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Block 2 PATH Exam -- Hypertension Lecture


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Breakdown of hypertension cases
Primary Hypertension -- 95%
Secondary Hypertension -- 5%
Benign Hypertension
Diastolic 90 - 120, slow rise
Pts. are usually middle-aged or elderly
Common (95%)
Very slow course
Malignant Hypertension
Diastolic > 120, rapid rise
Pts. are young or middle-aged
Uncommon (5%)
Very rapid course (months)
Glucocorticoid-Remediable Aldosteronism (GRA)
Autosomal Dominant
Chromosome 8q
Chimeric gene causes ectopic aldosterone production
Under control of ACTH
APPARENT Mineralocorticoid Excess (AME)
Autosomal recessive
Chromosome 16q
Inactivating mutation of beta-hydroxysteroid dehydrogenase
Increased levels of cortisol stimulate mineralocorticoid receptors
Liddle Syndrome
Autosomal dominant
Chromosome 16p
Gain of function mutation causes sustained sodium channel activity
Independent of mineralocorticoids
Lifestyle risk factors for hypertension
Alcohol Intake
High Sodium
Conn Syndrome
Primary Hyperaldosteronism
Caused by adrenal cortical adenoma
Or, Idiopathic Bilateral Adrenal Hyperplasia
CV system complications of hypertension
Aortic root dilatation
Eventual diastolic dysfunction
Acceleration of atherosclerosis
Renal complications due to hypertension
Nephrosclerosis (most common)
Due to either hyperfiltration or ischemia

Small arteries show hyalinized walls

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