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INPATIENT > Diseases of lungs and respiratory system > Flashcards

Diseases of lungs and respiratory system Flashcards

1
Q

List the most common extrapulmonary manifestations of tuberculosis.

A
  • Lymphadenitis
  • Pericarditis
  • Peritonitis
  • Nephritis
  • Vertebral osteomyelitis (Potts)
  • Hepatitis
  • Splenitis
  • Cutaneous
  • Arthritis
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2
Q

What disease is characterized by impaired chloride ion movements and decreased exocrine function?

A

cystic fibrosis

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3
Q

Name 5 main systems affected by cystic fibrosis.

A

–Male reproductive tract: missing epididymis, vas deferens

–Pancreas: obstruction & destruction

–Sinuses: polyps, opacification, abnormalities

–Intestines: decreased fluid secretion -> constipation

–Lungs: thicker mucus; affects conducting airways not alveoli

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4
Q

Top 3 organisms of typical community-acquired pneumonia:

A

S. pneumoniae

H. influenza

M. catarrhalis

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5
Q

Top 3 organisms of atypical community-acquired pneumonia:

A

M. pneumoniae

Chlamydia pneumoniae

Legionella

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6
Q

Organisms of aspiration pneumonia:

A

anaerobes

gram negs

Bacteriodes

Pseudomonas aeruginosa

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7
Q

Organisms of hospital-acquired pneumonia:

A

Pseudomonas aeruginosa

MRSA

Klebsiella

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8
Q

Treatment of community-acquired pneumonia:

A

If healthy & no abx < 3 months:

macrolide or doxycycline

If comorbidities or abx < 3 months:

respiratory fluoroquinolone or ceftriaxone + azithromycin

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9
Q

Treatments for aspiration pneumonia:

A

amoxicillin-clavulanate (augmentin)

OR

IV clindamycin

OR

piperacillin-tazobactam

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10
Q

Treatments for hospital-acquired pneumonia:

A

(antipseudomonal ceph, carbapenem, or PCN) + (fluoroquinolone or amikacin) + vancomycin

inpatient handout or purple book 6-2

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11
Q

What is Light’s Criteria for classifying pleural effusions?

A

Fluid is exudative (vs. transudative) if one of the following Light’s criteria is present:

  • (Effusion protein) / (serum protein) ratio greater than 0.5
  • Effusion lactate dehydrogenase (LDH)/serum LDH ratio greater than 0.6
  • Effusion LDH level greater than 2/3 the upper limit of the laboratory’s reference range of serum LDH
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12
Q

List some of the common pathogens associated with acute exacerbations of cystic fibrosis.

A

H. influenzae

P. aeruginosa

S. aureus

Burkholderia cepacia

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13
Q

How is cystic fibrosis definitively diagnosed?

A

BOTH of the following criteria must be met to diagnose cystic fibrosis (CF):

● Clinical symptoms consistent with CF in at least one organ system, AND

● Evidence of cystic fibrosis transmembrane conductance regulator (CFTR) dysfunction (any of the following):

  • Elevated sweat chloride ≥60 mmol/L (on two occasions)
  • Presence of two disease-causing mutations in CFTR from each parental allele
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14
Q

What is the most common type of lung cancer?

A

Non-Small Cell Lung Cancer

This is the most common type of lung cancer. About 85% of lung cancers are non-small cell lung cancers. Squamous cell carcinoma, adenocarcinoma, and large cell carcinoma are all subtypes of non-small cell lung cancer.

Small Cell Lung Cancer

Small cell lung cancer is also called oat cell cancer. About 10%-15% of lung cancers are small cell lung cancers. This type of lung cancer tends to spread quickly.

Lung Carcinoid Tumor

Fewer than 5% of lung cancers are lung carcinoid tumors. They are also sometimes called lung neuroendocrine tumors. Most of these tumors grow slowly and rarely spread.

cancer.org

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15
Q

How are the pulmonary manifestations of CF managed?

A
  1. Antibiotics, esp. azithromycin
  2. Bronchodilators
  3. Inhaled hypertonic saline
  4. Chest physiotherapy, e.g. postural drainage and percussion
  5. Vaccinations
  6. Double lung transplant
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16
Q

How is the pancreatic insufficiency of CF managed?

A

pancreatic enzyme replacement therapy

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17
Q

What are the risk factors for lung cancer?

A

The primary risk factor for the development of lung cancer is cigarette smoking, which is estimated to account for approximately 90 percent of all lung cancers.

Other factors: radiation therapy, pulmonary fibrosis, HIV infection, genetic factors

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18
Q

What is the standard treatment for stage I and stage II non-small cell lung cancer?

A

Surgery (lobectomy), followed by adjuvant chemotherapy

If patient cannot undergo surgery due to significant comorbidities, then radiation therapy

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19
Q

What is the prognosis for non-small cell lung cancer?

