Respiratory

Question 1

During which week of embryonic development does lung development start?

Describe the general process of lung development. How many stages are there?

Name all the stages of lung development, in order.

Answer 1

Week 4

5 stages

Lung bud develops from distal end of respiratory diverticulum; bud divides into 2 bronchial buds that branch off to form bronch

Embryonic (weeks 4–7), pseudoglandular (weeks 5–16), canalicular (weeks 16–26), saccular (week 26–birth), and alveolar (week 32–8 years)

Question 2

What happens during the saccular stage of lung development? Which gestational weeks does this stage encompass?

Answer 2

Alveolar ducts become terminal sacs, which are separated by primary septae, and pneumocytes develop;

week 26–birth

Question 3

Describe the difference in vascular resistance (VR) between the respiratory system in utero and at birth.

Answer 3

In utero “breathing” occurs via aspiration/expulsion of amniotic fluid, increasing VR;

at birth, replacement of fluid with air, decreases VR

Question 4

Give estimates of the alveoli count at birth and at full development. By what age are lungs fully developed?

Answer 4

At birth: 20–70 million alveoli;

by the age of 8 years (full development): 300–400 million alveoli

Question 5

At what gestational age does respiration become possible?

Which stage of lung development is this?

Answer 5

End canalicular stage ( @25 weeks) when airways increase in diameter;

respiration capable at 25 weeks

Before then, development is incompatible with life -pseudoglandular stage (5-16 weeks)

Question 6

A baby is born with a tracheoesophageal (TE) fistula.

At what stage of lung development did this likely arise? Which gestational weeks?

Answer 6

The embryonic stage

weeks 4 to 7

Question 7

A baby is born with Potter sequence. Name the three classic components of this sequence.

What is the cause?

Answer 7

Pulmonary hypoplasia,

congenital diaphragmatic hernia

bilateral renal agenesis

Babies who can’t pee in utero –> POTTER

Pulomnary hypoplasia

Oligohydraminos (TRIGGER)

Twisted face/flat face

Twisted skin

Extremity defects

Renal failure in utero

mxn:

Oligohydramnios –> compression of developing fetus –> limb deformities, facial anomalies (e.g., low-set ears and retrognathia [arrows
in A ]), compression of chest and lack of amniotic fluid aspiration into fetal lungs –> pulmonary hypoplasia (cause of death).

associated with: ARKD, obstructive uropathy, bilateral renal agenesis

Question 8

A neonate is born with pulmonary hypoplasia. What is this? Does this more commonly affect the right or left lung?

Answer 8

Pulmonary hypoplasia is a term for a poorly developed bronchial tree with abnormal histology;

>the right lung

Question 9

A newborn’s chest x-ray reveals discrete, round. sharply defined, air-filled densities. What are these and how are they formed?

You are speaking with the parents of a baby born with bronchogenic cysts. What can they expect in terms of infections?

Answer 9

These are bronchogenic cysts, which are caused by abnormal budding of the foregut and dilation of terminal or large bronchi

These cysts can cause chronic infections, since they drain poorly

Question 10

Histologically, how do type I pneumocytes appear? What about type II pneumocytes?

What is their important functions:

Answer 10

Squamous and thin (97% of pneumocytes are type I); cuboidal and clustered

Thin type I are necessary for maximum gas exchange is permitted by thin cells (squamous morphology)

Type II: They secrete surfactant (which prevents alveolar collapse) and serve as precursors to other pneumocytes (both types I and II)

Question 11

Describe club cells/clara cells (histologically) and their three functions

Answer 11

Nonciliated columnar/cuboidal pneumocytes w/secretory granules that:

• secrete a surfactant component,*
• degrade toxins,*
• & act as reserve cells*

Question 12

Explain the law of Laplace using the equation for calculating collapsing pressure (P).

Answer 12

P = 2 (Surface tension) ÷ Radius;

alveoli have a tendency to collapse on expiration, because as their radius decreases –> P increases

Question 13

What is dipalmitoylphosphatidylcholine? What is its function?

Answer 13

A type of lecithin and an important component of surfactant;

SURFACTANT decreases alveolar surface tension and prevents atelectasis

Question 14

A neonate is born at 32 weeks. Why is this neonate more likely to have respiratory problems?

Describe the mechanism of surfactant preventing alveolar collapse.

Answer 14

Surfactant synthesis starts at 26 weeks but does not mature until 35 weeks, so this neonate is more likely to have respiratory distress

Lecithin-to-spingomyelin ratio >2.0 in amniotic fluid indicated fetal lung maturity

Surfactant: decreases alveolar surface tension, preventing alveolar collapse,

decreasing lung recoil,

and increasing compliance

Question 15

Neonatal respiratory distress syndrome =

What is used as a measure of lung maturity in neonates? What values are expected in neonatal respiratory distress syndrome (NRDS)?

What are three risk factors for neonatal respiratory distress syndrome?

A newborn diagnosed with neonatal respiratory distress syndrome is at risk for what complications?

Answer 15

SURFACTANT DEFICIENCY!

