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Drug Formulary Y3 > Endocrine & Analgesic Drugs > Flashcards

Endocrine & Analgesic Drugs Flashcards

1
Q

Name 4 types of insulin?

A
  1. Insulin aspart
  2. Insulin glargine
  3. Biphasic insulin
  4. Soluble insulin
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2
Q

What are the common indications for use of insulin? (4)

A
  1. Type 1 diabetes: for insulin replacement
  2. Type 2 diabetes: for control of blood glucose where oral hypoglycaemic treatment is inadequate or poorly tolerated
  3. Diabetic emergencies: DKA, hyperglycaemic hyperosmolar syndrome, perioperative glycaemic control.
  4. Hyperkalaemia: used in treatment, alongside glucose.
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3
Q

What is the basic mechanism of action of insulin?

A

Exogenous insulin functions similarly to endogenous insulin. It stimulates glucose uptake from the circulation into tissues, including skeletal muscle and fat, and increases use of glucose as an energy source. Insulin stimulates glycogen, lipid and protein synthesis and inhibits gluconeogenesis and ketogenesis.

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4
Q

What is the mechanism of action of insulin in treating hyperkalaemia?

A

Insulin drives K+ into cells, reducing serum K+ concentrations. However once insulin treatment is stopped, K+ leaks back out of the cells into the circulation, therefore this is a short-term measure while other treatment is commenced.

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5
Q

Which type of insulin is used in medical emergencies, e.g. DKA and hyperkalaemia?

A

When IV insulin is required, soluble insulin e.g. Actrapid is usually used.

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6
Q

Name a rapid acting form of insulin and its characteristics, e.g. duration?

A

Insulin aspart e.g. Novorapid - immediate onset, short duration

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7
Q

Name a short acting form of insulin?

A

Soluble insulin e.g. Actrapid

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8
Q

Name an intermediate acting form of insulin?

A

Isophane (NPH) insulin e.g. Humulin I

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9
Q

Name two long acting forms of insulin?

A
  1. Insulin glargine e.g. Lantus

2. Insulin detemir e.g. Levemir

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10
Q

Name a biphasic insulin and its characteristics?

A 
Novomix 30 (insulin aspart/insulin aspart protamine). 
Preparations containing a mixture of rapid- and intermediate- acting insulins.
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11
Q

What is the main adverse effect of insulin?

A

Hypoglycaemia

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12
Q

What can occur when insulin is repeated injected subcutaneously in the same site?

A

Lipohypertrophy (fat overgrowth) - can be uncomfortable and unsightly

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13
Q

What is the warning associated with insulin use in people with renal impairment?

A

The insulin clearance will be reduced, so there is an increased risk of hypoglycaemia

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14
Q

Use of which type of drugs can increase insulin requirements?

A

Systemic corticosteroids

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15
Q

Why should you avoid treating unexpected high blood glucose concentrations with subcutaneous Actrapid (short-acting insulin) ?

A

As the time to peak effect (2-3 hours) is longer than often appreciated, and trying to correct hyperglycaemia quickly is often unnecessary and can be dangerous. Understanding why the hyperglycaemia has occurred is more important, and making small alterations to the patient’s regular insulin regimen.

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16
Q

What type of drug is gliclazide?

A

A sulphonylureas

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17
Q

What is the indication for use of gliclazide?

A

Type 2 diabetes

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18
Q

What is the mechanism of action of sulphonylureas?

A

The sulfonylureas act mainly by augmenting insulin secretion and consequently are effective only when some residual pancreatic beta-cell activity is present; during long-term administration they also have an extrapancreatic action.

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19
Q

When are sulphonylureas contraindicated? (1)

A

Presence of ketoacidosis

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20
Q

When/why should sulphonylureas be used with caution?

A
  1. Can encourage weight gain (should be prescribed only if poor control and symptoms persist despite adequate attempts at dieting)
  2. In the elderly
  3. In someone has a G6PD deficiency
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21
Q

Which antibiotic has a known interaction with sulphonylureas?

A

Chloramphenicol - it is known to increase the exposure to gliclazide

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22
Q

Why should sulphonylureas be avoided during pregnancy?

A

Can cause hypoglycaemia in neonates

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23
Q

What are the side effects associated with sulphonylureas? (2)

A

Weight gain

Rarely: hypoglycaemia

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24
Q

What is the risk when using sulphonylureas in patients wit hepatic/renal impairments?

A

Hypoglycaemia

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25
Q

What is the only type of biguanide licensed for use?

A

Metformin

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26
Q

What is the indication for use of metformin?

A

Type 2 diabetes: first choice medication for control of blood glucose, used alone or in combination with other oral hypoglycaemic drugs (e.g. sulphonylureas) or insulin

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27
Q

What is the mechanism of action of metformin?

A

Metformin (a biguanide) lowers blood glucose by increasing the response (sensitivity) to insulin. It suppresses hepatic glucose production (glycogenolysis and gluconeogenesis), increases glucose uptake and utilisation by skeletal muscle and suppresses intestinal glucose absorption. It achieves this by diverse intracellular mechanisms, which are incompletely understood.

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28
Q

Why does metformin not cause hypoglycaemia?

A

It does not stimulate pancreatic insulin secretion and therefore does not cause hypoglycaemia.

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29
Q

How is metformin helpful in preventing worsening of insulin resistance and progression of type 2 diabetes?

A

It reduces weight gain and can induce weight loss, which helps to slow deterioration of diabetes.

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30
Q

What common adverse effects are caused by metformin? (3)

A
  1. GI upset - including nausea, vomiting and diarrhoea
  2. Taste disturbance
  3. Anorexia
    (these adverse effects may contribute to weight loss)
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31
Q

What rare adverse effect is associated with metformin use?

A

Lactic acidosis - this doesn’t occur in stable patients, but can be precipitated by intercurrent illness, including renal impairment, illness that results in increased lactate production (e.g. sepsis, hypoxia, cardiac failure) or reduced lactate metabolism (e.g. liver failure).

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32
Q

What are the contraindications for metformin use? (3)

A
  1. Severe renal impairment
  2. AKI
  3. Severe tissue hypoxia
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33
Q

What are the warnings for using metformin, often including advise on dose reduction? (4)

A
  1. Moderate renal impairment
  2. Hepatic impairment
  3. Acute alcohol intoxication
  4. Chronic alcohol overuse
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34
Q

What are the important drug interactions associated with metformin? (3)

A
  1. IV contract media - metformin must be withheld before and for 48 hours after injection
  2. Any drugs with potential to impair renal function e.g. NSAIDs, ACE inhibitors, diuretics, should be used with caution
  3. Prednisolone, thiazide and loop diuretics all elevate blood glucose, therefore reduce the efficacy of metformin
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35
Q

Why is metformin the first-choice treatment for type 2 diabetes, as opposed to sulphonylureas or insulin?

A

Metformin does not cause weight gain

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36
Q

Name 2 thyroxine drugs?

A
  1. Levothyroxine

2. Liothyronine

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37
Q

What are the indications for use of thyroxine drugs? (3)

A
  1. Primary hypothyroidism
  2. Hypothyroidism secondary to hypopituitarism
  3. Thyroid excision secondary to hyperthyroidism
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38
Q

What is the mechanism of action of thyroxine drugs?

A

Thyroid hormones regulate metabolism and growth. Deficiency of these hormones cause hypothyroidism, with clinical features including lethargy, weight gain, constipation and slowing of mental progression. Levothyroxine (synthetic T4) is a long-term replacement of the hormones. Liothyronine (synthetic T3) has a shorter half-life and quicker onset (a few hours) and offset (24-48 hours) of action than levothyroxine.

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39
Q

When is liothyronine used?

A

For emergency treatment of severe or acute hypothyroidism.

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40
Q

What are the adverse effects associated with levothyroxine use?

A

They are related to excessive doses, so similar to that of hyperthyroidism.

  1. GI disturbances: diarrhoea, weight loss, vomiting
  2. Cardiac manifestations: palpitations, arrhythmias, angina
  3. Neurological manifestations: tremor, restlessness, insomnia
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41
Q

What are the warnings/cautions associated with taking thyroxine?

A
  1. Coronary artery disease: as thyroid hormones increase heart rate and metabolism, they can precipitate cardiac ischaemia in people with coronary artery disease therefore a low dose will be required with careful monitoring.
  2. Hypopituitarism: corticosteroid therapy must be initiated before thyroid hormone replacement to avoid precipitating Addisonian crisis
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42
Q

Which drugs need to be taken at different times to levothyroxine due to their effect in reducing absorption of levothyroxine? (2)

A
  1. Antacids

2. Calcium or iron salts

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43
Q

In whom would an increased dose of levothyroxine be required due to the process of metabolism of the drug?

A

Patients who take cytochrome P450 inducers (phenytoin, carbamazepine).

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44
Q

Name two anti-thyroid drugs?

A
  1. Carbimazole

2. Propylthiouracil

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45
Q

What is the indication for use of carbimazole and propylthiouracil?

A

Hyperthyroidism.

Carbimazole is first-line treatment, whereas propylthiouracil is reserved for when patients cannot tolerate carbimazole.

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46
Q

When is the use of carbimazole contraindicated? (1)

A

In people with severe blood disorders

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47
Q

What are the common side effects associated with carbimazole? (8)

A
  1. Arthralgia
  2. Fever
  3. Headache
  4. Jaundice
  5. Malaise
  6. Mild gastro-intestinal disturbances/nausea
  7. Pruritus/rash
  8. Taste disturbance
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48
Q

What is the mechanism of action of carbimazole?

A

Carbimazole is a carbethoxy derivative of methimazole. Once converted to its active form of methimazole, it prevents the thyroid peroxidase enzyme from coupling and iodinating the tyrosine residues on thyroglobulin, hence reducing the production of the thyroid hormones T3 and T4.

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49
Q

What can rashes and pruritus be treated with to allow continuation of carbimazole therapy?

A

Antihistamines

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50
Q

What important adverse effect can carbimazole induce, and what symptoms are patients advised to inform their doctors of?

A

Bone marrow suppression –> patients need to report any symptoms that suggest an infection, especially a sore throat and mouth ulcers.

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51
Q

When carbimazole is used in the hyperthyroidism blocking-replacement regime, which other drug is it used in combination with?

A

Levothyroxine

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52
Q

Propylthiouracil has very similar side effects to carbimazole, however there is one side effect it can cause that carbimazole doesn’t, what is it?

A

Hepatotoxicity - Severe hepatic reactions have been reported, including fatal cases and cases requiring liver transplant—discontinue if significant liver-enzyme abnormalities develop.

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53
Q

There is a big difference in the dosing between carbimazole and propylthiouracil, what is the dose conversion between the two?

A

Carbimazole 1mg is considered the equivalent of 10mg of propylthiouracil

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54
Q

Name 3 examples of Bisphosphonates?

A
  1. Alendronic acid
  2. Disodium pamidronate
  3. Zoledronic acid
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55
Q

What are the common indications for use of bisphosphonates? (4)

A
  1. Osteoporosis/Osteoporotic fragility fractures - alendronic acid is the first-line drug treatment options for at risk patients.
  2. Severe hypercalcaemia of malignancy - pamidronate and zoledronic acid are used, after appropriate IV rehydration.
  3. Myeloma/Breast cancer with bone metastases.
  4. Paget’s disease - first-line treatment of metabolically-active Paget’s disease,
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56
Q

Which bisphosphonates are indicated for use in myeloma or breast cancer with mets? (2)

A
  1. Pamidronate

2. Zoledronic acid

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57
Q

How do pamidronate/zoledronic acid help in patients with myeloma/breast cancer mets?

A

They reduce the risk of pathological features, cord compression and the need for radiotherapy or surgery

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58
Q

How do bisphosphonates help in Paget’s disease?

A

The aim is to reduce bone turnover and pain

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59
Q

What is the mechanism of action of bisphosphonates?

A

They reduce bone turnover by inhibiting the action of oestoclasts, the cells responsible for bone resorption. Bisphosphonates have a similar structure to naturally occurring pyrophosphate, hence are readily incorporated into bone. As bone is resorbed, bisphosphonates accumulate in osteoclasts, where they inhibit activity and promote apoptosis. The net effect is reduction in bone loss and improvement in bone mass.

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60
Q

What are the side effects that bisphosphonates can cause? (4)

A
  1. Oesophagitis
  2. Hypophosphataemia
  3. Osteonecrosis of the jaw (rare but serious - more likely in high dose IV therapy)
  4. Atypical femoral fracture
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61
Q

Due to the possible side effect of osteonecrosis of the law, when taking bisphosphonates, what is important for patients to be aware of?

A

Good dental hygiene, and to visit their dentist on a regular/recommended basis

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62
Q

What are the contraindications for using bisphosphonates? (3)

A
  1. Severe renal impairment
  2. Hypocalcaemia
  3. Upper GI disorders (oral administration contraindicated)
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63
Q

When should bisphosphonates be prescribed with caution? (2)

A

Due to the risk of jaw osteonecrosis;

  1. Smokers
  2. Dental disease
64
Q

If a patient with osteoporosis has hypocalcaemia, but needs to be taking bisphosphonates, what is the option for treatment?

A

Calcichew 6 days a week, alendronic acid to be taken on the one day when calcichew isn’t taken.

65
Q

What is the important drug interaction to be aware of with bisphosphonates?

A

Bisphosphonates bind to calcium, their absorption is therefore reducing if taken with claim salts (including milk), as well as antacids and iron salts.

66
Q

What are the different types of calcium and vitamin D in terms of drug prescriptions?

A
  1. Calcium carbonate
  2. Calcium gluconate
  3. Colecalciferol
  4. Alfacalcidol
67
Q

What are the indications for use of calcium and vitamin D?

A
  1. Osteoporosis (used to ensure positive calcium balance)
  2. CKD
  3. Severe hyperkalaemia
  4. Hypocalcaemia
  5. Vitamin D deficiency (prevention and treatment of - including for rickets (in children) and osteomalacia (in adults)
68
Q

Why are calcium and vitamin D prescribed in patients with CKD?

A

They are used to treat and prevent secondary hyperparathyroidism and renal osteodystrophy

69
Q

Why is calcium (as calcium gluconate) used in patients with severe hyperkalaemia?

A

It prevents life-threatening arrhythmias, other treatments e.g. insulin, are given to lower the potassium concentration

70
Q

What are the symptoms of hypocalcaemia?

A
  1. Paraesthesia
  2. Tetany
  3. Seizures
71
Q

At what level is hypocalcaemia classified as severe? (in terms of mmol/L)

A

<1.9mmol/L

72
Q

What is the mechanism of action of calcium and vitamin D?

A

Calcium is essential for normal function of muscles, nerves, bone and clotting. Calcium homeostasis is controlled by parathyroid hormone and vitamin D, which increase serum calcium levels and bone mineralisation, and calcitonin which reduces serum calcium levels.

73
Q

In osteoporosis, what is the mechanism of action of calcium and vitamin D?

A

In osteoporosis there is a loss of bone mass, which increases the risk of fracture. Restoring calcium balance (either by dietary means or by administering calcium and vitamin D) may reduce the rate of bone loss (though whether this prevents fractures is less clear).

74
Q

How do calcium and vitamin D help in patients with CKD?

A

In CKD, impaired phosphate excretion and reduced activation of vitamin D cause hyperphosphataemia and hypocalcaemia. This stimulates secondary hyperparathyroidism, which leads to a range of bone changes called renal osteodystrophy. Treatment may include oral calcium supplements to bind phosphate in the gut, and alfacalcidol to provide vitamin D that does not depend on renal activation.

75
Q

How do calcium and vitamin D help in hyperkalaemia?

A

Calcium raises the myocardial threshold potential, reducing excitability and the risk of arrhythmias. It has no effect on the serum potassium level.

76
Q

What are the possible side effects caused by oral calcium? (2)

A

Oral calcium may cause:

  1. Dyspepsia
  2. Constipation
77
Q

What can calcium gluconate cause, if administered IV for the treatment of hyperkalaemia?

A

Cardiovascular collapse (if administered too fast) and/or local tissue damage if accidentally given into subcutaneous tissue

78
Q

When should calcium and vitamin D use be avoided? (1)

A

In patients with hypercalcaemia

79
Q

Oral calcium reduces the absorption of which drugs? (4)

A
  1. Iron
  2. Bisphosphonates
  3. Tetracyclines
  4. Levothyroxine
    …and many others
80
Q

What is the dose for IV calcium gluconate in patients with life-threatening hyperkalaemia?

A

10mL of calcium gluconate 10% IV over 5-10 minutes

81
Q

What is the mineralocorticoid drug?

A

Fludrocortisone acetate

82
Q

What is the indication for use of fludrocortisone?

A
  1. Neuropathic postural hypotension
  2. Mineralocorticoid replacement in adrenocortical insufficiency
  3. Adrenocortical insufficiency resulting from septic shock (in combination with hydrocortisone)
83
Q

What is the mechanism of action of fludrocortisone?

A

Fludrocortisone binds the mineralocorticoid receptor (aldosterone receptor). This binding (or activation of the mineralocorticoid receptor by fludrocortisone) in turn causes an increase in ion and water transport and thus raises extracellular fluid volume and blood pressure and lowers potassium levels.
Mineralocorticoids act on the distal tubules of the kidney to enhance the reabsorption of sodium ions from the tubular fluid into the plasma; they increase the urinary excretion of both potassium and hydrogen ions.

