neutral

inverse

10mg for analgesia (PO)

100mg lethel (PO)

1. structural activity relationships
2. receptor isolation and purification
3. charecterization of receptor binding profiles
4. charecterizzation of receptor and second messenger system
5. receptor cloning
6. investigation of knock out mice
7. molecular modeling
8. crystal structure

1. pro-enkephalin-(leu-enkephalin, met enkephalin)
2. pro opioimelanocortin( beta-endorphin)
3. pro-enkephalin( dynorphin A and B,  alpha and beta neoendorphin)

respiratory depression

pupil constriction

reduced GI motility

euphoria

sedation

physical dependence

dysphoria

sedation

and sometimes dimerizze with the mu receptor

MU

morphine, codeine, methadone, meperidine, etropine, fentanyl

kappa receptor

nalorphine

bupenorphine

pentazocine

they are used for overdose or heroin addiction

naloxone (overdose go to)

naltrexone (heroin addiction some overdose)

glucoronide formation at hydroxy groups (morphine and codeine)

hydrolysis of esters (remifentanil)

N-demethylation (methadone, meperidine)

1. receptors it targets, potency, efficacy, duration of action
2. quantity frequency, duration of administration, route
3. elimination rate (ADME)

some recepters internalize in the membrane

some are metabolized by endozomes

1. no it is not reccommended since the high dose of the opioid will depress the vomitting center
2. you should give the opioid antagonist naloxone

action in the brain which varies by agent

in the periphery brdykinin capsacion blocking may work

16-60mg for analgesia

12mg for antitussive

5-30 mg IR

10-160mgSR

promotes breakdown of body tissue

increases metoblic rate, blood clotting, water retnentin

impairs immune function

activates fight or flight response

Physical

spiritual

social

psychological

let the patient tell you about it

charecterize the pain

develop a therapeutic stratagy

1. Admission- this will establish a baseline and find out all the areas of pain
2. after each intervention- assess before a dose and at peak onset of a dose (maybe use a pain diary)
3. with each new report of pain

• p-palliative/precipitating/previous therapy (what helps relieve the pain and what bings it on)
• Q-quality (what does the pain feel likesomatic nociceptice, visceral nociceptive, neuropathic)
• R-region/radiating (where does it hurt and does it spread)
• s-site/severity (find out the worst the best now average and where they would like to be)
• T-temporal (onset duration variation frequency patterns acute chronic)
• Aassociated symptoms(how does the pain affect you  (sleep, appetite, work mood)

facial expression

muscle tension

gestures

whinceing 

1. observe pain site
2. monitor GR, BP, RR (dont rely soley on the patient for pain)
3. look for signs and non-verbal symptoms

1. Step1-problem definition (data base observations, subjective, objective, knowledge of pathology)
2. step 2 - assessment (why now what etiology how severe)
3. step 3- define the therpeutic objective (re-visit your personalized pain goal, pain rating, associated symptoms)
4. step 4- identify indices of therapeutic effect( use subjective and objective measures)
5. step 5- indentification of available modalities (non-opiod therapy, opioid, adjuvant. co-analgesics)
6. step 6- identification of variables affecting therapy (agent related, patient related)

• liver disease
• use of EToH
• malnutritoin or fasting
• sore throat for more then 2 days with fever headache nausea rash or vomit
• pain >5days child and >10days adult or worsening fever>3 days
• children<2

why do NSAIDs give increase cardovascular risk

• increase water retention- which worsens blood pressure and heart failure
• also blocking cox two will force the cox-1 pathway- this will increase platelet aggregation

• history of allergies
• history of GI ulceration, bleeding
• renal impairment
• hepatic impairment
• CHF, fluid retention edema
• bleeding risk
• history of alco use
• self limiting illnesses that do not resolve

• anticoagulants
• aspirin (take aspirin first)
• corticosteroids
• methotrexate (reduced excretion increased toxicity)
• furosemide (reduced effect)
• lithium (reduced renal clearance)

sedation

dizziness and confusion

N/V

constipation

dry mouth

sweating

physical dependence

respiratory depression

pupillary constriction

CNS depressants

alcohol drugs of abuse

1. age- non one under 12 for transdermal fentanyl, no one under 18 and less then 50kg unless for research
2. renal impairment/ dialysis- should use methadone or fentanyl but can use ocycodone or hydromorphone
3. hepatic dysfunction- all opioids go through the liver
4. race- Azns may not metabolize codeine
5. body build- frail cachectic ppl may have altered pharmacokintetics/pharmacodynamics with
6.  trandermal fentanyl
7. patients ability to swallow
8. and so much more

tricyclic antidepressants

SSRI and selective norepinephrine reuptake inhibitors

calcium channel alpha2- ligands (gabapentin

lidocaine

opioids 

tramadol

antiepileptics

antidepressants

mexiletine

NMDA receptor antagonist

topical capsaicin

cardiovascular disease

claucoma

urinary retention

autonomic neuropathy

risk of suicide

use of tramadol or methadone

during titrations of a first line

episodic exacerbations of sever pain

acute neuropathic pain

neuropathic cancer pain

• follows injury to body and generally disappears when injury heals
• lasts less then 3 months

• pain is harmless
• pain masks diagnosis
• not recognized
• lack of assessment and reassessment
• fears of addication and respiratory depression
• inadequate preoperative patient education
• patient reluctant to ask for drugs
• interpatient variableitiy to opioids
• lack of education on opioid dosing
• accountability for pain management

1. etiology of pain
2. patient variables
3. potential for adverse effects
4. potential for drug interaction
5. comorbidities that may be exacerbated by non-analgesic properties of drug
6. costs of therapy
7. risks of medication abuse
8. risks of overdose

coagulopathy

orthopedic surgeries involving bone infusion

following coronary bypass surgery

the naive patient should use bolus

the tolerant patient should have a continuous infusion

PSA terms

1. loading dose
2. bolus dose
3. lockout
4. cumulative dose limits

1. loading dose- is the initial dose given at the start of a PCA (not always given)
2. bolus dose- these are the doses they get everytime they push the button (machine can also give a continuous drip at the same time)
3. lockout-- this is the predetermined time interval between doses (typically at onset of drug so the doses don't overlap)
4. cumulative dose limits- the max allowed in 1 or 4 hours

1. never titrate by altering lockout
2. typically increase doseages 25-50%
3. verify pca program is correct and working

acute soft-tissues injuries (strains sprains)

repetative strain injury

low back pain

rheumatoid and osteoarthritis

heat

swelling

pain

redness

• 48-72 hours
• rest affected area
• Ice the affected area 15-20 min every 2 hours for 48 hours
• compression-begin wrapping the bandage at the most distal point to the injury firmly but not too tight
• elevate above hear level

acetaminophen, NSAIDs (rarely opiods)

topicals

decision points (patient prefrences, extent of injury, patient related variables

1. topical NSAIDs voltaren gel (osteoarthritis), flector patch(sprains and strains)
2.  local anesthetics lidocaine benzocaine ()work to decrease discharge in superficial nerves to cause numbness)
3. counterirritants 4 types those that produce redness, cooling, vasodilation, irritate without causing redness

ally isothiocyanate

ammonia water

methyl salicylate (bengay ultra caution W/aspirin allergy)

trolamine salicylate (aspercreme)

camphor (jointflex)

menthol (bengay, icyhot)

3-5 times a day

externally only

small serface area

wash hands after

avoit eyes and mouth

do not use heating pad

do not wrap in bandage after

call dr if symptoms worsen persist over 7 days resolve and recure

10-15% of patients

most prevalent 35-45

women

two of the following

2 or more of the following

rapid pain relief over the short term

the long term is to diminish recurrence

• short term-analgesics, serotonin receptor agonists (triptans), start trreatment early
• long term management focus one lifestyle modifications, and screen for red flags

patient education- have them keep a record

limit exposure to triggers

behavioral

APAP, NSAID, opioid, 

triptans, ergotamines, caffeine

main is TCA

skeletal muscle relaxants,botulinum

main is verapamil

may use lithium

beta 2 causes relaxation

M3 causes accomadation

bimatoprost

latanoprost

travoprost

unoprostone

block beta 2 on the cilliary epithilium (stoping aquous humor production)

binds to beta 2 receptor in veins to decrease ultrafiltrate

corneal anesthesia

inflammation

systemic effects- hypotension, bradycardia, syncope 

upto 50% of patients will have an allergy to it

tolerance builds up

MAOI

anticholinergic use

renal failure, hepatic issues

lowered K and Na

COPD

Reduce IOP by contracting pupillary sphincter muscle of the iris and ciliary muscle to physically open the canal of Schlemm and the trabecular network.

this is a sudden  spike in IOP typically to over 40

which is caused by pupillary block (lens and iris connect blocking canal of schlem)

maybe one red eye

vomitting

IOP 40-90

primary reduce IOP by 20-30%

secondary decrease below 21

1. preserve visual function decrease IOP 25-30% in open angle and 40-50% in closed angle
2. then the secondary goal is to reduce below 21
3. if disease is advanced reduce IOP below 10
4. prevent further optic nerve damage

retinal thickening in macular area 

this is something that a patient with retinopothy will get

Optimize glycemic control

Optimize blood pressure control