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Year 3 > Block 32 Pharm > Flashcards

Block 32 Pharm Flashcards

1
Q

Antacids and alginates examples

A
  • Magnesium trisilicate
  • Aluminium/magnesium mixtures (Maalox) - Alginates
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2
Q

what are antacids and alginates used for?

A

dyspepsia, GORD

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3
Q

Mag trisillicate mechanism?

A

-antacid
- inc pH of gastric juicr via neutrilisation

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4
Q

CI of magnesium triscillicate?

A

Hypophosphataemia

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5
Q

mag tricillicate interactions?

A
  • amlodepine
  • nifedipine
  • verapamil
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6
Q

mag trisillicate side effects?

A
  • diarrhoea
  • nephrolithiasis (long term use)
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7
Q

Co-magaldrox (Maalox) mechanism?

A
  • mix of mag hydroxide and al hydroxide
  • neutralises acid
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8
Q

Co-magaldrox indications?

A

dyspepsia

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9
Q

Co-magaldrox side effects?

A

constipation and diarrhoea

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10
Q

Co-magaldrox and renal impairment?

A

There is a risk of accumulation and aluminium toxicity with antacids containing aluminium salts

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11
Q

alginates mechanism?

A
  • reacts w gastric acid to form a raft of alginic acid gel
  • raft had a neutral pH
  • acts as a barrier to impede reflux
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12
Q

CI of alginic acid?

A
  • intestinal obstruction
  • where excessive water loss likely (e.g. fever, diarrhoea, vomiting, high room temperature)
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13
Q

alginates and renal impairment?

A

avoid - risk of hypernatremia

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14
Q

alginic acid (gaviscon) side effects?

A
  • ankle swelling
  • constipation
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15
Q

H2-receptor antagonists?

A

rantidine

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16
Q

rantidine indications?

A

dyspepsia, GORD, peptic ulceration, prophylaxis of NSAID associated peptic ulceration

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17
Q

cautions with H2 receptor antagonits like ranitidine?

A

signs and symptoms of gastric cancer can be masked

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18
Q

ranitidine side effects?

A
  • bone marrow depression
  • nephritis
  • acute pancreatitis
  • dyskinesia
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19
Q

ranitidine mechanism?

A
  • normally after a meal, gastrin -> histamine release -> H2 activation -> acid secretopm
  • ranitidine blocks H2 receptors on gastric parietal cells -> less acid produced
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20
Q

PPIs?

A
  • Lansoprazole
  • Omeprazole
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21
Q

PPIs mechanism?

A
  • inhition of the H+/K+/ATPase pump
  • inhibition of acid production
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22
Q

PPIs and H pylori eradication?

A
  • PUD associated w H pylori infection
  • acid inhibition in H pylori eradication therapy raises gastric pH discouraging growth of H pylori
  • PPI inhibit urease enzyme
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23
Q

PPIs indications?

A
  • dyspepsia
  • GORD
  • oesophagitis
  • peptic ulceration
  • prophylaxis of NSAID associated peptic ulceration
  • H. pylori eradication
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24
Q

cautions of PPIs?

A
  • risk of fractures - high doses in the elderly
  • C diff infection risk
  • masking gastric cancer symptoms
  • B12 abs reduced w long term use
  • osteoporosis risk
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25
Q

side effects of all PPIs?

A
  • abd pain
  • constipation
  • diarrhoea
  • headache
  • skin reactions
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26
Q

Opiate based anti-motility agents =

A

codeine

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27
Q

indications of codiene?

A
  • diarrhoea
  • short term pain relief
  • dry cough
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28
Q

CI of codeine and all opiods?

A
  • ARD
  • comatose
  • raised ICP
  • risk of paralytic ileus
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29
Q

CI for codeine?

A
  • active UC
  • ab associated colitis
  • children under 18
  • known ultra-rapid codeine metabolisers
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30
Q

codeine interactions?

A
  • buprenorphine
  • clozapine
  • naltrexone
  • fluoxetine
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31
Q

side effects of codeine?

