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Top 100 drugs Flashcards

1
Q

What are Dipeptidylpeptidase-4 inhibitors indicated for?

A

Type 2 Diabetes: In combination with metformin (or other hyperglycaemic agents) where blood glucose is inadequately controlled.
As a single agent where metformin is contraindicated or not tolerated.

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2
Q

What is the mechanism of action for DPP-4 inhibitors?

A

Incretins and glucose-dependent insulinotropic peptide are released by the intestine throughout the day, and particularly in response to food - these promote the secretion of insulin and suppress glucagon release, thus lowering blood glucose. Incretins are rapidly inactivated by the enzyme DPP-4. DPP-4 inhibitors therefore prevent the degradation of incretins and increase plasma concentrations of their active forms, lowering blood glucose concentrations.

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3
Q

Which are less likely to cause HYPOglycaemia, DPP-4 inhibitors or sulphonylureas ?

A

DPP-4 inhibitors - As the action of incretins are glucose dependent they do not stimulate the secretion of insulin at normal blood glucose levels or suppress glucagon release in response to hypoglycaemia. This means DPP-4 inhibitors are less likely to cause hypoglycaemia than sulphonylureas which stimulate insulin secretion irrespective of blood glucose.

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4
Q

Name the DDP-4 inhibitors

A

Alogliptin, Sitagliptin, Linagliptin and Saxagliptin

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5
Q

What are the potential adverse effects associated with the use of DPP-4 inhibitors?

A
  • HYPOglycaemia where DPP-4 inhibitors are being used in combination with sulphonylureas and/or insulin
  • All DPP-4 inhibitors are associated with acute pancreatitis which typically presents as persistent abdominal pain resolved upon stopping of the drug
  • GI upset
  • Headache
  • Nasopharyngitis
  • Peripheral oedema
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6
Q

Can DPP-4 inhibitors be used to treat Type 1 diabetes?

A

No

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7
Q

Can DPP-4 inhibitors be used to treat ketoacidosis?

A

No

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8
Q

Can DPP-4 inhibitors be used during pregnancy or breastfeeding?

A

No

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9
Q

How are DPP-4 inhibitors excreted?

A

Renally

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10
Q

When should DPP-4s be dose adjusted?

A

During moderate to severe renal impairment

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11
Q

When are DPP-4 inhibitors contraindicated?

A

DPP-4 inhibitors are contraindicated in patients with hypersensitivity to the drug class

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12
Q

When should DPP-4 inhibitors be used with caution?

A
  • Elderly (>80 years)
  • History of pancreatitis
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13
Q

Use of which other drug classes increases the risk of HYPOglycaemia in concurrent use with DPP-4 inhibitors?

A
  • Sulphonylureas
  • Insulin
  • Alcohol
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14
Q

Which drug class may mask the symptoms of HYPOglycaemia?

A

Beta-blockers

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15
Q

What is the typical dosing of DPP-4 inhibitors?

A

Once daily

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16
Q

What quantity of the the daily dose of a DPP-4 inhibitor dose a combined formulation with metformin contain?

A

Half the daily dose

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17
Q

What is the key counselling point when advising a patient on the use of a DPP-4 inhibitor?

A

Acute Pancreatitis - seek medical attention if you develop severe or acute stomach pain radiating to the back

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18
Q

Which indicator is used to assess glycaemic control when using a DPP-4 inhibitor?

A

HbA1c

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19
Q

What are the target HbA1c levels for monotherapy and combined therapy with a DPP-4 inhibitor?

A

Monotherapy - <48mmol/mol
Combination therapy - <53mmol/mol

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20
Q

What HBA1c is generally a trigger to intensify treatment with an additional agent when using a formulation of a DPP-4 inhibitor?

A

> 58mmol/mol

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21
Q

What advantage do metformin and SGLT2 inhibitors have over use of DPP-4 inhibitors?

A

They reduce the risk of vascular complications

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22
Q

The efficacy of DPP-4 inhibitors is reduced by which medications that elevate levels of blood glucose?

A
  • Prednisolone
  • Thiazide
  • Loop diuretics
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23
Q

What is the indication for metformin?

A

Type 2 diabetes as a a monotherapy or in combination with DPP-4 inhibitors, Sulphonylureas, or insulin

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24
Q

What is the mechanism of action for metformin?

A

Metformin (a biguanide) lowers blood glucose by reducing hepatic glucose output (glycogenolysis and gluconeogenesis)) and to a lesser extend increasing the uptake and utilisation of glucose by skeletal muscle. Metformin achieves its mechanism of action through activation of AMP (adenosine monophosphate- activated) kinase which acts as a metabolic sensor.

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25
Q

What are some key adverse effects of metformin use?

A

GI upset
- Nausea
- Vomiting
- Taste disturbance
- Diarrhoea
- Lactic acidosis

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26
Q

When should metformin be used with caution?

A

Renal impairment
Hepatic impairment
Chronic alcohol abuse

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27
Q

At what eGFR does metformin require dose adjusting, and what level dose it require stopping metformin?

A

Dose reduction - <45ml/min per 1.73m2
Stopped - <30ml/min per 1.73m2

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28
Q

When should metformin be held?

A

AKI
Severe tissue hypoxia (e.g. in sepsis, cardiac or respiratory failure, or myocardial infarction)
Acute alcohol intoxication

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29
Q

Which three medications reduce the efficacy of metformin?

A

Prednisolone
Thiazide
Loop diuretics

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30
Q

When and for how long should metformin be withheld regarding IV CONTRAST MEDIA?

A

Metformin must be withheld before and for 48 hours after the injection of IV contrast media when there is an increased risk of renal impairment, metformin accumulation, and lactic acidosis.

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31
Q

Which other drugs that have the potential to impair renal function should be used in caution with metformin?

A

ACE inhibitors
NSAIDs
Diuretics

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32
Q

What formulation of metformin should patients be started on initially, and why?

A

Standard release to minimise GI side effects

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33
Q

What is a common starting regimen for metformin?

A

500mg OD with breakfast, increasing by 500mg weekly to 500-850mg TDS with meals

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34
Q

What are the key points when counselling a patient who has been newly started on metformin?

A
  • Inform their Dr they are taking metformin before having an X-ray or operation
  • Seek urgent medical advice if they develop significant illness such as breathlessness, fever, or chest pain, as, in addition to treating the illness, metformin may need to be stopped or withheld due to the risk of a side effect called lactic acidosis
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35
Q

Ideally when should renal function be measured in patients taking metformin?

A

Before starting treatment and then at least annually during treatment. Renal function should be measured more frequenty (at least twice per yer) in patients with deteriorating renal function or at increased risk of renal impairment.

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36
Q

How should glycaemic control be measured in patients taking metformin and what is the target level when metformin is being used as a single agent?

A

HbA1c - <48mmol/mol

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37
Q

Does metformin stimulate insulin scretion?

A

No

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38
Q

When and how should treatment of type 2 diabetes be intensified when using metformin as a single agent?

A

A second agent should be added if HbA1c >58mmol/mol and a new target of <53 mmol/mol is set (balancing the risk of hyperglycaemia against the risk of treatment, in particular hypoglycaemia)

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39
Q

At what point and for long should increased physical activity be recommended before meformin is initiated?

A

HbA1c >48 mmol/mol
At least three months before metformin initiation

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40
Q

What primarily increases insulin resistance?

A

Increased body weight

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41
Q

What kind of hormone is insulin?

A

Anabolic

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42
Q

Does metformin cause weight gain?

A

No. Unlike the sulphonylureas, metformin does not stimulate the secretion of insulin, which as an anabolic hormone causes weight gain and can worsen diabetes mellitus over the long term.

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43
Q

What are the sulphonylureas indicated for?

A

Type 2 diabetes in combination with metformin (and/or other hyperglycaemic agents) or as a single agent to control blood glucose levels where metformin is contraindicated

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44
Q

What drug class is gliclazide

A

Sulphonylurea

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45
Q

What is the mechanism of action of sulphonylureas?

A

They stimulate pancreatic insulin secretion by blocking ATP dependen K+ channels in pancreatic beta-membranes causing depolarisation of the cell membranes and the opening of Ca2+ channels. This increases intracellular Ca2+ concentrations, stimulating the secretion of insulin. Sulphonylureas are only effective in patients with residual pancreas function.

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46
Q

What are the potential adverse effects associated with the use of sulphonylureas?

A
  • GI upset
  • HYPOglycaemia
  • Rare sensitivity reactions (hepatic toxicity, drug hypersensitivity syndrome, and haematological abnormalities)
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47
Q

Where are the sulphonylureas metabolised?

A

The liver

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48
Q

How are the sulphonylureas excreted?

A

Unchanged drug and metabolites are excreted renally

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49
Q

Can sulphonylureas be used in renal impairment?

A

Yes, they should be used with caution in those with mild-moderate renal impairment due to the risk of hypoglycaemia. The lowest possible dose should be used and blood glucose should be carefully monitored

Gliclazide can be used in renal impairment but careful monitoring of blood glucose is essential

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50
Q

When should sulphonylreas be used with caution?

A

In those with increased risk of HYPOglycaemia:
- Hepatic impairment (reduced gluconeogenesis)
- Malnutrition
- Adrenal or pituitary insufficiency (lack of counter-regulatory hormones)
- Elderly

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51
Q

When is a dose adjustment required for the use of sulphonylureas?

A

In patients with hepatic impairment

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52
Q

The risk of HYPOglycaemia is increased by the co-prescription of which other drugs with the sulphonylureas?

A

Alchohol
Antidiabetic drugs:
- Metformin
- DPP-4 inhibitors
- Thiazolidinediones (*glitazones)
- Insulin

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53
Q

The efficacy of sulphonylureas are effected by which other drugs that elevate blood glucose?

A
  • Prednisolone
  • Thiazide
  • Loop diuretics
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54
Q

What dose of standard release gliclazide has the same glucose lowerin effect as 30mg MR gliclazide?

A

80mg

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55
Q

What is a standard starting regimen for gliclazide?

A

40-80mg OD, then increased of 160-320mg if necessary (in 2x divided doses when exceeding 160mg)

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56
Q

When/how should sulphonyolureas be taken?

