week 9 calcification & pigmentation.pdf
TRANSCRIPT
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Calcification &Pigment
AccumulationPresented
ByAhmed El-Rashedy
Professor & Previous Headof Pathology DepartmentAl-Azhar University
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Pathologic Calcification
Def.:
Deposition of calcium salts (ca phosphate & ca carbonate) in soft
tissues probably leading to malfunction.
Normally, precipitates of calcium salts are found only in
bones, otoliths and teeth.
Pathological calcification may be radiologically evident and
diagnostically useful.Types:
1. Metastatic calcification.
2. Dystrophic calcification.
Calcinosis Cutis:A calcification of the skin & subcutaneous (S.C.) tissue.
Calcinosis Universalis:
A widespread calcification of the muscles and tendons as well as
that of the skin & S.C. tissue.
Prof. Dr. Ahmed Elrashedy
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Differences Between Metastatic & Dystrophic Calcification
DystrophicMetastatic
Normal (9-11 gm%)(>11gm%)1.Serum
ca++ level:
Deposition of calcium salts in:1. Previously damaged tissues:
as thrombus, infarcted area,atheromatous plaques,congenitally bicuspid aorticvalve, calcified mitral valvering, old caseous tubercle,
bilharzial ova, old scars, fatnecrosis, breast lesions,
calcinosis cutis.2. Necrotic tumors: eitherA) Benign: Fibromyoma,
meningioma, thyroid adenoma.B) Malignant: mammary duct
carcinoma & carcinosarcoma.
calciumabsorption from GIT: inhypervitaminosis D. calcium mobiliz-ation from the bones asin case of :1. Hyperparathyroidism.2. Chronic renal failure.3. Osteolytic bone
metastasis.
2. Causes:
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DystrophicMetastatic
No Harmful Effects onthe functions.
An exception is:
Calcified congenitally
bicuspid aortic valve. Abicuspid aortic valve can
function quite normally
but when it becomes
calcified, the valve cusps
become thick and rigid.
This causes finally heart
failure.
1. Nephrocalcinosis: withimpaired renal function.
2. Calcification of the
GIT mucosa:with
defective absorption &digestion.
3. Calcification of the
alveolar walls:with
lack of oxygenation.
4. Calcifications of
arterial media:with
loss of its elastic recoil.
3. Effects:
Differences Between Metastatic & Dystrophic Calcification
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N.B.:1. Metastatic calcification must not be confused with
the process of metastasis of tumours.
2. Metastatic
calcification means being widespreadwhile dystrophic means occurring in a tissue alreadyaffected by disease.
Diagnosis:
1) Cl inical ly: At surgery, calcification is felt extremely hard.
2) Biochemically: Dystrophic calcification in case of fat
necrosis (due to trauma to adipose tissue or acute
pancreatitis), the liberated fatty acids bind calcium to form
insoluble calcium soaps, sometimes causing hypocalcaemia
and tetany.
3) Radiologically: The calcified lesions will often appear on
plain X-ray as opacities (white shadows).
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Diagnosis:
4. Pathologically:
A) Dystrophic calcification:
a) In some breast carcinomas as one of the abnormalities
detected in the mammography (breast X-rays) done for breast
cancer
(microcalcifications).
b) Some tumours contain minute concentric lamellated calcifiedbodies called psammoma bodies (psammos in Greek means
sand). These tumors are :
1. Meningiomas.
2. Papillary carcinomas of thyroid.
3. Papillary ovarian carcinomas.
Significance: Psammoma bodies help the histopathologist in
the correct diagnosis of the type of tumour.
Prof. Dr. Ahmed Elrashedy
P f D Ah d El h d
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B) Metastatic calcification (In hypercalcemia):
I. In alveolar walls:Appears as a purple-staining material deposited on
alveolar walls.
II. Widespreadcalcification:Occurs in normal tissues.Common causes of metastatic calcification :
1) Hyperparathyroidism due to adenoma or diffuse hyperplasia of the
parathyroid glands.
2) Hypercalcemia of malignancy. In adenoma or diffuse hyperplasia of the parathyroid glands: There
is a secretion of an excess parathyroid hormone which releases
calcium from the bone leading to hypercalcemia.
In some malignant neoplasms, hypercalcemia results from either thesecretion of a parathyroid hormone-like substance or extensive bone
erosion due to skeletal metastases. In this condition the calcium salts
are precipitated on to connective tissue fibres (e.g. collagen & elastic
fibers).
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Intracellular Pigment Accumulation
Pigment accumulated inside the cells may come into the body from
the external environment (exogenous) or synthesized within the
body itself (endogenous).
I) Exogenous pigmentation
Def.: Abnormal accumulation of pigment coming to the body
from outside.
