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Drugs studied Flashcards

1
Q

how does activated charcoal work?

A

1) adsorption of toxin onto the surface of the charcoal, reducing its absorption into the blood
2) increasing the rate of elimination

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2
Q

which drugs are most effectively removed by activated charcoal

A

weakly ionic drugs like benzodiazepines and methotrexate

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3
Q

common side effects of activated charcoal?

A

black stools, vomiting, intestinal obstruction

Aspiration- pneumonitis, bronchospasm, airway obstruction

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4
Q

When to give single and repeat doses of activated charcoal

A 
single dose (50mg)  if poison ingested less than 1 hour ago 
additional doses can be given after 4 hours if they are on aspirin, opioids or TCAs as these delay gastric emptying
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5
Q

how does adrenaline work in anaphylaxis

A

acts at adrenoreceptors to bring about the fight or flight response- vasoconstriction of the blood vessels supplying the skin, increased heart rate, increased force of contraction, vasodilation of blood vessels supplying the heart, bronchodilator and suppression of inflammatory release from mast cells

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6
Q

adrenaline side effects

A

adrenaline-induced hypertension, anxiety, tremor, headache, palpitations
angina, mi and arythmia in patients with existing heart disease

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7
Q

adrenaline interactions

A

interacts with beta blockers to cause wide-spread vasoconstriction

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8
Q

anaphylaxis dose of adrenaline

A

500mg IM

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9
Q

list 3 aminoglycoside antibiotics

A

gentamicin, amikacin, neomycin

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10
Q

what are the indications of aminoglycosides? [4]

A

severe infections caused by gram negative aerobes (e.g. pseudomonas aeruginosa)

1) severe sepsis
2) complicated UTI and pyelonephritis
3) biliary and intrabdominal sepsis
4) skin, eye or ear infections

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11
Q

MOA if aminoglycosides

A

inhibit protein synthesis by binding to ribosomes - bacteriocidal

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12
Q

adverse effects of aminoglycosides [2]

A

nephrotoxicity (more likely in combo with cyclosporin, cephalosporin, vancomycin and platinum chemotherapy)
ototoxicity (more likely in combo with loop diuretics and vancomycin)

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13
Q

in which groups are aminoglycosides used with caution [4]

A

neonates, elderly, renal impairment, myasthenia gravis

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14
Q

aminoglycosides ROA and dosing

A

Intermittent IV infusion OD - dose depends on weigh and renal function
dosing interval determined by plasma level monitoring ( usually 24 hours but can be longer in renal impairment)

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15
Q

aminoglycosides length of course

A

less than 7 days

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16
Q

monitoring parameters for aminoglycosides

A

temp, crp

renal function, plasma conc 18-24 hrs after first dose

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17
Q

Indications of amitriptyline

A

1) depression

2) neuropathic pain

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18
Q

amitriptyline side effects

A

antimuscarinic block- dry mouth, constipation, urinary retention, blurred vision
sedation, hypotension
arrhythmia, ECG changes
convulsions, hallucinations, mania
dopamine block- breast changes, sexual dysfunction, EPSEs

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19
Q

amitriptyline overdose

A

severe hypotension, arrhythmia, convulsions, coma, respiratory failure- death

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20
Q

amitriptyline withdrawal effects

A

sleep disturbances, flu like symptoms, GI upset

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21
Q

interactions of amitriptyline

A

monoamine oxidase inhibitors-> serotonin syndrome

TCAs- can augment side effects

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22
Q

Amitriptyline starting dose in neuropathic pain

A

10mg ON

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23
Q

amitriptyline counselling points

A

carry on for at least 6 mo after you start feeling better

dont stop treatment suddenly- withdrawal effects - reduce slowly over 4 weeks

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24
Q

list 4 antihistamines

A

cetirizine, loratadine, fexofenadine, chlorphenamine

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25
Q

how do antihistamines work?

A

h1 receptor antagonist- prevents histamine binding
histamine causes oedema (due to increased capillary permeability) erythema (vasodilation) and itching (sensory nerve stimulation)
used as an adjunct to adrenaline in anaphylaxis

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26
Q

antihistamine SEs

A

chlorphenamine- 1st gen- sedation

others dont cross bbb so no CNS side effects

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27
Q

in which population should antihistamines be avoided and why

A

severe liver disease- may precipitate hepatic encephalopathy

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28
Q

chlorphenamine in anaphylaxis- dose and route

A

10mg IV or IM

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29
Q

antihistamines counselling point

A

hay fever- should improve sneezing, itching, runiness- not so good for nasal congestion
chlorphenamine- sedative effect- might want to take at night - driving risk, avoid taking with alcohol

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30
Q

list 3 anti-platelet ADP-receptor antagonist drugs

A

clopidogrel, ticagrelor, prasugrel

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31
Q

3 indications of anti platelet drugs in combo with aspirin

A

1) acute coronary syndrome
2) prevention of occlusion of coronary artery stent
3) secondary prevention in cardiovascular/ cerebrovascular/ peripheral artery disease

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32
Q

MOA of clopidogrel (ticagrelor and prasugrel)

A

bind to pY12 subtype of G protein coupled ADP receptors on the surface of platelets- down stream events lead to platelet aggregation

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33
Q

side effects of ADP-receptor antagonists

A

bleeding, GI upset, thrombocytopenia (platelet deficiency)

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34
Q

ADP-receptor antagonists are not appropriate for

A

should not be used in patients with active bleeds
caution in renal and hepatic impairment
should be stopped 7 days before elective surgery

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35
Q

interactions of clopidogrel

A

clopidogrel is a pro drug

interacts with cyp 450 inhibitors- omeprazole, ciprofloxacin, erythromycin, antifungals, SSRIs

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36
Q

ticagrelor interactions

A

not a pro drug- interacts with cyp inhibitors and inducers

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37
Q

which drugs increase bleed risk of adp receptor antagonists?

A

antiplatelets, anticoagulants like heparin, NSAIDs

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38
Q

clopidogrel dose

A

loading dose= 300mg
maintenance dose= 75mg

oral only

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39
Q

clopidogrel counselling

A

purpose- to prolong life and prevent heart attacks and strokes
stent?- stress importance of taking every day as directed to keep stent clear
check if they are actively bleeding
if they start bleeding it may take loner for it to stop
report unusual bleeding to doctor

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40
Q

aspirin indications

A

1) ACS/ stroke

2) secondary prevention for cardiovascular/ cerebrovascular/ peripheral arterial disease

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41
Q

MOA of aspirin

A

irreversible inhibition of COX

(reduces production of thromboxane from arachidonic acid) which prevents platelet aggregation

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42
Q

aspirin SEs

A

GI irritation
peptic ulceration, haemorrhage
bronchospasm
high dose- tinnitus

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43
Q

aspirin overdose

A

hyperventilation, hearing loss, metabolic acidosis, confusion -> convulsions, cardiovascular collapse, respiratory arrest

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44
Q

when should aspirin be avoided

A

children under 16- Reyes syndrome
aspirin sensitivity (or NSAID sensitivity)
third trimester pregnancy- can cause premature closure of ductus arteriosus
caution- peptic ulcers, gout

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45
Q

doses of aspirin

A 
LD= 300mg
maintenance= 75mg
stroke= 300mg od for 2 weeks pain= 4g
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46
Q

aspirin gastroprotection

A

should be considered if lots of risk factors for go complications / NSAIDs/ prednisolone
omeprazole 20mg

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47
Q

aspirin counselling

A

take after food

watch out for indigestion/ bleeding issues- report them to ur doctor

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48
Q

list 5 beta blockers

A

bisoprolol, atenolol, propranolol, metoprolol, carvedilol

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49
Q

5 indications of beta blockers

A

1) ischaemic heart disease- angina
2) chronic HF
3) AF
4) SVT
5) hypertension

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50
Q

how do beta blockers work?

