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PATHOLOGY > ca haemostasis > Flashcards

ca haemostasis Flashcards

1
Q

what are the roles of ca

A

skeleton and muscle function
metabolic - action potentials, intracellular signalling

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2
Q

molecular levels in
* osteoporosis
* osteomalacia/rickets
* paget’s
* parathyroid bone disease
* renal bone disease

A
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3
Q

forms of ca in serum

A

Free (ionised) = 50% = biologically active
Protein bound = 40% = bound to albumin
Complexed = 10% = citrate/phosphate

1% of all ca is in plasma

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4
Q

what is normal total ca and what is corrected ca

A

2.2-2.6 mmol/L = normal ca

corrected = serum ca + 0.02 x (40-serum albumin in g/L)

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5
Q

why do we use corrected ca

A

if albumin was normal what would the ca be - would hope is the same as total ca. if low albumin = less bound ca = higher proportion as free
Corrected ca = serum ca + 0.02*(40-serum albumin)
Normal albumin is 40 - so if had normal albumin corrected ca = total ca
Low albumin = low bound ca and normal free ca
Therefore corrected ca tells you if problem is with the calcium or the albumin
note - can measure ionised ca too

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6
Q

summarise response to low Ca

A

detected by parathyroid gland
Releases PTH
Gets Ca from bone, gut absorption and resorption from kidney and renal 1 a hydroxylase (regulatory step - only works when PTH turns it on)

1 a OH - activates Vit D - increased intestinal ca absorption

Result in rise in plasma ca

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7
Q

what type of hormone is vit D

A

steroid

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8
Q

summarise PTH

A
  • 84aa protein
    • Only released from parathyroids
    • Bone and renal ca resorpyion
    • Stimulates 1 a OH vit D sythn to make 1,25 (OH)2 vit D synthesis
    • Also stimulates renal phosphate wasting
    • Maintain normal Ca-phos product
    • If Ca too high - crystalises so don’t want this to happen = stones
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9
Q

summarise vit D synthesis

A

Sun - then make some vit D
In liver - first pass metabolism -> 25-OH-Vit D (what measure when do assay - but inactive, stored vit D)
PTH turn on kidney - add OH to vit D (enzyme is 1a hydroxylase) = active vit D

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10
Q

types of vit D

A

Vit D3 is synth is skin - cholecalciferon
Vit D2 plant vitamin - ergocalciferol
Both are active - both do the same thing

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11
Q

why is vit D activated in sarcoid

A

lung condition with granulomata in lung - ectopic 1 a OH and not regulated - might become hyperca

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12
Q

what is calcitriol

A

Calcitriol same thing as 1,25 OH vit D
Active form - give when have no kidneys

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13
Q

roles of 1,25 OH Vit D

A

Increases intestinal ca absorption and intestinal phos absorption
Critical for bone formation

Vit D receptor controls many genes for cell proliferation, immune system

Vit D deficiency associated with ca, autoimmune disease, metabolic syndrome

Vit D levels are linked to poverty - which is what causes the conditions

Vit D will prevent fractures in much later life - prevent osteomalacia

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14
Q

role of PTH

A

stim osteoclasts - rise in ca and phos from bone
Phos lost from bone

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15
Q

use of bone alkaline phosphtase

A

can see if normal PTH activity because bone releases alk phos
Can see if have normal bone degrading too fast - see if have osteoporisis - see if increased bone transfer

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16
Q

role of skeleton

A

Structural framework
Strong
Lightwht
Mobile
Protects vital organs
Capable of orderly growth and remodelling

Metabolic role in ca homeostasis

Main resevoir of ca and phos

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17
Q

what are the metabolic bone diseases

A

osteoporosis - bone is normal but weak - less bone per unit volume
osteomalacia - bones decalcified, more protein and less ca than normal
paget’s - thought to have been caused by virus but never found
parathyroid bone disease - tumour of the parathyroid
renal osteodystrophy - no 1a hydroxylase

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18
Q

summarise vitamin D deficiency

A

Defective bone mineralisation
In childhood = rickets, in adulthood = osteomalacia
Rickets - end of bone gets wider
Osteomalacia - fracture when young

