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Pathology Block 1 > Block 1 Immunopathology > Flashcards

Block 1 Immunopathology Flashcards

1
Q

Types of hypersensitivity rxns

A

1- immediate
2- Ab-mediated
3- Ag-Ab complex
4- T-cell mediated/ delayed type

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2
Q

Timing of type 1 HS rxn

A

Immediate/initial: 5-30 min post exposure, subsides in 60 min
Late phase: 2-24 hrs lasting days

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3
Q

Cells of type 1 HS rxn

A

Im: mast cell
Late: eos, neutros, basos, monocytes, CD4+ T-cells

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4
Q

Risk factors for type 1 HS rxn

A

Atopy (predisposition bc of increase IgE or IL-4 producing TH2 cells, family hx)
Non-atopic: temp extremes/exercise - no IgE or TH2, but sensitive mast cells to non-immune stimuli

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5
Q

Genetic factors in type 1 HS rxn

A

Genetically determined, family hx important

5q31: cytokines IL-3,4,5,9,13
6p: close to HLA complex

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6
Q

Type 2 HS rxn mechanism

A

IgM or IgG Abs -> classical complement -> C3b, C4b -> MAC & lysis
ADCC: no phagocytosis but cell lysis; monos, neutros, eos, NK cells

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7
Q

Myasthenia gravis & Graves disease

A

Type 2 HS rxn
MG: Ab against ACh-R -> downregulates ACh-R -> mm weakness, paralysis
GD: Ab against TSH-R -> hyperthyroidism

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8
Q

AI hemolytic anemia & AI thrombocytopenic purpura

A

Type 2 HS by opsonization & phago of red cells (AHA) or platelets (ATP)
AHA: Ab against Rh antigen on RBC -> hemolysis, anemia
ATP: Ab against GP3b/2a integrin -> bleeding

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9
Q

Pemphigus vulgaris

A

Type 2 HS by Ab-mediated activation proteases, disruption intercellular adhesions
Ab to epidermal cadherins -> skin vesicles/bullae

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10
Q

ANCA vasculitis

A

Type 2 HS by neutro degran & inflam

Ab to neutro granule proteins -> vasculitis

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11
Q

Goodpasture syndrome

A

Type 2 HS by complement and FcR-mediated inflam

Ab to noncollagen protein in BM kidney glomeruli, lung alveoli -> nephritis, lung hemorrhage

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12
Q

Acute rheumatic fever

A

Type 2 HS by inflam, MF activation

Ab to strep cell wall Ag cross-rx with myocardial Ag -> myocarditis, arthritis

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13
Q

Insulin-resistant diabetes

A

Type 2 HS by Ab inhibiting binding of insulin

Ab to insulin-R -> hyperglycemia, ketoacidosis

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14
Q

Pernicious anemia

A

Type 2 HS rxn by neutralization of IF, decreasing absorption of B12
Ab to IF of gastric antrum parietal cells -> abnormal erythropoiesis, anemia

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15
Q

Type 3 HS mechanism

A

Ag-Ab complex elicits inflam at site of deposition; systemic or localized

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16
Q

SLE

A

Type 3 HS rxn

Ag = nuclear antigens -> nephritis, skin lesions, arthritis, etc.

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17
Q

PSGN

A

Type 3 HS rxn

Ag = strep cell wall Ag “planted” in glomerular BM -> nephritis

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18
Q

Polyarteritis nodosa

A

Type 3 HS rxn

Ag = hep B virus Ag in some cases -> systemic vasculitis

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19
Q

Reactive arthritis

A

Type 3 HS rxn

Ag = bacterial Ag (e.g. Yersinia) -> acute arthritis

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20
Q

Serum sickness

A

Type 3 HS rxn

Ag = various proteins like foreign serum protein (horse anti-thymocyte globulin) -> arthritis, vasculitis, nephritis

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21
Q

Arthus reaction

A

Type 3 HS rxn
Ag = various foreign proteins that diffuse into vascular wall & binds preformed Ab -> precipitate complex in vessel wall -> fibrinoid necrosis
*Ischemia made worse by superimposed thrombus

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22
Q

Morphology of type 3 HS rxn

A

H&E: necrotic tissue and deposits of immune complexes, complement, plasma protein -> smudgy eosinophilic deposit
Immunofluorescence: granular lumpy deposits of Ig and complement
EM: electron-dense deposits along glomerular BM

