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Peripheral Neuropathies Flashcards

1
Q

Define polyneuropathy

A

Symmetric distal sensory loss with burning or weakness

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2
Q

Etiologies of polyneuropathy

A

Adverse effect of medication

Manifestation of systemic disease

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3
Q

Pathogenesis of Guillain-Barre Syndrome

A

Acute immune-mediated group of polyneuropathies, usually provoked by preceding infection
Acute inflammatory demyelinating polyneuropathy (AIDP)

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4
Q

Types of infections which commonly bring on Guillain-Barre Syndrome

A

Campylobacter jejuni
Respiratory tract infection
CMV
EBV

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5
Q

Guillain-Barre antibodies to what

A

Gangliosides which cause axonal injury or immune response to myelin

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6
Q

Guillain-Barre Clinical Features

A 
Ascending symmetric muscle weakness
Severe respiratory muscle weakness (intubation)
Paraesthesia's common
Sensory abnormalities frequently mild
Severe back pain
Dysautonia
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7
Q

What is Dysautonia?

A

Tachycardia alternating with bradycardia, urinary retention, HTN alternating with hypotension, orthostatic hypotension, ileus, loss of sweating

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8
Q

Guillian Barre Syndrome Diagnostics

A

Lumbar puncture
Electromyography (EMG)
Nerve conduction studies
Glycolipid antibodies to gangliosides

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9
Q

Features that make Guillian-Barre Syndrome doubtful

A

Sensory level
Marked, persistent asymmetry of weakness
Severe/persistent bowel/bladder dysfunction
More than 50 WBC in the CSF

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10
Q

Define Bell’s Palsy

A

Acute peripheral facial palsy of unknown origin

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11
Q

Bell’s Palsy Anatomy

A

Fibers for motor output to facial muscles
Parasympathetic fibers to the lacrimal, submandibular, & sublingual salivary glands
Afferent fibers for taste from the anterior 2/3 of tongue
Somatic afferents for external auditory canal and pinna

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12
Q

Pathogenesis of Bell’s Palsy

A

Most common- herpes simplex
Other infectious causes: EBV, adenovirus, rubella, mumps, influenza B, herpes zoster, coxsackie virus
Ischemia

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13
Q

Clinical Presentation of Bell’s Palsy

A 
Sudden onset
Unilateral facial paralysis
Eyebrow saggio
Inability to close the eye
Disappearance of the nasolabial fold
Mouth drawn to the non affected side
Decreased tearing
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14
Q

Physical Exam for Bell’s Palsy

A

Assess facial movement
General physical and neurologic exam
Attention to external ear for vesicles or scabbing
Attention to parotid for mass lesions

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15
Q

Bell’s Palsy Course

A

Onset over hours to 2 days
Progressive with maximal paralysis within 3 weeks of onset
Recovery of some degree of function by 6 months

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16
Q

Bell’s Palsy Management

A

Glucocorticoid therapy

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17
Q

Patient Information for Bell’s Palsy

A

Usually caused by a virus
As nerve cell swells, it becomes compressed & it’s protective covering breaks down
Takes time to recover

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18
Q

What is Myasthenia Gravis?

A

Autoimmune disorder characterized by weakness and fatiguability of skeletal muscle

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19
Q

Pathogenesis of Myasthenia Gravis

A

Autoantibodies against acetylcholine receptors (AChR-Ab)
Decrease # of acetylcholine receptors due to binding
Destruction of receptors by a compliment-mediated process
T cells bind to acetylcholine receptors and activate B cells
Most have thyme abnormalities

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20
Q

Bimodal distribution of Myasthenia Gravis

A

Female- 20-30s

Male- 60-80s

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21
Q

Key Symptoms of Myasthenia Gravis

A

Fluctuating skeletal muscle weakness
Worsened by contractile force
True muscle fatigue not tiredness

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22
Q

Ocular Symptoms of Myasthenia Gravis

A

Ptosis
EOM often involved leading to diplopia
Ptosis increases with sustained upward gaze or by holding up the opposite eyelid

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23
Q

Bulbar Symptoms of Myasthenia Gravis

A

Weakness with prolong chewing, jaw weakness
Dysarthria
Dysphagia
Nasal regurgitation of liquids

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24
Q

Facial Symptoms of Myasthenia Gravis

A

Patient appears expressionless
“Lost their smile”
Weakness of orbicular Doris muscle
Weakness of orbicular oculi

