Neuro- GBS, MG, Critical Illness polyneuropathy, PD Flashcards

1
Q

What is Guillian Barre Syndrome

A

GBS: The clinical syndrome is classically characterized by ascending weakness, distal paresthesias, and areflexia.

Classically, GBS follows a viral infection, vaccination, or surgery, but in many instances, no prodrome is identified.

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2
Q

GBS path:

A

GBS results from an attack of peripheral myelin or axons mediated by autoantibodies originally generated in response to an infection that typically precedes the onset of neuropathy symptoms by days to weeks. These antibodies cross-react with the myelin or nodal axolemma antigens via molecular mimicry.

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3
Q

GBS presentations

A

progressive, symmetric ascending paralysis.

hypoactive or absent reflexes

Sensory symptoms, such as paresthesias(tingling) in the hands and feet, are often present,

Pain in the back, hips, and thighs

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4
Q

Diagnostic tests for GBS

A

Lumbar puncture

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5
Q

The CSF protein in GBS is usually

A

elevated

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6
Q

GBS treatment

A

Plasma exchange (PLEX) and IV immunoglobulin (IVIG)

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7
Q

What’ is Myasthenia Gravis?

A

an autoimmune disorder that involves antibody- mediated postsynaptic dysfunction of the neuromuscular junction of skeletal muscle resulting in fatigable weakness

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8
Q

Myasthenia gravis presentation:

A
  • fluctuating weakness that is worse after exercise or prolonged activity and improves with rest.

Presenting signs include ptosis, diplopia (double vision), dysarthria, dysphagia (difficulty swallowing), extremity weakness, and respiratory difficulty.

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9
Q

Diagnostics for MG

A

Serum AChR binding antibodies are detected in 85%–90%

MuSK antibodies are detected in about 30%–70% of AChR antibody– negative MG patients.

Chest CT is indicated to screen for a thymoma.

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10
Q

Treatment for MG

A

Plasmapheresis and IVIG are both used to treat MG

Pyridostigmine should be started at 30–60 mg PO tid–qid and titrated for symptom relief.

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11
Q

What is Parkinson’s disease

A

a chronic, progressive neurodegenerative disease characterized by at least two of three cardinal features: resting tremor, bradykinesia, and rigidity.

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12
Q

presentation of Parkinson’s disease

A

resting pill rolling tremor (3–7 Hz) that is often asymmetric.

Bradykinesia is characterized by generalized slowness of movement, especially in finger movement dexterity and gait (often shuffling).

Cogwheel rigidity

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13
Q

Diagnostic testing for Parkinsons disease

A

MRI Brain

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14
Q

first line treatment for parkinsons disease

A

Carbidopa–levodopa

Dopamine agonists (pramipexole, ropinirole) can be used as monotherapy or in combination with other PD medications.

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15
Q

Second line treatment for parkinsons disease

A

Amantadine and catechol-O-methyl transferase inhibitors

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16
Q

Third line treatment for parkinsons disease

A

Deep brain stimulation and Duodopa (intestinal infusion of carbidopa/levodopa gel) have benefit in PD patients who progress to develop motor fluctuations and dyskinesias unresponsive to oral medications.

17
Q

The sudden withdrawal of levodopa or dopamine agonists and following exposure to neuroleptics or other antidopaminergic drugs can cause

A

neuroleptic malignant syndrome (NMS)

18
Q

Serotonin syndrome can occur when monoamine oxidase inhibitors (MAOIs) are combined with

A

TCAs or SSRIs.

19
Q

Critical Illness Polyneuropathy

A

is the acute or subacute onset of extensive symmetric weakness in critical ill patients , usually with sepsis, respiratory failure, multisystem organ failure, or septic inflammatory response syndrome (SIRS).

20
Q

Critical illness polyneuropathy presentation

A

distal extremity weakness, wasting, and sensory loss, as well as paresthesia and decreased or absent deep tendon reflexes

21
Q

Gold standard for the diagnosis of critical illness neuropathy

A

nerve conduction studies and needle electromyography.

EMG is the best way to of making a diagnosis of CIP

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