Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MEDICINE > CEP WK6 - PARATHYROID GLAND & CA HOMEOSTASIS > Flashcards

CEP WK6 - PARATHYROID GLAND & CA HOMEOSTASIS Flashcards

1
Q

JOBS OF SKELETON

A
  • protect vital organs
  • support muscles
  • provide reservoir of calcium
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

CALCIUM HOMEOSTASIS

A
  • must maintain serum calcium conc. of 2.1-2.6 mM

- can be absorbed back (after being released to) from bone, intestine, kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

NORMAL BODY LEVELS

A

PTH = 1.6-6.9 pmol/L
Serum Ca = 2.1-2.6mM
1,25D3 = 50-150 pmol/L
Creatinine = 74.3-107 mmol/L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

PARATHYROID GLANDS

A

secrete PTH in response to low calcium or high phosphate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

JOBS OF PTH

A
  • binds to GPCR in kidney or osteoblast to do response
    KIDNEY - increase calcium reabsorption in renal distal tube
    INTESTINE - increase calcium reabsorption indirectly (by activating vit D)
    BONE increase calcium release from bone (by stimulating osteoclast activity)
  • decrease phosphate reabsorption
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

HYPOCALCAEMIA (low Ca level)

A
  • low Ca = more PTH secretion in parathyroid glands to kidney to decrease Ca in urine, increase phosphate in urine & produce 1,25D3 enzyme which produces vitamin D (goes to intestine to increase Ca absorption)
  • in very worst case scenario, we can reabsorb calcium from bone (not ideal)
    LOOK AT DIAGRAM ON CEP W7
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

HOW PTH REGULATED

A
  • PTH transcription inhibited by 1,25D3 (high 1,25D3 production lowers amount of PTH)
  • PTH translation inhibited by increased serum calcium (less PTH made if low calcium)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

CALCITONIN

A
  • produced by C-cells in thyroid in response to hypercalcaemia & works by inhibiting bone reabsorption
  • not essential to life as shown by no problems after a thyroidectomy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

VITAMIN D FROM?

A
  • obtained from diet or UV (hits skin & converts 7-dehydrocholesterol to vit D3) & D3 enters blood then converted to 25D3 in liver then converted to 1,25D3 by PTH in kidney
  • Active form is 1,25D3 & inactive is 25D3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

EFFECTS OF VIT D

A

binds to vit D receptors (intracellular & is a steroid receptor) & acts as TF &

  • promotes Ca & PO4 intestine absorption
  • promotes bone resorption (increase osteoclast number) - inhibits PTH transcription
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

SIGNS OF VITAMIN D DEFICIENCY

A

bone pain, seizures, renal signs, osteomalacia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

OTHER THAN VIT-D & PTH, WHAT INFLUENCES BONE STATUS (4)

A
  • age (bone density decreases with age)
  • oestrogen levels (oestrogen deficiency following menopause increases bone remodelling rate & degree of bone reabsorption)
  • levels of phosphate & calcium
  • steroid therapy (risk of bone loss due to steroid meds)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

HYPERCALCAEMIA

A

parathyroid glands clock the high Ca so decrease PTH secretion which leads to these things below to decrease the serum calcium level

  • less bone resorption
  • less urine phosphate & 1,25D3 production BUT higher urinary calcium
  • lower calcium & phosphate absorption in intestine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

HYPERPHOSPHATAEMIA (HIGH SERUM PO4)

A
  • FGF23 produced by osteocytes (bone cells) & released in response to high serum PO4 to increase urinary PO4 & suppress renal synthesis of active vitamin D (1,25D3) to decrease
  • FGF23 effectively overrides effects of PTH
  • FGF23 os inhibited by 1,25D3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

STRUCTURE OF BONES

A
  • main bone growth & activities happens in epiphysis

- strong part of bone is in diaphysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

WHAT IS BONE MADE OF

A

specialised connective tissue, extracellular matrix, collagen

17
Q

OSTEOCYTES

A
  • produce FGF 23

- have long processes used to communicate with other osteocytes & osteoblasts

18
Q

OSTEOBLASTS

A
  • bone forming cells

- produce matrix constituents & aid calcification

19
Q

OSTEOCLASTS

A
  • bone reabsorbing cells
  • produce acid (to reabsorb minerals) & enzymes (to reabsorb matrix)
  • have integrins to attach to bone surface
20
Q

HOW CALCIUM CONC RELATED TO SPASMS

A

low plasma calcium increases permeability of membranes to NA= which leads to depolarisation. If Ca2+ conc. is less than 50% of normal, AP may be spontaneously generated which leads to involuntary contraction of muscles

21
Q

OSTEOCLAST DEVELOPMENT

A
  • osteoblasts have a RANK ligans which goes to osteoclast precursor (has a RANK receptor) to form an osteoclast
  • drugs that can bind to RANK receptor to inhibit this are denosumabs & OPG’s
22
Q

BONE REMODELLING

A

osteoclasts bind to bone -> bone resorption -> resorption pit formed -> Ca2+/PO4/collagen all taken out of bone -> osteoblasts come in to form a new layer of mineralised bone (using collagen & PO4 & calcium)

23
Q

HYPERPARATHYROIDISM (raised serum PTH)

A

PRIMARY - caused by parathyroid tumour & leads to hypercalcaemia & low serum PO4 (loss of negative feedback loop from hypercalcaemia)
- treated by surgery
SECONDARY - caused by kidney disease & leads to increased phosphate and decreased activation of vitamin D
- treated with phosphate binders to bring phosphate level down
LOOK AT PG6 OF CEPW7

24
Q

OSTEOMALACIA

A
  • vitamin D & calcium deficiency due to diet & lack of sunlight
  • leads to lack of mineralisation of collagen component of bone (osteoid) & failure to absorb sufficient calcium from GI tract
  • symptoms are legs curving out at knees (bow-legs)(as osteoid at growth plate is weak) & swollen joints (growth plate expands to compensate)
  • treated by giving vitamin D
25
Q

OSTEOPOROSIS

A
  • loss of bone mass/density due to lack of mineral (you have normal bone but just less of it so increased fracture risk)
  • all bad effects are due to the osteoclasts
  • happens at ageing (less bone density as older), postmenopausal (decline in female bone density following oestrogen decline), steroid-induced (using steroids leads to decline in bone density)
  • prevented by exercise (enhanced osteocyte activity through bone stress)
26
Q

TREATING OSTEOPOROSIS

A
  • hormone replacement (replace oestrogen)
  • inhibit osteoclast development using RANK antibody e.g. denosumab (to block RANK receptor so less differentiation of pre-osteoclasts)
  • inhibition of osteoclast activity using bisphosphonates (disrupt intracellular enzymes needed for osteoclast activity)
  • stimulation of osteoblast activity

MEDICINE (27 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions