Term
| Describe the basic structure of the tracheobronchial tree. |
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Definition
Conducting Airway (Deliver air to alveoli, remove particles, humidify and heat air)
**16 generations by 16 weeks gestation**
1) Trachea divides into bronchi (right is shorter and straighter).
2) Bronchi divide into bronchioles, which eventually branch into TBL
Respiratory Airway (Gas exchange0
3) RBL becomes alveolar ducts/sacs and alveoli (called a single "Acinus") |
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Term
| How does the respiratory epithelial lining change moving distally along the tracheobronchial tree? |
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Definition
1) Ciliated, pseudostratified columnar in trachea and bronchi (with C-rings of cartilage)
2) Simple columnar in TBL
3) Simple cuboidal in RBL
4) Squamous in Alveoli (Type 1 pneumocytes)
** 7% of SA is covered in granular type 2 pneumocytes)** |
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Term
| What types of non-ciliated respiratory cells are seen moving distally along the tracheobronchial tree? |
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Definition
1) Goblet cells are seen in trachea, bronchi and bronchioles, but are absent in the TBL and beyond.
2) Basal and Kulchitskey (APUD) cells are seen in respiratory mucosa of trachea and bronchi
3) Clara cells begin to appear in bronchioles and have replaced goblet cells in TBL. |
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Term
Which of the following does not describe the bronchial circulation.
1) High resistance
2) Arises from aorta
3) Forms continuous sheet through lungs
4) Returns to left atrium via pulmonary veins
5) Supplies lungs only up to TBL |
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Definition
3- The PULMONARY arterial circulation forms this continuous sheet and gives rise to alveolar capillary networks.
The bronchial circulation is a high resistance, high pressure systemic blood supply that arises from the aorta and supplies the lungs as far as the TBL. |
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Term
| Describe the basic structure of the pleural space? |
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Definition
- A "potential" space between the visceral and parietal pleura, somewhat resembling two glass slides with water in between.
- Small amount of pleural fluid enters the pleural space through the parietal pleura and is removed by pulmonary lymphatics
- Pressure is negative relative to Patm |
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Term
| What are the important passive/active muscles of inspiration and expiration? |
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Definition
1) Passive inspiration
- Diaphragm (C3-C5 phrenic)
2) Active inspiration
- SCN, scalenes and external intercostals
3) Passive expiration
- None (relies on elastic recoil)
4) Active expiration
- Internal intercostals, transversus and rectus abdominus, obliques |
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Term
| What are the effects of sympathetic (upper thoracic ganglia) and parasympathetic (vagus) stimulation on the lungs? |
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Definition
1) Sympathetic
- bronchial smooth muscle dilation (beta 2 receptors)
- constriction of pulmonary vessels (alpha 1 receptors)
- decreased glandular secretion
2) Parasympathetic
- Bronchoconstriction (M3 receptors)
- Vessel dilation
- Increased glandular secretions |
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Term
| What are the 4 layers of the respiratory tree in the trachea and bronchi. |
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Definition
1) Mucosa
- Respiratory epithelium (pseudostratified, ciliated, columnar epithelium, goblet cells, kulchitsky cells, basal cells)
- BM (open-network)
- Adventitia (lymphocytes, C fibers and mast cells)
2) Submucosa
- serous and mucous secreting glands and vessels
3) Musclularis/cartilage
- C-shaped rings in trachea
- Plates in bronchi
4) Adventitia
- Blends into general connective tissue of central mediastinum |
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Term
| Why is the presence of clara cells in bronchioles so critical? |
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Definition
They produce surfactant proteins that reduce surface tension and maintain lumen patency during expiration.
NO CARTILAGE distal to bronchi. |
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Term
| What important structures are found in the bronchioles, TBL and RBL? |
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Definition
1) Bronchioles (within lung segment)
- No cartilage (full circle of smooth muscle)
- Simple columnar epithelium
- Few cilia, mucus glands and goblet cells
2) TBL (within lung lobule)
- No goblet cells or cilia
- Simple cuboidal epithelium
- Clara cells emerge
- Patches of smooth muscle
3) RBL (within lung acini)
- Low cuboidal epithelium with alveoli outpocketings
- Patches of smooth muscle |
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Term
| What important cells form the alveolar wall? |
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Definition
Surfactant:Type 1 pneumocytes: BM: Capillary endothelium: Plasma
1) Flat, squamous Type 1 pneumocytes cover 95% of SA
2) Round, granular Type 2 pneumocytes cover 5% and produce/secrete surfactant in lamellar bodies
3) Alveolar macrophages (recruited by SurfA) |
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Term
| What is the major determinant of PO2 and PCO2? |
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Definition
V:Q matching
A:a gradient > 1 at apex, where V>>P
A:a gradient < 1 at base, where P >>V
High V/Q units create anatomic deadspace (apex)
Low V/Q units lower PaO2 and increase PA:aO2 |
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Term
| What are the 2 major opposing forces that must be overcome during respiration and how are they determined? |
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Definition
Elastic Recoil (Chest and Lungs) and Viscous Force (dynamic)
1) Elastic recoil is combination of tissue forces (chest wall) and Surface forces (Surfactant).
At FRC, the elastic recoil of the lungs is pulling them to collapse and the elastic recoil of the chest wall is pushing it to expand. These forces are equal and opposing at FRC, so PL + PW (or Pa -Ppl + Ppl)= O
** Elastic recoil is inverse of compliance **
2) Viscous forces (arising during inspiration/expiration)
- Frictional forces produced by flow of gas through airways
**Related to Resistance, which is 8nL/(pi)r^4** |
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Term
| Why does such a small proportion of the total viscous forces that must be overcome during respiration arise from the smaller, lower airways? |
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Definition
We know that viscous forces are proportional to resistance, which is inversely related to radius (to the 4th power!).
However, as airways get smaller, their total number (i.e. surface area) gets very large, slowing down flow and decreasing the amount of resistance to flow! |
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Term
| Why does intrapleural pressure increase during inspiration in static pressure-volume experiments, but decrease with inspiration in real life? |
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Definition
The static experiments are performed while a subject breathes against a closed upper airway. This causes the parietal pleura to press down on the visceral pleura, generating a positive pressure.
In real life, the airway would be open, and the visceral pleura would actually "tug" down on the parietal pleura. |
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Term
| How is sufficient force applied during inspiration and expiration to overcome opposing forces? |
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Definition
1) Inspiration
- Diaphragm (C3-C5: phrenic nerve) contracts from equilibrium dome shape, increasing the volume of the thorax and lungs and decreasing intra-abdominal volume (generating intra-abdominal pressure that causes ribs to expand).
- To get from Vt to TLC, external intercostals, scalenes and SCN assist.
2) Expiration
- Expiration to FRC is passive, and due totally to elastic recoil of chest wall and lungs from TLC.
- Active expiration to RV requires internal intercostals, transversus and rectus abdominus muscles and obliques. |
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Term
| Why is Ppl negative at end-expiration? |
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Definition
Opposing elastic recoil of lungs and chest wall "tug" in opposing directions.
During inspiration, they are separated further, and pressure gets even more negative. |
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Term
| What happens to intrapleural pressure, lung volume from FRC, alveolar pressure and airway during inspiration? |
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Definition
1) Intrapleural pressure becomes more negative
2) Lung volume from FRC increases
3) Alveolar pressure decreases (don't fill as fast as mouth), but then increases to baseline by Vt
4) Airflow increases to a maximum at the point where alveolar pressure is most negative, at which point it ncreases to baseline. |
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Term
| Describe what is meant by "expiratory flow limitation." |
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Definition
Bottom line: Maximum expiratory flow is determined by lung elastic recoil, which is determined by LUNG VOLUME.
At maximum lung volumes of <85% of VC, a maximum expiratory flow is reached and cannot be increased regardless of amount of effort.
There is a critical points of airway narrowing at the equal pressure point (EPP), where pressure is equivalent inside and outside of the airways and flow can therefore not be increased.
Expiratory flow is therefore driven by the pressure gradient between the alveoli and this "CHOKE POINT." |
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Term
| Why do small airways not collapse on expiration? |
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Definition
Length dependent surface-tension minimization by surfactant.
When molecules get close together as airway shrinks, they interact more and reduce collapsing pressure further. |
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Term
| What are the standard lung volumes and capacities? |
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Definition
TLC = 6L
VC= 4.5L and RV= 1.5L
FRC= 3L and IC= 3L
Vt= 0.5 L and IRV= 2.5L and ERV =1.5L and RV= 1.5L |
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Term
| What is the A;a gradient of a patient with an PaCO2 of 60 mm Hg and a PaO2 of 50 mm Hg under normal atmospheric conditions? Is this normal? |
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Definition
150- (60/0.8)= 75= PAO2 by alveolar gas
75-50= 25 mm HG, which is mildly elevated above the normal 12 mm Hg. There is V/Q mismatching, so there will be a decrease in PaO2 (because of low V/Q units) and increased Vd (because of high V/Q units) |
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Term
| What is the minute ventilation, dead space ventilation and alveolar ventilation of a patient with a respiratory rate of 22, a tidal volume of 0.5L and a dead space volume of 0.1L? |
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Definition
Minute ventilation (Ve)= RR X Vt= 22 X 0.5L= 11
Dead space ventilation= RR X Vd= 22 X 0.1:= 2.2
Alveolar ventilation= Ve - Vd= 11 -2.2= 8.8 |
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Term
| How do minute ventilation, alveolar ventilation, dead space ventilation and CO2 production influence alveolar and arterial PCO2? |
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Definition
PACO2= K X VCO2/ (Ve-Vd)
= K X VCO2/ (Ve)(1- (vd/vt))
Increasing minute ventilation will decrease PACO2 and PaCO2
Increasing CO2 production or Dead Space Ventilation will increase PACO2 |
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Term
What happens to pleural pressure at the end of expiration going from apex to base in the lungs?
What is the impact of this on ventilation:perfusion? |
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Definition
| Pleural pressure increases from apex to base (gravity), so the lower regions will collapse under expiratory pressure first (higher ventilation at APEX). |
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Term
| How do lung volume, CO and gravity influence pulmonary vascular resistance? |
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Definition
1) Lung Volume
- Alveolar vessels are compressed with increasing lung volume on inspiration
- Extra-alveolar vessels are dilated on inspiration with increasing lung volume.
**PVR is lowest near FRC!**
2) CO
- Increased CO causes a decrease in PVR because of RECRUITMENT and DISTENTION
3) Gravity
- Think of column of water. Base-distension (decreased PVR) and Apex- narrowing (increased PVR) |
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Term
| How is fluid flow across the pulmonary capillaries regulated? |
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Definition
Qf= Kf {(Pc- Pi) - sigma (pi:p - pi: i)}
Fluid will flow out of capillaries when Pc increases or pi:c decreases
If Kf increases, there is greater permeability and greater flow
If sigma increases, the capillaries are more able to retain solute, and less fluid to go into interstium |
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Term
| What local factors might cause interstitial and alveolar pulmonary edema? |
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Definition
What gets fluid to move out of capillaries?
Clinically, capillary hydrostatic pressure (HTN) and permeability are most important (Damage in emphysema, for example).
1) Increased capillary hydrostatic pressure
2) Increased filtration coefficient or decreased retention coefficient
3) Decreased capillary oncotic pressure. |
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Term
| Why does mixed arterial PO2 fall with V/Q mismatching despite an increase in average alveolar PO2? |
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Definition
Hemoglobin saturation is nonlinear.
High V/Q units cannot compensate for low V/Q units in terms of PO2. This is NOT the case for PCO2, which can be compensated for, since its saturation curve is linear. |
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Term
| Why do high V/Q ratios cause an increase in physiologic dead space and an increased minute ventilation requirement? |
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Definition
1) High V/Q means that ventilated oxygen is being delivered in an amount that exceeds the amount of perfused alveolar space (some can't participate, so it is alveolar dead space).
2) Increased physiologic dead space impairs CO2 excretion by by lungs, but increased PCO2 comes from BLOOD LEAVING LOW V/Q REGIONS.
Since CO2 builds up, you need to ramp of Ve to prevent acidosis. Therefore, low V/Q units create Ve need |
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Term
How can you calculate a measure of V/Q mismatching mathematically?
PaCO2= 35 mm Hg
PeCO2= 18 mm Hg |
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Definition
Bohr Equation
Vd/Vt= (PaCO2- PeCO2)/PaCO2
Vd/Vt= 17/18= 0.95
This means the amount of dead space ventilation is equal to the tidal ventilation.
Therefore, the difference between arterial and exhaled PCO2 increases with the proportion of dead space to tidal breath. |
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Term
| Why does minute ventilation increase during exercise? |
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Definition
Since more CO2 is being produced by muscles, you need to ramp up PeCO2 to balance PaCO2 and decrease Vd/Vt ratio.
Vd/Vt= (PaCO2- PeCO2)/ PaCO2 |
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Term
| What are the major factors that determined the rate at which O2 and CO2 diffuse across the alveolar-capillary interface? |
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Definition
Ficks Law Vgas= [A X D X (P1-P2)]/ T
Gas will diffuse FASTEST if there is
1) More surface area of contact
2) higher diffusion coefficient (solubility)
**CO2 has higher MW than water, but >>> solubility**
3) greater partial pressure gradient
**Greater for O2 than CO2
4) a thinner interface. |
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Term
Why do patients will lung impairment get hypoxic during exercise?
Why don't these patients typically get hypercapnic all the time? |
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Definition
If there are some dead areas of lung, the increased CO will be spread between the healthy areas and will decrease the transit time of O2 at the capillary interface such that there is insufficient time for diffusion to take place!
The partial pressure gradient for CO2 is MUCH smaller and their is precise neural regulation of PCO2. For these reasons, it is more stable. |
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Term
| What should the PO2a:c gradient be normally? |
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Definition
O!
This is not the A-a gradient and there should be no difference between alveolar and capillary oxygen partial pressures if there is no disease. |
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Term
How does partial pressure of a gas differ from solubility?
How does solubility influence alveolar:capillary partial pressure equilibration? |
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Definition
Partial pressure is the force exerted by gas molecules relative to the entire gaseous population. It is the same in the alveoli, blood and all tissues and organs.
2) Concentration depends on partial pressure and SOLUBILITY. Highly soluble gasses have much higher blood and tissue concentrations
**Solubility is inversely proportional to the rate of equilibration between the partial pressure in blood and alveolar gas (O2 and CO2 equilibrate quickly!)** |
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Term
| What are the 5 mechanisms of hypoxemia? |
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Definition
Hypoventilation and Reduced Pb do NOT change the A-a gradient!
1) Hypoventilation- increase in PACO2 causes PaO2 to fall
2) Reduced Pb or FiO2 (altitude)- Alveolar Air Eq.
3) V:Q mismatch
4) Shunt (mixed venous blood added to arterial circulation)
5) Impaired diffusion (emphysema) |
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Term
| Why is arterial hypercapnia produced and identify 2 possible causes? |
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Definition
Inadequate alveolar ventilation (hypoventilation), such as the case in CF or ICD
1) Abnormally low Ve in restrictive disease due to kyphoscoliosis or obesity
2) Inadquate increase in Ve in cases of extreme V;Q mismatch |
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Term
| How is oxygen transported in the blood? |
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Definition
Dissolved (minor form) and in Combination with Hbg (major form)
CaO2= 1.34 X Hgb X SaO2 + 0.003 X PaO2
1) Dissolved= 0.003 X PaO2 (linear)
2) Combined with Hb is non-linear
- lowered pH, increased temperature, increased 2,3 BPG all "right-shift" curve and decrease affinity |
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Term
| What is the arterial blood oxygen delivery (DLco) of a patient with a CO of 50 dl/min, a PaO2 of 80 mm Hg, a Hgb of 15 g/dl and a SaO2 of 100%? |
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Definition
DLco= CaO2 (mlO2/dl blood) X CO (L/min) X 10
= [(1.34)(15)(1.0) + (0.003)(80)] X 50 X 10
= approximately 1000 ml/min |
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Term
| What factors can cause a decrease in arterial blood oxygen delivery? |
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Definition
DLco depends on Hemoglobin concentration, % SaO2, PaO2 and Cardiac Output.
Conditions like Anemia (Hb decreases), decreased saturation, V:Q mismatching (PaO2 decreases) and HF (CO decreases) can all cause hypoxia. |
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Term
| What is CO2 transferred in the blood? How do the Bohr and Haldane effects relate to this? |
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Definition
Dissolved in RBC (minor), bound to Hb, and hydrated via CA (major form).
1) Bohr effect explains how increased PCO2 in tissues leads to decreased pH (increased H+ and hydration of CO2), and decreased affinity of Hb for Oxygen.
2) Haldane effect explains how deoxygenated Hb likes to bind CO2 (helps loading).
So, in tissues, increased PCO2 causes O2 to be delivered and CO2 to be taken up by Hb.
In lungs, increased Hb oxygenation causes CO2 unloading (Haldane) and decreased CO2 facilitates O2 loading (Bohr) |
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Term
| What factors may cause a right-shift in the hemoglobin saturation curve and what would that mean? |
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Definition
Right shift means decreased affinity for Oxygen (as seen in tissues).
1) Decreased pH
2) Increased temperature
3) increased 2,3 BPG |
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Term
| How does neuro-regulation compensate for decreased PO2? How does this relate to normal respiratory neural regulation? |
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Definition
When PaO2 falls below 60 mmHg, peripheral chemical sensors in carotid body and aortic body sense low O2 tension and relay signals to the brainstem "pacemaker" via carotid sinus nerve and CN IX to stimulate ventilation.
1) Normally, brainstem motor neurons (pre-botzinger complex) send signals to dorsal (inspiratory) and ventral (expiratory) respiratory groups in lateral medulla.
2) These signals are sent to the chest wall (diaphragm and accessory muscles) as well as upper airways (patency) to initiate respiration.
**The magnitude of the alveolar ventilation regulates PaCO2, [H+] and PaO2** |
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Term
| How do central chemoreceptors regulate respiration? |
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Definition
Found in the ventrolateral medulla, these receptors are sensitive to carbon dioxide tension (PCO2), via H+ concentration in the brain.
CO2 can diffuse through BBB, while H+ and HCO3- cannot. After crossing, CO2 is rapidly hydrated to HCO3- and H+, and the H+ ions augment ventillary drive.
**20% of PCO2 response IS mediated by peripheral receptors (faster than central) |
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Term
| Explain the basis and 3 primary receptor types that regulate non-chemical control of breathing. |
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Definition
1) Slowly adaptive stretch receptors (myelinated) in airway smooth muscle cells stimulated by lung inflation that are innervated by afferent vagal fibers.
- Basis of Hering-Breuer Inflation Reflex, where prolonged inspiration is followed by apnea.
2) Rapidly adapting stretch receptors among airway epithelial cells stimulated by particulate matter and endogenous agents such as histamine/PGE that re innervated by myelinated vagal fibers
-cough, hyperpnea, bronchoconsriction
3) J-receptors in pulmonary interstitium near bronchial and pulmonary circulations that are stimulated by pulmonary congestion and are innervated by de-myelinated vagal C-fibers
- produces apnea, following by rapid shallow breathing (producing bradycardia and hypotension). |
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Term
What non-chemical receptors produce the following responses in the respiratory system and where are they located?
1) Cough, Hyperpnea and Bronchoconsriction
2) Apnea following prolonged lung inflation.
3) Apnea following by rapid shallow breathing, bradycardia and hypotension. |
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Definition
1) "Hering Breuer Inflation Reflex" mediated by fast-adaptive "irritant receptors" found among airway epithelial cells that are innervated by myelinated vagal fibers and respond to exogenous particulate matter and endogenous chemicals (histamine/PGE).
2) Slow-adaptive stretch receptors in bronchial smooth muscle that are innervated by myelinated vagal fibers and respond to lung inflation
3) "Pulmonary chemoreflex" in conditions of pulmonary congestion mediated by J-receptors found in pulmonary interstitium that are innervated by non-myelinated, vagal C- fibers. |
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Term
| What is the condition called where patients lose autonomic control of respiration, but maintain voluntary control? |
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Definition
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Term
| Why is cardiac rate, but not respiratory rate often altered in the case of Heart-Lung transplant? |
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Definition
| The trachea remains innervated, so loss of vagal afferent input is compensated for. |
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Term
| What normal respiratory changes take place during sleep? |
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Definition
1) Reduced Vt without change in RR, so Ve falls.
2) Reduced Ve leads to decreased PaO2 and increased PaCO2
**More irregular during REM sleep |
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Term
| Why might some patients with CHF or at high altitudes experience waxing and waning periods of hyperventilation and apnea? |
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Definition
Cheyne-Stokes respirations occur because of 3 major factors.
1) Pulmonary congestion (CHF)
2) Delay in circulation time between lungs and central chemoreceptors due to cardiac insufficiency (CHF)
3) Alterations in threshold for PaCO2 to stimulate breathing |
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Term
| What hormonal factor might be important for respiratory compensation for mechanical loads imposed by severe obesity? |
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Definition
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Term
| How are volume and flow measurements obtained during PFT? |
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Definition
1) Spirometry (measurements are taken 3 times for 4s and must be more than 20% away from the mean value to be considered abnormal)
- FVC is measured as patient blows as hard as they can through tube that is measured as a pressure.
- SVC can also be measured, and should be equal to FVC
- FEV1 is measure of rate of expiratory flow
If FEV1:FVC <0.7, you are looking at obstructive disease
If FEV1:FVC > 0.7, you are looking at restrictive disease
CANNOT measure FRC, RV or TLC |
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Term
| Why is a metacholine challenge sometimes useful? |
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Definition
Use this histamine-derivative to induce vasospasm in patients with episodic disease.
Drop in PEF of greater than 20% is considered + test. |
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Term
| How might looking at a flow volume loop help you tell between Extrathoracic variable upper airway obstruction and Intrathoracic variable upper airway obstruction? |
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Definition
1) Extrathoracic, intraluminal obstructions such as glottic strictures, tumors, and vocal-cord paralysis, will increase on inspiration
PEAK ON INSPIRATION
2) Intrathoracic, obstruction such as malignant tumors and tracheomalacia will improve on inspiration.
PEAK ON EXPIRATION |
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Term
| How can you measure FRC, RV and TLC? |
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Definition
Can't get them by spirometry
1) Helium Dilution
- measure change in spirometer helium concentration during inspiration to estimate gas volume change.
2) Body plethysmography
- Glass box |
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Term
| How is diffusion capacity measured clinically? |
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Definition
Single Breath CO diffusing capacity to assess gas exchange at pulmonary-capillary membrane.
Value less than 80% of normal is considered abnormal
and are seen in disorders like emphysema, interstitial lung disease and pulmonary vascular disease.
Increased capacity may be seen with polycythemia, mild CHF and pulmonary hemorrhage. |
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Term
Which condition would not cause a decrease in diffusing capacity by single breath CO testing?
1) Emphysema
2) Pulmonary vascular disease
3) Pulmonary hemorrhage
4) Interstitial lung disease |
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Definition
| Pulmonary hemhorrage would actually increase diffusing capacity! |
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Term
| What changes to pulmonary physiology take place during pregnancy? |
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Definition
1) Decreased FRC, but constant TLC and VC
2) Primary respiratory alkalosis with renal compensation (7.4-7.47) because increased Ve overcompensates for increased PCO2 due to metabolic changes
3) Increased Ve increases PaO2 and decreases PaCO2
**increased Ve from progesterone can cause dyspnea** |
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Term
What happens to normal respiratory mechanics and gas exchange during diving?
What 3 things should you watch out for if you are a diver? |
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Definition
1) As depth increases, lung volume decreases because of increased pressure and more O2, CO2 and N2 are dissolved in the blood.
2) FRC and TLC are reduced because extra-thoracic pressure opposes normal outward recoil of chest wall. Muscles have to work really hard, and cannot compensate at deeper than 1 meter with only a surface tube.
Watch out for
1. Barotrauma on rapid ascent (high pressure injury causing alveolar hemorrhage and/or air embolism)
2. Decompression illness where gas bubbles form in vessels and tissues on ascent (give hyperbaric O2 chamber)
3. Nitrogen narcosis where high PN2 alters CNS function. |
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Term
| What are the 3 major respiratory complications of Diving? |
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Definition
1. Barotrauma on rapid ascent (high pressure injury causing alveolar hemorrhage and/or air embolism)
2. Decompression illness where gas bubbles form in vessels and tissues on ascent (give hyperbaric O2 chamber)
3. Nitrogen narcosis where high PN2 alters CNS function. |
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Term
Why do Breath-hold divers hyperventilate prior to diving?
Why do they sometimes lose consciousness during ascent? |
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Definition
1) This reduces PaCO2 and increases the time until PaCO2 will rise and induce neurogenic ventilation.
2) PO2 and PCO2 both drop as pressure decreases, but PO2 is already low because of absent ventilation during breath-holding! |
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Term
| How does breathing at high altitudes produce arterial hypoxemia and hypocapnia? |
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Definition
1) Hypoxia
- As you ascend, Pb decreases and PAO2/PaO2 decrease by the alveolar air equation.
- Peripheral chemoreceptors in carotid body signal to brainstem and increase Ve, causing arterial pH to rise (respiratory alkalosis).
- Hypoxia is reduced by Acclimatization via HIF-1-alpha (quick changes as opposed to adaptation)
2) Hypocapnia occurs because of increase in Ve |
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Term
A young man who lives at a low altitude decides to ascend a 13,000 ft peak in 1 day.
When he arrives at the top, he is dizzy, dyspneic, weak, nauseous and has a severe headache.
What is the pathophysiological basis of this condition? How would you treat? |
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Definition
Acute Mountain Sickness due to hypoxia-induced cerebral vasodilation causing hyperperfusion and edema
2) Treat with Dexamethasone, Acetazolamide (accelerates acclimatization) and a slow decent.
If it gets worse, you are worried about HACE! |
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Term
| Why do you see Cheyne-Stokes respirations at high altitudes? |
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Definition
| Hypoxia and Alkalosis cause over-stimulatoin of carotid chemoreceptors that produce hyperpnea following by compensatory apnea. |
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Term
Why might you give a beta agonist as prophylaxis to a patient with High altitude pulmonary edema (HAPE)?
How would you treat HAPE? |
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Definition
1) Increase sodium channel expression in lung epithelium to increases sodium and water absorption
2) Gamov Bag and Supplemental O2 |
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Term
| What is the pathophysiological basis of the three types of respiratory failure? |
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Definition
1) Oxygenation
- Lung disease with V/Q mismatch and impairment of gas diffusion
- A-a gradient with increased Ve
2) Ventilation
- Neuromuscular or Chest wall disease with a primary drop in Ve, leading to increased PaCO2 and decreased PaO2
- no V/Q mismatching or increase in A:a ratio
3) Oxygenation-ventilation
- Like oxygenation failure, but with profound abnormality in lung compliance and/or resistance so that Ve cannot be ramped up
- ARDS, cardiogenic pulmonary edema, COPD and severe acute asthma |
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Term
| What factors determine FiO2 during supplemental oxygen administration? |
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Definition
1) FO2 being delivered
2) Flow rate of delivered gas
3) Patient's spontaneous inspiratory flow rate.
The lower the selected FO2 and the higher the spontaneous flow rate, the more air is entrained and the lower the actual FiO2 |
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Term
| Why is shunt physiology resistant to high FIO2? |
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Definition
Normally, the relationship between FIO2 and resulting PaO2 varies with severity of V/Q inequality (exact improvement is impossible to predict)
However, in shunt, there is a more linear relationship and there are units that are not perfused AT ALL, so increasing Fi-O2 will not increase the PaO2 no matter how high it is. |
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Term
| What are the 3 major indications for mechanical ventilation and what options are available? |
|
Definition
1) Respiratory acidosis resulting from acute increase in PaCO2
2) Impending ventilation failure
3) Arterial hypoxemia that is refractory to oxygen supplementation.
A/C ventilation (volume-set) best for critically ill
- physician set RR and Vt
- pressure-variable
PSV (pressure set, volume-variable).
- More patient control of Vt and RR, so it is more comfortable, but patients must make effort
- Usually used to see if patient actually needs A/C |
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Term
Why might a patient with ARDS be placed on PEEP?
How does this work and what are the benefits/risks? |
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Definition
In ARDS, PEEP will keep alveoli open at end-expiration and prevent premature collapse (restrictive phenotype).
PEEP increases volume remaining lungs at end-expiration (FRC) and increases pleural pressure.
1) Can reduce shunting by holding alveoli open
2) Can cause over-distension and rupture (barotrauma), - - Increase Hb and %SaO2, but decrease CO because of elevated right atrial pressure and decreased flow gradient. |
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Term
| A patient presents with deep regular breaths and you smell a fruity scent. What is going on? |
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Definition
This is Kussmaul respirations in Diabetic Ketoacidosis.
The patient is trying to compensate for the acidosis since dead space is minimized and CO2 elimination is most efficient. |
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Term
| Why should you be especially worried if the abdominal wall moves inward on inspiration? |
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Definition
This means diaphragm is failing and it is a sign of impending respiratory failure.
SCN is pulling diaphragm up |
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Term
| What are the 3 main respiratory signs that can be detected on Palpation? |
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Definition
1) Chest excursion
- asymmetric expansion may be seen in paralyzed diaphragm, localized pain, fibrosis or airspace disease.
2) Tactile Fremitus
- vibration felt through chest wall indicating lung consolidation
- decreased fremitus indicates airway obstruction (tumor), pleural effusion or pneumothorax
3) Crepitation
- Sub-Q air due to thoracic disease implying bronchopleural fistula
- Seen in trauma patients, pneumothorax and airway obstruction |
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Term
| Under what conditions might you expect to detect increased/decreased tactile fremitus? |
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Definition
1) Increased in lung consolidation
2) Decreased
- Pneumothorax
- Pleural effusion (effusion moves airways farther from chest wall)
- Airway obstruction from tumor |
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Term
| What 4 qualities of sound are you looking for on percussion? |
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Definition
1) Resonant (normal over lung)
2) Hyper-resonant (over emphysematous lung)
3) Tympanitic (gastric bubble)
4) Dull (pleural effusion or consolidated lung)
**Pneumothorax can be hyperresonant or amphoric (bottle/jar sound)** |
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Term
| How might you distinguish between Pleural effusion and Pneumonia on PE? |
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Definition
| Both will be dull to percussion, but you will have decreased tactile fremitus in effusion and increased tactile fremitus in Pneumonia |
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Term
What breath sound is described by each of the following?
1) Inspiratory phase> expiratory phase: audible over anterior and posterior chest walls
2) Inspiratory phase= Expiratory phase
3) Expiration > Inspiration phase heard over trachea
4) Continuous, low-pitched sound heard on expiration |
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Definition
1) Normal Vesicular
2) Bronchovesicular suggesting slight consolidation
3) Bronchial (Tubular) sounds reflection conduction fo sound from large airways indicating consolidation (Pneumonia)
4) Rhonchi found in airway disease like asthma, COPD and secretions |
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Term
When might you hear each of the following breath sounds?
1) Rales/Crackles
2) Rhonchi
3) Wheezing
4) Rubs |
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Definition
1) Parenchymal disease such as HF, Pneumonia or fibrosis
2) Airway disease such as Asthma, COPD or secretions
3) Turbulent airflow in airway obstructive disease or bronchial obstruction from tumor/foreign body
4) Inflammation of either/both pleural surfaces seen in Pneumonia, PE, rheumatological disease and malignancy. |
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Term
| What are the 3 important voice changes that indicate lung consolidation (fluid-filled)? |
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Definition
1) Bronchophony
- Words sound clear and loud over consolidation
2) Whispered pectoriloquy
- Audible patient whispering through stethescope
3) Egophony
- "E" to "A" at periphery of lung |
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Term
A patient displays the following PE findings. What is your diagnosis?
