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First Aid Respy > FA Respy I > Flashcards

FA Respy I Flashcards

1
Q

What structures make up the conducting zone?

A

Anatomic Dead Space that consists of Nose, pharynx, trachea, bronchi, bronchioles, and terminal bronchioles
Brings air in and out,

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2
Q

What structures make up the conducting zone?

A

Brings air in and out. Humidifies, warms, and filters air.

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3
Q

What structures make up the conducting zone?

A

Smooth Muscle

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4
Q

What structures make up the conducting zone?

A

Respiratory bronchioles, alveoli and alveolar ducts.

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5
Q

What structures make up the conducting zone?

A

Participates in gas exchange.

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6
Q

What structures make up the conducting zone?

A

Fetal Lung Maturity

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7
Q

What structures make up the conducting zone?

A

Squamous cell Pneumocytes that line 97% of alveoli.

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8
Q

What structures make up the conducting zone?

A

Allow gas diffusion to occur.

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9
Q

What structures make up the conducting zone?

A

Clustered, Cuboidal cells (3% of alveolar surfaces) that secrete pulmonary surfactant (dipalmitoyl phosphatidylcholine), which decreases alveolar surface tension.

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10
Q

What structures make up the conducting zone?

A

Type I cells and other Type II cells.

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11
Q

What structures make up the conducting zone?

A

Lung Damage?

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12
Q

What structures make up the conducting zone?

A

Nonciliated, columnar cells with secretory granules. Secrete component of surfactant, degrade toxins, act as reserve cells.

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13
Q

What structures make up the conducting zone?

A

Respiratory bronchioles

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14
Q

What structures make up the conducting zone?

A

Bronchi

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15
Q

What structures make up the conducting zone?

A

Clear Debris

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16
Q

What structures make up the conducting zone?

A

They are swept toward the mouth by ciliated cells.

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17
Q

What does each bronchopulmonary segment contain?

A

A Tertiary segmental bronchus and 2 arteries (bronchial and pulmonary in the center). Veins and lymphatics drain along the borders

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18
Q

What does the pulmonary artery contain?

A

Deoxygenated blood from the right side of the heart.

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19
Q

What do elastic walls do?

A

Maintain pulmonary arterual pressure at relatively constant levels throughout the cardiac cycle.

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20
Q

How many lobes does the right lung contain?

A

3 lobes

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21
Q

How many lobes does the left lung contain?

A

2 Lobes and a lingula (homologue of right middle lobe

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22
Q

What site is most common for inhaled foreign bodies?

A

Right side since it is more vertical and wider than the left.

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23
Q

If you aspirate a peanut while upright, where does it end up?

A

Lower portion of right inferior lobe

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24
Q

If you aspirate a peanut wile supine, where does it end up?

A

Superior portion of right inferior lobe

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25
Q

What is the relation of the pulmonary artery to the bronchus at each lung hilus?

A

RALS
Right- Anterior
Left- Superior

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26
Q

How many lobes do you see on the anterior view of the right and left lung?

A

3

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27
Q

How many lobes do you see on the posterior view of the right and left lung

A

2 (Superior and Inferior) for each side.

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28
Q

What structures perforate the diaphragm and at what level?

A

Inferior Vena Cava perforates at T8
Esophagus perforates at T10
Aorta, thoracic duct, and azygos vein perforates at T12

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29
Q

What is the diaphragm innervated by?

A

Phrenic Nerve- C3, C4, C5

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30
Q

What are the muscles of respiration used for quiet breathing?

A

Inspiration is the diaphgram. Expiration is passive

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31
Q

What are the muscles of respiration used during exercise?

A

Inspiration- external intercostals, scalene muscles, and sternocleidomastoids
Expiration- Rectus abdominus, internal and external obliques, transversus abdominus, and internal intercostals

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32
Q

What are some important lung products?

A

Surfactant, Prostaglandins, Histamine, Angiotensin-Converint Enzyme, Kallikrein

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33
Q

What does Surfactant due?

A

Produced by Type II cells

Decrease alveolar surface tension, increase comliance, and decrease work on inspiration.

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34
Q

What does histamine do?

