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PATHOLOGY (2nd year) > BLOOD VESSELS > Flashcards

BLOOD VESSELS Flashcards

1
Q
  1. What is the risk of rupture of abdominal aortic aneurysm if it is more than 6cms
    a. 1%
    b. 10%
    c. 20%
    d. 25%
A

Rationale: [d] 25%- larger than 6cm . Risk of rupture is directly related to the size of aneurysm (size is directly proportional to degree of rupture): 1%- 4-5cm; 11%- 5-6cm; 25%- larger than 6cm; 20%- expands rapidly (0.2-0.3cm/yr.)

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2
Q
  1. All vessels have a three-layered architecture, consisting of an intima, tunica media and adventitia, except:
    a. veins
    b. aorta
    c. arterioles
    d. capillaries
A

[d] capillaries. They have an endothelial lining but without tunica media and with variable number of pericytes

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3
Q
  1. Which form of Kaposi Sarcoma is associated with HHV8?
    a. Classic KS
    b. Endemic KS
    c. Epidemic KC
    d. Transplant associated KS
A

A. Chronic, Classic or European KS: Associated with a second malignant tumor or altered immune state but NOT associated with HIV.
B. Lymphadenopathic, African or Endemic KS: Localized or generalized lymphadenopathy and disorder occasionally involves the viscera.
C. AIDS associated (epidemic) KS: HHV 8.
D. Transplant Associated KS: Post op in solid organ transplant recipients who receive high doses of immunosuppressive therapy.

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4
Q
  1. A 23 years old man presents with fever, weight loss,
    malaise, abdominal pain, and myalgias. Work up reveals that the patient has polyarteritis nodosa (PAN) . Which of
    the following is associated with this form of vasculitis?
    a. Chlamydia
    b. Hepatitis B
    c. HHV8
    d. HIV
A

[b] Hepatitis B. Vasculitis secondary to infections. Antibodies to microbial constituents can form immune complexes that circulate and deposit in vascular lesions. In up to 30% of patients
with polyarteritis nodosa, the vasculitis is attributable to immune complexes composed of hepatitis B surface antigens (HBsAg) and anti-HBsAg antibody.

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5
Q
  1. 19 years old women presents with fever, malaise, myalgias and arthritis and “coldness” in her upper extremities. She has a weak radial pulse. Angiography shows stenosis of the aorta. Which among the following rheumatic condition does
    the patient have?
    a. Buerger Disease
    b. kawasaki Disease
    c. Reynaud disease
    d. Takayasu disease
A

[d] Takayasu disease/arteritis characterized by ocular disturbances and marked weakening of pulses in the upper extremities (pulseless disease) classically involves the aortic arch with pulmonary, coronary and renal artery involvement.

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6
Q

This condition is the result from exaggerated vasoconstriction of digital arteries and arteriole and there paroxysmal pallor of the hands and feet.
a. Buerger Disease
b. kawasaki Disease
c. Reynaud Phenomenon
d. Takayasu disease

A

[c] Reynaud phenomenon is an exaggerated vasoconstriction resulting in red, white and blue discoloration proximal to distal. Buerger disease or Thromboangitis obliterans is a segmental thrombosing acute and chronic inflammation of tibial and radial artery almost exclusively to heavy smoker less than 35 y.o. Kawasaki disease is the leading cause of acquired heart disease in children with anti-endothelial antibody. While Takayasu disease also known as pulseless disease is a granulomatous vasculitis with ocular disturbance and marked weakening of pulse in upper extremities.

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7
Q
  1. This vasculitis is almost exclusive to heavy smokers less than 35 y/o
    a. Buerger Disease
    b. kawasaki Disease
    c. Reynaud Phenomenon d. Takayasu disease
A

[a] Buerger disease or Thromboangitis obliterans is a segmental thrombosing acute and chronic inflammation of tibial and radial artery almost exclusively to heavy smoker less than 35 y.o. Reynaud phenomenon is an exaggerated vasoconstriction resulting in red, white and blue discoloration proximal to distal. Kawasaki disease is the leading cause of acquired heart disease in children with anti-endothelial antibody. While Takayasu disease also known as pulseless disease is a granulomatous vasculitis with ocular disturbance and marked
weakening of pulse in upper extremities.

