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STEP Pharm II > Tx of COPD/Asthma > Flashcards

Tx of COPD/Asthma Flashcards

1
Q

SNS innervates what in the lung?

A

primarily blood vessels releasing Nor which causes vasoconstriction via a-1 and a-2 receptors (blood vessels also have B2 receptors but Nor has very little affinity for them). B2 can be activated with Epi but there is very little there isn’t much PNS to vessels

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2
Q

PNS (cholinergic) innervates what in the lung?

A

bronchial smooth muscle (no SNS)

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3
Q

Where are Muscarinic receptors highest in the lung?

A

trachea and large bronchi

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4
Q

Where are adrenergic (B2) receptors highest in the lung?

A

small bronchioles

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5
Q

What do pre-synaptic M2 receptors do?

A

attenuate PNS constriction

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6
Q

What happens to M2 receptors in asthma/COPD?

A

eosinophils release basic proteins (cationic) that damage M2 receptors so increased Ach is released

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7
Q

What does nicotine from smoking do?

A

stimulates PNS and acts on nerve terminals (pre and post) and helps releases Ach (can release other neurotransmitters as well)

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8
Q

What other things can make Ach?

A

inflammatory cells like macrophages, T cells, and epithelial cells

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9
Q

M3 receptors are linked to what GCPR?

A

Gq

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10
Q

M2 receptors are linked to what GCPR?

A

Gi (reduced levels of cAMP)- particularly when B2 agonists are given

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11
Q

What else does M3 stimulation cause?

A

remodeling of bronchial smooth muscle via a-actin deposition on ECM

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12
Q

How is M3 stimulation on vessel different from bronchial smooth muscle?

A

stimulation (on intact endothelium) causes NO release and relaxation but in damaged endothelium, M3 agonism will cause contraction

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13
Q

What are the B2 specific, quick-onset short duration agonists?

A

-Albuterol-Terbutaline

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14
Q

What are the B2 specific, slow-onset long duration agonists?

A

-Salmeterol and Formoterol (used always with steroids)duration =12 hrs

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15
Q

What are the cholinergic antagonists?

A

Atropine, Ipratropium, Tiotropium, Imeclidinium

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16
Q

What are the methylxanthines (bronchodilators and antiinflammatory)?

A

TheophyllineAminophylline

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17
Q

What are the leukotriene receptor blockers (antiinflammatory)?

A

Monteleukast and Zafirlukast

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18
Q

What are the leukotriene synthesis inhibtiors?

A

Zileuton

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19
Q

What are the Anti-IgE ABs?

A

Omalizumab and Dupilumab

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20
Q

What are the Anti-IL-5 ABs?

A

Mepolizumab and Reslizumab

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21
Q

T or F. Anticholinergic agents will not cause a change in BP when given alone

A

T. Although there will be M3 binding in the vessels, you will not see a change (there must be a tonic release for change to occur) but you will see some increase in HEART RATE (but not CO)

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22
Q

What is Advair?

A

Salmeterol + Flucticasone (LABA)

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23
Q

How do B2 agonists work?

A

It causes increases in cAMP!! (via Gs), which activate PKA, which phosphorylates Myosin light chain kinase (MLCK), deactivating it, and decreasing muscle contraction OR harbor Ca2+ in the ER ANDcAMP can activate EPAC (exchange protein activated by cAMP) which can reduce bronchial smooth muscle proliferation

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24
Q

T or F. Frequent use of LABA can cause de-sensitivity of the receptor

A

T. The GCP dissociates

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25
Q

How can B2 agonists stimulate inflammation?

A

activation via Gq of PLC and B-arrestin-2 (which acts via p38 and PI3K)

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26
Q

Other effects of B2 agonists?

A

-inhibition of mast cell mediator release (only acutely)-inhibition of microvascular permeability increase and protein leakage-increase in mucociliary clearance

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27
Q

How do B2 agonists increase mucociliary clearance?

A

increasing frequency of cilia beating

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28
Q

What else do LABAs do?

A

increase transcription of glucocorticoid receptors (and glucocorticoids increase B2 receptor density)

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29
Q

AEs of B2 agonists?

