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Flashcards in Secondary HTN 1 Deck (16):
1

1. Define secondary and essential hypertension.

essential HTN= primary HTN (unknown cause)
secondary hypertension (known cause/ treatable) 5-10% of all HTN

2

2. Describe the pathology and pathogenesis of blood pressure elevation in unilateral renal artery stenosis.

HTN cause by sodium and water retention or greater than normal amounts production of renin

renal vascular disease reduces blood flow to the JG apparatus and stimulates renin release (primarily renal artery stenosis)

stenosis causes down stream vessels to dilate until they can no longer cope; only when auto regulation is exhausted will renin production increase; excessive stenosis kills kidney

causes include atherosclerosis and fibromuscular dysplasia (middle aged women), nurofibromatosis (children) or obstruction (inflammatory lesions, extrinsic pressure form tumors, cysts or trauma

3

2. Describe the pathology and pathogenesis of blood pressure elevation in chronic kidney disease.

acute disease damage to JG cells (acute)

chronic kidney disease (defect in sodium excretion) and HTN can cause damage to renal artery

rare causes include renin-secreting tumors (children) or Liddle Syndrome (abnormal ENaC channels)

4

2. Describe the pathology and pathogenesis of blood pressure elevation in primary aldosteronism.

increased secretion of aldosterone that is inappropriate, or maladaptive (not accompanied by elevated renin)

mineralocorticoids are increased until 'mineralocorticoid escape' causes pressure naturesis and system reaches new higher equilibrium; desperate attempts to hold on to sodium lead to increased potassium naturesis

common causes: adrenal adenomas (Conn syndrome), adrenal hyperplasia (defects in enzymes that catalyze cortisol

1. check urine potassium
2. check blood aldosterone
3. check blood renin
4. complete confirmatory imaging

5

3. Identify the diagnostic hallmarks of renal artery stenosis.

onset before 25 or after 50 yo esp with no FH

rapid worsening of pre-existing HTN, esp when there is vascular disease elsewhere

severe HTN requiring multiple drugs

coexistence of severe hypertension and impaired renal function (arterial pressure worsened by a drug)

recurrent pulmonary edema without obvious cardiac cause

reduction in diameter or length of kidney, collateral vessels or poststenoic dilation on arteriogram

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3. Identify the diagnostic hallmarks of primary aldosteronism.

low renin and high aldosterone; hypkalemia, unless Na intake is low

HTN that may be severe

lab findings: high aldosterone in blood and urine, low plasma renin, high urine potassium, low serum possum and metabolic alkalosis; most sensitive test is the plasma aldosterone to plasma renin activity

CT and MRI can localize ademonas or iodocholesterol scans when fasiculata is suppressed, tumors will continue to produce

7

4. Describe the principal therapies for renal artery stenosis.

balloon dilation (percutaneous trans-luminal renal angioplasty) and sometimes stunting

revascularization is preferred when narrowing if further from the branch point

antihypertensive drugs most popular currently, although they have contraindications and side effects (ACEI ARE CONTRAINDICATED IN BILATERAL STENOSIS- to blocks the normal compensation in the kidney and can lead to kidney failure)

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4. Describe the principal therapies for primary aldosteronism.

surgical removal of the gland

medical blockade of RAAS

9

What does the pneumonic RECAPS ABCDEF stand for?

renal disease (renal stenosis)
Estrogens and eclampsia
coarctation of the aorta
aldosteronism
pheochromocytoma
sleep apnea

alcoholism
brain lesions
cushing syndrome
drugs
endocrine diseases
fat

10

Discuss the methods dx. of renal artery stenosis.

gold standard is contrast arteriography

UA used for diagnosis or MRI with contrast, (CT with contrast less so)

renogram using radioactive tracer (administration of ACEI can highlight physiologically significant stenosis)

plasma levels of renin below and above the renal veins can also be helpful diagnostically

11

Describe the role of estrogens and eclampsia in the pathogenesis of HTN.

high doses of estrogens can cause HTN, although individual susceptibility varies; odds increase with obesity, FH and older age

estrogens are know to have Na retaining effects, stimulate hepatic renin substrate synthesis and potentiate actions of catecholamines

preeclampsia includes HTN, proteinura (+300mg/d, non-specific) and edema (most predictive in hands and face but specific);
usually initiates in 20th week of pregnancy

eclampsia: most sever HTN complication of pregnancy (preeclampsia, convulsions, coma and death) onset during or just after labor begins; known to arise from the fetal-placental unit; causes decreased fetal perfusion

12

1. Describe the pathology and pathogenesis of hypertension in coarctation of the aorta. How would you dx. coarctation?

fibrous narrowing of the aorta representing the failure of a segment of the aorta to grow with the rest (closer to heart, more dangerous)

pressure is elevated in proximal branches but and lower distally; HTN due to narrowing but also RAAS response (like bilateral stenosis)

cardinal finding is lower measured blood pressure in the legs as compared to the arms

other symptoms include pain or weakness in the legs, diminished pulse in the ankle, systolic murmur (hear best between scapula) and bruits in chest wall; imaging can review abnormal aortic shadow, enlarged intercostal vessels

13

1. Describe the pathology and pathogenesis of hypertension in pheochromocytoma.

tumors (derived from the neural crest) that secrete pressor catecholamines and can occur in some very obscure places; catecolamines increase cardiac output and peripheral resistance

characterized by paroxysms of HTN, headache, sweating; measure catecholamines and their metabolites in 24h sampling

14

2. Identify the hallmarks of the 10 causes of secondary HTN.

Renal disease- RA stenosis
Estrogen/eclampsia- pregnancy
Coartation of aorta: lower BP in lower limbs
Aldosteronism: high aldosterone, low renin
Pheochromocytoma: spikes in catecholamines
Sleep apnea: sympathetic arousals

Alcohol: strong correlation
Brain lesions: inter cranial pressure
Cushing's syndrome: mineralocorticoid activity
Drugs: stimulate adrenergic nervous system
Endocrine disorders: i.e. hyperthyroid (increased pulse pressure)

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3. State when to suspect secondary HTN in the average patient with elevated blood pressure.

.every person who presents with hypertension should e examined with an eye toward finding or ruling out secondary conditions (RECAPS ABCDEF)

16

Name common drugs that can negatively effect blood pressure.

nasal decongestants
appetite suppressants
cocain
ergot alkaloids
cyclosporine
MAOI with tyramine
Epo
glucocoriticoids