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HMS Homeostasis I > COPD and Asthma > Flashcards

COPD and Asthma Flashcards

1
Q

Bronchus cross section cartoon

A
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2
Q

How will the bronchus shown change in an acute asthma attack?

A
  1. Swelling
  2. Bronchoconstriction
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3
Q

Most of the long-term, chronic changes to the bronchi seen in asthma are due to ___ released during an allergic attack.

A

Most of the long-term, chronic changes to the bronchi seen in asthma are due to TNFa released during an allergic attack.

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4
Q

Salmeterol

A

Long-acting beta 2 agonist

Taken for chronic asthma

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5
Q

Not only to beta 2 agonists relieve bronchoconstriction due to their effects on smooth muscle, but they also ____.

A

Not only to beta 2 agonists relieve bronchoconstriction due to their effects on smooth muscle, but they also decrease mast cell degranulation by binding to beta 2 receptors on the mast cells themselves.

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6
Q

Most common side effect of fluticasone

A

Thrush

Think about it: It decreases local immune activity. So, whatever infects the airways will be more likely to do so. As it happens, that is often Candida albicans.

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7
Q

What is the fundamental physical reason why emphysema patients can reach a new tidal breath pattern at a higher EELV?

A

Because the recoil forces of lung tissue are greater at higher volumes

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8
Q

In a state of dynamic hyperinflation, ___ is higher, but ___ is also higher. This is because ___.

A

In a state of dynamic hyperinflation, elastic recoil is higher, but work of inspiration is also higher. This is because muscles start at a lower length (beneath Lmax) and the respiratory system as a whole is less compliant.

So dyspnea is also increased.

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9
Q

“hyperresponsiveness” of airways

A

exaggerated response of airway smooth muscle to a wide variety of stimuli.

Seen in asthma, likely due to underlying inflammation

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10
Q

Extrinsic vs intrinsic asthma

A

extrinsic = atopic asthma

intrinstic = nonatopic asthma

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11
Q

Types of changes associated with asthmatic airway remodeling

A
  • epithelial damage (probably from proteases)
  • airway fibrosis
  • smooth muscle hyperplasia
  • nerve exposure
  • Abundant eosinophils and lymphocytes
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12
Q

Some hypothesized effects from nerve exposure in asthma

A
  • Low threshold for reflexes (irritant receptors are twitchy, cause bronchoconstriction)
  • Release of tachykinin mediators (susbstance P, neurokinin A)
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13
Q

Tachykinins

A

Released from neurons. Short peptides with common C-term domain. Can stimulate neuron depolarizaiton, potent vasodilators, cause smooth muscle contraction

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14
Q

Where do leukotrienes vs histamine come from within the mast cell?

A

Histamine is presynthesized and stored.

Leukotrienes are synthesized immediately before release.

This and the fact that leukotrienes have such short half lives makes them excellent substrates for transcellular metabolism-modifiable signaling, where as histamine pretty much does what it does.

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15
Q

LOX pathways starting with linoleic acid or arachadonic acid

A
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16
Q

Lipoxygenases from 10,000 ft

A
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17
Q

Leukotrienes are all downstream of ____

A

Leukotrienes are all downstream of 5-LOX

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18
Q

Resolvins are all downstream of ____

A

Resolvins are all downstream of 15-LOX

(and acetylated COX-2)

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19
Q

In many patients, the return of FEV1 to normal is followed by . . .

A

In many patients, the return of FEV1 to normal is followed by a secondary delayed fall in FEV1 occurring hours after antigen exposure

This “late phase response” is due to the influx of the inflammatory cells called by the mast cell.

immediate repsonse = effects of mast cell’s mediators on local cells

late response = the effects of the cells that the mast cell called upon

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20
Q

___ can frequently provoke bronchoconstriction in patients with hyperreactive airways. This has to do with ___

A

Exercise can frequently provoke bronchoconstriction in patients with hyperreactive airways. This has to do with the inhalation of relatively cool, dry air. If the exercising asthmatic pathient is inhaling warm, water-saturated air, this will not occur.

