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Cardio Exam 1 > 10 - Cardiovascular Pathology II > Flashcards

10 - Cardiovascular Pathology II Flashcards

1
Q

Define ischemia

A
  • Reversible cellular injury
  • Therapeutic salvage may be possible
  • No tissue death
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2
Q

Define infarction

A
  • Irreversible injury
  • Myofiber coagulative necrosis
  • Once these fibers die, they don’t come back
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3
Q

What are the presenting factors in ischemic heart disease (IHD)?

A
  • Angina pectoris
  • Myocardial infarction
  • Chronic IHD with heart failure
  • Sudden cardiac death
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4
Q

How does IHD lead to heart failure?

A

Cardiac myocytes weaken, atrophy, leads to heart failure

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5
Q

What is myocardial ischemia?

A
  • Insufficient oxygen supply to myocardial fibers
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6
Q

Is myocardial ischemia reversible?

A

Yes

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7
Q

What causes myocardia ischemia?

A

Decreased myocardial blood supply and/or Increased myocardial oxygen demand

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8
Q

There are three types of agina pectoris - what are they?

A
  • Stable (typical) angina
  • Unstable or crescendo angina
  • Prinzmetal variant angina
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9
Q

Describe stable (typical) angina

A
  • Most common form, produced by physical activity, emotional excitement, or any other cause of increased cardiac workload resulting in an imbalance in coronary perfusion relative to myocardial demand.
  • Relieved by rest or administering nitroglycerin.
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10
Q

Describe unstable or crescendo angina

A
  • Pattern of increasingly frequent pain, often of prolonged duration, that is precipitated by progressively lower levels of physical activity or that even occurs at rest.
  • Caused by the disruption of an atherosclerotic plaque with superimposed partial thrombosis and possibly embolization or vasospasm (or both).
  • Unstable angina thus serves as a warning that an acute MI may be imminent.

Example
- Sitting on the couch and you start getting chest pain

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11
Q

Describe prinzmetal variant angina

A
  • Uncommon, episodic myocardial ischemia that is caused by coronary artery spasm.
  • The anginal attacks are unrelated to physical activity, heart rate, or blood pressure.
  • Responds promptly to vasodilators, such as nitroglycerin and calcium channel blockers.
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12
Q

What is the ABPI?

A

Ankle brachial pressure index

  • Assesses risk of peripheral artery disease (blockage in arms/legs)
  • Compares your blood pressure measured at your ankle with your blood pressure measured at your arm
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13
Q

What does ABPI tell you? What does a high ABPI tell you?

A
  • An ABPI number below 0.9 can indicate calcification or narrowing/blockage of the arteries in your legs, leading to circulatory problems, heart disease or stroke.
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14
Q

How can ABPI be used as a predictor for mortality?

A

ABPI may be an independent predictor of mortality, as it reflects the burden of atherosclerosis

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15
Q

What is the most important form of IDH?

A

Myocardial infarction

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16
Q

How many people suffer from an MI annually in the US?

A

1.5 million

Nearly 10% of myocardial infarcts occur in people under age 40, and 45% occur in people under age 65. African Americans and whites are equally affected.

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17
Q

Are men or women at a higher risk?

A

Men

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18
Q

What contributes to the rising trend of MI in women?

A
  • The decrease of estrogen following menopause is associated with rapid development of CAD, and IHD is the most common cause of death in elderly women
  • Postmenopausal hormonal replacement therapy is not currently felt to protect against atherosclerosis and IHD
  • Once you reach the age of 70, the rate of MI in men and women is equal
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19
Q

What are the symptoms of MI?

A
  • Chest pain
  • Dyspnea and diaphoresis (SOB and sweating)
  • Weakness, light-headedness, nausea, vomiting, palpitations
  • Loss of consciousness and sudden death
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20
Q

Describe the chest pain seen in MI

A
  • Levine’s sign: clenching their fist over the sternum.
  • Pain radiates most often to the left arm, but may also radiate to the lower jaw, neck, right arm, back, and epigastrium, where it may mimic heartburn.
  • Diabetics can have “silent MI’s” due to neuropathy
    = Very elderly do not usually have the typical presentation
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21
Q

How does an EKG change due to MI?

A
  • ST segment depression or T wave inversion (suspicious for ischemia)
  • ST segment elevation (indication of MI)
  • Non-diagnostic or normal ECG (need to then check enzymes)
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22
Q

What are the two serum markers we look for?

A
  • Troponin (from cardiac muscle)

- CK-MB (creatinine kinase)

23
Q

Which enzyme will peak first?

A

Creatinine kinase (0-1 day)

Troponin (1-2 days)

24
Q

What is the most important consideration for treating an MI?

A

TIMING TIMING TIMING

25
Q

Why is timing so important?

A
  • If you get to your patient in a half hour and you can reperfused the tissue, you have a chance of salvaging the myocardium and you can actually prevent any cell death
  • If hours goes on and you don’t get to your patient, you will not be able to prevent an MI – cell death will occur
26
Q

What determines the severity of an MI?

