Term
|
Definition
| Failure of the movable, synovial-lined joint |
|
|
Term
| In what gender OA is more common? |
|
Definition
|
|
Term
| What pecent of women <45 has OA? |
|
Definition
|
|
Term
| What percent of women betweem 45 and 64 y.o.has OA? |
|
Definition
|
|
Term
| What perceent of women >65 y.o. has OA? |
|
Definition
|
|
Term
| What kind of OA women are more likely to have? |
|
Definition
| Women are more prone to inflammatory OA of proximal and distal joints of hands |
|
|
Term
| How does race influence distribution of OA? |
|
Definition
Knee OA is 2X as likely in black women than white
Chinese, East Indian, Native American have lower incidence of hip OA than Caucasian |
|
|
Term
True/False
Older women are twice as likely as men to have OA of knee and hands |
|
Definition
|
|
Term
| What are risk factors for OA? |
|
Definition
Age, Female sex,Race,Genetic factors
Major joint trauma,Repetitive stress
Obesity,
Congenital/develop-mental defects
Prior inflammatory joint disease,
Metabolic/endocrine disorders |
|
|
Term
| What is a role of chondrocytes in OA? |
|
Definition
Produce collagen and PG as well as playing a role in degradation
Undergo active cell division and are active metabolically leading to thickened cartilage and compensated, stable OA |
|
|
Term
| What is going on in early OA? |
|
Definition
the cartilage is thicker than normal
Extra-cellular matrix is damaged and water content increased
Primary changes begin in the cartilage with a change in the arrangement and size of the collagen fibers |
|
|
Term
| What is going on later in OA? |
|
Definition
, joint surface thins, cartilage softens, integrity of the surface is breached, vertical clefts develop
Areas of repair develop but function is inferior
Bone growth occurs altering the contour of the joint and reducing mobility
Osteophyte – new bone growth at the joint margin away from the area of destruction
Synovitis leads to thickening of the joint capsule
Periarticular muscle wasting is common |
|
|
Term
| What are clinical finding for OA? |
|
Definition
Pain – deep ache, localized to the joint, aggravated by joint use, relieved by rest
Nocturnal pain is seen in advanced OA of the hip
Stiffening after inactivity
Joint motion limitation
Crepitus – grating or crackling with motion |
|
|
Term
True/False
People with OA complain about joint ache during weather change. |
|
Definition
| True (due to the change in barimetric pressue) |
|
|
Term
| What joints are more commonly affected by OA? |
|
Definition
DIP (Heberden’s nodes)
PIP (Bouchard’s nodes)
First carpometacarpal
Knees
Hips
Cervical and lumbar spine
First MTP joints (big toe) |
|
|
Term
| What joints are less commonly affected? |
|
Definition
Shoulder
Elbow
MCP (finger base) |
|
|
Term
| What are the sources of pain in OA? |
|
Definition
Cartilage contains few nerve endings
Pain can result from:
Osteophyte growth with stretching of the periosteum
Microfractures
Synovitis
Damage to ligaments and meniscus |
|
|
Term
| What is first line in the treatment of OA? |
|
Definition
| Nonpharmacological therapy |
|
|
Term
| What is a role of the meds in OA? |
|
Definition
| Medications do not alter disease course, but are used to treat symptoms |
|
|
Term
| What are the goals for treatment of OA? |
|
Definition
Relieve pain and stiffness
Maintain or improve joint mobility
Limit functional impairment
Maintain or improve quality of life |
|
|
Term
| What is a key in nondrug therapy of OA? |
|
Definition
|
|
Term
| On what side should be crutch used in OA? |
|
Definition
|
|
Term
| What is a first line agent for treatment of mild to moderate symptms of OA? |
|
Definition
|
|
Term
| What is a typical dose of acetameinophen for OA? |
|
Definition
| 325-1000 mg four times a day |
|
|
Term
| What is a max dose of APAP for OA? |
|
Definition
|
|
Term
| What is a major advantage of acetaminophen? |
|
Definition
|
|
Term
Acetamenophen is safest drug for patients with renal disease
True/False |
|
Definition
|
|
Term
| What is a big concern with acetamenophen? |
|
Definition
| Potentially fatal hepatotoxicity in ovedse. |
|
|
Term
Caution should be exercised when using acetamenophen in liver disease and alcohol abuse.