A

With meals (OD with breakfast or BD with breakfast and dinner for higher doses)

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57
Q

What are the key points when counselling a patient about the use of sulphonylureas such as gliclazide?

A
  • Should be used in addition to healhy lifestyle measures
  • Watch out for the symptoms of HYPOglycamia (dizziness, sweating, nausea, and confusion)
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58
Q

How is glycaemic control measured when using sulphonylureas?

A

HbA1c

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59
Q

What is the target HbA1c of a patient using gliclazide as a single agent to treat type-2 diabetes

A

<48 mmol/mol

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60
Q

When and how is treatment intensified for a patient using gliclazide as a single agent to treat type-2 diabtes

A

Treatment is itensified with the addiion of a second agent when HbA1c exceeds >58 mmol/mol and a new target of <53 mmol/mol is set

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61
Q

Which are more expensive; sulphonylureas or DPP-4 inhibitors

A

DPP-4 inhibitors are newer and more expensive

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62
Q

When are sulphonylureas contraindicated?

A

In the presence of ketoacidosis

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63
Q

Can sulphonylureas be used in pregnancy or breastfeeding?

A

No, due to the possible risk of neonatal or infant hypoglycaemia

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64
Q

During acute illness what should happen to treatment with sulphonylureas?

A

During acute illness, insulin resistance increases and renal and hepatic function may be impaired. As such oral hypoglycaemics become less effective at controlling blood glucose and side effects are more likely. Insulin treatment may be required temporarily as the dosage can be adjusted more easily than that of oral medications.

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65
Q

What drug class is prednisolone?

A

Corticosteroid

(Glucocorticoids)

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66
Q

What drug class is hydrocortisone?

A

Corticosteroid

(Glucocorticoids)

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67
Q

What drug class is dexamethasone?

A

Corticosteroid

(Glucocorticoids)

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68
Q

What are he indications for corticosteroids (glucocorticoids)

A
  1. To treat allergic and inflammatory disorders
  2. Supression of autoimmune disease
  3. In the treatment fof some cancers as part of chemotherapy or to reduce tumour-associated swelling
  4. Hormone replacement in adrenal insufficiency hypopituitarism
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69
Q

What are the mechanismsof action of corticosteroids (glucocorticoids)?

A

These corticosteroids mainly exert glucocorticoid effects.They bind to the cytosolic glucocorticoid receptors, which then translocate to the nucleus and bind to the glucocorticoid-response elements, which regulate gene expression. They upregulate antiinflammatory genes and downregulate pro-inflammatory genes (e.g. cytokines, tumour necrosis factor-alpha etc). Direct actions on inflammatory cells include suppression of circulating monocytes and eosinophils.
Their metabolic effects include increased gluconeogenesis from increased circulating amino and fatty acids released by catabolism of muscle and fat.
These drugs also have mineralocorticoid effects, stimulating sodium and water retention and potassium excretion in the renal tubule.

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70
Q

What are the main adverse effects of cortcosteroid use (glucocorticoids)?

A
  • Immunosuppression
  • Diabetes mellitus
  • Osteoporosis
  • Cushing’s syndrome
  • Skin thinning
  • Gastritis and peptic ulcers
  • Proximal muscle weakness
  • Bruising
  • Insomnia
  • Confusion
  • Psychosis
  • Suicidal ideation
  • HYPERtension
  • HYPOkalaemia
  • Oedema
  • Adrenal supression
  • Glaucoma
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71
Q

What immune side effects can corticosteroid use cause?

A

Immunosuppression

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72
Q

What metabolic side effects can corticosteroid use cause?

A

Diabetes mellitus
Osteoporosis

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73
Q

What side effects can result from increased catabolism associated with corticosteroid use?

A

Skin thinning
Gastritis
Easy bruising
Proximal muscle weaknes

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74
Q

What behavioural side effects can result from corticosteroid use?

A

Insomnia
Confusion
Psychosis
Suicidal ideation

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75
Q

What side effects can be caused by the mineralcorticoid effects of corticosteroid use?

A

Hypertension
Hypokalaemia
Oedema

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76
Q

Why is slow withdrawal of corticoid sterioids required?

A

To prevent Addisonian crisis and to allow for the recovery of endogenous adrenal function, and to prevent chronic glucocorticoid deficiency which presents as fatigue, weight loss and arthralgia (joint stiffness)

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77
Q

What is the MHRA warning for the use of systemic cortcosteroids

A

Rare risk of central serous chorioretinopathy wih local as well as systemic administration (Augut 207)

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78
Q

When should corticosteroids be prescribed with caution?

A

People with infection
Children - in whom it may suppress growh

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79
Q

How do corticosteroids interact with NSAIDs?

A

They both increase the rik of peptic ulceration and GI bleeding

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80
Q

Which drug classes increases the risk of HYPOkalaemia when taken with corticosteroids such as prednisolone?

A

Beta2-agonists
Theophylline
Loop diuretics
Thiazide diuretics

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81
Q

Which medications reduce the efficacy of corticosteroids such as prednisolone?

A

Cytochrome P450 inducers e.g
- phenytoin
- rifampicin
- carbamazepine

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82
Q

List the medications that interact wih corticosteroids

A

NSAIDs
Loop diuretics
Thiazide diuretcs
Beta2-agonists
Phenytoin
Carbamazepine
Rifampicin

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83
Q

When in the day should OD corticostroids be given and why?

A

In the morning to mimic the body’s natural circadian rythm and avoid insomnia

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84
Q

Between prednisolone, hydrocortisone, and dexamethasone, which is more potent and what are the equivalent dosages?

A

Dexamethasone is the more potent of the three
750micrograms dex = 5mg pred = 20mg hydrocort

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85
Q

What dose of dexamethasone is typically prescribed in emergencies (e.g. treatment of vasogenic oedema that may surround brain tumours)?

A

8mg BD IV or orally - then weaned down slowly as symptoms improve

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86
Q

What should happen to corticosteroid therapy during acute illness?

A

The dose is typically doubled as patients on long term steroids are usualy unable to increase endogenous secretion of cortisol in times of stress, therefore additional exogenous corticosteroid may be required.

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87
Q

When should courses of prednisolone be tapered down in adults?

A
  • When the patient has received 40mg or more OD for 1 week or more
  • Been given repeat doses in the evening
  • Received more than 3 weeks of treatment
  • Recently received repeat courses (particulalry in the last 3 weeks)
  • Taken a short course within 1 year of stopping long term therapy
  • Other possible causes of adrenal suppression
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88
Q

What is the typical dose of prednisolone used in an adult with an acute exacerbation of COPD?

A

30mg OD PO for 7-14 days

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89
Q

What is the typical dose of prednisolone used in an adult with an acute exacerbation of asthma?

A

40mg OD PO for at least 5 days

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90
Q

When should courses of prednisolone be tapered down in children?

A
  • When the patient has received 40mg or more OD for 1 week or more / 2mg/kg OD for 1 week or more / 1mg/kg OD for 1 month or more
  • Been given repeat doses in the evening
  • Received more than 3 weeks of treatment
  • Recently received repeat courses (particulalry in the last 3 weeks)
  • Taken a short course within 1 year of stopping long term therapy
  • Other possible causes of adrenal suppression
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91
Q

What drugs can be given to limit adverse effects of corticosteroid use in patients with relevant risk factors?

A

Bisphosphonates
PPIs

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92
Q

Which corticosteroid is typically used and how when oral aministration is not appropriate (e.g. inflammatory bowel disease flares, anaphylaxis, etc)?

A

IV hydrocortisone

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93
Q

When may the co-prescription of steroid sparing agents be necessary to limit adverse effects with corticosteroids? Which agents are typically co-prescribed?

A

In long term treatment of consitions such as inflammatory arthritis where the lowest dose of oral prednisolone is used to treat the disease and limit adverse effects.
Commonly co-prescribed drugs in these consitions are methotrexate and azathioprine.

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94
Q

What are the key points when counselling a patient newly started on corticosteroids such as oral prednisolone?

A
  • Do not stop treatment suddnly
  • Carry a steroid card incase they need treatment
  • Discus the risks of long term steroid use such as osteoporosis, bone fracture, and diabetes so the patient can make an informed decision about their therapy
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95
Q

How should the efficacy of prednisolone treatment be monitored?

A

This depends on the condition being treated and the anticipated adverse effects
- Peak expiratory flow in excerbations of asthma and COPD
- Blood inflammatory markers for inflammaory arthritis
- HbA1c and blood gluose to monitor for potential diabetic levels
- DEXA scans to measure bone densiy for potntil osteoporosis

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96
Q

How do corticosteroids affect ACTH (pituitary adrenocorticotropic hormone) secretion and what are the consequences of this?

A

ACTH secretion is suppressed
- stimulus of normal adrenal cortisol production switched off
- Prolonged treatment causes adrenal atrophy which prevents endogenous cortisol secretion
- Sudden withdrawal can cause Addisonian crisis with cardiovascular collapse
- Chronic glucorticoid deficiency during withdrawal may present as fatigue, weight loss, and arthralgia

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97
Q

Concurrent therapy with drug class increases insulin requirements?

A

Systemic corticosteroids

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98
Q

What are the indications for insulin?

A
  1. Insulin replacement in people with type 1 diabetes and control of blood glucose in type 2 diabetes where oral hypoglycaemic treatment is inadequate or poorly tolerated
  2. Given intravenously, in the treatment of diabetic emergencies such as diabetic ketoacidosis and hyperglycaemic hyperosmolar syndrome
  3. Given alongside glucose to treat hyperglycaemia while other measures are being initiated
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99
Q

What are the main adverse effects of insulin use?

A
  • Hypoglycaemia
  • Fat overgrowth in repeated SC use at the site of injection
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100
Q

What are the 5 types of insulin?

A
  1. Rapid acting
  2. Short acting
  3. Intermediate acting
  4. Long acting
  5. Biphasic
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101
Q

What type of insulin is insulin glargine

A

Long acting

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102
Q

What type of insulin is insulin degludec?

A

Long acting

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103
Q

What type of insulin is insulin detemir?

A

Long acting

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104
Q

What type of insulin is insulin aspart?

