for elimination
197
Q

Give 2 examples of bisphosphonates

A
  1. Alendronic acid
  2. Disodium pamidronate
198
Q

Give 5 indications for bisphosphonate use

A
  1. Prevention of fragility fractures
  2. Paget’s disease of bone
  3. Hypercalcaemia of malignancy
  4. Bone metastases and myeloma
  5. Osteogenesis imperfecta
199
Q

Give the mechanism of action for bisphosphonates

A

Inhibit osteoclast activity. Enter cells and result in reduced activity and increased likelihood of apoptosis, subsequently reducing resorption of bone and decreasing bone turnover.

This results in overall increase in bone mass.

200
Q

Give 4 side effects of bisphosphonate use

A
  1. Oesophagitis
  2. Hypophosphataemia
  3. Osteonecrosis of the jaw
  4. Atypical femoral fracture - particularly in long-term use
201
Q

Give 3 cautions for bisphosphonate use

A
  1. Severe renal impairment
  2. Hypocalcaemia
  3. Upper GI disorders
202
Q

Give 3 examples of calcium and vitamin D supplements

A
  1. Colecalciferol
  2. Calcium gluconate
  3. Calcium carbonate
203
Q

Give 5 indications for calcium and vitamin D supplement use

A
  1. Osteoporosis
  2. CKD - to treat secondary parathyroidism
  3. Severe hyperkalaemia - acts as a protectant by increasing the myocardial threshold potential and preventing excitability, reducing risk of arrhythmia
  4. Hypocalcaemia
  5. Vitamin D deficiency
204
Q

Give 4 side effects of calcium and vitamin D supplementation

A
  1. Dyspepsia
  2. Constipation
  3. Cardiovascular collapse - if calcium gluconate delivered too fast
  4. Local tissue damage - if injected subcutaneously
205
Q

Give 1 caution for calcium and vitamin D supplementation

A
  1. Hypercalcaemia
206
Q

Give 4 examples of calcium channel blockers

A
  1. Amlodipine
  2. Nifedipine
  3. Verapamil
  4. Diltiazem
207
Q

Give 3 indications for calcium channel blocker use

A
  1. Hypertension
  2. Supraventricular arrhythmia
  3. Stable angina
208
Q

Give the mechanism of action of calcium channel blockers

A

Decrease calcium entry into vascular cells and myocytes, reducing intracellular calcium concentrations.

This causes cardiac relaxation and vasodilation of arterial smooth muscle, lowering arterial pressure.

Reduce myocardial contractility and suppress cardiac conduction - subsequently reducing heart rate and therefore oxygen demand.

There are 2 classes of calcium channel blocker:
1. Di-hydropiridines (e.g. nifedipine/amlodipine) - selective for vasculature
2. Non-di-hydropiridines (e.g. verapamil) - selective for heart

209
Q

Give 6 side effects of calcium channel blocker use

A
  1. Ankle swelling
  2. Flushing
  3. Palpitations
  4. Bradycardia
  5. Heart block
  6. Cardiac failure
210
Q

Give 4 cautions for calcium channel blocker use

A
  1. Poor left ventricular function
  2. AV nodal conduction delay
  3. Unstable angina - vasodilation causes a reflex increase in contractility and tachycardia, increasing myocardial oxygen demand.
  4. Severe aortic stenosis
211
Q

Give 1 drug interaction for calcium channel blockers

A
  1. Beta-blockers - alongside non-di-hydropiridines as they are both negatively inotropic and chronotropic, and together may cause heart failure, bradycardia and asystole.
212
Q

Give 2 indications for carbamazepine use

A
  1. Seizure prophylaxis in epilepsy - first line for generalised tonic-clonic seizures and focal seizures
  2. Trigeminal neuralgia
213
Q

Give the mechanism of action for carbamazepine

A

Inhibition of of neuronal sodium channels, stabilising resting membrane potentials and preventing depolarisation.

This reduces seizure spread in the brain, and prevents synaptic transmission of pain.