Fremitus: Decreased
Percussion: Dull
Breath sounds: Decreased
Tracheal deviation: None
Pectoriloquy: Absent
Rhales: Absent
Wheezing: Absent |
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Definition
Small pleural effusion that is pushing lungs away from chest wall (decreased fremitus and breath sounds) and dull to percussion.
No tracheal deviation rules out Atelactasis and bronchial plug |
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Term
A patient displays the following PE findings. What is your diagnosis?
Fremitus: Decreased
Percussion: Dull
Breath sounds: Decreased
Tracheal deviation: Left
Pectoriloquy: Absent
Rhales: Absent
Wheezing: Absent |
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Definition
Atalectasis (local collapse) with tracheal deviation to sight of volume loss.
Collapse is decreasing fremitus and breath sounds. |
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Term
A patient displays the following PE findings. What is your diagnosis?
Fremitus: increased
Percussion: Dull
Breath sounds: Bronchial
Tracheal deviation: None
Pectoriloquy: yes
Rhales: yes
Wheezing: Absent |
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Definition
| Massive consolidation in increasing fremitus vibrations, breath sounds at trachea and vocal indications of consolidation (Pectoriloquy and Rhales) |
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Term
A patient displays the following PE findings. What is your diagnosis?
Fremitus: Normal
Percussion: Normal
Breath sounds: Normal
Tracheal deviation: None
Pectoriloquy: No
Rhales: Yes
Wheezing: No |
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Definition
Pulmonary fibrosis.
Isolated rales suggests parenchymal disease |
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Term
| Why might you prefer to use a PA radiograph vs. a AP radiograph |
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Definition
1) PA taken during standing inspiration, quickly with less magnification of heart
2) AP is substituted if patient cannot stand- increases magnification and decreases image sharpness. |
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Term
| Why is left lateral CXR preferred to right lateral CXR? |
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Definition
| Keep the heart closer to the film to decrease magnification and increase sharpness |
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Term
| Why do denser structures like metal and bone show up as white on CXR? |
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Definition
They have a greater ability to absorb and block x-rays, causing less silver ion precipitate.
Air absorbs it all and turns black quick. That is why an "overexposed" CXR is black. |
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Term
| How is a helical (spiral) CT performed? |
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Definition
3-D volumetric data acquisition during a single breath
All CT scanners at UPMC are multi-detector CT |
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Term
| Why might a "silhouette sign" be absent on CXR? |
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Definition
Loss of normal interface between air in lung and soft tissue in heart
See in Pneumonia |
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Term
You look at a patient's X-ray and note a "smeared chalk" appearance of the lung fields bilaterally.
What is this? |
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Definition
| Ground Glass Opacity from partial filling of the alveoli, interstitial thickening or increased capillary blood flow. |
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Term
You are looking at a patient's X-ray and note decreased inflation of the right upper lung with increased opacity.
What could be going on? |
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Definition
Atelectasis due to mucous plug, stricture, tumor or extrinsic compression (spontaneous pneumothorax?).
Non-involved lung will over-inflate! |
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Term
| If you see a nodulo-reticular pattern on an X-ray of the lungs, what would you expect to see on CT and biopsy? |
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Definition
IPF
On CT, honeycombing
On Biopsy, UIP with temporal and geographical heterogenity |
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Term
| What is the differential for nodular lung deposits on CXR? |
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Definition
1) Infectious- Miliary TB, fungi, CMV
2) Non-infectious granulomatous- Sarcoid
3) Neoplastic
4) Inhalation- Silicosis |
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Term
| Why might the lungs appear to be "too black" on x ray? |
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Definition
1) Air-trapping
- Emphysema
2) Oligemia (lack of BF)
- PAH, PE |
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Term
| Why might the lungs appear "too white" on CXR? |
|
Definition
1) Airspace (Acinar) consolidation
- Edema, Inhalation, Pneumonia or ARDS
2) Ground Glass opacity |
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Term
| What is the "anaerobic threshold" of exercise testing? |
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Definition
Point during exercise at which CO reaches a maximum, and CV system will longer be able to meet O2 demands, shifting toward anaerobic metabolism as a result.
**Determined by measuring the VO2 at which the rate of rise in CO2 production and Ve increases**
R will increase from 0.8 to >1. |
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Term
| Why might Ve exceed CO2 production during exercise? |
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Definition
To compensate for lactic acidosis.
It matches CO2 production after the anaerobic threshold is met, but later will have to compensate further.
This may cause respiratory alkalosis! |
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Term
| In the absence of CV and pulmonary disease, what is the primary limitation on exercise? |
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Definition
| The amount of oxygen that can be delivered to skeletal muscles by the CV system prior to reaching the anaerobic threshold. |
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Term
| How can you distinguish between Cardiovascular and Respiratory limitations in exercise? |
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Definition
CV= VO2at <0.4 (abnormal) and VEmax <0.7, with HRmax >0.9
**They reach anaerobic threshold quickly**
Resp= VO2at >0.4, Ve max 0.7 (abnormal) and HRmax< 0.9 (abnormal)
**Never reach anaerobic threshold**
1) VO2 max will be <90% of predicted value for both .
2) HRmax will be normal for CV limitation, but low for respiratory (respiratory reaches VO2max too quickly)
3) VO2at will be normal for respiratory limitation, but <0.4 for CV limitation
4) VEmax (MVV- breath out as strongly and quickly as possible for 12s and multiply by 5) is <0.7 for CV limitation (normal), but >0.7 for respiratory. |
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Term
| What is the normal CV and respiratory responses to exercise? |
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Definition
When anaerobic threshold is reached, ATP production decreases and lactic acid production increases. Exercise is usually terminated shortly thereafter.
1) To increase ATP production, the CV system needs to supply O2, so CO increases (HR and SV)
2) To increase CO2 excretion, the respiratory system increases Ve |
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Term
| Why might you use a pulse oximeter? |
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Definition
Noninvasive technique that measures oxygen saturation.
1) Rapid evaluation and monitoring of potentially compromised patients
2) Titrating O2 therapy in situations where O2 toxicity is a worry |
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Term
| Why administer NO and what are the important complications to be aware of? |
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Definition
NO preferentially dilates pulmonary vasculature in well-ventilated areas, and can therefore improve V/Q balance.
1) Given to newborns to treat persistent Pulmonary HTN or to adults for pulmonary embolism, HTN and acute chest syndrome in sickle cell patients.
2) Watch out for NO2 in presence of high O2 levels, as well as Methemoglobinemia in infants |
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Term
| Why administer Helium (g) and what are the important complications to be aware of? |
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Definition
Low density, low solubility, inert gas with high thermal conductivity that is used in
1) Pulmonary function testing to measure RV, FRC and related volumes.
2) Low density decreases work of breathing in patients with elevated airway resistance.
3) Slow down ignition of flammable components during laser surgery on airway
4) contrast agent in pulmonary MRI |
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Term
| What are the known physiological signaling effects of CO? |
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Definition
Inhalation of CO treats inflammation, HTN, organ transplant, vascular injury and ventilator-induced injury in animal models.
1) Modulates sGC, leading to cGMP production and pulmonary vasodilation
2) Modulates MAPK activation to stimulate Ca-dependent K+ (BK) channel activity to promote muscle relaxation |
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Term
What does Minimum alveolar concentration (MAC) have to do with anesthetic potency?
What are the potential drawbacks of using MAC as an indicator of potency? |
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Definition
1) MAC that prevents movement in 50% of patients is used as a measure of potency, where the lower the MAC, the MORE potent the drug.
2) MAC is consistent and reproducible within a given patient population, but decreases with age and body temperature and during pregnancy.
**measure in Vt** |
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Term
| Why are general anesthetics very dangerous drugs? |
|
Definition
1) Steep dose-response relationships
2) Low therapeutic indices
3) No available antagonists |
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Term
| How does the action of general anesthetics relate to GABAa signaling? |
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Definition
Increase sensitivity of inhibitory GABAa receptor to GABA (chloride channel gating)
**DOES NOT bind GABA site**
Other ligand-gated channels are also effected, with the general effect of inhibiting excitatory neurotransmission and potentiating inhibitory signaling. |
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Term
| How are general anesthetic partition coefficients defined pharmacokinetically? |
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Definition
| The ratio of anesthetic concentration in two tissues when the partial pressures of that anesthetic are equal (thus, difference in solubility). |
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Term
| How does anesthetic solubility relate to drug potency? |
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Definition
| The higher the solubility, the higher the partition coefficient and the lower the MAC (more potent). |
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Term
| What 3 important factors determine anesthetic uptake from the lungs? |
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Definition
| Blood solubility * CO * partial pressure driving drug from lung phase into venous blood phase |
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Term
| What factors influence FA/FI ratio and what does this have to do with the speed of anesthesia induction? |
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Definition
Fa is alveolar partial pressure and FI is inspired partial pressure (this ratio is the point of no net movement between alveoli and circulation)
Factors that increases the rate of FA/FI equilibration will speed up induction
Insoluble drugs that are inhaled quickly at high concentrations, in the context of low CO will act the fastest. |
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Term
| What are the 4 main body compartments with regard to uptake and distribution of anesthetics? |
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Definition
1) Vessel-rich: CNS and visceral organs
- Equilibrate rapidly with inspired drug because of high BF and low capacity**
2) Muscle group: skin andmuscle
- Moderate flow and high capacity
3) Fat group:
- Low flow and high capacity
4) Vessel poor: Bone, cartilage and ligaments
- Minimal effects on anesthetic uptake and distribution. |
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Term
| How is Hydrogen Sulfide utilized clinically? |
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Definition
Inhibits cytochrome C oxidase, limiting mitochondrial respiration.
- May limit some forms of cellular injury when delivered in dose-controlled manner. |
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Term
| What central neurological sites are affected by anesthetic action? |
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Definition
1) Spinal chord (pain and immobility).
2) Tuberoumamillary nucleus of hypothalamus (sedative/anxiolytic)
3) Hippocampus (amnestic)
4) Thalamic inhibition (awake-anesthetized transition) |
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Term
| What is the "concentration effect" of anesthetic delivery? |
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Definition
| More soluble drugs like halothane will take less time to equilibrate (e.g. take effect) when they are delivered at higher inspired partial pressures. |
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Term
| What are the effects of inhaled anesthetics on circulation and respiration? |
|
Definition
1) Decrease systemic BP in dose-related manner (CO is maintained for isoflurance and desflurane)
2) Reduced spontaneous Ve in dose-dependent manner
**if ventilation is not controlled, this may increase PaCO2 |
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Term
| Why is there increased airway resistance and decreased expiratory flow in obstructive lung disease? |
|
Definition
OLD= Asthma, COPD (emphysema + bronchitis), Bronchiolitis, Bronchiectasis
1) Airway Resistance
1a) In emphysema, you lose "tethering" of pulmonary parenchyma on small, non-cartilaginous airways, so they do not remain patent during expiration.
1b) In chronic bronchitis, asthma, bronchiolitis and bronchiectasis, inflammation and edema narrow the airway lumen
2) Decreased Expiratory Flow
- Due to increased airway resistance
- ONLY in emphysema, decreased elastic recoil (increased compliance) also decreases expiratory flow. |
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Term
| What changes to lung volumes occur in obstructive lung diseases like Emphysema? |
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Definition
- FRC (decreased recoil) and TLC increase
- RV increases because of "air-trapping," where small airways collapse prematurely, and "dynamic hyperinflation," where there is intrinsic PEEP
**makes compression/collapse even worse!**
- VC decreases |
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Term
| Why do hypoxia and hypercapnia occur in obstructive lung disease? |
|
Definition
1) Hypoxia
- Airway narrowing causes V/Q mismatching
- Low V/Q units lower PaO2 and increase PaCO2
- High V/Q units create alveolar dead space
**Exercise-induce hypoxia is only seen in emphysema, where there is capillary:alveolar damage**
2) Hypercapnia
- Increased dead space ventilation (low V/Q units) and impaired respiratory muscle function. |
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Term
| Why does obstructive lung disease impair the function of the diaphragm? |
|
Definition
Increased pressure must be generated to overcome viscous forces and respiratory muscle work and energy consumption increase.
1) Air-trapping and hyperinflation causes it to lose its dome-shaped configuration, which reduces its efficiency
2) Intrinsic PEEP from dynamic hyperinflation increases energy expenditure even further. |
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Term
Why do you see each of the following spirometric and PFT changes in obstructive lung disease?
1) Decreased FEV1/FVC
2) Increased FRC
3) Increased RV
4) Decreased DLco |
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Definition
1) Both FEV1 and FVC decrease, both FEV1 decreases more because flow is impeded.
2) FRC may be increased because expiration volume is decreased
3) RV is increased because of dynamic hyper-inflation and air-trapping
4) DLco is decreased because of alveolar:capillary damage (in emphysema) and V/Q mismatching in all obstructive diseases. |
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Term
| What are the major long-term complications of obstructive lung disease? |
|
Definition
| Pulmonary HTN with increased PVR leads to RVF (cor pulmonale) with systemic edema, JVD and hepatomegaly, ultimately leading to LHF and death. |
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Term
| What major factors produce exercise limitation and dyspnea in patients with Emphysema? |
|
Definition
1) increased airway resistance leads to increased muscle load, dynamic hyperinflation and V/Q mismatching; Diffusion impairment
- Respiratory muscle fatigue and decreased Vt increase Vd/Vt and cause dyspnea
2) Alveolar/capillary destruction produces V/Q inequality; Diffusion impairment.
- Decreased PaO2 and increased Vd leads to dyspnea |
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Term
| Why is exercise-induced hypoxemia seen in emphysema but not bronchitis? |
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Definition
There is alveolar/capillary damage in Emphysema, which means the increased CO will be spread in a smaller space, decreasing diffusion time.
This is not true in asthma, where you are more worried about bronchoconstriction and inflammation. |
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Term
| Provide a clinical definition of COPD, chronic bronchitis and emphysema. |
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Definition
1) COPD is not fully reversible obstructive disease that is characterized by airflow limitation (BOTH bronchitis and emphysema can occur without airflow limitation).
2) Chronic Bronchitis is a productive cough for 3 months during each of two successive years.
3) Emphysema is abnormal, permanent enlargement of air spaces distal to TBL (acinar) accompanied by destruction of their walls. |
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Term
| What are the primary risk factors for COPD? |
|
Definition
1) Exposure to toxic fumes and gases
2) Asthma
3) Mucus hyper-secretion
4) Perinatal and childhood respiratory infections. |
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Term
A 65 year old mane with a 40 pack year h/x of smoking presents with a productive cough, expectoration and dyspnea.
You perform PFT and notice prolonged expiratory time (6 seconds). The FEV1/FVC ratio is 0.5 and the DLco is decreased by 50%.
You then order a CXR and notice hyperinflation, oligemia and bullae.
What is the pathophysiology/treatment of this condition? |
|
Definition
This is clearly COPD with evidence of bronchitis and emphysema.
Stop them from smoking, start them on long-acting bronchodilators like Salmeterol and Tiotropium and give them continuous oxygen therapy as needed.
PP
1) PMNs accumulate in lung
2) Imbalance between PMN elastase:alpha-1-anti-trypsin leads to emphysema
3) Loss of matrix-attachments from elastase activity leads to cel death and airspace enlargement
4) Repair follows with abnormally arranged collagen. |
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Term
| How does airway inflammation in asthma cause bronchoconstriction, airway edema and increased mucous production? |
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Definition
| Early (mast cell activation) and Late (inflammatory cell infiltrate) responses |
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Term
| What are the defining clinical and PE features of Asthma? |
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Definition
1) Intermittent wheezing, cough, chest tightness and dyspnea, often attributable to a certain trigger
2) Severity and frequency of attacks and bronchodilator responsiveness.
3) Spirometry shows non-specific obstructive signs
4) Can try metacholine challange if lung function appears normal |
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Term
| What is the basic therapeutic management strategy for Asthma? How do they differ from COPD? |
|
Definition
Anti-inflammatory drugs don't work for COPD. You need the LABAs
1) Drugs that inhibit smooth muscle contraction (B2 agonists, methylxanthines and anticholinergics)
2) Drugs that prevent inflammation (GCs, LTC inhibitors, mast-cell stabilizing cromones)
Use anti-inflammatory drugs for chornic asthma, but combining them with bronchodilators can aid symptomatic relief. |
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Term
How do each of the following bronchodilators work to inhibit bronchoconstriction?
1) B-agonists
2) Methylxanthines
3) Anticholinesterases |
|
Definition
1) Beta agonists stimulate beta adrenergic receptors, leading to increased cAMP, PKA and phosphorylation of calcium-activated-BK channels leading to smooth muscle relaxation.
**also inhibit mast cell mediator release and enhance mucociliary clearance**
2) Methylxanthines like Theophylline are PDE5 inhibitors that prevent breakdown of cGMP/cAMP (reserved for severe, unresponsive cases)
3) Drugs like Tiotroprium inhibits M3 receptors in smooth muscle, and it dissociates more slowly from M3 than from M2 in pre-ganglionic sites (maintaining M2-mediated NE release inhibition).
**used predominantly in COPD** |
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Term
| Why might you use a short acting beta-agonist like Albuterol vs. a LABA like Formeterol? |
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Definition
Short-acting Albuterol is good for rapid symptomatic relief of dyspnea associated with asthmatic bronchoconstriction.
LABA in combination with ICS is recommended for long-term maintenance. |
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|
Term
| How/Which anti-infalmmatory agents used to treat asthma? |
|
Definition
Reduce fibrosis resulting from chronic inflammation from later allergic response.
1) GCs are great, but can cause systemic effects (limited by aerosol delivery) like immunosuppression
-Bind GR, which translocates to nucleus and recruits HATs and HDACs to activate and suppress various target genes, respectively
- Fluticasone proprionate is synthetic variant that is rapidly innactivated by CYP3A4 pathway systemically.
2) Cromones terminate inflammatory molecule release from Mast cells and inhibit IgE synthesis from B lymphocytes
**used mostly in pediatrics**
3) Anti-Leukotrienes
- Zileutin (LOX-5 inhibitor)
- Zafirlukast and Montelukast (Leukotriene receptor inhibitor)
4) Anti-IgE with Omalizumab |
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|
Term
How are glucocorticoids delivered in asthma treatment?
How are side effects minimized? |
|
Definition
1) Aerosol delivery is preferred to avoid systemic side effects, especially in less severe, chronic asthma.
2)
- Some oral bioavailability still present (goes to gut)
- Pulmonary retention limits systemic circulation and is increased by Lipid conjugation (lipophilicity correlate with lung retention) |
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Term
Why might you give Ciclesonide to treat asthma?
Why give it instead of Fluticasone proprionate? |
|
Definition
1) Novel GR agonist with high pulmonary deposition compared to fluticasone proprionate, that is preferentially activated in lungs compared to the oropharynx, where they are esterified and inactivated.
**Esterases are present in other tissues, so watch out for systemic side effects**
2) Better pulmonary deposition, but chance of systemic side effects (oral bioavailability is comparable, however). |
|
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Term
| What are "dissociated" glucocorticoids and how might they be used to treat asthma? |
|
Definition
Unleash gene repression activity of GR while having little impact on gene activation of the receptor (Get the HDACs moving without increasing the HATs)
Hoped to maintain anti-inflammatory properties while minimizing side effects. |
|
|
Term
| What is glucocorticoid resistance and why is it a problem? How should these patients be treated? |
|
Definition
1) Corticosteroid-dependent (CD asthma) results in a situation of reduced responsiveness among SMOKERS that requires very high doses (You can't lower them, but high doses aren't enough!)
Rarely, it can be totally resistant (CR)
2) CD and CR forms of asthma changes to GR function such as reduced nuclear transcription of GR or disruptions in histone modifications
- Increased GRb expression (as opposed to active GRa form) may also contribute.
3) Long-acting inhaled B2-agonists or Theophyllines (Decreasing chromatin-associated histone protein acetylation by increasing HDAC) |
|
|
Term
A 28 year old man presents with a chronic sputum-producing cough (significant amounts) and dyspnea. You notice clubbing of his feet and mid-inspiratory crackles.
What innate immune defenses must have been overcome to produce this condition? |
|
Definition
Presentation fits non-resolving infection/inflammation from bronchiectasis.
Mucociliary escalator and Ion transport throughout the airway. Proximally, in bronchus, goblet cells and ciliated cells defend, while more distally, in bronchioles, Clara cells take over.
1) Secreted proteins with anti-microbial activity
2) Mucus blanket (gel layer)
3) PLC layer
4) Synchronous ciliary action
5) Alveolar macrophages |
|
|
Term
| What adaptive immune responses are overcome in bronchiectasis to produce persistent inflammation and airway surface remodeling? |
|
Definition
| Airway becomes floppy and dilated because leukocyte end products overcome native anti-protease activity (alpha-1 anti-trypsin) to produce remodeling. |
|
|
Term
| What 2 major pathophysiological processes lead to obstructive lung disease in Bronchiectasis? |
|
Definition
1) Mucus/inflammatory cell plug of airway
2) Airway collapse (bronchial cartilage damage and chronic inflammation) |
|
|
Term
| How can various mutations in CFTR lead to the characteristic pulmonary manifestations of CF? |
|
Definition
Basic: AR CFTR mutations prevent inhibition of ENaC and lead to over-absorption of sodium and water from airway lumen into interstitial and plasma, DRYING IT OUT. Mucus cannot be cleared (obstruction) and infections take root, leading to bronchiectasis.
1) Class 1 mutations cause premature stop codon and truncated, non-functional protein
2) Class 2 mutation (most common), deltaF508 leads to abnormal folding of CFTR, after which it is targeted for degradation.
3) CLass III/IV mutations leads to defective channel regulation or conductance.
4) Class V mutations involve normal channels, but too little mRNA being translated. |
|
|
Term
| What are the major extra-pulmonary effects of CFTR mutations? |
|
Definition
1) Sweat glands cannot reabsorb salt and produce hypertonic sweat
2) In pancreas, bicarbonate secretion is impaired and neutralization of pancreatic enzymes/proteases is prevented.
3) In vas deferens, there is congenital bilateral absence. |
|
|
Term
| What are the primary CXR and CT findings of the diseases that present with chronic, sputum-producing cough, dyspnea, clubbing of feet and mid-inspiratory crackles? |
|
Definition
Bronchiectasis
1) CXR
- Interstitial pattern with peri-bronchial haziness
2) CT
- Dilatation and thickening of conducting airways with "tree and bud" appearance of distal airway
- Nodular opacities (mucus-filled airways) and thick walled cysts. |
|
|
Term
What do each of the following clinical findings indicate about etiology of Bronchiectasis?
1) Sweat chloride >60 mEq 2X with lack of chloride secretion on nasal potential difference
2) Decreased clearance of saccharin and radionucleide mucus, with lack of dynein arms on ciliary microtubules from EM analysis
3) Decreased IgA, IgG or IgG sub-class
4) Elevated IgE
5) Reduced serum level of anti-protease |
|
Definition
1) CF
2) Immotile Cilia Syndrome
3) Immunodeficiency
4) Aspergillus fungal infection
5) Alpha-1 antitripsin deficiency. |
|
|
Term
| What determines absorption of nicotine? |
|
Definition
) Aborption
- pH dependent (weak base, so well-absorbed in alkaline environment when it is de-ionized)
- pH of the lung is 7.4, allowing for a large fraction of non ionized nicotine Alveolar surface area of the lung is large Capillary system in the lung is extensive. Results in extremely high, transient blood levels of nicotine with each inhalation. |
|
|
Term
| How is nicotine distributed in the body? |
|
Definition
1) After inhalation (higher and less-prolonged than buccal absorption), non-charged nicotine is absorbed across pulmonary epithelium to enter circulation
2) Delivered to CNS (rapidly crosses BBB) |
|
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Term
| What about its metabolism makes tobacco users tobacco users repeat administration of nicotine during the day? |
|
Definition
| It is metabolized in the liver rather quickly, with a half-life of 2 hours, and cotinine is subsequently glucoronidated and excreted in the urine. |
|
|
Term
| How does nicotine exert its pharmacodynamic effects? |
|
Definition
1) Bind nAChR in brain, mimicking effects of ACh (does NOT bind muscarinic AChR)
2) nAChR acts as ion channel, increasing permeability to sodium (NMJ) and calcium (CNS and ganglia)
**alpha subunit contains ACh binding site** |
|
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Term
| How does nicotine exert its effects on mood and the CVS? |
|
Definition
1) Mood
- binds to pre-synaptic nAChRs and increased Ca2+ influx causing more neurotransmitter release
- Dopamine (pleasure reward)
- NE (Arousal, appetite suppression)
- Glutamate (Learning, memory)
- 5-HT (mood modulation)
- GABA (anxiety and tension)
2) CVS
- Sympathetic stimulation of arterioles
- Sympathetic stimulation of veins
- Tachycardia (adrenal stimulation overwhelms parasymp)
- Increased GI motility and secretions |
|
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Term
| What is the receptor-based mechanism of nicotine addiction? |
|
Definition
Activation and Desensitization
1) Sustained low-levels of nicotine shift receptors into desensitized state (higher affinity, but less ion flow)
2) Compensatory up-regulation of receptor # |
|
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Term
| What precautions should be taken when starting NRT therapy? |
|
Definition
Watch out for in TMJ disease, pregnancy, lactation and CVD!
1) Post MI (within 2 weeks0
2) Arrhythmias
3) Worsening AP
**Lower than continued tobacco use though!** |
|
|
Term
| What psychotropic drugs have proven to be useful in treating nicotine addiction? |
|
Definition
1) Buproprion (Zyban)- Look out for DEPRESSION
- inhibits re-uptake of NE, 5-HT and dopamine, reducing urge.
- long half life and slow steady-state achievement (give it before they stop smoking)
- GREAT option for patients with DRD2-A2 allele and SLC6A3-9 allele (also protective against addiction).
2) Varencicline tartrate (Chantix)- Nausea
- a4b2 (neuronal) partial agonist that inhibits pre-synpatic nicotine effects (blunts rewarding affects)
- Be be better than buproprion in long-term.
3) NicVAX
- Conjugates nicotine to carreir protein that elicits an immune response in bloodstream, preventing BBB crossing. |
|
|
Term
| What population benefits most strongly from Buproprion treatment? |
|
Definition
Those with protective Dopamine processing alleles like DRD2-A2 and SLC6A3-9, that increase dopamine responsiveness.
1) SLC6A3 encodes a dopamine reuptake transporter 9-repeat allele shows diminished dopamine reuptake compared to other alleles due to decreased protein expression (more dopamine remains in synapse).
2) DRD2-A2 allele higher density of dopamine receptors (more dopamine signaling).
3) DRD4-S allele shows increased dopamine affinity (heightened overall response to dopamine) |
|
|
Term
A 65 year old patient who lives in NYC presents with a chronic, sputum producing cough and shortness of breath.
You get a bronchial biopsy and see the following.
- Goblet cell and Squamous metaplasia
- Mucus gland hyperplasia
- Chronic inflammation of submucosa
- Airways filled with macrophages
what is your diagnosis |
|
Definition
Sounds like Chronic bronchitis (Reid index would be high since mucus glands are so big).
Remember, this can involve airway obstruction, but does not have to (in this case, it seems to).
Grossly, you would see extensive mucus plugging or air passages
You can treat with LABAs |
|
|
Term
A smoker from NYC presents with dyspnea and chest pain.
Grossly, his lungs are voluminous with bullae and he has a barrel chest deformity.
You order a lung biopsy and note the following.
1) Cystic spaces in the center of the acinus
2) Carbon deposition in surrounding connective tissue |
|
Definition
Centrilobular Emphysema
- PMN-mediates elastase activation and alveolar walls damage, leading to irreversible expansion of small airways.
Treat with LABAs
**If this was pan-lobular (more common in smokers) you would see destruction of the alveolar duct, with small cysts evenly disbursed throughout the pulmonary acinus. |
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|
Term
A 34 year old women presents complaining of intermittent chest tightness, dyspnea, cough and wheezing.
You order a CXR and notice distended lungs with segmental mucus plugging.
You order a biopsy and note the following.
1) Epithelial hyperplasia with goblet cell metaplasia/hypertrophy
2) Hyperplasia of tracheobronchial glands, with eosinophils and Charcot-Leyden crystals and Curschmann's spirals
3) BM thickening
4) Submucosal eosinophillic and lymphocytic infiltrates
5) Hypertrophy/hyperplasia of bronchial smooth muscle
What is the diagnosis and treatment options? |
|
Definition
Obstructive asthma treated with GCs and a LABA (albuterol acutely for symptoms perhaps)
Squamous/goblet metaplasia with tracheobronchial gland hyperplasia could be asthma or COPD, but Charcot-Leyden crystals and Curschmann' spirals are more specific for asthma.
Additionally, smooth muscle hypertrophy and BM thickening are characteristic of asthma. |
|
|
Term
You are examining a gross lung sample post-mortem from a patient who suffered from chronic, sputum-producing cough and trouble breathing.
You note dilatation of the lower lobe airways. The distal lung appears collapsed and fibrotic.
On histology, you note the following:
1) Acute inflammation and squamous metaplasia
2) Submucosa fibrosis and inflammation.
3) Enlarged, hyperplastic bronchial arteries in submucosa
What is your diagnosis? |
|
Definition
Bronchiectastis due to obstruction (tumor), post-inflammatory dilation (Pseudomonas) or congenital abnormality (CF or ICS)
Inflammatory is most common |
|
|
Term
| How do the 3 major types of restrictive disorders alter lung volumes? |
|
Definition
1) Disorders causing increased elastic recoil (IPF, Pneumoconiosis, Sarcoidosis)
- Decrease Vt, FRC, VC, TLC and RV
2) Diseases limiting expansion of chest wall (Obesity, Ascites, Kyphoscoliosis)
- Decrease Vt, FRC, VC, TLC and RV
3) Diseases causing impaired respiratory muscle function (ALS, Polio, Myasthenia Gravis)
- Decrease Vt, VC and TLC. FRC remains the same (determined only be elastic recoil) and RV increases (more air left after expiration). |
|
|
Term
| How can the three major types of restrictive disorders alter gas exchange? |
|
Definition
1) Interstitial disorders causing increased elastic recoil (IPF, Pneumoconiosis, Sarcoidosis)
- Inflammatory/fibrotic damage to pulmonary capillary bed causes V:Q mismatching and perfusion defect.
- Equilibration time decreases
2) Chest wall expansion and Respiratory muscle dysfunction
- Low Vt can cause atalectasis, leading to V/Q mismatch, shunt and arterial hypoxemia. |
|
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Term
| What are the characteristic PFTs of the 3 most common types of restrictive lung diseases? |
|
Definition
FEV1 decreases because of low VC, not because of decreased expiratory flow. Since there is just less lung volume to be exhaled, FEV1:FVC is normal or elevated.
1) Interstitial (IPF, Pneumoconiosis, Sarcoid) and Chest wall disorders (Kyphoscoliosis, obesity)
- FRC and RV decreased
2) Muscle disorder
- FRC normal and RV increased |
|
|
Term
| Why do patients with IPF and Pneumoconiosis get dyspnea and exercise limitation? |
|
Definition
1) Interstitial thickening
- Increased elastic recoil, leading to decreased Vt and increased muscle load
- Diffusion impairment
2) Alveolar/capillary destruction
- V/Q inequality and Diffusion impairment |
|
|
Term
| What are the most notable CXR/CT findings and current explanations for IPF pathogenesis? |
|
Definition
Restrictive interstitial lung disease (most common kind of idiopathic interstitial pneumonia) presenting in older males
- Progressive dyspnea on exertion
- "Velcro" crackles at lung bases
- Paroxysmal, non-productive cough
1) CXR shows reticulonodular infiltrates and CT shows honeycombing and "traction bronchiectasis"
**See UIP on pathology**
2) Pathogenesis
- Repetitive injury to alveolar micro-envioronment followed by abnormal healing (TGF-b, MMPs).
- Genetic association with Surfactant C mutations |
|
|
Term
| What are the characteristic pathologic findings in IPF and what are the treatments available? |
|
Definition
1) UIP with Geographical and Temporal heterogeneity of honeycombing fibrosis and smooth muscle hyperplasia.
- Fibroblastic foci are characteristic
- Thickened and normal interstitium
2) Prognosis is 3.5 years and only current option is transplant
- Future efforts with triple-kinase inhibitor, nintedanib may prove useful |
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Term
Diagnose each of the following described conditions and list the important pathological characteristics.
1) Gradual development of dyspnea is a foundry worker with nodules 2 cm nodules on CXR and massive fibrosis on biopsy
2) Slowly developing dyspnea with paroxysmal dry cough and IPF on radiograph
3) Coal worker with 0.2 cm opacities on CXR |
|
Definition
1) Complicated Silicosis with progressive massive fibrosis
- Look for silicotic nodule grossly and bifringnent silica particles on histology
**Likely to get mycobacterial infections in cavitations**
2) Asbestosis
- Ferruginous Asbestos body and iron-laden macrophages on histology
- No lymph node involvement or massive fibrosis
3) CWP
- Coal macule |
|
|
Term
| Describe the 4 radiographic stages of sarcoidosis |
|
Definition
Remember, Sarcoid is a disease mostly of "intrathoracic organs" affecting the Lungs, hilar LN, Liver, Eyes, Kidney, Skin.
1) Hilar and/or mediastinal adenopathy without pulmonary infiltrates. Good prognosis with spontaneous remission
2) Adenopathy and Infiltrates
- May have normal lung volumes and decent prognosis (50% remission, 25% progression to fibrosis and 25% relapse)
3) Absence of adenopathy with infiltrates in the upper lobes.
4) Absence of adenopathy with diffuse infiltrates and notable volume loss that is lacking in stage III
- Myceotomas from Aspergillus are common at this stage with hemoptysis |
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Term
| What is "Hypersensitivity Pneumonitis"? What histopathological features are characteristic of HP? |
|
Definition
1) Diffuse inflammatory lung disease seen in patients exposed to organic dusts (Extrinsic allergic alveolitis).
- Farmer's lung
- Bird-fancier's lung
2) Airway-centered cellular interstitial pneumonia with poorly formed non-nectrotizing granulomas (Type IV hypersensitivity) |
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Term
| What 3 features are often seen in the non-nectrotizing granulomas of Sarcoidosis? |
|
Definition
1) Epithelioid histiocytes
2) Fibrous rim
3) Multinucleated giant cells |
|
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Term
| What are the primary pathological findings in sarcoidosis? |
|
Definition
1) Granulomatous inflammation with well formed non-necrotizing granulomas (looks for epithelioid histiocytes, giant cells and fibrous rim) in a LYMPHANGITIC distribution (follows both bronchovascular bundles and veins along septa and pleura)
2) "Schaumann bodies" (laminated concretions composed of calcium and proteins"
3) "Asteroid bodies" (stellate inclusions containing degraded cytoskeletal protein enclosed in multi-nucleated giant cell. |
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Term
| How can you distinguish Hypersensitivity Pneumonitis from Sarcoidosis histologically? |
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Definition
Since both involve type IV hypersensitivity (T-cell mediated) with non-necrotizing granulomas, it can be confusing.
1) Sarcoid granulomas are WELL-formed, with epithelioid histiocytes, multi-nucleated giant cells and a clear fibrous ring.
2) HP granulomas are loosely formed will few inflammatory cells. |
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Term
| What is the supposed pathogenesis of Sarcoidosis? |
|
Definition
1) CD4+, Th1 cells are activated by MHC-II APCs (B cells and macrophages) that interact with TCR
2) Clonal expansion of stimulated Th1 cells occurs (specific variable regions) and inflammation ensues
**see gamma and delta chains that recognize TB bacteria**
3) SNPs in TNF-a, TGF-b, complement receptors and Ig light chains have all been identified.
**small contribution of HLA haplotypes to risk** |
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Term
| What is the basic immune cells involved in pathogenesis of Sarcoidosis? |
|
Definition
Th1-dominant response suggests presence of specific "sarcoidosis antigens"
**Low Th2 response may experience lack of cleared antigens**
1) CD4+ Th1 cells are activated
- Express high affinity IL-2 receptors
- Express MHC II antigens
- CD45RO+ (primed for specific antigens)
- Produce IFN-y, IL-2, IL-12 and IL-15
2) Macrophages
- Produce IL-12 (activate T cells)
- Become "epithelioid" via IL-1 and TNF-a
3) B cells (hypergammaglobulinemia) |
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Term
| What are the definitive geographic and racial differences in those affected by Sarcoidosis? |
|
Definition
Peak incidence between 25-40
1) Increase with degrees latitude from the equator
2) African americans 10X more likely ONLY in US
2b) High in asians living in london
3) Higher in health care workers |
|
|
Term
| What are the effects of airspace filling diseases on lung compliance and lung volumes |
|
Definition
ARDS, Pneumonia, Pleural Effusion, Alveolar hemorrhage
- Lung volumes are reduced because fewer "empty" alveoli are left V:Q mismatching since perfusion is intact, but ventilation is impaired.
- Compliance may be reduced since it is harder to inflate lungs filled with fluid.
You get hypoxia because CO is rushing through a limited area |
|
|
Term
| How do airspace filling diseases adversely affect gas exchange. |
|
Definition
1) V:Q mismatching because decreased alveolar ventilation area
- Low V:Q units decrease PaO2 and increase PaCO2 and A:a gradient.
- High V:Q units make deadspace and with decreased Vt, Vd/Vt increases leading to hypercapnia.
2) CO floods smaller area and diffusion time decreases |
|
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Term
| Why do patients with airspace filling diseases like Pneumonia and ARDS get dyspnea? |
|
Definition
1) Alveolar filling decreases Vt, which forces Ve to increase.
2) V/Q inequality increases dead space ventilation and decreases PaO2, further increasing Ve |
|
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Term
| What are the criteria required to make a diagnosis of ARDS? |
|
Definition
1) Bilateral airspace pulmonary airspace edema
2) Non-cardiogeneic edema secondray to damaged capillary:alveolar surface with increased hydrostatic pressure (PAP < 18 mmHg)
3) Hypoxemia (secondary to alveolar filling)
Hypoxemic respiratory failure with loss of compliance and due to loss of surfactant. Severity determined by P/F ratio
Clinically, ARDS presents with dyspnea, severe hypoxemia, tachycardia and hyperpnea. |
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Term
A patient presents with dyspnea, severe hypoxemia, tachycardia and hyperpnea.
On CXR, you notice bilateral pulmonary airspace edema and you measure PAP as 15 mm Hg.
What is the pathological process going on in this condition?
What are the predisposing/modifying factors? |
|
Definition
ARDS (bilateral, non-cardiogenic alveolar space edema with hypoxemia) associated with "predisposing factors"(Sepsis, aspiration, emergency surgery) and "modifying factors" (Alcohol)
Exudative Phase (3-7d)
- epithelial injury with hyaline membrane formation and interstitial PMN infiltrates
- DIFFUSE ALVEOLAR DAMAGE (DAD)
Proliferative Phase
- Organization of infiltrates with fibroblast proliferation, collagen deposition and type II cell hyperplasia
GROSS
- boggy, firm, red and HEAVY lungs (acutely)
- dark and fibrotic (proliferative) |
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Term
patient presents with dyspnea, severe hypoxemia, tachycardia and hyperpnea.
On CXR, you notice bilateral pulmonary airspace edema and you measure PAP as 15 mm Hg.
What are the best indicators of outcome in this patient? |
|
Definition
ARDS
1) Dead Space is best physiological predictor
- Pulmonary HTN is also a good indicator
- Severity of P/F defect DOES NOT predict
2) Sepsis is associated with worst outcome (may progress to DIC and death) and trauma has best outcome. |
|
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Term
| What are the major challenges of managing a patient with bilateral, non-cardiogenic pulmonary edema and severe hypoxemia? |
|
Definition
ARDS
Lung injury is HETEROGENEOUS
1) Hypoxemia demands PEEP to reduce shunt physiology, but must avoid bio/volu/baro trauma
2) FiO2 can improve oxygenation, but has Oxygen toxicity risk
Should use low Vt (12 ml/kg) ventilator management to avoid barotrauma (extra-alveolar pneumothorax), volutrauma (over-inflation of alveoli) and biotrauma and add Cisatracurium if in the first 48h |
|
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Term
| What does the paralytic agent, Cisatracurium, have to due to management of ARDS? |
|
Definition
| If you give it during first 48 hours of ventilator support, people survive more. |
|
|
Term
| What paradox of ARDS makes fluid management especially challenging? |
|
Definition
Pressure makes edema, but you need pressure for CO
1) Capillary leakage leads to greater Pulmonary edema for given LVED (wedge) pressure.
2) Heart has undergone shift of starling curve to right, so cardiac function NEEDS higher filing pressure to maintain CO
DRY strategy is better, since it reduces transfusion need and ventilator dependence. |
|
|
Term
| What is the disease associated with the emergence of DAD in a previously healthy individual? |
|
Definition
| Acute Interstitial Pneumonia or "Hamman-Rich disease." |
|
|
Term
| What are the two gross patterns of bacterial Pnuemonia? |
|
Definition
Both tend to occur in lower lobes and may be overlapping/caused by same organisms!
1) Lobar
- acute infection involving large amount of lobe
- S. pneumo
2) Bronchopneumonia (lobular)
- Patchy consolidation of parenchyma. |
|
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Term
| What are the 4 major pathological stages of Lobar Pneumonia? |
|
Definition
1) Congestion (>24h)
- dilated alveolar capillaries
- air spaces filled with eosinophilic fluid with few PMNs
2) Red hepatization (24h-2d)
- Red, firm and airless
- Numerous pnuemococci in PMNs.
3) Grey hepatization (2-3d)
-Decreased capillary congestion and leukocyte migration to alveoli.
4) Resolution
- Macrophage ingestion of debris or fibroblast organization into permanent adhesions. |
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Term
| What are the gross and histopathalogical signs of bronchopneumonia? |
|
Definition
S. aureus, S. pyogenes, H. influenzae, K. pnuemonia, Legionella
1) Gross
- Patchy yellow white tan infiltrates
2) Microscopically
- PMNs in bronchi, broncioles and adjacent airspaces |
|
|
Term
| What are the classic causes of Pneumonia in the immnocompromised host? |
|
Definition
1) Bacteria
Gram-negative and Gram-positive including Pseudomonas aeruginosa, Mycobacterium sp, Legionella pneumophilia and Listeria monocytogenes)
2) Viral
- CMV, HSV
3) Fungal
- PJP, Candida sp, Aspergillus sp, the Phycomycetes, Cryptococcus neoformans |
|
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Term
| What are the 2 classic histopathologic features of Atypical pneumonia due to mycoplasma infection? |
|
Definition
1) Airway obstruction/bronchiectasis
2) Micro-abscesses and Ill-defined granulomas (no necrosis and few giant cells) |
|
|
Term
| What infections are commonly associated with CMV pneumonia? |
|
Definition
Immunocompromised so think Pnuemocystis
Remember, usually there is interstitial pneumonia without necrosis |
|
|
Term
| What are the classic histopathalogical findings in Pnuemocystis Pneumonia? |
|
Definition
Organisms are in hyaline membranes within alveolar spaces (no budding)
1) Frothy, foamy or honeycomb exudate within airspaces associated with interstitial pnuemonia (associated with CMV pneumonia as well).
**most often seen in AIDS patients with pneumocystis**
2) DAD in non-AIDS patients
3) Helmet-shaped cysts on GMS staining |
|
|
Term
| What are the 3 typical histopathological signs of Aspergilliosis? |
|
Definition
1) Hemorrhagic infarction with minimal inflammation.
2) Fungal hyphae invades blood vessel walls and alveolar septa
3) Arterial lumens can be completely occluded by plugs of fungi |
|
|
Term
| What immune mechanisms must be overcome in Pneumonia pathogenesis? |
|
Definition
1) Upper airway (colonized by virridens streptococci, Neisseria and Candida) uses filtration, mucociliarty transport and sneezing, along with antimicrobial substances.
2) Glottis
- closure and cough reflex
3) Bifurcating airway
- Mucociliary escalator and anti-microbials
4) Alveolar macrophages (recruit PMNs) and immunoglobulins |
|
|
Term
What are the most common bacterial etiologies of Pneumonia in the following CAP contexts?
1) Outpatient- no co-morbidity
2) Outpatient- co-morbidity
3) Hospitalized
4) Hospitalized with severe disease |
|
Definition
1) Treat with Doxy or Azith (Macrolide)
- Strep. pneumoniae
- Mycoplasma pnemoniae
- Chlamydia
- Viral (adeno, RSV)
- Haemophilus influenza
2) Treat with Azithromcin or FQ
- Streptococcus pneumonia
- Haemophilus influenzae
- Chlamydia and Mycoplasma
- Viruses
- Legionella
3) Azithromycin with a Beta-lactam
- Strep pneumoniae
- Haemophilus influenzae
- Polymicrobia
- Viruses
- Legionella
4) Give Macrolide (Azythromycin) + beta lactam
Strep pneumoniae
- Legionella
- Pseudomonas and other gram - (give
- Staph aureus
- Viruses |
|
|
Term
| What is the rationale for the empiric antibiotic regimens for CAP and HAP? |
|
Definition
1) CAP
- Remember, no pathogen responsible for CAP is identified in 50% of patients, so CAP therapy must cover S. pnuemo and the Atypical causes
- If there is structural disease, recent Ab therapy or ICU stay, consider Pseudomonas also
- Give Macrolide with a beta-lactam (if hospitalized) and anti anti-pseudomonal if needed
2) HAP (If VAP, get a BAL)
- Early VAP (S. pneumo, S. aureus, H. influenzae)
Ampicillin/Sulbactam
- Late VAP (Pseduomonas, MRSA, Enteric gram negative)
VANCOMYCIN, CEFEPIME, TOBRAMYCIN
- Non-VAP (E. coli, Klebsiella, Proteus)
PIPERACILLIN/TAZOBACTAM |
|
|
Term
What drugs should be given for each of the following Pneumonia scenarios?
1) CAP (previously healthy)
2) HAP (Early VAP)
3) CAP (co-morbidity)
4) CAP (ICU stay)
5) HAP (non-VAP)
6) HAP (later-VAP) |
|
Definition
1) Macrolide like Azithromycin for S. pnuemo and atypicals
2) Amp/Sulbactam for S. pneumo, H. influenzae and S. aureus
3) Macrolide or FQ
4) Macrolide + Beta lactam
5) Piperacillin/Tazobactam for gram negative Klebsiella, E. coli and Proteus
6) Give Vancomycin, Cefepime or Tobramycin for MRSA, Pseudomonas and gram negative rods |
|
|
Term
What organisms produce following CXR findings and clinical symptoms?
1) Alveolar patterns that are sometimes lobar in distribution with Rapid onset fever/chills, pleurisy and cough with sputum
2) Interstitial pattern with dry cough and subacute onset in young adults
3) Alveolar pattern with patchy, segmental distribution accompanying Upper respiratory symptoms (sore throat, hoarseness) and a dry cough
4) Alveolar pattern, from patchy to more extensive consolidation in the context of a cough and extra-pulmonary manifestations (elevated liver enzymes, CNS symptoms, hyponatremia)
5) Interstitial pattern, bilaterally with a flu-like illness (high fever, headache, myalgias) |
|
Definition
1) S. pneumo, H. influenzae, Gram negative bacilli (e. coli or enterobacter)
2) Mycoplasma
3) Chlamydia pneumoniae
4) Legionella
5) Influenza |
|
|
Term
A patient presents with rapid onset fever/chills, pleurisy, cough and sputum.
On CXR you determine an alveolar pattern of consolidation, following a lobular distribution.
What is the diagnosis/treatment |
|
Definition
This is Pneumonia do to Strep pneumonia, H. influenza or gram-negative bacilli.
