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From Flashcardlet > Respiratory First Aid > Flashcards

Respiratory First Aid Flashcards

I do not own any of the included images, which are purely for educational use.

0
Q

What are the airways of the conducting zone?

A

nose, pharynx, trachea, bronchi, bronchioles and terminal bronchioles

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1
Q

What is the conducting zone?

A

the larger airways that warm, humidify, and filter air without participating in gas exchange; i.e., “dead space”

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2
Q

To what level of the conducting zone will cartilage and goblet cells extend?

A

bronchi

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3
Q

To what level of the conducting zone will psuedostratified ciliated columnar cells extend?

A

terminal bronchioles

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4
Q

To what level of the conducting zone will smooth muscle cells extend?

A

terminal bronchioles

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5
Q

What is the respiratory zone?

A

the airways participating in gas exchange

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6
Q

What are the airways of the respiratory zone?

A

lung parenchyma: respiratory bronchioles, alveolar ducts, alveoli

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7
Q

What is the histology of the respiratory bronchioles?

A

cuboidal cells

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8
Q

What is the histology of the alveoli?

A

simple squamous cells

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9
Q

You see simple squamous cells on a histology slide. From what level of the respiratory system is the slide?

A

alveoli or alveolar ducts

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10
Q

You see psuedostratified ciliated columnar cells on a histology slide. From what level of the respiratory system is the slide?

A

terminal bronchioles or above

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11
Q

You see cartilage on a histology slide. From what level of the respiratory system is the slide?

A

bronchi or above

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12
Q

You see goblet cells on a histology slide. From what level of the respiratory system is the slide?

A

bronchi or above

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13
Q

You see cuboidal cells on a histology slide. From what level of the respiratory system is the slide?

A

respiratory bronchioles

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14
Q

Are cilia present in the respiratory zone?

A

no

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15
Q

Where in the respiratory system may macrophages be found?

A

alveoli; predominantly in the lower lobes

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16
Q

What are Type I pneumocytes?

A

thin squamous cells present in the alveoli, functioning in optimal gas diffusion

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17
Q

Where are Type I pneumocytes found?

A

97% of alveolar surfaces

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18
Q

How is collapsing pressure calculated?

A

P = (2 x surface tension) / radius

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19
Q

What is the function of Type II pneumocytes?

A

secrete pulmonary surfactant –> decrease alveolar surface tension; prevent alveolar collapse

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20
Q

What type of cells, histologically, are Type II pneumocytes?

A

cuboidal

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21
Q

Do Type II cells originate from Type I cells, or are Type II cells progenitors for Type I cells?

A

Type II cells are progenitors for Type I cells. Type II cells can also give rise to other Type II cells.

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22
Q

When do Type II cells proliferate?

A

in lung damage

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23
Q

What is the Law of Laplace?

A

As the radius decreases upon expiration, alveoli have an increased tendency to collapse.

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24
Q

What does “atelectasis” mean, and how is it caused?

A

DEFINITION collapse of alveoli
CAUSES obstruction, compression, or contraction
–> damage to Type II pneumocytes –> loss of surfactant

NOTE Even reinflation may not return full function due to the loss of surfactant.

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25
Q

What IS surfactant, chemically?

A

a complex mix of lecithins, most importantly DIPALMITOYLPHOSPHATIDYLCHOLINE

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26
Q

What are Clara cells?

A

nonciliated, columnar cells with secretory granules

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27
Q

What do Clara cells secrete?

A

a “watery” component of surfactant

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28
Q

What are the functions of Clara cells?

A

to secrete a component of surfactant, to degrade toxins, and to act as reserve cells

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29
Q

When does surfactant synthesis begin?

A

around week 26 of gestation

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30
Q

When are mature levels of surfactant reached?

A

around week 35 of gestation

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31
Q

If a child is born premature, is it likely that they will produce sufficient levels of surfactant? If not, what is the child at risk of developing?

A

no

atelectasis

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32
Q

What measurement indicates if a fetus has mature lung function?

A

lecithin : sphingomyelin above 2

This can be measured in the amniotic fluid.

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33
Q

Which lung has three lobes?

A

right lung

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34
Q

Which lung has two lobes?

A

left lung; in place of the middle lobe, the lung accommodates the space necessary for the heart.

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35
Q

Which lung has a lingula?

A

left lung

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36
Q

Which lung is the more common site for inhaled foreign bodies and why?

A

right lung; right main stem bronchus is wider and more vertical

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37
Q

In relation to the lung hili, where is the pulmonary artery?

A

anterior to the right and superior to the left

–RALS: Right Anterior, Left Superior–

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38
Q

If a patient aspirates a peanut while upright, where in the lungs will it be found?

A

lower portion of the right inferior lobe

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39
Q

If a patient aspirates a peanut while supine, where in the lungs will it be found?

A

superior portion of the right inferior lobe

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40
Q

What structures perforate the diaphragm at T8, T10, and T12, respectively?

A

IVC, esophagus, aortic hilus

–I 8 10 Eggs At 12–

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41
Q

Where do the two trunks of the vagus nerve perforate the diaphragm?

A

T10

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42
Q

Where do the thoracic duct and azygous vein perforate the diaphragm?

A

T12

–at T 1-2, it’s the red (aorta), white (thoracic duct) and blue (azygous vein).–

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43
Q

What is the innervation of the diaphragm?

A

C3, C4, C5

–C3, 4, and 5 keep the diaphragm alive–

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44
Q

Where might pain from the diaphragm be referred?

A 
shoulder (C5)
trapezius ridge (C3, C4)
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45
Q

On a Ct scan, which is located more inferiorly: aorta, esophagus, IVC?

A

aorta

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46
Q

In quiet breathing, what muscle is responsible for inspiration?

A

diaphragm

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47
Q

In quiet breathing, what muscle is responsible for expiration?

A

none (passive process)

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48
Q

In exercise, what muscles are responsible for inspiration?

A

external intercostals, scalenes, sternocleidomastoid

–inSpiration: external, Scalene, Scm–

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49
Q

In exercise, what muscles are responsible for expiration?

A 
rectus abdominus
internal obliques
external obliques
transversus abdominis
internal intercostals
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50
Q

Graph: Normal Lung

A

.

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51
Q

What is the IRV?

A

Inspiratory Reserve Volume

the air that can still be breathed in after normal inspiration

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52
Q

What is the TV?

A

Tidal Volume

air that moves into lung with each quiet inspiration

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53
Q

What is the normal TV?

A

500

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54
Q

What is ERV?

A

Expiratory Reserve Volume

air that can still be breathed out after normal expiration

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55
Q

What is RV?

A

Residual Volume

the air in lung after maximal expiration

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56
Q

Which lung volume measurement cannot be read by spirometry?

A

RV (residual volume)

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57
Q

How is IC calculated?

A

Inspiratory Capacity = IRV + TV

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58
Q

How is FRC calculated?

A

Functional Residual Capacity = RV + ERV

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59
Q

How is VC calculated?

A

Vital Capacity = IRV + TV + ERV

This is the maximal volume of gas that can be expired.

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60
Q

How is TLC calculated?

A

Total Lung Capacity = IRV + TV + ERV + RV

This is the volume of gas present in the lungs after a maximal inspiration.

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61
Q

How is dead space calculated?

A

Vd = Vt x [(PaCO2 - PeCO2) / PaCO2]
–Taco, PAco, PEco, PAco–

PaCO2 = arterial PCO2
PeCO2 = expired air PCO2
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62
Q

What is physiologic dead space?

A

anatomic dead space of conducting airways plus functional dead space in alveoli; volume of inspired air that does NOT take place in gas exchange

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63
Q

What is the largest contributor of functional dead space?

A

apex of the lung

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64
Q

There is a tendency for the lungs to _____ _____ and chest wall to ____ ______.

A

collapse inward

spring outward

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65
Q

At FRC, what is the system pressure?

A

atmospheric; the inward pull of the lung is balanced by the outward pull of the chest wall.

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66
Q

What determines the combined volume of the chest wall and lungs?

A

their elastic properties

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67
Q

At FRC, what is the airway pressure?

A

0

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68
Q

At FRC, what is the alveolar pressure?

A

0

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69
Q

At FRC, what is the intrapleural pressure?

A

negative

This prevents pneumothorax.

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70
Q

What is compliance?

A

the change in lung volume for a given change in pressure

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71
Q

In what processes does compliance decrease?

A

pulmonary fibrosis
pneumonia
pulmonary edema

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72
Q

What are the causes of pulmonary edema?

A

HEMODYNAMIC increased vascular pressure, decreased oncotic pressure
MICROVASCULAR DAMAGE infection, ARDS, DIC
UNCLEAR neurogenic, high altitude

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73
Q

In what processes does compliance increase?

A

emphysema

normal aging

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74
Q

Pressure-Volume Curves of Lung and Chest Wall

A

.

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75
Q

What are the subunits of hemoglobin?

A

2 alpha

2 beta

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76
Q

Which form of hemoglobin has a low affinity for oxygen?

A

T (taut)

–Taut in Tissues–

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77
Q

Which form of hemoglobin has a high affinity for oxygen?

A

R (relaxed)

–Relaxed in Respiratory–

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78
Q

Hemoglobin exhibits ____ cooperativity and negative _____.

A

positive cooperativity

negative allosterity

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79
Q

What are the subunits of fetal hemoglobin (HbF)?

A

2 alpha

2 gamma

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80
Q

HbF has a lower affinity for _____ than adult hemoglobin, allowing it a _____ affinity for O2.

A

lower affinity for 2,3-BPG –> higher affinity for O2

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81
Q

Which binds oxygen better: adult or fetal hemoglobin?

A

fetal

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82
Q

What factors favor the taut form over the relaxed form of hemoglobin?
Does this mean it favors unloading or loading of oxygen?
How does the dissociation curve shift?

A

taut: Cl-, H+, CO2, 2,3-BPG

Since the taut form has low affinity for O2, it favors UNLOADING of oxygen into tissues.

This then shifts the dissociation curve right.

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83
Q

In sickle cell anemia, why do HbS molecules sickle?

A

HbS allows hydrophobic interaction among hemoglobin molecules –> polymerization of HbS –> sickling in hypoxia

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84
Q

What effect do modifications to hemoglobin have on O2 saturation and content?

A

decreased O2 saturation and content –> TISSUE HYPOXIA

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85
Q

What is methemoglobin?

A

an oxidized form of hemoglobin (Fe2+ –> Fe3+) that does NOT bind O2 as readily

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86
Q

If not oxygen, for what does methemoglobin have an increased affinity?

A

cyanide

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87
Q

How do you treat methemoglobinemia?

A

methylene blue

–METHemoglobin needs METHylene blue.–

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88
Q

What effect do nitrates have on iron?

A

They oxidize Fe2+ –> Fe3+

NOTE there will be normal readings of PO2 (plasma oxygen content is NOT changed; only hemoglobin binding), but DECREASED levels of Hb O2 saturation.

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89
Q

How is cyanide poisoning treated?

A

(1) give nitrates (such as amyl nitrate) to oxidize hemoglobin –> methemoglobin
(2) the cyanide present in plasma binds methemoglobin –> cytochrome oxidase is permitted to function
(3) give thiosuflate to bind cyanide –> thiocyanate –> renal excretion

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90
Q

How will the skin of a patient with methemoglobinemia appear?

A

dusky

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91
Q

What is carboxyhemoglobin?

A

form of hemoglobin bound to CO in place of O2

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92
Q

Compared to O2, what is the affinity of CO for hemoglobin?

A

200X that of O2

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93
Q

How does the oxygen-hemoglobin curve shift in carboxyhemoglobinemia?

A

left (decreased oxygen-binding capacity) –> decreased oxygen unloading in tissues

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94
Q

How are PO2, percent saturation and O2 content changed in carboxyhemoglobinemia (CO poisoning)?

A

PO2: unchanged
percent saturation: decreased
O2 content: decreased

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95
Q

Oxygen-Hemoglobin Dissociation Curve: Myoglobin

A

.

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96
Q

What shape does the oxygen-hemoglobin dissociation curve have? Why?

A

sigmoidal due to positive cooperativity
[Tetrameric hemoglobin molecule can bind 4 oxygen molecules and has a HIGHER affinity for EACH subsequent oxygen molecule bound.]

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97
Q

What shape does oxygen-myoglobin dissociation curve have? Why?

A

hyperbolic due to monomeric nature that does NOT show positive cooperativity

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98
Q

What does a right shift of the oxygen-hemoglobin dissociation curve denote?

A

decreased affinity of hemoglobin for O2 = UNLOADING of O2 to tissue

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99
Q

What causes a right shift of the oxygen-hemoglobin dissociation curve?

A 
CO2 (hypoxemia) / CHF / Chronic lung disease
BPG (2,3-BPG)
Exercise
Acid/Altitude/Anemia
Temperature
--CBEAT--
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100
Q

An increase in all factors (except pH) shifts the curve ____, while a decrease in all factors (except pH) shifts the curve ___.

A

right

left

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101
Q

Which direction is the HbF curve shifted and why?

A

left: fetal hemoglobin has a greater affinity for O2

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102
Q

Oxygen-Hemoglobin Dissociation Curve: 50% CO, Anemia

A

CARBOXYHEMOGLOBINEMIA (1) normal Hb but decreased HbO2 –> decreased total O2 content (2) normal PO2 (3) decreased percent saturation
with LEFT shift

ANEMIA (1) decreased Hb –> decreased O2 + HbO2 = decreased total O2 content (2) normal PO2 (3) normal percent saturation
with RIGHT shift

BOTH SHOW DECREASED CARRYING CAPACITY

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103
Q

Does a decrease in PAO2 cause a vasoconstriction or vasodilation? Where does blood move due to this?

A

hypoxic vasoconstriction; this shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung

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104
Q

How can diffusion across perfusion limited lung membranes increase?

A

if blood flow increases

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105
Q

What is the equation for diffusion?

A 
Vgas = A/T x Dk(P1-P2)
A = area
T = thickness
Dk(P1-P2) = difference in partial pressures
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106
Q

In emphysema, how does the diffusion equation change?

A

area decreases in emphysema

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107
Q

In pulmonary fibrosis, how does the diffusion equation change?

A

thickness increases

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108
Q

In normal, healthy lungs, is the circulation perfusion or diffusion limited?

A

perfusion

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109
Q

In perfusion limited circulation, when does gas equilibrate?

A

early along the length of the capillary

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110
Q

In diffusion limited circulation, when does gas equilibrate?

A

at no point; gas does not equilibrate by the time the blood reaches the end of the capillary

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111
Q

Perfusion or diffusion limited: O2 in normal health?

A

perfusion

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112
Q

Perfusion or diffusion limited: O2 in emphysema or fibrosis?

A

diffusion

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113
Q

Perfusion or diffusion limited: CO2?

A

perfusion

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114
Q

Perfusion or diffusion limited: N2O?

A

perfusion

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115
Q

Perfusion or diffusion limited: carbon monoxide?

A

diffusion

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116
Q

Graph: perfusion limited

A

.

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117
Q

Graph: diffusion limited

A

.

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118
Q

Graph: oxygen in diffusion/perfusion

A

.

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119
Q

What is the normal pressure of the pulmonary artery?

A

10-14 mmHg

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120
Q

What levels of pressure indicate pulmonary HTN, both at rest and during exercise?

A

rest: >25 mmHg
exercise: >35 mmHg

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121
Q

What is the characterization of pulmonary HTN?

A 
arteriosclerosis of pulmonary trunk 
smooth muscle (medial) hypertrophy of pulmonary arteries
intimal fibrosis
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122
Q

What causes primary pulmonary HTN?

A

inactivating mutation in the BMPR2 gene, classically seen in young females
NOTE this is a poor prognosis

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123
Q

What is the normal function of the BMPR2 gene?

A

inhibition of vascular smooth mucle proliferation

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124
Q

What are the causes of secondary pulmonary HTN?

A
  • obstructive lung disease: destruction of lung parenchyma
  • recurrent thromboemboli / restrictive lung disease: decreased cross-sectional area of pulmonary vascular bed
  • left-to-right shunt / CHF: increased volume in the pulmonary circuit –> increased shear stress –> endothelial injury
  • mitral stenosis: increased resistance –> increased pressure
  • autoimmune disease: systemic sclerosis; inflammation –> intimal fibrosis –> medial hypertrophy
  • sleep apnea: decreased PAO2 –> hypoxic vasoconstriction
  • living at high altitude: decreased PAO2 –> hypoxic vasoconstriction
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125
Q

What is the course of disease for pulmonary HTN?

A

severe respiratory distress –> cyanosis and RVH –> death from decompensated COR PULMONALE

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126
Q

What is the equation for pulmonary vascular resistance?

A

PVR = [P(pulmonary artery) - P(left atrium)] / CO

P(pulmonary artery) = pressure in the pulmonary artery
P(left atrium) = pulmonary wedge pressure
CO = cardiac output

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127
Q

What is the equation for resistance in a vessel?

A

R = (8ηl) / (πr^4)

η = viscosity of blood
l = vessel length
r = vessel radius
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128
Q

What is the equation for flow in a vessel?

A

F = (P2 - P1) / R

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129
Q

What is O2 content?

A

O2 content = (O2 binding capacity x % saturation) + dissolved O2

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130
Q

What is the normal amount of hemoglobin in the blood, and what level of hemoglobin denotes cyanosis?

A
  • 15 g/dL

- when deoxygenated Hb > 5 g/dL

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131
Q

How much O2 can be bound by 1 gram of normal Hb?

A

1.34 mL O2

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132
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - (PaCO2/R)

PAO2 = alveolar PO2 (mmHg)
PIO2 = PO2 in inspired air (mmHg)
PaCO2 = arterial PCO2 (mmHg)
R = respiratory quotient = CO2 produced per O2 consumed
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133
Q

How can you normally approximate the alveolar gas equation?

A

PAO2 = 150 - (PaCO2 / .8)

PAO2 = alveolar PO2 in mmHg
PaCO2 = arterial PCO2 in mmHg
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134
Q

What is the A-a gradient?

A

PAO2 - PaO2 = 10 to 15 mmHg

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135
Q

What may result from an increased A-a gradient?

A

hypoxemia

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136
Q

What are the potential causes of increased A-a gradient?

A

shunting
V/Q mismatch
fibrosis (impairs diffusion)

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137
Q

If hypoxemia exists (decreased PaO2), but the A-a gradient is normal, what may be the causes?

A

high altitude

hypoventilation

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138
Q

If hypoxemia exists (decreased PaO2), and the A-a gradient is increased, what may be the causes?

A

V/Q mismatch
diffusion limitation
right-to-left shunt

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139
Q

If hypoxia exists (decreased O2 delivery to tissues), what might be the causes?

A

decreased cardiac output
hypoxemia
anemia
carbon monoxide poisoning

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140
Q

If ischemia exists in the lung (loss of blood flow), what might be the causes?

A

impeded arterial flow

reduced venous drainage

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141
Q

What is the V/Q mismatch at the apex of the lung?

A

3 (wasted ventilation)

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142
Q

What is the V/Q mismatch at the base of the lung?

A

.6 (wasted perfusion)

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143
Q

What area of the lung do organisms that thrive in high O2 prefer?

A

apex

EXAMPLE TB

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144
Q

In exercise, what is the V/Q?

A

near 1

EXERCISE increases cardiac output –> vasodilation of apical capillaries

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145
Q

Where are both ventilation and perfusion the greatest?

A

base of the lung

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146
Q

IF V/Q approaches 0, what is the cause?

A 
airway obstruction (shunt)
NOTE giving 100% oxygen will NOT improve PO2
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147
Q

If V/Q approaches infinity, what is the cause?

A

blood flow obstruction (physiologic dead space)

NOTE assuming <100% dead space, 100% oxygen WILL improve PO2

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148
Q

What zone of the lung: PA > Pa > Pv?

A

Zone 1 (apex)

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149
Q

What zone of the lung: Pa > PA > Pv?

A

Zone 2

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150
Q

What zone of the lung: Pa > Pv > PA?

A

Zone 3

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151
Q

What are the three forms of transported carbon dioxide?

A

bicarbonate (90%)
carbaminohemoglobin, HbCO2 (5%)
dissolved CO2 (5%)

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152
Q

Where does CO2 bind hemoglobin?

A

N-terminus of globin, NOT heme

NOTE carbon monoxide binds the heme group

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153
Q

What form of hemoglobin does CO2 binding favor?

A

taut (O2 unloaded)

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154
Q

What is the Haldane effect?

A

oxygenation of Hb –> H+ dissociates from Hb –> equilibrium shifted to CO2 formation –> CO2 is released from RBCs

IN LUNGS

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155
Q

What is the Bohr effect?

A

increased H+ from tissue metabolism –> curve shifted right –> O2 unloaded

IN TISSUES

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156
Q

How is the majority of blood CO2 carried?

A

as bicarbonate

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157
Q

What channel is necessary in the RBC membrane for release of CO2 (as HCO3-) from the RBC?

A

Cl- / HCO3- antiporter

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158
Q

What enzyme is required in the RBC for CO2 to be converted to HCO3-?

A

carbonic anhydrase

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159
Q

What is the acute ventilation response to high altitude?

A

acute increase in ventilation with decrease in PO2 and PCO2

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160
Q

What is the chronic ventilation response to high altitude?

A

increased ventilation

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161
Q

How does erythropoetin change in response to high altitude?

A

increased erythropoietin –> increased hematocrit, hemoglobin (chronic hypoxia!)

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162
Q

How does 2,3-BPG change in response to high altitude?

A

increased 2,3-BPG –> binds to hemoglobin –> curve shifts right –> O2 unloading favored –> hemoglobin releases more O2

163
Q

What cellular changes are seen in response to high altitude?

A

increased mitochondria

164
Q

How does renal excretion of bicarbonate change in response to high altitude?

A

respiratory alkalosis –> increased renal excretion of bicarbonate –> metabolic compensation

165
Q

What is the result of chronic hypoxic pulmonary vasoconstriction?

A

RVH

166
Q

How does the respiratory system respond to exercise?

A

increased CO2 production –> increased venous CO2 content*
increased O2 consumption –> decreased venous O2 content*
increased ventilation rate to meet O2 demand
V/Q ration from apex to base becomes more uniform, approaches 1
increased cardiac output –> increased pulmonary blood flow
lactic acidosis –> decreased pH during strenuous exercise

  • NOTE no change in PaO2 and PaCO2
167
Q

What is the most common, normally fatal, congenital pulmonary anomaly?

A

diaphragmatic hernia

168
Q

What is Virchow’s triad, and what is its significance?

A

TRIAD stasis, hypercoagulability, endothelial damage

SIGNIFICANCE predisposition to DVT

169
Q

What is the most common cause of hypercoagulability?

A

FACTOR V LEIDEN (most common defect in coagulation cascade proteins)

170
Q

What is the complication of DVT?

A

pulmonary embolus

171
Q

What physical examination provocative test is most indicative of DVT?

A

HOMANS’ SIGN dorsiflexion of foot –> calf pain

172
Q

What is used for prevention and acute management of DVT?

A

heparin

173
Q

What is used for chronic prevention of DVT recurrence?

A

warfarin

174
Q

What is the presentation of pulmonary embolus?

A

SYMPTOMS
dyspnea, hemoptysis, pleuritic chest pain, and pleural effusion
MAY PRESENT AS SUDDEN DEATH: large saddle embolus blocking both left and right pulmonary arteries or with significant occlusion of a large pulmonary artery –> electro-mechanical dissociation (pulseless electrical activity / PEA)

LABS
V/Q scan: mismatch; perfusion normal
Spiral CT: vascular filling defect in lung
Doppler: useful to detect DVT
hemorrhagic, wedge-shaped infarct

NOTE normal D-Dimer eliminates pulmonary embolism. do not use D-dimer for any other interpretation regarding pulmonary embolism

175
Q

What are the types of pulmonary emboli?

