Resp Flashcards
1
Q
Lung development stages?
A
stage 1: embryonic (wks 4-7) stage 2: pseudoglandular (wks 5-17) stage 3:canalicular (wks 16-25) stage 4: saccular (wks 26-birth) stage 5:alveolar (wk 36-8 years)
2
Q
Embryonic stage of lung development
A
lung bud –> trachea –> bronchial buds –> mainstem bronchi –> secondary (lobar) bronchi –> tertiary (Segmental) bronchi
3
Q
error at what stage of lung development results in a tracheoesophageal fistula
A
at the embryonic stage at wks 4-7
4
Q
Pseudoglandular stage of lung development (wks 5-17)
A
endodermal tubules –> terminal bronchioles
surrounded by modest capillary network
respiration impossible and incompatible with life
5
Q
Canalicular stage of lung development (wks 16-25)
A
Terminal bronchioles –> respiratory bronchioles –> alveiolar ducts
surrounded by a prominent capillary network
airways increase in diameter
6
Q
respiration is capable at what week
A
25 wks
7
Q
pneumocytes develop starting at
A
20 weeks
8
Q
Saccular stage of lung development (wks 26-birth)
A
alveolar ducts –> terminal sacs which are separated by primary septae
9
Q
Alveolar stage of lung development (wks 36- 8 years)
A
Terminal sacs become adult alveoli due to secondary septation
10
Q
In utero breathing occurs via aspiration and expulsion of amniotic fluid which increases vascular resistance through gestation. What happens/changes at birth?
A
at birth fluid gets replaced with air and there is a decrease in pulmonary vascular resistance
11
Q
This congenital lung malformation is a poorly developed bronchial tree with abnormal histology
A
pulmonary hypoplasia
associated with congenital diaphragmatic hernia thats usually on the left side and bilateral renal agenesis (potter sequence)
12
Q
Congenital lung malformation that is caused by abnormal budding of the foregut and dilation of terminal or large bronchi. Discrete, round, sharply defined, fluid filled densities on CXR (air filled if infected)
A
bronchogenic cysts
usually asymptomatic but can cause respiratory infections
13
Q
__ cells are located in bronchioles and are important for degrading toxins and secreting a component of surfactant
A
Club cells
nonciliated
low columnar/cuboidal with secretory granules
act as reserve cells
14
Q
Type 1 pneumocytes
A
97% of alveolar surfaces
line the alveoli
squamous
Thin for optimal gas diffusion
15
Q
Type II pneumocytes
A
Secrete surfactant from lamellar bodies and decrease alveolar surface tension –> prevent alveolar collapse, decrease lung recoil, and increase compliance
cuboidal and clustered
16
Q
What type of pneumocyte proliferates during lung damage
A
Type II pneumocyte
serve as a precursor for type I cells and other type II cells
17
Q
Collapsing pressure equation
A
P=(2*surface tension)/radius
on expiration: radius decreases therefore higher chance of collapse
18
Q
Pulmonary surfactant is a complex mix mix of lecithins, the most important of which is ______
A
DPPC
dipalmitoylphosphatidylcholine
19
Q
when does surfactant synthesis begin? when are mature levels reached?
A
beings at 20 wk
mature levels reached at week 35
20
Q
______ are important for fetus surfactant production and lung development
A
corticosteroids
21
Q
Alveolar macrophage function to ____________ and release ________ and _________
A
phagocytose foreign materials
release cytokines and alveolar proteases
22
Q
__________ macrophages may be seen in pulmonary hemorrhage
A
hemosiderin-laden
23
Q
Surfactant deficiency in a neonate can result in? why? how does it appear on xray?
A
neonatal respiratory distress syndrome
low surfactant will increase surface tension and ultimately alveolar collapse
“ground glass appearance”
24
Q
Important risk factors for neonatal respiratory distress syndrome
A
1) prematurity
2) maternal diabetes due to increase in fetal insulin
3) c section delivery due to decrease of fetal glucocorticoids because it is less stressful than vaginal delivery
25
Treatment for neonatal respiratory distress syndrome
maternal steroids before brith
exogenous surfactant for infant
26
Therapeutic supplemental O2 can result in what three things?
1) retinopathy of prematurity
2) intraventricular hemorrhage
3) bronchopulmonary dysplasia
"RIB"
27
What is the screening test for fetal lung maturity
lecithin-sphingomyelin ratio in amniotic fluid
>= 2 is healthy
<1.5 is predictive of neonatal respiratory distress syndrome
can also look at foam stability index and surfactant-albumin ratio
28
persistently low O2 tension can increase the risk of
PDA
29
Where is there the least airway resistance
terminal bronchioles because there is a large number in parallel
30
conducting zone of the lung
(Trachea --> bronchi --> bronchioles --> terminal bronchioles
anatomic dead space because it does not participate in gas exchange
31
cartilage and goblet cells extend to the end of ____
bronchi
32
Cell types within the respiratory tree
- Trachea and bronchi : pseudostratified ciliated columnar epithelium + basal cells + goblet cells
- Bronchioles: simple ciliated columnar epithelium + club cells
- Terminal bronchioles: simple cuboidal epithelium + club cells
- Respiratory bronchioles: simple cuboidal and squamous epithelium + club cells
- Alveolar sacs: Type I pneumocytes + type II pneumocytes +alveolar macrophages (clear debris and immune response)
33
Respiratory zone
respiratory bronchioles --> alveolar sacs
participate in gas exchange
34
cilia terminate in the _________
respiratory bronchioles
35
Left lung
"Left is Less"
2 lobes + lingula (homolog of R middle lobe)
only an oblique fissure
instead of a middle lobe, the left lung has a space occupied by the heart
36
Right lung
3 lobes
37
carina is ____ to the ascending aorta and ___ to the descending aorta
posterior
anteromedial
38
Where do inhaled foreign bodies usually go to
right lung because the right mainstem bronchus is wider and more vertical and shorter
39
If you inhale a peanut while supine? while laying on right side? while upright?
if suprine --> right lower lobe
If lying on R side --> right upper lobe
If upright --> right lower lobe
40
needle for tension pneumothorax should be positioned between the
2nd and 3rd left ribs
41
diaphragm structures @ T8
IVC and R phrenic nerve
42
diaphragm structures @ T10
esophagus and vagus nerve
43
diaphragm structures @ T12
aorta
thoracic duct
azygos vein
1 and 2 is red,white, and blue
44
diaphragm structures mnemonic
I 8 10 eggs at 12
8=IVC
10=esophagus
12=aorta
45
Diaphragm is innervated by C____ (phrenic nerve). Pain can be referred to the shoulder via C ___ and trapezius ridge via C __ and ___
C3,4,5
C5 --> shoulder
C3 and 4 --> trapezius ridge
46
The common carotid bifurcates at?
bi"four"cates therefore C4
47
The trachea bifurcates at?
bi"four"cates therefore T4
48
The abdominal aorta bifurcates at?
bi"four"cates therefore L4
49
Air that can still be breathed in after normal inspiration
inspiratory reserve volume
50
Ait that moves into lung with each quiet inspiration typically 500 ml
tidal volume
51
Air that can still be breathed out after normal expiration
expiratory reserve volume
52
Air in lung after maximal expiration
residual volume
53
what cannot be measured by spirometry in terms of lung volumes
residual volume and anything that includes residual volume (functional residual capacity and total lung capacity)
54
Air that can be breathed in after normal exhalation
inspiratory capacity
IRV + TV
55
Volume of gas in lungs after normal expiration
functional residual capacity
RV+ERV
56
Maximum volume of gas that can be expired after a maximal inspiration
Vital capacity
TV+IRV +ERV
57
Volume of gas present in lungs after a maximal inspiration
total lung capacity
IRV+TV+ERV+RV
58
What is the largest contributor to alveolar dead space
apex of a healthy lung
59
Vd or physiologic dead space
Vd=physiologic dead space= anatomic dead space of conducting airways + alveolar dead space
it is the volume of inspired air that does not take part in gas exchange
60
physiologic dead space equation
Vs=Tidal volume ((arterial PCO2-expired air PCO2)/arterial PCO2)
"Paco Peco Paco"
61
physiologic dead space is _____ to anatomic dead space in normal lungs
approx. equivalent
may be greater than anatomic dead space in lugn diseases with V/Q defect
62
Minute ventilation equation
total volume of gas entering lungs per minute
Ve=Vt x RR
Vt= 500 mL/breath
RR=12-20
63
Alveolar ventilation equation
volume of gas that reaches alveoli each minute
Va=(Vt-Vd)RR
Vt=500 mL/breath
Vd=150 mL/breath
RR=12-20
64
Elastic recoil
tendency for lungs to collapse inward and chest wall to spring outward
this is balanced at the functional residual capacity or the volume of gas in lungs after normal expiration
65
compliance
change in volume/ change in pressure
ex) high compliance is seen in old age and emphysema
66
what is surfactants effect on compliance
it increases compliance
67
Hysteresis
lung inflation curve follows a different curve than the lung deflation curve due to need to overcome surface tension forces in inflation
68
Respiratory system changes in the elderly
- increase lung compliance
- decrease chest wall compliance
- increase residual volume
- decreased FVC and FEV1
- Normal TLC
- Increase ventilation/perfusion mismatch
- increased A-a gradient
- decreased resp muscle strength
69
Hemoglobin is composed of _____ polypeptide subunits. ____ alpha and ___ beta.
