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Pharm 141 > Minor Ailments Pharmacology > Flashcards

Minor Ailments Pharmacology Flashcards

1
Q

Decongestants: Used for? What receptor does it bind to? Mechanism of Action?

A

Topical (nasal, ophthalmic) and systemic decongestants are widely used in cough-cold preparations and in anti-allergy medications

Decongestants are α1 adrenergic receptor agonists that act in the nasal mucosa to produce vasoconstriction

Vasoconstriction decreases resistance to airflow and improves ventilation by decreasing the volume of the nasal mucosa and reduced delivery and secretion of fluids to the nasal mucosa

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2
Q

Ephedrine. What class does it belong to? What receptors does it bind to? What does it cause the release of?

A

Decongestant: Natural product, mixed-acting sympathomimetic drug

Directly stimulates α1-adrenergic receptors of respiratory mucosa causing vasoconstriction

Directly stimulates β-adrenergic receptors causing bronchial relaxation, increased heart rate and contractility

Enhances release of NE from sympathetic neurons

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3
Q

Pseudoephedrine: What receptors does it bind to? How does it compare to ephedrine?

A

Stereoisomer of ephedrine, but less potent than ephedrine in producing tachycardia, increasing blood pressure, and CNS stimulation

Directly stimulates α1-adrenergic receptors of nasal mucosa causing vasoconstriction;

Directly stimulates β-adrenergic receptors causing bronchial relaxation, increased heart rate and contractility

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4
Q

Phenylephrine: Class? Receptor?

A

Decongestant, and is a selective a1 adrenergic agonist

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5
Q

What is the onset of action for oral decongestants? And the adverse effects depends on?

A

Onset of action ~ 30 minutes

Adverse effects depend on the degree of α1 receptor selectivity
insomnia, tremor, irritability, nervousness, restlessness, dizziness, headache, tachycardia, palpitation, increased blood pressure (particularly in hypertensive patients

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6
Q

Topical nasal decongestants onset of action?

A

Onset of action – 5-10 minutes

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7
Q

Xylometazoline (Otrivin) 0.1%
Oxymetazoline (Dristan) 0.5%

What are these? Dosing? And are these short or long acting ?

A

Topical nasal decongestants, long-acting, and dosing is 2-3 sprays in each nostril q10-12 up to BID.

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8
Q

Phenylephrine Nasal. Dosing? Type of medication?

A

Short acting topical nasal decongestant.
Dose will be 2-3 sprays in each nostril q4h

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9
Q

Antitussives: Examples, MOA

A

Codeine and dextromethorphan
MOA: act centrally on medulla to increase cough threshold
Image: See the different parts of the medulla?

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10
Q

Opioid Antitussives

A

Codeine is both an opiate and an opioid
Acts on opioid receptors in the medullary cough centre

May also have additional peripheral action on cough receptors in proximal airways

Note – codeine itself has antitussive properties (does not require metabolism to morphine, which is needed for its full analgesic action)
Little evidence for effectiveness at OTC doses ADRs: sedation, constipation

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11
Q

Dextromethorphan. Does it have analgesic or euphoric properties? Where does it Act? Side effects compared to codeine?

A

No analgesic or euphoric properties
Does not act through opioid receptors
Acts centrally to elevate threshold for coughing
Produces fewer subjective and GI side effects compared to codeine

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12
Q

Dextromethorphan Metabolism: What happens if its taken in poor metabolizers or with 2D6 inhibitors?
What happens if you take it with MAOIs?

A

Metabolized by CYP 2D6, increased CNS effects in poor metabolizers/drug interactions with 2D6 inhibitors

Occasional dizziness, drowsiness, nausea

Risk of serotonin syndrome with MAOIs (contraindicated, blocks serotonin reuptake)

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13
Q

Expectorants

A
  • Compounds that helps bring mucous and other materials from the bronchi
  • Guaifenesin is an expectorant found in many cough-cold products
  • Thought to act as an expectorant by stimulating respiratory tract secretions, thereby increasing respiratory fluid volumes and decreasing mucous viscosity
  • May also promote mucociliary activity
  • Evidence for efficacy is very limited, but so is the evidence for adverse effects, no known drug interactions
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14
Q

Histamine

Stored in which cells, tissues?

