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Rapid Review Pathology > Chapter 4 - Immunopathology > Flashcards

Chapter 4 - Immunopathology Flashcards

0
Q

List the different types of effector cells in innate immunity.

A

Effector cells: phagocytic cells, NK cells, mucosal/endothelial cells

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1
Q

What is innate immunity?

A

Innate immunity: nonadaptive immune response to microbial pathogens

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2
Q

What do TLRs do?

A

TLRs: recognize nonself antigens on pathogens and damaged tissue antigens

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3
Q

What are PAMPs?

A

PAMPs: pathogen-associated molecular patterns

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4
Q

What are DAMPs?

A

DAMPs: damage-associated molecular patterns

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5
Q

What is NFκβ?

A

NFκβ: “master switch” to nucleus for induction of inflammation

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6
Q

What are NLRs?

A

NLRs: cytosolic receptors in monocytes/macrophages, dendritic cells

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7
Q

NLRs function in concert with what?

A

NLRs: function in concert with TLRs

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8
Q

What do activated NLRs form?

A

Activated NLRs: form multiprotein inflammosome complexes

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9
Q

What do inflammasomes activate resulting in what?

A

Inflammosomes activate caspase-1 → ↑secretion IL-1β and IL-18 → attract immune cells to sites of infection

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10
Q

What does hepcidin do?

A

Hepcidin: keeps iron away from bacteria

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11
Q

What is IL-6?

A

IL-6: key cytokine for stimulating APR synthesis/release from liver

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12
Q

Name four protective APRs.

A

Protective APRs: CRP, C3b, C5a, ferritin

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13
Q

What do protective gut bacteria do?

A

Protective gut bacteria: limit dominance, compete for nutrients, activate host defenses

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14
Q

What do defensins do?

A

Defensins: attract neutrophils, prevent microbial colonization of mucosa

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15
Q

Name two physical barriers.

A

Physical barriers: skin, mucous membranes

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16
Q

What does fever inhibit?

A

Fever: inhibits viral/bacterial reproduction

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17
Q

What does IFN-γ activate?

A

IFN-γ: activates macrophages

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18
Q

What do IFN-α and IFN-β inhibit?

A

IFN-α and IFN-β: inhibit viral growth

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19
Q

What do B lymphocytes produce?

A

B lymphocytes: humoral response (antibodies)

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20
Q

What do antibodies do?

A

Antibodies: destroy extracellular microbial pathogens

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21
Q

What do naive B cells produce?

A

Naïve B cells produce IgM and IgD

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22
Q

Class (isotype) switching to produce other Igs involves what?

A

Class (isotype) switching to produce other Igs involves changes in the heavy chain locus in the constant region of the gene

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23
Q

What is involved in isotype switching?

A

CD40 ligands, cytokines, and CD4 helper T cells are involved in isotype switching

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24
Q

CD4 and CD8 T lymphocytes are part of what type of immunity?

A

CD4 and CD8 T lymphocytes: cell-mediated immunity

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25
Q

What does CMI do?

A

CMI: destroys intracellular microbial pathogens

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26
Q

Where is MHC located and what is it collectively known as?

A

MHC: HLA system; chromosome 6

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27
Q

MHC is located on what cells?

A

MHC: located on all nucleated cells/platelets except RBCs

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28
Q

HLA genes are transmitted from whom to whom?

A

HLA genes: transmitted from parents to child

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29
Q

Class I molecules are encoded on what three loci?

A

Class I molecules: HLA-A, HLA-B, and HLA-C loci

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30
Q

How molecules encoded by the HLA-A, HLA-B, and HLA-C loci are expressed?

A

HLA-A, HLA-B, and HLA-C loci: molecules codominantly expressed

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31
Q

What two cell types recognize class I molecules?

A

Class I molecules: recognized by CD8 T cells/NK cells

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32
Q

Where are class II molecules encoded?

A

Class II molecules: HLA-D region (DP-DQ-DR subregions)

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33
Q

Class II molecules are located on what cell types?

A

Class II molecules on APCs: B cells, macrophages, dendritic cells

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34
Q

Name two applications of HLA testing.

A

HLA testing: transplantation workup for graft compatibility, disease risk

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35
Q

Developing anti-HLA antibodies can occur in what three scenarios?

A

Developing anti-HLA antibodies: pregnancy, blood transfusion, previous transplant

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36
Q

What is type I hypersensitivity?

A

Type I: IgE activation of mast cells/basophils

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37
Q

In type I HSR, allergens are first processed by what?

A

Allergens first processed by APCs (macrophage/dendritic cells)

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38
Q

APCs interact with what cell type?

