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MPharm Year 2 > Clinical > Flashcards

Clinical Flashcards

1
Q

Asthma treatment pathway according to NICE?

A

1) SABA
2) low-dose ICS and SABA
3) add in LTRA
4) LABA with ICS (with or without LTRA)
5) MART with ICS
6) MART with higher dose ICS or trial additional drug such as antimuscarinic or theophylline
7) specialist

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2
Q

Prescribing advice for LABA?

A
  • only add if ICS failing
  • do not initiate in rapidly deteriorating asthma
    -introduce at a low dose
  • discontinue if no benefit
  • not for exercise-induced asthma unless also using ICS
  • review as appropriate with aim to step down
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3
Q

Signs of theophylline toxicity?

A

Nausea and vomiting

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4
Q

Why do asthma deaths still occur?

A

Underuse of ICS
Over use of B2 agonists
Failure to recognise symptoms
Failure to recognise severity of attack
Incorrect use of inhalers
Underuse of monitoring devices
Lacks of education and training

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5
Q

What is classed as uncontrolled asthma?

A

3 or more days a week with symptoms or with SABA use or 1 or more nights awakening with asthma

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6
Q

Key features of asthma?

A

Chronic airway inflammation
Cough
Wheeze
Breathlessness
Chest tightness
Reversibility
Trigger factors

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7
Q

What is FEV1?

A

forced expiratory volume in 1 second the maximum amount of air that the subject can forcibly expel during the first second following maximal inhalation.

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8
Q

Normal FEV1 for age 8-19 years?

A

85%

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9
Q

Normal FEV1 for age 20-39 years?

A

80%

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10
Q

Normal FEV1 for age 40-59 years?

A

75%

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11
Q

Normal FEV1 for age 60-80 years?

A

70%

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12
Q

Common types of asthma?

A

Allergic
Non-allergic
Late-onset
Asthma with fixed airflow limitation
Asthma with obesity

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13
Q

Physiology of asthmatic airways?

A

Wall inflamed and thickened
Excess mucus production
Tightened airway muscles
Smaller lumen
Dysynchronisd cilia

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14
Q

Immune cells involved in mild/moderate asthma?

A

Eosinophils
Macrophages
CD4+ T-cells
Mast cells

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15
Q

Immune cells involved in severe refractory asthma?

A

Neutrophils
Macrophages
CD4+ T-cells
CD8+ T-cells

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16
Q

Key mediators in mild/moderate asthma?

A

Eotaxin
IL-4
IL-5
IL-13
Nitric oxide

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17
Q

Key mediators in severe refractory asthma?

A

IL-8
IL-5
IL-13
Nitric oxide

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18
Q

Activators of asthma exacerbations?

A

Viruses
Bacteria
Allergens
Occupational exposure (chemicals)
Irritants (smoke, pollution)
Aspirin
Cold air
Exercise

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19
Q

What causes airway inflammation?

A

Cytokines/chemokines
Cell adhesion
Cellular infiltrate/oedema
Increased mucus
IgE increase

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20
Q

What happens when mast cells in the airways degranulate?

A

Already inflammation and bronchoconstriction

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21
Q

What is Th2 imbalance in allergic asthma?

A

Normally it is an equal balance or favours Th1 but in asthma patients Th2 is greater

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22
Q

Local side effects of ICS?

A

Dysphonia
Candidiasis
Cough
Pneumonia

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23
Q

Systemic side effects of ICS?

A

Adrenal suppression
Growth suppression
Skin thinning
Osteoporosis
Cataracts
Glaucoma
Metabolic abnormalities
Psychiatric disturbance

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24
Q

What are the two response stages of asthma?

A

Acute response
Late response

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25
Q

What is the acute asthmatic response?

A

Bronchoconstriction
Hypersecretion of mucus
Mucosal oedema
Caused by mast cell degranulation
Lasts around an hour

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26
Q

What is the late asthmatic response?

A

Eosinophils attract Th2 T-cells and neutrophils. Causes:
Inflammation
Tissue destruction
Tissue remodelling
2-8 hours after exposure and lasts 1-2 days

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27
Q

What are the most common cells to be affected in testicular cancer?

A

Germ cells

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28
Q

Risk factors for developing testicular cancer?

A

Family history
Cryptorchidism (undescended testicles)
Previous testicular cancer
Testicular carcinoma in situ
Ethnic background
HIV

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29
Q

Symptoms of testicular cancer?

A

Testicular lump that is usually painless
Lumbar back pain
Cough
Dyspnoea
Difficulty swallowing
CNS symptoms

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30
Q

How to diagnose testicular cancer?

A

Ultrasound
MRI
Chest X-ray
Blood tests: AFP, LDH, beta-HCG

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31
Q

What is stage 1 testicular cancer?

A

Tumour confined to testes

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32
Q

What is stage 2 testicular cancer?

A

Tumour spread to abdominal lymph nodes

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33
Q

What is stage 3 testicular cancer?

