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Medicine year 2 semester 1 > Case 19- Pathology and Anatomy > Flashcards

Case 19- Pathology and Anatomy Flashcards

1
Q

Multiple Sclerosis

A

A disease of the CNS only, an autoimmune disease though the cause is not fully understood. The immune system attacks the oligodendrocytes. Doesn’t affects the PNS because it doesn’t contain Oligodendrocytes.

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2
Q

Causes of Multiple Sclerosis

A

Loss of myelin affects conduction of action potential down nerves, leading to conduction block and loss of function in affected nerves. The inflammatory process in MS leads to degradation of myelin, apoptosis of oligodendrocytes, disruption to the energy and nutrient supply of the neurons, ionic imbalance and eventually neurodegeneration.

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3
Q

MS onset and treatment options

A

Onset between 15 and 50 years of age

Treatment options- corticosteroids, beta interferons 1A and 1B and Glatiramer acetate.

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4
Q

Key clinical signs and symptoms of MS

A
  • Visual disturbance in one eye; optic neuritis, blurred vision, pain moving eye, loss of colour discrimination
  • Strange sensory sensations; feeling of a patch of wetness or burning, tingling sensation/sensory loss on one side of the body.
  • Lhermitte’s sign; feeling of electric shock down spine and on to limbs
  • Other possible sensory disturbances upon neurological examination.
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5
Q

Other signs and symptoms MS

A
  • Foot dragging; onset of weakness after walking
  • Leg cramping
  • Fatigue
  • Spasticity/increased muscle tone
  • Imbalance/loss of coordination
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6
Q

Types of MS

A

1) Relapsing remitting multiple sclerosis (RRMS)
2) Primary Progressive Multiple Sclerosis (PPMS)
3) Secondary Progressive Multiple Sclerosis (SPMS)

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7
Q

Relapsing remitting Multiple sclerosis

A

RRMS need MRI scan to confirm. The relaxing and remitting nature of the disease is due to damage to the myelin causing symptoms, followed by repair and remyelination that restores some function. However, the repairs are not complete and each new relapse causes a deterioration in symptoms.

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8
Q

Primary progressive multiple sclerosis (PPMS)

A

This is MS without the remission phases. PPMS is characterised by a continual degeneration without periods of recovery/remission

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9
Q

Secondary Progressive Multiple Sclerosis (SPMS)

A

After an initial phase of RRMS the symptoms get progressively worse similar to PPMS

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10
Q

Examination findings that would occur in lower but not upper motor neurone disease

A
  • Fasciculations
  • Muscle wasting
  • Hypotonia
  • Reduced reflexes
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11
Q

Three things a doctor should consider before breaking bad news

A
  • Setting up the appointment as soon as possible
  • Allow enough uninterrupted time, ensuring no interruptions
  • Aim for a comfortable, familiar environment
  • Encouraging the patient to invite support such as relatives or close friends
  • Ensure preparedness regarding the clinical case, including background, progress and management options
  • Put aside personal feelings / biases wherever possible
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12
Q

Good practise in breaking bad news

A
  • Assessing perception- how much they remember
  • Obtaining invitation- how much the patient wants to know
  • Clear information
  • Addressing emotions
  • Preparing a strategy
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13
Q

Why do many patients hide their conditions from their family?

A
  • Not wanting to burden them
  • Fearing judgement/stigma
  • Avoiding awkward conversations
  • Protecting their job
  • A feeling of wanting to regain some control
  • Not wanting to appear weak
  • Facing difficulty in accepting the diagnosis and by telling people this often cements the reality
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14
Q

Motor neurone disease

A

Death of motor neurones

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15
Q

The 2 types of motor neurones

A

1) Upper- starts in the cortex or brainstem

2) Lower- starts in the spinal cord

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16
Q

Different mechanisms for how motor neurons disease develops

A
  1. Dysfunction RNA transport through nuclear membrane
  2. Dysfunction RNA metabolism (RNA-binding proteins end up in cytoplasm)
  3. Impaired proteostasis – protein deposition
  4. Impaired DNA repair
  5. Mitochondrial dysfunction and oxidative stress
  6. Oligodendrocyte dysfunction – less support neurones
  7. Neuroinflammation – activated astrocytes and microglia
  8. Defective axon transport
  9. Defective vesicular transport
  10. Excitotoxicity
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17
Q

