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Neuro first semester 23-24 > Block II: CC1 > Flashcards

Block II: CC1 Flashcards

1
Q

WHta is the endoneurium?

A

is a supporting structure around individual axons within each fascicle.

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2
Q

WHat is a fascicle?

A

number of axons together in a circular structure surrounded by perineurium

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3
Q

WHta is the perineurium?

A

Collagenous tissue binding each fascicle with elastic fibers and mesothelium cells

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4
Q

Whta si the epineurium?

A

Collagen, elastic fibers and fatty tissue binding individual fascicles together. Outmost layer of supportive tissue. Contains vasa nervorum.

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5
Q

Rate nerve fibers by size (um)

A

Aa > AB > Ay > Ag > B >C

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6
Q

Rate nerve fibers by conduction speed (ms-1)

A

Aa > AB > Ay > Ag > B >C

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7
Q

Which fibers are myelinated?

A

Aa (thickest)
AB
Ay
Ag (thinnest)
B

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8
Q

Which fibers are NOT myelinated?

A

C

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9
Q

General functions of Aa?

A

Motor, propioception

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10
Q

General functions of AB?

A

Touch, pressure, vibration

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11
Q

General functions of Ay

A

Motor to muscle spindle

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12
Q

General functions of Ag

A

Touch, coldness, fast pain

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13
Q

General functions of B

A

Pre-ganglionic autonomic

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14
Q

General functions of C

A

Touch, warmth, itch, slow pain; post-ganglionic autonomic

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15
Q

What is slow transport in axonal transport?

A

0.5-10mm/day

-unidirectional always anterograde

-moves enzymes, cytoskeletal components and new axoplasm down the axon during repair and regeneration of damaged axons

-Damaged nerve fibers regenerate at a speed governed by slow axonal transport

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16
Q

what is fast transport in axonal transport?

A

20-400mm/day

-bi-directional

-anterograde transport: organelles, enzymes, synaptic vesicles and small molecules

-Retrograde: for recycle material and pathogens- rabies, herpes simplex, tetanus, polio viruses.

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17
Q

What is wallerian degeneration?

A

Following focal interruption of axons (as trauma or vasculitis). From injury downward. atrophic muscle

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18
Q

What is axonal degeneration?

A

Dying -back phenomenon from metabolic derangement of the neuron. Injuty occurs in the whole nerve, but dies from distal to proximal. atrophic muscle.

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19
Q

What is segmental demyelination?

A

affects myelin, slowing the conduction velocity. patched pattern

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20
Q

What is neuraplaxia?

A

Class I nerve injury
-milder form of damage
-nerve does not suffer major changes after injure, myelin regenerates
-cause:compression or ischemia
-good prgnosis

21
Q

What is axonotmesis?

A

-class II nerve injury
-axonal damage results in loss of continuity and wallerian degeneration distally.
-Basal lamina and endoneurial tissue is intact
-recovery depends on nerve regeneration (1-3mm/d)

22
Q

What is neuronotmesis?

A

Class III nerve injury
-results in separation of entire nerve including supportive tissue, ranging from endoneurial and schwann cell tube transection to total nerve serverance
-limited axonal regeneration
-neuroma formation and aberrant regeneration is common

23
Q

What type of fibers are injured in patient has trouble with motor and sensory axons responsible for propioception, vibration and light tough?

A

Large myelinated axons

24
Q

What type of fibers are injured in patient has trouble with sensory fibers responsible for light touch, pain, temperature, and preganglionic autonomic fucntions?

A

thinly myelinated axons

25
Q

What type of fibers are injured if the patient has trouble with pain, temperature and postganglionic autonomic factors?

A

small unmyelinated fibers

26
Q

what is diffuse (symemtric spatial distribution?

A

polyradiculopathu ex. sensory/motor diabetic neuropathy

27
Q

what is focal spatial distribution?

A

mononeuropathies, ex. entrapment neuropathies as in carpal tunnel or local trauma

28
Q

what is multifocal-lower spatial distribution?

A

usually assymetric; multiple mononeuropathy; ex. vasculitis

29
Q

What are symptoms of large fiber neuropathy?

