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System Pathology I -- Roecker > Exam 3: The Heart Pt2 > Flashcards

Exam 3: The Heart Pt2 Flashcards

1
Q

What is a general term that involves any situation involving myocardial injury following myocardial ischemia?

A

Ischemic Heart Disease (IHD)

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2
Q

How fast will significant ischemia cause cardiac dysfunction? What about a myocardial infarction?

A

dysfunction –> w/in 1-2 minutes

M.I.–> w/in 20-40 mins

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3
Q

What do most cases (90%) of Ischemic Heart disease develop following?

A

coronary artery disease = the presence of atheromas within the coronary arteries

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4
Q

We know CAD causes 90% cases of Ischemic Heart Disease, what can cause the other 10%?

A
  1. Reduced Coronary artery blood flow (90%)
  2. increased cardiac demand for blood/oxygen
  3. a reduction in total blood volume
  4. a reduction in red blood cell oxygenation
  5. diminished oxygen-carrying capacity
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5
Q

What related pathologies may cause the “reduced coronary artery blood flow” that may cause Ischemia Heart Disease?

A
  • coronary artery disease

- distributive forms of shock

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6
Q

What related pathologies may cause the “increased cardiac demand for oxygen” that may cause Ischemia? Heart Disease?

A
  • HTN

- Tachycardia

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7
Q

What related pathologies may cause the “reduced blood volume” that may cause Ischemia? Heart Disease?

A

hypovolemic shock

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8
Q

What related pathologies may cause the “reduced oxygenation” that may cause Ischemia? Heart Disease?

A
  • pneumonia
  • COPD
  • congestive heart failure
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9
Q

What related pathologies may cause the “reduced oxygen-carrying capacity” that may cause Ischemia? Heart Disease?

A
  • acute carbon monoxide poisoning

- severe anemia

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10
Q

What is it called when 70% or more of the available cross-sectional diameter of a coronary artery is occluded?

A

critical stenosis–> now become symptomatic

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11
Q

What will one experience who has Critical stenosis of a coronary artery?

A
  • chest pain = angina pectoris; that is provoked by physical activity
  • if at rest and have symptoms = 90% occlusion
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12
Q

What is the most common reason for a sudden (acute) myocardial infarction to occur?

A

acute plaque change of a coronary artery atheroma

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13
Q

What are teh cardiac syndromes that Ischemic Heart Disease may manifest as, regardless of what caused it?

A
  • angina pectoris
  • myocardial infarction
  • sudden cardiac death or chronic ischemic heart disease/CHF
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14
Q

What are the three forms of Angina Pectoris?

A

(aka “chest pain”)

  1. Stable Angina
  2. Prinzmetal Angina
  3. Unstable Angina
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15
Q

T/F. The level of ischemia associated with angina pectoris is sufficient enough to cause pain and myocyte death.

A

False—yes it can cause pain, but it does NOT cause myocyte death

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16
Q

What is the typical pain distribution of angina pectoris? How is the pain described?

A

chest, neck, jaw, left shoulder/arm, and epigastric region

as “crushing” or “squeezing” sensation, freq ass. with dyspnea, nausea, and sweating

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17
Q

What involves episodic angina pectoris that is predictably stimulated by increase in physical activity?

A

Stable angina

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18
Q

What is the pain associated with Stable Angina described as? Where does it typically go? How is the pain relieved?

A

“crushing” or “squeezing”

substernal or radiating into left jaw, neck, and arm

relieved by rest or with vasodilatory medications

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19
Q

What angina type occurs at rest and is the result of coronary artery vasospam?

A

Prinzmetal angina (aka variant angina)

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20
Q

What are the risk factors for coronary artery vasospasm associated with Prinzmetal Angina?

A
  • atherosclerotic plalques (CAD)
  • vascular inflammation
  • SNS stimulation
21
Q

Does Prinzmetal angina respond to vasodilatory medications?

A

yes

22
Q

When are myocardial infractions highest during the day? why?

A

b/w 6am and noon

think due to surge of adrenergic stimulation that occurs with awakening

23
Q

What occurs in patients that have a history of stable angina, but are experiencing an increasing severity of their signs and symptoms?

A

Unstable Angina

24
Q

What will Unstable Angina characteristically produce?

A

angina that is increasing in frequency, intensity, and is provoked by less exertion of may even develop at rest

25
Q

In what people is Unstable angina most likely to develop in?

A

patients who develop critical stenosis and freq ass. with development of an acute plaque change or thromboembolism

26
Q

What describes ischemia necrosis of myocardial cells?

A

myocardial infarction (MI, acute myocardial infarction, or heart attack)

27
Q

What are the vast majority of M.I.s caused by?

A

acute thrombosis w/in coronary artery at sites of preexisting atherosclerotic plaques

28
Q

What are risk factors for developing a myocardial infarction?

