UWorld 3 Flashcards
What is the main cause of hypercapnia in COPD?
Increased dead space ventilation. It acts to worsen the respiratory acidosis.
How does the body compensate for chronic hypercapnia?
By increasing renal bicarb retention and creating a compensatory metabolic alkalosis
Significant smoking history, hypercalcemia and a hilar mass
Think squamous cell carcinoma of the lung. sCAmous
The hyperCa is from PTHrP.
Supplemental oxygen improves hypoxia in COPD but can cause CO2 retention by what mechanisms? (3)
1) Loss of compensatory vasoconstriction in areas of ineffective gas exchange worsens the V/Q mismatch
2) Increase in oxyhemoglobin reduces the uptake of CO2 from the tissues by the Haldane effect
3) Decreased respiratory drive and slowing of the respiratory rate causes reduced minute ventilation
Goal oxyhemoglobin level is 90-93% in these patients.
Origin of hypoxia in COPD
In advanced COPD, destruction of the terminal bronchioles and alveoli causes areas of physiologic dead space to develop. The affected regions have limited surface area available for gas exchange, which leads to V/Q mismatch causing local hypoxia and hypercapnia.
Hypoxia induces selective vasoconstriction in these areas of the lung and redirects blood flow to better ventilated alveoli, reducing V/Q mismatch.
What does the acidosis in COPD cause?
It increases brain gamma-amino butyric acid and glutamine and decreases brain glutamate and aspartate, causing a change in level of consciousness.
The hypercapnia that caused the acidosis also causes reflex cerebral vasodilation and may induce seizures.
Oxygen should be used cautiously with a goal SaO2 of 90-93% or PaO2 60-70. Patients who develop significant acidosis or have severely reduced LOC require mechanical ventilation.
Hypertrophic osteoarthropathy
Condition where digital clubbing is accompanied by sudden-onset arthropathy, commonly affecting the wrist and hand joints. Hypertrophic pulmonary osteoarthropathy is a subset of HOA where the clubbing and arthropathy are attributable to underlying lung disease like lung cancer*, TB, bronchiectasis, or emphysema (look out for chronic smoking)
CXR is appropriate test for identifying underlying cause of suspected HPOA.
Ddx based on carbon monoxide diffusing capacity of the lung
1) Low DLCO and obstructive PFTs - emphysema
2) Normal DLCO and obstructive PFTs - chronic bronchitis or asthma
3) High DLCO and obstructive PFTs - asthma
4) Low DLCO and restrictive PFTs - ILD, sarcoid, asbestosis or heart failure
5) Normal DLCO and restrictive PFTs - MSK deformity or NM disease
6) High DLCO and restrictive PFTs - Morbid obesity
7) Low DLCO and normal PFTs - Anemia, PE, or pHTN
8) High DLCO and normal PFTs - Pulmonary hemorrhage or polycythemia
Respiratory alkalosis in ventilated patient (with appropriate TV)
Lower the RR.
Ventilation is defined as product of RR and TV. Respiratory alkalosis is from hyperventilation.
Avoid lowering the TV - this can trigger an increased ventilatory rate and exacerbate the situation.
Centriacinar vs panacinar emphysema
Centriacinar (centrilobular) is smoking induced. Usually in upper lobes lungs.
Panacinar is from AATD and results in destruction of lower lobes.
Goodpasture’s Disease
Most common in young adult males. Renal findings include nephritic range proteinuria (less than 1.5 g/d), acute renal failure and urinary sediment with dysmorphic red cells and red cell casts.
Pulm findings include SOB, cough, and hemoptysis caused by pulmonary hemorrhage.
Systemic symptoms (fever, weight loss, arthralgias) are uncommon.
Underlying cause is formation of antibodies to the alpha-3 chain of type 4 collagen, a protein expressed most strongly in the glomerular and alveolar basement membranes.
Renal bx demonstrating linear IgG deposition along glomerular BM on IF is diagnostic.
The different lung cancer cell types.
1) Adenocarcinoma - 40-50% incidence. Peripheral location. Associated with clubbing and hypertrophic osteoarthropathy. Most common one in nonsmokers. It is also the most common one in smokers.
2) SCC - 20-25%. Central location. Necrosis and cavitation. Associated with hypercalcemia.
3) Small cell - 10-15%. Central location. Associated with Cushing syndrome, SIADH, Lambert Eaton syndrome.
4) Large cell carcinoma - 5-10%. Peripheral location. Associated with gynecomastia and galactorrhea.
R mainstem bronchus intubation
Relatively common complication of ET intubation. It causes asymmetric chest expansion or absent breath sounds on the left side on auscultation. I.E., one side of the chest will be overinflated and one side will be underinflated.
Repositioning the ET tube by pulling it back slightly will move the tip between the carina and vocal cords and solve the problem. Ideal location is 2-6cm above carina.
Bronchogenic carcinoma
The most common malignancy associated with asbestos exposure. Smoking adds an extra effect. Asbestos exposure alone increases cancer risk by 6 fold. Asbestos plus smoking increases it 59 fold.
Mediastinal tumor locations
1) Thymoma - Anterior mediastinum. About 20% of myasthenia gravis patients have a thymoma. Other anterior masses are retrosternal thyroid, teratoma, and lymphoma. If mass is large, patient may complain of chest heaviness or discomfort. Hoarseness, Horner’s, and facial/upper extremity edema may occur if tumors invade locally.
2) Bronchogenic cyst - Benign. Middle mediastinum. Other middle mediastinal entities are tracheal tumors, pericardial cysts, lymphoma, LN enlargement, and aortic aneurysms of the arch.
3) Neurogenic tumors - Posterior mediastinum. These include meningocele, enteric cysts, lymphomas, diaphragmatic hernias, esophageal tumors, and aortic aneurysms. MRI is best test for a posterior mediastinum mass.
