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STEP 2: Inflammation PATHOMA > ACUTE INFLAMMATION > Flashcards

ACUTE INFLAMMATION Flashcards

1
Q

What are the 2 main stimuli of acute inflammation?

A

INFECTION

TISSUE NECROSIS

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2
Q

What is the most typical pathogen associated molecular pattern (PAMP) recognized by macrophages? What does this response activate?

A

CD14 (on macrophage surface) recognizes LPS PAMP of all Gm- bacteria outer surface

Activates TOLL-LIKE RECEPTOR (on dendritic cells/macrophages)

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3
Q

Which nuclear Tx factor is activated with Toll-like receptor (TLR) activation from PAMP? What does this result in?

A

NF-kappaB (RANK) activated with PAMP-mediated TLR activation

Results in upregulation of multiple immune response mediators

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4
Q

Which prostaglandin specifically mediates fever and pain?

A

PGE2

pgE2 = fEver (EEEE)

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5
Q

Which leukotriene attracts and activates neutrophils?

A

LTB4

B4 - Neutrophils BEFORE other immune system players

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6
Q

What are the 4 key mediators of attracting and activating neutrophils?

A

LTB4
IL-8
C5a
Bacterial products

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7
Q

What is the general principle of action of LTC4, LTD4, LTE4?

A

Smooth muscle contraction - vasoconstriction (arteriolar SM) bronchospasm (bronchus SM), Increased vascular permeability (Pericyte SM)

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8
Q

What are the 3 main stimuli of mast cell activation?

A
  1. Tissue Trauma
  2. Cross-linking of cell-surface IgE by Ag on mast cell
  3. Complement proteins C3a and C5a
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9
Q

What is the IMMEDIATE response of mast cell activation?

A

Release of pre-formed histamine granules:
1. ARTERIODILATION
2. INCREASED VASCULAR PERMEABILITY OF POST-CAPILLARY VENULE
Same actions as Prostaglandins

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10
Q

What is the DELAYED response of mast cell activation?

A

Production of arachidonic acid metabolites (particularly LTB4, LTC4/LTD4/LTE4)

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11
Q

Several hours later, an acute inflammatory response continues in a pt with mast cell activation What is the predominant mechanism for which the acute inflammatory response will progress?

A

ARACHIDONIC ACID (LEUKOTRIENES) PRODUCTION

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12
Q

What are the 5 key mediators of ACUTE INFLAMMATION?

A
  1. Toll-like receptors (TLR)
  2. Arachidonic acid metabolites (COX and LIPOXYGENASE)
  3. Mast cells
  4. Complement
  5. Hageman factor (FXII)
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13
Q

What are the 3 pathways of complement activation?

A
  1. CLASSICAL PATHWAY (C1 Binds to IgG or IgM)
  2. ALTERNATIVE PATHWAY (Microbial products directly activate complement)
  3. MANNOSE-BINDING LECTIN (MBL) PATHWAY (MBL binds mannose of micro-organisms)
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14
Q

END result of all pathways of complement activation:

A

C3 convertase: C3 conversion into C3a + C3b
C3b joins to form C5 convertase: C5 conversion into C5a + C5b
C5 joints C6-C9 to form MAC (membrane attack complex)

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15
Q

What are the 2 key complement proteins that activate mast cell degranulation?

A

C3a + C5a = ANAPHYLATOXINS

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16
Q

What is the complement protein that attracts and activates neutrophils?

A

C5a

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17
Q

What is the complement protein that acts as an opsonin for phagocytosis?

A

C3b

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18
Q

Which complement proteins does MAC consist of?

A

C5bC6-9

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19
Q

What are the two mediators of pain? (Hint: Prostaglandin and hormone)

A

PGE2 + Bradykinin

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20
Q

What pathology is associated with Gm- bacteria and Factor XII?

A

DIC

21
Q

Describe the pathophysiology of Gm-bacterial sepsis resulting in DIC.

A

Gm-bacteria -> Activation of Factor XII -> Activation of coagulation + fibrinolytic pathway -> DIC

22
Q

What pathways are activated by Factor XII in acute inflammation?

A
  1. Coagulation + Fibrinolytic Pathway
  2. Complement
  3. Kinin pathway - Kinin cleaves HMWKininogen -> Bradykinin
23
Q

What are the actions of bradykinin?

A

All of what histamine does (arteriodilation + increased vascular permeability in post-capillary venule) + Pain

24
Q

What are the 3 key mediators of REDNESS (RUBOR) and WARMTH (CALOR)? Which is the primary mediator?

A

Due to arteriodilation-mediated increase in blood flow

  1. PG (especially PGI2, PGD2, PGE2)
  2. HISTAMINE** PRIMARY mediator
  3. BRADYKININ (always think with histamine)
25
Q

What are the 2 key mediators of SWELLING (tumor)?

A
  1. HISTAMINE - Causes endothelial cell CONTRACTION

2. TISSUE DAMAGE - Actually DISRUPTS the endothelial cells

26
Q

What are the key mediators of PAIN?

A

Bradykinin + PGE2

27
Q

What is the key mediator of FEVER? Describe the molecular process that causes fever with exposure to PYROGENS (e.g. Bacterial LPS)

A

PYROGEN (e.g. LPS) -> Recognized by **MACROPHAGES -> Release IL-1 + TNF-a -> Enter hypothalamus perivascular cells -> Increases COX activity -> Increases PGE2 -> Raises temperature setpoint = FEVER

28
Q

What two selectins are upregulated on endothelial cells during neutrophil rolling?

