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Year Two > Semester One - Cognition and Perception > Flashcards

Semester One - Cognition and Perception Flashcards

1
Q

What is described as the fifth vital sign?

A

Pain.

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2
Q

What are the two components of pain?

A
  • The physical:
    Sensation of pain – nociceptors are pain receptors involving PNS and CNS
  • The psychological
    Emotional responses to pain sensation
    Pain is fairly consistent in humans but perception is influenced by other factors
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3
Q

What can influence the experience of pain?

A

Culture, age, gender, previous experiences of pain (pain management), peer influence, stress/anxiety.

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4
Q

What are the classifications of pain?

A
  • Acute
  • Chronic
  • Nociceptive somatic
  • Nociceptive visceral
  • Neuropathic
  • Psychogenic
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5
Q

What is the difference between nociceptive somatic pain and nociceptive visceral pain?

A
  • Viseral pain comes from the tissue associated with the internal organs
  • Somatic pain comes from the skin and deep tissues.

Nociceptive pain is caused by normal activation of neural pathways in response to potentially tissue-damaging stimuli.

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6
Q

What are the four basic processes involed in nociception?

A

TRANSDUCTION: stimulus detected by the nociceptive receptors
TRANSMISSION: Messages relayed from the receptors in the CNS
PERCEPTION: Brain perceives the sensation of pain
MODULATION: messages are modified by other activity

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7
Q

What key things are involved in pain assessment?

A
  • Assessment of the factors that may influence a patients experience and expression of pain
  • Awareness of the barriers that may affect nurses assessment and management of pain - knowledge, attitudes and beliefs about pain and the nurses experience
  • Accurate documentation of pain - assessment, management and re-evaluation
  • Use of pain assessment tools
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8
Q

What does PQRST stand for in relation to pain assessment?

A

P – Provocation/palliation – what makes it better or worse
Q – Quality/Quantity – burning, shooting, sharp, dull, nagging
R – Region/radiation – where is it? Where does it travel too.
S – severity
T – timing – how long does it last? When did it start? Is it constant?

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9
Q

How is a pain impulse generated?

A

Transduction.
- Pain impulse is generated by an exchange of sodium and potassium ions (de-polarisation and re-polarisation) at the cell membranes

  • Results in an action potential
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10
Q

What parts of the nervous system are responsible for pain perception?

A
  • The reticular system: This is responsible for the autonomic and motor response to pain and for warning the individual to do something
  • Somatosensory cortex: This is involved with the perception and interpretation of sensations
  • Limbic system: Responsible for the emotional and behavioural responses to pain
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11
Q

What are some barriers to pain management?

A
  • Lack of or inadequate pain assessment
  • Lack of agreement between nurse and patient about the patient’s level of pain, resulting in inadequate analgesia being given
  • Failure to recognise and respond to a patient’s pain
  • Failure to administer prescribed doses of medication
  • Lack of knowledge and misconceptions
  • Patienec reluctance to report pain
  • Concerns regarding addiction
  • Concerns regarding side-effects
  • A belief that pain is inevitable
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12
Q

Why do a neurological assessment? What is being monitored?

A
  • As part of an initial assessment to establish baseline recordings
  • Determine changes
  • Deterioration
  • Stability
  • Improvement
  • Identify neurological problems
  • Identify life threatening situations
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13
Q

What are some early signs of raised ICP?

A
  • Altered mental state
  • Headache
  • Vomiting (often projectile, without nausea)
  • Pupillary changes
  • Ptosis (drooping of eyelid), palsy of the 3rd and 6th cranial nerves
  • Sudden restlessness or quietness
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14
Q

What are some later signs of raised ICP?

A
  • Motor changes (hemiparesis),
  • Raised blood pressure and widening pulse pressure,
  • Slow irregular pulse
  • Seizures
  • Diaphoresis (sweating)
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15
Q

What is ‘Cushing’s triad’?

A

Cushing’s triad describes the physiological nervous system response to increased (ICP) that results in

  1. Hypertension (progressively increasing systolic blood pressure)
  2. Bradycardia
  3. Widening pulse pressure (an increase in the difference between systolic and diastolic pressure over time)
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16
Q

What does AVPU stand for?

A

A - alert
V - voice, unresponsive to voice?
P - pain, unresponsive to pain?
U - unresponsive

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17
Q

What is the ‘Glasgow Coma Scale’?

A 
Used to assess conditions where consciousness levels are in question
Assesses:
Eye responses : 1- 4
Verbal response: 1 -5
Best motor response : 1-6

Lowest = 3 / Highest = 15

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18
Q

When giving a verbal handover, what does ISBAR stand for?

