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PHARM 141 > OTC Pharmacology > Flashcards

OTC Pharmacology Flashcards

1
Q

What do decongestants do?

A

Alpha-1 adrenergic receptor agonists and/or indirect sympathomimetics (release NE)
Act in the nasal mucosa to produce vasoconstriction

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2
Q

What are examples of decongestants? (3)

A

Ephedrine
Pseudoephedrine
Phenylephrine

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3
Q

What is ephedrine?

A

Natural product, directly stimulates alpha-1 adrenergic receptors to cause vasoconstriction and beta-adrenergic receptors.
Enhances release of NE from sympathetic neurons.

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4
Q

What is pseudoephedrine?

A

Stereoisomer of ephedrine and less potent
Directly stimulates alpha-1 adrenergic receptors, causing vasoconstriction and has some direct stimulation of beta-adrenergic receptors

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5
Q

What is phenylephrine?

A

Selective alpha-1 adrenergic agonist

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6
Q

What is the major AE of topical decongestants?

A

Rebound congestion which can be worse than the original congestion

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7
Q

What are examples of antitussives?

A

Dextromethorphan and codeine.

Opioids are also potent antitussives but are not first line

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8
Q

How do expectorants work? What is an example?

A

Thought to stimulate olfactory tract secretions, increasing fluid and decreasing mucous viscosity.
Ex. Guaifenasin. Not much evidence that it does anything, but not much evidence that they’re harmful either.

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9
Q

How is histamine released during an allergic reaction?

A

Antigens interact with IgE antibodies on the surface of mast cells.
IP3 is produced, which increases intracellular calcium.
Calcium interacts with vesicles and facilitates release of stored histamine

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10
Q

What does activation of H1 and H2 receptors lead to?

A

Arterial dilation
Smooth muscle constriction
Increased capillary permeability–> extravasion of fluid and edema

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11
Q

What is the difference between first and second generation antihistamines?

A

Second generation antihistamines:
- do not cross the blood brain barrier
- have less affinity for muscarinic receptors
- longer half lives
First gen:
- block muscarinic receptors, resulting in anticholinergic side effects

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12
Q

Define eicosanoids vs autocoids

A

Eicosanoids: lipid signaling molecules related to or derived from arachidonic acid
Autocoids: substances that act locally to modulate the activity of tissues

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13
Q

What are prostanoids?

A

Derived from COX and other enzyme that convert arachidonic acid to PGH2 and then into prostanoids
Some are also produced from linoleic acid.

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14
Q

What are leukotrienes?

A

Derived from HPETE, which is converted into leukotrienes by enzymes

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15
Q

What happens during acute inflammation?

A
  • Release of local inflammatory mediators and accumulation of neutrophils
  • Swelling to bring plasma into the area to dilute present toxins and bring antibodies, complement and initiate blood clotting to prevent spread to other parts of the body.
  • Increased blood flow to bring oxygen and nutrients to cells responsible for inflammation
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16
Q

What happens during chronic inflammation?

A

Accumulation of additional blood cells, including macrophages and others

17
Q

Which compounds directly stimulate sensory pain neurons and which reduce the threshold at which neurons will fire?

A

Directly stimulate: histamine, bradykinins

Reduce threshold: histamine, prostaglandins

18
Q

How does acetaminophen exerts its antipyretic effects?

A

Inhibits COX in the thermoregulatory centre

Inhibit synthesis/release of PGE2 in the thermoregulatory centre of the anterior hypothalamus

19
Q

What are the three indications for NSAIDs?

A

Pain
Inflammation
Fever

20
Q

How do NSAIDs exert their effects?

A

Inhibit COX to prevent conversion of arachidonic acid to PGH2, preventing prostaglandin production

21
Q

Compare ibuprofen and naproxen

A

Naproxen has a longer half life than ibuprofen (14h vs 2-4h)

naproxen is very slightly COX-1 selective, while ibuprofen is almost equally selective for COX1 and 2

22
Q

How do corticosteroids exert their effects?

A

Target the first enzyme in the arachidonic acid cascade, phospholipase A2.
This shuts down all arachidonic acid products
Also have additional anti-inflammatory and immunosuppressant effects

23
Q

How do PPIs exert their effects?

A

Structurally related to H2 histamine receptor antagonists

24
Q

What are drug interactions to be concerned about when using PPIs?

A

Some anti-platelet medications and kidney adverse effects

25
Q

What were H2 receptor antagonists used for? How do they work?

A

To suppress acid production in the GI tract before PPIs were developed
Block H2 receptors on parietal cells in the stomach

26
Q

What do bismuth containing compounds do?

A

Coat erosions and ulcers
Stimulate prostaglandin production
Stimulate mucous and bicarbonate secretion
Decreases GI secretions to treat diarrhea
Direct antimicrobial effects, including H. pylori

27
Q

How does sucralfate work?

A

It’s a sucrose salt plus aluminum hydroxide that forms a viscous substance that coats ulcers in acidic environments

28
Q

Does dextromethorphan act through opioid receptors? What enzyme is it metabolized by? What is a drug interaction?

A

No– acts centrally to elevate threshold for cough
Metabolized by 2D6 inhibitors
Risk of serotonin syndrome with MAOIs

29
Q

What is an example of a drug that stimulates histamine release

A

Acetylcholine

Non-immunologic histamine releasors (ex. opioids, some food components)

30
Q

Describe the distribution of H1 receptors

A

Widely distributed in the CNS and periphery, particularly on smooth muscle and endothelial cells

31
Q

Describe the distribution of H2 histamine receptors

A

Gastric parietal cells

32
Q

Describe the distribution of H3 and H4 histamine receptors

A

H3: Autoreceptors on histamine containing neurons
H4: On white blood cells, play a role in inflammation and allergy

33
Q

What promotes acid secretion in the stomach?

A

Muscarinic, histamine and gastrin receptors promote the activity of the proton pump.
We can block these receptors (ex. by prostaglandins) to stop proton pump activity (or can block proton pump itself)

34
Q

Describe the effect of PPIs vs H2 histamine blockers on stomach acidity?

A

PPIs: way better at reducing acid secretion throughout the day,
H2 blockers: mostly good for nocturnal acid secretion

35
Q

Which receptors are involved in nausea and vomiting?

A 
M1 muscarinic receptors
H1 histamine receptors
NK1 neurokinin receptors
5-HT3 serotonin receptors
D2 dopamine receptors
36
Q

What are additional treatments for nausea and vomiting?

A

Cannabinoids
Benzodiazepines
Phenothiazines

37
Q

How much evidence exists for using cannabis to treat nausea and vomiting?

A

Little to none, but some evidence that it’s effective for chemotherapy induced vomiting

38
Q

How do opioids treat diarrhea?

A

mu receptor agonists reduce the tone of the GI smooth muscle

39
Q

Describe melatonin 1 and 2 receptors

A

Melatonin 1 receptors: coupled to G-alphai and thought to promote sleep when activated
Melatonin 2: Gq-coupled, thought to serve a coordinating function in the light-dark cycle

PHARM 141 (9 decks)

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