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Clin Med I- PULMONARY > OSA > Flashcards

OSA Flashcards

1
Q

Is COPD reversible?

A

Partially, but not fully reversible

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2
Q

What systemic manifestations is severe COPD associated with?

A

Cachexia, generalized weakness, osteoporosis, depression, anxiety, coronary artery disease

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3
Q

In which disease is there permanent enlargement of airspaces?

A

Emphysema

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4
Q

Role of alpha-1-antitrypsin

A

Inhibits elastase, keeping the balance of breakdown of elastic fibers in check

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5
Q

Name 5 risk factors for COPD

A

Smoking, exposure to occupational dusts, family history of COPD, alpha-1-antitrypsin deficiency, and older than 45 years

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6
Q

How is DLCO affected in asthma?

A

Increased

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7
Q

How are DLCO, RV, and TLC affected in COPD, particularly emphysema?

A

Decreased DLCO because of decrease in capillary bed due to lung parenchyma loss in COPD, and increased RV and TLC due to air trapping causing hyperinflated lung indicative of air trapping, in emphysema

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8
Q

Top causes of chronic cough (more than or equal to 8 weeks)

A

UACS (upper airway cough syndrome) or post-nasal drip (sinusitis leads to excessive mucus which accumulates in back of throat), asthma, GERD, and chronic bronchitis. Also, role of ace inhibitors and bordatella pertussis.

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9
Q

Expiratory time in COPD

A

Forced expiration time greater than 6 seconds, normal is 3

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10
Q

COPD classifications according to GOLD criteria

A

Stage 1 mild, 2-moderate, 3-severe, 4-very severe

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11
Q

Normal FEV1/FVC ratio

A

greater than or equal to 80%

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12
Q

FVC and FEV1 normals

A

should be greater than or equal to 80%

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13
Q

5 A’s and R’s in behavior interventions of COPD smoking management

A

Ask, advise, assess, assist, arrange. Relevance, risks, rewards, roadblocks, repeat.

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14
Q

Bronchodilators used in COPD management

A

Beta 2 agonists and anticholinergics

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15
Q

Beta 2 agonist short acting and long acting

A

short acting- albuterol, levalbuterol, pirbuterol. long acting- salmeterol, formoterol, indacaterol

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16
Q

anticholinergics as bronchodilators- name

A

Short acting- ipratropium. long acting- tiotropium

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17
Q

Inhaled corticosteroids for management of COPD

A

Fluticasone, budesonide

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18
Q

COPD medications-name

A

Bronchodilators, corticosteroids, combinations, methylxanthines, phosphodiesterase-4 inhibitors, mucolytic agents (little management), and antibiotics for acute exacerbations

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19
Q

What is methylxanthine and name a couple

A

Phosphodiesterase inhibitors- theophylline and aminophylline

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20
Q

Side effect of inhaled corticosteroids?

A

Thrush- tell patients to swish and spit 3 x

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21
Q

What are different ways in which bronchodilators can be administered?

A

Metered dose inhalers, dry powder inhalers, and nebulizers

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22
Q

How do phosphodiesterase-4 inhibitors work?

A

Increase intracellular cAMP and decrease inflammation. Promote airway smooth muscle relaxation. Decrease exacerbations if frequent of chronic bronchitis. Ex: Roflumilast PO.

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23
Q

What is pirbuterol?

A

Short acting Beta 2 agonist used for bronchodilation

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24
Q

What is theophylline?

A

Methylxanthine, phosphodiesterase inhibitor

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25
Q

What is Roflumilast?

A

Phosphodiesterase-4 inhibitor

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26
Q

What is budesonide

A

Inhaled corticosteroid to suppress immune system

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27
Q

What is tiotropium?

A

Long acting anticholinergic

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28
Q

What is indacaterol?

A

Long acting beta 2 agonist for bronchodilation

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29
Q

What is ipratropium?

A

Short acting anticholinergic

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30
Q

Mucolytic agents

A

Guaifenesin, N-acetylcysteine

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31
Q

Meds for acute exacerbations in COPD

A

Abx- macrolides, sulfa drugs, tetracyclines, penicillins, cephalosporins, and/or FQs. Chronic azithromycin.

32
Q

What would help in reducing frequency of acute exacerbations in COPD?

A

Azithryomycin

33
Q

Predominant organisms causing acute exacerbations in COPD?

A

H. influenzae, strep pnuemo, moraxella catarrhalis, although usually viral infection precedes exacerbations

34
Q

Advanced COPD complications

A

Pulmonary HTN, cor pulmonale, chronic respiratory failure

35
Q

Cardinal features of asthma

A

Reversible airway obstruction, airway inflammation, and airway hyperresponsiveness to a multiplicity of stimuli

36
Q

In which disease state would you see a lot of eosinophils, mast cells activated, subepithelial fibrosis, and mucous gland and goblet cell hyperplasia and what would this lead to?

A

Asthma- lots of mucus, leads to mucus plugging and further narrowing/blockage of airways

37
Q

When is the onset of asthma most common?

A

in childhood. If in adulthood, often occupation related.

38
Q

What is the predominant symptom in asthma patients?