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23
Q

Type 1 DM

A

Type 4 HS rxn

T-cell directed to panc islet beta cells -> insulitis (islet inflam), destruction of islet beta cells, diabetes

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24
Q

MS

A

Type 4 HS rxn
T-cell directed to protein Ag in CNS myelin -> demyelination in CNS with perivascular inflammation, paralysis, ocular lesions

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25
Q

RA

A

Type 4 HS rxn

T-cell directed to unknown Ag in joint synovium -> chronic arthritis with inflam, destruction articular cartilage, bone

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26
Q

Crohn disease

A

Type 4 HS rxn

T-cell directed to unknown Ag (role for commensal bacteria) -> chronic intestinal inflam, obstruction

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27
Q

Peripheral neuropathy/ Guillan-Barre syndrome

A

Type 4 HS rxn

T-cell directed to protein Ag of peripheral nerve myelin -> neuritis, paralysis

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28
Q

Contact sensitivity (dermatitis)

A

Type 4 HS rxn

T-cell directed to various environmental Ag (poison ivy urushiol) -> skin inflam with blisters

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29
Q

Cytokines involved in type 4 HS rxn

A

APC -> IL-12 -> activate TH1 cell
TH1 -> IFN-g, TNF -> activate MF; & IL-2 to self-activate
TH17 -> IL-17, IL-22 -> inflammation

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30
Q

Important genes for autoimmunity

A

PTPN-22: most frequently implicated in AI
NOD-2 polymorphisms: cytoplasmic sensor of microbes
IL-2-R (CD25) & IL-7-R alpha chains

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31
Q

Methods of triggering AI

A

Induction of costimulators on APCs by microbe; molecular mimicry

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32
Q

SLE antibodies & susceptibility

A

Numerous, especially ANA (anti-nuclear)

F>M, childbearing age, AA & Hispanics 2-3x higher

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33
Q

Criteria for SLE (must meet 4 of 11)

A

Malar rash, discoid rash, photosensitivity, oral ulcers, arthritis, serositis, renal disorder, neurologic dis, hematologic dis, immunologic dis, ANAs

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34
Q

Types of ANAs possibly seen in SLE

A

Anti- DNA, histone, nonhistone protein bound to RNA, nucleolar antigen

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35
Q

Anti-dsDNA Abs

A

Often seen in SLE

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36
Q

Anti-histone Abs

A

Drug-induced lupus, and SLE

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37
Q

Anti-Smith (core proteins of small nuclear RNP particles) antibody

A

SLE

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38
Q

Anti-RNP/U1RNP Ab

A

Systemic diffuse & limited (CREST) sclerosis

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39
Q

Anti-RNP Abs: SS-A (Ro) and SS-B (La)

A

Sjögren syndrome

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40
Q

Anti-DNA topoisomerase Ab (Scl-70)

A

Diffuse systemic sclerosis

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41
Q

Anti-centromere Abs

A

CREST (limited scleroderma)

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42
Q

Anti-histidyl-tRNA synthetase Ab Jo-1

A

Inflammatory myopathies

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43
Q

Indirect immunofluorescence: homogenous or diffuse nuclear staining

A

Chromatin, histones, dsDNA (sometime)

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44
Q

Indirect immunofluorescence: rim or peripheral staining

A

dsDNA

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45
Q

Indirect immunofluorescence: speckled pattern

A

Most commonly observed but least specific: Abs to non-DNA nuclear constituents, including Sm-antigen, RNP, SS-A & SS-B reactive antigens

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46
Q

Indirect immunofluorescence: nucleolar pattern

A

Few discrete spots within nucleus: anti-RNA Abs (systemic sclerosis)

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47
Q

Anti-phospholipid-B2-glycoprotein complex Abs

A

Bind cardiolipin Ag -> false positive syphilis test in lupus patients
Interferes with in vitro clotting tests (aka Lupus anticoagulant): increases PTT, hypercoagulable state (spont miscarriages, venous and arterial thromboses)

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48
Q

Genetic risk for SLE

A

HLA-DQ locus (anti-dsDNA, anti-Sm, anti-PL Abs)

Early complement component deficiency: C2, C4, C1q (can’t remove Ag-Ab complex)

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49
Q

Pathogenesis of SLE

A

Failure of self-tolerance in B cells (make ANAs), CD4+ helper T for nucleosomal Ag also escape tolerance
? role of type 1 IFNs
TNF-like BAFF promotes B-cell survival

