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PATHOMA/FA SYSTEMS > RESPIRATORY > Flashcards

RESPIRATORY Flashcards

1
Q

Where do the small airways technically begin?

A

bronchioles and end at terminal bronchioles

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2
Q

Give a description of what the “anatomic dead space” is (no equation)

A

This is the air that is in the conducting zone of the respiratory system

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3
Q

Which structures are no longer found after the bronchi (2)? Which are no longer found after the terminal bronchioles?

A

Cartilage and Goblet cells; Pseudostratified ciliated epithelium and smooth muscle (it is sparse beyond here)

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4
Q

Which “bronchioles” are present in the respiratory zone?

A

Respiratory bronchioles; terminal bronchioles are the last structures of the conducting zone

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5
Q

What is the epithelium of the conducting zone? The Respiratory zone?

A

Conducting zone = pseudostratified columnar; Respiratory zone = Cuboidal in respiratory bronchioles and then simple squamous

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6
Q

Histology of Type I pneumocyte

A

Simple squamous

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7
Q

Why are alveoli most likely to collapse in expiration?

A

The Collapsing pressure = 2(surface tension)/Radius? Since the radius decreases in expiration, the pressure to collapse is greatly increased

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8
Q

What is the significance of the lecithin to sphingomyelin ratio?

A

indicates fetal lung maturity? >2 is adequate

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9
Q

How do type II pneumocytes decrease the collapsing pressure?

A

P = 2(surface tension)/R? By decreasing surface tesnion, surfactant decreases the numerator leading to lower collapsing pressure

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10
Q

When does surfactant synthesis begin? When are lungs mature? What ratio do you use?

A

26, 35, Lecithin:sphingomyelin >2

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11
Q

What is the homologue of the right lung middle lobe in the left lung?

A

Lingula

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12
Q

Where will a peanut go if aspirated when upright? When supine?

A

Upright = lower portion of right inferior lobe; Supine = superior portion of right inferior lobe

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13
Q

Discuss the relation of the right and left pulmonary arteries with respect to the right and left mainstem bronchi

A

Right pulmonary artery is anterior to right bronchus; Left pulmonary artery is superior to left bronchus

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14
Q

What 2 structures pierce the diaphragm at T10?

A

Esophagus and Vagal trunks

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15
Q

What 3 structures pierce the diaphragm at T12?

A

Aorta, Thoracic duct, Azygos vein

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16
Q

Air that can still be breathed in after normal inspiration

A

Inspiratory reserve volume (IRV)

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17
Q

Air that moves into lung with each quiet inspiration (typically 500 mL)

A

Tidal volume (TV)

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18
Q

Air that can still be breathed out after normal inspiration

A

Expiratory reserve volume (ERV)

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19
Q

Air in lung after maximal expiration and cannot be measured on spirometry

A

Residual volume

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20
Q

IRV + TV

A

Inspiratory capacity

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21
Q

RV + ERV (volume in lungs after normal expiration)

A

Functional Residual capacity

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22
Q

TV + IRV + ERV (maximum volume of gas that be expired after maximal inspiration)

A

Vital Capacity

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23
Q

IRV + TV + ERV + RV

A

TLC (volume of gas in lungs after a maximal inspiration)

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24
Q

What is the inspiratory reserve volume?

A

Air that can be breathed in after a normal inspiration

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25
Q

What is the tidal volume?

A

Normal amount of air moving into lung with each inspiration (500 mL)

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26
Q

What is the expiratory reserve volume?

A

Air that can still be breathed out after normal expiration

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27
Q

What is the residual volume?

A

The amount of air in the lung after a maximal expiration

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28
Q

What is the inspiratory capacity?

A

IRV + TV (That is the normal amount inspired plus that which can be inspired on top of it)

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29
Q

What is the Functional residual capacity?

A

RV +ERV (volume in lungs after normal expiration? So the amount of air that can be breathed out after a normal expiration (ERV) plus that which remains after that (RV))

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30
Q

What is the vital capacity?

A

TV + IRV + ERV (maximum volume of gas that can be expired after a maximal inspiration)

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31
Q

What is the total lung capacity?

A

IRV + TV + ERV + RV (volume of gas in lungs after maximal inspiration)

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32
Q

How do you calculate Physiologic dead space?

A

Vd = Vt [(PaCo2 - PeCO2)/PaCO2]

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33
Q

What is the physiological deadspace? Explain in words

A

It is the anatomic deadspace plus the functional deadspace in alveoli

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34
Q

What part of the healthy lung is the largest contributor of functional deadspace?

A

Apex of lung

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35
Q

Regarding the physiology of the lung and chest wall, what is the significance of FRC?

A

FRC (i.e. the volume of air in the lungs after normal expiration (RV +ERV)) is the point at which the outward pull of the chest wall is balanced by the inward pull of the lungs

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36
Q

What forms of Hb (T and R) have high and low affinity for O2?

A

Taut form has low affinity for O2, relaxed form has high affinity for O2

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37
Q

Chloride, H, CO2, temperature, and 2,3-DPG favor (T or R) form of Hb?

A

Taut (i.e. the low affinity form) this way, Hb gives off O2

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38
Q

What 5 factors favor the taut form of Hb over the relaxed form?

A

Chloride, CO2, H, temperature, and 2,3-DPG

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39
Q

Which form of hemoglobin has the lowest affinity for 2,3 DPG?

A

Fetal Hb (allows it to be left-shifted and therfore to have higher affinity for O2 than mom leading to fetal oxygenation)

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40
Q

Which tissues have taut Hb and relaxed Hb?

A

Taut is in (peripheral) tissues; R (relaxed) form is in respiratory tissues

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41
Q

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

A

Because fetal Hb has a lower affinity for 2,3, DPG which normally causes a right shift

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42
Q

EXPLAIN the treatment of cyanide poisoning (2 aspects)

A

Nitrites oxidize hemoglobin to methemoglobin which will bind up the cyanide, this allows cytochrome oxidase (complex IV) to function; Thiosulfate is given to bind up the cyanide to form thiocyanate which is renally excreted

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43
Q

How do you treat methemoglobinemia?

A

Methylene blue

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44
Q

Why are nitrites toxic to Hb? This is exploited in the Tx of what?

A

They oxidize Fe2 to Fe3 (methemoglobin); This is exploited in cyanide poisoning because Fe3 (methemoglobin) will bind to cyanide which allows cytochrome oxidase to fxn

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45
Q

What is the shift in O2 binding curve when carboxyhemoglobin is present?

A

Left shift (this is carbon monoxide poisoning)

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46
Q

Why does the myoglobin-O2 curve lack a sigmoidal shape?

A

Myoglobin is a monomer and thus, cannot display cooperativity with its subunits like Hb

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47
Q

What would alkaline blood do to the HbO2 curve?

A

It would cause a left shift, (Haldane effect)

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48
Q

When is gas equilibration with capillary diffusion limited? Perfusion limited?

A

Diffusion limited in fibrosis and emphysema; perfusion limited in normal health

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49
Q

What does perfusion limited gas equilibration mean?

A

It means more gas can diffuse into the bloodstream only if there is an increase in perfusion to the lung

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50
Q

What does diffusion limited gas equilibration mean?

A

it means that the gas has not equilibrated by the time it reaches the end of the capillary, more perfusion will not help!

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51
Q

How do you know if someone ahs pulmonary HTN?

A

>25 mmHg resting or >35 exercising

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52
Q

An activating mutation of the BMPR2 gene is likely to cause __________

A

Primary pulmonary HTN (normally funtions to inhibit smooth muscle proliferation)

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53
Q

What is the genetic basis of primary pulmonary HTN?

A

Activating mutation of BMPR2 (normally functions to inhibit smooth muscle proliferation)

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54
Q

Why do recurrent PE’s lead to pulmonary HTN?

A

it decreases the cross-sectional area of the pulmonary vascular bed

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55
Q

How do you calculate pulmonary vascular resistance?

A

PVR = (Ppulm artery - P left atrium)/CO

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56
Q

How much O2 can be bound by 1g of Hb?

A

1.34 mL O2

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57
Q

How do you calculate O2 content?

A

O2 content = (O2 binding capacity x %sat) + dissolved O2

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58
Q

How do you approximate the alveolar gas equation?

A

PAO2 = 150 - (PaCO2/0.8)

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59
Q

What would increase the A-a gradient?

A

This is how much more O2 is in the alveoli than the blood; shunting, V/Q mismatch, and fibrosis (impairs diffusion)

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60
Q

What are 2 causes of normal A-a gradient hypoxemia?

A

Hypoventilation and High altitude

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61
Q

What is V/Q at the apex? What is V/Q at the base?

A

Apex V/Q = 3; Base V/Q = 0.6 (Apex has wasted ventilation, ideal for TB; Base has wasted perfusion!)

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62
Q

What is greater at the base of the lung? Ventilation or perfusion?

A

BOTH! But V/Q ratio is greater at the apex

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63
Q

What happens to the V/Q ratio at the apex of the lung in exercise?

A

Decreases because Q is increasing!

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64
Q

What happens to V/Q in a shunt?

A

Approaches 0 (airway obstruction)

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65
Q

What happens to V/Q in a blood flow obstruction?

A

Approaches infinity, i.e. physiologic dead space increases

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66
Q

What are the 3 forms that CO2 is transported from tissues to lungs?

A

Bicarb (most), Carbaminohemoglobin (HBCO2)? CO2 bound to N-terminis of GLOBIN not heme, and dissolved CO2

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67
Q

Where on Hb does CO2 bind?

A

to N-terminis of the GLOBIN (carbaminohemoglobin)

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68
Q

What is the Haldane effect?

A

This is when oxygenation in the lungs promotes H dissociation from Hb leading to CO2 formation

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69
Q

Why could living at a high altitude lead to RVH?

A

Since there is a low PO2, there is chronic hypoxic pulmonary vasoconstriction that leads to increased resistance

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70
Q

What is the most common cause of hypercoagulability?

A

Factor V Leiden

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71
Q

What is a likely cancer to cause a tumor pulmonary embolus?

A

Renal Cell CA

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72
Q

What increase in Reid index is observed in Chronic bronchitis?

A

greater than 50%

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73
Q

What airways are affected by chronic brochitis?

A

Small airways

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74
Q

What is the timeline for chronic bronchitis?

A

Productive cough for > 3 months (doesnt have to be consecutive) for over 2 years

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75
Q

Why do emphysema pts exhale through pursed lips?

A

increases airway pressure to prevent airway collapse during expiration

76
Q

What is the main association with centriacinar emphysema?

A

smoking

77
Q

What is a Curschmann spiral?

A

Shed epithelium in mucus plugs

78
Q

What is a Charcot Leyden crystal

A

breakdown product of eosinophil membrane protein

79
Q

What test is used for asthma?

A

Methacholine challenge test

80
Q

Which obstructive airway disease involves smooth muscle hypertrophy?

A

Asthma

81
Q

Which colonizing disease can cause bronchiectasis?

A

Allergic Bronchopulmonary Aspergillosis

82
Q

What are 2 causes of poor breathing due to structural abnormalities?

A

Scoliosis and morbid obesity

83
Q

4 drugs that can cause restrictive lung disease

A

Methotrexate, Busulfan, Bleomycin, and Amiodarone

84
Q

Which interstitial lung disease is associated with pathologic fractures?

A

Langerhans histiocytosis (Eosinophilic granuloma)

85
Q

What is the cause of idiopathic pulmonary fibrosis?

A

repeated cycles of lung injury with wound healing and collagen deposition in interstitium

86
Q

Which pneumoconiosis increases susceptibilities to TB and why?

A

Silicosis because silica may inhibit phagolysosomal fusion

87
Q

What causes “Eggshell” calcifications of hilar lymph nodes?

A

Silicosis

88
Q

Silicosis increases risk for what 2 things?

A

Bronchogenic carcinoma and TB

89
Q

Which pneumoconioses affect the upper lobes? Lower lobes?

A

Upper lobes = Silicosis and Anthracosis; Lower lobes = Asbestosis

90
Q

Ivory white calcified pleural plaques

A

pathognomonic feature of asbestos exposure, NOT precancerous

91
Q

Which pneumoconisosis is associated with shipbuilding, roofing, and plumbing?

A

Asbestosis

92
Q

What lecithin:sphingomyelin ratio is predictive of neonatal RDS?

A

2 is normal

93
Q

What are 2 untoward effects of giving supplemental O2 to neonatal respiratory distress syndrome

A

Retinopathy of prematurity; Bronchopulmonary dysplasia

94
Q

3 risk factors for neonatal RDS

A

Prematurity (not enough surfactant); maternal diabetes (too much fetal insulin); cesarian delivery = not enough glucocorticoids from stress of birth which causes development of surfactant

95
Q

What are 2 ways to treat neonatal RDS?

A

Can give artificial surfactant but can also give maternal steroids before birth

96
Q

What is the hallmark of ARDS?

A

DIFFUSE ALVEOLAR DAMAGE with formation of intra-alveolar hyaline membrane

97
Q

Where is the tracheal deviation in 1) Atelectasis from bronchial obstruction 2) Spontaneous pneumothorax 3) Tension pneumothorax

A

1) toward 2) toward 3) away

98
Q

Which peripherally located lung cancer bares a poor prognosis?

A

Large cell carcinoma

99
Q

What is a Kulchitsky cell?

A

A neuroendocrine cell in small cell carcinoma (chromogranin positive)

100
Q

What is the most common thing to see on Xray of lung CA?

A

Calcified Coin lesion

101
Q

What is the most common cause of metastasis to adrenals?

A

lung cancer

102
Q

What lung cancer is associated with k-ras activating mutations? Which amplifies myc oncogenes?

A

k-ras = adenocarcinoma; L-myc = small cell carcinoma

103
Q

What would be a likely V/Q in lung cancer?

A

0; airway obstruction

104
Q

Which lung cancer is associated with hypertrophic osteoarthropathy?

A

adenocarcinoma

105
Q

What mutation is seen in adenocarcinoma of the lung? What other type of cancer displays this?

A

K-ras; also seen in colorectal carcinoma

106
Q

Which type of lung cancer looks most similar to pneumonia?

A

Bronchioloalveolar because follows the bronchioles

107
Q

What genetic mutation is implicated in small cell carcinoma?

A

myc oncogene amplification

108
Q

What is the eponym for the malignant cells of small cell CA?

A

Kulitschky cells

109
Q

Where do lung carcinoid tumors occur?

A

In bronchi

110
Q

What can be seen on the histology of mesothelioma?

A

Psammoma body (keratin pearls are eosinophilic, psammoma bodies are basophilic)

111
Q

What is facial plethora?

A

impaired blood drainage from the head (SVC syndrome)

112
Q

3 populations at risk for aspiration pneumonia (Abscess)? Bugs involved?

A

Epileptics; alcoholics, diabetics (gastroparesis), also stroke pts with bulbar probs (nucleus ambiguus)–bacteroides, fusobacterium, peptostreptococcus

113
Q

What kind of hypersensitivity is hypersensitivity pneumonitis?

A

a mixed III/IV

114
Q

What situation leads to increased tactile fremitus?

A

pneumonia (consolidation)

115
Q

Rhinovirus receptor

A

ICAM-1

116
Q

Name 2 diseases associated with nasal polyps

A

Aspirin intolerant asthma and Cystic fibrosis

117
Q

Who is the most likely to have a nasal angiofibroma?

A

Adolescent male

118
Q

Pleomorphic keratin-positive epithelial cells in a background of lymphocytes

A

Nasopharyngeal carcinoma (Asians with EBV); classically also involves cervical lymph nodes

119
Q

Why is acute epiglottitis a medical emergency?

A

it risks airway obstruction

120
Q

How do you treat a vocal cord nodule?

A

rest the voice

121
Q

What is a vocal cord nodule composed of? 2 other diseases with this?

