Neuro Test 3 Set 1

Front 1

Hypoxia

Back 1

reduction of oxygen supply to tissue

Front 2

Ischemia

Back 2

deficiency of blood, due to constriction or obstruction of blood vessel

Front 3

Infarct

Back 3

area of coagulation necrosis due to ischemia resulting from interruption in circulation to the area

Front 4

Transiet Ischemic Attac (TIA)

Back 4

REVERSIBLE brief impairment of neurological fxn due to interruption of regional cerebral blood flow (several sec up to 24h & 1 in 5 progress to CVA)

Front 5

Reversible Ischemic Neurologic Deficit (RIND)

Back 5

neurologic deficit lasting more than 24h, but resolves before 3wks

Front 6

CVA

Back 6

IRREVERSIBLE neurological injury caused by interruption of cerebral blood flow (85%) or hemorrhage (15%)

Front 7

Rates of stroke (2)

Back 7

1)M > F; but 62% of stroke deaths are F
2)death rate in blacks is 2x that of whites

Front 8

Unmodifiable ISCHEMIC stroke risk factors (5)

Back 8

1)age
2)sex (M>F, but F have greater chance of dying)
3)race (blacks/hispanics have higher prevalence)
4)family history (risk goes up 4x if both parents have had one)
5)low birth wt (<2.5kg)

Front 9

Modifiable ISCHEMIC stroke risk factors***** (8)

Back 9

1)HTN
2)DM
3)smoking
4)A.fib
5)obesity
6)physical inactivity
7)hyperlipidemia
8)OCs/HRT

Front 10

3 categories of ISCHEMIC stroke

Back 10

1)thrombus
2)embolus
3)hypoxia

Front 11

Thrombus ISCHEMIC stroke
a)consists of...(4)

Back 11

Aggregation of:
a1)platelets
a2)fibrin
a3)clotting factors
a4)cellular elements of blood
ATTACHED TO THE INTERIOR WALL OF VEIN/ARTERY

Front 12

Embolus ISCHEMIC stroke
a)can be... (4)
b)other

Back 12

a1)foreign object
a2)quantity of air/gas
a3)bit of tissue or tumor
a4)piece of thrombus

b)circulates in bloodstream until it lodges in a vessel

Front 13

LARGE VESSEL thrombus stroke (3 and ex)

Back 13

1)less common cause of ischemic stroke
2)caused by atherosclerosis of intracranial arteries
3)gradual in onset or may "stutter"

ex)clot in carotid artery grows and extends directly to middle cerebral artery causing occlusion

Front 14

LACUNAR/SMALL VESSEL thrombus stroke (4)

Back 14

1)common cause of stroke (incr rate in blacks)
2)caused by thrombotic occlusion of small intracranial vessels
3)major risk factors are long-standing HTN/DM
4)multiple tiny lacunar infarcts can lead to VASCULAR DEMENTIA****

Front 15

2 types of Thrombosis stroke

Back 15

1)large vessel
2)lacunar/small vessel

Front 16

3 types of Embolism stroke

Back 16

1)cardioembolic
2)cryptogenic
3)artery

Front 17

Cardioembolic embolism stroke
a)other (2)
b)causes (5)

Back 17

a1)presents as a sudden onset of neurologic dysfxn (usually broken off piece of thrombus)
a2)originated in heart/aorta

b1)A.fib
b2)mural thrombus
b3)acute MI
b4)prosthetic valves
b5)rheumatic heart disease

Front 18

PARADOXICAL CARDIOEMOBLIC stroke (def and ex)

Back 18

a)can occur in pts w/ patent foramen ovale

b)thrombosis in leg proximal vein causes a stroke when the embolus travels to the brain (instead of pulmonary system/lung)

Front 19

Artery embolism stroke
a)2 other
b)causes (3)

Back 19

a1)presents as a sudden onset of neurologic dysfxn (usually broken off piece of thrombus)
a2)released clot/embolism travels until it occludes a distal vessel and prevents distal cerebral blood flow

b1)atherosclerotic plaque on aortic arch
b2)carotid bifurcation
b3)intracranial vessel that embolizes

Front 20

Cryptogenic embolism stroke (4)

Back 20

a1)presents as a sudden onset of neurologic dysfxn (usually broken off piece of thrombus)
a2)UNKNOWN CAUSE
a3)extensive workup reveals no clear cause
a4)about 30% of strokes

Front 21

Hypoxia embolic stroke (5)

Back 21

a1)presents as a sudden onset of neurologic dysfxn (usually broken off piece of thrombus)
a2)decr oxygen supply to brain
a3)hypotension and poor cerebral perfusion may lead to infarction; no vascular occlusion present (SO VASCULAR OCCLUSION NOT REQD)
a4)elevated blood glc at time of hypoxia increases brain lactate production and makes brain more vulnerable to damage
a5)other causes: carbon monoxide, cyanide, sulphide

Front 22

Risk factors for HEMORRHAGIC stroke (6)

Back 22

1)HTN (causes 50% of em)
2)atherosclerosis

3)blood dyscrasias (acquired, iatrogenic, congenital)
a)acquired- liver disease= coagulopathy= decr clotting factors
b)iatrogenic/meds- thrombolytics, anticoagulants, antiplatelets, cocaine, meth
c)congenital- genetic blood disease like hemophilia

Front 23

2 types of Hemorrhagic stroke

Back 23

1)subarachnoid hemorrhage
2)intracerebral hemorrhage

Front 24

Subarachnoid Hemorrhage
a)3 characteristics
b)3 symptoms

Back 24

1)rupture of cerebral aneurysm, most commonly in an artery @ base of brain
2)bleeding quickly disseminates thruout the subarachnoid space and can lead to sudden incr in intracranial pressure
a3)indifferent to age but F>M

b1)HA
b2)vomiting
b3)mental status changes

Front 25

Intracerebral Hemorrhage
a)3 characteristics
b)4 causes

Back 25

a1)bleeding into brain parenchyma
a2)blood is released into the brain under arteriolar or capillary pressure and effects a localized area
a3)direct contact of blood w/ brain tissue irritates and damages brain cells (and incr pressure in brain)

b1)thrombolytics
b2)anticoagulants
b3)cocaine
b4)meth

Front 26

Alteplase
a)MOA
b)3 characteristics
c)dose
d)2 other

Back 26

a)stimulates the conversion of plasminogen into plasmin (plasmin breaks down fibrin clots into solulbe fragments)

b1)currently only thrombolytic approved for ischemic stroke
b2)recombinant DNA form of tPA
b3)efficacy is highly dependent on timing of dose

c)0.9mg/kg IV (max 90mg) as 10% of total dose by IV bolus, then rest as continuous infusion over 1h

d1)DO NOT SHAKE WHEN MIXING
d2)100mg vial is $3000

Front 27

Antiplatelet agents
a)ASA (MOA)
b)Thienopyridines (MOA and 2ex)
c)Dipyridamole (MOA) (2)

Back 27

a)irreversible inactives COX leading to inhibition of TXA2

b)irreversibly inhibit platelet adhesion and aggregation by blocking ADP receptors on platelets (ticlopidine/plavix)

c1)inhibits platelet phosphodiesterase=incr cAMP=inhibits platelet aggregation
c2)stimulates prostacyclin release and inhibits TXA2

Front 28

General types of stroke (2) and general therapy/prevalence

Back 28

1)Hemorrhagic: 15-20% of strokes; therapy is supportive care

2)Ischemic: 80-85% of strokes; therapy is multifaceted

Front 29

Acute ISCHEMIC stroke has 3 types of tx

Back 29

1)rtPA (if within 3hrs of onset and NO CI)
2)ASA
3)Anticoagulation

Front 30

Acute Complications of ISCHEMIC Stroke (5)

Back 30

1)Arterial HTN
2)arrhythmias
3)seizures
4)incr intracranial pressure
5)DVT/PE

Front 31

Arterial HTN and ISCHEMIC stroke (4)

Back 31

1)in pt getting tPA maintain BP under 185/110
2)in pt NOT getting tPA maintain BP under 220/140
3)NEVER GIVE Nifedipine (because long acting)
4)BUT incr pressure may be beneficial to maintain cerebral perfusion

Front 32

ISCHEMIC stroke
a)arrhythmias (3)
b)seizures (2)

Back 32

a1)rare
a2)tx on prn basis
a3)monitor by EKG

b1)treat as needed in ischemic stroke
b2)prophylaxis in SAH

Front 33

ISCHEMIC stroke
a)incr intracranial pressure
b)DVT/PE (2)

Back 33

a1)tx as needed w/ surgery &/or diuresis

b1)common in pts w/ decr mobility
b2)PROPHYLAXIS (NOT TREATMENT) w/ SQ UFH, SQ LMWH, fondaparinux, mechanical/compression)

Front 34

Thrombolysis in ISCHEMIC stroke
a)drug
b)FDA approved for... (3)
c)when to give
d)clinical outcomes (3)

Back 34

a)Alteplase (activase)
b)ischemic stroke, PE, AMI
c)WITHIN 3HRS of stroke onset, improves clinical outcomes at 3 and 12 months

d1)incr neurological fxn
d2)decr fxnal disabilities
d3)NO MORTALITY BENEFIT

Front 35

Alteplase (ISCHEMIC stroke)
a)risk w/ it
b)dosage
c)monitoring (3)

Back 35

a)incr risk of intracranial hemorrhage (worsens with incr age)
b)0.9mg/kg (max 90mg) with 10% of total dose as bolus over 1minute then remander as continuous infusion over 1hr

c1)BP every 15min for 2hrs, then every 30min for 6hrs, then every hour
c2)if BP is over 185/110 for 2 consecutive reading give Labetalol then Nitroprusside if it fails
c3)AVOID use of antiplatelet/anticoagulant for 24h after giving alteplase

Front 36

Candidates for ALTEPLASE therapy (ISCHEMIC stroke) (6)

Back 36

1)onset of stroke symptoms was less than 3h ago
2)glucose b/w 50-400
3)CT scan of head showing no hemorrhage or edema
4)clinically meaningful neurological deficit
5)no evidence of improving s/sx
6)rule out excessive bleeding risk factors

Front 37

Excessive bleeding risk factors w/ ALTEPLASE (ISCHEMIC stroke) (10)

Back 37

1)BP over 185/110
2)currently taking anticoagulant (heparin within 48h, INR over 1.7)
3)platelets less than 100,000 (thrombocytopenia)
4)stroke or head injury within 3 months
5)history of hemorrhagic stroke
6)GI or urologic bleeding within 3wks
7)seizure activity at stroke onset
8)major surgery/trauma within 14d
9)active internal bleeds
10)history of lumbar puncture within 1wk

Front 38

ASA and ISCHEMIC stroke (3)

Back 38

1)use of ASA within 48h of stroke = reduction in recurrent stroke and decr mortality
2)maintain BP under 220/140
3)use in pts who are NOT elgible for alteplase OR if pt was give alteplase start ASA 24h after it

Front 39

Anticoagulation and ISCHEMIC stroke (3)

Back 39

1)UFH can be used in ONLY progressing stroke (stroke in evolution), large artery ischemic stroke OR cardioembolic stroke
2)TREATMENT dose is IV (prophy dose is SQ)

1)LMWH HAVE NO ROLE IN TREATMENT OF ISCHEMIC STROKE ONLY PROPHY

Front 40

Prevention of Ischemic Stroke (NON-CARDIOEMBOLIC) use what drugs (6)

Back 40

1)ASA
2)ticlopidine
3)plavix
4)dipyramidaloe
5)warfarin
6)lipid control

Front 41

ASA and NON-CARDIOEMBOLIC ISCHEMIC STROKE (3)

Back 41

1)doses over 325mg incr GI ADR's without incr benefit in secondary prevention
2)recommend dose of 50-325mg
3)questionable primary prevention of ischemic stroke (show to only work in females)

Front 42

Ticlopidine and NON-CARDIOEMBOLIC ISCHEMIC STROKE
a)dose
b)use
c)ADR's (3)
d)monitoring (2)

Back 42

a)250mg BID w/ food
b)more effective than ASA @ secondary prevention of ischemic stroke

c1)neutropenia
c2)TTP
c3)rash/diarrhea

d1)CBC w/ differential every 2wks for 3months
d2)LFTs every 4months

Front 43

Plavix and NON-CARDIOEMBOLIC ISCHEMIC STROKE
a)use (3)
b)dose
c)ADR's (3)

Back 43

a1)as effective as ticlopidine @ secondary prevention of ischemic stroke
a2)better safety profile than ticlopidine
a3)option for prevention of ischemic stroke, (particularly in those than can NOT take ASA)

b)75mg qd w/ or w/o food

c1)no neutropenia
c2)rash/diarrhea
c3)almost NO TTP

Front 44

Dipyridamole and NON-CARDIOEMBOLIC ISCHEMIC STROKE
a)place in therapy
b)use/dosing

Back 44

a)option for prevention of ischemic stroke (has decr cost, but BID dosing and incr ADR's over ASA monotherapy)

b)ONLY USE XR (aggrenox) 200mg w/ 25mg ASA for secondary prevention of ischemic stroke

Front 45

Warfarin and NON-CARDIOEMBOLIC ISCHEMIC STROKE
a)when to use

Back 45

a)DONT, ACCP dose NOT recommend it over ASA for non-cardioembolic stroke

Front 46

BP control in NON-CARDIOEMBOLIC ISCHEMIC STROKE (3)

Back 46

1)MOST IMPORTANT MODIFIABLE STROKE RISK FACTOR, importance increases with age
2)goal of under 140/90 OR 130/80 w/ DM or CKD
3)use thiazide +/- ACEI

Front 47

Dyslipidemia Control in NON-CARDIOEMBOLIC ISCHEMIC STROKE
a)general info (3)
b)multiple mechanisms by which statins decr stroke risk (6)

Back 47

a1)use Statins especially in ppl with CHD and incr LDL levels
a2)goal is under 100
a3)use simvastatin, pravastatin, or atorvastatin

b1)result of lipoprotein alterations
b2)improved endothelial fxn
b3)plaque stabilization
b4)antithrombotic effect
b5)antiinflammatory effect
b6)neuroprotective properties

Front 48

Smoking Cessation and NON-CARDIOEMBOLIC ISCHEMIC STROKE (4)

Back 48

1)decr # of cigs/day does not improve risk of stroke
2)MUST HAVE COMPLETE CESSATION
3)5yrs after cessation they will be at stroke risk of nonsmokers
4)avoid chronic second hand smoke as well

Front 49

Surgical Interventions and NON-CARDIOEMBOLIC ISCHEMIC STROKE (3)

Back 49

1)CEA decr risk of stroke and death in pts w/ TIA or nondisabling stroke w/ over 70% stenosis (best for old males)
2)good for asymptomatic high-grade stenosis
3)risk factor mod and antiplatelet tx are vital components of postop management

Front 50

Other beneficial changes in NON-CARDIOEMBOLIC ISCHEMIC STROKE (6)

Back 50

1)diet (fresh fruit/veggies and EtOH J curve)
2)manage insulin resistance
3)wt loss
4)physical activity
5)CRP (want to decr by diet exercise/wt loss)
6)decr homocysteine

Front 51

____ is responsible for 50% of CARDIOEMBOLIC STROKE (ISCHEMIC STROKE)

Back 51

A.fib

Front 52

Risk factors for CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) (A.fib +...) Intermediate ones... (4)

Back 52

1)DM
2)CAD w/o LV dysfxn
3)65-75yo
4)pts with more than 1 intermediate risk factor are considered HIGH risk

Front 53

Risk factors for CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) (A.fib +...) High ones... (7)

Back 53

1)prior stroke or TIA
2)prior systemic embolism
3)age over 75yo
4)LV dysfxn (EF less than 40%)
5)history of HTN
6)prosthetic heart valve
7)rheumatic mitral valvular disease

Front 54

A.fib and CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) efficacy/drugs (4)

Back 54

1)w/ no therapy annual risk of stroke is 2-20%
2)w/ ASA stroke risk reduction of 21%
3)w/ warfarin stroke risk of 70% with no incr in major bleeding events
4)SO in CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) use ASA or warfarin

Front 55

In CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) recommendations for less than 65yo
a)w/ NO risk factors
b)w/ 1 intermediate risk factor
c)high risk

Back 55

a)ASA 325mg QD
b)ASA or warfarin
c)warfarin (INR 2-3)

Front 56

In CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) recommendations for 65-75yo
a)w/ NO risk factors
b)high risk

Back 56

a)ASA or warfarin
b)warfarin (INR 2-3)

Front 57

In CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) recommendations for over 75yo (ALL PATIENTS)

Back 57

warfarin INR 2-3

Front 58

Cardioversion (AF of unknown duration or over 48h) (2)

Back 58

a)warfarin with target INR 2-3 for 3wks prior to cardioversion
b)warfarin for atleast 4wks post-cardioversion and consider dc ONLY if pt is in normal sinus rhythm

Front 59

Indications for post-MI anticoagulation in prevention of CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) (6 and tx)

Back 59

1)severe LV dysfxn
2)HF
3)anterior infarction
4)echocardiography evidence of mural thrombus
5)hx of embolism
6)a.fib

a)pts w/ any of above risk factors should be tx w/ warfarin to INR (2-3) for up to 3months (indefinetly in post-MI pts w/ A.fib)