Multiple sclerosis

A

Death of Oligodendrocytes, autoimmune disease

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18
Q

What causes multiple sclerosis

A

Microglial cells activated, produce chemicals, they degrade the blood brain barrier, activate other immune cells which can get into the brain because of degraded barrier, produce more cytokines, attack/degrade myelin
Cytotoxic damage to myelin, damages oligodendrocytes
Inflammation/immune response drives the pathology - lots of potential mechanisms for the damage.
Driven by inflammation

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19
Q

The possible pathological mechanisms of MS

A

• Chronic inflammation -> Increase reactive oxygen species (ROS)
• Energy deficiency – Damage to mitochondria neurones and oligodendrocytes
• Loss of Oligodendrocytes -> loss of trophic support for neurones
• Ion channel redistribution, functional impairment of ATPase – Ionic imbalance
• Excitotoxicity – increased release of glutamate
Apotosis of oligodendrocytes and, ultimately, neurones

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20
Q

Fissures of the Cerebellum

A
  • Primary-between the anterior and posterior lobes
  • Horizontal- in the posterior lobe (structural)
  • Postereolateral
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21
Q

Cerebellum- Afferent nerves

A
  • Towards Central Nervous system
  • Group of nerve fibres (axons)
  • Various Sensory Modalities
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22
Q

Efferent nerves

A
  • Away from Central Nervous System

* Motor nerve fibres to effector organs (muscle etc)

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23
Q

Vestibulocerebellum

A
  • Regions of the Cerebellum- Flocculonodular lobe, Vermis
  • Cerebellar nuclei- fastigial
  • Associated with inferior Cerebellar Peduncle
  • Function- balance, equilibrium, posture, extensor muscles
  • Input- vestibular nucleus, dorsal spinocerebellar. Receives input from mechanoreceptors, golgi tendon organs etc- proprioceptive information
  • Output- vestibular and reticular nuclei (in brainstem)
24
Q

How information travels in the Vestibulocerebellum

A
  1. Input from the vestibular nerve and dorsal spinocerebellar tract via the vestibular nuclei to the ipsilateral flocculonodular lobe
  2. Cortical efferent Purkinje fibres to the fastigial nucleus
  3. Projections to the reticular and vestibular nuclei
  4. Some fibres from the reticular nuclei returns to cerebellum. Many fastigial efferent fibres decussate to the contralateral brainstem
  5. Descend via the reticulospinal and vestibulospinal tracts to the extensor neurons in the spinal cord
25
Q

Spinocerebellum

A
  • Regions of the cerebellum- Anterior lobe, paravermal region
  • Cerebellar nuclei- interposed (globose and emboliform), fastigial
  • Associated with the superior and inferior Cerebellar Peduncle
  • Function- muscle tone, stability, ongoing movement regulation (coordination)
  • Input- dorsal and ventral spinocerebellar tract. From the mechanoreceptors, golgi tendon organs etc
  • Output- red nucleus
25
Q

Spinocerebellum

A
  • Regions of the cerebellum- paravermal region and possible the whole of the anterior lobe
  • Cerebellar nuclei- interposed (globose and emboliform), fastigial
  • Associated with the superior and inferior Cerebellar Peduncle
  • Function- muscle tone, stability, ongoing movement regulation (coordination)
  • Input- dorsal and ventral spinocerebellar tract. From the mechanoreceptors, golgi tendon organs etc
  • Output- red nucleus
26
Q

How information travels through the Spinocerebellum

A
  1. Afferents from the spinocerebellar tracts enter the cerebellum via the superior and inferior peduncles
  2. Both project to the ipsilateral paravermal region
  3. Purkinje fibres project to the interposed and fastigial nuclei
  4. They project to the contralateral red nucleus via the superior cerebellar peduncle
  5. Fibres descend through the spinal cord via the rubrospinal tract on the contralateral side to flexors
  6. Some projections go to the inferior olivary complex
27
Q

