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Phase 2a > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What are the 3 major ways that antibiotics can kill bacteria?

A
  • Inhibit cell wall synthesis
  • Inhibit nucleic acid synthesis
  • Inhibit protein synthesis
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2
Q

What two types of antibiotics inhibit cell wall synthesis?

A

Glycopeptides, beta lactams

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3
Q

What are the 3 types of beta lactams?

A

Penicillins, Cephalosporins, carbapenems

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4
Q

Name a glycopeptide antibiotic

A

Vancomycin

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5
Q

What is vancomycin used to treat?

A 
C diff (Second line), 
Severe staph infections e.g. MRSA
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6
Q

List 3 types of penicillins

A

Benzylpenicillin, flucloxacillin and amoxicillin/ampicillin

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7
Q

What is benzylpenicillin used to treat?

A

General resp infections ( pneumonia, strep throat). Also syphilis, gonococcal infection

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8
Q

What is flucloxacillin used to treat?

A

Cellulitis and other skin infections (diabetic skin infections, ulcers etc)
Staph Aureus, Strep Pyogenes

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9
Q

What is ampicillin/amoxicillin used to treat?

A

Community Acquired pneumonia, COPD exacerbations, UTIs (2nd line)

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10
Q

What are the three generations of cephalosporins?

A

1st gen: Cephalexin
2nd gen: Cefuroxime
3rd gen: Ceftazidime= Ceftriaxone

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11
Q

What are cephalosporins used to treat?

A

Chlamydia and Gonnohea

Staph Aureus, streptococci, nisseriae, haemophillus, coliforms

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12
Q

Name a carbapenem antibiotic

A

Imipenems, ertapenems

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13
Q

What are the cautions of glycopeptides?

A

Caution in renal impairment, history of deafness, pregnancy

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14
Q

What are the contraindications of penicillins?

A

Penicillin hypersensitivity

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15
Q

What are the side effects of benzylpenicillin and flucloxacillin?

A

Hypersensitivity reactions

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16
Q

What are the side effects of ampicillin/amoxicillin?

A

Nausea, vomitting

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17
Q

What are the four ways that antibiotics can inhibit nucleic acid synthesis?

A

Inhibit folate synthesis
Inhibit DNA gyrase
Bind to RNA polymerase
DNA strand breaks

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18
Q

Which antibiotics inhibit folate synthesis?

A

Trimethoprim, sulfamethoxazole, and co-trimoxazole (both combined)

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19
Q

Which antibiotics inhibit DNA gyrase?

A

Fluoroquinolones: Ciprofloxacin

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20
Q

Name an antibiotic that binds to RNA polymerase

A

Rifampicin

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21
Q

Which antibiotics causes DNA strand breaks?

A

Nitrodimazoles: metronidazole

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22
Q

What is trimethoprim used to treat?

A

UTI, prostatitis, acute/chronic bronchitis

Co-trimoxazole= PCP treatment and prophylaxis

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23
Q

What is Ciprofloxacin used to treat?

A

Acute pyelonephritis, gastroenteritis

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24
Q

What is rifampicin used to treat?

A

Mycobacteria- used as part of the quadruple TB treatment

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25
Q

What are nitrodimazoles used to treat?

A

Anaerobes, parasites

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26
Q

What are the cautions of Trimethoprim?

A

Pregnancy as inhibit folate synthesis

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27
Q

What are the side effects of trimethoprim?

A

Hyperkalaemia, depression of haematopoesis

Co-trimoxazole= Hyperkalaemia, Rash

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28
Q

What are the cautions of Fluoroquinolones?

A

Epilepsy, D6PD deficiency, myasthenia gravis

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29
Q

What are the contraindications of rifampicin?

A

Jaundice

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30
Q

What are the side effects of rifampicin?

A

Orange discolouration of saliva and urine, anorexia, nausea and vomitting, haemolytic anaemia

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31
Q

What are the contraindications of metronidazole?

A

Interaction with alcohol= profuse vomitting

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32
Q

What are the four types of antibiotics that inhibit protein synthesis?

A

Chloramphenicol
Macrolides
Tetracyclines
Aminoglycosides

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33
Q

List two macrolide antibiotics

A

Clarithromycin and erythromycin

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34
Q

List two tetracycline antibiotics

A

Tetracycline, doxycycline

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35
Q

List two aminoglycoside antibiotics

A

Gentamycin and streptomycin

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36
Q

What are macrolides used to treat?

A

General alternative to penicillin

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37
Q

What are tetracyclines used to treat?

A

Broad spectrum antibiotic.

Acne, Chlamydia, SIADH

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38
Q

What is gentamycin used to treat?

A

Staph, aureus, gram -ve bacilli, used for severe sepsis

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39
Q

What are the contraindications of tetracyclines?

A

Children <12 due to deposition in bone and teeth leading to hypoplasia, renal disease

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40
Q

What are the contraindications of aminoglycosides?

A

Myasthenia gravis

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41
Q

What antibiotic is usually used to treat non severe community acquired pneumonia?

A

Amoxicillin +/- clarithromycin

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42
Q

What antibiotic regime is usually used to treat TB?

A

RIPE= Rifampin (6), Isoniazid (6) , Pyrazinamide (2), and Ethambutol (2)

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43
Q

What antibiotic is usually used to treat atypical community acquired pneumonia?

A

Clarithromycin

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44
Q

What antibiotic is usually used to treat cellulitis?

A

Flucloxacillin

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45
Q

What antibiotic is usually used to treat infrequent exacerbations of COPD?

A

Amoxicillin/ Clarithromycin/ Doxycline

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46
Q

What antibiotic is usually used to treat UTIs?

A

Trimethoprim/ Nitrofurantoin

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47
Q

What antibiotic is usually used to treat hospital acquired pneumonia?

A

Co-amoxiclav

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48
Q

What antibiotic is usually used to treat acute pyelonephritis?

A

Co-amoxiclav/ Ciprofloxacin

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49
Q

What antibiotic is usually used to treat gonorrhoea?

A

Ceftriaxone (IM)

Azithromycin (PO)

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50
Q

What antibiotic is used to treat chlamydia?

A

Doxycycline/ Azithromycin (PO)

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51
Q

What antibiotic is used to treat syphilis?

A

Benzylpenicillin

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52
Q

What antibiotic is used to treat gastroenteritis?

A

(Campylobacter) Clarithromycin

(Salmonella/ Shigella) Ciprofloxacin

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53
Q

What antibiotic is used to treat C.Difficile?

