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Vascular Pathology Flashcards

1
Q

What are the two main mechanisms of disease of the vasculature?

A
  1. narrowing or obstruction of the vessel lumen

2. weakening of the vessel wall making it prone to rupture

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2
Q

What are the three main vascular congenital anomalies?

A
  1. berry aneurysm
  2. arteriovenous fistulas
  3. fibromuscular dysplasia
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3
Q

What is a berry aneurysm?

A

A saccular outpouching of the vessel wall in the circle of Willis.
It can rupture and lead to hemorrhage and potentially death

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4
Q

What is an arteriovenous fistula?
In addition to being congenital, what are 3 other causes of AV fistulas?

What is it called if an AV fistula forms a mass?

A

Abnormal connection between an artery and vein that bypasses the capillaries and transport unused blood increasing work of the heart causing high-output heart failure.

They can be congenital or due to:

  1. inflammation
  2. trauma
  3. dialysis

If the AV fistula forms a mass, it is called a AV malformation.

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5
Q

What is fibromuscular dysplasia?
What are the two main arteries where it occurs?
What are the outcomes?

A

Segmental thickening of the muscular layer of medium and large muscular arteries (renal and carotid) due to fibrosis and hyperplasia of the intima and media.
It can lead to secondary hypertension if it occurs in the renal arteries.

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6
Q

What are the6 major products of endothelium?

A
  1. anticoagulants (prostacyclin) and antithrombotics (thrombomodulin)
  2. PROthrombotic- thromboxane, vWF
  3. ECM
  4. substances to modulate flow (vasoconstrictors like endothelin and dilators like NO)
  5. factors that regulate immunity (VCAM, IL1 ICAM)6. factors that inhibit and stimulate growth

It also oxidizes LDL

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7
Q

What are things that can damage endothelium?
In the case of endothelium damage or dysfunction, what is stimulated to migrate from the media into the intima? What is the result?

A

Infection, trauma, inflammation, immune injury, toxic exposure

Smooth muscle cells migrate into the intima, become proliferative and synthetic and make ECM thickening the intima.

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8
Q

What is arteriosclerosis?

What are the 3 main forms (using the old classification scheme)?

A

It is the hardening of the arteries (thickening and loss of elasticity of the vessel wall).

  1. atherosclerosis
  2. arteriosclerosis
  3. Monckeberg medial calcification
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9
Q

What is Monckeberg medial calcification?
What are the 2 arteries it affects most?
Who does it affect?

A 
When the media of the muscular arteries is filled with calcified deposits 
1. Radial 
2. Ulnar 
In individuals over the age of 50.
It RARELY causes stenosis
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10
Q

What are the two main types of arteriosclerosis?

A
  1. Hyaline

2. hyperplastic

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11
Q

What are the 5 classifications of arteriosclerosis according to Robbins?

A
  1. atherosclerosis
  2. primary arterial calcification (Monckeberg and internal lamina calcifications)
  3. fibrinomuscular intimal thickening (dysplasia and hyperplastic)
  4. arterial hyalinosis
  5. oxalosis and amyloidosis
    4.
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12
Q

What is atherosclerosis?
What is it composed of?
Where in the world is it seen most frequently?

A

formation of atherosclerotic plaques in the intima.
The plaque is an eccentric mass composed of fibrous cap and lipid/necrotic core.
It protrudes into the lumen and blocks blood flow

It is seen in developed nations

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13
Q

What are the three categories of risk factors for atherosclerosis?

A
  1. major and modifiable
  2. major and non-modifiable
  3. uncertain risk
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14
Q

What are the 3 major non-modifiable risk factors for atherosclerosis?

A
  1. Age- plaques present around 40-60yrs
  2. Sex- males are at greater risk until females reach menopause and then the risk is relatively equal (or females may surpass)
  3. Genetics- multifactorial disease but associated with familial hypercholesterolemia (atherosclerosis sequelae by 20 years)
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15
Q

What are the 4 major modifiable risks for atherosclerosis?

