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Neuroscience > Module E-05 > Flashcards

Module E-05 Flashcards

1
Q

Myasthenia

A

Muscle weakness

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2
Q

Atrophy

A

decrease in size of cell , tissue or organ

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3
Q

Paresis

A

slight or incomplete paralysis

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4
Q

Lesions of the Motor Unit : Soma

A

ALS , Poliomyelitis

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5
Q

Lesions of the Motor Unit : Axon

A

Toxins, drugs and axotomy

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6
Q

Lesions of the Motor Unit : Schwann cell

A

Guillian - Barre syndrome, Diptheria

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7
Q

Lesions of the Motor Unit : Nerve ending

A

Botulism, Lambert-Eaton disease

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8
Q

Lesions of the Motor Unit : Synaptic cleft

A

acetylcholine esterase absent

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9
Q

Lesions of the Motor Unit : End plate

A

Myasthenia Gravis, nACh receptor defects

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10
Q

Lesions of the Motor Unit : Muscle Fiber

A

Myotonia , muscualr dystrophy

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11
Q

Variety of lesions of the nerve Soma or Axon

A
  • Diseases
  • Toxins
  • Drugs
  • Trauma
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12
Q

Signs/symptoms of lesions of the nerve Soma or Axon

A
  • Muscle atrophy and weakness
  • Fibrillations and fasciculations
  • Eventual loss of muscle fibers (replacement by noncontractile fibrous connective tissue)
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13
Q

What is Poliomyeltis

A

Infection with the polio virus can affect the whole body but mainly affects the muscles and nerves, particularly the motor neurons of the spinal ventral horns. Severe cases yield permanent paralysis or death.

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14
Q

Transmission of Polio virus occurs by

A

By direct person-to-person contact and through oral, nasal
and anal secretions.
Enters through mouth and nose then proliferates in the throat and intestinal tract and spreads through vascular and lymphatic systems

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15
Q

Prevention of Poliomyelitis

A

immunization prevents in 90% of cases

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16
Q

Variety of Lesions of Schwann cells

A
  • Autoimmune disease

- Toxins

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17
Q

Manifestations of lesion of Schwann cells

A

Demyelination-dependent conduction slowing or conduction block

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18
Q

Toxins that affect Nerve ending, Synaptic Cleft and End-Plate

A

1) Botulism
2) Alpha-Latrotoxin
3) Beta-Bungarotoxin
4) Curare (delta- Tubocurarine)

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19
Q

Cause of Botulism

A

Toxic protease from anaerobic bacteria , Clostridium Botulinum

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20
Q

Effect of Botulism

A

reduces ACh release by acting on presynaptic proteins involved in exocytosis

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21
Q

Transmission of Botulism

A
  • Eating food that contains the botulism toxin
  • Infection of a wound with Clostridium botulinum
  • Consuming spores of Clostridium botulinum
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22
Q

Source of Alpha-Latrotoxin

A

The black widow spider (Latrodectus mactans) synthesizes a neurotoxic venom

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23
Q

Effect of Alpha-Latrotoxin

A
  • causes massive release of ACh
  • venom reaches the blood via the lymphatic system
  • The venom acts at the nerve endings, causing tetanus, a continuous, painful contraction of the muscle (occasional patchy flaccid paralysis)
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24
Q

Source of Beta-Bungarotoxin

A

venom of snake

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25
Q

Effect of Beta-Bungarotoxin

A

reduces ACh release by acting on proteins in nerve terminals involved in exocytosis

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26
Q

Effect of Curare (delta- Tubocurarine)

A

a non-depolarising muscle relaxant that blocks the acetylcholine receptors at the neuromuscular junction

27
Q

What is Lambert-Eaton?

A

Autoimmune disease, where circulating antibodies
are directed against voltage-gated Ca2+ channels in
motor neuron terminals.
causes insufficient release of ACh into the synaptic cleft

28
Q

Why is strength increased with repeated contraction in Lambert-Eaton?

A

allow the synaptic concentration of synaptic ACh to rise sufficiently to increase force of contraction

29
Q

Lambert Eaton Syndrome is associated ______________

A

oat cell carcinoma (of the lung) as a paraneoplastic syndrome.

30
Q

Characteristics of Lambert-Eaton

A

– Muscle weakness and ‘facilitating neuromuscular block’
– Often found in patients with small cell cancers of the lung
– Culture of these cells express voltage-gated calcium
channels
– Immune system makes antibodies to these proteins
– Antibodies cross-link voltage-gated calcium channels in motor nerve terminals
– Reduced ACh release
– Reflexes are decreased

31
Q

Physiological Changes at End Plate in Lambert-Eaton syndrome

A

– Reduced amplitude of EPP
– Many EPPS do not attain threshold in muscle fibers
– Amplitude of MinEPP is unchanged

32
Q

Tests to confirm Lambert-Eaton syndrome

A

EMG and nerve conduction velocity

33
Q

Results seen in EMG for Lambert-Eaton syndrome

A

Waxing is evident in the EMG inresponse to repeated nerve

stimulation.

