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Block B - Respiration > Pathology/clinical/diseases > Flashcards

Pathology/clinical/diseases Flashcards

1
Q

What is the pulmonary lobule?

A

Lung tissue surrounded by interlobular septae

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2
Q

What is pulmonary acinus?

A

The lung parenchyma distal to a terminal bronchiole

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3
Q

What is pulmonary interstitium?

A

The connective tissue in the alveolar and interlobular septae, and around vessels and airways

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4
Q

What are the 3 types of emphysema and their characteristics?

A
  1. Centrilobular (proximal acinar) most common in clinic – upper lobe predominance – black due to cigarette smoking
  2. Panlobular (panacinar) less common – lower zone predominance, whole of acinus is affected, then whole lobule – alpha 1 antitrypsin (antiprotease) deficiency (gene PiMM - 90% population- or PiZZ)
  3. Paraseptal (distal acinar) – subpleural distribution, really close to the pleura – not common – upper lobe
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5
Q

What is Bronchiolitis?

A
  • An inflammation of the bronchioles, is associated with cigarette smoking, is characterized by
    • mural chronic inflammation
    • mural fibrosis
    • epithelial goblet cell hyperplasia and luminal mucus accumulation = lumen obstruction
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6
Q

What’s a clear symptom of chronic Bronchitis?

A
  • Expectoration (coughing up) of mucous on most days for at least 3 consecutive months for at least 2 years
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7
Q

What is Bronchiectasis?

A
  • An irreversible dilation of a portion of the bronchial tree
    • ​often grouped with COPD because there’s a lot of mucus in the airways and distal bronchiolitis
  • 3 types (based on morphology)
    • Cylindrical
    • Varicose
    • Saccular
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8
Q

What is the DEFINITION of COPD?

A

A common, preventable, and treatable disease that is characterized by persistent respiratory symptoms (breathless, cough, sputum) and airflow limitation that is due to airway and/or alveolar abnormalities usually caused by significant exposure to noxious particles or gases.

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9
Q

What is the epidemiology of COPD?

A
  • Major public health problem (1/10 men, 1/13 women over 40 y.o.
  • mortality rate of COPD is increasing
  • most admissions to hospitals (burden to the health system)
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10
Q

What are the risk factors of COPD?

A
  • Cigarette or environmental smoke
  • Occupational dust and chemicals
  • Pollution
  • Genes
  • Infections
  • Lung development
  • Asthma
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11
Q

Describe the pathophysiology of COPD.

A

calculate airflow limitation by using a volume/tine graph. If your FEV1/FVC is ↓ 0,7 and stays this way after administration of bronchodilator.

Key pathophysiological mechanism of dyspnea in COPD =

  1. Exhaling each breath requires time, but airflow limitation slows exhalation
  2. With insufficient time to exhale each breath, one breathes in before exhalation is complete
  3. This results in hyperinflation
  4. Breathing at a higher lung volume (hyperinflation) requires more effort
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12
Q

How do you diagnose COPD?

A
  1. Symptoms (dyspnea, chronic cough, sputum)
  2. Exposure to risk factors (tobacco, occupation, pollution)
  3. Spirometry (FEV1/FVC < 0.7 post bronchodilator) : REQUIRED TO ESTABLISH DIAGNOSIS
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13
Q

When diagnosing and/or evaluating a patient with COPD, there are some essential things we need to assess. What are those things ?

In that case, is spirometry enough to quantify the disease impact on patient lives ?

A
  1. Presence of persistent airflow limitation
  2. the severity of airflow limitation
  3. symptoms and exarcerbation risk (really important in order to caracterize the disease, is the patient breathless only during exercise, when he walks, too breathless to leave the house, etc.)

Spirometry is then not enough to quantify the disease impact on patient lives : symptoms severity, disability and risk of exacerbation.

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14
Q

What are the goals of management of COPD?

A
  • Alleviate breathlessness and other respiratory symptoms
  • Prevent disease progression
  • Treat exacerbations and complications
  • Reduce the frequency and severity of exacerbations
  • Improve exercise tolerance, physical activity
  • Improve health status
  • Reduce mortality
  • Assess and manage co-morbidities
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15
Q

What are the interventions with COPD?

A
  • Smoking cessation
    • ​if you quit smoking, you slow down the course of the disease (the slope is less severe, but you can never come back to what you were before smoking)
  • Vaccination
  • Bronchodilators
  • Anti-inflammatories
  • Anti-microbials
  • Pulmonary rehabilitation (self-management, exercise, cessation)
  • Supplemental oxygen
  • Assisted ventilation
  • Surgical: lung volume reduction, transplant
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16
Q

What is acute exacerbations in COPD?

A

Exacerbation and symptom burdens are important to characterize the disease.

Definition of exacerbation = Sustained (≥48 h, différencie acute exacerbation from the normal day-to-day variations in COPD symptoms) worsening of dyspnea, cough or sputum production that induces :

  • an increase on the use of regular medications
  • Supplementation with additional medications.

Exacerbation impacts all aspects of this vicious cycle and contribute to impired HRQL and more rapid decline of lung function over time

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17
Q

What constitutes and characterizes asthma?

A

Asthma is a chronic inflammatory disorder associated with reversible airway obstruction, bronchial hyper-responsiveness, and airway inflammation

  1. Variable degree of airway obstruction
  2. Airway inflammation
  3. Bronchial hyperresponsive
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18
Q

What are the inflammatory components of asthma sensitive to steroid?

A
  • eosinophils
  • mast cells
  • Th2-lymphocytes
  • dendritic cells
  • IL-4, IL-5, IL-13,
  • IgE
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19
Q

What are the inflammatory components of asthma NOT sensitive to steroid?

A
  • Th17 lymphocytes
  • neutrophils
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20
Q

When should an M.D. suspect asthma?

A
  • Recurrent episodes of wheezing
  • Troublesome cough, especially at night
  • Cough or wheeze after exercise
  • Cough, wheeze or chest tightness after exposure to airborne allergens or pollutants
  • Prolonged cough or wheeze following a respiratory infection. Colds “go to the chest” or take more than 10 days to clear.
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21
Q

What triggers asthma?

A
  • Respiratory tract infections.
    • Rhinovirus is by far the number 1 trigger for asthma exacerbation.
  • Allergens
    • ​human dust mite, fungal spores, animal danders, cockroach, pollens
  • Pollutants, irritants
    • ​smoke, perfumes, cleansing agents
  • Medications
    • ​ aspirin, beta blockers (blood pressure, angina, arrhythmia)
  • Physical factors
    • ​ exercise, cold air
  • Physiological factors
    • ​stress, gastro-œsophageal reflux, sinus disease, obesity, pregnancy
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22
Q

How is asthma diagnosed?

A
  • History and patterns of symptoms
  • Measurements of lung function
    • Spirometry (OBLIGATOIRE POUR UN DIAGNOSTIC)
    • Peak expiratory flow (if impossible to do spirometry)
  • Measurement of airway responsiveness
    • Following the administration of a bronchodilator such as salbutamol, an improvement in FEV1 of at least 12% and at least 200ml within 30 minutes.
    • We administrate histamine or methacholine and see how you respond
  • Measurements of inflammatory status of the airways (sputum analysis with hypertonic saline)
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23
Q

What are the long term goals of asthma management?