A

Fat: associated with long bone fractures and lipsuction
Air
Thrombus
Bacteria
Amniotic fluid: can lead to DIC, especially post-partum
Tumor
–an embolus moves like a FAT BAT–

176
Q

What do lines of Zahn in a pulmonary embolus indicate?

A

that the thrombi is pre-mortem

NOTE lines of Zahn are interdigitating areas of pink (platelets and fibrin) and red (RBCs)

177
Q

From where do the majority of pulmonary emboli arise?

A

deep leg veins

178
Q

What is the best imaging test of choice for a pulmonary embolism?

A

CT pulmonary angiography

DIAGNOSIS: V/Q mismatch on scan (perfusion normal)

179
Q

In obstructive lung diseases, how do the RV, FEV1, FVC, FEV1/FVC ratio, and V/Q change?

A 
RV increased
FEV1 greatly decreased
FVC normal or slightly decreased
FEV1/FVC decreased
V/Q mismatch
180
Q

Graph: Obstructive Lung Disease

A

.

181
Q

Why does the FVC decrease in obstructive lung disease?

A

volume of air that can be forcefully expired decreases

182
Q

Why is TLC increased in obstructive lung disease?

A

air trapping

183
Q

At what percentage is the FEV1 considered “very severe”?

A

<30%

184
Q

At what percentage is the FEV1 so severe that dyspnea at rest will be seen?

A

<25%

NOTE there will also be increased PCO2

185
Q

How much of the lung capacity may be lost before onset of dyspnea?

A

3/4

186
Q

How is COPD defined?

A

chronic lung disease with obstructive physiology (usually, chronic bronchitis + emphysema)

Epidemiologically, COPD is responsible for at least 100,000 deaths per year and accounts for 10% of all American disability.

187
Q

What are the diagnostic criteria for chronic bronchitis?

A

productive cough for >3 months per year (not necessarily consecutive) for > 2 years
especially in a smoker

188
Q

What is the pathogenesis of chronic bronchitis?

A

hypertrophy of bronchial mucinous glands –> increased thickness of mucus glands relative to overall bronchial wall thickness –> increased radius –> increased resistance –> decreased air flow

189
Q

What is the Reid index?

A

thickness of gland layer / total thickness of bronchial wall

190
Q

Of what is a Reid index of <40% indicative?

A

normal bronchi

191
Q

Of what is a Reid index of >50% indicative?

A

chronic bronchitis

192
Q

In chronic bronchitis, what changes will be seen in RV, TLC and diffusion?

A

RV increased
TLC normal
diffusion normal

193
Q

What are the findings in chronic bronchitis?

A

productive cough due to mucus production
“flare ups”
increased risk of infection and cor pulmonale
wheezing
crackles
cyanosis (“blue bloaters:” mucus plugs trap carbon dioxide –> shunting –> decreased PaO2, increased PaCO2 –> early-onset hypoxemia)
late-onset dyspnea

194
Q

What is the effect of bronchodilators in chronic bronchitis?

A

some response, but will not return patient to normal

195
Q

How is chronic bronchitis treated?

A

bronchodilators
glucocorticoids
broadspectrum antibiotics
O2

196
Q

What is the pathogenesis of emphysema?

A

imbalance of proteases and antiproteases –> increased elastase release by neutrophils –> excessive inflammation; lack of A1ATin the lower lobes –> destruction of alveolar air sacs –> increased compliance –> permanent enlargement of air spaces, decreased recoil –> collapse of airways during exhalation –> obstruction, air trapping

197
Q

What is A1AT, and what is its function?

A

alpha1-antitrypsin, inherited in an autosomal co-dominant pattern; neutralizes proteases in the lower lobes

198
Q

In emphysema, what changes will be seen in RV, FRV, TLC, and diffusion?

A

RV increased
FRC increased
TLC increased
diffusion decreased

199
Q

What is the cause of centriacinar emphysema?

A

smoking

200
Q

What is the cause of panacinar emphysema?

A

alpha-1 antitrypsin (A1AT) deficiency

201
Q

What is the result of A1AT deficiency?

A

misfolding of protein –>

(1) lack of antiprotease –> air sacs vulnerable to protease mediated damage –> panacinar emphysema
(2) accumulation of mutant A1AT in endoplasmic reticulum of hepatocytes –> liver damage

202
Q

What will a biopsy of the liver in A1AT deficiency emphysema reveal?

A

Note the pink, PAS-positive globules in hepatocytes

203
Q

Where in the lung is panacinar emphysema most severe?

A

lower lobe

204
Q

Where in the lung is centracinar emphysema most sever?

A

upper lobes

205
Q

What is the normal allele in A1AT deficiency?

A

PiM; two copies are usually expressed (PiMM)

206
Q

What is the most common clinically relevant mutation in A1AT deficiency?

A

PiZ

207
Q

What heterozygotes in A1AT deficiency are usually asymptomatic? What greatly increases this individual’s risk for emphysema?

A

PiMZ; smoking

208
Q

Which homozygotes are at significant risk for panacinar emphysema and cirrhosis?

A

PiZZ

209
Q

What are the clinical features of emphysema?

A

dyspnea and cough with minial sputum
prolonged expiration with pursed lips (“pink puffer;” this increases airway pressure and prevents airway collapse during respiration)
weight loss
increased AP diameter (“barrel chest”)

210
Q

What are the late complications of emphysema?

A

destruction of capillaries in the alveolar sac –> hypoxemia

cor pulmonale

211
Q

What is the pathogenesis of allergic asthma?

A

GENETIC SUSCEPTIBILITY allergens induce TH2 phenotype in CD4+ T cells –> TH2 cells secrete

(1) IL-4 –> class switch to IgE
(2) IL-5 –> attracts eosinophils
(3) IL-10 –> stimulation of TH2 cells, inhibition of TH1 cells

EARLY PHASE (minutes) REACTION reexposure to allergen –> IgE-mediated activation of mast cells –> release of preformed histamine granules, generation of LC4, LD4, LE4 –>

(1) smooth muscle spasm –> bronchoconstriction –> inflammation
(2) increased vascular permeability –> edema
(3) increased mucus production –> impaired mucociliary activity

LATE PHASE (12-24 hours) REACTION inflammation (especially major basic protein from eosinophils) –> damage of cells, perpetuation of bronchoconstriction (vagus nerve stimulation)

REPAIR OR REMODELING narrow and/or shortened airway

212
Q

What is the pathogenesis of nonallergic asthma?

A

?

follows URI

213
Q

What are the associations of asthma?

A 
childhood
allergic rhinitis
urticaria
eczema
family history of atopy
214
Q

What type of hypersensitivity reaction is asthma?

A

Type I

215
Q

What are the clinical features of asthma?

A

cough, wheezing (especially nocturnal episodes)
tachypnea, dyspnea
hyperinflation and atelectasis
hypoxemia
decreased I/E ratio (inspiration:expiration)
pulsus paradoxus
mucus plugging
productive cough with spiral-shaped mucus (Curschmann’s spirals)
eosinophil-derived crystals (Charcot-Layden crystals)
wheals, flare skin tests

severe, unrelenting attack –> status asthmaticus, death

216
Q

I say “Curschmann’s spirals,” you say…?

A

asthma

217
Q

I say “Charcot-Leyden crystals in sputum,” you say…?

A

note the numerous eosinophils also

asthma

218
Q

How will the FEV1, RV, FRC, and resistance change in asthma?

A

FEV1 decreased
RV increased
FRC increased
resistance increased

219
Q

What is bronchiectasis?

A

permanent dilatation of bronchioles and bronchi; loss of airway tone –> air trapping

220
Q

What is the pathogenesis of bronchiectasis?

A

necrotizing inflammation –> damage to airway cells –> permanently dilated airways

221
Q

What are the possible causes of bronchiectasis?

A

POOR CILIARY FUNCTION cystic fibrosis, Kartagener syndrome, smoking
OBSTRUCTION tumor or foreign body
INFECTIOUS necrotizing infection (H. influenza, P. aeruginosa), allergic bronchopulmonary aspergillosis

222
Q

What is Kartagener syndrome?

A

inherited defect of the dynein arm –> no ciliary movement –> sinusitis, bronchitis, infertility, siuts inversus

223
Q

Which individuals are most prone to allergic bronchopulmonary aspergillosis?

A

asthmatics, cystic fibrosis patients

hypersensitivity reacion to Aspergillus –> chronic inflammatory damage

224
Q

What are the clinical features of bronchiectasis?

A

cough, dyspnea
purulent, foul-smelling sputum
recurrent infections
hemoptysis

225
Q

What are the complications of bronchiectasis?

A 
hypoxemia with cor pulmonale
secondary amyloidosis (AA)
226
Q

How do you treat COPD?

A

STOP SMOKING
vaccinate against influenza, Streptococcus pneumonia
treat acute purulent bronchitis with bronchodilators (beta adrenergic, anticholinergic)
inhaled steroids for partial response
regular exercise
oxygen tank in chronic hypoxemia

227
Q

What are the obstructive lung diseases?

A 
COPD
chronic bronchitis
emphysema
asthma
bronchiectasis
228
Q

What are the restrictive lung diseases (interstitial lung diseases)?

A

ARDS, neonatal RDS (hyaline membrane disease)
idiopathic pulmonary fibrosis
idiopathic pulmonary hemosiderosis (seen in children)
sarcoidosis
Langerhans cell histiocytosis (eosinophilic granuloma)
PNEUMOCONIOSES Coal Workers’ pneumoconiosis, silicosis, berylliosis, asbestosis, anthracosis; hypersensitivity pneumonitis
HEMORRHAGIC Wegener’s (granulomatosis with polyangiitis); Goodpasture’s syndrome
CHEST WALL ABNORMALITIES polio, myasthenia gravis, scoliosis morbid obesity

NOTE always check occupational and drug history!

229
Q

How are TLC, FEV1, FVC, and the FEV1:FVC ratio changed in restrictive lung diseases?

A

TLC decreased
FEV1 decreased
FVC decreased
FEV1/FVC ratio normal or increased (>80%)

230
Q

Graph: Restrictive Lung Disease

A

.

231
Q

Why does the TLC decrease in restricted lung disease?

A

restricted lung expansion –> decreased lung volumes –> decreased TLC

232
Q

What issues of poor muscular effort may result in poor breathing mechanics sufficient enough to cause restrictive lung disease?

A

polio

myasthenia gravis

233
Q

What issues of poor structural apparatus may result in poor breathing mechanics sufficient enough to cause restrictive lung disease?

A

scoliosis

morbid obesity

234
Q

If restrictive lung disease is due to poor breathing mechanics, what labs will be seen?

A

extrapulmonary
peripheral hypoventilation
normal A-a gradient

235
Q

If restrictive lung disease is due to interstitial lung diseases (the most common causes), what labs will be seen?

A

pulmonary
lowered diffusing capacity
increased A-a gradient

236
Q

What drugs can cause restrictive lung disease?

A

bleomycin
busulfan
amiodarone
methotrexate

NOTE always check drug history!

237
Q

What are the pulmonary function results in interstitial fibrosis?

A 
TLC 81%
FVC 69%
FEV1 80%
FEV1/FVC .80
DCO 53%
PaO2 61 mmHg
238
Q

What is bleomycin used to treat, and what is its mechanism of action?

A

USES testicular cancer, Hodgkin’s lymphoma

MOA antitumor antibiotic: induces free radical formation –> breaks in DNA strangs

239
Q

What are the side effects of bleomycin?

A

pulmonary fibrosis
flagellate skin changes
minimal myelosuppression

240
Q

What is busulfan used to treat, and what is its mechanism of action?

A

USES CML; ablation of bone marrow before transplantation

MOA alkylating agent: alkylates DNA

241
Q

What are the side effects of busulfan?

A

pulmonary fibrosis

hyperpigmentation

242
Q

What is amiodarone used to treat, and what is its mechanism of action?

A

USES ventricular tachycardia, off label for atrial fibrillation and atrial flutter
MOA K+ channel blocker: act at atrial and ventricular muscle, His-Purkinje fibers to increase AP duration and ERP

243
Q

What are the side effects of amiodarone?

A 
increase QT --> TORSADES DE POINTES (but less than the other K+ channel blockers)
alteration of the lipid membrane
pulmonary fibrosis
hepatotoxicity
hypothyroidism/hyperthyroidism
corneal deposits (yellow-brown)
skin deposits (blue-gray) --> photodermatitis
neurologic effects
constipation
bradycardia, heart block, CHF
244
Q

What is methotrexate used to treat, and what is its mechanism of action?

A

USES leukemias, lymphomas, choriocarcinoma, sarcoma, abortion, ectopic pregnancy, RA, psoriasis
MOA antimetabolite: folic acid analog –> inhibition of dihydrofolate reductase –> decrease dTMP –> decrease DNA and protein synthesis

245
Q

What are the side effects of methotrexate?

A 
myelosuppression (reverse with leucovorin)
macrovesicular fatty change in liver
mucositis
teratogenic
lung injury
246
Q

55 year old man with progressive dyspnea and bilateral pulmonary infiltrated.
How would you make a diagnosis of interstitial lung disease?
What are the important diseases with known causes in the differential?

A

DIAGNOSING spirometry, Xray or CT scan
DIFFERENTIAL any acute disease; drug toxicities, environment exposure, connective tissue diseases, infectious disease; systemic diseases

247
Q

What is idiopathic pulmonary fibrosis (UIP), and to what is it likely related?

A

fibrosis of lung interstitium

cyclical alveolar injury: injured pneumocytes –> (1) proliferation of Type II pneumocytes with replacement of Type I pneumocytes –> release of TGF-beta-1 –> increased collagen deposition –> fibroblastic foci –> fibrosis (MACROPHAGE INVOLVEMENT) –> end stage lung
(2) alveolar exudation –> thickening of the interstitial space –> interference of gas exchange –> difficulty breathing

NOTE if a one time injury, there is a possibility of repair with resolution and scarring

248
Q

What is the presentation of general interstitial lung disease, as per Dr Nugent?

A

progressive dyspnea and cough (increased work of breathing)
crackles
possibly, pulmonary HTN (increased pulmonary artery pressure)
fibrosis of lung CT (subpleural pathches –> diffuse fibrosis –> end-stage “honeycomb” lung)
CXR: diffuse reiculonodular changes
hypoxemia in exercise
right heart failure

REDUCED DIFFUSING CAPACITY, LUNG VOLUMES, AND COMPLIANCE:

  • stiff, noncompliant alveolar walls
  • increased resistance in small bronchioles
  • impaired ventilation of alveoli
  • thickened alveolar walls
  • loss of capillary bed
249
Q

What are the clinical features of idiopathic pulmonary fibrosis?

A

progressive dyspnea and cough

fibrosis of lung CT (subpleural pathches –> diffuse fibrosis –> end-stage “honeycomb” lung)

250
Q

What is the treatment for pulmonary fibrosis?

A

lung transplant

251
Q

What is the pathogenesis of pneumoconioses?

A

chronic exposure to small, fibrogenic particles –> alveolar macrophages engulf foreign particles –> induction of fibrosis –> increased risk of cor pulmonale and Caplan’s syndrome

AFFECTS UPPER LOBES

252
Q

What are the pathologic findings of anthracosis / Coal Worker’s pneumoconiosis?

A

massive exposure to carbon dust –> diffuse fibrosis (“black lung;” progressive massive fibrosis)

ASSOCIATIONS RA, Caplan’s syndrome

253
Q

What is cryptogenic organizing pneumonia (COP)?

A

fibrosing variant of interstitial lung disease

  • all lesions same age
  • fibrous plugs in or around bronchioles
  • heal spontaneously OR WITH STEROIDS
  • highly variable lung pattern; “mimics everything”
254
Q

What is Caplan’s syndrome?

A

a combination of rheumatoid arthritis and pneumoconiosis (most commonly, anthracosis)

CXR shows multiple, round, well defined nodules, usually 0.5-2.0 cm in diameter, which may cavitate and resemble tuberculosis

255
Q

What is the pathogenesis of silicosis?

A

exposure to silica (foundries, sandblasters, silica miners, potters) –> macrophages release fibrogenic factors –> fibrotic nodules in upper lobes of lung with lymph node involvement

impairment of phagolyosome formation by macrophages –> increased risk for TB

256
Q

What are the complications of silicosis?

A

early pulmonary HTN due to involvement of periarterial nodules
increased risk for TB
increased risk for bronchogenic carcinoma

257
Q

What will be seen on chest Xray in silicosis and anthracosis?

A

“eggshell” calcification of hilar lymph nodes

258
Q

What is the pathogenesis of asbestosis?

A

exposure to asbestos fibers (construction workers, roofers, plumbers, shipyard workers) –> fibrosis of lung and plaque-ing of pleura

AFFECTS LOWER LOBES

259
Q

What are the complications of asbestosis?

A 
mesothelioma
bronchogenic carcinoma (more common)

NOTE the carcinogenicity of asbestosis is poorly understood

260
Q

What will be seen histologically in asbestosis?

A

asbestos/ferruginous bodies (long, golden-brown fibers with associated iron)

261
Q

What will be seen on CXR in asbestosis?

A

“ivory white” calcified pleural plaques, pathognomic of asbestos exposure BUT NOT precancerous (black arrows show profile view)

most commonly found in the 6th-9th interspaces, usually sparing the apices and lung bases and involve the parietal pleura

262
Q

What is the pathogenesis of berylliosis?

A

beryllium exposure (miners, aerospace workers) –> noncaseating granulomas in lung, hilar lymph nodes, and systemic organs

263
Q

What is the complication of berylliosis?

A

lung cancer

264
Q

Which pneumoconioses affect the upper lobes?

A

anthracosis (Coal Workers’)

silicosis

265
Q

Which pneumoconioses affect the lower lobes?

A

asbestosis

266
Q

What is the pathogenesis of sarcoidosis?

A

unknown
likely due to CD4+ helper T-cell response to an unknown antigen –> systemic disease

characterized by noncaseating granulomas in multiple organs

267
Q

What do the granulomas of sarcoidosis most commonly involve?

A

hilar lymph nodes (“potato” nodes)

lung (reticulonodular infiltrate)

268
Q

Aside from noncaseating granulomas, what will be seen histologically in sarcoidosis?

A

“asteroid bodies:” stellate inclusions within giant cells of the granulomas

Please note this finding is characteristic of a given disease but NOT specific.

269
Q

What other tissues, other than hilar lymph nodes and lung, may be involved in sarcoidosis?

A

uvea –> uveitis
skin –> cutaneous nodules, erythema nodosum
salivery and lacrima glands –> mimicry of Sjogren’s syndrome
liver

almost any tissues may be involved

270
Q

What are the clinical features of sarcoidosis?

A

dyspnea or cough
elevated serum ACE
hypercalcemia (1-alpha hydroxylase activity of epithelioid histiocytes –> vitamin D converted to active form

271
Q

What is the pathogenesis of hypersensitivity pneumonitis?

A

inhaled organic antigens (“pigeon breeder’s lung”) –> granulomatous reaction –> diffuse interstitial/reticulonodular lung fibrosis

NOTE the injury mechanisms vary and are commonly mixed: Type II and IV hypersensititivy, increased CD4+ and CD8+, granulomata, obliterative bronchiolitis

272
Q

What is the presentation of hypersensitivity pneumonitis?

A

fever, cough, and dyspnea hours after exposure

resolves with removal of exposure

273
Q

What is respiratory bronchiolitis?

A

associated interstitial lung disease

  • macrophage collections, mild peri-airway fibrosis in long-term smokers
  • variably symptomatic
274
Q

What will be seen histologically in pulmonary HTN?

A

plexiform lesions seen with severe, long-standing disease

CIRCLE angioma-like thin-walled vessels can be seen, referred to as “angiomatoid” or “dilation” lesions

275
Q

What is the cause of neonatal respiratory distress syndrome?

A

inadequate surfactant –> increased surface tension –> alveolar sac collapse after expiration –> formation of hyaline membranes

276
Q

What lecithin:sphingomyelin ratio in amniotic fluid is predictive of neonatal RDS?

A

ratio <1.5

277
Q

With what is neonatal RDS associated?

A

prematurity: adequate surfactant levels are not reached until week 35
caesarian: lack of stress-induced steroids –> no increased synthesis of surfactant
maternal diabetes: insulin decreases surfactant production

278
Q

What are the clinical features of neonatal RDS?

A

increasing respiratory effort after birth
tachypnea with use of accessory muscles
grunting
hypoxemia with cyanosis
CXR showing “ground-glass” appearance of lung

279
Q

What are the complications of neonatal RDS?

A

(1) persistently low O2 tension –> hypoxemia –> increased risk of PDA, necrotizing enterocolitis
(2) supplemental oxygen –> increased risk of free radical injury –> (A) retinopathy of prematurity –> blindness; (B) lung damage –> bronchopulmonary dysplasia

280
Q

What is the treatment for neonatal RDS?

A

maternal steroids before birth

artificial surfactant for infant

281
Q

What is the presentation of ARDS?

A

rapid onset dyspnea
tachypnea
cyanosis
refractory hypoxemia

282
Q

What are the causes of ARDS?

A 
trauma
sepsis
shock, DIC
gastric aspiration
uremia
acute pancreatitis
amniotic fluid embolism
hypersensitivity reaction
drugs
283
Q

What is the main risk factor for ARDS?

A

alcoholism

284
Q

What is the pathogenesis of ARDS?

A

neutrophil activation –> protease-mediated, coagulation cascade, and free radical damage of Type I and II pneumocytes –> diffuse damage to alveolar-capillary interface –> leakage of protein-rich fluid –> edema, formation of intra-alveolar hyaline membranes –> atelectasis –> cell death, sloughing

285
Q

What changes will be seen pathologically in ARDS?

A

acute bilateral pulmonary infiltrates, consistent with non-cardiogenic pulmonary edema

286
Q

What is the process of organizing diffuse alveolar damage?

A

Type II cell proliferation –> interstitial fibrosis, macrophages –> TGF, PDGR

287
Q

What are the possible outcomes of organizing diffuse alveolar damage due to ARDS?

A

recovery
interstitial fibrosis
death (common)

288
Q

How is ARDS treated?

A

address underlying cause
ventilation with positive end-expiratory pressure (PEEP)

NOTE recovery may be complicated by interstitial fibrosis; damage and loss of Type II pneumocytes leads to scarring and fibrosis

289
Q

CD4+, TH2, eosinophils, mast cells: asthma or COPD?

A

asthma

290
Q

CD8+, PMNs, macrophages: asthma or COPD?

A

COPD

291
Q

Thick basement membrane: asthma or COPD?

A

asthma&raquo_space;> COPD

292
Q

Hypertrophic and hyperplastic bronchial smooth muscle: asthma or COPD?

A

asthma&raquo_space;> COPD

293
Q

Mucus plugs: asthma or COPD?

A

BOTH

294
Q

With emphysema: asthma or COPD?

A

COPD

295
Q

Large airways: asthma or COPD?

A

asthma

296
Q

Small airway: asthma or COPD?

A

COPD

297
Q

What is sleep apnea?

A

DEFINITION repeated cessation of breathing lasting 10 seconds or longer during sleep –> disrupted sleep –> daytime somnolence
TYPES (1) central: no respiratory effort, (2) obstructive: respiratory effort against airway obstruction

298
Q

What are the associations of obstructive sleep apnea?

A 
obesity
loud snoring
systemic or pulmonary HTN
arrhythmias
sudden death
299
Q

What is the treatment for sleep apnea?

A

weight loss
CPAP
surgery (very seldom)

300
Q

What labs are associated with sleep apnea?

A

increased EPO

(hypoxia –> EPO release –> increased erythropoiesis

301
Q

What are the physical findings (breath sound, percussion, fremitus, and tracheal deviation) in pleural effusion?

