exam 3 Flashcards
Fatal genetic disorder that causes progressive breakdown of nerve cells in the brain
Physical and mental abilities deteriorate over time
No cure
Ability to reason, walk and speak are affected
Affects entire brain, not just 1 area - caused by degeneration of nerve cells within brain
Is autosomal dominant - Genetic
Brain isn’t impaired, so trapped in own body
Family cares for them
NM:
-No treatment will alter the course of the disease
-Medications can help control symptoms of movement and psychiatric
-Medications that help with chorea:
–Tetrabenazine (Xenazine)
–Levetiracetam (Keppra) helps with involuntary movements
–Clonazepam (Klonopin)
-Antipsychotic drugs
–Quetiapine (Seroquel), risperidone (Risperdal) - can help depression but in some pts with HD can do opposite and make worse
-Goal: manage S/S and reserve quality of life
-Speech therapy
–Help with speech, eating, and swallowing
-PT/OT
–Safety, exercises to maintain strength, provide assistive devices for home, adaptive utensils for eating/drinking
-Psychotherapy
–Talk therapy, manage behavioral problems, coping strategies
Huntington’s Disease
Usually appear between 30-50 years of age Worsen over 10-25 year period -Personality changes, mood swings, and depression* -Forgetfulness and impaired judgment -Unsteady gait -Involuntary movements (chorea) -Slurred speech* -Difficulty swallowing* -Significant weight loss* -Dysponia ? unsteady? -uncoordinated jerkey movements Diagnosis -Physical examination --Neurological --Psychiatric --Family medical history -Clinical manifestations -CT or MRI – structural changes of brain – used for rule out -Genetic testing
Huntington’s disease 2
The immune system mistakenly attacks the peripheral nervous system
Acute inflammatory demyelinating polyneuropathy
Immune mediated neuropathy – Lymphocytes and macrophages strip myelin from axons
-Causes a loss of our nerve impulses being sent
Seen in PNS, cranial nerves, and spinal nerve roots
Disease follows GI/resp illness - Demyelination of nerves that control the diaphragm and intercostal muscles result in respiratory failure. Require mechanical ventilation.
- immune system is primed and cant recognize normal/abnormal and it attacks the nerves
Guillain-Barre Syndrome
Ascending* paralysis develops quickly: concern = lungs/ability to breath
-Ground to Head* – happens in lower extremities first
Symmetrical weakness & paralysis*
-Respirations, Bowel and bladder paralysis: bowel: paralytic ileus (sedment of bowel stops function) - cuts of stimulation -> ischemia necrosis; bladder: urinary retention -> pathogens -> UTI
-Swallowing, talking disrupted
-Sensory loss
Areflexia – absent or depressed - may progress to complete paralysis all all 4 limbs
Tenderness and Pain – due to exposed axons
Respiratory Compromise*
At risk pts: autoimmune disease (vaccinations (rabies) r/t activate immune system
Guillain-Barre Syndrome 2
Complete functional recovery can take up to 2 years for some people. Some may develop residual symptoms because the axons were damaged permanently after demyelination.
If the cranial nerves are affected – optic nerve demyelination can cause blindness. Become unable to swallow or clear secretions due to demyelination of vagus nerve and glossopharyngeal nerve.
DOES NOT affect cognition of LOC.
Diagnosis:
-Depends greatly on patient medical history & progression of symptoms
–GI or respiratory disorder 1-4 weeks earlier???
-Lumbar Puncture - not definitive
–Increased proteins* (found in only 50% of patients with early GBS) (late see 90% of time)
-Electromyography – nerve conduction study
-Pulmonary function tests to get baseline and anticipate progression
NM:
-Great risk for respiratory compromise
-DVT Prophylaxis
-Monitor cardiovascular system
–Telemetry, blood pressure
-Plasmapheresis: machine to clean plasma in body - central line double lumen needed to eat macrophages (prevents progression)
-IVIG
Concern = mobility (DVT heparin/lovenox, SCD) - PT/OT to preserve muscle function and prevent atrophy
NM:
-Neurological Assessments: see progression/plateau : reflexes/strength
-Cardiovascular Assessments: affects SNS big BP swings -> risk of dysrhythmias
-Respiratory Status
-Gastrointestinal and Urinary Function: bowel/UI retention
-Mobility – PT/OT will be huge!
