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CPR II Exam 2 > Hubbard DSA's > Flashcards

Hubbard DSA's Flashcards

1
Q

How long does acute cough last?

A

less than 3 weeks

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2
Q

What is a subacute cough?

A

cough lasting 3-8 weeks

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3
Q

What is the most common cause of acute cough?

A

viral upper respiratory infection

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4
Q

What viruses are most often associated with cough?

A

lower respiratory tract disease: influenza A/B, parainfluenza virus, RSV

upper respiratory tract disease: coronavirus, adenovirus, rhinovirus

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5
Q

Diagnosis of influenza includes a temperature greater than 100 (37.7C) and at least one of the following 3 symptoms?

A
  1. cough
  2. pharyngitis
  3. rhinorrhea
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6
Q

When should neuraminidase inhibitor treatment be started for influenza?

A

within the first 2 days of symptom onset

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7
Q

What 3 organisms are non-viral causes of uncomplicated acute bronchitis and cough in adults?

A

bordatella pertussis, mycoplasma pneumoniae, chlamydophila pneumoniae

NOTE: gram stain and culture of sputum will not reliably detect these

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8
Q

Does routine antibiotic treatment have an effect on acute bronchitis?

A

no

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9
Q

What is the diagnostic gold standard for B. pertussis?

A

recovery of bacteria in culture or by PCR

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10
Q

What is the third most common (and most serious) cause of acute cough?

A

pneumonia

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11
Q

What are the treatments of acute cough?

A

antitussive agents, expectorants, mucolytic agents, antihistamines, nasal anticholinergic agents

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12
Q

What is considered a chronic cough?

A

cough lasting more than 8 weeks

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13
Q

What is the initial workup for a patient with chronic cough?

A

smoking cessation, discontinuation of ACE-I for 4 weeks before additional workup

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14
Q

What three disorders are responsible for 90% of cases of chronic cough in nonsmokers?

A

upper airway cough syndrome (UACS), asthma, and gastroesophageal reflux disease (GERD)

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15
Q

What is recommended for patients with allergic rhinitis?

A

avoiding allergens and the daily use of intranasal glucocorticoids or cromolyn sodium

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16
Q

What is recommended treatment for GERD patients before invasive testing?

A

therapeutic trial with a proton pump

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17
Q

Chronic cough with airway eosinophilia. But normal findings on chest radiography, normal spirometry and a negative methacholine challenge test?

A

nonasthmatic eosinophilic bronchitis (NAEB)

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18
Q

What is the hallmark symptom of chronic bronchitis?

A

cough with sputum

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19
Q

CT results showing thickened bronchial walls in a “tram line” pattern

A

bronchiectasis

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20
Q

How long does it take for ACE-I cough to disappear

A

median time to resolution is 26 days

NOTE: can substitute and androgen receptor blocker for ACE-I

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21
Q

What must the differential diagnostic of hemoptysis include?

A

upper airway (nasopharyngeal) sources of bleeding and GI bleed

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22
Q

What should all patients with hemoptysis undergo?

A

chest radiography

- chest CT and fiberoptic bronchoscopy if a clear cause of hemoptysis is not identified

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23
Q

What is the treatment for patients with lower respiratory tract infection and normal chest radiograph?

A

oral antibiotics

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24
Q

What is considered massive hemoptysis?

A

blood loss greater than 200mL/day

NOTE: death results from asphyxiation, not exsanguination

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25
Q

What should be considered in massive hemoptysis?

A

urgent bronchoscopy

NOTE: surgery is considered last resort treatment for massive hemoptysis

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26
Q

not troubled by breathlessness except on strenuous exercise

A

MRC dyspnea scale grade 1

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27
Q

short of breath when hurrying on the level or walking up a slight hill

A

MRC dyspnea scale grade 2

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28
Q

walks slower than most people on the level, stops after a mile, or after 15 minutes walking at own pace

A

MRC dyspnea scale grade 3

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29
Q

stops for a breath after walking about 100 yards or after a few minutes on level ground

A

MRC dyspnea scale grade 4

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30
Q

too breathless to leave the house, or breathless when undressing

A

MRC dyspnea scale grade 5

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31
Q

what are the cardiovascular causes of acute dyspnea related to?

A

decrease in left ventricular function, or any event that increases pulmonary capillary pressure

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32
Q

what are the respiratory causes of acute dyspnea?

A

airway dysfunction, disruption of gas exchange by parenchymal disease, vascular disease, or disturbance of the ventilatory pump

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33
Q

what does low oxygen saturation suggest in acute dyspnea?

