First Aid - Respiratory

Front 1

Respiratory tree - conducting zone - details?

Back 1

Consists of nose, pharynx, trachea, bronchi, bronchioles, and terminal bronchioles. Cartilage is present only in the trachea and bronchi. Brings air in and out. Warms, humidifies, filters air. Anatomic dead space. Walls of conducting airways contain smooth muscle.

Front 2

Respiratory tree - respiratory zone - details?

Back 2

Consists of respiratory bronchioles, alveolar ducts, and alveoli. Participates in gas exchange.

Front 3

What type of epithelial cells exist in the respiratory conducting zone?

Back 3

Pseudostratified ciliated columnar cells extend up to and including the terminal bronchioles, at which point the cells become cuboidal ciliated (macrophages clear debris in the alveoli)

Front 4

Pneumocytes - Type I cells

Back 4

97% of alveolar surfaces. Line the alveoli. Squamous; thin for optimal gas diffusion.

Front 5

Pneumocytes - Type II cells

Back 5

3% of alveolar surface. Secrete pulmonary surfactant (dipalmitoyl phosphatidylcholine, a.k.a. Lecithin), which decreases alveolar surface tension. Cuboidal and clustered epithelial cells.
Also serve as precursors to type I cells and other type II cells. Type II cells proliferate during lung damage.

Front 6

Pneumocytes - Clara cells

Back 6

nonciliated; columnar with secretory granules. Secrete components of surfactant; degrade toxins; act as reserve cells.

Front 7

What substance composes respiratory surfactant?

Back 7

Dipalmitoyl phosphatidylcholine, a.k.a. Lecithin

Front 8

Epithelial cell type of Type I vs. Type II pneumocytes? Clara cells?

Back 8

Type I - Squamous
Type II - Cuboidal and clustered
Clara cells - nonciliated, columnar with secretory granules

Front 9

What is the ratio that is the cutoff in amniotic fluid for indicating fetal lung maturity?

Back 9

Lecithin-to-sphingomyelin ratio > 2.0

Front 10

Gas Exchange barrier - histology

Back 10

Continuous endothelium with tight junctions is juxtaposed to Type I epithelial cells to create the Air-Blood barrier. Type II epithelial cells are sporadically placed one cell layer deep to the Type I cells and have Lamellar bodies. Surfactant is secreted constitutively. Macrophages are also scattered throughout, one cell layer deep to type I cell layer.

Front 11

Lung relations - Left vs. Right lung - details?

Back 11

Right lung has 3 lobes; Left has 2 lobes and a Lingula (homologue of right middle lobe). Right lung is more common site for inhaled foreign body because the right main stem bronchus is wider and more vertical than the left.

Instead of a middle lobe, the left lung has a space occupied by the heart. The relation of the pulmonary artery to the bronchus at each lung hilus is described by RALS - Right Anterior; Left Superior

Front 12

Aspirating a peanut - where does it go while upright? While supine?

Back 12

Upright - lower portion of right inferior lobe
Supine - superior portion of right inferior lobe

Front 13

Name 2 fissures of the R lung. Relation in space?

Back 13

Horizontal fissure and oblique fissure.

Horizontal fissure is superior to oblique fissure.

Front 14

Diaphragm structures

Back 14

Structures perforating the diaphragm:
At T8: IVC
At T10: Esophagus
At T12: Aorta, thoracic duct, azygous vein

Diaphragm is innervated by C3, 4 and 5 (phrenic nerve). Pain from the diaphragm is referred to the shoulder.

Front 15

What three structures pierce the diaphragm at T12?

Back 15

Aorta, azygous vein, thoracic duct

Front 16

Muscles of respiration - quiet breathing

Back 16

Inspiration - diaphragm
Expiration - passive

Front 17

Muscles of respiration - exercise

Back 17

Inspiration - external intercostals, scalene muscles, sternomastoids
Expiration - rectus abdominis, internal and external obliques, transversus abdominis, internal intercostals

Front 18

5 important lung products

Back 18

1. Surfactant - produced by type II pneumocytes, decreased alveolar surface tension, increased compliance, decreased work of inspiration
2. Prostaglandins
3. Histamine - increases bronchoconstriction
4. Angiotensin-converting enzyme (ACE) - angiotensin I -> angiotensin II; inactivates bradykinin (ACE inhibitors increase bradykinin and cause cough, angioedema)
5. Kallikrein - activates bradykinin

Front 19

Equation for Collapsing pressure in alveoli?

Back 19

Collapsing Pressure = P = 2(surface tension) / radius

Tendency to collapse on expiration increases as radius decreases (law of Laplace)

Front 20

Lung volumes - Residual volume (RV)

Back 20

air in lung after maximal expiration; cannot be measured on spirometry

Front 21

Lung volumes - Expiratory reserve volume (ERV)

Back 21

air that can still be breathed out after normal expiration

Front 22

Lung volumes - Tidal volume (TV)

Back 22

air that moves into lungs with each quiet inspiration, typically 500 mL

Front 23

Lung volumes - Inspiratory reserve volume (IRV)

Back 23

air in excess of tidal volume that moves into lung on maximum inspiration

Front 24

Lung volumes - vital capacity (VC)

Back 24

everything but the residual volume
VC = TV + IRV + ERV

Front 25

Lung volumes - Functional residual capacity (FRC)

Back 25

RV + ERV (volume in lungs after normal expiration)

Front 26

Lung volumes - Inspiratory capacity (IC)

Back 26

IRV + TV

Front 27

Lung volumes - Total lung capacity (TLC)

Back 27

IRV + TV + ERV + RV

Front 28

Physiologic dead space

Back 28

Vd = Vt x (PaCO2 - PeCO2) / PaCO2

Vd = physiologic dead space = anatomical dead space of conducting airways plus functional dead space in alveoli; apex of healthy lung is largest contributor of functional dead space. Volume of inspired air that does not take part in gas exchange.

Front 29

Lung and Chest Wall - compliance curves

Back 29

There is a tendency for the 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.
Elastic properties of both chest wall and lungs determine their combined volume.
At FRC, airway and alveolar pressure are 0, and intrapleural pressure is negative (prevents pneumothorax).
Compliance - change in lung volume for a given change in pressure; decreased in pulmonary fibrosis, insufficient surfactant, and pulmonary edema

Front 30

Hemoglobin molecule - details?

Back 30

Composed of 4 polypeptide subunits (2 alpha and 2 beta) and exists in 2 forms:
1. T (taut) form has low affinity for O2
2. R (relaxed) form has high affinity for O2 (300x). Hemoglobin exhibits positive cooperativity and negative allostery (accounts for the sigmoid-shaped O2 dissociation curve for hemoglobin), unlike myoglobin.

Increased Cl-, H+, CO2, 2,3-BPG, and temperature favor T form over R form (shifts dissociation curve to right, leading to increased O2 unloading).

Front 31

What is different about fetal hemoglobin characteristics that make its O2 binding affinity different from adult hemoglobin?

Back 31

2 alpha and 2 gamma subunits, has lower affinity for 2,3-BPG than adult hemoglobin (HgA) and thus has higher affinity for O2.

Front 32

Methemoglobin - details?

Back 32

Methemoglobin is the oxidized form of hemoglobin (ferric, Fe3+) that does not bind O2 as readily, but has increased affinity for CN-.
Iron in hemoglobin is normally in a reduced state (ferrous, Fe2+).

To treat cyanide poisoning, use nitrites to oxidize hemoglobin to methemoglobin, which binds cyanide, allowing cytochrome oxidase to function. Use thiosulfate to bind this cyanide forming thiocyanate, which is renally excreted.

Front 33

How to treat cyanide poisoning?

Back 33

Methemoglobin binds to CN- readily, so convert hemoglobin to methemoglobin by administering Nitrites. This allows cytochrome oxidase to function in peripheral tissue cells. Then use thiosulfate to bind this cyanide to form thiocyanate which is renally excreted.

Front 34

Carboxyhemoglobin - details?

Back 34

Form of hemoglobin bound to CO in place of O2. Causes decreased oxygen-binding capacity with left shift in the oxygen-hemoglobin dissociation curve. Decreased oxygen unloading in tissues.
CO has 200x greater affinity than O2 for hemoglobin.

Front 35

Oxygen-hemoglobin dissociation curve - details?

Back 35

Sigmoidal shape due to positive cooperativity, i.e., hemoglobin can bind 4 oxygen molecules and has higher affinity for each subsequent oxygen molecule bound. Myoglobin does not show positive cooperativity; curve lacks sigmoidal appearance.

When curve shifts to the right, decreased affinity of hemoglobin for O2 (facilitates unloading of O2 to tissue).
An increase in all factors (except pH) causes a shift of the curve to the right, and vice-versa.
Fetal Hb has a higher affinity for oxygen than adult Hb, so its dissociation curve is shifted left.
Hb saturation increases at any given PO2 in the presence of CO due to positive cooperativity.

Front 36

Pulmonary Circulation - details?

Back 36

Normally a low-resistance, high-compliance system. PO2 and PCO2 exert opposite effects on pulmonary and systemic circulation. A decrease in PAO2 causes a hypoxic vasoconstriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung.

Front 37

Pulmonary circulation - perfusion limited substances

Back 37

Perfusion limited - O2 (normal health), CO2, N2O. Gas equilibrates early along the length of the capillary. Diffusion can be increased only if blood flow increases. (See First Aid for graphs, p. 564)

Front 38

Pulmonary circulation - diffusion limited substances

Back 38

O2 (emphysema, fibrosis), CO. Gas does not equilibrate by the time blood reaches the end of the capillary. (See First Aid for graphs, p. 564)

Front 39

Pulmonary circulation - Diffusion equation

Back 39

Vgas = A/T x Dk(P1 - P2)
where A = Area, T = thickness, and Dk(P1-P2) = difference in partial pressures.
A decreases in emphysema.
T increases in pulmonary fibrosis.

Front 40

Pulmonary hypertension - details?

Back 40

Normal pulmonary artery pressure = 10-14 mmHg; pulmonary hypertension >/= 25 mmHg or >35 mmHg during exercise.
Results in atherosclerosis, medial hypertrophy, and intimal fibrosis of pulmonary arteries.

Course: severe respiratory distress --> cyanosis and RVH --> death from decompensated cor pulmonale

Front 41

Pulmonary hypertension - Primary

Back 41

Due to an inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation); poor prognosis.

Front 42

What gene is altered in primary pulmonary hypertension?

Back 42

BMPR2 is inactivated (normally functions to inhibit vascular smooth muscle proliferation)

Front 43

Pulmonary Hypertension - Secondary

Back 43

Due to COPD (destruction of lung perenchyma); mitral stenosis (increased resistance --> increased pressure); recurrent thromboemboli (decreased cross-sectional area of pulmonary vascular vascular bed); autoimmune disease (e.g., systemic sclerosis; inflammation --> intimal fibrosis --> medial hypertrophy); left-to-right shunt (increased shear stress --> endothelial injury); sleep apnea or living at high altitude (hypoxic vasoconstriction)

Front 44

Name 6 diseases associated with development of pulmonary hypertension.

Back 44

1. COPD (destruction of lung perenchyma)
2. Mitral Stenosis (increased resistance --> increased pressure)
3. Recurrent thromboemboli (decreased cross-sectional area of pulmonary vascular bed)
4. Autoimmune disease (e.g., systemic sclerosis; inflammation --> intimal fibrosis --> medial hypertrophy)
5. left-to-right shunt (increased shear stress --> endothelial injury)
6. sleep apnea or living at high altitude (hypoxic vasoconstriction)

Front 45

Equation for Pulmonary Vascular Resistance

Back 45

PVR = [P (pulm artery) - P (L atrium)] / Cardiac Output

P (pulm artery) = pressure in pulmonary artery
P (L atrium) = Pulmonary capillary wedge pressure

Front 46

Oxygen content of blood

Back 46

O2 content = (O2 binding capacity x % saturation) + dissolved O2
Normally 1 g Hb can bind 1.34 mL O2; normal Hb amount in blood is 15 g/dL. Cyanosis results when deoxygenated Hb > 5 g/dL.
O2 binding capacity = 20.1 mL O2/dL
O2 content in arterial blood decreases as Hb falls, but O2 saturation and arterial PO2 do not.
Arterial PO2 decreases with chronic lung disease because physiologic shunt decreases O2 extraction ratio.
Exercise decreases venous PO2.
Oxygen delivery to tissues = cardiac output x oxygen content of blood

Front 47

Alveolar gas equation

Back 47

PAO2 = PIO2 - PaCO2/R
Can normally be approximated as:
PAO2 = 150 - PaCO2/0.8

PAO2 = alveolar PO2 (mmHg)
PIO2 = PO2 in inspired air (mmHg)
PaCO2 = arteriolar PCO2 (mmHg)
R = respiratory quotient = CO2 produced/O2 consumed
A-a gradient = PAO2 - PaO2 = 10-15 mmHg
Increased A-a gradient may occur in hypoxemia; causes include shunting, V/Q mismatch, fibrosis (impairs diffusion)

Front 48

Oxygen deprivation - Hypoxemia with a normal A-a gradient

Back 48

High altitude, Hypoventilation

Front 49

Oxygen deprivation - Hypoxemia with increased A-a gradient

Back 49

V/Q mismatch, Diffusion limitation, Right-to-left shunt

Front 50

V/Q mismatch - details?

Back 50

Ideally, ventilation is matched to perfusion (V/Q = 1) in order for adequate gas exchange to occur.
Lung zones:
1. Apex of the lung - V/Q = 3 (wasted ventilation)
2. Base of the lung - V/Q = 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 (increased Cardiac Output), there is vasodilation of apical capillaries, resulting in V/Q ratio that approaches 1.
Certain organisms that thrive in high O2 (e.g. TB) flourish in the apex.
V/Q --> 0 = airway obstruction (shunt). In shunt, 100% O2 does not improve PO2.
V/Q --> infinity = blood flow obstruction (physiologic dead space). Assuming <100% dead space, 100% O2 improves PO2.

Front 51

Explain the V/Q mismatch in the apices and base of the lung.

Back 51

Gravity makes blood pressure/flow low in the apices.
PA > Pa > Pv

Gravity pools blood in the bases, pushes air out.
Pa > Pv > PA

In the middle lobes, there is balance and the artery pressure is high enough to push spurts of blood during the cardiac cycle, while the venous pressure is low enough to allow the alveoli to be ventilated adequately.
Pa > PA > Pv

Front 52

CO2 transport - 3 forms in blood

Back 52

1. Bicarbonate (90%)
2. Bound to globin as carbaminohemoglobin (5%)
3. Dissolved CO2 (5%)

Front 53

CO2 transport - details?

Back 53

Carbon dioxide is transported from tissues to the lungs in 3 forms:
1. Bicarbonate (90%)
2. Bound to hemoglobin at N terminus of globin (not heme) as carbaminohemoglobin (5%). CO2 binding favors taut form (O2 unloaded).
3. Dissolved CO2 (5%)

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 tissues, increased H+ from tissue metabolism shifts curve to right, unloading O2 (Bohr effect).
Majority of blood CO2 is carried as bicarbonate in the plasma.

Front 54

Respiratory response to high altitude - details?

Back 54

1. Acute increase in ventilation, decreased PO2 and PCO2
2. Chronic increase in ventilation
3. Increased erythropoietin --> increased hematocrit and hemoglobin (chronic hypoxia)
4. Increased 2,3-BPG (binds to hemoglobin so that hemoglobin releases more O2).
5. Cellular changes (Increased mitochondria)
6. Increased renal excretion of bicarbonate (e.g., can augment by use of acetazolamide) to compensate for the respiratory alkalosis
7. Chronic hypoxic pulmonary vasoconstriction results in RVH

Front 55

Respiratory response to exercise - details?

Back 55

1. increased CO2 production
2. Increased O2 consumption
3. Increased ventilation rate to meet O2 demand
4. V/Q ratio from apex to base becomes more uniform
5. Increased pulmonary blood flow due to increased cardiac output
6. Decreased pH during strenuous exercise (secondary to alctic acidosis)
7. No change in PaO2 and PaCO2, but increase in venous CO2 content

Front 56

Oxygen deprivation - hypoxia examples

Back 56

Decreased cardiac output, Hypoxemia, Anemia, Cyanide poisoning, CO poisoning

Front 57

Oxygen deprivation - ischemia details

Back 57

Impeded arterial flow, reduced venous drainage

Front 58

Embolus types

Back 58

Fat, Air, Thrombus, Bacteria, Amniotic Fluid, Tumor

Fat emboli are associated with long bone fractures and liposuction. Amniotic fluid emboli can lead to DIC, especially postpartum.

Pulmonary embolus - Chest pain, tachypnea, dyspnea

Approximately 95% of pulmonary emboli arise from deep leg veins. Helical CT is the imaging test of choice for PE.

Front 59

How to remember the types of embolism?

Back 59

An embolus moves like a FAT BAT.
Fat
Air
Thrombus
Bacterial
Amniotic fluid
Tumor

Front 60

Pulmonary thromboembolism - histology findings

Back 60

"Lines of Zahn" - interdigitating areas of pink and red in embolus, representing layers of RBCs, platelets, and fibrin laid down if thrombus formed before death

Front 61

Deep venous thrombosis - details?

Back 61

Can lead to pulmonary embolus.
Homan's sign - dorsiflexion of foot --> tender calf muscle
Prevent and treat with heparin

Predisposed by Virchow's triad:
1. Stasis
2. Hypercoagulability (e.g., defet in coagulative cascade proteins)
3. Endothelial damage (exposed collagen triggers clotting cascade)

Front 62

Obstructive Lung Disease (COPD)

Back 62

Obstruction of air flow resulting in air trapping in the lungs. Airways close prematurely at high lung volumes, resulting in increased RV and decreased FVC.

PFTs: very decreased FEV1, decreased FVC --> decreased FEV1/FVC ratio (hallmark), V/Q mismatch

Front 63

Obstructive Lung Disease - Chronic Bronchitis

Back 63

"Blue Bloater"
Hypertrophy of mucus-secreting glands int he bronchi --> in COPD, Reid index >50% (Reid index = gland depth/total thickness of bronchial wall)

Productive cough for >3 months per year for > 2 years. Disease of small airway.
Findings: wheezing, crackles, cyanosis (early-onset hypoxemia due to shunting), late-onset dyspnea

Front 64

Obstructive Lung Disease - Emphysema

Back 64

"Pink puffer," barrel-shaped chest
Enlargement of air spaces and decreased recoil resulting from destruction of alveolar walls; increased compliance.

Increased elastase activity, increased lung compliance due to loss of elastic fibers.
Exhalation through pursed lips to increase airway pressure and prevent airway collapse during respiration.

Front 65

Emphysema - histology findings

Back 65

Enlarged alveoli are seen separated by thin septa, some of which appear to float in alveolar spaces.

Front 66

Emphysema - gross pathology findings

Back 66

Gross specimen shows multiple cavities linked by heavy black carbon deposits.

Front 67

Obstructive lung disease - Asthma

Back 67

Bronchial hyperresponsiveness causes reversible bronchoconstriction. Smooth muscle hypertrophy and Curschmann's spirals (shed epithelium forms mucous plugs).

Can be triggered by viral URIs, allergens and stress.
Test with methacholine challenge.
Findings: cough, wheezing, tachypnea, dyspnea, hypoxemia, decreased I/E ratio, pulsus paradoxus, mucus plugging

Front 68

What are Curschmann's spirals?

Back 68

Seen with asthma. Represent shed epithelium from mucous plugs on histology of lung biopsy.

Front 69

Obstructive Lung Disease - Bronchiectasis

Back 69

Chronic necrotizing infection of bronchi --> permanently dilated airways, purulent sputum, recurrent infections, hemoptysis.

Associated with bronchial obstruction, poor ciliary motility (smoking), Kartagener's syndrome. Aspergillus is a possible risk factor.

Front 70

Describe pulsus paradoxus.

Back 70

>10 mmHg drop in SBP measurement during maximal inspiration. Associated with asthma exacerbations.

Front 71

Restrictive Lung Diseases - details and 2 major categories

Back 71

Restricted lung expansion causes decreased lung volumes (decreased FVC and TLC). PFTs - FEV1/FVC ratio >80%
Types:
1. Poor breathing mechanics (extrapulmonary, peripheral hypoventilation)
2. Interstitial lung diseases (pulmonary, lowered diffusing capacity)

Front 72

Restrictive Lung Diseases - Poor breathing mechanics

Back 72

Poor muscular effort - polio, myasthenia gravis
Poor structural apparatus - scoliosis, morbid obesity

Front 73

Restrictive Lung Diseases - Interstitial lung diseases

Back 73

1. Acute respiratory distress syndrome (ARDS)
2. Neonatal respiratory distress syndrome (hyaline membrane disease)
3. Pneumoconioses (coal miner's, silicosis, asbestos)
4. Sarcoidosis: bilateral hilar lymphadenopathy, noncaseating granuloma, increased ACE and calcium
5. Idiopathic pulmonary fibrosis (repeated cycles of lung injury and wound healing with increased collagen deposition)
6. Goodpasture's syndrome
7. Wegener's granulomatosis
8. Eosinophilic granuloma (histiocytosis X)
9. Drug toxicity (bleomycin, busulfan, amiodarone)

Front 74

Pneumoconioses - Coal miner's

Back 74

Associated with coal mines. Can result in cor pulmonale, Caplan's syndrome (rheumatoid arthritis involvement)

Affects upper lobes.

Front 75

What is Caplan's syndrome?

Back 75

Rheumatoid arthritis associated with Coal Miner's Pneumoconiosis

Front 76

Pneumoconioses - Silicosis

Back 76

Associated with foundries, sandblasting, 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.
Affects upper lobes. "Eggshell" calcifications of hilar lymph nodes (see picture).

Front 77

Pneumoconioses - Asbestosis

Back 77

Associated with shipbuilding, roofing, and plumbing. Results in "ivory white," calcified pleural plaques. Associated with an increased incidence of bronchogenic carcinoma and mesothelioma.

Affects lower lobes. Asbestos bodies are golden-brown fusiform rods resmbling dumbbells, located inside macrophages (see picture).

Front 78

Which pneumoconioses affect upper lobes? Lower lobes?

Back 78

Upper - Coal miner's, silicosis
Lower - Asbestosis

Front 79

Neonatal respiratory distress syndrome (Hyaline membrane disease)

Back 79

Surfactant deficiency leading to increased surface tension, resulting in alveolar collapse. Surfactant is made by type II pneumocytes most abundantly after 35th week of gestation. The lecithin-to-sphingomyelin (L:S) ratio in the amniotic fluid, a measure of lung maturity, is usually < 1.5 in neonatal respiratory distress syndrome. Persistently low O2 tension --> risk of PDA. Therapeutic supplemental O2 can result in retinopathy of prematurity.
Surfactant - dipalmitoyl phosphatidylcholine
Risk factors: prematurity, maternal diabetes (due to elevated insulin), cesarean delivery (decreased release of fetal glucocorticoids)
Treatment: maternal steroids before birth; artificial surfactant for infant; thyroxine

Front 80

Supplemental O2 for treatment of neonatal RDS can result in what complication?

Back 80

Retinopathy of Prematurity

Front 81

Name 3 risk factors for neonatal RDS.

Back 81

Prematurity
Maternal diabetes (due to elevated insulin)
Cesarean delivery (dec. release of fetal glucocorticoids)

Front 82

Why is maternal diabetes associated with an increased risk of neonatal respiratory distress syndrome?

Back 82

Elevated insulin

Front 83

Acute Respiratory Distress Syndrome - Details?

Back 83

May be caused by trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, or amniotic fluid embolism.

Diffuse alveolar damage --> increased alveolar capillary permeability --> protein-rich leakage into alveoli. Results in formation of intra-alveolar hyaline membrane (see picture). Initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, and oxygen-derived free radicals.

Front 84

Name 7 causes of ARDS

Back 84

Trauma
Sepsis
Shock
Gastric aspiration
Uremia
Acute Pancreatitis
Amniotic fluid embolism

Front 85

Obstructive vs. Restrictive Lung disease

Back 85

Normal - FEV1/FVC = 80%
Obstructive - FEV1/FVC < 80%
Restrictive - decreased TLC

Obstructive lung volumes > normal (Increased TLC, FRC, RV); restrictive lung volumes < normal. In both obstructive and restrictive FEV1 and FVC are reduced, but in obstructive, FEV1 is more dramatically reduced, resulting in a decreased FEV1/FVC ratio. (see First Aid p 570 for graphs)

Front 86

Sleep Apnea

Back 86

Person stops breathing for at least 10 seconds repeatedly during sleep.
Central sleep apnea - no respiratory effort
Obstructive sleep apnea - respiratory effort against airway obstruction

Associated with obesity, loud snoring, systemic/pulmonary hypertension, arrhythmias, and possibly sudden death.
Individuals may become chronically tired.
Treatment: weight loss, CPAP, surgery
Hypoxia --> increased EPO release --> increased erythrocytosis

Front 87

Lung-physical findings - Bronchial obstruction

Back 87

Absent or decreased breath sounds over affected area.
Decreased resonance.
Decreased fremitus.
Tracheal deviation toward the side of lesion.

Front 88

Lung-physical findings - Pleural effusion

Back 88

Decreased breath sounds over effusion.
Hyporesonance.
Decreased fremitus.
No tracheal deviation.

Front 89

Lung-physical findings - Pneumonia (lobar)

Back 89

May have bronchial breath sounds over lesion.
Hyporesonance.
Increased fremitus.
No tracheal deviation.

Front 90

Lung-physical findings - Tension pneumothorax

Back 90

Decreased breath sounds.
Hyperresonant.
Absent fremitus.
Tracheal deviation away from side of lesion.

Front 91

Lung-physical findings - Spontaneous pneumothorax

Back 91

Decreased breath sounds.
Hyperresonant.
Decreased fremitus.
Tracheal deviation toward the side of the lesion.

Front 92

Lung cancer - basics?

Back 92

Lung cancer is the leading cause of cancer death.
Presentation: cough, hemoptysis, bronchial obstruction, wheezing, pneumonic "coin" lesion on x-ray film or noncalcified nodule on CT

Metastases to lung are most common, often from breast, colon, prostate, and bladder cancer.
Sites of metastases - adrenals, brain (epilepsy), bone (pathalogic fracture), liver (jaundice, hepatomegaly)

Front 93

How to remember complications of lung cancer?

Back 93

SPHERE of complications
Superior vena cava syndrome
Pancoast tumor
Horner's syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal symptoms (hoarseness)
Effusions (pleural or pericardial)

Front 94

Lung cancer - Small cell (oat cell) carcinoma

Back 94

Location: central
Characteristics:
Undifferentiated --> very aggressive; often associated with ectopic production of ACTH or ADH; may lead to Lambert-Eaton syndrome (autoantibodies against calcium channels). Responsive to chemotherapy. Inoperable.

Histology: Neoplasm of neuroendocrine Kulchitsky cells --> small dark blue cells. "Salt and pepper" neuroendocrine-type chromatin (see picture).

Front 95

What are Kulchitsky cells?

Back 95

Small dark blue cells of neuroendocrine origin associated with Small cell carcinoma of the lung

Front 96

Lung cancer - Adenocarcinoma (Bronchial type)

Back 96

Location: Peripheral
CHaracteristics:
Develops in site of prior pulmonary inflammation or injury (most common lung cancer in nonsmokers and females).

Both bronchial and bronchioalveolar have Clara cells --> type II pneumocytes; multiple densities on x-ray of chest

Front 97

Lung cancer - Adenocarcinoma (Bronchioalveolar type)

Back 97

Location: peripheral
Characteristics: Not linked to smoking; grows along airways; can present like pneumonia. Can result in hypertrophic osteoarthropathy.

Both bronchial and bronchioalveolar types: Clara cells --> type II pneumocytes; multiple densities on x-ray of chest

Front 98

Lung cancer - Squamous cell carcinoma

Back 98

Location: Central
Characteristics:
Hilar mass arising from bronchus; Cavitation; Clearly linked with smoking; parathyroid-like activity (PTHrP)

Histology: keratin pearls and intercellular bridges

Front 99

Lung cancer - Large cell carcinoma

Back 99

Location: peripheral
Characteristics:
Highly anaplastic undifferentiated tumor; poor prognosis; less responsive to chemotherapy. Removed surgically.

Histology: pleomorphic giant cells with leukocyte fragments in cytoplasm (Giant Cells - think Large Cell Carcinoma)

Front 100

Lung cancer - Carcinoid tumor

Back 100

Characteristics:
Secretes serotonin, can cause carcinoid syndrome (flushing, diarrhea, wheezing, salivation). Fibrous deposits in right heart valves may lead to tricuspid insufficiency, pulmonary stenosis, and right heart failure.

Front 101

Lung cancer - Mesothelioma

Back 101

Location: pleural
Characteristics:
Malignancy of the pleura associated with asbestosis. Results in hemorrhagic pleural effusions and pleural thickening.
Histology: Psammoma bodies

Front 102

Small cell carcinoma of the lung - histology findings

Back 102

Sheets of tumor cells with nuclear modling, highmitotic rate, necrosis, and "salt-and-pepper" neuroendocrine-type chromatin.

Front 103

Squamous cell carcinoma of the lung - histology findings

Back 103

Sheets of large squamous cells with dysplasia and keratin "pearls"

Front 104

Pancoast tumor

Back 104

Carcinoma that occurs in apex of lung and may affect cervical sympathetic plexus, causing Horner's syndrome.

Front 105

Horner's syndrome - classic triad

Back 105

Ptosis, miosis, anhidrosis

Front 106

Superior vena cava syndrome

Back 106

An obstruction of the SVC that impairs blood drainage from the head ("facial plethora"), neck (jugular venous distension), and upper extremities (edema). Most commonly caused by neoplasms and thromboses. Can raise intracranial pressure (if obstruction is severe), which presents as headaches and dizziness and can increase the risk of aneurysm/rupture of cranial arteries.

Front 107

Pneumonia - Lobar - Organisms? Characteristics?

Back 107

Pneumococcus most frequently, Klebsiella

Intra-alveolar exudate --> consolidation; may involve entire lung.

Front 108

Pneumonia - Bronchopneumonia - organisms? characteristics?

Back 108

S. aureus, H. flu, Klebsiella, S. pneumoniae

Acute inflammatory infiltrates from bronchioles into adjacent alveoli; patchy distribution involving >/= 1 lobes.

Front 109

Pneumonia - Interstitial (atypical) pneumonia - organisms? characteristics?

Back 109

Viruses (RSV, adenoviruses), Mycoplasma, Legionella, Chlamydia

Diffuse patchy inflammation localized to interstitial areas at alveolar walls; distribution involving >/= 1 lobes. Generally follows a more indolent course than bronchopneumonia.

Front 110

Bronchopneumonia - histology findings

Back 110

Neutrophils in alveolar spaces.

Front 111

Bronchopneumonia - gross pathology findings

Back 111

Large area of consolidation

Front 112

Lung abscess

Back 112

Localized collection of pus within perenchyma. Caused by: bronchial obstruction (e.g., cancer); aspiration of oropharyngeal contents (especially in patients predisposed to loss of consciousness, e.g., alcoholics or epileptics)

Air-fluid levels often seen on CXR. Often due to S. aureus or anaerobes (Bacteroides, Fusobacterium, Peptostreptococcus)

Front 113

Hypersensitivity Pneumonitis

Back 113

Mixed type III/IV hypersensitivity reaction to environmental antigen --> dyspnea, cough, chest tightness, headache. Often seen in farmers and those exposed to birds.