A
  • Achieve and maintain control of symptoms
  • Maintain normal activity levels, including exercise
  • Maintain pulmonary function as close to normal levels as possible
  • Prevent asthma exacerbations
  • Avoid adverse effects from asthma medications
  • Prevent asthma mortality
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24
Q

What types of medication are used to treat asthma? Is there another way to treat it ?

A
  • Medication
    • blue/green puffers : bronchodilators («ols, «iums»)
      • rescue medication
        • ​short-acting bronchodilator agents (SABA)
      • ​controller medication
        • long-acting bronchodilators (LABD)
          • LABA (beta2-agonist)
          • LAMA (anticholinergics muscarinic)
    • orange/red/purple puffers : controllers
      • ​Inhaled corticosteroids (ICS) «-ides, -ones »
      • ICS-LABA (combination therapy)
    • oral medication : controllers
      • ​anti-IgE
      • prednisone (oral corticosteroid)
  • Non-medication (stop exposure, lifestyle)
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25
Q

What are the 2 less common (oral corticosteroids) treatment only used for severe asthma?

A
  1. Prednisone: very cheap and effective for SHORT periods of time because a lot of side effects
  2. Monoclonal antibodies: very expensive
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26
Q

What are the Canadian Asthma Consensus Guidelines criteria for acceptable control of asthma?

A
  1. Daytime symptoms < 4 days/week
  2. Night-time symptoms < 1 night/week
  3. Normal physical activity
  4. Mild, infrequent exacerbations
  5. No absenteeism due to asthma
  6. Fewer than 4 doses/week of SABA needed
  7. FEV1 or PEF >85% of personal best or greater (ideally 90%)
  8. Diurnal variability in PEF less than 15%
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27
Q
  • What are the 2 main caracteristic of COPD ?
  • It’s a slowly progressive disorder resulting from __________ and/or ______________
A
  • Main caracteristics :
    • Increased airway resistance to airflow
    • decreased lung/chest wall elastic recoil
  • It’s a slowly progressive disorder resulting from emphysema and/or irreversible reduction in the caliber of the small airways (non-respiratory bronchioles) aka bronchiolitis
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28
Q

What is emphysema ?

A
  • A condition of the lung characterized by abnormal and permanent enlargement of airspaces accompanied by the destruction of alveolar walls without significant fibrosis
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29
Q
  • explain the pathogenesis of emphysema
  • Why is cigarette smoke a risk factor for emphysema
A
  • Neutrophils in the lungs die and release proteolytic enzymes (proteases) that can digest elastin and collagen, and then destroy the underlying lung. Macrophages produce the same thing in the alveoli.
    • naturally, the body uses serum alpha 1 antiproteases produced by the liver to block the effect of those proteases (there’s a balance)
  • Cigarette smoke lead to an increase of neutrophils in lung tissue, delay their transit, augment the amount of neutrophil elastase and increase the neutrophil elastase release leading to a debalancement of this equilibrum leading to ephysema
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30
Q

what’s a bullae ?

A

When the cystic spaces of emphysema becomes larger than a centimeter = bullae in the case of paraseptea emphysema

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31
Q

In COPD, by what is caused the airway limitation ?

A
  1. ↓ lung elastic recoil pressure : reduces the driving pressure flow because of the destruction of the elastic alveolar walls
  2. ↓ airway tethering : destruction of elastic recoil leads to narrower luments = increased resistance to airflow
  3. augmentation of airway resistance (e.g. mucus plugging) : the airways are narrowed by remodelling or mucus
  4. dynamic compression of the airways
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32
Q

On what is based pharmacologic therapies in the case of COPD ?

A

On symptoms and exacerbation risk

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33
Q

Appart from medications, what are the possible treatment for COPD ?

A
  • patient-tailored multi-component intervention (cornerstone of managing COPD)
    • exercise training
    • disease education
    • self-managment
    • smoking cessation
  • long-term oxygen therapy to achieve a saturation of >90%
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34
Q

what’s the eiology and who do you manage exacebation in COPD ?

A
  • etiology
    • infectious (70%)
      • bacterial
      • viral
    • non-infectious (30%)
      • pollution
      • non-compliance
      • pulmonary embolism
      • unknown
  • management
    • antibiotic and corticosteroids are key component of acute COPD exacerbation
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35
Q

What is the prevalence of asthma in Canada ?

A
  • 8,4% canadians older than 12 y.o
  • 12% in canadian children
  • asthma prevalence has increased over time in adults
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36
Q

How do the component of airway inflammation determine response to therapy ?

A

Dépendamment si les cells/mediators sont sensible ou non aux stéroides, les course of treatments peuvent être différents pour régler des symptomes différents

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37
Q

how can you mesure lung function to do an asthma diagnosis ?

A
  • PEAK EXPIRATORY FLOW
    • if you have a low liability = athma bad
  • SPIROMETRY
    • obligatoire pour un diagnosis
    • key points
      • FEV1 and PEF are decreased
      • FVC is decreased or unchanged
      • FEV1/FVC is decreased
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38
Q

What criteria determine significant reversibility in airflow after bronchodilator administration ?

A
  • Following the administration of a bronchodilator such as salbutamol, an improvement in FEV1 of at least 12% and at least 200ml within 30 minutes.
    • Examples:
      • FEV1 improves from 1 liter to 1.15 liters after a bronchodilator: not significant bronchodilation
      • FEV1 improves from 2 liters to 2.25 liters after a bronchodilator: significant bronchodilation
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39
Q

how do we classify asthma severity ?

A

by what kind of medication the patient takes to get as good as he can be

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40
Q

Why do ICS is still used today ? What’s the ideal dose ?

A
  • dose-response effect
    • asthma mortality rate is reduced with each additionnal cartridge of ICS used and 3 month after stopping the treatment
    • asthma exacerbations is reduced. The effect is dose-dependant as weel ad higher ICS doses are more effective
  • the ideal dose is 500 mcg daily (1 inhalation twice a day of any of the ICS)
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41
Q

What do we do if high dose ICS don’t work in patient with asthma ?

A
  • add LABA in adults only (rather than upping the ICS dose)
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42
Q

What factors are associated with more severe athsma and a poor response ?

A
  • female
  • obesity
  • smoking
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43
Q

diffenrentiate asthma and COPD on those clinical features

  • age onset
  • smoking history (pre-onset)
  • allergy
  • airflow obstruction
  • FEV1 reversibility
  • noctural symptoms
  • dyspnea
  • corticosteroid responsivness
A
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44
Q

What treatment is longer: TB or non-tuberculous mycobacterial disease?

A

Non-tuberculous mycobacterial disease is longer (2 years) therefore the compliance is very low.

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45
Q

What promotes and inhibits sleep ?

