Pulmonology Flashcards

1
Q

Describe the primary pathophysiology of asthma.

A

Bronchial hyperreactivity, inflammation of airways, increased mucus production.

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2
Q

Define atopy.

A

The genetic tendency to develop allergic diseases

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3
Q

What is the atopic triad associated with asthma?

A

wheeze, eczema, seasonal rhinitis

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4
Q

What findings in pulmonary function testing are indicative of asthma?

A

FEV1:FVC ratio < 75%

< 12% inc in FEV1 after bronchodilator therapy

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5
Q

WHat ABG findings are indicative of severe asthma?

A

PaO2 < 60 and PaCO2 > 45

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6
Q

When is CXR indicated in the evaluation of an asthma patient?

A

Only if pneumonia or other Dx is suspected –> asthma will show hyperinflation

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7
Q

How are hand-held peak expiratory flow meters used in the management of asthma?

A

Can be used at home to estimate variability and quantify the severity of attacks.

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8
Q

When asthma is suspected but spirometry is non-diagnostic, what testing is performed and what result indicates asthma?

A

Histamine/Methacholine challenge –> FEV1 decrease of more than 20% is diagnostic for asthma.

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9
Q

Describe the pharmacologic options for long term asthma management.

A

inhaled corticosteroids, cromolyn (MAST cell stabilizer), nedocromil (anti0inflamatory), LABA, leukotriene antagonists (reduce mucus), theophyline.

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10
Q

Describe the pharmacologic options for short term asthma management.

A

SABAs, systemic corticosteroids, ipratropium bromide (anti-Ach)

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11
Q

What is the most effective anti-inflammatory for the management of chronic asthma?

A

Inhaled corticosteroids

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12
Q

Describe the 6 steps of therapy recommended in the management of asthma.

A

1: SABA PRN
2: Low dose inhaled corticosteroid (ICS)
3: Low dose ICS + LABA or medium dose ICS
4: Medium dose ICS + LABA
5: High dose ICS + LABA
6: High dose ICS, LABA, and PO cosrticosteroid

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13
Q

Define normal FEV1:FVC ratio by age.

A

< 20: 85%
20 - 39: 80%
40 - 59: 75%
>/= 60: 70%

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14
Q

Describe the PFT findings associated with mild, moderate, and severe asthma.

A

mild: FEV1 > 80% predicted, ratio normal
moderate: FEV1 60-80% of predicted, ratio dec by 5%
severe: FEV1 < 60% predicted, ratio dec by > 5%

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15
Q

What is the cardinal sign of bronchitis?

A

Cough for at least 1 week

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16
Q

T/F: Color of sputum is predictive of bacterial involvement in bronchitis.

A

False

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17
Q

Describe how a diagnosis of bronchitis is made.

A

Mostly clinical –> CXR negative for pneumonia

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18
Q

What supportive therapy may be used in the management of bronchitis?

A

hydration, expectorants, analgesics, B2 agonists, antitussives

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19
Q

T/F: Non-prescription cough and cold products should not be used in children less than 2.

A

True

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20
Q

What is the most common etiology of an acute exacerbation of chronic bronchitis and what is the recommended treatment?

A

Usually bacterial –> empiric first line treatment is 2nd gen cephalosporin, second line is Bactrim or a second gen macrolide (azithromycin/clarithromycin)

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21
Q

When should antibiotics be used in the management of bronchitis?

A

Elderly, immunocompromised, underlying respiratory disease –> no statistical benefit of antibiotics in healthy patients.

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22
Q

What is the most common etiology of bronchitis not related to a COPD exacerbation?

A

Viral –> usually adenovirus

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23
Q

Define COPD.

A

Progressive, largely irreversible airflow obstruction due to loss of elastic recoil and increasing airway
resistance

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24
Q

Describe the relationship of emphysema and chronic bronchitis.

A

Both are COPDs that usually coexist with one being more predominant than the other.

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25
Q

What are the risk factors for COPD?