A

The overall five-year survival in non-small cell lung cancer (NSCLC) is between 10 and 15 percent, primarily because approximately 70 percent of patients present with either locally advanced (stage III) or distant metastatic (stage IV) disease.

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20
Q

What is the general treatment approach for advanced non-small cell lung cancer?

A

Advanced non-small cell lung cancer (NSCLC) generally requires the sequential use of systemic chemotherapies in an effort to prolong overall survival while maintaining quality of life.

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21
Q

What is the general treatment approach for small cell lung cancer?

A

Chemotherapy is the mainstay of treatment for patients with SCLC because of the high frequency of early dissemination.

In addition to chemotherapy, there is a significant role for radiation therapy (RT) in the treatment of LS-SCLC.

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22
Q

What is the prognosis for the patient with small cell lung cancer?

A

The most important prognostic factor in patients with SCLC is the extent of disease (stage) at presentation.

Limited stage disease:

–Median survival ranges from 15 - 20 months

–Five-year survival rate is 10 - 13%.

Extended stage disease:

–Median survival is 8 - 13 months

–Five-year survival rate is 1 - 2%.

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23
Q

What is the top cause of transudative pleural effusion?

And 2 other causes?

A

HEART FAILURE (>90% of cases)

cirrhosis with ascites

PE

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24
Q

What is the top cause of exudative pleural effusions?

A

INFECTION

CANCER

chylothorax

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25
Q

Describe the classification system for pulmonary hypertension.

A

Class I:

  • NO limitation of physical activity
  • NO DOE, chest pain, or near-syncope

Class II:

  • SLIGHT limitation of physical activity
  • NO symptoms at rest but ordinary activity -> dyspnea, chest pain, near-syncope

Class III:

  • MARKED limitation of physical activity
  • NO symptoms at rest but less than ordinary activity -> dyspnea, chest pain, near-syncope

Class IV:

  • Inability to perform any physical activity without symptoms
  • At rest, dyspnea, fatigue
  • Evidence of right heart failure
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26
Q

What are the normal ranges for the components of an ABG?

A
  • pH: 7.38 - 7.44
  • PaCO2: 35 - 40 mm Hg
  • PaO2: 95 - 100 mm Hg
  • bicarb/total CO2 (calculated): 24 - 30 mEq/L

Basic Skills in Interpreting Lab Data

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27
Q

What are some indications for ABG?

A

Indications for ABG sampling include the following:

  • Identification of respiratory, metabolic, and mixed acid-base disorders
  • Measurement of the partial pressures of respiratory gases involved in oxygenation and ventilation
  • Monitoring of acid-base status, as in patient with diabetic ketoacidosis (DKA) on insulin infusion
  • Assessment of the response to therapeutic interventions such as mechanical ventilation in a patient with respiratory failure
  • Determination of arterial respiratory gases during diagnostic evaluations
  • Quantification of oxyhemoglobin, which, combined with measurement of arterial oxygen tension (PaO2), provides useful information about the oxygen-carrying capacity of the patient
  • Quantification of the levels of dyshemoglobins (eg, carboxyhemoglobin and methemoglobin)
  • Procurement of a blood sample in an acute emergency setting when venous sampling is not feasible (many blood chemistry tests could be performed from an arterial sample)

Medscape

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28
Q

What is this?

A

consolidation

pneumonia

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29
Q

What is this?

A

blunted costophrenic angles

pleural effusion

30
Q

What is this?

A

pulmonary edema

in very bad CHF

31
Q

What is this?

A

emphysema

hyperinflation - flattening of diaphragm, can see lots of ribs

32
Q

What is this?

A

lung cancer

33
Q

Review this

A

chest xray structures

34
Q

Review this too

A

another review of chest xray structures

35
Q

How many people in the U.S. are infected with TB?

A

10-15 million

purple book 6-15

36
Q

What populations are more likely to develop TB or progress to active disease if infected?

A

More likely to be exposed:

  • Immigrants from high-prevalence area
  • Homeless
  • Residents or workers in jails

More likely to progress to active disease if infected:

  • HIV
  • Uncontrolled DM & smoking
  • Close contact with active TB patient
  • Underweight
  • CKD
  • Organ transplant
  • IVDU
  • EtOH
  • Malnourished
  • Cancer

purple book 6-15

37
Q

What organism causes TB and how is it spread?

A

Mycobacterium tuberculosis

small-particle aerosols (droplet nuclei)

38
Q

How is the PPD skin test interpreted for different populations?

A

Considered to be positive > 5mm in HIV pts and close contacts of person with active TB

Considered to be positive > 10mm in high-risk or high-prevalence populations (this includes you)

Considered to be positive > 15mm in everyone else

purple book 6-15

39
Q

What are the clinical manifestations of primary TB pneumonia?

