CPC COPD/Lung cancer Flashcards

1
Q

smoker with chronic cough that was hospitalized many times in the past – why?

A

most probably due to either COPD exacerbation or LRT infections

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2
Q

what is JVP?

A

A physical examination technique to estimate jugular venous pressure. The patient is placed in supine position with the torso elevated to 45 degrees and the head rotated away from the examiner. Tangential lighting can help elicit the finding. Determine the vertical distance between the upper limit of visible distention of the internal jugular vein and the sternal angle. A distance > 4 cm is considered elevated. Conditions associated with elevated JVP include right-sided heart failure, fluid overload, pulmonary hypertension, cardiac tamponade, and constrictive pericarditis.

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3
Q

what is the pitting edema?

A

type of edema characterized by residual indentation left after applying pressure to the site of the swelling. Etiologies include fluid retention (e.g., in patients with heart failure or as an adverse effect of medications, such as calcium channel blockers), protein deficiency (e.g., hypoalbuminemia), venous insufficiency, and increased capillary permeability (e.g., from burns).

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4
Q

what are the causes of elevated JVP?

A

right heart failure, fluid overload, tricuspid valve dysfunction, SVC syndrome, pericardial effusion, tamponade, pulmonary hypertension

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5
Q

what is the parasternal heave?

A
  • -a heaving motion felt over the left parasternal area (palpate with a right hand and straightened elbow)
  • -Suggests RV hypertrophy (e.g., pulmonary hypertension)
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6
Q

coarse bilateral basal pulmonary crackles signify…

A

pulmonary edema

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7
Q

dullness on lung percussion suggests…

A

Sign of fluid inside the thoracic cavity: pneumonia, pleural effusion

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8
Q

wheezes on lung auscultation are heard in obstructive or restrictive diseases?

A

obstructive

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9
Q

what investigations should be performed in suspected COPD?

A
  • Sputum culture: to rule out infection
  • -FBC, LFT’s
  • -Blood cultures –
  • -CXR – to look for infection, edema
  • -ABG –to assess acid-base status
  • -ECG – to look for signs of RVH
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10
Q

How does FEVI / FVC ratio help separate obstructive and restrictive lung disease?

A

The ratio of FEV1 (maximum volume of air that can be forcefully expired within 1 second after maximal inspiration) to forced vital capacity expressed as a percentage. The normal value is 70–85%. FEV1/FVC is decreased in obstructive lung disease. In restrictive lung diseases, FEV1/FVC will be normal or increased.

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11
Q

type 1 vs 2 respiratory failure?

A

1) A type of respiratory failure characterized by hypoxemia (↓ PₐO₂) and normocapnia or hypocapnia (↓ PₐCO₂) on arterial blood gas analysis
2) A type of respiratory failure characterized hypercapnia (↑ PₐCO₂) and normoxemia or hypoxemia (↓ PₐO₂) on arterial blood gas analysis.

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12
Q

example of a cause of type 1 respiratory failure?

A
  • -alveolar flooding
    • It is typically caused by a ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs.
  • -This type of respiratory failure is caused by conditions that affect oxygenation such as:
    1) Low ambient oxygen (e.g. at high altitude)
    2) Ventilation-perfusion mismatch (parts of the lung receive oxygen but not enough blood to absorb it, e.g. pulmonary embolism)
    3) Alveolar hypoventilation (decreased minute volume due to reduced respiratory muscle activity, e.g. in acute neuromuscular disease); this form can also cause type 2 respiratory failure if severe
    4) Diffusion problem (oxygen cannot enter the capillaries due to parenchymal disease, e.g. in pneumonia or ARDS)
    5) Shunt (oxygenated blood mixes with non-oxygenated blood from the venous system, e.g. right to left shunt)
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13
Q

example of a cause of type 2 respiratory failure?

A
  • -COPD
  • -Type 2 respiratory failure is caused by inadequate alveolar ventilation; both oxygen and carbon dioxide are affected. Defined as the buildup of carbon dioxide levels (PaCO2) that has been generated by the body but cannot be eliminated. The underlying causes include:
    1) Increased airways resistance (chronic obstructive pulmonary disease, asthma, suffocation)
    2) Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)
    3) A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis)
    4) Neuromuscular problems (Guillain–Barré syndrome,[3] motor neuron disease)
    5) Deformed (kyphoscoliosis), rigid (ankylosing spondylitis), or flail chest
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14
Q

in COPD CXR shos…

A
  • -Signs of hyperinflated lungs (barrel chest)
    1) Hyperlucency of lung tissue (decreased lung markings)
    2) Increased anteroposterior diameter
    3) Diaphragm pushed down and flattened
    4) Horizontal ribs and widened intercostal spaces
    5) Long narrow heart shadow
  • -Can be used to determine the etiology for an acute COPD exacerbation (e.g., pneumonia, congestive heart failure)
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15
Q

what is the acute exacerbation of COPD?

