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Pathology > Ch 2 Pathoma > Flashcards

Ch 2 Pathoma Flashcards

1
Q

Acute Inflammation characterized by

A

Presence of edema and neutrophils in tissue

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2
Q

Acute inflammation arises in response to

A

infection (to eliminate pathogen) or tissue necrosis (to clear necrotic debris) - it’s an immediate response with limited specificity

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3
Q

5 mediators of acute inflammation

A

TLRs, arachidonic acid metabolites, mast cells, complement, hageman factor (factor XII)

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4
Q

TLRs are present on

A

cells of innate immune system (macrophages, dendritic cells) - also present on cells of adaptive immunity (lymphocytes) so they play a role in acute and chronic inflammation

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5
Q

TLRs are activated by _______ and up regulate _______, a nuclear transcription factor that activates immune response genes

A

PAMPs (pathogen associated molecular patterns); NF-KB (acts as an on switch)

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6
Q

______ on macrophages recognizes LPS found on gram ______ bacteria

A

CD14 (a co-receptor for TLR4); negative (LPS acts as a PAMP)

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7
Q

Arachidonic acid is released by ________ and acted upon by ____ or _____ (2 possible pathways with distinct products)

A

phospholipase A2 (from phospholipid cell membrane); cyclooxyrgenase or 5-lipoxygenase

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8
Q

Cyclooxygenase produces ________ and 5-lipoxygenase produces ________.

A

prostaglandins; leukotrienes

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9
Q

Which three prostaglandins mediate vasodilation and increased vascular permeability and which one mediates pain and fever?

A

PGI2, PGD2, and PGE2; PGE2

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10
Q

4 key mediators that attract and activate neutrophils

A

LTB4 (leukotriene), C5a (complement), IL8 (cytokine), and bacterial products

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11
Q

LTC4, LTD4, and LTE4 (slow reacting substances of anaphylaxis) mediate these three things

A

vasoconstriction, bronchospasm, increased vascular permeability

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12
Q

Mast cells are activated by these three things

A

tissue trauma, complement proteins C3a and C5a, or cross linking of cell surface IgE by antigen

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13
Q

Immediate and delayed response of mast cells involve production of _______ and ______ respectively

A

histamine (which causes vasodilation and increased vascular perm); arachidonic acid metabolites particularly leukotrienes

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14
Q

Complement activations occurs via these three pathways

A
  1. classical - C1 binds IgG or IgM that is bound to antigen (GM makes classic cars); 2. alternative - microbe products directly activate complement; 3. MBL (mannose binding lectin) - MBL binds to mannose on microorganisms and activates complement
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15
Q

Complement activation pathways result in

A

production of C3 convertase (mediates C3 –> C3a and C3b), which in turn produces C5 convertase (mediates C5 –> C5a and C5b). C5b complexes with C6-C9 to form MAC (membrane attack complex - creates hole in microbe cell membrane)

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16
Q

This complement is chemotactic for neutrophils and this one is opsonin for phagocytosis

A

C5a; C3b

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17
Q

________ is an inactive pro inflammatory protein produced in the liver that is activated upon exposure to sub endothelial or tissue collagen

A

Hagemon factor (factor XII) (can lead to DIC)

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18
Q

Hagemon factor (factor XII) activates these three things

A

coagulation and fibrinolytic systems (can lead to DIC) - most impt; complement; kinin system (kinin cleaves high-molecular weight kininogen HMWK to bradykinin which mediates vasodilation and increased vascular perm and pain)

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19
Q

2 key mediators for pain

A

PGE2 and bradykinin

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20
Q

5 cardinal signs of inflammation

A

redness (rubor), warmth (calor), swelling (tumor), pain (dolor), and fever

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21
Q

The key mediators of redness and warmth are (3); the key mediators of swelling are (2); the key mediators of pain are (2)

A

histamine, prostaglandins, bradykinin; histamine, tissue damage; bradykinin and PGE2

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22
Q

Pathway of fever

A

pyrogens (like LPS from bacteria) cause macrophages to release IL1 + TNF –> increases COX activity in perivascular cells in hypothalamus –> increase PGE2

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23
Q

Leukocyte arrival in tissues (steps)

A

Margination, rolling, adhesion, and transmigration

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24
Q

Vasodilation slows blood flow in _________ which cause leukocytes to ________

A

postcapillary venules; marginate

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25
Q

Rolling occur by the up regulation of _______ on endothelial cells, which binds with ________ on leukocytes

A

selectin; sialyl Lewis X

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26
Q

This type of selectin is released from Weibel Palade bodies mediated by histamine; and this type of selectin is induced by TNF and IL1

A

P-selectin (W-P bodies also release von Willebrand factor); E-selectin

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27
Q

CAMs are unregulated on endothelium by ___ and _____. Integrins are unregulated on leukocytes by ____ and _____