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8
Q
  1. What are the antibodies present in the following vasculitis?
    Churg-strauss
    a. MPO ANCA
    b. PR3 ANCA
    c. Anti-endothelial antibodies
A

a. MPO ANCA

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9
Q
  1. What are the antibodies present in the following vasculitis?
    Kawasaki Disease
    a. MPO ANCA
    b. PR3 ANCA
    c. Anti-endothelial antibodies
A

c. Anti-endothelial antibodies

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10
Q
  1. What are the antibodies present in the following vasculitis?
    Granulomatosis with Polyangitis
    a. MPO ANCA
    b. PR3 ANCA
    c. Anti-endothelial antibodies
A

b. PR3 ANCA

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11
Q
  1. This type of vessels provides conduit to return interstitial tissue fluid and inflammatory cells to the bloodstream.
    a. Post capillary venules
    b. lympathics
    c. arterioles
    d. small artery
A

b. LYMPHATICS
are Thin-walled channels lined by
specialized endothelium. Returns interstitial tissue fluid and inflammatory cells to the blood stream. Can also transport microbes and tumor cells, thus constituting an important potential pathway for disease dissemination.

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12
Q
  1. This vasculitis is almost exclusive to heavy smokers less than 35%
    a. Buerger disease
    b. Kawasaki disease
    c. Reynaud phenomenon
    d. Takuyasu dise
A

Buerger’s disease (also known as thromboangiitis obliterans) affects blood vessels in the body, most commonly in the arms and legs. Blood vessels swell, which can prevent blood flow, causing clots to form. This can lead to pain, tissue damage, and even gangrene (the death or decay of body tissues). The exact cause of Buerger’s disease is unknown, however tobacco use is strongly linked to its development. Researchers believe that chemicals in tobacco may irritate the lining of the blood vessels, causing them to swell. Almost everyone diagnosed with Buerger’s disease smokes cigarettes or uses other forms of tobacco, such as cigars and chewing tobacco.

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13
Q

dislodge thrombosis which may lead to stroke when lodge to the blood vessels of the brain

A

Embolism

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14
Q

mainly elastic and muscular arteries

A

ATHEROSCLEROSIS

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15
Q

small muscle arteries and arterioles

A

HYPERTENSION

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16
Q
  • derived from mesoderm which will differentiate to single layer epithelium to allow diffusion of oxygen and nutrients
A

TUNICA INTIMA

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17
Q
  • Innermost layer of the vessel
A

TUNICA INTIMA

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18
Q
  • Normally consists of a single layer of endothelial cells - These cells sit in basement membrane
A

TUNICA INTIMA

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19
Q
  • is distinct from the media by internal elastic
    lamina
A

TUNICA INTIMA

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20
Q
  • thick layer
  • Concentric layers of smooth muscle cells
A

TUNICA MEDIA

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21
Q
  • Veins - arranged haphazardly
  • Media of elastic arteries (e.g., Aorta) - has high
    elastin content allowing these vessels to expand during systole and recoil during diastole, a property that serves to propel the blood towards the tissues
  • Media of muscular arteries- predominantly circumferentially arranged smooth muscle cells
A

TUNICA MEDIA

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22
Q

are the principal point of physiologic resistance to blood flow

A

Arterioles

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23
Q
  • Outermost layer of vessel
  • External to the media and is separated by external elastic
    lamina
  • Loose connective tissue containing nerve fibers and the
    vasa vasorum
A

TUNICA ADVENTITIA

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24
Q

literally “vessels of the vessels”

A

VASA VASORUM

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25
Q

 Approximately the diameter of an RBC (7-8um) – capillaries are smaller than this about 5um
 They have an endothelial lining but without tunica media and with variable number of pericytes

A

CAPILLARIES

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26
Q

 Have large diameter, large lumen, thin wall
 Has the capacity to contain about 2/3 of the circulating blood
 Reverse flow (due to gravity) is prevented in the extremities
by venous valves.

A

VEIN

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27
Q

 Thin-walled channels lined by specialized endothelium
 Returns interstitial tissue fluid and inflammatory cells to the blood stream
 Can also transport microbes and tumor cells, thus constituting an important potential pathway for disease dissemination

A

LYMPHATIC

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28
Q

 Developmental or berry aneurysm
- Occur in 2 cerebral vessels namely:

A
  1. ACOM - ANTERIOR COMMUNICATING ARTERY
  2. ACA - ANTERIOR CEREBRAL ARTERY
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29
Q
  • Direct connections between an artery and vein
  • can shunt blood from arterial to venous side
A

AV FISTULA
ARTERIOVENOUS FISTULA

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30
Q
  • Focal irregular thickening in medium and large
    muscular arteries, including renal, carotid,
    splanchnic and vertebral vessels
A

FIBROMUSCULAR DYSPLASIA

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31
Q
  • Segments of the vessel wall are focally thickened by a combination of intimal and medial hyperplasia and fibrosis resulting in stenosis
A

FIBROMUSCULAR DYSPLASIA

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32
Q

It is a medical procedure which gives a contrast media or a dye and by utilizing radiologic imaging it yields a rosary like appearance or string of beads appearance.

