pathophysiology Flashcards

1
Q

what is delirium?

A

Delirium: disturbance of consciousness and cognition that develops over a short period of time (hours to days) and fluctuates over time

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2
Q

what type of conditions can include delirium?

A

o ICU psychosis
o ICU syndrome – type of organic brain syndrome manifested by variety of psychological reactions including fear, anxiety, depression, hallucinations and delirium
o Acute confusional state
o Encephalopathy
o Acute brain failure

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3
Q

hoe prevalent is delirium?

A

occurs in between 20-80% of medical and surgical patients

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4
Q

what is seen in hypoactive delirium?

A

decreases responsiveness, withdrawal and apathy

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5
Q

what is seen in hyperactive delirium?

A

agitation, restlessness and emotional lability

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6
Q

which type of delirium has better outcomes?

A

hyperactive

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7
Q

the pathophysiology of delirium is poorly understood, what are potential hypothesis behind it?

A

o Neurotransmitter imbalance: excess of dopamine and depletion of Ach, but other NT are likely to be involved
o Inflammation: abnormalities induced by endotoxin and cytokines play a role. The mediators that cross BBB in animal studies  increase vascular permeability  changes seen on EEG. Inflammation may also reduce cerebral blood flow via formation of microaggregates of fibrin, platelets, neutrophils and erythrocytes
o Impaired oxidative metabolism: the reduction is in oxidative metabolism

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8
Q

what can cause delirium?

A
  1. D: drugs
  2. E: eyes and ears
  3. L: low O2 – MI, ARDS, PE, CHF, COPD
  4. I: infection
  5. R: retention of stool/ urine
  6. I: ictal
  7. U: underhydrated and under nutrition
  8. M: metabolic
  9. S: shock, sleep deprivation
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9
Q

if cerebellum pathology what signs would be seen?

A

affects fine motor
ataxia
speech/ language deficits
dysdiachokinesia
past pointing
uncoordinated walking

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10
Q

what is intentional tremor?

A

tremor on nose to finger exam
rhythmic, oscillatory, and high amplitude tremor during a directed and purposeful motor movement, worsening before reaching the endpoint

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11
Q

how would an upper motor lesion present?

A

flexed
hypertonia
spasticity
positive toe test - flexed toe on babinski test

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12
Q

how would lower motor lesion present?

A

hypotonia
floppy
fasculitations

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13
Q

how is bells palsy managed?

A

50mg 10 day course of pred - step down
eye drops for lubrication

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14
Q

what are the signs of cerebellar dysfunction?

A

DANISH
D: dtsdiachokinesia
- A: ataxia
- N: nystagmus (coarse)
- I: intention tremor
- S: scanning speech
- H: hypotonia

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15
Q

what is nystagmus?

A

involuntary repetitive eye movements
side to side
up and down
circular motions

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16
Q

what is the function of the midbrain?

A
  • Helps with sleep cycle
  • Pain
  • Movement
  • Transmitting info about hearing
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17
Q

what info does the ascending tracts relay?

A

sensory from peripheries to brain

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18
Q

what are the two tracts within ascending tracts?

A
  • Conscious: dorsal column-medial lemniscal and anterolateral
  • Unconscious: spinocerebellar
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19
Q

the conscious ascending tract is the dorsal column-medial, what info does it carry?

A

tactile sensation - fine touch ]
vibration and proprioception

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20
Q

the anterolateral conscious tracts is split into anterior and lateral spinothalamic, what info do they carry?

A

anterior spinothalamic: crude touch and pressure
lateral spinothalamic: pain and temperature

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21
Q

what info does the spinocerebellar - unconscious tracts send?

A

proprioception

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22
Q

are tracts contralateral?

A

Most is contralateral  opposite side (90%)

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23
Q

why can some people recover from spinal tract injury?

A

10% of info remains ipsilateral
can relearn using these tracts if not damaged

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24
Q

what pathology would be seen with damage to dorsal column medial tract?

A

affects conscious
deficits in fine touch eg cotton wool - can not feel
can not feel vibration
proprioception - moving toe/ thumb up or down

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25
Q

what pathology would be seen if damage to spinothalamic ascending tract?

A

conscious sensory
anterior: can not detect pressure
lateral: can not detect pain (pin prick) or temperature (distinguish between hot or cold)

26
Q

how would spinocerebellar pathology present?

