HTN

Question 1

At what level should BP be?

Answer 1

Below 140/90 mmHg

Question 2

Primary vs secondary HTN

Answer 2

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

Question 3

Non-pharmacological treatments

Answer 3

• stop smoking
• reduce weight
• increase aerobic exercise
• reduce alcohol consumption
• Mediterranean diet
• reduce sodium intake

Question 4

ACE inhibitors - MOA, examples, AE

Answer 4

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

Question 5

Sartans - MOA, examples, AE

Answer 5

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

Question 6

What are the two types of calcium channel blockers w/ examples?

Answer 6

Dihydropyridines - amlodipine, nifedipine, felodipine
non-dihydropyridines - verapamil, diltiazem

Question 7

Calcium channel blocker MOA

Answer 7

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

Question 8

Adverse effects in non-dihydropyridine CCB specifically?

Answer 8

constipation (due to reduced peristalsis)

Question 9

Calcium channel blocker adverse effects?

Answer 9

hypotension, headache, flushes

peripheral oedema (due to increased permeability)

bradycardia

constipation

Question 10

What is the triple whammy?

Answer 10

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

Question 11

What happens if ACEI or A2RA are taken in pt with renal artery stenosis

Answer 11

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

Question 12

What are 3 types of diuretics and their distinctions?

Answer 12

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

Question 12

Loop diuretics - example, MOA, AE

Answer 12

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

Question 12

Thiazide diuretics - exampels, MOA, AE

Answer 12

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

Question 13

Which diuretic is known for highest risk of diabetes and should not be used in younger pt?

Answer 13

thiazide diuretics

Question 14

potassium sparing diuretics examples

Answer 14

E.g. spironolactone, amiloride, triamterene

Question 15

How does spironolactone differ from amiloride and triamterene?

Answer 15

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

Question 16

What are 2 adverse effects of sprinololactone?

Answer 16

hyperkalaemia
gynaecomastia in males (due to androgenic activity)

Question 17

What receptors do selective beta-blockers work on?

Answer 17

B1 receptors

Question 18

What are the effects of beta blockers on the body to reduce BP?

Answer 18

1. Blocks B1 receptors in kidney –> prevents renin release in the event of reduced BP –> no breakdown of angiotensinogen into angiotensin 1
2. Blocks B1 receptors of heart –> reduced HR and CO
3. turns of SNS –> reduces peripheral resistance

Question 19

When can beta blockers not be given?

Answer 19

ASTHMA
- will cause bronchoconstriction –> wheezing and asthmatic attacks

Question 20

What is the triple whammy?

Answer 20

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

Question 21

What effect do A2RA and ACEI have on renal stenosis?

Answer 21

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

Question 22

When should BP treatment commence?

Answer 22

when BP remains 140/90 (Stage 2 HTN)

Question 23

Comorbidities affecting antihypertensive choice

Answer 23

• kidney disease/renal failure - ACEI and ARBs renally cleared
• HF - cant use DCCB
• gout - cant use thiazide diuretics
• asthma and COPD - cant use BB

Question 24

Uncomplicated treatment

Answer 24

ACEI (or startan) OR thiazide diuretic OR DCCB

If not working,
- ACEI/sartan + thiazide diuretics

if still not working
- ACEI/sartan + thiazide diuretic + DCCB