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Pulmonary - Pathophysiology > COPD/Emphysema > Flashcards

COPD/Emphysema Flashcards

1
Q

What is the most common cause of COPD around the world?

A

Exposure to smoke from Buring Wood

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2
Q

T of F: in addition to being associated with limition of airflow, COPD is also characterized by an enchanced inflammatory response.

A

True, this response is to the noxious gas and particles that are inhaled.

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3
Q

Note: of the six major causes of death that were listed in 1970 the only one that has risen in incidence instead of decline it COPD

A

Note: of the six major causes of death that were listed in 1970 the only one that has risen in incidence instead of decline it COPD

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4
Q

Other than the inhalation of noxious and toxic chemicals, what are 4 other risk factors for developing COPD?

A
  • Genes (alpha-1 anti-trypsin)
  • Infections
  • Socio-economic status
  • Aging Populations
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5
Q

If you stop smoking will your FEV1 ever correct to be on pace with that of a non-smoker?

A

No

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6
Q

What two types of disease and destruction combine to give you the symptoms of COPD?

A

Small airways disease - from Airways inflammation, fibrosis, luminal plugs that increase small airway resistance

Parenchymal Destruction - Loss of alveolar attachements and decrease of elastic recoil

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7
Q

What defines chronic bronchitis?
• how is it diagnosed?

A

Chronic Bronchitis: recurrent/persistent cough on most days for a minum of 3 months in a year for not less than 2 years

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8
Q

What are some of the key characterisitics that occur in the pathophysiology of Chronic Bronchitis?

A

• Inflammation of the epithelium of the central airway by CD4 and Neutrophil and increased mucous glands (reid index above 0.4) as well as globlet cell metaplasia leading to more mucous and decreased mucociliary clearance

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9
Q

What is the Reid Index?

A

Reid Index = Mucous Gland Depth / Total Bronchial wall Thickness; in ppl. with chronic bronchitis this should be greater than 0.4

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10
Q

What classifies a small airway?
• what is the pathogenesis of small airway obstruction?

A

Small Airways = airways that do not have cartilage

Pathogensis:
• CD8 lymphocytes and Neutrophils infiltrate and you see goblet cell extention as well as squamous metaplasia. All of this inflammation causes collagen deposition in the small airway walls…a place where you shouldn’t see collagen

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11
Q

Emphysema is the abnormal enlargement of airspaces in the lung. Where does this occur?
• what inflammatory infiltrates do we see in people with emphysema?

A

• Abnormal airspace enlargment in emphysema happens distal to the terminal bronchioles - aka the damage starts right where gas exchange can take place

Inflammatory Infiltrates:
• CD8 lymphocytes, neutrophils, and macrophages - remember this inflamation will likely persist even after the person stops smoking

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12
Q

People with emphysema don’t have extremely inflammed airways and don’t have muscle weakness in their diaphragm. So why do they have trouble exhaling?

A

Loss of attachments between alveoli causes dynamic airway collapse in exhalation - (remember airway pressure drops at the edges as gas moves through)

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13
Q

What are the 3 IREVERSIBLE limitations to airflow that occur in COPD?
• which is the most important?

A

3 COPD airflow Limitations:
MOST IMP: Destruction of alveolar attachments that provide the support that maintains the patency of small airways (especially in exhalation)

  • Loss of elastic recoil in lungs due to alveolar destruction
  • Fibrosis and narrowing of the airways
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14
Q

What will you look for on the CXR of someone with emphysema?

A
  • Large Dark hollow looking Lungs
  • Diaphragm Flattening
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15
Q

What are the 3 REVERSIBLE limitations to airflow that occur in COPD?
• which is the most important?

A

3 REVERSIBLE changes in COPD:
• Accumulation of inflammatory cells, mucous, and plasma exudate

  • Smooth muscle contraction in peripheral and central airways
  • Dynamic hyperinflation

**For these just think about the way we treat COPDs, corticosteroids to reduce inflammatin, ß2’s and anti Muscarinics to relax smooth muscle**

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16
Q

What is dynamic hyperinflation?
• when does it get better or worse?

A

Dynamic Hyperinflation may occur at rest and get worse with excercise. Manifests as an increase in FRC which puts the respiratory muscles at a mechanical disadvantage thus increasing weakness of breath and reducing exercise tolerance during excercise.

17
Q

In whom should you consider a diagnosis of COPD?
• what MUST you have to make a diagnosis fo COPD?

A

• any patient with dyspnea, chronic cough or sputum production, and history of exposure to risk factors for the disease (tobacco, occupation, pollution)

• COPD is diagnosed by spirometry; FEV1/FVC less than 0.70 confirms the presence of a COPD

18
Q

Compare the blood gas values of someone with COPD to someone with Chronic Bronchitis.

