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USMLE Step 1 > Respiratory - First Aid > Flashcards

Respiratory - First Aid Flashcards

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USMLE® Step 1 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:

Pseudoglandular (weeks 5–17)

A
  • endodermal tubules → terminal bronchioles
  • surrounded by modest capillary network
  • respiration impossible, incompatible with life
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4
Q

Lung Development:

Canalicular (weeks 16–25)

A
  • terminal bronchioles → respiratory bronchioles → alveolar ducts
  • surrounded by prominent capillary networ
  • airways increase in diameter
  • respiration capable at 25 weeks
  • pneumocytes develop starting at 20 weeks
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5
Q

Lung Development:

Saccular (week 26–birth)

A
  • alveolar ducts → terminal sacs
  • terminal sacs separated by 1° septae
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6
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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7
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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8
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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9
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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10
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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11
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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12
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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13
Q

Alveolar Cell Types:

  • phagocytose foreign materials
  • release cytokines and alveolar proteases
  • hemosiderin-laden macrophages may be seen in pulmonary hemorrhage
A

Alveolar Macrophages

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14
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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15
Q

Respiratory Tree

A
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16
Q

Respiratory Tree:

Conducting Zone

A
  • large airways consist of nose, pharynx, larynx, trachea, and bronchi
  • small airways consist of bronchioles that further divide into terminal bronchioles (large numbers in parallel → least airway resistance)
  • warms, humidifies, and filters air but does not participate in gas exchange → “anatomic dead space”
  • cartilage and goblet cells extend to the end of bronchi
  • pseudostratified ciliated columnar cells primarily make up epithelium of bronchus and extend to beginning of terminal bronchioles, then transition to cuboidal cells
  • clear mucus and debris from lungs (mucociliary escalator)
  • airway smooth muscle cells extend to end of terminal bronchioles (sparse beyond this point)
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17
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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18
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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19
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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20
Q

Lung Volumes

A

A capacity is a sum of ≥ 2 physiologic volumes.

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21
Q

Lung Volumes:

air that can still be breathed in after normal inspiration

A

Inspiratory Reserve Volume

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22
Q

Lung Volumes:

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

Tidal Volume

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23
Q

Lung Volumes:

air that can still be breathed out after normal expiration

A

Expiratory Reserve Volume

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24
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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25
Q

Lung Volumes:

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

Inspiratory Capacity

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26
Q

Lung Volumes:

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

Functional Residual Capacity

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27
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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28
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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29
Q

Determination of Physiologic Dead Space

A
  • 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.
  • Taco, Paco, Peco, Paco (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
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30
Q

Ventilation:

  • total volume of gas entering lungs per minute
  • VE = VT × RR
A

Minute Ventilation

Normal Values:

  • Respiratory rate (RR) = 12–20 breaths/min
  • VT = 500 mL/breath
  • VD = 150 mL/breath
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31
Q

Ventilation:

  • volume of gas that reaches alveoli each minute
  • VA = (VT − VD) × RR
A

Alveolar Ventilation

Normal Values:

  • Respiratory rate (RR) = 12–20 breaths/min
  • VT = 500 mL/breath
  • VD = 150 mL/breath
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32
Q

Lung and Chest Wall

A
  • 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
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33
Q

Respiratory System Changes in the Elderly

A
  • ↑ 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
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34
Q

Hemoglobin

A
  • 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.
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35
Q

Hemoglobin Modifications

A

Lead to tissue hypoxia from ↓ O2 saturation and ↓ O2 content.

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36
Q

Hemoglobin Modifications:

Methemoglobin

A
  • Oxidized form of Hb (ferric, Fe3+), does not bind O2 as readily as Fe2+, but has ↑ affinity for cyanide. Fe<strong>2</strong>+ binds O2.
  • Iron in Hb is normally in a reduced state (ferrous, Fe<strong>2</strong>+; “just the 2 of us”).
  • Methemoglobinemia may present with cyanosis and chocolate-colored blood.
  • Methemoglobinemia can be treated with methylene blue and vitamin C.
  • Nitrites (eg. from dietary intake or polluted/high altitude water sources) and benzocaine cause poisoning by oxidizing Fe2+ to Fe3+.
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37
Q

Hemoglobin Modifications:

Carboxyhemoglobin

A
  • 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.
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38
Q

Cyanide Poisoning

A
  • 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).
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39
Q

Oxygen-Hemoglobin Dissociation Curve

A
  • 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.
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40
Q