34
Q

Therapy for Lambert-Eaton syndrome

A

– Remove underlying tumor and give immunosuppressive drugs
– Do plasma exchange
– Calcium gluconate to enhance calcium influx into nerve terminal
– Give 4-aminopyridine to prolong presynaptic action potential and improve transmitter release

35
Q

Congenital Forms of Myasthenia (Muscle Weakness)

A

1)Deficiency of ACh-esterase in synaptic cleft
2)Slow Channel Syndrome
3)Other forms
a)One form where the binding of ACh to nAChR is
abnormal
b) One form where the ACh-gated channels have very
brief opening times

36
Q

Effect of congenital myasthenia due to deficiency of ACh-esterase in synaptic cleft

A
  • EPP amplitude is larger and longer than normal
  • Single motor nerve stimuli delivered at low frequency cause single muscle twitches
  • High-frequency motor nerve stimuli produce temporal summation of EPPs and cause depolarization block of muscle
37
Q

Effect of congenital myasthenia due to Slow Channel Syndrome

A
  • Inherited rare condition presents at birth or early childhood
  • Muscle weakness
  • Rapid fatigue
  • Progressive atrophy
  • ACh binding to nAChRs causes prolonged opening of ACh receptor channels and, consequently, depolarization block
38
Q

Age of onset of congenital myasthenias

A

appear before the age of 2

39
Q

What is Myasthenia Gravis?

A

a chronic disease due to an autoimmune process. Antibodies to nAChRs develop and reduce transmission at the skeletal NMJ and other peripheral synapses with nAChRs. There is a genetic susceptibility to Myasthenia Gravis.

40
Q

Main sign indicative of Myasthenia Gravis

A

weakness of voluntary muscles, which improves after rest and worsens with muscular activity

41
Q

Symptoms of Myasthenia Gravis

A

– Weakness in muscles innervated by cranial nerves (eg,
ptosis)
*Ocular changes: Diplopia (double vision)Ptosis
(drooping eyelids)
*Patients with generalized disease may experience:
Difficult swallowing and frequent choking
– Weakness in limb muscles
*usually later in the day and recovery with rest
– Weakness not associated with denervation
– Serum from patients causes disease symptoms in animals

42
Q

Tests for myasthenia Gravis

A 
EMG 
Tensilon Test (acetylcholinesterase inhibitor)
43
Q

Results seen in EMG for Myasthenia Gravis

A

In repetitive stimulation, ‘waning pattern’

44
Q

Results seen in Tensilon test for

A

Positive test

45
Q

Describe the effect of antibodies at the nAChR in Myasthenia Gravis

A

– Antibodies bind to alpha subunits of nAChR
– Antibodies do not compete with ACh for binding sites on
subunits
– Antibodies cross link neighboring nAChRs hastening
resorption.

46
Q

Normal turn over time for ACh receptors

A

5-7 days

47
Q

Turnover time for ACh receptors in Myasthenia Gravis

A

2-5 days

48
Q

Who does myasthenia Gravis mostly affect?

A

Young Women and Older men

49
Q

Describe the resorption of ACh receptors

A

– Endocytosis of nAChRs in end plate membranes
– Lysosomal destruction
– Enhanced removal rate of nAChRs but no enhanced rate of insertion of nAChRs into end plate membrane

50
Q

Treatment of Myasthenia Gravis

A

1) AChesterase Inhibitors- Neostigmine or pyridostigmine
2) Prednisone (Cortisone) or immune suppressors such as azathioprine or cyclosporine can be applied after dissatisfying responses to other drugs.
3) Remission sometimes follows thymectomy.

51
Q

Myasthenia gravis is associated with ________

A

Tumors of thymus gland

52
Q

Structural changes at the Motor Endplate in Myasthenia Gravis

A

– Fewer nAChRs
– Wider synaptic cleft
– Smaller junctional folds

53
Q

What is a Myasthenic Crisis

A

Breathing difficulty may be life threatening.

54
Q

Myotonia Congenita aka

A

Chloride channel Syndrome

55
Q

What is Myotonia Congenita?

A

Autosomal dominant disease, influencing the gene
encoding chloride channels in the muscle membrane
Fewer chloride channels are expressed and inserted in the cell membrane

56
Q

Function of Chloride channels in normal muscle

A

the numerous chloride channels help to keep the
membrane potential close to ECl during recovery from an
action potential when potassium ions are accumulating in
the transverse tubular system (TTS)

57
Q

Effect of Myotonia Congenita

A

– Increased excitability: smaller depolarization is required to evoke an action potential and may even cause a train of
action potentials
– Potassium accumulation in TTS causes some depolarization leading to spontaneous firing of the muscle after the end of nerve stimulation

58
Q

relaxation?

A

repetitive firing?

59
Q

What is Duchenne’s Muscular dystrophy?

A

– X-linked–recessive disorder of muscles in males
– Onset of disease in early childhood (3-5 yrs)
– Muscle weakness develops progressively
– Patients die from cardiovascular and respiratory insuffiency
– Cause: absence of muscle protein - dystrophin

60
Q

Causes of Lower Motor Neuron Syndrome

A
  • Viral infections (e.g. poliomyelitis)
  • Trauma
  • Degenerative disease
61
Q

Signs of LMN syndrome

A 
 Muscle weakness (paresis)
 Flaccid paralysis
 Loss of reflexes
 Fasciculations
 Fibrillations
 Muscular atrophy progressing to complete myocytic death
62
Q

Expression of nAChR in embryo vs adult

A

In embryonic muscle fiber the nAChRs are distributed across the entire surface of muscle cells
In adult muscle fibers, normal nerve stimulation leads to aggregation of nAChRs under nerve endings

63
Q

What happens to expression of nAChR after denervation of muscle?

A

nAChRs return to a supersensitive embryonic state, with an

adult state re-emerging with reinnervation

Neuroscience (32 decks)

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