Unit 3

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Description and Tags

Pathophysiology

69 Terms

1

Pulmonary Edema

Abnormal accumulation of fluid from pulmonary vascular system into lung parenchyma

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2

Anatomical Changes of Pulmonary Edema

  1. Interstitial Edema

  2. Alveolar Flooding

  3. Increased Surface Tension of Alveolar Fluids

  4. Alveolar Shrinkage and Atelectasis

  5. Frothy White/Pink Secretions

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3

Cardiogenic Pulmonary Edema

Occurs when left ventricle is unable to pump out sufficient amount of blood during ventricular contraction

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Noncardiogenic Pulmonary Edema

Develops due to damage to the lungs

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5

What causes cardiogenic pulmonary edema?

  1. CHF and Other Heart Diseases

  2. Congenital Heart Defects

  3. Excessive Fluid Administration

  4. Pulmonary Emboli

  5. Renal Failure

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How do you diagnose cardiogenic pulmonary edema?

Echocardiogram

LVEF = < 40% may confirm heart failure

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What are possible causes of noncardiogenic pulmonary edema?

  1. Increased Capillary Permeability

  2. Lymphatic Insufficiency

  3. Decreased Intrapleural Pressure

  4. High-Altitude

  5. Decreased Oncotic Pressure

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Examples of Decreased Oncotic Pressure

Severe Malnutrition

Over Transfusion of Hypotonic IV Fluids

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Abnormal Labs Found with Pulmonary Edema

  1. Low Potassium

  2. Low Sodium

  3. Low Chloride

  4. Elevated BNP ——> Cardiac Indicator

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X-Rays Findings of Cardiogenic Pulmonary Edema

  1. Enlarged Heart - Cardiomegaly

  2. ‘Bat’s Wing’ or ‘Butterfly’ Patterns

  3. Pleural Effusion

  4. Kerley A and B Lines

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X-Ray Findings of Noncardiogenic Pulmonary Edema

  1. Granular / Ground Glass Appearance

  2. Reticulograndular or Honeycombing

  3. Bilateral Fluffy Opacities with a Predominantly Central Position in the Chest

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Management of Cardiogenic Pulmonary Edema

  1. Initial Management

  2. Therapeutic Intervention

    1. Preload Reduction

    2. Afterload Reduction

    3. Treatment of Reduced Cardiac Contractility

    4. Other Agents

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Management of Noncardiogenic Pulmonary Edema

Largely Supportive (i.e. adequate oxygenation and ventilation)

No Specific Treatment, except for Specific Infections or High Altitude

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Pleural Effusion

Fluid that accumulates in pleural space

Restrictive Disorder

Shunt

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15

Empyema

When fluid in the pleural space is infected

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16

Hydrostatic Pressure

Mainly a function of the arterial circulation

Creates the ‘push’ pressure on the walls of the vessels

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Oncotic Pressure

Reflects largely the protein concentration in the blood and lymphatic vessels

Creates the ‘pull’ pressure to pull fluid into the vessels

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Transudative Pleural Effusions

Develops when fluid from the pulmonary capillaries moves into pleural space

  1. Thin

  2. Watery

  3. Contains Few Blood Cells

  4. Contains Little Protein

  5. High Hydrostatic Pressure

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Exudative Pleural Effusions

Develops when pleural surfaces are diseases

  1. High Protein Content

  2. High Cellular Debris

  3. Lymphatic System is Not Working Properly

  4. Usually Caused by Infection or Cancer

  5. High Oncotic Pressure

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Causes of Transudative Pleural Effusions

  1. CHF - Most Commom

  2. Pulmonary Embolism

  3. Peritoneal Dialysis

  4. Nephrotic Syndrome

  5. Hepatic Hydrothorax

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Causes of Exudative Pleural Effusions

  1. Empyema

  2. Fungal Diseases

  3. TB

  4. Pneumonia

  5. Cancer

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Signs and Symptoms of Pleural Effusions

Tachypnea, Tachycardia, Increased BP, Chest Pain, Dry Nonproductive Cough, Dyspnea, Decreased Chest Expansion, Cyanosis, Chest Pressure when Effusions is about 500-1500mL, Tracheal Shift Away from Affected Side, Dull Percussion Note, Pleural Friction Rub (Occasionally), Decreased Tactile and Vocal Fremitus

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23

ABG’s of Mild Pleural Effusion

High pH

Low PaCO2

Low PaO2

Normal HCO3

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ABG’s of Moderate/Severe Pleural Effusion

Low pH

High PaCO2

Low PaO2

Normal HCO3

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General Treatment of Pleural Effusions

Best Way to Resolve Pleural Effusion is to Treat Underlying Cause.

