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Year 2 > HNN Week 4 > Flashcards

HNN Week 4 Flashcards

1
Q

What is ‘attention’?

A

A cognitive process encompassing multiple sensory modalities and operating across sensory domains

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2
Q

What is ‘arousal’ and what is it called if impaired?

A

State of wakefulness and responsitivity

Drowsiness

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3
Q

What is ‘vigilance’ and what is it called if impaired?

A

Capacity to maintain attention over long time periods

Impersistence

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4
Q

What is ‘divided attention’ and what is it called if impaired?

A

Ability to respond to more than once task at once

Distractible

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5
Q

What is ‘selective attention’ and what is it called if impaired?

A

Ability to focus on one stimulus while suppressing competing stimuli
Distractible

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6
Q

What is the difference between focal and global attention?

A

Focal attention = spatial awareness and visual functions

Global attention = a more overall function of the body

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7
Q

How is global attention controlled?

A

There are interactions between the ascending reticular activating system (ARAS and spinal pathways) and the cortex of the brain.

Knocking out of the ARAS causes drowsiness, delirium or coma.

Knocking out of the upper cortex causes inattention

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8
Q

What are the two broad classifications of memory?

A

Long term and immediate (working)

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9
Q

Describe immediate (working) memory:

A
  • immediate recall of small amounts of verbal/spatial information
  • controlled by dorsolateral prefrontal cortex
    -> ‘visual sketch pad’ is found in the parieto-occipital lobe for spatial and visual awareness and information
    -> ‘phonological store’ is in the language areas and stores short term information about words, numbers and melodies
    = Wernicke’s area is in the posterior temporal lobe and receives information from the auditory and visual cortices and comprehends information.
    = Wernicke’s area is attached to Brocca’s area (in the posterior inferior frontal lobe) which produces meaningful language
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10
Q

What can long term memory be divided into?

A

Implicit (procedural)

Explicit (declarative)

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11
Q

What is implicit memory?

A

memories not available to conscious reflection i.e. you can remember them without effort or awareness

  • procedural memory e.g. riding a bike, typing shoe laces, playing piano
  • networks involve basal ganglia and cerebellum
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12
Q

What is explicit memory?

A

memories available to conscious reflection e.g. requires effort for conscious reflection, doesn’t come easily

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13
Q

What can explicit memory be broken down into?

A

Episodic and semantic

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14
Q

What is episodic memory?

A

Having memory of EVENTS and what you have personally experienced e.g. what you ate for breakfast.

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15
Q

What is semantic memory?

A

Having memory with KNOWLEDGE of factual information e.g. what the capital of France is.

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16
Q

How can you test semantic memory?

A
  • genera knowledge tests e.g. what is the name of the Prime Minister?
  • fluency e.g. name as many animals as possible in 60 seconds
  • test verbal knowledge e.g. what colour is a banana
  • carry out person based tasks e.g. naming famous celebrities to face
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17
Q

How do you test episodic memory in clinical practice?

A
  • recognition of newly encountered names/faces
  • recall of geometric shapes
  • recall of what you did yesterday
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18
Q

What is the biochemical abnormality in Alzheimer’s?

A

decreased cholinergic transmission

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19
Q

What is the limbic cortex?

A
  • set of brain structures found on either side of the thalamus just below the cerebrum
  • is not a separate system but a collection of other brain structures e.g. hippocampus, cingulate gyrus, orbital and prefrontal cortex, basal ganglia, fornix and amygdala…
  • involved in motivation, learning, EMOTION
  • the circuit of papez is an emotion system that lies on the medial wall of the brain and links the cortex to the hypothalamus and governs the behavioural expression of emotion
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20
Q

What type of memory is affected in dementia and Alzheimer’s?

A

Semantic memory

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21
Q

Describe the location and function of the 4 tonsils in the head:

A

1) pharyngeal/adenoid tonsil: a mass of lymphatic tissue found on roof of posterior nasal cavity behind the uvula
2) palatine tonsils: in oropharynx, on either side between palatoglossal and palatopharyngeal arches
3) tubal tonsil: collection of lymphatic tissue around the base of the eustachian tube opening
4) lingual tonsils: collective name for many lymphoid tissue aggregates found on the posterior 1/3 of the tongue

  • tonsils are lymphatic organs filled with dendrites, macrophages and other immune cells and are an important component of the immune system, for fighting infection
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22
Q

What are the three parts of the external ear lobe?

A
  • helix
  • pinna
  • lobule
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23
Q

What is the composition of the external acoustic meatus?

A
  • outer 1/3 = elastic cartilage

- inner 2/3 = bone

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24
Q

Describe the anatomy of the tympanic membrane:

A
  • pars flaccida = area at the top under less tension
  • pars tensa = tense area which vibrates less around the bottom
  • umbo = central part where malleus attaches
  • light cone at bottom corner
  • malleus handle crosses the surface
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25
Q

What is the size difference between the tympanic membrane and the oval window?

A
  • 20x smaller = lots of amplification
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26
Q

Describe the anatomy of the inner ear:

A
  • semi-circular canals
  • cochlea (3.5 turns)
  • otolith organs (utricle = horizontal acceleration, saccule = vertical acceleration)
  • mastoid antrum (air-filled space in petrous part of temporal bone) that contains mastoid air cells to reduce the mass of the cranium and provide protection
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27
Q

What type of epithelium lines the tympanic membrane?

A
  • pseudostratified ciliated columnar epithelium
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28
Q

Name the three ear bones and describe their articulations and structure:

A
  1. Malleus = base of handle in contact with tympanic membrane at umbo, then head of malleus articulates with…
  2. Incus which attaches to…
  3. Stapes, the footplate of which attaches to round window
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29
Q

What two important muscles are found within the inner ear and what are their innervations?

A
  • Tensor tympani muscle: attaches to the handle of the malleus and is supplied by trigeminal nerve CN5, dampens vibrations of ossicles when they tense to quieten chewing sounds
  • Stapedius muscle: stabilises the stapes and also dampens vibrations, supplied by facial nerve CN7
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30
Q

Briefly describe the physiology of hearing:

A
  • pinna collects sound which passes through external auditory canal and meets tympanic membrane
  • high frequency sound = faster vibration
  • tympanic membrane in contact with handle of malleus
  • ossicles transmit sound to footplate of stapes which presses onto oval window
  • labyrinth filled with perilymph which can be displaced due to round window
  • vibrations sent UP cochlea to apex via scala vestibuli
  • vibrations travel DOWN cochlea via scala tympani
  • scala’s are filled with perilymph
  • cochlear duct is between the two scalas and is filled with endolymph
  • different membranes on cochlear duct are flexible and move in response to fluid vibrations
  • Reissner’s membrane: between scala vestibuli and cochlear duct
  • Basilar membrane: between cochlear duct and scala tympani (organ of corti here and there are hair cells on the organ of corti)
  • fluid vibrations pass between the scalas and cause hair cells in the organ of corti to move
  • hair cells covered by tectorial membrane and when inner hair cells are pushed against this it causes AP’s to be fired and signals travel in the cochlear branch of CN8 to the auditory cortex in the superior region of the temporal lobe
  • outer hair cells are motile and can change their shape and stiffness when stimulated to amplify vibrations
  • HAIR CELLS CANNOT REGROW
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31
Q

Describe tonotopic organisation:

A
  • low fq. sounds cause the basilar membrane near the apex of the cochlea to vibrate
  • high fq. sounds cause the basilar membrane near the base of the cochlea to vibrate
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32
Q

Describe types of ear infection:

A
  • acute otitis media: rapid onset with signs and symptoms of middle ear infection
  • otitis media effusion: presence of fluid in the middle ear without any signs/symptoms of a middle ear infection
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33
Q

Describe the aetiology of ear infections:

A
  • AOM and EOM are inter-related
  • AOM caused by upper respiratory tract infection which reaches middle ear via eustachian tube (H.influenza and S.pneumonia are common bacteria)
  • acute infection -> effusion -> predisposition to recurrent infection
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34
Q

Name some risk factors for glue ear:

A
  • male
  • pre-school age
  • bottle fed
  • your eustachian tube is shorter, wider and more horizontal as a child
  • native american/inuit
  • low socio-economic status
  • premature
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35
Q

Describe the pathophysiology of ear infection:

A
  • upper respiratory infection
  • inflammation of nasal passages
  • eustachian tube and tonsils hypertrophy
  • eustachian tube becomes blocked and air cannot enter the middle ear
  • respiratory epithelium and mucous secreting goblet cells increase mucous production
  • the mastoid air cells become inflammed and fluid builds up in the inner ear
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36
Q

How do you diagnose ear infection?

