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Respirology > Respirology Combined > Flashcards

Respirology Combined Flashcards

1
Q

What are the risk factors for decompression sickness?

A

Ascension rate, dive time, dive depth, air travel within 12 hours, right to left shunt.

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2
Q

List the complications of barotrauma.

A

Non cardiogenic pulmonary edema, pneumothorax, pneumomediastinum, gas embolism, ear/sinus/dental trauma.

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3
Q

Explain the difference in barotrauma mechanisms between descent and ascent.

A

Descent causes lung squeeze, edema, hemorrhage. Ascent leads to overinflation, potential rupture.

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4
Q

What are the symptoms supporting an asthma diagnosis?

A

Variable intensity, worsens at night or after infections, triggered by exercise or allergens.

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5
Q

Name the different TH2 mediators and their roles.

A

IL-5: eosinophil maturation, IL-4: IgE production, IL-13: mucous, IgE: mast cell degranulation.

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6
Q

What is Samter’s triad composed of?

A

Chronic rhinosinusitis with nasal polyposis, asthma, NSAID/ASA intolerance.

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7
Q

What are the cutoffs for VO2 max in post-operative planning?

A

<10 mL/kg/minute (high), 10-20 (moderate), >20 (>75% predicted) (low)

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8
Q

List patient factors that increase post-op complications from non-pulmonary surgery.

A

Age, Smoking, ASA class, OSA, COPD (FEV1 <60%), Pulmonary hypertension, Low albumin

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9
Q

How can post-operative complications be prevented?

A

Optimize lung disease, Smoking cessation, Avoid GA, Shorter surgery, Laparoscopic, CPAP, Lung expansion, Pain control

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10
Q

Describe physiological changes after a pneumonectomy.

A

Decrease in FEV1, FVC, lung volumes, DLCO, compliance; Increased resistance; RV EF reduces; No change in blood gases

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11
Q

What complications can occur post-pneumonectomy?

A

Post-pneumonectomy syndrome, Empyema, Bronchopleural fistula, Pulmonary embolism, Pneumothorax, Hemorrhage, Arrhythmias, MI

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12
Q

When does post-pneumonectomy syndrome occur?

A

After 6 months following surgery; Almost exclusively after right-sided pneumonectomy

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13
Q

What are the inclusion criteria for NSLT?

A

Age 55-74, Current smoker/quit within 15 years, 30 pack-year smoking history, Experienced centers

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14
Q

What are the exclusion criteria for NSLT?

A

Lung cancer, Hemoptysis, Lost >15 lb in last year, Chest CT in prior 18 months

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15
Q

Name general features of different lung cancers.

A

Small cell - central, Squamous cell - central and bulky, Adenocarcinoma - peripheral

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16
Q

What are the risk factors for lung cancer?

A

Smoking, Exposures (nickel, radon, asbestos, etc.), Underlying conditions (IPF, COPD, etc.), Radiation exposure

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17
Q

What are the Health Canada recommendations for radon levels?

A

If >200, professional hire needed; 200-600 have 2 years to fix; >600 must fix within 1 year

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18
Q

What treatments are associated with HARM in the management of obesity hypoventilation syndrome?

A

Oxygen and respiratory stimulants

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19
Q

What are the primary classification criteria for hypersomnolence?

A

Idiopathic hypersomnia, Kleine Levin syndrome, and narcolepsy

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20
Q

List some secondary classification criteria for hypersomnolence.

A

Genetic disorders, CNS disorders (e.g., stroke), Parkinson’s, post-traumatic causes, metabolic encephalopathy

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21
Q

What are some causes of recurrent SOREMPs?

A

Narcolepsy, idiopathic hypersomnolence, Parkinson’s disease, post-traumatic conditions, genetic disorders, central tumors, metabolic issues

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22
Q

What is required prior to Multiple Sleep Latency Testing (MSLT)?

A

Polysomnography (PSG) the night before, at least 6 hours of sleep on PSG, and discontinuation of REM suppressing medications for 2 weeks

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23
Q

Name some features of narcolepsy.

A

Sleep attacks, excessive daytime sleepiness, hypnagogic hallucinations, sleep paralysis, and sometimes cataplexy

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24
Q

List some drug categories used in the treatment of narcolepsy.

A

Selective dopamine reuptake inhibitors (e.g., Modafinil), selective norepinephrine and dopamine reuptake inhibitors (e.g., Methylphenidate, Solriamfetol), sodium oxybate, and Venlafaxine for cataplexy

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25
Q

What conditions are associated with REM sleep behavior disorder?

A

Parkinson’s disease, Multiple System Atrophy (MSA), dementia, stroke, tumors, narcolepsy, and SSRIs

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26
Q

List some disorders that can occur secondary to Parkinson’s disease.

A

Insomnia, hypersomnolence, REM sleep behavior disorder, restless leg syndrome, and excessive daytime sleepiness

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27
Q

Provide examples of opioid-related sleep disorders.

A

Central sleep apnea, hypoventilation, obstructive sleep apnea, and insomnia

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28
Q

What are the 4 parameters needed for aerobic exercise prescription?

A

Frequency, intensity, time, type

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29
Q

What are the 4 parameters needed for strength exercise prescription?

A

Frequency, intensity, time, type

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30
Q

What are the minimum health outcomes that need to be measured before and after PR?

A

Aerobic exercise endurance, muscle function, health status, others

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31
Q

What are the indications for referral to Pulmonary Rehabilitation (PR)?

A

COPD, ILD, PHTN

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32
Q

What are the proven benefits of Pulmonary Rehabilitation (PR) for COPD?

A

Improved VO2 max, improved O2 pulse, decrease in HR, increased AT, increased muscle mass, decrease in dynamic hyperinflation

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33
Q

Who are appropriate for Pulmonary Rehabilitation (PR) referral among post-COVID patients?

A

Patients with new respiratory symptoms post-COVID and specific criteria

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34
Q

What are the causes of eosinophilic lung diseases?

A

Acute/chronic eosinophilic pneumonia, EGPA, HES, ABPA, Infections, Neoplastic, PLCH, Lung transplantation

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35
Q

What are the causes of Acute Eosinophilic Pneumonia (AEP)?

A

Idiopathic, smoking, inhalation drugs, medications, occupational exposures, infections

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36
Q

What are the imaging findings in eosinophilic pneumonia?

A

Acute: diffuse, bilateral GGO, bronchovascular thickening, effusion, LN; Chronic: peripheral, bilateral GGO, upper lobe, migrating

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37
Q

What are the key differences between Acute Eosinophilic Pneumonia (AEP) and Chronic Eosinophilic Pneumonia (CEP)?

A

Causes, clinical manifestations, relapse, imaging, peripheral eosinophils, elevated IgE, BAL eos >25%, treatment with steroids

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38
Q

What are the diagnostic criteria for Acute Eosinophilic Pneumonia (AEP)?

A

Acute onset, <30 days, patchy infiltrates on CXR/CT, BAL eos >25%, absence of other specific eosinophilic diseases

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39
Q

What are the diagnostic criteria for Chronic Eosinophilic Pneumonia (CEP)?

A

Similar criteria to AEP but timeline is 4-5 months, imaging shows peripheral infiltrates

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40
Q

How is surfactant produced in the lungs?

A

Type II pneumocytes secrete surfactant, which is a mix of proteins and lipids

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41
Q

What are the causes of Pulmonary Alveolar Proteinosis (PAP)?

A

Idiopathic, primary (hereditary, autoimmune), secondary (infections, inhalation exposures, transplantation, hematological malignancies, immunodeficiencies)

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42
Q

What are the bronchoalveolar lavage (BAL) findings in Pulmonary Alveolar Proteinosis (PAP)?

A

Cloudy appearance, foamy macrophages, PAS+ macrophages on background of PAS material

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43
Q

What are the pathological findings in Pulmonary Alveolar Proteinosis (PAP)?

A

Normal alveolar structure with lipo-proteinaceous material filling terminal bronchioles and alveoli

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44
Q

Define apnea in sleep medicine.

A

Apnea: Decrease in airflow >/90% from baseline x >/10 seconds

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45
Q

Define hypopnea in sleep medicine.

A

Hypopnea: Decrease in airflow >/30% from baseline x >/10 seconds accompanied by desaturation of SaO2 by 3% or arousal

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46
Q

Differentiate obstructive vs. central hypopneas.

A

Obstructive: Snoring, paradoxical breathing, flattened nasal pressure. Central: None of the above.

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47
Q

Explain mixed apneas in sleep disorders.

A

Mixed apneas start as central then become obstructive.

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48
Q

What is the definition of a RERA?

A

RERA: Increased respiratory effort or nasal pressure flattening, causing arousal or desaturation.

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49
Q

Define hypoventilation in sleep medicine.

A

Hypoventilation: Increase in PaCO2 >55 mmHg x 10 mins or increase by >/10 mmHg to value above 50 mmHg x 10 mins.

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50
Q

Distinguish between AHI and RDI in sleep studies.

A

AHI = Apnea + hypopnea/total sleep time, RDI = Apnea + hypopnea + RERA/total sleep time.

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51
Q

What are some differential diagnoses for excessive daytime sleepiness (EDS)?

A

Insufficient sleep, sleep disordered breathing, neurologic disorders, hypothyroidism, adrenal insufficiency, anemia, etc.

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52
Q

List medical conditions prompting screening for OSA.

A

OHS, difficult-to-control HTN, recurrent AF post cardioversion or ablation.

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53
Q

What are the neurological controls of upper airway muscles?

A

Cranial nerves 5, 7, 9, 10, 11, 12.

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54
Q

What are the risk factors for OSA?

A

Smoking, elevated BMI, family history, increased age, male gender, mallampati score, tonsil hypertrophy, etc.

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55
Q

Explain the mechanism of hypoxemia in OSA.

A

Hypoxemia in OSA due to lung issues, supine SaO2, low FRC, apneic/hypopneic episode duration and frequency, respiratory efforts.

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56
Q

List possible complications of untreated OSA.

A

Hypertension, CAD, arrhythmias, stroke, heart failure, PH, diabetes, cognitive deficits, etc.

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57
Q

Name screening questionnaires used for OSA.

A

Berlin questionnaire, STOP-Bang questionnaire.

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58
Q

What are the diagnostic criteria for OSA?

A

Symptoms/complications + AHI >/5 or AHI >/15.

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59
Q

Describe the severity levels of OSA.

A

Mild: >/5 - 14.9, Moderate: 15 - 29.9, Severe: >/30.

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60
Q

Explain positional sleep apnea in sleep studies.

A

Positional sleep apnea: Supine AHI is at least double non-supine AHI.

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61
Q

What are the indications for PAP treatment in OSA?

A

Moderate to severe OSA (AHI >/15), mild symptoms (EDS), reduced QOL, hypertension, critical occupation.

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62
Q

State the starting and max pressures for PAP therapy.

A

Start at 4 cm H2O, switch to BPAP at 15 cm H2O, absolute max at 20 cm H2O.

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63
Q

Specify the min and max pressures for a BPAP machine.

A

Min 4 cm H2O, max 30 cm H2O, min difference of 4 cm H2O, max difference of 10 cm H2O.

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64
Q

What criteria are considered for titrating to the next pressure during a sleep study?

A

> /2 apneic events, >/3 hypopneic events,>/5 RERAs, >/3 mins snoring, any within 5 min period, want >/30 mins without a breathing event.

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65
Q

What are the criteria for optimal titration in sleep studies?

A

Optimal: RDI <5 for at least 15 mins, supine position.

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66
Q

How is asbestosis diagnosed?

A

Positive BeLT (blood or BAL), non-caseating granuloma and/or mononuclear cells on biopsy.

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67
Q

What are the main imaging findings of asbestosis?

A

Lower lobe distribution and reticular changes.

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68
Q

Where do pleural plaques usually occur?

A

Pleural plaques usually occur on the diaphragmatic pleura and peripheral lung bases.

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69
Q

What are the fluid features of benign asbestos related pleural effusion (BAPE)?

A

Exudative, eosinophilic usually, can be bloody, usually spontaneously resolves, can recur.

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70
Q

What occupations are associated with beryllium exposure?

A

Electronics, nuclear industry, nuclear weapons, aerospace industry, beryllium mining, ceramics.

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71
Q

How do you differentiate beryllium sensitization from chronic beryllium disease (CBD)?

A

Sensitization: sensitization, no symptoms, normal biopsy. CBD: sensitization, positive biopsy, presence of symptoms/radiographic findings.

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72
Q

What are the pulmonary manifestations of silicosis?

A

Includes acute silicoproteinosis, accelerated proteinosis, chronic simple silicosis, and complicated silicosis with progressive massive fibrosis.

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73
Q

What are the complications associated with silicosis?

A

Complications include tuberculosis, non-tuberculous mycobacteria (NTM), lung cancer, CTD/Erasmus syndrome, PAP, and fibrosing mediastinitis.

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74
Q

What is the causative agent of Silo Filler’s disease?

A

Silo gas, a combination of nitrogen dioxide and carbon dioxide.

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75
Q

List exposures associated with the development of lung cancer.

A

Uranium mining, beryllium exposure, asbestos exposure, silica exposure.

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76
Q

What are the benefits of the BCG vaccine?

A

Prevent CNS tuberculosis, prevents disseminated TB, mainly effective in childhood.

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77
Q

Name the organisms in the Mycobacterium TB complex.

A

Mycobacterium tuberculosis, Mycobacterium bovis, Mycobacterium carnetti, Mycobacterium africanum, Mycobacterium microti.

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78
Q

What are the risk factors for developing primary TB infections?

A

Age < 5, being immunocompromised e.g. HIV.

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79
Q

List risk factors for CNS TB.

A

Age < 5, HIV infection.

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80
Q

What factors increase the probability of TB transmission?

A

Cavitary disease, upper lung zone disease, AFB smear positive disease, close contact, coughing, sneezing.

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81
Q

When does a positive TBST or IGRA typically develop after exposure?

A

3-8 weeks.

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82
Q

What are the modes of transmission for TB?

A

Airborne, droplet, percutaneous, ingestion.

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83
Q

How long does isolation typically last for smear-negative TB cases?

A

2 weeks.

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84
Q

When is hospitalization indicated for TB cases?

A

In complicated TB, comorbid conditions, acute complications like hemoptysis, non-compliance with treatment.

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85
Q

What are the conditions for someone to isolate at home?

A

No shared ventilation, household contacts exposed and tested, <5 or immunocompromised receiving treatment.

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86
Q

Describe the imaging findings of primary TB.

A

Lower lobe distribution, consolidation, cavities, miliary TB, hilar, mediastinal LN enlargement, pleural effusion.

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87
Q

What are the imaging findings of secondary TB?

A

Upper lobe distribution, consolidation, cavitation, upper lobe fibrocalcific changes in 5% cases.

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88
Q

When is latent TB testing not required?

A

In low pretest probability, diagnosis of active TB in >12 years old, checking treatment response, mass testing programs for immigrants.

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89
Q

What are the indications for latent TB testing?

A

Apical fibronodular changes on CXR, recent exposure to active TB, certain occupations, HIV, drug use, immunosuppressive therapy, specific diseases.

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90
Q

On what immune response does the TBST rely?

A

Type IV delayed type hypersensitivity.

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91
Q

When is TBST preferred over IGRA?

A

For contact tracing purposes.

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92
Q

What are the causes of proliferative bronchiolitis/organizing pneumonia?

A

a. Idiopathic b. Immune deficiency c. Inhalational injury d. Infections e.g. COVID e. Malignancy, chemotherapy, radiation f. CTD g. Medications h. Aspiration i. Post transplantation

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93
Q

List the causes of obliterative bronchiolitis.

A

a. Post allograft transplantation (HSCT, lung) b. Inhalational injury e.g. silo, sulfur, silica, diacetyl c. Infection d. CTD, especially RA

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94
Q

What are the causes of follicular bronchiolitis?

A

a. Idiopathic b. CTD, especially Sjogren’s; RA, SLE c. Infection e.g. TB, HIV d. Immunodeficiency e. Chronic inflammatory e.g. bronchiectasis, CF, asthma

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95
Q

Outline the causes of diffuse panbronchiolitis.

A

a. CTD e.g. RA b. Ulcerative colitis c. Lymphoma

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96
Q

How should proliferative bronchiolitis be treated?

A

a. Steroids

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97
Q

What is the recommended treatment for obliterative bronchiolitis?

A

b. Depends on cause

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98
Q

What is the typical treatment approach for follicular bronchiolitis?

A

c. Steroids

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99
Q

How should diffuse panbronchiolitis be managed?

A

d. Erythromycin, bronchodilators

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100
Q

What treatments can be considered for COP if not responding to steroids?

A

a. Azathioprine b. MMF c. Treat underlying cause

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101
Q

Name the pulmonary manifestations of immunodeficiency.

A

a. GLILD b. LIP c. Follicular bronchiolitis d. Bronchiectasis e. Organizing pneumonia f. PAP g. Recurrent pneumonias

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102
Q

List the non-pulmonary manifestations of immunodeficiency.

A

a. Granulomas in other organs b. Non hodkin’s lymphoma c. Pernicious anemia d. Thyroiditis

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103
Q

Describe the imaging findings of GLILD.

A

a. Hilar and mediastinal LN b. Bronchiectasis c. GG and solid nodular opacities

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104
Q

Which malignancies are at the highest risk for radiation induced lung disease?

A

a. Lung cancer b. Mediastinal lymphoma c. Breast cancer

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105
Q

What are the risk factors for developing radiation pneumonitis?

A

a. Dose of radiation b. Volume of lung irradiated c. Form of radiation d. Fraction of radiation e. Previous chemotherapy f. Underlying lung disease g. Concomitant chemotherapy h. Female > male i. Smoker j. Older age

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106
Q

Enumerate the phases of development of radiation pneumonitis.

A

a. Initial = increased capillary permeability b. Latent = increased goblet cells c. Acute exudative = radiation pneumonitis d. Intermediate = 3-6 months e. Fibrosis = >6 months

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107
Q

Provide the timeline of radiation induced lung disease.

A

a. Radiation pneumonitis - within 1-3 months b. Radiation fibrosis - 6-12 months c. Radiation recall pneumonitis - anytime

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108
Q

What are the symptoms of radiation pneumonitis?

A

a. Fever, malaise, weight loss b. Dyspnea c. Dry cough d. Pleuritic chest pain

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109
Q

Describe the imaging findings in radiation pneumonitis.

A

a. GGO b. Consolidation c. Straight line pattern, radiation port edges d. Small pleural effusion

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110
Q

What are the pathological findings of radiation pneumonitis?

A

a. Epithelial and endothelial cell sloughing b. Fibrin rich alveolar exudate c. Hyaline membrane formation d. Microvascular thrombosis

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111
Q

What lung diseases are associated with smoking?

A

a. DIP b. RB ILD c. PLCH

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112
Q

Outline the causes of exogenous lipoid pneumonia.

A

a. E cigarettes b. Mineral based laxatives c. Petroleum jelly lubricants

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113
Q

List three risk factors for primary graft dysfunction (PGD).

A

Age >20 <45 donor, African American donor, Female donor

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114
Q

What is a common presentation of PGD?

A

Usually within 72 hours, bilateral patchy opacities, DAD on pathology

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115
Q

How is acute rejection diagnosed?

A

Cellular: TBBx, Antibody mediated: DSA, TBBx, CD4 staining

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116
Q

Describe the histological findings in acute rejection.

A

Perivascular and interstitial mononuclear infiltrates, Lymphocytic bronchiolitis

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117
Q

What are the treatment approaches for PGD vs. acute rejection?

A

PGD: Supportive, ARDS ventilation; Acute: steroids, PLEX/IVIG in antibody mediated

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118
Q

Define Chronic Lung Allograft Dysfunction (CLAD).

A

FEV1 decline by >/20% for at least 3 months, BOS: FEV1/FVC <0.7, RAS: TLC<90% baseline

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119
Q

What are the risk factors for CLAD post lung transplant?

A

Previous PGD or acute rejection, Infection, GERD, Aspiration

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120
Q

Explain the difference in imaging findings between BOS and RAS.

A

BOS: Mosaic attenuation, centrilobular nodules; RAS: Pleuroparenchymal fibroelastosis

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121
Q

What are the treatments for BOS vs. RAS post lung transplant?

A

Address risk factors, Optimize immunosuppression, Consider azithromycin

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122
Q

List some early complications post lung transplant.

A

Acute rejection, Infectious complications, Bleeding, Dehiscence, Anastomotic leak, Phrenic nerve injury

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123
Q

Provide a timeline for infectious complications post lung transplant.

A

First month: MRSA, VRE, pseudomonas, candida; Month 1-6: PJP, aspergillus, CMV, EBV

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124
Q

Name examples of post-transplant malignancies.

A

PTLD, non-melanomatous skin cancer, Primary lung cancer, Breast cancer

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125
Q

What causes Post-Transplant Lymphoproliferative Disorder (PTLD)?

A

EBV virus, serostatus, Degree of immunosuppression

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126
Q

List some diseases with recurrence post transplantation.

A

Bronchogenic carcinoma, Sarcoidosis, Giant cell interstitial pneumonitis

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127
Q

Differentiate between CMV infection and CMV disease post lung transplant.

A

Infection: Active replication without symptoms; Disease: Attribute signs/symptoms, tissue invasive

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128
Q

What are some risk factors for CMV post lung transplant?

A

R-/D+, R+/D+, R+/D-

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129
Q

Name 3 causes of PA obstruction.

A

CTEPH, foreign body emboli, Schistosomiasis/parasitic infection

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130
Q

List 3 causes of group 5 PHTN.

A

Polycythemia vera, Essential thrombocytosis, Paroxysmal nocturnal hemoglobinuria

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131
Q

State 4 pathogenesis factors of PAH.

A

Altered tone, smooth muscle medial hypertrophy, neointimal formation/hyperplasia, microthrombi

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132
Q

Provide 2 mechanisms for sarcoidosis-related PH.

A

Interstitial lung disease, granulomatous inflammation and vessel involvement

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133
Q

What are 3 physical examination findings of PH?

A

Loud P2, RV heave, elevated JVP

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134
Q

List 3 features associated with poor prognosis in PAH.

A

NYHA IV, syncope, 6MWD <165 m

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135
Q

Name 3 poor prognostic factors in RHC.

A

CI <2, RAP >14, SvO2 <60%

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136
Q

What are 4 echocardiographic features of PH?

A

TRV >2.8 m/s, RVSP 35-40 mmHg, RV hypertrophy, tricuspid regurgitation

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137
Q

State 4 ECG findings of PH.

A

RV strain pattern, right axis deviation, RBBB, RV hypertrophy

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138
Q

List 3 CXR findings in PH.

A

Vascular pruning, enlarged pulmonary arteries, enlarged heart

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139
Q

Name 3 ways of measuring CO in PH.

A

Direct Fick method, indirect Fick method, thermodilution method

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140
Q

State 2 indications for iron replacement in PH therapy.

A

Ferritin <100, Ferritin 100-299 but tSAT <20%

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141
Q

List 4 agents used in vasodilator testing.

A

Inhaled nitric oxide, IV epoprostenol, IV adenosine, selexipag

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142
Q

Provide the MOA of prostacyclin in medication.

A

Activates cAMP, inhibits platelet activation, promotes vasodilation

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143
Q

Name 3 side effects associated with prostacyclin medications.

A

Hypotension, flushing, headaches

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144
Q

What are the treatment options for diaphragmatic weakness?

A

Unilateral: plication, Bilateral: NIV, pacing.

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145
Q

What are the causes of kyphoscoliosis?

A

Idiopathic, Congenital, Cartilage disorders, Bony disorders, Neuromuscular disorders, Post thoracoplasty.

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146
Q

What are the risk factors for respiratory failure in kyphoscoliosis?

A

Cobb’s angle >110 degrees, VC <45 degrees in surgically untreated, Concomitant NMD, Concomitant lung disease.

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147
Q

When do we start screening for NIV needs in patients with kyphoscoliosis?

A

Once FVC <50%, look for hypercapnic resp failure.

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148
Q

What are the benefits of airway clearance?

A

Secretion clearance, reduce airway resistance, improve compliance, prevent atelectasis, pneumonia, respiratory failure, decrease work of breathing.

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149
Q

What are markers of a weak cough?

A

PCF <270 L/min, MEP <60 cm H2O, Bulbar dysfunction, absence of cough spikes on flow tracing.

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150
Q

What are the secretion management strategies in DMD?

A

Atropine, Scopolamine, Botox injection into salivary glands, Salivary gland RT.

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151
Q

What are the indications to start a cough support device in NMD?

A

PCF <270 L/min.

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152
Q

What are the methods to enhance cough in NMD?

A

Lung volume recruitment, manually assisted cough, mechanical insufflation and exsufflation device.

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153
Q

What are the contraindications to lung recruitment in NMD?

A

Unconsciousness, increased ICP, severe TBI, significant hypotension, pneumothorax, barotrauma risk, hemoptysis, severe bulbar weakness.

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154
Q

What are the contraindications to NIV?

A

Loss of consciousness, inability to protect airway, requiring intubation, hemodynamic instability, facial trauma/deformity, hemoptysis, upper GI issues.

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155
Q

What are the causes of hypercapnia in NMD patients on BPAP?

A

Non-compliance/low duration, suboptimal pressures, disease progression, underlying lung disease, compensation for metabolic alkalosis.

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156
Q

Other than BPAP, what ways can optimize respiratory status in NMD?

A

Cough assist, secretion mobilization, daytime mouthpiece ventilation, smoking cessation, vaccination.

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157
Q

What are the differential diagnoses for a lymphocyte predominant BAL pattern?

A

Lymphoproliferative disorders, Connective tissue diseases, Cryptogenic organizing pneumonia, Radiation pneumonitis, Sarcoidosis, NSIP, Drug induced pneumonitis.

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158
Q

What are the differential diagnoses for an eosinophilic predominant BAL pattern?

A

Infections, ABPA, Hodgkin’s lymphoma, Eosinophilic pneumonia, Asthma, EGPA, Drug induced pneumonitis, Bone marrow transplant.

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159
Q

What are the differential diagnoses for a neutrophil predominant BAL pattern?

A

Infection, Bronchitis, Aspiration pneumonia, UIP/IPF, Asbestosis, ARDS, DAD, Connective tissue diseases.

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160
Q

What BAL value of lymphocytes suggests granulomatous inflammation?

A

> 25%, >50% is especially suggestive of HP or cellular NSIP.

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161
Q

What are the pulmonary manifestations of drug-induced disease?

A

Eosinophilic pneumonia, Hypersensitivity pneumonitis, Organizing pneumonia, Occupational asthma, Diffuse alveolar hemorrhage, ARDS, Drug induced sarcoid reaction, vasculitis, lupus, Bronchiolitis, Pulmonary hypertension, Alveolar hypoventilation.

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162
Q

What are the risk factors for developing amiodarone-induced lung toxicity?

A

Older age, >/=2 months of therapy.

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163
Q

What are possible triggers for an IPF flare?

A

Bad disease at baseline, infection, pulmonary embolism, aspiration, procedures, immunosuppressive therapy.

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164
Q

What is the prognosis of an IPF flare in terms of hospital mortality?

A

50-90% in hospital mortality.

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165
Q

What are the diagnostic criteria for an IPF flare?

A

Acute respiratory deterioration, <1 month duration, bilateral GGO with or without consolidation, not fully explained by another cause.

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166
Q

What are the criteria for progressive pulmonary fibrosis?

A

Need two of three criteria occurring in the past year.

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167
Q

What are some causes of PPFE?

A

Idiopathic, connective tissue diseases, chronic HP, occupational exposures, chemotherapy, post HSCT.

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168
Q

What are the imaging findings in PPFE?

A

Pleural thickening, associated subpleural fibrosis, concentrated in the upper lobes.

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169
Q

What are the histopathological findings in PPFE?

A

Upper zone pleural fibrosis, subjacent intra-alveolar fibrosis.

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170
Q

What are the radiographic findings of CPFE?

A

Emphysema in upper lobes, fibrosis (usually UIP pattern) in lower lobes.

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171
Q

What are notable complications of CPFE?

A

Lung cancer, pulmonary hypertension.

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172
Q

What are the diagnostic criteria for IPAF?

A

Presence of interstitial pneumonia, exclusion of CTD criteria, exclusion of other etiologies, presence of at least 2 criteria.

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173
Q

What are the secondary causes of NSIP?

A

Idiopathic, connective tissue diseases, drugs/medications, exposures like hypersensitivity pneumonitis, infections including HIV.

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174
Q

What are the pulmonary manifestations of sarcoidosis?

A

Interstitial lung disease, progressive massive fibrosis, alveolar sarcoid, tracheal stenosis, lower airway obstruction, lymphadenopathy, pulmonary hypertension.

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175
Q

What are non-pulmonary manifestations of sarcoidosis?

A

Neurological symptoms, ocular sarcoidosis, cardiac sarcoid, renal sarcoid, hepatic sarcoid, hypercalcemia, skin manifestations, other organ involvement.

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176
Q

How does small fiber neuropathy present?

A

Paresthesias, numbness, pain, autonomic dysfunction.

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177
Q

How is Erdheim Chester syndrome differentiated from sarcoidosis?

A

By BRAF V600 somatic mutation and CD68 marker on biopsy.

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178
Q

What are the pulmonary manifestations of IgG4 disease?

A

Lymphadenopathy, nodules or masses, interstitial lung disease, fibrosing mediastinitis, subglottic stenosis, pleural involvement.

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179
Q

How is IgG4 disease diagnosed?

A

Serum and BAL IgG4 levels can be suggestive, biopsy is definitive.

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180
Q

What are the categories of adherence based on the RDI in sleep studies?

A

Good, Adequate, Unaccepted

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181
Q

List the potential causes of persistent sleepiness in OSA post-treatment.

A

Non-adherence, Additional medical conditions, Additional sleep disorders, Treatment emergent central sleep apnea, Inadequate pressures, Sleep deprivation

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182
Q

Name medications used for treating excessive daytime sleepiness (EDS) in OSA patients.

A

Modafinil, Solriamfetol

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183
Q

What are the indications for using modafinil in OSA?

A

Ongoing EDS despite treatment, Concomitant narcolepsy, Concomitant circadian rhythm disorder, Certain occupations like shift workers

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184
Q

How can adherence to PAP therapy be increased?

A

Education, Humidity, Nasal mask vs. full face mask, Treatment of nasal congestion, Polypectomy, Oral appliance, APAP

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185
Q

List the benefits of PAP, OA, and MMA treatment in sleep disorders.

A

Improved AHI, Improved symptoms, Decreased blood pressure, Potential improvement in Afib responsiveness, Possible better stroke outcomes

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186
Q

What are the contraindications to APAP therapy?

A

Chronic lung disease, Previous UPPP, Heart failure, Central sleep apnea, OHS/hypoventilation syndrome, Medications causing hypoventilation, Neuromuscular disease, Chest wall disorders

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187
Q

Name alternative treatments for OSA aside from PAP therapy.

A

Positional therapy, Oral appliances, Surgery, Hypoglossal nerve stimulation, Weight loss

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188
Q

What are the indications for using an oral appliance in sleep disorders?

A

Primary snoring disorder without OSA, OSA intolerance to PAP, To lower PAP pressures, Lack of responsiveness to CPAP

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189
Q

What complications are associated with the use of oral appliances?

A

Dental malocclusion, TMJ pain, Gum pain, Drooling or dry mouth

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190
Q

List the surgical options available for treating OSA.

A

UPPP, Mandibular advancement, Tonsillectomy, adenoidectomy, Tracheostomy

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191
Q

When should tracheostomy be considered for the treatment of sleep disorders?

A

Intolerance to PAP/high pressures, Inadequate control with other treatments, Mask fitting issues, Craniofacial weakness, Patient preference

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192
Q

What parameters should be assessed during overnight oximetry?

A

Mean nocturnal saturation, Nadir SpO2, Time spent below 88%, Percentage of study time below 90%

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193
Q

Provide the cutoffs for the ODI scale used in sleep studies.

A

<10, 10-30, >30

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194
Q

What defines an oxygen desaturation event in an ODI measurement?

A

A reduction in SpO2 of 4% or more for at least 10 seconds

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195
Q

What are the components of insomnia according to the course notes?

A

Difficulty sleeping, adequate opportunities for sleep, affecting functioning

196
Q

List common medical causes of insomnia mentioned in the notes.

A

Medications like stimulants, coffee, psychiatric conditions, neurological issues, chronic pain, diabetes, hypertension, cancer

197
Q

Name the medication categories that could lead to Central Sleep Apnea.

A

Opioids, Benzodiazepines, Gabapentinoids, Antidepressants

198
Q

What are the manifestations of pulmonary blastomycosis?

A

Acute focal, acute diffuse, chronic, and disseminated pulmonary blastomycosis.

199
Q

Which imaging findings are characteristic of Pneumocystis jirovecii pneumonia (PJP)?

A

Reticular changes, perihilar distribution, crazy paving, and pneumatoceles.

200
Q

What are the general blood work tests used to assess for PJP?

A

LDH and Beta D glucan are sensitive tests for PJP.

201
Q

What are the causes of a positive Beta D glucan test result?

A

Pseudomonas infection, IVIG, and IHD using cellulose membrane.

202
Q

When is Beta D glucan usually negative?

A

Mucormycosis, Cryptococcus, and Blastomycosis infections.

203
Q

What is the standard treatment regimen for Pneumocystis jirovecii pneumonia (PJP)?

A

Septra for 21 days, 15-20 mg/kg IV of TMP component.

204
Q

What are the indications for treating PJP with steroids?

A

PaO2 <70 mmHg, A-a gradient >/35 mmHg, U2D: SpO2 <92%.

205
Q

When are steroids indicated for Pneumocystis jirovecii pneumonia (PJP) prophylaxis in HIV patients?

A

CD4 <200 or CD4 <14% in HIV patients.

206
Q

What are the risk factors for invasive candidal infection?

A

Neutropenia, immunosuppression, broad-spectrum abx use, necrotizing pancreatitis, TPN, CVC, intra-abdominal surgical procedures.

207
Q

What are the risk factors for mucormycosis?

A

Diabetes (especially DKA), iron overload, hematological malignancies, HSCT, SOT, glucocorticoid treatment, COVID-19 pneumonia.

208
Q

What are the imaging findings typically seen in mucormycosis?

A

Similar to invasive pulmonary aspergillosis (IPA) with more pleural effusion.

209
Q

What are the risk factors for the development of Nocardia infection?

A

HIV with CD4<100, SOT (especially lung), long-term steroids, other immunosuppressive therapy, lymphoma, PAP, COPD, bronchiectasis.

210
Q

What are the extra pulmonary manifestations of Nocardia infection?

A

Brain abscess, meningitis, skin abscess, bone, and muscle involvement.

211
Q

What imaging findings are characteristic of congenital lobar emphysema (CLE)?

A

Unilateral hyperlucent lung, larger affected lung, decreased vascularity, contralateral mediastinal shift.

212
Q

What are the indications for treating congenital pulmonary airway malformation (CPAM)?

A

Treatment is indicated for symptomatic or asymptomatic cases.

213
Q

Which fungi require T cell mediated defense?

A

PJP, endemic fungi, NTM/TB, crypto.

214
Q

Which fungi require phagocytosis for immune defense?

A

Candida, aspergillus, mucormycosis.

215
Q

List some disease manifestations of aspergillus.

A

ABPA, aspergillus nodule, aspergilloma, chronic cavitating pulmonary aspergillosis, chronic fibrosing pulmonary aspergillosis, semi-invasive pulmonary aspergillosis, invasive pulmonary aspergillosis, tracheobronchitis.

216
Q

What are the available microbiological tests for aspergillus?

A

Aspergillus IgG, Serum/BAL PCR, Serum/BAL galactomannan, Sputum/BAL/tissue/blood/other culture.

217
Q

List risk factors for chronic cavitation aspergillosis.

A

Pre-existing structural lung disease, COPD, Tuberculosis, Cystic fibrosis, Others.

218
Q

What are the risk factors for invasive pulmonary aspergillosis?

A

Prolonged neutropenia, Transplantation, Hematological malignancy, Steroids, Chemotherapy, HIV/AIDS, Chronic granulomatous disease.

219
Q

How is chronic pulmonary aspergillosis generally diagnosed?

A

At least 3 months duration, Consistent clinical and imaging features, Evidence of Asp IgG or positive culture.

220
Q

What are some imaging findings for invasive aspergillosis?

A

Nodules, Reverse halo sign, Atoll sign, Air crescent sign, Wedge-shaped infarcts.

221
Q

What is the treatment for a pulmonary aspergilloma?

A

Single - observe or surgery/embolization if symptomatic, Multiple - antifungals (itraconazole), Antifungals pre/post surgery if high risk spillage.

222
Q

What is the treatment for chronic cavitary pulmonary aspergillosis?

A

Observe or Itraconazole, vori, posi for 6 months.

223
Q

How long is voriconazole typically used to treat invasive pulmonary aspergillosis?

A

Voriconazole for over 6 weeks.

224
Q

What are some imaging findings for allergic bronchopulmonary aspergillosis?

A

Finger in glove, mucous plugging, Bronchial wall thickening, Central bronchiectasis, Pulmonary fibrosis.

225
Q

What is one of the treatment options for allergic bronchopulmonary aspergillosis?

A

Prednisone, Itraconazole for 16 weeks, Anti-IL5 agent.

226
Q

What are the risk factors for disseminated disease from endemic fungi?

A

Medications (e.g., TNF-alpha inhibitors, steroids, IST), HIV/AIDS, Immune disorders, Hodgkin’s lymphoma, Extremes of age.

227
Q

List the pulmonary manifestations of histoplasmosis.

A

Acute localized pulmonary, Diffuse pulmonary, Chronic pulmonary, Disseminated histoplasmosis.

228
Q

What are some radiographic manifestations of histoplasmosis?

A

Acute localized - Local infiltrates/pneumonitis, Diffuse - Reticulonodular & miliary, Chronic - Apical fibrocavitary, Disseminated - Miliary.

229
Q

How is histoplasmosis diagnosed for the different manifestations?

A

Use antigen + antibody for acute or disseminated disease; Use culture for chronic disease.

230
Q

What is the treatment for mediastinal manifestations of histoplasmosis?

A

Observation, bronchoscopic preferred for broncholithiasis, surgical removal if needed for mediastinal granuloma.

231
Q

List the manifestations of pulmonary coccidioidomycosis.

A

Local primary, Diffuse, Chronic fibrocavitary disease, Disseminated.

232
Q

What are the diagnostic criteria for coccidioidomycosis?

A

Provide the specific diagnostic criteria for coccidioidomycosis.

233
Q

What are the physical exam findings in SVC syndrome?

A

Confusion, facial plethora, proptosis, facial and neck edema, elevated JVP, collateralization of superficial vessels, cyanosis, hypoxemia.

234
Q

List some causes of SVC syndrome.

