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Medical Sciences B > Symptoms, signs, pathological processes, cerebral haemodynamics > Flashcards

Symptoms, signs, pathological processes, cerebral haemodynamics Flashcards

1
Q

What are the words describing different levels of loss of sensation?

A

loss- Anaesthesia
heightened- Hyperasthesia
altered- Parasthesia

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2
Q

What are the words describing different levels of sense of smell?

A

lost- Anosmia

diminished- Hyposmia

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3
Q

What are the words describing different levels of sense of taste?

A

lost- Ageusia

diminished- agueusie

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4
Q

What is the difference between monoplegia, paraplegia, hemiplegia and quadriplegia?

A

Muscle paralysis of:

one limb -Mono
2 limbs -Para
one side of the body -Hemi
4 limbs -Quadri

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5
Q

What are the words describing different types of altered movements?

A

Kinesia:

Hyper- excess normal or abnormal movements
Dys- impairment of voluntary movement
Hypo- decreased bodily movement
A- lost movement
Brady- slow movement
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6
Q

List examples of hyperkinesias

A
  • tremors
  • convulsions
  • chorea
  • athetosis
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7
Q

Convulsion

A
  • seizure

* sudden, violent, irregular movement of the body, caused by involuntary contraction of muscles

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8
Q

Chorea

A

• jerky involuntary movements

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9
Q

Athetosis

A
  • abnormal muscle contraction causes involuntary writhing movements
  • ex. pill rolling in cerebral palsy
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10
Q

What are the words describing different types of altered speech?

A

Dysphasia -deficiency in the generation of speech

Aphasia -inability to generate speech

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11
Q

dysarthria

A

difficult or unclear articulation of speech that is otherwise linguistically normal

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12
Q

apraxia and dyspraxia

A

difficulty planning a movement, even though they know what it is and how to do it

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13
Q

What are the words describing different types of altered reflexes?

A

hyperreflexia

hyporeflexia

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14
Q

Pathologic changes in the NS can be classified in what 3 broad groups?

A

a) Focal lesions
b) Diffuse/generalised disorders
c) Systemic nervous diseases

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15
Q

What is a NS focal lesion?

A

causes localized disturbance of function

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16
Q

What is a NS diffuse/generalised disorder?

A
  • infective, metabolic, toxic, vascular

* affect NS and supporting elements throughout NS

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17
Q

What is a NS systemic nervous disease?

A
  • pathologic process shows predilection for a particular neuronal structure or group
  • anterior horn cells, cerebellum, corticospinal tracts
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18
Q

Gliosis

A

Damage to brain -> multiplication and enlargement of neuroglia with increased fibril production -> cell atrophy -> dense meshwork of fibres -> scarring

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19
Q

Satellitosis

A
  • oligodendrocytes increased in number and size when neurones are damaged
  • microglia phagocytose damaged cells and their degradation products
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20
Q

What are the fundamental types of nerve injury?

A

a) neuropraxia
b) axonotmesis
c) neurotmesis

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21
Q

What is neuropraxia?

A
  • transient iteration of nerve conduction WITHOUT loss of axonal continuity
  • Schwann cells start to remyelinate the axon
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22
Q

What is axonotmesis?

A
  • transection of axons (or loss of integrity) with preservation of endoneurium
  • wallerian degeneration -> repair if cell body intact
  • Schwann cells functional -> some scar tissue
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23
Q

What is neurotmesis?

A
  • complete disruption of nerve fibre and connective tissue surrounds
  • loss of normal architecture
  • wallerian degeneration
  • needs surgical intervention repair
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24
Q

What occurs following axon damage?

A

a) chromatolysis- nissl bodies break into finer masses
b) (distal) Wallerian degeneration- swelling, neurofilament hypertrophy, myelin sheath shrinks and disintegrates, neurolemma remains; axon disappears
c) (proximal) swelling and dispersal of Nissl substance, cell increase metabolic activity, protein synthesis, mitochondrial activity; new terminal sprouts project

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25
Q

What occurs during axon regeneration?

