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Phase 2A > Pharmacology - Drug List > Flashcards

Pharmacology - Drug List Flashcards

1
Q

Explain 3 effects β-blockers have on the body

A

Reduced force and speed of contraction in the heart (relieving myocardial ischaemia), prolongation of the refractory period of AV node (slowing ventricular rate) and reduction of renin secretion from the kidney (lowering blood pressure)

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2
Q

Which receptors do β-blockers act upon?

A

β1-adrenoreceptors (G-protein linked receptor)

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3
Q

How are β-blockers administered?

A

Usually orally as regular medication however they can be administered IV when rapid effect necessary

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4
Q

Name 5 adverse effects of β-blockers

A

Cold extremities, headaches, nausea, fatigue, sleep disturbance/nightmares

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5
Q

2 situations when β-blockers should not be used

A

In patients with asthma (can cause life threatening bronchospasm) and should not be used with non-dihydropyridine calcium channel blockers (can cause heart failure and bradycardia)

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6
Q

Name 2 relatively selective β-blockers and one non selective

A

Atenolol and Bisoprolol are relatively β-1 selective

Propranolol is non selective

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7
Q

Name 5 conditions ACEIs are used for

A

Hypertension, chronic heart failure, ischaemic heart disease, diabetic nephropathy and CKD with proteinuria

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8
Q

How do ACEIs work?

A

Block ACE, prevent conversion of angiotensin 1 to angiotensin 2 (vasoconstrictor and stimulates aldosterone). Blocking it’s production reduces afterload which lowers blood pressure. Reduction of aldosterone promotes sodium and water excretion which reduces preload

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9
Q

Name 3 side effects of ACEIs

A

Hypotension (especially after first dose), persistent dry cough (increased bradykinin which is usually inactivated by ACE) and hyperkalaemia (low aldosterone level promotes potassium retention)

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10
Q

Which drugs shouldn’t be prescribed with ACEIs?

A

Potassium elevation drugs, including potassium supplements and potassium sparing diuretics
(NSAIDs will also increase the risk of renal failure so should be avoided)

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11
Q

How are ACEIs administered?

A

Orally

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12
Q

Name 3 ACEIs

A

Ramipril, lisinopril, perindopril

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13
Q

What is digoxin used for?

A

In atrial fibrillation/atrial flutter to reduce ventricular rate (however a non dihydropyridine calcium channel blocker is more effective).
In severe heart failure when patient is already taking ACEI, BB and aldosterone antagonist/ARB

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14
Q

Name 5 conditions beta blockers are used for

A

Ischaemic heart disease, chronic heart failure, atrial fibrillation, supraventricular tachycardia, hypertension (when CCBs/ACEIs insufficient)

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15
Q

How does digoxin work?

A

Negatively chronotrophic (decreases heart rate), positively inotrophic (increases force of contraction) and reduces conduction at AV node to reduce ventricular rate

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16
Q

Name 5 adverse effects of digoxin

A

Bradycardia, dizziness, GI disturbance, rash, visual disturbance (blurred or yellow vision)

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17
Q

Name 4 drugs that can increase the plasma concentration of digoxin and therefore increase the risk of toxicity

A

amiodarone, CCBs, spironolactone, quinine

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18
Q

Name 3 conditions where loop diuretics would be prescribed

A

Relief of breathlessness in pulmonary oedema, fluid overload in acute heart failure, fluid overload in other oedematous states (due to renal disease or liver failure)

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19
Q

Which part of the nephron do loop diuretics act on?

A

Ascending limb of loop of henle where they inhibit Na/K/2Cl co-transporter, preventing sodium, potassium and chloride ions crossing from the lumen into the epithelial cells therefore inhibiting the transport of water and providing a potent diuretic effect

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20
Q

As well as acting on the nephron, what other effect do loop diuretics have on the body?

A

Direct effect on blood vessels causing dilatation of capacitance veins, reducing preload and improving contractile function of overstretched heart muscle

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21
Q

Name 2 loop diuretics

A

Furosemide, Bumetanide

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22
Q

Name 4 adverse effects of loop diuretics

A

Dehydration, hypotension, low electrolyte state (Na/K/Cl/Ca/Mg), at high doses tinnitus/hearing loss

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23
Q

When should loop diuretics not be prescribed?

