EXAM 3 PATHO

Part 1: Concepts of Pulmonary Pathophysiology

1. Homeostatic Adjustments in Chronic Lung Disease

  • (a) Chronic elevation of paCO2:

    • Definition: paCO2 refers to the partial pressure of carbon dioxide in arterial blood. Chronic elevation leads to acclimatization of the central chemoreceptors in the medulla oblongata.
    • Mechanism:
    • Initial response to elevated CO2 involves increased respiratory drive.
    • Over time, the chemoreceptors adapt to higher CO2 levels, resulting in a "resetting" of the respiratory set point, potentially leading to hypoventilation in response to a further increase in CO2.

  • (b) Caution when administering oxygen:

    • Importance: Patients with chronic lung disease often rely on hypoxemia (low oxygen levels) rather than hypercapnia (high CO2 levels) to stimulate breathing.
    • Risk: Administering supplemental oxygen can reduce their respiratory drive, potentially leading to CO2 retention and respiratory failure.

2. Airway and Tissue Resistance

  • (a) Airway Resistance vs. Tissue Resistance:

    • Airway Resistance: Resistance to airflow in the respiratory tract, primarily influenced by airway diameter.
    • Tissue Resistance: Resistance of the lung tissue to expansion; influenced by lung compliance and elastance.

  • (b) Airway Resistance:

    • Decreased Airway Radius: A decrease in the diameter of airways (e.g., in asthma) significantly increases airflow resistance due to Poiseuille's Law, where resistance is inversely proportional to the fourth power of radius (R ∝ 1/r^4).
    • **Factors Increasing Resistance:
    • Airway wall edema
    • Mucus obstruction
    • Bronchoconstriction: These lead to narrowing of the airways and increased resistance to airflow.

  • (c) Tissue Resistance:

    • Compliance vs. Elastance:
    • Compliance: A measure of the lung's ability to stretch and expand; high compliance means easy expansion.
    • Elastance: The lung's tendency to recoil after stretching; high elastance means it returns to its original shape easily.
    • **Impact on Gas Exchange:
    • Decreased compliance leads to reduced lung expansion and inefficient gas exchange due to insufficient surface area being used.
    • Decreased elastance can lead to difficulties in expiration, trapping air and reducing gas exchange.

3. Gas Diffusion Impairment

  • Factors decreasing gas diffusion across the alveolar-capillary membrane:
    • Decreased Inflated Alveoli: Inadequate lung inflation reduces surface area for gas exchange.
    • Decreased Blood Flow: Reduced pulmonary perfusion decreases the amount of blood available to pick up oxygen and expel CO2.
    • Interstitial Pathology: Increased fluid or fibrosis in the interstitial space impairs gas transfer by increasing diffusion distance.

4. Work of Breathing

  • (a) Meaning: The "work of breathing" includes the energy expended to inhale and exhale air and overcome airway resistance.
  • (b) Impact of pulmonary pathophysiology: Such conditions typically cause an increase in the work of breathing due to factors like airway resistance, decreased lung compliance, or respiratory muscle fatigue.
  • (c) Clinical manifestations reflect an increase in work of breathing:
    • Increased respiratory rate
    • Use of accessory muscles
    • Nasal flaring, wheezing, or chest retractions
  • (d) Increased work of breathing raises energy demands, which can lead to higher calorie consumption and potential fatigue.

5. Diagnostic Assessments of Respiratory Function

  • Oxygen Saturation Levels:
    • SpO2: Peripheral oxygen saturation measured by pulse oximetry; a non-invasive method. Normal range is typically 95-100%.
    • SaO2: Arterial oxygen saturation measured from arterial blood gases (ABGs); provides insight into oxygen loading efficiency in lungs.
  • Arterial Blood Gases (ABG):.
    • pH, paO2 (partial pressure of oxygen), paCO2 (partial pressure of CO2), and bicarbonate levels indicate lung function and acid-base balance.
  • Pulmonary Function Tests (PFTs):
    • Assess airflow and lung capacity; notable measures include FEV1 (forced expiratory volume in one second), DLCO (diffusion capacity of carbon monoxide), and pre/post bronchodilator tests for reversibility of obstruction.
  • Peak Expiratory Flow Rate (PEFR): Measurement of maximum speed of expiration; often used in asthma to assess airflow limitation.

