MUSCULOSKELETAL SYSTEM DRUGS

Card Set Information

Author:
xjessicax3
ID:
10624
Filename:
MUSCULOSKELETAL SYSTEM DRUGS
Updated:
2010-03-15 17:16:31
Tags:
Pharm test 2
Folders:

Description:
MUSCULOSKELETAL SYSTEM DRUGS-Pharm test 2
Show Answers:

Home > Flashcards > Print Preview

The flashcards below were created by user xjessicax3 on FreezingBlue Flashcards. What would you like to do?


  1. Prostaglandin synthesis

    -Prostaglandin modulate some components of:
    -_______
    -_______temperature
    -_______ temperature
    -platelet aggregation (formation of _______)
    -prostaglandins come from _______ Acid which is liberated from cells in response to _______, _______, _______, _______ & other stimuli.
    Prostaglandin synthesis

    • -Prostaglandin modulate some components of:
    • -inflammation
    • -body temperature
    • -pain temperature
    • -platelet aggregation (formation of platelet plugs)
    • -prostaglandins come from Arachidonic Acid which is liberated from cells in response to physical, chemical, hormonal,bacteria & other stimuli.
  2. Prostaglandin Synthesis

    -Prostaglandin is the result of conversion from ________ acid by the enzyme ________ (COX)
    -In order for prostaglandin to be made ________ acid must be metabolized through ________ (an enzyme)
    -There are two forms of cyclooxygenase (COX)
    -1. COX I- which is found in ________ cells
    -2. COX II- which is found in ________ cells
    -There are a variety of prostaglandins implicated in the _______ associated with inflammation. However, the key ones are PGE1 & PGE 2
    Prostaglandin Synthesis

    • -Prostaglandin is the result of conversion from Arachidonic acid by the enzyme cyclooxygenase (COX)
    • -In order for prostaglandin to be made arachidonic acid must be metabolized through cyclooxygenase (an enzyme)
    • -There are two forms of cyclooxygenase (COX)
    • -1. COX I- which is found in non-inflamed cells
    • -2. COX II- which is found in inflamed cells
    • -There are a variety of prostaglandins implicated in the pain associated with inflammation. However, the key ones are PGE1 & PGE 2
  3. Prostaglandins

    -Prostaglandins are needed for normal cell _____
    -Current NSAIDS inhibit COX __ as much as or more than they inhibit COX __
    -When NSAIDS inhibit _____ cells the stores of prostaglandins are _____ and normal cell function is _____
    -The action of NSAIDS accounts for numerous _____ effect of the drugs.
    Prostaglandins

    • -Prostaglandins are needed for normal cell functions
    • -Current NSAIDS inhibit COX I as much as or more than they inhibit COX II
    • -When NSAIDS inhibit non-inflammatory cells the stores of prostaglandins are depleted and normal cell function is disrupted.
    • -The action of NSAIDS accounts for numerous adverse effect of the drugs.
  4. NSAIDS

    -1. ________
    -Prototype: ________
    -Variety of________ uses
    -used for ________ to ________ pain
    -Interferes with prostaglandin synthesis by irreversibly inhibiting ________
    -Causes bleeding by interfering with ________ cascade.
    NSAIDS

    • -1. Salicylates
    • -Prototype: Aspirin
    • -Variety of therapeutic uses
    • -used for mild to moderate pain -Interferes with prostaglandin synthesis by irreversibly inhibiting COX
    • -Causes bleeding by interfering with coagulation cascade.
  5. Salicylates

    -Contraindicated in children with ___ illness including chicken pox (___) or flu-like illness due to association with ___ Syndrome.
    Salicylates

    -Contraindicated in children with viral illness including chicken pox (varicella) or flu-like illness due to association with Reye's Syndrome.
  6. Salicylates

    -Adverse Effects
    -A. Salicylism: Mild _______ toxicity seen either in long term use of high dose _______ therapy
    -B. Salicylate Poisoning:
    - ______-threatening
    -no _______
    -syrup of _______
    -Treatment includes gastric _______
    -activated _______
    -S &S: High _______ and _______
    Salicylates

    • -Adverse Effects
    • -A. Salicylism: Mild aspirin toxicity seen either in long term use of high dose aspirin therapy -
    • B. Salicylate Poisoning:
    • -Life-threatening
    • -no antidote-syrup of ipecac
    • -Treatment includes gastric lavage
    • -activated charcoal
    • -S &S: High fever and coma
  7. NSAIDS CONTINUED

    -2. _______ Synthetase Inhibitors (PSI)
    -Prototype: _______
    -Sub group of NSAIDS
    -PSI'S are group by _______ synthesis
    -Chronic use can --> _______, _______ & ___ bleed.
    -Contraindicated in those with a history of _______ disease
    -Used with caution in _______, _______ or _______ disease.
    NSAIDS CONTINUED