A
  • HTN
  • male sex
  • post-menopausal females
  • cardiac amyloidosis
  • family Hx
  • smoking
  • sickle cell anemia
  • obesity or metabolic syndrome
  • diabetes mellitus
  • advanced age
  • hypercholesterolemia
  • type A personality (stress)
29
Q

What is the most commonly involved artery to cause a myocardial infarction and is associated with nearly 50% of all M.I.s?

A

left anterior descending (LAD) artery

30
Q

What is the left anterior descending (LAD) artery considered as? why?

A

the “widow maker”–> b/c is ass. with 50% of all M.I.s

31
Q

Where is a myocardial infarction most likely to develop and where will it spread to?

A

first develop at subendocardial zone of heart wall and proceed externally to involve the entire thickness of the cardiac wall

32
Q

Following what, may reperfusion of blood supply to ischemic myocardium occur?

A
  • enzymatic thrombolysis (tPA or tissue plasminogen activator)
  • coronary artery angioplasty and endovascular stent placement
  • placement of bypass graft
33
Q

Reperfusion of blood to previously ischemic myocardium may result in significant myocardial dysfunction, what may this cause?

A
  • increased oxidative stress
  • mitochondrial dysfunction
  • myocyte hypercontracture
  • increased platelet and compliment activity
  • –> all increasing inflammation and irritability–> put at risk of developing prolonged cardiac arrhythmia (“V-fib”)–> may lead to lethal sudden cardiac death
34
Q

When dos a M.I. start to show gross cellular changes?

A

12-24 hrs–> grossly red-blue discoloration becomes evident

if survive–> lesion becomes well-demarcated w/in 10-14 days ane becomes more fibrotic w/in wks of injury

35
Q

When will acute inflammatory cells become evident microscopically at the site of M.I.?
When to macrophages become evident?
What happens in 1-2 weeks? What occurs at 6 weeks?

A

within 1-3 days –> inflam cells

5-10 days–> macrophages are more predominant

1-2 weeks –> area becomes filled with granulation tissue
6 wks–> prominent scar tissue

36
Q

What are the traditional features of an acute myocardial infarction?

A
  • substernal chest pain–> “crushing” sensation that lasts several mins-hrs
  • pain radiates to neck, jaw, epigastric region, or left should and arm

likely to NOT be relieved by vasodilators or rest

37
Q

How is pain from a M.I. distinguishable from pain associated with angina pectoris?

A

with a M.I. that pain will most likely NOT subside with vasodilators (nitroglycerine) or with rest

38
Q

What features besides the pain will inds suffering from a M.I. have?

A
  • dyspnea
  • nauseaous
  • diaphoretic (sweaty)
  • rapid but weak pulse–> “thready”
39
Q

What will massive M.I.s that involved almost half of the myocardium lead to?

A

cardiogenic shock

40
Q

Do women have different features with a M.I.? If so, what?

A

yes

  • nausea
  • dizziness
  • referred pain to back
  • epigastric pain
  • pain in lower thorax
  • dyspnea
  • fatigue
41
Q

What are the two “cardiac markers” that leak out of necrotic myocardial cellular membranes and enter the blood and help with a M.I. diagnosis?

A
  1. Troponins

2. CK-MB

42
Q

What are the most sensitive and most specific cardiac marker for Dx of a M.I.? When do they become elevated and peak? How long do they remain elevated?

A

troponins–> become elevated about 4 hours after M.I. and peak around 24-48 hrs

remain elevated for 10 days (longer than CK-MB)

43
Q

What was historically the cardiac marker for M.I.?

A

CK-MB
- rise w/in 2-4 hrs of M.I.
- peak around 24 hrs
(MAY allow for a more rapid lab confirmation of recent M.I. over troponins)–but use troponins MC now

44
Q

What describes the progressive heart failure that develops secondary to ischemia myocardial injury, such as surviving a myocardial infarction or long-term coronary artery disease?

A

Chronic Ischemic Heart Disease (ischemic cardiomyopathy)

45
Q

When is Chronic Ischemic Heart Disease said to begin?

A

when the compensatory mechanisms begin to fail

46
Q

What may Chronic Ischemic heart Disease involve progessively worsening of?

A
  • angina
  • heart failure (contractile failure)
  • arrhythmias
  • development of M.I.s
47
Q

What does the morphology of Chronic Ischemic Heart Disease involve?

A

prominent LV hypertrophy (concentric) and cardiac fragmentation/dilation may occur in advanced stages

48
Q

What are complicating factors that may worsen the progression of Chronic Ischemic Heart Disease?

A
  • presence of cardiac fibrosis form previous sites of MIs
  • cardiac mural thrombi–> embolize due to sluggish blood flow
  • coronary arteries contain sig. luminal stenosis –> cause cont myocardial injury

System Pathology I -- Roecker (14 decks)

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