Part 2: Common Respiratory Disorders

6. Acute Respiratory Failure

  • Pathophysiology:
    • Failure of respiratory system to maintain adequate gas exchange, resulting in hypoxemia and/or hypercapnia.
  • Clinical Diagnostics:
    • Requires assessment via arterial blood gas measurements, imaging studies, and clinical observation of symptoms like dyspnea and altered mental state.

7. Upper vs. Lower Respiratory Tract Infections

  • (a) Differences in Pathophysiology:
    • Upper: Generally localized inflammation affecting nasopharynx, sinus tissues, larynx.
    • Lower: Involves the bronchial tubes and lungs, often with more severe systemic effects.
  • (b) Common Infections:
    • Upper: Common cold, rhinitis, sinusitis, laryngitis, influenza.
    • Lower: Acute bronchitis, bronchiolitis.

8. Pathophysiology of Pneumonia

  • (a) Affected Lung Areas:
    • Primarily affects the alveoli and surrounding lung tissues, leading to impaired gas exchange as alveoli fill with exudate.
  • (b) Microbial Pathogens:
    • Bacterial, viral, and fungal pathogens can cause pneumonia; examples include Streptococcus pneumoniae and Mycoplasma pneumoniae.
  • (c) Hospital-acquired vs. Community-acquired:
    • Hospital-acquired pneumonia (HAP) develops during hospital stay, often involving antibiotic-resistant organisms; community-acquired pneumonia (CAP) occurs outside of health care settings.
  • (d) Lobar vs. Bronchopneumonia:
    • Lobar pneumonia affects a segment or lobe of the lung with consolidation, while bronchopneumonia affects patches throughout both lungs.
  • (e) Phases of Acute Bacterial Pneumonia:
    • Edema: Initial inflammation and fluid accumulation.
    • Red Hepatization: Alveoli fill with red blood cells and fibrin.
    • Grey Hepatization: Lysis of red blood cells leads to a grey appearance of lung tissue.
    • Resolution: Restoration of the alveoli and re-absorption of inflammatory fluid.
  • (e) Rust-colored sputum:
    • Often associated with bacterial pneumonia due to blood mixing with mucus in inflamed alveoli.

9. Pathophysiology of Tuberculosis (TB)

  • Affected Lung Area: Primarily the upper lobes (apices) due to higher oxygen tension.
  • Causative Organism: Mycobacterium tuberculosis, characterized by a thick, waxy cell wall providing resistance to environmental threats and antibiotics.
  • Hypersensitivity Response: Type IV hypersensitivity reaction; reflects a cellular immune response primarily involving T-lymphocytes.
  • Granuloma Formation: Granulomas (Ghon foci) form around TB bacteria as part of the immune response to contain and wall off the infection.

10. Risk Factors for Fungal Respiratory Infections

  • Individuals with compromised immune function:
    • e.g., HIV/AIDS, cancer patients, chronic steroid use. Fungal infections thrive in lower immune competence due to reduced ability to fight infections.

11. Respiratory Tract Malignancies

  • (a) General Pathophysiology:
    • Fueled by processes like chronic inflammation, exposure to carcinogens, and genetic mutations.
  • (b) Clinical Manifestations:
    • Laryngeal cancer: Hoarseness, difficulty swallowing.
    • Lung cancer: Persistent cough, hemoptysis, weight loss.

12. Acute Respiratory Infection Risks in Children

  • Anatomic and Immunologic Characteristics:
    • Smaller airways lead to increased resistance.
    • Underdeveloped immune system contributes to a higher susceptibility to infections.

