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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
what are the example of histamine H2 receptor antagonists
cimetidine ranitidine
26
when are histamine H2 receptor antagonists used
used in peptic ulcers and reflux oesophagi's
27
what are the pharmacokinetics of histamine H2 receptor antagonists
- rapidly absorbed orally - dosage varies with conditions - potent inhibitor of cytochrome p450s
28
what are the adverse effects of histamine H2 receptors
diarrhoea, dizziness, muscle pain cimetidine has slight antiandrogenic actions potent inhibitor of cytochrome p450 - reduces metabolism of anticoagulant and tricyclic antidepressants
29
what are antacids
bases that raise gastric luminal pH by neutralising gastric acid
30
what are the examples of antacids
sodium bicarbonate mg2+/al3+ hydroxide
31
what are the uses of antacids
dyspepsia oesophageal reflux
32
what are the pharmacokinetics of antacids
relatively slow action effects often short lived acid rebound
33
what are the adverse effects of antacids
diarrhoea, constipations, belching acid rebound alkalosis care must be taken with sodium content
34
what is helicobacter pylori
gram negative bacillus
35
what are helicobacter pylori infections
important factor in peptide ulcer formation risk factor in gastric cancer forms routine testing in patients with GI symptoms - urea breath tests
36
how can you treat helicobacter pylori infections
- treatment with combination therapy - PPI, antibacterials and cytoprotective agent
37
what are cytoprotective agents
- enhance mucosal protection mechanisms that form barriers over ulcer formations
38
what are the examples of cytoprotective agents
- bismuth chelate - sucralfate - misoprotosol
39
what is bismuth chelate
- toxic to bacillus - coats ulcer base, prostaglandin and bicarbonate synthesis
40
what is sucralfate
- stimulates mucus production and prevents degradation - increases prostaglandin and bicarbonate synthesis
41
what is misoprostol
- prostaglandin analogue - direct action on parietal cells (acid secretion)
42
what are the examples of NSAID that disrupt of mucosa
prostaglandins non-steroidal anti-inflammatory
43
how do prostaglandins disrupt mucosa
- synthesised by gastric mucosa (cycle-oxygenase 1) - increased mucus and bicarbonate secretion - decreased acid secretion
44
how do NSAIDs disrupt mucosa
- inhibit prostaglandin formation - causes gastric bleeds, erosion --> ulcer formation - specific COX2 inhibitors cause less GI damage
45
what are pacemaker cells in gastric contractions
- smooth muscle cells in upper fungus - rhythmic, autonomous, partial depolarisation
46
when do gastric contractions occur
- slow wave potentials sweep down stomach - slow wave exceeds resting membrane potential - usually 3 peristaltic waves/minute
47
how is gastric contraction force affected
neural - increased vagal activity, decreased by adrenergic activity hormonal - increased by gastrin, decreased by secretin
48
what is the gastric response to intake of food
- waves of peristaltic contraction throughout stomach - forceful contractions and increased pressure in antrum - retropulsion of food against close pylorus - mixing and grinding of food
49
what is the gastric response to the intake of food after a meal
- stretch receptors - activation of vagal inhibitory neurones - relaxation of smooth muscle -little change in pressure
50
what is emesis
-forceful evacuation of stomach contents
51
what are the stimuluses what trigger emesis
pain repulsive sights/smells emotional factors endogenous toxins/drugs stimuli from pharynx/stomach motion
52
where is emesis controlled
- vomiting centre - chemoreceptor trigger zone
53
which neurotransmitters are sensitive to stimulus
acetylcholine histamine 5-HT dopamine
54
what are emetics
occasionally necessary to stimulate vomiting e.g. toxin ingestion ipecacuanha
55
what is ipecacuanha
locally acting in stomach irritant effects of alkaloids emetine and cephaeline
56
examples of anti-emetics
- H1 receptor antagonists - muscarinic antagonists - D2 receptor antagonists - 5-HT3 antagonists
57
examples of 5-HT3 antagonists
cannabinoids antipyschotics steroid/neurokinin antagonists
58
examples of H1 receptor antagonists
- cyclising - promethazine
59
what are H1 receptor antagonists used for
- most effective for motion sickness - should be given before onset of nausea and vomiting - act on vestibular nuclei not CTZ
60
what are the adverse effects of H1 receptor antagonists
mild - drowsiness and sedation
61
what is an example of muscarinic antagonists
hyoscine
62
what are muscarinic antagonists used for
- useful in motion sickness effective against vestibular apparatus stimuli and local gut stimuli - ineffective on CTZ stimuli
63
adverse effects of muscarinic antagonists
mild - dry mouth, blurred vision sedation - less than H1 antagonsits
64
examples of D2 receptor antagonists
metoclopramide phenothiazines e.g. prochlorperazine
65
