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pathoma > Pathoma Inflammation, inflammatory disorders, wound healing > Flashcards

Pathoma Inflammation, inflammatory disorders, wound healing Flashcards

1
Q

Inflammation allows what to happen?

A

Inflammatory cells, plasma proteins, and fluid to exit from vessel to enter interstitial space

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2
Q

Cells seen in acute inflammation

A

Neutrophil

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3
Q

Cells in chronic inflammation

A

Lymphocytes

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4
Q

Acute inflammation characterized by

A

Edema and neutrophils

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5
Q

Acute inflammation arises in response to what 2 things

A

Infection or tissue necrosis - eliminate pathogen or clear necrotic debris

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6
Q

What is included in innate immunity

A

epithelium, mucus secreted by cells, complement system, cells (mast, macrophages, neutrophils, eosinophils, basophils)

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7
Q

Acute inflammation mediated by what factors?

A

TLRs: present on cells of innate immunity

AA: from phospholipase A2 (acted on by COX/5-lipooxygease)

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8
Q

What do TLRs recognize?

A

PAMPs - pathogen associated molecular patterns

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9
Q

What TLR is found on macrophages and recognizes LPS on outer membrane of G- bacteria

A

CD14

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10
Q

TLR activation results in upregulation of?

A

NF-kappaB

activates immune response genes

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11
Q

COX pathway produces what?

A

PG
I2, D2, E2
Mediate vasodilation (arteriole) and vascular permeability (post-capillary venule)

E2 - also mediates fever and pain

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12
Q

5-lipooxygenase produces?

A

LT
B4 - attracts and activates neutrophils

C4, D4, E4 - vasoconstriction, bronchospasm, increased vascular permeability - contract smooth muscle

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13
Q

What attracts/activates neutrophils?

A

LTB4, C5A, IL8, bacterial products

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14
Q

mast cells activated by

A

tissue trauma
complement proteins C3a, C5a
Crosslinking of cell surface IgE by antigen

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15
Q

what does histamine do

A

mediates vasodilation of arterioles and increase vascular permeability

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16
Q

Delayed response of mast cell

A

production of AA metabolites - leukotrienes to maintain inflammatory response

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17
Q

Complement for acute inflammation activation

A 
classical pathway (C1) binds IgG/IgM bound to antigen 
"GM makes classic cars"

alternative pathway - microbial products directly activate complement

mannose binding lectin pathway - MBL binds mannose on microorganisms and activates complement.

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18
Q

complement pathways result in

A

C3 convertase: C3 - C3a/b which activates
C5 convertase: C5 - C5a/b which creates formation of MAC
Binds with C6-9 to form MAC complex

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19
Q

C3a and C5a trigger what?

A

Mast cell degranulation

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20
Q

C5a is chemotactic for what?

A

neutrophils

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21
Q

C3b action

A

opsonin for phagocytosis

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22
Q

MAC complex does what?

A

Lyses microbes by creating holes in cell membrane

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23
Q

Hageman Factor

A

Activated up subendothelial or tissue collage

Produced in liver - important role in DIC (Gram - Sepsis)

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24
Q

What does Hegeman factor activate?

A

Coagulation and fibrinolytic systems
Complement
Kinin system (cleave HMWK to bradykinin - mediates vasodilation, vascular permeability, pain

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25
Q

Cardinal signs of inflammation

A

Rubor, calor, tumor, swelling, dolor, fever

Redness - d/t vasodilation (arteriole) resulting in increased blood flow

Relaxation of arteriolar smooth muscle

Leakage of fluid from postcapillary venules

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26
Q

Key mediators of rubor and color

A

Histamine, PG, bradykinin

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27
Q

Key mediators of swelling (tumor)

A

histamine, tissue damage

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28
Q

Key mediators of pain

A

Bradykinin and PGE2 by sensitizing nerve endings

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29
Q

Key mediators of fever

A

Pyrogens cause macrophages to release IL-1 & TNF

Increase in COX (perivascular cells of hypothalamus)

PGE2 - raise temp set point

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30
Q

Neutrophil phase peaks at what time?

A

24 hours

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31
Q

Macrophage phase peaks at what time?