A

Malignancy (lung ca, lymphoma), thrombosis, indwelling intravascular device, post radiation fibrosis, fibrosing mediastinitis, external compression from sarcoidosis, thyroid goiter.

235
Q

How is SVC syndrome managed in emergencies?

A

Stent placement; radiation if not a surgical candidate.

236
Q

Name some paraneoplastic syndromes associated with lung cancer.

A

Encephalitis, LEMS, Cushing’s syndrome, hyponatremia, hypercalcemia, hypertrophic pulmonary osteoarthropathy, various rashes.

237
Q

What are the imaging findings of hypertrophic pulmonary osteoarthropathy?

A

Symmetrical, increased linear uptake along diaphyseal and metaphyseal surfaces of long bones on bone scan; smooth periosteal reaction on XR.

238
Q

When is serial testing required?

A

Contact investigation or serial testing of HCW and other populations.

239
Q

What are the preferred scenarios for using IGRA?

A

When patient return is unclear, vaccine history is unclear, facilities for TST are lacking, TST contraindicated, or prior NTM infection.

240
Q

What are the contraindications to TB skin testing?

A

Previous allergic or blistering reaction.

241
Q

List causes of false positive TB skin tests.

A

Technical limitations, prior vaccination, sensitization to NTM, or rupture of a venule.

242
Q

What factors can lead to false negative TB skin tests?

A

Technical limitations, HIV, active TB or fungal infection, recent live virus vaccination, steroids, or waning immunity.

243
Q

What are the potential causes of false negative IGRA results?

A

Immunosuppression such as HIV, technical variability.

244
Q

Compare the sensitivity of TB skin tests and IGRA for latent TB.

A

TB skin test: 77%, IGRA: 60-95%.

245
Q

When are both IGRA and TST indicated?

A

After a negative test to increase sensitivity or after a positive TST to increase specificity.

246
Q

What are the cutoffs for a positive TB skin test?

A

<5, >/5, >/10.

247
Q

List the available tests for diagnosing TB.

A

AFB smear, PCR, culture, histopathology.

248
Q

Describe the diagnosis criteria for active TB.

A

Positive TB culture, positive TB PCR +/- AFB with appropriate clinical and imaging findings.

249
Q

What are potential samples collected for diagnosing TB?

A

Sputum, induced sputum, BAL, tissue, urine, blood, gastric aspirate, stool.

250
Q

What pathological findings indicate tuberculosis?

A

Caseating granulomatous inflammation, organisms may be present, AFB stain may be positive.

251
Q

What are the possible differentials for positive AFB stains?

A

Tuberculosis, NTM (MAC), Nocardia, Rhodococcus, Actinomyces.

252
Q

What percentage of patients with latent TB develop active TB in their lifetime?

A

5-10%, with 50% of the risk in the first 2 years.

253
Q

List drug regimens for treating latent TB.

A

3HP, Rifampin, Isoniazid x6/9 months, Isoniazid & Rifampin x3 months.

254
Q

Explain pretreatment testing before latent TB treatment.

A

Assess for active TB, LFTs, creatinine, CBC, HIV, hepatitis B, hepatitis C.

255
Q

What are the indications to treat pregnant patients with latent TB?

A

Recent close contact with active TB, immunosuppression, HIV.

256
Q

How is latent TB treated in pregnant patients?

A

Rifampin for 4 months.

257
Q

What are the benefits of non-resistant active TB drug regimens?

A

Isoniazid, Rifampin, Ethambutol, Pyrizinamide are bactericidal.

258
Q

List alternative treatment regimens for active TB.

A

R/I/E x2 months then extend, or drugs in continuation phase 3 times per week.

259
Q

Mention some potential side effects of TB treatment.

A

Isoniazid: peripheral neuropathy, hepatic toxicity, drug-induced SLE.

260
Q

What are the agents used to treat hypercalcemia in sarcoidosis?

A

Steroids, Ketoconazole, Possibly TNF alpha inhibitors

261
Q

How can fatigue in sarcoidosis be managed?

A

Exercise training, Inspiratory muscle training, Methylphenidate, modafinil

262
Q

What is the preferred treatment for skin manifestations of sarcoidosis?

A

Infliximab has the best evidence, followed by Oral steroids and MTX.

263
Q

How is small fiber neuropathy (SFN) treated?

A

Symptomatic with gabapentin or TNF alpha inhibitors, IVIG

264
Q

What is the treatment approach for neurosarcoidosis?

A

Steroids, MTX, Infliximab are commonly used treatments.

265
Q

How is cardiac sarcoidosis typically managed?

A

Primarily with steroids, although other immunosuppressive therapies are also considered.

266
Q

What are some poor prognostic variables in cardiac sarcoidosis?

A

Age >50, Ventricular tachycardia, NYHA III-IV, LVEF <40%, abnormal echo findings, thinning interventricular septum, Elevated BNP or trop, cardiac inflammation by PET, late gadolinium enhancement by MRI

267
Q

What symptoms should prompt a cardiac workup in sarcoidosis?

A

Palpitations, chest pain, syncope, tachycardia, bradycardia, new ECG findings

268
Q

What vision changes warrant a vision workup in sarcoidosis?

A

Floaters, blurry vision, visual field loss

269
Q

Who is suspected to have pulmonary hypertension in sarcoidosis?

A

Those with fibrotic lung disease, exertional chest pain, syncope, prominent P2, S4, reduced 6MWD, desaturation with exercise, increased PA diameter on CT, elevated BNP

270
Q

What are potential differentials for dyspnea disproportionate to lung function impairment?

A

Cardiac sarcoidosis, Pulmonary hypertension

271
Q

What are the benefits of steroids in pulmonary sarcoidosis?

A

Improvement in symptoms, quality of life, FVC, and radiographic disease burden

272
Q

What are clinical features highly suggestive of Hypersensitivity Pneumonitis (HP)?

A

Female non-smoker, relevant exposure history, symptoms worsen with exposure and improve away, presence of squawks on examination.

273
Q

What are some poor prognostic markers for HP and potential causes of increased mortality?

A

Older age, male, smoker, unidentified or ongoing exposure, low FVC or DLCO, evidence of fibrosis, UIP pattern on imaging or histology, fibrotic NSIP pattern, lower BAL lymphocytosis

274
Q

What are the usual radiographic findings in non-fibrotic and fibrotic Hypersensitivity Pneumonitis (HP)?

A

Non-fibrotic: see figure; Fibrotic: see figure

275
Q

What are the features of pathology in non-fibrotic and fibrotic HP?

A

See figure for details.

276
Q

What is the preferred mode of biopsy in Hypersensitivity Pneumonitis?

A

Transbronchial biopsy is preferred for HP, cryobiopsy for fibrotic HP, surgical if others fail.

277
Q

What is the recommended approach to treatment for HP?

A

Observation, Prednisone at a dose of 0.5-1 mg/kg/day x 4-6 weeks then taper over 3 months, steroid-sparing agents, antifibrotics

278
Q

Which steroid-sparing agents are commonly used in Hypersensitivity Pneumonitis?

A

Mycophenolate mofetil (MMF), Azathioprine

279
Q

How does autoPEEP affect lung compliance?

A

AutoPEEP decreases lung compliance.

280
Q

What is a potential consequence of autoPEEP on cardiac function?

A

AutoPEEP can decrease preload, cardiac output, and increase PVR.

281
Q

List two mechanisms of hypotension with PEEP.

A

Reduced preload to RV and LV, Increased RV afterload.

282
Q

What are the treatment options for autoPEEP?

A

Treat bronchospasm, decrease RR, TV, increase expiratory time.

283
Q

What are the relative contraindications to PEEP?

A

High ICP, Hypotension, RV failure, Right to left shunt.

284
Q

What are the ventilatory parameters for obstructive lung disease?

A

Mode: volume, FiO2: SpO2 88-92, PEEP: minimal, RR: 10-12%.

285
Q

What are the ventilatory parameters for ARDS?

A

Mode: volume, FiO2: 88-95%, PEEP: Modest, RR: 25-35.

286
Q

What are the possible complications of permissive hypercapnia?

A

Increased ICP, Decrease seizure threshold, Arrhythmias, Increased PVR.

287
Q

How do you treat autoPEEP?

A

Treatment includes treating bronchospasm, decreasing RR, TV, increasing expiratory time.

288
Q

What are the causes of ARDS?

A

Inhalation exposures, Aspiration, Fat embolism, Infections (pneumonia, sepsis).

289
Q

What are non-malignant causes of pleural masses?

A

Solitary fibrous tumour of the pleura, lipoma, mesothelial cyst, pleural endometriosis, pleural plaques (not really masses)

290
Q

What are the associated paraneoplastic syndromes with solitary tumour of the pleura?

A

Hypoglycemia, Doege-Potter syndrome (elevated IGF), hypertrophic pulmonary osteoarthropathy

291
Q

What are concerning features of pleural malignancy on imaging?

A

Thickness > 1 cm, circumferential thickening, involvement of the mediastinal pleura, diaphragmatic thickening > 7, nodular thickening

292
Q

What is the sensitivity of pleural fluid for malignancy overall?

A

60%, increases by 15% with the second tap

293
Q

What is the definition of non-expandable lung in malignant pleural effusion?

A

> /25% of the lung is not opposed to the chest wall, based on CXR

294
Q

What is the treatment for malignant pleural effusion?

A

Aspiration has shorter LOS but more need for intervention, IPC vs chest tube with talc slurry or poudrage

295
Q

What is the benefit of malignant pleural effusion management?

A

Improved dyspnea, improved QOL

296
Q

What are the agents for pleurodesis?

A

Talc, doxycycline, bleomycin

297
Q

What is the rate of spontaneous pleurodesis once an IPC is inserted?

A

25%

298
Q

What are possible side effects from pleurodesis?

A

Chest pain, fever, ARDS

299
Q

What is the approximate time frame after asbestos exposure for mesothelioma to occur?

