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Pharmacology > Pulmonary Drugs > Flashcards

Pulmonary Drugs Flashcards

1
Q

what is aerosol?

A

drug delivery by suspension of liquid or fine solid particles

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2
Q

what are some examples of aerosol:

A 
bronchodilators
mucolytics
antibiotics
surfactants
etc.
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3
Q

why use aerosol delivery?

A

drug can be delivered to site of action, often with limited systemic effects

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4
Q

can aerosolized agents produce significant systemic effects?

A

YES

it all has to do with the chemicals of the drug and the target tissue (usually the lungs and getting drugs to the brain)

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5
Q

typical drugs of abuse:

A

heroine, crack, marijuana

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6
Q

how do vaporizing drugs work?

A

uses the lungs to transport drug to the blood

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7
Q

what does insufflation mean?

A

snorting

has a rapid effect and terminating effect

(meth is unusually bc it has a rapid effect and also a long half life)

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8
Q

how are aerosolized drugs delivered?

A

nebulizers: liquid –> fine mist

Dry powder inhaler (DPI)- powder for inhalation
more expensive

Metered dose inhalers (MDI)- propellant

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9
Q

what are the disadvantages to aerosol therapy?

A

largely related to being able to use the product correctly:

  • correct dose?
  • altered breathing pattern?
  • deposition of drug in oral mucosa?

can use a different delivery system to solve these problems

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10
Q

what is asthma? what are the features of asthma?

A

a chronic disease affecting millions worldwide

features:
- airway inflammation
- airway hyper responsiveness
- bronchoconstriction
- hyper-secretion of mucus

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11
Q

what is atopy?

A

refers to the inherited predisposition to allergic diseases such as asthma, allergic rhinitis or eczema

atopy underlies almost all asthma in children and most asthma in adults

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12
Q

what are the differences of an inflamed airway?

A

increased mucus

eosinophils

enlarged mucus gland

edema

plasma leakage

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13
Q

what is pharmacotherapy?

A

treatment of disease through the administration of drugs

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14
Q

what are 3 goals of pharmacotherapy?

A

terminate acute bronchial constriction

reduce inflammation

reduce hyper secretion of mucus

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15
Q

what is COPD? what diseases does it include?

A

chronic obstructive pulmonary disease

a term for chronic lung conditions where airflow limitation is NOT reversible

includes:
chronic bronchitis
emphysema

generally related to cigarette smoke and other means of assaulting the body

COPD- increased secretions –> increased risk for infection
when an infection does occur it tends to involve more tissues

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16
Q

what are 4 treatment goals for COPD?

A

1- reduce inflammation
2- relieve bronchoconstriction
3- reduce risk of/treat infection
4- control cough

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17
Q

B2 adrenergic agonists are used for:

A

the treatment of acute bronchoconstriction

stimulate the B2 receptors found in the smooth muscle of the bronchi and bronchioles–> causes an increase in the activity of the enzyme adenylcyclase

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18
Q

induction of adenylcyclase leads to :

A

an increase in the production of intracellular cyclic AMP

the increase of cyclic AMP leads to the activation of protein kinase A which inhibits the phosphorylation of myosin and lowers intracellular ionic calcium concentrations, resulting in relaxation of the bronchioles

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19
Q

what drug stimulates both B1 and B2 receptors?

A

epinephrine- doesn’t favor 1 over the other

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20
Q

what is the advantage of selective B2 agonists vs. non-selective agents?

A

limits effects of the drug that aren’t helpful in specific case

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21
Q

what can epinephrine be used during ____ and provides ______:

A

during an acute bronchoconstriction

provides rapid therapeutic effect

epinephrine (racemic) is also used to treat bronchiolitis, RSV and can be used for status asthmaticus

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22
Q

what is status asthmaticus?

A

a severe prolonged form of asthma that is unresponsive to standard drug treatment

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23
Q

B2 adrenergic agonists are classified by:

A

duration of action

  • ultra-short acting
  • short acting
  • intermediate-acting
  • long acting
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24
Q

ultra short acting B2 adrenergic agonists:

A

2-3 hours

isoproterenol (Isuprel)
Isoetharine (Bronkosol)

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25
Q

Short acting B2 adrenergic agonists:

A

3-6 hours

metaproternol (Metaprel, Alupent)
Terbutaline ( Brethine)
Pirbuterol (Maxair)

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26
Q

Intermediate-acting B2 adrenergic agonists:

A

8 hours

Albuterol (Proventil)
Levalbuterol (Xopenex)
Bitolterol (Tornalate)

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27
Q

Long acting B2 adrenergic agonists:

A

12 hours

Salmeterol (Servent)
Formoterol (Foradil)

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28
Q

side effects of B2 adrenergic agonists:

A

high dose inhaled:

shaking, nervousness, tachycardia

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29
Q

a1 receptors are found in ____?

activation leads to ___?

