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Human Pathophyisology: Midterm > Lecture 6: CV Pathophysiology IV > Flashcards

Lecture 6: CV Pathophysiology IV Flashcards

1
Q

What factors influence myocardial oxygen delivery?

A
  • O2 carrying capacity of blood
  • coronary blood flow
  • coronary perfusion pressure
  • coronary vascular resistance
  • metabolic factors (adenosine, lactate, H+, CO2 - vasodilators)
  • endothelial factors (NO and prostacyclin vasodilator, endothelin-1 constricts)
  • neural factors (SNS leads to vasodilation because of increased O2 demand, PNS has no effect)
  • atherosclerosis
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2
Q

What influences myocardial oxygen demand?

A
  • HR
  • cardiac contractility
  • ventricular wall stress (enlarged ventricles need more O2; Law of Laplace)
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3
Q

What are the sex differences for CAD?

A
  • leading cause of death for both
  • more common in women
  • estrogen has an anti-inflammatory effect but not if its synthetic
  • men have more localized plaques –> easier to visualize and treat but more symptomatic
  • women are more likely to have extensive plaques that minimize obstruction to blood flow
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4
Q

chest pain; too brief to cause cell death

A

angina pectoralis

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5
Q

irreversible necrosis of cardiac muscle cells

A

MI

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6
Q

What can be used to treat after an episode of angina?

A
  • lifestyle changes
  • vasodilators
  • anti-coagulants
  • beta-blockers
  • statins
  • PCI (angioplasty and stenting)
  • coronary bypass surgery
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7
Q

insufficient blood flow (but not death)

A

ischemia

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8
Q

What is the difference in anterior and posterior wall MIs?

A

anterior - association with SNS; increased HR, contractility, and BP
posterior - association with vagus nerve; decreased HR an BP

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9
Q

What is angina typically preceded by?

A

increase in O2 demand (exercise, stress, sympathetic nerve activation)

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10
Q

What is stable angina?

A

when atherosclerotic coronary vessels reduce blood flow to critical levels

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11
Q

What is unstable angina?

A

when a clot causes ischemia but breaks down before necrosis occurs

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12
Q

How do you distinguish an MI from unstable angina?

A

enzymes tests that show enzymes released from dead myocardial cells

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13
Q

What events lead to coronary thrombosis?

A
  • exposure of sub endothelial collagen (injury)
  • turbulent flow contributes to clotting
  • hemorrhage narrows vessel
  • dysfunction of endothelium (low NO and prostacyclin levels)
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14
Q

Describe the symptoms of ischemia in men vs. women.

A

men - angina before and during MI
women - fatigue, sleep disturbances, and indigestion prior to an MI and SOB, weakness, fatigue, cold sweat, nausea during an MI

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15
Q

What changes occur on a molecular level during an MI?

A
  • less ATP produced slows ion pumps leading the cell death
  • lactic acid accumulates –> lower pH (results in functional changes in myocardium)
  • rising K+ levels can cause arrhythmias
  • rising Ca+ levels activate lipase that lead to cell death
  • inflammation and myocardial edema
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16
Q

What changes occur on a molecular level after an MI?

A

-dead cells are cleared by macrophages and replaced by fibrotic scar tissue within 7 weeks

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17
Q

What changes occur on a functional level after an MI?

A
  • decreased contractility/CO
  • “stunned” or “hibernating” cells may region function
  • ventricular remodeling (dilation of ventricle increases CO)
  • ultimately will lead to heart failure though
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18
Q

What does a non-STEMI on an ECG indicate?

A
  • partial occlusion or transient total occlusion of a vessel
  • mild ischemia
  • associated with high risk of MI but lower risk of death
19
Q

What does a STEMI on an ECG indicate?

A
  • total occlusion of a blood vessel

- greater risk of death

20
Q

What are the serum markers for MI and what do they indicate?

A

creatine kinase - found in heart cells, indicative of damage
myoglobin - early indication of MI but less specific (found in other muscle)
troponin T and troponin I - cardiac specific
lactate dehydrogenase - peaks 3-5 days post MI

21
Q

What can be used to treat an MI acutely?

A
  • PCI (angioplasty and stenting)
  • aspirin or heparin
  • anti-ischemic therapy to decrease O2 demand including nitrates (veNOdilation), beta-blockers (decrease HR), calcium channel blockers (decrease HR and contractility)
22
Q

What are potential causes of arrhythmia related to MI?