A
  • arrhythmias
  • constipation
  • hallucinations
  • nausea and vomiting on initiation
  • urinary retention
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32
Q

Non-opiate based anti-motility agents =

A

loperamide

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33
Q

codeine mechanism?

A
  • mu opiod receptors agonism
  • g protein response
  • hyperpolarisation of nociceptive neurons -> impaired pain transmission
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34
Q

loperamide mechanism?

A
  • used for diarrhoea
  • mu opiod agonist on the circ and longitudinal intestinal muscle
  • inhibits release of ACh and prostaglandins -> reducing peristalsis -> inc intestinal transit time
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35
Q

loperamide indications?

A
  • diarrhoea - acute and chronic
  • faceal incontinence
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36
Q

loperamide CI?

A
  • Active UC
  • ab assoc colitis
  • abd distension
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37
Q

loperamide interactions?

A
  • clozapine
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38
Q

cautions of loperamide?

A

children under 12

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39
Q

side effects of loperamide?

A
  • GI disorders
  • headache
  • nausea
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40
Q

Aminosalicylates?

A
  • e.g. mesalazine
  • IBD
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41
Q

mesalazine mechanism?

A
  • induce and maintains remission
  • inhibition of nuclear factor kappa B and blocks production of pro-inflamm cytokines
  • blocks COX pathways - less leukotrienes
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42
Q

mesalazine CI?

A
  • blood clotting abn
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43
Q

side effects of aminosalicyclates?

A
  • cough
  • fever
  • leucopenia
  • proteinuria
    -*** pancreaTitis **
  • ** agranulocytosis**
  • peripheral neuropathy
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44
Q

corticosteroids?

A

Hydrocortisone,Prednisolone, Budesonide

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45
Q

corticosteroids indications?

A

IBD - Crohs earlier than UC

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46
Q

corticosteroids mechanism?

A
  • neutrophil apoptosis
  • inhibits phospholipase A2, and NF-Kappa B
  • promote anti-inflammatory genes like IL10
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47
Q

CI for all corticosteroids?

A
  • avoid live viruses
  • systemic infection
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48
Q

steroids side effects?

A
  • cushings syndrome
  • psychotic disorder
  • hirtutism
  • HTN
  • osteoporosis
  • peptic ulcer
  • inc weight
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49
Q

steroids and adrenal suppression?

A

During prolonged therapy with corticosteroids, particularly with systemic use, adrenal atrophy develops and can persist for years after stopping. Abrupt withdrawal after a prolonged period can lead to acute adrenal insufficiency, hypotension, or death

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50
Q

Immunosuppressants =

A

azathioprine -> Crohns

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51
Q

azathioprine mechanism?

A
  • IS
  • Purine synthesis inhibition
  • inhibition of B and T cells
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52
Q

azathioprine Cl?

A

Reduced TPMT activity

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53
Q

azathioprine interactions?

A
  • allopurinol
  • BCG vaccine
  • captopril
  • HZ vaccine
  • ACEi
  • trimethoprim
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54
Q

azathioprine side effects?

A
  • bone marrow depression
  • leucopenia
  • pancreatitos
  • inc infection risk
  • thrombocytopenia
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55
Q

pre-treament screening for azathioprine?

A
  • TPMT activity
  • increased risk of myelosuppression with reduced TPMT activoty
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56
Q

azathioprine monitoring?

A
  • FBC weekly for first 4 weeks
  • then at least every 3 months
  • for risk of myelosuppression
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57
Q

cytokine inhibitors?

A
  • Infliximab
  • Adalimumab
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58
Q

cytokine inhibitors Ix?

A

Crohns

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59
Q

infliximab mechanism?

A
  • binds to TNF-a
    -> Downregulation of IL1 and IL6
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60
Q

adalimumab mechanism?

A
  • TNF-a inhibition
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61
Q

CI of infliximab/ adalimumab?

A

moderate/ severe HF, severe infections

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62
Q

infliximab interactions?

