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Cardiology > Pulmonary Disease > Flashcards

Pulmonary Disease Flashcards

1
Q

What test results would indicate asthma?

A
  1. Pulmonary function testing: FEV1/FVC 12% after bronchodilator (from baseline FEV1)
  2. Peak expiratory flow variability >20%
  3. Eosinophilia
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2
Q

What is the consequence of uncontrolled chronic asthma?

A

Affects airways like smoking! Fixed obstructive disease

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3
Q

What are reliever medications and how should they be used?

A

Short term relief of symptoms of asthma. Includes beta agonists, which causes bronchodilator ( act on smooth muscle).

Should be used sporadically with worsening symptoms. Should not be used prophylactically.

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4
Q

What is an asthma controller medication, and how should it be used?

A

Controllers are anti-inflammatory, slow onset, long acting medications.

Use for prophylaxis.

Try to use minimum does for maximum control

Examples: inhaled steroids, leukotrine receptor antagonists, combo steroids and long acting beta agonists.

Biological therapies are becoming a new area!

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5
Q

How are asthma and COPD differentiated?

A
  1. Age: asthma tends to be younger
  2. Smoking: COPD smoker or past smoker
  3. Cough: asthma nocturnal, COPD morning/productive
  4. Peak flow: variable in asthma, not in COPD
  5. Bronchodilator: asthma responds usually, COPD not
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6
Q

What are the types of pneumothorax?

A

Priamary=spontaneous

Secondary=underlying disease process

Iatrogenic

Traumatic

ALL CAN TURN INTO TENSION PNEUMOTHORAX!

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7
Q

What are the physical exam findings for pneumothorax?

A 
Tachycardia
Hyperesonance (percuss down each intercostal space)
Absent breath sounds
Tracheal shift (if more severe)
Profound hypoxia-tension
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8
Q

What are the recurrence rates for primary spontaneous pneumothorax?

A

30-40% after first incident

50% after second (may intervene now)

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9
Q

What are the risk factors for pneumothorax?

A 
Tall
Slim
Male
Younger
Smoker
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10
Q

When do we treat a pneumothorax?

A 
Symptomatic
Large (>2-3cm at apex)
Secondary 
Tension
Ventilated patient

Primary patients who are not breathless and have a small one can be discharged home with early follow up

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11
Q

What are the physical exam findings in pulmonary embolism?

A 
Tachycardia
Tachypnea
Fever
Pleural rub (squeak)
Right sided S4 (due to strain on right heart)
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12
Q

What are the physical exam findings of pericardial effusion?

A 
Tachycardia
Hypotension
Elevated JVP
Pulsus paradoxus
Muffled or quiet heart sounds
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13
Q

What are the physical exam and investigations findings for pericarditis?

A

Friction rub- scratching noise with heartbeat

ECG: diffuse concave upwards ST elevation

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14
Q

How do glucocorticosteroids help treat asthma?

A
  1. Block several pathways of inflammation
  2. Thereby reducing exacerbation frequency
  3. Watch out for side effects (oral thrush)
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15
Q

What is more effective in escalating asthma therapy, rather than increasing corticosteroid dose?

A

Add a long-acting beta agonist- this is much more effective than increasing dose of steroids alone. NEVER give LABA monotherapy (BAD)

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16
Q

What characterizes asthma?

A
  1. Variable airflow obstruction
  2. Airway hyper responsiveness
  3. Chronic airway inflammation
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17
Q

What characterizes asthma?

A
  1. Variable airflow obstruction
  2. Airway hyper responsiveness
  3. Chronic airway inflammation
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18
Q

Diagnostic testing COPD?

A

Spirometry:
FEV1/FVC less than 70%
Post bronchodilator FEV1: will tell you severity
Flow volume loop shows scooped out expiration

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19
Q

What are the causes of airflow limitation that are irreversible?

A

Fibrosis and narrowing of the airways
Loss of elastic recoil in alveoli
Destruction of alveolar supports

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20
Q

What are reversible causes of airway limitation?

A

Accumulation of inflammatory cells, mucus, plasma
Smooth muscle contraction
Dynamic hyperinflation during exercise

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21
Q

Emphysema

A

Abnormal, permanent enlargement of the airspace distal to the terminal bronchioles, accompanied by destruction of the walls

22
Q

Chronic bronchitis

A

Cough and sputum production (2 years, no other cause)

23
Q

Dynamic hyperinflation

A

Gas trapping in lungs during exercise.
Despite recruitment of expiratory muscles, COPD patients cannot exhale the volume they inhale during exercise (airways compress or collapse during exhalation).
Progress inflation of lungs, dyspnea on exertion

24
Q

What are the 5As of smoking cessation?

A 
Ask-about tobacco use
Advise- to quit
Assess- willingness to try
Assist- offer counselling, pharmacology
Arrange- follow up with patient
25
Q

What treatments give a mortality benefit in COPD?

A

Smoking cessation
Vaccination
Home oxygen

26
Q

What pharmacological interventions do we use in COPD?

A
  1. Bronchodilators: short acting (beta agonist) or long acting (cholinergic antagonist)
  2. Steroids: not that effective on their own
  3. The more acute exacerbations that occur, the more combination therapy that is used
27
Q

How do bronchodilators work and what would an ideal one accomplish?

A
  1. Increase inspiratory capacity
  2. Decrease exercise induced dynamic hyperinflation

Ideally: improve spirometry, dyspnea, lung hyperinflation, exercise performance in a sustained way

28
Q

How do we treat an acute COPD flare?

A
  1. Confirm with history, investigations
  2. Increase doses of SABA/LABA
  3. oral corticosteroids (course of prednisone)
  4. Antibiotics if new sputum (tailor to risks-are they going to be susceptible to resistant organisms?
29
Q

With a right sided pneumothorax, which way will the trachea deviate?

A

To the left- away from the tension!

30
Q

What can cause airway narrowing and increased resistance?

A
  1. Secretions (mucus, pus, fluid)
  2. Spasm (smooth muscle contraction)
  3. Swelling
31
Q

When in bronchospasm, what will happen to 1. Peak expiratory flow rates? 2. Inspiratory flow rates?

A
  1. Expiratory: these will decrease, as airways already tend to get smaller with expiration (made worse)
  2. Inspiration: may decline but not to same degree (airways pulled open during inspiration)
32
Q

What happens to muscles when there is increased airway resistance?

A
  1. Need higher pressure to expire the same tidal volume
  2. Muscles work harder
  3. This can cause acidosis
33
Q

In pulmonary fibrosis, what happens to PFTs?

A
  1. Peak flow rate increases as airways are held open
34
Q

Why is it unwise to give oxygen to a COPD patient in distress?

A
  1. Often they are in respiratory acidosis from hypoventilation
  2. Oxygen will affect respiratory centre in brain
  3. Making them hypoventilate further
35
Q

Bird Fancier’s Disease

A

Hypersensitivity to bird dander

36
Q

When someone completely drops their O2 sats with exercise, what does that indicate?

A

A diffusion defect- can’t get O2 across fast enough

37
Q

What are the four common presentations of interstitial lung disease?

A
  1. Cough
  2. Dyspnea
  3. Abnormal imaging
  4. Hypoxemia
38
Q

What drugs commonly cause interstitial lung disease?

A
  1. Nitrofurantoin (abx)
  2. Methotrexate (anti-metabolite)
  3. Amiodarone (anti-arrythmic)
  4. Bleomycin (chemotherapeutic)
  5. Radiation
39
Q

Physical exam findings in interstitial lung diease?

A
  1. Hands: cyanosis, clubbing
  2. Chest: velco crackles, inspiratory squeaks, expiratory wheezes
  3. CVS: signs of pulmonary HTN, right heart failure
  4. Check out for signs of autoimmune/connective tissue diseases
40
Q

What is the gold standard of ILD diagnosis?

A

Multi-disciplinary discussion; team of rheum, resp, rad, etc

41
Q

What findings indicate invasive pulmonary aspergillosis?

A
  1. Chest X-ray not sensitive

2. CT: halo sign

42
Q

What are the pathological signs of asthma?

A
  1. Mucus plugs
  2. Airway inflammatory cells
  3. Sub basement membrane thickening
  4. Epithelial shedding
  5. Goblet cell hyperplasia
  6. Airway wall edema
  7. Smooth muscle hyperplasia
43
Q

Asbestosis

A
  1. Caused by exposure to asbestos, occurs decades later
  2. Diffuse interstitial fibrosis, pleural plaques,
  3. Dyspnea, may see dry inspiratory crackles
  4. Increased risk of mesothelioma of pleura
44
Q

Hypersensitivity pneumonitis

A
  1. Lung reaction to specific antigen exposure (animals etc)
  2. Acute: mononuclear cell infiltrate, giant cells, granulomas, fever, cough,
  3. Chronic: patchy fibrosis, progressive dyspnea, weight loss
  4. CXR: ground glass opacity, mainly upper lobes
45
Q

Goodpastures Syndrome

A
  1. Antibodies against glomerular basement membrane (type 2 rxn)
  2. Common most in young men
  3. Lungs will have intra alveolar hemmorhages, kidneys will have issues
  4. Sx= hemoptysis
46
Q

Sarcoidosis

A
  1. Autoimmune dysfunction?
  2. Most common in African American women (20-40)
  3. Involves lung, lymph nodes, spleen, liver….
  4. Non caseating granulomas
  5. Sx= interstitial lung disease, erythema nodosum
  6. CXR: hilar lymphadenopathy
47
Q

Idiopathic pulmonary fibrosis

A
  1. Progressive, irreversible fibrosis of lung parenchyma. NO identifiable cause
  2. Affects males, 50-60. Survival 3-5 years
  3. Sx= progressive dyspnea, non productive cough, tired legs, low energy, constitutional Sx
  4. Spirometry shows decreased total lung capacity and vital capacity and diffusion (restrictive pattern)
    CT: reticular pattern, maybe honey combing
  5. Lung transplant only real treatment
48
Q

What are the possible causes for interstitial lung disease?

A
  1. Environmental/occupational (hypersensitivity, asbestos, silicosis..)
  2. Inflammatory/connective/vascular ( rheumatoid, sarcoidosis, lupus, scleroderma, Wegeners)
  3. Drugs (amiodarone, bleomycin, methotrexate, nitrofurantoin, radiation)
  4. Unknown cause (idiopathic pulmonary fibrosis)
49
Q

Manifestations of sarcoidosis

A
  1. Brain: meningitis
  2. Chest: lymph node granulomas, pericarditis, arrhythmias, lung granulomas
  3. Abdomen: hepatitis, splenomegaly, lymph nodes
  4. MSK; Arthritis
  5. Skin: erythema nodosum, nodules
50
Q

What is the differential for hilar lymphadenopathy?

A
  1. Sarcoidosis
  2. Lymphoma
  3. Cancer- primary or mets
  4. Infection
51
Q

How do you differentiate between parenchymal and non parenchymal causes of lung restriction?

A
  1. Parenchymal disease will have a reduced diffusion coefficient
  2. Non parenchymal will have a normal diffusion, even in lung volumes are limited ( ie neuro or obestity)

Cardiology (20 decks)

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