Internal Med- Pulmonology Flashcards

1
Q

What is the main difference between Asthma and COPD?

A

Asthma is a reversible bronchoconstriction

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2
Q

What are the 2 most common associations with Asthma?

A

Atopic disorders and obesity

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3
Q

What clinical presentation would make Asthma the most likely diagnosis?

A

The clear presence of wheezing with the acute onset of shortness of breath,
cough, and chest tightness

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4
Q

What are some of the associations / findings in a Pt with Asthma?

A
  • Symptoms worse at night
  • Nasal polyps and sensitivity to aspirin
  • Eczema or atopic dermatitis on physical examination
  • Increased length of expiratory phase of respiration
  • Increased use of accessory respiratory muscles (e.g., intercostals)
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5
Q

What is the best initial test in an acute exacerbation of asthma?

What is the most accurate diagnostic test?

A

The best initial test is based on the severity of presentation.
Peak expiratory flow (PEF) or
arterial blood gas (ABG).

Pulmonary function test (PFT) [Spirometry]
FEV1/FVC => The FEV1 decreases more than the FVC.
If asymptomatic on presentation=> methacholine challenge or histamine

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6
Q

A 15-year-old boy comes to the office because of occasional shortness of breath every few weeks. Currently he feels well. He uses no medications and denies any other medical problems. Physical examination reveals a pulse of 70 and a respiratory rate of 12 per minute. Chest examination is normal.

Which of the following is the single most accurate diagnostic test at this time?

a. Peak expiratory flow.
b. Increase in FEV1 with albuterol.
c. Diffusion capacity of carbon monoxide.
d. >20% decrease in FEV1 with use of methacholine.
e. Increased alveolar-arterial oxygen difference (A-a gradient).
f. Increase in FVC with albuterol.
g. Flow-volume loop on spirometry.
h. Chest CT scan.
i. Increased pCO2 on ABG.

A

*D.
When a patient is currently asymptomatic, it is less likely to find an increase in FEV1 with the use of short-acting bronchodilators like albuterol.
When the patient is asymptomatic, the most accurate test of reactive airway disease is a 20% decrease in FEV1 with the use of methacholine or histamine.
Chest CT, like an x-ray, shows either nothing or hyperinflation. The ABG and PEF are useful during an acute exacerbation. Flow-volume loops are best for fixed obstructions such as tracheal lesions or COPD.

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7
Q

When diagnosing Asthma with a PFT, what do we expect to see with the FEV1 with either Albuterol or Methacholine?

A

FEV1 ↑ (>12%): albuterol

FEV1 ↓ (>20%): methacholine

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8
Q

When diagnosing Asthma what can the CBC show?

A

CBC may show an increased eosinophil count

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9
Q

What immunologic test can be done in an Asthma Pt?

A

IgE levels. Increased levels suggest an allergic etiology.

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10
Q

What medication in relation to increased IgE in an Asthma Pt can be given?

A

Anti-IgE medication=> omalizumab

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11
Q

Apart from Asthma what other disease is associated with increased IgE levels?

A

allergic bronchopulmonary aspergillosis

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12
Q

How would you Mgx a Pt with Asthma?

A

Asthma is managed in a stepwise fashion of progressively adding more types of treatment if there is no response.

Step 1. inhaled short-acting beta agonist (SABA):
Albuterol, Levalbuterol

Step 2. Add a long-term control agent to a SABA. Low-dose inhaled corticosteroids (ICS): fluticasone, budesonide

Step 3. Add a long-acting beta agonist (LABA) [salmeterol or formoterol] to a SABA and ICS, or increase the dose of the ICS.

Step 4. Increase the dose of the ICS to maximum in addition to the LABA and
SABA. Add tiotropium, an antimuscarinic agent.

*Oral corticosteroids such as prednisone are added when all the other therapies are not sufficient to control symptoms.

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13
Q

What are some of the adverse effects of inhaled steroids?

A

Dysphonia and oral candidiasis?

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14
Q

What are some of the alternative long-term control agents?

A

Cromolyn inhibits mast cell mediator release and eosinophil recruitment

Theophylline

Leukotriene modifiers: montelukast (best with
atopic patients)

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15
Q

What are some of the adverse effects of systemic steroids?

A

Osteoporosis
Cataracts
Hyperlipidemia, hyperglycemia, acne, and hirsutism (particularly in women)
Thinning of skin, striae, and easy bruising

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16
Q

Which vaccines are mandatory in all asthma Pt?

A

Influenza and pneumococcal vaccine

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17
Q

A 47-year-old man with a history of asthma comes to the emergency department with several days of increasing shortness of breath, cough, and sputum production. On physical examination his respiratory rate is 34 per minute. He has diffuse expiratory wheezing and a prolonged expiratory phase.

Which of the following would you use as the best indication of the severity of his asthma?

a. Respiratory rate.
b. Use of accessory muscles.
c. Pulse oximetry.
d. Pulmonary function testing.
e. Pulse rate.

A

*A.
A normal respiratory rate is 10 to 16 per minute. By itself, a respiratory rate of 34 indicates severe shortness of breath. Accessory muscle use is hard to assess and is subjective.
Pulse oximetry will not show hypoxia until the patient is nearly at the point of imminent respiratory failure. Oxygen saturation can be maintained above 90% by hyperventilating. Pulmonary function testing cannot be done when a patient is acutely short of breath.

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18
Q

How can the severity of an asthma exacerbation be quantified?

A
  • Decreased peak expiratory flow (PEF)

- ABG with an increased A-a gradient

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19
Q

How would you manage an acute exacerbation of Asthma?

A

The best initial therapy is oxygen combined with inhaled short-acting beta agonists such as albuterol and a bolus of steroids. Corticosteroids need 4 to 6 hours to begin to work, so give them right away.

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20
Q

When can Magnesium be used in Asthma?

A

Magnesium is used only in an acute, severe asthma exacerbation not responsive to several rounds of albuterol while waiting for steroids to take effect.

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21
Q
If a Pt with Asthma does not respond to oxygen, albuterol, and steroids OR develops
respiratory acidosis (increased pCO2), what is the next best step?
A

The Pt may have to endotracheal intubation for mechanical ventilation.
These patients should be placed in the intensive care unit.

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22
Q

Why is Tobacco smoking associated with COPD?

A

Tobacco destroys elastin fibers

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23
Q

If a Pt presents with a clinical picture like COPD but is young and a nonsmoker, what is the most likely cause?

