Neuro Flashcards

1
Q

Sensory (Afferent) Division

A
  • Ascending: sensory receptors → spinal column
  • Conducts: signals from receptors to CNS
  • Composed of: sensory neurons
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2
Q

Motor (Efferent) Division

A
  • Descending: innervates muscles and glands
  • Conducts: signals from CNS to effectors
  • Composed of: motor neurons
  • Continues to have Autonomic Nervous System (ANS) & Somatic Nervous System (SNS):
    • ANS: controls involuntary responses
      • Sympathetic Division: “fight or flight” response that mobilizes body systems (epi/norepi)
      • Parasympathetic Division: “rest and digest” responses that conserves energy (acetylcholine)
    • SNS: controls voluntary movements
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3
Q

Stroke Identification

A
  • BE FAST
  • Balance Issues
  • Eyesight Changes
  • Facial Drooping
  • Arm Weakness
  • Speech Difficulties
  • Time to Call 911
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4
Q

Stroke Causes

A
  • Ischemic: interruption of blood circulation ⇒ occlusion of cerebral artery ⇒ brain partially deprived of oxygen and nutrients
    • Caused mainly by: A-fib & atherosclerosis ⇒ makes thrombosis made of fibrin
      • A-fib bc it’s a dysrhythmia of heart where 2 top chambers are just shaking bc of continuous firing of atrial nodes ⇒ forms clots that lodges itself on vessels ⇒ occlusion of arteries to brain ⇒ stroke
  • Hemorrhagic: extreme amts of pressure on small vessels feeding brain stem ⇒ ruptures cerebral artery wall (vessel rupture) ⇒ bleeding into brain
    • Caused mainly by: uncontrolled HTN
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5
Q

Stroke Risk Factors

A
  • Age: affects all range
  • Sex: males >
  • Race: African Americans >
  • HTN: bc of persistent vasoconstriction and actively forms clots
  • A-fib: bc it actively forms clots
  • Asymptomatic carotid stenosis: bc of atherosclerotic buildup in carotid arteries that supply brain cells
  • Sickle cell disease: bc of abnormal sickle shape that makes it easier for RBCs to lodge itself in vessels and cause occlusion
  • Hyperlipidemia: bc of cholesterol buildup that can lodge itself in vessels to cause occlusion
  • Smoking: bc of damage to blood vessels
  • FHx
  • DM
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6
Q

Management of Acute Strokes (goals for ischemic vs hemorrhagic)

A
  • Goal: determine cause (ischemic or hemorrhagic) → CT Scan First !!!
    • If ischemic → thrombolytics within 4. 5 hr window to try and re-establish perfusion to affected brain area to prevent and reduce irreversible ischemic damage
    • If hemorrhagic → get BP down + prevent expansion of bleeding, reduce intracranial pressure, and address the cause
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7
Q

Thrombolytic Therapy Treatment

A
  • For ischemic strokes only !!!
  • MOA: dissolves blood clots that causes ischemic
  • Goal: re-establish perfusion to affected brain area to prevent irreversible ischemic damage and reduce disability extent
  • Time-Sensitive Treatment:
    • Most effective when given as soon as possible after symptom onset.
    • Give within time window of within 4.5 hours from Sx onset
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8
Q

Transient Ischemic Attack (TIA)

A
  • What: temporary interruption of blood flow to brain ⇒ causing stroke-like Sxs that resolves within 24 hrs
  • Duration of Sxs: mins-hrs
  • Severity of Sxs: mild-moderate
  • Risk of recurrence: high
  • Prognosis: usually good
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9
Q

Cerebrovascular Accident (CVA)

A
  • What: sudden interruption of blood flow to brain ⇒ can cause permanent damage
  • Duration of Sxs: permanent
  • Severity of Sxs: can be severe
  • Risk of recurrence: high
  • Prognosis: can be poor
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10
Q

Neurotransmitters: Dopamine

A
  • Produced by brain’s basal ganglia’s substantia nigra’s dopaminergic neurons
  • Causes:
    • Vasoconstriction bc they’re alpha adrenergics
    • ↑ BP & HR
    • Fluid coordination/movement
      • No dopamine ⇒ no fluidity or coordination ⇒ extrapyramidal (or involuntary/automatic) motor function impairment
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11
Q

Neurotransmitters: Acetylcholine (ACh)

A
  • Depending on receptor type:
    • Muscarinic receptors (parasympathetic effects): Slows heart rate, stimulates digestion, and increases glandular secretions.
    • Nicotinic receptors (somatic and autonomic effects): Excitatory effects like muscle contraction
  • The relaxation of muscles after contraction is due to acetylcholine esterase (AChE) that cleans up remaining ACh ⇒ restores resting conditions
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12
Q

Parkinson’s Disease (Pathophysiology, Types)

A
  • Motor problem
  • Pathophysiology: lack of/reduced dopamine level
  • Types:
    • Dysfunction/degeneration of brain’s substantia nigra’s dopaminergic neurons that normally secretes dopamine ⇒ lacks dopamine secretion ⇒ not enough dopamine binds to receptors (dopamine deficiency)
    • Not enough receptors to bind w/ normal amt of secreted dopamine
    • Imbalance of both receptors and dopamine neurotransmitters
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13
Q

Parkinson’s Treatment Med + Considerations (MOA, Toxicity Signs, Nurs Considerations)

A
  • Treatment: Levodopa Considerations
  • MOA: crosses BBB to be converted to dopamine ⇒ ↑ dopamine lvls ⇒ ↓ Sxs
  • Toxicity Signs
    • Dyskinesias: involuntary movements like ticks or chorea
    • Neuropsychiatric: hallucinations, confusion, or psychosis
    • NV, esp early in treatment
  • Nurs Considerations
    • Dark colored urine is normal and harmless
    • Contraindicated w/ MAOIs or any other meds that ↑ dopamine bc they allow for more dopamine ⇒ increases HR and BP ⇒ risks for HTN crisis
    • Heavily protein-bound med ⇒ so if pt is HYPERalbumic ⇒ doesn’t allow carbidopa-levodopa to reach therapeutic effectiveness
    • Adherence of taking it at same time everyday important bc if you abruptly halt ⇒ dopamine receptors don’t have enough dopamine ⇒ prior Parkinson’s Sx onset recurs
    • Full therapeutic effect may take 3+ wks - months
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14
Q

Myasthenia Gravis (MG) (Pathophysiology + S&S)

A
  • Autoimmune disease
  • Pathophysiology: specific antibodies along skeletal muscles that destroys acetylcholine receptors (AChRs) ⇒ prevents ACh from binding ⇒ impaired transmission of nerve signals to muscles ⇒ prevents skeletal muscle contraction ⇒ muscle weakness bc ACh can’t sufficiently stimulate muscle
    • Weakness worsens with activity
    • Weakness improves with rest
  • S&S: WEAKNESS
    • Weakness of face, neck, arms, legs
    • Eyelid drooping (ptosis)
    • Appearance of blank expression
    • Keeps choking or gagging
    • No energy
    • Extraocular movement like diplopia
    • Slurred speech
    • SOB
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15
Q

Multiple Sclerosis (MS) (Pathophysiology)

A
  • Autoimmune disease
  • Pathophysiology: attacks myelin sheaths that’s needed for fast and efficient nerve signal transmission ⇒ degraded myelin sheaths ⇒ pot holes along axon ⇒ doesn’t allow for smooth signaling pathway transmission bc it’s all jagged up ⇒ interruptions of muscle contractions occur
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16
Q

MS Types: Relapsing-Remitting

A

Sxs comes and go but worsens each time they appear

17
Q

MS Types: Secondary Progressive

A
  • immune attack becomes constant ⇒ steady progression of disability
  • After initial relapsing-remitting course → disease begins to progress steadily over time
  • Immune attacks become constant ⇒ ongoing damage and increasing disability even without distinct relapses
18
Q

MS Types: Primary Progressive

A
  • one constant attack ⇒ causes steady progression of disability
  • From onset → there’s no relapsing-remitting phase
  • Disease progresses steadily from beginning w/o periods of remission or recovery
  • Symptoms gradually worsen over time without significant recovery
19
Q

MS Types: Progressive-Relapsing

A
  • one constant attack but disability happens even faster
  • Steady progression of Sxs from start but w/ acute relapses (periods of significant Sx worsening) superimposed on progression