Intracellular Accumulations Question And Answers

Intracellular Accumulations Important Notes

1. Endogenous pigments

• It includes lipofuscin, melanin, and certain derivatives of hemoglobin
• Lipofuscin is a yellowish-brown intracellular lipid pigment
• Found in
  • Atrophied cells of old age so-called wear and tear pigment
  • Myocardial fibres
  • Hepatocytes
  • Leydig cells of the testes
  • Neurons of senile dementia

Intracellular Accumulations Long Essays

Question 1. Mention types of degeneration. Discuss pathogenesis and macroscopic appearance of fatty liver.
Answer:

Degeneration Types:

Fatty Liver Pathogenesis:

In fatty liver: Intracellular accumulation of triglycerides can occur due to defect at one/ more of the following 6 steps:

• Increased entry of fatty acids into the liver.
• Increased synthesis of fatty acids by the liver.
• Decreased conversion of fatty acids into ketone bodies resulting in increased esterification of fatty acids to triglycerides.
• Increased a-glycerophosphate causes increased esterification of fatty acids to triglycerides.
• Decreased synthesis of lipid acceptor protein resulting in decreased formation of lipoprotein from triglycerides.
• Block in the excretion of lipoprotein from the liver into plasma.

Read And Learn More: Pathology Question And Answers

Macroscopic Appearance of Fatty Liver:

1. Gross appearance

• Size- liver is enlarged
• Color-yellow
• Capsule- tense and glistening capsule
• Margins are rounded

2. Cut surface

• It bulges slightly
• Color varies from pale yellow to yellow
• The surface is greasy to the touch

Question 2. Define and classify degeneration. Discuss etiopathogenesis and pathology of fatty liver,
(or)
Mention types of degeneration. Discuss patho¬genesis and microscopic appearance of fatty liver
Answer:

Degeneration Definition:

• Degeneration is a process by which a tissue deteriorates, loses its functional activity, and may become con¬verted into or replaced by other kinds of tissue.

Fatty Liver:

• Fatty liver or steatosis is the intracellular accumulation of neutral fat within parenchymal cells
• It is common in the liver as it plays a central role in fat metabolism

Microscopic Appearance:

• The fatty liver shows numerous lipid vacuoles in the cytoplasm of hepatocytes
• It is seen as a clear area that may vary from minute droplets to an extension of the entire cytoplasm

1. Initially

• Vacuoles are small
• They are present around the nucleus
• Centrilobular hepatocytes are affected

2. Later

• Vacuoles enlarge
• They push the nucleus to the periphery of the cells
• Fat accumulation involves the entire lobule
• Occasionally adjacent cells containing fat may rupture producing fatty cysts
• Rarely, lymphogranuloma may appear consisting of a collection of microphones, lymphocytes, and multi-nucleate giant cells

Intracellular Accumulations Short Essays

Question 1. What is fatty liver? What are its causes?
Answer:

• Fatty change/steatosis is the intra-cellular accumula¬tion of neutral fat within parenchymal cells.
• It is especially common is the liver as it plays a central role in fat metabolism,
• It may occur in other non-fatty tissues like the heart, skeletal muscles, kidneys, and other organs.

Fatty Liver Types:

• Fatty change may be
  • Mild and reversible
  • Severe and irreversible resulting in cell death.

Etiology: Fatty change in the liver results from.

Question 2. Wear and tear pigment
Answer:

• Lipofuscin is known as wear and tear pigment.
• Lipofuscin/lipochrome is a yellowish-brown intra-cellular lipid pigment.
• It is a hemoprotein-derived pigment

Site of Appearance:

• In atrophied cells of old age and Lence known as wear and tear pigment.
• It is seen in myocardial fibers, hepatocytes, Leydig cells of the testis, and neurons in senile dementia.

Significance:

• Lipofuscin represents the collection of indigestible material in the lysosomes after intra-cellular lipid peroxi¬dation and is therefore an example of residual bodies.

