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Phase 3b > MSK > Flashcards

MSK Flashcards

1
Q

List red flags for MSK disease

A

Bone pain: Pain all the time - at rest, activity and at night - cancer, infection, fracture
Inflammatory pain
Osteroarthritis
Neuralgic pain - nerve root compression - pain and paraesthesia in dermatomal distribution
Referred - unaffected by local movement

Hx of cancer
Weight loss
Fever
Recent serious illness/ infection (bone infection, eg discitis)
Bladder/ bowel dysfunction 
Saddle paraesthesia 
Any new neuro symptoms- foot drop etc
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2
Q

explain how you would distinguish between inflammatory vs degenerative disease

A 
Inflammatory: 
Pain in joint better with use/ moving
Stiff - new 30 mins or longer in AM 
Swelling (often - this is fluid in joint or joint thickening)
Hot and red joint 
Young patient
Family hx of autoimmune disease 
Distribution - eg RA hands and feet 
Responds to NSAIDs

Degenerative:
Osteoarthritis - stiffness less than 30 mins in morning
Swelling - boney
Distribution - single joint, base of thumb - common for osteoarthritis

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3
Q

Commonly used DMARDs*

Why? When? What to look out for?

A

Methotrexate:
Interactions - trimethoprim, septrin
Complications - pneumonitis (ARDS) - baseline chest xr
Monitoring - FBC (can get pancytopaenia), LFT (hepatotoxic), U&E (renally excreted, so need to monitor kidney function, only nephrotoxic at egrf <20). Every 3 months.
Unusual circumstances, eg pregnancy - teratogenic - used for medical abortions, need counselling not to get pregnant - dont do standard pregnancy test

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4
Q

give some examples of systemic complications of rheumatoid arthritis

A

Fibrosis - interstitial lung disease - can be hidden bc patient isnt as mobile so dont notice change in lung function
Cardiomegaly - pericardial effusion
Pleural effusion - protein rich exudative effusion
Pitting odema - nephrotic syndrome
Vasculitis - digital vascuilitis

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5
Q

give some examples of systemic complications of rheumatoid arthritis

A

Fibrosis - interstitial lung disease - can be hidden bc patient isnt as mobile so dont notice change in lung function
Cardiomegaly - pericardial effusion
Pleural effusion - protein rich exudative effusion
Pitting odema - nephrotic syndrome
Vasculitis - digital vascuilitis (more common in smokers - RF positive arthritis)
abdominal pain - at risk of gastric ulcers bc of immunosuppresant drugs - can present more sub-acutely than normal ulcers

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6
Q

What is the most common sign of methotrexate toxicity in blood results

A

Pancytopaenia

Albumin ? also important

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7
Q

How frequently are bloods monitored for methtrexate

A

Every 3 months

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8
Q

What is the biggest risk for patient pregnant on methotrexate

A

Miscarriage
Must stop methotrexate for 3 months before pregnancy
Cant use in breastmilk either

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9
Q

What is used instead in pregnancy

A

sulfasalazine

hydroxychloroquine

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10
Q

Interactions for methotrexate

A

Trimethoprim
Septrin
NEVER EVENTS - BONE MARROW FAILURE

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11
Q

What should you NEVER prescribe with methotrexate

A

Trimethoprim

Septrin

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12
Q

What must you prescribe with methotrexate

A

Folate

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13
Q

List some anti TNF drugs used for RA

A

Infliximab, adalimumab

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14
Q

If an immune suppressed placement comes into hospital ill what should you do

A

Take them off immunosupressant

Stop drug for duration of antibiotics and 2 weeks afterwards

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15
Q

how should a patient acutely unwell on steroids be managed

A

sick day rules - double the dose

if cant tolerate orally - need IV

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16
Q

list some common drugs to consider for low mg

A

PPIs
Frurosemide
Chemotherapy

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17
Q

What is the level for severe hypo mg

A

<1.9

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18
Q

how long does it take to normalise mg2+ with oral replacement

A

6-8 weeks

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19
Q

when should you check mg2+ after stopping replacement and why

A

1 week as can get rebound hypo mg

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20
Q

what should you always check on a patient with hypo mg2+

A

ecg

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21
Q

what axis/ gland is involved in calcium homeostasis

A

Parathyroid

Low plasma calcium = raised PTH

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22
Q

What is the action of PTH

A

RAISES PLASMA CALCIUM
promotes osteoclasts = release of calcium and phosphate from bones
promotes resorption of calcium from renal tubules
promotes excretion of phosphate from renal tubules (low phosphate)
promotes vit d synthesis and excretion from kidneys to gut for increased calcium absorption

