Intracellular Accumulations Lecture

60 question-and-answer style flashcards covering the key concepts of intracellular accumulations, pigments, and pathologic calcification from Dr. Mai’s lecture.

What is the definition of fatty change (steatosis)?

Intracellular accumulation of triglycerides within parenchymal cells.

Which organ is the most common site of fatty change?

The liver.

Name two other organs, besides the liver, where fatty change can occur.

Heart and skeletal muscle (it can also occur in kidney and other organs).

Free fatty acids reach hepatocytes from which two major sources?

Adipose tissue lipolysis and ingested dietary fat.

In hepatocytes, free fatty acids are primarily esterified to form what substance?

Triglycerides.

When triglycerides combine with apoproteins for export, what complex is produced?

Lipoproteins that enter the circulation.

A defect in which general steps can lead to hepatic lipid accumulation?

Uptake, catabolism, or secretion of lipids.

Give three conditions that cause excessive entry of free fatty acids into the liver.

Diabetes mellitus, starvation, and obesity.

Which common toxin disrupts mitochondria and SER, leading to fatty liver?

Alcohol (ethanol).

List four common causes of fatty change.

Alcohol abuse, diabetes mellitus, obesity, and protein malnutrition/starvation (anoxia is another).

Describe the gross appearance of a fatty liver.

Enlarged, tense capsule, rounded margin, smooth, soft, greasy, and yellow.

What term describes early small cytoplasmic fat vacuoles around the nucleus?

Microvesicular steatosis.

Macrovesicular steatosis is commonly seen in which three conditions?

Diabetes mellitus, obesity, and alcoholic liver disease (also non-alcoholic steato-hepatitis).

During macrovesicular steatosis, what happens to the hepatocyte nucleus?

It is displaced to the cell periphery.

Is mild fatty change reversible?

Yes, mild fatty change is reversible.

Which toxin can cause irreversible fatty change by lethal cell injury?

Carbon tetrachloride (CCl₄).

What are foam cells?

Macrophages filled with lipid vacuoles, giving their cytoplasm a foamy appearance.

Name five conditions associated with cholesterol/cholesteryl-ester accumulation.

Foam cells in necrosis, atherosclerosis, xanthomas, cholesterolosis, and Niemann-Pick disease type C.

In atherosclerosis, which two cell types in the arterial intima accumulate cholesterol?

Smooth muscle cells and macrophages.

What are xanthomas?

Tumorous masses of cholesterol-laden macrophages in skin or tendons occurring in hyperlipidemias.

Where does cholesterol accumulate in cholesterolosis?

The lamina propria of the gallbladder.

Which lysosomal storage disease features cholesterol accumulation?

Niemann-Pick disease, type C.

Heavy protein leakage in the kidney causes which tubular condition?

Protein reabsorption droplets in proximal convoluted tubules (seen in nephrotic syndrome).

How do protein reabsorption droplets appear histologically?

Pink, eosinophilic hyaline cytoplasmic droplets.

Russell bodies are composed of what material?

Aggregated immunoglobulins in the rough endoplasmic reticulum of plasma cells.

Russell bodies are characteristic of which malignant plasma-cell disorder?

Multiple myeloma.

Mallory bodies are composed predominantly of aggregates of which filaments?

Intermediate (cytokeratin) filaments.

Mallory bodies are highly characteristic of which liver disease?

Alcoholic liver disease.

The neurofibrillary tangle in Alzheimer disease is an aggregation of what?

Cytoskeletal (microtubule-associated) proteins.

In poorly controlled diabetes, glycogen accumulates in which three cell types?

Renal tubular epithelium, cardiac myocytes, and pancreatic islet β-cells.

Which stain gives glycogen deposits a rose-to-violet color in tissue sections?

Periodic acid–Schiff (PAS) reaction.

Define an exogenous pigment.

A colored substance that enters the body from an external source.

What is the most common exogenous pigment?

Carbon (soot).

Inhaled carbon pigment produces what benign condition in the lung?

Anthracosis (blackening of lung and lymph nodes).

Heavy carbon accumulation in miners can cause which serious lung disease?

Coal workers’ pneumoconiosis.

Why do tattoo pigments remain permanently in the dermis?

They are taken up by dermal macrophages and remain in connective tissue without significant inflammation.

List the three major endogenous pigments discussed.

Lipofuscin, melanin, and hemosiderin.

What nickname is given to lipofuscin?

“Wear-and-tear” pigment.

What is the biochemical origin of lipofuscin pigment?

Free-radical–induced lipid peroxidation of subcellular membranes (lipid-protein complexes).

Large amounts of lipofuscin produce what gross change in organs?

Brown atrophy.

What protective function does melanin serve in the skin?

Acts as a screen against harmful ultraviolet radiation.

Which cells synthesize melanin?

Melanocytes located in the epidermis.

Hemosiderin is derived from the breakdown of what blood component?

Hemoglobin (it is a storage form of iron).

What special stain is used to identify hemosiderin, and what color results?

Prussian blue stain, which colors iron deposits blue.

How does hemosiderosis differ from hemochromatosis regarding tissue damage?

Hemosiderosis shows iron in macrophages without tissue damage; hemochromatosis shows iron in parenchymal cells with damage and organ dysfunction.

Which gene is commonly mutated in hereditary hemochromatosis?

The Hfe gene on chromosome 6.

Name three organs most affected by iron deposition in hereditary hemochromatosis.

Liver, heart, and pancreas.

What classic clinicopathologic triad can develop in advanced hereditary hemochromatosis?

Liver cirrhosis, heart failure, and diabetes mellitus (“bronze diabetes,” often with skin pigmentation).

Define pathologic calcification.

Abnormal deposition of calcium salts in tissues other than bone or teeth.

How do dystrophic and metastatic calcification differ regarding serum calcium levels?

Dystrophic occurs with normal serum calcium; metastatic occurs with hypercalcemia.

Give four common sites of dystrophic calcification.

Areas of necrosis (coagulative, caseous, liquefactive), damaged heart valves, atheromatous plaques, and dead parasites/tumors (e.g., psammoma bodies).

What are psammoma bodies?

Lamellated concentric calcified structures seen in certain tumors such as meningiomas and papillary carcinomas.

How do calcium salts appear on gross examination?

Fine white, chalky granules or gritty clumps.

Which special histologic stain turns calcium salts black?

Von Kossa stain.

What is metastatic calcification?

Deposition of calcium salts in normal tissues due to deranged calcium metabolism and hypercalcemia.

Name three organs commonly affected by metastatic calcification.

Systemic arteries, kidneys (interstitium), and lungs (also gastric mucosa and pulmonary veins).

List four causes of hypercalcemia that may lead to metastatic calcification.

Hyperparathyroidism, vitamin D intoxication, bone destruction from tumors/multiple myeloma, and sarcoidosis (others include thyrotoxicosis, immobilization, milk-alkali syndrome).

How can chronic renal failure promote metastatic calcification?

It causes secondary hyperparathyroidism, producing hypercalcemia and phosphate retention.

Why are stomach, kidneys, and lungs frequent sites of metastatic calcification?

These organs secrete or excrete acids, creating an alkaline environment that favors calcium salt precipitation.

In which blood vessel wall was metastatic calcification illustrated in the lecture?

The wall of the uterine artery.