A

2-3 days

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32
Q

Step 1 of neutrophil arrival

A

Margination

Vasodilation slows blood flow in postpapillary venule
Cells marginate from center to periphery

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33
Q

Step 2 of neutrophil arrival

A

Rolling

Selectin - speed bumps upregulates

P selectin from Weibel Palade bodies (histamine)

E selectin by TNF and IL-1

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34
Q

Where does P selectin come from

A

Weibel Palade bodies

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35
Q

What are 2 key proteins from Weibel Palade body

A

vWF

P selectin

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36
Q

E selectin induced by

A

TNF & IL-1

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37
Q

What do selectins bind?

A

Sialyl Lewis X on leukocytes - results in rolling of leukocytes along vessel wall

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38
Q

Step 3 of neutrophil arrival

A

Adhesion

binding to wall by cellular adhesion molecules (upregulated by TNF and IL-1)

Bind integrins on leukocytes (upregulated by C5a, LTB4)

Results in firm adhesion to vessel wall

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39
Q

Leukocyte adhesion deficiency

A

CD18 subunit
Ar defect integrin - can’t be drawn into tissue

Delayed separation of umbilical cord - (normally neutrophils destroy tissue to allow separation)
Increased circulating neutrophils
Recurrent bacterial infections that lack pus formation (pus is dead neutrophils)

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40
Q

Step 4 neutrophil arrival

A

Transmigration and chemotaxis

Leukocyte transmigrate across endothelium of postcapillary venule

Move toward chemical attractants (C5a, LTB4, bacterial products, IL-8)

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41
Q

Step 5 neutrophil arrival

A

Phagocytosis

Enhanced by opsonins (IgG & C3b)

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42
Q

Chediak Higashi Syndrome

A

Protein trafficking defect - impaired phagolysosome formation (microtubule defect so can’t merge phagosome + lysosome)

  1. Increased risk pyogenic infection
  2. Neutropenia - (can’t divide properly)
  3. Giant granules in leukocytes (can’t be moved)
  4. Defective primary hemostasis - dependent on platelets - granules not properly distributed
  5. Albinism
  6. Peripheral neuropathy - can’t move proteins from nucleus to nerves
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43
Q

Step 6 of neutrophil arrival

A

Destrocion of phagocytosed material

O2 dependent

  • most effective
  • HOCl generated by oxidative burst in phagolysosomes

O2 independent
- enzyme present in leukocytes

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44
Q

Which is more effective? O2 dependent or independent killing?

A

O2 dependent

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45
Q

O2 - to O2.- to H2O2 to HOCl

A

O2 to O2.- by NADPH oxidase
O2.- to H2O2 by superoxide dismutate
H2O2 to HOCl (bleach) by myeloperoxidase

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46
Q

CGD (chronic granulomatous dz)

A

poor O2 dependent killing
D/T NADPH oxidase defect

can’t generate bleach: granuloma infections with catalase + organisms

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47
Q

Catalase + organism associated with CGD (chronic granulomatous dz)

A

Catalase destroys H2O2 so can’t produce bleach

S aureus
Pseudomonas cepacia

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48
Q

Test to screen for CGD?

A

Nitroblue tetrazolium

Is O2 to O2.- intact by NADPH oxidase? NO - dye remains colorless

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49
Q

MPO deficiency

A

can’t produce bleach but most pt will be asymptomatic

Increase risk in candida infections

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50
Q

what will happen in NBP (nitroblue tetrazolium) test in MPO deficiency?

A

It will turn blue because the O2 to O2.- reaction is intact

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51
Q

Step 7 neutrophil arrival

A

Resolution

Neutrophil undergoes apoptosis

Disappear within 24 hours after resolution of inflammatory stimulus

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52
Q

Monocytes arrive how?

A

Same as neutrophils:

margination, rolling, adhesion, transmigration

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53
Q

What is primary enzyme in macrophages?

A

Lysozyme

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54
Q

What are anti-inflammatory cytokines?

A

IL-10 and TGF-beta

55
Q

What cytokine continues inflammation?

A

IL-8 - macrophages call in neutrophils

56
Q

Does time or response define acute inflammation?

A

RESPONSE - IL-8 Secreted calling more macrophages, production of pus

57
Q

What characterizes chronic inflammation

A

Lymphocytes and plasma cells in tissue

58
Q

CD4+ T cell actiavtion

A

Extracellular antigen phagocytosed, processed, presented to MCH class II

B7 on APC binds CD28 on CD4+ T cells providing 2nd activation signal
28/7=4

59
Q

What do CD4+ T cells secrete?