-GOAL = Prevent infection and complications of immobility
-Aspiration Precautions
-Communication
-Respiratory Status
-Cardiac Monitoring
-Comfort Measures
-Psychosocial support
Guillain-Barre Syndrome 3
Caused by the unilateral inflammation of the facial nerve or cranial nerve VII
Results in weakness or paralysis of the facial muscle
Cause is unknown but theories include:
-Vascular ischemia: decrease blood supply to nerve
-Viral infections (herpes simplex, herpes zoster): virus
-Autoimmune disorders
nerve inflammation: not lack of sheath like others
Test: close eye against force
all 1 side: droop eyes (ptosis), corner mouth droops r/t muscle not working
Bell’s palsy
7th cranial nerve: smile, tongue, scrunch eye and face muscle
S/S:
-Unilateral facial paralysis
-Decreased lacrimation: stop making tears so dry eyes
-Painful sensations to the face: weird sensation like foot fell asleep
-Speech difficulties – decreased salivation: muscle to make lip/jaw move is compromised
-“Mask like” appearance of affected side: can’t move 1/2 of face
NM:
-Corticosteroid therapy
-Antiviral medications
-Analgesics for pain
–Heat can be applied to aid circulation
-*Protect affected eye from injury and corneal ulcerations: eye patch/shield r/t muscle can’t hold eye closed - give eye drops r/t decrease tear/dry eyes to preserve eye function
Bell’s Palsy 2
Chronic pain condition that affects the trigeminal or cranial nerve V
AKA tic douloureux
Form of neuropathic pain
Causes: Variety of conditions
-Blood vessel pressing on trigeminal nerve -> compression which cause pain - surgery to cut out blood
-MS patient – deterioration of nerves myelin sheath
-Injury to the nerve – sinus/oral surgery, stroke, facial trauma: car accident, surgery where nerve was nicked/cut
Extremely painful - 1 side
-Hallmark S/S: acute pain on 1 side of face
Trigeminal Neuralgia - 5th cranial nerve
S/S:
-Intense flashes of pain
–Extreme, sporadic, sudden burning
–Shock-like facial pain
—Can last seconds to minutes
–Aching, burning, stabbing pain (neurologic pain)
-Pain can be triggered by vibration or contact
–Brushing teeth, eating, drinking, talking, exposed to the wind
Diagnosis:
-History
-Clinical manifestations
-Physical & Neurological assessments
-Rule out other causes
–Shingles (activated by herpes), headaches/migraines, TMJ
-Diagnosis can be difficult
-MRI – rule out tumor, check for nerve compression (check to see if something is there they can remove it)
-No test/lab - must rule out, check progression and S/S
trigeminal neuralgia - 5th cranial nerve
Eye, cheek, jaw
sensation effects it (trigger)
trigger sets off pain - can be above or below or side (depends what nerve it effects)
Treatment:
-Anticonvulsant medications – block nerve firing
-Tricyclic antidepressants – help treat pain
-Surgery:
–Rhizotomy – nerve fibers damaged to block pain (meant to kill nerve with probe/electrical currents - for syatic/low back pain)
—Balloon compression – pain relief only lasts 1-2 years (push blood supply away from nerve)
—Gylcerol injection (kills nerve root - med to damage nerve ending to stop sending signal)
-Depression/isolation
-Sleep disturbances
-Non-pharmacological methods
NM:
-Ways to manage the pain using non-pharmacological methods to avoid triggers
–Chew food on unaffected side
–Rinse mouth when using a toothbrush is too painful
–Limit touch to face when possible
–Eat room temperature food
–Extreme hot or cold can cause increased pain
trigeminal neuralgia - 5th cranial nerve
Declining rates- more than 50%
70% burn injuries are men on hands/mouth from electrical wires
Average size is 10% TBSA
½ of patients are treated at specialized centers- less hospitalizations to prevent infection and keep segregated from others
Classifications: causative agent, depth, severity
burns
Thermal (temp/direct heat)
-70% of injuries
-Can be flame, explosion, scald, steam, or heat transfer via object
Chemical
-Exposure to acids and alkali (bleach)
-Contact time is critical*
-Will continue to burn as long it’s on skin
*Wash/flush up to 3 hours (reversal agents can –> complications) *wash it
Electrical (current moves through you - entrance/exit)
-Type of current is important (alternating or direct)
-Low voltage common with electrical cords on hands and in mouths (especially children) - Concentrated at point of burn
-For high voltage, look for entrance and exit wounds, leathery appearance, muscle flexion/contractures (claw like)
causative agent classification for burn
Factors include: -Temperature of the agent -Duration of the exposure -Areas of body exposed Discussed in terms of superficial (1st), partial-thickness (2nd), full-thickness (3rd) Table 53-1, pg 1186
depth classification for burn
Epidermal layer only- minimal intervention needed
Painful, then itches
3-5 days of healing, no scarring
-Skin might not be broken, heals itself in 3-5 days, no scars, starts painful/sore but skin still blanches
Treat: aloe, ice, Tylenol/ibuprofen, or lidocaine with aloe
superficial burns (1st degree) in depth classification
Superficial vs deep
Superficial: epidermal and top of dermal layers (minimal intervention, 10-14 days healing)
-Blister (don’t squeeze it), heal itself in 10 days-2 weeks, tissue regenerates
-Treat: Neosporin, soap/water, ointment, voer it, non-adheasive, keep granulated tissue separate
Deep: all of epidermis, lots of dermis. Consider fluids, nutrition, comorbidities
Deep partial-thickness burns require surgery if size is significant
-higher risk for infection
-IND to cut out old/dirty tissue, skin graft or silvidene cream
-hydrate, nutrition, protein to help rebuilt tissue
partial thickness (2nd degree) in depth classification