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23
Q

in a patient with raised calcium what PAIRED test must you do, and why

A

calcium and PHT
PHT very reactive, if dont do paired with calcium the result is meaningless, can only interpret if know what calcium was at time of pth

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24
Q

what are the symptoms of hypercalcaemia

A

grones, moans, bones, stones

polyuria (osmotic diuresis?), polydipsia, dehydration

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25
Q

what would be your assessment of a patient with hypercalcaemia

A

ECG, fluid status (dehydrated?)
Rehydrate - 0.9% saline 4-6 litres/24hrs
Consider IV bisphosphonate - discuss this with senior - pamidronate 30-90mg
Consider secondary treatments - steroids, calcimimetics, denosumab

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26
Q

what level of adjusted raised calcium is severe

A

> 3.4

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27
Q

what level of adjusted low calcium is severe

A

<1.9

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28
Q

at what (raised) plasma calcium level would someone become symptomatic

A

> 3

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29
Q

describe what raises in calcium are linked to symptoms

A
  1. 6-3.0 - asymptomatic
  2. 0-3.4 - may be tolerated if chronic, otherwise symptoms
  3. 4 - severe
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30
Q

what are the serious (life threatening) complications of hypercalcaemia

A

short QT (high calcium means when ca channels open, intracellular ca concentration is reached sonner and channels close = shorter plateau stage of depolarisation)
arrhythmia
HTN
Death

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31
Q

what are the ecg changes for hyper and hypo calcaemia

A

Hyper - short QT

Hypo - long QT

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32
Q

what are the symptoms of hypocalcaemia

A 
muscle excitability (as depolarisation isnt stable) - twitching
nerves (numbness/ paraesthesiae)
Cognitive dysfunction
Seizures
Stridor (laryngeal weakness)
Long QTc/ arrhythmias/ death
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33
Q

symptoms of hypercalcaemia

A

Cognitive dysfunction (moans)
Nausea/ vomiting/ constipation (groanes - abdo pain)
Abdominal pain
Nephrolithiasis/-calcinosis (stones)
Polyuria
Short QTc/ arrhythmias/ hypertension/death
Asymptomatic

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34
Q

what are the key blood tests do you need to request for hypercalcaemia

A

PTH - high/ normal = primary hyperparathyroid
normal/ low = malignancy (or other rarer causes)
Phosphate - can tell you if parathyroid as will drop
Albumin - can tell you about dehydration or malignancy
raised - dehydration
low - more likely to be malignancy

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35
Q

what are the most common causes for hypercalcaemia

A

Primary hyperparathyroid

Malignancy

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36
Q

What additional investigations could you do for hypercalcaemia after initial bloods

A

24 hour urine calcium
bone density
x-rays ? malignancy work up
electrophoresis

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37
Q

what is the most common cause of hypercalcaemia with a raised PTH

A

Primary hyperparathyroid (90%) of time

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38
Q

what is the most common cause of hypercalcaemia with a low PTH

A

Malignancy (90%) of the time

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39
Q

what are the key blood tests to request for hypocalcaemia

A

Mg - low mg can cause low PTH
Vit D - starts affecting calcium when vit d is <0.5 - usually causes a mild calcium deficiency
PTH

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40
Q

what are the causes of hypo mg

A 
gut losses 
low intake (alcoholics)
malabsorption
renal failure
drugs 
oral mg rehydration
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41
Q

how long does it take to correct low mg with sachets

A

6-8 weeks - must test mg 1 week after as can get rebound low mg

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42
Q

what are the action limits for low vit d

A

< 25 nmol/L – high dose supplementation
25-50 nmol/L – if bone health an issue standard dose supplementation
50-125 nmol/L – no action required

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43
Q

what is the management of severe hypocalcaemia

A

ECG - admit to hospital
IV calcium gluconate 10mls 10%
Arrythmias or digoxin- need continuous monitoring
Different guidance for renal failure - alfacalcidol

44
Q

common causes for hypocalcaemia

A 
poor intake (mild)
vit D deficiency (mild) 
CKD 
Low mg 
Malabsorption 
Diabetes 
drugs - ppi, furosemide, chemo
45
Q

what is the management of hypo mg

A 
Severe = Mg <0.4 mmol/L
IV Mg
Symptoms of hypomagnesaemia
Significant hypokalaemia or hypocalcaemia
Digoxin therapy
46
Q

what are the symptoms of low mg

A

same as low calcium

muscle twitches/ cramps

47
Q

what should you consider when giving oral mg relpacement

A

that it can cause rebound hypo mg

need to do mg repeat in 1 week

48
Q

what is the normal mg range

A

1.7-2.2

49
Q

what is the main thing you need to exclude with hypercalcaemia

A

malignancy

50
Q

what is the function of rank ligand

A

stimulates bone resorption via activating clasts

51
Q

what is the function of osteoprogenerator (OPG)

