COPD and Asthma

Mitzi W.

Created: 2011-11-13
Last Modified: 2011-11-13

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Related Textbooks:

CURRENT Medical Diagnosis and Treatment 2012, Fifty-First Edition (LANGE CURRENT Series)

COPD definition

Disease defined by airflow limitation that is…

-Progressive

-Not fully reversible

-Associated with inflammatory response to noxious agent

-May or may not have emphysema

-Varies greatly from one individual to another

Chronic bronchitis

Chronic cough/sputum for 3 months, 2 yrs consecutive

-Pathologically different from emphysema

-R/O other causes for chronic cou

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Emphysema

Irreversible increase in air spaces distal to terminal bronchioles, wall destruction

-May or may not have elements of chronic bronchitis

-No Fibrosis

an anatomical description characterized by weakening and permanent enlargement of the airspaces distal to the terminal bronchioles and destruction of the alveolar walls

COPD risk factors

smoking- primary cause of cb and emphysema

Indoor/Outdoor Pollution

-Occupational

-Perinatal Lung Development

-Socioeconomic Status

-Recurrent Respiratory Illness

-Gender

-Airway Hyperreactivity/Asthma

-Diet

-Genes (α one antitrypsin def)

Chronic Bronchitis Patho

submucosal gland enlargement and goblet cell hyperplasia lead to overproduction of mucous

Bronchial wall edema

These 2 factors together narrow airwayand increase airway resistance

Emphysema Patho

loss of elastic recoil/ loss of alveolar capillary surface area

Enlarge/destruction air spaces

- Weakening of distal airways

Loss of Elastic Recoil

-Destruction of pulm capillaries

Loss of Cap-Alv SA

leads to increase compliance, increase airway resistance, decrease exp flow rates, hyperinflation

VQ mismatch->hypoxia->pulm vasc comstriction->pulm htn

Types of emphysema

centrilobular- caused by smoking, Proximal portion terminal bronchiole affected, upper lobe prominence

Panlobular-bronchioles and airsacs affected, has lower lobe prominence, alpha 1 antitrypsin def.

clinical presentation

Cough

Sputum Production

Dyspnea (Exertional typically)

Fifth decade of Life

Recurrent Respiratory Infections

Clinical presentation- physical exam

Thin (severe)

-Pursed Lip breathing (severe)

-Central Cyanosis

-Odor

-Distress? Watch them walk, talk etc….observe

-Depression? Anxiety

-Co-morbidities

-PMH

Assess for presence of heart failure, resp illnesses, GERD, MI, Osteoporosis, Diabetes, Lung Cancer

-Assess for previous history of exacerbations, familial history, smoking history etc

clinical presentation- pulm and cv assessment

Increase A/P diameter (barrel)

-Tachypnea

-Accessory Muscles, Hoover’s Sign

-Increased resonance to percussion

-Expiratory wheezing

-Decreased breath sounds

Distant heart sounds (listen over xiphoid)

-Check neck veins

COPD labs

α1 Anti-Trypsin Deficiency:

-<45yrs, caucasian, family history….test everyone?>> ATS says yes

-Serum concentration < 15-20% of norm = highly suggestive

ABG: (not sensitive)

-Hypoxemia?

-Compensated respiratory acidosis

-Check if O2 Sat <92% on RA

Hematocrit:

-May be elevated above normal with chronic hypoxemia

COPD radiographs

Non-diagnostic

-Flattened Diaphragms

-Enlarged Retrosternal Air Space

-Hyperlucency

-Bullous disease?

-Long and Narrow Heart

Chest CT (HRCT):

-Not part of diagnostics > want you to know what to look for

if you have it

-Location of abnormalities (upper lobes vs lower lobes)

COPD diagnosis

Spirometry is the best way to diagnose COPD and to monitor its progression and health care workers to care for COPD patients should have assess to spirometry

A diagnosis of COPD should be considered in any patient who has cough, sputum production, or dyspnea and/or a history of exposure to risk factors. The diagnosis is confirmed by spirometry.

Spirometry terms

FVC : Forced Vital Capacity

Total volume of air that can be forcibly exhaled in one breath

FEV1 : Forced Expiratory Volume (1st second)

Volume of air expired in first second of forced exhalation

FEV1/FVC Ratio :

Fraction of air exhaled in the first second to total exhalation volume

VC : Vital Capacity

Maximal volume of air that can be inhaled and exhaled in one breath

TLC : Total Lung Capacity

Vital Capacity + Residual Volume

Staging COPD by spirometry

Stage I: Mild FEV1/FVC < 0.70 FEV1 < 80% predicted

Stage II: Moderate FEV1/FVC < 0.70 50% < FEV1 < 80% predicted

Stage III: Severe FEV1/FVC < 0.70 30% < FEV1 < 50% predicted

Stage IV: Very Severe FEV1/FVC < 0.70 FEV1 < 30% predicted or FEV1 < 50% predicted

plus chronic respiratory failure

BODE Index

Tool to assess severity of disease. Better predictor of mortality vs FEV1 alone.

