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NUR 406 > Neuro A&P, migraines, PD, MG, MS > Flashcards

Neuro A&P, migraines, PD, MG, MS Flashcards

1
Q

Explain the diagnostic requirements for migraine

A

2 features must occur: Unilateral head pain, throbbing pain, worsens with activity, moderate/severe pain.
& one of these: N/V, Photophobia, phonophobia.

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2
Q

photophobia

A

avoidance of light

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3
Q

phonophobia

A

avoidance of sound

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4
Q

Define the classifications of migraine

A

Aura present (visual, sensory, or motor)
Aura not present (most common)
Chronic: 15 days/month for 3 months

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5
Q

risk factors for developing a migraine

A

Family history
Estrogen and progesterone
Genetic and environmental factors

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6
Q

Triggers for migraines

A

Fatigue
Sleep Disturbance: too much or too little
Missed meals
Overexertion
Weather change
Stress
Hormonal changes
Alcohol: red wine
Bright lights or strong smells

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7
Q

Pathophysiology for migraines

A

Change in neurotransmitter levels in CNS.
Blood vessel tone.

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8
Q

what are the clinical phases of a migraine?

A

premonitory phase
migraine aura
headache phase
recovery phase

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9
Q

describe the premonitory phase

A

Hours to days before the onset of the aura or the headache.
1/3 have fatigue, irritability, loss of concentration, stiff neck, food cravings.

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10
Q

describe the migraine aura

A

Up to 1/3 have aura symptoms lasting up to 1 hr.

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11
Q

describe the headache phase

A

Throbbing pain: begins on one side then spreads to the entire head.
Fatigue, N/V, dizziness, hypersensitivity to touch on head.
Last 4 to 72 hrs.

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12
Q

describe the recovery phase

A

Irritability, fatigue, or depression.
Can linger for hours to days

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13
Q

Abortive (Symptomatic) Therapy

A

Aspirin-like drugs: ASA, acetaminophen, NSAIDs.
Serotonin1B/1D Receptor Agonists: sumatriptan (Imitrex).
Calcitonin Gene-related Peptide (CGRP) Antagonist: rimegepant (Nurtec).

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14
Q

sumatriptan

A

Class: Serotonin1B/1D Receptor Agonists
MOA: Constrict intracranial blood vessels, Suppress release of inflammatory neuropeptides, Block brain pathways for pain
indication: migraines
Route: Sub-q, PO, intranasal
SE: injection site reaction (SQ), chest pressure, flushing, weakness, headache, bad taste (nasal)
Considerations: avoid with ischemic stroke or heart disease, and angina

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15
Q

rimegepant

A

Class: Calcitonin Gene-related Peptide (CGRP) Antagonist
MOA: Mediates pain transmission
indication: migraines
Route: PO
SE: GI upset
Considerations: CYP substrate

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16
Q

preventative therapy for migraines

A

Beta-blockers: Propranolol (Inderal)
Tricyclic antidepressants: amitriptyline
Antiepileptic drugs: divalproex (Depakote), topiramate (Topamax)
Estrogens: Menstrual migraine

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17
Q

migraines: Preventative Therapy Goals

A

Reduce attack frequency, severity, and duration.
Improve responsiveness to treatment of acute attacks.
Improve function and reduce disability.
Prevent progression or transformation of episodic migraine to chronic migraine.

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18
Q

Discuss the basic organization of the nervous system.

A

A highly specialized system responsible for control and integration of the body’s activities.
Can be divided into the central nervous system (CNS) and the peripheral nervous system (PNS)

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19
Q

the CNS

A

consists of the brain and spinal cord.
Ascending tracts carry sensory information from the periphery, muscles, and organs to the higher levels of the CNS.
Descending tracts carry impulses from the brain and result in voluntary muscle movement.

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20
Q

the PNS

A

consists of the cranial/spinal nerves and the autonomic nervous system

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21
Q

Neurons

A

the primary functional unit of the nervous system.
Neurons (in general) do not divide or replace themselves.
However, some new neurons may generate from stem cells after a brain injury.

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22
Q

Neuroglial cells

A

more numerous and are supportive to the neuron.
can replicate. provide support, nourishment, and protection to neurons.
They make up almost half the brain and spinal cord and are 5-10x more numerous than neurons.
Different types of glial cells have different functions.

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23
Q

Define the 4 main parts of a neuron:

A

the cell body: the metabolic center of the neuron.
axon: extend varying distances from the cell body and carry nerve impulses. They can be myelinated or unmyelinated.
dendrites: short extensions from the body that receive and conduct nerve impulses.
myelin sheath: a white lipid substance that insulates and helps conduct the impulses.

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24
Q

Describe the 3 types of neuroglia

A

Oligodendrocytes: produce the myelin sheath for nerve fibers in the CNS and help make up the “white matter” of the brain.
Schwann cells: myelinate the nerve fibers in the periphery.
Astrocytes: provide structural support to neurons and form the blood-brain barrier. They are found in the “gray matter” of the brain.

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25
Q

Describe how a nerve impulse travels from neuron to neuron.

A

The initiation of a nerve impulse involves the generation of an action potential.
After the action potential is initiated, a series of action potentials travel along the axon.
When it reaches the end of the nerve fiber, it is transmitted across the junction (gap) between nerve cells by neurotransmitters.

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26
Q

neurotransmitter

A

a chemical agent involved in the transmission of an impulse across this junction

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27
Q

Examples of neurotransmitters

A

acetylcholine, epinephrine, norepinephrine, serotonin, and dopamine

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28
Q

Define Parkinson’s disease

A

a progressive, degenerative disorder of the basal ganglia function

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29
Q

PD is Characterized by…

A

rest tremors, rigidity, & bradykinesia

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30
Q

PD: Primary

A

Idiopathic = Parkinson’s disease, genetic or sporadic.

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31
Q

PD: secondary

A

Acquired= infection, intoxication, trauma, drug-induced

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32
Q

PD: risk factors

A

age (after 50, peaks at 70, average onset 60), gender: men, genetics: both dominant & recessive, environmental exposures, depression, head trauma, hysterectomy, coffee consumption (protective)

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33
Q

PD: Pathogenesis

A

-Destruction of substania nigra in basal ganglia
-Dopamine levels decrease
-Imbalance between dopamine & ACH
-excess of ACH
-Loss of controlled movement & balance

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34
Q

why is the substantia nigra significant?

A

has cells that produce dopamine

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35
Q

how does the basal ganglia work in PD?

A

the basal ganglia works with the cerebellum to make smooth, coordinated movement.

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36
Q

dopamine

A

Inhibitory neurotransmitter
Function = message transmission
Controls movement and balance
Helps muscles work smoothly, controllably, and without unwanted movement

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37
Q

Acetylcholine (ACh)

A

Excitatory neurotransmitter
Works in conjunction with dopamine system
Balance is CRUCIAL!!
Works best when in balance with dopamine

38
Q

PD: Manifestations

A

Bradykinesia (slowness of movement)
Cogwheel rigidity (stiff muscles)
Resting tremor (pill rolling tremor)
Shuffling gait
Mask-like expression
Postural instability

39
Q

classic triad of PD

A

Tremors (@ rest)
Rigidity
bradykinesia

40
Q

PD: onset?

A

gradual onset and progression

41
Q

true or false: PD involves both sides of the body at first

A

FALSE. it may only involve 1 side of the body at first.

42
Q

tremor

A

Often the first sign
Handwriting effected
More prominent at rest
Aggravated by stress or concentration
“Pill roll”

43
Q

Essential tremor

A

results from faulty neurological impulses
Tremors occur with motor function
No other manifestations of Parkinson’s Disease

44
Q

Parkinsons tremor

A

Results from dopamine deficiency
Tremors occur with rest and improve with movement
Presents with other manifestations of Parkinson’s disease

45
Q

rigidity

A

Defined = resistance to passive movement
“Cogwheel rigidity”: Movements are jerky and slow
Associated complaints: Muscle soreness, aches, pain

46
Q

PD: Why does rigidity happen?

A

Sustained muscle contraction
Too much ACh in comparison to dopamine

47
Q

Bradykinesia

A

Defined = Loss of automatic movements
No blinking
No swinging of arms
No swallowing of saliva = DROOLING
No self-expression with hands and face = Flat expression
Overall lack of spontaneous movement

48
Q

PD: Complications

A

Dementia (40%)
Sleep disturbances
Fatigue
Depression/anxiety
Decreased mobility: malnutrition, aspiration, pneumonia, UTI’s, skin breakdown
Drug related complication

49
Q

Treatment goal for PD

A

to help individuals to maintain motor function

50
Q

How does the pharmacology work for PD?

A

by correcting the imbalance between dopamine & ACh.
Drugs either ENHANCE dopamine or BLOCK the effects of ACH

51
Q

Levodopa/Carbidopa (sinemet)

A

MOA: Levodopa= converts to dopamine in the brain & activates dopamine receptors; Carbidopa= blocks destruction of levodopa
Advantages: most effective drug for PD
Disadvantages: takes several months to see improvement, does not work long-term, adverse effects.
SE: SE d/t levodopa, N/V- give low dose with food (not protein rich foods), BUT this reduces drug absorption, Dyskinesias- range from annoying to disabling, CV- postural hypotension, dysrhythmias, Psychosis- hallucinations, nightmares, paranoia, Darken sweat & urine, active malignant melanoma.
Drug interactions: decreases effects of Levodopa- vitamin B6 (pyridoxine), antipsychotics, protein. Increases effects of levodopa- carbidopa, anticholinergics, MOA inhibitors (can cause toxicity).

52
Q

sinemet: “loss of effects”

A

Gradual loss of drug effect
* Dose wears off
* May need shorter dose intervals
Abrupt loss of effect
* Called the “on-off” phenomenon
* Can occur anytime during dosing interval
* “Off” periods increase overtime
* Can be reduced with drugs and avoiding high-protein meals

53
Q

Duopa

A

Carbidopa-levodopa infusion
instilled via feeding tube into small intestine
Gel form (suspension)
Continuous infusion for continuous blood level: Up to 16 hours per day.
Patients who respond to drug but response fluctuates

SE: Falling asleep w/o warning, orthostatic hypotension, hallucinations (visual, auditory, tactile), unusual urges, depression, dyskinesia. Also has SE r/t placement of tube
Drug interactions: Do not take within 2 weeks of nonselective MAOI, for depression.

54
Q

Pramipexole (Mirapex)

A

Class: Dopamine receptor agonist
MOA: binds with D2 receptors
Indication: Monotherapy in early PD. Combined with Sinemet in advanced PD. Restless leg syndrome.
SE: Nausea, sleep attacks, pathologic gambling & other compulsive behaviors.
SE In combo w/ Levodopa: orthostatic hypotension, dyskinesias, hallucinations risk doubles.

55
Q

ropinirole (Requip)

A

Class: Dopamine receptor agonist
Indication: idiopathic PD
MOA: Unknown but thought to cause an increase in nerve impulses w/in the substantia nigra.
SE: similar to other PD drugs; Long term: increased risk of DM & acromegaly.

56
Q

Describe why Levodopa and Carbidopa are given together.

A

o Carbidopa prolongs the effects of levodopa

57
Q

MS: definition

A

Chronic, inflammatory autoimmune disorder
Potentially disabling disease
Brain and Spinal cord: White and gray matter

58
Q

MS: characteristics

A

Inflammation
Demyelination
Scar development (Gliosis)

59
Q

MS: risk factors

A

Age: 20-40
Gender: Women
Location: Moderately cool climate (Northern US)
Race: Caucasian
Genetics: Family history

60
Q

MS: possible RF

A

Smoking
Vitamin D deficiency
Obesity
Infection: Including Epstein-Barr

61
Q

MS: etiology

A

unknown, autoimmune may be triggered by infection, genetic predisposition.

62
Q

MS: pathogenesis

A

Consists of an autoimmune attack against the myelin sheath
T lymphocytes migrate to the CNS and cross the blood-brain barrier
Antigen-antibody reaction inCNS initiates an inflammatory response
Axons are de-myelinated and plaques/sclerosis forms
Axons are destroyed

63
Q

how are the Neurons affected by MS in early disease?

A

Nerve fiber not affected
Impulses still transmitted
May notice weakness

64
Q

how are the Neurons affected by MS later on in disease?

A

Axons are destroyed
Impulses are totally blocked
Permanent loss of function

65
Q

Describe the different types of progression of MS

A

Benign: after exacerbation they go back to baseline, no loss of function
Relapsing-remitting= RRMS: 80-90%, stable between exacerbation, returns a little weaker than baseline.
Primary-progressive= PPMS: gradual progression w/o attacks
Secondary-progressive= SPMS: initial relapsing/exacerbation followed by remission with some loss of function with each exacerbation
Progressive-relapsing= PRMS: gradual progression of symptoms, fewer remission.

66
Q

MS: CM

A

Cognitive problems: Cog Fog
Vision problems
Depression
Fatigue
Pain: Chronic or acute, Burning or stabbing
Bowel/bladder
Weakness: Including paralysis
Sexual issues
Muscle stiffness/spasm: Numbness/tingling
Walking/balance: Vertigo

67
Q

Is there a cure for MS?

A

NO

68
Q

MS: goals of therapy

A

Slow disability
Reduce frequency of relapses
Reduce new brain lesions

69
Q

what are the drugs for MS used for?

A

Modify the disease process
Treat an acute relapse
Manage symptoms

70
Q

Avonex

A

class: interferon beta-1a/b
MOA: Inhibit pro-inflammatory WBCs from crossing BBB
SE: Flu-like reactions, Liver toxicity, Bone marrow suppression, Depression, Drug interactions
Naturally occurring substance
Decrease relapse rate by up to 30%
Route: injectable

71
Q

Copaxone

A

class: glatiramer acetate
MOA: Increased production of anti-inflammatory T cells which cross the BBB and suppress inflammation
Similar efficacy
SE: Injection site reactions; Post-injection reactions-Flushing, palpitations, chest pain, rash, laryngeal constriction, Lasts 15 – 20 minutes, Treatment not necessary.

72
Q

fingolimod(Gilenya)

A

MOA: Retain lymphocytes in the lymph nodes, preventing them from crossing the BBB – decreasing inflammation
Indication: RRMS
route: PO

73
Q

dimethyl fumarate (Tecfidera® )

A

Developed specifically for MS
Thought to inhibit immune cells and may have anti-oxidant properties.
Route: PO

74
Q

natalizumab (Tysabri)

A

MOA: Prevents circulating T cells from leaving the vasculature and crossing BBB
Therapeutic uses: Multiple sclerosis (reduce relapse by 68%) and Crohn’s disease
Monotherapy only: Not used with any other agent, Relapsing form of MS.
Route: infusion
SE: Most common = Headache, fatigue, Progressive Multifocal Leukoencephalopathy (PML), Hepatotoxicity, Hypersensitivity.

75
Q

alemtuzumab (Lemtrada)

A

Reserved for patients with poor response to 2 or more MS medications

76
Q

mitoxantrone (Novantrone)

A

Secondary progressive
Progressive-relapsing
Worsening RRMS: Without complete remission

77
Q

MS: treating an acute relapse

A

Preferred treatment: High-dose IV glucocorticoid, Frequent use or long-term use should be avoided.
Another option = IV gamma globulin: Used for patients intolerant to glucocorticoids.
ACTH (H.P. Acthar Gel): Adrenocorticotropin hormone in gel form, Prolonged release of ACTH after injection, Unable to tolerate steroids or they have not been effective.

78
Q

meds to manage MS symptoms

A

Urinary frequency/retention- anticholinergics, cholinergic.
Constipation- bulk-forming laxatives
Fatigue- Amantadine (Symmetrel)
Muscle spasms- muscle relaxants
Cognitive dysfunction- donepezil (Aricept)

79
Q

what is Myasthenia Gravis?

A

An autoimmune disease.
Characterized by fluctuating weakness of certain muscle groups.
Course of the disease is variable: Short-term remission, Stabilization, Severe, progression

80
Q

MG: RF

A

Age: 10-65 yrs
Gender: Women

81
Q

MG: Etiology

A

Same as every other autoimmune disease!
genetic
environmental trigger

82
Q

MG: pathogenesis

A

Antibodies attack ACh receptors: AKA “anti-AChR antibodies”
Decrease in ACh receptor sites at the neuromuscular junction
This prevents ACh molecules from attaching and stimulating muscle contraction

83
Q

MG: manifestations

A

Fluctuating weakness of skeletal muscle
Strength comes back after resting
Muscles involved? Eyes/eyelids, Facial, Speaking, Breathing

84
Q

myasthenic crisis

A

Acute exacerbation of muscle weakness
Triggered by a stressor: Infection, Surgery, Emotional distress, Pregnancy/menses, Inadequate pharmacotherapy or other drugs.
Major complication? Breathing muscle weakness
Not enough stimulation or acetylcholine
Muscles are not stimulated and weak
Leading to Respiratory failure

85
Q

cholinergic crisis

A

Extreme muscle weakness or paralysis
S/S of excessive muscarinic stimulation
Treatment: Mechanical ventilation
Antidote for muscarinic sx = atropine
What should the patient wear at all times?Med-alert bracelet

Too much acetylcholine or nystigmine
overstimulation of muscles and muscles are worn out leading to respiratory failure

86
Q

Name the 2 classes of drugs that are used to treat MG

A

Immunosuppressants (steroids)
Cholinesterase inhibitors

87
Q

Are cholinesterase inhibitors a cure or symptomatic relief?

A

symptomatic relief

88
Q

How do cholinesterase inhibitors work?

A

Prevent inactivation of ACh by cholinesterase.
Intensify the effects of Ach released from motor neurons– increases muscle strength.
Give 30 – 45 min prior to eating to strengthen swallowing muscles

89
Q

Neostigmin (Prostigmin)

A

Class: Cholinesterase inhibitor (anticholinesterase)
Indication: MG
MOA: Enhances cholinergic action by facilitating transmission of impulses across neuromuscular actions. In therapeutic doses, this drug affects both muscarinic and nicotinic* receptors
route: multiple routes

90
Q

Muscarinic vs. Nicotinic adverse effects of Neostigmin.

A

Muscarinic: Increased secretions, GI motility, Urinary urgency, Bradycardia, Bronchial constriction, Miosis, near-sightedness
Neuromuscular (nicotinic): Therapeutic doses = increased muscle contraction, Toxic doses = reduced contraction, What could toxicity lead to? cholinergic crisis.

91
Q

your patient presents with respiratory insufficiency, extreme muscle weakness, what do you do next to determine if its a MG or cholinergic crisis?

A

Give EDROPHONIUM: A SHORT ACTING CHOLINESTERASE INHIBITOR, INCREASES ACETYLCHOLINE TEMPORARILY.
If they are in a MG crisis, they will improve because there is an increase in acetylcholine.
If they are in a cholinergic crisis, they will worsen because they already have too much acetylcholine.

NUR 406 (7 decks)

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