A

Tumour spread to lymph nodes above diaphragm

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34
Q

What is stage 4 testicular cancer?

A

Tumour invading organs other than lymph nodes

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35
Q

How to monitor treatment in testicular cancer?

A

Changes in tumour markers: AFP HCG

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36
Q

Drugs used to treat testicular cancer?

A

Bleomycin
Etoposide
Cisplatin
Ifosfamide

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37
Q

Bleomycin indication?

A

Metastatic testicular cancer
Non-Hodgkin lymphoma

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38
Q

Bleomycin route of administration?

A

Intramuscular

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39
Q

Side effects of bleomycin?

A

Rigors
Fever
Malaise
Interstitial pneumonia
Nausea and vomiting
Pulmonary fibrosis

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40
Q

Etoposide indication?

A

Carcinoma of bronchus
Testicular cancer
Lymphoma

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41
Q

Etoposide route of administration?

A

Intravenous infusion

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42
Q

Side effects of etoposide?

A

Hypertension
Nausea and vomiting
Abdominal pain
Diarrhoea
Fatigue
Alopecia
Cytopenias

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43
Q

Cisplatin indication?

A

Testicular cancer
Lung cancer
Cervical cancer
Bladder cancer
Head and neck cancer
Ovarian cancer

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44
Q

Cisplatin route of administration?

A

Intravenous infusion

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45
Q

Side effects of cisplatin?

A

Severe nausea and vomiting
Myelosuppression
Nephrotoxic
Hearing loss
Tinnitus
Peripheral neuropathy
Hyperurcaemia
Anaphylaxis

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46
Q

Ifosfamide indication?

A

Testicular cancer

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47
Q

Ifosfamide route of administration?

A

Intravenous infusion

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48
Q

Side effects of ifosfamide?

A

Nephrotoxic
Neurotoxic
Encephalopathy
Nausea and vomiting
Hypersensitivity
Haemorrhagic cystitis

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49
Q

Risk factors for cervical cancer?

A

HPV
Unprotected sex
Chemicals
Age
Smoking
Social deprivation
Muliparity
Early onset of sexual intercourse

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50
Q

What are CIN changes?

A

Cervical intraepithelial neoplasia changes
Grades abnormal cells that lead to cancer

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51
Q

Types of cervical cancer?

A

Squamous cell
Adenocarcinoma
Adenosquamous carcinoma
Small cell cancer

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52
Q

Symptoms of cervical cancer?

A

Unusual bleeding
Smelling vaginal discharge
Post-coital bleeding
Backache
Blood in urine
Bone pain
Weight loss
Loss of appetite

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53
Q

What type of test is a smear test?

A

Liquid-based cytology

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54
Q

How often are women aged 25-49 invited for cervical screening?

A

Every three years

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55
Q

How often are women aged 50-64 invited for cervical screening?

A

Every five years

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56
Q

What stage of cervical cancer is treated with chemotherapy?

A

4

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57
Q

Drugs used to treat cervical cancer?

A

Paclitaxel
Cisplatin/carboplatin
Topotecan
Bevacizumab

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58
Q

Paclitaxel indication?

A

Brest and cervical cancer

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59
Q

Paclitaxel route of administration?

A

Intravenous infusion

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60
Q

Side effects of Paclitaxel?

A

Bone marrow suppression
Neurotoxicity
Hypersensitivity (steroids and antihistamines should be given prior to treatment)
Extravasation

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61
Q

Topotecan indication?

A

Cervical cancer
Small cell lung cancer
Metastatic ovarian cancer

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62
Q

Topotecan route of administration?

A

Intravenous infusion
Oral capsules

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63
Q

Side effects of Topotecan?

A

Diarrhoea
Bone marrow suppression
Hypersensitivity
Sepsis
Alopecia
Mucositis

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64
Q

Bevacizumab indication?

A

Cervical cancer
Metastatic breast cancer
Metastatic colorectal cancer
Metastatic renal cancer
Ovarian cancer

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65
Q

Bevacizumab route of administration?

A

Intravenous infusion

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66
Q

Side effects of bevacizumab?

A

Osteonecrosis of the jaw
Fatigue
Pain
Lack of energy
GI effects

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67
Q

Monitoring required for bevacizumab?

A

Blood pressure

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68
Q

Three types of anaesthesia?

A

Local
Regional
General

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69
Q

What is local anaesthesia?

A

Localised response by inhibiting excitation of nerve endings or by blocking conduction in peripheral nerves. Usually used for minor procedures involving specific tissues

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70
Q

What is regional anaesthesia?

A

Usually involves a larger body area/region

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71
Q

What is general anaesthesia?

A

Involves most of the surgical procedures where patients need to be in an unconscious state

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72
Q

How do local anaesthetics work?

A

Bind reversibly and inactivate sodium channels

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73
Q

Examples of amino amide local anaesthetics?

A

Lidocaine
Prilocaine
Bupivacaine

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74
Q

Examples of amino ester local anaesthetics?

A

Cocaine
Procaine
Tetracaine
Benzocaine

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75
Q

Which type of local anaesthetics are more likely to cause hypersensitivity reactions?

A

Amino esters

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76
Q

Why can adrenaline be used with local anaesthetics?

A

Constricts the surrounds blood vessels to limit the diffusion of the anaesthetic agent, extending its duration of action

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77
Q

Contraindications of spinal anaesthesia?

A

Local infections
Sepsis
Bleeding disorders
Increased inter-cranial pressure
Hypovolaemia

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78
Q

What is the difference between spinal and epidural anaesthesia?

A

The main difference is the placement. With an epidural, anesthesia is injected into the epidural space. With a spinal, the anesthesia is injected into the dural sac that contains cerebrospinal fluid. The direct access means that a spinal gives immediate relief.

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79
Q

What adjuvants need to be added to general anaesthesia?

A

NMBA
Benzodiazepines
Opioids
Anti muscarinic agents

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80
Q

What is stage 1 of anaesthesia?

A

Stage of analgesia
Patient is still conscious but drowsy, usually exhibits a reduced response to painful stimuli

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81
Q

What is stage 2 of anaesthesia?

A

Stage of excitement
Occurs because inhibition is lost before consciousness

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82
Q

What is stage 3 of anaesthesia?

A

Surgical anaesthesia
Reflexes are lost, respiration becomes regular and a muscle tone eventually lost

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83
Q

What is stage 4 of anaesthesia?

A

Medullary depression
Respiratory and cardiovascular control is lost, usually resulting in death

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84
Q

What are the five main classes of general anaesthetic agents?

A

Intravenous anaesthetics
Inhaled anaesthetics
Intravenous sedatives
Synthetic opioids
Neuromuscular blocking drugs

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85
Q

Examples of group one general anaesthetics?

A

Etomidate
Propofol
Barbituates

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86
Q

How do group 1 anaesthetic agents work?

A

Actions mediated by a subset of GABA receptors

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87
Q

Examples of group two general anaesthetics?

A

Nitrous oxide
Xenon
Cyclopropane
Ketamine

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88
Q

How do group 2 anaesthetic agents work?

A

Potently inhibit NMDA receptors

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89
Q

Example of group 3 general anaesthetics?

A

Halogenated volatile anaesthetics
Isoflurane, halothane

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90
Q

How do group 3 anaesthetic agents work?

A

Positive modulation of GABA receptors
Activate 2P potassium channels and inhibit a variety of excitatory cation channels

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91
Q

Three main actions of anaesthesia?

A

Hypnosis
Analgesia
Relaxation

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92
Q

Symptoms of malignant hyperthermia?

A

Rapid rise in temperature
Increased muscle rigidity
Tachycardia
Acidosis

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93
Q

Malignant hyperthermia treatment?

A

IV dantrolene

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94
Q

Causes of nausea and vomiting?

A

Intracranial
Vestibular
Endocrine/metabolic
Radiotherapy
Psychogenic
Drug induced
Gastrointestinal
Surgery
Pain related

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95
Q

Receptors involved in nausea and vomiting?

A

Histaminergic H1
Cholinergic M1
Dopaminergic D2
Serotonergic 5HT3
Neurokinin-1 NK1

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96
Q

What is a volume disturbance?

A

When the volume of body fluids are altered

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97
Q

What is an osmolarity imbalance?

A

When the concentration of constituents in body fluids are altered

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98
Q

What is hypovolaemia?

A

Depletion of extracellular fluid. Concomitant loss of water and sodium

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99
Q

Cause of hypovolaemia?

A

Insufficient fluid intake
Haemorrhage
Diarrhoea
Burns
Vomiting
Endocrine imbalances

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100
Q

Symptoms of hypovolaemia?

A

Thirst
Weakness
Abdominal pains
Nausea
Hypotension
Elevated heart rate
Elevated respiratory rate

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101
Q

Treatment of hypovolaemia?

A

Volume replacement: crystalloids, colloids, blood products

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102
Q

What is hypervolaemia?

A

Excess extracellular fluid. Concomitant gain of water and sodium

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103
Q

Cause of hypervolaemia?

A

Excessive administration of fluids
Glucocorticoids
CKD
Liver disease
CCF
Endocrine imbalances

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104
Q

Symptoms of hypervolaemia?

A

Weight gain
Cough
Distended abdomen
Hypertension
Oedema

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105
Q

Treatment of hypervolaemia?

A

Diuretics

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106
Q

Normal plasma sodium range?

A

136-145mmol/l

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107
Q

What is hyponatremia?

A

Loss of sodium from body fluids or excessive gain of extracellular water

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108
Q

Cause of hyponatraemia?

A

Inadequate sodium intake
SIADH
Diuretic therapy
Adrenal insufficiency
Hypotonic solutions
Heart failure
Nephrosis
Cirrhosis

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109
Q

Symptoms of hyponatraemia?

A

Peripheral oedema
Hypotension
Nausea
Vomiting
Rapid heart rate
Cell swelling leads to cerebral oedema, headache and coma

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110
Q

Treatment of hyponatraemia?