A

cytokines

TH1: IL-2 (T cell GF and CD8+ T cell activator) INF- gamma (marcophages activator)

TH2: B cells
IL-4 - class switching to IgG and IgE
IL-5 - eosinphilia chemotaxis and activation, maturation of B cells to plasma cells, class switching to IgA
IL-10 - inhibits TH1 phenotype
60
Q

CD8+ T cell activation

A

MHC I - intracelluar antigen

IL-2 from CD4+ TH1 cell produces 2nd activation signal

Cytotoxic T cells activated for killing (kill cell)

61
Q

CD8+ kills cells how?

A

Perforins & granzyme inducing apoptosis
(caspase is key mediator)

Express FasL bind Fas activating apoptosis

62
Q

B cell activation

A

Antigen binding by IgM or IgD

B cell antigen presentation to CD4+ helper T cell via MHC II

CD40 receptor on B cell binds CD40L on helper T cell providing 2nd activation signal

63
Q

Defining feature of granuloma

A

Epitheloid histocyte! macrophages with abundant pink cytoplasm

64
Q

Noncaseating granulomas lack what? and what are the causes

A

Central necrosis

Reaction to foreign material
Sacroidosis
Beryllium exposure
Crohn dz (noncaseating dz)
Cat scratch dz
65
Q

Differential dx for caseating granuloma

A

TB & FUNGAL

AFB for TB
GMS (silver stain) for Fungal infection

66
Q

Steps in granuloma formation

A

Macrophage and CD4+TH1 helper T cell interaction
Find antigen on present via MCH II
IL-12 secreted from macrophages -> CD4+ helper cells to TH1 subtype which secrete TNF-gamma to convert macrophages into epithelioid histocytes

67
Q

DiGeorge - failure of what pharyngeal pouches and what deletion?

A

3rd/4th pouch

22q11 microdeletion

68
Q

DiGeorge presents with what?

A

T cell deficiency d/t lack of thymus
Hypocalcemia d/t lack of parathyroids
Abnormalities of heart, great vessels, face

69
Q

SCID

What are the etiologies

A

defective cell mediated and humoral immunity

  1. cytokine receptor defects
  2. Adenosine deaminase deficiency*** (enzyme for deamination of adenosine and deoxyadenosine - build up is toxic to lymphocytes)
  3. MHC class II deficiency
70
Q

What enzyme is can be deficient in SCID?

A

Adenoside deaminase

71
Q

SCID characteristics

A

Fungal, viral, bacteria, protozal infection

Opportunistic infection & live vaccines

72
Q

SCID tx

A

Sterile isolation and stem cell transplant - can generate normal B & T cells

73
Q

X linked agammaglobulinemia

A

Lack Ig in blood - x linked

Disordered B cell maturation so Niave B cell can’t mature into plasma cels

74
Q

What is Bruton tyrosine kinase mutation associated with

A

X linked agammaglobinemia

Signal for B cell to become plasma cell normally

75
Q

X linked agammaglobulinemia presentation

A 
After 6 mo
Recurrent bacterial (can't opsonize), enterovirus (no IgA) and Giardia infections (no IgA)

Live vaccines must be avoided

76
Q

Common Variable Immunodeficieny (CVID)

A

Low immunoglobin d/t B cell or helper T cell defect

Risk for bacterial, enterovirus, Giardia late in childhoood

Increase risk for AI dz and Lymphoma

77
Q

Common Variable Immunodeficieny (CVID) has increased risk for what 2 things

A

Autoimmune

Lymphoma

78
Q

IgA def

A

Mucosal infection risk
Most asymptomatic
Celiac dz association

79
Q

Hyper IgM syndrome

A

Too much IgM
Mutation in CD40L or CD40 receptor (B cells)

Can’t produce IL4/IL5
Low IgA, IgG, IgE
Recurrent pyogenic infections especially at mucosal sites

80
Q

Wiskott Aldrich Syndrome Triad

A

Thrombocytopenia
Eczema
Recurrent Infections

81
Q

what is the defect in wiskott aldrich syndrome and inheritance?

A

WASP gene and X linked

82
Q

Complement deficiency

A

C5-C9 - at risk for Neisseria infection

C1 inhibitor - edema of skin and mucosal surfaces (called hereditary edema) - especially periorbital

83
Q

What is the etiology of autoimmune?

A

Loss of self tolerance

84
Q

Central tolerance occurs where?

A

Thymus & Bone marrow

Stem cells from bone marrow to thymus to Double + cells (CD4 & CD8 & T cell receptor) then turn to Single + cells which progress to niave mature T cells

Undergo check points

85
Q

DP+ cell undergo + or - selection?

A

+ selection
Need to recognize MHC and antigen
If they can recognize MHC they turn to SP+ cells

If not undergo apoptosis

86
Q

SP+ cell undergo + or - selection?

A
  • selection
    If recognize self antigen, they will undergo apoptosis

Remove self reactive lymphocytes

87
Q

Central tolerance in Thymus for t Cells

AIRE mutation results in?

A

AI polyendocrine syndrome - destroys endocrine glands

Can’t express some subset of self antigen so some self recognizing antigens escape and go into the periphery

  1. hypoparathyroidism
  2. Adrenal failure
  3. candida infection (chronic)
88
Q

Where does negative and positive selection occur in thymus?

A

Negative in medulla

Positive in cortex

89
Q

Central tolerance for B cells occurs where?

A

Bone marrow

Stem cell in bone marrow changes to immature (Ig) then escapes bone marrow to naive mature b cell

90
Q

If B cell recognizes self antigen what happens?

A

Ig - undergo
1. B cell receptor editing (Rag genes will be re-expressed and edit the light chain so won’t bind self antigen)
OR
2. undergo apoptosis thru mito pathway

91
Q

Peripheral tolerance

A

If central tolerance failed - then peripheral tolerance - antigen recognized without co-stimulatory signal - then lymphocyte will undergo anergy (shut down) or undergo apoptosis

92
Q

CD4+ T cell has CD95 present known as what?

A

FAS- expressed when recognizes self-antigen & binds FAS Ligand inducing apoptosis

93
Q

ALPS

AI Lymphoproliferative Syndrome

A

mutation in FAS apoptosis pathway

Need FAS, FAS L & caspases (particularly 10)

Can’t undergo apoptotic pathway so self reactive lymphocytes can survive

AI: IgG production (self reactive) - cytopenia, anemia
LP - can’t get rid of self reactive lymphocytes - so lymph node enlargement, HSM (can get lymphoma)

94
Q

Regulatory T cells: CD4+ T cells

A

Block T cell activation

Needs second signal - CTLA4 can bind B7 decreasing second signal so cell undergoes anergy

Cytokines - IL-10 & TGF-beta - IL10 inhibits macrophages/dendritic cell limiting TCR, limit B7, TGF-beta inhibits macrophages

95
Q

CD4+ CD25+ FOXP3+

Regulatory T cells

A

CD25+ = IL-2R

FOXP3+ transcription factor

96
Q

CD25 polymorphisms are related to?

A

AI (MS & DM1)

Essential for regulatory T Cells

97
Q

FOXP3 mutations related to?

A

IPEX
Immune dysfunction Polyendocrinopathy Enteropathy

Thryoiditis, DM1 (islet of pancreas), Diarrhea, Skin
X linked

98
Q

What might be the effect of estrogen on B cells?

A

decrease apoptosis

99
Q

AI gene associations

A 
HLA subtypes (code for MHC)
Strongest is HLA-B27 (anklyosising spondylitis)

PTPN22 - tyrosine phosphatase - gain of function decreasing signaling for tolerance

100
Q

2 ethnicities in LUPUS

A

Af Am/Hispanics

101
Q

What complement deficiency is associated with lupus?

A

Early complement
C1a, C4, C2
*Most commonly C2

102
Q

what are the 11 criteria of Lupus?

