CPT Flashcards Preview

Final Year > CPT > Flashcards

Flashcards in CPT Deck (1448)
Loading flashcards...
1
Q

Def: pharmacokinetics

A

Study of factors which determine the amount of drugs at their sites of biological effect at various times.

Includes

ADME

Absorption

Distribution

Metabolism

Excretion

2
Q

Def: Pharmacodynamics

A

What the drug does to the body

3
Q

Def: clearance

A

Volume of plasma cleared of a drug per unit time

4
Q

Def: half-life

A

Time taken for drug concentration to decline to half its original valu

Depends on volume of distribution and clearance

5
Q

Def: volume of distribution

A

Volume into which a drug appears to distribute

Theoretical volume that would be necessary to contain the total amount of a drug administered at the same concentration that it is observed in the blood plasma.

High for lipid-soluble drugs

Low for water-soluble drugs

6
Q

What factors can increase the volume of distribution?

A

Higher Vd indicates a greater amount of tissue distribution.

High lipid solubility (non-polar drugs), low rates of ionisation or low plasma binding capabilities have higher volumes of ditribution than drugs which are more polar, more highly ionised or exhibit high plasma binding.

Vd may be increased by renal failure (due to fluid retention) and liver failure (due to altered body fluid)

7
Q

Vd=

A

Total amount of drug in body/drug blood plasma concentration

8
Q

What is first order kinetics?

A

Clearance of durg is always proportional to plasma concentration

Most drugs are in this category

9
Q

What is zero order kinetics?

A

Clearance of drug is not always proportional to plasma concentration

Saturation of metabolism-> constant rate of elimination regardless of plasma levels

10
Q

Give some examples of drugs with zero order kinetics

A

Phenytoin

Salicylates

Ethanol

11
Q

What is bioavailability?

A

Percentage of the dose of a drug which reaches the systemic circulation

100% for IV administration

12
Q

How long is ~ required for a drug to reach a steady state?

A

Around 5 half lifes

13
Q

What does a loading dose do?

A

Reduces the time needed to reach a steady state, useful if long or short half life

14
Q

What are some drugs that use loading doses?

A

Phenytoin

Digoxin

Amiodarone

Theophylline

15
Q

What are the indications for therapeutic drug monitoring?

A

Ix lack of drug efficacy (possibility of poor compliance)

Suspected toxicity

Prevention of toxicity

16
Q

What are three drugs that must have therapeutic drug monitoring?

A

Aminoglycosides

Vancomycin

Li

17
Q

What are some dugs that have therapeutic monitoring?

A

Phenytoin

Carbamazepine

Digoxin

Ciclosporin

18
Q

Does Warfarin undergo therapeutic drug monitoring?

A

Not monitored per se, it is the biological effect that is monitored rather than the plasma drug level

19
Q

What is first pass metabolism?

A

Metabolism and inactivation of a drug before it reaches the systemic circulation

i.e. pre-systemic elimination

Occurs in gut wall and liver

20
Q

Gives some examples of drugs that undergo FPM

A

Propranolol

Verapamil

Morphine

Nitrates

21
Q

What are the pathways of drug metabolism and elimination?

A

Excreted unchanged by the kidney e.g. frusemide

Phase 1 metabolism and then renal excretion

Phase 2 metabolism and then renal excretion

22
Q

What is phase 1 metabolism

A

Creation of reactive, polar functional groups.

Oxidation: usually by cytochrome P450 system

Reduction and hydrolysis

23
Q

What is phase 2 metabolism?

A

Production of polar compounds for renal elimination

Either the drug or its phase 1 metabolite

Conjugation reactions: glucuronidation, sulfonation, acetylation, methylation

24
Q

What is the principle method of elimination?

A

Renal, depends on GFR

25
Q

How many subtypes of CyP450 are there?

A

>11

26
Q

What is the most important CyP?

What proportion of drugs does it metabolise?

A

CyP3A4

>30% e.g. CCBs, beta blockers, statins, benzos

27
Q

What is the second most important CyP?

What proportion of drugs does it metabolise?

A

CyP2D6

>20% e.g. antidepressants, some beta blockers, opiates

28
Q

Prodrugs: –>

L-DOPA

A

Dopamine

29
Q

Prodrugs: –>

Enalpril

A

Enalprilat

30
Q

Prodrugs: –>

Ezetimibe

A

Ez-glucuorinde

31
Q

Prodrugs: –>

Methyldopa

A

alpha-methylnorepinephrine

32
Q

Prodrugs: –>

Azathioprine

A

6-mercaptopurine (by xanthine oxidase)

33
Q

Prodrugs: –>

Carbimazole

A

Methimazole

34
Q

Prodrugs: –>

Cyclophosphamide

A

4-hydroxycyclophosphamide

35
Q

What are pharmacogenomics?

A

Genetically determined variation in drug response

36
Q

What is the significance of acetylation in terms of pharmacogenomics?

A

Fast vs slow acetylators e.g. fast in Japan vs Europe

37
Q

Variations in acetylation affects which drugs?

A

Isoniazid

Hydralazine

Dapsone

38
Q

Which CyP doesn’t have polymorphisms?

A

CyP3A4

39
Q

What is the signifcance of G6PDD?

A

Oxidative stress-> haemolysis

40
Q

What are some drugs that can precipitate haemolysis in G6PDD?

A

Quinolones, primaquine, nitrofurantoin, dapsone

41
Q

How can ADRs be classified?

A

Type A

Type B

Long term ADR

Delayed ADR

42
Q

Features of Type A ADR

A

Common, predictable reactions

Dose-related but may occur at therapeutic doses

Consequences of known pharmacology of the drug

43
Q

Features of Type B ADR

A

Rare, idiosyncratic reactions

Usually not dose related

E.g. allergies and pharmacogenetic variations

44
Q

Features of LT ADR

A

Dependence, addiction

Withdrawal phenomena

Adaptive changes e.g. tardive dyskinesia

45
Q

Features of delayed ADR?

A

Carcinogenesis

Teratogenesis

46
Q

What are the drug determinants of ADR?

A

Pharmacodynamics

Pharmacokinetics

Dose

Formulation

Route of administration

Rate of administration

47
Q

What are the patient specific determinants of ADR

A

Age

Co-morbidities

Renal- digoxin, aminoglycosides

Hepatic: warfarin, opiates

Organ dysfunction

Genetic predisposition

48
Q

Examples of drug that can cause T1HS?

A

Penicllins, contrast media

Anaphylaxis

49
Q

Examples of drugs that can cause T2HS?

A

e.g. causing haemolysis

Penicillins, cephalosporins, oral hypoglycaemics

Methyldopa

50
Q

Examples of drugs that can cuase T3HS reactions

A

Immune-complex

Serum sickness-like reaction

Penicillins, sulphonamides

51
Q

Examples of drugs that can cause T4HS

A

Cell-mediated

Topical Abx, antihistamine cream

52
Q

What are pseudoallergies?

A

Pharmacological ADRs not immune

53
Q

NSAID pseudoallergy

A

Bronchospasm

Shift metabolism from prostaglandins-> leukotrienes-> bronchoconstriction

May occur in non-asthmatic populations but commoner if asthmatic

54
Q

ACEI pseudoallergy

A

Cough and angioedema (anaphylactoid)

ACEI inhibit bradykinin metabolism

55
Q

Drugs associated with withdrawal

A

Opiates

Benzos

Corticosteroids

56
Q

Def: rebound

A

Worse on withdrawing the drug than before starting

57
Q

Drugs in which rebound ADR may be seen?

A

Clonidine

Beta-blockers

Corticosteroids

58
Q

Adaptive LT ADR?

A

Neuroleptics-> tardive dyskinesia

59
Q

Delayed ADRs

Oestrogens

A

Endometrial Ca

Breast Ca

60
Q

Delayed ADRs

cytotoxics

A

Leukaemia

61
Q

Drugs causing immune urticaria

A

Penicllins

Cephalosporins

62
Q

Drugs causing non-immune urticaria?

A

Contrast

Opiates

NSAIDs

63
Q

Drugs causing erythema multiforme?

SNAPP

A

Sulfonamides

NSAIDs

Allopurinol

Phenytoin

Penicllin

64
Q

Drugs causing erythema nodosum

A

Sulponhamides

OCP

65
Q

Drugs causing photosensitivity?

A

Amiodarone

Thiazides

Sulfonylureas

66
Q

Drugs causing fixed eruptions

A

Erythromycin

Sulphonamides

67
Q

Drugs causing lupus like reactions

A

Hydralazine

Isoniazid

Penicillamine

68
Q

Drugs causing cholestatic hepatotoxicity

A

Clavulanic acid (may be delayed)

Fluclox: may be delayed

Erythromycin

Sulfonylureas (glibenclamide)

OCP

Tricyclics

Chlorpromazine, prochlorperazine

69
Q

Drugs causing hepatocellular damage

A

Paracetamol

VPA, phenytoin, CBZ

Rifampicin, Isoniazid, Pyrazinamide

Halothane

Methotrexate

Statins

70
Q

Drugs causing chronic hepatitis

A

Isoniazid

Methyldopa

Methotrexate

71
Q

Drugs causing gallstones

A

OCP

72
Q

Drugs causing pancytopenia/aplastic anaemia

A

Cytotoxics

Phenytoin

Chloramphenicol

Penicillamine

Phenothiazines

Methyldopa

73
Q

Drugs causing neutropenia

A

Carbamezapine

Carbimazole

Clozapine

Sulfasalazine

74
Q

Drugs causing thrombocytopenia

A

Valproate

Salicylates

Chloroquine

75
Q

Drugs causing peripheral neuropathy

A

Isoniazid

Vincristine

Amiodarone

Nitrofurantoin

Penicilliamine

76
Q

Drugs causing pulmonary fibrosis

A

Bleomycin

Busulfan

Amiodarone

Nitrofurantoin

Sulfasalazine

Methotrexate

Methysergide

77
Q

Drugs causing gynaecomastia

A

Spironolactone

DIgoxin

Verapamil

Cimetidine

Metronidazole

78
Q

Drugs causing SIADH

A

Carbamezapine

Cyclophosphamide

Chlorpropamide

SSRIs

TCAs

79
Q

Drugs causing gingival hypertrophy

A

Nifedipine

Phenytoin

Ciclosporin

80
Q

Drugs causing prolonged QT

FVN MATCH

A

Fluoroquinolones: ciprofloxacin

Venlafaxine

Neuroleptics: phenothiazines, haldol

Macrolides

Anti-arrhythmics 1a/III: quinidine, amiodarone, sotalol

TCAs

Histamine antagonists

81
Q

Cholinergic side effects

SBLUDGEMS

Caused by?