A

Rapid acting

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105
Q

What type of insulin is insulin isophane?

A

Intermediate acting

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106
Q

What type of insulin is insulin lispro?

A

Rapid acting

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107
Q

What type of insulin is insulin glulisine?

A

Rapid acting

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108
Q

What type of insulin is soluble insulin?

A

Short acting

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109
Q

What types of insulin are usually in a biphasic insulin preparation?

A

Rapid and intermediate

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110
Q

What type of insulin is in Lantus preparations?

A

Glargine

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111
Q

What type of insulin is in Humalog preparations?

A

Lispro

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112
Q

What type of insulin is in Toujeo preparations?

A

Glargine

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113
Q

What type of insulin is in Levemir preparations?

A

Detemir

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114
Q

What kind of insulin is in Tresiba preparations?

A

Degludec

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115
Q

What kind of insulin is in Actrapid preparations?

A

Soluble insulin

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116
Q

What kind of insulin is in Fiasp prepaprations?

A

Aspart

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117
Q

What kind of insulin is in Humalog S preparations?

A

Soluble insulin

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118
Q

What kind of insulin is in Humalin I preparations?

A

Isophane

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119
Q

What kind of insulin is in Semglee preparations?

A

Glargine(-yfgn)

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120
Q

What is the mechanism of action of insulin in the treatment of HYPERkalaemia?

A

Insulin drives potassium ions into the cells, reducing serum K+ levels. However, when insulin treatment is stopped K+ leakback out of cells, so this is only a short-term measure while other treatments are initiated.

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121
Q

What is the general mechanism of action of insulin in the treatment of type 1 and 2 diabetes?

A

Insulin stimulates th uptake of glucose from circulaion into tissues, including skeletal muscle and fat, and increasess the use of glucose as an energy source. It also stimulates glycogen, lipid and protein synthesis and inhibits gluconeogenesis and ketogenesis.

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122
Q

Which yp of insulin is used whn IV insulin is required?

A

Soluble inulin (Actrapid)

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123
Q

Which types of insulin (inc. brand names) are typically used in a basal-bolus regimen?

A

Inulin glargine (Lantus) and insulin aspart (NovoRapid)

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124
Q

What is soluble insulin administered with in the treatment of HYPERkalaemia and why?

A

Glucose (20%), to avoid hypoglycaemia

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125
Q

What are the key points when counselling a patient on insulin use?

A
  • Treatment does not replace the need to maintain helthy lifestyle such as exercise and diet
  • Risk of hypoglycaemia and symptoms (i.e. dizziness, agitation, nausea, sweating and confusion)
  • If they should develop hypoglycaemia they should take a sugary snack followed something starchy (i.e. sandwich etc)
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126
Q

If a correction dose of insulin is necessary what kind of insulin should be used and why?

A

Rapid acting insulin such as insulin aspart. Short acting insulins (Actrapid) should be avoided due to the 2-3 hour delay to their peak effect)

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127
Q

Where insulin is being given as a continuous IV infusion what should be monitored in addiion to serum glucose and how often?

A

Serum potassium ion (K+) levels should be monitored every 4 hours ideally to assess whether replacement is required

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128
Q

What should be considered in patients with renal impairment during insulin therapy?

A

The clearance of insulin will be reduced and there will therefore be an increased risk of hypoglycaemia

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129
Q

What are the 3 main types of long acting insulin?

A

Detemir, Glargine and Degludec

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130
Q

What are the 2 main types of rapid acting insulin

A

Aspart and Lispro

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131
Q

What is the main type of intermediate acting insulin?

A

Isophane

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132
Q

What is the main type of short acting insulin?

A

Soluble insulin

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133
Q

Which type of insulin preparations are used in a “twice daily” regimen?

A

Biphasic (rapid acting in combination with a intermediate acting insulin)

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134
Q

What are the indications for thyroid hormones?

A
  1. The treatment of primary hypothyroidism
  2. The treatment of hypothyroidism secondary to hypopituitarism
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135
Q

Levothyroxine is a synthetic version of which thyroid hormone?

A

Thyroxine (T4)

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136
Q

Liothyronine is a synthetic version of which thyroid homone?

A

Triiodothyronine (T3)

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137
Q

What is the mechanism of action of thyroid replacement hormones?

A

The thyroid gland produces thyroxine (T4) which is converted into the more active triiodothyronine (T3) in target tissues. These hormones regulate metabolism and growth and deficiency of these hormones causes hypothyroidism which presents as lethargy, weight gain, constipation and the slowing of mental processes.

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138
Q

Which thyroid hormone replacement is usually reserved for the treatment of severe or acute hypothyroidism?

A

Liothyronine as it has a shorter half-life and quicker onset (a few hours) and offset than levothyroxine.

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139
Q

What are the potential adverse effects associated with the use of thyroid replacement hormones?

A

Usually du to excessive dosing these symptoms are typically similar to those of hyperthyroidism:
Gastrointestinal
- diarrhoea
- weight loss
- vomiting
Cardiac
- palpittions
- arrythmias
- angina
Neurological
- tremor
- restlessness
- insomnia

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140
Q

Do thyroid replacement hormones increase heart rate?

A

Yes

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141
Q

What are the warnings associated wih thyroid hormone replacement therapies such as levothyroxine and liothyronine?

A
  • As thyroid hormones increase heart rate and metabolism they can precipitate cardiac ischaemia in people with coronary artery disease, in whom therapy should be started at a low dose and with careful monitoring
  • In hypopituitarism, corticosteroid therapy must be started before thyroid hormone replacement to avoid the precipitation of Addisonian crisis
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142
Q

How should treatment with thyroid hormone replacement be initiated in patients with coronary artery disease and why?

A

Thyroid replacement should be initiated carefully at a low dose and monitored closely to prevent the preciptation of cardiac ischaemia

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143
Q

How should thyroid hormone replacement therapy be started in patients with hypopituitarism and why?

A

Before thyroid hormone replacement is initiated the patient should be started on coticosteroid therapy to prevent the precipitation of Addisonian crisis

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144
Q

Which medications interact with thyroid hormones?

A
  • Antacids
  • Iron an calcium salts
  • Cytochrome P450 inducers (carbemazepine and phenytoin)
  • Insulin
  • Warfarin
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145
Q

How do thyroid hormones interact with antacids and calcium and iron salts, and what precautions need to be taken?

A

The GI absorption of levothyroxine is reduced by antacids, calcium and iron salts, and as such adminitration of these drugs needs to be separated by at least 4 hours

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146
Q

When does a dose adjustment of levothyroxine need to be considered?

A

In patients taking cytochrome P450 inducers such as carbemazepine or phenytoin

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147
Q

How do thyroid hormones intract with warfarin?

A

Levothyroxine-induced chnges in metabolism can enhance the effects of warfarin

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148
Q

How does levothyroxine interact with insulin?

A

Levothyroxine-induced changes in metabolism can increase insulin and oral hypoglycaemic requirements

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149
Q

What is a typical starting dose of levothyroxine?

A

50-100 micrograms OD

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150
Q

What is a typical starting dose of levothyroxine in elderly patients with cardiac disease?

A

25 micrograms OD

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151
Q

How is liothyronine typically administred?

A

Intravenously

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152
Q

What is a typical maintenance dose of levothyroxine?

A

50-200 micrograms OD

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153
Q

What are the key points when counselling a patient on the use of levothyroxine?

A
  • Treatment is for life
  • It may take some time for them to feel back to “normal”
  • Calcium or iron replacement and antacids should be taken at least 4 hours between these treatments and levothyroxine
  • The signs of too much treatment include shakiness, anxiety, sleeplessness and diarrhoea
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154
Q

How often should thyroid function tests be performed for a patient taking levothyroxine?

A

3 months after initiation and then annually afterwrds

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155
Q

How is dosing guided in the initial weeks and months of treatment with levothyroxine?

A

Dosing is adjusted an guided according to symptoms

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156
Q

What measurement is used as the main guide to dosing with levothyroxine after the first 3 months of treatment?

A

TSH

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157
Q

What symptoms might patients experience shortly after initiating levothyroxine? How should this be dealt with and why?

A

Patients may begin to experience hyperthyroid symptoms shortly after starting levothyroxine. If this happens therapy should be continued at a lower dose while monitoring for reemergence of symptomsof hypothyroidism. Thyroid function tests will be unhelpful at this stage as TSH and T4 will likely be increased; TSH as this takes several weks for this to decrease following initiation of therapy and T4 because of the levothyroxine therapy.

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158
Q

What is a possible cause for a patient to develop symptoms of thyroid dysfunction during treatment with levothyroxine?

A

Switching to a different formulation of levothyroxine

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159
Q

What is the MHRA warning associated with levothyroxine?

A

New prescribing advice for patient who experience symptoms when switching between different levothyroxine products (May 2021)

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160
Q

What should be considered if a patient is switching to a different formulation of levothyroxine?

A

Thyroid function tests should be performed if the patient starts to experience symptoms of thyroid dysfunction. If symptoms are persistent, prescribing a formulation of levothyroxine that the patient is known to consistently tolerant of is recommended. If the patient remains symptomatic try switching the patient to an oral solution formulation.

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161
Q

Can levothyroxine be used in pregnancy and breastfeeding?

A

Yes, the amount excreted in breastmilk is too small to affect neonatal hypothyroidism tets

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162
Q

What are th clinical indications for the use of SGLT2 inhibitors?

A
  • Type 2 diabetes in combination with other antidiabetic drugs or as a monotherapy if metformin is not tolerated
  • Symptomatic chronic heart failure wih reduced ejection fraction, inadequately controlled with a bta-blocker, ACEi, and an aldosterone antagonist
  • Chronic kidney disease with albuminuria, alongside an ACEi or ARB
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163
Q

Name the SGLT2 inhibitors

A
  • Dapagliflozin
  • Empagliflozin
  • Canagliflozin
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164
Q

What is the mechanism of action of SGLT2 inhibitors with regards to the treatment of type 2 diabetes?

A

These drugs selectively and reversibly inhibit the sodium-glucose co-transporter 2 (SGLT2) in the proximal convuluted tubule of the nephron.
SGLT2 mediates active transport of glucose and sodium from filtrate into the blood, controlling the sodium content of the filtrate and recovering most of the filtered glucose.
SGLT2 inhibition impairs glucose resorption in the nephron increasing renal excretion of glucose an treating hyperglycaemia.

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165
Q

What is the mechanism of action of SGLT2 inhibitors with regards to the treatment of chronic heart failure?

A

These drugs selectively and reversibly inhibit the sodium-glucose co-transporter 2 (SGLT2) in the proximal convuluted tubule of the nephron.
SGLT2 mediates active transport of glucose and sodium from filtrate into the blood, controlling the sodium content of the filtrate and recovering most of the filtered glucose.
By increasing renal sodium excretion and water excretion, SGLT2 inhibitors reduce extracellular water volume, blood pressure an cardiac preload.

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166
Q

What is the mechanismof action of SGLT2 inhibitors with regards to the teatment ofchronic kidney disease wih albuminuria?

A

These drugs selectively and reversibly inhibit the sodium-glucose co-transporter 2 (SGLT2) in the proximal convuluted tubule of the nephron.
SGLT2 mediates active transport of glucose and sodium from filtrate into the blood, controlling the sodium content of the filtrate and recovering most of the filtered glucose.
Increased sodium delivery to the macula densa triggers tubuloglomerular feedback mechanisms that reduce intraglomerular pressure

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167
Q

What are the MHRA warnings asociated with the use of SGLT2 inhibitors?

A
  • Risk of diabetic ketoacidosis (April 2016)
  • Monitor ketone levels during treatment interuption for surgical procedures or acute serious medical illness (March 2020)
  • Reports of Fournier’s gangrene (necrotising fasciitis of genitalia or perineum) (February 2019)
  • Dapagliflozin specific -5mg should no longer be used inthetreatment of type 1 diabetes mellitus (November 2021)
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168
Q

When should SGLT2 inhibitors be withheld?

A

SGLT2 inhibitors should be withhld during acute illness (sick day rules) that causes or presnts a risk of volume depletion or hypotension

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169
Q

Which other drugs do SGLT2 inhibitors interact wih and to what effect?

A
  • Glucose lowering medications such as insulin or sulphonylureas, etc - augments their effects - increases the risk of hypogycamia
  • Blood pressure lowering medications - augments their effects - increased risk of hypotension
  • Diuretics - augments their effects - increased risk of volume depletion
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170
Q

What are the most clinically significant potential adverse effects of the use of SGLT2 inhibitors?

A
  • Hpoglycaemia (when use with other hypoglycaemic agents)
  • Increased thirst (due to increased osmotic diuresis
  • Increased risk of genital and urinary infections (due to glycosuria)
  • Euglycaemic ketoacidosis (more common in the treatment of type 1 diabetes mellitus)
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171
Q

What general prescribing advice is given when starting an SGLT2 inhibitor for the treatmen of heart failure or CKD in a diabetic patient?

A

Other antihyperglycaemic medications may have to be ose adjusted to accomodate the glucose lowerin effect of theSGLT2 inhibitor

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172
Q

What is a typical dose of canagliflozin?

A

100mg OD

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173
Q

What is a typical dose of dapagliflozin?

A

10mg OD

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174
Q

What is the simplified mechanism of action of SGLT2 inhibitors?

A

Thy increase the amount of suger passed in the urine, which in turn increases the amount of water passed

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175
Q

How would you establish if a patient being treated with an SGLT2 inhibitor has euglycaemic dibetic ketoacidosis?

A

Check for urinary ketones - withhold the drug, check acid base status (e.g.by arterial blod or venous blood gas analysis) and seek expert advise

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176
Q

When should SGLT2 inhibitors be restarted after they have been withheld in acute illness?

A

When the patient feels better (i.e. is asymptomatic)

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177
Q

When should renal function be checked with regards to the use of SGLT2 inhibitors?

A

Before initiation and at least annually afterwards

178
Q

When should SGLT2 inhibitors be stopped and what monitoring should be carried out?

A

In acute illness, especially if it requires hospital admission.
The patient should be monitored for signs of dehydration, hypovalaemia, and hypotension.

179
Q

How long does treatment with an SGLT2 inhibitor typically last for?

A

Indefinitely

180
Q

What are some conditions in which corticosteroids are typically used?

A
  • Inflammatory conditions of the skin
  • Ulceratice colitis
  • Crohn’s disease
  • Haemorrhoids
  • Postural hypotension (fludrocortisone acetate)
  • Septic shock resulting from adrenal insufficiency (hydrocortisone and fludrocortisone)
  • Adrenal hyperplasia (dexamethasone and betamethasone)
  • Raised intracranial pressure or cerebral oedema
  • Asthma and COPD
  • Rheumatoid arthritis
  • Autoimmune hepatitis
181
Q

In which conditions may high doses of corticosteroids need to be given?

A
  • Exfoliative dermatitis
  • Pemphigus
  • Acute luekemia
  • Transplant rejection
182
Q

What is an unlicensed use for dexamethasone?

A

Bacterial meningitis

183
Q

Which corticosteroids are licensed for adjunct treatment of Covid-19 requiring supplemental oxygen?

A

Dexamethasone
Hydrocortisone (when dex is unavailable)

184
Q

What is the most common endogenous cause of Cushing’s syndrome?

A

Tumours secreting adrenocototrophic hormone or cortisol

185
Q

Which medications are used to treat Cushing’s syndrome?

A
  • Ketoconazole
  • Metyrapone
  • Osilodrostat
186
Q

What is the basic mechanism of action of oral ketoconazole for the treatment of Cushing’s syndrome?

A

Ketoconazole is an imidazole derivative which acts as a potent inhibitor of cortisol and aldosterone synthesis

187
Q

What is the aim of treatment when treating a patient with Cushing’s syndrome?

A

To lower cortisol to normal endogenous levels

188
Q

What does HbA1c represent?

A

HbA1c reflects the average plasma glucose over the previous 2-3 months

189
Q

What HbA1c level is considered diabetic?

A

> 48mmol/mol

190
Q

What is a normal HbA1c in a non-diabetic person?

A

<36 mmol/mol

191
Q

What are the clinical indications for the use of bisphosponates?

A
  1. Prevention of osteoporotic fragility fractures (alendronic acid is the first line)
  2. Severe hypercalcamia of malignany (pamidronate and zoledronic acid)
  3. Myeloma and breat cancer wih bone metatases (pamidronate and zoledronic acid)
  4. Paget’s disease of the bone
192
Q

What is the mechanism of action of bisphosphonates?

A

They reduce bone turnover by inhibiting the action and promote apoptosis of oseoclasts, the cells responsible for bone resorption. Bisphosphonates have a similar structure tonaturally occurring pyrophosphate and hence they are readily incorporated into the bone.

193
Q

What are the MHRA warnings associated with the use of bisphosphonates?

A
  • Atypical femoral fractures
  • Osteonecrosis of the jaw
  • Osteonecrosis of the external auditory canal
194
Q

What are the most prevalent side effects of biphosphonate use?

A
  • Oesophagitis
  • Hypophosphataemia
  • Osteonecrosis of the jaw
  • Atypical femoral fractures
195
Q

How are bisphosphonates excreted?

A

Renally

196
Q

Can bisphosphonates be used in renal impairment?

A

They should be avoided in severe renal impairment

197
Q

In the presence of which conditions is the use of bisphosphonates contraindicated?

A

Hypocalcaemia
Upper GI disorders

198
Q

Which substances reduce the absorption of bisphosphonates?

A
  • Calcium salts
  • Iron salts
  • Antacids
199
Q

How are zoledroic acid an pamidronate typically administered?

A

Intravenously

200
Q

After what duration of alendronic acid use should a “bisphosphonates holiday” be considered?

A

5 years

201
Q

What are the key points when counselling a patient on the use of alendronic acid, particularly with regards to administration?

A
  • Take 30 minutes before any food, drink or other medication
  • Must remain upright for at least minutes after taking
  • Maintain good oral hygeine
  • Be vigilant for hip or lower limb pain
202
Q

What are the clinical indications for the use of oestrogens and progestogens?

A
  1. Hormonal contraception in patients who required highly effective and reversible contraception, particularly if the may also benefit its other effects such as improved acne symptoms with oestrogens
  2. Hormone replacement therapy to delay early menopause in woen <50yo and to treat distressing menopausal symptoms at any age
203
Q

What is the mechanism of action of oestrogens and progestogens as contraceptives and as hormone replacement therapy?

A

Luteinising homone (LH) and follicle-stimulating hormone (FSH) control ovulation and ovarian production of oestrogen an progesterone.
In turn oestrogen and progesterone exert negative feedback on LH and FSH release.
In contraception, oestrogen and and/or progestrogens are given to suppress LH and FSH release and therefore ovulation.
They also act outise of the ovary. Their action in the cervix and endometrium contribute to their contraceptive effect.
Where in menopause, ymptoms are predominantly caused by a drop in oestrogen and progestrogen levels, replacement of these hormones can alleviate the symptoms.

204
Q

What are some important adverse effects associated with the use of oestrogens and progestrogens?

A
  • Irregular bleeding
  • Mood changes
  • 2x the risk of venous thromboembolism (Oestrogens in CHC)
  • Increased risk of cardiovascular disease and stroke (Oestrogens in CHC)
  • Increased risk of breast and cervical cancer
205
Q

Do oestrogens and progestrogens cause weight gain?

A

No

206
Q

Which kind of oral contraceptive does not increase the risk of VTE or cardiovascular disease?

A

Progesterone-only pills

207
Q

In what condition is the use of all oestrogens and progestrogens contraindicated in?

A

Breast cancer

208
Q

In which conditions should the use of CHCs be avoided?

A
  • VTE
  • Cardiovascular disease
209
Q

Which group of medications may reduce the efficacy of contraceptives, particularly progestrogen-only formulations?

A

Cytochrome P450 inducers:
- Rifampicin
- Carbemazepine

210
Q

The efficacy of which anti-epileptic medication is lowered in concurrent use with oral contraception?

A

Lamotrigine

211
Q

What dose of ethinylestradiol is appropriate for most women?

A

30-35 micrograms

212
Q

What is an appropriate alternative oral contraceptive where CHC is contraindicated?

A

Progesterone-only pill

213
Q

What is the preferred formulation/therpy type of HRT for most women?

A

Combined oestrogen-progestrogen therapy

214
Q

What type of formulation is best for treating women with just vaginal symptoms during menopause?

A

Vaginal oestrogen preparations

215
Q

How many days of missed oral contraception necessitates use of additional contraeptive precautions, and for how longshoul these precautions be taken?

A

2 doses
7 days

216
Q

If started when during a women’s cycle, does no additional contraceptive method need to be used when initiating oral contraceptive pills?

A

In the first 6 days - if started from day 7 onwards a barrier contraceptive should be used in addition to the pill

217
Q

How are most combined formulations of hormonal contracetion meant to be taken?

A

Take for 21 days followed by a 7 day pill-free interval

218
Q

Is continuous use (without pill-free intervals) of COC pills licensed?

A

No, but it is safe and effctive

219
Q

What is one benefit (subjective) of the continued use of COC pills without pill-free period?

A

It eliminates or reduces withdrawal bleeding which some women may find desirable

220
Q

What are the monitoring requirements when initiating COC pills?

A

Baseline BMI and BP
Repeated after 3 months and then annually thereon

221
Q

What is the risk of starting combined HRT more than 10 years after menopause?

A

Increased risk of coronary heart disease

222
Q

Which preparation type of HRT has an associated increased risk of breast cancer?

A

Combined oestrogen-progestrogen prepartions

223
Q

To which drug class does gentamicin belong to?

A

Aminoglycosides

224
Q

To which drug class does amikacin belong to?

A

Aminoglycosides

225
Q

To which drug class does neomycin belong to?

A

Aminoglycosides

226
Q

Which aminoglycoside is typically used topically?

A

Neomycin

227
Q

Which aminoglycosides are typically used systemically?

A

Gentamicin and amikacin

228
Q

Aminoglycosides are typically indicated for the treatment of which kinds of bacteria?

A

Gram-negative aerobes

229
Q

What are the clinical indications for the use of aminoglycoside antibiotics?

A
  1. Treatment of severe sepsis (inclusing those where the source is unidentified)
  2. Pyelonephritis and complicated urinary tract infections
  3. Biliary and intraabdominal sepsis
  4. Endocarditis
  5. Bacterial skin, eye, or external ear infections
230
Q

What should aminoglycoside antibiotics be paired with when the cause of an infection is unknown?

A

Penicillin and/or metronidazole

231
Q

Do aminoglycosides have any activity against anaerobes?

A

No

232
Q

What MHRA warning is associated with the use of all aminoglycosides?

A

Increased risk of deafness in patients with mitochondrial mutations (January 2021)

233
Q

What MHRA warning is associated with the use of gentamicin?

A

Potential of histamine-related adverse reactions with some batches (November 2017)

234
Q

What are the most important adverse effects associated with the use of aminoglycosides?

A
  • Nephrotoxicity
  • Ototoxicity

Ototoxicity may be irreversible and usually not noticed until treatment of acute infection is finished

235
Q

How are aminoglycosisdes excreted?

A

Renally

236
Q

In which condition is the use of all aminoglycosides contraindicated?

A

Myasthenia gravis

237
Q

Ototoxicity is more likely when aminoglycosides are co-prescribed with which other drugs?

A
  • Loop diuretics
  • Vancomycin
238
Q

Nephrotoxicity is more likely when aminoglycosides are co-prescribed with which other drugs?

A
  • Ciclosporin
  • Cephalosporins
  • Platinum chemotherapies
  • Vancomycin
239
Q

Can aminoglycosides be given orally?

A

No, they are highly polarised and therefore cannot cross the lipid membranes of the gut

240
Q

How should amoniglycosides be administered?

A

They should be diluted in NaCl 0.9% solution and infused slowly as to not expose the ears to high bolus concentrations that may lead to to ototoxicity

241
Q

How is treatment with aminoglycosides monitored?

A
  • Symptomatically - C-reactive protein levels
  • Safety - Reanl function measured before and during treatment
  • Serum drug concentrations - the next dose should only be given if this concentration is within safe levels
242
Q

During aminoglycosides therapy, if the pre-dose (trough) serum drug concentration is too high what action must be taken in both adults and children?

A

The interval between doses must be increased

243
Q

When should serum drug levels be measured in patients receiving gentamicin therapy?

A

Pre-dose and 1 hour after administration

244
Q

In a ‘multiple daily dose’ regimen of gentamicin what should the pre- and post-dose serum concentrations levels ideally be in both adults and children?

A

Pre-dose (trough) = 5 -10mg/L
Post-dose = <2mg/L

245
Q

In a ‘multiple daily dose’ regimen of gentamicin specifically for the treatment of endocarditis what should the pre- and post-dose serum concentrations levels ideally be in both adults and children?

A

Pre-dose (trough) = 3 - 5mg/L
Post-dose = <1mg/L

246
Q

To which rug class does tobramycin belong to?

A

Aminoglycosides

247
Q

What is the basic mechanism of action of the aminoglycosides and which microbes are they effective against

A

Aminoglycosides bind irreversible to bacterial ribosomes and inhibit protein synthesis.They enterbacterial cells through oxygen-dependent transport systems whichstreptococci and anaerobic bacteria lack, making them ineffective in the treatment of these organisms.
Aminoglycosides are effective against Gram-negative anaerobic bacteria.

248
Q

Name some antifungal medications

A
  • Clotrimazole
  • Fluconazole
  • Nystatin
249
Q

What are the clinical indications for the use of antifungal agents?

A
  1. Treatment of local fungal infections (oropharynx, vagina, and skin) orally or topically
  2. Treatment of invasive or disseminated fungal infections
250
Q

What is the basic mechanism of action of the antifungal agents?

A

Fungal cell membranes contain ergostrel, which is not found on animal or human cells, and it is this that is the target for the antifungals. Imidazole and triazole antifungals prevent the synthesis of ergostrel, which in turn inhibits cell membrane synthesis, while polyene antifungals bind to ergostrel and allow ions to leak through the cell membrane.

251
Q

What are the the 3 main types of antifungal agents?

A
  1. Imidazole (clotrimazole)
  2. Polyene (nystatin)
  3. Triazole (fluconazole)
252
Q

What are he adverse effects associated with the use of topical antifungals such as clotrimazole and nystatin?

A

There are very few except for occasional local irritation

253
Q

What are the most common adverse effects associated with the use of systemic antifungals such as fluconazole?

A
  • GI upset
  • Headache
  • Hepatitis
  • Hypersensitivity skin reactions
254
Q

What severe adverse effets are associated with the use of systemic antifungal agents such as fluconazole?

A
  • QT interval prolongation which can lead to arrythmias
  • Severe hepatic toxicity
  • Hypersensitivity reactions such as anaphylaxis and severe cutaneous reactions
255
Q

Can fluconazole be used in pregnancy and breastfeeding?

A

It should be avoided in pregnancy but can be used during breastfeeding

256
Q

When should caution be advised with the use of fluconazole?

A

In patients with hepatic impairment due to the increased risk of hepatic toxicity
Dose adjustments are required in patients with moderate renal impairment

257
Q

Fluconazole interacts with which drugs and to what extent?

A
  • Drugs that are metabolised by P450 enzymes such as carbemazepine, phenytoin, warfarin, diazepam, simvastatin, and sulphonlyureas
  • Reduces the antiplatelet effect of clopidogrel which is metabolised in the liver
  • Increases the risk of arrythmias when used in combination with drugs that potentially prolong the QT interval such as amiodarone, antipsychotics, quinine, quinolones, macrolides, and SSRIs
258
Q

How should oral nystatin be administered?

A

It should be taken after food and held in the mouth to allow for good contact with lesions - dentures must be removed before use

259
Q

What is a typical topical dose of nystatin for the treatment of thrush?

A

100,000 units QD for 7 days

260
Q

What is a typical short course dose of fluconazole?

A

150mg OD

50mg OD for prolonged (2 weeks) courses

261
Q

How long after symptoms after resolved should treatment be continued for topical antifungals?

A

1 - 2 weeks after symptoms have resolved

262
Q

What should be monitored in prolonged courses of fluconazole?

A
  • Liver enzymes
  • Symptoms of liver dysfunction
263
Q

Which type of drugs increase the risk of oral thrush?

A

Inhaled corticosteroids

When used in addition to antibiotic and antimuscarinics this risk is increased further

264
Q

What are the common clinical indications for the use of antivirals such as aciclovir?

A
  1. Treatment of acute episodes of herpesvirus infections
  2. Suppression of recurrent herpes simplex attacks (where they are occurring 6 or more times a year)
265
Q

What is the basic mechanism of action of aciclovir?

A

Aciclovir inhibits herpes-specific DNA polymerase which stops any further viral DNA synthesis

266
Q

What are the potentail adverse effects of associated with the use of aciclovir?

A
  • GI upset
  • Headache
  • Dizziness
  • Skin rash
  • Acute renal failure (IV administration only)
267
Q

When is aciclovir contraindicated?

A

Aciclovir has no major contraindications

268
Q

Can aciclovir be used in pregnancy and breastfeeding?

A

Aciclovir does cross into the placenta and is expressed in breastmilk so caution is advised or its use during pregnancy and breastfeeding

The potential harm caused by viral conditions with which aciclovir is used to treat often outweight the risks of using aciclovir itself in pregnancy and breastfeeding

269
Q

When is a dose adjustment of aciclovir required?

A

In severe renal impairment

270
Q

Which drugs interact with aciclovir?

A

Aciclovir has no clinically important drug interactions

271
Q

Name some of the viral conditions in which the use of aciclovir is indicated

A
  • Oral herpes
  • Genital herpes
  • Herpes simplex encephalitis
  • Varicellar-zoster (chickenpox and shingles)
272
Q

What should be monitored during the use of aciclovir?

A
  • Symptomatic efficacy
  • Renal function
273
Q

What are the clinical indications of cephalosporins and carbapenems?

A
  1. Oral cephalosporins are second- and third-line options for the treatment of urinary and respiratory tract infections
  2. Parenteral cephalosporins and cerbapenems are reserved for severe infections and complicated infections caused by antibiotic resistance
274
Q

What spectrum of action to cephalosporins and carbapenems have?

A

Broad spectrum

275
Q

What kind of bacteria do cephalosporins have increasing activity against?

A

Gram-negative bacteria

276
Q

What is the basic mechanism of action of cephalosporins and carbapenems?

A

Cephalosporins and carbapenems inhibit the enzymes responsible for cross-linking peptidoglycans in bacterial cell walls using their beta-lactam rings. This causes a weakened cell wall, lysis and bacterial cell death

277
Q

Name the most commonly prescribed cephalosporins

A
  • Cefalexin
  • Ceftriaxone
278
Q

Name the most commonly prescribed carbapenems

A
  • Meropenem
  • Ertapenem
279
Q

What are the important adverse effects related to the use of cephalosporins and carbapenems?

A
  • GI upset
  • Increased risk of c.diff
  • Antibiotic collitis
  • Hypersensitivity reactions
  • Increased risk of neurological toxicity leading to seizures

Neurological toxicity is is a risk particularly where carbapenems are being used in high doses in patients with renal impairment

280
Q

Which group of antibiotics do cephalosporins and carbapenems share allergic cross-sensitivity?

A

Penicillins

281
Q

When is the use of cephalosporins and carbapenems contraindicated?

A

History of allergy to penicillin - particularly if it was a serious reaction such as anaphylaxis

282
Q

When should carbapenems be used with caution?

A

R- Patients with epilepsy
- Patients at risk of c.diff
- renal impairment

283
Q

When should cephalosporins be used with caution?

A
  • Patients at risk of c.diff
  • Renal impairment
284
Q

Which drugs do cephalosporins and carbapenems interact with?

A
  • Warfarin - Increases the anticoagulant effect by killing gut flora that synthesises vitamin K
  • Aminoglycosides - Increases the nephrotoxicity of aminoglycosides (Cephalosporins
  • Valproate - Reduces the plasma concentration and efficacy of valproate (carbapenems)
285
Q

How are carbapenems administered?

A

Intravenously

286
Q

When are IV cephalosporins used?

A

In severe infections

287
Q

How often is ertapenem administered?

A

Once daily

288
Q

What drug class does ertapenem belong to?

A

Carbapenems

289
Q

How is treatment with cephalosporins and carbapenems monitored?

A

Symptomatically and using blood test markers such as c-reactive protein

290
Q

Why is the use of second- and third-generation cephalosporins particularly restricted in most hospital trusts?

A

Because of the frequency of which antibiotic-associated collitis occurs with the use of these medications

291
Q

What are the clinical indications for the use of chloramphenicol?

A
  1. Bacterial conjuctivitis using eye drops
  2. Otitis externa using ear drops
292
Q

Why is oral chloramphenicol rarely used?

A

It is highly toxic to bone marrow when used systemically

293
Q

What spectrum of activity does chloramphenicol have?

A

Chloramphenicol has a broad spectrim of activity and is effective against gram-positive and gram-negative bacteria, as well as aerobes and anaerobes

294
Q

What is the basic mechanism of action of chloramphenicol?

A

Chloramphenicol binds to bacterial ribosomes inhibiting protein synthesis. It is therefore bacteriostatic meaning that it simply prevents the growth of bacteria

AT high enough doses it can be bactericidal

295
Q

What are the most common adverse effects of chloramphenicol use when applied topically?

A
  • Stinging
  • Burning
  • Itching
296
Q

When is a dose adjustment of systemic chloramphenicol required?

A

In patients with hepatic impairment

297
Q

Where is chloramphenicol metabolised?

A

Liver

298
Q

When is the use of chloramphenicol contraindicated?

A
  • In patients with personal or family history of bone marrow disorders
  • In patients with previous hypersensitivity reactions
  • Third trimester of pregnancy
  • Breastfeeding
  • Children <2 years of age
299
Q

What significant interactions does chloramphenicol have with other drugs?

A

Chloramphenicol has no significant interactions with other medications when used topically

300
Q

How often should chloramphenicol 0.5% eye drops be applied?

A

Every 2 hours, then reduced to QD when infection comes under control

301
Q

How often should chloramphenicol (5-10%) ear drops be applied?

A

4 drops, 2 - 3 times daily for 7 days

302
Q

How often should chloramphenicol (1%) eye ointment be applied?

A

3 - 4 times daily

303
Q

Can chloramphenicol eye drops be used in the ear, and can chloramphenicol ear drops be used in the eye?

A

Chloramphenicol eye drops can safely be used in the ear, though they will be less effective than ear drops. Chloramphenicol ear drops cannot be used in the eyes.

304
Q

What advice regarding contact lenses needs to be given to patients using chloramphenicol eye drops?

A

Eye drops can become damaged by the preservatives in the eye drops, causing transient blurred vision. All contact lenses should be avoided in eye infection.

305
Q

Which group of antibiotics end in the suffic ‘mycin’

A

Macrolides

306
Q

List the macrolides

A
  • Erythtomycin
  • Clarithromycin
  • Azithromycin
307
Q

What are the clinical indications for the use of macrolides?

A
  1. Treatment of respiratory, skin and soft tissue infections as an alternative to penicllin when its use is contraindicated
  2. Severe pneumonia in addition to a penicillin to cover atypical organisms such as Legionella pneumophilia and Mycoplasma pneumoniae
  3. Elimination of Helicobacter pylori in combination with a PPI and either amoxicillin or metronidazole
308
Q

What spectrum of antibacterial activity do the macrolides possess?

A

Erythromycin possess a broad spectrum of activity against gram-negative and gram-positive bacteria.
Newer synthetic macrolides (clarithromycin and azithromycin) have increased activity against gram-negative bacteria, particularly Haemophilus influenzae.

309
Q

What is the basic mechanism of action of macrolide antibiotics?

A

Macrolides inhibit bacterial protein synthesis by binding to the 50S subunit of the bacterial ribosome and blocking translocation. They are therefore bacteriostatic as they do not actually kill the bacteria.

310
Q

Why is resistance to macrolides common?

A

Due to mutations in the bacterial ribosome

311
Q

Which macrolide has an increased adverse effects profile?

A

Erythromycin

312
Q

What are the important adverse effects associated with the use of all macrolides?

A
  • Macrolides are irriatants and cause GI upset such as nausea, vomiting, diarrhoea, and abdominal pain when given orally, and when thrombophlebitis when given intravenously
  • Antibiotic-associated colitis
  • Cholestatic jaundice
  • Prolongation of the QT interval
  • Ototoxicity
313
Q

When is dose adjustment required for the administration of macrolides?

A

Macrolides are excreted hepatically with a small renal component, and as such need dose reducing in severe hepatic and renal impairment

314
Q

Which drugs interact with macrolides and to what extent?

A
  • Warfarin - enhances their anticoagulant effect increasing the risk of bleeding
  • Statins - increased risk of myopathy
  • Amiodarone - risk of QT prolongation
  • Antipsychotics - risk of QT prolongation
  • Quinines - risk of QT prolongation
  • Quinolones - risk of QT prolongation
  • SSRIs - risk of QT prolongation
315
Q

How are each of the macrolides dosed?

A

Erythromycin - 250 - 500mg 6 hourly
Clarithromycin 250 - 500mg 12 hourly
Azithromycin 250 - 500mg daily

The frequency of dosing is dictated by how heavily each is concentrated in the tissues

316
Q

How must macrolides be administered intravenously?

A

They must be diluted in a large volume of NaCl 0.9% and infused over at least 60 minutes. They cannot be given as IM injections or as bolus IV.

317
Q

In LRTIs when should macrolides be added and why?

A

Macrolides should only be added in LRTIs when there is evidence of pneumonia, as macrolides provide atypical cover of Legionella pneumophila and Mycoplasma pneumoniae which cause pneumonia but nother LRTIs such as COPD exacerbations.

318
Q

What is the spectrum of activity for metronidazole?

A

Anaerobic bacteria and protozoa

319
Q

What are the clinical indications for the use of metronidazole?

A
  1. Antibiotic-associated colitis caused C.diff
  2. Oral infections or aspiration pneumonia caused by gram-negative anaerobes
  3. Surgical and gynaecological infections caused by gram-negative anaerobes
  4. Protozoal infections
320
Q

What type of organism is C.diff?

A

Gram-positive anaerobic bacteria

321
Q

What is the basic mechanism of action of metronidazole?

A

Metronidazole is reduced by anaerobic bacteria generating a free radical which binds to bacteria DNA causing widespread degradation and cell death

Aerobic bacteric cannot reduce metronidazole in this manner

322
Q

What are the main adverse effects associated with the use of metronidazole?

A
  • GI upset
  • Hypersensitivity reactions
  • Neurological effects such as: seizures, peripheral and optical neuropathy, and encephalopathy (mainly when used at high doses for prolonged duration)
  • Sensitivity to sunlight when used topically
323
Q

How is metronidazole metabolised?

A

Metronidazole is metabolised by hepatic cytochrome P450 enzymes

324
Q

What should be avoided during metronidazole treatment?

A

Alcohol should not be consumed during treatment with metronidazole

Metronidazole inhibits the enzyme responsible for clearing the immediate metabolic product of alcohol, and concurrent use of the two causes disuliram-like reactions such as flushing, headache, vomiting

325
Q

Is metronidazole an inducer or an inhibitor?

A

Inhibitor of cytochrome P450

326
Q

What are some important interactions between metronidazole and other drugs/classes?

A
  • Warfarin - increased risk of bleeding
  • Phenytoin - increased risk of otoxicity / reduced efficacy of metronidazole
  • Rifampicin - reduced efficacy of metronidazole
327
Q

What is a typical oral dose and frequency of oral metronidazole?

A

400mg every 8 hours

328
Q

What is a typical IV dose and frequency of IV metronidazole?

A

500mg every 8 hours

IV metronidazole is reserved for severe infections of where patients are nil by mouth

329
Q

Which antibiotics interact with alcohol?

A
  • Metronidazole (disulfarim-like reaction)
  • Co-trimoxazole (dislfarim-like reaction - rare)
  • Doxycycline (delays effectiveness)
  • Erythromycin (delays effectiveness)
330
Q

What needs to be monitored during treatment with metronidazole?

