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Respiratory - First Aid Flashcards

1
Q

Lung Development

A
  • occurs in five stages
  • initial development includes development of lung bud from distal end of respiratory diverticulum during week 4
  • Every Pulmonologist Can See Alveoli.
    • Embryonic (weeks 4–7)
    • Pseudoglandular (weeks 5–17)
    • Canalicular (weeks 16–25)
    • Saccular (week 26–birth)
    • Alveolar (week 36–8 years)
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2
Q

Lung Development:

Embryonic (weeks 4–7)

A
  • lung bud → trachea → bronchial bud → mainstem bronchi → secondary (lobar) bronchi → tertiary (segmental) bronchi
  • errors at this stage can lead to tracheoesophageal fistula
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3
Q

Lung Development:

Saccular (week 26–birth)

A
  • alveolar ducts → terminal sacs
  • terminal sacs separated by 1° septae
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4
Q

Lung Development:

Alveolar (week 36–8 years)

A
  • terminal sacs → adult alveoli (due to 2° septation)
  • in utero, “breathing” occurs via aspiration and expulsion of amniotic fluid → ↑ vascular resistance through gestation
  • at birth, fluid gets replaced with air → ↓ in pulmonary vascular resistance
  • At birth: 20–70 million alveoli
  • By 8 years: 300–400 million alveoli
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5
Q

Congenital Lung Malformations:

  • poorly developed bronchial tree with abnormal histology
  • associated with congenital diaphragmatic hernia (usually left-sided) and bilateral renal agenesis (Potter sequence)
A

Pulmonary Hypoplasia

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6
Q

Congenital Lung Malformations:

  • caused by abnormal budding of the foregut and dilation of terminal or large bronchi
  • discrete, round, sharply defined, fluid-filled densities on CXR (air-filled if infected)
  • generally asymptomatic but can drain poorly, causing airway compression and/or recurrent respiratory infections
A

Bronchogenic Cysts

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7
Q

Respiratory Embryology:

  • nonciliated
  • low columnar/cuboidal with secretory granules
  • located in bronchioles
  • degrade toxins
  • secrete component of surfactant
  • act as reserve cells
A

Club Cells

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8
Q

Alveoli

A
  • Alveoli have ↑ tendency to collapse on expiration as radius ↓ (law of Laplace).
  • Pulmonary surfactant is a complex mix of lecithins, the most important of which is dipalmitoylphosphatidylcholine (DPPC).
  • Surfactant synthesis begins around week 20 of gestation, but mature levels are not achieved until around week 35.
  • Corticosteroids important for fetus surfactant production and lung development.
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9
Q

Alveolar Cell Types:

  • 97% of alveolar surfaces
  • line the alveoli
  • squamous
  • thin for optimal gas diffusion
A

Type I Pneumocytes

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10
Q

Alveolar Cell Types:

  • secrete surfactant from lamellar bodies → ↓ alveolar surface tension, prevents alveolar collapse, ↓ lung recoil, and ↑ compliance
  • cuboidal and clustered
  • also serve as precursors to type I cells and other type II cells
  • proliferate during lung damage
A

Type II Pneumocytes

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11
Q

Neonatal Respiratory Distress Syndrome

A
  • surfactant deficiency → ↑ surface tension → alveolar collapse (“ground-glass” appearance of lung fields)
  • Risk Factors:
    • prematurity
    • maternal diabetes (due to ↑ fetal insulin)
    • C-section delivery (↓ release of fetal glucocorticoids; less stressful than vaginal delivery)
  • Complications:
    • PDA
    • necrotizing enterocolitis
  • Treatment:
    • maternal steroids before birth
    • exogenous surfactant for infant
  • Therapeutic supplemental O2 can result in (RIB):
    • Retinopathy of prematurity
    • Intraventricular hemorrhage
    • Bronchopulmonary dysplasia
  • Screening Tests:
    • lecithinsphingomyelin (L/S) ratio in amniotic fluid(≥ 2 is healthy; < 1.5 predictive of NRDS)
    • foam stability index
    • surfactant-albumin ratio
  • persistently low O2 tension → risk of PDA
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12
Q

Respiratory Tree

A
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13
Q

Respiratory Tree:

Respiratory Zone

A
  • lung parenchyma
  • consists of respiratory bronchioles, alveolar ducts, and alveoli
  • participates in gas exchange
  • mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli
  • cilia terminate in respiratory bronchioles
  • alveolar macrophages clear debris and participate in immune response
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14
Q

Lung Anatomy

A
  • Right lung has 3 lobes.
  • Left has Less Lobes (2) and Lingula (homolog of right middle lobe).
  • Instead of a middle lobe, left lung has a space occupied by the heart.
  • Relation of the pulmonary artery to the bronchus at each lung hilum is described by RALS:
    • Right Anterior
    • Left Superior
  • Carina is posterior to ascending aorta and anteromedial to descending aorta.
  • Right lung is a more common site for inhaled foreign bodies because right main stem bronchus is wider, more vertical, and shorter than the left.
  • Aspiration:
    • while supine—usually enters right lower lobe
    • while lying on right side—usually enters right upper lobe
    • while upright—usually enters right lower lobe
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15
Q

Diaphragm Structures

A
  • Structures perforating diaphragm:
    • T8: IVC, right phrenic nerve
    • T10: esophagus, vagus (CN 10; 2 trunks)
    • T12: aorta (red), thoracic duct (white), azygos vein (blue) (“At T-1-2 it’s the red, white, and blue”)
    • I (IVC) ate (8) ten (10) eggs (esophagus) at (aorta) twelve (12).
  • Diaphragm is innervated by C3, 4, and 5 (phrenic nerve).
    • C3, 4, 5 keeps the diaphragm alive.
  • Pain from diaphragm irritation (eg. air, blood, or pus in peritoneal cavity) can be referred to shoulder (C5) and trapezius ridge (C3, 4).
  • Number of Letters = T Level:
    • T8: vena cava
    • T10: “oesophagus”
    • T12: aortic hiatus
  • Other bifurcations:
    • The common carotid bifourcates at C4.
    • The trachea bifourcates at T4.
    • The abdominal aorta bifourcates at L4.
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16
Q

Lung Volumes

A

A capacity is a sum of ≥ 2 physiologic volumes.

