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Pulmonary Block > Pharmacology Histamines/Drugs&Delivery/PAH > Flashcards

Pharmacology Histamines/Drugs&Delivery/PAH Flashcards

1
Q

Process of Histamine Release

A

IgE binds to mast cells which release histamine by exocytosis

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2
Q

Uses of H1 antagonists

A

Amelioration of allergy and hay fever symptoms; treatment of symptoms of insect bites and stings and contact flora poisoning; attenuation of motion sickness and vertigo

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3
Q

Side Effects of H1-antagonists

A

sedation, impaired cognition, decreased alertness, slowed reaction time, confusion, dizziness, dystonia, potentiation of nasal congestion

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4
Q

H1 Antagonists selectivity and specificity

A

They are highly selective for H1 but are not specific for that receptor
Diohenhydramine active muscarinic
Promethazine activate alpha and muscarinic

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5
Q

Side effects Second generation H1 antagonists

A

Mild cognitive disturbance; appetite stimulation

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6
Q

Uses of 2nd gen H1 antagonists

A

Relief of allergy and hay fever symptoms; treatment of symptoms from insect bites, stings, and contact with flora poisonings; attenuation of motion sickness and vertigo; treatment of asthma (experimental)

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7
Q

Fexofenadine (Allegra)

A

Strong H1 blockade; anti asthmatic; 8-24hr duration; hepatic metabolism?

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8
Q

Loratadine (Claritin)

A

Strong H1 blockade; anti asthmatic; 24hr duration

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9
Q

Cetirizine (Zyrtec)

A

Strong H1 blockade; slight sedation; anti asthmatic; 12 hr duration

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10
Q

Promethazine (phenagren)

A

Strong H1 blockade; highly sedative; highly anticholinergic; slight GI effects; 4-6hr duration

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11
Q

Diphenhydramine (Benadryl) and Dimendyrinate (Dramamine)

A

Strong H1 blockade; strong sedative; strong anticholinergic; slight GI effects; 4-6hr duration

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12
Q

Chlorpheniramine (Chlor-Trimeton)

A

Strong H1 blockade; mildly sedative; mild anticholinergic; mild GI effects; 4-6hr duration

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13
Q

Characteristics of first generation Antihistamines

A

Based on the structure of histamine, often short lived, multiple dosing, highly sedative, anticholinergic side effects

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14
Q

Histamine effect on vasulature

A

H1 mediated microvasodilation (also H2), capillary permeability, vasoconstriction

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15
Q

Histamine effect on lungs

A

H1 bronchoconstriction; H2 bronchodilation

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16
Q

Histamine effect on Neuro

A

H1, H3 nerve ending stimulation and wakefulness and sedation

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17
Q

H1 effect on endothelial cells and smooth muscle

A

smooth muscle contraction, stimulation of NO formation, endothelial cell contraction, increased vascular permeability

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18
Q

Sites of Histamine biosynthesis

A

Mast cells and basophils

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19
Q

Disadvantages of inhaled medium of drug delivery

A

expense, contamination possible, device preparation required before treatment, cleaning required after dose, not all medication available, less efficient (dead volume loss)

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20
Q

Benefits of inhalation drug therapy

A

lung is more permeable to macromolecules than any other portal, small molecules do not require complex metabolites, noninvasive route with quick onset of action

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21
Q

Practical issues with inhalers

A

Drug must be very small particles, patient must inhale correctly and size of aerosol is critical; 30-60% device efficiency; deposition in conducting airway; deposition in mouth and other epithelium causing adverse effects; epithelium is a barrier (think in trachea; thin in alveoli)

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22
Q

Mechanism of Absorption for Inhaled Drugs

A

Morer lipid soluble = more rapid absorption

Less ionized = more rapid

Insoluble compounds must use para-cellular route, pass through aqueous pores in intercellular tight junctions

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23
Q

Pulmonary issues treated with anti-inflammatory agent

A

Asthma, COPD, allergic rhinitis, restrictive lung disease, PAH

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24
Q

Pulmonary issues treated with anti-infective agents

A

Tuberculosis, Pneumonia (bacterial, fungal, viral)

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25
Q

Pulmonary issues treated with anti cancer agents

A

SCLC, NSCLC, Adenocarcinoma, Squamous cell

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26
Q

Treatment of Pneumoconiosis

A

There is no curative treatment for deposited material; patients should avoid further exposure to causative agent (asbestos, silica, etc)

