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MOD Genetic, Immuno, and Hematopoesis > Immunopathology > Flashcards

Immunopathology Flashcards

1
Q

List types of PRRs

A

1) Toll-Like
2) NOD-Like
3) C-type Lectin

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2
Q

Activation of NK cells

A

1) MHC I

2) NKG2D Ligands

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3
Q

Inhibition of NK cells

A

Presentation of MHC I

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4
Q

Describe Type I Hypersensitivity

A

1) IgE Mediated

2) Sensitization and Second exposure

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5
Q

Function of Leukotrienes and Prostaglandins

A

1) Leukocyte Infiltration
2) Epithelial Damage
3) Bronchospasm

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6
Q

Histamine Function

A

Vasodilation
Vascular Leakage
smooth Muscle Spasm

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7
Q

What causes late phase reaction in Type I hypersensitivity

A

Cytokines –> leukocyte recruitment

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8
Q

What cells are recruited during Type I hypersensitivity

A

Eosinophils
Basophils
Neutrophils

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9
Q

Examples of type I hypersensitivity

A

1) Asthma
2) Seasonal Allergies
3) Food allergies
4) Severe Allergic rxns
5) eosinophilic esophagitis
6) skin prick test

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10
Q

Characteristics of Asthma

A

Bronchoconstriction
Bowel peristalsis
Vasodilation Permeability

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11
Q

List some Severe Allergic Reactions

A

1) Urticaria
2) Angioedema
3) Anaphylaxis

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12
Q

Describe Eosinophilic Esophagitis

A 
Recurrent Dysphagia 
Weight Loss (due to painful to swallow)
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13
Q

What causes Eosinophilic Esophagitis

A

Food Driven antigen

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14
Q

Morphology of Type II Hypersensitivity

A

Smooth Linear

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15
Q

Mechanism of Type II Hypersensitivity

A

1) Opsonization and Phagocytosis
2) Complement and Fc Receptor-mediated Inflammation
3) Antibody-Mediated Cellular Dysfunction

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16
Q

Type II Hypersensitivity: Opsonization/Phagocytosis Examples

A

1) Autoimmune Hemolytic Anemia
- RBC membrane Proteins (Rh; I antigen)

2) Autoimmune thrombocytopenia Purpura
- GpIIb:IIIa

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17
Q

Type II Hypersensitivity: Complement and Fc receptor-mediated inflammation Mechanism

A

1) Basement membrane proteins

2) Streptococcal Proteins that Cross-react w/ Myocardium

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18
Q

Describe a Lentivirus

A

Goes under extensive latency

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19
Q

Type II Hypersensitivity: Complement and Fc receptor-mediated inflammation examples

A

1) Vasculitis
2) Goodpasture
3) Acute Rheumatic Fever

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20
Q

What is the cause of Vasculitis

A

Neutrophil Degranulation

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21
Q

What type of antibodies are present in vasculitis

A

ANA

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22
Q

MOA of Good pastures syndrome

A

1) Type II Hypersensitivity

2) Basement Membrane

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23
Q

What are some common clinical manifestations in Goodpasture’s syndrome

A

1) Nephritis

2) Lung Hemorrhage

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24
Q

MOA of Acute Rheumatic Fever?

A

Molecular Mimicry

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25
Q

Clinical Manifestations of Acute Rheumatic Fever

A

Arthritis

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26
Q

Type II Hypersensitivity: Anti-Mediated Cellular Dysfunction mechanisms

A

1) Disrupted Endocrine Signaling

2) Disrupted Neural Signaling

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27
Q

Type II Hypersensitivity: Anti-Mediated Cellular Dysfunction Examples

A

1) Disrupted Endocrine Signaling
- Graves Disease
- Insulin-Resistant Diabetes

2) Disrupted Neural Signal
- Myasthenia Gravis

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28
Q

What is the MOA of Graves Disease

A

Ab to TSH receptor

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29
Q

MOA of Type II Diabetes

A

Ab to insulin

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30
Q

MOA of Myasthenia Gravis

A

Ab inhibits ACh receptors

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31
Q

MOA of Type III Hypersensitivity

A

Ag-Ab Complexes

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32
Q

Morphology of Type III Hypersensitivity

A

Granular

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33
Q

Examples of Type III Hypersensitivity

A

1) Serum Sickness
2) Arthus Reaction - Local Rxn
3) Lupus Erythematosus

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34
Q

MOA of Type IV hypersensitivity

A

Cell Mediated (T Cell-mediated)

