Hypertension and Target Organ Damage - Feb 12 Flashcards
Why is hypertension as risk for cardiovascular disease (2 reasons)
1) Is a risk for cardiovascular disease because it accelerates artherosclerosis
2) those with hypertension often have other cardiovasc. disease risk factors (diabetes, hypercholesterolemia..)
Diagnosis of hypertension
- Initial presentation, only if hypertensive urgency/emergency
- On first hypertension visit if SBP > 140 and/or DBP> 90 at least 2 more readings (discard first reading and average last 2). Diagnostic tests to assess for end organ damage.
- Visit 2 for assessment of hypertension if SBP > 180 mHg and/or DBP > 110 mmHg. OR at visit 2 patients with microvascular target organ damage, diabetes mellitus or chronic kidney disease can be diagnosed if SBP >140 mmHg or DBP > 90mmHg
- SBP >160 mmHg and/or DBP >100mmHg across first 3 visits
- SBP > 140 mmHg and/or DBP > 90 mmHG acorss first 5 visits
Hypertensive urgencies and emergencies
1 + 8
- Asymptomatic diastolic BP > 130 mmHg
- severe elevations BP in the setting of any of:
1. Hypertensive encephalopathy
2. Acute aortic dissection
3. Acute left ventricular failure
4. Acute coronary syndrome
5. Acute kidney injury
6. Intracranial hemorrhage
7. Acute ischemic stroke
8. Eclampsia of pregnancy
Systems that regulate blood pressure (think general)
- Neural (autonomic nervous system)
2. Humoral (endocrine)
Neural pathway for regulation of blood pressure components (what system, what does it connect)
- sympathetic nervous system
- spans/connects regulatory centers in the midbrain and brainstem (hypothalamus and medulla) to effectors (the heart, kidney, adrenal glands and blood vessels)
RAAS pathway regulation of blood pressure MOA (i.e. humoral regulation of bp)
- Renin-angiotensin-aldosterone system:
1) Decrease in perfusion of kidney
2) Release of renin from juxtaglomerular apparatus
3) Renin convert Angiotensinogen in liver to angiotensin I
4) Angiotensin I converted to Ang II via angiotensin converting enzyme (ACE) in pulmonary capillary endothelium
5) angiotensin II causes:
i) release of aldosterone from the adrenal cortex
ii) direct vasoconstriction
iii) secretion of ADH from the hypothalamus
iv) feeling of thirst
Function of aldosterone (how it increases BP)
- act at kidney tubules (distal convoluted tubule) to increase Na+ re-absorption into extracellular space
- water follows osmotically
- increase water back to extracellular space = increased blood volume = increased BP
Function of ADH (how it increases BP)
- acts at collecting tubule
- increase reabsorption of water (via aquaporin in membrane)
- increased blood volume = increase BP
Primary hypertension
Diagnosis with hypertension with cause unknown (idiopathic)
Factors linked to primary hypertension (6)
- genetics (ex: Little’s syndrome)
- obesity
- diabetes mellitus
- hyperlipidemia
- increased circulating endogenous catehcholamines
- environment
Little’s syndrome
- mutation in genes encoding subunits on renal tubular sodium channels
- increased sodium and water retention
- leading to hypertension in some patients
Most common cause of hypertension
Primary hypertension
1-10% of patients have a potentially correctable (secondary) cause
In what situations should secondary hypertension be suspected (5)
1) When it occurs at the extremes of age with unexpected target organ damage
2) When it occurs abruptly
3) When the response to therapy is atypical
4) When renal failure is present
5) When hypokalemia (low K+) and hypercalcemia (high Ca2+) are present
Causes of secondary hypertension (A-3, B-2, C-3, D-2, E-2)
A: accuracy, obstructive sleep apnea, primary aldosteronism
B:
i) Bad kidneys (chronic renal failure)
ii) Bruits (turbulent flow due to narrowing of renal arteries -renaovascular hypertension leading to increased activation of RAS)
C:
i)Catecholamines (adrenal medullary turns - pheochromocytoma- increased CO and vasoconstriction)
ii) Cushing’s syndrome-increased stimulation of pituitary = increased circulating levels of cortisol = increase Na+ and H2O retention
iii) Coarctation of the aorta-upper limb hypertension due to congenital narrowing just beyond subclavian artery
D:
i) Diet (increase Na+)
ii) Drugs (prescription and non-prescription)
E:
-erythropoietin- increased circ RBCs = increased viscosity and SVR
-endocrine disorders (hyper/hypothyroidism, hypeparathyroidism)
Drugs linked to secondary hypertension (3+3)
A) prescription -corticosteroids (prednisone) -non-steroidal anti-inflammatory drugs -oral contraceptives containing high doses of estradiol B) non-prescription drugs -nicotine in tobacco -herbal preparations containing ephedra -methamphetamines and cocaine