A

act at beta 1 receptors in the heart to reduce force of contraction and rate of conductivity in heart which reduces cardiac work & oxygen consumption of heart

arrhythmia- prologue refractory period of AV node

reduce renin secretion by kidney to lower blood pressure

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51
Q

SEs of beta blockers

A

fatigue, cold extremities, headache, GI disturbances, sleep disturbances & nightmares
impotence in men

52
Q

cautions and contraindications - beta blockers

A

contraindicated in asthmatics (bronchospasm) and heart block

can use in copd but chose bisoprolol/ metoprolol (more b1 selective)
HF- start at low dose and up titrate slowly
caution- haemodynamic instability,
dose reduction in hepatic failure

53
Q

which class interact with beta blockers?

A

non- dihydropyridine calcium channel blockers (verapamil, diltiazem) - HF, bradycardia, asystole

54
Q

beta blockers counselling

A

explain rationale for treatment, discuss side effects (impotence!)
HF- may cause worsening of symptoms at first (seek attention if this happens)
obstructive airway diseases- stop and seek attention if breathing difficulties arise

55
Q

list 2 cephalosporins

A

cefalexin, cefotaxime

56
Q

list 2 carbapenems

A

meropenem, ertapenem

57
Q

indications of cephalosporins and carbapenems

A

1) urinary and respiratory tract infections

2) parenteral- very severe and complicated or caused by resistant organisms

58
Q

target organism of cephalosporins

A

broad spectrum antibiotic- targeting gram-negative bacteria (e.g. pseudomonas aeruginosa) - first to fifth generation get more activity against them , variable activity agains gram positive organisms

59
Q

why are cephalosporins and carbapenems less susceptible to resistant mutations

A

cephalosporins and carbapenems are naturally more resistant to beta lactamases because beta lactic ring is fused to another bulky group

60
Q

mode of action of cephalosporins and carbapenems

A

inhibit enzymes responsible for the cross linking of peptidoglycan in bacterial cell walls - weakens cell wall preventing the bacterial cell from maintaining osmotic gradient-> cell wall swells-> lysis-> cell death

61
Q

Side effects of cephalosporins and carbapenems

A

GI upset, antibiotic-associated colitis
C diff overgrowth (due to death of gut flora)
hypersensitivity ( can be cross reactive in penicillin allergy)
neurological toxicity including seizure

62
Q

contraindications and cautions cephalospronis and carbapenems

A

caution- at risk of c diff, epilepsy, renal impairment

ci- allergy, penicillin allergy

63
Q

interactions- cephalosporins, carbapenems

A

warfarin- enhance anticoagulant effect- kill gut flora which synthesise vit K
aminoglycosides- nephrotoxicity
valproate- reduce plasma conc

64
Q

Roa of carbapenems

A

iv only

65
Q

counselling carbapenems and cephalosporins

A

check no penicillin/ b-lactam antibiotic allergy
seek medical advice if rash or other unexpected symptom develops
if you get a reaction- tell them not to take this class of antibiotics in future

66
Q

list 3 systemic glucocorticosteroids

A

prednisolone, hydrocortisone, dexamethasone

67
Q

indications of systemic glucocorticosteroids

A

1) allergic inflammatory disorders e.g. asthma
2) autoimmune diseases e.g. IBS
3) cancer
4) adrenal insufficiency, hypopituitarism

68
Q

Moa of glucocorticosteroids

A

bind to glucocorticoid receptors in cytosol -> translate to the nucleus and bind to glucocorticoid-response elements on DNA to regulate gene expression

up regulate anti-inflammatory genes and down regulate pro-inflammatory genes (like cytokines and TNF alpha)

  • suppress circulating monocytes and eosinophils
  • increase gluconeogenesis by increasing circulating amino acids and fatty acids
  • mineralocorticoid receptor- increase sodium and water retention and increase potassium execretion
69
Q

glucocorticosteroids should be used in caution in…

A

people with infections and children

70
Q

gluco-corticosteroids interact with

A

NSAIDs- increase bleed risk
b2 agonists, theophylline, loop/ thiazide diuretics- enhance hypokalaemia
cyp p450 inducers (carbamazepine, phenytoin, rifampicin)
vaccines- reduce immune response

71
Q

dose of prednisolone in acute asthma

A

40mg od

72
Q

when should corticosteroids be taken?