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35
Q

Morphology of Type IV Hypersenitivity

A

Immune Granulomas

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36
Q

Examples of Type IV Hypersensitivity

A

1) Type I Diabetes
2) RA
3) MS
4) IBD
5) Psoriasis
6) Contact Sensitivity

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37
Q

Inhibitory receptors and their ligands

A

1) CD80/86 and CTLA4

2) PDL-1/2 and PD-1

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38
Q

Which inhibitory receptors/ligands do APCs have?

A

1) CD80/86

2) PDL-1/2

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39
Q

Ankylosing SPondylitis is associated with which type of gene?

A

HLA- B27

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40
Q

Clinical Manifestations of Ankylosing Spondylitis

A

1) Neck and Lower Back Pain

2) Bamboo Spine

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41
Q

Pathogenesis of Ankylosing Spondylitis

A

Vertebral Disc Degeneration

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42
Q

Etiology of Rheumatoid Arthritis

A

1) Abnormal B and T Cells
2) Type IV Hypersensitivity
3) Absence of Central/Peripheral Tolerance

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43
Q

Genetic association of RA

A

PTPN22 Polymorphism

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44
Q

Clinical Manifestation of RA

A

1) Swollen Joints
2) Stiffness
3) Redness

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45
Q

What cell dysfunction is present in chron’s disease

A

Paneth Cells

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46
Q

What receptor is dysfunction in Chrons

A

NOD-2

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47
Q

Pathogenesis of Chron’s Disaese

A

Microbial Overgrowth

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48
Q

Clinical Presentations of Rheumatic Fever

A

1) Pharyngitis
2) PGST Complication
3) Heart Valve Destruction

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49
Q

MOA of Oral Lichen planus

A

Epitope Spreading

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50
Q

Etiology of Oral Lichen Planus

A

Epithelial Damage due to T Cell response

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51
Q

Pathogenesis of Oral Lichen Planus

A

Basement membrane destruction –> DAMPs

52
Q

Exposure to DAMPs leads to a ___ B cell response

A

Secondary

53
Q

Clinical Manifestaitons of Oral Lichen Palnus

A

1) Keratosis

2) Secondary Pemphigoid –> Blistering

54
Q

List ANA + Disorders

A

1) Lupus
2) Systemic Sclerosis
3) Sjogren Syndrome

55
Q

What are ANA disorders

A

Abs against nuclear content w/in nucleus of cells

56
Q

How would you diagnose:

1) Lupus
2) Systemic Sclerosis
3) Sjogren Syndrome

A

1) Lupus: Anti DS DNA and Anti Smith
2) Systemic Sclerosis: Anti DNA Topoisomerase (ScI-70)
3) Sjogren Syndrome: Anti Ro/SS-A and Anti La/SS-B

57
Q

What is the ANA pattern in Lupus?

A

Homogenous

58
Q

What is the ANA pattern in Systemic Sclerosis

A

Nucleolar

59
Q

What is the ANA pattern in Sjogren

A

Speckled

60
Q

Young female pt presents with Malar Rash, Renal and/or Heart

A

Systemic Lupus Erythematosus

61
Q

What is Diffuse Lupus?

A

Lupus Nephritis

62
Q

Pathogenesis of Diffuse Lupus

A

1) Increased Cellularity

2) Type II HS: Immune Deposits

63
Q

Clinical Manifestations of Diffuse Lupus

A

1) Proteinuria

2) Hematuria

64
Q

Cardiovascular Complications in Systemic Lupus

A

Libman-Sacks Endocarditis

65
Q

Pathogenesis of Libman-Sacks Endocarditis

A

Warty valve deposits of fibrin - LSE

66
Q

Morphology of Libman-Sacks Endocarditis

A

L-E Cells: Neutrophil or Macrophage engulfed damage lymphocytes

67
Q

When you suspect amyloid and see a bubble gum pink appearance what would you want to do next?