A

Smoking by far #1. Other is alpha 1 antitrypsin deficiency (protects elastin in lungs from damage by WBCs)

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26
Q

What are the hallmark signs of emphysema and chronic bronchitis?

A

emphysema: dyspnea on exertion
bronchitis: productive cough

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27
Q

Differentiate emphysema from chronic bronchitis in terms of S/S.

A

Emph: resp alkalosis, matched V/Q, mild hypoxemia and normal CO2, pink puffers (chachexia and pursed lip breathing), hyperresonant with dec lung sounds.
Bronch: resp acidosis, severe V/Q mismatch, severe hypoxemia and hypercapnea, blue bloaters (obese and cyanotic), rhonchi, rales, wheezing lung sounds.

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28
Q

What is the gold standard testing used for diagnosis of COPD?

A

PFTs/Spiriometry

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29
Q

What value of spirometry is an important prognostic factor in COPD?

A

FEV1 –> < 1L indicates increased risk of mortality.

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30
Q

What spirometry findings are expected in COPD?

A

Obstruction: dec FEV1, FVC, and ratio
Hyperinflation: Increased RV, TLC, FRC

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31
Q

What is the most effective choice of bronchodilators in long term management of COPD?

A

Combo therapy with B-2 agonist and inhaled anti-Ach

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32
Q

What anti-Ach’s are commonly used in the management of COPD?

A

Tiotropium (Spiriva) - long acting

Ipratropium (Atrovent) - short acting

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33
Q

What are the contraindications of Anti-Ach use in COPD?

A

Glaucoma and BPH

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34
Q

What B-2 agonists are commonly used in the management of COPD?

A

Albuterol and terbutaline - short acting

Salmeterol - long acting

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35
Q

What are the contraindications and precautions in the use of B-2 agonists?

A

CI: severe CAD, precautions: DM, hyperthyroid

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36
Q

Describe the use of theophyline in management of COPD.

A

B-2 agonist that is rarely used s/p narrow therapeutic window. Smokers require a higher dose.

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37
Q

Describe the use of corticosteroids in management of COPD.

A

Adjunct - not monotherapy

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38
Q

What is the only therapy proven to decrease mortality in COPD, what is the MOA, and when is it indicated?

A

O2 –> reduces pulmonary vasoconstriction s/p hypoxia. Use when SpO2 < 88%

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39
Q

What is the first and most important step in the management of COPD?

A

smoke cessation

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40
Q

What vaccinations are recommended for COPD patients?

A

Pneumococcal and flu

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41
Q

Why is azithromycin a particularly useful abx in COPD patients?

A

It has anti-inflamatory properties in the lungs.

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42
Q

How is chronic bronchitis defined?

A

Productive cough more than 3 months for 2 consecutive years.

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43
Q

Describe the PFT values associated with stage I, II, III< and IV COPD.

A

I: FEV1 > 80% of predicted
II: FEV1 50-80% of predicted
III: FEV1 30-50% of predicted
IV: FEV1 < 30% of predicted

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44
Q

Describe the management associated with stage I, II, III< and IV COPD.

A

I: SABA PRN and decrease risk factors
II: SABA PRN + LABA or LAMA
III: SABA, LABA + LAMA, pulmonary rehab, ICS
IV: SABA, LABA + LAMA, rehab, ICS, O2

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45
Q

What two types of cancer make up the vast majority of lung cancers?

A

Small cell carcinoma (15%)

Non-small cell carcinoma (85%)

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46
Q

What are the primary risk factors for lung cancer?

A

Smoking, occupational exposures, poor indoor air quality, genetics, oncogenic viruses.

47
Q

What is the most common type of lung cancer in a non-smoker?

A

Adenocarcinoma (a type of non-small cell)

48
Q

Describe the cellular pathogenesis in the development of lung cancer.

A

normal epithelium –> squamous metaplasia –> dysplasia –> carcinoma in situ –> invasive carcinoma

49
Q

What symptoms are common in lung cancer and how many symptoms are usually found on initial presentation?

