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endo > w5 - bone disorders inc OP > Flashcards

w5 - bone disorders inc OP Flashcards

1
Q

define osteoporosis

A

progressive systemic skeletal disease
low bone mass, micro-architecture deterioration
incr in bone fragility + fracture susceptibility

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2
Q

how much of the adult keleton is remodelled each year

A

10%

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3
Q

bone remodelling occurs at discrete foci called bone remodelling units. OUtline

A

osteoclasts - appear on inactive surface, begin to absorb bone

osteoblasts - replace OC, fill cavity with osteoid, mineralised to form new bone

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4
Q

in OP there is a problem with bone remodelling, what is it

A

incr in resorption over formation, leading to bone loss

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5
Q

regulating factors for peak bone mass 5

A 
genetics 
body weight
sex hormones 
diet 
exercise
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6
Q

regulating factors for bone loss 7

A 
sex hormone deficiency 
body weight 
genetics
diet 
immobility 
diseases 
drugs (glucocorticoids, aromatase inhibitors)
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7
Q

common fracture sites in OP

A

neck of femur
vertebral body
distal radius
humeral neck

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8
Q

how is bone density measured

A

DEXA scans

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9
Q

ranges of normal, osteopenia, oP, sev. OP in BMD

A

normal: BMD within 1 SD of young adult reference

Osteopenai (low bone m.): BMD: 1-2.5 SD below young a. ref.

OP: BMD >2.5 below young a. ref.

Sev. OP: BMD >2.5 below + fragility fracture

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10
Q

in OP target therapeutic inervention is for those at high risk of …

A

low impact fracture

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11
Q

SIGN guideline is based on fracture risk and not BMD, and treatment based on addressing risk factures, what are modifiable/non-modifiable risk factors

A 
modifiable 
BMD 
alcohol 
smoking 
weight
inactivity 
pharmacological factors 
non-mod 
age
gender
ethnicity 
pre. fracture 
FH
menopause <45yrs
comorbidities
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12
Q

tool used to assess risk of fracture

A

WHO fracture risk calculator

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13
Q

who to assess? when to refer to DXA

A

> 50yrs

<50 + early menopause or on glucocorticoids

if risk >10%

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14
Q

investigations for OP

A 
U+Es
LFTs
Bone biochem 
FBC
PV 
TSH 
protein electrophoresis/bence jones proteins 
coeliac antibodies 
testosterone 
250H  VitD 
PTH
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15
Q

2ndary causes of OP can be due endo, GI, resp, or others. give examples

A

endocrine

  • hypothyroid
  • hypoparathyroid
  • cushings

GI

  • coeliac
  • IBD
  • chronic liver disease
  • chronic pancreatitis

resp

  • CF
  • COPD

chronic kidney disease

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16
Q

lifestyle advice for management of OP includes high intensity strength training, avoiding excess alcohol and smoking. name 2 more

A

low impact weight bearing exercise

fall prevention

17
Q

diet for op

A 
700mg calcium (2-3portion from dairy) 
if post menopause - 1000mg calcium (3-4portions)
18
Q

non-dairy sources of caclium

A

bread and cereals
fish with bones
nuts
green veg

19
Q

drug treatments for OP

A 
calcium + Vit D supplemwents 
biphosphonates
denosumab 
teriparatide 
HRT 
SERMS 
Testosterone
20
Q

vit D deficiency at risk patients

A

low exposure to suun

house-boound

21
Q

calcium supplements should not be taken within 2 hours of oral __

A

biphosphonates

22
Q

t.f if dietary calcium is adequate, 700mg Vit D is preferred

A

true

23
Q

biphosphonates are ___ agents, examples are alendronate and risedronate. They work by preventing bone loss at all sites vulnerable to OP.

They are 1) anologues of ____, that absorb onto bone within matin the matrix
2) ingested by ___, leading to cell death

A

biphosphonates are anti-resorptive agents, examples are alendronate and risedronate. They work by preventing bone loss at all sites vulnerable to OP

They are 1) anologues of pyrophosphates, that absorb onto bone within matin the matrix
2) ingested by osteoclasts, leading to cell death

24
Q

duration of biphosphonate therapy

A

5yrs

10yrs if vertebral fracture

25
Q

zoledronic acid is given through

A

1 yearly IV infusion for 3yrs

26
Q

1 in 3 patients suffer an acute phase reaction with the first infusion of zoledronic acid, what is given

A

paracetamol

27
Q

denosumab is a monoconal antibody that targets ___. preventing activation of its receptor, inhibiting development and activity of ____, decreasing bone ___

A

denosumab is a monoconal antibody that targets RANKL. preventing activation of its receptor, inhibiting development and activity of Osteoclasts, decreasing bone resorption

28
Q

how is denosumab administered?
adverse effects of denosumab?
contraindicated in renal impairment t.f?

A

6mnthly SC injection

adverse: hypocalcaemia, eczema, cellulitis

false

29
Q

teriparatide is a recombinant ___ hormone, it stimulates bone growth (anabolic). when is it considered?

A

parathyroid

> 65yrs T

30
Q

when to treat OP with antiresorptive therapy

A

T < -2.5

if ongoing steroid requiremnt >7.5mg prednisolone for 3mnths, or vertebral fracture, consider treatment with T

31
Q

what are 3 direct iimpacts and 1 non-direct impact of glucocorticoids and bone

A

direct

  • reduces Osteoblast activity + lifespan
  • suppresses replication of OB precursors
  • reduces calcium absorption

indirect
inhibits gonadal + adrenal steroid productio n

32
Q

glucocorticoids effect on calcium metabolism

A

incr excretion and reduces absorption in gut
reduces matrix synthesis resorption
impact of pit and kidneys too

33
Q

pagets disease is abnormal ___ activity, followed by incr __ activity. leading to abnormal bone structure with reduced strength and incr fracture risk. name for single site and multiple sites

A

pagets disease is abnormal osteoclastic activity, followed by incr osteoblastic activity. leading to abnormal bone structure with reduced strength and incr fracture risk.

monostotic =single
polyostotic = multiple

34
Q

bones usually affected by pagets

A

long bones
pelvis
lumbar spine
skull

35
Q

pagets presentation

A

bone pain
deformity
deafness
compression neuropathies

36
Q

pagets is diagnosed on __, isotope bone scan used to show ___, biochem shows raised ___ ___ with otherwsie normal __ . Treated with ___ if pain not responding to analgesia

A

pagets is diagnosed on XR,
isotope bone scan used to show distribution, biochem shows raised alkaline phosphatase with otherwsie normal LFTs. Treated with biphosphonates if pain not responding to analgesia

37
Q

osteogenesis is inherited through __ __ pattern, most are secondary mutations of __ ___ __ genes (COL1A1, COL1A2)

A

autosomal dominant

type 1 collagen

38
Q

associations of osteogenesis imperfecta 2

A

dentinogenesis imperfects

blue sclerae

39
Q

more sev. form of osteogeneis imperfecta presents with __ in __. No cure, only fracture fixing/surgery for deformities/biphosphonates.

A

fractures

childhood

endo (21 decks)

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