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HLSC 222 Pathophysiology 🧫 > Chapter 15 > Flashcards

Chapter 15 Flashcards

1
Q

What is cognitive behavioural functional competence?

A

Integrated processes of cognitive, sensory and motor systems

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2
Q

Full Consciousness

A

State of awareness of oneself and appropriate responses to the environment

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3
Q

What are the 2 components of Consciousness?

A

Arousal
Awareness

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4
Q

Arousal

A

State of awakeness

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5
Q

Awareness

A

Content of thought

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6
Q

How are structural alterations divided?

A

According to their location of dysfunction

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7
Q

What are the 2 divisions of structural alterations?

A

Supratentorial disorders
Infratentorial disorders

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8
Q

What are Supratentorial disorders?

A

Above tentorium cerebelli
-Produces changes in arousal

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9
Q

What are Infratentorial disorders?

A

Below tentorium cerebelli
-Produces decline in arousal by dysfunction of the reticular activating system or brainstem

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10
Q

What do metabolic alterations in arousal produce?

A

Disorders produce a decline in arousal by alterations in the delivery of energy substrates

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11
Q

What are the five patterns of neurological functions?

A
  1. Level of consciousness
  2. Pattern of breathing
  3. Pupillary reaction
  4. Oculomotor responses
  5. Motor responses
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12
Q

What is the most critical index of the nervous system function?

A

level of consciousness

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13
Q

What do changes in the level of consciousness indicate?

A

Indicate improvement or deterioration

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14
Q

What is the highest level of consciousness?

A

Person is alert and oriented to oneself, others, place and time

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15
Q

How does the level of consciousness diminish from the normal state level?

A

Normal state level —> confusion —> Disorientation —> Coma

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16
Q

What is normal breathing?

A

Rythmic pattern

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17
Q

How does breathing respond to consciousness diminishing?

A

Breathing responds to changes in PaCO2 levels

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18
Q

What is Cheyne-Stokes?

A

Altered period of tachypnea and apnea directly related to PaCO2

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19
Q

What are other patterns related to reduced arousal related to breathing?

A

Apneusis
Ataxic breathing

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20
Q

Apneusis

A

Prolonged inspiratory time and a pause before expiration

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21
Q

Ataxic breathing

A

Complete irregularity of breathing with increasing periods of apnea

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22
Q

What does Pupillary reaction indicate?

A

Presence/level of brainstem dysfunction

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23
Q

The brainstem area that controls arousal also controls?

A

Pupils

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24
Q

What happens to the pupils during Ischemia?

A

Dilated/fixed pupils

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25
Q

What happens to the pupils during Hypothermia or opiates?

A

Pinpoint pupils

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26
Q

What changes at various levels of brain dysfunction?

A

Oculomotor responses
-resting, spontaneous and reflexive eye movements

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27
Q

What is the normal oculomotor response?

A

Eyes move together to side opposite from the turn of the head

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28
Q

What is the abnormal oculomotor response?

A

Eyes do not turn together

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29
Q

What is the absent oculomotor response?

A

Eyes move in the direction of head movement

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30
Q

What is the caloric Ice water test?

A

Ice water is injected into the ear canal to test oculomotor responses

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31
Q

What is a normal oculomotor response to the caloric ice water test?

A

Eyes turn together to the side of the head where ice water is injected

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32
Q

What is an abnormal oculomotor response to the caloric ice water test?

A

Eyes do not move together

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33
Q

What is an absent oculomotor response to the caloric ice water test?

A

No eye movement

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34
Q

What do motor responses determine?

A

Determines brain function and indicates the most severely damaged side of the brain

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35
Q

What are the 3 possible patterns of motor response?

A
  1. Purposeful
  2. Inappropriate, generalized movement
  3. Not present
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36
Q

What do motor signs indicate a loss of?

A

Cortical inhibition

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37
Q

What does a loss of cortical inhibition mean?

A

Decreased consciousness associated with the performance of primitive reflexes and rigidity (paratonia)

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38
Q

What is vomiting, yawning and hiccups?

A

Complex reflex-like motor responses integrated in the brainstem

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39
Q

A compulsive/repetitive production of vomiting, yawning and hiccups is caused by what?

A

A dysfunction of medulla oblongata

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40
Q

What are the two categories of outcomes of alterations in arousal?