A
  • The size of the vascular bed perfused by the obstructed vessels
  • The duration of the occlusion
  • The metabolic/oxygen needs of the myocardium at risk
  • The extent of collateral blood vessels
  • The presence, site, and severity of coronary arterial spasm
  • Other factors, such as heart rate, cardiac rhythm, and blood oxygenation
27
Q

What is the breakdown of arteries occluded in MIs?

A
  • Left anterior descending coronary artery (40-50%)
  • Right coronary artery (30-40%)
  • Left circumflex (15-20%)
28
Q

Describe a left anterior descending coronary artery MI

A

infarcts involving the anterior wall of left ventricle near the apex; the anterior portion of ventricular septum; and the apex circumferentially

29
Q

Describe a right coronary artery MI

A

infarcts involving the inferior/posterior wall of left ventricle; posterior portion of ventricular septum; and the inferior/posterior right ventricular free wall in some cases

30
Q

Describe a left circumflex artery MI

A

infarcts involving the lateral wall of left ventricle except at the apex

31
Q

What will we see within 1/2 to 4 hours post MI?

A

Wavy red fibers (see slide 61 for image)

32
Q

What will we see within 12-24 hours post MI?

A

Early coagulation necrosis

33
Q

What will we see within 1-3 days post MI?

A

Peak neutrophil levels

34
Q

What will we see within 3-7 days post MI?

A

Myocardial rupture

  • All the mechanisms of wound healing have not occurred yet
  • The actual site of the MI can rupture

KNOW THIS

35
Q

What will we see after a couple months post MI?

A

Over a couple months, the wound healing will take over

Dense white tissue will form in the wall of the heart

36
Q

List the possible complications following acute MI

A
  • Contractile dysfunction
  • Arrhythmias
  • Myocardial rupture
  • Pericarditis
  • Right ventricular infarction
  • Infarct extension
  • Infarct expansion
  • Mural thrombus
  • Ventricular aneurysm
  • Papillary muscle dysfunction or rupture
  • Progressive late heart failure
37
Q

What are the three types of myocardial rupture?

A
  • Rupture of the free wall of the left ventricle
  • Rupture of the papillary muscle
  • Rupture of the ventricular septum
38
Q

What does a rupture of the free wall of the left ventricle lead to?

A

Cardiac tamponade

Compression of the heart by an accumulation of fluid in the pericardial sac

39
Q

What does a rupture of papillary muscle lead to?

A

Acute mitral valve incompetence

40
Q

What does a rupture of the ventricular septum lead to?

A

Acutely acquired VSD (ventricular septal defect)

Eventually causes right heart failure

41
Q

What is pericarditis?

A

Inflammation of the pericardium

  • Occurs over time following an MI
  • The area of the MI rubs against the pericardium causing inflammation
42
Q

What is delayed Dressler’s syndrome?

A
  • An autoimmune inflammatory reaction to myocardial neo-antigens that form as a result of an MI
  • Typically occurs 2 weeks post-myocardial infarction (up to a few months)
43
Q

What is a ventricular aneurysm?

A
  • A complication occurring post-MI
  • Arises from a patch of weakened tissue in a ventricular wall
  • Balloon or bubble filled with blood pouches out
  • Usually doesn’t burst, but can block blood flow out of the heart
44
Q

What are some non-cardiac complications of MI?

A
  • Acute pulmonary edema and congestion
  • Hepatic congestion (acute and chronic)
  • Splenic congestion
  • Renal failure (congestive and/or ischemic)
  • Systemic thrombo-embolism
  • Cerebrovascular insufficiency (due to not pumping enough blood to take care of your brain)
45
Q

What is the prognosis of a patient who has had an MI?

A
  • 16% mortality within 30 days
  • 5% mortality per year after that due to…
    • 33% sudden death
    • 33% re-infarction
    • 33% CHF
46
Q

Describe the etiology of coronary heart disease

A

Coronary heart disease is responsible for 1 in 5 deaths in the U.S.

  • Massive killer
  • Due to arthrosclerosis and coronary artery disease
47
Q

What are therapeutic options for heart failure?

A 
1 - Preventative measures
2 - Coronary care unit at hospital
3 - Thrombolytic therapy 
4 - Stent placement 
5 - CABG (coronary artery bypass graft)
48
Q

What are the preventative measures?

A
  • Diet
  • Not smoking
  • Blood pressure control
  • Exercise

An ounce of prevention = a pound of

49
Q

What is a thrombolytic therapy?

A

TPA

Give ASAP after occlusion to dissolve the clot

50
Q

How many patients in the US have a CABG each year?

A

400,000

51
Q

What do we make grafts out of?

A
  • Reversed autologous saphenous vein

- Left internal mammary artery (the only artery in the body that isn’t affected by artherosclerosis)

52
Q

How long does a saphenous vein graft last?

A

Long-term patency (openness) of saphenous vein grafts is only 50% at 10 years

53
Q

How long a mammary artery graft last?

A

Greater than 90% of internal mammary artery grafts are patent (open) at 10 years.

Cardio Exam 1 (15 decks)

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