Obstructive Pulmonary Conditions (Exam 1b) Flashcards by Isaiah Smith

What does obstructive mean?

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

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Obstructive airway causes

Increase work of breathing

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

Forced expiratory volume in 1 second (FEV1)

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All obstructive disease cause

V/Q mismatch and hypoxemia (watch video)

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Air trapping results in

Hypoventilation and hypercapnia

Build up CO2 and decrease O2

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Obstructive Pathophysiology: Air Trapping

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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Air trapping causes

Chronically HIGH CO2 and Low O@

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Asthma

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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Asthma is a chronic disease (not curable) state with

Acute exacerbations

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Risk factors for Asthma

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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Pathophysiology of Asthma

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

Hypersecretion of Mucus
Airway Muscle Constriction
Swelling Bronchial Membranes
Causes

Narrow Breathing Passages

Wheezing, cough, SOB, Tightness in chest

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Common Asthma Triggers

Exercise (most common)

Second Hand Smoke (2nd)

Climate (3rd)

Dust mite
Pets
Pollen

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Early Response Asthma

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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Late Asthmatic Response

4-8 hours after early response

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

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Untreated Asthma Inflammation

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

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Two Responses of Asthma

Bronchoconstriction = 1# symptoms of asthma attack

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

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How do we diagnose Asthma

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

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What is the gold standard for diagnosing Asthma?

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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Symptoms of asthma

Wheezing

SOA

Cough

Chest tightness

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Severe Asthma Attacks

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

Asthma Management

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-Avoidance of irritants

-Use peak flow meter

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

-Immunotherapy (allergy shots)

Severe asthma managment

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

How to monitor treatment

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Use peak flow meter and keep an action plan

Status Asthmaticus

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Severe symptoms = pCO2> 70 mm hg

Unrelenting asthma attack and silent chest because no air movement

Life Threatening Emergency

Chronic Bronchitis

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

Chronic Bronchitis: Etiology

90% smoke cigs Form of COPD

Chronic Bronchitis: Presentation

May have acute exacerbation of chronic bronchitis = AECB

Prognosis of Chronic Bronchitis

Premature morbidity and mortality

Chronic Bronchitis: Clinical Manifestations

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

Chronic Bronchitis: Diagnosis

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

Who gets chronic bronchitis

SMOKERS AND VAPERS

Chronic Bronchitis: Pathophysiology

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)

Initially the process of chronic bronchitis

only affects bronchi but eventually all airways involved Obstruction of airway results particularly during expiration when airways are narrowed

Chronic Bronchitis: Late Clinical manifestations

Pulmonary Hypertension: Advanced disease (syncope-DOE-Fatigue) Right sided heart failure = cor pulmonale

cor pulmonale

right sided heart failure cause by pulmonary hypertension

Chronic Bronchitis: Treatment

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

Chronic Bronchitis Treatment Cont

Bronchodilators Expectorants CPT Steroids late in disease ( or with acute exacerbations)

Emphysema

Abnormal, PERMANENT enlargement of gas exchange airways, accompanied by DESTRUCTION of alveolar walls Obstruction results from inflammatory and dexctruces changes in lung tissues

Major mechanism of airflow limitation in Emphysema

Loss of elastic recoil with collapse of the airways during expiration

Emphysema

Disease of alveoli Permanently enlarger

Emphysema is defined by

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

What causes Emphysema and loss of Elastic recoil

SMOKING SMOKING SMOKING Air pollution Childhood Respiratory Infections

Genetic Emphysema

Primary emphysema Inherited deficiency of enzyme --> alpha antitrypsin protein

Emphysema: Clinical Manifestations

-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

Emphysema: Diagnosis

PFT's FEVI decreased CXR - Hyperinflation of lungs ABGS - Respiratory Acidosis ( really high CO2 causing low ph)

Emphysema: Treatment

Smoking cessation Bronchodilators and Anti Inflammatory agent O2 supplementation Breathing retraining Relaxation techniques Antibiotics for acute infections

Blue Bloaters and Pink Puffers

SLIDE

COPD Umbrella

Term that can be used to describe a range of pulmonary conditions, including: Chronic Bronchitis Emphysema Irreversible or refractory asthma

Hallmark sign of emphysema

Decrease breath sounds throughout

Obstructive Pulmonary Conditions (Exam 1b) Flashcards

(49 cards)