Cerebro/Ponto/Neocerebellum

A
  • Regions of the Cerebellum- anterior and posterior lobes, possibly just posterior
  • Cerebella nuclei- dentate
  • Associated with the middle (mainly) and superior Cerebellar Peduncle
  • Function- initiation and planning of movement, motor learning
  • Input- Cerebral cortex via the pontine nuclei (pontocerebellar fibres)
  • Output- to the premotor cortex, supplementary motor area and motor cortex via the thalamus (and association somatosensory cortex)
28
Q

How information travels through the Neocerebellum

A
  1. Corticopontine fibres project onto the deep pontine nuclei
  2. Pontocerebellar fibres decussate and enter the cerebellum via the middle cerebellar peduncle to terminate in the cerebellar cortex
  3. Purkinje cells project onto the dentate nucleus
  4. Fibres leave the superior cerebellar peduncle and project to the contralateral thalamus- some via the red nucleus
  5. Fibres project to the cortex
29
Q

How the Neocerebellum is involved in motor learning, Practise makes perfect

A
  • Repeated stimulation of mossy and climbing fibres changes the structure of purkinje cells
  • This leads to a permanent change at the level of the cerebellar cortex, which leads to learning
30
Q

The symptoms associated with cerebellar damage

A 
DANISH
• Dysdiadochokinesia
• Ataxia
• Nystagmus
• Intention tremor
• Slurred speech
• Hypotonia
31
Q

Symptoms caused by damage to the Vestibulocerebellum

A

1) Staggering gait- Ipsilateral, falling to affected side

2) Nystagmus on lateral gaze (contralteral)

32
Q

Symptoms caused by damage to the Spinocerebellum

A

1) Ataxia

2) Hypotonia / Hyporeflexia- due to loss of activity of pontoreticulospinal fibres

33
Q

Symptoms caused by damage to the Neo/Ponto/Cerebrocerebellum

A

1) Slow movement onset
2) Speech impairement- slurred
3) Dysmetria- undershooting or overshooting
4) Dysdiadochokinesis
5) Rebound phenomena
6) Intention/action tremor
7) Decompoisition of movements (intention/action tremors)

34
Q

Peripheral nerves

A
  • Afferent nerves- towards central nervous system, a group of nerve fibres (axons), various sensory modalities
  • Efferent nerves- away from the CNS, motor nerve fibres to effector organs
35
Q

Motor and Sensory nerves

A
  • Motor- multipolar, cell body in the spinal cord, fast, myelinated
  • Sensory- unipolar, cell body in the dorsal root ganglion. Different types, different speeds. Myelinated, unmyelinated
36
Q

Classification of peripheral nerves

A
  • Roman numeral system- only to sensory nerve fibres

* Letter system- both sensory (afferent) and motor (efferent)

37
Q

Classification of peripheral nerves- Roman numericals

A 
Ia = muscle spindle = A alpha
Ib = Golgi tendon organs = A alpha
II = muscle spindle, touch, pressure = A beta
III = pain, cold receptors = A delta
IV = pain, temperature = C
38
Q

Classification of peripheral nerves- letter system

A
  • A alpha = 13-22µm, VC = 70-120, alpha motor neurones, touch, muscle spindle, Golgi tendon organs
  • A beta = 8-13µm, VC = 40-70, touch, kinaesthesia, muscle spindle
  • A gamma = 4-8µm, VC = 15-40, touch, pressure, gamma motor neurones
  • A delta = 1-4µm, VC = 5-15, pain, crude touch, pressure, temperature
  • B = 1-3µm, VC = 3-14, preganglionic autonomic
  • C = 0.1-1µm, VC = 0.2-2, pain, touch, pressure, temp, postganglionic autonomic
39
Q

Sensation and Perception

A

• Sensation- conscious/subconscious awareness of external environment
• Perception- interpretation of sensation (cortex)
• Sensory nerves convert stimulus (chemical, mechanical, physical) into action potentials
The two types of sensory modalities are general senses and special senses (smell, taste, hearing, equilibrium, balance)

