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CPR II Exam 1 > Chapter 11/Lecture 4: Veins/Lymph, DVT, Vascular Tumors > Flashcards

Chapter 11/Lecture 4: Veins/Lymph, DVT, Vascular Tumors Flashcards

1
Q

Which 3 types of vessels are most often affected by vasculitis?

A
  • Arterioles
  • Capillaries
  • Venules
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2
Q

Why is distinguishing between infectious and immune-mediated causes of vasculitis important as far as tx goes?

A
  • Immune-mediated can be treated w/ immunosuppressive therapy
  • This tx would be counter-productive for infectious causes
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3
Q

How can a non-infectious vasculitis be indirectly triggered by an infection?

A

Generation of immune complexes or triggering cross-reactive immune response

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4
Q

Infectious causes of vasculitis do so through ________ invasion

A

Direct

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5
Q

Which non-infectious vasculitis is the only one to affect the aorta amongst other vessels?

A

Giant Cell (Temporal) Arteritis

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6
Q

Which lesions are most common for Drug Hypersensitivity Vasculitis?

A

Skin lesions

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7
Q

Immune complex-associated vasculitis may be seen in which systemic immunologic disorder?

A

SLE

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8
Q

A pt >40 yo with history ± polymyalgia rheumatica is most likely to have what type of vasculitis?

A

Giant Cell (Temporal) Arteritis

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9
Q

Immune complex vasculitis is due to the production of what?

What deposits in the vascular walls?

A
  • Production of autoantibodies and formation of immune complexes
  • Deposition of antigen-antibody complexes in vascular walls
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10
Q

Why is it important to consider Drug Hypersensitivity as a cause of vasculitis as far as treatment goes?

A

Stop drug –> resolution of vasculitis!

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11
Q

What are very useful diagnostic markers of non-infectious vasculitis and their titers mirror clinical severity?

A

ANCAs

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12
Q

MPO-ANCA’s are found in what 2 types of non-infectious vasculitis?

A
  • Microscopic polyangiitis
  • Churg-Strauss syndrome
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13
Q

ANCAs can directly activate which immune cells and cause the release of?

A

Neutrophils, stimulating release of ROS and proteolytic enzymes

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14
Q

Why are ANCA-associated vasculitides often described as “pauci-immune”?

A

ANCA Ab directed against cellular constituents and do NOT form circulating immune complexes

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15
Q

Giant cell arteritis stems from an immune response by which cells and causes inflammation of arteries where?

A
  • T cell mediated (CD4+ > CD8+)
  • Inflammation of arteries in the head, especially temporal a.
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16
Q

Which 2 types of antibodies are seen in 2/3 of pt’s with Giant Cell (temporal) Arteritis?

A

anti-endothelial cell and anti-SM cell

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17
Q

What do the classic lesions associated with Giant Cell (Temporal) Arteritis exhibit morphologically?

A
  • Granulomatous inflammation w/ multinucleated giant cells
  • Fragmentation of the elastic lamina and intimal thickening
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18
Q

What are the common signs/sx’s of Giant Cell (Temporal) Arteritis?

A
  • Facial pain or HA, most intense along course of superficial temporal a.; painful to palpation***
  • Diplopia or complete vision loss
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19
Q

Why is biopsy of at least a 1-cm segment required for diagnosis of Giant Cell (Temporal) Arteritis?

A

As it can be extremely PATCHY and FOCAL

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20
Q

Treatment for Giant Cell (Temporal) Arteritis?

A

Corticosteroidsoranti-TNF therapies

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21
Q

Granulomatous vasculitis of medium and large arteries characterized by ocular disturbances and marked weaking of the pulses and low BP in the UE’s is characteristic of?

A

Takayasu Arteritis (aka pulseless disease)

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22
Q

Takayasu arteritis has similar histological findings as those seen in giant cell arteritis, except involves which vessels?

