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neuro > Pathoma: inflammation, inflammatory disorders, wound healing > Flashcards

Pathoma: inflammation, inflammatory disorders, wound healing Flashcards

1
Q

acute inflammation is characterized by

A

edema and neutrophils and tissue
arises in response to infection (to elim. pathogen) or tissue necrosis (to clear necrotic debris)
immediate response with limited specificity (innate immunity)

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2
Q

Toll-like receptors

A

present on cells of the innate immune system
activated by PAMPs (pathogen-associated molecular patterns)
activation results in up rgulation of NF-kB -> nuclear transcription factor that activates immune response genes leading to production of multiple immune mediators
also present on cells of adaptive immunity and are involved in mediating chronic inflammation

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3
Q

CD14

A

co-receptor for TLR4 on macrophages recognizes lipopolysaccharide on the outer membrane of G- bacteria

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4
Q

Arachidonic acid metabolites

A

released from phospholipidcell membrane by phospholipase A2 and then acted upon by COX or 5-lipoxygenase

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5
Q

COX produces

A

prostaglandins

PGI2, PGD2, and PGE2 - mediate vasodilation and increase vascular permeability

PGE2 also mediates pain and fever

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6
Q

5-lipoxygenase produces

A

leukotrienes

LTB4 attracts and activates neutrophils

LTC4, LTD4, LTE4 (slow reacting substances of anaphylaxis) mediate vasoconstriction, bronchospasm, and increased vascular permeability

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7
Q

Mast Cells

A

throughout connective tissue
activated by - tissue trauma
- complement proteins C3a and C5a
- cross-linking of cell-surface IgE by antigen

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8
Q

Immediate response of Mast Cells

A

release of preformed histamine granules, which mediate vasodilation of arterioles and increased vascular permeability

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9
Q

Delay response of Mast Cells

A

production of arachidonic acid metabolites - particularly leukotrienes

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10
Q

Complement

A

proinflammatory serum proteins that complement inflammation

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11
Q

Activation of complement occurs via 3 pathways

A

classical
alternative
mannose-binding lectin pathway

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12
Q

Classical Complement Pathway

A

C1 bind IgG or IgM that is bound to antigen

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13
Q

Alternative Complement Pathway

A

microbial products directly activate complement

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14
Q

mannose-binding lectin Complement Pathway

A

MBL binds to mannose on microorganisms and activates complement

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15
Q

All complement pathways result in production of

A 
C3 convertase (C3 -> C3a and C3b) -> activates C5 convertase (C5 -> C5a and C5b)
C5b complexes with C6-C9 to form the membrane attack complex
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16
Q

C3a and C5a

A

Anaphalytoxins

trigger mast cell degranulation -> histamine-mediated vasodilation and increased vascular permeability

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17
Q

C5a

A

chemotactic for neutrophils

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18
Q

MAC

A

lyses microbes by creating a hole in the cell membrane

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19
Q

Hageman Factor

Factor XII

A

inactive proinflammatory protein produced in the liver

activated upon exposure to subendothelial or tissue collagen

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20
Q

Activated Hageman Factor activates

A

coagulation and fibrinolytic systems
complement
kinin system - kinin cleaves high molecular weight kininogen(HMWK) to bradykinin, which mediates vasodilation and increase vascular permeability as well as pain

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21
Q

Cardinal Signs of Inflammation

A 
Redness - rubor
warmth - calor
swelling - tumor
pain - dolor
fever
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22
Q

redness - rubor

warmth - calor

A

due to vasodilation - increased blood flow

occurs via relaxation of arteriolar smooth muscle, key mediator are histamine, prostaglandins, and bradykinin

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23
Q

swelling - tumor

A

leakage of luid from postcapillary venules into the interstitial space (exudate)
key mediators are histamine (causes endothelial cell contraction) and tissue damage (endothelial cell disruption)

