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Pulmonary Week 1 > Pharm I > Flashcards

Pharm I Flashcards

1
Q

What are some advantages to pulmonary delivery of drug?

A

The lung is more permeable to macromolecules and even more permeable to small molecules than the GI tract and has extremely fast onset of action

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2
Q

What are some disadvantages to pulmonary delivery of drug?

A

-inhaled corticosteroids can deposit a
significant portion of the drug dose in the oral cavity, with opportunistic infections
like candidiasis arising from diminished immune function.

Acidic powders are
also a concern for the integrity of tooth enamel.

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3
Q

What routes do drugs take for absorption in the lung?

A

para and trans-ceullar

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4
Q

How are lipid-soluble drugs absorbed?

A

They can dissolve in the lipid bilayer and are absorbed trans-cellularly

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5
Q

How are insoluble drugs absorbed?

A

para-cellularly via aqueos pores in the tight junctions

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6
Q

T or F. The less ionized a molecule, the faster its absorption rate

A

T. because it forms fewer interactions with the proteins and lipids lining the pore

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7
Q

What are the three major categories of disease that require treatment of the lung?

A
  • inflammation
  • infection
  • cancer
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8
Q

What types of inflammation diseases require lung treatment?

A
  • asthma
  • COPD
  • allergic rhinitis
  • cystic fibrosis
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9
Q

What are some classes of drugs that act in the upper respiratory tract?

A
  • mucolytics
  • vasoconstrictors
  • antihistamines
  • drugs acting in the CNS cough center
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10
Q

What are some major uses of antihistamines?

A
  • allergic rhinitis

- hay fever

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11
Q

What is the major use of vasoconstrictors in the URT?

A

permit someone to breath more easily, by

relieving nasal congestion.

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12
Q

What is ivacaftor?

A 
Recently gained approval as the first in a new class of CTFR (cystic fibrosis
transmembrane conductance regulator) potentiators.
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13
Q

What part of the ANS dominates lung function?

A

PNS, it provides direct innervation of smooth muscle and glandular tissue

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14
Q

T or F. In humans, bronchial smooth muscle has no direct neural connection from the SNS

A

T. SNS activity can only modulate the activity of the PNS via hetero-receptors

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15
Q

What other way can the SNS affect the lung?

A

beta-2 receptors can respond to circulating Epinephrine or to exogenous drug treatment

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16
Q

What classes of drugs can be used to control bronchospasm in asthma?

A

B2 adrenergic agonists and muscarinic anatgonists

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17
Q

What is the role of muscarinic M1 receptors?

A

They transduce vagal signal to both sub-mucosal glands and the airway smooth muscle AND increase glandular secretions in nasal mucosa

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18
Q

What is the role of muscarinic M2 receptors?

A

they are inhibitory auto receptors on the pre-synaptic membrane of PG fibers AND are found in bronchial smooth muscle where they oppose the increase in cAMP produced by B2 adrenergic stimulation

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19
Q

What is the role of muscarinic M3 receptors?

A

promotes bronchoconstriction of airway smooth muscle and mucus secretion

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20
Q

How do non-selective drugs, like atropine and ipratropium affect the lungs?

A

they non-selectively antagonize M-2 and M-3 receptors equally well

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21
Q

How does blockade of the M2 auto-receptors affect the release of endogenous Ach?

A

it increases the release, which serves to partially offset any bronchodilatory drug effects. (So the non-selective nature is not good)

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22
Q

How selective is Tiotropium?

A

it is selective for M1 and M3 receptors

23
Q

T or F. Tiotropium has a longer duration of action than other muscarinic antagonists

A

T. But a slower onset of effect

24
Q

How would anticholinergic drugs affect glandular secretions?

A

it dries them and potentially thickens them

25
Q

What other drugs have anticholinergic activity and thus induce drying of secretions?

A

1st gen antihistamines

26
Q

What are the 1st generation antihistamines?

A
  • Chloropheniramine
  • Doxylamine
  • Diphenhydramine
27
Q

What kinds of drugs potentiate cholinergic activity?

A

Acetylcholinestase inhibitors

28
Q

What are some Acetylcholinestase inhibitors?

A
  • Neostigmine

- Edrophonium

29
Q

What are some off-label uses of marijuana?

A
  • anorexia
  • cachexia
  • glaucoma
  • N/V
30
Q

What effect does marijuana have on secretions?

A

increases them

31
Q

Where are B2 receptors most common?

A

the lungs (70-80%)

32
Q

What is the main effect of albuterol on the lungs?

A

bronchodilation and relaxation of smooth muscle and most effective against early (bronchospastic) response to inhaled antigens

33
Q

T or F. Albuterol is ineffective against late (inflammatory) phase of inhaled antigen

A

T.

34
Q

Are B2 agonists all good?

A

No, some with M-2 agonizing action have the potential to produce bronchoconstriction by increasing PNS tone

35
Q

How does B2 stimulation affect mast cells?

A

reduces histamine release

36
Q

How does ANS stimulation affect mucocilliary clearance?

A

Goblet cells and submucosal glands primarily receive PNS innervation but circulating epinephrine can give SNS effects

37
Q

What do a-agonists do to mucocillary clearance?

A

increase fluid secretion volume

38
Q

What do B-agonists do to mucocillary clearance?

A
  • increase glycoprotein composition

- increase beat frequency of cilia to promote more clearance

39
Q

How do B-agonists affect micro-vasculature?

A

They decrease microvascular leakage which reduces airway obstruction in asthma

40
Q

T or F. B2 receptors exist in the heart

A

T. Some

41
Q

At high conc, how do B2 agonists affect the heart?

A
  • CV stimualtion
  • QT prolongation, especially in hypokalemia
  • widening pulse pressure
  • arterial dilation in coronary, pulmonary, and skeletal muscle
42
Q

One of the classical adverse effects that a patient who has taken too much beta-2 agonist
might display is a twitching or fasciculation of skeletal muscle. Why?

A

B2 stimulation increases Na/KATPase activity which increases intracellular K+

43
Q

What are some DD interactions with B2 agonists?

A
  • TCAs
  • MAOIs
  • Saquinavir
  • Loop and thiazide diuretics
  • Non-specific Beta-blockers
44
Q

What are some common TCAs?

A
  • amitriptyline

- Despiramine

45
Q

Why are TCAs a potential DD interaction with B2 agonists?

A

block reuptake of drug

46
Q

What are some common MAOIs?

A
  • selegilene

- rasagilene

47
Q

Why are MAOIs a potential DD interaction with B2 agonists?

A

they block metabolism of amines by monoamine oxidase-B

48
Q

Why are Saquinavir and loop/thiazide diuretics potential DD interactions with B2 agonists?

A

they promote hypokalemia, QT prolongation, and arrhythmia

49
Q

Both muscarinic and beta-adrenergic receptors are G protein-coupled receptors. M1 and
M3 are coupled to stimulatory ____ signaling,

A

Gq

50
Q

What GCPR does M2 receptors work with?

A

Gi (inhibitory)

51
Q

What GCPR does B2 receptors work with?

A

Gs mediated

52
Q

Too frequent stimulation of B2 receptor causes what?

A

Too frequent a

stimulation of the beta-receptor leads to internalization and loss of physiologic function.

53
Q

How are corticosteroids used in asthma treatment?

A

they transcriptionally upregulate the expression of the beta-adrenergic
receptor, leading to renewed response to the beta-2 agonist inhaler treatment.

Pulmonary Week 1 (17 decks)

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