A

Increases bronchoconstriction

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35
Q

What does Angiotensin-Converting Enzyme do?

A

Converts Angiotensin I to Angiotensin II, inactivates bradykinin

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36
Q

How do ACE inhibitors affect bradykinin levels?

A

They increase it which can cause cough and angioedema.

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37
Q

What does Kallikrein do?

A

Activates bradykinin.

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38
Q

What is collapsing pressure

A

2X Surface Tension/ (Radius)

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39
Q

What can cause tendency to collapse on expiration?

A

Radius decreasing

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40
Q

What is deficient in neonatal RDS

A

The surfactant dipalmitoyl phosphatidylcholine (lecithin)

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41
Q

What is residual volume?

A

Air in lungs after maximal expiration. Cannot be measured on spirometry

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42
Q

What is expiratory reserve volume?

A

Air that can still be breathed out after normal expiration.

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43
Q

Tidal Volume

A

Air that moves in and out of lungs with each quiet inspiration, typically 500 ml

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44
Q

Inspiratory Reserve Volume

A

Air in excess of tidal volume that moves into lungs on maximum inspiration

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45
Q

What is capacity?

A

Sum of two volumes

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46
Q

What is vital capacity?

A

VC= TV+IRV+ERV, everything but the residual volume

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47
Q

What is functional residual capacity?

A

FRC= RV+ERV (volume in normal lungs after expiration)

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48
Q

What is inspiratory capacity?

A

Inspiratory Reserve volume+ Tidal Volume, = IRV+ TV

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49
Q

What is total lung cacapcity?

A

IRV+TV+ERV+RV

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50
Q

What is Vd? What is a large contributor of Vd?

A

Volume of inspired air that does not take part in gas exchange. Physiologic space consisting of Anatomic dead space of conducting airway plus functional dead space in alveoli. Apex of healthy lung is largest contributor of functional dead space.

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51
Q

How is Vd calculated?

A

Vd= Vt x (PaCo2-PeCo2)/(PaCo2)

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52
Q

How many polypeptide subunits does hemoglobin contain?

A

Composed of 4 subunits (2 a and 2 B)

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53
Q

How many forms does hemoglobin exist in? Which one has a higher affinity for O2.

A

Two: One relaxed and one taut. Relaxed form (R) has higher affinity.

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54
Q

How many polypeptide subunits does hemoglobin have?

A

Fetal hemoglobin has 2a and 2 gamma subunits.

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55
Q

Why does fetal hemoglobin have a higher affinity for O2 than adult hemoglobin?

A

Since fetal hemoglobin has lower affinity for 2,3 BPG than Adult Hemoglobin

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56
Q

What substances favor T form over the R form? What does this due to the dissociation curve?

A

Increased Cl-, H+, CO2, and 2,3-BPG, Shifts dissociation curve to right, leads to increased O2 unloading.

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57
Q

What are some common hemoglobin modifications What do they lead to?

A

Methemoglobin, Carboxyhemoglobin, Can lead to tissue hypoxia from decreased O2 saturation and decreased O2 content.

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58
Q

What is Methemoglobin?

A

Oxidized form of hemoglobin (Fe3) that does not bind O2 as readily. Increased affinity for Cyanide.

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59
Q

What can methemoglobin be treated with?

A

Methylene blue

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60
Q

What will you use to treat cyanide poisoning

A

-Nitrates to oxide hemoglobin to methemoglobin.
Methemoglobin will bind the cyanide, allowing cytochrome oxidase to function.

-Use thiosulfate to bind this cyanide, forming thiocyanate, which is renally excreted.

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61
Q

What is carboxyhemoglobin? What does it cause??

A

Form of hemoglobin bound to CO in place of O2.Decreased O2 binding capacity with a left shift in the oxygen-hemoglobin dissociation curve. Decreases oxygen unloading in the tissues.

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62
Q

Compare CO affinity for hemoglobin compared to O2’s?

A

CO has 200 x greater affinity than O2 for hemoglobin.

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63
Q

Describe positive cooperativity in oxygen-hemoglobin dissociation curve?

A

Hemoglobin can bind 4 oxygen molecules and has higher affinity for each subsequent oxygen molecule bound.

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64
Q

What happens when Oxygen-hemoglobin dissociation curve shifts to the right?

A

Decreased affinity for O2 (Facilitates unloading of O2 to tissue)

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65
Q

Is fetal hemoglobins curve shifted to the left or right relative to adult hemoglobin?

A

Shifted to the left. Has a stronger affinity.

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66
Q

What are the things that cause the O2 hemoglobin dissociation curve to shift to the right?

A

CO2, Cl-, H+, Altitude, DPB, Exercise, Temperature

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67
Q

In the respiratory system, cartilage is only present where?

A

In the trachea and bronchi

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68
Q

What is compliance with regards to the respiratory system? What is compliance decreased in?

A

Change in lung volume for a given change in pressure. Pulmonary fibrosis, insufficient surfactant, and pulmonary edema

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69
Q

What happens to the lung and chest wall when it reaches Funcitonal residual capacity?

A

Inward pull of lungs is balanced by outward pull of chest wall and system pressure is atmospheric. Airway and Alveolar pressure are 0. Intrapleural pressure is negative (prevents pneumothorax)

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70
Q

What determines combined volume of chest wall and lungs?

A

The elastic properties of chest wall and lungs.

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71
Q

What can cause Acute Respiratory Distress Syndrome?

A

Trauma, Sepsis, Shock, Gastric Aspiration, Uremia, Acute Pancreatitis, or amniotic fluid embolism

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72
Q

What happens in Acute Respiratory Distress Syndrome?

A

Diffuse Alveolar damage which causes alveolar capillary permeability and protein-rich leakage into alveoli. This results in formation of intra-alveolar hyaline membrane. Initial damage is due to neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, or oxygen-derived free radicals.[object Object]

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73
Q

What happens in Neonatal Respiratory Distress Syndrome?

A

Surfactant deficiency leading to increased surface tension, resulting in alveolar collapse. Persistent low O2 tension cause increased risk of PDA. Therapeutic supplemental O2 can result in retinopathy of prematurity.

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74
Q

What and when is surfactant made?

A

Surfactant is made by type II pneumocytes most abundantly after 35th week of gestation.

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75
Q

What happens to the lecithin to sphingomyelin ratio is NRDS?

A

Usually <1.5 in neonatal respiratory distress syndrome.

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76
Q

What are risk factors of neonatal respiratory distress syndrome?

A

Prematurity, Maternal Diabetes (Due to elevated insulin), cersarean delivery (decreased release of fetal glucocorticoids)

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77
Q

What is the treatment for neonatal respiratory distress syndrome?

A

Maternal steroids before birth, Artificial surfactant for infant and thyroxine.

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78
Q

What are the pneumoconioses?

A

Coal miner’s, Silicosis, and Asbestos

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79
Q

What happens in Coal Miner’s?

A

Associated with coal mines. Can result in Cor pulmonale, Caplan’s Syndrome. Affects upper lobe.

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80
Q

What happens in Silicosis?

A

Associated with foundries, sandblasting, and mines. Macrophages respond to silica and release fibrogenic factors leading to fibrosis.

Possibly silica may disrupt phagolysomes and impair macrophages. Increases susceptibility to Tb.

Affects Upper lobes with eggshell calcification of hilar lymph nodes.

81
Q

What happens in asbestos?

A

Associated with shipbuilding, roofing, and plumbing. Results in “ivory white”, calcified pleural plques.

Affects lower lobes. Associated with an increased incidence of bronchogenic carcinoma and mesothelioma.

82
Q

Whats an abestos body?

A

Golden-brown fusiform rods, resembling dumbbells located inside macrophages.[object Object]

83
Q

What is Virchow’s Triad (In Deep Vein Thrombosis)

A

Stasis, Hypercoagulabiity, Endothelial damage (Exposed collagen provides impetus for clothing cascade)- SHE

84
Q

What can Deep Vein Thrombosis lead to? How do you prevent it?

A

Can lead to pulmonary embolus, heparin

85
Q

What is homan’s sign?

A

Dorisflexion of foot causing tender calf muscle.

86
Q

What are the embolus types?

A

Fat, Air, Thombus, Bacteria, Amniotic Fluid, Tumor

87
Q

What fat emboli are associated with?

A

Long bone fractures and liposuction.

88
Q

What signs will you see with pulmonary embolus?

A

Chest pain, tachypnea, dyspnea.

89
Q

Where do most pulmonary emboli arise?

A

Deep vein of the leg

90
Q

What is the imaging test of choice for a pulmonary embolus?

A

Helical CT

91
Q

How is pulmonary vascular resistance calculated

A

(Pulmonary Artery Pressure- Left Atrium Pressure)/ Cardiac Output

92
Q

What is resistance equal to?

A

8(n)(l)/ (pi)r^4

N= viscosity, l=length, r=radius

93
Q

What happens in obstructive lung disease?

A

Obstruction of air flow resulting in air trapping in the lungs. Airways close prematurely at high lung volumes, resulting in increased RV and Decreased Functional Vital Capacity.

94
Q

What will you see on a pulmonary function test for someone with obstructive lung disease or COPD?

A

Decreased FEV1, Decreased FVC, Decreased FEV1/ FVC Ratio (hallmark), V/Q mismatch

95
Q

What are the obstructive lung diseases (COPD)

A

Chronic Bronchitis, Asthma, Brochiectasis, Emphysema

96
Q

What happens in Chronic Bronchitis?

A

“Blue Bloater”, Hypertrophy of mucus-secreting glands in bronchioles.
Productive Cough for greater than 3 consecutive months in greater than 2 or more years. Disease of small airways.

97
Q

What findings will you see with chronic bronchitis?

A

Wheezing, Crackles, Cyanosis (early-onset hypoxemia due to shunting), late-onset dyspnea

98
Q

What is Reid Index? What is the reid index in COPD.

A

Gland Depth/Total thickness of bronchial wall. Reid Index is greater than 50%

99
Q

What happens in Asthma?

A

Bronchial hyperresponsiveness causes reversible bronchoconstriction. Smooth muscle hypertrophy and Curschman’s spirals (shed epithelium from mucous plugs).

Can be triggered by viral URIs, allergens, and stress

100
Q

What can you test Asthma with?

A

Test with methacholine challenge

101
Q

What findings will you see with asthma

A

Cough, wheezing, dyspnea, tachypnea, hypoxemia, Decreased I/E Ratio, Pulsus Paradoxus, Mucus Plugging

102
Q

What happens in Bronchiectasis

A

Chronic Necrotizing infection of bronchi leading to permanently dilated airways, purulent sputum, and recurrent infections, and hemoptysis

103
Q

What is bronchiectasis associated with?

A

Associated with bronchial obstruction, CF, poor ciliary motility, Kartagener’s syndrome.

104
Q

What can you develop with bronchiectasis?

A

Aspergillosis.

105
Q

What happens in Emphysema

A

“Pink Puffer” Barrel Shaped Chest, Enlargement of air spaces and decreased recoil resulting from destruction of alveolar walls, increased compliance.

Increased elastase activity, increased lung compliance due to loss of elastic fibers. Exhale through pursed lips to increase airway pressure and prevent airway collapse during exhalation.

106
Q

What are the different types of emphysema? What are they caused by?

A

Centriacinar- caused by smoking
Panacinar- A1-antitrypsin deficiency (also liver cirrhosis)
Paraseptal Epmhysema- associated with bullae -> can rupture -> spontaneous pneumothorax, often in young otherwise health males.

107
Q

What are the findings seen with emphysema?

A

Dyspnea, Decreased breath sounds, tachycardia, late-onset hypoxemia due to eventual loss of capillary beds (occurs with loss of alveolar walls), early onset dyspnea

108
Q

What is O2 content equal to?

A

O2 binding capacity x % saturation + dissolved O2

109
Q

How much can 1g hb bind?

A

1 g of hemoglobin can bind 1.34 ml O2.

110
Q

How much is the normal HB amount in blood?

A

Normal Hb amount in blood is 15 g/dl

111
Q

What is deoxygenated hemoglobin level during cyanosis?

A

Cyanosis results when deoxygenated Hb> 5g/dl

112
Q

What is O2 binding capacity?

A

20.1 ml O2/ dl

113
Q

What happens to O2 content of blood as Hb falls?

A

O2 content of arterial blood decreases but O2 saturation and arterial PO2 do not fall.

114
Q

Oxygen Delivery to the tissues is equal to?

A

Oxygen delivery is equal to cardiac output x oxygen content of blood.

115
Q

What happens to Arterial PO2 with chronic lung disease? Why?

A

Arterial PO2 decreases because physiologic shunt decreases O2 extraction ratio.

116
Q

What is the alveolar gas equation?

A

PAO2= PIO2- (PACO2/R)

Alveolar PO2= PO2 in inspired air- alveolar PCO2/Respiratory Quotient

117
Q

What can the alveolar gas equation normally be approximated to?

A

150-PAco2/0.8

118
Q

What is the respiratory quotient?

A

CO2/Produced per O2 consumed.

119
Q

What is the A-a gradient? What’s a normal value for A-gradient?

A

Alveolar PAO2- PaO2, 10-15 mmHg

120
Q

What causes an increases A-a gradient

A

Increased A-a gradient may occur in hypoxemia, including shunting, V/Q mismatch, and fibrosis.

121
Q

What is the difference between hypoxemia, hypoxia, and ischemia?

A

Hypoxemia is decreased partial pressure of O2.
Hypoxia is decreased O2 delivery to tissue.
Ischemia- Loss of blood Flow

122
Q

What are some conditions that can cause hypoxemia?How will that affect the (A-a gradient)

A

High altitude (normal A-a gradient)
Hypoventilation (normal A-a gradient)
V/Q mismatch (Increased A-a gradient)
Diffusion Limitation (Increased A-a gradient)
Right to Left Shunt (Increased A-a gradient)

123
Q

What are some causes of ischemia

A

Impeded arterial flow

Reduced Venous Drainage

124
Q

What are some causes of hypoxia?

A

Decreased Cardiac output, hypoxemia, anemia, cyanide poisoning, and CO poisoning.

125
Q

What does a V/Q Ratio of 1 mean?

A

Ventilation is matched to perfusion

126
Q

Describe the v/q ratios of the apex and Base

A

Apex of the lung- V/Q= 3 (Wasted ventilation)

Base of the lung- V/Q= 0.6 (Wasted Perfusion)

127
Q

Are ventilation and perfusion greater at the base or the apex?

A

The Base

128
Q

A V/Q ratio of 0 means?

A

Airway obstruction (Shunt). In shunt, 100 O2 does not improve PO2

129
Q

A V/Q ratio that approaches infinity?

A

Blood Flow Obstruction (Physiologic Dead space). Assuming <100% dead space, 100% O2 improves PO2

130
Q

What happens with exercise to apical capillaries?

A

Vasodilation of apical capillaries results in a V/Q ratio that approaches 1.

131
Q

What organism thrives in high O2? Where would it flourish?

A

TB, the apex

132
Q

What are the relative pressures of alveoli, arteries, and veins in the apex and base?

A

Apex PA>Pa>PV, high alveolar pressure compresses capillaries.
Base Pa>Pv>PA

133
Q

What are the three ways in which CO2 can be transported from tissues to the lungs? What are the relative percentages?

A

Bicarbonate (90%), Bound to Hemoglobin at N terminus (not heme) as carbaminohemoglobin (5%), Dissolved CO2 (5%)

134
Q

Increased H from tissue metabolism does what to O2 curve?

A

Shifts it to the right. Increases unloading (Bohr Effect)

135
Q

Describe the pathway CO2 takes as it enters a blood cell

A

CO2 combined with water to form Carbonic Acid which can split into H+ ion and bicarbonate. Hydrogen can bind to hemoglobin while Carbonic Acid can be transported out of blood cell while Cl- comes in.

136
Q

What does oxygenation of Hb do to Co2?

A

Oxygenation of hemoglobin promotes dissociation of H+ from hemoglobin. Shifts equilibrium toward CO2 formation. Therefore, CO2 is released from RBCs.

137
Q

What does CO2 binding to hemoglobin do?

A

Favors the Taut conformation. Increases O2 unloaded.

138
Q

What is sleep apnea?

A

Person stops breathing for at least 10 seconds repeatedly during sleep.