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24
Q

pain - dolor

A

bradykinin and PGE2 sensitize sensory nerve endings

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25
Q

Fever

A

pyrogens (LPS from bacteria) cause macrophages to release IL-1 and TNF which increase cyclooxygenase activity in perivascular cells of the hypothalamus

increased PGE2 raises temperature set point

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26
Q

Neutrophil Arrival and Function

A

1) margination
2) rolling
3) adhesion
4) transmigration and chemotaxis
5) phagocytosis
6) destruction of phagocytosed material
7) resolution

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27
Q

margination

A

vasodilation slows blood flow in postcapillary venules

cells marginate from center of flow to the periphery

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28
Q

rolling

A

selectin is upregulated on endothelial cells
P-selectin release from Veibel-Palade bodies mediated by histamine
E-selectin - induced by TNF and IL-1
selectins bind sialyl Lewis X on leukocytes
interaction results in rolling of leukocytes along vessel wall

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29
Q

adhesion

A

ICAM and VCAM are upregulated on endothelium by TNF and IL1
integrins upregulated on leukocytes by C5a and LTB4
interaction creates firm adhesion of leukocytes to vessel wall

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30
Q

transmigration and chemotaxis

A

leukocytes transmigrate across the endothelium of postcapillary venules and move toward chemical attractants
neutrophils are attracted by bacterial products, IL8, C5a, and LTB4

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31
Q

phagocytosis

A

consumption of pathogens or necrotic tissue

enhanced by opsonins - IgG and C3b

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32
Q

destruction of phagocytosed material

A

O2-dependent killing is most effective mech

HOCL generated by oxidative burst in phagolysosomes destroys phagocytosed microbes

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33
Q

resolution

A

neutrophils undergo apoptosis and disappear within 24 hours after resolution of inflammatory stimulus

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34
Q

leukocyte adhesion deficiency is most commonly due to

A

AR defect of integrins (CD18 subunit)
delayed separation of umbilical cord, increased circulating neutrophils (due to impaired adhesion), and recurrent bacterial infection that lack pus formation

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35
Q

Chediak- Higashi

A 
AR - protein trafficking defect
impaired phagolysosome formation
increased risk of pyogenic infections
neutropenia
giant granules in leukocytes
defective primary hemostasis
albinism
peripheral neuropathy
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36
Q

chronic granulomatous disease

A

poor O2 dependent killing
due to NADPH oxidase defect ( x-linked or AR)
recurrent infection and granuloma formation with catalase + organisms (s. aureus, pseudomonas cepacia, serratia marcescens, nocardia, and aspergillus)
screen with nitroblue tetrazolium test - colorless if NADPH is defective, turns blue if it convers O2 to O2-

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37
Q

MPO deficiency

A

defective conversion of H2O2 to HOCL

increased risk for candida infections

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38
Q

Macrophages

A

predominate after neutrophils
peak 2-3 days after inflammation
derived from monocytes in the blood

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39
Q

IL-10 and TGF - B

A

anti-inflammatory cytokines produced by macrophages

involved in resolution and healing

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40
Q

continued acute inflammation

A

persistent pus formation

IL-8 from macrophages recruits additional neutrophils

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41
Q

Abscesses

A

acute inflammation surrounded by fibrosis

macrophages mediate fibrosis via fibrogenic growth factors and cytokines

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42
Q

macrophages in chronic inflammation

A

present antigen to activate CD4+ helper T cells which secrete cytokines that promote chronic inflammation

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43
Q

chronic inflammation is characterized by

A

presence of lymphocytes and plasma cells in tissue

delayed response, more specific adaptive immunity

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44
Q

chronic inflammation stimuli

A 
persistent infection
infection with viruses, mycobacteria, parasites, and fungi
autoimmune disease
foreign material
some cancers
45
Q

where are T lymphocytes produced

A

bone marrow as progenitor T cells

46
Q

Further development of T cells occurs in the

A

thymus
T Cell receptor undergoes rearrangement and progenitor cells become CD4+ or CD8+ cells
-T cells use TCR complex (TCR and CD3) for antigen surveillance
- TCR complex recognizes antigen presented on MHC
- CD4+ - MHC II
- CD8+ - MHC I
- activation of T cells requires binding of antigen/MHC complex and an additional second signal