A

Aortic arch (aortitis) and major branch vessels

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23
Q

Since many features of Takayasu arteritis are shared with Giant Cell arteritis, the distinction between the 2 is primarily made how?

A
  • AGE of the pt
  • Takayasu = younger (<50 yo)
  • Giant cell = older (>50 yo)
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24
Q

Which vessels are the major ones affected in Takayasu Arteritis?

A
  • Aortic arch and major branch vessels
  • Pulmonary a. (1/2 of cases)
  • Coronary and renal arteries
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25
Q

Major signs/sx’s associated with Takayasu Arteritis?

Sx’s associated w/ involvement of renal, pulmonary, and distal aorta?

A
  • Reduced BP and pulses in carotids and UE’s
  • Ocular disturbances + Neuro deficits
  • If distal aorta involved –> claudication of legs
  • Pulmonary a. involvement –> pulmonary HTN
  • Renal a. involvement –> systemic HTN
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26
Q

In 1/3 of pt’s with polyarteritis nodosa the vasculitis is attributable to chronic infection by which virus?

Immune-complexes composed of what?

A

HBsAg and anti-HBsAg = Chronic HBV

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27
Q

List the 4 vessels most often involved in Polyarteritis Nodosa in descending order of frequency.

A
  • Kidneys
  • Heart
  • Liver
  • GI tract
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28
Q

Vessels of which organ are characteristically spared in Polyarteritis Nodosa?

A

Pulmonary

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29
Q

Lesions seen in Polyarteritis Nodosa involve which part of the vessel and have a predileciton for which areas?

A

Only part of the vessel circumference w/ predilection for branch points

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30
Q

Classic Polyarteritis Nodosa is characterized by what morphological pattern of inflammation?

A

Segmental TRANMURAL necrotizing inflammation of small- to medium-sized arteries

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31
Q

During acute phase of Polyarteritis Nodosa the transmural inflammation of arterial wall shows a mixed inflammatory infiltrate and is often accompanied by what type of necrosis?

A

Fibrinoid necrosis

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32
Q

Polyarteritis Nodosa is typically a disease affecting which age group?

Typical course of the disease?

A
  • Primarily young adults, but can also affect geriatric and pediatric pts
  • Course is remitting and episodic, with long sx-free intervals
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33
Q

What is a “classic” presentation (signs/sx’s) of Polyarteritis Nodosa?

A
  • Rapidly accelerating HTN + abdominal pain + bloody stools
  • Diffuse myalgias and peripheral neuritis
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34
Q

What type of treatment can yield remissions or cures in 90% of pt’s with Polyarteritis Nodosa?

A

Immunosuppression

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35
Q

Acute arteritis affecting large, medium, and small-sized vessels, seen in infants and small children (<4 yo) is characteristic of what disease?

A

Kawasaki disease

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36
Q

Clinical significance of Kawasaki Disease stems from its predilection for which artery?

Leading to what manifestations?

A
  • Coronary a.
  • Aneurysms —> thrombosis or rupture –> acute MI
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37
Q

Vascular damage in Kawasaki Disease is primarily mediated by which immune cells?

A

T cells and monocytes/macrophages

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38
Q

What is the morphology of the vasculitis seen in Kawasaki Disease; differs from PAN how?

A

Dense transmural inflammatory infiltrate w/ LESS prominent fibrinoid necrosis than in PAN

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39
Q

Kawasaki disease typically presents with what signs/sx’s?

*First Aid Mnemonic

A

*CRASH and burn

- Conjunctival injection

  • Rash (polymorphous -> desquamating)
  • Adenopathy (cervical LN enlargement = mucocutaneous LN syndrome)
  • Strawberry tongue (erythema and blistering of oral mucosa)
  • Hand-foot changes (edema and erythema)
  • Burn = FEVER
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40
Q

If Kawaksaki Disease is recognized early in its course treatment with what will sharply reduce the risk of symptomatic coronary artery disease?

A

IV immunoglobulin and Aspirin

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41
Q

Microscopic polyangiitis generally affects which type of vessels?