Front 60

LV dysfxn tx in CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) prevention (3)

Back 60

1)anticoagulation recommended if pt also has A.fib or hx of PE
2)consider anticoag in pts w/ SEVERE LV dysfxn who are in normal sinus rhythm
3)warfarin (INR 2-3)

Front 61

Prosthetic/mechanical heart valves in CARDIOEMBOLIC STROKE (ISCHEMIC STROKE) (listed in order of highest to lowest of thrombogenicity) (6)

Back 61

1)Caged-ball (prosthetic) (HIGHEST CLOT RISK)
2)Single-tilting (prosthetic)
3)Bileaflet-tilting (prosthetic)
4)Porcine (bioprosthetic)
5)Bovine (bioprosthetic)
6)Homograft (human-bioprosthetic) (LOWEST CLOT RISK)

Front 62

Therapy recommendations for prosthetic valves (4)

Back 62

1)Warfarin (2-3) for bileaflet or single-tilting in aortic
2)Warfarin (2.5-3.5) for bileaflet or single-tilting in mitral
3)warfarin (2.5-3.5) for bileaflet in any pt W/ A.FIB
4)warfarin and ASA (80-100mg) for caged-ball

Front 63

Therapy recommendations for bioprosthetic valves (3)

Back 63

1)ASA (80mg) bioprosthetic valve in pts w/ normal sinus rhythm
2)Warfarin (2-3) for first 3 months post-op bioprosthetic valve in mitral or aortic
3)Warfarin (2-3) long term w/ bioprosthetic valve in pts w/ A.FIB

Front 64

When to start secondary stroke prevention

Back 64

after pt has atleast a TIA

Front 65

MS epidemiology (2)

Back 65

1)dx b/w 20-45yo
2)2:1 ratio women to men (but men's prognosis is worse)

Front 66

MS etiology theories (2)

Back 66

1)autoimmune
2)microbial

Front 67

Autoimmune theory of MS (6)

Back 67

1)autoimmune attack against self-myelin or self-oligodendrocyte antigens
2)macrophages, killerT, lymphokines, Ig cause myelin destruction
3)T-helper (CD4) attach to BBB
4)production of metalloproteinases, allows entry into CNS
5)production of cytokines allows entry of B cells, complement, macrophages, Ig
6)interaxn w/ microglia and astrocytes which enhances production of proinflammatory cytokines and other mediators of CNS damage

Front 68

Microbial theory of MS (4)

Back 68

1)virus or bacteria
2)direct attack on myelin and/or oligodendrocyte
3)stimulation of autoimmune response
4)multiple agents have been id'd as possible causes

Front 69

Demyelination and inflammation in MS lead to... (3)******* and result of this...

Back 69

plaque formation in:
a)brain
b)sprinal cord
c)optic nerves

disrupt the transmission of nerve impulses

Front 70

Demylelination and axonal transection disrupt the transmission of nerve impulses causes (2)

Back 70

1)neurologic symptoms
2)may involve several nervous system fxns as these plaques can extend across several nerve pathways

Front 71

In MS plaques there are decr # of....

Back 71

oligodendrocytes

Front 72

Oligodendrocytes and MS (3)

Back 72

1)oligodendrocytes (which produce myelin) could be the target of the immunologic attack
2)nonspecific destruction of oligo's occur in early/acute MS
3)selective destruction occurs in chronic stages in MS

Front 73

3 categories of MS s/sx

Back 73

1)primary symptoms are directly due to conduction disturbances (depending on where lesion is)
2)secondary symptoms are complications from primary symptoms
3)tertiary symptoms are the (-) impact the disease has on the pt's life in general

Front 74

Primary MS symptoms (9)

Back 74

1)spasticity
2)bladder dysfxn
3)bowel dysfxn
4)fatigue
5)sensory symptoms
6)tremors
7)cognitive dysfxn
8)depression
9)sexual dysfxn

Front 75

Secondary MS symptoms (6)

Back 75

1)recurrent UTI
2)urinary calculi
3)decubiti ulcer
4)muscle contractions
5)respiratory infexns
6)poor nutrition

Front 76

Tertiary MS symptoms (5)

Back 76

1)financial problems
2)personal/social problems
3)vocational problems
4)martial problems
5)emotional problems

Front 77

Relapsing Remitting (RRMS) (3)

Back 77

1)85% of cases @ presentation
2)have acute attacks followed by complete/partial remission
3)neurologic recovery is good early on BUT tends to be less complete over time