Front 114

What are two risk factors for developing Hypersensitivity Pneumonitis?

Back 114

Farmers and being exposed to birds

Front 115

Pleural Effusions - 3 types and details of each

Back 115

Transudate - decreased protein content. Due to CHF, nephrotic syndrome, or hepatic cirrhosis.
Exudate - Increased protein content, cloudy. Due to malignancy, pneumonia, collagen vascular disease, trauma (occurs in states of increased vascular permeability). Must be drained in light of risk of infection.

Lymphatic - also known as chylothorax. Milky-appearing fluid; increased triglycerides

Front 116

Pneumothorax - Signs and Symptoms?

Back 116

Unilateral chest pain and dyspnea, uilateral chest expansion, decreased tactile fremitus, hyperresonance, diminished breath sounds

Front 117

Spontaneous pneumothorax

Back 117

Accumulation of air in the pleural space. Occurs most frequently in tall, thin, young males because of rupture of apical blebs. Trachea deviates toward affected lung.

Front 118

Tension pneumothorax

Back 118

Usually occurs in setting of trauma or lung infection. Air is capable of entering pleural space but not exiting. Trachea deviates away from affected lung.

Front 119

H1 blockers - details

Back 119

Reversible inhibitors of H1 histamine receptors.

Front 120

H1 blockers - 1st generation - Examples? clinical uses? toxicity?

Back 120

Diphenhydramine, dimenhydrinate, chlorpheniramine
Clinical uses: allergy, motion sickness, sleep aid
Toxicity: Sedation, antimuscarinic, anti-alpha-adrenergic

Names usually contain "-en/-ine" or "-en/-ate"

Front 121

H1 blockers - 2nd generation - Examples? Clinical uses? Toxicity?

Back 121

Loratidine, fexofenadine, desloratadine, cetirizine
Clinical uses: Allergy
Toxicity: Far less sedating than 1st generation because of decreased entry into CNS.

Names usually end in "-adine"

Front 122

Asthma drugs - details

Back 122

Bronchoconstriction is mediated by (1) inflammatory processes and (2) parasympathetic tone; therapy is directed at these two pathways.

Front 123

Asthma drugs - nonspecific Beta-agonist

Back 123

Isoproterenol - relaxes bronchial smooth muscle (Beta-2). Adverse effect is tachycardia (Beta-1).

Front 124

Asthma drugs - Beta-2 agonists

Back 124

Albuterol - relaxes bronchial smooth muscle (Beta-2). Use during acute exacerbation.

Salmeterol - long-acting agent for prophylaxis. Adverse effects are tremor and arrhythmia.

Front 125

Asthma drugs - methylxanthines

Back 125

Theophylline - likely causes bronchodilation by inhibiting phosphodiesterase, thereby decreasing cAMP hydrolysis. Usage is limited because of narrow therapeutic index (cardiotoxicity, neurotoxicity); metabolized by P-450. Blocks actions of adenosine.

Front 126

Asthma drugs - Muscarinic antagonists

Back 126

Ipratropium - competitive blocker of muscarinic receptors, preventing bronchoconstriction. Also used for COPD.

Front 127

Asthma drugs - Cromolyn

Back 127

Prevents release of mediators from mast cells. Effective only for the prophylaxis against asthma. Not effective during an acute asthmatic attack. Toxicity is rare.

Front 128

Asthma drugs - Corticosteroids

Back 128

Beclomethasone, prednisone - inhibit snthesis of virtually all cytokines. Inactivate NF-kappaB, the transcription factor that induces the production of TNF-alpha, among other inflammatory agents. 1st line therapy for chronic asthma.

Front 129

Asthma drugs - antileukotrienes - Zileuton

Back 129

A 5-lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes.

Front 130

Asthma drugs - antileukotrienes - Zafirlukast, montelukast

Back 130

Block leukotriene receptors. Especially good for aspirin-induced asthma.

Front 131

What drug is particularly good at treating aspirin-induced asthma?

Back 131

Leukotriene receptor blockers (Montelukast, Zafirlukast)

Front 132

Guaifenesin

Back 132

Expectorant - removes excess sputum, does not suppress cough reflex

Front 133

N-acetylcysteine

Back 133

Mucolytic - can loosen mucous plugs in CF patients. Also used as an antidote for acetaminophen overdose.

Front 134

Bosentan

Back 134

Used to treat pulmonary hypertension. Competitively antagonizes endothelin-1 receptors, decreasing pulmonary vascular resistance.

Front 135

Dextromethorphan

Back 135

Antitussive (antagonizes NMDA glutamate receptors). Synthetic codeine analog. Has mild opioid effect when used in excess. Naloxone can be given for OD. Mild abuse potential.

Front 136

How does dextromethorphan elicit its antitussive effects?

Back 136

antagonizes NMDA glutamate receptors

Front 137

Pseudoephedrine, phenylephrine - Mechanism? Clinical use? Toxicity?

Back 137

Mechanism: sympathomimetic alpha-agonist nonprescription nasal decongestants
Clinical use: reduces hyperemia, edema, and nasal congestion; opens obstructed Eustachian tubes. Pseudoephedrine also used as a stimulant.
Toxicity: Hypertension. Can also cause CNS stimulation/anxiety (pseudoephedrine).

Front 138

Methacholine - mechanism? clinical use?

Back 138

Mechanism: Muscarinic receptor agonist
Clinical use: Used in asthma challenge testing.

Front 139

Explain bronchial tone mediators

Back 139

cAMP causes bronchodilation while ACh and Adenosine cause bronchoconstriction.

Beta-agonists increase Adenylate Cyclase activity, thus increasing cAMP and bronchodilation. Theophylline blocks phosphodiesterase which prevents hydrolysis of cAMP and promotes bronchodilation.

Muscarinic antagonists block acetylcholine's bronchoconstrictive effect. Theophylline also blocks adenosine's bronchoconstrictive effect directly.

Front 140

How long does it take for hemoglobin levels to elevate to the point where blood oxygen content is near normal after moving to a high altitude environment (>4000 meters above sea level).

Back 140

EPO begins being secreted after several hours but it takes 10-14 days for hemoglobin concentrations and blood oxygen content to have adjusted adequately.

Therefore, blood PaO2 will be low (~60 mmHg) for many days following the move.

Front 141

Chronic rejection after lung transplant affects what anatomical region of the lung?

Back 141

Small airways (small bronchioles) - termed "bronchiolitis obliterans"

Front 142

In a patient with suspicion of CF but a normal sweat test, what other test should be performed?

Back 142

Nasal transepithelial potential difference - measures the charge on the respiratory epithelial surface as compared to the interstitial fluid

CF patients have a significantly more negative nasoepithelial surface than normal due to increased luminal sodium absorption

Front 143

Why do CF patients have increased sodium absorption in ductal epithelial cells?

Back 143

CFTR has a tonic inhibitory effect on the opining of apical sodium channels (which absorb sodium into the cell) - if CFTR is nonfunctioning, sodium absorption goes on unchecked

Front 144

Explain the "Chloride shift"

Back 144

RBCs have a higher chloride content in the venous circulation than the arterial circulation (systemically) because chloride shifts into the RBCs to maintain electrical neutrality, given the excretion of HCO3- ions out of the cells

Front 145

What finding points you away from left heart failure and towards ARDS, most notably?

Back 145

Normal PCWP in ARDS.

Front 146

Which leukotriene stimulates neutrophil chemotaxis?

Back 146

Leukotriene B4

Front 147

Panacinar emphysema occurs in patients with what risk factor, most commonly?

Back 147

alpha1-antitrypsin deficiency

Front 148

The process by which centriacinar emphysema develops is mediated by many proteases and oxidant molecules. Which molecule plays a particularly central role, and what cell secretes it?

