NEURO 110 Peripheral Neuropathy Flashcards Preview

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Flashcards in NEURO 110 Peripheral Neuropathy Deck (31)
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1
Q

What is neuropathy?

A

Nerve disease

2
Q

How do you classify a neuropathy?

A

The type of and number of nerves affected, aetiology, timing and pathology

3
Q

How would a motor neuropathy present?

A

Weakness, wasting, fasiculations and areflexia

4
Q

How can a sensory neuropathy present?

A

Parasthesia, burning, allodynia, ataxia, loss of pain sensation or hypersensitivity, ulcers, loss of vibration sense, loss of proprioreception, areflexia

5
Q

What would an autonomic neuropathy present?

A

Dry eyes, dry mouth, GI disturbance, impotence, loss of heart rate variability, bladder hypersensitivity, excessive/inadequate sweating, orthostatic hypotension

6
Q

Describe a compression neuropathy

A

Focal demyelination where compression occurs, and reduced conduction velocity across compression area
Usually a mononeuropathy

7
Q

What are the two common mononeuropathies/compression neuropathies

A

Median nerve compression - Carpal Tunnel Syndrome

and Ulnar nerve compression

8
Q

What are the risk factors for carpal tunnel syndrome

A

Diabetes, pregnancy, acromegaly, weight gain, repetiitive wrist movements, wrist fracture, artritis

9
Q

What are the signs and symptoms of carpal tunnel syndrome?

A

Numbness - waking at night and with certain daytime postures, in the lateral 3.5 fingers, weak thumb abduction and wasting of the thenar eminence

10
Q

What are the treatments for carpal tunnel syndrome?

A

Wrist splints, steroids, decompression surgically

11
Q

what are the risk factors for ulnar nerve compression?

A

elbow trauma, RA, leaning on elbow

12
Q

what are the signs and symptoms of ulnar nerve compression?

A

hypothenar wasting, weakness of finger abduction and opposition of little finger, sensory changes to medial 1.5 fingers

13
Q

What are the treatments for ulnar nerve compression?

A

Avoid resting on elbows, night time splints, nerve gliding exercises, decompression surgery

14
Q

What is guillian barre syndrome?

A

Acute demyelinating polyneuropathy with preceding infection

15
Q

What are the signs and symptoms and GBS?

A

Numbness and paralysis beginning distally

16
Q

What will investigations show in GBS?

A

increased protein concentration in the CSF, slowed nerve conduction belocities and action potential delay and dispersion

17
Q

What are the treatments for GBS?

A

Intravenous immunoglobulin pooled from blood donations, or plasma exchange
Both expensive and high risk

18
Q

What is the potential difference between ICF and ECf?

A

~70mV

19
Q

What ion concentrations are higher extracellularly

A

Sodium, calcium and chloride

20
Q

What ion concentration is higher intracellularly and what maintains this balance?

A

Potassium - the Na+/K+ pump

21
Q

How is an AP initiated?

A

Na ligand gated channels open after binding of excitatory NT and Na+ floods in

22
Q

What is the rising phase of an AP?

A

Threshold reached due to ligand mediated Na+ influence and there is further Na+ influx and K+ efflux

23
Q

Why does the membrane hyperpolarise?

A

Due to the magnitude of K+ extracellularly

24
Q

What is the refractory period of an AP?

A

Peak depolarisation to hyperpolarisation and where Na+ channels become inactive for 1ms after closing

25
Q

What is the relative refractory period of an AP?

A

Re-establishment of resting potential

26
Q

What occurs when acetylcholine binds to its receptors at the NMJ?

A

It causes K+ channels to open post synaptically and triggers AcH reuptake

27
Q

What is Lambert Eaton Myasthenic syndrome?

A

An autoimmune disease with antibodies against the voltage gated calcium channel

28
Q

What is neuromyotonia?

A

When the muscles don’t relax there is twitches and cramp

29
Q

What is myasthesia gravis due to?

A

Antibodies against the acetylcholine receptor

30
Q

What does myasthesia gravis present with?

A
Fatiguable weakness
Eyes: diplopia, ptosis
Speech, chewing and swallowing trouble
Neck extension weakness
Respiratory failure
Late onset: thymic atrophy
31
Q

How would you treat Myasthesia gravis?

A

IV immunoglobulin exchange or plasma exchange, acetylcholinesterase inhibitors, immunosuprresants