Surfactant deficiency leads to an increase in surface tension, resulting in collapse of the alveoli –> impairing gas exchange in the lungs

The lecithin-sphingomyelin ratio in amniotic fluid

> 2 is healthy;

< 1.5 is predictive of NRDS

Risk Factors: Prematurity, maternal diabetes (due to elevated fetal insulin), and cesarean delivery (due to decreased release of fetal glucocorticoids)

Metabolic acidosis, PDA, necrotizing enterocolitis

Question 16

What vascular pathology is associated with persistently low oxygen tension due to neonatal respiratory distress syndrome?

Answer 16

Patent ductus arteriosus

Question 17

Medical management of neonatal respiratory distress syndrome includes what treatments for the mother and infant?

A newborn receives supplemental oxygen therapy for neonatal respiratory distress syndrome. This can lead to what three complications?

Answer 17

Administration of steroids to the mother before delivery

administration of artificial surfactant to the newborn

RIB:

Retinopathy of prematurity

Intraventricular hemorrhage

Bronchopulmonary dysplasia

Question 18

Which structures make up the large airways of the conducting zone of the respiratory tree? The small airways?

Which part of the conducting zone of the respiratory tree has the least airway resistance?

three functions of the conducting zone of the respiratory tree.

Answer 18

Large airways: nose, pharynx, larynx, trachea, bronchi; small airways: bronchioles, terminal

The terminal bronchioles (A large number of them run in parallel.)

The conducting zone warms, humidifies, and filters air; it does not participate in gas exchange (“anatomic dead space”)

Question 19

Cartilage and goblet cells extend to the end of what part of the conducting zone?

Describe the types of epithelium in the parts of the conducting zone.

What type of muscle is found in the walls of the conducting airways? To which area does it extend?

Answer 19

The bronchi

Pseudostratified ciliated columnar cells arise in bronchi/early terminal bronchioles; cuboidal cells arise in terminal bronchioles onward

Smooth muscle; it extends to the end of the terminal bronchioles (Beyond that point, it is sparse.)

Question 20

What anatomic area does the respiratory zone encompass? What is its major function?

What type of epithelial cell is found in respiratory bronchioles?

Answer 20

The lung parenchyma: respiratory bronchioles, the alveolar ducts, and the alveoli; its major function is gas exchange

Predominantly cuboidal cells

Question 21

What is the relation of the pulmonary artery to the bronchus at each lung hilium?

The oblique fissure divides which two lobes in the right lung? The left lung?

In the posterior aspect of both the right and left lungs, which fissure divides the superior and inferior lobes?

Answer 21

RALS = Right Anterior; Left Superior

The middle and inferior lobes; the superior and inferior lobes

[horizontal fissure divides superior and middle lobes of the left lung]

The oblique fissure

Question 22

mneumonics for diaphgram structures:

Answer 22

Structures perforating the diaphragm:

I (IVC) ate (8) ten (10) eggs (esophagus) in Vegas (vagus) at (aorta) twelve (12)

IVC @ T8

esophagus and vagus @ T10

Aorta, thoracic duct and azygos vein @ T12

The aorta (red), thoracic duct (white), and azygos vein (blue) (AtT-1-2, it’s the red, white, and blue.)

BiFOURcations:

C4 - Common Carotid

T4- Trachea

L4- abdominal aorta

Phrenic nerve = C3, C4, C5 (C3, 4, 5 keeps the diaphragm alive.)

Question 23

A man with diaphragmatic trauma has no pain there. To which anatomic regions is the pain referred? What is the innervation of these regions?

Answer 23

The shoulder (C5) and the trapezius ridge (C3, C4)

Question 24

Which tendon can be found on the inferior aspect of the diaphragm surrounding the caval and esophageal hiatuses?

Answer 24

The central tendon

Question 25

A man comes in with severe pain, and you determine that his phrenic nerve is irritated. What are three possible clinical causes?

Answer 25

Air, blood, or pus in his peritoneal cavity can all irritate the diaphragm (phrenic nerve)

Question 26

The inspiratory reserve volume plus the tidal volume equals what? The residual volume plus the expiratory reserve volume equals what? A pt exhales as much as he can, inhales as much as he can, and then exhales as much as he can again. What volume of air has he moved = vital capacity; Vital capacity equals the sum of what three lung volumes?

Answer 26

Inspiratory capacity Functional residual capacity *cannot use spirometry b/c residual volume can't be measured.* Tidal volume, inspiratory reserve volume, and expiratory reserve volume = maximum volume of air that can be inhaled and exhaled

Question 27

What is pathologic dead space? What is the volume of inspired air that does not contribute to gas exchange?

Answer 27

When part of the respiratory zone becomes unable to perform gas exchange (ventilation without perfusion) Physiologic dead space, VD = *It is approximately equivalent to the anatomic dead space in normal lungs, plus any alveolar dead space;* inspired air that does not contribute to gas exchange In a pt has a lung disease with a V/Q defect, likely greater than the anatomic dead space in normal lungs, vs health individual these two spaces are more or less equivalent

Question 28

What is minute ventilation (VE)? How do you calculate it? What are normal values for respiratory rate (RR), tidal volume, and physiologic dead space? What is alveolar ventilation (VA)? How do you calculate it?

Answer 28

The total volume of gas entering the lungs each minute; VE = VT × respiratory rate (RR) RR: 12 to 20 breaths/min; tidal volume: 500 mL/breath; physiologic dead space: 150 mL/breath The volume of gas per unit time that reaches the alveoli; VA = (VT− VD) × respiratory rate

Question 29

At what point in the respiratory cycle is the inward pull of the lung equal to the outward pull of the chest wall?

Answer 29

At functional residual capacity (FRC)

Question 30

At the point of functional residual capacity (FRC), what is the value of the air pressure within the lungs?

Answer 30

At FRC, the pressure within the lungs is equal to atmospheric pressure

Question 31

A pt takes a deep breath. What determines the combined volume of the chest wall and lungs?

Answer 31

Elastic properties of both

Question 32

In terms of lung pressures, explain how a pneumothorax is prevented.

Answer 32

At FRC, lung pressures are atmospheric, and opposing forces of the lung and chest wall create negative pressure in the intrapleural space

Question 33

At what lung volume is the pulmonary vascular resistance at a minimum?

Answer 33

At functional residual capacity (FRC)

Question 34

What is compliance?

Answer 34

The change in lung volume for a given change in pressure, expressed as ΔV/ΔP, and inversely proportional to wall stiffness

Question 35

What is hysteresis in relation to the pulmonary system?

Answer 35

Lung inflation curve follows a different curve than lung deflation curve because the surface tension needs to be overcome during inflation

Question 36

Is the lung easier or harder to fill with high compliance? What about low compliance?

Answer 36

High compliance: easier to fill; low compliance: harder to fill

Question 37

Hemoglobin: What are the two conformational forms of hemoglobin?

Answer 37

Relaxed (oxygenated) and taut (deoxygenated) **R**elaxed 300 X more affinity for oxygen [think: **R**espiratory *ie) whats to pick up oxygen in the lungs]* Positive cooperativity **T**aut [Think: **T**aut in **T**issues, whats to have decreased affinity to *release oxygen in the tissues*] Negative allostery

Question 38

An increase in which five factors will **favor the taut form** of hemoglobin over the relaxed form and will decrease affinity for oxygen (release oxygen)?

Answer 38

Chloride (Cl−), protons (H+)/acidity, carbon dioxide, 2,3-bisphosphoglycerate, and temperature Think of exericse - you're hot, increasing lactic acid production, increasing PvCO2 you need Hb to have a decrease affinity for oxygen so that it can release in the tissues = favors oxygen unloading

Question 39

What interaction with 2,3-BPG allows fetal hemoglobin to have a greater affinity for oxygen?

Answer 39

**Decreased affinity for 2,3-BPG** allows for greater affinity for oxygen

Question 40

Hemoglobin can act as a buffer for which ions?

Answer 40

H+

Question 41

What is the state of iron in hemoglobin needed for oxygen binding?

Answer 41

Iron in Hb ins normally in a REDUCED state = ferrous Fe2+ Fe**2**+ binds O**2** **["reduced" compared to Fe3+ = ferric, does not bind O2 readily but has an increased affinity fo cyanide]**

Question 42

When another molecule, such as carbon monoxide, binds to hemoglobin in place of oxygen, what are the systemic effects?

Answer 42

CO causes a left shift in the oxygen-hemoglobin curve, resulting in tissue **hypoxia** from decreased oxygen unloading

Question 43

A pt has **cyanide poisoning**. What two treatments do you provide?

Answer 43

**Nitrites first and then thiosulfate** (induced methemoglobinemia) nitrates and benzocaine cause poisoning by oxidizing Fe2+ --\> Fe3+

Question 44

A pt who spends much of his time mountaineering is cyanotic; a blood sample is chocolate colored. What caused this?

Answer 44

Poisoning by nitrites found in high-altitude water

Question 45

What is the name of a form of hemoglobin in which carbon monoxide is bound instead of oxygen?

Answer 45

Carboxyhemoglobin CO has 200 times the affinity of oxygen for hemoglobin

Question 46

A man presents with a headache, nausea, and confusion. He was found in a small unventilated room with a space heater. Treatment?

Answer 46

This is likely carbon monoxide poisoning: **100% O2 and hyperbaric O2**

Question 47

Hemoglobin modifications causing decreased oxygen saturation and content may lead to what?

Answer 47

Hypoxia from decreased oxygen saturation and content

Question 48

What is the difference between hemoglobin and methemoglobin?

Answer 48

Iron in hemoglobin is in reduced form (ferrous, Fe2+), while iron in methemoglobin is in oxidized form (ferric, Fe3+)

Question 49

A cyanotic pt is found to have chocolate-colored blood. Treatment?

Answer 49

Methylene blue (This pt has methemoglobinemia.)

Question 50

A man has cyanide poisoning. What property of methemoglobin makes it useful for treatment? A child has cyanide poisoning. What is the mechanism of action of nitrites used in the treatment?

Answer 50

The ferric (Fe3+) state of methemoglobin has decreased affinity for O2 but increased affinity for cyanide \*\*important to think of a person recently in a fire for cyanide poisoning\*\* Nitrites oxidize iron to form methemoglobin, which readily binds cyanide, **restoring function to cytochrome oxidase** [cyanide has a double wammy - binds hemoglobin more avidly AND disrupts cytochorme oxidase activity --\> Cyanide poisoning is a form of **histotoxic hypoxia** because the **cells of an organism are unable to use oxygen**, primarily through the **inhibition of cytochrome c oxidase** **[***It receives an electron from each of four cytochrome cmolecules, and transfers them to one oxygen molecule, converting molecular oxygen to two molecules of water. In the process, it binds four protons from the inner aqueous phase to make water, and in addition translocates four protons across the membrane, helping to establish a transmembrane difference of proton electrochemical potential that the ATP synthase then uses to synthesize ATP]*

Question 51

When the oxygen-hemoglobin dissociation curve shifts to the right... what happens to the affinity of hemoglobin for oxygen? what happens to the O2 saturation (%) at a PO2 of 50 mm Hg? Increases in the amount of which six factors cause a right shift of the oxygen-hemoglobin dissociation curve?

Answer 51

A right shift decreases the affinity of hemoglobin for oxygen = facilitates oxygen unloading A right shift **decreases oxygen saturation** =Higher oxygen pressure is required to saturate hemoglobin Right shift: **ACE BAT**s **right** handed (Acid, CO2, Exercise, 2,3-BPG, Altitude,Temperature)

Question 52

When the oxygen-hemoglobin dissociation curve shifts to the left, what happens to the affinity of hemoglobin for oxygen? what happens to the O2 saturation (%) at a PO2 of 50 mm Hg? Why is fetal hemoglobin shifted to the left?

Answer 52

A left shift increases the affinity of hemoglobin for oxygen A left shift **increases oxygen saturation** Less oxygen pressure is required to saturate hemoglobin **Fetal hemoglobin (2 alpha, 2 gamma)** has higher affinity for oxygen than adult hemoglobin because it has a **lower affinity for 2,3 BPG** than adult Hb thus **higher affinity for O2**

Question 53

What are the likely levels of a person with anemia? Hb, % O2 saturation of Hb, dissolved O2 (PaO2), and total O2content? polycythemia?

Answer 53

Anemia: Hb is decreased, % O2 saturation of Hb is normal, PaO2 is normal, and total O2 content is decreased Polycythemia: Hb is increased, % O2 saturation of Hb is normal, PaO2 is normal, and total O2 is content increased Anemia and polycythemia are opposites while both express normal %O2 sat of Hb (hemoglobin remains unchanged!), and dissolved O2 in the blood

Question 54

What is the equation for oxygen content in the blood? How do you calculate oxygen delivery to the tissues?

Answer 54

O2 content = (O2 binding capacity × Percent saturation) + Dissolved O2 Normal Hb amount = 15 g/dL; each gram can bind 1.34 mL of oxygen Normal value of the O2 binding capacity: 20.1 mL O2/dL Hb O2 delivery to tissues = Cardiac output × O2content of blood

Question 55

A previously healthy pt develops blue lips and fingertips. What does this say about the value of her deoxygenated hemoglobin level?

Answer 55

Her deoxygenated hemoglobin must be \< 5 g/dL ## Footnote **CYANOSIS**

Question 56

A woman has CO poisoning. What are the likely levels of her Hb, % O2 saturation of Hb, dissolved O2 (PaO22 content?

Answer 56

*Hb - normal* %O2 sat of Hb - **DEC** [CO competes with O2] Dissolved O2/PaO2+ content - **decreased**

Question 57

What is the resistance and compliance in pulmonary circulation?

Answer 57

Low resistance, high compliance * compliance ~ comply, they stretch out* * but recoil is needed for alveoli to come back!* * High elastic = low compliance = high recoil*

Question 58

Within the lungs, a decrease in PAO2 causes what process to occur within the vasculature in the area?

Answer 58

**Hypoxic vasoconstriction** **Note this is different from the systemic system** The purpose of this is to shift AWAY from the poorly ventilated areas of the lung to those that are well-ventilated!

Question 59

Perfusion-limited gases What are some examples where along the length of the pulmonary capillary do the partial pressures of a gas equilibrate?

Answer 59

O2 in healthy and normal lungs, CO2, N2O PP equilibrate early - gas exchange is NOT limited by its ability to cross the membrane, only by the supply of the blood; thus gas exchange CAN be increased via increasing blood flow

Question 60

Diffusion-limited gases Name examples Where along the length of the pulmonary capillary does the gas equilibrate?

Answer 60

Oxygen in damaged lungs - emphysema, fibrosis, CO Gas does NOT equilibrate - characteristic of the gas cause it to diffuse SLOWLY across the alveolar membrane

Question 61

A pt with untreated pulmonary hypertension presents with jugular venous distention, edema, and hepatomegaly. What caused this?

Answer 61

The pt is showing signs of **cor pulmonale** =right heart failure, a complication of pulmonary hypertension

Question 62

What is the equation for diffusion of a gas across a membrane? How does emphysema or fibrosis affect this equation?

Answer 62

Vgas = (A/T) × Dk(P1 − P2) where A = area, T = thickness, Dk(P1 − P2) = difference in partial pressures A pt with *emphysema* = **destruction of membranes**, **decreases the AREA** available for gas transfer causing a *_DEC in diffusion_* A pt with *fibrosis*, **thickenss of the alveolar membrane** is **increased,** causing a *_DEC in diffusion_*

Question 63

How is pulmonary vascular resistance calculated? How do you measure pulmonary vascular resistance using flow and the difference in pressure across it?

Answer 63

PVR = (Pressure in the pulmonary artery − Pressure in the left atrium) ÷ Cardiac output left atrial pressure measured = pulmonary wedge pressure **R = ΔP ÷ Q**, *where R is resistance, P is pressure, and Q is flow*

Question 64

How is pulmonary vascular resistance affected by vessel length and radius?

Answer 64

Directly prop. to length & inversely prop. to radius; R = (8η1) ÷ (πr4), *where η = viscosity of blood, 1 = vessel length, and r = vessel radius*

Question 65

What is the alveolar gas equation?

Answer 65

PAO2 = PIO2 − PaCO2/R. * PAO2 = alveolar PO2* * PI02 [typically = .21X(Patoms-water vapr), unless giving 100% oxygen or at a different altitude = .21 (760-47) ~150]* * = PO2 in inspired air,* * PaCO2 = arterial PCO2,* * R = respiratory quotient = CO2 produced/O2 consumed ~.8*

Question 66

By using the alveolar gas equation, what important measure of pulmonary function can be determined? What could affect this #

Answer 66

The alveolar-arterial gradient normal alveolar-arterial gradient: 10–15 mm Hg A-a gradient could increase due to hypoxemia, such as shunting, V/Q mismatch, fibrosis (impairs diffusion)

Question 67

Name five processes that can lead to hypoxemia (decreased arterial oxygen). Which could lead to hypoxemia with a normal A-a gradient? an increased A-a gradient?

Answer 67

NL gradient: High altitude, hypoventilation (opiod use) INC gradient: ventilation/perfusion ratio mismatches, diffusion limitations (fibrosis), and right-to-left shunting

Question 68

What does hypoxia mean? Nmae 4 processes that can lead to hypoxia

Answer 68

= decreased oxygen DELIVERY to tissue Decreased cardiac output, hypoxemia, anemia, and carbon monoxide poisoning

Question 69

Name two processes that can lead to ischemia (loss of blood flow).

Answer 69

Impeded arterial flow and reduced venous drainage

Question 70

What is the difference between hypoxemia and hypoxia?

Answer 70

Hypoxemia is decreased arterial partial pressure of oxygen, whereas hypoxia is decreased oxygen delivery to tissue

Question 71

A hiker is weak after rapidly ascending a mountain. What is his likely A-a gradient?

Answer 71

His A-a gradient is likely normal, as this is a case of hypoxemia caused by a high altitude

Question 72

A pt is found to have a diffusion limitation in his lungs. How would the A-a gradient help you show this? A pt develops a pulmonary embolus. What is his likely A-a gradient? A pt is found to have a right-to-left shunt. How is his likely A-a gradient affected?

Answer 72

Diffusion limitation would lead to an increased A-a gradient This is a case of V/Q mismatch, which would cause an increased A-a gradient A-a is increased with right to left shunts

Question 73

What is the ideal ventilation/perfusion ratio for gas exchange? What does the V/Q look like at the apex of the lung? At the base?

Answer 73

Ideal = 1:1, ventilation = perfusion **At apex: V/Q ~ 3** --\> *_wasted ventilation_*; which means there is more ventilation than there is perfusion (**both V and Q are reduced** but Q is reduced more than V) **At base: V/Q ~ .6** --\> *_wasted perfusion;_* which means there is more perfusion than there is ventilation (**both V and Q are increased** BUT Q is increased more, decreasing the ratio)

Question 74

A pt exercises. The vasodilation of the apical capillaries of the lung results in what change to the ventilation/perfusion ratio?

Answer 74

The ventilation/perfusion ratio approaches 1, maximizing gas exchange to meet the metabolic demands of exercise ***Vasodilation of apical capillary***, allows ratio to approach 1

Question 75

A pt has tuberculosis. This and other microorganisms that thrive in high-oxygen environments flourish in which part of the lungs?

Answer 75

**The apex** **zone 1** **most oxygen rich zone of the lungs**

Question 76

What part of the lung is ventilation greater? What part is perfusion greater?

Answer 76

Ventilation AND perfusion are greater at the BASE = zone 3

Question 77

A woman chokes and aspirates a peanut. What is her ventilation/perfusion ratio likely to be?