A

inhibits rank ligand - therefor inhibits bone resorption

52
Q

what makes up the bone matrix

A

Organic - mainly collagen scaffold (structural support)

Inorganic - hydroxyapatite - calcium and phosphate (mineral that provides strength)

53
Q

what are typical osteoperotic fractures

A

(colles) wrist, femur, vertebral

54
Q

how common are osteroperotic fractures in men and women over 50

A

1/2 of women

1/5 of men

55
Q

by how much does osteoperotic medication reduce this risk

A

by half

56
Q

what is the morbidity associated with osteoperosis fractures

A

20% die within first year after fracture

57
Q

what are common causes of osteoperotic fractures

A

can be fall

vertebral fracture - sitting down too quickly, changing the bed

58
Q

explain the bone remodelling cycle, how does this link to osteoperosis

A

injury/ physical activity (any changes to pressure on bones) will stimulate bone remodelling
bone remodelling is clast activation - resorption - and the blasts - deposition. So you have new bone.
When bone turnover is going too fast - eg after menopause - greatly increases fracture risk
Medications aim to slow down clast activity and restore balance between clasts and blasts

59
Q

how do osteoperotic medications work

A

Inhibit osteo clasts to rebalance normal bone remodelling

60
Q

who is at risk of osteopersosis

A 
Post menopausal 
Inflammatory disease (including IBD) 
Endocrine - early menopause conditions, hyperthyroid, cushings syndrome 
Immobility- problems with bone loading 
Malabsorption - coaeliac
Low BMI 
Family history - has your parent fractured a hip 
Alcohol excess 
Vitamin D deficiency
61
Q

what medications can cause osteoperosis

A

Steroids - downregulate (inhibit) whole calcium homeostasis axis
Any meds that lower oestrogen
eg GnRH analogues
Depo
Aromatase inhibitors (used in breast cancer)

62
Q

how is fracture risk assessed

A

QRisk or FRAX

Bone densitometry - DEXA, vertebral fracture assessment

63
Q

what is a T-score from DEXA scan

A

DS score of bone density for gender matched young adult - so essentially looking at how much bone have you lost since you were an adult with peak bone mineral density
-1 - within normal (normal bone loss)
-2.5 - osteoperosis
in between osteopenia

64
Q

what is vertebral fracture assessment

A

use dexa - low dose xray to get image of spine
Look for fractures
vertebral fractures indicate very high risk for future fractures
Only around 30% of vertebral fractures are diagnosed at the time - so many people could have these and be at high risk of future fractures and not know

65
Q

what is first line investigation for osteoperosis

A

DEXA scan

Vertebral fracture assessment

66
Q

What are second line investigations of osteoperosis - why are they done

A 
Bloods - to look at secondary causes that need treatment. Think: Endocrine, inflammatory, malabsorption, reproductive, malignancy
Calcium, phosphate, ALP (tells you about bone turn over)
PTH - primary hyperparathyroid 
TSH - hyperthyroid 
vit D 
ESR and FBC
Coeliac antibodies 
Sex hormnes
Serum and urine electrophoresis
67
Q

what is the management of osteoperosis

A

1.Treat secondary causes
2.Lifestyle causes - alcohol, exercise, adequate calcium and vit D, smoking
3.medicines - decided by metabolic done disease team
first line - BISPHOSPHONATES- alendronic acid - reduce fractures by 50%. Can have oral (PO, weekly) or IV - 3 monthly, or yearly
2nd lines - HRT, denosumab

68
Q

what is recommended calcium intake and vit D

A

800 mg of calcium a day (2-3 portions of diary a day)

69
Q

what are the actions of anti-osteoperotic medications

A
  1. Anti resorbative (decrease osteoclast activity)
    Alendronic acid, HRT, denosumab
  2. Anabolic (drive osteoblast activity)
    Teriparatide
70
Q

side effects of bisphosphonates

A

oesophagitis - need to give v specific dosing
IV can cause flu like symptoms
AF - not that common - usually not a problem in stable well controlled AF
Osteonecrosis of the jaw - rare but serious - usually occurs when had dental procedure and bone has taken a while to remodel/ heal because of bisphosphonate - usually been on meds long time with this
Atypical femoral fractures - to do with reducing bone resorption and makes bone stiff so fractures in unusual way - if someone on bisphosphonates been on for long time have hip pain - get xray as could be atypical fracture

