Pharmacology III Flashcards
(40 cards)
Topical and systemic corticosteriods
work in the same action
Natural corticosteriod cortisol
natural physiological antagonist to insulin
considered a stress hormone due to this reason
MOA of natural corticosteriod cortisol
cortisol will limit the inflammation by limiting availability of WBC
Administration of cortisol and its derivatives
There will be a redistribution of WBC - increased plasma concentration of neutrophils but the rest are decreased from plasma conc. **
via inhibition of PMN from extravasating from the vasculature (can’t get through to the site of inflammation) = reduce inflammation
Administration of cortisol and its derivatives
all non-PMNs will be reassigned to lymph nodes, even the ones that are activated already and causing inflammation
will decrease macrophage release of IL1
which is very proinflammatory
decrease MMP and plasminogen factor -> will inhibit vascular porosity = more tightness
decrease COX2 expression = antiinflammatory
Fludrocortisone
acts like aldosterone
synthesized corticosteriod different from natural corticoids - longer half life
SALT RETENTION OF FLUDROCORTISONE (EVEN HIGHER THAN ALDOSTERONE EFFECT)
Beta>Dexa>Fludro are the most anti-inflammatory activity
Bursitis
fluid filled sac in a joint can also be reduced with cortisol (as w/ tenosynovitis)
Arthritis is highly indicated with anti-inflammatory
Chronic use of corticosteriods
Cause ulcers, bone fragility (do not give to elderly)
Corticosteriods in asthma, dermatitis, and irritable bowel syndrome due to crohn’s disease/ulceritis
Tx with corticosteriods - but has same effects on ulcers for instance if chronic use of the drugs
Major side effects of corticosteriods
sodium retention = hypertension hypokalemia osteoporosis infections hyperglycemia ulcers obviously, the drugs are contraindicated with peptic ulcers, HTN, osteoporosis/osteopenia, Heart failure
NSAIDs
inhibit COX1 or 2
depending on the drug
GI bleeding is a major side effect
contraindicated in ulcers and hemorrhage
cause decreased GFR and kidney failure
decreased levels of prostacyclin in afferent arterioles
->differential distribution of prostaglandin and cyclins will either cause constriction or dilation in kidney afferent/efferent arterioles
Acetaminophen
not a true NSAID
not antiinflammatory
Aspirin MOA
MOA is irreversible binding to COX1/2
inhibits all Prostaglandins and prostacyclins and thromboxanes
Decreased NADPH oxidase will inhibit PMN from using oxidative bursts
COX and LOX are competitors
-COX inhibit will create aspritin-triggered LOX synthesis
Tx MI/angina, analgesic
Which COX inhibitor drugs inhibit NADPH oxidase
INDOMETHACIN
PIROXICAM
IBUPROFEN
Aspirin adverse/side effects
Cause Reye’s syndrome in pediatrics
cause airway hyperactivity (asthmatic)
Propionic acid derivatives
IBUPROFEN
Tx. gout, ankylosing spondylitis, arthritis and primary dysmenorrhea
NAPROXEN - very long half life - 20x more poten than aspirin
directly inhibits leukocyte function and cause less severe adverse effects than aspirin
Piroxicam
prodrug like Sulidac better tolerated but not good efficacy it is an oxicam Tx as effective as aspirin, naproxen, ibuprofen against arthritis inhibits MMP and NADPH oxidase
Acetaminophen toxicity
kidney and liver
Colecoxib
Ischemic toxicity
MI
stroke
Adalimumab
complete human IgG1 for arthritis
No activity on TNFb
Monoclonal antibodies
mimics/inhibit inflammatory cytokine
Etanercept
given with methotrexate to decrease proliferating of lymphocytes
For arthritis
Dimeric fusion protein against TNFa/b
Main targets of Monoclonal Ab anti-infammatories
TNFa and granulocyte macrophage stimulating factor
Abatacept
Blood t-cell activation with decrease in TNFa
Tx. sever resistant rheumatoid arthritis
