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STEP > Respiratory > Flashcards

Respiratory Flashcards

1
Q

peculiar feature about newborn respiratory physiology

A

obligate nose breathers

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2
Q

RV vs. ERV

A

RV is the volume of air remaining after a maximal expiration. ERV is the volume remaining after normal expiration.

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3
Q

Characteristic of NRDS

A

Atelectasis. This is because without surfactant, the surface tension of the small alveoli collapse into the large aveoli.
- Lack of surfactant also decreases compliance.

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4
Q

When does surfactant appear?

A

Around week 24

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5
Q

Asthma physiology

A

Wheezing + tachypnea. Hypoxemia causes tachypnea, which drives PCO2 down.

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6
Q

What happens to intrapleural pressure with inspiration?

A

Becomes more negative than it is at rest or during expiration.

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7
Q

When airway pressure is equal to atmospheric pressure…

A

This is equilibrium and there is no airflow. ***Volume in the lungs = FRC.

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8
Q

What happens to alveolar PO2 with a PE?

A

Alveolar PO2 is equal to the PO2 in inspired air.

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9
Q

Blood flow in the systemic vs. pulmonary circulations…

A

Blood flow in the systemic and pulmonary circulations is nearly equal. Pulmonary flow is slightly less than the systemic flow because about 2% of systemic CO bypasses the lungs.

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10
Q

Resistance in pulmonary circulation

A

Resistance in the pulmonary circulation is lower than in the systemic circulation.

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11
Q

Compared with the apex of the lung, the base of the lung has…

A

a higher pulmonary capillary **PCO2

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12
Q

Mean arterial PO2 and PCO2 during exercise…

A

There is no change in mean arterial PO2 or PCO2. This is because ventilation rate increases to match the increased O2 consumption and CO2 production.
BUT venous pCO2 increases.

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13
Q

Central chemoreceptor location

A

Medulla. (medullary chemoreceptors).

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14
Q

Peripheral chemoreceptor location

A

Carotid and aortic bodies

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15
Q

If an area of the lung is not ventilated because of bronchial obstruction, the pulmonary capillary blood serving that area will have a PO2 that is…

A

Equal to mixed venous PO2. This is because pulmonary blood will NOT equilibriate with alveolar PO2 but will have a Po2 equal to that of mixed venous blood.

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16
Q

What happens with transporting CO2 from tissues to lungs?

A

CO2 is hydrated to form H+ and HCO3- in RBCs. H+ is buffered inside the RBCs by deoxyhemoglobin, which ACIDIFIES RBCs. HCO3- leaves RBCs in exchange for Cl- and is carried to the lungs in the plasma.

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17
Q

Carbonic anhydrase

A

Sits in RBCs and CO2 + H2O H2CO3.

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18
Q

What buffers H+ in RBCs?

A

Deoxyhemoglobin

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19
Q

hypoxemia

A

Decreased arterial PO2

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20
Q

Causes of hypoxemia

A

1) high altitude
2) hypoventilation
3) right to left cardiac shunt

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21
Q

Which cause of hypoxemia is associated with an increased AA gradient?

A

Right-to-left cardiac shunt. This is because the shunt “dilutes” the PO2 of the normally oxygenated blood thus decreasing the arterial O2.

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22
Q

Causes of hypoxemia with normal A-a gradient?

A

High altitude + hypoventilation

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23
Q

Causes of hypoxemia with increased A-a gradient?

A

1) V/Q mismatch
2) Diffusion limitation (fibrosis)
3) right-to-left shunt

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24
Q

Why is pH of venous blood only slightly more acidic than the pH of arterial blood?

A

H+ generated from CO2 and H2O is buffered by deoxyhemoglobin in venous blood.

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25
Q

Function of J (juxtacapillary) receptors

A

Receptors located in the alveolar walls, close to the capillaries. Engorgement of pulmonarry capillaries such as with left HF stimulates J receptors, which then cause rapid, shallow breathing.

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26
Q

How do you calculate dead space?

A

Tidal volume x ((arterial PCO2-expired PCO2)/arterial PCO2))

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27
Q

Initial development of lungs and when it happens

A

Lung bud buds off from distal end of respiratory diverticulum during week 4

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28
Q

embryonic stage events + timeframe

A

4-7 weeks

lung bud –> trachea –> mainstem bronchi –> secondary (lobar) bronchi –> tertiary (segmental) bronchi

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29
Q

what do errors in embryonic stage lead to?

A

TE fistula

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30
Q

pseudoglandular stage events + timeframe

A

5-16 weeks.

Endodermal tubules –> terminal bronchioles. Surrounded by modest capillary network.

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31
Q

Canalicular stage events + timeframe

A

16-26 weeks.
Terminal bronchioles –> respiratory bronchioles –> alveolar ducts. Surrounded by prominent capillary network.
*increase in airway diameter.

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32
Q

When is respiration possible?

A

Canalicular stage, at 25 weeks

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33
Q

Saccular stage events + timeframe

A

Weeks 26-birth.

Alveolar ducts –> terminal sacs. Terminal sacs separated by primary septa. Pneumocytes develop.

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34
Q

Alveolar stage events + timeframe

A

Weeks 32-8 years.

Terminal sacs–> adult alveoli (due to secondary separation)

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35
Q

of alveoli at birth and at 8 ye

A

At birth: 20-70 million

By 8 years: 300-400 million

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36
Q

How does breathing in utero work?

A

Aspiration and expulsion of amniotic fluid, which leads to increased vascular resistance.

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37
Q

Changes in pulmonary vascular resistance at birth.

A

At birth, fluid gets replaced with air, leading to decreased pulmonary vascular resistance.

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38
Q

Pulmonary hypoplasia

A

Poorly developed bronchial tree with abnormal histology.

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39
Q

Which lung does pulmonary hypoplasia usually involve?

A

Right lung

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40
Q

bronchogenic cysts

A
  • Code: Jeep broncho in living room/bronchogenic cysts. Bronchi hanging overhead + guts hanging on top/caused by abnormal budding of the foregut (lung buds arise from the ventral foregut) and dilation of terminal or large bronchi. Metal railing around broncho + round cysts all over car + air tanks in back spraying air everywhere/discrete + round + sharply defined + air-filled densities on CXR. Chelsea on top with drains in her chest + bugs flying into mouth/Drain poorly and cause chronic infections.
  • Location: Living room
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41
Q

Collapsing pressure equation

A

P = (2(surface tension))/radius

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42
Q

surfactant mechanism

A

decreases alveolar surface tension, preventing alveolar collapse, DECREASING lung recoil and increasing compliance.

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43
Q

Club cell histology

A

Conciliated; low-columnar/cuboidal with secretory granules.

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44
Q

Club cell function

A

1) Secrete component of surfactant.
2) Degrade toxins
3) Act as reserve cells

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45
Q

NRDS presentation on CXR

A

ground glass

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46
Q

L/S ratio predictive of NRDS

A

less than 1.5

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47
Q

Screening tests for fetal lung maturity

A

1) L/S ratio
2) Foam stability index test
3) surfactant-albumin ratio

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48
Q

Sequela of NRDS

A

1) PDA
2) metabolic acidosis
3) necrotizing enterocolitis

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49
Q

NRDS RF’s

A

1) prematurity
2) maternal diabetes (due to increased fetal insulin)
3) C-section delivery

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50
Q

Why is C-section a risk factor for NRDS?

A

Decreased release of fetal glucocorticoids.

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51
Q

NRDS management

A

Maternal steroids before birth; artificial surfactant for infant.

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52
Q

Therapeutic O2 can cause…

A

RIB
Retinopathy of prematurity
Intraventricular hemorrhage
Bronchopulmonary dysplasia

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53
Q

Large airways

A

Nose –> bronchi

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54
Q

Small airways

A

Bronchioles –> terminal bronchioles

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55
Q

Function of conducting zone

A

Warm, humidify and filter airs but no gas exchange (dead space).

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56
Q

Extent of cartilage and goblet cells

A

End of bronchi

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57
Q

Epithelium of bronchus

A

psuedostratified ciliated columnar cells

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58
Q

Extent of psuedostratified ciliated columnar cells

A

Extend to beginning of terminal bronchioles, then transition to cuboidal cells

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59
Q

Extent of airway smooth muscle cells

A

End of terminal bronchioles.

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60
Q

Respiratory zone components

A

Lung parenchyma; respiratory bronchioles + alveolar ducts + alveoli.

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61
Q

Histology of respiratory bronchioles

A

Mostly cuboidal

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62
Q

Histology after respiratory bronchioles up to alveoli

A

simple squamous

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63
Q

When do cilia terminate?

A

Respiratory bronchioles

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64
Q

Relation of pulmonary artery to bronchus at each lung hilum

A

RALS – Right Anterior; Left Superior

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65
Q

Lingula…

A

left lung

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66
Q

If you aspirate a peanut upright where will it end up?

A

Inferior segment of right inferior lobe.

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67
Q

If you aspirate a peanut while supine where will it end up?

A

superior segment of right inferior lobe

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68
Q

central tendon

A

big tendon in the diaphragm

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69
Q

Where does IVC perforate diaphragm?

A

T8

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70
Q

Where does vagus perforate diaphragm?

A

T10

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71
Q

Where does aorta perforate diaphragm?

A

T12

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72
Q

Where does esophagus perforate diaphragm?

A

T10

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73
Q

Where does thoracic duct perforate diaphragm?

A

T12

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74
Q

Where does azygos vein perforate diaphragm?

A

T12

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75
Q

Where does the trachea bifurcate?

A

T4 (bifourcate)

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76
Q

Where does the common carotid bifurcate?

A

C4 (bifourcate)

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77
Q

What innervates the diaphragm?

A

C3,C4,C5 (Phrenic nerve, C3,C4C5 keeps the diaphragm alive). This explains why pain can be referred to shoulder (C5) and trapezius ridge (C3,4)

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78
Q

Typical tidal volume

A

500 mL

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79
Q

What can you not measure by spirometry

A

1) RV
2) FRC
3) *TLC

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80
Q

Dead space equation

A

FA 633

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81
Q

physiologic dead space

A

anatomic dead space + alveolar dead space

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82
Q

Largest contributor to alveolar dead space

A

Apex of lung

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83
Q

anatomic dead space

A

dead space of conducting airways

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84
Q

Pathologic dead space

A

ventilated but not perfused

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85
Q

Minute ventilation equation

A

Vt x RR

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86
Q

alveolar ventilation

A

VA = (Vt-Vd) x RR

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87
Q

Normal dead space volume

A

150 mL/breath

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88
Q

Why is system pressure atmospheric at FRC?

A

Inward pull of lung is balanced by outward pull of chest wall.

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89
Q

When is PVR at minimum?

A

FRC

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90
Q

When is alveolar pressure at FRC?

A

0

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91
Q

compliance expression

A

deltaV/deltaP. Change in lung volume for a change in pressure.

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92
Q

When is compliance increased?

A

1) emphysema
2) normal aging
* surfactant increases compliance.

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93
Q

Hysteresis

A

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

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94
Q

Taut form of hemoglobin

A

Deoxygenated; low affinity for O2, thus promoting release/unloading.

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95
Q

Relaxed form of hemoglobin

A

High affinity for O2 (300x). Hb exhibits positive cooperatively and negative allostery.

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96
Q

Cl affect of hemoglobin

A

Favors taut form over relaxed form.

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97
Q

Fetal Hb structure

A

2alpha and 2gamma

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98
Q

Why does fetal Hb have higher O2 affinity?

A

Decreased affinity of HbF for 2,3BPG

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99
Q

Oxidized Hb

A

decreased O2 affinity but increased cyanide affinity

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100
Q

What do you use to induce methemoglobinemia?

A

Nitrites, followed by thiosulfate.

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101
Q

Other things that can cause methemoglobin

A

benzocaine

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102
Q

carboxyhemoglobin

A

Hb bound to CO

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103
Q

left shift vs. right shift

A

Right shift = decreased affinity

Left shift = increased affinity

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104
Q

CO poisoning management

A

100% O2 + hyperbaric O2

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105
Q

O2 content of blood equation

A

= (1.34 x Hb x SaO2) + (0.003 x PaO2

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106
Q

normal Hb amount in blood

A

15 g/dL

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107
Q

normally 1 g Hb can bind…

A

1.34 mL O2

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108
Q

O2 binding capacity =

A

20.1 mL O2/dL blood

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109
Q

physiologic effects of decreased Hb on

1) arterial O2 content
2) O2 saturation
3) PaO2

A

1) decreased
2) no change
3) no change

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110
Q

Calculating O2 delivery to tissues

A

= CO x O2 content of blood

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111
Q

CO poisoning effect on total O2 content

A

Decreased

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112
Q

Anemia effect on…

1) Hb concentration
2) %O2 sat of Hb
3) dissolved O2 (PaO2)
4) total O2 content

A

1) decreased
2) normal
3) normal
4) decreased

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113
Q

Polycythemia effect on

1) Hb concentration
2) %O2 sat of Hb
3) dissolved O2 (PaO2)
4) total O2 content

A

1) increased
2) normal
3) normal
4) increased

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114
Q

V/Q mismatch

A

Either shunt physiology or dead space.

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115
Q

Examples of low V/Q

A

1) chronic bronchitis
2) asthma
3) hepatopulmonary syndrome
4) acute pulmonary edema

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116
Q

Perfusion limited gases

A

1) O2 (normal health)
2) CO2
3) N2O

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117
Q

Perfusion limited gas characteristics

A

1) Gas equilibrates early along the length of the capillary.

2) Diffusion can only be increased if blood flow increases.

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118
Q

Diffusion limited gases

A

1) O2 (emphysema, fibrosis)

2) CO

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119
Q

Diffusion limited gas graph + characteristic

A

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

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120
Q

Diffusion equation

A

FA 613

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121
Q

What is the underlying diffusion problem with emphysema?

A

Decreased area for diffusion

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122
Q

DLCO

A

Extent to which oxygen passes from air sacs of lungs into blood.

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123
Q

Hypoxia

A

Decreased O2 delivery to tissue

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124
Q

Causes of hypoxia

A

1) decreased CO
2) hypoxemia
3) anemia
4) CO poisoning

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125
Q

Causes of ischemia

A

1) impeded arterial flow

2) decreased venous drainage

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126
Q

V/Q at apex of lung

A

3 (wasted ventilation), both perfusion and ventilation are reduced, but perfusion is reduced to a greater extent

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127
Q

Lung zones

A

Zone 1 is apex, 2 is middle lobe, 3 is base

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128
Q

V/Q at base of lung

A

0.6 (wasted perfusion)

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129
Q

When is ventilation greatest?

A

base of the lung

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130
Q

When is perfusion greatest?