A
  • Ascending arousal system (monoaminergic, orexinergic) promotes wakefulness
  • Inhibition of arousal system by ventro-lateral pre-optic (VLPO) area promotes sleep
  • Sleep-wake neuronal systems project to respiratory control centres
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46
Q

What is Obstructive apnea-hyopopnea?

A

An upper airway collapse during sleep that has many determinants and causes.

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47
Q

What are the causes of Central apnea-hypopnea?

A
  • Hypercapnic
  • “Idiopathic”
  • Central nervous system lesions
  • Congestive Heart Failure: Cheyne-Stokes Respiration: the feed-back is impaired
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48
Q

What is the treatment of Treatment of Cheyne-Stokes Respiration?

A

Adaptive Servo-Ventilation

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49
Q

What sleeping disorder is associated with severe cardio-vasculaire complications ?

A

Obstructive apnea-hyopopnea is associated with:

  • Hypertension
  • Arrhythmias
  • Acute coronary events
  • Transient ischemic attack/Stroke
  • Pulmonary Hypertension
  • Congestive Heart Failure
  • Increased mortality
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50
Q

Who plays the role of central regulators of hemostasis ?

A

endothelial cells

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51
Q

What does an endothelial cell injury cause?

A
  1. Release endothelin
  2. Release/activation of pro-coagulants (eg. tissue factor, aka factor III)
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52
Q

What are the 3 elements that control the balance CLOT/BLEEDING in both hemostasis and thrombosis?

A
  1. Endothelial cells and vascular wall
  2. Platelets
  3. Coagulation cascade
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53
Q

Main steps of hemostasis after injury occurs?

A
  1. Arteriolar Vasoconstriction
  2. Primar hemostasis (formation of initial platelet plg)
  3. Secondar hemostasis (stabilization of platelet plug)
  4. Fibrinolysis and dissolution
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54
Q

What causes vasoconstriction?

A

Endothelin released because of the injury

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55
Q

Who is responsible for the vasoconstriction?

A

Smooth muscle cells

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56
Q

What are the 3 main steps of primary hemostasis?

A

Platelet adhesion, activation and aggregation

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57
Q

What are the 2 roles of initial platelet plug?

A

Form hemostatic plug that seals vascular defects

Provide surface to recruit & concentrate activated coagulation facotrs

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58
Q

What is a platelet?

A

Anucleate fragment from megakaryocyte that circulate in blood

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59
Q

What are the 3 components of platelet adhesion

A
  1. Adhesion via special receptors (glycoprotein 1b) on von Willebrand factor (on exposed ECM)
  2. Other receptors link to other platelets via platelet-fibrinogen complex
  3. Continues until platelets fill vascular defects
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60
Q

Describe platelet activation.

A
  • Platelets undergo irreversible shape change after adhesion
  • Granules secretion for coagulation & wound headling (calcium: required for several coagulation factors & thromboxane a2: activate additional nearby platelets & role in platelet aggregation)

ALso, wound healing allows re-endothelialisation of vessels.

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61
Q

Platelet aggregation

A

Shape changes in platelets –> allow for binding to fibrinogen with receptors on other platelets

Leads to aggregation to fill defect & finish forming primary plug

Increasing surface area available for interaction with coagulation factors for secondary hemostasis

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62
Q

In a normal Platelet-Endothelial Interaction, who vasodilates and usually inhibit platelet aggregation?

A

Prostaglandin PGI2 & NO - synthetized by normal endothelium.

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63
Q

In the platelet-endothelial interaction, during an endothelial injury/thrombosis, who vasoconstricts & enhance platelet aggregation?

A

TxA2 - synthetized by activated platelets

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64
Q

What drug can help inhibit platelet aggregation?

A

Cyclo-oxygenase inhibitor, ex ASA (aspirin)

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65
Q

Short definition of secondary hemostasis

A

Local activation of coagulation cascade (stabilization of platelet plug)

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66
Q

What is the end result of the coagulation cascade, a pathway of multiple factors acting in concert?

A

Activation of thrombin, which cleaves fibrinogen and forms an insoluble fibrin polymer.

Thrombin also activates more platelets to reinforce plug.

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67
Q

What does fibrin polymerization do?

A

It leads to cementing the platelets into a definitive secondary hemostatic plug that is more large and stable than the first one; contains entrapped red cells and leukocytes.

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68
Q

What is the only thing we need to know about the coagulation cascade?

A

A successive series of amplifying enzymatic reactions.

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69
Q

Where do the coagulation factors assemble on a platelet?

A

On the phospholipid surface

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70
Q

Why is it important to control the coagulation factors?

A

To prevent inappropriate and potentially dangerous clotting elsewhere in the vascular tree.

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71
Q

How is coagulation restricted to sites of injury? 3 choses

A
  1. Blood flow washes away coagulations factors & platelets to limit size of platelet plug
  2. Limiting enzymatic activation to phospholipid surfaces provided by activated platelets or injured endothelium
  3. Normal endothelial cells have surface receptors/proteins that are natural anticoagulants (antithrombin iii, protein C)
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72
Q

What other cascade is activated by platelet plug formation? (We say it’s the end-product of the coagulation cascade)

A

Fibrinolytic cascade

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73
Q

What is the role of fibrinolytic cascade?

A

Limits the size of the clot and contributes to its later dissolution.

  • Largely done with enzymatic activation of plasmin, which breaks down fibrin.
  • Plasmin generated from plasminogen, by plasminogen activators
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74
Q

What is the Thrombosis Virchow’s Triad

A

Endothelial injury/dysfunction

Hypercoagulability

Abnormal blood flow

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75
Q

What bacterial product can be use to lyse clots?

A

Streptokinase

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76
Q

What will we find in blood that could help us diagnose abnormal thrombotic state and why?

A

Elevated levels of FSPs: fibrin split products. Something that is produced when fibrinolysis happens.

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77
Q

What can be 2 characteristics of a dysfunctional endothelium?

A
  1. More procoagulant factors (ex,tissue factor)
  2. Less antifibrinolytic factors (ex,thrombomodulin, PGI2, t-PA)
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78
Q

What can cause an endothelial injury/dysfunction in a thrombosis?

A
  • Myocardial infarction
  • Atherosclerosis
  • Traumatic/inflammatory injury(vasculitis)
  • Hypertension
  • Turbulent blood flow
  • Bacterial products
  • Radiation injury
  • Metabolic abnormalities (Hypercholesterolemia,homocystinuria)
  • Toxins(cigarette smoking)
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79
Q

In a normal blood flow, what is the type of flow and where are platelets/blood cells ?

A

Laminar blood flow and found in the center of the lumen

(Plasma is on the sides)

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80
Q

Why does abnormal blood flow lead to coagulation?

A

Because it activates the endothelial cells because of the flow-induced changes in endothelial gene expression

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81
Q

2 types of abnormal blood flow ? What are they factor for ?

A
  • statis (something physically blocks the flow)
    • factor for venous blood clots
  • turbulence (clotthing factors are on th e border instead of the middle where they usually are)
    • factor for cardiac and arterial thrombi
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82
Q

What does turbulence flow cause?