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50
Q

Environmental factors for SLE

A

UV light exacerbates disease (may induce apoptosis, alter DNA to make immunogenic)
Sex hormones (pregnancy, menses)
Drugs: hydralazine, procainamide, d-penicillamine -> SLE-like response

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51
Q

Mechanism of tissue injury in SLE

A

Immune complexes (type 3 HS), autoAb to RBC, WBC, platelets

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52
Q

LE (lupus eryth.) cell

A

Neuto or MF that has engulfed the denatured nucleus of an injured cell

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53
Q

Acute necrotizing vasculitis

A

Can be b/c of SLE, fibrinoid deposits in tissue b/c immune comlpexes -> eventual fibrosis

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54
Q

Morphologic classes of lupus nephritis

A

1: minimal mesangial
2: mesangial proliferative
3: focal proliferative
4: diffuse proliferative
5: membranous
* None is specific for lupus

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55
Q

Mesangial lupus glomerulonephritis (GN)

A

Mesangial cell proliferation, immune complex deposition without involvement of glomerular capillaries; increase in mesangial matrix & # cells

56
Q

Focal proliferative GN

A
57
Q

Diffuse proliferative GN

A

Global, >50% glomeruli involved; hematuria & proteinuria, hypertension, mild-severe renal insufficiency; most severe form of lupus nephritis & most common

58
Q

Membranous GN

A

Diffuse thickening of capillary walls (“wire loop”), severe proteinuria or nephrotic syndrome

59
Q

Skin morphology of SLE

A

H&E: vacuolar degeneration of epidermal basal layer, dermal edema, perivascular inflam, vasculitis w/ fibrinoid necrosis
Immunofl: Ig, complement deposits at dermo-epidermal jxn (also seen in scleroderma, dermatomyositis)

60
Q

SLE heart morphology

A

Pericarditis, non-bacti verrucous endocarditis, other serial cavity involvement, warty deposit on either side of any valve, CAD
Acute: fibrinous exudate
Chronic: thickened, opaque, shaggy fibrous tissue

61
Q

SLE joint morphology

A

Nonerosive synovitis, little deformity, different from RA, but painful joints

62
Q

SLE CNS morph

A

Not clear pathogenesis; psychoses or convulsions, ? Ab against synaptic membrane protein, ? acute vasculitis vs. intimal proliferation -> occlusion small vessels

63
Q

SLE spleen morphology

A

Splenomegaly, capsular thickening, follicular hyperplasia

Onion-skin lesions (central arteries concentric intimal/SM hyperplasia)

64
Q

SLE lung morph

A

Pleuritis, pleural effusion (50% pts), alveolar injury w/ edema/hemorrhage, chronic interstitial fibrosis & 2’ pulm HTN

65
Q

SLE bone marrow, lymph node morph

A

BM: hematoxylin bodies (also in other organs)
LN: enlarged, hyperplastic follicles, necrotizing lymphadenitis, “infections”

66
Q

Course & prognosis SLE

A

Variable, flare-ups and remissions, acute cases rarely -> death
Tx: corticosteroids, immunosuppressants
90% 5-y, 80% 10-y survival
Most common COD: renal failure, infections

67
Q

Chronic discoid lupus erythematosus

A

Skin manifestations of SLE, rarely systemic
Skin plaques, variable edema, scaliness, follicular plugging
Skin atrophy w/ elevated red border (face, scalp)

68
Q

Immune characteristics of discoid lupus

A

35% positive ANA test, rarely dsDNA Abs

Ig & C3 at dermoepidermal junction (like SLE)

69
Q

Subacute cutaneous lupus

A

Predominant skin involvement, widespread superficial rash w/o scarring (usually), mild systemic symptoms

70
Q

Subacute cutaneous lupus immune characteristics

A

Abs to SS-A Ag and HLA-DR3 genotype

71
Q

Drug-induced lupus: drugs causing it, symptoms

A 
Hydralazine, procainamide, INH, d-penicillamine
Multiple organs (renal and CNS uncommonly), only ⅓ patients with ANAs have symptoms, which remit with drug withdrawal
72
Q

Drug-induced lupus: immune characteristics

A

ANAs, anti-histone Abs, rarely anti-dsDNA

73
Q

Rheumatoid arthritis

A

Chronic inflammation affecting primarily jj, sometimes extra-articular tissues, skin, blood vessels, lungs, heart
Due to unknown synovial Ag

