Brainscape's Knowledge GenomeTM

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


See full index

old patho 154 > pvd-up to Cardiomyopathy > Flashcards

pvd-up to Cardiomyopathy Flashcards

1
Q

where does PVD usually occur

A

lower limbs. usually in arteries but can also be in veins, cap, lymphatics

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

how are PVD and atherosclerosis different

A

the changes are atherosclerotic but they take place in diff vessels.
similar to changes int he coronary artery

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

acute arterial occlusion

does it occur quickly or slowly

A

may be due to a clot which has developed elsewhere (embolism) or my form in vessel (thrombosis)
-quickly. it leads to inadequate perfusion and tissue is compromised

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

atherosclerotic occlusive disease

A

develops gradually
occurs in lower extremities
inc in elderly and diabetes mellitus pts

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

why does atherosclerotic occlusive disease inc in elderly adn diabetic pts

A

elderly because atherosclerotic changes only mnft after decades
in diabetics because one of the chronic complications of diabetes is vascular damage

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

mfft of atherosclerotic occlusive disease

A

-intermittent claudication
(pain upon walking.)
- tissue distant to occlusion gets ischemic due to impeded perfusion which leads to infarction and pain
-dec venous return -> venous stasis. the pressure will build up and cause edema. the lymphatics get overwhelmed and this leads to lymph stasis and wastes and fluids accumulate

  • intermittent claudication
  • ischemia (infarction & pain)
  • edema (lymph stasis, waste, fluid accum)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

collateralization=

A

formation of new vessels around an obstruction which may or may not be useful

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

compensation for atherosclerotic occlusive disease

A

vasodilation, anaerobic metabolism and collateralization

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

what happens if theres no Tx for atherosclerotic occlusive disease

A

leads to ulceration and gangrene and then amputation

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

aneurysms=

A

localized dilation of an artery that is permanent

d/t degenerative changes in the vesel wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

where do aneurysms generally develop

A

in certain regions of the vessel where they bend or bifurcate

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

risks for aneurysms

A

HTN, atherosclerosis, congenital defects

C-HTN-Aneurysms everywhere?

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

3 types of anuerysms

A

fusiform eg abdominal aorta
saccular
dissecting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

common sites of aneurysms

A 
abdominal aorta
thoracic aorta
femoral 
iliac
popliteal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

are aneurysms always detectable

A

if in a body cavity they may go undetected within limits

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

what is a dissecting aneurysm and how is it different from fusiform and saccular

A

dissecting seem to bleed in between the vessel layers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

complications of aneurysms

A
  • pressure on adjoining structures
  • the most serious complication is rupture
  • thrombosis (with a bulge the speed of flow will be dec which puts pt at risk of clotting and thrombi)
  • distal embolization
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

do complications always develop for a disease

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

coronary artery disease
causes what
due to what
where does it occur

A

major cause of death
mostly d/t atherosclerosis
occurs in coronary artery and other branches of coronary circuit

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

2 types of CAD

A

acute coronary syndromes

chronic ischemic heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

acute coronary syndrome is what type of CVD

wat is it

A

CAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is CAD

A

it is heart disease caused by impaired coronary blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

which types of conditions fall under acute coronary syndrome

char of ACS

A

MI
unstable angina
sudden cardiac death

hppens quickly but whatever is predisposing the person doesnt have to happen quickly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

chronic ischemic heart disease vs acute coronary syndromes

A

fig 4-5
-stable angina has a fixed atherosclerotic plaque (it is CIS)
-

25
Q

chronic ischemic heart disease

A

stable angina

congestive heart failure (issue with blood flow)

26
Q

why is stable angina stable

A

because the atherosclerotic plaque isnt going anywhere

27
Q

stable angina is pain on exertion T or F
what is it?
how is unstable angina different in rt pain

A

true
stable is transient pain

unstable is pain at rest and during exertion
-it is severe, longer, also at rest & or nocturnal

28
Q

angina pectoris is a _____ of CAD

A

is a mnft of CAD

29
Q

etiology of angina pectoris

A
  • atherosclerosis mostly
  • vasospasm
  • thrombosis
30
Q

pathophysiology of angina ectoris

A

-inadequate perfusion->myocardial ischemia->angina

(under normal circumstances the arteries would dilate on demand but they are unable to dilate d/t atherosclerosis

31
Q

mnfts of angina pectoris

A 
chest pain (triggered by exertion, emotion, cold)
(cold because it causes vasoconstriction)
32
Q

stable angina
is
triggered by

A
  • fixed plaque
  • perfusion impeded
  • transient pain (~5 min)
  • triggered by exertion, relieved by rest
33
Q

how could you assist a pt w stable angina nonpharmacologically

A

relax, stop exerting yourself

come out of cold

34
Q

unstable angina

A

unstable plaque
-plaque collects platelets, fibrin and cellular debris
-if ruptured it leads to thrombosis
-platelets aggregate->prostaglandin release->vasospasm
(int he capillary it had the effect of inc cap permb, vasodilation)
-pain is severe, longer, also at rest and or nocturnal. it can lead? to acute coronary syndrome and therefore MI if not managed well

