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Applied Pharmacology > Musculoskeletal System > Flashcards

Musculoskeletal System Flashcards

1
Q

What are the main indications of NSAIDs

A
  • mild-moderate pain
  • pain related to inflammation
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2
Q

What is the MOA of NSAIDs?

A

Inhibit COX (cyclo-oxygenase) to inhibit prostaglandin synthesis.

COX exists as 2 main isoforms:
- COX-1 = constitutive form: stimulates prostaglandin synthesis essential to preserve integrity of gastric mucosa, dilates afferent glomerular arterioles which maintains renal perfusion, and inhibits thrombus formation at the vascular endothelium
- COX-2 = inducible form, expressed in response to inflammatory stimuli. It stimulates production of prostaglandins that cause inflammation and pain

  • Therapeutic benefits principally mediated by COX-2 inhibition
  • Adverse effects principally mediated by COX-1 inhibition
  • Although there is some overlap between the 2

Selective COX-2 inhibitors (e.g. etoricoxib) were developed to reduce the adverse GI effects

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3
Q

What are the main side effects of NSAIDs?

A
  • GI toxicity
  • Renal impairment
  • increased risk of cardiovascular events.
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4
Q

What are the key contraindications of NSAIDs?

A
  • Severe renal impairment
  • HF
  • Liver failure
  • Known NSAID hypersensitivity

pts at high risk of adverse effects e.g:
- PUD
- GI bleeding
- CVD
- Renal impairment

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5
Q

What are the key interactions of NSAIDs?

A

Peptic ulceration
- Low-dose aspirin
- Corticosteroids e.g. prednisolone

GI bleeding
- Antioagulants e.g. warfarin, DOACs
- SSRIs
- Venlafaxine

Renal impairment
- ACEi
- Diuretics

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6
Q

Give some examples of bisphosphonates?

A
  • Alendronic acid
  • Pamidronate and zoledronic
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7
Q

What are the main indications for Bisphosphonates?

A
  • those at risk of osteoporotic fragility fractures.
  • severe hypercalcaemia
  • Paget’s disease
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8
Q

What is the MOA of Bisphosphonates?

A

Inhibit the action of osteoclasts (which are responsible for bone resorption) and promotes apoptosis of osteoclasts which:
- Reduces bone turnover
- Reduction in bone loss
- Improvement in bone mass

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9
Q

What are the main side effects of Bisphosphonates?

A

common:
- oesophagitis
- hypophosphatemia

Rare:
- osteonecrosis of the jaw
- atypical femoral fracture

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10
Q

Whom are Bisphosphonates contraindicated in?

A
  • severe renal impairment
  • hypocalcaemia
  • GI disorders don’t give oral
  • caution- smokers, dental disease
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11
Q

What are the key interactions of Bisphosphonates?

A
  • calcium salts (including milk)
  • antacids
  • iron salts
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12
Q

What are the main indications of Allopurinol

A
  • to prevent recurrent gout attacks
  • to prevent uric acid and calcium oxalate renal stones
  • to prevent hyperuricaemia and tumor lysis syndrome associated with chemotherapy
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13
Q

What are the key contraindications of Allopurinol?

A
  • acute attacks of gout
  • Recurrent skin rash or signs of more severe hypersensitivity to allopurinol

Reduce doses in pts with:
- Renal impairment
- Hepatic impairment

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14
Q

What are the common side effects of Allopurinol?

A
  • starting it can trigger/ worsen a gout attack

Common Side effects:
- skin rash (stevens-johnson syndrome or toxic epidermal necrolysis)

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15
Q

What are the rare side effects of Allopurinol?

A

Rare, life-threatening: allopurinol hypersensitivity syndrome
- Fever
- Eosinophilia
- Lymphadenopathy
- Involvement of other organs e.g. skin and liver

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16
Q

What are the key interactions of allopurinol?

A
  • Azathioprine increases the risk of toxicity of allopurinol

Risk of hypersensitivity reaction increased by co-prescription with:
- ACE inhibitors
- Thiazides
- Amoxicillin (increases the risk of skin rash)

17
Q

What are the main indications for Colchicine?

A
  • acute gout
  • short-term prophylaxis of gout flares
  • familial mediterranean fever
18
Q

What are the main side effects of colchicine?

A
  • abdominal pain
  • Diarrhoea
  • Nausea
  • vommiting
  • Agranulocytosis
  • Thrombocytopenia
19
Q

What are the key contraindications of Colchicine?

A
  • hepatic impairment
  • pregnancy
  • breastfeeding
  • eGFR <10
20
Q

What are the key interactions og Colchicine?