A

Nonproductive cough

39
Q

Associated conditions with asthma

A

Nasal polyps (have allergic etiology), rhinitis, and sinusitis

40
Q

8 year old girl presents describes periods of dyspnea, chest tightness, and coughing. Upon auscultation, you hear wheezes, decreased breath sounds. Hyperinflation of lungs and use of accessory muscles to breathe. She also has a history of getting nasal polyps frequently. Diagnosis?

A

Asthma

41
Q

How would you diagnose asthma?

A

Bronchoprovocation testing with methacholine if normal spirometry and you are suspicious. Allergy skin test or radioallergosorbent test, ABG

42
Q

If you see a severe asthma patient with normal PaCO2 levels, what do you suspect?

A

Respiratory failure

43
Q

What is a radioallergosorbent test?

A

Tests serum IgE levels

44
Q

What are the classifications in asthma based on?

A

frequency of daytime/nighttime symptoms, need for rescue inhaler, limitation in activity, and lung function. Severity is based on worse feature present

45
Q

Which obstructive diseases are very prone for recurrent bacterial infections?

A

CF and chronic bronchitis

46
Q

What is the most common genetic cause of bronchiectasis?

A

CF

47
Q

Etiology of CF

A

Genetic defect of chromosome 7 which produces a defective CFTR gene

48
Q

What cells are effected by CF

A

Of epithelial origin- lungs, sinuses, GI system, sweat glands, hepatobiliary system, reproductive tract

49
Q

In which age of CF would you find clinical features of tachypnea, feeding problems, retractions, and recurrent sinopulmonary infections?

A

Infant

50
Q

In which age of CF would you find clinical symptoms of rectal prolapse, jaundice, and meconium ileus?

A

Neonate

51
Q

In which age of CF would you find clinical features of diffuse rhonchi/rales, clubbing, cough, and hemoptysis?

A

Child or adolescent

52
Q

What is the most common cause of clubbing in children?

A

CF

53
Q

16 year old presents with cough, recurrent hemoptysis. You note diffuse rhonch and rales, clubbing of the extremities, and steatorrhea. Hyperresonance to percussion. Mother complains that child is unable to gain weight, no matter how much he eats. Delayed sexual maturity. Diagnosis?

A

CF

54
Q

Why would you get a sputum culture in CF?

A

To monitor if bronchiectasis has developed within the patient- most common organisms affecting are Staph and H. influenzae

55
Q

Diagnosis of CF

A

Sweat chloride test, genetic test to look for 2 CF alleles, family history with first degree relative of CF, nasal potential difference, cXR, PFT, sputum culture, fecal fat analysis, semen analysis,

56
Q

Why do a semen and fecal fat analysis in CF?

A

Because of pancreatic insufficiency, the small intestine is not digesting the fats. This leads to steatorrhea in which theres excessive discharge of fat in the feces. Semen analysis will show decreased sperm.

57
Q

What would CXR tell you in CF?

A

Do this if suspicious of bronchiectasis. May see hyperinflation and ring shadows and cysts.

58
Q

What is nasal potential difference testing?

A

Measures how well sodium and chloride flow across the mucous membranes in the nose

59
Q

False positives for sweat chloride test in CF

A

AAddisons, hypothyroidism, nephrogenic diabetes insipidus

60
Q

When is the sweat chloride test positive?

A

when chloride is greater than 60mmol/L in children

61
Q

What is death usually due to in CF?

A

Respiratory failure

62
Q

Median survival age of CF

A

36 years

63
Q

Lung transplantation for CF should not occur if chronic infection with this organism

A

Burkholderia cenocepacia

64
Q

How does Ivacaftor work

A

Is a CFTR modulator in CF patients with G551D mutation. It increases the amount of time the CFTR channel remains open.

65
Q

4 components of therapy for CF

A

Mobilization of secretions, nutritional interventions, ATB therapy of chronic bronchiectasis, and control of airway inflammation

66
Q

Patient presents with chronic cough, purulent, foul smelling sputum, fever, weakness, weight loss. Rale, rhonchi, and wheezes heard on auscultation. CXR shows bronchial wall thickening and airway dilation. What is the diagnosis?

A

Bronchiectasis- suspect diagnosis if chronic bacterial infection and the production of large quantities of foul-smelling sputum

67
Q

Are recurrent infections with bronchiectasis common?

A

Yes

68
Q

Diagnosis for bronchiectasis

A

Definitive test by HRCT- dilated airways that are thickened due to mucopurulent plugs (tree in bud pattern). CXR shows bronchial wall thickening, ring shadows with cysts. CBC, sputum culture and smear to check if bacterial cause, PFT, bronchoscopy

69
Q

What condition can bronchiectasis lead to?

A

Pulmonary HTN

70
Q

Who does bronchiolitis most commonly affect?

A

Infants and kids

71
Q

Most common cause of bronchiolitis?

A

RSV- especially in witner months, and rhinovirus

72
Q

3 main types of bronchiolitis in adults

A

Proliferative, constrictive, or follicular

73
Q

Clinical features of bronchiolitis in children

A

Tachypnea, retractions, wheezing on expiration, grunting, nasal flaring cyanosis

74
Q

Clinical features of bronchiolits in adults

A

Sneaky onset of cough and dyspnea

75
Q

How is bronchiolitis diagnosed?

A

Clinically

Clin Med I- PULMONARY (7 decks)

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