A

Review diuretics
Treat cause
Administer/restrict electrolytes and fluids
V2 receptor antagonist (tolvaptan)
Demeclocycline

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111
Q

What is hypernatraemia?

A

Increased intake of sodium or excessive loss of water

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112
Q

Cause of hypernatraemia?

A

Excessive sodium intake
Corticosteroids
Renal insufficiency

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113
Q

Symptoms of hypernatraemia?

A

Hypotension
Tachycardia
Excessive thirst
Cell shrinking can lead to CNS irritability

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114
Q

Treatment of hypernatremia?

A

Treat underlying cause
IV fluids, such as glucose
Enteral water

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115
Q

Normal plasma potassium range?

A

3.6-5mmol/l

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116
Q

Cause of hypokalaemia?

A

Insufficient intake
Abnormal loss
Drugs: diuretics, corticosteroids, amphotericin, insulin
Endocrine imbalance
Trauma
Burns

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117
Q

Symptoms of hypokalaemia?

A

Mild: mostly asymptomatic
Severe: muscle weakness, ECG changes, arrhythmias

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118
Q

Treatment of hypokalaemia?

A

Potassium replacement, enteral or parenteral

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119
Q

Cause of hyperkalaemia?

A

Renal insufficiency
Increased tissue catabolism
Increase fragility of blood cells
Drugs: ACEi, potassium supplements, potassium-sparing diuretics

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120
Q

Symptoms of hyperkalaemia?

A

Life-threatening cardiac arrhythmias

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121
Q

Treatment of hyperkalaemia?

A

Mild: loop diuretics and NaCl infusion
Severe: calcium gluconate
Insulin/glucose infusion
B-2 agonist infusion
Cation exchange resins such as resonium/zirconium
Sodium bicarb, if acidosis present

122
Q

What is hypocalcaemia?

A

Decrease calcium intake/absorption or increased calcium excretion

123
Q

Cause of hypocalcaemia?

A

CKD
Deficient intake/absorption of calcium/vitamin D
Hypoparathyroidism
Hyperphosphataemia

124
Q

Symptoms of hypocalcaemia?

A

Increased neuromuscular excitability
Prolonged action potentials in the heart

125
Q

Treatment of hypocalcaemia?

A

IV calcium replacement
Oral calcium or vitamin D replacement

126
Q

What is hypercalcaemia?

A

Increased calcium intake/absorption or decreased calcium excretion or movement of calcium from the bones to the extracellular fluid

127
Q

Causes of hypercalcaemia?

A

Hyperparathyroidism
Thiazide diuretics
Excessive intake of calcium/vit D
Bone carcinomas

128
Q

Symptoms of hypercalcaemia?

A

Nausea
Vomiting
Fatigue
Muscle weakness
Diminished reflexes
Cardiac arrhythmias

129
Q

Treatment of hypercalcaemia?

A

Phosphates
Calcitonin
Bisphosphonates
Loop diuretics

130
Q

Normal plasma calcium range?

A

2.15-2.65mmol/l

131
Q

Normal plasma phosphate range?

A

1.12-1.45mmol/l

132
Q

Main types of antiplatelet drugs?

A

Theinopyridines
Glycoprotein IIb/IIIa inhibitors
Others

133
Q

Examples of theinopyridines?

A

Clopidogrel
Prasugrel
Ticlopidine

134
Q

Examples of glycoprotein IIb/IIIb inhibitors?

A

Abciximab
Eptifibatide
Tirofiban

135
Q

Examples of ‘other’ antiplatelet drugs?

A

Aspirin
Dipyridamole
Ticagrelor

136
Q

What does the cycloxygenase enzyme produce?

A

Thromboxane A (TXA2)
Prostacyclin 2 (PGI2)

137
Q

What does Thromboxane A (TXA2) do?

A

Promotes platelet aggregation

138
Q

What does Prostacyclin 2 (PGI2) do?

A

Inhibits platelet aggregation

139
Q

Low dose aspirin mode of action?

A

Irreversibly inhibits cyclooxygenase, which reduces the synthesis of thromboxane A for the life of the platelet

140
Q

Common side effects of low dose aspirin?

A

GI irritation
Prolonged bleeding time
Allergy

141
Q

Rarer side effects of low dose aspirin?

A

GI bleed
Intracranial bleed

142
Q

Can low dose aspirin be used in pregnancy?

A

Category C in pregnancy
Low doses are considered safe but should be avoided where possible in the third trimester

143
Q

Clopidogrel/prasugrel mode of action?

A

Block the platelet ADP receptor (P2Y12) which prevents activation of the platelet glycoprotein IIa/IIIb complex, preventing platelet aggregation and thrombus formation

144
Q

When would clopidogrel be used alongside aspirin?

A

After having a CV event whilst on aspirin or after stenting

145
Q

When should aspirin be taken with prasugrel?

A

In most cases

146
Q

Comparison of prasugrel and clopidogrel in ACS after PCI?

A

Prasugrel superior in primary outcomes (death, stroke, MI) and secondary outcomes (stent thrombosis)
Prasugrel had an increased risk of bleeding
Overall mortality did not differ between the two groups

147
Q

Prasugrel dose?

A

Loading dose of 60mg then 10mg daily. Reduced to 5mg daily if over 75 years old or less than 60kg

148
Q

Dipyridamole mechanism of action?

A

Inhibits platelet function by inhibiting phosphodiesterase, thereby increasing cAMP, which blocks platelet response to ADP

149
Q

Dipyridamole indications?

A

In combination with warfarin in patients with prosthetic heart valves
In combination with aspirin for the secondary prevention of stroke

150
Q

Dipyridamole side effects?

A

Headache
Hot flushes
Hypotension
Tachycardia
Allergic reactions

151
Q

Ticagrelor mechanism of action?

A

Binds reversibly to P2Y12 receptor inhibiting platelet aggregation

152
Q

Ticagrelor indication?

A

For use in ACS with aspirin.

153
Q

Ticagrelor with aspirin VS clopidogrel with aspirin?

A

Ticagrelor more effective in preventing CV events in ACS patients
Significant reduction in MI and vascular death but a non-significant increase in stroke noted
Total bleeding similar but rate if ICH higher with ticagrelor
Risk-benefit of ticagrelor less favourable when used with aspirin doses above 150mg daily

154
Q

Side effects of ticagrelor?

A

Bleeding
Nausea
Diarrhoea
Headache
Non-cardiac chest pain

155
Q

How are glycoprotein IIb/IIIa receptor inhibitors administered?

A

Intravenously

156
Q

Mechanism of action of glycoprotein IIb/IIIa receptor inhibitors?

A

Prevent binding of fibrinogen to platelet by occupying platelet glycoprotein IIb/IIIa receptor, reducing platelet aggregation

157
Q

Main groups of anticoagulants?

A

Indirect parenteral anticoagulants
Direct thrombin inhibitors
Vitamin K antagonists
Factor Xa inhibitors

158
Q

Examples of indirect parenteral anticoagulants?

A

Heparin
LMWH
Danaparoid

159
Q

Examples of direct thrombin inhibitors?

A

Dabigatran
Bivalirudin

160
Q

Examples of vitamin K antagonists?

A

Warfarin
Phenindione

161
Q

Examples of factor Xa inhibitors?

A

Apixaban
Edoxaban
Rivaroxaban
Fondaparinux

162
Q

Heparin onset of action?

A

Almost immediate

163
Q

Heparin mechanism of action?

A

Heparin binds to antithrombin III, causing a conformational change allowing antithrombin to rapidly
combine and inhibit thrombin
It also inactivates factor Xa

164
Q

Can heparin be used in pregnancy?

A

Yes, it does not cross the placenta as it has a large molecular weight

165
Q

How can heparin be administered?

A

IV or SC

166
Q

Why can heparin not be administered intramuscularly?

A

Risk of haematoma

167
Q

Heparin side effects?

A

Haemorrhage
Bruising or pain at injection site
HIT
Hypersensitivity reactions

168
Q

Heparin monitoring?

A

Platelet count on days 0, 3, 5 and then on alternative days if treatment continued
APTT target range of 1.5-2.5 times of control

169
Q

LMWH mechanism of action?

A

Enhance effects of antithrombin III but have a higher ratio for factor Xa than IIa, so has a more selective Xa activity

170
Q

Which is more Xa selective LMWH or danaparoid?

A

Danaparoid

171
Q

LMWH monitoring?

A

AntiXa levels but only in at-risk patients

172
Q

LMWH vs heparin in regards to bleeding?

A

Similar incidences of bleeding but protamine only partially effective with LMWH

173
Q

LMWH vs heparin in regards to renal impairment?

A

Incidence of bleeding higher with LMWH

174
Q

LMWH vs heparin in regards to HIT?

A

Lower risk with LMWH but there is 90% cross-reactivity, so LMWH is not an alternative to heparin in a patient with HIT

175
Q

LMWH vs heparin in regards to preventing VTE in general surgery patients?

A

Similar efficacy, but LMWH can be given once daily, although it is more expensive

176
Q

LMWH vs heparin in regards to preventing VTE in orthopaedic patients?

A

LMWH seen to be more effective

177
Q

LMWH vs heparin in regards to treating DVT?

A

LMWH are at least as effective as heparin in preventing recurrence and reducing overall mortality in hospital patients. LMWH is more expensive, but since monitoring is not required and can be used for outpatients, this may offset the cost

178
Q

Warfarin mode of action?

A

Impairs utilisation of vitamin K and reduces the synthesis of some clotting factors and proteins. thought to interfere with clotting factor synthesis by inhibition of the regeneration of vitamin K1 epoxide

179
Q

Which clotting factors and anticoagulant proteins does warfarin reduce the synthesis of?

