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
potassium sparing diuretics examples
E.g. spironolactone, amiloride, triamterene
How does spironolactone differ from amiloride and triamterene?
Spirinolactone blocks aldosterone receptors in late distal tubule whereas amiloride and triamterene block potassium channels in sodium and potassium exchange
sprinolactone reverses aldosterone effects - increased sodium and water excretion, increased potassium reabsorption
BOTH PRODUCE HYPERKALAEMIA
What are 2 adverse effects of sprinololactone?
hyperkalaemia
gynaecomastia in males (due to androgenic activity)
What receptors do selective beta-blockers work on?
B1 receptors
What are the effects of beta blockers on the body to reduce BP?
- Blocks B1 receptors in kidney –> prevents renin release in the event of reduced BP –> no breakdown of angiotensinogen into angiotensin 1
- Blocks B1 receptors of heart –> reduced HR and CO
- turns of SNS –> reduces peripheral resistance
When can beta blockers not be given?
ASTHMA
- will cause bronchoconstriction –> wheezing and asthmatic attacks
What is the triple whammy?
The triple whammy is one 3 specific drug classes are combined, resulting in the inhibtion of the body’s compensatory response to changes in BP –> can lead to renal failure
- NSAIDs - inhibit prostaglandin release –> prevents vasoconstriction of efferent arterioles and vasodilatation of afferent arterioles
- ACEI/A2RA - inhibits vasodialation and sodium/water retention –> reduced BP
- diuretics - fluid secretion
What effect do A2RA and ACEI have on renal stenosis?
in RAS afferent arterioles narrow, reduced blood flow to the glomerular apparatus
- kidneys vasoconstrict afferent artioles to improve BP to increase peripheral resistance
In A2RA/ACEI, this vasoconstriction is prevented –> no increase in BP –> renal failure
When should BP treatment commence?
when BP remains 140/90 (Stage 2 HTN)
Comorbidities affecting antihypertensive choice
- kidney disease/renal failure - ACEI and ARBs renally cleared
- HF - cant use DCCB
- gout - cant use thiazide diuretics
- asthma and COPD - cant use BB
Uncomplicated treatment
ACEI (or startan) OR thiazide diuretic OR DCCB
If not working,
- ACEI/sartan + thiazide diuretics
if still not working
- ACEI/sartan + thiazide diuretic + DCCB
