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Basics of Path > Inflammation, Inflammatory Disorders, and Healing > Flashcards

Inflammation, Inflammatory Disorders, and Healing Flashcards

1
Q

What is the main inflammatory cell involved in acute inflammation?

A

Neutrophils (polys)

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2
Q

What are the two main stimuli of acute inflammation?

A

Infection and tissue necrosis

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3
Q

Acute inflammation is an _________ response with _______ specificity.

A
  1. Immediate

2. Limited (innate immunity)

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4
Q

Where are TLR’s found?

A

Macrophages and dendritic cells

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5
Q

CD14

A

A TLR on macrophages - recognizes LPS on the outer membrane of GN bacteria

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6
Q

TLR activation results in upregulation of ______

A

NF-kB

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7
Q

True or False: TLRs are only present on cells of innate immunity.

A

False. TLRs are present on lymphocytes and play a role in mediating chronic inflammation as well.

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8
Q

Cyclooxygenase acts on arachidonic acid to generate what? What do these mediate?

A

PGI2, PGD2, PGE2 - vasodilation (arteriole) and inc. vasc. perm (post. cap venule)
PGE2 - fever and pain

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9
Q

5-lipooxygenase acts on AA to produce what? What do these mediate?

A

LTB4 - attracts/activates neutrophils

LTC4, LTD4, LTE4 - vasoconstriction, bronchospasm, and inc. vasc. perm

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10
Q

What are the 4 key mediators that attract and activate neutrophils?

A
  1. LTB4
  2. C5a
  3. IL-8
  4. Bacterial products
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11
Q

Mast cells are activated by which 3 things?

A
  1. Tissue trauma
  2. C3a and C5a
  3. Cross-linking of cell-surface IgE by antigen
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12
Q

Once activated, mast cells release ___________, that mediates _____________ and _________________.

A
  1. Histamine granules
  2. Vasodilation of arterioles
  3. Inc. vasc. perm at post. cap venule
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13
Q

What is the delayed response of mast cells?

A

Production of AA metabolites – leukotrienes

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14
Q

Classical complement pathway

A

C1 binds to IgG or IgM that is bound the antigen

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15
Q

Alternative complement pathway

A

Microbial products directly activate complement

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16
Q

Mannose-binding lectin pathway

A

MBL binds mannose on microorganisms and activates complement

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17
Q

What is the result of the activation of complement?

A
  1. C3 convertase
  2. C5 convertase
  3. Formation of MAC
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18
Q

What role does C3b play?

A

Opsonin for phagocytosis

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19
Q

Hageman factor

A

Inactive proinflammatory protein made in liver - activated upon exposure to subendothelial or tissue collagen

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20
Q

What does Hageman factor activate? What can this cause?

A
  1. Coagulation and fibrinolytic system - DIC in GN sepsis
  2. Complement
  3. Kinin system –> bradykinin (VD, VP, pain)
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21
Q

What are the cardinal signs of inflammation?

A
  1. Redness & Warmth
  2. Swelling
  3. Pain
  4. Fever
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22
Q

What mediates redness and warmth?

A

VD of arteriole - histamine, PGI2, PGD2, PGE2, and bradykinin

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23
Q

What mediates swelling?

A

Leakage of fluid from postcap venule into interstitial space - histamine & tissue damage

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24
Q

What mediates pain?

A

Bradykinin and PGE2 - sensitize sensory nerve endings

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25
Q

What mediates fever?

A

Pyrogens cause macrophages to release IL-1 and TNF –> Inc. COX activity in perivascular cells of hypothal –> Inc. PGE2 raises temp set point

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26
Q

Margination

A

VD slows blood flow in postcap. venule – cells marginate from center of flow to periphery

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27
Q

Rolling

A

Endothelial cells upregulate selectin to slow down neutrophils

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28
Q

P-selectin

A

Released from Weibel-Palade bodies, mediated by histamine

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29
Q

E-selectin

A

Induced by TNF and IL-1

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30
Q

Selectins bind ____________ on leukocyte, which results in ________ of leukocytes along the vessel wall.

A
  1. Sialyl Lewis X

2. Rolling

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31
Q

Leukocytes

A

Neutrophils and macrophages

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32
Q

What upregulates cellular adhesion molecules and what do they bind?

A
  1. TNF and IL-1

2. Integrins on the leukocyte

33
Q

What triggers upregulation of integrins on the leukocytes?

A

LTB4 and C5a

34
Q

What interaction results in a firm adhesion between leukocytes and the endothelium?

A

Cellular adhesion molecules and integrins

35
Q

Leukocyte Adhesion Deficiency

A

Autosomal recessive defect of integrin (CD18) –>

Delayed separation of umbilical cord, inc. circ. neutrophils, recurrent bacterial infections that lack pus

36
Q

Leukocytes transmigrate across the endothelium of the ____________.

A

Post capillary venules

37
Q

Neutrophils are attracted by which 3 things?

A

IL-8, C5a, and LTB4

38
Q

Neutrophil phagocytosis is enhanced by which opsonins?

A

IgG and C3b

39
Q

How do neutrophils phagocytose necrotic cells and pathogens?

A

Pseudopods from leukocytes extend to form phagosomes which are internalized and merge with lysosomes –> phagolysosome

40
Q

Chediak-Higashi Syndrome

A

Protein trafficking defect - MT defect (ARec)

Inc. risk of pyogenic infection, neutropenia, giant granules in leukocytes, defective primary hemostasis, albinism, peripheral neuropathy

41
Q

How do neutrophils destroy phagocytosed material?

