Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardio II Midterm > Vascular Pathology 1 > Flashcards

Vascular Pathology 1 Flashcards

1
Q

Berry aneurysms

A

Typically found in the Circle of Willis

Associated with AD polycystic kidney disease

Rupture can cause fatal subarachnoid hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Arteriovenous fistulas

A

artery –> vein

most commonly a developmental defect, may arise secondary to inflammation, trauma, rupture

may lead to rupture and hemorrhage, or to high-output cardiac failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Fibromuscular dysplasia

A

Focal thickening of intima and media of middle to large muscular arteries, resulting in stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Vascular response to injury - endothelial cell activated state

A 
Stimuli:
Turbulent blood flow
HTN
Complement, bacterial products, lipid products, glycation end products
Viruses
Hypoxia, acidosis
Components of tobacco smoke

Characterized by expression of:
Adhesion molecules
procoagulants and anticoagulants
vasoactive factors, growth factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Endothelial dysfunction

A

prolonged activated state

characterized by:
pro coagulation
pro inflammation
smooth muscle stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Vascular injury

A

loss of endothelial cells secondary to tissue damage or prolonged endothelial dysfunction

Response: intimal thickening

  • smooth muscles cells from the media migrate to the intima, where they proliferate and elaborate ECM
  • Intima thickened, potentially affecting blood flow in that vessel

Vascular intimal thickening seen in response to any injury to the vessel, regardless of cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

HTN is a risk factor for:

A

Atherosclerosis, aortic dissection
Hypertensive heart disease
Stroke
Hypertensive renal disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Factors that alter cardiac output

A

Blood volume - sodium, mineralocorticoids, ANP

Cardiac factors - HR, contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Factors impacting peripheral resistance

A

Humoral factors:
Constrictors: AngII, catecholamines, thromboxane, leukotrienes, endothelin
Dilators: prostaglandins, kinins, NO

Neural factors
Constrictors: alpha-adrenergic
Dilators: beta-adrenergic

Local factors: auto regulation, pH, hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Renin

A

released by juxtaglomerular cells in afferent arterioles in the kidney in states of low volume or low peripheral resistance, or decreased GFR

Cleaves angiotensinogen to angiotensin I

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Angiotensin II

A

ACE converts angiotensin I to angiotensin II

short lived vasoconstrictor

stimulates adrenal cortex release of aldosterone - renal reabsorption of Na+ and water

Resistance and volume increased, raising BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Atrial natriuretic peptide

A

released by myocardial cells in response to volume expansion.

Leads to Na+ excretion and diuresis as well as vasodilation –> lower BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hyaline arteriolosclerosis

A

Increased smooth muscle matrix synthesis

Plasma protein leakage across damaged endothelium

Homogenous pink (hyaline) thickening of the vessel wall, with associated luminal narrowing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hyperplastic arteriolosclerosis

A

Occurs in severe hypertension

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Constitutional risk factors for Atherosclerosis

A

family hx
age
gender

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Modifiable risk factors (major) for Atherosclerosis

A

Hyperlipidemia (especially LDL)
HTN
Smoking
DM

17
Q

Minor modifiable risk factors for Atherosclerosis

A

inflammation
hyperhomocystinemia
Metabolic syndrome

18
Q

Response to injury model for atherosclerosis pathogenesis

A

chronic injury and/or dysfunction of endothelium, leading to chronic inflammation and attempting to repair the tissue

1) chronic endothelial injury due to: hyperlipidemia, HTN, smoking, homocysteine, hemodynamic factors, toxins, viruses, immune reactions
2) Endothelial dysfunction (increased permeability leukocyte adhesion), monocyte adhesion and emigration
3) macrophage activation, sm.m. recruitment
4) macrophages and sm.m. cells engulf lipid
5) Sm.m. proliferation, collagen and other ECM deposition, extracellular lipid

19
Q

Fibrofatty atheroma characteristics

A

Fibrous cap - smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization

Necrotic center - cell debris, cholesterol crystals, foam cells, calcium

Media

20
Q

Hemodynamic turbulence associated with endothelial injury and dysfunction in the pathogenesis of atherosclerosis

A

◦ Atherosclerosis does not occur randomly in vessels, nor does it occur everywhere uniformly

◦ Most lesions tend to occur at openings of exiting vessels, branch points, posterior abdominal aorta—due to flow disturbances normally seen in these locations

21
Q

Circulating lipids associated with endothelial injury and dysfunction in the pathogenesis of atherosclerosis

A

◦ Lipids in atheromatous plaques are predominantly cholesterol and cholesterol esters

◦ Accumulate in the intima, are taken up by macrophages and partially oxidized

◦ This modified LDL further accumulates within macrophages and smooth muscle cells, forming foam cells and a lesion known as a “fatty streak”

◦ This stimulates an inflammatory response to accumulation of this toxic form of LDL

22
Q

Inflammation in the pathogenesis of atherosclerosis

A

◦ Accumulation of cholesterol crystals within macrophages is recognized by the inflammasome, which leads to IL-1 secretion

◦ More macrophages and T-lymphocytes are recruited and activated

◦ Inflammatory cytokines further activate endothelial cells, and growth factors stimulate smooth muscle cells to migrate to the intima and proliferate

23
Q

Smooth muscle proliferation and matrix deposition in the pathogenesis of atherosclerosis

A

◦ Proliferating smooth muscle cells synthesize extracellular matrix, including collagen

◦ Due to the intimal expansion from foam cells and extracellular lipid, recruited inflammatory and smooth muscle cells and increased ECM, an atheromatous plaque is formed

◦ Over time, a soft fibrofatty plaque becomes covered with a fibrous cap (dense collagen fibers). The center of the plaque is necrotic, containing lipid, debris, foam cells and thrombus, surrounded by a zone of inflammatory and smooth muscle cells.

