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
Q

Neck and Limb Symptoms of Myasthenia Gravis

A

Weight of head overcome extensors
Limbs proximal weakness
Wrist & finger extensors & foot dorsiflexors

26
Q

Respiratory Symptoms of Myasthenia Gravis

A

Respiratory insufficiency

Pending respiratory failure

27
Q

Myasthenia Gravis Clinical Course

A

Early symptoms transient

Gets worse throughout the day

28
Q

Myasthenia Gravis Diagnostics

A

Serologic testing immunologic assay

Electrophysiologic studies

29
Q

Electrophysiologic Studies

A

Repetitive nerve stimulation studies

Single fiber electromyography

30
Q

Treatment for Myasthenia Gravis

A

Anticholinesterase agents
Chronic immunotherapies
Rapid immunotherapies
Surgery

31
Q

Anticholinesterase Agent for Myasthenia Gravis

A

Pyridostgigmine (Mestinon)

32
Q

Chronic Immunotherapy for Myasthenia Gravis

A

Corticosteroids

33
Q

Rapid Immunotherapy for Myasthenia Gravis

A

Plasmapheresis

IV immunoglobulin

34
Q

Surgery for Myasthenia Gravis

A

Thymectomy

35
Q

Etiologies for Polyneuropathy

A
Diabetic polyneuropathy
Patients with AIDS
Vitamin B12 deficiency
Toxins: alcohol, chemotherapy, heavy metals
Other vitamin deficiencies
Uremia
36
Q

Pathophysiology of Polyneuropathy

A

Axonal: most common
Demyelinating: seen more in autoimmune and diabetic polyneuropathy

37
Q

Clinical Presentation of Polyneuropathy

A

Slowly progressive with feet 1st
Dysesthesias: burning, pain
Mild gait abnormalities

38
Q

Polyneuropathy Diagnostics

A
Electrodiagnostic testing
CBC
ESR
TSH
Glucose
Vitamin B12 level
Antinuclear antibodies
UA
39
Q

Risk Factors for Polyneuropathy

A
Duration and severity of hyperglycemia
Increased triglyceride level
BMI
Smoker or not
Presence of HTN
40
Q

Pathogenesis of Diabetic Polyneuropathy

A
Accumulation of advanced glycosylation end products
Accumulation of sorbitol
Increased oxidative stress
Nerve ischemia
Peripheral nerve repair
41
Q

Diabetic Polyneuropathy Physical Findings

A
Loss of vibratory sensation
Altered proprioception
Impairment of pain, light touch, and temperature
Decreased/absent reflexes
Motor Weakness (late finding)
42
Q

Complications of Diabetic Polyneuropathy

A

Can’t walk properly

Amputations

43
Q

Treatment of Diabetic Polyneuropathy

A

Tight glycemic control

44
Q

Prevention of Diabetic Polyneuropathy

A

Tight glycemic control
Weight management
Smoking cessation

45
Q

Symptomatic Prescription for Polyneuropathy

A
Gabapentin (Neurontin)
TCAs
Carbamazepine (Tegretol
Phenytoin (Dilantin)
Pregabalin (Lyrica)
Duloxetine (Cymbalta)
46
Q

How Gabapentin Treats Polyneuropathy

A

Reduces pain

Well tolerated

47
Q

How TCA’s Treats Polyneuropathy

A

Amitriptyline

Desipramine

48
Q

How Pregabalin Treats Polyneuropathy

A

Targeted for Diabetics

Trying for other etiologies

49
Q

How Duloxetine Treats Polyneuropathy

A

Antidepressant

Control Pain

50
Q

Alcoholic Polyneuropathy Pathogenesis

A

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
Q

Vitamin B12 Deficiency

A

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
Q

Vitamin B12 Deficiency Diagnostics

A
Serum B12 level
Serum gastrin
Parietal cell antibodies
Anti-intrinsic factor antibodies
Check for H. pylori
53
Q

Treatment for B12 Deficiency

A

IM B12 injections twice weekly for 2 weeks
Weekly injections for 2 months
Monthly injections for life

54
Q

Vitamin E Deficiency

A
Variable peripheral nerve involvement
Ataxia
Hyporeflexia
Proprioceptive
Vibratory loss
55
Q

Vitamine E Deficiency Diagnostics

A

Serum alpha-tocopherol/( serum cholesterol + triglycerides)

56
Q

Thiamine Deficiency

A

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
Q

Thiamine Deficiency Diagnostics

A

Urinary thiamine

Serum thiamine

58
Q

Treatment for Thiamine Deficiency

A

Thiamine and then glucose