Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Patho Flash cards 2016 Pics > V - Diseases of the Immune System > Flashcards

V - Diseases of the Immune System Flashcards

1
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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).

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Indicate type of hypersensitivity reaction:SLE

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Indicate type of hypersensitivity reaction:Multiple sclerosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Indicate type of hypersensitivity reaction:Transplant rejection

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Indicate type of hypersensitivity reaction:Anaphylaxis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Indicate type of hypersensitivity reaction:Goodpasture syndrome

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Indicate type of hypersensitivity reaction:Serum sickness

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Indicate type of hypersensitivity reaction:Arthus reaction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Indicate type of hypersensitivity reaction:Autoimmune hemolytic anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Indicate type of hypersensitivity reaction:Allergies

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Indicate type of hypersensitivity reaction:Type I DM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Indicate type of hypersensitivity reaction:Tuberculosis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Indicate type of hypersensitivity reaction:Bronchial asthma

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Indicate type of hypersensitivity reaction:Acute rheumatic fever

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Indicate type of hypersensitivity reaction:Poststreptococcal glumerulonephritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Indicate type of hypersensitivity reaction:Polyarteritis nodosa

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Indicate type of hypersensitivity reaction:Rheumatoid arthritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Indicate type of hypersensitivity reaction:Inflammatory bowel disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Indicate type of hypersensitivity reaction:Tuberculin reaction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Indicate type of hypersensitivity reaction:Reactive arthritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Indicate type of hypersensitivity reaction:Graves disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Indicate type of hypersensitivity reaction:Acute rheumatic fever

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Indicate type of hypersensitivity reaction:Myasthenia gravis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Indicate type of hypersensitivity reaction:Insulin resistant DM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Indicate type of hypersensitivity reaction:Pernicious anemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

SOAP BRAIN MD mnemonic for SLE stands for?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

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.

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

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.

A

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

48
Q

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

A

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

49
Q

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.

A

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

50
Q

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

A

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

51
Q

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

A

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

52
Q

HIV viral surface proteins essential for viral entry into cells.

A

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

53
Q

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

A

Pneumocystis carinii pneumonia (PCP)(TOPNOTCH)

54
Q

Main cellular target of HIV.

A

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

55
Q

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

A

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

56
Q

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

A

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

57
Q

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

A

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

58
Q

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

A

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

59
Q

Tissues of the immune system

A

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

60
Q

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

A

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

61
Q

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:

A

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

62
Q

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:

A

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

63
Q

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

A

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

64
Q

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:

A

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

65
Q

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:

A

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

66
Q

The result of hypoplasia or lack of thymus in DiGeorge Syndrome

A

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

67
Q

The hallmark of AIDS

A

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

68
Q

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:

A

Systemic Lupus Erythematosus (TOPNOTCH)

69
Q

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

A

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

70
Q

The fundamental defect in SLE

A

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

71
Q

Most common manifestation of SLE

A

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

72
Q

Most common hematologic finding in SLE

A

Anemia(TOPNOTCH)

73
Q

Most common and most severe form of lupus nephritis

A

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

74
Q

The most common causes of death in SLE

A

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

75
Q

Cytokine most firmly implicated in the pathogenesis of Rheumatoid arthritis

A

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

76
Q

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

A

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

77
Q

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

A

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

78
Q

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

A

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

79
Q

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.

A

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

80
Q

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

A

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

81
Q

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

A

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

82
Q

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

A

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

83
Q

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

A

True. (TOPNOTCH)

84
Q

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.

A

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

85
Q

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

A

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

86
Q

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

A

Herpes simplex virus infection(TOPNOTCH)

87
Q

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

A

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

88
Q

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

A

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

89
Q

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?

A

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

90
Q

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

A

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

91
Q

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

A

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

92
Q

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

A

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

93
Q

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

A

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

94
Q

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

A

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
Q

Hallmarks of immune complex injury

A

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

96
Q

Autoantibody associated with: SLE

A

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
Q

Autoantibody associated with: Mixed CT disease

A

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

98
Q

Autoantibody associated with: Sjogren Syndrome

A

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

99
Q

Autoantibody associated with: Systemic Sclerosis

A

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

100
Q

Autoantibody associated with: Inflammatory myopathies

A

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

101
Q

Autoantibody associated with: Primary biliary cirrhosis

A

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

102
Q

Autoantibody associated with: Dermatitis herpetiformis and celiac disease

A

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

103
Q

Autoantibody associated with: Various vasculitides

A

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

104
Q

Autoantibody associated with: Chronic autoimmune hepatitis

A

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

105
Q

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

A

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

106
Q

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

A

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

107
Q

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

A

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

108
Q

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.

A

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

109
Q

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

A

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

110
Q

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

A

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

111
Q

Histopathologic and IF microscopy findings in SLE

A

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
Q

Characteristic feature of vegetatations caused by Libman-Sacks endocarditis

A

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
Q

First event that triggers extensive fibrosis in systemic sclerosis

A

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
Q

Disease associated with “sago spleen” and “lardaceous spleen”

A

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

115
Q

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

A

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

116
Q

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

A

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

Patho Flash cards 2016 Pics (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions