HTN Flashcards
At what level should BP be?
Below 140/90 mmHg
Primary vs secondary HTN
Primary - no identifiable cause for elevated BP (still increases risk of CV event) - more common
Secondary - cause can be identified e.g. renal disease, smoking, medications
Non-pharmacological treatments
- stop smoking
- reduce weight
- increase aerobic exercise
- reduce alcohol consumption
- Mediterranean diet
- reduce sodium intake
ACE inhibitors - MOA, examples, AE
Examples - captopril, ramipril
MOA - inhibits ACE enzyme –> stops conversion of A1 into A2 –> stops vasoconstriction, aldosterone secretion, sodium/water retention
AE
- orthostatic HT
- first dose HT - lightheadedness, dizziness
- cough due to increased bradykininlevels
- rash
- increased bradykinin levels
- hyperkalemia - due to reduced potassium secretion
Sartans - MOA, examples, AE
Examples - ibesartan, valsartan
MOA - binds to AT1 receptors and prevents A2 from binding (competitive antagonist) - no increase in bradykinin levels
ONLY ACTS ON AT1 RECEPTORS
AE
- postral hypotension, dizziness
- NO COUGH
- hyperkalaemia
What are the two types of calcium channel blockers w/ examples?
Dihydropyridines - amlodipine, nifedipine, felodipine
non-dihydropyridines - verapamil, diltiazem
Calcium channel blocker MOA
Binds to votage gated calcium channels and blcoks binding –> prevents polarisation of cells –> prevents vasoconstriction of smooth muscle
In non-dihydropyridines - also reduced heart and CO and reduced GI motility
Adverse effects in non-dihydropyridine CCB specifically?
constipation (due to reduced peristalsis)
Calcium channel blocker adverse effects?
hypotension, headache, flushes
peripheral oedema (due to increased permeability)
bradycardia
constipation
What is the triple whammy?
When 3 specifc drug classes are used together, impairing body’s natural compensatory response in the event of BP changes –> significant renal impairment
- ACEI, A2RA - prevent sodium/water retention and vasoconstriction
- NSAIDs - act on COX2 receptor and reduce prostagladin secretion –> stops constriction of efferent arterioles and dialation of afferent arterioles
- Diuretics - promotes fluid loss
What happens if ACEI or A2RA are taken in pt with renal artery stenosis
In pt with renal artery stenosis, afferent arterioles narrow, reducing blood flow to glomerular apparatus
–> body vasoconstricitions afferent arterioles to compensate
- if ACEI or A2RA are taken, vasoconstriction will be prevented –> renal failure
What are 3 types of diuretics and their distinctions?
Loop diuretics - act on thick ascending limb of loop of henle
Thiazide diuretics - act on distal convoluted tubule
Potassium sparing diuretics - act on late distal tubule
Loop diuretics - example, MOA, AE
E.g. Frusemide
MOA - inhibts NA/K/Cl co transporters in thick ascending loop of henle –> prevents sodium, potassium and chloride reabsorption
–> most potent diuretics - 20-25% effectivness as distal tubule and collecting duct cannot compensate for increased sodium load
AE
- hypokalaemia - increases potassium secretion at LOH, distal tubule and collecting duct
- uric acid build up - sodium and chloride compete with uric acid at co-transporter
- may increase blood glucose levels
- urinary frequency and urgency
Thiazide diuretics - exampels, MOA, AE
e.g. hydrochlorothiazide
Inhibit sodium and chloride reabsorption in distal convoluted tubule
- less potent - 5-10% of sodium reabsorbed
AE
- electrolyte disturbances - hypokalaemia, hyponatraemia
- increased blood glucose levels
- can increase blooc uric acid levels (due to competitve effect on uric acid co-transporters) –> gout risk
- urinary frequency and urgency
- hypokalaemia - some sodium is reabsorbed in Na/K exchange in late distal tubule due to higher sodium than potassium concentration in filtrate
Which diuretic is known for highest risk of diabetes and should not be used in younger pt?
thiazide diuretics