A

APCs interact with CD4 TH2 cells

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39
Q

What does IL-4 do?

A

IL-4: plasma cells switch from IgM to IgE synthesis

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40
Q

What does IL-5 do?

A

IL-5: stimulates production/activation of eosinophils

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41
Q

What happens during mast cell activation?

A

Mast cell activation: allergens cross-link allergen-specific IgE antibodies

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42
Q

Describe what occurs during the early phase reaction of type I HSR.

A

Early phase: release preformed histamine, eosinophil chemotactic factor

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43
Q

Describe how the mediators released by mast cells differ between the early phase and late phase.

A

Mast cell releases mediators: early phase preformed, late phase synthesized

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44
Q

Name three late phase mediators.

A

Late phase mediators: PGs, LTs, PAF

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45
Q

List two test used to evaluate for type I HSR.

A

Type I testing: scratch test, RAST test

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46
Q

What is type II HSR?

A

Type II: antibody directed against antigens on cell membrane/in extracellular matrix

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47
Q

Give two clinical examples of cell lysis IgM-mediated.

A

Cell lysis IgM-mediated: cold IHA, ABO mismatch

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48
Q

Give two examples of cell-lysis that is IgG-mediated.

A

Cell lysis IgG-mediated: Goodpasture syndrome, acute rheumatic fever

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49
Q

Give two examples of phagocytosis in type II HSR.

A

Phagocytosis: warm autoimmune hemolytic anemia, ABO hemolytic disease of newborn

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50
Q

Give two examples of ADCC that is IgG-mediated.

A

ADCC IgG-mediated: NK attaching to IgG in virally infected cell or cancer cell

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51
Q

Give an example of IgE-mediated ADCC.

A

ADCC IgE-mediated: eosinophil destruction of IgE-coated helminth

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52
Q

Give two examples of IgG autoantibodies against cell surface receptors.

A

IgG autoantibodies against cell surface receptor: myasthenia gravis, Graves disease

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53
Q

Name two tests to evaluate type II HSR.

A

Type II tests: indirect/direct Coombs tests

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54
Q

What is type III HSR?

A

Type III: circulating antigen-antibody complexes that damage tissue

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55
Q

Describe the mechanism of tissue damage in type III HSR.

A

Type III: ICs activate complement that attract neutrophils, leading to tissue damage

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56
Q

What is an Arthus reaction?

A

Arthus reaction: localization of ICs

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57
Q

Give an example of an Arthus reaction.

A

Arthus reaction: farmer’s lung

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58
Q

Which types of HSRs are antibody-mediated?

A

Antibody-mediated HSRs: types I, II, III

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59
Q

What is type IV HSR?

A

Type IV: T cell-mediated immunity; often delayed

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60
Q

Name three functions of CMI.

A

CMI functions: infection control (e.g., TB), graft rejection, tumor surveillance

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61
Q

What cell types are involved in DTH?

A

DTH: involves macrophages (APCs) and CD4 T cells

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62
Q

In DTH, macrophages interact with what cell type via what?

A

Macrophages interact via their class II antigen sites with naïve CD4 T cells

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63
Q

In DTH, Naïve CD4 cells differentiate into what cell type? What is the stimulus for this differentiation? How do these cells continue to differentiate?

A

Naïve CD4 cell → CD4 TH1 memory cells: IL-12 activated macrophage, γ-IFN memory T cell

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64
Q

What do activated CD4 TH1 cells release? What results?

A

Activated CD4 TH1 cells release IFN-γ: ↑macrophage phagocytosis/killing phagocytosed pathogen

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65
Q

What do activated macrophages become?

A

Activated macrophages become epithelioid cells

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66
Q

In DTH, what does a granuloma consist of?

A

Granuloma: epithelioid cells, multinucleated giant cells, rim CD4 T cells

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67
Q

A PPD reaction is an example of what type of HSR?

A

PPD reaction: example of DTH

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68
Q

What are Langerhans cells?

A

Langerhans cells: APC of skin; dendritic cell

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69
Q

PPD reaction is dependent on what?

A

PPD reaction dependent on CMI competency

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70
Q

CMI is diminished in what types of people?

A

CMI diminished in elderly/people with AIDS

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71
Q

The CD4 TH17 subset secretes what in order for what to occur?

A

CD4 TH17 subset: cytokines recruit neutrophils/monocytes

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72
Q

DTH in chronic asthma involves what cell types?

A

DTH chronic asthma: macrophages, CD4 TH2 subset cells, eosinophils

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73
Q

Give four examples of what may cause allergic contact dermatitis.