A

Countercurrents and local pockets of stasis –> leads to endothelial injury and dysfunction

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83
Q

What are the 2 types of hypercoagulability states

A

Primary (genetic) and secondary (acquired)

84
Q

what is hypercoagulability

A

Abnormally high tendency of blood to clot, alterations in coagulation factors

85
Q

What could be the reasons for an acquired hypercoagulability state?

A

Immobilisation

Oral contraceptives & pregnancy

Mucinfrom some adenocarcinomas

86
Q

Clinically, for a thrombosis, if a young patient comes in with the condition, what would you consider as a primary cause ?

A

Patients under 50: hypercoagulability states altered (acquired or genetic)

87
Q

What is a thromboembolus?

A

When the area of propagation of a thrombi break off migrating in blood

88
Q

What is an emboli?

A

Solid, liquid or gas carried by blood distant to site

Ex, bone marrow embolus, amniotic fluid embolus.

89
Q

3 characteristics of an arterial thrombi

A

Rich in platelets

Zones of epithelial injury with turbulence

Usually on ruptured atherosclerotic plaque, vasculitis or trauma

90
Q

4 characteristics of venous thrombi - phlebothrombosis

A
  1. increase in activity of coagulation (more than in platelets)
  2. zones of statis
  3. SLower venous flow leads to increased trapped RBCs = red thrombi
  4. most comonly veins of legs (90%)
91
Q

2 other types of thrombi and brief definition

A

Mural: in heart chambers/aortic lumen

Vegetations: on heart valves

92
Q

4 possible fates of a thrombus after formation

A

Propagation

Embolization

Dissolution (fibrinolytic factors)

Organisation & recanalization (ingrowth of endothelial cells, smooth musclescells & fibroblasts )

93
Q

In which of these 2 is embolisation most important - arterial thrombi or venous thrombi? And when it is where in particular?

A

In venous thrombi, especially when the Deep venous thrombi is above the knee,

94
Q

Migratory thrombophlebitis: what is it?

A

Formation of thrombi in multiple venous beds because of adenocarcinomas/tumor-associated procoagulatn state. Often pancreatic or lung.

95
Q

Disseminated Intravascular Coagulation: what is it

A
  • Widespread thrombosis in the microcirculation
  • Can be slow or all of a sudden.
  • Divers associations: obstetric complications, heat stroke, infections, etc.
  • Cause consumption of platelets and coagulation proteins at the same time as fibrinolytic mechanism activation = EXCESSIVE CLOTTING AND BLEEDING AT THE SAME TIME
96
Q

Definition of infarction

A
  • Ischemic necrosis because of occlusion of vascular supply to the downstream affected tissue.
    • leads to organ dysfunction and sometimes death
  • Caused by arterial thrombi, arterial/venous embolism obstructing distnat vessel, others (vasospasm, vascular twisting)
97
Q

Factors affecting infarct development (4)

A
  1. Collateral blood supplies (2 feeding slupplu, that organ will be safe)
  2. Rate of occlusion (how fast the cloth forms)
  3. Intrinsic tissue susceptibility to ischemic injury : different parts are more susceptible (brain, heart, very susceptible. Require lots of oxygen.)
  4. Blood oxygenation (if COPD, cant keep good oxygenation à more susceptible to have an infarct).
98
Q

what are the 2 types of infarct and short definition

A
  • red hemorrhagic
    • With venous occlusions(e.g., Ovarian torsion).
    • In tissues with dual circulations(lung, small intestine).
    • In previously congested tissues.
    • When flow is reestablished after infarction has occurred(after angioplasty of an arterial obstruction)
  • white anemic
    • With arterial occlusions in solid organs with end arterial circulations(e.g., heart, spleen, and kidney).
99
Q

Definition of pulmonary embolism

A

The most serious form of venous thrombo-embolism occurs when a thrombosis (blood clot) dislodges from a deep vein usually in the lower extremity, and embolizes (travels) through the right side of the heart to the pulmonary circulation. It terminates in one or more branches of the pulmonary artery where it produces a number of clinical consequences that can vary from asymptomatic, to circulatory collapse and sudden death.

  • could also be other material traveling through the venous circulation (fat, tumor, amniotic fluid)
100
Q

Name all the interstitial lung disease (IDL) seen in class ?

A
  1. pulmonary edema
  2. pneumonia presenting as IDL
  3. idiopathic pulmonary fibrosis (IPF, patho = UIP)
  4. sarcoidosis
  5. acute interstitial pneumonitis (AIP - patho = DAD)
  6. cryptogenic organizing pneumonia (COP ; patho = organizing pneumonia)
101
Q

What is interstitial lung tissue?

A

The interstitial tissue of the lung provides a supporting framework for the airways, vessels and alveolar airspaces. It can be considered in two interconnecting “compartments”:

  1. Parenchymal: in the alveolar wall and surrounding small vessels and lymphatics
  2. Non-parenchymal: in the pleura, interlobular septa surrounding the large vessels and airways
102
Q

How does pulmonary edema evolve?

A

In pulmonary edema, the edema starts as a non-parenchymal interstitium (fluid leaks out of the capillaries into the adjacent instertitial space) but is accumulated in the non-parenchymal and then in the alveolar airspace.

CRX findings:

  1. Engorged blood vessels
  2. Kerley B lines + Thickened fissures because of fluid accumulation
  3. Air bronchograms «Consolidation»
103
Q

What is Sarcoidosis?

A
  • It is a multi-system disease (non-parenchymal interstitial disease)
  • There is generally involvement of the lungs at some point in the illness trajectory
    • formation of granulomas to isolate the infectious agent
    • can also lead to fibrosis
  • Precise etiology is not known
  • It is asymptomatic in many patients (i.e. discovered incidentally on a routine CXR)
104
Q

What are the 3 types of Interstitial Pneumonia (pathology and clinical names)?

A
  1. Usual interstitial pneumonia (UIP) (PATHO) or Idiopathic pulmonary fibrosis (IPF) (CLINICAL)
  2. Diffuse alveolar damage (PAHTO) or Acute interstitial pneumonia (CLINICAL)
  3. Organizing pneumonia (PAHTO) or Cryptogenic Organizing Pneumonia (COP) (CLINICAL)
105
Q

What is the clinical presentation of Sarcaidosis?

A
  • Loefgren’s syndrome : Fever, polyarthritis, erythema nodosum, and an abnormal CXR
  • Heerfordt’s syndrome : Fever, enlarged parotid and uveitis
  • Lupus Pernio : Violaceous papules on nose, lips and cheeks
106
Q

How do you diagnose a sarcoidosis ?

A
  • CXR : bilateral hilar adenopathy +/- an interstitial pattern
  • Bronchoscopy and lymph node biopsy (EBUS) or lung biopsy to confirm the diagnosis
  • Pulmonary Function Test (PFTs) usuallu reveal a mixed restrictive/obstructive pattern
107
Q

What are the different stages of sarcoidosis on CXR ?

A
  1. enlarged lymph nodes
  2. enlarged lymph nodes + lungs markings
  3. lymph nodes regress
  4. fibrosis
108
Q

what’s the treatment for sarcoidosis ?

