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3 - Physio Genetics > Inflammation > Flashcards

Flashcards in Inflammation Deck (16):
1

innate immunity

-we have this naturally --> this is INFLAMMATION
-Impact could just be diluting whatever is going on
-Innate protects you in the gap between exposure and the more specific immune response that is adaptive or acquired

2

what are the chemical mediators that drive inflammation

chemokines and cytokines

3

relationship between prostaglandins and pain

directly related to pain! Directly stimulates nerve endings to cause pain response AND create inflammation that also causes pain

4

phases of inflammation

-acute vascular response
-acute cellular response
-chronic cellular response
-resolution

5

characteristics of gout

-circumferential and “dusky red” swelling
-Exquisitely painful, swollen and hot to touch

6

hallmarks of inflammation

-rubor
-tumor
-calor
-dolor
-loss of function

7

acute phase reactants

-Molecules detectible in blood that rise reliably with inflammatory processes
-Reflect a change in homeostatic mechanisms in response to pathology
-Defined as proteins whose serum concentrations rise or fall by 25% or more in inflammatory states
-Made in liver – serve as marker of liver metabolism

8

CRP

-First identified APR
-Levels vary widely – no known “normal”
-Can increase 1000 fold or more
-Binds damaged cells
-Binds nuclear proteins
-Binds pathogens
-This is a sticky molecule, binds to everything
-Activates compliment pathway --> focuses immune response
-Activates proinflammatory cytokines
-THERE IS NO KNOWN NORMAL LEVEL OF CRP

9

erythrocyte sedimentation rate

-One of the LEAST specific tests you do
-Indirect, non-specific measure of inflammation
-Less useful when occurs in isolation, but considered more significant if CRP elevated (happens normally in obesity due to IL-6 from adipose tissue)
-Measures the change in viscosity of blood that may be created by enhanced APR protein content, particularly fibrinogen
-The more sticky stuff (inflammatory) = elevated sed rate
-Cells in more viscous medium settle to bottom of vertical tube more slowly (RATE is lower))
-In anemia, absence of red cells reduces viscosity and RATE rises (sed happens faster)

10

action of NSAIDs

-NSAIDs (and steroids) inhibit cyclo-oxygenase, AKA Prostaglandin synthase, reducing inflammation
-Pain effect of NSAIDs in 20-30 minutes
-Anti-inflammatory effect in 7-10d
-If you inhibit cox-1, kidney problems, ulcers, altered blood clotting

11

role of inflammation in other conditions

-“Inflammation” indicated as cardiac risk
-Thought to be involved in “softening” arterial plaques leading to thromboembolic events
-Renal patients don’t clear pro-inflammatory molecules well
-Kidneys don’t work as well to get the inflammatory molecules out of the system
-Assessment of APR in autoimmune inflammatory conditions – RA, SLE, giant cell arteritis

12

Giant cell arteritis

-Inflammation of temporal artery
-Migraines
-Presents in older adults
-GOLD STANDARD DIAGNOSTIC = temporal artery biopsy where you visualize inflammation in microscopic
-Back in the day, the test was a sed rate

13

angioedema

-Self-limited, localized swelling of skin or soft tissue
-Doesn’t involve the rest of it --> allergy is more systemic in nature
d/t loss of vascular integrity
-Occurs alone or as a component of urticaria
-Probably mast cell (histamine) or bradykinin mediated
-Treat with antihistamine and ORAL steroids
-lisinopril is one cause
-ACE inhibitors can cause angioedema --> African American population is more susceptible to it
Around the mouth is most common place

14

allergy

-Isolated angioedema rare
-IgE mediated immune response
-Anaphylaxis treated with epinephrine
-Urticaria treated with leukotriene inhibitors, antihistamines, topical steroids, rarely systemic steroids
-Urticaria = hives

15

Eczema

-Pruritic, inflammatory skin disease
-Factors: Skin barrier dysfunction, Inappropriate immune response, Altered flora
-Immune response: Skin breakdown allows enhanced allergen penetration
-Acute response characterized by enhanced cytokine production
-Clinical feature – epidermal spongiosis (edema)

16

Psoriasis

-Complex immune mediated disorder
-Characterized by defined plaques and scale (Immune mediated response)
-Pathophysiology begins with immune cells – dendritic cells, macrophages, neutrophils present in higher numbers in psoriasis patients
-Presence of antigens activates cells
-Native skin cells release proinflammatory cytokines which recruit more immune cells and cause release of more inflammatory mediators
-EXAMPLE OF POSITIVE FEEDBACK!!!