Clin Med: Pulm I Flashcards

1
Q

What kind of disorder is asthma?

A

chronic inflammatory airway disorder w/ obstruction

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2
Q

What can predispose you to asthma? (endogenous)

A
  • genetic predisposition
  • atopy
  • airway hyperresponsiveness
  • gender
  • ethnicity
  • obesity
  • early viral infx
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3
Q

What can predispose you to asthma? (environmental)

A
  • indoor & outdoor allergens
  • occupational sensitizers
  • passive smoking
  • respiratory infxs
  • air pollution
  • diet
  • dampness & mold exposure
  • acetaminophen
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4
Q

Asthma triggers

A
  • allergens
  • viral URI
  • exercise & hyperventilation
  • cold air
  • sulfur dioxide & irritant gases
  • drugs (B-blockers, aspirin)
  • stress
  • irritants
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5
Q
A
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6
Q

Asthma pathophysiology

A

1) trigger
2) airway inflammation
3) combo: hypersecretion of mucus, airway muscle constriction, swelling bronchial membranes
4) narrow breathing passages
— small & large airways
5) wheezing, cough, SOB, tightness in chest

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7
Q

Asthma: History

A
  • recurrent wheezing
  • difficulty breathing
  • chest tightness
  • cough
  • can be WORSE AT NIGHT
  • family history of asthma, allergy, atopy
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8
Q

It is unlikely asthma if

A
  • lack of improvement after Tx w/ bronchodilator
  • onset after 50
  • Hx of >20 pack year history smoking
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9
Q

Asthma: clinical findings

A
  • EXPIRATORY wheezing
  • multiple pitches starting & stopping in the resp cycle
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10
Q

Asthma: clinical finding if severe airflow obstruction

A
  • tachypnea
  • tachycardia
  • decreased 02 saturation
  • accessory muscle usage
  • tripod position
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11
Q

Asthma: signs of atopy

A
  • cobblestone appearance of pharynx (allergic rhinitis)
  • nasal polyps
  • atopic derm
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12
Q

Which cell has an excessive reaction during asthma

A

TH2 cells (involved in atopic triad)

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13
Q

What does IL-4 do?

A
  • activated IgE antibodies
  • they bind to mast cells & release histamines, leukotrienes, & prostaglandins
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14
Q

What does IL-5 do?

A
  • activates eosinophils
  • stimulates release of cytokines & leukotrienes
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15
Q

With obstructive disorders, patients cannot fully ___.

A

exhale

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16
Q

With restrictive disorders, patients cannot fully ___.

A

inhale

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17
Q

Test to run when there is clinical suspicion of asthma.

A
  • PFT or chest x-ray
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18
Q

Pulmonary Function testing involves___

A
  • spirometry measuring FEV1 & FVC
  • bronchodilator response
  • Bronchoprovocation testing
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19
Q

What is spirometry measuring

A

how much air is being exhaled at any time

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19
Q
A
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20
Q

Chest x-ray involves___

A
  • done if Dx is unclear
  • CXR almost always normal in asthma
  • Helpful if Pt. has fever, chronic purulent sputum, hemoptysis, weight loss (rules things in/out)
  • Possible CT if CXR abnormal
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21
Q

Review: FEV1 & FVC

A
  • forced expiratory volume in 1 sec
  • forced vital capacity (total exhaled air)
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22
Q

Describe Asthma: intermittent

A
  • symptoms </= 2x a week
  • night symptoms </= 2x monthly
  • rescue meds </= 2days/week
  • asymptomatic b/t flares
  • FEV1 > 80% of predicted
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23
Q

Describe asthma: mild persistent

A
  • symptoms > 2x a week but not daily
  • night symptoms 3-4x monthly
  • rescue meds > 2 days/wk but not > 1x/day
  • minor limitations b/t flares
  • FEV1 > 80% predicted
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24
Q

