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MP322 > week 6 > Flashcards

week 6 Flashcards

1
Q

where are parietal cells absent from?

A

the antrum

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2
Q

what controls saliva secretion?

A

reflexes mediated by the ANS

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3
Q

What causes increase in watery saliva, rich in amylase and mucous.

A

parasympathetic nervous system

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4
Q

What causes increase in thicker mucous and reduction in saliva glands?

A

Sympathetic nervous system

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5
Q

What is logD a measure of?

A

lipophilicity in all states

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6
Q

Agonists that stimulate acid secretion

A

Histamine, gastrin, acetylcholine.

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7
Q

Histamine receptor antagonist

A

Racecadotril

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8
Q

Dyspepsia symptoms

A

upper abdominal pain/discomfort, heartburn, gastric reflux, nausea, vomiting.

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9
Q

Peptic ulcers; what are they, where are they found?

A

sores that develop in the lining of the stomach, lower oesophagus or small intestine (duodenum). Duodenum ulcers are most common

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10
Q

What is peritonitis?

A

When peptic ulcers perforate, and bacteria that live in the stomach are able to escape and infect the lining of the abdomen. Can rapidly spread to sepsis, symptoms including sudden sudden, intense steady abdominal pain.

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11
Q

__ ulcer pain is classically aggravated by meals whereas, __ ulcer is relived.

A

gastric, duodenal

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12
Q

Factors that protect the walls of the stomach from being digested - Alkaline mucus

A

1- Alkaline mucus ; mucosa surface lined with secretory cells that release alkaline mucus that forms a thin layer over the luminal surface. Protein content of mucus and its alkaline nature, neutralize H+ in the immediate area of the epithelium. Mucus forms a chemical barrier between the highly acidic contents of the lumen and the cell surface.

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13
Q

Factors that protect the walls of the stomach from being digested - tight junctions between epithelial cells

A

these tight junctions between the epithelial cells lining of the stomach limit the diffusion of H+ into the underlying tissues.

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14
Q

Factors that protect the walls of the stomach from being digested - replacement of damaged cells every few days

A

damaged epithelial cells are replaced every few days by new cells arising by the division of cells within gastric pits.

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15
Q

Describe ulcer formation.

A

involves breaking down the mucosal barrier and exposing the underlying tissue to the corrosive action of acid and pepsin.

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16
Q

Factors affecting acid and pepsin levels, therefore increased chance of peptic ulcer disease.

A

smoking, genetic factors, stress and helicobacter pylori.

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17
Q

How do NSAIDs increase risk of peptic ulcer disease?

A

can impair mucosal defence and therefore also increase peptic ulcer formation. They allow back diffusion of hydrogen ions

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18
Q

Duodenal ulceration associated with

A

excess acid secretion

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19
Q

Gastric ulceration associated with

A

breakdown of the protective function of the gastric mucosa

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20
Q

H.Pylori stimulates increased __ release thereby increased acid secretion.

A

gastrin

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21
Q

How does H.Pylori act?

A

It causes inflammation of the gastric mucosa and infects the lower part of the stomach. It uses chemotaxis to avoid areas of low pH, and also neutralizes the acid in the environment by producing large amounts of urease, which breaks down the urea present in the stomach to carbon dioxide and ammonia. This ammonia neutralizes stomach acid.

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22
Q

How can H.Pylori be tested for?

A

urea breath test, stool antigen test to detect antigens in an active infection

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23
Q

What is secreted in the stomach body?

A

mucus pepsinogen and HCl

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24
Q

What is secreted in the antrum?