A

An acute worsening of the manifestations of chronic obstructive pulmonary disease (typically characterized by increased frequency or severity of cough, increased sputum volume or change in sputum consistency, and/or increased dyspnea). Caused by an underlying infection (e.g., viral or bacterial pneumonia) in ~ 80% of cases.

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16
Q

what is the red hepatization of pneumonia?

A

An inflammatory stage of lobar pneumonia. Characterized by neutrophils, red blood cells, and fibrin in the alveoli, which results in a liver-like consistency of the affected lung. Precedes gray hepatization.

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17
Q

what is the gray hepatization of pneumonia?

A

An inflammatory stage of lobar pneumonia that follows red hepatization. Characterized by the destruction of red blood cells that have infiltrated the alveoli, which results in a fibrinosuppurative exudate that gives the affected lung a gray appearance on gross examination. Infiltration of macrophages and fibroblasts.

18
Q

why culture and sensitivity are performed in acute exacerbation of COPD?

A

Culture and sensitivity of expectorated sputum to identify causative organisms and to determine its sensitivity to antibiotics +/- Blood culture

19
Q

how a patient with acute exacerbation of COPD should be managed?

A
  • -O2
  • -Antibiotics
  • -Physiotherapy
  • -Bronchodilator
  • -Advice regarding smoking cessation
20
Q

Do we have to be careful administering O2 in respiratory failure?

A

1) if O2 < 92%, but be mindful that inappropriate O2 therapy poses a risk of life-threatening hypercapnia (CO2 narcosis)
2) Although the causes are not entirely understood, hypercapnia is theorized to occur via a combination of two mechanisms if too much O2 is given (inappropriate O2 therapy):
- -↓ Hypoxic pulmonary vasoconstriction: ↑ FiO2 → ↑ alveolar O2 tension → ↓ hypoxic pulmonary vasoconstriction → ↑ V/Q mismatch and hypercapnia
- -Haldane effect: ↑ FiO2 → ↑ oxygenated Hb, which has less affinity to bind CO2 (right shift in the CO2 dissociation curve) → CO2 is released from Hb and RBCs → ↑ PaCO2
3) Another commonly taught mechanism for O2-induced hypercapnia is that giving O2 causes hypercapnia by inactivating the hypoxic respiratory drive, but studies have disproven this theory.

21
Q

what is a bronchoscopy?

A

An endoscopic procedure for visualizing the airways. Can be performed as a diagnostic (e.g., bronchoalveolar lavage, biopsies, cytology, transbronchial needle aspiration, and endobronchial ultrasound) or therapeutic (e.g., balloon dilatation, ablation, brachytherapy, and stent placement) measure.

22
Q

what is the pathology of SCC of the lung?

A
  • -Solid, epithelial tumor
  • -Subtypes: keratinizing, nonkeratinizing, basaloid
  • -Histology: intercellular bridges (desmosomes), keratin pearls
  • -Immunohistochemistry: expression of cytokeratin subtypes CK5 and CK6
23
Q

What factors determine the stage of lung carcinoma?

A

The staging of NSCLC is based on the UICC TNM staging system. This classification defines four stages from I to IV, corresponding to cancer spread.

  • -Stages IA-IIB: Tumor size ≤ 7 cm, No lymph node involvement beyond the ipsilateral hilar nodes, No mediastinal invasion, No metastases
  • -stage IIIA: Tumor size > 7 cm, Mediastinal lymph node involvement and/or regional spread, No mediastinal invasion or metastases
  • -stages IIIB and IV: Mediastinal invasion, Distant nodes and/or distant metastases
24
Q

How does lung cancer present?

A

1) Effect of the primary
- -Site dependent eg cough, hemoptysis, pneumonia, chest pain, Pancoast’s tumor
2) Effect of metastases
- -Lymph nodes, liver, adrenal glands, brain, bone, skin, other
3) General effects of malignancy
- -Weight loss, fatigue, etc.
4) Paraneoplastic effects
5) Hormone secretion
6) Asymptomatic – abnormal CXR

25
Q

how the tissue is obtained for histopathological diagnosis of lung cancer?

A

1) Sputum
2) Bronchoscopy
- -Bronchial washings
- -Biopsy of a visible lesion
3) EBUS TBNA (diagnostic and staging)
4) CT guided biopsy
- -Primary lung parenchymal lesion
- -Metastasis

26
Q

what is the classification of lung malignancies?