A

BREATH SOUNDS decreased
PERCUSSION dull
FREMITUS decreased
TRACHEAL DEVIATION no change

302
Q

What are the physical findings (breath sound, percussion, fremitus, and tracheal deviation) in atelectasis?

A

BREATH SOUNDS decreased
PERCUSSION dull
FREMITUS decreased
TRACHEAL DEVIATION toward side of lesion

303
Q

What are the physical findings (breath sound, percussion, fremitus, and tracheal deviation) in spontaneous pneumothorax?

A

BREATH SOUNDS decreased
PERCUSSION hyperresonant
FREMITUS decreased
TRACHEAL DEVIATION toward side of lesion

304
Q

What are the physical findings (breath sound, percussion, fremitus, and tracheal deviation) in tension pneumothorax?

A

BREATH SOUNDS decreased
PERCUSSION hyperresonant
FREMITUS decreased
TRACHEAL DEVIATION away from side of lesion

305
Q

What are the physical findings (breath sound, percussion, fremitus, and tracheal deviation) in consolidation (lobal pneumonia, pulmonary edema)?

A

BREATH SOUNDS bronchial; late inspiratory crackles
PERCUSSION dull
FREMITUS increased
TRACHEAL DEVIATION no change

306
Q

What type of cancer carries the greatest mortality?

A

lung cancer

307
Q

Are primary lung neoplasias common or rare in infancy?

A

rare

308
Q

How do all lung cancers present?

A 
cough
hemopytsis
bronchial obstruction
wheezing
chest pain
dyspnea
weight loss
CXR: pneumonia "coin" lesion
CT: noncalcified nodule

NOTE biopsy is required for diagnosis of cancer

309
Q

What are the complications of lung cancer?

A

Superior vena cava syndrome
Pancoast tumors (enophthalmos, prosis, miosis, anhidrosis)
Horner’s syndrome
Endocrine (paraneoplastic)
Recurrent laryngeal symptoms (hoarseness)
Effusions (pleural or pericardial)
–SPHERE–

310
Q

What is superior vena cava syndrome?

A

obstruction of the SVC –> impaired blood drainage from head, neck, and upper extremities –> distended head and neck veins –> JVD, edema, blue discoloration of arms and face

CAN raise intracranial pressure –> headaches, dizziness, increased risk of aneurysm / rupture of cranial arteries

MEDICAL EMERGENCY

311
Q

What is the most common cause of cancer?

A

metastatic cancer; most commonly from breast, colon, prostate, or bladder cancer

312
Q

Which lung cancers are NOT associated with smoking?

A

bronchioalveolar

bronchial carcinoid

313
Q

What is the percentage of lung cancer occurring in smokers?

A

85%

314
Q

How many carcinogens are in cigarette smoke, and what are the major carcinogens?

A

60

polycyclic aromatic hydrocarbons, arsenic

315
Q

Aside from cigarette smoke and asbestos, what is the other key risk factor for lung cancer?

A

radon, formed by radioactive decay of uranium, present in soil

316
Q

Where does radon accumulate?

A

closed spaces such as basements

317
Q

What is responsible, currently, for the majority of public exposure to ionizing radiation?

A

radon

By the way, ionizing radiation is the reason you should opt out of the full body scanners at the airport. Not good for you.

318
Q

What is the average American age of presentation with lung cancer?

A

60

319
Q

Which benign lung lesions, commonly seen in children, also produce a “coin lesion” on CXR?

A 
granuloma (often caused by TB or Histoplasma)
bronchial hamartoma (benign tumor comprised of lung tissue and cartilage; often calcified on imaging)
320
Q

What is the overall 5-year survival percentage in lung cancer?

A

15%

321
Q

You suspect malignant mesothelioma. What does your differential include?

A

carcinoma
sarcoma
solitary fibrous tumors (focal, pedunculated, fibroblastic looking)

NOTE immunoperoxidase Ag staining may be helpful

322
Q

What are the two major divisions of lung carcinoma?

A

SMALL CELL 15% of cancers; normally not amenable to surgical resection and treated instead with surgery; demonstrate early metastasis
NON-SMALL CELL 85% of lung cancers; treated upfront with surgical therapy as they do not respond to chemotherapy; slow growing and with poor prognosis

323
Q

What are the subtypes of non-small cell lung carcinoma?

A

adenocarcinoma 40%
squamous cell carcinoma (30%)
large cell carcinoma (10%)
carcinoid tumor (5%)

324
Q

Which lung cancer commonly demonstrates pleural involvement?

A

adenocarcinoma

325
Q

What is the most common lung cancer in nonsmokers and females?

A

adenocarcinoma

326
Q

What lung cancers are centrally located?

A 
squamous cell carcinoma
small cell (oat cell) carcinoma
327
Q

Which lung cancer results in hemorrhagic pleural effusions and pleural thickening/plaque-ing?

A

mesothelioma

328
Q

What lung cancers are peripherally located?

A

adenocarcinoma

large cell carcinoma

329
Q

What lung cancer demonstrates pleomorphic giant cells?

A

large cell carcinoma

330
Q

What lung cancer demonstrates keratin pearls and intracellular bridges?

A

squamous cell carcinoma

331
Q

What is the associated histology of bronchioloalveolar adenocarcinoma?

A

growth along alveolar septa –> apparent “thickening” of alveolar walls

332
Q

What lung cancer has an excellent prognosis and rarely metastasizes?

A

bronchial carcinoid tumor

333
Q

What lung cancer demonstrates neuroendocrine Kulchitsky cells?

A

small cell (oat cell) carcinoma

Kulchitsky cells are small dark blue cells

334
Q

What lung cancer is correlated with Cavitation, Cigarettes, and hyperCalcemia?

A

squamous cell carcinoma

335
Q

What lung cancer is associated with ACTH, ADH, Antibodies against presynaptic calcium channels (Lambert-Eaton syndrome), and Amplification of myc?

A

small cell (oat cell) carcinoma

336
Q

What lung cancer demonstrates nests of neuroendocrine cells and is also chromogranin positive?

A

bronchial carcinoid tumor

337
Q

Which lung cancer is inoperable and treated with chemotherapy?

A

small cell (oat cell) carcinoma

338
Q

Which lung cancer shows hazy infiltrates similar to pneumonia on CXR?

A

adenocarcinoma, bronchioloalveolar subtype

339
Q

Which lung cancer is located in the pleural?

A

mesothelioma

340
Q

Which lung cancer is associated with k-ras mutations?

A

adenocarcinoma

341
Q

Which lung cancer demonstrates psammoma bodies?

A

mesothelioma

342
Q

Where do Pancoast tumors occur?

A

apex of the lung; may affect cervical sympathetic plexus

343
Q

What are the symptoms of Horner’s syndrome?

A

ipsilateral ptosis
miosis
anhidrosis

344
Q

What is the most common cause of rhinitis?

A

Rhinovirus

345
Q

What is allergic rhinitis?

A

subtype of rhinitis, due to Type I hypersensitivity reaction (e.g., pollen)

346
Q

What are the associations of allergic rhinitis?

A

asthma

eczema

347
Q

What is the characterization of allergic rhinitis?

A

inflammatory infiltrate with eosinophils

348
Q

What is a nasal polyp, and how is it commonly caused?

A

DEFINITION protrusion of edematous, inflamed nasal mucosa

CAUSE secondary to repeated bouts of rhinits; also occurs in CF and aspirin-intolerant asthma

349
Q

What is the triad of aspirin-intolerant asthma?

A

asthma
aspirin-induced bronchospasms
nasal polyps

NOTE seen in 10% of asthmatic adults

350
Q

What is an angiofibroma, and how does it present?

A

DEFINITION benign tumor of nasal mucosa composed of large blood vessel and fibrous tissue
PRESENTATION epistaxis in adolescent males

351
Q

What is a nasopharyngeal carcinoma, and with what is it associated?

A

DEFINITION malignant tumor of nasopharyngeal epithelium

ASSOCIATION EBV; African children and Chinese adults

352
Q

What does a biopsy of nasopharyngeal carcinoma demonstrate?