A
  • BCG vaccine
  • cholera vaccine
  • MMR vaccine
  • HZ vaccine
  • influenza vaccine
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63
Q

side effects of infliximab?

A
  • alopecia
  • arrhythmias
  • hypotension/ hTN
  • neutropenia
  • vasodilation
  • sepsis
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64
Q

pre-Tx screening w infliximab/ adalimumab?

A

TB

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65
Q

adalimumab side effects?

A
  • agranulocytosis
  • anx
  • haemorrhage
  • leucopenia, neutropenia, thrombocytopenia
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66
Q

adalimumab is assoc w ?

A

infections, sometimes severe, including tuberculosis, septicaemia, and hepatitis B reactivation.

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67
Q

Metronidazole & Vancomycin are used for

A

C diff assoc diarrhoea - colitis

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68
Q

metronizadole mechanism?

A
  • high activity against anaerobic bacteria and protozoa
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69
Q

metronidazole interactions?

A
  • disulfiram
  • fluorouracil
  • lithium
  • warfarin
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70
Q

side effects of metronidazole - IV?

A
  • Vomiting
  • metallic taste
  • nausea
  • dry mouth
  • vomiting
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71
Q

rare side effects w metronidazole

A
  • panc
  • agranulocytosis
  • peripheral neuropathy
  • cerebellar syndrome
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72
Q

metronidazole mechanism?

A
  • nucleic acid synthesis inhibition
  • anaerobic bacteria
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73
Q

vancomycin mechanism?

A
  • prevens crosslinkage of peptidoglycan subunits
  • prevents cell wall formation
  • glycopeptide ab
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74
Q

cautions of vancomycin?

A

Systemic absorption may be enhanced in patients with inflammatory disorders of the intestinal mucosa or with Clostridioides difficile-induced pseudomembranous colitis (increased risk of adverse reactions)

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75
Q

side effects of vancomycin?

A
  • agran
  • eosinophilia
  • hypersensitivity
  • renal failure
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76
Q

Antiprotozoal agent e.g.

A

metronidazole

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77
Q

anti-fungal agents?

A
  • Nystatin
    -Fluconazole
78
Q

nystatin mechanism?

A
  • forms channels in the membrane
  • changes membrane permeability
  • affinity for ergosterol
79
Q

nystatin indications?

A
  • oral candidasis
80
Q

nystatin side effects?

A
  • abd distress
  • angioedema
  • face oedema
  • SJS
81
Q

fluconazole mechanism?

A
  • selective inhibitor of P450 dependent enzyme lansterol 14-a demethylase
  • this enzyme converts lanosterol to ergosterol, which is necessary for fungal cell wall synthesis
82
Q

fluconazole Ix?

A
  • candidasis
83
Q

CI of fluconazole?

A

acute porphyrias

84
Q

cautions of fluconazole?

A

Susceptibility to QT interval prolongation

85
Q

interactions of fluconazole?

A
  • alc
  • amiodarone -> hepatotoxicity
  • amphotericin B
  • apiprazole
  • atorvostatin
  • bendroflumethaizide
86
Q

side effects of fluconazole?

A
  • GI discomf
  • diarrhoea
  • headache
  • skin reactions
  • agranulocytosis
  • QT prolongation
  • torsades
87
Q

other antispasmodics?

A

Mebeverine & Peppermint oil

88
Q

IBS drugs?

A
  • Mebeverine
  • Peppermint oil
  • Hyoscine (Buscopan)
89
Q

hyoscine mechanism?

A
  • muscarinic receptor antagonism
  • anticholinergic effect
  • relaxes/ spasmolytic effect on SM
90
Q

Safety info for hyoscine?

A
  • risk of serious adverse effects
  • including tachycardia, hypotension, and anaphylaxis
91
Q

CI for all antimuscarinics?

A
  • closed angle glaucoma
  • GI obstruction
  • MG
  • paralytic ileus
  • pyloric stenosis
  • severe UC
  • significant bladder outflow obstruction
  • toxic megacolon; urinary retention
92
Q

Interactions of hyoscine?

