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Pathoma > Acute inflammation > Flashcards

Acute inflammation Flashcards

1
Q

Acute inflammation is characterized by the presence of what?

A

edema and neutrophils

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2
Q

What type of response is AI?

A

Immediate with limited specificity (innate immunity)

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3
Q

What are the major mediators of AI?

A

Toll-like receptors (TLRs), Arachadonic acid metabolites, Mast cells, Complement, and Hagemen factor (factor XII)

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4
Q

Where do you find TLRs?

A

On cells of innate immunity (e.g., macrophages and dendritic cells)

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5
Q

How are TLRs activated?

A

Pathogen-associated molecular patterns (PAMPs)

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6
Q

CD 14 (TLR4 co-receptor) on macrophages recognizes…

A

Lipopolysaccaride (a PAMP) on outer membrane of gram-negative bacteria

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7
Q

What happens upon TLR activation?

A

Upregulation of NF-kB (a nuclear transcription factor), which activates immune response genes that produce multiple immune mediaters

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8
Q

Where can you find TLRs that help with chronic inflammation?

A

Cells of adaptive immunity (e.g., lymphocytes)

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9
Q

What enzyme releases AA from phospholipid cell membrane?

A

Phospholipase A2

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10
Q

What two enzymes act on AA? What do they produce?

A

Cyclooxygenase –> produces prostaglandins (PG) and

5-lipoxygenase –> produces leukotrienes (LT)

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11
Q

What role do PGI2, PGD2, and PGE2 play in AI?

A

Mediate vasodilation (at arteriole level) and increased vascular permeability (at post-capillary venule)

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12
Q

What else does PGE2 do with regards to AI?

A

Mediates pain and feeeeever

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13
Q

LTB4 function?

A

Attracts and activates neutrophils

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14
Q

LTC4, LTD4, and LTE4 function?

A

Mediate vasoconstriction, bronchospasm, and increased vascular permeability. (–>smooth muscle contraction)
They are slow reacting substances of anaphylaxis.

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15
Q

What are the main activators of neutrophils?

A

LTB4, C5a, IL-8, and bacterial products

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16
Q

Where are mast cells present?

A

Widely distributed throughout connective tissue

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17
Q

How are mast cells activated?

A

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

18
Q

What is the immediate response of mast cells?

A

Release of preformed histamine granules. Mediates vasodilation or arterioles and increased vascular permeability.

19
Q

What is the delayed response of mast cells?

A

Production of AA metabolites, particularly leukotrienes. Allows for maintenance of acute inflammation.

20
Q

What are complement proteins?

A

Proinflammatory serum proteins that “complement” inflammation

21
Q

What are the three pathways of activation?

A

Classical, Alternative, and Mannose-binding lectin (MBL)

22
Q

How is the classical pathway activated?

A

C1 binds IgG or IgM that is bound to antigen

–> “GM makes CLASSIC cars”

23
Q

How is the alternate pathway activated?

A

Microbial products directly activate complement

24
Q

How is the MBL pathway activated?

A

MBL binds to mannose on microorganisms and activates complement

25
Q

Where is the earliest all common pathways meet?

A

Production of C3 convertase (mediates C3–> C3a and C3b)

–> produces C5 convertase (mediates C5–> C5a and C5b)

26
Q

How is the membrane attack complex (MAC) formed?

A

C5b complexes with C6-C9

27
Q

What are the roles of C3a and C5a?

A

Trigger mast cell degranulation (anaphylatoxins)–> histamine-mediated vasodilation and increased vascular permeability
C5a also is chemotactic for neutrophils

28
Q

What is the role of C3b?

A

Opsonin for phagocytosis

29
Q

What does MAC do?

A

lyses microbes by creating a hole in the cell membrane

30
Q

What is Hageman factor (XII)?

A

Inactive proinflammatory protein produced in liver

31
Q

How is factor XII activated?

A

Exposure to subendothelial or tissue collagen

32
Q

What does an activated factor XII activate?

A

(1) Coagulation and fibrinolytic systems (mechanism by which DIC can occur)
(2) Complement
(3) Kinin system

33
Q

How does the kinin system work?

A

Kinin cleaves high-molecular-weight kininogen (HMWK) to bradykinin

34
Q

What does bradykinin do?

A

Mediates vasodilation and vascular permeability (like histamine), also mediates pain

35
Q

What are the Cardinal signs of inflammation?

A

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

36
Q

Why do you see redness and warmth?

A

Due to vasodilation –> increased blood flow

–> Occurs via relaxation of arteriolar smooth muscle

37
Q

What are the key mediators of relaxation of arteriolar smooth muscle in inflammation?

A

Histamine, prostaglandins, and bradykinin

38
Q

Why do you have swelling in inflammation?

A

Leakage of fluid from postcapillary venules into the interstitial space (exudate)

39
Q

What are the key mediators of swelling?

A

(1) Histamine - endothelial cell contraction

(2) tissue damage - endothelial cell disruption

40
Q

What are the key mediators of pain?

A

Bradykinin and PGE2 –> sensitize sensory nerve endings

41
Q

Why does fever occur in inflammation?

A

Pryogens (e.g., LPS from bacteria) cause macrophages to release IL-1 and TNF

  • -> increase COX activity in parivascular cells of hypothalamus
  • -> Increased PGE2 raises temperature set point

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