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s3 - MSK, Derm, Cardio, Neuro, Pharm > Musculo-Skeletal > Flashcards

Musculo-Skeletal Flashcards

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1
Q

Myosin heavy chain isoform that splits ATP fastest supplying energy from glyolysis alone.

A

MHC 2B

high impact resistance training increases levels

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2
Q

Why are MHC 1 containing fibres “red”?

A

High myoglobin

low impact CV training increases levels –> fatigue resistance

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3
Q

How does the Growth Factor Endocrine Axis relate to muscle growth?

A

GH stimulates IGF-1 release from the liver.
IGF-1 activates satellite cells and protein synthesis leading to increased muscle filaments

NB: prolonged contraction releases IGF-1 from muscle (autocrine) to stimulate their own hypertrophy

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4
Q

Fill in the profile for a myopathy:

Weakness: 
Reflexes:
Sensation:
CK:
EMG:
A 
Weakness: proximal (from girdles)
Reflexes: normal (unless severe wasting)
Sensation: normal
CK: raised 
EMG: more muscle recruitment to get certain force
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5
Q

Duchenne Muscular Dystrophy inheritance is …
Caused by a mutation in…this gene…
Onset age:

A

…X linked
…Dystrophin Xp21 gene…forms protein that links muscle cytoskeleton to the ECM
…3-5yrs

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6
Q

3 symptoms of DMD

A
  • pseudohypertrophy of legs (scar tissue)
  • Gowers manoevre and toe walking
  • scoliosis
  • cardiomyopathy, resp faliure
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7
Q

Difference between DMD and Becker’s MD?

A

DMD has a frameshift mutation, more severe.

Beckers is non frameshift so protein function is reduced but OK

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8
Q

2 Gene therapies for DMD

A

Ataluren - ribosomes cant bind to stop codon so its not read and protein is not truncated, better function

Eteplirsen - antisense oligon. for a specific exon 51 mutation, binds to RNA and restores reading frame so DMD –> Beckers.

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9
Q

Fill in the profile for a NMJ Disorder:

Weakness: 
Reflexes:
Sensation:
CK:
EMG:

+feature

A

Weakness: proximal and extraocular muscles as smaller ratio of axon:muscle fibre
Reflexes: normal
Sensation: normal
CK: normal
EMG: amplitude of muscles AP reduces with repetitive stimulation

+fatiguability as Ach released from end plates is used up, takes time to replenish

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10
Q

What kind of condition is Myasthenia Gravis?

What is this condition associated with?

A

an aquired neurological autoimmune disease where the patient develops antibodies to Nic AchR on muscle membrane interferes with Ach action

associated with thymic abnormalities (thymus)

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11
Q

3 treatments for Myasthenia Gravis

A

-The enzyme Pryridostigmine which inhibits ACh-esterase so blocks ACh breakdown in cleft

Immunosuppresants e.g. azathioprine to reduce antibody and T cell functions

Thymectomy-removes driver of the autoimmunity

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12
Q

What does the botulism toxin do?

A

Stops Ach vesicles merging with the pre-synaptic membrane causing severe flaccid paralysis

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13
Q

What is Lambert Eaton Myasthenic Sydrome (LEMS)?

A

Antibodies to the VGCa2+C so no calcium can enter channel/no depolarisation –> flaccid muscle weakness

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14
Q

Fill in the profile for a Neuropathy:

Weakness: 
Wasting:
Reflexes:
Sensation:
CK:
EMG:

+feature

A

Weakness: distal (long ones more vulnerable)
Wasting: early and rapid (no regeneration signal)
Reflexes: reduced/absent
Sensation: abnormal
CK: may be elevated/notmal
EMG: particular neurogenic pattern

+feature: spontaneous fasiculations

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15
Q

How can pathological classifications of neuropathies as axonal or de-myelinating be done?

A

NCS-Nerve Conducting Studies

to see how fast the conduction is to see if Schwaan cells are affected.

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16
Q

Common Mononeuropathies:

  • Median
  • Ulnar
  • Radial
  • Common Peroneal
A
  • Median-carpal tunnel
  • Ulnar-handlebar
  • Radial-sat night palsy-wrist drop
  • Common Peroneal-foot drop
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17
Q

Inflammation, Guillan Barre Syndrome, brachial neuritis, diabetes, B12 deficiency, chemotherapy, alcohol, lead, leprosy and HIV are examples of causes of what?

A

Polyneuropathy

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18
Q

What is Charcot-Marie Tooth Disease?

A

CMTD is mostly AD length-dependent genetic condition.

Symptoms e.g. wasting of lower leg “champagme bottel-like”, pes callus/high arches, wasting of hand muscles.

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19
Q

At what levels does Erbs Palsy plexopathy damage the brachial plexus?

A

C5 and C6

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20
Q

Describe the most common cause of radiculopathy (nerve root)?

A

IV herniation, annulus ruptures and nucleus pulposus leaks out and compresses the motor root (can also be sensory root) leading to weakness (numbness if sensory)

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21
Q

Motor Neurone Disease is primary degredation in the..

It starts…
And affects…

A

..anterior horn of spinal cord

It starts…in one area e.g hand up arm to other then to face
And affects…all VOLUNTARY muscles

22
Q

Explain the steps that occur at a skeletal NMJ leading up to sufficient AP to exceed threshold for contraction?

