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CBL MSK > lectures 2 > Flashcards

lectures 2 Flashcards

1
Q

Make up of bones

A 
Mineral phase 
Organic phase 
water 
Hydroxyapatite( calcium phsophate)
Collagen and other proteins
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2
Q

Calcium- where is it sotred

A

99% in bones

1% in serum

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3
Q

Why is calcium level important

A

For bodily functions eg blood clotting, nerve cell activity and other cellular activities

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4
Q

How is calcium levels maintained

A

Controlling rate of calcium resorption from bone into the blood and calcium deposition into the bones

Regulated by 3 main hormones - pth, vitamin d and

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5
Q

How can calcium be bounded

A

Protein bound

Diffusible- free

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6
Q

PTH - parathyroid hormone effect on bone calcium

A

FALL in blood calcium- detected by PTH receptors, PTH synthesis increased and released into teh blood

PTH binds to pTH receptors on osteoblasts, which produce RANKL, this stimulates osteoclast cells to proliferate which increases the resorption of bone which causes release of calcium from bone into the blood

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7
Q

What is PTH

A

amino acid peptide secreted by chief cells within teh 4 parathyroid glands, located on back of thyroid gland in the neck

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8
Q

PTH effect on kidneys and vitamin D

A

When theres low calcium
- decreased loss of calcium in the urine

Vitamin D is released - enhanced absorption of calcium from intestine

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9
Q

Vitamin D effect on calcium levels when low

A

Stimulates calcium and phosphate absorption in the intestine into the blood

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10
Q

Vitamin D role

A

Necessary for bone mineralisation

lack = osteomalacia

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11
Q

Why might you not have enough vitamin D

A

Not enough UV
Dietary requirements
Supplements

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12
Q

What is Calcitonin

A

secreted from parafollicular cells of the parathyroid gland in response to rising serum Ca2+ conc

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13
Q

How does calcitonin regulate calcium levels

A

When increased blood calcium levels
Inhibits osteoclast activity, inhibits ca2+ absorption by the intestines and inhibits renal tubular ca2+ reabsorption, reducing plasma ca2+ and phosphate concs

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14
Q

Increased ca2+ blood levels - HYPERCALCAEMIA

A

Thyroid gland releases calcitonin
Osteoclast acitivity is inhibited
Ca2+ reabsorption in the kidneys decreased
Ca2+ level in blood decreased

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15
Q

decreased Ca2+ blood levels - hypocalemia

A

Parathyroid glands release PTH
Osteoclasts release Ca2+ from bone
Calcium is reabsorbed from urine by teh kidneys
Calcium absorption int eh small intestine increases via vitamin D synthesis
Ca2+ level in blood increases

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16
Q

What is bone density

A

Measure of the amount of mineral ( hydroxyapatite) present in the bone
Used to diagnose osteoporosis

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17
Q

What can affect bone density

A

Availability of substrates
- Calcium intake, calcium absorption, functionality of PTH

Physiological factors
- weight bearing exercise, smoking, BMI, healthy diet

Biochemical factors
- steroid hormones, oestrogen, thyroid hormones

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18
Q

Bone density variation with age

A

Reduces whit age

In women- reduces after menopause- decreasing ostrogen levels

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19
Q

Do people need calcium supplements?

A

Vegans

Lactose intolerance

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20
Q

Fracture risk

A 
Previous fracture 
Age
Smoking status 
Medication ( steroids) 
Bone density 
Alcohol intake
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21
Q

Bone remodelling

phases names

A 
Activation 
Resorption 
Reversal
Formation 
Quinesence
22
Q

Activation - bone remodelling

A

Preosteoclasts are attracted to the remodelling sites

Preosteoclasts fuse to form multinucelated osteoclasts

23
Q

Resorption- bone remodelling

A

Osteoclasts dig out a cavity, called a resorption pit, in spongey bone or burrow a tunnel in compact bone
Calcium can be released into the blood for use in various bodily functions
Osteoclasts disappear

24
Q

Reversal - bone remodelling

A

Mesenchymal stem cells appear along burrow where they PROLIFERATE(increase in no.s) and differentiate into pre osteoblasts