13. Pathophysiology of Epiglottitis

  • (a) Location/Function:
    • Epiglottis is located at the base of the tongue; it covers the trachea during swallowing to prevent aspiration.
  • (b) Clinical Manifestations:
    • Difficulty breathing, stridor, high fever, drooling, inability to swallow.
  • (c) Life-Threatening Risks: Airway obstruction due to swelling can develop rapidly, necessitating immediate medical intervention.

14. Pathophysiology of Common Childhood Respiratory Infections

  • Infections include:
    • Epiglottitis, croup (laryngotracheobronchitis), bronchiolitis.
  • Each has distinctive clinical findings; for example, croup often presents with a characteristic barking cough.

15. Neonatal Respiratory Distress Syndrome (NRDS)

  • Pathophysiology:
    • Caused by insufficient surfactant production in premature infants leading to alveolar collapse and impaired gas exchange.

Part 3: Disorders of Oxygenation & Ventilation

16. Aspiration and Pneumonia

  • Increased Risk Situations:
    • Occurs when foreign substances enter the lungs, often due to impaired swallow or consciousness, higher likelihood of reaching the right mainstem bronchus due to its straighter path.

17. Pathophysiology of Atelectasis

  • Definition: Collapse of lung tissue affecting oxygen exchange.
  • Compression Atelectasis: Due to external pressure (tumors, fluid).
  • Absorption Atelectasis: Loss of lung volume due to air absorption, often seen in obstructive diseases.

18. Pathophysiology of Pulmonary Edema

  • Mechanisms contributing includes:
    • Increased hydrostatic pressure, reduced oncotic pressure, inflammation, and capillary permeability.
  • Surfactant helps prevent pulmonary edema by lowering surface tension in alveoli, promoting uniform expansion.

19. Pathophysiology of Pneumothorax

  • Definition: Air in the pleural space causing lung collapse.
  • (b) Spontaneous Pneumothorax:
    • Occurs without trauma, often in tall young men.
  • (c) Open vs. Tension Pneumothorax:
    • Open allows air to enter and exit pleural space; tension traps air causing pressure buildup. Tension is more immediately life-threatening due to compressive effects on the lungs and heart.

20. Pathophysiology of Pleural Effusion

  • Types:
    • Transudative: Clear fluid; occurs in heart failure.
    • Exudative: Contains proteins and cells; seen in infections (empyema).
    • Hemothorax: Blood in the pleural space.
    • Chylothorax: Lymph fluid due to trauma/infections.

21. Acute Respiratory Distress Syndrome (ARDS)

  • (a) Pathophysiology involves lung injury leading to widespread inflammation and pulmonary edema.
  • (b) Lung injuries can arise from infections, trauma, or inhalation of harmful substances.
  • (c) ARDS vs. Neonatal RDS:
    • Neonatal RDS is primarily marked by surfactant deficiency, while ARDS results from acute inflammatory processes damaging alveoli.

22. Pathophysiology of Asthma

  • Clinical manifestations include wheezing, shortness of breath, chest tightness.
  • (a) Inflammation leads to airway changes by narrowing air passages, causing difficulty in airflow. Reducing inflammation can relieve symptoms.
  • (b) Components contributing to obstruction:
    • Airway edema, mucus secretion, bronchoconstriction.
  • (c) Diagnostic Tests:
    • FEV1: Measures forced expiratory volume in 1 second to assess airflow limitations.
    • PEFR: A quick measure of outflow rates ensuring patient is within safe parameters.
  • (d) Mechanism of Air Trapping: airway inflammation can restrict airflow leading to trapped air in lungs.
  • (e) Types of Asthma:
    • Allergic asthma has immediate reactions involving IgE, while non-allergic occurs without preceding allergic reactions (e.g. exercise-induced).
  • (f) Triggers include allergens, cold air, exercise, emotional stress.

23. Chronic Bronchitis vs. Emphysema

  • Different pathophysiologic changes of airways lead to unique symptomatology in each:
  • Chronic Bronchitis: Characterized by chronic cough, mucus production, and airway inflammation.
  • Emphysema: Results in destruction of alveoli and poor elastic recoil leading to air trapping.
  • Clinical manifestations: Chronic bronchitis often leads to cyanosis and obesity, while emphysema patients are typically thin.
  • Polycythemia in Chronic Bronchitis: Increased red blood cell production occurs as an adaptive mechanism to chronic hypoxemia in the early stages of the disease, not prominent in emphysema due to overall lower oxygenation.

