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SRNAAnatomy II > Lilly Ch 5-7 Atherosclerosis, Ischemic Heart Disease, ACS > Flashcards

Lilly Ch 5-7 Atherosclerosis, Ischemic Heart Disease, ACS Flashcards

1
Q

Leading cause of mortality/morbidity in the

developed world______

A

Atherosclerosis

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2
Q

**Atherosclerosis is a _______

A

Chronic inflammatory condition involving endothelial cells, smooth muscle cells, lipids, macrophages and thrombosis

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3
Q

3 layers of the Normal Arterial Wall (MIA)

A

3 layers:
Intima (interna)
Media
Adventia (externa)

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4
Q

**What are the different parts of the Intima Layer **

A

Endothelial cells
– Basement membrane
– Internal elastic lamin

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5
Q

What are the different parts of the Media layer

A

– Smooth muscle cells

– External elastic lamina

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6
Q

Endothelial cells of the intima in contact with

A

the blood.

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7
Q

_________overlies smooth muscle of the media.

A

Internal elastic lamina

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8
Q

separates media from adventitia

A

External elastic lamina

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9
Q 
The endothelial cells
Some Vasodilators (2)
Some Vasoconstrictors (1)
A 
Produce substances that modulate smooth muscle - 
Vasodilators
- Prostacyclin
- nitric oxide (NO)
Vasoconstrictors:
• endothelin
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10
Q

In addition, Endothelial cells

A

oppose local inflammation

Resist leukocyte adhesion

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11
Q

***Do smooth muscle cells play a role in inflammation. Explain

A 
– They produce Vasoconstriction/dilation
– Produce extra cellular matrix
– Synthesize vasoactive inflammatory mediators:
• IL-6
• TNF- α
Promote leukocyte proliferation
Induce endothelial expression of LAM (leukocyte adhesion
molecules)
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12
Q

*****2 vasoactive inflammatory MEDIATORS

A

Il-6

TNF-α

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13
Q

***Explain the 6 steps of Plaque evolution

A

Evolution of Plaque
- 1. Various stressors cause endothelial dysfunction
allows entry of lipids into subendothelial space
2 and 3 - Oxidized lipids cause cytokine release from
endothelium = chemoattractant for monocytes
4 - Monocytes take in lipids, become foam cells
5 - Impaired foam cells produce superoxide anion O2-
and MMP (Matrix Metalloproteinases)
6- Smooth muscle cells migrate into intima
7 - Muscle cells divide and produce matrix, enlarging
plaque
8-Some muscle cells undergo apoptosis, fibrofatty
lesion forms, lipid core with fibrous cap

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14
Q

**Endothelial Stressors
• Endothelial dysfunction from cell injury secondary to various
•* Laminar flow favors production of NO which is a
–
–
–
****Turbulent flow impairs ____________ functions
****Places where turbulent flow occurs? ***

A 
Endothelial Stressors
• Endothelial dysfunction from cell injury secondary to  various agents, chemical irritants, physical forces,
hydrodynamic stress
• Laminar flow favors production of NO
– Vasodilator
– Inhibits platelet aggregation
– Has anti-inflammatory effects
Turbulent flow impairs atheroprotective functions
– Occurs at bifurcations
• ***Common carotid
• ***Left coronary artery
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15
Q

Stages of Plaque Development

A
  • Fatty streak forms
  • Plaque forms
  • Plaque rupture with Thrombus
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16
Q

Describe how inflammation alters plaque stability

A

Inflammatory cytokines stimulate foam cells to
secrete ***MMP – Breaks down collagen & elastin – Weakens fibrous cap predisposing it to rupture
(Thin fibrous cap & large lipid core predispose
to rupture and thrombus formation)

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17
Q

Stable plaque

Vulnerable Plaque

A

thick

thin

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18
Q

**Biomarkers of Risk: Homocysteine

A
  • Elevated levels found in coronary, cerebral & PAD

– Promotes oxidative stress, vascular inflammation & platelet aggregation

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19
Q

**Biomarkers of Risk: Lipoprotein

A

– Variant of LDL
– Competes with normal plasminogen activity
– Encourages inflammation & thrombosis

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20
Q

**Biomarkers of Risk: CRP

A

– Elevated in systemic inflammation with atherosclerosis
– High sensitivity predictor for MI, CVA, PAD & sudden cardiac
death

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21
Q

**Ischemic Heart Disease **

A

Arises from an imbalance between myocardial

oxygen supply & demand

22
Q

***Determinants of O2 SUPPLY

A 
Coronary blood flow
Coronary Perfusion Pressure
Coronary vascular resistance
External compression
Intrinsic Regulation/tone
Local Metabolites
Endothelial factors
Neural innervation
23
Q

**Myocardial Oxygen Supply

• Depends on 2 things

A

coronary flow And O2 content of the blood
directly proportional to Pressure &
inversely proportional to Resistance

24
Q

**O2 content determined by

A

Hb & degree of systemic oxygenation

25
Q

***** Coronary flow

A

directly proportional to Pressure and Resistance relationship Q =P/R

26
Q

***Coronary Perfusion Pressure predominace of

A

coronary perfusion takes place during diastole (unlike systemic arteries in systole)
Systolic coronary flow in smallr branches IMPAIRED BY COMPRESSION of CONTRACTING MYOCARDIUM

27
Q

**Perfusion pressure approximated by

A

Aoric Diastolic Pressure

28
Q

**Conditions that Decrease aortic diastolic pressur e

A

decrease coronary perfusion and O2 supply.