A
  • middle or lower lob consolidation
  • +/- effusion
  • +/- cavitation

purple book 6-15

40
Q

What are the diagnostic studies for active TB?

A
  • acid-fast bacilli smear and culture
  • PCR
  • CXR

purple book 6-15

41
Q

What is the preventive therapy regimen for TB and when is it given?

A
  • Treat patients who are positive PPD test, or any exposed HIV patient
  • Isoniazid + pyroxidine 6-9 months OR 12 weeks observed isoniazid + rifapentine
  • HIV: Isoniazid + pyroxidine for 9 months
  • if isoniazid resistant, then rifampin for 4 months

purple book 6-16

42
Q

COPD

A

purple book 2-5

43
Q

What are the GOLD criteria for staging COPD?

A
  • I mild FEV1 > 80%
  • II mod FEV1 50-80%
  • III severe FEV1 30-50%
  • IV very severe FEV1 < 30%
44
Q

What is alpha-1 antitrypsin deficiency?

How does it present?

A
  • Alpha-1 antitrypsin (AAT) deficiency is a clinically under-recognized inherited disorder affecting the lung, liver, and rarely, skin.
  • AAT is a protease inhibitor of the proteolytic enzyme elastase.
  • So if you have a deficiency of the inhibitor, then your proteolytic enzymes will be out of control.
  • The clinical manifestations of AAT deficiency during the first two decades of life is that of liver disease, specifically chronic elevation of liver enzymes or cirrhosis.
  • Beyond the first two to three decades of life, patients with severe deficiency of AAT have an accelerated rate of lung function decline, especially with cigarette smoking and some occupational exposures.

UTD

45
Q

How is alpha-1 antitrypsin deficiency treated?

A

Intravenous augmentation via the infusion of pooled human AAT (alpha-1 antiprotease) is currently the most direct and efficient means of elevating AAT levels in the plasma and in the lung interstitium.

UTD

46
Q

What is hemothorax?

A

Hemothorax is a collection of blood in the space between the chest wall and the lung (the pleural cavity).

47
Q

What is the most common cause of hemothorax?

What are some other causes?

A

The most common cause of hemothorax is chest trauma. It can also occur in patients who have:

  • Blood clotting defect
  • Chest (thoracic) or heart surgery
  • Death of lung tissue (pulmonary infarction)
  • Lung or pleural cancer
  • Tear in a blood vessel when placing a central venous catheter
  • Tuberculosis

Medline

48
Q

What is the clinical presentation of hemothorax?

A
  • Anxiety
  • Chest pain
  • Low blood pressure
  • Pale, cool and clammy skin
  • Rapid heart rate
  • Rapid, shallow breathing
  • Restlessness
  • Shortness of breath
49
Q

What are some diagnostic studies that can reveal hemothorax?

A
  • Chest x-ray
  • CT scan
  • Pleural fluid analysis
  • Thoracentesis
50
Q

How is hemothorax treated?

A
  • chest tube to drain
  • if severe, may need thoracotomy to stop bleeding
  • obv treat cause of hemothorax
51
Q

What is chylothorax?

A

Chylothorax is caused by disruption or obstruction of the thoracic duct or its tributaries that results in leakage of chyle (lymphatic fluid of intestinal origin) into the pleural space. Chylous ascites can also flow into the pleural space. The fluid typically has a high triglyceride content and often a turbid or milky white appearance.

UTD

52
Q

What are the top 2 causes of chylothorax?

A
  1. Malignancy
  2. Trauma/surgery
53
Q

What is the clinical presentation of chylothorax?

A
  • Patients with chylothoraces usually present with signs and symptoms induced by the mechanical effects of a pleural effusion. Patients with nontraumatic chylothoraces frequently experience a gradual onset of decreased exercise tolerance, dyspnea, a heavy feeling in the chest, and fatigue. Fever and chest pain are rare because chyle within the pleural space does not evoke an inflammatory response.
  • The onset of a posttraumatic chylothorax may be delayed for as long as 10 days after the traumatic event.

UTD

54
Q

What are some treatment options for chylothorax?

A
  1. Treat underlying condition
  2. Pleural drainage
  3. Dietary (fasting or low fat diet)
  4. Pleurodesis
  5. Thoracic duct ligation

UTD

55
Q

What is the approach to a mystery pleural effusion?

A
  1. Thoracentesis to get some fluid
  2. Pleural fluid analysis:
  • appearance
  • transudate/exudate
  • chemical analysis - protein, LDH, cholesterol, glucose, pH, etc.
56
Q

How is empyema treated?

A
  • Sterilization of the empyema cavity with appropriate systemic antibiotics; at least 4 to 6 weeks of therapy are required.
  • Complete pleural fluid drainage, as evidenced by minimal chest tube output and CT documentation that no residual loculations persist.
  • Obliteration of the empyema cavity by adequate lung expansion.