A

present in arteriolar smooth muscles

activation leads to vasoconstriction

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30
Q

a2 receptors are found in ___?

activation leads to ___?

A

found pre-ganglionically and in the CNS

activation leads to decrease in the sympathetic flow from the CNS

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31
Q

b1 receptors are found in ___?

activation leads to ___?

A

found in the heart and kidney

activation leads to increase HR, force of contraction, and release of renin from the kidney

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32
Q

b2 receptors are found it ___?

A

smooth muscles of blood vessels and bronchi

activation leads to vasodilation and bronchodilation

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33
Q

what is levalbuterol (xopenex)?

A

intermediate acting B2 adrenergic agonist

R-Enantiomer (mirror image) of the short acting B2 receptor agonist albuterol

34
Q

why use levabuterol (xopenex)?

A

B2 selective drugs typically a mixture of R and S isomers. Only the R isomer activates the B2 receptor

35
Q

what if formoterol (foradil)?

A 
a highly selective B2 agonist with a long duration of action
Long acting (LABAs) B2 adrenergic agonist

How?
formoterol is highly lipophilic entering the plasma cell membrane in the form of a “depot” and is gradually released into the aqueous phase to activate the B2 receptors resulting in a long duration of action

the aqueous phase activity is not demonstrated by salmeterol

36
Q

how does tolerance happen?

A

if short acting B2 agonists are overused, tolerance may occur as B2 receptors may become unresponsive to stimulation

37
Q

can tolerance be reversed?

A

tolerance can be slowly revered through the use of inhaled corticosteroids

38
Q

tolerance is not observed with:

A

long acting B2 agonists

39
Q

inhaled anticholinergics block:

A

muscarinic cholinergic receptors (non-specific anti-cholinergic)

“muscarinic antagonists”??

40
Q

what is the mechanism of action of inhaled anticholinergics?

A

inhaled anticholinergic drugs cause a decrease in the formation of cGMP

  • decreasing contractility of smooth muscle in the lung
  • inhibiting bronchoconstriction
  • inhibiting mucus secretion
41
Q

cholinergic=

A

parasympathetic

42
Q

adrenergic=

A

sympathetic

43
Q

M receptors are present in:

A

the neuro-effector junction of the parasympathetic division

44
Q

inhaled anticholinergics are most often used for?

A

the symptomatic relief of COPD

45
Q

examples of inhaled anticholinergics:

A

ipratropium bromid (atrovent)
ipratropium & albuterol (combivent)
tiotripium (Spiriva)

46
Q

what are the side effects of inhaled anticholinergics?

A 
dry mouth
nervousness
GI upset
headache
worsening of narrow-angle glaucoma
prostatic hypertrophy
47
Q

atropine derivatives will block:

A

M receptors in the lung

48
Q

inhalation administration of opratropium bromide (atrovent) or tiotropium (Spiriva) are commonly used for:

A

anticholinergics for COPD

49
Q

tiotropium (Spiriva) is a:

A

longer-acting, structural analog of ipratropium bromide

approved for maintenance of COPD

the long action is thought to be due to slowed dissociation rate from M receptors

50
Q

what are the primary actions of inhaled corticosteroids in the lungs?

A

1- SUPPRESS INFLAMMATION in the airways
decreases mucous cell secretions
reduce edema
assist in repair of damaged epithelium

2-INCREASE THE NUMBER & SENSITIVITY OF B2 RECEPTORS
restores and/or enhances the effectiveness of B2 agonist agents

51
Q

In most acute severe asthma attacks, IV administration of corticosteroids offers:

A

little advantage over PO dosing

52
Q

the full action of systemic corticosteroids will take:

A

48-72 hours

53
Q

oral corticosteroids should be taken for:

A

7-10 days with doses titrated down

should not D/C rapidly

54
Q

inhaled vs. systemic corticosteroids:

A

inhaled corticosteroids, even at high doses, do not appear to cause significant adverse effects

long term systemic corticosteroid treatment is associated with serious adverse effects

55
Q

what are adverse effects of systemic corticosteroids?

A 
adrenal gland atrophy
peptic ulcers
hyperglycemia
osteopenia & osteoporosis
aseptic necrosis of the hip
immune suppression
56
Q

what are unpleasant side effects of systemic corticosteroids?

A 
"moon face"
redistribution of weight
thin skin
acne
fatigue
GI disturbance
57
Q

examples of inhaled corticosteroids:

A 
fluticasone (Flovent Diskus)
budesonide (Pulmicort)
triamcinolone (Azmacort)
flunisolide (Aerobid)
beclomethasone (Qvar, Beclovent)
58
Q

examples of oral corticosteroids:

A

methylprednisolone (Depo-medrol)

prednisone (deltasone, etc)

59
Q

what is fluticasone propionate (Flovent)?

