Step Up - Resp Flashcards

1
Q

What are the two predominant findings in COPD? What is the cause of COPD (4)?

A

1) Chronic bronchitis and empysema

2) Smoking, A1AT, Environmental factors, chronic asthma

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2
Q

What are the SSx of COPD (7)?

A

1) Cough with sputum production
2) Exertional dyspnea
3) Prolonged expiratory time
4) decreased breath sounds on auscultation
5) Cyanosis
6) Accessory muscle use in respiration
7) Hyperressonance on percussion

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3
Q

How is COPD diagnosed and classified? What lung capacities and volumes are affected by COPD?

A

1) Dx - PFTs
a) FEV1 > 80% - mild disease
b) FEV1 50-80% - moderate disease
c) FEV1 30-50% - severe disease
d) FEV1 less than 30% - very severe
2) Increased RV, FRC, TLC. Decreased VC.

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4
Q

Outline the treatment of mild-moderate COPD (4).

A

1) Bronchodilator in metered-dose inhaler - anticholinergic drug and/or B-agonist
2) Anti-inflammatory - Inhaled glucocorticoids
3) Theophylline (improve mucocilliary clearance and resp drive) if refractory
4) Annual flu shot and Strep pneumo vaccine if >65yo.

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5
Q

Outline the treatment of Severe COPD (4).

A

1) As in mild-moderate: bronchodilator, anti-inflammatoy, theophylline, immunization
2) Continuous O2 therapy
3) Pulmonary rehabilitation
4) Triple inhaler therapy - long-acting B-agonist plus long-acting anticholinergic plus inhaled glucocorticoid

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6
Q

Outline the management of an acute COPD exacerbation (6).

A

1) Bronchodilators - B-agonist and/or anticholinergic
2) Systemic (IV) corticosteroids (methylprenisolone)
3) IV Antibiotics
4) Supplemental O2. Sats 90-93% ideally
5) BiPAP/CPAP as needed
6) Mechanical ventilation if severe

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7
Q

What are the indications for O2 therapy in COPD (3)?

A

1) PaO2 55mmHg -or-
2) O2 sat less than 88% -or-
3) PaO2 55-59mmHg with polycythemia or cor pulmonale.

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8
Q

What are the symptoms of Asthma (4)?

A

1) SOB
2) Wheeze - inspiratory and expiratory
3) chest tightness
4) cough
- symptoms worse at night. obstructive pattern is reversible

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9
Q

When diagnosing asthma, what is seen on PFTs, spirometry before/after bronchodilators, CXR, and ABGs?

A

1) PFTs - obstructive pattern, low FEV1, low FVC, low FEV1/FVC (less than 70%)
2) Spirometry - Increase in FEV1 or FVC by 12% following bronchodilator is diagnostic
3) CXR - hyperinflation only if disease severe
4) ABGs - Hypocarbia. If PaCO2 normal or high, could indicate decompensation

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10
Q

What test can be used when suspicion of asthma is high, but PFTs are normal?

A

Bronchoprovocation test with methacholine or histamine - Dx if FEV1 falls by >20%.

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11
Q

Describe the treatment for mild intermittent asthma (2 or fewer attacks per week) (1).

A

1) Short-acting B-agonist for acute attacks

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12
Q

Describe the treatment for mild persistent asthma (2 or more attacks per week) (2).

A

1) Short-acting B-agonist for acute attacks

2) Low dose inhaled corticosteroid

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13
Q

Describe the treatment for moderate persistent asthma (daily symptoms) (4).

A

1) Short-acting B-agonist for acute attacks
2) Low dose inhaled corticosteroid
3) Long-acting B-agonist
4) Consider addition of leukotriene modifier or theophylline

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14
Q

Describe the treatment for severe persistent asthma (constant symptoms) (5).

A

1) Short-acting B-agonist for acute attacks
2) Med-High dose inhaled corticosteroid
3) Long-acting B-agonist
4) Omalizumab (anti-IgE)
5) Consider systemic corticosteroid if poorly controlled

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15
Q

Describe the management of an acute severe asthma exarcebation in the ER (6).

A

1) Inhaled B-agonist - nebulizer or MDI
2) Corticosteroids - IV or oral
3) IV magnesium - if refractory to above, bronchodilates
4) O2 - sats >90%
5) Abx if exacerbation may be infection related
6) Intubate if respiratory failure occurs or impending.

