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Flashcards in V - Diseases of the Immune System Deck (116):
1

Type of immunity mediated by neutrophils, macrophages and natural killer cells and includes epithelial barriers of the skin, GIT and respiratory tract.

Innate immunity (natural/native)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108

2

Type of immunity mediated by lymphocytes and their products, and is normally silent and responds to the presence of microbes by becoming active, expanding and generating potent mechanisms for neutralizing and eliminating microbes.

Adaptive immunity (acquired/specific)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108

3

Type of adaptive immunity mediated by soluble antibody proteins that are produced by B lymphocytes. Effective against extracellular microbes.

Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109

4

Type of adaptive immunity mediated by T lymphocytes. Designed to combat cell-associated microbes (e.g. Phagocytosed microbes and microbes in the cytoplasm of infected cells).

Cell-mediated or cellular immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109

5

Results from activation of TH2 CD4+ helper T cells by environmental antigens, leading to the production of IgE antibodies, which become attached to mast cells.

Type I Hypersensitivity (immediate)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120 *SEE SLIDE 5.1

6

Caused by antibodies that bind to FIXED TISSUE AND CELL ANTIGENS and promote phagocytosis and destruction of the coated cells or trigger pathologic inflammation in tissues.

Type II Hypersensitivity (Antibody-mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120 *SEE SLIDE 5.1

7

Caused by antibodies binding to antigens to form COMPLEXES that circulate and may deposit in vascular beds and stimulate inflammation, secondary to complement activation.

Type III Hypersensitivity (immune complex mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120 *SEE SLIDE 5.1

8

Cell-mediated immune responses in which T lymphocytes cause tissue injury, either by producing cytokines that induce inflammation and activate macrophages, or by directly killing cells.

Type IV Hypersensitivity (T-cell mediated/Delayed)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120 *SEE SLIDE 5.1

9

Indicate type of hypersensitivity reaction:SLE

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

10

Indicate type of hypersensitivity reaction:Multiple sclerosis

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

11

Indicate type of hypersensitivity reaction:Transplant rejection

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

12

Indicate type of hypersensitivity reaction:Anaphylaxis

Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

13

Indicate type of hypersensitivity reaction:Goodpasture syndrome

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

14

Indicate type of hypersensitivity reaction:Serum sickness

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

15

Indicate type of hypersensitivity reaction:Arthus reaction

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

16

Indicate type of hypersensitivity reaction:Autoimmune hemolytic anemia

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

17

Indicate type of hypersensitivity reaction:Allergies

Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

18

Indicate type of hypersensitivity reaction:Type I DM

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

19

Indicate type of hypersensitivity reaction:Tuberculosis

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

20

Indicate type of hypersensitivity reaction:Bronchial asthma

Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

21

Indicate type of hypersensitivity reaction:Acute rheumatic fever

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

22

Indicate type of hypersensitivity reaction:Poststreptococcal glumerulonephritis

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

23

Indicate type of hypersensitivity reaction:Polyarteritis nodosa

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

24

Indicate type of hypersensitivity reaction:Rheumatoid arthritis

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

25

Indicate type of hypersensitivity reaction:Inflammatory bowel disease

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

26

Indicate type of hypersensitivity reaction:Tuberculin reaction

Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

27

Indicate type of hypersensitivity reaction:Reactive arthritis

Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

28

Indicate type of hypersensitivity reaction:Graves disease

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

29

Indicate type of hypersensitivity reaction:Acute rheumatic fever

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

30

Indicate type of hypersensitivity reaction:Myasthenia gravis

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

31

Indicate type of hypersensitivity reaction:Insulin resistant DM

Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

32

Indicate type of hypersensitivity reaction:Pernicious anemia

Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

33

A special form of graft rejection occuring in the setting where PREFORMED ANTIDONOR ANTIBODIES are present in the circulation of the host before transplant. Occurs within minutes to a few hours after transplantation.

Hyperacute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133

34

Rejection which occurs within days to weeks (but may aslo be months or years) of transplantation in a nonimmunosuppressed host. Caused by both cellular and humoral immune mechanisms.

