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Pod Med III > 7) Lower Extremity Manifestations Of The Autonomic Nervous System > Flashcards

7) Lower Extremity Manifestations Of The Autonomic Nervous System Flashcards

1
Q

Hypothalamus main function

A
  • Homeostasis
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2
Q

Hypothalamus afferent input

A
  • Visceral sensory – blood pressure, gut distention
  • Reticular formation – skin temperature
  • Intrinsic receptors – temperature and ionic balance
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3
Q

Hypothalamus efferent input

A
  • Vagal – heart rate, vasoconstriction, digestion

- Pituitary regulation

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4
Q

Wernicke’s syndrome

A
  • Nutritional deficiency in thiamine

- Often occurs in chronic alcoholics

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5
Q

Wernicke’s syndrome triad

A
  • Mental status changes (short term memory loss, maintain cognitive function)
  • Ataxia (Broad based gait)
  • Ophthalmoplegia (cranial nerve IV palsy, gaze-evoked nystagmus)
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6
Q

Role of thiamine

A
  • Co-factor in carbohydrate catabolism
  • Areas with highest metabolic rate at greatest risk
  • Paraventricular hemorrhages occur
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7
Q

Wernicke’s syndrome treatment

A
  • 100 mg thiamine along with magnesium
  • Repeat until symptoms subside
  • Symptoms may lessen but persist → Korsakoff’s Syndrome
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8
Q

Autonomic nervous system

A
  • Regulates glands, smooth and cardiac muscle
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9
Q

ANS sympathetic component

A
  • Fight or flight
  • Catabolic
  • Thoracolumbar
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10
Q

ANS parasympathetic component

A
  • Rest and digest
  • Anabolic
  • Caudocranial
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11
Q

Sympathetic nervous system preganglionic fibers

A
  • Arise within intermediolateral columns of spinal cord
  • Course from T1 – L2
  • Exit column to enter paravertebral chain (sympathetic chain)
  • May travel up or down prior to synapsing
  • First synapse – cholinergic
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12
Q

Sympathetic nervous system postganglionic fibers

A
  • Second synapse – adrenergic

- Exception – sweat ducts - cholinergic

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13
Q

Parasympathetic nervous system nerves originate in the medulla oblongata

A
  • Cell bodies within intermediolateral columns from S2 – S4
  • Cranial nerves III, VII, IX and X
  • Synapses lie close to or within viscera
  • First and secondary synapses – cholinergic
  • Exceptions – some secondary synapses use nitric oxide
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14
Q

Autonomic neuropathy CVS manifestations

A
  • Resting tachycardia
  • Vagal nerve dysfunction
  • Fail to do valsalva maneuver
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15
Q

Diagnosing CVS manifestations of autonomic neuropathy

A
  • Valsalva maneuver – normally 4 phases
  • Phase 1 – transient HR
  • Phase II – ↑ HR
  • Phase III – further ↑ HR
  • Phase IV – transient ↓ HR
  • With neuropathy – no transient changes in HR
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16
Q

Postural hypotension

A
  • Fall of systolic pressure
  • From supine to standing
  • Drop >30 mm/Hg significant
  • Fall in diastolic pressure
  • “isometric” test
  • Maintain hand grip
  • Drop >10 mm/Hg significant
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17
Q

Painless of silent MI

A
  • Greater general anesthesia risk
  • Damages afferent innervation
  • Risk greatest in the morning
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18
Q

Diurnal variation

A
  • BP normally declines at night

- BP increases at night with neuropathy

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19
Q

Established acute MI ECG readings

A
  • Prominent Q wave
  • Elevated ST segment
  • Inverted T waves
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20
Q

Esophageal symptoms (autonomic neuropathy)

A
  • Dysphagia – uncommon

- Occasional heartburn

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21
Q

Gastric dysfunction (autonomic neuropathy)

A
  • Gastroparesis
  • Early satiety
  • Nausea and vomiting (undigested food)
  • Emesis of undigested food
  • Abdominal bloating and epigastric pain
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22
Q