24
Q

Atherosclerosis - Common sites of involvement

A 
In decreasing order of frequency/severity of involvement: ◦ Abdominal aorta
◦ Coronary arteries
◦ Popliteal arteries
◦ Internal carotid arteries 
◦ Circle of Willis
25
Q

Complications of atherosclerotic plaques

A

Rupture and ulceration
◦ May lead to thrombosis

Hemorrhage
◦ May follow plaque rupture

Embolism
◦ May follow plaque rupture

Aneurysm formation

26
Q

Stenosis of the arterial lumen in atherosclerosis

A

◦ Plaques tend to continually grow because of repeated cycling through the injury-healing process

◦ The lumen of the affected vessel gradually shrinks, eventually leading to ischemia downstream (a point known as critical stenosis – approximately 70% occluded)

◦ This may lead to chronic ischemia of myocardium, bowel, brain, the extremities, etc.

27
Q

Acute plaque change

A

An acute thrombus may form over the plaque, occluding the artery. This may occur secondary to
◦ Rupture of the plaque
◦ Erosion or ulceration of the plaque surface

Hemorrhage into the plaque may acutely expand its volume

28
Q

Factors making some plaques more prone to rupture than others

A

◦ The fibrous cap is continually being degraded and resynthesized (remodeled)

◦ Increased inflammation in the plaque can accelerate fibrous cap degradation and inhibit its resynthesis, thus reducing the amount of collagen in the cap and weakening it

◦ Physical stresses can cause plaque rupture

  • Changes in blood pressure
  • Vasoconstriction
29
Q

Aneurysm

A

Localized abnormal dilation of a blood vessel or the heart that may be congenital or acquired

30
Q

True vs false aneurysm

A

True: characterized by an intact, but thinned, muscular wall at the site of the dilation

False: defect through the wall of the vessel or heart, communicating with an extravascular hematoma

31
Q

Aneurysm pathogenesis

A

Occur whenever connective tissue of vascular wall is weakened

◦ Defective vascular wall connective tissue
-Marfan syndrome (defective fibrillin synthesis)

◦ Net degradation of vascular wall connective tissue
-Inflammatory conditions (such as atherosclerosis) → increased matrix metalloprotease

◦ Weakening of the vascular wall by ischemia

  • Atherosclerosis → ischemia of inner media
  • Hypertension → ischemia of outer media
  • Tertiary syphilis → ischemia of outer media (thoracic aorta)
32
Q

Cystic medial degeneration

A

loss of vascular wall elastic tissue or ineffective elastin synthesis

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

final common result of different conditions (ischemic medial damage, Marfan syndrome)

33
Q

Most common causes of aortic aneurysms

A

atherosclerosis

HTN

34
Q

Abdominal aortic aneurysm

A

usually below renal arteries, often involve common iliac arteries

More frequent in men, smokers, 60s

Characterized by severe atherosclerosis of the aorta, covered with mural thombus

Pulsating mass in abdomen

35
Q

Complications of AAA

A

rupture (risk related to size) and hemorrhage
Occlusion of branching arteries and downstream ischemia
Embolism
Impingement on another structure

36
Q

Thoracic aortic aneurysm

A

Often due to HTN or Marfan

Clinical presentation:
Impingement: lower respiratory tree, esophagus, recurrent laryngeal nerves

Aortic valvular insufficiency
Rupture

37
Q

Aortic dissection

A

Occurs when blood enters a defect in the intima and travels through a tissue plane within layers of the aortic media.

Aortic dissection occurs in
◦ Hypertensive males, 40-60
◦ Patients with disorders of vessel connective tissue (Marfan)

The primary risk factor is hypertension.

Classic presentation: severe chest pain, radiating to the back between the scapulae

38
Q

Aortic dissection pathogenesis

A

Blood enters aortic wall via an intimal tear (cause generally unknown), forming an intramural hematoma

Hypertensive patients, there is some degree of cystic medial degeneration (many there is little or none)

Most dissections arise in the ascending aorta

39
Q

Type A vs Type B aortic dissections

A

Type A: involve ascending aorta, more common, higher morbidity and mortality; treated with antihypertensive therapy and surgical repair of intimal tear

Type B: does not involve ascending aorta

Most common cause of death is rupture

Dissection may extend along arterial branches causing occlusion of those vessels

Cardio II Midterm (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions