earliest changes of rheumatoid arthritis occur where?

and erosions are usually first seen at the:

earliest changes occur in wrists or feet

erosions usually first seen at ulnar styloid

PT/OT

systemic and articular rest

exercise and weight loss

heat or cold - pt preference

asistive devices

splints

what is the first line treatment for rheumatoid arthritis

and this drug does or does not prevent erosions, altering disease progression?

NSAIDs

they provide relief, but do NOT prevent erosions or alter disease progression (just decrease the inflammation and pain)

true or false

NSAIDs should initially be given as monotherapy for rheumatoid arthritis

FALSE

no appropriate for monotherapy, should be used with DMARDs

methotrexate is the initial DMARD of choice

should see a beneficial effect within 2 - 6 weeks

what drug can be added to methotraxate for treating rheumatoid arthritis, when methotrexate alone has been inadequate

(or is commonly used as intial tx in combo WITH methotrexate for pts w/poor prognositic factors)

biologic DMARDs - tumor necrosis factor inhibitors

(etanercept, infliximab, adalimumab, golimumab, certolizumab pegol)

corticosteroids

(not in lecture notes, but in CMDT: often used a bridge to decrease dz activity until the slower acting DMARDs take effect OR as adjunctive therapy for active dz that persists despite tx w/DMARDs)

biologic DMARDs - rituximab or tocilizumab

(but not really used very often)

NSAIDS

indomethacin thought to be the most effective

OR

sulfasalazine

radiographic findings:

marginal erosions of bone and irregular destruction of joints and bones that are NOT symmetric - giving a "sharpened pencil" appearance to the phalanges

suspiscious of what?

initial treatment of psoriatic arthritis

change to what if refractive to first line drug

change to what is refractive to second line drug

NSAIDs

if resistant to NSAIDs - give methotrexate

if refracotry to methotrexate - give TNF inhibitor (bunting said in class though, that normally in clinic providers go straight from NSAIDs to TNF inhibitors)

treatment of reactive arthritis

treatment for reactive arthritis specifically caused by chlamydia

NSAIDs are mainstay of treatment

tetracycline for 3 months can reduce duration of symptoms for reactive arthritis cause by chlamydia

procainamide

hydralazine

isoniazid

malar rash

discoid rash

oral ulcers

arhtritis

neurologic complications (psychosis/seizures)

photosensitivity

serositis

renal dz (proteinuria/cellular casts/glomerulonephritis)

hematologic d/o's (hemolytic anemia/leukopenia/thrombocytopenia)

immunologic abnormalities (anti-DNA/anti-Sm/false pos syphilis)

positive ANA

ANA - sensitive but NOT specific

anti-DNA and anti-Sm - specific but not sensitive

complement levels and anti-DNA

anti-Sm does NOT correlate w/dz activit

treatment of serois cases of SLE

and what associated condition may require an increase in dosage of this specific drug

corticosteroids are required for more serious disease

CNS disease may require higher doses

what does CREST stand for?

what is it describing

Calcinosis (Ca deposits in the skin)

Raynaud's phenomenon

Esophageal dysfunction (reflux and decrease in motility)

Sclerodactyly (thickening and tightening of skin on fingers and hands)

Telangiectasias (dilation of capillaries, causing red marks on skin)

it is describing the symptoms of limited scleroderma

positive ANA (almost always)

scleroderma antibody (SCL-70) - 33% w/diffuse, and 20% in limited

ESR elevation = unusual

symptomatic and supportive

no known medication will alter disease progression

if pt has:

raynauds --> CCB (nifedipine) or ARB (losartan)

esophageal reflux --> PPI, avoid late night meals

malabsorption --> tetracycline

renal crisis --> ACE-I

pulmonary fibrosis --> cyclophosphamide

to prevent digital ulcers --> bosentan

positive for anti-SS-a and anti-SS-b

schirmer test (measures quantity of tears produced)

topical cyclosprine

(and artificial tears applied frequently)

pilocarpine

(or cevimiline is alternative)

can also advise all pts dealing with dry mouth to sip water frequently, chew sugar free gum or hard candies and use oral fluoride rinse

treatment for henoch-schonlein purpura

what could be used for a pt w/renal disease

corticosteroids may be effective for some pts

azathioprine may be used for renal disease

initial treatment of granulomatosis with polyangitis

treatment once remission has been achieved

what can be used for relapses (typically better than cyclophosphamide for relapses)

prednisone and ORAL cyclophosphamide for induction treatment

(methotrexate can be used in place of cyclophosphamide in mild cases)

change from cyclophosphamide to azathioprine once remission has been achieved

rituximab (reduces ANCA levels) may be better at treating relapses

high dose corticosteroids

cyclophosphamide

treatment of behcet's syndrome

for severe ocular or CNS dz

for mucocutaneous findings

corticosteroids are mainstay of therapy

(may use azathioprine instead)

cyclophosphamide or chorambucil for severe ocular or CNS dz

colchicine and thalidomide for mucocutaneous findings

prednisone, 10 - 20 mg daily

slowly taper after 2 - 4 weeks

most require some sort of low dose for atleast 1 year

daily exercise

good sleep hygeine

healthy diet

stress reduction

alternative/complimentary medicine

True or False

NSAIDs are not an effective form of treatment for fibromayalgia

TRUE

use tylenol or tramadol

anti-depressants are first line (typically SSRI before a TCA)

fluoxetine (prozac) - SSRI

amitriptyline (Elavil) - TCA

duloxetine (cymbalta) - SNRI

treatment of polymyositis and dermatomyositis

if resistant or intolerant to first line drug

drug specific for dermatomyositis that is resistant to first line drug

drug that can help ameliorate skin disease

corticosteroids

start with oral high dose, then taper down; long term use is often needed

if resistant or intolerant to prednisone - methotrexate or azathioprine

IVIG or rituximab is effective for dermatomyositis resistant to prednisone

hydroxychloroquine can help ameliorate skin dz

non-narcotic analgesics

behavoiral approaches (relaxation) are also effective

treatment of chronic tension HAs

what drug is NOT helpful in the treatment of pure tension HAs

amitriptyline is the only proven tx for chronic tension HAs/prevention

(other anti-depressants may be useful as prophy)

triptans are NOT helpful w/pure tension HAs

often responds well to therapy with anti-depressants

consider psychiatric consultation/counseling

rest in a dark, quiet room (avoiding light and sounds)

regulated lifestyle: healthful diet, regular sleep patterns, avoid excess caffeine/alcohol

treatment of mild symptoms of a migraine HA

(best if used right away to prevent worsening of the migraine)

NSAIDs, ASA +/- caffeine derivatives

possibly w/dopamine antagonists (metoclopramide) as adjunctive therapy (if NSAIDs are failing - can help improve absorption and decrease N/V)

treatment of migraine (more so than just a "mild" case)

what is the fastest acting non-parental antimigraine therapy

ergotamine drugs (nonselective): cafergot

OR

triptans (selective): most efficacious oral pills = rizatriptan or eletriptan

nasal 5-HT1-A: migranol, zomig, or sumitriptan

when should triptans be given to a migraine pt with an aura

co-administration of what drug is useful to add to triptans for the tx of migraines (giving longer lasting effects)

triptans are not effective in migraine with aura unless given AFTER aura is completed and HA has initiated

co-administration of a longer-acting NSAID is useful: naproxen

(bc of short duraction of action of the triptan)

worst HA of my life

first severe HA

worsening over days or weeks

vomiting preceding HA

pain that disturbs sleep, or presents immediately upon wakening

older age at onset

worsening or presistent HA

abrupt onset

age > 50s

change in characteristics, increased frequency

signs of increased ICP

meningeal signs

new HA in immunocompromised

they act to alter the pain sensation - therefore they do NOT treat the underlying HA mechanish

(suboptimal for tx of pts w/recurrent HAs bc craving or w/drawal can aggravate and accentuate migraine)

when is typically the only time narcotics are used as the tx of migraines

(what type of circumstances)

propranolol

TCAs - amitriptyline, nortriptyline

anticonvulstants - topiramate, valproate, gabapentin

NO EFFECT from: clonidine, nimodipine, SSRIs

atleast 5 attacks w/in 10 days

daily bouts of 1 - 2 attacks for 8 - 10 weeks a year

pain free interval averaging little less than a year

atleast 1 of the daily attacks recurs at same time of day for duration of cluster bout

oxygen inhalation for 15 - 20 mins @ 10 - 12 L/min

imitrex (sumatriptan) - SUBQ or INTRANASAL

OR

lidocaine - INTRANASAL

oral agents = ineffective

prophylaxis therapy for short bout cluster HAs

prophylaxis therapy for long bout cluster HAs

short bouts: prednisone X 7 days and taper

long bouts: verapamil (typically high dose)

