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CM2001 > PED2006 > Flashcards

PED2006 Flashcards

1
Q

what is the importance of gastrointestinal importance

A
  • function - major metabolic and endocrine system
  • pathology - wide range of disease
  • economic - £5 million per year in Newcastle
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2
Q

what is the pharmacological importance of the gastrointestinal system

A
  • gastric secretion
  • vomiting (emesis)
  • bowel motility
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3
Q

what is included in the GI tract hormonal innervation

A
  • endocrine secretions (bloodstream)
  • paracrine secretions (local)
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4
Q

what hormones are included in endocrine secretions

A

gastrin
cholecystokinin - synthesis in endocrine cells of mucosa

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5
Q

what hormones are included in paracrine secretions

A
  • histamine
  • acetylcholine
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6
Q

what is the function of parental cells in the walls of the gastric gland

A

to keep pH between 6-7

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7
Q

what is the structure of parietal cells in the walls of the gastric gland

A

canalicular membrane
canaliculus - releases HCL
tubulovesicles - release hydrogen and potassium
mitochondria
basolateral membrane

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8
Q

what is the action of the proton pump in the canalicular membrane

A
  • H+/K+ ATPase
  • Cl- co-transporter
  • release isotonic HCl
  • requires extrinsic stimulation
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9
Q

what is the action of the hydrogen potassium pump

A

pulls potassium back in and hydrogen out, keeping the pH isoelectrically neutral
gastrin is a key driver in this process

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10
Q

how does gastrin control acid secretion

A
  • peptide hormone
  • stimulates acid secretion, pepsinogen secretion (indirectly), blood flow and increases gastric motility
  • increases cytosolic ca2+
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11
Q

how does acetylcholine control acid secretion

A
  • neurotransmitter
  • released from vagal neurones
  • increases cytosolic ca2+
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12
Q

how does histamine control acid secretion

A
  • sub-type specific action (H2 receptors)
  • increases cAMP
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13
Q

what diseases are associated with acid dysregulation

A
  • dyspepsia
  • peptide ulceration
  • reflex oesophagitis
  • zoloinger-ellison syndrome
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14
Q

what is dyspepsia

A
  • indigestion
  • upper abdominal pain
  • bloating
  • nausea
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15
Q

what causes peptide ulceration

A
  • prolonged excess acid secretion leading to gastric and duodenal ulceration
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16
Q

what is reflux oesphagitis

A
  • damage to oesophagus by excess acid secretion
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17
Q

what is Zollinger-Ellison syndrome

A
  • gastrin producing tumour
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18
Q

how do we decrease secretion of gastric acid

A
  • reducing proton pump function
  • blocking histamine receptor function (H2 receptor antagonism
  • neutralising acid secretion with antacids
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19
Q

what is the action of proton pump inhibitors

A
  • irreversibly inhibit H+/K+ ATPase
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20
Q

what are example drugs of proton pump inhibitors

A

omeprazole
lansoprazole

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21
Q

what conditions are proton pumps used to treat

A

peptide ulcers
reflux oesophagitis
Zollinger-ellison

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22
Q

what are the pharmacokinetics of proton pump inhibitors

A
  • inactive at neutral pH
  • weak bases - allows accumulation in acidic environment
  • degraded rapidly at low pH (enteric coating)
  • single dosing –> 2-3 day acid secretion inhibition
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23
Q

what are the adverse effects of proton pump inhibitors

A

headache, diarrhoea, rash
can mask the symptoms of gastric cancer
care must be taken in high risk groups - i.e. liver failure and pregnancy

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24
Q

what are histamine H2 receptor antagonists

A
  • competitive inhibitors of H2 histamine receptors
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25
Q

what are the example of histamine H2 receptor antagonists

A

cimetidine
ranitidine

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26
Q

when are histamine H2 receptor antagonists used

A

used in peptic ulcers and reflux oesophagi’s

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27
Q

what are the pharmacokinetics of histamine H2 receptor antagonists

A
  • rapidly absorbed orally
  • dosage varies with conditions
  • potent inhibitor of cytochrome p450s
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28
Q

what are the adverse effects of histamine H2 receptors

A

diarrhoea, dizziness, muscle pain
cimetidine has slight antiandrogenic actions
potent inhibitor of cytochrome p450 - reduces metabolism of anticoagulant and tricyclic antidepressants

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29
Q

what are antacids

A

bases that raise gastric luminal pH by neutralising gastric acid

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30
Q

what are the examples of antacids

A

sodium bicarbonate
mg2+/al3+ hydroxide

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31
Q

what are the uses of antacids

A

dyspepsia
oesophageal reflux

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32
Q

what are the pharmacokinetics of antacids

A

relatively slow action
effects often short lived
acid rebound

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33
Q

what are the adverse effects of antacids

A

diarrhoea, constipations, belching
acid rebound
alkalosis
care must be taken with sodium content

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34
Q

what is helicobacter pylori

A

gram negative bacillus

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35
Q

what are helicobacter pylori infections

A

important factor in peptide ulcer formation
risk factor in gastric cancer
forms routine testing in patients with GI symptoms - urea breath tests

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36
Q

how can you treat helicobacter pylori infections

A
  • treatment with combination therapy
  • PPI, antibacterials and cytoprotective agent
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37
Q

what are cytoprotective agents

A
  • enhance mucosal protection mechanisms that form barriers over ulcer formations
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38
Q

what are the examples of cytoprotective agents

A
  • bismuth chelate
  • sucralfate
  • misoprotosol
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39
Q

what is bismuth chelate

A
  • toxic to bacillus
  • coats ulcer base, prostaglandin and bicarbonate synthesis
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40
Q

what is sucralfate

A
  • stimulates mucus production and prevents degradation
  • increases prostaglandin and bicarbonate synthesis
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41
Q

what is misoprostol

A
  • prostaglandin analogue
  • direct action on parietal cells (acid secretion)
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42
Q

what are the examples of NSAID that disrupt of mucosa

A

prostaglandins
non-steroidal anti-inflammatory

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43
Q

how do prostaglandins disrupt mucosa

A
  • synthesised by gastric mucosa (cycle-oxygenase 1)
  • increased mucus and bicarbonate secretion
  • decreased acid secretion
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44
Q

how do NSAIDs disrupt mucosa

A
  • inhibit prostaglandin formation
  • causes gastric bleeds, erosion –> ulcer formation
  • specific COX2 inhibitors cause less GI damage
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45
Q

what are pacemaker cells in gastric contractions

A
  • smooth muscle cells in upper fungus
  • rhythmic, autonomous, partial depolarisation
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46
Q

when do gastric contractions occur

A
  • slow wave potentials sweep down stomach
  • slow wave exceeds resting membrane potential
  • usually 3 peristaltic waves/minute
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47
Q

how is gastric contraction force affected

A

neural - increased vagal activity, decreased by adrenergic activity
hormonal - increased by gastrin, decreased by secretin

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48
Q

what is the gastric response to intake of food

A
  • waves of peristaltic contraction throughout stomach
  • forceful contractions and increased pressure in antrum
  • retropulsion of food against close pylorus
  • mixing and grinding of food
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49
Q

what is the gastric response to the intake of food after a meal

A
  • stretch receptors
  • activation of vagal inhibitory neurones
  • relaxation of smooth muscle
    -little change in pressure
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50
Q

what is emesis

A

-forceful evacuation of stomach contents

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51
Q

what are the stimuluses what trigger emesis

A

pain
repulsive sights/smells
emotional factors
endogenous toxins/drugs
stimuli from pharynx/stomach
motion

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52
Q

where is emesis controlled

A
  • vomiting centre
  • chemoreceptor trigger zone
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53
Q

which neurotransmitters are sensitive to stimulus

A

acetylcholine
histamine
5-HT
dopamine

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54
Q

what are emetics

A

occasionally necessary to stimulate vomiting e.g. toxin ingestion
ipecacuanha

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55
Q

what is ipecacuanha

A

locally acting in stomach
irritant effects of alkaloids emetine and cephaeline

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56
Q

examples of anti-emetics

A
  • H1 receptor antagonists
  • muscarinic antagonists
  • D2 receptor antagonists
  • 5-HT3 antagonists
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57
Q

examples of 5-HT3 antagonists

A

cannabinoids
antipyschotics
steroid/neurokinin antagonists

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58
Q

examples of H1 receptor antagonists

A
  • cyclising
  • promethazine
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59
Q

what are H1 receptor antagonists used for

A
  • most effective for motion sickness
  • should be given before onset of nausea and vomiting
  • act on vestibular nuclei not CTZ
60
Q