Acute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133

35

Acute rejection most commonly seen within the first months after transplantation, typically accompanied by signs of renal failure. Extensive CD4+ and CD8+ T-cell (MONONUCLEAR) infiltration with edema and mild interstitial hemorrhage.

Acute cellular rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133

36

Acute rejection caused by antidonor antibodies. May take the form of necrotizing VASCULITIS with endothelial cell necrosis, neutrophilic infiltration, deposition of antibody, complement, and fibrin, and thrombosis.

Acute humoral rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133

37

Rejection which present clinically months to years after transplantation with a progressive rise in serum creatinine levels. Dominated by arteriosclerosis, interstitial fibrosis and loss of renal parenchyma. *SEE SLIDE 5.2

Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133

38

A multisystem autoimmune disease which principally affects the skin, kidneys, serosal membranes, joints and heart. Associated with autoantibodies including ANAs.

Systemic Lupus Erythematosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.139

39

SOAP BRAIN MD mnemonic for SLE stands for?

SerositisOral ulcersArthritisPhotosensitivityBloodRenal disorderANA positiveImmunologic disorderNeurologic disorderMalar rashDiscoid rash(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140

40

How many symptoms must be present in a patient for her/him to be diagnosed as having SLE?

4 out of 11 symptoms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140

41

A systemic, chronic inflammatory disease affecting many tissues but principally attacking the joints to produce a nonsuppurative proliferative synovitis that frequently progress to destroy articular cartilage and underlying bone with resulting disabling arthritis.

Rheumatoid arthritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.145

42

Characteristic lesion in RA, formed by proliferating synovial-lining cells admixed with inflammatory cells, granulation tissue and fibrous connective tissue.

Pannus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146

43

Cytokine which plays a central role in the pathogenesis of RA.

TNF(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146

44

A clinicopathologic entity with a triad of dry eyes, dry mouth and arthritis.

Sjogren syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.148

45

Characterized by progressive fibrosis involving the skin, GIT and other tissues. May be a result of activation of fibroblasts by cytokines produced by T cells.

Systemic sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.149

46

A vascular disorder characterized by reversible vasospasm of the arteries. Typically the hands turn white due to vasospasm, then blue due to cyanosis, then red due to reactive hyperemia.

Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.151

47

One of the more common forms of primary immune deficiency characterized by absent or markedly decreased numbers of B-cells in the circulation, with depressed serum levels of all classes if immunoglobulin.

X-linked agammaglobulinemia (Bruton disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.152

48

Most common of all the primary immune deficiencies characterized by recurrent sinopulmonary infections and diarrhea.

Isolated IgA deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154

49

A constellation of genetically distinct syndromes with common feature of defects in both humoral and cell-mediated immune responses, making affected infants susceptible to severe recurrent infections by bacteria, viruses, fungi, protozoans, and opportunistic infections.

Severe Combined Immunodeficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154

50

Autosomal recessive form of SCID is due to deficiency of what enzyme?

Adenosine deaminase (ADA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154

51

An X-linked recessive disease characterized by thrombocytopenia, eczema, and marked vulnerability to recurrent infection ending in early death.

Wiskott-Aldrich Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.155

52

HIV viral surface proteins essential for viral entry into cells.

gp41 and gp120(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.157

53

A form of pneumonia in HIV patients caused by a yeast-like fungus.

Pneumocystis carinii pneumonia (PCP)(TOPNOTCH)

54

Main cellular target of HIV.

CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.158

55

P.carinii pneumonia occurs in AIDS patients with CD4+ T cell count of ______.

Less than 200 cells/uL(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163

56

Most common secondary infection of the CNS in patients with AIDS.

Toxoplasmosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163

57

Most common neoplasm in AIDS patients, caused by HHV8. Characterized by cutaneous lesions with or without internal involvement.

