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Pulmonology > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

What are some key differences of pulmonary vessels compared to systemic vessels?

A
  • Larger diameters
  • Shorter, more branches
  • Higher # of arterioles
  • Arterioles do not direct flow
  • Lower resistance from lower resting muscle tone in arterioles
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2
Q

What occurs to pulmonary vessels during exercise?

A

Increased cardiac output leads to a decrease in resistance and increase in blood flow: recruitment and distension

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3
Q

How does lung volume affect vascular diameters and resistance?

A

Alveolar vessels are compressed at higher lung volumes, which increases R
Extra-alveolar vessels are pulled open by expansion of attached parenchyme, which decreases R
Results in a drop in total R followed by an increase

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4
Q

What is hypoxic vasoconstriction?

A

Constriction of pulmonary vessels below avleolar PO2

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5
Q

What three things affect intravascular pressure (Piv)?

A

Cardiac cycle - high compliance system does not dampen pulse
Vertical position - gravity leads to high Q at base, low Q at apex
Respiratory cycle - Inspiration: PA Patm

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6
Q

What is the relationship of arterial, alveolar, and venous pressure in the three zones (of West)?

A

Zone 1: Above LA, decr. Piv.; alv. capillaries crushed –> low Q
PA > Pa > Pv
Zone 2: At LA; arterioles dilated but venules squeezed leading to incr. R and low Q
Pa > PA > Pv
Zone 3: Below LA, causing incr. Piv; Ptm along vessel dilates it causing decr. R
Pa > Pv > PA

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7
Q

How is left atrial pressure measured?

A

Swan-Ganz catheter threaded through R heart to pulm aa., measuring pulmonary capillary wedge pressure (PCWP), usually 7-8mmHg

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8
Q

What determines the rate of fluid flux out of capillaries?

A

According to Starling’s Law:

  • Difference in capillary and interstitial hydrostatic P
  • Difference in oncotic pressure of lung interstitium and plasma multiplied by the reflection coefficient of the membrane
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9
Q

What is Poiseuille’s equation and how does it relate to pulmonary hypertension?

A

Ppa = Q x PVR + PCWP

The difference in P b/t the pulmonary a. P and left atrial P depends on the blood flow and pulm. vascular R

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10
Q

What are some causes of pulmonary HTN?

A

Incr. Q: L to R shunts
Incr. Rp: hypoxic vasoconstr., clot, tumor, inflammation
Incr. left atrial P: left ventricular cardiomyopathies, valvular dz

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11
Q

What happens in fetal circulation after birth?

A

Ductus arteriosus, foramen ovale close due to decr. in R atrial P
Fetal pulm. circulation incr. P due to incr. PO2 and PGI2/PAF

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12
Q

How does PCWP cause pulmonary edema?

A

When PCWP > 18-25mmHg, fluid moves from the capillaries into the interstitium. If the rate of clearance is exceeded pulmonary edema (interstitial first, then alveolar) will occur

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13
Q

What are the steady state values of PAO2/PaO2 and PACO2/PaCO2? How are these calculated?

A 
PAO2 = 104mmHg
PACO2 = 40mmHg
PaO2 = 100mmHg
PaCO2 = 40mmHg

Pressure of a gas in air present in alveoli (Pi) depends on humidity (PH2O) and the total P of inspired air
Pi = (Ptot - PH2O)(%Pi)

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14
Q

What is anatomic dead space? How can it be measured?

A

The 150mL of inspired air that remains in the conducting airways after each breath.
Measured by Fowler N2 washout method: pt inhales 100% O2, exhaled air is analyzed for N2. N2 in dead space mixes with inhaled O2

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15
Q

What is physiologic dead space?

A

VD(phys) = VD(anat) + VD(alv)
Proportion of dead space in each breath:
VD/VT = (PACO2 - PTCO2) / PACO2); normally ~30%

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16
Q

How is alveolar ventilation measured?

A

Alv V: flow of air into alveoli taking part in gas exchange; must be sufficient for CO2 removal, so PACO2 ~ VCO2 / VA

VA = 0.863 (VCO2 / PACO2)

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17
Q

How do parasympathetic and sympathetic NS affect airflow?

