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363 Cards in this Set
- Front
- Back
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ALS
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Amyotrophic lateral sclerosis AKA Lou Gahrig’s Disease
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ALS Pathophysiology
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Rapidly Progressive neurodegenerative disease that attacks upper and lower motor neurons.
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What neurotransmitter do ALS pts have in excess? How is it harmful?
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Glutamate- it's toxicity is apparently due to Ca flooding the cell. Ca is supposed to briefly enter the neuron with each signal and triggers the cell to fire off its own signals and adjust its own activities accordingly. But prolonged Ca inside the cell evidently can do damage, and will even activate programmed cell death
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Is ALS slow or quick onset?
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Very quick progression and very short lifespan
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Major problems for ALS pts?
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No known cause, cure, specific treatment, standard pattern of progression, and no method of prevention.
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What is the suspected cause of ALS?
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Genetic (10%)- small gene mutation maybe overstimulation by glutamate→ cell injury degeneration (ALS patients have higher levels of glutamate)
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Age and gender ALS usually affects?
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ages 40-60
Men > women |
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ALS: what is the overall problem?
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Brain can no longer send impulses to muscles (therefore can no longer control muscle movement)
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Does ALS start as being widespread throughout the body?
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Starts in one area of body and spreads until entire body is involved
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Major clinical manifestations of ALS
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Atrophy → Progressive muscle weakness
Muscle wasting Spasticity → paralysis Fatigue Cramps Twitching especially of face (fasciculation) Less motor control in hands and arms Talk, swallow, and breathing affected (will eventually need to be put on a ventilator) |
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What are the biggest concerns for ALS pts?
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• Compromised respiratory
• Pneumonia |
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Does ALS cause death?
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Not from ALS itself, but death due to respiratory failure
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What is the avg lifespan for ALS pt?
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3-5 yrs d/t respiratory failure
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Are cognitive/intellictual functinos affected by ALS?
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No- Intellectual functioning remains intact! Worst part of this desease ☹ (Think Steven Hawkings)
May see cognitive changes in thinking and planning processes |
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Are the senses affected by ALS?
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No- Does not affect sight, sound, smell, taste, hearing
• Control of eyes, bladder, etc. will be lost |
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How to diagnose ALS?
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No Specific test to diagnose ALS (all tests are used only to rule out other diseases )
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Tests used to determine if pt has ALS?
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• Electromyelogram (EMG): Looks at fibrillations and muscle twitching
• Muscle Biopsy: Shows abnormalities • PFTs: To make sure no other respiratory problems are the cause of fatigue |
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Why do we want to diagnose ALS early on?
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The earlier it is diagnosed, the slower the disease progresses = can have longer lifespan (d/t lifestyle and environmental changes)
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Can ALS be treated to stop progressing>
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No- no matter what, the disease WILL progress
100% fatal |
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How to manage ALS?
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No specific treatment
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What is the only drug approved by the FDA to manage ALS?
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Rilutek
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What type of drug is Rilutek?
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glutamine antagonists
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What labs to monitor for pts on Rilutek?
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LFTs- drugs harsh on liver
AST/ALT |
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How long does Rilutek work for ALS pts?
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Only 2-3 months!
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What does Rilutek do for the ALS pt?
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slows progression and may prolong need to be trached- Does not relieve symptoms
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What other meds will ALS pts be Rx?
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Meds also prescribed for pain, fatigue, spasticity, excessive secretions, sleep disturbances, and other complications as they occur
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What nursing care for ALS pts?
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Support!
Patient may feel pain, depression, panic attacks, fear, etc. Pastoral care? Palliative/comfort care, refer to support groups, hospice programs, help w/ spasticity, help/advise about putting final affairs in order |
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What are some of the issues ALS pts and families will have to deal with?
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Adaptive devices to maintain independence
Alternative means of communication Consider mechanical ventilator (up to patient and family) Remember- No Cure |
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GB- Guillan Barre
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It is demylination/INFLAMMATION OF THE PERIPHERAL NERVES AFFECTS NODES OF RANVIER, SLOWS TRANSMISSION OF IMPULSES→progressive motor weakness and sensory abnormalities.
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How common is Guillan Barre?
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Rare!
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Does Guillan Barre affect more men or women?
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Men- esp middle aged
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Most common form of Guillan Barre?
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ASCENDING PARALYSIS,
LEGS UPWARD DTR (deep tendon reflexes)s, flaccid paralysis, paresthesias |
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Descending type of Guillan Barre affects...
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Starts in the jaw, tongue larynx- on its way down compromises respiratory function
Facial weakness, dysphagia, difficulty speaking, diplopia As it goes down cranial nerve 10 is affected- difficulty swallowing and BP drops d/t vagal, bradycardia, orthostatic BP, bottom out, arrhythmias, shock |
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IF GB STARTS TO AFFECT AUTONOMIC NERVOUS SYSTEM AND RESP. SYSTEM...
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MAJOR COMPLICATIONS AND EVENTUALLY RESP FAILURE→DEATH!!!!
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How does GB happen?
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Acute illness causes an autoimmune response that interferes with T-suppressor cell circuits. Causative antigen has similar cell markers as myelin. Body mistakes myelin for causative agent and attacks= invasion of spinal and cranial nerves.
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Three acute stages of GB
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Acute/Initial period
Plateau Recovery phase |
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What is the Acute/Initial period of GB?
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1-4 weeks- onset of symptoms (NUMBNESS AND TINGLING), PROGRESSIVE WEAKNESS) and ends when no further deterioration occurs
Can Cause complete paralysis If spread to Resp & ANS- pt in danger- on vent in ICU |
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Plateau phase of GB?
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Several days to 2 weeks- NO RECOVERY, NO FURTHER PROGRESSION OF DISEASE→ Most discouraging phase to patients- they need complete emotional support, and information from HCP they are very frustrated and need help in moving forward
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Recovery phase for GB
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4-6 months ,sometimes up to 2 years- HEALING OCCURS IN REVERSE ORDER (whatever was affected last heals first), CAN BE PAINFUL WHEN NERVES REMYELINATE, SOME PTS MAY HAVE RESIDUAL DEFICITS THAT NEVER HEAL.
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Cause of GB?
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NO actual known cause
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What are potential causes linked to GB?
