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Semester 3 > MSK > Flashcards

MSK Flashcards

1
Q

3 type of joints

A

fibrous
cartilaginous
synovial

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2
Q

structure/layout of cartilage

A

mainly made up of proteoglycans:
aggrecan = GAG + core protein

they produce high osmotic pressure –> inflating the cartilage –> high gel swelling pressure

many proteoglycans held via hyaluronan

these are held by collagen type II

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3
Q

what cell secretes lubricin and hyaluronan

A

type B synoviocyte cell

lubricin - for high load low velocity
hyaluronan - for low load high velocity

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4
Q

what cell is osteoclasts and osteoblasts differentiated/derived from

A 
osteoclasts = haematopoietic
osteoblasts = mesenchymal (but also can be from haematopoietic)
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5
Q

describe how PTH stimulates resorption of bone

A

PTH receptors on osteoblasts

osteoblasts produce RANK ligand

RANK receptors on osteoclast PRECURSORS

stimulates differentiation into osteoclasts –> resorption

osteopotegrin binds to RANK ligand = antagonist

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6
Q

what do osteoblasts and osteoclasts produce

A

osteoblasts = uOCN

  • stimulates b-cells (Pancreas)
  • Increase insulin
  • increases glucose uptake for energy for bone growth

osteoclasts = FGF-23

  • acts on kidney
  • increases phosphate excretion
  • decreases 1a-hydroxylation = dec. vit D function
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7
Q

how is PTH produced

A

in parathyroid gland by chief cells

pre-prohormone–> ER—> prohormone–> golgi–>released into circulation–> hormone–> broken down in blood–> 1-34 is active

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8
Q

PTH function

A
  • increase vit D production via stimulating 1a-hydroxylase
  • increase ca absorption in DCT
  • increase phosphate excretion
  • stimulate resorption by increase CM-CSF + RANK in osteoblasts
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9
Q

describe function of CaSR

A

calcium sensing receptors on chief cells of parathyroid gland
when ca rises

  • Gi —> decrease PKA –> decreases PTH
  • Gq–> DAG/IP3–> increases PKC and Ca–> decreases PTH
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10
Q

synthesis of vitamin D

A

cholesterol —–> cholecalciferol (D3) when light hits skin
ergosterol —–> ergocalciferol (D2) from diet

these go to liver –> 25-OH—> kidney —> 1a-hydroxylase–> 1,25 triol

(1a-hydroxylase stimulated by PTH and inhibited by FGF23)

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11
Q

what type of receptor does vitamin D bind to

A

type 2 nuclear

binding = dimerisation with retinoic acid receptor

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12
Q

describe how production of vitamin d leads to its own negative feedback inhibition

A

increases Ca –> decreases PTH–> decreases 1a-hydroxylase

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13
Q

transport of calcium in gut (2 ways)

A
  1. paracellular route

2. TPRV –> calbindin–> Ca/3Na or CaATPase

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14
Q

does vitamin D increase or decrease insulin resistance when acts on pancreatic cells

A

decrease

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15
Q

how many somites formed in humans

A

44

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16
Q

what are somites formed from

A

presomitic mesoderm

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17
Q

what do somites differentiate into and what do they form (4)

A

1) dermamyotome + sclerotome
2) myotome + dermatome + sclerotome
3) syndetome

sclerotome = vertebrae
myotome = epimere(extensor of vertebral column)/hypomere(chest wall + limb muscles)
dermatome = dorsal dermis
syndetome = tendons
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18
Q

3 tiers of control of somitogenesis

A

1) bottom = within cell (time for transcription etc.)
2) middle = between cells (delta-notch signals)
3) top = cranial+caudal ends (cranial -retinoic acid + caudal - wnt+FGF)

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19
Q

what bones do not undergo endochondrial ossification

A

flat bones of face
cranial bones
clavicle

they undergo intramembranous ossification

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20
Q

explain how symmetry and elongation of limb muscles are controlled

A

FGF from apical ectodermal ridge = keeps the zone of proliferation from differentiating = elongates

SHH from zone of polarising activity controls the symmetery of AER

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21
Q

explain myotome —> myofibre

A

myotome—-myf5/myoD—-> myoblast—myogenin—-> myotubes (primary and secondary –mrf4—> myofibre

22
Q

what is secreted from growth cone for a NMJ to form

A

agrin

acts as a signal by binding to MUSK (tyrosine-kinase receptor) on myofiber

23
Q

what is Duchenne muscular dystrophy

A

mutated dystrophin gene (responsible for connecting sarcomere with sarcolemma = muscle integrity)

due to frameshift deletion

  • risk of death
  • but satellite cells are not affected
24
Q

oestrogen effect on bone

A

inhibits osteoclasts

therefore as you age, decrease of oestrogen, more osteoclasts resorbing = osteoporosis

localised = paget’s

25
Q

what is osteomalacia

A

lack of vit D–> lack of absorption of calcium –> weak/undermineralised bones

in children = rickets

26
Q

4 stages of fracture healing

A
  1. inflammation
  2. soft callus
  3. hard/bony callus
  4. bone remodelling
27
Q

treating gout (inflammatory mono)