Answer 77

***_Approaching 0_***, as airway obstruction creates a blood flow shunt, which isn't part of gas exchange ***0 = "oirway" obstruction*** ***if the airway obstruction leads to perfusion with NO ventilation = SHUNT***

Question 78

A man has a pulmonary embolus. What is his ventilation/perfusion ratio likely to be?

Answer 78

***_Approaching ∞_***, as the pulmonary embolus is a blood flow obstruction, causing physiologic dead space ## Footnote **∞ = bl∞d flow obstruction**

Question 79

A pt has hypoxia due to a suspected shunt and you begin treating with 100% oxygen. Will the pt's condition improve?

Answer 79

If the pt truly has a shunt, it is **unlikely** that his or her condition will improve with 100% oxygen

Question 80

A pt has hypoxia with a V/Q ratio approaching infinity. How will you treat her?

Answer 80

**Physiologic dead space should be suspected**; *assuming dead space is less than 100%*, **oxygen should improve her condition**

Question 81

What enzyme catalyzes the conversion of carbon dioxide and water into carbonic acid? In which forms is carbon dioxide transported from the tissues to the lungs? What is the percentage of each form? Once inside a red blood cell, carbon dioxide combines with which molecule to eventually become bicarbonate?

Answer 81

Carbonic anhydrase 90% as bicarbonate (HCO3−) 5% bound to hemoglobin as carbaminohemoglobin (HbCO2- *bound to the N-terminus of globin not heme*) 5% dissolved CO2 Water

Question 82

Within a red blood cell, the carbonic acid formed from the combination of carbon dioxide and water dissociates into what two compounds? What is the fate of the two compounds after their dissociation?

Answer 82

Hydrogen and bicarbonate ions Bicarb (HCO3-) leaves the RBC adn is replaced by a chloride *Chloride shift* The hydrogen binds to Hb --\> HHb

Question 83

In the lungs, the oxygenation of hemoglobin promotes what? What is this shift effect called?

Answer 83

The dissociation of a proton from hemoglobin and therefore a decrease in pH, which favors formation of carbon dioxide from bicarbonate /**left** shift CO2 therefore can be released from RBC and exhaled =**HALDANE** effect *LHBT (in the lungs = haldane, bohr in tissues)*

Question 84

A woman has lactic acidosis. How will this pH reduction in the peripheral tissues relative to the lungs shift the oxygen dissociation curve? What is the name of this shift?

Answer 84

It will shift it to the **right**, favoring dissociation of oxygen from hemoglobin **= BOHR effect** *LHBT (in the lungs = haldane, bohr in tissues)*

Question 85

A hiker ascends to a high altitude. What happens to his ventilation, PaO2, and PaCO2? What happens to his level of 2,3-bisphosphoglycerate? what is the purpose of this?

Answer 85

*PaO2 and PaCO2 decrease*, as **ventilation is increased** In response to high altitude, the 2,3-BPG level increases --\> binds to hemoglobin so that **hemoglobin releases more oxygen as a physiologic response to high altitude**

Question 86

A pt has been living high in the mountains for years. What happens to his erythropoietin levels?

Answer 86

In response to high altitude, erythropoietin levels are increased, as are hematocrit and hemoglobin

Question 87

A hiker climbs up a tall mountain. Which organelle in his tissues increases in quantity?

Answer 87

The number of **mitochondria** increases in response to high altitude

Question 88

What happens as a man ascends up a mountain to his pH? What efect will this have on his system?

Answer 88

DEC atmos oxygen (PO2) --\> DEC PaO2 --\> **INC ventilation** --\> DEC PaCO2 --\> **respiratory alkalosis** --\> **Altitdue sickness** In response, there will be **increased renal excretion of HCO3-** to compensate for respiratory alkalosis

Question 89

The increased renal excretion of bicarbonate that is seen in response to high altitude can be augmented by using which drug?

Answer 89

Acetazolamide

Question 90

A man decides to live in the mountains for several years. What condition develops in response to chronic hypoxic pulmonary vasoconstriction?

Answer 90

Right ventricular hypertrophy

Question 91

A man undergoes an exercise test. What happens to carbon dioxide production in his muscles, oxygen consumption, and rate of ventilation? What happens to the ventilation/perfusion ratio? What happens to pulmonary blood flow?

Answer 91

They all increase V/Q ratio becomes more uniform from apex to base Pulmonary blood flow increases due to increased cardiac output

Question 92

A personal trainer performs strenuous exercise. How does the pH of the body change?

Answer 92

The pH decreases during strenuous exercise due to lactic acidosis

Question 93

What happens to PaO2 and PaCO2 in response to exercise? In response to exercise, what happens to the venous CO2 and venous O2 content?

Answer 93

No change no arterial concentrations Venous CO2 increases, and venous O2 decreases

Question 94

What are nasal polyps? What should you consider if you have repeating bouts?

