ANTI-HYPERTENSIVE AGENTS Flashcards
DEFINITION OF HYPERTENSION AND AETIOLOGY
sustained elevated BP over 24h period.
essential HTN: cause unknown, multifactoral risks ( hyperlipidemia, diabetes, genetic, high salt diet, stress)
secondary HTN: identifiable cause ( Renal artery stenosis, narrowing of the aorta, tumor of adrenal glands, Cushing disease, primary aldosteronism)
the aim of HTN therapy is to reduce the risk of _________, such as _____ and ______________. therapeutic targets are BP =________ in all pt, = to ______________ in diabetic pts.
complications, stroke,m coronary artery disease, 140/90, 130/80
the pathways of BP regulation
- blood volume, fluid loss or retention
- peripheral resistance/diameter of the arterioles, (how much the vessels dilate or restrict with the change of volume
- cardiac output, stroke volume ( preload, contractility, afterload) and heart rate.
BP= ______x________
4 sites of BP regulation
cardiac output, peripheral vascular resistance
- cardiac output
- venules capacitance
- baroceptors in the kidneys
- peripheral resistance
NAC OF DIURETICS
N. sodium/chloride symporter antagonist, in the epithelial lumen of the kidney nephron (thiazine works in the distal tubule)
A. reduce intake of sodium and water, causing a reduction in blood volume and extracellular fluid
C. reduce the cardiac output (less blood goes back to the heart), reduction in total peripheral resistance
S/E. electrolytes depletion, in particular potassium, alkalosis ( alkaline pH of blood)
Indication. treat HTN noncomplicated in combination with ACE inhibitors, profound edema with loop diuretics, mild heart failure.
types of beta-adrenoceptors
- beta1, increase cardiac properties, renin and insulin release and lipolysis
- beta 2, vasodilatation, relaxation of NON-VASCULAR smooth muscles, increase liver and muscles glycogenolysis
- beta 3. unknown
BETA BLOCKERS NAC
N. beta adrenoceptors antagonist,
A. they block the binding of adrenaline to the beta receptors,
C. reduction of CO, renin release, sympathetic activity
Clinical Use. HTN+ angina/heart failure/arrhythmias, younger pts.
S/E. non-selective cardiac receptors, they bind to beta2 receptors causing bronchoconstriction, exercise-induced hypoglycemia, bradycardia, cardiac failure, fatigue, depression.
difference between Propranolol and Atenolol/metoprolol
propanolol, noncardioselective, crosses BBB causing depression and insomnia, no more first-line drug
atenolol, cardioselective, less central effects and bronchoconstriction
same effect in lowering BP
NAC ALFA-ADRENERGIC RECEPTOR ANTAGONIST
N. alfa adrenergic receptor antagonist
A. block the binding of adrenaline to their receptor
C. vasodilatation and reduced peripheral vascular resistance
S/E, postural hypotension, dizziness, fatigue
at which level of the RAAS is the ACE produced?
the angiotensin-converting enzyme is produced by the vascular epithelium in response to low BP and converts the angiotensin 1 into angiotensin 2 in the plasma then causes vasoconstriction and changes into aldosterone in the adrenal cortex which stimulates sodium reabsorption at the kidney
ACE Inhibitors NAC and S/E
N. ACE antagonists, they mimic the angiotensin 1 structure and they bind on their same binding sites in the enzyme blocking the action.
A. reduction of cardiac load+ vessels resistance.
C. reduction of HTN, little effect in normotensive patents, more effective if associated with diuretics.
S/E. dry cough, compliance issues, poor renal perfusion in renal artery stenosis, hyperkalemia, rashes and taste disturbances, less effective in African-American people because of polymorphisms of Ace enzyme
NAC OF ARAs
N. angiotensin receptor antagonist, AT1 recept
A. block the binding between angiotensin 2 and AT1 receptors
C. equal effect in lowering BP, slow progress of the renal disease
S/E. same as ACE-I but no cough ( ACE also breaks down bradykinin so ACEI causes accumulation of this that leads to cough because bradykinin causes contraction on non-vascular smooth muscles in the airways)
Calcium channel blockers bind to the ____ subunit of the ______ calcium channels, reducing ______ and ______ calcium.
they cause generalized ___________ and they target ____ and ______ muscle
________ is an example that effect smooth muscle.
S/E._____________
alfa 1, L-type, calcium entry, intracellular, arterial vasodilatation, heart and smooth, nifedipine.
headaches, ankle swelling, constipation
therapeutic regimen if HTN over 55 and black american origin
CCB (monotherapy) step 1
CCB+ ACE/ARA step 2
CCB+ ACEI/ARA + thiazide diuretics step 3
confirm compliance, add alfa bloccker / beta blocker if uncontrolled BP, seek expert advice step 4