A

In patients with severe hypovolemia or dehydration. In patients with gout and hepatic encephalopathy they should be used with caution

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24
Q

When would potassium sparing diuretics be prescribed?

A

For the treatment of hypokalemia arising from loop/thiazide like diuretic use. Spiranolactone may be used as an alternative

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25
Name a potassium sparing diuretic and how it is administered
Amiloride (commonly prescribed as co-amilofruse which contains furosemide aswell) and is taken orally
26
How do potassium sparing diuretics work?
They act on the distal convoluted tubule inhibiting the resorption of sodium, and therefore water, by epithelial sodium channels.
27
Which drugs should not be prescribed alongside potassium sparing diuretics?
Potassium elevating drugs including supplements and aldosterone antagonists due to the risk of hyperkalaemia.
28
Who shouldn't potassium sparing diuretics be prescribed to?
Patients with severe renal impairment, hyperkalaemia or hypovolemia
29
Name 3 adverse effects of potassium sparing diuretics
Hypotension, GI upset, urinary symptoms
30
Name 1 thiazide diuretic and 2 thiazide like diuretics
Bendroflumethiazide (thiazide) , indapamide, chlortalidone
31
Which condition are thiazide like diuretics prescribed for?
Hypertension, either when a CCB is unsuitable (oedema/heart failure) or as an add on treatment when inadequately controlled by CCB + ARB/ACEI
32
How do thiazide diuretics work?
Act on distal convoluted tubule, inhibiting Na/Cl transporter preventing sodium (and water) reabsorption. Long term anti-hypertensive effects are not completely understood but are likely due to vasodilatory mechanisms
33
Name 3 side effects of thiazide diuretics
Hyponatraemia, hypokalaemia, cardiac arrhythmias
34
Which class of drugs reduces the effectiveness of thiazide diuretics?
NSAIDs
35
What is acetylcysteine most commonly prescribed for?
Paracetamol overdose
36
How does acetylcysteine work?
Replenishes body with glutathione which can conjugate with hepatotoxic NAPQI to detoxify it
37
How is acetylecysteine administered?
Intravenously as a weight adjusted dose
38
List 3 conditions aldosterone antagonists are used for
Ascites/oedema due to liver cirrhosis (Spiranolactone is first line diuretic), chronic heart failure (in addition to a BB + ACEI/ARB), primary hyperaldosteronism
39
How do aldosterone antagonists work?
Competitively binds to aldosterone receptor, increasing sodium and water excretion, and potassium retention
40
Name 2 main adverse effects of spiranolactone
Hyperkalaemia (can lead to muscle weakness, arrhythmias and cardiac arrest) and gynaecomastia
41
When shouldn't aldosterone antagonists be used?
Patients with severe renal impairment, hyperkalaemia or addisons disease
42
What is amiodarone used for?
Tachyarrhythmias - AF, atrial flutter, supraventricular tachycardia, ventricular tachycardia, and ventricular fibrillation
43
2 effects amiodarone has on myocardial cells
Blockade of sodium, calcium and potassium channels. | Antagonism of α and β-adrenergic receptors
44
6 adverse effects of amiodarone
Pneumonits, bradycardia, AV block, hepatitis, photosensitivity, thyroid abnormalities
45
When are angiotensin receptor blockers prescribed?
When ACEI is not tolerated due to cough. Same indications (Hypertension, chronic heart failure, ischaemic heart disease, diabetic nephropathy & CKD with proteinuria)
46
How do ARBs work?
Block the action of angiotensin 2 on AT1 receptor, reducing afterload which lowers blood pressure. Dilates efferent glomerular arteriole reducing intraglomerular pressure and reducing progression of CKD.
47
3 adverse effects of ARBs
Hypotension (particularly after first dose), hyperkalaemia and renal failure. No cough because ACE (and therefore bradykinin) is not affected
48
What shouldn't be prescribed with ARBs?
Potassium elevating drugs including supplements and potassium sparing diuretics
49
Name 4 calcium channel blockers
Amlodipine, nifedipine, diltiazem, verapamil
50
3 indications for calcium channel blockers