A

base of the lung

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131
Q

Pa,PA,PV in Zone 1

A

PA greater than Pa greater than Pv

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132
Q

Pa,PA,PV in Zone 2

A

Pa greater than PA greater than PV

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133
Q

Pa,PA,PV in Zone 3

A

Pa greater than Pv greater than PA

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134
Q

What happens to V/Q with exercise?

A

With increased CO, apical capillaries vasodilator, V/Q approaches 1.

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135
Q

Relative forms of CO2 transport

A

1) HCO3- (90%)
2) carbaminohemoglobin (HbCO2) (5%)
3) dissolved CO2 (5%)

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136
Q

carbaminohemoglobin

A

CO2 bound to Hb at N-terminus of globin (not heme)

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137
Q

Haldane effect

A

In lungs, oxygenation of Hb promotes dissociation of H+ from Hb. This shifts equilibrium toward CO2 formation; therefore, CO2 is released from RBCs. (shifts equation to the left)

138
Q

Bohr effect

A

In peripheral tissue, increased H+ from tissue metabolism shifts curve to right, unloading O2.

139
Q

Pulmonary vasculature response to high altitude

A

Chronic hypoxic pulmonary vasoconstriction results in pulmonary HTN + RVH.

140
Q

Renal response to high altitude

A

Increased renal excretion of HCO3- to compensate for respiratory alkalosis (this is why acetazolamide is also given for altitude sickness).

141
Q

Rhinosinusitis pathophys

A

Obstruction of sinus drainage into the nasal cavity, leading to inflammation and pain over affected area

142
Q

Sinuses typically affected in rhinosusitis and drainage

A

Maxillary sinuses, which drain into the middle meatus.

143
Q

Common bacterial causes of rhinosinusits

A

S Pneumonia + H influenza + M cattarhalis

144
Q

Most common area for epistaxis

A

Anterior segment of nostril (Kiesselach plexus)

145
Q

Life-threatening hemorrhages location?

A

Posterior segment (sphenopalatine artery)

146
Q

Sphenopalatine branches from…

A

Maxillary artery

147
Q

Field cancerization

A

Carcinogen damages wide mucosal area leading to multiple tumors

148
Q

Virchow triad

A

Stasis + hyper coagulability + endothelial damage

149
Q

Endothelial damage and thrombosis mechanism

A

Exposed collagen triggers clotting cascade

150
Q

D-dimer characteristics as a test

A

High sensitivity, low specificity

151
Q

Homan sign

A

Sign of DVT. Dorsiflexion of foot –> calf pain.

152
Q

Acute management of DVTs

A

unfractionated heparin or low-molecular weight heparins

153
Q

DVT prophylaxis

A

unfractionated heparin or low-molecular weight heparins

154
Q

DVT long-term prevention

A

warfarin + rivaroxaban

155
Q

Imaging test of choice for DVTs

A

compression ultrasound

156
Q

acid-base disturbance with PEs

A

Respiratory alkalosis (tachypnic)

157
Q

What composes lines of Zahn?

A

areas of pink = platelets, fibrin

red = RBCs

158
Q

Fat emboli triad

A

hypoxemia + neurologic abnormalities + petechial rash

159
Q

amniotic fluid emboli association

A

DIC

160
Q

Imaging test of choice for PE

A

CT pulmonary angiography

161
Q

Cardiac sequela of obstructive lung disease

A

Chronic hypoxic pulmonary vasoconstriction can lead to cur pulmonale

162
Q

Reid index

A

Thickness of mucosal gland layer to thickness of war between epithelium and cartilage. (NOT just surface area ratio)

163
Q

Chronic bronchitis diagnosis

A

Productive cough for greater than 3 months (don’t need to consecutive) for over 2 consecutive years.

164
Q

CXR in chronic bronchitis

A

Normal (mucus buildup is etiology)

165
Q

Centriacinar vs. panacinar emphysema location

A

centriacinar usually in upper lobes, panacinar frequently in lower lobes.

166
Q

emphysema pathophys

A

Increased elastase activity leads to loss of elastic fibers leading to increased lung compliance.

167
Q

Breathing pattern in emphysema

A

Exhalation through pursed lips to increase airway pressure and prevent airway collapse.

168
Q

recoil and compliance in emphysema

A

Increased compliance, decreased recoil

169
Q

CXR finding in asthma

A

Peribronchial cuffing

170
Q

Inspiratory/expiratory ratio in asthma

A

Decreased

171
Q

Bronchiectasis pathophys + presentation

A

Chronic necrotizing infection of bronchi leading to permanently dilated airways + purulent sputum + recurrent infections + hemoptysis + digital clubbing

172
Q

FEV1/FVC in restrictive lung disease

A

greater than or equal to 80%

173
Q

ILD characteristics

A

Decreased diffusing capacity + increased A-a gradient

174
Q

Pulmonary langerhans cell histiocytosis (eosinophilic granuloma)

A

…

175
Q

Hypersensitivity pneumonitis hypersensitivity type

A

Mixed type III/IV

176
Q

Hypersensitivity pneumonitis presentation

A

Dyspnea + cough + chest tightness + headache

177
Q

Pneumoconioses cardiac sequela

A

Increased risk of cor pulmonale

178
Q

asbestosis professional RF’s

A

Shipbuilding + roofing + plumbing

179
Q

Pathognomonic finding of asbestosis

A

“Ivory white” calcified, supra diaphragmatic and pleural plaques.

