Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

8 Cardiac Pathology > 8.1 Ischemic Heart Disease (IHD) > Flashcards

8.1 Ischemic Heart Disease (IHD) Flashcards

1
Q

types of angina (3)

-what’s the difference

A
  1. stable–chest pain on exertion
  2. unstable–chest pain at rest
  3. prinzmetal–episodic chest pain unrelated to exertion (coronary vasospasm)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Difference between angina and MI

A

angina: reversible myocyte damage (less than 20 min ischemia)

MI: myocyte necrosis

-timeframe: after 20 minutes of ischemia, necrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

main immediate cause:

  1. Stable angina
  2. unstable angina
  3. prinzmetal angina
A
  1. 70% stenosis from atherosclerosis
  2. thrombosis formation from plaque rupture, with incomplete occlusion
  3. coronary vasospasm
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How to relieve angina?

is it different for different types of angina?

A
  • Use nitoglycerin for all angina types.
  • Calcium channel blockers also work for prinzmetal angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Angina:

-EKG reading for each angina type

A
  1. Stable and unstable: ST depression
    - subendocardial ischemia
  2. Prinzmetal: ST elevation
    - transmural ischemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

MI: immediate causes

  • most common immediate cause
  • 3 other causes
A
  1. thrombosis from plaque rupture, with full occlusion
  2. coronary vasospasm (prinzmetal’s)
  3. embolism
  4. vasculitis (eg Kawasaki disease)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Does nitroglycerin relieve MI symptoms?

A

No–Nitroglycerin relieves angina, but not MI. This is an important clinical finding.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

List the 3 most likely coronary vessels occluded in MI, starting with most common.

-what areas of the heart does each affect?

A
  1. LAD–anterior wall and anterior septum of LV
  2. RCA–posterior wall, posterior septum, and papillary muscles of LV
  3. Left circumflex–lateral wall of LV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

MI:

initial vs continued phases, as indicated on EKG reading

A
  1. initial phase: subendocardial infarction–ST depression
  2. continued ischemia: transmural infarction–ST elevation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MI:

  • what lab tests to dx (2)
  • timeframe of each
  • advantages/disadvantages
A
  • Cardiac enzymes
    1. Troponin I
  • levels rise 2-4 hrs post-infarct, peak 24 hrs, regress 7-10 days
    2. CK-MB (creatine kinase MB)
  • levels rise 4-6 hrs, peak 24 hrs, regress 3 days
  • Troponin I is gold standard, but cannot detect a reinfarct that occurs before 7-10 days. This is where CK-MB is useful.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

MI treatment:

-list usual drugs (6)

A
  1. Aspirin–antiplatelet to limit thrombosis
  2. Heparin–anticoagulant, limit thrombosis
  3. Nitrates (vasodilate veins+coronary a)
  4. Beta blockers–decrease O2 demand
  5. ACE inhibitor–decrease LV dilation by reducing venous return
  6. tPA–fibrinolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are 2 complications in opening a blocked vessel in MI?

A
  1. contraction band necrosis
    - calcium influx into necrosed cells causes myofibril hypercontraction. (visible as bands on histology)
  2. reperfusion injury
    - return of O2 and inflammatory cells leads to free radical generation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Why do you see increase in cardiac enzymes after opening an occluded coronary artery in MI?

A
  • reperfusion injury
  • free radicals continue to cause myocyte damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

morphologic changes in MI:

  • 4 stages
  • timeframe
A

(see diagram–1 day, 1 week, 1 month)

  1. coagulative necrosis
    - within 1 day
  2. Acute inflammation (neutrophils, then macrophages)
    - 1 day to 1 week
  3. Healing (granulation tissue)
    - 1 week to 1 month
  4. scarring (fibrosis)
    - after 1 month
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MI coagulative necrosis stage

-what complications at this stage?

A

-arrythmia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

MI acute inflammation stage:

-what complications? (4)

A
  1. fibrinous pericarditis (chest pain with friction rub)
    - caused by neutrophil invasion of pericardium
  2. Cardiac tamponade
    - rupture of ventricular free wall
  3. Shunt formation
    - rupture of interventricular septum
  4. Mitral regurg
    - rupture of papillary muscle
17
Q

MI scarring stage (fibrosis)

-what complications? (3)

A
  1. aneurysm (weakened wall)
  2. mural thrombus
  3. Dressler syndrome (Ab against pericardium, autoimmune)
18
Q

Dressler syndrome

A
  • autoimmune Ab against pericardium
  • occurs post-MI during the scarring/fibrosis stage
  • causes pericarditis
19
Q

What is sudden cardiac death?

-most common cause

A
  • Death within 1 hr of cardiac problems, with or w/o symptoms
  • usu due to ventricular arrhythmia from acute ischemia
20
Q

Chronic ischemic heart disease

A
  • poor myocardial fxn due to chronic ischemic damage (with or w/o infarction)
  • leads to CHF

8 Cardiac Pathology (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions