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Resp Flashcards

1
Q

Lung development stages?

A 
stage 1: embryonic (wks 4-7)
stage 2: pseudoglandular (wks 5-17)
stage 3:canalicular (wks 16-25)
stage 4: saccular (wks 26-birth)
stage 5:alveolar (wk 36-8 years)
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2
Q

Embryonic stage of lung development

A

lung bud –> trachea –> bronchial buds –> mainstem bronchi –> secondary (lobar) bronchi –> tertiary (Segmental) bronchi

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3
Q

error at what stage of lung development results in a tracheoesophageal fistula

A

at the embryonic stage at wks 4-7

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4
Q

Pseudoglandular stage of lung development (wks 5-17)

A

endodermal tubules –> terminal bronchioles

surrounded by modest capillary network

respiration impossible and incompatible with life

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5
Q

Canalicular stage of lung development (wks 16-25)

A

Terminal bronchioles –> respiratory bronchioles –> alveiolar ducts

surrounded by a prominent capillary network

airways increase in diameter

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6
Q

respiration is capable at what week

A

25 wks

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7
Q

pneumocytes develop starting at

A

20 weeks

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8
Q

Saccular stage of lung development (wks 26-birth)

A

alveolar ducts –> terminal sacs which are separated by primary septae

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9
Q

Alveolar stage of lung development (wks 36- 8 years)

A

Terminal sacs become adult alveoli due to secondary septation

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10
Q

In utero breathing occurs via aspiration and expulsion of amniotic fluid which increases vascular resistance through gestation. What happens/changes at birth?

A

at birth fluid gets replaced with air and there is a decrease in pulmonary vascular resistance

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11
Q

This congenital lung malformation is a poorly developed bronchial tree with abnormal histology

A

pulmonary hypoplasia

associated with congenital diaphragmatic hernia thats usually on the left side and bilateral renal agenesis (potter sequence)

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12
Q

Congenital lung malformation that is caused by abnormal budding of the foregut and dilation of terminal or large bronchi. Discrete, round, sharply defined, fluid filled densities on CXR (air filled if infected)

A

bronchogenic cysts

usually asymptomatic but can cause respiratory infections

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13
Q

__ cells are located in bronchioles and are important for degrading toxins and secreting a component of surfactant

A

Club cells

nonciliated

low columnar/cuboidal with secretory granules

act as reserve cells

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14
Q

Type 1 pneumocytes

A

97% of alveolar surfaces

line the alveoli

squamous

Thin for optimal gas diffusion

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15
Q

Type II pneumocytes

A

Secrete surfactant from lamellar bodies and decrease alveolar surface tension –> prevent alveolar collapse, decrease lung recoil, and increase compliance

cuboidal and clustered

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16
Q

What type of pneumocyte proliferates during lung damage

A

Type II pneumocyte

serve as a precursor for type I cells and other type II cells

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17
Q

Collapsing pressure equation

A

P=(2*surface tension)/radius

on expiration: radius decreases therefore higher chance of collapse

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18
Q

Pulmonary surfactant is a complex mix mix of lecithins, the most important of which is ______

A

DPPC

dipalmitoylphosphatidylcholine

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19
Q

when does surfactant synthesis begin? when are mature levels reached?

A

beings at 20 wk

mature levels reached at week 35

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20
Q

______ are important for fetus surfactant production and lung development

A

corticosteroids

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21
Q

Alveolar macrophage function to ____________ and release ________ and _________

A

phagocytose foreign materials

release cytokines and alveolar proteases

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22
Q

__________ macrophages may be seen in pulmonary hemorrhage

A

hemosiderin-laden

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23
Q

Surfactant deficiency in a neonate can result in? why? how does it appear on xray?

A

neonatal respiratory distress syndrome

low surfactant will increase surface tension and ultimately alveolar collapse

“ground glass appearance”

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24
Q

Important risk factors for neonatal respiratory distress syndrome

A

1) prematurity
2) maternal diabetes due to increase in fetal insulin
3) c section delivery due to decrease of fetal glucocorticoids because it is less stressful than vaginal delivery

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25
Q

Treatment for neonatal respiratory distress syndrome

A

maternal steroids before brith

exogenous surfactant for infant

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26
Q

Therapeutic supplemental O2 can result in what three things?

A

1) retinopathy of prematurity
2) intraventricular hemorrhage
3) bronchopulmonary dysplasia

“RIB”

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27
Q

What is the screening test for fetal lung maturity

A

lecithin-sphingomyelin ratio in amniotic fluid

> = 2 is healthy

<1.5 is predictive of neonatal respiratory distress syndrome

can also look at foam stability index and surfactant-albumin ratio

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28
Q

persistently low O2 tension can increase the risk of

A

PDA

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29
Q

Where is there the least airway resistance

A

terminal bronchioles because there is a large number in parallel

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30
Q

conducting zone of the lung

A

(Trachea –> bronchi –> bronchioles –> terminal bronchioles

anatomic dead space because it does not participate in gas exchange

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31
Q

cartilage and goblet cells extend to the end of ____

A

bronchi

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32
Q

Cell types within the respiratory tree

A
  • Trachea and bronchi : pseudostratified ciliated columnar epithelium + basal cells + goblet cells
  • Bronchioles: simple ciliated columnar epithelium + club cells
  • Terminal bronchioles: simple cuboidal epithelium + club cells
  • Respiratory bronchioles: simple cuboidal and squamous epithelium + club cells
  • Alveolar sacs: Type I pneumocytes + type II pneumocytes +alveolar macrophages (clear debris and immune response)
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33
Q

Respiratory zone

A

respiratory bronchioles –> alveolar sacs

participate in gas exchange

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34
Q

cilia terminate in the _________

A

respiratory bronchioles

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35
Q

Left lung

A

“Left is Less”

2 lobes + lingula (homolog of R middle lobe)

only an oblique fissure

instead of a middle lobe, the left lung has a space occupied by the heart

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36
Q

Right lung

A

3 lobes

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37
Q

carina is ____ to the ascending aorta and ___ to the descending aorta

A

posterior

anteromedial

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38
Q

Where do inhaled foreign bodies usually go to

A

right lung because the right mainstem bronchus is wider and more vertical and shorter

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39
Q

If you inhale a peanut while supine? while laying on right side? while upright?

A

if suprine –> right lower lobe
If lying on R side –> right upper lobe
If upright –> right lower lobe

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40
Q

needle for tension pneumothorax should be positioned between the

A

2nd and 3rd left ribs

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41
Q

diaphragm structures @ T8

A

IVC and R phrenic nerve

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42
Q

diaphragm structures @ T10

A

esophagus and vagus nerve

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43
Q

diaphragm structures @ T12

A

aorta
thoracic duct
azygos vein

1 and 2 is red,white, and blue

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44
Q

diaphragm structures mnemonic

A

I 8 10 eggs at 12

8=IVC
10=esophagus
12=aorta

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45
Q

Diaphragm is innervated by C____ (phrenic nerve). Pain can be referred to the shoulder via C ___ and trapezius ridge via C __ and ___

A

C3,4,5

C5 –> shoulder

C3 and 4 –> trapezius ridge

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46
Q

The common carotid bifurcates at?

A

bi”four”cates therefore C4

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47
Q

The trachea bifurcates at?

A

bi”four”cates therefore T4

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48
Q

The abdominal aorta bifurcates at?

A

bi”four”cates therefore L4

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49
Q

Air that can still be breathed in after normal inspiration

A

inspiratory reserve volume

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50
Q

Ait that moves into lung with each quiet inspiration typically 500 ml

A

tidal volume

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51
Q

Air that can still be breathed out after normal expiration

A

expiratory reserve volume

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52
Q

Air in lung after maximal expiration

A

residual volume

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53
Q

what cannot be measured by spirometry in terms of lung volumes

A

residual volume and anything that includes residual volume (functional residual capacity and total lung capacity)

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54
Q

Air that can be breathed in after normal exhalation

A

inspiratory capacity

IRV + TV

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55
Q

Volume of gas in lungs after normal expiration

A

functional residual capacity

RV+ERV

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56
Q

Maximum volume of gas that can be expired after a maximal inspiration

A

Vital capacity

TV+IRV +ERV

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57
Q

Volume of gas present in lungs after a maximal inspiration

A

total lung capacity

IRV+TV+ERV+RV

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58
Q

What is the largest contributor to alveolar dead space

A

apex of a healthy lung

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59
Q

Vd or physiologic dead space

A

Vd=physiologic dead space= anatomic dead space of conducting airways + alveolar dead space

it is the volume of inspired air that does not take part in gas exchange

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60
Q

physiologic dead space equation

A

Vs=Tidal volume ((arterial PCO2-expired air PCO2)/arterial PCO2)

“Paco Peco Paco”

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61
Q

physiologic dead space is _____ to anatomic dead space in normal lungs

A

approx. equivalent

may be greater than anatomic dead space in lugn diseases with V/Q defect

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62
Q

Minute ventilation equation

A

total volume of gas entering lungs per minute

Ve=Vt x RR

Vt= 500 mL/breath
RR=12-20

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63
Q

Alveolar ventilation equation

A

volume of gas that reaches alveoli each minute

Va=(Vt-Vd)RR

Vt=500 mL/breath
Vd=150 mL/breath
RR=12-20

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64
Q

Elastic recoil

A

tendency for lungs to collapse inward and chest wall to spring outward

this is balanced at the functional residual capacity or the volume of gas in lungs after normal expiration

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65
Q

compliance

A

change in volume/ change in pressure

ex) high compliance is seen in old age and emphysema

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66
Q

what is surfactants effect on compliance

A

it increases compliance

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67
Q

Hysteresis

A

lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation

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68
Q

Respiratory system changes in the elderly

A
  • increase lung compliance
  • decrease chest wall compliance
  • increase residual volume
  • decreased FVC and FEV1
  • Normal TLC
  • Increase ventilation/perfusion mismatch
  • increased A-a gradient
  • decreased resp muscle strength
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69
Q

Hemoglobin is composed of _____ polypeptide subunits. ____ alpha and ___ beta.

A

4

2 alpha and 2 beta

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70
Q

Deoxygenated form of hemoglobin

A

low affinity for O2

so that it can release/unload O2

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71
Q

Oxygenated form of hemoglobin

A

high affinity for O2 (x300)

+ cooperativity
- allostery

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72
Q

Right shift on the hemoglobin dissociation curve indicates

A

increased O2 unloading (deoxygenated form)

due to increased Cl-, H+, CO2, 2,3 BPG, temp

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73
Q

Left shift on the hemoglobin dissociation curve indicated

A

decreased O2 unloading (oxygenated form of hemoglobin)

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74
Q

Fetal hemoglobin components and O2 affinity compared to adult

A

2alpha
2gamma

higher affinity for O2 –> drives O2 diffusion from mother to child across placenta

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75
Q

Why does fetal hemoglobin have an increased affinity for O2

A

-oxygenated form of hemoglobin /decreased O2 unloading due to low affinity of HbF for 2,3 BPG. This shifts the curve to the left

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76
Q

Hemoglobin acts as a buffer for ___ ions

A

H+

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77
Q

Myoglobin

A

single polypeptide chain associated with one heme moiety

higher affinity for oxygen than Hb

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78
Q

Patient presents with cyanosis and chocolate colored blood. What is the patient likely suffering from? What causes it? What is the pathophys? how is it treated?

A

Methemoglobin- Oxidized form of Hb (ferric Fe 3+) does not bind O2 as readily as Fe2+ (normal reduced form) but has greater affinity for cyanide

Can be caused by nitrites and benzocaine which cause poisoning by oxidizing Fe2+ to Fe3+

treat with methylene blue and vitamin C

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79
Q

Carboxyhemoglobin

A

Form of Hb bound to CO in place of O2

causes decrease in oxygen binding capacity with left shift in oxygen hemoglobin dissociation curve –> lower O2 unloading in tissues

CO binds competitively to hemoglobin and with 200X greater affinity than O2

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80
Q

Patient presents with headaches, dizziness, and cherry red skin

A

CO poisoning

treat with 100% O2 and hyperbaric O2

81
Q

Patient presents with almond breath odor, pink skin, and cyanosis

A

Cyanide poisoning

Inhibits aerobic metabolism via complex 4 inhibition –> hypoxia unresponsive to supplemental O2 and increase anaerobic metabolism

82
Q

how do you treat cyanide poisoning

A

first give nitrites which oxidizes hemoglobin to methemoglobin (can trap cyanide as cyanmethemoglobin)

Then give thiosulfates which convert cyanide to thiocyanate –> renally excreted

83
Q

The hemoglobin curve is ___ shaped due to ____. The myoglobin curve lacks this shaped because it is monomeric and does not show _____

A

sigmoid shaped

positive cooperativity

positive cooperativity

84
Q

Shifting the oxygen dissociation curve to the right results in

A

decreased Hb affinity for O2 which facilitates unloading of O2 to tissue. Therefore the P50 increases indicating that a higher PO2 is required to maintain 50% saturation

  • increased H+
  • drop in PH or increase acid
  • Exercise
  • Increase 2,3-BPG
  • High altitude
  • Increased temperature
85
Q

Shifting the oxygen dissociation curve to the left

A

means there is decreased O2 unloading

think left=lower O2 unloading

  • drop in H+
  • increase in pH or base
  • drop in 2,3-BPG
  • drop in temperature
86
Q

Decreased O2 unloading results in renal hypoxia which increases

A

EPO synthesis and results in compensatory erythrocytosis

87
Q

O2 content in blood

A

(1.34 x (hemoglobin level) x (arterial O2 saturation) ) + (0.003xPaO2)

88
Q

normal hemoglobin amount

A

15 g/dL

89
Q

If there is a drop in Hb, what happens to the O2 content of blood, the O2 saturation, and the partial pressure of O2 in arterial blood

A

O2 content drops
No change in O2 saturation
No change in PaO2/Partial pressure of O2 in arterial blood

90
Q

A decrease in pAO2 causes what response?

A

hypoxic vasocontriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung

91
Q

Perfusion limited

A

Rate at which gas is transported away from functioning alveoli and into tissues is principally limited by the rate of blood flow through the pulmonary capillaries and thus across the alveolar membrane.

on graph it increases and then plateau early. Gas equilibrates early along the length of the capillary. Diffusion can be increased only if increase in blood flow

related to O2 (normal health), CO2, N2O

92
Q

Diffusion limited

A

Gas does not equilibrate by the time blood reaches the end of the capillary

O2 (emphysema, fibrosis, exercise) and CO

93
Q

What is a consequence of pulmonary hypertension

A

cor pulmonale or abnormal enlargement of R side of heart

subsequent right ventricular failure

94
Q

Diffusion eq

A

V gas= Area x Diffusion coefficient x ((different in partial pressures)/alveolar wall thickness)

area decreases in emphysema
alveolar wall thickness increases in fibrosis

95
Q

Dlco

A

the extent to which CO a surrogate for O2 passes from air sacs of lungs into blood

96
Q

PVR or pulmn vasc. resistance equation

A

(pressure in pulm artery - pulmonary capillary wedge pressure) / cardiac output

97
Q

Alveolar gas eq

A

PAO2=150-PaCO2/0.8

0.8 is resp quotient= CO2 produced/O2 consumed

98
Q

A-a gradient

A

PAO2-PaO2 = normal is 10-15 mm Hg

gradient increases in hypoxemia which is caused by shunting, V/Q mismatch, fibrosis because they impair diffusion

99
Q

Define hypoxia

A

decreased O2 delivery to tissue

100
Q

Define hypoxemia

A

decrease PaO2

101
Q

What causes hypoxemia

A

a decrease in PaO2 is caused by:

high altitude and hypoventilation - these have normal A-a gradient

V/Q mismatch, Diffusion limitation, Right to left shunt - these have increased A-a gradient

102
Q

V/Q mismatch

A

ventilation/perfusion mismatch

103
Q

Where in the lung is there wasted ventilation and what does this show in reference to the V/Q mismatch

A

V/Q mismatch at apex of lung = 3 which indicated wasted ventilation. Increase in V but great decrease in Q

organisms that thrive in O2 like TB flourish in the apex

104
Q

Where in the lung is there wasted perfusion and what does this show in reference to the V/Q mismatch

A

V/Q mismatch at base of lung=0.6 which indicated wasted perfusion. Increase in V but greater increase in Q

note: both ventilation and perfusion are greater at the base of the lung

105
Q

What happens to the V/Q mismatch during these changes:

1) exercise
2) airway obstruction
3) blood flow obstruction

A

1) increase in cardiac output which causes vasodilation of apical capillaries and thus V/Q ratio approaches 1
2) V/Q=0 during airway obstruction (shunt). In a shunt, 100% O2 does not improve PaO2. ex is foreign body aspiration
3) V/Q=infiniti during blood flow obstruction (physiological dead space). Assuming <100% dead space, 100% O2 improves the PaO2. ex is pulmonary embolus

106
Q

Co2 is transported from tissue to lungs in 3 forms:

A

1) HCO3 (70%)
2) Carbaminohemoglobin or HbCO2 (21-25%)
3) Dissolved CO2

note: CO2 bound to Hb at N-terminus of globin (not heme). CO2 favors deoxygenated form (O2 unloaded)

107
Q

In the lung, oxygenation of Hb promotes dissociation of ____ from Hb. This shifts equilibrium towards CO2 formation and therefore CO2 is released from RBCs. This is called the

A

Halfane effect

108
Q

In peripheral tissues, increase in _____ in tissue metabolism shifts curve to the right, and unloading O2. This is called the

A

bohr effect

109
Q

CO2 enters RBC and is converted to HCO3 via

A

carbonic anyhdrase

first becomes H2CO3 then converts to HCO3

110
Q

What is your bodies response to high altitude

A

decrease in atmospheric oxyen causes a drop in PaO2 and an increase in ventilation. The increase in ventilation causes a drop in PaCO2. This causes respiratory alkalosis aka altitude sickness

111
Q

Besides resp alkalosis causing high altitude sickness, what other changes occur in the body

A
  • increase in erythropoietin due to chronic hypoxia which increase hct and hv
  • increase 2,3 BPG which binds to Hb and causes a right shift so that Hb releases more O2
  • increase in mitochondria
  • increased renal excretion of HCO3 to compensate for resp alkalosis
  • chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH
112
Q

Bodies response to exercise

A

V/Q ratio from apex to base become more uniform

decrease in pH during strenuous exercise thats secondary to lactic acidosis

No change in PaO2 and PaCO2

113
Q

Rhinosinusitis

A

obstruction of sinus drainage into nasal cavity

114
Q

Rhinosinusitis typically affects what sinuses and why

A

typically affects maxillary sinuses which drain against gravity due to ostia located superomedially

115
Q

What is the most common cause of rhinosinusitis

A

most common acute cause is viral URI but it may lead to superimposed bacterial infections, most commonly S. pneumo, H influenzae, M catarrhalis

116
Q

Infections in sphenoid or ____ sinuses may extend to the cavernous sinus and cause

A

cavernous sinus syndrome - ophthalmoplegia, proptosis, ocular and conjunctival congestion, trigeminal sensory loss and Horner’s syndrome. These signs and symptoms result from the involvement of the cranial nerves passing through the cavernous sinus.

117
Q

Epistaxis define? Where does it occur most commonly? related to what plexus?

A

epistaxis is nose bleed

most commonly occurs in anterior segment of nostril

at the kiesselbach plexus - superior labial artery, anterior and posterior ethmoidal arteries, greater palatine artery, sphenopalatine artery

118
Q

Life threatening hemorrhages occur in the ____ segment of the nose. This is because of what artery?

A

posterior segment

sphenopalatine artery, a branch of maxillary artery

119
Q

Head and neck cancers are mostly

A

Squamous cell carcinomas

Oropharyngeal - HPV16
Nasophayngeal - EBV

field cancerization is when carcinogen damages wide mucosal area and results in multiple tumors that develop independently after exposure

120
Q

Deep venous thrombosis

A

presents with swelling, redness, warmth, and pain

predisposed by the Virchow triad (stasis, hypercoagulability, endothelial damage)

can use D-dimer to rule out DVT but it is not very specific

treat with

121
Q

Most pulmonary emboli arise from

A

proximal deep veins of lower extremity

122
Q

Patient presents with sudden onset dyspnea, pleuritic chest pain, tachypnea, and tachycardia, Patient dies and on autopsy you find a saddle embolis

A

Pulmonary emboli causing electromechanical dissociation

123
Q

How do you know a thrombi was formed before death vs after death

A

Lines of zahn are interdigiting areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death

they help distinguish pre and post mortem thrombi

124
Q

Patient presents with triad of hypoxemia, neurologic abnormalities, and petechial rash

A

fat emboli

125
Q

decompression sickness/caisson disease

A

air emboli - nitrogen bubbles precipitate in ascending divers

tx with hyperbaric O2

126
Q

Amniotic fluid emboli can lead to

A

DIC

especially post partum

127
Q

Obstructive lung disease

RV
FRC
TLC
FEV1
FVC
FEV1/FVC
A 
RV increased
FRC increased
TLC increased
FEV1 very low
FVC decreased
FEV1/FVC decreased (HALLMARK)

loop shifts to the left and looks like a slide

128
Q

Restrictive lung disease

RV
FRC
TLC
FEV1
FVC
FEV1/FVC
A 
RV decreased
FRC decreased
TLC decreased
FEV1 decreased
FVC decreased
FEV1/FVC normal or increased because FEV1 decreased proportionately to FVC

loop shifts to the right

129
Q

Obstructive lung disease

A

chronic bronchitis
emphysema
Asthma

130
Q

Patient presents with wheezing, crackles, cyanosis, dyspnea, CO2 retention, secondary polycythemia. She mentions having a productive cough for more than 3 months in the past year and that this has happened for 2 consecutive years. What does she have? what kind of lung disease is it? and what is the pathology?

A

Chronic bronchitis - obstructive lung disease

hypertrophy and hyperplasia of mucus-secreting glands in bronchi –> reid index > 50%

reid index is thickness of mucosal gland layer to thickness of wall between epithelium and cartilage

DLCO normal

131
Q

Patient presents with a barrel shaped chest and complain that she only feels comfortable upon exhalation through pursed lip. What does she have? what kind of lung disease? why does she purse her lips?

A

Emphysema- obstructive lung disease

increases airway pressure and prevents airway collapse

chest xray shows increased AP diameter, flattened diaphragm, and increased lung field lucency

drop in DLCO from destruction of alveolar walls

imbalance of proteases and antiproteases causes increased elastase activity and increased loss of elastic fibers –> increased lung compliance

132
Q

Centriacinar emphysema

A

associated with smoking because smoke rises up to upper lobes

133
Q

Panacinar emphysema

A

associated with alpha1-antitrypsin deficiency frequently in lower lobes

134
Q

Patent presents with coughing, wheezing, decreased inspiratory/expiratory ratio, pulsus paradoxus, mucus plugging and was unable to do the methacholine challenge

A

Asthma- obstructive lung disease

hyperresponsive bronchi - reversible bronchoconstriction

smooth mm hypertrophy and hyperplasia

curschmann spirals (shed epithelium forms whorled mucous plugs)

charcot leyden crystals (eosinophilic hexagonal double pointed crystals formed from breakdown of eosinophils in sputum)

DLCO normal or increased

135
Q

Patient has cystic fibrosis and presents with purulent sputum, recurrent infections, hemoptysis, and digital clubbing. What type of lung disease are we most worried about

A

bronchiectasis- obstructive lung disease

chronic necrotizing infection of bronchi or obstruction that permanently dilates airways

associated with bronchial obstruction, poor ciliary motility, CF, and allergic bronchopulmonary aspergillosis

136
Q

Restrictive lung diseases

A

decreased FVC
increased FEV1/FVC ratio

can be due to poor breathing mechanics (poor mm effort of structural apparatus) OR interstitial lung diseases that decrease pulmonary diffusing capacity and increase A-a gradient

137
Q

hypersensitivity pneumonitis

A

mixed type III/IV hypersensitivity reaction to environmental antigen

dyspnea, cough, chest tightness, headache

reversible in early stages

usually associated with farmers and those exposed to birds

138
Q

Sarcoidosis

A

immune mediated widespread noncaseating granulomas, elevated serum ACE levels, and elevated CD4+/CD8+ ratio in bronchoalveolar lavage fluid

patients are often asymptomatic except for enlarged lymph nodes, CXR of bilateral adenopathy and coarse reticular opacities, CT of chest better demonstrates the extensive hilar and mediastinal adenopathy

139
Q

What is sarcoidosis associated with

A
  • Bells palsy
  • Uveitis
  • Granulomas - contain schaumann and asteroid bodies
  • Lupus pernio - skin lesions on face resemble lupus
  • Interstitial fibrosis (restrictive lung dz)
  • Erythema nodosum
  • Rheumatoid arthritis-like arthropathy
  • Hypercalcemia due to increased 1αhydroxylase –mediated vitamin D activation in macrophages
140
Q

Treat patients with sarcoidosis with

A

steroids

141
Q

Inhalation injury

A

chemical tracheobronchitis,edema,pneumonia, ARDS

142
Q

Patient is a roofer that has “ivory white”, calcified supradiaphragmatic and pleural plaques. What does the patient have and in what lobes do you commonly see affect? What are the risks?

A

asbestos is a form of pneumoconioses

lower lobes

risk of bronchogenic cancer

143
Q

What is the hallmark sign on prussian blue stain of bronchoalveolar lavage

A

ferruginous bodies are golden-brown fusiform rods resembling dumbbells

144
Q

berylliosis

A

beryllium is a form of pneumoconioses

upper lobes

granulomatous (noncaseating)

increased risk of cancer and cor pulmonale

145
Q

Coal workers pneumoconiosis

A

macrophages laden with carbon cause inflammation and fibrosis in upper lobes

called black lung disease

affects upper lungs

increased risk of caplan syndrome or rheumatoid arthritis and pneumoconiosis with intrapulmonary nodules

146
Q

Anthracosis

A

asymptomatic condition found in many urban dwellers exposed to sooty air

147
Q

silicosis

A

macrophages respond to silica and release fibrogenic factors that lead to fibrosis

form of pneumoconiosis that affects upper lobes

silica may disrupt phagolysosomes and impair macrophages and increase susceptibility to TB. Increased risk of cancer, cor pulmonale, and caplan syndrome

see eggshell calcification of hilar lymph nodes on CXR

148
Q

Mesothelioma

A

malignancy of the pleura associated with asbestosis

hemorrhagic pleural effusion (exudative) and pleural thickening

psammoma bodies and calretinin +

smoking is not a risk factor

149
Q

The most common cause of acute respiratory distress syndrome

A

sepsis

150
Q

ACute respiratory distress syndrome pathophys

A

alveolar insult causes release of proinflammatory cytokines

these cytokines result in neutrophil recruitment, activation,and release of toxic mediators causing capillary endothelial damage and increased vessel permeability

protein rich fluid leaks into alveoli and causes formation of intra alveolar hyaline membranes and noncardiogenic pulmonary edema

151
Q

diagnosis of ARDS (acute resp distress syndrome)

A
  • Abnormal chest xray (bilateral lung opacities)
  • Respiratory failure within 1 week of alveolar insult
  • Decreased PaO2/FiO2 (ratio <300, hypoxemia due to shunting and diffusion abnormalities
  • Symptoms of respiratory failure are not due to HF/fluid overload
152
Q

sleep apnea involves the cessation of breathing for greater than ___ seconds

A

10 seconds

results in nocturnal hypoxia which causes systemic/pulmonary hypertension, arrhythmias (a fib/flutter), sudden death

153
Q

obstructive sleep apnea in adults vs children

A

adults have excess parapharyngeal tissue

children have adenotonsillar hypertrophy

154
Q

central sleep apnea

A

impaired respiratory effort due to CNS injury/toxicity, HF, opioids

may be associated with cheyne-stokes repirations - oscillation between apnea and hyperpnea

treat with positive airway pressure

155
Q

obesity hypoventilation syndrome /Pickwickian syndrome

A

obesity >= 30 BMI

hypoventilation causes increased PaCO2 during waking hours (Retention) and a drop in PaO2 and increase PaCO2 during sleep

156
Q

pulmonary hypertension is defined as a mean pulmonary artery pressure >=

A

25 mm Hg

normal is 10-14 mm hg

results in arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries, plexiform lesions

157
Q

pulmonary hypertension course

A

severe respiratory distress causes cyanosis and RVH –> death from decompensated cor pulmonale

158
Q

Heritable PAH (pulm art. hypertension)

A

Inactivating mutation in BMPR2 gene (normally inhibits vascular smooth mm proliferation)

159
Q

PAH can also be due to pulmonary vasculature endothelial dysfunction which results in

A

increased vasocontrictors (endothelin) and decreased vasodilatory (NO and prostacyclins)

160
Q

pulmonary hypertension can also be caused by chronic thromboembolic

A

recurrent microthrombi which decreased cross sectional area of pulmonary cascular bed

161
Q

Breath sounds in:

1) pleural effusion
2) atelectasis (bronchial obstruction)
3) simple pneumothroax
4) tension pneumothorax
5) consolidation

A

decreased in all except in consolidation we see bronchial breath sounds, late inspiratory crackles, egophony, whispered pectoriloquy

162
Q

Percussion in :

1) pleural effusion
2) atelectasis (bronchial obstruction)
3) simple pneumothroax
4) tension pneumothorax
5) consolidation

A

1) pleural effusion - dull
2) atelectasis (bronchial obstruction) - dull
3) simple pneumothroax - hyperresonant
4) tension pneumothorax - hyperresonant
5) consolidation - dull

163
Q

fremitus in

1) pleural effusion
2) atelectasis (bronchial obstruction)
3) simple pneumothroax
4) tension pneumothorax
5) consolidation

A

decreased except in consolidation (lobar pneumo or pulm edema)

164
Q

Tracheal deviation in

1) pleural effusion
2) atelectasis (bronchial obstruction)
3) simple pneumothroax
4) tension pneumothorax
5) consolidation

A

1) pleural effusion –> none if small ; away from side of lesion if large
2) atelectasis (bronchial obstruction) –> toward side of lesion
3) simple pneumothroax –> none
4) tension pneumothorax –> away from side of lesion
5) consolidation –> none

165
Q

tension vs simple pneumothorax

A

Tension pneumothorax is the progressive build-up of air within the pleural space, usually due to a lung laceration which allows air to escape into the pleural space but not to return. Positive pressure ventilation may exacerbate this ‘one-way-valve’ effect.

A simple pneumothorax is a non-expanding collection of air around the lung. The lung is collapsed, to a variable extent.

166
Q

pleural effusion

A

excess accumulation of fluid between pleural layers that cause restricted lung expansion during inspiration

can be treated with thoracentesis to remove/reduce fluid

167
Q

pleural effusion: transudate

A

decreased protein content

due to increased hydrostatic pressure or decreased oncotic pressure

168
Q

pleural effusion: exudate

A

increased protein content, cloudy

due to malignancy, pneumonia, collagen vascular disease, trauma

occurs in states of increase vascular permeability

must be drained due to risk of infection

169
Q

pleural effusion: lymphatic

A

chylothorax

due to thoracic duct injury from trauma or malignancy

milky appearing fluid

increased triglycerides

170
Q

Primary spontaneous pneumothorax

A

due to rupture of apical subpleural bleb or cysts

occurs most frequently in tall, thin, young males and smokers

171
Q

Secondary spontaneous pneumothorax

A

due to diseased lung, mechnical ventilation with use of high pressures which result in barotrauma

172
Q

Traumatic pneumothorax

A

caused by blunt, penetrating, or iatrogenic trauma ( central line placement,lung biopsy, barotrauma due to mechanical ventilation)

173
Q

tension pneumothorax

A

can be from any trauma pneumothorax causes

air enters the pleural space but cannot exit. Increased trapped air causes tension pneumothorax. Trachea deviates away from the affected lung

174
Q

Lobar pneumonia typical organisms

A

S pneumo most common

legionella
klebsiella

175
Q

lobar pneumonia characterisitcs

A

intra alveolar exudate leading to consolidation

can involve entire lobe or whole lung

176
Q

bronchopneumonia typical organisms

A

S pneumo, S aureus, H influenzae, Klebsiella

177
Q

bronchopneumonia characteristics

A

acute inflammatory infiltrates from bronchioles into adjacent alveoli

patchy distribution involving >=1 lobe

178
Q

Interstitial atypical pneumonia typical organisms

A 
mycoplasma
chlamydophila pneumo
chlamydophila psittaci
legionella
viruses (RSV,CMV, influenza, adenovirus)
179
Q