A

~40 years

300
Q

What are the three main subtypes of mesothelioma?

A

Epithelioid, biphasic, sarcomatoid

301
Q

What are the causes of mesothelioma?

A

Asbestos (+ dose response), erionite fibers, thoracic radiation, SV40 infection, chronic pleural disease

302
Q

What are the imaging features concerning for mesothelioma?

A

Pleural thickening with concerning features, presence of asbestos exposure, local invasion, usually unilateral changes

303
Q

How is mesothelioma diagnosed?

A

Image-guided biopsy, medical pleuroscopy, surgical pleuroscopy/VATS

304
Q

What is the management of mesothelioma?

A

Double immunotherapy, debulking surgery if candidate, both improve survival

305
Q

What are poor prognostic markers in mesothelioma?

A

Histology, stage, age, poor performance status

306
Q

What are the malignant causes of lymphangitic carcinomatosis?

A

Cervical, colon, stomach, breast, prostate, pancreas, thyroid, lung

307
Q

What is the post-operative equation for lobectomy PPO?

A

PPO FEV1 = FEV1 x [1 - (resected segments/19)]

308
Q

What are examples of important post-operative complication predictors?

A

VO2 max, FEV1, DLCO

309
Q

How many segments are there in the right upper lobe of the lung?

A

3

310
Q

What are the surgical indications for pulmonary sequestration?

A

Symptomatic, complications, >/20% hemithorax, characteristics concerning malignancy/pleuropulmonary blastoma

311
Q

What are the imaging abnormalities in Scimitar syndrome?

A

Anomalous pulmonary venous return, right lung hypoplasia, pulmonary artery hypoplasia, mediastinal shift, dextroposition, pulmonary sequestration

312
Q

List the causes of tracheobronchomalacia.

A

Previous intubation, tracheostomy, surgery, Marfan’s syndrome, Ehlers danlos syndrome, autoimmune conditions, chronic inflammation, recurrent infections

313
Q

What are the diagnostic criteria for tracheobronchomalacia?

A

Non-contrast dynamic CT and bronchoscopy; <70% normal, 70-80 mild, 80-90 moderate, >90% severe

314
Q

How is tracheobronchomalacia treated?

A

Underlying cause, PAP therapy, airway clearance techniques, stent trial leading to tracheobronchoplasty

315
Q

What are the causes of tracheal and subglottic stenosis?

A

Congenital, previous intubation/tracheostomy/surgery, inflammatory, infectious, malignancy, radiation

316
Q

What are the benign causes of tracheal masses?

A

Chondroma, leiomyoma, lipoma, amyloidoma, squamous cell papilloma, hamartoma, hemangioma, tracheobronchomalacia osteochondroplastica

317
Q

List the malignant causes of tracheal masses.

A

Squamous cell carcinoma, chondrosarcoma, carcinoid tumour, adenoid cystic carcinoma, mucoepidermoid carcinoma, metastatic disease

318
Q

What are the differential diagnoses for mediastinal masses?

A

Anterior - teratoma, thymoma/thymic tumors, thyroid, terrible lymphoma; Middle - adenopathy, aneurysms, anomalies, others; Posterior - neural tumors, esophageal processes, aortic aneurysm, extramedullary hematopoiesis, Bochdalek hernia

319
Q

What blood work is used in the assessment of teratoma?

A

Beta HCG, AFP, LDH

320
Q

Provide examples of thymic tumors.

A

Thymoma, thymic carcinoma, thymic lymphoma, thymic neuroendocrine (carcinoid tumour), thymolipoma

321
Q

What percentage of sleep is spent in N2 stage?

A

50%

322
Q

What percentage of sleep is spent in N3 stage?

A

20%

323
Q

What are the typical characteristics of REM sleep?

A

Low amplitude, mixed frequency, rapid eye movements, REM atonia.

324
Q

What is another term for N3 sleep?

A

Slow wave sleep or deep sleep.

325
Q

What type of waves are seen in N2 sleep?

A

Sleep spindles, fast bursts of 0.5-2 seconds of 12-15 Hz activity.

326
Q

What is the purpose of K complexes in sleep?

A

They go up first, then down in N2 stage.

327
Q

What are the causes of REM rebound?

A

Depression, medication withdrawal, REM sleep deprivation, CPAP titration.

328
Q

How much theta waves are required in N1/N2 sleep?

A

At least 50% of the epoch.

329
Q

What does a short REM latency suggest?

A

Narcolepsy.

330
Q

What medications stimulate breathing during sleep?

A

Theophylline, acetazolamide, progesterone, thyroid hormone.

331
Q

What is the effect of aging on sleep stages?

A

Decrease in N3, increase in N1 and N2, no change in REM.

332
Q

What physiological changes occur during sleep?

A

Decreased BP, HR, CO; increased upper airway resistance.

333
Q

What are the components of a typical PSG?

A

EEG, EOG, EMG, ECG, airflow, respiratory efforts, SpO2, CO2 measurement.

334
Q

What are ways to measure airflow in sleep studies?

A

Oronasal thermistor for apnea, nasal pressure transducer for hypopnea.

335
Q

When should patients with sleep apnea be followed up on?

A

Within 4 weeks if high risk, within 6 months for all others.

336
Q

What are the diagnostic criteria for cystic fibrosis?

A

See figure. Tests include clinical NBS, family history, sweat chloride test, genetic testing, and functional assays.

337
Q

What tests are used to diagnose CF?

A

Clinical tests like NBS, family history, sweat chloride test, genetic testing, and functional assays.

338
Q

List the DDx of positive sweat chloride test.

A

Malnutrition, anorexia, bulimia, pancreatitis, untreated adrenal insufficiency, untreated hypothyroidism, hypophysitis, technical/test factors.

339
Q

Provide the DDx of negative sweat chloride test.

A

Dehydration, physiologic low sweat rate, hypoproteinemic states, drugs (e.g., mineralocorticoids), CFTR modulators, technical/test factors, malnutrition.

340
Q

What are the airway clearance techniques for CF patients?

A

Active cycle of breathing, autogenic drainage, positional therapy, Oscillating PEP devices (Aerobika, Acapella, flutter valve), percussive vest.

341
Q

What are the risk factors for acquiring MRSA in CF?

A

Younger age, F508 delta mutation, higher admissions, Pseudomonas aeruginosa coinfection.

342
Q

What is the role of antibiotics in CF management?

A

Eradication of bacteria, prevention of exacerbations, treatment during exacerbations.

343
Q

Which mutations make a patient eligible for CFTR modulator therapy?

A

F508 del, Gating mutation (e.g., G551D), R117H.

344
Q

List the benefits of CFTR modulator therapy.

A

Improved symptoms, quality of life, lung function (FEV1), weight, sweat chloride levels, reduced exacerbations and admissions, improved mortality.

345
Q

What are the major criteria for diagnosing MTX toxicity?

A

HP by histopathology without evidence of infection, Imaging findings, Negative blood culture and sputum culture

346
Q

What are the minor criteria for diagnosing MTX toxicity?

A

Dyspnea <8 weeks, Non productive cough, SpO2 <90% on RA, WBC <15,000, DLCO <70

347
Q

What are the common patterns of drug-induced lung disease?

A

Pulmonary edema, Pulmonary hemorrhage, DAD, OP, NSIP, UIP, EoPNA

348
Q

What are the extrapulmonary manifestations of MTX toxicity?

A

Transaminitis, Stomatitis, Macrocytosis, myelosuppression

349
Q

What are the normal pulmonary pressures?

A

sPAP: 15-30, dPAP: 4-12, mPAP: 8-20

350
Q

What drugs are associated with the development of PH?

A

Toxic rapeseed oil, Amphetamines, Dasatinib, Fenfluramine, St John’s Wort, Cocaine, Cyclophosphamide

351
Q

How should tubing be cleaned when there is visible soiling?

A

Clean tubing when there is visible soiling.

352
Q

What is a complication of strep pneumonia involving pus in a body cavity?

A

Empyema

353
Q

What are some risk factors for invasive pneumococcal disease?

A

Age, chronic heart disease, chronic lung disease, liver disease, kidney disease, diabetes, malnutrition, immunodeficiency, splenectomy, HIV infection, transplants, leukemia, lymphoma, immunosuppressive therapy.

354
Q

When should legionella be tested for?

A

Severe CAP, lack of response to beta-lactam, epidemiological factors.

355
Q

What are the different diagnostic tests for legionella?

A

Urine legionella antigen, PCR, culture.

356
Q

What is the treatment regimen for legionella infections?

A

Azithromycin 500 or levofloxacin 750 for 7-14 days depending on severity.

357
Q

Name some viral causes of pneumonia.

A

COVID-19, Influenza A and B, RSV, Parainfluenza, Rhinovirus, Adenovirus.

358
Q

What are some risk factors for a severe response to influenza?

A

Age over 65, pregnancy, postpartum up to 2 weeks, chronic medical conditions, immunosuppression.

359
Q

List common superinfections post-influenza.

A

Staphylococcus aureus, Streptococcus.

360
Q

What are the diagnostic options for influenza and COVID-19?

A

Rapid antigen test, RT-PCR, cultures.

361
Q

What are the benefits of oseltamivir in influenza treatment?

A

Reduce duration of symptoms, reduce risk of death, best outcomes within 48 hours.

362
Q

What are some imaging findings associated with COVID-19?

A

Ground-glass opacities, consolidation, crazy paving, bronchovascular thickening, pleural effusion, lymphadenopathy.

363
Q

Name some current therapies for COVID-19 based on severity.

A

Mild: budesonide, remdesivir, Paxlovid.
Moderate: dexamethasone, remdesivir, tocilizumab, baricitinib.
Severe: dexamethasone, tocilizumab, baricitinib.

364
Q

What vaccines are available for COVID-19 and what are their associated side effects?

