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CPR > Test 3: Mara Rendi review > Flashcards

Test 3: Mara Rendi review Flashcards

1
Q

What is the general definition of arteriosclerosis?

A

hardening and thickening of blood vessels

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2
Q

Name 3 arterioscelreosis diseases

A

Mockeberg’s arteriosclerosis

arteriolosclerosis

atherosclerosis

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3
Q

What is this?

A

Mockeberg’s arteriosclerosis

It is the calcification of the media

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4
Q

Does Mockeberg’s arterioscleosis obstruct arterial flow?

A

Nope

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5
Q

What is arteriolosclerosis?

A

hyaline thickening or proliferation of small vessels. The type of thickening depends on the type of arteriolosclerosis

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6
Q

What are the two types of arteriolosclerosis?

A

Hyaline arteriolosclerosis

hyperplastic arteriolosclerosis

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7
Q

What is this?

A

hyaline arteriolosclerosis

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8
Q

Does hyaline arteriolosclerosis obstruct flow?

A

Yes!

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9
Q

What is this?

A

hyperplastic arteriolosclerosis

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10
Q

Does hyperplastic arteriolosclerosis obstruct flow?

A

Yes!

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11
Q

What is atherosclerosis?

A

The formation of atheromas within the INTIMA

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12
Q

What are the components of a atheroma-plaque?

A

central core

fibrous cap

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13
Q

What is in the central core?

A

cholesterol

foam cells (macrophages with lipid inside of them)

necrotic debris

calcium

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14
Q

What is in the fibrous cap?

A

collagen

fibrin

smooth muscle

foam cells

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15
Q

What are these pictures trying to show?

A

fatty streaks

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16
Q

What is this trying show show?

A

More fatty streaks

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17
Q

Why are fatty streaks important to know about?

A

They are the first steps in becoming an atheroma-plaque

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18
Q

What is this?

A

a god damn fatty streak!

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19
Q

What is this?

A

A atheroma-plaque.

Notice the fibrous cap and the necrotic core

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20
Q

What is this?

A

early atherosclerosis

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21
Q

What is this slide? What is the arrow showing?

A

Atherosclerosis

the arrow is pointing to calcification

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22
Q

What is this? What are the “red chunks”?

A

late atherosclerosis

thrombi that are forming due to the ruptured plaques

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23
Q

What are the “needle” shapes in the central core?

A

Cholesterol needles

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24
Q

Name the components

A
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25
What is the difference between these two pictures?
A - Atheroma-plaue B- Ruptured atheroma-plaque
26
What are the major complications of atherosclerosis?
Ruptured plaques result in thrombus formation which can lead to emboli. These emboli, depending on where the thrombus formation occured, can cause occlusion which is bad. Atheroscleorsis can also lead to aneurysms, which are also bad
27
What are the modifiable and non-modifiable risk factors for atherosclerosis?
Non-Modifiable: advanced age, male sex, family history, genetics Modifiable: smoker, diabetes, hypertension, hyperlipidemia,
28
Is atherosclerosis an inflammatory process?
Yes
29
Where does venous thrombosis occur?
Usually in the deep veins of the legs
30
What three factors make you at high risk for a DVT?
stasis of blood flow endothelial injury hypercoagulability
31
What is this? Bonus: Where is this?
embolus Bonus: in the lungs
32
What is the difference between ischemia and hypoxia?
ischemia is the lack of blood flow hypoxia is the lack of oxygen
33
What is this picture showing? What would happen is you started to increase physical exertion?
atherosclerosis of a coronary artery Ischemia leading to angina
34
This is a slide of a coronary artery. What is going on here?
Ruptured plaque that resulted in thrombus formation. This is a STEMI
35
Evolution of MI What changes can bee seen grossly and histologically within 12 hours?
no gross changes not much histologic changes
36
Evolution of MI What changes can bee seen grossly and histologically within 12 - 24 hours?
- Grossly: blue-gray discoloration caused by stagnant blood - Histologically: coagulative necrosis and contraction bands
37
How old is this MI? What is the arrow pointing to?
This is between 12-24 hours You can see coagulative necrosis (notice there are **no nuclei**) and you can see contraction bands indicated by the arrow
38
How old is this infarction?
12-24 hours Myocardium on the right is normal while the myocardium on the left is undergoing coagulative necrosis
39
Evolution of MI What changes can bee seen grossly and histologically within 1 - 4 days?
- Grossly: blue-gray discoloration caused by stagnant blood - Histologically: neutrophils within the necrotic myocardium
40
How old is this infarct?
1 - 4 day old Notice the presence of neutrophils
41
Evolution of MI What changes can bee seen grossly and histologically within 4-10 days?
- Grossly: tan-yellow and soft at the area of infarction with hyperemic boarders (red due to recruitment of blood vessels) - Histologically: macrophages arrive to clean up the scene
42
Why is the 4-10 period a very danegrous time for the patient?
The area of infarction is the point of maximal weakness and is susceptible for rupture
43
Where is the point of maximal weakness?
44
How old is this infarct?
4 - 10 days
45
How old is this infarct?
4 - 10 days notice the macrophages and the nearly complete removal of the necrotic caridomyocytes
46
How old is this infarct?
4 - 10 days notice the macrophages and the nearly complete removal of the necrotic caridomyocytes
47
Evolution of MI What changes can bee seen grossly and histologically within 10 days - 3 weeks?
- Grossly: mottled yellowish tan and gray depressed area - Histologically: granulation tissue present
48
How old is this infarct?
10 day to 3 weeks Note: grossly, it would be VERY difficult to distinguish between 4-10 days and 10 days - 3 weeks, which is why you would want to look at it histologically
49
How old is this infarct?
10 days - 3 weeks old Granulation tissue characterized by **loose connective tissue** and **abundant capillaries**.
50
Evolution of MI What changes can bee seen grossly and histologically within 3 - 8 weeks?
Grossly: white scar Histologically: dense scar tissue
51
How old is this infarct?
3 - 8 weeks notice the white scar
52
How old is this infarct?
3 - 8 weeks notice the dense fibrous connective tissue and residual myocardiocytes
53
How old is this infarct?
3 - 8 weeks notice the dense fibrous connective tissue and residual myocardiocytes
54
How old is this infarct?
1 - 4 days
55
What's going on here?
Reperfusion causes hemorrhage in area of infarction
56
What are 5 complications of MI?
arrhythmias heart failure tamponade (4-10 days) mural thrombosis ventricular aneurysm
57
What is this?
58
What is this?
59
What is this?
60
What is this?
61
What is this?
62
What is this?
63
What is this?
64
What are aneurysms?
Abnormal dialtions of arteries and veins that can rupture
65
What are the 3 causes of aneurysms that we should know for this test?
hypertenstion atherosclerosis marfans syndrome
66
What is this?
ruptured abdominal aortic aneurysm
67
What is this?
ascending aortic aneurysm
68
What is this?
69
What is patent foramen ovale?
The foramen ovale is not closed, but the pressures from the valve keep the flap closed
70
What is a paradoxical embolization?
It is an embolism that forms on in the venous system but can travel through a septal defect into the arterial system
71
What is a VSD?
hole in the ventricular septum
72
What is patent ductus arteriosus? What can it lead to?
failure of the ductus arteriosus to close pulmonary hypertention
73
What is coarctation of the aorta?
constriction of the aorta
74
Who develops coarctation of the aorta?
men\>women turner's syndrome (female with one X)
75
What is this?
coarctation of the aorta
76
What is this?
patent ductus arteriosus
77
Do patients with coarctation of the aorta have higher blood pressure in the upper extermities?
yes
78
What is tetralogy of fallot? Is this a left to right flow?
1. Sub-pulmonary Stenosis (obstruction of right ventricular outflow tract) 2. Right ventricular hypertrophy 3. Overriding aorta 4. Ventricular Septal Defect NO! this is a right to left flow
79
What is transposition of the great arteries?
The reveral of pumlonary trunk and aorta
80
is transposition of the great vessels a cyanotic disease? How can a fetus survive this?
yes they need a large VSD or a patent ductus arteriosus

CPR (27 decks)

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