9.1 Hypertension Flashcards

1
Q

HTN

Definition

A

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)

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2
Q

Isolated systolic HTN

A

≧140 / <90

Progressive ↓ vascular compliance (elasticity)

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3
Q

Accelerated HTN

A

↑ BP with evidence of vascular damage on fundoscopy BUT WITHOUT papilledema

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4
Q

Malignant HTN

A

↑ BP with vascular damage (encephalopathy or nephropathy) AND papilledema in fundoscopy

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5
Q

HTN urgency

A

sBP >210 or dBP >120 with minimal or not target-organ damage

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6
Q

HTN emergency

A

↑ BP and acute target-organ damage

Acute symtomps

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7
Q

Resistant HTN

A

Failure to reach BP control with full doses of 3-drug tx (diuretic included)

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8
Q

Mechanisms of HTN

A

Intravascular volume
Autonome nervous system
Renin-Angiotensin-Aldosterone
Vascular

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9
Q

Intravascular volume physiology

A

Na+ is predominantly extracellular and primary determinant of extracellular volume
↑NaCl intake → ↑extracel. volume → ↑cardiac output

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10
Q

Autonome nervous system

A

Via pressure, volume and chemoreceptor signals
Adrenergic reflexes {short term} + (hormonal + volume-related factors) = long term
Norepinephrine, Epinephrine & Dopamine

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11
Q

Adrenergic receptor physiology

A

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)

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12
Q

Renin physiology

A

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

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13
Q

Angiotensin II physiology

A
  • Vasoconstriction

- Smooth muscle myocyte growth (artherosclerosis pathogenesis and cardiac hypertrophy)

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14
Q

Aldosterone physiology

A

Stimulated by AT2 and ↑K⁺

Na⁺ retention (exchange Na⁺ for K⁺)

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15
Q

Vascular physiology

A

Elasticity of the vessel
Hypertrophy = ↓elasticity
Nitric oxide = vasodilator
Endotelin = vasoconstriction

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16
Q

Investigation in HTN

labs

A

-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)

17
Q

Causes of Secondary HTN

A
-ABCDE-
A Apnea, Aldosteronism
B Bruits, Bad kidneys
C Coarctation, Cushing's, Catecholamines, Calcemia, Contraceptives
D Drugs
E Endocrine disease
18
Q

Physical findings

A

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⁺

19
Q

Lifestyle modifications

may be sufficient in stage 1 HTN

A
  • 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)
20
Q

Tx Target BP in HTN

A

<140/90 in the rest

Pregnant with crisis: dBP 90-100 (to avoid hypoperfusion of placenta)

21
Q

Who to treat?

A

dBP >90 despite 3- to 6-month with lifestyle modifications

22
Q

First line Tx

A

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”)

23
Q

How to combine anti-HTN drugs

A

ACEI β-Blockers Younger px / Heart failure
| x | —————–
CCB Diuretic >50 yr / low-renin HTN

24
Q

Tx for Specific HTN groups

A
  • 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)
25
Q

HTN emergency Tx

A
  • 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
26
Q

Renal Artery Stenosis

Causes, Dx and Tx

A
  • 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)
27
Q
Primary Hyperaldosteronism
(Causes, Dx and Tx)
A
  • 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
28
Q

Pheochromocytome

Causes, Dx and Tx

A
  • 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
29
Q

Cushing Disease

Causes, Dx and Tx

A
  • 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
30
Q

Coarctation of the Aorta

Causes, Dx and Tx

A
  • Causes: Aorta narrows where ductus arteriosus
  • Dx: HTN greater in upper extremities than in lower + murmur posterior left interscapular area → transesophageal echocardiography
  • Tx: Qx
31
Q

When to investigate secondary HTN?

A
  • Very young or very old
  • Those with key features
  • HTN refractory to therapy