Chapter 2 - Cell Injury, Adaptations, and Maladaptive Changes (Capriotti/Davis Advantage)

A comprehensive set of Q&A flashcards covering etiology, cell adaptations, injury mechanisms, endothelium-related pathology, and programmed cell death concepts from Chapter 2.

What is disease etiology?

The original cause of a cell alteration or disease.

What are etiologic agents?

Causes of the cell alteration or disease (e.g., infection, trauma, inflammation, etc.).

What can happen in response to an etiologic agent?

Cells may develop adaptive/compensatory changes or maladaptive changes.

What is histology?

The microscopic study of tissue.

What is a biopsy?

A sample of tissue taken for histological analysis.

What is an autopsy?

Examination of tissue of a deceased organism.

What are pathognomonic changes?

Unique, identifying disease presentations.

Give examples of pathognomonic changes.

Crater-like stomach formations indicate ulcers; rice-water stools indicate cholera.

What is atrophy?

Cells revert to a smaller size due to reduced metabolic demand (e.g., paralysis or immobilization).

What is hypertrophy?

Increase in the size of individual cells; can be physiological or pathological.

What is hyperplasia?

Increase in the number of cells; occurs in cells capable of mitosis and can be hormone-driven.

What is metaplasia? ex

Replacement of one mature cell type with another better suited to stress.

ex: gerd

What is dysplasia?

Deranged cell growth; often chronic inflammation and a precancerous state.

• cells can vary in shape and organization compared with normal

What is Barrett’s metaplasia progression in GERD?

Esophageal squamous cells transform to columnar (stomach-like) cells, potentially advancing to low- and high-grade dysplasia and adenocarcinoma.

What is neoplasia?

New growth; disorganized, uncoordinated, uncontrolled cell growth; can be benign or malignant.

What distinguishes benign from malignant neoplasms?

Benign: resembles normal cells, non-metastatic, well-defined borders. Malignant: poorly differentiated, metastasis-prone, poorly defined borders.

What are the basic concepts of cell injury?

Dysfunction of the Na+/K+ pump,

plasma membrane damage,

decreased protein synthesis,

intracellular accumulations (including water),

DNA damage.

What happens when the Na+/K+ pump fails due to reduced ATP?

Loss of electrochemical gradient;

Na+ and water influx cause cell swelling;

Ca++ accumulates inside the cell.

What occurs when the plasma membrane integrity is lost?

Harmful substances enter the cell;

essential substances are lost;

electrolyte and fluid balance is disrupted.

How does decreased protein synthesis relate to cell injury, with the lack of ATP

cells can’t synthesize necessary proteins, potentially leading to death.

What are intracellular accumulations?

Excess deposits that disrupt cell function

(e.g., fatty liver; storage diseases).

What causes hypoxic injury?

Decreased oxygen to tissues

; most common cause of cell damage, from ischemia, anemia, or pulmonary/cardiac issues.

What is ischemia and its common causes?

Reduced blood flow; caused by atherosclerosis or thrombosis leading to chronic hypoxia.

What are cellular responses to hypoxia?

Decreased ATP, pump failure (Na+/K+ and Na+/Ca++ exchange),

cell swelling,

vacuolation,

reduced protein synthesis.

What is vacuolation in hypoxic injury?

Endoplasmic reticulum swells and forms vacuoles; may be reversed if oxygen is restored.

What happens after vacuolation in hypoxia?

Lysosomes and mitochondria swell, release calcium, activate enzymes leading to autolysis and cell death.

What are free radicals (ROS)?

Highly reactive molecules formed during metabolism that can damage proteins, membranes, and DNA.

How do cells defend against free radicals?

Antioxidant enzymes (e.g., SOD) and antioxidants like glutathione, vitamins C and E.

What is chemical injury?

Damage from endogenous or exogenous chemicals/drugs

; examples include acetaminophen overdose and carbon monoxide.

How can infections injure cells?

Infectious agents (bacteria, viruses, fungi, parasites)

e.g., botulinum toxin causes paralysis, HIV kills T helper cells.

What is the endothelium and what does it secrete?

Cells lining blood vessels;

secrete VEGF ( vascular endothelial growth factor which causes growth of new blood cells)

NO ( nitric oxide, vasodilator)

and endothelin (vasoconstrictor

How does endothelial injury relate to atherosclerosis?

Injury to the endothelium initiates inflammation and plaque formation in arteries.

What factors injure the endothelium?

Hypertension - increased blood pressure

, hyperglycemia- elevated blood glucose levs

free radicals,

hyperlipidemia- increased levels of lipids especially LDL

(often together).

What is the effect of hypertension on the endothelium?

Increased shear forces damage endothelium; inflammation and aneurysm risk increase.

How does diabetes affect the endothelium?

Hyperglycemia forms advanced glycation end products (AGEs) that damage endothelium and cause inflammation; endothelin rises, increasing BP; oxidative stress ensues.

What role do free radicals play in endothelial injury?

ROS from factors like smoking damage endothelial cells.

What is the role of angiotensin II in endothelial injury?

Potent vasoconstrictor that raises BP and shear stress; countered by ACE inhibitors or ARBs.

What is atherogenesis?

Formation of atherosclerotic plaques initiated by endothelial injury and inflammatory responses to LDL deposition. which form foam cells

What are foam cells?

Macrophages that have taken up LDL cholesterol and become lipid-laden, contributing to plaque formation.

What happens after plaques form in vessels?

Luminal narrowing;

plaques can rupture

, causing clots;

NO reduction reduces vasodilation,

worsening ischemia.

What is apoptosis?

Programmed cell death; organized, without inflammation; cellular contents are neatly removed by macrophages.

How does apoptosis differ from necrosis?

Necrosis is due to injury and irreversible with the lysosomal activation and autolysis the membrane disintegrates and has inflammatory reaction

infarction is death of tissue results from prolonged ischemia

What is infarction?

Ischemic necrosis; tissue death due to prolonged ischemia (e.g., myocardial infarction).

What is gangrene?

Prolonged ischemia leading to infarction and infection; gas gangrene is caused by Clostridium perfringens.

occurs in skin,intestine, deep wounds

what happens if hyperplasia evolves into maladaptive compensation

Keloid formation

what are mutations

genetic Damage injuring DNA changing the function of the cell

what are some long term complications of diabetes

include neuropathy, retinopathy, nephropathy, and cardiovascular diseases.

most of the many long term complications of diabetes are due to

damaged blood vesselsh and the problems that result from it

how does high blood glucose harm blood vessels

• excessive glucose reacts forming advanced glycation end products by inflammation

• endothelin- potent vasoconstrictor increasing BP

• Hypoglycemia- which causes oxidative stress

what is oxidative stress

imbalance between free radicals and antioxidants in the body,

often leading to cellular damage and contributing to various diseases.