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21
Q

The greatest difficulty with expiration in asthma patients occurs when the patienst are asked to . . .

A

The greatest difficulty with expiration in asthma patients occurs when the patienst are asked to perform a forced expiration

With forced expiration, pleural pressure becomes much more positive, thereby promoting airway narrowing and closure as well as air trapping.

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22
Q

The most common pattern of arterial blood gases for acute asthma patients

A

a low Po2 accompanied by a low Pco2 (respiratory alkalosis)

Mechanism is V/Q mismatch

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23
Q

Samter syndrome

A

also known as the asthma triad

  1. Asthma
  2. Aspirin sensitivity
  3. Nasal polyps

Not uncommon among chronic asthma patients

24
Q

Major symptoms during an acute asthma attack are:

A
  1. Cough
  2. Dyspnea
  3. Wheezing
  4. Chest tightness
25
Q

status asthmaticus

A

State of an asthma patient during a particularly severe attack that is refractory to treatment with bronchodilators. This is an emergency.

May require assisted ventilation, and may even die as a result of the acute attack.

26
Q

Classification and Treatment of Asthma by Severity

A
27
Q

Useful tips for asthma diagnosis

A
  • If the patient produces sputum, check it for eosinophils. If they’re there, probably asthma
  • Skin and allergen inhalation tests not as helpful as you might expect
  • Better to test for hyperreactive airways generally than the above, this is done with methacholine (cholinergic agonist) or histmaine inhalation test. Asthma patients will respond to very low inhaled dosage.
  • Reversible airway obstruction test (with albuterol) is great
28
Q

Treatments for asthma (table)

A
29
Q

“chronic obstructive pulmonary disease”

A

chronic disorders that disturb airflow, whether the most prominent process is within the airways or within the lung parenchyma. The two disorders generally included in this category are chronic bronchitis and emphysema

30
Q

Genetic contribution to COPD

A

inherited deficiency of the protein α1-antitrypsin, encoded by the gene SERPINA-1

31
Q

Physiological changes in chronic smoking

A
  1. Increased # and size of mucous glands
  2. Thickening of airway wall due to hypertrophied and hyperplastic mucous glands
  3. Chronic airway inflammation
  4. Reduced cilia function
  5. Areas of fibrosis
32
Q

Protease-antiprotease hypothesis

A

Suggests that emphysema is the result of destruction of the connective tissue matrix of alveolar walls by proteolytic enzymes (proteases) released by inflammatory cells in the alveoli. In smokers, the balance between proteases and protease inhibitors is thought to be disturbed by multiple mechanisms.

Ex, neutrophil elastase and its inhibition by the α1-antitrypsin produced by lung tissue. If there is an increase in neutrophil elastase, the antitrypsin gets overwhelmed.

33
Q

Mechanisms that skew the protease-antiprotrease ratio in smokers

A
  1. Neutrophilic inflammation = more neutrophil elastase
  2. Oxidants derived from smoke or from inflammatory cells deactivate critical amino acid residues on antitrypsin
  3. Increased TRMs produce matrix metalloproteases
34
Q

Prominent lung proteases and their respective antiproteases

A
  • Matrix metalloproteases : TIMPs
  • Neutrophil elastase : α1-antitrypsin and secretory leukoprotease inhibitor
35
Q

Reid index

A

Relative thickness of the mucous glands with the total thickness of the airway wall

One way to assess hypertrophy and hyperplasia of mucous glands in chronic bronchitis

36
Q

panacinar/panlobular emphysema

A

Characterized by a relatively uniform involvement of the acinus, the region beyond the terminal bronchiole, including respiratory bronchioles, alveolar ducts, and alveolar sacs

37
Q

Centriacinar/centrilobular emphysema

A

In centrilobular emphysema, the predominant involvement and dilation are found in the proximal part of the acinus, the respiratory bronchiole.