    • -2. Prostaglandin Synthetase Inhibitors (PSI)
    • -Prototype: Ibuprophen
    • -Sub group of NSAIDS
    • -PSI'S are group by chemical synthesis
    • -Chronic use can --> gastritis, ulceration & GI bleed.
    • -Contraindicated in those with a history of GI disease
    • -Used with caution in hematopoetic, hepatic or renal disease.
  8. Disease Modifying Antirheumatoid Drugs

    -Used when _______ are not tolerated or a ineffective.
    -Called _______ because they can arrest the progression of rheumatoid arthritis & induce _______ in some patients.
    -Also known as Slow Acting Antirheumatic Drugs (SAARDS) because of the _______ in achieving a response.
    Disease Modifying Antirheumatoid Drugs

    • -Used when PSI'S are not tolerated or a ineffective.-Called DEMARDS because they can arrest the progression of rheumatoid arthritis & induce remission in some patients.
    • -Also known as Slow Acting Antirheumatic Drugs (SAARDS) because of the delay in achieving a response.
  9. DMARDS

    -most common DMARDS are gold salts _________ (an antineoplastic used for a variety of _________ disorders)
    -The major disadvantages induce:
    -______ onset of action
    -______ in achieving a therapeutic response
    -potential for serious _______ & even _____ reactions
    -prototype : ________ (_______ - gold salt)
    DMARDS

    • -most common DMARDS are gold salts methotrexate (an antineoplastic used for a variety of malignant disorders)
    • -The major disadvantages induce:
    • -slow onset of action
    • -delay in achieving a therapeutic response
    • -potential for serious adverse & even fatal reactions
    • -prototype : auranofin (Ridaura - gold salt)
  10. Gold Salt Theory

    -Adminstration of gold salts is called ________
    -________ contains 29% gold
    -mechanism of actions is ________
    -chrysotherapy can produce serious,______ reactions
    -most serious effect is lethal ____ ____ suppression
    -most common effect is ________
    -gold can deposit in the ________ -> skin pigment changes ________ to ________ coloration
    -can cause ________ syndrome.
    Gold Salt Theory

    • -Adminstration of gold salts is called chrysotherapy
    • -Auranofin contains 29% gold
    • -mechanism of actions is unknown
    • -chrysotherapy can produce serious, toxic reactions
    • -most serious effect is lethal bone marrow suppression
    • -most common effect is diarrhea
    • -gold can deposit in the tissue -> skin pigment changes grey to blue coloration
    • -can cause nephrotic syndrome.
  11. Anti-gout

    -gout is aka the rich man's disease because it is associated with a diet high in _______ (_______ cream, _______ meats)
    -prototype: _______
    -used to treat gout since 1763
    -Colchicine_______ leukocyte phagocytosis which inhibit further _______ deposits
    -Contraindicated in patients with severe_______ , _______or _______ disease due to risk of cumulative toxicity
    -most adverse effect is ____
    -S&S that must be reported immediately include:
    -fever, chills, sore throat, difficulty _______ & muscle _______ (drug cause _______)
    Anti-gout

    • -gout is aka the rich man's disease because it is associated with a diet high in purines (whipped cream, organ meats)
    • -prototype: Colchicine-used to treat gout since 1763
    • -Colchicine opposed leukocyte phagocytosis which inhibit further urate deposits
    • -Contraindicated in patients with severe heart , liver or kidney disease due to risk of cumulative toxicity
    • -most adverse effect is GI
    • -S&S that must be reported immediately include:
    • -fever, chills, sore throat, difficulty breathing & muscle weakness (drug cause myoneuropathy)
  12. Uricosurics

    -prototype: _______ (_______)
    -Used in _______ gout
    -keeps the uric acid level _______ saturation to prevent the formation of uric _______
    -must not be used during _______ attacks since it can _______ the anti- inflammatory response
    -contraindicated in patients with uric acid _______ and bone marrow _______
    -should not be used in ______ impairment
    -probenecid reduce renal failure secretion of many drugs -> _______ -> toxicites
    Uricosurics

    • -prototype: probenecid (Benmid)
    • -Used in chronic gout
    • -keeps the uric acid level below saturation to prevent the formation of uric crystals
    • -must not be used during acute attacks since it can prolong the anti- inflammatory response
    • -contraindicated in patients with uric acid stones and bone marrow depression
    • -should not be used in renal impairment
    • -probenecid reduce renal failure secretion of many drugs -> accumulation -> toxicites

What would you like to do?

Home > Flashcards > Print Preview