A

1st: Metronidazole
2nd: Vancomycin

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54
Q

What antibiotic is used to treat appendicitis?

A

Ceftriaxone and metronidazole

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55
Q

What is pharmodynamics?

A

How the drugs affects the body

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56
Q

What can drugs target?

A

Receptors, enzymes, transporters and ion channels

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57
Q

Name some types of receptors

A

Ligand-gated ion channels
G protein coupled receptors
Kinase-linked receptors
Nuclear receptors

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58
Q

What are the two types of G protein coupled receptors?

A

M3R and beta-2adrenoreceptors

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59
Q

What is potency?

A

A measure of how well a drug works

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60
Q

What is EC50?

A

The concentration of a drug that gives half the maximal response

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61
Q

What is an agonist?

A

A compound that binds to a receptor and activates it

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62
Q

What is an antagonist?

A

A compound that reduces the effect of an agonist

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63
Q

What is competitive antagonism?

A

When an antagonist competes with the agonist to bind receptors, thereby preventing agonists from having an effect.

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64
Q

What is non-competitive antagonism?

A

When an antagonist binds near the receptor causing a conformational change, so the agonist cannot activate the receptor

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65
Q

What effect does competitive antagonism have?

A

It causes the dose response curve to shift right, meaning that more agonist is required to illicit the same response

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66
Q

What effect does non-competitive antagonism have?

A

A right shift and down of the dose response curve= meaning that even more agonist is required to illicit the same response

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67
Q

What are the two types of cholinergic receptors?

A

Muscarinic ACh receptor and Nicotinic ACh receptor

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68
Q

What is affinity?

A

Describes how well a ligand binds to the receptor (shown by both antagonist and agonist)

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69
Q

What is efficacy?

A

Describes how well a ligand activates the receptor (only agonists show efficacy)

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70
Q

What is signaling transduction and amplification?

A

When a ligand binds at a receptor it sets off a signalling cascade which is then amplified. This can determine how powerful a response is

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71
Q

What is allosteric modulation?

A

When binding of an allosteric ligand to a receptor can affect an agonists effect on a receptor either positively (allosterically) or negatively (orthosterically)

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72
Q

What is inverse agonism?

A

When a drug binds to the same receptor as an agonist and induces a pharmacological response opposite to that agonist

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73
Q

What is tolerance?

A

The reduction in drug effect over time. It is seen with continuous, repeated high concentration over drug over time

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74
Q

Give an example of a selective drug

A

Salbutomol is a selective B2 adrenoceptor agonist (whereas isoprenaline is non selective so it activates both B1 and B2 receptors)

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75
Q

How do NSAIDs work?

A

They inhibit the enzyme cyclooxygenase by competitive inhibition, which is the enzyme that converts arachidonic acid to prostaglandin H2

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76
Q

Are NSAIDs selective?

A

Most are selective- celecoxib is COX2 selective

Aspirin is non-selective so acts on both COX1 and COX2

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77
Q

Where is COX found?

A 
COX1= Normally and widely around the body
COX2= Induced and found in inflammation only
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78
Q

What is the role of uniporters?

A

Use energy from ATP to pull molecules in

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79
Q

What are symporters?

A

Use the movement of one molecule to move another molecule in against its concentration gradient

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80
Q

What are antiporters?

A

One substance moves against its conc gradient using energy from the second substance moving down its gradient (opposite directions)

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81
Q

What is the route of formation of dopamine?

A

L-Tyrosine forms L dopa

L dopa then forms dopamine via dopa decarboxylase

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82
Q

What is synergy?

A

Where the actions of two drugs combine, such as paracetamol and codeine to increase analgesic effect

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83
Q

What are some patient risk factors for drug interactions?

A 
Polypharmacy
Old age
Genetics
Hepatic disease 
Renal disease
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84
Q

What are some drug risk factors for interactions?

A

Narrow therapeutic index
Steep dose/response curve
Saturable metabolism

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85
Q

What is saturable metabolism?

A

When after a certain point, the drug cannot be metabolised anymore

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86
Q

What things can affect drug absorption?

A

Motility, Acidity, Solubility, Complex formation, enterocyte action

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87
Q

What interactions affect motility?

A

Antibiotics often cause diarrhoea, so interacts with the absorption of the oral contraceptive

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88
Q

What can affect the solubility of a drug?

A

Eating high fat food whilst taking a fat soluble drug will cause the drug to dissolve and thus not be absorbed

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89
Q

What four major things affect pharmokinetics?

A

Aborption
Distributions
Metabolism
Excretion

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90
Q

How might distribution of a drug be affected?

A

Protein binding in the plasma

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91
Q

How might metabolism of a drug be affected?

A

Things affecting Cytochrome P450

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92
Q

How might excretion of a drug be affected?

A

Renal excretion is pH dependent= Weak bases are cleared faster if urine is acidic, and vice versa

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93
Q

Name some acidic drugs

A

Aspirin, Ibuprofen, paracetamol, warfarin

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94
Q

Name some basic drugs

A

Amphetamine, atropine, propranolol, salbutamol

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95
Q

Name some ways to avoid drug interactions

A

Prescribe rationally= BNF
Medicines information service
Technological mechanisms

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96
Q

Name some foods that have drug interactions

A

Avocado, grapefruit juice, garlic, Soya, Ginger

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97
Q

Name 3 drug targets

A

Receptors, enzymes, transporters, ion channels

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98
Q

The action of a drug can be either receptor-related or tissue-related, which of these do the principles of affinity and efficacy influence? (1) What do agonists / antagonists show?

A

Affinity and efficacy relate to receptors

Agonists show affinity & efficacy / antagonists show affinity only

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99
Q

Describe the difference between tolerance and desensitisation?

A

Tolerance - reduction in drug effect over time (continuously repeated high conc)
Desensitisation - receptors become degraded / uncoupled / internalised

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100
Q

What class of drug is Candesartan?

A

Angiotensin II Receptor Blocker

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101
Q

Which common condition often diagnosed in childhood is a contraindication of beta-blockers and why?

A

Asthma

Beta-Blockers cause bronchoconstriction

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102
Q

Approximately 60% of the body is comprised of water. In an average 70Kg male this constitutes 42 L of water. Approximately how many liters of water would you expect to find in the following compartments of this patient: Intracellular, Extracellular, Plasma?

A
  • Intracellular ~ 28L (2/3),
  • Extracellular~ 14L (1/3).
  • Plasma ~3 L (a component of the extracellular compartment)
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103
Q

What are the 4 stages of Pharmacokinetics?

A
  • Absorption
  • Distribution
  • Metabolism
  • Excretion
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104
Q

What is pharmacokinetics?

A

The fate of the drug in the body after administration

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105
Q

What is a first order reaction?

A

Where rate of diffusion is directly proportional to the concentration of the drug

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106
Q

What is a second order reaction?

A

Where Rate of diffusion is directly proportional to the square of the conc of the drug

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107
Q

What is a third order reaction?

A

Where Rate of diffusion is directly proportional to the cube of the conc of the drug

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108
Q

What is a zero order reaction?

A

Where rate of diffusion is unrelated to the conc of the drug

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109
Q

What are the three compartments of the body?

A

Plasma
Interstitial
Intracellular

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110
Q

What are the 5 ways that a drug can move between compartments?

A 
Simple diffusion
Facilitated diffusion
Active transport
Extracellular spaces
Non-ionic diffusion
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111
Q

What is the relationship between pH, and the ionisation of drugs?

A

When pH is increased- weak acids become more ionised, and weak bases become less ionised
and Vice Versa

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112
Q

What is pinocytosis?

A

A form of carrier mediated entry into the cytoplasm. Usually involved in the uptake of endogenous macro molecules.

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113
Q

What is bioavaiability?

A

Amount of drug taken up as a proportion of the amount administered

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114
Q

What route of administration gives the highest bioavailability?

A

Intravenous

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115
Q

List some routes of administration

A

Oral, IV, IM, Transcut, Intrathecal, sublingual, inhalation, topical, rectal

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116
Q

What can vary the bioavailability of oral medication?

A

Surface area of gut, pH of gut, stomach motility, diarrhoea etc.

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117
Q

Which route of administration works the fastest?

A

Intravenous

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118
Q

Why is it necessary for an oral drug to be lipid soluble?

A

To allow for it to be absorbed in the gut

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119
Q

What is volume of distribution?

A

The total amount of drug in the body/ the concentration of drug in the plasma

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120
Q

In which component are proteins/large molecules active?

A

Plasma

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121
Q

In which component are water soluble molecules active?

A

Plasma and interstitial compartment

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122
Q

In which component are lipid soluble molecules active?

A

Intracellular fluid

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123
Q

What is clearance?

A

The volume of plasma that can be completely cleared of drug per unit time

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124
Q

What is kidney clearance?

A

rate of appearance in urine/ plasma concentration

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125
Q

What substance is used as a marker in the kidneys?

A

Creatinine

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126
Q

What is renal blood flow?

A

1l/min

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127
Q

What properties would make a drug more likely to be eliminated by the kidney?

A

Water soluble and small molecules

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128
Q

What is hepatic extraction ratio?

A

The proportion of a drug that can be removed by one passage through the liver

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129
Q

What is high first pass metabolism?

A

A high hepatic extraction ratio, meaning that a high proportion is removed by one passage through the liver

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130
Q

What is the function of phase I reactions?

A

To make drugs more reactive = expose OH or other reactive sites

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131
Q

What enzyme is used in phase I reactions?

A

Cytochrome P450 enzymes

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132
Q

Give some examples of phase I reactions

A

Hydroxylation, delalkylation, deamination, hydrogen removal, reduction, hydrolysis

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133
Q

What is the aim of phase II reactions?

A

Glucuronidation= Make the molecule hydrophillic

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134
Q

What enzyme is used in phase II reactions?

A

Glucuronosyltransferase (UGT)

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135
Q

What is enterohepatic circulation?

A

When some drug from the bile rediffuses from the gut back into the blood, and is then reconjugated

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136
Q

Why are IV infusions used?

A 
Enable steady state plasma
Enables accurate drug delivery
Fast
100% Bioavailability
Useful if oral medication isn't possible
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137
Q

When does steady state normally occur?

A

4-5 half lives

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138
Q

How do you calculate loading dose?

A

Loading dose = steady state x volume of distribution

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139
Q

How do you calculate rate of elimination during a steady state?

A

Clearance x drug conc between peaks and troughs

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140
Q

How do you calculate steady state?

A

Rate of infusion/ Clearance

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141
Q

How is insulin administered?

A

Sub cutaneously

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142
Q

What is the oral bioavailability of morphine?

A

50%= due to first pass metabolism of the liver

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143
Q

What percentage of the population cannot metabolism morphine?

A

10%

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144
Q

Name some naturally occurring opioids

A

Morphine, Codeine

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145
Q

Name some synthetic opioids

A

Pethidine, fentanyl, alfentanil

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146
Q

Name an opioid antagonist

A

Nalaxone

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147
Q

How do opioids work?

A

Opioids block the descending pain transmission
They use the natural opioid receptors (G proteins) and inhibit the release of pain transmitters at the spinal cord and midbrain, and modulate pain perception in higher centres

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148
Q

What are the opioid receptors?

A

MOP, KOP, DOP, NOP

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149
Q

Where are opioid receptors found?

A

Midbrain, spine, GI tract, and breathing centre

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150
Q

What is dependence?

A

Psychological (craving of euphoria) and physical dependence

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151
Q

What are some side effects of opioids?

A

Respiratory depression, Sedation, Nausea and vomiting, Constipation, Itching. Immune suppression, Endocrine effects

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152
Q

How do you treat opioid induced respiratory depression?

A

Airways, breathing, circulation

IV Naloxone and titrate to effect

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153
Q

List some local anaesthetics

A

lidocaine and procaine

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154
Q

How do local anaethetics work?

A

Local anesthetics block the conduction of the nerve by blocking Na+ channels thereby preventing the depolarisation of the nerve and the propagation of the action potential

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155
Q

Why do patients often get constipated with opioid use?

A

Opioid receptors are located in the GI tract

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156
Q

How long does opioid withdrawal take?

A

It begins at 24 hrs and lasts about 72 hrs

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157
Q

Which branch of the nervous system is voluntary and what neurotransmitter(s) does it use?

A

Somatic

Uses acetyl choline

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158
Q

Which branch of the nervous system is involuntary and what neurotransmitter(s) does it use?

A

Autonomic

Uses Ach and noradrenaline

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159
Q

What are the two branches of the autonomic nervous system?

A

Parasympathetic and sympathetic

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160
Q

Is the post-synaptic ganglion closer to the spinal cord in the sympathetic or the parasympathetic system?

A 
Sympathetic= Ganglion lies closer to the spinal cord
Parasympathetic= Ganglion lies closer to the effector organ
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161
Q

What type of receptors are used in parasympathetic and sympathetic systems?

A

Both use nicotinic for the first synaptic ganglion
Parasympathetic uses muscarinic receptors in effector organs
Sympathetic uses alpha or beta receptors in effector organs

162
Q

What neurotransmitters does the parasympathetic and sympathetic systems use?

A

Both use ACh in the first synaptic ganglion
Parasympathetic also uses ACh in effector organ
Sympathetic uses noradrenaline at effector organ

163
Q

What are NANCs and where are they found?

A

Non-adrenergic, non-cholinergic autonomic transmitters

Found in the enteric nervous system

164
Q

Briefly explain what happens at a neuromuscular junction

A
  1. Choline acetyl transferase enzyme makes ACh
  2. ACh is packaged into a vesicle
  3. The vesicle is exocytosed and ACh is released
  4. ACh acts on receptor
  5. ACh is broken down by acetylcholinersterase
165
Q

What is botulinum toxin and how does it work?

A

It prevents vesicle fusion thus inhibiting the release in ACh release.
It results in paralysis, and is used for spasticity, and cosmetically (botox)

166
Q

How does nerve gas cause paralysis?

A

It irreversibly inhibits acetylcholinesterase meaning ACh remains indefinately

167
Q

Where are M1 receptors found?

A

Mainly in the brain

168
Q

Where are M2 receptors found?

A

The heart- their activation slows the heart

169
Q

Where are M3 receptors found?

A

Glandular and smooth muscle. Cause bronchoconstrictition, sweating, salivary gland secretion

170
Q

Where are M4/5 receptors found?

A

Mainly in the CNS

171
Q

How does atropine help in cardiac arrest and bradycardia?

A

It blocks M2 receptors so will oppose the parasympathetic nervous system and stop slowing of the heart

172
Q

List some functions of the parasympathetic nervous system

A 
Rest and digest
Constricts pupils
Stimulates tears and salivation
Lowers heart rate
Reduces respiration
Contract bladder
Erection
173
Q

List some functions of the sympathetic nervous system

A 
Fight or flight 
Dilates pupils
Inhibits tears and salivation
Increases heart rate and respiration
Relaxes bladder
Ejaculation
174
Q

What is the consequence of Alpha 1 receptor innervation?

A

Contraction of smooth muscles (pupils, blood vessles), Vasoconstriction, increased blood pressure

175
Q

What is the consequence of alpha 2 receptor innervation?

A

Lowers blood pressure, Increased glucagon release, reduced insulin

176
Q

What is the consequence of beta 1 receptor innervation?

A

Chronotropic and inotropic effects on heart

= Increases heart rate and myocardial contractility

177
Q

What is the consequence of beta 2 receptor innervation?

A

Relaxes smooth muscle (vasodilation, bronchodilation)= lowers blood pressure

178
Q

What is the consequence of beta 3 receptor innervation?

A

Enhances lipolysis, relaxes detrusor muscle

179
Q

Which beta blockers are beta 1 selective?

A

Atenolol, bisoprolol, metoprolol

180
Q

What is the effect of adrenaline?

A

Targets blood vessels (alpha-1), heart (Beta-1) and bronchial smooth muscle (Beta-2), causing vasoconstriction, positive inotropic effects and bronchodilation

181
Q

What type of drug is atenolol?

A

B1 selective Beta blocker

182
Q

List a medication a that is derived from plants.

A 
Morphine= Poppy
Atropine= Deadly nightshade
183
Q

Name a drug that was derived by chance

A

Penicillin and sildenafil

184
Q

Why are sulphonamide nuclei added to drugs?

A

It is rigid and unreactive, so adds stability to the drug

185
Q

Name a drug that was derived by rational receptor approach

A

Proponalol

Cimetidine

186
Q

What are sterioisomers?

A

Molecules that have chiral carbons, and are mirror images of one another= rotate plane polarised light in an opposite direction

187
Q

What are the two types of stereoisomers and which is used more?

A

D (S form) or L (R form). Biological systems use L-amino acids (R form).

188
Q

Who invented the first vaccine and what was the vaccine for?

A 
Edward Jenner (in 1796)
Smallpox
189
Q

List some recombinant proteins in clinical drug use

A 
Insulin
Erythropoietin
Growth hormone
Interleukin 2
Gamma interferon
Interleukin 1 receptor antagonist
190
Q

What is

Combinatorial chemistry?

A

Biochemical modification of natural products

191
Q

What is Combinatorial biosynthesis?

A

Large enzyme complexes generate natural products, and then manipulate biosynthetic machinery to generate structural analogues

192
Q

Briefly explain antibody based immunotherapy

A

Serum from patients who have had a certain disease can be taken and their antibodies can be isolated and given to other patients as a treatment

193
Q

Briefly explain monoclonal antibody formation

A

Mouse is immunised against specific antigen. B cells are isolated to check they are producing antibodies. If it is, B cells in the spleen are removed and then cultured along with myeloma tumour cells. Solution is added to fuse the B cells with the tumour cells to produce hybridomas that can divide indefinitely and produce antibodies. The hybridomas are then cloned. Antibodies are produced and then used for clinical purposes

194
Q

What are humanised antibodies?

A

Chimeric (humanised) antibodies have a mix of human and mouse antibody chains

195
Q

How does azathioprine prevent DNA formation?

A

Blocks incorporation of thiopurine analogues into the DNA structure, causing chain termination and cytotoxicity

196
Q

What is high-throughput screening?

A

Robotics and data processing software to screen millions of chemical, genetic or pharmacological tests to find targets. It looks at the biological activity of compounds

197
Q

What is an adverse drug reaction?

A

An unwanted or harmful reaction following administration of a drug or combination of drugs under normal conditions of use and is suspected to be related to the drugs

198
Q

What is the different between adverse drug reactions and side effects?

A

Adverse drug reactions have to be negative
Side effects can be beneficial
Generally minor and predictable ADR’s are called side effects

199
Q

What can make a patient more susceptible to an ADR?

A 
Age- elderly or neonates
Gender- More common in females
Pregnancy- Negative effect on baby etc
Disease- Liver or renal in particular
Drug interactions
Diet or alcohol intake changes
Genetics
200
Q

What is a hyper-susceptibility effect?

A

A very small amount of a drug below the theraputic range, that still causes an ADR

201
Q

What are collateral effects?

A

ADRs that occur within the theraputic range

202
Q

What are toxic effects?

A

ADRs that occur above the theraputic range

Can occur if dose is too high or drug excretion is reduced

203
Q

What are some drug risk factors for ADRs?

A

Steep dose-response curve
Low therapeutic index
Commonly causes ADRs

204
Q

What are the Rawlins Thompson categories for adverse drug reactions?

A 
Augmented
Bizarre
Chronic
Delayed
End of use 
Failure of therapy
205
Q

What are augmented adverse drug reactions?

A

Commonest and predictable
An extension of the clinical effect
Dose related and self-limiting

206
Q

Give an example of an augmented adverse drug reaction

A

Examples include diuretic causing dehydration, anticoagulants causing bleeding, hypertensive drug causing hypotension.

207
Q

What are bizarre adverse drug reactions?

A

Not predictable and not dose dependent ABRs

208
Q

List some categories of time dependent reactions

A 
Rapid reactions
First dose reactions
Early reactions
Intermediate reactions
Late reactions
Delayed reactions
209
Q

Give an example of a drug that has a delayed reaction

A

Thalidomide

210
Q

What are end of treatment adverse drug reactions?

A

Drug reactions that occur after drug withdrawal e.g. withdrawal

211
Q

Give an example of a bizarre drug reaction

A

Anaphylaxis

212
Q

What does DoTS stand for (regarding ADRs)?

A

Dose relatedness
Timing
Susceptibility

213
Q

What are chronic adverse drug reactions?

A

Drug reactions that occur after long term treatments of a drug

214
Q

Give an example of a chronic drug reaction

A

Steroids can cause osteoporosis

215
Q

What is a failure adverse drug reaction?

A

When a medication fails to work properly- oral contraceptive etc.

216
Q

What is the yellow card scheme?

A

A form to report adverse drug reactions

217
Q

What are the clinical features of anaphylaxis?

A

CVS- Vasodilation, increased vascular permeability, lowered BP, angio-oedema
Respiratory- Dyspnoea due to bronchoconstriction, mucus production
Skin- Urticaria Rash, swelling
GI- Pain, vomiting

218
Q

How is anaphylaxis treated?

A

Commencement of basic life support- Airways, Breathing, Circulation
Stop drug if infusion
Adrenaline IM 500 micrograms Or 300 micrograms in epi-pen
High flow oxygen
IV anti histamine (Chlorphenamine 10mg)
IV hydrocortisone (100-200mg)

219
Q

When do ADRs need to be reported via the yellow card system?

A

All suspected ADRs for new medicines
All ADRs in children
All serious reactions to include fatal, life threatening, disabling, or incapacitation ADRs

220
Q

What is non-immune anaphylaxis?

A

Due to direct mass cell degranulation
Doesn’t require prior exposure
Clinically identical to immune anaphylaxis

221
Q

What is the effect of adrenaline?

A

Vasoconstriction- increases peripheral vascular resistance to increase BP
Stimulation of beta1- adrenoceptors- positive inotropic and chronotropic affects on heart
Attenuates anaphylactic response from mast cells
Reduces oedema

222
Q

What type of hypersensitivity reaction is anaphylaxis?

A

Type 1- IgE mediated

223
Q 
A drug given through IV route is assumed to have a bioavailability of..
A) 50%
B) 75%
C) 100%
D) 10%
A

Correct answer= C

224
Q

What is meant by the term parenteral administration?

A

The drug is delivered to the systemic circulation, bypassing the GI tract (e.g. IV, IM, Sub Cut)

225
Q

What is meant by the term enteral administration?

A

The drug is delivered via the GI tract (e.g. oral, rectal)

226
Q

What is meant by the term pharmacodynamics?

A

What a drug does to the body

227
Q

Why should you not give propanolol to patients with asthma?

A

It is a non-selective Beta blocker, so also affects B2= causing bronchoconstriction

228
Q

NAPQI is a toxic metabolite that builds up in the liver and causes acute liver necrosis. Levels of which antioxidant are depleted in paracetamol OD?

A

glutathione

229
Q

What drug is used to treat paracetamol OD?

A

Acetylcysteine

230
Q

Activation of which type of adrenoreceptor leads to tachycardia, increased myocardial contractility and renin release?

231
Q 
Which of the following processes do beta lactam antibiotics intefere with...
A) Bacterial protein synthesis
B) Bacterial cell wall synthesis
C) Bacterial nucleic acid synthesis
D) Viral protein synthesis
A

Correct answer= B

232
Q 
Which of the following is an irreversible enzyme inhibitor...
A) Enalapril
B) Aspirin
C) Ibuprofen
D) Salbutamol
A

Correct answer= B

233
Q

What is the first line for s. pyogenes?

A

Penicillin

234
Q

Name a beta lactamase inhibitor antibiotic?

A

Clavulanic acid, sulbactam, and tazobactam

235
Q

What is co-amoxiclav?

A

amoxicillin and clavulanic acid

236
Q

Briefly explain how ramipril works

A

Ramipril targets Angiotensin Converting Enzyme (ACE), and competitively inhibits it. This inhibits synthesis of potent vasoconstrictor peptide angiotensin II leading to vascular smooth muscle relaxation and vasodilatation.
Overall effect: Reduced blood pressure

237
Q

When should renal function be monitored when using a ACE inhibitor?

A

Renal impairment — monitor renal function 1–2 weeks after starting an ACE-inhibitor, after each dose increase, and regularly throughout treatment

238
Q

Why do Afro-Caribbean patients respond less well to ACE inhibitors?

A

Angiotensin converting enzyme (ACE) inhibitors, β blockers, and angiotensin receptor antagonists are generally less effective as monotherapy in black hypertensives, because of the tendency towards a low renin state and a lower cardiac output, with increased peripheral resistance.

239
Q

What is St. Johns Wort?

A

St John’s wort is a herbal remedy that has been used for hundreds of years to treat mental health problems. Today it is mainly used as an over-the-counter remedy to treat mild and moderate depression, and sometimes seasonal affective disorder (SAD), mild anxiety and sleep problems.

240
Q

List some medications that St. Johns Wort is known to interact with?

A

Alprazolam (Xanax), Some contraceptives, Aminolevulinic acid, Amitryptiline, Cyclosporine, Digoxin, Fenfluramine, Medications changed by the liver, Antidepressants , Medications for HIV/AIDS, Medications for pain (Narcotic drugs), Warfarin

241
Q

In a patient with a new diagnosis of depression what class of drug would initially be used?

A

SSRIs are usually the first choice medication for depression because they generally have fewer side effects than most other types of antidepressant

242
Q

How does methotrexate work for inflammation?

A

Methotrexate has antiinflammatory and immunosuppressive effects which are due to inhibition of inflammatory mediators such as IL-6, IL-8 and tumour necrosis factor

243
Q

Why is Folic Acid given to RA patients on Methotrexate?

A

Methotrexate (As a cancer treatment) acts by inhibiting the conversion of folic acid to tetrahydrofolate therefore preventing protein synthesis. As this is not required in rheumatoid arthritis, the patient should take folic acid to prevent deficiency

244
Q

Doxazosin and Tamsulosin are both alpha 1-blockers and both used for benign prostatic obstruction, which receptors do they act on?

A

They are highly selective for alpha-1 adrenoceptors which are found mainly on smooth muscle, including blood vessels and urinary tract
Blocking these receptors therefore causes relaxation, so vasodilation and reduced resistance to bladder outflow

245
Q

An elderly gentleman needs cataract surgery and is taking Tamsulosin for his lower urinary tract symptoms (LUTS), why is it important that he lets his surgeon know that he is taking it?

A

It may slightly lower his blood pressure, so is important to consider during the anaesthetics

246
Q

The patient complains of dizziness when standing up quickly after taking Tamsulosin with his breakfast, how would you advise him?

A

Start taking the medicine at bedtime to minimise the impact of the dizziness (although if they get up from the bed at night time, they will need to be careful)

247
Q

How should alendronate be taken?

A

In the morning, at least 30 minutes before eating with plenty of water. The patient should remain upright for 30 minutes after taking.

248
Q

Why would a patient be taking letrozole?

A

For early and locally advanced oestrogen-receptor positive breast cancer

249
Q

How would you treat a P. aeruginosa infection?

A

Ciproflolaxin

250
Q

What is Clenil Modulite?

A

Beclomethosone (ICS)- given for prophylaxis of asthma attacks

251
Q

What is salbutamol?

A

A SABA. Given for acute flares of asthma/ after exercising.

252
Q

What class of drug is contraindicated with non DHP CCBs?

A

Beta blockers (precipitate heart failure)

253
Q

What medication is given in PCI?

A

CABG

Aspirin + Prasugrel (or clopidogrel if on anticoagulant)

254
Q

What medication is given in fibrinolysis for STEMI?

A

Alteplase + aspirin + ticagrelor

255
Q

When is fibrinolysis indicated in STEMI?

A

If over 120 mins but below 12 hrs

256
Q

What is the immediate treatment of NSTEMI?

A

Aspirin+ fondaparinux

257
Q

What is the typical basic dual antiplatelet therapy for STEMI/NSTEMI?

A

Aspirin + ticagrelor

258
Q

What is the higher risk dual antiplatelet therapy for NSTEMI/STEMI?

A

Aspirin + prasugrel

259
Q

What is the long term management post MI?

A 
ABAAC
AceI/ARB, 
Beta Blocker
Aspirin 
Atorvstatin
Clopidogrel / prasugrel/ ticagrelor
260
Q

What is prescribed for heart failure?

A

DABAD

  1. Diuretics (loop)= furosemide 40mg
  2. ACEi
  3. Beta blocker= Carvedilol 3.125 mg
  4. Aldosterone antagonist= Spironlactone 25 mg
  5. Digoxin
261
Q

What condition are beta blockers contraindicated for?

262
Q

What would you do for a non haemodynamically stable AF?

A

DC Cardioversion

263
Q

What would you do for a haemodynamically stable AF with a rate over 200bpm?

A

DC Cardioversion

264
Q

What would you do for a haemodynamically stable AF with a rate under 200bpm, and onset less than 48hrs?

A

Rhythm control+ LMWH

  • Electrical DC cardioversion
  • Amiodarone
265
Q

What would you do for a haemodynamically stable AF with a rate under 200bpm, and onset morethan 48hrs?

A

Rate Control

- Beta blocker or CCB

266
Q

What does a CHA2DS2-VASc score of over 1(males) or over 2(females) indicate?

A

Anticoagulate with DOAC

267
Q

What is not indicated in heart failure

  • Ramipril
  • Furosemide
  • Verapamil
  • Carvedilol
  • Spironlactone
268
Q

What type of drug is Carvedilol?

A

Beta blocker

269
Q

What are the ADPr antagonists?

A

Clopidogrel
Prasugrel
Ticagrelor

270
Q

What is the main side effect of aspirin?

A

GI irritation (Give with PPI)

271
Q

What is the main caution with digoxin?

A

Narrow therapeutic window

272
Q

What clotting factors are inhibited by warfarin?

A

10, 9, 7, 2

273
Q

What is the target INR?

274
Q

What do DOACs inhibit?

A

Factor Xa (prothrombin cannot be converted to thrombin)

275
Q

When is fondaparinux prescribed?

A

Immediate treatment of NSTEMI

276
Q

How is heparin typically administered?

A

SubCut (5000 units SC daily)

277
Q

When is fresh frozen plasma given?

278
Q

What are the K+ sparing diuretics?

A

Spronlactone, amiloride

279
Q

What drug class is flecianide and when is it given?

A

Na+ channel blocker

Block channels responsible for depolarisation

280
Q

When would EPO often be given?

A

Chronic disease

In Jehovah’s witnesses if blood products are refused

281
Q

What is the immediate management of a STEMI?

A 
MONA
Morphine
Oxygen
Nitrate
Aspirin 300mg
282
Q

A patient comes in with massive bleed. He is currently on warfarin. How is this reversed in an acute setting?

A

Prothrombin complex concentrate and vitamin K

283
Q

Which P2Y12 inhibitor is reversible?

A

Ticagrelor

284
Q

What are whole blood products indicated for?

A

Massive blood loss

285
Q

What blood products would be given for DIC?

A

First line- Platelets

Second line- Cryoprecipitate

286
Q

What blood product would be given first line for warfarin overdose?

A

Prothrombin complex concentrate

287
Q

What blood product would be given for TTP?

A

Fresh frozen plasma

288
Q

What blood product would be given for VWD?

A

Cryoprecipitate

289
Q

How is DKA monitored/treated?

A

FIG-PICK

  • Fluids
  • Insulin; actrapid
  • Glucose monitoring
  • Potassium monitoring
  • Infection- find and treat
  • Chart fluid balance
  • Ketone monitoring
290
Q

What would you prescribe for stable angina?

A
  1. Beta blocker/ calcium channel blocker

2. Nitrate

291
Q

What is the first pharmacological intervention for type 2 diabetes?

292
Q

What are the main side effects of metformin?