  1. Thoracentesis

  2. Appropriate Antibiotic

  3. Chest Tube in Severe Cases

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Specific Treatment for Transudative Pleural Effusion

  1. Lower BP

  2. Diuretics

  3. Give Proteins

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Specific Treatment for Exudative Pleural Effusion

  1. Test for Bacteria and Give Antibiotics

  2. Cytologic Exam to Identify Cancer

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28

2 Disorders of COPD

  1. Emphysema

  2. Chronic Bronchitis

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Chronic Bronchitis

Chronic Productive Cough for 3 Months in each of 2 Successive Years in a Patient in Whom Other Causes of Productive Chronic Cough Have Been Excluded

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Emphysema

The Presence of Permanent Enlargement of the Air Spaces Distal to the Terminal Bronchioles, Accompanied by Destruction of Bronchiole Walls and Without Obvious Fibrosis

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Structures Affected by Chronic Bronchitis

Conducting Airways Especially the Bronchi

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Structures Affected by Emphysema

Alveoli

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Dysfunction Caused by Chronic Bronchitis

  1. Smooth Muscle Constriction

  2. Mucus Plugging

  3. Hyperinflated Alveoli

  4. Enlarged Submucosal Glands

  5. Mucus Accumulation

  6. Epithelial Inflammation

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Why are Patients Who Have Chronic Bronchitis Called Blue Bloaters?

  1. Cyanosis

  2. Overweight

  3. Fluid Retention

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Why are Patients Who Have Emphysema Called Pick Puffers?

  1. Flushed Skin

  2. ‘Puffing’ from Pursed-Lip Breathing

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2 Types of Emphsema

  1. Panacinar (Panlobular)

  2. Centriacinar (Centrilobular)

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Panacinar (Panlobular) Emphysema

Abnormal Weakening and Enlargement of ALL Alveoli Distal to the Terminal Bronchioles

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Centriacinar (Centrilobular) Emphysema

Involves the Respiratory Bronchioles Proximal (Central) Portion of the Acinus

Most Common Form of Emphysema

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Acinus

A region of the lung supplied with air from one of the terminal bronchioles

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Emphysema Percussion Sound

Hperresonnant due to Air Trapping

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Polycythemia

High Levels of RBCs

Common in Patients with Chronic Bronchitis

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Genetic Disorder that Causes Early Onset of Emphysema/COPD

Alpha-1 Antitrypsin Deficiency (ATT1)

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Alpha-1 Antitrypsin Deficiency (AAT1)

Protease Inhibitor

Without it Patient Experiences Damaged Airways

Normal Range: 150 - 350mg

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Spirometry Test for Diagnosing COPD

Post-Bronchodilator FEV1/FVC

For Diagnosis Patient must Score Less than 70%

Normal Range is Greater Than or Equal to 70%

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Score on mMRC to be Considered High-Risk for Severe COPD Exacerbations

Score > 2 is High-Risk

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Score on CAT to be Considered High-Risk for Severe COPD Exacerbations

Score > 10 is High Risk

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SpO2 Goals for COPD Patients

Target is 88% - 92%

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Symptoms of Cor Pulmonale

  1. Enlarged Heart

  2. Right-Sided Heart Failure

  3. Swollen Ankles and Legs

  4. Distended Neck Veins

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Gold 1 Standard for COPD - Mild

FEV1 80% Predicted

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Gold 2 Standard for COPD - Moderate

50% ≤ FEV1 < 80% Predicted

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Gold 3 Standard for COPD - Severe

30% ≤ FEV1 < 50% Predicted

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Gold 4 Standard for COPD - Very Severe

FEV1 < 30% Predicted

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53

Cystic Fibrosis

Progressive Genetic Disease that can Affect Lungs, Pancreas, Liver, and Sweat Glands

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What Causes CF?

Mutations of the CFTR Gene Causes to Become Dysfunctional

Creates an Inability to Transport Sodium and Chloride Across Epithelial Surfaces

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Most Common Defect of CF

ΔF508

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Gating Defect (Class III) of CF

Channel Doesn’t Open

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Conductance Defect (Class IV) of CF

Channel is Open, but Chloride Doesn’t Move Effectively

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Common Gram Negative Bacteria Found in CF Patients

  1. Pseudomonas Aeruginosa

  2. Burkholderia Cepacia Complex (Most Dangerous)

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Common Gram Positive Bacteria Found in CF Patients

  1. Staphylococcus Aureus

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Immunoreactive Trypsin (IRT)

Test Performed on All Newborns on Birth

Detection of Atleast 1 CF Mutation is Considered a Positive Screen for CF

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Most Reliable Test in Diagnosing CF?

Sweat Chloride Test

x > 60 mmol/L

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62

Nonallergic / Nonatopic / Intrinsic Asthma

Onset Seen in Adults After Age 40

Not Related to Hypersensitivity to Antigens

Does Not Respond Well to ICS Therapy

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Causes / Irritants of Intrinsic Asthma

  1. Cold Air

  2. Infections

  3. Emotional Stress

  4. Exercise

  5. Dust

  6. Drugs

  7. Smoke

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Allergic / Atopic / Extrinsic Asthma

Typically Appears in Childhood

Sputum Contains Eosinophils

Is Considered Type 1 (Immediate Hypersensitivity Reaction)

Elevated IgE Levels

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Common Vital Signs of Asthma Exacerbation

  1. Tachypnea

  2. Tachycardia

  3. Hypertension

  4. Pulsus Paradoxus

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Bronchial Provocation Test

Most Often Using Inhaled Methacholine to Provoke Bronchospasm in a Controlled Environment

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Atopy

Genetic Disposition to Develop Allergic Diseases

Associated with Overproduction of IgE to Specific Antigen

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68

FeNO

Fractional Concentration of Nitric Oxide

Increased Levels are Caused by Airway Inflammation

Normal Range:

  1. Adult: < 25 ppb

  2. Children = < 20ppb

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What is Prescribed for High FeNO Levels?

Inhaled Corticosteroids (ICS)

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