A

Allergic contact dermatitis: poison ivy, topical drugs, rubber, chemicals

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74
Q

Describe what occurs during the induction phase of contact dermatitis.

A

Induction phase: CD4 TH1 subset memory cells in lymph nodes; effector cytotoxic CD8 memory T cells in circulation

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75
Q

Describe the elicitation phase of contact dermatitis.

A

Elicitation phase: cytokine release from circulating effector T lymphocytes

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76
Q

Describe the key clinical findings of allergic contact dermatitis.

A

Allergic contact dermatitis: pruritus, erythema, edema, vesicles

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77
Q

In CD8 T cytotoxicity, what do T cells interact with?

A

CD8 T cytotoxicity: T cells interact with altered class I antigen sites

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78
Q

In CD8 T cell cytotoxicity, which cell types are lysed?

A

CD8 T cell cytotoxicity: lysis of neoplastic, virus-infected, donor graft cells

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79
Q

What test is used to confirm allergic contact dermatitis?

A

Patch test: confirm allergic contact dermatitis

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80
Q

What is anergy?

A

Anergy: no response to mitogenic assays and/or skin response to Candida

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81
Q

What is the most important requirement for successful transplantation?

A

ABO blood group compatibility: most important requirement for successful transplantation

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82
Q

List two factors that enhance graft viability.

A

Graft viability: absence preformed anti-HLA antibodies; close matches for HLA-A, HLA-B, HLA–C-DR loci

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83
Q

What is an autograft? How does the survival rate compare to other types of grafts?

A

Autograft: self to self; best survival rate

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84
Q

What is a syngeneic graft?

A

Syngeneic graft: graft between identical twins

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85
Q

What is an allograft?

A

Allograft: graft between genetically different individuals of same species

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86
Q

What is a xenograft?

A

Xenograft: graft between two different species

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87
Q

Hyperacute rejection is what type of reaction and what type of HSR?

A

Hyperacute rejection: irreversible; type II

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88
Q

Describe the pathogenesis of hyperacute rejection.

A

Hyperacute rejection: small vessel vasculitis; neutrophils, fibrinoid necrosis, thrombosis

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89
Q

Name two causes of hyperacute rejection.

A

Causes: ABO mismatch, anti-HLA antibodies

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90
Q

What is the most common type of rejection? Is it reversible? What type of HSR is this type of rejection?

A

Acute rejection: most common (MC) rejection; reversible; type II/IV

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91
Q

What is the key cell in donor grafts?

A

Key cell in donor graft: dendritic cells with classes I and II MHC molecules

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92
Q

Acute rejection type IV is characterized by what?

A

Acute rejection type IV: endothelialitis, interstitial tissue inflammation

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93
Q

What are the key cells in the recipient in type IV HSR?

A

Key cells in recipient in type IV: CD4 T cell (DTH), CD8 T cell (cytotoxicity)

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94
Q

What is acute rejection type II caused by?

A

Acute rejection type II: anti-HLA antibodies

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95
Q

Describe a finding of less severe/late onset acute rejection.

A

Acute rejection less severe/late onset: vessels show thicker intima similar to atherosclerosis

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96
Q

Describe chronic rejection.

A

Chronic rejection: irreversible; months/years; previous acute rejection immunosuppression

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97
Q

What is the most common infection in transplantation recipients?

A

CMV: MC infection in transplantation recipients

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98
Q

What is the most common infection in solid organ transplantation?

A

Solid organ transplantation: Candida MC infection

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99
Q

What is the most common infection in bone marrow transplantation?

A

Bone marrow transplantation: Aspergillus MC infection

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100
Q

HLA matching of the donor and recipient is very important in what types of transplantations, preventing what?

A

HLA matching donor/recipient: very important in kidney/bone marrow transplants; prevents hyperacute rejections

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101
Q

How do you test for compatibility of the recipient and donor class II antigens?

A

Compatibility donor/recipient lymphocytes: mix together to see if mitoses occur (incompatible)

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102
Q

Describe lymphocyte cross-match.

A

Lymphocyte cross-match: recipient serum against donor lymphocytes; test for anti-HLA antibodies (concept similar to blood transfusion cross-match)

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103
Q

Describe three key prerequisites for GVH.

A

GVH reaction: graft has T cells; recipient immunocompromised; recipient has foreign MHC antigens

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104
Q

List four different causes of GVH.

A

Causes GVH: bone marrow/liver transplant; blood transfusion to T cell–immunodeficient patient, newborn

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105
Q

What occurs during acute GVH?

A

Acute GVH: donor CD8 cells attack foreign MHC antigens

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106
Q

List four clinical findings of acute GVH.

A

Clinical: jaundice, diarrhea, dermatitis, hepatosplenomegaly

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107
Q

Define autoimmune.

A

Autoimmune: lose self-tolerance; host tissue considered foreign

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108
Q

List four types of self-antigens.

A

Self-antigens: class I/II MHC, nuclear/cytoplasmic

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109
Q

In autoimmune diseases, class I-related diseases and class II-related diseases are more common in men or women?

A

Autoimmune: class I–related men > women; class II-related women > men

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110
Q

In genetically susceptible individuals, what is required to initiate an autoimmune disease?

A

Autoimmune: genetic predisposition involving HLA system + environmental trigger

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111
Q

If an infection is the environmental trigger for autoimmune disease, what does the infection do?

A

Infections as trigger: upregulates co-stimulators on APCs

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112
Q

What are co-stimulators?

A

Co-stimulators: APCs with both class I and II antigens

113
Q

What are self-reactive lymphocytes?

A

Self-reactive lymphocytes: IL-2 causes clonal proliferation of CD4 and CD8 T cells

114
Q

What is molecular mimicry? Provide an example.

A

Sharing antigens between host and pathogen: S. pyogenes−rheumatic fever

115
Q

Name three polyclonal B cell activators. Polyclonal activation of B lymphocytes results in what?

A

Polyclonal B cell activators: EBV, HIV, CMV; produces autoantibodies

116
Q

Name six viruses that may act as a trigger for autoimmune disease.

A

Viruses as triggers: coxsackievirus, measles virus, CMV, EBV, HHV-6, influenza virus

117
Q

Name four bacterial triggers for autoimmune disease.

A

Bacterial triggers: S. pyogenes, C. trachomatis, M. pneumoniae, C. jejuni

118
Q

How can procainamide and hydralazine act as an environmental trigger for autoimmune disease?

A

Procainamide, hydralazine: autoantibodies against histones; lupus-like syndrome

119
Q

Give an example of drug alteration resulting in autoimmune disease.

A

Drug alteration: methyldopa alters Rh antigens on RBCs; AIHA

120
Q

Describe the role of hormones as a trigger for autoimmune disease.

A

Autoimmune disease women > men: ? role of estrogen

121
Q

List four tissues with sequestered antigens.

A

Tissues with sequestered antigens: sperm, lens, uveal tract, CNS

122
Q

Name two types of intracellular sequestered antigens.

A

Intracellular sequestered antigens: DNA, histones

123
Q

Describe how UV light may trigger autoimmune disease.

A

UV light: apoptosis keratinocytes; autoantibodies against nuclear antigens with formation of ICs

124
Q

What do non-MHC genes do?

A

Non-MHC genes: interfere with immune regulation and self-tolerance

125
Q

The PTPN-22 gene is implicated in what two autoimmune diseases?

A

PTPN-22 gene: rheumatoid arthritis, type 1 DM

126
Q

The NOD-2 gene is implicated in what autoimmune disease?

A

NOD-2 gene: implicated in Crohn disease

127
Q

List two important markers of autoimmune disease.

A

IRF5, STAT4: important markers of autoimmune disease

128
Q

List two organ-specific autoimmune disorders.

A

Organ-specific: Addison disease, pernicious anemia

129
Q

List three systemic autoimmune disorders.

A

Systemic: SLE, rheumatoid arthritis, systemic sclerosis

130
Q

What are serum ANA?

A

Serum ANA: antibodies against DNA, histones, acidic proteins, nucleoli

131
Q

What is the most useful screening test in autoimmune disease?

A

Serum ANA: most useful screening test in autoimmune disease

132
Q

Anti-dsDNA is positive in patients with what disease?

A

Anti-dsDNA: SLE with glomerulonephritis

133
Q

Anti-histone antibodies are present in what disease?

A

Anti-histone: drug-induced lupus

134
Q

Anti-Sm antibodies are present in what disease?

A

Anti-Sm: SLE

135
Q

Anti-RNP antibodies are present in what two diseases?

A

Anti-RNP: systemic sclerosis, SLE

136
Q

Anti-nucleolar antibodies are present in what disease?

A

Anti-nucleolar: systemic sclerosis

137
Q

Describe the serum ANA test.

A

Serum ANA: fluorescent antibody test; pattern and titer

138
Q

The presence of a rim pattern of fluorescence in a serum ANA test is associated with what?

A

Rim pattern: associated with anti-dsDNA antibodies

139
Q

Who does SLE primarily affect?

