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Hypertension (primary and secondary)
Terms in this set (42)
Hemodynamics: Blood pressure
Regulation: Blood pressure
- High pressure
- Low pressure
Mechanism: Baroreceptor reflex (high pressure)
Mechanoreceptors on sensory neurons located on the carotid sinus (IX) and aortic arch (X) detect changes in BP as there are (+) by changes in stretch - an increase in BP → (+) baroreceptors → (+) NTS to direct changes in several cardiovascular centres in the RF of medulla/pons → (-) symp/(-) ADH release and (+) parasymp
Location/Function: Cardiopulmonary (Low-Pressure) Baroreceptors
+ Large systemic veins
+ Pulmonary vessels
+ Walls of RA/VA
Function: Sense changes in blood volume and thus changes in blood volume → changes in venous/arterial pressure → changes in LP baroreceptor action
Mechanism: Low pressure baroreceptors
↑ in blood volume (∴ ↑ in pressure in LP baroreceptors) -> mechanisms to ↑ Na+/H2O excretion (∴ ↓ blood volume)
+ ↑ ANP secretion from atria → vasodilation of afferent arteriole ∴ ↑ GFR ∴ ↑ Na+/H2O secretion
+ ↓ ADH secretion - pressure receptors project to hypothalamus and (-) ADH release -> ↓ H2O reabsorption
Abnormally high arterial blood pressure
As a general guide:
> 140/90mmHg or higher (or 150/90mmHg or higher if you're over the age of 80)
Ideal BP is usually considered to be between 90/60mmHg and 120/80mmHg
Repeated measurements on both arms → HTN is diagnosed if the average BP of ≥ 2 readings obtained on ≥ 2 separate visits is elevated!
Helps if you do it at different times/after different events - more comprehensive
Most common/important risk factor for cardiovascular/cerebrovascular disease!
Affects > 1 billion people worldwide; more common in the developed world
Hypertension rates are much higher in black Africans (40-45% of adults).
Approximately 90 % who are non-hypertensive at 55-65 years will develop hypertension by the age of 80-85.
- Primary; essential
Define: Primary HTN
HTN of unknown etiology - MULTIFACTORIAL (approx 95% of cases)
a.k.a essential HTN
Risk factors: Primary HTN
Non-modifiable risk factors
- Positive family history
- Ethnicity (more common in black people)
- Advanced age (stiffening)
Modifiable risk factors
- Physical inactivity
- High sodium diet (→ fluid retention)
- Low K+ in diet (<3.5g/d)
- Diabetes (hyperinsulinemia → renal Na+ retention/proliferation vascular SM (→ ↑ vascular resistance).
- Excessive alcohol intake
- Excessive caffeine intake
- Psychological stress
Recommended salt intake
<5g salt/day = just under a teaspoon!
<2g of sodium/day
All salt should be IODISED or fortified with iodine!
- essential for brain development/mental function in general
How can obesity → HTN?
+ Physical compression of renal arteries → (+) RAAS → vasoconstriction/↑ BV → hypertension
+ Obesity - release of angiotensinogen from adipocytes → AAS (+)
Genetics: Primary HTN
+ Usually polygenic - affects SNS, RAAS, sodium transport mechanisms, vasodilation etc...
+ Rare monogenic forms - Liddle's syndrome - overactivity of ENaC
Define: Secondary HTN
HTN of known aetiology (approx 5% of cases; adults)
< 10 yrs old, secondary HTN >> than primary! (mainly due to renal disease)
Common types: Secondary HTN
+ Renal hypertension
+ Endocrine hypertension
+ Coarctation of the aorta
+ Drug induced
+ Isolated systolic hypertension
Etiology: Renal hypertension
Potentially ALL RENAL DISEASES can cause hypertension!
+ Reno-vascular HTN
+ Glomerulonephritis, renal failure (failure to excrete Na+/H20 → ↑ intravascular volume)
+ Polycystic kidney disease
Causes: Renovascular hypertension
+ Fibromuscular dysplasia
Pathogenesis via RV HTN?
