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Pharm III > Flood chapter 25: Resp pharmacology > Flashcards

Flood chapter 25: Resp pharmacology Flashcards

1
Q

Medications delivered to the lungs can have what effects

A

Direct effects on the airway
Systemic effects
Both direct and systemic

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2
Q

Pharm agents administered via the lungs allow for rapid uptake of drugs into ________or immediate ________

A

the blood stream

use by the cells of the airway

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3
Q

Action of inhaled anesthetics on the brain

A

Anesthesia

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4
Q

Action of inhaled anesthetics on the lungs

A

Bronchodilation

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5
Q

Direct effects of inhaled anesthetics

A

Bronchodilation from action on the lungs

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6
Q

Systemic effects of inhaled anesthetics

A

Anesthesia from action on the brain

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7
Q

Beta-adrenergic agonists delivered via aerosol exert direct effect on bronchial smooth muscle with few systemic effects. This would be an example of?

A

direct effect only

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8
Q

Drugs administered via airway are excellent for parenchymal diseases such as asthma and COPD because?

A

They take advantage of the rapid exposure to blood and pulmonary parenchymal cells.

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9
Q

Autonomic Nervous System (ANS) is divided into?

A

Divided into Sympathetic Nervous System (SNS) and Parasympathetic Nervous System (PNS)

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10
Q

Regulates airway caliber (diameter), airway, glandular activity and airway microvascular.

A

Parasympathetic Nervous System (PNS)

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11
Q

__________ provides the preganglionic fibers

A

Vagus Nerve

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12
Q

Preganglionic fibers synapse with postganglionic fibers in the_________

A

airway parasympathetic ganglia

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13
Q

Acetylcholine activates _____________ to produce bronchoconstriction.

A

the muscarinic (M3) receptor of postganglionic fibers of the PNS

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14
Q

Anticholinergics can provide bronchodilation even in the resting state because?

A

the PNS produces a basal level of resting bronchomotor tone.

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15
Q

Plays no direct role in control of airway muscle tone.

A

SNS

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16
Q

________ adrenergic receptors (a lot of them) are present on airway smooth muscle cells and cause bronchodilation (via stimulatory G mechanisms)

A

Beta-2

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17
Q

What is exact role of NANC?

A

Not well defined

It has excitatory and inhibitory neuropeptides that influence inflammation and smooth muscle tone respectively.

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18
Q

ANS also influences bronchomotor tone through

A

NANC system

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19
Q

the main inhibitory transmitters thought to be responsible for airway smooth muscle relaxation are?

A

Vasoactive Intestinal Peptide (VIP) and Nitric Oxide (NO)

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20
Q

The main excitatory transmitters shown to cause neurogenic inflammation, including bronchoconstriction are?

A

Substance P (SP) and Neurokinin A (NKA)

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21
Q

The mainstay therapy for bronchospasm, wheezing, and airflow obstruction is

A

Beta-adrenergic agonists.

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22
Q

Identify features of beta-adrenergic agonists used in clinical practice

A

Typically delivered via inhalers or nebulizers

Beta-2 selective

Divided into short and long acting therapies

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23
Q

Identify systemic adrenergic agonists

A

Terbutaline
Epinephrine
Albuterol

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24
Q

Identify short acting inhaled adrenergic agonists

A

Albuterol
Levalbuterol
Metaproterenol
Pirbuterol

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25
Q

Identify long acting inhaled adrenergic agonists

A

Salmeterol
Formoterol
Arformoterol

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26
Q

Name short acting Inhaled cholinergic antagonists

A

Ipratropium

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27
Q

Name long acting Inhaled cholinergic antagonists

A

Tiotropium

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28
Q

Name systemic cholinergic antagonists

A

Atropine
Scopolamine
Glycopyrrolate

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29
Q

Short acting Beta-2 Agonist Therapy is effective for

A

rapid relief of wheezing, bronchospasm and airflow obstruction.

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30
Q

____________ are used as maintenance therapy providing improved lung function and reduction in symptoms and exacerbations.

A

Long acting Beta-2 Agonists Therapy

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31
Q

Short acting Beta-2 agonists Bind to the Beta-2 adrenergic receptor located on the plasma membrane of

A

smooth muscle cells
epithelial
endothelial
and many other types of airway cells.

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32
Q

How does cAMP cause smooth muscle relaxation?