25
Q

Formation- bone remodelling

A

Mature into osteoblasts at surface of borrow and release osteoid at the site, forming a new soft nonmineralised matrix
New matrix is mineralised with calcium and phosphorus

26
Q

Quiescence- bone remodelling

A

Site with resting lining cells remains dormant until the next cell

27
Q

Wolffs law

A

Everyday remodeling in response to stress

Bones will adapt based on teh stress or demands placed on them

28
Q

Osteopenia

A

Midway point to osteoporosis - bone density is lowering but not as severe

On a scan, bones look darker - less mass

When loose bone mass and your bones get weaker

29
Q

Disuse osteopenia

A

Loss of bone due to lack of normal stress

30
Q

Bone breakage

A

Force to one side

Compresses on side where force is applied
On the other side - tension is caused= BREAK

31
Q

TYPES OF BONE HEALING and when are they used

A

Primary - absolute stability and compression ( plates and screws) , no callous formed- good for joints

Secondary- relative stability, normal biological process of healing
CALLOUS formation

32
Q

3 phases of healing

A

Reactive phase
reparative phase
remodelling

33
Q

Reactive phase of healing

A

Haematoma formed
Blood clot
Blood supply to the bone cells that lie on either side of fracture is disrupted and they begin to die. Dead cells induce macrophages and osteoclasts to start removing the dead bone debris and cells from fracture site. Localized swelling

34
Q

Reparative phase of healing

Hard and soft callous

A

SOFT CALLOUS – fibroblasts make fibrous tissue, new blood vessels add stability as they contain connective tissue, fibroblasts mature and differentiate into chondroblasts,

HARD CALLOUS- osteogenic progenitor cells form into osteoblasts and secrete bone matrix- woven bone

35
Q

Remodelling phase of healing

A
  • Woven bone lattice is rearranged itno the normal cortical and spongey bone arrangement. Woven bone is removed gradually by osteoclasts and replaced by osteoblasts
36
Q

Factors influencing healing - 2 types and examples

A

FRACTURE VARIABLES
blood supply, complexity, immobilisation

PATIENT VARIABLES
nictoine, diabetes, diet, HIV ( affects osteoblasts, difficult to heal bone

37
Q

What is non union

A

When bone doesnt heal

38
Q

Atropic non union

A

Intermediate fragments are missing and scar tissue that lacks osteogenic potenital is left in their place
No callus forms

39
Q

Hypertropic non union

A

Callus is formed, but the bone fractures have not joined

Can be due to inadequate fixation of the fracture and treated with rigid immobilisation or in a joint

40
Q

Functions of skeletal muscle

A 
Movement 
Control posture 
remove and store glucose 
Generate heat 
Metabolically active
41
Q

Isometric contractions

A

Tension increases, muscle length remains the same. Important in maintaining posture

42
Q

Contraction

A

Movement or generation of force

43
Q

Isotonic contraction

A

Tension remains the same, muscles shorten, used in movement.

44
Q

Concentric vs eccentric

A 
Concentric = shortening muscle 
Eccentric = lengthening muscle
45
Q

EMG
EEG
ECG

A 
ecg = heart 
emg = skeletal muscle 
eeg= brain active
46
Q

Egs of skeletal muscle relaxants

A

Botulinum toxin
Curare
Succinylcholine

47
Q

Botulinum toxin

A

Prevents release of ACh containing vesicles

Causes paralysis of muscle and inhibition of secretion from exocrine glands normally stimulated by parasympathetic NS

48
Q

Curare

A

Blocks nAChRs to cause paralysis ( used during surgery to prevent muscle spasm )

49
Q

Succinylcholine

A

Short acting block of nAChR

50
Q

Function of SR

A

Stores calcium
In musscles
Rapidly releases calcium ( triggered by action potential)
Rapidly restore calcium (using ATP driven calcium pumps

51
Q

T tubules

A

Convey quickly the action potential deep inside the fiber

T tubules are continuous with surface membrane

CBL MSK (6 decks)

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