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52 Cards in this Set

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What is Osteoarthritis(OA)?
-Thee most prevelent rheumatic dz
-Increases with age
-50% over 65, and almost everyone by 75
How does OA present?
-Slowly progressive and affects diarthrodial joints
-Minimal inflammation involved
What body area does OA affect?
-Articular cartilage
-subchondral sclerosis
-osteophyte production
Clinical manisfestaions of OA?
-Gradual onset of joint pain
-Stiffness
-Limitation of motion
Risk factors of OA?
Obesity
repetitive stress
low quadriceip strenght
advancing age
genetic factors
Goals of OA tx
1) educate the pt, caregivers and relatives
2) relive pain and stiffness
3) Maintain or improve joint mobility
4) mantain or improve the Quality of Life
Pain management is the primary goal of OA tx. T or F?
True
Pharm tx OA:
-DMARDS do not work
-Acetominophen up to 4 gms/days should be tried initially.
-Try NSAID if acetominophen ineffective
Pharm tx OA:
-Capsaicin (Zostrix)
-Glucosamine and Chondroitin
Capsaicin:
-Active ingredient of hot chili peppers
-Depletes substance P form afferent nicoreceptors
-Apply 2-4 times daily to affected joints
-Takes up to 2 weeks to work
-Advise pts to wash hands well after touching and do not get in eyes
Glucosamine and Chondrotin (OA)
-Stim Proteoglycan synthesis from articular carglige in vivo
-Excellent safety profile
-Well tol
Gout?
Is a Rheumaltologic DZ due to Uric Acid Crystals
What is Uric Acid?
-Waste product of Purine Metabolism
Serum urate concentration with risk of Gout correlates with?
-age, serum creatinine level, BUN, Male gender, BP, body weight, and alcohol intake.
Solubility of Uric Acid (weak acid)?
-7mg/dl at physiologic PH
pKa=5.5
Risk of Gout increases with?
-Increasing Uric acid levels but:
many pts will have normal levels of uric acid somw will never have an attack despite very high levels of Uric Acid.
Bascically with Increased Uric Acids Levels?
= increased Gout attack
Drugs that cause Hyperuricemia and Gout?
-Diuretics
-Nicotinic Acid
-Salicylates
-Ethanol
-Pyranzanmide
-Levodopa
-Ethambutol
-Cytotoxic Drugs
-Cyclosporine
Presentation of Gout:
Gout typically involves acute attacks of:
-arthritis
-nephrolithiasis
-gouty neuropathy
-aggregated deposits of Sodium Urate (Tophi) in cartligae, tendons, synovial membranes, and elsewhere.
Tophi (with Gout)?
Tophi= aggregated deposits of sodium Urate
Acute Gouty arthritis?
Most common form of Gout
-rapid onset of excruciating pain, swelling and inflammation.
Monoarticular at first then great toe, and then order of freq: insteps, ankles, heels, knees, wrists, fingers, and elbows
TX of Gouty arthritis?
-Indomethacin
-Naproxen
-Ibuprofen
-Sulindac
Indomethacin = most potent NSAID but very toxic too.
Kidney stones?
10-20% of pts with Gout.
Risk factors for Stones:
-excessive urinary excretion of uric acid, acidic urine, highly concentrated urine.
TX Kidney stones with Gout?
-Urine output 2-3 ml/day
-alkalinazation of Urine (PH 6-6.5)
-avoidance of purine rich foods
-moderation of protein intake
-reduction of urinary acid secretion
Prevention of Kidney stones with Gout?
-Allopurinol is the mainstay.
Prevents formation of Uric acid in bloodstream
-which prevents fromation of calculi
Gouty Nephropathy
Two types?
-Acute Uric acid Nephropathy
-Chronic Urate Nephropathy
* see notes
For pts with myeloproliferative disorders undergoing chemotherapy-what is the Drug of choice?
-Allopurinol
DOC to prevent Acute Nephropathy
Tophaceous Gout?
-late complication of hyperuricemia
-affects: base of great toe, helix of ear, olecranon bursa, Achilles tendon, knees, wrists, and hands.
See notes for more crap
Can lead to Carpal Tunnel syndrome*
Labs of Tophaceous Gout?