A

pleumorphic keratin-positive epithelial cells (poorly differentiated squamous cell carcinoma) in a background of lymphocytes

353
Q

What is the most common cause of acute epiglottitis?

A

H. influenza B, especially in non-immunized children

354
Q

What is the presentation of acute epiglottitis?

A 
high fever
sore throat
drooling with dysphagia
muffled voice
inspiratory stridor
355
Q

What is a possible complication of epiglottitis?

A

airway obstruction

356
Q

What is the presentation of laryngotracheobronchitis (croup)?

A

hoarse, “barking” cough

inspiratory stridor

357
Q

What is the composition of a vocal cord nodule (singer’s nodule)?

A

degenerative (myxoid) connective tissue

358
Q

What is a laryngeal papilloma, and what is its cause?

A

DEFINITION benign papillary tumor of the vocal cord

CAUSE HPV 6, 11

359
Q

What is the presentation of a laryngeal papilloma?

A

single in adults; multiple in children

hoarseness

360
Q

What is a laryngeal carcinoma, and what is its presentation?

A

DEFINITION squamous cell carcinoma usually arising from the epithelial lining of the vocal cord
PRESENTATION hoarseness; cough, stridor

361
Q

What are the risk factors for laryngeal carcinoma?

A

alcohol
tobacco

rarely, arising from laryngeal papilloma

362
Q

What is the presentation of pneumonia, generally?

A 
fever, chills
productive cough with yellow-green (pus) or rusty (bloody) sputum
tachypnea 
pleuritic chest pain
decreased breath sounds
dullness to percussion
elevated WBC count
363
Q

How is a diagnosis of pneumonia made?

A

CXR
sputum gram stain & culture
blood cultures

364
Q

When does pneumonia occur?

A

when normal defenses are impaired: impaired cough reflex, damage to mucociliary escalator, mucus plugging

365
Q

What are the organisms involved in lobar pneumonia?

A

S. pneumoniae (95%)

Klebsiella

366
Q

What are the four classic gross phases of pneumonia?

A

CONGESTION due to congested vessels and edema
RED HEPATIZATION due to exudate, neutrophils, and hemorrhage filling the alveolar air spaces –> solid consistency of lung instead of spongy
GRAY HEPATIZATION due to degradation of red cells within exudate
RESOLUTION

367
Q

What are the characteristics of lobar pneumonia?

A

intra-alveolar exudate –> consolidation; may involve entire lung

368
Q

What are the infectious agents in bronchopneumonia?

A

S. pneumoniae
S. aureus
H. influenzae
Klebsiella

369
Q

What is the characterization of bronchopneumonia?

A

acute inflammatory infiltrates from bronchioles into adjacent alveoli –> scattered patchy consolidation centered around bronchioles; often multifocal and bilateral

370
Q

What are the infectious agents in interstitial (atypical) pneumonia?

A

viruses (influenza, RSV, adenoviruses)
Mycoplasma
Legionella
Chlamydia

371
Q

What is the characterization of interstitial (atypical) pneumonia?

A

diffuse patchy inflammation localized to interstitial areas at alveolar walls; distribution involving > 1 lobe

372
Q

What is the presentation of interstitial (atypical) pneumonia?

A

mild UR symptoms: minimal sputum and low fever

373
Q

What are the common agents involved in aspiration pneumonia?

A

anaerobic bacteria in the oropharynx (Bacteroides, Fusobacerium, Peptococcus)

374
Q

What populations are most at risk for aspiration pneumonia?

A

alcoholics

comatose patients

375
Q

What infectious agent causes a “current jelly” sputum?

A

Klebsiella pneumoniae

sputum is gelatinous due to a thick mucoid capsule

376
Q

What population is at risk for lobar pneumonia caused by Klebsiella pneumoniae?

A

malnourished, debilitated individuals
elderly in nursing homes
alcoholics
diabetics

377
Q

What is the most common cause of secondary pneumonia?

A

S. aureus; often will be complicated by abscess or empyema

378
Q

What is the most common cause of pneumonia in CF patients?

A

Pseudomonas aeruginosa

379
Q

What infectious agents are a common cause of community-acquired bronchopneumonia?

A

Moraxella catarrhalis

Legionella pneumophila

380
Q

What is the most common cause of atypical pneumonia in young adults?

A

Mycoplasma pneumoniae

381
Q

What are the complications of atypical pneumonia as caused by Mycoplasma pneumoniae?

A

IgM against I antigen on RBCs causes cold hemolytic anemia –> autoimmune hemolytic anemia
erythema multiforme

382
Q

What is the second most common cause of atypical pneumonia in young adults?

A

Chlamydia pneumoniae

383
Q

What is the most common cause of atypical pneumonia in infants?

A

RSV (respiratory syncytial virus)

384
Q

What is the common cause of atypical pneumonia in postttransplant immunosuppressive therapy?

A

CMV

385
Q

How is Coxiella distinct from most rickettsiae?

A

(1) causes pneumonia
(2) does not require arthropod vector for transmission (survives as highly heat-resistant endospores)
(3) does not produce a skin rash

386
Q

Where will an abscess most commonly be seen in atypical pneumonia?

A

right lower lobe (less acute angle)

387
Q

What is the cause of TB?

A

Mycobacterium tuberculosis

388
Q

What happens in primary TB?

A

focal, caseating necrosis in the lower lobe of the lung and hilar lymph nodes –> fibrosis and calcification –> Ghon complex

389
Q

What happens in secondary TB?

A

reactivation of Mycobacterium tuberculosis in the apex of lung due to high O2 tension –> cavitary foci of caseous necrosis, may also lead to miliary pulmonary TB or tuberculosis bronchopneumonia

390
Q

If secondary TB spread systemically, what tissues will be most commonly affected?

A

meninges –> meningitis
cervical lymph nodes
kidneys –> pyuria
lumbar vertebrae –> Pott disease

391
Q

What are the clinical features of secondary TB?

A

fevers
night sweats
cough with hemoptysis
weight loss

392
Q

What is the CXR finding on lung abscess?

A

air-fluid level

393
Q

What are the common causative agents of lung abscesses?

A

S. aureus

anaerobes (Bacteroides, Fusobacterium, Peptostreptococcus)

394
Q

What is the cause of a lung abscess?

A 
bronchial obstruction (cancer)
aspiration of oropharyngeal contents (especially in patients predisposed to loss of consciousness such as alcoholics or epileptics)
395
Q

What is hypersensitivity pneumonitis, and how does it present?

A

DEFINITION mixed type III/IV hypersensitivity reacion to environmental antigen
PRESENTATION dyspnea, cough, cheat tightness, headache

396
Q

What are the causes of transudate in pleural effusions?

A

CHF
nephrotic syndrome
hepatic cirrhosis

397
Q

What are the causes of exudate in pleural effusions?

A

malignancy
pneumonia
collagen vascular disease
trauma

398
Q

What are the causes of lymphatic pleural effusion / chylothorax?

A

thoracic duct injury from trauma or malignancy

399
Q

What are the findings in lymphatic pleural effusion / chylothorax?

A

milky-appearing fluid

increased triglycerides

400
Q

What is a pneumothorax?

A

accumulation of air in the pleural space

401
Q

What is the general presentation of a pneumothorax?

A 
unilateral chest pain and dyspnea
unilateral chest expansion
decreased tactile fremitus
hyperresonance
diminshed breath sounds
402
Q

What is a spontaneous pneumothorax?

A

accumulation of air in the pleural space due to rupture of an emphysematous bleb –> collapse of a portion of the lung

403
Q

Which direction does the trachea shift in spontaneous pneumothorax?

A

toward the side of collapse

404
Q

Which direction does the trachea shift in tension pneumothorax?

A

away from the side of injury

405
Q

What causes a tension pneumothorax?

A

penetrating chest wall injury or lung infection; air can enter pleural space but cannot exit

406
Q

How do you treat a tension pneumothorax?

A

insertion of a chest tube

From Flashcardlet (18 decks)

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