A

Congo Red Stain

68
Q

Lab Findings for Discoid Lupus

A

1) + ANA

2) - DS DNA

69
Q

Clinical Manifestations of Discoid Lupus

A

Disseminated Skin Lesion: Looks similar to burns and contracted appearance

70
Q

Common Causes for Graft V. Disease

A

1) bone Marrow
2) Thymus
3) Liver Transplant

*** Anything with increased immune cells

71
Q

Manifestation of Graft v. Host Disease.

A

1) Skin: Rash –> Desquamation
2) Liver - Jaundice –> Cholestasis
3) Intestines - Bloody Diarrhea –> Strictures

72
Q

Lab finding for Drug-induced Lupus

A

+ Anti-Histone Ab

73
Q

Clinical Manifestations of Drug induced lupus

A

1) Cutaneous Lesions

2) Arthralgias and Fever

74
Q

Clinical Manifestations of Sjogren Syndrome

A

1) Dry, Irritated Eyes
- Sand in eyes

2) Dry Mouth (xerostomia) and Difficulty Swallowing
3) Root Caries
4) Smooth Tongue w. Candida Yeast

75
Q

Complications of Sjogren Syndrome

A

1) Pulmonary Fibrosis

2) Lymphoma

76
Q

Etiology Sjogren Syndrome

A

Lacrimal and Salivary Gland Tissue Destruction

77
Q

Pathogenesis of Sjogren Syndrome

A

B and T- Cell mediated inflammatory rxn

- Fibrotic Destruction Follows

78
Q

Systemic Sclerosis Morphology

A

1) Loss of Subcutaneous Tissue
- Replaced by collagen and fibrosis
2) Vascular Hyalinization

79
Q

Clinical Features of Systemic Sclerosis

A

1) Sclerodactyly
2) Raynaud Phenomenon
- Episodic vessel obstruction in hands
- Leads to Necrosis
3) Gastrointestinal Tract
- GERD
- Esophageal Ulceration
4) Renal Vascular Disease
5) Pulmonary
- Pulmonary HTN
- Pulmonary Fibrosis

80
Q

CREST Syndrome ANA Pattern

A

Centromere

81
Q

What is CREST Syndrome

A

limited sclerosis w/ less visceral involvement (Better prognosis)

82
Q

Clinical Manifestations of CREST

A

1) Calcinosis
2) Raynaud’s Phenomenon
3) Esophageal Dysfunction
4) Sclerodactyly
5) Telangiectasias - Vascular Malformations
- Blotchy Skin Appearance

83
Q

IgG4-Releated Disease Etiology

A

Autoinflammatory Disease

84
Q

Pathogenesis of IgG4 Related Disease

A

IgG4 - producing plasma cells –> Fibrosis

85
Q

Clinical Manifestations of IgG4 Related Disease

A

Autoimmune Pancreatitis
Fibrous Bile Duct: Sclerosing Cholangitis
Submandibular Fibrosis w/ IgG4 abs

86
Q

Types of Allorecognition

A

1) Direct

2) Indirect

87
Q

Types of Direct Allorecognition

A

1) Acute

2) Chronic

88
Q

Types of Indirect Allorecognition

A

1) Hyperacute Rejection

2) Acute/Chronic Antibody-Mediated Rejection

89
Q

Describe Acute Cellular Rejection

A

W/in days months and years of transplant

90
Q

Clinical Manifestation of Chronic Cellular Manifestation

A

Arteriosclerosis

91
Q

Morphology of Chronic Cellular Rejection

A

Fibrosis/Sclerosis

92
Q

Pathogenesis of acute/chronic antibody mediated rejection

A

Inflammation and Complement

93
Q

What allows you to detect an acute/chronic antibody-mediated rejection

A

C4d

94
Q

List Treatments for Rejections

A

1) Corticosteroids
2) Tacrolimus
3) Rituximab (anti CD20 recombinant ab)