Complications with GI autonomic neuropathy

A
  • Compromised nutrient delivery to small bowel

- Interferes with glucose absorption

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23
Q

Autonomic neuropathy GI treatment

A
  • Good glucose control aids gastric motor function

- Eat multiple small meals

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24
Q

Neurogenic bladder

A
  • ↓ Bladder sensation due to afferent nerve damage
  • Bladder enlarges up to 3x
  • Inability to void completely
  • Increased risk of urinary infection
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25
Q

Neurogenic bladder treatment

A
  • Parasympathomimetics
  • Alpha-1 blocker
  • Self catheterization
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26
Q

Autonomic neuropathy sexual dysfunction

A
  • Erectile dysfunction
  • Retrograde ejaculation
  • Female dysfunction
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27
Q

Sudomotor symptoms of autonomic neuropathy

A
  • Disturbances with thermal regulation
  • Hyperhidrosis – upper body
  • Anhidrosis - lower body
  • Dry, brittle skin
  • Increase risk of ulceration
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28
Q

Sudomotor symptoms palliative treatment

A
  • Emollients (helps exfoliate)

- Patient education

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29
Q

Charcot joint disease hypertrophic form

A
  • Proliferative dense osseous reaction
  • Coalescence resulting in “healing”
  • Results in significant deformity
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30
Q

Hypertrophic charcot joint disease etiology

A
  • Neurotraumatic theory

- Neurovascular theory”

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31
Q

Neurotraumatic theory (charcot joint)

A
  • Loss of pain and proprioception
  • Unable to recognize joint subluxation
  • Presence of periarticular fragmentation
  • Seen Radiographically
  • Repetitive microtrauma
  • Glycosylated collagen
  • Abnormal weight bearing load distribution
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32
Q

Autonomic neuropathy (CJD)

A
  • Increased osseous circulation
  • Periarticular osteopenia
  • Decreased mineralization
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33
Q

Motor neuropathy (CJD)

A
  • Intrinsic minus foot
  • Abnormal distribution of weight bearing load
  • Micro stress fracture
  • Non-enzymatic glycosylation of collagen
  • Weakened ligaments
  • Decreased capsular strength
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34
Q

CJD stage 0

A
  • Clinical

- Erythema, edema, and increased temperature

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35
Q

CJD stage I

A
  • Development
  • Generalized demineralization
  • Periarticular fragmentation
  • Loose body formation
  • Joint dislocation
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36
Q

CJD stage II

A
  • Coalescence
  • Organization and early healing of fragments
  • Periosteal new bone formation
  • Resorption of bony debris
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37
Q

CJD stage III

A
  • Reconstruction/consolidation
  • Greater definition of bony spurs
  • Reconstruction or ankylosis of bones
38
Q

CJD anatomic classification (Brodsky)

A
  • Type 1 = midfoot = rare instability, symptomatic plantar prominences
  • Type 2 = hindfoot = grossly deformed and unstable, longer immobilization
  • Type 3a = ankle = leads to more severe instability
  • Type 3b = calcaneal fracture = leads to pes planus, creates Achilles insufficiency
39
Q

CJD midtarsus deformity classification (Schon)

A
  • Type 1 = met-cuneiform/met-cuboid joints = plantar medial process
  • Type 2 = nav-cun/met-cub = plantar lateral prominence
  • Type 3 = perinavicular region = plantar central prominence, plantar lateral prominence
  • Type 4 = transverse tarsal = variable prominences
40
Q

CJD clinical recognition

A
  • Bounding pedal pulses
  • Red, hot, swollen foot
  • Generally painless
41
Q

CJD differential diagnosis

A
  • Osteomyelitis
  • Bone tumor
  • Cellulitis
  • Deep venous thrombosis
42
Q

CJD diagnosis

A
  • Clinical presentation
  • Radiographic findings
  • Osseous shards with synovial biopsy
43
Q

CJD treatment

A
  • Early recognition!!!
  • Prevention of additional trauma
  • Wide distribution of weight bearing load
44
Q

CJD surgical intervention indications

A
  • Chronic ulceration from deformity
  • Joint instability that cannot be braced
  • Recurrent ulceration from bony prominences
  • Acute displaced fractures – good circulation
45
Q

CJD surgical intervention timing

A
  • Avoid acute and subacute phases – fixation failure
  • Simon et al* – good results with early arthrodesis
  • He did this during Stage I
  • Heal all ulcers if possible
46
Q

