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Pao's Pulmonary > All of it! > Flashcards

All of it! Flashcards

1
Q

In what stage of development is surfactant made?

A

Cannalicular

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2
Q

In what stage of development are terminal bronchioles formed?

A

Pseudoglandular

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3
Q

What cell type makes surfactant?

A

Type II pneumocyte

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4
Q

Where are mesothelial cells?

A

Lining inside of parietal and visceral pleuras

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5
Q

In what layer of the bronchial wall are leukocytes?

A

Lamina Propria

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6
Q

In what layer of the bronchial wall are MALTs (mucosal-associated lymph tissue)?

A

Submucosa

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7
Q

How many cell membranes must an oxygen molecule pass through to reach Hemoglobin?

A

5 (two membranes of Type I pneumocyte, two membranes of capillary, one membrane of RBC)

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8
Q

How often is a Type I pneumocyte replaced?

A

~20 days

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9
Q

What is the main component of surfactant?

A

Phospholipid

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10
Q

What is the usual range of intrapleural pressure?

A

-5 - -30 cm H2O (1cm H2O is about 1 Torr)

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11
Q

What is the formula for compliance?

A

∆V/∆P

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12
Q

Where is intrapleural pressure larger (more negative): apex or base of lung?

A

Apex

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13
Q

Where are bronchioles and alveoli larger: apex or base of lung?

A

Apex

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14
Q

Is the apex or base more well-ventilated?

A

Base (more change in volume of alveoli)

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15
Q

What is a normal tidal volume?

A

~400mL per breath

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16
Q

What is a normal FEV1/FVC?

A

80%

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17
Q

Define hypoxemia

A

Low O2 in blood

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18
Q

Define hypoxia

A

Low O2 at tissue level

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19
Q

Does a right or left shift of the oxyhemoglobin dissociation curve represent an increase in off-loading?

A

Right shift

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20
Q

A decrease in pH shifts the curve in what direction?

A

To the right, more dissociation of oxygen

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21
Q

What is normal arterial free oxygen concentration?

A

70-90 Torr

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22
Q

What is the barometric pressure at sea level?

A

760 mmHg

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23
Q

What is the barometric pressure in Denver?

A

630 mmHg

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24
Q

What is the normal concentration of bicarb?

A

24 mM

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25
Q

What is the normal concentration of CO2 in the blood?

A

40

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26
Q

What are causes of Anion Gap Metabolic Acidosis?

A

MUDPILES

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27
Q

What is a normal Anion Gap value?

A

12 +/- 2

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28
Q

What is Winter’s formula used for?

A

To find the expected PCO2

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29
Q

What is Winter’s formula?

A

expected PCO2 = 1.5(HCO3) + 8 +/- 2

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30
Q

What is the relationship between the increase in CO2 and the decrease in pH in an acute setting?

A

For every 10 Torr increase in CO2, pH decreases by 0.08

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31
Q

What is the relationship between an increase in CO2 and an increase in bicarb?

A

For every 1 Torr increase in CO2, bicarb increases by 0.4 meq/L

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32
Q

Where in the brain is the respiratory center?

A

Medulla

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33
Q

What is the sole detector of arterial pH in the body that can mediate ventilatory changes?

A

Peripheral carotid chemoreceptors

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34
Q

What chemoreceptor is important in the rapid response of elevated CO2 (only 20% of the response)?

A

Carotid & aortic peripheral chemoreceptors

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35
Q

Is low O2 or high CO2 the main driver of peripheral chemoreceptors?

A

Hypoxemia

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36
Q

Do central chemoreceptors respond to O2 or CO2?

A

CO2 (C for central)

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37
Q

Are there any central chemoreceptors for O2?

A

No

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38
Q

How do the central chemoreceptors respond to CO2?

A

CO2 crosses blood-brain barrier, interacts with H2O to create protons and bicarb. Central chemoreceptors bind protons and send signals to increase ventilation. Strong response, takes minutes. This is an important day-to-day regulator.

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39
Q

What vessels are most often the source of hemoptysis?

A

Bronchial circulation

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40
Q

What is the source of the bronchial circulation?

A

Aorta

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41
Q

What is the equation to calculate Pulmonary Vascular Resistance (PVR)?