A

Para: bronchoconstr
Sympa: bronchodilates
Act via increasing [cAMP] in smooth muscle cells

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18
Q

What is vital capacity?

A 
VC = ERV + IC
VC = ERV + VT + IRV

Max. vol. of air that can be expelled after a maximal inspiration

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19
Q

What is residual volume?

A

RV = FRC - ERV

Volume of gas remaining in lungs after forced expiration

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20
Q

What is expiratory reserve volume?

A

Volume of air beyond normal tidal volume that can be forcibly expired

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21
Q

What is inspiratory reserve volume?

A

Volume of air beyond normal tidal volume that can be forcibly inspired

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22
Q

What is functional residual capacity?

A

FRC RV + ERV

Volume of gas remaining in lungs after tidal expiration; cannot be directly measured

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23
Q

What two factors contribute to lung collapsibility?

A

Alveolar surface tension: surfactant lowers T when r reduced, preventing collapse of smaller alveoli into larger ones
Elastic fibers: alveoli tethered by fibers in interstitium tend to pull and hold alveoli open - lowers R – radial traction

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24
Q

What is the differential diagnosis for obstructive lung disease?

A 
F - foreign body
A - asthma
C - chronic bronchitis/bronchiectasis
E - emphysema
S - small airway disease
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25
Q

What is the PFT hallmark of obstructive lung disease? Emphysema? Chronic bronchitis?

A 
Decr. FEV1
Decr. FVC
Decr. FEV1/FVC 
Incr. TLC
Decr. DLCO
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26
Q

What is the differential diagnosis for restrictive lung disease?

A 
P - Pleural disease
A - alveolar filling disease (ARDS)
I - Interstitial lung diseases
N - neuromuscular
T - thoracic cage abnormalities (kyphoscoliosis)
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27
Q

What PFTs are indicative of restrictive lung disease?

A 
Decr. FEV1
Decr. FVC
Incr. or nl FEV1/FVC
Decr. or nl FEF25-75
Decr. TLC
Decr. FRC
Decr. DLCO
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28
Q

What is compliance and how is it affected by increasing volume?

A

Change in volume as transmural pressure is changed
∆V / ∆Ptm

Compliance decr. as volume incr. and walls approach maximum stretch

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29
Q

Why does the slope of the compliance curve differ from inhalation to exhalation? What is this called?

A

Greater P is needed to open a previously closed airway than to keep an open airway from closing. This effect is called hysteresis

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30
Q

How do restrictive and obstructive lung diseases affect lung compliance?

A

Restrictive - scarring causes incr. interstitial tissue, reducing compliance, incr. WOB
Obstructive - emphysema: destroy parenchyma, increasing compliance

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31
Q

Why is expiratory flow limited in COPD?

A

Loss of radial traction - airway collapse in expiration

Loss of elastic recoil - decr. alv. driving P

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32
Q

What factors affect normal PFT values?

A

Age - older lower
Sex - women lower
Race - blacks lower
Height - shorter lower

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33
Q

How are flow volume loops changed in disease states?

A

Obstructive: shifted left, characteristic “scoop” on expiration, reduced total flow

Restrictive: Normal shape, shifted right, reduced total flow

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34
Q

What determines the diffusion of a gas across a membrane?

A

Gas solubility, pressure difference, area of diffusion, thickness of membrane

Diffusion ~ (A x G x ∆P) / T

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35
Q

Why do O2 and CO2 diffuse at similar rates in the lung?

A

Driving force for diffusion is ∆P. Since ∆PO2 > ∆PCO2 (60mmHg vs. 6mmHg) they diffuse similarly

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36
Q

How are diffusion and perfusion capacities measured?

A

Diffusion: DLCO - measures ability of CO to cross into bloodstream independent of blood flow
Perfusion: N2O - amount taken up depends on blood flow and not barrier

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37
Q

How is the alveolar PO2 estimated?

