Old material on the final Flashcards
Distinguish between the 3 names that a drug might have
chemical name - N-acetyl-para-aminophenol (APAP)
generic name - acetominophen
brand name - tylnon
define what is meant by drug dose
precise amount of active ingrediet in medication - often combien with other materials to increase affectiveness/abodorption and ifll out the meds
Describe the 3 phases of drug action
1.pharmaceutical - how drug progressed from administered to beng dissolved
- enteral: oral, rectal, sublingual
- parenteral
- injections, inhaltion, teansdermal
2. Pharmacodynamic - the effect of the body on the drug
aborption - have to get drug acoss cell
distribution
metabolism
elimination
3 Pharmacokinetic
- how body acts on the drug
waht is least effective method of drug absorptuon
oral - has t go thru frstpass metabolism + gi contenets and dug coating can impact
what is potency? Whcih way does it go on the graph
The strength of a drug at a particular dose - right to left
what is efficacy and which way does it go on the graph?
down to up
the max effect a drug has on the body
what is therapeutic index?
The ration. between toxic and minimum effective dose - macimize desired effect + mniimize toxin ones
what are the 2 xompinents of pain?
sensor comonent + affective and cognitive component
what is the difference between nocireceptive and neuropathic pain
nocireceptive arises from tissue damge (physical, mechanical, chemical)
- somatic (ss nerves detect) or visceral (sns detect) - referred pain
neuropathic is by a dysfucntion in the nervous systme - often no tissue damage
referred pain is ___ localized an dccurs in waht source of pain
poorly localized - nocireceptive visceral pain - eg pain. in arm due to inflmamaion of the galbladder
chronic pain is if it occurs ___
for loigne than 3 months
compare and contast acute vs chronic pain
acute
- less than 2 moths
Delat A fibrers
sudden shorterm
protective fucntion
resolve cause and relive pain
chronic
- c fibres
linger than 3 months
- nereve hyeprsensitibity 0 could eb lcoalzied within CNS
what does current research indicated cause of chronic apin as? treatment.
chronic inflammation fo the NS - malfucntionin glail cells
treatment - fish oil, exrcise,neuromoduatlion
what aer the 4 ways t manage pain? Example for each
prevention
- nutrition
psychologucal
- mindfulness, relaxation
phsycial
- safe movement and exrcise
pahrmacetuical - analgesisc. (perception) +anaeesthetics (Sensation)
waht is neuromodualtion
magnetic pulse stimualted nerve cells in brain to trate chronic depression +neurpoathic pain
Describe the 5 cardinal signs of acute inflammation
- swelling
- rednesss
heat - pain
- loss of function
5.
Explain the local action of chemical mediators during an acute inflammatory response
pain response - bind to nocireepetors
vascular response - vasodilation + increased capillary permeabilty
cellular respsonse - attract immune cells to injury cite ( chemotaxis)
escribe the 3 potential healing fates of damaged cells, following an acute inflammatory response
resolution
- damged cells tecover
regeneration
- damged cells are replaced by identical cell type (epithelail)
replacement
- damged cells replaced by connective tissue/scar tissue - loss of function
scar tissue = collagen crosslinking
compare acute vs chronic inflmamation
acute
- fast onset
- antiinflammatory response
- neutrophils
rominents signs
chronic
- no antiinflammtory compnoent
- monocyted, macrophages ;ymphocytes
what immune cells are involved with chronic inflammtion vs acte/
acute- neutrophil
chronic - monocytes, macrophages, lymphocytes