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1. ACUTE ILLNESS
2. UPPER RESP INFECTIONS 3. TRAUMA 4. IMMUNIZATIONS 5. SURGERY 6. INFECTION→VIRAL EXPOSURE→EPSTEIN BARR (GET IT? GUILLAN BARRE) 7. SYSTEMIC LUPUS 8. UNDERCOOKED CHICKEN…NASTY. :/ |
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S/S of GB
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• DECREASED DEEP TENDON REFLEXES
• FLACCID PARALYSIS • TONE REMAINS INTACT • PARESTHESIAS • WEAKNESS • FATIGUE • FACIAL PARALYSIS • DYSPHAGIA • DIFFICULTY SPEAKING • DIPLOPLIA (DOUBLE VISION) • LABILE BP • CARDIAC ARRYTHMIAS • TACHYCARDIA • LOSS OF BOWEL AND BLADDER FUNCTION • ATAXIA |
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Most dangerous symptom of GB in severe cases?
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IN SEVERE CASES→RESP FAILURE→PNEUMONIA→DEATH!!!!!
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What test to diagnose GB?
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NO SINGLE DEFINITIVE TEST- tests are only used to rule out other diseases/disorders
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Tests to help diagnose GB?
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Lumbar puncture
Blood Studies EMG NCV Hx of viral illenss in past few weeks or immunization |
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If pt has GB, what will Lumbar Puncture show?
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Cerebral Spinal Fluid will have proteins (from inflammation)
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What will blood studies show if pt has GB?
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Leukocytosis (only in early phase of illness)
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What will EMG show if pt has GB?
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electromyelogram MEASURES THE MUSCLES ABILITY TO FIRE IMPULSES (ACTIVITY)- will be diminished
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What will NCV show if pt has GB?
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Nerve Conduction Velocity (MEASURES THE SPEED AT WHICH MUSCLES/NERVES CONDUCT AN IMPULSE) will be slowed
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What is the cure for GB?
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No known Cure
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What are treatments for GB?
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Plasmapharesis
IV Immunoglobulins |
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What is Plasmapharesis?
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Plasma Is Removed From Whole Blood, Antibodies That Circulate In Plasma Are Thus Removed, And The Pt Receives The Remaining Blood Cells. Done Several Days After Onset Of Symptoms. 3-4 Treatments 1-2days Apart
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How does Plasmapharesis work to help GB?
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Limits the amount of circulating antibodies that are attacking the myelin
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What nursing responsibilities for pts undergoing plasmapheresis?
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Support/Reassurance
Weigh The Pt Monitor Shunt (Patency, Bleeding, Obstructions Listen For The Bruits!!!!) Pt May Experience Bradycardia Because Of Loss Of Plasma |
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What do we give pt if they are experiencing bradycardia d/t loss of plasma?
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Atropine!
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Atropine
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atropine counters the "rest and digest" activity of all muscles and glands regulated by the PNS. This occurs because atropine is a competitive antagonist of the muscarinic acetylcholine receptors (acetylcholine being the main neurotransmitter used by the parasympathetic nervous system). Atropine dilates the pupils, increases HR, and reduces salivation and other secretions.
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Major A/E of plasmaphresis?
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1. Hypovolemia
2. Hypokalemia These both can lead to cardiac problems! |
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What is Iv Immunoglobulin therapy?
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Pt Is Treated With Immunoglobulins From A Pool Of Donors, When Given Can Lessen Attack On Nervous System
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Major A/E of Iv Immunoglobulin therapy?
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1. Chills
2. Fever 3. Headache 4. Myalgia |
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Interventions for GB?
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Monitor Resp status
Monitor for cardiac dysfunction Improve mobility Manage Pain Promote communication Nutrition Provide Support |
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What to give for hypotension (GB)?
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IVF
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What to give for Bradycardia (GB)?
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Atropine
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What to give for Hypertension (GB)?
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Beta Blockers (Nitroprusside)
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Hot to improve mobility (GB)?
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ROM exercises- active and passive, PT, OT, Assist w/ transfers, assistive devices, balance rest with activity
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How to manage pain (GB)?
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Opiates With A Pca Pump, Positioning, Deep Breathing, Distraction, Humor, Guided Imagery, Ice, Heat (Not Excessive!!!!!), Massage
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What is MS?
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Multiple Sclerosis is a chronic autoimmune disease that affects the myelin sheath and conduction pathway of the CNS. It’s one of the leading causes of neurological disability in persons 20-40yrs
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Cause of MS?
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Unknown- may have genetic predisposition and environmental factors (also geographic)
Viral- inflammation process could be a cause |
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MS is an ______ response that destroys the ___ ___ (______-)
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inflammatory
myelin sheath (demylination) |
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Pathway of MS-
___________--> _________--> ________--> interference of normal ______ _________ |
Inflammation --> Scarring --> plaques --> interference of normal nerve transmission
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MS is characterized by an ______ response that results in diffuse random or patchy areas of _____ in the white matter of the CNS. When this happens, the ____ ______ is damaged and its thickness is reduced (__________).
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inflammatory
plaque myelin sheath (demyelinated) |
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Myelin is responsible for...
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The electrochemical transmission of impulses between the brain and spinal cord and the rest of the body.
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Are impulses still transmitted in MS pts?
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Yes- but they are less effective
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What areas are most affected by MS?
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optic nerves, pyramidal tracts, posterior columns, brainstem nuclei and the periventricular regions of the brain
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4 types of MS?
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Relapsing Remitting (RRMS)
Primary Progressive (PPMS) Secondary progressive (SPMS) Progressive Relapsing (PRMS) |
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Relapsing Remitting (RRMS):
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MOST COMMON. periods of exacerbation and remission- clearly defined for about 4-5 yrs. The course of the disease may be mild or moderate, depending on the degree of disability. Symptoms may develop and resolve in a few weeks to months after which the patient returns to baseline.
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Primary Progressive (PPMS):
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continuous progressive worsening of mobility, balance, increased spasticity and pain involves a steady and gradual neurological deterioration without remission of symptoms. The patient has progressive disability with no acute attacks. Patients with this type of MS tend to be between 40-60yrs at onset of disease.
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Secondary progressive (SPMS):
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begins with relapsing-remitting course that later becomes steadily progressive. Functioning begins to decline with no clear times of remission
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Progressive Relapsing (PRMS):
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characterized by frequent relapse with some partial recovery but not a return to baseline. Progressive, cumulative symptoms and deterioration occur over several years.
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MS S/S
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Fatigue/weakness
Visual disturbances Cognitive changes Mental Health Spinal Cord dysfunctions |
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What type of visual disturbances with MS?
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Blind spots (holes in vision)
Blurred vision Diplopia (double vision) Decreased visual acuity Scotomas (change in peripheral vision) Nystagmus (involuntary, rapid eye movement) |
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What type of cognitive changes with MS?