A

ANGIOGRAPHY
-FIBROMUSCULAR DYSPLASIA

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33
Q
  • Specialized lining of blood vessels (found in tunica intima)
  • Fenestrated and impermeable
  • They have several constitutive activities that are critical for vessel homeostasis and circulatory function
A

ENDOTHELIAL CELLS

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34
Q
  • Endothelial cells can respond to various stimuli by adjusting their steady-state (constitutive) functions and by expressing newly acquired (inducible) properties
A

ENDOTHELIAL ACTIVATION

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35
Q
  • Regulated predominantly at the level of the arterioles
    by neural and hormonal inputs.
A

PERIPHERAL RESISTANCE

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36
Q
  • Have the ability to proliferate (to prevent any further
    damage of the injury but narrowing the lumen of the
    blood vessel)
  • Synthesizes collagen, elastin, proteoglycans and elaborate growth factors and cytokines
  • Responsible for vasoconstriction and vasodilation
A

VASCULAR SMOOTH MUSCLES

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37
Q

VASCULAR PATHOGENESIS OF HYPERTENSION
It is associated with 2 forms of blood vessel disease:

A

It is associated with 2 forms of blood vessel disease:
1. HYALINE ARTERIOSCLEROSIS
2. HYPERPLASTIC ARTERIOSCLEROSIS

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38
Q
  • Arterioles show homogenous pink hyaline thickening
    associated with luminal narrowing
  • Reflect both plasma protein leakage across the injured
    endothelial cell and increased matrix synthesis of smooth
    muscle
A

HYALINE ARTERIOSCLEROSIS

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39
Q
  • A common feature of diabetic microangiography AND neprosclerosis
A

HYALINE ARTERIOSCLEROSIS

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40
Q
  • In severe hypertension, exhibits concentric laminated
    thickening of the walls with luminal narrowing
  • Laminations consist of smooth muscle with thickened,
    reduplicated basement membrane.
A

HYPERPLASTIC ARTERIOSCLEROSIS

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41
Q

necrotizing arteriolitis and onion skinning

A

HYPERPLASTIC ARTERIOSCLEROSIS

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42
Q
  • is the most insignificant form of arteriosclerosis (atherosclerosis and arteriosclerosis are significant because of arterial luminal narrowing).
  • It is more common in the elderly.
A

MOCKENBERG MEDIAL SCLEROSIS
[M-M-S]

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43
Q

you have these purplish calcifications and the lumen appears unaffected. Incidental finding. The process would be, if there are risk factors as in the Virchow’s triad, other areas like the neck and the lymph will be involved.

A

MOCKENBERG MEDIAL SCLEROSIS

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44
Q

 Accumulation of lipid in the vascular wall

A

ATHEROSCLEROSIS

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45
Q

ATHEROSCLEROSIS
 Constitutional Risk Factors (Non-modifiable)

A
  • GENETICS
  • AGE(40 ABOVE)
  • GENDER (premenopausal women are protected
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46
Q

ATHEROSCLEROSIS
 Modifiable Risk Factors

A

**HYPERLIPIDEMIA
o Hypertension
o Cigarette smoking
o Inflammation
o Hyperhomocystenemia
o Metabolic Syndrome
o Lipoprotein A- an altered form of LDL. Associated
with MI and CVD

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47
Q

PATHOGENESIS OF ATHEROSCLEROSIS

A
  1. ENDOTHELIAL INJURY AND DYSFUNCTION
  2. LIPOPROTEINS ACCUMULATION
  3. MONOCYTE ADHESION TO THE EPITHELIUM
  4. PLATELET ADHESION
  5. FACTOR RELEASE FROM ACTIVATED PLATELETS
  6. SMOOTH MUSCLE PROLIFERATION, ECM PRODUCTION
  7. FURTHER LIPID ACCUMULATION
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48
Q

In a nutshell, endothelium is good, media, intima adventitia but if you have hypertension,

A

endothelium will be damaged that would trigger the recruitment of your macrophage plus the addition of your platelet, secretion of your inflammatory cytokines

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49
Q

In a nutshell, endothelium is good, media, intima adventitia but if your patient is hyperlipidemic, smoker,

A

it will lead to atherosclerosis.