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16
Q

Describe the pathophysiology of brochiectasis. What are the main causes (5)?

A

1) Chronic inflammation leads to ciliary dysfunction/loss

2) Causes: recurrent infections, CF, primary ciliary dyskinesia, autoimmune disease, humoral immunodeficiency

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17
Q

What are the clinical features of bronchiectasis (4)? How is it diagnosed?

A

1) Chronic cough with foul smelling sputum
2) Dyspnea
3) Hemoptysis - due to bronchial wall vessel rupture
4) recurrent or persistent pneumonia
5) Dx - CT chest

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18
Q

What is the treatment of bronchiectasis (3)?

A

1) Abx for acute exacerbation
2) Hydration and chest physio
3) Inhaled bronchodilators

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19
Q

Discuss the etiology of lung cancer (2). How are they staged?

A

1) Small cell lung cancer (25%) vs nonsmall cell lung cancer (75%)
2) SCLC staging:
a) limited - confined to chest and supraclavicular lymphnodes
b) extensive - beyond region of limited disease
3) NSCLC - TNM staging

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20
Q

What are the risk factors for lung cancer (4)?

A

RF:

a) Smoking / second-hand smoke
b) Asbestos
c) Radon
e) COPD - independent risk factor

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21
Q

What are the clinical features of lung cancer (5)?

A

1) Local manifestations - cough, obstruction, wheeze
2) Constitutional symptoms - anorexia, wt loss, weakness
3) Local invasion - SVC syndrome, recurrent laryngeal nerve palsy, horner syndrome, pancoast tumor (shoulder and arm pain), malignant plural effusion
4) Metastatic disease
5) Paraneoplastic syndromes - Eaton-lambert syndrome (SCLC - similar to myasthenia gravis), digital clubbing

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22
Q

How is lung cancer diagnosed (4)?

A

1) CXR - if lesion stable over 2-yrs, then benign
2) CT/PET - useful for staging
3) Cytologic examination of sputum - useful for central tumors
4) Bronchoscope/thransthoracic needle biopsy - useful for visualization and biopsy or central and peripheral lesions respectively.
- Biopsy required for Dx of LC.

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23
Q

How is SCLC (2) and NSCLC (2) treated?

A

1) SCLC - chemo/rad for limited disease, chemo only for extensive disease. Nonresectable lesions.
2) NSCLC - surgery, radiation as adjunct. No chemo.

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24
Q

What features are suggestive of malignancy in the finding of a solitary pulmonary nodule (6)?

A

1) Age - >50 = 50% chance malignant
2) Hx of smoking
3) Size - >3cm
4) Borders - irregular
5) Eccentric/asymmetric calcification
6) Change in size

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25
Q

Provide a work-up for a solitary pulmonary nodule found incidentally on CXR ()?

A

1) Compare to old CXR - if no change in size in 2 yrs, then likely benign. STOP.
2) If change, or no past CXR. Stratify into low, intermediate, and high-probability based on risk factors for malignancy (Age, smoking, size, borders, calcification, change in size)
a) Low - serial CT scan
b) Intermediate - PET, biopsy if positive
c) High - biopsy, resect as appropriate

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26
Q

What are the most common causes of anterior (4), middle (3), and posterior (3) mediastinal masses?

A

1) Anterior (four Ts) - thyroid, teratogenic tumors, thymoma, terrible lymphoma
2) Middle - LC, lymphoma, aneurysm
3) Posterior - neurogenic, esophageal, aneurysm

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27
Q

What are the clinical features of a mediastinal mass (6)? How is it Dx?

A
  • Usually asymptomatic, symptoms caused by mass effect.
    1) Cough
    2) Chest pain, dyspnea
    3) Postobstructive pneumonia
    4) dysphagia
    5) SVC syndrome
    6) Compression of nerves - phrenic paralysis, hoarseness, horners
  • Dx via CT
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28
Q

Describe the pathophysiology of transudative pleural effusions. Provide the common causes (7)

A

1) Pathophys: due to elevated pressures in capillaries of the pleura or due to decreased plasma oncotic pressure.
2) Causes:
a) CHF
b) atelectasis
c) PE
d) Cirrhosis
e) Nephrotic syndrome
f) Peritoneal dialysis
g) Hypoalbuminemia

29
Q

Describe the pathophysiology of exudative pleural effusions. What are the most common causes (5)?

A

1) Pathphys: caused by increased permeability of pleural surfaces or decreased lymphatic drainage
2) Causes
a) Bacterial pneumonia, TB
b) Malignancy
c) Viral infection
d) PE
e) collagen vascular disease

30
Q

Describe the (Light’s) criteria for exudative effusions in terms of protein and LDH (3).

A

1) Protein (pleural)/Protein (serum) > 0.5
2) LDH (pleural)/LDH (serum) > 0.6
3) LDH (pleural) > 2/3 up limit of normal serum LDH

31
Q

What are the clinical features of pleural effusions (5)?

A
  • Often asymptomatic
    1) dyspnea on exertion
    2) Peripheral edema
    3) Orthopnea, PND
    4) Dullness to percussion
    5) Decreased breath sounds/ tactile fremitus
32
Q

How are pleural effusions Dx (3)? What is the Tx (3)?

A

1) CXR (visible if >250ml), CT, Thoracentesis (helpful in determining etiology)
2) Tx: transudative - diuretics, sodium restriction, therapeutic thoracentesis
3) Tx: exudative - treat underlying disease
4) Tx: parapneumonic - Abx if uncomplicated, Chest tube or surgical lysis if complicated.

33
Q

What are the causes (1), diagnostic tests (2), and treatment (2) for empyemas?

A

1) Cause: complication of bacterial pneumonia
2) Dx: CT or CXR
3) Tx: drainage (thoracentesis), Abx

34
Q

Describe the types of pneumothorax (3)

A

1) Traumatic - often iatrogenic
2) Spontaneous (simple) - rupture of subpleural blebs
3) Spontaneous (complicated) - underlying lung disease (COPD), more threatening as limited pulm reserve in these pts.

35
Q

What are the clinical features of pneumothorax (6)?

A

1) Ipsilateral chest pain
2) Dyspnea
3) Cough
4) Decrease breath sounds/ tactile fremitus
5) Hyperresonance to percussion
6) Mediastinal shift towards affected side

36
Q

How is a spontaneous pneumothorax treated (3)?

A

1) Primary spontaneous (small)- observation, resolves in 10 days
2) Primary spontaneous (large) - O2, chest tube
3) Secondary spontaneous - chest tube

37
Q

What are the causes of a tension pneumothorax (3)?

A

1) Mechanical ventilation with barotrauma
2) CPR
3) Trauma

38
Q

What are the clinical features of a tension pneumothorax (5)?

A

1) Hypotension - cardiac filling impaired
2) Distended neck veins
3) Shift of trachea away from affected side
4) Decrease breath sounds on affected side
5) Hyperresonance to percussion

39
Q

What is the appropriate treatment for a tension pneumothorax

A

1) Medial emergency - decompress with needle in second intercostal space, mid-clavicular line

40
Q

Describe the pathophysiology of interstitial lung disease

A

Inflammatory process of alveolar wall leading to fibrosis, distortion of lung architecture, and impaired gas exchange

41
Q

Describe the clinical features of interstitial lung disease (6).

A

1) Dyspnea
2) nonproductive cough
3) Fatigue
4) Rales at base
5) Digital clubbing
6) Pulm HTN in advance disease

42
Q

How is interstitial lung disease diagnosed (4)?

A
  • diagnosis is clinical picture + biopsy findings
    1) CXR - nonspecific diffuse changes
    2) CT - extensive fibrosis
    3) PFTs - restrictive pattern, all volumes and capacities reduced, FEV1/FVC ration increased
    4) Tissue biopsy
43
Q

Describe the clinical features (4), diagnostic work-up (3) and treatment of Sarcoidosis. What type of interstitial lung disease is it?

A

1) Clinical features: Young (less than 40), Black, Erythema Nodosum, Anterior Uveitis
2) Diagnosis: CXR shows bilateral hilar adenopathy, ACE elevated, biopsy shows noncaseating granuloma
3) Treatment: self-resolve in 2 years, systemic corticosteroids if symptomatic, methotrexate if refractory to steroids.
- instertitial lung disease associated with granulomas

44
Q

What are the forms of interstitial lung disease associated with granulomas (4)?