A

Salivation

Bronchoconstriction

Lacrimation

Urination

Diarrhoea

GI upset

Emesis

Miosis

Sweating

e.g. anti-cholinesterases

82
Q

Anti-muscarinic side effects

CUMBBD

A

Constipation

Urinary retention

Mydriasis

Blurred vision

Bronchodilation

Drowsiness

Dry eyes/skin

83
Q

Causes of anti-muscarinic side effect profile?

A

Ipratropium

Anti-histamines

TCAs

Anti-psychotics

Procyclidine

Atropine

84
Q

Causes of dopamine excess

A

L-Dopa

Da agonists

85
Q

Clinical features of dopamine excess?

A

Behaviour change

Confusion

Psyhcosis

86
Q

Causes of dopamine deficit

A

Anti-psychotics

Anti-emetics: metoclopramide, prochlorperazine

87
Q

Features of dopamine deficit?

A

EPSEs

Increased prolactin

Neuroleptic malignant syndrome

88
Q

Cerebellar disease

DANISH

A

Dysdiadochokinesia, dysmetria, rebound

Ataxia

Nystagmus

Intention tremor

Scanning dysarthria/slurred speech

Hypotonia

89
Q

Pharmacological causes of cerebellar syndrome

A

EtOH

Phenytoine

90
Q

Causes of EPSEs?

A

Typical antipsychotics

Rarely: metoclopramide, prochlorperazine: especially in youing women

Dyskinesias and dystonias are common with anti-parkinsonian drugs

91
Q

Mechanism of EPSEs?

A

D2 block in the nigrostriatal pathway

Excess AChM- hence the effect of anti-AChM

92
Q

What are the types of EPSEs?

A

Parkinsonian

Acute dystonia

Akathisia

Tardive dyskinesia

Neuroleptic malignant syndrome

93
Q

Explain mechanism of EPSEs

A
94
Q

Features of Parkinsonian EPSEs?

A

Occurs within months

More common in the elderly

Bradykinesia tremor, rigidity

95
Q

Rx of parkinsonian EPSEs?

A

Procyclidine

96
Q

Features of acute dysonia

A

Occurs within hours-days of starting drugs

Commoner in young males

Involuntary sustained muscle spasm

e.g. lock jaw, spasmodic torticollis, oculogyric crisis

97
Q

Rx in acute dystonia?

A

Procyclidine

98
Q

Features of akathisia

A

Occurs within days to months

Subjective feeling of inner restlessness

99
Q

Rx of akathisia?

A

Propranolol (crosses BBB)

100
Q

Features of tardive dyskinesia?

A

Rhythmic involuntary movement of head, limbs and trunk

Chewing, grimacing

Protruding, darting tongue

Occur in 20% of those on long term neuroleptics

101
Q

Rx in tardive dyskinesia?

A

Switch to atypical neuroleptic

Clozapine may help

Procyclidine worsens symptoms

102
Q

Features of neuroleptic malignant syndrome

A

4-10d after initiation or change of dose

Mostly in young males

Motor: severe muscular rigidity

Mental: fluctuating consciousnsess

Autonomic: hyperthermia, increased HR, sweating, hyper/hypotensive

Blood: rasied CK, leukocytosis

103
Q

Rx neuroleptic malignant syndrome?

A

Dantrolene: inhibits muscle Ca release

Bromocriptine/apomorphine: reverse Da block

Cool patient

104
Q

Where do pharmaceutical drug interactions take place?

A

Outside the body

Mainly with IV drugs being mixed together

e.g. Ca and NaHCO3-> precipitation

105
Q

What are the pharmacokinetic forms of drug interactions

A

Altered absorption

Displacement from plasma proteins

Metabolism- inhibitors and inducers

Excretion

106
Q

Give an example of altered absorption

A

Tetracyclines and quinolones with Ca, Fe, Al

Drugs chelate the metals and are not absorbed

107
Q

Give an example of drug displacement from plasma proteins

A

Warfarin + some NSAIDs

often clinically insignificant as clearance increases proportionally with displacement

108
Q

What are some enzymes that can be inhibited by drugs?

A

P450

Xanthine oxidase: allopurinol

DOPA decarboxylase: carbidopa

Acetaldehyde dehydrogenase: disulfiram, metronidazole

109
Q

How do diuretics affect Li?

A

Reduce Li clearance

110
Q

How do loop diuretics affect aminoglycosides

A

Increase aminoglycoside ototoxicity

111
Q

What are some examples of indirect drug interactions

A

Diuretics and steroids-> increase risk of digoxin toxicity by reducing K

NSAIDs and warfarin increase risk of GI bleed

Abx and warfarin increase bleeding risk as Abx kill GI microflora that make Vit K

112
Q

What are some important P450 inducers

PC BRAGS

A

Phenytoin

Carbamezapine

Barbiturates

Rifampicin

Alcohol (chronic)

Griseofulvin

St John’s Wort

113
Q

What are some important P450 Inhibitors?

VIP C CEO GFF

A

Valproate

Isoniazid

Protease inhibitors

Ciprofloxacin

Cimetidine

Erythromycin and clarithromycin

Omeprazole

Grapefruit juice

Fluconazole, fluoxetine

114
Q

What are some important drugs metabolised by p450?

COWEST

A

Ciclosporin

OCP

Warfarin

Epileptic drugs: phenytoin, CBZ

Statins

Theophylline

115
Q

What classes of drugs increase Warfarin action?

A

Enzyme inhibitors

EtOH

Simvastatin

NSAIDs

Dipyridamole

Amiodarone

116
Q

What drugs reduce warfarin action?

A

Enzyme inducers

117
Q

What drugs do diuretics potentiate?

A

ACEI

Li

Digoxin

118
Q

What do k-sparing diruetics do with ACEI?

A

Increase risk of hyperkalaemia

119
Q

Pharmacokinetics of the edlerly: Distribution

A

Reduce body water- increased {water soluble drugs}

Increased body fat- {reduced fat soluble drugs}

Reduced albumin- [increased protein bound drugs]

Reduced weight: therefore at standard dose- {increased]

120
Q

Pharmaokinetics in the elderly: metabolism

A

Reduced oxidation

Reduced FPM

Reduced induction of liver enzymes

Therefore with age there is an increased t1/2 of hepatically metabolised drugs

121
Q

Pharmacokinetics in the elderly: elimination

A

Reduced GFR

Reduced tubular secretion

122
Q

Bottom line of pharmacokinetics in the elderly

A

Increased age tends to lead to greater and longer drug effects

123
Q

Altered organ sensitivity in the elderly

ANS

A

Defective compensatory mechanisms

Reduced beta receptor density: therefore reduced effectiveness of drugs targeting them

124
Q

Altered organ sensitivity in the elderly:

CNS

A

Increased sensivity to anxiolytics and hypnotics

125
Q

Altered organ sensitivity in elderly:

Reduced cardiac function

A

Reduced perfusion of liver and kidneys: reduced function: reduce metabolism or elimination of drug

126
Q

What are some issues with compliance in the elderly

A

Confusion

Reduced vision

Arthritic hands

Living alone

Polypharmacy

127
Q

What are the major problem drugs in the elderly affecting the CVS?

A

Anti-HTNs

Digoxin

Diuretics

128
Q

What are the major problem drugs in the elderly affecting the CNS?

A

Anti-depressants

Anti-parkinsonian

Hypnotics

129
Q

Pharmacokinetics in the neonate

A

A: reduced gastric motility

D: immature BBB

Increased body water: {reduced water soluble drug]

Reduced body fat [increased fat soluble drugs]

Reduced albumin {increased]

M:

Reduced P450 activity

Reduced conjugation

E:

Reduced GFR and tubular secretion

Bottom line: reduced age leads to greater and longer drug effects

130
Q

Mechanisms of teratogen action?

A

Orally active= crosses placenta

Implantation-> abortion

Embryonic-> structural defets

Fetogenic-> relatvely less dangerous

131
Q

Common teratogens and their effects

A

ACEI: affect kidney growth

AEDs: NTDs

LI: Ebstein’s anomaly

Anti-folate e.g. trimeth-> NTDs

Tetracyclines-> stains teeth

Warfarin: cardiac defects, reduced IQ, saddle nose, blindness

Statins

132
Q

What are some drugs to avoid in late pregnancy and why?

A

Asprin: haemorrhage, kernicterus

Aminoglycosides: CN8 damage

Anti-thyroid: goitre, hypothyroidism

Benzos: floppy baby syndrome

Chloramphenicol: grey baby syndrome

Warfarin: haemorrhage

Sulphonylureas: kernicterus

133
Q

Mx of HTN in pregancny

A

NB don’t prescribe ACEI to fertile young women

Labetalol

Methyldopa

Nifedipine

Hydralazine

134
Q

Mx of DM in pregnancy

A

Poor glucose control associated with increased congenital abnormalities

Use insulin and or metformin

135
Q

Mx of epilepsy in pregnancy

A

Folic acid pre-conception

Drug level tends to fall in pregnancy

Increased risk of malformations

Increased risk of haemorrhagic disease of newborn

Avoid VPA

Use LTG or CBZ

136
Q

Atnicoagulation in 1st trimester

A

LMWH

137
Q

Anticoagulation in 2nd trimester-36w

A

LMWH or warfarin

138
Q

Anticoagulation 36w- term

A

LMWH

139
Q

Mx of anticoagulation term onwards

A

Warfarin

140
Q

Sedatives and breast feeding

A

Drowsiness

141
Q

Anti-thyroid and breast feeding

A

Goitre

142
Q

Tolbutamide and breast feeding

A

Hypoglycaemia in infant

143
Q

What are some important drugs affected by renal impairment?

DGAAC

A

Digoxin

Gentamicin

Atenolol

Amoxicillin

Captopril

144
Q

Digoxin in renal impirment

A

T1/2: 36-90 hours

Low therpaeutic index, shoulde be monitored

145
Q

Nausea, xanthopsia, gynaecomastia

AV tachyarrythmias, heart block

A

Digoxin toxicity

146
Q

Gentamicin in renal disease

A

T1/2:2.5-> 50h

MUST be monitored

Increased risk of toxicity if reduced Na e.g. diuretics or dehydrated

147
Q

Hearing and vestibular issues

Nephrotoxicity

A

Gentamicin

148
Q

Atenolol in renal disease

A

T1/2: 6->100hours

149
Q

CI to atenolol

A

Asthma/bronchospasm

Severe heart failure

PVD

150
Q

Bradycardia, hypotension

Worsening of PVD and HF

Confusion

A

Atenolol toxicity

151
Q

Amoxicillin in renal disease

A

T1/2 2-> 15hrs

Toxcity:

seizures (in meningitis, impaired BBB), rashes

152
Q

Hypotension

Taste distrubrance

Cough

reduced GFR

Angioedema

A

Captopril toxicity

153
Q

What form of VitD should be used in renal impairment?

A

Alfacalcidol (1 alpha-hydoxylated)

154
Q

What are some important nephrotoxic drugs?