A

abnormalities of gas exchange
- points to processed such as asthma, acute exacerbation of COPD, ARDS, heart failure, pulm fibrosis, or pulm vascular disease

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34
Q

What is the primary diagnostic tool of acute dyspnea?

A

chest radiography

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35
Q

what do focal infiltrates on CXR indicate?

A

pneumonia

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36
Q

what does air in pleural space on CXR indicate?

A

pneumothorax

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37
Q

what does the presence of basal opacity with a meniscus on CXR indicate?

A

pleural effusion

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38
Q

what do cardiomegaly and vascular congestion on CXR indicate?

A

heart failure

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39
Q

when would high resolution CT be useful in patient with dyspnea?

A

when chest radiography is nondiagnostic and there’s a high suspicion of parenchymal lung disease

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40
Q

when would laryngoscopy and broncoscopy be useful to diagnose dyspnea?

A

suspected foreign body aspiration, airway obstruction and vocal cord dysfunction

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41
Q

what can dry crackles on lung examination signify in patient with dyspnea?

A

presence of pulmonary parenchymal disease

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42
Q

what is the workup of suspected pulmonary causes of chronic dyspnea?

A

chest imaging (plain chest radiography or CT) and pulmonary function testing

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43
Q

what is conjunctival pallow, tachycardia and a flow murmur suggestive of in pt with dyspnea?

A

anemia

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44
Q

what would a goiter and tachycardia indicate in pt with dyspnea?

A

hyperthyroidism and high output heart failure

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45
Q

what might kyphoscoliosis indicate in pt with dyspnea?

A

pulmonary restriction

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46
Q

what further workup should be considered in patients whose history, exam, and initial workup are unrevealing in pt with dyspnea?

A

cardiopulmonary exercise testing

- arterial blood gas measurements

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47
Q

what is considered mild oxygenation on the Berlin definition of ARDS?

A

PaO2 < 300 with PEEP or CPAP >5cm H2O

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48
Q

what is considered moderate oxygenation on the Berlin definition of ARDS?

A

PaO2 < 200 with PEEP >5cm H2O

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49
Q

what is considered severe oxygenation on the Berlin definition of ARDS?

A

PaO2 < 100 with PEEP >5cm H2O

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50
Q

what is part of the diagnostic criteria of ARDS?

A

severe hypoxemia

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51
Q

what indicates failure of compensatory ventilation, is especially worrisome and warrants immediate attention?

A

concominant hypercapnia (CO2 retention)

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52
Q

what are some direct predisposing causes of ARDS?

A

pneumonia, gastric aspiration, chest trauma/lung contusion, inhalation injury, near drowning

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53
Q

what are some indirect predisposing causes of ARDS?

A

non-pulmonary sepsis, acute pancreatitis, severe non-chest trauma, blood transfusions, surface burns

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54
Q

what is the typical physical exam finding of ARDS?

A

tachypnea and auscultation of rales

NOTE: may also present with heart failure, pneumonia, occult interstitial lung disease

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55
Q

what will CXR show of ARDS pt?

A

bilateral, diffuse airspace infiltrates

- patchy infiltrates may become more confluent as the syndrome evolves

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56
Q

what causes the exudative stage of ARDS?

A

vascular hydrostatic and protein osmotic pressures, together with vascular integrity, set the stage for accumulation of proteinaceous pulmonary edema

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57
Q

what other disorders can be indistinguishable from ARDS?

A

acute infectious pneumonias that cause either interstitial pattern or diffuse airspace disease

NOTE: P. jiroveci may present with a similar CXR and refractory hypoxemiawithout the same cellular toxicity seen in ARDS

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58
Q

have coticosteriods been shown to work in ARDS?

A

no

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59
Q

what is the best treatment for ARDS?

A

low tidal volume ventilation or high frequency oscillatory ventilation (HFOV) -> very high respiratory rates with very low tidal volumes

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60
Q

what are the management strategies for ARDS?

A
  • low tidal volumes
  • prone ventilation
  • fluid management
  • cardiopulm monitoring

NOTE: simple interventions like daily ventilator liberation, proper oral care, venous thomboembolic dz prophylaxis and OMM can improve ventilation

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61
Q

what are the most significant risk factors for head and neck cancer?

A

alcohol and tobacco

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62
Q

what is EBV infection frequently associated with?