A

in the morning (reduce insomnia)

73
Q

what classes are commonly prescribed with corticosteroids

A

steroid sparing agents- azathioprine, methotrexate
bisphospates
PPIs

74
Q

corticosteroid counseling points

A
  • start to feel better in 1-2 days
  • dont stop suddenly- withdrawal effects
  • steroid card to carry with them
  • risks and benefits- oesteoporosis, fractures, diabetes
75
Q

list 4 DOACs

A

apixaban, dabigatran, edoxaban, rivaroxaban

76
Q

indications of DOACs

A

VTE secondary prevention

AF primary prevention

77
Q

how do DOACs work?

A

act on final common pathway- inhibit factor Xa- prevent conversion of prothrombin into thrombin
dabigatran inhibits thrombin directly and prevents fibrin -> fibrinogen conversion

78
Q

SEs of DOACs

A 
bleeding (epistaxis and GI)
anaemia, 
GI upset,
 dizziness, 
elevated liver enzymes
79
Q

in which people should DOACs be avoided

A

active bleeding, risk factors of major bleed (e.g. peptic ulcer/ cancer/ recent surgery),
preg/ BF
dose reduction needed in renal and liver disease

80
Q

DOAC interactions

A

other antithrombotic drugs- heparin, anti platelets, NSAIDs
anticoagulant effect increased by macrolides, protease inhibitors, fluconazole
decreased by rifampicin, phenytoin

81
Q

rivaroxaban dosing regimen

A

rivaroxaban- 15mg every 12hrs for vte
20mg OD in AF lifelong
10mg od for 14 days VTE prophylaxis after knee replacement

82
Q

rivaroxaban, but not the other DOACs should be taken…

A

with food

83
Q

counselling for DOACs

A
  • risk of bleed
  • provide alert card, show card to all health care providers especially if have an accident/ surgery/ new meds)
  • contact doc if serious bleed/ weakness/ tiredness/ breathlessness (anaemia)
84
Q

what are 3 indications of gabapentin and pregabalin

A

1) add-on for focal epilepsies
2) neuropathic pain
3) pregabalin- anxiety

85
Q

how do gabapentin and pregabalin work?

A

bind to voltage sensitive calcium channels which inhibits the release of NTs which reduces neuronal excitability in the brain

86
Q

side effects gabapentin

A

drowsiness, dizziness, ataxia - usually improve over first few weeks of treatment

87
Q

cautions and contraindications gabapentin

A

dose reduction in renal impairment

88
Q

gabapentin interactions

A

benzodiazepines and other sedating drugs- enhance sedative effect

89
Q

gabapentin counselling

A
  • diziness and drowsiness- this is why we start low and uptitrate- should improve over next few weeks
  • avoid driving/ operating heavy machinery til settled
90
Q

4 indications of metronidazole

A

1) antibiotic associated collitis
2) oral infections
3) surgical and gynaecological infection
4) protozoal infections

91
Q

metronidazole is effective against

A

anaerobic bacteria and protozoa

92
Q

Mao of metronidazole in anaerobes

A

reduced to nitroso free radical which binds to DNA causing damage-> cell death

93
Q

metronidazole SEs

A

GI upset, hypersensitivity reactions

long term/ high dose= neurological effects: peripheral and optic neuropathy, seizures, encephalopathy

94
Q

warnings- metronidazole

A

dose reduction in severe liver disease

avoid alcohol -> flushing, headache, nausea, vomitting

95
Q

interactions of metronidazole

A

inhibits CYP- reduces warfarin metabolism & phenytoin
CYP inducers (rifampicin) - reduces antibiotic effect
increases toxicity of lithium

96
Q

usual oral dose metronidazole

A

400mg every 8 hours

97
Q

metronidazole councelling

A

check allergy
if allergy develops tell them not to take metronidazole in future
dont drink alcohol until 48hrs after treatment

98
Q

naloxone indication

A

opioid overdose

99
Q

how does naloxone work?