71
Q

when is pneumonitis most likely to start with methotrextae

A

first 6 months

72
Q

if methotrexate does cause pulmonary fibrosis what would be this clinical picture

A

chronic clinical picture - not acute

73
Q

can you be on methotrexate and biologic

A

yes, but only try to use 1 DMARD with biologic not mutiple

74
Q

what is DAS-28, and what is it used for

A

activity score to grade patients with inflammatory disease

75
Q

what bloods should you do first line for gca

A

crp and esr

bc esr can have false negative so want crp as well as less prone to false positives

76
Q

what should you give stat from gca

A

pred 60 mg

77
Q

red flags for septic discitis

A

Point pain

diffuse pain more likely to be myeloma

78
Q

in a patient with AKI and on methotrexate - what should you do

A

Stop methotrexate

Stop ACE and diuretics

79
Q

when would you re-start methotrexate in someone who had it stopped for AKI

A

depends on renal function - may need to dose adjust depending on kidney function
(if patient been on abx and normal kidney function - can wait 2 weeks)

80
Q

how long should you wait after abx to re start dmards

A

2 weeks

81
Q

when could you use trimethoprim in a patient who has previously been on a dmard

A

at least 6-8 weeks - minimum

82
Q

differences in PMR and RA

A

PMR - older patients >50 years
sero negative
PMR - acute ish presentation (weeks)

83
Q

what are the instructions for taking a bisphosphonate and why

A

First thing in the morning
Empty stomach (bc poor absorption - 5%)
Big glass of water (prevent sticking in oesophagus)
Dont eat/ drink for 3 mins (bc of poor absorption)
Dont lie down (prevent reflux/ oesophagitis)

84
Q

what should you always check when you see a patient who is taking bisphosphonates

A

that they are taking correctly in the morning

85
Q

how does denosumab work

A

monoclonal ab to RANKL

Blocks the action of RANKL activating osteoclasts

86
Q

what are contraindications to HRT for osteoperosis

A

PMHx breast cancer
CVD risk factors
VTE risk factors
if over 60 - hrt less beneficial

87
Q

what is teriparatide

A

PTH analogue

88
Q

what should you do a junior dr to prevent osteoperosis

A

Think about and know Risk factors for osteoperosis
If see vertebral fracture on a report and not been followed up - refer for DEXA scan
If DEXA scan actions not been followed up - do this
Make sure they are taking their bisphosphonates correctly

89
Q

what is pagets disease and what are symptoms

A

Disease of clast hyperactivity - increase in bone remodelling but disorganised - leads to deformity and pain
Triad of symptoms - pain, fracture deformity

90
Q

what investigations should you do for pagets

A
  1. XRay
  2. biochemistry
    ALP - if active disease will be raised (ALP raised when lots of bone remodelling happening)
    Ca/ phophate - usually normal. Ca not high because local disease, not systemic metabolic disease
  3. can do isotope scan with IV bisphosphonate to see where disease is
91
Q

what is the management of pagets

A

Depends if they are symptomatic
Only treat with bisphosphonates if symptomatic
Be aware that pagets disease radiologically is common, but symptomatically uncommon

92
Q

what age group usually presents with pagets

A

> 40/50s

93
Q

what drug group can cause hypercalcaemia

A

thiazides

94
Q

what is a t score in DEXA

A

SD

95
Q

what does inflammatory disease put you at risk of osteoperosis

A

because inflammation drives osteoclast activity

96
Q

what age should patient be to be put on bisphosphonate regardless of bone mineral density

A

over 65 and on steroids

97
Q

does a dexa of -2.5 always mean osteoperosis diagnosis

A

No - low bone density also seen in osteomalacia

98
Q

what is the differential diagnosis for a dexa result of -2.5

A

Osteomalacia

99
Q

what are the blood results for osteomalacia

A

Low calcium
High PTH
High ALP (bc of PTH driven bone turnover)
Low urine calcium

100
Q

what does a raised ALP tell you

A

high bone turnover

101
Q

other non dairy sources of calcium

A

calcium supplement

102
Q

when are z scores used in DEXA

A

under 25
z score looks at BMD for matched age group
t score looks at BMD in comparison to gender matched young adult

103
Q

osteomalacia management

A

High dose vit D (cholecalciferol) plus calcium
Have to give both
Long term Adcal-D3

104
Q

what is active vit d, when is this given

what is normal vit D, when is this given

A

calcitriol - CKD

cholecalciferol - normal vit D (pre kidney activation) - give this to anyone who doesnt have kidney disease

105
Q

what medications should you consider stopping in severe hypercalcaemia

A

any calcium supplements and diuretics

discuss with snrs about when to restart

Phase 3b (13 decks)

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