RF: lack of sun, dark skin, dietary, malabsorption

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19
Q

clinical features of osteomalacia

A

Looser zones - pseudofractures - part way through bone, don’t break until trauma. Increased fracture risk
Sx - bone and muscle pain

Low Ca and phos and raised ALP - both not absorbed from the gut

20
Q

clinical features of rickets

A

bowed legs, costochondral swelling, widened epiphyses at the wrists, myopathy - waddling gate and nerve->muscle function doenst work

Risk - after childbirth and in lactation because baby take ca

21
Q

causes of osteomalacia

A

renal fauilure=don’t activate Vit D,
anticonvulsants induce breakdown of vit D (phenytoin),
lack of sunlight,
chappatis (contain phytic acid = chelate vit D)

Anticonvulsant rickets - counteract by giving vit D when give anticonvulsants. anticonvulsant - induce enzyme that makes inactive vit D

22
Q

biochemistry for osteomalacia

A

low ca
low phos
high ALP

23
Q

summarise osteoporosis

A

Losing bone mass
Cause of pathological fracture
Occuring more often as people live longer

Lack of use of bone: immobilisation, caused by progressive slow loss - excess steroid and thyroxine and lack of oestrogen all contribute

Post-menopausal

Biochem - completely normal - ca, phos and PTH are all completely normal
Reduced bone mineraldensity, asymptomatic until fracture (1st sx!)
Typical fracture - neck of femur fracture, vertebral, wrist (colles)

24
Q

dx of osteoporosis

A

Bone density scan - DEXA - hip, spine, wrist
Compare with normal healthy young person of same gender - T score
We know as everyone gets older they will get fracture
Z score is age matched - show much worse than everyone else. Useful to show accelarated bone mass in younger population
T <-2.5 SD from mean - then by definition have osteoporosis
T -1 - -2.5 = osteopenia

25
Q

causes/RF for osteoporosis

A

Between 45-60 lose bone faster than other ages
Childhood illness (ie failure to make peak bone mass)/early menopause
Early menopause causes big change in risk of fracture - use HRT unless cant eg FHx of breast cancer
Sedentary
Alcohol - causal
Smoking - association
Low BMI/nutritional
Steroids - need vit D prophylaxis
Genetic
Prolonged intercurrent illness
Prolactinoma - turn off oestrogen and testosterone
Hyperthyroid/cushings

26
Q

what does DEXA stand for

A

dual energy X-ray absorptiometry

27
Q

treatment for osteoporosis

A

Wht bearing exercise
Stop smoking
Reduce alcohol
Vit D and ca
Bisphosphonates - alendronate = reduce bone resorption
* Oral - gastric irritation. Need to take it by itself binds to ca - so if ca in stomach, then it will bind and be excreted - so need to take once a week w/ water and NO milk etc, and need to stay upright. Has phos and nitrogen - if make bone from it = not biodegradable = really strong and not as fast turnover - unnatural phosphate.
* IV - give once a year - zelondronate
Teriparatide - injection daily - PTH analonge - build bone
Strontium - anabolic and anti-resorbative. Not very effective
HRT - oestrogen
Selective oestrogen receptor modulator - raloxifene/tamoxifen. Tamoxifen block E2 receptor in breast, in bone agonist. Both worsen sx of menopause - so not popular with menopausal women

28
Q

symptoms of hypercalcaemia

A

Polyuria/polydipsia
Constipation
Neuro - confusion/seizures/coma
Unlikely unless ca >3
Overlap with sx of primary hyperPTH

29
Q

if high ca and PTH is detectable - what does that suggest

A

overactive thyroid glands

30
Q

what is the approach to a high Ca level

A

High ca - check again, make sure not a lab error
Then check what the PTH is:

If suppressed - then appropriate and likely diagnosis is malignancy - cancer invades bone = release ca (metastatic) - some patients with cancer present with high ca. Rare: sarcoid, vit d excess, thyrotoxicosis, milk alkali syndrome

If pth normal - inappropriate making PTH = primary hyperPTH, rare is Familial hypocalciuric hypercalcaemia

31
Q

summarise primary hyperparathyroidism

A

Commonest cause of high ca
Parathyroid adenoma/hyperplasia/cancer
Hyperplasia associated with MEN1 - more common in women - high ca PTH, low phosphate, high urine ca

Bones - get Colles fractures
STONES
MOANS - constipation/pancreatitis
GROANS - psychiatric confusion

32
Q

biochem of primary hyperparathyroidism

A

high Ca,
high or inappropriately normal PTH,
low serum phosphate
high urine ca (due to high serum Ca)

33
Q

what does the calcium sensing receptor do

A

parathyroids - regulate PTH release
renal - influence Ca resorption (PTH independent)

34
Q

summarise Familial hypocalciuric (/benign) hypercalcaemia (FBH or FHH)

A

no cells see ca -> PTH normal
born with mutation - measure high ca but body cant see it.
Gene means don’t urinate ca -> so don’t have stones.
Measure high ca in blood but not causing any harm - so don’t treat.
There is a higher set point for PTH to be released.

35
Q

what are the types of hypercalcaemia of malignancy

A

Hormonal hypercalcaemia of malignanncy - eg small cell lung ca - PTHrP - ca increases because bone looses it

Locally ca invades the bone - local bone osteolysis

Haematological malignancy eg myeloma - cytokines

36
Q

non-PTH driven causes of hypercalcaemia

A

Sarcoid - non-renal 1a OH - give steroids
Thyrotoxicasis - thyroxine - bone resorption
Hypoadrenalism - renal ca transport
Thiazide diuretics - make you lose less ca
Excess vit D eg sunbeds

37
Q

Rx for hypercalcaemia

A

Acute mx
Loads of fluids!! - SALINE as much as you can safely give 4L/day if no heart failure. Keep going if Ca still high

Bisphosphonates if cause is cancer - good at reducing bone pain - causes indestructable bone and cancer cant invade it as well. Don’t give it to people without cancer too early - because when stop become very hypocalcaemic and then very hard to manage because bone is not destructale

Treat the underlying cause

38
Q

clinical signs of hypocalcaemia

A

Neuromusclar excitability
Chvostek’s sign - face twitch
Blood pressure cuff - trousseau’s sign - carpal spasm
Hyperreflexia
Laryngeal spasm - stridor
Convulsions
Prolonged QT interval on ECG

39
Q

rx for hypocalcaemia

A

Ca and vit D - usually activated unless cause is just simple Vit D def

40
Q

IX and causes for hypoca

A

Is it real - repeat test
What is PTH

NON PTH DRIVEN - PTH will be raised = secondary hyperPTH
Vit D deficiency
Chornic kidney disease - 1a OH
PTH resistance - pseudohypoPTH

DUE TO LOW PTH
Surgical inc post thyroidectomy
Autoimmune hypoPTH
Congenital absence of parathyroids - DiGeorge syndrome
Mg deficiency - PTH regulation

41
Q

pathophysiology of tertiary hyperparathyroidism

A

Renal failure = low ca = high PTH to compensate = low bones = take ca. Transplant - new kidneys - parathyroid glands keep producing PTH - because tumourous = tertiary hyperparathyroidism

42
Q

what is paget’s disease of the bone

A

Focal disorder of bone remodelling
Focal pain
Warmth
Deformity
Fracture
SC compressuon
Malignancy
Cardiac faulure - Risk of heart failure - bone shunts blood through it

43
Q

biochemistry of paget’s disease

A

evated Alkaline phosphtase and everything else is normal

44
Q

ix for paget’s

A

nuclear med scan or XR

45
Q

what are the other metabolic bone disorders

A

Primary high PTH
- Loss of cortical bone = fracture
- Osteitis fibrosia (long term untreated primary high PTH)
- Then go onto get:

Renal osteodystropghy
- Due to secondary high PTH and retention of albumin from dialysis fluid
- Have no 1 a hydroxylase

PATHOLOGY (94 decks)

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