Types of exogenous pigments:
1) Carbon or coal dust (Anthracosis).
2) Inoculated pigment (Tattooing).
1)Anthracosis
Inhalation and trapping of carbon or coal dust within the alveolar
macrophages that will transport it into the draining
tracheobronchial LNs through intervening lymphatics black
discoloration of the lung tissues & the involved L.Ns.
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1) Anthracosis
Examples:
1. Coal miners.2. Those living in a heavily air polluted environment.
Complications:
1. Pulmonary fibrosis.
2. Emphysema.
3. Pulmonary hypertension followed by right sided heart
failure (Cor-pulmonale ).
2) Tattooing
Def.: A localized cutaneous exogenous pigmentation with
trapping of the inoculated pigment within the dermal
macrophages and remains for life.
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II) Endogenous Pigmentation
Def.:Abnormal accumulation inside the tissue cells of
pigment synthesized within the body itself.
Types of endogenous pigments:
1. Lipofuscin (Lipochrome; Ageing pigment).
2. Melanin.3. Hemosiderin.
4. Bilirubin.
Prof. Dr. Ahmed Elrashedy
P f D Ah d El h d
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BilirubinHemosiderinMelaninLipofuscin
Hb-derived
pigment
Hb-derived pigment
(Small aggregates of
ferritin molecules)
Oxidation of
tyrosine into
dihydroxy-
phenyl
alanine
Lipid peroxid-
ation of poly-
unsaturated
lipids of the
cell &
subcellular
membranes.
1. Origin:
Normal major
pigment in thebile.
Iron conjugated with
apoferritin protein.
Amino acid.Lipid
polymers +phospholipids
complexed
with proteins.
2. Chemical
nature:
1. Liver :
(bile sinusoids,kupffer phagocytic
cells& hepatocytes
2. Kidney: renal
tubular
epithelium.
A) Localized: Inside
the macrophages.B) Systemic:
Many organs &
tissues (liver, spleen,
kidney, LNs, B.m.,
pancreas, endocrine
glands ).
Melanocytes
&melanophors
of the skin
Liver cells +
cardiacmuscles
(cytoplasmic)
3. Sites:
Prof. Dr. Ahmed Elrashedy
P f D Ah d El h d
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BilirubinHemosiderinMelaninLipofuscin
Hyperbilirubinemia due to :
1. Biliary Obstruction.
2. Hemolysis.
3. Liver cell failure
Hemorrhage or
hemolysis.
iron absor-
ption fromdiet.
iron utili-
zation
Prolonged
exposure
to sunlight
Ageing
process
4. Cause:
1) Obstructive jaundice:
a) Cancer head of pancreas.b) Cholangiocarcinoma: of
common bile duct.
2) Hemolytic jaundice: in all
hemolytic anemias.
3) Hepatocellular jaundice:
a) Hepatitis.b) Liver cirrhosis.
c) Hepatocellular tumors.
A) Localized:
1) Contusion(Bruise).
2) Local Hge.
B) Systemic:
1) Hemolytic
anemias.
2) Hemolytic3) blood
transfusion.
Prolonged
exposureto sunlight
1) Brown
atrophy ofheart
2) Severe
malnutrition
3) Cancer
cachexia
5. Examples
Orange-red.
N.B.: Bile itself is green
brown - to - black
Golden yellow-
brown
Brown-
black
Yellow-
brown
6. Color:
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BilirubinHemosiderinMelaninLipofuscin
1) Pigment gall
stones.
2) Pigmentary
livercirrhosis.
3) Kernicterus
particularly
in neonates
with brain
atrophy.
1.Localized:
Noharmful effects.
2. Systemic:
Anemia. Impaired functions of the
involved organs.
N.B.:
1) At first , the pigment will be
found inside the phagocytic
cells ,then, theparenchymal cells become
pigmented.
2) Prussian blue reaction:
This differentiates between
lipofuscin & hemosiderin. If
the color is changed from
yellow-brown into blue, this
is hemosiderin (+ve
reaction). Lipofuscin color
doesnt change (-ve
reaction).
Hyperpig-
mentation.
Shrinkage
of involved
organ
withoutharmful
effects on
its cells or
function.
7. Effects:
Pro
f.Dr.Ahmed
Elrashedy
P f D Ah d El h d
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1) Anthracosis 2) Tattooing
I. Exogenous Pigmentation
Prof. Dr. Ahmed Elrashedy
Prof Dr Ahmed Elrashedy
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1) Brown atrophy of the heart (right)
versus cardiac hypertrophy (left) 2)Melanin pigment
3) Hemosiderosis in
spleen & liver
4) Jaundice (left) & bilirubin (right)in small bile ductules in the liver
II. Endogenous Pigmentation
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Prof. Dr. Ahmed Elrashedy