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CP1 > Therapeutics > Flashcards

Therapeutics Flashcards

1
Q

Describe the clinical pharmacology of ACEis

A

Ramipril, Captopril, Enalapril, Perindopril
Angiotensin converting enzyme inhibitor
ACE predominantly located in the lungs
ACE converts the peptide AI into AII (vasocontrictor)
AII acts on AT1 receptors causing vasoconstriction
AII stimulates aldosterone release (Na+/H2O retaining)

ACE metabolises bradykinin (vasodilator)
ACEI increases bradykinin levels

ACEIs reduce vasoconstriction, BP, work of the heart, induce cough in 10%

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2
Q

Describe the clinical pharmacology of angiotensin AT1 receptor antagonists

A

Losartan, Valsartan
Angiotensin II receptor 1 antagonist
Blocks action of AII at AT1 receptor
Alternative if ACEI not tolerated (cough)

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3
Q

Describe the clinical pharmacology of calcium channel blockers

A

Dihydropyridines: Amlodipine, Felodipine, Nifepidine
Rate limiting agents: Diltiazem, Verapamil
Inhibit calcium channels on vascular smooth muscle –> vasodilation & reduced BP

Dihydropyridines: most widely used for HTN
Rate limiting agents: also act upon cardiac calcium channels –> decreasing HR by partially blocking AV node

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4
Q

Describe the clinical pharmacology of thiazide-like diuretics

A

Chlortalidone, Indapamide
Inhibit Na+/Cl- symporter in DCT preventing Na+ reabsorption, followed by H2O
Decreases circulating volume (can be restored over time)
Cause vasodilation
Ineffective with moderate renal impairment as they require excretion/secretion by PCT to act at DCT
Diabetogenic
Uric acid + thiazide compete for excretion/secretion in PCT
Hypokalaemia: thiazide-like diuretic causes hypovolaemia –> activates RAAS –> increases aldosterone (Na+ retaining & K+ losing)

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5
Q

Hypertensive regimen for a patient with asthma

A

Avoid beta-blocker
<55y = ACEI (e.g. ramipril)
>55y/afro-carribean = Calcium channel inhibitor (e.g. amlodipine/verapamil) - rate limiting or DHP???
A + C
A + C + thiazide-like diuretic (e.g. chlortalidone)
Add alpha blocker (Prazocin, Doxazocin)
or spironolactone - K+ sparing diuretic
or other diuretic
Or beta blocker (don’t combine with rate limiting Ca+ channel blocker)

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6
Q

Hypertensive regimen for a patient with diabetes

A

ACEI indicated for diabetic nephropathy

Thiazide-like diuretics are diabetogenic

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7
Q

Hypertensive regimen for a patient with renal impairment (elderly)

A

Calcium channel inhibitor
Renovascular disease = Avoid ACEI
Thiazide-like diuretics ineffective in moderate renal impairment as they require excretion by PCT to work on the DCT (except metolazone - chose in renal impairment??)

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8
Q

Ischaemic heart disease regimen including antiplatelet and statin therapty

A

GTN for symptomatic relief (release of NO –> venodilation & coronary vasodilation)

B-blocker: prophylaxis: -ve inotropic & -ve chromotropic effects reduce cardiac work
Decreased HR –> Increased diastole time = increased coronary perfusion

Aspirin/clopidogrel: antiplatelet
Statin: reduce overall CV risk
BP controlled: ACEI?

Calcium channel inhibitor: vasodilation. Verapamil = rate-limiting –> bradycardic action prolongs diastole so improves coronary perfusion

Potassium channel activators (Nicorandil): NO donor and activator of ATP-sensitive K+ channels on vascular smooth muscle = hyperpolarisation = vasodilation

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9
Q

Describe the clinical pharmacology of loop diuretics

A

Act on the Na+-K+-2Cl− symporter in the ascending limb of the loop of Henle to inhibit Na+, Cl- and K+ reabsorption
Inhibits magnesium and calcium reabsorption in the thick ascending limb
The collective effects of decreased blood volume and vasodilation decrease blood pressure and ameliorate oedema

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10
Q

Describe the clinical pharmacology of beta-blockers

A

Atenolol, Propanolol
Mechanism of action unclear
Inhibit sympathetically evoked renin release from kidneys
Reduces cardiac output via reducing beta-stimulation of the heart
Beta1-selective agents (atenolol) only weakly selective so still have significant action on bronchial beta2-adrenoceptors = contraindicated in asthma (& caution COPD)
Class 2 anti-arrhythmic effects: reduce risk of MI
Reduce hypoglycaemic awareness
Contraindicated in heart block
Labetalol licenced for pregnancy

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11
Q

Describe the clinical pharmacology of digoxin

A

+ve inotrope by inhibiting Na+/K+ ATPase –> Na+ accumulates in myocytes and is exchanged for Ca2+ = increased contractility
Impairs AV conduction & increases vagal activity (via CNS) = heart block & bradycardia

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12
Q

CHF drug regimen for a patient with asthma

A

ACEI: (elanapril/lisinopril/ramipril) inhibit RAAS
ATRA if ACEI not tolerated (cough)
Furosemide: oedema
Spironolactone: aldosterone receptor antagonist, low non-diuretic dose (25mg) inhibits heart fibrosis. ACEI + spironolactone = hyperkalaemia risk
ACEI + ATRA if disease refractory (+hydralazine & nitrate)
Digoxin: +ve inotropic effect. Diuretic induced hypokalaemia increases the risk of digoxin toxicity
Avoid beta-blocker
Avoid low-dose aspirin?