74
Q

Sjögren syndrome

A

Immune-mediated destruction of lacrimal and salivary glands (keratoconjunctivitis sicca, xerostomia)

75
Q

Sicca syndrome

A 
Primary = isolated disorder
Secondary = more common, in association with other AI disorders like lupus, RA
76
Q

Mechanism of Sjögren syndrome

A

Lymphocytic infiltration and fibrosis of lacrimal and salivary glands (CD4+ Th, B, plasma cells)

77
Q

Immune characteristics of Sjögren syndrome

A

75% have rheumatoid factor (reactive with self-IgG)
50-80% ANAs
90% Anti-SS-A (Ro), SS-B (La)
*None are diagnostic

78
Q

HLA associations with Sjögren syndrome

A

Primary: H8, DR3, DRW52; DQA1,B1 loci

Anti-SS-A or B Abs: DQA1,B1 loci

79
Q

Possible pathogenesis of Sjögren syndrome

A

Aberrant T- and B-cells, ? triggered by viral infection of salivary glands -> cell death = released tissue self-Ag (? a-fodrin cytoskeletal protein, ? viruses EBV, HCV, human retrovirus T-cell lymphotropic virus type 1)

80
Q

Morphology of Sjögren syndrome

A

Periductal, perivascular lymphocytic infiltration; ductal epithelium hyperplasia then atrophy/scar

81
Q

Comorbidities/ risk factors of Sjögren syndrome

A 
Women 50-60 years old
Increased risk lymphoma (40x)
Keratoconjunctivitis
Xerostomia
Bronchitis, pneumonia
⅓ extra glandular disease (SS-A Ab), rarely glomerular lesions, tubular fxn defect frequent (renal tubular acidosis, uricosuria, phosphaturia, tubulointerstitial nephritis)
60% patients have other AI disorder
82
Q

Mikulicz syndrome

A

Lacrimal, salivary gland inflam from any etiology (sarcoidosis, leukemia, lymphoma, AI, etc.)

83
Q

Essential test to dx Sjögren syndrome

A

Biopsy of the lip (minor salivary glands)

84
Q

Characteristics of systemic sclerosis

A

Chronic inflammation (AI), widespread damage to small blood vessels, progressive interstitial and perivascular fibrosis in skin and multiple organs

85
Q

Most commonly affected organs in systemic sclerosis & COD

A

Skin, GI, kidneys, heart, mm, lungs
May be confined to skin for years, usually progresses to visceral involvement
COD: renal or cardiac failure, pulmonary insufficiency, intestinal malabsorption

86
Q

Diffuse vs. limited systemic sclerosis

A

Diffuse: widespread skin involvement at onset
Limited: skin confined to fingers, forearms, face, late visceral involvement, benign clinical course

87
Q

CREST syndrome

A

Occurs in some patients with limited systemic sclerosis
Calcinosis
Raynaud’s phenomenon
Esophageal dysmotility
Sclerodactyly
Telangectasia
*Rare/late inv of viscera, esophagus, pulmonary HTN, biliary cirrhosis

88
Q

Antibodies associated with CREST syndrome

A

Anti-centromere antibodies

89
Q

Causes of extensive fibrosis in systemic sclerosis

A

? exogenous agent trigger activates T/B cells, other leukocytes; cytokines/trigger -> blood vessel injury, narrowing; cytokines & ischemia -> fibroblasts increase ECM deposition

90
Q

ANAs associated with systemic sclerosis

A

DNA-topoisomerase 1 (anti-Scl-70): highly specific, 10-20% patients, increases pulmonary fibrosis, peripheral vascular disease
Anti-centromere Ab: 20-30% patients, CREST or limited cutaneous SS
Rarely, pts have both

91
Q

Clinical features of systemic sclerosis

A

Raynaud’s phenomenon, dysphagia, abdominal pain/ weight loss/ anemia, malignant HTN, mild proteinuria, pulmonary disease (major COD b/c renal treatments effective)

92
Q

Inflammatory myopathies

A

Immune-mediated injury and inflam of mainly sk mm
E.g. dermato-, poly-, inclusion body -myositis
Occurs alone or with other immune diseases