UTD

57
Q

What is the management for primary spontaneous pneumothorax?

A

Depends on size of pneumothorax…

  1. oxygen
  2. needle aspiration
  3. chest tube
  4. thoracoscopy or chemical pleurodesis

UTD

58
Q

What is respiratory failure?

A

Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, it may be classified as either hypoxemic (PaO2 < 60) or hypercapnic (PaCO2 > 50).

59
Q

Describe an algorithm for deciding whether to intubate.

A
60
Q

What are some causes of acute respiratory failure?

A
  • Airway disorders, e.g. asthma
  • Pulmonary edema
  • Parenchymal lung disorders, e.g. pneumonia
  • Pulmonary vascular disorders, e.g. PE
  • Chest wall, diaphragm, pleural disorders, e.g. pneumothorax, rib fx
  • Neuromuscular disorders, e.g. myasthenia gravis
  • CNS disorders, e.g. drugs, infections
  • Increased CO2 production, e.g. fever, drugs

CURRENT

61
Q

What are the s/s of acute respiratory failure?

A

Symptoms and signs of acute respiratory failure are those of the underlying disease combined with those of hypoxemia or hypercapnia.

Hypoxemia: dyspnea, cyanosis, restlessness, confusion, anxiety, delirium, tachypnea, bradycardia or tachycardia, hypertension, cardiac dysrhythmias, and tremor.

Hypercapnia: dyspnea and headache are the cardinal symptoms; signs include peripheral and conjunctival hyperemia, hypertension, tachycardia, tachypnea, impaired consciousness, papilledema, and asterixis.

CURRENT

62
Q

What are CURRENT’s indications for intubation? Maybe you’ll like these better than UpToDate’s:

A

(1) hypoxemia despite supplemental oxygen
(2) upper airway obstruction
(3) impaired airway protection
(4) inability to clear secretions
(5) respiratory acidosis
(6) progressive general fatigue, tachypnea, use of accessory respiratory muscles, or mental status deterioration
(7) apnea

63
Q

What are CURRENT’s indications for mechanical ventilation?

A

(1) apnea
(2) acute hypercapnia that is not quickly reversed by appropriate specific therapy
(3) severe hypoxemia
(4) progressive patient fatigue despite appropriate treatment

64
Q

How does chronic respiratory failure differ from acute respiratory failure?

A
  • Chronic respiratory failure develops over several days or longer.
  • There is sufficient time for renal compensation and an increase in bicarbonate so the pH is usually only slightly decreased.
  • Clinical markers of long-standing hypoxemia include polycythemia and cor pulmonale.
65
Q

What are the s/s of pulmonary hypertension?

A

Exertional chest pain and dyspnea

Peripheral edema due to RHF

Anorexia and/or RUQ pain due to hepatic congestion

Increased intensity of S2, splitting of S2

Prominent A wave in JVP

UTD

66
Q

What are the diagnostic studies for pulmonary hypertension?

A

echocardiogram

CXR

EKG

PFTs

67
Q

What are some risk factors for pulmonary hypertension?

A
  • Scleroderma
  • HIV
  • Portal hypertension
  • Congenital heart disease
  • Left heart disease
  • COPD
  • Obstructive sleep apnea
  • Interstitial lung disease
  • Sickle cell

UTD

68
Q

How is pulmonary hypertension managed?

A

Depends on the cause, but could be:

  • Diuretics
  • Oxygen
  • Anticoagulation
  • Dobutamine
  • Vasodilators, e.g. CCBs, prostacyclin, PDE-5 inhibitors
  • Lung transplant

purple book 2-17

69
Q

What are the clinical manifestations of PE?

A
  • Dyspnea
  • Pleuritic chest pain
  • Cough
  • Hemoptysis
  • Increased RR, increased HR
  • Crackles, pleural friction rub
  • Massive: syncope, hypotension, PEA, increased JVP

purple book 2-14

70
Q

What are the Wells Criteria for PE?

A
  • Prior PE or DVT
  • Active cancer
  • Immobilization (bed rest, surgery)
  • Alternative dx less likely
  • Clinical signs of DVT
  • HR > 100
  • Hemoptysis

More than one of the above = “likely”

purple book 2-14

71
Q

What are the diagnostic studies for PE?

A
  • CXR
  • EKG
  • ABG
  • D-dimer
  • TTE
  • CT angiography

purple book 2-14

72
Q

What are the management options for PE?

A
  • Massive: thrombolysis, thrombectomy
  • Catheter-directed therapy (fibrinolysis, thrombus aspiration)
  • IVC filter
  • Long-term anticoagulation

purple book 2-15

INPATIENT (11 decks)

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