A

Alpha-1 antitrypsin deficiency

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24
Q

What are some of the clinical features of a COPD Pt?

A
  • Shortness of breath worsened by exertion
  • Intermittent exacerbations with increased cough, sputum, and shortness of breath often brought on by infection
  • “Barrel chest” from increased air trapping
  • Muscle wasting and cachexia
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25
Q

What is the best initial test in COPD? What are the features?

A

Chest x-ray:

  • Increased anterior-posterior (AP) diameter
  • Air trapping and flattened diaphragms
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26
Q

What is the accurate diagnostic test in COPD? What are the features?

A

PFT:

  • Decreased FEV1, decreased FVC, decreased FEV1/FVC ratio (under 70%)
  • Increased TLC because of an increase in residual volume
  • Decreased DLCO (emphysema, not chronic bronchitis)
  • Incomplete improvement with albuterol
  • Little or no worsening with methacholine
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27
Q

In COPD, what are the chances of reversibility with Inhaled Bronchodilators and what quantitative figure defines fines reversibility?

A

About 50% will have some degree of response.
About 50% will have some degree of response.
Full reversibility in response to bronchodilators is defined as greater than 12% or 200 mL increase in FEV1.

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28
Q

What changes do you expect to see with the ABG in a Pt with an acute exacerbation of COPD?

A

Increased pCO2 and hypoxia. Respiratory alkalosis but acidosis may be present if there is insufficient metabolic compensation

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29
Q

What changes may be present on the CBC in a Pt with COPD?

A

May have an increase in hematocrit from chronic hypoxia

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30
Q

What ECG findings may be consistent with a Pt with COPD?

A
  • Right atrial hypertrophy and right ventricular hypertrophy (Corplumonale)
  • Atrial fibrillation or multifocal atrial tachycardia (MAT)
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31
Q

What Echocardiography findings do you expect to find in a Pt with COPD?

A
  • Right atrial and right ventricular hypertrophy

- Pulmonary hypertension

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32
Q

What is the best initial treatment of COPD?

A

*Smoking cessation
O2 therapy=>
pO2 below 55 mm Hg or oxygen saturation below 88%
OR
If there are signs of right-sided heart disease/failure or an elevated hematocrit:
pO2 less than 60 mm Hg or oxygen saturation below 90%

Anticholinergic agents: tiotropium, ipratropium

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33
Q

Which vaccines are mandatory in COPD?

A

Influenza and pneumococcal vaccinations

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34
Q

What medication/therapy can improve symptoms but not decrease disease progression or mortality?

A
  • Short-acting beta agonists (e.g., albuterol)
  • Anticholinergic agents: tiotropium, ipratropium
  • Steroids
  • Long-acting beta agonists (e.g., salmeterol, formoterol)
  • Pulmonary rehabilitation
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35
Q

How would you Tx Acute Exacerbations of Chronic Bronchitis?

A

Bronchodilators (Ipratropium) and

corticosteroid therapy is combined with antibiotics

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36
Q

Why are antibiotics used in Acute Exacerbations of Chronic Bronchitis?
Which antibitics can be used in Acute Exacerbations of Chronic Bronchitis?

A

Because infection is by far the most commonly identified cause of Acute Exacerbations of Chronic Bronchitis.

  • Macrolides: azithromycin, clarithromycin
  • Cephalosporins: cefuroxime, cefixime
  • Amoxicillin/clavulanic acid (Amoxiclav)
  • Quinolones: levofloxacin, moxifloxacin
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37
Q

What are some of the causes of Bronchiectasis?

A

The single most common cause of bronchiectasis is cystic fibrosis, which accounts for half of cases. Other causes are:

  • Infections: tuberculosis, pneumonia, abscess
  • Immune deficiency
  • Foreign body or tumors
  • Allergic bronchopulmonary aspergillosis (ABPA)
  • Collagen-vascular disease such as rheumatoid arthritis
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38
Q

What clinical presentation would make Bronchiectasis the most likely diagnosis?

A

Recurrent episodes of very high volume purulent sputum production is the key to the suggestion of the diagnosis. Hemoptysis can occur. Dyspnea and wheezing are present in 75% of cases. Other findings are:

  • Weight loss
  • Anemia of chronic disease
  • Crackles on lung exam
  • Dyskinetic cilia syndrome
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39
Q

What is the best initial test to diagnose Bronchiectasis?

What is the most accurate test?

A

A chest x-ray:
Will show dilated, thickened bronchi,
sometimes with “tram-tracks,” which is the thickening of the bronchi

CT scan is the most accurate test

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40
Q

How would you Mgx Bronchiectasis?

A

Chest physiotherapy and postural drainage are essential for dislodging plugged-up bronchi.

Rotate antibiotics, 1 weekly each month.

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41
Q

What is Allergic Bronchopulmonary Aspergillosis (ABPA)?

A

Its a hypersensitivity of the lungs to fungal antigens that colonize the bronchial tree. ABPA occurs almost exclusively in patients with asthma and a history of atopic disorders.

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42
Q

What clinical presentation would make Allergic Bronchopulmonary Aspergillosis (ABPA) the most likely diagnosis?

A

An asthmatic patient with recurrent episodes of brown-flecked sputum
and transient infiltrates on chest x-ray.

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43
Q

What are some of the test that can be used to Dx Allergic Bronchopulmonary Aspergillosis (ABPA)?

A
  • Peripheral eosinophilia
  • Skin test reactivity to aspergillus antigens
  • Precipitating antibodies to aspergillus on blood test
  • Elevated serum IgE levels
  • Pulmonary infiltrates on chest x-ray or CT
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44
Q

How would you Mgx Allergic Bronchopulmonary Aspergillosis (ABPA)?

A
Oral steroids (prednisone) for severe cases because inhaled steroids are not
effective for ABPA

Itraconazole orally for recurrent episodes.

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45
Q

What is the pathophysiologic definition of Cystic fibrosis (CF)?

A

is an autosomal recessive disorder caused by a mutation
in the genes that code for chloride transport, the cystic fibrosis transmembrane regulator (CFTR). This leads to abnormally thick mucus in the lungs, as well as damage to the pancreas, liver, sinuses, intestines, and genitourinary tract. Neutrophils also dump tons of DNA into airway secretions, clogging them up.

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46
Q

What are the possible forms of clinical presentations consistent with Gastrointestinal Involvement in Cystic fibrosis (CF)?

A
  • Meconium ileus in infants with abdominal distention
  • Pancreatic insufficiency (in 90%) with steatorrhea and vitamin A, D, E, and K malabsorption
  • Recurrent pancreatitis
  • Distal intestinal obstruction
  • Biliary cirrhosis
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47
Q

Can Cystic fibrosis (CF) result in Diabetes Mellitus?

A

Not really because islets are spared. Beta cell function is normal until much later in life.

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48
Q

What are the possible forms of clinical presentations consistent with Genitourinary Involvement in Cystic fibrosis (CF)?

A

Men are often infertile; 95% have azoospermia, with the vas deferens missing in 20%.

Women are infertile because chronic lung disease alters the menstrual cycle and thick cervical mucus blocks sperm entry

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49
Q

What is the most accurate test to Dx Cystic fibrosis (CF)?

A

Increased sweat chloride test.

Pilocarpine increases acetylcholine levels which increases sweat production. Chloride levels in sweat above 60 meq/L on repeated testing establishes the diagnosis.

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50
Q

Why is genotyping with CFTR not the most accurate test to Dx Cystic fibrosis (CF)?

A

Because there are so many different types of mutations that can lead to CF.

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51
Q

What will PFT’s show in Cystic fibrosis (CF)?

A

Show mixed obstructive and restrictive patterns; decrease in FVC and total lung capacity; and decreased diffusing capacity for carbon monoxide.

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52
Q

How would you Mgx Cystic fibrosis (CF)?

A
  • Antibiotics are routine (Inhaled aminoglycosides)
  • Inhaled recombinant human deoxyribonuclease (rhDNase). This breaks down the massive amounts of DNA in respiratory mucus that clogs up the airways.
  • Inhaled bronchodilators such as albuterol
  • Ivacaftor increases the activity of CFTR in the 5% of patients who have a specific mutation
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53
Q

Which vaccines are mandatory in Cystic fibrosis (CF)?

A

Pneumococcal and influenza vaccinations

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54
Q

What is Community-Acquired Pneumonia?

A

CAP is defined as pneumonia occurring

before hospitalization or within 48 hours of hospital admission.

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55
Q

Which pathogen is the most common cause of Community-Acquired Pneumonia (CAP)?

A

Streptococcus pneumoniae

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56
Q

Name (8) common pathogens in Community-Acquired Pneumonia (CAP) and their associations

A
  1. Haemophilus
    influenzae- COPD
  2. Staphylococcus aureus- Recent viral infection (influenza)
  3. Klebsiella pneumoniae- Alcoholism, diabetes
  4. Anaerobes- Poor dentition, aspiration
  5. Mycoplasma
    pneumoniae- Young, healthy patients
  6. Legionella- Contaminated water sources, air conditioning, ventilation systems
  7. Chlamydia psittaci- Birds
  8. Coxiella burnetii- Animals at the time of giving birth, veterinarians, farmers
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57
Q

What are some of the clinical features of Community-Acquired Pneumonia (CAP)?

A
  • All forms of pneumonia present with fever and cough.
  • Cough, from any etiology, may be associated with hemoptysis.
  • Dullness to percussion is found if there is an effusion.
  • “Bronchial” breath sounds and egophony occur from consolidation of air spaces.
  • Rales, rhonchi, and crepitations are auscultatory findings from virtually any form of lung infection.
  • Abdominal pain or diarrhea can occur with infection in the lower lobes irritating the intestines through the diaphragm.
  • Chills or “rigors” are a sign of bacteremia often with bacterial pathogens.
  • Chest pain from pneumonia is often pleuritic, changing with respiration.
  • Hypothermia is just as bad as a fever in terms of pathologic significance.
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58
Q

How do you distinguish severe infections in Community-Acquired Pneumonia (CAP)?

A

Severe infections are distinguished by abnormalities of vital signs (tachycardia, hypotension, tachypnea) or mental status.

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59
Q

What are the main ways to distinguish pneumonia from bronchitis?

A

Dyspnea, high fever, and an abnormal chest x-ray

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60
Q
What are the associations on presentation of the following pathogens:
1. Klebsiella
pneumoniae
2. Anaerobes
3. Mycoplasma
pneumoniae
4. Legionella
5. Pneumocystis
A
  1. Hemoptysis from necrotizing disease, “currant jelly” sputum
  2. Foul-smelling sputum, “rotten eggs”
  3. Dry cough, rarely severe, bullous myringitis
  4. Gastrointestinal symptoms (abdominal pain, diarrhea) or CNS
    symptoms such as headache and confusion
  5. AIDS with <200 CD4 cells
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61
Q

Which organisms causing Community-Acquired Pneumonia (CAP) are often accompanied by a dry cough and why?

A
Viruses
Mycoplasma
Coxiella
Pneumocystis
Chlamydia

These infections preferentially involve the interstitial space and more often leave the air spaces of the alveoli empty. That is why there is less sputum production.

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62
Q

What is the best initial test to Dx Community-Acquired Pneumonia (CAP)?

A

The best initial test for all respiratory infections is a chest x-ray

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63
Q

What are the 2 best ways to first try determine a specific microbial etiology in pneumonia?

A

Sputum Gram stain and sputum culture.

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64
Q

What does the term atypical pneumonia mean?

A

It refers to an organism not visible on Gram stain and not culturable on standard blood agar.

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65
Q

In Pneumonia, why is the use of sputum stain and culture is somewhat controversial?

A

Even after thorough sputum examination, no etiology is found in at least 50% of cases. This is because Mycoplasma, Chlamydophila, Legionella, Coxiella, and viruses are not visible on Gram stain yet they’re not atypical pneumonia causing organisms but CAP.

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66
Q

Which organisms present with bilateral interstitial infiltrates on chest X-ray?

A
The same organisms that typically present with a nonproductive
cough.
Viruses
Mycoplasma
Coxiella
Pneumocystis
Chlamydia
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67
Q

What are the chances of the first X-ray being falsely negative in pneumonia?

A

at least 10% to 20% of cases.

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68
Q

What are the chances of blood cultures being positive in pneumonia?

A

<15% of cases of CAP

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69
Q

When is Thoracentesis indicated in Pneumonia?

A

When the diagnosis is unclear and to exclude an empyema.

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70
Q

What is an empyema? How is it managed?

A

It is an infected pleural effusion.

