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MCPHS PATHOPHYS EXAM 2 QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST £8.52   Add to cart

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MCPHS PATHOPHYS EXAM 2 QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST

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MCPHS PATHOPHYS EXAM 2 QUESTIONS AND ANSWERS WITH COMPLETE SOLUTIONS VERIFIED LATEST Developmental (berry) aneurysms Congenital aneurysm Occur in cerebral vessles Arteriovenous Fistulas Congenital abnormal connection between artery and vein Fibromuscular dysplasia Congenital abnormal cellular...

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  • November 2, 2024
  • 17
  • 2024/2025
  • Exam (elaborations)
  • Questions & answers
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MCPHS PATHOPHYS EXAM 2 QUESTIONS AND ANSWERS WITH

COMPLETE SOLUTIONS VERIFIED LATEST

Developmental (berry) aneurysms


Congenital aneurysm Occur in cerebral vessles


Arteriovenous Fistulas


Congenital abnormal connection between artery and vein


Fibromuscular dysplasia


Congenital abnormal cellular growth in medium and large muscular arteries (renal, carotid) leading to

stenosis and aneurysm


Endothelial dysfunction


Induced thrombogenic surface with high affinity for inflammatory cells


Intimal Thickening


Stimulation of smooth muscle cell growth and ECM production in Intima layer


High BP/Regular BP


140/90 - 120/80


BP = CO x PR


CO determined by Blood volume (sodium/ANP) and cardiac factors (HR/Contractility)

PR determined by Humoral (hormone constrict/dilate - ex: Ang II) and Neural (adrenergic) factors


Atrial Natriuretic Peptide

,Released from heart, causes vasodilation and Na excretion


Angiotensin II


Vasoconstrictor and aldosterone inducer (Na resorption)


Essential Hypertension


Idiopathic. Results from genetics, reduced Na excretion, vasoconstriction, and evironment (salt, smoke)


Atherosclerosis


intimal based plaques composed of lipids, smooth muscle, inflam cells, and ECM. Has Fibrous cap and

Necrotic center.

CHRONIC INFLAMMATION ALWAYS PRESENT, WOMEN PROTECTED BY ESTROGEN


2 important causes of endothelial dysfunction


Hemodynamic disturbance and hyperlipidemia


Pathogenesis of hyperlipidemia atherogenesis


Neutrophils oxidize lipoproteins in intima.

Macrophages engulf oxidized lipids and release cytokines.

Macrophages turn to "foam cells" and eventually burst leading to more inflammation and oxidized lipids


Vulnerable vs Stable atherosclerotic plaques


Vulnerable have large areas of foam cells/lipids, lots of inflammatory cells, and a THIN fibrous cap.

Stable is opposite


Clinical outcomes of Atherosclerotic plaques

, 1. Rupture, ulceration, erosion- leads to thrombosis

2.Hemorrhage in plaque

3. Atheroembolism

4. Aneurysm formation from increased pressure/ischemia


True Aneurysm


Bound by all wall layers, just weakening


False Aneurysm (pseudo)


Extravascular hematoma (rupture through entire vascular wall)


Dissection


When blood enters in between the layers of the vascular wall as a hematoma


Aneurysm cause


Loss of collagen by inflammation, poor intrinsic strength, and ischemia of medial layer


Abdominal Aortic Aneurysm


Caused by atherosclerosis, a true aneurysm. Usually in elderly smokers. Usually asymptomatic, but can

rupture and expand and cause embolisms.


Aortic Dissection (thoracic)


Caused by hypertension. Usually in 40-60 men. Often leads to rupture.

Medial degeneration in aorta. Sudden onset with excruciating pain in back and chest, similar to angina.


Immune Complex associated Vasculitis

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