A

nasopharyngeal cancer (esp in Mediterranean and far East)

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63
Q

what is HPV associated with in Western countries?

A

tumors of the oropharynx (tonsillar bed and base of tongue)

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64
Q

what effect do fruits and vegetables have on head and neck cancers?

A

cancer rates are higher in people with lowest consumption of fruits and vegetables

NOTE: certain vitamins, including carotenoids may be protective

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65
Q

when are HPV-related malignancies usually diagnosed?

A

40’s-50’s

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66
Q

when are EBV-related nasopharyngeal cancers diagnosed?

A

all ages, including teenagers

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67
Q

what can cause unilateral serous otitis media?

A

cancer of the nasopharynx, due to obstruction of the eustachian tube, nasal obstruction or epistaxis

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68
Q

what can advanced nasopharyngeal carcinomas cause?

A

neuropathies of the cranial nerves due to skull base involvement

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69
Q

how do carcinomas of the oral cavity present?

A

nonhealing ulcers, changes in the fit of dentures, or painful lesions

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70
Q

what can tumors of the tongue base or oropharynx cause?

A

decreased tongue mobility and alterations in speech

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71
Q

what is frequently the first sign of HPV-related tumors?

A

neck lymphadenopathy

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72
Q

what can be an early symptom of laryngeal cancer?

A

hoarseness

NOTE: requires referral to specialist for indirect laryngoscopy/radiography

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73
Q

if enlarged nodes are located in the upper neck and tumor cells are squamous cell histology, where did the malignancy most likely arise from?

A

mucosal surface in the head or neck

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74
Q

other than palpating the floor of the mouth, tongue and neck, what further workup should be considered in a malignancy is suspected?

A

CT scan, PET scan (to help ID/exclude distant metastases)

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75
Q

what is the definitive staging procedure to diagnose head/neck malignancy?

A

endoscopic examination under anesthesia

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76
Q

what is a stage 1 TNM definition tumor?

A

<2cm without extraparenchymal extension

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77
Q

what is a stage 2 TNM definition tumor?

A

> 2cm but not more than 4cm, without extraparenchymal extension

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78
Q

what is a stage 3 TNM definition tumor?

A

tumor >4cm, WITH extraparenchymal extension

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79
Q

what is a stage 4a TNM definition tumor?

A

tumor invades skin, mandible, ear canal and/or fascial nerve

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80
Q

what is a stage 4b TNM definition tumor?

A

tumor invades skull base and/or pterygoid plates and/or encases carotid artery

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81
Q

what are common sites of metastasis for T4 tumors?

A

lungs, bones, and liver

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82
Q

what should be performed is squamous cell carcinoma is found?

A

panendoscopy

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83
Q

where do HPV-positive tumors spread early?

A

locoregional lymph nodes

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84
Q

what is the treatment for stage 1 or 2 (localized) lesions?

A

radiation

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85
Q

what is the treatment for stage 3 and early 4 (intermediate) lesions?

A

concominant chemo-radiotherapy

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86
Q

what is the treatment for recurrent and/or metastatic disease?

A

supportive/palliative. can be given chemotherapy for pain control, but response is only 30-50%

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87
Q

what are complications of head/neck cancer treatment?

A

mucositis, dysphagia, xerostomia, loss of taste, decrease tongue mobility, hypothyroidism

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88
Q

what are the majority of lung cancers?

A

non-small cell cancer (85%)

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89
Q

what type of lung cancer is diagnosed almost exclusively in smokers?

A

small cell lung cancer

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90
Q

what are examples of paraneoplastic syndromes that patients with small cell lung cancer often present with?

A

acromegaly, Cushing syndrome, hypercalcemia, hypertrophic pulmonary osteoarthropathy, hyponatremia, superior vena cava syndrome, Trousseau syndrome, vocal cord paralysis, Horner syndrome

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91
Q

what is the workup if lung cancer is suspected?

A

CXR to look for masses

  • CT may be required to detect smaller lung cancers
  • peripheral node biopsy (will dx stage of cancer)
  • sputum cytology (only in pt with poor pulmonary function who cannot tolerate invasive procedures)
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92
Q

what is the staging evaluation in non-small cell lung cancer?

A

chest/abdomen CT, and PET-CT (may ID advanced disease and can preclude unnecessary thoracotomy)

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93
Q

what are small cell lung tumors exquisitely sensitive to?

A

radiation and chemotherapy

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94
Q

what is the mainstay treatment for patients with stage 1 or 2 lung cancer?

A

surgery

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95
Q

what is the treatment for patients with stage 4 (inoperable) non-small cell lung cancer?

A

combined tx, including local radiation for a symptomatic mass and/or palliative chemotherapy

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96
Q

what is the mainstay of treatment for small cell lunger cancer?

A

combination chemotherapy with a platinum-based agent

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97
Q

what is a stage 1 non-small cell lung cancer?

A

tumor surrounded by lung or pleura, more than 2 cm from carina

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98
Q

what is a stage 2 non-small cell lung cancer?

A

locally advanced disease without mediastinal involvement

99
Q

what is a stage 3 non-small cell lung cancer?

A

mediastinal involvement or two separate tumor nodules in same lobe without mediastinal involvement

100
Q

what is a stage 4 non-small cell lung cancer?

A

metastatic (including malignant pleural nodules and pleural/pericardial effusions)

101
Q

what are the differential diagnoses of COPD

A

asthma, bronchiectasis, cystic fibrosis, bronchiolitis, a1-AT deficiency

102
Q

what is the best way to prevent COPD?

A

smoking cessation

103
Q

what are the smoking-related changed the airway undergoes?

A

bronchial mucous gland hypertrophy, goblet cell metaplasia and inflammatory cell infiltrates -> squamous epithelial metaplasia, ciliary loss and dysfunction

104
Q

what are the signs of hyperinflation to look for in diagnosing COPD?

A

barrel chest, hyperresonant percussion, distant breath sounds, prolonged expiratory time.

also pursed lip breathing

105
Q

what are the cardiac symptoms in COPD?

A

cor pulmonale, split S2, ad a parasternal lift due to RV hypertrophy

106
Q

what is the gold criteria stage 1?

A

FEV > 80%

107
Q

what is the gold criteria stage 2?

A

FEV: 50-80%

108
Q

what is the gold criteria stage 3?

A

FEV 30-50%

109
Q

what is the gold criteria stage 4

A

FEV < 30%, or FEV <50% plus chronic respiratory failure

110
Q

what should be suspected with early-onset COPD, with panacinar emphysema?

A

a1-AT deficiency

111
Q

when would you give short acting b-agonists in COPD?

A

as needed for relief of persistent or worsening symptoms, to improve exercise tolerance (not continuous symptoms)

effects last 4-6 hours

112
Q

when would you give long acting b-agonists?

A

for more sustained/predictable improvement in lung function (for more chronic symptoms, decreasing the need for rescue medication)

effects last 12 hours

113
Q

what should tiotropium NOT be combined with?

A

short-acting anticholinergic drugs

NOTE: anticholinergic agents should be used with caution in patients with urinary obstruction and narrow-angle glaucoma

114
Q

what medication should not be used alone to treat COPD?

A

inhaled glucocorticoids

115
Q

what medication is indicated in stage 1 COPD?

A

short-acting bronchodilator

116
Q

what medication is indicated in stage 2 COPD?

A

regular treatment with one or more long-acting bronchodilators; add pulmonary rehabilitation

117
Q

what medication is indicated in stage 3 COPD?

A

add inhaled corticosteroids if repeated exacerbation

118
Q

what medication is indicated in stage 4 COPD?

A

add long-term oxygen therapy if chronic respiratory failure. consider surgical treatments

119
Q

what is the preferred treatment for COPD exacerbation?

A

short acting b-agonist

120
Q

what treatment alleviates respiratory acidosis, decreases respiration rate, severity of dyspnea, length of hospital stay and mortality in severe COPD patients?

A

noninvasive intermittent ventilation

121
Q

heterogenous involvement of the lung with different stages of progression of fibrosis in adjacent areas of the lung.
- starts in subpleural regions and honeycombing is seen

A

usual interstitial pneumonitis (UIP)

122
Q

uniform involvement of lung parenchyma with cellular infiltration or fibrosis
- bilateral/subpleural with ground-glass infiltrates on CT imaging

A

nonspecific interstitial pneumonitis (NSIP)

123
Q

small-airway bronchiolotis with granulation tissue and organizing pneumonia
- granulomas are hallmark (well-formed, noncaseating are typical for sarcoidosis, loosely formed granulomas are more commonly seen in hypersensitivity pneumonitis)

A

bronchiolitis obliterans organizing pneumonia (BOOP).cryptogenic organizing pneumonia (COP)

124
Q

patient presents with progressive dyspnea (over months), reduced exercise tolerance and persistent dry cough

A

DPLD

NOTE: history should look for underlying causes

125
Q

PE shows oxygen desturation with exertion, basilar inspiratory crackles on lung exam, digital clubbing, signs of autoimmune disease (systemic sclerosis or RA), and evidence of right side heart failure

A

DPLD

126
Q

what should plain CXR show in DPLD?