A

TNF and IL1; C5a and LTB4

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28
Q

Adhesion occurs by the interaction btwn _____ and ______

A

CAMs (on endothelium); Integrins (on leukocyte)

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29
Q

Leukocyte adhesion deficiency common cause and clinical presentation (3)

A

integrin defect (CD18 subunit); delayed separation of umbilical cord (neutrophils can’t come in after necrosis), increased circulating neutrophils (due to impaired adhesion of marginated pool), and recurrent bacterial infections that lack pus formation (pus is dead neutrophils sitting in fluid)

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30
Q

Phagocytosis is enhanced by _______

A

opsonins (C3b and IgG)

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31
Q

______ is a protein trafficking defect (autosomal recessive) characterized by impaired phagolysosome formation

A

Chediak-higashi syndrome

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32
Q

Clinical features of chediak higashi syndrome (6)

A

increased risk of pyogenic infections, neutropenia, giant granules in leukocytes, defective primary hemostasis, albinism (melanocytes can’t pass melanin to keratinocytes), peripheral neuropathy (can’t send proteins from cell body down long nerve)

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33
Q

O2 dependent killing pathway

A

O2 –(NADPH oxidase)–> O2^- –(SOD)–> H202 –(MPO)–> HOCl (bleach)

SOD = superoxide dismutase
MPO = myeloperoxidase
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34
Q

_____ is characterized by poor O2 dependent killing due to _____ defect

A

CGD; NADPH oxidase

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35
Q

Chronic granulomatous disease leads to recurrent infection and granuloma formation with _______ organisms, particularly _____ (5)

A

catalase positive; staph aureus, psuedomonas cepacia*, serratia marcescens, nocardia, aspergillus

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36
Q

_____ is used to screen for CGD

A

Nitroblue tetrazolium test (NBT) - it turns blue if NADPH oxidase can convert O2 to O2^-

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37
Q

MPO deficiency causes increased risk for _____ infections; pts have a normal/abnormal NBT

A

Candida; normal (O2 to H2O2 is intact)

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38
Q

Neutrophils peak after _____, and macrophages peak ______ after inflammation begins

A

24 hours; 2-3 days

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39
Q

Macrophages destroy phagocytosed material via _______

A

O2 independent killing; use enzymes in secondary granules (ex: lysozyme)

40
Q

Anti-inflammatory cytokines produced by macrophages (2)

A

IL10 and TGFB

41
Q

______ from macrophages recruits additional neutrophils

A

IL8 (continued acute inflammation)

42
Q

Abscesses are formed by _______ mediating fibrosis via fibrogenic growth factors and cytokines

A

macrophages

43
Q

Macrophages present antigen to activate ____ which secrete cytokines that promote chronic inflammation

A

CD4+ helper T cells

44
Q

Acute/chronic inflammation is characterized by the presence of lymphocytes and plasma cells in the tissue

A

chronic

45
Q

Chronic inflammation stimuli include (5)

A

persistent infection (most common); infection with viruses, mycobacteria, parasites, and fungi; autoimmune disease; foreign material; and some cancers

46
Q

T-Cell receptor complex includes both the TCR and ____

A

CD3

47
Q

CD4+ T cells recognize antigens presented on MHC class ___ and CD8+ T cells on MHC class ____

A

II; I

48
Q

Activation of T cells requires (2)

A

binding of antigen/MHC complex and an additional 2nd signal

49
Q

2nd signal for activation of CD4+ helper T cells and for CD8+ cytotoxic t cells

A

B7 on APC binds CD28 on CD4+ helper T cell; IL-2 (secreted by CD4+ TH1)

50
Q

TH1 secretes _____ (activating macrophage, promotes B cell class switching from IgM to IgG, promotes TH1 phenotype and inhibits TH2 phenotypes)

A

IFN-gamma

51
Q

TH2 secretes _____ (facilitates B cell class switching to IgE) and ______ (eosinophil chemotaxis and activation, and class switching to IgA), and ______ (function similar to first one)

A

IL-4; IL-5; IL-13 (function similar to IL-4)

52
Q

Two ways CD8+ cytotoxic T-cells kill

A
  1. secretion of perforin and granzyme; 2. expression of FasL, which binds Fas on target cells (both activate apoptosis)
53
Q

B cell activation occurs in these two ways

A

Antigen binding by surface IgM or IgD (results in maturation to IgM or IgD secreting plasma cells); B cell antigen presentation to CD4+ helper T cells via MHC class II (CD40 receptor on B cell binds CD40L on helper T cell

54
Q

What is the key cell of a granuloma?

A

epithelioid histiocyte (macrophage with abundant pink cytoplasm) - often also find giant cells and a rim of lymphocytes

55
Q

Caseating granulomas exhibit exhibit/lack central necrosis and are characteristic of ______ (2)

A

exhibit; TB and fungal infections

56
Q

Noncaseating granulomas exhibit/lack central necrosis. Common etiologies include _____ (5)

A

lack; rxn to foreign material, sarcoidosis, beryllium exposure, Crohn disease, and cat scratch disease

57
Q

Steps to forming a granuloma (3)

A

Macrophage process and present antigen via MHC class II to CD4+ helper T cells, which cause macrophages to release IL-12 inducing CD4+ t cells to differentiate to TH1 subtype; 3. TH1 cells secrete IFNgamma which converts macrophages to epithelioid histiocytes and giant cells

58
Q

DiGeorge’s syndrome is a developmental failure of the _________ due to a ____ microdeletion

A

3rd and 4th pharyngeal pouches; 22q11

59
Q

DiGeorge’s syndrome clinical presentations (3)

A

T-cell deficiency (lack of thymus), hypocalcemia (lack of parathyroids), abnormalities of heart, great vessels, and face

60
Q

Severe Combined Immunodeficiency (SCID) results in defective _____ and _____ immunity

A

cell mediated (T cell) and humoral (B cell)

61
Q

3 etiologies of SCID

A

cytokine receptor defects (necessary for proliferation and maturation of b and t cells); adenosine deaminase deficiency* (necessary to dominate adenosine and deoxyadenosine which otherwise build up and are toxic to lymphocytes); MHC class II deficiency (necessary for CD4+ helper t cell activation and cytokine production and subsequent CD8+ t cell and B cell development)

62
Q

SCID is characterized by susceptibility to ______ infections including opportunistic and live vaccines. And tx

A

fungal and viral (t cell defect), bacterial, and protozoal (b cell defect) - tx is sterile isolation and stem cell transplantation

63
Q

X-linked agammaglobulinemia

A

complete lack of immunoglobulin due to disordered b cell maturation (due to mutated bruton tyrosine kinase)

64
Q

X-linked agammaglobulinemia presents with

A

recurrent bacterial, enterovirus, and Giardia lamblia infections (maternal ABs present during first 6 mo of life are protective) - avoid live vaccines

65
Q

Immunodeficiency disorder due to low immunoglobulin due to B cell or helper T cell defects

A

Common variable immunodeficiency (CVID)

66
Q

CVID presents with increased risk for

A

bacterial, enterovirus, and giardia lamblia infections and increased risk for autoimmune disease and lymphoma

67
Q

IgA deficiency presents with increased risk for

A

mucosal infection, especially viral (most common Ig deficiency; most pts are asymptomatic) - IgA protects against mucosal enteric infxns

68
Q

Wiskott-Aldrich Syndrome cause and triad presentation

A

due to a mutation in WASP gene (x-linked); characterized by thrombocytopenia, eczema, and recurrent infxns (defective humoral and cellular immunity) - bleeding is major cause of death

69
Q

Increased risk of Neisseria infection (N gonorrhoeae and N meningitidis) is caused by

A

C5-C9 deficiencies (complement deficiency)

70
Q

______ deficiency results in hereditary angioedema (edema of skin especially periorbital and mucosal surfaces)

A

C1 inhibitor
causes over activation of C1 –> over activation of complement –> increased vasodilation, vascular permeability, and edema (inflammation)

71
Q

Central tolerance vs peripheral tolerance

A

central occurs in areas where lymphocytes develop (thymus or bone marrow); peripheral occurs in other tissues

central tolerance in thymus leads to apoptosis or generation of regulatory t cells; in bone marrow leads to receptor editing or apoptosis

peripheral tolerance leads to anergy or apoptosis of both t and b cells

72
Q

AIRE mutations

A

AIRE is a TF that causes dendritic cells in thymus to express self-antigen to ensure T-cells aren’t created that bind to self; mutations lead to autoimmune polyendocrine syndrome (hypoparathyroid, adrenal failure, and chronic candida infxns)

73
Q

_____ suppress autoimmunity by blocking T cell activation (by expressing CTLA4, which competes with CD28 on t cells to bind B7 on APCs) and producing anti-inflammatory cytokines (IL-10, TGF-B)

A

Regulatory T cells

They are CD4+, CD25+ (IL-2 receptor), and FOXP3+ (a TF needed for dvlpmnt and maintenance)

74
Q

FOXP3 mutations lead to _______

A

IPEX syndrome (Immune dysfunction, Polyendocrinopathy, Enteropathy, X-linked)

75
Q

Why autoimmune disorders are more common in women?

