Path slide set 1 Flashcards

1
Q

what causes a thoracic aortic aneurysm?

A

HTN

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2
Q

young women, renal artery, beads on string

A

Fibromuscular dysplasia

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3
Q

occurs when blood enter defect in intima and travels through tissue plane within layers of aortic media

A

Aortic dissection

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4
Q

What is the most frequent preexisting histologically detectable lesion of an aortic dissection?

A

cystic medial degeneration. inflammation generally absent

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5
Q

Where are most dissections?

A

Ascending aorta

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6
Q

what causes and abdominal aorta aneurysm

A

atherosclerosis

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7
Q

HTN has increased prevalence in who?

A

advancing age and african americans

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8
Q

What is the cause of most HTN?

A

idiopathic (essential HTN; 90-95%

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9
Q

vascular morphological changes of HTN?

A

hyaline or hyperplastic arteriolosclerosis

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10
Q

In the pathogenesis of an Aneurysm, what weakens the vascular wall by ischemia of inner media?

A

Atherosclerosis

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11
Q

prolonged activation of endothelium may lead to endothelial dysfunction, often characterized by what?

A
  • procoagulation
  • proinflammation
  • smooth muscle stimulation
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12
Q

In tact but thinned muscular wall at site of dilation

A

“true” aneurysm

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13
Q

what can an AAA impinge?

A

ureter or erosion of vertebrae

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14
Q

Other non major modifiable risk factors

A
  • inflammation (levels of C-reactive protein)
  • hyperhomocystinemia (>100umol/L)
  • metobolic syndrome
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15
Q

major modifiable risk factors of atherosclerosis

A
  • hyperlipidemia (LDL) based on diet and exercise
  • HTN
  • Smoking
  • DM
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16
Q

Most common locations for atherosclerotic lesions in decreasing frequency?

A
  • abdominal aorta
  • coronary arteries
  • popliteal arteries
  • Internal carotid arteries
  • Circle of Willis
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17
Q

Activated state of endothelium is characterized by expression of what?

A
  • adhesion molecules
  • procoagulants and anticoagulants
  • voasoactive factors, growth factors
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18
Q

Constitutional risk factors for atherosclerosis

A
  • Family history
  • Age
  • gender
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19
Q

Congenital conditions predisposing to aneurysm

A
  • Marfan syndrome - fibrillin
  • Ehlers Danlos - type 3 collagen
  • Loeys-Dietz - TGF beta receptor - synthesis of elastin and COL 1 and 3
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20
Q

explain the gender predisposition for atherosclerosis

A

Males more than females until women hit menopause then increases and they eventually pass men

21
Q

Advanced glycation end products can cause activation of endothelium due to what disorder?

A

uncontrolled diabetes

22
Q

besides HTN, when else would you see hyaline arteriolosclerosis?

A

long standing diabetes

23
Q

in the pathogenesis of an aneurysm, loss of vascular wall elastic tissue or ineffective elastin synthesis leads to what?

A

cystic medial degeneration

24
Q

describe cystic medial degeneration

A

disrupted and disorganized elastin filaments and increased ground substance (proteoglycans)

25
Q

what gives a “pulsating hematoma”

A

False aneurysm

26
Q

defect though wall of vessel or heart, communicating with an extravascular hematoma?

A

“false” aneurysm

27
Q

severe chest pain, radiating to back b/t scapulae

A

Aortic dissection

28
Q

When oxidized LDL accumulated within macrophages and smooth muscle cells it forms what?

A

foam cells and a “fatty streak”

29
Q

Clinically significant effects of large or multiple arteriovenous fistulas?

A

shunting of blood from arterial to venous and forcing heart to pump additional volume –> high-output cardiac failure

30
Q

Describe Hyaline arteriolosclerosis

A
  • increase smooth muscle matrix synthesis
  • plasma protein leakage across damaged endothelium
  • homogeneous pink thickening of vessel wall with luminal narrowing
31
Q

complications of atherosclerotic plaques

A
  • Rupture and ulceration
  • hemorrhage
  • embolism
  • Aneurysm
32
Q

what congenital vascular disorder are berry aneurysms associated with?

A

Autosomal dominant polycystic kidney disease

33
Q

primary risk factor for aortic dissection

A

HTN

34
Q

Accumulation of cholesterol crystals within macrophages is recognized by what? leading to what?

A

inflammasome, leading to IL-1 secretion and further macrophage and T cell recruitment and activation

35
Q

explain intimal thickening

A

-smooth muscle cells from media go to intima where they proliferate and elaborate ECM

36
Q

what is the more frequent epidemiology for an AAA

A

smoking men in their 50s

37
Q

descibe hyperplastic arteriolosclerosis

A
  • occurs in severe HTN

- smooth muscle cells form concentric lamellations (“onion skinning”) with resultant luminal narrowing

38
Q

Describe the Response to injury model for pathogenesis of atherosclerosis

A

1: chronic endothelial “injury”
2: endothelial dysfunction, monocyte adhesion and emigration
3: macrophage activation and smooth muscle recruitment
4: macrophages and smooth muscle cells engulf lipid, forming “foam cells”
5: smooth muscle proliferation, collagen and other ECM deposition, extracellular lipid

39
Q

HTN is what blood pressure?

A

> 140/90

40
Q

clinical sign of AAA

A

pulsating mass in abdomen

41
Q

epidemiology of aortic dissection

A
  • hypertensive males 40-60

- marfans

42
Q

Tertiary Syphilis affects what location?

A

Vaso vasorum of thoracic Aorta leading to ischemia of outer media

43
Q

Focal thickening of INTIMA and MEDIA of medium to large muscular arteries resulting in stenosis

A

fibromuscular dysplasia

44
Q

What is the stereotypical response to vascular injury?

A

intimal thickening

45
Q

Loss of endothelial cells secondary to tissue damage or prolonged endothelial dysfunction leads to what?

A

vascular injury

46
Q

Where is ACE found?

A

endothelial cells everywhere but especially in lungs

47
Q

In the pathogenesis of an Aneurysm, what weakens the vascular wall by ischemia of outer media?

A

HTN and Tertiary syphilis

48
Q

Clinical presentation of Thoracic Aortic aneurysm?

A

impingement of lower respiratory tree, esophagus, and recurrent laryngeal nerves - respiratory difficulty, difficulty swallowing and persistent cough