True/False |
|
Definition
|
|
Term
| What kind of activity acetamenopen does not have? |
|
Definition
|
|
Term
| What qualities does aspirin have? |
|
Definition
anti-inflamatory
analgesic
antipyretic
platelets inhibition |
|
|
Term
| At what dose ASA has anti-inflamatory effect? |
|
Definition
|
|
Term
| For what kind of pain ASA can be used for? |
|
Definition
|
|
Term
| What is a mechanism for antipyretic effect of ASA? |
|
Definition
| Heat dissipation through vasodilation |
|
|
Term
| Cardioprotective effect of ASA is due to what? |
|
Definition
Platelet inhibition
Decreased aggregation from inhibition of thromboxane synthesis
Irreversible inhibition, therefore 8 days required for normal platelet function |
|
|
Term
| How should be plain ASA be taken? |
|
Definition
| with foodor milk to min GI SEs |
|
|
Term
| Enteric coated ASA should be separated from antacids and milk |
|
Definition
|
|
Term
|
Definition
GI (from mild to peptic ulcers),Decreased platelet aggregation increases bleeding risk
CNS – tinnitis and vertigo
Intolerance
Reye’s Syndrome – children
Allergy |
|
|
Term
Dyspepsia can't predict GI bleed.
True/False |
|
Definition
|
|
Term
NSAIDs exibit antiinflamatory effect at higher doses.
True/False |
|
Definition
|
|
Term
NSAIDs exibit analgesic effect at higher doses.
True/False |
|
Definition
|
|
Term
|
Definition
| Mechanism is based on blockade of prostaglandin synthesis through inhibition of cyclooxygenase (COX-1 and COX-2) |
|
|
Term
| What toxicities do NSAIDs have? |
|
Definition
Gastrointestinal
Renal
Cardiovascular
Hematological
CNS |
|
|
Term
| What percent of pts will have dyspepsia, heartburn and pain while taking NSAIDs? |
|
Definition
|
|
Term
| What kind of GI SE another 20-30% ofpts will have? |
|
Definition
| mucosal erythema, erosions, peptic ulceration (endoscopy) |
|
|
Term
| What will increase risk of GI SE with NSAIDs? |
|
Definition
| age, history of peptic ulcer or bleeding, systemic glucocorticosteroids, increasing NSAID dose |
|
|
Term
| How one can reduce GI irritation with NSAIDs? |
|
Definition
| Take with food or antacids to reduce irritation |
|
|
Term
| What kind of products can't be taken with food or antacids? |
|
Definition
|
|
Term
| What can be use for treatment/prophylaxis against ulceration? |
|
Definition
Proton pump inhibitors (PPIs) -omeprazole (Prilosec)
Prostaglandin analogs –misoprostol/diclofenac (Arthrotec)
H2 blockers -famotidine (Pepcid), ranitidine (Zantac)
Antacids -calcium carbonate (Tums)
Sucralfate (Carafate) |
|
|
Term
| What i a SE of prostaglandin analogs misoprostol/diclofenac (Arthrotec)? |
|
Definition
| Diarrhea, cramping (unsafe in women) |
|
|
Term
| What drugs are often used with NSAIDs to prevent ulceration? |
|
Definition
| PPIs - omeprazole (Prolosec) |
|
|
Term
| What doses of H2 blockers -famotidine (Pepcid), ranitidine (Zantac) should be used for GI prophylaxis? |
|
Definition
|
|
Term
| What drugs have less degree of evidence long term for GI prophylaxis? |
|
Definition
Antacids -calcium carbonate (Tums)
Sucralfate (Carafate)
not used in combo |
|
|
Term
| What blood tests should be done while taking NSAIDs? |
|
Definition
|
|
Term
| In what condition prostaglandins are especially important? |
|
Definition
| Prostaglandins are especially important for renal function in patients with volume overload or diminished cardiac output |
|
|
Term
| What is an average BP increase on NSAIDs? |
|
Definition
|
|
Term
| NSAIDs should be used in caution in what group of pts? |
|
Definition
| in patients with congestive heart failure (CHF), liver disease with ascites, compromised renal function, or concomitant diuretic use |
|
|
Term
Neprotic syndrme is directly relate to previous renal problems
True/False |
|
Definition
| False, it s a rare SE, due to direct irritation of the nephrons, reversible on D/C |
|
|
Term
| NSAIDs can lead to CV events,thrombotic events, myocardial infarction, and stroke, which can be fatal. |
|
Definition
|
|
Term
| What will increase risk of CV, thrombosis, MI, stroke with NSAIDs? |
|
Definition
| prolonged use, CV disease or factors for CV disease |
|
|
Term
| What is CI contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery ? |
|
Definition
|
|
Term
| What drugs are linked to increased risk of CV events? |
|
Definition
|
|
Term
| What drug is safer in CV risk? |
|
Definition
|
|
Term
| When pt should take ASA while on therapy with NSAIDs? |
|
Definition
|
|
Term