214
Q

Give 6 side effects of carbamazepine

A
  1. GI upset
  2. Neurological effects - dizziness, ataxia
  3. Hypersensitivity - affects 10% on carbamazepine
  4. Antiepileptic hypersensitivity syndrome - consists of severe skin reactions (e.g. SJS, TEN) alongside fever, lymphadenopathy and systemic symptoms (e.g. haematological, hepatic and renal involvement)
  5. Oedema
  6. Hyponatraemia
215
Q

Give 5 cautions for carbamazepine use

A
  1. Pregnancy - folic acid should be taken prior to conception
  2. Antiepileptic hypersensitivity syndrome previously
  3. Hepatic impairment
  4. Renal impairment
  5. Cardiac disease
216
Q

Give 4 drug interactions for carbamazepine

A
  1. Drugs that are metabolised by CYP (e.g. warfarin, oestrogens, progestogens) - carbamazepine induces these enzymes, so these drugs would have decreased efficacy due to decreased concentrations.
  2. CYP inhibitors (e.g. macrolides, amiodarone, diltiazrm, fluconazole) - carbamazepine metabolised by CYP, and so it’s concentration and side effects are increased.
  3. Antiepileptic drugs
  4. Drugs which lower the seizure threshold (e.g. antipsychotics, tramadol)
217
Q

Give 2 examples of cephalosporins and 2 examples of carbapenems

A

Cephalosporins:
1. Cefotaxime

  1. Cefalexin

Carbapenems:
1. Meropenem

  1. Ertapenem
218
Q

Give 2 indications for cephalosporin and carbapenem use

A
  1. Urinary and respiratory tract infections - oral cephalosporins
  2. Very severe, complicated or resistant infections - parenteral cephalosporins and carbapenems
219
Q

Give the mechanism of action for cephalosporins and carbapenems

A

Broad spectrum of activity, including Gram +ve and -ve bacteria. Have more resistance to beta-lactamase than penicillins.

Bactericidal effect resulting from beta-lactam ring. Inhibit enzymes responsible for cross-linking the peptidoglycan cell wall, weakening cells and resulting in swelling, osmotic lysis and death.

220
Q

Give 4 side effects of cephalosporin and carbapenem use

A
  1. GI upset
  2. Antibiotic associated colitis - kill normal gut flora, allowing overgrowth of C. diff - can result in perforarion and death
  3. Hypersensitivity
  4. Neurological toxicity - resulting in seizures
221
Q

Give 4 cautions for cephalosporin and carbapenem use

A
  1. Allergy (including to penicillins)
  2. Epilepsy
  3. Renal impairment
  4. Risk of C. diff infection (e.g. in hospital, elderly)
222
Q

Give 2 drug interactions for cephalosporins and carbapenems

A
  1. Warfarin - increases it’s anticoagulatory effect by killing gut flora which produce vitamin K
  2. Valproate - decreases concentrations and therefore efficacy
223
Q

Give 2 indications for chloramphenicol use

A
  1. Bacterial conjunctivitis
  2. Otitis externa

(Rarely used systemically due to toxicity - only in severe infections where other drugs have failed - e.g. epiglottitis, typhoid fever)

224
Q

Give the mechanism of action for chloramphenicol

A

Broad activity against Gram +ve and -ve, aerobic and anaerobic organisms.

Binds to bacterial ribosomes to inhibit protein synthesis, and therefore is bacteriostatic.

225
Q

Give 5 side effects of chloramphenicol use

A
  1. Burning, itching, stinging
  2. Dose-related bone marrow suppression (systemic use)
  3. Aplastic anaemia (systemic use)
  4. Grey baby syndrome (circulatory collapse occurring in exposed neonates who are unable to metabolise and excrete the drug)
  5. Optic and peripheral neuritis
226
Q

Give 6 cautions for chloramphenicol use

A
  1. Third trimester of pregnancy
  2. Breast feeding
  3. Age < 2 years
  4. Bone marrow disorders
  5. Previous hypersensitivity reaction to chloramphenicol
  6. Hepatic impairment
227
Q

Give 3 examples of inhaled corticosteroid

A
  1. Budesonide
  2. Beclometasone
  3. Fluticasone
228
Q

Give 2 indications for inhaled corticosteroid use

A
  1. Asthma - for asthma not controlled by SABA alone
  2. COPD - alongside LABA
229
Q

Give the mechanism of action for inhaled corticosteroids

A

Enters the cytoplasm and reacts with receptors, which in turn enter the nucleus where they modify the transcription of a large number of genes.

