Ms And Gbs

Front 1

onset of MS

Back 1

20-40

Front 2

peak of MS

Back 2

30

Front 3

male/female ratio for MS

Back 3

1:2

Front 4

MS most prevalent

Back 4

areas far away from equator

Front 5

which races does MS affect?

Back 5

all, mostly whites

Front 6

percent of people with MS who have affected relative

Back 6

15%

Front 7

gene implicated in MS genetic susceptibility

Back 7

DR2

Front 8

how is genetic susceptibility determined?

Back 8

pattern of histocompatibility antigens (HLA, DR15, DQ6)

Front 9

second pathological feature of MS

Back 9

demyelinating lesions (plaques and diffuse lesions)

Front 10

plaques produce?

Back 10

slowing of conduction and finally a conduction block

Front 11

plaques involve ___ matter?

Back 11

CNS white matter

Front 12

areas of MS plaque involvement (5)

Back 12

around:
- periventricular regions
- optic nerves
- brainstem
- cerebellum
- spinal cord

Front 13

characteristic of acute stage

Back 13

process of perivenous demyelination

Front 14

characteristic of chronic stage

Back 14

gliosis (glial scarring w/late degeneration of axons)

Front 15

examples of precipitating factors for MS

Back 15

infection, trauma, pregnancy

Front 16

onset of symptoms after pregnancy

Back 16

3 months postpartum

Front 17

Relapsing-Remitting MS

Back 17

- clear relapses
- full recovery or partial recovery w/lasting disability
- no worsening b/w attacks
- 85% - most common

Front 18

Primary Progressive

Back 18

progression from onset w/occasional plateaus
fairly uncommon
involve diff. brain and spinal cord damage than other types

Front 19

Secondary Progressive

Back 19

begins w/patterns of clear-cut relapses and recovery
becomes steadily progressive over time
two-thirds develop eventually

Front 20

Progressive-Relapsing

Back 20

progressive from onset but also has clear acute attacks
rare type

Front 21

percentage that INITIALLY experience RR type

Back 21

90%

Front 22

percentage that have the mixed establishement after years

Back 22

50%

Front 23

Mixed Type optic neuritis symptoms

Back 23

impaired central vision and color perception

Front 24

Mixed Type optic neuritis signs

Back 24

decreased central visual acuity
scotoma (central or paracentral)
aquired color vision deficit (R or G)
defective pupillary reaction to light

Front 25

how many recover completely from these types?

Back 25

one-third

Front 26

Mixed type brain stem lesions

Back 26

involve cranial nerves 3-12 at root, nuclear, or corticobulbar level

Front 27

mixed type brain stem symptoms (9)

Back 27

opthalmoplegia
nystagmus
dysarthria
deafness
vertigo
tinnitus
facial weakness
facial sensory deficit
diplopia

Front 28

what is diagnostic of MS in young adults?

Back 28

bilateral internuclear opthalmoplegia

Front 29

mixed type cognitive dysfunction

Back 29

decreased short-term memory
recent memory impairment
decreased concentration
word-finding problems
planning difficulties
mood alterations

Front 30

percentage with Spinal Type MS?

Back 30

30-40%

Front 31

areas involved in spinal type

Back 31

spinal tract and dorsal root column

Front 32

initial symptoms of spinal type

Back 32

weakness, numbness, or both in one or more limbs

Front 33

spinal type subjective corticospinal symptoms (3)

Back 33

stiffness, slowness, weakness
often unilateral

Front 34

spinal type spinal signs

Back 34

bilateral more often affecting lower limbs and lower limbs affected more severely

Front 35

most common single neurological finding in spinal type MS

Back 35

spastic paraparesis

Front 36

area of bladder and bowel symptoms involvement

Back 36

spinal cord

Front 37

bladder and bowel symptoms

Back 37

urgency and hesitancy before incontinence
small, spastic or large, flaccid bladder
constipation common
bowel incontinence rare

Front 38

spinal type subjective dorsal column symptoms

Back 38

symmetric paresthesias with an unpredictable pattern but w/predilection for lower extremities

Front 39

percentage with Cerebellar Types MS?

Back 39

5%

Front 40

symptoms common initially

Back 40

nystagmus and ataxia (cerebellar and corticospinal involvement)

Front 41

symmetry of cerebellar type deficits

Back 41

symmetric w/all 4 limbs involved

Front 42

cerebellar type pure cerebellar symptoms (3)

Back 42

motor ataxia
hyptonia
asthenia (weakness)

Front 43

motor ataxia manifestations

Back 43

reduced movement
inability to perform rapid alternating movements
dysmetria

Front 44

charcot triad

Back 44

combo of dysarthria, intention tremor, nystagmus

Front 45

hypotonia manifestations (3)

Back 45

decreased resistance to passive movement
hypoactive deep tendon reflexes
pendular knee jerk

Front 46

mechanism of short-lived attacks of cerebellar type

Back 46

complete, reversible conduction block in partially demyelinated axons

Front 47

causes of short-lived attacks of cerebellar types

Back 47

1. minor increases in body temp or serum Ca concentrations
2. functional demands exceeding conduction capacity

Front 48

paroxysmal attacks of cerebellar type

Back 48

sensory or motor symptoms of abrupt onset and short duration

Front 49

paroxysmal attacks of cerebellar type SYMPTOMS (4)

Back 49

paresthesias
dysarthria
ataxia
tonic head turning

Front 50

paroxysmal attack mechanism

Back 50

nonsynaptic transmission where nerve impulses are DIRECTLY transmitted b/w adjacent demyelinated axons

Front 51

common symptom of paroxysmal attack

Back 51

LHermittes sign

Front 52

LHermittes sign

Back 52

momentary paresthesia that shoots down trunk or limbs during flexion of neck

Front 53

paroxysmal attack inciting events (4)

Back 53

sensory stimulaiton
voluntary movement
hyperventilation
emotional stress

Front 54

diagnostic tests for MS

Back 54

CSF
evoked response
CT scans of head
MRI

Front 55

amount w/elevated IgG

Back 55

2/3

Front 56

percentage w/oligoclonal (IgG) bands

Back 56

90%

Front 57

what does the evoked response show for MS?

