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
Name 2 H2 receptor antagonists?
Ranitidine Cimetidine -tidine
26
What adverse effect is associated with H2 receptor antagonists?
Masks gastric malignancy
27
How do compound alginates work?
Antacid and alginate function Antacid = increase pH in the stomach Alignate = foam layer that protects the oesophagus (think Gaviscon)
28
Name 2 compound alignates
Peptac | Gaviscon
29
What 2 substances reduce secretagogue action and inhibit gastric acid secretion? What else is known to inhibit gastric acid secretion?
Somatostatin Prostagladins Nausea
30
What do NSAIDs inhibit? | Why is this an issue?
COX-1 (involved in prostagladin production) Reduce production of prostagladins -> increase HCl -> increased risk of peptic ulcers
31
Name 4 NSAIDs that if you see on a drug history you must be thinking of peptic ulcers
Aspirin Ibuprofen Diclofenac Naproxen
32
What drug can be used for NSAID induced peptic ulcer prophylaxis?
Misoprostol
33
What anti-emetic MUST be avoided in bowel obstruction? | Why?
Metoclopramide Encourages gastric emptying
34
Define nausea
Unpleasant sensation normally felt in the throat and stomach
35
Define emesis
Forceful expulsion of gastric/intestinal contents out the mouth
36
Define retching
Rhythmic reverse peristalsis Involuntary abdo and diaphragm contraction
37
What stops to allow emesis? (2)
Intestinal slow wave activity Breathing
38
What "powers" emesis?
Vomiting centre of medulla oblongata
39
Are stomach muscles contracted or relaxed in emesis? What muscles are involved?
Relaxed Diaphragm and abdo muscles contract (common mistake)
40
What is the most common consequence of vomitting?
Dehydration
41
Which biochemical abnormality can occur in mass vomiting?
Metabolic alkalosis
42
What is a mallory Weiss tear?
Oesophageal damage
43
What type of antiemetic is commonly used for anti-nausea in chemo-therpay paitents?
5-HT3 anatagonists "setrons" Ondanesteron Palonosteron (Imagine Dan Ross in chemo)
44
What is the common antiemetic used for travel sickness?
Hyosine (high in plane - travel - hyosine) Muscarinic acetylcholine
45
Which antiemetic is used in conjunction with morphine?
Metoclopramide
46
Diarrhoea = ... loose stools in ...hrs
3 in 24 hrs
47
What are the 4 causes of diarrhoea?
- Activation of CFTR (e.g. by bacterial entertoxins) - Impaired absorption of NaCl - Non-absorable or poorly absorbable solutes in the lumen - Hypermotility
48
What recpetor do synthetic opiods act on? Where is this receptor expressed?
Opiod receptors Enteric neurons
49
What is the action of the synthetic opiods?
Inhibit ENS -> decreased peristalsis -> increased fluid absorption -> constipating
50
Name 2 synthetic opiods?
LOPERAMIDE | Codeine phosphate
51
What are the 4 contradicitions of synthetic opiods?
``` Remember ABCD Acute UC Babies C.diff infection Dysentary ```
52
What transporter is involved in the absorption of Na+ and glucose from the rehydration salts?
SGLT1
53
What "follows" the rehydration salts?
Water (absorbed too)
54
Metoclopramide MoA?
Dopamine antagonist
55
Describe and explain cyclizine?
Anti-histamine drug Bind to H1 in brain Indicated in motion sickness