A

PVR = (PAP-LAP)/CO

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42
Q

What is a normal PVR?

A
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43
Q

What are the four criteria for ARDS?

A
  1. Bilateral alveolar radiographic infiltrates
  2. PaO2/FiO2
  3. Not fully explained by cardiac failure or fluid overload
  4. Occurs within 1 week of a known clinical insult or of worsening respiratory symptoms
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44
Q

What is the definition (cutoff) for pulmonary hypertension?

A

MAP pulm > 25 mmHg (normal is 15-18 mmHg)

45
Q

What is the criteria for Pre-capillary pulmonary hypertension (PAH)?

A

Mean PAP > 25 mmHg, PCWP/LVEDP 3 Wood Units

46
Q

What is the criteria for Post-capillary pulmonary hypertension (PVH)?

A

Mean PAP > 25 mmHg, PCWP/LVEDP > 15 mmHg

47
Q

What are the five WHO classifications of pulmonary hypertension?

A
  1. PAH
  2. PH due to L heart disease
  3. PH due to lung diseases and/or hypoxia
  4. Thromboembolic PH
  5. PH with unclear/multifactorial mechanisms
48
Q

What is the prognosis of Idiopathic PAH?

A

Rare and fatal!! Median survival is 2.8 years without treatment, affects mostly young women

49
Q

Idiopathic PAH is mostly idiopathic but can also be due to a mutation in what?

A

Bon Morphogenic Protein Receptor Type 2 (BMPR2)

50
Q

What is the overall therapeutic treatment of PAH?

A

Pulmonary vasodilators

51
Q

What are the three pathways that can be exploited in vasodilation in PAH?

A

Endothelin pathway, NO pathway, and prostacyclin pathway

52
Q

What does increased fremitus usually indicate?

A

Pneumonia (vibrations travel well through fluid)

53
Q

Is the trachea pulled away from or towards a large pleural effusion?

A

Away from

54
Q

What does egophany usually indicate?

A

Pneumonia

55
Q

What does a pleural rub usually indicate?

A

Inflammation of the pleura

56
Q

What are the 5 causes of hypoxemia?

A
  1. Altitude
  2. Hypoventilation
  3. V/Q Mismatch
  4. Shunt
  5. Diffusion problem
57
Q

For every 1 L of supplemental O2, Fi02 increases by what?

A

3%

58
Q

What is a normal A-a gradient?

A

5-10

59
Q

NSCLC, specifically adenocarcinoma, has what kind of appearance on CXR?

A

Ground glass

60
Q

Squamous cell carcinoma is of what origin?

A

Epithelium

61
Q

SCLC is of what tissue origin?

A

Bronchial origin

62
Q

What is the most common cause of metabolic acidosis?

A

DKA

63
Q

A decreased FEV1/FVC ratio indicates what disease process?

A

Obstructive

64
Q

If there is an extra-thoracic obstruction, will there will be a change in the Flow-Volume loop on expiration or inspiration?

A

Inspiration

65
Q

If there is an intra-thoracic obstruction, will there will be a change in the Flow-Volume loop on expiration or inspiration?

A

Expiration

66
Q

If there is a fixed obstruction, will there will be a change in the Flow-Volume loop on expiration or inspiration?

A

Both! Won’t change based on expiration or inspiration.

67
Q

What are some things that can increase diffusing capacity of CO?

A

Polycythemia, early CHF, asthma, alveolar hemorrhage

68
Q

What are some things that can decrease diffusing capacity of CO?

A

Emphysema, pulmonary vascular disease, ILD, anemia

69
Q

In areas of the lung with high V/Q, how does the lung compensate?

A

Alveolar PCO2 drops, leading to an increase in local airway resistance and decreasing ventilation –> V/Q lowers

70
Q

In areas of the lung with low V/Q, how does the lung compensate?

A

Alveolar PO2 drops, leading to hypoxic vasoconstriction and decreasing local perfusion –> V/Q increases

71
Q

What is the extreme of low V/Q called?

A

Shunt

72
Q

What is the extreme of high V/Q called?

A

Dead space

73
Q

Is pneumonia an example of shunt or dead space?

