obstructive pulmonary conditions Flashcards

1
Q

obstructive pulmonary conditions

A

emphysema
chronic bronchitis
asthma

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2
Q

asthma

A

chronic inflammation of bronchial airways (NOT alveoli)

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3
Q

asthma risk factors

A

-genetic
-level of exposure to allergens
-urban residency
-exposure to pollution
-tobacco exposure/smoker
-recurrent respiratory viral infections & GERD

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4
Q

patho of ashtma

A
  1. exposure to trigger/antigen 2. airway inflammation
  2. hyper secretion of mucus, airway muscle constriction, swelling bronchioles
  3. narrow breathing passage
  4. wheezing, cough, SOB, tightness in chest
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5
Q

patho of ashtma

A
  1. exposure to trigger/antigen 2. airway inflammation
  2. hyper secretion of mucus, airway muscle constriction, swelling bronchioles
  3. narrow breathing passage
  4. wheezing, cough, SOB, tightness in chest
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6
Q

what immune cells are involved in asthma process?

A

dendritic
T helper
B lymphocytes
mast cells
neutrophils
basophils
eosinophils

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7
Q

early asthmatic response

A

responses activated immediately and release of inflammatory mediators occurs within minutes

-vasodilation
-increased capillary permeability
-mucosal edema
-bronchoconstriction
-mucus secretion

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8
Q

late asthmatic response

A

4-8 hours after early

-eosinophils, neutrophils, lymphocytes gather
-another release of inflammatory mediators again –> causing same process

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9
Q

airway remodeling

A

untreated inflammation

long-term airway damage - IRREVERSIBLE

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10
Q

1 sign of asthma attack

A

bronchoconstriction

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11
Q

what is the biggest problem r/t asthma?

A

inflammation

long-term problem that causes seriousness of disease

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12
Q

how is asthma diagnosed? gold standard

A

pulmonary functions test: measures lung function with respect to time
*decreased FEV-1
*decreased flow rate

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13
Q

classic asthma symptoms

A

wheezing, SOB, cough, chest tightness

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14
Q

severe asthma symptoms (attack)

A

use of accessory muscles, distant breath sounds, diaphoresis, inability to speak, RESPIRATORY FAILURE (inaudible breath sounds, repetitive hacking cough, pCO2 >70)

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15
Q

management of asthma

A

avoid triggers
*peak flow meter (measures FEV1 @ home)
*lose-dose corticosteroids
*SABA (mild)
*anti-inflammatory, inhaled corticosteroids, LABA, leukotriene antagonist (severe)
*immunotherapy

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16
Q

treatment for asthma attack

A

bronchodilators, corticosteroids, oxygen

17
Q

chronic bronchitis

A

hyper secretion of mucus and chronic productive cough for at least 3 months of the year for 2 years

18
Q

acute bronchitis

A

inflammation of bronchi and bronchioles
*caused by bacterial or viral infection - NO obstruction
*mild and self-limiting - usually better in 3-4 weeks

19
Q

chronic bronchitis

A

bronchitis for 3 months of of the year for 2 years

caused by SMOKING and OBSTRUCTION of airway

*may have acute exacerbation

20
Q

what is the prognosis of acute exacerbation?

A

premature morbidity and mortality

21
Q

chronic bronchitis: S/S

A

*persistent productive cough (purulent)
*frequent resp infections

as disease progresses…
increased cough, congestion, SOA

22
Q

chronic bronchitis: diagnosis

A

based on hx of symptoms, exam, chest imaging, PFTs

low FEV1

*typically disease is progressed and irreversible by the time pt seeks treatment

23
Q

patho chronic bronchitis

A
  1. inhaled irritants = airway inflammation
  2. infiltration of neutrophils, macrophages, lymphocytes into bronchial wall
  3. continual bronchial inflammation –> bronchial edema increase number and size of GOBLET cells and mucus glands
  4. causes thick mucus and can’t be cleared bc impaired ciliary fxn
24
Q

late clinical manifestations of chronic bronchitis

A

pulmonary HTN: increase in pulmonary artery pressure d/t elevated pulmonary venous pressure, increased pulmonary blood flow, pulmonary vascular obstruction or hypoxemia
^may result in right-sided heart failure (cor pulmonale)

S/S: DOE, syncope, fatigue

25
Q

treatment of chronic bronchitis

A

IRREVERSIBLE

stop smoking: halt progression

TEACH: if stopped before s/s occur, risk for bronchitis decreases considerably

*bronchodilators
*expectorants
*CPT
*steroids (late disease or acute exacerbations)
*O2 therapy

26
Q

emphysema

A

chronic, irreversible, progressive lung disease characterized by:
-loss of elastic recoil
-abnormal, permanent enlargement of air sacs distal to bronchioles –> destruction of alveolar walls and capillaries
*AIRWAY REMODELING
-lung hyperinflation

27
Q

destruction in emphysema results from

A

tissue changes NOT mucus production

28
Q

loss of elastic recoil in emphysema - caused by

A

SMOKING
air pollution
childhood resp infections
genetic emphysema (alpha-antitrypsin

29
Q

clinical manifestations of emphysema

A

*DOE
*SOA at rest (prolonged expiratory phase + O2 dependent)
*wheezing
*malnourished
*decrease muscle mass
*barrel chest
*pursed lip breathing
*decreased breath sounds !!!!!

30
Q

diagnosis of emphysema

A

PFT’s: FEV1 decreased

CXR: hyperinfiltration

ABG’s: respiratory acidosis (high CO2, decreased pH)

check alpha1-antitrypsin (AAT)

31
Q

treatment of emphysema

A

stop smoking
bronchodilators and anti-inflammatories
O2 therapy
breathing retraining
relaxation techniques
ATB for acute infections