what are the adverse effects of H1 receptor antagonists

A

mild - drowsiness and sedation

61
Q

what is an example of muscarinic antagonists

A

hyoscine

62
Q

what are muscarinic antagonists used for

A
  • useful in motion sickness
    effective against vestibular apparatus stimuli and local gut stimuli - ineffective on CTZ stimuli
63
Q

adverse effects of muscarinic antagonists

A

mild - dry mouth, blurred vision
sedation - less than H1 antagonsits

64
Q

examples of D2 receptor antagonists

A

metoclopramide
phenothiazines e.g. prochlorperazine

65
Q

what are D2 receptor antagonists used for

A

useful in vomiting cause by renal failure and radiotherapy
work centrally in the chemoreceptor trigger zone

66
Q

what are the adverse effects of D2 receptor antagonists

A

CNS effects (motor movement disorders - twitching, restlessness
prolactin stimulations –> menstrual disorders

67
Q

examples of 5HT3 antagonists

A

ondansetron

68
Q

what are 5-HT3 antagonists used for

A

useful anti-emetic in chemotherapy, post surgergy
primarily acts of CTZ
5-HT3 released in gut following some endogenous toxins and chemotherapy drugs

69
Q

adverse effects of 5-HT3 antagonists

A

mild - headache, diarrhoea

70
Q

what drugs can be used in issues with bowel motility

A

diarrhoea - anti-diarrhoeal
constipation - purgatives/laxatives
inflammatory bowel disease

71
Q

what can be the causes of diarrhoea

A

viral - rotavirus
bacterial - campylobacter
systemic disease - inflammatory bowel disease
drug-induced - antibiotics e.g. erythromycin

72
Q

what is the action of anti-diarrhoea

A
  • stimulation of opiate receptors in the bowel
  • increase tone of smooth muscle
  • suppress propulsive peristalsis
  • raise sphincter tone at Cleo-caecal valve and anal sphincter
  • reduce sensitively to rectal distension
  • resultant delay in passage of faeces through the gut and increased water and electrolyte absorption in small intestine and colon
73
Q

what are the examples of opioid agonists

A

codeine and morphine

74
Q

what is the action of opioid agonists

A
  • activate muw receptors on myenteric neurones
  • causes hyperpolarisation –> inhibition of acetylcholine release
  • reduce bowel motility
75
Q

examples of synthetic opioid analogues

A
  • loperamide (Imodium)
  • diphenoxylate
76
Q

function of loperamide

A

binds to opiate receptors in gut wall
relatively free of CNS side effect

77
Q

key points for diphenoxylate

A
  • marketed as a cophenotrope (iomotil)
  • atropine present to discourage abuse
78
Q

what are laxatives

A
  • bulk forming agents
  • osmotic laxatives
  • stimulants
  • faecal softeners
79
Q

examples of bulk forming agents

A
  • ispaghula
  • methylcellulose
  • brain
80
Q

features of bulk forming agents

A
  • contain polysaccharide and cellulose components
  • not digested and retain fluid
  • increase faecal bulk and stimulate peristalsis
  • onset action 12-36 hours
  • must be taken with plenty of fluids
81
Q

side effects of bulk forming agents

A

flatulence and bloating

82
Q

examples of osmotic laxatives

A
  • magnesium salts
  • polyethylene glycol
  • phosphate enemas
  • lactulose
83
Q

function of osmotic laxatives

A
  • act by osmosis to retain water in the bowel
  • softer, bulkier stool
84
Q

what is the onset of action for osmotic laxatives

A
  • 30 mins for rectal preparations
  • 2-5hrs for magnesium salts
  • 48hrs for lactulose
85
Q

what are the side effects of osmotic laxatives

A

abdominal cramps,
flatulence
electrolyte disturbance

86
Q

what are the examples of stimulant laxatives

A

Senna
bisacodyl
Danton

87
Q

what is the mechanism of actions of stimulant laxatives

A

-directly stimulate colonic nerves
- movement of faecal mass
- reduces transit time
- onset of action 8-12hrs