A

Capillaries + small arterioles and venules

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42
Q

How do the age and distribution of the lesions seen in Microscopic Polyangiitis differ from PAN?

A

Tend to be of the same age and are distributed more widely

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43
Q

Microscopic polyangiitis affects vessels of many organ systems, but which 3 systems are most common?

A
  • Renal (necrotizing glomerulonphritis)
  • Lungs (pulmonary capillaritis)
  • Skin (palpable purpura)
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44
Q

Hypersensitivity vasculitis or leukocytoclastic vasculitis are another name for what?

A

Microscopic Polyangiitis

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45
Q

Microscopic polyangiitis can be a feature of which 3 immune disorders?

A
  • Henoch-Schonlein purpura
  • Essential mixed cryoglobulinemia
  • Vasculitis assoc. w/ CT disorders
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46
Q

Segmental fibrinoid necrosis of the media and focal transmural necrotizing lesions w/ ABSENCE of granulomatous inflammation is characteristic of what type of vasculitis?

A

Microscopic polyangiitis

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47
Q

Which immune cells are seen infiltrating in microscopic polyangiitis, many of which are undergoing apoptosis and giving rise to the term leukocytoclastic vasculitis?

A

Neutrophils

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48
Q

What are the major clinical features (signs/sx’s) seen with microscopic polyangiitis?

A
  • Hemoptysis
  • Hematuria and Proteinuria
  • Bowel pain or bleeding
  • Muscle pain or weakness
  • Palpable cutaneous purpura
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49
Q

Churg-Strauss Syndrome is a vasculitis affecting which size vessels?

Classically associated with what systemic manifestations?

A
  • Small-vessel necrotizing vasculitis
  • ASTHMA, ALLERGIC rhinitis, lung infiltrates, peripheral HYPER-eosinophilia, and extravascular necrotizing granulomata
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50
Q

Churgg-Strauss syndrome may have inflammation that resembles PAN or microscopic polyangiitis with the addition of what 2 things?

A

Eosinophils and Granulomas = Granulomatous, necrotizing vasculitis w/ eosinophilia

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51
Q

What is the primary manifestation of Churg-Strauss Syndrome affecting the kidneys?

A

Focal and segmental glomerulosclerosis

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52
Q

What is the primary manifestation of Churg-Strauss Syndrome affecting the myocardium?

Clinically significant why?

A
  • Cardiomyopathy w/ eosinophilic infiltrates
  • Accounts for HALF the deaths in this syndrome
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53
Q

Cutanous involvement of Churg-Strauss Syndrome presents with what?

A

Palpable Purpura

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54
Q

Behcet Disease is a vasculitis of small-to medium-vessels what classically presents with what triad?

A

1) Recurrent oral apthous ulcers
2) Genital ulcers
3) Uvetis

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55
Q

Which HLA haplotype is associated with Behcet Disease?

A

HLA-B51

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56
Q

Vessel inflammation in Behcet Disease is due to what inflammatory cell type?

Recruited by which T cells?

A
  • Neutrophilic inflammation
  • Recruited by TH17 cells
57
Q

Mortality seen in Behcet Disease is related to what 2 complications?

A
  • Severe neurologic involvement
  • Rupture of vascular aneurysms
58
Q

Granulomatosis with Polyangitis (Wegener granulomatosis) is a necrotizing vasculitis characterized by a triad of what?

A

1) Necrotizing granulomas of upper or lower respiratory tract, or both
2) Necrotizing or granulomatous vasculitis most prominenetly in lungs
3) Focal necrotizing, often CRESCENTERIC, glomerulonephritis

59
Q

Granulomatosis with polyangiitis is a form of hypersensitivity mediated by what?

A

T-cell-mediated hypersensitivity

60
Q

PR3-ANCAs (aka c-ANCA) is associated with what form of non-infectious vasculitis?