A

Disability (morbidity) and mortality

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41
Q

What do outcomes of alterations in arousal depend on?

A

Cause
Damage
Duration of coma

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42
Q

What happens to some individuals who never retain consciousness?

A

Neurological death

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43
Q

What are the 2 forms of neurological death?

A
  1. Brain death
  2. Cerebral death
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44
Q

What is the neurological determination of death (NDD)?

A

Total brain death

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45
Q

What is brain death/

A

Brain is damaged and can’t recover (irreversible) and can no longer maintain homeostasis

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46
Q

What is the Canadian criteria for NDD?

A
  1. Unresponsive coma
  2. No brainstem functions
  3. No spontaneous respiration (apnea)
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47
Q

What parts of brain die during cerebral death?

A

Cerebral hemispheres die
-Brainstem and cerebellum still alive

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48
Q

What is cerebral death?

A

Irreversible coma
Permanent brain damage in which an individual never responds in a significant way. May continue to maintain homeostasis

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49
Q

What are the cerebral death states?

A
  1. Persistent vegetative state
  2. Minimally conscious state (MSC)
  3. Locked in Syndrome
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50
Q

What is a persistent vegetative state?

A

Complete unawareness of self or environment
Does not speak
Sleep-wake cycles present
cerebral function absent

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51
Q

What is a Minimally conscious state (MSC)?

A

Follow simple commands
Manipulate objects
Give yes/no responses

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52
Q

What is locked in syndrome?

A

Complete paralysis of voluntary muscles except for eye movement
Intact content of thought and level of arousal
Fully conscious
Blinking = communication

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53
Q

What is awareness?

A

Content of thought

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54
Q

What does awareness encompass?

A

All cognitive function

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55
Q

What mediates awareness?

A

Executive Attention Networks (EAN)

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56
Q

What are Executive Attention Networks (EAN)?

A

Networks include selective attention and memory and involve abstract reasoning, planning, decision-making, judgement and self-control

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57
Q

What is selective attention (orienting)?

A

Ability to select specific information and focus on related specific task
Also includes selective visual and auditory attention

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58
Q

What are the 3 executive attention deficits?

A

Initial detection
Mild deficit
Severe deficit

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59
Q

What is the initial detection of executive attention deficits?

A

Person fails to stay alert and orientate to stimuli

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60
Q

What is a mild deficit?

A

Grooming and social graces are lacking

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61
Q

What is a severe deficit?

A

Motionless
Lack of response
Doesn’t react with surroundings

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62
Q

What are some characteristics of executive attention deficits?

A

Inability to maintain sustained attention and inability to set goals and recognize when the goal is achieved

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63
Q

What is memory?

A

Recording, retention and retrieval of information

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64
Q

What is amnesia?

A

Loss of memory

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65
Q

What is retrograde amnesia?

A

Difficulty retrieving past memories

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66
Q

What is anterograde amnesia?

A

Inability to form new memories

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67
Q

What are Data-processing deficits?

A

problems associated with recognizing and processing sensory information

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68
Q

What are the 5 states of data-processing deficits?

A
  1. Agnosia
  2. Dysphasia
  3. Acute Confusional State and delirium
  4. Dementia (Alzheimer’s)
  5. Frontotemporal Dementia
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69
Q

What is Agnosia a defect of?

A

Pattern recognition

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70
Q

What is Agnosia?

A

Failure to recognize the form and nature of objects
-Normally one sense affected

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71
Q

Example of agnosia?

A

Unable to identify a safety pin by touching it but able to name it when looking at it

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72
Q

What is agnosia associated with?

A

Cerebrovascular accidents in specific brain areas

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73
Q

What is Dysphasia?

A

Impairment of comprehension or production of language

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74
Q

What are the two types of dysphasia?

A

Expressive dysphasia
Receptive dysphasia

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75
Q

What area of the brain is affected to cause expressive dysphasia?

A

Broca’s area

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76
Q

What is expressive/Broca dysphasia?

A

Loss of ability to produce spoken or written language
-Verbal comprehension is usually present

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77
Q

What area of the brain is affected to cause Receptive dysphasia?

A

Wernicke’s area

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78
Q

What is Receptive/Wernicke dysphasia?

A

inability to understand written or spoken language
Speech is fluent but words and phrases have no meaning

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79
Q

The pathology of dysphasia is due to what?

A

The occlusion of the middle cerebral artery

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80
Q

What is the middle cerebral artery?

A

One of three major arteries supplying blood to the brain

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81
Q

What are the Acute Confusional States and Delirium?

A

Transient disorders of awareness may have a sudden or gradual onset.

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82
Q

What causes acute confusional states and delirium?

A

Drug intoxication, alcohol withdrawal, post anesthesia
and electrolyte imbalance

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83
Q

What areas of the brain are disrupted to cause acute confusional states?

A

Reticular system
Thalamus
Cortex
Limbic system

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84
Q

What is delirium?

A

Hyperactive Acute confusional state

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85
Q

Where does delirium most commonly occur?

A

In Critical Care units over 2-3 days

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86
Q

What is disrupted to cause delirium?

A

Neurotransmitters: acetylcholine and dopamine

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87
Q

What is Excited Delirium Syndrome?

A

AKA agitated delirium
Hyperkinetic delirium that can lead to sudden death

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88
Q

What are the signs/symptoms of Excited Delerium Syndrome?

A

Rapid breathing
High pain tolerance
Superhuman strength

89
Q

How does delirium manifest?

A

Terrifying dreams
Hallucinations
Gross alteration of perception
Individuals can’t sleep

90
Q

How is delirium evaluated?

A

CAM-ICU: Confusion Assessment Method for Intensive Care Unit (ICU)

91
Q

What is dementia?

A

Deterioration/progressive failure of many cerebral functions

92
Q

What causes dementia?

A

Cerebral neuron degeneration, atherosclerosis and genetics

93
Q

Does dementia have a cure?

A

No specific cure exists
-help the family to understand

94
Q

How is dementia treated?

A

Maximizing remaining capacities

95
Q

What is Alzheimer’s disease?

A

The leading cause of severe cognitive dysfunction in older adults

96
Q

What is the cause of Alzheimer’s?

A

The exact cause is unknown

97
Q

What are the three forms of Alzheimer’s?

A
  1. Nonhereditary sporadic late-onset AD
  2. Early-onset Familial AD
  3. Early-onset AD
98
Q

What is the most common form of Alzheimer’s?

A

Nonhereditary sporadic late-onset AD
70%-90%
-Has no specific genetic association

99
Q

What is early-onset familial AD linked to?

A

Chromosomal 21 mutations

100
Q

What form of Alzheimer’s is very rare?

A

Early-onset AD

101
Q

What is Early-onset AD linked to?

A

Chromosomal 19 mutations

102
Q

What is the same across all forms of Alzheimer’s?

A

Pathological alteration

103
Q

What accumulates to lead to Alzheimer’s?

A

Accumulation of toxic fragments of amyloid plagues

104
Q

What is there a loss of to lead to Alzheimer’s?

A

Loss of acetylcholine in forebrain cholinergic neurons

105
Q

What are amyloid plagues?

A

Aggregates of misfolded proteins

106
Q

What happens when there is a loss of acetylcholine in forebrain cholinergic neurons?

A

Death of neurons

107
Q

What increases neural death to cause Alzheimer’s?

A

Tau proteins (microtubule) form neurofibrillary tangles within the neuron

108
Q

Where are neuroibrullary tangles concentrated?

A

In the cerebral cortex

109
Q

As neural death increases what happens to the brain?

A

Brain atrophy via widening of sulcus and shrinking of gyrus

Sulcus = grooves
Gyrus = Folds on the outermost layer of the brain

110
Q

What are the first symptoms of Alzheimer’s?

A

Memory loss
Impaired learning

111
Q

How do symptoms of Alzheimer’s continue?

A

Decrease in language, reasoning, social behaviour, dyspraxia (loss of movement and coordination) may occur

112
Q

What is ALzheimer’s progression of?

A

Short-term memory loss to total loss of cognitive function

113
Q

When can pathophysiological changes occur in dementia?

A

Decades before dementia

114
Q

What is Frontotemporal dementia?

A

Previously known as Pick Disease

115
Q

What is the second most common form of dementia?

A

Frontotemporal dementia

116
Q

What is Frontotemporal dementia an umbrella term for?

A

Disorders that affect frontal and temporal regions of the brain

117
Q

What are the first symptoms of Frontotemporal dementia?

A

Apathy
Poor judgement/reasoning
Break laws

118
Q

Does genetics determine frontotemporal dementia?