88
Q

what are the side effects of stimulant laxatives

A

abdominal cramps
colonial atony with long term use

89
Q

what is an example of faecal softeners

A

docusate sodium

90
Q

what is the mechanism of action of faecal softeners

A
  • non-ionic surfactant with stool softening properties
  • reduces surface tension
  • allows penetration of fluid into the faecal mass
  • also a weak stimulant
91
Q

names of diseases associated with inflammatory bowel diseases

A
  • crohns disease - affects entire gut
  • ulcerative colitis - affects only the large bowel
91
Q

characteristics of inflammatory bowel disease

A

cyclical bouts of diarrhoea, constipation and/or abdominal pain

92
Q

treatments for inflammatory bowel disease

A
  • glucocorticoids - oral or local anti-inflammatory
  • aminosalicylates
  • sulphasalazine
  • immunosuppression - infliximab (TNF-alpha)
92
Q

which drugs are predominately used to treat emesis

A
  • H1
  • muscarinic
    D2
    5-HT3 receptor antagonists
93
Q

how can constipation be controlled

A
  • increasing faecal bulk
  • stimulating faecal movement or
  • reducing faecal surface tension
94
Q

how are airway obstructions caused

A
  • smooth muscle contraction
  • inflammation
  • edema
  • mucus
  • airway structural changes
95
Q

what are the major symptoms of asthma

A
  • wheezing
  • chest tightness
  • dyspnea
  • cough
  • hypoxemia
96
Q

what are the stages of an asthma attack

A
  • early/acute (min) - bronchoconstriction
  • late/delayed (hrs) - inflammation, hyper responsiveness
  • chronic (days/months) - airway damage and remodelling
97
Q

which drugs are used to relax smooth muscle

A
  • beta blockers (SABA and LABA)
  • PDE blockers (theophylline)
  • LTRAs
98
Q

which drugs are needed to block inflammatory cascades

A
  • corticosteroids (esp. ICS)
  • LTRAs
  • [PDE blockers]
  • targeted biologics
99
Q

what is the resulting action of beta 2 adrenoreceptor agonists

A

causes relaxation of smooth muscle by increasing cAMP through Gs
physiological antagonists to bronchoconstrictors

100
Q

what are the examples of beta2 adrenoceptor agonists

A

adrenaline
isoprenaline (isoproterenol)

101
Q

what is the action of isoprenaline

A
  • selective beta agonists
  • bronchodilator and cardiac stimulation
102
Q

what are the routes of administration for beta2 adrenoceptor agonists

A
  • aerosol inhalation - metered dose inhaler
  • inhalation of nebulised solution
  • inhalation of powder
  • oral administration
  • parental –> IV, SC or IM injection
103
Q

what are the two examples of short acting beta2 agonists

A

salbutamol
terbutaline

104
Q

what are the two examples of longer acting beta2 agonists

A

salmeterol
formoterol

105
Q

how do some beta2 agonists work longer than others

A

lipophilic structures aid duration
used as an adjunct to corticosteroids

106
Q

what are the side effect of beta2 adrenceptor agonists

A

muscle tremor at high doses
tachycardia
cardiac dysrhymias
risk of paradoxical bronchospasm

107
Q

how do we minimise the side effect of beta2 adrenoceptor agonists

A

delivery via inhalation vs systemic routes

108
Q

how are leukotrienes linked to asthma

A

leukotrienes are synthesised and released during the acute response by mast cells; also produced by inflammatory cells

109
Q

what are cysteine LTs

A
  • potent constrictors of bronchial smooth muscle
  • increase vascular leakage, mucus production
  • chemoattractants for eosinophils/basophils
  • mainly via cos-LT1 receptors coupled to Gq-ca2+
110
Q

what are the names of the two leukotrienes receptor antagonists

A

zafirlukast
montelukast

111
Q

what is the name of the 5-lipoxygenase inhibitor

A

zileuton

112
Q

features of leukotriene receptors antagonists

A

selective
high affinity competitive antagonists for cystic-LT1 receptors

113
Q

what is action of leukotriene receptor antagonist

A
  • block LTC4 and LTD4 effects on smooth muscle
  • block some cyst-LT ‘inflammatory’ actions
  • don’t block LTB4 effect
114
Q

what is the action of zileuton

A
  • it inhibits the formation of all 5-LOX products from LTA4 synthesis (cyst-LTs, LTB4, other eicosanoids)
  • some LT effects via cos-LT2 receptors (vasoconstriction
115
Q

what is leukotriene modulator indication

A
  • do not produce rapid bronchodilator
116
Q

what are the indications of leukotrienes

A
  • asthma: prophylaxis + chronic treatment
  • montelukast - acute prevent of exercise-inducers bronchoconstrictions
  • montelukast - allergic and perennial rhinitis
117
Q

which group of patients use motelukast

A

adults and younger children

118
Q

which group of patients use zafirlukast

A

adults and older children

119
Q

which group of patients use zileuton

A

adults and teenagers

120
Q

how do leukotrienes effect mild to moderate asthma

A

improve basal lung function and symptoms; indicated as alternative to low dose ICS and/or add-on therapy