Downregulates pro-inflammatory chemicals, and upregulates antiinflammatory proteins. This results in reduced mucosal inflammation, widened airways and reduced mucus.

This improves symptoms and reduces exacerbation.

230
Q

Give 3 side effects of inhaled corticosteroid use

A
  1. Oral candidiasis
  2. Hoarse voice
  3. Pneumonia
231
Q

Give 2 cautions for inhaled corticosteroid use

A
  1. History of pneumonia
  2. Children - potential for growth suppression
232
Q

Give 3 examples of systemic corticosteroids

A
  1. Hydrocortisone
  2. Dexamethasone
  3. Prednisolone
233
Q

Give 4 indications for systemic corticosteroid use

A
  1. Allergic or inflammatory disorders (e.g. anaphylaxis)
  2. Autoimmune disease (e.g. IBD)
  3. Cancers - as part of chemotherapy
  4. Hormone replacement in adrenal insufficiency or hypopituitarism
234
Q

Give the mechanism of action for systemic corticosteroids

A

Exert glucocorticoid effects, regulating gene expression in the nucleus.

Upregulate antiinflammatory proteins, and downregulate pro-inflammatory genes (e.g. cytokines, TNF-a).

Have a mineralocorticoid effect - increasing Na+ and water retention and K+ excretion renally.

235
Q

Give 6 side effect of systemic corticosteroid use

A
  1. Immunosuppression
  2. Mood and behavioural changes
  3. Mineralocorticoid actions - hypertension, hypokalaemia, oedema
  4. Adrenal atrophy
  5. Addisonian crisis - due to sudden withdrawal - life threatening situation that results in low blood pressure, low blood levels of sugar and high blood levels of potassium
  6. Chronic glucocorticoid deficiency
236
Q

Give 2 cautions for systemic corticosteroid use

A
  1. Infection - due to immunosuppressive effect
  2. Children - due to risk of growth suppression
237
Q

Give 2 drug interaction for systemic corticosteroids

A
  1. CYP inducers (e.g. carbamazepine, phenytoin, rifampicin) - may reduce efficacy of corticosteroids
  2. NSAIDs - due to increased risk of peptic ulceration
238
Q

Give 2 examples of topical corticosteroids

A
  1. Hydrocortisone (mild)
  2. Betamethasone (potent)
239
Q

Give 1 indication for topical corticosteroid use

A
  1. Inflammatory skin disorders (e.g. eczema) - where emollients are ineffective
240
Q

Give the mechanism of action for topical corticosteroids

A

Downregulate proinflammatory genes, and upregulate antiinflammatory proteins.

241
Q

Give 2 side effects of topical corticosteroid use

A
  1. Local adverse effects - e.g. skin thinning, striae, telangiectasia, contact dermatitis
  2. Rebound worsening of the underlying condition
242
Q

Give 2 cautions for topical corticosteroid use

A
  1. Infection
  2. Facial lesions
243
Q

Give 2 indications for digoxin use

A
  1. Atrial fibrillation and atrial flutter
  2. Severe heart failure
244
Q

Give the mechanism of action for digoxin

A

Negatively chronotropic and positively inotropic (reduces heart rate and increases force of contraction).

Reduces conduction at the AV node to prevent some impulses travelling to the ventricles, reducing ventricular rate.

Inhibits Na+/K+ ATPase pumps on myocytes, increasing accumulation of Na+ in myocytes, increasing force of contraction.

245
Q

Give 6 side effects of digoxin use

A
  1. GI upset
  2. Bradycardia
  3. Rash
  4. Dizziness
  5. Visual disturbance
  6. Digoxin toxicity
246
Q

Give 6 cautions for digoxin use

A
  1. Second-degree heart block
  2. Ventricular arrhythmia
  3. Renal failure
  4. Hypokalaemia
  5. Hyponmagnesaemia
  6. Hypercalcaemia
247
Q

Give 2 examples of dipeptidylpeptidase-4 inhibitors

A
  1. Sitagliptin
  2. Linagliptin
248
Q

Give 1 indication for dipeptidylpeptidase-4 inhibitors

A
  1. Type 2 diabetes - alongside metformin
249
Q

Give the mechanism of action of dipeptidylpeptidase-4 inhibitors

A

Incretins are released in response to food and act to promote insulin secretion and suppress glucagon release, thus lowering blood glucose.

