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Respiratory > Obstructive Pulmonary Diseases > Flashcards

Obstructive Pulmonary Diseases Flashcards

1
Q

This is when elastin fibers are destroyed, leading to more compliance and an increase in FRC.

A

Emphysema

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2
Q

This is when there is decreased compliance, increased elasticity, and decrease in FRC.

A

Pulmonary fibrosis

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3
Q

This a slow waxing and waning respiration occuring about every 40-60s.

A

Cheyne-Stokes breathing

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4
Q

Which 2 types of patients get Cheyne-Stokes breathing?

A
  1. Cardiac failure- b/c blood flow is slow.

2. Brain dmg- cuz resp drive is slow.

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5
Q

This is the absence of spontaneous breathing during normal sleep.

A

Sleep apnea

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6
Q

This is when there is blockage of the upper airway which causes an absence of spontaneous breathing during sleep.

A

Obstructive sleep apnea

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7
Q

Besides your significant other trying to kill you, what causes obstructive sleep apnea?

A

be fat –> too much relaxation of pharyngeal muscles –> snoring gasps

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8
Q

This is the type of sleep apnea where the CNS drive to the ventilator muscles transiently ceases.

A

Central sleep apnea

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9
Q

What causes central sleep apnea?

A

Damage to the central respiratory centers or abnormalities of the respiratory neuromuscular apparatus (like from strokes)

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10
Q

Emphysema destroys capillaries –> ↑ pulmonary resistance –> pulmonary HTN –> ____ _______ _______

A

Right heart failure

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11
Q

What is the cause of asthma is 70% of the cases?

A

Allergic hypersensitivity (plants and smog)

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12
Q

What is the main chemical to cause bronchoconstriction in asthma?

A

Slow-reacting substance of anaphylaxis

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13
Q

What happens to inspiration an expiration problems in asthma?

A

pt can inspire normally but cannot expire

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14
Q

What are the 2 main diseases for COPD?

A

Emphysema

Chronic bronchitis

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15
Q

What makes asthma different than emphysema and chronic bronchitis?

A

It’s reversible.

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16
Q

In centriacinar emphysema, there is significant airway obstruction causing damage where, the bronchioles or distal alveoli?

A

bronchioles

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17
Q

What is typically found in the walls of the emphysematous spaces in centriacinar emphysema?

A

Black pigment

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18
Q

Where is panacinar emphysema located in the lung?

A

The acini from the bronchiole –> alveoli at the lower zones and anterior margins of the lungs.

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19
Q

What condition is panacinar emphysema associated with?

A

a1-antitrypsin deficiency

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20
Q

What is centricainar emphysema associated with?

A

smoking

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21
Q

this is the type of emphysema where the proximal portion of the acinus is normal and the distal part is predominantly involved.

A

Paraseptal (distal acinar) emphysema

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22
Q

Where in the lung is paraseptal emphysema located?

A

Against the pleura along the lobular connective tissue septa in the upper 1/2 of the lungs.

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23
Q

This is dilation of alveoli, but no destruction of septal walls in response to loss of lung substance elsewhere. It is best exemplified by hyperexpansion of the residual lung parenchyma that follows removal of a diseased lung or lobe.

A

Compensatory hyperinflation

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24
Q

This is the lung expands because air is trapped within it. A common cause is because of tumor or foreign object obstruction that lets air in, but doesn’t let it out.

A

Obstructive overinflation

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25
Q

This is a large subpleural bullae that occur in any form of emphysema. They represent localized accentuations of emphysema and occur near the apex, sometimes in relation to old tuberculosis scarring

A

Bullous emphysema

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26
Q

This is when alveolar tears in pulmonary emphysema provide the avenue of entrance of air into the stroma of the lung, but rarely, a wound of the chest that allows air to be sucked in or a fractured rib that punctures the lung substance may underlie this disorder

A

Intersitital emphysema

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27
Q

After how much parenchyma is destroyed in emphysema b4 u get Sx?

A

1/3

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28
Q

What causes death in emphysema?

A

Respiratory acidosis and coma, RHF, an massive collapse of the lungs secondary to pneumothorax.

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29
Q

How long must u have a persistent cough with sputum production to have chronic bronchitis?

A

at least 3 mo within 2 consecutive years

30
Q

What are the 4 hallmarks to asthma?

A
  1. episodic bronchoconstriction
  2. inflammation of the bronchial walls
  3. increased mucus secretion
  4. curshmann spiral, charcot laden
31
Q

This is the most common type of asthma hwere there is a type I IgE-mediated hypersensitivity rxn to environmental allergens.

A

Atopic asthma

32
Q

This is the type of asthma due to virus-induced inflammation of the respiratory mucosa which lowers the threshold of the subepthelail vagal receptors to irritants.