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Intention tremor (tremor when performing an activity)
Cognitive changes usually seen late in the course of the disease: decreased short term memory, concentration, and ability to perform calculations; inattentiveness; and impaired judgment |
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What type of mental health issues with MS?
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• depression
• isolation |
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What type of Spinal Cord Changes/dysfunctions with MS?
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• Bowel and bladder dysfunction
• Constipation and INCONTINENCE • Sexual dysfunction • muscle spasms (SPASTICITY) • tingling/numbness • decreased motor coordination (ATAXIA) |
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What is important to teach the pt about any type of MS medication therapy?
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***medications that work well now may not work later, and medications that do not work now may work later- it is all trial and error***
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What is the acronym for MS medical treatment?
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A-B-C
Avonex, Betaserone, Copoxone |
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Avonex or Betaserone
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MS med- interferons (Very expensive)
FIGHTS VIRAL INFECTION and regulates the immune system -mechanism of action is very unclear but it does help to FIGHT RELAPSE of symptoms-every other day SQ inj fights viral infections and regulates the immune system |
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Copoxone
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MS med- a glutimer acetate
decreases relapse rate and progression of disease. Blocks immune system’s attack of myelin. |
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Baclofen
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for the muscle spasms (muscle relaxer) (MS)
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Baclofen Most Common A/E?
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Sedation
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Gabapentin (Neurontin)
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decreases spasticity (MS)
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What labs to monitor for pts on Gabapentin?
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monitor renal function tests (BUN, CR)
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MS- Overall goals of meds?
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increase self care ability with ADLs
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What drugs are useful to decrease spasticity?
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Baclofen and valium
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What type of history to assess for MS pts?
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relatives with MS?
type of symptoms? how long do they last? triggers? |
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What is a neurological exam used for in pts with MS?
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TO see the progressino of the disease and any cognitive changes
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What is and EMG used for in pts with MS?
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looks at neurological electrical activity and conduction through muscle stimulation
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What are the two gold tests for MS???
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MRI and VEP (Visual Evoke Potential)
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what type of MRI and what are they looking for in pts with MS?
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MRI of Brain w/ contrast- looking for plaque
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What is the Visual Evoke Potential (VEP) and why is it used to help diagnose MS?
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measures electrical activity of brain in response to visual sensory input (demyelination will slow conduction)- in MS it will be severely slowed
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What is the overall goal for MS pts?
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GOAL= ↑ independence and self-care with ADL’s
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What pt teaching for MS pts?
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Energy Banking
Diet Prevent exacerbations Make appts later in morning to allow time for mobility |
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What diet is helpful for MS pts?
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↓ simple carbs, saturated fats
use of mustard under tongue to decrease spasticity |
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What can MS pts do to help avoid exacerbations?
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Avoid:
Over exertion Stress- physical and emotional Heat intolerance Sick people (Immunosuppressants) Sudden body changes |
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What are the three Movement Disorders?
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Multiple Sclerosis
Parkinson's Disease ALS |
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What system is responsible for coarse control of voluntary muscles (And is affected in movement disorders?)
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The EPS- Extrapyramidal System
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What is Dopamine?
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A neurotransmitter that is produced in the Substantia Nigra (basal ganglia) and adrenal glands. DA sends info to parts of the brain that control movement and coordination
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What other neurotransmitter is important in smooth movement, and communicates with DA?
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ACh
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what type of disorder is Parkinson's?
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A movement disorder
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Is Parkinson's curable?
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No
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What are causes of Parkinson's?
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Causes are UNKNOWN, but genetics and exposure to PESTICIDES and other chemical agents are suspected to have a role.
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What happens at a cellular level Parkinson's Disease?
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here is Death of the neuron (substantia nigra cells) that produce dopamine
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The substantia nigra is responsible for
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the production of dopamine.
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Dopamine (DA) and Acetylcholine (Ach) work together to
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to initiate and control smooth purposeful movement.
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What happens to Dopamine and ACh in Parkinson's Disease?
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Because there is a decrease in Dopamine, and a normal level of ACh there is now an imbalance between the two. The imbalance causes increased GABA action (an inhibitory neurotransmitter) which decreases signal conduction which leads to the manifestations of the disease.
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What are the 4 CLASSIC manifestations/symptoms of Parkinson's Disease?
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1) Tremors at rest (tremors when not engaged in purposeful movement)
2) Muscle rigidity (stiffness) 3) Slow movement (shuffling) 4) Postural instability (stooped posture) |
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Do Classic symptoms occur more at rest or during purposeful movement?
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At rest, during purposeful movement symptoms subside
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What are other symptoms of Parkinson's disease?
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orthostatic hypotension, “mask-face”, may get dementia, excessive perspiration
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Is Ach increased in Parkinson's?
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No, it stays the same, but because DA is deceased, there is now an imbalance
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What happens when ACh and DA become unbalanced?
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Movement becomes jerky
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Why does the imbalance of DA and ACh cause this type of jerky movement?
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The UNOPPOSED Ach causes a stimulation of GABA, and DECREASES the CELLS ABILITY TO FIRE
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Is Parkinsons Progressive?
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Yes
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Is Parkinson's fatal?
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No, and life expectancy is not decreased
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What types of drugs are used to treat Parkinson's?
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dopaminergics, dopamine agonists, anticholinergics, and COMT inhibitor
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What Dopaminergics are used to treat Parkinson's?
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Carbidopa and Levodopa
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Why is carbidopa and levodopa given in combination?
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Levadopa is a precursor to dopamine. It can cross the BBB but only 2% makes it past the BBB to be converted to dopamine where it can do its work. Levadopa is deactivated by DDC and COMT (enzymes)
•Carbidopa inhibits DDC, which allows a greater 10% of the levodopa to reach the BBB, allowing for smaller amounts of Levadopa to be administered, which decreases the chances for adverse effects. |
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Why can't Dopamine be given for Parkinson's?
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It cannot cross the BBB
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What two enzymes in the body break down Levodopa?
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Dopamine decarboxylase (DDC) &
catechol-O-methyl transferase (COMT) |
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How does Carbidopa work to increase the amount of Levodopa available to cross the BBB?
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Carbidopa inhibits the DDC enzyme- stops it from breaking down the levodopa
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How long does the Carbidopa-Levodopa combo take to see effects?
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1-2 months, sometimes up to six months.
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Where is Carbidopa-Levodopa metabolized into Dopamine?