A

Not precisely known

Decreases in calcium release

Alterations in membrane potential

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33
Q

What unique properties allow for longer duration of action of LABA

A

Salmeterol has a longer duration because of a side that chain binds to the Beta-2 receptor and prolongs the activation of the receptor.

Formoterol has a lipophilic side chain allowing for interaction with the lipid bilayer of the plasma membrane. This allows a slow and steady release prolonging its duration of action.

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34
Q

Clinical effects of short acting B2 agonists is seen in minutes and lasts?

A

up to 4-6 hours.

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35
Q

Used primarily as rescue therapy

A

short acting B2 agonists

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36
Q

Long Acting B2 agonists are prescribed for?

A

Symptom control when short acting used > 2 x week

Combination therapy with inhaled corticosteroid where they are effective in reducing symptoms, reducing exacerbation and improving lung function while minimizing the dose of inhaled corticosteroids.

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37
Q

Combination therapy of LABA with inhaled corticosteroid are effective in

A

reducing symptoms

reducing exacerbation

improving lung function while minimizing the dose of inhaled corticosteroids.

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38
Q

B2 agonist side effects

A

Tremors

Tachycardia

Temporary reduction of PO2 of 5 mmHg In severe asthma

Hyperglycemia

Hypokalemia

Hypomagnesemia

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39
Q

Tremors and Tachycardia with B2 agonist is secondary to

A

Direct stimulation of the Beta-2 adrenergic receptor in skeletal muscle or vasculature.

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40
Q

Temporary reduction of PO2 of 5 mmHg In severe asthma with B2 agonist use is secondary to?

A

Beta-2 mediated vasodilation in poorly ventilated lung regions.

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41
Q

These side effects of B-2 agonist therapy tend to decrease with regular use.

A

Hyperglycemia

Hypokalemia

Hypomagnesemia

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42
Q

Beta-2 adrenergic Tolerance likely reflects?

A

Beta-2 adrenergic receptors down regulation

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43
Q

Withdrawal of a Beta-2 agonist after regular use can produce

A

transient bronchial hyperresponsiveness (exaggerated bronchial restriction)

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44
Q

_____ is not affected by B2 agonist tolerance

A

bronchodilation

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45
Q

Tolerance to Beta-2 agonists can occur with regular use over _______period

A

period of weeks

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46
Q

Evidence of Beta-2 agonists tolerance

A

Decrease in duration of bronchodilation

Decrease in magnitude of side effects (such as tremors and tachy etc.).

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47
Q

Use of _______ without concomitant use of a steroid inhaler as been shown to be associated with fatal and near-fatal asthma attacks.

A

long acting Beta-2 agonist therapy

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48
Q

Prudent to reserve long acting Beta-2 agonists for those pts who?

A

Are poorly controlled on inhaled steroids alone.

Have symptoms perilous enough to warrant the potential added risk.

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49
Q

B2 agonist Inhalation route should be first line treatment d/t

A

possibilities of side effects with IV formulations

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50
Q

The side effects of systemic adrenergic agonists is similar to inhalational adrenergic agonists with _________ being the most common.

A

tremors and tachy

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51
Q

Inhaled anticholinergics are used for

A

maintenance therapy and tx of acute exacerbations in obstructive disease

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52
Q

Use of _________ in COPD as maintenance and rescue therapy is standard treatment.

A

inhaled anticholinergics

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53
Q

Anticholinergics are used for maintenance therapy in asthma. True/False

A

False

Anticholinergics are NOT used for maintenance therapy in asthma. Only recommended for use in acute exacerbations.

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54
Q

3 subtypes of muscarinic receptors in the airway are

A

M2: Not targeted by inhaled anticholinergics

M1 and M3: Targets of inhaled anticholinergic therapy.

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55
Q

M2 receptors are responsible for?

A

Responsible for limiting production of Ach and protect against bronchoconstriction.

Is NOT the target of inhaled anticholinergic, but is antagonized by them.

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56
Q

Muscarinic 1 (M1) and Muscarinic 3 (M3): These receptors are responsible for

A

bronchoconstriction and mucus production and are the targets of inhaled anticholinergic therapy.

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57
Q

M1 and M3 receptor action

A

Acetylcholine binds to the M3 and M1 receptors and causes smooth muscle contraction.

This smooth muscle contraction is produced from increases in cyclic guanosine monophosphate (cGMP) or by activation of a G protein (Gq)

Gq activates phospholipase C to produce inositol triphosphate (IP3)

IP3 causes release of calcium from intracellular stores and activation of myosin light chain kinase causing smooth muscle contraction.