139
Q

What are the types of Sleep Apnea?

A

Central Sleep Apnea- No respiratory Effort

Obstructive Sleep Apnea- Respiratory Effort against airway obstruction.

140
Q

What is Sleep Apnea associated with?

A

Associated with obesity, loud snoring, systemic/pulmonary hypertension, arrhythmias, and possibly sudden death. Individuals may become chronically tired.

141
Q

What is the treatment for sleep apnea?

A

Weight loss, CPAP, surgery

142
Q

How does hypoxemia affect erythropoeitin?

A

Causes increases in EPO release which causes erythrocytosis.

143
Q

What is normal pulmonary artery pressure?

A

10-14 mmHg

144
Q

What pressure value is classified for pulmonary hypertension?

A

Greater than 25 mmHg or greater than 35 during exercise

145
Q

What does pulmonary hypertension result in?

A

Atherosclerosis, medial hypertrophy, and intimal fibrosis of pulmonary arteries

146
Q

What is a primary cause of pulmonary hypertension

A

Inactivating Mutation of BMPR2, which normally functions to inhibit vascular smooth muscle proliferation (Poor Prognosis)

147
Q

What are secondary cause of pulmonary hypertension? Why do these cause pulmonary hypertension

A 
COPD (destruction of lung parenchyma), 
Mitral stenosis (increased resistance, increased pressure), recurrent thromboemboli (decreases cross-sectional area), autoimmune disease (systemic sclerosis; inflammation-> intimal fibrosis, medial hypertrophy)
Left to Right Shunt (Increased Shear Stress -> Endothelial injury
Sleep apnea or living at high altitude (hypoxic vasoconstriction)
148
Q

What is the normal course of pulmonary hypertension?

A

Severe respiratory distress-> cyanosis and RVH-> death from decompensated cor pulmonoale.

149
Q

What are responses to high altitude?

A
  • Acute increase in ventilation
  • Chronic increase in ventilation
  • Increased erythropoietin- increases hematocrit and hemoglobin (chronic hypoxia)
  • Increased 2,3 DPB (binds to hemoglobin so that hemoglobin releases more O2)
  • Increased cellular changes (
150
Q

What are the responses to exercise?

A
  • Increase CO production
  • Increase O2 consumption
  • Increased ventilation rate to meet O2 demand
  • V/Q ratio from apex to base becomes more uniform
  • Increased pulmonary blood flow due to increased cardiac output
  • Decreased pH during strenuous exercise (
151
Q

What happens in restrictive lung disease?

A

Restricted lung expansion causes decreased lung volume (Decreased FVC and TLC).

152
Q

What will you see on a pulmonary function test for restrictive lung disease?

A

FEV1/FVC ratio greater than 80

153
Q

What are the types of restrictive lung diseases?

A
  • Poor Breathing Mechanics (Extrapulmonary/Peripheral Hypoventilation)
  • Interstitial Lung Diseases (Pulmonary, lowered diffusing capacity
154
Q

What are the different categories of Poor breathing mechanics that occur in restrictive lung disease?

A
  • Poor muscular effort (polio, myasthenia gravis)

- Poor Structural Apparatus- scoliosis, morbid obesity

155
Q

What are the different categories of interstitial lung diseases seen in restrictive lung disease?

A

ARDS, Neonatal Respiratory Distress Syndrome, Pneumoconioses,
Sarcoidoises- bilateral hilar lymphadenopathy, noncaseating granuloma, increased ACE and calcium
Idiopathic Pulmonary fibrosis (repeated cycles of lung injury and wound healing with increased collagen)
Goodpasture’s
Wegener’s Granulomatous
Eosinophilic Granuloma (Histiocytosis X)
Drug Toxicity (Bleomycin, busulfan, amiodarone)

156
Q

What is sarcoidosis characterized by? Common in what population

A

Immune-mediated, widespread noncaseating granulomas and elevated serum ACE levels. Black females.[object Object]

157
Q

What is sarcoidosis associated with?

A
  • Restrictive lung disease
  • bilateral hilar lymphadenopathy, -erythema nodosum
  • Bell’s Palsy
  • Epithelial Granulomas containing microscopic schaumann and asteroid bodies
  • Uveoparotitis
  • Hypercalcemia due to conversion of Vitamin D to its active form in
158
Q

What will you use to treat Sarcoidosis with?