A

unconscious activity
gait ataxia, dysphagia, dysarthria, oculomotor disturbances
- deficits in proprioception
positive rhombergs

27
Q

what is the function of descending tracts?

A

motor signals from brain to lower motor neurones

28
Q

what is pyramidal?

A

originate in cerebral cortex, carry info from spinal cord to brain stem

29
Q

what type of blood collects in an extradural haematoma?

A

arterial

30
Q

where does an extradural haematoma occur?

A

: blood collecting between skull and periosteal layer of dura usually middle meningeal artery

31
Q

what shape is an extradural haematoma?

A

dome

32
Q

what type of blood is a subdural

A

venous

33
Q

what usually causes extradural haematoma?

A

trauma

34
Q

where does a subdural haematoma occur?

A

: venous blood collects between dura and arachnoid mater  no hole into skull.
venous sinuses

35
Q

what shape is subdural haematoma?

A

follows shape of skull
crescent

36
Q

what can disuse atrophy cause within an upper motor lesion?

A

not using muscles enough
fixed tightening of muscle, tendons, ligaments or skin

37
Q

how can increased tone present due to UM lesion?

A

spasticity/ rigidity

38
Q

what is the pathology within an UM lesion?

A

loss of inhib tone leading to constant contraction

39
Q

what can cause a UM lesion?

A

ischaemic/ haemorrhagic stroke, amyotrophic lateral sclerosis, MS

40
Q

how can lower MN lesion present?

A

marked atrophy
fasciculations
- Reduced tone
- Variable patterns of weakness
- Reduced or absent weakness
- Downgoing plantars or absent response

41
Q

what are fasciculations?

A

– involuntary rapid muscle twitches that are too weak to move limb

42
Q

what is the pathology of LM lesion?

A

no signal to tell muscles what to do

43
Q

what is the aetiology behind LM lesion?

A

peripheral nerve trauma/ compression, spinal muscular atropy, amyotrophic lateral sclerosis, GBS, poliomyelitis

44
Q

what is neuromyelinitis optica?

A

severe rare demyelinating disorder previously considered as a form of MS  rare and characterised by bilateral optic neuritis and transverse acute myelitis with no other neurological involvement

45
Q

what is useful is diagnostics in optic nerve neuropathies?

A

visual evoked potentials

46
Q

what does demyelination have within it?

A

conduction block and slowing conduction
related to modifications in distributions of voltage gated sodium

47
Q

what is seen within upper motor neurone damage?

A
  • Hypotonia
  • Due to no signalling
  • No tone/ power
  • Fistulations
  • Floppy/ droopiness
48
Q

what is the pathophys of myasthenia gravis?

A

autoimmune condition where antibodies are produced and affect NMJ
- They block, alter or destroy the receptors for Ach at NMJ which prevents muscle from contracting

49
Q

what are the symptoms of myasthenia gravis?

A
  • Symptoms: weakness of eye muscles, drooping of one or both eyelids, blurred/ double vision, changes in facial expressions, difficulty in swallowing, SoB, weakness in arms, legs, fingers, neck
50
Q

what is the management of myasthenia gravis?

A
  • Management: using immunosuppression drugs, anticholinesterase (neostigmine)
51
Q

what is the pathophys of MND?

A

variety of specific diseases affecting motor nerves
progressive degeneration of upper and lower motor neurones

52
Q

what is the most common type of MND?

A
  • Amyotrophic lateral sclerosis is most common and well known type of MND
53
Q

what are signs of MND?

A

lower motor  wasting, reduced tone, fasciculations, reduced reflexes and upper  increased tone or spasticity, brisk reflexes and upgoing plantar reflex

54
Q

what is riluzole used for in MND?

A

riluzole: can slow progression of disease and extend survival,

55
Q

what is measured within GCS?

A

eyes
voice
motor

56
Q

how do you mark eyes on GCS?

A

4 pt; spontaneous
3pt: speech
2: pain
1: none

57
Q

how do you mark verbal response on gcs?

A
  1. orientated
  2. confused
  3. inappropriate sounds
  4. incomprehensive sounds
  5. none
58
Q

how do you assess motor response on GCS?

A

O: obeys - 6
L: localises pain -5
D: draws back -4

B:bends - 3
E: extends -2
N: none -1

59
Q

what GCS requires airway management?

A

8 or less

60
Q

between vancomycin and gentamycin, which can not be used if there is MRSA resistance?

A

vancomycin

61
Q
A