A

an inhaled corticosteroid

outside of the airway, the bioavailability of fluticasone is minimal
because subject to rapid inactivation by the liver.
The metabolite that is produced is largely inactive and has limited affinity for the glucocorticoid receptor

60
Q

what are combination agents?

A

a few inhaled medications contain both a corticosteroid and a bronchodilator

fluticasone and salmeterol (Advair Diskus)

Budesonide and formoterol (Symicort)

61
Q

what are Methylxanthines?

A

bronchodilators that are chemically related to caffeine

theophylline (Theo-Dur, etc)
aminophylline (Somophyllin)

can be given PO or IV however their use has declined steadily due to a narrow margin of safety and significant adverse effects and toxicity

*serum drug levels must be monitored
WHY?

62
Q

in addition to bronchodilation, methylxanthines have other pulmonary effects including:

A
  • inhibit pulmonary edema by decreasing vascular permeability
  • increase the ability of the cilia to clear mucus etc.
63
Q

non-pulmonary effects of methylxanthines include:

A

increasing cardiac output
peripheral vasodilation
mild diuretic effect
CNS stimulation

64
Q

what are mast cell stabilizers?

A

inhibit the release of histamine from mast cells

used as prophylaxis to prevent acute asthma attacks

short life=2.5 hours; must be used long-term for significant benefit

cromolyn (Intal)
Nedocromil (Tilade)

65
Q

what are leukotriene modifiers?

A

strong chemical mediators of bronchoconstriction, inflammation and mucus secretion

formed by the lipoxygenase pathway of arachidonic acid metabolism is response to cellular injury

developed to counteract the effects of leukotrienes

66
Q

leukotriene modifiers are currently indicated for:

A

long-term treatment of asthma and allergies

67
Q

examples of leukotriene modifiers:

A

zileuton (Zyflo)- reduces formation of leukotrienes by blocking lipoxygenase

montelukast (Singulair) and zafirlukast (Accolate)- block leukotriene receptors

68
Q

what is omalizumab (Xolair)?

A

an immunosuppressant monoclonal antibody

binds to immunoglobulin E
prevents IgE attachment to mast cells and basophils

this prevents the release of pro-inflammatory and pro-allergic substances

69
Q

who is omalizumab mainly prescribed to?

A

patients with severe, persistent asthma, which cannot be controlled even with high doses of corticosteroids

70
Q

what are mucolytics and expectorants used for?

A

to reduce the viscosity of bronchial mucous and aid in its removal

OTC: guaifenesin (Robitussin, etc)

RX:
acetylcysteine (Mucomyst)
dornase alfa-recombinant (Pulmozyme)

71
Q

what are antitussives?

A

dampen the cough reflex

opiodes

non-opioids

**most antitrussives are used in combo with other agents such as mucolytic/expectorant

72
Q

antitussives:opioids:

A 
codeine
hydrocodone bitartrate (hycodan)
73
Q

antitussives: non-opioids

A

benzonatate (Tessalon)

dextromethorphan (PediaCare, etc)

74
Q

what is respiratory distress syndrome? (RDS)

A

condition where the lungs are not producing surfactant

occurs most often in premature infants

surfactant forms a thin layer on the inner surface of the alveoli allowing the lung to remain open during respiration

colfosceril (exosurf)
ceractant (survanta)

75
Q

what cell type produces surfactant?

A

type II alveolar cells????

76
Q

what is RSV?

A

respiratory syncytial virus

normally affects infants and young children

77
Q

what treatment would be used for RSV?

A

may include both non-selective and selective B adrenergic drugs, oxygen, ribavirin, supportive care, etc

78
Q

what prevention can be used for RSV?

A

a monthly injection consisting of RSV antibodies can be given during peak RSV season to reduce the risk of infection

79
Q

what is anaphylaxis?

A

a severe, sometimes life threatening allergic reaction to a variety of agents

FOOD: nuts, shellfish, milk and eggs
STINGING INSECTS: bees, wasps
MEDICATIONS: penicillin

80
Q

what are symptoms of anaphylaxis?

A 
flushing
urticaria (hives)
pruritis (itching)
bronchospasm
cramping
hypotension
81
Q

pathophysiology of anaphylaxis:

A

First exposure to allergen

–> IgE formation
IgE attached to mast cells and basophils

–>mediators (histamine) are released from mast cells

Mediators:

  • ->smooth muscle constriction leading to bronchospasm, cramping
  • ->increased vascular permeability (50% shift of vascular volume to tissues)
  • ->vasodilation
82
Q

what treatment would be used for anaphylaxis?

A

epinephrine S.C. or I.M. 0.3-0.5 mg

EFFECTS:

alpha agonist activity: increased peripheral vascular resistance, reverse vascular permeability

beta agonist activity: bronchodilation, positive ionotrophic effect

Pharmacology (8 decks)

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