Describe asthma: moderate persistent

A
  • symptoms are daily
  • night symptoms > 1x a week, but not nightly
  • rescue meds daily
  • some limitation b/t flares
  • FEV1 > 60% predicted
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25
Q

Describe asthma: severe persistent

A
  • symptoms throughout the day
  • night symptoms several times per day
  • rescue meds several times/day
  • extremely limitations
  • FEV1 < 60% predicted
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26
Q

GINA cycle of asthma care - 3 steps

A
  1. Assess: dx, inhaler comprehension, Pt. preferences, symptom control
  2. Tx: meds, non pharm strategies, Treat modifiable risk factors
  3. Review: symptoms exacerbations, SEs of meds, lung function, Pt. satisfaction
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27
Q

What are the two goals of asthma care?

A
  • decrease impairment
  • decrease risk of severe attack
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28
Q

Non-pharm Tx for asthma

A
  • encourage exercise
  • stop smoking
  • Pt. edu
  • control triggers
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29
Q

What are the starting points for treatment in asthma: stages and which severity stage

A

Stage 1: mild intermittent
Stage 2: mild persistent
Stage 3: moderate persistent
Stage 4: severe persistent

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30
Q

Asthma: stage 1 Tx

A
  • mild intermittent
  • low dose ICS - formoterol OR
    low dose ICS

-control & rescue are the same b/c this is the mild intermittent asthma

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31
Q

Asthma: stage 2 Tx

A
  • mild persistent
  • Con: low dose inhaled corticosteroid (ICS)
  • Res: ICS - formoterol
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32
Q

Asthma: stage 3 Tx

A
  • moderate persistent
  • Con: low dose ICS-LABA
  • Res: ICS formoterol or SABA
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33
Q

Asthma: stage 4 Tx

A
  • severe persistent
  • Con: medium dose ICS-LABA
  • Res: ICS - formoterol or SABA
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34
Q

Asthma: stage 5 Tx

A
  • Con: high dose ICS-LABA
  • Res: ICS-formoterol or SABA
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35
Q

Asthma is being controlled if…

A
  • daytime symptoms None (</= 2/wk)
  • no limits to activities
  • no night awakenings
  • rescue meds (</= 2/week)
  • normal lung function
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36
Q

Asthma is partially controlled if…

A
  • daytime symptoms >/= 2/week
  • any limits to activities
  • any night awakenings
  • rescue meds >2x/wk
  • < 80% predicted
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37
Q

Asthma: w/ kids, what is the preferred method of rescue?

A

SABA (albuterol)

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38
Q

Say you are in a primary care office and a patient comes in with the following symptoms, what would your treatment be?

broken sentences, not agitated, inc RR, HR 100-120, no acc. m. use, RA = 90-95%

A
  • mild/moderate asthma
  • SABA via MDI or neb
    prednisolone: oral or IV
    O2 if needed
  • reassess at 1 hour: if improved discharge with at home instructions
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39
Q

Say you are in a primary care office and a patient comes in with the following symptoms, what would your treatment be?

speaking in words, tripoding, rr>30, acc. m. use, HR= > 120

A

-severe asthma

  • call 911
  • SABA
  • ipratropium
  • O2
  • prednisolone
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40
Q

Asthma: mild (dyspnea w/ activity) Exacerbations Tx

A
  • SABA (inhaled or nebulizer)
  • short course oral corticosteroids
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41
Q

Asthma: moderate (dyspnea interferes w/ activity–> symptoms improve in 1-2 days) exacerbations Tx

A
  • SABA (may add ipratropium)
  • Oral corticosteroids
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42
Q

Asthma: severe (dyspnea at rest) last longer than 3 days exacerbations Tx

A
  • req hospitalization
  • SABA/ipratropium hourly or continuously
  • oral corticosteroids
  • adjunctive tx (02 therapy, IV MgSO4, intubation/mechanical ventilation)
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43
Q

When do you refer a patient w/ asthma to a specialist?