Empyema acts like an abscess and will improve more rapidly if it is drained with a chest tube.

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71
Q

How would you determine that fluid collected from thoracentesis is from an empyema?

A
  • LDH above 60% of serum level and protein above 50% of serum level.
  • A white cell count above 1000/μl or pH <7.2 is suggestive of infection.
72
Q

When is bronchoscopy indicated in pneumonia?

A

-In ICU Pts condition is worsening despite
empiric therapy.
-Pneumocystis pneumonia because noninvasive testing rarely reveals a diagnosis, and precise confirmation of the etiology is critical to guide therapy.

73
Q
What are the specific Dx tests for the following organisms:
1. Mycoplasma pneumoniae
2. Chlamydia psittaci
3. Legionella
4. Coxiella burnetii
5. Pneumocystis jiroveci
(PCP)
A
  1. PCR, cold agglutins, serology, special culture media
  2. Rising serologic titers
  3. Urine antigen, culture on charcoal-yeast extract
  4. Rising serologic titers
  5. Bronchoalveolar lavage (BAL)
74
Q

How would you Tx pneumonia in an Outpatient?

A

1) If previously healthy or no antibiotics in the past 3 months and mild symptoms=> macrolide (azithromycin or clarithromycin)
2) If Pt has Comorbidities or taken antibiotics in the past 3 months=> Respiratory fluoroquinolone (levofloxacin or moxifloxacin)

75
Q

How would you Tx pneumonia in an Intpatient?

A

1) Respiratory fluoroquinolone: levofloxacin or moxifloxacin
OR
2) Ceftriaxone and azithromycin

76
Q

What are the 2 single factors that are a sufficient reason to hospitalise a Pt with Pneumonia?

A

Hypoxia and hypotension

77
Q

What combination of factors are sufficient reasons to hospitalise a Pt with Pneumonia?

A

CURB65

  • Confusion
  • Urea
  • Respiratory rate above 30 per minute or pH below
    7. 35
  • BP (low)
  • Age 65 or older, or comorbidities such as cancer, COPD, CHF, renal failure (BUN above 30 mg/dL), or liver disease
78
Q

A 65-year-old woman is admitted to the hospital with CAP. Sputum Gram stain shows Gram-positive diplococci but the sputum culture does not grow a specific organism. Chest x-ray shows a lobar infiltrate and a large effusion. She is placed on ceftriaxone and azithromycin. Thoracentesis reveals an elevated LDH and protein level with 17,000 white blood cells per μl. Blood cultures grow Streptococcus pneumoniae with a minimal inhibitory concentration (MIC) to penicillin less than 0.1 μg/mL. Her oxygen saturation is 96% on room air. Blood pressure is 110/70, temperature is 102°F, and pulse is 112 per minute.

What is the most appropriate next step in the management of this patient?

a. Repeated thoracentesis.
b. Placement of chest tube for suction.
c. Add ampicillin to treatment.
d. Place patient in intensive care unit.
e. Consult pulmonary.

A

*B.
Infected pleural effusion or empyema will respond most rapidly to drainage by chest tube or thoracostomy. A large effusion acts like an abscess and is hard to sterilize. Each side of the chest can accommodate 2 to 3 liters of fluid. There is no benefit of adding ampicillin to ceftriaxone. A low MIC to penicillin automatically means that the organism is sensitive to ceftriaxone and, in fact, all cephalosporins.
There is no need to be in the ICU just because of an effusion or for chest tube drainage. The patient is not unstable and, despite the effusion, has no evidence of instability because her pulse is only mildly abnormal and the blood pressure and pulse oximeter are normal. Pulmonary consultation will not add anything, although it may be commonly done in practice.

79
Q

What is the relationship between Exudate and empyema?

A

LDH >60% of serum (0.6) or protein >50% of serum (0.5) suggest an exudate but if pH is <7.2 it suggests an empyema

80
Q

What are the 2 main causes of exudates?

A

infection and cancer.

81
Q

What is the format for Pneumococcal Vaccination?

A

13 polyvalent vaccine, followed in 6–12 months with the 23 polyvalent vaccine.
If the first vaccination is given before age 65 or with the other conditions previously described, a second dose should also be given 5 years after the first dose.

82
Q

Who should get Pneumococcal Vaccination?

A
  1. Everyone above the age of 65
  2. All those with chronic heart, liver, kidney, or lung disease (including
    asthma)
  3. Functional or anatomic asplenia (e.g., sickle cell disease)
  4. Hematologic malignancy (leukemia, lymphoma)
  5. Immunosuppression: diabetes mellitus, alcoholics, corticosteroid users, AIDS or HIV positive
  6. CSF leak and cochlear implantation recipients
83
Q

What is Hospital-acquired pneumonia (HAP) [Nosocomial pneumonia]?

A

is defined as a pneumonia developing more than 48 hours after admission or after hospitalization in the last 90 days.

84
Q

What is the most common etiology of Nosocomial pneumonia / Hospital-Acquired
Pneumonia?

A

Gram-negative bacilli such as E. coli or Pseudomonas

85
Q

How would you Tx Nosocomial pneumonia / Hospital-Acquired

Pneumonia (HAP)?

A

Antipseudomonal cephalosporins: cefepime or ceftazidime
OR
Antipseudomonal penicillin: piperacillin-tazobactam (always used in this combination or piperacillin with clavulanic acid)
OR
Carbapenems: imipenem, meropenem, or doripenem

86
Q

What is the pathophysiology behind Ventilator-Associated Pneumonia?

A

Mechanical ventilation interferes with normal mucociliary clearance of the respiratory tract such as the ability to cough. Positive pressure is tremendously damaging to the normal ability to clear colonization.

87
Q

What is incidence of Ventilator-Associated Pneumonia per day?

A

5% per day in the first few days

on a ventilator.

88
Q

What clinical features would make Ventilator-associated

pneumonia (VAP) the most likely diagnosis?

A
  • Fever and/or rising white blood cell count
  • New infiltrate on chest x-ray
  • Purulent secretions coming from the endotracheal tube
89
Q

How valuable is a sputum culture in Ventilator-associated

pneumonia (VAP)?

A

sputum culture is nearly worthless because of colonization of the endotracheal tube (ET)

Culturing an endotracheal tube is like culturing urine with a Foley catheter in place: It will always grow something because of colonization.

