SAP Flashcards

1
Q

what are the models of reactions to dying and bereavement?

A

Elizabeth-kubler ross model- change from curing to caring. 5 stages: denial/shock, anger, depression (preparatory grief), bargaining, acceptance
Greer and Watson- coping style for adjustment to cancer- fighting spirit, fatalism (what happens happens), helplessness/ hopelessness, anxious preoccupation (everything it to do with the disease), avoidance/ denial
William worden- tasks of grief: 1. accept the reality of the loss, 2. experience the pain of the loss, 3. adjustment to an environment where the deceased is missing, 4. emotionally relocate the deceased to an important but not central place
dual process model- not a linear process two orientations which a person can jump between: loss oriented- grief work, denial/avoidance, breaking ties/ bonds. restoration oriented- attending to life changes, distraction from grief, denial of grief, doing new things, new roles/identity/ relationships

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2
Q

what are the roles of the doctor at the end of life?

A

discuss adaptation to major life changes
contribute to the care if the patients and their families at the end of life, including management of symptoms, practical issues of law and certification
communicate appropriately in difficult situations including breaking bad news, uphold the wishes and customs of the patient

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3
Q

what are the signs of imminent death?

A
loss of appetite, unable to swallow
excessive fatigue or sleep
physical weakness
mental confusion/disorientation
laboured breathing, cheyne- stokes breathing (breathing deepens/gets faster then gets shallower/ slower before it stops temporarily)
decreased urinary output
cold cyanosed extremities, mottled skin
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4
Q

what is the medical definition of death?

A

irreversible loss of capacity for consciousness AND loss of capacity to breath

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5
Q

how should breaking bad news be approached?

A

preparation- know as much as possible about the patient and the information you are given, ensure privacy and adequate time, prepare the patient- tall them they may want a loved on present.
initiating and patient perception- establish initial rapport, check patients ICE, give warning that there is bad news
giving the information- assess the patients prior knowledge and how much they want to know, give factual and clear information in short chunks and check understanding and invite questions, allow news to settle- use silence
responding to patients reactions- be empathetic, address concerns, answer any questions, ask if they are ready to consider options/ making a plan, offer emotional support, be sensitive to cues, make use of information resources that the patient can take away, arrange a follow up

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6
Q

what are the cardinal symptoms of neurological disease?

A

headaches
nausea and vomiting
blurred/double vision or loss of vision hearing difficulty or tinnitus
speech or language difficulty
difficulty swallowing dizziness/ altered consciousness/ fits or faints
psychological changes
unsteadiness or loss of balance
motor- weakness, stiffness or tremor
difficulty with coordination/clumsiness sensory- numbness, pins and needles, tingling, pain
sphincter disturbances
loss of function

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7
Q

what are the ethical issues associated with withholding or withdrawing life saving treatment?

A

withholding- HCP are not obliged to provide CPR, income cases CPR is not recommended as it is contraindicated or very unlikely to work, patients must normally be consulted if HCP decide to enter a DNACPR order into their notes
withdrawing- in some cases it is appropriate to withdraw treatment such as artificial hydration and nutrition for example if the patient is in a persistent vegetative state and will never recover.

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8
Q

what are advanced decisions?

A

a decision made by a competent person about what they wish or do not wish to happen to them in particular circumstances that the may find themselves in at some point in the future, when they may not have the capacity to make the decision.
advance decisions cannot refuse actions that are needed to keep a person comfortable (warmth, shelter, offer of food and water by mouth)

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9
Q

what is the ‘doctrine of double effect’?

A

the theory that it is acceptable to cause a foreseen bad effect that is not intended, when the good effect cannot be obtained with out the (risk of) the bad effect and when there is good reason to allow the (risk of the) bad effect.
this is often invoked to justify the administration of pain relief (which may result in the person dying) when the patient is going to die.
for this to be lawful the death must not be intended even if it is foreseen, and the provision of alternative forms or quantities of pain relief are considered inadequate

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10
Q

what are the causes and clinical features of a spinal cord hemi-section?

A

causes- trauma resulting in damage to one half of the spinal cord, motor and sensory pathways damaged.
clinical features: mixed motor and sensory signs and symptoms:
ascending pathways- damage to:
dorsal column- changes in fine touch, proprioception (ipsilateral below lesion)
spinothalamic tract- changes in pain, temperature (contralateral below leision)
spinocerebellar tract- balance- unsteady gait
descending pathways:
lateral corticospinal tract- paralysis, weakness (ipsilateral below lesion)
rubrospinal, reticulospinal, vestibulospinal- balance, spacticty, abnormal reflexes

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11
Q

what are the clinical features of a slipped disk?