47
Q

CD4+ helper T cell activation

A

extracellular antigen is phagocytosed, processed, and presented on MHC II, which is expressed by APCs
B7 on APC binds CD28 on CD4+ providing 2nd activation signal
activated CD4+ helper T cells secrete cytokines that help inflammation and are divided into 2 subsets - Th1 and Th2

48
Q

Th1

A 
secretes IFN-gamma (activates macrophage, promotes B cell class switching from IgM to IgG
promotes Th1 and inhibits Th2
49
Q

Th2

A 
secretes IL-4 (facilitates B-cell class switching to IgE)
IL-5 (eosinophil chemotaxis and activation, and class switching to IgA)
IL-13 (function similar to IL-4)
50
Q

CD8+ cytotoxic T-cell activation

A

intracellular antigen is processed and presented on MHC I, which is expressed by all nucleated cells and patelets
IL-2 from CD4+ Th1 cells provides 2nd activation signal
activated for killing

51
Q

CD8+ killing occurs by

A

secretion of perforin and granzyme
perforin creates poes that allow granzyme to enter the target cell, activating apoptosis
expression of FasL, which binds Fas on target cells, activating apoptosis

52
Q

B-Lymphocytes are produced where

A

bone marrow

undergo immunoglobulin rearrangements to become naïve B cells that express surface IgM and IgD

53
Q

B-cell activation occurs via

A

antigen binding by surface IgM or IgD - maturation to IgM or IgD secreting plasma cells
B-cell antigen presentation to CD4+ helper T cells via MHC II
- CD40 receptor on B cell binds CD40L on helper T cell - 2nd signal
- helper T cell then secretes IL-4 and IL-5 (mediate B-cell isotype switching, hypermutation, and maturation to plasma cells

54
Q

granulomatous inflammation

A

subtype of chronic inflammation
characterized by granuloma, which is a collection of epithelioid histiocytes(macs with abundant pink cytoplasm)
usually surrounded by giant cells ad a rim of lymphocytes

55
Q

Non caseating granulomas

A

lack cental necrosis

reaction to foreign material
sarcoidosis
beryllium exposure
Crohn disease
cat scratch disease
56
Q

caseating granulomas

A

central necrosis

characteristic of tuberculosis and fungal infections

57
Q

steps involved in granuloma formation

A

1) macrophages process and present antigen via MHC II to CD4+ helper T cells
2) interaction leads macrophages to secrete IL-12 - inducing CD4+ to differentiate into Th1 subtype
3) Th1 cells secrete IFN-gamma - converts macs to epithelioid histiocytes and giant cells

58
Q

Primary Immunodeficiencies

A 
Digeorge Syndrome
Severe Combined Immunodeficiency
X-Linked Agammaglobulinemia
Common Variable Immunodeficiency
IgA Deficiency
Hyper IgM Syndrome
Wiskott-Aldrich Syndrome
Complement Deficiencies
59
Q

Digeorge Syndrome

A

developmental failure of the third an fourth pharyngeal pouches - due to 22q11 microdeletion
presents with T-cell deficiency (lack of thymus)
hypocalcemia (lack of parathyroids)
and abnormalities of heart, great vessels, and face

60
Q

SCID

A

defective cell-mediated and humoral immunity

cytokine receptor defects
adenosine deaminase (ADA) deficiency
MHC II deficiency

susceptibility to fungal, viral, bacterial, and protozoal infections

Tx - sterile isolation (bubble boy) and stem cell transplantation

61
Q

cytokine receptor defects

A

necessary for proliferation and maturation of B and T cells

62
Q

adenosine deaminase (ADA) deficiency

A

necessary to deaminate adenosine and deoxyadenosine for excreation as waste
buildup is toxic to lymphocytes

63
Q

MHC II deficiency

A

necessary for CD4+ activation and cytokine production

64
Q

X-Linked Agammaglobulinemia

A

complete lack of immunoglobulin due to disordered B cell maturation
pre and pro B cells cannot mature
X-linked - mutated Bruton tyrosine kinase
presents at 6 months after maternal antibodies are done
recurrent bacterial, enterovirus, and giardia lamblia infections
Avoid live vaccines (polio)