A

Degenerative myxoid tissue; atrial myxoma, mitral valve prolapse

122
Q

What will you see on the biopsy of nasopharyngeal carcinoma?

A

pleomorphic keratin-positive epithelial cells in a background of lymphocytes

123
Q

Another name for croup

A

laryngotracheobronchitis

124
Q

What causes a laryngeal papilloma?

A

HPV 6 and 11 (koilocytic change)

125
Q

What are the risk factors for laryngeal carcinoma?

A

Tobacco and alcohol; rarely from a laryngeal papilloma (HPV 6 and 11 are low risk)

126
Q

What are the 3 major patterns of pneumonia?

A

Lobar pneumonia; Bronchopneumonia; Interstitial pneumonia

127
Q

What causes grey hepatization of a lung with pneumonia?

A

Follows red hepatization and is when the RBCs breakdown

128
Q

What is a pneumonia that follows the bronchioles?

A

Bronchopneumonia

129
Q

What would happen if you lost type II pneumocytes?

A

pathcy atelectasis (loss of surfactant)

130
Q

CXR worse than clinical presentation?

A

interstitial pneumonia

131
Q

What is infected in interstitial pneumonia?

A

Literally, the interstices? i.e. the alveolar septae etc.

132
Q

What is the most common cause of secondary pneumonia?

A

S. pneumo! i.e. following a viral infection with influenza

133
Q

What complication may arise in K. pneumo pneumonia?

A

abscess formation (it is an aspirated pneumonia)

134
Q

What causes empyema?

A

S. aureus

135
Q

What pneumonia often leads to an exacerbation of COPD?

A

H. influenzae, M. catarrhalis, L. pneumophila

136
Q

Best way to visualize Legionella? 2 others?

A

Silver stain; H. pylori and P. jiroveci

137
Q

2 complications of mycoplasma pneumoniae?

A

Cold autoimmune hemolytic anemia; erythema multiforme

138
Q

Most common cause of atypical pneumonia in infants

A

RSV

139
Q

What are 3 ways that Coxiella is different from other Rickettsial organisms?

A

1) causes pneumonia 2) DOES NOT REQUIRE ARTHROPOD VECTOR 3) no skin rash

140
Q

Discuss primary TB

A

goes to lower lobe and hilar lymph node forming caseating granulomas and a calcified lesion = Gohn complex? USUALLY ASYMPTOMATIC

141
Q

Why would miliary TB cause sterile pyuria?

A

it is acid fast, wouldn?t show up

142
Q

Where does tuberculous meningitis tend to occur?

A

base of the brain

143
Q

Name 3 stains for TB

A

Auramine rhodamine, Ziehl Neehlsen, AFB

144
Q

What is a normal FEV1:FVC ratio?

A

0.8

145
Q

If mucus plugs trap CO2, what happens to O2?

A

PO2 drops, that is a general principle

146
Q

Which lobes are most affected in centriacinar emphysema? Why?

A

This is caused by smoking, since V/Q is highest in upper lobes they are the best ventilated

147
Q

Where does mutant A1AT accumulate?

A

endoplasmic reticulum of hepatocytes

148
Q

What is the normal allele for A1AT? Mutant Allele? What is the inheritance pattern?

A

PiM, PiZ; it is codominant so PiMZ is less serious unless they smoke and PiZZ is serious

149
Q

Why are ppl with emphysema usually skinny?

A

They need to do more “exercise” to get the air out

150
Q

Why does COPD lead to cor pulmonale?

A

Hypoxic vasoconstriction increases pulmonary resistance

151
Q

What is the usual cause of airway obstruction in asthma?

A

allergic stimuli

152
Q

Explain the pathogenesis of asthma (the immunology of)

A

allergens stimulate CD4 to differentiate into Th2 which produce IL-4, IL-5, and IL-10? The IgE produced from IL-4 induced class-switching will sensitize mast cells

153
Q

What interleukin is directly responsible for charcot-leyden crystals?

A

IL-5 attracts eosinophils (however, IL-4 causes IgE production which sensitizes mast cells and they release eosinophil chemotactic factor)

154
Q

What do leukotrienes C4, D4, and E4 do in asthma?