A

mucus pepsinogen and gastrin

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25
Treatment of peptic ulcer disease
Antacids, Antisecretory agents (Histamine receptor H2 antagonists, Proton pump inhibitors), Eradication of H.Pylori infection.
26
Antacids
neutralise free acids in the stomach and stimulate mucosal repair around ulcers. Symptomatic relief
27
Antisecretory agents - Histamine receptor H2 antagonists examples and their side effects
cimetidine, nizatidine, famotidine, ranitidine reduce acid secretion. diarrhoea, headache, confusion in the elderly, gynaecomastia with cimetidine. Potential interactions between cimetidine and warfarin, phenytoin and theophylline
28
Proton Pump Inhibitors examples and method of action.
omeprazole, lansoprazole, pantoprazole, esomeprazole. Inhibition of the pump almost completely blocks acid secretion, irreversible. Acid secretion is inhibited by around 90% for around 24 hours with a single dose.
29
When are PPIs most effective? Why is this?
More effective when taken at meals times as they only bind to active pumps.
30
PPI side effects.
GI upset, headache, skin rashes
31
Who discovered propranolol and cimetidine?
James Black
32
Drugs involved in the eradication of H.Pylori
triple therapy of a PPI, amoxicillin and clarithromycin (switch amoxicillin for metronidazole where penecillin allergy is found)
33
What is GORD?
The amount of acid secretion is normal, however there is an incompetent functionality in the lower oesophageal sphincter which allows reflux of gastric contents which can cause retrosternal burning.
34
GORD treatment
Antacids and antacid/alginate combinations. Alginate intended to provide additional coating to lower oesophagus reducing mucosal contact with the refluxed contents.
35
GORD is a __ condition and requires long term treatment.
chronic
36
Log P is a partition coefficient and a measure of __/__ in an __ state.
lipophillicty/hydrophilicity in an unionsed state
37
If logP =1.7 then P = __?
10^1.7
38
Log P > 0
lipophillic
39
log P < 0
hydrophilic
40
The more equilibrium that lies on the right, the more __ it is
acidic.
41
Log P equation
Log (C organic / C aqueous)
42
Acids like to __ protons
donate
43
Ka, acid dissociation constant equation.
Ka = products/reactants
44
higher Ka value suggests what?
stronger acid or weaker base
45
higher pKa value suggests what?
weaker acid or stronger base
46
The higher the Ka value, the greater the __ and so the __ the acid.
dissociation and so the stronger the acid
47
What does LogP assume?
no ionization and that molecules distribute between the two layers accordingly
48
Log D accounts for __
ionization
49
What is LogD dependent on
pH
50
Log D equation - for bases
LogD = logP + log (F unionised) where F unionised = 1 / (1+10^ pka-pH)
51
Log D equation - for acids
LogD = logP + log (F unionised) where F unionised = 1 / (1+10^ pH-pKa)
52
What does a negative logD suggest?
the molecule in equilibrium prefers the aqueous layer over the organic
53
Why does omeprazole been to be encapsulated?
to prevent the pro drug from changing into its active sulphenamide form in the stomach.
54
When will log D = log P?
if unionized in the environment
55
How does omeprazole work to give a therapeutic effect
acts specifically in the parietal cells due to ion trapping. pH of parietal cells ~ 1 causes omeprazole to become completely ionised and ions are trapped. A build up of this causes a chemical conversion into sulphenamide to occur due to the steep proton gradient. Sulphenamide reacts with thiol groups in H+, K-ATPase enzyme which forms a stable disulphide complex. No more acid is produced until new enzyme is made which results in long duration of inhibition of gastric production.
56
How long can a single 40mg omeprazole dose affect acid secretion for?
72 hours
57
Is esomeprazole more potent than omeprazole?
Yes
58
How do H2 antagonists work to reduce stomach acid?
Stomach acid is produced by H2 receptors, so if we inhibit these, acid production should halt. Ranitidine
59
Why is Ranitidine formulated as a salt?
Ranitidine hydrochloride - salt aids the drug to dissolve, therefore go into equilibrium and absorb.
60
How are drugs able to carry out their mechanism of action?
due to the functional group properties which complement the receptor and therefore bind
61
If pKa= -log10Ka then Ka = ?
Ka = 10^-pka
62
More severe side effects of PPIS
increased chance of bone fracture on prolonged use and increased risk of CDiff. Omeprazole decrease antiplatelet effect of clopidogrel.
63
Cimetidine H2 antagonist side effects
increases blood concentration of erythromycin. interactions between the hepatic cytochrome P450 - slowing metabolism of some drugs.
64
In UV/Vis, the stronger the concentration the __ the absorbance.
greater
65
Ulcerative Colitis
Only affects the large bowel and the inflammation is on the inner lining.
66
Crohn's disease
Can affect any area of the GI system and all layers of tissue can be inflamed. Diagnosis can be through small bowel enema and by small capsule endoscopies.
67
How can IBD be diagnosed?
blood testing for anaemia, vitamin deficiencies and inflammatory markers. X-ray examination, CT + MRI scans. Sigmoidoscopy and colonoscopy.
68
Causes of IBD
* Genetic links * Autoimmune disease * Environmental * Previous infection
69
Corticosteroid examples, what do they aim to do, what are the side effects?
Hydrocortisone, beclomethasone, budesonide, prednisolone. Aim to reduce inflammation. Insomnia, dyspepsia, Cushing’s Syndrome, impaired healing, adrenal suppression with long term use
70
Aminosalicylates examples, what do they aim to do, anyside effects?
Balsalazide, mesalazine, olsalazine, sulfasalazine. Aim to reduction inflammation. Rare side effects- unexplained bleeding, bruising, fever, sore throat.
71
Side effects of the amino salicylates sulfasalazine.
Colours urine and contact lenses orange. Decreases concentration of digoxin (moderate) and absorption of folates (moderate)
72
Cytokine modulators, what do they aim to do? Give examples
subcutaneous administration; infliximab, adalimumab, golimumab, vedolizumab. They inhibit pro-inflammatory cytokine, tumour necrosis factor alpha. Stop the expansion of activated T cells.
73
Immunosuppressants
Azathioprine, ciclosporin, mercaptopurine, methotrexate
74
Non-drug treatment of IBD
smoking cessation attention to diet- identify trigger foods surgery- stoma and resection operations

MP322 (5 decks)

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