A
  1. Diabetes- hypercholesterolemia to increase risk of ischemic heart disease by 2x
  2. Hyperlipidemia- LDL(eggs/animal fats) delivers cholesterol to tissue and is bad. HDL(exercise/alcohol) removes it from tissue.
  3. Smoking - ischemic heart disease by 200%
  4. Hypertension - increase risk of ischemia by 60%
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16
Q

What are “other risks” for atherosclerosis (5)?

A
  1. Elevated C-reactive protein
  2. Lipoprotein A
  3. Elevated procoagulants
  4. Hyperhomocysteinemia
  5. Metabolic syndromes
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17
Q

What is C- reactive protein?

A

An acute phase reactant that is a marker for the role of inflammation in the development of atherosclerosis plaques.
(MI, stroke, peripheral vascular disease)

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18
Q

What is lipoprotein A?

A

It resembles plasminogen so competitively inhibits the activation of plasmin allowing thrombosis to occur

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19
Q

Describe the process of formation of an atherosclerotic plaque?

A
  1. Endothelium gets injured
  2. Increased permeability, leukocyte adhesion
  3. monocyte adhesion and migration to intima
  4. Macrophages engulf oxidized lipoproteins and form the lipid core of the plaque
  5. Platelets adhere and contribute to the thrombus
  6. Platelets, macrophages and endothelial cells recruit smooth muscle cells from the intima to proliferate and secrete ECM
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20
Q

What are the 2 major pieces of evidence for the role of hemodynamic disturbance in endothelial injury?

A
  1. Atherosclerotic plaques commonly form at points of bifurcation and Ostia where there are altered flow patterns
  2. non-turbulent laminar flow induces atherosclerotic-protective genes
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21
Q

What are the 4 major causes of hyperlipidemia?

A
  1. increased dietary LDL
  2. decreased serum HDL
  3. familial dyslipoproteinemias
  4. secondary to alcoholism or DM
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22
Q

What does hyperlipidemia lead to?

A

It increases production of ROS that can:

  1. inactivate NO (a vasodilator)
  2. oxidize LDL which will accumulate in the intima to be taken up by macrophages to accumulate in the clot and be toxic to endothelial cells and smooth muscle cells
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23
Q

What is the role of inflammation in endothelial cell injury and plaque formation?

A

When inflamed, endothelial cells express vascular cell adhesion molecules to bind monocytes which: 1. become macrophages in the intima to engulf lipid
2. produce ROS
3. increase production of oxidized LDL
They also bind T cells which :
1. secrete cytokines to activate macrophages, endothelial cells and smooth muscle cells

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24
Q

What infectious agents have been found in plaques but not normal vessels?

A
  1. herpesvirus
  2. CMV
  3. Chlamydia pneumoniae
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25
Q

What signals stimulate smooth muscle cells to migrate from the media to the intima to proliferate and secrete ECM?
What else do smooth muscle cells do besides thicken the intima?

A

PDGF, FGF, TGFa

They engulf LDL

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26
Q

Secretion of ECM, mainly ________ by smooth muscle cells, helps promote plaque growth and expansion from ______ to ____________.

A

mainly collagen

Fatty streak –> atherosclerotic plaque

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27
Q

Describe the morphology of a fatty streak.

A

Linear, slight intimal elevations filled with lipid-laden foam cells
They appear in the aorta as young as 1 year old

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28
Q

What are the three components of an atherosclerotic plaque?

A
  1. cells (macrophages, T cells, smooth muscle cells)
  2. ECM (collagen, elastic fiber, proteoglycans)
  3. lipid (intracellular and extracellular)
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29
Q

What are the three principal areas of the atherosclerotic plaque?

A
  1. fibrous cap
  2. shoulder (slightly more cellular)
  3. lipid/necrotic core
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30
Q

What do plaques have that make them especially susceptible to hemorrhage?

A

neovascularization that can hemorrhage, rupture and form thrombus

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31
Q

What are the acute changes in a plaque?

A
  1. rupture
  2. ulceration
  3. erosion
  4. hemorrhage
  5. embolism
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32
Q

If a plaque ruptures and exposes the necrotic core, why is this a problem?

A

The core is thrombogenic meaning that it will promote thrombogenesis and occlude the vessel more

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33
Q

If there is hemorrhage in the atherosclerotic plaque, what are two potential outcomes?