180
Q

asbestosis association

A

Increased risk of pleural effusions

181
Q

Lung region affected in asbestosis

A

Lower lobes

182
Q

Lung region affected in asbestosis in berylliosis

A

Upper lobes

183
Q

Potential treatment for berylliosis

A

Occasionally responsive to steroids (granulomatous)

184
Q

Coal workers’ pneumoconiosis findings

A

inflammation + fibrosis

185
Q

Coal workers’ pneumoconiosis lung region affected

A

Upper lobes

186
Q

Silicosis professional RF’s

A

Foundries + sandblasting + mines

187
Q

Silicosis pathophys

A

Macrophages respond to silica and release fibrogenic factors, leading to fibrosis

188
Q

Silicosis and increased TB risk pathophys

A

Silica disrupts phagolysosomes and impairs macrophages, thus increasing susceptibility to TB.

189
Q

Silicosis lung region affected

A

Upper lobes

190
Q

PaO2/FIO2 in ARDS

A

decreased

191
Q

ARDS and fluid overload

A

no evidence of HF or fluid overload

192
Q

ARDS associations

A

SPARTAS: Sepsis, Pancreatitis, Pneumonia, Aspiration, uRemia, Trauma, Amniotic fluid embolism, Shock

193
Q

ARDS pathophys

A

endothelial damage leads to increased alveolar capillary permeability, leading to protein-rich leakage into alveoli, leading to diffuse alveolar damage and noncardiogenic pulmonary edema.

194
Q

ARDS management

A

Mechanical ventilation with low tidal volumes, address underlying cause.

195
Q

Initial ARDS damage pathophys

A

Release of neutrophilic substances toxic to alveolar wall –> activation of coagulation cascade –> oxygen derived free radicals

196
Q

PaO2 in sleep apnea

A

Decreased at night, normal during day

197
Q

Sleep apnea definition

A

Repeated cessation of breathing greater than 10 seconds during sleep.

198
Q

Sudden death in sleep apnea pathophys

A

Nocturnal hypoxia –> systemic/pulmonary HTN –> arrhythmias (atrial fibrillation/fluter)

199
Q

OSA etiology in adults and kids

A

Adults –> excess paraparyngeal tissue.

Kids –> adenotonsillar hypertrophy

200
Q

Central sleep apnea

A

No respiratory effort due to CNS injury/toxicity, HF, opioids

201
Q

Obesity hypoventilation syndrome labs

A

Decreased PaO2 and increased PaCO2 during sleep; increased PaCO2 during waking hours (retention).

202
Q

Normal mean pulmonary artery pressure

A

10-14 mm Hg

203
Q

Pulmonary HTN defined as..

A

greater than 35 mm Hg at rest

204
Q

Arterial sequela of pulmonary HTN

A

Pulmonary arteries..

1) Arteriosclerosis
2) medial hypertrophy
3) intimal fibrosis

205
Q

Heritable PAH genetics

A

Inactivating mutation in BMPR2 gene

206
Q

BMPR2 gene function

A

normally inhibits vascular smooth muscle proliferation

207
Q

Other causes of PAH

A

1) Amphetamines + cocaine
2) connective tissue disease
3) HIV infection
4) portal HTN
5) congenital heart disease
6) schistosomiasis

208
Q

ID associated with PAH…

A

schistosomiasis

209
Q

Microthrombi and pulmonary HTN mechanism

A

recurrent micro thrombi lead to decreased cross-sectional area of pulmonary vascular bed

210
Q

fremitus

A

Vibratory sensation transmitted through the lungs.

211
Q

Fremitus

1) Increased pathophys
2) decreased pathophys

A

1) Denser or inflamed lung tissue, eg pneumonia

2) air or fluid in pleural spaces, eg COPD or asthma

212
Q

tracheal deviation with atelectasis (bronchial obstruction)

A

Toward side of lesion

213
Q

Simple pneumo

1) breath sounds
2) percussion
3) fremitus

A

1) decreased
2) hyperresonant
3) decreased

214
Q

tracheal deviation in simple pneumo

A

None

215
Q

tracheal deviation in tension pneumo

A

Away from side of lesion

216
Q

Simple pneumo

1) breath sounds
2) percussion
3) fremitus

A

1) decreased
2) hyper resonant
3) decreased

217
Q

Consolidation (lobar pneumonia, pulmonary edema)

1) breath sounds
2) percussion
3) fremitus

A

1) bronchial breath sounds; late inspiratory crackles
2) dull
3) ***increased

218
Q

typical organisms in lobar pneumonia

A

1) s pneumo most frequently
2) legionella
3) klebsiella

219
Q

Lobar pneumonia characteristics

A

Intra-alveolar exudate leading to consolidation; may involve entire lobe or lung.

220
Q

typical organisms in bronchopneumonia

A

1) s pneumo
2) s aureus
3) H flu
4) klebsiella

221
Q

bronchopneumonia characteristics

A

1) Acute inflammatory infiltrates from bronchioles into adjacent alveoli
2) patchy distribution involving more than 1 lobe

222
Q

typical organisms in interstitial (atypical) pneumonia

A

1) mycoplasma
2) chlamydia
3) legionella
4) RSV
5) CMV
6) influenza
7) adenovirus

223
Q

interstitial (atypical) pneumonia characteristics

A

Diffuse patchy inflammation localized to interstitial areas at alveolar walls; diffuse distribution involving one or more than one lobe.

224
Q

lung abscess etiology

A

1) aspiration

2) bronchial obstruction (eg cancer)

225
Q

lung abscess treatment

A

Clindamycin

226
Q

Location of aspiration when upright

A

Basal segments of right lower lobe

227
Q

Location of aspiration when supine

A

Posterior segments of right upper lobe or superior segment of right lower lobe

228
Q

Sequela of mesothelioma

A

1) hemorrhagic pleural effusion (exudative)

2) pleural thickening

229
Q

caveat about mesothelioma

A

Smoking is not a risk factor

230
Q

mesothelioma markers

A

Cytokeratin + calretinin positive

231
Q

area affected in Horner syndrome

A

Superior cervical ganglion

232
Q

pan coast tumor associations

A

1) hoarseness
2) horner’s
3) SVC syndrome
4) sensorimotor deficit

233
Q

Physical exam findings in SVC syndrome

A

1) facial plethora
2) blanching after fingertip pressure
3) JVD
4) upper extremity edema

234
Q

SVC syndrome etiology

A

1) Pancoast tumor

2) thrombosis from indwelling catheter

235
Q

SVC syndrome sequela pathophys

A

Raised ICP –> headaches, dizziness + increased risk of aneurysm/rupture of intracranial arteries.

236
Q

Coin lesion on CXR…

A

lung cancer

237
Q

non calcified nodule on CXR…

A

lung cancer

238
Q

lung cancer mets

A

adrenals + brain + bone + liver

239
Q

most common mets to lung

A

Breast, colon, prostate, bladder

240
Q

lung cancer caveat

A

mets more common than primary neoplasms

241
Q

small cell management

A

chemo +/- radiation

242
Q

small cell origin

A

neoplasm of neuroendocrine Kulchitsky cells

243
Q

adenocarcinoma genetics

A

Activating mutations in KRAS + EGFR + ALK.

244
Q

adenocarcinoma association

A

Hypertrophic osteoarthropathy

245
Q

CXR of adenocarcinoma in situ

A

hazy infiltrates similar to pneumonia.

246
Q

adenocarcinoma in situ also known as…

A

bronchioloalveolar subtype

247
Q

SCC location

A

hilar mass arising from bronchus

248
Q

large cell carcinoma management

A

Less responsive to chemo; surgery.

249
Q

large cell carcinoma marker

A

Can secrete beta-hCG

250
Q

bronchial carcinoid tumor prognosis

A

Excellent; mets rare

251
Q

bronchial carcinoid presentation

A

Symptoms due to mass effect or carcinoid syndrome (flushing, diarrhea, wheezing).

252
Q

bronchial histology

A

Nests of neuroendocrine cells + chromogranin A positive.

253
Q

First generation antihistamines

A

1) Diphenhydramine
2) dimenhydrinate
3) chlorpheniramine

254
Q

Second generation antihistamines

A

1) Loratadine
2) fexofenadine
3) desloratadine
4) cetirizine

255
Q

Guaifenesin caveat

A

just thins respiratory secretions; doesn’t suppress cough reflex.

256
Q

N-acetylcysteine MOA

A

disrupts disulfide bonds

257
Q

N-acetylcysteine use

A

Liquefying mucus in COPD

258
Q

Dextromethorphan mechanism

A

1) antagonizes NMDA glutamate receptors

2) synthetic codeine analog

259
Q

abuse potential of dextromethorphan?

A

Mild

260
Q

pseudoephedrine mechanism

A

alpha-adrenergic agonist

261
Q

pseudoephedrine SE’s

A

HTN + CNS stimulation/anxiety

262
Q

Pulmonary HTN drugs

A

1) bosentan
2) sildenafil
3) epoprostenol, iloprost

263
Q

Bosnian mechanism

A

Competitively antagonizes endothelin-e receptors

264
Q

How can sildenafil be used for pulmonary HTN?

A

By inhibiting cGMP, prolongs vasodilatory effect of NO.