90
Q

List the diagnostic tests (5) for Ventilator-associated
pneumonia (VAP) from the least accurate but
easiest to do, to the most accurate but most dangerous.

A

Tracheal aspirate: A suction catheter is placed into the ET and aspirates the contents below the trachea when the catheter is past the end of the ET tube.

Bronchoalveolar lavage (BAL): A bronchoscope is placed deeper into the lungs where there are not supposed to be any organisms. Can be contaminated when passed through the nasopharynx.

Protected brush specimen: The tip of the bronchoscope is covered when passed through the nasopharynx, then uncovered only inside the lungs. Much more specific because of decreased contamination.

Video-assisted thoracoscopy (VAT): A scope is placed through the chest wall, and a sample of the lung is biopsied. This allows a large piece of lung to be taken without the need for cutting the chest open (thoracotomy). It is like sigmoidoscopy of the chest.

Open lung biopsy: The most accurate diagnostic test of VAP, but with much greater morbidity and potential complication of the procedure because of the need for thoracotomy.

91
Q

How would you Tx Ventilator-associated

pneumonia (VAP)?

A

Combine 3 different drugs (1 Antipseudomonal beta-lactam + 1 Antipseudomonal + 1 MRSA agent)

1) Antipseudomonal beta-lactam:
- Cephalosporin (ceftazidime or cefepime) or
- Penicillin (piperacillin/tazobactam) or
- Carbapenem (imipenem, meropenem, or doripenem)

2) Antipseudomonal:
- Aminoglycoside (gentamicin or tobramycin or amikacin) or
- Fluoroquinolone (ciprofloxacin or levofloxacin)

3) MRSA agent
- Vancomycin or
- Linezolid

92
Q

A patient is admitted to the hospital for head trauma and a subdural hematoma. The patient is intubated for hyperventilation and a subsequent craniotomy. Several days after admission, the patient starts to vomit blood and is found to have stress ulcers of the stomach. Lansoprazole is started. VAP develops and the patient is placed on imipenem, linezolid, and gentamicin. Phenytoin is started prophylactically. Three days later, the
creatinine rises. The patient then starts having seizures. A repeat head CT shows no changes.

What is the most appropriate next step in the management of this patient?

a. Switch phenytoin to carbamazepine.
b. Stop lansoprazole.
c. Stop imipenem.
d. Stop linezolid.
e. Perform an electroencephalogram.

A

*C.
Imipenem can cause seizures. Imipenem is excreted through the kidneys. The renal failure has caused a rise in imipenem levels leading to toxicity. This is much more likely than a failure of phenytoin. Carbamazepine is no more effective than phenytoin at stopping seizures.

93
Q

What is the etiology behind Lung abscesses?

A

-a patient with a large-volume aspiration of
oral/pharyngeal contents, usually with poor dentition, who is not adequately
treated for aspiration pneumonia.
-Stroke with loss of gag reflex
-Seizures
-Intoxication
-Endotracheal intubation

94
Q

What is the typical location of aspiration pneumonia?

A

upper lobe when lying flat

95
Q

What is the best initial test for a Lung Abscess?

What is the most accurate test?

A

Chest x-ray will show a cavity, possibly with an airfluid level.

Chest CT is more accurate than a chest x-ray, but only a lung biopsy can establish the specific microbiologic etiology.

96
Q

Which medications can be used in Lung Abscesses?

A

Clindamycin or
penicillins
*target anaerobes

97
Q

What is the etiology of Pneumocystis Pneumonia?

A

The agent causing pneumocystis pneumonia (PCP) has been renamed P. jiroveci instead of P. carinii. PCP occurs almost exclusively in patients with AIDS whose CD4 cell count has dropped below 200/μl and who are not on prophylactic therapy.

98
Q

If an X ray is done showing bilateral interstitial infiltrates and you suspect Pneumocystis Pneumonia from the other findings. What is the next best step?

A

Sputum stain for pneumocystis is quite specific if it is positive. If the stain is stated to be positive, there is no need to do further testing. A negative sputum stain means you do bronchoscopy as the best diagnostic test.

99
Q

What is the most accurate test for Pneumocystis Pneumonia?

A

Bronchoalveolar lavage

100
Q

What/Which lab value would make PCP “not” the most likely diagnosis?

A

A normal LDH. LDH levels are always elevated in PCP.

101
Q

How would you Tx PCP?

A

Trimethoprim/sulfamethoxazole (TMP/SMX) is unquestionably the best initial therapy both for treatment and for prophylaxis.

102
Q

What defines PCP to be severe and how is it Mgx?

A

Severe PCP is defined as a pO2 below 70 or an A-a gradient above 35.

Add steroids to Trimethoprim/sulfamethoxazole (TMP/SMX)

103
Q

Incase of toxicity from TMP/SMX which medications can be used?

A

Clindamycin and primaquine

104
Q

If hypoxia is mild which drug can be used as an alternative to TMP/SMX?

A

Atovaquone

105
Q

An HIV-positive African American man is admitted with dyspnea, dry cough, high LDH, and a pO2 of 63 mm Hg. He is started on TMP/SMX and prednisone. On the third hospital day he develops severe neutropenia and a rash. He has anemia and there are bite cells visible on his smear.

What is the most appropriate next step in the management of this patient?

a. Stop TMP/SMX.
b. Begin antiretroviral medications.
c. Switch TMP/SMX to intravenous pentamidine.
d. Switch TMP/SMX to aerosol pentamidine.
e. Switch TMP/SMX to clindamycin and primaquine.

A

*C.
Rash is the most common adverse effect of TMP/SMX and bone marrow suppression is the second most common adverse effect. Although clindamycin and primaquine may have more efficacy than pentamidine, the patient seems to have glucose 6 phosphate dehydrogenase (G6PD) deficiency and primaquine is contraindicated in G6PD deficiency. He is an African American man and there are bite cells suggestive of G6PD deficiency on his smear. For active disease, intravenous pentamidine is used, not aerosol. Starting antiretroviral medications should be done eventually, but they will not help an acute opportunistic infection. In addition, antiretrovirals are relatively contraindicated in acute opportunistic infections because of the possibility of immune reconstitution syndrome.

106
Q

When should PCP Prophylaxis be started?

A

in those with AIDS whose CD4 count is below 200/μl.

107
Q

If there is a rash or neutropenia from TMP/SMX what alternatives are there?

A

Atovaquone or dapsone

108
Q

What is the common contraindication of Dapsone and Primaquine?

