3.7 Cardiac Medications + Dental Side Effects Flashcards

1
Q

What are the main drug classes used in hypertension medications?

A
  1. ACE inhibitors
  2. Angiotensin II anatgonists
  3. Calcium channel blockers
  4. Thiazide diuretics
  5. Beta blockers
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2
Q

What are the two types of antianginal medication?

A
  1. Nitrates
  2. Aspirin
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3
Q

Blood pressure is determined by cardiac output (stroke volume x heart rate) and peripheral vascular resistace. What are the targets for the various hypertension drug classes?

A
  1. Cardiac output (gen) = angiotensin II antagonists
  2. Stroke volume specific = diuretics + ACE inhibitors
  3. Heart rate specific = beta blockers
  4. Vascular resistance = calcium channel blockers
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4
Q

How do beta blockers lower heart rate?

A

Baroreceptor reflex compares arterial pressure to set point

When arterial pressure decreases, signals CNS to increase cardiac output via sympathetic pathway

Beta blockers prevent sympathetic pathway being activated

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5
Q

How do ACE inhibitors, angiotensin II antagonists, and diuretics lower heart rate?

A

Interrupt renin-angiotensin system (RAS) at various points

ACE inhibitors = inhibit angiotensin converting enzyme (ACE)

Angiotensin II antagonists = block angiotensin II (AT) receptors

Diuretics = prevent kidney from H2O + NaCl reabsorption

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6
Q

What are examples of ACE inhibitors?

A

“-prils”

Catopril, Enalapril, Fosinopril, Lisinopril

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7
Q

What are the cardio-renal effects of ACE inhibitors?

A

Vasodilation (arterial + venous) to reduce pressure and ventricular afterload + preload

Decrease blood volume

Inhibit cardiac + vascular hypertrophy

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8
Q

What are the side effects of ACE inhibitors?

A

Electrolyte disbalance

Worsen renal function (if already impaired)

Contraindicated in preganancy (2.7x risk of malformation)

Anaphylaxis

Dry cough

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9
Q

What are examples of angiotenin II antagonists?

A

“-sartans”

Losartan, candesartan, temlisartan

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10
Q

Calcium channel blockers block voltage dependent Ca2+ channels to relax vascular smooth muscle cells. What are examples of this type of medication?

A

Dihydropyridines (-dipine)
Amlodipine, Nifedipine, Felodipine, Nimodipine

Non-nihydropyridines
Diltiszam, verapamil

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11
Q

What are the desired effects of calcium channel blockers?

A

Cardiac = decrease contractility, heart rate, and conduction velocity

Vascular = smooth muscle relaxation

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12
Q

What are the side effects of calcium channel blockers?

A

Vasodilation (ankle oedema, tachycardia, headache, flushing)

Constipation

Verapamil/ciltizem can decrease cardiac output to point of heart failure

Gingiva hyperplasia

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13
Q

How do thiazide diuretics work to decrease blood pressure?

A
  1. Inhibit Na+ and Cl- reabsorption in distal tubule, decreasing body water retention + blood volume
  2. Direct effect on vascular smooth mucle = less responsive to vasoconstrictors
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14
Q

What are potential side effects of thiazide diuretics?

A

Gout
Hypercalcemia
Hypokalaemia
Hypomagnesemia
Hyperglycaemia
Electrolyte imbalance
Dry mouth

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15
Q

Noradrenaline causes both excitatory and inhibitory sympathetics responses due to different membrane receptor proteins. What are these different receptors and their effects?

A

Alpha-1 = vasoconstriction
Alpha-2 = negative feedback
Beta-1 = Increase heart rate + force of contraction
Beta-2 = relaxes bronchial + vascular smooth muscle

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16
Q

What are examples of beta blockers / beta-adrenoreceptor antagonists?

A

“-lols”

Atenolol, metoprolol, propanolol, pindolol, oxprenolol, sotalol, bisprolol

17
Q

What are the two mechanims behind beta-adrenoreceptor antagonists?

A
  1. Decrease cardiac output by blocking B1 adrenoreceptors in heart
  2. Block CNS sympathetic outflow, inhibiting renin release (decreases peripheral resistance)
18
Q

What are th epreferred beta-adrenoreceptor agonists for use, and why?

A

Cardio selective B1 blockers (atenolol / metoprolol)

Reduction in stroke / MI

Alone = 50-60% effective
With diuretic = 60-80% effective

19
Q

What are possible side effects for beta-adrenoreceptor antagonists?

A

Bradycardia, reduced exercise capacity, heart failure, hypotension, and AV nodal conduction block

Asthamtic patient = bronchoconstriction

Diabetic patient = Hypotension from masking hypoglycemia

20
Q

What are the common cholesterol lowering medications?

A

“Statins”

Atorvastatin, fluvastatin, pravastatin, rosuvastatin, simvastatin

21
Q

How do statins lower cholesterol levels and what are the possible side effects?

A

Inhibits endogenous pathway of cholesterol synthesis

Common complaints = muscle pain

NOT SUITABLE FOR PREGNANT WOMEN

22
Q

How are aspirins and NSAIDs used in patients with heart disease?

A
  1. Prevents arachidonic acid cycle creating COX
  2. Small doses block COX 1 = blocks thromboxane + prevent splatelet aggregation / blood clotting
23
Q

What is the difference in effect between 100mg of aspirin and 300mg?

A

100mg = low dose, recommended for patients with previous cardiac issues eg angina

300mg at chest pain can prevent death + improve heart function immediately after MI

24
Q

Possible side effects of NSAIDs are inducing asthma attacks or actuallay causing cardiovascular disease. What kind of NSAID would cause, rather than prevent cardiovascular disease?

A

COX 2 specific NSAIDs

COX 2 = anti-inflammatory effects

25
Q

What are nitrates?

A

Nitrodilators are drugs that mimic the actions of Nitric Oxide (NO) by releasing NO or forming NO within tissues

26
Q

What are the primary cardiovascular actions of nitrodilators (nitrates)?

A
  1. Vasodilation (decrease venous pressure + arterial pressure less so)
  2. Cardiac = reduced preload + afterload, decrease O2 demand
  3. Coronary = prevents vasospasm, vasodilation, improves subendocardial perfusion, and increase oxygen delivery
27
Q

What are the possible side effects of nitrates?

A

Headache

Cutaneous flushing

Postural hyptension + reflex tachycardia

Adverse effect on cGMP-dependent phosphodiesterase inhibitors (erectile dysfunction meds)