A

-lower motor neuron pattern of weakness
-muscle loss, atrophy
-loss of tendon reflexes
-impaired propioception
-abnormal romberg test

30
Q

What are symptoms of large fiber neuropathy?

A

Contact hyperalgesia
-burning, aching, stabbing pain (non specific)
-mild distal disturbance in sharp dull discrimination
-normal DTR’s
-Orthostatic hypotension

31
Q

Axonal neuropathy pathologic features include:

A

-Impaired axonal transport
-failure of impulses generation in nerve terminal
-atrophy

32
Q

clinicopathologic correlation of axonal neuropathy

A

-initial findings in lower limbs
-sensory and motor loss
-tingling and pinprick
-decresed or loss ankle reflexes
-normal CSF protein level
-slow recovery

33
Q

what is demyelinating neuropathies?

A

-acquired conditions generally result of an immune mediated attack to PNS myelin
-primary myelin destruction sheath leaving axon intact
-begins at nodes of ranvier
-spinal roots involved
-schwann cells remyelinates the axon
-no atrophy

34
Q

demyalinated neuropathy clinicopathology correlationa

A

-fast (days)
-cranial nerves invovled
-weakness with mild sensory loss
-absent DTRs
-elevated CSF protein
-may recover
-segmental (multifocal) almost always acquired
-uniform - hereditary

35
Q

What is an evaluation method for patients with peripheral neuropathy?

A

EMG and nerve conduction

36
Q

Which is th emost commeon clinical neuropathy?

A

diabetes

37
Q

What are some characteristics of clinical diabetic neuropathy?

A

-majority have distal symmetric fiber-lenth-dependent pattern
-sensory and autonomic manifestations
-progressive distal axonopathy
-can develop focal and multifocal neuropathies

38
Q

What are cranial neuropathies?

A

-unilateral oculomotor nerve palsies
-third CN (pupillary reflex spared, pain 5%)
-6th cranial nerve

39
Q

What is proximal diabetic neuropathy of lower limbs?

A

-pain and sensory loss with unilateral proximal muscles weakness and atrophy
-acute onset
-burning type of pain in thigh
-good prognosis

40
Q

What is an example of demyelinating polyneuropathy?

A

guillain barre syndrome

41
Q

explain guullian barre

A

-bilateral acute, ascending, symmetric peripheral neuropathy
-progression may continue up to 4 weeks
-areflexia
-mild sensory symtoms
-bilateral facial weakness
-may require ventilator
-infection or gastroenteritis may be a predisposing factor (CMV, Campilobacter jejuni)
-csf protein elevated after first week
-elcectrodiagnostic studies (lumbar punction)

42
Q

What is molecular mimicry?

A

when there is a pathogen or unknown substance, the perivascular lymphocytic macrophages infiltrates causing a segmental inflammatory demyelination and edema by error attacks myelin from nerve since antibodies of virus seem similar to those of the nerve.

43
Q

What is vasculitic neuropathies?

A

A diverse group of disorders characterized by the acute-to-subacute onset of painfulsensory and motor deficits that result from inflammatory destruction of nerve blood vessels and subsequent ischemic injury.

44
Q

what are the two main pathways that lead to sichemic vasculitic nerve damage?

A

-Immune complex deposition within the vessel walls with complement deposition and release of proinflammatory cytokines.

-Cell-mediated immunity occurs when antigen-presenting cells present relevant antigens to circulating T cells producing proinflammatory cytokines and other inflammatory mediators that cause neutrophils and lymphocytes to adhere to and injure the blood vessel.

45
Q

Examples of primary vasculitis?

A

large vessel: giant cell (temporal) arteritis

-medium and small vessel vasculitis: polyarteritis nodosa, churg0strauss syndrome, wegner’s granulomatosis, microscopic polyaniitus, isolated angiitis of NS)

46
Q

Examples of secondary vasculitis?

A

-connective tissue disorder: RA, SLE
-Malignancies: small cell CA lung, lymphoma
-infections: herpes varicella zoster, CMV, HIV, hepatitis
-cryoglobulinemia

47
Q

example of focal neuropathies?

A

carpal tunnel syndrome
peroneal neuropathy
tarsal tunnel
meralgia parestehtica

48
Q
A

Neuro first semester 23-24 (9 decks)

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