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In the periphery of the body
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What disease can Carbidopa-Levodopa activate (if the person is already genetically predisposed to?)
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Malignant melanoma
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What pts is the Carbidopa-Levodopa combo contraindicated in?
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In pts with undiagnosed pigmented lesions, hx of melanoma,
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What effect can carbidopa-levodopa have on pts with preexisting conditions?
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Anyone with past cardiac disease, pulmonary disease, Peptic ulcer disease and DM may have exacerbation of symptoms
Can also cause mental status changes in pts with mental health hx (Depression, SI) |
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Why is it a goal to get more levodopa to the BBB?
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So that we can give less medication to begin with and decrease the A/E
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What are A/E of carbidopa-Levodopa?
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GI upset- N/V/D, anorexia, wt loss, orthostatic hypotension
Abnormal movements |
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What is the most serious A/E of carbidopa-Levodopa?
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Neuroleptic malignant syndrome (AKA parkinsonian crisis)- happens when drug is STOPPED ABRUPTLY-extreme rigidity/tremors
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Simultaneous admin of Carbidopa-Levodopa with MAOIs can result in...
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hypertensive crisis- MAOIs should be D/Cd 2-4 weeks before start of therapy
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What effect does B6 (pyroxidine) have on Carbidopa-Levodopa?
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It increases levadopa destruction.
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What (7) foods contain B6?
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bananas, avocado, oatmeal, sunflower seeds, chicken, halibut
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What Drug interaction happens with Carbidopa-Levodopa and TCAs?
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delays absorption
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What happens when Hydantions (aka phenytoin- dilantin) are given with Carbidopa-Levodopa?
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decreases effectiveness of levadopa
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What is very important to assess before giving Carbidopa-Levodopa as drug therapy?
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Psych Hx
Malignant melanoma- skin lesions? Cardiac Hx |
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What diet to follow while on Carbidopa-Levodopa?
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High protein diet can slow or prevent absorption of carbidopa-levodopa- therefore need to take protein in high amts- eat equally throughout the day
•Take on an empty stomach, but take food 15-30 mins after to decrease GI distess. |
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Is Carbidopa-Levodopa less effective for certain races/ethnicities ?
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Yes- Due to increased COMT in Chinese, Filipino, and Thai populations, this drug is less effective for them.
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How long does Carbidopa-Levodopa work for?
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2-5 years, so they need to alert HCP when symptoms start to worsen so they can be switched to something else
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Should pts on Carbidopa-Levodopa reduce their dietary intake of Vit B6?
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No! They need to eat the foods high in B6 or take supplements because they still need that vitamin for the body. Plus, only Levodopa ALONE interacts with B6- not the combo drug because the carbidopa inhibits the action of B6
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If taking Levodopa alone should pts avoid foods high in Vit B6?
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Yes!
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What are surgical treatments for Parkinson's?
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Pallidotomy
Fetal-Cells- Stem Cell implantation (still in research) Beep Brain Stimulation |
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Pallidotomy
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Can be very effective for controlling Parkinson's Symptoms- go in and destroy brain tissue
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Beep Brain Stimulation
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Put a pacemaker into the brain to interfere with the part of brain causing tremors and to inactivate parts of the brain that causes theose symptoms without purposly destroying the brain like pallidotomy
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What are 2 major nursing responsibility with Parkinson's patients?
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Aspiration precautions and
Maintain movement- Keep pt. as mobile & independent as possible |
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What is Meningitis?
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Inflammation of the meninges- the tissue that surrounds the brain and the spinal cord
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What causes meningitis?
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Inflammation is caused by viral, bacterial, fungal, or protozoal infection
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How do organisms enter the brain/meninges?
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Organisms enter brain via BBB- opened connection between the CSF and the organism following a trauma injury, surgery, ruptured cerebral abscess, or other open entry
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When will we see exudate with meningitis?
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If infection is bacterial
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What is something that must be constantly monitored with meningitis?
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Increased ICP d/t blockage of CSF flow that results in a change in blood flow leading to increased ICP, hypoxia, and infarction (stroke)
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How common and severe is viral meningitis?
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It is the most common; it is self-limiting and can get better on it's own.
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How does one get viral meningitis?
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results from viral illness- measles, mumps, herpes simplex, zoster (shingles) virus
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Is there anything found in the CSF to diagnose meningitis when it is a viral infection?
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No
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Viral menigitis AKA
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Aseptic Meningitis
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S/S Viral meningitis
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fever, photophobia, HA, myalgias, nausea
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Treatment for viral meningitis?
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symptomatic cases treated only- usually with acyclovir
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How serious is bacterial meningitis?
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VERY SERIOUS- MEDICAL EMERGENCY
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When do we see a lot of bacterial meningitis cases coming into the hospital?
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Seasonal when upper resp. infections are common (colds)
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What are the common organisms that cause bacterial meningitis?
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Bacteria organisms that cause meningitis: Neisseria meningitides (most often), Streptococcus pneumoniae, H. influenza
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Outbreaks of Meningococcal meningitis occurs in areas of increased populations in...
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Close quarters ex: college dorms, military barracks
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What is the classic triad of symptoms that are associated with bacterial meningitis?
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Fever
Nuchal Rigidity Decreased LOC |
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What other S/S are associated with Bacterial Meningitis?
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Seizures
ICP → decreased LOC Brudzinski’s sign Kernig’s Sign |
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Brudzinski’s sign
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neck and hip flexion
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Kernig’s Sign
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SEVERE cases only, passive extension of the knee while hips are flexed
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What causes the ICP in bacterial meningitis?
|
exudate and abnormal stimulation of hypothalamic area
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If bacterial meningitis is left un-treated...
|
If left untreated → herniation of brain → DEATH
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|
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Infant S/S meningitis
|
“flu-like”, increased irritability, arching, decreased feeding, nuchal rigidity,
**can be hospitalized for up to 6 months, lose all motor skills- relearn how to walk, talk, eat, etc. |
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What will we see when assessing Pupil reaction & Eye movements in bacterial meningitis?
|
nystagmus, photophobia
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What cranial nerve responsible for pupil reaction and eye movement?
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Cranial nerves 2,3,4,6,
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What motor response will we see when assessing bacterial meningitis?
|
decreased muscle tone
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What cranial nerves are involved in progression to decreased muscle tone?
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Cranial nerves 3, 4, 6, 7, 8
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Will we see memory and behavioral changes with bacterial meningitis?
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Yes
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What type of HA with bacterial meningitis?
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Severe HA that will not go away
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What is the best way to diagnose bacterial meningitis?