A

Shunt

74
Q

Is emphysema an example of shunt or dead space?

A

Dead Space

75
Q

How can we distinguish shunts from V/Q mismatch?

A

Monitor PaO2 on 100% oxygen. In cases of shunt, PaO2 will not substantially increase

76
Q

What is the action of a beta-2 adrenergic receptor agonist on bronchial smooth muscle?

A

Bronchodilation

77
Q

What is the action of a muscarinic receptor agonist on bronchial smooth muscle?

A

Bronchoconstriction

78
Q

What is the action of a Leukotriene receptor agonist on bronchial smooth muscle?

A

Bronchoconstriction

79
Q

What is the action of a Histamine H1 receptor agonist on bronchial smooth muscle?

A

Bronchoconstriction

80
Q

What is the action of a Muscarinic receptor agonist on secretory cells?

A

Increased secretion

81
Q

What is the action of a Muscarinic receptor agonist on blood vessels?

A

Vasoconstriction

82
Q

What is the action of an alpha-1 adrenergic receptor agonist on blood vessels?

A

Vasoconstriction

83
Q

What is the action of a Histamine H1 receptor agonist on blood vessels?

A

Vasodilation

84
Q

What is the action of a Bradykinin receptor agonist on sensory pain afferents?

A

Increase pain

85
Q

What is the action of a Mu opioid receptor agonist on the cough center in the medulla?

A

Suppress cough reflex

86
Q

What is the action of a Bradykinin receptor agonist on blood vessels?

A

Vasodilation

87
Q

What is the action of a Histamine H1 receptor agonist on sensory pain afferents?

A

Increase pain

88
Q

Is edema associated with a runny or stuffy nose?

A

Runny

89
Q

Is vasodilation associated with a runny or stuff nose?

A

Stuffy

90
Q

What are some advantages and disadvantages of first-generation antihistamines?

A

Additional blocking actions at non-H1 receptors. Penetrate more readily into CNS. Sedation. Prevent nausea and vomiting.

91
Q

What are some advantages and disadvantages of second-generation antihistamines?

A

Longer actions with metabolic and/or renal elimination. Much lower sedation. Do NOT prevent nausea and vomiting.

92
Q

All drugs ending in “-amine” are what?

A

First-generation antihistamine drugs

93
Q

What do second-generation antihistamines end in? (3)

A

-izine, -inate, -adine

94
Q

How do antihistamines block the H1 R?

A

Reversible & competitive

95
Q

What four receptors do antihistamines block?

A

Adrenergic Rs, H1 Rs, Muscarinic Rs, and Na channel block

96
Q

What are the three names of the decongestant drugs?

A

Pseudoephedrine (Sudafed), phenylephrine, oxymetolazine

97
Q

How do decongestant drugs works?

A

Sympathomimetic with vasoconstrictor action (stimulate alpha-1 receptors of vascular smooth muscle)

98
Q

What is a side effect of topical decongestants?

A

Rebound congestion

99
Q

What is the mainstream antitussive?

A

Codeine/Dextromethorphan

100
Q

With is the MOA of Codeine/Dextromethorphan?

A

Both central and peripheral actions. Agonists at endogenous opioid Rs that act to suppress cough center in brain stem.

101
Q

What is the name of the Expectorant drug?

A

Guaifenesin

102
Q

What is the MOA of guaifenesin?

A

Uncertain, possibly decreases viscosity of mucus

103
Q

What is the brand name of Guaifenesin?

A

Mucinex

104
Q

What is the name of the mucolytic drug?

A

N-Acetylcysteine (Mucomyst)

105
Q

What is the MOA of N-Acetylcysteine?

A

Splits disulfide linkages between mucoproteins resulting in decreased viscosity of pulmonary mucus secretions. Also possesses antioxidant properties.

106
Q

What is the route of administration of N-Acetylcysteine?

A

Inhalation

107
Q

What are the most common diseases that lead to ARDS?

A

Pancreatitis, sepsis, trauma, transfusion, and aspiration

108
Q

What is the treatment of ARDS?

A

Treat underlying condition. Also prone positioning and LOW tidal volume ventilation.

Pao's Pulmonary (1 decks)

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