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Cardiology Exam > CV Pathology 1 > Flashcards

CV Pathology 1 Flashcards

1
Q

organization of the vasculature into tunics

A
  1. intima:
    -endothelium = hemostasis regulation
    -internal elastic lamina layer
  2. media:
    -smooth muscle, helically arranged
    -elastic fibers
  3. aventitia:
    -connective tissues (loose/dense irregular)
    -+/- vaso vasorum
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2
Q

vasculature classifications

A
  1. elastic:
    -maintain BP
    -aorta, pulmonary artery
  2. muscular:
    -distribute blood to/from organs
  3. arterioles/venules:
    -control blood into/out of capillary bed
  4. capillaries:
    -tissue gas/nutrient exchange
    -types: continuous, fenestrated, sinusoidal
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3
Q

inflammatory markers - general

A

*certain proteins released into the bloodstream during inflammation
*if their concentrations increase or decrease by at least 25%, they can be used as systemic inflammatory markers
*help to identify generalized inflammatory state (NOT diagnostic for any particular condition)
*examples: C-reactive protein, erythrocyte sedimentation rate

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4
Q

C-reactive protein (CRP)

A

*a general inflammatory marker (reliable early indicator of active systemic inflammation)
*made in liver following IL6 secretion by macrophages/T cells
*helps to activate complement
*normal range: <3-10 mg/L
*infections/inflammatory conditions → several hundred-fold increase
*concentrations change rapidly in first 6-8 hours after injury, peak at 48 hours, then normalize once the issue has resolved

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5
Q

erythrocyte sedimentation rate (ESR; sed rate)

A

*a general inflammatory marker
*ESR = rate at which RBCs in anticoagulated whole blood descend in a standardized tube over a period of 1 hour
*indirect measurement of plasma protein concentrations
*normal values are specific to age and sex
*increased levels → inflammation, pregnancy, anemia, autoimmune disorders, infections, cancer

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6
Q

anti-neutrophilic cytoplasmic antibodies (ANCAs) - overview

A

*heterogenous autoantibodies directed against neutrophil primary granules and monocyte lysosomes
*directly ACTIVATE neutrophils, stimulating release of ROS and proteolytic enzymes, which in vascular beds → endothelial cell injury
*useful diagnostic markers

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7
Q

anti-myeloperoxidase (MPO-ANCA)

A

*specific type of perinuclear-ANCA (p-ANCA)
*elevated levels = EGPA (eosinophilic granulomatosis with polyangiitis)

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8
Q

anti-proteinase-3 (PR3-ANCA)

A

*specific type of cytoplasmic-ANCA (c-ANCA)
*elevated levels = GPA (granulomatosis with polyangiitis)

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9
Q

vasculitis - overview

A

*group of disorders defined by presence of vessel wall inflammation & destruction
*highly varied pathophysiology and clinical features
*any vessel in any organ may be affected
*> 20 primary forms, based on:
-vessel diameter
-role of immune complexes
-type of inflammation
-organ specificity
-population demographics

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10
Q

vasculitis - general clinical manifestations

A

*findings referable to the specific tissue(s) involved
*constitutional s/s associated with systemic inflammation: fever, myalgias, arthralgias, malaise

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11
Q

vasculitis - pathogenesis

A
  1. immune-mediated inflammation:
    -immune complex deposition
    -ANCA antibodies
    -anti-endothelial cell antibodies
    -autoreactive T cells
  2. direct invasion of vascular walls by infectious pathogens:
    -may generate immune complexes indirectly inducing immune-mediated process
  3. direct physical/chemical injury (irradiation, mechanical trauma, toxins)
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12
Q

giant cell arteritis - overview

A

*chronic granulomatous disorder that principally affects LARGE-SIZED ARTERIES in the head
*most common form of vasculitis among US elderly
*arteries commonly affected: TEMPORAL ARTERY, vertebral arteries, ophthalmic arteries, aorta

note - an example of large vessel arteritides

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13
Q

giant cell arteritis - pathogenesis

A

*T cell-mediated response to as-yet uncharacterized vessel wall antigen
*pro-inflammatory cytokines (TNF) and anti-endothelial cell antibodies
*granulomatous inflammation

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14
Q

giant cell arteritis - pathology

A

*GRANULOMATOUS INFLAMMATION IN A PATCHY DISTRIBUTION
-nonnecrotizing
-multinucleated giant cells
-fragmented internal elastic membrane
-involved segments exhibit intimal thickening impinging on lumen, causing distal ischemia

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15
Q

Kawasaki disease - overview

A

*acute, febrile, self-limited arteritis of infancy/childhood
*usually medium vessels/coronary arteries are affected

note - an example medium vessel arteritides

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16
Q

Kawasaki disease - clinical manifestations

A

*frequent involvement of coronary arteries → development of coronary artery aneurysms/thromboses
*FEVER > 5 days
*CRASH syndrome:
-Conjunctival infection
-Rash, desquamating
-Adenopathy (cervical)
-Strawberry tongue
-Hand/foot (edema/erythema)

