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immuno med wk 2 > Gout > Flashcards

Gout Flashcards

1
Q

@ site of inflammation 1

A

Macrophages ingest urate and release inflammatory cytokine IL-1beta, and chemokine IL-8

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2
Q

@ site of inflammation 2

A

IL-1b induces expression of adhesion molecules on endothelium

COX-2 in macs, monocytes, connective tissue and endothelium as well

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3
Q

@ site of inflammation 3

A

TOGETHER (emphasizeD) IL-1beta and IL-8 recruit neutrophils from the blood toward site of inflammation/activated macs/monos

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4
Q

@ site of inflammation 4

A

activated cells (monos/macs/connective tissue/neutrophils) increase enrichment of lipid mediators of inflammation + other factors (complement, coagulation, peptides).

Inflammatory environment manifests as redness/swelling, pain/heat

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5
Q

@ sit of inflammation alternative version

A

IL-1b induces expression of COX-2 in cells at site of inflammation and in adjacent endothelium.

COX-1, COX-2 generate prostaglandin mediators that cause dilation+increase permeability of vessels, especially post-cap venules

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6
Q

COX-2: where would you find this and how would it be affected by NSAIDs?

COX-1: compare to COX-2

A

This is the enzyme activated at sites of inflammaiton, and responsible for prostaglandin/leukotriene synthesis

NSAIDs block PG synthesis

COX-1 is constitutive
COX-2 is induced

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7
Q

PG synthesis 1

A

IL-1b induces

Phospholipase A + membrane phospholipids –> arachidonic acid (AA)

AA + COX-2 or COX-1 –> Prostaglandin H2 (PGH2)

PGH2 + Tissue isomerases –> PG-D,F,G + Prostacyclin + Thromboxane (TxA2)

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8
Q

How are prostaglandins degraded?

A

15-OH-dehydrogenase oxidizes them to inactive metabolites

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9
Q

How are prostacyclins degraded?

A

a hydrolase enzyme

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10
Q

Vasculature/Endothelium

Eicosanoid

A

PGI(2)

vasodilation, platelet aggregation

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11
Q

Blood Platelets

Eicosanoid

A

TxA(2)

vasoconstriction
platelet aggregation

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12
Q

Vasculature

Eicosanoid

A

PGE(2)

permeability

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13
Q

GI

Eicosanoid

A

PGE(2)

mucosal cytoprotection
muscle tone
motility

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14
Q

Renal

Eicosanoid

A

PGI(2), PGE(2)

Na+, H20 excretion

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15
Q

Uterus

Eicosanoid

A

PGF(2)a, PGE(2)

muscle contraction

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16
Q

CNS

Eicosanoid

A

PGE(2)

temperature

17
Q

PNS

Eicosanoid

A

PGE(2)

Pain sensitization

18
Q

Skeletal

Eicosanoid

A

PGE(2)

bone remodeling

19
Q

COX-1, PGs, & inflammation (3 things)

A

IL-1beta stimulates AA release
COX-1 converts AA into PGE2
PGE2 causes symptoms

20
Q

COX-2, PGs, & inflammation (3 things)

A

IL-1b induces COX-2 expression
COX-2 converts AA into PGE(2), PGI(2)
PGE(2), PG(I) amplifies symptoms

21
Q

PGE(2) and PGI() contribute functionally to….

A

vasodilation, vascular permeability, and local edema, and pain

22
Q

How do PGE2 and PGI2 contribute to edema?

A

PGE –> permeability of endothelia
PGI –> vasodilation of endothelia

together this causes “extravasation” of plasma into interstitial space

23
Q

“marginating pool”

A

neutrophils induced by Ig-1b to express adhesion molecules, making them “sticky”

24
Q

the Cytokine response and Involvement toward

LPS, bacterial components, fungal components

A

robust TNF-alpha, cytokines, and interleukins, IFN, IL-1, IL-8 etc

often system: sepsis possible

25
Q

The cytokine response and involvement toward

uric acid buildup

A

IL-1b and IL-8

26
Q

Bacteria engulfed —> inflammatory cytokines

A

TNF-alpha, IL-1, IFN, chemotactic sytokiens

27
Q

LPS itself —> inflammatory cytokines

A

TNF-alpha/IL-1 –> adhesion molecules expression on endothelia + COX-2 expression in macs, monocytes, connective tissues, and endothelium

28
Q

systemic inflammation can be caused by

A

sepsis, during which time the entire body launches an inflammatory response

the response overwhelms the body: organs, shock, death

29
Q

Sepsis: Physiology, Pathology

A

Phys: Autocoid mediators act locally, briefly
Pathology: Autocoid mediators act systemically and persistently

30
Q

What two components cause systemic inflammation during sepsis?

What then causes widespread damage to the host?

A

TNF-alpha in response to LPS

induction of COX-2 and adhesion molecules, activation of myeloid cells

extravasation of plasma from the blood to the interstitial spaces leads to a drop in blood pressure from a septic shock

31
Q

What does “Extravasation” do to the body?

A

when blood leaks out of the epithelium into the tissues and causes a drop in blood pressure

32
Q

COX-1 an Gout versus COX-2 and Gout

A

IL-1b stimulates release of AA
Cox- 1 converts AA into PGE2
PGE2 causes symptoms (Erythema/Edema/Pain)

L-1b induces COX-2 expression (inducible)
Cox-2 converts AA into PGE(2) and PGI(2)
PGE and PGI amplify symptoms (WORSE Erythema, Edema, Pain)

33
Q

PGI(2) on the endothelium

PGE(2) on the endothelum

A

PGI - vasodilation
PGE - permeability

they work together

immuno med wk 2 (27 decks)

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