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Pulmonary > ANS and Bronchial Tone > Flashcards

ANS and Bronchial Tone Flashcards

1
Q

Mechanism of Drug Absorption in Lung

A
  • Lipid soluble compounds via trans-cellular route
  • Insoluble compounds transverse the epithelium via para-cellular route in which they pass through the acquous pores in the intercellular tight jxn
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2
Q

What determines the rate at which molecules pass through?

A

Molecular weight and degree of ionization!

The less ionized a molecule, the faster its absorption rate, because it forms fewer interactions with the proteins and lipids that line the pore

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3
Q

Does the SNS innervate bronchial smooth muscle?

A

NO! The SNS does NOT directly innervate bronchial smooth musle.

  • Adrenergic receptors are found throughout the lung in airway SM, epithelial cells, mast cells, and type II alveolar cells.
  • **Sympathetic (B2) agonists and parasympathetic (M1-M3) antagonists produce relaxation of BSM and modulate bronchial secretions. **

The PNS assumes a dominat role

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4
Q

Which agonist/antagonists are used to control bronchospasm

A

B2 adrenergic agonists

Muscarinic antagonists

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5
Q

What is the mneumonic to remember the different G proteins for receptors?

A

Mnemonic: Qiss (kiss) and qiq (kick) till your siq (sick) of sqs (super qinky sex)

Sympathetic: Alpha 1 (Q), Alpha 2 (I), Beta 1 (S), Beta 2 (S)

Parasympathetic: M1 (Q), M2 (I), M3 (Q)

Dopamine: D1 (S) D2 (I)

Histamine: H1 (Q) H2 (S)

Vasopressin: V1 (Q) V2 (S)

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6
Q

Describe major functions of alpha-1

A
  • increase vascular smooth muscle contraction
  • increase pupillary dilator muscle contraction (mydriasis)
  • increase intestinal and bladder sphincter muscle contraction
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7
Q

Describe the major functions of alpha-2

A
  • Decreased sympathetic outflow
  • Decreased insulin release
  • Decreased lipolysis
  • Increased platelet aggregation
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8
Q

Describe the major functions of beta-1

A
  • increase heart rate
  • increase contractility
  • increase renin release
  • increase lipolysis
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9
Q

DESCRIBE THE MAJOR FUNCTIONS OF BETA-2*

A
  • vasodilation
  • bronchodilation
  • increase HR
  • increase contractility
  • increase lipolysis
  • increase insulin release
  • decrease uterine tone (tocolysis)
  • ciliary muscle relaxation
  • increase aqueous humor production
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10
Q

Describe the major functions of M1

A

CNS, enteric nervous system

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11
Q

Describe major functions of M2

A

Decrease HR and contractility of atria

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12
Q

DESCRIBE THE MAJOR ROLES OF M3*

A
  • increase exocrine gland secretions (e.g., lacriminal, salivary, gastric acid)
  • increase gut peristalsis
  • increase bladder contraction
  • bronchoconstriction
  • increase pupillary sphincter muscle contraction (miosis)
  • increase ciliary muscle contraction (accommodation)
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13
Q

Describe the major functions of dopamine receptors

A
  • D1: relaxes renal vascular smooth muscle
  • D2: modulates transmitter release, especially in brain
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14
Q

Describe the major functions of histmaine receptors

A
  • H1: increase nasal and bronchila mucus production, increase vascular permeability, contraction of bronchioles, pruritis, and pain
  • H2: increase gastric acid secretion
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15
Q

Describe the major functions of vasopressin receptors

A
  • V1: increase vascular smooth muscle contraction
  • V2: increase H20 permeability and reabsorption in the collecting tubules (“V2 is found in the 2 kidneys”)
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16
Q

Describe action on Gq receptors

A

Mnemonic: “HAVe 1 M&M”

  • H1, A1, V1, M1, M3

Act on Gq

Release of PLC, which converts PIP2 into IP3 and DAG

  • DAG stimulates PKC
  • IP3 leads to increaed intracellular calcium, which causes smooth muscle contraction
17
Q

Describe actions on Gs and Gi receptors

A

Mnemonic: “MAD 2’s”

  • M2, A2, D2 act on Gi, which inhibits Adenylyl Cyclase

B1, B2, D1, H2, V2 act on Gs which stimulatse Adenylyl cyclase, which converts ATP to cAMP. cAMP produces PKA which stimulates an increase in intracellular calcium within the heart, and inhibits myosin light-chain kinase in smooth muscle causing a decrease in intracellular calcium and relaxation.