Tendo-Achilles off-loading techniques

A
  • Limited ankle joint dorsiflexion increases forefoot plantar pressures
  • Tendon thickening may occur secondary to glycosylation
47
Q

Tendo-Achilles lengthening

A
  • Benefits: temporary relief of forefoot pressures

- Downfalls: increased rearfoot pressures

48
Q

CJD midfoot surgical intervention

A
  • Most common area for neuropathic arthropathy

- Exostectomy

49
Q

CJD midfoot exostectomy

A
  • Stable midfoot
  • Consideration of ulcer location if present
  • Consideration of rotational flap
50
Q

CJD midfoot surgical intervention arthrodesis

A
  • Importance of restoring lateral arch
  • Unstable midfoot
  • May require multiple multi-planar osteotomies
  • Plate is stronger construct that cannulated screws
  • Consider external fixation if ulcer present
51
Q

CJD hindfoot and ankle surgical intervention

A
  • Maintain weight bearing alignment
  • Prevent progression of deformity
  • Fixation may be a challenge
52
Q

CJD hindfoot and ankle surgical intervention considerations

A
  • Tendo Achilles lengthening
  • Anatomic alignment of rearfoot to leg with restoration of calcaneal inclination angle
  • Restoration of the forefoot to rearfoot relationship
  • Use of bone stimulator
  • Many options available – internal and external
53
Q

CJD sequelae

A
  • Rocker bottom foot
  • Bony abnormalities
  • Neurotrophic ulcerations
54
Q

CJD treatment

A
  • Insensate foot measures
  • Accommodative shoe gear
  • Surgical intervention
55
Q

Diabetic osteolysis

A
  • Less common variety
  • Occurs in response to hyperemia
  • Tubular bones develop atrophic bone changes
  • Classic “penciling” of metatarsal heads
  • Hourglass resorption of phalanges
56
Q

Clinical signs of sympathetic nervous dysfunction

A
  • Visible color changes
  • Temperature alterations
  • Hydration changes
57
Q

Sympathetic nervous system dysfunction with overactivity

A
  • Vasoconstriction and hyperhidrosis

- Cyanotic, cool and clammy extremity

58
Q

Sympathetic nervous system dysfunction with underactivity

A
  • Vasodilation and anhidrosis

- Bounding pulses, erythema and anhidrosis

59
Q

Hyperhidrosis

A
  • Increased SNS activity

- Hands affected more than feet

60
Q

Hyperhidrosis predilection for

A
  • Tinea
  • Cutaneous diphtheroid infections
  • Bromhidrosis
61
Q

Hyperhidrosis treatment

A
  • Glutaraldehydes

- Anti-perspirant creams

62
Q

Anhidrosis

A
  • Complete loss of sympathetic input

- Total loss of sweating with lesion above T7

63
Q

Prolonged anhidrosis leads to

A
  • Decreased muscle bulk
  • Demineralization of bone
  • Significant xerosis
64
Q

Anhidrosis treatment

A
  • Emollients

- Physical therapy

65
Q

Raynaud’s Disease

A
  • Vasomotor instability

- Tri-phasic color response (pallor, cyanosis, rubor)

66
Q

Raynaud’s incidence

A
  • Females > males

- May co-exist with several collagen vascular diseases

67
Q

Raynaud’s Disease symptoms

A
  • Paresthesias
  • Digital stiffness
  • Exacerbated by cold
68
Q

Raynaud’s Disease diagnosis

A
  • Rule out underlying disorders
  • CBC with differential
  • Rheumatoid profile
  • ESR
69
Q

Raynaud’s management

A
  • Medical management of underlying etiology – if present
  • Minimize stress and anxiety (Yoga)
  • “insulate” the digit
70
Q

Digit insulation for Raynaud’s

A
  • Multiple layers of socks
  • Petroleum jelly on digits
  • Nitroglycerin paste
  • Drug therapy to reduce peripheral vasoconstriction
71
Q

Acrocyanosis

A
  • SNS overactivity
  • Etiology unknown
  • Persistence of cyanosis
  • Females > males
72
Q