A

-fall in BP and reflex tachycardia-Hypokalemia (prolonged QT) AT HIGH DOSE -NV, headache-agitation, convulsions, comaAlbuterol= TREMORS

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30
Q

What are the non-selective antimuscarinics?

A

-Atropine -Ipratropium (Adrovent= local contact in eyes can cause pupillary dilation and ironies in intra-ocular pressure)M1, M2, and M3 (3-5 hr duration)

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31
Q

What is a long acting (24hr) antimuscarinic?MAIN AE?

A

Tiotropium (Spiriva) binds mostly M3 (but does bind M1 and very little M2)CONSTIPATION and urinary retention

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32
Q

What are the effects of antimuscarinics?

A

-reduce smooth muscle contraction and mucus secretion

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33
Q

T or F. COMBINED use of antimuscarinics and B2 agonists provides a greater effect than individual use

A

T.

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34
Q

What are the AEs of of antimuscarinics?

A

-pupillary dilation and cycloplegia-constipation-urinary retention-tachycardia and confusion

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35
Q

Contraindications to antimuscarinics?

A

-glaucoma-stomach, bowel or urinary blockage-cardiac disease

36
Q

What are the methylxanthines?

A

-Aminophylline-Theophylline

37
Q

How do Methylxanthines work?

A

-increases cAMP-blocks adenosine -decrease inflammatory mediators

38
Q

Effects of Methylxanthines?

A

-bronchodilaiton-anti-inflammatory-increased CNS activity, gastric acid secretion, and skeletal strength -weak diuretic-inotropic and chronotropic effect

39
Q

T or F. At very low doses (1-5ug/ml) Theophylline will not produce bronchodilation or inhibit adenosine but will have anti-inflammatory effects

A

T. Induces the activity of histone deacetylase 2

40
Q

What are some AEs of Methylxanthines at 5-10ug/ml?

A

N/V, nervousness, headache, insomnia

41
Q

What are some AEs of Methylxanthines at 20+ug/ml?

A

-hypokalemia, vomiting-hypergylcemia-tremor-seizures -tachycardia and arrhythmia

42
Q

What are Methylxanthines best for?

A

nocturnal wheezing

43
Q

What does cromolyn sodium do?

A

-inhibits mast cell degranulation-alter Cl- channel activity-inhibits inflammation, cough, and reduced bronchial hypersensitivity in exercise- and antigen-induced asthma

44
Q

AEs of Cromolyn?

A

unpleasnat taste and irritation of trachea (rarely, chest pain, N/V)

45
Q

What are some glucocorticoids?

A

-Budesonide-Fluticasone-Budesonide-Mometasone-Dexamethasone

46
Q

How do glucocorticoids works?

A

-decrease the production go inflammatory cytokines-reduce mucus secretion and bronchial hypersensitivity-enhance B2 agonist effect

47
Q

What are some anti-inflammatory genes upregulated by glucocorticoids?

A

-SLPI-MKP-1-GILZ

48
Q

What are some inflammatory genes down-regulated by glucocorticoids?

A

-TNF-a-IL-6-CM-CSF-COX-2does this through histone deacetylase

49
Q

What else do glucocorticoids do?

A

reduce production of IL-4, IL-13 and IL-5 via reduced TH2 production by competiting with GATA-3 for import to the nucleus (carrier is importin-alpha) AND activate MAPK-1 dephosphoryase to dephosphorylate p38-MAPK and GATA-3 (thus inactivating them)

50
Q

What are the AEs of inhaled GCs?

A

-orophyarngeal candidiasis, hoarseness, and dry mouth-sore throat -decrease growth rates

51
Q

T or F. Inhaled GCs can increase bone mineral density in pre-menopausal women

A

T. They can Decrease it

52
Q

AEs of prolonged use of Oral GCs?

A

-adrenal crisis-glucose intolerance-Cataracts-increased BP and wet-growth retardation (in early phases only-will catch up)-Osteoporosis/penia

53
Q

Another potential AE of GCs is Cushingoid syndrome. What is this?