* is a characteristic but not diagnostic

A
  1. Malar “butterfly” rash
  2. Discoid rash - circle, erythematous, scaling - scars
  3. Rash upon exposure to sunlight
  4. Oral/nasopharyngeal ulcers
  5. Arthritis
  6. Serositis
  7. Psychosis/seizures
  8. Renal damage (Most common/most damaging - Diffuse proliferative glomerulonephritis or membranous glomerulonephritis)
  9. Antibodies to cells in blood: anemia, thrombocytopenia, leukopenia (Type II specifically even though Lupus is type III Hypersensitivity)
    * Libman-sacks endocarditis - small vegetations of both sides of mitral valve
  10. Antinuclear antibodies
  11. Anti-dsDNA or Anti-Sm antibodies/Antiphospholipid Ab
103
Q

what are the 3 antiphospholipid antibodies generally tested?

A 
Anticardiolipin (False + VDRL & RPR - false positive for Syphillis)
Lupus anticoagulant (falsely elevates PTT test) 
Anti-Beta2-glycoprotein I
104
Q

APA syndrome

A

Anitphospholipid antibody + hypercoagulable state
DV, hepatic vein, placental, cerebral thrombosis
Requires lifelong anticoagulant

105
Q

Drug induced Lupus causing drus + antibody

A

Hydralazine, procainamide, isoniazid

ANA+

106
Q

Most common causes of death in Lupus

A

Renal failure and infection

  1. from immunosuppressions
  2. antibodies to WBC
107
Q

Late common cause of death in Lupus

A

Accelerated coronary atherosclerosis

108
Q

Sjrogren syndrome - destruction of what glands?

A

lacrimal - dry eyes
salivary glands - dry mouth/dental caries

Type IV hypersensitivity

109
Q

Antibodies in sjrogen syndrome

A

ANA
anti-ribonucleoprotein (anti-SSA/SSB) - related to extraglandular associations
SSA can cross placenta and develop neonatal lupus

110
Q

Neonatal lupus - develop what condition?

A

Heart block

111
Q

Additional diagnostic criteria for Sjrogen - what biopsy and what are you looking for?

A 
Lymphocytic sialadenitis
(on lip biopsy of minor salivary glands)
112
Q

Increase risk of what cancer with Sjrogens

A

B cell lymphoma

113
Q

Systemic sclerosis - sclerodoma

A

Deposition of collagen by fibroblasts

114
Q

Limited scleroderma has limited skin involvement

What does CREST mean?

A 
C:alcinosis/anti-Centromere bodies
R:aynaud
E:sophageal dysmotility
S:clerodactyly
T:elangiectasias of skin
115
Q

Diffuse type scleroderma

A

Early visceral involvement

Vessels
GI 
Lungs
Kidney
Heart
DNA topo 1 antibodies
116
Q

Wound healing beings when?

A

Initiated when inflammation beings

Regeneration or repair (scarring)

117
Q

What are the 3 types of regenerative capacity?

A

Labile - continuously regenerating = stem cells
(BONE: CD34 hematopoietic stem cell)
Stable - quiescent (Go - re-enter cell cycle)
Permanent - lack significant regenerative potential

118
Q

What are the permanant tissues in the body?

A

Myocardium
Skeletal muscle
Neurons

119
Q

Repair places damage with?

A

fibrous scar

120
Q

What is the initial phase of repair?

A

Granulation tissue…

Firborblasts (deposit collagen type III)
Capallaries
Myofibroblasts

121
Q

In a scar what collagen replaces the initial collage III deposition?

A

Collagen I removed by collegenase (requires Zn cofactor)

122
Q

Collagen I

A

Bone
B”one”
Strong tensile strenght

123
Q

Collagen II

A

Cartilage

Car”two”lage

124
Q

Collagen III

A

pliable

BV, granulation tissue, embryonic tissue

125
Q

Collagen IV

A

Basement membrane

126
Q

What type of signaling mediates regeneration and repair?

A

Paracrine signlaing by GR

127
Q

TFG-alpha

A

epithelial and fibroblast GF

128
Q

TGF-beta

A

fibroblast GF

Inhibits inflammation

129
Q

PDGF

A

endotheilum, SM, fibroblast GF

130
Q

FGF

A

angiogensis

Skeletal development

131
Q

VEGF

A

angiogenesis

132
Q

Secondary intention of wound healing

A

Granulation tissue fills in defect so scar will from

Cause contraction of wound - by myofibroblasts

133
Q

Most common cause of delayed wound healing

A

Infection

Less common:
Vit C, Copper, Zn def
Foreign body, ischemia, diabetes, malnutrition

pathoma (12 decks)

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