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Analysis of CSF
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What will results of CSF analysis be if pt has bacterial meningitis?
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Appearance cloudy
High WBCs and High protein Low Glucose CSF pressure will be elevated |
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What will results of CSF analysis be if pt has viral meningitis?
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Appearance clear
High WBCs and slightly High protein normal or low Glucose CSF pressure varies |
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What is the VERY FIRST thing that is prescribed when bacterial meningitis is even suspected?
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Broad spectrum Antibiotic – 1st thing!!! prophylaxis
very important, patient can die during testing |
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What position should a pt be in after a LP?
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patient MUST lay flat for 8 hrs after procedure to avoid CSF leakage
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What nursing interventions for bacterial meningitis?
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• monitor VS
• FREQUENT neuro and vascular assessments- Q2Hr **change in neuro may indicate increased ICP- esp. LOC changes • reduce environmental stimuli • monitor peripheral pulses • medication management |
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What meds are prescribed for bacterial meningitis?
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antibiotics, steroids, hyperosmolor, anti epileptics (seizures d/t increased ICP)
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The increased ICP in bacterial meningitis increases the likelihood of what?
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seizures
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Encephalitis
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inflammation of the brain tissue itself and meninges
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What is encephalitis usually caused by?
|
Viral infection
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What is encephalitis patho?
|
inflammation of the brain tissue and meninges, usually caused by viral infection which causes inflammation which leads to the 2D’s ( neurological degeneration and demylination) where white matter can be destroyed, then swelling or edema occurs resulting in compression and increased ICP, herniation of the brain and ultimately DEATH
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Is encephalitis serious?
|
YES LIFE THREATENING-leads to neurological deficits, motor issues, learning disabilities, memory problems, and epilepsy
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**CLASSIC TRIAD of clinical manifestations of encephalitis**
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**FEVER, N/V, STIFF NECK **
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Other s/s encephalitis
|
change in mental status
neurological deficits motor dysfunction light and/or noise sensitivity fatigue |
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What changes in mental status come with encephalitis?
|
more severe change than meningitis- personality and behavioral
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What neurological defecits happen in encephalitis?
|
optic nerve paralysis, nystagmus, facial weakness
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optic nerve paralysis, nystagmus, facial weakness in encephalitis- what cranial nerves are involved?
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Cranial nerves 2, 4, 6
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What type of motor dysfunction comes with encephalitis?
|
difficulty swallowing
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What cranial nerve is affected if there is difficulty swallowing?
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Cranial nerve 10
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How to diagnose encephalitis?
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CSF specimen
Polymerase Chain Reaction (PCR) |
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What information will CSF give in the case of encephalitis?
|
obtained via lumbar puncture, determines specific infection organism
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What information will PCR give in the case of encephalitis?
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detects viral DNA/RNA chains in CSF
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What is the number 1 intervention for encephalitis?
|
Prompt recognition and treatment for increased ICP
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Other interventions for encephalitis?
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frequent VS including O2 sat and neuro checks – Q2Hr
HOB elevated between 35-45- not too high to reduce risk of increasing ICP darkened, quiet environment to reduce stimuli |
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What med to give to pts with encephalitis?
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antiviral medication therapy- acyclovir
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What to teach pts and family about encephalitis?
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family support and care- possibility of long term care: fall precautions, signs and symptoms of decreased LOC and mental status changes, aspiration, swallowing precautions, etc.
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What are the outcomes of encephalitis?
|
recovery VERY SLOW, may have full recovery or may have some permanent disabilities
Medical management is long term therapy |
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What is a seizure?
|
Abnormal, sudden, excessive, uncontrolled electrical discharge of neurons w/in brain
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What is epilepsy?
|
two or more seizures
Chronic disorder, repeated unprovoked seizures occur |
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What can be causes of epilepsy?
|
May be caused by:
An abnormality in electrical neuronal activity Imbalance of neurotransmitters (GABA) both |
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Triggers for seizures?
|
Increased physical exertion
Emotional stress Stimulants (caffeine) Fatigue Foods Chemicals Bright lights, strobes |
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Three broad categories of seizures
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1. Generalized seizures- both hemispheres
2. Partial seizures- one hemisphere 3. Unclassified seizures |
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Generalized Types of seizures affect which hemisphere?
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Affects Both Hemispheres
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4 types of generalized seizures
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Tonic Clonic (Grand Mal)
Absent Myoclonic Atonic |
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Tonic Clonic (Grand Mal) seizure
|
(generalized-both hemi)
Lasts 2-5 Mins Tonic Phase→Stiff, Rigid, LOC Clonic Phase→Jerky Uncontrolled Movements Post-Ictal→Resting Phase May Last Up To 2 Hours, Do Not Wake The Pt, Allow Them To Wake Up On Their Own! |
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What is the tonic phase?
|
Stiff, Rigid, LOC
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What is the clonic phase?
|
Jerky Uncontrolled Movements of extremities, biting down, sometimes incontinence
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What is the post-ictal phase?
|
Lethargy Phase after seizure. May Last Up To 2 Hours, Do Not Wake The Pt, Allow Them To Wake Up On Their Own!
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What sometimes happens right before a seizure?
|
Person will feel an aura or sensation that something is about to happen
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Absent (Petite Mal) seizure
|
Mostly Children
Day-Dreamers Short Seizure Activity Blank Stare Brief Loss Of Consciousness Automatisms→Lip Smacking, Picking At Clothing Abrupt Return To Baseline (generalized-both hemi) |
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Automatisms
|
Lip Smacking, Picking At Clothing
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Why does it sometimes take a long time for absent seizures to be diagnosed in children?
|
This can take a long time to be diagnosed because parents think their kids just dayderam, the longer it goes on the more and more it can happen and can start to interfere of their activities and daily lives
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What can happen if absent seizures are left untreated?
|
If Untreated May Result In Learning Disabilites And Problems In School
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|
Myoclonic seizures
|
(generalized-both hemi)
Short In Duration seconds to minutes Jerky/Stiff/Rigid Movements of extremities Unilateral and/or Bilateral (generalized-both hemi) |
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|
Atonic seizure
|
Rapid Loss Of Muscle Tone
Pt Loses Consciousness Post-ictal Confusion Upon Awakening (generalized-both hemi) |
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What is the biggest danger of atonic seizures?
|
Injury! They have falls
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Partial seizures affect how many hemispheres?