A 
PAO2 = PIO2 - (PaCO2/0.8)
PAO2 = 150 - (PaCO2/0.8)
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38
Q

What is the Aa gradient, how is it calculated, and what is its significance?

A

The Aa gradient measures the difference in PO2 b/t alveolar gas and mixed arterial blood; a large Aa gradient indicates pathology of gas exchange (nl 5-10mmHg; or age x 0.3).

Aa = 150 - PCO2/0.8 - PaO2

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39
Q

Why does helium dilution underestimate lung volume in obstructive lung disease?

A

Helium doesn’t reach portions of the lungs distal to the obstruction

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40
Q

Why is diffused O2 so important for normal gas exchange?

A

Due to cooperative binding of O2 to Hb, the presence of extracellular O2 diffused in the plasma ensures that O2 is delivered where it is needed–small ∆ in SaO2 drastically changes Hb binding of O2

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41
Q

What is the equation for the amount of O2 carried in the blood?

A

CaO2 = (1.34 x Hb x SaO2) + (0.003 x PaO2)

Total amount carried by hemoglobin plus dissolved plasma O2

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42
Q

What factors occur in actively working tissue and how do they affect Hb binding O2?

A

Incr. tempr
Incr. PCO2
Incr. 2,3-DPG
Incr. acidity (decr. pH)

All 4 decrease Hb affinity for O2

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43
Q

What effect do drugs or chemicals such as nitrites and sulfonamides have on Hb? How is this dealt with?

A

Oxidize Hb to MetHb, which can’t bind O2. Reduced by MetHb reductase, so only 1.5% of Hb is in MetHb state

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44
Q

How is CO2 transported in the blood (3 forms)?

A 
Dissolved CO2 (6%)
Bicarbonate (70%) - carbonic anhydrase in RBCs
Carbamino compounds (24%) - carbaminoHb formed by CO2 combining with free amine groups
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45
Q

What is the Haldane effect?

A

Oxygenation of blood decreases its ability to carry CO2

Deoxygenation of blood increases its ability to carry CO2

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46
Q

What is the equation to calculate alveolar O2?

A

PAO2 = FIO2 x (Patm - PH2O) - (PACO2 / R)

Normally 100mmHg

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47
Q

What are some causes of hypoxemia (6)?

A 
V/Q mismatch (most common)
Reduced DLCO (increased Aa gradient)
Alveolar hypoventilation
Reduced PIO2 (altitude)
Reduced FIO2 (fire)
Shunt (V/Q = 0)
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48
Q

What equation describes the relationship between arterial PCO2, CO2 production, and alveolar ventilation?

A

PaCO2 = K(VCO2 / VA)

The arterial PCO2 is proportional to the volume of CO2 produced by the tissues divided by the alveolar ventilation

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49
Q

What are four common causes of hypercapnia?

A

Alveolar hypoventilation (decr. VA)
Incr. VD/VT (rapid, shallow breathing)
Incr. CO2 production (w/ fixed ventilation)
Severe V/Q mismatch

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50
Q

How does the lung respond to high V/Q due to changes in perfusion?

A

Hypocapnic bronchoconstriction

VA is decreased to compensate for decreased blood flow. VA is increased elsewhere to accommodate increased Q caused by blocked vessels.

If Q is increased, VA is increased.

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51
Q

How does the lung respond to low V/Q?

A

Hypoxic vasoconstriction, in order to offset effects of shunt (hypoxemia)

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52
Q

What is a normal Aa gradient?

A

0-10mmHg, increases w/ age

When hypoxemia is present and PaCO2 is reduced, the Aa gradient MUST be wide

53
Q

What interstitial lung diseases are associated with smoking?

A

Desquamative interstitial pneumonia (DIP)
Respiratory bronchiolitis-associated interstitial lung disease (RB-ILD)
Pulmonary Langerhans cell histiocytosis (PLCH)
Idiopathic pulmonary fibrosis (IPF)

54
Q

What is the DDx for interstitial lung disease that is granulomatous?

A

Sarcoidosis
Infection
Hypersensitivity pneumonitis

55
Q

What part of the brain acts as a respiratory rhythm generator? What structure initiates inspiration?

