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Case Pres > 5. Cardiovascular Drugs > Flashcards

5. Cardiovascular Drugs Flashcards

1
Q

What are ace inhibitors and angiotensin 2 inhibitors used for? (2)
- Mechanism?

A
  1. Hypertension and congestive heart failure

2. Suppression of renin-angiotensin-aldosterone system

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2
Q

ACE inhibitor - example

- Mechanism

A

Lisinopril
- Blocks synthesis of angiotensin 2 and allows for vasodilatory effect of bradykinin

(Angiotensin 2 causes direct vasoconstriction and increases aldosterone which increases fluid retention)

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3
Q

Angiotensin 2 blocker - example

- Mechanism

A

Valsartan

- Blocks action of angiotensin 2 (limiting direct vasoconstriction)

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4
Q

ACE inhibitors / Angiotensin 2 blockers - Side effects (4)

A
  1. Persistent cough
  2. Dizziness, fatigue
  3. Dry mouth, dysgeusia
  4. Oral ulcerations
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5
Q

ACE inhibitors / Angiotensin 2 blockers - Interactions

A

ASA & NSAIDs interact to decrease antihypertensive effects

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6
Q

ACE inhibitors / Angiotensin 2 blockers - Dental considerations (3)

A
  1. Oral ulcers, persistent cough
  2. Orthostatic hypotension
  3. Assess patient’s salivary flow
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7
Q

Ca++ channel blockers

  • Uses (5)
  • Mechanism
A
  1. Angina, HTN, coronary vasospasm, MI, CHF
  2. Decrease Ca++ influx in cardiac and smooth muscle, decrease myocardial contractility and O2 demand, dilate coronary arteries
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8
Q

CA++ channel blockers - Side effects (4)

A
  1. Dizziness, headache
  2. Dry mouth
  3. Bradycardia
  4. Gingival hyperplasia
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9
Q

Ca++ channel blockers

- Interactions (3)

A
  1. Protein-bound drugs (ASA, NSAIDs)
  2. Grapefruit juice
  3. Erythromycin (5x sudden death risk)
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10
Q

Ca++ channel blockers - Dental considerations (5)

A
  1. Orthostatic hypotension
  2. Assess salivary flow
  3. Gingival enlargement
  4. Use NSAID with caution
  5. Avoid Erythromycin
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11
Q

Beta blockers - which are selective and which are non-selective
- Metoprolol, atenolol, propanolol

A

Selective: Metoprolol and atenolol (A-M)

Non-selective (N-Z): Propanolol

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12
Q

Beta blockers - Uses

- Mechanism

A

Use: Angina, HTN, MI
Mechanism: Blockage of B-1 receptors, slowing HR and depress renin secretion

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13
Q

Beta blockers - Side effects (5)

A
  1. Dizziness, fatigue
  2. Dry mouth
  3. Hypotension
  4. Bradycardia
  5. Asthmatic issues if non-selective
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14
Q

Beta blockers - interactions (2)

A

Epinephrine and NSAIDs

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15
Q

Beta blockers - Dental considerations

A
  1. Monitor vital signs
  2. Minimize stress
  3. Orthostatic hypotension
  4. Monitor salivary flow
  5. Use epi/NSAIDs with caution
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16
Q

Vasodilators - Nitrates

  • Mechanism
  • Side effects
A

Decrease cardiac preload by increasing venous capacitance

Headache, postural hypotension, dry mouth, tolerance

17
Q

Vasodilators - Nitroglycerine - Mechanism

- Metabolized where?

A

Causes vascular smooth muscle relaxation and vasodilation

- Metabolized in liver

18
Q

Vasodilators - Alpha 1 blockers

- Mechanism

A

Blockage of catecholamine binding sites on vascular alpha-1 adrenoreceptors, causing decrease in arteriolar resistance

19
Q

Cardiac glycosides - Digoxin

  • Mechanism
  • Uses? (2)
A

Inhibits Na-K ATPase to increase Calcium and contractility (increases CO/EF)
Increase PS tone to heart, reducing SA firing and conduction velocity through AV node

Uses: A-fib and CHF

20
Q

Cardiac glycosides - digoxin - What are the dangers? (3)

A

Very narrow therapeutic index and may result in worsening CHF or increased mortality with a-fib

21
Q

Diuretics - Uses (2)

- Mechanism?

A

HTN and edema

Inhibits reabsorption of Na+ and Cl- in distal tubule/loop of Henle

22
Q

Diuretics

- Side effects

A

Hypokalemia and hypotension

23
Q

Diuretics - Dental considerations

A
  1. Oral ulcers
  2. Assess patient’s salivary flow
  3. K+ supplementation
24
Q

Coumadin - Uses

- Mechanism

A

Peripheral thrombi, a-fib, pulmonary embolism, MI, prosthetic heart valves
Mechanism: Inhibit synthesis of Vital K dependent coagulation factors (II, VII, IX, X)

25
Q

Coumadin - Side effects (1)

- Interactions (3)

A

Hemorrhage

  1. Salicylates, NSAIDs
  2. Acetaminophen
  3. Cephalosporins, Cipro, antibiotics
26
Q

Coumadin - Dental considerations (4)

A
  1. Lab test (check PT/INR)
  2. Local hemostasis measures
  3. Provide OHI
  4. Many drug interactions
27
Q

Plavix - Use and MoA

A
  1. Treatment and prophylaxis of atherothrombotic events

2. Inhibits platelet aggregation by inactivating receptors linked to ADP pathways

28
Q

Plavix - side effects and interactions

A

Hemorrhage

  1. Salicylates
  2. Proton Pump Inhibitors
29
Q

Plavix - Dental Considerations

A
  1. Local hemostasis measures / increased risk of intra-operative bleeding
  2. Provide OHI
30
Q

Pradaxa - Use and complications

A

Reduction of ischemic stroke risk; a-fib

Bleeding complication

31
Q

Xarelto - Use and complications

A

DVT prophylaxis TJR surgery. Ischemic stroke prevention, A-fib

32
Q

Antilipid agents (HMG CoA reductase inhibitor) - Use and mechanism (3)

A

Hypercholesterolemia and hyperlipidemia

MoA: Inhibit HMB COA reductase (statins), modify lipoproteins, interfere with cholesterol absorption

33
Q

HMG CoA Reductase inhibitors - Side effects

A
  1. Nausea, ab pain, diarrhea
  2. Liver enzyme elevation
  3. Dysgeusia
34
Q

HMG CoA Reductase inhibitors - Interactions and Dental considerations (1)

A

Interacts with erythromycin, so avoid erythromycin

Case Pres (7 decks)

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