4
2 alpha and 2 beta
70
Deoxygenated form of hemoglobin
low affinity for O2
so that it can release/unload O2
71
Oxygenated form of hemoglobin
high affinity for O2 (x300)
+ cooperativity
- allostery
72
Right shift on the hemoglobin dissociation curve indicates
increased O2 unloading (deoxygenated form)
due to increased Cl-, H+, CO2, 2,3 BPG, temp
73
Left shift on the hemoglobin dissociation curve indicated
decreased O2 unloading (oxygenated form of hemoglobin)
74
Fetal hemoglobin components and O2 affinity compared to adult
2alpha
2gamma
higher affinity for O2 --> drives O2 diffusion from mother to child across placenta
75
Why does fetal hemoglobin have an increased affinity for O2
-oxygenated form of hemoglobin /decreased O2 unloading due to low affinity of HbF for 2,3 BPG. This shifts the curve to the left
76
Hemoglobin acts as a buffer for ___ ions
H+
77
Myoglobin
single polypeptide chain associated with one heme moiety
higher affinity for oxygen than Hb
78
Patient presents with cyanosis and chocolate colored blood. What is the patient likely suffering from? What causes it? What is the pathophys? how is it treated?
Methemoglobin- Oxidized form of Hb (ferric Fe 3+) does not bind O2 as readily as Fe2+ (normal reduced form) but has greater affinity for cyanide
Can be caused by nitrites and benzocaine which cause poisoning by oxidizing Fe2+ to Fe3+
treat with methylene blue and vitamin C
79
Carboxyhemoglobin
Form of Hb bound to CO in place of O2
causes decrease in oxygen binding capacity with left shift in oxygen hemoglobin dissociation curve --> lower O2 unloading in tissues
CO binds competitively to hemoglobin and with 200X greater affinity than O2
80
Patient presents with headaches, dizziness, and cherry red skin
CO poisoning
treat with 100% O2 and hyperbaric O2
81
Patient presents with almond breath odor, pink skin, and cyanosis
Cyanide poisoning
Inhibits aerobic metabolism via complex 4 inhibition --> hypoxia unresponsive to supplemental O2 and increase anaerobic metabolism
82
how do you treat cyanide poisoning
first give nitrites which oxidizes hemoglobin to methemoglobin (can trap cyanide as cyanmethemoglobin)
Then give thiosulfates which convert cyanide to thiocyanate --> renally excreted
83
The hemoglobin curve is ___ shaped due to ____. The myoglobin curve lacks this shaped because it is monomeric and does not show _____
sigmoid shaped
positive cooperativity
positive cooperativity
84
Shifting the oxygen dissociation curve to the right results in
decreased Hb affinity for O2 which facilitates unloading of O2 to tissue. Therefore the P50 increases indicating that a higher PO2 is required to maintain 50% saturation
- increased H+
- drop in PH or increase acid
- Exercise
- Increase 2,3-BPG
- High altitude
- Increased temperature
85
Shifting the oxygen dissociation curve to the left
means there is decreased O2 unloading
think left=lower O2 unloading
- drop in H+
- increase in pH or base
- drop in 2,3-BPG
- drop in temperature
86
Decreased O2 unloading results in renal hypoxia which increases
EPO synthesis and results in compensatory erythrocytosis
87
O2 content in blood
(1.34 x (hemoglobin level) x (arterial O2 saturation) ) + (0.003xPaO2)
88
normal hemoglobin amount
15 g/dL
89
If there is a drop in Hb, what happens to the O2 content of blood, the O2 saturation, and the partial pressure of O2 in arterial blood
O2 content drops
No change in O2 saturation
No change in PaO2/Partial pressure of O2 in arterial blood
90
A decrease in pAO2 causes what response?
hypoxic vasocontriction that shifts blood away from poorly ventilated regions of lung to well-ventilated regions of lung
91
Perfusion limited
Rate at which gas is transported away from functioning alveoli and into tissues is principally limited by the rate of blood flow through the pulmonary capillaries and thus across the alveolar membrane.