A

cough, anorexia, weight loss, fatigue, anemia, fever, pain –> more than 80% have at least 3 symptoms

50
Q

What symptoms usually develop when pulmonary lesions are present.

A

cough, hemoptysis, dyspnea, chest pain

51
Q

Define pancoast tumor.

A

Rare form of lung cancer that forms at the very top of the lung. Invasion to surrounding tissue causes shoulder and arm pain.

52
Q

What two types of cancer are most associated with smoking?

A

Small cell carcinoma (highest association) and squamous cell carcinoma

53
Q

Differentiate small cell carcinoma from squamous cell carcinoma in terms of their location.

A

Small: always occurs centrally
Squamous: usually central but can be peripheral

54
Q

When and how does small cell lung carcinoma typically present?

A

Present at very late stage often as ACTH (Cushing’s Syndrome) or ADH (SIADH) secreting tumors.

55
Q

Name and describe the most common type of adenocarcinoma.

A

Bronchioalveolar cell carcinoma (BAC) –> associated with non-smokers, very slow growing, can be mucinous, non-mucinous, or mixed.

56
Q

What is a carcinoid tumor?

A

A neuroendocrine tumor (NET) that can be a type of lung cancer.

57
Q

What is carcinoid syndrome?

A

Functional NET that secretes a high amount of serotonin causing one or more of: facial flushing, sweating, diarrhea, dyspnea, wheezing, weakness, tachycardia, HTN.

58
Q

Differentiate between typical and atypical carcinoid tumors.

A

Typ: slow growing and rarely metastasize
Atyp: faster growing and more likely to met.
Typical accounts for 90% of carcinoid tumors.

59
Q

In what patients are typical and atypical carcinoids usually seen?

A

Young, non-smokers

60
Q

What are the most aggressive types of lung cancer and in what patients are they seen?

A

Small cell carcinoma large cell neuroendocrine tumors –> both more common in smokers.

61
Q

What is the definition of a solitary pulmonary nodule?

A

Asymptomatic lesion <3cm diameter surrounded by normal lung parenchyma

62
Q

What are the risk factors for a solitary nodule to be malignant?

A

Advanced age, smoking, prior malignancy

63
Q

What diagnostic findings indicate a solitary nodule is more likely to be malignant?

A
  • Larger size increases chance of malignancy
  • Doubling in size within 400 days inc malignancy
  • Lobulated or spiculated borders indicate malignancy
  • Ground glass or part solid nodules inc malignancy
  • Calcification > 200 hounsfield units
  • Location in upper lobes more likely malignant
64
Q

What are the most common characteristics of a benign lung nodule?

A

Solid, smooth borders, unchanged in size over two years.

65
Q

What imaging is used to evaluate pulmonary nodules?

A

CT initially –> PET scan and biopsy definitive

66
Q

Which lung cancer patients are best candidates for primary surgical therapy?

A

Stage 2 and some stage 1. Stage 1 non-surgical candidates get radiotherapy.

67
Q

Describe the prognosis for small cell lung carcinoma.

A

Initial response to chemo is very good. But remission tends to be short lived. Two year survival = 20-40% in early stages and 5% in late stages.

68
Q

What are the most common pathogens responsible for community acquired and hospital acquired penumonia?

A

CAP: Strep pneumo (H. Flu in Pts with pulm disease)
HAP: Pseudomonas

69
Q

Differentiate community acquired from hospital acquired pneumonia.

A

CAP: Not in a hospital, SNF, pneumonia < 48 hours after hospital admission.
HAP: Pneumonia develops > 48 hours after admission

70
Q

What are the most common pathogens responsible for aspiration pneumonia?

A

Outpatient: anaerobes

In-patient: Staph aureus and gram neg bacteria

71
Q

Differentiate between typical and atypical pneumonia.

