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pulmonary 2 Flashcards

1
Q

What is the flow of events in COPD?

A

Lungs encounter a decrease in PAO2 -> chronic pulmonary vasoconstriction -> chronic pulmonary HTN -> cor pulmonale & subsequent right ventricular failure (JVD, edema, hepatomegaly)

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2
Q

What is the equation for pulmonary vascular resistance?

A

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

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3
Q

What do P(pulmonary artery), P(left atrium), and CO represent?

A

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

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4
Q

What is the equation for resistance in a vessel?

A

R = (8?l) / (?r^4)

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5
Q

What do ?, l, and r represent in the resistance equation?

A

? = viscosity of blood; l = vessel length; r = vessel radius

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6
Q

What is the normal amount of hemoglobin in the blood?

A

15 g/dL

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7
Q

What level of hemoglobin denotes cyanosis?

A

When deoxygenated Hb > 5 g/dL

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8
Q

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

A

1.34 mL O2

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9
Q

What is the formula for O2 delivery to tissues?

A

O2 delivery to tissues = CO x O2 content of blood

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10
Q

What is the alveolar gas equation?

A

PAO2 = PIO2 - (PaCO2/R)

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11
Q

What do PAO2, PIO2, PaCO2, and R represent in the alveolar gas equation?

A

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

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12
Q

How can you normally approximate the alveolar gas equation?

A

PAO2 = 150 - (PaCO2 / .8)

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13
Q

What is the A-a gradient?

A

PAO2 - PaO2 = 10 to 15 mmHg

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14
Q

When does an increased A-a gradient occur?

A

Hypoxemia

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15
Q

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

A

Shunting; V/Q mismatch; fibrosis (impairs diffusion through an increase in barrier thickness)

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16
Q

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

A

High altitude; hypoventilation (i.e. opioid use)

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17
Q

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

A

V/Q mismatch; diffusion limitation (i.e. fibrosis); right-to-left shunt

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18
Q

If hypoxia exists, what might be the causes?

A

Decreased cardiac output; hypoxemia; anemia; carbon monoxide poisoning

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19
Q

If ischemia exists in the lung, what might be the causes?

A

Impede arterial flow; reduced venous drainage

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20
Q

What is the ideal ventilation & perfusion ratio for adequate gas exchange?

A

1

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21
Q

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

A

3 (wasted ventilation) due to a decrease in perfusion; part of the physiologic dead space

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22
Q

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

A

.6 (wasted perfusion) due to too much blood (this is called shunting as there is venous blood leaving the lung without O2)

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23
Q

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

A

Apex

Example: TB

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24
Q

What is the V/Q during exercise?

A

Exercise increases the CO, there is vasodilation of apical capillaries causing an increase in perfusion -> V/Q = 1

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25
Q

Where are both ventilation and perfusion the greatest?

A

Base of the lung due to gravity pulling more blood to the base

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26
Q

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

A

Airway obstruction (shunt)

NOTE: Giving 100% oxygen will NOT improve PO2 due to nothing getting to the alveoli anyway

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27
Q

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

A

Blood flow obstruction (physiologic dead space)

NOTE: Assuming <100% dead space, 100% oxygen WILL improve PO2

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28
Q

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

A

Zone 1 (apex)

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29
Q

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

A

Zone 2

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30
Q

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

A

Zone 3

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31
Q

Compare V & Q at the base of the lung to the apex.

A

Both V & Q are increased at the base of the lung due to gravity, however perfusion increases way more!

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32
Q

What are the three forms of transported carbon dioxide?

A

Bicarbonate (HCO3- - 90%); carbaminohemoglobin or HbCO2 (5%); dissolved CO2 (5%)

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33
Q

Where does CO2 bind hemoglobin?

A

N-terminus of globin, NOT heme

NOTE: Carbon monoxide binds the heme group

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34
Q

What form of hemoglobin does CO2 binding favor?

A

Taut (O2 unloaded)

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35
Q

What is the Haldane effect?

A

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

IN LUNGS

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36
Q

What is the Bohr effect?

A

Increased H+ (CO2) from tissue metabolism –> curve shifted right (favors ‘T’ form of Hb) –> O2 unloaded

IN TISSUES

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37
Q

How is the majority of blood CO2 carried?

A

As bicarbonate

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38
Q

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

A

Cl- / HCO3- antiporter

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39
Q

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

A

Carbonic anhydrase

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40
Q

What is the acute body response to being in high altitude?

A

Decrease in Po2 -> decrease in PaO2 -> increase in ventilation -> decrease in PaCO2 (due to breathing more you blow off more CO2) -> respiratory alkalosis -> altitude sickness

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41
Q

What is the chronic ventilation response to high altitude?

A

Increased ventilation

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42
Q

How does erythropoietin change in response to high altitude?

A

Increased erythropoietin –> increased hematocrit AKA 40->65 & hemoglobin AKA 15->20 (chronic hypoxia!)

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43
Q

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

A

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

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44
Q

What cellular changes are seen in response to high altitude?

A

Increased mitochondria

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45
Q

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

A

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

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46
Q

What is the result of chronic hypoxic pulmonary vasoconstriction?

A

Pulmonary HTN & RVH

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47
Q

How does the respiratory system respond to exercise?

A

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

NOTE: No change in PaO2 and PaCO2

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48
Q

What is Rhinosinusitis?

A

Obstruction of sinus drainage into the nasal cavity -> inflammation & pain over affected area (typically maxillary sinuses, which drain into the middle meatus, in adults)

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49
Q

What is the most common acute cause of Rhinosinusitis?

A

Viral URI; may be superimposed bacterial infection (i.e. S. pneumoniae, H. influenzae, M. catarrhalis)

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50
Q

What is an Epistaxis?

A

Nosebleed

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51
Q

Where does Epistaxis most commonly occur?

A

Anterior segment of nostril (Kiesselbach plexus)

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52
Q

Where do life-threatening Epistaxis hemorrhages occur?

A

Posterior segment (i.e. sphenopalatine artery, a branch of the maxillary artery)

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53
Q

What is the most common type of head & neck cancer?

A

Squamous cell carcinoma

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54
Q

What are the risk factors for head & neck cancer?

A

Tobacco; alcohol; HPV-16 (oropharyngeal); EBV (nasopharyngeal)

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55
Q

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

A

Diaphragmatic hernia

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56
Q

What is a DVT?

A

Blood clot within a deep vein (i.e. femoral, popliteal, iliofemoral) -> swelling, redness warmth & pain

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57
Q

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

A

TRIAD (‘SHE gets a lot of clots’) 1) stasis (i.e. post-op, long drive/flight) 2) hypercoagulability (i.e. defect in coagulation cascade proteins, such as factor V Leiden) 3) endothelial damage (i.e. exposed collagen triggers clotting cascade

SIGNIFICANCE: predisposition to DVT

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58
Q

What is the most common cause of hypercoagulability?

A

Factor V Leiden (most common defect in coagulation cascade proteins)

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59
Q

What is the complication of DVT?

A

Pulmonary embolus

60
Q

What physical examination provocative test is most indicative of DVT?

A

Homan’s sign = dorsiflexion of foot –> calf pain

61
Q

What is used for prevention and acute management of DVT?

A

Heparin

62
Q

What is used for chronic prevention of DVT recurrence?

A

Warfarin, rivaroxaban

63
Q

What clinical test is used to RULE OUT DVT?

A

D-Dimer lab test (high sensitivity, low specificity)

64
Q

What clinical test is used to RULE IN DVT?

A

Imaging test (Ultrasound)

65
Q

What is the effect to the body of getting a PE?

A

PE causes hypo perfusion of affected lung parenchyma, which leads to a redistribution of pulmonary blood flow & a V/Q mismatch. The resulting hypoxemia stimulates hyperventilation & acute respiratory alkalosis. ABG shows an increase in pH & a decrease in PaCO2, along with a decrease in PaO2

66
Q

What are the symptoms of a PE?

A

Sudden-onset dyspnea, chest pain, tachypnea & tachycardia

67
Q

What happens with a large or saddle embolus of the pulmonary artery?

A

May cause sudden death

68
Q

What do lines of Zahn in a pulmonary embolus indicate?

A

That the thrombi is pre-mortem

NOTE: Lines of Zahn are interdigitating areas of pink (platelets and fibrin) and red (RBCs) found only in thrombi formed before death

69
Q

From where do the majority of pulmonary emboli arise?

A

Deep leg veins

70
Q

What are the types of pulmonary emboli?

A

Fat; Air; Thrombus; Bacteria; Amniotic fluid; Tumor

–an embolus moves like a FAT BAT–

71
Q

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

A

CT pulmonary angiography (look for filling defects)

72
Q

Describe obstructive lung diseases.

A

Obstruction of air flow resulting in air trapping in lungs. **Extended expiratory phase; can’t get rid of air in lungs!

73
Q

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

A

RV increased; FRC increased; TLC increased; FEV1 greatly decreased; FVC decreased; FEV1/FVC decreased; V/Q mismatch

74
Q

What is FEV1?

A

Air expired in 1 second

75
Q

What is FVC?

A

Total air expired in a forced breath

76
Q

Why does the FVC decrease in obstructive lung disease?

A

Volume of air that can be forcefully expired decreases

77
Q

Why is TLC increased in obstructive lung disease?

A

Air trapping

78
Q

Why does diffusion decrease in obstructive lung diseases?

A

Decrease in surface area

79
Q

At what percentage is the FEV1 considered ‘very severe’?

A

<30%

80
Q

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

A

<25%

NOTE: There will also be increased PCO2

81
Q

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

A

3/4

82
Q

How is COPD defined?

A

Chronic lung disease with obstructive physiology

**(usually, chronic bronchitis + emphysema)

83
Q

What are the diagnostic criteria for chronic bronchitis?

A

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

84
Q

What is the pathogenesis of chronic bronchitis?

A

Hypertrophy of mucus-secreting glands in bronchi –> Reid index > 50% (thickness of mucosal gland layer to thickness of wall between epithelium & cartilage) –> decreased air flow

**More than 1/2 of bronchial wall is compromised of mucus-secreting glands

85
Q

What is the formula for the Reid Index?

A

Mucosal glands layer / (mucosal gland layer & epithelium)

**Cartilage is NOT included

86
Q

Is chronic bronchitis caused by smoking?

A

Yes

87
Q

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

A

Normal bronchi

88
Q

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

A

Chronic bronchitis

89
Q

What happens to the dLCO in chronic bronchitis?

A

Normal

90
Q

What happens to the RV & TLC in chronic bronchitis?

A

RV increases; TLC does not increase as much as emphysema

91
Q

What are the findings in chronic bronchitis?

A

-Productive cough due to mucus production; ‘flare ups’; increased risk of infection and cor pulmonale; wheezing, crackles, cyanosis, early-onset hypoxemia due to shunting, mucus plugs trap carbon dioxide (hypercapnia), secondary polycythemia

92
Q

What are the chronic complications of chronic bronchitis?

A

Pulmonary HTN, cor pulmonale

93
Q

What is a trick name for chronic bronchitis patients?

A

‘Blue bloaters’

94
Q

What is the effect of bronchodilators in chronic bronchitis?

A

Some response, but will not return patient to normal

95
Q

How is chronic bronchitis treated?

A

Bronchodilators; glucocorticoids; broad-spectrum antibiotics; O2

96
Q

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

A

RV increased; FRC increased; TLC increased; diffusion decreased (i.e. decreased dLCO)

97
Q

Describe the overall criteria for emphysema.

A

Enlargement of air spaces; decrease elastic recoil; increased compliance; decrease diffusing capacity for CO from destruction of alveolar walls

98
Q

Is emphysema caused by smoking?

A

Yes

99
Q

What is a trick name for emphysema?

A

‘Pink puffers’

100
Q

What is the cause of centriacinar emphysema and its location?

A

Smoking (upper lobes); destruction of central portion of acini

‘Smoke rises to the UPPER LOBES’

101
Q

What is the cause of panacinar emphysema and its location?

A

Alpha-1 antitrypsin (A1AT) deficiency (lower lobes); destruction of entire acini

102
Q

What is A1AT, and what is its function?

A

Alpha1-antitrypsin, inherited in an autosomal co-dominant pattern

103
Q

What is the cause of centriacinar emphysema? Location?

A

Smoking (upper lobes); destruction of central portion of acini.

104
Q

What is the cause of panacinar emphysema? Location?

A

Alpha-1 antitrypsin (A1AT) deficiency (lower lobes); destruction of entire acini.

105
Q

What is A1AT, and what is its function?

A

Alpha1-antitrypsin, inherited in an autosomal co-dominant pattern; neutralizes proteases (i.e. elastase) in the lower lobes.

106
Q

What is the result of A1AT deficiency?

A

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

107
Q

Describe the pathway once the A1AT deficiency goes into effect.

A

Increased elastase activity -> loss of elastic fibers -> increase lung compliance.

108
Q

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

A

Note the pink, PAS-positive globules in hepatocytes.

109
Q

Where in the lung is panacinar emphysema most severe?

A

Lower lobe.

110
Q

Where in the lung is centracinar emphysema most severe?

A

Upper lobes.

111
Q

What is the normal allele in A1AT deficiency?

A

PiM; two copies are usually expressed (PiMM).

112
Q

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

A

PiZ.

113
Q

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

A

PiMZ; smoking.

114
Q

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

A

PiZZ.

115
Q

What are the clinical features of emphysema?