Anticholinergics inhibit this cascade and reduce smooth muscle tone by decreasing release of calcium from intracellular stores.

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58
Q

Ipratropium (Atrovent)

A

Classified as a short acting anticholinergic.

Commonly used as maintenance therapy for COPD.

Also used as rescue therapy or both COPD and asthmatic exacerbations (not indicated for routine management of asthma).

Ipratropium treatment increases in exercise tolerance, decrease in dyspnea, and improved gas exchange.

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59
Q

Tiotropium (Spiriva):

A

Only long acting anticholinergic available for COPD maintenance therapy.

Reduces COPD exacerbations, respiratory failure, and all-cause mortality

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60
Q

This drugs is associated with CV and CVA complications however, studies do not consistently support this claim

A

Tiotropium

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61
Q

Inhaled Anticholinergics _________ absorbed and serious side effects are uncommon

A

Poorly

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62
Q

Inflammatory cell types present in COPD

A

Neutrophils
macrophages
CD 8 + T lymphocytes
eosinophils

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63
Q

prominent cells in the inflammatory composition of Asthma

A

Eosinophils (Most)

mast cells (2nd most)

CD 4 + T lymphocytes

macrophages

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64
Q

Anti-Inflammatory response in COPD and asthma can be predicted by?

A

Inflammatory cell types present in sputum; biopsy specimens; and bronchoalveolar lavage fluid.

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65
Q

the primary target of ICS is?

A

Glucocorticoid receptor alpha (GRα) located in the cytoplasm of airway epithelial cells

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66
Q

In asthma, treatment with ICS will?

A

ICS reduces inflammatory changes associated with the disease.

Improves lung function; reducing exacerbations that result in hospitalization and death.

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67
Q

ICS treatment in COPD

A

ICS as a monotherapy is discouraged.

ICS are used in combination therapy with a long-actin B-adrenergic agonists (LABA).

The synergistic effect reduces inflammation

Combination of ICS and LABA are recommended for severe to very severe COPD pts.

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68
Q

ICS are added to the asthma regimen when ?

A

When there is an increase in frequency or severity of exacerbations

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69
Q

Evidence does show ICS decrease ___________ in asthma.

A

hospitalizations and deaths

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70
Q

Combination of ICS and LABA are recommended for

A

severe to very severe COPD pts.

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71
Q

ICS/LABA has been shown to improve mortality in COPD pts. T/F?

A

FALSE : It hasn’t been shown to improve mortality.

The combination has been reported to improve lung function and reduce exacerbations

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72
Q

Steroid receptor MOA

A

Steroid enters the cell through passive diffusion leading to binding of the steroid ligand to the glucocorticoid receptor alpha, dissociation of heat shock proteins, and subsequent translocation to the nucleus.

This complex can bind to promoter regions of DNA sequences and either induce or suppress gene expression.

Its can also Interact with transcription factors such as the one responsible for pro-inflammatory mediators (without binding to DNA) and repress expression of those genes

It can also affect chromatin structure; influence the winding of DNA; reduce access of RNA and thus reduce expression of inflammatory gene products

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73
Q

Passive diffusion of steroids into the cell allows for

A

Binding of the steroid ligand to the glucocorticoid receptor alpha.

Dissociation of heat shock proteins.

Subsequent translocation to the nucleus.

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74
Q

After translocation to the nucleus, the steroid- glucocorticoid receptor alpha complex can?

A

Bind to promoter regions of DNA sequences and either induce or suppress gene expression.

Interact with transcription factors such as the one responsible for pro-inflammatory mediators (without binding to DNA) and repress expression of those genes

Affect chromatin structure; influence the winding of DNA; reduce access of RNA and thus reduce expression of inflammatory gene products

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75
Q

ICS has reported increase in pneumonia and severe pneumonia in patients with?

A

COPD

However no reported increase in death

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76
Q

What are the side effects of ICS in patients with COPD and Asthma

A

candidiasis

pharyngitis

easy bruising

osteoporosis

cataracts

elevated intraocular pressure

dysphonia and growth retardation in children.

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77
Q

The recommended duration of Systemic corticosteroids in COPD patients should not exceed 2 weeks because

A

Side effects with No added benefit to longer duration.

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78
Q

In Asthma, systemic Corticosteroids are recommended for exacerbations that are?

