17 - ASCVD Flashcards

1
Q

ASCVD Pathogenesis

FATTY STREAK FORMATION

A
  • LDL Particles -> enter the endothelium
    • ​become Modified** / **Oxidized
      • COAGULATION
        • plasminogen activator inhibitor
      • ​↑VASOCONSTRICTION
        • ↑endothelin / ↓NO
      • ​↑INFLAMMATION
  • Leukocyte Recruitment / adhesion & accumulation
    • Engulf the LDL -> FOAM CELLS
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2
Q

ASCVD Pathogenesis

Atherosclerotic plaque formation

A
  • Weakened fibrous cap
    • COLLAGEN production
    • collagen DEGRADATION
  • Foam Cells
    • ↑TISSUE FACTOR production
      • –> COAGULATION
  • Foam Cell DEATH / DEGRADATION
    • reduced clearance =
      • NECROTIC CORE
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3
Q
  • *ASCVD Pathogenesis**
  • *2 Pathways for ARTERIAL REMODELING**
A

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

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4
Q

Clinical Sequelae of ASCVD

CVD

A

BRAIN
Cerebrovascular Disease = CVD

TIA = Transient Ischemic Attact

Stroke

Seizures

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5
Q

Clinical Sequelae of ASCVD

RAS

A

KIDNEYS
Renal Artery Stenosis = RAS

Acute & Chronic Kidney Disease

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6
Q

Clinical Sequelae of ASCVD

Misentery

A

Misentery

Mesenteric ISCHEMIA

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7
Q

Clinical Sequelae of ASCVD

CAD = CHD

A

HEART
Coronary ARTERY/HEART Disease

Angina

MI

Heart Failure

Arrhythmias

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8
Q

Clinical Sequelae of ASCVD

PAD = PVD

A

LIMBS
Peripheral ARTERIAL / VASCULAR Disease

Intermittent Claudication

Critical Limb Ischemia

GANGRENE

Acute Limb Ischemia

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9
Q

_ASCVD
Etiologies of Vascular Disease
_

5

A

IntraCRANIAL Atherosclerosis

Carotid Plaque
with arteriogenic emboli

Carotid Stenosis
causing flow REDUCTION

Cardiogenic EMBOLI

ARTERY SPASM

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10
Q

ASCVD
Fluid Mechanics Across Stenoses

A

Resistance is
INVERSELY RELATED
to SQUARE of Cross-sectional Area

Small changes in luminal area
VVV
LARGE RESISTANCE & PRESSURE GRADIENT changes
across stenosis

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11
Q

​Coronary Artery Disease

What affects:
OXYGEN SUPPLY

A
  • *Arterial pO2**
  • *Oxygenation + Hemoglobin Stores**
  • *Diastolic Filling Time**
  • *HR**

Coronary BLOOD FLOW

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12
Q

​Coronary Artery Disease

What affects:
OXYGEN DEMAND

A

HEART RATE

Myocardial CONTRACTILITY

Ventricular Wall Tension

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13
Q

Cerebrovascular Disease

What does
CPP

equal & stand for?

A

CPP = Cerebral Perfusion Pressure
driving force for cerebral capillary

CPP = MAP - ICP

MAP = Mean Arterial Pressure

ICP = Intracranial Pressure

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14
Q
  • *Cerebrovascular Disease**
  • *Ischemic Cycle**

↓CCP
Directly affects what?

A

CPP = Cerebral Perfusion Pressure

↓CPP –> ↑VD

VD = Vasodilation

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15
Q
  • *Cerebrovascular Disease**
  • *Ischemic Cycle**

ICP
Directly affects what?

A

ICP = Intracranial Pressure

ICP –> CPP

CPP = Cerebral Perfusion Pressure

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16
Q
  • *Cerebrovascular Disease**
  • *Ischemic Cycle**

VD
Directly affects what?

A

VD = Vasodilation

VD -> ↑CBV

CBV = Cerebral Blood Volume

CBV ~ 150
skull limits tolerance for increased CBV

17
Q
  • *Cerebrovascular Disease**
  • *Ischemic Cycle**

CBV
Directly affects what?

A

CBV = Cerebral Blood Volume

CBV -> ↑ICP

ICP = Intracranial Pressure

18
Q

Collateral Circulation

A

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

19
Q

INFARCTION

A

Irreversible CELL DEATH / NECROSIS
Caused by:
Severe / Prolonged ISCHEMIA

For Brain:
4-10 minutes

Heart:
20 minutes

20
Q

Ischemic Penumbra

A

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