95
Q

____ inhibits T cell proliferation and is important for Cell Mediated Rejection

A

Tacrolimus

96
Q

____ inhibits reactive B cells

A

Rituximab

97
Q

Manifestations of Graft v. Host disease

A

1) Skin: Rash –> Desquamation
2) Liver: Jaundice –> Cholestasis
3) Intestine: Bloody Diarrhea –> Strictures

98
Q

Clinical Manifestations of Chediak-Higshi Syndrome

A

1) Grey Hair
2) Albinism
3) Easy Bleeding

99
Q

Morphology of Chediak-Higshi Syndrome

A

Giant Granules in Leukocytes

100
Q

Complication of Chediak-Higshi Syndrome

A

1) Increased bacterial infecion risk w/ catalase - bacteria
- Streptococcus
- Enterococcus
- Staphylococcus

101
Q

MAC def leads to

A

Sus. Neisseria Infections

-Meningitis

102
Q

Pathogenesis and Inheritance of Chediak-Higshi

A

1) AR

2) Failed Phagolysosome

103
Q

Inheritance of Hereditary Angioedema

A

1) AD

104
Q

PAthogenesis of Hereditary Angioedema

A

Def. C1-INH

105
Q

Clinical manifestations of Hereditary Angioedema

A

1) Kinin-Mediated Edema at multiple sites

2) Corkscrew pattern of bowel on CT

106
Q

Types of Leukocyte Adhesion Deficiency

A

1) LAD Type I: Lack of selectin (no Fucosyl Transferase)

2) LAD Type 2: Defective B2 integrin

107
Q

Severe Combined Immunodeficiency Inheritance

A

X Linked or Autosomal Recessive

108
Q

Population for Severe Combined Immunodeficiency X Linked

A

Males

109
Q

Pathogenesis of Severe Combined Immunodeficiency : X Linked

A

Mutated IL receptors

- Reduced T Cell # –> no b cell response

110
Q

Autosomal Recessive SCIDS Pathogenesis

A

1) Adenosine Deaminase Deficiency
- Toxic Purine Accumulation
- Blocks t Cell formation
- Suppresses Humoral Response

111
Q

Gene associated with X-Linked Agammaglobulinemia

A

BTK (Burotn Tyrosine Kinase) on X Chromosome

112
Q

1) Pathogenesis of X-Linked Agammaglobulinemia

2) Complications

A

1) B cells can’t mature ( no light chain rearrangement)

2) Increased infections w/ encapsulated bacteria, viruses and protozoa

113
Q

Gene associated with DiGeorge

A

22q11 Deletion

114
Q

Clinical Manifestations of DiGeorge Syndrome

A

1) Underdeveloped Thymus
2) Hypoparathyroidism –> Hypocalcemia –> Tetany
3) Heart and Great Vessel Abnormalities

115
Q

Hyper-IgM Syndrome Pathogensis

A

CD40/CD40L Mutation: Can’t class switch

116
Q

Complications of Hyper IgM

A

Encapsulated Bacterial Infections: Lack of opsonizing antibodies

117
Q

Isolated IgA syndrome conplication

A

1) Less defense against inhaled and ingested pathogens

118
Q

Clinical Manifestations of Isolated IgA deficiency

A

1) Sinus and Respiratory Infections
2) Urinary bladder infections
3) Gastrointestinal infectionss
4) Autoimmune disease and allergies

119
Q

When someone has isolated IgA def. and gets a blood transfusion … what occurs

A

Anaphylactic Rxn

120
Q

Gene association with Wiskott Aldrich Syndrome

A

WASP

121
Q

Clinical Manifestations of Wiskott Aldrich

A

1) thrombocytopenia
2) eczema
3) recurrent infections

122
Q

Pathogenesis of Wiskott-Aldrich

A

1) T cell loss

2) Hypogammaglobulinemia

123
Q

Ataxia-telangiectasia is a def, of what?

A

1) IgG

2) IgA

124
Q

Consequences of Ataxia-telangiectasia

A

1) Respiratory infections
2) autoimmune disease
3) cancer

125
Q

Inheritance of Ataxis Telangiectasia

A

AR

126
Q

Gene mutation associated with Ataxia Telangiectasia

A

ATM

- Defective DNA repair

MOD Genetic, Immuno, and Hematopoesis (3 decks)

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