A

vertebral disc displaces and presses on spinal cord, most often compress the spinal nerve.
symptoms- weakness, pain, numbness, tingling in myotome/ dermatome at level of injury

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12
Q

what are the causes and features of tabes dorasalis?

A

causes- tertiary syphilis infection (treponema palladium) can cause demyelination of the dorsal column neurones
signs/ symptoms:
hypoesthesia- reduced touch sensation, sensory ataxia- coordination- +ve rombergs sign,
paresthesia- pins and needles
if infection spreads to grey matter of the dorsal horn- diminished reflexes, muscle hypotonia

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13
Q

what are the causes and features of syringomyelia?

A

cyst which grows inside spinal cord (central canal), many causes- tumour, etc. start in the centre and works outwards.
symptoms:
affects crossing fibres of the spinothalamic tract- gradual loss of pain and temperature sensation bilaterally.
back pain, stiffness
spread to ventral horn- muscle weakness LMN signs

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14
Q

what are the causes and features of anterior spinal cord syndrome?

A

caused by occulsion of anterior spinal artery leading to damage to pathways in the anterior portion of the spinal cord:
ventral horns- LMN signs- weakness, diminished reflexes
anterior and lateral spinothalamic tracts- impaired pain and temperature sensation
anterior spinocerebellar tract- less of balance

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15
Q

what are the barriers to spinal cord regeneration?

A

infiltration of immune cells- inflammation
release of chemicals from damaged cells- further spread of damage (excitoxicity)
formation of glial- astrocytes, OPCs and microglia
inhibitory debris- proteins

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16
Q

what treatments are there to engineer regeneration of the spinal cord?

A
  1. degrade glial scar- chondroitinase- enzyme which breaks down glial scar
  2. olfactory ensheathing cells- transplanted into spinal cord to promote cell growth
  3. stem cells
17
Q

what experimental neurotechnologies are there to treat spinal cord injury?

A
  1. neuromodulation- spinal cord stimulation by electrodes enable weak connections at the site if injury. useful for managing pain
  2. microelectrode array recording- microelectrode array inserted into cortex and brain signals recorded, amplified and filtered
  3. brain spine interfaces- combining microelectrode array recording with delivering electrical impulses to the spinal cord
18
Q

what are the signs and symptoms of cerebellar damage?

A

vestibulocerebellum- staggering gait (ipsilateral), nystagmus on lateral gaze (contralateral)
spinocerebellum- ataxia (slurred speech, stumbling, falling, incoordination), hypotonia/hyporeflexia- due to loss of pontoreticulospinal fibres
neo/ponto/cerebrocerebellum- slow movement onset, speech impairment, dysmetria (undershoot or overshoot movement), dysdiadochokinesis (impaired ability to perform rapid, alternating movements), intention/action tremor, decomposition of movements

19
Q

what are the signs pf upper motor neurone and lower motor neurone lesions?

A

UMN- hypertonia, hypereflexia, clonus (involuntary, rhythmic muscle contractions), positive babinski sign (toes splay out), muscle weakness.
LMN- hypotonia, hyporeflexia, muscle weakness, fasciculation’s, muscle atrophy/wasting

20
Q

what are the clinical consequences of demyelinating disease?

A

multiple sclerosis- autoimmune disease which targets oligodendrocytes leading to the degradation of myelin, disruption to energy and nutrient supplies to neurones, ionic imbalance and eventually neurodegeneration.
signs/symptoms- visual disturbance, strange sesnory sensations (burning, tingling, sensory loss), Lhermitte’s sign (feeling of shock down spine), foot dragging, leg cramping, fatigue, spasticity, increased muscle tone, imbalance

21
Q

what are the types of MS?

A

relapsing remitting MS- relapsing remitting nature is due to damage to the myelin causing symptoms, followed by repair and demyelination that restores some function. however the repairs are not complete and each relapse causes deterioration in symptoms
primary progressive- MS without remission phase, continual degradation
secondary progressive MS- after initial RRMS the symptoms get worse similar to PPMS.

22
Q

what is the clinical presentation of motor neurone disease?

A

mixture of UMN and LMN symptoms:
UMN- spasticity, brisk reflexes, upward plantar reflex (+ve babinski)
LMN- wasting, fasciculation’s such as of the tongue
weakness in ankle/leg, slurred speech, weak grip