Microscopy:

• By light microscopy, the pigment is coarse, golden brown granular, and often.’ accumulates in the central part of the cells around the nuclei.
• In heart muscle, change is associated with wasting of the muscle and is commonly refered to as brown atrophy.
• By electron microscopy, lipofuscin appears. J as integrally- ribosomal electron-dense granules in perinuclear location. Granules are composed of did-protein complexes.

Question 3. Hemosiderosis
Answer:

Hemosiderosis Definition:

• Excessive storage of hemosiderin is called he-mosiderosis

Hemosiderosis Causes:

• Increased breakdown of red cells
• Systemic overload of iron due to
  • Primary causes
    • Idiopathic
    • Hereditary
  • Secondary causes
    • Thalassaemia
    • Sideroblastic anemia
    • Alcoholic cirrhosis

Hemosiderosis Effects:

1. Localized hemosiderosis

• Black eye occurs due to bilirubin and biliverdin
• Brown induration in the lungs occurs due to small hemorrhages

2. Generalized hemosiderosis

• Parenchymatous deposition of hemosiderin in the liver, kidney, pancreas
• Reticuloendothelial deposition in the liver, spleen, and bone marrow

Intracellular Accumulations Short Question And Answers

Question 1. Melanin pigment
Answer:

• Melanin is an endogenous pigment
• Melanin is a brown-black, non-hemoglobin-derived pigment normally present in the hair, skin, choroid of the eye, meninges, and adrenal medulla.

Melanin pigment Synthesis:

• It is synthesized in the melanocytes and dendritic cells

Melanin pigment Storage:

• Stored in the form of cytoplasmic granules in the phagocytic cells called as melanophores.

Melanin pigment Disorders:

Various disorders of melanin pigmentation cause gen¬eralised and localized hyperpigmentation and hypopigmentation.

1. Generalised hyperpigmentation is seen during.

• Addison’s disease
• Chloasma
• Chronic arsenal poisoning.

2. Focal hyperpigmentation.

• Cafe-au-lait spots in Albright’s syndrome.
• Peutz-Jeghers syndrome.
• Melanosis coli.
• Melanotic tumors
• Dermatopathiclymphadentis.

3. Generalised hypopigmentation.

• Albinism

4. Localised hypopigmentation.

• Leukodema
• Vitiligo
• Acquire focal hypopigmentation.

Question 2. Exogenous pigment
Answer:

Exogenous pigments are the pigments introduced into the body from outside such as by inhalation, ingestion, or inoculation.

Inhaled pigments:

• The most commonly inhaled substances are carbon/coal, dust, silica/stone dust, iron oxide, asbestos, and various other organic substances.
• These substances may cause occupational lung disease called pneumoconiosis.
• Extensive deposition of particulate material over many years provides low-grade inflammation, fibrosis, and impaired respiratory function.

Ingested pigments:

• Chronic ingestion of certain metals may produce pigmentation. E^/Argyria, chronic lead poisoning, melanosis coli.

Injected pigments:

• Examples of injected pigments are prolonged use of ointments containing mercury, dirt left accidentally in a wound, and tattooing by pricking the skin with dyes.
• In it pigment is taken by the macrophages and lies permanently in the connective tissue

Question 3. Fatty degeneration/ fatty change
Answer:

• Fatty degeneration or fatty change is the intracellular accumulation of neutral fat within parenchymal cells
• It occurs in the cytosol and represents an absolute increase in the intracellular lipids

Fatty change Types:

• Depending upon the cause and amount of accumulation, fatty change can be

1. Mild and reversible
2. Severe and irreversible- Causing cell death

Question 4. Causes of Ketonuria.
Answer:

• Metabolic abnormalities – diabetes, renal glycosuria
• Dietary conditions – starvation, fasting, prolonged vomiting, anorexia
• Hyperthyroidism, fever, pregnancy, lactation

Question 5. Ketone bodies.
Answer:

• Ketone bodies are water-soluble molecules – acetone, acetoacetate, and beta-hydroxybutyrate
• They are produced by the liver from fatty acids during low food intake, starvation, prolonged intense exercise, alcoholism or untreated diabetes mellitus
• Ketone bodies are readily picked up by the extrahepatic tissues and converted into acetyl CoA which enters the citric acid cycle
• It is oxidized in mitochondria for energy