Brainscape's Knowledge GenomeTM

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


See full index

Pathology-Cardio > introduction to cardiac pathology > Flashcards

introduction to cardiac pathology Flashcards

1
Q

coronary arteries originate from

A

ostia behind aortic valve

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

coronary arteries

A
  • run in connective tissue on surface of heart

- supply blood from outer to inner layers of myocardium

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

most of coronary blood flow occurs

A

during diastole

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

LAD

A

apex of heart
anterior LV
anterior 2/3 of ventricular septum

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

RCA

A

RV free wall
posterior 1/3 of ventricular septum
posterior LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Left circumflex

A

lateral left ventricular wall

can also supply posterior aspect of LV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

left main

A

both LAD and left circumflex

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

occulsio to what CA(s) results in damage to LV wall and ventricular septum

A

RCA or LCA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

endocardium

A
  • thickness varies inversely with myocardium

- subendocardial region at greatest risk of ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

anatomy of conduction system

A
  • specialized myofibers
  • myocytes have a certain automaticity without impulse conduction will either fire an impulse aberrantly (premature complexes) or contract in an unorganized fashion (fibrillation)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SA anatomy

A

location at junction of SVC and right atrium

serves as pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

AV anatomy

A

AV node near atrium-ventricular junction

organizes and fires impulses into Bundle of His

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

bundle of his anatomy

A
  • runs thru ventricular septum to insure coordination contraction of both ventricles
  • movement of contraction in a wave of depolarization to maximize pumping action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

P wave

A

atrial contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Q wave

A

atrial systole

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

R wave

A

atrial diastole

17
Q

S wave

A

ventricular contraction

18
Q

T wave

A

ventricular systole

19
Q

chamber function

A
  • left/right synchronous
  • dependent on directional wave of depolarization
  • sequential upper chamber to lower chamber contraction to help in directional flow
20
Q

valvular function

A
  • one directional flow valve to prevent back flow
  • essential for maintaining stroke volume and attaining pressure differential across valve
  • most passive, mitral valve is assisted papillary muscle and chordae tendonae, tricuspid has similar structures
21
Q

valvular dysfunction

A

stenosis
insufficiency
anatomic distortion
loss of papillary muscle

22
Q

inflow

A
  • systemic-> inflow through IVC, dependent on systemic blood pressure and ventricular volume
  • pulmonary-> interruption of flow secondary to pulmonary emboli
23
Q

outflow

A
  • pulmonary: specialized vessels to pump large volume of blood through lungs under low pressure
  • two main problems:
    1. pulmonary HTN resulting in cor pulmonale
    2. pulmonary emboli

-systemic: collective peripheral resistance, blood volume, vessel diameter, elasticity, HTN

24
Q

cardiac cycle

A

diastole systole
[————————][——————————-]
S2 S1 S2

25
Q

starlings law

A

stretch versus contractility

26
Q

cardiac dysfunction: primary causes of cardiovascular dysfunction

A
  1. Hypovolemia
  2. Arrhythmia
  3. Cardiac muscle failure
    - ischemia (hypertrophy+ cardiac artery disease)
    - metabolic
  4. Decreased end diastole volumes
    - decreased diastolic relaxation
    - decreased ventricular volume
27
Q

cardiac failure

A

hypertrophied muscle may lead to end stage dilation and heart failure

28
Q

left heart failure

A

->80% ischemia, 1-3% HTN, 1% rheumatic

29
Q

signs and symptoms of left heart failure

A
  1. cardiac enlargement with:
    LVH-> heart increases in both volume and mass
    actual cardiac dilatation is end point decompensation
    2.Obstruction to venous return-> pulmonary congestion
  2. obstruction of systemic outflow
    -insufficient renal perfusion leads to fluid retention and further exacerbation of problem
    -hypoxic encephalopathy
    -coronary insufficiency and cardiac ischemia
  3. LA enlargement may be secondary to left ventricular enlargement or may be primary (MS) often associated with atrial fibrillation
  4. atrial fibrillation is associated with formation of mural thrombi (stasis of atrial blood flow) increased risk of embolic stroke
30
Q

right heart failure

A
  • occurs in only a few diseases
  • usually consequence of left sided (global) failure
  • most common pure form-> cor pulmonale (pul. HTN)
  • associated with valvular disease
31
Q

right heart failure

A
  1. engorgement of systemic and portal congestion (nutmeg liver, dependent pitting edema)
  2. liver congestion: chronic passive congestion (nutmeg liver)
    - stasis of blood in central vein with hypoxia of adjacent cells
    - vascular congestion with local hemorrhage, phagocytosis of red cells
    - fibrosis of long-standing ischemic tissue cardiac sclerosis
32
Q

global heart failure

A
  • long standing right or left sided failure
  • constrictive disease (tamponade)
  • massive infarct
  • shock
33
Q

signs of symptoms of global heart failure

A

degree of symptomology depends on the rapidity of development of cardiac failure

34
Q

pressure of volume overload

A

response: Hypertrophy

Microscopic features:

  • increased myocyte size with prominent and sometimes reduplicated nuclei
  • decreased capillary density
  • increased deposition of ECM
35
Q

chronic ischemia

A

response: myocardial atrophy, apoptosis

microscopic changes:

  • decreased cell numbers
  • increased fibrosis
36
Q

acute ischemia

A

response: necrosis, accompanying inflammation around margins

microscopic features: coagulative necrosis, with evolving inflammatory infiltrates, eventual replacement by fibrosis and scar

37
Q

reperfusion

A

response: reperfusion injury

microscopic features: contraction bands

38
Q

infection

A

response: acute inflammation

microscopic features: depends on nature of infectious agent, variable infiltration of inflammatory cells and myocyte damage

39
Q

aging

A 
microscopic features: 
fewer myocytes
increased collagen
senile amyloidosis
basophillic degeneration (by product of glycogen metabolism)
brown atrophy-> lipofuschin
pericardial fat

Pathology-Cardio (11 decks)

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