A
  • many patients : no treatments
  • steroids (improvement, but relapse once the therapy is done)
  • lung transplant in certain cases
  • other therapies : chemotherapeutic agents, anti-malarial agents, anti-TNF agents
109
Q

what are clear pathological finds of usual interstitial pneumonia ? What’s the prognosis ?

A

IDIOPATHIC PULMONARY FIBROSIS (clinical name)

  • honeycomb change (architectural remodeling)
  • patchy distribution (variable intra- and inter- lobular severity)
    • biphasic fibrosis - active and remote : appears to be 2 phases «alveolitis» and «fibrosis», the first one being more amendable to treatment
  • mild inflammation

Poor prognosis, less then 1/3 of patients improve with steroids

110
Q

What are typical clinical presentation of UIP (as weel as most other ILDs). Are the following capacities improved or worsen?

  • compliance
  • elasticity
  • elastic recoil
  • lung volume
  • diffusion capaicty
  • large airway caliber
  • small airway caliber
A
  • compliance ↓
  • elasticity ↑
  • elastic recoil ↑
  • lung volume ↓
  • diffusion capacity ↓
  • large airway caliber : ↑ often or sometimes will increase
  • small airway caliber ↓

You’ll sometimes have as clinical presentation

  • dyspnea (progressive, first with exertion and then at rest)
  • cough (non-productive)
  • finger clubbing
  • may be cyanosis
  • the respiratory pattern will be rapid and shallow
111
Q

what can help differenciate the acute interstitial pneumonia from the idiopathic pulmonary fibrosis ?

A
  • in acute interstitial pneumonia, the disease is diffuse; all of the alveoli are abnormal (something is accumulation within them) and capillaries are enlarged
112
Q

what is the pathological finding of organizing pneumonia ?

A

Clinical : Cryptogenic organising pneumonia (COP)

  • patchy distribution (variable intra- and inter- lobular severity)
  • fibroblastic tissue in respiratory bronchiolar/alveolar duct lumens and alveolar airspaces
  • mild - moderate interstitial inflammation
113
Q

How is mycobacterium tuberculosis transmitted ?

A

Transmission is airbone - exclusively

  • the probability of transmission is the probability of inhaling a viable bacterium which is proportionnal to the concentration in the air
    • volume of air that TB bacteria are dilluted in
      • big room = lower concentration
    • production vs elimination
      • production : related to the source
      • elimination : by sunlight or drying, and removal of airbone bacteria by ventilation
114
Q

Exposure to TB result in infection or no infection. How is that ? How can it influence the course of the disease ?

A
  • Exposure results in new infection or no infection determined by innate immunity
    • The initial immune response to primary infection is largely ineffective for TB
      • CMI is defective in
        • very young and very old
        • HIV infection
        • other immunocompromising conditions/treatments
        • co-morbidities (diabeter, renal failure)
    • Following the primary infection, development of effective cell mediated immunity determines if diseases develops or infection becomes dormant (latent) about 4-7 weeks after initial infection
      • special immune cells from hard shell called granuloma to contain the bacteria
        • latent state is a dynamic state where the mycobacterium is trying to get out, but the host defense constantly trying to hold ‘em back
        • «dormant» TB can remain viable for 40 years or more, are asymptomatic, but a tuberculing skin test will be positive
      • if CMI defective - primary TB infection is not controlled and symptomatic diseases develops within 3-6 months
      • If CMI deteriorates, then granulomas «release» TB bacteria and the person develops active TB disease (environ 10% des dormant TB cases)
115
Q

What are the different phases of progression of TB ?

A
  1. Exposure
  2. Primary infection : bacteria reach the alveolus.
  3. TB bacteria spread to the regional lymph nodes (2-4 weeks)
  4. Hematogenous dissemination (4+ weeks)
116
Q

What are the main risk factors for the development of active diseases of TB? How does it happen ?

A

Happens in environ 10% of latent infection

Risk factors :

  • Interval since infection (highest risk in the first 1-2 years)
  • HIV/AIDS : strongest known risk factor, around 7-10% per year
  • other immune suppresion : i.e. transplant
  • age (more in young children)
  • smoking, alcohol use
  • under-weight
  • diabetes, renal failure
  • silicosis - pulmonary diseases only

Reactivation process

  • hard shell breaks and tubercle escape and multiply
117
Q

Is the TB only in the lungs ?

A

No, pulmonary disease isn’t the only form and many forms of TB can appear at different time

118
Q

How can you diagnose active TB ? What seams to be the best confirmation test ?

A
  • Clinical: symptoms of cough, sputum – for weeks to months.
    • Fever and sweating at night are classical
    • Hemoptysis (coughing up blood) – late in course
  • Physical exam – chest exam usually normal
    • low grade fever, thin
  • Chest X-ray – usually first step
    • Sensitive (not many cases missed)
    • But not very specific (a lot of false diagnoses)
  • Microbiology is essential
    • Sputum–at least 3 samples
      • Microscopic exam of sputum smearStained for acid fast organisms
      • Rapid but not sensitive (~50-60% of all pulmonary cases)
    • Cultures – most sensitive and specific
      • But take 4 weeks or more for final result
    • Nucleic acid amplification – rapid and fairly sensitive (+++ OUI OUI OUI)
      • Same day test
      • More sensitive than acid-fast smear
119
Q

How do you diagnose latent TB ?

A
  • Clinical – no symptoms. Exam normal
  • All routine tests for TB disease are negative
    • Chest Xray usually normal, or at least stable
    • All cultures are negative
  • Two immune based tests available
    • Do not provide any information about duration of infection; both have known limitations
    • Tuberculin Skin Test – “PPD”
      • In-vivo test. Inject purified protein derivative in forearm
    • Interferon gamma release assays (IGRA’s)
      • ​In-vitro assays. Use whole blood
    • Fairly low predictive value for future active TB
      • About 10%
120
Q

How do you treat active TB ?

A
  • Multiples drugs (at least 2 drugs at all times)
    • prevents resistance (TB can mutate rapidly and develop resistance if only 1 drug is given)
    • At least 3 (usually 4) drugs initially
  • prolonged therapy
    • minimum 6 months
    • longer if drug resistance
  • most important drugs :
    • Isoniazid (INH) and Rifampin (RIF)
    • Bactericidal (kill TB bacteria)
      • Pyrazunamide (PZA)
121
Q

Hoe do you treat a latent infection of TB ?

A
  • single drug therapy
    • no risk of drug resistance
  • therapy is prolonged
    • isoniazid - daily 9 months (highly efficacious) when taken completely
    • completion is poor, hence new 3-4 month regiments
  • not everyone needs treatment
    • balance of risks vs benefits of treatment
122
Q

Epidemiology of TB in Canada? Reasons ?

A
  • Overall TB rates (mortality + incidence) in Canada have declined from the early 1900s
  • The situation in Inuit communities is totally different, it has increased
    • account for 20% of all canadian cases
    • affects adolescents and young adults
    • WHY ?
      • Housing conditions
      • smoking and alcohol
      • malnutrition
      • diabetes
      • genetic factors
123
Q

What’s the most important cause of TB worldwide ?