A

2,7,9,10
Proteins C and S

180
Q

Why does warfarin take time to exert its full anticoagulant effect?

A

It has not direct action on the coagulation factors present in the blood so the effects start once these factors are cleared. The factors have half-lives between 24 and 50 hours

181
Q

Warfarin contraindications?

A

Bleeding disordered
Previous GI bleed
Haemorrhagic retinopathy
Intracerebral haemorrhage
Severe hypotension
Bacterial endocarditis
Alcoholism
Unsupervised dementia
Frequent falls

182
Q

Warfarin in renal and hepatic impairment?

A

Cautioned

183
Q

Warfarin in pregnancy?

A

Avoid- teratogenic and can cause placental haemorrhage

184
Q

How can warfarin interact with other drugs?

A

Decreased hepatic synthesis of procoagulant factors
Inhibition of enzymatic metabolism of warfarin
Increased receptor affinity for warfarin
Decreased vitamin K synthesis
Displacement of warfarin from protein binding sites
Increased metabolism of warfarin

185
Q

INR range for AF, DVT, PE and bio-prosthetic heart valves?

A

2.0-3.0

186
Q

INR range for mechanical prosthetic heart valves?

A

2.5-3.5

187
Q

How often is INR monitored?

A

2-3 times weekly until three consecutive readings are within 0.5 of each other, then weekly for four weeks and then every 4-6 weeks when stable

188
Q

Warfarin counselling points?

A

?Do not change brands
Take at same time of day
Stabilise vitamin K intake
Avoid excessive alcohol intake
Care with OTC and herbal products
Warn about early signs of haemorrhage

189
Q

Warfarin antidote?

A

Phytomenadione

190
Q

How does dabigatran/bivalirudin work?

A

Binds directly to thrombin to block its effect

191
Q

Which type of anticoagulants also have an antiplatelet affect?

A

Dabigatran
Bivalirudin

192
Q

Dabigatran indications?

A

Prevention of VTE after elective hip or knee replacement
Treatment of acute VTE and prevention of subsequent VTE
Non-valvular AF and a high risk of stroke or systemic embolism

193
Q

Common dabigatran drug interactions?

A

Clarithromycin
Verapamil
Ketoconazole

194
Q

Common dabigatran side effects?

A

Gastritis
Dyspepsia
GI bleed

195
Q

Dabigatran counselling points?

A

Importance of not missing doses
Do not open capsules or chew or crush as it can increase the risk of bleeding
Take at the same time of day
Monitor for signs of bleeding

196
Q

Dabigatran reversal agent?

A

Idarucizumab

197
Q

Factor Xa inhibitor mechanism of action?

A

Selectively inhibits factor Xa, blocking thrombin production, conversion of fibrinogen to fibrin and thrombus development

198
Q

Can factor Xa inhibitors be used in valvular AF?

A

No

199
Q

Common DOAC interactions?

A

Ketoconazole
Itraconazole
HIV protease inhibitors
Rifampicin
St Johns wort
Carbamazepine

200
Q

When to consider DOACs over warfarin?

A

Lots of interacting medicines or frequent antibiotic courses
High alcohol intake
Unable to cope with variable dosing

201
Q

Warfarin vs DOAC in renal impairment?

A

Warfarin clearance less affected by renal function

202
Q

DOAC positives?

A

No INR monitoring
No known food interactions

203
Q

DOAC negatives?

A

Cannot be used in valvular AF
High cost
Shorter half-life so greater effect with compliance issues
Less evidence for reversal agents

204
Q

Warfarin positives?

A

Longer half-life so compliance less of an issue
Cheap
Lots of experience with its use
Can be used in valvular AF
Reversal agent

205
Q

Warfarin negatives?

A

INR monitoring
Food interactions

206
Q

Appropriate starting dose of beclometasone ICS in ages 5-16?

A

50mcg BD

207
Q

Appropriate starting dose of beclometasone ICS in ages 17+?

A

100mcg BD

208
Q

What is low-dose budesonide ICS in adults?

A

<400mcg daily

209
Q

What is moderate-dose budesonide ICS in adults?

A

> 400<800mcg daily

210
Q

What is high-dose budesonide ICS in adults?

A

> 800mcg daily

211
Q

What is low-dose budesonide ICS in under 16s?

A

<200mcg daily

212
Q

What is moderate-dose budesonide ICS in under 16s?

A

> 200<400mcg daily

213
Q

What is high-dose budesonide ICS in under 16s?

A

> 400mcg daily

214
Q

How often to clean a spacer?

A

Monthly

215
Q

How often to change a spacer?

A

6-12 months

216
Q

Difference between NICE and GINA?

A

NICE: LTRA after ICS
GINA: LABA after ICS
GINA does not recommend SABA alone

217
Q

Why does NICE use LRTA second line?

A

Cost-effective, even though evidence shows LABA more effective

218
Q

Chlamydia treatment?

A

Doxycycline 100mg BD for seven days
OR azithromycin 1g stat (useful in pregnancy)

219
Q

Gonorrhoea treatment?

