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phar 301 > Lecture 19 > Flashcards

Lecture 19 Flashcards

1
Q

What is Rhinitis

A

When airflow is blocked due to inflammation of the nasal mucous membrane
Symptom of common cold (rhinovirus) and allergic reactions (allergic rhinitis)

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2
Q

Things that cause Rhinitis

A

1) Vasodilation (blood supply increases)
2) Edema (fluid leaking out from between cells)
3) Mucous secretion (rhinorrhea), resulting in a runny nose

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3
Q

What can treat rhinorrhea (mucous secretion from rhinitis

A

Muscarinic receptor antagonist (suppresses parasympathetic nervous system)

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4
Q

Main approaches to treat a stuffy nose

A

1) Sympathomimetic nasal decongestants (rhinitis from common cold)
2) Antihistamines (allergic reaction)

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5
Q

Receptors in blood vessels of nose

A

Alpha 1 and alpha 2 adrenergic receptors (stimulation induces vasoconstriction)
Vasodilation causes swelling inwards resulting in nasal congestion

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6
Q

Raynaud’s syndrome

A

Severe vasoconstriction due to excessive sympathetic tone
Lack of blood flow to extremities

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7
Q

Mechanism of Indirect Sympathomimetics

A

ex. pseudoephedrine and PPA
Indirect sympathomimetics act presynaptic ally on sympathetic terminals to stimulate release of noradrenaline–>release of NA increases stimulation of alpha 1 and alpha 2 receptors–>induces vasoconstriction

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8
Q

Mechanism of Direct Sympathomimetics

A

ex. Phenylephrine
Phenylephrine selectively stimulate the alpha-1 receptor–>inducing vasoconstriction

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9
Q

Pathway of Alpha 1-receptor vasoconstriction

A

Stimulation of alpha-1 receptor–>Activates GPCR–>activates Phospholipase C (PLC)–>increase in IP3 (second messenger)–>IP3 stimulates Ca2+ release–>Ca2+ activation calcium dependent protein kinase–>increasing smooth muscle tone–>vasoconstriction

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10
Q

Pathway of Alpha 2-receptor vasoconstriction

A

Stimulation of alpha-2 receptor–>activates G protein alpha subunit–>inhibits adenylate cyclase–>decrease [cAMP]–> decrease in PKA activity–>increase in smooth muscle tone–>vasoconstriction

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11
Q

Downside of Adrenaline injection for asthma exacerbation

A

Adrenaline is quickly metabolized by monoamine oxidase in blood stream (short action)

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12
Q

Alternative to adrenaline injection for asthma exacerbation

A

Ephedrine
Orally available, longer half life in bloodstream than adrenaline

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13
Q

Alternative (bad) to Ephedrine

A

Amphetamine
Stable and widely available but addictive

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14
Q

Treatment for common cold

A

NONE, just drugs to alleviate symptoms

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15
Q

Topically vs orally available sympathomimetics

A

Topically–>Phenylephrine and PPA
Orally–>Phenylephrine, ephedrine, amphetamine, and PPA

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16
Q

Sympathomimetics susceptibility to degradation

A

Stable to degradation by monoamine oxidase (long lifetime)–>pseudoephedrine, ephedrine, and PPA

Degraded by MAO–> Phenylephrine, adrenaline, and noradrenaline

Completely resistant to catechol-O-methyltransferase (COMT, degrades adrenaline and noradrenaline)–>Phenylephrine, pseudoephedrine, ephedrine, and PPA

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17
Q

What sympathomimetic synthesizes methamphetamine

A

Pseudoephedrine can be made into methamphetamine so is restricted, replaced with phenylephrine (less effective drug)
Methamphetamine causes early aging and meth mouth

18
Q

What is rebound withdrawal

A

When the body fights the drug administered and attempts to counter its effect, even when the drug is no longer present

19
Q

Effect of inhalation administration

A

Very fast onset, moderate decongesting effect, very fast offset

20
Q

Effect of nasal spray administration

A

Very strong decongestant effect, fast onset and fast offset

21
Q

Effect of syrup administration

A

Very slow onset, moderate decongesting effect, very slow offset

22
Q

Which sympathomimetic has NO effect when taken orally

A

Phenylephrine (gets metabolized quickly in bloodstream by MAO

23
Q

Decongestants effect on blood pressure

A

Increase heart rate and blood pressure due to increasing sympathetic drive
Stimulation of beta-1 adrenergic receptors–>minor increase of heart rate
Stimulation of alpha 1 adrenergic receptors (peripheral blood vessels)–>vasoconstriction

24
Q

Why is PPA banned?