A

The rostral VRG, the Botzinger complex. It contains pacemaker cells.
The DRG contains primarily inspiratory neurons that generate APs of increasing intensity: ramp signal

56
Q

What structures in the brain modulate respiration and fine tune respiratory rhythm?

A

Apneustic center - prolong ramp action potentials

Pneumotaxic center - switch off inspiration, regulate inspiratory volume

57
Q

What are the chemosensors in the aortic and carotid bodies, and how do they communicate with the DRG?

A

Glomus cells - depolarized by low PaO2, high PaCO2, and low pH. Signal DRG to increase ventilation

58
Q

How do central chemoreceptors sense changes in pH?

A

Central chemoreceptors sense increase [H+], which is produced when CO2 diffuses across the BBB into the CSF, which reacts with H2O to form HCO3- and H+

59
Q

What is the Hering-Breuer reflex?

A

Cessation of inspiration following signals from slowly-adapting pulmonary stretch receptors within the tracheobronchial tree when the lungs overinflate

60
Q

What function do J receptors serve?

A

J receptors in the alveoli and small conducting airways respond to interstitial edema and engorgement of pulmonary capillaries. They mediate closure of the larynx and apnea followed by rapid shallow breathing. They also mediate tachypnea in response to PE

61
Q

What is the main difference between OSA and central sleep apnea?

A

Both OSA and CSA have >5 apneic episodes/night but CSA is characterized by lack of respiratory drive during apneic episodes

62
Q

What are the main advantages to inhaled treatments over systemic treatments for respiratory pharmacologic agents?

A

Delivery to respiratory tissues decreases systemic absorption and thus side effect profiles
The portion of inhaled drugs that are absorbed are passed through the liver and inactivated via first pass metabolism, thereby decreasing systemic side effects

63
Q

What are the inhaled vasodilators and their mechanism of action?

A

NO - cause pulmonary vasodilation to acutely lower pulmonary arterial P; improves oxygenation but not survival in ARDS
Prostacyclin - causes pulmonary vasodilation; has anticoagulation/antiproliferative actions

64
Q

What are the inhaled mucolytics?

A

N-Acetylcysteine (NAC) - breaks S-H bonds to break down proteins; can irritate bronchial mucosa and induce cough
DNase - breaks up DNA of degenerating neutrophils/bacteria in order to reduce sputum viscosity (not approved for chronic bronchitis)

65
Q

What are the beta agonists and how do they work?

A

Stimulate beta-2 receptors, incr. cAMP levels via IP3, increasing Ca2+ efflux.
Albuterol (fast onset, short duration)
L-albuterol - B2 > B1, decr. side effects
Salmeterol (slow onset, long duration)
Formoterol (fast onset, long duration)

66
Q

What are the anti-cholinergics and how do they work?

A

Block muscarinic receptors to block cholinergic mediated bronchoconstriction; better for COPD than asthma (due to increased musc. tone in COPD)

Ipratropium - short acting, blocks M1, M2, M3 receptors
Tiotropium - long acting, blocks M1, M3 receptors

67
Q

How do anti-leukotrienes exert their effect?

A

Leukotrienes are involved in IgE mediated inflammation and bronchoconstriction; blocking LKTs cause a decr. in eosinophils and incr. in FEV1 in asthma

Zileuton - blocks 5-lipoxygenase
Montelukast/zafirlukast - blocks binding of LTE4 to receptors in lung tissue –> bronchodilation

68
Q

What is the mechanism of PDE4 inhibitors, and for what condition(s) are they prescribed?

A

PDE4 inhibition increases cAMP levels in airway smooth muscle cells and inflammatory cells, leading to mild bronchodilation and anti-inflammatory effects.

Roflumilast - Rx in COPD exacerbations, but monitor liver tox.

69
Q

How do inhaled steroids work to decrease inflammation? What are some examples?