38
Q

In cases of COPD with pure airway disease, ___ should be unchanged.

A

In cases of COPD with pure​ airway disease, FRC should be unchanged.

39
Q

Transpulmonary pressure by volume for emphysema

A
40
Q

How can COPD lead to pulmonary hypertension?

A

Hypoxia!

The V/Q mismatch and shunt physiology creates hypoxic vasoconstriction in non-oxygenated alveoli. If there are enough of these, then pulmonary circuit resistance gets pretty high, thus increasing the pressure necessary to drive fluid through the lung capillaries.

41
Q

Type A COPD

A

“Pink Puffer”

Underlying emphysema, high minute ventilation, and relatively normal PaO2

Represents “pure” emphysema

42
Q

Type B COPD

A

“Blue Bloater”

Chronic bronchitis, hypoxemia, and hypercapnia

Represents “pure” airway disease

43
Q

Rhonchi

A

Coarse gurgling sounds that may be heard in airways full of profuse airway secretions.

44
Q

Cor Pulmonale

A

Disease of the right ventricle secondary to lung disease

45
Q
A

Chest radiograph showing hyperinflated lungs

Emphysema patient

46
Q

Treating COPD

A
  • Bronchodilators
  • Corticosteroids during acute exacerbation
  • Phosphodiesterase-4 inhibitors
  • Supplemental oxygen (especially for pulmonary hypertension)
  • Vaccination against all preventable respiratory infections (particularly infleunza and pneumococcus)
  • Lung transplant
  • Mechanical ventilation
47
Q

“Respitarory failure”

A

Inability to breathe in a manner that supports the basic metabolic needs of the body

48
Q

‘Adaptation’ to hypercapnia

A

Acutely, hypercapnia will increase ventilation due primarily to effects on central chemoreceptors

Within days (chronically), however, kidneys will compensate and pH of blood and CSF will approach normal levels, and ventilation will come back down. And, because of the buffers now present in the blood, new increases in PaCO2 will have a diminished effect on ventilation.

49
Q

In patients with acute on chronic respiratory disease and chronic hypercapnia, if you give 100% oxygen, . . .

A

. . . their PaCO2 will go up by about 20 mmHg, but they will not decrease their ventilation.

The increase in PaCO2 is due to 1) vasodilation of alveoli with trapped CO2, and 2) the Haldane effect, more CO2 is released.

50
Q

Alveolar ventilation and carbon dioxide proportionality

A
51
Q

Visualization of Haldane effect

A
52
Q

____ is the most accurate spirometric measure of dynamic hyperinflation

A

Inspiratory capacity is the most accurate spirometric measure of dynamic hyperinflation

53
Q

In a patient with airflow obstruction on spirometry, what would be most indicative of COPD as the diagnosis?

A

Elevated residual volume

54
Q

In COPD, airway inflammation is notable for ___.

In asthma, airway inflammation is notable for ___.

A

In COPD, airway inflammation is notable for neutrophils.

In asthma, airway inflammation is notable for eosinophils.

55
Q

A 67 year old man with a confirmed diagnosis of COPD presents to clinic for evaluation. His only medication is a short-acting beta-agonist that he uses as needed for intermittent shortness of breath. His FEV1 today is 45% predicted. He relays to you that he was hospitalized once in the last year for an acute exacerbation of COPD. He describes being able to walk for only 2-3 minutes before having to stop to catch his breath. On exam today, he has decreased air movement bilaterally but no wheezing or crackles on pulmonary auscultation. He states that he feels at his baseline, with resting shortness of breath, but not markedly different from over the past few months.

Which are the most important next steps in his management?

A

Provide a long-acting beta agonist inhaler and an inhaled corticosteroid inhaler

HMS Homeostasis I (62 decks)

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