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50
Q

Principal point of physiologic resistance to blood flow

A

ARTERIOLES

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51
Q

They have an endothelial lining but without tunica media
and with variable number of pericytes

A

CAPILLARY

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52
Q

Focal irregular thickening in medium and large muscular
arteries, including renal, carotid, splanchnic and vertebral vessels

A

FIBROMUSCULAR DYSPLASIA

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53
Q

BP of greater than or equal to 200/120 mmHg

A

MALIGNANT HYPERTENSION

54
Q

Arterioles show homogenous pink hyaline thickening
associated with luminal narrowing

A

HYALINE ARTERIOSCLEROSIS

55
Q

A localized abnormal dilatation of blood vessel or the heart that may be congenital or acquired.

A

ANEURYSM

56
Q

Occurs when blood separates the laminar planes of the
media to form a blood-filled channel within the aortic walls

A

AORTIC DISSECTION

57
Q

Vessel wall inflammation

A

VASCULITIS

58
Q

Granulomatous vasculitis of medium and larger arteries
characterized principally by ocular disturbances and marked
weakening of pulses in upper extremities, hence, the name
pulseless disease.

A

TAKAYASU ARTERITIS

59
Q

A small to medium sized vessel neutrophilic vasculitis that
classically presents as a clinical triad of recurrent oral aphthous
ulcers, genital ulcers and uveitis

A

BEHCET DISEASE

60
Q

Tumors have a preference to travel through

A

Veins

61
Q

Favorite transport route of metastatic cancers.

A

LYMPHATIC

62
Q

For example a person had a wound caused by an abrasion:
● The endothelium would start to bleed then produce cytokines.
● The cytokines would then cause:

A

○ Inflammation
○ Hypotension
○ Hemorrhagic Shock

63
Q

● Stereotyped response to vascular injury.
● Formation of neointima

A

INTIMAL THICKENING

64
Q

● Stereotyped response to vascular injury.

A

○ Smooth muscle recruitment.
○ Smooth muscle proliferation
○ Matrix synthesis

65
Q

Most Important Determinant of Stroke Volume

A

FILLING PRESSURE

66
Q

○ Heart rate and myocardial contractility: Regulated by:

A

ɑ- and β- adrenergic systems.

67
Q

Dilators

A
  • Prostaglandin
  • Kinins
  • NO (Nitric Oxide)
68
Q

Examples of hypertensive drugs are

A

ACE INHIBITORS

69
Q

RELATIONSHIP OF PERIPHERAL RESISTANCE AND BP

A

Increased Peripheral Resistance = Increased BP

70
Q

● Neural Factors: (what is constrictor/dilator?)

○ ɑ- androgenic -
○ β- adrenergic -

A

○ ɑ- androgenic (constriction)
○ β- adrenergic (dilator)

71
Q

● Local Factors:

A

○ Autoregulation
○ pH
○ Hypoxia

72
Q

WHERE IS Angiotensinogen

A

LIVER

73
Q

WHERE IS Angiotensin Converting Enzyme

A

LUNGS

74
Q

If a patient has High Blood, a non-pharmacologic solution to treat them would be

A

decreasing the salty food intake

75
Q

○ Inadequate organ perfusion.
○ Can lead to tissue dysfunction or death.

A

Low Blood Pressure (hypotension)

76
Q

○ Can cause end-organ damage.
○ Can damage capillaries like in kidneys.

A

High Blood Pressure (hypertension)

77
Q

Fibrinoid deposits and
vessel wall necrosis (necrotizing arteriolitis).

A

MALIGNANT HYPERTENSION

78
Q

● From the greek root words: “gruel” and “hardening”
● Most frequent and clinically important pattern.

A

ATHEROSCLEROSIS

79
Q

consists of a raised lesion with a soft grumous core of lipid (mainly cholesterol and cholesterol esters) covered by a fibrous cap.

A

ATHEROMATOUS PLAQUE

80
Q

smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastin, proteoglycans, neovascularization and there will be new blood vessel formation).