A
  • Dyspnea and cough with minimal sputum, hyperventilation, wheezing.
  • Prolonged expiration with pursed lips (‘pink puffer’; this increases airway pressure and prevents airway collapse during respiration).
  • Weight loss.
  • Barrel-shaped chest.
  • CXR shows increased AP diameter, flattened diaphragm, increased lung field lucency.
116
Q

What are the late complications of emphysema?

A

Destruction of capillaries in the alveolar sac –> hypoxemia; cor pulmonale.

117
Q

Describe asthma.

A

Bronchial hyper-responsiveness that causes REVERSIBLE bronchoconstriction.

118
Q

What happens to the smooth muscle during asthma?

A

Hypertrophy (b/c muscles are working harder).

119
Q

Key findings in asthmatic patients?

A

Curschmann spirals (shed epithelium forms whorled mucus plugs); Charcot-Leyden crystals (eosinophilic, hexagonal, double-pointed, needle-like crystals formed from breakdown of eosinophils in sputum).

120
Q

What are the triggers of asthma?

A

Viral URIs; allergens; stress.

121
Q

What type of hypersensitivity reaction is asthma?

A

Type I.

122
Q

Clinical diagnosis of asthma?

A

Supported by spirometry & methacholine.

123
Q

What are the clinical features of asthma?

A

Cough; wheezing; tachypnea; SOB; hypoxemia; decreased inspiratory/expiratory ratio; pulsus paradoxus (drop in SBP > 10 mmHg during inspiration).

124
Q

What is a finding on CXR during asthma?

A

Peribronchial cuffing.

125
Q

I say ‘Curschmann’s spirals,’ you say…?

A

Asthma.

126
Q

I say ‘Charcot-Leyden crystals in sputum,’ you say…?

A

Note the numerous eosinophils also; asthma.

127
Q

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

A

FEV1 decreased; RV increased; FRC increased; resistance increased.

128
Q

What is bronchiectasis?

A

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

129
Q

What is the pathogenesis of bronchiectasis?

A

Chronic necrotizing infection/inflammation of bronchi –> damage to airway cells –> permanently dilated airways, purulent sputum, recurrent infections, hemoptysis & digital clubbing.

130
Q

What are the possible causes of bronchiectasis?

A

Poor ciliary function: cystic fibrosis, Kartagener syndrome, smoking; obstruction: tumor or foreign body; infectious: necrotizing infection (H. influenza, P. aeruginosa), allergic bronchopulmonary aspergillosis.

131
Q

What is Kartagener syndrome?

A

Inherited defect of the dynein arm –> no ciliary movement –> sinusitis, bronchitis, infertility, situs inversus.

132
Q

Which individuals are most prone to allergic bronchopulmonary aspergillosis?

A

Asthmatics, cystic fibrosis patients (hypersensitivity reaction to Aspergillus –> chronic inflammatory damage).

133
Q

What are the clinical features of bronchiectasis?

A

Cough, dyspnea; purulent, foul-smelling sputum; recurrent infections; hemoptysis.

134
Q

What are the complications of bronchiectasis?

A

Hypoxemia with cor pulmonale; secondary amyloidosis (AA).

135
Q

How do you treat COPD?

A

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

136
Q

What are the obstructive lung diseases?

A

COPD; chronic bronchitis; emphysema; asthma; bronchiectasis.

137
Q

What is the basic criteria for restrictive lung diseases?

A

Restricted lung expansion causes a decrease in lung volumes; can’t fill lung very well; decreased diffusion d/t thickened tissue.

138
Q

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

A

ARDS, neonatal RDS (hyaline membrane disease); pneumoconioses (Coal Workers’ pneumoconiosis, silicosis, berylliosis, asbestosis, anthracosis); sarcoidosis; idiopathic pulmonary fibrosis; Goodpasture’s syndrome; Wegener’s (granulomatosis with polyangiitis); pulmonary Langerhans cell histiocytosis (eosinophilic granuloma); hypersensitivity pneumonitis; drug toxicity (bleomycin, busulfan, amiodarone, methotrexate).

139
Q

What are the restrictive lung diseases (poor breathing mechanics; outside lung)?

A

Poor muscular effort (polio, myasthenia gravis, Guillain-Barre); poor structural apparatus (scoliosis, morbid obesity).

140
Q

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

A

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

141
Q

Why does the TLC decrease in restricted lung disease?

A

Restricted lung expansion –> decreased lung volumes –> decreased TLC.

142
Q

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

A

Polio; myasthenia gravis.

143
Q

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

A

Scoliosis; morbid obesity.

144
Q

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

A

Extrapulmonary; peripheral hypoventilation; normal A-a gradient.

145
Q

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

A

Pulmonary; lowered diffusing capacity; increased A-a gradient.

First Aid (18 decks)

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