35
Q

stable and unstable angina

what is the other kind of angina called

A

variant/vasospastic/Prinzmetal’s angina

36
Q

variant/vasospastic/Prinzmetal’s angina

A

-pin can occur nocturnally, at rest

  • differs from the other two types of angina in that theres no atherosclerosis
  • the coronary vessels undergo vasospasm
  • to detect ECG changes the patient must be in pain at tht time
37
Q

mnfts of vasospastic angina

A
  • transient, mild to moderate chest pain
    • squeezing, burning (heartburn or indigestion? this is what the pt often think and they dont seek attention because of this)
  • can radiate to L shoulder and upper arm
  • the pain can be migratory (starts somewhere and moves elsewhere)
38
Q

tx of variant or Prinzmetal’s angina

A 
dec activity
use ntroglycerin (a vasodilator)

the more episodes of angina a person has the more likely they are to hve an MI

39
Q

Myocardial infarctions (STEMI)
where is this in r/t CAD
how does this affect life
is it acute or chronic

A

it is end point of CAD
its life threatening
it has acute onset

40
Q

etiology of STEMI

A

atherosclerosis
hemmorhage
coronary vessel spasm

the problem is that the heart isnt getting eough blood

41
Q

patho of STEMI

A

atherosclerosis->complicated lesion->ischemia->cardiac hypoxia->anaerobic metb->acidosis??->arrythmias (irreg heart rate)->inability to pump and infarction

some area of heart wall will die and it is irreplaceable

42
Q

size of infarction is based on

A
  • affected vessel-how much tissue is affected
  • extenet of occlusion
  • duration of occlusion
  • metabolic status of hert
  • HR, BP and rhythm (status of person)
  • collateral circulation (two vessels supplying area or more this would give alternate routes for the blood to arrive)
43
Q

2 Types of MI infarction

A

-subendocardial infarction

transmural infarction

44
Q

subendocardial infarction

A 
inner 1/3 to 1/2 of ventricle wall
distal occlusion (branches)
45
Q

transmural infarction

A

1 artery is obstructed
the entire ventricle wall is affected
the occlusion is proximal

46
Q

what is a STEMI

A

an acute STEMI is char by the ischemic death of myocardial tissue assoc w elevation of the ST-segment of the ECG, and serum markers (cardiac) indicating myocardial damage

47
Q

sme mnfts of MI

A

-chest pain (radiate to L shoulder, neck, jaw, arm)
-crushing pain that is severe
-anxiety, tachycrdia
-nausea, vomiting, fatigue
( severe pain is often assoc w nausea and vomiting. The electrical activity that is taking place in the centre in the brain that senses pain will affect the nearby vomit reflex center)
-less common (from him talking) palor, dizziness, palpitations, SOB, weakness. women often present with some of these symptoms as well as the pain often radiates to back

48
Q

review ECGs and what happens when

A

at minimum during the St segment there is no electrical activity
the atria is in diastole and filling since the Av valves are closed
the ventricles are in systole ad building up pressure until semilunar valves can open
the ventricles eject blood into the pulmonary and aortic arteries

49
Q

dx of Mi

A
  • ECG (can show you where occlusion is and the extent of it. eg look for St depression and know it is subendocardial injury or St elevation and it is transmural
  • angiogram (insert a catheter into an artery. Once near the occlusion or heart, release contrast medium. Then visualize the circuit on the screen. Dangerous because most pts have atherosclerosis. v precise. If obstruction found they will fix it)
  • serum markers: Troponin I &T, myoglobin, CKnB
50
Q

TRoponins T& I and MI

when do they peak and appear

A

troponins are regulatory proteins in the heart. (specifica to heart)
difficult to use as a serum marker because they are present in blood in various amounts depending on the time post MI
-I & T will begin to appear 3-4hrs after and peak 8-12hrs

51
Q

myoglobin as a serum marker for MI

peaks and appears

A

it is a resp pigment in the blood nonspecific to the heart. Stores oxygen. appears 1-2hrs after Mi and peaks early

52
Q

CKMB vs CKMM

A

CKMM is nonspecific to heart vs CKMB

53
Q

Tx of MI

A
  • stat attention to preserve life
  • thrombolytics, anti-arrythmics & anticoagulants
  • oxygen for hypoxia
  • morphine PRN
  • post-stabilization: IV diuretics, inotrope + vasodilator
  • revascularization Sx (angioplasty, bypass)
54
Q

how do diuretics help the heart post MI

A

diuretics lead to fluid loss->dec blood volume which allows dec cardiac workload

55
Q

inotrope

A

a drug class :affects the force of contraction but not the rate
-there are positive inotropes and negative.
Negative will dec the force of contraction.
if the heart was failing and not forceful enought then could give positive inotrope

56
Q

is nitroglycerin useful post MI or during MI

A

it is not useful during MI because the thrombus has already caused vasodilation but once it is gone post MI it can be useful to have a vasodilator

57
Q

revascularization surgery on the heart is aka

A

angioplasty or bypass

58
Q

types of surgery to help with MI

A 
balooning angioplasty (isnt used as often now
-stent. (a metal bracket put into vessel to hold it open. may have platelet aggregation.)

old patho 154 (18 decks)

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