A

clozapine

93
Q

side effects of all antimuscarinics?

A
  • const
  • dry mouth
  • flushing
  • dyspepsia
  • tachycardia
  • urinary retention
94
Q

mebeverine?

A
  • antispasmodic
  • anticholinergic
  • relaxes SM
95
Q

Mebeverine CI?

A

paralytic ileus

96
Q

side effects of mebeverine?

A
  • angioedema
  • face oedema
  • skin reactions
97
Q

peppermint oil mechanism?

A
  • contains L-menthol
  • blocks CC in SM -> antispasmodic effect
  • reduces calcium influx
98
Q

side effects for peppermint oil?

A
  • bradycardia
  • GI discomfort
  • reflux
  • tremor
  • paraesthesia
99
Q

what are the laxatives?

A
  • Methylcellulose
  • Ispaghula husk
  • Senna Lactulose
  • Sodium picosulphate
100
Q

methylcellulose mechanism?

A
  • bulk forming laxative
  • inc water content of stool
  • Methylcellulose absorbs water in the gastrointestinal lumen thereby increasing the bulk of the stool.
  • This leads to distension and stimulation of peristalsis
101
Q

isphalga husk mechanism?

A
  • bulk forming
  • increasing faecal mass which stimulates peristalsis
102
Q

CI of isphalga husk?

A
  • faceal impaction
  • intestinal obstruction
  • undiagnosed rectal bleeding
  • reduced gut motility
103
Q

cautions w isphalga husk?

A
  • adequate fluid intake to avoid oesophageal or intestinal obstruction
104
Q

side effects of ispaghula husk?

A
  • abd distension
  • bronchospasm
  • conjunctivitis
105
Q

senna mechanism?

A
  • stimulant laxative
  • stimulates peristalsis thereby increasing the motility of the large intestine.
106
Q

senna CI?

A
  • atony
  • intestinal obs
  • undiagnosed abd pain
107
Q

side effects of senna?

A
  • albuminuria
  • fluid imbalance
  • GI discomfort
  • haematuria
  • pseudomelanosis coli
108
Q

prolonged/ excessive senna use can cause?

A

hypokalaemia

109
Q

lactulose indications?

A
  • constipation
  • hepatic encephalopathy
110
Q

lactulose CI?

A
  • galactosaemia
  • GI obstruction
  • GI perf
111
Q

side effects of lactulose?

A
  • diarrhoea
  • flatulence
  • nausea
  • vomiting
  • abd pain
112
Q

lactulose mechanism?

A
  • osmotic laxative
  • causes retention of water through osmosis leading to softer easier to pass stool
113
Q

Sodium picosulphate mechanism?

A
  • stimulant laxative
  • inhibits abs of water and electrolytes and increases their secretion into intestinal lumen to form an active metabolite which acts directly on colonic mucosa to stimulate peristalsis
114
Q

CI of Sodium picosulphate?

A

intestinal obst

115
Q

side effects of Sodium picosulphate

A
  • diarrhoea
  • GI discomfory
116
Q

summary of the laxatives?

A
  • methylcellulose and ispaghula husk: BF
  • senna: faecal softner
  • lactulose: osmotic
  • Sodium picosulphate: stimulant
117
Q

Local anaesthetics =

A
  • Lidocaine
  • Bupivacaine
  • used for suturing
118
Q

lidocaine CI?

A

all grades of AV block, severe myocardial depression

119
Q

SE of lidocaine?

A
  • AV block
  • cardiac arrest
  • hypotension
  • methaemglovinaemia
120
Q

lidocaine mechanism?

A
  • blocks sodium channels
  • preventing nerve depolarisation
121
Q

bupivacaine mechanism?

A
  • sodium channel blocker
122
Q

CI of bupivacaine?

A
  • Bier’s block
  • injection into inflamed tissues
123
Q

SE of bupivacaine?

A
  • arrythmias
  • dizziness
  • hTN
  • parasthesia
  • neurotoxicity
124
Q

IV anaesthetics?