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17
Q

Lung Volumes:

air that can still be breathed in after normal inspiration

A

Inspiratory Reserve Volume

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18
Q

Lung Volumes:

  • air that moves into lung with each quiet inspiration
  • ttypically 500 mL
A

Tidal Volume

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19
Q

Lung Volumes:

air that can still be breathed out after normal expiration

A

Expiratory Reserve Volume

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20
Q

Lung Volumes:

  • air in lung after maximal expiration
  • _____ and any lung capacity that includes _____ cannot be measured by spirometry
A

Residual Volume

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21
Q

Lung Volumes:

  • IRV + TV
  • air that can be breathed in after normal exhalation
A

Inspiratory Capacity

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22
Q

Lung Volumes:

  • RV + ERV
  • volume of gas in lungs after normal expiration
A

Functional Residual Capacity

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23
Q

Lung Volumes:

  • TV + IRV + ERV
  • maximum volume of gas that can be expired after a maximal inspiration
A

Vital Capacity

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24
Q

Lung Volumes:

  • IRV + TV + ERV + RV
  • volume of gas present in lungs after a maximal inspiration
A

Total Lung Capacity

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25
Determination of Physiologic Dead Space
* VD = physiologic dead space * anatomic dead space of conducting airways plus alveolar dead space * apex of healthy lung is largest contributor of alveolar dead space * volume of inspired air that does not take part in gas exchange * VT = tidal volume * Paco2 = arterial Pco2 * Peco2 = expired air Pco2. * **T**aco, **Pa**co, **Pe**co, **Pa**co (refers to order of variables in equation) * Physiologic Dead Space * approximately equivalent to anatomic dead space in normal lungs * may be greater than anatomic dead space in lung diseases with V˙/Q˙ defects
26
Ventilation: * total volume of gas entering lungs per minute * VE = VT × RR
Minute Ventilation Normal Values: * Respiratory rate (RR) = 12–20 breaths/min * VT = 500 mL/breath * VD = 150 mL/breath
27
Ventilation: * volume of gas that reaches alveoli each minute * VA = (VT − VD) × RR
Alveolar Ventilation Normal Values: * Respiratory rate (RR) = 12–20 breaths/min * VT = 500 mL/breath * VD = 150 mL/breath
28
Lung and Chest Wall
* Elastic Recoil * tendency for lungs to collapse inward and chest wall to spring outward * At FRC, inward pull of lung is balanced by outward pull of chest wall, and system pressure is atmospheric. * At FRC, airway and alveolar pressures equal atmospheric pressure (called zero), and intrapleural pressure is negative (prevents atelectasis). * The inward pull of the lung is balanced by the outward pull of the chest wall. * System pressure is atmospheric. * PVR is at a minimum. * Compliance * change in lung volume for a change in pressure * expressed as ΔV/ΔP and is inversely proportional to wall stiffness * hig compliance = lung easier to fill (emphysema, normal aging) * lower compliance = lung harder to fill (pulmonary fibrosis, pneumonia, NRDS, pulmonary edema) * surfactant increases compliance * **Compliant** lungs **comply** (cooperate) and fill easily with air. * Hysteresis * lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation
29
Respiratory System Changes in the Elderly
* ↑ lung compliance (loss of elastic recoil) * ↓ chest wall compliance (↑ chest wall stiffness) * ↑ RV * ↓ FVC and FEV1 * Normal TLC * ↑ ventilation/perfusion mismatch * ↑ A-a gradient * ↓ respiratory muscle strength
30
Hemoglobin
* Hemoglobin (Hb) is composed of 4 polypeptide subunits (2α and 2β) and exists in 2 forms: * Deoxygenated form has low affinity for O2, thus promoting release/unloading of O2. * Oxygenated form has high affinity for O2 (300×). Hb exhibits positive cooperativity and negative allostery. * ↑ Cl−, H+, CO2, 2,3-BPG, and temperature favor deoxygenated form over oxygenated form (shifts dissociation curve right → ↑ O2 unloading). * Fetal Hb (2α and 2γ subunits) has a higher affinity for O2 than adult Hb, driving diffusion of oxygen across the placenta from mother to fetus. ↑ O2 affinity results from ↓ affinity of * HbF for 2,3-BPG. * Hemoglobin acts as buffer for H+ ions. * Myoglobin is composed of a single polypeptide chain associated with one heme moiety. Higher affinity for oxygen than Hb.
31
Hemoglobin Modifications
Lead to tissue hypoxia from ↓ O2 saturation and ↓ O2 content.
32
Hemoglobin Modifications: Methemoglobin
* Oxidized form of Hb (ferric, Fe3+), does not bind O2 as readily as Fe2+, but has ↑ affinity for cyanide. Fe2+ binds O**2**. * Iron in Hb is normally in a reduced state (ferro**us**, Fe2+; “just the **2** of **us**”). * Methemoglobinemia may present with cyanosis and chocolate-colored blood. * **Meth**emoglobinemia can be treated with **meth**ylene blue and vitamin C. * Nitrites (eg. from dietary intake or polluted/high altitude water sources) and benzocaine cause poisoning by oxidizing Fe2+ to Fe3+.
33
Hemoglobin Modifications: Carboxyhemoglobin
* Form of Hb bound to CO in place of O2. Causes ↓ oxygen-binding capacity with left shift in oxygen-hemoglobin dissociation curve. ↓ O2 unloading in tissues. * CO binds competitively to Hb and with 200× greater affinity than O2. * CO poisoning can present with headaches, dizziness, and cherry red skin. May be caused by fires, car exhaust, or gas heaters. Treat with 100% O2 and hyperbaric O2.
34
Cyanide Poisoning
* Usually due to inhalation injury (eg. fires). * Inhibits aerobic metabolism via complex IV inhibition → hypoxia unresponsive to supplemental O2 and ↑ anaerobic metabolism. * Findings: * almond breath odor * pink skin * cyanosis * Rapidly fatal if untreated. * Treat with induced methemoglobinemia: first give nitrites (oxidize hemoglobin to methemoglobin, which can trap cyanide as cyanmethemoglobin), then thiosulfates (convert cyanide to thiocyanate, which is renally excreted).
35
Oxygen-Hemoglobin Dissociation Curve
* Sigmoidal shape due to positive cooperativity (ie. tetrameric Hb molecule can bind 4 O2 molecules and has higher affinity for each subsequent O2 molecule bound). * Myoglobin is monomeric and thus does not show positive cooperativity; curve lacks sigmoidal appearance. * Shifting the curve to the right → ↓ Hb affinity for O2 (facilitates unloading of O2 to tissue) → ↑ P50 (higher Po2 required to maintain 50% saturation). * Shifting the curve to the left → ↓ O2 unloading → renal hypoxia → ↑ EPO synthesis → compensatory erythrocytosis. * Fetal Hb has higher affinity for O2 than adult Hb (due to low affinity for 2,3-BPG), so its dissociation curve is shifted left.
36
Oxygen Content of Blood
* O2 content = (1.34 × Hb × Sao2) + (0.003 × Pao2) * Hb = hemoglobin level * Sao2 = arterial O2 saturation * Pao2 = partial pressure of O2 in arterial blood * Normally 1 g Hb can bind 1.34 mL O2; normal Hb amount in blood is 15 g/dL. * O2 binding capacity ≈ 20.1 mL O2/dL of blood. * With ↓ Hb there is ↓ O2 content of arterial blood, but no change in O2 saturation and Pao2. * O2 delivery to tissues = cardiac output × O2 content of blood.
37
Pulmonary Circulation
* Normally a low-resistance, high-compliance system. Po2 and Pco2 exert opposite effects on pulmonary and systemic circulation. A ↓ in Pao2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung. * Perfusion Limited * O2 (normal health), CO2, N2O * gas equilibrates early along the length of the capillary * diffusion can be ↑ only if blood flow ↑ * Diffusion Limited * O2 (emphysema, fibrosis, exercise), CO * gas does not equilibrate by the time blood reaches the end of the capillary * A consequence of pulmonary hypertension is cor pulmonale and subsequent right ventricular failure.
38
Pulmonary Vascular Resistance
* Ppulm artery = pressure in pulmonary artery * PL atrium ≈ pulmonary capillary wedge pressure * Q = cardiac output (flow) * R = resistance * η = viscosity of blood * l = vessel length * r = vessel radius
39
Alveolar Gas Equation
* Pao2 = alveolar Po2 (mmHg) * PIo2 = Po2 in inspired air (mmHg) * Paco2 = arterial Pco2 (mmHg) * R = respiratory quotient = CO2 produced/O2 consumed * A-a gradient = Pao2 – Pao2 * ​Normal Range = 10–15 mm Hg * ↑ A-a gradient may occur in hypoxemia. * causes include shunting, V˙/Q˙ mismatch, and fibrosis (impairs diffusion)
40
Oxygen Deprivation: * ↓ cardiac output * hypoxemia * anemia * CO poisoning
Hypoxia (↓ O2 delivery to tissue)
41
Oxygen Deprivation: * Normal A-a gradient * high altitude * hypoventilation (eg. opioid use) * ↑ A-a gradient * V˙/Q˙ mismatch * diffusion limitation (eg. fibrosis) * right-to-left shunt
Hypoxemia (↓ Pao2)
42
Oxygen Deprivation: * impeded arterial flow * ↓ venous drainage
Ischemia (loss of blood flow)
43
Ventilation/Perfusion Mismatch
* Ideally, ventilation is matched to perfusion (ie. V˙/Q˙ = 1) for adequate gas exchange. * Lung zones: * V˙/Q˙ at apex of lung = 3 (wasted ventilation) * V˙/Q˙ at base of lung = 0.6 (wasted perfusion) * Both ventilation and perfusion are greater at the base of the lung than at the apex of the lung. * With exercise (↑ cardiac output), there is vasodilation of apical capillaries → V˙/Q˙ ratio approaches 1. * Certain organisms that thrive in high O2 (eg. TB) flourish in the apex. * V˙/Q˙ = **0** = “**o**irway” **o**bstruction (shunt). In shunt, 100% O2 does not improve Pao2 (eg. foreign body aspiration). * V˙/Q˙ = ∞ = blood flow obstruction (physiologic dead space). Assuming \< 100% dead space, 100% O2 improves Pao2 (eg. pulmonary embolus).
44
Carbon Dioxide Transport
* CO2 is transported from tissues to lungs in 3 forms: ① HCO3− (70%) ② Carbaminohemoglobin or HbCO2 (21–25%) * CO2 bound to Hb at N-terminus of globin (not heme) * CO2 favors deoxygenated form (O2 unloaded) ③ Dissolved CO2 (5–9%) * In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore, CO2 is released from RBCs (Haldane effect). * In peripheral tissue, ↑ H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect). * Majority of blood CO2 is carried as HCO3− in the plasma.
45
Response to High Altitude
* ↓ atmospheric oxygen (PO2) → ↓ Pao2 → ↑ ventilation → ↓ Paco2 → respiratory alkalosis → altitude sickness * chronic ↑ in ventilation * ↑ erythropoietin → ↑ Hct and Hb (due to chronic hypoxia) * ↑ 2,3-BPG (binds to Hb causing left shift so that Hb releases more O2) * cellular changes (↑ mitochondria) * ↑ renal excretion of HCO3− to compensate for respiratory alkalosis (can augment with acetazolamide) * chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH
46
Response to Exercise
* ↑ CO2 production * ↑ O2 consumption * ↑ ventilation rate to meet O2 demand * V˙/Q˙ ratio from apex to base becomes more uniform * ↑ pulmonary blood flow due to ↑ cardiac output * ↓ pH during strenuous exercise (2° to lactic acidosis) * no change in Pao2 and Paco2, but ↑ in venous CO2 content and ↓ in venous O2 content
47
Respiratory Pathology: * nose bleed * most commonly occurs in anterior segment of nostril (Kiesselbach plexus) * life-threatening hemorrhages occur in posterior segment (sphenopalatine artery, a branch of maxillary artery) * common causes include foreign body, trauma, allergic rhinitis, and nasal angiofibromas (common in adolescent males)
Epistaxis **Kiesselbach** drives his **Lexus** with his **LEGS**: * superior **L**abial artery * anterior and posterior **E**thmoidal arteries * **G**reater palatine artery * **S**phenopalatine artery
48
Deep Venous Thrombosis
* blood clot within a deep vein → swelling, redness, warmth, pain * Predisposed by Virchow triad (**SHE**): * **S**tasis (eg. post-op, long drive/flight) * **H**ypercoagulability (eg. defect in coagulation cascade proteins, such as factor V Leiden; oral contraceptive use) * **E**ndothelial damage (exposed collagen triggers clotting cascade) * d-dimer lab test used clinically to rule out DVT (high sensitivity, low specificity) * Most pulmonary emboli arise from proximal deep veins of the lower extremities. * Use unfractionated heparin or low-molecular-weight heparins (eg, enoxaparin) for prophylaxis and acute management. * Use oral anticoagulants (eg. warfarin, rivaroxaban) for treatment (long-term prevention). * Imaging test of choice is compression ultrasound with Doppler.
49
Pulmonary Emboli
* V˙/Q˙ mismatch, hypoxemia, and respiratory alkalosis * sudden-onset dyspnea, pleuritic chest pain, tachypnea, and tachycardia * Large emboli or saddle embolus may cause sudden death due to electromechanical dissociation. * Lines of Zahn are interdigitating areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death; help distinguish pre- and postmortem thrombi. * Types (**FAT BAT**): * **F**at * **A**ir * **T**hrombus * **B**acteria * **A**mniotic fluid * **T**umor * Fat Emboli * associated with long bone fractures and liposuction * classic triad of hypoxemia * neurologic abnormalities * petechial rash * Air Emboli * nitrogen bubbles precipitate in ascending divers (caisson disease/decompression sickness) * treat with hyperbaric O2 * can be iatrogenic 2° to invasive procedures (eg. central line placement) * Amniotic Fluid Emboli * can lead to DIC * especially postpartum * CT pulmonary angiography is imaging test of choice for PE (look for filling defects). * May have S1Q3T3 abnormality on ECG.
50
Flow-Volume Loops
51
Obstructive Lung Diseases
* obstruction of air flow → air trapping in lungs * airways close prematurely at high lung volumes → ↑ **FRC**, ↑ **RV**, ↑ **TLC** * PFTs: ↓↓ FEV1, ↓ FVC → ↓ FEV1/FVC ratio (hallmark), * V˙/Q˙ mismatch * Chronic, hypoxic pulmonary vasoconstriction can lead to cor pulmonale. * Chronic obstructive pulmonary disease (**COPD**) includes chronic bronchitis and emphysema. * “**FR**i**C**kin’ **RV** needs some increased **TLC**, but it’s hard with **COPD**!”
52
Obstructive Lung Diseases: * Findings: * wheezing, crackles, cyanosis (hypoxemia due to shunting), dyspnea, CO2 retention, 2° polycythemia * hypertrophy and hyperplasia of mucus-secreting glands in bronchi → Reid index (thickness of mucosal gland layer to thickness of wall between epithelium and cartilage) \> 50% * DLCO usually normal. * Diagnostic Criteria: * productive cough for \> 3 months in a year for \> 2 consecutive years
Chronic **B**ronchitis (“**b**lue **b**loater”)
53
Obstructive Lung Diseases: * Findings: * barrel-shaped chest, exhalation through pursed lips (increases airway pressure and prevents airway collapse) * Centriacinar * associated with smoking * frequently in upper lobes (smoke rises up) * Panacinar * associated with α1-antitrypsin deficiency * frequently in lower lobes * Enlargement of air spaces ↓ recoil, ↑ compliance, ↓ DLCO from destruction of alveolar walls. * Imbalance of proteases and antiproteases → ↑ elastase activity → ↑ loss of elastic fibers → ↑ lung compliance. * CXR: * ↑ AP diameter * flattened diaphragm * ↑ lung field lucency
Em**p**hysema (“**p**ink **p**uffer”)
54
Obstructive Lung Diseases: * Findings: * cough, wheezing, tachypnea, dyspnea, hypoxemia, ↓ inspiratory/expiratory ratio, pulsus paradoxus, mucus plugging * Triggers: * viral URIs * allergens * stress * Diagnosis is supported by spirometry and methacholine challenge. * hyperresponsive bronchi → reversible bronchoconstriction * smooth muscle hypertrophy and hyperplasia, Curschmann spirals (shed epithelium forms whorled mucous plugs), and Charcot-Leyden crystals (eosinophilic, hexagonal, double-pointed crystals formed from breakdown of eosinophils in sputum) * DLCO normal or ↑ * type I hypersensitivity reaction * Aspirin-induced _____ is a combination of COX inhibition (leukotriene overproduction → airway constriction), chronic sinusitis with nasal polyps, and _____ symptoms.
Asthma
55
Obstructive Lung Diseases: * Findings: * purulent sputum, recurrent infections, hemoptysis, digital clubbing * Chronic necrotizing infection of bronchi or obstruction Ž permanently dilated * airways. * Associated with bronchial * obstruction, poor ciliary * motility (eg, smoking, * Kartagener syndrome), * cystic fibrosis H, allergic * bronchopulmonary * aspergillosis.
Bronchiectasis
56
Restrictive Lung Diseases
* Restricted lung expansion causes ↓ lung volumes (↓ FVC and TLC). PFTs:↑ FEV1/FVC ratio. * Patient presents with short, shallow breaths. * Poor Breathing Mechanics (extrapulmonary, peripheral hypoventilation, normal A-a gradient): * Poor Structural Apparatus—scoliosis, morbid obesity * Poor Muscular Effort—polio, myasthenia gravis, Guillain-Barré syndrome * Interstitial Lung Diseases (pulmonary ↓ diffusing capacity, ↑ A-a gradient): * Pneumoconioses (eg. coal workers’ pneumoconiosis, silicosis, asbestosis) * Sarcoidosis: bilateral hilar lymphadenopathy, noncaseating granuloma; ↑ ACE and Ca2+ * Idiopathic Pulmonary Fibrosis (repeated cycles of lung injury and wound healing with ↑ collagen deposition, “honeycomb” lung appearance and digital clubbing) * Goodpasture Syndrome * Granulomatosis with Polyangiitis (Wegener) * Pulmonary Langerhans Cell Histiocytosis (eosinophilic granuloma) * Hypersensitivity Pneumonitis * Drug Toxicity (Bleomycin, Busulfan, Amiodarone, Methotrexate)
57
Respiratory Pathology: * mixed type III/IV hypersensitivity reaction to environmental antigen * causes dyspnea, cough, chest tightness, and headache * often seen in farmers and those exposed to birds * reversible in early stages if stimulus is avoided
Hypersensitivity Pneumonitis
58
Respiratory Pathology: * characterized by immune-mediated, widespread noncaseating granulomas, elevated serum ACE levels, and elevated CD4+/CD8+ ratio in bronchoalveolar lavage fluid * more common in African-American females * often asymptomatic except for enlarged lymph nodes findings on CXR of bilateral adenopathy and coarse reticular opacities * CT of the chest better demonstrates the extensive hilar and mediastinal adenopathy * Associated with: * Bell palsy * Uveitis * Granulomas (epithelioid, containing microscopic Schaumann and asteroid bodies) * Lupus pernio (skin lesions on face resembling lupus) * Interstitial fibrosis (restrictive lung disease) * Erythema nodosum * Rheumatoid arthritis-like arthropathy, * hypercalcemia (due to ↑ 1α-hydroxylase–mediated vitamin D activation in macrophages) * Treatment: steroids (if symptomatic)
Sarcoidosis A **facial droop** is **UGLIER**. * **Bell Palsy** * **U**veitis * **G**ranulomas * **L**upus pernio * **I**nterstitial fibrosis * **E**rythema nodosum * **R**heumatoid arthritis-like arthropathy
59
Respiratory Pathology: * complication of smoke inhalation from fires or other noxious substances * caused by heat, particulates (\< 1 μm diameter), r irritants (eg. NH3) → chemical tracheobronchitis, edema, pneumonia, and ARDS * many patients present 2° to burns, CO inhalation, cyanide poisoning, or arsenic poisoning * singed nasal hairs common on exam * bronchoscopy shows severe edema, congestion of bronchus, and soot deposition
Inhalation Injury and Sequelae
60
Pneumoconioses
* **Asbestos** is from the **roof** (was common in insulation), but affects the **base** (lower lobes). * **Silica** and **coal** are from the **base** (earth), but affect the **roof** (upper lobes).
61
Pneumoconioses: * associated with shipbuilding, roofing, and plumbing * “ivory white,” calcified, supradiaphragmatic and pleural plaques are pathognomonic * risk of bronchogenic carcinoma \> risk of mesothelioma * affects lower lobes * ferruginous bodies are golden-brown fusiform rods resembling dumbbells, found in alveolar sputum sample, visualized using Prussian blue stain, often obtained by bronchoalveolar lavage * ↑ risk of pleural effusions
Asbestosis
62
Pneumoconioses: * associated with exposure to beryllium in aerospace and manufacturing industries * granulomatous (noncaseating) on histology and therefore occasionally responsive to steroids * ↑ risk of cancer and cor pulmonale * affects upper lobes
Berylliosis
63
Pneumoconioses: * prolonged coal dust exposure → macrophages laden with carbon → inflammation and fibrosis * also known as black lung disease * ↑ risk for Caplan syndrome (rheumatoid arthritis and pneumoconioses with intrapulmonary nodules) * affects upper lobes * small, rounded nodular opacities seen on imaging
Coal Workers’ Pneumoconiosis
64
Pneumoconioses: asymptomatic condition found in many urban dwellers exposed to sooty air
Anthracosis
65
Pneumoconioses: * associated with sandblasting, foundries, and mines * macrophages respond to silica and release fibrogenic factors, leading to fibrosis * it is thought that silica may disrupt phagolysosomes and impair macrophages, increasing susceptibility to TB * ↑ risk of cancer, cor pulmonale, and Caplan syndrome * affects upper lobes * “eggshell” calcification of hilar lymph nodes on CXR
Silicosis The **silly** **egg** **sand**wich I **found** is **mine**!
66
Respiratory Pathology: * malignancy of the pleura associated with asbestosis * may result in hemorrhagic pleural effusion (exudative) and pleural thickening * Psammoma bodies seen on histology * Calretinin ⊕ in almost all \_\_\_\_\_, ⊝ in most carcinomas * smoking not a risk factor
Mesothelioma
67
Respiratory Pathology: * alveolar insult → release of pro-inflammatory cytokines → neutrophil recruitment, activation, and release of toxic mediators (eg. reactive oxygen species, proteases, etc.) → capillary endothelial damage and ↑ vessel permeability → leakage of protein-rich fluid into alveoli → formation of intra-alveolar hyaline membranes and noncardiogenic pulmonary edema (normal PCWP) * loss of surfactant also contributes to alveolar collapse * caused by sepsis (most common), aspiration, pneumonia, trauma, and pancreatitis * diagnosis of exclusion with the following criteria: * abnormal chest X-ray (bilateral lung opacities) * respiratory failure within 1 week of alveolar insult * decreased Pao2/Fio2 (ratio \< 300, hypoxemia due to ↑ intrapulmonary shunting and diffusion abnormalities) * symptoms of respiratory failure are not due to HF/fluid overload * causes impaired gas exchange, ↓ lung compliance and pulmonary hypertension * treat the underlying cause * Mechanical Ventilation: * ↓ tidal volumes * ↑ PEEP
Acute Respiratory Distress Syndrome **ARDS**: * **A**bnormal chest X-ray (bilateral lung opacities) * **R**espiratory failure within 1 week of alveolar insult * **D**ecreased Pao2/Fio2 (ratio \< 300, hypoxemia due to ↑ intrapulmonary shunting and diffusion abnormalities) * **S**ymptoms of respiratory failure are not due to HF/fluid overload
68
Sleep Apnea: * aespiratory effort against airway obstruction * associated with obesity, loud snoring, and daytime sleepiness * caused by excess parapharyngeal tissue in adults and adenotonsillar hypertrophy in * children * Treatment: * weight loss * CPAP * surgery
Obstructive sleep Apnea
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Sleep Apnea: * impaired respiratory effort due to CNS injury/toxicity, HF, and opioids * may be associated with Cheyne-Stokes respirations (oscillations between apnea and hyperpnea) * treat with positive airway pressure
Central Sleep Apnea
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Sleep Apnea: * obesity (BMI ≥ 30 kg/m2) → hypoventilation → ↑ Paco2 during waking hours (retention); ↓ Pao2 and ↑ Paco2 during sleep * also known as Pickwickian syndrome
Obesity Hypoventilation Syndrome
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Respiratory Pathology: * results in arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries, and plexiform lesions * Course: * severe respiratory distress → cyanosis and RVH → death from decompensated cor pulmonale
Pulmonary Hypertension (≥ 25 mm Hg) * normal mean pulmonary artery pressure = 10–14 mmHg
72
Pulmonary Hypertension: * oten idiopathic * heritable PAH can be due to an inactivating mutation in BMPR2 gene (normally inhibits vascular smooth muscle proliferation); poor prognosis * pulmonary vasculature endothelial dysfunction results in ↑ vasoconstrictors (eg. endothelin) and ↓ vasodilators (eg. NO and prostacyclins) * other causes include drugs (eg. amphetamines, cocaine), connective tissue disease, HIV infection, portal hypertension, congenital heart disease, and schistosomiasis
Pulmonary Arterial Hypertension
73
Lung—Physical findings
74
Pleural Effusions: * ↓ protein content * due to ↑ hydrostatic pressure (eg. HF) or ↓ oncotic pressure (eg. nephrotic syndrome, cirrhosis)
Transudate
75
Pleural Effusions: * ↑ protein content, cloudy * due to malignancy, pneumonia, collagen vascular disease, and trauma (occurs in states of ↑ vascular permeability) * must be drained due to risk of infection
Exudate
76
Pleural Effusions: * also known as chylothorax * due to thoracic duct injury from trauma or malignancy * milky-appearing fluid * ↑ triglycerides
Lymphatic
77
Pneumothorax: * due to rupture of apical subpleural bleb or cysts * occurs most frequently in tall, thin, young males and smokers
Primary Spontaneous Pneumothorax
78
Pneumothorax: * diseased lung (eg. bullae in emphysema, infections) * mechanical ventilation with use of high pressures → barotrauma
Secondary Spontaneous Pneumothorax
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Pneumothorax: * air enters pleural space but cannot exit → increasing trapped air * trachea deviates away from affected lung * needs immediate needle decompression and chest tube placement * may lead to ↑ intrathoracic pressure → ↓ venous return → ↓ cardiac function
Tension Pneumothorax
80
