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USMLE Step 1 > Respiratory > Flashcards

Respiratory Flashcards

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USMLE® Step 1 flashcards
1
Q

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.

A

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)

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2
Q

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

A

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

week 26–birth

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3
Q

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

A

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

at birth, replacement of fluid with air, decreases VR

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4
Q

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

A

At birth: 20–70 million alveoli;

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

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5
Q

At what gestational age does respiration become possible?

Which stage of lung development is this?

A

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)

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6
Q

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

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

A

The embryonic stage

weeks 4 to 7

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7
Q

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

What is the cause?

A

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

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8
Q

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

A

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

>the right lung

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9
Q

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?

A

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

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10
Q

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

What is their important functions:

A

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)

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11
Q

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

A

Nonciliated columnar/cuboidal pneumocytes w/secretory granules that:

  • secrete a surfactant component,*
  • degrade toxins,*
  • & act as reserve cells*
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12
Q

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

A

P = 2 (Surface tension) ÷ Radius;

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

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13
Q

What is dipalmitoylphosphatidylcholine? What is its function?

A

A type of lecithin and an important component of surfactant;

SURFACTANT decreases alveolar surface tension and prevents atelectasis

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14
Q

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.

A

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

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15
Q

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?

A

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

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16
Q

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

A

Patent ductus arteriosus

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17
Q

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?

A

Administration of steroids to the mother before delivery

administration of artificial surfactant to the newborn

RIB:

Retinopathy of prematurity

Intraventricular hemorrhage

Bronchopulmonary dysplasia

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18
Q

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.

A

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”)

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19
Q

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?

A

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.)

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20
Q

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

What type of epithelial cell is found in respiratory bronchioles?

A

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

Predominantly cuboidal cells

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21
Q

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?

A

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

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22
Q

mneumonics for diaphgram structures:

A

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.)

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23
Q

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

A

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

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24
Q

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

A

The central tendon

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25
Q

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

A

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

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26
Q

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?

A

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

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27
Q

What is pathologic dead space?

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

A

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

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28
Q

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?

A

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

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29
Q

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

A

At functional residual capacity (FRC)

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30
Q

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

A

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

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31
Q

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

A

Elastic properties of both

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32
Q

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

A

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

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33
Q

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

A

At functional residual capacity (FRC)

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34
Q

What is compliance?

A

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

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35
Q

What is hysteresis in relation to the pulmonary system?

A

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

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36
Q

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

A

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

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37
Q

Hemoglobin:

What are the two conformational forms of hemoglobin?

A

Relaxed (oxygenated) and taut (deoxygenated)

Relaxed

300 X more affinity for oxygen

[think: Respiratory ie) whats to pick up oxygen in the lungs]

Positive cooperativity

Taut

[Think: Taut in Tissues, whats to have decreased affinity to release oxygen in the tissues]

Negative allostery

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38
Q

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)?

A

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

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39
Q

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

A

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

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40
Q

Hemoglobin can act as a buffer for which ions?

A

H+

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41
Q

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

A

Iron in Hb ins normally in a REDUCED state

= ferrous Fe2+

Fe2+ binds O2

[“reduced” compared to Fe3+ = ferric, does not bind O2 readily but has an increased affinity fo cyanide]

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42
Q

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

A

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

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43
Q

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

A

Nitrites first and then thiosulfate

(induced methemoglobinemia)

nitrates and benzocaine cause poisoning by oxidizing Fe2+ –> Fe3+

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44
Q

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

A

Poisoning by nitrites found in high-altitude water

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45
Q

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

A

Carboxyhemoglobin

CO has 200 times the affinity of oxygen for hemoglobin

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46
Q

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

A

This is likely carbon monoxide poisoning:

100% O2 and hyperbaric O2

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47
Q

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

A

Hypoxia

from decreased oxygen saturation and content

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48
Q

What is the difference between hemoglobin and methemoglobin?

A

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

49
Q

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

A

Methylene blue (This pt has methemoglobinemia.)

50
Q

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?

A

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]

51
Q

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?

A

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 BATs right handed (Acid, CO2, Exercise, 2,3-BPG, Altitude,Temperature)

52
Q

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?

A

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

53
Q

What are the likely levels of a person with anemia?

Hb, % O2 saturation of Hb, dissolved O2 (PaO2), and total O2content?

polycythemia?

A

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

54
Q

What is the equation for oxygen content in the blood?

How do you calculate oxygen delivery to the tissues?

A

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

55
Q

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

A

Her deoxygenated hemoglobin must be < 5 g/dL

CYANOSIS

56
Q

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

A

Hb - normal

%O2 sat of Hb - DEC [CO competes with O2]

Dissolved O2/PaO2+ content - decreased

57
Q

What is the resistance and compliance in pulmonary circulation?

A

Low resistance, high compliance

  • compliance ~ comply, they stretch out*
  • but recoil is needed for alveoli to come back!*
  • High elastic = low compliance = high recoil*
58
Q

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

A

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!

59
Q

Perfusion-limited gases

What are some examples

where along the length of the pulmonary capillary do the partial pressures of a gas equilibrate?

A

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

60
Q

Diffusion-limited gases

Name examples

Where along the length of the pulmonary capillary does the gas equilibrate?

A

Oxygen in damaged lungs - emphysema, fibrosis, CO

Gas does NOT equilibrate - characteristic of the gas cause it to diffuse SLOWLY across the alveolar membrane

61
Q

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

A

The pt is showing signs of cor pulmonale

=right heart failure, a complication of pulmonary hypertension

62
Q

What is the equation for diffusion of a gas across a membrane?