Oxygen Content of Blood

A
  • 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.
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41
Q

Pulmonary Circulation

A
  • 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.
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42
Q

Pulmonary Vascular Resistance

A
  • 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
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43
Q

Alveolar Gas Equation

A
  • 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)
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44
Q

Oxygen Deprivation:

  • ↓ cardiac output
  • hypoxemia
  • anemia
  • CO poisoning
A

Hypoxia (↓ O2 delivery to tissue)

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45
Q

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
A

Hypoxemia (↓ Pao2)

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46
Q

Oxygen Deprivation:

  • impeded arterial flow
  • ↓ venous drainage
A

Ischemia (loss of blood flow)

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47
Q

Ventilation/Perfusion Mismatch

A
  • 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 = “oirway” obstruction (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).
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48
Q

Carbon Dioxide Transport

A
  • 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.
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49
Q

Response to High Altitude

A
  • ↓ 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
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50
Q

Response to Exercise

A
  • ↑ 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
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51
Q

Respiratory Pathology:

  • obstruction of sinus drainage into nasal cavity → inflammation and pain over affected area
  • typically affects maxillary sinuses, which drain against gravity due to ostia located superomedially
  • most common acute cause is viral URI
  • may lead to superimposed bacterial infection, most commonly S. pneumoniae, H. influenzae, and M. catarrhalis
  • infections in sphenoid or ethmoid sinuses may extend to cavernous sinus and cause complications (eg. cavernous sinus syndrome)
A

Rhinosinusitis

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52
Q

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)
A

Epistaxis

Kiesselbach drives his Lexus with his LEGS:

  • superior Labial artery
  • anterior and posterior Ethmoidal arteries
  • Greater palatine artery
  • Sphenopalatine artery
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53
Q

Respiratory Pathology:

  • mostly squamous cell carcinoma
  • risk factors include tobacco, alcohol, HPV-16 (oropharyngeal), aand EBV (nasopharyngeal)
  • Field Cancerization
    • carcinogen damages wide mucosal area → multiple tumors that develop independently after exposure
A

Head and Neck Cancer

54
Q

Deep Venous Thrombosis

A
  • blood clot within a deep vein → swelling, redness, warmth, pain
  • Predisposed by Virchow triad (SHE):
    • Stasis (eg. post-op, long drive/flight)
    • Hypercoagulability (eg. defect in coagulation cascade proteins, such as factor V Leiden; oral contraceptive use)
    • Endothelial 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.
55
Q

Pulmonary Emboli

A
  • 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):
    • Fat
    • Air
    • Thrombus
    • Bacteria
    • Amniotic fluid
    • Tumor
  • 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.
56
Q

Flow-Volume Loops

A
57
Q

Obstructive Lung Diseases

A
  • 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.
  • “FRiCkin’ RV needs some increased TLC, but it’s hard with COPD!”
58
Q

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
A

Chronic Bronchitis (“blue bloater”)

59
Q

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
A

Emphysema (“pink puffer”)

60
Q

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.
A

Asthma

61
Q

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.
A

Bronchiectasis

62
Q

Restrictive Lung Diseases

A
  • 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)
63
Q

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
A

Hypersensitivity Pneumonitis

64
Q

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)
A

Sarcoidosis

A facial droop is UGLIER.

  • Bell Palsy
  • Uveitis
  • Granulomas
  • Lupus pernio
  • Interstitial fibrosis
  • Erythema nodosum
  • Rheumatoid arthritis-like arthropathy
65
Q

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
A

Inhalation Injury and Sequelae

66
Q

Pneumoconioses

A
  • 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).
67
Q

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
A

Asbestosis

68
Q

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
A

Berylliosis

69
Q

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
A

Coal Workers’ Pneumoconiosis

70
Q

Pneumoconioses:

asymptomatic condition found in many urban dwellers exposed to sooty air

A

Anthracosis

71
Q

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
A

Silicosis

The silly egg sandwich I found is mine!

72
Q

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
A

Mesothelioma

73
Q

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
A

Acute Respiratory Distress Syndrome

ARDS:

  • 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
74
Q

Respiratory Pathology:

  • repeated cessation of breathing > 10 seconds during sleep → disrupted sleep → daytime somnolence
  • diagnosis confirmed by sleep study
  • normal Pao2 during the day
  • nocturnal hypoxia → systemic/pulmonary hypertension, arrhythmias (atrial fibrillation/flutter), sudden death
  • hypoxia → ↑ EPO release → ↑ erythropoiesis
A

Sleep Apnea

75
Q

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
A

Obstructive sleep Apnea

76
Q

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
A

Central Sleep Apnea

77
Q

Sleep Apnea:

  • obesity (BMI ≥ 30 kg/m2) → hypoventilation → ↑ Paco2 during waking hours (retention); ↓ Pao2 and ↑ Paco2 during sleep
  • also known as Pickwickian syndrome
A

Obesity Hypoventilation Syndrome

78
Q

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
A

Pulmonary Hypertension (≥ 25 mm Hg)

  • normal mean pulmonary artery pressure = 10–14 mmHg
79
Q

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
A

Pulmonary Arterial Hypertension

80
Q

Pulmonary Hypertension:

sauses include systolic/diastolic dysfunction and valvular disease

A

Left Heart Disease

81
Q

Pulmonary Hypertension:

  • destruction of lung parenchyma (eg. COPD)
  • lung inflammation/fibrosis (eg. interstitial lung diseases)
  • hypoxemic vasoconstriction (eg. obstructive sleep apnea, living in high altitude)
A

Lung Diseases or Hypoxia

82
Q

Pulmonary Hypertension:

recurrent microthrombi → ↓ cross-sectional area of pulmonary vascular bed

A

Chronic Thromboembolic

83
Q

Pulmonary Hypertension:

causes include hematologic, systemic, and metabolic disorders, along with compression of the pulmonary vasculature by a tumor

A

Multifactorial

84
Q

Lung—Physical findings

A
85
Q

Respiratory Pathology:

  • excess accumulation of fluid between pleural layers → restricted lung expansion during inspiration
  • can be treated with thoracentesis to remove/reduce fluid
A

Pleural Effusions

86
Q

Pleural Effusions:

  • ↓ protein content
  • due to ↑ hydrostatic pressure (eg. HF) or ↓ oncotic pressure (eg. nephrotic syndrome, cirrhosis)
A

Transudate

87
Q

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
A

Exudate

88
Q

Pleural Effusions:

  • also known as chylothorax
  • due to thoracic duct injury from trauma or malignancy
  • milky-appearing fluid
  • ↑ triglycerides
A

Lymphatic

89
Q

Respiratory Pathology:

  • accumulation of air in pleural space
  • dyspnea and uneven chest expansion
  • chest pain, ↓ tactile fremitus, hyperresonance, and diminished breath sounds, all on the affected side
A

Pneumothorax

90
Q

Pneumothorax:

  • due to rupture of apical subpleural bleb or cysts
  • occurs most frequently in tall, thin, young males and smokers
A

Primary Spontaneous Pneumothorax

91
Q

Pneumothorax:

  • diseased lung (eg. bullae in emphysema, infections)
  • mechanical ventilation with use of high pressures → barotrauma
A

Secondary Spontaneous Pneumothorax

92
Q

Pneumothorax:

  • caused by blunt (eg. rib fracture) or penetrating trauma (eg. gunshot)
  • can be iatrogenic (eg. central line placement, lung biopsy, barotrauma due to mechanical ventilation)
A

Traumatic Pneumothorax

93
Q

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
A

Tension Pneumothorax

94
Q

Pneumonia:

  • S. pneumoniae most frequently, also Legionella and Klebsiella
  • Intra-alveolar exudate Ž consolidation A ; may
  • involve entire lobe B or the whole lung.
A

Lobar pneumonia

95
Q

Pneumonia:

  • S. pneumoniae, S. aureus, H. influenzae, Klebsiella
  • acute inflammatory infiltrates from bronchioles into adjacent alveoli
  • patchy distribution involving ≥ 1 lobe
A

Bronchopneumonia

96
Q

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)
A

Interstitial (Atypical) Pneumonia

97
Q

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
A

Cryptogenic Organizing Pneumonia

98
Q

Natural History of Lobar Pneumonia

A
99
Q

Lung Cancer

A
  • 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:
    • Superior vena cava/thoracic outlet syndromes
    • Pancoast tumor
    • Horner syndrome
    • Endocrine (paraneoplastic)
    • Recurrent laryngeal nerve compression (hoarseness)
    • Effusions (pleural or pericardial)
  • Risk factors include smoking, secondhand smoke, radon, asbestos, and family history.
  • Squamous and Small cell carcinomas are Sentral (central) and often caused by Smoking.
100
Q

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 ⊕
A

Small Cell (Oat Cell) Carcinoma

101
Q

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.
A

Adenocarcinoma

102
Q

Lung Cancer:

  • non–small cell
  • central hilar mass arising from bronchus, cavitation
  • cigarettes, hypercalcemia (produces PTHrP)
  • keratin pearls and intercellular bridges
A

Squamous Cell Carcinoma

103
Q

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
A

Large Cell Carcinoma

104
Q

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 ⊕
A

Bronchial Carcinoid Tumor

105
Q

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
A

Lung Abscess

106
Q

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
A

Pancoast Tumor

107
Q

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
A

Superior Vena Cava Syndrome

108
Q

Respiratory Drugs:

reversible inhibitors of H1 histamine receptors

A

Histamine-1 Blockers

109
Q

First Generation Histamine-1 Blockers

A
  • Diphenhydramine
  • Dimenhydrinate
  • Chlorpheniramine
110
Q

Respiratory Drugs:

  • used for allergy, motion sickness, and sleep aid
  • causes edation, antimuscarinic and anti-α-adrenergic effects
A

First Generation Histamine-1 Blockers

  • Diphenhydramine
  • Dimenhydrinate
  • Chlorpheniramine
111
Q

Second Generation Histamine-1 Blockers

A
  • Loratadine
  • Fexofenadine
  • Desloratadine
  • Cetirizine
112
Q

Respiratory Drugs:

  • used for allergies
  • far less sedating than 1st generation because of ↓ entry into CNS
A

Second Generation Histamine-1 Blockers

  • Loratadine
  • Fexofenadine
  • Desloratadine
  • Cetirizine
113
Q

Respiratory Drugs:

  • expectorant
  • thins respiratory secretions
  • does not suppress cough reflex
A

Guaifenesin

114
Q

Respiratory Drugs:

  • mucolytic
  • liquifies mucus in chronic bronchopulmonary diseases (eg. COPD, CF) by disrupting disulfide bonds
  • also used as an antidote for acetaminophen overdose
A

N-Acetylcysteine

115
Q

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
A

Dextromethorphan

116
Q

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
A
  • Pseudoephedrine—CNS stimulation/anxiety
  • Phenylephrine
117
Q

Pulmonary Hypertension Drugs:

  • competitively antagonizes endothelin-1 receptors → ↓ pulmonary vascular resistance
  • hepatotoxic (monitor LFTs)
  • Example: Bosentan
A

Endothelin Receptor Antagonists

118
Q

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
A

PDE-5 Inhibitors

119
Q

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
A

Prostacyclin Analogs

120
Q

Asthma Drugs

A
  • Bronchoconstriction is mediated by:
    • inflammatory processes
    • parasympathetic tone
  • Therapy is directed at these 2 pathways.
121
Q

Asthma Drugs:

  • β2-agonist
  • relaxes bronchial smooth muscle (short acting β2-agonist)
  • used during acute exacerbation
A

Albuterol

122
Q

Asthma Drugs:

  • β2-agonist
  • long-acting agents for prophylaxis
  • adverse effects are tremor and arrhythmia
A
  • Salmeterol
  • Formoterol
123
Q

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
A

Inhaled Corticosteroids

  • Fluticasone
  • Budesonide
124
Q

Asthma Drugs:

  • competitively block muscarinic receptors, preventing bronchoconstriction
  • also used for COPD
A

Muscarinic Antagonists

  • Tiotropium—long acting
  • Ipratropium
125
Q

Asthma Drugs:

  • antileukotrienes
  • block leukotriene receptors (CysLT1)
  • especially good for aspirin-induced and exercise-induced asthma
A
  • Montelukast
  • Zafirlukast
126
Q

Asthma Drugs:

  • antileukotriene
  • 5-lipoxygenase pathway inhibitor
  • blocks conversion of arachidonic acid to leukotrienes
  • hepatotoxic
A

Zileuton

127
Q

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
A

Anti-IgE Monoclonal Therapy

  • Omalizumab
128
Q

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
A

Methylxanthines

  • Theophylline
129
Q

Asthma Drugs:

  • prevent release of inflammatory mediators from mast cells
  • used for prevention of bronchospasm, not for acute bronchodilation
A

Mast Cell Stabilizers

  • Cromolyn
  • Nedocromil
130
Q

Respiratory Drugs:

  • nonselective muscarinic receptor (M3) agonist
  • used in bronchial challenge test to help diagnose asthma
A

Methacholine

USMLE Step 1 (18 decks)

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