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85 Cards in this Set

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What is MOA for ASA/NSAIDS
inhibt periperally acting COX-1 and COX -2
and centrally acting mechanismm
What does COX-I do?
synthesis protaglandins
Why is COX-I good?
it increases the mucous layer which protects the stomach, and it dialates afferent artery-maintain adequate perfusion
What happens when COX-I inhibitied
PG decrease, decrease mucosal layer, and constricts afferent artery in kidney, so kidney retatins (Na/H20)
Wht does Cox-II do
sytnehsis protaglandins,
Why is COX-II bad
increases inflammation
What happens when COX-II inhbiited
PG decrease, resulting in decrease of inflammation
ASA and platelet activation
ASA irrevesible binds, inhibiting platlet activation for life--(7-10 days)
Benfits of ASA
analagesic, anytpyeric (central mechansism)
COX II--antiinflammatory
Side effects of ASA
GI/irratation damage,
Kidney irration damage
Irreversible platlet inactivation
How do you manage sides effects of ASA
Stomach--take with food
Kidneys--take with 6oz water
Platelets--be aware of brusing and increasedriske of bleeding
What is HF and general result
HF, ultimately results in inability of the heath provide adequre pumping and blood supply to heart--becuase of this, patietns have fluid overload in many body parts
What is NSAID/ASA bad for HF patients
constrict afferent artery of kidney, decreases perfusion (usaually happens from dehydration), body retatins more fluid, adds to fulid overload in HF paitents (makes HF worse)
Can pt with HF take low dose of ASA
yes, is accetable
Most common use for ASA
cardio-protective activity, as decreases risk of heart attack, stroke,and blood clots
What is MOA of APAP
central inhibition of prostaglandin syntheisis of (COX 3)
Benefits of APAP
antipyretic, and analgesic, easy on stomach
Where is APAP metabolized?
APAP is extenively metabolized in Live and cytochrome P-450
What is normal mechanism of APAP metabolism
95% is metabolized by Glucuronidation, adn sulfate conjugation, 5% is by Cytochrome P450--
Why is Cytochrome P450 bad metabolism
b/c APAP is broken down into a toxic metabolite,
Usually what happens to toxic metabolite
quickly converted to non-toxic by (GSH) Glutathione
APAP and Alcohol problem
Problem b/c both are metabolized in liver
What happens when patient take too much APAP or ETOH with APAP
the Glucuronidation and fulfate conjugation process become saturated, so more is procress by P450..making more toxic metabolics--if their is not enough GSH to make non-toxic,
What happens when more toxic metabolites than GSH
they react with liver cell macromolecules, and result in liver death
Why is alcohol also a problem with Nsaid and ASA
1. COX I decrease mucusol layer,
2.NSAIDs ASA, adn Etoh..all acidic,
both can lead to irriation, erosion then uleraction
3. inactive platelets which increases risk of bleeding
What pathophysiology of HA
vasodialtion--puts pressure on tissue in brain
What generally causes tension-type headaches
stress, anxiety, depression, fatigue
What is Location of tension HA
bilateral, over the top of the head, extends to neck and shoulders
What is nature of tension HA
diffuse, aching pain (TIGHT, pressing and constricting)
Onset of tension HA
gradual
Duration of Tension HA
mintutes to days
What generally cuases Migranes
stress, fatigue, FASTING, FOOD, meications, and menses
Location of migraine
ONE-SIDED
Nature of migraine
THROBBING
Onset of migraine
Sudden!
Why does migrane with aura similar to stroke
b/c of vasoconstriction--difficulty speaking, one-side muscle weakness
Other symptoms of aura (non-stroke)
flashing areas, blinds spots
How long does Aura last
up to 1/2 hour
What is duration of migraine
HOURS-to 2 days!!!
Location of sinus headache
face, forehead, and around eyes (peri-orbital)
Nature of sinus headache
pressure behind eyes or face, pain in teeth
Onset of sinus HA
with sinus symptoms, and prulent nasal discharge
Duration of sinus HA
resolves with sinus symptoms
When a symptoms worse with sinus HA pain
upon awaking
What are exculsion for Self-treatment of HA
Severe head pain, Secondary headache, Symptoms consitant with migraine, but NO dianosis, serious infection headache that persist more than 10 days, history of liver disease or alcoholism
Until what age should patient avoid ASA adn why
15, can cause Reye's Syndrome
Why should older patient and patients with Renal disease avoid ASA and nsaids
older more sentivie to GI upset, and side effects and all nsaids and asa, metbolized by KIDNEY
Dosage of Iburofen
200-400 mg every 4-6 hours

max 1200
Dose of ASA
650-1000 every 4-6 hrs max 4000
Dose of APAP
325-1000 every 4-6 hours max 4000
Dose of naproxen
220mg every 8-12 hrs and at least 12 yrs old
Dose of Ketoprofen
12.5-25 mg 4-6 hours max 75 and at least 16
What causes Myalgia
strains, trauma, overexertion, sysyemic infections, alcohol, statins
Location of myalgia
body muscles
Signs of myalgia
pain, increase CPK, and rare (swelling)
Symptoms of myalgia
dull, constant ache, weakness, and fatigue of muscle
Onset of myaliga
trauma-acute
drugs-insidous (gradual)
Excerbating factors of myalgia
contraction of muscle
Nonpharm for Myalgia
streching and warming up, elminating cause, rest, RICE,
Where is location of OA
Weight-bearing joints, kness, hip, spine, hands
Signs of OA
NON-infammatory joints, possible joint deformities
Symptoms of OA
Dull join pain relived by REST <20-30 minutes
Onset of OA
gradual--over the years
What causes OA
softening and destruction of the cartilage between bone
What are excerbating factors of OA
obesity, lack of activity, heavy physical activity
Non-pharm for OA
continous light-moderate activity, or weight loss, shock absorbing shoes, canes, walkers
Location of RA
small joings of fingers, wrists and feet
Signs of RA
joint swelling and deformities
Symptoms of RA
Pain worse in moring >30 minutes
Onset of RA
autoimmune diesase--weeks to months
What is treatment of choice for OA, should we treat RA
APAP, b/c no inflammtion, don't treat RA--see a RA
Exculsion for Self-Treatment of OA, Myalgia
Severe pain, Serious infection, pain last >10 with.out treatment, pevlic or abdominal pain, visual deformity or <7 yrs
What is a an OTC recommened for OA
Glucosamine
What is Glucosamine and treats
Building block for cartilage, reduces pain, and reduces the progression of the disease
What 2 brands are recommend by Glucosamine or what certification
Kirkland Brand and Nature's way----USP verified
Who should stay away from Glucosamine
Diabetics, and allergies to shellfish
What is non-pharm for tension HA
relaxation exercise and PT
What is non-pharm for mirgrane
regular sleeping, eating schedule, practice methods for coping with stress, avoid wines, cheese, caffiene
What is RICE
REst, ICE , compression, adn elevation
How should one ice
ASAP to the injured area in 10 minue increments 3-4 times for 1-3 days
What is compression
wrap the injured area from the most distal part, if icing at same time wet bandange with cold water
What is elevation
elevate the injured area at or above the level of the heat to decrease swelling and relieve pain
What is heat helpful
for patients that have NON-INFLAMMATORY pain..reduces pain by increasing blood flow
How often should heat be used for myalgia and who
DO NOT USE on recently injured area or INFLAMED--can increase vacodialtion--should be applied every 15-20 minutes 3-4 times a day
What is onset of relief from Glucosamine
Take same time each time, may take up a month to see a relief in symptoms----