A

1) Sarcoidosis
2) Histiocytosis X - Tx: Corticosteroids, Lung Transplant
3) Wegener Granulomatosis - cANCA positive. Tx: immunosuppressive agents and glucocorticoids
4) Churg-Strauss Syndrome - pANCA and associated eosinophilia. Tx: glucocorticoids.

45
Q

What are the four types of environmental lung disease (ILD)? Describe the CXR findings for 2 of them.

A

1) Coal worker’s pneumoconiosis
2) Asbestosis - CXR: lower lobe pleural plaques
3) Silicosis - CXR: Nodular upper lobe fibrosis
4) Berylliosis

46
Q

What are the two forms of interstitial lung disease associated with hypersensitivity? What are some exposures that may lead to a hypersensitivity reaction (4)?

A

1) Hypersensitivity pneumonits - IgG and IgA mediated - allergen’s: moldy hay, avian droppings, moldy sugar cane, compost
2) Eosinophilic pneumonia

47
Q

What are the two alveolar filling diseases (ILD)? Briefly describe each one.

A

1) Goodpastures - IgG antibodies against GM and alveolar BM. Result is GN and hemoptysis. Tx: plasmapheresis, cyclophosphamide, corticosteoids
2) Pulmonary alveolar proteinosis - rare. CXR shows ground glass appearance. Dx with biopsy.

48
Q

Provide three interstitial lung disease classified as Miscellaneous ILDs.

A

1) Idiopathic pulmonary fibrosis
2) Cryptogenic organizing pneumonitis
3) Radiation pneumonitis

49
Q

Describe the clinical features (3), diagnosis (3), and treatment (3) of idiopathic pulmonary fibrosis.

A

1) CF: unknown etiology, men + smoker, survival 3-7 years
2) Dx: CXR - groundglass/honeycomb, lung biopsy, r/o other causes
3) Tx: O2, lung transplantation, palliative

50
Q

Define Acute Respiratory Failure (2).

A

1) Hypoxemic - PaO2 less than 60mmHg
2) Hypercapnic - PCO2 > 50 mmHG
- can be a mix of both

51
Q

Define Hypoxemic respiratory failure (2). What are the causes? What are the pathophysiologic processes at play (2)?

A

1) PaO2 less than 60mmHg, Sat less than 90% despite FiO2 of >0.6. PaCO2 may be low or normal.
2) Caused by disease process of the lung - ARDS, pneumonia, pulm edema
3) V/Q mismatch and shunt

52
Q

Define Hypercapnic respiratory failure (2). What are the causes(2)? What is the pathophysiologic process?

A

1) Decrease in minute ventilation or increase in dead space
2) May be caused by underlying lung disease - COPD, Asthma, CF. May be cause by non-lung process such as CNS depression, MSK limitation of chest wall.
3) Hypoventilation

53
Q

Discuss V/Q mismatch and shunt in terms of pathophys, presence of hypercapnia, and response to oxygen treatment.

A

1) V/Q
a) Pathophys - deficit in ventilation or perfusion (spectrum: from shunt to deadspace)
b) hypoxia, no hypercapnia
C) responsive to O2 treatment
2) Shunt
a) Pathophys - deficit in ventilation of a perfused area (V/Q = 0)
b) Hypoxia and hypercapnia
c) Not responsive to O2

54
Q

Provide an algorithm for determining cause of acute respiratory failure based on ABG findings.

A

1) Examine PaCO2:
a) If normal, move to A-a gradient
b) If elevated, hypoventilation is cause. Also look at A-a, if normal - then hypoventilation accounts for hypoxemia
2) A-a gradient:
a) If normal - low inspired PaO2 is the cause (hypoventilation)
b) If elevated - V/Q mismatch or shunt is cause. If responsive to O2, then V/Q. If not responsive to O2, then shunt.

55
Q

What is the pathophysiology of ARDS (2)? How is it defined (Berlin 2012) (4)? What are the values for mild/moderate/severe disease?

A

1) Neutrophil activation leading to lung inflammation. Massive shunting.
2) Acute onset, bilateral infiltrates on CXR, Pulm edema not caused by CHF, abnormal Pa02/Fi02 ratio
3) Severity
a) mild - Pa02/Fi02 200-300
b) moderate - Pa02/Fi02 100-200
c) severe - Pa02/Fi02 less than 100.