A

Severe with a peak expiratory low of <40% of baseline.

Mild to moderate exacerbation with no immediate response to short acting Beta-adrenergic agonists.

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79
Q

Recommend duration for systemic corticosteroids in asthma is?

A

3-10 days without tapering.

80
Q

Some Asthma and COPD pts will receive long term oral corticosteroid therapy b/c?

A

their disease is difficult to manage

81
Q

SYSTEMIC CORTICOSTEROIDSSIDE EFFECTS

A 
Hptn
Hyperglycemia
Adrenal Suppression
Increased Infections
Cataracts
Dermal Thinning
Psychosis
PUD
82
Q

Arachidonic acid is converted to leukotrienes via?

A

the 5-lipoxygenase pathway

83
Q

What are the end products of the 5-lipoxygenase pathway.

A

Leukotrienes C4, D4 and E4

84
Q

Leukotrienes will cause?

A

bronchoconstriction

tissue edema

migration of eosinophils

increased airway secretions.

85
Q

2 types of leukotriene modifiers are?

A

Leukotriene Receptor Antagonists

Leukotriene Inhibitors i.e Zileuton

86
Q

antagonizes the 5-lipoxygenase inhibiting the production of leukotrienes

A

Leukotriene Inhibitors i.e Zileuton

87
Q

Leukotriene Modifiers therapeutic effects in asthma

A

Improve lung function

Reduce exacerbations

Used a long-term asthma therapy

88
Q

First line for long term treatment of asthma

A

ICS

ICS are superior to leukotriene modifiers for long term therapy and should be first line treatment. Both used together improve control of asthma symptoms as opposed to ICS alone.

89
Q

_________ is known to cause a reversible hepatitis in 2% - 4% of patients.

A

Zileuton

90
Q

An unclear link exists between _____________ and Churg-Strauss Syndrome

A

Leukotriene Antagonists

91
Q

A form of necrotizing vasculitis in which there is a prominent lung involvement with severe asthma, eosinophilia, and granulomatous reactions. Will have skin lesions that are tender SQ nodules and bruise like spots

A

Churg-Strauss Syndrome

92
Q

_____ stabilize submucosal and intraluminal mast cells

A

Mast Cell Stabilizers e.g. Cromolyn Sodium and Nedocromil

93
Q

MOA of mast cell stabilizers

A

They interfere with the antigen-dependent release of mediators, such as histamine and slow-reacting substances of anaphylaxis that cause bronchoconstriction, mucosal edema, and increased mucus secretions.

94
Q

Most common side effects of mast cell stabilizers are

A

GI upset
coughing
throat irritation

95
Q

used as preventative tx before exercise or known allergen exposure

A

Mast Cell Stabilizers e.g. Cromolyn Sodium and Nedocromil

96
Q

Mast Cell Stabilizers are not first line therapy for asthma but provides alternative tx when?

A

when conventional therapies are not optimal

97
Q

Nonselective inhibitor of phosphodiesterase and increases levels of cAMP and cGMP causing smooth muscle relaxation.

A

Theophylline

98
Q

Theophylline MOA

A

Nonselective inhibitor of phosphodiesterase and increases levels of cAMP and cGMP causing smooth muscle relaxation.

Antagonizes A1 and A2 adenosine receptors causing smooth muscle relaxation via inhibition of the release of histamine and leukotrienes from mast cells.

Activates histone deacetylase and reduces the expression of inflammatory genes.

Theophylline and aminophylline are reported to improve diaphragmatic function however data is inconsistent

99
Q

In asthma theophylline reduces ______

A

Reduces number of eosinophils in bronchial specimens and has anti-inflammatory effect

100
Q

In COPD theophylline reduces ______

A

reduces the number of neutrophils in sputum, and has an anti-inflammatory effect

101
Q

Theophylline is used as an alternative therapy for COPD and Asthma due to

A

Requires monitoring of blood levels

Side effects prominent at blood levels > 20 mg/L

102
Q

Most common side effects of Theophylline are?

A 
headache
nausea
vomiting
restlessness
abdominal discomfort
GERD
diuresis
103
Q

Most significant side effects of Theophylline are?

