Essential and secondary hypertension

Question 1

What causes essential HPTN

Answer 1

Genetics and environment

Question 2

What is stage 1 HPTN clinic vs AMPB/HMPB

Answer 2

140-159/90-99
135-149/85-94 - AMP

Question 3

What is stage 2 HPTN

Answer 3

160-179/100-119 - clinci
AMP >150/95 <180/120

Question 4

Stage 3 or severe HPTN

Answer 4

> 180/120mmHg

Question 5

Requirements for taking BP

Answer 5

Quiet room
No smoking, exercise or caffeine for 30 mins before
after 5 mins seated
Arms at chest level
3 measurements 1 min apart and average 2
Check both arms use higher reading
Check standing and sitting BP for postural HPTN

Question 6

What can cause postural hypotension

Answer 6

Drug induces
Autonomic neuropathy related postural hypotension

Question 7

What is discrepancy between arms in BP?

Answer 7

Aortic stenosis

Question 8

Risk factors for modifiable HPTN

Answer 8

Salt consumption
Low intake fruit and veg
Sat fats and trans fats
Being overweight and obese
Harmful use of alcohol
Lack of physical activity
Smoking

Question 9

Consequences HPTN

Answer 9

Heart attack
Stroke
Kidney failure
Blindness

Question 10

How often should over 60s have their blood pressure monitored

Answer 10

Annually

Question 11

Investigations of patients with HPTN

Answer 11

ECG
Urinalysis
U+Es, electrolytes, eGFR, HBa1c, lipid profile
CXR or ECHO only if LVH sus

Question 12

Ways to decrease HPTN non phramaceutical

Answer 12

Weight loss - 2/1 per kg

DASH diet - 8/6 per kg

Substitiuting sodium chloride to potassium chloride (low salt )

Decrease alcohol

Increase fibre

Exercise moderate

Question 13

When to seek immediate advice/referral for HPTN

Answer 13

Stage 3 or higher

Question 14

Drugs causing HPTN

Answer 14

Corticosteroids
COX-2 inhibitors, NSAIDs
Erythropoietin
Oral contraceptive pill
SSRIs
MAOIs

Question 15

Erythropoietin indications

Answer 15

• treatment of anemia due to Chronic Kidney Disease (CKD) in patients on dialysis and not on dialysis.
• treatment of anemia due to zidovudine in patients with HIV-infection.
• treatment of anemia due to the effects of concomitant myelosuppressive chemotherapy, and upon initiation, there is a minimum of two additional months of planned chemotherapy.
• reduction of allogeneic RBC transfusions in patients undergoing elective, noncardiac, nonvascular surgery.

Question 16

What two categories cause secondary HPTN

Answer 16

Renal
Endocrine

Question 17

Renal causes of secondary HPTN

Answer 17

Primary renal disease
Renovascular disease

Question 18

Endocrine causes of secondary HPTN

Answer 18

Mineralcorticoid excess
Catecholamine excess

Question 18

Primary renal disease causes

Answer 18

(polycsytic kidneys, chronic renal disease from diabetes, SLE et

Question 19

Renovascular disease causes

Answer 19

Fibromuscular hyperplasia if young, atherosclerosis older ppl

Question 20

Mineralcorticoid excess cuases

Answer 20

Aldestorne excess - Conns syndrome
Cortisol - cushings

Question 21

What can cause catecholamine excess

Answer 21

Phaeochromocytomas
Acromegaly
Hypoparathyroidism

Question 22

What are the macula dnsa

Answer 22

Highly metabolically active cells next to arterioles in JGM responsible for activating RAAS

Question 23

How is RAAS activated

Answer 23

Macula densa sense changes in blood flow and modify release of renin in reaction to this

Question 24

What happens in unilateral renovascular disease to plasma renin activity?

Answer 24

It is elevated

Question 25

Why does unilateral renovascular disease cause increased renin activity

Answer 25

One kidney underperfused -> RAS increased, angiotensin dependent hypertension One overperfused outweighed, does cause increased Na excretion

Question 26

Why can RAS blocking treatment cause unilateral kidney failure in unilateral renovascular disease?

