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(3) Cardio-Pulmo-Renal Rehabilitation > S2 L2.3: Atherosclerosis > Flashcards

S2 L2.3: Atherosclerosis Flashcards

1
Q

LDL ( ___ cholesterol) will find its way into the ______ and it will be causing the migration of the smooth muscles bc ____ _____ will form

A

LDL (bad cholesterol) will find its way into the endothelium and it will be causing the migration of the
smooth muscles bc foam cell will form

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2
Q

T/F:

Foam cell makes up the bulk of lipid clots, and
these clots may rupture and cause a heart attack

A

False

Foam cell makes up the bulk of CHOLESTEROL clots, and
these clots may rupture and cause a heart attack

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3
Q

Medical term for cholesterol plaque

A

Atheroma

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4
Q

EVOLUTION OF ATHEROMA

Arrange the following in order from 1 - 10:

Calcification and fibrosis continues

SMCs in the intima divide and migrate into the intima
from the media

Accumulation of lipoprotein particles in the intima

Increase expression of adhesion molecules

Expression of scavenger receptors

Extracellular matrix accumulation in the growing
atherosclerotic plaque.

Oxidative stress can induce local cytokine elaboration

Development of foam cells

A
  1. Accumulation of lipoprotein particles in the intima
  2. Oxidative stress can induce local cytokine elaboration
  3. Increase expression of adhesion molecules
  4. Expression of scavenger receptors
  5. Development of foam cells
  6. SMCs in the intima divide and migrate into the intima
    from the media
  7. Extracellular matrix accumulation in the growing
    atherosclerotic plaque.
  8. Calcification and fibrosis continues
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5
Q

Covers the plaque

A

Cap

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6
Q

SIMPLIFIED VERSION OF ATHEROMA EVOLUTION

Arrange the following from 1 - 4

Atheroma Formation

Fibrosis Healing

Clot Formation

Plaque Rupture

A

A. Atheroma Formation
B. Plaque Rupture
C. Clot Formation
D. Fibrosis or Healing (reduced lumen, limitation of blood flow)

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7
Q

EVOLUTION OF ATHEROMA

Thin caps can be ruptured easily due to ____,
____, ____, _______ _____

A

smoking,
htn, alcohol, inflammatory events

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8
Q

T/F regarding EVOLUTION OF ATHEROMA:

Cap ruptures → blood clot formation due to bleeding → Injures the endtholeium → clot too
big which obstructs the artery completely

A

False

Cap ruptures → Injures the endothelium →
blood clot formation due to bleeding → clot too
big which obstructs the artery completely

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9
Q

Modified T/F regarding EVOLUTION OF ATHEROMA:

  1. The amount of clot formation will tell how severe the
    situation is.
  2. A resolved clot but has thickened cap leads to reduced lumen which will result in limitation of blood flow
A

TT

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10
Q

Arrange the following in accordance with the ATHEROSCLEROSIS TIMELINE (from 1 to 6)

Complicated lesion/rupture

Foam cells

Fatty streak

Atheroma

Intermediate lesion

Fibrous plaque

A
  1. Foam cells
  2. Fatty streak
  3. Intermediate lesion
  4. Atheroma
  5. Fibrous plaque
  6. Complicated lesion/rupture
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11
Q

Match the following items:

1.Growth mainly by lipid accumulation
2. Thrombosis, hematoma
3. Smooth muscle and collagen
4. 0 days - 10 years old
5. 21 - 30 years old
6. 31 - 40 years old

A. From first decade
B. From third decade
C. From fourth decade

A
  1. A and B
  2. C
  3. C
  4. A
  5. B
  6. C
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12
Q

Is a life threatening disease that may have begun to develop during childhood

A

Atherosclerosis

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13
Q

Is a process in which deposits of fatty
material called plaque, build up inside the walls of
arteries reducing or completely blocking blood flow

A

Atherosclerosis

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14
Q

Give me at least three (3) risk factors for atherosclerosis

A

Risk factors for atherosclerosis:
○ High blood pressure
○ High cholesterol
○ Tobacco smoke
○ Diabetes
○ Obesity
○ Physical inactivity
○ Hyperlipidemia

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15
Q

T/F:
1. Scientists are sure that it begins with damage to endothelium, inner
wall of an artery
2. Over time, substances traveling in the blood such as
cholesterol, fats, and cellular wastes products
accumulate inside the damaged area the arterial wall

A
  1. F. Although exact causes are not clear, many scientists think that it begins with damage to endothelium, inner
    wall of an artery
  2. T
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16
Q