A

increased interstitial reticular or nodular infiltrates

127
Q

what is crucial tool in diagnostic evaluation of DPLD?

A

high-resolution CT, provides detail about the distribution and extent of disease (often times don’t need a biopsy)

128
Q

what drug is a common cause of lung disease? what is the therapeutic intervention?

A

amiodarone

- discontinuation (glucocorticoids may also benefit)

129
Q

what two other drugs are commonly associated with DPLD?

A

methotrexate and nitrofurantoin

130
Q

what is the management of connective-tissue associated DPLD?

A

focused on the underlying connective tissue disease and supportive care for the lung manifestations

131
Q

why is diagnosing idiopathic pulmonary fibrosis important?

A

because it has a poor prognosis

NOTE: no medical treatment has shown consistent improved mortality

132
Q

dyspnea on exertion, exercise intolerance, dry cough, crackles on inspiration

imaging shows lower lung zone and subpleural linear reticular markings, volume loss, honeycombing and traction bronchiectasis

A

idiopathic pulmonary fibrosis

133
Q

what is the next line of treatment in idiopathic pulmonary fibrosis?

A

patients with acute exacerbations should be evaluated for underlying and treatable infection or volume overload

134
Q

rare illness, acute/abrupt onset

imaging shows bilateral alverolar disease with ground-glass changes. histology shows diffuse alveolar damage

A

acute interstitial pneumonia (aka Hamman-Rick syndrome)

135
Q

how is AIP diagnosed?

A

open lung biopsy

136
Q

small airway bronchiolitis with granulation tissue, presents as flu-like illness and radiography shows peripheral opacities that change over time

A

BOOP/COP

137
Q

do BOOP/COP respond to glucocorticoids?

A

yes

138
Q

granulomatous disease of unclear cause that affects multiple organs, including the lung. highest incidents of age groups under 18 and 50-60. those with lung involvement commonly present with cough, dyspnea, and chest heaviness.

A

sarcoidosis

139
Q

what would imaging of sarcoidosis show?

A

bilateral hilar adenopathy and/or interstitial infiltrates

140
Q

what is the treatment for DPLD?

A

smoking cessation, supplemental oxygen

- symptomatic treatment for reactive airways or cough, maintenance of nutrition/fitness, treatment of infections

141
Q

what do many patients with severe \/chronic DPLD develop?

A

pulmonary hypertension

142
Q

what occurs in people with repeated episodes of inhalation of antigens with immunologic reaction?

A

hypersensitivity pneumonitis

NOTE: clues should be fungal elements or bird droppings, etc

143
Q

how does hypersensitivity pneumonitis present?

A

acute flu-like symptoms, crackles on physical exam, labs show leukocytosis

hi-res CT shows ground-glass opacities with **centrilobular nodules and noncaseating granulomas

144
Q

what is the treatment for hypersensitivity pneumonitis?

A

avoidance of causative antigen. can also use systemic steroids for patients with chronic symptoms

145
Q

what are the clinical features of obstructive sleep apnea (OSA)?

A

habitual snoring, nighttime awakening, insomnia, daytime fatigue, erectile dysfunction

146
Q

what is the most important risk factor for OSA?

A

excess body weight

NOTE: post-menopausal women also at risk)

147
Q

what physical exam findings are likely with OSA?

A

crowded pharynx, nasal obstruction, retrognathia, systemic HTN, decreased oxygen saturation, accentuated pulmonic component of S2, or S3 gallop

148
Q

what labs can be done for OSA?

A
  • *polysomnography** (test of choice)

- overnight oximetry, CBC, serum TSH, ECG, arterial blood gas

149
Q

what are the differential diagnoses of OSA?

A

central sleep apnea, upper airway resistance syndrome, periodic limp movements of sleep, narcolepsy, obstructive or restrictive lung disease, GERD, sinusitis, heart failure, epilepsy, sleep deprivation, hypothyroidism, acromegaly

150
Q

what is the treatment of OSA?

A
  • *lifestyle changes and CPAP** are the cornerstones of therapy
  • it aims to improve daytime sleepiness and cognitive performance, and to prevent long-term sequelae
151
Q

what are the physical exam findings of pneumothorax?