Incretins are inactivated by the enzyme dipeptidylpeptidase-4, and therefore DPP-4 inhibitors lower blood glucose by preventing incretin degredation.

Incretin action is glucose dependent - therefore DPP-4 inhibitors are less likely to cause hypoglycaemia.

250
Q

Give 2 side effects of dipeptidylpeptidase inhibitors

A
  1. Acute pancreatitis
  2. Hypoglycaemia
251
Q

Give 8 cautions for dipeptidylpeptidase-4 inhibitors

A
  1. Hypersensitivity
  2. History of acute pancreatitis
  3. Severe renal impairment
  4. The elderly
  5. Type 1 diabetes
  6. Ketoacidosis
  7. Pregnancy
  8. Breastfeeding
252
Q

Give 3 examples of direct oral anticoagulants

A
  1. Edoxaban
  2. Rivaroxaban
  3. Apixaban
253
Q

Give 2 indications for direct oral anticoagulant drugs

A
  1. Venous thromboembolism - prevention
  2. Atrial fibrillation - to prevent thrombotic events
254
Q

Give the mechanism of action for direct oral anticoagulant drugs

A

Act on the final common pathway of the coagulation cascade - directly inhibiting factor Xa (activated factor X). This prevents the conversion of prothrombin to thrombin, and therefore inhibiting the conversion of fibrinogen to fibrin.

255
Q

Give 5 side effects of direct oral anticoagulant use

A
  1. Bleeding
  2. GI upset
  3. Anaemia
  4. Dizziness
  5. Elevated liver enzymes
256
Q

Give 6 cautions for direct oral anticoagulant use

A
  1. Active bleeding
  2. Risk factors for bleeding - e.g. surgery, peptic ulceration
  3. Hepatic disease
  4. Renal disease
  5. Pregnancy
  6. Breastfeeding
257
Q

Give 3 drug interactions for direct oral anticoagulants

A
  1. CYP inhibitors (e.g. macrolides, fluconazole, protease inhibitors) - increase anticoagulant effect of DOACs
  2. CYP inducers (e.g. rifampicin, phenytoin)- decrease anticoagulant effect
  3. Other antithrombotic medications
258
Q

Give 2 examples of loop diuretics

A
  1. Furosemide
  2. Bumetanide
259
Q

Give 3 indications for loop diuretic use

A
  1. Acute pulmonary oedema
  2. Chronic heart failure - to manage fluid overload
  3. Oedematous states
260
Q

Give the mechanism of action for loop diuretic use

A

Inhibit Na+/K+/2Cl- co-transporter in the loop of Henle, normally transporting ions from the tubular lumen of the nephron back into the circulation. Inhibiting this pump has a profound diuretic effect.

Dilate capacitance veins, reducing preload and improving contractile force - this is their effect in acute heart failure.

261
Q

Give 4 side effects of loop diuretic use

A
  1. Dehydration
  2. Low electrolyte state
  3. Hypotension
  4. Hearing loss and tinnitus
262
Q

Give 6 cautions for loop diuretic use

A
  1. Gout
  2. Hypovolaemia
  3. Hyponatraemia
  4. Dehydration
  5. Hypokalaemia
  6. Hepatic encephalopathy
263
Q

Give 1 drug interaction for loop diuretics

A
  1. Drugs which are excreted by the kidney (e.g. lithium, digoxin) - can result in reduced excretion and accumulation
264
Q

Give 2 examples of thiazide diuretcs

A
  1. Bendroflumethiazide
  2. Indapamide
265
Q

Give 2 indications for thiazide diuretic use

A
  1. Alternative first-line treatment in hypertension - where a CCB would normally be used but is otherwise contraindicated
  2. Add-on treatment for hypertension if not adequately controlled by CCB plus an ACE inhibitor/ARB.
266
Q

Give the mechanism of action for thiazide diuretics

A

Inhibit the Na+/Cl- co-transporter in the distal renal tubule, preventing reabsorption of Na+ (and therefore water) and having a profound diuretic effect.