A

Steroids

159
Q

What is the mnemonic “Grain” for sarcoidosis stand for?

A

Gammaglobulinemia, Rheumatoid Arthritis, Ace-Increase, Interstitial Fibrosis, Noncaseating granulomas.

160
Q

Name a nonspecific B-agonist. What is its mechanism of action.

A

Isoproterenol- relaxes bronchial smooth muscle (B2), Adverse effect is tachycardia (B1)

161
Q

Name B2 Agonists what are there mechanisms of action.

A

Albuterol- relaxes bronchial smooth muscle (B2). Use during acute exacerbation.

Salmeterol- long acting agent for prophylaxis. Adverse effects are tremors and arrhythmias

162
Q

Name an example of Methylxanthines. What is the mechanism of action

A

Theophylline likely causes bronchodilation by inhibiting phosphodiesterase, thereby decreasing cAMP hydrolysis. Usage is limited because of narrow therapeutic index, metabolized by P-450. Blocks actions of Adenosine.

163
Q

Name a muscarinic antagonist used in asthma.

A

Ipratropium- competitive block of muscarinic receptors, prevents bronchoconstriction, also used for COPD.

164
Q

What is cromolyn’s mechanism of action

A

Prevents release of mediators from mast cells. Effective only for prophrylaxis of asthma. Not effective during an acute asthmatic attack. Toxicity is rare.

165
Q

What are some corticosteroids used in asthma?

A

Beclomethasone, Prednisone- inhibits the synthesis of virtually all cytokines. Inactivates NF-kb, the transcription factor that induces the production of TNFa, among other inflammatory agents. 1st line therapy for chronic asthma.

166
Q

Name some antileukotrienes used in asthma? What are there mechanisms of action?

A

Zileuton- 5 lipoxygenase pathway inhibitor. Blocks conversion of arachidonic acid to leukotrienes.

Zafirlukast, Monetlukast- blocks leukotriene receptors. Especially good for aspirin-induced asthma.

167
Q

What is a method used to prevent exposure to antigen (dust, pollen, etc.)?

A

Avoidance

168
Q

What is a method used When antigen and IgE are on mast cells?

A

Use cromolyn or steroids.

169
Q

What prevents the early response (Bronchoconstriction) of asthma?

A

B-agonists, Theophylline, and Muscarinic Antagonists.

170
Q

What prevents the late response (Inflammation) of asthma ?

A

Bronchial Hyperreactivity

171
Q

Name two expectorants. Name their mechnisms of action.

A

Guaifenesin- Expectorant- removes excess sputum, does not supress cough reflex.

N-acetylcysteine- Mucolytic- can loosen mucous plugs in CF patients. Also used as an antidote for acetaminophen overdose.

172
Q

What is the mechanism of Bosentan

A

Used to Treat pulmonary hypertension. Completely antagonizes endothelin-1 receptors, decreases pulmonary vascular resistant.

173
Q

What will you see in lobar pneumonia? What organisms are common causes of lobar pneumonia?

A

Intraalveolar exudate, consolidation, may involve entire lung
Streptococcus Pneumonia and Klebsiella are common causes

174
Q

What will you see in Bronchopneumonia? What organisms are common causes of Bronchopneumonia?

A

S. Aureus, H. flu, Klebsiellla, S. Pyogenes.

Acute inflammatory infiltrates from bronchioles into adjacent alveoli, patchy distribution involving >1 lobes

175
Q

What will you see in interstitial pneumonia? What organisms commonly cause interstitial pneumonia?

A

Diffuse patchy inflammation localized to interstitial areas at alveolar walls, distribution involving greater than >1 lobe. Generally follows a more indolent course than bronchopneumonia.
Viruses (RSV, Adenovirus), Mycoplasma, Legionella, Chlamydia.

176
Q

What’s the difference between transudate and exudate?

A

Transudate is protein poor. Exudate is protein rich, cloudy.

177
Q

What are conditions in which you will see a transudate?