A

Gentamicin

Li

Ciclosporin

ACEI/ARB

NSAIDs

155
Q

Gentamicin: renal toxicity mechanism

A

Renal tubular damage-> accumulation-> increased nephro and ototoxcicity

MUST monitor levels

156
Q

Li: renal toxicity mecahnism

A

Inhibits Mg-dependant enzymes e.g. adenylate cyclase

ADH requires adenylate cyclase therefore Li causes nephrogenic DI

Also causes direct tubular damage

Must monitor drug levels

157
Q

How does Li cause nephrogenic DI

A

ADH requires adenylate cycle, an Mg-dependant enzyme inhibited by Li

158
Q

Ciclosporin: renal toxciity mechanism

A

Reduced GFR: reversible

Damages renal tubules: irreversible

P450 substrate

Consider monitoring

159
Q

ACE/ARB nephrotoxcity mechanism

A

Reduce GFR: inhibit efferent arteriolar vasoconstriction may be profound in RAS or CoA

160
Q

NSAIDs: nephrotoxicity mechanism

A

Reduce GFR: prevent afferent arteriolar vasodilation

Leading to papillary necrosis

161
Q

What should be considered in prescribing in hepatic impairment

A

Albumin levels

Clotting factors synthesis

Reduced FPM

Reduce alpha 1 acidic glycoprotein

Encephalopathy

Hepatorenal syndrome

162
Q

Prescribing in hyopalbuminaemia

A

Increased proportion of free drug

e.g. phenytoin, CBZ, predniosolne, diazepam, tolbutamide

163
Q

Redcued FPM, what Rx should be assessed

A

Opiates

Phenothiazine

Imipramine

164
Q

What are some drugs bound by alpha-1acidic glycoprotein

A

Chlorpromazine

Quinidine

Imipramine

165
Q

What is a consideration in hepatic encephalopathy regarding Rx

A

Sedatives/opiates-> coma

Caution with drugs that may cause constipation

Anxiolytis: temazepam safest due to short t1/2

TCAs safer but avoid MOAIs

166
Q

Considerations in Rx with hepatorenal syndrome

A

Withdraw nephrotoxic drugs

Modify doses of renally-excreted drugs

167
Q

What are some drugs causing cholestatic heaptotoxicity

A

Clavulanic acid: may be delayed

Fluclox: may be delayed

Erythromycin

Sulfonylureas

OCP

Tricyclics

Chlorpromazine, prochlorperazine

168
Q

What drug is associated with gallstones?

A

OCP

169
Q

What drugs are associated with chronic hepatitis

A

Isoniazid

Methyldopa

170
Q

What drugs are associated with hepatocellular damage

A

Paracetamol

VPA, Phenytoin, CBZ

Rifampicin, isoniazid, pyrazinamide

Halothane

Methotrexate

Statins

171
Q

Drugs and doses used as morning after pill

A

Levonorgesterl 1.5mg PO STAT

Ulipristal 30mg PO STAT

172
Q

MOA of beta agonists

A

Act at bronchial B2 receptors:

SM relaxation and reduce secretions

173
Q

Side effects of beta agonist bronchodilators

A

Tachycardia

Tremor

174
Q

Interactions of beta agonist bronchodilators

A

Reduce K in high doses with corticosteroids, loop/thiazide diuretics/theophylline

175
Q

SABA features

A

Short acting, fast onset

2-4 hrs

176
Q

Give 2 examples of SABA

A

Salbutamol (ventolin)

Terbutaline (Bricanyl)

177
Q

MOA muscarinic antagonist bronchodilation

A

Bronchodilation

Mucus secretion

178
Q

Side effects of muscarinic antagonist bronchodilators

A

Dry mouth

179
Q

Caution re muscarinic antagonist bronchodilators

A

Closed angle glaucoma

Prostatic hypertrophy

180
Q

Features of SAMAs

A

3-6hrs

Short acting

181
Q

e.g. SAMA

A

Ipratropium (Atrovent)

182
Q

e.g. LAMA

A

Tiotropium (Spiriva)

183
Q

e.g. of ICS

A

Beclometasone: Becotide

Budenoside: Pulmicort

Fluticasone: Flixotide

184
Q

What is symbicort?

A

Budenoside and fomoterol

185
Q

Gives examples of LABA

A

Salmeterol

Formoterol

186
Q

What is seritide

A

Fluticasone and salmeterol

187
Q

MOA of ICS

A

Act over weeks to reduce inflammation:

Reduce cytokine produciton

Reduce prostaglanding/leukotriene synthesis

Reduce IgE secretion

Reduce leukocyte recruitment

Prevent long term decline in lung function

188
Q

Side effects of ICS

A

Oral candidiasis

High doses may lead to typical steroid SEs

189
Q

Fluticasone vs other ICS

A

2x as potent: use lower dose

190
Q

Symbicort usage

A

Can be used as a preventer or a reliver because of formoterol’s fast onset

191
Q

Use of ICS advice

A

Use a spacer

Rinse mouth after use

192
Q

Theophylline MR

Aminophylloine

Drug class

A

Methylxanthines

193
Q

Methylxanthine MOA

A

PDE inhibitors: increase cAMP-> bronchodilation

194
Q

Side effects of methylxanthines?

A

Nausea

Arrhythmias

Seizures

Hypokalaemia

195
Q

Interactions of methylxanthines leading to reduced levels

A

Smoking

EtOH

CYP inducers

196
Q

Interactions of methylxanthines to increase levels

A

CCBs

CYP inhibitors

197
Q

Additional detail re methylxanthines

A

Aminophylline is IV form:

give IVI slowly

Too fast -> VT

Monitor with ECG and check plasma levels

CYP metabolism

NB if pt already on theophylline cannot have IV aminophylline

198
Q

MOA

Montelukast

Zafirlukast

A

Leukotreine receptor antagonists

Block cysteinyl leukotrienes

199
Q

Side effects for leukotriene R antagonists

A

?Churg Strauss

200
Q

What are leukotriene antagonists particulalrly useful for?

A

NSAID and exercise induced asthma

201
Q

Roflumilast MOA

A

PDE-4i

202
Q

Side effects roflumilast

A

GI

203
Q

CI for roflumilast

A

Severe immunological disease

204
Q

Omalizumab MOA

A

Humanised anti-IgE mAb

205
Q

Features of omalizumab

A

SC injection every 2-4w

Used for severe asthma

206
Q

Carbocysteine

A

Mucolytic

207
Q

Side effects of carbocysteine

A

GI bleed (rare)

208
Q

CI carbocystiene

A

Active peptic ulceration

209
Q

Dornase ALFA (Dnase) MOA

used in?

A

Mucolytic

CF

210
Q

Non-sedating H1R antagonists

A

Certrizine

Loratidine

Fexofenadine

211
Q

Sedating H1R inverse agonists (antagonists)

A

Chlorphenamine

212
Q

Inverse agonist

A

In the field of pharmacology, an inverse agonist is an agent that binds to the same receptor as an agonist but induces a pharmacological response opposite to thatagonist. A neutral antagonist has no activity in the absence of an agonist or inverse agonistbut can block the activity of either

213
Q

Side effects of H1R inverse agonists

A

hypotension

Arrhythmia: long QT

Older agents: drowsiness

Anti-AChM

214
Q

CI for H1R inverse agonists

A

Severe hepatic disease

215
Q

Caution in H1R inverse agonists

A

Long QT

BPH

Closed-angle glaucoma

216
Q

LMWH in pregnancy

A

Does not cross the placenta

217
Q

ST effects of pred in asthma

A

Candidiasis

Hypokalaemia

218
Q

What is important to remember re LMWH in pregnancy

A

Must remember to stop it due to risk of osteoporosis

219
Q

Indapamide

A

Thiazide like diuretic

220
Q

Which 2 of the following are most likely to cause hyponatraemia

INdpamide

Perindopril

Rivaroxaban

Amlodipine

Citalopram

Simvastatin

Paracetamol

A

Indapamide- will cause sodium loss-> hyponatraemia

Citalopram-> SIADH (obscure adverse effect)

Periondopril will cause hyponatraemia but hyperkalaemia

221
Q

Why should you take short acting statins at night (simvastatin)

A

Because cholesterol synthesis is thought to happen prinicipally during the night

222
Q

%w/v units

A

grams in 100 millilitres gives you the percentage

223
Q

v/v %

A

millilitres in 100 millllitres

224
Q

Abciximiab

A

2b3a antagonist

225
Q

Cough ADR in ACEi

A

Dose independent

226
Q

Colchicine in gout

A

Recommended in patients with HF as unlikely to make HF worse.

Diclofenac should not be used as it has a high risk of cardiovascular events

227
Q

1:1000 adrenaline

A

1mg per ml

228
Q

1:10000

A

0.1mg per ml

229
Q

Mx of acute dystonia

A

Procyclidine 5mg IM

230
Q

What is the limit of morphine per 24h

A

200mg/24 hours

231
Q

Which medication is often associated with gout

A

Thiazide diuretics: increase Na clearance at the expense of uric acid excretion

232
Q

Two common side effects of metronidazole

A

N+V

Furred tongue

Metallic taste in mouth

233
Q

Reversal of warfarin overdosing with Vit K PO or IV

A

IV and PO both same onset of action

If plan is to restart warfarin, give IV as PO action takes longer to turn off than IV

234
Q

What drugs require obligatory TDM?

A

Aminoglycosides

Vancomycin

Lithium

235
Q

What are some drugs that commonly have TDM?

A

Aminoglycosides

Vancomycin

Lithium

Digoxin

Phenytoin

236
Q

Does Warfarin have TDM?

A

Technically not as it is not the [plasma] being monitored, rather the biological effect

237
Q

What are the 3 pathways of drugs through the body?

A

Excreted unchanged by the kidney e.g. furosemide

Phase 1 metabolism-> kidney or phase 2

Phase 2 metabolism: undergoes phase 2 transformation and then excreted

238
Q

Phase 1 metabolism=

A

Oxidation

Reduction

Hydrolysis

Molecule itself is directly altered usually by cytochrome p450 (oxidation)

239
Q

Phase 2 metabolism

A

Either the original drug or its modified form is then conjugated e.g. glucuronidation, sulphation, acetylation

This tends to make compound more polar, allowing excretion more readily

240
Q

What is the most important cytochrome subtype

A

CYP3A4: accounts for 30% of prescribed drugs e.g. CCBs, statins, BZDs

241
Q

CYP2D6

A

Next most important cytochrome, metabolises 20% of drugs e.g. antidepressants, beta blockers, some opiates

242
Q

CYP1A2 metabolises

A

Paracetamol

Caffeine

Theophylline

243
Q

CYP2C9 metabolises

A

Warfarin

Ibuprofen

244
Q

CYP2C19 metabolises

A

Diazepam

Omeprazole

245
Q

Enalpril

A

Prodrug, ACEi

converted to enlaprilat

246
Q

Azathioprine

A

Prodrug, converted to 6-mercaptopurine

247
Q

Ezetimibe

A

Ez-glucuorine

Converted to the glucuronide in the liver which is the active form. This reaches the lumen of the small intestine where it blocks cholesterol absorption

248
Q

What is the single most important determinant in the elimination of most drugs?

A

GFR

249
Q

What is pharmacogenetics?

A

The study of genetically determined varaitions in the response to drugs

250
Q

What is the significance of acetylation polymorphisms?

A

A small number of drugs are metabolised by acetylation, there are fast and slow acetylators, which is genetically determined and which may have different side-effects

Drugs that udnergo acetylation include isoniazid, hydralazine, dapsone

251
Q

What are some examples of variations in clinical pharamacogenetics?

A

Pseudocholinesterase

G6PD

Porphyria

252
Q

Significance of pseudocholinesterase

A

Patients lacking this enzyme had prolonged recovery after anaesthesia

253
Q

Type A ADRs

A

Predictable reactions

Common

Dose-related but can occur at therapeutic doses

Consequence of known pharmacology of drugs

254
Q

What is a type B ADR

A

Idiosyncratic reactions

Rare to very rare

Usually not dose related

Include true allergies

Include some pharmacogenetic variations

255
Q

What are long term ADR?

A

Dependence/addiciton e.g benzos

Withdrawal phenomena inc rebound e/g/ clonidine

Adaptive changes e.g. typical antipsychotics-> tardive dyskinesia

256
Q

What are delayed ADR

A

Carcinogenesis

Teratogenesis

257
Q

ABCDE classification of ADRs

A

Augmented pharmacological effect

Bizarre

Chronic

Delayed

End of treatment

258
Q

What are the drug determinants of ADRs?

A

Pharmacodynamics:

pharmacokinetic properties e.g. digoxin

Dose e.g. beta blockers

Formulation e.g. digoxin

ROA e.g. phenytoin

Rate of administration e.g. aminophylline

259
Q

Digoxin excretion

A

Renally

260
Q

ROA phenytoin

A

Oral- rarely CV problems

IV: bradycardia/hypotension

261
Q

Rate of administration aminophylline

A

Given too quickly-> ventricular arrythmia

262
Q

liver disease + opiates

A

Increases risk of hepatic encephalopathy and worsening liver failure

263
Q

What are some examples of pseudoallergies

A

Non-immune mechanisms, pharmacolgoical

e.g. salicylates, other NSAIDs-> bronchospasm. shift metabolsim from prostaglandins to leukotrienes which leads to bronchospasm

ACEi-> cough, angioedema (anaphylactide)

264
Q

Drugs causing urticaria

A

Penicllins, contrast media, opiates

265
Q

Drugs causing erythema multiforme

A

Penicllins, sulfonamides

266
Q

Drugs causing erythema nodosum

A

Sulfonamides, OCP

267
Q

Drugs causing photosensitivity

A

Amiodarone

Thiazides

Sulfonylureas

268
Q

Drugs causing fixed eruptions

A

Erythromycin

Sulfonamides et.c

269
Q

Drugs causing lupus-like reactions

A

Penicllins, isoniazid, hydralazine

270
Q

Fixed eruption

A

Drug causes rash in a fixed distribution

Drug stopped, if restarted rash appears in same distribution

271
Q

Drugs causing intrahpeatic cholestasis

A

Phenothiazines (formerly used as an antihelminthic)

TCA

Sulfonylurea

Erythromycin

Clavulanic acid (may be delayeed)

Carbimazole

Anabolic steroids (dose related)

272
Q

Drugs causing hepatocellular damage

A

Isoniazid

Pyrazinamide

Methyldopa

TCA

Phenytoin

All of the above can occur from acute or chronic use

Pracetamol (dose dependant)

Methotrexate (dose dependant) (causes liver fibrosis)

273
Q

Drugs causing chronic hepatitis

A

Isoniazid

Methyldopa

274
Q

Drugs causing gallstones

A

Fibrates

Oestrogens

275
Q

Drugs causing pancytopenia (aplastic anaemia)

A

Cytotoxics (Type A)

Type B:

Chloramphenicol( (1/10000, tends to be lethal)

Phenytoin

Peniclliamine

Phenothiazines

276
Q

Drugs causing neutropenia

A

All type B

Carbamazepine

Carbimazole

Clozapine

Mianserin- withdrawn

Sulfasalazine

277
Q

Mianserin

A

It is classified as a noradrenergic and specific serotonergic antidepressant (NaSSA)

278
Q

Drugs causing thrombocytopenia

A

All type B

Chloroquine

Captopril

Quinidine

Salicylates

VPA (most important)

279
Q

Drugs causing peripheral neuropathy

A

Amiodarone

Nitrofurantoin

Penicillamine

Isoniazid

Dose dependant:

Vincristine

Cis-platin

280
Q

Drugs causing pulmonary fibrosis

BBC MAN

A

B-Bleomycin

B-Busulfan

C-Cyclophosphamide

M-Methylsergide

A-Amiodarone

N-Nitrofurantoin

Methotrexate

281
Q

Azathioprine enzyme moniotring

A

Azathioprine is a purine analogue that interferes with DNA synthesis and inhibits the proliferation of quickly growing cells, especially cells of the immune system. It is used as an immunosuppressant in patients undergoing organ transplantation, and its metabolite 6-mercaptopurine is used in the treatment of autoimmune diseases and acute lymphoblastic leukemia.

During metabolism, hypoxanthine-guanine phosphoribosyltransferase (HGPRT) converts 6-mercaptopurine to cytotoxic 6-thioguanine nucleotide analogues, while thiopurine methyltransferase (TPMT) inactivates 6-mercaptopurine through methylation to form 6-methylmercaptopurine.

Approximately 11% of the population has reduced TPMT activity and 0.3% of the population has true deficiency of TPMT. [1] In these patients, active 6-mercaptopurine accumulates, and a larger proportion of 6-mercaptopurine is converted to the cytotoxic 6-thioguanine nucleotide analogues, which can lead to bone marrow toxicity and myelosuppression

282
Q

Withdrawal reactions

important drugs

A

Opiates

BZDs

Corticosteroids

283
Q

Rebound reactions

common drugs

A

Clonidine

Beta-blcokers

Corticosteroids

284
Q

Oestrogen carcinogenesis

A

Endometrial ca

?breast ca

285
Q

Types of clinical trials

A

Phase 1: normal volunteers (50)

Phase 2: patients, open study (200)

Phase 3: clinical trials: DB-RCT

Phase 4: post marketing

286
Q

What are the 3 methods for detecting ADR post approval

A

Post-marketing: yellow card

Cohort studies

Prescription event monitoring

287
Q

Black triangle drugs

A

Newly licensed usually <2y

Report any suspected adverse reaction

288
Q

Established drugs in yellow card scheme

A

Only report serious adverse reactions: fatal, life-threatneing, needing hospital admission, disabling

289
Q

What are pharmacetuical drug interactions

A

Ones taking place outside the body

Generally IV drugs being mixed together e.g. Ca and bicarbonate precipitating out

Always read instruction

290
Q

Altered absorption: drug interactions

A

Tetracyclines, quinolones + Ca, Fe, Al

Altered absorption if given with any metal due to chelation

Think about drug timing

291
Q

Displacement from plasma proteins

Most important

A

Warfarin + NSAIDs

292
Q

Cytochrome p450 inhibitors

SICKFACES.COM Group

A

Sodium VPA

Isoniazid

Cimetidine

Ketoconazole

Fluconazole

Alcohol- binge drinking

Chloramphenicol

Erythromycin and other macrolides

Sulfonamides

Ciprofloxacin

Omeprazole

Metronidazole

Grapefruit juice

293
Q

Allopurinol + 6 mercaptopurine

A

Makes it more cyotoxic

294
Q

Cheese reaction

A

MAOI and cheese-> hypertensive reaction. e.g. cheese, marmites (foods containing tyramine)

295
Q

P450 inducers

CRAP GPS

A

Carbamezapine

Rifampicin

Alcohol (chronic)

Phenytoin

Griseofulvin

Phenobarbitone

Sulphonylureas

296
Q

Diuretics + lithium

A

Increased Na clearance but decreased Li clearance

297
Q

Loop diuretics + aminoglycosides

A

Inihbit each others excretion and increase toxicitiy, particularly ototoxicity

298
Q

What are some exmaples of indirect interactions?

A

Diuretics, corticosteroids + digoxin (low K)

NSAIDs and warfarin: damage to stomach, increased risk of GI bleed

Antibiotics and warfarin. reduced gut bacteria (involved in K production)

299
Q

How can renal disease impact pharmacology

A

Drugs that are eliminated by the kidney

Drugs that are metabolised by the kidney

Nephrotoxic drugs

300
Q

What are the clinically most important drugs effected by renal impairment

A

DIgoxin

Gentamicin

Atenolol

Amxocivillin

Captopril

301
Q

Nause

Dysrhythmias

Anthopsia

Breast enlargement

A

Digoxin

302
Q

Ototoxcitiy

Nephrotoxicity

Increased risk of toxicity in hyponatraemia and dehydration

A

Gentamicin

303
Q

Bradycardia

Confusion

Hypotension

Fatigue

PVD

Heat failure at higer doses

A

Atenolol

304
Q

Hypotension

Reduced GFR

Cough

Taste distrubance

Angioedema

GI distrubance

A

Captopril

305
Q

When dose amoxicllin toxicity become important and why

A

Generally nontoxic

In patients with renal impairment the half life of the drug is substantially increased( 14h)

In patients with menigitis, the BBB is disrupted and this allows amoxiillin to accumulate in the CSF

These patients may develop seizures.

The allergic manifestation of drugs may also appear more commonly in this group of patients

306
Q

Dry cough proportion of ACEi patients

A

15%

307
Q

What is an important drug metabolised by the kidney and the significance of this?

A

Vit D3 (cholecalciferol- formed in skin). Vit D (made by uv irradiation of ergosterol)

Both forms are activated sequentially. 25a in liver

1a in the kiney

to yield 1,25 di(OH)D3 and 1,25 di(OH)D2

308
Q

Mechanism of 2o hyerparathyroidism

A

Hypocalcaemia with relative conseuqence of hypophosphataemia lead to hyperparathyroid

Consequnece of failure in VtiD/ renal pathway

309
Q

Gentamicin mechanism of nephrotoxicity

A

Renal tubular damge

Important in that damage occus with an accompanying degree of reduciton in GFR leading to gentamicin accumulation.

Causes a cycle.

Importance of appropriate gentamicin TDM

310
Q

LI mecahnism of nephrotoxicity

A

Nephrogenic DI: through inhibiting Mg dependent enzymes (adenylate cyclase) which is activated in renal tubule by ADH.

and

Tubular damage

311
Q

Cyclosporin A mechanism of nephrotoxicity

A

Reduced GFR

and

Tubular function

Used in renal transplant immunosuppression. Physician needs to distinguish between rejection episode causing decline in renal function or cyclosporin toxicity.