A

1) Carcinoma
- -Small cell carcinoma
- -Non-small cell carcinoma
- -Adenocarcinoma
- -Squamous cell carcinoma
- -Large cell Neuroendocrine tumours
2) Carcinoid tumours
- -Typical vs atypical
3) Lymphoma
4) Sarcoma
5) Metastases to the lung
- -Carcinoma
- -Melanoma
- -Sarcoma
- -Germ cell tumours

27
Q

Why is small cell carcinoma separated from adenocarcinoma and squamous cell carcinoma?

A
It is a neuroendocrine tumor
1)Cytology:
--Small round blue cells
--Necrosis
2)Immunohistochemistry:
-- Cytokeratin positive
 --Neuroendocrine markers
positive  - - CD56
3)Usually high stage
4)Usually treated with chemotherapy 
and not surgery
28
Q

what are the features of lung adenocarcinoma?

A
  • Malignant cells forming glands
  • TTF-1 positive in nuclei of
    malignant cells
    –Peripheral
    –Most common type of lung cancer overall and in women
    –Most common lung cancer in non-smokers
    –Associated mutations: EGFR , ALK , and KRAS
    –Distant metastases are common
    –Noninvasive subtype: bronchioloalveolar carcinoma
    –Hypertrophic osteoarthropathy
29
Q

what are the features of the SCC of the lung?

A
  • -Keratin production
  • -Positive for Ck5/6 and p63
  • -Central airways
  • -Strong association with smoking!
  • -Cavitary lesions are common
  • -Direct spread to hilar lymph nodes
  • -↑ Parathyroid hormone-related protein (PTHrP) leads to hypercalcemia
30
Q

what is the management of NSCLC?

A

–Stage 1/2: Surgical resection ± adjuvant chemotherapy (radiation therapy is only required if the resection margins are not tumor free)
If surgery is not possible: radiation therapy + polychemotherapy
–Stage 3A:Polychemotherapy + radiation therapy
Consider surgery if tumor size decreases significantly after initial treatment
Prophylactic cranial irradiation does not improve survival
–Stage 3B and 4: Polychemotherapy ± targeted therapy
Alternative: symptom-oriented palliative support
Radiation therapy may be considered for management of metastases and complications (e.g., bone pain, brain metastasis, SVC syndrome)

31
Q

molecular targeted therapy in lung cancer?

A
  • -EGFR inhibitors (e.g., gefitinib) in advanced-stage NSCLC that is EGFR-positive
  • -ALK tyrosine kinase inhibitors (e.g., crizotinib) in advanced-stage NSCLC that is ALK-positive
32
Q

Why test lung cancer for molecular events?

A
  • -To find a mutation that is susceptible to molecular targeted therapy
  • -This has resulted in more frequent mutation testing in NSCLC
  • -Likelihood of finding a mutation depends on histologic subtype
  • -Currently, most mutations that are susceptible to targeted therapies have been detected in adenocarcinomas
33
Q

common mutations in lung cancer?

A
  • -EGFR
  • -ALK
  • -PDL1
34
Q

what is the significance of EGFR expressing cancers?

A
  • -Cancers that overexpress EGFR have been shown to have increased resistance to therapy, increased metastatic potential, and poorer prognosis
  • -EGFR mutations are present in approximately 10% of lung adenocarcinomas
  • -Stimulation of the EGFR pathway leads to increased autophosphorylation of a tyrosine kinase pathway associated with EGFR, which leads to increased tumor growth and ability to metastasize
  • -Tyrosine kinase inhibitors can block activation of the EGFR pathway
  • -Examples of tyrosine kinase inhibitors: Gefitinib (Iressa) and Erlotinib
35
Q

EGFR mutations are commonly seen in SCC of lung.T/F

A

False

–EGFR mutations are present in approximately 10% of lung adenocarcinomas

36
Q

does EGFRmakeslung cancer more treatable?

A

No
–Cancers that overexpress EGFR have been shown to have increased resistance to therapy, increased metastatic potential, and poorer prognosis

37
Q

examples of EGFR inhibitors?

A

Examples of tyrosine kinase inhibitors: Gefitinib (Iressa) and Erlotinib

38
Q

what is the significance of ALK mutations?

A
  • -Chromosomal rearrangement of Anaplastic lymphoma kinase (ALK) occurs in approx. 5% of pulmonary adenocarcinomas
  • -ALK inhibitors (Crizotinib and Ceritinib) have been approved for treatment of patients with metastatic ALK positive NSCLC
39
Q

examples of ALK inhibitors?

A

Crizotinib and Ceritinib

40
Q

what is nivolumab?

A
  • -Nivolumab is a monoclonal antibody inhibitor of programmed death protein-1 (PD-1). This drug has activity on CD8, which restores cytokine secretion and T cell proliferation.
  • -Early stage of trials but may have potential in NSCLC