Diseases Of The Immune System Flashcards

1
Q

This term refers to protection against infections.

A

Immunity

(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

It is the collection of cells and molecules that are responsible for defending against pathogenic microbes.

A

Immune system

(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 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
4
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
5
Q

Type of adaptive immunity mediated by soluble antibody proteins that are produced by B lymphocytes.

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
6
Q

Type of adaptive immunity mediated by T lymphocytes.

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
7
Q

Mediated by antibodies and is 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
8
Q

Reaction of T-lymphocytes, designed to combat cell-associated microbes (e.g. Phagocytosed microbes and microbes in the cytoplasm of infected cells).

A

Cell-mediated immunity

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.109

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

Reaction of immune system against one’s own cells.

A

Autoimmunity

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.119

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

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

Caused by antibodies that bind to fixed tissue or cell surface 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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
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
15
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
16
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
17
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
18
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
19
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
20
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
21
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
22
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
23
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
24
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
25
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
26
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
27
Q

Indicate type of hypersensitivity reaction:

Poststreptococcal glumerulonephritis

A

Type III

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

28
Q

Indicate type of hypersensitivity reaction:

Polyarteritis nodosa

A

Type III

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

29
Q

Indicate type of hypersensitivity reaction:

Rheumatoid arthritis

A

Type IV

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

30
Q

Indicate type of hypersensitivity reaction:

Inflammatory bowel disease

A

Type IV

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

31
Q

Indicate type of hypersensitivity reaction:

Tuberculin reaction

A

Type IV

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

32
Q

Indicate type of hypersensitivity reaction:

Reactive arthritis

A

Type III

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

33
Q

Indicate type of hypersensitivity reaction:

Graves disease

A

Type II

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

34
Q

Indicate type of hypersensitivity reaction:

Acute rheumatic fever

A

Type II

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

35
Q

Indicate type of hypersensitivity reaction:

Myasthenia gravis

A

Type II

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

36
Q

Indicate type of hypersensitivity reaction:

Insulin resistant DM

A

Type II

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

37
Q

Indicate type of hypersensitivity reaction:

Pernicious anemia

A

Type II

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.120

38
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

39
Q

Rejection which occurs within days to weeks 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

40
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 infiltration with edema and mild interstitial hemorrhage.

A

Acute cellular rejection

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.133

41
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

42
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.

A

Chronic rejection

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.133

43
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

44
Q

SOAP BRAIN MD mnemonic for SLE stands for?

A

Serositis
Oral ulcers
Arthritis
Photosensitivity

Blood
Renal disorder
ANA positive
Immunologic disorder
Neurologic disorder

Malar rash
Discoid rash

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.140

45
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

46
Q

Most serious and most common form of renal lesion in SLE. “Wire-loop” appearance of glomerular capillary walls.

A

Diffuse proliferative glomerulonephritis (Class IV)

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.142

47
Q

Cardiac manifestation of SLE, which occurs as nonspecific mononuclear infiltrates and the presence of irregular 1-3mm warty deposits on either surface of the leaflets.

A

Libman-Sacks Endocarditis

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.144

48
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

49
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

50
Q

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

A

TNF

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.146

51
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

52
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

53
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

54
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

55
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

56
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

57
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

58
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

59
Q

HIV viral surface proteins essential for viral entry into cells.

A

gp41 and gp120

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.157

59
Q

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

A

Pneumocystis carinii pneumonia (PCP)

TOPNOTCH

60
Q

Main cellular target of HIV.

A

CD4+ helper T cells

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.158

62
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

63
Q

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

A

Toxoplasmosis

TOPNOTCH
Robbins Basic Pathology, 8th Ed p.163

64
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

64
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.

A

Amyloidosis

(TOPNOTCH)

Robbins Basic Pathology, 8th Ed p.166