Arrange the folllowing in order of the sequence of the formation of atherosclerosis from 1 to 11 (this is from atheroscleorsis (2009) nucleus medical media):

Chemical reactions occurring within the build up of
material cause cholesterol molecules to oxidize which will initiate an inflammatory response wherein
endothelial cells at the damaged site release
chemicals that signal call for help. In response, monocytes from the bloodstream travel
to the damaged site

Stimulation from the oxidized cholesterol converts
monocytes into macrophages

As the plaque increases in size, the arterial wall thickens and hardens

Most of the smooth muscle cells move to the
surface of the plaque

The macrophages then eat and digest the cholesterol
molecules which changes these macrophages
into foam cells. Such foam cells would eventually accumulate to form plaque

Smooth muscle cells within the arterial
wall begin to multiply

The smooth muscle cells contribute to the formation of a firm, fibrous cap, covering the plaque

Over time, the cap may erode and break open, releasing plaque into bloodstream

Limited blood supply is available to the area
surrounding the partially blocked artery degrading and potentially killing the neighboring tissue

The plaque can flow downstream and contribute to the formation of a blood clot, which can stop blood flow

Significant damage in organs such as the heart or brain can result in a heart attack or stroke

A
  1. Chemical reactions occurring within the build up of
    material cause cholesterol molecules to oxidize which will initiate an inflammatory response wherein
    endothelial cells at the damaged site release
    chemicals that signal call for help. In response, monocytes from the bloodstream travel
    to the damaged site
  2. Stimulation from the oxidized cholesterol converts
    monocytes into macrophages

3.The macrophages then eat and digest the cholesterol
molecules which changes these macrophages
into foam cells. Such foam cells would eventually accumulate to form plaque

  1. As the plaque increases in size, the arterial wall thickens and hardens
  2. Smooth muscle cells within the arterial
    wall begin to multiply
  3. Most of the smooth muscle cells move to the
    surface of the plaque
  4. The smooth muscle cells contribute to the formation of a firm, fibrous cap, covering the plaque
  5. Over time, the cap may erode and break open, releasing plaque into bloodstream
  6. The plaque can flow downstream and contribute to the formation of a blood clot, which can stop blood flow
  7. Limited blood supply is available to the area
    surrounding the partially blocked artery degrading and potentially killing the neighboring tissue
  8. Significant damage in organs such as the heart or brain can result in a heart attack or stroke
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17
Q

ATHERSCLEROSIS TO ATHEROTHROMBOSIS

Modified T/F:
1. It is not the plaque but the rupture of the plaque that predisposes one to have an Acute myocardial infarction

  1. Over time, if you don’t get to control the cholesterol
    plaque formation, it will just progressively diminish the
    lumen of the arteries making chest pains progressive
A

TT

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18
Q

Is the following description unstable or stable plaque?

  1. Fibrous cap is gonna decrease the lumen
  2. If you have a plaque rupture, you’ll have the plaque
    formation at the thrombus, wherein there is a
    complete obstruction
  3. Distal to the obstruction, there will be a deprivation of blood flow, which will give the potential heart attack, myocardial infarction, myocardial death, or myocardial necrosis
A
  1. Stable
  2. Unstable
  3. Unstable
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19
Q

Give me the three (3) acute risk factors that is rooted from certain triggers for the formation of disruption/thrombosis from a vulnerable plaque

A
  1. Hemodynamic
  2. Vasoconstrictive
  3. Prothrombotic
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20
Q

Arrange the following into the correct sequence using arrows:

Atherosclerosis Chronic risk factors

Triggers

Acute risk factors (hemodynamic, vasconstrictive, prothrombotic)

Vulnerable plaque

Non-vulnerable plaque

Disruption, thrombosis

Plaque progression (Unstable angina, myocardial infarction, sudden cardiac death)

SAMPLE ANSWER:
Disruption → Non-vulnerable plaque → Plaque progression

A

Atherosclerosis Chronic risk factors →Non-vulnerable plaque → vulnerable plaque → triggers → acute risk factors (hemodynamic, vasconstrictive, prothrombotic) → Disruption, thrombosis → Plaque progression (Unstable angina, myocardial infarction, sudden cardiac death)

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21
Q

A plaquet hat is strong becomes vulnerable plaque over time if you cannot control risk factors

A

Non-vulnerable plaque

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22
Q

What is being described?

Fluctuation in blood pressure (It goes up and down vice versa)

A

Hemodynamic triggers

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23
Q

What is being described?

Blood becomes thicker with hypertension (especially
when you are already predisposed to Htn)

A

Prothrombotic

24
Q

Means that you are predisposed to
blood clot

A

Prothrombotic

25
Q

Due to this: disruption of blood flow, thrombosis
occurs, myocardial infarction, plaque
progression occurs

A

Prothrombic

26
Q

ISCHEMIC TRIGGERS

Classify the following:

  1. Exercise
  2. Pulse pressure
  3. Assuming upright posture
  4. Cigarette smoking
  5. Cold exposure
  6. heart rate
  7. Systolic BP
  8. Increased vascular
    resistance
  9. Catecholamine levels

A. Trigger
B. Mediator

A
  1. A
  2. B
  3. A
  4. A
  5. A
  6. B
  7. B
  8. B
  9. B
27
Q

The following are included under ischemic triggers, EXCEPT:
A. Exercise
B. Assuming upright posture
C. Cigarette smoking
D. Cold exposure
E. None of the Above

A

E

28
Q

Selec the items that are included under mediators for ischemic triggers?
A. Exercise
B. Pulse pressure
C. Assuming upright posture
D. Cigarette smoking
E. Cold exposure
F. heart rate
G. Systolic BP
H. Increased vascular
resistance
I. Catecholamine levels

A

B and F to I

29
Q

Arrange the following items regarding ischemic triggers in sequence using arrows:

Trigger

Plaque fissure, thrombin and platelet activation, and vasospasm

Mediator

A

Trigger → Mediator → Plaque fissure, thrombin and platelet activation, and vasospasm

30
Q

What are the three (3) possible result fron ischemic triggers?

A

Plaque fissure, thrombin and platelet activation, and vasospasm

31
Q

T/F

Exercise can increase heart rate, blood pressure; So when doing exercises for patients with heart diseases, you want to be watchful over heart rates and blood pressure because you do not want wide swings on them

A

True

32
Q

T/F

PTs do not need to be careful when it comes to positioning when it comes to cardiac patients

A

False

We have to be careful when making patients assume upright posture; This is why in PT sessions, they would train the pt and not make patient stand right away as circulatory system cannot adjust yet

33
Q

What possible factors and/or activities causes vasconstriciton?

A

Cigarette smoking and cold environment

When applying cold packs → could have a negative impact on CAD pts

34
Q

Difference of SBP and DBP, ____ pulse pressure (___/___) = more dangerous, ____ pulse pressure (___/___) = also can be dangerous

A

Difference of SBP and DBP, higher pulse pressure (160/60) = more dangerous, lower pulse pressure (100/80) = also can be dangerous

35
Q

Modified T/F:

  1. You want your patients stress free during treatments; don’t want them to be too excited
  2. Monitor BP and HR; cannot measure vascular resistance during sessions
A

TT

36
Q

T/F
Not all CADs are brought upon by atherosclerotic lesions

A

True

37
Q

NON-ATHEROSCLEROTIC CAUSES OF CAD

Give me at least four (4) fixed lesions for Non-Atherosclerosis Causes of CAD

A

● Congenital Anomalies
● Myocardial Bridges
● Aortic Dissection
○ Coming from a weak artery (aorta) it bulges
(aneurysmal) and is torn d/t HTN
● Granulomas
● Tumors
● Scarring from trauma, radiation

38
Q

MYOCARDIAL BRIDGING

Normally, the _____ arteries are called _____

A

Normally, the coronary arteries are called epicardial (epi - on top & outside the epicardium)

● Normal left anterior descending artery or epicardial
artery is just on top and outside the muscle wall

39
Q

MYOCARDIAL BRIDGING

It could be called bridging because the ____ bridged
over the _____

A

It could be called bridging because the muscle bridged
over the artery

40
Q

What is the role of myocardial bridging in CAD?

A

It is one of the fixed lesions under non-atherosclerotic causes of CAD

41
Q

Match the following items about myocardial bridging:
1. The artery dove deep into the muscle such
that when the muscle contracts, the blood vessel gets
constricted (like an obstruction). Causes chest pain when heart contracts more (i.e.
exercise, tachycardia)
2. Part of the arteries penetrates into the
myocardium such that when the heart contracts, they pinch the myocardial arteries
3. When the heart contracts during systole, the patient
may feel chest pain
4. Slightly buried into the muscle; not
embedded into the myocardium (no symptoms)

A. Deep bridging
B. Shallow bridge

A

1-3. A
4. B

42
Q

DEEP BRIDGING in myocardial bridging

The artery dove deep into the muscle such
that when the muscle contracts, the blood vessel gets
_____ (like an ______). Causes _____ ______ when heart ______ _____ (i.e.
exercise, tachycardia)