A
  1. acute expansion of the plaque can cause rupture and acute thrombosis
  2. the hemorrhage can resolve but contribute to the size of the plaque (chronic)
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34
Q

What are chronic changes that can occur to an atherosclerotic plaque?

A

pressure of the plaque on the intima causes atrophy and weakening of the media which can lead to:

  1. aneurysm
  2. rupture
  3. hemorrhage
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35
Q

Chronic changes in plaque size are due to what?

Acute changes in plaque size are due to what?

A

Chronic- increasing accumulation of LDL and continued collagen production and/or hemorrhage resolution

Acute- thrombosis or hemorrhage

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36
Q

What is the critical degree of stenosis that must occur for an atherosclerotic plaque to cause symptoms?

A

> 70-75% obstruction of the vessel

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37
Q

If atherosclerotic plaques form in the vessels of the lower extremities, what happens?
What is the pain referred to as?

A

The muscles become ischemic with exercise (walking).

The ischemia produces pain called claudication which ceases when exercise stops

38
Q

What are the two types of hypertension?

A

Pulmonary hypertension and systemic hypertension

39
Q

BP = ____x_____

A

COxSVR

40
Q

What is the main regulator of blood volume?

What is the main regulator of peripheral resistance?

A

volume is regulated by the concentration of sodium

PVR is controlled by the arterioles which are regulated by neural and hormonal factors

41
Q

Describe the renin-angiontensin-aldosterone system.

A
  1. When blood volume or pressure is low, the kidney secretes renin.
  2. Renin converts angiontensinogen to angiotensin I
  3. Ang I is converted to Ang II by ACE
  4. Angiotensin II contracts smooth muscles raising peripheral resistance and increasing BP
  5. Angiotensin II also stimulates aldosterone which reabsorbs Na to increase H20 retention to increase volume
42
Q

What is the difference between essential (primary) hypertension and secondary hypertension?
What percent of cases of systemic hypertension are primary?

A

Secondary has an identifiable underlying cause. Primary hypertension is idiopathic (no identifiable cause)

90-95% have no identifiable underlying cause (but are most likely the result of multiple genetic and environmental factors)

43
Q

What are the characteristics of malignant hypertension?

A
  1. Acute and marked increase in BP (diastolic >120)

2. association with renal failure

44
Q

Essential hypertension most likely is the result of __________ and ________ factors that result in reduced __________ and _________.

A

genetic and environmental factors that result in reduced Na excretion (causing increased volume) and vasoconstriction

45
Q

What are the 4 main causes of secondary hypertension?

A
  1. Renal
  2. endocrine
  3. cardiovascular
  4. neurologic causes
46
Q

What are the 4 renal causes of secondary hypertension?

A
  1. acute glomerulonephritis
  2. chronic renal disease
  3. renal artery stenosis
  4. renin-producing tumors
47
Q

How does renal artery stenosis contribute to secondary systemic hypertension?

A

The kidney at the distal end of the vessel perceives low volume and will release renin to compensate. This will raise the pressure in the kidney to a normal level but will raise the BP in the rest of the body to a hypertensive level

48
Q

What are the endocrine causes of hypertension?

A
  1. Cushing syndrome
  2. primary aldosteronism (tumor of adrenal cortex that release aldo and retains sodium)
  3. pheochromocytoma- catecholamine releasing tumor
  4. hyper/hypothyroidism
49
Q

What are the 3 main cardiovascular causes of secondary hypertension?

A
  1. coartation (narrowing) of the aorta
  2. increased CO
  3. intravascular increase in volume
50
Q

What are the neurologic causes of hypertension?

A
  1. acute stress
  2. phsychogenic
  3. increased intracranial pressure (the brain perceives low flow and raises the body BP to compensate)
51
Q

Hypertension can predispose patients to ________ and _________ and can damage small vessels leading to _________ and _______ arteriosclerosis.

A

cerebral hemorrhage and aortic dissection

hyaline and hyperplastic arteriosclerosis

52
Q

Describe the morphology of hyaline arteriosclerosis. What type of hypertension is it seen in?