A
  1. HISTORY - sleep disturbance, look for younger children tugging at ears, ear pain
  2. EXAMINE - tympanic membrane, opaque, decreased motility and air bubbles
  3. TYMPANOMETRY: probe with speaker, microphone and air pump is placed in the inner ear and causes changes in ear pressure, the probe measures sound that is reflected back from the ear drum to see how mobile the middle ear is and reduced movement suggests effusion and infection
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37
Q

What is conductive hearing loss?

A
  • due to an external ear condition (wax, foreign body) or a middle ear condition (trauma, otitis media, otosclerosis)
  • the auditory stimuli is not adequately transmitted through the auditory canal and ossicle chain to reach the tympanic membrane
  • most blockages are temporary (cotton wool) but some can be more permanent (osteosclerosis, Paget’s disease (which can affect the ossicles)
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38
Q

What is sensorineural hearing loss?

A
  • also called perceptive hearing loss
  • due to hair cell damage, CNS damage (meningitis), atherosclerosis, tumours, ototoxic drugs (anti-malarials and loop diuretics) or idiopathic (Méniere’s disease)
  • due to disorders affecting the inner ear and auditory pathways to the brain
  • sound waves ARE conducted into the inner ear but there are cochlear abnormalities or nerve impulse issues
  • can also be genetic cause
  • can also be environmental cause from loud sound exposure
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39
Q

How what two tests can you use to distinguish between conductive or sensorineural hearing loss and describe the results you would see in the known defective ear:

A
  1. Weber’s test: place a vibrating tuning fork onto the centre of the forehead and if there is conductive hearing loss, the vibration will sound louder in the defective ear. If there is sensorineural hearing loss the vibrations will be louder in the normal ear.
  2. Rinne’s test: place vibrating tuning fork on mastoid process and then once vibrations no longer heard move to outside near and normally air conduction is greater than bone conduction. In conductive hearing loss, -VE Rinne’s test and bone conduction will be greater than air conduction in the defective ear. In sensorineural hearing loss, there will be a +ve Rinne’s test and air conduction will be greater than bone conduction in the defective ear.
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40
Q

How do you treat otitis media?

A
  • most cases resolve spontaneously
  • antimicrobial therapy
  • corticosteroid therapy
  • analgesics
    SURGERY
  • insertion of grommet/ventilation tube
  • most common and effective treatment of glue ear
  • performed under general anaesthetic ~15mins
  • small incision made in ear drum and then grommet inserted
  • drains fluid in middle ear and maintains middle ear pressure keeping the ear drum open for several months until 6-15 months later the grommets fall out as the tympanic membrane heals
  • 30% of children require more than one session of grommet insertion
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41
Q

What are the dangers of child deafness?

A
  • delayed speech development
  • delayed communication skills development
  • learning issues
  • reduced academic achievement
  • isolation and self-confidence issues
42
Q

What are the tests for child screening?

A

SCREENING carried out in first few weeks of life by 1/2 simple tests

1) OAE test - otoacoustic emmisions test
- the cochlea produces a fake echo when stimulated by sound
- small speaker and microphone placed into ear and if cochlea is functioning properly then ear piece detect echo
- may be invalid results from birthing fluid in childs ear or background noise

2) AABR - automated auditory brainstem response
- records the brain activity in response to sound
- headphones play a clicking noise and small electronic sensors placed on baby’s head
- the brains electrical activity can be measured on a computer
- the test checks if the cochlea is converting auditory stimuli into electrical impulses

43
Q

Describe how movement is controlled:

A
  • can be voluntary or involuntary
  • voluntary movement involves motor learning and different memory types including:
  • > declarative (explicit) memory = memory that is easily formed and forgotten and takes effort to recall e.g. what you had for breakfast, capital cities
  • > non-declarative memory (implicit) = memory that is not easily formed or forgotten e.g. riding a bike
  • normally movement involves a combination of both of these
  • ways of controlling voluntary movements involve:
  • > ballistic approach (pre-programmed movements, rapid and cannot compensate change)
  • > visual feedback = can compensate
44
Q

What cortical brain areas are involved in controlling movement?