A

CHF, Nephrotic Syndrome, Hepatic Cirrhosis

178
Q

What are conditions in which you will see an exudate?

A

Malignancy, Pneumonia, Vascular Collagen Disease, trauma (occurs in states of increased vascular permeabiltiy), Must be drained in light of risk of infections.

179
Q

What is lymphatic fluid like?

A

Milky white, rich in triglycerides.

180
Q

What is a lung abscess?

A

A localized collection of pus within parenchyma, usually resulting from bronchial obstruction (cancer) or aspiration of oropharyngeal contents (especially patients predisposed to loss of consciousness and epileptics). Often due to S. Aureus or Anaerobes.

181
Q

What do H1 blockers do?

A

Reversible inhibitors of histamine receptors.

182
Q

What are the 1st generation Histamine Blockers, Uses, and Clinical Toxicities?

A

Diphenhydramine, Dimenhydraminate, Chlorpheniramine
Used in allergies, motion sickness, sleep aid.

Toxicities include Sedation, Antimuscarinic, alpha-adrenergic.

183
Q

What are the 2nd generation histamine blockers, uses, and clinical toxicites?

A

Loratidine, Fexodenadine, Desloratidine, Cetirizine

Used in allergies
Far less sedating than 1st generation because of decreased entry into the CNS.

184
Q

What is Pancoast’s Tumor?

A

Carcinoma that occurs in the apex of the lung and may affect cervical sympathetic plexus

185
Q

What will you see in Horner’s?

A

Ptosis, Anhidrosis, Meiosis

186
Q

What is the leading cause of cancer death?

A

Lung cancer

187
Q

What is the presentation you will see with lung cancer?

A

Cough, Hemoptysis, bronchial obstruction, wheezing, pneumonic “coin lesion on x-ray film or noncalficed nodule on CT”

188
Q

Where can metastasis to the lung arrive from?

A

Breast, Colon, Prostate, and Bladder Cancer

189
Q

Where are the sites of metastases from the lung?

A

Adrenals, brain (epilepsy), bone (pathologic fracture), liver (jaundice, hepatomegaly)

190
Q

What is the mnemonic for remembering lung cancer complications?

A 
Superior Vena Cava Syndrome
Pancost's Tumor
Horner's Syndrome
Endocrine (Paraneoplastic)
Recurrent laryngeal symptoms (hoarseness)
Effusions (pleural or pericardial)
191
Q

What are the physical findings you will see for a bronchial obstruction?

A

Decreased/Absent breath sounds over affected areas, Decreased resonance, Decreased fremitus, Trachea deviates toward the size of the lesion.

192
Q

What are the physical findings you will see on a pleural effusion?

A

Decreased breath sounds over pleural effusion, Dullness, Decreased fremitis

193
Q

What are the physical findings you will see in Lobar Pneumonia

A

May have bronchial breath sounds over lesion, Increased fremitis, dullness

194
Q

What are the physical findings you will see in tension pneumothorax?

A

Decreased breath sounds, Trachea Deviated toward size of lesion, Hyperresonance, Absent fremitus

195
Q

What happens to TLC, FRC, and RV in obstructive vs restrictive lung disease compared to a normal lung.

A

The TLC, FRC, and RV are greater than normal in obstructive.

TLC and FRC are less than normal in restrictive.

196
Q

Is the pulmonary circulation low resistance or high resistance? Low Compliance or High Compliance

A

Low-Resistance, High Compliance

197
Q

What will a decrease in PO2 do to pulmonary circulation? Why?

A

Hypoxic vasoconstriction, shifts blood away from poorly ventilated regions of lungs to well-ventilated regions of lung.

198
Q

What is a consequence of pulmonary hypertension?

A

Cor pulmonale, subsequent right ventricular failure (JVD, Edema, Hepatomegaly)

199
Q

What is the difference between perfusion limited and diffusion limited?

A

Perfusion limited is where gas (O2 normal, CO2, N2O) equilibrates early along length of the capillary. Diffusion can only be increased if blood flow increased.

Diffusion limited- Gas (CO, O2 in emphysema) does not equilibrate by the time blood reaches the end of the capillary (Emphysema, Fibrosis)

First Aid Respy (2 decks)

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