A

binds to opioid receptors- competitive antagonist (displaces morphine)

100
Q

adverse effects of naloxone

A

opioid withdrawal effect- pain, restlessness, nausea and vomiting, dilated pupils cold dry skin, goose bumps

101
Q

cautions with naloxone

A

opioid dependence- risk of withdrawal

lower doses in palliative care

102
Q

acute opioid toxicity treatment

A

400-1200 micrograms naloxone

103
Q

indications of nitrofurantoin

A

1) UTI

2) UTI prophylaxis (recurrent infections)

104
Q

nitrofurantoin moa

A

damages bacterial DNA-> cell death

105
Q

nitrofurantoin SEs

A 
gi upset, hypersensitivity, 
dark yellow/ brown urine
chronic pulmonary reactions 
hepatitis, 
peripheral neuropathy 
neonates- haemolytic anaemia
106
Q

CIed groups for nitrofurantoin

A

pregnant women close to term, babies under 3 mo, renal impairment

107
Q

acute uncomplicated UTI treatment

A

nitrofurantoin 50-100mg every 6 hours

108
Q

how should nitrofurantoin be taken

A

take with food or milk

109
Q

counselling nitrofurantoin

A

check allergies, urine colour (yellow/ dark brown)

report pins and needles and breathlessness

110
Q

what are COX 1 and 2 responsible for

A

COX 1- GI mucosal integrity, maintains renal perfusion

COX-2- inducible in response to inflammation

111
Q

which NSAID has highest gi risk and lowest cardiovascular risk?

A

Naproxen

112
Q

which NSAID has the lowest GI risk and the highest cardiovascular risk?

A

Diclofenac

113
Q

NSAID interactions

A

aspirin, corticosteroids, anticoagulants, SSRIs, venlafaxine, ACEi, diuretics

114
Q

counselling NSAIDs

A

indigestion- stop treatment & contact doc
longterm (>10 days)- not recommended bc SEs
stop if unwell/ dehydrated (reduce kidney damage)

115
Q

who needs a PPI with NSAIDs?

A

> 65/ previous peptic ulcer/ co-morbidity/ aspirin/ prednisolone

116
Q

opioids SEs

A 
respiratory depression
nausea and vomitting- tends to settle
small pupils
constipation
itching
tolerence & dependence
withdrawal effects on cessation
117
Q

morphine dosing

A

oramorph for breakthrough -about 1/6th dose of MR MST continus maintenance

118
Q

morphine counselling

A

addiction isn’t an issue when used for pain relief- dont worry
may need to increase dose due to tolerance effect- dont be alarmed
take slow release every 12 hours, if that’s not covering the pain take fast acting
may expiernce but this should improve- offer metoclopramide
constipation- offer Senna, stay hydrated
drowsy? dot drive

119
Q

weak opioids (tramadol/ codeine/ dihydrocodeine) councelling

A

weaker version of morphine
take at regular intervals for best results
laxative?
drowsy? dont drive
out of reach of children
careful if contains paracetamol dont take paracetamol

120
Q

paracetamol counselling

A

feel effect half an hour after taking
dont exceed max dose- liver poisoning
remind them that paracetamol in cold & flu pills and stuff- avoid overdose

121
Q

penecillin interactions

A

reduces excretion of methotrexate

122
Q

penicillin counselling

A

check allergy- if it develops they shouldn’t take it again (rash)
complete course

123
Q

PPI counselling

A

reduce stomach acid- allowing symptoms to improve

report weight loss/ difficulty swallowing

124
Q

triptan counselling

A

reduce severity of migraines by constricting cranial arteries
should shorten duration and make pain less intense
take as soon as you feel migraine coming on
can be taken with paracetamol and ibuprofen if needed
SEs- heaviness/ pressure on chest - should pass quickly- if it doesnt seek medical help- small risk of MI
return if you get more than 4 a month for something stronger

125
Q

tetracyclines- counselling

A

allergy check
take treatment during a meal with a full glass of water sitting/ standing up
avoid indigestion remedies containing iron/ zinc 2 hours before antibiotic
potent skin from sunlight even on cloudy days

126
Q

vancomycin counselling

A

report ringing in the ears- only reversible if promptly stopped

127
Q

warfarin councelling

A

risk benefit (bleeds, preventing clots)
anticoagulant yellow book- record doses, blood test results, duration
alcohol- increases risk of bleed
food- high vit K (garlic, grapefruit, cranberry juice)
drugs- CYP inhibitors & inducers, st johns, antibiotics

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