A

Typ: Strep pneumo, lobar on CXR, fever, productive cough, pleuritic C/P, PE –> dull percussion, bronchial breath sounds, inc tactile fremitus and egophony.
Atyp: Mycoplasma, diffuse patchy infiltrates on CXR, low fever, dry cough, malaise, sore throat, HA, N/V/D, physical exam normal

72
Q

Correlate specific types of pneumonia with CXR findings.

A

Abscess = staph aureus

Right upper lobe with bulging fissure and cavitations = Klebsiella

73
Q

T/F: Clinicians can track the effectiveness of pneumonia treatment based on improvements in repeat CXRs.

A

False: CXR resolution lags behind clinical improvement for weeks

74
Q

Correlate sputum findings to likely pathogen.

A

Rusty / blood tinged = strep pneumo
Currant jelly = klebsiella
Green = h.flu / pseudomonas
Foul smelling = anaerobes

75
Q

State the common abx administered for different types of pneumonia.

A

CAP outpatient: macrolide or doxy (FQ only if co-morbid conditions / recent abx use)
CAP inpatient: B lactam + macrolide OR broad spectrum FQ
CAP ICU: B lactam + macrolide OR B lactam + broad spectrum FQ
HAP (pseudomonas): anti-pseudomonal B lactam, anti pseudomonal aminoglycoside or FQ
Aspiration: clindamycin or augmentin +/- metronidazole

76
Q

Describe the vaccine recommendations for pneumonia.

A

PCV 13 = childhood vaccination
PPV 23 Age >65 = revaccinated every 5 years
PPV 23 Age < 65 = revaccinate every 5 years if chronic disease.

77
Q

What is the most common cause of pneumonia from an atypical bacteria and what is the classic presentation?

A

Mycoplasma –> aka walking pneumonia

78
Q

Patients in what circumstances are at risk for contracting Legionella pneumonia and how do they present?

A

Cooling towers, AC, contaminated water

S/S: anorexia, N/V/D, increased LFTs, HypoNa

79
Q

What patients are at highest risk for Klebsiella and what is the hallmark finding on CXR?

A

Alcoholics –> cavitation lesions on CXR

80
Q

What are the three types of atypical bacteria that cause pneumonia?

A

Myoplasma, Chlamydia, Legionella

81
Q

What is the most common location and pathogen in an aspiration pneumonia?

A

Anaerobes in right lower lobe

82
Q

What is the most common bacterial pathogen to cause pneumonia in an immunocompromised patient?

A

Pseudomonas

83
Q

What are the most common causes of viral pneumonia in children and adults?

A

Kids: RSV and parainfluenza
Adults: flu

84
Q

What is the most common fungal pathogen to cause pneumonia in an immunocompromised patient and what are the S/S?

A
Pneumocystis jiroveci (PCP)
S/S: fatigue, dry cough, dyspnea on exertion, pleuritic chest pain
85
Q

What fungal pathogen is common in the Mississippi and Ohio river valleys?

A

Histoplasmosis

86
Q

Define the terms insomnia, hypersomnia, and parasomnia and state which is more associated with obstructive sleep apnea.

A

Ins: Difficulty falling and staying asleep
Hyper: Excessive daytime sleepiness
Para: Abnormal behavior during sleep –> sleep walking, terrors, nightmares, etc.
Hypersomnia higher association with sleep apnea

87
Q

What are the risk factors for sleep apnea?

A

obese, middle aged, HTN, CHF

88
Q

Describe narcolepsy.

A

Sudden, brief sleep attacks, cataplexy, sleep paralysis, hypnagogic hallucinations (occur at start of sleep), which may precede sleep

89
Q

Define cataplexy.

A

Condition in which strong emotion or laughter precipitates sudden collapse, though remaining conscious.

90
Q

Define and describe polysomnography.

A

Sleep study –> evaluates EEG, HR, RR, SpO2

91
Q

In addition to a sleep study, what other test is important to evaluate in a person complaining of sleep disturbances?

A

TSH

92
Q

What components are involved in counseling a person to improve sleep hygiene?