A

Ceftriaxone 500mg IM/IV stat AND azithromycin 1g stat OR doxycycline 100mg BD for 10 days

220
Q

Early/late latent syphilis treatment?

A

Benzathine penicillin 1.8g IM stat OR procaine penicillin 1.5g IM daily for 10 days

221
Q

Tertiary syphilis treatment?

A

Ben pen 1.8g every four hours for 15 days

222
Q

Trichomoniasis treatment?

A

Metronidazole 2g stat OR tinidazole 2g stat
In relapse metronidazole 400mg BD for 5 days

223
Q

First episode of genital herpes treatment?

A

Aciclovir 400mg TDS for 10 days
(Stop treatment after 5 days if worked)

224
Q

Episodic genital herpes treatment?

A

Aciclovir 800mg TDS for two days

225
Q

Prevention of genital herpes?

A

Aciclovir 400mg BD

226
Q

Treatment of pubic lice?

A

Permethrin

227
Q

Microbiological features of chlamydia?

A

Gram-negative (ish)
Lacks cell wall
Non-motile
Has two forms: elementary bodies, which are cocci, and articulate bodies, which are pleomorphic

228
Q

Is chlamydia an intracellular or extracellular pathogen?

A

Intracellular
Grows in host cells as does not have genes for ATP production

229
Q

What causes chlamydia?

A

Chlamydia trachomatis

230
Q

Which form of chlamydia bodies are infective?

A

Elementary

231
Q

Which form of chlamydia bodies can replicate and how?

A

Reticulate. Through binary fission within phagosomes

232
Q

What cells can chlamydia infect?

A

Conjunctiva
Trachea
Bronchi
Urethra
Uterus
Anus
Rectum

233
Q

Does chlamydia cause genital lesions?

A

Yes. Initially a lesion forms as bacteria multiply. This is I ften missed though, internal in women

234
Q

How can chlamydia be transmitted?

A

Drops
Hands
Fomites
Flies

235
Q

Chlamydia symptoms in women?

A

85% asymptomatic
Unusual vaginal discharge
Pain when urinating
Low abdominal pain
Bleeding between periods or after sex
Pain during sex

236
Q

Chlamydia symptoms in men?

A

75% have symptoms
White/cloudy/watery discharge
Pain/burning when urinating
Testicular pain or swelling

237
Q

Diagnosis of chlamydia?

A

Urine test or swab

238
Q

Cause of gonorrhoea?

A

Neisseria gonorrhoeae

239
Q

Microbiological features of gonorrhoea?

A

Gram-negative
Diplococci
True pathogen

240
Q

What cells can gonorrhoea infect?

A

Genital mucosal membranes, urethra, digestive tract, cervix, uterus, rectum, pharynx, mouth

241
Q

Gonorrhea secretes?

A

A protease that cleaver IgA

242
Q

Gonorrhoea symptoms in men?

A

Usually symptomatic
Acute inflammation
Painful urination
Purulent discharge
Can cause infertility

243
Q

Gonorrhoea symptoms in women?

A

Often asymptomatic
Often mistaken for bladder infection
Infects cervix
Can lead to pelvic inflammatory disease

244
Q

Diagnosis of gonorrhoea?

A

Urine sample or swab

245
Q

Why do athletes use drugs?

A

Legitimate therapeutic use
Performance continuation
Recreationally
Performance enhancement

246
Q

What is WADA?

A

World anti-doping agency

247
Q

Five main groups of performance enhancing drugs?

A

Stimulants
Anabolic steroids
Diuretics
Narcotic analgesics
Peptides/hormones

248
Q

Activation of what receptors in the gut can cause nausea and vomiting?

A

5HT3
D2
NK1

249
Q

Activation of what receptors in the chemoreceptor trigger zone can cause nausea and vomiting?

A

5HT3
D2
M1

250
Q

Where is the chemoreceptor trigger centre found?

A

Area postrema

251
Q

Activation of what receptors in the cerebral cortex can cause nausea and vomiting?

A

NK1
GABA
5HT

252
Q

Activation of what receptors in the vestibular nuclei can cause nausea and vomiting?

A

M1
H1

253
Q

Activation of what receptors in the vomiting centre can cause nausea and vomiting?

A

M1
H1
Mui opioid
5HT3
NK1

254
Q

What gene is defective in CF?

A

CFTR

255
Q

What does the CFTR gene stand for?

A

Cystic fibrosis transmembrane conductance regulator

256
Q

What does the CFTR gene control?

A

Transport of chloride

257
Q

Is CF dominant or recessive?

A

Recessive

258
Q

What is the most common CFTR gene mutation?

A

Delta-F508

259
Q

Common places to find CFTR channels?

A

Sweat glands
Lungs
Pancreatic duct
GI tract

260
Q

How many functional mutation classes of CF are there?

A

Six

261
Q

How is CF tested for in newborns and when?

A

Heel prick blood test on day six of life

262
Q

Ways to diagnose CF?