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1
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Are partial seizures common in adults or children?
|
adults
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Are partial seizures more responsive or less responsive to treatment?
|
Less responsive
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Types of partial seizures?
|
Complex Partial
Simple Partial |
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Complex Partial seizure
|
1-3 Minutes In Duration
Loss Of Consciousness Amnesia Afterwards Automatisms |
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Simple Partial Seizure
|
1-2 minutes (+ or-)
Aura beforehand Unilateral Movement Of Extremity Pt Is Conscious Weird Sensations- Metallic Taste, Pain, Offensive Smells Memory intact afterward |
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Standard Seizure precautions
|
Pad The Side Rails (Side Rails Up X 4)
Have O2 w/ face mask ready IV access Ready to go Suction ready to go Remove Restrictive Clothing |
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|
What to do for pt during seizure?
|
Do Not Restrict Their Movements
Turn Pt On Side Time The Seizure Notice Characteristics |
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|
What to do immediately after a seizure?
|
Supplemental O2 Via Mask, Not Nasal Cannula
Suction After The Pt Is Done Seizing |
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Why do we NOT put anything in persons mouth during a seizure?
|
Chipped Teeth→Airway Obstruction
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What to do with family during their loved ones seizure?
|
If Family Is Present→ Keep Them Busy With Helpful Jobs, “Hold My Pen”, “Please Time The Seizure”, “Sit And Relax, Talk To Your Family Member In Postictal Period”
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Status Epilepticus
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Seizure Activity Lasting Longer Than 5 Minutes Or Recurring Seizures Lasting Longer Than 30 Minutes
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Is Status Epilepticus serious?
|
Yes! This Is A Medical Emergency
Medications Are Required |
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|
What meds to give in status epileptics?
|
Benzos (Short Acting)
Dilantin Tegretal/Depakote |
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|
Meds used to treat seizures?
|
Dilantin
Benzos Tegretal Valporic Acid (Depakote/Depakene) |
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|
What is one of the oldest drugs used to treat seizures?
|
Dilantin
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Which seizures is Dilantin useful for?
|
Status epilepticus and tonic-clonic (grand mal)
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|
What drug classification is Dilantin (phenytoin)?
|
Anti-epileptic- HYDANTOINS "the toins"
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What is the action of Dilantin?
|
Controls seizures by reducing the amount of sodium influx into the cells. This causes decreased Depolarization and activity of the cells to fire
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How long does Dilantin take to take effect?
|
Long Half Life 7-10 Days To Trake Effect
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If Dilantin given PO...
|
TAKE WITH MEALS
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If Dilantin given NGT
|
Dilute
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If Dilantin given IV/IVP...
|
Give SLOWLY!!! Can Cause Cardiovascular Collapse!!!!! Give 50mg/Min
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What rate to give Dilantin IV/IVP?
|
50mg/Min
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What drugs does Dilantin interact with?
|
ETOH, Benzos, Ibuprofen
Barbiturates Acetaminophen |
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|
What is the effect if Dilantin interacts with ETOH, Benzos, Ibuprofen?
|
Inhibit The Metabolism Of Dilantin=Drug Toxicity
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What is the effect if Dilantin interacts with Barbiturates?
|
Inhibit Absorption Of Dilantin=Decreased Effects
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What is the effect if Dilantin interacts with Acetaminophen?
|
Accelerates The Metab Of Aceta. Causing Decreased Analgesic Effects Of Acetaminophen and more Aceta circulating so more liver damage potential
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Dilantin most common A/E?
|
Nausea, Dizziness, Blurred Vision, Ataxia
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Dilantin most SERIOUS A/E?
|
Cardiovascular Collapse
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Can Dilantin and Benzos be given in the same IV line?
|
No- they will precipitate
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|
What medications can be used to ABORT a seizure?
|
Dilantin
Benzos Tegretal Valporic Acid (Depakote/Depakene) |
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Examples of Benzos?
|
Valium/Ativan/Lorazepam
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How do Benzos work to stop seizures?
|
They increase the effect of the neuro-inhibitor GABA
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What is GABA?
|
inhibitory neurotransmittor that works in opposition to glutamate
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|
Benzos action
|
Keep Chloride Channels Open Longer→ Raises Cells Threshold To Fire→Produces Inhibitory Effect Decreasing Electrical Activity In The Brain
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|
In what case is Benzo the first choice when having to do with seizures?
|
In status epilepticus they are the first choice before any other seizure aborting drug
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Are the Benzos given over long periods of time for seizures?
|
No- they are on the BEERs criteris of meds to watch out for- they have a very high addictive rate, so only used short term
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What drugs to avoid when giving benzos?
|
Any other sedative drugs- ETOH and CNS depressants!
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What to closely monitor with Benzos?
|
ABGs
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A/E of benzos?
|
Cann
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How does Tegretal (Carbamazipine) work to control seizures?
|
Reduces Influx Of Na Ions, Thus Decreases Cells Ability To Fire
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What is important to monitor when ot taking Tegretal?
|
Monitor Blood Levels 2-4mcg/Ml,
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When is Tegretal used for seizures?
|
When other meds are ineffective
|
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How does Valporic Acid (Depakote/Depakene) work to reduce seizures? (Action)
|
Reduces Influx Of Na Ions, Thus Decreases Cells Ability To Fire
|
|
|
What is important to monitor for in pts taking Valporic Acid?
|
Monitor Blood Levels 50-150mcg/Ml, Monitor Liver (Hepatotoxic Alt, Ast) And Renal Function Tests)
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|
A/E of Valporic Acid?
|
Sedation, Dizziness, Agitation
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|
What should nurses teach pts that have seizures... a good way to document for complete hx?
|
Patients Should Keep A Seizure Diary (Characteristics, Triggers, Reactions To Meds)
|
|
|
If pts miss a dose of their seizure meds, can they double up the next time?
|
NO
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|
|
Should seizure pts wear anything special on a day to day basis?
|
Wear a medic alert bracelet
|
|
|
What is the antidote to Heparin (and should be on hand during dialysis?)
|
Protamine Sulfate
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|
|
MG
|
Myasthenia Gravis “Grave Muscle Weakness"
|
|
|
What type of disease?
|
chronic Autoimmune disorder that affects the Peripheral Nervous System.
|
|
|
What happens in Myasthenia gravis?
|
Skeletal/voluntary muscles cannot hold a contraction.
|
|
|
What happens at the cellular level in Myasthenia gravis?
|
• Normally ACh is the neurotransmitter that causes muscles to contract, Cholinesterase comes in to break down Ach in the synapse, causing muscles to contract.