A

Granulomatosis w/ polyangiitis (Wegener granulomatosis)

61
Q

Which non-infectious vasculitis is characterized by the presence of granulomas and a dramatic response to immunosuppressive therapy?

A

Granulomatosis w/ polyangiitis (Wegener granulomatosis)

62
Q

Which sex is more often affected by granulomatosis with polyangiitis and at what age?

A

M > F; average age 40 yo

63
Q

What are the classic features (signs/sx’s) of granulomatosis with polyangiitis?

A
  • Persistent pneumonitis w/ bilateral nodular and cavitary infiltrates
  • Chronic sinusitis
  • Nasopharyngeal ulcerations
  • Evidence of renal disease
64
Q

How serious is granulomatosis with polyangiitis if left untreated?

A

Rapidly fatal w/ 80% mortality at one year

65
Q

What are the morphological characteristics of the granulomas seen in the upper respiratory tract of someone with granulomatosis with polyangiitis?

A

Granulomas w/ geographic patterns of CENTRAL necrosis

66
Q

The necrotizing granulomas seen in granulomatosis with polyangiitis are surrounded by zones of what?

Resembles?

A
  • Zones of proliferating fibroblasts assoc. w/ giant cells and leukocytic infiltrate
  • Reminiscent of mycobacterial or fungal infections
67
Q

What may be seen radiographically in the lower respiratory tract of pt w/ granulomatosis with polyangiitis as multiple necrotizing granulomas coalesce?

A

Radiographically visible nodules that can also cavitate

68
Q

Which renal lesions may be seen early on in granulomatosis with polyangiitis?

Eventually progress to what in late stages?

A
  • Focal and segmental glomerulonephritis
  • Crescenteric glomerulonephritis
69
Q

Thromboangiitis obliterans (Buerger disease) is characterized by what type of vasculitis and especially in which arteries?

Occasional secondary extension to affect what?

A
  • Segmental, thrombosing, acute and chronic vasculitis of small- and medium-vessels
  • Principally the radial and tibial arteries w/ occasional 2’ extension to veins and nerves of the extremities
70
Q

Thromboangiitis obliterans (Buerger disease) occurs almost exclusively in which patients and at what age?

A

Heavy cigarette smokers before age 35

71
Q

Most patients with Thromboangiitis obliterans (Buerger disease) have hypersensitivity to intradermally injected what?

A

Tobacco products

72
Q

What are 3 ethnic groups have higher incidences of Thromboangiitis obliterans (Buerger disease)?

A
  • Israeli
  • Indian subcontinent
  • Japanese
73
Q

The acute and chronic inflammation seen in Thromboangiitis obliterans (Buerger disease) is accompanied by what other morphological feature?

A

Luminal thrombus w/ small microabscesses composed of neutrophils surrounded by granulomatous inflammation

74
Q

What are the early manifestations of Thromboangiitis obliterans (Buerger disease)?

A
  • Raynaud’s
  • Leg pain induced by exercise that is relieved on rest
  • Instep foot pain induced by exercise
  • Superficial nodular phlebitis (venous inflammation)
75
Q

The vascular insufficiency of Thromboangiitis obliterans (Buerger disease) tends to be accompanied by what type of pain/when?

Chronic extremity ulcerations eventually progress to?

A
  • Severe pain even at rest - due to neural involvement
  • Progress to frank gangrene of extremities
76
Q

Which 3 organisms can directly invade vessels and cause infectious vasculitis?

A
  • Pseudomonas
  • Aspergillus
  • Mucor
77
Q

Vascular invasion by organisms resulting in infectious vasculitis typically occurs in association with what, but can also less commonly occur via which route?

A
  • Part of localized tissue infection
  • Less commonly via hematogenous spread
78
Q

Vascular infections can weaken arterial walls and can result in what clinically significant events?

A
  • Mycotic aneurysms

or

  • Induce thrombosis and infarction (i.e., thrombosis of meningal vessels in meningitis —> infarction of underlying brain)
79
Q

How does Primary Raynaud’s vs. Secondary differ in their symmetry of involvement of the digits?

