Diabetic neuropathy Flashcards

1
Q

Diabetic neuropathy

A
  • common complication associated with DM
  • progressive disorder with nerve fiber loss, atrophy, manifested by deteriorating neural function, progressively decreasing sensation and strength

-neuropathies can be focal or diffuse and involve the ANS or somatic PNS

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2
Q

Diabetic neuropathy incidence

A
  • can occur in type I (54%) or Type II diabetes (30%).

- 50% of people with diabetes never develop S/S of neuropathy

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3
Q

Diabetic neuropathy : etiology

A
  • individual with good glycemic control can still develop neuropathies, although a clear relationship does exist between the length of time that the individual has diabetes and development of neuropathy
  • there may be a genetic predisposition
  • caused by chronic metabolic dstrubances that affect nerve cells and schwann cells
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4
Q

Diabetic neuropathy Pathology

A
  • loss of both myelinated and unmyelinated axons associated with exposure of nerves and schwann cells to glucose. the nerves are affected more distally than proximally
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5
Q

diabetic neuropathy: hyperglycemia

A
  • chqracterized by increased sorbital and fructose
  • coincide with deficiencies in ATP that alter peripheral nerve function
  • excess sorbital also damages schwann cells
  • leads to abnormalities in microcirculation creating endothelial capillary changes and local ischemia
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6
Q

diabetic neuropathy: pathology vascular changes

A
  • vascular changes can also aaffect the peripheral nerves
  • endoneurial and microvascular thickening is present with closed capillaries that are associated with multifocal regions of ischemia and hypoxia to the nerve
  • decreased blood supply leads to axonal degeneration
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7
Q

diabetic neuropathy: pathology impaired nerve nutrition

A
  • the nerve may also be nutrionally deprived
  • the concentration of nerve growth factor is similar molecularly to insulin and is reduced which reduces the nutrition to the nerve
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8
Q

Summary of pathophysiology

A
  • metabolic disturbances affect nerve cells and schwann cells
  • hyperglycemia coincides with deficiencies in ATP that alter peripheral nerve function
  • excess sorbital also damages Schwann cells
  • hyperglycemia leads to abnormalities in microcirculation
  • the nerve may also be nutritionally deprived
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9
Q

diabetic neuropathy : diagnosis

A
  • at leasttwo abnormalities have been recommended for diagnosis
  • electrodiagnotic studies
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10
Q

diabetic neuropathy: clinical manifestations

A
  • stocking and glove distribution of sensory loss
  • progression of disease moves distal to proximal
  • insidious onset
  • loss of ankle reflexes
  • muscle wasting
  • loss of sensation and thermal awarenes
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11
Q

Rapidly reversible neuropathy

—Hyperglycemic neuropathy

A
  • occurs in individuals with uncontrolled DM or newly diagnosed cases
  • presents with sensory changes, paresthesias, tenderness of the feet and legs
  • symptoms disappear when blood sugar is controlled although nerve conduction may be abnormal
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12
Q

acute sensory neuropathy

A
  • rapid onset of severe burning pain, deep aching a sudden sharp “electric shock” sensation and hypersensitivity of the feet
  • sx are often worse at night
  • sensory loss may be mild
  • motor exams are normal
  • DTRs are normal or reduced at the ankles
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13
Q

chronic sensorimotor neuropathy

A
  • most common type of diabetic polyneuropathy
  • 50%of patients may develop this
  • insidious onset
  • S/S include sensory loss, burning pain and paresthesias because of small fiber loss.
  • large fiber loss results in non-painful paresthesias decrease proprioception, impaired vibration, loss of touch sensation, diminished DTRs
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14
Q

autonomic neuropathy

A
  • sympathetic and parasympathetic involvement
  • after 10-15 years 30% of patients have subclinical manifestations of autonomic involvement
  • cardiovascular: tachycardia, exercise intolerance, orthostatic hypotension, dizziness
  • gastrointestinal: esophageal motility dysfunction, diarrhea, constipation
  • genitourinary: neurogenic bladder, bladder urgency, incontinence, erectile dysfunction
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15
Q

mononeuropathy

A
  • single neuropathy in the limb
  • occur less often than symmetric patterns
  • median , ulnar and peroneal nerves are the most commonly affected
  • somatic division of the oculomotor nerve can be affected
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16
Q

diabetic neuropathy: management

A
  • control of hyperglycemia and measures to address sympotomatic management of the disorder
  • physical therapy for strategies to compensate for sensory loss and balance training
17
Q

diabetic neuropathy medications

A
  • gangliosides
  • NGFs
  • angiotensin-converting enzyme inhibitors
  • antidepressants
  • gabapentin: focal neuropathies
  • topical capsaicin: allodynia
  • b12- for pain & parasthesias
18
Q

diabetic neuropathy Prognosis

A
  • metabolic disorder and multiple organs are affected

- strict preventative procedures and early detection can greatly alter the progression of the disease

19
Q

alcoholic neuropathy: etiology

A
  • peripheral neuropathy that appears after years of chronic alcohol abuse.
  • patients without a co-existing thiamine deficiency tend to have a slower progressing course
  • nutritional deficiencies
20
Q

alcoholic neuropathy: pathology

A
  • segmental demyelination progressing to axonal degeneration

- changes occur distally at first and become more marked and proximal

21
Q

alcoholic neuropathy: clinical manifestation

A
  • mild forms are associated with minor loss of muscle bulk, sensory impairment, diminished ankle reflexes, aching in calves
  • distal sensory changes include pain, paresthesia, and numbness in stocking glove pattern
  • begins insidiously, most cases involve all four extremities. occasionally the onset may be more acute
  • weakness and atrophy of distal musculature should be anticipated
  • foot drop and wrist drop. peripheral muscle weakness
  • LE are more affected that UE
22
Q

compression neuropathies

A
  • may develop from prolonged positions of nerve compression when patients passs out in awkward positions after intoxication
23
Q

Rhabdomyolysis

A
  • characterized by proximal muscle wasting, swelling, pigmented urine, result of renal failure
24
Q

chronic renal failure

A
  • uremic encephalopathy characterized by recent memory loss, inability to concentrate, perceptual errors and decreased alertness
25
Q

alcoholic neuropathy anemia

A
  • decreased hemoglobin in blood levels, moderate to severe is 7-8g/dl. normal is 11-12 g/dl for females and 13-14 g/dl for males
26
Q

alcoholic neuropathy: diagnosis

A
  • made by clinical presentation and history
  • nerve biopsy demonstrates greater small fiber axonal loss inpatient w/o a thiamine deficiency. greater large fiber loss with segmental demyelination in those with a deficiency
  • electrodiagnostic testing shows loss of action potential amplitude
27
Q

alcoholic neurpathy: management

A
  • quit drinking
  • treatment is symptomatic
  • recovery depends on demyelination or degeneration
  • equipment evaluation
  • orthotic evaluation for AFOs and wrist splints
  • medication for management of paresthesias
28
Q

alcoholic neuropathy: prognosis

A
  • if the individual abstains from alcohol, mild improvement can be expected
  • recovery is slow and dependent on whether demyelination or degeneration has occurred. careful review of EMG studies are needed