NUR306- Patho Day 1

Pathophysiology

The study of how normal physiological processes are altered by disease.

Homeostasis

The body's ability to maintain relatively stable internal conditions even when exposed to external or internal stressors.

5 Basic Needs of Cells

Oxygen (95-100), water, nutrients, stable temperature (98.6), and acid-base balance (7.35-7.45).

Cellular Adaptation

Cells changing their structure and function in response to stress to maintain homeostasis.

Atrophy

A decrease in cell size (making them more efficient) in response to a decreased workload.

Atrophy Causes

Disuse (e.g. casted limb), denervation (nerve damage), decreased hormones, malnutrition, and decreased blood flow.

Catabolism in Atrophy

A metabolic process that breaks down complex molecules (like proteins) into simpler ones, increasing during atrophy to cause cells to shrink.

Hypertrophy

An increase in cell size and tissue mass of an involved organ/tissue in response to an increased workload.

Hypertrophy Causes & Examples

Increased skeletal muscle workload (exercise), pathologic hypertension (causing cardiac muscle hypertrophy), or physiologic pregnancy (uterine enlargement).

Hyperplasia

An increase in the number of cells due to an increased rate of cell division.

Compensatory Hyperplasia Example

Normal organ regeneration, such as the liver growing back after a partial hepatectomy.

Hormonal Hyperplasia Example

Normal cell multiplication stimulated by hormones, such as estrogen causing breast and uterine tissue growth during pregnancy.

Pathologic Hyperplasia Danger

Abnormal hormonal stimulation, such as excess estrogen causing endometrial bleeding, which can undergo malignant transformation (cancer).

Metaplasia

Reversible conversion of one adult cell type to another simpler, less specialized cell type of the same lineage to survive chronic irritation.

Metaplasia Clinical Example

Chronic smoking converting ciliated columnar airway cells into stratified squamous cells, which lack protective cilia for mucus clearance.

Dysplasia

Abnormal growth of cells with deranged size, shape, and organization; often called atypical hyperplasia.

Dysplasia Precancerous Risk

Although adaptive and potentially reversible if the irritant is removed, persistent dysplasia can progress to cancer (e.g. cervical HPV dysplasia).

Reversibility of Adaptations

Metaplasia and Dysplasia are adaptive and potentially reversible if the irritating causative agent/stressor is removed.

Loss of Sodium-Potassium Pump

Without ATP, potassium (K+) leaks out, sodium (Na+) moves in, and water follows sodium, causing the cell to swell.

Hypoxia to Anaerobic Metabolism

Lack of oxygen forces cells to convert to anaerobic metabolism, leading to lactic acid buildup, decreased pH, and decreased protein synthesis.

Reversible vs. Irreversible Injury (NCLEX Pearl)

ATP depletion and cell swelling indicate reversible injury; mitochondrial failure and cell membrane damage indicate irreversible cell injury/death.

Cell Swelling and Vacuoles

Failed ion transport causes water to accumulate in the cytoplasm, forming membrane-bound sacs called vacuoles (vacuolar degeneration).

Intracellular Accumulations (Infiltrates)

Normal or abnormal substances (lipids, proteins, calcium/plaque, pigments) produced in excess that build up in the cell's cytoplasm.

Systemic Manifestations of Cell Injury

Fatigue, malaise, loss of appetite, fever, pain, elevated white blood cells (WBCs), and cell-specific enzymes in the blood.

Coagulative Necrosis

Cell death caused by ischemia/hypoxia (commonly in heart and kidney) where tissue remains firm and swollen, resembling a cooked egg white.

Liquefactive Necrosis

Cell death (commonly in brain or abscesses) where cells are completely digested by enzymes, resulting in soft, liquid tissue and pus.

Caseous Necrosis

Cell death (classic in Tuberculosis) resembling a cheesy appearance, representing a combination of coagulative and liquefactive necrosis in the lungs.

