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CRP scenarios > CRP Scenarios > Flashcards

CRP Scenarios Flashcards

1
Q

Pathophysiology in chronic COPD

A

Emphysaema and chronic bronchitis
Cardinal symptoms (dyspnoea, cough and sputum)
Risk factors

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2
Q

Assessment for chronic COPD

A

Subjective
Obs (sats)
Chest expansion
Tactile fremitus
Auscultation

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3
Q

Treatment for chronic COPD

A

ACBT
Add an adjunct (aerobika which is an oscillating PEP)

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4
Q

Physiology for exacerbation of COPD

A

emphysaema and bronchitis
risks for exacerbation
what happens in exacerbation all the way through to being ventilated etc

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5
Q

Assessment in exacerbation of COPD

A

subjective
confusion
chest expansion
auscultate
tactile fremitus

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5
Q

What happens in an exacerbation of COPD?

A
  • acute event with worsening of symptoms
  • inflammation > bronchoconstriction, sputum hypersecretion > cough reflex
  • increased resistance in airways > fast and shallow breathing is easier than filling lungs - air trapped in alveoli > dynamic hyperinflation
  • inner range activity of diaphragm > weakens
  • hypercapnia and hypoxia
  • accessory muscles
  • type II resp failure > fatigue > ventilation
  • cardiac
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6
Q

Treatment for exacerbation of COPD

A

sit out
ACBT
add aerobika
pursed lip breathing

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7
Q

what are the inspiratory muscles?

A

diaphragm, external intercostals, scalene, sternocleidomastoid, trapezius

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8
Q

what are the accessory expiration muscles?

A

internal intercostals, internal and external obliques, transverse abdominis, rectus abdominis

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9
Q

what is the main impact of inspiratory weakness?

A

reduced diaphragmatic excursion

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10
Q

how does cheyne stokes respiration happen?

A

high co2 > hyperventilation > low Co2 > apnoea

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11
Q

how can central control of breathing be damaged?

A

change in consciousness
intracranial pressure
damage to brain stem

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12
Q

treatment for neuromuscular weakness

A

sit out (w help) and ACBT
position on ‘good’ lung and perform percussion

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12
Q

assessment in neuromuscular weakness respiratory

A

observe
chest expansion
tactile fremitus
auscultate
cough strength with peak flow meter, 140L/min

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13
Q

why do surgical patients get pneumonia?

A
  • reduced mobility
  • pain so don’t breathe / cough
  • anaethesia reduces central respiratory drive
  • atelectasis because all gas is absorbed from alveoli under GA
  • new microflora
  • already compromised
  • already inflammatory response
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14
Q

treatment for pneumonia

A

sit out and ACBT with scar support
incentive spirometry or PEP

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14
Q

assessment for pneumonia

A

subjectively
obs and bloods
auscultate
tactile fremitus

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15
Q

assessment for bronchiectasis

A

subjective
obs
sputum
auscultation
tactile fremitus

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16
Q

important contraindications for manual techniques in neuromuscular weakness (stroke) patient

A

recent anticoagulants
increased intracranial pressure
broken ribs
osteoporosis

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16
Q

explain what happens in bronchiectasis

A
  • abnormal irreversible dilation of bronchi
  • initial infection starts the inflammatory process
  • neutrophils and lymphocytes recruited
  • cilia dysfunction
  • mucus hypersecretion
  • epithelial damage
    = inflammation
    MMPs, elastases, cytokines
    mucus causes airway obstruction
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17
Q

pathophysiology acute stroke

A
  • ischaemic vs haemorrhagic
  • location
  • hemiplegia
18
Q

assessment acute stroke patient

A
  • mention safety!! stand on left (weak side)
  • rolling / bridging
  • lie to sit
  • sitting balance
  • stand
  • standing weight shifts
19
Q

treatment acute stroke patient

A

pelvic tilts > bridging
sitting balance - side and behind
STSs
weight shifts

20
Q

what can MCA obstruction cause?

A
  • contralateral hemiparesis
  • facial paresis > dysarthria
  • sensory loss UL and upper extremities
  • LL is stroke is deep enough
  • neglect
  • visual field loss
  • aphasia
21
Q

what functions does the PCA supply?