doses are ORAL for prophylactic therapy

reduce dose of analgesic and ultimately eliminate it

add small dose of NSAID to relieve residual pain as analgesic is reduced

prednisone 60 - 80 mg PO qd for 4 - 6 weeks and THEN taper

consider low dose ASA to possibly prevent loss of vision or decrease risk of stroke

optimistic encouragement

graduated rehabilitation

avoidance of sports until resolved

simpe analgesics (NSAIDs)

if severe - amitiptylene, or anticonvulsants, or propranolol

indomethacin 25 - 50 mg BID or TIB

possible LP (decreases ICP)

vomiting preceding HA by weeks is highly characteristic of what

de novo HA in pt w/known malignancy suggests what

intracranial mass (posterior fossa brain tumors)

suggests mets, carcinomatous meningitis or both

treatment of pseudotumor cerebri

what is ineffective in treating this

treatment if medical management fails

acetazolamide PO TID (reduces formation of CSF)

may need to add oral steroids

any specific cause warrants tx (d/c OCP, treat infections, etc)

repeat LP to remove CSF to lower pressure is ineffective

consider placing a shunt to decrease pressure on optic n.

treatment of complicated temporomandibular joint dysfunction

treatment of uncomplicated

complicated (fx): oral maxillofacial surgeon referral

uncomplicated: simple analgesics

pt should eat soft foods until improved

reassurance

artificial tears and tape eye at night

prednisone taper

+/- antiviral (valcyclovir or acyclovir)

DOC for the treatment of trigeminal neuralgia

second choice drug?

carbamazepine (tegretol) = DOC

do not w/draw abruptly

avoid UV light while on this medication

phenytoin

treatment of postherpetic neuralgia

if first line fails, consider?

what are the possible topical treatments

trial of simple analgesics (consider narcotics)

if that fails, consider TCAs +/- phenothiazine

topical: capsaicin cream or lidocaine cream

usually tx is not necessary

if tx is needed: propranolol

2nd line option: primidone

resting tremor

rigidity

bradykinesia

impaired gait and mobility

postural instability

muscle strength (there is no muscle weakness present)

tendon reflexes (there is no alteration in reflexes)

plantar responses (no alteration)

levodopa (dopamine precursor)

(co-administer w/carbidopa to prevent SEs from peripheral metabolism to dopamine)

(levodopa/carbidopa = Sinemet)

dopamine agonists - 2nd generations used most often

ropinirole or pramipexole

effective in early and advanced disease

COMT inhibitors (entacapone or tolcapone)

leads to more sustained plasma levels and more constant DA stimulation - reducing fluctuation b/t levo doses

*decrease dose of Sinemet by 1/3 when COMT-I is added*

list the two possible non-drug therapies for parkinson's

and which one is preferred?

surgical treatment - thalamotomy or pallidotomy (reserved for unresponsive pts, or pts w/intolerable SEs to meds)

deep brain stimulation - preferred surgical approach

symptomatic - no cure, and cannot halt progression

for symptoms:

tetrabenazine

reserpine

haloperidol

amantadine

haloperidol

clonazepam

clonidine

pimozide in unable to tolerate haloperidol

relapsing/remitting (RRMS)

85%

discrete attacks

between attacks - neurologically stable

which clinical type of MS always begings as RRMM

and pt experiences steady deterioration in function that is unassociated with their acute attacks

methylprednisolone IV (solumedrol) for 3 - 5 days

AND

prednisone PO, after the first 3 days, for 14 - 21 days

interferon beta1 b or a

natalizumab IV

Immunoglobulin IV

immunosuppressive tx for SPMS

symptomatic tx for:

spasticity

paroxysmal pain

urinary urgency

fatigue

depression

fecal incontinence

spasticity: baclofen

paraoxysmal pain: amitriptyline

urinary urgency: oxybutynin

fatigue: amantadine

depression: SSRIs

fecal incontinence: fiber supplementation, poss anti-diarrheals

supportive measures

plasmapheresis or IVIG

anticholinesterase: neostigmine, pyridostigmine or both

thymectomy - esp considered for pts < 60 yo

tx in ICU

early and effective abx therapy, respiratory assistance, pulmonary physiotherapy

plasmapheresis and IVIG may hasten recovery

abx (AG, quinolones, macrolides)

anesthetics

beta blockers

botulinum toxin

quinine derivatives

Mg

penicillamine

no effective drug or therapy

riluzole

symptomatic - splints, tracheotomy

emotional support

what is the most important diagnostic test to confirm acute viral meningitis

and what are the findings that would be present?