A 
I - introduction 
S - situation 
B - background 
A - assessment 
R - reccomendation
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19
Q

What are some early signs of neurological deterioration?

A
  • Altered level of consciousness
  • Reflexes (pupillary light reflex, knee jerk)
  • Verbal response
  • Motor response
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20
Q

During transmission what are the two fibres involved and what kind of pain is associated with them?

A

C Fibres:

  • Dull
  • Burning
  • Aching
  • Referred to as slow or second pain

A-delta fibres:

  • Well-localised
  • Sharp
  • Stinging
  • Pricking
  • Referred to as fast or first pain
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21
Q

Vomiting is a protective mechanism. What are three things that can cause vomiting?

A
  • noxious stimuli
  • bacteria
  • vestibular distirbunces
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22
Q

What is ‘emisis’?

A

It means ‘to vomit’

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23
Q

What neurotransmitters are involved in vomiting? (6)

A
  • dopamine (D2): toxin stimulated vomit
  • acetylcholine (M1): motion sickness
  • histamine (H1): motion sickness
  • opioids
  • serotonin (5-HT3): stomach, intestine stimulated vomit
  • substance P (NK1): toxin stimulated vomit
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24
Q

How does the vestibular system (motion sickness) cause nausea and vomiting?

A
  1. Stimulation of the labrynth (inner ear) and along vestibular nerve and in to vestibular nuclei (in brain stem)
  2. Vestibular nuclei have M1 and H1 receptors.
  3. Activation of this causes a stimulation in the chemorecpetor trigger zone which simulates the vomit center - making the person vomit.
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25
Q

How do toxins cause nausea and vomiting?

A

The chemoreceptor trigger zone is situated in the medulla outside of the blood-brain barrier. This means it is able to detect toxins in the blood.
When toxins are present, the CTZ is activated - stimulating the vomit centre making the person vomit.

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26
Q

How does the stomach, intestines etc. cause vomiting?

A

Seratonin receptors and sensory nerve fibres send messages to the chemoreceptor trigger zone stimulating the the vomit centre, making the person vomit. Caused by food poisoning etc.

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27
Q

If vomiting is because of things related to higher centers, what is usually the cause?

A

Smell, taste, memory, anxiety, disgust.

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28
Q

How does metaclopromide stop/reduce/prevent vomiting and nausea?

A

Due to its antagonist activity at D2 receptors in the chemoreceptor trigger zone in the central nervous system. It prevents nausea and vomiting triggered by most stimuli. At higher doses, 5-HT3 antagonist activity may also contribute to the antiemetic effect.

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29
Q

How can opiods cause vomiting and nausea? (3)

A
  • Increased vestibular sensitivity
  • Direct effect on CTZ
  • Delayed gastric emptying
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30
Q

Metaclopromide is used for nausea and vomiting. In which situations could it be effective?

A
  • chemotherapy
  • radiation
  • delayed gastric emptying
  • PONV
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31
Q

How does ondansetron stop/reduce/prevent nausea and vomiting?

A

Ondansetron is a serotoin antagonist.

Selective serotonin antagonists inhibit visceral effect and CTZ stimulation in the small bowel, vagus nerve, CTZ.

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32
Q

How can an antihistamine stop/reduce/prevent nausea and vomiting?

A

Used for motion sickness, vestibulocochlear disease
- Decrease Ach (acetylcholine) stimulation
- Block H1 receptors
= No transmission of signal to vomit centre

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33
Q

Pathopysiology impacting on cognition and perception fall in to which six categories?

A
  • Infection
  • Autoimmune
  • Neurodegenerative
  • Space occupying lesions
  • Trauma
  • Cardiovascular
34
Q

What can cause a raised ICP?

A 
Aneurysm
Subarachnoid haemorrhage
Tumour
Encephalitis
Traumatic brain Injury (TBI)
Hydrocephalus 
Intraventricular haemorrhage
Meningitis
Subdural hematoma
Status epilepticus
Stroke
35
Q

What is the pathophysiology of Alzeimer’s?

A
  • Plaques develop and commonly occur in the hippocampus and in other areas of the cerebral cortex
  • Neuron destruction and loss of brain tissue
  • Loss of acetylcholine
36
Q

How are abcess and empyemas of the nervous system treated?

A
  • Antibiotic therapy
  • Surgery to drain the infected site-this allows immediate relief of pressure on the brain or spinal cord
  • Sample is taken for bacterial identification-drug therapy can be altered to a more specific antibiotic.
37
Q

What are some common features of neurodegenerative conditions?

A 
Insidious onset
Fatigue
Delayed and/or difficult diagnosis
Progress may be very rapid eg MND or over a period of many years eg. MS, Huntington's Disease
Mobility issues
Communication issues
Cognition
Continence
Nutrition
Breathing/secretions
38
Q

What is the difference between agonist and antagonist?

A
  • Agonist: a substance that fully activates the neuronal receptor that it attaches to
  • Antagonist: a substance that attaches to a receptor but does not activate it or if it displaces an agonist at that receptor it seemingly deactivates it thereby reversing the effect of the agonist.
39
Q

What is bipolar disorder?

A

A mood disorder associated with recurrent (one or more) episodes of mania, or mixed episodes of mania and depression.

40
Q

What are some symptoms of bipolar disorder?

A

Grandiosity, depression, racing thoughts, distorted perception, risk taking behaviour

41
Q

What are the neurotransmitters involved in bipolar disorder?

A

serotonin, dopamine, norepinephrine, GABA

42
Q

What are symptoms of depression?

A

low mood, tearfulness, feelings of helplessness, hopelessness, loss of interest in activities, appetite or weight changes, sleep changes, anger or illritability, loss of energy, self-loathing, reckless behaviour, recurrent thoughts of death

43
Q

What is SIGECAPS?

A

An assessment tool for mood disorder symptoms.

S - Sleep 
I - interest (lack of)
G - guilt, low self esteem 
E - energy (lack of) 
C - concentration (lack of)
A - apetite 
P - psychomotor (agitated/retardation)
S - suicidal ideation/thoughts of death
44
Q

What can cause manic and depressive episodes?

A

Stress, lack of sleep, subtance abuse, conflict.

45
Q

What does SSRI stand for and what does it do?

A

Selective serotonin reuptake inhibitors (SSRI)

Acts as a re-uptake inhibitor of the neurotransmitter serotonin by blocking the action of the serotonin transporter.

46
Q

What does SRNI stand for? What does it do?

A

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)

Blocks reuptake of serotonin and norepinephrine, increasing concentration in the synapse.

47
Q

How do tricylic antidepressants work?

A

Inhibits the reuptake of serotonin and norepinephrine at the neuronic synapses.

48
Q

What is lithium for and what does it do? How are the levels monitored?

A

Bipolar disorder.
Lithium carbonate provides a source of lithium ions that may act by competing with sodium ions at various sites in the body. Therapeutic range is 0.8-1.6 – blood test every three months

49
Q

What are some side effects of lithium?

A
  • Thirst
  • Nausea
  • Frequent urination
  • Weight gain
  • Toxicity can occur
50
Q

What are the neurotransmitters involved in depression?

A
  • serotonin
  • dopamine
  • noradrenaline
51
Q

What are some signs and symptoms of serotonin syndrome?

A

Triad of clinical features -
Cognitive effects: headache, agitation, hypomania, mental confusion, hallucinations, coma
Autonomic effects: shivering, sweating, hyperthermia, vasoconstriction, tachycardia, nausea, diarrhea.
Somatic effects: myoclonus (muscle twitching), hyperreflexia (manifested by clonus), tremor.

Generalised hyperreflexia most important neurological sign (overresponsive reflexes)

52
Q

Glutemate

A
  • Excitatory neurotransmitter, acts as accelerator in the brain
  • Closely associated with GABA, balance between the two is important
53
Q

GABA

A
  • The main inhibitory neurotransmitter
  • Acts as a ‘break’ in the brain
  • Too little and the person may become anxious and excited, too much and the person becomes drowsy and sedated
  • Used in seizure medication
  • Opens ion channels = hyperpolarisation
54
Q

Serotonin

A

Serotonin

  • Inhibitory
  • Blood pressure
  • Gut control
  • Nausea
  • Controls mood
  • Anxiety
  • Emotions
  • Sleep/wakefulness
  • Feeding
  • Temperature control
  • Associated with schizophrenia
55
Q

Histamine

A
  • Inhibitory monoamine
  • Sleep, wakefulness
  • Hormonal secretions
  • Cardiovascular control
  • Thermoregulation
  • Food intake
  • Memory formation
  • Mediation of allergy and inflammation
  • Usually associated with allergies
  • Involved in neurotransmission affecting emotions and behavior
  • Sleep wake cycles
56
Q

Dopamine

A
  • Involved in regulation of emotions
  • Cognition
  • Motor function
  • Perception
  • Parathyroid secretions
  • Pituitary hormone secretion
  • Several regions of brain
  • Inhibitory and excitatory
  • Coordination of voluntary body movements
  • Behaviour
  • Motivation, reward and reinforcement
  • Sleep, dreaming, mood, attention, memory, learning
57
Q