A

seizures
cardiac arrhythmias
death

104
Q

Inhaled anesthetic with most bronchodilation

A

Sevo

Sevo produces greater reduction in respiratory system resistance than Iso or halothane

105
Q

All inhaled anesthetic produce bronchodilation except

A

Desflurane

106
Q

Volatile Agents likely induce bronchodilation by

A

↓intracellular calcium, partly mediated by an ↑ in intracellular cAMP

↓ sensitivity of calcium mediated by protein kinase C.

107
Q

Volatile induced bronchodilation Effect is seen in distal airway smooth muscle secondary to?

A

T-type voltage-dependent calcium channel which is sensitive to volatile anesthetics.

108
Q

Limitations of using volatile anesthetics as sole agents for status asthmaticus are?

A

Potential although rare for MH

Hypotension

Issues using outside an OR

109
Q

Airway smooth muscles are relaxed when using which IV anesthetics

A

Propofol

Ketamine

Midazolam

110
Q

Etomidate or thiobarbiturates do not affect bronchomotor tone. T/F

A

True

111
Q

What is the mechanism of reduction of bronchomotor tone for IV Anesthetics?

A

Not known

Ketamine is thought to have a direct relaxant effect on smooth muscle.

Propofol is thought to reduce vagal tone and have a direct effect on muscarinic receptors by interfering with cellular signaling and inhibiting calcium mobilization

112
Q

_________ found in propofol prevents the inhibition of vagal-mediated bronchoconstriction.

A

The preservative metabisulfite

113
Q

Systemic Local anesthetics are Primarily used to?

A

suppress cough and blunt hemodynamic response to tracheal intubation.

Some studies suggest LA may cause bronchial smooth muscle relaxation, it is limited by toxicity and other more potent bronchodilators

114
Q

Reynolds number indicating mixture of laminar and turbulent flows

A

2,000 and 4,000

115
Q

Reynolds number indicating laminar flows

A

< 2,000

Air during quiet breathing are < 2,000 throughout most of the upper and lower airway

116
Q

Reynolds number associated with turbulent flow

A

> 4,000

117
Q

When a gas or liquid flows through a straight unbranched tube, flow will usually be laminar and resistance is directly proportional to _________ of the gas or liquid and inversely proportional to ______________

A

the viscosity

the radius (actually the 4th power of the radius).

(Poiseuille’s law)

118
Q

At very high flow rates or when gas flows through an irregular tube or orifice, flow tends to be more turbulent and resistance becomes proportional to _______________ of the gas and inversely proportional to _____________

A

the density

the radius (actually to the 5th power of the radius)

119
Q

A dimensionless number that allows estimation of whether a flow is turbulent or laminar

A

Reynolds Number (velocity x diameter x density / viscosity)

120
Q

Heliox

A

A combination of Helium and O2, (80%/20%) has a density approx. 0.33 that of air and 0.30 that of O2 .

Conditions of high turbulent flow in large airways due to a mass or edema, breathing a mixture of helium and oxygen (having a low Reynold’s Number) will decrease dyspnea for some patients.

Does not help in COPD or Asthma:

121
Q

__________ release from mast cells and basophils is responsible for airway inflammation and bronchoconstriction in asthma

A

Histamine

122
Q

ANTIHISTAMINES

A

Histamine release from mast cells and basophils is responsible for airway inflammation and bronchoconstriction in asthma

Not standard therapy for asthma. However using antihistamines and leukotrienes modifiers for allergen-induced bronchoconstriction has shown promise for diminishing early and late allergen responses

Allergen induced asthma or patients having an allergic reaction in the OR may benefit from antihistamines to attenuate the role that histamine plays in bronchconstriction.

123
Q

Magnesium Sulfate

A

Not standard therapy for asthma exacerbations

Can be used as in nebulized form for bronchodilation.

Not a first line drug

Potential benefit when nebulized with a Beta-adrenergic agonists

124
Q

The main principles of PHTN management are?

A

Reduce RV afterload

Preserve coronary perfusion

Avoid reduction in BP

125
Q

Patients with PHTN have High risk for ________ and ______________surgeries.

A

High risk for cardiac and non-cardiac surgeries.

126
Q

Patients with PHTN Have poor cardiorespiratory reserve and are at risk of pulmonary hypertension crisis resulting in

A

heart failure
respiratory failure
dysrhythmias

127
Q

Primary goal of Pulmonary Vasodilators is?

A

reducing the consequences of an elevated pulmonary vascular resistance and the resulting RV dysfunction.