Answer 26

Underperfused kidney even less perfused with reduced BP -> eGFR failure

Question 27

Mechanism behind bilateral RA stenosis

Answer 27

Reduced overall kdiney perfusion, increased RAS, impaired Na and H20 secretion inhibits RAS, volume increase is what causes increased BP

Question 28

Plasma renin acitvity in bilateral renovascular disease

Answer 28

normal or low angiotensin (attmepting to compensate)

Question 29

Why is RAAS blockage mediation so dangerous in bilateral renovascular disease?

Answer 29

Both kidneys already readuced perfusion, if BP lowered -> AKI or significant kidney impairement

Question 30

What features would warrant further investigation for renal hypertension

Answer 30

Isolated HPTN in young women HPTN with reduced eGFR Resistant HPTN (3+ agents) ACEi treat -> reduced eGFR or abnormal urinalysis with protein or haematuria Acute pulmonary oedema with no cardiac disease Coincidental atherosclerotic vascular disease and renal artery bruits, absent peripheral pulses

Question 31

Further investigations for renal causes of HPTN

Answer 31

Renal imaging with US nad doppler flow along renal arteries Peripheral pulses

Question 32

Manageing primary renal disease

Answer 32

Treat underlying cause Treat BP as per CKD guidelines if primary renal disease not treatable

Question 33

Renovascular disease management

Answer 33

AVOID RAS blocking agents Stenting of renal artery stenosis if possible

Question 34

When do you consider mineralcorticoid excess as a cause o secondary HPTN

Answer 34

Hypokalemia (not always present) Drug resistant HPTN (2+) Isolated metabolic alkalosis (Na always normal, bicarb raised)

Question 35

Why get isolated hypokalemia in mineralcorticoid excess

Answer 35

Potassium reabsorption exchanged for H+ is mechanism for correcting hypokalemia -> reduced H+ in body

Question 36

Causes of mineralcorticoid excess

Answer 36

Adrenocortical adenoma (tumour-> aldosterone) Bilateral adrenocortical hyperplasia (bilaterally -> excess aldosteroe)

Question 37

What plasma aldosterone:renin ratio is diagnostic for mineralcorticoid excess

Answer 37

>300pmol/L

Question 38

What to do if positive aldosterone:renin ratio

Answer 38

Image renal glands with CT, US +/-selective venous sampling from adrenal veins

Question 39

Management of mineralcorticoid excess

Answer 39

Surgery - single adenoma Spironolactone (K+ receptor blockers)

Question 40

What syndrome can present with mineralcorticoid excess

Answer 40

Cushings (metabolic alkalosis, hyperkalaemia and HPTN caused by excess cortisol)

Question 41

What are the biologically active catecholamines

Answer 41

Dopamine Norepinephrine Epinephrine Secerted from adrenal medulla - autonomic

Question 42

What effect does beta receptors have when activated

Answer 42

Increase in HR and force of contraction

Question 43

What effect does alpha receptors have when activated

Answer 43

Increased venous return to heart Increased peripheral resistance

Question 44

Phaeochromocytoma symptoms

Answer 44

BP v high fluctuates Headaches - intermittnet, parozysmal, severe Excess sweating Racing heart - tachycardia, palpitations Anxiety/nervous, impednding doom Tremors Pain in lower chest or upper abdomen Nausea w/wout vomit Weight loss Heat intolerance Diabetes mellitus Posutral hypotension - autonomic overactivity

Question 45

Investigation/management phaeochromocytoma

Answer 45

Plasma or 24 hour irnary metanephries or catecholamines Avoid beta blockers - unstopped alpha adrenergic activity Imaging by CT (outside adrenal glands)

Question 46

Management of phaechromcytoma

Answer 46

Surgical removal best - pre op prep with alpha and beta blockers essential May require cortisol replacement if removed

Question 47

Sites of phaechromocytomas

Answer 47

85% adrenal glands Within sympathetic nerve chain along spinal cord Overlying distal aorta or major vessels Within ureters Within urinary bladder