A

mRNA (myocarditis, pericarditis, Bell’s palsy, anaphylaxis), Vector (VTE, GBS, anaphylaxis)

365
Q

How can an echinococcal cyst be treated?

A

Antiparasitic therapy, surgical resection, percutaneous aspiration.

366
Q

What are the general criteria for central sleep apnea?

A

Cessation or reduction in ventilatory effort, most common in N1/N2 sleep, no effort seen via RIP belt or diaphragmatic EMG.

367
Q

How is Cheyne-Stokes respiration defined in a PSG?

A

Over 5 central apneas/hypopneas per hour associated with crescendo, decrescendo breathing patterns.

368
Q

What distinguishes CSR from CSA?

A

CSR has longer cycle lengths, prolonged hyperpnea periods, delayed O2 saturation nadir, and arousals during hyperpnea.

369
Q

List some causes of Cheyne-Stokes respiration.

A

Heart failure, renal failure, central diseases like stroke, tumors, and certain medications such as sedatives.

370
Q

Describe the pathophysiology of CSR.

A

Involves apnea, increased circulatory time, heightened chemoreceptor response to CO2, and increased loop gain leading to apnea.

371
Q

How does CSR impact heart failure?

A

It is associated with increased mortality and occurs in around 30% of heart failure patients.

372
Q

What are some treatment options for Cheyne-Stokes respiration?

A

General disease-modifying therapy for heart failure, nocturnal oxygen, CPAP therapy, phrenic nerve stimulation, and acetazolamide/theophylline with limited evidence.

373
Q

Explain the benefits of CPAP in treating CSR.

A

It can improve Apnea-Hypopnea Index (AHI), arrhythmias, and may lead to improved left ventricular function.

374
Q

What were the findings of the SERVE-AF trial regarding ASV in HFrEF patients?

A

ASV increased all-cause mortality in patients with Heart Failure with Reduced Ejection Fraction (<45%) and is contraindicated.

375
Q

How should management of central sleep apneas be approached?

A

For idiopathic cases, consider BPAP-ST, ASV, or CPAP based on the type of central apnea present.

376
Q

What changes occur in sleep architecture at higher altitudes?

A

Increased wake after sleep onset, more N1 and N2 sleep, and decreased N3 sleep, somewhat comparable to aging.

377
Q

Name common side effects of riociguat.

A

Headaches, flushing, volume overload, priapism.

378
Q

What are contraindications to specific PAH therapies?

A

Teratogenicity for ERAs and riociguat, heart failure for prostacyclins.

379
Q

What cardiopulmonary comorbidities are considered in PH treatment?

A

Conditions associated with left ventricular diastolic dysfunction, such as obesity, hypertension, diabetes, and CAD.

380
Q

What tests should be done at every PH follow-up?

A

WHO FC, 6MWD, BNP, ECG, ABG, or pulse oximetry.

381
Q

What is the percentage of patients with acute PE that develop CTEPH?

A

3%.

382
Q

What are possible post-endarterectomy complications?

A

Reperfusion injury.

383
Q

What differentiate non-severe from severe group 3 PH?

A

PVR greater than 5.

384
Q

Define platypnea and orthodeoxia.

A

Platypnea: dyspnea in upright position, improves supine. Orthodeoxia: SaO2 drops when upright.

385
Q

List treatment options for HPS.

A

Supplemental oxygen, liver transplantation.

386
Q

What are manifestations of PAVMs?

A

Brain abscess, embolic events.

387
Q

Name risk factors for developing bleomycin-induced lung toxicity.

A

Older age, cigarette smoking, higher doses (>400 units), concomitant radiation, concurrent cisplatin or cyclophosphamide, high FiO2 administration, underlying lung disease.

388
Q

List medications causing mediastinal lymphadenopathy.

A

Phenytoin, Methotrexate.

389
Q

What are potential adverse events post surgical lung biopsy?

A

Prolonged air leak, Pneumothorax, Hemothorax, Pleural effusion, Infection, Delayed wound healing, ILD exacerbation, Requirement for intubation.

390
Q

What prognostic factors are associated with poor outcomes in Initial IPF diagnosis?

A

Older age, Male, FVC <50%, DLCO <35%, Greater extent of fibrosis on CT, Hypoxemia at rest or with exertion, Low 6MWT, especially <250 meters, Lower BMI, Certain comorbidities e.g. PH.

391
Q

List poor IPF prognostic factors on follow-up.

A

Absolute reduction in FVC by 10%, Absolute reduction in DLCO by 15%, Worsening fibrosis on HRCT, Worsening level of dyspnea.

392
Q

What are the benefits of antifibrotic therapies in IPF?

A

Improved QOL, Reduced decline of FVC, Reduced rate of exacerbation and hospitalization, Reduced mortality.

393
Q

What are the requirements for antifibrotic initiation/who would benefit?

A

Age >40, FVC >/50, DLCO >/30.

394
Q

Name comorbidities that should be managed in IPF patients.

A

GERD, Pulmonary hypertension, Obstructive sleep apnea, Lung cancer.

395
Q

Which therapies improve survival in IPF?

A

Antifibrotics: nintedanib and pirfenidone, Lung transplantation.

396
Q

In IPF, what conditions are associated with UIP pattern?

A

IPF, Familial IPF, CTD-ILD, Drugs, Asbestosis, Chronic hypersensitivity pneumonitis.

397
Q

What are the red flags for cough?

A

Age, smoking history, hemoptysis, dysphonia, recurrent pneumonia, dyspnea, systemic symptoms, vomiting.

398
Q

What are the endogenous causes of lipoid pneumonia?

A

Bronchial obstruction, PAP, lipid storage disorders, chronic inflammatory disorders.

399
Q

How does albuterol cause lactic acidosis?

A

By creating a hyperadrenergic state, enhancing glycogenolysis, leading to more glucose and pyruvate production.

400
Q

Name some important bacteria for individuals with reduced cell counts.

A

<200: PJP, endemic fungi, aspergillus, candida <100: Toxoplasmosis <50: MAC, CMV.

401
Q

What are the manifestations of Kaposi sarcoma?

A

Skin disease, parenchymal disease, endobronchial disease, mediastinal lymphadenopathy.

402
Q

What are some publicly reported illnesses?

A

Legionella, invasive pneumococcal disease, influenza, H. influenza, TB, HIV, SARS, COVID-19.

403
Q

List some causes of pulmonary disease in HIV patients.

A

ILD, PAP, emphysema, bronchiectasis, bronchiolitis, pulmonary hypertension, various infections, malignancies.

404
Q

What are the common imaging features of viral pneumonia?

A

Interstitial infiltrates, miliary pattern, airspace opacities, peribronchial thickening.

405
Q

When is 5 days of antibiotic treatment considered sufficient?

A

When the patient is afebrile for 48 hours and has less than 1 sign of instability.

406
Q

What are the complications of MSSA pneumonia?

A

Abscess formation, cavitation, pleural effusion, bacteremia, potential resistance to MRSA.

407
Q

List the CTD causes of UIP.

A

RA, SSc, SLE, DM/PM

408
Q

Name extraparenchymal CT findings suggesting CTD-ILD.

A

Esophageal dilatation, Pleural or pericardial effusion, Lymphadenopathy, C1-2 subluxation

409
Q

What are risk factors for development of RA-ILD?

A

Male, Older, Smoking, RF positive, Anti-CCP positive, Disease activity, MUC5B

410
Q

List pulmonary manifestations of RA.

A

RA-ILD (UIP, NSIP, LIP, OA, CPFE), Diffuse alveolar hemorrhage, RA pulmonary nodules, etc.

411
Q

What are the imaging features of RA-related lung disease?

A

Nodules, Cavities, Pleural effusions, Pneumothorax, Bronchiectasis, PH findings, etc.

412
Q

Describe BAL cell count and differential in RA-ILD.

A

Lymphocytic in NSIP, Neutrophilic in UIP

413
Q

How often should patients with SSc-ILD be followed?

A

6 months x 5 years, Annually after 5 years if stable

414
Q

What are the pulmonary manifestations of myositis?

A

ILD, Respiratory muscle weakness, Aspiration pneumonia, Pneumothorax, Pulmonary hypertension

415
Q

List the treatment options for myositis-ILD.

A

Cyclo if very sick, MMF, azathioprine

416
Q

What are the pulmonary manifestations of lupus?

A

ILD (NSIP, UIP, LIP), Acute pneumonitis, Organizing pneumonia, DAH, Pleural effusion, etc.

417
Q

Name the skin manifestations of lupus.

A

Acute cutaneous lupus erythema, Panniculitis, Discoid lesion, Chilblain lupus erythematosus

418
Q

What are the potential side effects of Rifampin?

A

Drug-drug interaction, body fluid discoloration, hepatic toxicity, rash

419
Q

What side effect is associated with Ethambutol?

A

Optic neuropathy, red-green color blindness

420
Q

Which drug is associated with hepatotoxicity?

A

Pyrazinamide

421
Q

List examples of drug-drug interactions with Rifampin.

A

DOACs, warfarin, oral contraceptives, antifungals, Tacro, cyclo, methadone, phenytoin

422
Q

When should liver toxicity be a concern with TB drugs?

A

Billi >3, ALT > 3 ULN with symptoms, ALT >5 ULN without symptoms

423
Q

What are the indications to extend active TB treatment to 9 months?

A

BASELINE Cavitary ON CXR + smear/culture positive at 2 months, Diabetes and cavitary disease, HIV not on ART therapy, Solid organ transplant recipients, On TNF alpha inhibitors, TB meningitis, TB bone disease if elevated inflammatory markers at end of 6 months

424
Q

When do you start ART therapy in a patient with active TB and HIV?

A

TB meningitis - after 2 weeks, No TB meningitis - within 2 weeks

425
Q

What are the monitoring requirements for patients on TB treatment?

A

CBC, crea, LFTs monthly, HIV, hepatitis B/C at start, CXR at baseline then q2 months, Sputum smear, culture q2 weeks until negative, PFT within 6 months after treatment

426
Q

Differentiate between recurrence, relapse, and reinfection in TB.