A
  • Area 4 = primary motor cortex, contains homunculus and initiates movement
  • Area 6 = premotor area (lateral - controls movement of proximal motor units) and supplementary motor area (medial - controls movement of distal motor units)
45
Q

What non-cortical brain areas are involved in controlling movement?

A
  • cerebellum: controls gait and smooth execution of movements
  • receives input from the sensory cortex and output is sent via the thalamus to the premotor area
  • basal ganglia:
  • output from basal ganglia tends to be inhibitory (GABAinergic neurons and GABA is an inhibitory neurotransmitter)
  • the inhibitory and excitatory output from the basal ganglia is what maintains normal motor function
46
Q

Describe how and where dopamine is synthesised and what happens to the dopamine after it is released into the synapse:

A
  • produced in the brain from the amino acid tyrosine
    Tyrosine —(tyrosine hydroxylase - rate limiting step)—> DOPA —(DOPA decarboxylase - decarboxylation)—> Dopamine
  • after release into the synapse, not all dopamine is up taken by other nerve cells and some is recaptured by monoamine transporters and then metabolised
  • monoamine oxidase and catecholomethyl transferase convert dopamine into DOPAC and homovallinic acid (HVA) which are then excreted and can be measured to look at dopamine release from the body
47
Q

Describe the anatomical routes and functions of the main dopamine pathways in the brain:

A

1) Tuberohypophyseal (the only one which doesn’t have fibres that pass through the medial forebrain bundle) and goes from hypothalamus to pituitary gland - involved in controlling prolactin and GH secretion for lactation and growth
2) Mesolimbic pathway: from VTA through medial forebrain bundle to areas of the limbic system including the amygdala and hypothalamus: involved in motivation, reward and emotion
3) Mesocortical pathway: from VTA through medial forebrain bundle to the prefrontal cortex: for behaviour control
4) Nigrostriatal pathway: from substantia nigra to the corpus striatum: for motor control

NOTE: VTA = ventral tegmental area, located next to the substantia nigra

48
Q

What are the different types of dopamine receptors and their actions?

A

‘D1 family’ = D1 and D5

  • Gs receptors
  • cAMP and adenyl cyclase activated
  • PKA activated
  • phosphorylation of voltage gated Ka/Ca channels

‘D2 family’ = D2,3,4

  • Gi/o receptors
  • K channels activated
  • Ca channels inhibited
  • adenyl cyclase inhibited and so there is less phosphorylation
49
Q

Where are the various dopamine receptors found?

A

D1 - corpus striatum, hypothalamus and limbic system
D2 - “” “” + pituitary gland
D3 - limbic system
D4 - weak expression in cortex and limbic areas

50
Q

Does dopamine have any effects not on the brain?

A

YES - can act peripherally by increasing myocontractility and increasing renal vasodilation

51
Q

Can dopamine act pre-synaptically and post-synaptically?

A

YES:

  • presynaptic: if dopamine is in plentiful supply, it will bind to its pre-synaptic terminals and prevent further synthesis and release (negative feedback)
  • post-synaptically: dopamine can act as an antagonist and increase dopamine synthesis and release
52
Q

Name two other monoamines except dopamine:

A

Noradrenaline

Serotonin

53
Q

Describe the noradrenaline pathways in the brain and the function of noradrenaline

A
  • function: mood, anxiety, sleep patterns, attention, learning, pain
  • most prominent cluster of cell bodies of NA neurons is in LC (locus coerulus) in the pons
  • from LC, branches extend through medial forebrain bundle to cortex, hippocampus, thalamus, hypothalamus and cerebellum
  • no direct synapses, diffuse neurotransmitter release onto 250,000 neurons
  • there are a small cluster of neurons more ventrally in the brainstem that release adrenaline rather than NA
  • contain the enzyme phenyl-ethanolamine N methyl transferase to convert NA into A
  • axons from these adrenergic neurons project to pons, medulla and hypothalamus
54
Q

Which brain parts are involved in the ascending reticular activating system?