Treat with Macrolide antibiotic like Azithromycin |
|
|
Term
A 13 year old boy presents with dry cough and you order a CXR, on which you notice an interstitial pattern of consolidation.
What is the diagnosis/treatment |
|
Definition
Mycoplasma Pneumonia
Azithromycin |
|
|
Term
A 18 year old women presents with sore throat, hoarseness and a dry cough.
You order a CXR and notice alveolar consolidation in a patchy and segmental pattern.
What is the diagnosis/treatment? |
|
Definition
Chlamydia Pneumonia CAP
Use Macrolide |
|
|
Term
A 37 year old man presents acutely with a sputum-producing cough, elevated liver enzymes and dizziness/confusion.
On CXR you see an alveolar pattern of consolidation that is patchy.
What is the diagnosis? |
|
Definition
Sounds like atypical Pneumonia from Legionella species.
Macrolide |
|
|
Term
Patient presents with high fever, headache and myalgias.
A CXR reveals bilateral interstitial consolidation
What is the diagnosis? |
|
Definition
| Sounds like Pneumonia due to influenza |
|
|
Term
What congenital causes of immunodeficiency predispose young patients to Pneumonia?
What organisms are associated? |
|
Definition
1) T lymphocyte (Viruses, PJP)
- Di George/Thymic aplasia with reduced CD4+ and CD3
2) B lymphocyte (S. pneumo and H. influenzae)
- Bruton's X_linked agammaglobulinemia (no B, plasma or IG)
- Selective IgG subclass
- IgA deficiency
3) Mixed T and B
- CVID
- SCID
- Wiskott-aldrich
4) Phagocyte (staph aureus, pseudomonas, aspergillus))
- Chronic granulomatous disease (NADPH oxidase)
- Chediak-Higashi |
|
|
Term
| What are the 4 major categories of immunocompromised patients affected by Pneumonia? |
|
Definition
1) Chemotherapy for hematologic malignancy and solid tumor
- Neutropenia (Aspergillus and Pseudomonas)
- Splenectomy (S. pneumo, N. meningiditis, H. influenzae)
- Cyclosporine ( fungal, viral and mycobacterial)
2) Immunosuppression in solid-organ transplant
- Early post-transplant (CMV) and iatrogenic immunosuprresion (re-activation of CMV, TB or histo)
3) Corticosterodis, methotraxate, anti-TNFa for Rheumatic Arthritis
- Fungal infection
- TB
4) HIV
- CD4 count <200 is key
- PJP, S. pneumo, CMV, TB/MAC, |
|
|
Term
A patient with a hematological malignancy or solid tumor may undergo chemotherapy, splenectomy and/or treatment of graft versus host disease in case of stem cell transplant.
What sorts of infections occur in these conditions? |
|
Definition
1) Chemotherapy produces Neutropenia
- Pseudomonas and Aspergillus
2) Splenectomy for lymphoma
- Encapsulated (S. pneumoniae, H. influenzae, N. meningitidis)
3) Tacrolimus/Cyclosporine
- Fungal
- Mycobacterial
- Viral (CMV) |
|
|
Term
| Why do patients with Rheumatoid arthritis and Autoimmune disorders tend to get Pneumonia? |
|
Definition
TREATMENT with corticosteroids and anti-rheumatic agents
TB is an issue and requires a PPD. |
|
|
Term
What do each of the following hints tell you about Pneumonia etiology in an immunocompromised patient?
1) Travel to southwestern US (New Mexico, California, Arizona)
2) Travel to Ohio River Valley (Ohio, Tennessee)
3) Construction in hospital
4) Swimming in lakes.
5) Donor:recipient serotype mismatch |
|
Definition
1) Coccidiomycosis
2) Histoplasma
3) Aspergillosis
4) Legionella, Aspergilliosis or Pseudomonas
5) CMV or Toxo |
|
|
Term
A patient presents with cutaneous nodules on their skin and a severe respiratory infection.
What is the diagnosis? |
|
Definition
| Pneumonia due to Cryptococcus |
|
|
Term
A patient who recently received a solid organ transplant presents with a pulmonary infection that you suspect in Pneumonia.
What do each of the following timepoints, post-transplant tell you about the likely organism?
1) <1 month
2) 1-6 months
3) > 6 months |
|
Definition
1) **MRSA**, Gram negative bacilli, Legionella, Aspergillus
2) **CMV** Aspergillus, Legionella, Gram negative bacilli (if ventilated- E. coli)
3) Nocardia, Mycobacteria, Cryptococcus, Coccidiodes immitus |
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Term
| How does a CD4+ count of > 200 or < 200 change your diagnosis of Pneumonia etiology? |
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Definition
You don't see PJP until less than 200
1) > 200 think S. pneumonia or M. tuberculosis
2) < 200, think S. pneumonia, PJP, M. tuberculosis |
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Term
When a patient with Multiple myeloma gets a stem cell transplant, they are treated prophylactly for graft versus host disease using cyclosporine/tacrolimus with corticosteroids.
What bugs are they at risk for? |
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Definition
1) Fungal
2) Mycobacterial
3) Viral (CMV) |
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Term
| What are the histological features of UIP, Sarcidosis and Hypersensitivity Pneumonitis? |
|
Definition
1) UIP is pathology and IPF is clinical
-Geographical and Temporal Heterogeneity (see Fibroblastic foci)
- Fibrosis with distortion of architecture (honeycomb change)
2) Sarcoidosis
- Granulomatous inflammation with well formed non-necrotizing granulomas (composed of epithelioid histiocytes, and multinucleated giant cells)
- Lymphangitic distribution (along bronchovascular bundles and septa and pleura)
3) Hypersensitivity Pneumonitis (HP)
- Airway-centered cellular interstitial pnuemonia
- Poorly formed non-necrotizing granulomas |
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Term
| What is an "interstitial pnuemonia"? |
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Definition
1) Damage to alveolar structure.
2)Inflammatory infiltrates involving the interstitium leading to further damage to alveolar structure
3) Alveolar macrophages and lymphocytes come and lead to fibrosis eventually |
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Term
What is the basic anatomy routes of arteries, veins and lymphatics in the lungs?
What diseases of the interstitium follow these distributions? |
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Definition
Pulmonary arteries, bronchial arteries and airways run in centri-lobular distribution, while veins follow inter-lobular septa to pleural surface. Lymphatics show both.
1) Pulmonary arteries run in Bronchovascular bundles in the center of lung lobules (Centrilobular)
2) Airways run in bronchovascular bundles in center of lobules (Centrilobular)
3) Bronchial arteries run with airways they supply (Centrilobular)
4) Veins form in lobules and run along interlobular septum to pleural surface
**Hypersensitivity pneumonitis follows this distribution**
5) Lymphatics follow both routes.
**Sarcoidosis follows this distribution** |
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Term
| How does pulmonary vascular disease alter gas exchange and CV function? |
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Definition
These diseases do not affect parenchyma or airways, so elastic recoil, compliance and airway resistance are normal (Normal PFTs but decreased DLco)
1) Gas exchange
- V/Q mismatching leading to increased A-a gradient and Ve
- See fall in PaO2 with exercise because of large decreases in surface area (like interstitial disease and emphysema)
2) Cardiovascular function
- Cause pulmonary hypertension, increasing RV afterload and leading to RVF
- RVF reduces LV output by reducing blood pumped to left heard and reducing LV size/compliance (RV is too big)
(LV preload is too low) |
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Term
| Why do patients with pulmonary vascular disease get dyspnea and exercise limitation? |
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Definition
PVD causes pulmonary HTN, diffusion impairment and V/Q inequality.
- Increased CO in exercise further increases PAP, increasing RV afterload and leading to RV dysfunction.
RV dysfunction impairs LV function and metabolic demands of body are not met. |
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Term
| What are the major risk factors for venous thromboembolism? |
|
Definition
"VIrchow's Triad"
1) Hypercoagulability
- Inborn (factor V leiden and prothrombin 20210A mutation)
- Acquired (Malignancy, estrogens, preegnancy, anti-phospholipid antibodies)
2) Stasis of blood
- Surgery
- Lower extremity paralysis
- Immobilization
3) Vessel injury
- Surgery or trauma
**ALSO Prior thromboembolism, and AGE (>40) |
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Term
| How doe PE affect gas exchange and hemodynamics? |
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Definition
Come from femoral/popliteal veins (Deep).
1) Gas Exchange
- Blood cannot reach ventilated alveoli, so you get V/Q mismatching (NOT SHUNTING).
2) Hemodynamics
- Cross-sectional area decreased, increasing PVR and RV afterload.
- RV dysfunction leads to LV dysfunction |
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Term
| What important imaging and laboratory studies are used to evaluate a patient who presents with acute onset dyspnea and tachypnea if you are worried about DVT/PE? |
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Definition
1) D-dimer
- High NPV
2) CT angiography to see PE
3) Venous ultrasound to see DVT (loss of vein compressibility) |
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Term
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Definition
Anticoagulation with bolus of heparin followed by infusion with added oral Warfarin.
Can use altepase acutely and use IVC filters in patients for whom drugs are ineffective or who have a high recurrent risk of PE. |
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Term
| How is Pulmonary hypertension classified? |
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Definition
> 25 mmHg at rest or >30 mmHg during exercise
1) PAH
- Sporadic, Familial, Collagen vascular, congenial shunts, portal, HIV, drugs and toxins
2) PVHTH
- left-side heart disease
3) Hypoxemia
- COPD, interstitial disease, sleep disorder, hypoventilation, high altitude
4) Chronic thrombotic/embolic
5) Miscellaneous
- Sarcoid
- Histiocytosis |
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Term
| What are the causes of pulmonary hypertension? |
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Definition
1) Idiopathic
2) Familial
3) Collagen vascular disease
4) Congenital systemic-pulmonary shunts
5) Liver Disease
6) HIV
7) Drugs
8) Hemoglobinopathy
9) Interstitial disease
10) Sleep disorderss
11) Chronic thromboembolic
12) Left heart disease |
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Term
| What kinds of mutations are associated with familial PAH? |
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Definition
1) BMPR-2 mutation with smooth muscle growth
2) ALK-1 (TGF-b like) mutation in patients with Osler-Weber-Rendu
3) 5-HTT transporter |
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Term
| What is the basic pathophysiological process underlying PAH? |
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Definition
1) Endothelial dysfunction leads to increased Endothelin, THXA2 (constrictive) and Decreased NO and Prostacyclin (dilating)
2) Smooth muscle activation and dysfunction
- dysfunction of voltage-gated K+ channels lead to K+ efflux and increased intracellular calcium (furthering constriction)
3) Fibrosis and angiogenesis
4) Progressive remodeling |
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Term
What disease is not associated with the onset of PAH?
1) Osler-Weber-Randu
2) Collagen Vascular disease
3) HIV
4) Hepatopulmonary syndrome
5) Protopulmonary Hypertension |
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Definition
4) Hepatopulmonary syndrome involves progressive hypoxemia due to oxygenation defect form intrapulmonary vascular dilations. It does not cause PAH and resolves after transplant.
This is different from Portopulmonary Hypertension, which presents with PAH but not hypoxemia
It can involves a) hyperdynamic circulatory state, b) excess volume and c) vasoproliferative disease.
- Osler-Weber-Randu, Collagen Vascular Disease and HIV are all associated with PAH. |
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Term
| What are the 3 subsets of Portopulmonary hypertension that can produce PAH? |
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Definition
You can tell by looking at CO and PVR.
1) Hyperdynamic circulatory state
- Moderate increase in pulmonary pressure and severe increase in CO
- REDUCED PVR
2) Excess volume
- moderately increased pulmonary pressure and CO
- NORMAL PVR
3) Vasoproliferative disease
- rare with increased pulmonary pressure and PVR
- DECREASED CO (need t/x) |
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Term
| Why is PAH seen in HIV patients? |
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Definition
HHV-8 producing Kaposi sarcoma is implicated.
Give them HART! |
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Term
Which of the following conditions is not associated with PAH?
1) Anorexinogen use
2) Sick-cell disease
3) Idiopathic pulmonary fibrosis
4) Obstructive sleep apnea
5) Chronic thromboembolic PAH |
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Definition
| NONE! They are all associated |
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Term
| How does the endothelin-1 system function under normal conditions? |
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Definition
Vasoconstriction, cell proliferation and differentiation determined by ET-A:ET-B balance.
1) ET-1 synthesized and released by endothelial cells (as well as many other cell types) under conditions of hypoxemia, pulsatile stretch, low shear stress and inflammation.
2) Endothelin released into cytoplasm as prepro-endothelin, where it is cleaved by furin-like enzyme to Big-endothelin (bET-1)
3) bET-1 is cleaved by ECE into ET-1, which binds ET-A (vascular smooth muscle) and ET-B (endothelial cells)
3a) ET-A on smooth muscle leads to smooth muscle contraction via PLC pathway
3b) ET-B on endothelial cells leads to NO-dependent vasodilation and ET-1 clearance. |
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Term
| How does ET-1 dysfunction produce PAH pathogenesis? |
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Definition
ndothelial damage causes imbalance of vasoconstrictive (Endothelin-1 and Thromboxane A2 increase) and vasodilating (Prostacyclin and NO decrease) factors
Normally, ET-1 reduces heart rate, decreases coronary BF and coronary sinus O2 saturation and increases cardiac contractility.
Under pathological conditions
1) Acute
- vasoconstriciton and inflammation
2) Chronic
- Fibroblast proliferation and ECM components
- Increase ACE activity
- Cardiac myocyte hypertrophy |
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Term
| How can dysfunction in the Prostacyclin pathway contribute to PAH pathogenesis? |
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Definition
Remember, Prostacyclin and NO inhibit ET-1
1) Major lipid-mediator product on endothelium, which relaxes smooth muscle by increasing cAMP and inhibiting platelet aggregation and smooth muscle proliferation.
2) In IPAH, prostacyclin synthase is down-regulated (especially in collagen vascular disease) |
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Term
| How is NO signaling impaired in PAH? |
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Definition
NO increases cGMP (broken down by PDEs) via soluble GC leading to smooth muscle relaxtion.
1) Reduced eNOS expression in lungs of PAH with impaired activity of soluble GC prevents appropriate dilation.
2) PDE5 may be a good target to prevent cGMP breakdown. |
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Term
| How does hypoxic pulmonary vasoconstriction occur in the pulmonary vasculature? |
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Definition
1) Hypoxia sensed by endothelium.
2) Inhibition of pulmonary vascular smooth muscle K+ channel (more K+ efflux and more intracellular Ca2+) |
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Term
| What are the major physiological issues that limit pharmacological options in PAH? |
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Definition
Low SA and CO
1) Loss of cross-sectional area of pulmonary vasculature limits RV CO and is difficult to change
2) Limited RVCO limits LVCO, leading to bi-ventricular CO reduction (patients cannot tolerate agents that cause systemic vasodilation).
** Need to find vascular-bed specific receptor populations** |
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Term
| How is NO signaling regulated? |
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Definition
1) Receptor-medited increases in Ca2+ induce eNOS to make NO in endothelium.
**NO synthesized from L-arginine**
2) NO diffuses into the vascular smooth muscle, binds sGC and increases cGMP, which produces vasodilation |
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Term
| How is inhaled NO delivered selectively to the lungs? |
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Definition
1) NO combines with and is deactivated by oxygenated (forming Methemoglobin and NO3-) and deoxygenated (nitrosylhemoglobin) Hb
2) Vasodilation occurs in well-ventilated alveolar units, |
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Term
| Why is inhaled NO generally only used in the ICU for neonates with PAH? |
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Definition
It has a short half life (2-6s) and can cause rebound hypertension.
metabolized to nitrate by kidneys and excreted in the urine at rate of GFR. |
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Term
| Why might you prescribe Epoprostenol, Treprotinil or Iloprost? |
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Definition
All 3 PGI2 analogues directly induce pulm/systemic vasodilation and inhibit platelet aggregation.