A

diminished breath sounds, decreased tactile fremitus, decreased movement of the chest

152
Q

physical exam findings of tension pneumothorax?

A

marked tachycardia, hypotension, and mediastinal/trachial shift

153
Q

what would left sided primary pneumothorax produce of ECG?

A

QRS and precordial T-wave changes that may be misinterpreted as AMI

154
Q

what imaging should be ordered for pneumothorax? what does it show?

A

expiratory CXR

- tension pneumothorax: show a large amount of air in the affected hemithorax and contralateral shift of the mediastinum

155
Q

what is the treatment for pneumothorax

A

(depends on the severity of the pneumothorax and nature of underlying disease)
- simple aspiration drainage of pleural air with small-bore catheter for spontaneous primary pneumothoraces that are large or progressive

156
Q

when would a patient need a chest tube with a pneumothorax?

A

secondary pneumothorax, large pneumothorax, tension pneumo, or severe symptoms

157
Q

when would thoracoscopy or ope thoracotomy be indicated in pneumothorax?

A

recurrence of spontaneous pneumothorax, any occurrence of bilateral pneumothorax and failure of tube thoracostomy for the first episode

158
Q

what two mechanisms lead to the accumulation of excessive fluid in the pleural space?

A
  1. increased capillary hydrostatic pressure

2. decreased plasma oncotic pressure

159
Q

what are the leading causes of pleural effusion in the US?

A

heart failure, pneumonia, cancer

160
Q

what are the physical exam findings of pleural effusion (large accumulations of fluid)?

A

dull to percussion, diminished/absent tactile fremitus, decreased/absent breath sounds on auscultation, and a pleural friction rub

161
Q

what is the workup of pleural effusion?

A

CXR and CT, because it can more effectively define the size and location of the pleural effusion and distinguish parenchymal from pleural disease

NOTE: thoracentesis should also be considered

162
Q

what are bilateral transudative effusions commonly associated with?

bilateral exudative effusions?

A

heart or liver failure

malignancy or pleuritis due to SLE

163
Q

what is the major complication of thoracentesis?

A

pneumothorax

164
Q

what causes exudative pleural effusions?

A

inflammation, infection, malignant conditions

165
Q

what causes transudative pleural effusions?

A

unbalanced hydrostatic forces, heart failure and cirrhosis

166
Q

what is the treatment of pleural effusions?

A

large effusions should be evacuated

NOTE: shouldn’t remove more than 1.5L at a time to minimize the likelihood of re-expansion pulmonary edema

167
Q

what are the most common lesions in the anterior mediastinum?

A

thymomas, lymphomas, teratomas, thyroid masses

168
Q

what are the most common lesions in the middle mediastinum?

A

vascular masses, lymph node enlargement from metastases/granulomatous dz, pleuropericardial and bronchogenic cysts

169
Q

what are the most common lesions in the posterior mediastinum?

A

neurogenic tumors, meningoceles, meningomyoloceles, gastroenteric cysts, esophageal diverticula

170
Q

what is the best imaging technique for mediastinal masses?

A

CT**

- only one that should be done in most cases

171
Q

what is the appropriate treatment of acute mediastinitis?

A

exploration of the mediastinum with primary repair of the esophageal tear and drainage of the pleural space

172
Q

what are most cases of chronic mediastinitis caused by?

A

histoplasmosis or tuberculosis

- can also be sarcoidosis silicosis and other fungal diseases

173
Q

what are the symptoms of fibrosing mediastinitis?

A

compression of a mediastinal structure (SVC or large airway, phrenic or recurrent laryngeal nerve paralysis)

174
Q

what is the treatment of chronic mediastinitis?

A

antituberculous therapy

NOTE: no other medical or surgical therapy has been shown to work

175
Q

gas in the interstices of the mediastinum

A

pneumomediastinum

176
Q

what are the 3 main causes of pneumomediastinum?

A
  1. alveolar rupture
  2. perforation/rupture of esophagus, trachea, or main bronchi
  3. dissection of air from the neck or abdomen into mediastinum
177
Q

what are the symptoms of pneumomediastinum?

A

severe substernal check pain with or without radiation into the neck/arms

178
Q

what physical exam findings in pneumomediastinum?

A

subcutaneous emphysema in the suprasternal notch, Hamman’s sign (crunching/clicking with the heartbeat)

179
Q

how is diagnosis of pneumomediastinum confirmed?

A

chest radiograph

180
Q

how is compression relieved in pneumomediastinum?