24. Cystic Fibrosis Pathophysiology

  • Genetic disorder affecting the CFTR gene leading to thick mucus production, affecting lungs and other organs like pancreas and GI tract.
  • Diagnostic tests include sweat chloride test and genetic testing. Pathophysiologic effects include malabsorption and respiratory infections.

25. Idiopathic Pulmonary Fibrosis

  • A type of interstitial lung disease characterized by progressive lung scarring affecting gas exchange, often leading to respiratory failure.

26. Ventilation/Perfusion Ratio (V/Q Ratio)

  • (a) Definition: Ratio of air reaching the alveoli to blood flow in pulmonary capillaries.
  • (b) Effects of V/Q Mismatch:
    • Low V/Q ratio indicates poor ventilation relative to perfusion, causing hypoxemia.
    • High V/Q ratio indicates wasted ventilation where air reaches well-perfused but poorly functioning alveoli.

27. Pulmonary Embolism Pathophysiology

  • (a) Risk from DVT arises from thrombi breaking loose and traveling to pulmonary system.
  • (b) Other substances: fat globules, air bubbles, and amniotic fluid can cause embolism in specific risk scenarios.
  • (c) Clinical presentations differ, with massive PE causing acute respiratory distress and cardiovascular collapse while small PE may present less acutely yet remain significant.

28. Pathophysiology of Pulmonary Hypertension

  • (a) Pathophysiology involves elevated blood pressure in pulmonary arteries, leading to reduced perfusion and consequent heart strain.
  • (b) Primary vs. Secondary:
    • Primary originates idiopathically, while secondary is often due to chronic lung disease-induced hypoxia leading to vasoconstriction.

29. Hypoxia-Induced Pulmonary Vasoconstriction

  • (a) Definition: Alveolar hypoxia leads to vasoconstriction of pulmonary arterioles; a compensatory mechanism to redirect blood flow to better ventilated areas.
  • (b) Adaptive Purpose: To optimize V/Q matching, ensuring efficient gas exchange.
  • (c) Effects on Pulmonary Resistance: Increased vascular resistance increases right ventricular workload.

30. Cor Pulmonale Pathophysiology

  • Right heart failure due to lung pathology (e.g., COPD) causing hypoxia-induced pulmonary vasoconstriction, leading to right ventricular hypertrophy.

31. Blood Flow Dynamics

  • (a) Blood flow influenced by vessel length, radius, and blood viscosity; radius has the largest effect on flow according to Poiseuille's law (R ∝ r^4).
  • (b) Anemia vs. Polycythemia:
    • Anemia leads to reduced oxygen delivery, while polycythemia can risk hyperviscosity and resultant reduced flow.
  • (c) Laminar vs. Turbulent Flow: Laminar is smooth, efficient flow; turbulent flow increases resistance and can produce murmurs which indicate abnormal blood flow.

32. Cardiac Output Factors

  • (a) Four factors: preload (ventricular filling), afterload (pressure against which heart works), contractility (strength of heart muscle contractions), heart rate.
  • (b) Changes in any factor impact CO; for example, decreased preload reduces stroke volume.

33. Pathogenesis of Atherosclerosis

  • Risk factors: hypertension, inflammation, high LDL, and formation of foamy macrophages contribute to plaque formation and narrowing of arteries, subsequently reducing CO, primarily affecting afterload.

34. Lipid Profile Components

  • Distinguishing between triglycerides and cholesterol; HDL is protective, while LDL increases risk of atherosclerosis.

35. Aneurysm Pathophysiology

  • Aneurysms often arise from arterial weakening due to atherosclerosis. Risk of rupture increases with aneurysm increases in size.

36. Peripheral Vascular Disorders

  • (a) Peripheral arterial vs. venous disorders differ in occlusion types and etiology; arterial disorders lead to ischemia, while venous disorders can produce swelling and clotting issues.

