OMK Week 16 Flashcards

Block 3 OMK OMS-I

Airflow Direction

Air moves from higher to lower pressure; no active transport of gases.

Driving Force Inspiration

Occurs when alveolar pressure drops below atmospheric pressure.

Driving Force Expiration

Occurs when alveolar pressure exceeds atmospheric pressure.

Boyle’s Law

Pressure and volume are inversely related in a closed system; increasing thoracic volume lowers alveolar pressure.

Intrapleural Pressure

Pressure in pleural space; normally negative due to opposing elastic forces of lungs (inward) and chest wall (outward).

Transmural Pressure

Transpulmonary pressure = alveolar − intrapleural pressure; maintains alveolar inflation; lungs collapse when zero.

Alveolar Pressure Rest

Equal to atmospheric at end of quiet breathing.

Intrapleural Pressure Rest

Approximately −4 mmHg; balances lung and chest wall recoil.

Alveolar Pressure Inspiration

About −1 mmHg; air flows inward.

Intrapleural Pressure Inspiration

Becomes more negative (≈−6 mmHg) to prevent lung collapse.

Alveolar Pressure Expiration

About +1 mmHg; air flows outward.

Transpulmonary Pressure Maximal Inspiration

Highest when alveoli are most distended.

Primary Muscles Inspiration

Diaphragm and external intercostals increase thoracic volume.

Accessory Muscles Inspiration

Sternocleidomastoid, scalenes, pectoralis minor elevate upper ribs and sternum.

Passive Expiration

Relies on elastic recoil of lungs and chest wall; no muscle contraction.

Active Expiration

Internal intercostals and abdominal muscles contract to force air out during exercise or disease.

Conducting Zone

Nasal cavity through terminal bronchioles; warms, humidifies, filters air; no gas exchange.

Respiratory Zone

Respiratory bronchioles to alveoli; site of gas exchange at alveolar-capillary interface.

Spirometric Volumes

Tidal = 500 mL; IRV, ERV, VC = TV + IRV + ERV; IC = TV + IRV.

Non-Spirometric Volumes

RV, FRC, TLC cannot be measured directly; require gas-dilution or body plethysmography.

Helium Dilution

Method using inert helium; change in concentration after equilibration allows FRC or RV calculation.

Elastic Recoil

Lung tendency to collapse due to elastin/collagen and surface tension opposed by outward chest wall force.

Pulmonary Surfactant

Phospholipid-protein mix from type II cells reducing surface tension, increasing compliance, preventing alveolar collapse.

Alveolar Interdependence

Shared walls tether alveoli; collapse of one resists due to surrounding tension; aided by pores of Kohn.

Compliance

ΔV/ΔP; measure of distensibility; lung ≈ 150–200 mL/cm H₂O; total ≈ 100 mL/cm H₂O.

Hysteresis

Difference between inflation and deflation compliance curves due to surfactant behavior.

High Compliance

Easy inflation, poor recoil (e.g., emphysema).

Low Compliance

Difficult inflation, strong recoil (e.g., fibrosis, IRDS).

Poiseuille’s Law

Flow = (ΔP π r⁴)/(8ηL); flow proportional to radius⁴; small radius change greatly alters airflow.

Airway Resistance

Raw = ΔP / flow; depends on radius, length, viscosity, airway generation, lung volume, and smooth-muscle tone.

Airway Resistance Lung Volume

High volumes open airways → lower resistance; low volumes narrow → higher resistance.

Laminar Flow

Streamlined, parallel flow in small airways; quiet breathing.

Turbulent Flow

Chaotic flow in large airways; increases resistance; associated with loud breath sounds.

Transitional Flow

Occurs at branch points or high inspiratory rates; mix of laminar and turbulent.

Dynamic Properties Inspiration

Diaphragm contracts → intrapleural pressure more negative → alveolar pressure falls → air in.

Dynamic Properties Expiration

Passive recoil → intrapleural pressure less negative → alveolar pressure exceeds atmosphere → air out.

Static Compliance

Elastic property measured with no airflow; decreased in fibrosis, increased in emphysema.

Dynamic Compliance

Measured during breathing; affected by elasticity and airway resistance; decreased in obstructive disease.

Dynamic Airway Compression

Positive pleural pressure during forced expiration compresses small bronchioles; limits flow.

Equal Pressure Point

Location where airway pressure = pleural pressure; distal collapse beyond EPP.

Work of Breathing

Elastic + airway + tissue resistance work; increased in restrictive (elastic) and obstructive (resistive) disease.

Autonomic Control Airway Resistance

Sympathetic β₂ → bronchodilation; parasympathetic M₃ → bronchoconstriction; basal tone maintained by vagus.

Sympathetic Activation

Epinephrine → β₂ receptors → ↑cAMP → bronchodilation, ↓mucus.

Parasympathetic Activation

ACh → M₃ receptors → IP₃/Ca²⁺ → bronchoconstriction, ↑mucus.

Pulmonary Stretch Receptors

Sense inflation; inhibit inspiration (Hering–Breuer reflex); cause bronchodilation; vagal afferents.

Irritant Receptors

Rapidly adapting; respond to smoke/dust; cause cough, bronchoconstriction, mucus; vagal afferents.

Juxtapulmonary Receptors

Located in alveolar capillaries; respond to edema/inflammation; cause tachypnea, dyspnea.

Pulmonary Function Tests Obstructive

↓FEV₁ and FVC, FEV₁/FVC < 0.7, ↑TLC RV FRC, scooped expiratory loop.

Pulmonary Function Tests Restrictive

↓FEV₁ and FVC, FEV₁/FVC normal or ↑, ↓TLC RV FRC, tall narrow loop.

Compliance Obstructive

Emphysema ↑ compliance (air trapping); Asthma ↓ dynamic compliance during attack.