A
  • Primary has symmetrical involvement of the digits
  • Secondary has asymmetrical involvement of the digits
80
Q

Secondary Raynaud’s may be a component of other arterial diseases such as what?

A
  • SLE
  • Scleroderma
  • Thromboangiitis obliterans
81
Q

Excessive vasoconstriction of myocardial arteries or arterioles which may cause ischemia or infarct is known as what?

A

Cardiac Raynaud

82
Q

What are endogenous and exogenous agnts which are vasoactive mediators and can precipitate prolonged myocardial vessel contraction?

A
  • Endogenous = epinephrine, pheochromocytoma
  • Exogenous = cocaine or phenylephrine
83
Q

Varicose veins are abnormally dilated, tortous veines produced by prolonged, increased intraluminal pressure and most often affect which veins?

A

Superficial veins of the upper and lower legs

84
Q

Secondary tissue ischemia resulting from chronic venous congestion and poor vessel drainage results in what skin abnormalities?

A
  • Stasis dermatitis (aka “brawny induration”)
  • Ulcerations
  • Poor wound healing and superimposed infections
85
Q

How frequent do emboli arise from superficial LE veins?

A

Rarely

86
Q

What is the most serious potential complication associated with DVT’s and is often the first manifestation of thrombophlebitis?

A

Pulmonary Embolism

87
Q

Patients with what types of cancer and in which locations are at increased risk for thrombophlebitis, why?

A
  • Adenocarcinoma of lung, ovary, pancreas
  • Mucin-producing adenocarcinomas (mucin is thrombogenic)
  • May occur as paraneoplastic syndrome, related to elaboration of procoagulant factors by tumor cells
88
Q

Which factors associated with slow venous return increase the risk for DVT’s?

A
  • Prolonged immobilization = MAJOR
  • Pregnancy
  • CHF
  • Obesity
89
Q

In the setting of systemic hypercoagulability, including genetic hypercoagulability, and cancers, what is the classical sign of venous thromboses?

A
  • Appear at one site, dissapear, and then occur at another site
  • Migratory thrombophlebitis (Trousseau sign)
90
Q

What are the major causes of Superior Vena Cava Syndrome?

A
  • Neoplasms (i.e., bronchogenic carcinoma or mediastinal lymphoma)
  • Less commonly aortic aneurysms
91
Q

Obstruction associated with superior vena cava syndrome produces what characteristic clinical complex?

A
  • Marked DILATION of the veins of the: head, neck, and arms w/ CYANOSIS
  • If pulmonary vessels compressed –> respiratory distress
92
Q

Which 2 cancers have a tendency to grow within veins and may ultimately lead to inferior vena cava syndrome?

May also be caused by thrombosis from where?

A
  • Hepatocellular carcinoma
  • Renal cell carcinoma
  • Thrombosis of the hepatic, renal, or LE veins which propogate cephalad
93
Q

What are the signs/sx’s associated with inferior vena cava syndrome?

With renal involvement?

A
  • Marked LE edema + distention of superficial collateral veins of lower abdomen
  • Renal involvement —> MASSIVE proteinuria
94
Q

Which bacteria is most commonly responsible for Lymphangitis?

A

group A β-hemolytic strep

95
Q

Red, painful subcutaneous streaks w/ painful enlargement of the draining LN’s, is characteristic of what?

A

Lymphangitis

96
Q

Port wine stains a special form of nevus flammeus, found within the distribution of the trigeminal nerve are associated with what congenital disorder?

A

Sturge-Weber Syndrome (encephalotrigeminal angiomatosis)

97
Q

Sturge-Weber syndrome is associated with what clinical findings?

A
  • Port wine nevi in trigeminal distribution
  • Ipsilateral venous angioma in cortical leptomeninges
  • Mental retardation + Seizures
  • Hemiplegia
  • Skull radio-opacities
98
Q

What are the common sites for hemangiomas?