A
  • S/S are atypical
  • Difficulty achieving or maintaining control of asthma
  • Persistent asthma requiring step 4 care or higher
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44
Q

Asthma: Pt. Edu

A
  • smoking cessation
  • avoid triggers
  • pneumococcal/flu vaccine recommended
  • caution w/ NSAIDS/ASA (esp. aspirin)
  • asthma diary
  • properly use inhalers
  • clear asthma tx plan w/ an emergency care plan in place
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45
Q

Risk of asthma related death increased if ___

A
  • previous severe exacerbation
  • 2 or more hospitalization in the past year
  • 3 or more ED visits in the past year
  • 2 or more canisters of SABA per month
  • low socioeconomic status or inner-city resident
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46
Q

COPD is characterized by

A

persistent respiratory symptoms & airflow limitation that is not fully revisible

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47
Q

COPD includes what 3 conditions? (that occur together)

A
  • chronic bronchitis
  • emphysema
  • small airway disease
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48
Q

Chronic bronchitis clinical dx is defined by___

A

excessive secretion of mucous & daily cough for 3 months or more in 2 consecutive year

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49
Q

Emphysema is a pathologic dx with ___

A

abnormal enlargement of air spaces distal to the terminal bronchiole, w/ destruction of alveolar walls

(Look at lung tissue itself. can be seen on CT)

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50
Q

Risk factors for COPD

A
  • cigarette smoking
  • occupational exposures
  • ambient air pollution
  • 2nd hand smoke
  • genetic (alpha 1 antitrypsin deficiency)
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51
Q

Chronic bronchitis large airways pathophys

A

oxidants from cigarette smoke cause mucous gland hyperplasia –> increased mucous production–> chronic cough

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52
Q

chronic bronchitis small airways pathophys

A

edema/increases mucous production/fibrosis–> airway narrowing/airway resistance

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53
Q

Chronic bronchitis alveoli pathophys

A
  • macrophages release enzymes that digest alveolar walls–> decreases area for gas exchange–> damage to capillaries
  • damage to elastin fibers causes airway collapse
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54
Q

Emphysema pathophys

A
  • structural changes in alveoli
  • inflammatory reaction in the alveoli attract immune cells, release chemicals/enzymes–> breaks down collagen & elastin
  • airways collapse during exhalation, causing air trapping
  • alveoli eventually coalesce into large air filled spaces (reduced surface area for gas exchange)
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55
Q

Chronic bronchitis: pink puffer s/s

A

-CO2 retention*
-min cyanosis*
-pursed lip breathing*
-dyspnea
-hyperressonance
-barrel chest*
-prolonged expiration
-anxious
-accessory muscle use
-thin

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56
Q

Chronic bronchitis: blue bloater s/s

A

-airway flow problem
-cyanotic
-recurrent cough and sputum
-hypoxia
-hypercapnia
-resp. acidosis
-inc Hgb
-digital clubbing
-enlarged heart
-accessory m use
-right side heart failure: bilateral pedal edema, JVD

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57
Q

Age when COPD presents…

A

40-50 years old

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58
Q

COPD Hx symptoms that may be present for months-years…

A
  • cough
  • sputum production
  • exertional dyspnea
  • physical activity changes?
  • smoking?
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59
Q

Symptoms in Hx for advanced COPD

A
  • hypoxemia
  • pneumonia
  • pulmonary HTN
  • Cor pulmonale
  • Respiratory failure
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60
Q

PE findings in early stages of COPD

A

usually normal exam

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61
Q

PE findings in later stages of COPD

A
  • prolonged expiratory phase
  • expiratory wheezing
  • signs of hyperinflation
  • accessory muscle use/ cyanosis in acute exacerbation
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62
Q

PE findings in advanced COPD

A

cachexia (very poor Px factor)

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63
Q

PE findings in acute exacerbation of COPD

A
  • wheezing, tachypnea, decreased mental status
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64
Q