65
Q

Common Variable Immunodeficiency

A

low immunoglobulin due to B cell or helper T cell defects
increased risk for bacterial, enterovirus, and giardia lamblia infections in late childhood
increased risk for autoimmune disease and lymphoma

66
Q

IgA Deficiency

A

low serum and mucosal IgA
most common immunoglobulin deficiency
increased risk for mucosal infection - esp. viral
most pts are asymptomatic

67
Q

Hyper IgM Syndrome

A

elevated IgM
mutated CD40L (on T helper Cells) or CD40 R (on B cells)
2nd signal cannot be delivered to helper T cells during B cell activation -> cytokines required for immunoglobulin class switching are not produced
low IgA, IgG, and IgE -> recurrent pyogenic infections (due to poor opsonization) especially at mucosal sites

68
Q

Wiskott-Aldrich Syndrome

A

characterized by thrombocytopenia, eczema, and recurrent infections (defective humoral and cellular immunity)
bleeding is major cause of death
mutation in WASP gene
X-linked

69
Q

Complement Deficiencies

A

C5-C9 deficiencies
increased risk for Neisseria infection (gonorrhoeae and meningitides)
C1 inhibitor deficiency -> hereditary angioedema, characterized by edema of the skin (esp. periorbital) and mucosal surfaces

70
Q

Central tolerance in the thymus leads to

A

T-cell apoptosis or generation of regulatory T cells

AIRE mutations -> autoimmune polyendocrine syndrome

71
Q

central tolerance in the bone marrow leads to

A

receptor editing or B-cellapoptosis

72
Q

peripheral tolerance leads to

A

anergy or apoptosis of T and B cells

Fas apoptosis pathway mutations result in autoimmune lymphoproliferative syndrome (ALPS)

73
Q

Regulatory T cells suppress autoimmunity by blocking

A

T-cell activation and producing anti-inflammatory cytokines - IL-10, TGF-B
CD25 polymorphisms assoc. with autoimmunity (MS and type I DM
FOXP3 mutations -> IPEX syndrome

74
Q

Autoimmune disorder etiology

A

more common in women - estrogen may decrease apoptosis of self reactive B cells
HLA B27 and PTPN22 association

75
Q

SLE

A

antigen-antibody complexes damage multiple tissues (type III HSR)
poorly cleared apop. debris activates self-reactive lymphocytes -> produces antibodies to host nuclear antigens
Can effect any tissue

76
Q

SLE common findings

A

fever, weight loss, fatigue, lymphadenopathy, and Raynaud phenomenon
malar rash or discoid rash - esp. after exposure to sunlight
oral or nasopharyngeal ulcers
arthritis
serositis
psychosis or seizures
renal damage
anemia, thrombocytopenia, or leukopenia (type II HSR)
Libmann-Sacks endocarditis
antinuclear antibody
anti-dsDNA or anti-Sm antibodies
anti-phospholipid AB assoc with 1/3 of pts -> characterized by hypercoagulable state

77
Q

Anti-histone antibody

A

characteristic of drug-induced lupus
procainamide, hydralazine, and isoniazid
ANA is positive by definition (anti-nuclear antibody)

78
Q

sjogren syndrome

A

autoimmune destruction of lacrimal and salivary glands
lymphocyte mediated damage (type IV HPR) with fibrosis
dry eyes, mouth and recurrent dental caries in an older woman
can be primary or assoc. with rheumatoid arthritis
lymphocytic sialadenitis on lip biopsy is a diagnostic criterion

79
Q

sjogren syndrome is characterized by what antibodies

A

ANA and anti-ribonucleoprotein antiodies

80
Q

systemic sclerosis (scleroderma)

A

autoimmune disorder characterized sclerosis of skin and visceral organs - middle aged females
fibroblast activation leads to deposition of collagen
autoimmune damage to mesenchyme is possible initiating event
endothelial dysfunction leads to inflammation, vasoconstriction, and secretion of growth factors (TGF-B and PDGF)
fibrosis, initially perivascular, progresses and causes organ damage