A

SLE: women of childbearing age

140
Q

List two genetic factors in SLE.

A

Genetic factors: HLA associations; complement deficiencies

141
Q

List four environmental triggers for SLE.

A

Environmental triggers: EBV, UV light, estrogen, medications

142
Q

Describe two mechanisms of injury in SLE.

A

Mechanism injury: ICs (type III); autoantibodies (type II)

143
Q

Name four constitutional symptoms in SLE.

A

Constitutional: fatigue (MC), fever, arthralgia, weight loss

144
Q

Name four hematologic findings in SLE.

A

Hematologic: anemia, neutropenia, lymphopenia, thrombocytopenia

145
Q

Name two lymphatic findings in SLE.

A

Lymphatic: generalized lymphadenopathy, splenomegaly

146
Q

Describe two features of arthralgias in SLE.

A

Arthralgia (joint pain): very common initial complaint; morning hand stiffness

147
Q

Describe four features of arthritis in SLE.

A

Arthritis: symmetrical; hands (PIP, MCP), wrist; nonerosive, nondeforming

148
Q

Describe three features of a malar rash.

A

Malar rash: photosensitive; cheeks/bridge of nose, sparing nasolabial folds

149
Q

What do immunofluorescence studies of a malar rash show?

A

IF: basement membrane involved/uninvolved skin

150
Q

What is the most common visceral organ involved in SLE?

A

Kidney MC visceral organ involved

151
Q

What is the most common cardiac manifestation in SLE?

A

Fibrinous pericarditis with/without effusion: MC cardiac manifestation

152
Q

What are two features of Libman-Sacks endocarditis?

A

Libman-Sacks endocarditis: sterile vegetations MV; MV regurgitation

153
Q

Give two examples of serositis, a key finding in SLE.

A

Pleuritis, pericarditis: example is serositis, key finding in SLE

154
Q

In SLE, interstitial fibrosis leads to what?

A

Interstitial fibrosis: restrictive lung disease, hypoxemia

155
Q

List four CNS findings in SLE.

A

CNS: headache (MC), psychosis, stroke (APL), seizures

156
Q

Name two pregnancy-related findings in SLE.

A

Pregnancy: complete heart block in newborn (IgG anti-SS-A antibodies); recurrent spontaneous abortions (placental vessel thrombosis; APL)

157
Q

What is the most common drug involved in drug-induced lupus?

A

Procainamide: MC drug in drug-induced lupus

158
Q

List three ways drug-induced lupus differs from SLE.

A

Drug-induced lupus vs SLE: antihistone antibodies, ↓incidence renal/CNS disease, symptoms disappear when drug removed

159
Q

What is the best screening test for SLE?

A

Serum ANA best screen for SLE

160
Q

How can you confirm the diagnosis of SLE?

A

Confirm SLE: anti-dsDNA/anti-Sm antibodies; high specificity

161
Q

APL antibodies may be present in the SLE patient with what two clinical findings?

A

APL antibodies: strokes, recurrent abortions

162
Q

What is an LE cell?

A

LE cell: neutrophil containing phagocytosed altered DNA

163
Q

What is the band test?

A

Band test: IF along basement membrane skin biopsy; ICs

164
Q

What are the two most common causes of death in SLE?

A

MC causes of death: infection, CRF

165
Q

List three features of systemic sclerosis.

A

Systemic sclerosis: vascular dysfunction, fibrosis skin/visceral organs, immune dysfunction

166
Q

What are the two major forms of systemic sclerosis?

A

Types: diffuse/limited systemic sclerosis

167
Q

Describe the epidemiology of systemic sclerosis.

A

Systemic sclerosis: female dominant, ↑black females

168
Q

Describe the etiology of systemic sclerosis.

A

Systemic sclerosis: ↑CD4 TH2 cells; ↑DNA-topoisomerase, centromere antibodies

169
Q

What is the earliest manifestation of systemic sclerosis? What does this manifestation lead to?

A

Endothelial dysfunction: earliest manifestation; vasculitis

170
Q

Describe the role of vasoconstrictors and vasodilators in endothelial dysfunction in systemic sclerosis.

A

Endothelial dysfunction: ↓NO, PGI2; ↑endothelin

171
Q

Describe the mechanism of fibrosis in systemic sclerosis.

A

Mechanism of fibrosis: ↑PDGF, TGF-β

172
Q

What is the most common initial sign of systemic sclerosis?

A

Raynaud phenomenon: MC initial sign of systemic sclerosis

173
Q

List two digital findings in systemic sclerosis.