Most acute exacerbations of COPD are triggered by___

A

resp infx

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65
Q

Dx testing for COPD

A
  • PFT
  • Chest x-ray
  • CT
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66
Q

Dx results of PFT for COPD

A

reduction in FEV1 & FEV1/FVC

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67
Q

Dx results for chest x-ray in COPD

A

normal or show hyperinflation w/ emphysema

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68
Q

Why run a CT in pt. with COPD

A

more sensitive/specific for dx of emphysema

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69
Q

What is used to assess the severity of COPD

A

“CAT” score

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70
Q

Describe the “CAT” score

A

used to assess progression, decline in functional status, & gauge effectiveness of pulm rehab

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71
Q

COPDL: initial Tx is based on

A

GOLD classification:
this is the CAT score + number of exacerbations

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72
Q

COPD: what is the Tx for a pt. w/ a CAT <10 & >2 moderate exacerbations w/ 1 leading to hospitalizations?

A

LAMA
Group C

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73
Q

COPD: what is the tx for a pt w/ a CAT <10 & 1 or 2 exacerbations w/o hospitalization?

A

bronchodilator
Group A

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74
Q

COPD: what is the Tx for a pt. w/ a CAT of 10 or more & >2 exacerbations w/ a hospitalization?

A

LAMA + LABA or
ICS + LABA
Group D

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75
Q

COPD: what is the Tx for a pt. w/ a CAT of 10 or more & 0-1 exacerbations leading to no hospitalizations?

A

LABA or LAMA
Group B

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76
Q

Describe the group categories for COPD.

A
  • Group A: less symp, low risk
  • Group B: more symp, low risk
  • Group C: less symp, high risk
  • Group D: more symp, high risk
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77
Q

Describe COPD: Group A

A

less symp, low risk

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78
Q

Describe COPD: Group B

A

more symp, low risk

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79
Q

Describe COPD: Group C

A

less symp, high risk

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80
Q

Describe COPD: Group D

A

more symp, high risk

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81
Q

COPD: medications for acute exacerbations

A
  • albuterol (SABA) (inhale or neb)
  • ipratropium (anticholinergic)
  • prednisone (oral glucocorticoids)
  • Abx (mod or severely ill patients)
  • O2, bipap, intubation if needed
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82
Q

COPD: Abx that can be used to treat acute exacerbations

A
  • levofloxacin
  • moxifloxacin
  • doxycycline
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83
Q

COPD: Pt. Edu

A
  • smoking cessation
  • get flu & pneumococcal vaccine
  • careful exercise programs
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84
Q

Make a COPD referral if…

A
  • onset before 40yo
  • 2+ exacerbations/year
  • severe or rapid progression
  • need for long term O2 therapy
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85
Q

Make a COPD admission to hospital if…

A
  • failing to respond to outpatient tx
  • worsening hypoxemia, peripheral edema
  • can’t maintain nutrition/hydration due to symptoms
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86
Q

With COPD, what is alpha 1 antitrypsin (A1AT)deficiency?

A

an autosomal dominant genetic disorder that leads to an overproduction of elastace

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87
Q

COPD: What is elastace?

A

an enzyme that breaks down elastin in the lungs & liver

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88
Q

When to suspect A1AT deficiency in a Pt?

A

develop COPD earlier than age 40

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89
Q

COPD: Dx test for A1AT deficiency

A
  • serum level of A1AT
  • genetic testing
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90
Q

COPD: Tx for A1AT deficiency

A
  • COPD Tx + infusions of A1AT
  • Lung transplant
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91
Q

Bronchiectasis is a disease of what?