A

LC, Raphe nuclei

55
Q

What is the function of serotonin and describe its pathways in the brain:

A

Functions: sleep, appetite, thermoregulation, pain, anxiety

  • cell bodies are clustered together called ‘Raphe Nuclei’ (there are 9)
  • the more rostral nuclei project to cortex, hippocampus, hypothalamus, limbic system, basal ganglia
  • the more caudal project to the cerebellum, medulla and spinal cord
56
Q

Why does serotonin have a precursor and what is it?

A
  • serotonin cannot cross the BBB so is synthesised as 5-hydroxytryphtophan (5-HTP) and then is converted into serotonin once across the BBB
57
Q

What is Parkinsonism?

A

The generic term for the symptoms of parkinson’s disease, but a patient can have these symptoms caused by another illness/disease/condition as it is not just PD that causes them

58
Q

Define Parkinson’s disease (PD) and its aetiology (causes):

A
  • a disease involving disordered motor control due to deficiency of dopamine in the nigrostriatal pathway
  • found in 1:200 people 80yrs+
  • 1.5 males to 1 female
  • increasing risk with age
  • environmental factors: pesticides, rural living
  • SMOKING IS PROTECTIVE
  • genetic factors: some genetic loci (PARK1-11) that cause the autosomal recessive form are found in early onset PD before 40yrs
  • majority of cases are idiopathic
59
Q

What is the pathophysiology of PD?

A
  • presence of abnormal protein aggregates called Lewy bodies are in nerve cells and become more widespread over time
  • causes a loss of dopaminergic neurons in the pathway from the substantia nigra to the corpus striatum that contains the basal ganglia (the nigrostriatal pathway)
  • there may be auto-oxidation of dopamine and this injures the neurons in the substantia nigra
  • there may be a genetic mutation which causes the autosomal dominant form in the gene that encodes the production of the protein ‘alpha-synuclein’ and this protein is a major constituent of Lewy bodies
60
Q

What are the signs and symptoms of PD?

A
  • pathological changes occur early on and are not seen until 70% dopaminergic neurons are lost
    MOTOR SYMPTOMS
  • hypokinetic: akinesia, bradykinesia, dyskinesia
  • hyperkinetic features: tremor, leadpipe rigidity, cogwheel rigidity (combo of previous two)
  • stooped posture
  • gait changes
  • speech and swallowing issues
  • tremor unilateral and then spreads, starts in hands

NON MOTOR:
- dementia, impaired cognitive function, aches/pains, constipation, asomnia (90% people have affected olfactory bulbs)

61
Q

How can you investigate and diagnose Parkinson’s?

A
  • no lab tests
  • MRI not useful
  • history
  • recognise physical signs
  • dopamine transporter imaging (uses radioactive ligand that binds to dopamine terminals to show the extent of nigrostriatal neuron loss)
  • GIVE DOPAMINE to see if symptoms are relieved
62
Q

What are the main strategies in the treatment of Parkinson’s disease?

A
  • education
  • physical activity encouraged where possible
  • control motor symptoms with dopamine focussed treatment
  • control non motor symptoms e.g. constipation, depression, sleeping disorders
63
Q

Describe the medications used to target the motor symptoms of Parkinson’s:

A

Levodopa:

  • metabolic precursor of dopamine that can cross the BBB
  • it enhances dopamine synthesis in the remaining substantia nigra, effective even if only 20% dopaminergic neurons left
  • large doses required as it is decarboxylated into dopamine in the periphery, although is taken with carbidopa to try and reduce the large doses and to reduce the side effects of nausea and vomiting

CARBIDOPA:

  • dopa-decarboxylase inhibitor
  • reduces the dose of L-dopa required by 5x
  • lowers L-dopa breakdown in the periphery so that there is more available in the CNS

DOPAMINE AGONISTS:

  • cabergoline
  • not as effective or well tolerated as L-DOPA but less side effects over 5 years
  • apomorphine (short acting subcutaneous pen for relief or IV pump)

SELEGILINE:
- monoamine oxidase Beta inhibitor, reduces dopamine breakdown in the brain

AMANTADINE:
- weak glutamate receptor antagonist which increases dopamine release

ANTICHOLINERGICS:
- block ACh and help reduce tremor

64
Q

What are some non-pharmacological ways to treat PD?

