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BASIC - MSK Flashcards

1
Q

Names of NSAIDs?

A

Ibuprofen, diclofenac, etoricoxib

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2
Q

Indications of NSAIDs?

A
  • PRN for mild-to-moderate pain

- Regular treatment of pain related inflammation

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3
Q

Mechanism of NSAIDs?

A
  • Inhibit synthesis of prostaglandins from arachidonic acid by inhibiting cyclooxygenase (COX
  • COX-1 stimulates prostaglandin synthesis essential to preserve gastric mucosa, maintain renal perfusion (by dilating afferent glomerular arterioles) and inhibit thrombus formation at the vascular endothelium
  • COX-2 expressed in response to inflammatory stimuli stimulates production of prostaglandins that cause inflammation and pain
  • Therapeutic benefits of NSAIDs are principally COX-2 inhibition and adverse effects by COX-1 inhibition
  • Selective COX-2 inhibitors (e.g. etoricoxib) developed to reduce the adverse effects
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4
Q

Side effects of NSAIDs?

A
  • GI ulcers/gastritis
  • Renal impairment
  • Increased risk of MI/CVA
  • Fluid retention
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5
Q

Interactions of NSAIDs?

A 
-	GI Ulceration
o	Aspirin, corticosteroid
-	GI bleeding
o	Anticoagulants, SSRIs, venlafaxine
-	Renal Impairments
o	ACEi, diuretics
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6
Q

Contraindications of NSAIDs?

A

o Severe renal impairment
o Heart Failure
o Liver failure

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7
Q

Cautions of NSAIDs?

A

o Peptic ulcer disease
o GI bleeds
o CVD

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8
Q

Prescription of NSAIDs?

A
  • Available as tablets, suspensions, gels, suppositories, injectable
  • Acute pain treatment should be stopped when resolved
  • Taken with food to minimise GI upset
  • Can use gastroprotection for patients at increased risk
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9
Q

Names of oral glucocorticoids?

A

Prednisolone, hydrocortisone, dexamethasone

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10
Q

Indications of oral glucocorticoids?

A

Allergic or inflammatory disorders (anaphylaxis, eczema, asthma, COPD)
Severe croup
Autoimmune disease (IBD, ITP, inflammatory arthritis)
Cancer treatment
Myasthenia Gravis, Polymyalgia rheumatica, GCA, Lupus
Proctitis
Joint injections
Adrenal insufficiency/Hypopituitarism

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11
Q

Mechanism of oral glucocorticoids?

A
  • Bind to cytosolic glucocorticoid receptors which upregulate anti-inflammatory genes and downregulate pro-inflammatory genes (cytokines, TNFa)
  • Suppression of circulating monocytes and eosinophils
  • Metabolic effects
    o Increased gluconeogenesis
    o Increased catabolism
  • Mineralocorticoid effects
    o Stimulate Na and water retention and K excretion
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12
Q

Side effects of oral glucocorticoids?

A
  • Immunosuppression
  • Diabetes mellitus
  • Insomnia, psychosis and suicidal ideas
  • Osteoporosis
  • Metabolic
    o Proximal muscle weakness, skin thinning with easy bruising and gastritis
  • Mineralocorticoid
    o Hypertension, hypokalaemia and oedema
  • Prolonged
    o Adrenal atrophy leading to Addisonian crisis if withdrawn suddenly
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13
Q

Cautions of oral glucocorticoids?

A
  • Infection
  • Children (suppress growth)
  • Hepatic or Renal impairment
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14
Q

Interactions of oral glucocorticoids?

A

Risk of peptic ulceration – NSAIDs
Hypokalaemia – B2-agonists, theophylline, loop and thiazide diuretics
Affected by CYP450 enzymes

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15
Q

Prescription of oral glucocorticoids?

A

o Can be given orally, IM, IV
o OD, taken in the morning to mimic natural circadian rhythm
o Consider use of bisphosphonates and PPIs if long-term and risk

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16
Q

Monitoring of oral glucocorticoids?