A

Trigger eosinophil apoptosis, decrease mast cell degranulation and macrophage proliferation
Act on epithelial cells, decreasing cytokine and mitogen release
Bind to smooth muscle cells and mucus gland cells

Beclomethasone
Fluticasone
Budesonide
Mometasone

70
Q

What are cromolyn and how does it work?

A

Blocks the release of histamine and LKTs from mast cells
Tx exercise-induced bronchoconstriction, limited use in standard asthma

Nedocromil is related but also blocks mediator release from eosinophils, macrophages, and platelets; used infrequently

71
Q

What are anti-tussives?

A

Cough suppressants/expectorants
Codeine - act on mu receptor
Dextromethorphan - non-opiate with affinity for mu receptor, modest effectiveness
Benzonatate - local anesthetic in upper airway
Guaifenesin - draws free water into airway to assist sputum clearance

72
Q

What causes expiratory flow limitation in COPD? In chronic bronchitis?

A

COPD - loss of radial traction leads to airway collapse; loss of elastic recoil results in decr. alveolar driving pressure

Chr. bronchitis - edema, smooth muscle constriction, incr. mucus production, mucus gland hyperplasia, inflammation –> incr. airway resistance

73
Q

What treatment options are there for COPD?

A 
Smoking cessation
SABA - albuterol
LABA - salmeterol
LAMA - tiotropium (COPD > Asthma)
Theophylline (systemic bronchodilator)
PDE4 inh.
Corticosteroids
Surgery - reduce lung volume
Pulm rehab
O2 if hypoxemic
74
Q

What are some causes of acute exacerbations of COPD? What treatments are available?

A 
Bacterial infxn (most common)
Viral infxn
Environmental exposures (pollution)

Life threatening event, can result in permanent loss of lung fxn

Tx: Bronchodilators - SABA, LAMA, theophylline
Anti-inflammatory - systemic/inhaled corticosteroids
Abx
Alpha-1-antitrypsin
Immunization - influenza, pneumococcus
PDE-4 inh.

Expectorants/mucolytics NOT EFFECTIVE

75
Q

What is the biggest factor that influences the development of asthma?

A

Atopy - predisposition toward developing hypersensitivity; may have genetic component

76
Q

What are the hallmarks of asthma?

A 
Airway inflammation
Airway hyperresponsiveness (AHR)
Airflow obstruction
77
Q

What are the key factors involved in the early and late stages of asthma?

A

Early - bronchospasm - mast cells, and macrophages

Late - bronchospasm, edema, inflammation - recruitment & activation of eosinophils; cytokines (IL-4, -5, -13) released

78
Q

What occurs during airway remodeling in chronic asthma?

A

Mucus gland hyperplasia
Angiogenesis
Subepithelial fibrosis
Airway smooth muscle hypertrophy/hyperplasia

79
Q

What is aspirin induced asthma and how does it develop?

A

Aspirin inh. COX, incr. arachidonic acid pathway towards lipoxygenase pathway –> incr. LKTs –> edema, bronchoconstr., mucus, eosinophils

Tx: avoidance, standard asthma tx
LKT modifiers (montelukast, zileuton)
80
Q

How is methacholine used to dx asthma?

A

Asthmatics have incr. rxn at low conc. of methacholine - 20% reduction in FEV1 at low doses
Nl test in untreated pt r/o asthma; nl tests in treated pts

81
Q

What are the key factors involved in the early and late stages of asthma?

A

Early - bronchospasm - mast cells, and macrophages

Late - bronchospasm, edema, inflammation - recruitment & activation of eosinophils; cytokines (IL-4, -5, -13) released

82
Q

What infection are CF pts prone to get, and how can it be prevented?

A

Pseudomonas aeruginosa

Tx: inhaled tobramycin

83
Q

What are the main differences between CF and non-CF bronchiectasis?

A

Non-CF: acquired disorder characterized by permanent dilation and destruction of bronchial walls; requires infectious insult plus impairment of drainage, airway obstruction, and/or defect in host defense

CF: pulmonary manifestation of a multi-organ dz

84
Q

What is required for a CF dx in an adult?

A

Clinical sx consistent w/ CF in at least one organ system

Evidence of CFTR dysfunction

85
Q

What are characteristic microscopic findings in asthma?