A

Recurrence can be due to either, Relapse involves the same strain, Reinfection involves a different strain

427
Q

How is active TB treated in pregnancy?

A

RIE x 9 months (omit P)

428
Q

What are the clinical manifestations of ALS related to bulbar symptoms?

A

Dysphagia, dysarthria, tongue atrophy, jaw jerk reflex

429
Q

What are the upper motor neuron (UMN) symptoms associated with ALS?

A

Spasticity, hyperreflexia, extensor plantar response

430
Q

What are lower motor neuron (LMN) symptoms in ALS characterized by?

A

Muscle atrophy and fasciculations

431
Q

List the common causes of nocturnal hypoxemia in ALS.

A

Concomitant OSA, hypoventilation, central hypoventilation, underlying lung or heart diseases, upward shift in ventilatory setpoint for PaCO2

432
Q

In hypoventilation due to muscle weakness, describe the progression of symptoms.

A

From REM to NREM to daytime, loss of accessory muscles in REM

433
Q

What are the key parameters to monitor every 2-6 months in ALS?

A

Clinical symptoms, FVC sitting, supine FVC, MIP, MEP, SNP, cough history, PCF, arterial blood gas/TcCO2, Nocturnal oximetry/PSG

434
Q

What are the indications to initiate non-invasive ventilation (NIV) in ALS patients?

A

Orthopnea, FVC <50% predicted, FVC <80% predicted with symptoms, low MIP or SNIP, high daytime PaCO2, presence of SDB criteria

435
Q

Name the best predictors of death at 6 months in ALS.

A

FVC <50% predicted, SNP <-40, MIP <-40

436
Q

What are the benefits of NIV in ALS patients?

A

Improvement in quality of life, slowing down the decline in VC, reducing daytime PaCO2 levels, and decreasing mortality

437
Q

Identify medications that should be avoided in myasthenia gravis.

A

Fluoroquinolones, aminoglycosides, macrolides, beta blockers, procainamide, checkpoint inhibitors, iodinated contrast

438
Q

What are the risk factors for severe asthma exacerbation?

A

Current smoker, SABA overuse, history of severe exacerbation, poorly controlled asthma, low FEV1, older age, female gender, elevated BMI, depression, anxiety

439
Q

What are the risk factors for near fatal asthma exacerbation?

A

History of near fatal asthma, history of severe asthma, recurrent ED or hospitalizations, non adherence, missed appointments, depression, anxiety, substance use, elevated BMI

440
Q

What are the benefits of using aerochambers in asthma management?

A

Reduced oropharyngeal deposition and side effects, improved pulmonary deposition and benefits, easier actuation coordination

441
Q

What defines uncontrolled asthma?

A

Poor control based on criteria, frequent exacerbations requiring oral steroids, serious exacerbations requiring hospitalizations or ICU, airflow limitation below 80% of personal best

442
Q

What are the biomarkers for TH2 inflammation and their cut offs?

A

FENO greater than 25 ppb, sputum eosinophils over 2%, serum eosinophils exceeding 150, clinically-driven asthma allergen responses

443
Q

What is the role of FENO in asthma management?

A

Evaluates respiratory inflammatory etiology, predicts response to steroids, monitors response, guides management decisions, assesses adherence

444
Q

What are the causes of increased FENO levels?

A

Atopic asthma, atopy, allergic rhinitis, eczema, eosinophilic bronchitis

445
Q

What are possible interventions for COPD?

A

LVRS, Bullectomy, Endoscopic procedures, Lung transplant

446
Q

Who is eligible for LVRS?

A

Patients symptomatic from emphysema, not CB/asthma, meeting specified criteria

447
Q

What are the contraindications to LVRS?

A

Comorbid disease with life expectancy <2 years, severe CAD, high BMI, specific lung function criteria

448
Q

What are the benefits of LVRS?

A

Improved dyspnea, HRQOL, exercise tolerance, lung function, possible mortality benefit

449
Q

What are the risk factors for COPD exacerbations?

A

Older age, low FEV1, previous exacerbations, eosinophils >300, chronic mucous hypersecretion

450
Q

How is an AECOPD treated?

A

SABA, SAMA, oral steroids, antibiotics based on criteria, IV magnesium in severe cases

451
Q

What antibiotics can be used for treating AECOPD?

A

Amoxi-clav, fluoroquinolones, macrolides, tetracyclines like doxycycline

452
Q

What are the indications for NIV in AECOPD?

A

Low pH, high PcO2, worsening work of breathing, persistent hypoxemia

453
Q

What are the genotype variants in A1AT deficiency?

A

Normal - M, Deficient - Z/S, Dysfunctional - F, Null

454
Q

What are the benefits of supplemental oxygen therapy in COPD?

A

Mortality benefit, improved dyspnea, exercise tolerance, physiological effects

455
Q

What are the notable side effects of biologic therapy?

A

Injection site pain, nasopharyngitis, headaches; anaphylaxis for omalizumab and hypereosinophilia for dupilumab.

456
Q

List the benefits of biologic therapy.

A

Improves symptoms, FEV1, reduces exacerbations and oral corticosteroid use.

457
Q

What are the causes of decreased Fractional Exhaled Nitric Oxide (FENO)?

A

Smokers, leukotriene receptor antagonists, rhinosinusitis, non-eosinophilic asthma, RADS, vocal cord dysfunction, COPD, bronchiectasis, and cystic fibrosis.

458
Q

Name some treatment options for Type 2 asthma.

A

LAMA, azithromycin, anti-TSLP drugs, and bronchial thermoplasty.

459
Q

What investigations confirm the diagnosis of occupational asthma?

A

PEF variability >20%, NSBHR >3.2 fold, specific inhalation challenge test FEV1 drop >15%, increased sputum eosinophils, and less sensitive spirometry.

460
Q

What are the stages in the Stages of Change model for COPD?

A

Pre-contemplative, contemplative, preparation, action, and maintenance.

461
Q

Describe the 5A’s of smoking cessation.

A

Assess, advise, ask, assist, arrange.

462
Q

What factors increase the risk of developing sensitizer-induced occupational asthma?

A

Atopy, higher and more frequent exposure, and cigarette smoking.

463
Q

Can you name some work-related asthma causative agents?

A

Chlorine, nitrogen oxides, acetic acid, sulfur dioxide, and isocyanates.

464
Q

What are 3 treatments for CMV disease?

A

Oral valganciclovir, IV ganciclovir, Foscarnet

465
Q

What should be considered in reduction of IST for CMV disease treatment?

A

Reduction in immunosuppressive therapy

466
Q

Name 3 congenital causes of non-CF bronchiectasis.

A

Cystic fibrosis, Primary ciliary dyskinesia, Young syndrome

467
Q

List 4 pulmonary manifestations of cystic fibrosis.

A

Bronchiectasis, Bacterial colonization, Recurrent pulmonary infection, Mucous plugging

468
Q

What are the 3 classic bacteria causing colonization in CF patients?

A

Staphylococcus aureus, Pseudomonas, H. Influenza

469
Q

What technique is used for airway clearance in bronchiectasis?

A

Active cycle of breathing technique

470
Q

What is the median age of survival for CF after Trikafta?

A

68 years

471
Q

Name 4 extrapulmonary manifestations of cystic fibrosis.

A

Sinusitis, Meconium ileus, Pancreatic insufficiency, Male/female infertility

472
Q

What are the 2 most common causes of non-CF bronchiectasis exacerbations?

A

PsA, H. influenzae

473
Q

What bacterial species can cause bronchiectasis exacerbations in those with PSA?

A

Anti pseudomonas - tobra, collistin, gentamicin

474
Q

What pleural fluid characteristics are typical of chylothorax?

A

Milky white, exudative, lymphocyte predominant, TG >124 mmol/L or chylomicrons, normal pH, glucose, LDH

475
Q

What is the treatment for chylothorax?

A

Dietary changes, fat soluble vitamins, chest tube (if large or symptomatic), somatostatin/octreotide, sirolimus in LAM

476
Q

What is the triad seen in yellow nail syndrome?

A

Yellow nails, lymphedema, pulmonary symptoms (sinusitis, bronchiectasis, recurrent PNA, effusions)

477
Q

List some causes of pleuritis.

A

Association with lupus flare, more likely to be bilateral, requires treatment with NSAIDs or prednisone

478
Q

What are some complications of pleural infections?

A

Bronchopleural fistula, pleural calcifications, pleural thickening, empyema necessitans, fibrothorax

479
Q

What are signs of pleural infection on CT scan?

A

Lentiform shape, split pleura sign, compresses surrounding lung, obtuse angle with pleura, contrast enhancement, extrapleural fat hypertrophy

480
Q

What are the surgical options for pleural infections?

A

Drainage, debridement, decortication

481
Q

What is recommended for parapneumonic effusion treatment?

A

Beta lactam + beta lactamase inhibitor, ceftriaxone/FQ + metronidazole, carbapenems, clindamycin, carbapenem + vancomycin if HAP, duration 2-6 weeks

482
Q

What is the maximum dose of lidocaine for bronchoscopy?

A

5 mL/kg without epinephrine, 7 mg/kg with epinephrine

483
Q

What are the cardiovascular changes during pregnancy?

A

SVR decreases, PVR decreases, BP decreases

484
Q

What are the changes that occur in high altitude physiology?

A

Hyperventilation, increased HR and CO, hypoxic vasoconstriction

485
Q

Name complications associated with high altitude.

A

AMS, HAPE, HACE, Periodic breathing of altitude

486
Q

What are the indications for large bore chest tube insertion?

A

Pneumothorax not responding to chest tube, pneumothorax on mechanical ventilation

487
Q

Which antibiotics are contraindicated in pregnancy?

A

Fluoroquinolones, aminoglycosides, Septra, sulfa drugs, tetracyclines

Respirology (3 decks)

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