CSF examination - LP

elevated WBCs - w/prominant lymphocytes

normal (or lsightly elevated) protein

normal glucose

normal (or mildly elevated) opening pressure

primarily symptomatic - analgesics, antipyretics, and antiemetics

monitor fluids and electrolytes

oral or IV acyclovir (if very ill: start IV, then change to oral; less ill: oral only)

pt is immunocompromised

has significant alterations in consciousness

has seizures

has focal S&S suggesting poss encephalitis

has an atypical CSF profile

medical emergency

dexamethasone, AND

empiric therapy (until culture results are back)

then cater to culture results

N. meningitides and S. pneumoniae (two of the most common): Pen G

IV abx combined with surgical drainage (aspiration or excision)

broad spectrum abx first and then alter once C&S is available

dexamethasone - if need to reduce any associated edema

abx tx is continued parenterally for 6 - 8 weeks, and then orally for another 2 - 3 weeks

tx in ICU

start empiric acyclovir

then specific antiviral therapy when appropriate

therapy aimed at preventing further attacks or strokes (warfarin, ASA)

stop smoking

treat underlying disease (HTN, DM, etc)

carotid endarterectomy - when surgically accessible and high grade stenosis

anticoagulation

coumadin (more effective than ASA)

ASA can be used for people who cannot tolerate coumadin

(coumadin is more effective than ASA)

ASA + dipyridamole (aggrenox) is optimal for stroke prevention

(to prevent strokes - it is more effective than ASA alone)

for pt w/noncardioemoblic TIAs - what drug can be given is place of first line drug for decreasing frequency of future TIAs (and also used to prevent strokes) if they are intolerant of the first line drug

(sorry - long question)

plavix can be used instead of ASA if pt is intolerant of ASA

(don't give plavix and ASA together!)

what imaging study should be done EARLY in the management of an acute stroke

and this study is done to rule out what?

CT of the head - do it early!

done to r/o cerebral hemorrhage

(therefore, CT is preferable to MRI in acute stages)

IV heparin to limit further deterioration - immediately

IV thrombolytic therapy WITHIN 3 hours

if cardiac source of embolization: coumadin

physical therapy (passive first and then active ROM)

OT

speech therapy

use of mechanical aids to assist w/ADLs

clinical dx of stroke

onset of symptoms < 3 hrs

CT scan: NO hemorrhage or edema of > 1/3 of MCA territory

age > 18 yo

consent by pt or surrogate

sustaine BP > 185/110

platelet < 100,00, HCT < 25%

use of heparin w/in 48 hr, prolonged PTT or elevated INR

rapidly improving symptoms

prior stroke/head injury w/in 3 mo

major surgery in last 14 day

minor stroke symptoms

GI bleeding past 21 days

recent acute MI

coma or stupor

generally conservative and supportive

ventricular drainage may be required

if cerebellar hemorrhage: prompt surgical evacuation

tx of underlying structural lesions

confine to bed, avoid exertion or straining

treat the symptoms (HA, constipation)

Lower BP gradually keeping diastolic below 100

phenytoin to prevent seizures

treatment of an intracranial aneurysm

and what is the definitive treatment

primary goal is to prevent hemorrhage

CCBs to reduce vasospasm

definitive tx: requires surgical clipping or coil embolization

injection of vascular occlusive polymer

gamma knife

(if doesn't say whether these are 3rd and 4th line, or when they are done, they are just listed)

phenytoin

carbamazepine

valproic acid

phenobarbital

Primidone

Gapapentin

lamotrigine

topiramate

ethosuximide

valproic acid

clonazepam

valproic acid

clonazepam

maintain airway

50% D50 IV

lorazepam 4mg IV bolus @ 2mg/min

OR

diazepam 10 mg IV or rectally

phenytoin 20 mg/kg IV @ 50 mg/kg

in a pt w/staticus epilepticus; if seizures continue after the administration of phenytoin, what is given next

if that also fails - what is then given

if seizures continues: add phenobarbital

if all above fails and seizures continue: general anesthesia - midazolam