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ICM > Pulmonary > Flashcards

Pulmonary Flashcards

1
Q

COPD

A
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2
Q

Definition of chronic bronchitis?

A

Chronic productive cough for 3 months of each of 2 successive years

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3
Q

Definition of Emphysema?

A

Abnormal permanent enlargement of alveoli with destruction of alveolar walls without fibrosis

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4
Q

Definition of Asthma?

A

Airway responsiveness that leads to recurrent episodes of wheezing, breathlessness, chest tightness, and coughing

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5
Q

When is asthma NOT considered COPD?

A

Not all asthma is COPD; if asthma is REVERSIBLE it is not considered COPD

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6
Q

What patients are not considered to have COPD yet they have airflow obstruction?

A

These would be patients with a KNOWN etiology or specific pathology (CF, bronchiectasis, or obliterative bronchiolitis)

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7
Q

Number one cause of COPD?

(If you dont get this right youre a dumdum and should no longer be in medical school :-P)

A

Smoking

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8
Q

Technical definition of COPD?

A

Disease state characterized by airflow limitation not fully reversible. Airflow limitation is usually progressive and associated with an abnormal inflammatory response of the lungs to noxious particles of gasses

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9
Q

What three main things occur in COPD?

A
  1. Mucus hypersecretion
  2. Disrupted alveolar attachment (desmosomes?)
  3. Mucosal and peribronchial inflammation and fibrosis
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10
Q

What happens to diffusion capacity in emphysema?

A

Decreases (an easy obvious answer)

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11
Q

Exposure risk factors for COPD?

A
  • Tobacco smoking
  • Passive smoking
  • Air pollution
  • Occupational exposure
  • Infections
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12
Q

Host factors for COPD?

A
  • Genetic mutations
    • Such as Alpha-1-antitrypsin deficiency
  • Reduced Lung growth
  • Airway responsiveness
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13
Q

Variants of alpha-1antitrypsin deficiency and the way their effects?

A
  • S varient
    • 60% of normal levels with no pulmonary effects
  • Z varient
    • 10% of normal levels
    • Accumulation of alpha-antitrypsin in the RER of the liver
    • Predisposition of juvenile hepatitis, cirrhosis, and hepatocellular carcinoma
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14
Q

FEV1 percentage representing severe disability?

A

25%

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15
Q

What are key indicators in the diagnosis of COPD?

A
  • Chronic cough
  • Chronic sputum production
  • Dyspnea
  • History of exposure to risk factors
    • Tobacco smoke
    • Occupational exposure
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16
Q

Diagnosis of COPD?

A
  • H & P
  • Lab exam
    • Imaging: XR, CT
    • Pulmonary function testing
      • FEV1/FVC<0.7 (hallmark of obstruction)
      • Decreased IC and Increased TLC/RV/FRC
      • DLCO decrease
  • Arterial blood gases
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17
Q

What is a key early finding on the physical exam of COPD?

A

Decreased breath sounds at the bases

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18
Q

Upon initial visualization of a patient with severe COPD, what action is indicative of an obstructive disorder?

A

Pursing the lips while breathing

(they also use accessory respiratory muscles)

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19
Q

What are 2 very noticible things on an XR of an emphysema patient?

A

Hyperinflation

Flattened diaphragm

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20
Q

What is most important in the diagnosis of COPD?

A
  • Pulmonary functions testing
  • Understand the flow volume curves
    • Obstructive moves to the lefts
    • Restrictive moves to the right (R.. R)
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21
Q

In what COPD will you find decreased DLCO?

Normal DLCO?

A
  • Decreased
    • Emphysema
  • Normal
    • Bronchitis
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22
Q

Lung Cancer

A
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23
Q

What is occuring to the incidence of lung cancer in men?

Women?

A

Men: declining

Women: plateauing

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24
Q

Risk factors?

A
  • Smoking/second hand smoke
  • Prior radiation therapy
  • Environmental/occupational exposure:
    • Asbestos
    • Beryllium
    • Radon
  • Systemic disease
    • HIV or scleroderma
  • Pulmonary disease
    • COPD and Idiopathic pulmonary fibrosis
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25
Q

Is there any prevention?

A

Suggested CXR but not effective due to cost and likelihood.

No chemoprevention

Smoking cessation

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26
Q

Thoracic/pulmonary clinical presentation?