what are D2 receptor antagonists used for
useful in vomiting cause by renal failure and radiotherapy work centrally in the chemoreceptor trigger zone
66
what are the adverse effects of D2 receptor antagonists
CNS effects (motor movement disorders - twitching, restlessness prolactin stimulations --> menstrual disorders
67
examples of 5HT3 antagonists
ondansetron
68
what are 5-HT3 antagonists used for
useful anti-emetic in chemotherapy, post surgergy primarily acts of CTZ 5-HT3 released in gut following some endogenous toxins and chemotherapy drugs
69
adverse effects of 5-HT3 antagonists
mild - headache, diarrhoea
70
what drugs can be used in issues with bowel motility
diarrhoea - anti-diarrhoeal constipation - purgatives/laxatives inflammatory bowel disease
71
what can be the causes of diarrhoea
viral - rotavirus bacterial - campylobacter systemic disease - inflammatory bowel disease drug-induced - antibiotics e.g. erythromycin
72
what is the action of anti-diarrhoea
- 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
what are the examples of opioid agonists
codeine and morphine
74
what is the action of opioid agonists
- activate muw receptors on myenteric neurones - causes hyperpolarisation --> inhibition of acetylcholine release - reduce bowel motility
75
examples of synthetic opioid analogues
- loperamide (Imodium) - diphenoxylate
76
function of loperamide
binds to opiate receptors in gut wall relatively free of CNS side effect
77
key points for diphenoxylate
- marketed as a cophenotrope (iomotil) - atropine present to discourage abuse
78
what are laxatives
- bulk forming agents - osmotic laxatives - stimulants - faecal softeners
79
examples of bulk forming agents
- ispaghula - methylcellulose - brain
80
features of bulk forming agents
- 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
side effects of bulk forming agents
flatulence and bloating
82
examples of osmotic laxatives
- magnesium salts - polyethylene glycol - phosphate enemas - lactulose
83
function of osmotic laxatives
- act by osmosis to retain water in the bowel - softer, bulkier stool
84
what is the onset of action for osmotic laxatives
- 30 mins for rectal preparations - 2-5hrs for magnesium salts - 48hrs for lactulose
85
what are the side effects of osmotic laxatives
abdominal cramps, flatulence electrolyte disturbance
86
what are the examples of stimulant laxatives
Senna bisacodyl Danton
87
what is the mechanism of actions of stimulant laxatives
-directly stimulate colonic nerves - movement of faecal mass - reduces transit time - onset of action 8-12hrs
88
what are the side effects of stimulant laxatives
abdominal cramps colonial atony with long term use
89
what is an example of faecal softeners
docusate sodium
90
what is the mechanism of action of faecal softeners
- non-ionic surfactant with stool softening properties - reduces surface tension - allows penetration of fluid into the faecal mass - also a weak stimulant
91
names of diseases associated with inflammatory bowel diseases
- crohns disease - affects entire gut - ulcerative colitis - affects only the large bowel
91
characteristics of inflammatory bowel disease
cyclical bouts of diarrhoea, constipation and/or abdominal pain
92
treatments for inflammatory bowel disease
- glucocorticoids - oral or local anti-inflammatory - aminosalicylates - sulphasalazine - immunosuppression - infliximab (TNF-alpha)
92
which drugs are predominately used to treat emesis
- H1 - muscarinic D2 5-HT3 receptor antagonists
93
how can constipation be controlled
- increasing faecal bulk - stimulating faecal movement or - reducing faecal surface tension
94
how are airway obstructions caused
- smooth muscle contraction - inflammation - edema - mucus - airway structural changes
95
what are the major symptoms of asthma
- wheezing - chest tightness - dyspnea - cough - hypoxemia
96
what are the stages of an asthma attack
- early/acute (min) - bronchoconstriction - late/delayed (hrs) - inflammation, hyper responsiveness - chronic (days/months) - airway damage and remodelling
97
which drugs are used to relax smooth muscle
- beta blockers (SABA and LABA) - PDE blockers (theophylline) - LTRAs
98
which drugs are needed to block inflammatory cascades
- corticosteroids (esp. ICS) - LTRAs - [PDE blockers] - targeted biologics
99
what is the resulting action of beta 2 adrenoreceptor agonists
causes relaxation of smooth muscle by increasing cAMP through Gs physiological antagonists to bronchoconstrictors
100
what are the examples of beta2 adrenoceptor agonists
adrenaline isoprenaline (isoproterenol)
101
what is the action of isoprenaline
- selective beta agonists - bronchodilator and cardiac stimulation
102
what are the routes of administration for beta2 adrenoceptor agonists
- aerosol inhalation - metered dose inhaler - inhalation of nebulised solution - inhalation of powder - oral administration - parental --> IV, SC or IM injection
103
what are the two examples of short acting beta2 agonists
salbutamol terbutaline