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27
Q

Drugs that can cause ARDS

A

aspirin, cocaine, opioids, phenothiazines, tricyclic antidepressants

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28
Q

Idiosyncratic drug reactions that cause ARDS

A

chemotherapeutics and radiologic contrast media

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29
Q

Alcohol abuse’s role in ARDS

A

can increase risk of ARDS due to other causes such as sepsis and trauma, but it does not cause ARDS

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30
Q

Perfect drug treatment for ARDS

A

no drug has demonstrated a consistent and unequivocal benefit in the treatment of ARDS

31
Q

Drugs used for ARDS

A

B2 agonists, albuterol IV, inhaled NO, inhaled PGI2, corticosteroids, dietary oil supplementation (anti-inflammatory action by modulation of arachidonic acid metabolism)

32
Q

Most common cause of respiratory failure in newborns and death in premies

A

Newborn Respiratory Distress Sydnrome (NRDS) due to surfactant deficiency in immature lung tissue

33
Q

Steroids MOA in NRDS

A

antenatal corticosteroids to all women at risk of delivery before 34 weeks; exogenous surfactant

34
Q

Steroids MOA in NRDS

A

enhances maturational changes in fetal lung architecture and increases synthesis and release of surfactant

35
Q

Poractant alfa, Calfactant, Beractant

A

Exogenous surfactant that is from animal derived products rich in surfactant proteins B/C, neutral lipids, and Dipalmitoylphosphatidyl-choline (DPCC) which is the primary active component that lowers alveolar surface tension.

36
Q

Treatment of Sarcoidosis

A

Glucocorticoids or off label use of methotrexate

37
Q

Glucocorticoid MOA

A

most potent anti-inflammatory agent; bind to glucocorticoid receptors, modulating transcriptional regulation in the nucleus; inhibit production of IL-1beta and TNF while promoting production of anti-inflammatory cytokines like IL-10 by macrophages and dendritic cells; promote apoptosis of macrophages, dendrites, T cells, leading to inhibition of immune response

38
Q

Adverse effects associated with chronic Corticosteroid use

A

suppression of the hypothalamic pituitary adrenal (HPA) axis; osteoporosis, pancreatitis, steroid induced DM, cataracts, glaucoma, psychosis, oral candidiasis, other opportunistic infections, immunosuppression, weight gain, skin atrophy

39
Q

Methotrexate MOA

A

DHFR inhibition (antineoplastic); increases adenosine-mediation immunosuppression by causing intracellular AMP build up which causes increased extracellular Adenosine, leading to activation of A2 receptor, causing increased cAMP and immunosuppression

40
Q

Methotrexate adverse effects

A

not used as front-line therapy because: severe dermatologic reactions, birth defects, malignant lymphoma, increased risk of incection, potentially fatal pulmonary issues including acute or chronic interstitial pneumonitits and pulmonary fibrosis

41
Q

Drugs that help with Idiopathic Pulmonary Fibrosis

A

not a chronic inflammatory disease, so even the most potent anti-inflammatory drugs have no therapeutic effect. No drugs have shown therapeutic benefit

42
Q

Treatment of Goodpasture Syndrome

A

Treat with plasmapheresis since the disease is caused by Type II Hypersensitivity to alpha3-chain of type IV Collagen in basement membranes of kidney and lungs

43
Q

Treatment of Wegener’s Granulomatosis

A

Rituximab, azathioprine, cyclophosphamide, corticosteroids

44
Q

Rituximab MOA

A

immunsuppressing monoclonal AB that binds to CD20 on B cells - depleting the cell population for 6-9months

45
Q

Azathioprine MOA

A

a DNA and RNA synthesis inhibitor that also produces immunosuppression, possibly by facilitating apoptosis of T cell populations

46
Q

Cyclophosphamide MOA

A

an alkylating agent that also produces Ba and T cell lymphopenia, selective suppression of B lymphocyte activity and decreased immunoglobulin secretion

47
Q

Rituximab toxicities

A

hypertension, asthenia, pruritis, urticarial, rhinitis, arthralgia

48
Q

Azathioprine toxicities

A

neoplastic, mutagenic, leukopenic, and thromboytopenic toxicity. Increases risk of infection

49
Q

Cyclophosphamide toxicities

A

Associated with neutropenia, thrombocytopenia, bladder cancer, myeloproliferative or lymphoproliferative malignancies

50
Q

Prostanoids

A

induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation; Epoprostenol, Iloprost, Treprostinil