Physiological roles?

A

Primary storage site in tissues is in mast cells

Tissues with large numbers of mast cells include skin, bronchial mucosa, intestinal mucosa, also stored in basophils

Physiological roles in early phases of allergic reactions, GI acid secretion, immune system function, and sleep-wake cycles

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15
Q

Histamine in Allergic Responses

A

Mast cells after interacting with antigen through IgE antibodies= Ip3 is increased= increases intracellular calcium, this calcium causes exocytosis of histamine from secretory granules .

Other allergic mediators like leukotrienes also secreted

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16
Q
A

Mast cell with signaling pathways. Physically stimulated, or antigens, or compliment pathway during immune response. Drugs can also promote or inhibit release.

Beta adrenergic agents )epinephrine, isoproterenol) can inhibit, as can prostaglandins, and Ach can promote the release (but can be blocked by atropine).

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17
Q

Once activated, Histamine can bind to:

A

H1, H2, H3, H4

All are GPCRs

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18
Q

H1 receptors:

A

H1 receptors:

Distributed widely in CNS** and **periphery, particularly on smooth muscle and endothelial cells

Many of the common effects of histamine are due to activation of H<u>1 </u>receptors (itching, stimulation of nasal secretion, sedation associated with antihistamines, etc.)

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19
Q

H2 receptors:

A

Distributed in gastric parietal cells (involved in gastric acid secretion), cardiac muscle, mast cells, CNS

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20
Q

H3 Receptors

A

Autoreceptors on histamine-containing neurons, activation inhibits further histamine release

21
Q

H4 Receptors

A

Located on cells of hematopoietic origin, white blood cells

Involved in inflammation, allergy, less understood than H1 receptors

22
Q

Vascular Effects of Histamine

A

Dilation of resistance vessels - involves H1 (and H2)

Constriction of veins

  • Due to activation of H1 receptors on vascular smooth
  • muscle, contributes to extravasation of fluid and edema
  • Increased capillary permeability Also contributes to edema

Effect on the vasculature

  • Large amounts of histamine (e.g. during anaphylaxis) cause profound reduction in blood pressure due to vasodilation and plasma escape from circulation
23
Q

Other Effects of Histamine

A
  • Altered cardiac contractility and electrical conductance (H1 and H2)
  • Contraction of non-vascular smooth muscle (H1), contributes to bronchoconstriction in patients with asthma
  • Wheal formation, itching, pain (H1)
24
Q

Difference Between 1st gen and 2nd gen antihistamines?

A

First generation antihistamines:

  • Cross the blood-brain barrier and cause sedation by blocking histamine
  • Most are not selective for H1 receptors, and also block muscarinic receptors (i.e. have anticholinergic activity)

Second generation antihistamines:

  • Non-sedating, do not cross BBB
  • More selective for H1 receptors, not associated with significant anticholinergic activity
  • Typically have longer half-lives, may only require one dose daily
25
Q

Adverse Effects of Antihistamine Drugs

A

CNS effects:

Sedation, dizziness, tinnitus, incoordination, fatigue, blurred vision, sometimes euphoria, nervousness, insomnia, tremors

All significantly reduced with second-generation agents

Anticholinergic effects:

Dry mouth, urinary retention, dysuria, constipation, increased heart rate

Reduced with second-generation agents

26
Q

Arachidonic Acid Metabolites. From where do you get them? and Structure?

A

From diet and/or membranes. Long chain carbon molecules with a carboxylic acid functional group

27
Q

Pathway of Arachidonic Acid

A

Arachidonic acid is made from phospholipids by enzyme Phospholipase A2

AA is then broken down into 2 pathways by 2 different enzymes : LOX enzymes break them down into leukotrienes, while COX enzymes break them down into prostaglandins

28
Q

Eicosanoids

A

They are all the lipid signaling molecules related to or derived from arachidonic acid.

29
Q

Autacoids (definition and examples?)

A

Include eicosanoids and histamine, serotonin, kinins. DEFINITION: substances produced by neural and non neural tissues that act LOCALLY to modulate the activity of smooth muscles, nerves, glands, platelet, and other tissues.