93
Q

Mixed connective tissue disease

A

Mixed clinical features of SLE, SScl, polymyositis
U1-RNP-Abs
Modest renal involvement (responds to c-steroids)
Can evolve to SLE, SScl
Complications: pulmonary HTN, renal disease ~SScl

94
Q

Polyarteritis nodosa, other vasculitides

A

Noninfectious, involve any type of vessel, many clinical settings
PN: necrotizing inflam of vessel walls, strong evidence of immunological pathogenetic mechanism

95
Q

Primary immunodeficiencies

A

Genetically determined
Affect adaptive (T, B, or T/B) & innate immunity (NK, phagocytes, complement)
Most manifest in infants with recurrent infection

96
Q

Bruton’s X-linked agammaglobulinemia mechanism

A

Failure of B cell dev d/t Btk mutation

On Xq21.22: no light chains = pre-B cell R can’t deliver signal to continue maturation

97
Q

Bruton’s X-linked agammaglobulinemia clinical

A

Appears ~6 mos b/c maternal IgG

Recurrent bacterial URI, viral infections (GI), polio vaccine -> poliomyelitis, Giardia lamblia (dec IgA)

98
Q

Bruton’s X-linked agammaglobulinemia lab features

A

Absent/dec B cells, Ig, plasma cells
Normal pre-B cells in BM, normal T-cell med rxns
Underdeveloped germinal centers

99
Q

Bruton’s X-linked agammaglobulinemia comorbidities and tx

A

AI diseases increase in frequency - paradoxical, arthritis, dermatomyositis, breakdown of self-tolerance ? d/t chronic infxns; *Paradoxical
Tx: Igs

100
Q

Common variable immunodeficiency characteristics

A

Hypogammaglobulinemia, affecting all the classes or only IgG, sx in later childhood/ adolescence
M=F, sporadic and inherited, relatives have high incidence of IgA def

101
Q

CVID comorbidities

A

High fx AI diseases (20%, including RA)

Inc risk of lymphoid malignancy, and gastric cancer

102
Q

CVID morphology

A

Hyperplastic B-cell areas in lymphoid tissues d/t defective regulation (normal feedback inh by IgG absent)

103
Q

Mechanism of CVID

A

Intrinsic B cell defects and abnormal Th cell-mediated activation of B cells
BAFF-R, ICOS

104
Q

CVID clinical

A

Recurrent sinopulmonary pyogenic infections, ~20% recurrent herpesvirus infxn, enterovirus -> meningoencephalitis, G. lamblia diarrhea

105
Q

IgA deficiency characteristics

A

1/600 of Euro descent in US
Low levels serum and secretory IgA
Familiar/acquired (toxoplasmosis, measles)

106
Q

IgA def symptoms

A

Asymptomatic: decreased mucosal defense, resp infxn, GI, UTI
Symptomatic: recurrent sinopulmonary infxns, diarrhea

107
Q

IgA def mechanism

A

Impaired differentiation of naive B cells to IgA-producing cells
*BAFF gene

108
Q

IgA def comorbidities

A

May also be IgG2,4 def = prone to infxns
Inc risk resp tract allergy, AI disease (SLE, RA)
Assc. with CVID
*Fatal anaphylaxis with blood transfusion

109
Q

Hyper IgM syndrome mechanism

A

Make IgM, no class switching b/c defective Th cells
X-linked (70%): CD40L gene on Xq26
AR: CD40 gene, AID (DNA editor)

110
Q

Hyper IgM comorbidities

A

Can cause AI hemolytic anemia, thrombocytopenia, neutropenia
Recurrent pyogenic infxns (low level IgG to opsonize)
Pneumocystitis jiroveci pneumonia

111
Q

DiGeorge syndrome

A

Dev failure of 3,4 pharyngeal arches: thymus, parathyroids, thyroid clear cells
Abnormal mouth, ears, facies
22q11 deletion in 90% pts or T-box TF gene family

112
Q

DiGeorge clinical

A

T-cell mediated immunity impaired = fungal, viral infxns

Also tetany, congenital defects of heart and great vessels

113
Q

DiGeorge lab

A

Depleted T cell zones in tissues (paracortex in LN, periarteriolar sheath of spleen)
Normal or dec Ig levels

114
Q

SCID characteristics, clinical, tx

A

Humoral and cell-mediated problems
Sx in infants: oral thrush, diaper rash, failure to thrive, morbilliform rash
Numerous severe infxns
BM transplant in 1 year, ? retroviral gene therapy

