Nursing 280: Pathophysiology Examination

1
Nursing 280 PathophysiologyExamination
6Module V Alterations in Central Nervous
System Function and Special Sensory FunctionPart
C Pathophysiologic ProcessesSection II

• Presented by
• Ronda M. Overdiek, M.S.N., R.N.

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Part C Section IIPathophysiologic Processes

• Objectives 15-17
• Chapter 15

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Objectives in Part CSection II

• Objective 15
• Identify pathophysiology and clinical
  manifestations of infections.
• Objective 16
• Identify degenerative diseases as to the clinical
  manifestations and pathophysiology.
• Objective 17
• Identify disorders of myoneural junction.

4
Objective 15 Identify pathophysiology and
clinical manifestations of infections.

• Meningitis
• Infection of meninges (dura, arachnoid, pia
  mater).
• Caused by
• Bacteria, viruses, fungi, parasites, or toxins.
• Bacterial 25 mortality in adults
• Viral meningitis
• Fungal meningitis

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Objective 15 Identify pathophysiology and
clinical manifestations of infections.

• Bacterial Meningitis
• Infection of the pia mater and arachnoid, the
  subarachnoid space, the ventricular system, and
  the CSF.
• Infectious agents
• Meningococcus (Neisseria meningitidis)
• pneumococcus (streptococcus pneumoniae)
• URI---blood borne---CNS entry
• Inflammatory response by meninges, CSF,
  ventricles.
• Neutrophils migrate producing exudate that plugs
  off CSF flow around the brain and spinal cord.
• Increase in ICP

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Objective 15 Identify pathophysiology and
clinical manifestations of infections.

• Bacterial Meningitis
• Signs/Symptoms
• Fever, tachycardia, chills, petechial rash,
  throbbing headache, photophobia, nuchal rigidity,
  decrease in LOC, focal neurologic deficits,
  seizures, projectile vomiting.
• Treatment
• Antibiotic therapy, supportive.

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Objective 15 Identify pathophysiology and
clinical manifestations of infections.

• Encephalitis
• Viral, bacterial, fungal, autoimmune response
• Caused by
• Arthopod-borne (mosquito) virus
• Herpes Simplex Type I
• Meningeal involvement w/nerve cell degeneration

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Objective 15 Identify pathophysiology and
clinical manifestations of infections.

• Encephalitis
• S/S
• Fever, delirium, confusion progressing to
  unconsciousness, seizures, paresis, paralysis,
  increased ICP.
• Evaluation
• Medical history, CSF, CT/MRI scan.
• Treatment
• Herpes encephalitis acyclovir/steroids
• Supportive therapy, decrease ICP

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Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• Parkinson Disease
• Degenerative disorder of the basal ganglia
  involving the depletion of the inhibitory
  neurotransmitter dopamine.
• Imbalance of dopaminergic (inhibitory) and
  cholinergic (excitatory) activity causes
  symptoms. Balance of the two produced normal
  motor function.
• Possible Causes
• Genetic, viral, and toxic.
• Figure 15-16 Page 415

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Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• Parkinson Disease
• Clinical Manifestations
• Tremors at rest, rigidity (muscle stiffness),
  akinesia (decrease in voluntary
  movements-disturbance in time it takes to make a
  movement), postural abnormalities.
• Associated with depression and dementia.
• Treatment Drug therapy

11
Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• Alzheimer Disorder
• Cause is unknown
• Loss of neurotransmitter stimulation, chromosomal
  mutations, viral causes, etc.
• Pathophysiology
• Neuronal proteins become distorted and twisted
  causing degeneration and development of plaques
  (senile plaques) causing decrease in neuronal
  transmission.

12
Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• Alzheimer Disease
• Clinical Manifestations
• Forgetfulness, emotional upset, disorientation,
  confusion, behavioral changes (irritability,
  agitation, restlessness), deterioration of
  language, rigidity, posturing.
• Treatment
• Memory aids, assisting with ADLs.

13
Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• Multiple Sclerosis
• Destruction of CNS myelin
• Most prevalent CNS demyelinating disorder and
  leading cause of neurologic disability in early
  adulthood.
• Cause
• Previous viral insult to the nervous system has
  occurred in a genetically susceptible individual
  with a subsequent abnormal immune response in the
  CNS. (T-cells become autoreactive to a single
  myelin protein).

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Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• M.S.
• Clinical Manifestations (variable)
• Paresthesias, ataxia, blindness, tonic head
  turning, bowel/bladder symptoms, vomiting,
  fatigue, weakness, vertigo, ataxia, pain,
  depression, progressive deterioration of motor
  function due to demyelinating lesions (plaques)
  that produce slowing of conduction then finally a
  conduction block, etc.

15
Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• M.S.
• Evaluation/Treatment
• CSF, CT, MRI
• Steroids, immunosuppressant therapy, drug
  therapy. Supportive management of fatigue,
  weakness, tremors, etc.

16
Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• Amyotrophic Lateral Sclerosis
• Lou Gehrig Disease (Classic ALS)
• Degenerative disorder involving lower and upper
  motor neurons resulting in progressive muscle
  weakness leading to respiratory failure and
  death.
• Cause is unclear
• Genetic factors, virus, environmental agents,
  autoimmune.

17
Objective 16Identify degenerative diseases as
to the clinical manifestations and
pathophysiology.

• ALS
• Lower/upper motor neuron degeneration
• Clinical Manifestations
• Weakness, paralysis, muscle atrophy. Normal
  intellectual and sensory functions are sustained
  until death.
• Treatment
• Supportive, drug (put off ventilatory use).

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Objective 17Identify disorders of the
myoneural junction.

• Myasthenia Gravis
• Chronic autoimmune disease that effects the
  neuromuscular junction.
• Characterized by
• Muscle weakness and fatigability
• Pathophysiology
• Defect in nerve impulse transmission at the
  neuromuscular junction.
• Postsynaptic acetylcholine receptors on the
  muscles cells plasma membrane are no longer
  recognized as self and elicit the generation of
  autoantibodies.

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Objective 17Identify disorders of the
myoneural junction.

• Myasthenia Gravis
• Clinical Manifestations
• Weakness, fatigue, muscles of facial expression,
  mastication, swallowing, and speech are impaired.
  Pts at risk for aspiration/respiratory
  infections. Eventually, require ventilatory
  support.
• Treatment
• Drugs (steroids, immunosuppressants), supportive
  measures (respiratory needs).