All may have jaw pain, flushing, syncope (less pronounced in Iloprost)
Difference is method of administration and half life (Epoprostenol is shorter half life and given IV)
1) Epoprostenol is given IV to central venous circulation (t1/2 6min)
2) Treprostinil is given by sub-q infusion with 100% bioavailability (t1/2 2-4h)
3) Iloprost is 4R:4S diasteromer mixture administered by aerosol and lasting 30-60min |
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Term
You start a hypovolemic patient on a drug to increase their blood pressure but notice an immediate drop in arterial blood pressure.
You are concerned, but the BP starts to increase.
What happened? |
|
Definition
You gave an ET-1 analouge.
1) ET-1 causes rapid and transient decrease in BP because of ET-B-mediated PGI2 and NO release from vascular endothelium.
2) This is countered by ET-A activation in vascular smooth muscle, which produces constriction. |
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Term
| Why might you prescribe Ambrisentan, Bostentan, or Sitaxsentan for PAH? |
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Definition
"Entan"= ET-1 inhibitors.
ETA-selectivity is really the issue here and Abrisentan/Sitaxsentan are better than Bostentan
1) Abrisentan is a highly selective ETA antagonist
- dose-dependent hepatotoxicity (not major issue)
2) Bostentan is competitive antagonist of ETA and ETB (slightly more ETA)
3) Sitaxsentan is the BEST ETA-selectivity, with drug interactions (only available in research).
- Hepatotoxic
- Don't give with anti-glycemic agents, cyclosporine A or during pregnancy! |
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Term
| Why might you prescribe Sildenefil or Tadalafil in PAH? |
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Definition
Both are orally administered PDE 5 inhibitors that prevent cGMP breakdown and prolong NO action.
Both have minor headache, flushing and nasal congestion.
1) Sildenefil (viagra)
- drug-drug interactions are issue
- some PD3 (cardiac contractility) and PD6 (color vision) activity |
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Term
An older patient presents to your office complaining that he is having difficulty "seeing the color of his wife's eyes). He also says he has been having abnormal heart rythms.
What could be going on? |
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Definition
| He might be on Viagra for PAH and/or ED and these are side effects due to PDE6 and PDE3 inhibition (supposed to hit only PDE5) |
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Term
| What are the major histological features of Bacterial Pneumonia? |
|
Definition
1) Lobar (large portion of one lobe
4 stages
- Congestion (<24h) with wet cut, eosinophilic froth
- Red hepatitization (1-3d) with dry cut, PMNs and edema
- Grey hepatitization (3 d) with leukocytes in alveoli
- Resolution with pathcy ingestion by macrophages
2) Bronchopneumonia (patchy consolidation)
- Patchy yellow white tan infiltrates (S. aureus, S. pyogenes, H. influenzae, Klebsiella and Legionella) |
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Term
| What are the major histological features of ARDS? |
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Definition
| DAD (all parts of one alveolus) during exudative stage with hyaline membranes (fibrosis in proliferative stage) |
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Term
What are the major histological features of
1) Pneumocystis Pneumonia
2) Aspergillus Pneumonia |
|
Definition
1) Prominent frothy, foamy honeycomb exudate in airspaces
with round, helmet-shaped cysts
- No yeast budding and can be visualized with Ab
2) long, thin hyphae, which branch at about 45 degree angles.
- Caseous necrosis |
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Term
| What are the major histological features of PE? |
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Definition
Airspace filling with RBCs and hemosiderinladen macrophages
**Resolution results in reconstitution of pre-existing architecture** |
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Term
| How can you clinically detect Obstructive Sleep Apnia or Hypoapnia? |
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Definition
Apnea is lack of airway measured at nose and meath for 10 seconds longer during sleep despite effort to breathe
1) Decrease in oxyhemoglobin saturation
2) ECG changes |
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Term
| What is the basic pathophysiology of OSAH? |
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Definition
Airway closure with negative intrathoracic pressure
1) Airway size determined by craniofacial structure/function and obesity
2) In sleep, muscle tone decreases and airway collapse becomes an issue.
3) Ventilatory related arousal is precipitated by airway resistance (snoring), hypopnea or apnea.
4) Persistant sympathetic arousal to wake patients up leads to CVD over time. |
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Term
| Why might you see elevation of C-reactive protein in OSAH? |
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Definition
| Intermittent hypoxia because of ischemia-reperfusion leads to expression of markers of oxidative stress. |
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Term
| What are the important co-morbidities of OSAH? |
|
Definition
1) CV
- prevents normal decrease in BP and HR
- toll over time can lead to hypertension, HF, MI or stroke.
2) Metabolic
- Elevated leptin inhibits neuropeptide Y synthesis, which is a stimulator of food intake
3) Neurocognitive
- Sleepiness and cognitive function
- Depression |
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Term
| What is the typical clinical presentation of a patient who suffers from OSAH? |
|
Definition
- Nightly loud snoring
- breathing pauses during sleep
- choking
- daytime sleepiness |
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Term
| How do you definitively diagnose OSAH? |
|
Definition
Need labs for objective measurement.
Portable polysomnography is typical
EEG, bilateral electroculogrpahic and submental electromyographic (chin) activity.
Cardiopulmonary measures are also taken. |
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Term
| What are the recommended treatments for OSAH? |
|
Definition
1) First-line is positive pressure ventilation (CPAP) to treat airway closure
- improves insulin sensitivity, LVF, pulmonary hypertension, endothelial function and mortality.
- Adherence is issue because of nasal dryness (humidifiers added)
2) Oral Appliance (OAP)
- increase upper airway size and prevent collapse
- takes a long time, compliance is poor and effectiveness is not 100%
- Tongue-retaining (TRD) and mandibular advancement (MAD)
3) Surgical therapy
- Tracheostomy (bypass upper airway)
- Reconstruction of upper airway (better cosmetically, but less certain results) |
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Term
| What are the critical elements of a pediatric history for diagnosis airway disease? |
|
Definition
Birth, when did it begin, triggers, what makes it better, what is it like, does it wake you?
1) Birth history
2) Did it arise in 1st 6 months?
- congenital?
3) What are the triggers of cough or wheeze?
- Viral RI?
4) Response or lack of response to therapy?
5) Nature of cough (wet or dry)?
- asthma is dry in infants
- wet means bacterial, CF or primary ciliary dyskinesia (PCD)
6) Does the cough wake you from sleep?
- RED FLAG. |
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Term
| What is the "Atopic triad" that should be asked about in Family h/x? |
|
Definition
1) Asthma
2) Eczema
3) Allergies |
|
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Term
| What are the most important ROS for a pediatric respiratory exam? |
|
Definition
1) GER
2) Recurrent OM (PCD but NOT CF), sinusitis, and pneumonia/bronchitis/bronchiolitis |
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Term
| What is meant by a child who is a "happy wheezer"? |
|
Definition
compliant in first 6 months.
1) Kids with Large airway diseases (floppy trachea or bronchus) have chronic noisy breathing but NEVER have respiratory distress (NO HYPOXEMIA). |
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Term
| What does the "time constant" have to do with pediatric respiratory disease physiology? |
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Definition
Time constant (s)= Resistance (viscous flow) * Compliance (elastic recoil)
**approximately 1/3 the time for lungs to empty fully**
1) Resistance
- Small changes in airway size create large changes in Resistance
- 8nL/(pi)r^4
2) Compliance is change in volume per a change in pressure.
- Increased compliance in bronchopulmonary dysplasia (BPD) and focally in congenitl lobar emphysema (CLE) |
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Term
| Why in small airway disease of children is the time constant (t) increased, but RR also increased? |
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Definition
T is 1/3 the time for a lung unit to empty and depends on R * C
- In small airway disease like RSV, T increases because R increases.
- HOWEVER, there is V/Q mismatching, so Ve increases and "air trapping" occurs, leading to over-expansion of the lungs and pressure pushing the diaphragm from the chest wall (you see subcostal retractions). |
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Term
What do each of the following findings on pediatric chest inspection indicate?
1) RR= 50 in a 1 week old
2) Subcostal RTX
3) Intercostal/suprasternal RTX |
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Definition
1) RR of 50 is normal for 2 week and 32 is normal for 1 year)
2) Subcostal retractions (RTX) means small airway disease
3) Intercostal/suprasternal RTX means excessive negative pleural pressure in Pneumonia, RDS and interstitial lung disease.
2) Palpation
3) Percussion
4) Ascultation |
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Term
What do the following PE findings indicate?
1) Unilateral vibrations on palpation
2) Crackles (discontinuous)
3) Polyphonic Wheezing (continuous)
4) Monophonic Wheezing (continuous) |
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Definition
1) Bronchomalacia, foreign body or mucus plug
2) Interstitial lung disease (coarse or fine)
3) Polyphonic means asthma or bronchiolitis
4) Monophonic tracheo- and bronchomalacia or bronchial foregin body (single location of partial obstruction) |
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Term
A 1 year old child presents with difficulty breathing. On palpation, you notice unilateral vibrations which are accompanied by monophonic wheezing.
What are the possible diagnoses? |
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Definition
| Bronchomalacia, Tracheomalacia or Foreign body. |
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Term
| Why are symptoms from bronchiolar obstruction much more common in infants and young children than in adults? |
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Definition
Bronchioles contribute 50% of airway resistance in the younger cohort, while only 10% in the older.
Bronchiolitis is commonly acute in kids and chronic in adults. |
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Term
| What is the most common etiological agent of acute infectious bronchiolitis in kids? |
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Definition
RSV- most kids <2
- ssRNA virus that enters through nasal or conjunctival mucosa and first infects upper airway (increased secretory and circulating Ab production)
- Infects secretions are aspirated into lower airway and infect epithelial cells (replicates inside cell and is released with lysis)
- Peribronchiolar edema and mononuclear and lymphocytic infiltration occur, with stimulation of mucous production
Mycoplasma pneumoniae is also a concern. |
|
|
Term
| What is the basic pathogenesis of RSV infection of infants? |
|
Definition
Most common cause of hospitalization in kids <1
1) ssRNA virus that enters through nasal or conjunctival mucosa and first infects upper airway (increased secretory and circulating Ab production)
2) Infectious secretions are aspirated into lower airway and infect epithelial cells (replicates inside cell and is released with lysis)
3) lysed cells cause inflammation: Peribronchiolar edema and mononuclear and lymphocytic infiltration occur, with stimulation of mucous production
4) V/Q mismatching occurs and hypoxemia follows, with low compliance and high resistance |
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|
Term
A 1 month-old boy presents with profuse rhinorrhea and a prominent cough. He is breathing at a RR of 60 and is working hard with "short, shallow breaths."
On PE, you notice intercostal, sternal and subcostal RTX.
You also note crackles and wheezing
Why do you see this breathing pattern and what should you do next? |
|
Definition
RSV for sure
1) Short rapid breathing because of decreased compliance and increased resistance (needs to conserve work).
2) Try and identify organism with nasopharyngeal wash or viral culture (ELISA and PCR are fast and reliable)
3) Treat with fluid replacement (careful), supplemental O2 and maybe bronchodilators
**Not anti-inflammatory and anti-viral agents** |
|
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Term
| What is Bronchopulmonary dysplasia and who does it affect? |
|
Definition
BPD is lung disease of small, premature infants.
- Infants are born with RDS because of surfactant deficiency and lung immaturity.
- Multifactorial pathogenesis with ventilator-induced volutrauma and barotrauma, as well as oxidant injury, nutrition, corticosteroids (RSD) |
|
|
Term
| How should babies with BPD be managed? |
|
Definition
Oxygen (retinopathy concern), bronchodilators, anti-inflammatories, ect.
The clinical status of children with BPD should improve over time with continued somatic and pulmonary growth...
If it doesn’t, consider:
Airway complications
Gastroesophageal reflux, aspiration
Cardiac complications |
|
|
Term
| What are the cardiovascular and neurological complications of BPD? |
|
Definition
1) CV (monitor oximetry and BP closely)
- Pulmonary hypertension
- Cor pulmonale
- Heart failure
- Systemic hypertension
- Shunts
2)
- Neuromotor feeding disorders
- Developmental delay
- Spasticity - hypotonia
- Auditory loss
- Visual loss |
|
|
Term
| What are the 2 major types of lung cancer. |
|
Definition
2 types of Bronchogenic carcinoma
1) Non-small cell carcinoma (NSCLC)
- Adenocarcinoma (35% of all), squamous carcinoma, large cell, undifferentiated carcinoma (most common)
2) Small cell lung carcinoma
- Agressive with early metastasis and poor prognosis |
|
|
Term
| What are the most common exposures that lead to lung cancer? |
|
Definition
1) Tobacco smoke (Second worst)
2) Radon (uranium miners)
3) Asbestos (the worst!)
4) Wood smoke/air pollution |
|
|
Term
What kinds of cancer are each of the following associated with?
1) N-nitrosamines
2) PAH |
|
Definition
1) Adenocarcinoma
2) Squamous cell tumors |
|
|
Term
| What are the 3 best described oncogenes in human lung cancer? |
|
Definition
1) c-myc in small cell lung cancer (alters transcription)
2) K-ras in cell:cell signal transduction (proto-oncogene becomes oncogene with SNPs)
3) c-erbB2 is TK that regulates EGFR |
|
|
Term
| What proto-oncogenes are most commonly mutated in pulmonary adenocarcinoma and how do these mutations contribute to the pathobiology of cancer? |
|
Definition
K-ras and EGFR
Mutation prevents auto-inhibition of TK on EGRF and leads to constitutive activation, leading to proliferation, invasion and metastasis |
|
|
Term
What pathological findings define each of the following?
1) Adenocarcinoma
2) Bronchioloalaveolar Cell Carcinoma (BAC)
3) Squamous cell carcinoma
4) Large cell, undifferentiated
5) Small cell |
|
Definition
1) Peripheral nodule or mass with pseudo-gland formation and intracytoplasmic mucin
2) subtype of 1 with alveolar septal growth, presenting as nodule or alveolar infiltrate (BRONCHORRHEA)
3) Bronchogenic tumor of central airways leading to obstruction. Look for "Keratin "earls" on H & E
4) Large, bulky mass with necrosis
5) central chest with early LN involvement and metastasis to brain, liver, bone marrow.
- Pleomorphic population of small cells with hyperchromatic nuclei and dispersed chromatin. |
|
|
Term
What kind of lung cancer matches each of the following pathological descriptions?
1) Peripheral nodule or mass with pseudo-gland formation and intracytoplasmic mucin
2) Bronchorrhea
3) "Keratin Pearls" on H & E
4) Large, bulky mass with necrosis
5) Pleomorphic population of small cells with hyperchromatic nuclei and dispersed chromatin. |
|
Definition
1) Adenocarcinoma
2) Bronchioloalveolar cell carcinoma (BAC)
3) Squamous cell carcinoma
4) Large cell carcinoma
5) Small cell carcinoma |
|
|
Term
| How are lung cancer tumors staged in small-cell carcinoma? |
|
Definition
1. Evaluation of the primary tumor
- Primary tumors are staged from T0 (no evidence of tumor) to T4 (extensive tumor)
2) Evaluation of regional lymph node metastases
- Regional lymph nodes are staged from N0 (no metastases) to N3 (contralateral metastases)
3) Evaluation of distant metastases
- M0 - no metastases; M1 - distant metastases present
The three parameters are combined together to establish pathologic stage of the disease (from I to IV). |
|
|
Term
What medical therapies are suggested for each of the following NSMC?
1) Stage 1 A/B and II A/B
2) Stage IIIA
3) Stage IIIB
4) Stage IV |
|
Definition
1) Lobectomy
2) Surgery + chemo is superior to surgery alone
3) Thoracic radiation and chemotherapy only.
4) Palliation (chemotherapy to be 3-9 months extra) |
|
|
Term
| What are the important paraneoplastic syndromes to be aware of with lung cancers? |
|
Definition
1) Hypertrophic Pulmonary Osteoarthropathy (HPO)
- Clubbing and painful arthropathy of knees, ankles and wrists.
2) Hypercalcemia
- PTH-related peptide causes bone turnover and increases calcium reabsorption and sodium wasting through kidney.
