Case Based Learning

Question 2

How does heparin work?

Answer 2

Heparin binds to antithrombin and accelerates the inhibition of thrombin and factor Xa (as well as factors IXa and XIa)

Question 3

How is Heparin monitored?

Answer 3

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)

Question 4

How could ou confirm a diagnose of Heparin-Induced Thrombocytopenia?

Answer 4

The diagnosis can be confirmed by testing for antibodies to the heparin-platelet factor 4 (PF4) complex

Question 5

. Briefly describe the pathophysiology of TTP

Answer 5

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.

Question 6

If there is clinical suspicion for TTP, what should be done for treatment?

Answer 6

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

Question 7

emesis

Answer 7

vomiting

Question 8

Finding A-a gradient

Answer 8

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

Question 9

Despite a very high dead space, a patient’s PCO2 is 33. What does this tell you about her alveolar ventilation and minute ventilation?

Answer 9

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)

Question 10

What causes the exercise-induced hypoxemia in a patient with pulmonary fibrosis?

Answer 10

Reduced transit time of the RBCs through a “fixed” capillary bed (diffusion impairment leads to exercise induced hypoxemia)

Question 11

COPD with hypoxemia and high PCO2 – what factors are contributing to hypexmia if at sea level?

Answer 11

V/Q mismatch and hypoventilation

Question 12

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?

Answer 12

Oxyhemoglobin curve shifts to the left, 2-3-DPG is synthesized, red cell mass increases

Question 13

Summary of CO Effects on Hemoglobin

Answer 13

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)

Question 14

Which spirometric measurements is the most affected by variation in patient effort?

Answer 14

Peak flow—data collected entirely from effort dependent part of flow-volume curve

Question 15

How does the presence of air trapping affect the vital capacity?

Answer 15

Decreases VC because residual volume is increased (ERV is also reduced)

Question 16

plethysmography measures which component of lung volumes that cannot be assessed by spirometry?

Answer 16

Residual volume (volume remaining in the chest at end expiration that cannot be measured through spirometry)

Question 17

What spirometry observation occurs in most cases of pure restrictive AND in some cases of pure obstructive disorders?

Answer 17

Reduced FVC (can be true for both obstruction and restriction)

Question 18

During variable intrathroacic obstruction, what is the mechanism of airway collapse?

Answer 18

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.)

Question 19

DLCO decreased or normal: emphysema

Answer 19

decreased

Question 20

DLCO decreased or normal: asthma

Answer 20

normal

Question 21

DLCO decreased or normal: lung fibrosis

Answer 21

decreased

Question 22

DLCO decreased or normal: dyspnea due to obesity

Answer 22

decreased

Question 23

DLCO decreased or normal: dyspnea due to severe anemia

Answer 23

decreased

Question 24

DLCO decreased or normal: dyspnea due to mild congestive heart failure

Answer 24

normal

Question 25

What is the appropriate management for a patient with pulmonary hypertension due to left side heart failture?

Answer 25

diuretics

Question 26

What is an AQI score?

Answer 26

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.

Question 27

Why does ARDS lead to restrictive ventilatory physiology?

Answer 27

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

Question 28

List and discuss some of the major causes of ARDS. What do they have in common?

Answer 28

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

Question 29

What is the pathogenesis of hyaline membrane formation in ARDS?

Answer 29

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

Question 30

What is the appropriate initial management for a patient with ARDS?

Answer 30

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.

Question 31

what condition can result in a similar presentation to IPF?

Answer 31

connective tissue disease

Question 32

What is needed to establish an asbestosis diagnosis for legal purposes?

Answer 32

Occupational history and a chest radiograph interpreted by specialist with additional training related to pneumoconiosis

Question 33

how can you make a specific diagnosis for hypersensitivity pneumonitis?

Answer 33

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.

Question 34

How would you improve and then preserve a patient’s lung function if they have hypersensitivity pneumonitis?

Answer 34

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.

Question 35

Why does leaning forward help a COPD patient breath more easily?

Answer 35

The increased abdominal pressure at the end of exhalation causes the diaphragm to start from a more mechanically advantageous position

Question 36

Cause of hypoxemia in Pulmonary Embolism

Answer 36

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.

Question 37

bone fracture can be a risk for what kind of pulmonary problem?

Answer 37

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.

Question 38

what is treatment for hemodynamically unstable patients due to thromboembolism?

Answer 38

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

Question 39

how is fremitus affected by an effusion?

Answer 39

Fremitus over an effusion will be decreased

Question 40

how does lung consolidation affect fremitus?

Answer 40

In the presence of consolidation, fremitus becomes more pronounced