on graph it increases and then plateau early. Gas equilibrates early along the length of the capillary. Diffusion can be increased only if increase in blood flow
related to O2 (normal health), CO2, N2O
92
Diffusion limited
Gas does not equilibrate by the time blood reaches the end of the capillary
O2 (emphysema, fibrosis, exercise) and CO
93
What is a consequence of pulmonary hypertension
cor pulmonale or abnormal enlargement of R side of heart
subsequent right ventricular failure
94
Diffusion eq
V gas= Area x Diffusion coefficient x ((different in partial pressures)/alveolar wall thickness)
area decreases in emphysema
alveolar wall thickness increases in fibrosis
95
Dlco
the extent to which CO a surrogate for O2 passes from air sacs of lungs into blood
96
PVR or pulmn vasc. resistance equation
(pressure in pulm artery - pulmonary capillary wedge pressure) / cardiac output
97
Alveolar gas eq
PAO2=150-PaCO2/0.8
0.8 is resp quotient= CO2 produced/O2 consumed
98
A-a gradient
PAO2-PaO2 = normal is 10-15 mm Hg
gradient increases in hypoxemia which is caused by shunting, V/Q mismatch, fibrosis because they impair diffusion
99
Define hypoxia
decreased O2 delivery to tissue
100
Define hypoxemia
decrease PaO2
101
What causes hypoxemia
a decrease in PaO2 is caused by:
high altitude and hypoventilation - these have normal A-a gradient
V/Q mismatch, Diffusion limitation, Right to left shunt - these have increased A-a gradient
102
V/Q mismatch
ventilation/perfusion mismatch
103
Where in the lung is there wasted ventilation and what does this show in reference to the V/Q mismatch
V/Q mismatch at apex of lung = 3 which indicated wasted ventilation. Increase in V but great decrease in Q
organisms that thrive in O2 like TB flourish in the apex
104
Where in the lung is there wasted perfusion and what does this show in reference to the V/Q mismatch
V/Q mismatch at base of lung=0.6 which indicated wasted perfusion. Increase in V but greater increase in Q
note: both ventilation and perfusion are greater at the base of the lung
105
What happens to the V/Q mismatch during these changes:
1) exercise
2) airway obstruction
3) blood flow obstruction
1) increase in cardiac output which causes vasodilation of apical capillaries and thus V/Q ratio approaches 1
2) V/Q=0 during airway obstruction (shunt). In a shunt, 100% O2 does not improve PaO2. ex is foreign body aspiration
3) V/Q=infiniti during blood flow obstruction (physiological dead space). Assuming <100% dead space, 100% O2 improves the PaO2. ex is pulmonary embolus
106
Co2 is transported from tissue to lungs in 3 forms:
1) HCO3 (70%)
2) Carbaminohemoglobin or HbCO2 (21-25%)
3) Dissolved CO2
note: CO2 bound to Hb at N-terminus of globin (not heme). CO2 favors deoxygenated form (O2 unloaded)
107
In the lung, oxygenation of Hb promotes dissociation of ____ from Hb. This shifts equilibrium towards CO2 formation and therefore CO2 is released from RBCs. This is called the
Halfane effect
108
In peripheral tissues, increase in _____ in tissue metabolism shifts curve to the right, and unloading O2. This is called the
bohr effect
109
CO2 enters RBC and is converted to HCO3 via
carbonic anyhdrase
first becomes H2CO3 then converts to HCO3
110
What is your bodies response to high altitude
decrease in atmospheric oxyen causes a drop in PaO2 and an increase in ventilation. The increase in ventilation causes a drop in PaCO2. This causes respiratory alkalosis aka altitude sickness
111
Besides resp alkalosis causing high altitude sickness, what other changes occur in the body
- increase in erythropoietin due to chronic hypoxia which increase hct and hv
- increase 2,3 BPG which binds to Hb and causes a right shift so that Hb releases more O2
- increase in mitochondria
- increased renal excretion of HCO3 to compensate for resp alkalosis
- chronic hypoxic pulmonary vasoconstriction results in pulmonary hypertension and RVH
112
Bodies response to exercise
V/Q ratio from apex to base become more uniform
decrease in pH during strenuous exercise thats secondary to lactic acidosis
No change in PaO2 and PaCO2
113
Rhinosinusitis
obstruction of sinus drainage into nasal cavity
114
Rhinosinusitis typically affects what sinuses and why
typically affects maxillary sinuses which drain against gravity due to ostia located superomedially
115
What is the most common cause of rhinosinusitis
most common acute cause is viral URI but it may lead to superimposed bacterial infections, most commonly S. pneumo, H influenzae, M catarrhalis
116
Infections in sphenoid or ____ sinuses may extend to the cavernous sinus and cause
cavernous sinus syndrome - ophthalmoplegia, proptosis, ocular and conjunctival congestion, trigeminal sensory loss and Horner's syndrome. These signs and symptoms result from the involvement of the cranial nerves passing through the cavernous sinus.