Hypertension (amlodipine and nifedipine), stable angina, supraventricular arrhythmias (diltiazem and verapamil)
51
How do calcium channel blockers work?
Decrease Ca entry into vascular/cardiac cells reducing intracellular calcium concentration causing relaxation and vasodilation. Reduce myocardial contractility and suppress cardiac conduction across AV node slowing ventricular rate. Reduced rate, afterload and contractility reduces oxygen demand preventing angina.
52
How are the calcium channel blockers split into classes?
Dihydropyridines (amlodipine and nifedipine) are relatively selective for vessels whereas non-dihydropyridines are more selective for the heart (verapamil more so that diltiazem)
53
4 adverse effects of dihydropyridines
Flushing, headaches, ankle swelling and palpitations
54
4 adverse effects of verapamil
Constipation, bradycardia, heart block and cardiac failure
55
What class of drug should non-dihydropyridines be prescribed with?
β-blockers - both drugs are negatively inotropic and chronotrophic and may cause heart failure, bradycardia and asystole
56
4 indications for clopidogrel
Acute coronary syndrome, prevent occlusion of coronary artery stents, long term secondary prevention of thrombotic arterial events (patients with cardiovascular, cerebrovascular and peripheral arterial disease) and to reduce the risk of embolic stroke in AF when warfarin contraindicated
57
How does clopidogrel work?
Prevents platelet aggregation by binding irreversibly to ADP receptors on the surface of platelets. This process is independent of the cyclooxygenase pathway and is synergistic with the actions of aspirin
58
3 adverse effects of clopidogrel
Bleeding, GI upset, thrombocytopenia
59
What may reduce the efficacy of clopidogrel?
Cytochrome p450 inhibtors
60
Name 3 systemic corticosteroids
Prednisolone, hydrocortisone, dexamethasone
61
6 indications for systemic corticosteroids
Allergic disorders, inflammatory disorders, autoimmune disease, some cancers, adrenal insufficiency, hypopituitarism
62
Which receptors do corticosteroids act upon?
Cytosolic glucocorticoid receptors (nuclear)
63
How do corticosteroid receptors work?
Upregulate anti-inflammatory genes and downregulate pro-inflammatory genes (TNFα, cytokines)
64
8 adverse effects of corticosteroids
Immunosuppression increases risk and severity of infection, diabetes mellitus, osteoporosis, muscle weakness, skin thinning, gastritis, mood changes, hypertension, insomnia
65
Name 3 inhaled corticosteroids
Beclametasone, budesonide, fluticasone
66
Two indications when inhaled corticosteroids would be prescribed
Asthma (2nd step after SABA), COPD (in combinations with LABA)
67
3 effects inhaled corticosteroids have to improve asthma symptoms?
Reduced mucosal inflammation, widening of airways, reduced mucus secretion
68
2 adverse effects of inhaled corticosteroids
Oral candidiasis, hoarse voice
69
When would dipyramidole be prescribed?
First line therapy for TIA , second line therapy following an ischaemic stroke where clopidogrel is contraindicated, to induce tachycardia during a myocardial perfusion scan
70
How does dipyramidole work?
antiplatelet effect - increased cAMP inhibits platelet aggregation. Blocks uptake of adenosine - vasodilatory effect
71
5 adverse effects of dipyramidole
Headaches, flushing, dizziness, GI upset, thrombocytopenia
72
Name 2 nitrates
Isosorbide mononitrate, Glyceryl trinitrate
73
2 indications for GTN
Acute angine, acute coronary syndrome
74
1 indication for isosorbide mononitrate
angina prophylaxis where BB/CCB is intolerated
75
How do nitrates work?
Converted to NO which increases cGMP synthesis and reduces intracellular calcium in vascular smooth muscle cells causing them to relax. This leads to venous and arterial vasodilatation, reducing cardiac preload/work therefore relieving angina
76
3 conditions where nitrates should not be prescribed?
Severe aortic stenosis, haemodynamic instability, hypotension
77
Name 3 NSAIDs
naproxen, ibuprofen, etoricoxib
78
How do NSAIDs work?
Inhibit synthesis of prostaglandins from arachidonic acid by inhibiting COX

Phase 2A (9 decks)

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