A
  • bronchi & bronchioles
  • permanent dilation & destruction of bronchial walls
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92
Q

Bronchiectasis: focal development

A

obstruction (aspirated foreign body, mass)

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93
Q

Bronchiectasis: diffuse development

A

infection
immunodeficiency (AIDs)
genetic
autoimmune
recurrent aspiration
idiopathic (most common)

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94
Q

Bronchiectasis: infectious pathophysiology

A

poor mucociliary clearance results in microbial colonization

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95
Q

Bronchiectasis: non infections pathophysiology

A

immune mediated reactions that damage the bronchial wall

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96
Q

Bronchiectasis: biggest pathophys concern

A

IMPAIRED SECRETION CLEARANCE

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97
Q

Bronchiectasis: History

A

persistent productive cough w/ ongoing production of thick sputum

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98
Q

Bronchiectasis: Physical

A
  • crackles & wheezing on lung auscultation
  • In later stages, may have clubbing of digits
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99
Q

Bronchiectasis: Dx labs/imaging

A
  • CXR: “tram tracks”–> lacks sensitivity
  • Chest CT: “tram tracks” or “signet ring” appearance–> more more sensitive & specific
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100
Q

Bronchiectasis: treatment

A

-treat underlying disease
-hospitalization if tachy, hypotensive, fever, hypoxemia, failure to improve with abx
-mucolytic agents/airway hydration
-bronchodilators, oral/inhaled glucocorticoids

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101
Q

Bronchiectasis: acute exacerbation Tx

A

(based on culture results)
fluoroquinolone empirically (levofloxacin, moxifloxacin)

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102
Q

CF: genetic factor

A

autosomal recessive exocrinopathy

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103
Q

CF is a ___, ___, & ___ disease

A

respiratory, pancreatic, hepatobiliary

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104
Q

CF: which gene regulates chloride

A

CFTR

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105
Q

CF: pathophys

A

CFTR gene is affected–> Cl- channels don’t function right–> abnormal transport of Cl- & NA+ across epithelium–> results in abnormal secretions in the lungs & GI tract

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106
Q

CF: clinical findings

A
  • resp findings: productive cough, very thick sputum, wheezing, recurrent pneumonia, exercise intolerance, dyspnea
  • chronic airway infx begin in infants leading to bronchiectasis
  • severe sinus disease
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107
Q

CF: What is the cause of chronic airway infx?

A
  • S. aureus
  • pseudomonas
  • h. influenzae
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108
Q

CF: acute exacerbations hx/PE

A

increased cough, sputum production

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109
Q

CF: Dx - labs/imaging

A
  • ** Elevated sweat chloride (>60mmol/L)
  • genetic testing: presence of 2 dz causing mutations
  • abnormal nasal potential difference if other results are inconclusive
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110
Q

CF: Tx for airway clearance

A
  • inhaled tx (albuterol, hypertonic saline, Dnase)
  • Chest PT
  • Exercise
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111
Q

CF: prevention of infx tx

A
  • seasonal flu vaccine
  • pneumococcal vaccine
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112
Q

Influenza A & B cause seasonal epidemics during what time of the year?

A

October to May

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113
Q

Flu: Pathophys has what two types of glycoproteins in the outer membrane?

A
  • Hemagglutinin
  • Neuraminidase
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114
Q

Flu viruses are exceptionally good at:

A
  • Antigenic drift: mutations during replication that occur in HA & NA
  • Antigenic shift: complete change in HA, NA, or both
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115
Q

How is the flu spread?

A

via air droplets or contaminated hands

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116
Q

The flu virus ____ viscosity of ___, promoting _____.

A

lowers; mucous, spread of the virus

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117
Q

Flu: incubation time & viral shedding time

A

Incubation: 1-4 days
Viral shedding: from one day prior to sx to day 5

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118
Q

Flu: History/Physical

A
  • Sudden onset fever, chills, fatigue, myalgia, malaise
  • appears ill w/ sweating, coughing, diffuse pharyngeal erythema
  • lung exam w/ scattered rales, rhonchi, wheezes
  • may have muscle pain elicited w/ pressure
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119
Q

Flu: Dx - Labs/Imaging

A
  • largely based on clinical findings
  • nasal swab for rapid test
  • nasal swab for PCR
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120
Q

Flu: tx

A

oral oseltamivir

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121
Q

Who should get vaccinated for the flu?

