Essential and secondary hypertension Flashcards
What causes essential HPTN
Genetics and environment
What is stage 1 HPTN clinic vs AMPB/HMPB
140-159/90-99
135-149/85-94 - AMP
What is stage 2 HPTN
160-179/100-119 - clinci
AMP >150/95 <180/120
Stage 3 or severe HPTN
> 180/120mmHg
Requirements for taking BP
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
What can cause postural hypotension
Drug induces
Autonomic neuropathy related postural hypotension
What is discrepancy between arms in BP?
Aortic stenosis
Risk factors for modifiable HPTN
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
Consequences HPTN
Heart attack
Stroke
Kidney failure
Blindness
How often should over 60s have their blood pressure monitored
Annually
Investigations of patients with HPTN
ECG
Urinalysis
U+Es, electrolytes, eGFR, HBa1c, lipid profile
CXR or ECHO only if LVH sus
Ways to decrease HPTN non phramaceutical
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
When to seek immediate advice/referral for HPTN
Stage 3 or higher
Drugs causing HPTN
Corticosteroids
COX-2 inhibitors, NSAIDs
Erythropoietin
Oral contraceptive pill
SSRIs
MAOIs
Erythropoietin indications
- 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.
What two categories cause secondary HPTN
Renal
Endocrine
Renal causes of secondary HPTN
Primary renal disease
Renovascular disease
Endocrine causes of secondary HPTN
Mineralcorticoid excess
Catecholamine excess
Primary renal disease causes
(polycsytic kidneys, chronic renal disease from diabetes, SLE et
Renovascular disease causes
Fibromuscular hyperplasia if young, atherosclerosis older ppl
Mineralcorticoid excess cuases
Aldestorne excess - Conns syndrome
Cortisol - cushings
What can cause catecholamine excess
Phaeochromocytomas
Acromegaly
Hypoparathyroidism
What are the macula dnsa
Highly metabolically active cells next to arterioles in JGM responsible for activating RAAS
How is RAAS activated
Macula densa sense changes in blood flow and modify release of renin in reaction to this
What happens in unilateral renovascular disease to plasma renin activity?
It is elevated
Why does unilateral renovascular disease cause increased renin activity
One kidney underperfused -> RAS increased, angiotensin dependent hypertension
One overperfused outweighed, does cause increased Na excretion
Why can RAS blocking treatment cause unilateral kidney failure in unilateral renovascular disease?
Underperfused kidney even less perfused with reduced BP -> eGFR failure
Mechanism behind bilateral RA stenosis
Reduced overall kdiney perfusion, increased RAS, impaired Na and H20 secretion inhibits RAS, volume increase is what causes increased BP
Plasma renin acitvity in bilateral renovascular disease
normal or low angiotensin (attmepting to compensate)
Why is RAAS blockage mediation so dangerous in bilateral renovascular disease?
Both kidneys already readuced perfusion, if BP lowered -> AKI or significant kidney impairement
What features would warrant further investigation for renal hypertension
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
Further investigations for renal causes of HPTN
Renal imaging with US nad doppler flow along renal arteries
Peripheral pulses
Manageing primary renal disease
Treat underlying cause
Treat BP as per CKD guidelines if primary renal disease not treatable
Renovascular disease management
AVOID RAS blocking agents
Stenting of renal artery stenosis if possible
When do you consider mineralcorticoid excess as a cause o secondary HPTN
Hypokalemia (not always present)
Drug resistant HPTN (2+)
Isolated metabolic alkalosis (Na always normal, bicarb raised)
Why get isolated hypokalemia in mineralcorticoid excess
Potassium reabsorption exchanged for H+ is mechanism for correcting hypokalemia -> reduced H+ in body
Causes of mineralcorticoid excess
Adrenocortical adenoma (tumour-> aldosterone)
Bilateral adrenocortical hyperplasia (bilaterally -> excess aldosteroe)
What plasma aldosterone:renin ratio is diagnostic for mineralcorticoid excess
> 300pmol/L
What to do if positive aldosterone:renin ratio
Image renal glands with CT, US +/-selective venous sampling from adrenal veins
Management of mineralcorticoid excess
Surgery - single adenoma
Spironolactone (K+ receptor blockers)
What syndrome can present with mineralcorticoid excess
Cushings (metabolic alkalosis, hyperkalaemia and HPTN caused by excess cortisol)
What are the biologically active catecholamines
Dopamine
Norepinephrine
Epinephrine
Secerted from adrenal medulla - autonomic
What effect does beta receptors have when activated
Increase in HR and force of contraction
What effect does alpha receptors have when activated
Increased venous return to heart
Increased peripheral resistance
Phaeochromocytoma symptoms
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
Investigation/management phaeochromocytoma
Plasma or 24 hour irnary metanephries or catecholamines
Avoid beta blockers - unstopped alpha adrenergic activity
Imaging by CT (outside adrenal glands)
Management of phaechromcytoma
Surgical removal best - pre op prep with alpha and beta blockers essential
May require cortisol replacement if removed
Sites of phaechromocytomas
85% adrenal glands
Within sympathetic nerve chain along spinal cord
Overlying distal aorta or major vessels
Within ureters
Within urinary bladder