Interstitial atypical pneumonia characteristics

A

diffuse patchy inflammation localized to interstitial areas at alveolar walls

diffuse distribution involving >=1 lobe

“walking pneumonia”

180
Q

Cryptogenic organizing pneumonia

A

caused by chronic inflammatory disease or medication side effects

negative sputum and blood cultures, no response to antibiotics

noninfectious pneumonia characterized by inflammation of bronchioles and surrounding structures

used to be called bronchiolitis obliterans organizing pneumonia

181
Q

natural history of lobar pneumonia

A

congestion –> red hepatization –> gray hepatization –> resolution

182
Q

sites of metastasis for lung cancer:

A

adrenals

brain

bone

liver

183
Q

lung cancer most commonly from

A

breast

colon

prostate

bladder cancer

184
Q

lung cancer complications

A 
superior vena cava/thoracic outlet syndromes
pancoast tumor
horner syndrome
endocrine (paraneoplastic)
recurrent laryngeal nerve compression
Effusions
185
Q

lung cancers most commonly caused by smoking

A

squamous and small cell carcinomas

which are also centrally located

186
Q

small cell carcinoma lung cancer

A

central location

undifferentiated and very aggressive

may produce ACTH(cushing syndrome), SIADH, or antibodies against presynaptic Ca channels (lambert eaton myasthenic syndrome) or neurons (paraneoplastic myelitis, encephalitis, subacute cerebellar degeneration)

amplification of myc oncogenes

187
Q

histology of small cell carcinoma lung cancer

A

neoplasm of neuroendocrine Kulchitsky cells causing small dark blue cells

chromogranin A +, neuron specific enolase +, synaptophysin +

188
Q

non small cell lung cancers

A
  • adenocarcinoma
  • squamous cell carcinoma
  • large cell carcinoma
  • bronchial carcinoid tumor
189
Q

adenocarcinoma of lung

A
  • found in periphery
  • most common primary lung cancer
  • nonsmokers
  • activating mutations: KRAS, EGFR,ALK
  • associated with hypertrophic osteoarthropathy (clubbing)
  • bronchioalveolar subtype
  • glandular pattern on histology which stains mucin +
190
Q

bronchioloalveolar is subtype of

A

adenocarcinoma in situ

CXR shows hazy infiltrates similar to pneumonia

grows along alveolar septa with apparent thickening of alveolar walls. Tall columnar cells containing mucus

191
Q

what two lung cancers have less association with smoking

A

bronchial carcinoid and bronchioloalveolar cell carcinoma

192
Q

squamous cell carcinoma

A

central

hilar mass arising from bronchus

cavitation, cigarettes, hypercalcemia (produces PTHrP)

keratin pearls and intercellular bridges

193
Q

Large cell carcinoma

A

peripheral

highly anaplastic undifferentiated tumor with poor prognosis

strong association with smoking

pleomorphic giant cells

194
Q

Bronchial carcinoid tumour

A

central or peripheral

excellent prognosis, metastasis is rare

symptoms due to mass effect of carcinoid syndrome (flushing, diarrhea, wheezing)

nests of neuroendocrine cells, chromogranin A +

195
Q

Lung abscess on chest xray

A

air fluid levels often see on CXR

presence suggests cavitation due to anaerobes or s aureus

196
Q

what side of the lung do you commonly see a lung acscess that secondary to aspiration

A

right lung

197
Q

This is a carcinoma that occurs in the apex of the lung and may cause destructive lesions of the thoracic inlet and involvement of the brachial plexus and cervical sympathetic nerves (stellate ganglion)

A

pancoast tumor or superior sulcus tumor causing pancoast syndrome by invading cervical sympathetic chain

198
Q

pancoast tumor can compress locoregional structures:

recurrent laryngeal:
stellate ganglion:
superior vena cava:
brachiocephalic vein:
brachial plexus:
A

recurrent laryngeal: hoarseness
stellate ganglion: horner syndrome (ipsilateral ptosis, miosis, anhidrosis)
superior vena cava: SVC syndrome
brachiocephalic vein: brachiocephalic syndrome (unilateral symptoms)
brachial plexus: sensorimotor deficits

199
Q

Superior vena cava syndrome

A

an obstruction of the SVC that impairs blood drainage from the head ( facial plethora)

note blanching after fingertip pressure

JVD

edema in UE

commonly caused by malignancy and thrombosis

can rise ICP if severe and cause headaches, dizziness, increased risk of aneurysm, rupture of intracranial arteries

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