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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
what functions does the PCA supply?
occipital lobe - vision temporal lobe - communication thalamus - cognitive impairment, ataxia
21
what does ACA obstruction caise?
contralateral motor and sensory deficits in LL
22
why is there hemiparesis?
- loss of facilitatory drive from motor cortex -motor cortex > corticospinal tract > motor neurones in anterior horn > muscles - weakness leads to stiffness
23
chronic stroke / shoulder patient pathophysiology?
ischaemic and haemorrhagic strokes hemiparesis = MCA occlusion normally the stability of the shoulder is maintained by shoulder subluxation differentials
24
chronic stroke / shoulder patient assessment?
- palpate - fingerbreadth and tenderness - apprehension-relocation test - sulcus sign test - active and then passive ROM (checking for weakness/stiffness) - strength
25
chronic stroke/shoulder patient treatment?
- 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
what muscles are weak in shoulder sublux?
trapezius and serratus anterior rotator cuff
27
what muscles are spastic in shoulder sublux?
pecs, rhomboids, levator scapulae, latissimus dorsi
28
where is the shoulder most likely to be if spasticity is the cause of pain?
internally rotated and adducted
29
what cells are damaged in parkinsons?
dopaminergic in pars compacta of substantia nigra
30
why do cells die in PD?
aggregation of alpha synuclein
31
excitatory and inhibitory pathways in PD?
ex - direct - d1 in - indirect - d2
32
how do the different pathways cause symptoms in pd?
too much inhibition and not enough excitation = slowness of movement too much excitation and not enough inhibition = tremour and inhibition
33
assessment in pd
TUG (12 / 14.7) -look at gait -add cognitive component -add motor component
34
features of freezing in PD
flexion at hip, ankle and knee incomplete stops residual trembling higher, smaller steps
35
treatment in PD
cognitive tasks eg colour recognition and stop/go/turn/backwards steps hurdles comment on safety
36
explain the pathophysiology of MS
- 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
causes of ataxia
dorsal column cerebellum - midline = gait and trunk - vermis = speech - posterior = vertigo, eye movement - hemispheres = gait sensory - proprioceptive damage vestibular
38
features of an ataxic gait
wide irregular step pattern uncoordinated reduced ankle rom not a straight line
39
how is the blood brain barrier disrupted in ms?
t cell mediated allows b cells in
40
how could transfers be affected in ms?
balance proprioception (LL, spinothalamic tract, dorsal column, thalamus) motor weakness spasticity pain vision cognitive
41
assessment for ataxia ms patient
- gait - balance - co ordination heel / toe, finger/nose
42
treatment for ataxia ms patient
- balance - toe stand -- one leg w progressively more knee / hip flexion - star excursion - tandem stance w progressively closer feet
43
assessment for transfers ms patient
sitting balance STS w all 4 phases TUG standing balance
44
treatment for transfers ms patient
sitting marching standing marching with support squats to STS
45
phases of STS
flexion (trunk, hip, knee, pelvis) seat off (hip extensors) extension (hip and knee extensors) stabilisation

CRP scenarios (1 decks)

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