A

Those with glucose 6 phosphate

dehydrogenase deficiency. (G6PD deficiency)

109
Q

An HIV-positive woman with 22 CD4 cells/μl is admitted with PCP and is treated successfully with TMP/SMX. Prophylactic TMP/SMX and azithromycin are started. She is then started on antiretroviral medication and her CD4 rises to 420 cells for the last 6 months.

What is the most appropriate next step in the management of this patient?

a. Stop TMP/SMX.
b. Stop both TMP/SMX and azithromycin.
c. Stop all medications and observe.
d. Stop all medications if the PCR-RNA viral load is undetectable.
e. Continue all the medications.
f. Stop the azithromycin.

A

*B.
If the CD4 count is maintained above 200/μl for several months, prophylactic TMP/SMX can be stopped. Azithromycin is used as prophylaxis for atypical mycobacteria and is used when the CD4 count drops below 50/μl. You cannot stop the antiretroviral medications because her CD4 count will drop. It is the antiretroviral medications that are maintaining her CD4 count. If the CD4 rises and is maintained high, there is no need for prophylactic medications. These cells are fully functional and
they will prevent opportunistic infections. The use of prophylactic medications is based on the CD4 count, not the viral load.

110
Q

What would make TB the most likely diagnosis?

A

A Pt with risk factors presenting with fever, cough, sputum, weight loss, hemoptysis, and night sweats, a cavity
on the chest x-ray, or a positive smear.

111
Q

What is the best initial test for TB?

What is the most accurate test

A

The best initial test is a chest x-ray as with all respiratory infections. Sputum stain and culture specifically for acid-fast bacilli (mycobacteria) must be done 3 times to fully exclude TB.

Pleural biopsy is the single most accurate diagnostic test.

112
Q

How would you Tx TB?

A

4 Drugs: Rifampin, Isoniazid, Pyrazinamide, and Ethambutol (RIPE).
After using RIPE for the first 2 months, stop ethambutol and pyrazinamide and continue rifampin and isoniazid for the next 4 months. The standard of care is 6 months total of therapy.

113
Q

Does knowing the sensitivity of the organism to all TB medications change the 4-drug empiric therapy

A

Yes. You do not need the ethambutol if it is known at the beginning of therapy that the organism is sensitive to all TB medications.

114
Q

What would warrant extension of TB Tx to >6 months?

A
  • Osteomyelitis
  • Miliary tuberculosis
  • Meningitis
  • Pregnancy or any other time pyrazinamide is not used
115
Q

Which TB drugs cause hepatotoxicity and when are they to be stopped?

A

All of the TB medications cause hepatoxicity, but are not stopped till the transaminases rise to 3 to 5 times the upper limit of normal.

116
Q

What are the adverse effects of the following antituberculosis therapy and how would you manage each;

  1. Rifampin
  2. Isoniazid
  3. Pyrazinamide
  4. Ethambutol
A
  1. Red color to body secretions- No Mgx, benign finding
  2. Peripheral neuropathy- Use pyridoxine to prevent
  3. Hyperuricemia- No Tx unless symptomatic
  4. Optic neuritis/color vision- Decrease dose in renal failure
117
Q

What is the benefit of using Glucocorticoids in some Pt with TB?

A

They decrease the risk of constrictive pericarditis in those with pericardial involvement. They also decrease neurologic complication in TB meningitis.

118
Q

In which group of Pt is a purified protein derivative (PPD) and an interferon gamma release assay (IGRA) not useful?
What should be done instead?

A

Those who are symptomatic or those with abnormal chest x-rays.
These patients should have sputum acid fast testing done.

119
Q

Explain the Two-Stage Testing with the PPD

A

If the patient has never had a PPD skin test before, a second test is indicated within 1 to 2 weeks if the first test is negative. This is because the first test may be falsely negative. If the second test is negative, it means the patient is truly negative. If the second test is positive, it means the first test was a false negative.

But if the first test is positive, a second test is not necessary

120
Q

If a PPD or IGRA is positive but chest X-ray is negative, how would you Mgx the Pt?

A

9 months of isoniazid.
A positive PPD or IGRA confers a 10% lifetime risk of tuberculosis. Isoniazid results in a 90% reduction in this risk; after isoniazid, the lifetime risk of TB goes from 10% to 1%.

121
Q

What are the types of Pulmonary fibrosis?

A

Idiopathic and Secondary Pulmonary Fibrosis

Idiopathic AKA idiopathic fibrosing interstitial pneumonia.

122
Q

What are some of the types (6) of Pneumoconioses?

A
  1. Coal worker’s pneumoconiosis- Coal
  2. Silicosis- Sandblasting, rock mining, tunneling
  3. Asbestosis- Shipyard workers, pipe fitting, insulators
  4. Byssinosis- Cotton
  5. Berylliosis- Electronic manufacture
  6. Bagassosis- Moldy sugar cane
123
Q

What are some of the general clinical features of Pulmonary fibrosis?

A
  • Dyspnea, worsening on exertion
  • Fine rales or “crackles” on examination
  • Loud P2 heart sound
  • Clubbing of the fingers
124
Q

What is the best initial test for Pulmonary fibrosis?

What is the most accurate test?

A

The best initial test is always a chest x-ray. High resolution CT scan is more accurate than a chest x-ray, but the most accurate test is a lung biopsy.

125
Q

What are the likely findings of an Echocardiography in Pulmonary fibrosis?

A

Pulmonary hypertension and possibly right ventricular hypertrophy.

126
Q

What are the likely findings of on the PFT’s in Pulmonary fibrosis?

A

PFTs: Restrictive lung disease with decrease of everything proportionately.
The FEV1, FVC, TLC, and RV will all be decreased, but since everything is decreased, the FEV1/FVC ratio will be normal. The DLCO is decreased in proportion to the severity of the thickening of the alveolar septum.

127
Q

How would you Mgx Interstitial Lung Diseases?

A

Most types of interstitial lung diseases are untreatable.
If the biopsy shows white cell or inflammatory infiltrate, prednisone should be used.

In patients who do respond to steroids, switch to azathioprine for long-term treatment to get the patient off steroids. If there is no response to steroids or azathioprine, try cyclophosphamide.

128
Q

Which type of pneumoconioses, is the most likely to

respond to treatment with steroids and why?

A

Berylliosis.

This is due to the presence of granulomas, which are a sign of inflammation.