A
  • damage to conduction pathway
  • pH and ion permeability changes
  • autonomic stimulation (PNS or SNS)
23
Q

When does congestive heart failure occur and what are the consequences?

A
  • develops when >40% of LV is damaged
  • severely decreased CO and hypotension
  • leads to further ischemic damage
  • decreased SV leads to LV hypertrophy, which increased O2 demand
  • mortality is >70%
24
Q

What are some treatments for CHF?

A
  • ionotropic agents (increase contractility and CO)
  • arterial vasodilators (decrease afterload)
  • intraaortic balloon pump (helps perfuse coronary and peripheral tissues
25
Q

What are some long-term treatments for MI?

A
  • daily aspirin
  • beta-blockers
  • ACE inhibitors
  • statins/cholesterol-lowering drugs
  • stop smoking
  • exercise
26
Q

What is SCD and what causes it?

A

sudden cardiac death; results from cardiac arrhythmia or dramatic bradycardia; often a result of CAD

27
Q

Treatment for SCD?

A

defibrillation ASAP - brain dead can occur within 4-6 min after cardiac arrest

28
Q

What are some triggers for cardiac events?

A
  • anything that activates SNS (waking up, emotional stress, physical exertion, etc.)
  • drugs
  • exposure to air pollution
29
Q

inability of the heart to pump blood at a sufficient rate to meet metabolic demands of the body (forward failure) or the ability to do so only under abnormally high cardiac filling pressures (backward failure)

A

congestive heart failure

30
Q

What can cause CHF?

A
  • MI

- pulmonary hypertension (increases after load of right heart)

31
Q

What can cause pulmonary hypertension?

A
  • atherosclerosis
  • drug use
  • congenital factors
  • sleep apnea
32
Q

What factors influence CO?

A
  • HR
  • SV
  • preload
  • afterload
  • ventricular wall stress
  • contractility
33
Q

type of heart failure that results in an inability to pump blood out of the heart; typically due to impaired myocardial contractility or increased afterload

A

systolic dysfunction

34
Q

type of heart failure with problems with filling; often due to an inability of the ventricle relax during diastole or ventricular stiffness

A

diastole dysfunction

35
Q

How does the body compensate during heart failure?

A
  • increase EDV by increasing blood volume or venous return
  • increased thirst and fluid retention
  • increase SNS activity and contractility
  • cardiac hypertrophy (increases ability to pump)
36
Q

How do the body’s compensatory mechanism for CHF become detrimental over time?

A
  • increased blood volume leads to pulmonary congestion
  • pulmonary edema leads to dyspnea or orthopnea and decreased O2 availability
  • peripheral edema, especially in feet
  • ascites, enlargement of liver, GI discomfort
37
Q

How can you treat CHF?

A
  • ACE inhibitors (most important)
  • diuretics
  • inotropic drugs (increase force of contraction)
  • beta-blockers
  • vasodilators
38
Q

How is blood supply in the brain protected?

A
  • anastomoses (interconnections between blood vessels, aka. circle of Willis)
  • only 20% of people have a complete circle of Willis –> decrease chance of stroke
39
Q

when a portion of the blood flow to the brain is blocked (85%)

A

ischemic (occlusive) stroke

40
Q

when a blood vessel in the brain ruptures (15%); often results from congenital abnormalities

A

intracranial hemorrhagic stroke

41
Q

area in which blood flow is at

A

ischemic core

42
Q

area in which blood flow is at 20-50% and cells will remain viable for several hours; target of treatment

A

ischemic penumbra

43
Q

Describe the mechanism of cell death.

A
  • insufficient levels of glucose and O2 causes ATP depletion
  • no ATP for ion pumps means that ion gradient can’t be maintained
  • neuron undergoes anoxic depolarization where concentrations begin to equilibrate
  • neurotransmitters released in massive quantities due to depolarization
  • release of high levels of glutamate is toxic to adjacent neurons
  • when blood flow is restored, oxygen reacts with accumulated substrates, creating free radicals which cause more oxidative injury (reperfusion injury)
44
Q

What are some treatments for strokes?

A

ischemic - thrombolytic drugs (must be administered within 3 hours)
hemorrhagic - treated surgically or with blood-clot promoting and anti-hypertensive drugs

Human Pathophyisology: Midterm (6 decks)

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