Back 148

Elastase, neutrophils

Front 149

How are particles of different sizes cleared from the respiratory tract?

Back 149

10-15 um - trapped in upper respiratory tract
2.5 - 10 um - enter the trachea and bronchi and are cleared by mucociliary transport
< 2um - reach terminal bronchioli and alveoli and are phagocytized by macrophages

Front 150

what epithelial cell type covers the true vocal cords?

Back 150

stratified squamous epithelium

Front 151

What epithelial cell type covers the paranasal sinuses, laryngeal vestibule, false vocal cords, and tracheal bifurcation?

Back 151

ciliated, pseudostratified, columnar, mucus-secreting epithelium

Front 152

what is Potter syndrome?

Back 152

congenital condition marked by pulmonary hypoplasia, limb deformities and characteristic facies (suborbital creases, a depressed nasal tip, low-set ears, and retrognathia) as a result of oligohydramnios from bilateral renal agenesis

Front 153

why do patients with restrictive lung disease typically have relatively high expiratory flow rates?

Back 153

increased elastic recoil pressure and increased radial traction on the conducting airways by the fibrotic pulmonary interstitium leads to less conducting airway resistance

Front 154

what is the most common mutation in CF patients?

Back 154

Delta508 - deletes the three nucleotides that code for phenylalanine at amino acid position 508 (70% of cases)

this causes abnormal protein folding and failure of glycosylation - the CFTR protein is degraded before it reaches the cell surface, causing its complete absence fromt he apical membrane of exocrine ductal epithelial cells

Front 155

what marker of mast cell activation is elevated in an anaphylactic reaction (besides Histamine)

Back 155

tryptase

Front 156

what mechanism triggers vasoactive substance release by mast cells?

Back 156

IgE-Fc receptor aggregation on mast cell surface -> produces various intracellular cascades that ultimately cause mast cell degranulation

Front 157

how does suppurative destruction of lung parenchyma within an abscess cavity induced?

Back 157

lysosomal content release by macrophages

Front 158

how does surfactant reduce the variation in distending pressure amongst spheres of varying sizes?

Back 158

Surfactant decreases the surface tension as a sphere decreases in size. As the inside area of the sphere decreases, the surfactant becomes more concentrated and thus is able to decrease surface tension to a greater extent. Conversely, as a sphere grows larger, the surfactant molecules become more spread out and do not reduce the surface tension as much.

Front 159

what molecule do both amphotericin B and nystatin bind to in fungal cell wall that allows them to create pores?

Back 159

ergosterol - they will not work if ergosterol is not synthesized adequately by the fungal cells

Front 160

what are the Echinocandins?

Back 160

Caspofungin and Micafungin (antifungals) - inhibit glucan synthesis (a component of the fungal cell wall)

Front 161

Name three mechanisms for the development of lung abscesses.

Back 161

1. aspiration of oropharyngeal contents (most commoN) - Fusobacterium, Peptostreptococcus, and bacteroides species are usually found
2. Complication of bacterial pneumonia - immunosuppressed, old age and underlying chronic diseases - usually nosocomial and caused by S. aureus, E. coli, K. pneumoniae, or S. pneumoniae type 3
3. Hematogenous spread - in sepsis or infective endocarditis, usually multiple abscesses are found - staphylococcus and streptococcus are most common (may also be e. coli and fungi)

Front 162

what are the four stages of a lobar pneumonia?

Back 162

Congestion (first 24 hours) - grossly red, heavy and boggy; microscopically vascular dilation, alveolar exudate containing mostly bacteria

Red hepatization (days 2-3) - grossly red, firm lobe (liver-like consistency) - alveolar exudate contains erythrocytes, neutrophils and fibrin

Gray hepatization (days 4-6) - gray-brown firm lobe - RBCs disintegrate, alveolar exudate contains neutrophils and fibrin

Resolution - restoration of normal architecture - enzymatic digestion of the exudate

Front 163

how does amphoterocin B cause most of its side effects

Back 163

has some activity against human cell cholesterol molecules

Front 164

main toxicities of Amphotericin B

Back 164

1. acute infusion related reactions
2. dose-dependent nephrotoxicity
3. Electrolyte abnormalities (hypomagnesemia and hypokalemia)
4. Anemia
5. Thrombophlebitis at site of injection may occur

Front 165

How does N-acetylcysteine induce its mucolytic effects?

Back 165

Reducing intermolecular disulfide bridges within mucus glycoproteins

Front 166

explain the mechanism of panacinar emphysema development in alpha1-antitrypsin deficiency

Back 166

Unopposed action of neutrophil elastase on alveolar walls

Front 167

explain two ways that smoking is thought to contribute to panacinar emphysema development in patients with alpha1-antitrypsin deficiency

Back 167

Oxidant products of smoke (include free radicals) can inactivate endogenous alpha1-antitrypsin, producing a "functional" alpha1-antitrypsin deficiency.

Smoking also enhances elastase activity in macrophages and macrophage elastase (unlike neutrophil derived elastase) is not inhibited by alpha1-antitrypsin.

Front 168

vitamin D (calcitriol) is thought to be secreted in what respiratory conditions?

Back 168

granulomatous disorders (sarcoidosis, tuberculosis, Hodgkin's disease, non hodgkin's lymphoma)

Front 169

if you are given a PaO2 and a PaCO2, how can you calculate the A-a gradient?

Back 169

alveolar gas equation

PAO2 = 150 - PaCO2 / 0.8

A-a gradient = PAO2 - PaO2

Front 170

streptomycin inhibits what step of protein translation?

Back 170

Aminoglycosides inhibit the INITIATION step

Front 171

recurrent respiratory infections with pseudomonas, chronic diarrhea and weight loss with the death of a 9-year-old sibling due to respiratory infection suggest what disease?

Back 171

Cystic Fibrosis

Front 172

what enzyme can be replaced in CF patients to help with chronic diarrhea and weight loss?

Back 172

pancreatic lipase

Front 173

reduced pulmonary parenchymal compliance is the hallmark of what disease?

Back 173

pulmonary fibrosis

Front 174

In the Reid index, what layer of the bronchial wall is not included in the measurement?

Back 174

the outer cartilage layer is excluded

Front 175

if a question mentions long, branched lipids within some bacterial cells, it is most likely referring to what?

Back 175

mycolic acid in M. tuberculosis

Front 176

why do patients with CF develop squamous metaplasia of exocrine ducts in the pancreas?

Back 176

Vitamin A deficiency from long-standing pancreatic insufficiency

Vitamin A and its metabolite, Retinoic acid, are required to maintain orderly differentiation of specialized epithelia, including mucus-secreting columnar epithelium. When a deficiency state exists, the epithelium undergoes squamous metaplasia to a keratinizing epithelium.

Front 177

What is Bosentan used for?

Back 177

Given to patient's with pulmonary hypertension while awaiting lung transplantation.

It is an oral endothelin-receptor antagonist recently approved for treatment of pulmonary hypertension. Endothelin is a potent vasoconstrictor and stimulant of endothelial proliferation.

Front 178

What drug inhibits synthesis of the fungal cell wall?

Back 178

Caspofungin (and other echinocandin antifungals such as micafungin)

Blocks glucan synthesis (glucan is a major polysaccharide component of the fungal cell wall.)

Front 179

How many days does it take for the kidneys to compensate for severe respiratory acid-base disturbances?

Back 179

3-5 days

Front 180

A white newborn develops bilious vomiting and laparotomy reveals an inspissated green fecal mass obstructing the small bowel lumen.

What disease does the baby have?

Back 180

Cystic Fibrosis leading to a meconium ileus

Front 181

what is the major enzyme that is released by eosinophils in atopic asthma?

Back 181

Major Basic Protein

Front 182

in a chronic smoker, metaplasia from what cell type to what cell type occurs in the bronchi?

Back 182

From ciliated pseudostratified epithelium to stratified squamous epithelium

Front 183

what is the most likely mechanism of tissue damage in patients with caseating granuloma from reactivation TB?

Back 183

Delayed-type hypersensitivity (the mechanism by which granuloma is formed) - this leads to collateral damage from inflammation

Front 184

What is the most potent mediator of cerebral blood flow?

Back 184

PaCO2 - direct, linear relationship

Front 185

what gives sputum its green color in patients with lobar pneumonia?

Back 185

Myeloperoxidase - a blue green, heme-based pigment molecule contained in azurophilic granules of neutrophils that catalyzes the production of hypochlorous acid (HOCl) from chloride and hydrogen perxoide during the phagocytic respiratory burst

Front 186

why is blood in the left atrium slightly less oxygenated than blood in the pulmonary capillaries?

Back 186

Bronchial blood is mixed in which is deoxygenated - bronchioles are supplied from branches off the descending aorta and much of this blood flow then returns to the heart via the pulmonary arteries

Front 187

what two gene mutations lead to TB resistance to Isoniazid in the setting of monotherapy administered to a patient with active TB?

Back 187

Decreased expression of catalase-peroxidase enzyme that is required for isoniazid activation once the drug enters the bacterial cell.

Modification of the protein target binding site for Isoniazid

Front 188

What is the most common cause of death in patients with Asbestos exposure?

Back 188

Lung Cancer - specifically bronchogenic carcinoma

NOT MESOTHELIOMA - that is the second most common cause of death

Front 189

what type of NMJ blocker is succinylcholine?

Back 189

depolarizing - action is more rapid than with most non-depolarizing NMJ blockers (such as rocuronium)

Front 190

What is train-of-four stimulation? Explain what it looks like in a patient on succinylcholine.

Back 190

used to assess the degree of muscle relaxation induced by NMJ-blocking agents

Depolarizing blockers show sustained and equal reduction of all 4 twitches during phase 1 blockade. Continued administration of succinylcholine results in eventual transition to phase II blockage. Twitch response during this phase mimics those seen in nondepolarizing NMJ bloackade and show a fading pattern with progressive reduction in each of the 4 responses.

Front 191

Ethambutol works by what mechanism?

Back 191

Inhibits arabinosyl transferase, an enzyme that polymerizes arabinose into arabinan and then arabinogalactan (a constituent of the mycobacterial cell wall). This carbohydrate polymerization is necessary for mycobacterial cell wall synthesis.

Front 192

Superior vena cava syndrome is most commonly caused by what?

Back 192

Bronchogenic carcinoma is most common, but any mediastinal mass can cause it

Front 193

what finding on a biopsy of a lung coin lesion would suggest hamartoma?

Back 193

Cartilage tissue - hamartoma (a.k.a. pulmonary chondroma) is the most common benign lung tumor.

Hamartoma is an excessive growth of a tissue type native to the organ of involvement. Lung hamartomas often contain islands of mature hyaline cartialge, fat, smooth muscle and clefts lined by respiratory epithelium.

Front 194

What separates silica from the other pneumoconioses in terms of x-ray findings and histology?

Back 194

Eggshell calcification of hilar nodes on CXR and birefringent silica particles surrounded by fibrous tissue in the nodes themselves.

Front 195

which lung cancer is inoperable in all cases?

Back 195

small cell carcinoma

Front 196

What lung disease can develop in patients with OSA?

Back 196

Pulmonary Hypertension --> Cor Pulmonale

Front 197

Fat embolism syndrome - describe

Back 197

Triad of acute-onset neurologic abnormalities, hypoxemia, and a petechial rash in a patient with severe long bone and/or pelvic fractures.

Traumatic event dislodges fat globules from the bone marrow, allowing them to travel through the marrow vascular sinusoids and into the pulmonary microvessels. The release of free fatty acids from the fat globules causes local toxic injury to the endothelium (with the potential to cause ARDS.)

Thrombocytopenia and petechiae that are associated with the fat embolism syndrome arise secondary to platelet adherence to and coating of the fat microglobules.

Front 198

What is the mechanism of action of Terbinafine?

Back 198

Inhibition of squalene epoxidase inhibits synthesis of ergosterol of the fungal membrane.

Front 199

Which TB drug works best in acidic environments and therefore works well against intracellular TB organisms?

Back 199

Pyrazinamide

Front 200

Why is minute ventilation different from alveolar ventilation?

Back 200

Minute ventilation incorporates dead space while alveolar ventilation only accounts for air that is involved in gas exchange.

Front 201

What two ways does COPD lead to obstructive flow-volume loop profile?

Back 201

increased bronchial resistance (due to anatomic narrowing as in chronic bronchitis) and/or from decreased lung elasticity (e.g. due to destruction of interalveolar walls as in emphysema)

Front 202

How can you distinguish Absolute versus relative erythrocytosis?

Back 202

Need to check for increased total RBC mass - increased suggests absolute erythrocytosis, nromal suggests relative erythrocytosis - can check this with 51Cr-tagged RBC infusion test

Front 203

What SaO2 is the cutoff for developing secondary polycythemia?

Back 203

<92% (PaO2 < 65 mm Hg)

NOTE THAT THE SaO2 is a percentage - use the PaO2

Front 204

How can you tell primary from secondary erythrocytosis?

Back 204

EPO is low in primary (myeloproliferative disorders)

EPO is high in secondary (chronic hypoxia)

Front 205

How does Cromolyn work?

Back 205

Prevents release of mediators from mast cells.

Front 206

At what point on the spirometry graph showing all the various possible lung volumes, is the pulmonary vascular resistance the lowest?

Back 206

Functional residual capacity (end of normal exhalation) - if you exhale more forcibly, although the alveoli are less expanded and exert less force on the vaculature, the chest wall and muscles is pushing down on the vessels from increased intrathoracic pressure - therefore the end expiratory volume of a normal breath is where pressure is the lowest

Front 207

What are possible symptoms of locally invasive superior sulcus tumor in the lung?

Back 207

1. Severe pain in the shoulder that radiates toward the axilla and scapula (most common). Can also have arm parasthesia, weakness, and muscle atrophy.
2. Horner's syndrome
3. Compression of the subclavian vessels may cause edema of the upper extremity
4. Extension of the tumor into the intervertebral foramina may lead to spinal cord compression and paraplegia.

Front 208

Why is it theorized that apical subpleural blebs form and lead to spontaneous pneumothorax in tall, thin young men?

Back 208

It is thought that intrapleural pressure is more negative in the apical lung in this patient population.

Front 209

Why is haptoglobin lower in patients with sickle cell anemia?

Back 209

Haptoglobin is a free plasma protein that binds hemoglobin in order to prevent its renal excretion. haptoglobin levels are decreased in patients with hemolytic anemias because the half-life of the haptoglobin-hemoglobin complex is about 90 minutes (the complex is hepatically cleared); in contrast, free haptoglobin has a half-life of 5 days.

Front 210

Increased HR and CO with preservation of PaO2 and PaCO2 is consistent with what integrated response?

Back 210

Cardiorespiratory response to exercise

Front 211

stab wound just superior to the clavicle and lateral to the manubrium could damage what structure?

Back 211

lung pleura --> tension pneumothorax

Front 212

Patient with normal PaO2, normal SaO2 and low oxygen content likely has what?

Back 212

Anemia - low concentration of hemoglobin but saturation of hemoglobin molecules would remain unchanged, and PaO2 is independent of Hg concentration

Front 213

What drug can improve postmenopausal osteoporosis and simultaneously reduce the chance of developing breast cancer?

Back 213

Raloxifene, a selective-estrogen receptor modulator (SERM) - binds to estrogen receptors and exhibits tissue-specific behavior that can imitate or antagonize the effects of natural estrogen.

Raloxifene has estrogen agonist activity on bone leading to a decrease in net bone resorption. In the breast and uterus, however, raloxifene behaves as an estrogen antagonist.

Front 214

Describe breathing patterns in Cheyne-Stokes breathing.

