Chapter 2: Altered Cells and Tissues; Inflammation and Tissue Repair (Lecture Notes)

A comprehensive set of Q&A flashcards covering cellular structure and function, cellular responses to stress and injury, inflammation and healing processes, and common inflammatory diseases and case-study concepts from the notes.

What is the hierarchical organization of the human body from simplest to most complex structures?

Cells, tissues, organs, and organ systems.

What is the composition of the plasma membrane?

A phospholipid bilayer with polar, hydrophilic heads and nonpolar, hydrophobic tails, containing integral, transmembrane, channel, and peripheral proteins.

Name some organelles found in the cytoplasm.

Endoplasmic reticulum, Golgi apparatus, lysosomes, peroxisomes, proteasomes, mitochondria, nucleus, and cytoskeleton.

List key cellular functions.

Transportation, ingestion, secretion, respiration, communication, and reproduction.

Differentiate passive transport, facilitated transport, and active transport.

Passive transport does not require energy (diffusion, osmosis); facilitated transport is passive with protein assistance; active transport requires energy (ATP) to move substances against a gradient.

What processes involve ingestion of materials by the cell?

Endocytosis, including pinocytosis (small vesicles) and phagocytosis (large particles like bacteria).

What process involves the release of cellular products from the cell?

Exocytosis.

How do aerobic and anaerobic respiration differ?

Aerobic respiration uses oxygen; anaerobic respiration does not.

Name the major cellular responses to stress.

Atrophy, hypertrophy, hyperplasia, metaplasia, and dysplasia.

Differentiate apoptosis and necrosis.

Apoptosis is programmed cell death; necrosis is death from injury.

What are common causes of cellular injury?

Physical, mechanical, thermal, or chemical factors.

What is reversible vs irreversible cell injury?

Mild stress is reversible; severe or persistent stress can cause irreversible injury and necrosis.

What is the pathophysiology of cerebral atrophy?

Reduction in the size of cells in the cerebrum and neurons, often due to reduced stimulation or injury.

What are the clinical manifestations of cerebral atrophy?

Focal (localized) or global (affecting the entire brain) symptoms.

What drives cardiac hypertrophy, and what is secondary hypertrophy?

Increased cardiac workload or increased functional demand or inherited traits; secondary hypertrophy results from an underlying condition that raises left ventricular workload.

What are the clinical manifestations of cardiac hypertrophy?

Shortness of breath, chest pain, and syncope.

What causes acromegaly Pathophysiology?

Excessive growth hormone and IGF-1 leading to hyperplasia and excessive growth after epiphyseal plates close.

What are the clinical manifestations of acromegaly?

Soft tissue swelling, altered facial features, hand numbness, and deepening of the voice.

Where does cervical metaplasia and dysplasia occur and what is metaplasia?

In the transformation zone of the cervix; metaplasia is a change in cell type in response to stress.

What are risk factors for cervical metaplasia and dysplasia?

Early onset of sexual activity, more than three sexual partners, HPV exposure, and smoking.

What are the three lines of defense?

First line: skin and mucous membranes; Second line: inflammatory response; Third line: immune response.

What triggers acute inflammation and what are its goals?

Tissue injury triggers it; goals are to increase blood flow and recruit healing cells for tissue repair.

Describe the vascular response in acute inflammation.

Chemical mediators cause vasodilation and increased capillary permeability, leading to redness and swelling.

What are the sources of inflammatory mediators?

Cell-derived mediators from white blood cells, platelets, or damaged tissue, and plasma-derived mediators from complement, kinin, and clotting systems.

What is the cellular response to inflammation?

Chemotaxis, cellular adherence, and cellular migration; phagocytes move to the site to engulf and destroy harmful substances.

What are local manifestations of acute inflammation?

Heat, incapacitation, pain, edema, and redness.

What are systemic manifestations of inflammation?

Fever and an increase in circulating leukocytes and plasma proteins.

What are the phases of healing?

Inflammatory phase, proliferative phase, and remodeling phase.

What are common complications during healing?

Infection, ulceration, dehiscence, keloids, and adhesions.

What characterizes chronic inflammation?

Persistent or recurrent inflammation lasting weeks or longer, with prominent involvement of monocytes, macrophages, and lymphocytes, and possible granuloma formation and scarring.

What are the acute and chronic sinusitis pathophysiologies?

Acute: ostial blockage and mucus outflow obstruction due to allergies, viruses, or irritants; Chronic: multifactorial with environmental factors, persistent infection, and allergens.

What are the clinical manifestations of acute vs chronic sinusitis?

Acute: facial pain, fever, nasal congestion; Chronic: nasal congestion, foul breath, chronic cough.

How are burns classified by depth and what are their clinical manifestations?

Depths: superficial partial-thickness, deep partial-thickness, full-thickness. Superficial: heat, swelling, pain, redness; deep partial-thickness: blistering; full-thickness: eschar.

What is the pathophysiology of rheumatoid arthritis?

Chronic inflammation of the synovial membranes with autoimmune etiology; genetics and triggers contribute.

What are the clinical manifestations of rheumatoid arthritis?

Symmetrical joint pain, stiffness, redness, heat, swelling, and decreased mobility.

What are the pathophysiology and risks of gastritis?

Acute gastritis: acute inflammation of gastric mucosa due to irritants or poor perfusion, causing epithelial necrosis. Chronic gastritis: persistent infection (H. pylori) or autoimmune, leading to atrophy.

What are the pathophysiology features of pancreatitis (acute vs chronic)?

Acute pancreatitis: injury to acinar cells, zymogens, and pancreatic duct often due to gallstones or alcohol. Chronic pancreatitis: long-term alcohol use with duct obstruction and ischemia, causing atrophic and fibrotic acinar cells and loss of function.

How do Crohn disease and ulcerative colitis differ in pathophysiology?

Crohn disease: chronic, noncontinuous inflammation with penetrating ulcers and fibrosis anywhere in the GI tract. Ulcerative colitis: continuous, superficial inflammation beginning in the rectum and ascending the colon, with ulceration and risk of perforation/hemorrhage.