115
Q

SCID genetics

A

X-linked: 50-60% cases, mutation in y-chain subunit of cytokine receptors
AR: ADA def -> ? accumulation toxic products; also other AR forms

116
Q

SCID lab

A

Thymus small, no lymph cells; lobules of undiff epithelial cells (fetal thymus, X-linked); hypoplastic lymphoid tissue in all T or T/B cell areas

117
Q

Wiskott-Aldrich syndrome symptoms, genetics, tx

A

Immunodeficiency with thrombocytopenia and eczema
Xp11.23 link membrane receptors
Inc risk lymphoma
Tx: BM transplant

118
Q

WAS lab

A

Thymus normal, progressive 2’ depletion T-cells, variable loss cellular immunity
*No Abs to polysaccharide Ags, poor response to protein Ags
Dec IgM, normal IgG, inc IgA & E

119
Q

C2 deficiency

A

Little or no increase in infection susceptibility, but inc incidence of SLE-like AI disease
*Alt pathway adequate b/c properdin, factor D def rare
Recurrent pyogenic infxns

120
Q

C3 deficiency

A

Needed for class, alt pathways = susc to serious recurrent pyogenic infxns
Inc risk immune-complex mediated glomerulonephritis -> MAC def = susc to Neisseria

121
Q

Hereditary angioedema

A

AD: C1 inhibitor def
Edema in skin, larynx, GI tract -> life-threatening asphyxia or n/v/d after minor trauma/ emotional stress
Tx: C1-I concentrates

122
Q

PNH

A

Mutation in GPI linkage enzymes (CD55/DAF and CD59)

Uncontrolled complement act -> hemolysis

123
Q

Factor H mutations

A

Complement regulator; 10% of hemolytic uremic syndrome; microvascular thrombosis in kidneys

124
Q

Amyloid

A

Pathogenic proteinaceous substance deposited in extracellular space in various tissues/organs

125
Q

Amyloidosis onset, diagnosis, lab findings

A

Insidious onset, biopsy required for dx
On H&E, amorphous eosinophilic, hyaline, extracellular substance accumulating and encroaching on adjacent cells -> atrophy
Congo red stain has apple green birefringence d/t amyloid polarization

126
Q

Chemical makeup of amyloid

A

95% fibril proteins, 5% P component, other GPs

3 common forms: AL, AA, A-beta

127
Q

AL amyloid

A

Amyloid light chain: Ig light chain produced by plasma cells

lambda > kappa

128
Q

AA amyloid

A

Amyloid-assc: unique non-Ig protein synth by liver

SAA = inflam state as part of acute phase response

129
Q

A-beta amyloid

A

beta amyloid precursor protein -> cerebral lesions in AD

130
Q

Other proteins in amyloid deposits

A

TTR, B2-microglobulin, prion disease of CNS

Other minor include serum amyloid P component, proteoglycans, highly sulfated glycosaminoglycans

131
Q

Transthyretin (TTR)

A

Normal serum protein transports thyroxine, retinol
Mutant form in familial amyloid polyneuropathies
Dep in heart of aging: senile systemic amyloidosis

132
Q

B2-microglobulin

A

Normal serum protein; amyloid fibril subunit AB2m in hemodialysis assc amyloidosis

133
Q

2 categories of amyloid proteins

A

Normal: inherent tendency to fold improperly, associate, and form fibrils *when production inc
Mutant: prone to misfolding and aggregation

134
Q

Amyloidosis morphology

A 
Enlarged, firm, waxy spleen
Congo red birefringence
Spleen deposits are sago (deep in splenic follicles) or lardaceous (in sinuses, CT, red pulp)
Liver replaced, fxn ok
Heart conduction sys
Tongue deposits -> macroglossia
135
Q

Amyloidosis clinical

A

Proteinuria, nephrotic syndrome, failure, uremia; cardiac insidious CHF, conduction, disturbances, arrhythmias, restrictive pattern
GI: asx, malabsorption, diarrhea (tongue, speech, swallowing probs)

136
Q

Amyloid dx and prognosis

A

Dx: biopsy of kidney, rectum, gingiva, fat pad -> CONGO RED stain
Serum/urine protein electrophoresis for light chains
Radiolabeled SAP - follow for binding to deposits
Prog: poor, 2 yr median survival rate, worse if plasma cell-assc myeloma

Pathology Block 1 (12 decks)

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