A
  • cough
  • shortness of breath
  • hemoptysis
  • post-obstructive pneumonia (from endobronchial tumor or bronchial compression from surrounding tumor)
  • Pleural effusion
  • SVC syndrome
    • from high mediastinal tumor. Facial edema
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27
Q

If there is fluid in the pleural space on the right side, which way will the mediastium shift?

A

Towards the left

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28
Q

Common metastasis?

A
  • Bone (Ribs)
  • CNS
  • Liver
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29
Q

Extrapulmonary symptoms?

A
  • Wt loss
  • fatigue
  • fever
  • **digital clubbing
  • paraneoplastic syndromes
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30
Q

What is a paraneoplastic syndrome?

A

Disease/symptom related to but not directly caused by the anatomic presence of cancer

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31
Q

Examples of paraneoplastic syndromes?

A
  • Hypercalcemia
  • SIADH
    • common with hyponatremia and will present with seizures
  • Lambert-Eaton
    • mimics myasthenia gravis but increased strength of contraction with increased stimulation
  • Dermatomyositis
  • Cushings
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32
Q

In what cancer is hypercalcemia more common?

SIADH?

Lambert-Eaton?

A
  • Hypercalcemia
    • Squamos cell
  • SIADH
    • Small cell (responds to chemo)
  • Lamber Eaton
    • Small cell
    • Fatigueable weakness
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33
Q

Diagnosis?

A

“No meat, no treat”

MUST BIOPSY

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34
Q

Types of biopsies?

A
  • Bronchoscope
    • Endobronchial brush or EBUS
  • Fine needle aspirate
    • CT guided for distant
  • Surgical biopsy (less common)
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35
Q

Subtypes of NSCLC?

A
  • Adenocarcinoma
  • Adenosquamos
  • Large cell
  • Squamos
  • Other
    • Mesothelioma
    • Combinations
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36
Q

Small cell carcinoma (formerly “oat cell”):

Aggressiveness?

Shape of cells? Stain?

What does it look like at time of diagnosis?

A
  • Highly aggressive
  • Round/oval cells that are highly basophilic
  • Necrotic at time of diagnosis
    • cancer is expanding faster than the vasculature
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37
Q

3 ways to stage? (NOT TNM)

A
  • By ability to resect (surgery)
    • mediastenoscopy
    • not resectable if metastatic
  • PET scan
    • radiolabled glucose for highly metabolic areas
  • Bronchoscope/EBUS
38
Q

What does TNM staging refer to? (what is the TNM acronym)

A
  1. T = tumor
  2. N = nodes
  3. M = metastasis
39
Q

What is a pancoast tumor?

How may it present?

A
  • A highly apical NSCLC tumor
  • Presenting symptoms can mimic Horner’s
    • compression of sympathetic ganglia?
40
Q

Prognosis of NSCLC vs Small cell?

A
  • NSCLC
    • Stage 1: median survival of 59 months
      • most die of non-cancer related disease
    • Stage IV: 4 months
  • Small cell
    • Minimal 5 year survival even if caught early and treated
41
Q

What does the Karnovsky performance status scale measure?

A

Implications for treatment via the level of functional capacity

42
Q

GAS EXCHANGE AND ABGs

A

I DONT EVEN KNOW WHAT THE HELL ABG STANDS FOR?

43
Q

How much CO2 is produced from each molecule of acetic acid in the TCA cycle?

Equation?

A
  • 2 molecules
  • R = VCO2/VO2
    • R = 1 for carbs
    • R = .8 for protein
    • R = .7 for fat
44
Q

What is the equation for alveolar ventilation?

A

VA= VT - VD

  • VA = alveolar ventilation
  • VT = tidal volume
  • VD = dead space
    • 1ml/ lb of body wt
45
Q

Venous blood perfuses the alveoli at a rate equal to?

A

Cardiac output (Q)

So this is saying V/Q = 1?

46
Q

What is the equation for oxygen content?

A
  • O2 content = [Hb] x 1.39 x Hb saturation %
    • = PO2 x .003
47
Q

6 causes of hypoxemia?

A
  • Reduction in inspired PO2
  • Abnormal diffusion
  • Hypoventilation
  • Ventilation perfusion mismatch
  • Shunt
  • Nonpulmonary factors affecting PaO2
48
Q

Normal inspired PO2:

  • What is PO2 at sea level?
  • What is the PAO2? Why is it different from PO2?
A
  • PO2 = FO2 (% in atmosphere) x Patm
    • = .21 x 760 = 160mmHg
  • PAO2 = FO2(Patm-47) - (PaCO2/.8)
49
Q

What are two causes of hypoxemia due to reduction in inspired PO2?

