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110 Peripheral Neuropathy > Peripheral Neuropathy > Flashcards

Peripheral Neuropathy Flashcards

1
Q

What is the value of a resting membrane potential

A

-65mV

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2
Q

What are the relative concentrations of Cl, Na and K in a RMP

A

Cl and Na high outside.

K higher inside.

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3
Q

What maintains the RMP, and how?

A

Na-K transporter (pump) transports 3 Na out to every 2 K in, using ATP.

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4
Q

what are the 2 types of channels enabling RMP/APs?

A

LGIC, VGIC

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5
Q

Initial trigger for AP

A

ligand gated Na channel (ligand it the neurotransmitter), Na starts to move into cell.

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6
Q

What causes the fast rising phase of depolarisation?

A

after some Na has entered through LGICs, VG Na channels open, allowing Na to flood in.

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7
Q

what does the membrane potential reach in a full AP?

A

40mV

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8
Q

What causes the fast depolarisation to stop, and repolarisation to begin?

A

LGIC and VGIC for Na close (depolarisation stops). This level of depolarisation causes VGIC for K to open. Electrochemical gradient causes K to efflux - depolarisation.

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9
Q

What is Myelin?

A

80% lipid, 20% protein.
White matter.
insulates and speeds up APs.

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10
Q

pathology of Lambert-Eaton syndrome

A

Antibodies are generated against calcium channels at the NMJ. This can be due to small cell lung carcinoma. Not enough Ca influx to elicit an AP, but continuous effort may enable a response.

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11
Q

What is the course of events to transfer an AP from one neurone to another?

A

AP arrives and is sensed by a VG Ca channel.
Ca influx onto presynaptic terminal
Vesicles release neurotransmitter into cleft
Neurotransmitter binds to post synaptic receptors.

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12
Q

How does the initiation of an AP from an excitatory neurotransmitter differ from an inhibitory neurotransmitter?

A

Excitatory neurotransmitters allow influx of Ca, whereas inhibitory neurotransmitters open Cl channels.

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13
Q

What are the two divisions of the PNS?

A

Somatic and ANS.

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14
Q

From where does the SNS arise?

A

T1-L2

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15
Q

What is the sympathetic chain?

A

para-vertebral ganglia into which myelinated sympathetic axons enter, and unmyelinated post ganglionic sympathetic axons leave.

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16
Q

what do post ganglionic sympathetic neurones release?

A

NA (onto adrenergic receptors)

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17
Q

from where does the PSNS arise?

A

brainstem and sacrum

18
Q

What neurotransmitter do posts ganglionic parasympathetic neurones release?

A

ACh (onto muscarinic or nicotinic receptors)

19
Q

What are nicotinic receptors?

A

excitatory
LGICs
activated by ACh

20
Q

What are muscarinic receptors?

A

Metabotropic receptors (eg GPCRs)
activated by ACh
on effectors of PSNS

21
Q

What does ACh activate?

A

Muscarinic and nicotinic receptors.
Initiates all pre ganglionic neurones.
released from PSNS post ganglionic neurones to effectors

22
Q

What does NA activate?

A 
Adrenergic receptors (alpha and beta).
released from SNS post ganglionic neurones.
23
Q

What can CMAP studies show?

A

Compound Muscle Action Potential
the velocity and the
amplitude of the AP

24
Q

What would be a feature of CMAP study in a demyelinating pathology?

A

slow conduction velocity, dispersed AP (not all firing at once)

25
Q

What would be a feature of CMAP in an axonal injury?

A

reduced AP amplitude - not all firing, but ones that are, are fine, so conduction velocity is normal.

26
Q

Explain carpel tunnel syndrome

A

Compression neuropathy of median nerve at wrist.
Index, middle and half of ring finger loss os sensation.
Loss of thumb abduction
Thenar eminence wasting.

27
Q

what are the symptoms of ulnar nerve compression?

A

little and half of ring finger loss of sensation/function.

28
Q

Pain, loss of sensation on top of foot. Weakness lifting foot.

A

Peroneal Nerve (at knee) compression.

29
Q

Wrist drop. Lateral posterior of hand numb.

A

Radial nerve compression.

30
Q

pain/numbness/burning sensation on outer thigh.

A

compression of lateral cutaneous nerve.

31
Q

What is the pathology of GBS?

A

following an infection, autoimmune response causing Wallerian demyelination of PNS neurones. SELF LIMITING

32
Q 
Weakness:
Rapid onset,
distal,
bilateral
following infection.
A

GBS.

33
Q

Treatment for GBS

A

GBS is self limiting, but pt can be very ill.
Reduce autoimmune response: IV Ig, Plasma exchange
Reduce risk of DVT - heparin
Monitor resp - poss ITU.

34
Q

What is the pathology of LEMS?

A

Antibodies against VG Ca channels, prevents ACh release at NMJ.
60% of Pts have had lung cancer.

35
Q

Areflexia, proximal muscle weakness - improves as effort is sustained, reflexes may return too.

A

Lamber Eaton Myasthetnic Syndrome

36
Q

What’s the pathology of myasthenia gravis?

A

Antibodies against ACh receptor. There are fewer receptors to excite - when prolonged excitation occurs, they get saturated rapidly and weakness progresses.
There is an association with thymus hyperplasia/atrophy.

37
Q 
Progressive weakness esp in:
Face/mouth:
difficulty speaking
dysphagia
difficulty breathing
*symptoms improve is pt relaxes for a while
A

Myasthenia Gravis (ACh receptors become available (unsaturate) upon relaxation and are able to elicit a response again.

38
Q

Treatment for Myasthenia Gravis

A

Reduce excitation: AChase to reduce ACh in NMJ
reduce antibodies: IV Ig, plasma exchange, immunosuppressants.
Thymectomy.

39
Q

COPS Maintain myelin.

What is the Mnemonic?

A

in the CNS - Oligodendrocytes

in the PNS - Schwann cells

40
Q

Child
Foot drop
Curled toes
Loss of sensation - feet, hands.

A

Charcot-Marie-Tooth

41
Q

What is the pathology of Charcot-Marie-Tooth?

A

Genetic - peripheral demyelination

110 Peripheral Neuropathy (1 decks)

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