NR 283 FINAL EXAM STUDY GUIDE
Neurological
Clinical Manifestations for alterations in arousal
o Changes in LOC is the most critical piece on information we have
o LOC: are early changes, first thing you will see when something goes
wrong neurologically
o Pattern of breathing: assess the rate, rhythm and pattern; can have
changes in any of those. Respiratory rate can be low or labored. Could
have Cheyne stroke respirations
o Pupillary Changes: biggest thing to look for fixed and dilated pupils.
(Pupils are wide and don’t move). This is not good, its sign of brain
hypoxia or ischemia.
o Oculomotor Responses: just looking for changes and or things your not
supposed to have.
Resting, spontaneous, reflexive eye movements
o Motor Responses: Can help evaluate level of dysfunction and damaged
side ( just looking for changes or things that shouldn’t be there)
Purposeful, inappropriate, or not present
o Consciousness: state of awareness of oneself and the environment
Arousal: state of being awake and being able to respond
Awareness: state of being aware
These are all mediated by the RAS, in brainstem
If you get damage to cerebrum then the RAS will maintain you in a
vegetative state- will keep you alive if something happens severely
to your brain tissue.
o Structural: could be due to a tumor, bleeding in the brain
o Metabolic: anything that effects the metabolism like hypoxia, electrolyte
changes, medications or drugs
o Psychogenic: patients with psychiatric diseases like schizophrenia
o Outcomes: Long-term disabilities, or patients could die.
Brain Death: body can no longer maintain internal homeostasis
o Occurs when the brain has been damaged so severely that it can never
recover. Death or damage to the brain stem. These patients are
considered legally dead
, Cerebral death : irreversible damage to the cerebrum but the cerebellum and
brain stem maintain intact- because the cerebellum and brainstem are intact, all
vitals can be maintained, your still alive, just not where you want to be
o 4 types:
o Remain in coma for life: they will have vital signs, but will not move,
talk or open their eyes etc.
o Emerge into a persistent vegetative state: the only thing they can do is
open their eyes and have normal sleep patterns. Will have vital signs
o Progress into a minimal conscious state (MCS): may follow simple
commands, may have small motor movements, and could be able to say
yes or no.
o Locked in syndrome: patient is fully conscious but completely
paralyzed, only thing they can do is move their eyes. They are completely
aware of what’s going on. They will be in this syndrome for the rest of
their life.
Seizures: sudden transient (temporary) alteration of brain function caused by an
abrupt explosive, disorderly discharge of cerebral neurons. – Usually a small
group of neurons
o Cause: could be tumor, trauma, a chemical disorder, or due to flashing
lights, loud noises.
o Epilepsy: a disease, someone has seizures but do NOT know the cause.
Could be genetic combined with environmental factors.
Epileptic neurons: hyper sensitive and fire more frequently
o Phases – Tonic clonic: has two phases
Tonic phase: the phase of continuous muscle contractions
Clonic phase: alternating of contraction and relaxation. The
neurons that aren’t part of seizure are trying to stop the seizure
activity.- the periods of relaxation will get longer and longer until
the seizure stop.
Neurons cannot bring seizure to an adrupt stop, that’s why you
get periods of relaxation.
o post-ictal: the phase that immediately following the end of the seizure,
this is when seizure stops. Patient can be semi conscious, fatigued
o Manifestations
Aura: sign or symptom that the patient will have right before the
seize. (Seconds). It’s the warning sign that a seizure is coming
, Prodroma: sign or symptom that occurs hours or days before a
seizure. Could be a headache, or feeling of malaise, it’s a warning
sign of seizure coming.
Increase in oxygen consumption: a lot of oxygen is used during
seizure because of a lot of energy is being used.
Anaerobic metabolism: If your patient runs out of
oxygen then they will start building up lactic acid
o Prolonged seizure can cause brain damage
Dysphasia: problem with communication (speech) – 3 types
o Agnosia- a problem with the ability to recognize patterns or objects.
Theres a problem with one of there senses,
have to use one of there other senses to recall. Ex) see pen, can see
it but cant recall what it is
o Expressive dysphasia-problem with brocas area- they know what they
want to say but they cant express themselves
Deficit of expression
o Receptive dysphasia- problem with wernicke area- problem with
comprehension –when someone speaks you have no idea what they are
saying (almost like they are speaking in another language)- see a lot of
with stroke patients.