A

estrogen may reduce apoptosis of self-reactive B cells

76
Q

Wound healing occurs via a combination of ______ and ______

A

regeneration and repair

77
Q

Three types of regenerative capacity and tissues that exhibit each type

A

Labile (small/large bowel - stem cells in crypts, skin - stem cells in basal layer, bone marrow - hematopoietic stem cells);
Stable (liver - regenerate tissue only when necessary, otherwise the cells are quiescent (G0));
Permanent (myocardium, skeletal muscle, neurons - lack regenerative potential)

78
Q

_____ formation is the initial phase of repair

A

granulation tissue

79
Q

Granulation tissue consists of these 3 major things

A

fibroblasts (deposit type III collagen), capillaires (provide nutrients), and myofibroblasts (contract wound - aka make it smaller)

80
Q

In scar formation, type ____ collagen is replaced with type ____ collagen

A

III; I
(III is pliable and present in granulation tissue, embryonic tissue, and keloids - I has high tensile strength and is found in skin, bone, tendons)

81
Q

Regeneration and repair are mediated by paracrine signaling via growth factors that interact with receptors and result in gene expression and cellular growth. Name 5 examples of mediators.

A

TGF-alpha (epithelial and fibroblast GF)
TGF-beta (fibroblast GF; inhibits inflammation)
PDGF (GF for endothelium, smooth muscle and fibroblasts)
Fibroblast GF (impt for angiogenesis; mediates skeletal development)
Vascular endothelial GF (VEGF - impt for angiogenesis (growing bv’s))

82
Q

Delayed wound healing occurs in

A

Infection (most common); vitamin C, copper, or zinc deficiency (all involved in strengthening collagen); foreign body, ischemia, diabetes, and malnutrition

zinc is a cofactor for collagenase, which replaces type III collagen of granulation tissue with type I

83
Q

______ is excess production of scar tissue that is out of proportion to the wound and is characterized by excess _______. (genetic predisposition in african americans)

A

Keloid; type III collagen

classically affects earlobes, faces, and upper extremities

84
Q

An autoimmune disease in which flares and remissions are common, classically arises in middle aged females, can present with a malar butterfly rash or discoid rash

A

Systemic lupus erythematosus (SLE)

85
Q

A sensitive test for SLE and 2 highly specific tests for SLE

A

Antinuclear antibody (ANA); Anti-dsDNA or anti-Sm antibodies

86
Q

This autoimmune disorder causes destruction of lacrimal and salivary glands and often presents with dry eyes, lymphocytic sialadenitis, and ANA + anti-SSA/SSB + rheumatoid factor

A

Sjogren syndrome

87
Q

This autoimmune disorder is characterized by hardening of the skin and visceral organs - fibroblast activation leads to deposition of collagen

A

systemic sclerosis (Scleroderma)

endothelial dysfunction leads to inflammation (increased adhesion molecules), vasoconstriction (increased endothelin and decreased NO), and secretion of growth factors (TGF-B and PDGF which both can activate fibroblasts)

88
Q

Limited type or diffuse type of systemic slcerosis presents with CREST syndrome

A

Limited; CREST = calcinosis/anti-Centromere antibodies, Raynaud’s, Esophageal dysmotility, Sclerodactyly (tight skin), and Telangiectasias of skin (red marks from dilated capillaries)

Diffuse type is highly associated with antibodies to DNA topoisomerase I

89
Q

This autoimmune disease is characterized by ANA along with serum antibodies to U1 ribonucleoprotein

A

Mixed connective tissue disease (has mixed features of SLE, systemic sclerosis, and polymyositis)

90
Q

Which hypersensitivity reaction is characterized by IgE-related release of chemical mediators from mast cells and basophils?

A

Type I (immediate) - anaphylactic type

91
Q

Which hypersensitivity reaction is mediated by sensitized T lymphocytes?

A

Type IV (cell mediated type) - delayed type = granuloma formation by CD4+ TH1-cells; cytotoxic type - CD8+ destroy antigen containing cells

92
Q

Type III hypersensitivity reaction are characterized by the formation of _______.

A

Immune complexes (antibody-antigen complexes) - deposit in tissue resulting in inflammation and tissue injury

93
Q

Which hypersensitivity reaction is characterized by IgG and IgM antibody directed against a specific target cell or tissue with complement usually involved?

A

Type II (antibody mediated) - complement dependent cytotoxicity results in lysis of cell; antibody dependent cell mediated cytotoxicity (ADCC) causes killing of antibody coated cells

94
Q

Anaphylaxis and asthma are what type of hypersensitivity reaction?

A

Type 1

95
Q

Serum sickness and autoimmune diseases like SLE and rheumatoid arthritis, and glomerulonephirits are what type of hypersensitivity reaction?

A

Type III

96
Q

Name 4 types of type II hypersensitivity reactions

A

Transfusion reactions, hemolytic anemia, graves disease, and myasthenia gravis

97
Q

Name 5 types of type IV hypersensitivity reactions

A

Graft rejection, viral infection, immune reaction to tumors, granulomatous disease, and delayed skin reactions (poison ivy)

Pathology (21 decks)

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