37. Hypertension

  • (a) Primary vs. Secondary Hypertension: Primary Hypertension has no identifiable cause; Secondary originates from underlying diseases.
  • (b) Target Organ Damage: Chronic elevation can damage organs such as the heart and kidneys due to ongoing ischemic episodes or pressure overload.

38. Orthostatic Hypotension Pathophysiology

  • Definition: Drop in blood pressure upon standing leading to lightheadedness due to impaired autonomic regulation.

Part 2: Dysrhythmias & Myocardial Disorders

39. Cardiac Dysrhythmias

  • (a) Rhythm alterations include:
    • PACs and PVCs differ in origin and consequence on HR.
    • SVT vs. V-Tach differ in potential for significant drop in CO.
    • A-Fib carries increased stroke risk due to irregular heartbeats.

40. Myocardial Ischemia and CAD

  • (a) CAD pathophysiology involves plaque buildup leading to ischemia via vascular lumen stenosis; risk factors include hypertension and atherosclerosis.
  • (b) Ischemia reduces CO, especially affecting contractility.
  • (c) Angina pectoris defined by chest pain from myocardial ischemia, with classic presentations during exertion

41. Acute Coronary Syndromes

  • (a) Unstable angina indicates a more serious condition than stable angina, necessitating immediate intervention.
  • (b) Differences in pathophysiology include:
    • NSTEMI vs. STEMI regarding the depth of myocardial damage and EKG changes.

42. Electrocardiogram Changes

  • (c) Changes from ischemia include:
    • T-wave inversions in NSTEMI, ST-elevations in STEMI, and pathological Q-waves indicating myocardial damage.

43. Healing Post-Myocardial Infarction

  • (d) Myocardial necrosis leads to scar formation, losing functional heart muscle capabilities; scar cannot conduct electrical signals like muscle.
  • (e) Serum biomarkers like troponins indicate myocardial injury; released upon cell damage.

44. Myocardial Infarction Complications

  • (f) Include immediate dangers (arrhythmias, rupture) and long-term effects (heart failure, remodelling).

Part 3: Pericardial & Endocardial Disorders, Heart Failure & Circulatory Failure

45. Heart Wall Disorders

  • (a) Distinct types: pericarditis, pericardial effusion, cardiac tamponade, cardiomyopathy, and infective endocarditis reflect varying severity and types of effects.

46. Rheumatic Heart Disease

  • (a) Primary risk from streptococcal infections highlighting need for prophylaxis in at-risk populations.

47. Valvular Heart Disorders

  • Pathophysiology reflects altered blood flow in scenarios like valvular insufficiency (regurgitation) or stenosis, impacting cardiac efficiency.

48. Heart Failure Definition

  • (a) Heart failure is impairment in heart function leading to fluid overload and congestion. Clinical manifestations include fatigue, dyspnea, and edema.
  • (b) BNP elevation reflects worsening heart failure; BNP promotes natriuresis and diuresis to counteract fluid overload.
  • (c) Classifications: left vs. right heart failure, systolic vs. diastolic dysfunction impact symptoms and clinical management distinctly.

49. Clinical Manifestations of Heart Failure

  • Symptoms of left heart failure include pulmonary congestion and dyspnea.
  • Right heart failure symptoms include systemic congestion leading to hepatomegaly and peripheral edema.

50. Circulatory Failure and Shock

  • (a) Circulatory failure leads to systemic hypoperfusion, risking cellular injury and organ dysfunction.
  • Compensated Shock vs. Hypotensive Shock:
    • Compensated: Body attempts to stabilize; hypotensive is progressive state often leading to organ failure if unaddressed.

51. Types of Shock

  • Pathophysiology differs among species:
    • Cardiogenic, hypovolemic, obstructive, and distributive shocks (including neurogenic, anaphylactic, and septic) highlighting variability in causes, diagnostics, and management.

52. Complications of Shock

  • Include lactic acidosis, lung injury, organ failure, leading to long-term health consequences or mortality.