• In the case of MG there is an autoantibody attack on the Ach receptors in muscle end plate membranes, limiting the number of receptors, and so those nerve impulses are not transmitted to the muscles. |
|
|
Causes of Myasthenia gravis?
|
o Over growth (hyperplasia) of the Thymus Gland
o Thymoma (encapsulated thymus gland tumor) o Strong relationship with hyperthyroidism |
|
|
Myasthenia gravis symptoms?
|
o Weakness and fatigue (esp. muscles that are innervated by cranial nerves, skeletal, and respiratory muscles)
o Ocular muscles affected- Ptosis (drooping eyelids- like Sleepy), diplopia- dbl vision o Bulbar involvement (muscles used for facial expression) o Chewing, swallowing, speech difficulty o Muscle weakness that increases w/ exertion and improves with rest |
|
|
What is a blood test looking for in Myasthenia Gravis?
|
To detect Ach receptor antibodies- will be increased
|
|
|
What pharmacology test is used to diagnose Myasthenia Gravis?
|
Tensilon Test (Challenge)-
|
|
|
Why is the Tensilon Test (Challenge)- used to help diagnose Myasthenia Gravis?
|
It is a Cholinesterase inhibitor and within minutes with will temporarily increase levels of ACh and relieve weakness- this tells us that there is a problem with ACh and it is MG
|
|
|
What is the antidote to Tensilon?
|
Atropine
|
|
|
What diagnostic tests are used to help diagnose MG?
|
EMG
CT PFT |
|
|
What will EMG tests show in cases of MG?
|
nerve conduction study which tests for specific muscle “fatigue” be repetitive nerve stimulation- shows muscles decreased response to repetitive stimulation
|
|
|
What will CT tests show in cases of MG?
|
Abnormal thymus gland- useful to identify if there is any thymus gland present or a thymoma
|
|
|
What will PFT tests show in cases of MG?
|
measure breathing strength- helps predict whether respiratory system may fail and lead to myasthenic crisis
|
|
|
What two Anticholinesterase/ cholinesterase hinibitor/ cholinergic agonist drugs are used to treat Myasthenia Gravis?
|
neostigmine (Prostigmin)
and pyridostigmine (Mestinon) |
|
|
What is the drug of choice for Mysathenia Gravis?
|
pyridostigmine (Mestinon)
|
|
|
Ho do the anticholinesterase drugs work to treat MG?
|
ONLY FOR SYMPTOMS
increases amount of Ach available at the receptor site- resulting in enhanced muscle contraction. |
|
|
Most common A/E of the Anticholinesterase drugs?
|
N/V/D, bradycardia, miosis, diaphoresis
|
|
|
Most serious A/E of the Anticholinesterase drugs?
|
cholinergic crisis
|
|
|
How to admin Anticholinesterase drugs?
|
PO- Admin with small amount of food to minimize GI effects- 45 min to 1 hr after taking med to prevent aspiration
|
|
|
What other drugs to avoid while pt is on Anticholinesterase drugs?
|
Mg, morphine, hypnotics, etc. should be avoided- they may increase pts weakness
|
|
|
What is the antidote to the Anticholinesterase drugs?
|
Atropine
|
|
|
How does the dosing of Pyridostigmine (Mestonin) work?
|
the dose depends on that say’s symptoms- like a sliding scale. Given PO. A/E and antidote same as Neostigmine
|
|
|
Why are Corticosteroid Meds given to treat Myasthenia Gravis?
|
• Used to induce remission
• Immunosuppression • Used if pt doesn’t respond well to Anticholinesterase drugs |
|
|
Why are Immunosuppression Meds (Imuran, Cytoxin) given to treat Myasthenia Gravis?
|
Used to induce remission
|
|
|
How do immunosuppression meds improve muscle strength in myasthenia gravis?
|
• Improves muscle strength by suppressing the production of abnormal antibodies
|
|
|
Major side effects of Immunosuppressant Meds (Imuran, Cytoxin)?
|
• Infection
• Leukocytosis (Low WBC count) • Liver Dysfunction (Monitor LFTs- AST/ALT) • Hair loss |
|
|
What medications are used to induce remission in Myasthenia Gravis?
|
Corticosteroids
and Immunosuppressants |
|
|
What medications are used to relieve symptoms in Myasthenia Gravis?
|
the anticholinesterase drugs
|
|
|
What surgeries have been helpful in treating myasthenia gravis?
|
Thymectomy
|
|
|
How does the Thymectomy help with Myasthenia Gravis?
|
removing the thymus in order to (hopefully) rebalance the immune system- takes about 2 year post op to be effective
|
|
|
What is important nursing care post op thymectomy?
|
• Post op- pay extra attention to pulmonary hygiene (suction PRN)
• Provide chest tube care • Sterile technique for wound care • Observe for s/s pneumothorax or hemothorax (Major Complications!) |
|
|
What are s/s pneumothorax or hemothorax?
|
• Chest pain, SOB, dim chest wall expansion, dim breath sounds, change in V/S
|
|
|
What to do if nurse suspects pneumothorax or hemothorax?
|
• Call surgeon STAT, Provide O2, raise HOB 45 degrees
|
|
|
How does plasmaphoresis helpin Myasthenia Gravis?
|
• Plasma taken out and replaced. Done to DECREASE the amount of Ach ANTIBODIES
|
|
|
How long does plasmaphoresis relieve Myasthenia Gravis symptoms?
|
only lasts a couple months if treatment done alone- that is why thymectomy is usually done after this
|
|
|
What is a Myasthenic Crisis
|
• Sudden worsening of symptoms
|
|
|
What causes a myasthenic crisis?
|
TOO LITTLE cholinesterase inhibitor drugs
|
|
|
S/S Myasthenic crisis?
|
• Increase HR, BP, absence of cough, swallow reflex absent or decreased
|
|
|
Nursing focus during myasthenic crisis?
|
• Treatment- focus on respiratory support. Most pts on mechanical vent
|
|
|
Do we give more cholinesterase drugs during myasthenic crisis?
|
• Even though this is due to too little cholinesterase drugs, we still do not want to increase drugs during crisis because it would cause an increase in secretions and the pt is already having respiratory problems.
|
|
|
What is a Cholinergic Crisis
|
• Acute exacerbation of symptoms
|
|
|
What causes a Cholinergic Crisis
|
TOO MUCH cholinesterase inhibitor drugs
|
|
|
S/S Cholinergic Crisis
|
• Increase in weakness, Twitching especially around the eyes, general facial weakness
• Inability to clear secretions, swallow, or breathe adequately |
|
|
Do we give more cholinesterase drugs during Cholinergic Crisis?