A

Digital findings: sclerodactyly, infarction

174
Q

What is the most common target organ in systemic sclerosis?

A

Skin: MC target organ

175
Q

List four skin findings in systemic sclerosis.

A

Skin: edema, fibrosis, dystrophic calcification, radial furrowing around mouth

176
Q

List four esophageal findings in systemic sclerosis.

A

Esophagus: dysphagia solids/liquids, dysmotility, strictures/ulceration, Barrett esophagus

177
Q

List two stomach findings in systemic sclerosis.

A

Stomach: dysmotility/bloating

178
Q

List three small intestine findings in systemic sclerosis.

A

Small intestine: malabsorption, dysmotility, diverticula

179
Q

List two large intestine findings in systemic sclerosis.

A

Large intestine: dysmotility, constipation

180
Q

List two respiratory findings in systemic sclerosis.

A

Respiratory: PH, interstitial fibrosis

181
Q

What is the most common cause of death in systemic sclerosis?

A

Systemic sclerosis: respiratory failure MCC death

182
Q

List two renal findings in systemic sclerosis.

A

Renal: hyperplastic arteriolosclerosis, malignant hypertension

183
Q

What is CREST syndrome?

A

CREST: calcinosis, Raynaud phenomenon, esophageal dysmotility, sclerodactyly, telangiectasia

184
Q

What tests are positive in systemic sclerosis?

A

Systemic sclerosis: +ANA, anti-topoisomerase/centromere antibodies

185
Q

What tests are positive in CREST syndrome?

A

CREST syndrome: centromere antibodies, +ANA

186
Q

Name two noninfectious inflammatory myopathies.

A

Noninfectious inflammatory myopathies: PM, DM

187
Q

Describe the epidemiology of polymyositis.

A

PM: female dominant; ↑blacks; ↑risk malignancies (lung, bladder, lymphoma)

188
Q

Describe the etiology and pathogenesis of polymyositis.

A

PM: CD8 T cells/CD4 TH1, viruses (HIV, HTLV-1), environmental triggers → autoantibodies

189
Q

List the muscles involved in polymyositis.

A

PM muscle involvement: upper/lower extremity, trunk, shoulders/hips, neck extensors

190
Q

Describe the dysphagia present in PM.

A

PM: oropharyngeal/upper esophagus dysphagia solids/liquids

191
Q

Respiratory difficulties in PM are related to what?

A

PM: interstitial fibrosis

192
Q

What are the lab findings in PM?

A

PM: ↑serum CK/aldolase; +ANA; ↑anti–Jo-1

193
Q

In PM, what do the EMG and biopsy show?

A

PM: EMG (myopathic dysfunction); biopsy (lymphocytic/macrophage infiltrate, atrophy not prominent)

194
Q

What is the first-line treatment for PM?

A

PM: corticosteroids first-line treatment

195
Q

Describe the etiology and pathogenesis of DM.

A

DM: CD4 T cells target skeletal muscle capillaries; antibody/complement involvement

196
Q

List two cutaneous findings in DM.

A

DM: Gottron patches over knuckles/PIP joints; heliotrope eyes

197
Q

What do muscle biopsies show in DM?

A

DM: muscle atrophy; lymphocytic infiltrate

198
Q

What is MCTD?

A

MCTD: signs/symptoms ∼SLE, systemic sclerosis, PM

199
Q

Describe the epidemiology of MCTD.

A

MCTD: female dominant, renal disease uncommon

200
Q

Describe the etiology and pathogenesis of MCTD.

A

MCTD: B/T cell activation; antibodies against ribonucleoprotein

201
Q

List two vascular findings in MCTD.

A

MCTD: Raynaud phenomenon, sclerodactyly

202
Q

List two MSK findings in MCTD.

A

MCTD: arthralgia/arthritis hands

203
Q

List one GI finding in MCTD.

A

MCTD gastrointestinal: esophageal dysmotility

204
Q

List two MCTD respiratory findings.

A

MCTD respiratory: pulmonary hypertension, pleuritis

205
Q

List one cardiovascular, hematologic, and CNS finding in MCTD.

A

MCTD: pericarditis, leukopenia, trigeminal neuralgia

206
Q

List two lab findings in MCTD.

A

MCTD: +ANA, anti-ribonucleoprotein (U1-RNP antibodies)

207
Q

List four risk factors for immunodeficiency disorders.

A

Risk factors: prematurity, autoimmune disease, lymphoma, HIV, immunosuppressive agents

208
Q

What is the most common cause of death due to infection worldwide?

