Obstructive Pulmonary Conditions (Exam 1b) Flashcards

1
Q

What does obstructive mean?

A

Narrowed airways (causes airway obstruction worse on EXPIRATION) (Air trapped in the lungs)

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2
Q

Obstructive airway causes

A

Increase work of breathing

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3
Q

With obstruction the emptying of lungs is slowed and this is measured by

A

Forced expiratory volume in 1 second (FEV1)

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4
Q

All obstructive disease cause

A

V/Q mismatch and hypoxemia (watch video)

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5
Q

Air trapping results in

A

Hypoventilation and hypercapnia

Build up CO2 and decrease O2

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6
Q

Obstructive Pathophysiology: Air Trapping

A

Occurs when person is not able to fully exhale so air cannot get out

Build up of CO2 in blood

Air trapped in the alveoli –> person works harder to breathe, lungs are Hyperinflated

Therefore: Normal exhalation is obstructed

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7
Q

Air trapping causes

A

Chronically HIGH CO2 and Low O@

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8
Q

Asthma

A

Chronic inflammation of bronchial airways

(not alveoli like other Obstructive conditions)

Chronic inflammation causes bronchial HYPERRESPONSIVENESS, constriction of the airways and variable airflow obstruction that is reversible

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9
Q

Asthma is a chronic disease (not curable) state with

A

Acute exacerbations

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10
Q

Risk factors for Asthma

A

Usually starts in childhood –> highly associated with allergies

Familial link

Levels of allergen exposure

Urban residency

Exposure to indoor and outdoor air pollution

Tobacco exposure and smoke

RI and GERD

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11
Q

Pathophysiology of Asthma

A

Exposure to antigen (trigger factor)

Lots of immune cells involved in these process –> dendritic cells-T helper-B lymphocytes-mast cells-neutrohphils-basophils-EOSINOPHILS

Trigger factors (antigen) causes

Bronchial airway inflammation which causes

  1. Hypersecretion of Mucus
  2. Airway Muscle Constriction
  3. Swelling Bronchial Membranes
    Causes

Narrow Breathing Passages

Wheezing, cough, SOB, Tightness in chest

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12
Q

Common Asthma Triggers

A

Exercise (most common)

Second Hand Smoke (2nd)

Climate (3rd)

Dust mite
Pets
Pollen

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13
Q

Early Response Asthma

A

These cellular responses are activate immediately and the cascade of release of inflammatory mediators

Vasodilation, increased capillary permeability, mucosal edema, bronchial smooth muscle contraction and mucus secretion

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14
Q

Late Asthmatic Response

A

4-8 hours after early response

Recruitment of WBC causes another realse of inflammatory mediators inciting same process

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15
Q

Untreated Asthma Inflammation

A

Can lead to long term airway damage that is IRREVERSIBLE and is known as airway remodeling (CHRONIC ASTHMA)

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16
Q

Two Responses of Asthma

A

Bronchoconstriction = 1# symptoms of asthma attack

Inflammation: Biggest problem and causes the seriousness of the disease (airway remodeling)

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17
Q

How do we diagnose Asthma

A

History of allergies, recurrent episodes of wheezing, dyspnea, and exercise intolerance

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18
Q

What is the gold standard for diagnosing Asthma?

A

PFT’s

Measures lung function with respect to time (seconds)

-Decreased expiratory flow rate

-Decreased FEV1 (how much air can a patient blow out in one second)

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19
Q

Symptoms of asthma

A

Wheezing

SOA

Cough

Chest tightness

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20
Q

Severe Asthma Attacks

A

-Use of accessory muscles
-Distant breath sounds
-Diaphoresis
-Can not speak
-Respiratory failure (Silent chest)
-Repetitive hacking cough

21
Q

Asthma Management

A

-Avoidance of irritants

-Use peak flow meter

-Low does corticosteroids (mainstay for exacerbations), short acting beta-agonist inhaler for milder forms

-Immunotherapy (allergy shots)

22
Q

Severe asthma managment

A

Add anti inflammatory medications that are inhaled corticosteroid, long acting beta agonist inhalers, or leukotriene antagonists

23
Q

How to monitor treatment

A

Use peak flow meter and keep an action plan

24
Q

Status Asthmaticus

A

Severe symptoms = pCO2> 70 mm hg

Unrelenting asthma attack and silent chest because no air movement

Life Threatening Emergency

25
Q

Chronic Bronchitis

A

Hypersecretion of mucus and chronic productive cough for at least 3 months of the year for at least 2 consecutive years