A

It is acellular, eosinophilic hyaline that surrounds the vessel due to leakage of plasma proteins and overproduction of ECM by smooth muscle cells.
It is seen in benign hypertension

53
Q

Describe the morphology of hyperplastic arteriosclerosis. What type of hypertension is it seen in?

A

It is cellular, concentric rings that laminate and thicken the arteriole wall (onion skin)
It is due to smooth muscle cells and duplicated BM.

Malignant hypertension

54
Q

What is an aneurysm?

What is a dissection?

A

An aneurysm is a localized abnormal dilation of the vessel wall or wall of the heart.
A dissection occurs when a tear in the intima of a vessel allows blood to seep into the media

55
Q

What is the difference between a true aneurysm and a false aneurysm?

A

True aneurysms are dilations that involve all three layers of the vessel wall (atherosclerotic, syphilitic, congenital, ventricular)

False aneurysms are hematomas outside the wall of the vessel due to damage to the vessel

56
Q

What is the difference between a saccular and fusiform aneurysm?

A

Saccular is an eccentric outpouching involving a segment of the vessel wall.

Fusiform is generalized concentric dilation of the wall of the vessel

57
Q

What are the two most common causes of aneurysms?

What are other causes?

A 
Most commonly:
1. atherosclerosis
2. cystic medial degeneration 
Other:
1. Mycotic aneurysms (due to infections like syphilis)
2. trauma
58
Q

Mycotic aneurysms can result by what 3 mechanisms?

A
  1. local extension of an adjacent infection
  2. embolization of infective endocarditis
  3. circulating organisms in the blood that infect the wall
59
Q

What is an AAA? Where does it most commonly occur? What is the most common cause?

A

Abdominal aortic aneurysm from atherosclerosis that occurs below the renal arteries above the iliac bifurcation.

60
Q

AAA occurs more frequently in_____ than ______. It is most common over the age of ______.
It (does/does not) have a genetic component.

A

men > women
50
does

61
Q

How does an AAA form?

A
  1. intimal plaques from atherosclerosis compress the media and vasculature impairing delivery of O2 and nutrients to the wall of the vessel
  2. Necrosis occurs
  3. Matrix metalloproteinases degrade ECM and are usually in balance with tissue inhibitors of metalloproteinases. An imbalance is created
  4. The wall is weak and expands out
62
Q

What are the 3 major factors in the development of an AAA?

A
  1. aortic wall proteolysis by matrix metalloproteinases
  2. aortic wall inflammation
  3. oxidative stress
63
Q

Describe the process of formation of a syphilitic aneurysm. What vessels are involved?

A

Obliterative endarteritis involves the vasa vasorum so it causes ischemic damage to the media allowing for dilation of the vessel.
It involves the thoracic aorta, specifically the aortic root.
It leads to aortic insufficiency and LV dilation

64
Q

What are complications of a thoracic aortic aneurysm?

A
  1. pressure on mediastinal structures:
    - cough bc of irritation of recurrent laryngeal nerve
    - trouble breathing bc pressure on lungs
    - compression of esophagus
  2. pain due to bone erosion
  3. aortic insufficiency (if the hemorrhage extends to the aortic valve ring)
  4. aortic rupture
65
Q

What is an aortic dissection?
What are the 2 possible routes?
What are most aortic dissections due to?

A

tearing of the intima allowing blood to enter the medial of the vessel and travel within the vessel wall. then the blood can:

  1. exit back into the vessel at a point distal to the tear
  2. tear through the adventitia and into the pericardial sac, pleural cavity or retroperitoneum

Most are due to hypertension (increased pressure on the aortic wall compresses the vaso vasorum, decreasing nutrient/O2 delivery. the wall is weakened and can tear)

66
Q

Epidemiologically, who is most likely to get an aortic dissection?

A
  1. 40-60 year old males with hypertension
  2. Marfan’s or EDS
  3. pregnant women
  4. during coronary artery catheterization
67
Q

How does Marfan’s syndrome cause aortic dissection?

A

It is a defect in fibrillin protein which is a structural protein that allows elastin to organize. Elastin gives strength to the wall and makes it resistant to tear

68
Q

Describe the morphology of an aortic dissection.
Where in the media is the hemorrhage?
What is found by the tear?