18
Q

Muscarinic Antagonists

A
  • Non-selective drugs, like atropine and ipratropium, antagonize M2 and M3 receptors
  • Blocakde of M2 auto-receptors actually increases the release of endogenous ACh, which serves to partially offset any bronchodilatory drug effects.
  • Tiotropium, an agent that possess a functional selectivity for M1 and M3 receptors has higher muscarinic receptor binding affinity, longer duration of action, and slower onset of effect.
19
Q

If muscarinic receptors are responsible for increasing glandular secretions, then what class of drugs produces a drying/thickening of secretions?

A

ANTICHOLINERGIC DRUGS!

  • 1st generation antihistamines with anticholinergic activity: available as an OTC product in combination wtih NSAIDs and as a phenylephrine (vasoconstrictor used to treat rhinitis, coughs and colds)
  • Chlorpheniramine
  • Doxylamine
  • Diphenhydramine
20
Q

If muscarinic receptors are responsible for increasing glandular secretions, then what class of drugs produces an increase in secretions?

A
  1. Acetylcholinesterase inhibitors (prevent almost immediate metabolic degradation fo ACh)
  2. Edrophonium and Neostigmine
  3. Marijuana
21
Q

Beta-2 Adrenergic Agonists

A
  • B2 receptors predominate in the lung (70-80%)
  • The MAJOR response to administration of albuterol is relaxation of the bronchial smooth muscle and BRONCHODILATION
  • EFFECTIVE against early (bronchospastic) response to inhaled antigen. INEFFECTIVE against late (inflammatory) phase
  • B2 agonists, like M2 agonists, have the potential to produce bronchoconstriction, by increasing the PNS tone. Overall effect of B2 agonist therapy is therefore a balance between opposing forces.
22
Q

Describe the effects of Beta-2 Receptor Activation in Pulmonary Tissue

A
  • Mast cells: stimulation reduces histamine release
  • Mucociliary clearence: goblet cells and submucosal glands receive primarily PNS innervation
  • SNS effects from circulating epinephrine
  • alpha-agonists increase fluid secretion volume
  • Beta-agonist change compostion (increase glycoprotein)
  • Beta-agonist increase beta frequency of cilia, thereby facilitating mucociliary clearence
  • Vascular endothelial permeability: beta-2 adrenergic agonists decrease microvascular leakage and thus decrease airways obstruction in asthma
23
Q

Describe how beta receptor location along the lines of “one heart - two lungs” is an oversimplification

A

Oversimplification because beta-2 receptors exist in the heart and beta-1 receptors in the lung.

At high concentrations, beta-2 agonists produce:

  • CV stimulatory effects
  • Prolongation of the QT interval, especially in the presence of hypokalemia (avoid with drugs also producing hypokalemia)
  • Stimulation of skeletal muscle Na/K ATPase leads to increased intracellular K+ and **decreased serum K+ **(activity against ATPase thought to be responsible for muscle tremor/twitching/fasciculation experienced when taking B2 agonists)
24
Q

List the 3 most common types of drug interactions

A
  1. Drugs that prolong the pharmacologic effect of the adrenergic agonists (e.g. TCAs and MAOIs)
  2. Drugs that themselves produce hypokalemia, which, when combined with a beta-2 agonist would lead to additive toxicity (e.g. saquinavir, loop and thiazide diuretics)
  3. Non-speicifc beta-blockers (contraindicated in patients with asthma; remember nonselective antagonists mostly go from N to Z such as propranolol)
25
Q

What happens with too frequent a stimulation of the beta-receptor?

A

Internalization and loss of physiologic function (no receptors, no drug response)! This phenomenon also occurs with opiate therapy

  • Repeated stimulation of G-proteins results in phosphorylation by PKA and/or B-adrenergic receptor kinase.
  • B-arrestin binds to phosphorylated domain and blocks Gs binding, thereby decreasing adenylyl cyclase activity.
  • Binding of arrestin leads to endosomal localization of receptors, effectively neutralizing B-adrenergic activity.
  • Prolonged receptor occupancy can lead to down-regulation and eventual receptor degradation. Cells can also reduce receptor number by inhibiting transcription or translation of gene encoding receptor.
26
Q

What class of drugs leads to a renewed response to beta-2 agonists?

A

CORTICOSTEROIDS! Patients will recieve a short course of corticosteroids that increase transcriptional activity in favor of producing newly functional B2 receptors, thereby restoring drug sensitivity

Pulmonary (10 decks)

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