Deficit of comprehension
o Transcortical dysphasia (not as common)- echolalia-repeats a word or
phrase over and over-speech is clear but makes no sense – fixed on a
certain word or syllable
Echolalia
Acute confusion state and delirium-
o Acute Confusion State: Transient (temporary) disorders of awareness
that result from cerebral dysfunction. Temporary state of confusion.
Cause: patient disease or condition, drugs
Wont be able to concentrate, restless, wont know where they
are.
Ex: patient that keeps climbing out of bed or they need bed alarms
or sitters
o Delirium: more severe state of confusion. – see this a lot with patients
withdrawing from drugs and alcohol.
Will be confused, irritable, mis-interrupt things, could hallucinate,
hostile, violent.
, Alzheimer’s Disease: form of dementia (umbrella term), most common form
of dementia
o Don’t know the cause: could be chemical problem in brain, too much
trauma. Could be genetic ( 2 chromosomes)
o Pathologic Features:
Neurofibrillary tangles: tangles of protein on the neurons
themselves.
Neuritic plaques: deposits of protein in the brain
Neural Degeneration: destruction of the neurons
o Pathologic features leads to:
o Neuron Death: when neurons die and get a loss of
neurotransmitters- the brain will atrophy
CM: Start with forgetfulness and emotional upset- they are going to get
upset that they are forgetting things.
Progressive CM: memory loss, confusion, mood changes, problem
solving, they become completely different
Increased intracranial pressure (ICP): caused by increase in intracranial
content
o Stage 1: no change in pressure due to body compensating. Blood vessels
in brain constrict in attempt to keep pressure low.
o Stage 2: Expansion of intracranial content.
Slight pressure rise and subtle CM
Will have change in LOC.
o Stage 3: Pressure continues to increase, becomes hypoxic and patient
deteriorates
o Pupil changes, respiratory changes, motor response changes
o Stage 4: Pressure in cranium is so high that brain tissue herniates
Herniation of brain tissue- the brain tissue goes somewhere else
( the foramen magnum)
Herniation= death
Cerebral edema: increase in the fluid content (intracellular or extracellular)
within the brain tissue itself.
o Occurs after brain injury
o **Vasogenic: Most common/important, increased capillary permeability
Brain got injured, inflammatory response became stimulated, get
vasodilation that increased capillary permeability and leaks fluid
into the tissue
Neurological
Clinical Manifestations for alterations in arousal
o Changes in LOC is the most critical piece on information we have
o LOC: are early changes, first thing you will see when something goes
wrong neurologically
o Pattern of breathing: assess the rate, rhythm and pattern; can have
changes in any of those. Respiratory rate can be low or labored. Could
have Cheyne stroke respirations
o Pupillary Changes: biggest thing to look for fixed and dilated pupils.
(Pupils are wide and don’t move). This is not good, its sign of brain
hypoxia or ischemia.
o Oculomotor Responses: just looking for changes and or things your not
supposed to have.
Resting, spontaneous, reflexive eye movements
o Motor Responses: Can help evaluate level of dysfunction and damaged
side ( just looking for changes or things that shouldn’t be there)
Purposeful, inappropriate, or not present
o Consciousness: state of awareness of oneself and the environment
Arousal: state of being awake and being able to respond
Awareness: state of being aware
These are all mediated by the RAS, in brainstem
If you get damage to cerebrum then the RAS will maintain you in a
vegetative state- will keep you alive if something happens severely
to your brain tissue.
o Structural: could be due to a tumor, bleeding in the brain
o Metabolic: anything that effects the metabolism like hypoxia, electrolyte
changes, medications or drugs
o Psychogenic: patients with psychiatric diseases like schizophrenia
o Outcomes: Long-term disabilities, or patients could die.
Brain Death: body can no longer maintain internal homeostasis
o Occurs when the brain has been damaged so severely that it can never
recover. Death or damage to the brain stem. These patients are
considered legally dead
, Cerebral death : irreversible damage to the cerebrum but the cerebellum and
brain stem maintain intact- because the cerebellum and brainstem are intact, all
vitals can be maintained, your still alive, just not where you want to be
o 4 types:
o Remain in coma for life: they will have vital signs, but will not move,
talk or open their eyes etc.
o Emerge into a persistent vegetative state: the only thing they can do is
open their eyes and have normal sleep patterns. Will have vital signs
o Progress into a minimal conscious state (MCS): may follow simple
commands, may have small motor movements, and could be able to say
yes or no.
o Locked in syndrome: patient is fully conscious but completely
paralyzed, only thing they can do is move their eyes. They are completely
aware of what’s going on. They will be in this syndrome for the rest of
their life.