A

Nausea and diarrhoea

293
Q

How does metformin work?

A

Decrease hepatic glucose production

Increase muscle glucose uptake and utilisation

294
Q

How is thyrotoxic storm treated?

A 
Fluids
Propranolol
Digoxin
Hydrocortisone
Carbimazole
295
Q

What are the methods of treating hyperthyroidism?

A
  • Radioactive iodine
  • Thionamides
  • Surgery
  • Beta blockers
296
Q

How is hypothyroidism treated?

A

Levothyroxine for secondary and primary causes

297
Q

How would acute hypothyroidism be treated?

A

Liothyronine IV (T3)

298
Q

What class is metformin?

299
Q

What class is gliclazide?

A

Sulphonyurea

300
Q

What class is dapagliflozin?

A

SGLUT2 Inhibitor

301
Q

What class is pioglitazone?

A

Thiazolidinedione

302
Q

What class is sitagliptin?

A

DPP4 Inhibitor

303
Q 
Which of these is the priority in the treatment of a DKA
A) Potassium monitoring
B) Insulin administration
C) Ketone monitoring
D) Fluid resuscitation
E) Glucose monitoring
304
Q

A 41-year-old lady has recently been started on carbimazole for Grave’s disease. She attends her GP as she believes she is having side effects from the medication.
Which of these would not be a potential side effect of taking carbimazole?
A) Palpitations
B) Constipation
C) Hair loss
D) Fatigue

305
Q

What surgical treatments could be given for OA?

A
  • Arthoscopy for loose bodies in joints
  • Osteotomy- removal of bone
  • Arthroplasty (joint replacement)
  • Fusion of joint
306
Q

What is the first line treatment for OA?

A

Education, Exercise, weight loss, physio

- Initially paracetamol

307
Q

What should be co-prescribed with NSAIDs?

A

Lansoprazole (15mg daily)

308
Q

Should NSAIDs or paracetamol be given first in degenerative arthritis?

A

Paracetamol

309
Q

What are the contranidications of NSAIDs?

A

Renal impairment
Heart failure
Liver failure
Peptic ulcers

310
Q

How quickly should treatment for rheumatoid arthritis start?

A

Within 3 weeks of symptoms

311
Q

Give an example of an Anti-TNF

A

Adalimumab
Infliximab
Entercept

312
Q

Give an example of an ANTI-CD20

313
Q

Give an example of an Anti-IL6

A

Sarliumab

Tocilzumab

314
Q

Give an example of a JAK inhibitor

A

Tofactinib

Barictinib

315
Q

What drug gives temporary male infertility?

A

Sulfasalazine

316
Q

What is the first line treatment for RA?

A

Methotrexate, leflunomide or sulfasalazine

317
Q

What are the side effects of methotrexate?

A

Pneumonitis, pulmonary fibrosis, liver toxicity, pancytopenia, tetratogenic

318
Q

What must be coprescribed with methotrexate?

A

Folic acid

319
Q

What are the side effects of lefunomide?

A

Increased BP, Peripheral neuropathy, liver toxicity

320
Q

How does methotrexate work?

A

Dihydrofolate reductase inhibitor, prevents cell replication and production of inflammatory mediators

321
Q

What is the second line treatment for RA?

A

Combination of= Methotrexate, leflunomide or sulfasalazine

322
Q

What is the third line treatment for RA?

A

Methotrexate plus biological DMARD (Usually TNF Inhibitor such as adalimumab)

323
Q

What type of drug is a rituximab?

324
Q

What is the fourth line treatment for RA?

A

Methotrexate plus rituximab

325
Q

What is the treatment for spondyloarthropathies

A
  1. Exercise +NSAID
  2. DMARD, Anti-TNF
  3. Secukinumab (ank spon), ustekinumab (Psoriatic)
326
Q

Are paracetamol or NSAIDs prescribed first in spondyloarthropathies??

327
Q

What does HRT increase the risk of?

A

Breast cancer and CVD

328
Q

What is denosumab prescribed for?

A

Osteoporosis (3rd line after adcal, bisphophonates and HRT)

= It is a MAb to RANKL

329
Q

What is secukinumab prescribed for?

330
Q

What is ustekinumab prescribed for?

A

Psoriatic arthritis

331
Q

How is osteomalacia treated?

A

Vit D (50000 IU before tapering down to 800IU daily) +/- Calcium

332
Q

How often is zoledronic acid given for osteoprosis?

A

IV once yearly

333
Q

What are the common side effects of allopruinol?

A

Gout if given during acute flare, skin rash, Stevens-Johnson syndrome

334
Q

What drug would be suitable first line for a patient with RA

  • Topical diclofenac
  • Leflunomide
  • Etanercept
  • IM methylprednisolone
A

Leflunomide

335
Q

What are the side effects of Isoniazid?

A

Hepatitis, neuropathy

336
Q

What are the side effects of pyrazinamide?

A

Gout, rash, nausea, myalgia

337
Q

What are the side effects of ethambutol?

A

Visual changes (optic neuritis)

338
Q

How does citalopram affect an ecg?

A

It prolongs the QT interval

339
Q

What should be avoided when on metronidazole?

340
Q

What antibiotic causes “red man” syndrome?

A

Vancomycin

341
Q

What antibiotic can cause tendon rupture?

A

Ciproflolaxin

342
Q

How do you treat undiagnosed dyspepsia?

A

1 month of PPI (Omeprazole)

343
Q

How do you treat GORD?

A

2 months of PPI

344
Q

What is the triple therapy for h. pylori?

A

PPI (omeprazole) + Clarithromycin + metronidazole or amoxicillin

345
Q

How do you treat a non-variceal upper GI bleed?

A

Adrenaline injection at bleeding site on endoscopy+ thermal/mechanical ligation + IV PPI for 72 hrs

346
Q

How do you treat a variceal upper GI bleed?

A

Terlipressin + prophylactic Abx + band ligation (oesophageal varices)

347
Q

How do you treat choleystitis?

A

IV Abx, IV fluids, analgesia, cholecystectomy

348
Q

How do you treat acute cholangitis?

A

Fluid resus, IV abx, analgesia, ERCP

349
Q

How do you treat chronic pancreatitis?

A

Analgesia, enzyme replacement therapy

350
Q

What hepatitis is best treated with pegylated interferon alpha?

A

B (can use in D but poor evidence)

351
Q

What hepatitis is common in East-Asia?

352
Q

How do you treat hepatic encephalopathy?

353
Q

How do you treat a mild flare of UC?