A
  • Symptoms
  • Inflammatory markers (CRP)
  • In a course exceeding 10 days - FBC and LFTs
331
Q

What is the MHRA warning associated with the use of nitrofurantoin?

A

Reminder of the risk of pulmonary and hepatic adverse drug reactions (April 2023)

332
Q

What are the clinical indications for the use of nitrofurantoin?

A
  1. Treatment of uncomplicated lower urinary tract infection
  2. Prophylaxis of recurrent UTI
333
Q

What are some alternatives to nitrofurantoin for the treatment of uncomplicated UTI?

A
  • Trimethoprim
  • Amoxicillin
  • Cefalexin
334
Q

What is the spectrum of activity of nitrofurantoin?

A

Nitrofurantoin has a broad spectrum of activity against most UTI causing organisms

E.coli (Gram-negative) and S.saprophyticu (Gram-positive)

335
Q

What is the basic mechanism of action of nitrofurantoin?

A

The primary metabolite when nitrofurantoin is reduced by bacteria damages bacterial DNA and causes cell death

336
Q

What are some important adverse effects associated with the use of nitrofurantoin?

A
  • GI upset
  • Hypersensitivity reactions
  • Discolouration of urine to dark yellow or brown
  • Chromic pulmonary reactions
  • Hepatitis
  • Peripheral neuropathy
337
Q

When is the use of nitrofurantoin contraindicated?

A
  • In pregnant women approaching term
  • In babies in their first 3 months of life
  • Renal impairment
338
Q

What interactions are there between nitrofurantoin and other drugs/classes?

A

There are no significant interactions between nitrofurantoin and other comonly prescribed drugs

339
Q

What is the typical duration of treatment with nitrofurantoin for women with an uncomplicated lower UTI infection?

A

3 days is usually sufficient

340
Q

When is a 7 day or longer course of nitrofurantoin required?

A
  • UTIs in men
  • More complicated lower UTIs
341
Q

What are the key points when counselling a patient on the use of nitrofurantoin?

A
  • May colour urine dark yellow or brown, this is harmless
  • Notify Dr if they experince symptioms of peripheral neuropathy or pulmonary reactions such as pins and needles or breathlessness respectively
342
Q

What are the common clinical indications for the penicillins benzylpenicillin and phenoxymethylpenicillin?

A
  1. Streptococal infection, including tonsilitis, pneumonia (with a macrolide or tetracycline), endocarditis (with gentamicin) and skin and soft tissue infections (with flucloxacillin)
  2. Meningococcal infection
  3. Clostridial infection
343
Q

What is the spectrum of activity of benzylpenicillin and phenoxymethylpenicillin?

A

Narrow - activity against some gram-positive and gram-negative organisms

344
Q

What is the basic mechanism of action of the penicillins benzylpenicillin and phenoxymethylpenicillin?

A

Using their beta-lactam rings they inhibit the enzymes responsible for cross-linking peptidoglycans in bacterial cell walls; this creates an osmotic imbalance (draws in water) that causes cell lysis and death

345
Q

What are some important adverses effects associated with the use of penicillins?

A
  • Allergic reactions inclusing skin reactions or anaphylaxis
  • Neurological toxicity (when used at very high doses or due to renal impairment)
346
Q

When is the use of penicillins contraindicated?

A

In peniciliin allergy

347
Q

What are the important interactions between penicillins and other drugs/classes?

A

Penicillins reduce the renal excretion of methotrexate increasing the risk of toxicity

348
Q

How is benzylpenicllin administered?

A

It can only be administered via IV or IM injection as it cannot be absorbed by the GI tract

349
Q

Which antibiotic should be used to treat sore throat or a young person caused by an unknown organism and why?

A

Phenoxymethylpenicillin should be used as opposed to amoxicillin. This is because amoxicillin commonly causes rash if the causative agent is Epstein-Barr virus

350
Q

What is the most commonly prescribed antipseudomonal penicillin?

A

Piperacillin with tazobactam (Tazocin)

351
Q

What are the common indications for the use of Tazocin?

A
  1. LRTIs
  2. UTIs
  3. Intraabdominal sepsis
  4. Skin and soft tissue infections
352
Q

What is the spectrum of activity of Tazocin?

A

Broad range of activity against gram-positive, gram-negative, and anaerobic organisms

353
Q

What are the important adverse effects associated with the use of Tazocin?

A
  • GI upset
  • Antibiotic colitis
  • Increased risk of C.diff (all broad spectrum antibiotics)
  • Hypersensitivity reactions
354
Q

When should antipseudomonal antibiotics be used with caution?

A
  • In patients with C.diff
  • Dose adjusted in patients with moderate/severe renal impairment
355
Q

Which drugs/classes interact with Tazocin and to what effect?

A
  • All penicillin reduce the renal excretionof methotrexate and therefore increse the risk of toxicity
  • As a broad spectrum Abx, Tazocin enhances the effect of warfarin by killing GI flora that synthesise vitamin K
356
Q

How long is a typical course of Tazocin?

A

5 - 14 days

4.5g every 4 - 6 hours

357
Q

What needs to be taken into account when considering electrolyte replacement for a patient being treated with Tazocin?

A

Each dose of Tazocin contains 11mmol of Na and is often infused in NaCl 0.9%

358
Q

What are the most commonly prescribed broad-spectrum penicillins?

A

Co-amoxiclav
Amoxicillin

359
Q

What are the common clinical indications for the use of the broad spectrum penicillins?

A
  1. Amoxicllin is used to treat a variety of infections such as CAP, otitis media, sinusitis, and UTIs
  2. Helicobacter pylori-associated infections (amoxicillin used with clarithromycin or metronidazole and a PPI)
  3. Co-amoxiclav is used for the treatment of severe hospital-acquired infections)
360
Q

What is the spectrum of activity of amoxicillin?

A

Broad spectrum

361
Q

What is the spectrum of activity of co-amoxiclav?

A

Broad spectrum

362
Q

What are the important potential adverse effects associated with the use of broad-spctrum penicillins?

A
  • GI upset
  • Increased risk of C.diff
  • Antibiotic-associated colitis
  • Allergic reactions
363
Q

What is an adverse effect associated with the use of co-amoxiclav but not amoxicillin?

A

Acute liver injury (generally self-limiting)

364
Q

When should broad-spectrum penicillins be used with caution?

A
  • Patients with C.diff
  • Patients with a history of acute liver injury
  • Dose adjustments required in severe renal impairment
365
Q

With drugs do the broad-spectrum penicillins interact with?

A
  • Warfarin - broad spectrum antibiotics kill the GI flora that synthesise vitamin K
366
Q

What are the benefits of prompt IV-to-oral switching of antibiotics?

A

Reduces the adverse effect risk profile and cost of treatment

367
Q

What is the most commonly prescribed penicillinase-resistant penicillin?

A

Flucloxacillin

368
Q

What are the common clinical indications for the use of penicillinase-resistant penicillins?

A

Straphylococcal infection, usually as part of a combination therapy, including:
1. Skin and soft tissue infections
2. Osteomyelitis and septic arthritis
3. Other infections including endocarditis

369
Q

How does flucloxacillin differ from other penicillins?

A

It has a acyl side chain that protects its beta-lactam ring making it effective against beta-lactamase-producing staphylococci

370
Q

Which organism resists the activity of flucloxacillin by reducing its binding activity?

A

MRSA

371
Q

What are some important adverse effects associated with the use of flucloxacillin?

A
  • GI upset
  • Allergic reactions
  • Liver toxicity
372
Q

When is the use of flucloxacillin contraindicated?

A
  • Penicillin allergy
  • History of flucloxacillin-related hepaticotoxicity
373
Q

Which drugs interact with flucloxacillin and to what extent?

A

Flucloxacillin reduces the renal excretion of methotrexate and increases the ris of toxicity

374
Q

What are the common clinical indications for quinine sulfate?

A
  1. Leg cramps (depending on the severity of the case)
  2. Treatment of Plasmodium falciparum malaria
375
Q

What is the basic mechanism of action of quinine sulfate?

A

It reduces the excitability of the motor end plate in response to acetylcholine, helping to reduce leg cramps
The exact mechanism of action in the treatment of malaria is unknown outside of the fact it kills the malaria parasites

376
Q

What are some important adverse effects associated with the use of quinine?

A
  • GI upset
  • Tinnitus, deafness, blindness
  • Prolongation of the QT interval
  • Potentially fatal overdose
377
Q

When should be quinine be used with caution?

A
  • Patients with a history of sight or hearing loss
  • It is teratogenic and should be avoided in the first trimester of pregnancy but the ebenefits may outweigh the risks
  • It should be avoided in patients with G6PD deficiency
378
Q

Which drugs interact with quinine?

A

Drugs that prolong the QT interval:
- Quinolones
- Macrolides
- SSRIs
- Amiodarone
- Antipsychotics

379
Q

What is quinine sulfate commonly given alongside for the treatment of malaria?

A

Doxycycline

380
Q

At what dose and for how long is a trial of treatment of nocturnal leg cramps with quinine sulfate?

A

200 - 300mg ON for 4 weeks

If after 4 weeks there is no benefit then treatment should be stopped

381
Q

If trial treatment of nocturnal leg cramps is successful when should quinine treatment be reviewed and potentially stopped?

A

After 3 months of treatment

382
Q

Which group of drugs uses the suffix ‘floxacin’?

A

Quinolones

383
Q

What are the most commonly prescribed quinolones?

A

Ciprofloxacin
Moxifloxacin
Levofloxacin

384
Q

What are the common clinical indications for the use of the quinolones?

A

Quinolines are reserved as second- and third-line treatments of:
- UTIs (mostly gram-negative)
- Severe gastroenteritis
- LRTIs (gram-positive and gram-negative)

385
Q

What is the spectrum of activity of quinolones?

A

Broad spectrum of activity with particular activity against gram-negative bacteria

386
Q

Newer quinolones such as moxifloxacin and levofloxacin have enhanced activity against which spectrum of bacteria?

A

Gram-positive

387
Q

How is ciprofloxain unusual as an oral antibiotic?