312
Q

Cyclosporin AEs

A

TDM

Hypertension

Reduced GFR

313
Q

Mechanism of ACEi nephrotoxicity

A

A2Rs located principally on the efferent arteriole. Have a vasoconstrictive effect.

If you administer ACEi which blocks biosynthesis of AngII or you give ARB there will be dilatation of the efferent arteriole.

As a consequent of that, renal blood flow through glomerulus increases.

However, the pressure within the glomerular tuft decreases.

The GFR is dependent on the perfusion pressure within the glomerular tuft, as perfusion pressure reduces, GFR reduces.

If a patient has a pathological reduction in pressure in the afferent arteriole e.g. RAS,(or more rarely in CoARc sited proximally to the renal arteries) there is a danger that if you inhibit ACEI/ARB for the pressure within glomerular tuft to reach pathologically low levels with a consequent critical reduction in GFR.

314
Q

NSAIDs mechanism of toxicity

A

Inhibit COX and reduce PG concentration.

In the kidney and renal vasculature, most of the PGs are vasodilator. Effects are mediated by prostaglandin E2 and prostacycline.

These molecules regulate the diameter of blood vessels around the glomerulus.

LT use of NSAIDs. particularly in patients with preexisting renal damage, may result in a further reduciton in GFR and Na retention.

May also cause papillary necrosis. Papilla receives blood supply from surrounding bvs that require PGs to maintain their diameter, thus patients receiving high concentrations of NSAIDs may develop relative ischaemia of the renal papilla-> necrosis if sustained. Necrotic papilla may become detached from renal cortex, fall into renal pelvis and block ureturs

315
Q

What are the hepatic synthetic functions important in pharmacology

A

Albumin: hypoalbuminaemia may increase proportion of the free drug, more of a problem if drug clearance is reduced.

e.g. Diazepam, tolbutamide, phenytoin

A1-acidic glyocoprotein: binds basic drugs

e.g. quinidine, chlorpromazine and imipramine

Reduced synthesis of Clotting factors

Warfarin and synthesis of Vit-K dependant clotting factors

316
Q

What are the Vit K dependent clotting factors?

A

2, 7, 9, 10

317
Q

What are drugs that should be prescribed with care in current or recent encepahlopathy?

A

Opiates (most important):

prolonged elimination, may precipitate encephalopathy

Anti-psychotics: phenothiazine and butyrophenones

Anxiolytes and hyponotics: oxazepam and temazepam are safest

Antidepressants: TCAs are safest, avoid MAOs: idiosyncractic hepatotoxicity

318
Q

Hepatorenal syndrome precipitated by

A

Opiates

Major tranquilisers etc.

319
Q

Patient with hepatic disease and declining renal function

A

?hepatorenal syndrome

R/v drug chart and withdraw drugs that may be contributing

320
Q

What are the groups of drugs that are likely to present problems in patients with liver disease?

A

Those with high FPM

High plasma protein binding

Low TI

Those with CNS depressant effect

321
Q

Importance of drugs with extensive FPM

A

Normally only a small proportion of ingested blood enters blood, liver disease-> very reduced FPM

e.g.

Clormethiazole

Chlorpromazine

Imipramine

Morphine

Pethidine

322
Q

Importance of drugs with high plasma protein binding in context of liver disease

A

Combination of high protein binding and reduced elmination likely to precipitate a prolbem

e.g.

Chloral hydrate

Phenytoin

323
Q

Importance of durgs with low TI in context of liver disease

A

Any incapacity of liver to metabolise drug and reduce toxic levels likely to precipiate toxicity

e.g. barbiturates

324
Q

Importance of drugs with CNS effect in context of liver disease

A

Principally because of capacity to control through autonomic NS the important CV and respiratory functions likely to become hypotensive, develop bradycardias and stop breathing.

Drugs include opiates, phenothiazine and othrers with known sedative effects

325
Q

How can the mecahnisms of hepatotoxicity be classified?

A

Non-covalent

or

Covalent

326
Q

What are the mechanisms of non-covalent hepatotoxcitty?

A

Occur as a consequence of the activity of cytochrome p450.

During these reaction oxygen radicals can be generated e.g. peroxides, superoxides, hydroxyl radicals. Highly reactive molecular species that may damage the structure of lipids, aas and other molecules.

Normally glutathione is there to protect the cell and serves as free radical scavenger, however in established liver disease glutathione may become depleted and this may increase the propensity of oxudative products to cause issues

327
Q

What is the mechanism of covalent hepatotoxicity

A

Involve adduct formation between drug/metabolite and DNA/proteins/lipids within the cell

328
Q

What are the common hepatotoxic drgus?

A

Hepatocellular necrosis:

Paracetamol- reactive intermediate

Halothane: repeated use

Anticonvulsants Carbamazepine, phenytoin and valproate

MAOIs, isoniazid, nitrofurantoin, sulphonamides

Hydralazine, methyl dopa

Cholestasis:

Chlorpromazine

Sulphonylureas (glibenclamide)

Carbimazole

329
Q

This drug has 100% bioavailability in an oral formulation

A.

Metformin

B.

Captopril

C.

Levodopa

D.

Amiodarone

E.

Gentamicin

F.

Methotrexate

G.

Isoniazid

H.

Ciprofloxacin

I.

Phenytoin

J.

Diltiazem

A

Ciprofloxacin

330
Q

Probenecid competitively inhibits the secretion of which drug?

A.

Lithium

B.

Beclometasone

C.

Penicillin

D.

Metronidazole

E.

Theophylline

F.

Azathioprine

G.

Suxamethonium

H.

Lignocaine

I.

Propofol

J.

Dapsone

A

Penicillin

331
Q

A.

Lithium

B.

Beclometasone

C.

Penicillin

D.

Metronidazole

E.

Theophylline

F.

Azathioprine

G.

Suxamethonium

H.

Lignocaine

I.

Propofol

J.

Dapsone

A prodrug that interacts with allopurinol

A

Azathioprine

332
Q

Drug metabolised by acetylation, used to treat leprosy

A

Dapsone

333
Q

Smoking increases the metabolism of this drug.

A.

Lithium

B.

Beclometasone

C.

Penicillin

D.

Metronidazole

E.

Theophylline

F.

Azathioprine

G.

Suxamethonium

H.

Lignocaine

I.

Propofol

J.

Dapsone

A

Theophylline

334
Q

An anti-platelet drug that may cause a rare thrombotic syndrome that is characterised by a classic triad

A

Clopidogrel

335
Q

A drug used to treat Wilson’s disease, that may cause a myasthenia gravis-like syndrome

A

Penicillamine

336
Q

A centrally acting antihypertensive that may give rise to a positive Coombs test

A

Methyldopa

337
Q

If this antidepressant is given with amiodarone it increases the risk of an arrhythmia

A

Amitryptilline

338
Q

If this drug is given to a patient with bipolar affective disorder, there is increased risk of toxicity of a particular mood stabiliser

A

Frusemide

339
Q

Which drug causes ‘floppy baby syndrome’?

A

Diazepam

340
Q

Which drug, when given to a mother in the late stages of pregnancy, can cause a low platelet count in the neonate?

A

Bendroflumethiazide

341
Q

Which drug causes Ebstein’s anomaly in the baby?

A

Li

342
Q

Effects of this drug on the fetus include frontal bossing, midface hypoplasia, saddle nose, cardiac defects, short stature, blindness and mental retardation.

A

Warfarin

343
Q

Drug that may cause liver adenoma.

A.

Penicillamine

B.

Sumatriptan

C.

Oral contraceptive

D.

Cimetidine

E.

Hydroxychloroquine

F.

Methotrexate

G.

Rifampicin

H.

Cyclophosphamide

I.

Atenolol

J.

Diclofenac

A

Rifmapicin

344
Q

Renally excreted drug that can cause impotence, nightmares and type 2 Diabetes

A

atenolol

345
Q

Renally excreted drug used to treat Zollinger Ellison Syndrome

A

Cimetidine

346
Q

Detemir

A

Longer acting insulin that binds to albumin in the circulation

347
Q

Glargine

A

Longer acting aa-altered insulin, thus prolonged absorption from subcutaneous tissue

348
Q

Action of insulin at the liver

A

Switches off hepatic glucose output:

gylcogenolysis

gluconeogensis

Inhibits ketogenesis

349
Q

Action of insulin at adipose tissue

A

Increaes lipoprotein lipase activity:

reduces hypertriglyceridaemia

Increases GLUT4 activity-> glucose stored as fat

Decreased lipolysis: reduced [glycerol], [non-esterified fatty acids reduced]

350
Q

Insulin action at muscle

A

Decreased proteolysis: decreased aa delivery to liver for gluconeogenesis

Increased GLUT4 activity-> [reduced glucose]

351
Q

Can a bolus of insulin be useful?

A

Short t1/2 of IV insulin means bolus is never useful. Should be given by infusion

352
Q

When is human insulin used?

A

IV

353
Q

Features of basal-bolus QDS insulin

A

Short acting with breakfast

Second dose with lunch

Third with evening meal

Intermediate insulin given OD

ACTrapid given 15 mins before meal

Intermediate given before patient goes to bed

354
Q

Preprandial glucose

A

Doesn’t tell you how much insulin is needed

Post prandial tell you how much you should have given

355
Q

Fasting glucose

A

Tells us how much long acting needs to have been given night before

356
Q

Issues with actrapid

A

Human insulin.

Forms hexamers under skin and is abosrbed over 3-4h

Needs to be given 15 mins before meal

Can lead to late post prandial hypoglycaemia

Can lead to immediate post-prandial hyperglycaemia that may lead to diabets cx

357
Q

Insulin lispro

A

Short acting insulin that has modified aa so doesn’t form hexamers under skin

Faster onset and shorter duration of action

Can be given at beginning of food or even after food.

358
Q

Possible T2D insulin regimes

A

Long acting insulin + sulphonylurea

BD mixtrrd

Full basal bolus

Insulin + metformin

359
Q

Advantage of metformin and insulin

A

Didn’t gain weight that is seen in intensive insulin alone

360
Q

Glucagon in EtOH induced hypo

A

May not be as effective as EtOH uses glycogen in metabolism

361
Q

Dietary advice in T2DM

A

Control total calories/increase exercise

Reduced refined carbohydrate

Increase complex carbohydrate as a proportion of carbohydra

Reduce fat as proportion of caloires

Increase unsaturated fat as a proprotion of fat

Increase soluble fibre

Address Na intake

362
Q

Oriistat dose

A

120mg TDS

363
Q

Metformin

A

Insulin sensitiser

Biguanide

Increases hepatic insulin sensitivity

Inhibits hepatic gluconeogenesis

364
Q

Insulin sensitiser

Biguanide

Increases hepatic insulin sensitivity

Inhibits hepatic gluconeogenesis

A

Metformin

365
Q

Metformin iniitial dose

A

500mg BD

366
Q

Side effects of metformin

A

GI disturbance: nausea and diarrhoea

Lactic acidosis (rare)

Do not use if severe liver, severe cardiac, or mild renal failure (elevated Cr + radiological contrast media)

367
Q

Act on beta cell to acutely cause insulin release independent of glucose concentration

Stimulate second phase insulin secretion

A

Sulphonylureas

Metaglinides

368
Q

Sulphonylurea MOA

A

Act on insulin secretagogue

Act on beta cell to acutely cause insulin release independent of glucose concentration

Stimulate second phase insulin secretion

369
Q

Starting dose of sulphonylureas

A

2.5mg BD

370
Q

Draw MOA of sulphonylureas

A
371
Q

Cx of sulphonylureas

A

Hypoglycaemia: can be severe, prolonged, or even fatal

Especially a problem in elderly, alcoholics and those with poor nutirtion- not enough stored glyocgen

Weight gain

Rarer complications: rashes, blood dyscrasia

372
Q

Hypoglycaemia: can be severe, prolonged, or even fatal

Especially a problem in elderly, alcoholics and those with poor nutirtion- not enough stored glyocgen

Weight gain

Rarer complications: rashes, blood dyscrasia

A

Sulphonylureas

373
Q

What are the non-sulphonylurea secretagogues?

A

Repaglanide

Nataglinide

374
Q

Gliclazide

Glibenclamide

A

Sulphonylureas

375
Q

MOA Thiazolidinediones

A

Reduce lipotoxicity

Increase muscle insulin sensitivity

Favourable fat distribution

Suppression off fatty acid release through PPARg agonism

376
Q

Reduce lipotoxicity

Increase muscle insulin sensitivity

Favourable fat distribution

Suppression off fatty acid release

All rthrough PPARg agonism

A

Thiazolidinediones

377
Q

Rosiglitazone

Pioglitazone

A

Glitazone: PPARg agonists

378
Q

MOA PPARg

A

Act on intranuclear PPARg

Adipose tissue>liver and muscle

Affect lipoprotein lipase, FA transporter, CoA synthase, GLUT4

Insulin resistance reduced

379
Q

Act on intranuclear PPARg

Adipose tissue>liver and muscle

Affect lipoprotein lipase, FA transporter, CoA synthase, GLUT4

Insulin resistance reduced

A

PPARg agonist e.g. glitazone

380
Q

Side effects of pioglitazone

A

Peripheral weight gain

Oedema

Should not be used with insulin

381
Q

E.g. of alpha glucosidase inhibitors

A

Acarbose

382
Q

MOA acarbose

A

Delay oligosaccharide absorption

383
Q

S/E acarbose

A

Flatulence

384
Q

MOA GLP-1

A

Inhibit glucagon release

Cause acute insulin release

Stimulate insulin biosynthesis

Improve beta cell differentiation

385
Q

Inhibit glucagon release

Cause acute insulin release

Stimulate insulin biosynthesis

Improve beta cell differentiation

A

GLP1

386
Q

Pramitide MOA

A

Slow gastric eptying

Inhibit glucagon release

Cause acute insulin release

387
Q

Why should thyroxine be introduced gradually, especially in the elderly

A

Can exacerbate pre-existing ischaemic heart disease

388
Q

What are the risks of suppressing TSH

A

Osteopenia/osteoporosis

AF (especially in older patients)

Should not aim to suppress TSH, should aim to bring it within normal range

389
Q

Mx of low uptake thyroxtocisosis

A

Use beta blockers as thionamides won’t work

390
Q

Sore throat on carbimazole

A

Warn patient to stop due to risk of agranulocytosis

391
Q

When is 131I not used in thyroid disease

A

Opthalmopathy/tracheal compression

392
Q

MOA Mg Triscillate

A

Antacid

Neutralises gastric acid

393
Q

MOA AI hydroxide

A

Antacid

Neutralises gastric acid

394
Q

MOA Gaviscon

A

Alginate

Reduces reflux: increased stomach content viscosity

Forms a raft on top of stomach contents

395
Q

MOA

Omeparzole

Lansoprazole

Pantoprazole

A

PPIs

Activated in acidic pH

Irreversibly inhibit H/K ATPase

More effective than H2R antagonsits

396
Q

MOA

Cimetidine

Ranitidine

A

H2 R antagonists

Reduce gastric parietal cell H secretion

397
Q

MOA

Misoprostol

A

Prostaglandin analgoue

Acts on parietal cells to reduce secretion

398
Q

Side effects:

Mg Triscillate

A

Diarrhoea

399
Q

Side effects: AI hydroxide

A

Constipation

400
Q

Side effects: PPIs

A

GI distrubance

Headache

401
Q

Side effects: H2R antags

A

Mainly with cimetidine: GI disurbance

402
Q

Side effects:

Misoprostol

A

Diarrhoea is very common

403
Q

Interactions:

Mg Triscillate

A

Interfere with drug absorption- take separately

404
Q

Interactions:

AI hydroxide

A

Interfere with drug absorption- take separately

405
Q

Interactions:

PPIs

A

P450 inhibitor

406
Q

Interactions:

Cimetidine

A

P450 inhibitor

407
Q

Additional notes:

Mg Triscillate, AI hydroxide

A

Take when symptoms occur/expected

408
Q

Additional notes:

PPIs

A

Masy mask symptoms of gastric carcinoma

409
Q

Additional notes:

H2R antags

A

May mask symptoms of gastric Ca

410
Q

Additional notes:

Misorpostol

A

Mainly used to prevent NSAID-associated PUD

Often in combination with NSAID e.g. diclogenac + misoprostol= arthrotec

411
Q

MOA:

Bran Ispaghula

A

Bulk laxatives

Increase feacal mass-> increased peristalsis

412
Q

MOA:

Docusate

Glycerin (PR)

Senna

Picosulfate

A

Stimulant laxatives

Increase intestinal motility

413
Q

MOA:

Lactulose

Macrogol

Phosphates

Mg Salts

A

Osmotic laxatives

Increse stool water content

414
Q

MOA:

Liquid paraffin

A

Stool softener

415
Q

Side effects:

Bulk forming laxatives

A

Bloating

416
Q

Side effects:

Liquid paraffin

A

Reduced ADEK absorption

Granulomatous reactions

417
Q

Contraindication to all laxatives

A

Bowel obstruction

418
Q

What is co-danthrusate

A

A mild stimulant laxative used in Rx of opioid induced constipation

419
Q

MOA:

Hyoscine butylbromide (Buscopan)

A

Antimuscarinic- antispasmodic

420
Q

MOA:

Mebeverine

Peppermint oil

A

Antispasmodic

421
Q

MOA:

Loperamide

A

Opioid receptor agonist

Doesn’t cross BBB therefore no central effects

422
Q

MOA:

Sulfasalzine

Mesalazine

A

5-ASA
Unknown MOA

423
Q

MOA:

Budesonide

A

Steroid

More potent than prednisolone

High FPM therefore less systemic effects

424
Q

MOA:

Infilixmab

A

Chimeric anti-TNF mAB

425
Q

MOA:

Etanercept

A

P75 TNFRFc fusion protein

426
Q

MOA:

Adalimumab

A

Human anti-TNF mAb

427
Q

Side effects:

Hyoscine

A

Anti-AChM SEs: dry mouth, palpitations

428
Q

Side effects:

Loperamide

A

Abdo cramps

429
Q

Side effects:

5-ASAs

A

Sulfasalzine has increased SEs:

blood dyscrasias

hepatitis

rash, urticaria

Oligospermia

pulmonary fibrosis

430
Q

Side effects:

Infliximab, etanercept, adalmimuab

A

Severe infections

TB

Allergic reactions

CCF

CNS demyelination

431
Q

Points of interest:

5-ASA

A

Monitor FBC

Topical in distal disease

432
Q

Points of interest:

Budesonide

A

Use to induce remission in ileal crohn’s

433
Q

Points of interest:

Biologics used in IBD

A

Screen for TB before parenteral admin

Give hydrocortisone to reduce allergic SEs

434
Q

SABAs

A

Salbutamol

Terbutaline

435
Q

LABAs

A

Salmeterol

Formoterol

436
Q

MOA:

beta agonists

A

Act @ bronchial B2 receptors- smooth muscle relaxation

reduced mucus secretion

437
Q

MOA:

Muscarinic antagonists

A

Bronchodilation

Mucus secretion

438
Q

SAMA

A

Ipratropium

439
Q

LAMA

A

Tiotropium

440
Q

E.g. ICS

A

Beclometasone

Budesonide

Fluticasone

441
Q

Symbicort

A

Budesonide + formoterol

442
Q

Seretide

A

Fluticasone + salmeterol

443
Q

MOA:

ICS

A

Act over weeks to reduce inflammation

Reduce cytokine production

Reduce prostaglanding/leukotriene synthesis

Reduce IgE secretion

Reduce leukocyte recrutiement

Prevent long term decline in lung function

444
Q

MOA:

Theophylline

Aminophylline

A

Methylxanthines

PDE inhibitors: increse cAMP-> bronchodilation

445
Q

MOA:

Montelukast

Zafirlukast

A

Leukotriene antagonists

Block cysteinyl leukotirenes

446
Q

MOA:

Roflumilast

A

PDE4 inhibitor

447
Q

MOA:

Omalizumab

A

Humanised anti-IgE mAb

448
Q

MOA:

Carbocystine

A

Mucolytic

449
Q

MOA:

Dornase ALFA

A

DNAse (mucolytic)

450
Q

MOA:

Certirizine/loratidine/fexofenadine

Chlorphenamine (piriton)

A

Selective H1R inverse agonists aka H1 antagonists

451
Q

What are the non-sedating antihistamines

A

Certirizine

Des/ loratidine

Feoxfenadine

452
Q

Give an example of a sedating antihistamine

A

Chlorphenamine

453
Q

Side effects:

H1R partial agonists

A

Hypotension

Arrhthmia: long QT

Older agents:

drowsiness

Anti-AChM

454
Q

Side effects:

Carbocystiene

A

GI bleed (rare)

455
Q

Side effects:

Roflumilast

A

GI

456
Q

Side effects:

Leukotriene antagonsits

A

?Churg-Strauss

457
Q

Side effects:

Methylxanthines

A

Nausea

Arrhythmias

Seizures

Hypokalaemia

458
Q

Side effects:

ICS

A

Oral candidiasis

High doses may -> typical steroid SEs

459
Q

Side effects:

Muscarinic antagonsits

A

Dry mouth

460
Q

Side effects:

Beta agonsits

A

Tachycardia

Tremor

461
Q

CI:

Muscarinic antagonists

A

Closed angle glaucoma

Prostatic hypertrophy

462
Q

CI:

Roflumilast

A

Severe immunological disease

463
Q

CI:

Carbocysteine

A

Active peptic ulceration

464
Q

CI:

