9.1 Hypertension Flashcards
HTN
Definition
Normal <80 (no tx)
Prehypertension 120-139 / 80-89 (tx only if end-organ damage)
Stage 1 HTN 140-159 / 90-99 (tx)
Stage 2 HTN ≧160 / ≧100 (2 drug dx)
Isolated systolic HTN
≧140 / <90
Progressive ↓ vascular compliance (elasticity)
Accelerated HTN
↑ BP with evidence of vascular damage on fundoscopy BUT WITHOUT papilledema
Malignant HTN
↑ BP with vascular damage (encephalopathy or nephropathy) AND papilledema in fundoscopy
HTN urgency
sBP >210 or dBP >120 with minimal or not target-organ damage
HTN emergency
↑ BP and acute target-organ damage
Acute symtomps
Resistant HTN
Failure to reach BP control with full doses of 3-drug tx (diuretic included)
Mechanisms of HTN
Intravascular volume
Autonome nervous system
Renin-Angiotensin-Aldosterone
Vascular
Intravascular volume physiology
Na+ is predominantly extracellular and primary determinant of extracellular volume
↑NaCl intake → ↑extracel. volume → ↑cardiac output
Autonome nervous system
Via pressure, volume and chemoreceptor signals
Adrenergic reflexes {short term} + (hormonal + volume-related factors) = long term
Norepinephrine, Epinephrine & Dopamine
Adrenergic receptor physiology
alfa 1 postsynaptic smooth muscle cells (vasoconstriction)
alfa 2 presynaptic membranes in postganglionic nerve terminal that synthesizes epinephrine (negative feedback inhibiting norepinephrine release)
beta 1 ↑cardiac output by ↑HR + ↑contraction. ↑renin release from kidney.
beta 2 relaxation of smooth muscle (vasodilatation)
Renin physiology
Synthesized in renal afferent arteriole
Secretion stimulated by:
1. ↓NaCl (distal ascending loop of Henle)
2. ↓pressure in renal afferent arteriole (baroreceptor)
3. β1 stimulation
Angiotensin II physiology
- Vasoconstriction
- Smooth muscle myocyte growth (artherosclerosis pathogenesis and cardiac hypertrophy)
Aldosterone physiology
Stimulated by AT2 and ↑K⁺
Na⁺ retention (exchange Na⁺ for K⁺)
Vascular physiology
Elasticity of the vessel
Hypertrophy = ↓elasticity
Nitric oxide = vasodilator
Endotelin = vasoconstriction
Investigation in HTN
labs
-Evaluate end-organ damage and rule-out secondary causes-
Urinalyisis (Proteinuria)
Hto. (Is HTN killing the Kidney?)
Electrolytes (K⁺) (Is HTN killing the Kidney?)
Serum Cr & BUN (Is HTN killing the Kidney?)
EKG (Left-ventricular hypertrophy)
Blood Glucose (DM?)
Lipid profile (risk factors)
Causes of Secondary HTN
-ABCDE- A Apnea, Aldosteronism B Bruits, Bad kidneys C Coarctation, Cushing's, Catecholamines, Calcemia, Contraceptives D Drugs E Endocrine disease
Physical findings
Renovascular: abdominal bruit (renal artery stenosis most common cause)
Cushing: weight gain, moon-like facies, striae and ecchymoses
Pheochromocytoma: episodic HTN with headache, palpitations and sweating
Primary aldosteronism (Conn Syndrome): muscular weakness + polyuria/polydipsia from ↓K⁺
Lifestyle modifications
may be sufficient in stage 1 HTN
- Diet: DASH (↓colesterol & ↓saturated fats) & limit sodium intake to 65-100 mmol (1.5-2.3 g)
- Exercise: 30-60 min, 4-7 x/wk
- Smoking cessation
- ↓OH
- Weight loss (most important= 1kg:1mmHg)
Tx Target BP in HTN
<140/90 in the rest
Pregnant with crisis: dBP 90-100 (to avoid hypoperfusion of placenta)
Who to treat?
dBP >90 despite 3- to 6-month with lifestyle modifications
First line Tx
Diuretic, ACEI, β-Blockers, CCB
In absence of specific indication or contraindication, diuretics should be first tx (morality benefit)
Stage 2 HTN, a two-drug tx should be used (diuretic + “X”)
How to combine anti-HTN drugs
ACEI β-Blockers Younger px / Heart failure
| x | —————–
CCB Diuretic >50 yr / low-renin HTN
Tx for Specific HTN groups
- DM: ACEI or ARB
- Post-MI: β-Blockers
- ↓left-ventricular systolic function: ACEI ± β-Blockers
- Blacks: least effective with ACEI
- Pregnant: methyldopa / hydralazine (eclampsia) (NEVER ACEI nor ARB)
HTN emergency Tx
- EKG more important as an initial test to exclude MI
- IV tx: Nitroprusside (nitroglycerine if MI)
- Goal: ↓MAP by no more than 25% in first 1-2 hrs
Renal Artery Stenosis
Causes, Dx and Tx
- Causes: Artherosclerotic disease OR fibromuscular dysplasia in young women.
- Dx: Upper abdominal bruit → best initial test: Abdo USG → Confirmation test: Arteriogram.
- Tx: Percutaneous transluminal angioplasty (if Qx fails=ACEI)
Primary Hyperaldosteronism (Causes, Dx and Tx)
- Cause: Adenome (most common) or Bilateral Hyperplasia
- Dx: HTN + ↓K⁺ (muscular weakness + polyuria/polydipsia) → ↑aldosterone in urine and blood (with normal renin)
- Tx: Adenome = Qx / Hyperplasia = Spironolactone
Pheochromocytome
Causes, Dx and Tx
- Cause: Adrenal gland benign tumor
- Dx: EPIsodic HTN + headaches, sweating, palpitations and ↑HR → urinary vanillylmandelic acid (VMA), metanephrine and free urinary catecholamines. (metabolites: EPInephrine→metanephrine→VMA)
- Tx: alfa-blockers (Fenoxibenzamina or Phentolamine) followed by Qx
Cushing Disease
Causes, Dx and Tx
- Cause: Pituitary adenoma (most common)
Glucocorticoids inhibit protein production (amino-acids are turned into glucose) - Dx: HTN + Truncal obesity, buffalo hump, menstrual abnormalities, striae, hyperpigmentation and impaired healing → best initial test: Dexamethasone suppression test + 24-hour urine cortisol (DO NOT START WITH CT)
- Tx: Qx
note
If dexa test is positive = look for ACTH?
↑ACTH = pituitary
↓ACTH = adrenal or ectopic
Coarctation of the Aorta
Causes, Dx and Tx
- Causes: Aorta narrows where ductus arteriosus
- Dx: HTN greater in upper extremities than in lower + murmur posterior left interscapular area → transesophageal echocardiography
- Tx: Qx
When to investigate secondary HTN?
- Very young or very old
- Those with key features
- HTN refractory to therapy