A

CHECK 100 DRUG BOOK

21
Q

What are the main indications of Paracetamol?

A
  • acute and chronic pain
  • Antipyretic that can reduce fever and its associated symptoms (e.g. shivering)
22
Q

What is the MOA of paracetamol?

A

A weak inhibitor of COX which is involved in prostaglandin metabolism.

COX inhibition increases pain threshold and reduces prostaglandin E2 concentrations in the thermoregulatory region of the hypothalamus, controlling fever.

Has specificity for COX-2 however is a weak anti-inflammatory
- Actions limited by the presence of peroxides

23
Q

What are the main side effects of paracetamol?

A

In overdose may cause liver failure
- Hepatotoxicity can be prevented by treatment with the glutathione precursor acetylcysteine

24
Q

What are the key contraindications of Paracetamol?

A
  • liver toxicity
  • chronic excessive alcohol use
  • low body weight
25
Q

What are the key interactions of Paracetamol?

A

After paracetamol overdose, CYP inducers e.g. phenytoin and carbamazepine:
- Increase rate of NAPQI production 5
- Increase risk of liver toxicity

26
Q

Give an example of a weak/ moderate opioid?

A
  • codiene
27
Q

What are the main indications of weak/ moderate opioids?

A

Mild-to-moderate pain, including post-operative pain
- As 2nd line agent when simple agents e.g. paracetamol are insufficient

2nd ‘rung’ of the WHO pain ladder

28
Q

What is the MOA of very weak opioids such as Codeine/ Dihydrocodeine?

A
  • Metabolised in liver which produce relatively small amounts of morphine from Opioid – these metabolites, which are stronger agonists of opioid mu receptor probably account for most of the analgesic effect.
29
Q

What is the MOA of moderate-strength opioids such as Tramadol?

A

Like codeine, tramadol and its active metabolite are mu-receptor agonists
- Unlike other opioids, it also affects serotonergic and adrenergic pathways – thought to act as a SNRI (serotonin and noradrenaline reuptake inhibitor) which contributes to its analgesic effect

30
Q

What are the common side effects of weak/ moderate opioids?

A
  • nausea
  • constipation
  • dizziness
  • drowsiness
31
Q

What can a opioid overdose present with?

A
  • Neurological depression
  • Respiratory depression
32
Q

Whom is weak/ moderate opioids contraindicated in?

A

Used with caution in significant respiratory disease

Reduce doses in:
- Hepatic failure
- Renal impairment
- Elderly

Tramadol lowers seizure threshold
- Avoid in pts with epilepsy
- Contraindicated in pts with uncontrolled epilepsy

Avoid in biliary colic
- May cause spasm of sphincter of Oddi

33
Q

What other drugs does weak/moderate opioids interact with?

A

Should ideally not be used with other sedating drugs e.g.:
- Antipsychotics
- Benzodiazepines
- Tricyclic antidepressants

Tramadol
- Should not be used with other drugs that lower the seizure threshold e.g. antipsychotics

34
Q

Give an example of a strong opioid?

A

Morphine
Oxycodone

35
Q

What are the main indications of strong opioids?

A

Raid relief of acute severe pain, including:
- Post-operative pain
- Pain associated with acute MI

Relief of chronic pain, when paracetamol, NSAIDs and weak/moderate opioids are insufficient (‘rung 3’ of the WHO pain ladder)

End-of-life care: relief of breathlessness

Relief of breathlessness and anxiety in acute pulmonary oedema, alongside:
- O2
- Furosemide
- Nitrates

36
Q

What are the main side effects of strong opioids?

A

Reduce resp drive  respiratory depression

May cause:
- Euphoria
- Detachment

In higher doses, may cause neurological depression

nausea and vomiting

Pupillary constriction
- Due to stimulation of Edinger-Westphal nucleus

Constipation

In the skin, may cause histamine release
- Itching
- Urticaria
- Vasodilation
- Sweating

Continued use can lead to:
- Tolerance
- Dependance

37
Q

What is the MOA of strong opioids?

A

Therapeutic action:
Binds opioid mu receptors in the CNS to activate GPCR leading to several effects that, overall, reduce:
- Neuronal excitability
- Pain transmission

In medulla, they blunt response to hypoxia and hypercapnia which reduces respiratory drive and breathlessness

By relieving pain, breathlessness and associated anxiety, they reduce SNS activity
- Thus in MI and acute pulmonary oedema, they may reduce cardiac work and O2 demand, as well as relieving symptoms

38
Q
A

Applied Pharmacology (7 decks)

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