26
Q

Chronic Bronchitis: Etiology

A

90% smoke cigs

Form of COPD

27
Q

Chronic Bronchitis: Presentation

A

May have acute exacerbation of chronic bronchitis = AECB

28
Q

Prognosis of Chronic Bronchitis

A

Premature morbidity and mortality

29
Q

Chronic Bronchitis: Clinical Manifestations

A

Persistent Productive Cough

Purulent if superimposed respiratory infection (mucus becomes a favorable breeding ground for infections)

30
Q

Chronic Bronchitis: Diagnosis

A

Based on history of symptoms, physical exam, chest imagining, pulmonary function test

Typically by the time people seek treatment, disease is in a progressive state and the pathological changes that have occurred are IRREVERSIBLE

31
Q

Who gets chronic bronchitis

A

SMOKERS AND VAPERS

32
Q

Chronic Bronchitis: Pathophysiology

A

Inhaled irritants result in airway inflammation –> infiltration occurs with neutrophils, lymphocytes into the bronchial walls

Continual bronchial inflammation –> bronchial edema, increase number and size of the GOBLET cell and mucus glands

Thick, tenacious mucus produced and cannot be cleared because of impaired ciliary function

Accumulation of inflammatory cells

Leads to thickened smooth muscles secondary to chronic bronchospasm (fibrosis)

33
Q

Initially the process of chronic bronchitis

A

only affects bronchi but eventually all airways involved

Obstruction of airway results particularly during expiration when airways are narrowed

34
Q

Chronic Bronchitis: Late Clinical manifestations

A

Pulmonary Hypertension: Advanced disease (syncope-DOE-Fatigue)

Right sided heart failure = cor pulmonale

35
Q

cor pulmonale

A

right sided heart failure cause by pulmonary hypertension

36
Q

Chronic Bronchitis: Treatment

A

Prevent if you can :/

If smoking is stopped before symptoms occurs, the risk for bronchitis decreases considerably and eventually reaches that of a person who have never smoked

37
Q

Chronic Bronchitis Treatment Cont

A

Bronchodilators

Expectorants

CPT

Steroids late in disease ( or with acute exacerbations)

38
Q

Emphysema

A

Abnormal, PERMANENT enlargement of gas exchange airways, accompanied by DESTRUCTION of alveolar walls

Obstruction results from inflammatory and dexctruces changes in lung tissues

39
Q

Major mechanism of airflow limitation in Emphysema

A

Loss of elastic recoil with collapse of the airways during expiration

40
Q

Emphysema

A

Disease of alveoli

Permanently enlarger

41
Q

Emphysema is defined by

A

Chronic, Irreversible, Progressive, and Destructive lung disease characterized by:

Loss of elastic recoil = Decrease Recoil

Abnormal PERMANENT enlargement of air spaces distal to terminal bronchioles

Lung hyperinflation

Destruction results from tissue changes and not mucus production

42
Q

What causes Emphysema and loss of Elastic recoil

A

SMOKING SMOKING SMOKING

Air pollution

Childhood Respiratory Infections

43
Q

Genetic Emphysema

A

Primary emphysema

Inherited deficiency of enzyme –> alpha antitrypsin protein

44
Q

Emphysema: Clinical Manifestations

A

-Gradual increase in breathlessness with any exceptions. = DOE

-Eventually SOA at REST (With prolonged expriartory phase) (May become oxygen dependent)

-Wheezing

-Malnourished (r/t increased WOB)

-Decrease Muscle Mass

-Barrel Chest

-Pursed lip breathing

-Decreased Breath Sounds Throughout

45
Q

Emphysema: Diagnosis

A

PFT’s FEVI decreased

CXR - Hyperinflation of lungs

ABGS - Respiratory Acidosis ( really high CO2 causing low ph)

46
Q

Emphysema: Treatment

A

Smoking cessation

Bronchodilators and Anti Inflammatory agent

O2 supplementation

Breathing retraining

Relaxation techniques

Antibiotics for acute infections

47
Q

Blue Bloaters and Pink Puffers

A

SLIDE

48
Q

COPD Umbrella

A

Term that can be used to describe a range of pulmonary conditions, including:

Chronic Bronchitis
Emphysema
Irreversible or refractory asthma

49
Q

Hallmark sign of emphysema

A

Decrease breath sounds throughout