A

1) macrophage phagocytose debris
2) protein synthesis accelerates
3) Schwann cells multiply and connect both ends
4) regenerating axon evade Schwann tube, growing toward distal part of axon (if gap not too large)

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26
Q

What factors influence cerebral oxygenation?

A
  • cerebral blood volume
  • cerebral blood flow
  • cerebral perfusion pressure
  • intracranial pressure
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27
Q

What determines cerebral blood volume?

A
  • diameter of blood vessels
  • arterial blood pressure
  • total blood volume
  • brain activity
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28
Q

What determines cerebral blood flow?

A

cerebral perfusion pressure divided by cerebrovascular resistance (influenced by length, diameter, laminar flow, arrangement of vessels)

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29
Q

What is cerebral perfusion pressure? what influences it?

A
  • pressure gradient btw arteries and veins
  • influenced by mean arterial pressure and intracranial pressure
  • usually constant
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30
Q

What is intracranial pressure (ICP)? influenced by?

A
  • pressure in skull, external to blood vessels
  • normal is 7-15mmHg
  • influenced by: brain volume, blood volume, CSF volume
31
Q

What are the compensatory mechanisms to increases in ICP?

A
  • CSF reabsorption outside cranial vault
  • vasoconstriction and compression of veins to reduce blood volume
  • then systemic blood pressure increases (due to systemic vasoconstriction)
32
Q

What are the causes of increased ICP?

A
  • tumour
  • cerebral oedema
  • increased CSF: production, obstruction, absorption
  • haemorrhage
  • craniosyntosis
  • cerebral venous thrombosis
  • increase intracranial venous pressure
33
Q

What are the consequences of increased ICP?

A
  • vascular damage: papilloedema
  • intracranial nerve damage (CNIII and VI)
  • obstruction of CSF flow
  • changes skull bones
  • reduced cerebral blood flow and perfusion pressure (causes more ischemia)
  • distortions and dislocations of brain substance (herniation)
34
Q

What are the clinical manifestations of increased ICP?

A
  • consciousness change (confused, drowsy, coma)
  • increased arterial blood pressure
  • decreased HR
  • altered respiration (hyperventilation, cheyne-strokes resp.)
  • nausea, vomiting
  • headache
  • pupils dilated (CNIII damage from herniation)
35
Q

List the major types of cerebral oedema?

A
  • vasogenic
  • cytotoxic
  • interstitial
36
Q

What is vasogenic cerebral oedema?

A
  • disruption in integrity of BBB, so that plasma proteins and water move into interstitial tissue
  • mostly occurs in white matter
  • caused by: infarcts, neoplasms, abscesses
37
Q

What is cytotoxic cerebral oedema?

A
  • cellular injury -> disruption of active transport systems
  • water enters cells -> swell
  • occurs in grey matter
  • caused by: general ischaemia, infarcts
38
Q

What is interstitial cerebral oedema?

A
  • trans-ependymal movement of CSF from ventral to extracellular spaces
  • caused by non-communicating hydrocephalus
39
Q

What are the effects of cerebral oedema?

A
  • increases ICP
  • disturbs level of consciousness
  • focal neurological deficits
  • progress -> more ischemia -> more oedema
  • herniation
40
Q

Define herniation

A

abnormal movement of tissue through an opening

41
Q

List the different types of brain herniation?

A
  • uncle
  • cerebellar tonsillar
  • cingulate
  • transcalvarial
42
Q

Uncal herniation

A
  • uncut is medial projection of temporal lobe
  • herniates under tentorium cerebella
  • compresses oculomotor nerve (pupil dilation, strabismus)
  • compress posterior cerebral artery (occipital lobe infarct)
  • alter respiration (cheyne-strokes resp)
43
Q

Cerebellar tonsillar herniation

A
  • cerebellar tonsils go into foramen magnum
  • compresses brainstem (cardiac, resp, consciousness)
  • cheyne-stroke resp
  • death
44
Q

Cingulate herniation

A
  • cingulate gyrus herniates under falx cerebri

* anterior cerebral artery maybe compressed (infarct)

45
Q

Transcalvarial herniation

A
  • result of post-surgical oedema or trauma

* brain through defect in skull

46
Q

Neuron vs neuroglia

A

Neuron:
• functional unit of NS
• propagate electrical impulses
• 3 types

Neuroglia:
• supportive cells
• 6 types

47
Q

List and describe the glial cells of the PNS?

A

PNS:
• Schwann- myelin production
• Satellite- regulate and support

CNS:
• Oligodendrocytes- myelin production
• Astrocytes- regulate and support BBB
• Microglia- phagocytosis
• Ependymal cells- produce and circulate CSF in choroid plexus
48
Q

Graded potentials

A
  • small changes in resting membrane potential due to opening of ion channels in response to signal
  • don’t propagate
  • at synapse or sensory receptor
  • summate up to threshold potential
49
Q

List the sequence of events occurring in an action potential?

A

1) Resting membrane potential: voltage-gated Na+ channels rest, voltage-gated K+ channels closed
2) Stimulus depolarized to threshold
3) Voltage-gated Na+ channel gates open
4) Voltage-gated K+ channels open and Na+ channels inactive
5) Voltage-gated K+ channels remain open, Na+ channels rest

50
Q

Absolute vs relative refractory period

A

Absolute
• voltage-gated Na+ gates are open and cannot be opened more (cant get 2nd AP)

Relative
• Na+ channels are in resting state
• need higher than usual stimulus for 2nd AP

51
Q

What determines speed propagation of APs in neurons?

A
  • amount of myelination
  • axon diameter
  • temperature
52
Q

What are the words describing different levels of loss of muscle tone?

A

decrease- hypotonia
loss- atonia
increase- hypertonia

53
Q

Rigidity

A

increase in muscle tone which does not alter with the speed of passive movement

54
Q

Clasp knife spasticity

A

increase in muscle tone which changes with the speed of passive movement and at the extremes of the movement arc

55
Q

What are the words describing different levels of loss of tactile sensation?

A

decrease- hypoesthesia
loss- anesthesia
peculiar (pins and needles)-paraesthesia
heightened- hyperaesthesia

56
Q

Loss of ability to contract skeletal muscle

57
Q

Decrease in the ability contract skeletal muscles

58
Q

Slow, irregular, twisting movement of 1 part of the body

59
Q

Irregular, jerky, involuntary movements no purpose

60
Q

Involuntary movement of part or parts of the body, resulting from alternating contractions of skeletal muscles

61
Q

A lack of muscle co-ordination. Often used to describe a ‘staggering’

A

Ataxic gait

62
Q

Inability to perform a purposeful, learned motor activity, although they are willing to do so and there is no associated motor or sensory deficit

63
Q

Reduced ability to perform a purposeful, learned motor activity, although they are willing to do so and there is no associated motor or sensory deficit

64
Q

Presence of involuntary movements

A

hyperkinesia ???

65
Q

What are the words describing different levels of loss of voluntary movement?

A

without- Akinesia
slowness- Bradykinesia
reduced- hypokinesia

66
Q

Absence in either comprehension or expression of speech

67
Q

Disturbance in comprehension or expression of speech

68
Q

Decrease in bulk of 1 or more muscles

69
Q

Type of dizziness where individual feels as if they or the environment is moving or spinning

70
Q

Partial or complete loss of memory

71
Q

Alteration in the level of consciousness, characterised by varying degrees of disorientation, with impairment in perceiving, thinking, responding and remembering events currently occurring

72
Q

What is the importance of cerebral autoregulation to normal neuronal functioning?

A
  • neurons exclusively run on glucose
  • can only get it from blood supply
  • neurons use 20% of body blood glucose
  • small changes have big effects
73
Q

What are the possible consequences of cerebral oedema?

A
  • increase ICP
  • herniation
  • disturbance in consciousness level
  • focal neurological deficit
74
Q

What is the difference between supratentorial and infratentorial brain herniation?

A

above vs below the tentorium cerebellae (divides cerebellum from cortex)

Medical Sciences B (23 decks)

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