Case Based Learning Flashcards
How does heparin work?
Heparin binds to antithrombin and accelerates the inhibition of thrombin and factor Xa (as well as factors IXa and XIa)
How is Heparin monitored?
It is usually monitored using the aPTT. The goal aPTT is typically between 1.5 and 2.5 times normal. (Direct measurements of heparin blood levels are also available)
How could ou confirm a diagnose of Heparin-Induced Thrombocytopenia?
The diagnosis can be confirmed by testing for antibodies to the heparin-platelet factor 4 (PF4) complex
. Briefly describe the pathophysiology of TTP
Autoimmune destruction of ADAMTS-13 allows persistence of very large VWF multimers. These can spontaneously bind to platelets and generate microthrombi consisting of platelets and VWF in small vessels. This causes mechanical RBC destruction and organ dysfunction due to decreased perfusion.
If there is clinical suspicion for TTP, what should be done for treatment?
it is imperative that the patient receive treatment. The mainstay of treatment is plasmapheresis with plasma replacement. This provides two benefits – 1) it reduces the levels of anti-ADAMTS13 antibodies and 2) it replaces the ADAMTS13 by giving back normal donor plasma
emesis
vomiting
Finding A-a gradient
PAO2 = (Patm - Pwater) FiO2 - PaCO2/0.8
PAO2 = PiO2 – PaCO2/0.8
IF at room air at sea level:
PAO2 = 150 mm Hg - PaCO2/0.8
Despite a very high dead space, a patient’s PCO2 is 33. What does this tell you about her alveolar ventilation and minute ventilation?
Alveolar ventilation is high, minute ventilation is high (in addition to alveolar ventilation being high, the dead space fraction is elevated (normal is around 0.2), thus you can conclude that minute ventilation is high (VE = VA + VD)
What causes the exercise-induced hypoxemia in a patient with pulmonary fibrosis?
Reduced transit time of the RBCs through a “fixed” capillary bed (diffusion impairment leads to exercise induced hypoxemia)
COPD with hypoxemia and high PCO2 – what factors are contributing to hypexmia if at sea level?
V/Q mismatch and hypoventilation
Patient with alkalosis and hypoxemia goes to high altitude. What is the most likely order of changes that occur in response to the alkalosis (lower PaCO2) and to compensate for the decline in oxygen content?
Oxyhemoglobin curve shifts to the left, 2-3-DPG is synthesized, red cell mass increases
Summary of CO Effects on Hemoglobin
Reduced binding of O2 to Hgb due to increased affinity of CO
Inaccurate measurement of oxygenation through pulse oximetry
Reduced delivery of oxygen to the tissues due to change in hemoglobin molecule reducing release of oxygen in the peripheral tissues (Left Shift)
Which spirometric measurements is the most affected by variation in patient effort?
Peak flow—data collected entirely from effort dependent part of flow-volume curve
How does the presence of air trapping affect the vital capacity?
Decreases VC because residual volume is increased (ERV is also reduced)
plethysmography measures which component of lung volumes that cannot be assessed by spirometry?
Residual volume (volume remaining in the chest at end expiration that cannot be measured through spirometry)
What spirometry observation occurs in most cases of pure restrictive AND in some cases of pure obstructive disorders?
Reduced FVC (can be true for both obstruction and restriction)
During variable intrathroacic obstruction, what is the mechanism of airway collapse?
pleural pressure exceeds airway pressure in the large airways (the plateau on the expiratory limb of the flow volume loop doesn’t happen in regular obstructive diseases; its presence suggests a mass in the trachea etc. or some other large airway that is usually stented open by cartilage etc.)
DLCO decreased or normal: emphysema
decreased
DLCO decreased or normal: asthma
normal
DLCO decreased or normal: lung fibrosis
decreased
DLCO decreased or normal: dyspnea due to obesity
decreased
DLCO decreased or normal: dyspnea due to severe anemia
decreased
DLCO decreased or normal: dyspnea due to mild congestive heart failure
normal
What is the appropriate management for a patient with pulmonary hypertension due to left side heart failture?
diuretics
What is an AQI score?
