Cardiovascular Flashcards

(20 cards)

1
Q

Mechanism of action for blood pressure

A
  1. Blood volume (plasma)
  2. Heart rate (stress, calcium)
  3. Stroke volume
  4. Blood viscosity
  5. Peripheral resistance (blood vessel constriction)
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2
Q

Cardiovascular drugs glossary

A

Lipids
1. Statin - production
2. Bile acid resin - excretion
3. Fibric acid
4. Ezetimibe - absorption
5. Ezetimibe/Statin fixed etc. Vytorin
6. CETPi (Cerivastatin, did not pass QC) - transport

Hypertension
1. Diuretics
2. Calcium channel blockers
3. ACEi / angiotensin-receptor blockers (etc. Vasotec)
4. Alpha & beta-andrenergic blockers
5. vasodilators

Angina Pectoris
1. Glyceryl titrate spray

Myocardial Infarction
1. Thrombolytics - restore blood supply
2. Beta blockers or calcium channel blockers - reduce myocardial O2 demand
3. Aspirin, beta-blockers or ACEi - reduce BP and stress
4. Antiplatelet/ anticoagulant

Dysarrythmia
1. Channel blockers (Sodium, beta-adrenergic, potassium, calcium)

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3
Q

Cardiovascular diseases glossary

A
  1. Atherosclerosis
  2. Coronary heart disease (CHD)
  3. Chest pain (angina pectoris)
  4. Irregular heartbeat (arrhythmia)
  5. Congestive heart failure (CHF)
  6. Congenital and rheumatic heart disease
  7. Stroke
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4
Q

Types of Lipid disorders

A
  1. Atherosclerosis: plaque buildup
  2. Hyperlipidemia: high lipid level in blood
  3. Hypercholesterolemia: elevated blood cholestrol
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5
Q

Types of lipoproteins (water soluble, free-moving in blood)

A
  1. low-density lipoprotein (plauqe buildup & atherosclerosis)
  2. high-density lipoprotein (reverse lipid transport; beneficial)
  3. very low-density lipoprotein (primary triglyceride carrier; unideal)
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6
Q

reduce blood lipid levels

A

Statin; inhibit cholestrol levels (reduce LDL, VLDL, increase HDL)

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7
Q

Mechanism of Statin

A

Aim: to reduce LDL levels

acts as competitive inhibitor of HMG-CoA reductase (enzyme that converts HMG-CoA to mevalonate; precurosor of cholestrol)

By inhibiting HMG-CoA, cholestrol production is reduced, and increased expression of LDL receptor is triggered and LDL uptake increases, hence reducing LDL levels.

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8
Q

Examples of Statin

A
  • Atorvastatin (Liptor)
  • Simvastatin (Zocor)

Statin to be administered enteral in the evening (after meal digestion -> LDL increase)

  • Cerivastatin (Baycol, Lipobay) withdrawal due to rhabdomyolysis
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9
Q

Other drugs to lower blood cholestrol

A
  1. Bile acid resin
    - aid in fat digestion, reduce LDL
  2. Fibric acid (etc. Tricor)
    - treat high triglycerides
  3. Combination approach (ezetimibe + statin; etc Vytorin, Advicor)
    - ezetimibe blocks absorption of dietary cholestrol -> reduce LDL & triglycerides
    - lower dose, increased compliance benefits
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10
Q

CETPi

A

stands for CholesterylEster Transfer Protein Inhibitor
- to prevent transfer of cholestrol from HDL to VLDL or LDL

Did not pass QC

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11
Q

Hypertension

A

can lead to stroke, heart failure or myocardial infarction

primary factors responsible for blood pressure are cardiac output,
resistance of the small arteries & blood volume

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12
Q

Anti-hypertensive therapy

A

Vasodilation:
Calcium channel blockers (CCBs) → relax vascular smooth muscle

Vasodilators → direct smooth muscle relaxation (e.g. hydralazine)

Angiotensin receptor blockers (ARBs) → block angiotensin II = vasodilation
[blocks stress response]

ACE inhibitors (ACEi) → ↓ angiotensin II = vasodilation ✅
[blocks hormonal activity]

Reduce cardiac output:
Alpha & Beta blockers → ↓ heart rate, ↓ myocardial contractility

Some CCBs (like verapamil/diltiazem) also ↓ HR and contractility

Increase urine output & reduce blood volume:
Diuretics (1st choice) → e.g. thiazide diuretics (hydrochlorothiazide), loop diuretics
→ ↓ blood volume → ↓ preload → ↓ BP

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13
Q

Angina Pectoris

A

Acute chest pain due to insufficient oxygen to heart muscles, commonly caused by atherosclerosis

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14
Q

Drug mechanism to for angina pectoris treatment

A
  1. Beta blockers → prevent angina pain
  2. Organic nitrates (etc. Glyceryl trinitrate spray) → terminating angina pain
  3. Calcium channel blockers → substitue for beta blockers
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15
Q

Myocardial Infarction

A

heart attack; blood flow to the heart is suddenly cut off

Usually caused by blood clot from rupture at pre-existing atherosclerosic site

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16
Q

Myocardial infarction treatment

A
  1. Thrombolytics → restore blood supply by dissolving clot
  2. Beta blockers → reduce myocardial oxygen demands
  3. Calcium channel blockers → prevent another MI
  4. Asprin & ACEi (or beta blockers) → reduce post MI mortality
  5. Analgesis → manage severe chest pains
  6. Antiplatelets or anticoagulants → prevent new clot
17
Q

Disarthymias

A

Arrhythmias; abnormal heartbeat, can be harmless (palpitations) or life-threatening (asystole lol)

18
Q

types of disarthymias

A
  1. SVT (Supraventricular tachycardia): arrythmia, sudden burst of rapid heartbeats
  2. A-Fib (Atrial fibrilliation): heart palpitations
  3. V-Tach (Ventricular tachycardia): >100bpm, indicate pre-existing heart disease
  4. V-Fib (Ventricular fibrillation): due to untreated V-Tach, usually becomes heart attack
19
Q

Disarthymia treatment

A

1-3 slows HR
1. Sodium channel blockers: slow the rate of impulse conduction through the
heart

  1. Beta-adrenergic blockers: reduce automatically and slow conduction velocity in the heart
  2. Potassium blockers: prolong the refractory period of the heart
  3. Calcium channel blockers: treats SVT
20
Q

生脉散(Generate the Pulse Powder)

A
  1. Increases myocardial contractility
  2. Prevents arrythmia, improves blood perfusion to coronary artery and body peripherals
  3. Cardio protective effect against post-ischemic myocardial dysfunction
  4. Immune stimulant: increases white blood cells and T-lymphocytes
  5. Mild sedative effect on CNS
  6. Anti-inflammatory