H1R inverse agonsists

A

Severe hepatic disease

Caution:

long QT

BPH

Closed angle glaucoma

465
Q

Interactions:

Methylxanthines

A

Reduced levels:

smoking, EtOH, CyP inducers

Increased levels:

CCBs

CyP inhibitors

466
Q

Interactions:

Beta agonsits

A

Reduced K in high doses with corticosteroids, loop/thiazide diuretics

Theophylline

467
Q

Additional info:

Salbutamol

A

Can be given IV in acute severe asthma

468
Q

Additional info:

ICS

A

Decreases risk of complications: use spacer, rinse mouth after use

Fluticasone is 2x as potent so use at lower dose

Symbicort can be used as a reliever or a preventer because of formoterol’s fast onset

469
Q

Additional info:

Methylxanthines

A

Aminophylline is IV form

Give IVI slowly, too fast-> VT

Monitor with ECG and check plasma levels

470
Q

Additional info:

Leukotriene antagonsits

A

Particularly useful for NSAID and exercise induced asthma

471
Q

Additional info:

Omalizumab

A

SC injection every 2-4w

Used for severe asthma

472
Q

Use: carbocystine

A

COPD

473
Q

Use: DNAse

A

CF

474
Q

Standard dose:

Amoxicillin

A

500mg TDS PO

475
Q

Standard dose:

Clarithromycin

A

500mg BD PO

476
Q

Standard dose:

Trimethoprim

A

200mg BD PO

477
Q

Standard dose:

Co-amox

A

1.2g TDS IV

478
Q

Standard dose:

Simvastatin

A

20mg OD Nocte PO

479
Q

Standard dose:

Nifedipine MR

A

20mg OD PO

480
Q

Standard dose:

Lisinopril HTN

A

10mg OD PO

481
Q

Standard dose:

Lisinopril HF

A

2.5mg OD PO

482
Q

Standard dose:

Bisorprolol HF

A

1.25mg OD PO

483
Q

Standard dose:

Paracetamol

A

1g QDS PO

484
Q

Standard dose:

Codeine phosphate

A

30mg every 4h PRN PO

Max 240mg daily

485
Q

Standard dose:

Tramadol

A

50mg ever 4h PRN PO

Ma 300mg daily

486
Q

Standard dose:

Enoxaparin

A

Treatment: 1.5mg/kg/24h SC

Prophlyaxis: 40mg OD SC

487
Q

MOA:

Cyclophosphamide

A

Alkylates DNA

Affects B cells> T cells

488
Q

MOA:

Cisplatin

A

Alkylates DNA

489
Q

MOA:

Azathioprine

A

Blocks de novo nucleotdie synthesis

Affects T cells > B cells

490
Q

MOA:

Mycophenolate mofetil

A

Blocks de novo nucleotide synthesis

Affects T cells > B cells

491
Q

MOA:

Methotrexate

A

Dihydrofolate reductase inhibitor

492
Q

MOA:

Chlorambucil

A

Alkylates DNA

493
Q

Antiproliferative agents

A

Cyclophosphamide

Cispaltin

Azathioprine

Mycophenolate mofetil

Methotrexate

Chlorambucil

494
Q

Inihibitors of cell signalling

A

Ciclosporin

Tacrolimus

Sirolums

495
Q

MOA:

Ciclosoprin

Tacrolimus

A

Calcineruin inhibitors

Block IL-2 production

496
Q

MOA:

Sirolimus

A

Blocks mTOR pathway

497
Q

What are the anti-T cell monoclonal antibodies

A

Murnomab-CD3

Basiliximab

Toilizumab

Abatecept

498
Q

MOA:

Muromonab-CD3

A

Blocks CD3 on T cells

499
Q

MOA:

Basiliximab

A

Blocks CD25R (alpha chain of Il-2R)

500
Q

MOA:

Tocilizumab

A

Blocks IL-6 R

501
Q

MOA:

Abatecept

A

Anti CTLA-4 Ig

Blocks costimulation of T cells

502
Q

MOA:

Prednisolone

A

Inhibits phosophilapse A2:

Reduces platelet activating factor

Reduced arachidonic acid

Reduced trafficlking of phagocytes (hence transient increase in phagocyte count)

Lymphopenia, apoptosis of T+V cells

503
Q

MOA:

Ustekinumab

A

Binds to p40 subunit of IL-12 and IL-23

504
Q

MOA:

Rituximab

A

Anti-CD20

Redcues B cells (not plasma cells)

used for lymphoma and autoimmune disease

505
Q

MOA:

Alemtuzumab

A

Binds to CD-52

Used in CLL

506
Q

MOA:

Natalizumab

A

Anti-a4 integrin

Used in MS and Crohn’s

507
Q

Side effects:

Cyclophosphamide

A

Bm suppresswion

Haemorrhagic cystitis

Alopecia

Sterility

508
Q

Side effects:

Cisplatin

A

BM suppression

Severe n/v

Nephrotoxic

Ototoxic

Peripheral neuropathy

509
Q

Side effects:

Azathiorpine

A

Bm suppression

Hepatotoxicity

n/v/d

Arthralgia

510
Q

Side effects:

Mycophenolate

A

BM suppression

Skin malignancy

GI upset

511
Q

Side effects:

Methotrexate

A

Pulmonary fiboris

Hepatotoxic

Mucositis

512
Q

Side effects:

Chlorambucil

A

BM suppression

EM-> SJS

513
Q

Side effects:

Ciclosporin

A

Nephrotoxic

Hepatic dysfunction

Tremor

Hypertrichosis

Gingival hypertrophy

Encephalopathy

514
Q

Side effects:

Tacrolimus

A

Nephrotoxic < cf ciclosporin

Diabetogneic

Neurotoxic > cf ciclopsoinr

515
Q

Side effects:

Sirolimus

A

Dyslipidaemia

516
Q

Side effects:

Pred

A

Diabetes

Central obesity

Adrenal suppression

Cataracts

Glaucoma

Pancreatitis

Osteopororis

Cushingoid

Hirstutism

Neutrophilia

517
Q

Interactions:

Azathioprine

A

Allopurinol-> increased toxicity

518
Q

Interactions:

Methotrexate

A

Increased toxicity with NSAIDs, ciclosporin, Crohn’s

519
Q

Interactions:

Ciclosporin

Tacrolimus

A

P450 inhibitors

520
Q

Use:

Cyclophosphamide

A

Cancer

RA

SLE

Systemic sclerois

Wegener’s

521
Q

Use:

Cisplatin

A

Cancer

522
Q

Use:

Azathioprine

A

Prevent Tx rejection

Steroid sparing agent: IBD, SLE, RA

523
Q

Use:

Mycophenolate

A

Prevent Tx rejection

AI disease

524
Q

Use:

Methotrexate

A

Cancer

RA

Psoriasis

Crohn’s

525
Q

Use:

Chlorambucil

A

Cancer e.g. CLL

526
Q

Use:

Ciclopsporin

A

Prevent Tx rejection

GvHD

UC

RA

Psoriasis

527
Q

Use:

Tacrolimus

A

Prevent Tx rejection

528
Q

Additional info:

Cyclophosphamide

A

Give mensa to prevent haemorrhagic cystitis

Activated by p450

529
Q

Additional info:

Cisplatin

A

Carboplatin is associated with less severe SEs

Requires pre-admin hydration

530
Q

Additional info:

Azathioprine

A

Do TPMT assay before use

50% of patients intolerant of azathioprine tolerate 6-MP

531
Q

Additional info:

Methotrexate

A

Give folinic acid to reduce risk of myelosuppression

Monitor U+E, FBC, LFT

532
Q

Additional info:

Ciclosporin

A

Monitor LFTs

533
Q

What are the important cytotoxic classes

A

Aklyating agents

Antimetabolites

Cytotoxic Abx

Microtubule inhibitors

Topoisomerase inhibitors

Immune modulators

MAbs

Tyrosine kinase inhibitors

Endocrine modulators

534
Q

Alkylating agents

A

Cyclophosphamide

Chlorambucil

Busulfan

Cisplatin

535
Q

MOA alkylating agents

A

DNA x-linking

Base mis pairing

Excision of alkylated DNA-> strand breaks

536
Q

Antimetabolites

A

Methotrexate

5-FU

537
Q

Cytotoxic Abx

A

Anthracycline: doxorubicin, daunorubicin

Bleomycin

538
Q

MOA cytotoxic Abx

A

Intercalate with DNA

Free radical formation

539
Q

MT inhibitors

A

Vinca alklaoids: vincristine, vinblastine

Taxanes: paclitaxel

540
Q

Topoisomerase inhibotrs

A

Etoposide

541
Q

Immune modualtors

A

Thalidomide, lenalidomide

542
Q

Trastuzumab

A

Anti-Her 2: breast Ca

543
Q

Bevacizumab

A

Anti-VEGF

544
Q

Cetuximab

A

Anti-EGFR (CRC)

545
Q

Rituximab

A

Anti-CD20 NHL

546
Q

Tyrosine kinase inhiibots

A

Erlotonib

Imatinib

Sinitimib

547
Q

Erlotinib

A

Lung Ca

548
Q

Imaitinb

A

CML

549
Q

Sunitinib

A

RCC

550
Q

Common side effects of CTx

A

N/v: prophylactic anti-emetics

Alopecia

Neutropenia: 10-14d post chemo

Extravasation of chemo agents:

pain, burning brusing at infusion site. Stop infusion, give steroids, apply cold pack. Liaise early with plastics

Hyperuricaemia

Oral mucositis

551
Q

Specific problems:

Cyclophosphamide

A

Haemorrhagic cystitis: give mensa

Hair loss

BM suppression

552
Q

Specific problems:

Doxorubicin and other anthracylcines

A

Cardiomyopathy

Extravasation reactions

553
Q

Specific problems:

Bleomycin

A

Pulmonary fibrosis

554
Q

Specific problems:

Vincristine

A

Peripheral neuropathy

Don’t give intrathecal

555
Q

Specific problems:

Paclitaxel

A

Peripheral neuropathy

Hypersensitivity

Pre rx with anti-histamines and steroids

556
Q

Specific problems:

5-FU

A

Palmar-plantar erythrodysthesia

Mucositis

557
Q

Mx of chemo-induced emesis

A

Low risk: domperidone/metoclopramide started pre Rx

High risk:

ondanestron + dex + aprepitant

558
Q

Breast Ca: FEC

A

5- FU

Epirubicine

Cyclophospamide

559
Q

Breast Ca: CMF

A

Cyclophosphamide

Methotrexate

5-FU

560
Q

Testicular teratoma: BEP

A

Bleomycin

Etoposide

cisPlatin

561
Q

CTx ovarian

A

Carboplatin

Pacliatzel

562
Q

R-CHOP

A

NHL

Ritxuimab

Cyclophosphamide

Hydroxydaunomycin (doxorubicin)