A

The artery dove deep into the muscle such
that when the muscle contracts, the blood vessel gets
constricted (like an obstruction). Causes chest pain when heart contracts more (i.e.
exercise, tachycardia)

43
Q

DEEP BRIDGING in myocardial bridging

Part of the arteries ______ into the
myocardium such that when the heart contracts, they _____ the myocardial arteries

A

Part of the arteries penetrates into the
myocardium such that when the heart contracts, they pinch the myocardial arteries

44
Q

DEEP BRIDGING in myocardial bridging

When the heart contracts during ______, the patient
may feel _____ _______

A

When the heart contracts during systole, the patient
may feel chest pain

45
Q

What do you call the event wherein the aorta is torn which leads to compromised aortic branches?

A

AORTIC DISSECTION:
Aorta is torn, can compromise its branches

46
Q

What is the role of aortic dissection in CAD?

A

It is one of the fixed lesions under non-atherosclerotic causes of CAD

47
Q

Match the following items regarding aortic dissection:

  1. Proximal aorta involvement (L)
  2. Distal aorta involvement (R)
  3. All dissections involving the ascending aorta
  4. Anything outside the proximal portion
  5. All dissections NOT involving the ascending aorta
  6. More dangerous
  7. Patient may die instantly since it is near the heart
  8. Tear in the proximal portion of aorta

A. Type A
B. Type B

A
  1. A
  2. B
  3. A
  4. B
  5. B
  6. A
  7. A
  8. A
48
Q

The following describes Type A aortic dissection, EXCEPT (there can be more than one answer):

A. Anything outside the proximal portion
B. All dissections NOT involving the ascending aorta
C. More dangerous
D. Patient may die instantly since it is near the heart
E. Tear in the proximal portion of aorta

A

A and B

49
Q

Which of the following describes Type B aortic dissection? (there can be more than one answer):

A. Distal aorta involvement (R)
B. All dissections NOT involving the ascending aorta
C. Anything outside the proximal portion
D. Patient may die instantly since it is near the heart
E. Proximal aorta involvement (L)

A

A, B, C

50
Q

T/F regarding Aortic Dissection:

  1. R & L coronary artery came from the sinuses of the aorta
  2. Dissection of one of the arteries produces a functional obstruction = myocardial infarction
  3. From the true lumen, blood enters through the
    tear creating another lumen (the false lumen)
  4. False lumen impinges on RCA and creates an
    obstruction
  5. Deadly case, straight to emergency operation (OR)
A

All are TRUE

51
Q

AORTIC DISSECTION

Dissection of one of the arteries produces a_____ _____ that leads to ______ ______

A

Dissection of one of the arteries produces a functional obstruction that leads to myocardial infarction

52
Q

AORTIC DISSECTION

How is a false lumen created?

A

From the true lumen, blood enters through the
tear creating another lumen (the false lumen)

53
Q

AORTIC DISSECTION

The formed false lumen impinges on ______ ____ _____ (hint: an artery) and creates an _______

A

The formed false lumen impinges on right coronary artery or RCA and creates an obstruction

54
Q

T/F regarding Aortic Dissection:
1. Dissection of one of the arteries is a deadly case (straight to emergency operation (OR)) and a difficult case
2. Death rate is >50%
3. In all cases, the patients always suffer from ischemia

A

1-2. True
3. False. If there is still blood flow, the patient may not suffer from ischemia

55
Q

Give me the three (3) transient causes under non-atherosclerotic causes of CAD

A
  1. Vasospasm
  2. Embolus
  3. Thrombus in situ
56
Q

TRANSIENT CAUSES under non-atherosclerotic causes of CAD

Match the following items:

  1. Vasoconstriction in blood vessels causes angina
    pectoris
  2. From the Situ*, there’s clot formation there and then
  3. Patients who are in hypercoagulable states
  4. Not necessarily cholesterol
  5. Any blood clot that can enter in coronary arteries can obstruct
  6. In patients with Raynaud’s disease, they can also
    have chest pain most likely caused by vasospasm
    (Prinzmetal Angina)
  7. Patients who take contraceptive pills
  8. Patients whose blood is very sticky (high platelet
    count), the can develop thrombus

A. Vasospasm
B. Embolus
C. Thrombus in situ*

*In situ means “in the normal location” or “in its original place” (source: google)

A
  1. A
  2. C
  3. C
  4. B
  5. B
  6. A
  7. C
  8. C

(3) Cardio-Pulmo-Renal Rehabilitation (34 decks)

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