129
Q

Which medications can decrease the rate of progression of Idiopathic Pulmonary Fibrosis (IPF)?

A

Pirfenidone and Nintedanib. Pirfenidone is an antifibrotic agent that inhibits collagen synthesis. Nintedanib is a tyrosine kinase inhibitor that blocks fibrogenic growth factors and inhibits fibroblasts.

130
Q

What is sarcoidosis?

A

It is an idiopathic inflammatory disorder predominantly of the lungs but can affect most of the body. Sarcoidosis is more common in African American women.

131
Q

What clinical features would make sarcoidosis the most likely diagnosis?

A

Shortness of breath on exertion and occasional fine rales on lung exam, but without the wheezing of asthma. Erythema nodosum and lymphadenopathy, either on examination or especially on chest x-ray *Bilateral Hilar Lymphadenopathy

  • Parotid gland enlargement
  • Facial palsy
  • Heart block and restrictive cardiomyopathy
  • CNS involvement
  • Iritis and uveitis
132
Q

What is the best initial test for Sarcoidosis?

What is the most accurate test?

A

Chest x-ray is the best initial test. Hilar adenopathy is present in more than 95% of patients with sarcoidosis.

Lymph node biopsy is the most accurate test. The granulomas are noncaseating.

133
Q

What are some of the Lab values that may show changes in a Pt with Sarcoidosis?

A

Elevated ACE level: 60%
Hypercalciuria: 20%
Hypercalcemia: 5% (granulomas in sarcoidosis make vitamin D)

134
Q

What are the PFT’s likely to show in Sarcoidosis?

A

PFTs: restrictive lung disease (decreased FEV1, FVC, and TLC with a normal FEV1/FVC ratio)

135
Q

What is a Bronchoalveolar lavage likely to show in Sarcoidosis?

A

An elevated level of helper cells.

136
Q

How is Sarcoidosis Mgx?

A

Prednisone is the clear drug of choice. Few patients fail to respond.
Asymptomatic hilar adenopathy does not need to be treated.

137
Q

What is the relationship between Pulmonary embolism (PE) and deep venous thrombosis (DVT)?

A

PE and DVT are essentially treated as a spectrum of the same disease. Pulmonary emboli derive from DVT of the large vessels of the legs in 70% and pelvic veins in 30%, the risks and treatment are the same

138
Q

What is etiology of Pulmonary embolism (PE) and deep venous thrombosis (DVT)?

A

DVTs arise because of stasis from immobility, surgery, trauma, joint replacement, or thrombophilia such as factor V Leiden mutation and antiphospholipid syndrome. Malignancy of any kind leads to DVT

139
Q

What clinical presentation would make a PE the most likely diagnosis?

What are some of the other supporting findings?

A

Sudden onset of shortness of breath with clear lungs on
examination and a normal chest x-ray.

  • Tachypnea, tachycardia, cough, and hemoptysis
  • Unilateral leg pain from DVT
  • Pleuritic chest pain from lung infarction
  • Fever can arise from any cause of clot or hematoma
  • Extremely severe emboli will produce hypotension
140
Q

What is the best initial test for a PE?

What is the most accurate?

A

Chest x-ray, EKG,
and ABG are the best initial tests.

Angiography, is the most accurate test, nearly 100%, but can be fatal in 0.5% of cases. It is rarely done

141
Q

When suspecting a PE, after doing an ABG, chest x-ray, and EKG, what is the
best next step?

A

Spiral CT scan: Also called a CT angiogram,

142
Q

What changes would you expect to find on a chest X-ray when suspecting a PE?

A

Usually normal in PE. The most common abnormality is atelectasis. Wedge-shaped infarction, pleural-based lesion (Hampton hump), and oligemia of one lobe (Westermark sign) are much less common than simple atelectasis.

143
Q

What changes would you expect to find on an ECG when suspecting a PE?

A

Usually shows sinus tachycardia. The most common abnormality is nonspecific ST-T wave changes. Only 5% will show right axis deviation, RV hypertrophy or right bundle branch block.

144
Q

What changes would you expect to find on an ABG when suspecting a PE?

A

Hypoxia and respiratory alkalosis (high pH and low p CO2) with a normal chest x-ray is extremely suggestive of PE.

145
Q

A 65-year-old woman who recently underwent hip replacement comes to the emergency department with the acute onset of shortness of breath and tachycardia. The chest x-ray is normal, with hypoxia on ABG, an increased A-a gradient, and an EKG with sinus tachycardia.

What is the most appropriate next step in management?

a. Enoxaparin.
b. Thrombolytics.
c. Inferior vena cava filter.
d. Embolectomy.
e. Spiral CT scan.
f. Ventilation/perfusion (V/Q) scan.
g. Lower-extremity Doppler studies.
h. D-dimer.

A

*A.
When the history and initial labs are suggestive of PE, it is far more important to start therapy (with LMW heparin or enoxaparin or with a NOAC) than to wait for the results of confirmatory testing such as the spiral CT or V/Q scan. D-dimer is a poor choice when the presentation is clear because its specificity is poor. Embolectomy is rarely done and is performed only if heparin is ineffective and there is persistent hypotension, hypoxia, and tachycardia. There is no benefit of IV unfractionated heparin except a short half-life.

146
Q

A Spiral CT scan (CT angiogram) can not be done in pregnancy, what is the alternative?

A

Ventilation/Perfusion (V/Q) scan

147
Q

What is the main limitation of a Ventilation/Perfusion (V/Q) scan when diagnosing a PE?

A

The chest x-ray must be normal for the V/Q scan to have any degree of accuracy.

148
Q

What is the value of a D-dimer when diagnosing a PE?

A

This test is very sensitive, but the specificity is poor since any cause of clot or increased bleeding can elevate the d-dimer level. A negative test excludes a clot, but a positive test doesn’t mean anything.

149
Q

If a Lower extremity (LE) Doppler study confirms a clot in the legs, should you confirm the PE with a spiral CT or V/Q scan?

A

You do not need a spiral CT or V/Q scan to confirm a PE if there is a clot in the legs because they will not change therapy. The patient will still need heparin and 6 months of warfarin.

150
Q

What are the main adverse effects of angiography?

A

allergy, renal toxicity, and death

151
Q

How would you Mgx a PE or DVT?

A

Low-molecular-weight (LMW) heparin or enoxaparin followed by a NOAC or warfarin is an acceptable therapy.

