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MSK Flashcards

0
Q

What is a sarcomere?

A

1 repeat unit of the thick and thin filaments.

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1
Q

What is a Myofibril?

A

Arrangement of thick and thin filaments in cytoplasm into cylindrical bundles

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2
Q

What is the thick filament and what does it form cross bridges with?

A

Myosin, it forms cross bridges with actin

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3
Q

What does actin contain and what do they do?

A

Actin contains Tropomysin and Troponin.
Tropomysin lies over actin filaments blocking myosin binding sites
Troponin changes shape and moves Tropomysin out the way when Ca2+ binds

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4
Q

What is a motor end plate?

A

Region of muscle fibre membrane directly under the terminal portion of an axon

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5
Q

What is the neuromuscular junction?

A

Junction of axon terminal with motor end plate

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6
Q

What is the neurotransmitter at the NMJ and what receptor does it bind to?

A

Acetylcholine and it binds to Nicotinic receptors

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7
Q

What does an end plate potential cause?

A

Depolarisation of the t-tubules causing a calcium influx into the Sarcoplasmic reticulum. This activates the contractile machinery

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8
Q

What poison blocks Ach Nicotinic receptors?

A

Curare

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9
Q

What are the sources of ATP?

A

Dephosphorylation of phosphocreatine
Oxidation of free fatty acids
Aerobic metabolism of carbohydrates
Anaerobic metabolism of glycogen

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10
Q

What is an isometric contraction?

A

Muscle develops tension but doesn’t shorten

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11
Q

What is an isotonic contraction?

A

Contraction where a muscle shortens while the load remains constant

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12
Q

What’s and eccentric muscle contraction?

A

Muscle lengthens whilst resisting a load

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13
Q

What are the types of muscle fibre?

A

Type 1- slow twitch, oxidative. Red and high in myoglobin and mitochondria
Type 2a- fast twitch. Oxidative. Contain machinery for anaerobic but also vascular with myoglobin
Type 2b- fast twitch, glycolytic. Low in myoglobin with large glycogen stores

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14
Q

Where are stains or pulls most common?

A

At the Myotendinous jct. Most associated with eccentric contractions

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15
Q

What are the Fibrillar collagens?

A

Type 1, 2, 3, 5 and 11.

They have mechanical/ tensile strength

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16
Q

What are fibril associated collagens (FACIT)?

A

Types 9, 12, 14, 19

These link Fibrillar collagens to each other

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17
Q

What is the main collagen found in tendons?

A

Type 2

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18
Q

What are Proteoglycans?

A

They regulate collagen fibril size and act as a shock absorber. Made up of glycosaminoglycans and hyaluronic acid.

E.g. Aggrecan

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19
Q

What is the site where ligaments and tendons join bones called?

A

Enthesis.

Injuries to this are called Enthesonopathies

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20
Q

What is the main collagen component of ligaments?

A

Type 1.

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21
Q

What is Articular cartilage arranged into and what are the zones called?

A

Benninghoff arcades.

  • superficial zone
  • mid zone
  • deep zone
  • calcified cartilage
  • bone
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22
Q

Where does Articular cartilage gets it’s nutrients from?

A

Synovial fluid. Via diffusion, assisted by compression and movement

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23
Q

What do Metalloproteinases do?

A

Matrix-Metalloproteinases degrade collagen and matrix

Aggrecanases (ADAMTs) degrade Aggrecan

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24
Q

What are bones made up of?

A

Osteocytes, osteoblasts, osteoclasts and mineralised ECM

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25
Q

What are the main parts of the skeleton?

A

Axial and appendicular

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26
Q

What is the ECM of bone made up of?

A

Organic (40%)- type 1 collagen, Proteoglycans

Inorganic (60%)- calcium hydroxyapatite crystals

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27
Q

What’s the difference between trabecular (cancellous) bone and cortical bone?

A

Trabecular bone is ‘spongy’ with a high turnover

Cortical bone is ‘compact’ forms a shell around the trabecular bone

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28
Q

What is osteogenesis inperfecta?

