Previous Exam Questions Flashcards

1
Q

Discuss the three main histological features of Alzheimer’s

A

The senile plaque (neuritic plaque)
o occur mainly in the hippocampus (also in other areas of cortex and deep grey matter)
o up to 200 m in diameter
o initially is a collection of dilated pre-synaptic neuronal processes which contain many organelles
o with maturation observe:
➢ enlargement
➢ degeneration of the neuronal processes
➢ core of aluminosilicates and amyloid protein develops
➢ reactive astrocytes and microglia collect at the periphery of the plaque
o burnt out phase of plaque development
➢ the neuronal processes have degenerated completely
➢ the plaque is an extracellular collection of amyloid protein

Neurofibrillary tangles (developing in cytoplasm of affected cells)
o appear in the cytoplasm of neurons
o occur mostly in hippocampal neurons (occur in other parts of CNS also)
o observe the following changes:
➢ thickening of fibrils in the neuronal cytoplasm
➢ the fibrils form tortuous, elongated, cork-screw like structures
➢ the fibrils resemble neurofilament and microtubule associated proteins

Diffuse Neuronal Loss
As name suggests

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2
Q

List the causes of Guillan Barre Syndrome

A

Factors predisposing to GBS:

  • follows infection (bacterial and viral agents)
    • Campylobacter jejuni (onset variable; affected patients commonly experience more rapid deterioration)
    • EBV
    • Herpes
    • Lyme disease
    • HIV
    • Zika virus
    • Gangliosides (grey matter lipids in the brain) are targeted by immunoglobulins and share antigenic epitopes with some bacterial and viral antigens
  • Linked to vaccines
    • swine flu
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3
Q

Discuss the clinical features of GBS

A

Painless onset of mild weakness in the lower extremities

  • the pt often does not notice the weakness unless walking up hill/climbing stairs etc.
  • may have tingling/paraesthesia in toes and fingers
  • deep tendon reflexes are diminished

Weakness becomes more profound

  • after a few days since onset
  • often extends to involve upper limbs and eventually the face (landry’s ascending paralysis)
  • deep tendon reflexes disappear
  • loss of proprioception in arms and legs
  • breathing and swallowing becomes difficult
  • clinical findings include: symmetrical motor weakness (both proximal and distal mm of all limbs

Weakness progresses for several days to a couple of weeks, and finally stabilises, remaining constant for a variable period of time.
Recovery then begins (85% of pt. healing is complete in several weeks to months)

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4
Q

Write notes on complex partial seizures

A

It is synonyms with the temporal lobe = psychomotor seizures
- usually originating in one of the temporal lobes
- the seizure results in an impairment or loss of consciousness
Observe 2 variants:
1st
- an initial partial seizure with symptoms and signs reflecting its origin in the temporal lobe
- a change in the initial symptoms and signs in which we observe motor complaints (automatisms) e.g. lip smacking, chewing, fumbling of hands, complex behaviour
- the pt gradually experiences varying degrees of impaired consciousness and memory (may have postictial amnesia)

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5
Q

Define mononeuritis multiplex

A

When several peripheral nerves are affected in a specific point in time

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6
Q

What is the main cause of mono neuritis multiplex?

A

Vasculitis

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7
Q

Discuss the diagnosis of Fibromyalgia

A

week 11

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8
Q

Define and describe the three types of neuronal degeneration and their key features

A

Axonal degeneration
- primary degeneration of the axon followed by secondary degeneration of the myelin sheath
- results in degeneration of the distal axon (then degeneration follows a distal to proximal pattern)
- usually symmetric
- most common pathologic reaction occurring in polyneuropathies
- often secondary to metabolic aetiology
Following manifestations can be evident:
- symmetrical glove and stocking sensorimotor disturbances
- diminished/loss of deep tendon reflexes
disordered ANS function

Segmental demyelination
is the focal degeneration of the myeline sheath with sparing of the axon. occurring mainly in focal mononeuropathies; also seen in generalised sensorimotor or predominantly motor neuropathies
*Can be acquired (caused by immune ir inflammatory conditions) or hereditary (Charcot-Marie-Tooth disease)
*classification:
Primary: schwann cell is damaged
Secondary: follows axon degeneration

Wallerian degeneration
When the axon degenerates distal to a focal lesion that interrupts its continuity

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9
Q

Define and describe the three types of neuronal degeneration and their key features

A

Axonal degeneration
- primary degeneration of the axon followed by secondary degeneration of the myelin sheath
- results in degeneration of the distal axon (then degeneration follows a distal to proximal pattern)
- usually symmetric
- most common pathologic reaction occurring in polyneuropathies
- often secondary to metabolic aetiology
Following manifestations can be evident:
- symmetrical glove and stocking sensorimotor disturbances
- diminished/loss of deep tendon reflexes
disordered ANS function

Segmental demyelination
is the focal degeneration of the myeline sheath with sparing of the axon. occurring mainly in focal mononeuropathies; also seen in generalised sensorimotor or predominantly motor neuropathies
*Can be acquired (caused by immune ir inflammatory conditions) or hereditary (Charcot-Marie-Tooth disease)
*classification:
Primary: schwann cell is damaged
Secondary: follows axon degeneration

Wallerian degeneration
When the axon degenerates distal to a focal lesion that interrupts its continuity
* caused by:
- trauma
- infarction of peripheral nerve (diabetic mononeuropathy, vasculitis)
- neoplastic infiltration

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10
Q

Write notes on MS plaques

A

The characteristic feature of MS is the “plaque” i.e. an area of demyelination. (abnormal area in CNS)

a) acute plaque (i.e. early lesion)
- occurs during acute inflammatory episode in CNS
- 0.1 - several centimetres in diameter
- often occurs in periventricular areas of CNS
- plaque is soft and pink
- ill-defined borders
- oedema **
- histologically: breakdown of myelin & phagocytosis by macrophages
- perivascular infiltration and accumulation (cuffing) of inflammatory cells (T-cells, plasma cells)
- perivascular (around blood vessel) infiltration of monocytes & lymphocytes (found in infection – immune system activated)

b) chronic plaque: (i.e. myelin breakdown & inflammation subsides)
- lesion that occurs as acute inflammatory episode in CNS dies down
- reactive fibrillary gliosis occurs
o gliosis = specialized CNS scar tissue produced by the enlargement of astrocyte cellular processes.
o When CNS is damaged astrocyte processes enlarge & expand to fill gaps left behind by dead cells
o Process referred to as gliosis, but resulting permanent scar tissue is called a chronic plaque
- sharply defined, grey/translucent areas of demyelination (as previous inflammatory process has destroyed the myelin sheath)
- few/absent oligodendrocytes
- subsidence of perivascular infiltrates
- induration (hardening / stiffening) of affected tissues (hence sclerosis = scaring)

• Commonest sites of development of the patches of demyelination is the white matter of the brain & spinal cord. The following areas are characteristically involved:

  • optic nerves (= the commonest initial site)
  • brain stem
  • cerebellar peduncles
  • dorsal and lateral (pyramidal) spinal tract
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11
Q

Clinical features of MS

A

• Observe sudden development of a focal neurological deficit which spontaneously recovers (very first manifestation)
• Frequency of initial symptoms and signs:
- limb weakness 40-50%
- optic neuritis 20% → pale optic nerve → visual field . lost in L eye on R side
- bladder dysfunction 5%
- paraesthesia 20% (fingers & toes arise 1st)
- diplopia 10%
- vertigo 5%

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