265
Q

epoprostenol, iloprost SE’s

A

flushing + jaw pain

266
Q

epoprostenol, iloprost MOA

A

PGI2 (prostacyclin)

267
Q

formoterol

A

like salmeterol

268
Q

salmeterol, formoterol AE’s

A

tremor + arrhythmia

269
Q

1st line for chronic asthma

A

fluticasone, budesonide (inhaled corticosteroids0

270
Q

fluticasone, budesonide MOA

A

1) inhibit synthesis of virtually all cytokines

2) inactivate NF-kappaB

271
Q

NF-kappaB

A

TF that induces production of TNF-alpha and other proinflammatory agents

272
Q

tiotropium vs. ipratropium

A

tiotropium is long acting

273
Q

methacoline receptor

A

M3 agonist

274
Q

best treatment for aspirin-induced asthma

A

Montelukast, zafirlukast

275
Q

Montelukast, zafirlukast mechanism

A

block leukotriene receptors (CysLT1)

276
Q

Zileuton SE

A

hepatotoxic

277
Q

Zileuton MOA

A

5-lipoxygenase inhibitor

278
Q

Omalizumab clinical use

A

allergic asthma with increased IgE levels resistant to inhaled steroids and LABAs

279
Q

theophylline MOA

A

bronchodilator via phosphodiesterase inhibition, leading to increased cAMP levels due to decreased cAMP hydrolysis

280
Q

theophylline caveats

A

1) limited usage due to narrow therapeutic index (cardiotoxic + neurotoxic)
2) adenosine

281
Q

Phosphodiesterase (PDE)

A

cAMP –> AMP

282
Q

cAMP respiratory mechanism

A

bronchodilator

283
Q

molecules that cause bronchoconstriction

A

1) ACh

2) adenosine

284
Q

Phospholipase A2 in arachidonic acid pathway

A

Converts membrane phospholipids to arachidonic acids

285
Q

What activates COX-2?

A

NF-kB

286
Q

5-lipoxygenase

A

Arachidonic acid –> 5-HPETE (eicosanoid)

287
Q

COX-1 action in arachidonic acid pathway

A

arachidonic acid –> cyclic endoperoxides

288
Q

arachidonic acid pathway

A

1) membrane phospholipids –> arachidonic acid –> 5-HPETE –> Leukotrienes
2) membrane phospholipids –> arachidonic acid –> cyclic endoperoxides –> prostacyclin + PGs + thromboxane

289
Q

Leukotrienes that increase bronchial tone

A

1) LTC4
2) LTD4
3) LTE4

290
Q

Dinoprostone

A

PGE2

291
Q

Alprostadil

A

PGE1

292
Q

Carboprost

A

PGF2alpha

293
Q

thromboxane actions

A

1) increase platelet aggregation

2) increase vascular tone

294
Q

PGE1 actions

A

Decreases vascular tone

295
Q

PGE2 actions

A

Increases uterine tone

296
Q

PGF2alpha actions

A

Increases uterine tone

297
Q

Prostacyclin (PGI2) action

A

1) decreases platelet aggregation

2) decreases vascular tone

298
Q

Pulmonary hypertension characteristic finding

A

Coronary sinus dilation is a characteristic finding (coronary sinus contains venous blood and communicates freely with the RA and therefore may become dilated secondary to any factor that causes right atrial dilatation).

299
Q

Causes of transudate

A

1) increased hydrostatic pressure

2) decreased oncotic pressure

300
Q

examples of transudate

A

1) nephrotic syndrome

2) cirrhosis

301
Q

Conditions that cause exudate

A

1) malignancy
2) pneumonia
3) collagen vascular disease
4) trauma
* states of increased vascular permeability.

302
Q

chylothorax

A

AKA lymphatic effusion

303
Q

Cause of lymphatic effusion

A

thoracic duct injury from trauma or malignancy

304
Q

lymphatic effusion presentation

A

1) Milky-appearing fluid

2) increased TGs

305
Q

Pneumothorax

1) breath sounds
2) percussion
3) fremitus

A

1) diminished
2) hyperresonant
3) decreased

306
Q

Cause of secondary spontaneous pneumo

A

1) Diseased lung (eg bullae in emphysema, infections).

2) mechanical ventilation with use of high pressures leading to barotrauma.

307
Q

Tension pneumothorax

A

Can be any of other types. Air enters pleural space but cannot exit. Increased trapped air leads to tension pneumothorax.

308
Q

tension pneumo management

A

Immediate needle decompression + chest tube placement.

309
Q

tracheal deviation in tension pneumo

A

Trachea deviates away from affected lung.

310
Q

Phases of lobar pneumonia

A

 Hippo with cold in lawn chair/congestion. Red lungs + covered in blood vessels + francis’s climbing all over it/1) congestion (first 24 hrs): red, heavy and boggy lobe + vascular dilation + alveolar exudate contains mostly bacteria.
 red hippo in lawn chair/red hepatization. Red lungs + newts crawling around everywhere + big RBCs on the ground + lawn chair covered in fibrin/2) red hepatization (2-3 days): red, firm lobe (liver-like consistency + alveolar exudate contains erythrocytes + neutrophils + fibrin.
 Grey hippo in lawn chair/grey hepatization. Grey lobe + disintegrating RBCs on ground + lawn chair covered in fibrin + newts crawling around/3) grey hepatization (4-6 days): gray-brown firm lobe + RBCs disintegrate + alveolar exudate contains neutrophils and fibrin.
 Hippo dancing around/4) resolution: restoration of normal architecture + enzymatic digestion of the exudate.