How does emphysema or fibrosis affect this equation?

A

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

63
Q

How is pulmonary vascular resistance calculated?

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

A

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

64
Q

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

A

Directly prop. to length & inversely prop. to radius;

R = (8η1) ÷ (πr4),

where η = viscosity of blood, 1 = vessel length, and r = vessel radius

65
Q

What is the alveolar gas equation?

A

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*
66
Q

By using the alveolar gas equation, what important measure of pulmonary function can be determined?

What could affect this #

A

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)

67
Q

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?

A

NL gradient: High altitude, hypoventilation (opiod use)

INC gradient: ventilation/perfusion ratio mismatches, diffusion limitations (fibrosis), and right-to-left shunting

68
Q

What does hypoxia mean?

Nmae 4 processes that can lead to hypoxia

A

= decreased oxygen DELIVERY to tissue

Decreased cardiac output, hypoxemia, anemia, and carbon monoxide poisoning

69
Q

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

A

Impeded arterial flow and reduced venous drainage

70
Q

What is the difference between hypoxemia and hypoxia?

A

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

71
Q

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

A

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

72
Q

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?

A

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

73
Q

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?

A

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)

74
Q

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

A

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

75
Q

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

A

The apex

zone 1

most oxygen rich zone of the lungs

76
Q

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

A

Ventilation AND perfusion are greater at the BASE

= zone 3

77
Q

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

A

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

78
Q

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

A

Approaching ∞, as the pulmonary embolus is a blood flow obstruction, causing physiologic dead space

∞ = bl∞d flow obstruction

79
Q

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

A

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

80
Q

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

A

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

81
Q

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?

A

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

82
Q

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?

A

Hydrogen and bicarbonate ions

Bicarb (HCO3-) leaves the RBC adn is replaced by a chloride

Chloride shift

The hydrogen binds to Hb –> HHb

83
Q

In the lungs, the oxygenation of hemoglobin promotes what?

What is this shift effect called?

A

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)

84
Q

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?

A

It will shift it to the right, favoring dissociation of oxygen from hemoglobin

= BOHR effect

LHBT (in the lungs = haldane, bohr in tissues)

85
Q

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?

A

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

86
Q

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

A

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

87
Q

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

A

The number of mitochondria increases in response to high altitude

88
Q

What happens as a man ascends up a mountain to his pH?

What efect will this have on his system?

A

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

89
Q

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

A

Acetazolamide

90
Q

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

A

Right ventricular hypertrophy

91
Q

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?

A

They all increase

V/Q ratio becomes more uniform from apex to base

Pulmonary blood flow increases due to increased cardiac output

92
Q

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

A

The pH decreases during strenuous exercise due to lactic acidosis

93
Q

What happens to PaO2 and PaCO2 in response to exercise?

In response to exercise, what happens to the venous CO2 and venous O2 content?

A

No change no arterial concentrations

Venous CO2 increases, and venous O2 decreases

94
Q

What are nasal polyps?

What should you consider if you have repeating bouts?

A

= 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]

95
Q

Angiofibroma

A

benign tumor of nasal mucosa composed of large blood vessels and fibours tissue

classically seen in ADOLSECNET MALES

presents with perofuse epistaxis (nose bleeds)

96
Q

Nasopharyngoma

A

malignant tumor

associated with EBV

seen in african children and chinese adults

invovled cervical lymph nodes

Biopsy: pleomorphic keratin-positive epithelial cells in background of lymphocytes

97
Q

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

A

Bradykinin and prostaglandin E2

98
Q

Lobar pneumo:

what does it look like?

Common causes?

Phases

A

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)
99
Q

Bronchopneumo:

description

A

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]

100
Q

interstitial pneumo:

A

1 cause = mycoplasm pneumo - affecting young adults such as college students or military recruits

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)

101
Q

What are the common bugs seen with aspiration pneumo?

Who is at high-risk?

A

Bacteroides, fusobacterium, peptococcus

pt at high risk = alcoholics, comatose pt

Classically results in right lower lobe abscess

102
Q

What is a ghon complex?

A

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*
103
Q

Chronic Bronchitis

A

1 cause: smoking

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

104
Q

Emphysema

A

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,

105
Q

Asthma

Key players

A

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 vascular 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

106
Q

Bronchiectasis

A

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

107
Q

What drug toxicities could lead to interstitial lung disease?

A

Bleomycin, busulfan, amidorarone, methotrexate

108
Q

What is caplan syndrome?

A

pneumoconiosis with intrapleural nodules (particularly coal workers’) + rheumatoid arthritis

109
Q

Ivory white calcified supradiaphragmatic and pleural plaques are pathognomonic of…

A

asbestosisi

110
Q

What could be seen histologically in someone with asbestosisi?

A

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

111
Q

How does silicosis cause penumoconioses?

A

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

112
Q

where do the different types of pneumoconioses affect the lung?

A

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)

113
Q

Sarcoidosis typical presentation?

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

A

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)

114
Q

What is hypersensitivity pneumonitis?

A

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

115
Q

What classifies as pulmonary hypertension?

A

>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

116
Q

What mutation is associated with primary pulmonary HTN?

some consequences?

A

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

117
Q

ARDS

pathogen

findings

A

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

118
Q

NRDS

A

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

119
Q

what are the common complications associated with lung CA

A

SPHERE of complications!

Superior vena cava syndrome

Pancost tumor

Horner syndrome

Endocrine/paraneoplastic syndrome

Recurrentlaryngeal nerve compresison/hoarseness

Effusions-pericardial or pleural

USMLE Step 1 (15 decks)

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