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66 Cards in this Set

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Acute inflammation
Immediate response to local mediators
What are the Autacoids
Histamine, serotonin, bradykinin, prostaglandins, leukotrienes

*locally acting substances
What is the affect of autacoids?
Vasodilation, increased vascular permeability chemotaxis, pain
Chronic inflammation occurs in response to what mediators?
Interleukins
Granulocyte-macrophage colony-stimulating factor (GM-CSF)
TNF alpha and beta
Interferons
PDGF
Most common chronic inflammatory condition
Rhematoid Arthritis
Which enzyme converts Aracodonic Acid(AA) to Leukotrienes
Lipoxygenase
Which enzyme converts AA to prostacyclins, thromboxanes, and prostaglandins
Cyclooxygenase
What do leukotrienes cause?
Bronchoconstricion
What does thromboxane cause?
Platelet aggregation
What do Prostacyclins (PGX, PGI) cause?
Antiaggregating factor release
What does PGE2 cause?
Edema, erythema, pain, fever
What does PGF2alpha cause?
Uterine contraction
Prostacyclin (PGI2) and PGE2 have what local effect?
Vasodilation
Phospholipase A2 is inhibited by what?
Glucocorticoids
Inhibits Cyclooxygenase
NSAIDS
COX 1 Expression
Constitutively in most tissues, generates LOW levels of prostaglandins
Function of COX-1
Protective function (gastric mucosa), vasodilator- determines peripheral resistance to kidney
Other Functions of COX-1
Blood clotting, uterine contraction, muscle growth, synaptic transmission at some CNS synapses
COX-2 constituive or inducible?
Inducible
COX-2: Yields high or low levels of prostaglandins and thromboxanes
HIGH
When is COX-2 expressed in high concentration
After induction by inflammatory mediators
What is the major inflammatory mediator product
Prostaglandin E2
NF-kB
Induces expression of cytokines (IL-1, IL-6), interferon beta, and cell adhesion molecules = ENHANCED INFLAMMATION
What stimulates NF-kB?
TNF alpha
DMARD
Disease Modifying Anti-Rheumatic Drugs
- they delay the disease process
Examples of DMARDs
Methotrexate
Gold
Low-dose corticosteroids
Leflunomide
TNF alpha inhibitors
Selective Cox-2 inhibitor
Celecoxib (sell a kox' ib)
Non selective COX inhibitors (hint: there are 7)
Aspirin
Sodium salicylate
Indomethacin
Ibuprofen
Naproxen
Phenylbutazone
Acetaminophen
Immunosuppresive Agents
(hint: 4 + 3 for gout)
Glucocortocoids
Gold sodium thiomalate
Methotrexate
Leflunomide
Drugs for gout: allopurinol, probenecid, sulfinpyrazole
TNF alpha blockers
Etanercept
Infliximab
How long does it take to have a therapeutic response to DMARD
weeks or months
Current recommendation for DMARD
Early in the course of RA
Methotrexate
most widely used DMARD
anti-inflammatory
How long does it methotrexate to work?
4-6 weeks
Side effects of Methotrexate
Anorexia, vomiting, abdominal cramps, increased hepatic enzyme activity, immuno-suppresion, bone marrow supression, lymphomas
What would you combine with methotrexate to make it more effective?
Cyclosporine or infliximab
Gold preparations MA
Retard progression of bone and articular destruction
Gold sodium thiomalate MA
Gold accumulates in macrophages decreasing activation, migration, and therefore immune response
How is Gold sodium thiomalate excreted?
Urine (60-90%)
Feces (10-40%)
Gold sodium thiomalate admin.
I.m.
Adverse effects of gold sodium thiomalate
~1/3 of patients
Dermatitis, thrombocytopenia, aplastic anemia(rare), proteinuria
Etanercept
TNF alpha antagonist
Structure of Etanercept
composed of p75 TNF RECEPTOR coupled to Fc fragments of immunoglobulin
MA of Etanercept
Binds TNF alpha and blocks stiumlation of the receptors
Infliximab
TNF alpha chimeric monoclonal antibody
(* on exam: Fc region of IgG + Fab sequences of mouse ANTI-TNF ANTIBODY)
Structure of Infliximab
Human Fc of IgG + Fab sequence of mouse anti-TNF Ab
MA of Infliximab
Binds free TNF alpha
Reduces joint swelling and damage
Infliximab admin
I.v.
Side effects of TNF alpha antagonist?
Increased risk for infection, allergic rxns, and possibly malignancies
Aspirin
Irreversible non-selective COX enzyme inhibitor
Aspirin MA
Acetylates COX enzymes
Ibuprofen/Naproxen
Reversible non-selective COX enzyme inhibitors
Side effects of Ibuprofen/Naproxen
Due to (-) of COX 1, mainly gastric ulceration and bleeding, impaird kidney fxn
Salicylate
Weak COX inhibitor, probably a better NF-kB inhibitor (decreased IL-1,IL-6, and INF B)
Celecoxib
-advantages?
COX-2 selective inhibitor
Reduced gastroduodenal damage, platelet aggregation is not impaired
Which COX-2 selective inhibitor was recently taken off the market?
Rofecoxib (Vioxx)- increased risk of thromboembolic events due to unchecked Thromboxane A2 production
Acetominophen
Analgesic and anti-pyretic
weak COX 1 and 2 inhibitor
New findings about Tylenol
COX-3 expressed in CNS is very sensitive to acetaminophen inhibition
Glucocorticoid 3 possible MA
Inhibition of AA production by (-) of phospholipase A2

Inhibition of inflam. cytokines (Interleukins,TNFa, IFNy)

Inhibition of NF-kB
Side effect of glucocorticoids
Cushing's
Why give aspirin to patients with heart conditions
Reduces incidence of MI by 40%
What cancer can aspirin provide protection against?
Colorectal
* 4 aspirin/week for 10 years of more
Bartter's Syndrome
hyperplasia of renal JG apparatus -- hyperreninemia, hyperaldosteronism, hypokalemic alkalosis, normal BP, elevated PG excretion

USE NSAIDS
Why use NSAIDs to treat Bartter's syndrome
Reverses the symptoms
PDA and NSAIDs
patent ductus arteriosus treatment with NSAIDs as 60-90% success in closing duct
What is salicylate?
The deacetylated metabolite of aspirin