A
  • Deep brain stimulation with electrodes for therapeutic relief when medication is not effective
  • Tissue transplantation still being researched
65
Q

What specialists/interventions are used to treat PD?

A
  • physiotherapists
  • OT
  • Physical aids
  • Speech therapy

All these help with management, reducing disability and injury, improving mobility and speech issues

66
Q

What is the vestibular apparatus and its components?

A
  • Organs of balance
  • There are 2 components:
  • > semi-circular canals (detect angular acceleration) arranged in 3 different planes
  • otolith organs (utricle detects horizontal acceleration and saccule detects linear acceleration and TILT)
67
Q

What are the ampulla of the semi-circular canals?

A
  • swellings containing the sensory neurons where signal transduction occurs
68
Q

What is the vestibulo-ochlear reflex?

A

Direction of eyes remains constant when head moved

69
Q

What happens if there is disturbance of the vestibulo-ochlear reflex?

A

Nystagmus (constant, uncontrolled eye movement)

70
Q

Describe how the vestibulo-ochlear reflex works:

A
  • inertia causes endolymph to lag behind in semi-circular canals and when head moves cilia are deflected and an AP produced from signal transduction
  • impulses travel to brainstem via CN8
  • there is then sensory input to the extrinsic eye muscles
  • the pupils have to stay in position to focus images onto the retina during head movements so this is why the direction of the eyes has to stay constant when the head moves
  • there is activation of lateral rectus muscle of one eye and the medial rectus muscle of the other eye which causes the eyes to be pulled in a direction contrary to the direction of the head’s rotation
  • the semi-circular canal on the other side of the head is inhibited and there is less AP fired -> less activation of respective eye muscles and the image is stabilised on the retina
71
Q

What direction do the eyes move in horizontal nystagmus?

A

Horizontally

72
Q

What direction do the eyes move in rotational nystagmus?

A

Round in circles as though you are looking round the edge of a clock face

73
Q

What direction do the eyes move in vertical nystagmus?

A

^ (up) and down

74
Q

How does caloric stimulation work and why is its use relevant?

A
  • injection of water at temperature slightly above body temperature into the external acoustic meatus
  • heat is transferred and convection currents occur in the horizontal SCC (as it is anatomically closest)
  • vestibulo-ochlear reflex initiated and causes horizontal nystagmus
  • can be used to test the integrity of the brainstem in an unconscious patient as can other brainstem reflexes (pupillary light reflex)
  • horizontal nystagmus may be triggered by the same mechanism of caloric stimulation when removing ear wax from ears with water and syringe
75
Q

What can happen if there is excessive stimulation of semi-circular canals?

A

Motion sickness -> disorientation -> disability

76
Q

What determines the severity of a stroke and where is the disability found?

A

The extent of the haemorrhage

The disability will be on the contralateral side of the body to the haemorrhage

77
Q

What happens in Huntington’s disease?

A

There are random involuntary movements which are produced due to basal ganglia dysfunction

78
Q

What type of inherited disorder is Huntington’s and what is one of its key features?

A

Autosomal dominant

Choreas = jerky, involuntary movements involving head, face and upper limbs especially

79
Q

What is the motor control of walking and taking steps?

A
  • alternating flexor and extensor muscle activity

- activity generated in the spinal cord and there is no brain involvement

80
Q

What is a motor unit?

A

A single motor neuron and all the motor fibres that it innervates

81
Q

What are the 4 sinuses found in the head and their functions?