A
  • Malnutrition (27%)
  • smoking and alcohol (20%)
  • HIV infection (14%)
124
Q

Non-tuberculous mycobacterium

A
  • most do not cause human disease
  • no direct spread between humans (may be present in humans without causing disease)
  • they do not automatically require treatment and not reportable
  • Mycobacterium avium are most frequently associated with human diseease in Canada .Major syndromes :
    • nodular lung infiltrates on CXR, associated with bronchiectasis
    • TB «mimic»
    • seen in people with previous underlying lung disease
      • _​_also in people with uncontrolled AIDS
    • manifest as indolent symptoms (cought, sputum, weight loss)
125
Q

Name example of sleep tracings and associated sleep stage

A
126
Q

Explain the effects of normal changes in respiratory control during system and what they are ?

A
  • Changes
    • loss of the «wakefulness drive to breath»
      • ↓ drive output from controller
    • ↓ muscle activity (inhibition during REM)
      • affects non-diaphragmatoc respiratory muscles
    • ↓ end-expiratory lung volume
    • ↑ upper airway resistance
    • impaired compensation for added loads
    • ↓ responses to ventilatory stimuli : hypoxia, hypercapnia, airway receptors
  • Effects
    • ↓ minute ventilation during sleep and increase in PaCO2
    • Normal brief period of breathing instability
    • ↑ susceptibility to blood gas disturbances during sleep in pathologic conditions (stage R most suseptible)
127
Q

Types of sleep disordered breathing (SDB)

A
  • obstructive sleep apnea (most common)
  • central sleep apnea
  • sleep-associated hypoventilation
128
Q

What are the different types of sleep-disordered breathing events ?

A
  • Discrete episodes, lasting ≥ 10 sec, of absent (apnea) or reduced (hypopnea) breathing
  • Sleep-associated hypoventilation: sustained reduction in breathing associated with hypercapnia (and hypoxemia)
129
Q

What are OSA (upper airways collapse during sleep) symptoms ?

A
  • Nocturnal
    • heavy, habitual snoring
    • apneas witnessed by bedpartner
    • noctural choking (uncommon)
    • restless sleep
    • nocturia
    • sweating
    • morning headache
    • awakening unrefreshed
  • Daytime
    • excessive daytime sleepiness
    • impaired concentration
    • memory problem
    • mood disturbances
    • increased motor vehicule accidents
130
Q

How is OSA linked with cardiovascular complications ?

A

Cardiovascular changes associated with breathing events, reflected by heart rate (pulse) increases.

  • cardiovascular complications
    • hypertension
    • arrhythmias
    • acute coronary events
    • transient ischemic attack
    • pulmonary hypertension
    • congestive heart failure
    • increased mortality
131
Q

What is a loop gain ?

A

Relationship between magnitude of ventilatory disturbance / ventilatory response

  • high LG = respiratory instability
132
Q

OSA treatment option

A
  • weight loss
  • avoidance alchool, sedatives
  • positioning therapy
  • phamacotherapy
  • upper airway surgery
  • hypoglossal nerve stimulation
  • madibular advancement devides
  • positive airway pressure (cPAP - continuous positive airway pressure)
    • ​effective when used (compliance problem)
133
Q

What are the causes of central sleep apnea ?

A
  • hypercapnic
  • idiopathic
  • central nervous system lesions
  • congestive heart failure
134
Q

What are the causes of sleep-associated hypoventilation ? What’s the treatment ?

In what phase of sleep do you see it more often ?

A

WORSE IN REM THAT NREM

  • Causes
    • Central nervous system disease
    • Drug-induced
    • Metabolic
    • Neuromuscular disease
    • Diffuse; localized eg diaphragm
    • Chest wall deformities
    • Chronic Obstructive Lung Disease
    • Obesity Hypoventilation Syndrome
  • Treatment
    • treat underlying cause
    • ventilaroty stimulant medication
    • oxygen
    • non-invasive ventilation
      • bipap
135
Q

what inhibits calcium activation ? What does it lead to in the coagulation cascade ?

A
  • Calcium activation requires vitamin K a cofactor
    • this reaction is inhibited by coumadin (warfarin), one of the most populat anticoagulant in the clinic
136
Q

Usually, because of the increase in dead space during a pulmonary emboli, what should you see in the blood gases . ? Why don’t you see it ?

A
  • Assuming that minute-ventilation stays the same, increasing dead space automatically decreases alveolar ventilation and hence CO2 excretion –> hypercapnia
  • HOWEVER, it’s an unusual consequence of pulmonary embolus because of ventilatory compensation
    • increase in minute-ventilation to compensate for the increase in dead space.
    • the body compenses so much, an usual consequence of a pulmonary embolus is hyperventilation and hypocapnia
137
Q

Types of thrombi ?

A
  • Arterial or venous
  • mural
  • vegetations
138
Q

what are the risk factors of pulmonary embolism ?

A
  • endothelial injury
    • trauma
    • post operative
    • previous VTE
  • stasis
    • immobility
      • post-operative
        • orthopedic
        • cancer
      • medical illness
        • congestive heart failure
        • stroke
      • travel
        • economy flight syndrome
    • obstruction of venous flow
      • pregnancy
      • previous VTE (or family history)
      • malignancy
      • anatomic variants
  • hypercoagulabiity
    • congenital
      • high factor VIII
      • factor V. Leiden
    • acquired (medications or other things)
      • smoking
      • medical illness
        • anti-cardio-lipin
        • nephrotic syndrome
      • medications
        • hormones
        • chemo
      • malignancy
      • ​hormones
        • pregnancy
        • oral contraceptive pill
        • replacement
        • chemo
139
Q

A thrombi result in realease of chemical mediators. What’s the source ? What effect do they have on the lungs?

A
  • Exact source and nature is unknown, but platelets that adhere to the thrombus are an important source of mediators such as histamine, serotonine and prostaglandine
  • secondary effects on both airways and blood vessels of the lungs
    • bronchoconstriction
      • contribute to the hypoxemia that commonly accompanies pulmonary embolism
    • affect areas of low ventilation and inappropriately high perfusion
      • ​hypoxic vasoconstriction becomes compromised
      • vasoconstriction of pulmonary arteries and arteriols can occur and add to the likelihood of major cardiovascular compromise
140
Q

what are the 2 mechanical obstruction of the pulmonary artery caused by pulmonary embolism ? Explain.

A
  • increased pulmonary resistance
    • takes a while to get there since the pulmonary circulation first recruit new vessels and dilate the existing ones. You need at least 40% of the occluded lung to see a rise in pressure
  • increased dead space
    • ​when a vessel is occluded by an embolus perfusion of pulmonary capillaries normally supplied by that vessel ceases. If the ventilation to the corresponding alveoli continues, then the ventilation is wasted and the region of the lung serves as a dead space.
141
Q

What is the leading cause of cancer death in both males/females

A

Lung cancer

142
Q

True or false, incidence rate of LC is higher in men than women

A

True, because of differences in tobacco use.

143
Q

What is the leading etiology of LC

A

Tobacco

144
Q

Tobacco industry made changes in composition of cigarettes & filter-tip cigarettes appeared. How did it impact the types of cancer incidences?

