angina pectoris Flashcards

1
Q

angina pectoris is a manifestation of?

A

coronary artery disease but also a disorder itself

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

angina=

A

angina= pain
pectoris= chest
chest pain

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

what kind of pain?

A

ischemic pain

-inadequate perfusion to area of heart wall, not meeting demand

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

etiology of angina pectoris?

A
  • d/t atherosclerosis in most cases
  • thrombus
  • hemorrhage
  • vasospasm (vessel constricts and stays in constricted position, tissue distal is ischemic)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

pathophysiology of angina pectoris?

A

arteries NORMALLY dilate on demand BUT if vessel has atherosclerotic change it may be already compensating by vasodilating and CANT any further!
—> inadequate perfusion —> ischemic —> chest pain

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

manifestations of angina pectoris?

A
  • CHEST PAIN
    -heart wall is impacted from vessels in coronary circuit not providing adequate blood and oxygen to heart cells
    -“squeezing, burning” pain
    -transient to severe
    -radiates to UPPER ARM SHOULDER NECK JAW
    typically LEFT UPPER ARM and SHOULDER
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

types of angina?

A

stable
variant/vasospastic/prinzmetals
unstable

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

what is stable angina?

A

FIXED plaque within wall of vessel
PROTRUDING into lumen
at REST, pt has enough adequate blood flow
PAIN occurs when metabolic demand of heart INCREASES
d/t:
a) exertion (physical activity)
b) emotional stress
c) cold- vessels automatically constrict to reduce BF to periphery so heat is not lost, causes systemic response and arteries, decreased BF to heart
^^ all perfusion to heart is IMPAIRED= pain

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

what is unstable angina?

A

atheroma/plaque can rupture through wall of vessel into lumen, causing bleeding
-atheroma contains necrotic and foam cells that LEAK out fibrin and cell debris and platelets
-THROMBUS forms in lumen once plaque ruptures and has potential to dislodge “unstable”
-prostaglandin released from platelet aggregation —> triggers vasospasm —> vessel constricts —> cuts off lumen even further
PAIN more SEVERE, LONGER PAIN
-cannot withdraw trigger! pain occurs ANYTIME, ECG changes

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

what is variant/vasospastic/prinzmetals angina?

A
  • SPASM of artery in CORONARY circuit
  • unclear etiology, could be:
    a) abnormal epithelium- SM in vessel wall constricting when doesnt need to
    b) calcium ions- calcium channel blocked, SM cells inadequately handling Ca
    c) sympathetic ns- hyperactivity of SNS, excessive stimulation of SM cells
    d) nitric oxide- chemical compound involved in vasodilation, if decreased conc, vasoconstriction
  • triggered at ANYTIME
  • TRIGGER UNKNOWN so difficult to manage
  • DIFFICULT TO ASSESS bc can not be triggered on demand when usually u would watch the ECG by triggering angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

treatment of angina?

A

-rest/cease activity
-nitroglycerin!! (increase nitric oxide in cells, vasodilator)
comes in aerosal spray, patch, sublingual
systemic vasodilation
-avoid trigger to prevent recurrent episodes and decrease risk of MI!

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