25
Neck and Limb Symptoms of Myasthenia Gravis
Weight of head overcome extensors Limbs proximal weakness Wrist & finger extensors & foot dorsiflexors
26
Respiratory Symptoms of Myasthenia Gravis
Respiratory insufficiency | Pending respiratory failure
27
Myasthenia Gravis Clinical Course
Early symptoms transient | Gets worse throughout the day
28
Myasthenia Gravis Diagnostics
Serologic testing immunologic assay | Electrophysiologic studies
29
Electrophysiologic Studies
Repetitive nerve stimulation studies | Single fiber electromyography
30
Treatment for Myasthenia Gravis
Anticholinesterase agents Chronic immunotherapies Rapid immunotherapies Surgery
31
Anticholinesterase Agent for Myasthenia Gravis
Pyridostgigmine (Mestinon)
32
Chronic Immunotherapy for Myasthenia Gravis
Corticosteroids
33
Rapid Immunotherapy for Myasthenia Gravis
Plasmapheresis | IV immunoglobulin
34
Surgery for Myasthenia Gravis
Thymectomy
35
Etiologies for Polyneuropathy
``` Diabetic polyneuropathy Patients with AIDS Vitamin B12 deficiency Toxins: alcohol, chemotherapy, heavy metals Other vitamin deficiencies Uremia ```
36
Pathophysiology of Polyneuropathy
Axonal: most common Demyelinating: seen more in autoimmune and diabetic polyneuropathy
37
Clinical Presentation of Polyneuropathy
Slowly progressive with feet 1st Dysesthesias: burning, pain Mild gait abnormalities
38
Polyneuropathy Diagnostics
``` Electrodiagnostic testing CBC ESR TSH Glucose Vitamin B12 level Antinuclear antibodies UA ```
39
Risk Factors for Polyneuropathy
``` Duration and severity of hyperglycemia Increased triglyceride level BMI Smoker or not Presence of HTN ```
40
Pathogenesis of Diabetic Polyneuropathy
``` Accumulation of advanced glycosylation end products Accumulation of sorbitol Increased oxidative stress Nerve ischemia Peripheral nerve repair ```
41
Diabetic Polyneuropathy Physical Findings
``` Loss of vibratory sensation Altered proprioception Impairment of pain, light touch, and temperature Decreased/absent reflexes Motor Weakness (late finding) ```
42
Complications of Diabetic Polyneuropathy
Can't walk properly | Amputations
43
Treatment of Diabetic Polyneuropathy
Tight glycemic control
44
Prevention of Diabetic Polyneuropathy
Tight glycemic control Weight management Smoking cessation
45
Symptomatic Prescription for Polyneuropathy
``` Gabapentin (Neurontin) TCAs Carbamazepine (Tegretol Phenytoin (Dilantin) Pregabalin (Lyrica) Duloxetine (Cymbalta) ```
46
How Gabapentin Treats Polyneuropathy
Reduces pain | Well tolerated
47
How TCA's Treats Polyneuropathy
Amitriptyline | Desipramine
48
How Pregabalin Treats Polyneuropathy
Targeted for Diabetics | Trying for other etiologies
49
How Duloxetine Treats Polyneuropathy
Antidepressant | Control Pain
50
Alcoholic Polyneuropathy Pathogenesis
Axonal neuropathy complicated by demyelination when coexisting nutritional deficiency Reduction in density of small myelinated and unmyelinated fibers with normal thiamine Alcohol is direct neurotoxin
51
Vitamin B12 Deficiency
Defect in myelin formation leading to subacute degeneration of dorsal and lateral spinal columns Paresthesias Ataxia with loss of vibration/position sense Severe weakness, spasticity, clonus, & paraplegia
52
Vitamin B12 Deficiency Diagnostics
``` Serum B12 level Serum gastrin Parietal cell antibodies Anti-intrinsic factor antibodies Check for H. pylori ```
53
Treatment for B12 Deficiency
IM B12 injections twice weekly for 2 weeks Weekly injections for 2 months Monthly injections for life
54
Vitamin E Deficiency
``` Variable peripheral nerve involvement Ataxia Hyporeflexia Proprioceptive Vibratory loss ```
55
Vitamine E Deficiency Diagnostics
Serum alpha-tocopherol/( serum cholesterol + triglycerides)
56
Thiamine Deficiency
Seen in anorexia nervosa, malnutrition, alcoholism bariatric surgery Dry beriberi: neuropathy with calf cramps, muscle tenderness, burning feet, autonomic neuropathy Wet beriberi: high-output CHF + neuropathy
57
Thiamine Deficiency Diagnostics
Urinary thiamine | Serum thiamine
58
Treatment for Thiamine Deficiency
Thiamine and then glucose

Neurology (10 decks)

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