CALCIFICATIO
N
• Submitted
by:-
TECHI TARIN
Roll no.
23MBBS017
DEFINITIO
N-
Deposition of calcium salts in tissues other than
osteoid or enamel is called pathological
calcification.
DYSTROPHIC
CALCIFICATION:- 囚
• Calcification of dead and dying tissues.
• The level of calcium in blood is usually
normal.
PATHOGENESIS:-
囚囚
囚
SITES OF
CALCIFICATION
• Dead tissues:-
• Caseation eg:
Tuberculosis.
• Dead parasites.
• Fat necrosis.
• Infarcts
• Thrombi
• Haematoma
• Degenerative
tissues:-
• Atherosclerosis – Moncke berg
sclerosis.
• Damaged heart valves.
• Infected lymph
nodes.
• Degenerating
tumours.
METASTATIC CALCIFICATION
• Deposition of calcium salts in tissues which may
be normal and it is associated with disorders of
calcium metabolism (Hypercalcemia).
• It may occur widely throughout the body hence
the term metastatic.
PATHOGENESIS:-
~ Those organs that lose
acid .
~ Underlying alkaline
compartment.
~ An alkaline internal component of cell is susceptible to
calcification.
~ Increase
cel andamount
gets of calcium in blood move from the blood
deposited
ls
vessel s to there.
SITES OF CALCIFICATION:-
1. Basement membrane and tubular lamina of
kidney.
2. Pulmonary veins.
3. Alveolar wall of
lung.
4. Cornea and
conjuntiva.
5. Gastric mucosa.
6. Synovium of the
joints.
7. Systemic arteries.
CAUSES OF HYPERCALCEMIA:-
1. Hyperparathyroid ism –
• Primary (due to neoplasm )
• Secondary (nutritional or renal
failure)
2. Hypervitaminosis-D ( vitamin-D
toxicosis)
• Increased absorption of calcium from
intestine.
• Lymph osarcoma and apocrine adenocarcinoma secretes
3. Neoplasm-
parathyroid hormones like peptides and cause
hypercalcemia.
GROSS:- 囚
. CALCIFICATION APPEARS AS PALE CHALKY WHITE AREAS IN
THE
TISSUES. 囚
. EVEN IF NOT VISIBLE, CALCIFICATION CAN SOMETIMES BE
DETECTED BY THE COARSE GRITTY FEEL OF THE TISSUES
WHEN SCRAPPED OR INCISED WITH A KNIFE OR SCALPEL
BLADE .
MICROSCOPIC APPEARANCE:- 囚
• Single necrotic cells act like little grains of sands around which a pearl
• Calcium salts appears as blue granules ( deep basophil ic ) on
H&E.
of calcium is deposited. This is called PSAMMOMA BODY.
• Special stains like Von Kossa gives a black colour and Alizarin
red S produces red staining.
Defi
nition:-
。 Cellular ageing is the result of a progressive decline in cellular function and viability caused by genetic abnormalities and the
accumulation of cellular and molecular
damage due to the effects of exposure to exogenous influences.
Cellular basis of
ageing:-
。 Individuals age because their cells slowly decline to function. This is reflected in structural and functional changes in
different organs and systems of the human body with ageing. Changes at cellular and subcellular level linked with ageing
are supported by the following theories:
1. Free radical theory of ageing.
2. Telomere shortening and cellular senescence.
3. Caloric regulation theory.
4. Mitochondrial dysfunction.
5. DNA damage.
6. Altered gene expression.
7. Reduced autophagy.
8. Activation of tumour suppressor genes.
[Link] radical theory of
囚 ageing:-
In normal cells , very small amount 3% of total oxygen consumed by the cell is converted into
reactive oxygen species ROC. With ageing, there is low metabolic rate with generation of toxic
oxygen radicals which fail to get eliminated causing their accumulation and hence cell damage
due to mitochondrial injury.
[Link] shortening and
cellular senescence:
。 Cells divide approximately only 60-70 times in their entire life span, Hayfl ick limit.
。 After a fixed number of divisions cells become arrested in terminally nondividing state,known as replicative senescence of cells .
。 Telomere ( short repeated sequence of DNA present at the ends of linear chromosomes) are present as a protective mechanism that prevents
the chromosomes from fusion and
degradation.
。 During every cell division there is progressive shortening of telomere present at the ends of linear chromosomes, telomere attrition .
。 In normal somatic cells , there is no telomerase activity which exists in germ cells for repairing the loss of telomere.
。 Thus, progressive loss of telomere in somatic cells in ageing results in exit of senescent cells from the cell cycle and inability to renew lost
cells.
[Link] regulation theory:-
。 It has been observed that caloric restriction delays
ageing.
。 Caloric restriction reduces the release of growth factors
suchGH,
as insulin and insulin like growth factor
1(IGF-1).
。 These hormnes
delays are activated by nutrients but restricted
nutrients
ageing.
Sirtuins:-
They are NAD dependent protein deacetyl ases.
。 They inhibit insulin
increasing cellularsensitivity,
ageing by increasing
reducing free
DNAradical
injury, repairs.
。 Sirtuins levels can be increased by-
1. Calorie restriction.
2. Wine consumption.
[Link] Damage:-
。 Long duration of exposure to several exogenous agents (physical,
chemical and biologic), endogenous agents ROS targets the
nuclear and mitochondrial DNA of the cell.
。 Normally, damaged DNA is repaired by DNA repair enzymes
but in ageing the repair mechanisms start to weaken or fail .
。 Example:-
Werner Syndrome – Syndrome of premature ageing.
- Premature ageing due to defect in DNA he
licase. Bloom Syndrome
Organ changes in
ageing:- 囚
1. Cardiovascular system – Atherosclerosis, arteriosclerosis with calcification,
Möncke berg medial calcification, brown atrophy of the heart , loss of elastic tissue
from aorta and major arterial trunks causing their dilatation.
2. Nervous system – Atrophy of gyri and sul ci , Alzheimer’s disease, Parkinson’s disease.
3. Muscul oskeletal system – Degenerative bone disease , frequent fractures due to loss of bone density, age related muscular
degeneration.
4. Eyes- Deterioration of vision due to cataract and vascular changes in retina.
5. Hearing Disability in hearing due to senility is related to
otosclerosis.
6. Immune system, Reduced IgG response to antigens,
frequent and more several infections.
7. Skin laxity of skin due of elastic tissue.
[Link] – 80% of cancers occur in the age range of 50-
80years.
。 Thank
you!