Answer 94

= protrusion of edematous, inflammed nasal mucosa usually secondary to repeated rhiniits also occurs in **CYSTIC FIBROSIS** and **aspirin-intolerant asthma** **[aspirin-intolerant asthma -- asthma, aspirin-induced bronchospasms, nasal polyps]**

Question 95

Angiofibroma

Answer 95

benign tumor of nasal mucosa composed of large blood vessels and fibours tissue classically seen in ADOLSECNET **MALES** **presents with perofuse epistaxis (nose bleeds)**

Question 96

Nasopharyngoma

Answer 96

malignant tumor associated with **EBV** seen in **african children** and c**hinese adults** invovled cervical lymph nodes Biopsy: pleomorphic **keratin-positive** _epithelial cells_ in *background of lymphocytes*

Question 97

what are the key mediators to pain, during a pulmonary infection?

Answer 97

Bradykinin and prostaglandin E2

Question 98

Lobar pneumo: what does it look like? Common causes? Phases

Answer 98

consolidation of an entire lobe Typically, bacterial: **Strep Pneumo (95%)** **Klebsiella pneumo!** _Histo_: airsaces, high neutrophils + frothy = exudate of pneumo _Phases:_ 1. Congestion 2. Red hepatization (liver like change to normal spongy lung) - becomes solid; exudate, neutrophils, hemorrhage filling the alveolar air space 3. Grey hepatization - degeneration of red cells within exudate 4. Resolution -\> heal lung via regeneration (type II pneumocyte, stem cell that helps to regenerate)

Question 99

Bronchopneumo: description

Answer 99

scattered pathcy consolidations centered around bronchiles, often multifocal and bilateral caused by various bacterial organisms **[s. aureus, h. influ, pseudo aeruginosa, moraxella catarrhalis, legionella pneumo]**

Question 100

interstitial pneumo:

Answer 100

characterized by DIFFUSE INTERSTITIAL infiltrates CXR - inflammation of the wall --\> increased interstitial appearance and lung markings presents with relatively mild upper respiratory tract symptoms (minimal sx, low fever) caused by various bacteria and viruses (mycoplasm pneumo, Chlamydia pneumo, RSV, CMV, influenza, coxiella burnetti) #1 cause = mycoplasm pneumo - affecting young adults such as college students or military recruits

Question 101

What are the common bugs seen with aspiration pneumo? Who is at high-risk?

Answer 101

Bacteroides, fusobacterium, peptococcus pt at high risk = alcoholics, comatose pt Classically results in right lower lobe abscess

Question 102

What is a ghon complex?

Answer 102

Seen in TB focal, caseating necrosis --\> under go fibrosis and calcification; classically **subpleural** indicate primary TB (usually asympto! + ppd) **--\> reactivation leads to secondary TB!** * usually at apex, because higher O2, poor lymphatic draining* * Biopsy: caseating granulomas, AFB stains reveal acid-fast bacilli*

Question 103

Chronic Bronchitis

Answer 103

Chronic productive cough lasting \>3 months for min of 2 years hypertrophy of bronchial mucinous glands --\> increase mucus secretion (cough up buckets of mucus) Reid index \> 50% Clinical features: cyanosis/blue bloaters, increase Co2 due to mucus plugs, leads to a shunt and early hypoxemia Increase risk for infection and cor pulmonale #1 cause: smoking

Question 104

Emphysema

Answer 104

Pink puffer Due to enlargement of airspace, DEC recoil, INC compliance, DEC diffusiong capacity due to either increase proteases, or decrease anti-protease activity INC elastase --\> loss of elastic fibers --\> inc compliance _two types:_ **Centriacinar** - associated with smoking due to increased inflammation, increase protease; more severe on upper lobe **panacinar** - associated with anti-trypsin deficiency; decrease anti-protease activity, seen with liver cirrhosis due to the accumulation of the misfolded protein in the ER of hepatocytes; **PAS +** [PiM = normal, PiZ = mutant; PiMZ hetero, asympto; PiZZ inc risk for emphysema and cirrhosis] SX: **prolong expiration w/ pursed lips** breathing to inc airway pressure and prevent collapsing, bare-shapped chest,

Question 105

Asthma Key players

Answer 105

Allergens induce Th2 in CD4+ T cells ***_Th2 secrete:_*** **IL 4** (induces class switch to IgE) **IL5** (attracts eosinophils) **IL 10** (stimulates Th2, inhibits Th1) RE-EXPOSURE: **IgE** mediates activation of **mast cells** (early phase) --\> *_by crosslinking IgE_* =\> activates mast cells -- \> dumps preformed **histamine** granules [results in histamine induced **vasodilation _@ arterioles_** and v**ascular permeability _@ post-capillary venule_**] THEN, mast cells generate leukotrienes C4, D4, E4 --\> bronchoconstriction, inflammation and edema 2nd phase --\> tissue damage and inflammation and presence of major basic proteins from eosinophils will perpetuate bronchoconstriction (late phase) Clinically: SOB, wheezing, productive cough **Curchmann spirals** [spiral shaped mucus plug from shed epithelium] **Charcot-leyden crystals** [crystalin aggregated from breakdown of eosinophils] hypoxemia, dec insp/expir ratio, pulsus paradoxus, mucus plugging

Question 106

Bronchiectasis

Answer 106

**Necrotizing infection/inflammation of damaged to airway walls** --\> permanetn dilation of bronchioles and bronchi --\> purulent sputum, recurrent infections, hemoptysis Causes: **Cystic Fibrosis**, poor ciliary movement (smoking, **kartagener** syndrome- defect in the ***_dynein_*** ***_arm_***, which is necessary for ciliary movement), **allergic bronchopulonary aspergillosis** Complications: hypoxemia, cor pulmonale and **secondary amyloidosis**

Question 107

What drug toxicities could lead to interstitial lung disease?