(Attempting to improve contractility of the RV are generally not effective)

128
Q

An increase in PAP may be the result of

A

increased Peripheral Vascular Resistance (PVR)

increased CO

an increase in Left Arterial Pressure (LAP)

129
Q

[PVR X CO] + LAP

A

PAP

130
Q

N-methyl-D-aspartic acid (NMDA) receptor antagonist that also binds to opioid receptors and muscarinic receptors

A

Ketamine

131
Q

Ketamine should be used with caution in patients with PHTN because?

A

It is thought to cause pulmonary vasoconstriction

132
Q

Ketamine MOA

A

Not fully understood.

It is an N-methyl-D-aspartic acid (NMDA) receptor antagonist and also binds to opioid receptors and muscarinic receptors

Appears to stimulate release as well as inhibit neuronal uptake of catecholamines which may account for its cardiostimulatory and bronchodilatory effects.

133
Q

The hemodynamic effects of a bolus of Ketamine can be attenuated or abolished with premedicants such as

A

droperidol, dexmedetomidine, or benzodiazepines.

134
Q

The concern of using propofol in PHTN is?

A

The decrease in SVR which can effect intracardiac shunting (if present) and can lead to decreased in coronary artery perfusion of the RV resulting in RV dysfunction.

135
Q

In animal studies have shown that during increased tone conditions in the pulmonary vasculature propofol may act as _______________?

A

a pulmonary vasoconstrictor.

136
Q

Etomidate

A

Is an imidazole (2 of 5 atoms is Nitrogen) mediates clinical actions primarily at GGABA-A receptors

Appears to have vasorelaxant properties in isolated pulmonary arteries

Stable hemodynamic profile

Pts with cardiac disease: induction dose increases MAP, decreased SVR and decreased PAP

In Peds without PHTN no significant change in hemodynamics was shown with induction dose of etomidate.

137
Q

In pts with cardiac disease etomidate induction dose will?

A

increases MAP
decreased SVR
decreased PAP

138
Q

Nitrous oxide typically avoided in PHTN because?

A

It is believed to cause pulmonary vasoconstriction. This constriction may be release of catecholamines from sympathetic nerves supplying the pulmonary vasculature.

139
Q

Rocuronium, Cisatracruium and Vecuronium have little to no effect on most cardiac indices in pts undergoing CABG. T/F

A

True

140
Q

Magnesium use in PHTN

A

Vasodilator in both systemic and pulmonary circulations

MOA of mag ability to cause vasodilation is likely though its effects on membrane channels involved in calcium flux and through its action in the synthesis of cAMP.

Mag has been used with controversy to treat persistent PHTN of newborns

141
Q

Thoracic Epidural Anesthesia (TEA) may decrease PAP through?

A

decreases in CO or attenuation of pulmonary sympathetic outflow.

142
Q

TEA depresses ______ in acute PHTN

A

RV function

143
Q

Unilateral thoracic paravertebral block with lidocaine has been shown to decrease _____________ up to _________% and significantly decrease systemic pressure. This may be attenuated by using epinephrine

A

myocardial contractility

30%

144
Q

Decreases myocardial contractility up to 30% and significantly decrease systemic pressure.

A

Unilateral thoracic paravertebral block

145
Q

Can patients with PHTN receive regional and TEA?

A

YES

Potential benefits outweighs risks of hypotension and RV dysfunction

Pts with PHTN, careful titration and monitoring must be done.

146
Q

Neurotransmitter receptors of the pulmonary vasculature includes:

A 
Adrenergic
Cholinergic
Dopaminergic
Histamine
Serotonin
Adenosine
Purines
peptides
147
Q

Pulmonary vasculature

A

Sympathetic activation will generally result in an increase in PVR.

Administration of acetylcholine induces pulmonary relaxation.

Pts with chronic secondary PHTN undergoing anesthesia for cardiac surgery show norepinephrine and phenylephrine increase PAP and PVRI with minimal change in CI.

Norepinepherine decreases mPAP to MAP ratio but phenylephrine did not. This suggest phenylephrine may be a better choice of vasopressor

148
Q

Vasodilator in PHTN

A

rapid onset
short half-life
produce regional pulmonary vasodilation

This would:
Avoid systemic hypotension
Avoid potential adverse effect on ventilation perfusion matching that limit use of systemic agents in critically ill pts

Therefore inhaled vasodilators are attractive as they preferentially dilate ventilated alveoli and have less systemic effects.