A

There is a genetic component

119
Q

When does the onset of frontotemporal dementia occur?

A

At less than 60 years old

120
Q

What genes are mutated in frontotemporal dementia?

A

Mutation of tau encoding genes

121
Q

What do seizures represent?

A

Represent a manifestation of a disease, not a specific

122
Q

What are seizures?

A

Sudden disruption in brain electrical function caused by abnormal excessive discharges of cortical neurons (interneurons)

123
Q

What is Epilepsy?

A

Recurrence of seizures where no known cause for seizures can be found

124
Q

What are convulsions?

A

Jerky, contact-relax movements associated with seizures?

125
Q

What is the probable cause of seizures in young adults?

A

Alcohol/drug withdrawal
Brain tumour
Peri-natal insults (occurring between 28 weeks of gestation to 28 days after birth)

126
Q

What is the probable cause of seizures in older adults?

A

Alcohol/drug withdrawal
Metabolic disorders
CNS degeneration

127
Q

What is the epileptogenic focus?

A

Brain site where the seizure originates
-aka Epileptogenic zone

128
Q

What happens to neurons in the epileptogenic focus?

A

They are hypersensitive and activated by numerous stimuli
Fire more frequently and with greater amplitude than other neurons

129
Q

During a seizure what can the focus be determined by?

A

Activated SPECT
-a test that detects blood flow changes in the brain

130
Q

What are the 2 phases of a seizure?

A

Tonic
Clonic

131
Q

What is the tonic phase?

A

Muscle contraction with increased muscle tone
– associated with loss of consciousness

132
Q

What is the clonic phase?

A

Alternating contraction and relaxation of muscles

133
Q

What does the clonic phase begin with?

A

Begins when inhibitory neurons in thalamus and basal ganglia react to cortical excitation

134
Q

What is the result of the clonic phase?

A

Seizure discharge is interrupted = intermittent contractions that diminish and finally cease

135
Q

If the number of seizures increases, what else increases?

A

Brain damage

136
Q

How do seizures end?

A

Epileptogenic neurons are exhausted

137
Q

What happens to the brain during the clonic phase?

A

Reduced oxygen causes a switch to anaerobic metabolism and an accumulation of lactic acid

138
Q

What are the 3 injury states that Cerebral Blood Flow (CBF)?

A
  1. Inadequate cerebral perfusion
  2. Normal perfusion but with elevated intracranial pressure (ICP)
  3. Excessive blood volume (CBV)
139
Q

What is normal ICP?

A

1-15 mmHg

140
Q

How does increased ICP occur?

A

Increase in intracranial content
-Tumour, edema, hemorrhage, etc.

141
Q

What is displaced to try to make room for the increased intracranial content?

A

Cerebral spinal fluid

142
Q

What happens when high ICP continues?

A

Alterations in cerebral blood volume and blood flow

143
Q

What is the result of increased ICP?

A

Four stages of ICP that lead to Death

144
Q

What is Stage 1 increased ICP?

A

Cranial vasoconstriction and systemic adjustments result in a decrease in ICP
ICP does not increase due to these compensations
No detectable symptoms of ICP

145
Q

What is Stage 2 increased ICP?

A

Continual expansion of intracranial contents = ICP exceeds compensatory mechanisms
Pressure begins to affect neuron oxygenation
Manifestations of confusion, restlessness and lethargy
Pupils and breathing remain normal
Surgical intervention is best here

146
Q

What is Stage 3 increased ICP?

A

Autoregulation: mechanism to alter diameter of intracranial blood vessels to
maintain a constant blood flow during changes in ICP
˜ Autoregulation is lost in Stage 3 = ICP approaches arterial pressure
˜ Severe hypoxia, hypercapnia and acidosis occur = severe deterioration of individual condition
˜ Pupils: small, sluggish
˜ Widening of pulse pressure
˜ Manifestations of loss of peripheral vision/blindness, tinnitus
˜ Surgical intervention needed here

147
Q

What is stage 4 increased ICP?

A

˜ Brain tissue shifts (herniates) from greater pressure to lesser pressure
˜ Herniated brain tissue = reduction in blood supply
˜ Herniations rapidly increases ICP
˜ Pupils: progress to bilateral dilation and fixation
˜ Breathing: Cheyne-Stokes breathing /Mental status: progresses to deep coma
˜ Surgical intervention futile here / Death occurs

148
Q

What are the 3 types of cerebral edema?

