cellular injury ( part 3) l General pathology revision for dental students

cellular injury ( part 3) , INTRACELLULAR ACCUMULATIONS AND EXTRACELLULAR DEPOSITIONS l General pathology revision for dental students

 

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MISCELLANEOUS INTRACELLULAR ACCUMULATIONS AND EXTRACELLULAR DEPOSITIONS

The following substances may accumulate inside the cells (INTRACELLULAR ACCUMULATIONS) :

1. Water: In cloudy and hydropic swelling.
2. Fat: In fatty change of parenchymatous organs , atherosclerosis, lipid storage diseases and skin xanthoma.
3. Mucin: In mucoid change.
4. Glycogen: In glycogen storage disease.
5. Protein: In hyalinosis.
6. Pigments.

HYALINOSIS(Hyaline Change)

• A microscopic change in the tissues which become homogenous, structureless and stains pink with eosin. The chemical basis of hyaline change is not known.

CONNECTIVE TISSUE HYALINOSIS

A physic chemical change in the collagen fibers which fuse to form a homogenous structureless tissue. Examples of connective tissue hyalinosis are:

 The wall of the blood vessels ; The vessels wall becomes thickened and structureless and the lumen narrowed , e.g. :

1. The arteries in atherosclerosis.
2. The arterioles in benign hypertension.
3. The kidney glomeruli in chronic diffuse glomerulonephritis.
4. The central arterioles of the lymph follicles of the spleen in old age and hypertension.
5. The blood vessels of atrophic organs as the blood vessels of the ovary in old age.
6. Old scars and keloids.
7. Mesodermal tumours particularly leiomyoma.

CELLULAR HYALINOSIS

1. In old thrombi.
2. In the islets of Langerhan's in diabetes mellitus.
3. The basophil cells of the pituitary gland in Cushing's syndrome.
4. The degenerated liver cells in alcoholic cirrhosis show round hyaline masses called Mallory bodies.
5. Plasma cell in old chronic inflammation undergoes hyalinosis and changes to a red oval a nuclear body called Russel body.
6. After middle age and in senile hyperplasia of the prostate, the epithelial lining of the prostatic acini is shaded off. In the acinar lumen the cells undergo hyaline change and fuse forming concentrically laminated round or oval bodies called corpora amylacea.
7. Zenker's degeneration:

• Hyaline change in the voluntary muscles in fatal cases of typhoid fever and other severe infections as pneumonia.
• The change is caused by the bacterial toxins and the excess lactic acid accumulation in the muscle. The lesion is best seen in the rectus abdominis and diaphragm. Grossly the muscle appears pale and friable.
• Microscopically the muscle fibers swell, lose the cross striations and nuclei and show a hyaline appearance. Rupture and small hemorrhages complicate the lesion.

MUCOID CHANGE ( Mucoid or Mucinous Degeneration )

• Abnormal accumulation of excess mucin inside the epithelial cells. The cell becomes swollen and the nucleus flattened and pushed against the cell membrane(signet ring appearance).

• Some of the cells may rupture with release of mucin. It affects the epithelial cells of the mucous membranes in catarrhal inflammation e.g. catarrhal rhinitis and the cells of mucoid carcinoma.

Melanin Pigments (ENDOGENOUS PIGMENTS)

• Melanin is the pigment which colors the skin, hair, iris and choroid. It varies in color from pale yellow to dark brown.
• It is formed in the skin by the melanocytes from the amino acid tyrosine. Tyrosinase enzyme converts tyrosine to melanin. Macrophages engulfing melanin are called mclanophores.

Deficiency of Melanin Pigment:

• Albinism: Hereditary condition characterized by absence of melanin due to deficiency of the enzyme tyrosinase. The hair is white. The skin, iris and choroid are pink.

• Leucoderma: White skin patches due to melanin loss. It may be idiopathic or secondary to leprosy or syphilis.

Increase of Melanin Pigment:

• Prolonged exposure to the sun causes dark coloration of the skin.

• Chloasma: Brown patches in the skin of the face, nipple and genitalia caused by excess oestrogens.It occurs in pregnancy, ovarian diseases and with oral contraceptives.

• Benign and malignant melanomas are pigmented skin tumors of melanocytes.

• In Addison's disease caused by chronic adrenal cortical insufficiency brown pigmentation affects the skin (face, breast, axilla and scrotum) and mucous membranes (mouth, vagina and rectum).Pigmentation is caused by loss of hormonal control of the adrenal cortex on the activity of the pituitary melanocyte-stimulating hormone ,so excess melanin is formed.

II. Lipochrome Pigments (Lipofuscins Pigments) ENDOGENOUS PIGMENTS

• Yellowish brown pigments of lipid origin. Normally present in small amounts in the corpus luteum, testis, adrenal cortex, ganglion cells, heart muscles and other tissues.
• The pigments increase in old age and in atrophic conditions as a result of "wear and tear" of the tissues.

Brown Atrophy of the Heart:

• Cause: Old age and wasting diseases.