A
  1. Topical 5-aminosalicylate
  2. Oral 5-aminosalicylate
  3. Oral steroids
354
Q

How to you treat a severe flare of UC?

A
  1. IV steroids
  2. Ciclosporin
  3. Surgery
355
Q

How do you maintain remission after a mild flare of UC?

A

5-Aminosalicylate

356
Q

How do you maintain remission after a severe flare of UC?

A

Azathioprine or mercaptopurine

357
Q

How do you treat a flare of Crohns?

A
  1. Steroids
  2. 5-Aminosalicylate
    • Methotrexate
    • Infliximab
358
Q

How do you maintain remission of Crohns?

A
  1. Azathioprine or mercaptopurine

2. Methotrexate

359
Q

What is tenesmus?

A

Cramping rectal pain where the patient feels that they need to pass stool

360
Q

What is the first line treatment for asthma?

361
Q

What is the second line treatment for asthma?

362
Q

What is the third line treatment for asthma?

A

SABA+ICS+LABA

363
Q

What is the fourth line treatment for asthma?

A

SABA+ICS+LABA+Ipratropium

364
Q

What classifies as severe asthma?

A
  • Inability to complete sentances in one breath
  • Resp rate over 25
  • PEF 33-50%
  • Heart rate over 110
365
Q

What classifies as life threatening asthma attack?

A

Severe plus

  • o2<92%
  • Normal paCO2
  • Altered consciousness
366
Q

What classifies as near fatal asthma?

A

Life threatening plus hypercapnia (type 2 resp failure)

367
Q

What is the treatment of acute asthma attack?

A

O SHIT ME

  1. Oxygen if needed= Severe
  2. Salbutamol = Moderate/ Severe
  3. (Hydrocortisone or) prednisolone= Moderate/Severe
  4. Ipratropium= Add on for life threatening
  5. Theophylline
  6. Magnesium sulphate
  7. Escalate
368
Q

What is the best treatment for COPD?

A

Smoking cessation

369
Q

Give an example of a LAMA

A

Tiotropium

Ipratropium

370
Q

What is the first line treatment for COPD?

371
Q

What is the “triple therapy” for COPD?

A 
LABA= Salmeterol
LAMA= Tiotropium
ICS= Beclomethasone
372
Q

What are the rules of oxygen therapy?

A
  • Over 15 hrs a day
  • Patients with pO2 <7.3 kpa
  • No smoking !
373
Q

What is the main treatment for a COPD exacerbation that isn’t due to bacteria?

A

Prednisolone

374
Q

What are the classic symptoms of glucocorticoids?

A

CUSHINGOID MAP
Cataracts, ulcers, Striae, Hypertension, Incfection risk, Necrosis of bone, growth restriction, Osteoporosis, increased ICP, Diabetes, Myopathy, Adipose tissue hypertrophy, pancreatitis

375
Q

How do you treat mild CAP(curb 65 0-1)?

A

Oral Amoxicillin 5 days

376
Q

How do you treat moderate CAP (CURB65 2)?

A

Admit, IV fluids, analgesia, oxygen

IV Co-amoxiclav or Tazocin + Clarithromycin

377
Q

How do you treat severe CAP (CURB65 3+)?

A

Admit, IV fluids, analgesia, oxygen

IV Co-amoxiclav or Tazocin + Clarithromycin

378
Q

What should be co-prescribed with isoniazid?

A

Pyridoxine (Vitamin B6)

379
Q

How do you treat a haemodynamically stable patient with PE?

A

DOAC (Apixaban or rivaroxaban)= 3 months if known cause, 6 months if unknown cause

380
Q

How do you treat a haemodynamically unstable patient with PE?

A

Thrombolysis with alteplase

381
Q

If a Wells score is over 4, how should you investigate?

382
Q

If a Wells score is under 4, how should you investigate?

A

Plasma D dimer

383
Q

How would you generally initially treat a severe asthma attack?

A

Nebulised salbutamol and PO prednisolone

384
Q

How would you generally initially treat a life threatening asthma attack?

A

Nebulised salbutamol and tiotropium and PO prednisolone

385
Q

How do you treat stress incontinence?

A

Pelvic floor training
Duloxetine (SNRI)
Surgery

386
Q

How do you treat urge incontinence?

A

Bladder retraining
Antimuscarinics= oxybutynin
Mirabegron

387
Q

What is the treatment scheme of BPH?

A
  1. Alpha 1 antagonist e.g. doxazosin, Tamsulosin
  2. 5 Alpha reductase inhibitor e.g. finasteride
  3. TURP
388
Q

What is the main side effect of doxazosin/ tamsulosin?

A

Hypotension

389
Q

How do you treat migraine?

A

Triptan (CI in CHD and hypertension) + simple analgesia = NSAID or paracetamol
= Prophylaxis beta blocker

390
Q

How do you treat tension-type headache?

A

Simple analgesia, stress relief

391
Q

How do you treat cluster headache?

A

Subcut sumatriptan + high flow O2

= Beta blocker or tricyclic antidepressant for prophylaxis

392
Q

How do you treat trigeminal neuralgia?

A

Carbamazepine

= Calcium channel blocker for prophylaxis

393
Q

How do you treat temporal arteritis?

A

High dose Prednisolone and aspirin

394
Q

How do you treat generalised epilepsy?

A
  1. Sodium valproate

2. Lamotrigine/ Carbamazepine

395
Q

How do you treat focal epilepsy?

A
  1. Lamotrigine/ Carbamazepine

2. Levetiracatam/ Sodium valproate

396
Q

How do you treat absence epilepsy?

A
  1. Sodium valproate

2. Ethosuximide

397
Q

How do you treat myoclonic epilepsy?

A
  1. Sodium valproate

2. Lamotrigine

398
Q

In which types of epilepsy should carbamazepine be avoided?

A

Absence and myoclonic

399
Q

What is status epilepticus?

A

Continuous seizure lasting over 5 minutes or repeated seizures with no recovery of consicousness in between

400
Q

How do you treat status epilepticus?

A
  1. Benzodiazepine (diazepam or lorazepam)
  2. Phenytoin, sodium valproate, levetircetam, phenobarbital
  3. Induction of general anaesthetic with propofol
401
Q

How do you treat meningitis?

A
  • IM Benzylpenicillin in community
  • IV ceftriaxone or cefotaxime + amoxicillin if over 50 or very young
  • IV dexamethosone to reduce chance of long term consequences
402
Q

How do you treat encephalitis?

A

IV aciclovir stat

Phase 2a (31 decks)

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