Dry Gangrene

A type of coagulative necrosis in extremities characterized by dry, wrinkled, black skin with a clear line of demarcation and few systemic symptoms.

Wet Gangrene

A rapid, severe type of necrosis with active bacterial infection, characterized by moist, swollen, black tissue with no line of demarcation and severe systemic symptoms.

Gas Gangrene

A surgical emergency caused by Clostridium bacterial infection in trauma/fractures, producing toxins and gas bubbles in tissue.

Crepitus

A crackling sensation felt and heard under the skin caused by the presence of gas bubbles in tissues (characteristic of gas gangrene).

Negative Feedback System

The body's primary control mechanism to maintain homeostasis by sensing a deviation from normal and triggering a response to counteract that change.

Selye's Triad of Stress

Orchestrated bodily response consisting of: 1) Enlargement of adrenal glands, 2) Atrophy of the thymus gland, and 3) Development of bleeding gastric ulcers.

GAS Stage 1: Alarm Reaction

The rapid mobilization of resources (SNS fight-or-flight) where the body releases adrenaline and cortisol to prepare to respond.

GAS Stage 2: Resistance

The body attempts to cope with and adapt to the persistent stressor, maintaining high stress resistance while trying to return to homeostasis.

GAS Stage 3: Exhaustion

Occurs when reserves are completely depleted due to chronic, prolonged stress, leading to system failure, illness, or death.

Sympathetic Nervous System (SNS) Stress Role

A very rapid 'fight-or-flight' response necessary for basic survival, shifting blood and resources to vital organs to get out of harm's way.

Norepinephrine (NE) Stress Function

A catecholamine that promotes vasoconstriction and supports blood pressure (increased systemic vascular resistance) to maintain perfusion.

Epinephrine (EPI) Stress Function

A catecholamine that increases heart rate, cardiac output, bronchodilates airways, dilates pupils, increases skeletal muscle flow, and increases blood glucose.

Endorphins in Stress

Endogenous opiates released to increase the pain threshold and produce well-being or euphoria; levels decrease with chronic stress.

HPA Axis Pathway

Hypothalamus (releases CRH) -> Anterior Pituitary (releases ACTH) -> Adrenal Cortex (releases Cortisol).

Cortisol

A glucocorticoid steroid hormone released by the adrenal cortex in response to physical or emotional stress.

Cortisol-Induced Hyperglycemia

Cortisol increases gluconeogenesis (glucose production in the liver), raising blood sugar to conserve energy for critical nerve cells.

Cortisol-Induced Immune Suppression

Cortisol suppresses antibodies and inflammation, resulting in thymus/lymph node atrophy and masking subtle signs of infection (fever may be absent).

Cortisol-Induced Poor Healing

Cortisol decreases fibroblasts and collagen production, resulting in thin skin, bruising, and slow wound healing.

Cushingoid Features

Systemic signs of high cortisol or chronic steroid use, including gastric ulcers, moon face, buffalo hump, and truncal obesity.

Adaptive (Good) Effects of Cortisol

In short bursts, it conserves energy for nerve cells and reduces destructive cytokines, preventing excessive tissue damage from inflammation.

Corticosteroids MOA

Synthetic glucocorticoids (like Prednisone and Solu-Medrol) that act as potent anti-inflammatories and suppress immune function.

Prednisone vs. Solu-Medrol

Prednisone is administered orally (PO) for chronic conditions (e.g. asthma, COPD); Solu-Medrol is given IV or IM for acute exacerbations.

NSAIDs vs. Corticosteroids

NSAIDs block COX to reduce pain/fever (risk GI bleeds/AKI); Corticosteroids suppress the entire immune response (risk hyperglycemia/infection).

Corticosteroid NCLEX Alerts

Never stop corticosteroids abruptly (requires tapering to avoid adrenal crisis), and monitor blood glucose closely ('Steroids = SUGAR').