Pneumonia: * *S. pneumoniae* most frequently, also *Legionella* and *Klebsiella* * Intra-alveolar exudate Ž consolidation A ; may * involve entire lobe B or the whole lung.
Lobar pneumonia
81
Pneumonia: * *S. pneumoniae*, *S. aureus*, *H. influenzae*, *Klebsiella* * acute inflammatory infiltrates from bronchioles into adjacent alveoli * patchy distribution involving ≥ 1 lobe
Bronchopneumonia
82
Pneumonia: * *Mycoplasma*, *Chlamydophila pneumoniae*, *Chlamydophila psittaci*, *Legionella*, viruses (RSV, CMV, influenza, adenovirus) * diffuse patchy inflammation localized to interstitial areas at alveolar walls * diffuse distribution involving ≥ 1 lobe * generally follows a more indolent course (“walking” pneumonia)
Interstitial (Atypical) Pneumonia
83
Pneumonia: * etiology unknown * secondary organizing pneumonia caused by chronic inflammatory diseases (eg. rheumatoid arthritis) or medication side effects (eg. amiodarone) * ⊝ sputum and blood cultures, no response to antibiotics * formerly known as bronchiolitis obliterans organizing pneumonia (BOOP) * noninfectious pneumonia characterized by inflammation of bronchioles and surrounding structure
Cryptogenic Organizing Pneumonia
84
Natural History of Lobar Pneumonia
85
Lung Cancer
* leading cause of cancer death * Presentation: * cough, hemoptysis, bronchial obstruction, wheezing, pneumonic “coin” lesion on CXR or noncalcified nodule on CT * Sites of Metastases from Lung Cancer: * adrenals * brain * bone (pathologic fracture) * liver (jaundice, hepatomegaly) * In the lung, metastases (usually multiple lesions) are more common than 1° neoplasms. Most often from breast, colon, prostate, and bladder cancer. * **SPHERE** of Complications: * **S**uperior vena cava/thoracic outlet syndromes * **P**ancoast tumor * **H**orner syndrome * **E**ndocrine (paraneoplastic) * **R**ecurrent laryngeal nerve compression (hoarseness) * **E**ffusions (pleural or pericardial) * Risk factors include smoking, secondhand smoke, radon, asbestos, and family history. * **S**quamous and **S**mall cell carcinomas are **S**entral (central) and often caused by **S**moking.
86
Lung Cancer: * central * undifferentiated → very aggressive * may produce ACTH (Cushing syndrome), SIADH, or antibodies against presynaptic Ca2+ channels (Lambert-Eaton myasthenic syndrome) or neurons (paraneoplastic myelitis, encephalitis, subacute cerebellar degeneration) * amplification of myc oncogenes common * managed with chemotherapy +/– radiation * neoplasm of neuroendocrine Kulchitsky cells → small dark blue cells * Chromogranin A ⊕, Neuron-Specific Enolase ⊕, Synaptophysin ⊕
Small Cell (Oat Cell) Carcinoma
87
Lung Cancer: * non–small cell * peripheral * most common 1° lung cancer * more common in women than men, most likely to arise in nonsmokers * activating mutations include KRAS, EGFR, and ALK * associated with hypertrophic osteoarthropathy (clubbing) * Bronchioloalveolar subtype (in situ): * CXR often shows hazy infiltrates similar to pneumonia * better prognosis * bronchial carcinoid and bronchioloalveolar cell carcinoma have lesser association with smoking * glandular pattern on histology, often stains mucin ⊕ * Bronchioloalveolar subtype: * grows along alveolar septa * Ž apparent “thickening” * of alveolar walls. Tall, * columnar cells containing * mucus.
Adenocarcinoma
88
Lung Cancer: * non–small cell * central hilar mass arising from bronchus, cavitation * cigarettes, hypercalcemia (produces PTHrP) * keratin pearls and intercellular bridges
Squamous Cell Carcinoma
89
Lung Cancer: * non–small cell * peripheral highly anaplastic undifferentiated tumor * poor prognosis * less responsive to chemotherapy * removed surgically * strong association with smoking * pleomorphic giant cells
Large Cell Carcinoma
90
Lung Cancer: * non–small cell * central or peripheral * excellent prognosis * metastasis rare * symptoms due to mass effect or carcinoid syndrome (flushing, diarrhea, wheezing) * nests of neuroendocrine cells * Chromogranin A ⊕
Bronchial Carcinoid Tumor
91
Respiratory Pathology: * localized collection of pus within parenchyma * caused by aspiration of oropharyngeal contents (especially in patients predisposed to loss of consciousness [eg. alcoholics, epileptics]) or bronchial obstruction (eg. cancer) * Treatment: antibiotics * air-fluid levels often seen on CXR * fluid levels common in cavities * presence suggests cavitation * due to anaerobes (eg. *Bacteroides*, *Fusobacterium*, *Peptostreptococcus*) or *S. aureus* * _____ 2° to aspiration is most often found in the right lung * location depends on patient’s position during aspiration
Lung Abscess
92
Respiratory Pathology: * also known as Superior Sulcus Tumor * carcinoma that occurs in the apex of lung may cause _____ syndrome by invading cervical sympathetic chain * compression of locoregional structures may cause array of findings: * recurrent laryngeal nerve → hoarseness * stellate ganglion → Horner syndrome (ipsilateral ptosis, miosis, anhidrosis) * superior vena cava → SVC syndrome * brachiocephalic vein →brachiocephalic syndrome (unilateral symptoms) * brachial plexus → sensorimotor deficits
Pancoast Tumor
93
Respiratory Pathology: * an obstruction of the SVC that impairs blood drainage from the head (“facial plethora”; note blanching after fingertip pressure), neck (jugular venous distention), and upper extremities (edema) * commonly caused by malignancy (eg. mediastinal mass, Pancoast tumor) and thrombosis from indwelling catheters * medical emergency * can raise intracranial pressure (if obstruction is severe) → headaches, dizziness, ↑ risk of aneurysm/rupture of intracranial arteries
Superior Vena Cava Syndrome
94
Respiratory Drugs: reversible inhibitors of H1 histamine receptors
Histamine-1 Blockers
95
First Generation Histamine-1 Blockers
* Diph**en**hydram**ine** * Dim**en**hydrin**ate** * Chlorph**en**iram**ine**
96
Respiratory Drugs: * used for allergy, motion sickness, and sleep aid * causes edation, antimuscarinic and anti-α-adrenergic effects
First Generation Histamine-1 Blockers * Diphenhydramine * Dimenhydrinate * Chlorpheniramine
97
Second Generation Histamine-1 Blockers
* Lorat**adine** * Fexofen**adine** * Deslorat**adine** * Cetirizine
98
Respiratory Drugs: * used for allergies * far less sedating than 1st generation because of ↓ entry into CNS
Second Generation Histamine-1 Blockers * Loratadine * Fexofenadine * Desloratadine * Cetirizine
99
Respiratory Drugs: * expectorant * thins respiratory secretions * does not suppress cough reflex
Guaifenesin
100
Respiratory Drugs: * mucolytic * liquifies mucus in chronic bronchopulmonary diseases (eg. COPD, CF) by disrupting disulfide bonds * also used as an antidote for acetaminophen overdose
N-Acetylcysteine
101
Respiratory Drugs: * antitussive (antagonizes NMDA glutamate receptors) * synthetic codeine analog * has mild opioid effect when used in excess * Naloxone can be given for overdose * mild abuse potential * may cause serotonin syndrome if combined with other serotonergic agents
Dextromethorphan
102
Respiratory Drugs: * α-adrenergic agonists * used as nasal decongestants * used to reduce hyperemia, edema, and nasal congestion * open obstructed eustachian tubes * causes hypertension * rebound congestion if used more than 4–6 days * can also cause CNS stimulation/anxiety
* Pseudoephedrine—CNS stimulation/anxiety * Phenylephrine
103
Pulmonary Hypertension Drugs: * competitively antagonizes endothelin-1 receptors → ↓ pulmonary vascular resistance * hepatotoxic (monitor LFTs) * Example: Bosentan
Endothelin Receptor Antagonists
104
Pulmonary Hypertension Drugs: * inhibits PDE-5 → ↑ cGMP → prolonged vasodilatory effect of NO * also used to treat erectile dysfunction * contraindicated when taking nitroglycerin or other nitrates * Example: Sildenafil
PDE-5 Inhibitors
105
Pulmonary Hypertension Drugs: * PGI2 (prostacyclin) with direct vasodilatory effects on pulmonary and systemic arterial vascular beds * inhibits platelet aggregation * Side Effects: flushing, jaw pain * Examples: Epoprostenol, Iloprost
Prostacyclin Analogs
106
Asthma Drugs
* Bronchoconstriction is mediated by: * inflammatory processes * parasympathetic tone * Therapy is directed at these 2 pathways.
107
Asthma Drugs: * β2-agonist * relaxes bronchial smooth muscle (short acting β2-agonist) * used during acute exacerbation
Albuterol
108
Asthma Drugs: * β2-agonist * long-acting agents for prophylaxis * adverse effects are tremor and arrhythmia
* Salmeterol * Formoterol
109
Asthma Drugs: * inhibit the synthesis of virtually all cytokines * inactivate NF-κB, the transcription factor that induces production of TNF-α and other inflammatory agents * 1st-line therapy for chronic asthma * use a spacer or rinse mouth after use to prevent oral thrush
Inhaled Corticosteroids * Fluticasone * Budesonide
110
Asthma Drugs: * competitively block muscarinic receptors, preventing bronchoconstriction * also used for COPD
Muscarinic Antagonists * Tiotropium—long acting * Ipratropium
111
Asthma Drugs: * antileukotrienes * block leukotriene receptors (CysLT1) * especially good for aspirin-induced and exercise-induced asthma
* Montelukast * Zafirlukast
112
Asthma Drugs: * antileukotriene * 5-lipoxygenase pathway inhibitor * blocks conversion of arachidonic acid to leukotrienes * hepatotoxic
Zileuton
113
Asthma Drugs: * binds mostly unbound serum IgE and blocks binding to FcεRI * used in allergic asthma with ↑ IgE levels resistant to inhaled steroids and long-acting β2-agonists
Anti-IgE Monoclonal Therapy * Omalizumab
114
Asthma Drugs: * likely causes bronchodilation by inhibiting phosphodiesterase → ↑ cAMP levels due to ↓ cAMP hydrolysis * usage is limited because of narrow therapeutic index (cardiotoxicity, neurotoxicity) * metabolized by cytochrome P-450 * blocks actions of adenosine
Methylxanthines * Theophylline
115
Asthma Drugs: * prevent release of inflammatory mediators from mast cells * used for prevention of bronchospasm, not for acute bronchodilation
Mast Cell Stabilizers * Cromolyn * Nedocromil
116
Respiratory Drugs: * nonselective muscarinic receptor (M3) agonist * used in bronchial challenge test to help diagnose asthma
Methacholine

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