A

needle aspiration

181
Q

what is the most common pathogen causing CAP?

A

strep pneumo

other pathogens = H. influenzae, mycoplasma pneumo, chlamydophila pneumo, legionella

182
Q

what can cause severe pneumonia in patients with alcoholism?

A

Klebsiella pneumo

183
Q

what pathogen is more common to cause pneumonia in patients with structural lung disease?

A

Pseudomonas

184
Q

who is the PCV13 vaccine indicated for?

A

adults over 65, patients with immunocomprimising conditions, asplenia, CSF leaks, or cochlear implants

NOTE: PCV23 and 13 are NOT administered together

185
Q

pneumonia symptoms + chronic heart and lung disease?

A

Pneumococci, H. influenzae

186
Q

pneumonia + travels to SW US?

SE Asia?

A
  • Coccidioides

- Mycobacterium

187
Q

pneumonia + IV drug use?

A

Staph aureus, M. tuberculosis

188
Q

pneumonia + bats?

A

Histoplasmosis

189
Q

pneumonia + farm animals?

A

Coxiella burnetii

190
Q

what are the physical exam findings of pneumonia?

A

tachypnea, fever, crackles, bronchial breath sounds, pleural effusion (egophony and dullness to percussion)

191
Q

how many CURB-65 criteria must be met for a patient to be hospitalized?

A

2

192
Q

what is the workup for patient with pneumonia?

A

CXR

193
Q

what do the presence of cavities with air-fluid levels suggest on a CXR of patient with pneumonia?

A

abscess formation

194
Q

what should you do if a pleural effusion is present in patient with suspected pneumonia?

A

decubitus film or chest CT

195
Q

what is the treatment for outpatient pneumonia?

A

macrolide or doxycycline

196
Q

what is treatment for patient with cardiopulm disease?

A

respiratory quinolone or combination of beta-lactam + macrolide or doxycycline

197
Q

what medication is given to hospitalized patient when aspiration is suspected?

A

clindamycin or beta-lactam/beta-lactamase inhibitor

198
Q

how long should you treat patients with Legionella infection?

A

5-10 days with quinolone is used

NOTE: mild-moderate <7days

199
Q

pneumonia that develops at least 48 hours after hospitalizaition, including ventilator-associated pneumonia and post-op pneumo

A

HCAP

200
Q

what is the most common type of HCAP?

A

ventilator-associated (VAP)

201
Q

what is the most common cause of HCAP?

A

microaspiration of bacteria that colonize the oropharynx/upper airway

202
Q

what are common pathogens of HCAP?

A

Enterobacter, pseudomonas, Klebsiella, E.coli, Strep and S. aureus

203
Q

what is VAP diagnosis based on?

A

clinical presentation, leukocytosis, new/changing CXR findings

204
Q

how does treatment of PAH differ from most other causes of PH?

A

treatment is focused on vasodilator therapy

205
Q

what causes over 80% of PH cases?

A

conditions causing elevation of left-sided heart filling pressures or pulmonary disease

206
Q

what are the most common symptoms of PH?

A

fatigue and dyspnea with exertion

- may also have palpitations or chest pain

207
Q

how is a diagnosis of PH confirmed?

A

ONLY by right heart catheterization and direct measurement of mean pulmonary artery pressure
- can also do CMP, BNP, 6 minute walk test

208
Q

what is group 1 pulmonary hypertension?

A

idiopathic PAH: resting mPAP >25mmHg, PCWP<15mmHg

209
Q

what is group 2 PH?

A

secondary left heart disease: mPAP>25mmHg, PCWP elevated

- systolic, diastolic or valvular dysfunctions

210
Q

what is HIV/AIDS a major risk factor for?

A

primary progression and reactivation of quiescent tuberculosis

211
Q

why should you consider retesting or treating high-risk TB patients empirically?

A

because skin test result may not become positive for up to 12 weeks

212
Q

what is an IGRA screen?

A

it assesses the T-cell response to specific M. tuberculosis antigens
- ** is the preferred screen for those who are BCG vaccinated**

213
Q

what is mandatory to rule out active disease in all patients with a positive skin test or IGA result?

A

CXR and history, PE

214
Q

what do hemoptysis and chest pain from pleural involvement indicate?

A

advances stage tuberculosis

215
Q

what are radiologic abnormalities of reactivation Tb?

A

lesions in the apical posterior segments of the upper lung and superior segments of the lower lobe

216
Q

what is the standard treatment for active Tb?