-Elevated serum uric acid levels
-overprod or underproduction of uric acid
-Excretion primarily renal(2/3) but also GI(1/3)
-Leukocytosis
TX for Tophaceous Gout?
1) Tx for acute attack:
-NSAIDS (no aspirin_
-Colchicine
-Intrarticular steriod
-Probencid
2) Prev of recurrent attacks
-Allopurinol
-ARBS(losartin) and Probencid increase urinary excretion of uric acid.
Colchicine?
pg 512
Tx for accute Gouty attacks
and prevention of recurrent attacks
MOA Colchicine?
MOA
-reduciton in lactic acid production by leukocytes, which results in a decrease in uric acid deposition, and a reduction in phagocytosis with abatement of inflammatory response
ADX of Colchicine?
Many:
Alopecia, N&V, Gi disturbances, diahrrea, agranulocytosis/aplastic anemia, alopecia
Allopruinol(Zyloprim)
Use: Prevention of recurrent attacks, prev of neuropathy from chemo, mgmt of pts with signs and sxms of primary or secondary gout.
Allopruinol MOA
-Xanthine oxidase inhibitor
-Prevents formation of Uric acid
-Lowers serum uric acid levels (goal <6)
-Results in a fall in both serum and urinary uric acid within 2-3 days-dose dependant
Adverse effects of Allopruinol?
-Severe rash(SJS,TEN)
-DC at first signs*
-Renal elimination
-Drink extra fluid to maintain dilute and neutral to alkaline urine.
Lactation-use caution
Uricosuric acid?
-increase renal clearance of uric acid by inhibit renal tubular reabsorption
-start low dose to avoid poss stone formation
-Maintain urin flow alk with Sodium bicarb first few days to reduce uric acid stone formation
Probenicid?
-Tx of hyperuricemia associated with Gout and Gouty arthritis
MOA for Probenicid?
Inhibits tubular reabsorption urate, thus increasing the urinary excretion of uric acid and decreasing serum urate levels.
ADVSE rxn:
Acute sxms at first, start Chochiicin or NSAID first
Hypersensit rxn
Preg cat B
Many rxns.
Ankylosing Spondylitis?
A rheumatic disease that causes arthritis of the spine and sacroiliac joints and can cause inflammation of the eyes, lungs, and heart valves
Ankylosing Spondylitis
-varies from intermittaent episodes of back paing and sever chronic dz that attacks spine, peripheral joints, and other body organs resulting in severe joint stiffness, loss of motion and deformity
-Genetic marker HLA-B27
-Predisp post bowel or UTI
-adolescents and young adult males
Most common is Native Amreicans**
What is the most effective NSAID For AS?
Indomethacin
Hypnotic effects with Benzo's
-Hyonosis is a characteristic of ALL sedatives/hypnotics if a large enough dose is given
--Goal induce sufficient drowsiness to induce sleep!
Most sedative/hypnotics:?
-decrease time to get to sleep (latency)
-increase time spent in stage 2 NREM sleep*
-dec time spent in REM sleep*
-both of those are good for sleep*
Discontinuation of sedative/hypnotics results in?
-REM Rebound
*Tolerance to effects on sleep patterns often develops post 2 weeks.
Anasthesia effects of Benzo's?
-Some agents will depress CNS to achieve stage III anesthesia
-*Benzo's are NOT suitable for induction of anesthesia
-Contribute to Postanesthetic respiratory depression
Anticonvuslant effects of Benzo's?
-some benzo's can inhibit the spread of seizure activity W/I the CNS
-Clonazepam
-Lorazepam
-Diazepam
-Nitrazepam
Bezo tx should not exceed....?
4 months
Short term for anxiety insomnial only!
Advse RXN with Benzos?
-majority of effects involve CNS
-drowsiness, sedation, psychomotor impairment, disinhibition, and ataxia
Many others see notes**
Benzo's for anti-anxiety:?
-Alprazolam (Xanax)
-Clonazepam(Klonopin)
-Diazepam (Valium)
-Lorazepam (Ativan)
Benzo's for sleep:?
-Temazepam (restoril)
Non-benzo's anitanxiety?
-Busiprone(Buspar)
-Zolpidem(Ambien)