| What patients population at increased risk for GI AEs? |
|
Definition
|
|
Term
| Hematological SE of NSAIDs are due to what? |
|
Definition
Inhibition of COX-1 causes reduced platelet adhesiveness and prolonged bleeding time
Rarely -thrombocytopenia and bone marrow toxicity |
|
|
Term
| What CNS SE do NSAIDs HAVE? |
|
Definition
| Cognitive dysfunction, confusion, somnolence, dizziness, behavioral changes, headache |
|
|
Term
| What is respiratory SE of NSAIDs? |
|
Definition
|
|
Term
| What is dermatological SE of NSAIDs? |
|
Definition
|
|
Term
| What factors increae risk of GI renal SE? |
|
Definition
| Moderate to high dose (Naproxen, Ibuprofen, diclofenac)and increased age |
|
|
Term
| NSAIDs decrease antihypertensive effect of which drugs? |
|
Definition
| ACE inhibitors, beta blockers, diuretics |
|
|
Term
|
Definition
|
|
Term
| bisphosphonates + NSAIDs =? |
|
Definition
| increased risk of GI irritation |
|
|
Term
| What is effect of salicylates on NSAIDs? |
|
Definition
|
|
Term
| Phenytoin/Lithium + NSAIDs = ? |
|
Definition
| increased level of phenytoin/lithium |
|
|
Term
| Methotrexate + NSAIDs = ? |
|
Definition
| increased toxicity of methotrexate |
|
|
Term
| What pts can't take celecoxib? |
|
Definition
|
|
Term
| What SEs are similar for nonselective NSAIDs and COX-2 inhibitors? |
|
Definition
| Sodium retention and decreased glomerular filtration |
|
|
Term
| When we target COX-2 we interfere with? |
|
Definition
platelet aggregation, vasodilation, antiproliferative effects
Naproxen and diclofenac have bad outcomes |
|
|
Term
| When we target COX-1 we interfere with? |
|
Definition
| platelet aggregation, vasoconstriction, smooth muscle proliferation |
|
|
Term
True/False
Combo (naproxen + PPI) is effective as celecoxib in pts with GI risk? |
|
Definition
|
|
Term
| Celecoxib risk increases with which dose? |
|
Definition
|
|
Term
| How ibuprofen should be dosed when ASA is used for cardioprotection? |
|
Definition
| Dose ibuprofen 8 hours before or 30 minutes after immediate-release ASA |
|
|
Term
| When ASA is used for cardioprotection what should be used for pain management? |
|
Definition
|
|
Term
| What is most COX-2 selective agent? |
|
Definition
|
|
Term
| What are some characteristics of Non-acetylated Salicylates? |
|
Definition
Less GI irritation than ASA
Less effective than ASA at inhibiting COX
Smaller effect on platelet aggregation than ASA Potential benefit in asthma, bleeding risk, renal dysfunction |
|
|
Term
| What agents are Non-acetylated Salicylates? |
|
Definition
Salsalate
Diflunisal
Choline salicylate
Choline magnesium salicylate |
|
|
Term
| What opioids can be used for OA? |
|
Definition
Tramadol (Ultram®)
Codeine w/ APAP
Propoxyphene |
|
|
Term
| What opioid is not a first line agent? |
|
Definition
|
|
Term
|
Definition
| nausea, vomiting, dizziness, constipation, tolerance, dependence, respiratory depression |
|
|
Term
|
Definition
| Endogenous substance made from glucose and used in biosynthesis of proteoglycans and glycosaminoglycans, the building blocks of cartilage |
|
|
Term
| What is simptomatic improvement with glucosamine similar to? |
|
Definition
|
|
Term
true/false
Glucosamine is C/I in pts with diabetes |
|
Definition
|
|
Term
| What dose of glucosamine is used for OA? |
|
Definition
| 1500 mg QD (or divided BID-TID) |
|
|
Term
| What are SE of glucosamine? |
|
Definition
|
|
Term
|
Definition
| Mucopolysaccharide found in most mammalian cartilaginous tissues |
|
|
Term
| What is daily dose of chondroitin? |
|
Definition
|
|
Term
| What classes of agents chondroitin may interact with? |
|
Definition
| anticoagulants and antiplatelets: INR will increase |
|
|
Term
True/false
one should start combo (glucosamine+chondroitin) since the beginning |
|
Definition
False
A pt should start with one product for a month and see if there is any improvement. |
|
|
Term
| What drugs glucosamine may interact with? |
|
Definition
|
|
Term
| What are indications for orthopedic referral in OA? |
|
Definition
Severe OA that has failed to respond to medications
Progressive limitation in ADLs |
|
|
Term
| What are indications for total hip replaement? |
|
Definition
Radiographic evidence of joint damage
Moderate to severe persistent pain or disability
Not substantially relieved by an extended course of therapy |
|
|
Term
| What agents have evidence in OA disease progression and inflamation? |
|
Definition
| Doxicycline and minocycline |
|
|