A

Vasogenic edema
Cytotoxic (metabolic) edema
Interstitial edema

149
Q

What is most important type of edema?

A

Vasogenic

150
Q

What causes vasogenic edema?

A

Increased capillary permeability
Disruption of BBB

151
Q

What leaks into cranial ECF during Vasogenic edema?

A

Plasma proteins/fluid

152
Q

What happens when fluid accumulates in white matter during vasogenic edema?

A

Separation of myelinated fibers

153
Q

How does Vasogenic edema manifest?

A

Consciousness disturbances and increases in ICP

154
Q

What is the resolution to Vasogenic edema?

A

Slow diffusion

155
Q

What is brain edema?

A

Lateral ventricles compressed (long
arrows)
Gyri flattened (short arrows)

156
Q

What is cytotoxic (metabolic) edema?

A

Toxic factors affect neural, glial, and endothelial cells = loss of active transport mechanisms
= loss of K+ and gain large amounts of Na+ = change in intracellular osmolarity = cells swell

157
Q

What is interstitial edema?

A

Movement of cerebral spinal fluid from ventricles into interstitial space = edema

fluid volume increases around ventricles = increased pressure within white matters = disappearance of myelination

158
Q

What is Hydrocephalus?

A

Condition of excess cerebral spinal fluid (CSF) in
ventricles or subarachnoid space.

159
Q

What causes Hydrocephalus?

A

Increased CSF production
obstruction in ventricles
defective reabsorption of CSF fluid into systemic blood

160
Q

What are the types of Hydrocephalus?

A

Communicating
Noncommunicating

161
Q

What does ‘communicating’ mean?

A

refers to fact that CSF can still flow between the ventricles

162
Q

Who is affected by communicating hydrocephalus?

A

Infancy through adulthood

163
Q

What is communicating hydrocephalus?

A

Impaired absorption of CSF from
subarachnoid space

164
Q

What causes communicating hydrocephalus?

A

Infection

165
Q

Who is affected by noncommunicating hydrocephalus?

A

Adults

166
Q

What is noncommunicating hydrocephalus?

A

Obstruction of CSF between ventricles

167
Q

What causes noncommunicating hydrocephalus?

A

Congenital
-present from birth

168
Q

What leads to Hydrocephalus (HC)?

A

Obstruction of CSF flow = increase pressure and dilation of ventricles
= atrophy of cerebral cortex and degeneration of white matter

169
Q

How does acute hydrocephalus manifest?

A

Rapidly developing ICP = deep coma

170
Q

How does normal pressure HC manifest?

A

Dilation of ventricles without increased pressure
HC develops slowly
Family notices declines in memory, etc.
Progression to triad symptoms: broad- based gate / falling / incontinence

171
Q

How is Hydrocephalus treated?

A

Shunting procedure

172
Q

What is the shunting procedure?

A

Shunt used for ventricular bypass into normal intracranial/extracranial channels where fluid can be absorbed
-One of three most common neurosurgical procedures

173
Q

What is normal muscle tone?

A

Slight resistance to passive movement
resistance is smooth, constant, and even.

174
Q

What is Hypotonia?

A

Decreased muscle tone
Tire easily
Difficulty rising from a sitting position
Muscle mass atrophy/muscles appear flabby and flat
Joints hyperflexible (can acquire positions requiring extreme joint mobility)

175
Q

What is Hypertonia?

A

Increased muscle tone
Passive movement occurs with increased
resistance
Symptoms: enlargement of muscle mass, development of firm muscles, muscle spasms

176
Q

What causes alterations in Muscle Movement?

A
  1. Neurotransmitter dopamine involved in several disorders (too little or too much dopamine)
  2. Other disorders are neurological disorder = excessive or insufficient movement
177
Q

What is Hyperkinesia?

A

Excessive, purposeless movement

178
Q

What are the 3 types of Hyperkinesia?

A

Paroxysmal dyskinesias
Tardive dyskinesias
Ballism

179
Q

What is Paroxysmal dyskinesias?

A

Involuntary movements that occur as spasms

180
Q

What is Tardive dyskinesias?

A

Involuntary movement of face, lips, tongue and extremities

181
Q

What causes tardive dyskinesias?

