Nursing 280: Pathophysiology Examination

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

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

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Part C Section IPathophysiologic Processes

• Objectives 8-14
• Chapter 14
• Chapter 15

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Objectives in Part CSection I

• Objective 8 Define/differentiate brain and
  cerebral death.
• Objective 9 Define seizure. Describe the
  neurophysiology of a seizure.
• Objective 10 Identify different types of
  seizure disorders.
• Objective 11 Correlate clinical manifestations
  and pathophysiology of motor dysfunction.

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Objectives in Part CSection I Continued

• Objective 12 Discuss increased intracranial
  pressure and complications of unrelieved
  intracranial pressure.
• Objective 13 Identify traumatic injuries to the
  CNS.
• Objective 14 Correlate pathophysiology and
  clinical manifestations of vascular problems to
  the CNS.

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Objective 8 Define/differentiate brain and
cerebral death.

• Brain Death (brain stem death)
• Occurs when irreversible brain damage is so
  extensive that the brain has no potential for
  recovery and no longer can maintain the bodys
  internal homeostasis.
• Destruction includes the brain stem and
  cerebellum.
• Postmortem brain is autolyzing or is autolyzed.

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Objective 8 Define/differentiate brain and
cerebral death.

• Cerebral Death
• Death of the cerebral hemispheres exclusive of
  the brain stem and cerebellum.
• Brain damage is permanent
• Individual is forever unable to respond
  behaviorally in any significant way to the
  environment.
• The brain may continue to maintain internal
  homeostasis.

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Objective 9 Define seizure. Describe the
neurophysiology of a seizure.

• Seizure
• Results from a sudden, explosive, disorderly
  discharge of cerebral neurons.
• Characterized by
• Sudden, transient alteration in brain function
  usually involving motor, sensory, autonomic, or
  psychic clinical manifestations and altered level
  of arousal.
• Epilepsy

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Objective 9 Define seizure. Describe the
neurophysiology of a seizure.

• Etiology of Seizure
• Cerebral lesions
• Biochemical Disorders
• Cerebral Trauma
• Epilepsy
• The tendency to have a seizure. General term for
  the primary condition that causes seizures.
• Precipitated by
• Hypoglycemia, fatigue, lack of sleep, stress,
  febrile illness, hyponatremia, constipation,
  withdrawal of depressant drugs, hyperventilation,
  blinking lights, loud noises, music, odors,
  patient being startled, for females PMS/Menses.

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Objective 9 Define seizure. Describe the
neurophysiology of a seizure.

• Seizure Activity
• Maintenance requires a 250 increase in ATP,
  cerebral oxygen consumption is increased by 60.
• Available glucose and oxygen are readily
  depleted.
• Cerebral blood flow increases approximately 250.

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Objective 9 Define seizure. Describe the
neurophysiology of a seizure.

• Seizure pathophysiology
• Group of neurons have depolarization shift and
  sudden changes in membrane potential
  (epileptogenic focus).
• Primary abnormality membrane defect leading to
  instability of resting potential.
• Firing of neurons becomes increasingly greater in
  frequency and amplitude.
• Triggered by
• Hyperthermia, hypoxia, hypoglycemia,
  hyponatremia, repeated sensory stimulation, and
  certain sleep phases.

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Objective 9 Define seizure. Describe the
neurophysiology of a seizure.

• Tonic Phase
• Phase of muscle contraction and increased muscle
  tone
• Associated with loss of consciousness
• Apnea may be present
• Clonic Phase
• Phase of alternating contraction and relaxation
  of muscles
• Interruption in seizure discharge
• Bursts become more and more infrequent until they
  cease

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Objective 9 Define seizure. Describe the
neurophysiology of a seizure.

• Causes of seizures (Table 14-6 Page 364)
• Age Specific
• Hypoxia, trauma, infection, tumors, drugs use,
  cerebrovascular disease, metabolic disorders,
  etc.

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Objective 10Identify different types of
seizure disorders.

• Traditional Terminology
• Focal motor, temporal lobe/psychomotor seizures,
  limited grand mal, grand mal, petit mal, drop
  attacks, minor motor.
• New Nomenclature
• Partial seizures, Generalized seizures, Epileptic
  syndromes

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Objective 10Identify different types of
seizure disorders.

• Partial Seizures or Focal Seizures (beginning
  locally)
• Classified as simple or complex
• Simple without impairment of consciousness
• Complex with impairment of consciousness
• Involve neurons only unilaterally
• Often have focal onset
• Consciousness may be maintained as long as
  seizure activity is limited to one hemisphere,
  but the seizure activity may become generalized
  and consciousness is lost.

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Objective 10Identify different types of
seizure disorders.

• Generalized Seizures
• Account for 30 of seizures
• Involve neurons bilaterally
• Often do not have a focal onset
• Consciousness is ALWAYS impaired or lost.
• Partial vs. Generalized
• Table 14-7 Page 365.

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Objective 10Identify different types of
seizure disorders.

• Postictal State
• State that follows a seizure
• Fatigue, confusion, disorientation

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Objective 11Correlate clinical manifestations
and pathophysiology of motor dysfunction.

• Motor Dysfunction
• Alterations in Muscle Tone
• Hypotonia Decreased muscle tone.
• Passive movement of muscle occurs with little or
  no resistance.
• Causes patients to tire easily, weakness, muscle
  atrophies
• Hypertonia Increased muscle tone.
• Passive movement of a muscle occurs with
  resistance.
• Types of hypertonia spasticity, paratonia,
  dystonia, rigidity.
• Table 14-15 Page 377

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Objective 11Correlate clinical manifestations
and pathophysiology of motor dysfunction.

• Alterations in Movement
• Hyperkinesia
• Excessive movements
• Table 14-16 Page 379
• Hypokinesia
• Decreased movement loss of voluntary movement
  despite preserved consciousness and normal
  peripheral nerve and muscle function.
• Paresis (weakness) is partial paralysis with
  incomplete loss of muscle power.
• Paralysis loss of motor function so that a
  muscle group is unable to overcome gravity.
• Hemiparesis/hemiplegia is paresis/paralysis of
  the upper and lower extremities on one side.
• Paraparesis/paraplegia refers to the
  weakness/paralysis of the lower extremities.
• Quadraparesis/quadriplegia refers to
  paresis/paralysis of all four extremities.

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Objective 12Discuss increased intracranial
pressure and the complications of unrelieved
intracranial pressure.

• Cerebral Hemodynamics (Terms)
• Cerebral blood volume (CBV) Refers to the amount
  of blood in the intracranial vault at a given
  time. Determined by autoregulation mechanisms
  that control cerebral blood flow.
• Cerebral blood flow (CBF) Normally maintained at
  a rate that matches local metabolic needs of the
  brain-750 ml/min (15-20 of cardiac output).
  Regulated through constriction/dilation of
  cerebral vessels in response to oxygen/carbon
  dioxide levels.
• Cerebral perfusion pressure (CPP) Pressure
  required to perfuse the cells of the brain. CPP
  determines CBF. CPP MAP ICP.
• Cerebral oxygenation critical factor measured by
  oxygen saturation in the internal jugular vein.
• Intracranial pressure Normal is 5-15 mm Hg.

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Objective 12Discuss increased intracranial
pressure and the complications of unrelieved
intracranial pressure.

• Increase intracranial pressure
• Results from
• Increase in intracranial content (tumor)
• Edema
• Excess CSF
• Hemorrhage
• Stages of Compensation/Decompensation
• Stages I IV and Death
• Treatment Steroids, dehydrating agents, osmotic
  diuretics.

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Objective 12Discuss increased intracranial
pressure and the complications of unrelieved
intracranial pressure.Figure 14-8 Page 373
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Objective 12Discuss increased intracranial
pressure and the complications of unrelieved
intracranial pressure.

• Cerebral Edema
• Increase in the fluid content of brain tissue.
• Occurs after brain insult from
• Trauma, infection, hemorrhage, tumor, ischemia,
  infarct, or hypoxia.
• Harmful effects include
• Distortion of blood vessels, displacement of
  brain tissues, eventual herniation of brain
  tissue
• Four types of edema
• Vasogenic, cytotoxic, ischemic, interstitial.

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Objective 12Discuss increased intracranial
pressure and the complications of unrelieved
intracranial pressure.

• Cerebral Edema
• Vasogenic Edema
• Caused by increased permeability of the capillary
  endothelium of the rain after injury to the
  vascular structure.
• Results in disruption of blood brain barrier
• Promotes accumulation of more edema because
  promotes ischemia from increasing pressure

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Objective 12Discuss increased intracranial
pressure and the complications of unrelieved
intracranial pressure.

• Cerebral Edema
• Cytotoxic Edema
• Toxic factors affect the cellular elements of the
  brain causing failure of active transport
  systems.
• Cells loose potassium and gain larger amounts of
  sodium.
• Ischemic Edema
• Caused by cerebral infarction.
• Includes both vasogenic and cytotoxic edema.
• Interstitial Edema
• Seen with noncommunicating hydrocephalusmovement
  of CSF from the ventricles to the extracellular
  spaces of the brain tissue.

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Objective 13Identify traumatic injuries to the
CNS.

• Brain Trauma
• Traumatic insult to the brain capable of
  producing physical, intellectual, emotional,
  social, and vocational changes.
• Traumatic Brain Injury (TBI) Categories
• Closed (blunt) trauma
• More common, involves the head striking a hard
  surface or a rapidly moving object striking the
  head
• Dura remains intact and the brain tissues are not
  exposed
• Open (penetrating) trauma
• Exposure of cranial contents to the environment
• Caused by
• Transportation related events, falls,
  sports-related events, violence.

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Objective 13Identify traumatic injuries to the
CNS.

• Concussion
• Involves diffuse cerebral disconnection from the
  brain stem reticular activating system and is a
  phenomenon of physiologic, neurologic dysfunction
  w/o substantial anatomic disruption.
• Mild Concussion Characterized by immediate but
  transitory clinical manifestations. CSF pressure
  rises, initial confusional state lasts for one to
  several minutes. Patients may have head pain and
  c/o nervousness and not being themselves for up
  to a few days.
• Classic Cerebral Concussion is evidenced by
• Immediate loss of consciousness which lasts less
  than 6 hours
• Amnesia is present
• Reflexes fail which result in falls
• Breathing stops, bradycardia occurs, blood
  pressure falls
• Head pain, nausea, fatigue, attentional and
  memory system impairments and mood and affect
  change.

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Objective 13Identify traumatic injuries to the
CNS.

• Contusion (bruise) Page 79
• Bleeding into the skin or underlying tissues as a
  consequence of a blow that squeezes or crushes
  the soft tissues and ruptures blood vessels w/o
  breaking the skin.
• Contusions produce epidural, subdural, and
  intracerebral hematomas (collection of blood in
  soft tissues or an enclosed space, pg. 79).
• Damage results from compression of the skull at
  the point of impact and rebound effect.
• Severity of contusion varies with the amount of
  energy transmitted by the skull to underlying
  brain tissue.
• Intracranial pressure results from edema.
  Infarction, necrosis, multiple hemorrhages occur.
• Maximum effects peak 18-36 hours after injury.
• Mechanism of injury (Figure 15-1 Page 393).
• Coup injury impact against the object causing
  direct trauma, shearing of subdural veins, trauma
  to base of brain.
• Contrecoup injury site of injury where brain
  hits inside of skull and shearing forces through
  the brain.

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Objective 13Identify traumatic injuries to the
CNS.

• Extradural Hematoma
• Consist of epidural hematomas and hemorrhages.
• 1-2 of major head injuries
• Artery is source of bleeding in 85 of injuries
• 90 of patients have skull fractures
• Temporal fossa is most common site caused by
  injury to the middle meningeal artery or vein
• Results in temporal lobe herniation, ipsilateral
  pupil dilation, contralateral hemiparesis
• Treatment surgical evacuation, burr holes,
  ligation of bleeding vessel.
• Medical Emergency

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Objective 13Identify traumatic injuries to the
CNS.

• Subdural Hematoma
• 10-20 of persons with TBI.
• Types
• Acute Hematoma develops rapidly associated
  w/fractures such as occurs MVA
• Subacute signs and symptoms occur in one to
  several weeks, progresses more slowly
• Chronic more common in elderly due to
  anticoagulant therapy. S/S are occur slowly such
  as dementia and rigidity.
• Manifestations Headache, drowsiness, confusion,
  loss of consciousness, respiratory changes, pupil
  changes (s/s of herniation).
• Treatment Burr holes, craniotomy, supportive,
  manage increasing ICP.

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Objective 13Identify traumatic injuries to the
CNS.

• Intracerebral Hematoma
• 2-3 of persons with head injuries
• Caused by shearing forces that disrupt small
  blood vessels, increasing ICP w/compression of
  brain tissue.
• Signs/Symptoms decreasing LOC, coma,
  contralateral hemiplegia and s/s of herniation
• Treatment Surgical evacuation of single
  hematoma, management of increased ICP

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Objective 13Identify traumatic injuries to the
CNS.

• Open Head Injury
• Most patients loose consciousness
• Duration of coma related to location of injury,
  extent of damage, and amount of bleeding.
• Treatment debridement of traumatized tissue to
  prevent infection and to remove blood clots,
  reducing ICP, antibiotics.

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Objective 13Identify traumatic injuries to the
CNS.

• Spinal Cord Trauma
• Most commonly occur because of vertebral injuries
• Most often occur in C1 to C2, C4 to C7, and T10
  to L2.
• Injury causes hemorrhages and edema lending to
  ischemia and necrosis.
• Spinal shock reflex function is completely lost
  in all segments below the region. Lasts 7 to 20
  days.
• Loss of motor and sensory function depend on the
  level of injury.
• Treatment immobilize to decrease chance of more
  injury, surgical intervention, steroids,
  nutrition, lung function, skin integrity,
  bladder/bowel management.

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Objective 13Identify traumatic injuries to the
CNS.

• Autonomic Hyperreflexia
• May occur after spinal shock resolves usually in
  patients with injury at T6 level or above.
• Massive, uncompensated cardiovascular response to
  stimulation of the sympathetic nervous system.
• Condition is life threatening
• Signs/symptoms paroxysmal hypertension, pounding
  headache, blurred vision, sweating above the
  level of the lesion with flushing of the skin,
  nausea, bradycardia (30-40 beats/min).
• Cause distended bladder or rectum, pain.
• Treatment HOB elevated, stimulus should be found
  and removed. Antihypertensive agents given for
  elevated blood pressure (risk of CVA).
• Figure 15-8 Page 400

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Objective 14Correlate pathophysiology and
clinical manifestations of vascular problems to
the CNS.

• Cerebrovascular Accidents (CVA)
• Incidence is 600,000 per year, 3rd leading cause
  of death, leading cause of disability (40 billion
  dollars per year).
• Risk factors hypertension, smoking, diabetes,
  polycythemia, thrombocytopenia, presence of
  lipoprotein-a, impaired cardiac function, atrial
  fibrillation.
• Types
• Thombotic, embolic, hemorrhagic.

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Objective 14Correlate pathophysiology and
clinical manifestations of vascular problems to
the CNS.

• Thrombotic Stroke
• Arise from arterial occlusions caused by thrombi
  formed in the arteries supplying the brain or in
  the intracranial vessels.
• Most frequently attributed to atherosclerosis and
  inflammatory disease that damage vessel walls.
• Increased coagulation can lead to thrombus
  formation, conditions causing inadequate cerebral
  perfusion such as dehydration, hypotension)
  increases changes of stroke.
• Transient Ischemic Attacks (TIAs)
• Thrombotic particles that cause an intermittent
  blockage of circulation or spasm.
• Signs/symptoms resolve w/in 24 hours

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Objective 14Correlate pathophysiology and
clinical manifestations of vascular problems to
the CNS.

• Embolic Stroke
• Fragments that break from the thrombus formed
  outside the brain or in the heart, aorta, common
  carotid, or thorax.
• Cause ischemia by blocking the vessel
• Conditions associated
• Atrial fibrillation, myocardial infarction,
  endocarditis, rheumatic heart disease, valvular
  prosthesis, atrial-septal defects, etc.

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Objective 14Correlate pathophysiology and
clinical manifestations of vascular problems to
the CNS.

• Hemorrhagic Stroke
• Causes hypertension, ruptured aneurysms,
  vascular malformations, bleeding into a tumor,
  bleeding disorders or anticoagulation, head
  trauma, illicit drug use.
• Risk factors hypertension, previous cerebral
  infarct, coronary artery disease, diabetes.

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Objective 14Correlate pathophysiology and
clinical manifestations of vascular problems to
the CNS.

• Stroke
• Signs/symptoms are dependent on where stroke is
  located. They include, but are not limited to
• Motor contralateral hemiparesis or hemiplegia,
  decreased sensation, loss of speech,
  comprehension defects, cheyne-stokes
  respirations, headache, visual disturbances.
• Treatment
• Time is brain.
• Thrombotic/Embolic Prevention of ischemic injury
  and supportive management to control cerebral
  edema and increasing ICP.
• Hemorrhagic Stopping or reducing bleeding,
  controlling ICP, preventing rebleed, surgical
  interventions.

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Objective 14Correlate pathophysiology and
clinical manifestations of vascular problems to
the CNS.

• Arteriovenous Malformation
• Tangled mass of blood vessels creating abnormal
  channels between the arterial and venous systems.
• DO NOT have normal blood vessel structure and are
  abnormally thin. Dilation occurs over time,
  blood is shunted away from brain tissue.
• Signs/Symptoms Chronic headache, seizures,
  hemorrhage, systolic bruit can be heard over the
  carotid artery in the neck, the mastoid process
  or the eyeball.
• Treatment Surgical intervention or radiation.