A

Increased risk of hemorrhagic stroke, also associated with heart attacks

25
Q

Side effects of Alpha-1 agonists

A

Hypertension, stroke, insomnia, nervousness, and loss of appetite

26
Q

Main issue with Pseudoephedrine

A

Can be synthesized into methamphetamine

27
Q

Types of allergic rhinitis

A

Seasonal (produces IgE) or perennial (throughout the year)

28
Q

Effect of seasonal allergies

A

IgE production followed by mast cell degranulation and leukotrienes and histamine release–>histamine binds to H1 receptor

29
Q

What reduces inflammation and allergic rhinitis

A

Antihistamines (H1 blockers, first generation) to inhibit the action of histamine
Leukotriene receptor antagonists to decrease inflammation by blocking action of leukotrienes, but not as effective

30
Q

2 generations of H1 histamine receptor antagonists

A

1st–>cause sedation, cross BBB (diphenhydramine)
2nd–>non-sedating (terfenadine), cannot cross BBB

31
Q

Tests to see if terfenadine (2nd generation antihistamine) can cross BBB

A

1) Radiolabeling of terfenadine
2) Measuring of H1 receptor occupancy
3) Behavioural test

32
Q

Outcome of Radiolabeled terfenadine experiment

A

The concentration of terfenadine in the rats brains after death was very low
Terfenadine concentration was highest in the GIT
No radiolabeled terfenadine was present in the brain after death

33
Q

Outcome of H1 receptor occupancy in Vivo experiment

A

H1 receptor antagonists: terfenadine and mepyramine
1) Chlorpheniramine enters the brain (as 3H-mepyramine binding was lower when co-administered with chlorpheniramine)
2) Terfenadine cannot enter the brain (3H-mepyramine binding was the same when co-administered with terfenadine)
3) Absence of terfenadine in the brain is not due to experimental error (both chlorpheniramine and terfenadine showed near complete saturation of peripheral H1 receptors)
4) Terfenadine can act competitively in the brain (in vitro), but cannot pass BBB in vivo

34
Q

H1 receptor occupancy outcome with antihistamines

A

1) First generation antihistamines (chlorpheniramine and diphenhydramine)–>CAN cross BBB and bind H1 receptors in brain
2) Second generation antihistamines (terfenadine)–> canNOT cross BBB and canNOT bind H1 receptors in the brain

35
Q

Kinetics of H1 receptor block

A

Chlorpheniramine–>rapid and reversible onset, wears off after a few hours
Terfenadine–>slower onset, abnormal recovery, irreversible

36
Q

Explanation of abnormal Terfenadine dose response curve

A

Flattening (downward shift) of dose-response curve due to terfenadine’s slow (negligible) dissociation from the receptors and interaction with spare receptors
More spare receptors present while agonist is at 100%, more potent the agonist

37
Q

Terfenadine affinity with H1 receptors

A

Terfenadine has a very high affinity for H1 receptors with few spare receptors left, and a very strong antagonist block
Low concentrations–>enough spare receptors for histamine to achieve maximum effect and surmount terfenadine’s antagonist block
High concentrations–>nearly all spare receptors are blocked, even high concentrations of histamine cannot achieve maximal effect, so insurmountable block by terfenadine (flattens dose response curve)

38
Q

Behavioural test outcomes

A

Driving test
Terfenadine is NOT sedating as none of the doses affected the driver’s performance more than the placebo

39
Q

First vs second generation antihistamines

A

Same effectiveness
Second generation antihistamine + pseudoephedrine achieves stronger decongesting effect (synergistic)

40
Q

Side effects of Terfenadine

A

Drug-drug interactions with other medications and grapefruit (inhibiting CYP450 enzymes preventing terfenadine metabolism, leading to accumulation)
Accumulation of terfenadine can cause ventricular arrythmia

41
Q

Side effects of First generation H1 antagonists

A

1) Sedation through CNS H1 block
2) Alleviate motion sickness but inhibit salivation through Muscarinic block
3) Postural hypotension through Alpha-1 block
4) Drug-drug interactions through CYP450s competition
5) Allergic reaction

42
Q

Most effective at treating rhinitis

A

Glucocorticoids are more effective than antihistamines, but have slow onset and slow offset

phar 301 (23 decks)

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