117
Epistaxis define? Where does it occur most commonly? related to what plexus?
epistaxis is nose bleed
most commonly occurs in anterior segment of nostril
at the kiesselbach plexus - superior labial artery, anterior and posterior ethmoidal arteries, greater palatine artery, sphenopalatine artery
118
Life threatening hemorrhages occur in the ____ segment of the nose. This is because of what artery?
posterior segment
sphenopalatine artery, a branch of maxillary artery
119
Head and neck cancers are mostly
Squamous cell carcinomas
Oropharyngeal - HPV16
Nasophayngeal - EBV
field cancerization is when carcinogen damages wide mucosal area and results in multiple tumors that develop independently after exposure
120
Deep venous thrombosis
presents with swelling, redness, warmth, and pain
predisposed by the Virchow triad (stasis, hypercoagulability, endothelial damage)
can use D-dimer to rule out DVT but it is not very specific
treat with
121
Most pulmonary emboli arise from
proximal deep veins of lower extremity
122
Patient presents with sudden onset dyspnea, pleuritic chest pain, tachypnea, and tachycardia, Patient dies and on autopsy you find a saddle embolis
Pulmonary emboli causing electromechanical dissociation
123
How do you know a thrombi was formed before death vs after death
Lines of zahn are interdigiting areas of pink (platelets, fibrin) and red (RBCs) found only in thrombi formed before death
they help distinguish pre and post mortem thrombi
124
Patient presents with triad of hypoxemia, neurologic abnormalities, and petechial rash
fat emboli
125
decompression sickness/caisson disease
air emboli - nitrogen bubbles precipitate in ascending divers
tx with hyperbaric O2
126
Amniotic fluid emboli can lead to
DIC
especially post partum
127
Obstructive lung disease
```
RV
FRC
TLC
FEV1
FVC
FEV1/FVC
```
```
RV increased
FRC increased
TLC increased
FEV1 very low
FVC decreased
FEV1/FVC decreased (HALLMARK)
```
loop shifts to the left and looks like a slide
128
Restrictive lung disease
```
RV
FRC
TLC
FEV1
FVC
FEV1/FVC
```
```
RV decreased
FRC decreased
TLC decreased
FEV1 decreased
FVC decreased
FEV1/FVC normal or increased because FEV1 decreased proportionately to FVC
```
loop shifts to the right
129
Obstructive lung disease
chronic bronchitis
emphysema
Asthma
130
Patient presents with wheezing, crackles, cyanosis, dyspnea, CO2 retention, secondary polycythemia. She mentions having a productive cough for more than 3 months in the past year and that this has happened for 2 consecutive years. What does she have? what kind of lung disease is it? and what is the pathology?
Chronic bronchitis - obstructive lung disease
hypertrophy and hyperplasia of mucus-secreting glands in bronchi --> reid index > 50%
reid index is thickness of mucosal gland layer to thickness of wall between epithelium and cartilage
DLCO normal
131
Patient presents with a barrel shaped chest and complain that she only feels comfortable upon exhalation through pursed lip. What does she have? what kind of lung disease? why does she purse her lips?