A

FIBROUS CAP

81
Q

cell debris, cholesterol crystals, foam cells, calcium - too thick so the vasa vasorum cannot meet their metabolic demands so they will eventually die, so it will be forming cholesterol crystal, debris, and foam cells

A

NECROTIC CENTER

82
Q

● Composed of lipid-filled foamy macrophages.
● Begins as multiple minute flat yellow spots.
● Eventually coalesce into elongated streaks 1 cm
long or longer.
● These lesions are not sufficiently raised to cause any
significant flow disturbances.
● Can evolve into plaques.
● not all are destined to become advanced lesions.

A

FATTY STREAKS

83
Q

● Key processes: intimal thickening and lipid
accumulation .
● White-yellow
● Encroach (protrude) on the lumen of the artery.

A

ATHEROSCLEROTIC PLAQUE

84
Q

it’s a stage wherein the
occlusion is around 70%; with this degree of stenosis, chest pain may develop with exertion (so-called stable angina).

A

CRITICAL STENOSIS

85
Q

can lead to aneurysm and rupture.

A

Mural thrombosis
embolization
wall weakening

86
Q

Most important causes of aortic aneurysms:

A

1.ATHEROSCLEROSIS (AAA)
2.HYPERTENSION (TAA)

87
Q

Attenuated but intact arterial wall or thinned ventricular wall of the heart.

A

TRUE ANEURYSM

88
Q

Spherical outpouchings involving
only a portion of the vessel wall.

A

SACCULAR

89
Q

Diffuse, circumferential dilations of a long vascular segment.

A

FUSIFORM

90
Q

Defect in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular
space (pulsating hematoma”).

A

FALSE ANEURYSM

91
Q

Most common sites of atherosclerotic aneurysms:

A

ABDOMINAL AORTA
COMMON ILIAC ARTERIES

92
Q

ABDOMINAL AORTIC ANEURYSM usuallylocated:

A

below the renal arteries
above the bifurcation of the aorta

93
Q

in aortic dissection whatare more common and are more dangerous.

A

PROXIMAL LESIONS

94
Q

● Giant cell arteritis
● Takayasu arteritis
● Kawasaki disease
● Granulomatosis with polyangiitis

A

Autoreactive T-cells

95
Q

● Systemic lupus erythematosus (SLE)
● Drug Hypersensitivity
● Polyarteritis nodosa (PAN)

A

Immune complex deposition

96
Q

LARGE VESSEL

A

● Giant Cell Arteritis
● Takayasu Arteritis

LARGE - GT

97
Q

MEDIUM VESSEL

A

● Polyarteritis Nodosa (PAN)
● Kawasaki Disease

MEDIUM - PK

98
Q

NEUTROPHILIA

A

BEHCET DISEASE

99
Q

Most common form of vasculitis among older individuals.

A

GIANT CELL ARTERITIS

100
Q
  • Segmental transmural necrotizing inflammation.
  • Mixed infiltrate of neutrophils, eosinophils, and mononuclear cells.
  • Fibrinoid necrosis.
A

Polyarteritis Nodosa (PAN)

101
Q
  • Necrotizing glomerulonephritis
    (90% of patients will have a
    problem in the kidneys)
  • As well as the pulmonary capillaritis
    Associated with MPO-ANCA.
A

Microscopic Polyangiitis

102
Q

TRIAD

Necrotizing granuloma
Necrotizing or granulomatous vasculitis (most prominent in the lungs)
Focal necrotizing, glomerulonephritis - often crescentic.

○ (+) PR3-ANCA also known as CANCA previously.

A

Granulomatosis with Polyangiitis

Wegener granulomatosis.

103
Q

HYPEREOSINOPHILIA
MPO-ANCA

A

Churg-Strauss Syndrome

104
Q

○ Small- to medium-vessel neutrophilic
vasculitis, this one needs to haveneutrophil
○ TRIAD:
- Recurrent oral aphthous ulcers
- Genital ulcers (presence of“butlig”)
- Uveitis
○ Associated with certain HLA haplotypes
(HLA-B51).
○ TH17 cells recruit neutrophils which
infiltrate the vessel walls.

A

BEHCET DISEASE

105
Q
  • Focal acute and chronic vasculitis of small- and medium-sized arteries, predominantly of the extremities.
  • Luminal thrombosis with small microabscesses
A

BUERGER DISEASE

106
Q

● Direct invasion of infectious agents.
○ Positive agent like usually bacteria
(Pseudomonas) or fungi (Aspergillus and Mucor)
● Part of a localized tissue infection.
○ Bacterial pneumonia or adjacent to
abscesses.