84
Q

What are the effects of fludrocortisone toxicity?

A

Effects of overexposure include:

  1. Irritation
  2. Cardiac oedema
  3. Increased blood volume
  4. Hypertension
  5. Cardiac arrhythmias
  6. Enlargement of the heart
  7. Headaches
  8. Weakness of the extremities.
85
Q

What side effects can fludrocortisone cause? (59?!?!……59 side effects!)

A

As with all corticosteroids:

  1. Abdominal distension
  2. Acute pancreatitis
  3. Aggravation of epilepsy
  4. Aggravation of schizophrenia
  5. Amenorrhoea
  6. Anaphylaxis (in children)
  7. Bruising
  8. Candidiasis
  9. Congestive heart failure
  10. Corneal thinning
  11. Cushing’s syndrome (with moon face, striae and acne) 12. Dyspepsia
  12. Ecchymoses
  13. Exacerbation of ophthalmic fungal disease
  14. Exacerbation of ophthalmic viral disease
  15. Exophthalmos
  16. Facial erythema
  17. Glaucoma
  18. Headache
  19. Hiccups
  20. Hirsutism
  21. Hypercholesterolaemia
  22. Hyperglycaemia
  23. Hyperhidrosis
  24. Hyperlipidaemia
  25. Hypersensitivity reactions (in children)
  26. Impaired healing
  27. Increased appetite
  28. Increased intra-ocular pressure
  29. Increased intracranial pressure with papilloedema (usually after withdrawal) (in children)
  30. Increased susceptibility to and severity of infection
  31. Insomnia
  32. Leucocytosis
  33. Long bone fractures
  34. Malaise
  35. Menstrual irregularities
  36. Muscle weakness
  37. Myocardial rupture following recent myocardial infarction
  38. Nausea
  39. Negative calcium/nitrogen balance
  40. Oesophageal ulceration
  41. Papilloedema (in adults)
  42. Petechiae
  43. Posterior subcapsular cataracts
  44. Potassium loss
  45. Psychological dependence
  46. Reactivation of dormant tuberculosis
  47. Scleral thinning
  48. Skin atrophy
  49. Sodium retention
  50. Suppression of growth (in children)
  51. Telangiectasia
  52. Tendon rupture
  53. Thromboembolism
  54. Urticaria
  55. Vertebral fractures
  56. Vertigo
  57. Water retention
  58. Weight gain
86
Q

Name some commonly prescribed NSAIDs? (3)

A
  1. Naproxen
  2. Ibuprofen
  3. Etoricoxib
  4. Diclofenac
  5. High dose aspirin
87
Q

What are the common indications for use of NSAIDs?

A
  1. Mild-to-moderate pain

2. Pain related to inflammation, particularly MSK.

88
Q

Which drug is preferred to NSAIDs when used as an analgesic?

A

Paracetamol - a single dose of each has similar analgesic effects, so paracetamol is preferred as there are less side effects. Obviously often they are used in combination together.

89
Q

Give some examples of MSK conditions that NSAIDs are indicated for use in? (3)

A
  1. Rheumatoid arthritis
  2. Severe osteoarthritis
  3. Acute gout
90
Q

What is the mechanism of action of NSAIDs?

A

NSAIDs inhibit synthesis of prostaglandins from arachidonic acid by inhibiting cyclooxygenase (COX). COX exists as two main isoforms. COX-1 is the constitutive form. It stimulates prostaglandin synthesis that is essential to preserve integrity of the gastric mucosa; maintain renal perfusion (by dilating afferent glomerular arterioles); and inhibit thrombus formation at the vascular endothelium. COX-2 is the inducible form, expressed in response to inflammatory stimuli. It stimulates production of prostaglandins that cause inflammation and pain. The therapeutic benefits of NSAIDs are principally mediated by COX-2 inhibition and adverse effects by COX-1 inhibition, although there is some overlap between the two. Selective COX-2 inhibitors (e.g. etoricoxib) were developed in an attempt to reduce the adverse effects of NSAIDs.

91
Q

What are the main adverse effects associated with NSAID use? (3)

A
  1. GI toxicity
  2. Renal impairment
  3. CV events (e.g. increased risk of MI and stroke)
92
Q

Of all the non-selective NSAIDs, which one is associated with lowest risk of GI effects?

A

Ibuprofen

93
Q

Which two NSAIDs are associated with lowest risk of CV events?

A
  1. Ibuprofen

2. Naproxen

94
Q

What are COX-2 inhibitor NSAIDs associated with in terms of side effects?

A

They cause fewer GI side effects compared to non-selective NSAIDs, but are associated with an increased risk of CV events.

95
Q

Are any NSAIDs not associated with impaired renal function?

A

No, all NSAIDs including COX-2 inhibitors can cause renal impairment.

96
Q

What are adverse effects can NSAIDs cause? (2)

A
  1. Hypersensitivity reactions e.g. bronchospasm and angioedema
  2. Fluid retention (which can worsen heart failure and hypertension).
97
Q

When is NSAID use contraindicated?

A
  1. Severe renal impairment
  2. Heart failure
  3. Liver failure
  4. NSAID hypersensitivity
98
Q

When should NSAIDs be avoided/used with caution (4), and what is the advice given if they have to be used?

A
  1. Peptic ulcer disease
  2. GI bleeding
  3. Cardiovascular disease
  4. Renal impairment
    Use the safest NSAID at the lowest effective dose, for the shortest period of time
99
Q

Name some commonly prescribed compound-preparation opioids?

A
  1. Co-codamol

2. Co-dydramol

100
Q

What is the indication for use of co-codamol/co-dydramol?

A

Mild-to-moderate pain; as second-line agents when simple paracetamol/ibuprofen is insufficient.

101
Q

On the WHO ‘pain ladder’, which rung are co-codamol/co-dydramol on?

A

The second rung

102
Q

What is the mechanism of action of co-codamol?

A

Has two mechanisms of action - paracetamol and codeine. The mechanism of action of paracetamol is poorly understood, but it is a weak inhibitor of COX. In the CNS, COX inhibition appears to increase the pain threshold.
Codine and dihydrocodeine are weak opioids. They are metabolised by cytochrome P450 enzymes to morphine and morphine-related metabolites. These metabolites, which are agonists of opioid u-receptors, probably account for most of their analgesic effect.

103
Q

Why is it effective combining paracetamol and codeine?

A

As the two analgesics have different mechanisms of action, they may offer better pain control than can be achieved with either drug alone.

104
Q

What are the adverse effects associated with co-codamol/co-dydramol?

A
  1. Nausea
  2. Constipation
  3. Drowsiness
105
Q

What would be the clinical signs of a co-codamol overdose?

A
  1. Paracetamol overdose causes hepatotoxicity

2. Opioid toxicity causes neurological and respiratory depression

106
Q

What are the warnings associated with taking weak opioids/compound preparation opioids? (4)

A

Dose reduction/caution when prescribing to patients with:

  1. Significant respiratory disease
  2. Renal impairment
  3. Hepatic impairment
  4. Elderly
107
Q

What are the important drug interactions to note with co-compound preparations of opioids?

A

Opioids should not ideally be used with other sedating drugs:

  1. Antipsychotics
  2. Benzodiazepines
  3. Tricyclic antidepressants
108
Q

Name some weak prescription opioids?

A
  1. Codeine
  2. Tramadol
  3. Dihydrocodeine
109
Q

What is the indication for use of weak opioids?

A

Mild-to-moderate pain, including post-operative pain. It is one the same second ‘rung’ of the WHO pain ladder, as with compound preparation opioids.

110
Q

What is the key enzyme that metabolises opioids, that 10% of caucasians have a less active form of?

A

Cytochrome P450 2D6

111
Q

Where are weak opioids metabolised?

A

In the liver, to form small amounts of morphine

112
Q

What is tramadol?

A

It is a synthetic analogue of codeine, and is better classified as a moderate strength opioid.

113
Q

How is tramadols mechanism of action different to that of codines/dihydrocodeines?

A

Tramadol and its active metabolite are also u-receptor agonists (just like codeine) but in addition to this, tramadol also affects serotonergic and adrenergic pathways, where it is thought to act as a serotonin and noradrenaline re-uptake inhibitor. This is thought to contribute to its analgesic effects.

114
Q

What are the side effects associated with weak opioid use? (4)

A
  1. Nausea
  2. Constipation
  3. Dizziness
  4. Drowsiness
115
Q

What are the effects of an opioid overdose?

A

Neurological and respiratory depression

116
Q

Does tramadol cause more or less side effects than other opioids?

