17 - ASCVD Flashcards
ASCVD Pathogenesis
FATTY STREAK FORMATION
-
LDL Particles -> enter the endothelium
- become Modified** / **Oxidized
-
↑COAGULATION
- ↑plasminogen activator inhibitor
-
↑VASOCONSTRICTION
- ↑endothelin / ↓NO
- ↑INFLAMMATION
-
↑COAGULATION
- become Modified** / **Oxidized
-
Leukocyte Recruitment / adhesion & accumulation
- Engulf the LDL -> FOAM CELLS
ASCVD Pathogenesis
Atherosclerotic plaque formation
-
Weakened fibrous cap
- ↓ COLLAGEN production
- ↑collagen DEGRADATION
-
Foam Cells
-
↑TISSUE FACTOR production
- –> COAGULATION
-
↑TISSUE FACTOR production
- Foam Cell DEATH / DEGRADATION
- ↓ reduced clearance =
- NECROTIC CORE
- ↓ reduced clearance =
- *ASCVD Pathogenesis**
- *2 Pathways for ARTERIAL REMODELING**
After Plaque Rupturing & Thrombosis….
- *ARTERIAL OCCLUSION**
- *thrombus forms** –> endogenous fibrinolysis
- *Stroke / Death / MI**
OCCLUSIVE PLAQUE FORMATION
able to HEAL = endogenous fibrinolysis DEGRADES thrombus
Thrombin -induced fibrosis –> FIBROUS / OCCLUSIVE
SMALLER / NARROW LUMINAL AREA
Clinical Sequelae of ASCVD
CVD
BRAIN
Cerebrovascular Disease = CVD
TIA = Transient Ischemic Attact
Stroke
Seizures
Clinical Sequelae of ASCVD
RAS
KIDNEYS
Renal Artery Stenosis = RAS
Acute & Chronic Kidney Disease
Clinical Sequelae of ASCVD
Misentery
Misentery
Mesenteric ISCHEMIA
Clinical Sequelae of ASCVD
CAD = CHD
HEART
Coronary ARTERY/HEART Disease
Angina
MI
Heart Failure
Arrhythmias
Clinical Sequelae of ASCVD
PAD = PVD
LIMBS
Peripheral ARTERIAL / VASCULAR Disease
Intermittent Claudication
Critical Limb Ischemia
GANGRENE
Acute Limb Ischemia
_ASCVD
Etiologies of Vascular Disease_
5
IntraCRANIAL Atherosclerosis
Carotid Plaque
with arteriogenic emboli
Carotid Stenosis
causing flow REDUCTION
Cardiogenic EMBOLI
ARTERY SPASM
ASCVD
Fluid Mechanics Across Stenoses
Resistance is
INVERSELY RELATED
to SQUARE of Cross-sectional Area
Small changes in luminal area
VVV
LARGE RESISTANCE & PRESSURE GRADIENT changes
across stenosis
Coronary Artery Disease
What affects:
OXYGEN SUPPLY
- *Arterial pO2**
- *Oxygenation + Hemoglobin Stores**
- *Diastolic Filling Time**
- *HR**
Coronary BLOOD FLOW
Coronary Artery Disease
What affects:
OXYGEN DEMAND
HEART RATE
Myocardial CONTRACTILITY
Ventricular Wall Tension
Cerebrovascular Disease
What does
CPP
equal & stand for?
CPP = Cerebral Perfusion Pressure
driving force for cerebral capillary
CPP = MAP - ICP
MAP = Mean Arterial Pressure
ICP = Intracranial Pressure
- *Cerebrovascular Disease**
- *Ischemic Cycle**
↓CCP
Directly affects what?
CPP = Cerebral Perfusion Pressure
↓CPP –> ↑VD
VD = Vasodilation
- *Cerebrovascular Disease**
- *Ischemic Cycle**
↑ICP
Directly affects what?
ICP = Intracranial Pressure
↑ICP –> ↓CPP
CPP = Cerebral Perfusion Pressure
- *Cerebrovascular Disease**
- *Ischemic Cycle**
↑VD
Directly affects what?
VD = Vasodilation
↑VD -> ↑CBV
CBV = Cerebral Blood Volume
CBV ~ 150
skull limits tolerance for increased CBV
- *Cerebrovascular Disease**
- *Ischemic Cycle**
↑CBV
Directly affects what?
CBV = Cerebral Blood Volume
↑CBV -> ↑ICP
ICP = Intracranial Pressure
Collateral Circulation
Chronic Ischemia + NO production
STIMULATES the production of growth factors:
↑VEGF& ↑BFGF
VVV
ANGIOGENESIS / ARTERIOGENESIS
maturation of smaller / capillary-like vessels from pre-existing arteries
COLLATERAL FLOW to areas of ISCHEMIA
INFARCTION
Irreversible CELL DEATH / NECROSIS
Caused by:
Severe / Prolonged ISCHEMIA
For Brain:
4-10 minutes
Heart:
20 minutes
Ischemic Penumbra
Tissue that is SURROUNDING INFARCTION
that is
Ischemic / Metabolically active
VUNERABLE to INFARCTION
Metabolic Toxins & Oxygen Free Radicals
ACCUMULATE & ION SHIFTS occur
VVV
Depolarization of Adjacent Cells
VVV
SEIZURES / ARRHYTHMIAS
