Module 2: Cardiovascular And Hemodynamics Pathology Flashcards
(16 cards)
Two Classifications of Hypertension
• Secondary Hypertension
• Under 10% of cases
• Due to an underlying condition
• Renal or adrenal disease • Essential (Idiopathic)
Hypertension
• 90-95% of all hypertension cases
• No known direct cause
• Influenced by genetics and environmental factors
Mechanisms of Essential Hypertension
• Reduced renal sodium excretion —> Na in blood so water follows Na (increase blood volume and blood pressure)
• Increased vascular resistance
—Chronic vasoconstriction may result in permanent thickening of the walls of affected vessels
• Genetic factors
—Possible susceptible genes influencing the renin-angiotensin system
• Environmental factors
— Stress, obesity, smoking, physical inactivity, and high levels of salt consumption
• All can influence epigenetics which influence genes being expressed
HTN treatment
Lifestyle Changes
• DASH diet or diets less in salt • Exercise / Weight loss • Smoking cessation
Medications
• Thiazide Diuretics (water pills)
• Eliminate water and sodium • Angiotensin-converting enzyme (ACE) inhibitors • Angiotensin II receptor blockers (ARBs) • Beta blockers
• Decrease the workload on your heart
• Vasodilation
• Slows the heart rate
All of the options are true regarding hypertension, except?
• A. Secondary hypertension can be due to a renal disorder
• B. Reduced renal sodium excretion is associated with essential hypertension
• C. A complication of hypertension is cardiac hypertrophy
• D. Actually, all of the options are true
D
All of the statements are true, except?
• A. Increased risk of stroke is a complication of hypertension.
• B. Stage 1 hypertension needs both high readings of systolic and diastolic
• C. Decreased renal sodium excretion is a mechanism of hypertension
development • D. Medications that block the effect of RAAS is a treatment of hypertension
B
Tunic Intima and Tunic Media thicken
with damage
Referred to as: Intimal Thickening and
Intima-Media Thickness
Intimal Hyperplasia
• Process that the intimal layer of the blood
vessel becomes thickened • Due to presence and increase of smooth
muscle and extracellular matrix
components • Between the endothelium and internal
elastic membrane
Arteri/o
Refers to an artery or arteries
Sclerosis
Abnormal and pathological hardening of body tissue
• Mostly from scar tissue
Arteriosclerosis
Literally means hardening of an artery or arteries
• “Chronic disease characterized by abnormal thickening and hardening of the
arterial walls with resulting loss of elasticity”
Mainly associated with hypertension, diabetes mellitus, and smoking
Three Types Arteriosclerosis
- Arteriolosclerosis
—Arteriol/o = arterioles - Atherosclerosis
—Most common type of arteriosclerosis - Mönckeberg Medial Sclerosis
• Calcium deposits in muscular arteries
Arteriolosclerosis vs atherosclerosis • Arteriolosclerosis
• Arteriolosclerosis
— Hardening and thickening of arterioles
• Atherosclerosis
— Hardening of an artery specifically due to an atheromatous plaque
Atherosclerosis: Overview
Build of fat, cholesterol, and other substances
underneath the endothelium
• Build-up is called an Atherosclerotic Plaque
• Plaques also weaken the underlying media tunics
• Can lead to aneurysm
• Atherosclerosis basically hardens the vessel and narrows
the lumen space
** Coronary Artery Disease (CAD) & Peripheral Artery Disease (PAD)**
• Dangerous manifestation of atherosclerosis
• Deaths caused by ischemic heart disease (IHD)
• Myocardial infarction
• Lower extremity complications
Pathogenesis
Steps to Atherosclerosis Development
- Endothelial Damage
• Damage to the endothelium
• High blood pressure, smoking, high cholesterol
• Initiates the inflammatory process
- Accumulation of Lipoproteins and Monocytes
LDL (“bad” cholesterol) particles enter the damaged area and get stuck in
the vessel wall • Monocytes move to the area to “clean up” the excess LDL particles
- Immune Response and Fatty Streak Formation
Monocytes differentiate into macrophages that phagocytize the LDL
particles and become foam cells • Foam cells pile up and form a fatty streak, the earliest visible lesion • Fatty Streak is visible and thrombogenic
- Smooth Muscle Proliferation and Plaque Formation
Smooth muscle cells migrate from the tunica media into the intima
• Produce ECM components to form a fibrous cap over the lipid core
- Plaque Rupture or Calcification of Plaque
If the fibrous cap ruptures, the lipid core is exposed to the bloodstream
• Will cause a thrombosis (an abnormal blood clot) which can block the artery
• Leads to a heart attack or stroke or blood vessel blockage
6.*Calcification of plaque
Clinical complications of atherosclerosis
Atherosclerosis Leads To:
• Coronary Artery Disease (CAD)
• Peripheral Artery Disease (PAD)
• Transient Ischemic Attack
• Cerebral Vascular Accident
- infarction (partially block vessel lumen, clot forms and completely blocks vessel lumen)
- Aneurysm and rupture (plaque build up weakens vessel wall
- Embolism formation
All of the options are TRUE, except?
• A. Arteriosclerosis is hardening of the arterioles
• B. Foam cells are macrophages that phagocytize LDL particles
• C. The fatty streak is formed due to the foam cells
• D. Fibrous cap formation is due to smooth muscle cells
• E. Actually, all of the options are true
A
All of the options are TRUE, except?
• A. Tremendous and serious complications are associated with atherosclerosis
• B. Endothelial damage associated with atherosclerosis can be caused from
hypertension • C. Coronary artery disease is primarily associated with atherosclerosis • D. Intimal hypertrophy naturally occurs as an individual ages • E. The process of atherosclerosis occurs quickly, typically within months
E
