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

Pharmacology Histamines/Drugs&Delivery/PAH Flashcards

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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
Pulmonary issues treated with anti cancer agents
SCLC, NSCLC, Adenocarcinoma, Squamous cell
26
Treatment of Pneumoconiosis
There is no curative treatment for deposited material; patients should avoid further exposure to causative agent (asbestos, silica, etc)
27
Drugs that can cause ARDS
aspirin, cocaine, opioids, phenothiazines, tricyclic antidepressants
28
Idiosyncratic drug reactions that cause ARDS
chemotherapeutics and radiologic contrast media
29
Alcohol abuse's role in ARDS
can increase risk of ARDS due to other causes such as sepsis and trauma, but it does not cause ARDS
30
Perfect drug treatment for ARDS
no drug has demonstrated a consistent and unequivocal benefit in the treatment of ARDS
31
Drugs used for ARDS
B2 agonists, albuterol IV, inhaled NO, inhaled PGI2, corticosteroids, dietary oil supplementation (anti-inflammatory action by modulation of arachidonic acid metabolism)
32
Most common cause of respiratory failure in newborns and death in premies
Newborn Respiratory Distress Sydnrome (NRDS) due to surfactant deficiency in immature lung tissue
33
Steroids MOA in NRDS
antenatal corticosteroids to all women at risk of delivery before 34 weeks; exogenous surfactant
34
Steroids MOA in NRDS
enhances maturational changes in fetal lung architecture and increases synthesis and release of surfactant
35
Poractant alfa, Calfactant, Beractant
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
Treatment of Sarcoidosis
Glucocorticoids or off label use of methotrexate
37
Glucocorticoid MOA
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
Adverse effects associated with chronic Corticosteroid use
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
Methotrexate MOA
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
Methotrexate adverse effects
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
Drugs that help with Idiopathic Pulmonary Fibrosis
not a chronic inflammatory disease, so even the most potent anti-inflammatory drugs have no therapeutic effect. No drugs have shown therapeutic benefit
42
Treatment of Goodpasture Syndrome
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
Treatment of Wegener's Granulomatosis
Rituximab, azathioprine, cyclophosphamide, corticosteroids
44
Rituximab MOA
immunsuppressing monoclonal AB that binds to CD20 on B cells - depleting the cell population for 6-9months
45
Azathioprine MOA
a DNA and RNA synthesis inhibitor that also produces immunosuppression, possibly by facilitating apoptosis of T cell populations
46
Cyclophosphamide MOA
an alkylating agent that also produces Ba and T cell lymphopenia, selective suppression of B lymphocyte activity and decreased immunoglobulin secretion
47
Rituximab toxicities
hypertension, asthenia, pruritis, urticarial, rhinitis, arthralgia
48
Azathioprine toxicities
neoplastic, mutagenic, leukopenic, and thromboytopenic toxicity. Increases risk of infection
49
Cyclophosphamide toxicities
Associated with neutropenia, thrombocytopenia, bladder cancer, myeloproliferative or lymphoproliferative malignancies
50
Prostanoids
induce pulmonary artery vasodilation, retard smooth muscle growth and disrupt platelet aggregation; Epoprostenol, Iloprost, Treprostinil
51
Epoprostenol half life and administration
half life of 2-5 minutes; requires continuous IV infusion
52
Eproprostenol adverse effects
hypotension, muscle pains, HA, flushing; risk of catheter infection; monitor for bleeding, esp if receiving antithrombotics
53
Iloprost route and half life
half life 25 min. Requires 6-9 inhaled doses/day using approved pulmonary delivery device - takes 10 min/dose
54
Iliprost adverse effects
Hemoptysis, cough, flushing, HA, hypotension, muscle cramps, tongue/back pains; monitor for bleeding if receiving antithrombotics
55
Treprostinil route and administration
half life of 4 hours; contiuous SC (can be irritation) or IV infusion; more stable in solution
56
Treprostinil adverse effects
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
Endothelin-1 receptor antagonist MOA
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
Bosentan Route and Adverse effects
5-8hr half life; taken orally twice daily; AE: significantly elevated LFTs, anemia, nasopharyngitis, HA, extensive hepatic metabolism (CYP2C9 and CYP3A4 inducer), teratogen
59
Ambrisentan route and adverse effects
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
Endothelin 1 Receptor Antagonist drug list
Bosentan and Ambrisentan
61
Phosphodiesterase Type 5 Inhibitors
Sildenafil, Tadalafil; perpetuate endogenously generated cGMP leading to vasodilation and reduce cellular proliferation; not to used in patients taking organic nitrates
62
Sildenafil route and adverse effects
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
Tadalafil route and adverse effects
17hr half life; orally once daily; HA, back pain, dyspepsia, change in color vision (non-arteric anterior ischemic optic neuropathy NAION); CYP3A4 substrate
64
Calcium Channel Blockers MOA
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
Diltiazem immediate release route and adverse effects
3-6hr half life; orally three times/day; bradycardia, hypotension, HA, edema, CYP3A4 substrate
66
Nifedipine extended release route and adverse effects
2-5hr half life Orally once daily; flushing, edema, hypotension, heartburn, CYP3A4 substrate
67
Amlodipine route and adverse effects
35-50hr half life; orally once daily; edema, fatigue, hypotension, CYP3A4 substrate
68
Acetylcholinesterase inhibitors
used for myasthenia gravis, prevent the almost immediate metabolic degradation of acetylcholine. Increase secretions. Edrophonium and Neostigmine
69
Tricyclic antidepressants amitriptyline, desipramine effect on adrenergic agonists
prolong effect; block reuptake of drug and NE into nerve terminal
70
Monoamin Oxidase Inhibitors, selegilene, rasagilene effect on adrenergic agonists
prolong effect; block metabolism of amine by monoamine oxidase-B
71
Saquinavir with B2 agonist
promotes hypokalemia, QT prolongation, arrhythmias
72
Loop and Thiazide diuretics with B2 agonists
Predispose patient ot hypokalemia and increase likelihood of QT prolongation/arrhythmias - monitor serum K+
73
Non specific B blockers effects in asthmatics
removes the ability to treat acute bronchospasm with B2 agonist because the B1 and B2 cancel each other out

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