Back 57

decreased conduction velocity in visual, auditory, and somatosensory pathways

Front 58

MRI shows what that is not detected by CT?

Back 58

brain stem, optic nerve, and spinal cord lesions

Front 59

3 purposes of MS treatment

Back 59

1. acute management of relapses to prevent disability
2. reducing frequency of relapses or minimizing disease progression
3. management of symptoms

Front 60

treatment for acute episodes

Back 60

methylprednisolone and plasma exchange
- used to shorten duration of relapses

Front 61

disease modifying drugs (DMD)

Back 61

used to reduce relapse rate

Front 62

treatment in Relapsing-Remitting MS

Back 62

Betaseron
Avonex
Rebif
Copaxone
IV immunoglobulins

Front 63

treatment of secondary progressive MS

Back 63

interferon beta-1b and mitoxantrone (Novantrone)

Front 64

average duration of MS

Back 64

30 years

Front 65

characterization of GBS

Back 65

acute onset of motor paralysis of ascending nature (usually)

Front 66

incidence of GBS

Back 66

1-2 per 100,000

Front 67

GBS mortality rate

Back 67

4-6%

Front 68

GBS morbidity rate

Back 68

5-10% (permanent disability)

Front 69

GBS precipitating events

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mild respiratory or gastrointestinal viral or bacterial infection
surgical procedures
viral immunizations
lymphoma
other viral illnesses

Front 70

? found in GBS patient's serum

Back 70

IgM antibodies against myelin glycolipid

Front 71

when is Anti-GM1 found

Back 71

ppl WITHOUT sensory symptoms
ppl WITH prodromal diarrheal illness

Front 72

When is Anti-GD1b found

Back 72

ppl WITH sensory symptoms and ataxia

Front 73

when is Anti-GQ1b found

Back 73

almost all WITH cranial nerves signs and Miller-Fisher variant

Front 74

which antibodies are responsible for GBS peripheral demyelination and inflammation?

Back 74

those that are CELL-MEDIATED RESPONSES

Front 75

clinical manifestations of GBS (3)

Back 75

paresis of legs to complete quadriplegia
respiratory insufficiency
autonomic nervous system instability

Front 76

motor signs of GBS manifest as ?

Back 76

acute or subactue progressive paralysis

Front 77

proximal or distal muscles involved earlier and more significantly?

Back 77

proximal

Front 78

pattern of paresis/paralysis

Back 78

ascending, involving limbs, respiratory muscles, then bulbar muscles

Front 79

results of only bulbar muscle involvement

Back 79

dysphagia and dysarthria

Front 80

when does GBS weakness plateaus/improves?

Back 80

by 4th week in 90% of patients

Front 81

GBS sensory symptoms (3)

Back 81

paresthesias/dysthesias
pain (lower back, buttocks and legs)
numbness

Front 82

percentage that need ventilator support in GBS

Back 82

10-30% w/respiratory muscle weakenss

Front 83

manifestations of cranial nerve weakness in GBS

Back 83

facial weakness & bulbar weakness
- chewing, swallowing, cough

Front 84

autonomic dysfunction in GBS

Back 84

tachy/brady-cardia
hypo/hypertension
loss of or increase of sweating

Front 85

cause of hyponatremia in GBS

Back 85

syndrome of inappropriate antiduretic hormone (SAIDH)
especially in ventilated patients

Front 86

significant diagnostic signs of GBS

Back 86

paresthesia
paralysis
CSF findings

Front 87

CSF findings in GBS

Back 87

high protein levles (500 mg/dl) without cellular abnormality

Front 88

treatment w/in first 2 weeks of onset

Back 88

plasmapheresis or plasma exchanges

Front 89

other GBS treatment

Back 89

IV immune globulin and combination therapy

Front 90

mosquito that transmits West Nile

Back 90

Culex mosquito

Front 91

first emergence of WNV

Back 91

in NY in 1999

Front 92

incidental hosts of west nile

Back 92

human, horses, and other mammals

Front 93

life cycle hosts of west nile

Back 93

birds and mosquitoes

Front 94

peak times of west nile infection incidence

Back 94

summer and fall

Front 95

Stage 1 WNV infection

Back 95

febrile (feverish) illness of acute onset
clinically unrecognizable

Front 96

Stage 2 WNV infection

Back 96

mild infection after 3-4 day incubation period
symptoms last 4-6 days

Front 97

Stage 3 WNV infection

Back 97

severe infection (1 in 150)
advanced age is a risk factor

Front 98

symptoms of west nile (9)

Back 98

fever
weakness
nausea
vomiting
headache
mental status changes
diarrhea
rash
lymphadenopathy

Front 99

meningeal signs of infection

Back 99

severe HA
high fever
nuchal rigidity (stiffness of neck)

Front 100

encephalitis signs of infection (8)

Back 100

disorientation
stupor
coma
seizures
tremor
ataxia
extrapyramidal signs
paralysis

Front 101

what may the MRI show for WNV?

Back 101

abnormalities of:
thalamus
basal ganglia
cerebellum

Front 102

how is a preliminary diagnosis for west nile made?

Back 102

if IgM for virus is found in CSF or serum

Front 103

what test confirms WNV?

Back 103

plaque reduction neutralization assay (PRA)

Front 104

treatment for severe infection

Back 104

interferon-alpha w/supportive care