40
Q

The two types of general sense

A
  • Somatic- tactile, thermal, pain, proprioceptive

* Visceral- conditions of internal organs

41
Q

Types of sensory receptors

A
  • Microscopic features- free nerve endings, encapsulated nerve, separate cells
  • Receptor location and activating stimuli- Exteroceptors, Interceptors, Poprioceptors
  • Types of stimulus detected- Mechanoreceptors, thermo receptors, Nociceptors, Chemoreceptors, Photoreceptors, Osmoreceptors
42
Q

Sensory receptors in the skin

A 
• Hair follicle receptors
• Free nerve endings
• Meissner corpuscle
• Merkel cells
• Pacinian corpuscle
• Ruffini endings
All but nociceptors are low threshold mechanoreceptors.
43
Q

What receptors enter the spinal cord through the dorsal root ganglion

A

Pain, touch and proprioception receptors send connections straight to the brain

44
Q

Receptor fields

A

The region of the sensory surface that when stimulated causes a change in the firing rate of the neuron. The smaller the receptor field the higher the specificity. Two types:

1) Small, numerous, highly discriminatory i.e. fingertips
2) Large, sparse and low discriminatory i.e. the bacl

45
Q

Convergence

A

In some sensory pathways i.e. the convergence of rods in the retina. Can lead to one sensory modality modulating another, the gated theory of pain, multisensory processing. 2 receptor fields can combine to form one. Allows you to experience low threshold stimuli as they converge together so they get over the stimuli to send an action potential to the brain. Can’t tell where the stimuli is from

46
Q

Divergence

A

Signal amplifying, allows one signal to be sent to multiple areas in the body. Get a larger amount of signal towards the brain.

47
Q

Basic reflex arch

A

Sensory neurone -> interneurone -> motor neurone
(sensory neurone sending signal into spinal cord via dorsal root which sends signal to brain where it synapses on interneurone which acts on motor neurone). Fast, autonomic and independent of the brain. Relay on short local circuits in the brain

48
Q

Lateral inhibition

A
  • Stimulus centre of receptive field increases
  • Receptor field lateral to the stimulus decreases
  • This increases the contrast between the receptor fields
  • If one receptor is activating more than the other, it can have an inhibitory effect on the other receptors, allows for discrimination. Allows you to tell the boundary of the stimuli. Neurons are constantly firing but fire more when there is a stimuli, pattern is important
49
Q

Sensory transuction

A

The conversion of a sensory stimulus from one form to another

50
Q

Pacinian corpuscles

A

Sensitive to changes in mechanical pressure (mechanoreceptors). Pressure o nthe skin changes the shape of the Pacinian corpuscle. Alters the shape of the pressure sensitive sodium channels, the sodium channels open- depolarisation. Generator potential. Fast acting, large field. Vibration, pressure (60-300Hz). A-beta. Encapsulated endings

51
Q

Hair follicle receptors

A

Mechanoreceptors, motion and direction. II and A-beta receptors

52
Q

Free nerve ending receptors

A

Nociceptors and thermoreceptors, variable receptor fields and speeds. Pain A-delta.

53
Q

Meissner corpuscle, Merkel cells and Ruffini corpuscle

A

Meissner corpuscle- Mechanoreceptors, fast acting. Small receptive fields. Light touch, stroking, flickers, vibrations (5-40Hz). A-beta. Encapsulated endings
Merkel cell- mechanoreceptors, slow, small receptive field. Steady pressure, texture. A-beta
Ruffini corpuscle- mechanoreceptors and thermoreceptors. Slow acting, large receptive field. Steady pressure, stroking, heat perception. A-beta. Encapsulated endings

54
Q

Tonic action potential

A

Baseline action potential

55
Q

What does coding of sensory information depend on

A

Many sensory receptors fire tonic action potentials. Coding of sensory information occurs due to:
• Change in firing rates- increase/decrease
• Duration of time action potentials fire for
• Activation of different parts of the receptive field

56
Q

Rapid and slow acting receptors

A

1) Rapid adapting receptors- Meissner corpuscles, some hair follicle receptors and Pacinian corpuscles. Responds to application/removal of stimulus. Transient, phasic, vibratory stimulus. Fails to respond to maintained stimulus
2) Slow adapting receptors- Merkel cells, some hair follicles and Ruffini corpuscles. Encode stimulus intensely. Active for duration of maintained stimulus

Medicine year 2 semester 1 (53 decks)

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