30
Q

Eicosanoids

A

Ligands for GPCR, have multiple functions on multiple different tissues

31
Q

What is the net effect on a particular tissue with multiple eicosanoids and receptors?

A

The net effect involves both the NUMBER and TYPE of eicosanoid receptors, and….. THE TYPE and CONCENTRATION of eicosanoids

32
Q

Prostanoids

A

derived via actions of COX enzymes. AA→ PGH2→ Other prostanoids

33
Q

COX enzymes

A

2 types of COX enzymes.

COX1 → “housekeeping”, expressed in most tissues, responsible for carrying out most of the homeostatic activities

COX2 → ??

34
Q

Leukotrienes

A

Derived from HPETE, produced from arachidonic acid by lipoxygenase

35
Q

Local Inflammatory Hormones

A

Histamine, bradykinin, prostaglandins, leukotrienes, chemokines, cytokines, etc

36
Q

What compounds stimulate sensory pain neurons?

A

HISTAMINE and BRADYKININ

37
Q

What reduces the threshold at which neurons will fire?

A

HISTAMINE and PROSTAGLANDINS

38
Q

Acetaminophen vs NSAIDs MOA

A

Acetaminophen inhibit the synethesis and release of PGE2 in the thermoregulatory center, while NSAIDs inhibit COX enzyme

39
Q

Aspirin

A

inhibitor of COX-1 selective (1st gen)

40
Q

COX-1 and COX-2 . Inhibiting which one causes the therapeutic effects, and which one causes the adverse effects?

A

COX-1 inhibition is the Adverse effects

COX-2 is the therapeutic effects

41
Q

Ibuprofen binds to COX1 or COX2?

A

Ibuprofen is almost exactly equipotent for COX1 vs. COX2

42
Q

Naproxen, what is it selective for? And what is the difference between Naproxen and Ibuprofen?

A

Naproxen is slightly selective for COX-1.

Major difference is that it has a longer half life ~14 hours… compared to 2-4 hours for ibuprofen

43
Q

What does Corticosteroids target?

A

first enzyme of the process.. Phospholipase A2

Shut down all pathways: prostaglandins, bradykinins, leukotrienes

Additional functions of corticosteroids:

  • Lysis and redistribution of lymphocytes
  • Reduced circulating lymphocyte counts
  • Activation of NF-kappaB to increase apoptosis white blood cells
  • Down-regulation of IL-1 and IL-6
  • Inhibition of IL-2 in T-cells
  • Inhibition of cytotoxic T lymphocytes
  • Reduced neutrophil chemotaxis
44
Q
A

muscarinic receptors, gastrin receptors, histamine receptors all promote activity of the proton pump to cause the release of acid secretion from parietal cells.

PHE2 acts to STOP (turn down) this pathway. It inhibits acid secretion. NSAIDs, meanwhile, will block PGE2 formation, so acid secretion will go up

In addition, Prostaglandins also activate the superficial epithelial cell to make mucus and bicarbonate. Thus, by blocking this production, we damage the mucous layer

45
Q

Loperamide

A

anti diarrhea agent

Mu opioid receptor agonist, but doesnt cross the BBB

Reduces tone of the GI smooth muscle to cause constipation (usually ADR, but this time its used as a therapeutic effect)

46
Q

What promotes sleep?

A

GABA, Opioids, Melatonin, Leptin

47
Q

Duration of Insomnia (DSM-V)

A

transient = 1 week

short term insomnia= 4 episodes within 3 months

Chronic = persistent for >3 months

Risk Factors: women, older adults, more severe cases

48
Q

Antihistamines for sleep

A

1st generation. Cross the BBB and cause sedation by blocking the HISTAMINE receptor in brain. Most are not selective for H1 receptors, and also block muscarinic receptors (anticholinergic activity)

49
Q

Melatonin

A

NT derived from aa tryptophan

rleeased during dark cycle 9pm to 4am

binds 1,2,3 receptors, has antioxidant properties, etc etc

Melatonin 1= Galphai= promote sleep when activated

Melatonin 2= Gq coupled= coordinating function in the light dark cycle

Pharm 141 (8 decks)

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