L 19 Pharmacology of Hypertension Flashcards
The 90% of hypertension is ‘primarily’ the reason is?
unknown
What are the Therapy goal with Drug treatments for hypertension?
Dilate blood vessels
Reduce vasoconstriction
Reduce blood volume
Reduce cardiac load
What is RAAS?
Renin-angiotensin aldosterone system
What is the side effect of B1 blocker, if we anticipate(expect) a….what will happen to our heart?
Slow down the heart rate
If we give an Alpha blocker then we anticipate therapeutic effects?
Vasodilation results in a decrease in heart rate.
If we give a B blocker for our lungs what will happen?
bronchoconstriction ( B2 is more than B1)
Why are high dose selective B1 blockers (+example) and non-selective B-blockers (+example) avoided in asthmatics?why?
Because giving a non-selective B blocker or a high dose of a B1 selective blocker will cause bronchoconstriction, therefore should be avoided in asthmatics.
Non-selective B-blocker e.g propranolol
Selective B1 blocker e.g metoprolol
What is the side effect of Alpha blockers?
Dizziness/postural hypotension (light headedness when standing)
How many nephrons in each kidney?
Around One million perhaps
Nephrons are divided into two structures: what they are?
Glomerulus and Renal tubules
What is the Homeostasis of renal function?
Excrete of water and waste and xenobiotic substances
RAAS system controls these 2x things they are:
Extracellular fluid volume(ECF) and Electrolyte balance
Renin is released in response to
Reduced BP or renal blood flow
How does RAAS (Renin angiotensin aldosterone system work)?
ATS=>ATI=>ATII=>Aldosterone
ATS means=> Angiotensinogen
ATI means=> Angiotensin i
ATII means=>Angiotensin ii
What is the therapeutic effects of ACE inhibitor or angiotensin ii receptor blocker(ARB)
Cause vasodilation
Angiotensin II receptor blocker causes…
Vasoconstriction and aldosterone release
What are the therapeutic effects of Aldosterone?
K+ excretion, Na+ and water reabsorption
If we give an ACE inhibitor or an angiotensin receptor blocker we can expect…
Vasodilation
ATII causes vasoconstriction so blocking this path = vasodilation
What If we give an aldosterone antagonist (stops binding to mineralocort receptor) we can anticipate?
Decrease in Na+ and water reabsorption and increase in K+ (opposite effects to aldosterone)
Is an aldosterone antagonist used to treat hypertension?
No, more relevant to heart failure
What are the only diuretics used routinely to treat hypertension?
Thiazides
How do thiazides work?
Inhibit Na+Cl- transporter in DCT (Distal convoluted tubule) and PCT to increase NaCl excretion, therefore reducing BP as water is excreted too.
What are the Side effects of ACEI and ARBs x3
Dizziness/postural hypotension
Hyperkalaemia
ACEI can cause cough due to bradykinin build up (not being broken down by ACE anymore)
What are the side effects of thiazide diuretics?
Dizziness/postural hypotension
Hypo: K+, Na+, Cl-, Mg2+
Hyper: Ca2+, Urea, glycaemia
Where do Calcium Channel Blockers act?
Act at L-type voltage gated calcium channels
Where are L-type voltage-gated calcium channels found?
Skeletal, cardiac, and smooth muscle
What subunit do Calcium Channel Blockers bind to?
Bind to Alpha 1 subunit, of membrane-spanning proteins
Do Calcium channel blockers plug the hole of the channel?
No
What are the 2 classes of Calcium Channel Blockers?
Dihydropyridines and non-DHP CCBs
What are the CCB’s therapeutic effects?
Increase cardiac output
What are the Side effects of CCBs
Headache, flushing, dizziness, peripheral edema, constipation
What are the Side effects of Non-DHP CCBs?
cause bradycardia (slower than normal heart rate)
CCB examples (DHP and non-DHPs)
(Dihydropyridines)DHP CCBs: felodipine, amlodipine
Non-DHP CCBs: verapamil, diltiazem
Verapamil is a …. and interacts with…
Strong CYP3A4 inhibitor and interacts with simvastatin.
What is the Variability in beneficial effects and side effects related to CCBs?
Drugs PK and PD and other combinations with the drugs
