CV Drugs 1 Flashcards
What is the main cause of CV disease?
Atherosclerosis
Draw the CV disease continuum, showing the relationship bw each other
Other risk factors -> endothelial dysfunction HTN -> stroke
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Atherosclerosis -> thrombosis
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Angina. ACS. —> HF
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Arrhythmias & sudden C death
What’s the main effect of statins?
Mechanism of action?
Important in lowering cholesterol - driver of Atherosclerosis
In the liver, Statins block the rate-limiting enzyme (HMG-CoA reductase) involves in synthesis of cholesterol
(Also as a result causes Chol to be taken up into the liver from plasma)
Atorvastatin drug profile
- Rapid absorption & high 1st pass metabolism; some metabolites are also active against HMG-CoA reductase
- reaches its peak plasma conc in 1-2 hrs, and almost entirely bound to proteins in blood
- Half life ~ 14hrs, but activity against enzyme lasts 20-30hrs
- Excreted mainly into the bile
What is HTN?
An elevation of systolic and/or diastolic BP to the point where it increases the risk of CV disease.
~30% of population
Name the different stages
PreHTN: 80-90 and/or 130-139
Stage 1: 90-99 and/or 140-159
Stage 2:
Stage 3: > 110 and/or > 180
Major risk factors as a result of HTN?
Stroke
CAD
cHF
Very important to treat high BP because could also could damage to target organs
Diagnosis + assessment of HTN
Measure BP using Sphygmomanometer
Types of HTN
Primary - no identifiable cause in the patient (majority of cases)
Secondary - cause can be identified (minority)
Hypertensinogenic factors: primary or secondary?
-obesity, insulin resistance
Pathophysiology of primary HTN.
What is it that drives your BP up?
A lot of what increases these factors is driven by
Sympathetic and renin/ angiotensin/ aldosterone systems
BP formula
BP = CO*TPR
HTN represents a disorder of the processes which regulate long-term BP
Normal feedback control of Arterial BP
Regulatory systems:
Decrease in Firing of sympathetic neurons
Inhibition of RAAS
Renal component…
Vascular component…
What is the implication of the current concepts of long term BP regulation?
Successful lowering of BP requires the sustained reduction of blood volume and/or vascular tone.
All of the drugs used do one or the other. All (except b1 receptor blockers) have vasodilation effect and all (except a1 receptor blockers? + K+ channel agonists) have natriuretic effect.
Some have direct Decrease of CO effect (b1 receptor blockers + some Ca channel blockers)