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13
Q

CHF drug regimen for a patient with COPD

A

Caution beta-blockers (weigh up benefit/risk)
ACEI: (elanapril/lisinopril/ramipril) inhibit RAAS
ATRA if ACEI not tolerated (cough)
Furosemide: oedema
Spironolactone: aldosterone receptor antagonist, low non-diuretic dose (25mg) inhibits heart fibrosis. ACEI + spironolactone = hyperkalaemia risk
ACEI + ATRA if disease refractory (+hydralazine & nitrate)
Digoxin: +ve inotropic effect. Diuretic induced hypokalaemia increases the risk of digoxin toxicity

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14
Q

CHF drug regimen for a patient with renal impairment

A

Beta-blocker: metoprolol/bisoprolol/carvedilol/nebivolol: block sympthetic activity (slowly titrate up)
ATRA instead of ACEI?
Furosemide: oedema
Spironolactone: aldosterone receptor antagonist, low non-diuretic dose (25mg) inhibits heart fibrosis. ACEI + spironolactone = hyperkalaemia risk
Digoxin: +ve inotropic effect. Diuretic induced hypokalaemia increases the risk of digoxin toxicity
Digoxin 2/3 renally cleared so dose dependent on eGFR
NSAIDs + ACEIs = increased risk of renal damage
Diabetic nephropathy = ACEI
Renovascular disease = avoid ACEI - bilateral renal artery stenosis
Thiazides ineffective in moderate renal failure

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15
Q

CHF drug regimen for a patient with concurrent AF

A

Digoxin beneficial in AF
ACEI + beta-blocker: ACEI established 1st, then beta-blocker added
Warfarin/aspirin: thromboembolic prophylaxis. NSAID reduces antihypertensive effect of ACEI + in combination can cause renal damage.
Furosemide: oedema
Spironolactone: aldosterone receptor antagonist, low non-diuretic dose (25mg) inhibits heart fibrosis. ACEI + spironolactone = hyperkalaemia risk
ACEI + ATRA if disease refractory (+hydralazine & nitrate)
Diuretic induced hypokalaemia increases the risk of digoxin toxicity

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16
Q

Describe the clinical pharmacology of warfarin

A

Vitamin K antagonist
Inhibits the vitamin K-dependent synthesis of clotting factors II, VII, IX and X

Contraindicated alongside: antiplatelet drugs, non-steroidal anti-inflammatory drugs (NSAIDs), selective serotonin reuptake inhibitors (SSRIs), venlafaxine or duloxetine.

Dabigatran etexilate, rivaroxaban and apixaban are relatively newer oral anticoagulants. Dabigatran etexilate is a direct thrombin inhibitor, whilst rivaroxaban and apixaban inhibit activated factor Xa

17
Q

Describe the clinical pharmacology of heparin (including LMWH)

A

Unfractioned heparin activates antithrombin –> inactivates clotting factor Xa & thrombin
LMWH: (enoxaparin/dalteparin) preferentially inactivate factor Xa
Administered i.v. or subcut.

18
Q

Describe the clinical pharmacology of low dose aspirin

A

Inhibits endothelial and platelet cyclo-oxygenase (COX) –> inhibits production of prostaglandins (inhibit platelet aggregation) and thromboxane (stimulates platelet aggregation)
Endothelial cells can regenerate COX (platelets can’t due to lack of nucleus) therefore prostaglandins are favoured

Ibuprofen: COX inhibitor that may compete with aspirin and reduce its effects

19
Q

Describe the clinical pharmacology of clopidogrel

A

ADP receptor antagonist: prevents platelet aggregation

Used in patients who cannot have aspirin (e.g. asthma)

20
Q

What monitoring is required when using warfarin and heparin?

A

Warfarin: INR is checked daily until in the therapeutic range, twice a week for 1-2 weeks, weekly until stable, then every 6-12 weeks.
Change in a patient’s condition - eg, liver disease, intercurrent illness, a new drug started - necessitates more frequent testing.

Heparin: FBC to monitor platelet count?
Renal damage: accumulation of LMWH

21
Q

Clinical pharmacology of antacids

A

q

22
Q

Clinical pharmacology of H2 receptor antagonists

A

q

23
Q

Clinical pharmacology of proton pump inhibitors

A

q

24
Q

Clinical pharmacology of misoprostol

A

q

25
Q

Clinical pharmacology of ‘triple therapy’ when treating peptic ulceration

A

q

26
Q

Pharmacological management of non-ulcer dyspepsia

A

q

27
Q

Pharmacological management of peptic ulceration associated with H. Pylori

A

q

28
Q

Pharmacological management of peptic ulceration NOT associated with H. Pylori

A

q

29
Q

Pharmacological management of peptic ulceration associated with NSAID use

A

q

30
Q

Pharmacological management of GORD

A

q

31
Q

Pharmacological management of constipation

A

q

32
Q

Pharmacological management of diarrhoea

A

q

33
Q

Pharmacological management of irritable bowel syndrome

A

q

34
Q

Pharmacological management of inflammatory bowel disease

A

5-aminosalicylates
Corticosteroids
Immunosuppressives

35
Q

Interpret results of a liver function test

A

q

36
Q

Management of complications of liver failure

A

q

37
Q

Liver dysfunction in drug therapy

A

q

CP1 (12 decks)

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