A

at least 6 months of 4-drug regimen

- usually isoniazid, rifampin, pyrazinamide, ethambutol

217
Q

what is the recommended follow up of Tb?

A

monthly sputum cultures to monitor treatment response, and adjust the drug regimen based on susceptibilities and length of therapy

218
Q

what is the main cause of fat embolism syndrome (FES)?

A

long bone and pelvic fractures

219
Q

what is the clinical presentation of FES?

A

24-72 hours after initial insult, classic triad: hypoxemia, neurologic abnormalities, petechial rash

NOTE: can develop a syndrome indistinguishable from ARDS

220
Q

what are the imagine/lab findings in FES?

A
  • CXR normal, CT normal
  • MRI may show “starfield” pattern of diffuse, punctate, hyperintense lesions
  • CRP generally elevated in critical illness
221
Q

what is the treatment for FES?

A

therapy is largely supportive, no definitive tx

NOTE: do NOT give corticosteriods or heparin!!

222
Q

progressive lower extremity edema with achy pain in the legs (may be worse with standing)

  • shiny, atrophic skin, cutaneous telangiectasia (dilated blood vessels close to skin), varicose veins
  • breakdown of skin in severe cases, ulceration (especially around medial malleolus)
A

venous stasis

223
Q

lower extremity edema secondary to venous stasis must be differentiated from what?

A

CHF, mechanical venous obstruction, liver failure, chronic kidney disease

224
Q

what is the first line of treatment for venous stasis?

A

external compression, behavior modification

NOTE: ulcers are difficult to treat and often reoccur

225
Q

why is DVT of the upper extremities rising in incidence?

A

secondary to increasing use of indwelling venous catheters

226
Q

patient presents with erythema, swelling, tenderness of affected limb
- Homan sign (pain in calf on forced dorsiflexion)

A

lower extremity DVT

227
Q

what testing should be done for patient with low clinical liklihood of DVT?

A

D-dimer (blood clot test)

highly sensitive and specific test

228
Q

what does a positive D-dimer test indicate?

A

high clinical likelihood of DVT

229
Q

what are the differential diagnoses of DVT?

A

venous insufficiency, muscle strain, ruptured baker cyst, cellulitis, lymphedema

230
Q

what is the treatment for DVT?

A

immediate anticoagulation

  • IV unfractionated (or low MW) heparin
  • longer-term warfarin can be used simultaneously
231
Q

what should happen once a patient is on stable anticoagulation for DVT?

A

therapy should be continued for a duration based on their risk factor profile
-alll pt should be treated minimum of 3 months

232
Q

what treatment can be used if there is a strong contraindication for anticoagulation therapy?

A

IVC filter

233
Q

what does a Wells Criteria score of 3+ indicate?

A

DVT is likely

234
Q

what does a Wells Criteria score of 102 indicate?

A

moderate risk

  • should proceed to D-dimer testing
  • > negative D-dimer rules out DVT
  • > positive D-dimer –> US
  • > positive US is concerning for DVT
235
Q

what are the Wells criteria categories?

A
  • active cancer
  • bedridden recently
  • calf swelling
  • superficial (nonvaricose veins present)
  • entire leg swollen
  • localized tenderness
  • pitting edema
  • paralysis/immobilization
  • previously document DVT
236
Q

when should IVC filters not be used?

A

for perioperative prophylaxis for pulmonary embolism

237
Q

what are the most common symptoms of PE?

A

dyspnea, pleuritic chest pain, cough, hemoptysis, tachypnea, crackles, tachycardia, accentuated pulmonic component of S2

238
Q

what does CXR show in PE?

A

atelectasis, small pleural effusion, focal oligemia, wedge-shaped density

239
Q

what does a normal D-dimer value effectively rule out?

A

PE -> correlated with excellent outcome, no further workup required

240
Q

what is the initial imaging for PE?

A

contrast-enhanced CT (CT angiography), ventilation-perfusion (V/Q) scanning (measures alteration in pulmonary blood flow)

NOTE: only a totally normal V/Q scan can exclude PE

241
Q

what is the treatment for PE?

A

managed in the hospital until stable, including treatment of hypoxia and management of hemodynamic instability

242
Q

when is surgical embolectomy for massive PE indicated?

A

if patient is unstable and thrombolytic therapy is contraindicated

243
Q

what Wells criteria score is PE considered likely?

A

> 4

<4 is unlikely

CPR II Exam 2 (5 decks)

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