|
we do not want to increase drugs during crisis because it would cause an increase in secretions and the pt is already having respiratory problems.
|
|
|
What to do during a myasthenic or cholinergic crisis??
|
Do not give MG Drugs- Monitor Respiratory Status- Call DR, going to so the Tensilon Test
|
|
|
How to distinguish between myasthenic or cholinergic crisis
|
Tensilon Test
|
|
|
What will the Tessilon test show if it is myasthenic crisis?
|
a TEMPORARY IMPROVEMENT of symptoms in Myasthenic crisis
|
|
|
What will the Tessilon test show if it is Cholinergic crisis?
|
NO IMPROVEMENT of symptoms in Cholinergic Crisis
|
|
|
What nursing interventions if tensilon tests shows that it is myasthenic crisis?
|
• Monitor Resp status, mech vent possibly, drugs w/held, takes few days to recover
|
|
|
What nursing interventions if tensilon tests shows that it is cholinergic crisis?
|
• Give antidote- Atropine 1mg IV, repeat if necessary
• Monitor airway- secretions can thicken • Improves rapidly after antidote is given |
|
|
What is the overall goal for Myasthena Gravis?
|
Goal: Maintain muscle strength!
|
|
|
When should meds be given to Myasthenia Gravis pts?
|
Give meds before eating to prevent aspiration, but because some meds should be given with food to prevent GI upset, provide meal as soon as medication kicks in
|
|
|
When should myasthenia gravis pts expect peak activity?
|
peak activity in the morning- Weakness will increase throughout the day
|
|
|
Pt teaching for myasthenia gravis?
|
Teach that disease has exacerbations and remissions
Things that may cause exacerbation Take drugs at same time to maintain therapeutic level |
|
|
Things that may cause exacerbation of myasthenia gravis
|
fever, stress, infection, surgery, exercise, extreme heat/weather change, change in sleep habits (sedatives)- any sudden change in body
|
|
|
Is there a cure for MG... Can MG pts live long lives?
|
NO CURE FOR MG BUT LONG TERM REMISSION IS POSSIBLE, they can still live normal or near normal lives
|
|
|
What are the cranial nerve diseases?
|
Trigeminal
Bell’s Palsy |
|
|
What is Trigeminal Nerve Disease?
|
“tic douloureux”- PAINFUL TWITCH
Unilateral, sudden, intense facial spasms |
|
|
What facial nerve is affected in Trigeminal Nerve Disease?
|
affects Cranial Nerve 5- Trigeminal Nerve
|
|
|
What is the likely cause of trigeminal verve disease?
|
Cause is uncertain but most likely due to vascular compression.
|
|
|
Clinical Manfiestatios of Trigeminal Nerve Diasease
|
• unilateral sudden onset intense facial spasms
• sharp, shooting, piercing, burning pain |
|
|
What usually brings the onset of painful facial twitch?
|
provoked by stimulation at trigger zone
pt usually aware of what causes pain |
|
|
How long does the painful twitch last in Trigeminal nerve disease?
|
may go on for weeks to months- then no pain for a period of time
|
|
|
Trigeminal Nerve Disease- does it ever go away?
|
rarely does it go away forever
|
|
|
Medications to manage Trigeminal Nerve Disease?
|
Antiseizure Meds and
Pain Meds |
|
|
What antiseizure meds to help with Trigeminal Nerve Disease?
|
carbamazepine (Tegretol), phenytoin (Dilantin)
meds decrease nerve transmission TAKE WITH MEALS |
|
|
A/E of carbamazepine (Tegretol), phenytoin (Dilantin)
|
Adverse Effects: dizzy, drowsy
|
|
|
What types of pain medications are used for trigeminal nerve disease?
|
gabapentin ( Neurontin)
lidocaine- numbs pain calcitonin intranasal spray- temporary relief |
|
|
Are opioids effective for nerve pain?
|
No
|
|
|
How can Microvascular Decompression work to relieve trigeminal nerve disease?
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posterior craniotomy done microscopically
artery pressing is lifted to relieve pressure by use of a small prosthetic device |
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How can Radiofrequency Thermal Regulation work to relieve trigeminal nerve disease?
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small heat lesions made in nerve to stop conduction of pain; affected side will be permanently unresponsive to pain
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How can Balloon Microcompression work to relieve trigeminal nerve disease?
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balloon compresses the nerve root and vascular structures
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For balloon microcompression- what nursing int pre op
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no eating hot or cold foods or washing face with hot or cold water which can trigger pain
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For balloon microcompression- what nursing int post op
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CN ASSESMENT- ALL CRANIAL NERVES
ice pack to site – monitor closely d/t decreased sensations prevent chewing, rubbing eyes on affected side- can bite through tongue, can injure eye regular dental visits d/t absence of pain |
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What is Bell’s Palsy
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A Cranial Nerve Disease that causes Facial Paralysis
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How does Bells Palsy Manifest?
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unilateral paralysis of Cranial Nerve VII- Facial Nerve, can also affect Cranial Nerve V(Facial)
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Which cranial nerve is affected in Bells Palsy?
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7- facial Nerve (can also affect 5)
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Bells Palsy is caused by __________ which weakens or paralyzes facial muscles on affected side
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inflammation
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What can trigger Bells Palsy?
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inflammation process may be triggered by herpes simplex virus (HSV-1)
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Clinical Manifestations of Bells Palsy
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• pain: face, ear, eye
• quick onset of paralysis- full extent within 2-5days • distorted face- cannot move anything on affected side, increased tearing, speech and eating affected |
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Do pts ever recover from Bells Palsy?
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MOST recover completely with no residual effects
80% fully recover within a few weeks to months |
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What part of face is important to protect in cases of Bells Palsy?
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protection of eye- artificial tears, taped or shield at bedtime, goggles or sunglasses to protect from debris and sunburn
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What nsg interventions in regard to facial muscles for bells palsy?
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eat and drink on unaffected side to reduce injury- small meals are easier to tolerate
prevent facial muscle atrophy- massage, facila exercises facial exercises: wrinkling forehead, blowing out cheeks, whistling |
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Glasgow coma scale (GCS)
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tool used to help describe the patient’s level of consciousness. It has been shown to be very reliable for most patients
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What do the scores of Glasgow Come Scale mean?
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A score of 15 means the patient has normal neurologic function, where a score of 7 means the patient is comatose. The lower the score, the lower the patient’s level of consciousness.
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The GCS establishes baseline data in each of these areas (3):
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• Eye opening
• Motor response • Verbal response |