• Macroscopic picture: The heart is reduced in size and weight. The sub-pericardial fat is replaced by edematous jelly-like tissue (serous atrophy of fat). The coronaries are more tortuous. The myocardium is dark brown, thin and atrophic.

• Microscopic picture: The muscle fibers are thin and atrophic. Excess fine yellowish brown lipochrome pigments are seen on both sides of the nucleus in sections stained by haematoxylin only. The nuclei are pyknotic.

Haemoglobin Derived Pigments ENDOGENOUS PIGMENTS 

• Haemoglobin is a combination of a pigment complex "heme" and a protein "globin" .Three pigments may be formed from haemoglobin breakdown:

• Bilirubin: Iron-free pigment. Its normal formation and excretion are vital to health. Excess bilirubin pigment in cells and tissues occur in jaundice.

• Haemosiderin: Iron containing brown insoluble granules. Haemosiderin gives a blue color when stained with potassium ferrocyanide and hydrochloric acid(Prussian blue reaction).

• Hematin: A brown pigment formed by the action of acids or alkalies on haemoglobin. Hematin is not found normally in the body. It gives a negative Prussian blue reaction.

Pathological Increase in Haemoglobin Derived Pigments

Haemosiderosis

• Definition: Pathological excess haemosiderin deposit in the tissues.

Types:

• Localized Haemosiderosis: Occurs around areas of haemorrhage. The haemosiderin gives the tissue a brown color and stimulates fibrosis around. Haemosiderin gets phagocytosed by macrophages. Examples of localized haemosiderosis are:

1. In venous congestion of the lung and spleen.
2. Around infarcts, varicose veins, varicose ulcers and bone fractures.

• Generalized Haemosiderosis (Secondary Haemochromatosis), Causes:
• Excess destruction of red cells in the circulation as in haemolytic anemia.
• Increased iron content of the diet.
• Prolonged iron therapy and repeated blood transfusions.
• Pathology: Excess haemosiderin is deposited in the cells of the reticulo-endothelial system, liver cells and renal tubules. The deposit gives the tissue a brown color. Tissue damage is mild.

Hemochromatosis (Bronzed Diabetes)

Cause:

1. An inborn error of iron metabolism.
2. There is abnormality in the enzyme system controlling iron absorption from the duodenum.
3. Excess iron is absorbed from the diet and deposited in the tissues over a period of years.
4. Haemochromatosis most commonly affects middle aged men, women being protected by iron loss in the menstrual blood.

Pathology:

• The pigment is deposited in the liver cells, pancreas, heart, skin and other organs.The affected cells undergo necrosis and fibrosis follows.
• The organ appears enlarged, brown and hard. The level of plasma iron is elevated.

Effects:

1. Liver: Develops pigmentary cirrhosis. The liver is enlarged, nodular and firm. Pigmentary cirrhosis leads to esophageal varices and ascites. Hepatoma complicates 10%of the cases.
2. Pancreas: Enlarged, hard, pigmented and shows fibrosis. The lesion causes diabetes mellitus.
3. Heart: Its fibrosis leads to heart failure.
4. Skin: Has a bronzed color due to increased melanin and haemosiderin deposition.

Parasitic Pigmentation

• In malarial and bilharzial infection, the parasites feed on the red cells in the circulation. A brown pigment called haemozoin related to haematin is produced from the haemoglobin.

• The pigment is released in the blood stream,then removed by the cells of the reticulo-endothelial system mainly in the spleen and liver.

• The pigment gives a negative Prussian blue reaction as its iron is firmly bound.

EXOGENOUS PIGMENTS

• Pigments are introduced into the body from outside by three different means:

1. Inhalation: e.g. of carbon particles produce black pigmentation in the lung called anthracosis.
2. Ingestion: e.g. chronic lead poisoning (plumbism), in which blue pigmentation due to the formation of lead sulphide affects the oral mucosa and the gums.
3. Inoculation: e.g. tattooing, where india ink and other pigments are introduced in the dermis by certain needles.Part of the pigments are carried by the macrophages to the draining lymph nodes.

GOUT

• Disturbance in purine metabolism with sodium urates deposition in the tissue.

Causes:

1. Primary type: Hereditary and occurs mainly in middle aged males.
2. Secondary type: Caused by increased nucleoprotein breakdown as in chronic leukaemias.

Pathological Features:

• Increased level of blood uric acid to 6-12 mgm.per 100 ml.(normal level is 3-6 mgm.per 100 ml.).
• Monosodium urate crystals deposit in ; The deposit forms small masses called tophi :

1. Joint structures as the articular cartilage, synovial membrane, capsule, ligaments and tendons. The lesion mainly affects the metatarso-phalangeal joint of big toe.
2. Cartilage of the nose, ear and eyelids.
3. Interstitial tissue of the kidney.
4. Cardiac valves.

• The affected cartilage is thin, eroded and shows white plaques of urate deposits. The covering skin may ulcerate.
• Microscopically the tissue shows needle shaped mono-sodium urate crystals surrounded by a foreign body granuloma.
• Renal failure in chronic cases.