Exam Pt 4 Flashcards

1
Q

If a patient w PD has impaired balance, they are stage..

A

III

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2
Q

Brandyphrenia is.. & is a symptom of ..

A

Slowed thinking ; PD

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3
Q

What is the pharm intervention of UI in MS?

A

Anticholinergic drugs

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4
Q

What are the two common causes of death in pts w MS you should be on the alert to look out for?

A

UTIs and respiratory infection

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5
Q

What is a reasonable intervention for DiplopiA?

A

Eye patching

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6
Q

What neurotransmitter is deficient in PD?

A

Dopamine within the BG corpus striatum

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7
Q

What issues of perception/sensation occur in PD?

A

1 cramp-like sensation,

  1. Spatial organization deficit
  2. Perception of the vertical
  3. Extreme restlessness (akathisia)
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8
Q

What is festinating gait?

A

Abnormal involuntary increase in the speed of walking (occurs in PD)

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9
Q

What is the main medical mgmt for PD? How is its effect prolonged?

A

Sinemet (levodopa/carbidopa) or sustained release sinemet

  • -provides dopamine
  • -prolonged effect via LOW PROTEIN DIET & dopamine agonist drugs
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10
Q

In patients with PD, what are anticholinergic drugs used for?

A

Control of tremor

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11
Q

What does Amantadine do?

A

Enhances dopamine release

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12
Q

DBS for PD is used in what area of the brain?

A

Thalamus or subthalamus

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13
Q

Myasthenia gravis is an autoimmune attack on what receptors ? Where?

A

ACh receptors at NMJ

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14
Q

How do people with myasthenia gravis respond to continual contraction?

A

Muscular strength gets worse with continuing contraction , improved with rest

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15
Q

What is myasthenic crisis?

A

Myasthenia gravis w respiratory failure (MEDICAL EMERGENCY)

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16
Q

What ms are the most effected in myasthenia gravis?

A

Proximal ms

-ie getting out of a chair & going up stairs the most difficult functional activities

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17
Q

If a pt w PD has unilateral symptoms, they are H&Y stage ..

A

I

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18
Q

what are the 3 main pharmacological interventions used for Myasthenia Gravis? `

A
  1. ACh inhibitors
  2. Corticosteroids
  3. Immunosuppressants (ie IVIG)
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19
Q

what is the autonomic phenomenon associated with epilepsy?

A

sudden attack of : anxiety, tachycardia, sweating, piloerection, abnormal sensation in upper abdomen/chest

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20
Q

the cognitive phenomenon in epilepsy involves affective disturbances, such as..

A

intense feelings of hate, fear and anger

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21
Q

What is a possible cause of seizures if you are pregnant?

A

eclampsia (seizure caused by HTN, mother can subsequently become comatose)

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22
Q

grand mal seizures aka ..

A

tonic clonic seizures

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23
Q

a partial focal motor seizure involves..

A

clonic activity involving a specific area of the body

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24
Q

a temporal lobe seizure is characterized by ..

A

episodic changes in behavior, with complex hallucinations and automatisms

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25
Q

a complex partial seizure involves..

A

simple partial seizures followed by an impairment of consciousness

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26
Q

“status epilepticus” involves..

A

prolonged seizure OR series of seizures lasting >30 min, life threatening medical emergency if generalized

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27
Q

Dilantin (phenytoin) is used as a …

A

antiepileptic medication

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28
Q

what is unique about the cerebellar presentation of signs and symptoms?

A

they typically manifest themselves unilaterally

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29
Q

lesions to the archicerebellum lead to what?

A
  1. central vestibular symptoms
  2. gait and trunk ataxia
  3. little change in tone or dyssynergia of extremity movements
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30
Q

what are the central vestibular symptoms produced by a lesion to the archicerebellum?

A

ocular dysmetria
poor eye pursuit
dysfunctional VOR
impaired hand-eye coordination

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31
Q

what are the symptoms after a lesion of the paleocerebellum

A
  1. hypotonia
  2. truncal ataxia
  3. ataxic gait

normally responsible for equilibrium & ms tone

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32
Q

lesion to what aspect of the cerebellum causes an intention tremor?

A

neocerebellum (posterior lobe)

33
Q

in general, lesions of the neocerebellum cause..

A

ataxic limb movements

-dysdiadochokinesia, dysmetria, dyssynergia, errors in timing related to perceptual tasks, intention tremor

34
Q

what dynamic stability exercises should be used for patients with cerebellar ataxia?

A

promote small range control & smooth reversals of movement
movement transitions
using carefully graded resistance

35
Q

how do you improve stabilization of VOR in cerebellar lesions?

A

slow head movements with visual fixations (compensation)

36
Q

what motor learning strategies should be used in patietns with cerebellar ataxia?

A
  1. low stim environment (closed)
  2. focus on practice and repetition
  3. distributed practice (endurance may be low)
37
Q

what are 3 potential causes of bilateral vestibular disorders?

A
  1. Paget’s disease (vestibular neuropathy, otosclerosis)
  2. B/L infection : neuritis, meningitis
  3. toxicity (ototoxic drugs)
38
Q

what is Meneire’s disease?

A

recurrent and usually progressive vestib disease
-episodic attacks minute to severeal hours
-assoc w tinnitus, deafness, sensation of pressure/fullness within ear, etiology unknown
UNILATERAL vesitbular dysfxn

39
Q

what is the subj assessment rec for vestib dysfxn

A

DHI

40
Q

when examining VOR fxn, look for..

