CLASE TEÓRICA 2 - LESIÓN, ADAPTACIÓN Y DIFERENCIACIÓN CELULAR

Introduction to Cellular Adaptations and Injuries

Overview of the Virtual Session

• Dr. Gabriel Asís introduces herself and acknowledges the challenges of virtual learning, encouraging positivity and resilience during this time.

Cellular Responses to Stress

• The discussion begins with normal cells' adaptive mechanisms in response to harmful stimuli, emphasizing their ability to adapt through various processes.

Types of Cellular Adaptation

• Key forms of cellular adaptation are introduced:

• Hiperplasia: Increase in organ size due to an increase in cell number.

• Hipertrofia: Increase in organ size due to an increase in individual cell volume.

• Atrofia: Decrease in organ size due to a reduction in cell size or number.

• Metaplasia: Replacement of one mature epithelium with another more resilient type.

Cellular Injury Mechanisms

Transition from Adaptation to Injury

• The concept of "injury" is defined as a transitional state before actual cellular damage occurs, where cells have not yet sustained irreversible injury.

Reversible vs. Irreversible Injury

• Reversible injuries can lead back to normalcy if the harmful stimulus is removed; an example given is steatosis, characterized by lipid accumulation within cells.

• Irreversible injuries result in necrosis, which refers not just to cell death but also encompasses all subsequent changes that occur post-mortem.

Examples of Cellular Changes

Cardiac Muscle Response

• A specific case study on cardiac myocytes under pressure overload (e.g., hypertension), leading them to undergo hypertrophy as an adaptive response.

Histopathological Evidence

• Hypertrophy can be observed histologically and macroscopically; examples include concentric hypertrophy reducing ventricular lumen space due to pressure overload.

Injury Progression and Infarction

From Injury to Necrosis

• The progression from reversible injury (lipid accumulation) leads eventually to irreversible injury (cell death), particularly noted in cardiac tissue during infarction events.

Visual Representation of Infarction

• An illustration shows areas affected by myocardial infarction, highlighting necrotic zones that become functionally inactive and may lead to arrhythmias.

Cellular Adaptations Under Stress

Defining Cellular Adaptations

• Cellular adaptations are described as functional and structural responses that are reversible when faced with significant physiological stress or pathological stimuli.

Prostate Gland Example

• An example provided includes benign prostatic hyperplasia seen commonly in older men, characterized by nodular growth patterns upon examination.

Understanding Benign Prostatic Hyperplasia and Related Concepts

Benign Prostatic Hyperplasia (BPH)

• BPH is characterized as a benign nodular hyperplasia, which can cause complications due to the enlargement of the prostate gland that compresses the prostatic urethra.

Urinary Flow Interruption

• The compression from BPH leads to interrupted urine flow, resulting in urinary retention in the bladder and potentially affecting kidney structures.

Physiological Hypertrophy

• An example of physiological hypertrophy is observed in pregnant women, where the uterus enlarges significantly compared to a non-pregnant uterus, demonstrating normal histopathological changes.

Atrophy vs. Hypertrophy

• Atrophy refers to a decrease in organ size due to loss of cells or cell size; for instance, comparing a normal brain with one exhibiting significant atrophy shows profound sulci indicative of reduced parenchyma.

Cellular Adaptations and Injuries

Metaplasia Example: Barrett's Esophagus

• Metaplasia occurs when stratified squamous epithelium of the esophagus is replaced by columnar epithelium due to gastroesophageal reflux disease (GERD), illustrating adaptive cellular responses.

Causes of Cellular Injury

• Cellular injuries can arise from various factors including hypoxia, physical agents, chemical agents, infectious diseases, immune reactions, genetic mutations, and hormonal imbalances.

Reversible vs. Irreversible Cell Injury

• Cell injuries may be reversible if stimuli are removed early; however, persistent or intense stimuli lead to irreversible damage characterized by necrosis or apoptosis.

Types of Cell Death

Necrosis vs. Apoptosis

Understanding Cell Death: Apoptosis vs. Necrosis

Mechanisms of Cell Death

• Apoptosis is a programmed cell death process, meticulously regulated where cells activate enzymes to degrade nuclear DNA and cytoplasmic proteins.

• The result of apoptosis includes the formation of apoptotic bodies, which are eventually phagocytosed by macrophages.

Key Differences Between Necrosis and Apoptosis

• A critical morphological difference is that necrosis triggers an inflammatory response, while apoptosis does not elicit such a response.

• Various patterns of tissue necrosis exist, including coagulative, liquefactive, gangrenous, fatty, and fibrinoid necrosis.

Coagulative Necrosis

• Coagulative necrosis often results from ischemic factors due to lack of oxygen or nutrients caused by vascular obstruction (e.g., coronary artery blockage).

• In myocardial infarction (coagulative necrosis), cells appear ghost-like as they lose their nuclei and transform into acidophilic structures.

Caseous Necrosis in Tuberculosis

• Caseous necrosis is characterized by white areas in lung tissue resembling cheese; it is associated with tuberculosis caused by Mycobacterium tuberculosis.

• Granulomas form in response to chronic inflammation in tuberculosis; they consist of central areas of necrotic tissue surrounded by mononuclear infiltrates.

Fatty Necrosis

• Fatty necrosis occurs frequently in acute pancreatitis when pancreatic enzymes like lipase damage surrounding adipose tissue.

• This type of necrosis leads to the destruction of fat cells, resulting in visible signs of inflammation around the affected area.

Fibrinoid Necrosis

• Fibrinoid necrosis appears histologically as pink-stained deposits resembling fibrin within blood vessel walls; it typically indicates immune-mediated damage.

• This pattern is commonly observed during immunological reactions where immune complexes deposit on arteriolar walls, narrowing their lumens significantly.

Developmental Disorders Related to Organ Formation

• Agenesis refers to the complete absence of an organ and its embryonic precursor; atresia denotes a lack of opening in hollow organs like the trachea or intestines.

Understanding Organ Dysplasia and Anaplasia

Overview of Organ Dysplasia

• The term "dysplasia" refers to incomplete development or reduced size of an organ, characterized by a lower number of cells.

• A common example is esophageal atresia, where a segment of the esophagus is replaced by fibrous tissue due to lack of lumen, leading to feeding difficulties in infants.

Treatment and Implications

• Surgical intervention is the only corrective treatment for this defect, ideally performed shortly after birth to alleviate feeding issues.

• Organ dysplasia is defined as a malformative disorder resulting in disorganization of normally present elements within an organ's parenchyma.

Characteristics of Dysplastic Organs

• Classic examples include renal dysplasia, which presents with cystic cavities visible macroscopically and histopathologically.

• Dysplastic changes can lead to significant implications in specific organ pathology studied later in the year.

Epithelium and Its Changes

• Epithelial dysplasia signifies disordered growth often seen in metaplastic epithelium; however, not all metaplasia indicates dysplasia.

• Key characteristics include loss of cellular uniformity and architectural organization among epithelial cells.

Classification of Epithelial Dysplasia

• Epithelial dysplasias are classified into mild, moderate, or severe forms based on the extent of cellular alteration.

• Cervical intraepithelial neoplasia (CIN), categorized into types 1 through 3, reflects varying degrees of epithelial involvement from mild (affecting one-third) to severe (involving all layers).

Anaplasia: Loss of Differentiation

• Anaplasia denotes a significant loss in differentiation where cancerous cells deviate markedly from normal cell morphology.

• Features include hyperchromatic nuclei, pleomorphism, and atypical mitotic figures commonly observed in malignant tumors.