Emphysema- obstructive lung disease
increases airway pressure and prevents airway collapse
chest xray shows increased AP diameter, flattened diaphragm, and increased lung field lucency
drop in DLCO from destruction of alveolar walls
imbalance of proteases and antiproteases causes increased elastase activity and increased loss of elastic fibers --> increased lung compliance
132
Centriacinar emphysema
associated with smoking because smoke rises up to upper lobes
133
Panacinar emphysema
associated with alpha1-antitrypsin deficiency frequently in lower lobes
134
Patent presents with coughing, wheezing, decreased inspiratory/expiratory ratio, pulsus paradoxus, mucus plugging and was unable to do the methacholine challenge
Asthma- obstructive lung disease
hyperresponsive bronchi - reversible bronchoconstriction
smooth mm hypertrophy and hyperplasia
curschmann spirals (shed epithelium forms whorled mucous plugs)
charcot leyden crystals (eosinophilic hexagonal double pointed crystals formed from breakdown of eosinophils in sputum)
DLCO normal or increased
135
Patient has cystic fibrosis and presents with purulent sputum, recurrent infections, hemoptysis, and digital clubbing. What type of lung disease are we most worried about
bronchiectasis- obstructive lung disease
chronic necrotizing infection of bronchi or obstruction that permanently dilates airways
associated with bronchial obstruction, poor ciliary motility, CF, and allergic bronchopulmonary aspergillosis
136
Restrictive lung diseases
decreased FVC
increased FEV1/FVC ratio
can be due to poor breathing mechanics (poor mm effort of structural apparatus) OR interstitial lung diseases that decrease pulmonary diffusing capacity and increase A-a gradient
137
hypersensitivity pneumonitis
mixed type III/IV hypersensitivity reaction to environmental antigen
dyspnea, cough, chest tightness, headache
reversible in early stages
usually associated with farmers and those exposed to birds
138
Sarcoidosis
immune mediated widespread noncaseating granulomas, elevated serum ACE levels, and elevated CD4+/CD8+ ratio in bronchoalveolar lavage fluid
patients are often asymptomatic except for enlarged lymph nodes, CXR of bilateral adenopathy and coarse reticular opacities, CT of chest better demonstrates the extensive hilar and mediastinal adenopathy
139
What is sarcoidosis associated with
- Bells palsy
- Uveitis
- Granulomas - contain schaumann and asteroid bodies
- Lupus pernio - skin lesions on face resemble lupus
- Interstitial fibrosis (restrictive lung dz)
- Erythema nodosum
- Rheumatoid arthritis-like arthropathy
- Hypercalcemia due to increased 1αhydroxylase --mediated vitamin D activation in macrophages
140
Treat patients with sarcoidosis with
steroids
141
Inhalation injury
chemical tracheobronchitis,edema,pneumonia, ARDS
142
Patient is a roofer that has "ivory white", calcified supradiaphragmatic and pleural plaques. What does the patient have and in what lobes do you commonly see affect? What are the risks?
asbestos is a form of pneumoconioses
lower lobes
risk of bronchogenic cancer
143
What is the hallmark sign on prussian blue stain of bronchoalveolar lavage
ferruginous bodies are golden-brown fusiform rods resembling dumbbells
144
berylliosis
beryllium is a form of pneumoconioses
upper lobes
granulomatous (noncaseating)
increased risk of cancer and cor pulmonale
145
Coal workers pneumoconiosis
macrophages laden with carbon cause inflammation and fibrosis in upper lobes
called black lung disease
affects upper lungs
increased risk of caplan syndrome or rheumatoid arthritis and pneumoconiosis with intrapulmonary nodules
146
Anthracosis
asymptomatic condition found in many urban dwellers exposed to sooty air
147
silicosis
macrophages respond to silica and release fibrogenic factors that lead to fibrosis
form of pneumoconiosis that affects upper lobes
silica may disrupt phagolysosomes and impair macrophages and increase susceptibility to TB. Increased risk of cancer, cor pulmonale, and caplan syndrome
see eggshell calcification of hilar lymph nodes on CXR
148
Mesothelioma
malignancy of the pleura associated with asbestosis
hemorrhagic pleural effusion (exudative) and pleural thickening
psammoma bodies and calretinin +
smoking is not a risk factor
149
The most common cause of acute respiratory distress syndrome
sepsis
150
ACute respiratory distress syndrome pathophys
alveolar insult causes release of proinflammatory cytokines
these cytokines result in neutrophil recruitment, activation,and release of toxic mediators causing capillary endothelial damage and increased vessel permeability
protein rich fluid leaks into alveoli and causes formation of intra alveolar hyaline membranes and noncardiogenic pulmonary edema
151
diagnosis of ARDS (acute resp distress syndrome)