A

It has particular activity against Pseudomonas aeruginosa

388
Q

What is the basic mechanism of action of the quinolone antibiotics?

A

They kill bacteria by inhibiting bacterial DNA synthesis

389
Q

Which groups of antibiotics are most comonly associated with C.difficile colitis?

A

Cephalosporins
Quinolones

390
Q

What are the common adverse effects associated with the use of quinolone antibiotics?

A
  • GI upset
  • Hypersensitivity reactions
  • Lowering of the seizure threshold
  • Inflammation and rupture of tendons
  • Prolongation of QT interval
  • Increased risk of C.diff
391
Q

What are the MHRA warnings associated with the use of quinolone antibiotics?

A
  1. Systemic and inhaled fluoropuinolones: small increased risk aortic aneurysm and dissection (November 2018)
  2. Fluoroquinolone antibiotics: new restrictions and precautions for use due to very rare reports of disabling and potentially long-lasting or irreversible side effects (March 2019)
  3. Systemic and inhaled fluoroquinolones: small risk of heart valve regurgitation; consider other therapeutic options first in patients at risk (December 2020)
392
Q

When should quinolones be used with caution?

A
  • History of seizures
  • Children and growing young people
  • Those with other risk factors for QT prolongation
393
Q

Which drugs interact with quinolones and to what extent?

A
  • Drugs containing divalent cations (calcium and antacids) reduce the efficacy of quinolones
  • Theophylline - increased risk of theophylline toxicity
  • Co-prescription with NSAIDs increases the risk of seizures
  • Co-prescription with prednisolone increases the risk of tendon rupture
394
Q

Do quinolones extend the QT interval?

A

Yes

395
Q

When should quinolones be prescribed with caution?

A

In co-prescription with other drugs that prolong the QT interval:
- Amiodarone
- Antipsychotics
- Macrolides
- Quinine
- SSRIs

396
Q

Which antibiotic has good activity against organisms that cause traveller’s diarrhoea?

A

Ciprofloxacin

397
Q

What are the most commonly precribed tetracycline antibiotics?

A

Doxycyline
Lymecycline

398
Q

What are the common clinical indications for the use of tetracycline antibiotics?

A
  1. Acne vulgaris
  2. LRTIs including infective exacerbations of COPD and pneumonia
  3. Chlamydial infections
  4. Other infectiosn such as typhoid, malaria, lyme disease, and anthrax
399
Q

What is the spectrum of activity of tetracyclines?

A

Broad

Use is limited however due to increasing resistance

400
Q

What is the basic mechanims of action of tetracycline antibiotics?

A

Tetracyclines inhibit bacterial protein synthesis and are therefore bacteriostatic

401
Q

Of the broad spectrum antibiotics, which class has a lower risk of causing C.diff infections?

A

Tetracyclines

402
Q

What are the important adverse effects associated with the use of tetracyclines?

A
  • GI upset
  • Oesophageal irritation, ulceration and dysphagia
  • Photosensitivity
  • Discolouration of teeth in children
  • Hepatotoxicity
  • Intracranial hypertension
403
Q

Can tetracyclines be used during pregnancy and breastfeeding?

A

No, they bind to teeth and bones during fetal development, infancy and early childhood

404
Q

When should tertracyclines, particularly doxycyline be used with caution?

A
  • Alcohol dependence
  • Renal impairment
405
Q

Which drugs interact with tetracyclines and to what extent?

A
  • Divalent cations and so there should be a 2 hour gap betwen administration of tetracyclines and calcium or antacids
  • Warfarin - increased anticoagulant effect as tetracyclines kill GI flora that synthesise vitamin K
406
Q

What is a typical regimen for treatment using doxycyline?

A

200mg OD on day 1,then 100-200mg OD for 4-6 days

407
Q

What are the key points when counselling a patient on the use of tetracyclines?

A
  • Should be taken with a meal
  • Protect their skin from the sun
  • Avoid indigestion remedies
408
Q

What are some other, non-antibiotic, properties of tetracyclines that are being explored?

A
  • Anti-inflammatory
  • Immune-modulation
  • Neuroprotective effects
409
Q

Trimethoprim is the first line treatment for what indications?

A
  1. Acute lower UTIs
  2. Prophylaxis of recurrent UTI
410
Q

What is the spectrum of activity of trimethoprim?

A

Broad against gram-positive and gram-negative bacteria though it is becoming limited due to resistance - hence the addition of sulfonamide in co-trimaxazole

411
Q

What is the basic mechanism of action of trimethoprim?

A

Trimethoprim inhibits the synthesis of bacterial folate. It is therefore bacteriostatic.

412
Q

What are the important adverse effects associated with the use of trimethoprim?

A
  • GI upset
  • Skin rash
  • Hypersensitivity reactions
  • Haematological disorders such as thrombocytopenia, megaloblastic anaemia, and leucopenia (due to its action as a folate antagonist)
  • Hyperkalaemia
413
Q

Can trimethoprim be used in pregnancy and breastfeeding?

A

It should be avoided in the first trimester of pregnancy due toits teratogenic effects
It is not known to be harmful in breastfeeding

414
Q

When should trimethoprim be used with caution?

A
  • People with folate deficiency
  • Renal impairment
  • Neonates and the elderly
  • HIV infection
415
Q

Which drugs interact with trimethoprim and to what extent?

A
  • Potasium elevating drugs such as aldosterone antagonists, ACE inhibitors, and ARBs
  • Other folate antagonists such as methotrexate
  • Drugs that increase folate metabolism such as phenytoin
  • Warfarin - increased anticoagulant effect
416
Q

Why is trimethoprim less effective in patients with renal impairment?

A

As trimethoprim inhibits creatinine secretion by the renal tubules leading to small and reversible increase in serum creatinine concentrations. Serum creatinine and trimethoprim then compete to be excreted into the urinary tract, the site of action of trimethoprim

417
Q

What is a typical dose of trimethoprim for the treatment of UTI?

A

200mg BD

418
Q

What is a typical dose of trimethoprim for prolonged prophylaxis of recurrent UTI?

A

100mg OD

419
Q

Which drug class does vancomycin belong to?

A

Glycopeptides

420
Q

What are the common clinical indications for the use of vancomycin?

A
  1. Treatment of gram-positive infections (e.g. endocarditis) where the infection is severe or penicillins cannot be used
  2. Treatment of antibiotic-associated colitis cause dby C.difficile (second line where metronidazole is ineffective or poorly tolerated)
421
Q

What is the spectrum of activity of vancomycin?

A

Narrow - effective against only gram-positive bacteria, notably MRSA and C.diff

422
Q

What is the basic mechanims of action of vancomycin?

A

Vancomycin inhibits the growth and cross-linking of peptidoglycan chains, inhibiting the synthesis of the cell wall of gram-positive bacteria, making it bactericidal

423
Q

What are the important adverse effects associated with the use of vancomycin?

A
  • Thrombophlebitis
  • Allergic reactions
  • ‘Red man syndrome’
  • Nephrotoxicity (IV)
  • Ototoxcity (IV)
  • Neutropenia (IV)
  • Thrombocytopenia (IV)
424
Q

When should vancomycin be used with caution?

A
  • Renal impairment
  • Elderly
425
Q

Which drugs interact with vancomycin and to what extent?

A

Vancomycin increases the risk of ototoxicity and/or nephrotoxicity when prescribed with:
- Aminoglycosides
- Loop diuretics
- Ciclosporin

426
Q

How is vancomycin given for the treatment of C.diff infections

A

Orally as it acts topically in the GI system - 125mg 6-hrly for 10-14 days

427
Q

What is the target serum concentration range when using IV vancomycin?

A

Between 10 - 15mg/L

428
Q

What should be monitored in prolonged courses of vancomycin?

A
  • Plasma drug concentrations
  • Renal function
  • Platelets
  • Leukocytes
  • WCC
  • CRP
429
Q

Which drug class does teicoplanin belong to?

A

Glycopeptides

430
Q

List some enzyme inducing drugs

A
  • Carbemazepine
  • Rifampicin
  • Phenytoin
  • Phenobarbitone
  • Sulphonylureas
  • Griseofulvin
  • St John’s wort
431
Q

List some enzyme inhibiting drugs

A
  • Metronidazole
  • Sodium valproate
  • Erythromycin
  • Isoniazid
  • Cimetidine
  • Chloramphenicol
  • Ciprofloxacin
  • Omeprazole
  • Sulfonamides
  • Ketoconazole
432
Q

List some drugs that have an anticholinergic burden

A
  • Amitriptyline
  • Paroxetine
  • Chorphenamine
  • Promethazine
  • Olanzapine
  • Quetiapine
  • Solifenacin
  • Tolterodine
433
Q

What are the most commonly prescribed acetylcholinesterase inhibitors?

A

Donepezil
Rivastigmine

434
Q

What are the acetylcholinestaerase inhibitors indicated for?

A
  1. Mild to moderate Alzheimer’s
  2. Mild to moderate Parkinson’s (rivastigmine)
435
Q

What are some important adverse effects associated with the use of acetylcholinesterase inhibitors?

A
  • GI upset
  • Exacerbation of asthma and COPD symptoms
  • Peptic ulcers
  • Bradycardia
  • Heart block
  • Hallucinations
  • Altered behaviour
  • Neuroleptic malignant syndrome
436
Q

When should acetylcholinesterase inhibitors be used with caution?

A
  • Asthma and COPD
  • Peptic ulcers
437
Q

When should the use of acetylcholinesterase inhibitors be avoided?

A
  • Bradycardia
  • Heart block
438
Q

Which drugs do acetylcholinesterase inhibitors interact with an to what extent?

A
  • NSAIDs - increased risk of ulcers and GI blleds
  • Corticosteroids - increased risk of ulcers and GI bleeds
  • Beta-blockers - increased risk of bradycardia and heart block
  • Antipsychotics - increased risk of neuroleptic malignant syndrome
439
Q

Which drug class does donepezil belong to?

A

Acetylcholinesterase inhibitors

440
Q

Which drug class does rivastigmine belong to?

A

Acetylcholinesterase inhibitors

441
Q
A

Pre-Registration Pharmacy (20 decks)

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