81
Q

systemic sclerosis (scleroderma)

limited type

A 
skin involvement is limited to hands and face with late visceral involvement
Prototype is CREST syndrome
Calcinosis/anti-centromere ABs
Raynaud phenomenon
esophageal dysmotility
sclerodactyly
telangiectasias of the skin
82
Q

systemic sclerosis (scleroderma)

diffuse type

A

skin involvement is duffuse with early visceral involvement
any organ can be involved
commonly:
vessels (Raynaud’s)
GI tract (esophageal dysmotility and reflux)
lungs (interstitial fibrosis and pulmonary hypertension)
kidneys (scleroderma renal crisis)

highly assoc. with ABs to DNA topoisomerase I (anti-Scl-70)

83
Q

Mixed connective tissue disease

A

autoimmune-mediated tissue damage with mixed features of SLE, systemic sclerosis, and polymyositis
characterized by ANA along with serum ABs to U1 ribonucleoprotein

84
Q

wound healing - regeneration

A

replacement of damaged tissue with native tissue, dependent on regenerative capacity of tissue

85
Q

three types of tissue based on regenerative capacity

A

labile, stable, and permanent

86
Q

labile tissues

A

possess stem cells that continuously cycle to regenerate tissue
small and large bowel (stem cells in mucosal crypts)
skin (stems in basal layer)
bone marrow (hematopoietic stems)

87
Q

stable tissues

A

cells that are quiescent but can reenter the cell cycle to regenerate when necessary

88
Q

permanent tissues

A

lack significant regenerative potential

myocardium
skeletal muscle
neurons

89
Q

wound healing - repair

A

replacement of damaged tissue with fibrous scar
when regenerative stem cells are lost (deep skin cut) or when a tissue lacks regenerative capacity (healing after myocardial infarction)

90
Q

initial phase of repair

A

formation of granulation tissue
consists of fibroblasts(deposit type III collagen)
capillaries (provide nutrients)
and myofibroblasts (contract wound)

91
Q

scar formation

A

type III collagen is replaced with type I collagen

92
Q

type III collagen

A

pliable and present in granulation tissue, embryonic tissue, uterus, and keloids

93
Q

type I collagen

A

high tensile strength

present in skin, bone, tendons, and most organs

94
Q

collagenase

A

removes type III collagen

requires zinc as cofactor

95
Q

TGF-alpha

A

epithelial and fibroblast growth factor

96
Q

TGF-B

A

important fibroblast growth factor, also inhibits inflammation

97
Q

platelet-derived growth factor

A

growth factor for endothelium, smooth muscle, and fibroblasts

98
Q

fibroblast growth factor

A

important for angiogenesis, also mediates skeletal development

99
Q

vascular endothelial growth factor - VEGF

A

angiogenesis

100
Q

regeneration and repair is mediated by

A

paracrine signaling via growth factors

101
Q

primary intention

A

wound edges are brought together (suturing)

minimal scar formation

102
Q

secondary intention

A

edges are not approximated
granulation tissue fills the defect
myofibroblasts then contract the wound - forming a scar

103
Q

delayed wound healing occurs in

A

infection (S. Aureus is most common)
vitamin C, copper and zinc deficiency
foreign body, ischemia, diabetes, and malnutrition

104
Q

vitamin C deficiency

A

important cofactor in the hydroxylation of proline and lysine procollagen residues
hydroxylation is necessary for eventual collagen cross-linking

105
Q

copper deficiency

A

cofactor for lysyl oxidase

which cross-links lysine and hydroxylysine to form stable collagen

106
Q

zinc deficiency

A

cofactor for collagenase

replaces the type III collagen of granulation tissue with stronger type I collagen

107
Q

dehiscence

A

rupture of a wound

most commonly seen after abdominal surgery

108
Q

hypertrophic scar

A

excess production of scar tissue that is localized to the wound

109
Q

keloid

A 
excess production of scar tissue that is out of proportion to the wound
characterized by type III collagen
genetic predisposition (African americans)
classically affects earlobes, face, and upper extremities

neuro (18 decks)

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