This document discusses pathological calcification and summarizes its main types:
1) Dystrophic calcification refers to the local deposition of calcium salts in necrotic or degenerate tissues regardless of normal serum calcium levels.
2) Metastatic calcification reflects deranged calcium metabolism and systemic deposition of calcium salts associated with increased serum calcium levels.
3) Pigments that accumulate in tissues include exogenous pigments like carbon and tattoos, as well as endogenous pigments such as lipofuscin, melanin, hemosiderin, and bile.
Intracellular accumulation refers to the abnormal build-up or accumulation of substances within the cells of an organism. This phenomenon occurs when cells are unable to process, utilize, or eliminate certain substances effectively. These accumulated substances can be diverse and include lipids, proteins, carbohydrates, pigments, and other cellular components.
The accumulation may result from various factors such as genetic mutations, impaired enzymatic activity, or exposure to toxins. Intracellular accumulation can lead to cellular dysfunction, impaired organ function, and, in some cases, contribute to the development of diseases.
Examples of intracellular accumulation include lipid accumulation in hepatocytes (fatty liver disease), protein accumulation in neurodegenerative disorders like Alzheimer's disease, and pigment accumulation in conditions such as hemosiderosis or lipofuscinosis. Understanding the underlying causes and consequences of intracellular accumulation is crucial for developing effective strategies for diagnosis and treatment in medical and research contexts.Intracellular accumulation can manifest in different forms, each associated with specific substances and underlying mechanisms. Here are some additional details on notable types of intracellular accumulation:
1. **Lipid Accumulation:**
- Lipid accumulation, often seen in hepatocytes, can lead to conditions like fatty liver disease. Excessive triglycerides accumulate within liver cells, compromising liver function and potentially progressing to more severe liver disorders.
2. **Protein Accumulation:**
- In neurodegenerative diseases such as Alzheimer's and Parkinson's, misfolded proteins accumulate within neurons, forming aggregates that disrupt cellular function. This can contribute to the progressive degeneration of the nervous system.
3. **Glycogen Accumulation:**
- Glycogen storage disorders result from impaired metabolism of glycogen, leading to its abnormal accumulation within cells. This can affect various organs, including the liver, muscles, and heart, causing functional impairments.
4. **Pigment Accumulation:**
- Abnormal accumulation of pigments can occur, such as hemosiderin in conditions like hemochromatosis, leading to iron overload. Additionally, lipofuscin, often referred to as the "wear and tear" pigment, accumulates in cells over time and is associated with aging.
5. **Calcium Accumulation:**
- Dysregulation of cellular calcium levels can result in calcium accumulation within organelles. This can disrupt cellular signaling and contribute to conditions like calcific vasculopathy or dystrophic calcification in tissues.
Understanding the specific type of intracellular accumulation and its implications is crucial for developing targeted therapeutic interventions. Research in this field plays a vital role in unraveling the complexities of various diseases and advancing our knowledge of cellular biology and pathology.
Fa1zanS: Disorder of exchange of Chromoprotein (endogenous pigment). Disorder...Faizan Siddiqui
Disorder of exchange of Chromoprotein (endogenous pigment).
Disorder of exchange of nucleic acids.
Disorder of mineral exchange.
Pathological calcification.
Formation of Stone.
1. PATHOLOGICAL CALCIFICATION
Definition:-
Abnormal deposition of calcium salts
together with smaller amount of Mg++ ,Fe++ &
other minerals in tissues other than osteoid or
enamel
3. • Dystrophic calcification
refers to local deposition of calcium salts in
necrotic or degenerate tissues, whatever the
type of necrosis, in spite of normal serum Ca++
4. Pathologic Calcification
Dystrophic Calcification
- Area of tissue necrosis
- Aging or damage heart valve
- Atherosclerosis
- Single necrotic cell
“psammoma body”
6. Metastatic calcification
reflects deranged calcium metabolism
in contrast to dystrophic calcification and
is associated with increase serum calcium
level & systemic deposition of Ca++salts
in interstitial tissue of gastric mucosa,
kidney,lungs,systemic arteries&
pulmonary veins.