Front 78

Secondary-Progressive (SPMS) (2)

Back 78

1)begins as RRMS but then there is a steady deterioration in fxn unrelated to acute attacks (are RRMS then NO acute attacks but still decline)
2)50% of RRMS will have SPMS after 15yrs

Front 79

Primary-Progressive (PPMS) (4)

Back 79

1)15% of cases @ presentation
2)slow, continuous worsening w/ no acute attacks
3)presents later in life w/ more distribution b/w gender
4)NO TREATMENT OPTIONS FOR THIS CATEGORY

Front 80

Progressive-Relapsing (PRMS) (2)

Back 80

1)like PPMS but have occasional attacks during progressive course
2)early stages are indistinguishable from PPMS

Front 81

Dx of MS (3)

Back 81

1)2 eps of neurological disturbance separated by time that reflect sites of damage to CNS
2)eps must have lasted atleast 24h and occurred more than 1 month apart
3)OR have gradual progression over atleast 6mon

Front 82

MRI for MS (2)

Back 82

1)highly selective in detecting MS lesions
2)can differentiate b/w new and old lesions

Front 83

Lumbar puncture for MS (3)

Back 83

1)90% of MS pts have increased IgG proteins
2)oligoclonal bands are commonly present
3)nonspecific so generally used to rule out other conditions that might mimic MS

Front 84

Evoked potential tests for MS (2)

Back 84

1)measure electrical activity of brain after stimulation (EEG)
2)useful to ID areas of demyelination that are clinically silent

Front 85

Mortality is LOW in MS

Back 85

suidicide rate can be as high as 7x the general population

Front 86

Indicators of favorable prognosis of MS (6)

Back 86

1)female
2)under 40
3)initial symptom of optic neuritis or sensory symptoms
4)low frequency of attacks
5)minimal impairment after first 5yrs
6)RRMS course of disease

Front 87

Indicators of poorer prognosis of MS (5)

Back 87

1)male
2)over 40
3)initial symptom of motor or cerebellar symptoms
4)high frequency of attacks
5)progressive course of disease

Front 88

Most MS pts experience...******

Back 88

progressive neurologic disability

Front 89

Acute attack of MS
a)what is it
b)can be caused by...
c)goals of therapy (2)
d)when to tx

Back 89

a)acute deterioration or appearance of new symptoms that last at least 24h before stabilization or improvement
b)infexn, stress, lotsa stuff
c)shorten duration, reduce severity
d)when fxnal ability is affected

Front 90

MS acute attacks
a)DOC
b)efficacy
c)MOA (4)

Back 90

a)Methylprednisolone
b)effective in 75% of pts

c1)decr edema in areas of demyelination
c2)restore the integrity of BBB
c3)reduce the release of pro-inflammatory cytokines
c4)cause T-cell apoptosis

Front 91

Methylprednisolone
a)ADR's (7 of many)

Back 91

1)incr WBC count (if there is a left shift then infexn, w/o it no infexn)
2)HTN
3)hyperglycemia
4)hypokalemia
5)cognitive dysfxn
6)fluid retention
7)infexn

Front 92

Methylprednisolone
a)CI's (2)
b)precautions (3)
c)Monitoring parameters (3)

Back 92

a1)hypersensitivity
a2)systemic fungal infexn

b1)DM
b2)HTN
b3)osteoporosis

c1)BP
c2)finger stick blood sugar
c3)electrolytes

Front 93

Alternative tx of Acute attacks (2)

Back 93

1)plasma exchange
2)IVIG

Front 94

MS Disease modifying therapies (6)

Back 94

ABC-R (TN are 2nd line)

Avonex
Betaseron
Copaxone (NOT INTERFERON)
Rebif

Tysabri (Natalizumab)
Novatrone (mitroxantrone)

Front 95

Disease modifying therapies should be con't indefinetly except... (4)

Back 95

1)when clear lack of benefit
2)intolerable AEs
3)new information
4)better tx available

Front 96

Goals of Disease modifying therapies (4)

Back 96

1)alter natural course of MS
2)reduce frequency/severity of relapses
3)prevent chronic progressive phase
4)slow progression of disability

Front 97

Interferon B-1b/a
a)indications
b)use (2)

Back 97

a)first line of RRMS, SPMS w/ exacerbations, and those who can't tolerate galtiramer acetate

b1)reduce # of exacerbations
b2)improve MRI measures