A

Type 1 collagen mutation –> weak bones

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29
Q

What are Chondrodysplasias?

A

Type 2 collagen mutations –>abnormal cartilage bone and joint deformities

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30
Q

What is Ehrlers-Danlos syndrome?

A

Type 3 collagen mutation–> fragile skin and blood blood vessels, hyper mobile joints

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31
Q

What are osteocytes and what are they in?

A

Modified osteoblasts and are contained in lacunae.

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32
Q

What causes scurvy?

A

Insufficient vitamin c. It’s the cofactor for the hydroxylases Hydroxyproline and Hydroxylysine which stabile the triple helix and form cross links, therefore vit c deficiency causes weak bones, tendons, skin and blood vessels

33
Q

What does osteoprotegerin (OPG) do?

A

Reduces resorption

34
Q

What does RANKL do? And what increases RANKL?

A

PTH, vit d3 and pge2 all increase RANKL. This causes increased bone resorption.

35
Q

What causes osteoporosis?

A

Negative bone balance. Formation increases, but resorption increases by more.

36
Q

What are osteoprogenitors?

A

Precursor cells that become bone cells.

37
Q

What is the purpose of calcium homeostasis?

A

To maintain constant blood calcium concentration

38
Q

what regulates calcium homeostasis?

A

Gut, bone and kidneys.

PTH, Vit D and Calcitonin

39
Q

Where is vitamin D converted to its active metabolite and what controls this?

A

It’s converted to 1,25(OH)2 vitamin D3 in the kidneys by 1a- hydroxylase. This is controlled by PTH.

40
Q

What are the functions of vitamin D?

A
  1. Stimulate transepithelial transport of Ca2+ & PO42- in small intestine
  2. Stimulate differentiation of OC directly and via OB increasing serum Ca2+ from bone.
  3. Inhibit PTH gene trascription (-ve feedback)
41
Q

Where is PTH produced?

A

Chief cells of the parathyroid gland. These are embedded in the thyroid gland.

42
Q

What are the functions of PTH?

A

Preserve blood Ca2+ by:

  • Stimulating bone resorption
  • Stimulating renal tubular reabsorption of Ca2+
  • Stimulating 1a-hydroxylase (Vit D) indirectly increasing intestinal absorption.
43
Q

How is PTH controlled?

A

-ve feedback control. Via calcium sensing receptor in the parathyroids. This receptor is also present in the kidneys

44
Q

What is the function of Calcitonin?

A

Inhibits osteoclast resorption. No role in day to day plasma Ca2+ levels.

45
Q

What does hypercalcaemia cause?

A

Generally causes suppression of activity (blocks Na+ channels).
-Stones, bones, groans, thrones, psychiatric overtones.

46
Q

What are the signs and symptoms of hypocalcaemia?

A

Pins and needles (1st), tetany, facial spasms, Arrhythmias, increased tendon reflexes.

47
Q

What is Rickets?

A

Vit D deficiency in children causing bowing of long bones which are soft and easily fractured.

48
Q

What is osteomalacia?

A

Vitamin D deficiency in adults –> unmineralised osteoid.

49
Q

What must be ruled out in patients presenting with monoarthritis?

A

Infection

50
Q

Cause of monoarthritis?

A

Gout, trauma (haemarthrosis), osteoarthritis, psoriatic/IBD, sarcoid, reactive, infection.

51
Q

How does septic arthritis present?

A

Acute inflammation of a joint. Sudden onset, pain and swelling, erythematous.

52
Q

What investigations would you perform for suspected septic arthritis?

A

FBC, U&Es, LFT, CRP, Urate, Cultures, gram stain, AFB, X-ray. Aspirate fluid if no prosthetic)

53
Q

What causes gout?

A

Inflammatory response to monosodium urate monohdrate crystals- can form from hyperuricaemia.

54
Q

Non biochemical causes of gout?