A
  • Etomidate
  • Ketamine
  • Propofol
  • Thiopental
125
Q

What are IV anaesthetics used forr?

A

Rapid induction of anaesthesia, total intravenous anaesthesia, prolonged sedation

126
Q

etomidate mechanism?

A
  • short acting IV
  • binds to GABA-A increasing duration of time
  • post inhib effect of GABA is prolonged
127
Q

etomidate cautions?

A
  • acute circ failure
  • adrenal insufficiency
  • hypovolaemia
  • cardiovascular disease
128
Q

etomidate - adrenal insufficiency?

A
  • suppresses adrenocortical function
  • should not be used for maintenance of anaesthesia
129
Q

SE of etomidate?

A
  • hypotension
  • resp disorders
  • vascular pain
  • adrenal insufficiency
130
Q

Ketamine mechanism?

A
  • rapid acting GA
  • NMDA antagonist used for induction of anaesthesia
131
Q

ketamine CI?

A
  • HTN
  • pre-eclampsia
  • raised ICP
  • stroke
132
Q

side effects of ketamine?

A
  • anx
  • hallucination
  • nystagmus
  • vomiting
133
Q

which anaesthetic can cause cystitis haemorrhagic?

A

ketamine

134
Q

reducing hallucinations with ketamine?

A

Incidence of hallucinations can be reduced by premedicaton with a benzodiazepine (such as midazolam).

135
Q

Propofol mechanism?

A
  • positive modulation of the inhibitory function of GABA-A
136
Q

propofol indications?

A
  • induction and maintenance of anaesthesia
137
Q

cautions of propofol?

A
  • shock
  • cardiac impairment
  • hypovolaemia
  • raised ICP
138
Q

SE of propofol?

A
  • apnoea
  • arrhythmias
  • hypotension
  • nausea and vomiting
139
Q

what else can occur w propofol?

A
  • pulm oedema
  • urine discoloration
  • pancreatitis
140
Q

Thiopental mechanism?

A
  • barbituate
  • binds to CI- ionophore at GABA receptor, enhancing effect of GABA
141
Q

thiopental SE?

A
  • decreased cardiac contractility
  • arrhythmia
  • circ collapse
  • resp disorders
142
Q

IV opiods during anaesthesia?

A
  • Fentanyl
  • Remifentanil
143
Q

use of iV opiods during anaesthesia?

A

Reduction in the dose requirement of anaesthetic agents, sedation and respiratory depression during assisted ventilation in intensive care

144
Q

fentanyl Mx?

A
  • mu opiod receptor agonist
  • hyperpolarises cell and inhibits nerve activity
145
Q

CI of fentanyl?

A

opiod naive ppts

146
Q

SE of fentanyl?

A
  • apnoea
  • HTN
  • muscle rigidity
  • resp disorders
147
Q

Remifentanil mechanism?

A

µ-opioid agonist with rapid onset and peak effect, and short duration of action.

148
Q

CI of remifentanil?

A

analgesia in conscious patients

149
Q

remifentanil SE?

A
  • Apnoea
  • hypotension
  • muscle rigidity
150
Q

remifentanil metabolism?

A

In contrast to other opioids which are metabolised in the liver, remifentanil undergoes rapid metabolism by plasma esterases; it has short duration of action which is independent of dose and duration of infusion

151
Q

inhalation anaesthetics =

A
  • Desflurane
  • Halothane
  • Isoflurane
  • Nitrous oxide
  • Sevoflurane
152
Q

Desflurane indications?

A

indication and maintenance of anaesthesia

153
Q

CI of all volatile halogenated anaesthetics?

A

Susceptibility to malignant hyperthermia

154
Q

side effects of all volatile halogenated anaesthethics?

A
  • agitation
  • chills
  • resp disorders
  • cough
155
Q

SE of desflurance/

A

coagulation disorders, conjunctivitis

156
Q

desflurane mechanism?

A
  • agonises GABA-A and glycine receptors
  • antagonises glutamate receptors
157
Q

Halothane mechanism?