29
Q

**CORONARY VASCULAR RESISTANCE influenced by 2 factors

A

EXTERNAL COMPRESSION

INTRINSIC CORONARY VASCULAR TONE

30
Q

***CVR influncer: external compresion

A

Myocardial contraction ↑intraventricular pressure
– Subendocardium adjacent to ↑intraventricular
pressure has ↓perfusion
– Subendocardium most vulnerable to ischemic change

31
Q

***CVR influencer: Intrinsic Coronary Vascular Tone

A

– Heart cannot ↑ O2 extraction : ↑demand must be met

by ↑flow ( controlled by coronary vascular Tone)

32
Q

**Intrinsic Coronary Vascular Tone (MEN)

Influenced by 3 items:

A 
A) METABOLITES
 During hypoxia, ADP & AMP accumulate, degrade into
Adenosine = vasodilation =↑flow
B) ENDOTHELIAL FACTORS
– Prostacyclin & NO = vasodilators
– Endothelin 1 = vasoconstrictor
C) NEURAL INNERVATION 
– Sympathetic effects on receptors in coronary vessels
α1 = vasoconstrict
β2 = vasodilate
33
Q

**3 Determinents of Oxygen demand (HCV)

A

Ventricular Wall stress
HR
Contractility

34
Q

*Ventricular Wall Stress caused by
Related to :
Formula is ?

A

1) Stretching force on myocardial fibers pulling them apart 2) and the energy expended in opposing that force.
• Wall stress related to: – Intraventricular pressure (P) – Radius of the ventricle (r) – Wall thickness (h)
= Px R/ 2h

35
Q

**Pathophysiology of Ischemia from
atherosclerosis
• The 2 most important factors:

A

1) FIXED VESSEL NARROWING
– Radius has biggest effect on flow in Poiseuille’s Law:
Q= Change in P x Pi X r ^4 / 8 nL

2)ABNORMAL VASCULAR TONE
– Dysfunctional endothelial cells in atherosclerosis fail to
release vasodilators
– vasoconstriction occurs instead = ischemia
– Also loss of antithrombotic effect = ↑risk of ischemia

36
Q

**4 consequences of ISCHEMIA (SACC)

A

Consequences of Ischemia

  1. SOB
  2. Chest pain
  3. Arrhythmias
  4. Cardiogenic Shock
37
Q

***SOB with ISCHEMIA how? (TICC)

A

SOB
– Ischemia results in ↓ contraction & relaxation
– Causes elevated LV diastolic pressure
– Transmitted back to pulmonary capillaries
– Causes pulmonary congestion & SOB

38
Q

***Chest Pain with ISCHEMIA how ?

A

– Accumulated metabolic products activate pain receptors

39
Q

**Arrhythmias with ISCHEMIA how?

A

– Damaged myocytes undergo altered ion transport

40
Q

***Cardiogenic Shock with ISCHEMIA how?

A

– Impaired myocardial function =↓ C.O.

41
Q

***3 forms of Angina (SUV)

A

Three forms: – Stable – Variant – Unstable

42
Q

**Stable angina

A
  • Transient
  • Precipitated by physical activity / emotional stress
  • Relieved by rest (within a few minutes)
  • EKG: temporary ST Depression
43
Q

** VARIANT ANGINA

A

Pain at rest
• Caused by spasm, not ↑O2 demand
• EKG: ST elevation
• a.k.a. “Prinzmetal Angina

44
Q

**UNSTABLE ANGINA

A

Increased frequency & duration of Pain at Rest
• EKG: ST depression
• High risk of progression to MI if untreated

45
Q

***Non-ST segment elevation MI

A

• Partial occlusion of main coronary artery, or total
occlusion of small branch
• Partial thickness wall damage
• ST seg depression and/or T wave inversion

46
Q

**What are the 3 markers of NSTEMI and STEMI?

A

Markers: – Troponin I – CKMB – troponin T – (also ↑wbc, ESR, CRP)

47
Q

*****ST elevation MI

Comment on thickness

A

Complete acute thrombus occlusion of main
coronary vessel
• Full thickness wall damage

48
Q

***** EKG changes of STEMI

A
  • ST elevation - indicates full thickness wall injury
  • Pathologic Q - indicates muscle necrosis
  • T wave inversion - indicates muscle ischemia
49
Q 
****ACS summary
Partially occlusive thrombus
EKG  changes :\_\_\_\_\_\_and/or\_\_\_\_\_
If biomarkers POSITIVE \_\_\_\_\_
If biomarkers NEGATIVE \_\_\_\_\_\_\_
A

ST segment depression and/or T- wave inversion
NSTEMI
Unstable angina

50
Q

**ACS summary
Occlusive thrombus
EKG changes :______and___ (later
biomarkers POSITIVE _____

A

ST elevation and Q waves later

STEMI

SRNAAnatomy II (16 decks)

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