3) SIADH
- Euvolemic hyponatremia
4) Cushing's
- Small cell cancers leading to ectopic ACTH production |
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Term
| Why do patients with small cell lung cancer sometimes present with HTN, moon facies and abdominal striae? |
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Definition
Cushing's syndrome with ectopic ACTH production.
Too much cortisol. |
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Term
| What neurological disorders are associated with small cell carcinoma? |
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Definition
1) Neuropathy
- anti-neuronal antibodies
2) Limbic encephalitis
- decreased cognitive ability and easy confusion (looks like dementia)
3) Lambert-Eaton Syndrome
- Proximal muscle weakness and hyporeflexia
- partial blockage of ACh release from NMJ by antibodies against Ca channels.
**decreases with remission** |
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Term
A 75 year old man who is a non-smoker presents with localized chest pain. He was previously asymptomatic.
You order an CXR and see a peripheral sub-pleural mass that has spread to the hilar and peribronchial lymph nodes.
What do you see on gross examination and histological analysis of his lungs? |
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Definition
This is Adenocarcinoma, the most common cause of lung cancer in non-smokers.
The asymptomatic history and older age fits well.
1) Gross
- Usually a peripheral, sub-pleural mass
2) Histology
- Infiltrating "pseudo" glands in cribriform, tubular or papillary configuration (80% of mucus)
- Desmoplastic stroma. |
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Term
| What types of lung cancers are close to the mediastinum, deriving from the mucosa of the main, lobar or segmental bronchi? |
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Definition
These are Central Lesion and often arise in areas of squamous metaplasia.
Carcinomas are Squamous Cell or Small Cell and are prone to distal atalectasis, necrosis/cavitation and microorganism colonization. |
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Term
A 69 year old male with a 80 pack year h/x of smoking presents with chest pain. He is hypercalcemic. You order a CXR are discover a mediastinal mass.
What do you see on gross/histological analysis of the mass? |
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Definition
This is squamous cell carcinoma. Age and smoking h/x fit, as well as central lesion (vs. peripheral lesion in adenocarcinoma) and hypercalcemia.
**Squamous pearls wrapping keratin plug like an ONION**
1) Gross
- Central lesion
2) Histological
- Squamous metaplasia/dysplasia, which may progress to carcinoma in situ and invasive squamous carcinoma.
- Intercellular bridges desmosomes.
- Intracytoplasmic keratinization. |
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Term
A 72 year old female with a 30 pack year history of smoking presents presents with a bloody cough.
You order a chest X-ray and see a Central mass with metastases.
What do you see on gross/histological analysis of the mass? |
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Definition
Small cell carcinoma
1) Grossly
- Central lesion with or w/o cavitation
2) Histology
- Sheet-like arrangement of malignant cells with vesicular nuclei, prominent nucleoli, and abundant cytoplasm.
- No keratin pearls, intercellular bridges, or mucin production |
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Term
A 82 year old male presents with a bloody cough, HTN, moon face and abdominal striae. He is also hypokalemic.
You order a CXR and see a central tumor mass with small primary and extensive nodal disease.
What are the gross/histological findings? |
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Definition
Older individual with bloody cough and paraneoplastic syndromes (Cushing's and SIADH described here), as well as central mass with small primary lesion means SMALL CELL CARCINOMA.
1) Gross
- Centrally located / mediastinal mass
- Frequently necrotic
- Mediastinal lymphadenopathy
2) Histological
- Small cells with dense hyperchromatic nuclei, scant cytoplasm, nuclear molding
- Extensive necrosis
- Lymphatic invasion
- Presence of neurosecretory granules (neuroendocrine differentiation |
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Term
A 74 year old male roof-worker presents with pleuritic chest pain and a bloody pleural effusion.
On CXR you see diffuse pleural thickening.
What are the gross/histological findings? |
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Definition
Asbestos exposure in older individual with pleural effusion and pain indicates Mesothelioma.
**look for ferruginous body!**
1) Gross
- White nodules and plaques covering the parietal and visceral surfaces (initially unilateral)
2) Histological
- Epithelial variant (papillary or tubular structures resembling adenocarcinoma)
- Spindle (sarcomatoid) variant (elongated spindle cells in fascicles)
- Mixed type (Epithelial and spindle cells) |
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Term
| What is the diagnostic test of choice for patients with small peripheral tumors or pleural tumors? |
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Definition
Video-assisted thoracoscopy
- Thorascope is passed through a small incision in the chest to remove a sample of lung tissue. |
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Term
| In which type of lung cancer do neoplastic cells recapitulate Clara cells, goblet cells or Type 1 and II pneumocytes? |
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Definition
Bronchioloalveolar adenocarcioma (Adenocarcinoma varient), which is commonly seen in non-smokers and young individuals.
Cells grow along septa. |
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Term
| What are the 2 types of tumors formed in Large cell carcinoma? |
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Definition
1) Anaplastic
- undifferentiated squamous or adenocarcinomas
2) Neuroendocrine
- uniform, medium-size cells that grow in clusters (express neuroendocrine peptides and you may see neuroendocrine granules on EM). |
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Term
Which of the following statements is CORRECT?
1) Throughout a tidal inspiration, the respiratory muscles must overcome the elastic recoil of the lungs and the chest wall.
2) At FRC, the elastic recoil pressure generated by the lungs (i.e. trans-pulmonary pressure) is zero.
3) The elastic equilibrium point of the chest wall (i.e. when the pressure gradient across the chest wall is zero) occurs at approximately 60% of the vital capacity.
4) To reach RV, the respiratory muscles must overcome the elastic recoil of both the lungs and the chest wall. |
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Definition
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Term
During spontaneous breathing, all of the following statements are correct, EXCEPT:
1) Pleural pressure becomes increasingly more negative as lung volume increases during inspiration.
2) Pleural pressure normally becomes positive (greater than atmospheric pressure) during a passive exhalation.
3) During passive exhalation, pleural pressure increases to its normal negative value.
4) Pleural pressure becomes positive only during forced or active expiration.
5) Alveolar pressure is zero at the end of inspiration.
Alveolar pressure becomes positive during exhalation. |
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Definition
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Term
After inhaling 2000 ml and reaching TLC, a subject relaxes his respiratory muscles, and the pressure in front of an occluded mouthpiece is found to be 40 cmH2O. Which of the following statements is TRUE?
1) At this volume, the elastic recoil pressure of the lungs is 40 cmH2O.
2) The compliance of the respiratory system is 0.02 cmH2O/ml
3) The measured pressure reflects, in part, the pressure required to overcome frictional or viscous forces during inspiration.
4) During inspiration, the respiratory muscles generated a pressure of at least 40 cmH2O. |
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Definition
4
During inspiration, the respiratory muscles must overcome both elastic recoil of the lungs and chest wall and frictional/viscous forces. To get to TLC, therefore, the muscles must generate at least the 40 cmH2O, which is required to overcome elastic recoil. |
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Term
All of the following statements are true, EXCEPT:
1) During inspiration, the respiratory muscles must generate sufficient pressure to overcome both elastic recoil and viscous forces.
2) Pleural pressure decreases throughout a spontaneous inspiration.
3) The elastic recoil of the lungs progressively increases throughout inspiration.
4) Alveolar pressure is negative (relative to atmospheric pressure) at the end of a spontaneous inspiration. |
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Definition
4)
At the end of a spontaneous inspiration, flow stops and the pressure inside and outside the lungs becomes equal. Alveolar pressure must, therefore, equal atmospheric pressure. |
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Term
If a subject with a baseline PaCO2 of 40 mmHg doubles his/her minute ventilation, PaCO2 would be expected to decrease to 20 mmHg only if:
1) Dead space ventilation is unchanged
2) Tidal volume does not change
3) CO2 production is cut in half
4) Respiratory rate does not change |
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Definition
| 2) If tidal volume does not change, both minute ventilation and dead space ventilation will double, as will alveolar ventilation. This will cause the PCO2 to decrease by one-half. |
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Term
Which of the following statements is INCORRECT?
1) At end-expiration, alveolar volume is greater at the bottom than at the top of the lungs.
2) During inspiration, more air enters the alveoli at the bottom of the lungs than at the top of the lungs.
3) Pleural pressure increases from the top to the bottom of the lungs.
4) At end-expiration, alveolar pressure is zero (atmospheric) throughout the lungs. |
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Definition
| 1) Since pleural pressure increases from the top to the bottom of the lungs and alveolar pressure at end-expiration is zero (atmospheric) everywhere, transpulmonary pressure and lung volume at end-expiration increase from the bottom to the top of the lungs. |
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Term
Which of the following do NOT cause a decrease in pulmonary vascular resistance (PVR)?
1) Increased cardiac output
2) Increased hydrostatic pressure
3) Increasing lung volume from RV to FRC
4) PGE2
5) PGI2 |
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Definition
| PGE2 is a protaglandin that causes vasoconstriction and therefore increases PVR |
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Term
Which of the following statements about ventilation-perfusion relationships is FALSE?
1) The PO2 and PCO2 of the gas in an alveolus are determined by the ratio of ventilation and perfusion to that alveolus.
2) As the V/Q of an alveolus falls, alveolar PO2 decreases and PCO2 rises.
3) High V/Q ratios increase alveolar and physiologic dead space.
4) A right to left intra-pulmonary shunt produces a V/Q of infinity. |
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Definition
| 4) A shunt produces a V/Q of zero. A V/Q of infinity indicates the absence of blood flow (dead space) |
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Term
Which of the following statements about diving is INCORRECT?
1) Lung volume decreases and the partial pressure of O2, CO2, and N2 increase with depth.
2) Decompression illness results from a rapid decrease in the partial pressure of nitrogen.
3) Barotrauma during ascent most commonly occurs during a breath-hold dive.
4) It is impossible to breathe through a tube connected to the surface beyond a depth of about 1 meter. |
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Definition
| 3) Barotrauma occurs when gas inhaled at high pressure causes the lungs to expand rapidly as ambient pressure falls during a rapid ascent. This will occur only if a SCUBA diver holds his breath during ascent. |
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Term
If rapid decompression of an airplane flying at 30,000 feet occurs, passengers will experience all of the following EXCEPT:
1) Increased PaCO2
2) Decreased PN2
3) A marked drop in barometric pressure
4) Decreased PaO2 |
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Definition
| 1: Like other gases, PCO2 depends on the barometric pressure and its fractional concentration. When barometric pressure falls, the partial pressure of all gases in the lungs and body fluids also decreases. |
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Term
Which of the following signs would help you to distinguish between complete lung atelectasis (collapse) and a pneumothorax?
1) Decreased or absent unilateral breath sounds
2) Dullness to percussion
3) Reduced vocal fremitus
4) Absent egophony |
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Definition
| Complete lung atelectasis will lead to dullness over the dense, collapsed lung, whereas a pneumothorax leads to hyper-resonance over the air-filled chest. |
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Term
Which of the following statements is INCORRECT?
1) The major densities distinguished by CT are air, fat, fluid, soft tissue, and bone/calcium.
2) The right hilum is almost always higher than the left hilum on the PA CXR.
3) The right hemidiaphragm is almost always higher than the left on the PA CXR.
4) The trachea is contained within the mediastinum. |
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Definition
| 2: The LEFT hilum is almost always higher than the right. |
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Term
Which of the following does NOT contribute to the dyspnea experienced during maximal exercise?
1) Increased CO2 production by the muscles
2) Increased VD/VT
3) Lactic acidosis
4) Increased inspiratory and expiratory flow rates |
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Definition
| 2: Because of the increased tidal volume and reduced dead space volume, VD/VT normally falls during exercise. |
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Term
A patient stops exercising when her VO2 is 65% predicted, her HR is 70% predicted, and her maximum VE is 30% of MVV. You find that she has not reached anaerobic threshold. Which of the following statements is CORRECT?
1) This patient has no cardiovascular or pulmonary limitation to exercise.
2) Her exercise limitation could be caused by use of a beta-blocker, which limits her maximum heart rate and cardiac output.
3) This patient has a pulmonary limitation to exercise.
4) This patient has a cardiovascular limitation to exercise. |
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Definition
| 1: At maximum VO2, this patient has a submaximal heart rate, has not reached anaerobic threshold, and has a large ventilatory reserve. |
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Term
In some patients with severe COPD, administration of supplemental oxygen leads to worsening hypercapnia. The most likely mechanism for this is:
1) Increased physiologic dead space
2) Loss of the "hypoxic" respiratory drive
3) Decreased minute ventilation
4) Increasing shunt |
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Definition
| 1: Studies have shown that patients who become more hypercapnic during O2 administration do not have a reduced minute ventilation. This means that the increased PCO2 is most likely due to increased physiologic dead space from worsening ventilation-perfusion imbalance. |
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Term
Each of the following statements is correct, except:
1) Intrinsic PEEP will increase as expiratory airway resistance decreases.
2) Intrinsic PEEP is determined by the combined elastic recoil of the lungs and chest wall.
3) Intrinsic PEEP increases with end-expiratory lung volume.
4) Intrinsic PEEP is associated with dynamic hyperinflation. |
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Definition
| 1: Intrinsic PEEP is the elastic recoil pressure of the respiratory system that remains at end-expiration. Therefore, the same factors that cause dynamic hyperinflation will cause intrinsic PEEP. A decrease in expiratory resistance will increase expiratory flow and reduce any intrinsic PEEP. |
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Term
Side effects of inhaled corticosteroids include all of the following, EXCEPT:
1) Thinning of skin and easy bruising
2) Oro-pharyngeal candidiasis (Thrush)
3) Hypothalamic-pituitary-adrenal (HPA) suppression
4) Immunosupression, with increased risk of infections |
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Definition
| 4. Inhaled corticosteroids have been shown to suppress the HPA axis, but they have not been found to produce immune suppression. |
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Term
All of the following statements about interstitial lung disease are true, EXCEPT:
1) The expiratory flow rate at a given lung volume is often increased above normal.
2) The pressure required to generate a given lung volume is increased.
3) Tidal volume is abnormally low and respiratory rate and 4) VD/VT are abnormally elevated.
5) Arterial hypoxemia is due largely to shunting. |
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Definition
| 5) Arterial hypoxemia is due to V/Q mismatch and diffusion impairment. Shunt is minimal, since these diseases do not produce regions of absent ventilation (V/Q=0). |
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Term
In patients with an airspace filling disease, arterial hypoxemia is largely due to:
1) Diffusion impairment
2) Shunt
3) Ventilation perfusion imbalance
4) Hypoventilation |
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Definition
| 2: Airspace filling causes lack of ventilation to perfused lung regions, and this leads to intrapulmonary shunting. |
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Term
All of the folloing statement about airspace filling diseases are true, EXCEPT:
1) Airspace filling leads to a decrease in lung volumes.
2) Airspace filling diseases are associated with an increase in airway resistance.
3) Airspace filling causes an increase in lung elastic recoil (stiffnes).
4) PFTs typically show a decrease in FVC and TLC. |
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Definition
| 2: Since they only affect the lung parenchyma, airspace filling diseases do not usually alter airway resistance. |
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Term
All of the following diseases may cause ARDS, EXCEPT:
1) Sarcoidosis
2) Bowel perforation
3) Alveolar hemorrhage
4) Massive aspiration
5) Pneumonia |
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Definition
| 1: Interstitial lung diseases do not lead to ARDS because they do not cause airspace filling. |
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Term
Which of the following causes of pulmonary hypertension is not associated with an increase in pulmonary vascular resistance?
1) LV failure
2) Severe COPD
3) Recurrent pulmonary embolism
4) Idiopathic pulmonary arterial hypertension |
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Definition
| 1: In patients with LV failure, elevated ventricular pressure is transmitted to the pulmonary circulation, but PVR remains normal. |
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Term
In infants and children, bronchiolitis causes small airway narrowing and increased airway resistance through all of the following mechanisms, except:
1) Airway edema
2) Increased mucous production
3) Epithelial cell sloughing
4) Smooth muscle constriction |
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Definition
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Term
In infants, GE reflux may cause all of the following, except:
1) Bronchiolitis
2) Asthma
3) Laryngospasm
4) Apnea |
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Definition
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