cardiac physiology Q8

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Questions and Answers

what r the modifiable risk factors of primary/essential hypertension?

excess salt consumption, obesity, smoking, inactivity, alcohol,

unmodifiable risk factors of primary/essential hypertension?

age, race, genetic factors

risk factors of the secondary hypertension (5-10%):

renal disease, excess aldosterone, pheochromocytoma, and other disorders,

what hormone contribute to secondary hypertension?

aldosterone. Signup and view all the answers

what's the initial event in the pathogenesis of atherosclerosis?

injury to the epithelium. Signup and view all the answers

atherosclerosis pathogenesis.

injury to vascular endothelium>LDL is deposited on the endothelium and oxidised>enters the tunica intima>ingested by macrophages>(lipid-filled foam cells)> fatty streak>increase in size and narrow the lumen. LDL acts as an antigenic and attracts inflammatory cells into the arterial wall>inflammatory mediators are released>more lymphocytes. smooth muscles migrate to the surface of age plaque>(fibrous cap), if thin can rupture and cause thrombosis>plaque calcified/hard. Signup and view all the answers

Flashcards

Modifiable risk factors of primary hypertension

Lifestyle factors that can be changed to reduce the risk of primary hypertension, including excess salt consumption, obesity, smoking, inactivity, and alcohol use.

Unmodifiable risk factors of primary hypertension

Factors that cannot be changed, including age, race, and genetic predisposition.

Secondary hypertension cause

High blood pressure caused by an underlying medical condition, e.g., renal disease, aldosterone excess, or pheochromocytoma.

Hormone in secondary hypertension

Aldosterone, a hormone, can contribute to secondary hypertension.

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Atherosclerosis' initial event

Damage to the inner lining of the artery (endothelium) is the first step in atherosclerosis.

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Atherosclerosis pathogenesis steps

Starts with endothelial injury, followed by LDL oxidation, macrophage ingestion, fatty streaks, and fibrous cap formation. More inflammation and the potential for plaque rupture.

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