A

Increase of adenocarcinomas and decrease of squamous cell carcinoma.

145
Q

Name 2 other etiologies of cancer except tobacco.

A

Radon and asbestos

146
Q

What are more popular tumor amongts the 5 tumor categories according to WHO

A
  • Epithelial (95% of tumor are epithelial)
  • Other kinds :
    • Mesenchymal
    • Lymphohistocytic
    • Tumors of ectopic origin
    • Metastatic tumor
147
Q

Nom du chat pref a Isa

A

Henri

148
Q

4 types of lung cancers we study

A

Squamous cell carcinoma

Adenocarcinoma

Small cell lung cancer

Carcinoid tumours

149
Q

For the 4 cancers we study: is it associated with smoking/to which degree?

A

Squamous cell: strongly associated with smoking

Adenocarcinoma: yes but less, 15% of diseased are non-smokers in NA/Europe

Small cell carcninoma: STRONGEST ASSOCIATION

Carcinoids tumors: no clear relation with tobacco

150
Q

What does a squamous cell carcinoma show? How can you catch it ?

A
  • Kertinization and/or intercellular bridges
  • expresses certain immunohistochemical markers of squamous differentation : p40, CK5/6
151
Q

Squamous cell carcinoma: proximal or distal tumors? What does it leads to ?

A
  • Proximal tumors - associated with main bronchi
  • often : intraliminal growth +/- associated with obstructive pneumonitis
152
Q

How can we define adenocarcinoma?

A

Malignant epithelial tumor with glandular differentiation, mucin production OR pneumocyte marker expression TTF-1

153
Q

Adenocarcinoma: peripheral or proximal tumors

A

Peripheral

154
Q

Macroscopic appearance of adenocarcinoma

A

Grey nodules with scarring & anthracotic pigmentation (black carbon pigment)

Poorly defined border

155
Q

What are the different patterns and a brief description of each that an adenocarcinoma can have

A

Acinar - associated with glands

Papillary - along a fibrovascular core (chemins blancs partout entre)

Micropapillary - growing in papillary tufts in the alveoles.

Lepidic - tumor cells growing along the surface of alveolar walls

Solid - sheet of tumor cells, poorly differentiated

156
Q

Can we have many patterns of tumors inside of one adenocarcinoma, or only one?

A

We can have many - often an adenocarcnioma is described as, for instance: 60% acinar, 10% papillary, 5% micropappilary, etc.

157
Q

What are the steps of preinvasive lesions for adenocarcinoma?

A
  • there is a continuum
    • Atypical adenomatous hyperplasia (AAH)
    • Adenocarcinoma in situ
    • Minimally invasive adenocarcinoma
158
Q

What are the 4 categories of neuroendocrine tumours?

A

High grade: small cell carcinoma, large cell neuroendrocine carcnima

Low/intermediate grade: typical carcinoids, atypical carcinoids (both subtypes of CARCINOID TUMORS)

159
Q

3 characteristics of the definition of small cell carcinoma

A

Scant cytoplasm

Finely dispersed chromatin

Absent/inconspicuous nucleoli

160
Q

what is the classic clinical presentation of pulmonary embolism ?

A
  • dyspnea (most common complaint)
  • chest pain
    • pleuritic
  • hemoptysis
  • palpitations
  • syncope
  • swollen, tender leg
  • can be assymptomatic
161
Q

Characteristics of macroscopic appearance of small cell carcinoma?

A

Proximal large hilar tumors

Bulky Mediastinal lyph nodes

Metastases

Paraneoplastic syndromes (linked with ectopic secretion of hormones)

162
Q

High mitotic rate and necrosis are common in… (what cancer)

A

Small cell carcinoma (really small nucleus)

163
Q

What findings in a clinical exam should you expect to find in a patient with P.E

A
  • vitals
    • low BP
    • tachycardia
    • Low O2 sat
  • chest
    • decreased air-entry
    • pleural friction
  • cardiac
    • loud P2
    • elevated JVP
    • edema (distented right ventricule)
  • Extremeties
    • tender, swoller, erythematous lower limb
164
Q

What are the characteristics of the outcome of small cell (prognosis, resectable or no, metastases)?

A

Poor prognosis with a 2-year survival rate 10%

Usually non resectable, CTherapy treatment

Distant metastases: brain, bone, adrenal glands

165
Q

What percentage of newly diagnosed lung cancers are carcinoid tumors?

A

1%

166
Q

What are the main characteristics of macroscopic appearance of carcinoid tumors?

A
  • Arise mainly in central airways < 1/3 peripheral

Well circumscribed

Bronchial obstruction

Rare metastases (mediastinal lymph nodes)

167
Q

what test can you use to diagnose a PE ? Gimmie a little detail please

A
  • V/Q scanning
    • ​you give a radiolabelled gaz and see how the perfusion is going
    • normal = exclude PE
  • compression ultrasonography :
    • ​imaging a venous defects that persist, most-reliable sign is non-compressibility of the vein
  • computerized tomorgaphic pulmonary angiography (CTPA)
    • ​non-invasive
    • has become the most common, and reliable diagnostic test (you see the clot)
  • conventional pulmonary angiography
    • ​historically gold standard for diagnosis, now replaced by CTPA
168
Q

What can bronchial obstruction cause in a carcinoid tumor?

A

Cough,hemoptysis and recurrent obstructive pneumonitis.

169
Q

What is the most popular mutation and its percentage of frequency? Highest in what gender, nationality and smoking habits?

A

EGFR with 10-15%.

Non/light smokers, female, Asian

170
Q

How does pTNM work?

A

T: size

N: nodes

M: metastases

171
Q

Compare the incidence of lung cancer in NA/Europe with China.

A

NA/Europe –> incidence is declining

China –> epidemic, mainly because largest consumer of tobacco

172
Q

In cases of PE, do you wait for diagnosis results to begin therapy ?

A

No, you begin therapy when diagnosis is suspected while waiting for diagnostic tests

173
Q

How would you treat PE ? Explain how the things work

(imagine you’re a good doctor and not a fucking medical student who still has 208 years of school to do)

A
  • ensure vital signs stable
    • oxygen
    • fluid
  • mainstay of therapy is anticoagulation
    • unfractionnated or low molecular weight heparin
      • _​_fast
      • sub-cutaneous injection
      • stable levels of anti-coagulation without need for monitoring
    • warfarin
      • _​_vitamin K antagonist
      • 4-7 days to take effect
      • needs careful monitoring
    • newer fancy stuff (like CAVIAR)
      • oral thrombin inhibitors : dabigatran
      • factor Xa inhibitors : rivaroxaban, apixaban
        • oral agent
        • no monitoring
        • usually minimal interactions with other medications
        • can’t give with renal failures
  • in critical cases
    • consider thrombolysis
    • surgery
174
Q

The proportion of LC in non-smokers is increasing or decreasing?