A

Less side effects

117
Q

Which opioids must never be given intravenously, due to a severe reaction similar to anaphylaxis? (2)

A

Codine and dihydrocodeine

118
Q

Is the severe reaction to IV codeine/dihydrocodeine an allergic response?

A

No, although it is mediated by histamine release

119
Q

What is the contraindication for tramadol use?

A

Tramadol lowers the seizure threshold so is best avoided in patients with epilepsy and contraindicated in people with uncontrolled epilepsy

120
Q

Which drugs should tramadol not be prescribed alongside?

A

Other drugs that lower seizure threshold; SSRIs and tricyclic antidepressants

121
Q

Why might patients have a red patch on their thigh after an operation in which the anaesthetist administered post-operative analgesia?

A

Anaesthetists may give an IM infection of codeine towards the end of an operation, to provide post-operative analgesia. A red patch can form at the site of injection.

122
Q

Name two strong opioids?

A
  1. Morphine

2. Oxycodone

123
Q

What are the common indications for use of strong opioids?

A
  1. Acute severe pain; for rapid relief, including post-operative pain, and pain associated with acute MI
  2. Chronic pain; ‘rung’ 3 of the WHO pain ladder, where all other analgesics beforehand were insufficient
  3. Breathlessness - in the context of end of life care
  4. Acute pulmonary oedema - to relieve breathlessness and anxiety
124
Q

What are drugs are prescribed alongside strong opioids when treating acute pulmonary oedema? (3)

A
  1. Oxygen
  2. Furosemide
  3. Nitrates
125
Q

What is the mechanism of action of strong opioids?

A

Opioids encompasses naturally-occurring opiates e.g. morphine, and synthetic analogues e.g. oxycodone. The therapeutic action of opioids arises from activation of opioid (mu) receptors in the CNS. Activation of these G protein-coupled receptors has several effects that, overall, reduce neuronal excitability and pain transmission. In the medulla, they blunt the response to hypoxia and hypercapnoea, reducing respiratory drive and breathlessness.

126
Q

By relieving pain and breathlessness, what overall effect do opioids have on the sympathetic nervous system?

A

Opioids reduce the sympathetic nervous system (fight or flight) activity.

127
Q

As opioids reduce sympathetic nervous systemic activity, what is their contribution to helping people with an acute MI or pulmonary oedema?

A

Opioids reduce cardiac work and oxygen demands, as well as relieving symptoms. Although the efficacy of morphine in acute pulmonary oedema is not fully understood/firmly established.

128
Q

What side effect do strong opioids have on the respiratory system?

A

They cause respiratory depression by reducing respiratory drive.

129
Q

What side effects can strong opioids cause, other than respiratory depression? (5)

A
  1. Euphoria and detachment, which can lead to neurological depression
  2. Nausea and vomiting
  3. Pupillary constriction
  4. Constipation
  5. Itching, urticaria, vasodilation and sweating
130
Q

Why do strong opioids cause nausea and vomiting?

A

They can activate the chemoreceptor trigger zone

131
Q

Why do strong opioids cause pupillary constriction?

A

They stimulate the Edinger-Whestphal nucleus.

132
Q

What effect do strong opioids have on the colon, leading to constipation?

A

They activate u (mu)-receptors, which increases muscle tone and reduces motility, leading to constipation.

133
Q

Why can opioids cause itching, urticaria etc.?

A

They mediate the release of histamine

134
Q

What are the symptoms/clinical signs of opioid withdrawal (particularly when patient has become dependent)? (5)

A

The opposite of the clinical effects of opioids:

  1. Anxiety
  2. Pain
  3. Breathlessness
  4. Pupils dilate
  5. Skin is cool and dry
135
Q

What are the warnings associated with strong opioid use? (4)

A

Same as with any other opioids:

  1. Hepatic failure
  2. Renal impairment
  3. Respiratory failure
  4. Biliary colic (can worsen pain as cause spasm of the sphincter of Oddi)
136
Q

What is the drug interaction associated with strong opioid use? (same as with other opioids)

A

Opioids should not be used with other sedating drugs: e.g. antipsychotics, benzodiazepines and tricyclic antidepressants.

137
Q

What are the common indications for use of paracetamol?

A
  1. Acute and chronic pain : first-line analgesic

2. Antipyretic : can reduce fever and its associated symptoms e.g. shivering

138
Q

What is the mechanism of action of paracetamol?