A
  • AP conducted via motor nerves. Cause VGCC to open and Ca2+ influx -> Ach vesicle release
  • ACh binds on LG-receptor, opens Na+. EJP.
23
Q

If muscles stop producing enough force to support ‘x’, what happens?

A
  • spindles in the muscles are stretched, signal sent up spinal cord
  • increased MN excitation for muscle to contract more
24
Q

What happens if you want to/voluntarily put ‘x’ down/stretch?

A
  • brain signal to anatgonist’s muscle to contract (and a-MNs to agonist muscle inhibited)
  • gamma MNs shorten poles so muscle is sensitive to stretch under the new tension
25
Q

What is the purpose of the Golgi Tendon Organ?

A

-Ib afferents wrapped around collagen signal when the tendon is stretched/muscle contraction

26
Q

What pattern is seen in LMN lesions?

A

Flaccid Paralysis:

  • denervated muscle, weakness, wasting, areflexia
  • fasiculations
27
Q

What pattern is seen in UMN lesions?

A

Spastic Paralysis:

-weakness, hypertonia and hyper-reflexia

28
Q

What are group II afferents involved in?

A
  • slower, indirect connection to a-MNs

- respond to muscle length, maintain limb position and posture for resting muscle tone

29
Q

What are group I afferents involved in?

A
  • faster, monosynaptic connections to a-MNs
  • respond to the rate of change/velocity of muscle
  • correct rapid, unintended movements
30
Q

Give 3 treatments that improve UMN damage by increasing spinal cord inhibition?

A
  • oral benzodiazepines (boost GABAa inhibition)
  • intrathecal baclofen (activates GABAa R on group I)
  • intramusclular botox (weakens NMJs)
31
Q

What is osteoarthritis a result of?

A
  • Increased chondrocyte activity and matrix production in response to cartilage damage
  • disrupts structure + abnormal collagen and proteoglycan structure
32
Q

What is a BMEL?

How do they appear on X-Ray?

A
  • Bone Marrow Oedema-Like Lesion (painful as richly innervated)
  • end stage cyst seen as a shadow at edge of joint
33
Q

What are aggrecanases and collagenases?

What endogenously inhibits them?

A
  • MMPs-Matrix Metalloproteinases

- TIMPs inhibit their action

34
Q

Give 2 inflammatory changes in Osteo Arthritis.

A
  • lining cell hyperplasia
  • increased vascularity
  • subintimal fibrosis
35
Q

What 3 areas are currently targeted for OA treatment?

A
  • central pain processing e.g. amitryptiline
  • DRG e.g. opiates
  • OA joint e.g. corticosteroids, NSAIDS
36
Q

Where does CT originate from?

What are its 4 classes?

A

Mesodermal origin

Proper (loose&dense), cartilage, bone and blood

37
Q

How do proteoglycans lead to tugor?

A

They are negatively charged and v.hydrophilic, they bring in Na+ attracting lots of water via osmosis

38
Q

Where are the following mainly found?

  • collagen I
  • collagen II
  • collagen III
A

collagen I - bone
collagen II - hyaline cartilage
collagen III - woven bone

39
Q

Give an example of a mutation in the following genes:

  • collagen I
  • collagen II
  • collagen III
A
  • collagen I - osteogenesis imperfecta (brittle, short)
  • collagen II - achondrogenesis
  • collagen III - Ehlers Danlos (hypermobile joints/skin..)
40
Q

Elastin is arranged in ECM, made as tropo-elastin that polymerises to elastin. What is involved in its degredation?

A
  • elastase degrades it

- a-1 anti-trypsin inhibits elastase

41
Q

What is the elastin core covered in?

A

A sheath of microfibrils comprised of glycoproteins (mostly fibrilin)

42
Q

What is crutis laxa?

A

Not enough elastin in skin

43
Q

What is Marfan’s Syndrome a mutation in?

A

Fibrilin gene. Can get dilation of aorta and displacement of lens

44
Q

What is a keloid scar a result of?

A

Too much collagen made

45
Q

Bone marrow holds adipose tissue. What ion do the hydroxyapatite crystals hold?

A

Calcium

46
Q

Osteoblasts lay down osteiod, what happens to them as the osteoid mineralises?

A

Osteoblasts become entombed between lamellae (layers of ECM) in lacunae where they mature into osteocytes which monitor minerals/proteins and regulate bone mass

47
Q

How do osteoclasts (derived from MOs) reabsorb bone?

A

They release H+ ions and lysosomal enzymes

48
Q

When is woven bone/1ry bone present?

A

In embryonic development

In fracture repair

49
Q

What is the difference in woven bone and lamellar/2ndry bone?

A

Woven has osteoid (unmineralised ECM) and collagen is arranged randomly
Lamellar bone has organised sheets of strong mineralised osteoid. Can be outer compact bone or inner spongy bone.

50
Q

The functional unit of Compact Bone (a type of lamellar bone) is an “osteon”. Name 3 features of it:

A
  • lamellae in concentric circles surround a vertical Haversian canal
  • Haversian canals are connected by horizontal Volkmanns canals
  • osteocytes are located between the lamallae in lacunae interconnected by canaliculi (tunnels)
51
Q

Spongy bone (aka cancellous/trabecullar) is light and porous but strong against multidirectional lines of force. What does this bone have?

A
  • many large spaces, honeycomb like
  • spongy lightness allows body to move
  • 3D next work of fine columns cross linking to form irregular trabeculae.
  • spaces between trabeculae often filled with marrow

s3 - MSK, Derm, Cardio, Neuro, Pharm (9 decks)

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