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RCA Test 2 > neuromuscular diseases > Flashcards

neuromuscular diseases Flashcards

0
Q

Multiple sclerosis causes

A

Unsure (genetic?)
Mineral deficiency ?
Vitamin D3
Virus? Epistein bar, herpies

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1
Q

Multiple sclerosis physiology

A 
Upper motor neuron 
Inflammatory response 
Glial cells destroyed 
Demyelination of white matter
Impulses are slowed or blocked 
Increase in sodium channels 
Myelin sheath and cells destroyed
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2
Q

Multiple sclerosis prevalence

A

Northern climates

20-30 years of age

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3
Q

Multiple sclerosis

A

Optic neuritis - 25% partial or total loss of vision
Any part of CNS
Brain and spinal cord

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4
Q

Multiple sclerosis signs and symptoms (early)

A 
1st symptom in 50% numbness in one or more limbs 
Weakness 
Spastic 
Babinski sign 
Emotional instability 
Bladder disfunction
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5
Q

Multiple sclerosis symptoms (late)

A 
Severe muscle spasm 
Urinary incontinence 
Difficulty swallowing 
Contractures 
Spastic ataxic 
URTI
Surgery 
Stress
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6
Q

Multiple sclerosis (course)

A 
Recovery over weeks to months 
Incomplete 
Exacerbations and remission
Slurred speech, bed ridden, Incontinence
12 to 15 years
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7
Q

Multiple sclerosis (diagnosis)

A

CSF - increase # of gamma globulin and immunoglobulin

MRI - scarred lesions in brain

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8
Q

Multiple sclerosis treatment

A 
Steroids 
Decadron
Interferon (proteins formed when cells are exposed to a virus) 
ACTH
Decrease inflammation 
Physical therapy, supportive
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9
Q

Myasthenia gravis (patho)

A

Nerve impulse fails to pass muscles at myoneural junction

Motor end plate

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10
Q

Myasthenia gravis

A 
Rare disease occurring in young adults 
Auto immune 
Women effected more then men (2 to1) 
aspiration is common
URTI occur due to ineffective cough 
May require artifical airway
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11
Q

Eaton lambert syndrome

A

Special form of myasthenia gravis
Found in people with oat cell carcinoma
Visual symptoms less frequent
Trunk , pelvic and shoulder girdle involved
Weakness with exertion, but temp in muscle power at first

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12
Q

Myasthenia gravis (patho)

A

Inability of motor end plate to secrete acetylcholine
Excessive cholinestrase at nerve endings
Non response of muscle fiber to acetylcholine
Antibodies to acetylcholinestetase receptors at end plate

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13
Q

Myasthenia gravis (clinical)

A

Droopy eyelids (ptosis)
Usually muscles of eyes, face, jaws, neck first then limbs
Proximal greater than distal (vision)
Muscle weakness with gravis prognosis
Repeated use of muscle leads to progressive weakness restored by rest

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14
Q

Myasthenia gravis (diagnosis)

A

EMG -electromyography
IV edrophonium chloride (Tensilon) test
-short acting anticholinestrase
-increase in muscle strength test is positive

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16
Q

Myasthenia gravis (treatment)

A 
*Anticholinesterase 
Neostigmine
Pyridostigmine 
*Steroids 
Plasmapheresis 
Atropine - blocks acetylcholine 
Tensilon (underdosage and overdosage decrease muscle strength)
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17
Q

Myasthenia Gravis (general)

A 
in advance stages: effects all muscles 
NO cardiac or sensory involvement 
Rapid or slow with exacerbation and remission 
Thymic turmors 25% 
thymic hyperplasia 80%
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18
Q

Myasthenia Gravis (drugs to avoid)

A

Muscle relaxants - Morephine
barbiturates
tranquilizers
neomycin

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19
Q

ALS (general)

A 
Lou Gehrig Disease 
Upper or lower motor neurons 
Effects men more than women 
Maybe Genetic - SOD type 1
Slow viral infection ?
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20
Q

ALS (patho)

A 
myelin sheath destroyed - scar tissue 
Anterior horn cells are affected
Loss of motor NOT sensory
spinal cord lateral tracts / medulla ventral tracts 
nerve impulses blocked
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21
Q

ALS (Clinical)

A

fatigue, awkwardness of fine finger movements
Dysphagia (difficulty swallowing)
Spasticity of flexor muscles
progressive muscle weakness, atrophy, fasciculations (muscle twitching)
Jaw Clonus

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22
Q

ALS (theories)

A

excess naturally glutamate in synaptic cleft,- cell death
oxidative injury (malfunction of SOD1
Protein aggregates
axonal strangulation

23
Q

ALS (outcomes)

A

One side of body more involved with progression
person remains alert no sensory loss
death within 5 to 10 years (resp or bulbar) paralysis

24
Q

ALS (medical management)

A

Heparin prophylactically to decrease P.E.
Nasogastric tube
home care ventilation for respiratory failure

25
Q

Poliomyelitis (general)

A

Acute febrile diaseae
Cause by three types of virus
Paralysis common with type 1
Salk vaccine, safe “live virus”

26
Q

Poliomyelitis (patho)

A

Incubation 7 to 21 days
virus attacks anterior horn cells of spinal cord
Motor pathways damaged, NOT sensory
Motor units become enlarged with recovery

27
Q

Bulbar Poliomyelitis

A

attacks medulla and basal structures of brain and cranial nerves

28
Q

Poliomyelitis (clinically)

A

No symptoms 90 to 95% of time
mild systemic symptoms
aseptic meningitis 3 to 4 days after
muscle weakness in 48 hours to weeks

29
Q

Poliomyelitis (clinically2)

A 
spinal cord (limb weakness) 
brain stem, crainal nerves, cerebral 
lower motor neurons 
decrease reflexes 
atrophy, no sensory loss, pain
30
Q

Poliomyelitis (outcomes)

A

Some recovery after 3 to 4 months
Resp failure -due to involvement of resp control center, muscles of diaphragm, intercostals
lose neurons at a faster rate than normal

31
Q

Poliomyelitis (treatments)

A

Supportive: Physiotherapy

ventilation/suctioning

32
Q

Post polio syndrome

A

progressive weakness with aging

33
Q

Musclar Dystrophy (general)

A 
gradual wasting of skeletal muscle 
progressive with increased weakness 
diminution of muscle mass 
confined to wheel chair
NO REMISSION
34
Q

Muscular Dystrophy (general)

A

Four clinical forms of the disease

Microscopic abnormalities of skeletal muscles

35
Q

Muscular Dystrophy (Form of)

A 
Duchenne 
Symptoms noted before age of 5
spinal deformity waddling gait, muscle wasting
involves HEART muscles! (leads to death)
X-linked recessive (ALL BOYS)
36
Q

Muscular Dystrophy (Becker)

A

milder form of Duchenne musclar dystrophy

37
Q

Facio-Scapulo-Humeral MD

A

type of muscle dystrophy
M/F equally effected
weakness/wasting of shoulder girdle/upperarms
onset puberty
weakness of facial muscles first years of life

38
Q

Limb-Girdle MD

A

type of muscular dystrophy
M/F equally, early or late in life, slow course
most of the muscles of the body affected

39
Q

Myotonic MD

A

type of muscular dystrophy
M/F equally effected
occurs earlier and more severe later gens
delayed relaxation of muscles
cataracts in both eyes may occur, reproductive functions distrubed

40
Q

Muscular Dystrophy (treatment)

A

origins in genetic mutation

supportive treatment: physical and occupational therapy

41
Q

Miscellaneous causes of resp muscle weakness

A

Malnutrition,
electrolytes (hypokalemia, hypomagnesemia, hypophosphatemia, hypochloremia)
Iatrogenic causes due to treatment with corticosteroids
Botulism, tetanus (infectious causes)

42
Q

Guillain-Barre syndrome (general)

A

an inflammatory disease that effects PNS
autoimmune response
rapid symmetrical limb weakness ascending pattern

43
Q

Guillain-Barre syndrome (general)

A

1 cause of acute NM weakness

Acute inflammatory Neuropathy
all ages commonly in 30-50 yr, Males

44
Q

Guillain-Barre syndrome (etiology)

A

occurs 2 wks after recent URTI or GI infection
Campylobacter jejuni (major cause)
occurs with: HIV, mycoplasma, Hep, epstine
occurs after immunizations
associated with hodgkins lymphoma

45
Q

Guillain-Barre syndrome (patho)

A

Injury to PNS ONLY! immunological
cell mediated/humoral (antibody) reaction
lymphocytes sensitized and attach to myelin sheaths on peripheral nerves. Demyelination by macrophages remove damaged myelin

46
Q

Guillain-Barre syndrome (patho)

A

all peripheral nerves affected become inflamed
impediment of nerve impulses -myelin damage
schwann cells proliferate+remyelination

47
Q

Guillain-Barre syndrome (clinical)

A

3 main stages of disease
acute onset 1-3 weeks
Plateau symptoms remain but dont get worse
Recovery few weeks to 2 yrs, full recovery
Glove and stocking distribution
entrance complaint- difficulty walking, trouble up and down stairs, trouble rising from chair

48
Q

Guillain-Barre syndrome (symptoms)

A

progressive ascending skeletal muscle paralysis
tingling sensation + numbness (distal paresthesia)
Loss of deep tendon reflexes
SENSORY nerve impairment
under and over reaction of SNS or PNS
CARDIAC arrhythmias
malignant hypertension

49
Q

Guillain-Barre syndrome (symptoms)

A

peripheral facial weakness
decrease gag reflex; cranial nerve 9,10
decrease ability to swallow
muscle paralysis involves ab, diaphragm, arms
postural hypoten, thermal reg, reten urine
mechanical vent

50
Q

Guillain-Barre syndrome (clinical assessment)

A

ABG - acute ven failure, resp acidosis hypoemia
PFT’s - reduce lung vol & capac
diminish B/S w/crackles + wheezes
CXR - normal

51
Q

Guillain-Barre syndrome (clinical assessment)

A

past hx - preceding infection, weakness
lumbar puncture - CSF - protein
reduced nerve conduction (blocked/slow)
electromyography- single muscle fiber activate
progressive motor weakness >1 limb+areflexia

52
Q

Guillain-Barre syndrome (treatment)

A

plasmapheresis or TPE (shorten course)
IV immunoglobulin
all pts need hospitalized high risk vent fail

53
Q

plasmapheresis

A

removes portion of patients circulating blood, centrifuged, separate elements, mixed with 50% ALBUMIN 50% SALINE, reinfused, old plasma discarded
5 treatments in a row lasting 90 mins
not for mild symptoms
contraindicated: acute MI, angina, sepsis, autonomic dysfunction .

54
Q

Guillain-Barre syndrome (Prognosis)

A

80% of pts make total recovery in 1 year
25% req mech vent
10% relapse

RCA Test 2 (4 decks)

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