Inflammation Flashcards
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
what are the chemical mediators that drive inflammation
chemokines and cytokines
relationship between prostaglandins and pain
directly related to pain! Directly stimulates nerve endings to cause pain response AND create inflammation that also causes pain
phases of inflammation
- acute vascular response
- acute cellular response
- chronic cellular response
- resolution
characteristics of gout
- circumferential and “dusky red” swelling
- Exquisitely painful, swollen and hot to touch
hallmarks of inflammation
- rubor
- tumor
- calor
- dolor
- loss of function
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
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
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)
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
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
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
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
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
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)