A

Overproduction or underexcretion of urate either caused by a high purine diet, or renal impairment (90%)

55
Q

What drugs decrease urate excretion (therefore increase risk of gout)?

A

Low dose aspirin, thiazides, frusemide, ethambutol, nicotinic acid, pyrazinomide

56
Q

Symptoms of acute gout?

A

Pain, swelling & erythema, >50% in 1st MTP but can be any joint, mild= 1-2 days, severe= 7-10 days. 90% is monoarticular

57
Q

What can result from chronic gout?

A

Tophi can form. These are firm, nodular fusiform swellings.

58
Q

Investigations for gout?

A

Joint fluid –> urate crystals.

Bloods –> Urate, urea & creatinine.

59
Q

Treatment for gout?

A

Correct hyperurcauemia (diet, drugs)
NSAIDs.
Don’t start urate reducing therapy during an acute attack

60
Q

Examples of Urate lowering drugs?

A

Xanthine oxidase inhibitors - Allopurinol & Feboxostat

Uricosuric agents - Sulphinpyrisone.

61
Q

What are some problems with Allopurinol?

A

It needs to be titrated, interacts w/ warfarin and there are difficulties with renal impairment

62
Q

What are the different grades of cartilage lesions?

A

1- fissure to the superficial cartilage
2- multiple fissures up to 1/2 depth
3- fissures down tot he bone but no denuded bone
4- complete loss of cartilage and bone exposure

63
Q

Why does articular cartilage have limited capacity for repair?

A

It’s avascular and diffusion of nutrients is slow.

64
Q

What are the treatment options for articular cartilage damage?

A

TJA (v. serious), debridement, microfracture, osteochondral grafting (mosiacplasty), osteotomy, cell based therapies (ACI)

65
Q

What is autologous chondrocyte implantation (ACI)?

A

Autologous chondrocytes from healthy cartilage are taken for ex vivo expansion. reimplanted then cover the defects.

66
Q

What nerves combine to form the Sciatic nerve?

A

Common peroneal and tibial (L4-S3)

67
Q

What connects the lumbar plexus to the sacral plexus?

A

lumbosacral trunk

68
Q

What are the symptoms of femoral nerve palsy?

A

Pain in the inguinal region –> eases on flexion and external rotation, knee buckling, anterior knee pain (saphenous nerve supplies the patella), weak hip flexion & knee extension, reduced sensation in anteromedial thigh

69
Q

What are symptoms of tibial nerve palsy?

A

Tarsel tunnel syndrome, discomfort/pain/burning in plantar foot, night pain

70
Q

Symptoms of peroneal nerve palsy?

A

Foot drop due to paralysed ankle dorsiflexors, reduced sensation of superficial and deep peroneal nerves.

71
Q

Symptoms of sciatica?

A

Lower back pain, numbness of the lower thigh, pins and needles, uni/bilateral, weakness

72
Q

Possible causes of sciatic nerve pain?

A

Spinal stenosis, piriformis syndrome

73
Q

What sort of joint is the facet joint of the spine?

A

Synovial

74
Q

Where is the most common site for a vertebral fracture?

A

Where mobile areas meet immobile areas- e.g. T12-L1

75
Q

What is the difference between a stable spinal fracture and an unstable fracture?

A

A stable fracture generally only involves the anterior column, if any other columns are involved then it is generally considered to be unstable

76
Q

What makes up the anterior column of the spine?

A

Anterior longitudinal ligament and the anterior 1/2 of the vertebral column, disk and annulus.

77
Q

What makes up the middle column of the spine?

A

Posterior 1/2 of the vertebral body, disk and the posterior longitudinal ligament

78
Q

What makes up the posterior column?

A

Facet joints, ligamentum flavum, posterior elements and the interconnecting ligaments

79
Q

What is cervical spondylosis?

A

Degenerations of the intervertebral disks +/- facet joint degeneration, narrowing of disk spaces, protrusion and calcification of the annulus, osteophytes and thickening of the spinal ligaments

Revision (12 decks)

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