311
Q

methemoglobinemia presentation

A

dizziness + dyspnea + confusion + seizures + coma

312
Q

Complication of nitric oxide administered for pulmonary HTN disease of newborn

A

methemoglobinemia

313
Q

Systemic mastocytosis

A

o Code: Scott Massed: huge cat spewing acid from its mouth behind him/mast cell proliferation in the bone marrow and in other organs, resulting in increased histamine secretion gastric acid hypersecretion. Scott looking like below + flushed face + itching himself intensely + booting everywhere/presentation = pruritis + rash + flushing + GI symptoms (abdominal cramps, nausea, vomiting). Huge nests at top of all the sail boat masts + intestines in the nests/small bowel biopsy = nests of mast cells within the mucosa.
o Location: Boat yard, end of dock near exit from Royal River

314
Q

Worsening SOB + malaise + continued respiratory symptoms in a patient with pneumonia

A

pulmonary effusion

315
Q

CXR of pulmonary effusion

A

blunting of costophrenic angle + air fluid level.

316
Q

Physical exam findings of pleural effusion

A

pleural friction rub on auscultation.

317
Q

Characteristic finding in severe PAH

A

Lesions can progress to form plexiform lesions (interlacing tufts os mall vascular channels)

318
Q

presentation of IPF

A

insidious onset of dyspnea on exertion + dry cough present for more than 3 months + bibasilar rales clubbing + diffuse reticular opacities.

319
Q

inflammatory mediators of chronic bronchitis

A

monocytes + CD8+ T cells + neutrophil infiltration

320
Q

cough productive of yellow sputum…

A

chronic bronchitis

321
Q

common pathogen in smokers with chronic bronchitis

A

H flu

322
Q

sputum findings in bronchial asthma

A

Luke in corner and it’s hailing on him + eoss goddesses wrapped around all the hanging spiral/sputum findings = **eosinophils, which are recruited and activated by IL-5 secreted by TH2 type helper T-cells.

323
Q

bronchiectasis association

A

hypertrophic osteoarthropathy (HOA)

324
Q

leukocoria

A

White reflex

325
Q

leukocoria associations

A

1) retinoblastoma

2) congenital cataracts

326
Q

ARDS on CXR

A

bilateral radiographic opacities

327
Q

Brain abscess RF’s

A

endocarditis + bronchiectasis + IV drug use

328
Q

lung abscess presentato

A

indolent + fever + night sweats + weight loss + cough productive of foul-smelling sputum (indicative of anaerobes).

329
Q

How do enteric bacteria (e coli + klebsiella + enterococci) cause hepatic abscesses?

A

Ascend biliary tract

330
Q

other route of infection to hepatic abscess

A

portal vein pyemia

331
Q

How does staph aureus cause hepatic abscesses?

A

Francis with a blow dart gun shooting seeds at liver/another route of infection = hematogenous seeding of the liver with staph aureus.

332
Q

pneumoconiosis associated with insulation…

A

asbestosis/mesothelioma

333
Q

Mesothelioma histology

A

tumor cells with long, slender microvilli + abundant tonofilaments

334
Q

typical pneumonia

A

♣ Code: Margaret Lawrence: she’s sweating profusely + coughing up sputum all over her chest/presentation = high fever + lobar consolidation + productive sputum. Newts crawling around floor everywhere/these symptoms result from the primary responding immune cell, the neutrophil, which enters area, releases pyrogenic products (fever), causes innocent bystander damage to lung, and creates abscesses (lobar consolidation). /usually EXTRACELLULAR organisms, gram-negatives (1) s. pneumo + 2) H. influ + 3) M. cattarhalis + 4) S. aureus). /lobar infiltrate. Steph in a track suit flashing her tits + prostitutes sitting at table/treatment = empirical ceftriaxone + azithromycine.
♣ Location: Conference room in library first floor

335
Q

typical pneumonia treatment

A

ceftriaxone + azithromycine

336
Q

neonatal atypical pneumonia presentation

A

crackles + wheeze

337
Q

cold agglutinins

A

antibodies (usually IgM) produced in response to certain kinds of infection such as m. pneumoniae.

338
Q

Relation between lung volume and pulmonary vascular resistance

A

o Code: huge massive U/graph is U shaped. /This is because high lung volumes (eg following inspiration) increase PVR due to the longitudinal stretching of alveolar capillaries by the expanding alveoli. Decreased lung volumes also increase PVR due to decreased radial traction from adjacent tissues on the large extra-alveolar vessels. /thus, PVR is lowest at the FRC.
o Location: Above DIA

339
Q

What can you use to measure FRC and RV?

A

helium dilution technique

340
Q

Lamellar body or granule

A

Phospholipids are stored in lamellar bodies and serve as pulmonary surfactant.

STEP (85 decks)

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