A

-wgt gain, especially abdomen,, face (men face), neck, and buffalo hump-muscle weakness-thin hair-acanthosis-high BP

54
Q

Glucocorticoids inhibit ____

A

Cytosolic Phospholipase A2 (via lipcortin, macrocortin, lipomodulin)NOT the main effect of anti-inflammatory effect!!! See card 49 for main effect

55
Q

Phospholipase A2 breaks down membrane phospholipids into what?

A

Arachidonic acid

56
Q

Action of ____ on arachidonic acid produces PGG2.

A

COX1/COX2

57
Q

Action of ____ on arachidonic acid produces LTA4.

A

5-LO (acts with FLAP to translocate to nucleus)

58
Q

What inhibits the action of 5-LO?

A

Zileuton

59
Q

What is the effect of PGD2?

A

produced by mast cells and has inflammatory effects on eosinophils (causes eosinophilia)

60
Q

What drug can block the DP2 receptor for PGD2 effect on TH2 cells?

A

Seratrodast

61
Q

What happens to LTA4?

A

it is taken up by neutrophils and can be converted to LTB4 and then it is taken up by other cells and converted to LTC4 (which is transported to the cell surface), LTD4, and then LTE4

62
Q

LTC4, LTD4, and LTE4 do what?

A

bronchoconstriction, mucosal edema, and increase capillary permeability (can lead to anaphylaxis)mimic symptoms of asthma

63
Q

What drug can block action of LTD4 (and some LTC4 and LTE4) at a leukotriene 1 receptor?

A

Zafirlukast or Monteleukast effective in some aspirin-induced asthma

64
Q

What is the role of LTB4?

A

neutrophil chemoattractant

65
Q

What are the AEs of Zafirlukast?

A

GI disturbances, mild headache, and elevation of liver enzymes

66
Q

What are the AEs of Monteleukast?

A

-GI disorders-Laryngitis, -Pharyngitis-Otitis and sinusitis-Viral infections

67
Q

What is the effect of Zileuton?

A

-decreases smooth muscle contraction, blood vessel permeability, and leukocyte migration

68
Q

AEs of Zileuton?

A

-elevated LFTs-CYP1A2 inhibitor

69
Q

DD interaction of Zileuton

A

need to reduce Theophylline

70
Q

How does Omalizumab work?

A

Binds to IgE and prevents binding (decreases allergic response)

71
Q

AEs of Omalizumab?

A

-serious allergic rxns-redness, bruising, stinging, injection site rxn -MI, arrhythmias

72
Q

What cells produce IL-5?

A

Th2, eosinophils, mast cells, and basophils

73
Q

What is the effect of Il-5?

A

-stimulates proliferation, differentiation, maturation, and migration of eosinophils -promotes AB formation-contributes to airway inflammation and remodeling

74
Q

What monoclonal ABs target IL-5?

A

Mepolizumab (helps in eosinophilic asthma patients)Reslizumab

75
Q

What is Mepolizumab used for?

A

With other agents for maintenance of severe asthma in 12+ yoa asthma patients (injected subQ 1/month)

76
Q

AEs of Mepolizumab?

A

-Headahce, back pain, fatigue-Shingles-Hypersensitivity rxns

77
Q

AEs of Reslizumab?

A

-Hypersensitivity rxsn, anaphylaxis (rare)

78
Q

What is a monoclonal Ab for IL-5 receptor binding?

A

Benralizumab

79
Q

What is a monoclonal Ab for IL-4 receptor binding?

A

Dupilumab

80
Q

What does Dupilumab do?

A

-blocks Il-4 and IL-13 action-produces marked reduction in asthma exacerbation and significant improvement in FEV1 in TH2 eosinophilic asthmamade for atopic dermatitis

81
Q

Levalbuterol is an alternative for albuterol in patients that experience consistent _____.

A

tachycardia (R-isomer= know for test)

82
Q

T or F. Corticosteroid response in COPD is good

A

F. It is good in asthma though (usually the damage is irreversible in COPD)

83
Q

What is a good option for smoking cessation?

A

Bupropion

84
Q

Main AE of inhaled Ipratropium?

A

dryness of mouth

85
Q

Osteopenia (large doses) is seen more in ____ corticosteroids

A

systemic (oral)

STEP Pharm II (42 decks)

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