The AQI is an index for reporting daily air quality. EPA calculates the AQI for five major air pollutants regulated by the Clean Air Act: ground-level ozone, particle pollution (also known as particulate matter), carbon monoxide, sulfur dioxide, and nitrogen dioxide. Higher is worse.
Why does ARDS lead to restrictive ventilatory physiology?
ARDS is a diffuse inflammatory response in the lung either due to direct or indirect injuries. The hallmark of ARDS is the presence of protein-rich edema fluid in the alveoli due to an increased permeability of pulmonary capillary. As the alveoli become filled with this fibrin rich edema, the lung becomes less compliant. It requires greater intrathoracic pressure to generate similar volumes. This by definition is restrictive physiology
List and discuss some of the major causes of ARDS. What do they have in common?
Direct Lung injury:
- Pulmonary infections
- Aspiration: gastric contents, drowning
- Pulmonary contusion,
- Fat emboli
- Inhalational injury: high O2, chlorine, smoke, ozone
Indirect Lung Injury:
- Overwhelming infection: Sepsis
- Trauma
- Pancreatitis
- Drug overdose: narcotics
All of these (and many other possible causes) do damage to the alveolar capillaries throughout the lung
What is the pathogenesis of hyaline membrane formation in ARDS?
Alveolar lining cells are damaged. Fibrin-rich edema fluid mixed with the cytoplasmic and lipid remnants of necrotic epithelial cells then accumulates in the alveolar space, forming the alveolar hyaline membranes
What is the appropriate initial management for a patient with ARDS?
The treatment for ARDS is largely to minimize further injury to the lung and provide supportive care. Patients often require intubation and mechanical ventilation to assist with oxygenation and minute ventilation.
what condition can result in a similar presentation to IPF?
connective tissue disease
What is needed to establish an asbestosis diagnosis for legal purposes?
Occupational history and a chest radiograph interpreted by specialist with additional training related to pneumoconiosis
how can you make a specific diagnosis for hypersensitivity pneumonitis?
The best way to make the diagnosis is by performing bronchoscopy with transbronchial biopsy; tissue histopathology should demonstrate “loose” granulomata comprised of lymphocytes and mononuclear phagocytes and lymphocytes infiltrating alveolar septae. Bronchoalveolar lavage could also be performed; a large percentage of lymphocytes, particularly if the T4 to T8 lymphocyte ratio is low, is strongly supportive of the diagnosis.
How would you improve and then preserve a patient’s lung function if they have hypersensitivity pneumonitis?
The most important treatment is to cease exposure to the causative antigenic agent(s). Usually the inflammation will resolve quite well if this is done. However, continued exposure with persistent inflammation may lead to irreversible fibrosis. A brief course of corticosteroids may be beneficial for this patient with severe manifestations of the disease.
Why does leaning forward help a COPD patient breath more easily?
The increased abdominal pressure at the end of exhalation causes the diaphragm to start from a more mechanically advantageous position
Cause of hypoxemia in Pulmonary Embolism
Dead space does not result in hypoxemia unless the amount of physiologic dead space is so large that there are not enough lung units left to participate in gas exchange (i.e., until diffusion capacity becomes a limiting factor). Hypoxemia in P.E. is caused by areas of low V/Q and shunt. These areas may be the result of atelectasis, pulmonary hemorrhage, loss of surfactant, pneumoconstriction, and localized pulmonary edema. Rises in PA pressure following P.E. may also result in a right to left intracardiac shunt through a potentially patent foremen ovate.
bone fracture can be a risk for what kind of pulmonary problem?
a long bone fracture can put a patient at risk for a fat embolism
These tend to present within 24-72 hours of the injury. They are characterized by hypoxemia, neurologic abnormalities, and petechial rash. Patients can progress to develop ARDS.
what is treatment for hemodynamically unstable patients due to thromboembolism?
thrombolysis (AKA “clot busters”) and mechanical thrombectomy. Thrombolytics like streptokinase or alteplase are tissue plasminogen activators (tPA) which convert plasminogen to plasmin leading to fibrin breakdown. These agents work much more quickly than UFH or LMWH but also carry significant bleeding risks; may not be ideal if recently underwent surgery
how is fremitus affected by an effusion?
Fremitus over an effusion will be decreased
how does lung consolidation affect fremitus?
In the presence of consolidation, fremitus becomes more pronounced