A

Heel prick blood test
Sweat test
Genetic test

263
Q

What type of sweat is produced in individuals with CF and why?

A

Hypertonic (salty) as since Cl- cannot be reabsorbed so to balance the electrical charges, neither is Na+

264
Q

What is ASL in the lungs?

A

Airway surface liquid

265
Q

What is airway surface liquid?

A

Salt containing, mucus gel layer that traps bacteria and foreign particles breathed in. Then wafted out by cilia

266
Q

How is airway surface liquid affected by CF?

A

Excess Na+ reabsorbed from the ASL and water follows so it becomes sticky and dehydrated

267
Q

Lung management in CF?

A

Chest physiotherapy
Mucus modifying drugs
Vibrating vest
Regular sputum samples
Prophylactic antibiotics
Bronchodilators
Transplant
Gene therapy

268
Q

Effects of CF on the pancreas?

A

Pancreatic insufficiency
Nutrient malabsorption
Constipation
Bloating
Pancreatitis
Can lead to diabetes
Fats and fat-soluble vitamins not absorbed

269
Q

Effects of CF on the liver bile duct?

A

Obstruction of liver bile duct
Biliary cirrhosis
Inflammation
Scarring
Fibrosis

270
Q

Effects of CF on the GI system?

A

Malnutrition
Vitamin deficiency
Intestinal obstruction
Intussusception

271
Q

Effects of CF on the reproductive system?

A

Infertility

272
Q

Effects of CF on the sinuses?

A

Sinusitis
Nasal polyps

273
Q

Why is reproduction affected in patients with CF?

A

98% of males have no vas deferens
Females have thick cervical mucus

274
Q

What does HIV bind to?

A

CD4 antigens on lymphocytes, macrophage

275
Q

What to monitor when using antiretrovirals?

A

Clinical status and compliance
HIV viral load
CD4 cell count
Toxicity through FBC, U and Es every three months
Cardiovascular risk

276
Q

Common opportunistic infections in HIV?

A

PCP
CMV
MAC

277
Q

What causes pubic lice?

A

Phthirus pubis

278
Q

Drugs that target bacterial cell walls?

A

Beta-lactams
Glycopeptides

279
Q

Antibiotics that target bacterial protein synthesis?

A

Aminoglycosides
Chloramphenicol
Fusidic acid
Clindamycin
Macrolides
Tetracyclines

280
Q

Antibiotics that target folate synthesis?

A

Sulphonamides
Trimethoprim

281
Q

Antibiotics that target transcription of bacterial RNA?

A

Rifampicin

282
Q

Antibiotics that target bacterial DNA gyrase and topoisomerase IV?

A

Quinolones

283
Q

How do penicillins work?

A

Bind to penicillin-binding proteins resulting in weakness of the cell wall and lysis

284
Q

General penicillin spectrum of action?

A

Many Gram-positive organisms and gran-negative cocci

285
Q

Which penicillin does not need to be taken on an empty stomach?

A

Amoxicillin

286
Q

Examples of beta-lactam inhibitors?

A

Clavulanate
Tazobactam

287
Q

Common side effects of penicillin?

A

Diarrhoea
Nausea
Superinfection

288
Q

Rare side effects of penicillins?

A

Anaphylaxis
Bronchospasm
SJS
TEN

289
Q

Common penicillin drug interactions?

A

Probenecid
Oral contraceptives
Anticoagulants

290
Q

Benzylpenicillin spectrum of activity?

A

Neisseria meningitidis
Neisseria gonorrhoeae

291
Q

600mg of benpen in units?

A

100 million units (1 mega unit)

292
Q

Key points of benzathine penicillin?

A

Slowly released from IM injection site and is hydrolysed to benpen
Gives low serum concentrations for up to one month
Treatment for syphilis

293
Q

Key points of procaine penicillin?

A

Mix of procaine and benpen
Procaine slows absorption of penicillin which gives a plateau-type blood level at four hours which gradually falls over the next 15-20 hours

294
Q

First-generation cephalosporins?

A

Cefazolin
Cefalotin
Cefalexin

295
Q

Second-generation cephalosporins?

A

Cefaclor
Cefoxitin
Cefuroxime

296
Q

Third-generation cephalosporins?

A

Cefotaxime
Ceftriaxone
Ceftazidime

297
Q

Fourth-generation cephalosporins?

A

Cefipime

298
Q

Moderate spectrum cephalosporins?

A

Cefaclor
Cefalotin
Cefoxitin
Cefuroxime
Cefalexin
Cephazolin

299
Q

Broad spectrum cephalosporins?

A

Cefepime
Cefotaxime
Ceftaroline
Ceftazidime
Ceftriaxone

300
Q

What can happen with rapid IV administration of cephalosporins?

A

Seizures

301
Q

Monitoring with cephalosporins?

A

Renal function and FBCs with high doses or prolonged therapy

302
Q

What is the main macrolide used in STIs?

A

Azithromycin

MPharm Year 2 (6 decks)

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