Pulmonology Part II

  1. Where do pulmonary embolisms arise from
    • 1. Systemic venous circulation
    • 2. Right side of the heart
    • 3. Tumors that have invaded the venous circulation
    • 4. Clots in the deep vein of the lower extremities
    • 5. Air emboli from central veins
    • 6. Amniotic fluid from active labor
    • 7. Fat from long bone fracture
  2. what the MC place pulmonary emboli originate from?
    Clots from the deep veins of the lower extremities, 90%
  3. hypercoagulable state, venous stasis, and vascular intial inflammation...triad for
    Virchow’s triad, risk factors for pulmonary embolism
  4. surgical procedures, cancer, oral contraceptives, and pregnancy are risk factors for
    Pulmonary embolism
  5. Symptoms: pleuritic chest pain, dyspnea, apprehension, cough, hemoptysis, and diaphoresis
    Pulmonary embolism
  6. signs: tachycardia, tachypnea, crackles, accentuation of pulmonary component of second heart sound, low-grade fever
    Pulmonary embolism
  7. diagnostic test for pulmonary embolism
    • SPIRAL CT*
    • ABG- acute respiratory alkalosis 2nd to hyperventilation
    • EKG- tachycardia, non-specific ST-T wave changes, S1Q3T3 pattern-indicates cor pulmonale
    • CXR- nonspecific maybe basilar atelectasis, done to r/o other pathology
    • v/Q scan- if normal okay if ab, do further tests
    • D-dimer- low suspicion , neg is <250
    • Pulmonary angiography*-definitive test for diagnose, used if non-invasive test are uncertain (unclear spiral CT)
  8. treatment for pulmonary embolism
    • 1. Anticoagulation therapy: heparin IV: Initial: 10,000 units, then 50 to 70 units/kg (5,000 to 10,000 units) every 4 to 6 hours
    • 2. Failure of anticoagulant agents: thrombolytic therapy
  9. How long should a person with pulmonary embolism be treated for?
    3 months minimum
  10. how do you prevent pulmonary embolisms
    High risk ppl: early ambulatory, intermittent pneumatic compression stockings, low dose heparin and low molecular weight heparin, combo of pharaoh and mechanical measures
  11. These type of tumors orginate in the GI tract and metastasize to the lungs
    Carcinoid tumors
  12. MC type of carcinoid tumor
    Adenoma
  13. This tumor is slow growing, and has rare metastasizing capablility
    Adenoma
  14. Presents with haemoptysis, cough, focal wheezing or recurrent pneumonia...and (cutaneous flushing, diarrhea, wheezing and low blood pressure) (hallmark sign)
    Carcinoid syndrome is the hallmark sign, carcinoid tumor
  15. Carcinoid tumor CXR will show
    low grade CA seen as pedunculated sessile growth in the central bronchi
  16. <3 cm nodule is called
    Coin shaped
  17. >3 cm nodule is called
    Mass
  18. These are found incidentally most of the time on xrays
    pulmonary nodules
  19. If a pulmonary nodule is found on a CXR what should you do
    order a chest CT to further investigate
  20. If a CT of the chest is suspicious for malignancy ( a nodule >1cm )what should you do next?
    biopsy
  21. if nodule is less than 1 cm in chest what should you do?
    Monitor it for growth at 3 mo, 6 mo, 1 year and then yearly for 2 year, if too small chances of getting it in biopsy are slim, that is why you monitor it for growth
  22. Shape of cancerous vs benign nodule
    • Ill defined, lobular or spiculated suggests cancer
    • Calcification, smooth well-defined edges, suggests benign disease
  23. the most common of all interstitial lung diseases
    Idiopathic pulmonary fibrosis
  24. In order to be considered "idiopathic" you must be sure to
    rule out other common causes such as drugs, and environmental or occupational exposures