A 
Bronchial smooth muscle hypertrophy
Bronchial basement membrane thickening
Bronchial wall edema/inflammation - eosinophils and mast cell infiltrate
Goblet cell hyperplasia
Submucosal gland hypertrophy
86
Q

What are the two types of emphysema and how are they distinguished?

A

Panacinar - enlargement of airspaces in distal acinus initially, later whole pulmonary acinus is involved; lower lung zones more severely affected. Assoc. w/ alpha-1-antitrypsin deficiency

Centriacinar - enlargement of proximal acinar airspaces; emphysematous areas separated by relatively normal lung; more severe in upper lobes. Assoc. w/ smoking

87
Q

What is the clinical definition of chronic bronchitis?

A

Productive cough for at least 3 months during 2 consecutive years w/o other known cause
Reid index increased - nl 0.4

Assoc. w/ smoking, often coexists w/ emphysema

88
Q

What histologic changes are apparent in bronchiectasis?

A

Acute neutrophilic inflammation
Increased fibrosis - subepithelial collagen
Squamous metaplasia - ciliated –> cuboidal epithelium

89
Q

What is the blood supply to the layers of the pleura? Lymphatics?

A

Parietal: systemic aa. and vv.; stoma drain pl. space
Visceral: bronchial aa. and pulmonary vv.; lymph drains towards hila, not involved in clearance of pl. space

90
Q

What is the innervation to the layers of the pleura?

A

Visceral: None
Parietal:
Costal/peripheral - intercostal nn., pain referred to chest wall
Central - phrenic nn., pain referred to ipsilat. shoulder

91
Q

Why is gas in the pleural space absorbed by venous blood?

A

Due to decreased pO2 in venous blood (40mmHg), the total venous P (by Dalton’s law) is 68cmH2O below Ppl

92
Q

How is a transudate different from an exudate? How do they develop?

A

Transudate: plasma ultrafiltrate caused by either increased hydrostatic pressure or decreased osmotic pressure
Exudate: protein-rich fluid from capillary leakage secondary to inflammation or dz of pl. surface, independent of Starling forces

93
Q

What are some major etiologies of transudative effusions?

A

CHF - RV (parietal transudate) or LV (visceral transudate)
Nephrotic syndrome
Cirrhosis
Atelectasis

94
Q

What are some etiologies of exudative effusions?

A 
Tumors - primary & metastatic
Pneumonia - parapneumonic, empyema
TB
PE
Collagen vasc. dz - lupus, RA
Trauma
95
Q

What is needed for an effusion dx - trans. vs. exud.?

A

Pl fluid protein / serum protein > 0.5
Pl fluid LDH / serum LDH > 0.6
or pl fluid LDH > 2/3 upper limit of nl serum LDH

96
Q

How are pleural effusions treated?

A

Transudates: tx underlying cause, effusion should resolve
Exudates: tx underlying cuase but further intervention might be req’d

In pneumonia, thoracentesis indicated for effusion > 10mm
Chest tube drainage for empyema, complicated parapneumonic effusion

97
Q

What are CXR findings indicating a tension PTX?

A

Contralateral shifting of trachea, mediastinum
Compressed lung w/ hypoopaque lung field
Depressed/inverted diaphragm

98
Q

What are general physical exam findings in interstitial lung dz? CXR?

A 
Cyanosis
Tachypnea, tachycardia
Clubbing
Velcro rales, end-insp. squeaks
Left parasternal heave, loud P2, right S3
LE edema

CXR: diffuse reticular infiltrates, honeycombing

99
Q

What are some tx options for IPF?

A

Lung transplant
Nintedanib - VEGF-R, FGF-R, PDGF-R blockade - incr. exercise tolerance
Pirfenidone - inh. TGF-B expression

100
Q

What are the ILDs of known etiology or association?