Epinephrine and norepinephrine

A
  • Controls blood pressure
  • Myocardial contractility and force
  • Airway reactivity
  • Variety of metabolic functions
  • In CNS they control sleep/wakefulness, arousal, mood, emotion and drive.
  • Main neurotransmitter of the sympathetic nervous system
  • Key determinant of responses to metabolic or global challenges to homeostasis
  • Adrenaline is the main hormone secreted by the adrenal medulla
  • Responsible for tonic and reflexive changes in cardiovascular tone
  • Excitatory or inhibitory
  • Affects behavior: modulation of vigilance, arousal, attention, motivation, reward, and also learning and memory
58
Q

Acetylcholine

A
  • Involved in muscle contraction
  • Bradycardia
  • Negative inotropy (decrese cardiac contractility)
  • Exocrine secretion (saliva, sweat)
  • Brain and spinal cord
  • Neuromuscular junction of skeletal muscle
  • Memory
  • Wakefullness
  • Sexuality
  • Thirst
  • Associated with Alziemer’s disease and myasthenia gravis
  • It is responsible for much of the stimulation of muscles, including the muscles of the gastro-intestinal system.
  • It is also found in sensory neurons and in the autonomic nervous system, and has a part in scheduling REM (dream) sleep.
59
Q

How do opiods work?

A
  • When there is pain, signals move from the presynaptic neuron to post synaptic neurons.
  • Opioid particles attach to Mu receptor causing release of GABA which is picked up by presynaptic neuron.
  • This causes an increase in release of dopamine.
  • Opioids slow and block the Mu receptor from transmitting its signals meaning the pain signal is stopped.
60
Q

What is the difference between excitatory and inhibitory neurotransmitters?

A

Excitatory – produce depoalrisation

Inhibitory – decreased ability to produce action potential

61
Q

What is Parkonson’s disease associated with?

A 
Depletion of dopamine
Loss of  inhibitory neurotransmitter
Increased activity of ACH
Onset insidious
Depression
inappropriate sweating, orthostatic hypotension gastric retention, constipation urinary retention
Disorders of equilibrium:
Postural adjustments
Fall like a post
Festinating gate
Unable to upright self
Reflex status, sensory status and mental status all intact
62
Q

Describe the pathway of pain:

A
  1. Noxious stimuli eg. nail stabbing skin
  2. Chemicals are released stimulating nociceptors.
  3. They send a message to spinal cord from dorsal horn.
  4. Nocicptors relsease substance P and glutemate
  5. Second order neuron recieves in the info and takes it to the thalamus.
  6. Sensation then travels to the cerbral cortex - awareness of pain
63
Q

How does pain relief work in the pain pathway?

A

The pain signals that travel to the brain will cause the release of neurotransmitters called endorphins (endorphins are endogenous opiod)

These endorphins are released from the hypothatamus and pituitary. The hypothalamus is responsible for maintaining homeostasis.

So basically the pain is causing uneven equilibrium so therefor the endorphins are released.

The endorphins then land on their appropriate receptors ie the mu receptors. The sends a message to calm the nerve response by inhibiting the release of substance P

64
Q

What are some common side effects of opiods?

A
  • dizziness
  • sedation
  • constipation
  • nausea
  • respiratory depression
65
Q

What is psychosis

A
  • impaired reality testing; unable to distinguish personal subjective experience from the reality of the external world
  • Psychosis is a cluster of symptoms comprising one or more of the following:

Hallucinations
Delusions
Disorganised thoughts and behaviour

66
Q

What is the prodromal phase of schizophrenia associated with?

A
  • changes in behaviour and perception, known as a ‘prodrome’
  • Often evident in early adolescence. The prodromal period can last up to two years.

Symptoms include:

  • Worsening of usual work or school performance
  • Worsening intellectual and organisational functioning
  • Social withdrawal
  • Emerging unusual beliefs
  • Changes in perception such as experiencing instances of hearing sounds/voices not heard by others.
67
Q

What is the acute phase of schizophrenia associated with?

A

Acute phase may be preceded by days/weeks of deteriorating behaviour leading to intense emotional and psychological upheaval, and symptoms such as:

  • Hallucinations (mainly auditory)
  • Delusional thinking
  • Disorganized or bizarre behaviour,
  • Social and emotional withdrawal poor self care
  • Anxiety, paranoia, depression or euphoria may be seen
68
Q

In mental health what is the difference between positive and negative symptoms?

A

Positive symptoms are experiences that happen in addition to normal experience.

Negative symptoms incorporate a loss or decrease in normal functioning.

69
Q

What is an addiction?