A
  • Decreased FIO2
    • somehow oxygen content in the air is below .21
  • Increased elevation
    • causes a change in Patm
50
Q

Normal diffusion:

Gas transfer = ?

A
  • Gas transfer = diffusing capacity x (PA-Pcapillary)
    • Diffusing capacity of the membrane is proportional to the cross sectional area
    • Diffusing capacity is inversely proportional to the thickness of the membrane
51
Q

Causes of hypoxemia due to decreased diffusing capacity?

Decreased diffusing capacity in individuals at rest?

A
  • Fibrosis/inflammatory lung disease: membrane thickening
    • As Thickening increases D.C. decreases
  • Diffuse alveolar destruction: decreased cross sectional area
    • As surface area decreases D.C. decreases

At rest decreased diffusion capacity rarely leads to hypoxemia

52
Q

PACO2 = ?

Proportions?

A
  • PACO2 = (VCO2/VA) x K
    • K = constant
  • PaCO2 = PACO2
  • VE = VA

PaCO2 is inversely proportional to VE

53
Q

What occurs to PaCO2 with hypoventilation? PaO2?

A

Rise in PaCO2 in hypoventilation leads to a proportional decrease in PaO2

54
Q

Given PaCO2 = 80, calculate PAO2.

What is normal PAO2-PaO2?

A
  • Recall: PAO2 = FO2(Patm-47) - (PaCO2/.8)
    • PAO2 = (.21) (760-47) - (80/.8)
    • PAO2 = 50
  • Normal PAO2-PaO2 <15
55
Q

Causes of hypoventilation stimulated hypoxemia?

A
  • Decrease in central drive
  • Decrease in functioning of the respiratory pump
56
Q

What does V/Q = 0 indicate? Example?

What does V/Q = infinity indicate? Example

A
  • V/Q = 0
    • Perfusion but no ventilation
    • Example: a shunt
  • V/Q = infinity
    • Ventilation but no perfusion
    • Example: dead space
57
Q

What can cause a decrease in V/Q?

A
  • Decrease in V due to airway disease
  • Increase in perfusion
    • Example: pulmonary embolism with shunting to nonembolized areas
58
Q

What can cause an Increase in V/Q?

A
  • Decrease in perfusion
    • Example: there will be air in places without perfusion such as an area of embolus
  • Emphysema
    • lose of perfusion (due to alveolar destruction) is greater than the decrease in ventilation
59
Q

With a V/Q inequality, how does increased ventilation of normal alveoli affect CO2 elimination? O2?

A
  • CO2
    • Because CO2 elimination is proportional to alveolar ventilation, alveoli CAN compensate for abnormal alveoli
  • O2
    • The O2 content curve flattens out at higher PO2 and therefore increased ventilation CANNOT compensate for abnormal alveoli
60
Q

What are 3 causes of a shunt?

A
  1. Normal anatomical shunt
  2. Abnormal anatomical channels in patients with pulmonary hypertension
  3. Blood passing alveoli that are atelectatic or fluid filled
61
Q

3 nonpulmonary factors that decrease PO2?

A
  1. Decreased cardiac output
  2. Decreased Hb
  3. Increased utilization of O2 by tissues
62
Q

In a normal lung, how can decreased PO2 be increased (if caused by a nonpulmonary factor)

A

Increase in ventilation

63
Q

Causes of hypercarbia?

A
  • Decreased respiratory drive
    • Narcotics
    • Obesity hypoventilation syndrome
  • Mechanical impairments to ventilation
    • Neuromuscular disease
    • Thoracic deformity (kyphoscoliosis)
    • Obesity hypoventilation syndrome
  • Severely impaired V/Q matching

*** see last page of notes for acid-base disorders? its mostly just equations. to know or not to know…

64
Q

ILD Article

A

doin my best hurr

65
Q

Characterization of interstitial lung diseases?

A

Infiltration of cellular and/or noncellular material into the lung parenchyma. ( also alveolar airspaces,
blood vessels, and distal airways)

66
Q

Major physiological consequence of ILDs?

A

Impaired gas exchange

67
Q

Known causes of ILDs?

A
  • inhaled organic and inorganic substances
  • drugs
  • radiation
  • systemic disorders
    • connective tissue diseases (CTDs)
68
Q

Most common form of ILD seen clinically?

A

IPF, also called cryptogenic fibrosing alveolitis

69
Q

“definite” diagnosis of
IPF requires evidence of?