149
Q

Ideal Pulmonary Vasodilator Should have

A

rapid onset
short half-life
produce regional pulmonary vasodilation

150
Q

Dose of iNO is controversial but typical doses are?

A

10-40 ppm

151
Q

Studies demonstrate NO reduces

A

need for extracorporeal membrane oxygenation (ECMO)

requirement for O2 therapy following ICU discharge

152
Q

Methemoglobin levels need to be monitored when NO is administered for ?

A

more than 24 hours.

153
Q

In theory, heart and lung transplant pts should benefit from NO due to

A

pulmonary vasodilation and related improvement of acute RV failure.

154
Q

Prostaglandins actions are

A

relaxation of vascular smooth muscle

inhibition of growth of smooth muscle cells

powerful inhibition of platelet aggregation.

155
Q

Epoprostenol

A

Prostaglandin delivered by nebulizer through a ventilator circuit.

It has a short T1/2 causing inefficiencies with nebulization.

156
Q

Synthetic drugs such as prostanoids, treprostinil, and iloprost are

A

Prostaglandins being researched as vasodilators and may only required intermittent administration.

157
Q

Prostacyclin can be delivered by nebulizer into a ventilator circuit at a starting dose of _________ with clinical effects evident within ________

A

50 ng/kg/min

10 minutes

158
Q

Inhaled prostacyclin decreases ________with maintenance of favorable systemic pressures but does not change PaO2 during one lung ventilation (OLV)

A

PVRI and PAP

159
Q

Prostaglandins and iNO have what in common

A

Both affect platelet function

Although clinical relevance of platelet inhibition with these inhaled agents is unknown, they could theoretically contribute to periop bleeding in large surgeries; also a concern with neuraxial analgesia

160
Q

MOA of phosphodiesterase inhibitors

A

Phosphodiesterase inhibitors prevent the degradation of cGMP and cAMP which are activated by NO and are intermediaries in a pathway that leads to vasodilation.
This vasodilation is via the activation of protein kinases, and reduction in cytosolic calcium.

161
Q

An adenosine-3’, 5’- cAMP-selective phosphodiesterase enzyme (PDE) inhibitor

A

Milrinone

162
Q

Milrinone

A

Is an adenosine-3’, 5’- cAMP-selective phosphodiesterase enzyme (PDE) inhibitor

Milrinone nebulized has shown to lead to a relative reduction in PVR compared to SVR

Milrinone selectively dilates the pulmonary vasculature without systemic effects.

Milrinone (+) inhaled prostacyclin demonstrates a potentiation and prolongation of the pulmonary vasodilation effect.

163
Q

Phosphodiesterase __________ have a higher expression in pulmonary circulation versus the systemic circulation and thus their inhibitors have a relative selective effect on PVR as opposed to SVR.

A

Phosphodiesterase 5 (PDE5)

164
Q

________ have been demonstrated to enhance effects of NO and may blunt rebound pulmonary pressure that occur during weaning off of inhaled NO.

A

Sildenafil

165
Q

All volatile anesthetics inhibit HPV in dose dependent fashion. Rank from the most to least inhibition.

A

halothane>enflurane>isoflurane/desflurane/sevoflurane

166
Q

What is the effect of IV anesthetics on hypoxic pulmonary vasoconstriction

A

IV anesthetic agents have no effect on Hypoxic Pulmonary Vasoconstriction (HPV)

167
Q

HPV

A

At 1 MAC ISO, SEVO, DES are weak and equipotent HPV inhibitors

Nitrous inhibits HPV and is usually avoided during thoracic anesthesia

HPV decreased by vasodilators such as NTG and Nitroprusside.

Thoracic epidural sympathetic blockade probably has little or no direct effect on HPV

Thoracic epidural anesthesia can have an indirect effect on O2 if hypotension is allowed and a fall in CO

168
Q

Lungs

A

Receive essentially entire CO and has enormous vasculature bed surface area (70 – 100 m2 ).

Contain nearly half body’s endothelium

High perfusion of 14 ml/min/g tissue (next highest is renal at 4 ml/min/g tissue

169
Q

Lung perfusion in ml/min/g

A

14 ml/min/g tissue

170
Q

Pulmonary Uptake (or extraction)

A

is used to describe transfer from blood to lung: Does not indicate if the substance is metabolized for returned back to the blood with or without alteration.

