Vascular Disease part 1: Atherosclerosis Flashcards

1
Q

What are the earliest lesions seen in atherosclerosis?

A

Fatty streaks

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2
Q

What are the three layers in a blood vessel? -LB

A

Tunica Intima - epithelium
Tunica media - smooth muscle
Tunica adventitia - connective tissue, nerves, and vasa vasorum

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3
Q

Which layer of blood vessel creates connective tissue? -LB

A

Tunica Media (smooth muscle)

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4
Q

What percent of vessel occlusion is the typical threshold for angina? -LB

  • 15%
  • 50%
  • 70%
  • 80%
  • 90%
A

70% occlusion

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5
Q

What type of arteriosclerosis is palpable, in patients > 50 y.o., seen in muscular arteries, and presenting with ring-like calcifications?

A

Monckeberg

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6
Q

What can lead to the breakdown of endothelial tight junctions in blood vessels? -LB

A

Hemodynamics factors (Hypertension) and vasoactive agents (such as histamine)

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7
Q

What can result from breakdown of endothelial tight junctions in a blood vessel? -LB

A

Edema (through loss of protein and electrolyte out of vascular space), and inflammation (from lymphocytes leaving blood stream)

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8
Q

In which two patient populations do you see hyaline arteriolosclerosis? J

A

Diabetics and patients with benign hypertension

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9
Q

What are the two vasculitis conditions that effect large vessels? -LB

A

Giant Cell Arteritis and Takayasu Arteritis

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10
Q

What is the major differences between giant cell arteritis and takayasu arteritis? -LB

A

Age of the patient: Takayasu < 50; Giant cell > 50

Position of embolus: Takayasu more distal; Giant cell proximal (at aortic branches)

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11
Q

A 28 year old Asian female presents to the emergency department complaining of a severe headache. On physical exam she is also found to have visual field impairments, jaw claudication, and a pulseless right upper extremity. What is the first line drug class used to treat this patient empirically? -LB

A

Steroids (treatment same for giant cell arteritis and Takayasu [this case]), as it is a granulomatous vasculitis.

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12
Q

Name three vasculitis conditions effecting medium sized vessels -LB

A

Polyarteritis Nodosa
Kowasaki’s disease
Buerger’s disease

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13
Q

What causes the ‘string of pearls’ sign often seen with Polyarteritis Nodosa? -LB

A

Alternating early and late lesions from the disease on the same vessel, leading to some spots of thinning with aneurism, and other spots with fibrous tissue ‘nodes’.
=O=O=O=O=

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14
Q

A three year old Asian child presents to your office with a erythematous rash on his hands and feet, as well as conjunctivitis. His mother reports that he has had a fever for a few days as well. Later, the child starts to experience severe chest pain and EKG shows that he is suffering a myocardial infarction. What vasculitis effecting muscular blood vessels does this child have, and what is the primary treatment? -LB

A

Kawasaki’s disease, treated with aspirin (although Aspirin is often contraindicated in children with viral illnesses)

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15
Q

A 72 year old female two pack per day smoker presents to your office for a yearly checkup. She has COPD and hypertension, but reports that nothing has changed much health wise over the past year. She does notice that her hands sometimes turn pale and cold, then turn blue, and eventually red. What is causing this and how is it treated? -LB

A

Burger disease - vasospasms in the hands and feet resulting in loss of blood flow to the far extremities. Smoking cessation is the treatment.

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16
Q

Your patient comes into the office with complaints of chest pain that happen randomly with or without exercise. He also mentions having a history of cocaine usage. What is the cause of this angina?

A

Coronary artery vasospasms

this is Prinzmetal angina

17
Q

What are the potential harms of using angioplasty to treat MI?

A
  1. Calcium influx into irreversibly damaged cells leading to hyper-contraction of myofibrils
  2. Return of oxygen and inflammatory cells may possibly lead to free radical formation, which can damage myocytes.
18
Q

True or False? Fibrinous pericarditis secondary to subendocardial MI occurs ~ 1-3days after infarction.

A

False.

It only occurs if the infarction is a TRANSMURAL MI.

19
Q

When I say heart failure cells you say..?

A

Hemosiderin-Laden Macrophages.

These are seen in left sided CHF

20
Q

List the four characteristics or Tetralogy of Fallot.

A
  1. Stenosis of pulmonary artery
  2. Right ventricular hypertrophy
  3. Ventricular septal defect (VSD)
  4. Aorta overriding the VSD(a right-to-left shunt)
21
Q

BL: Hyaline arteriosclerosis and hyperplastic arterisclerosis is commonly found in what disease?

A

mild hypertension in hyaline arteriosclerosis

malignant or accelerated hypertension in hyperplastic arterisclerosis

22
Q

BL: Ring like calcifications in Monckeberg arteriosclerosis is located in what layer? What blood vessel type would be impossible to find calcifications?

A

tunica Media in muscular arteries.

capillaries cause they contain no muscles

23
Q

BL: Atherosclerotic plaques are located in what layer of the blood vessel?

A

tunica intima

24
Q

BL: What are the top 5 places that atherosclerosis could be located?

A
  1. Lower abdominal aorta:
  2. Coronary arteries
  3. Popliteal arteries
  4. Internal carotid arteries
  5. Vessels of the Circle of Willis

• Abdominal aorta > thoracic aorta, more prominent
around ostia

25
Q

BL: Consequence of artherosclerosis: Describe acute plaque changes. (3). What are other consequences of artherosclerosis? (2)

A

• Rupture/fissuring – exposes thrombogenic plaque
constituents
• Erosion/ulceration – exposes thrombogenic
basement membrane
• Hemorrhage into the plaque – expands volume of
plaque

• Thrombosis
Forms on disrupted plaque
Causes partial or complete occlusion
May embolize

• Vasoconstriction
Stimulated by circulating or local factors
May make a partial occlusion complete

26
Q

BL: Describe a “vulnerable” plaque.

A
•Fibrous cap is thinner
•Lipid core is larger
•Often do not cause
clinically significant
stenosis
•It is difficult to predict
which plaques are
vulnerable to acute
plaque change