A

1) treat acute attack
- NSAIDs
- colchicine
- steroid

2) prevent
- reduce serum uric acid below crystallising threshold
- xanthine oxidase inhibitors
- uricosuric drugs

28
Q

what joints are affected in RA vs osteoarthritis

A

RA = PIP/wrist/MCP

OA = DIP/1st CMC joints

29
Q

what gene can cause ankylosing spondylitis(arthritis affecting spine)

A

HLA B27+

30
Q

3 types of hyperparathyroidism

A

primary - high ca/PTH due to tumour causing high production of PTH

secondary - low Ca so you get high PTH

tertiary - after secondary when you get a transplant so high ca due to high PTH that body is used to

31
Q

what is probably the cause if there is low PTH but high Ca

A

cancer–> inflammatory response–> mediators–> stimulate osteoclasts–> high resorption of Ca

granulomatous disease
(granulomas contain 1a-hydroxylase–> stimulates vit D)

32
Q

treatment for hypercalcaemia

A
  • hydrate with saline (stimulates 3Na/Ca)
  • loop diuretics (furosemide) to help pee/flush out ca
  • bisphosphonates (stops osteoclasts)
  • calcitonin (only hormone to decrease calcium levels)
  • prednisolone (steroid to suppress immune response)
  • calcimimetics to activate CaSR to decrease PTH
  • surgery to remove parathyroid tumour (primary)
33
Q

2 types of hypoparathyroidism

A

primary = congenital/autoimmune causing faulty production from parathyroids

secondary = due to injury/surgery

34
Q

why might you get low calcium despite having high PTH

A

pseudoparathyroidism

PTH receptors are not working

35
Q

gene therapy option for Duchenne

A

ataluren - stop codon read through

eteplisren - antisense oglionucleotide for exon 51 (specific)

36
Q

what degrades joint tissue

A

aggrecanase
MMP

their products (bind to TLR4) cause positive feedback to keep degrading

37
Q

what is the extracellular matrix made up of

A

ground substance
fibrous proteins (collagen/elastin from fibroblasts)
water
minerals

38
Q

how is elastin formed

A

tropoelastin—-polymerisation–> elastin

laid down due to microfibrils composed of fibrilin

39
Q

what is elastin degradation controlled by

A

elastase = degrades

alpha 1 anti-trypsin = inhibits elastase = prevents degrading

40
Q

what is pulmonary emphysema and Marfan syndrome

A

PE = lack of anti-trypsin so elastase degrades elastin

MS = mutation of fibrillin gene so elastin not deposited properly

41
Q

what type of collagen causes the conditions:

  • osteogenesisimperfecta (glycine >taurine disrupts alpha helix)
  • achondrogenesis (lack of ossification)
  • ehlers-danlos syndrome
A
  • type I (bone/tendons)
  • type I
  • type III/V (skin/blood vessels)
42
Q

what can muscle fibre number be affected by

A

fibre # is set from birth

but it can be affected by temp/nutrition/hormones/ innervation

43
Q

4 main myosins

A

type 2 = fast

  • IIx
  • IIalpha
  • IIbeta

type1 = slow
-beta-slow

44
Q

4 types of pseudo hypothyroidism

A

(all have high PTH levels)

1a - low urine cAMP / clinical phenotype
1b- low urine cAMP / non-clinical phenotype
1c - normal cAMP/ clinical phenotype
2 - normal cAMP / non-clinical phenotype

45
Q

4 types of pseudo hypothyroidism

A

(all have high PTH levels)

1a - low urine cAMP / clinical phenotype
1b- low urine cAMP / non-clinical phenotype
1c - normal cAMP/ clinical phenotype
2 - normal cAMP / non-clinical phenotype

phenotype =

  • short 4th/th metacarpals
  • round/obese face
  • ecptopic calcification
  • short
  • reduced IQ
  • issues w/ pituitary hormones
46
Q

what are looser zones

A

pseudo fractures that don’t penetrate the whole way through

47
Q

difference between myasthenia graves and botulism

A

both cause muscle weakness / NMJ disease

MG - Ach nic receptors are blocked by autoantibodies

botulism - prevention of release of Ach from synaptic vesicles

48
Q

mononeuropathy vs radiculopathy

A

focal pattern of neuropathy

mono = affecting 1 nerve
radiculopahty = nerve root
49
Q

organisation of collagen fibres in tendons/ligaments, bone and cartilage

A

tendons and ligaments (I) = parallel

bone (I) = spirals

cartilage (II) = meshwork

50
Q

pulmonary emphysema and Marfan syndrome

A

PE = lack of anti-trypsin—> high elastase activity

Marfan = mutation of fibirillin = can’t lay down elastase –> fragile tissue/unstable joints

51
Q

what occurs during hypertension in terms of elastin/collagen

A

increased synthesis and deposition —>

  • thicker vessel walls
  • reduced vessel diameters
  • slower turnover of elastin/collagen

Semester 3 (6 decks)

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