Oncovin

Pred

563
Q

ABVD

A

HL

Adriamycin

Bleomycine

Vinblastine

Dacarbazine

564
Q

Advies with pred

A

Don’t stop steroids suddenly

Consult doctor when unwell

Increase does with illness or stress

Carry steroid card

Avoid OTcs e.g. NSAID

Osteoporosis and PUD prophylaxis (Ca+ vit D, bisphosphonates, PPI)

565
Q

SEs of steroids

A

GI:

Candidiasis, PUD, oesophageal ulceration, pancreastitis

Cardio:

HTN, CCF

MSK:

Proximal myopathy

Osteoporosis

Endo:

Growth suppression, HPA suppression, Cushing’s

Metabolic:

Na and fluid retention

Raised PMN

Reduced K

CNS:

Depression, psychosis

Eye:

Cataracts, glaucoma

Immune:

Increased susceptibility to infection

566
Q

Liver transplant regime

A

Tacrolimus

Azathioprine

Pred: withdraw at 3m

567
Q

Renal transplant regime

A

Pre-op:

Alemtuzumab

Post op

Pred

Tacrolimus LT

568
Q

Drugs used in rheumatic disease

A

5-ASAs

Methotrexate

Hydroxychloroquine

Penicllamine

Infliximab

569
Q

MOA:

Hydroychloroquine

A

Reduced activation of dendritic cells

570
Q

Anti-Gout Drugs

A

Colchcine

Allopurinol

Feboxustat

Probenecid

Rasburicase

571
Q

MOA:

Allopurinol

A

XO inhibitor

572
Q

MOA:

Feboxustat

A

XO inhibitor

573
Q

MOA:

Probenecid

A

Urcisouric

574
Q

MOA:

Rasburicase

A

Recombinant uric oxidase

575
Q

MOA:

NSAIDs

A

Non-selective COX inhibitors

Analgesic

Antipyretic

Anti-inflammatory

576
Q

MOA:

Celecoxib

A

Selective COX2 I

577
Q

Rank NSAIDs from least to most toxic

A

Ibuprofen

Diclofenac

Aspirin

Naproxen

Indomethacin

Ketoprofen

578
Q

Neuromusuclar durgs

A

Stigmines

Baclofen

Dantrolene

579
Q

MOA:

stigmines

A

Anticholinesterases:

Increase ACh in the synpatic cleft

Enhacne neuromuscular transmission

580
Q

MOA:

Baclofen

A

GABA agonist

Skeletal muscle relaxant

581
Q

MOA:

Dantrolene

A

Prevents Ca release from sarcoplasmic reticulum

Skeletal muscle relaxant

582
Q

Side effects:

Hydroxychloroquine

A

Visual change: rarely retinopathy

Seizures

BM suppression

583
Q

Side effects:

Penicillamine

A

Nephrotic syndrome

Drug-induced lupus

Taste change

584
Q

Side effects:

Infliximab

A

Severe infectsion

TB

Allergic reactions

CCF

CNS demyelination

Increased AI disease and C

585
Q

Side effects:

Colchicine

A

Diarrhoea

Renal impairment

586
Q

Side effects:

Allopurinol

A

Severe skin reactions -> SJS

GI upset

Hepatotoxic

587
Q

Side effects:

Feboxustat

A

Headache

Rash

Abnormal LFTs

588
Q

Side effects:

Probenecid

A

GI upset

589
Q

Side effects:

NSAIDs

A

Gastritis and PUD

Reduced GFR

Interstitial nephritis

Papillary necrosis

hyperkalaemia

Peripheral oedema

Bronchospasm

EM-> SJS

590
Q

Side effects:

Stigmines

A

Cholinergic

591
Q

Side effects:

Baclofen

A

Sedation

Reduced tone

Nausea

Urinary distrubance

592
Q

Side effects:

Dantrolene

A

Hepatotoxicity

GI upset

593
Q

CI:

Hydroxychloroquine

A

Caution in G6PDD

594
Q

CI:

Penicillamine

A

SLE

595
Q

CI:

Infliximab

A

TB

596
Q

CI:

Colchicine

A

Caution in renal impairment

597
Q

CI:

Allopurinol

A

Caution in R + L: reducce dose

598
Q

CI:

Methotrexate

A

R+L disease

599
Q

CI:

Febroxustate

A

R+L disease

600
Q

CI:

NSAIDS

A

Renal or cardiac failure
PUD

Severe hepatic impairment

Caution in: the elderly, asthma

601
Q

CI:

Celecoxib

A

IHD

Cerebrovascular disease

L+R disease

602
Q

CI:

Stigmines

A

Asthma

Inestinal/urinary obstruction

603
Q

CI:

Baclofen

A

PUD

604
Q

CI:
Dantrolene

A

Hepatic impairment

605
Q

Interactions:

Allopurinol

A

Reduces metabolism of azathioprine: avoid

606
Q

Interactions:

NSAIDs

A

Increased bleeding with warfarin

Reduces effects of ACEi and ARBs

Increases toxicity of methotrexate

607
Q

Interactions:

Celecoxib

A

Reduces effects of ACEis and ARBs

Increases toxicity of methotrexate

608
Q

Interactions:

Baclofen

A

Increased by TCAs

609
Q

Additional notes:

Hydroxychloroquine

A

Monitor vision

610
Q

Additional notes:

Penicillamine

A

Chelates Cu and Pb

Prevents stones in cystinruia

611
Q

Additional notes:

Allopurinol

A

Initial Rx can increase gout

Initiate with NSAID/colchicine cover

612
Q

Additional notes:

NSAIDs

A

Can be given with other agents for gastroprotection: PPI, H2Ras, misoprostol

613
Q

Additional notes:

Celecoxib

A

Assess CV risk before use

Only used for short periods in young patients with intolerance for other NSAIDs

614
Q

Additional notes:

Stigmines

A

Edrophonium preferred for Dx of MG

Pyridostigmine preferred for the Rx of MG (long t1/2)

615
Q

Additional notes:

Dantrolene

A

Used to relieve chronic spasiticity and malignant hyperthermia

616
Q

A 62-year-old man with a history of type 2 diabetes mellitus and ischaemic heart disease presents to his GP with erectile dysfunction. Which one of the following medications would contraindicate the prescription of sildenafil?

Metformin

Isosorbide mononitrate

Gliclazide

Atorvastatin

Clopidogrel

A

Viagra? - contraindicated by nitrates and nicorandil

Patients taking nitrates cannot take sildenafil concurrently as this may potentiate the vasodilating effects of such drugs

617
Q

Contraindications to sildenafil

A

Patients taking nitrates and related drugs such as nicorandil

Hypotension

Recent stroke or MI (NICE recommend waiting 6 months)

618
Q

Side effects of Sildenafil

A

Visual disturbances e.g. blue discolouration, non-arteritis anterior ischaemic neuropathy

Nasal congestion

Flushing

GI side-effects

Headache

619
Q

Aldosterone antagonsits following MI

A

Patients who have had an acute MI and who have symptoms and or signs of heart failure and left ventricular systolic dysfunction should be treated with an aldosterone antagonist licensed for post-MI therapy e.g. eplerenone 3-14d post MI, preferrably after ACEI therapy

620
Q

Causes of raised prolactin- the p’s

A

Pregnancy

Prolactinoma

Physioloical

PCOS

Primary hypothyroidism

Phenothiazines, metocloPramide, domPeridone

(oestrogens, acromegaly)

621
Q

Drugs causing raised prolactin

A

Metoclopramide, domperidone

Phenothiazines

Haloperiodl

SSRIs, opioids

622
Q

What cardiovascular drugs require drug monitoring

A

Statins

ACEi

Amiodarone

623
Q

Statin drug monitoring

A

LFTs at baseline, 3m, 12m

624
Q

ACEi drug monitoring

A

U+E,

Prior to treatment

After increasing dose

at least annually

625
Q

Amiodarone drug monitoring

A

TFT, LFT

TFT, LFT, U+E, CXR prior to treatment

TFT, LFT every 6m

626
Q

Rheumatology drugs that require monitoring

A

Methotrexate

Azathioprine

627
Q

Methotrexate drug moniotring

A

FBC, LFT, U+E

The Committee on Safety of Medicines recommend ‘FBC and renal and LFTs before starting treatment and repeated weekly until therapy stabilised, thereafter patients should be monitored every 2-3 months’

628
Q

Azathioprine drug monitoring

A

FBC, LFT

FBC, LFT before treatment
FBC weekly for the first 4 weeks
FBC, LFT every 3 months

629
Q

Neuropsychiatric drugs that require monitoring

A

Lithium

LFT

630
Q

Lithium drug monitoring

A

Lithium level, TFT, U&E

TFT, U&E prior to treatment
Lithium levels weekly until stabilised then every 3 months
TFT, U&E every 6 months

631
Q

VPA drug monitoring

A

LFT

LFT, FBC before treatment
LFT ‘periodically’ during first 6 months

632
Q

Glitazones drug monitoring

A

LFT before treatment
LFT ‘regularly’ during treatment

633
Q

Drugs causing pulmonary fibrosis

A

Amiodarone

Cytotoxic agents: busulphan, bleomycin

Anti-rheumatoid drugs: methotrexate, sulfasalazine, gold

Nitrofurantoin

Ergot-derived dopamine R antagonists: bromocriptine, cabergoline, pergolide

634
Q

Alpha 1 agonist

A

Decongestants e.g. phenylephrine/oxymetazoline

635
Q

Alpha 2 agonist

A

Topical briminodine in glaucoma

636
Q

Alpha R antagonist

A

BPH e.g. tamsulosin

HTN e.g. doxazosin

637
Q

Beta 1 agonist

A

Inotropes e.g. dobutamine

638
Q

Beta 2 agonist

A

Bronchodilators e.g. salbutamol

639
Q

Dopamine agonist

A

PD e.g. ropinirole

Prolactinoma

640
Q

GABA agonist

A

BZD

Baclofen

641
Q

Muscarinic agonist

A

Glaucoma e.g. pilocarpine

642
Q

Nicotinic agonist

A

Nicotine

Varenicline (uesd for smoking cessation)

Depolarising muscle relaxant e.g. suxamethonium

643
Q

Oxytocin agonist

A

Inducing labour e.g. syntocinon

644
Q

Serotonin agonist

A

Triptans e.g. for acute migraine (zolmitriptan)

645
Q

Beta 1 antagonists

A

Non-selective and selective e.g. atenolol and bisoprolol

646
Q

Beta 2 antagonists

A

Non-selective beta-blockers e.g. propranolol, labetalol

647
Q

Dopamine antagonists

A

Schizophrenia e.g. haloperidol

Anti-emetics e.g.s metoclopramide/domperidone

648
Q

GABA antagonists

A

Flumezanil

649
Q

H1R antagonists

A

Antihistamines e.g. loratidine

650
Q

Muscarinic antagonists