A

avoid alcohol, caffeine, nicotine, exercise

prior to bed; establish regular sleep hours; relaxation techniques; avoid prolonged daytime naps.

93
Q

What are the primary treatments for sleep apnea and narcolepsy?

A

Apnea: Weight reduction and CPAP
Narc: dextroamphetamine and modafinil (stimulants)

94
Q

Define nocturnal myoclonus and state the most appropriate treatment.

A

Def: involuntary muscle twitches during sleep
Treatment: clonazepam

95
Q

What is the treatment for sleep terrors or sleep walking?

A

Benzos

96
Q

Define and describe tuberculosis.

A

Chronic infection with mycobacterium tuberculosis that involves formation of a granuloma.

97
Q

What is the hallmark symptom of tuberculosis?

A

Persistent, dry cough for about 3 weeks. Can have hemoptysis in advanced stages.

98
Q

Aside from the hallmark symptom, what other S/S are commonly present in tuberculosis?

A

Fever, night sweats, anorexia, weight loss, pleuritic chest pain, dyspnea, post-tussive rales

99
Q

What is the gold standard diagnostic evaluation for tuberculosis?

A

Acid fast bacillus cultures x 3 days –> need 3 negative cultures to deem non-infectious.

100
Q

Describe the use of radiography to evaluate TB.

A

Used for yearly screening in PPD positive patient or to exclude active TB.

101
Q

What is required for definitive diagnosis of TB?

A

m. tuberculosis from culture (6-8 weeks to grow) or DNA/RNA amplification techniques (1-2 days)

102
Q

Describe what is indicated by a positive PPD test and state the parameters for a positive test.

A

Identifies presence of infection but doesn’t differentiate active from latent.
> 5mm in HIV/immunosuppressed, recent contact with active TB or CXR indicating TB.
> 10mm in IVDU, recent immigrants, healthcare workers, Hx of DM, CKD, scoliosis, and age < 4
> 15mm everyone else - no risk factors

103
Q

Differentiate between primary, latent, and secondary TB.

A

1: First exposure, usually isolated to the middle of the lungs forming an area called a Gohn focus
Lat: Inactive period of the Gohn focus after the first exposure
2: Latent TB that becomes active TB with lesions most common in the lung apices.

104
Q

T/F: Primary TB can become active without entering a latent phase.

A

True: But this is rare –> called Primary progressive TB

105
Q

Describe 2 ways latent TB can become active TB.

A

Reactivation of the latent infection (most common) or from a reinfection after an additional exposure to TB

106
Q

Describe the pathophysiology of secondary TB.

A

Formation of a granuloma described a casseous, cheese-like necrosis on gross exam.

107
Q

Describe the treatment for latent TB.

A

Isoniazid for 9 months …or…
Rifampin for 4 months …or…
Rifampin and Pyrazinamide for 2 months

108
Q

Describe the treatment for active TB.

A

Some combination of isoniazid, rifampin, pyrazinamide, and ethambutol for 6-9 months. HIV patients require treatment for at least 1 year.

109
Q

When are patients with active TB considered to no longer be infectious?

A

2 weeks after initiation of therapy.

110
Q

How are patients with latent TB treated prophylactically?

A

Isoniazid for 6-12 months

111
Q

What are the AEs associated with each of the TB treatment drugs?

A

Iso: peripheral neuropathy, hepatitis
Rif: orange body fluid and skin
Pyr: hyperuricemia and photosensitive rash
Eth: optic neuritis (reg-green vision)

112
Q

What must be coadministered with isoniazid?

A

Vitamin B6

113
Q

Describe 4 steps for maintenance of public health after diagnosing a case of active TB.

A
  1. Report the infection
  2. Isolate patient for minimum of 2 weeks
  3. BCG vaccine for patients in high risk areas
  4. Kids or immunocompromised with known exposure should be treated for at least 12 weeks then given a PPD skin test –> stop treatment if negative.