Lecture 10 -Gastrointestinal Flashcards

(59 cards)

1
Q

What are the control of gastric acid secretion?

A

Vagus: sight, smell, taste Release of gastric: presence of food (protein) Histamine CCK GIP Somatostatin

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2
Q

What is the PH in the stomach controlled by?

A

Gastric acid secretion

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3
Q

Why is secretion of HCL needed?

A

To get a low PH to get activation of relevant stomach enzymes (e.g. pepsin)

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4
Q

Why is carbonic anhydrase needed?

A

Generation of free H+ ions

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5
Q

What are the forms gastric secretion can take?

A

HCL Pepsinogen Mucus Bicarbonate ions

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6
Q

What is the acidic environment in the stomach maintained by?

A

Action of parietal cells

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7
Q

What do parietal cells do?

A

Secrete H+ against concentration gradient

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8
Q

Where does ATPase get hydrogen ions from?

A

Carbon dioxide and water

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9
Q

What are the bicarbonate ions exchanged for?

A

Chloride ions, the chloride ions will be transported along with K+ into gut lumen via a symporter mechanisms

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10
Q

When do peptic ulcers arise?

A

When the protective layer is disrupted Elevated prolonged acidity in the gut

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11
Q

What are the causes of peptic ulcer?

A

Stress: activation of vagus nerve NSAIDs: e.g. aspirin Diet: disrupt gut favouring breakdown and degradation of cell types within cell wall Alcohol Zollinger-Ellison Syndrome: tumour of cells tjat product gastric leading to altered HCL Bacterial: helicobacter

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12
Q

What may Helicobacter pylori be involved in?

A

Pathology of peptic ulcer

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13
Q

Why was it difficult to establish cultures?

A

Gut helicobacter pylori takes longer period to be established in the gut

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14
Q

What does G cell create?

A

Gastrin

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15
Q

What does gastrin interact with?

A

Cholecystokinin receptors to promote the release of local hormone histamine

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16
Q

What does histamine act upon?

A

Histamin receptor (H2) that stimulate the production of pumping of H+ ions in the target cell (parietal cells)

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17
Q

What does somatostatin regulate?

A

H+ ion level at many different sites at 3 different cell types

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18
Q

How may you be prone to stress ulcers?

A

Activation of the parasympathetic nerve system and the vagus nerve Elevation of ACH -> activate muscarinic receptors and cause reduction in HCL

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19
Q

What does prostaglandin receptor have negative effect on?

A

Histamine release

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20
Q

What is Aspirin mode of action?

A

Inhibit the enzyme that concert arachidonic acid into prostaglandin Inhibit enzyme: cyclooxygenase

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21
Q

What is Aspirin involved in?

A

Inflammatory pathways

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22
Q

What happens in the presence of Aspirin?

A

Prolonged and elevated secretions of H+ and formation of HCL in the gut which can lead/contribute to peptic ulcer

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23
Q

How can Aspirin contribute to peptic ulcer?

A

Manipulation of gastrin, enterochrokaffin-like, parietal cell axis

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24
Q

What are Antacids?

A

Medicines that counteract (neutralise) the acid in your stomach to relieve indigestion and heartburn

25
Antacids
Buffer/neutralise acid, raise PH Promote healing over time Magnesium and Aluminium salt Sodium bicarbonate Alginates, simeticone (affect viscosity of mucus)
26
What is magnesium salt produce?
Diarrhoea
27
What does aluminium salt produce?
constipation
28
Histamine H2 receptor antagonist
Histamine receptor subtypes identified in the early 1970s
29
What is the effect of Histamine H2 receptor antagonists?
Basal and stimulated acid and pepsinogen secretion Promote healing Ulcer relapse
30
Proton pump inhibitors
Irreversible inhibitors of H+/K+ ATPase Produces fastest rate of healing
31
What are advantages of proton pump inhibitors ?
Better tolerated and cheaper than other drugs
32
What is the action range of proton pump inhibitors?
Long term action: 2-3 days Maximum effectiveness: 5 days
33
What are proton pump inhibitors associated with?
Increased risk of infection Pneumonia and C.difficile
34
Where are proton pump inhibitors administered ?
Enteric coating
35
What can happen to drug at low PH?
Drug can be easily and rapidly broken down
36
H.pylori Therapy
Present in peptic ulcers Healing of peptic ulcers (80% vs 20% re-occurrence when eradicated)
37
Where are Bismuth chelate used in?
resistant cases
38
Bismuth Chelate
Toxic to H.pylori and prevent adherence Coat ulcer base, adsorb pepsin, stimulate PG synthesis and bicarbonate secretion Minimally absorbed and normally fully excreted
39
Sucralfate
Aluminium hydroxide and sulfated sucrose Form complex gels with mucus, Inhibit pepsin, stimulate secretion of mucus, PGs and bicarbonate Requires acidic environment and block absorption of some other drugs May cause constipation
40
What is misoprostol?
Prostaglandin E1 analogue
41
What is a drawback of Bismuth Chelate?
Form a paste than can form obstruction within gut
42
What can control of emesis be?
central or local
43
What does the reflex of vomiting bring?
Contraction of the gut
44
What does CNS component give rise to?
Vomiting or nausea feeling
45
Centrally mediated vomiting reflexes
Stimulation of vomiting centre via the CTZ or chemoreceptors trigger in Medulla of brain
46
How can the antiemetic effect be generated?
Interference with the function of the CTZ or vomiting centre
47
Motion sickness
Disturbance within labyrinth in the ears in the vestibular system
48
What can be found in the vestibular nucleus?
Histamine receptor (H1) Antagonist Mach antagonist
49
What can be used to treat nausea?
5HT3 antagonist
50
H1 receptor antagonist
Effective against motion sickness Morning sickness in pregnancy
51
What are the side effects of H1 receptor antagonist ?
Drowsiness sedation
52
Muscarinic Antagonist
Block muscarinic receptor common motion sickness prophylactic
53
What are the side effects of muscarinic antagonist?
Dry mouth Blurred vision Less drowsiness than antihistamine
54
What are the side effects of selective 5-HT3 receptor antagonist?
GI effects and headaches
55
What are the frequent side effects of Antipsychotics?
Drowsiness Hypotension Motor disorders
56
What are Benzodiazepine?
Adjunct Therapy In circumstances where Anxiety is a factor
57
D2 receptor antagonist
Increase GI motility - used for other GI conditions
58
What can metoclopramide have?
Serious CNS side effects
59
What is Neurokinin-1 antagonist ?
Aprepitant inhibiting the action of substance P; inhibitor of P450