A

AIDS: MCC death due to infection worldwide

209
Q

Name two features of HIV.

A

HIV: retrovirus; reverse transcriptase

210
Q

What is reverse transcriptase?

A

Reverse transcriptase: converts viral RNA to proviral dsDNA

211
Q

What is the most common virus causing AIDS in the U.S.?

A

HIV-1: MC virus causing AIDS in U.S.

212
Q

Describe two features of HIV-2.

A

HIV-2: more restricted than HIV-1; most prevalent in Western Africa

213
Q

HIV cannot penetrate what?

A

HIV cannot penetrate intact skin/mucosa

214
Q

What does the gag gene in HIV do?

A

Gag gene: synthesis p24 core antigen

215
Q

What does the env gene in HIV do?

A

Env gene: synthesis gp120

216
Q

What does the pol gene in HIV do?

A

Pol gene: synthesis of reverse transcriptase, integrase, protease

217
Q

What is the most common cause of AIDS?

A

Sexual transmission MC cause AIDS

218
Q

What increases the risk for HIV?

A

STDs ↑risk for HIV

219
Q

What is the second most common cause of AIDS?

A

IVDA: 2nd MCC AIDS

220
Q

What is the most common cause of pediatric AIDS?

A

Pediatric AIDS: MC due to vertical transmission

221
Q

What is the most common cause of HIV in health-care workers?

A

Accidental needlestick: MCC HIV in health-care workers

222
Q

How do blood banks screen blood products for HIV?

A

Blood products: blood bank screens for HIV with p24 antigen assay

223
Q

List four body fluids with HIV.

A

Body fluids with HIV: blood, semen/vaginal secretions, breast milk

224
Q

List the different cell types that can be infected by HIV.

A

Cells infected by HIV: CD4 T cells, macrophages, dendritic cells, astrocytes

225
Q

HIV is cytotoxic to what cell type?

A

HIV cytotoxic to CD4 T cells

226
Q

What two cell types are important reservoirs for HIV?

A

Macrophages/dendritic cells: reservoirs for HIV

227
Q

How does HIV enter the body?

A

HIV enters interrupted mucosal surfaces genital tract/anus

228
Q

What cell type is the major reservoir for HIV during latency?

A

Follicular dendritic cells: major reservoir for HIV during latency

229
Q

Describe the process of HIV binding.

A

HIV binding: gp120, chemokine co-receptors

230
Q

What does viral protease do?

A

Viral protease: uncoats virus, releasing RNA

231
Q

What does reverse transcriptase do?

A

Reverse transcriptase: viral RNA → dsDNA

232
Q

What does viral integrase do?

A

Viral integrase: inserts viral DNA into host DNA; provirus

233
Q

In HIV infection, activation of the host cell leads to what?

A

Activation of host cell: transcription for IL-2 + receptor

234
Q

Describe the role of cytokines in the HIV life-cycle.

A

Cytokines: HIV genome transcribes viral RNA

235
Q

What is the HIV core structure?

A

HIV core structure: protein surrounding viral RNA

236
Q

Describe the role of the HIV core structure in the life-cycle of HIV.

A

HIV core structure: acquires lipid bilayer from cell membrane → forms bud → detaches as infective viral particle

237
Q

Describe the acute phase of HIV infection.

A

Acute phase: 3–6 weeks postinfection; flu-like symptoms; greatest risk coital contraction HIV

238
Q

Describe the asymptomatic carrier phase of HIV infection.

A

Asymptomatic carrier phase: virus replicates in follicular dendritic cells/macrophages

239
Q

Describe the early symptomatic phase of HIV infection.

A

Early symptomatic phase: lymphadenopathy, hairy leukoplakia, oral candidiasis

240
Q

What are the criteria for AIDS?

A

AIDS: CD4 T-cell count ≤200 cells/mm3 and/or AIDS-defining lesion

241
Q

List four AIDS-defining malignancies.

A

AIDS-defining malignancies: Kaposi sarcoma, Burkitt lymphoma 1° CNS lymphoma, cervical carcinoma

242
Q

What is the cause of death in AIDS?

A

Death in AIDS: disseminated infection (CMV, MAI)

243
Q

In AIDS, hypergammaglobulinemia results from what?

A

AIDS: hypergammaglobulinemia due to polyclonal B cell stimulation by EBV/CMV

244
Q

In AIDS, decreased CD4 T cells results in what?

A

↓CD4 T cells: lymphopenia, anergy, CD4/CD8 ratio <1

245
Q

What treatment can be given to pregnant women with AIDS in order to decrease transmission to newborns?