56
Q

How is ARDS diagnosed (3)?

A

1) CXR - bilateral infiltrates
2) ABG - PaO2 less than 60, PaCO2 increases as work or breathing increase and resp failure begins.
3) No CHF - PCWP less than 18mmHg

57
Q

What is the treatment for ARDS (5)?

A

1) O2 to keep sats at >90%
2) Mechanical ventilation with PEEP
3) Fluid management - diuretics and vasopressors
4) Treat underlying cause
5) Tube feed

58
Q

Define Pulmonary Hypertension. What are the WHO classifications for pulmonary hypertension (5).

A
  • mean pulmonary arterial pressure >25 mmHg
    1) Pulmonary arterial hypertension - idiopathic, familial, veno-occlusive disease, PAH with associated conditions (SLE, HIV)
    2) Left Heart disease
    3) Lung disease/chronic hypoxemia - ILD, COPD, OSA
    4) Chronic thromboembolic disease - recurrent PE
    5) Misc - pulmonary vascular compression (tumors), sarcoidosis, histiocytosis
59
Q

What are the clinical features of pulmonary hypertension (7)

A

1) dyspnea, fatigue, chest pain, syncope
2) Loud P2
3) RV heave
4) RVF - JVD, hepatomegaly, ascites, peripheral edema

60
Q

What is seen on EKG, CXR, Echo, cath during the work-up of Pulm Htn?

A

1) EKG - RVH, R axis deviation
2) CXR - enlarged vascularture
3) Echo - dilated RA, RV, and pulm artery
4) cath - high pulm artery pressure

61
Q

How is pulm HTN treated (4)

A

1) Treat underlying disease
2) Vasodilators in WHO Group 1 - sildenafil, oral CCBs, prostacyclins
3) O2, diuretics, inotropes (digoxin)
4) Lung transplant

62
Q

Define Cor pulmonale. What are the causes? What is seen on EKG (3)? What is the treatment (2)?

A
  • RVH/RVF from pulm HTN secondary to pulmonary disease (not cardiac)
    1) Causes - Lung disease: COPD, PE, ILD, asthma, CF, OSA, pneumoconioses
    2) EKG - R axis deviation, peaked p-waves, RVH
    3) Treat underlying disease, O2
63
Q

What are the risk factors for DVT/PE (10)?

A

1) Age >60
2) Malignancy
3) Prior Hx
4) Hereditary hypercoagulable states
5) Prolonged travel or immobilization
6) Cardiac disease - CHF
7) Nephrotic syndrome
8) Major surgery - pelvis
9) Major trauma
10) Pregnancy, estrogen use (oral contraceptives)

64
Q

What are the clinical features of PE (10)

A

1) Dyspnea
2) Pleuritic chest pain
3) Cough
4) Hemoptysis
5) Syncope/Shock if large PE
6) Tachypnea
7) Rales
8) Tachycardia
9) S4
10) Loud P2

65
Q

Provide an algorithm for the work-up of PE dependent on clinical suspicion level.

A

1) Clinically unlikely - do D-dimer first. If positive, then proceed to CT scan. If negative, then no PE.
2) Clinically likely - Do spiral CT first. If positive, initiate treatment. If inconclusive, do leg ultrasound to look for DVT.

66
Q

Outline the treatment for PE and describe indications and goals for each(6).

A

1) O2
2) Acute anticoagulation - IV LMWH for 5-10 days, aPTT 1.5-2.5 control
3) Oral anticoagulation - Warfarin, INR 2-3, 3-6 months treatment
4) Thrombolytic therapy - tPA if hemodynamically unstable or RVF
5) Surgical thrombectomy - if hemodynamically unstable
6) IVC Filter - if anticoagulation contraindicated or high risk of death with PE

67
Q

What are the most common causes of dyspnea (SOB) (5)?

A

1) CHF exacerbation
2) Pneumonia
3) Bronchospasm (asthma)
4) PE
5) Anxiety

68
Q

What are the most common causes of hemoptysis (5)?

A

1) Bronchitis
2) Lung cancer
3) TB
4) Bronchiectasis
5) Pneumonia