A

o For children – height and weight monitored annually – refer to paediatrician if slow
o Prolonged treatment – HbA1c or DEXA scan

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17
Q

Cessation of oral glucocorticoids?

A

o Abrupt withdrawal can lead to adrenal insufficiency

o Gradual withdrawal used if treatment >3 weeks, received >40mg, repeated evening doses

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18
Q

Communication of oral glucocorticoids?

A

o Should feel better in 1-2 days
o Do not stop immediately
o Steroid card to carry round at all times

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19
Q

Indications of methotrexate?

A
  • Rheumatoid arthritis
  • Crohn’s disease
  • Chemotherapy – e.g. leukaemia, lymphoma and some solid tumours
  • Severe psoriasis
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20
Q

Mechanism of methotrexate?

A
  • Inhibits dihydrofolate reductase, which converts dietary folic acid to tetrahydrofolate (FH4)
    o FH4 needed for DNA and protein synthesis, so lack of it prevents cellular replication
    o Actively dividing cells particularly sensitive so good for cancer
  • Anti-inflammatory and immunosuppressive effects
    o Inhibition of IL-6, IL-8 and TNF alpha
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21
Q

Side Effects of methotrexate?

A
  • Sore mouth, GI upset (diarrhoea, nausea, vomiting)
  • Neutropenia, leukopenia, thrombocytopenia (Agranulocytosis)
  • Hepatitis, pneumonitis
  • Long term use – hepatic cirrhosis, pulmonary fibrosis
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22
Q

Contraindications of methotrexate?

A
  • Active infection
  • Pregnancy – teratogenic (both men and women taking drug need effective contraception during and for 3 months after stopping treatment
  • Severe renal impairment
  • Hepatic impairment in non-malignant conditions
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23
Q

Cautions of methotrexate?

A
  • Abnormal liver function
24
Q

Interactions of methotrexate?

A
  • Methotrexate toxicity more likely with:
    o NSAIDs, penicillins
  • Risk of haematological abnormalities in trimethoprim and phenytoin
  • Risk of neutropenia increased in clozapine
25
Q

Prescription of methotrexate?

A
  • Oral dose, once weekly 7.5-20mg, adjusted according to response
  • Folic acid prescribed to be taken on the other 6 days when methotrexate isn’t taken
  • For cancer – given IV/IM/intrathecal
26
Q

Important communication to patient of methotrexate?

A
  • Report symptoms of sore throat, fever, bruising, bleeding, nausea, abdominal pain, dark urine, breathlessness
  • Need contraception
  • Give folic acid to reduce side effects
27
Q

Monitoring of methotrexate?

A
  • Before treatment – FBC, LFT, U&E and a pregnancy test
  • 1-2 weekly until established
  • 2-3 monthly thereafter
28
Q

Indications of allopurinol?

A
  • Prophylaxis of gout and uric acid/calcium oxalate renal stones
  • Prophylaxis of hyperuricaemia in cancer
29
Q

Mechanism of allopurinol?

A
  • Xanthine oxidase inhibitor

- Reduces xanthine to uric acid – lowers concentrations of uric acid

30
Q

Side effects of allopurinol?

A
  • Skin rash – mild to severe SJS or TENs
  • Drug hypersensitivity syndrome
    o Fever, eosinophilia, lymphadenopathy
  • Acute gout triggered
31
Q

Contraindications of allopurinol?

A
  • Acute gout

- Recurrent skin reaction

32
Q

Cautions of allopurinol?

A
  • Ensure adequate fluid intake (2-3 litres/day)

- Start allopurinol before cancer treatment

33
Q

Dose changes in renal/hepatic impairment of allopurinol?

A
  • Dose reduction
34
Q

Interactions of allopurinol?

A
  • Allopurinol and amoxicillin risk of rash

- Allopurinol and ACEi/thiazides – risk of hypersensitivity reactions

35
Q

Prescription of allopurinol?