A

The hemorrhage is in the middle and outer thirds of the media but can vary in thickness.

Cystic medial degeneration- elastic tissue at the tear site fragments and become separated by an amorphous acellular proteoglycan ECM

69
Q

What is vasculitis? What vessels does it affect?

What are the two main ways it occurs?

A

Inflammation of any vessel wall (aorta to capillaries to venules and veins)

  1. infection
  2. immune-mediated inflammation
70
Q

What are the 3 mechanisms of immune-mediated vasculitis?

A
  1. Immune complex associated
  2. anti-neutrophil cytoplasmic Ab (pANCA or cANCA)
  3. anti-endothelial Ab
71
Q

What are three examples of immune-complex associated vasculitis?

A
  1. SLE
  2. drug hypersensitivity
  3. viral infections
72
Q

What are the two main anti-neutrophilic cytoplasmic antibodies?
Where are they located? What are they against?
What diseases are each associated with?

A
  1. pANCA
    - against myeloperoxidase
    - perinuclear localization
    - Churg-Strauss and microscopic polyangitis
  2. cANCA
    - against proteinase-3
    - cytoplasmic localization
    - Wegener granulomatosis
73
Q

What is the mechanism by which the ANCAs work?

A

Neutrophils release PR3 or myeloperoxidase promoting ANCA formation.
Then a disorder may express PR3 and myelo abbherently on the vascular cell surface leading to ANCA binding and neutrophil degranulation

74
Q

Describe Giant-cell (temporal) arteritis.

  1. vessels involved
  2. histology
  3. clinical presentation
  4. Pathogenesis
A
  1. temporal, vertebral, ophthalmic, aorta
  2. granulomas, fragmented internal elastic lamina, nodular intima thickening
  3. OVER 50 (headache, vision changes)
    4, T-cell mediated inflammation
75
Q

Describe Takayasu arteritis.

  1. vessels involved
  2. histology
  3. clinical presentation
  4. Pathogenesis
A
  1. aorta and branches, pulmonary
  2. granulomas, narrowing of lumen (collagen scarring and inflammation)
  3. “pulseless” in upper extremities, ocular disturbances, aortic insufficiency, MI, 50 OR YOUNGER
  4. ???
76
Q

Describe polyarteritis nodosa.

  1. vessels involved
  2. histology
  3. clinical presentation
  4. Pathogenesis
A
  1. small and medium muscular arteries (renal, visceral NOT PULMONARY)
  2. segmental and transmural necrotizing inflammation that is TEMPORALLY DISSIMILAR thrombus
  3. Young adults- symptoms associated to what artery is affected
  4. HBsAg-HBsAb immune complexes
77
Q

Describe Kawasaki disease (mucocutaneous lymph node syndrome)

  1. vessels involved
  2. histology
  3. clinical presentation
  4. Pathogenesis
A
  1. coronary arteries
  2. transmural inflammation with less prominent fibrinoid necrosis than PAN
  3. Infants and children under 4
    - Acute phase= conjunctival and oral erythema, edema of hands/feet, lymph node enlargement
    - chronic= coronary artery ectasia or aneurysm–> thrombus or rupture
  4. Delayed type hypersensitivity with autoantibodies against endothelial cells and smooth muscle
78
Q

Describe Microscopic Polyangiitis (leukoclastic vasculitis)

  1. vessels involved
  2. histology
  3. clinical presentation
  4. Pathogenesis
A
  1. capillaries, arterioles, venules
  2. segmental and tranmural necrotizing inflammation that is temporally similar
  3. Lung is commonly involved as well as skin, mucous membrane, GI heart brain kidneys muscle
  4. Immune complex deposition with Ab to drugs, microorganisms, tumor proteins . pANCA
79
Q

Describe Wegener granulomatosis.

  1. vessels involved
  2. histology
  3. clinical presentation
  4. Pathogenesis
A
  1. small vessels
  2. TRIAD
    - acute necrotizing granulomas in the upper respiratory tract
    - necrotizing/granulomatous vasculitis in the lungs
    - focal necrotizing glomerulonephritis
  3. Males >40 with pneumonia, sinusitis, renal disease
  4. cANCA
80
Q

Describe Churg-Strauss.