A

Prolonged antipsychotic medication use

182
Q

What is a characteristic of tardive dyskinesias?

A

Rapid, repetitive stereotypical movements
-Continually chewing, or tongue protrusions

183
Q

What syndrome is associated with tardive dyskinesias?

A

Tourette Syndrome

184
Q

What is Ballism?

A

Muscle disorder with wild, flinging movement of limbs

185
Q

What is the other name for Huntington’s disease?

A

Chorea

186
Q

What is HD symptoms the hallmark of?

A

Hyperkinesia

187
Q

What is Huntington’s disease?

A

relatively rare degrative hyperkinetic disorder

188
Q

What part of brain is involved in Huntington’s?

A

Basal ganglia and cerebral cortex

189
Q

When is the onset of HD?

A

25-45 years old

190
Q

What is the most common manifestation of huntington’s disease?

A

Begins in face and arms and eventually whole body is affected

191
Q

What are manifestations of HD?

A

Thinking is slow
Alterations in euphoria and depression are common
Involuntary fragmented movements

192
Q

How does one get Huntington’s?

A

Inherited
-Autosomal dominant trait

193
Q

What causes Huntington’s?

A

Mutation in chromosome 4 results in abnormally long protein caused by a cytosine-adenine-guanine (CAG) trinucleotide

194
Q

The altered amino acid chain in HD does what to neurons?

A

It is toxic to neurons

195
Q

How is the age of onset of HD determined?

A

by the number of repeated amino acid chains

= increased chains = increased toxicity of protein = earlier age of onset.

196
Q

How many repeats does a healthy gene have vs HD gene?

A

Healthy = 10-26 repeats
HD = 37-80

197
Q

What is Hypokinesia?

A

Decreased movement
Loss of voluntary movement despite preserved consciousness

198
Q

What are the 2 types of Hypokinesia?

A

Akinesia
Bradykinesia

199
Q

What is Akinesia?

A

lack of spontaneous movement (facial expressions) or associated movements (arm swinging while walking)

200
Q

What is Bradykinesia?

A

Slowing of movement

201
Q

What is Parkinson’s?

A

Complex motor disorder accompanied by systemic nonmotor and neurological symptoms

202
Q

What is Primary parkinson’s?

A

Begins after 40 yoa with increased incidence after 60 years old

-Leading cause of neurological disability in people over 60 yoa

203
Q

What is Secondary PD?

A

Parkinson’s caused by disorder other than PD (head trauma, infections, toxins, medication intoxication)

204
Q

What is the most common secondary PD?

A

Medication intoxication
-Most often reversible

205
Q

What medications lead to medication intoxication?

A

-Neuroleptics: antipsychotics (treat hallucinations, delusions, etc.)
-Antiemetics: prescribed to address nausea and vomiting
-Anti-hypertensives

206
Q

What is Parkinson’s disease due to?

A

Several gene mutations

207
Q

What causes PD?

A

Basal ganglia dysfunction due to misfolded proteins

208
Q

What do misfolded proteins due in regards to PD?

A

Loss of dopamine-producing neurons in substantia nigra

209
Q

What causes tremors and rigidity associated with PD?

A

Loss of dopamine (inhibitory neurotransmitter) and excess production of cholinergic (excitatory neurotransmitters)

210
Q

What is the classic manifestation of PD?

A

resting tremor, rigidity, bradykinesia
(slowness of movement), dysarthria

211
Q

Dysarthria

A

loss of control of muscles you speak
with = slurring speech

212
Q

What can be an early symptom of PD?

A

Loss of smell

213
Q

What can’t people with PD make adjustments to?

A

Tilting
-Fall like a post

214
Q

What is the principal feature of ALS/Lou Gehrig’s?

A

Degeneration of both lower and upper motor neurons

215
Q

What happens to upper motor neurons in ALS?

A

Decrease in large motor neurons in CNS
-Motor neurons death results in demyelination and glia proliferations and sclerosis (scarring)

216
Q

What happens to lower motor neurons in ALS?

A

Denervation of motor units

217
Q

How does ALS manifest?

A

-Muscle weakness starting in arms and legs and
progressing to difficulty speaking and swallowing
-No associated mental or sensory symptoms

218
Q

How is ALS treated?

A

Medication Rilutek extends time before ventilatory
assistance is required

HLSC 222 Pathophysiology 🧫 (16 decks)

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