V - Diseases of the Immune System Flashcards
Innate immunity (natural/native)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
Type of immunity mediated by neutrophils, macrophages and natural killer cells and includes epithelial barriers of the skin, GIT and respiratory tract.
Adaptive immunity (acquired/specific)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.108
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.
Humoral immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
Type of adaptive immunity mediated by soluble antibody proteins that are produced by B lymphocytes. Effective against extracellular microbes.
Cell-mediated or cellular immunity(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.109
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).
Type I Hypersensitivity (immediate)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120 *SEE SLIDE 5.1
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 II Hypersensitivity (Antibody-mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120 *SEE SLIDE 5.1
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 III Hypersensitivity (immune complex mediated)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120 *SEE SLIDE 5.1
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 IV Hypersensitivity (T-cell mediated/Delayed)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120 *SEE SLIDE 5.1
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 III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:SLE
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Multiple sclerosis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Transplant rejection
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Anaphylaxis
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Goodpasture syndrome
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Serum sickness
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Arthus reaction
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Autoimmune hemolytic anemia
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Allergies
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Type I DM
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Tuberculosis
Type I(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Bronchial asthma
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Poststreptococcal glumerulonephritis
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Polyarteritis nodosa
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Rheumatoid arthritis
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Inflammatory bowel disease
Type IV(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Tuberculin reaction
Type III(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Reactive arthritis
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Graves disease
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Acute rheumatic fever
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Myasthenia gravis
Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Insulin resistant DM
Type II(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
Indicate type of hypersensitivity reaction:Pernicious anemia
Hyperacute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
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.
Acute rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
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 cellular rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
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 humoral rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
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.
Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.133
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
Systemic Lupus Erythematosus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.139
A multisystem autoimmune disease which principally affects the skin, kidneys, serosal membranes, joints and heart. Associated with autoantibodies including ANAs.
SerositisOral ulcersArthritisPhotosensitivityBloodRenal disorderANA positiveImmunologic disorderNeurologic disorderMalar rashDiscoid rash(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
SOAP BRAIN MD mnemonic for SLE stands for?
4 out of 11 symptoms(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.140
How many symptoms must be present in a patient for her/him to be diagnosed as having SLE?
Rheumatoid arthritis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.145
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.
Pannus(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
Characteristic lesion in RA, formed by proliferating synovial-lining cells admixed with inflammatory cells, granulation tissue and fibrous connective tissue.
TNF(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.146
Cytokine which plays a central role in the pathogenesis of RA.
Sjogren syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.148
A clinicopathologic entity with a triad of dry eyes, dry mouth and arthritis.
Systemic sclerosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.149
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.
Raynaud phenomenon(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.151
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.
X-linked agammaglobulinemia (Bruton disease)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.152
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.
Isolated IgA deficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
Most common of all the primary immune deficiencies characterized by recurrent sinopulmonary infections and diarrhea.
Severe Combined Immunodeficiency(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
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.
Adenosine deaminase (ADA)(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.154
Autosomal recessive form of SCID is due to deficiency of what enzyme?
Wiskott-Aldrich Syndrome(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.155
An X-linked recessive disease characterized by thrombocytopenia, eczema, and marked vulnerability to recurrent infection ending in early death.
gp41 and gp120(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.157
HIV viral surface proteins essential for viral entry into cells.
Pneumocystis carinii pneumonia (PCP)(TOPNOTCH)
A form of pneumonia in HIV patients caused by a yeast-like fungus.
CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.158
Main cellular target of HIV.
Less than 200 cells/uL(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163
P.carinii pneumonia occurs in AIDS patients with CD4+ T cell count of ______.
Toxoplasmosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.163
Most common secondary infection of the CNS in patients with AIDS.
Kaposi sarcoma(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.164
Most common neoplasm in AIDS patients, caused by HHV8. Characterized by cutaneous lesions with or without internal involvement.
Amyloidosis(TOPNOTCH)Robbins Basic Pathology, 8th Ed p.166
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
Bone marrow, thymus, lymph nodes, spleen, mucosal and cutaneous lymphoid tissue. (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 193
Tissues of the immune system
Dendritic cells(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 191
The most important antigen-presenting cells for initiating T-cell responses against protein antigens
Hyperacute rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 233
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:
Acute cellular (T-cell mediated) rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 234
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:
Hyperacute rejection (TOPNOTCH) Robbin Basic Pathology, 9th ed., p. 233
Preformed antidonor antibodies present in the circulation of the recipient is implicated in what type of rejection pattern?
Acute antibody-mediated rejection (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 234
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:
Chronic rejection(TOPNOTCH)Robbins Basic Pathology, 9th ed., p.234
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:
Variable loss of T-cell mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p.241
The result of hypoplasia or lack of thymus in DiGeorge Syndrome
Profound immune deficiency, primarily cell-mediated immunity (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 245
The hallmark of AIDS
Systemic Lupus Erythematosus (TOPNOTCH)
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:
Deposition of immune complexes in a variety of tissues. (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 128
Morphologic changes in SLE are primarily a result of what key factor in its pathogenesis?