  25. What diagnostics test are ordered to investigate idiopathic fibrosising interstitial pna?
    • CXR: evidence of progressive fibrosis over the years
    • CT chest: diffuse patchy fibrosis with pleural based honeycombing
    • PFTs will demonstrate a restrictive pattern - opposite of what you would see with asthma Decreased lung volume with a normal to increased FEV1/FVC ratio
    • Bronchoalveolar lavage, transbronhial biopsy, surgical lung biopsy
  26. Management for Idiopathic fibrosing interstitial pna
    • controversial; none shows improvement for survival or quality of life compared to no treatment
    • Trial therapy of oral corticosteroids
    • definitive: lung transplant, 5 year survival rate 50%
  27. This disease affects many organs and is idiopathic causes; 90% have lung involvement
    Sarcoidosis
  28. sarcoidosis affects these type of people most
    high in North American blacks (esp women) and Northern European whites
  29. Diagnostic studies for sarcoidosis
    • Serum blood tests: leukopenia, eosinophilia, elevated ESR, hypercalcemia, hypercalciuria
    • Angiotensin-converting enzyme: elevated in 40-80%
    • CXR:bilateral hilar and right paratracheal adenopathy and bilateral diffuse reticular infiltrates
    • Transbronchial biopsy of lung or fine needle biopsy confrims the diagnosis
    • biopsy: noncaseating granulomas
  30. cough, dyspnea of insidious onset, chest discomfort (common)
    malaise, fever, and symptoms consistent for various symptoms
    Other common: erythema nodosum, enlargement of parotid glands, lymph nodes, liver or spleen
    sarcoidosis= lung findings and systemic
  31. what are the clinically important pneumoconioses?
    Coal workers, silicosis, berylliosis, and asbestosis
  32. what is a chronic fibrotic lung disease abused by inhalation of coal dust or various inert, inorganic or silicate dusts
    Pneumoconioses
  33. people who work in insulation, demolition, and construction are most prone to this lung infection?
    Asbestosis pneumoconiosis
  34. high technology fields, aerospace, nuclear power, ceramics, foundries, tool and die manufacturers are most prone to this lung infection
    Berylliosis pneumoconiosis
  35. miners, sand blasters, stone workers are most prone to this lung infection
    Silicosis pneumoconiosis
  36. abestosis has the highest risk of developing
    Lung cancer: mesothelioma, especially if a smoker
  37. complicated cases of pneumoconiosis symptoms:
    Dyspnea, inspiratory crackles, clubbing of the fingers, and cyanosis
  38. pneumoconiosis simple cases’ symptoms present as
    Asymptomatic
  39. People with silicosis are at highest risk of developing
    Tuberculosis
  40. treatment for pneumoconiosis
    • Supportive therapy: oxygen, vaccinations, and rehab
    • corticosteroids for silicosis and berylliosis
  41. managment for sarcoidosis
    • There is no cure
    • corticosteroids and can be controlled with modest maintenance doses: 90% respond
    • Immunosuppressant cytotoxic drugs for patient with refractory to CS
  42. Acute onset of respiratory insufficiency with hypoxemia and bilateral radiographic infiltrates and without left atrial hypertension
    ARDS
  43. What are the three clinical setting that account for 75% of ARDS cases
    • 1. Sepsis syndrome (single most important)
    • 2. Severe multiple trauma
    • 3. Aspiration of gastric contents
  44. shock, toxic inhalation, near drowning, and multiple transfusions can cause this
    ARDS
  45. what is the underlying abnormality in ARDS?
    Increased permeability of the alveolar capillary membranes, this leads to development of protein-rich pulmonary edema
  46. event followed by rapid onset of profound dyspnea occuring 6 hrs to 72 hrs after, PE shows tachypnea, frothy pink or red sputum, diffuse crackles (rales), cyanotic with increasing severe hypoxia that is refractory to administered oxygen, SOB, diaphoresis, cough
    signs/ symptoms of ARDS
  47. diagnostic studies for ARDS
    • CXR: may be normal, infiltrates tend to be peripheral not in the angles, with air broncho grams- bilateral fluffy
    • MULTIPLE organ failure is common if other labs show it
    • BNP: <100 pg/ ml is normal, if above is this
    • abg: show hypoxemia and can be metabolic acidosis, respiratory alkalosis to acidosis
    • order others to rule out DDX
  48. management of ARDS
    • 1. Identification and specific treatment for severe respiratory dysfunction
    • -sedation, hemodynamics monitor with central cath
    • 2. Supportive care is req’d to compensate for respiratory dysfunction- oxygen via ET tube + low level of PEEP < 4 (2-6 Normal)
    • 3. Mortality rate is high so treat quickly
    • 4. Death occurs within 3 days of onset of symptoms. Remaining death occurs within 2 weeks of diagnosis and are caused by infection and multiple organ failure
  49. What is hyaline membrane disease now called?
    Respiratory distress syndrome
  50. what is the most common cause of respiratory disease in the preterm infant
    RDS
  51. what causes hyaline membrane disease or RDS?
    Deficiency of surfactant
  52. What does the infant with RDS look like
    Signs of respiratory distress
  53. what are diagnostic studies for RDS?