A

COPD patients will have near normal blood gas values (hence they are pink -oxygenated puffers). In conrast those with chronic bronchitis are hypercapnic and hypoxemic

• Chonic bronchitis patients are the obese people who forget to breathe

19
Q

What do you expect to see in the flow-volume loop of someone with COPD?

A

Scooping during the expiratory phase (the part that is not under our control)

20
Q

What are some things you should look for when doing the clinical assessment of a COPD patient?

A
  • Distant/Decrease heart sounds - caused by hyperinflation of the chest
  • Pursed lip breathing
  • Barrel chest deformity
  • Prologation of Expiratory time
  • Use of accessory muscles
21
Q
A
22
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23
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A
24
Q

Describe the findings in the following pulmonary function tests that would lead you to a diagnosis of PURE CHRONIC BRONCHITIS.
• Flow-Volume Loop
• Treatment with bronchodilators
• Spirometry

A

Flow-Volume:
• Flow-Volume loop reveals airflow obstruction during expiration and inspiration, this tells you obstruction is fixed

Obstruction:
• Obstruction does not improve with bronchodilators (aka FEV1 doesn’t increase by more than 15% or 200ml)

Spirometry:
• Reduced FEV1/FVC

***Diffusing capacity and everything else is normal**

25
Q

Describe the findings in the following pulmonary function tests that would lead you to a diagnosis of PURE EMPHYSEMA.
• Flow-Volume Loop
• Treatment with bronchodilators
• Spirometry

A

Flow-Volume Loop:
• Obstruction (scooping) durings expiration but not change in inspiration (this is slightly different than chronic bronchitis because the obstruction isn’t persistent)

Bronchodilator Response:
• No ACUTE improvement with bronchodilators (aka FEV1 doesn’t increase more than 15% or 200 ml)

Spirometry:
• Reduced FEV1/FVC

26
Q

What does an increased RV/TLC ratio tell you?

A

The patient is HYPERINFLATED - you’re probably looking at something like emphysema because TLC has increased as a consequence of creating more unusable space.

27
Q

How does the mMRC grading 0-4 work?

A

0 - only get breathless with strenuous excercise

1 - I get short of breath when hurrying on the level or walking up a slight hill

2 - I walk slower than people may age or have to stop to breathe while walking

3 - I have to stop to breath after about 100 meters

4 - I am too breathless to leave the house or I am breathless when dressing or undressing

28
Q

How does the GOLD ranking system work?

A

Gold 1 Mild: FEV1 greater than 80%

Gold 2 Moderate: 50% to 80% FEV1

Gold 3 Severe: 30% to 50% FEV1

Gold 4 Very Severe: 30% FEV1

29
Q

What is the main thing that you should always screen people with COPD for?

A

Depression

30
Q

T or F: someone hospitalized with a COPD exacerbation may or may not be high risk

A

False, anyone hospitalized with a COPD exacerbation is High Risk

31
Q

What are some comorbidities to look out for in obstructive lung Diseases?

A
  • Cardiovascular Diseases
  • Osteoporosis
  • Repiratory Infections
  • Anxiety and Depression
  • Diabetes
  • Lung cancer
  • Bronchietasis
32
Q

What vaccines should you make sure anyone with COPD gets?

A

Flu and Pneumococcal vaccines

33
Q

T or F: Cigarette smoke induces an inflammatory response that increases the activity of proteases and leads to alveolar wall destruction and increased mucus secretion

A

True

34
Q

What is the MOA of ß2 agonists?

A

ß2 agonists increase cAMP via a GPCR which activates PKA and ultimately results in decreased activity of Myosin Light Chain Kinase (MLCK), PKA also acts on channels to hyperpolarize cells and prevent them from contracting

35
Q

Why are glucocorticoids used in asthma therapy?

A

• Act on histone DEacytylase to reduce histone acetylation via NfKB thus reducing the production of inflammatory genes

36
Q

How do you progress the Medication as someone’s COPD becomes more uncontrolld?

A
  1. Start with Short Acting Beta 2 Agonists or SA Muscarinic Antagonists
  2. Use Long Acting Beta 2 Agonist or LA Muscarinc Antagonist
  3. Use (LABA or LAMA) + inhaled corticosteroids
  4. Use (LABA AND/or LAMA) + inhaled corticosteroids
37
Q

What is this?

A

Collapsed lung with mediastinal shift and depressed diaphragm, this is a TENSION pneumothorax.

Patient will get hypotensive and hypoxemic, need to put in a needle immediately

Pulmonary - Pathophysiology (13 decks)

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