Hypoperfusion to JGA → increased renin secretion → increased AT-II (vasoconstriction of arterioles, increasing TPR) and aldosterone - (reabsorption of Na+ via luminal ENaC channel in collecting tubules ∴ H20 → expanding plasma volume)
Etiology: Hormonal hypertension
+ Hyperaldosteronism -
Primary = Conn's syndrome (adenoma/carcinoma)
Secondary (renal ischemia - as mentioned above)
+ Cushing's syndrome (cortisol (+) aldosterone receptors - similar structure/α1 vasoconstriction)
+ Pheochromocytoma (↑ adrenaline/noradrenaline → → HR/peripheral vasoconstriction)
+ Hyperthyroidism (↑ CO)
+ Primary hyperparathyroidism (→ hypercalcemia → renal dysfunction/vasoconstriction)
Which congenital diseases can cause hypertension?
Drug induced hypertension
Caffeine (not sustained)
2) Iatrogenic and OTC
Clinical features: Hypertension
Usually asymptomatic until organ damage occurs!
- high pressure → damage to the endothelium!
Hypertensive emergency/crisis (>180/120mmHg) → acute organ damage; must be treated with IV anti hypertensives immediately (oral if no signs of organ damage)!
Signs of hypertensive crisis
- Chest pain
- Severe headache
- Blurry vision
- Heart failure (↑ after-load → concentric LV hypertrophy → LHF)
- MI (damage to coronary arteries)
- Aortic dissection
- Aortic aneurysm
- Stroke (mostly hemorrhagic)
- Cognitive changes
- Nephrosclerosis (chronic HTN → narrowing of AA/EA → reduced GFR → ischemia → sclerosis/fibrosis → renal failure)
Retinopathy; required fundoscopy!
Quantify CV risk
End organ damage
Exclude secondary causes
- Lifestyle changes
- Drug treatment
Medication is required with BP ≥160/100mmHg (or ABPM ≥150/95mmHg). For those ≥140/90, the decision depends on the risk of coronary events, presence of diabetes, or end-organ damage!
Clinic blood pressure between 140/90 - 180/120mmHg?
- Offer ABPM (ambulatory BP monitoring) or HBPM; at least 4 days (home monitoring) to confirm the diagnosis
Whilst waiting for confirmation; carry out
- Assessment of CV risk
- Investigations for target organ damage
- Exclusion of secondary causes
Assessment of CVD risk
QRISK score; https://qrisk.org/three/
+ Fasting bloods for lipids (tot and HDL chol)/glucose
↑ 10yr risk of vascular disease ≥20%; requires pharma treatment!
Organ damage assessment/exclude secondary causes
U&E, creatinine (renal function, ↓K+ in Conns, ↑ Ca2+ in hyperPTHism...)
ECG (LV hypertrophy, past MI...)
Urine dipstick test (blood, protein)
These baseline tests, if abnormal → further investigations!
What can indicate secondary hypertension?
Recurrent hypertensive crises
Susp. of renal hypertension?
Elevated creatinine/urea from baseline investigation
Examination; renal artery bruits, palpable kidneys, haematuria, proteinuria...
US, arteriography (PKD, renal artery stenosis)
Susp. of Cushing syndrome?
↑ serum cortisol
Susp of Conn syndrome?
- Aldosterone: renin ratio ↑
Susp. of pheochromocytoma?
Young patients with a history of endocrine tumors. MEN type 2 is likely in patients who also have hyperparathyroidism.
+ Sweating, shaking, palpitations
↑ 24 hr urinary metanephrines
Susp. of hyperthyroidism?
↑ free T4
Susp. of hyperparathyroidism
Hypercalcemia symptoms (stones, groans, moans; confusion, polyuria)
Diet (low sodium, fat, high in fruit/veg/whole-grains)
Limit alcohol intake
Lose weight (if overweight/obese)
Indications for pharmacological treatment of hypertension
All with BP ≥160/100mmHg (or ABPM ≥150/95mmHg).
CV risk >20%
DM/CKD + 140/90mmHg
DM or existing renal or CV disease; <130/80mmHg
K+ ↑ (lack of aldosterone)
Dry cough (common cause of chronic cough in adults)
Dihydropyridine (vasoselective) are used in HTN:
- Peripheral edema
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