A

Increasing :(

175
Q

What are LC main risk factors (appart fumer mettons)

A
  • first degree relatives
  • exposure to biomass and wood smoke in developing countries (AKA DON’T GO CAMPING)
  • parenchymal scarring : old TB scars and pulmonary fibrosis

you should also ask patient

  • work
  • family-history
  • smoking and second-hand smoke
176
Q

What is the specific goal of screening?

A

Reduce the disease’s specific mortality - NOT JUST DIAGNOSE EARLIER

177
Q

What was the conclusion of a study in 1970s concerning CXRs and sputum tests as screening?

A

No reduction in disease specific mortality.

178
Q

What is the conclusion concerning recent methods of screening for LC?

A

Screening with low-dose CT (when compared to CXR) : decrease of 20% in LC deaths.

When screening with high-risk asymptomatic men: 26% reduction in LC deaths in a 10-year follow-up. Even better for women.

179
Q

What are the 2 main categories of lung cancer and their incidence?

A

Small cell 14% and non-small-cell 85%

180
Q

What is included in the category of non-small cell?

A

Adenocarcinoma, squamous, large cells

181
Q

How do we treat a mixed SCLC/NSCLC tumor?

A

We treat it as a small cell tumor since it’s the most aggressive one.

182
Q

Class adeno, small cell and squamous in terms of best prognosis to worst prognosis.

A
  1. Squamous
  2. Adenocarcinoma
  3. Small cell
183
Q

Un ptit summary brainscape: central or periphery for small cells, adeno, squamous?

A

Small cell: central

Adenocarcinoma: periphery

Squamous: central

184
Q

Which cancer can be associated with hypercalcemia?

A

Squamous cell

185
Q

Which cancer can develop in old scars

A

Adenocarcinoma (scar carcinoma lolz no shit)

186
Q

Which cancer tends to cavitate?

A

Squamous cell

187
Q

Which cancer which location is variable behaves similar to adenocarcinoma, and spreads to nodes & distnatly?

A

Large cell lung cancer

188
Q

Name 3 signs/symptoms of lung cancer.

A

Change in character of smoker’s cough

Stridor (if large tumor compresses the trachea externally). Inspiratory sound. (unilateral wheeze - expiratory sound - may be hear if airway obstructed by endobronchial tumor)

Minor hemoptysis should be investigated - even if most of the time it’s a bronchitis

189
Q

Name paraneoplastic syndromes for SCLC and NSCLC.

A
  • More commonly seen with SCLC – not common but when they DO happen, SCLC.
    • Cushing syndrome (ectopic ACTH, ectopic production of hormones)
    • SIADH (Syndrome of Inappropriate Antidiuretic Hormone Secretion – hyponutriema)
    • Neurologic syndromes (Lambert Eaton, peripheral neuropathy, cerebellar degeneration)
  • In NSCLC
    • Hypercalcemia
    • Hypertrophic osteoarthropathy and clubbing
      • Painful symmetrical joint pain in ankles, knees, wrists, elbows)
    • Dermatomyositis (muscle weakness, rash)
190
Q

Name 4 locoregional symptoms.

A
  • Cough, bronchorrhoea, hemoptysis, obstructive pneumonia, chest pain from invasion of the chest wall, neck nodes, hoarseness (recurrent laryngeal nerve invaded at the hilum), swallowing problems (esophageal compression)
  • SVCO syndrome (obstruction of the superior vena cava). Symptoms include early morning headache, edema of the upper limbs, facial congestion and distension of the jugular vein and veins on the chest.
  • Pancoast syndrome (tumor at the lung apex): hand or arm pain from brachial plexus involvement, Horner’s syndrome from involvement of the sympathetic chain (ptosis, miosis, anhydrosis)
  • Dyspnea from pleural or pericardial effusions
191
Q

Name some disseminated disaase than could happen in lung cancer.

A
  • weight loss, bony pain, headache,
  • Soft tissue masses
  • skeletal symptoms; pathological fractures, spinal cord compression
  • focal neurologic deficits, seizure
192
Q

Hematologic disease in lung cancer?

A

Thrombophlebitis & thromboembolic disease

193
Q

How does staging work for small cell LC?

A
  • Since 90% of the patient present with stage 3, we use limited or extensive staging
    • ​Limited: tumor is in an hemithorax or regional lymph nodes that can fit within a single radiation field
    • Extensive: anything else
194
Q

What could be false positives and false negatives when using pet scans for staging? Should you use PET scans ?

A
  • False + : inflammatory diseases
  • False -: bronchioalveolar cell, carcinoids, <1cm, brain

yes, you should use it since it has an accuracy of 89-100% for malignancy

195
Q

Briefly describe the treatments for SCLC.

A

Limited: Chemotherapy & radiation

Extensive: chemotherapy

Here, the performance status is less important because 90% of patients actually respond to the treatment so it’s worth it.

196
Q

Generally, for a LC, what is the treatment when comparing early stage/locally advanced/metastatic?

A

Early: surgery for resection

Locally advanced: chemo/radiation:

Metastatic: palliative chemo

197
Q

Is there a pre-invasive leasion in squamous cell carcinoma ?

A

Yes, squamous cell carcinoma in situ has no maturation from base to luminal surface with cellular crowding and atypia.

198
Q

if you see solid and micropapillary patterns on a adenocarcinoma, what shoudl you do ?

A
  • lobectomy
    • since in early lung adenocarcinoma (stage IA), solid and micropapillary patterns are related with an increase risk of recurrence.
199
Q

immunohistochemistry of small cell carcinomas. What cancer has the same ?

A
  • CD56
  • chromogranin
  • synaptophysin

same as carcinoid tumors

200
Q

What are the most frequently tested molecular markers in all high stages adenocarcinomas ?

A
  • EGFR
  • ALK
  • ROS1
  • PD-L1 (to know if there’s gonna be a response to therapy)
201
Q

what are the main molecular abberations tested in lung cancer ? Explain each a little

A
  • KRAS : most frequent mutation in smokers
  • EGFR : highest in non-light smokers
  • ALK : highest in non-smokers/light smokers
  • ROS1
202
Q

Why do we test PD-L1 ?

A
  • tested in all non-small cell carcinomas
  • high expression is linked with higher response rate to immunotherapy
203
Q

what are the 2 main determinating factor of a cancer’s stage ?

A

size and invasion of the pleura

204
Q

what’s the cancer most commonly linked to asbestos exposure ? What happens if the patients smokes as well ? Are you gonna have lung cancer as soon as you’re exposed to asbestos ?

A
  • mesothelioma. Cigarette smoking and asbestos exposure have a multiplicative effect on the risk of developing lung cancer (increase the risk of LC by 20-50 times a non-smoker, non-exposed person)
  • no, there’s a lag-period of 20-30 years between exposure and development of LC
205
Q

how diagnosing of lung cancer works ?

A
  • histologic confirmation must be obtained
  • patient should be investigated and referred for treatment within 2-4 weeks of abnormal CXR
  • use procedure that can diagnose stage and kind of cancer
    • like sampling of large nodes
  • use bronchoscopy, EBUS (to biopsy lymph nodes) or thransthoracic needle aspirate (peripheral)

Block B - Respiration (8 decks)

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