7. Metastatic calcification
Hypercalcimia
• Increased secretion of parathyroid hormone
• Destruction of bone tissue 2ndry to primary tumor of
bone marrow ( multiple myeloma, leukemia), or diffuse
skeletal metastasis.
• Vitamin D-related intoxication
• Renal failure
•Excessive intake of calcium & absorbable antacids as
milk or calcium carbonate.
8. This is dystrophic calcification in the wall of the stomach. At
the far left is an artery with calcification in its wall
11. Accumulation of Pigments
• Exogenous pigments
Carbon ( anthracosis)
Coal dust ( pneumoconiosis)
Lung: pick up by alveolar macrophages
regional lymph nods
blackening the tissues of the lungs
(anthracosis)
16. Accumulation of Pigments
• Endogenous pigment
:Lipofuscin – aging pigment(fucus=brown)
lipid, phospholipid-protein complex (lipid
peroxidation) ,brown-yellow pigment
accumulated as the atrophic and dying cells
undergo autophagocytosis. Harmless,Sign of free
radical injury & lipid perioxidation, seen in aging patients
severe malnutrition & cancer cachexia.
17. Lipofuscin granules in a cardiac myocyte as shown by A, light microscope (deposits indicated by
arrows) , and B,Electron microscopy (perinuclear ,intralysosomal location).
22. :Hemosiderin – aggregates of ferritin micelles (iron + apoferritin =
ferritin)
Hemosiderosis:- Excess of hemosiderin granules in
mononuclear phagocytes without organ dysfunction
Causes:- Local (bruise)
Systemic as
Hemolytic anemia,
Increased absorption of dietary iron
Repeated blood transfusion
Hemochromatosis:- Excess of hemosiderin granules in
mononuclear phagocystic system & paranchymal cells causing
organ dysfunction ( liver fibrosis, DM, heart failure).
23. Hemosiderin granules in liver cells A, H&E section showing golden-brown,finely
granular pigment. B, Prussian blue reaction, specific for iron.
32. Ageing:
“Progressive time related loss of
structural and functional
capacity of cells leading to
death”
• Senescence, Senility, Senile
changes.
• Ageing of a person is intimately
related to cellular ageing.
33. Factors affecting Ageing:
• Genetic – Clock genes, (fibroblasts)
• Diet – malnutrition, obesity etc.
• Social conditions -
• Diseases – Atherosclerosis, diabetes etc.
• Werner’s syndrome.
34. Cellular mechanisms of
ageing
• Cross linking proteins &
DNA.
• Accumulation of toxic
by-products.
• Ageing genes.
• Loss of repair
mechanism.
• Free radicle injury
• Telomerase shortening.
36. Ageing –changes:
• Gradual atrophy of tissues and organs.
• Dementia
• Loss of skin elasticity
• Greying and Loss of hair
• BV damage – atherosclerosis/bruising.
• Loss of Lens elasticity opacity
vision
• Lipofuscin pigment deposition – Brown
atrophy in vital organs.
If you see a golden brown, slightly refractile pigment on routing light H&E microscopy, it is either hemosiderin, melanin, or bile derived. A few other degenerative pigments, such as lipofucsin, are also possible. Special stains can prove it is one or the other, if it is not abundantly clear from its cellular or pathologic setting and/or location
This tiny amount of microscopic tattoo pigment can make white skin look quite black! Is this EXogenous or ENDogenous?
Why does anthracosis look worse along the pleural surface than on cut sections? Why are MANY extrathoracic lymph nodes also anthracotic? What in the body is black and NOT due to EXOGENOUS pigments?
Why would somebody order a prussian blue stain, or a S-100 immunoperoxidase stain or a HMB-45 stain?