A

nystagmus, blurred vision w head & total body mvmt

41
Q

to examine for VSR function..

A

examine posture & balance

-examine for instability in sitting, standing, during fxnl activities and gait

42
Q

what is the definitive exam performed for BPPV?

A

Hallpike Dix
-check for vertigo or nystagmus
+ for BPPV on the side that produces symptoms

43
Q

to test for vertebral artery compression..

A

in supine, ext/lat flex/rotate head , hold 30 sec then test contralat side

44
Q

what are some disorders that you should avoid overwork fatigue when dealing with? & why?

A

MS, ALS, MD, PPS, GBS; all have degeneration of nerves (cranial or peripheral nerves with ALS, PPS, GBS), so overwork will actually cause the ms to break down

45
Q

canalith repositioning treatment is used for..

A

horizontal SCC BPPV & posterior SCC BPPV

46
Q

what is Wallerian degeneration?

A

transection that results in degernation of the axon and myelin sheath

47
Q

what is an example of segmental demyelination?

A

GBS - axons preserved, remyelination restores fxn

48
Q

what are the 3 classes of traumatic nerve injury

A

I - neurapraxia (transient loss of fxn)
II - axonotmesis (axon interruption, loss of fxn distal to lesion, REGEN POSSIBLE)
III - neurotmesis : complete loss of fxn 2/2 severance of nerve

49
Q

what are the characteristics of trigeminal neuralgia?

A

brief paroxysms of neurogenic pain (stabbing and/or shooting pain) reocurring freq ; 2/2 autonomic instability, this is exacerbated by stress and cold and relieved by relaxation

50
Q

Bell’s Palsy affects taste where?

A

anterior 2/3 of tongue

51
Q

what can you do to protect the cornea in bell’s palsy?

A

eye patching or artificial tears until restore fxn

52
Q

bulbar palsy refers to..

A

weakness or paralysis of the muscles innervated by the motor nuclei of the lower brainstem,

  • affects ms of face, tongue, larynx and pharynx
  • ALS is one type
53
Q

the 2 CNs most typically affected w bulbar palsy are..

A

Vagus & glossopharyngeal

-phonation, articulation, palatal action, gag reflex, swallowing

54
Q

GBS involves demylination of..

A

both CNs & peripheral nerves

55
Q

What are the UMN signs of ALS?

A

Spasticity and hyperreflexia; also demos LMN signs (atrophy, widespread weakness, ms cramping and ms twitching)

56
Q

What are the two main types of ALS ?

A

Bulbar onset - progressive bulbar palsy

Spinal cord onset - progressive ms atrophy

57
Q

At what stage of ALS are you a w/c user?

A

Stage IV

58
Q

What CNa tend to be affected in ALS and GBS?

A

VII , IX-XII

59
Q

What is the only pharm intervention that slows ALS disease progression?

A

Riluzole

60
Q

At what point should exercise be avoided with ALS?

A

If less than 1/3 of motor units are functioning

61
Q

Patients with PPS may have difficulty with what cognitive functions?

A

Concentration, memory and attn

Damage to reticular formation, hypothalamus, dopaminergic neurons

62
Q

What type of sensory deficits should you expect in PPS?

A

NONE

63
Q

To increase Aerobic capacity in PPS, what machine should you use?

A

Ergo meter that involves UE&LE

64
Q

What meds decrease fatigue and sleep disorders in PPS?

A

NT inhibitors ie serotonin, norepinephrine

65
Q

What pathway is fast pain transmitted via?

A

A delta fibers (poly modal non myelinated) ; for LOCALIZATION, discrimination of pain

66
Q

Slow pain is transmitted via.. And tells cortex ..

A

Via C fibers

- diffuse arousal (protective/adverse reactions), affective and motivational aspects of pain

67
Q

To be classified as chronic pain, must exist for..

A

> 6 mos

68
Q

Nociceptive pain is response to..

A

An immediate noxious stimulus signaling impending tissue damage

69
Q

Central neurogenic pain often presents as ..

A

Burning, aching and prickling (from injury/damage to CNS )

70
Q

What type of stroke produces central post stroke pain?

A

CVA of central posterolateral thalamus

-continuous intense central pain

71
Q

CRPS is an example of what type of pain?

A

Peripheral neurogenic pain

72
Q

What is allodynia?

A

Pain upon light touch

73
Q

What is hyper pathia?

A

Increased sensitivity to normal stimuli

74
Q

What is shingles ?

A

Herpes zoster (it’s a “peripheral neurogenic pain”)

  • acute painful mononeuropathy
  • infection can last 10 days to 5 weeks
  • post therapeutic neuralgia pain may persist for months or years
75
Q

Fibromyalgia vs myofascial pain syndrome :

A

F- widespread tenderness in ms, MPS - involves deep aching pain w trigger points

76
Q

Where does referred pain for the gallbladder manifest?

A

Right subscapular pain

77
Q

What is a valid subjective pain questionnaire to use with chronic pain?

A

McGill Pain Questionnaire

78
Q

what CN controls corneal reflex?

A

CN V trigeminal

79
Q

when do pts w MS typically have the LEAST amt of fatigue?

A

early AM