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Semestre 6: bloque 2 > Patho week 3 > Flashcards

Patho week 3 Flashcards

(65 cards)

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1
Q

Autoantibodies in SLE

A

Antinuclear antibodies (ANAs) → not specific
Anti-Smith and Anti-ds-DNA → specific

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2
Q

Epidemiology of SLE

A

Women → 20-40 years old
Hispanic and african american
HLA-DR2 and HLA-DR3

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3
Q

Hallmark of SLE

A

Production autoantibodies

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4
Q

Method for detecting ANAs

A

Immunofluorescence

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5
Q

Antibodies that can give a false-positive tests related to syphilis

A

Antibodies vs b-glycoprotein complex (also binds to cardiolipin)

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6
Q

Environmental factor that exacerbates SLE

A

Exposure UV light

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7
Q

Drugs that can contribute to SLE

A

Hydralazine, procainamide, D-penicillamine

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8
Q

Type of hypersensitivity in SLE

A

Type III: immune complex-mediated

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9
Q

Morphology of blood vessels in SLE

A

Vasculitis

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9
Q

Cutaneous characteristic of SLE

A

Butterfly rash → erythema affects face along bridge of nose and cheeks

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10
Q

Type of endocarditis found in SLE

A

Libman-Sacks endocarditis

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11
Q

Skin manifestations may mimic SLE but systemic manifestations are rare

A

Chronic discoid lupus erythomatosus

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12
Q

Features intermediate between SLE and chronic discoid lupus

A

Subacute cutaneous lupus erythematosus

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13
Q

Most common pattern of kidney disease in SLE

A

Class IV

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14
Q

Nephrotic (proteinuria) classes of kidney disease in SLE

A

Class I and V

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15
Q

Nephritic (hematuria) classes of kidney disease in SLE

A

Class II, III, IV

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16
Q

Class I of kidney disease in SLE

A

**Minimal mesangial lupus nephritis
Normal glomeruli but mesangial immune complex deposits

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17
Q

Class II of kidney disease in SLE

A

Mesangial proliferative lupus nephritis
Mesangial cell proliferation and granular mesangial deposits

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18
Q

Class III of kidney disease in SLE

A

Focal lupus nephritis
Involvement <50% glomeruli
Glomeruli exhibits swelling and proliferation of endothelial and mesangial cells

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19
Q

Class IV of kidney disease in SLE

A

Diffuse lupus nephritis
Half or more glomeruli affected)
Endothelial, mesangial and epithelial cells involved
Wire loops

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20
Q

Class V of kidney disease in SLE

A

Membranous lupus nephritis
Diffuse thickening of capillary walls due to deposition of subepithelial immune complexes
Subepithelial podocytes → non proliferative

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21
Q

Class VI of kidney disease in SLE

A

Advanced sclerosing lupus nephritis
Sclerosis >90% glomeruli, end stage renal disease

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22
Q

Epidemiology of rheumatoid arthritis

A

Women 20-40 years old
HLA-DR4 and HLA-DR1
Risk factors → infection & smoking

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23
Q

Pathogenesis of rheumatoid arthritis

A

Autoimmune response initiated by CD4 helper T cells
Autoantibodies specific for citrullinated peptides (CCPs) → arginine residues are converted to citrulline

