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Block 2 - non communicable diseases > Essential and secondary hypertension > Flashcards

Essential and secondary hypertension Flashcards

1
Q

What causes essential HPTN

A

Genetics and environment

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2
Q

What is stage 1 HPTN clinic vs AMPB/HMPB

A

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

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3
Q

What is stage 2 HPTN

A

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

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4
Q

Stage 3 or severe HPTN

A

> 180/120mmHg

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5
Q

Requirements for taking BP

A

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

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6
Q

What can cause postural hypotension

A

Drug induces
Autonomic neuropathy related postural hypotension

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7
Q

What is discrepancy between arms in BP?

A

Aortic stenosis

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8
Q

Risk factors for modifiable HPTN

A

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

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9
Q

Consequences HPTN

A

Heart attack
Stroke
Kidney failure
Blindness

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10
Q

How often should over 60s have their blood pressure monitored

A

Annually

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11
Q

Investigations of patients with HPTN

A

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

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12
Q

Ways to decrease HPTN non phramaceutical

A

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

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13
Q

When to seek immediate advice/referral for HPTN

A

Stage 3 or higher

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14
Q

Drugs causing HPTN

A

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

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15
Q

Erythropoietin indications

A
  • 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.
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16
Q

What two categories cause secondary HPTN

A

Renal
Endocrine

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17
Q

Renal causes of secondary HPTN

A

Primary renal disease
Renovascular disease

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18
Q

Endocrine causes of secondary HPTN

A

Mineralcorticoid excess
Catecholamine excess

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18
Q

Primary renal disease causes

A

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

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19
Q

Renovascular disease causes

A

Fibromuscular hyperplasia if young, atherosclerosis older ppl

20
Q

Mineralcorticoid excess cuases

A

Aldestorne excess - Conns syndrome
Cortisol - cushings

21
Q

What can cause catecholamine excess

A

Phaeochromocytomas
Acromegaly
Hypoparathyroidism

22
Q

What are the macula dnsa

A

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

23
Q

How is RAAS activated

A

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

24
Q

What happens in unilateral renovascular disease to plasma renin activity?

A

It is elevated

25
Q

Why does unilateral renovascular disease cause increased renin activity

A

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

26
Q

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

A

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

27
Q

Mechanism behind bilateral RA stenosis

A

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

28
Q

Plasma renin acitvity in bilateral renovascular disease

A

normal or low angiotensin (attmepting to compensate)

29
Q

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

A

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

30
Q

What features would warrant further investigation for renal hypertension

A

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

31
Q

Further investigations for renal causes of HPTN

A

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

32
Q

Manageing primary renal disease

A

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

33
Q

Renovascular disease management

A

AVOID RAS blocking agents
Stenting of renal artery stenosis if possible

34
Q

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

A

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

35
Q

Why get isolated hypokalemia in mineralcorticoid excess

A

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

36
Q

Causes of mineralcorticoid excess

A

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

37
Q

What plasma aldosterone:renin ratio is diagnostic for mineralcorticoid excess

A

> 300pmol/L

38
Q

What to do if positive aldosterone:renin ratio

A

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

39
Q

Management of mineralcorticoid excess

A

Surgery - single adenoma
Spironolactone (K+ receptor blockers)

40
Q

What syndrome can present with mineralcorticoid excess

A

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

41
Q

What are the biologically active catecholamines

A

Dopamine
Norepinephrine
Epinephrine
Secerted from adrenal medulla - autonomic

42
Q

What effect does beta receptors have when activated

A

Increase in HR and force of contraction

43
Q

What effect does alpha receptors have when activated

A

Increased venous return to heart
Increased peripheral resistance

44
Q

Phaeochromocytoma symptoms

A

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

45
Q

Investigation/management phaeochromocytoma

A

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

46
Q

Management of phaechromcytoma

A

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

47
Q

Sites of phaechromocytomas

A

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

Block 2 - non communicable diseases (8 decks)

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