A
  • Oral start at low dose and titrate according to uric acid levels to maintenance dose
  • Typical 100mg initial and then up to 200-600mg
  • Take after food
  • NSAID or colchicine prescribed for 1 month after serum uric levels normalise to avoid acute attack
36
Q

Communication of allopurinol?

A
  • Take after meals
  • Seek advice if rash develops
  • Do not stop allopurinol in acute attack
37
Q

Monitoring required of allopurinol?

A
  • Uric acid levels checked 4 weeks after start/dose change

- Aim for uric acid <300 and titrate dose

38
Q

Names of calcium salts?

A

Calcium carbonate, calcium gluconate

39
Q

Names of vitamin D analogue?

A

Colecalciferol

40
Q

Indications of calcium salts and vitamin D?

A
  • Osteoporosis
  • Chronic kidney disease
  • Severe hyperkalaemia (calcium gluconate)
  • Hypocalcaemia if symptomatic or severe (<1.9)
  • Vitamin D used in prevention and treatment of Vitamin D deficiency, including rickets (children) and osteomalacia (adults)
41
Q

Mechanism of action in calcium and vitamin D?

A
  • Calcium needed for muscles, nerves, bone and clotting
  • Homeostasis controlled by PTH and vitamin D, which increase serum Ca and calcitonin which reduces Ca level
  • Restoring positive Ca balance reduces rate of bone loss, restores Ca level in CKD
  • In hyperkalaemia, calcium gluconate raises myocardial threshold potential, reducing excitability
42
Q

Side effects of calcium salts?

A
  • Dyspepsia
  • Constipation
  • Nausea
43
Q

Interaction of oral calcium?

A
  • Oral calcium reduces absorption of:

o Iron, bisphosphonates, tetracyclines and levothyroxine

44
Q

Prescription of calcium salts & vitamin D?

A
  • Adcal D3 BDS contains calcium and vitamin D (cholecalciferol)
  • Chew then swallow tablets
  • Separate doses by 4 hours to medicines that interact
45
Q

Monitoring in calcium salts?

A
  • Check calcium levels regularly
46
Q

Names of bisphosphonates?

A

Alendronic acid, disodium pamidronate, zoledronic acid

47
Q

Indications of bisphosphonates?

A
  • Alendronic acid – patients at risk of osteoprotic fragility fractures
  • Pamidronate/Zoledronic acid – severe hypercalcaemia of malignancy, myeloma, breast cancer with bone mets
  • Paget’s Disease
48
Q

Mechanism of bisphosphonates?

A
  • Reduce bone turnover by inhibiting action of osteoclasts, cells responsible for bone resorption
  • Reduction in bone loss and improvement in bone mass
49
Q

Side effects of bisphosphonates?

A
  • Oesophagitis
  • Hypophosphatemia
  • Osteonecrosis of jaw
  • Osteonecrosis of external auditory canal
  • Atypical femoral fractures
50
Q

Contraindications of bisphosphonates?

A
  • Severe renal impairment (<35)
  • Hypocalcaemia
  • Upper GI disorders
51
Q

Cautions of bisphosphonates?

A
  • Smokers

- Dental disease

52
Q

Interactions of bisphosphonates?

A
  • Absorption reduced if taken with calcium salts (including milk), antacids and iron salts
53
Q

Prescription of bisphosphonates?

A
  • For osteoporosis – alendronic acid oral 70mg once weekly

- For severe hypercalcaemia – slow IV infusions

54
Q

Communication to patient of bisphosphonates?

A
  • Alendronic acid – swallowed whole >30 mins before breakfast or other medications with plenty of water, patient remain upright for 30 minutes afterwards to reduce oesophageal irritation
55
Q

Monitoring of bisphosphonates?

A
  • Osteoporosis – check Ca and Vit D before and during treatment, DEXA every 1-2 years
  • Hypercalcaemia – Ca levels

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