A

P-selectin

E-selectin

29
Q

What do Weibel-Palade bodies release? What is the stimulus for their release?

A

W - vWF
P - P-selectin

Histamine stimulates this release

30
Q

What induces E-selectin expression on endothelial cells to mediate neutrophil rolling?

A

TNF-alpha + IL-1 (Same mediators released by macrophages for FEVER)

31
Q

What do P-selectin and E-selectin on the endothelial cells bind to to mediate the slowing down of neutrophil rolling?

A

SELECTINS (on endothelial cells) bind SIALYL LEWIS X (on neutrophil and macrophage surface)

32
Q

What is the pathology related to DEFECTIVE NEUTROPHIL ADHESION?

A

LEUKOCYTE ADHESION DEFICIENCY: Autosomal recessive defect of CD18 subunit on integrin (expressed on neutrophil) - Can NOT bind ICAM/VCAM (expressed on endothelial cell)

33
Q

What is the inheritance pattern of LEUKOCYTE ADHESION DEFICIENCY?

A

AR - CD18 subunit of integrins on leukocyte

34
Q

What are the 3 clinical features of LEUKOCYTE ADHESION DEFICIENCY? (Hint: one finding in infancy, finding in CBC, another with infection)

A
  1. DELAYED UMBILICAL CORD SEPARATION: At birth, umbilical cord is dead -> Tissue necrosis -> Acute inflammation -> Insufficient neutrophils -> Delayed separation
  2. INCREASED CIRCULATING NEUTROPHILS (Shift of marginated pool to free pool of neutrophils)
  3. RECURRENT BACTERIAL INFECTION with NO PUS (dead neutrophils in tissue)
35
Q

What are two opsonins that enhance phagocytosis by recognition?

A

IgG + C3b

36
Q

What is the pathology of a MT protein trafficking defect that impairs phagolysosome formation for phagocytosis?

A

CHEDIAK-HIGASHI SYNDROME

37
Q

What is the inheritance pattern of CHEDIAK-HIGASHI SYNDROME?

A

Autosomal Recessive

38
Q

What are the key 6 features of CHEDIAK-HIGASHI SYNDROME

A
  1. PYOGENIC INFECTIONS - Impaired phagolysosome production
  2. NEUTROPENIA - Ineffective division
    3-4. GIANT FUSED GRANULES next to GOLGI in leukocytes/DEFECTIVE PRIMARY HEMOSTASIS - Defective trafficking of granules from Golgi/ in PLT
    5-6. ALBINISM/ PERIPHERAL NEUROPATHY - Defective railroad track
39
Q

What is the most effective mechanism of destructing phagocytosed material?

A

O2 dependent killing

40
Q

What is CHRONIC GRANULOMATOUS DISEASE (CGD)? Inheritance pattern?

A

Defect in NADPH Oxidase - Xlinked or AR

41
Q

Which infections are CGD pts most susceptible to?

A 
Pseudomonas cepacia 
S.aureus 
Serratia
Nocardia
Aspergillus
42
Q

What is the screening test for CGD? What is a positive result?

A

NITROBLUE TETRAZOLIUM TEST
-CGD (Effective NAPDH oxidase): Yes O2- produced, Turns NBT Dye BLUE
+CGD (Deficient NADPH oxidase): No O2- produced, NBT dye remains COLORLESS

Positive result (+CGD) = COLORLESS

43
Q

What infections are MPO deficiency pts most susceptible to?

A

CANDIDA INFECTIONS

44
Q

What result will MPO Deficiency pts have with the NITROBLUE TETRAZOLIUM TEST?

A

Negative Test: Since oxidative burst generation of O2- from O2 is still intact (O2- can still convert NBT to blue)
MPO Deficiency: Can not convert H2O2 to bleach (HOCl)

45
Q

How do NEUTROPHILS resolve within the tissue?

A

DIE/APOPTOSIS within 24hrs - resulting in PUS

46
Q

What is the primary mechanism of destruction of phagocytosed material in NEUTROPHILS? How about in MACROPHAGES?

A

Neutrophils - O2 DEPENDENT (NADPH oxidase, SOD, MPO) to produce bleach
Macrophages - O2 INDEPENDENT killing (LYSOZYME** in secondary granules of macrophages and major basic protein in eosinophils)

47
Q

What are the two anti-inflammatory cytokines produced by macrophages that mediate resolution and healing?

A

IL-10 + TGF-beta

48
Q

Pt presents with coughing up pus for the past 8 weeks. Is this inflammation acute or chronic?

A

ACUTE INFLAMMATION

Remember that acute inflammation is not defined by the time but by the response- EDEMA and NEUTROPHILIC PUS!

49
Q

What are the 4 possible outcomes of MACROPHAGE RESPONSE?

A
  1. Good Job to neutrophils! Resolution and healing by producing anti-inflammatory cytokines (IL-10, TGF-b)
  2. Not good enough neutrophils CONTINUED ACUTE INFLAMMATION- Produce IL-8 to attract/activate more neutrophils
  3. Let’s wall off! - Abscess formation
  4. Really not good enough neutrophils! Need something more - Macrophages present Ag on MHC Class II to CD4+ Tcells for chronic inflammation

STEP 2: Inflammation PATHOMA (4 decks)

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