A

bronchoconstriction

155
Q

Most severe sequela of asthma

A

status asthmaticus

156
Q

Tx of aspirin induced asthma

A

montelukast

157
Q

What 2 populations are most likely to get allergic bronchopulmonary aspergillosis?

A

Asthmatics and Cystic fibrosis

158
Q

What kind of amyloidosis would develop in ABPA?

A

Secondary amyloidosis i.e. SAA –> AA from chronic infection (anemia of chronic disease is also likely)

159
Q

What cells are responsible for fibrosis in idiopathic intersitial fibrosis?

A

TGF-B from type II pneumocytes leads to activation of fibroblasts

160
Q

Where does fibrosis usually begin in idiopathic pulmonary fibrosis? What is the end-stage?

A

subpleural; honeycomb lung

161
Q

What cells are responsible for fibrosis in pneumoconioses?

A

MO because they engulf antigen and cause fibrosis

162
Q

What pneumoconiosis can cause non-caseating granulomas?

A

Berryliosis; assoc. with aerospace stuff? Be sure to differentiate from sarcoidosis

163
Q

What inclusions are seen in sarcoidosis?

A

asteroid bodies

164
Q

Dermatologic finding in sarcoidosis

A

erythema nodosum

165
Q

What is coal workers pneumoconiosis with rheumatoid arthritis?

A

Caplan syndrome

166
Q

Who gets silicosis?

A

sandblasters and silica miners (increase risk of TB)

167
Q

What kind of inflammation occurs in hypersensitivity pneumonitis?

A

granulomatous

168
Q

What is seen on microscopy in severe, long-standing pulmonary HTN?

A

plexiform lesions (tufts of capillaries blown out from the artery)

169
Q

Diffuse alveolar damage characterizes

A

ARDS (along with hyaline membranes)

170
Q

What causes the formation of hyaline membranes in ARDS?

A

There is diffuse alveolar damage, the leakage of proteins into the necrotic mix causes hyaline membranes to form

171
Q

White out on CXR

A

ARDS

172
Q

The fact that ARDS can be complicated by fibrosis is a testament to the loss of which cell?

A

Type II pneumocyte (the basal cell of the lung)

173
Q

What is the point of PEEP in ARDS?

A

Their lungs collapse easily due to the damage. So Positive END EXPIRATORY pressure keeps them open a bit when finishing the expiration

174
Q

What is the difference between ARDS and neonatal RDS?

A

ARDS = diffuse alveolar damage; neonatal RDS = lack of surfactant so has patchy atelectasis; however, hyaline membranes can still form

175
Q

Diffuse granularity (ground glass) CXR of newborn

A

neonatal RDS

176
Q

What is the most likely cause of bronchopulmonary dysplasia in an infant?

A

Tx with supplemental O2 for neonatal RDS (other AE = retinopathy of prematurity)

177
Q

Why would someones basement give them lung cancer?

A

If there is radon it can decay to uranium leading to ionizing radiation of the lungs

178
Q

What is a benign tumor in the lung composed of lung tissue and cartilage?

A

bronchial hamartoma

179
Q

Most common tumor in male smokers

A

SCC of lung

180
Q

Where does bronchioloalveolar carcinoma come from?

A

Clara cells

181
Q

Lung cancer arising from Clara cells?

A

Bronchioloalveolar carcinoma (lepidic growth pattern, good prognosis)

182
Q

Which lung tumor is chromogranin positive?

A

Carcinoid tumor (bronchial polyp) NOTE there is another card in here that says small cell CA is, I am not sure if that is true, ignore

183
Q

What are the intercellular bridges of SCC of lung?

A

desmosomes

184
Q

Benign bronchial polypoid lesion; malignant? Stain?

A

Bronchial hamartoma; Carcinoid (chromogranin)

185
Q

Unique site of lung cancer metastasis

A

adrenal gland

186
Q

Which cancer is a primary pleural cancer? A metastasis to it?

A

mesothelioma; adenocarcinoma

PATHOMA/FA SYSTEMS (10 decks)

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