  1. vessels involved
  2. histology
  3. clinical presentation
  4. Pathogenesis
A
  1. small vessels
  2. transmural necrotizing inflammation with eosinophilic granulomas
  3. allergic rhinitis, asthma, peripheral eosinophilia
  4. pANCA
81
Q

Describe Buerger disease.

  1. vessels involved
  2. histology
  3. clinical presentation
  4. Pathogenesis
A
  1. medium and small vessels (tibial, radial)
  2. segmental acute and chronic vasculitis, thrombosis, microabscesses
  3. before 35 in heavy smokers with phlebitis and pain at rest which can chronically ulcerate the toes
  4. direct toxicity of tobacco products
82
Q

What is Raynaud’s phenomenon?

What are the 3 types?

A

exaggerated vasoconstriction of arterioles and arteries of the digits (fingers are white or blue with cyanosis and proximal to the constriction is red from dilation)

  1. Primary- young women when they are cold or with emotion. Benign
  2. Secondary- vasoconstriction with a disease process (SLE or atherosclerosis)
  3. Cardiac- in the heart which can lead to infarction resulting in sudden death or ischemic dilated myopathy
83
Q

What are varicose veins?

What are the 3 locations they mainly occur?

A

dilated veins produced by increased intraluminal pressure and loss of vessel wall support

  1. of the legs- stasis leads to congestion, edema, pain and thrombosis
  2. esophageal varices- due to cirrhosis of the liver because it is an alternate route of blood back to the heart
  3. hemorrhoids- prolonged pelvic vascular congestion- straining at stool that can cause pain, thrombose, hemorrhage
84
Q

What is thrombophlebitis?
What are risk factors?
What are the complications?

A 
It is inflammation and thrombus in veins
The risk factors are:
1. infection
2. factor V Leiden (hypercoagulable)
3. CHF
4. neoplasia
5. immobility
6. pregnancy
7. obesity

It can lead to embolism (DVT-> PE)

85
Q

What is lymphangitis?

A

inflammation of lymphatics due to bacterial infection

86
Q

What are the 3 types of hemangiomas?
What area of the body does each affect?
Do they persist or regress?
What type of person does each affect?

Benign or malignant?

A
  1. cavernous- deep structures (like liver) and do not regress. von Hippel-Lindau disease
  2. capillary- superficial (like skin) and regress. Children and infants.
  3. pyogenic granuloma- proliferating capillaries, chronic inflammatory exudate, edema. Skin and gingival surfaces. Associated with pregnancy.

Benign

87
Q

What is a glomus tumor?
Where is it common to see them?
Benign or malignant?

A

Benign but painful tumor from modified smooth muscle cells of the glomus body (part of the dermis that controls temperature regulation)
See them under the fingernails or at distal parts of the fingers

Benign

88
Q

What is Osler-Weber-Rendu disease?

Benign or malignant?

A

Hereditary hemorrhagic telangiectasia- AD disease where there are dilated capillaries and veins in the skin and oral mucous membranes

Benign

89
Q

What is Bacillary angiomatosis?

What bacteria is it associated with?

A

It is vascular proliferation of the bone, skin and brain due to a Bartonella infection

90
Q

What are the 4 forms of Karposi’s sarcoma?

What viral infection are they ALL associated with?

A
  1. Chronic (classic) presenting in older Europeans in their lower extremities. Locally persistant, not aggressive
  2. Endemic in Africa. Very aggressive and affects internal organs
  3. Transplant associated- aggressive
  4. AIDS-associated - skin and viscera

They are associated with HHV8 (herpes)

91
Q

What is the morphology/progression of Karposi’s sarcoma?

What cells are seen microscopically?

A

patches–> plaques–> nodules

Microscopically you see angulated blood vessels and spindle cells with extravasted RBCs

92
Q

What are the clinical scenarios that cause angiosarcoma?

What do the tumors look like?

A
  1. Vinyl chloride exposure
  2. lymphedema (common in upper extremity after axillary node dissection in breast cancer)

They range from well-differentiated (looking like hemangiomas) to poorly-differentiated (don’t look like blood vessels at all)

Cardio Block (25 decks)

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