Seizures: sudden transient (temporary) alteration of brain function caused by an
abrupt explosive, disorderly discharge of cerebral neurons. – Usually a small
group of neurons
o Cause: could be tumor, trauma, a chemical disorder, or due to flashing
lights, loud noises.
o Epilepsy: a disease, someone has seizures but do NOT know the cause.
Could be genetic combined with environmental factors.
Epileptic neurons: hyper sensitive and fire more frequently
o Phases – Tonic clonic: has two phases
Tonic phase: the phase of continuous muscle contractions
Clonic phase: alternating of contraction and relaxation. The
neurons that aren’t part of seizure are trying to stop the seizure
activity.- the periods of relaxation will get longer and longer until
the seizure stop.
Neurons cannot bring seizure to an adrupt stop, that’s why you
get periods of relaxation.
o post-ictal: the phase that immediately following the end of the seizure,
this is when seizure stops. Patient can be semi conscious, fatigued
o Manifestations
Aura: sign or symptom that the patient will have right before the
seize. (Seconds). It’s the warning sign that a seizure is coming
, Prodroma: sign or symptom that occurs hours or days before a
seizure. Could be a headache, or feeling of malaise, it’s a warning
sign of seizure coming.
Increase in oxygen consumption: a lot of oxygen is used during
seizure because of a lot of energy is being used.
Anaerobic metabolism: If your patient runs out of
oxygen then they will start building up lactic acid
o Prolonged seizure can cause brain damage
Dysphasia: problem with communication (speech) – 3 types
o Agnosia- a problem with the ability to recognize patterns or objects.
Theres a problem with one of there senses,
have to use one of there other senses to recall. Ex) see pen, can see
it but cant recall what it is
o Expressive dysphasia-problem with brocas area- they know what they
want to say but they cant express themselves
Deficit of expression
o Receptive dysphasia- problem with wernicke area- problem with
comprehension –when someone speaks you have no idea what they are
saying (almost like they are speaking in another language)- see a lot of
with stroke patients.
Deficit of comprehension
o Transcortical dysphasia (not as common)- echolalia-repeats a word or
phrase over and over-speech is clear but makes no sense – fixed on a
certain word or syllable
Echolalia
Acute confusion state and delirium-
o Acute Confusion State: Transient (temporary) disorders of awareness
that result from cerebral dysfunction. Temporary state of confusion.
Cause: patient disease or condition, drugs
Wont be able to concentrate, restless, wont know where they
are.
Ex: patient that keeps climbing out of bed or they need bed alarms
or sitters
o Delirium: more severe state of confusion. – see this a lot with patients
withdrawing from drugs and alcohol.
Will be confused, irritable, mis-interrupt things, could hallucinate,
hostile, violent.
, Alzheimer’s Disease: form of dementia (umbrella term), most common form
of dementia
o Don’t know the cause: could be chemical problem in brain, too much
trauma. Could be genetic ( 2 chromosomes)
o Pathologic Features:
Neurofibrillary tangles: tangles of protein on the neurons
themselves.
Neuritic plaques: deposits of protein in the brain
Neural Degeneration: destruction of the neurons
o Pathologic features leads to:
o Neuron Death: when neurons die and get a loss of
neurotransmitters- the brain will atrophy
CM: Start with forgetfulness and emotional upset- they are going to get
upset that they are forgetting things.
Progressive CM: memory loss, confusion, mood changes, problem
solving, they become completely different
Increased intracranial pressure (ICP): caused by increase in intracranial
content
o Stage 1: no change in pressure due to body compensating. Blood vessels
in brain constrict in attempt to keep pressure low.
o Stage 2: Expansion of intracranial content.
Slight pressure rise and subtle CM
Will have change in LOC.
o Stage 3: Pressure continues to increase, becomes hypoxic and patient
deteriorates
o Pupil changes, respiratory changes, motor response changes
o Stage 4: Pressure in cranium is so high that brain tissue herniates
Herniation of brain tissue- the brain tissue goes somewhere else
( the foramen magnum)
Herniation= death
Cerebral edema: increase in the fluid content (intracellular or extracellular)
within the brain tissue itself.
o Occurs after brain injury
o **Vasogenic: Most common/important, increased capillary permeability
Brain got injured, inflammatory response became stimulated, get
vasodilation that increased capillary permeability and leaks fluid
into the tissue