A
  • Skin and mucous membranes of HEAD and NECK
  • Liver
99
Q

What is the most common type of hemangioma and where are they found?

A
  • Capillary hemangioma
  • Skin, subcutaneous tissues, and mucous membranes of the mouth, lips, liver, spleen, and kidneys
100
Q

Which type of hemangioma is very common in newborns and often presents with multiple lesions, growing rapidly for a few months, and then regressing by age 7?

A

Juvenile Hemangioma (“strawberry type”)

101
Q

How do Cavernous Hemangiomas differ in terms of infiltration and regression as compared to Capillary Hemangiomas?

A
  • Are more infiltrative and frequently involve deep structures
  • Do NOT spontaneously regress
  • Locally destructive!
102
Q

How do Cavernous Hemangiomas appear histologically?

A
  • Unencapsulated mass
  • Large, cavernous blood-filled vascular spaces
  • Separated by CT stroma
103
Q

What is the characteristic histology of Capillary Hemangiomas?

A

Thin-walled capillaries w/ scant stroma

104
Q

Which type of hemangioma is commonly seen in VHL disease and where are the lesions most often seen?

A
  • Cavernous hemangiomas
  • Cerebellum, brain stem, retina, pancreas, and liver
105
Q

What are 3 sequelae commonly associated with Cavernous Hemangiomas?

A
  • Dystrophic calcifications
  • Traumatic ulceration
  • Intravascular thrombosis
106
Q

Which subtype of capillary hemangioma presents as a rapdily growing red pedunculated lesion on the skin, gingival, or oral mucosa which often ulcerate and bleed easily?

A

Pyogenic granulomas

107
Q

Simple (capillary) lymphangiomas can arise in the head, neck, and axillary regions and appear very similar to capillary hemangiomas, but can be differentiated how?

A

Absence of RBC’s

108
Q

Cavernous lymphangiomas (cystic hygromas) are typically found where and in whom?

Common features?

A
  • Neck or axilla of children
  • Can occasionally be enormous (up to 15 cm) and may fill axilla or produce gross deformities of the neck.
109
Q

Cavernous lymphangiomas (cystic hygromas) are a common feature of which congenital disorder?

A

Turner Syndrome

110
Q

What are the histologic findings associated with cavernous lymphangiomas (cystic hygromas)?

A
  • Massively dilated lymphatic spaces lined by endothelial cells
  • Separated by intervening CT stroma containing lymphoid aggregates
111
Q

What are the characteristics of Glomus Tumor (Glomangioma)?

Arise from what cells and are most often found where?

A
  • Benign but VERY painful tumor
  • Arising from modified smooth m. cells of the glomus bodies
  • Most commonly in distal portion of the digits, especially under fingernails
112
Q

Bacillary Angiomatosis is a vascular proliferation most commonly arising in whom and is due to what organism?

A
  • Immunocompromised hosts (i.e., AIDS)
  • Gram negative bacilli of Bartonella family
113
Q

The bacillary angiomatosis induced by B. henselae infection is caused by induction of which host factors and upregulation of?

A

HIF-1 –> ↑ VEGF

114
Q

How do the skin lesions in Bacillary Angiomatosis appear both grossly and microscopically?

A
  • Grossly = red nodules and papules, or rounded SQ masses
  • Histo = capillary proliferation w/ plump epitheloid endothelial cells exhibiting nuclear atypia and mitoses
115
Q

What stain can help visualize the Bartonella bacilli associated with Bacillary Angiomatosis?

A

Warthin-Starry Silver

116
Q

The infections and lesions associated w/ Bacillary Angiomatosis can be cleared with what med?

A

Macolide antibiotics (i.e., erythromycin)

117
Q

How does the gross morphology of the lesions associated with Bacillary Angiomatosis differ from Kaposi Sarcoma?

A
  • Bacillary = raised lesions
  • Kaposi = flat lesions
118
Q

Classic kaposi sarcoma is a disease most often seen in whom and where?

