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NSG 533 Advanced Pathophysiology Exam 3 Questions With All Correct Answers 2024/2025 $11.49
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NSG 533 Advanced Pathophysiology Exam 3 Questions With All Correct Answers 2024/2025

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NSG 533 Advanced Pathophysiology Exam 3 Questions With All Correct Answers 2024/2025

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  • September 24, 2024
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NSG 533 Advanced Pathophysiology
Exam 3


List the unconventional threat factors for CAD
1) markers of inflammation, ischemia, and thrombosis (expanded high sensitivity C-reactive
protein, troponin, fibrinogen) 2) adipokines (leptin, adiponectin) three) CKD four) air pollutants
and ionizing radiation 5) medicinal drugs (NSAIDs) 6) coronary artery calcification and carotid
wall thickness and seven) microbiome eight) small dense LDL debris and lipoprotein(a) 9)
Hyperhomocysteinemia




List nonmodifiable hazard elements for CAD
Advanced age, male gender or woman after menopause, and own family history (genetics,
shared environmental exposure).




List modifiable danger factors for CAD
Dyslipidemia, high blood pressure, cigarette smoking, diabetes and insulin resistance, weight
problems and sedentary lifestyle, and an atherogenic weight loss plan.


How does dyslipidemia make contributions to CAD?
High ranges of LDL within the bloodstream results in LDL oxidation, migration into the vessel
wall, and phagocytosis by way of macrophages, all key steps in the pathogenesis of
atherosclerosis.


Atherosclerosis
A continual inflammatory situation that results in damage to the arteries. Thickening and
hardening of the vessels are resulting from the accumulation of lipid-laden macrophages (foam
cells) inside the arterial walls, main to the formation of a plaque.


Optimal lipid panal results
Total ldl cholesterol (< two hundred), LDL (< 100), triglycerides (< one hundred fifty)

, What is the reaction-to-injury speculation inside the development of atherosclerotic lesions?
The earliest occasion in atherogenesis is injury to the endothelium, which might be induced
through high blood pressure, movement of ROS (smoking, pollutants), dyslipidemia, and
elevated A1C.




When foam cells collect in a tremendous quantity within the arterial wall, they shape ______ .
What is then launched?
A lesion called a fatty streak; inflammatory cytokines, unfavorable enzymes, and boom
elements.


Growth elements launched released in atherogenesis stimulate _______ , which ________ .
Clean muscle cell proliferation; produce collagen and migrate over the fatty streak to form a
fibrous plaque.




Plaques that have ruptured are known as ______ .
Complicated plaques


Plaque rupture happens due to the ______ .
Inflammatory activation of proteinases, apoptosis of cells inside the plaque, and bleeding within
the lesion (plaque hemorrhage).


What takes place once a plaque ruptures?
The underlying tissue is uncovered and reasons platelet adhesion, initiation of the clotting
cascade, and rapid thrombus formation which can occlude the vessel, resulting in ischemia and
infarction.


Stable atheromatous lesions
A fibrous plaque that has calcified, protruded into the vessel lumen, and obstructs blood float,
causing chest pain throughout workout (stable angina)


Unstable atheromatous lesions
Plaques which can be prone to rupture even earlier than they have an effect on blood float
(clinically silent until rupture). The fibrous cap is typically thinner in an volatile plaque.

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