Compliance Restrictive

Fibrosis ↓ compliance (stiff lungs); ↑ work of breathing.

Wheezes

Turbulent flow through narrowed airways; expiratory; asthma, COPD.

Crackles

Sudden reopening of collapsed alveoli or fluid; inspiratory; fibrosis, pneumonia, CHF.

Rhonchi

Low-pitched sounds from mucus in large airways; bronchitis.

Pleural Rub

Grating sound from inflamed pleura; heard in inspiration and expiration.

Stridor

High-pitched inspiratory sound from upper airway obstruction.

Atopy

Genetic predisposition to produce IgE to common allergens.

Atopic Asthma

Pathologic IgE-mediated hypersensitivity causing airway inflammation, remodeling, and hyperreactivity.

Sensitization Phase

Initial allergen exposure → Th2 activation (IL-4, IL-5, IL-13) → B-cell class switch → IgE → mast-cell arming.

Elicitation Phase

Re-exposure → allergen crosslinks IgE on mast cells → degranulation → histamine, PGs, LTs → bronchoconstriction.

Mast Cell Mediators

Histamine → vasodilation/bronchoconstriction; LTs/PGs → sustained bronchospasm; cytokines → eosinophil recruitment.

Adrenergic Receptors Lungs

β₂ → Gs → ↑cAMP → PKA → smooth-muscle relaxation (bronchodilation).

Cholinergic Receptors Lungs

M₃ → Gq → PLC → IP₃ → ↑Ca²⁺ → bronchoconstriction and mucus secretion.

Albuterol

Short-acting β₂ agonist; acute bronchospasm rescue; ↑cAMP → relaxes smooth muscle; AEs = tremor, palpitations, tachycardia.

Formoterol

Long-acting β₂ agonist (12–24 h); maintenance only with ICS; AEs = headache, muscle pain, exacerbation if alone.

Salmeterol

Long-acting β₂ agonist for control and prevention; AEs = tremor, arrhythmia; never monotherapy in asthma.

Ipratropium

Short-acting M₃ antagonist; COPD or adjunct asthma; ↓ACh-mediated bronchoconstriction; AEs = dry mouth, cough.

Tiotropium

Long-acting M₃ antagonist for COPD/asthma maintenance; AEs = dry mouth, constipation.

Theophylline

PDE inhibitor and adenosine antagonist → ↑cAMP bronchodilation; narrow TI; AEs = arrhythmia, seizures; CYP3A metabolism.

Fluticasone

Inhaled corticosteroid; inhibits COX-2 and cytokines (IL-4, IL-5); first-line controller; AEs = oral thrush, hoarseness, growth delay.

Budesonide

ICS reducing inflammation and eosinophilia; AEs = thrush, hoarseness; rinse mouth post-use.

Cromolyn

Mast-cell stabilizer; blocks Ca²⁺ influx → prevents degranulation; prophylactic only; AEs = throat irritation, bad taste.

Zileuton

5-lipoxygenase inhibitor → ↓ LTB₄ LTC₄ LTD₄; used chronic asthma; AEs = hepatotoxicity, insomnia, psychiatric effects.

Montelukast

CysLT₁ receptor antagonist; blocks leukotriene-mediated bronchoconstriction; use for asthma and allergic rhinitis; AEs = headache, Churg-Strauss, neuropsychiatric events.

Omalizumab

Anti-IgE monoclonal antibody; binds free IgE → prevents mast-cell sensitization; severe allergic asthma; AEs = anaphylaxis, injection reaction.

ICS Mechanism

Bind glucocorticoid receptor → ↓IL-4/IL-5 production, ↓eosinophils, ↑β₂ receptor expression.

LABA Mechanism

Stimulate β₂ receptor → Gs → ↑cAMP → PKA → smooth-muscle relaxation.

Anticholinergic Mechanism

Block M₃ receptors → inhibit IP₃-mediated Ca²⁺ release → bronchodilation and ↓mucus.

Leukotriene Modifier Mechanism

Zileuton blocks synthesis; Montelukast blocks receptor; both ↓ bronchoconstriction and inflammation.

Methylxanthine Mechanism

Inhibits PDE → ↑cAMP and blocks adenosine → bronchodilation.

Asthma Step 1

Intermittent symptoms <2 days/week → PRN albuterol.

Asthma Step 2

Mild persistent → low-dose ICS.

Asthma Step 3

Moderate persistent → ICS + LABA.

Asthma Step 4

Severe persistent → high-dose ICS + LABA ± LTRA or omalizumab.

Acute Asthma Treatment

Inhaled SABA, oxygen, systemic steroids if severe, add ipratropium as needed.

Asthma Diagnostic Test

Methacholine challenge (M₃ agonist) provokes bronchoconstriction to confirm hyperreactivity.

Drug Pregnancy Safety

ICS safe; β₂ agonists generally safe; avoid theophylline toxicity; avoid tetracyclines.

Drug Pediatric Use

ICS and SABA safe; LABA only with ICS; monitor growth on steroids.

Drug Contraindications

Theophylline in arrhythmia/seizure; Zileuton in liver disease; LABA monotherapy in asthma contraindicated.

Drug Interactions

Theophylline metabolized by CYP3A (erythromycin, ciprofloxacin ↑ levels); Zileuton ↑ warfarin and theophylline.

Asthma Pathologic Changes

Smooth muscle hyperplasia, basement-membrane thickening, goblet cell hyperplasia, mucus plugging, eosinophilic infiltration.

IL-25 and IL-33 Function

Epithelial alarmins enhancing mast cell degranulation and Th2 cytokine production.

Distal Airway Resistance

Main site of increased resistance due to smooth muscle hyperplasia, fibrosis, and mucus buildup.