121
Q

how do leukotrienes effect severe asthma

A

not effective if patient not controlled on ICS + LABA

122
Q

examples of antimuscarinics used in the treatment of asthma

A

ipratropium (derived from atropine)
tiotropium

123
Q

which muscarinic receptor is targeted with antimuscarinics

A

M3 receptor antagonist
leads to bronchodilator and reduced mucous secretion

124
Q

what is the effect of antimuscarinics

A

used as adjunct therapy to beta 2 agonists and steroids
may increase mucociliary clearance through action on cilia of peitherlial cells
main use in COPD

125
Q

How can muscarinic antagonists be used as bronchodilators

A
  • parasympathetic nerves synthesise and release acetylcholine and are the primary source of acetylcholine in the lung
  • they innervate all conducting airways, from the trachea to the bronchioles as well as pulmonary blood vessels
126
Q

what is an examples of a SAMA

A

ipratropium

126
Q

what is the use of ipratropium

A
  • slow onset of bronchodilators and is usually maximal 30-60min after inhalation but may persist for 6-8hrs - 3 to 4 times a day
127
Q

what are the different types of LAMAs

A
  • tiotropium bromide - once a day
  • glycopyrronium bromide - once a day
  • umeclidinium bromines - once a day
  • aclidinium bromide - twice a day
128
Q

what are the systemic anticholinergic side effects

A

dry mouth
gastrointestinal motility disorder
tachycardia
nausea

129
Q

which treatments are focussed on immunosuppression

A

ICS
biologics

130
Q

what are the effects of glucocorticoids

A
  • anti-inflammatory
  • inhibit inflammatory response to injury and allergic disease
131
Q

what can glucocorticoid inhibit the synthesis of

A

inflammatory mediators
cytokines
cell chemoattractants
vasoactive agents
decreased inflammatory cell infiltration and proliferation, vascular permeability and mucus secretion

132
Q

what are the examples of inhaled corticosteroids

A

beclomethasone
budesonide

133
Q

what are inhaled corticosteroids

A
  • not bronchodilators
  • preventative treatments
  • metered dose or dry powder inhaler
  • up regulate beta2 receptor expression
134
Q

what is the result of inhaled corticosteroids reducing transcription and decreasing formation of cytokines

A
  • Th2 cytokines
  • reduce activation of eosinophils
  • reduce production of IgE
  • reduce production of leukotrienes and PAF
  • inhibits induction of cyclooxyrgenase pathway
135
Q

what are the side effects of inhaled corticosteroids

A
  • oropharyngeal candidiasis - use of spacer helps prevent this
  • reduced systemic side effects
  • adrenal suppression
  • reduced bone mineral density when taken long term
136
Q

what are the examples of oral corticosteroids

A

prednisolone
hydrocortisone

137
Q

when are oral corticosteroids taken

A

taken in short term for severe episode and severe acute asthma attacks

138
Q

what can be the side effects of prolonged corticosteroid therapy

A
  • suppression of immune response to infection
  • Cushing syndrome
  • hyperglycaemia
  • muscle wasting
  • inhibition of growth in children
139
Q

what is the benefit of using eosinophils in allergic asthma

A

they secrete: Th2 cytokines, ROS, LTC4/LTD4;PGD2, TGF-beta, major basic protein

140
Q

what are the examples of IL-5 blockers

A

mepolizumab
reslizumab

141
Q

what is the action of IL5 blockers

A

bind to IL5 and prevent binding to IL-5R on eosinophils, decreasing eosinophil production and survival

142
Q

what is the use of benralizumab

A

bind IL-5 receptor on eosinophils, stopping IL-5 binding

143
Q
A

CM2001 (13 decks)

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