B - Body Mass Index

O - Obstruction

D - Dyspnea

E – Exercise

Higher the score = Higher Mortality Risk

BODE score 0-10

4 components of COPD management

Control stable COPD

Observe, assess and monitor disease

Prevent exacerbations

Decrease risk factors

Bronchodilators

Anticholinergics

Beta-agonists

Methylxanthines

Combination bronchodilators may have sustained effect

-LA bronchodilator treatment more effective and convenient

-Inhaled is preferred route except for methylxanthines

-Combo SABA & Anticholinergic =

Fenoterol Ipratropium & Albuterol Ipratropium

Anti Cholinergics

Blocks acetylcholine receptors M3 - bronchodilation

- LA Tiotropium bronchodilating effects longer than SABA, up to 24hrs

-Improves symptoms & FEV 1 acutely

-Common side effect dry mouth

-SA-Ipratropium Bromide, LA- Tiotropium

Beta-Agonists

B2 adrenergic agonists – relaxes airway smooth muscles and

antagonizes bronchoconstriction

-SA-Albuterol, Levobuterol, LA-Salmeterol, Formoterol

-Side Effects: Tachycardia (less tachyphylaxis than we think), Tremors

Methylxanthines

Non-selective Phosphodiesterase inhibitors? Inc exp flow rate?

-Theophylline, Aminophylline

-High risk for toxicity and drug, food interactions, levels

Not inhaled- theophylline and aminophylline

Inhaled Glucocorticoids

Patients with FEV1 < 50% (Stage III or IV)

-In addition to B2-Agonist more effective than alone

-Reduces exacerbations & improve symptoms

-Not been shown to alter natural history of disease

-Long term safety still not known

-Shown to decrease BMD long term, fracture risk?

-Can cause oral candidiasis

-Beclomethasone, Budesonide, Fluticasone, Triamcinolone

-Combo LABA/ICS = Formoterol/Budesonide,

Salmeterol/Fluticasone

Therapy for each stage of COPD

Stage 1- SA bronchodilator as needed

Stage 2: add LA bronchodilator and pulm rehab

Stage 3: add inhaled glucocorticoid if COPD exacerbations

Stage 4: add O2 if resp failur and consider surgical options

o2 therapy

Goal to preserve vital organ function

-Only non-pharmacologic treatment that reduces mortality

-Must have room air PaO2 ≤ 55 mmHg or O2Sat ≤ 88%

-If Pulm Htn, Peripheral edema, Polycthemia and PaO2 55-60 or

O2Sat ≤ 88%.

-Titrate flow to keep Sat 90% or above

-Mortality benefit for > 15hrs/day of oxygen therapy

-Also for exertional and nocturnal hypoxemia

COPD management of acute exacerbations

Most common causes:

-Infection of tracheobronchial tree

-Air pollution

-Up to 1/3 unknown etiology…? Evidence of disease

progression

Antibiotic Therapy

-Inhaled Bronchodilators (w/wo anticholinergics)

-Oral Glucocorticoids (Oral Prednisone, Methylpred)

-Supplemental O2

-ABG, CXR, CBC

antibiotic use for exacerbation

Mild- oral Beta Lactams, Tetra, Bactrim, Macrolides, Cephalosporins

Moderate- oral or IV Beta Lactams, Cephalosporins, or fluoroquinolone

Severe- Fluroquinolone Or Beta Lactam (with Pseudom coverage)

Management of COPD exac with rep failure

Noninvasive postive pressure ventilation vs ventilator

Asthma definition

Asthma is a chronic inflammatory disorder of the airways.

-Variable recurrent symptoms

-Airway obstruction (Reversible)

-Inflammation (Cellular component)

-Bronchial Hyperresponsiveness

Cellular component = mast cells, eosinophils, T-lymphocytes, macrophages and neutrophils

Asthma risk factors- Intrinsic

Ethnicity

Genetic Predisposition

Airway Hyperresponsive

Atopy- allergies

Gender

Asthma risk factors environmental

I/O Allergens

Occupational

Passive Smoking

Respiratory Infection

Obesity

Viral ?

Asthma triggers

Allergens

URI-viral

Exercise

Cold Air

Sulfur Dioxide

Meds

Stress

Irritants

Asthma patho key points

Inflammation >>> Chronic Repair >>> Eventual Irreversible Narrowing of the Airway in severe patients

Bronchoconstriction + Airway Edema + Vascular congestion + Luminal Mucous >>>

-Airflow Limitation

-Decrease FEV1 and FEV1/FVC ratio

-Decrease peak expiratory flow (PEF)

-Increased Airway Resistance

Asthma clinical presentation

Wheezing

Dyspnea

Coughing

Chest Tightness

Symptoms worse at night or early morning

Reflux

Mucous ?

Nasal mucosal swelling, nasal polyps >> allergic

Exam may be normal if controlled

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