A

Pneumoconioses
- Asbestosis, coal worker’s pneumoconiosis, silicosis, berylliosis
Hypersensitivity pneumonitis
- Humidifier lung, bird fancier’s dz, farmer’s lung
Direct tissue injury
- Silo filler’s lung (NO2 exposure), RADS
Airway dz - occupational asthma
- Baker’s asthma

101
Q

What are the idiopathic interstitial pneumonias?

A

Usual interstitial pneumonia/idiopathic pulmonary fibrosis (UIP/IPF)
Cryptogenic organizing pneumonia (COP)
Acute interstitial pneumonia (AIP)
Desquamative interstitial pneumonia (DIP)
Nonspecific interstitial pneumonia (NSIP)
Respiratory bronchiolitis-associated ILD (RB-ILD)
Lymphoid interstitial pneumonia (LIP)

102
Q

What are the histologic hallmarks of hypersensitivity pneumonitis?

A

Airway-centered lymphocyte-predominant inflammation extending into alveolar septa
Loosely formed granulomas

103
Q

What are the hallmarks of granulomatosis with polyangiitis?

A

Vasculitis - inflammation and invasion of blood vessels in the lung
c-ANCA positive cells

104
Q

How can Langerhans cell histiocytosis be identified?

A

Multiple small bilateral lung nodules by CT
Stellate lesions with adjacent traction emphysema
Langerhans cells w/ prominent nuclear grooves, S-100 positive
Eosinophils
Birbeck granules by EM

105
Q

What are some distinguishing features of cryptogenic organizing pneumonia (COP/BOOP)?

A

CT/CXR: Unilateral or bilateral consolidation, can have nodular opacities mimicking neoplasia
Histo: fibroblastic plugs within airspaces, variable inflammation of interstitium

106
Q

How can acute interstitial pneumonia be identified?

A

Sudden onset - days-weeks
Ground glass opacities
Diffuse alveolar damage - hyaline membranes (acute/exudative phase) becoming loose organizing fibrosis in alveolar septa (organizing phase)

107
Q

What are the defining features of desquamative interstitial pneumonia?

A

Mild interstitial fibrosis
Pigmented macrophages with light brown cytoplasmic pigment
More severe than RB-ILD

108
Q

What is the DDx for wheezing?

A 
B - bronchiolitis, bronchiectasis
E - eosinophilic lung dz
C - CHF
A - asthma
U - upper airway obstruction
S - strongyloides (parasite)
E - emboli
O - obstructive lung dz
F - foreign bodies
G - GERD
A - aspirin
S - sinusitis
109
Q

What is the DDx for bronchiectasis?

A 
M - Marfan's syndrome
U - ulcerative colitis
C - CF
O - obstructive lesions
P - postpneumonic
U - useless cilia (immotile cilia, Kartageners)
S - sarcoid
Y - Young's syndrome
A - ABPA (allergic bronchopulmonary aspergillosis)
I - Ig deficiency
R - right middle lobe syndrome
W - Williams-Campbell syndrome
A - alpha-1-antitrypsin deficiency
Y - Yellow Nail syndrome
S - Swyer-James syndrome
110
Q

What is the DDx for dysnpea/hypoxemia with normal CXR?

A 
C - crazy (psychogenic)
L - low hematocrit (anemia)
E - emphysema
A - asthma
R - respiratory muscle weakness
C - chest wall dz
H - heart dz
E - emboli
S - sleep apnea
T - tracheal dz
S - shunt
111
Q

What is the equation for O2 delivery or transport to tissues?

A 
DO2 = CaO2 x CO
DO2 = [1.34(Hb)(SaO2) + 0.003(PaO2)] x CO
112
Q

What is type I respiratory failure and some common causes?

A

Hypoxemic respiratory failure - PaO2

113
Q

What is type II respiratory failure and some common causes?

A

Hypercapnic respiratory failure - PaCO2 > 45mmHg

Incr. VD/VT, decr. resp. drive, decr. resp. pump, incr. WOB

Acute: Drug OD, spinal cord injury, acute NMD, COPD exacerbation, status asthmaticus
Chronic: chronic NMD, kyphoscoliosis, OHS, COPD

114
Q

How does tx for acute hypoxemia differ from chronic?

A

Acute: shoot for PaO2 70-80mmHg, SpO2 > 95% w/ high flow O2, face mask with FiO2 > 50%
Chronic: only need PaO2 ~ 60mmHg, SpO2 90%; avoid worsening hypercapnia w/ low flow O2 therapy by nasal cannula/mask

115
Q

What is the clinical definition of ARDS?

A

R - Respiratory failure (not CHF)
O - Onset (acute)
AC - Abnormal CXR - bilat. opacities, not explained by other processes
H - Hypoxemia (PaO2/FiO2

116
Q

What is the approach to ARDS treatment?

A

Mech. ventilation - support while lungs recover
- lower tidal volumes protect the lung
- PEEP prevents atelectasis, improving PaO2
Supportive care - prophylaxis for ulcers, thromboembolism
Drug tx - abx if needed, NM blockade

117
Q

What are four types of ventilator-induced lung injury?

A

Volutrauma - injury to lung indistinguishable from ARDS
Barotrauma - rupture of alveoli (PTX)
Biotrauma - cytokine-mediated injury secondary to initial lung injury
Atelectrauma - repetitive opening/closing of alveoli (prevented by PEEP)

118
Q

What are the definitions of pre- and post-capillary pulmonary hypertension?

A

Pre-capillary: pulmonary arterial HTN, nl or reduced PCWP (15mmHg)
Post-capillary: pulmonary venous HTN, PCWP > 15mmHg

Pulm. HTN is defined as mean Pa >25mmHg

119
Q

What is the WHO group I class of pulm HTN?

A

Pulmonary arterial HTN
Idiopathic & heritable
Assoc. w/ congen. heart dz, portopulmonary HTN, HIV, drugs, sickle cell

120
Q

What is the WHO group II class of pulm HTN?

A

Pulmonary venous HTN
LV systolic dysfxn
Valvular defects - AS/MS
LV diastolic dysfxn - LV doesn’t relax, resulting in decreased preload and increased P

121
Q

What is the WHO group III class of pulm HTN?

A 
Pulm HTN w/ lung dz and/or chronic hypoxia
Obstructive/COPD
Restrictive/interstitial
Hypoventilatory
Sleep apnea
High altitude
122
Q

What is the WHO group IV class of pulm HTN?

A

Pulm embolic HTN

Chronic thromboembolic PH (CTEPH)

123
Q

What is the WHO group V class of pulm HTN?

A

Misc. causes of PHTN
Sarcoid
Glycogen storage dz (Gaucher’s)
Hematologic, NF, tumor emboli, chronic renal failure

124
Q

What is endothelin and what is its role in treating pulmonary HTN?

A

Molecule secr. by vascular endothelium and binds to smooth m. receptors, triggering contraction and eventual remodeling.
Tx: selectively block ETA receptor (more than ETB) - ETB binding triggers release of NO/PGI2 which cause vasodilation

125
Q

What are some therapeutic measures than can be employed to treat pulmonary HTN?

A 
General: Diuretics, digoxin, phlebotomy
Anticoagulants
Tx underlying dz (WHO groups II-V)
Group I: vasodilators/anti-proliferative
 - Ca channel blockers
 - Prostacyclins
 - Endothelin receptor antagonists
 - PDE5 inh.
 -Guanylate cyclase stimulants
126
Q

What are the three main risk factors for PE Dx?

A

Virchow’s triad:

  • Stasis
  • Inflammation
  • Hypercoagulability
127
Q

What histologic findings are consistent with pulmonary edema?

A

Pink transudate in alveolar spaces
Hemosiderin-laden macrophages (heart-failure cells)
Fibrotic thickening of alveolar septa (chronic edema)

128
Q

What are three histologic hallmarks of severe, irreversible pulmonary HTN?

A

Plexiform lesion - vessels replaced by slit-like proliferative vascular spaces (resemble glomeruli)
Angiomatoid lesion - proliferation of thin-walled dilated and congested vessels
Necrotizing vasculitis - fibrinoid necrosis of intimal hyperplasia

Pulmonology (1 decks)

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