267
Q

Give 4 side effects of thiazide diuretic use

A
  1. Impotence
  2. Hypokalaemia
  3. Hyponatraemia
  4. Cardiac arrhythmias
268
Q

Give 3 cautions for thiazide diuretic use

A
  1. Gout
  2. Hyponatraemia
  3. Hypokalaemia
269
Q

Give 2 examples of dopaminergic drugs for Parkinson’s disease

A
  1. Levodopa
  2. Ropinirole
270
Q

Give 3 indications for dopaminergic drug use in Parkinson’s

A
  1. Early Parkinson’s - dopamine agonist (i.e. ropinirole) use
  2. Late Parkinson’s - Levodopa forms an integral part of treatment
  3. Secondary Parkinsonism
271
Q

Give the mechanism of action for dopaminergic drug use in Parkinson’s

A

L-dopa is a precursor for dopamine, which replenishes it’s deficient supply in the nigrostriatal pathway.

Ropinirole agonises the D2 receptors in this pathway.

272
Q

Give 5 side effects of dopaminergic drug use in Parkinson’s

A
  1. Nausea
  2. Drowsiness
  3. Confusion
  4. Hallucinations
  5. Hypotension
273
Q

Give 3 cautions for dopaminergic drug use in Parkinson’s

A
  1. Elderly
  2. Cognitive or psychiatric disease
  3. Cardiovascular disease
274
Q

Give 2 drug interactions for dopaminergic drug use in Parkinson’s

A

Drugs which have opposing actions on dopamine receptors:

  1. First-generation antipsychotics
  2. Metoclopramide
275
Q

Give 2 examples of emollients

A
  1. Aqueous creams
  2. Liquid paraffin
276
Q

Give 2 indications for emollient use

A

Dry and scaling skin disorders:

  1. Eczema
  2. Psoriasis
277
Q

Give the mechanism of action for emollients

A

Replace water content in dry skin, and reduce water loss by protecting against evaporation from the skin surface.

278
Q

Give 3 side effects of emollient use

A
  1. Greasiness
  2. Exacerbation of acne vulgaris
  3. Folliculitis
279
Q

Give 1 caution for emollient use

A

Paraffin based emollients are a significant fire hazard.

280
Q

Give 2 examples of fibrinolytic drugs

A
  1. Alteplase
  2. Streptokinase
281
Q

Give 3 indications for fibrinolytic drug use

A
  1. Acute ischaemic stroke
  2. Acute STEMI
  3. Massive PE with haemodynamic instability
282
Q

Give the mechanism of action for fibrinolytic drugs

A

Thrombolytic.

Catalyse the conversion of plasminogen to plasmin, acting to dissolve fibrinous clots and re-canalise occluded vessels.

283
Q

Give 6 side effects of fibrinolytic drug use

A
  1. Bleeding
  2. Allergic reaction
  3. Cardiogenic shock
  4. Cardiac arrest
  5. Cerebral oedema
  6. Arrhythmias
284
Q

Give 3 cautions for fibrinolytic drug use

A
  1. Bleeding
  2. Intracerebral haemorrhage
  3. Previous streptokinase treatment - due to development of anti-streptokinase antibodies
285
Q

Give 3 indications for pregabalin and gabapentin use

A
  1. Add-on therapy for focal epilepsies
  2. Neuropathic pain (carbamazepine is more appropriate for trigeminal neuralgia)
  3. Generalised anxiety disorder (pregabalin)
286
Q

Give the mechanism of action for pregabalin and gabapentin

A

Structurally related to GABA - the major inhibitory neurotransmitter in the brain.. Do not, however, bind to GABA receptors.

Bind to pre-synaptic voltage gated Ca2+ channels - inhibiting the release of excitatory neurotransmitters.

This results in a reduction in neuronal excitability.

287
Q

Give 3 side effects of pregabalin and gabapentin

A
  1. Drowsiness
  2. Dizziness
  3. Ataxia (the loss of full control of bodily movements)
288
Q

Give 1 caution for pregabalin and gabapentin use

A
  1. Renal impairment - depend on the kidneys for elimination
289
Q

Give 1 drug interaction for pregabalin and gabapentin

A
  1. Sedating drugs (e.g. bezodiazepines)
290
Q

Give 1 example of a H2-receptor antagonist

A
  1. Ranitidine
291
Q

Give 2 indications for H2-receptor antagonist use

A
  1. Peptic ulcer disease
  2. GORD and dyspepsia
292
Q

Give the mechanism of action for H2-receptor antagonist use

A

Reduce gastric acid secretion - normally produced by proton pumps of the parietal cell, the action of which is regulated by histamine.