Kaposi sarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.164

58

A disorder of protein misfolding, causing extracellular deposition of pink or red colored deposits stained with Congo red, with apple-green birefringence in polarized light. *SEE SLIDE 5.3

Amyloidosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.166

59

Tissues of the immune system

Bone marrow, thymus, lymph nodes, spleen, mucosal and cutaneous lymphoid tissue. (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 193

60

The most important antigen-presenting cells for initiating T-cell responses against protein antigens

Dendritic cells(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 191

61

A 48 y/o male patient underwent kidney transplant suddenly developed bloody urine few hours after the procedure. Nephrectomy was done and revealed a cyanotic, mottled, and flaccid kidney and necrotic kidney cortex. There is neutrophilic accumulation in the arterioles, glomeruli, and peritubular capillaries. Glomeruli undergo thrombotic occlusion of capillaries and fibrinoid necrosis in arterial walls. *SEE SLIDE 5.4 The most likely diagnosis is:

Hyperacute rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 233

62

A 45 y/o female presented with signs of kidney failure 2 months after her renal transplant. Immunohistochemical staining reveals both CD4+ and CD8+ lymphocytes. Morphologic findings showed an extensive interstitial inflammation with infiltration of tubules and focal tubular injury. This is a case of:

Acute cellular (T-cell mediated) rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 234

63

Preformed antidonor antibodies present in the circulation of the recipient is implicated in what type of rejection pattern?

Hyperacute rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 233

64

A 30 y/o male developed oliguria and subsequent renal failure 3 weeks after an uneventful kidney transplant. Renal findings showed inflammation of glomeruli and peritubular capillaries, deposition of complement breakdown and focal small vessel thrombosis. This is a case of:

Acute antibody-mediated rejection (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 234

65

A 24 y/o female diagnosed with renal failure underwent renal transplant. Four years later, increasing levels of creatinine was noted, and biopsy showed an interstitial fibrosis and tubular atrophy, glomerulopathy with duplication of basement membrane, and multilayering of peritubular capillary basement membranes. Interstitial mononuclear cell infiltrates, NK cells and plasma cells were also noted. *SEE SLIDE 5.2 This is a case of:

Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 9th ed., p.234

66

The result of hypoplasia or lack of thymus in DiGeorge Syndrome

Variable loss of T-cell mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.241

67

The hallmark of AIDS

Profound immune deficiency, primarily cell-mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 245

68

A 32-year old female, presents to the clinic with symptoms of fatigue, joint pains, and malar rash. CBC revealed anemia and low platelet count. The most likely diagnosis is:

Systemic Lupus Erythematosus (TOPNOTCH)

69

Morphologic changes in SLE are primarily a result of what key factor in its pathogenesis?

Deposition of immune complexes in a variety of tissues. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 128

70

The fundamental defect in SLE

Failure of mechanisms that maintain self-tolerance (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 219

71

Most common manifestation of SLE

Hematologic manifestation (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 218

72

Most common hematologic finding in SLE

Anemia(TOPNOTCH)

73

Most common and most severe form of lupus nephritis

Diffuse lupus nephritis/Class IV(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 224

74

The most common causes of death in SLE

Renal failure and intercurrent infections (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 225

75

Cytokine most firmly implicated in the pathogenesis of Rheumatoid arthritis

TNF (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 1210

76

Major cytokine produced by TH1, stimulates macrophage activation and IgG antibody production. Plays a role in autoimmune and other chronic inflammatory diseases.

IFN-gamma(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 198

77

The dominant immune reactions of these subset of helper cells are the stimulation of IgE production and activation of mast cells and eosinophils.

TH2(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 198

78

These are the mediators of adaptive immunity and the only cells that produce specific and diverse receptors for antigens

Lymphocytes(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 199

79

These are cells the help B cells to make antibodies, activate macrophages to destroy ingested microbes, stimulate recruitment of leukocytesand regulate all immune responses to protein antigens.

CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 9th Ed p.200

80

These are cells that express antigens in the cytoplasm that are seen as foreign, such as virus-infected and tumor cells.

CD8+ cytotoxic T lymphocytes(TOPNOTCH)Robbins Basic Pathology, 9th Ed p.200

81

The most potent vasoactive and spasmodic agents causing increasing vascular permeability and causing bronchial smooth muscle contraction.

Leukotrienes C4 and D4(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 203

82

A lipid mediator produced by some mast cell populations, not derived from arachidonic acid, causing platelet aggregation, increased vascular permeability, and vasodilation.

Platelet-activating factor(PAF)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 203

83

True or False. Atopic individuals tend to have higher serum IgE levels and more IL-4 producing Th2 cells.

True. (TOPNOTCH)

84

This disease presents with nephritis and lung hemorrhage due to complement and Fc receptor-mediated inflammation due to antibody against noncollagenous protein in basement membranes of kidney glomeruli and lung alveoli.

Goodpasture syndrome(TOPNOTCH)Robbbins Basic Pathology, 9th ed., p. 206

85

This disease causes demyelination in CNS is perivascular inflammation due to inflammation mediated by TH1 and TH17 cytokines, myelin destruction by activated macrophages.

Multiple sclerosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 209

86

Mucocutatnous ulcerations involving the mouth, esophagus, external genitalia, and perianal region in AIDS patient may be caused by

Herpes simplex virus infection(TOPNOTCH)

87

An 18 year old female presents with a day-old circular erythematous plaque with vesicles on her neck. She relates a history of wearing a new metallic pendant three days ago, and has had a similar history with other metallic jewelry. If the plaque is biopsied, which inflammatory cell is expected to predominate? (A) neutrophil (B) eosinophil (C) mast cell (D) lymphocyte

Lymphocyte (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp128-130

88

An 8 year old male with a strep throat four weeks ago develops tea-colored urine. A kidney biopsy showed hypercellular glomeruli with neutrophils. Electron microscopy showed subepithelial "humps." *SEE SLIDE 5.5. These findings are caused by (A) antibodies against glomerular basement membrane (B) antibodies against endothelium (C) immune complex deposition (D) T-cell mediated recruitment of neutrophils

immune complex deposition (TOPNOTCH) Robbins Basic Pathology, 8th ed. P126

89

A 5 year old female with a strep throat two weeks ago develops joint pains and fever. Auscultation revealed a friction rub. What type of hypersensitivity is responsible?

Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120

90

A 33 year old female presents with morning stiffness of the PIP and MCP joints of the hands. On workup, she is positive for rheumatoid factor. Which of the following is expected in the involved joints? (A) synovial hypertrophy with dense lymphoid aggregates (B) synovial atrophy with epithelioid macrophages (C) synovial hypertrophy devoid of leukocytes (D) synovial atrophy with dense lymphoid aggregates

synovial atrophy with dense lymphoid aggregates (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp145-146

91

A 50 year old female with chronic red eye is diagnosed with keratoconjunctivitis sicca and is referred to by her ophthalmologist for bilateral infraauricular masses. Her oral mucosa has multiple fissures. Biopsy of the infraauricular masses will likely show (A) epithelial and myoepithelial cells admixed with chondroid stroma (B) lymphoplasmacytic infiltration with ductal hyperplasia (C) basaloid cells in cribriform structures (D) highly pleomorphic epithelial cells and numerous atypical mitoses

lymphoplasmacytic infiltration with ductal hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp148-149 *SEE SLIDE 5.6

92

Patients with diffuse scleroderma have sclerotic atrophy of the skin. Which other organ is most commonly involved? (A) kidneys (B) heart (C) lungs (D) gastrointestinal tract

gastrointestinal tract (90% of patients) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 149-150

93

A 22 year old male has unprotected sex and develops generalized lymphadenopathy five days later. The following month, he tests positive on HIV screening. Excision biopsy of one of his lymph nodes would likely show (A) marked follicular hyperplasia (B) epithelioid macrophages and giant cells (C) diffuse infiltration by atypical mononuclear cells (D) subcapsular necrosis

marked follicular hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 165

94

A 68 year old female with multiple myeloma dies of acute renal failure. At autopsy, her kidneys and liver were pale gray, with waxy cut sections, while her spleen showed tapioca-like granules. On histology, these organs show deposits that (A) have empty vacuoles that uptake Sudan black (B) are infiltrated by neutrophils and histiocytes (C) will fluoresce an apple green color when stained with Congo red (D) are bluish, with concentric lamellations

will fluoresce an apple green color when stained with Congo red (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 169-170 *SEE SLIDE 5.3

95

Hallmarks of immune complex injury

Acute necrotizing vasculitis, microthrombi, ischemic necrosis, fibrinoid necrosis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 117

96

Autoantibody associated with: SLE

Mainly anti-dsDNA and Anti-Sm. Others: Anti-RNP UI (shared with mixed CT disease), Anti-SS-A and Anti-SS-B (shared with Sjogren syndrome), Anti-histones (especially with drug-induced lupus), Antiphospholipid (shared with APAS) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

97

Autoantibody associated with: Mixed CT disease

Anti-RNP UI (Shared with SLE) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

98

Autoantibody associated with: Sjogren Syndrome

Anti-SS-A (Ro) and Anti-SS-B (La) (Shared with SLE) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

99

Autoantibody associated with: Systemic Sclerosis

Anti-SCL-70 aka DNA topoisomerase I and anti-centromere (latter shared with limited scleroderma) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

100

Autoantibody associated with: Inflammatory myopathies

Anti-Jo I aka histidyl tRNA ligase(TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

101

Autoantibody associated with: Primary biliary cirrhosis

Anti-mitochondrial (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

102

Autoantibody associated with: Dermatitis herpetiformis and celiac disease

Anti-transglutaminase (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

103

Autoantibody associated with: Various vasculitides

ANCA (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

104

Autoantibody associated with: Chronic autoimmune hepatitis

Anti-smooth muscle (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127

105

SLE renal involvement morphologic classification (I, II, III, IV, V, or VI) : Immune complexes in mesangium only, no alterations detectable by light microscopy

I - MINIMAL mesangial lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7

106

SLE renal involvement morphologic classification (I, II, III, IV, V, or VI) : Immune complexes in mesangium with mild to mod increase in mesangial matrix and cellularity

II - Mesangial PROLIFERATIVE lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7

107

SLE renal involvement morphologic classification (I, II, III, IV, V, or VI): Lesions visualized in fewer than half of the glomeruli, segmentally or globally distributed within each glomerulus. With cell proliferation, swelling, and infiltration of neutrophils and fibrinoid deposits

III - FOCAL lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7

108

SLE renal involvement morphologic classification (I, II, III, IV, V, or VI): Most serious form and most commonly envountered. Involvement of HALF or MORE GLOMERULI. With diffuse hypercellularity and wire-looping due to extnsive subendothelial deposits.

IV- DIFFUSE lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7

109

SLE renal involvement morphologic classification (I, II, III, IV, V, or VI): Widespread thickening of capillary wall due to SUBEPITHELIAL immune complexes.

V - MEMBRANOUS lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7

110

SLE renal involvement morphologic classification (I, II, III, IV, V, or VI): Complete sclerosis of greater than 90% of glomeruli. End-stage renal disease.

VI - ADVANCED SCLEROSING lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 129 *SEE SLIDE 5.7

111

Histopathologic and IF microscopy findings in SLE

Light microscopy: Liquefactive degeneration of basal layer, edema at DEJ, mononuclear infiltrates around blood vessels and skin appendages. IF: Deposition of IMMUNOGLOBULIN and COMPLEMENT at DEJ (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 129

112

Characteristic feature of vegetatations caused by Libman-Sacks endocarditis

Can be seen on either surface of the leaflet (surface exposed to flow or on underside) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 130

113

First event that triggers extensive fibrosis in systemic sclerosis

ENDOTHELIAL INJURY, which produces a T-cell reaction. T-cells and macrophages then release cytokines that activate fibroblasts. (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 133

114

Disease associated with "sago spleen" and "lardaceous spleen"

Amyloidosis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 157

115

In amyloidosis involving the liver, deposits first appear in which part of the liver parenchyma?

Space of Disse (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 157

116

In patients receiving long-term dialysis, deposition of B2-microglobulin most commonly occur where?

Carpal ligaments of the wrist, producing carpal tunnel syndrome. (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 157