Quiz 1 - CV

Question 1

What kind of conditions cause aortic dissection?

Answer 1

Conditions that weaken or cause degenerative changes in the elastic or smooth muscle layers of the aorta

Question 2

Tell me 5 risk factors for aortic dissection

Answer 2

1. atherosclerosis
2. degeneration of the medial layer of the vessel wall
3. Marfan syndrom (connective tissue disease)
4. congenital defects of the aortic valve
5. aortic coarctation

Question 3

Tell me how cardiac surgery can contribute to development of aortic dissection (2)

Answer 3

1. You may see aortic dissection where the aorta was cross clamped or incised
2. you may also see it where the saphenous vein was sutured to the aorta during a CABG

Question 4

Define atherosclerosis

Answer 4

hardening of the arteries

Question 5

What are 5 risk factors for atherosclerosis?

Answer 5

1. hypercholesterolemia (esp LDLs)
2. HTN
3. obesity
4. DM
5. smoking

Question 6

Tell me about the 3 stages of development of an atherosclerotic plaque

Answer 6

First you see development of a fatty streak. Then you see the fatty streak turn into a fibrous plaque. The fibrous plaque then progresses into a complicated plaque

Question 7

How does a fatty streak develop?

Answer 7

First smoking or LDLs or some immune mediated mechanism causes injury to the vessel endothelium. This injury causes inflammation and attracts monocytes and other inflam mediators. The monocytes migrate in between the endothelial cells, oxidize the LDLs and gobble them up, forming foam cells. These monocytes/macrophages and foam cells also produce growth factors that cause the proliferation of SMCs.

Question 8

How does a fatty streak turn into a fibrous plaque?

Answer 8

Fatty streaks grow large and you see further proliferation of smooth muscle cells. A fibrous cap develops over the lipid core of the plaque. The plaque starts to encroach on the lumen of the vessel.

Question 9

What is a complicated plaque?

Answer 9

A complicated plaque contains hemorrhage, ulceration, and scar tissue deposits. It’s at high risk for rupture because blood flow over it becomes increasingly slow and turbid.

Question 10

What are the 4 clinical manifestations of atherosclerosis?

Answer 10

1. the vessel becomes narrowing, resulting in decreased blood flow and ischemia to the perfused tissues
2. vessel becomes suddenly obstructed due to plaque rupture or hemorrhage
3. you see thrombosis or emboli from ruptured plaque
4. you see aneurysm formation from weakening of the vessel wall

Question 11

What is the important complication of atherosclerosis in large vessels?

Answer 11

Thrombus formation and weakening of vessel walls

Question 12

What is the important complication of atherosclerosis in medium sized vessels such as coronary and cerebral arteries?

Answer 12

Ischemia and infarction due to vessel occlusion

Question 13

What are the systemic effects of Angiontensin II and what is the impact of this during and after an MI

Answer 13

Ang II is a powerful vasoconstrictor and also causes fluid retention. An increase in blood volume and increase in peripheral vascular resistance increase the workload on the heart, which is especially difficult when the myocardium is experiencing a decrease in contractility

Question 14

What are the local effects of Ang II on the myocardium during and immediately after an MI?

Answer 14

Ang II is a growth factor for myocytes, vascular smooth muscle cells, and fibroblasts. It also contribute to cathecholamine release, which causes coronary artery spasms

Question 15

What is Ang II involved in cardiac remodeling after an MI?

Answer 15

Ang II contributes to myocyte hypertrophy and scarring, thus contributing to the loss of contractility in myocardium distal to the infarction.

Question 16

So why would you give an ACE Inhib during the aerly and convalescent phases of an MI?

Answer 16

ACE inhibs will increased CO, reduce systemic pulmonary vascular resistance. This reduces left ventric dysfunction and SCD