A
  • An overwhelming compulsion to continually use a substance and a resulting drive to obtain it by any means necessary.
    • ‘tolerance’- over time a person will need increased amounts of the substance to get the desired effect
  • A high tendency to relapse even when the person has broken the cycle of habitual use for a period of time.
  • psychological and/or physical dependence on a substance where the person experiences withdrawal pain or discomfort when unable to obtain the substance
  • Use of the substance has a negative/ detrimental effect on the individual and/or society
70
Q

How do depressants work and what are some examples?

A

Depressants are substances that inhibit or depress the activity of the CNS (central nervous system). They are sometimes referred to as ‘downers’ because of their sedative effects. Depressants increase the effects of GABA receptors thereby increasing GABA’s inhibitory effects. It also reduces the ability of glutamate to excite a cell.

Depressants can decrease respirations and heart rate.

Examples of depressants:
Alcohol, benzodiazepines (e.g. Diazepam), opioids (heroin, morphine, methadone) and cannabis

71
Q

How do stimulants work and what are some examples?

A

Stimulants are substances which increase activity and arousal in the CNS. These are sometimes referred to as ‘uppers’ because they speed up mental and physical processes in the body.
Stimulants can increase blood pressure, heart rate, respiration and increased temperature (especially with amphetamine- based drugs). Can cause increased agitation and aggression.

Examples of stimulants:
Ecstasy, amphetamines, caffeine, cocaine, nicotine, synthetic drugs

72
Q

How do hallucinogens work and what are some examples?

A

Substances that alter the CNS and distort mood, perceptions, thinking, feelings, emotions, sense of time and place. These are also called psychedelics.
Can include experiences of paranoia and delusions.

Examples of Hallucinogens:
LSD, Magic mushrooms, Cannabis, Kronic, Daytura

73
Q

At the end of a brief interview with a client discussing addiction, you should SEW it up, what does this mean?

A

S- summarise- a summary of the clients statements in favour of change

E- emphasise- emphasise the clients strengths and their ability to make changes

W-what agreement has been reached?

74
Q

What are some common mental disorders in older adults?

A 
Delirium	
 Dementia
 Depression
 Anxiety 
 Schizophrenia
 Substance Use
75
Q

What is delirium?

A

Also known as acute confusion, Delirium is a syndrome that has characteristic pattern of signs and symptoms which are caused by anything that rapidly damages the brain.

This occurs over a period of hours to days and can fluctuate at different times of the day. It can be challenging to differentiate Delirium from Dementia.
It is important to recognise delirium early so that the cause can be treated and delirium resolved.
It is important in older adults to investigate any behavioural changes and not to pass it off as part of the aging process.

76
Q

What is dementia?

A

A Syndrome due to disease of the brain, usually of a chronic or progressive nature, in which there is disturbance of multiple higher cortical functions, including memory, thinking, orientation, comprehension, calculation, learning capacity, language and judgement.

the most common types are: Alzheimer’s disease, vascular dementia, Lewy body dementia and fronto-temporal dementia (e.g. Picks disease)

People with Dementia often experience delusions, hallucinations, sleep disturbances, personality changes, aggression and depression

77
Q

How does depression in an older adult differ from that in a younger person?

A

The symptoms of depression in an older adult can be subtly different to those in younger people. For example, older people are less likely to display affective symptoms, e.g. dysphoria, worthlessness and guilt, and more likely to show cognitive changes, somatic symptoms, e.g. sleep disturbance, agitation and general loss of interest.

78
Q

What is an intellectual disability?

A

I.Q below 70 (+ - 4)
Significant deficits in 2 or more areas of adaptive functioning measured in standard clinical tests
An onset that started before adulthood (before 18)with a lasting effect on development

Adaptive function: 
Conceptual skills
language
literacy 
money
time
number concepts
self-direction.
79
Q

The process of action potential

A

Stimulus reaches the threshold – channels open causing sodium to rush in to cell making membrane potential more positive = DEPOLARISATION
Now that it is very positive, potassium wants to leave. Channels open meaning potassium can leave. This means the membrane potential decreases = REPOLARISATION.
The membrane potential goes further away from the threshold making it more negative. = HYPERPOLARISATION
The resting state. Sodium is outside the cell and potassium is inside the cell. Awaiting stimulation = POLARISATION.

80
Q

What is the mode of action for morphine?

A

Morphine and other opioid agonists relieve pain by mimicking the actions of endogenous opioid peptides, primarily at mu receptors.

Opiod peptides and morphine bind to the same receptors in the CNS which are associated with pain perception.

81
Q

What drug is used to antagonise the action of morphine?

A

Naloxone.

Year Two (4 decks)

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