A

occipital lobe - vision
temporal lobe - communication
thalamus - cognitive impairment, ataxia

21
Q

what does ACA obstruction caise?

A

contralateral motor and sensory deficits in LL

22
Q

why is there hemiparesis?

A
  • loss of facilitatory drive from motor cortex
    -motor cortex > corticospinal tract > motor neurones in anterior horn > muscles
  • weakness leads to stiffness
23
Q

chronic stroke / shoulder patient pathophysiology?

A

ischaemic and haemorrhagic strokes
hemiparesis = MCA occlusion
normally the stability of the shoulder is maintained by
shoulder subluxation
differentials

24
Q

chronic stroke / shoulder patient assessment?

A
  • palpate - fingerbreadth and tenderness
  • apprehension-relocation test
  • sulcus sign test
  • active and then passive ROM (checking for weakness/stiffness)
  • strength
25
Q

chronic stroke/shoulder patient treatment?

A
  • scapula exercises - elevate/depress, protract/retract to strengthen serratus anterior and trapezius
    closed chain weight bearing activities eg wall/table push off
  • closed chain active-assisted ROM activities eg table/ wall shapes
    (closed chain = co-activation of deltoid and rotator cuff so increases neuromuscular activation and proprioception)
  • progress to active rom
26
Q

what muscles are weak in shoulder sublux?

A

trapezius and serratus anterior
rotator cuff

27
Q

what muscles are spastic in shoulder sublux?

A

pecs, rhomboids, levator scapulae, latissimus dorsi

28
Q

where is the shoulder most likely to be if spasticity is the cause of pain?

A

internally rotated and adducted

29
Q

what cells are damaged in parkinsons?

A

dopaminergic in pars compacta of substantia nigra

30
Q

why do cells die in PD?

A

aggregation of alpha synuclein

31
Q

excitatory and inhibitory pathways in PD?

A

ex - direct - d1
in - indirect - d2

32
Q

how do the different pathways cause symptoms in pd?

A

too much inhibition and not enough excitation = slowness of movement
too much excitation and not enough inhibition = tremour and inhibition

33
Q

assessment in pd

A

TUG (12 / 14.7)
-look at gait
-add cognitive component
-add motor component

34
Q

features of freezing in PD

A

flexion at hip, ankle and knee
incomplete stops
residual trembling
higher, smaller steps

35
Q

treatment in PD

A

cognitive tasks eg colour recognition and stop/go/turn/backwards steps

hurdles

comment on safety

36
Q

explain the pathophysiology of MS

A
  • unknown aetiology
  • inflammation, demyelination, gliosis, neuronal loss
  • myelin sheath surrounds neurones and is there for electrical insulation to speed up transmission of impulses, when it is lost impulses are slower
  • the inflammation also causes neuronal dysfunction / scarring / death through other processes
  • once demyelinated the axon is unprotected -> more risk of damage by inflammatory mediators
37
Q

causes of ataxia

A

dorsal column
cerebellum
- midline = gait and trunk
- vermis = speech
- posterior = vertigo, eye movement
- hemispheres = gait

sensory - proprioceptive damage
vestibular

38
Q

features of an ataxic gait

A

wide
irregular step pattern
uncoordinated
reduced ankle rom
not a straight line

39
Q

how is the blood brain barrier disrupted in ms?

A

t cell mediated
allows b cells in

40
Q

how could transfers be affected in ms?

A

balance
proprioception (LL, spinothalamic tract, dorsal column, thalamus)
motor weakness
spasticity
pain
vision
cognitive

41
Q

assessment for ataxia ms patient

A
  • gait
  • balance
  • co ordination heel / toe, finger/nose
42
Q

treatment for ataxia ms patient

A
  • balance
  • toe stand
    – one leg w progressively more knee / hip flexion
  • star excursion
  • tandem stance w progressively closer feet
43
Q

assessment for transfers ms patient

A

sitting balance
STS w all 4 phases
TUG
standing balance

44
Q

treatment for transfers ms patient

A

sitting marching
standing marching with support
squats to STS

45
Q

phases of STS

A

flexion (trunk, hip, knee, pelvis)
seat off (hip extensors)
extension (hip and knee extensors)
stabilisation

CRP scenarios (1 decks)

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