A
  1. O2 dependent

2. O2 independent

42
Q

O2-dependent killing

A

O2 converted to HOCl via oxidative burst to destroy organism - most effective mechanism

43
Q

What converts O2 to O2- (superoxide)?

A

NADPH oxidase - “Oxidative burst”

44
Q

What converts O2- (superoxide) to hydrogen peroxide?

A

Superoxide dismutase (SOD)

45
Q

What converts H2O2 to HOCl (bleach)?

A

Myloperoxidase (MPO)

46
Q

Chronic Granulomatous Disease

A

Poor O2-dependent killing - NADPH oxidase defect (X-linked or A. Rec.)

47
Q

What infections do pt w/ CGD typically get?

A 
Catalase-positive - 
S. Aureus
P. cepacia
Nocardia
Aspergillus
S. Marcescens
48
Q

Why are pts with CGD susceptible to catalase positive bacteria?

A

Catalase destroys bacterial H2O2 - can’t use it in lieu self-generated H2O2 (other bacteria produce some H2O2)

49
Q

Nitroblue tetrazolium test

A

Turns blue if NADPH can convert O2 to O2-

50
Q

What does a colorless nitroblue tetrazolium test indicate?

A

NADPH oxidase is defective - CGD

51
Q

DHR (Dihydrorhodamine) test for CGD preferred

A

Whole blood stained w/ DHR and stimulated to produce O2- which then oxidizes DHR to rhodamin

52
Q

MPO deficiency

A

Can’t produce bleach - asymptomatic - inc. risk for candida infections - NBT test is normal

53
Q

O2 independent killing

A

Less effective - occurs via enzymes present in leukocyte secondary granules e.g. lysozyme and major basic protein

54
Q

Neutrophils undergo _________ and disappear within _______ after resolution of inflammatory stimulus

A

Apoptosis

24 hours

55
Q

Macrophages peak ______ after inflammation begins.

56
Q

Monocytes arrive via the _________, rolling, adhesion, and ______________ sequence.

A
  1. Margination

2. Transmigration

57
Q

How do macrophages destroy material?

A
  1. Phagocytosis

2. O2 independent - enzymes in secondary granules - Lysozyme

58
Q

How do macrophages induce resolution and healing?

A

IL-10 and TGF-beta (anti-inflammatory)

59
Q

How do macrophages induce continued acute inflammation?

60
Q

Abscess formation

A

Macrophages create a wall of fibrosis around area of infection to wall off acute inflammation.

61
Q

Macrophages can call in _________________ by presenting on _______.

A
  1. Chronic inflammation

2. MCH II

62
Q

Chronic inflammation is characterized by what?

A

Presence of lymphocytes and plasma cells in tissue
Delayed
More specific - Adaptive

63
Q

What things stimulate chronic inflammation?

A
  1. Persistant infection
  2. Viruses, mycobacteria, parasites and fungi
  3. Autoimmune disease
  4. Foreign material
  5. Some cancers
64
Q

T cells develop in the ________ and undergo _______________ becoming CD4 and CD8 T cells.

A
  1. Thymus

2. TCR rearrangement

65
Q

Activation of CD4 T cells requires what 2 things?

A
  1. Extracellular antigen:MHC II

2. B7(APC):CD28(CD4)

66
Q

What 2 ways do CD8 T cells kill cells?

A
  1. Secrete perforins and granzyme

2. FasL expression to bind Fas on target cell

67
Q

Naive B cells express ____ and ____.

A

IgM and IgD

68
Q

What is the 2nd signal involved when B cells present to CD4 T cells?

A

CD40(Bcell):CD40L on T cell

69
Q

What are the 2 ways a B cell can be activated?

A
  1. IgM binds antigen

2. B-cell presents to CD4 w/ 2nd signal - IgG

70
Q

Granulomatous inflammation is characterized by a _________.

71
Q

What is the key cell that characterizes a granuloma?

A

Epitheloid histiocytes (Macrophages w/ abundant pink cytoplasm)

72
Q

What other things are seen in a granuloma

A

Giant cells w/ rim of lymphocytes

73
Q

Noncaseating granulomas lack ______________.

A

Central necrosis - cells all have their nuclei

74
Q

Noncaseating granulomas arise in reaction to what 5 things?

A
  1. Reaction to foreign material
  2. Sarcoidosis
  3. Beryllium exposure
  4. Crohn disease
  5. Cat scratch disease
75
Q

Caseating granulomas exhibit ___________ and are characteristic of ____ and _____________.

A
  1. Central necrosis
  2. TB (AFB stain)
  3. Fungal infections (GMS stain)
76
Q

How are granulomas formed?

A
  1. Macrophages present to CD4
  2. Macrophages secrete IL-12 –> Th1
  3. Th1 cells secrete IFN-gamma which converts the macrophages to epithelioid histiocytes and giant cells
77
Q

True or False: Both caseating and noncaseating granulomas are formed via the IL-12 from macrophages and IFN-gamma from Th1 cells?

78
Q

DiGeorge Syndrome

A

22q11 microdeletion - developmental failure of the 3rd and 4th pharyngeal pouches

Basics of Path (5 decks)

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