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Patho II > Chronic Neuro diseases (Parkinson's, Seizure Disorder, MS, MG) > Flashcards

Chronic Neuro diseases (Parkinson's, Seizure Disorder, MS, MG) Flashcards

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1
Q

Parkinson’s: Description

A

Progressive, degenerative disorder of the dopamine secreting neurons that control muscle movement.

There is no cure; not fatal but death may result from complications.

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2
Q

Acetylcholine and Dopamine

A

Acetylcholine is excitatory/ Dopamine is inhibitory.
Parkinson’s is the depletion of dopamine,
therefore the depletion of inhibitory inputs.

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3
Q

Forms of Parkinson’s

A

Primary: idiopathic
Secondary: caused by trauma, infection, tumor, atherosclerosis, toxins
–some block dopamine receptors

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4
Q

Parkinson’s: Diagnosis

A

15% under 50, most 60s-70s.
No lab test for it- diagnosis is clinical.
CT and MRI needed to rule out other causes

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5
Q

Parkinson’s: Patho

A

(Normal: dopamine and acetylcholine secretion from basal ganglia are balanced)

1) Extrapyramidal brain nuclei deep in basal ganglia affected - this influences initiation, modulation, completion of movement
2) Degeneration of dopaminergic neurons => deficiency of dopamine (and excess of ACh) - leads to rigidity, tremors, bradykinesia
3) Dopamine deficiency prevents affected brain cells from performing their normal inhibitory fxn in the CNS

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6
Q

Parkinson’s: Classic Manifestations

A

1) Resting tremor: asymmetric, rhythmic, low amplitude
- unilateral (usually hands and feet)
- “pill rolling”
- Disappears during sleep; worse with stress/anxiety
- intermittent but progressively worsens
2) Bradykinesia: slowness of voluntary mvmt
- failure of antagonistic muscles to relax
- loss of walking, blinking, swallowing saliva
3) Rigidity: contraction of striated muscle
- stiffness of limbs, resistance to ROM
- uniform: lead pipe or cogwheel
4) postural dysfunction: shuffling gait, balance issues
- loss of reflexes mean easy falls
- Stooped posture, lean to one side when seated
- Festinating gait: short, accelerating steps

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7
Q

Parkinson’s: Other Manifestations

A
  • fine motor deficits
  • microphagia (small handwriting)
  • hypomimia (mask-like faces)
  • dysarthria/ monotone, high-pitch, low-vol voice
  • freezing/stuck when initiating movement
  • foot drag on affected side (?)
  • lack of arm swing on affected side (?)
  • hesitant/ ‘en bloc’ turns
  • increase in dandruff, ,seborrhea
  • less blinking => conjunctivitis, blepharospasm
  • drooling and dysphagia
  • autonomic dysfunciton
  • depression and anxiety
  • intelligence NOT affected, but some late stage dementia
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8
Q

Parkinson’s: Complication

A
  • various degrees of disability or difficulty performing ADLs
  • injury from falls
  • aspiration d/t difficulty swallowing/eating
  • UTIs
  • pressure ulcers
  • Dementia
  • Side effects of meds
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9
Q

Parkinson’s: Treatment (general)

A
  • Goal is to relieve symptoms and maintain function. Through Rx, surgery, PT (PROM, walking, baths, massage).
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10
Q

Parkinson’s: pharmacological treatment

A

Dopaminergic (Levodopa-Carbidopa)
- needs to be given inactively so it can cross BBB
Anticholinergics (Artane, Cogentin)
Other drugs (Eldpryl, Tasmar, Symmetrel)

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11
Q

Parkinson’s: surgical treatment

A
  1. Pallidotomy by stereotactic neurosurgery: obliteration of ventrolateral nucleus of thalamus & globus pallidus (to prevent involuntary movement)
  2. Fetal tissue transplants: transplanting cells from the basal ganglia or adrenal medulla of fetuses into caudate
  3. Deep brain stimulation: pacemaker-like brain implants to decrease tremors
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12
Q

Parkinson’s: nursing care

A
  • education
  • refer to support groups
  • exercise to maintain mobility and safety
  • assess chewing, swallowing, nutrition, depression
  • speech therapy for dysarthria
  • home safety
  • clothing choices
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13
Q

Epilepsy: Description

A

Condition of the brain characterized by susceptibility to recurrent seizures
- paroxysmal events associated w/ abnormal electrical discharges of the brain

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14
Q

Seizure Disorder: Causes

A 
-primary = idiopathic (50%)
secondary = structural changes or metabolic alteration increase automaticity 
- birth trauma
- perinatal infection
- anoxia
- infection
- toxins
- brain tumors
- PKU or TB
- head injury/trauma
- metabolic disorders
- CVA
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15
Q

Seizure Disorder: Diagnostics

A

Dx based on occurrence of 1+ seizures

  • CT or MRI to reveal sructural abnormalities
  • EEG: high fast voltage in tonic clonic
  • Skull XR to assess bony structures
  • Serum chemistries to eval metabolic conditions
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16
Q

Seizure Disorder: Patho

A
  • Epileptogenic focus: Neurons in the brain depolarize/ become hyperexcitable, fire more readily
  • RMP is less negative or inhibitory connections are missing d/t GABA activity or electrolyte shifts (lower threshold)
  • Epileptogenic focus fires, spreads electrical current to surrounding cells (fire with greater amplitude)
  • Impulse cascades to 1 side of the brain (partial seizure) or both sides (generalized seizure) OR in the cortical, subcortical, and brain stem areas
  • Incr. met demand for O2 & nutrients (200%): if not met, brain damage
  • Firing of inhibitory neurons causes the excitatory neurons to slow firing & eventually stop
  • If action doesn’t occur, status epilepticus without Tx anoxia is fatal
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17
Q

Seizure Disorder: Manifestations

A
  • Recurrent seizures
  • Aura/ Prodrome - a sensory sign that a seizure is imminent
  • After generalized seizure (postictal state):
    • slow return to consciousness
    • combative or lethargic
    • confusion, headache, fatigue
    • loss of bladder/ bowel fxn
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18
Q

Simple Partial seizure (Jacksonian)

A

Begins locally, doesn’t cause change in consciousness

  • sensory Sx: flashing lights, smells, auditory hallucinations
  • autonomic sx: sweating, flushing, pupil dilation
  • psychic sc: dream states, anger, fear
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19
Q

Complex partial seizure

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A
  • alters consciousness
  • amnesia for events during and after seizure
  • patient may be able to respond to some commands during
  • 1-3 min avg
20
Q

Absence seizure (generalized)

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A

“petit mal”

brief change in LOC, lasts 1-10sec

21
Q

Myoclonic seizure (generalized)

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A
  • bilateral epileptic myoclonus
  • may be rhythmic
  • brief involuntary muscle jerks
  • consciousness often intact
22
Q

Tonic-Clonic seizures (generalized)

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A

grand mal

  • begins with loud cry
  • loss of consciousness
  • body falls, spasms (tonic), relaxes (clonic)
  • usually 2-5 min
23
Q

Atonic seizures (generalized)

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A

Drop seizure/ drop attack

  • loss of postural tone
  • temporary loss of consciousness
24
Q

Status Epilepticus

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A
  • medical emergency*
  • continuous seizure state
  • can occur in all seizure types, but tonic-clonic most dangerous
  • accompanied by resp distress, can lead to hypoxia/anoxia (which can lead to brain damage)

May be due to

  • anticonvulsant Rx withdrawal
  • hypoxic or metabolic encephalopathy
  • head trauma
  • septicemia d/t encephalitis/meningitis
25
Unclassified seizures
Don't fit characteristics of any partial, generalized, or status epi seizures
26
Seizure disorder: complications
- hypoxic brain damage - mental development changes - depression or anxiety - social isolation
27
Seizure disorder: treatment
- ID type (note time, activity) - reverse cause if possible - Pharm care based on seizure type - vagal nerve stimulators - counseling Surgeries (can have more effects...) - resective to excise epileptogenic focus - corpus collostomy removes connections b/t hemis
28
Seizure disorder: nursing care during
- protect from injury (move obstacles, protect head) - place on ground, side lying - maintain airway - apply oxygen, monitor response (don't hold down or put shit in their mouths my god!!!)
29
Seizure disorder: nursing care after
- administer anticonvulsants - monitor therapeutic lvls of meds - educate about precipitating factors
30
Pediatric febrile seizures
Likely arises from fever effects on the developing brain - b/t 3mo and 6y/o - w/ fevers >100.4 - lasts a few seconds to a few minutes * call 911 if it lasts more than 15 min or breathing difficulty - often outgrow before age 5
31
Multiple Sclerosis: Description
Demyelination of white matter in brain/SC. Damages nerves and their targets affects central nerves (Guillain Barre peripheral nerves) *thought to be auto-immune Age: avg 27 (b/t 20-40 onset sxs) Sex: Females 3x more likely Place: northern areas
32
Multiple Sclerosis: Syndromes
1) corticospinal: (cross at medulla obl) - symmetric muscle weakness/stiffness. - spastic paralysis, bowel/bladder incontinence 2) Brain stem (where cranial nerves exit) - dysfxn of CN III - CN XII => - nystagmus, ophthalmoplegia, dysarthria, ptosis, paresthesia 3) Cerebellar: spastic gait, ataxia, intention tremors, hypotonia 4) Cerebral - optic neuritis (clouding), impaired vision, intellectual and emotional deterioration
33
Multiple Sclerosis: Types (patterns over time)
1) Relapsing-remitting (25%): clear attacks w/ full or partial recovery to baseline. Disease does not worsen (much) with attacks) 2) Primary progressive (uncommon, 15%): steady progression with minor recovery or plateaus 3) Secondary progressive: begins w/ relapses and recovery, disability steadily progressive - worsens between attacks 4) progressive relapsing (rare): steadily progressive from the onset but w/ acute attacks
34
Multiple Sclerosis: Causes
- unknown but thought to be autoimmune - theory: slow acting or latent viral infection stim autoimmune response - genetics + environment - trauma, toxins, nutritional deficiencies
35
Multiple Sclerosis: Diagnosis
- evidence of 2+ neuro attacks - periodic testing and close observation - MRI shows white matter lesions - EEG abnormalities (1/3 of patients) - LP: nL CSF protein but high CSF IgG - CSF electrophoresis shows kappa light chains - EPs show slowed nerve impulses
36
Multiple Sclerosis: Patho
- Sporadic plaques (demyelination) of axons and nerve fiber loss through CNS. - can be destruction of axon w/ subsequent destruction of myelin (no fxn) - OR destruction of myelin leading to slow transmission - slowed impulses = alterations in movemvent, reflexes, change in mental status - Swelling & edema => further injury to neurons and dvlpmnt of scar tissue plaques
37
Multiple Sclerosis: Manifestations
* depends on extent and location of destruction, extent of remyelination, adequacy of restored synapse transmission* - Ocular disturbances: optic neuritis, diplopia, opthalmoplegia, blurred vision, nystagmus, scotoma - Sensory impairment: burning, pins & needles, electrical sensations - Muscle dysfunction: weakness, paralysis (monoplegia to quadriplegia), spasticity, hyperreflexia, intention tremor, gait ataxia - Urinary disturbances: incontinence, frequency, urgency, frequent infections - Bowel disturbances: involuntary evacuation or constipation - Fatigue: often the MOST debilitating Sx - Speech problems: poorly articulated and dysphagia Sx’s precipitated by stress and sometimes heat
38
MS: Secondary complications
``` Injuries from falls Urinary tract infection Constipation Joint contractures Pressure ulcers Rectal distention (can't evacuate) Pneumonia (hard to clear lungs w/o innervation) Insomnia ```
39
MS: tertiary complications
Depression – role changes & loss of independence Loss of social support – social isolation Family/spousal stress – divorce Financial problems - unemployment
40
MS: Treatment
GOALS: Treat acute exacerbations Treat disease process Treat related s/s PHARMA - Aggressive immunosuppressant therapy at the start of the disease & with any exacerbation - Antiviral drugs may slow progression of the disease - SQ immune substance interferon beta lowers # & severity of exacerbations - Innovative therapies to foster antigenic self-tolerance ED Bladder training, sexual functioning, avoidance of complications, avoidance of fatigue/stress
41
Myasthenia Gravis: Description
"Grave Muscular Weakness" A disorder of transmission at the neuromuscular jxn peak = 20-30y/o (women) or later in life (men)
42
Myasthenia Gravis: Patho
Autoimmune: antibody mediated destruction of ACh receptors in NMJ - accompanied by thymic abnormalities (75%): thymoma, thymomic hyperplasia - characterized by fluctuating weakness of muscle groups
43
Myasthenia Gravis: manifestations
Often starts as ocular weakness => general weakness extremity weakness greater proximally, not distally Symptoms quietest in the AM, worse with effort - ptosis and blurred/dbl vision (extraocular muscles) - arm and leg weakness - difficulty breathing - chewing and swallowing diff - slurred speech (face muscles) - chronic muscle fatigue
44
Myasthenia Gravis: crisis
A sudden exacerbations - affects respiratory muscles (may need ventilator) - occurs during stress - may be d/t dysregulation of drugs used to treat
45
Myasthenia Gravis: Diagnosis
- Hx and physical exam - Anticholinesterase test - Nerve and muscle stim studies - test for Ach receptor antibodies
46
Myasthenia Gravis: treatment
MEDS: - anticholinesterase drugs - immunosuppressants - corticosteroids for poor response Plasmapheresis to removie ABs - w/ immunosuppressants IV immunoglobulins (can be improvement but weeks to months) Thymectomy -- could have neg effect

Patho II (12 decks)

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