Acrocyanosis symptoms

A
  • Swelling
  • Decreased sensory perception
  • Paresthesias
  • Hyperhidrosis
73
Q

Acrocyanosis treatment

A
  • Minimize cold exposure
74
Q

Erythromelalgia characterized by

A
  • Erythema and swelling
  • Pain or “itching”
  • Triggered by a “critical temperature” (hotter climate exacerbates it)
75
Q

Erythromelalgia etiology

A
  • Unknown but may be due to congenitally small vessels
  • Unable to dissipate heat
  • Males > females
76
Q

Erythromalalgia diagnosis

A
  • Itching or burning with triggering temperature
  • Intact pedal pulses
  • Symptomatic relief with aspirin?
  • May have concomitant polycythemia vera
77
Q

Erythromelalgia treatment

A
  • Patient education
  • Elevation with cold compresses
  • Lumbar sympathectomy
78
Q

Complex regional pain syndrome

A
  • Occurs secondary to vasomotor instability mediated by the SNS
  • Pain out of proportion to injury
79
Q

Type I CRPS

A
  • Formerly known as Reflex Sympathetic Dystrophy
  • Sequalae of “minor” trauma
    No identifiable nerve lesion
80
Q

Type II CRPS

A
  • Formerly known as Causalgia
    Identifiable nerve lesion
  • Sympathetically maintained pain
  • Pain restricted to the distribution of a single nerve
81
Q

CRPS short circuit theory

A
  • Nociceptor efferent pathways lose insulation
  • Normal impulses are disrupted
  • Impulses are misdirected and cross stimulate afferent pain fibers
82
Q

CRPS internuncial neurons

A
  • Act as “liaisons” between afferent and efferent stimulus which governs reflex responses
  • Internuncial neurons are overstimulated by afferent input of irritated nerve
  • In turn overstimulate motor and smooth muscle efferent nerves
83
Q

Early CRPS diagnosis

A
  • Swelling (comes and goes)
  • Temperature (hot)
  • Agony (pain out of proportion)
  • Redness/purple discoloration
  • Tremors (sometimes w/ weakness)
84
Q

CRPS treatment

A
  • Nerve meds (gabapentin, pregabalin, duloxetine)
  • Opioids
  • Work outs (PT as well)
85
Q

CRPS Type I acute stage

A
  • Lasts 2-3 months
  • Presence of severe burning pain
  • Increased warmth, swelling and joint stiffness
  • Symptoms involve an entire region
  • Exacerbated by limb dependency, emotional stress of physical contact
  • Radiographs: maybe early demineralization
86
Q

CRPS Type I dystrophic stage (phase 2)

A
  • Several months
  • Warm edematous phase subsides
  • Extremity becomes firm, cyanotic and cool
  • Pain becomes constant and unrelenting
  • Symptoms exacerbated by any stimulus (hypersensitive to anything that can exacerbate their pain)
  • Radiographic Findings: diffuse osteoporosis (Sudeck’s atrophy), flexion contractures of digits begin to develop
87
Q

CRPS Type I atrophic stage (phase 3)

A
  • Irreversible
  • Pain may subside or become intractable
  • Skin and subcutaneous tissues become atrophic
  • Flexion contractures become irreversible
  • Radiographic findings: ground glass appearance of bone, advanced osteoporosis
88
Q

CRPS Type I incidence

A
  • Individuals of all ages
  • Female to male – 3:1
  • Psychological profile: “Type A” personalities, anxious, inquisitive
  • Minor trauma – especially crush injuries!
89
Q

CRPS diagnosis

A
  • Early recognition and treatment essential
  • Changes on radiographs
  • Triphasic technetium scan (intense, focal peri-articular uptake in phase 3)
  • Thermography
  • Symptomatic relief to sympathetic nerve block
90
Q

CRPS Type I imaging

A
  • Periarticular
  • Osteopenia
  • Diffuse midfoot uptake in phase 3
91
Q

CRPS treatment

A
  • Aggressive physical therapy (prevent joint contracture and muscle wasting)
  • Sympathetic nerve blocks (biweekly administration, break aberrant nerve impulses)
  • Pain management (Bier blocks, tricyclic anti-depressants, anticonvulsants, surgical sympathectomy)

Pod Med III (8 decks)

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