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Aaron-Exit: Championship Rounds > Pathoma Chapter 2A > Flashcards

Pathoma Chapter 2A Flashcards

1
Q

What does inflammation allow?

A

Allows inflammatory cells, plasma proteins (e.g., complement), and fluid to exit blood vessels and enter the interstitial space

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2
Q

Inflammation is divided into what?

A

Divided into acute and chronic inflammation

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3
Q

What is inflammation characterized by?

A

the presence of edema and neutrophils in tissue

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4
Q

Inflammation arises in response to what?

A

infection (to eliminate pathogen) or tissue necrosis (to clear necrotic debris)

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5
Q

innate immunity

A

Immediate response with limited specificity

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6
Q

What are the mediators of acute inflammation?

A

Toll-like receptors, Arachidonic acid (AA) metabolites, Mast cells, Complement, Hageman Factor

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7
Q

Toll-like receptors

A

Present on cells of the innate immune system (e.g., macrophages and dendritic cells)

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8
Q

How are TLRs attivated?

A

pathogen-associated molecular patterns (PAMPs) that are commonly shared by microbes, CD14 (a TLR) on macrophages recognizes lipopolysaccharide (a PAMP) on the outer membrane of gram-negative bacteria

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9
Q

TLR activation results in what?

A

upregulation of NF-kB, a nuclear transcription factor

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10
Q

What does NF-kB do?

A

activates immune response genes leading to production of multiple immune mediators

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11
Q

TLRs and chronic inflammation?

A

They are also present on cells of adaptive immunity (e.g., lymphocytes) and play an important role in mediating chronic inflammation.

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12
Q

Arachidonic acid (AA) metabolites

A
  1. AA is released from the phospholipid cell membrane by phospholipase A2 and then acted upon by cyclooxygenase or 5-lipoxygenase.
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13
Q

Cyclooxygenase

A

produces prostaglandins (PG) a. PGI2, PGD2 and PGE2 mediate vasodilation and increased vascular permeability. PGE2 also mediates pain.

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14
Q

5-lipoxygenase

A

produces leukotrienes (LT) a. LTB4 attracts and activates neutrophils. b. LTC4, LTD4 and LTE4 (slow reacting substances of anaphylaxis) mediate vasoconstriction, broncho spasm, and increased vascular permeability.

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15
Q

Where are Mast cells located?

A
  1. Widely distributed throughout connective tissue
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16
Q

How are Mast cells activated?

A

(1) tissue trauma (2) complement proteins C3a and C5a (3) cross-linking of cell-surface IgE by antigen

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17
Q

Mast cells immediate response is?

A

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

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18
Q

Mast cells delayed response is?

A

involves production of arachidonic acid metabolites, particularly leukotrienes.

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19
Q

Complement

A

proinflammatory serum proteins that complement inflammation

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20
Q

Where is complement located?

A

Circulate as inactive precursors;

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21
Q

Activation of complement occurs via what?

A

Classical pathway, Alternative pathway, MBL pathway

22
Q

Classical pathway

A

C1 binds IgG or IgM that is bound to antigen

23
Q

Alternative pathway

A

Microbial products directly activate complement.

24
Q

Mannose binding lectin pathway

A

mannose binding lectin (MBL) pathway MBL binds to mannose on microorganisms and activates complement

25
Q

All pathways of complement result in?

A

production of C3 convertase (mediates C3?>C3a and C3b, producing C5 convertase (mediates C5?>C5a and C5b)

26
Q

What forms the MAC?

A

C5b complexes with C6-C9 to form the membrane attack complex (MAC)

27
Q

C3a and C5a

A

(anaphylatoxins)?trigger mast cell degranulation, resulting in histamine-mediated vasodilation and increased vascular permeability

28
Q

C5a

A

chemotactic for neutrophils

29
Q

C5b

A

opsonin for phagocytosis

30
Q

MAC

A

Lyses microbes by creating a hole in the cell membrane

31
Q

Where is Hageman factor (Factor XII) produced?

A

Inactive proinflammatory protein produced in liver

32
Q

How is Hageman factor (Factor XII)?

A

Activated upon exposure to subendothelial or tissue collagen;

33
Q

Hageman factor (Factor XII) activates what?

A
  1. Coagulation and fibrinolytic systems 2. Complement 3. Kinin system
34
Q

Kinin system

A

Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin, which mediates vasodilation and increased vascular permeability (simitar to histamine), as well as pain.

35
Q

What are the cardinal signs of inflammation?

A

Redness (rubor) and warmth (calor), swelling, pain, fever

36
Q

What is Redness (rubor) and warmth (calor) due to?

A
  1. Due to vasodilation, which results in increased blood flow
37
Q

How does Redness (rubor) and warmth (calor) occur?

A

Occurs via relaxation of arteriolar smooth muscle;

38
Q

Key mediators of Redness (rubor) and warmth (calor) are?

A

histamine, prostaglandins, and bradykinin

39
Q

Swelling (tumor) is due to what?

A

Due to the leakage of fluid from postcapillary venules into the interstitial space (exudate)

40
Q

What are the Key mediators of swelling?

A

(1) histamine, which causes endothelial cell contraction and (2) tissue damage, resulting in endothelial cell disruption,

41
Q

Pain (dolor)

A

Bradvkinin and PGE2 sensitize sensory nerve endings.

42
Q

Fever

A
  1. Pyrogens (e.g., LPS from bacteria) cause macrophages to release IL-1 and TNF, which increase cyclooxygenase activity in perivascular cells of the hypothalamus, 2. Increased PGE2 raises temperature set point.
43
Q

What are the steps in neutrophil arrival?

A

Margination, Rolling, Adhesion, Transmigration and Chemotaxis, Phagocytosis, Destruction of phagocytosed material, resolution

44
Q

Step 1?Marginatum

A
  1. Vasodilation slows blood flow in postcapillary venules. 2. Cells marginate from center of flow to the periphery.
45
Q

Step 2?Rolling

A
  1. Selectin speed bumps are upregulaled on endothelial cells. 2. Selectins bind sialyl Lewis X on leukocytes. 3. Interaction results in rolling of leukocytes along vessel wall
46
Q

P-selectin is released from where and what does it mediate?

A

release from Weibel Palade bodies, is mediated by histamine.

47
Q

E-selectin is induced by what?

A

TNF and IL-1.

48
Q

Step 3?Adhesion

A
  1. Cellular adhesion molecules (ICAM and VCAM) are upregulated on endothelium by TNF and IL-1 2. Integrins are upregulated on leukocytes by C5a and LTB4 3. Interaction between CAMs and integrins results in firm adhesion of leukocytes to the vessel wall
49
Q

Leukocyte adhesion deficiency

A

is most commonly due to an autosomal recessive defect of integrins (CD18 subunit)

50
Q

What are the clinical features of LAD?

A

delayed separation of the umbilical cord, increased circulating neutrophils (due to impaired adhesion of marginated pool of leukocytes), and recurrent bacterial infections that lack pus formation.

Aaron-Exit: Championship Rounds (27 decks)

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