Inflammation and Wound Healing Flashcards

1
Q

Characterizes acute inflammation

A

edema and neutrophils

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2
Q

CD14

A

on macrophages, recognize lipopolysaccarides (a PAMP) on outer membrane

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3
Q

TLR activation results in upregulation of:

A

NF-kB, nuclear transcription factor that activates immune response

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4
Q

Arachidonic acid metabolites

A

cyclooxygenase or 5-lipooxygenase

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5
Q

Cyclooxygenase produces this:

A

PGs

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6
Q

5-Lipoxygenase produces this:

A

Leukotrienes (LTs)

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7
Q

Activates neutrophils

A

LTB4

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8
Q

Leukotrienes

A

Delayed response

LTC4, D4, and E4 cause vasoconstriction, bronchospasm, and increased perm

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9
Q

4 key products that activate neutrophils

A

LTB4, IL-8, C5a, bacteria products

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10
Q

C3a and C5a

A

anaphylatoxins, trigger mast cell degranulations (histamine)

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11
Q

Cardinal sign of inflammation

A

redness (palor), warmth (calor)

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12
Q

Swelling: leakage of fluid from:

A

postcapillary venules

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13
Q

Pain mediators

A

Bradykinin, PGE2, sensitize nerve endings

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14
Q

Fever

A

Pyrogens cause macrophages to release IL-1 and TNF, increase COX in perivascular cells, increase PGE2

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15
Q

Steps of Neutrophils

A

Margination, Rolling, Adhesion, Transmigration and Chemotaxis, Phagocytosis, Destruction of shit

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16
Q

Vasodilations occurs in the:

A

postcapillary venules

17
Q

E selectin is produced by

A

endothelial cells in response to IL1 and TNF

18
Q

Integrins are upregulated by

A

C5a and LTB4

19
Q

Baby has delayed separation of umbilical cord

A

Leukocyte adhesion deficiency

20
Q

Leukocyte adhesion deficiency

A

AD mutation located on CD18 subunit, will have increased circulating neutrophils

21
Q

Phagocytosis Opsonins

A

C3b, IgG

22
Q

Chediak Higashi Syndrome

A

protein trafficking defect (AR), impaired phagolysoosme defect. Clinical features:
increased risk of pyogenic infections, neutropenia, giant granules in leukocytes, defective primary hemostasis, albininsm, peripheral neuropathy

23
Q

Chronic granulomatous disease (CGD)

A

poor O2-dependent killing by neutrophils, due to a NADPH oxidase defect. Test with NBT test

24
Q

CGD recurrent infections

A

Staph Aureas, Serratia, Aspergillus, Pseudomonas, and Norcadia

25
Q

MPO Deficiency: increased risk for

A

Candida, most are asymptomatic

26
Q

Anti-inflammatory cytokines

A

IL10 and TGFbeta

27
Q

How CD8 T cells kill

A

secretion of perforin and granzyme

28
Q

B cells need this to make other types of antibodies

A

CD40 binding with Th2 cells, and then Th cell secretes IL4 and IL5 to change the shape of the B cell to make IgG, IgA, and IgE

29
Q

Hallmark of a granuloma

A

epithelioid histiocytes

30
Q

Process of granuloma formation

A
  1. Macrophages presents antigens to MHCII receptors on T helper cells (CD4)
  2. Interaction: leads macrophages to secrete IL-12, turning CD4 helper T cells to Th1 subtype
  3. Th1 subtype then releases INFgamma, which converts macrophages to epithelioid histiocytes and giant cells
31
Q

Digeorge Syndrome

A

Failure of 3rd and 4th pharyngeal pouches to form, causing no thymus, due to a 22q11 microdeletion

32
Q

Severe Combined Immunodecifiency (SCID)

A

both cell mediated and humoral deficiency
Main point: ADA deficiency (Adenosine Deaminase (ADA) is required to deaminate adenosine and deoxyadenosine as waste products, these accumulate and are toxic to lymphos)
susceptible to everything

33
Q

CVID is linked to:

A

autoimmune disease and lymphoma

34
Q

IgA Deficiency is linked to

A

Celiac Disease

35
Q

Hyper-IgM Syndrome

A

A lot of IgM because defective CD40 receptors or ligands, low IgA, IgE, and IgG result in recurrent pyogenic infections, especially mucosal sites

36
Q

Wiskott-Aldrich Syndrome

A

Thrombocytopenia, exzema, and recurrent infections

37
Q

C5-C9 deficiency: susceptible to:

A

Neisseria infection

38
Q

C1 deficiency

A

Results in angioedema, edema of the skin (especially periorbital)