A

Older men of Mediterranean, Middel Eastern, or Eastern European descent

119
Q

Which types of Kaposi Sarcoma are not associated with HIV?

A
  • Classic KS
  • Endemic African KS
  • Transplant-associated KS
120
Q

How does classic kaposi sarcoma typically manifest?

Most common location and spreads how?

A
  • Multiple red-purple skin plaques or nodules
  • Usually in distal LE; progressively ↑ in size and number and spread proximally
121
Q

Endemic African kaposi sarcoma differs from classic KS in that it more frequently involves what?

A

Lymph nodes

122
Q

How great of risk are transplant patients at for transplant-associated kaposi sarcoma?

A

100x ↑ risk

123
Q

Which structures are most often involved in Transplant-Associated KS?

A

Lymph nodes, viscera, and mucosa

124
Q

What is the most common HIV-related malignancy worldwide?

A

AIDS-associated (epidemic) KS

125
Q

AIDS-associated (epidemic) KS frequently involves what structures and follows what course?

A

Lymph nodes and disseminates widely to viscera EARLY in its course

126
Q

The nodular lesions seen in KS have what histological features and cells?

A

Sheets of plump, proliferating spindle cells

127
Q

In classic KS, the cutaneous lesions progress through what 3 stages?

A
  1. Patches –> red, purple macules confined to distal LE’s
  2. Raised plaques –> as lesions spread prox.
  3. Nodular lesions –> distinctly neoplastic; sheets of plump proliferating spindle cells in dermis and SQ tissues
128
Q

Which treatment is usually adequate for excellent prognosis in cases of Classic KS?

A

Surgical resection

129
Q

Which therapy has greatly reduced the frequency of KS in HIV infected patients?

A

Anti-retroviral therapy

130
Q

Vascular tumor occurring around medium and large-sized veins with neoplastic cells that are plump and often cuboidal is characteristic of?

A

Epitheliod Hemangioendothelioma

131
Q

Hepatic angiosarcoma is associated with exposures to what?

A
  • Arsenic (i.e., pesticides)
  • Thorotrast (radioactive constrast agent)
  • Polyvinyl Chloride (widely used plastic)
132
Q

Angiosarcomas most often occur in which sex?

A

Either = NO gender predilection; typically older adults

133
Q

Angiosarcomas may arise from lymph edema, classically where and in what setting?

Arise from which vessels?

A
  • Ipsilateral UE years after radical masectomy (i.e., w/ LN resection) for breast cancer
  • Arising from lymphatic vessels (lymphangiosarcoma)
134
Q

How invasive and what is the risk of metastasis for angiosarcomas?

5-year survivial?

A
  • Locally invasive and can readily metastasize
  • 5-year survival around 30%
135
Q

What is the gross morphology of cutaneous angiosarcomas?

A
  • Begin as multiple small and asymptomatic red papules or nodules
  • Eventually become large, fleshy masses of red-tan to gray-white tissue w/ margins blurring into surrounding structures
  • Central areas of necrosis and hemorrhage common
136
Q

In angiosarcomas what kind of differentiation can be seen?

A
  • ALL degrees of differentiation may be seen:
  • From plump, atypical endothelial cells forming vascular channels
  • Wildly undifferentiated tumors w/ solid spindled appearance and no discernible blood vessels
137
Q

The endothelial origin of Angiosarcomas can be demonstrated with staining for what?

A
  • CD31
  • von Willebrand factor
138
Q

Angiosarcomas most commonly is found in which 4 locations?

A
  • Skin
  • Liver
  • Breast
  • Soft tissue
139
Q

Small bore artificial grafts generally fail as a result of what 2 complications?

If small bore replacement required, best to use which grafted vessels?

A
  • Thrombosis or intimal hyperplasia at jct. of the graft
  • Use saphenous vein or left internal mammary arteries (best option)

CPR II Exam 1 (25 decks)

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