Blocking H2 receptors results in decreased gastric acid secretion.

293
Q

Give 1 caution for H2-receptor antagonist use

A
  1. Can disguise symptoms of gastro-oesophageal cancer
294
Q

Give 3 examples of heparins

A
  1. Enoxaparin
  2. Dalteparin
  3. Unfractionated heparin
295
Q

Give 2 indications for heparin use

A
  1. Venous thromboembolism (DVT and PE)
  2. Acute coronary syndrome
296
Q

Give the mechanism of action for heparins

A

Heparins enhance the anticoagulant effect of anti-thrombin - which normally acts to inactivate clotting factors to provide a natural break in the clotting process.

LMWH is more specific for factor Xa.

297
Q

Give 3 side effects of heparin use

A
  1. Haemorrhage
  2. Hyperkalaemia
  3. Heparin-induced thrombocytopenia
298
Q

Give 5 cautions for heparin use

A
  1. Clotting disorders
  2. Severe uncontrolled hypertension
  3. Recent surgery or trauma
  4. Invasive procedures
  5. Renal impairment
299
Q

Give 4 examples of insulins

A
  1. NovoRapid - fast acting
  2. Actrapid - short acting
  3. Humulin I - intermediate acting
  4. Lantus - long acting
  5. NovoMix - biphasic insulin, consists of a mixture of rapid and intermediate acting insulins.
300
Q

Give 3 indications for insulin use

A
  1. Diabetes mellitus types 1 and 2
  2. Diabetic emergencies - e.g. ketoacidosis
  3. Hyperkalaemia - alongside glucose
301
Q

Give the mechanism of action for insulins

A

In diabetes exogenous insulin reacts functionally similarly to endogenous insulin - stimulating glucose uptake from the circulation.

Insulin drives K+ into cells, reducing serum concentrations, helping to manage hyperkalaemia.

302
Q

Give 1 side effect of insulin use

A
  1. Hypoglycaemia
303
Q

Give 1 caution for insulin use

A
  1. Renal impairment - can result in reduced insulin secretion and subsequent hypoglycaemia
304
Q

Give 2 examples of iron supplements

A
  1. Ferrous sulfate
  2. Ferrous fumarate
305
Q

Give 2 indications for iron supplement use

A
  1. Iron-deficiency anaemia
  2. Prophylaxis of iron-deficiency anaemia
306
Q

Give the mechanism of action for iron supplement use

A

Replenishes iron stores.

307
Q

Give 1 side effect of iron supplement use

A
  1. GI upset (including nausea, epigastric pain, constipation, diarrhoea)
308
Q

Give 2 cautions for iron supplement use

A
  1. Intestinal disease - including IBD
  2. Atopic predisposition - risk of anaphylaxis
309
Q

Give 2 indications for lamotrigine use

A
  1. Epilepsy - first-line monotherapy in focal seizures, generalised tonic-clonic seizures and absence seizures
  2. Bipolar depression - but not in mania or hypomania
310
Q

Give the mechanism of action for lamotrigine

A

Binds to voltage-sensitive Na+ channels, impeding neuronal firing.

311
Q

Give 8 side effects of lamotrigine use

A
  1. Headache
  2. Drowsiness
  3. Irritability
  4. Blurred vision
  5. Dizziness
  6. GI symptoms
  7. Skin rash
  8. Severe hypersensitivity
312
Q

Give 3 cautions for lamotrigine use

A
  1. Hypersensitivity to antiepileptic drugs
  2. Hepatic impairment
  3. Pregnancy
313
Q

Give 2 drug interactions for lamotrigine

A
  1. Glucoronidation inducers - carbamazepine, phenytoin, oestrogens, rifampicin - cause lamotrigine concentration to fall
  2. Glucoronidation inhibitors - valproate - cause lamotrigine levels to rise
314
Q

Give 3 examples of osmotic laxatives

A
  1. Lactulose
  2. Macrogol
  3. Phosphate enema
315
Q

Give 3 indications for osmotic laxative use

A
  1. Constipation and faecal impaction
  2. Bowel preparation for surgery/endoscopy
  3. Hepatic encephalopathy
316
Q

Give the mechanism of action for osmotic laxatives

A

Based on osmotically active substances which are not digested or absorbed and therefore remain in the gut lumen - they therefore hold back water in the stool, maintaining its volume and stimulating peristalsis.