51
Q

Epoprostenol half life and administration

A

half life of 2-5 minutes; requires continuous IV infusion

52
Q

Eproprostenol adverse effects

A

hypotension, muscle pains, HA, flushing; risk of catheter infection; monitor for bleeding, esp if receiving antithrombotics

53
Q

Iloprost route and half life

A

half life 25 min. Requires 6-9 inhaled doses/day using approved pulmonary delivery device - takes 10 min/dose

54
Q

Iliprost adverse effects

A

Hemoptysis, cough, flushing, HA, hypotension, muscle cramps, tongue/back pains; monitor for bleeding if receiving antithrombotics

55
Q

Treprostinil route and administration

A

half life of 4 hours; contiuous SC (can be irritation) or IV infusion; more stable in solution

56
Q

Treprostinil adverse effects

A

injection site erythema, rash, pain, HA, N, diarrhea, vasodilation, jaw pain; monitor for bleeding w/ antithrombit users; CYP2C8 interactions (decrease clearance with gemfibrozil, increase clearance with rifampin)

57
Q

Endothelin-1 receptor antagonist MOA

A

block the smooth muscle proliferation and pulmonary arterial vasoconstriction produced by this vasoactive molecule up binding to type A (smooth muscle) and type B (endothelial cells) endothelin receptors

58
Q

Bosentan Route and Adverse effects

A

5-8hr half life; taken orally twice daily; AE: significantly elevated LFTs, anemia, nasopharyngitis, HA, extensive hepatic metabolism (CYP2C9 and CYP3A4 inducer), teratogen

59
Q

Ambrisentan route and adverse effects

A

15hr half life, taken orally once daily; cannot use in patients with hepatic dysfunction because it is major elimination route though no hepatoxicity; peripheral edema and HA; metabolized via CYP2C9, CYP3A4, OATP and P-gp

60
Q

Endothelin 1 Receptor Antagonist drug list

A

Bosentan and Ambrisentan

61
Q

Phosphodiesterase Type 5 Inhibitors

A

Sildenafil, Tadalafil; perpetuate endogenously generated cGMP leading to vasodilation and reduce cellular proliferation; not to used in patients taking organic nitrates

62
Q

Sildenafil route and adverse effects

A

3-4hr half life; orally or IVP three times/day; HA, epistaxis, flushing, insomnia, dyspepsia, dizziness, hearing loss, CYP3A4 and lesser so 2C9 substrate

63
Q

Tadalafil route and adverse effects

A

17hr half life; orally once daily; HA, back pain, dyspepsia, change in color vision (non-arteric anterior ischemic optic neuropathy NAION); CYP3A4 substrate

64
Q

Calcium Channel Blockers MOA

A

prevent access of calcium into cells during membrane depolarization, thus block the key mediator of smooth muscle contraction and permitting a vasodilation to occur; not all patients respond appropriately to these drugs

65
Q

Diltiazem immediate release route and adverse effects

A

3-6hr half life; orally three times/day; bradycardia, hypotension, HA, edema, CYP3A4 substrate

66
Q

Nifedipine extended release route and adverse effects

A

2-5hr half life Orally once daily; flushing, edema, hypotension, heartburn, CYP3A4 substrate

67
Q

Amlodipine route and adverse effects

A

35-50hr half life; orally once daily; edema, fatigue, hypotension, CYP3A4 substrate

68
Q

Acetylcholinesterase inhibitors

A

used for myasthenia gravis, prevent the almost immediate metabolic degradation of acetylcholine. Increase secretions. Edrophonium and Neostigmine

69
Q

Tricyclic antidepressants amitriptyline, desipramine effect on adrenergic agonists

A

prolong effect; block reuptake of drug and NE into nerve terminal

70
Q

Monoamin Oxidase Inhibitors, selegilene, rasagilene effect on adrenergic agonists

A

prolong effect; block metabolism of amine by monoamine oxidase-B

71
Q

Saquinavir with B2 agonist

A

promotes hypokalemia, QT prolongation, arrhythmias

72
Q

Loop and Thiazide diuretics with B2 agonists

A

Predispose patient ot hypokalemia and increase likelihood of QT prolongation/arrhythmias - monitor serum K+

73
Q

Non specific B blockers effects in asthmatics

A

removes the ability to treat acute bronchospasm with B2 agonist because the B1 and B2 cancel each other out

Pulmonary Block (8 decks)

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