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GI > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

When should laxative treatment be considered?

A

When other measures such as change to diet/ increased exercise haven’t made a difference

Only use for a short period of time

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2
Q

What is the MOA of bulking laxatives?

A

Cannot be digested by small intestine -> increased mass in stool

Increased mass -> increased water absorption

Bulkier stool -> peristalsis -> SHITTTTTT

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3
Q

Name 2 bulking laxatives?

A

Ispaghula husk

Methylcellulose

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4
Q

What are the 2 contradictions to bulking laxatives?

A

Bowel obstruction

Ileus

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5
Q

What is the MOA of osmotic laxatives?

A

Cause osmosis -> increase bulk of stool -> peristalsis -> SHITTTT

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6
Q

Name 2 osmotic laxatives

A

Lactulose

Macrogols

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7
Q

What is the contradiction for all osmotic laxatives?

A

Bowel obstruction

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8
Q

What is the MOA of stimulant laxatives?

A

Increase motility -> increase movement of stool

Increase water excretion -> increase bulk of stool -> peristalsis

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9
Q

Name 2 stimulant laxtaives

A

Senna

Glycerol suppository

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10
Q

What is the contradiction?
What is the result of prolonged use?

(of stimulant laxatives)

A

Bowel obstruction

Atonic colon

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11
Q

What is the side effect of stimulant laxatives in general and the specific side effect of Senna?

A

Abdo pain

Hypokalaemia

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12
Q

What cell produces HCl?

A

Parietal cell

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13
Q

How are HCO3- and H+ produced?

A

Breakdown of carbonic acid

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14
Q

What ion is HCO3- pumped out of the cell in exchange for?

A

Cl-

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15
Q

What is H+/K+ ATPase also called?

A

Proton pump

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16
Q

What do secretagogues do?

A

Agents that cause secretion

HAG - histamine, ACh, gastrin

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17
Q

Match the following secretagogues to their receptor found on parietal cells

  • Histamine
  • ACh
  • Gastrin

(HAG)

A

Histamine - H2
ACh - M3
Gastrin - G/CCK2

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18
Q

Fill the gaps:

Secretagogues can cause an increase in the number of …. which leads to ….. acid production

A

Proton pumps

Increased

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19
Q

How do PPIs decrease HCl production?

A

IRREVERSIBLY inhibit the proton pump

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20
Q

When should PPIs be taken?

A

20 mins before food

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21
Q

Name 2 PPIs

A

Omeprazole
Lansoprazole

-prazole

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22
Q

What 3 adverse effects are associated with PPIs

A

Increased risk of C.diff (less acidic stomach environment)

Masks symptoms of gastric malignancy

Osteoporosis

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23
Q

How do H2 receptor antagonists decrease HCl production?

A

Block H2 receptors so histamine cannot act on parietal cell

24
Q

Why are H2 antagonists less effective than PPIs?

A

They only block H2 receptors so ACh and gastrin can still act on the cell

25
Q

Name 2 H2 receptor antagonists?

A

Ranitidine
Cimetidine

-tidine

26
Q

What adverse effect is associated with H2 receptor antagonists?

A

Masks gastric malignancy

27
Q

How do compound alginates work?

A

Antacid and alginate function

Antacid = increase pH in the stomach

Alignate = foam layer that protects the oesophagus (think Gaviscon)

28
Q

Name 2 compound alignates

A

Peptac

Gaviscon

29
Q

What 2 substances reduce secretagogue action and inhibit gastric acid secretion?

What else is known to inhibit gastric acid secretion?

A

Somatostatin
Prostagladins

Nausea

30
Q

What do NSAIDs inhibit?

Why is this an issue?

A

COX-1 (involved in prostagladin production)

Reduce production of prostagladins -> increase HCl -> increased risk of peptic ulcers

31
Q

Name 4 NSAIDs that if you see on a drug history you must be thinking of peptic ulcers

A

Aspirin
Ibuprofen
Diclofenac
Naproxen

32
Q

What drug can be used for NSAID induced peptic ulcer prophylaxis?

A

Misoprostol

33
Q

What anti-emetic MUST be avoided in bowel obstruction?

Why?

A

Metoclopramide

Encourages gastric emptying

34
Q

Define nausea

A

Unpleasant sensation normally felt in the throat and stomach

35
Q

Define emesis

A

Forceful expulsion of gastric/intestinal contents out the mouth

36
Q

Define retching

A

Rhythmic reverse peristalsis

Involuntary abdo and diaphragm contraction

37
Q

What stops to allow emesis? (2)

A

Intestinal slow wave activity

Breathing

38
Q

What “powers” emesis?

A

Vomiting centre of medulla oblongata

39
Q

Are stomach muscles contracted or relaxed in emesis?

What muscles are involved?

A

Relaxed

Diaphragm and abdo muscles contract

(common mistake)

40
Q

What is the most common consequence of vomitting?

A

Dehydration

41
Q

Which biochemical abnormality can occur in mass vomiting?

A

Metabolic alkalosis

42
Q

What is a mallory Weiss tear?

A

Oesophageal damage

43
Q

What type of antiemetic is commonly used for anti-nausea in chemo-therpay paitents?

A

5-HT3 anatagonists “setrons”

Ondanesteron
Palonosteron

(Imagine Dan Ross in chemo)

44
Q

What is the common antiemetic used for travel sickness?

A

Hyosine (high in plane - travel - hyosine)

Muscarinic acetylcholine

45
Q

Which antiemetic is used in conjunction with morphine?

A

Metoclopramide

46
Q

Diarrhoea = … loose stools in …hrs

A

3 in 24 hrs

47
Q

What are the 4 causes of diarrhoea?

A
  • Activation of CFTR (e.g. by bacterial entertoxins)
  • Impaired absorption of NaCl
  • Non-absorable or poorly absorbable solutes in the lumen
  • Hypermotility
48
Q

What recpetor do synthetic opiods act on?

Where is this receptor expressed?

A

Opiod receptors

Enteric neurons

49
Q

What is the action of the synthetic opiods?

A

Inhibit ENS -> decreased peristalsis -> increased fluid absorption -> constipating

50
Q

Name 2 synthetic opiods?

A

LOPERAMIDE

Codeine phosphate

51
Q

What are the 4 contradicitions of synthetic opiods?

A 
Remember ABCD
Acute UC
Babies
C.diff infection 
Dysentary
52
Q

What transporter is involved in the absorption of Na+ and glucose from the rehydration salts?

A

SGLT1

53
Q

What “follows” the rehydration salts?

A

Water (absorbed too)

54
Q

Metoclopramide MoA?

A

Dopamine antagonist

55
Q

Describe and explain cyclizine?

A

Anti-histamine drug

Bind to H1 in brain

Indicated in motion sickness

GI (26 decks)

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