A

Paracetamol is weak inhibitor of COX, the enzyme involved in prostaglandin metabolism. In the CNS, COX inhibition appears to increase the pain threshold and reduce prostaglandin (PGE2) concentrations in the thermoregulatory region of the hypothalamus, controlling fever. Paracetamol has specificity for COX-2 (the isoform induced in inflammation) rather than COX-1 (the isoform involved in protecting the gastric mucosa and regulating renal blood flow and clotting).

139
Q

Why is paracetamol a weak anti-inflammatory drug, if it has COX-2 specificity?

A

Paracetamol is a weak anti-inflammatory, as its actions are inhibited in inflammatory lesions by the presence of peroxides.

140
Q

What are the side effects associated with paracetamol use?

A

Paracetamol is a very safe drug, with few side effects.

141
Q

What are the effects of paracetamol overdose?

A

In overdose, paracetamol causes liver failure.

142
Q

Why does paracetamol overdose cause liver failure?

A

Paracetamol is metabolised by cytochrome P450 enzymes to a toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI), which is conjugated with glutathione before elimination. After overdose, this elimination pathway is saturated and NAPQI accumulation causes hepatocellular necrosis.

143
Q

How can hepatotoxicity be avoided with a paracetamol overdose?

A

Treatment with the glutathione precursor - acetylcysteine.

144
Q

What are the warnings associated with paracetamol use?

A

Paracetamol dose should be reduced in people at increased risk of liver toxicity:

  1. Either because of increased NAPQI production: chronic excessive alcohol use …or…
  2. Due to reduced glutathione stores: malnutrition, low body weight and severe hepatic impairment.
145
Q

What are the important drug interactions with paracetamol use?

A

There are few clinically significant interactions. However cytochrome P450 induces, e.g. phenytoin and carbamazepine, increase the rate of NAPQI production and risk of liver toxicity after paracetamol overdose

146
Q

Name some xanthine oxidase inhibitors?

A
  1. Allopurinol (commonly prescribed)
  2. Aloprim
  3. Febuxostat
  4. Uloric
147
Q

What are the common indications for use of allopurinol? (3)

A
  1. To prevent acute attack of gout
  2. To prevent uric acid and calcium oxalate renal stones
  3. To prevent hyperuricaemia and tumour lysis syndrome associated with chemotherapy
148
Q

What is the mechanism of action of allopurinol?

A

Allopurinol is a xanthine oxidase inhibitor. Xanthine oxidase metabolises xanthine (produced from purines) to uric acid. Inhibition of xanthine oxidase lowers plasma uric acid concentrations and reduces precipitation of uric acid in the joints or kidneys.

149
Q

What are the side effects caused by allopurinol? (1)

A

The most common side effect is a skin rash, which may be mild or may indicate a more serious hypersensitivity reaction such as Stevens-Johnson syndrome or toxic epidermal necrolysis.

150
Q

As well as severe skin reactions leading to Stevens-Johnson syndrome, what are syndrome can allopurinol cause?

A

Drug hypersensitivity syndrome (aka drug rash with eosinophilia and systemic symptoms - DRESS). This is a rare, life-threatening reaction to allopurinol that can include fever, eosinophilia, lymphadenopathy and involvement of other organs, such as the liver and skin.

151
Q

What can allopurinol do if started during an acute gout attack?

A

Worsen the attack.

152
Q

What are the contraindications for use of allopurinol? (3)

A
  1. Acute attacks of gout
  2. Recurrent skin rash
  3. Severe hypersensitivity
153
Q

Where is allopurinol metabolised and where is it excreted, and what does this mean in terms of dosage?

A

Allopurinol is metabolised by the liver and excreted by the kidneys, therefore the dose should be reduced in patents with severe renal or hepatic impairment.

154
Q

In which drugs does allopurinol inhibit their metabolism, and therefore increase the risk of toxicity? (2)

A

The cytotoxic drug mercaptopurine and its pro-drug azathioprine, require xanthine oxidase for metabolism. When allopurinol is prescribed with these drugs, it inhibits their metabolism and increase the risk of toxicity.

155
Q

Co-prescription of allopurinol and which antibiotic, leads to a skin rash (or increases the chances of)?

A

Amoxicillin

156
Q

Co-prescription of allopurinol and which drugs, increase the risk of hypersensitivity reactions? (2)

A
  1. ACE inhibitors

2. Thiazides

157
Q

Which drugs can induce gout? (2)

A
  1. Thiazide or loop-diuretics

2. Aspirin

Drug Formulary Y3 (9 decks)

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