A

Pregnant woman AIDS: Rx reverse transcriptase inhibitors ↓transmission to newborns

246
Q

How does early treatment of AIDS affect survival?

A

Rx AIDS: early Rx improves survival

247
Q

What is the principal treatment to prevent immune deterioration in AIDS?

A

HAART: principal Rx to prevent immune deterioration

248
Q

Describe two features of complement.

A

Complement: liver synthesis; innate immunity

249
Q

Complement is only functional in what form?

A

Complement: cleavage factors functional

250
Q

What are the anaphylatoxins of complement?

A

C3a, C5a anaphylatoxins

251
Q

What is the role of C3b?

A

C3b opsonization

252
Q

What does C5a do?

A

C5a: activate neutrophil adhesion molecules, chemotaxis

253
Q

What do C5-C9 do?

A

C5-C9 cell lysis

254
Q

Describe the classical pathway of complement.

A

Classical pathway: C1, C4, C2; activated by ICs; requires antibody for activation

255
Q

What does C1 esterase inhibitor do?

A

C1 esterase inhibitor: inactivates protease activity of C1

256
Q

What are the components of the alternative pathway? How is it activated?

A

Alternative pathway: factor B, properdin, factor D; activated by endotoxins

257
Q

What is the importance of the lectin pathway?

A

Lectin pathway: important in destruction of bacteria, fungi, viruses

258
Q

What does the membrane attack complex consist of?

A

MAC: C5-C9

259
Q

What does decay accelerating factor do? It is deficient in what disease?

A

DAF: enhances degradation C3 and C5 convertase in classical/alternative pathways; deficient in PNH

260
Q

Describe how deficiencies in complement predispose to infection via two mechanisms.

A

Complement deficiencies: ineffective opsonization, defects in cell lysis

261
Q

How do opsonization defects present? What type of organism is responsible?

A

Opsonization defects: recurrent pyogenic infections; encapsulated bacteria

262
Q

How do deficiencies in C1, C4 and C2 present? What is the most common presentation?

A

Deficiencies in C1, C4, C2: autoimmune disease; SLE MC

263
Q

How does MAC deficiency present?

A

MAC deficiency: recurrent infection N. gonorrhoeae/meningitidis

264
Q

What is CH50?

A

CH50: functional ability complement systems

265
Q

Describe test results indicating activation of the classical pathway.

A

Classical pathway activation: decreased C4, C3; normal factor B

266
Q

Describe test results indicating activation of the alternative pathway.

A

Alternative pathway activation: decreased factor B, C3; normal C4

267
Q

What is amyloid?

A

Amyloid: fibrillar protein; deposited in interstitial tissue; pressure atrophy

268
Q

Describe the composition of amyloid.

A

Amyloid: linear filament; β-pleated sheet

269
Q

Describe Congo red staining of amyloid.

A

Amyloid: Congo red +; apple green birefringence when polarized

270
Q

What are the tree major precursor proteins of amyloid?

A

Major precursor proteins: λ light chains, SAA, APP

271
Q

List three other amyloid precursor proteins.

A

Other precursor proteins: transthyretin, β2-microglobulin, prion proteins

272
Q

Describe the pathogenesis of amyloidosis.

A

Pathogenesis: misfolded proteins in most cases; monocyte enzyme defects

273
Q

Describe kidney involvement in amyloidosis.

A

Kidney: proteinuria with nephrotic syndrome

274
Q

List two gastrointestinal findings in amyloidosis.

A

Gastrointestinal: malabsorption, macroglossia

275
Q

List three cardiac findings in amyloidosis.

A

Heart: restrictive cardiomyopathy, diastolic dysfunction LHF, conduction defects

276
Q

Describe nervous system involvement in amyloidosis.

A

CNS: dementia, peripheral/autonomic neuropathy

277
Q

Describe liver involvement in amyloidosis.

A

Liver: hepatomegaly, functional impairment uncommon

278
Q

Describe spleen involvement in amyloidosis.

A

Spleen: splenomegaly; white pulp sago spleen, red pulp lardaceous spleen

279
Q

List one clinical finding in hemodialysis-associated amyloidosis.

A

Hemodialysis-associated amyloidosis: carpal tunnel syndrome

280
Q

Describe three hemostasis abnormalities of amyloidosis.

A

Hemostasis: factor X deficiency, pinch purpura, periorbital hemorrhage

281
Q

List six techniques used to diagnose amyloidosis.

A

Diagnosis: serum/urine electrophoresis, BM aspirate, nuclear imaging, echocardiography, tissue biopsy

Rapid Review Pathology (14 decks)

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