Exam 1 Study Guide Notes

Exam 1 Study Guide - Summer 2025 N3517 Pathophysiology

Cell Adaptation and Injury

• Types, characteristics, and examples of cell adaptation.

• Cellular responses to and mechanisms of cell injury:

  • Ischemia: Pathophysiology of insufficient blood flow to tissues.

  • Hypoxic injury: Pathophysiology of cell damage due to oxygen deprivation.

  • Reactive Oxygen Species (ROS) and Oxidative Stress:

    • Pathophysiology: Imbalance between ROS production and antioxidant defenses, leading to cell damage.

    • Treatment: Strategies to reduce ROS production or enhance antioxidant capacity.

• Mechanisms and manifestations of cell death:

  • Necrosis: Unregulated cell death due to injury. Different types include:

    • Coagulative necrosis: Cell proteins denature, common in hypoxic environments.

    • Liquefactive necrosis: Cells are digested by enzymes, resulting in liquid debris (e.g., brain infarct).

    • Caseous necrosis: Cheese-like appearance, characteristic of tuberculosis.

    • Fat necrosis: Occurs in adipose tissue, often due to lipase enzymes.

    • Gangrenous necrosis: Death of tissue from severe hypoxic injury; can be dry or wet.

  • Apoptosis: Programmed cell death, a regulated process.

• Reperfusion injury: Pathophysiology of tissue damage caused when blood supply returns to tissue after a period of ischemia or lack of oxygen.

Acute Major Burn Injury

• Pathophysiology: Systemic response to burn injury affecting multiple organ systems. Includes zone of coagulation, stasis, and hyperemia.

• Complications and their pathophysiology: Inhalation injury, Infection, hypovolemic shock, hypermetabolism, and cardiac arrest.

• Clinical manifestations:

  • Fluid loss and electrolyte imbalances.

  • Inflammatory response.

  • Increased metabolic rate.

Fluid and Electrolyte Balance

• Water balance regulation: Mechanisms involving ADH, thirst, and kidney function.

• Mechanisms, clinical manifestations, and treatment of fluid alterations:

  • Dehydration/Hypovolemia: Fluid deficit in the body.

  • Edema: Abnormal fluid accumulation in interstitial spaces.

  • Hypertonic, hypotonic, and isotonic imbalances.

• Electrolyte regulation, mechanisms of alterations, and clinical manifestations:

  • Calcium: Role in muscle contraction, nerve transmission, and bone structure.

  • Potassium:

    • Regulation and function in neuromuscular excitability.

    • Alterations and clinical manifestations (hyperkalemia and hypokalemia).

    • Treatment of potassium imbalances.

  • Sodium: Regulation of fluid balance and nerve function.

• Acid-base balance:

  • Interpretation of arterial blood gases (ABGs): pH, PaCO2, HCO3-.

  • Physiology of compensatory mechanisms: Buffers, respiratory, and renal compensation.

  • Clinical manifestations of acid-base imbalances

Inflammation and Immunity

• Mechanisms and clinical manifestations of the inflammatory process:

  • Acute inflammation: Immediate response to injury or infection.

    • Local: Redness, swelling, heat, pain, loss of function.

    • Systemic: Fever, leukocytosis, acute phase proteins.

  • Chronic inflammation: Prolonged inflammatory response.

    • Involves macrophages, lymphocytes, and fibroblasts.

    • Can lead to tissue damage and fibrosis.

  • White blood cell count differential: Changes in WBC types during inflammation.

• Mechanisms, regulation, effects, and treatment of histamine release:

  • Histamine: Released from mast cells and basophils.

  • Causes vasodilation and increased vascular permeability.

• Plasma protein systems:

  • Complement cascade: Functions and mechanisms.

    • Opsonization, cell lysis, inflammation.

• Wound healing:

  • Pathophysiology: Process of tissue repair.

  • Complications: Infection, dehiscence, keloid formation.

• Physiology, pathophysiology, and clinical manifestations of the adaptive/acquired immune response:

  • Humoral immunity: B cells and antibodies.

  • Cell-mediated immunity: T cells.

• Types and examples of immunity:

  • Active: Acquired through exposure or vaccination.

  • Passive: Transfer of antibodies (e.g., mother to fetus).

• Mechanisms, clinical manifestations, complications, and treatment of hypersensitivity reactions:

  • Type I: Immediate hypersensitivity (e.g., allergy).

  • Type II: Antibody-mediated (e.g., transfusion reaction).

  • Type III: Immune complex-mediated (e.g., serum sickness).

  • Type IV: Cell-mediated (e.g., contact dermatitis).

Infection

• Bacterial toxins:

  • Gram-negative organisms: Endotoxins - pathophysiology.

• Viral: Pathophysiology, protection.

• Acquired Immunodeficiency Syndrome (AIDS):

  • Pathophysiology: HIV infection leading to immune deficiency.

  • Interpretation of laboratory tests: CD4+ cell count, viral load.

• Cytokine types and roles:

  • Endogenous pyrogens: IL-1, TNF-alpha - induce fever.

Stress

• Stages and sequelae of stress adaptation (General Adaptation Syndrome):

  • Alarm, resistance, and exhaustion stages.

• The stress response:

  • Pathophysiology: Activation of the HPA axis and sympathetic nervous system.

  • Stress hormones and their effects: Cortisol, epinephrine.

  • Clinical manifestations of stress.

• Allostatic overload:

  • Pathophysiology: Cumulative effects of chronic stress.

  • Sequelae: Cardiovascular disease, immune dysfunction.

• Stress activation of the immune response:

  • Pathophysiology: Cytokines released, especially endogenous pyrogens.

• Glucocorticoid therapy: Effects on immune function and inflammation.

Shock

• Anaphylactic: Pathophysiology; Severe allergic reaction leading to vasodilation and bronchoconstriction.

• Cardiogenic: Pathophysiology, compensatory responses; Heart failure leading to inadequate tissue perfusion.

• Hypovolemic: Etiology, pathophysiology, compensatory responses; Insufficient circulating blood volume.

• Neurogenic: Pathophysiology; Imbalance between parasympathetic and sympathetic nervous systems, leading to vasodilation and hypotension.

• Septic: Pathophysiology; Systemic response to infection, leading to vasodilation and inflammation.