Back 214

Cyclic breathing in which apnea is followed by gradually increasing tidal volumes, and then gradually decreasing tidal volumes until the next apneic period. It is commonly seen in cardiac disease (e.g., advanced congestive heart failure) and neurologic disease (e.g., stroke, brain tumors, traumatic brain injury). It is frequently a poor prognostic sign in individuals with either neurological or cardiac disease.

Front 215

What antibiotic is commonly used to treat lung abscess?

Back 215

Clindamycin

Front 216

What vessel has the highest oxygen content in a fetus besides the umbilical vein?

Back 216

IVC (what it dumps into)

Front 217

A patient with lung cancer, diplopia and erectile dysfunction likely has what?

Back 217

Lambert-eaton syndrome - can have autonomic symptoms such as dry mouth or impotence

Front 218

what areas of the lungs are most affected in panacinar emphysema 2/2 alpha1-antitrypsin deficiency? why?

Back 218

lower lobes - they receive relatively greater perfusion, allowing greater rate of neutrophil infiltration

Front 219

what is normal PO2 of inspired air, tracheal air, and alveolar air?

Back 219

Inspired - 160 mm Hg
Tracheal - 150 mm Hg (due to humidification)
Alveolar - 104 mm Hg (which is between tracheal air (150) and venous blood (40))

Front 220

What is normal PCO2 of tracheal air, alveolar air, and venous blood?

Back 220

Tracheal air - 0 mm Hg
Alveolar air - 40 mm Hg
Venous blood - 46 mm Hg

Front 221

How are presbyopia and age-related skin wrinkles related?

Back 221

They are both normal and age-related

Front 222

What CF mutation is more common in Ashkenazi Jews?

Back 222

mutation causing premature termination of the transmembrane protein, which leads to complete absence of membrane-bound CFTR protein

Front 223

what are the only indications for Rifampin monotherapy?

Back 223

prophylactic monotherapy for H. influenzae or N. meningitidis

Front 224

What is the intrapleural pressure at the FRC?

Back 224

-5 cm H2O -> during normal inspiration the inrapleural pressure drops to -7.5 which induces a slightly negative pressure in the alveoli that draws air into the lungs

Front 225

What is coagulative necrosis?

Back 225

Coagulative Necrosis: most common, characterized by relative preservation of cell outlines in the necrotic tissue. Most exogenous injuries, including a brown recluse spider bite, are associated with coagulative necrosis. Organ ischemia is the classic example. Cell cytoplasm becomes eosinophilic due to protein denaturation. The nucleus shrinks and there is chromatin clumping (pyknosis), fragmentation (karyorrhexis), and eventually lysis.

Front 226

What is liquefactive necrosis?

Back 226

usually occurs in the CNS, in sites of ischemic strokes. Necrotic cells undergo fragmentation and are phagocytized by macrophages with the formation of a cystic cavity.

Front 227

What is fat necrosis?

Back 227

Seen in acute pancreatitis. Pancreatic enzymes, including lipases, digest the perenchyma with formation of fatty acids. Saponification (soap formation) occurs when fatty acids combine with calcium.

Front 228

What is caseous necrosis?

Back 228

Occurs in tuberculosis. Necrotic tissue has a "cheesy" appearance and consists of fragmented cells and acellular material.

Front 229

The methacholine challenge is used to rule out asthma by assessing for bronchial hyperreactivity (BHR). What is the definition for confirming BHR?

Back 229

20% decline in FEV1 after inhalation of a bronchocontstrictive substance (e.g., methacholine).

Front 230

What do the lamellar bodies of type II pneumocytes hold?

Back 230

surfactant molecules

Front 231

Explain how the optimum breathing rate goes up in conditions with increased elastic resistance in the lungs while the optimum breathing rate goes down in conditions with increased upper airway resistance.

Back 231

In patients with increased elastic resistance, tidal volume needs to go down to minimize workload, as this is the main issue for these patients. Therefore, fast, shallow breaths are ideal.

In patients with upper airway obstruction (COPD, goiter, asthma), slow, deep breaths minimize work.

Front 232

Which portion of the bronchial tree has the highest airway resistance?

Back 232

Medium and small-sized bronchi greater than 2 mm in diameter (the first 10 generations of bronchi) provide the greatest summated frictional resistance. In contrast, airways smaller than 2 mm in diameter normally produce less than 20% of the total airway frictional resistance because they have a much larger total cross-sectional area.

Front 233

As epithelial cells transition as you go down the bronchial tree...which aspect of these cells is the last to stop being produced?

Back 233

Cilia are the last thing and stop being produced just before the alveoli begin.

Front 234

what TB-produced enzyme is necessary to activate Isoniazid molecules?

Back 234

catalase-peroxidase (KatG)

Front 235

If EM of a pleural biopsy shows numerous, long, slender microvilli and abundant tonofilaments, what are you seeing?

Back 235

Mesothelioma (distinguish this from adenocarcinoma which has short, plump microvilli)

Front 236

what cells are capable of dividing in response to alveolar injury?

Back 236

Type II pneumocytes (NOT clara cells)

Front 237

Why can oxygen supplementation be dangerous in patients with COPD?

Back 237

If they are chronically hypoxemic (PaO2 < 60 mm Hg), oxygen becomes an important mediator of respiratory drive via its effects on the carotid body and aortic arch chemoreceptors.

If you give a patient supplemental oxygen who has been chronically hypoxemic, their medullary respiratory center may be inhibited and respiratory drive may decrease dramatically.

Front 238

In what clinical situation would it be most appropriate to perform a methacholine challenge test?

Back 238

If a patient has normal spirometry values but a family history of allergic triad diseases. Can use methacholine challenge test as a good rule out (has good NPV).

Front 239

why can an axillary lymph node dissection lead to an inability to abduct the arm above the horizontal?

Back 239

long thoracic nerve injury leads to a denervation of the serratus anterior muscle...one of this muscles primary actions is to rotate the glenoid cavity superiorly in order to allow the humerus to be completely abducted

Front 240

how does theophylline intoxication present?

Back 240

abdominal pain, nausea, vomiting, cardiac arrhythmias and seizures

treat with gastric lavage, activated charcoal, and cathartics

Treat cardiac tachyarrhytmias with beta blockers. Treat seizures with benzos and barbiturates.

Front 241

Explain the theorized mechanism for the development of hereditary pulmonary hypertension.

Back 241

First insult is an autosomally dominant gene inheritence with variable penetrance. The gene is a Bone Morphogenic Protein receptor type 2 (BMPR2) gene mutation which predisposes the patient to pulmonary vascular disease.

The patient then receives a second insult such as a viral infection, ion channel defect, or drug side effect that activates the disease process, which is characterised by increased endothelin (vasoconstrictor), decreased prostacyclin (vasodilator and platelet inhibitor), and decreased nitric oxide (vasodilator).
The result is vasoconstriction, vascular smooth muscle proliferation, fibrosis, thrombosis of pulmonary arteries and arterioles, endothelial growth factor, and elevated pulmonary pressures.

Front 242

What are the four categories of lung cancer? Describe the commonly tested clinical presentations (not respiratory pathology) that are associated with them.

Back 242

1. small cell carcinoma - ACTH, lambert-eaton, and SIADH
2. squamous cell carcinoma - PTHrP
3. adenocarcinoma - clubbing, hypertrophic osteoarthropathy
4. large cell carcinoma - gynecomastia, galactorrhea

Front 243

what category of transmembrane ion channel is CFTR?

Back 243

ATP-gated

Front 244

What stain is used to look for fat in the lung perenchyma in fat embolism syndrome? What does it cause to change (color)?

Back 244

osmium tetroxide is used, imparts a black color to fat

Front 245

What is the first step in primary TB infection of a host?

Back 245

Gravity-assisted migration to the smallest airways and phagocytization by macrophages. Mycobacterium organisms then replicate intracellularly due to the presence of the sulfatide virulence factor.

Front 246

How long does it take for the Th1 cell activation to occur in primary TB infection?

Back 246

2-4 weeks!

Front 247

Treat acute RSV bronchiolitis in a child with what drug?

Back 247

Ribavirin - best results in immunocompromised patients