104
what are the two examples of longer acting beta2 agonists
salmeterol formoterol
105
how do some beta2 agonists work longer than others
lipophilic structures aid duration used as an adjunct to corticosteroids
106
what are the side effect of beta2 adrenceptor agonists
muscle tremor at high doses tachycardia cardiac dysrhymias risk of paradoxical bronchospasm
107
how do we minimise the side effect of beta2 adrenoceptor agonists
delivery via inhalation vs systemic routes
108
how are leukotrienes linked to asthma
leukotrienes are synthesised and released during the acute response by mast cells; also produced by inflammatory cells
109
what are cysteine LTs
- 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
what are the names of the two leukotrienes receptor antagonists
zafirlukast montelukast
111
what is the name of the 5-lipoxygenase inhibitor
zileuton
112
features of leukotriene receptors antagonists
selective high affinity competitive antagonists for cystic-LT1 receptors
113
what is action of leukotriene receptor antagonist
- block LTC4 and LTD4 effects on smooth muscle - block some cyst-LT 'inflammatory' actions - don't block LTB4 effect
114
what is the action of zileuton
- 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
what is leukotriene modulator indication
- do not produce rapid bronchodilator
116
what are the indications of leukotrienes
- asthma: prophylaxis + chronic treatment - montelukast - acute prevent of exercise-inducers bronchoconstrictions - montelukast - allergic and perennial rhinitis
117
which group of patients use motelukast
adults and younger children
118
which group of patients use zafirlukast
adults and older children
119
which group of patients use zileuton
adults and teenagers
120
how do leukotrienes effect mild to moderate asthma
improve basal lung function and symptoms; indicated as alternative to low dose ICS and/or add-on therapy
121
how do leukotrienes effect severe asthma
not effective if patient not controlled on ICS + LABA
122
examples of antimuscarinics used in the treatment of asthma
ipratropium (derived from atropine) tiotropium
123
which muscarinic receptor is targeted with antimuscarinics
M3 receptor antagonist leads to bronchodilator and reduced mucous secretion
124
what is the effect of antimuscarinics
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
How can muscarinic antagonists be used as bronchodilators
- 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
what is an examples of a SAMA
ipratropium
126
what is the use of ipratropium
- 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
what are the different types of LAMAs
- tiotropium bromide - once a day - glycopyrronium bromide - once a day - umeclidinium bromines - once a day - aclidinium bromide - twice a day
128
what are the systemic anticholinergic side effects
dry mouth gastrointestinal motility disorder tachycardia nausea
129
which treatments are focussed on immunosuppression
ICS biologics
130
what are the effects of glucocorticoids
- anti-inflammatory - inhibit inflammatory response to injury and allergic disease
131
what can glucocorticoid inhibit the synthesis of
inflammatory mediators cytokines cell chemoattractants vasoactive agents decreased inflammatory cell infiltration and proliferation, vascular permeability and mucus secretion
132
what are the examples of inhaled corticosteroids
beclomethasone budesonide
133
what are inhaled corticosteroids
- not bronchodilators - preventative treatments - metered dose or dry powder inhaler - up regulate beta2 receptor expression
134
what is the result of inhaled corticosteroids reducing transcription and decreasing formation of cytokines
- Th2 cytokines - reduce activation of eosinophils - reduce production of IgE - reduce production of leukotrienes and PAF - inhibits induction of cyclooxyrgenase pathway
135
what are the side effects of inhaled corticosteroids
- oropharyngeal candidiasis - use of spacer helps prevent this - reduced systemic side effects - adrenal suppression - reduced bone mineral density when taken long term
136
what are the examples of oral corticosteroids
prednisolone hydrocortisone
137
when are oral corticosteroids taken
taken in short term for severe episode and severe acute asthma attacks
138
what can be the side effects of prolonged corticosteroid therapy
- suppression of immune response to infection - Cushing syndrome - hyperglycaemia - muscle wasting - inhibition of growth in children
139
what is the benefit of using eosinophils in allergic asthma
they secrete: Th2 cytokines, ROS, LTC4/LTD4;PGD2, TGF-beta, major basic protein
140
what are the examples of IL-5 blockers
mepolizumab reslizumab
141
what is the action of IL5 blockers
bind to IL5 and prevent binding to IL-5R on eosinophils, decreasing eosinophil production and survival
142
what is the use of benralizumab
bind IL-5 receptor on eosinophils, stopping IL-5 binding
143

CM2001 (13 decks)

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