317
Q

Give 6 side effects of osmotic laxative use

A
  1. Flatulence
  2. Abdominal cramps
  3. Nausea
  4. Diarrhoea
  5. Local irritation
  6. Electrolyte imbalance
318
Q

Give 4 cautions for osmotic laxative use

A
  1. Intestinal obstruction
  2. Heart failure (phosphate enemas can cause a significant electrolyte shift)
  3. Ascites
  4. Electrolyte disturbance
319
Q

Give 3 examples of stimulant laxative

A
  1. Senna
  2. Docusate sodium
  3. Bisacodyl
320
Q

Give 2 indications for stimulant laxative use

A
  1. Constipation
  2. Faecal impaction
321
Q

Give the mechanism of action for stimulant laxatives

A

Increase water and electrolyte secretion, thereby increasing the volume of colonic content and stimulating peristalsis.

322
Q

Give 1 caution for stimulant laxative use

A
  1. Intestinal obstruction - risk of perforation

Do not give rectal preparations in anal fissure or haemorrhoids.

323
Q

Give 1 example of a leukotriene receptor antagonist

A
  1. Montelukast
324
Q

Give 6 examples of Cytochrome P450 inducers

A

Cytochrome P450 system in the liver is responsible for metabolising active drugs. Inducers hasten the metabolism of other drugs, and therefore reduce their concentrations.

PCBRAS:
-Phenytoin
-Carbamazepine
-Barbiturates
-Rifampicin
-Alcohol (chronic excess)
-Sulphonylureas

325
Q

Give 9 examples of Cytochrome P450 inhibitors

A

Inhibit metabolism of drugs, therefore increasing their concentrations.

AODEVICES
-Allopurinol
-Omeprazole
-Disulfiram
-Erythromycin
-Valproate
-Isoniazid
-Ciprofloxacin
-Ethanol
-Sulphonamides

326
Q

Give 4 side effects of leukotriene receptor antagonist use

A
  1. Headache
  2. Abdominal pain
  3. Hyperactivity and reduced ability to concentrate
  4. Churg-Strauss syndrome - an eosinophillic autoimmune disorder
327
Q

Give 2 drugs which may cause neutropenia

A
  1. Clozapine (antipsychotic)
  2. Carbimazole (anti thyroid)
328
Q

Give the mechanism of action for levetiracetam

A

Targets synaptic vesicle protein 2A which is expressed throughout the brain in synapses. Levetiracetam interferes with synaptic vesicle function to modulate neuronal excitability and reduce the risk of seizures.

329
Q

Give 2 drug classes which may cause hyperkalaemia

A
  1. ACE inhibitors
  2. Potassium sparing diuretics
330
Q

Give 1 indication for leukotriene receptor antagonist use

A
  1. Asthma - in adults alongside corticosteroid and LABA
331
Q

Give the mechanism of action for leukotriene receptor antagonists

A

Leukotrienes are produced by mast cells and activate the G protein coupled leukotriene receptor CysLT1.

This activates a cascade which results in inflammation and bronchoconstriction.

Antagonising leukotriene receptors results in reduced inflammation and reduced bronchoconstriction.

332
Q

Give 2 side effects of lidocaine use

A
  1. Stinging (when given locally)
  2. Hypotension
333
Q

Give 1 indication for leukotriene receptor antagonist use

A
  1. Asthma - where symptoms not adequately controlled by steroids and LABA. Or as alternative to LABA in children.
334
Q

Give the mechanism of action for leukotriene receptor antagonists

A

Leukotrienes are produced by mast cells, and act to activate the G protein-coupled leukotriene receptor CysLT1.

This activates a cascade that result in inflammation and bronchoconstriction.

Antagonising the leukotriene receptors results in reduced inflammation and reduced bronchoconstriction.