Failure of mechanisms that maintain self-tolerance (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 219
The fundamental defect in SLE
Hematologic manifestation (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 218
Most common manifestation of SLE
Anemia(TOPNOTCH)
Most common hematologic finding in SLE
Diffuse lupus nephritis/Class IV(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 224
Most common and most severe form of lupus nephritis
Renal failure and intercurrent infections (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 225
The most common causes of death in SLE
TNF (TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 1210
Cytokine most firmly implicated in the pathogenesis of Rheumatoid arthritis
IFN-gamma(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 198
Major cytokine produced by TH1, stimulates macrophage activation and IgG antibody production. Plays a role in autoimmune and other chronic inflammatory diseases.
TH2(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 198
The dominant immune reactions of these subset of helper cells are the stimulation of IgE production and activation of mast cells and eosinophils.
Lymphocytes(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 199
These are the mediators of adaptive immunity and the only cells that produce specific and diverse receptors for antigens
CD4+ helper T cells(TOPNOTCH)Robbins Basic Pathology, 9th Ed p.200
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.
CD8+ cytotoxic T lymphocytes(TOPNOTCH)Robbins Basic Pathology, 9th Ed p.200
These are cells that express antigens in the cytoplasm that are seen as foreign, such as virus-infected and tumor cells.
Leukotrienes C4 and D4(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 203
The most potent vasoactive and spasmodic agents causing increasing vascular permeability and causing bronchial smooth muscle contraction.
Platelet-activating factor(PAF)(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 203
A lipid mediator produced by some mast cell populations, not derived from arachidonic acid, causing platelet aggregation, increased vascular permeability, and vasodilation.
True. (TOPNOTCH)
True or False. Atopic individuals tend to have higher serum IgE levels and more IL-4 producing Th2 cells.
Goodpasture syndrome(TOPNOTCH)Robbbins Basic Pathology, 9th ed., p. 206
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.
Multiple sclerosis(TOPNOTCH) Robbins Basic Pathology, 9th ed., p. 209
This disease causes demyelination in CNS is perivascular inflammation due to inflammation mediated by TH1 and TH17 cytokines, myelin destruction by activated macrophages.
Herpes simplex virus infection(TOPNOTCH)
Mucocutatnous ulcerations involving the mouth, esophagus, external genitalia, and perianal region in AIDS patient may be caused by
Lymphocyte (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp128-130
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
immune complex deposition (TOPNOTCH) Robbins Basic Pathology, 8th ed. P126
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
Type II (TOPNOTCH)Robbins Basic Pathology, 8th Ed p.120
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?
synovial atrophy with dense lymphoid aggregates (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp145-146
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
lymphoplasmacytic infiltration with ductal hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp148-149 *SEE SLIDE 5.6
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
gastrointestinal tract (90% of patients) (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 149-150
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
marked follicular hyperplasia (TOPNOTCH) Robbins Basic Pathology, 8th ed. P 165
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
will fluoresce an apple green color when stained with Congo red (TOPNOTCH) Robbins Basic Pathology, 8th ed. Pp 169-170 *SEE SLIDE 5.3
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
Acute necrotizing vasculitis, microthrombi, ischemic necrosis, fibrinoid necrosis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 117
Hallmarks of immune complex injury
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
Autoantibody associated with: SLE
Anti-RNP UI (Shared with SLE) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127
Autoantibody associated with: Mixed CT disease
Anti-SS-A (Ro) and Anti-SS-B (La) (Shared with SLE) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127
Autoantibody associated with: Sjogren Syndrome
Anti-SCL-70 aka DNA topoisomerase I and anti-centromere (latter shared with limited scleroderma) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127
Autoantibody associated with: Systemic Sclerosis
Anti-Jo I aka histidyl tRNA ligase(TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127
Autoantibody associated with: Inflammatory myopathies
Anti-mitochondrial (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127
Autoantibody associated with: Primary biliary cirrhosis
Anti-transglutaminase (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127
Autoantibody associated with: Dermatitis herpetiformis and celiac disease
ANCA (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127
Autoantibody associated with: Various vasculitides
Anti-smooth muscle (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 127
Autoantibody associated with: Chronic autoimmune hepatitis
I - MINIMAL mesangial lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7
SLE renal involvement morphologic classification (I, II, III, IV, V, or VI) : Immune complexes in mesangium only, no alterations detectable by light microscopy
II - Mesangial PROLIFERATIVE lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7
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
III - FOCAL lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7
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
IV- DIFFUSE lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7
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.
V - MEMBRANOUS lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 128 *SEE SLIDE 5.7
SLE renal involvement morphologic classification (I, II, III, IV, V, or VI): Widespread thickening of capillary wall due to SUBEPITHELIAL immune complexes.
VI - ADVANCED SCLEROSING lupus nephritis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 129 *SEE SLIDE 5.7
SLE renal involvement morphologic classification (I, II, III, IV, V, or VI): Complete sclerosis of greater than 90% of glomeruli. End-stage renal disease.
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
Histopathologic and IF microscopy findings in SLE
Can be seen on either surface of the leaflet (surface exposed to flow or on underside) (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 130
Characteristic feature of vegetatations caused by Libman-Sacks endocarditis
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
First event that triggers extensive fibrosis in systemic sclerosis
Amyloidosis (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 157
Disease associated with “sago spleen” and “lardaceous spleen”
Space of Disse (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 157
In amyloidosis involving the liver, deposits first appear in which part of the liver parenchyma?
Carpal ligaments of the wrist, producing carpal tunnel syndrome. (TOPNOTCH) Robbins Basic Pathology, 9th ed. Pp 157
In patients receiving long-term dialysis, deposition of B2-microglobulin most commonly occur where?
