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
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