A
  • binds to potassium channels in cholinergic neurons
  • binds to NMDA and calcium channels causing hyperpolarisation
158
Q

SE of halothane?

A
  • hepatotoxicity
  • resp depression
  • irreg HB
159
Q

Isoflurane SE?

A
  • Carboxyhaemoglobinaemia
  • delirium
  • cognitive impairment
160
Q

isoflurane mechansim?

A
  • binds to GAB receptor, glutamate receptor and glycine receptor
161
Q

nitrous oxide cautions?

A
  • presence of intercranial air after head injury or trapped air after underwater dive
  • pneumothorax
162
Q

NO interacts w

A

methotrexate

163
Q

SE of NO?

A
  • Abd distension
  • agranulocytosis
  • parasthesia
  • subcaute combined cord degeneration
164
Q

NO mechanism?

A
  • induces opiod release in the brain stem
  • activates descending nociceptive process
165
Q

sevoflurane mechanism?

A
  • GABA and glycine receptors
  • inhibt excitatory activity by blocking nictonic ACh, serotonin and glutamate receptors
166
Q

uses of the inhalational anaesthetics?

A

Induction and maintenance of anaesthesia

167
Q

sevoflurane CI?

A

Susceptibility to QT-interval prolongation

168
Q

Sevoflurane SE?

A
  • Drowsiness
  • fever
  • hypothermia
169
Q

Depolarising neuromuscular-blocking drugs

A

suxamethonium (succinylcholine)

170
Q

use of suxamethonium?

A

Endotracheal intubation, muscle relaxation during surgery or on the ICU

171
Q

suxamethonium mechanism?

A
  • mimicks ACh at NM junction
  • but bc its hydrolsed much slower than ACh, depolarisation is prolonged leading to NM blockade
172
Q

CI of suxamethonium?

A
  • hyperkalaemia
  • low plasma cholinesterase activity - including severe liver dsisease
  • malignant hyperthermia
173
Q

suxamethonium interacts w

A

steroids - fludrocortisone, hydrocortisone, pred, beclomethasone

174
Q

SE of suxamethonium?

A
  • arrythymias
  • bradycardia
  • involuntary muscle contractions
  • myogloburia
175
Q

Competitive N2 receptor antagonists (non-depolarising blockers)

A
  • Atracurium
  • Cisatracurium
  • Mivacurium
  • Pancuronium
  • Rocuronium
  • Vecuronium
176
Q

atracurium uses?

A

NM blockade

177
Q

cautions for all non depolarising NM blocking drugs?

A
  • burns
  • CV disease
  • fluid dist
  • MG
178
Q

Atracurium interacts w?

A

steroids

179
Q

SE of all ND NM blocking drugs?

A
  • flushing
  • hypotension
180
Q

atraucrium and other non depolarising NM blockers mechanism?

A
  • competes w ACh for binding sites
181
Q

competitive N2 antagonists (ND NM blockers) are used for…

A

Endotracheal intubation, muscle relaxation during surgery or on the ICU

182
Q

acetylcholineesterase inhibitors =

A
  • Edrophonium
  • Neostigmine
  • Pyridostigmine
183
Q

edrophonium, neostigmine and pyridostigmine mechanism?

A
  • prolong ACh action
  • by inhibiting acetylcholineesterase action
184
Q

AChE inhibitors are used to treat

A
  • MG, and to
  • reverse non depolarising (competitive) NM blockade - neostigmine
185
Q

CI of all anticholinesterases?

A
  • intestinal or urinary obs
186
Q

side effects of all anticholinesterases?

A
  • abd cramps
  • diarrhoea
  • hypersalivation
  • nausea and vomiting
187
Q

Reversal of musle relaxants used during general anaesthesia =

A

neostigmine

188
Q

to test the therapeutic response to AChE inhibitors in myasthenia gravis =

A

edrophonium

189
Q

drug used for MG =

A

Pyridostigmine

190
Q
A

Year 3 (45 decks)

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