Antiinflammatory Drugs + Immune Rxn's Flashcards
3 stages of inflammation
- acute 1-3 days hot, red, and painful
- subacute 3 days - 1 month–cleaning
- chronic–month-years
plasma transporter of iron
Transferrin
clotting factor
Fibrinogen (can lead to clotting disorder)
in the hypothalamus, prostaglandins stimulte the production of nt’s which function to reset the temp set point at a higher leverl
Fever
damage to cells releases cytokines i.e. (4) that ______ and ______ local immune cells to site
chemokines, interferon, interleukins, TNF,–
attract and activate
Steps of inflammation
- injury occurs–invasion of organism
- Activation of local macrophages
- biochemical messages released (part of step 2)
- Dendritic cells = ^ espionage (gain info) and responses
- Arrival of killer T cells (specialized for viruses)
- Return to homeostasis
step 3 of inflammation
red, warm, edema, pain
T-cells kill by
neutrophils (earliest) kill by
dendritic cells kill by
- instructed cell death–apoptosis
- phagocytosis & degranulation & creates net (*bacteria)
- phagocytosis
- Inflammation can be (2) + cell mediators
acute (neutrophil mediated) vs.
chronic (monocyte, macro, lymphocyte mediated)
in phase 6 of inflammation–the tissue engineers are_____, may lead to ______ as after ab surgery
fibroblasts,
adhesions
chronic inflammation is often ______ and ________–usually due to overactive fibroblasts
severe and progressive
“SMOLDERING”
Acute inflammation is usually ____ and ___-______–local S&Ss are often _____
mild and self-limited,
prominent
inflammation is associated w/
almost every disease–get used to it
a distinctive pattern of chronic inflammation characterized by aggregates of activated macrophages w/ scattered lymphocytes (walling off isolated foreign materials and debris) i.e TB, Syphilis
Granulomatous inflammation (a type of chronic inflammation)
Systemic S&S of inflammation (3) PROSTAGLANDINS
- Fever (hypothalamus–adjusted “set-point”)
- Production of acute-phase proteins (C-reactive)
- Leukocytosis (^ WBCs)
the process of inflammation is fundamental to virtually…
all of clinical medicine!!!!!
leukocytosis in common to inflammatory rxn’s–esp those induced by ________
bacteria
- Plasma levels of _______ and _______ raise dramatically during inflammation–produced by LIVER–checked via “Sed rate” (sedimentation rate)/ ESR
C-reactive protein, Serum amyloid A
2 classes of antiinflammatory drugs
- steroidal (corticosteroids)
2. nonsteroidal (NSAIDS)
ESR tests:
how quickly red blood cells (erythrocytes) settle in a test tube in one hour. The more red cells that fall to the bottom of the test tube in one hour, the higher the sed rate.
really good gram+ antibiotic
gentimycin
___-______ not good at treating intracellular organisms
beta-lactams
cell membrane phospholipids can become -_______ ______ which can become _____________ —> inflammation
arachadonic acid,
prostaglandins
Corticosteroids (prednisone) blocks synthesis of ______ _____–blocking much downstream
arachidonic acid
most common cause of cushings (^ cortisol)
steroid treatment (prednisone)
glucocorticoids:
desired effects:
Undesired effects:
- antiinflammation, lower immune funciton
- lower immune function, ^gluconeogenesis, ^lipolysis, fat redistribution, ^insulin resistance, mood changes (ANGER)
glucocorticoid MO
involved in concentration, distribution and function of peripheral leukocytes–> suppression on cytokine release
*equivalent physiological dose of prednisone
5 mg
prednisone inhibits _________
phospholipases –/–> arachidonic acid
prednisone dosing and duration dictated by
seriousness of condition
- Prednisone dosing:
acute inflammation:
chronic:
- high dose short duration
- low dose long term–taper if over 2 weeks (over 2 is when ADRs emerge) (stunted growth in kids–monitor growth)
Prednisone distributes __________ quickly; metabolized into _________
everywhere; -
prednisolone (more active form)
Most common prednisone ADRs:
ADRs to concern us:
- GI upset and mood changes (anger)
- disturbance of HPA axis (Cushings)
All agents w/in these classes are antiinflammatory, antipyretic, and analgesic via inhibition of prostaglandin synthesis
NSAIDs–via cyclooxygenase inhibition selectively or non-selectively
antiinflammatory drugs in addition to steroids and NSAIDS
tetracyclines and macrolides–inhibit production of inflammatory mediators
Hypersensitivity Rxn mne: ACID mediator? A: C: I: D:
A: IgE–allergin binds to mast cells and basophils=> degran
C: IgG– Antigen=Antibody –>compliment mediated lysis
I: IgG – Compliment activation attracts POLYMORPHONUCLEAR cells–>release lysosomal enzymes
D: Cell– Help T cell –> lymphokines => inflammation + Macrophages
Type I hypersensitivity induces ____ ______ or eosinophile to release ______ (rhinnorrhea, anaphylaxis, angioedema)
mast cells,
histamine
angioedema mediated by
Type I or II (bradikinins or histamine)
hypersensitivity rxn often caused by ________ rather than direct allergen
metabolite
IgG binds to antigen on cell surface + compliment system => cytotoxic (cell is killed)
Type II hypersensitivity rxn (i.e. wrong blood type infusion–AUTOIMMUNE disorder)
anaphylaxis vs.
anaphylactoid
- IgE mediated
- drug itself acts as sensitivity mediator
Difference btwn type II and III (video)
type II: IgG attaches directly to cell surface antigen
type III: IgG attaches to antibody–> immune complexes
penicillin allergy most likely
Type I
serum sickness caused from type ____ hypersensitivity
III
ARTHUS reaction looks just like
cellulitis
Initiation of the T-helper cell
Type IV hypersensitivity rxn–activation of B and Killer T cells (can lead to most dangerous autoimmune diseases i.e. diabetes)
positive TB test is
type IV rxn
