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Drugs for Human diseases > CVS > Flashcards

CVS Flashcards

1
Q

What are the drugs that end in -pril? (i.e. Enalapril)

A

ACE inhibitors

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2
Q

How do ACE inhibitors work?

A
  1. Inhibit the conversion of angiotensin I to angiotensin II and prevent aldosterone dependent reabsorption of salt and water.
  2. Basically they reduce blood pressure by reducing excess salt and water retention
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3
Q

What are some side effects of taking ACE inhibitors?

A
  1. Chronic cough primarily but others too…
  2. Oral lichenoid reactions
  3. Postural hypotension (may effect when sitting patients up in the chair)
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4
Q

WHat should you be mindful of when prescribing NSAIDs (i.e ibuprofen, aspirin..) to someone on ACE inhibitors?

A

The interaction could reduce the anti-hypertensive effect as well as increase the risk of acute renal injury.

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5
Q

What are the drugs that end in -artan? (i.e Losartan, candesartan…)

A

Angiotensin II blockers

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6
Q

What is the mode of action of angiotensin II blockers?

A

Similar to how ACE inhibitors work EXCEPT; ACE inhibitors inhibit the conversion of angiotensin I to angiotensin II, while the ARBs antagonize receptor binding of angiotensin II to AT1 receptors.

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7
Q

What are some side effects of ARBs?

A

Renal impairment, cough, postural hypotension

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8
Q

What should you be mindful of prescribing for someone taking ARBs?

A

NSAIDs

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9
Q

What drugs (most often but not always) end in -ipine? (i.e Amlodipine, Nifedipine, verapamil, diltiazem..)

A

Calcium channel blockers

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10
Q

What is the mode of action of calcium channel blockers?

A

Calcium channel blockade affects smooth muscle and results in vasodilation and a reduction in heart rate (useful in treating some arrhythmias).

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11
Q

Which of the CCBs are more are more active on peripheral blood vessels compared with ones that are more active on the heart muscle?

A

Some drugs are more active on peripheral blood vessels (-ipines) and others are more active on the heart muscle (verapamil, diltiazem)

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12
Q

What are some dental implications of a patient taking calcium channel blockers?

A

gingival hyperplasia, postural hypotension

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13
Q

What antibiotic should you be cautious of prescribing for a patient on calcium channel blockers?

A

Macrolides

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14
Q

What bendroflumethiazide and furosemides?

A

Diuretics

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15
Q

Bendroflumethiazide

A

Thiazide diuretic

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16
Q

Furosemide

A

Loop diuretic

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17
Q

Thiazide compared with loop diuretics and indications for both

A

Thiazides are used to relieve oedema due to chronic heart failure and, in lower doses, to reduce blood pressure. Loop diuretics are used in pulmonary oedema due to left ventricular failure and in patients with chronic heart failure.

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18
Q

Mode of action of diuretics

A
  1. Used in Hypertension and for heart failure.
  2. Increase salt and water LOSS leading to reduced plasma volume and therefore reduced cardiac workload
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19
Q

What are some side effects of diuretics use?

A

SE: can lead to Na+/K+
imbalance if not monitored carefully

Dental: Dry Mouth

20
Q

What are the drugs ending in -olol? (i.e. bisoprolol, propranolol, atenolol…)

A

Beta-blockers

21
Q

Mode of action for beta-blockers

A

Beta-blockers work by blocking beta receptors, hindering the effects of adrenaline. This reduces heart rate and blood pressure, making them effective for conditions like hypertension and anxiety. Picture beta-blockers as “stress shields” that calm the heart’s response to adrenaline, like a protective barrier against excessive excitement and high blood pressure.

22
Q

Uses of beta blockers

A

Used in management of IHD, Hypertension AND Arrhythmias.
Stop arrhythmias leading to cardiac arrest (Ventricular fibrillation – VF). They prevent increase in heart rate by reducing heart muscle excitability.

23
Q

Side effects of beta blockers

A

worsen asthma, postural hypotension

24
Q

Drugs that end in -statin (atorvastatin, rosuvastatin, simvastatin etc)

A

HMG coA Reductase inhibitors

25
Q

Statins mode of action

A

HMG-CoA reductase inhibitors, commonly known as statins, act on a key enzyme called 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase in the liver. By inhibiting this enzyme, statins reduce the synthesis of cholesterol, lowering overall cholesterol levels in the blood. Including, LDL cholesterol.

26
Q

LDL cholestrol

A

Low-density lipoprotein (“bad cholestrol”)

27
Q

Side effects of statins

A

Myositis (“muscle” + “inflammation”) with some drug interactions - such as dental antifungals.

Fluconazole - stop taking the statin whilst on this anti fungal and then restart when course is over.

28
Q

Examples of anti-anginal drugs

A

Nitrates:
1. Isosorbide mononitrate - prevents angina
2. Glyceryl trinitrate (GTN spray) - short acting, useful in emergency management of angina symptoms

29
Q

Mode of action of nitrates

A

Dilate VEINS and reduce preload to the heart

Dilate resistance arteries and reduce cardiac workload (afterload) and cardiac oxygen consumption
Dilate collateral coronary artery supply and reduce anginal pain

30
Q

Side effects of nitrates

A

Headache, hypotension. No specific dental implications.

31
Q

What are some examples of anti-platelet drugs?

A

Aspirin, clopidogrel, dipyridamole, new antiplatelet drugs (Prasugrel, Ticagrelor etc.)

32
Q

Mode of action of aspirin

A

By inhibiting COX-1 in platelets, aspirin reduces the formation of thromboxane A2, a prostaglandin that promotes platelet aggregation.

Favouring; thromboxane A2 over prostaglandin may result in excessive platelet aggregation and vasoconstriction - aspirin corrects this ratio.

33
Q

Mode of action of clopidogrel

A

Requires metabolic activation in the liver to become effective. Once activated, clopidogrel inhibits a specific receptor called the P2Y12 receptor (ADP usually acts on this to form clots) on the surface of platelets.

34
Q

Mode of action of Dipyridamole

A

Inhibits platelet phosphodiesterase

35
Q

When would new antiplatelet drugs be prescribed?

A

They are only licensed in the management of ACS.

36
Q

Side effects of anti-platelet drugs

A

Increased bleeding risk. Bleeding implications - local haemostatic measures.

37
Q

Anti-coagulants examples

A

Warfarin

38
Q

Mode of action of warfarin

A

Inhibits synthesis of Vitamin K dependent clotting factors.

39
Q

Side effects of warfarin

A

SE: Multiple drug interactions – Assume ALL drugs interact with Warfarin!
Dental: Bleeding Risk – local haemostatic measures

40
Q

New oral anti-coagulants (NOACs) examples

A

• Rivaroxiban
• Apixaban
• Edoxaban
• Dabigatran

41
Q

NOACs - Factor Xa Inhibitors examples

A

• Rivaroxiban
• Apixaban
• Edoxaban

42
Q

NOACs - Direct Thrombin Inhibitor examples?

A

Dabigatran

43
Q

Factor Xa inhibitors mode of action

A

Directly inhibit prothrombinase complex and Factor Xa resulting in a reduction in thrombin.

44
Q

Direct Thrombin inhibitor mode of action

A

Targets Thrombin (Factor IIa) preventing thrombin-mediated activation of coagulation factors

45
Q

Side effects of NOACs

A

No significant drug interactions relevant to dentistry
Dental: Bleeding risk

Drugs for Human diseases (12 decks)

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