- Abnormal chest xray (bilateral lung opacities)
- Respiratory failure within 1 week of alveolar insult
- Decreased PaO2/FiO2 (ratio <300, hypoxemia due to shunting and diffusion abnormalities
- Symptoms of respiratory failure are not due to HF/fluid overload
152
sleep apnea involves the cessation of breathing for greater than ___ seconds
10 seconds
results in nocturnal hypoxia which causes systemic/pulmonary hypertension, arrhythmias (a fib/flutter), sudden death
153
obstructive sleep apnea in adults vs children
adults have excess parapharyngeal tissue
| children have adenotonsillar hypertrophy
154
central sleep apnea
impaired respiratory effort due to CNS injury/toxicity, HF, opioids
may be associated with cheyne-stokes repirations - oscillation between apnea and hyperpnea
treat with positive airway pressure
155
obesity hypoventilation syndrome /Pickwickian syndrome
obesity >= 30 BMI
hypoventilation causes increased PaCO2 during waking hours (Retention) and a drop in PaO2 and increase PaCO2 during sleep
156
pulmonary hypertension is defined as a mean pulmonary artery pressure >=
25 mm Hg
normal is 10-14 mm hg
results in arteriosclerosis, medial hypertrophy, intimal fibrosis of pulmonary arteries, plexiform lesions
157
pulmonary hypertension course
severe respiratory distress causes cyanosis and RVH --> death from decompensated cor pulmonale
158
Heritable PAH (pulm art. hypertension)
Inactivating mutation in BMPR2 gene (normally inhibits vascular smooth mm proliferation)
159
PAH can also be due to pulmonary vasculature endothelial dysfunction which results in
increased vasocontrictors (endothelin) and decreased vasodilatory (NO and prostacyclins)
160
pulmonary hypertension can also be caused by chronic thromboembolic
recurrent microthrombi which decreased cross sectional area of pulmonary cascular bed
161
Breath sounds in:
1) pleural effusion
2) atelectasis (bronchial obstruction)
3) simple pneumothroax
4) tension pneumothorax
5) consolidation
decreased in all except in consolidation we see bronchial breath sounds, late inspiratory crackles, egophony, whispered pectoriloquy
162
Percussion in :
1) pleural effusion
2) atelectasis (bronchial obstruction)
3) simple pneumothroax
4) tension pneumothorax
5) consolidation
1) pleural effusion - dull
2) atelectasis (bronchial obstruction) - dull
3) simple pneumothroax - hyperresonant
4) tension pneumothorax - hyperresonant
5) consolidation - dull
163
fremitus in
1) pleural effusion
2) atelectasis (bronchial obstruction)
3) simple pneumothroax
4) tension pneumothorax
5) consolidation
decreased except in consolidation (lobar pneumo or pulm edema)
164
Tracheal deviation in
1) pleural effusion
2) atelectasis (bronchial obstruction)
3) simple pneumothroax
4) tension pneumothorax
5) consolidation
1) pleural effusion --> none if small ; away from side of lesion if large
2) atelectasis (bronchial obstruction) --> toward side of lesion
3) simple pneumothroax --> none
4) tension pneumothorax --> away from side of lesion
5) consolidation --> none
165
tension vs simple pneumothorax
Tension pneumothorax is the progressive build-up of air within the pleural space, usually due to a lung laceration which allows air to escape into the pleural space but not to return. Positive pressure ventilation may exacerbate this 'one-way-valve' effect.
A simple pneumothorax is a non-expanding collection of air around the lung. The lung is collapsed, to a variable extent.
166
pleural effusion
excess accumulation of fluid between pleural layers that cause restricted lung expansion during inspiration
can be treated with thoracentesis to remove/reduce fluid
167
pleural effusion: transudate
decreased protein content
due to increased hydrostatic pressure or decreased oncotic pressure
168
pleural effusion: exudate
increased protein content, cloudy
due to malignancy, pneumonia, collagen vascular disease, trauma
occurs in states of increase vascular permeability
must be drained due to risk of infection
169
pleural effusion: lymphatic
chylothorax
due to thoracic duct injury from trauma or malignancy
milky appearing fluid
increased triglycerides
170
Primary spontaneous pneumothorax
due to rupture of apical subpleural bleb or cysts
occurs most frequently in tall, thin, young males and smokers
171
Secondary spontaneous pneumothorax
due to diseased lung, mechnical ventilation with use of high pressures which result in barotrauma
172
Traumatic pneumothorax
caused by blunt, penetrating, or iatrogenic trauma ( central line placement,lung biopsy, barotrauma due to mechanical ventilation)
173
tension pneumothorax
can be from any trauma pneumothorax causes
air enters the pleural space but cannot exit. Increased trapped air causes tension pneumothorax. Trachea deviates away from the affected lung