335
Q

Give 4 side effects of leukotriene receptor antagonist use

A
  1. Headache
  2. Abdominal pain
  3. Hyperactivity and reduced ability to concentrate
  4. Churg-Strauss syndrome - an eosinophillic autoimmune disorder
336
Q

Give 2 indications for levetiracetam use

A
  1. Seizure prophylaxis in epilepsy (focal seizures)
  2. Convulsive status epilepticus
337
Q

Give the mechanism of action for levetiracetam

A

Targets synaptic vesicle protein 2A which is expressed throughout the brain in synapses. Levetiracetam interferes with synaptic vesicle function to modulate neuronal excitability and reduce the risk of seizures.

338
Q

Give 3 cautions for macrolide use

A
  1. Allergy
  2. Renal impairment - due to renal elimination
  3. Hepatic impairment - due to hepatic elimination
339
Q

Give 2 indications for lidocaine use

A
  1. Local anaesthetic
  2. Antiarrhythmic - in VT and VF
340
Q

Give the mechanism of action for lidocaine

A

Blocks voltage-gated sodium channels, preventing initiation and propagation of action potentials in muscles and nerves.

Reduces action potential duration, slows conduction velocity and increases the refractory period in the heart to reverse arrhythmias.

341
Q

Give 2 side effects of lidocaine use

A
  1. Stinging (when given locally)
  2. Hypotension
342
Q

Give 1 caution for lidocaine use

A
  1. Reduced cardiac output - lidocaine relies heavily on hepatic blood flow for it’s elimination.
343
Q

Give 3 examples of macrolides

A
  1. Clarithromycin
  2. Azithromycin
  3. Erythromycin
344
Q

Give 3 indications for macrolide use

A
  1. Respiratory, skin and soft tissue infection - as alternative to penicillin
  2. Severe pneumonia - added to penicillin therapy to cover atypical organisms
  3. Helicobacter pylori eradication in peptic ulcer disease - alongside PPI
345
Q

Give the mechanism of action for macrolides

A

Broad spectrum of activity against Gram +ve and -ve organisms.

Inhibit bacterial protein synthesis by binding to bacterial ribosomes. This makes them bacteriostatic, and assists with the immune system’s destruction of these drugs.

346
Q

Give 6 side effects of macrolide use

A
  1. Irritant
  2. Ototoxicity
  3. Prolongation of QT interval - predisposing to arrhythmias
  4. Cholestatic jaundice
  5. Allergy
  6. Antibiotic-associated colitis
347
Q

Give 3 cautions for macrolide use

A
  1. Allergy
  2. Renal impairment - due to renal elimination
  3. Hepatic impairment - due to hepatic elimination
348
Q

Give 2 drug interactions for macrolides

A
  1. Drugs metabolised by CYP - e.g. warfarin
  2. Drugs that prolong the QT interval or cause arrhythmias - e.g. amiodarone, antipsychotics, quinine, SSRIs
349
Q

Give 1 indication for metformin use

A
  1. Type II diabetes - first choice medication
350
Q

Give the mechanism of action for metformin

A

Reduces hepatic glucose output (glycogenolysis and gluconeogenesis) and increases glucose uptake by skeletal muscle.

351
Q

Give 2 side effects of metformin use

A
  1. Lactic acidosis
  2. GI upset
352
Q

Give 6 cautions for metformin use

A
  1. Renal impairment
  2. Hepatic impairment
  3. AKI
  4. Tissue hypoxia - e.g. in shock
  5. Acute alcohol intoxication
  6. Chronic alcohol abuse
353
Q

Give 1 drug interaction for metformin

A
  1. IV contrast media - metformin must be withheld for 48 hours prior
354
Q

Give 3 indications for methotrexate use

A
  1. DMARD for rheumatoid arthritis
  2. Chemotherapy - including for leukaemia and lymphoma
  3. Psoriasis
355
Q

Which drugs are cytochrome P450 enzyme inducers?

A

PC BRAS

Phenytoin
Carbamazepine
Barbiturates
Rifampicin
Alcohol (chronic excess)
Sulphonylureas

356
Q

Which drugs are cytochromne P450 enzyme inhibitors?

A

AODEVICES

Allopurinol
Omeprazole
Disulfiram
Erythromycin
Valproate
Isoniazid
Ciprofloxacin
Ethanol (acute intoxication)
Sulphonamides

PSA (2 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions