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140/90 in most, for people with risk factor such as CAD, MI, DM2 should consider lowering threshold to 130/80.
Blood pressure =
cardiac output X peripheral resistance
Renin is secreted from the JGA of the kidneys. This reacts with angiotensinogen from the liver to create angiotensin I. Angiotensin I reacts with ACE in lung to create angiotensin II (responsible for vasocontriction). Angiotensin II stimulates aldosterone release from the adrenals, which lead to the kidneys retaining Na and H2O while secreting K (fluid retention).
Idiopathic or essential. 95% of HTN cases. Can be due to OSA, alcoholism, obesity, drugs, NSAIDS, etc. Black, mexican and white people have this because we are more prone to HTN without needing other contributing diseases.
5% of pts. Young, non-black, non-obese people who can be younger than 30 y/o. Renal disease is the largest cause. Can also be caused by thyroid disease, Cushings, pheochromocytoma & coarctation of the aorta.
- HTN with persistent hypokalemia. Aldosterone stimulates sodium and water retention w/ secretion of K.
- Test for this with aldosterone/renin ration. >50 is suspicious for hyperaldosteronism even when K is normal.
- Can be caused by adrenal aldosteronoma (can be seen on CT, trx with surgery). Can also be caused by bilateral adrenal hyperplasia (treat with spironolactone-aldactone or eplerenone-Inspra.
- Blocks aldosterone receptors at the kidney. Increased serum alosterone can lead to decreased serum renin due to negative feedback.
- Can see hyperkalemia, PCOS & severe acne
- Binds receptors at the aldosterone-dependent Na-K exchange site in the kidney (distal convoluted tubule). Causes diuresis - Na & H2O secretion with K being saved. Lowers BP by diuretic mechanism.
- Can see hyperkalemia, increase in BUN & creatinine.
- Can be used to counteract thiazides & loop diuretics (saves K+)
- Does not lead to increased uric acid
Cushing's syndrome (cause of secondary HTN)
- Increased cortisol can have mineralocorticoid effects - Na & H2O retention with activation of RAAS.
- Usually due to ACTH-producing pituitary tumor
- Diagnose with dexamethasone suppression test, 24-hr urine free cortisol level, CT or MRI looking for tumor.
- Catecholamine (epinephrine & norepinephine) secreting tumor of adrenal medulla.
- Can be life-threatening due to severe episodic HTN.
- Diagnose with plasma metanephrines or 24-hr urine catecholamines.
Acromegaly (cause of secondary HTN)
Can lead to HTN due to sleep apnea (a side-effect of having excess HGH in the blood)
Coarctation (narrowing) of the aorta (cause of scondary HTN)
- HTN in upper extremities (before point of coarctation) and low blood pressure in lower extremities (beyond point of coarctation).
- Usually seen in children
- Sudden onset, symptomatic, very high BP
- Medical emergency due to end organ failure (renal failure & changes in eye)
- Diastolic often above 130 (220/130)
- Most common in pregnant female
Thiazides (chlorthalidone, hydrocholothiazide)
- First line
- Mechanism: inhibit Na & chloride reabsorption in kidney, leading to mild diuresis. Lower BP by decreasing plasma volume initially, but in the long term, they also reduce peripheral vascular resistance.
- May need to give K due to K-wasting effects. Can precipitate gout.
- If you need to use in larger doses, should combine with K-sparig agent (ACE inhibitor or ARB)
- Compelling indications: HF, high CAD risk, Diabetes, stroke prevention
Loop diuretics (flurosemide, bumetanide)
- Strong diuretic
- Mechanism: Inhibits chloride reabsorption n thick ascending loop of henle.
- High loss of K, can cause dehydration, increases serum uric acid.
- Really only good in pts w/ HF due to volume depletion effects and in pts with CrCl < 30 (kidney dysfunction)
Aldosterone receptor antagonists (spironolactone)
- Increases Na & H2O secretion and K retention.
- Can see hyperkalemia
- Good in resistant HTN (added to top of 4-drug regimen)
- Indicated in salt-retaining states (HF, post MI & cirrhosis)
Nitrates (Isosorbde dinitrate, IMDUR)
- Direct venodilation by release of nitric oxide
- Good in renal pts w. resistant HTN in addition to 3-4 drug regimen.
- Compelling indication: angina
ACE inhibitors (Enalapril, Lisinopril)
- Inhibits vasocontriction by inhibiting ACE enzyme from converting angiotensin I to angiotensin II. Provides balanced vasodilation. Protect kidneys from end-organ damage.
- Compelling indications: Everything (black ppl for renal protection)
- When combined with Calcium channel blocker or diuretic, these are potent.
- Monitor serum creatinine & potassium (hyperkalemia) - can also see angioedema
ARB (angiotensin II receptor blockers) - Irbesartan, losartan
- Similar mechanism to ACE inhibitor, just later in RAAS.
- Compelling indications: HF, Diabetes, CKD
- Provides kidney protection as well.
Beta blockers (atenolol, metoprolol)
- Preferentially blocks B1 recepters, decreasing HR, cardiac output & renin release
- Compelling indications: Steady HF (not early), post-MI, high CAD risk & DM
- Not contraindicated in COPD or asthma, but use caution. Can cause ED - problems with compliance in males.
- Monitor: HR, blood glucose in DM
Calcium channel blocker (amlodipine & felodipine)
- Decrease Ca influx into cells of vascular smooth muscle causing peripheral vasodilation. Can be used as monotherapy - will control 60% of HTN.
- Good in black population.
- Don't combine with beta blocker.
diuretics and ace inhibitors
- ace inhibitors for renal protection & diabetes, thiazide.
- If that doesn't work, Ca channel blocker.
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