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CVPR Unit 2 > Lecture review > Flashcards

Lecture review Flashcards

1
Q

What contributes to coronary blood flow rate?

A
  1. perfusion pressure
  2. perfusion time
  3. vascular resistance
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2
Q

What contributes to myocardial O2 supply?

A

Coronary blood flow rate

Oxygen content of blood

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3
Q

As perfusion goes ↓, resistance vessels _____________
If perfusion goes ↑, resistance vessels _____________

what is this process called?

A

As perfusion goes ↓, resistance vessels dilate, so flow is maintained in spite of lower pressure

If perfusion goes ↑, resistance vessels constrict, so you don’t overperfuse the tissue

  • AUTOREGULATION
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4
Q

As perfusion goes ↓, resistance vessels _____________
If perfusion goes ↑, resistance vessels _____________

what is this process called?

A

As perfusion goes ↓, resistance vessels dilate, so flow is maintained in spite of lower pressure

If perfusion goes ↑, resistance vessels constrict, so you don’t overperfuse the tissue

  • AUTOREGULATION via arteriolar resistance vessels
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5
Q

What happens to pressure if stenosis increases?

A

P will drop (across the stenosis)
ie: 100 –> 70

body can compensate with arteriolar resistance vessels

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6
Q
  • Oxygen supply may be compromised by what two things?
A

Anemia: less hemoglobin per ml blood

Hypoxemia: incomplete saturation of hemoglobin

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7
Q

What happens to perfusion P with hypotension?

A

decreased perfusion pressure

- ie hypovolemia (massive bleeding) or septic shock

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8
Q

Cardinal symptom of acute MI

- what should we keep in mind though?

A

severe unremitting chest discomfort at rest (not angina) - more severe, longer)

  • 25-30% of MIs are silent
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9
Q

Cardinal symptom of acute MI

- what should we keep in mind though?

A

severe unremitting chest discomfort at rest (not angina) - more severe, longer)

  • 25-30% of MIs are silent
  • 1/3 of pts die suddenly
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10
Q

What mediators are released in AMI that can result in pain?

A

Adenosine, lactate from ischemic myocardial cells onto local nerve endings

but ischemia in AMI persists → necrosis → substances accumulate → activate nerves for longer periods

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11
Q

Possible Physical findings of AMI:

A

Possible Physical findings of AMI: (173)

- S4
- S3

Systolic murmur sometimes if:
○ Ischemia induced papillary muscle dysfxn → mitral valvular insufficiency (regurg)
○ Infarct ruptures through IV septum → VSD

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12
Q

• Drugs to treat coronary heart disease:

A 
○ Lipid-modifying:	
- Statins
○ Anti-platelet: 
- Aspirin, clopidogrel
○ Anti-anginal:		
- Nitrates, beta blockers, CCBs
○ LV dysfunction:	ACEI or ARBs
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13
Q

• Drugs to treat coronary heart disease:

A

○ Lipid-modifying:
- Statins

○ Anti-platelet:
- Aspirin, clopidogrel

○ Anti-anginal:
- Nitrates, beta blockers, CCBs

○ LV dysfunction:
- ACEI or ARBs

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14
Q

Primary prevention of anginal attacks

A

start a statin if LDL cholesterol > 190mg/dl

  • aspirin
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15
Q

Secondary prevention after MI:

A
  • Aspirin with or w/o clopidogrel or other thienopyridines (clop/thi esp after MI)
    • Statins
    • Beta blockers
    • ACE inhibitor
    • Smoking cessation
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16
Q

Profibrinolytics

  • examples
  • good to treat _____
A

profibrinolytics: tPA, uPA

Good to treat STEMI (not UA, or NSTEMI)

17
Q

Problems with stents

A

Stents are thrombogenic, so a combo of oral antiplatelet agents (aspirin + clopidogrel) is crucial after implantation

18
Q

Which vessels are commonly used for grafts?

A

○ Internal mammary artery

○ Saphenous vein

19
Q

Primary prevention of anginal attacks

A
  • start a statin if LDL cholesterol > 190mg/dl

- aspirin

20
Q

How to acutely treat stable angina vs unstable angina

A

stable:

  • Anti-anginal (nitrates, BBs)
  • Anti-hypertensives
  • Statins
  • Antiplatelets (aspirin)
  • if symp not relieved –> cor angiography

Unstable:

  • Hospitalization
  • IV nitroglycerin
  • Usually early Cath / cor intervention
  • Anti-anginal (nitrates, BBs)
  • AntiTHROMBOTICS (aspirin, heparin ect)
21
Q

How to acutely treat stable angina vs unstable angina vs acute STEMI

A

stable:

  • Anti-anginal (nitrates, BBs)
  • Anti-hypertensives
  • Statins
  • Antiplatelets (aspirin)
  • if symp not relieved –> cor angiography

Unstable:

  • Hospitalization
  • IV nitroglycerin
  • Usually early Cath / cor intervention
  • Anti-anginal (nitrates, BBs)
  • AntiTHROMBOTICS (aspirin, heparin ect)

AMI:

  • Immediate aspirin, nitroglycerin, maybe BBs
  • Reperfusion therapy ASAP: Coronary angioplasty if poss, or thrombolytic if not.
22
Q

Activated SMC actions

A
  1. ↑ed inflammatory cytokines (IL-6, TNF) → ↑ed Leukocyte Prolif and LAM expression
  2. ↑ed ECM synthesis
  3. ↑ed migration/prolif into subintima (almost like a malignancy)
23
Q

Good fxn of NO is activating cGMP to vasodilate, what is a negative fxn?

A

Recognize that abnormal endothelium and promote inflammatory state

24
Q

How is activation of SNS in normal endothelium beneficial? How can it be bad?

A

Normal: activate SNS → ↑ blood flow → ↑ NO → vasodilate
- relaxation effect of NO outweighs direct a-adrenergic constrictor effect of catecholamines

Abnormal endo: impaired NO → inappropriate vasoconstriction

25
Q

Atheroembolism vs Thromboembolism

A

atheroembolism: embolism from an atherosclerotic plaque

26
Q

Atheroembolism vs Thromboembolism

A

Both are embolism from an atherosclerotic plaque

Atheroembolism:

  • stroke, opthalmic artery.
  • cholesterol makes the occlusion

Thromboembolization:
-plaque dislodges from rupture
from L atrial appendage in setting of afib
- plaque rupture and occlusion via platelets and shizz

27
Q

2 manifestations of CAD

A

Myocardial infarction and chronic stable angina

28
Q

2 manifestations of CAD

A

Myocardial infarction
and
chronic stable angina

29
Q

2 manifestations of CAD

A

Myocardial infarction
and
chronic stable angina

30
Q

2 manifestations of PAD

A

Claudication
and
acute limb ischemia

31
Q

2 manifestations of PAD

A

Claudication
and
acute limb ischemia

*note: claudication is upon exertion

32
Q

Treatments:
Venous thrombosis
Arterial Thrombosis

A

Venous thrombosis
- anti-coagulation (bc fibrin rich)

Arterial Thrombosis
- antiplatelets

33
Q

Normal paracrine and endocrine functions of the endothelium

A

a) Defend against thrombosis. (For example, by producing antithrombotic molecules such as heparans and tissue plasminogen activator tPA.)
b) Provide anti-inflammatory properties. (For example, by downregulating expression of cell adhesion molecules thereby decreasing leukocyte recruitment.)
c) Promote vasodilatation (For example, by secreting vasodilatory molecules such as nitric oxide and prostacyclin.)

CVPR Unit 2 (6 decks)

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