    • CXR: air bronchograms, diffuse bilateral atelectasis causing ground-glass appearance, and doming of the diaphragm (reticular granular)
    • ABG: hypoxemia, hypercapnia
    • CBC /CRP
  54. treatment of RDS or hyaline membrane disease
    • Synchronized intermittent mandatory ventilation
    • admin of exogenous surfactants- use in delivery room as prophylaxis or as rescue in established RDS
    • Antenatal steroids (MAG To stop labor)-betamethasone- impairs fetal growth
    • prevent preterm delivery
  55. Unintentional inhalation of f/b into the airway MC occurs in what age groups?
    Children <3 (no molars to chew down food) and adults >50
  56. knowledge of what will be life saving if someone has a f/b stuck in their throat?
    Heinrich maneuver
  57. what can be aspirated to cause a foreign body?
    Gastric contents, inert material, toxic material, poorly chewed food. Degree of injury depends on what’s aspirated
  58. choking and coughing or unexplained wheezing or hemoptysis should raise the suspicion for what?
    foreign body aspiration
  59. what can occur as a results of aspiration of obstructing material?
    Asphyxia and death
  60. what diagnostic studies can be order for aspirated f/b?
    • Expiratory X-RAY: could reveal regional hyperinflation caused by a check valve effect. F/b could also show
    • culture: obtain if postobstructive pna is suspected
  61. The number one cause for ARDS
    Sepsis
  62. what are surfactants made of
    Phospholipids, helps lungs stay open
  63. barotrauma does what to aveoli
    Stretches them out—> pressures are affected, they activate cytokines...TNF, IL1-6-8–>they activate neutrophils, they come in...this changes the pressures water goes in for osmostic balance, causing cascade effect. (This all washes off surfactant)
  64. top of lungs, doesnt send as much blood not as not air, is this match or mismatch v/q
    V/q match
  65. what is v/q
    Ventilation(in coming in and going out) and perfusion (blood flow)
  66. what causes pulmonary artery vasoconstriction
    Airway pressures, hypercapnia, and hypoxia (pulmonary hypertension)
  67. what does wet stiff lungs do to pulmonary compliance
    Decreases pulmonary compliance
  68. Rales
    fluid in the aveoli
  69. rhonchi
    Fluid in the bronchi
  70. normal output in heart, rales bilaterally think of...
    ARDS
  71. How do you diagnose ARDS
    • Berlin criteria
    • respiratory symptoms < 1 week of insult
    • CXR: bilateral opacities not otherwise explainable
    • pulmonary edema not cardiac in origin
    • severity: determined by calculating PaO2/ FiO2 and on ventilator with PEEP or CPAP >5 mmHg
  72. Putting a patient prone does what for ventilation
    Allow diaphragm to expand better
  73. Is a f/b has been lodged long what do you expect to look like
    Fever, acute/chronic cough, hemptsis, chest pain, chest pain, recurrent pneumonia’s (could be like asthma or pna presentation)
  74. why would you do expiratory film for f/b
    The air will be stuck, you can see a mediastinal shift, but only present <20% of the time
  75. Treatment for f/b
    • -abdominal thrusts for adults and children
    • -back blows and chest thrust on infants
    • -direct laryngoscopes if suspected in URI (L)
    • -removal with McGill forceps
    • -emergency trachestomy
    • -rigid bronchscopy
    • -flexible for non emergent: basket, forceps, balloon, or thoracotomy with possible lobar resection for chronic obstruction
  76. What are some risk factors for RDS
    • <28 weeks at birth (28 weeks)
    • prenatal, prematurity, maternal diabetes (insulin dependent)
    • male gender
    • caucasion
  77. What can you do to reduce chance of RDS
    Stress the baby by giving antenatal steroids, tells the body to stop growing and switch over to function—> it will start making surfactant
  78. change in volume divided by change in pressure is
    Compliance
  79. is something is already open, does it take more or less pressure to open more
    less pressure to get it more open, so its takes less energy
  80. nasal flaring, retractions, grunting, cyanosis, diminished adventitious breath sounds, harsh quality and crackles, tachypnea...present as this disease
    RDS
  81. once a baby is born with RDS what can you do for treatment
    • ventilation management (NIPPV, intubation)- CPAP: maintains FRC, decreases intrapulmonary shunting
    • maintain O2 sat between 90-95%
    • PaCO2 between 40-60 mmHg
    • vascular access
    • blood transfusion prn
    • antibiotics prn
  82. what are the side effects of giving surfactants in premies
    Air leak (pnemothorax), pulmonary hemorrage
Author
Ctrempe3047
ID
339320
Card Set
Pulmonology Part II
Description
Pulmonary
Updated