Diabetic neuropathy Flashcards
Diabetic neuropathy
- 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
Diabetic neuropathy incidence
- can occur in type I (54%) or Type II diabetes (30%).
- 50% of people with diabetes never develop S/S of neuropathy
Diabetic neuropathy : etiology
- 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
Diabetic neuropathy Pathology
- 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
diabetic neuropathy: hyperglycemia
- 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
diabetic neuropathy: pathology vascular changes
- 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
diabetic neuropathy: pathology impaired nerve nutrition
- 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
Summary of pathophysiology
- 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
diabetic neuropathy : diagnosis
- at leasttwo abnormalities have been recommended for diagnosis
- electrodiagnotic studies
diabetic neuropathy: clinical manifestations
- 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
Rapidly reversible neuropathy
—Hyperglycemic neuropathy
- 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
acute sensory neuropathy
- 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
chronic sensorimotor neuropathy
- 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
autonomic neuropathy
- 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
mononeuropathy
- 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
diabetic neuropathy: management
- control of hyperglycemia and measures to address sympotomatic management of the disorder
- physical therapy for strategies to compensate for sensory loss and balance training
diabetic neuropathy medications
- gangliosides
- NGFs
- angiotensin-converting enzyme inhibitors
- antidepressants
- gabapentin: focal neuropathies
- topical capsaicin: allodynia
- b12- for pain & parasthesias
diabetic neuropathy Prognosis
- metabolic disorder and multiple organs are affected
- strict preventative procedures and early detection can greatly alter the progression of the disease
alcoholic neuropathy: etiology
- 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
alcoholic neuropathy: pathology
- segmental demyelination progressing to axonal degeneration
- changes occur distally at first and become more marked and proximal
alcoholic neuropathy: clinical manifestation
- 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
compression neuropathies
- may develop from prolonged positions of nerve compression when patients passs out in awkward positions after intoxication
Rhabdomyolysis
- characterized by proximal muscle wasting, swelling, pigmented urine, result of renal failure
chronic renal failure
- uremic encephalopathy characterized by recent memory loss, inability to concentrate, perceptual errors and decreased alertness
alcoholic neuropathy anemia
- 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
alcoholic neuropathy: diagnosis
- 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
alcoholic neurpathy: management
- 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
alcoholic neuropathy: prognosis
- 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