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STEP 2: Inflammation PATHOMA > ACUTE INFLAMMATION > Flashcards

ACUTE INFLAMMATION Flashcards

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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?

21
Q

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

Study These Flashcards
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?

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

What are the actions of bradykinin?

Study These Flashcards
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?

Study These Flashcards
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
What are the 2 key mediators of SWELLING (tumor)?
1. HISTAMINE - Causes endothelial cell CONTRACTION | 2. TISSUE DAMAGE - Actually DISRUPTS the endothelial cells
26
What are the key mediators of PAIN?
Bradykinin + PGE2
27
What is the key mediator of FEVER? Describe the molecular process that causes fever with exposure to PYROGENS (e.g. Bacterial LPS)
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
What two selectins are upregulated on endothelial cells during neutrophil rolling?
P-selectin | E-selectin
29
What do Weibel-Palade bodies release? What is the stimulus for their release?
W - vWF P - P-selectin Histamine stimulates this release
30
What induces E-selectin expression on endothelial cells to mediate neutrophil rolling?
TNF-alpha + IL-1 (Same mediators released by macrophages for FEVER)
31
What do P-selectin and E-selectin on the endothelial cells bind to to mediate the slowing down of neutrophil rolling?
SELECTINS (on endothelial cells) bind SIALYL LEWIS X (on neutrophil and macrophage surface)
32
What is the pathology related to DEFECTIVE NEUTROPHIL ADHESION?
LEUKOCYTE ADHESION DEFICIENCY: Autosomal recessive defect of CD18 subunit on integrin (expressed on neutrophil) - Can NOT bind ICAM/VCAM (expressed on endothelial cell)
33
What is the inheritance pattern of LEUKOCYTE ADHESION DEFICIENCY?
AR - CD18 subunit of integrins on leukocyte
34
What are the 3 clinical features of LEUKOCYTE ADHESION DEFICIENCY? (Hint: one finding in infancy, finding in CBC, another with infection)
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
What are two opsonins that enhance phagocytosis by recognition?
IgG + C3b
36
What is the pathology of a MT protein trafficking defect that impairs phagolysosome formation for phagocytosis?
CHEDIAK-HIGASHI SYNDROME
37
What is the inheritance pattern of CHEDIAK-HIGASHI SYNDROME?
Autosomal Recessive
38
What are the key 6 features of CHEDIAK-HIGASHI SYNDROME
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
What is the most effective mechanism of destructing phagocytosed material?
O2 dependent killing
40
What is CHRONIC GRANULOMATOUS DISEASE (CGD)? Inheritance pattern?
Defect in NADPH Oxidase - Xlinked or AR
41
Which infections are CGD pts most susceptible to?
``` Pseudomonas cepacia S.aureus Serratia Nocardia Aspergillus ```
42
What is the screening test for CGD? What is a positive result?
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
What infections are MPO deficiency pts most susceptible to?
CANDIDA INFECTIONS
44
What result will MPO Deficiency pts have with the NITROBLUE TETRAZOLIUM TEST?
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
How do NEUTROPHILS resolve within the tissue?
DIE/APOPTOSIS within 24hrs - resulting in PUS
46
What is the primary mechanism of destruction of phagocytosed material in NEUTROPHILS? How about in MACROPHAGES?
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
What are the two anti-inflammatory cytokines produced by macrophages that mediate resolution and healing?
IL-10 + TGF-beta
48
Pt presents with coughing up pus for the past 8 weeks. Is this inflammation acute or chronic?
ACUTE INFLAMMATION | Remember that acute inflammation is not defined by the time but by the response- EDEMA and NEUTROPHILIC PUS!
49
What are the 4 possible outcomes of MACROPHAGE RESPONSE?
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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