174
Lobar pneumonia typical organisms
S pneumo most common
legionella
klebsiella
175
lobar pneumonia characterisitcs
intra alveolar exudate leading to consolidation
can involve entire lobe or whole lung
176
bronchopneumonia typical organisms
S pneumo, S aureus, H influenzae, Klebsiella
177
bronchopneumonia characteristics
acute inflammatory infiltrates from bronchioles into adjacent alveoli
patchy distribution involving >=1 lobe
178
Interstitial atypical pneumonia typical organisms
```
mycoplasma
chlamydophila pneumo
chlamydophila psittaci
legionella
viruses (RSV,CMV, influenza, adenovirus)
```
179
Interstitial atypical pneumonia characteristics
diffuse patchy inflammation localized to interstitial areas at alveolar walls
diffuse distribution involving >=1 lobe
"walking pneumonia"
180
Cryptogenic organizing pneumonia
caused by chronic inflammatory disease or medication side effects
negative sputum and blood cultures, no response to antibiotics
noninfectious pneumonia characterized by inflammation of bronchioles and surrounding structures
used to be called bronchiolitis obliterans organizing pneumonia
181
natural history of lobar pneumonia
congestion --> red hepatization --> gray hepatization --> resolution
182
sites of metastasis for lung cancer:
adrenals
brain
bone
liver
183
lung cancer most commonly from
breast
colon
prostate
bladder cancer
184
lung cancer complications
```
superior vena cava/thoracic outlet syndromes
pancoast tumor
horner syndrome
endocrine (paraneoplastic)
recurrent laryngeal nerve compression
Effusions
```
185
lung cancers most commonly caused by smoking
squamous and small cell carcinomas
which are also centrally located
186
small cell carcinoma lung cancer
central location
undifferentiated and very aggressive
may produce ACTH(cushing syndrome), SIADH, or antibodies against presynaptic Ca channels (lambert eaton myasthenic syndrome) or neurons (paraneoplastic myelitis, encephalitis, subacute cerebellar degeneration)
amplification of myc oncogenes
187
histology of small cell carcinoma lung cancer
neoplasm of neuroendocrine Kulchitsky cells causing small dark blue cells
chromogranin A +, neuron specific enolase +, synaptophysin +
188
non small cell lung cancers
- adenocarcinoma
- squamous cell carcinoma
- large cell carcinoma
- bronchial carcinoid tumor
189
adenocarcinoma of lung
- found in periphery
- most common primary lung cancer
- nonsmokers
- activating mutations: KRAS, EGFR,ALK
- associated with hypertrophic osteoarthropathy (clubbing)
- bronchioalveolar subtype
- glandular pattern on histology which stains mucin +
190
bronchioloalveolar is subtype of
adenocarcinoma in situ
CXR shows hazy infiltrates similar to pneumonia
grows along alveolar septa with apparent thickening of alveolar walls. Tall columnar cells containing mucus
191
what two lung cancers have less association with smoking
bronchial carcinoid and bronchioloalveolar cell carcinoma
192
squamous cell carcinoma
central
hilar mass arising from bronchus
cavitation, cigarettes, hypercalcemia (produces PTHrP)
keratin pearls and intercellular bridges
193
Large cell carcinoma
peripheral
highly anaplastic undifferentiated tumor with poor prognosis
strong association with smoking
pleomorphic giant cells
194
Bronchial carcinoid tumour
central or peripheral
excellent prognosis, metastasis is rare
symptoms due to mass effect of carcinoid syndrome (flushing, diarrhea, wheezing)
nests of neuroendocrine cells, chromogranin A +
195
Lung abscess on chest xray
air fluid levels often see on CXR
presence suggests cavitation due to anaerobes or s aureus
196
what side of the lung do you commonly see a lung acscess that secondary to aspiration
right lung
197
This is a carcinoma that occurs in the apex of the lung and may cause destructive lesions of the thoracic inlet and involvement of the brachial plexus and cervical sympathetic nerves (stellate ganglion)
pancoast tumor or superior sulcus tumor causing pancoast syndrome by invading cervical sympathetic chain
198
pancoast tumor can compress locoregional structures:
```
recurrent laryngeal:
stellate ganglion:
superior vena cava:
brachiocephalic vein:
brachial plexus:
```
recurrent laryngeal: hoarseness
stellate ganglion: horner syndrome (ipsilateral ptosis, miosis, anhidrosis)
superior vena cava: SVC syndrome
brachiocephalic vein: brachiocephalic syndrome (unilateral symptoms)
brachial plexus: sensorimotor deficits
199
Superior vena cava syndrome
an obstruction of the SVC that impairs blood drainage from the head ( facial plethora)
note blanching after fingertip pressure
JVD
edema in UE
commonly caused by malignancy and thrombosis
can rise ICP if severe and cause headaches, dizziness, increased risk of aneurysm, rupture of intracranial arteries