A

Everyone

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122
Q

How is pertussis spread

A
  • aka whopping cough
  • caused by Bordetella pertussis
  • Lasts 6 wks
  • vaccine preventable, immunity decreases overtime
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123
Q

How is pertussis spread?

A

via respiratory droplets

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124
Q

Pertussis: pathophys

A

bacteria attach to ciliated cells & causes destruction of the cilia

leads to cough & inability to clear secretions
PT: pertussis toxin
TCT: tracheal cytotoxin
LPS: lipopolysaccharides

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125
Q

Pertussis Stage 1: catarrhal stage length

A

1-2 weeks

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126
Q

Pertussis Stage 1: catarrhal stage symptoms

A

runny nose, low-grade fever, mild, occasional cough
Highly contagious

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127
Q

Pertussis Stage 2: Paroxysmal stage length

A

1-6 weeks, may go up to 10

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128
Q

Pertussis Stage 2: Paroxysmal stage symptoms

A

numerous fits, rapid coughs w/ whoop sound; vomiting & exhaustions after coughing

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129
Q

Pertussis Stage 3: Convalescent stage length

A

2-3 weeks

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130
Q

Pertussis Stage 3: Convalescent Stage symptoms

A

recovery is gradual, cough lessens, but fits may return

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131
Q

Pertussis Dx - labs/imaging

A
  • nasopharyngeal swab or nasopharyngeal aspirate (PCR) or culture
  • serologic testing
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132
Q

Pertussis Tx: within 3 wks of onset

A
  • Azithromycin, Clarithromycin
  • eradicates bacteria , helps to prevent spread
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133
Q

Pertussis Tx: after 3 wks:

A
  • no tx needed - cough is related to tissue damage
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134
Q

Pertussis: Tx for cough

A

dextromethorphan (DM)

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135
Q

Pertussis: post exposure prophylaxis Tx

A
  • household contacts, regardless of vaccination history
  • same medication as tx
    (azithromycin, clarthromycin)
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136
Q

Pertussis: vaccine recommendations for infants & children

A
  • 5 doses DTaP 2mo, 4mo, 6mo, 15mo, 18mo, & 4-6 yo
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137
Q

Pertussis: vaccine recommendations for adolescents

A

single dose of Tdap, 11-12 yo

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138
Q

Pertussis: vaccine recommendations for pregnant women

A

single dose of Tdap during, 27-36 wks

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139
Q

Pneumonias is what type of dz?

A

infx of the lung paranchyma

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140
Q

Pneumonias classifications

A

Infecting organism
- bacteria, viral, fungal
Community acquired vs healthcare/hospital acquired

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141
Q

Lung parenchyma defintion

A

the portion of the lung involved in gas transfer
the alveoli, alveolar ducts, & respiratory bronchioles

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142
Q

Organisms that cause typical pneumonia.

A

S. pneumoniae, H. influenzae, S. aureus, Group A strep, Moraxella catarrhalis, anaerobes, & aerobic gram (-) bacteria

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143
Q

Organisms that causes atypical pneumonia

A

Legionella spp, M. pneumoniae, C. pneumoniae, & Chlamydia psittaci

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144
Q

Pneumonia: pathophys

A

infection of lung–> inflammatory response–> alveolar edema + exudate formation–> Alveoli & resp bronchioles fill w/ serous exudate, blood cells, fibrin, bacteria–> consolidation of lung tissues

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145
Q

Pneumonia: How is the sterile lower respiratory tract exposed to pathogens?

A
  • aspiration
  • inhalation of infective resp droplet or aerosols
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146
Q

Pneumonia: What should you ask pt. about?