A

Non-atopic asthma

33
Q

In drug-induced asthma, which drug causes asthmatic attacks by elabortating bronchoconstrictor leuktotrienes?

A

ASA

34
Q

Which type of asthma is stimualted by fumes, organic and chemical dusts, gases, and other chemicals?

A

Occupational asthma

35
Q

What is the severe form of asthma, where there is severe cyanosis and death from airflow obstruction?

A

Status asthmaticus

36
Q

This condition is when there is severe, persistent cough, expectoration of floul smelling blood sputum, dyspnea and orthopnea in severe cases, and occasiaonally life-treatening hemoptysis.

A

Bronchiectasis

37
Q

What are the SANS receptors to the lungs?

A

B2

38
Q

What are the PANS receptors to the lungs?

A

M3

39
Q

What happens with SANS receptors are activated?

A

Bronchodilation

40
Q

Which hormone stimulates SANS receptors the best?

A

Epinephrine

41
Q

What is the first line drug for the Tx of acute asthmatic Sx?

A

Albuterol

42
Q

What are the 2 indications for anticholinerigic agents?

A
  1. COPD

2. Acute asthma attacks when B2 agonists are contraindicated

43
Q

What are the 6 bronchoconstricting peptides?

A
  1. ) Neurokinin A
  2. ) Calcitonin gene-related peptide
  3. ) Substance P
  4. ) Bradykinin
  5. ) Tachykinin
  6. ) Neuropeptide Y
44
Q

What are the 2 bronchodilators released from nonadrenergic noncholinergic (NANC) fibers?

A
  1. NO

2. Vasoactive

45
Q

Which lymphocytes are the key role in the immune response in asthma?

A

T cells (CD8 and CD4)

46
Q

Case: your pt has ASTHMA but has cardiac ischemia. what is the DOC?

A

Ipratropium

47
Q

Why is ipatropium better than atropine for treating asthma?

A

Less side effects

48
Q

This is the drug for COPD which is a competitive antagonist at muscarinic (M3) receptors –> bronchorelaxation and decreased mucus secretion.

A

Tiotropium

49
Q

Terbutaline, albuterol, pirbuterol, and bitolterol are good for bronchidilation because they bind almost exclusively to which receptors and activate them?

A

B2

50
Q

What do you avoid using an albuterol inhaler rather than something oral?

A

Avoids systemic effects

51
Q

Since B2 receptors are also expressed in peripheral SkM, what can be a side effect of high B2 agonists?

A

Tremors

52
Q

Why are new drugs like Formoterol and Salmeterol good as prophylactic drugs for asthma?

A

They have a longer duration of action (12-24hr)

53
Q

Why must u use fomoterol and salmeterol with corticosteroids?

A

They control the asthma but do not treat the underlying inflammation

54
Q

How does methylxanthines cause bronchodilation?

A

nonspecific inhibition of PDE isoenzymes III and IV –> prevents cAMP degredation –> smooth muscle relaxation

55
Q

Which receptor does Theophylline block?

A

Adenosine

56
Q

Why can’t u give cimetidine with theophylline?

A

Cimetidine is a P450 inhibitor and theophylline is metabolized by P450 isoenzyme CYP3A

57
Q

What is the chief preventative agent for the Tx of asthma?

A

Inhaled corticosteroids

58
Q

Corticosteroids increase the transcription of which receptors, leading to a prophylacitic mechanism for asthma?

A

B2

59
Q

Corticosteroids decrease the transcription for which proteins?

A

pro-inflammatory proteins like IL4 and IL5

60
Q

Corticosteroids also decrease which cells in the airways for the Tx of asthma?

A

inflammatory cells

61
Q

What is the 1 limitation of coticosteroids in the Tx of asthma?

A

it cannot reverse airway remodeling

62
Q

Where is the substitution to cause corticosteroids to work as inhaled agents?

A

17-alpha

63
Q

This drug prevents the immediate allergic response in allergic asthma by decreasing the activity of mast cells.

A

Cromolyn

64
Q

What pathway do montelukast and zafirlukast inhibit for the Tx of asthma?

A

Leukotriene pathway

65
Q

Which receptor do montelukast and zafirlukast inhibit?

A

CysLT1 receptor

66
Q

How does omalizumab treat asthma?

A

It decreases the quantity of circulating IgE and prevents the remaining IgE from binding to mast cells.

67
Q

Which GI condition may exasterbate asthma?

A

GERD

68
Q

What must be coexisting in the pt to cause allergic bronchopulmonary aspergillosis?

A

Asthma or CF

69
Q

True or False: to treat allergic bronchopulmonary aspergillosis, you can give corticosteroids or antifungals.

A

FALSE. Antifungals don’t work.

70
Q

How do u treat obstructive sleep apnea?

A

CPAP or BiPAPmachine

Respiratory (9 decks)

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