171
Q

First Pass Uptake

A

describes the amount of substance removed from the blood on the first cycle through the lungs

172
Q

Clearance

A

describes a substance undergoing actual elimination

173
Q

Lung Effects

A

Lungs has a pronounced impact on the blood concentration of substances even when does not secrete or break down these substances

Happens because of simple uptake and retention of substances, often followed by release back into the blood

Capacitor Effect: a rapid rise or fall in concentration is attenuated

174
Q

Lungs found to have substantial concentration of Cytochrome P 450.
These are particularly located within?

A

Type II pneumocytes

Clara cells

Endothelial cells

175
Q

The activity of Cytochrome P 450 in the lungs are very small to ______ % of that of the liver

A

33%

176
Q

Compare first pass of opioids

A

Fentanyl has a first pass uptake of up to 90%.

Sufentanil demonstrates an first pass uptake a little more than half of Fentanyl

Morphine is about 10% first pass uptake

177
Q

Lidocaine first pass

A

Lidocaine: first pass uptake is ~ 50% with significant retention at 10 minutes.

Lidocaine demonstrates increased uptake with higher blood pH.

178
Q

Compare first pass of thiopental, ketamine and propofol

A

Thiopental ~ 15% first pass with little or no metabolism

Ketamine little less than 10% without metabolism

Propofol is thought to be 30% first pass and negligible metabolism by the lungs

179
Q

The lungs play a critical role in renin-angiotensin system because?

A

High concentrations of angiotensin-converting enzyme (ACE) reside in the pulmonary endothelium.

180
Q

Angiotensin formation

A

Kidney responds to changes in physiologic changes such as vascular volume, BP and adrenergic stimulation by the cleaving of prorenin, the resultant “renin” catalyzes the formation of angiotensin I from angiotensinogen.

ACE then converts angiotensin I to the vasoconstrictor angiotensin II

Angiotensin II is not taken up or further metabolized by the endothelial cell but immediately retuned to the blood.

Thus ACE inhibitors have been useful for systemic hypertension

181
Q

Bradykinin is produced from_________ through the action of _______.

A

kininogen

plasma kallikrein

182
Q

Bradykinins effects include:

A

Antithrombotic

Profibrinolytic activity in the coagulation s system

Modulation of NO and prostacyclin release

183
Q

Bradykinins metabolism

A

Its metabolized by several petidases

184
Q

Bradykinin eliminated

A

It is eliminated on first pass through the lungs

185
Q

Bradykinin in Lung

A

Bradykinin has a vasodilating effect on normal pulmonary vessels

Bradykinin is vasoconstriction in destroyed pulmonary endothelium

Bradykinin is a bronchoconstrictor

Side Effects of ACE inhibitors such as angioedema, cough, and some of the benefits such as decreased MI and improved renal function all involve modification of bradykinin metabolism.

186
Q

Norepinephrine demonstrates a ______to _____-% first-pass uptake. However, dopamine, isoproterenol, and epinephrine have essentially no uptake.

A

35% to 50%

187
Q

Biogenic amines are composed of?

A

Histamine

Serotonin (5-hydroxytryptamine or 5-HT);

Three naturally occurring catecholamines dopamine, norepinephrine, and epinephrine

188
Q

5-HT is produced predominately by.

A

the gastrointestinal tract’s chromaffin cells

189
Q

Ingested tryptophan undergoes a two-step conversion which is?

A

first by tryptophan-5-hydroxylase and then by L-amino acid decarboxylase to serotonin.

190
Q

Mast cells and neuroendocrine cells in the lung are also capable of producing serotonin by

A

uptake of tryptophan along the same enzymatic pathway.

191
Q

Once released from the gastrointestinal tract, there is avid uptake of 5-HT, particularly by

A

nerve endings and platelets.

192
Q

MAO inhibitors block the cytosolic metabolism of 5-HT but not its uptake, whereas several drugs, including volatile anesthetic agents, block __________

A

uptake but not intracellular metabolisms.

193
Q

________ is a useful marker of carcinoid syndrome with increased histamine turnover.

A

5-HIAA

194
Q

The pulmonary uptake of 5-HT by the lung is typically reported to be ___________ meaning that little 5-HT reaches the systemic vasculature under normal circumstances.

A

90% or greater

195
Q

In carcinoid the reason that the right heart shows the greatest myocardial and valvular injury in this syndrome is?

A

the right heart receives a high concentration of 5-HT before being extracted and metabolized by the pulmonary circulation.

Pharm III (11 decks)

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