152
Q

What are the 2 main advantages of using Novel Oral Anticoagulants (NOACs)?

A
  • NOACs cause less intracranial bleeding than warfarin.
  • NOACs do not need INR monitoring and do not need enoxaparin (heparin) first.
  • They reach a therapeutic effect in several hours, instead of several days like warfarin.
153
Q

For a PE or DVT, when is it most appropriate to use an inferior vena cava (IVC) filter?

A
  • Contraindication to the use of anticoagulants (e.g., melena).
  • Recurrent emboli while on a NOAC or fully therapeutic warfarin.
  • Right ventricular (RV) dysfunction with an enlarged RV on echo. In this case, disease is so severe that an IVC filter is placed because the next embolus, even if seemingly small, could be potentially fatal.
154
Q

For a PE when is it most appropriate to use thrombolytics?

A
  • Hemodynamically unstable patients (e.g., hypotension [systolic BP <90] and tachycardia)
  • Acute RV dysfunction
155
Q

What is the time frame that thrombolytics should be used, in a PE?

A

There is no specific time limit in which to use thrombolytics as there is in stroke or MI.

156
Q

What alternative drug can be used in In heparin-induced thrombocytopenia (HIT)?

A

Fondaparinux

157
Q

What examples in the components of Virchow’s Triad can influence the occurrence of a PE or DVT?

A

1) Stasis:
- immobility
- CHF
- recent surgery

2) Endothelial injury
- trauma
- surgery
- recent fracture

3) Hypercoagulability
- Factor V Leiden mutation
- any malignancy

158
Q

Define Pulmonary Hypertension and its etiology.

A

Pulmonary hypertension is systolic BP >25 mm Hg, diastolic BP >8 mm Hg. Any form of chronic lung disease such as COPD or fibrosis elevates the pulmonary artery pressure.

159
Q

What is the pathophysiology behind Pulmonary Hypertension?

A

Any form of chronic lung disease such as COPD or fibrosis elevates the pulmonary artery pressure. Hypoxemia causes vasoconstriction of the pulmonary circulation as a normal reflex in the lungs to shunt blood away from areas of the lung it considers to have poor oxygenation. This is why hypoxia leads to pulmonary hypertension, and pulmonary hypertension results in more hypoxemia.

160
Q

What is the best initial test for Pulmonary Hypertension?

What is the most accurate test?

A

Chest x-ray and CT: best initial tests showing dilation of the proximal pulmonary arteries with narrowing or “pruning” of distal vessels

Right heart or Swan-Ganz catheter: most accurate test and the most precise method to measure pressures by vascular reactivity

161
Q

In Pulmonary Hypertension what can the ECG reveal?

A

right axis deviation, right atrial and ventricular hypertrophy

162
Q

In Pulmonary Hypertension what can Echocardiography reveal?

A

RA and RV hypertrophy; Doppler estimates pulmonary artery (PA) pressure

163
Q

In Pulmonary Hypertension what can the CBC reveal?

A

Polycythemia from chronic hypoxia

164
Q

How would you Mgx Pulmonary Hypertension?

A
  1. Correct the underlying cause when one is clear.
  2. Idiopathic disease is treated, if there is vascular reactivity, with:
    - Prostacyclin analogues (PA vasodilators): iloprost
    - Endothelin antagonists: bosentan
    - Phosphodiesterase inhibitors: sildenafil
  3. Oxygen slows progression, particularly with COPD
165
Q

What are the types of Sleep Apnea?

A

1) Obstructive

2) Central

166
Q

What is the main etiology of Obstructive Sleep Apnea?

A

Obesity

167
Q

List the main features as well as the accompanying symptoms of Sleep Apnea?

A

Patients present with daytime somnolence and a history of loud snoring.

  • Headache
  • Impaired memory and judgement
  • Depression
  • Hypertension
  • Erectile dysfunction
  • “Bull neck”
168
Q

What is the most accurate test for Dx Sleep Apnea?

A

Polysomnography (sleep study) which shows

multiple episodes of apnea.

169
Q

What can an ECG and CBC reveal in a Pt with Sleep Apnea?

A

Arrhythmias and erythrocytosis

170
Q

How would you Mgx Sleep Apnea?

A
  1. Weight loss and avoidance of alcohol
  2. Continuous positive airway pressure (CPAP)
  3. Surgical widening of the airway (uvuloplatopharyngoplasty) if this fails
  4. Avoid use of sedatives
  5. Oral appliances to keep the tongue out of the way
171
Q

What is Acute Respiratory Distress Syndrome?

A

Acute respiratory distress syndrome (ARDS) is a severe inflammatory reaction of the lungs from overwhelming lung injury or systemic disease leading to severe hypoxia with a chest x-ray suggestive of congestive failure but normal cardiac hemodynamic measurements. ARDS decreases surfactant and makes the lung cells “leaky” so that the alveoli fill up with fluid.

172
Q

What do you expect to see on a Chest X-ray of Acute Respiratory Distress Syndrome?

A

Typically shows diffuse bilateral infiltrates (“butterfly pattern”).

173
Q

What does the PaO₂/FiO₂ ratio entail?

A

PaO₂=> The partial pressure of oxygen in arterial blood.
FiO₂=> The fraction of oxygen (by volume) in inspired air.

A rough estimate of the expected PaO₂ in a normal individual is five times that of the concentration of oxygen in inhaled air (FiO₂).

Patients who are on mechanical ventilation usually receive air with an FiO₂ between 0.21 and 0.5 in order to avoid oxygen toxicity.

So if the PaO₂ (as measured on an ABG) is 70 while breathing 50% oxygen, the ratio is 70/0.5 or 140.

174
Q

How can we asses the severity of Acute Respiratory Distress Syndrome (ARDS)?

A

Using the PaO₂/FiO₂ ratio.

  1. PaO₂/FiO₂ <300 = ARDS
  2. PaO₂/FiO₂ <200 = moderately severe
  3. PaO₂/FiO₂ <100 = severe
175
Q

How would you Mgx Acute Respiratory Distress Syndrome (ARDS)?

A
  1. The primary objective is achieving sufficient oxygen saturation (while avoiding oxygen toxicity).
    Goal: SaO2 >90% (or PaO2 >55 mmHg)
  2. Treat the underlying cause

Low tidal-volume mechanical ventilation is the best support while waiting to see if the lungs will recover. Use 6 mL per kg of tidal volume.