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24
Most implicated cytokine in rheumatoid arthritis
TNF
25
Diagnostic for rheumatoid arthritis
Anti-citrullinated peptide antibodies (ACPA)
26
What is affected in rheumatoid arthritis
Small joints of hands and feet
27
How is the synovium in rheumatoid arthritis
Grossly edematous, thickened and hyperplastic
28
Morphologic characteristics of synovial pannus
Synovial cell hyperplasia Dense inflammatory infiltrate Increased vascularity Fibrinopurulent exudate Osteoclastic activity
29
Morphologic characteristics of rheumatoid nodules
In subcutaneous tissue Similar to necrotizing granulomas
30
Joints affected in hands on rheumatoid arthritis
Metacarpophalangeal and proximal interphalangeal joints
31
Clinical characteristic of rheumatoid arthritis
Morning joint stiffness does not subside with activity
32
Rx hallmark of rheumatoid arthritis
Joint effusions and juxta articular osteopenia with erosions and narrowing of joint space
33
Treatment for rheumatoid arthritis
Corticosteroids & TNF antagonists
34
Major antigenic differences between donor and recipient that result in rejection of transplants
HLA alleles
35
Pathways in which recipients T cells recognize donor HLA antigens from the graft
Direct → graft antigens presented directly to recipient T cells by graft APCs Indirect → graft antigens are picked up by host APCs and presented to host T cells
36
Graft rejection mediated by preformed antibodies (IgM) specific for antigens on graft endothelial cells
Hyperacute rejection
37
Characteristics of hyperacute graft rejection
* Complement system activation * Endothelial damage * Inflammation * Thrombosis
38
Time in which each type of graft rejection takes to occur
Hyperacute: minutes Acute: days to weeks Chronic: months to years
39
Graft rejection mediated by T cells and antibodies that are activated by alloantigens in the graft
Acute rejection
40
Types of acute rejection and their characteristics
Cellular → CD8 CTLs directly destroy graft cells or CD4 cells secrete cytokines and induce inflammation Antibody-mediated → antibodies bind to vascular endothelium and activate classic pathway of complement
41
Indolent form of graft damage that leads to progressive loss of graft function
Chronic rejection
42
Characteristics of chronic rejection
Interstitial fibrosis Intimal thickening Vascular occlusion Glomerulopathy
43
How does tacrolimus (FK506) work against graft rejection
Inhibits phosphatase calcineurin, which is required for activation of NFAT (NFAT stimulates IL2)
44
Occurs when immunologically competent cells or their precursors are transplanted into immunologically compromised recipients, and then transferred cells recognize alloantigens in the host and attack host tissues
Graft vs Host Disease (GVHD)
45
Types of GVHD
Acute → involvement of immune system and epithelia of skin, liver and intestines Chronic → Extensive cutaneous injury, fibrosis of dermis, chronic liver disease
46
Modes of transmission of HIV
Sexual transmission → dominant route Parenteral transmission Mother-to-infant transmission
47
Polyprotein processes into p17, p24, p7, and p6
gag
48
Most abundant viral antigen (detected by ELISA)
p24
49
Hallmark of AIDS
Profound immune deficiency, death of CD4 T cells
50
Role of gp120 and gp41 in HIV
gp120: binds to coreceptors CCR5 (macrophages) and CXCR4 (T cells) gp41: medites fusion of viral & host membranes after gp120 binding
51
Enzyme that protects naive T cells from HIV infection
APOBEC3G
52
Protein that binds to APOBEC3G and promotes its degradation
Vif
53
Role of macrophages in HIV infection
Allow viral replication but are resistant to cytopathic effects → continued viral replication and reservoir
54
Role of dendritic cells in HIV infection
Mucosal DCs: transported to regional lymph nodes (transmission to CD4 T cells) Follicular DCs: germinal centers, potential reservoirs
55
Predominant cell type in brain affected by HIV
Microglia
56
Natural history of HIV infection
Primary infection: 3-6 weeks after exposure, resolves in 2-4 weeks, flu-like symptoms Chronic infection: silent but ongoing viral replication with progressive CD4 T cell loss AIDS: final stage, breakdown of immune defenses and many opportunistic infections
57
Long-term nonprogressor HIV patients
Untreated, stable CD4 counts, low viral loads +10 years
58
Elite controller HIV patients
Maintain undetectable viral load without treatment
59
Opportunistic infections in AIDS
Pneumocystis jirovecii → pneumonia Candidiasis → most common fungal infection Tuberculosis Cryptosporidium → persistent diarrhea
60
Most common neoplasms in AIDS
Kaposi sarcoma
61
Characteristics of Kaposi sarcoma
Vascular tumor Proliferation of spindle cells
62
Infection involved in development of lymphomas in AIDS patients
EBV
63
Most common CNS disease in AIDS patients
Progressive encephalopathy
64
Morphologic characteristc of HIV infection
"kissing cells"

Semestre 6: bloque 2 (10 decks)

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