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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
Formation- bone remodelling
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
Quiescence- bone remodelling
Site with resting lining cells remains dormant until the next cell
27
Wolffs law
Everyday remodeling in response to stress | Bones will adapt based on teh stress or demands placed on them
28
Osteopenia
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
Disuse osteopenia
Loss of bone due to lack of normal stress
30
Bone breakage
Force to one side Compresses on side where force is applied On the other side - tension is caused= BREAK
31
TYPES OF BONE HEALING and when are they used
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
3 phases of healing
Reactive phase reparative phase remodelling
33
Reactive phase of healing
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
Reparative phase of healing | Hard and soft callous
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
Remodelling phase of healing
- 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
Factors influencing healing - 2 types and examples
FRACTURE VARIABLES blood supply, complexity, immobilisation PATIENT VARIABLES nictoine, diabetes, diet, HIV ( affects osteoblasts, difficult to heal bone
37
What is non union
When bone doesnt heal
38
Atropic non union
Intermediate fragments are missing and scar tissue that lacks osteogenic potenital is left in their place No callus forms
39
Hypertropic non union
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
Functions of skeletal muscle
``` Movement Control posture remove and store glucose Generate heat Metabolically active ```
41
Isometric contractions
Tension increases, muscle length remains the same. Important in maintaining posture
42
Contraction
Movement or generation of force
43
Isotonic contraction
Tension remains the same, muscles shorten, used in movement.
44
Concentric vs eccentric
``` Concentric = shortening muscle Eccentric = lengthening muscle ```
45
EMG EEG ECG
``` ecg = heart emg = skeletal muscle eeg= brain active ```
46
Egs of skeletal muscle relaxants
Botulinum toxin Curare Succinylcholine
47
Botulinum toxin
Prevents release of ACh containing vesicles | Causes paralysis of muscle and inhibition of secretion from exocrine glands normally stimulated by parasympathetic NS
48
Curare
Blocks nAChRs to cause paralysis ( used during surgery to prevent muscle spasm )
49
Succinylcholine
Short acting block of nAChR
50
Function of SR
Stores calcium In musscles Rapidly releases calcium ( triggered by action potential) Rapidly restore calcium (using ATP driven calcium pumps
51
T tubules
Convey quickly the action potential deep inside the fiber | T tubules are continuous with surface membrane

CBL MSK (6 decks)

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