A
  • occupation
  • animal exposure
  • travel history
  • tobacco & alcohol
  • immune suppressive drugs (steroids & biologics)
  • malignancy
  • chronic lung disease
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147
Q

Pneumonia: symptoms

A
  • acute or subacute onset of fever, cough, w/ or w/o sputum, & dyspnea
  • rigors, sweats, chills, pleurisy, chest discomfort, & hemoptysis
  • fatigue, anorexia, HA, myalgias , & abdom pain
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148
Q

Pneumonia: physical findings

A
  • fever or hypothermia
  • tachypnea
  • tachycardia
  • arterial O2 desaturation
  • altered breath sounds or rales
  • dullness to percussion may be found in lobar consolidation
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149
Q

Pneumonia: Dx - labs/imaging for all patients & what will it show?

A

chest x-ray( will show infiltrate)

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150
Q

Pneumonia: Dx - labs/imaging for admitted patients

A
  • CBC
  • chemistries
  • arterial blood gases
  • sputum/blood cultures
  • UA assay for legionella & strep pneumo
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151
Q

Pneumonia: Treatment Protocol

A

Slide 96 & 97 notes

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152
Q

Pneumonia: Pt. Edu

A

Prevention:
- Pneumococcal vaccine
–>PCV13 for children 2-59 mo
–> PPSV23 for all 65+

Quit smoking, early mobilization, flu vaccine

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153
Q

Pneumonia: When to admit?

A

based on age, comorbidities, altered mental status, vital signs

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154
Q

Pneumonia: complications

A
  • effusion
  • empyema
  • sepsis
  • HF
  • increase risk of PE
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155
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503
Q

Hyaline membrane disease key factors

A
  • aka respiratory distress of the newborn
  • pulmonary insufficiency in neonates due to surfactant deficiency & structural immaturity of the lung
  • most common in infants <28 weeks gestation, males, mothers w/ DM
504
Q

Hyaline membrane disease clinical findings/history

A

consider RDS in any neonate with early respiratory distress symptoms, especially in premature neonates, including
- retractions
- tachypnea
- nasal flaring
- stridor
- cyanosis
- grunting

505
Q

Hyaline Membrane Dx: labs & imaging

A

chest x-ray
– ground glass appearance

evidence of oxygen requirement

506
Q

Hyaline Membrane disease Tx

A

Delivery room stabilization:
- oxygen
- positive end airway pressure (PEEP)

Surfactant (instilled in the trachea or via endotracheal tube)

507
Q

How can PEs be classified

A
  • gross appearance (blood, serous, pus)
  • underlying process (infectious, malignant)
  • characteristics of the fluid (transudative or exudative)
508
Q

Describe transudative pleural effusion

A
  • too much fluid leaves capillaries b/c either increased hydrostatic pressure or decreased oncotic pressure in BVs
509
Q

Example of where hydrostatic pressure creates transudative PE

A

HF causes blood to back up into the pulm vessels–> increased pressure–> fluid leaves capillaries & goes into pleural space

510
Q

Example of where oncotic pressure creates transudative PE.

A

cirrhosis–> liver makes less albumin–> decreased oncotic pressure in the BVs–> fluid moves into the pleural space

511
Q

Describe exudative pleural effusion

A
  • inflammation of the pulmonary capillaries makes them “leaky” allowing protein, immune cells, large proteins to leak out of the capillaries
  • could be due to infx, inflammation, malignancy
512
Q

General Pleural effusion pathophysiology

A

accumulation of fluid within the pleural space

513
Q

Examples of pleural effusion transudative

A

CHF, cirrhosis, nephrotic syndrome, PE, hypoalbuminemia

514
Q

Examples of pleural effusion exudative

A
  • e.g. pneumonia, cancer, TB, viral infection, PE, autoimmune
515
Q

Pleural effusion: clinical findings - History/Physical

A
  • Hx & symptoms depend on etiology
  • Pts will complain of dyspnea, cough, pleuritic chest pain
  • Ask about:
    –> Dyspnea on exertion (CHF)
    –> Sharp chest pain (pericarditis)
    –> Abdominal pain (pancreatitis)
    –> Hemoptysis (malignancy, PE, TB)
  • chest exam finding may include
    –> dullness to percussion
    –> decreased or absent tactile fremitus
    –> decreased breath sounds
  • other exam finding pertinent to underlying cause
516
Q

Pleural effusion Dx: labs & imaging

A
  • chest x-ray
  • thoracentesis w/ US guidance
  • pleural effusion evaluation
517
Q

What’s included in a Dx pleural effusion evaluation?