A

UIP ( usual intersitial pneumonia) characterized by patchy collagen fibrosis with associated scarring distributed in a peripheral, subpleural
fashion with honeycomb changes

70
Q

Clinical presentation for ILD of unknown cause?

A

Gradually worsening exertional dyspnea with inspiratory crackles (not heard in sarcoidosis) and restrictive lung disease or impaired gas exchange

71
Q

What will you see on a high resolution CT for ILD?

A

Presence of bilateral and peripheral opacities and subpleural honeycombing with basal predominance

72
Q

Second most common ILD = sarcoidosis.

Characterization of sarcoidosis?

A

Presence of noncaseating epitheloid granulomas (no finger clubbing or crackles; has nodules)

73
Q

High resolution CT findings of sarcoidosis?

A

Nodular infiltrates with an upper and mid lung predominance (instead of IPF: basal). Affects peribronchovascular regions, the interlobular
septa, and the pleural surface

74
Q

Common
forms of hypersensitivity pneumonitis in the United States?

A

just to fuck with you…

bird fancier’s disease, farmer’s lung disease and
“hot tub lung.” (those are real!!!)

75
Q

types of drugs associated with ilds?

A
  • chemo - bleomycin
  • cardiovascular drugs - amiodarone
  • abx - nitrofurantoin
76
Q

Drug induced ILD CT?

A

Shows diffuse alveolar damage, nonspecific interstitial pneumonia, eosinophilic pneumonia, and pulmonary hemorrhage

Histologically - nonspecific

77
Q

Pulmonary Langerhans cell histiocytosis characterization?

Where may there be extrapulmonary manifestations?

A

Characterized by the proliferation of Langerhans cells in the lung with destruction of lung parenchyma (cystic changes on CT) and architectural manifestations.

Extrapulmonary manifestations:

  • bone, skin, pituitary, liver, lymph nodes, and thyroid
78
Q

What is the most common ILD associated with a normal XR and sometimes even a normal high resolution CT?

A

Hypersensitivity pneumonitis

79
Q

What ILDs affect peripheral lung zones?

Central

A
  • Peripheral
    • Chronic eosinophilic pneumonia
    • IPF, cryptogenic organizing pneumonia
  • Central
    • sarcoidosis and berylliosis
80
Q

What is Traction bronchiectasis/bronchiolectasis?

A

dilatation and distortion of the
bronchi and bronchioles in areas of parenchymal fibrosis

81
Q

Pulmonary function testing in patients with ILDs typically reveals?

A

restrictive pattern with reduced diffusing capacity

82
Q

SHLEEEP

A
83
Q

What is obstructive sleep apnea?

A

Cessation/decrease in airflow in the presence of breathing effort > 10 seconds.

Apnea-Hypopnea index (AHI) > 5 + EDS

84
Q

What is Hypopnea?

A

Decreased airflow + 4% desaturation

85
Q

What parts of the airway are implicated in an OSA patient?

A
  • Nasopharynx
  • Velopharynx
    • tongue base and soft palate
  • Hypopharynx
    • lower pharynx
86
Q

What is a trend in the clinical findings of OSA patients?

A
  • Smaller airways
  • Larger structures that surround the airways
87
Q

What is transmural pressure and how is it related to sleep apnea?

A
  • Pt = difference between the intraluminal and surrounding tissue pressure
  • At Pt decreases so does the cross sectional area of the pharynx
  • When the net forces equal the closing pressure, OSA occurs
88
Q

Risk factors for OSA?

A
  • smoking
  • menopause
  • alcohol use
  • sedative use
  • supine sleeping position
89
Q

What is the “stop” mnemonic?

A
  • S: snoring (loudly, often)
  • T: tired
  • O: observation of apnea by another person
  • P: blood pressure increase
90
Q

What is the “BANG” mnemonic?

A
  • B: BMI>35
  • A: age>50
  • N: neck circumference>40cm
  • G: gender - male
91
Q

What is central sleep apnea?

Common findings?

A

Cessation/decrease in airflow in the ABSENCE of respiratory effort.

  • Males
  • A. fib
  • >60yo
  • hypocarbia
92
Q

Cardiovascular effects from OSA?

A
  • hypoxemia and hypercapnea
  • Increased negative intrathoracic pressure
  • hypertension
  • heart failure and arrhythmia
    • bradyarrhythmia common
  • Renal disease
  • Stroke
  • Sudden death
  • 2x prevalence of coronary artery disease

ICM (9 decks)

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