Answer 107

Bleomycin, busulfan, amidorarone, methotrexate

Question 108

What is caplan syndrome?

Answer 108

*_pneumoconiosis_* with intrapleural nodules (particularly coal workers') + **rheumatoid arthritis**

Question 109

Ivory white calcified supradiaphragmatic and pleural plaques are pathognomonic of...

Answer 109

asbestosisi

Question 110

What could be seen histologically in someone with asbestosisi?

Answer 110

asbestos/ferrruginous bodies - golden-brown fusiform rods resembling dumbels found in alveolar septum

Question 111

How does silicosis cause penumoconioses?

Answer 111

macrophages do respond, and release fibrogenic facotrs --\> fibrosis BUT thought that **silica may disrupt phagolysosomes and impair macrophages;** Increased risk for TB Increased risk for bronchogenic CA seen as eggshell calcifications in X-rays

Question 112

where do the different types of pneumoconioses affect the lung?

Answer 112

**Absbestos** is from the roof but affects the **BASE** (*lower lung*) **silica** and **coal** are from the base (earth) but affect the **roof** (*upper lobes*)

Question 113

Sarcoidosis typical presentation? What do we need to be careful not to confuse with sarcoidosis?

Answer 113

etiology unknow, probably due to a CD4+ helper T-cell responseto an unknow antigen young AA female NON-caseating granulomas with asteroid bodies INC ACE, Hypercalcemia (due to inc 1-alpha-hydroxylase activity of epithelioid histiocyte that coverts vitamin D to its active form) Tx: steroids, or spontenous involvement _Dont confuse with_: berylliosis (aerospace worker), sjogren syndrome (won't see non-caseating granulomas in SS)

Question 114

What is hypersensitivity pneumonitis?

Answer 114

**mixed III/IV** hypersensitivity reaction to environmental antigen --\> **GRANULOMATOUS REACTION** to inhaled organic antigen; will see *_eoinophils_* since it is a hypersensitivity reaction seen highly around bird breeders; usually goes away when exposure is removed BUT chronic exposure --\> interstitial fibrosis

Question 115

What classifies as pulmonary hypertension?

Answer 115

\>25 mmHg (normal is 10-14 mmHg) Results in arteriosclerosis, medial hypertrophy, intimal fibrosisi of pulmonary arteries WIth long-standing diease, **plexiform** lesions could be seen

Question 116

What mutation is associated with primary pulmonary HTN? some consequences?

Answer 116

**BMPR2** inactivating mutation, leads to proliferation of vascular smooth muscle (normally inhibits vascular smooth muscle) --\> plexiform lesions COuld lead to: arteriosclerosis, medial hypertrophy, intimal fibrosisi of pulmonary arteries

Question 117

ARDS pathogen findings

Answer 117

diffuse damage to the alveolar capillary interface -- diffuse alveolar damage --\> INC alveolar capillary permeability --\> protein-rich leakage into alveoli and noncardiogenic pulmonary edema --\> **intra-alveolar hyline membrane** --\> initial damage due to the release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade and oxygen-derived free radicals ---\> BOTH damage of type I and type II pneumocytes Diffuse white out on CXR thicekn diffusion barrier --\> hypoxemia, cyanosis and increased surface tension --\> collapse of air sacs

Question 118

NRDS

Answer 118

neonate respiratory distress syndrome [*syntheseized 26 weeks --\> 35 weeks*] **surfactant deficiency** --\> increase surface tension --\> alveolar collapse ground-glass appearance L:S ratio \<1.5 Findings: retinopathy of prematurity, intraventricular hemorrhage, bronchopulmonary dysplasia RIB (due to increase free radials with oxygen supplemental therapy) clinica pre: inc respiratory effort after birth, tachypnea, with use of accessory muscles and grunting --\> hypoxemia and cyanosis INC risk for persistence of PDA (hypoxemia induced) and necrotizing enterocolitis (dec o2), metabolic acidosos CXR- diffuse granularity of the lung - ground glass RF: prematurity, c section, maternal **diabetes**

Question 119

what are the common complications associated with lung CA

Answer 119

**SPHERE** of complications! **S**uperior vena cava syndrome **P**ancost tumor **H**orner syndrome **E**ndocrine/paraneoplastic syndrome **R**ecurrentlaryngeal nerve compresison/hoarseness **E**ffusions-pericardial or pleural