A
  1. Maxillary
  2. Frontal
  3. Sphenoid
  4. Ethmoid
  • contribute to humidifying air and decreasing the weight of the skull
  • form part of upper respiratory tract but become troublesome if infected and are the occasional site of malignant disease
82
Q

Describe the location of each of the 4 pair of sinuses:

A
  1. Maxillary: cheeks
  2. Frontal: forehead
  3. Sphenoid: lateral to cranial cavity, look as though directly behind nose from front on imaginary picture
  4. Ethmoid: between eyes
    - > there are 3 ethmoid pairs (anterior, middle and posterior)
83
Q

What is ‘sick role’?

A

Having sanctioned deviance = you can do something that is not socially acceptable because you are ill e.g. not going to work
- You still have rights and responsibilities e.g. try to get better and seek co-operation with help given

84
Q

What is ‘illness behaviour’?

A
  • the way individuals monitor the structure and function of their own bodies and interpret symptoms or take remedial action
85
Q

What is illness?

A

The expression and experience of ill health and psychological, social and cultural factors are crucial

86
Q

What beliefs does illness behaviour depend on?

A
  • the cause
  • the prognosis (duration, course and severity)
  • the possible consequences
  • social impact
  • adequacy of medical care
87
Q

What is ‘locus of control’ and why is it important in chronic illness?

A
  • whether a person believes that they are in control of their own illness or whether the responsibility of their recovery and treatment lies with someone else (do they think the person that can change things is them or the doctors?)
  • is important in chronic illness as it determines successful management and possible development of psychological disorders like anxiety and depression
  • internal locus of control: you know you are in control and try to improve things
  • external locus of control: you believe you have little control yourself and rely on others
88
Q

Describe some of the social impacts of illness:

A
  • work
  • relationships
  • incomes and financial stress
  • PIP (personal independent payment)
89
Q

What is secondary gain?

A

The advantage that occurs secondary to a real illness e.g. when you are not consciously seeking help but you are genuinely ill and people are helping you

90
Q

What is malingering?

A

When you are pretending to be ill and seeking benefits from it consciously

91
Q

What are the components in adjusting to illness?

A
  • managing uncertainties
  • searching for meaning
  • dealing with loss of control
  • having a need for medical and emotional support
92
Q

What are the 5 stages of grief?

A
  1. Denial
  2. Anger
  3. Bargaining
  4. Depression
  5. Acceptance
93
Q

Describe components of ‘good coping’:

A
  • optimistic
  • practical
  • willing to consider and use a range of strategies
  • own your own decisions and have an internal locus of control
94
Q

What 5 elements have been identified as facilitating successful adjustment to chronic illness?

A

1) successful performance of adaptive task
2) absence of psychiatric disorder (is avoidable and it is not the primary cause)
3) presence of high positive affect
4) adequate functional status
5) satisfaction and well-being in various life domains

95
Q

List symptoms which may be induced by cytokine activity in chronic illness:

A
  • weakness
  • fatigue
  • anorexia
  • lethargy
  • pro-inflammatory cytokines are released after diabetes, MRI, cancer e.g. TNF, interferon alpha, and they influence psychological symptoms
96
Q

What is involved in good self management?

A
  • good understanding and education of illness
  • use of medication where advised
  • symptom monitoring
  • decision making
  • diet
  • lifestyle
  • exercise
97
Q

What happens if people do not adjust to illness?

A
  • poor health outcomes
  • increased disability
  • co-morbidity
  • poor life quality
  • avoidance and alcohol
  • death
98
Q

What barriers stop people adjusting to illness?

A
  • characteristics of the illness e.g. pain, fatigue
  • characteristics of the treatment e.g. dialysis
  • societal e.g. stigmas and rejection
  • personality and locus of control
  • social circumstances (finances, social support)
99
Q

What can be used by psychiatrists to help people not coping with illness?

A
  • cognitive behavioural therapy
  • acceptance and commitment therapy
  • mindfulness
100
Q

What are the potential positive experiences of illness and how are there relevant to adjustment?

A
  • changing priorities (spend more family time)
  • improved health (diet, smoking)
  • adaptability
  • creativity
  • changes in life and relationship choices (divorce, more time with partner)
  • be more cautious of future life choices

Year 2 (22 decks)

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