A
  • gross appearance
  • RBC
  • WBC
  • Protein
  • LDH
  • Glucose
  • Cytology for malignancy
  • Culture
518
Q

Pleural effusion: transudates appearance

A

clear, straw colored

519
Q

Pleural effusion: transudates protein

A

< 3g/100mL

520
Q

Pleural effusion: transudates pH

A

> 7.2

521
Q

Pleural effusion: transudates glucose

A

> 40 mg/dL

522
Q

Pleural effusion: transudates LDH

A

Low, < 200IU/L

523
Q

Pleural effusion: transudates number of cells

A

< 1000/mm3

524
Q

Pleural effusion: exudates appearance

A

cloudy, purulent, opalescent

525
Q

Pleural effusion: exudates protein

A

> 3g/100mL

526
Q

Pleural effusion: Exudates pH

A

< 7.2

527
Q

Pleural effusion: Exudates glucose

A

<40 mg/dL

528
Q

Pleural effusion: Exudates LDH

A

high, >200 IU/L

529
Q

Pleural effusion: Exudates number of cells

A

> 1000/mm3

530
Q

Pleural effusion: Tx

A
  • treat underlying disease
  • thoracentesis can be diagnostic & therapeutic
531
Q

What is a potential complication of thoracentesis?

A
532
Q

Obstructive Sleep Apnea: Overview

A

sleep disorder causing repetitive complete (apnea) or partial (hypopnea) upper airway obstruction during sleep, w/ recurrent arousals & sleep fragmentation

533
Q

Describe excessive daytime sleepiness associated w/ obstructive sleep apnea

A
  • drowsiness
  • decreased concentration & memory
534
Q

Obstructive Sleep Apnea: Epidemiology/ Etiology

A

high-risk patients include those w/:
- obesity
- HF
- Afib
- HTN
- Type II DM
- Stroke
- Pulm HTN

535
Q

Obstructive Sleep Apnea: pathophysiology

A
536
Q

Obstructive Sleep Apnea: History clinical findings

A
  • sleep problems
  • excessive daytime sleepiness
  • morning headaches
  • nocturia
  • motor vehicle accidents
537
Q

Describe sleep problems associated w/ obstructive sleep apnea.

A
  • restless non refreshing sleep
  • snoring
  • awakenings (w/ gasping or paroxysmal nocturnal dyspnea)
  • witnessed apneas
  • sleep fragmentation
538
Q

Obstructive Sleep Apnea: Physical clinical findings

A
  • evaluate for obesity
  • evaluate for oropharyngeal anatomy associated w/ OSA
539
Q

Obstructive Sleep Apnea Dx: labs/imaging

A

Lab polysomnogram; it measures:
- respiratory effort
- oxygen saturation
- EKG, EEG, EOG, chin EMG
- body position
- anterior tibialis EMG

540
Q

Tx: Gen considerations for Obstructive Sleep Apnea

A
  • lifestyle modifications
  • weight reduction
  • positional therapy to keep patient in nonsupine position
  • oropharyngeal exercises may help snoring
  • continuous positive airway pressure (CPAP)
541
Q

Obstructive Sleep Apnea Pt. Edu

A
  • weight loss, ideally to BMI < or equal to 25 kg/m2
  • exercise
  • positional therapy
  • avoidance of alcohol & sedatives before bedtime