17
Q

Kawasaki disease - pathogenesis

A

*unknown
*seasonal variation in incidence (maybe a viral triggered immune response)
*?? anti-endothelial cell antibodies + delayed type IV hypersensitivity

18
Q

Kawasaki disease - pathology

A

*TRANSMURAL, FIBRINOID NECROSIS - SUPPARATIVE
*neutrophils & lymphocytes
*fibrin
*wall damage → aneurysm

19
Q

granulomatosis with polyangiitis (GPA) - diagnostic triad

A
  1. necrotizing granulomatosis vasculitis (small vessels)
  2. respiratory tract involvement (upper: ear, nose, sinuses, throat OR lower: lung OR both)
  3. renal involvement - necrotizing glomerulonephritis

note - an example of small vessel vasculitides

20
Q

granulomatosis with polyangiitis (GPA) - clinical features

A

*bilateral pneumonitis with cavitary lesions
*CHRONIC SINUSITIS with nasopharyngeal mucosal ulcerations (SADDLE NOSE)
*renal disease
*PR3-ANCAs present (c-ANCA)

21
Q

granulomatosis with polyangiitis (GPA) - respiratory tract pathology

A

*upper = sinusitis with ulcerating mucosal granulomas
-nose, palate, or pharynx, rimmed by granulomas with geographic patterns of central necrosis and accompanying vasculitis

*lower = NECROTIZING GRANULOMAS WITH GIANT CELLS
-leukocyte infiltrate surrounded by zone of fibroblasts
-coalesce to produce radiographically visible cavitary nodules

22
Q

granulomatosis with polyangiitis (GPA) - renal pathology

A

*mild = focal glomerular necrosis with isolated capillary loop thrombosis

*advanced = diffuse necrosis with parietal cell proliferation

23
Q

hemangioma - overview

A

*common BENIGN tumors composed of blood-filled vessels
*variants:
1. capillary hemangiomas (skin, SQ tissues, oral cavity, liver, spleen, kidneys)
2. juvenile hemangiomas (strawberry; skin)
3. cavernous hemangiomas (large, cystically dilated vascular channels)
4. pyogenic hemangiomas (skin of gingival or oral mucosa)

24
Q

hemangiomas - pathology

A

*composed of OBVIOUS VASCULAR CHANNELS lined by normal-appearing endothelial cells
*lumens are filled with blood cells or lymph
*usually circumscribed

25
Q

Kaposi Sarcoma - overview

A

*malignant vascular neoplasm caused by human herpesvirus-8 (HHV-8)
*most common in individuals with impaired T-cell function (AIDS)

26
Q

Kaposi Sarcoma - 4 clinical forms

A
  1. classic Kaposi Sarcoma = older men of Ashkenazi Jews descent
    -confined to skin/subcutis of lower extremities
  2. endemic [African] Kaposi Sarcoma = HIV-negative children/young adults
    -indolent or aggressive; involving lymph nodes/viscera
  3. transplantation-associated Kaposi Sarcoma = solid-organ transplant recipients
    -aggressive; involves lymph nodes, mucosa, viscera
    -lesions regress with attenuation of immunosuppression
  4. epidemic [AIDS-associated] Kaposi Sarcoma = AIDS-defining illness
    -most common HIV-related malignancy worldwide
    -involves lymph nodes and disseminates widely to viscera early in its course
27
Q

Kaposi Sarcoma - pathogenesis

A

*HHV-8 latently infected endothelial cells
*encodes homologs of IL6, cyclin D, p53 inhibitors
*absent effective T cell response, proliferation persists → clonal evolution → progression to full-fledged malignancy

28
Q

Kaposi Sarcoma - gross pathology

A

*3 sequential stages:

  1. patches = pink, red, or purple macules
    -dilated, irregular, and angulated blood vessels associated with an infiltrate of chronic inflammatory cells
  2. plaques = elevated lesions
    -dilated dermal vascular channels lined by plump spindle cells
  3. nodular lesions = overt tumors
    -increased proliferating spindle cells with interspersed slit-like spaces
    -accompanied by nodal/visceral involvement (Endemic African & Epidemic AIDS variants)
29
Q

Kaposi Sarcoma - microscopic pathology

A

*dilated, irregular, angular blood vessels
-slit like spaces
-extravasation of RBCs/hemorrhage
*infiltrate of lymphocytes
*nuclear expression of HHV-8 (latency associated nuclear antigen-1 = LANA1)

30
Q

angiosarcoma - overview

A

*malignant spindle cell neoplasm of ENDOTHELIAL PROLIFERATION
*more common in older adults
*affects skin, soft tissue, breast, liver
*highly aggressive tumors (invade locally & metastasize)

31
Q

angiosarcoma - pathogenesis risk factors

A

*LYPHEDEMA
*RADIATION

32
Q

angiosarcoma - pathology

A

*early = small, sharply demarcated, red nodules
*advanced = large with ill-defined margins
*range in differentiation:
-well differentiated = hemangioma-like
-poorly differentiated = wildly anaplastic lesions with pleomorphism, branching vascular channels, atypical mitoses

Cardiology Exam (52 decks)

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