A

INFECTIOUS VASCULITIS

107
Q

coronary arteries and myocardial arterioles

A

Myocardial Vessel Vasospasm

108
Q

-Exaggerated central and local vasomotor responses to cold or emotion
-Symmetric involvement of the extremities
-Extent and severity: static

A

Primary Raynaud Phenomenon

109
Q

-Due to arterial disease caused by other entities: SLE, scleroderma, Buerger disease, atherosclerosis
-Asymmetric involvement of the extremities
-Extent and severity: progressively worsen

A

Secondary Raynaud Phenomenon

110
Q

● Vasospasm of cardiac arterial or arteriolar beds has been called cardiac Raynaud and in a subset of cases leads to Prinzmetal angina (angina due to vasospasm).
● Intrinsic hyper-reactivity of medial smooth muscle cells.
● Vasoactive mediators can also precipitate prolonged myocardial vessel contraction.

A

MYOCARDIALVESSELVASOSPASM

111
Q

pain elicited on forced dorsiflexion of the foot.

A

HOMAN SIGN

112
Q

Most common serious clinical complication of DVT

A

PULMONARY EMBOLISM

113
Q

○ Venous thrombosis appears in one location, disappears, and then occurs in another site.
○ Hypercoagulability occurs as a paraneoplastic syndrome related to elaboration of procoagulant factors by
tumor cells (adenocarcinomas).

A

Migratory thrombophlebitis (Trousseau sign)

114
Q

● Acute inflammation elicited by bacterial infection into lymphatics
● Most common cause
○ Group A B-hemolytic streptococci

A

LYMPHANGITIS

115
Q

Peau d’orange (orange peel) appearance due to persistent edema and subsequent deposition of interstitial connective tissue.

A

LYMPHEDEMA

116
Q

○ Most common form of vascular ectasia.
○ Most ultimately regress spontaneously.

A

Nevus flammeus (birthmark)

117
Q

○ Radial arrays of dilated subcutaneous arteries about a central core.
○ Most frequently associated with hyperestrogenic states.

A

Spider telangiectasia

118
Q

Port wine stain

A

Sturge-Weber syndrome

119
Q

Hereditary hemorrhagic telangiectasia

A

Osler-Weber-Rendu disease

120
Q

Cavernous hemangioma

A

Von Hippel-Lindau disease

121
Q

Cystic hygroma

A

Turner disease

122
Q

● Tumors arising from modified smooth muscle cells
of the glomus bodies (arteriovenous structures
involved in thermoregulation).
● Benign but exquisitely painful.

A

GLOMUS TUMOR

123
Q
  • A necrotizing granulomatous disorder of lymph nodes) in immunocompetent hosts like those who have HIV.
  • Bartonella henselae
A

Cat-scratch disease

124
Q

Trench fever” in World War I.

A

Bartonella quintana

125
Q

● Not associated with HIV.
● Multiple red-purple skin plaques or nodules, usually
in the distal lower extremities;

A

CLASSIC Kaposi sarcoma

126
Q

● HIV-seronegative.
● A particularly severe form, with prominent lymph
nodes and visceral involvement, occurs in prepubertal children; prognosis is poor, with an almost 100% mortality within 3 years.

A

ENDEMIC AFRICAN Kaposi sarcoma

127
Q

Solid organ transplant recipients in the setting of
T-cell immunosuppression

A

TRANSPLANT-ASSOCIATED Kaposi sarcoma

128
Q

● AIDS defining illness.
● Most common HIV-related malignancy
● Involves lymph nodes and disseminates widely to
viscera early in its course.

A

AIDS-ASSOCIATED Kaposi sarcoma (epidemic)

129
Q

● Intermediate gray tumor.
● Spectrum of vascular neoplasms with clinical
T-cell immunosuppression.
behaviors intermediate between well-differentiated hemangiomas and anaplastic angiosarcomas.

A

HEMANGIOENDOTHELIOMA

130
Q

● Malignant endothelial neoplasm that primarily affects older adults.
● Most commonly involves skin, soft tissue, breast, and liver.

A

ANGIOSARCOMA

131
Q

marker for blood vessels

A

CD31

132
Q

● Considered as tumors that arise from pericytes, the
myofibroblast-like cells associated with capillaries
and venules.
● Recent studies suggest that tumors of pericytes are
very rare.

A

HEMANGIOPERICYTOMA

PATHOLOGY (2nd year) (6 decks)

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