📌 fatty change (steatosis)➡️ most comm site (liver)
🖇 alcohol and diabetes associated with obesity are the most common causes of fatty change
🖇 fatty ch is reversible except in CCI4 poisoning

📍 Russell bodies :in multiple myloma (Ig accumulation in plasma Cs)
📍 Mallory bodies or alcoholic hyalin :inclusions composed of aggregated intermediate cytokeratin filaments
📍 Neurofibrillary tangle : in alzheimer ds is an aggregated protein inclusion contain microtubule associated proteins

📌 in poorly controlled DM glycogen accumulates in renal tubular epithelium , cardiac myocytes , β cells

📌 Carbon is the most comm exogenous pigment
📍 Anthracosis
📍 coal workers pneumoconiosis

📌Lipofuscin "wear & tear pigment" insoluble brownish yellow ➡️brown Atrophy
. seen in ( heart , liver , brain ) as a function of age or atrophy
⚠️it is not injurious to the cell but imp as a marker of past free radical injury


📌 Melanin act as screen against harmful UV radiation

📌 Hemosiderin : golden yellow brown. can be identified by prussian blue dye .
📍 Hemosiderosis: acc of hemosiderin without organ damage
📍 hemochromatosis : extensive acc with tissue damage
🔸hereditary hemochromatosis caused by mutation in Hfe gene


📌 Dystrophic calcification
📍 normal Ca deposit in dead tissue
📍 mostly in area of necrosis

📌 Metastasis calcification
📍 Deposit Ca in living tissue because hypercalemia

📍Causes :
1_ hyperparathyrodism
2_ hyperthyroidism
3_ Vit D toxicity
4_ Addison disease
5_ sarcoidosis
6_ bone marrow tumor
7_ immobilization
8_ milk alliance syndrome
#pathology
Accumulation

#pathology
Accumulation

⛔atrophy
⬇️
decrease in size of the cell(atrophic cell not' dead but if stimulation continues ↪die by apoptosis.
increase autophagic vaculoes -residual bodies-lipofuscin pigment. (Brown atrophy)

🔹️mechanism of atrophy:
decrease protein synthesis
increase protein degradation
(by ubiquitin-proteasome pathway)

🔹️causes of atrophy➡
1/reduced workload(in case of cast)
2/inadequate nutrition
3/ageing
4/loss of innervation
5/decreed B.supply-
6/ loss endocrine stimulation.

🔹️types of atrophy:
🖇physiological atrophy➡
atrophy of ductus arteriosus
-atrophy of thymus in adult-
atrophy of gonads in old age.
🖇pathological atrophy
💥generalized atrophy ↪atrophy due to starvation-senile atrophy.
💥localized atrophy⬇️
🔸️ischaemic atrophy 👉small atrophic kidney in atherosclerosis of renal .A.
🔸️disuse atrophy👉 wasting of ms of limb immobilised in cast.
🔸️neuropathic atrophy👉 poliomyelitis.
🔸️endocrine atrophy👉hypopituitarism lead to atrophy of thyroid ;adrenal & gonads.
🔸️pressure atrophy➡. erosion of spine
by tumour in nerve root

🚫hypoplasia
incomplete growth of organ
🚫agenesis
complete failure of development of organe in embryogenesis.

🏷 hypertrophy----> increase in size of cell

✔✔hypertrophy without hyperplasia affect mainly perminant cell(heart-skeletal ms-nerve cell)
🔹️ physiological hypertrophy:
❗enlargment of uterus during pregnancy due to estrogen stimulation-
❗ breast enlargment during pregnancy
❗-skeletal .ms hypertrophy d/t increase workload.
🔹️pathological hypertrophy
❗hypertrophy of uterine smooth ms (effect of estrogen secreted by ovarian tumor)
❗lt.v.hypertrophy-
❗Rt.v.hypertrophy.

🏷 hyperplasia:
increase in number of cells.
Du to 1-hormonal stimulation
2-tissue loss(labile cells & stable cells).

🖇physiological
🔹️hormonal.
proliferation of epith.of breast at puberty& during pregnancy d/t estrogen stimulation.
🔹️compensatory:
occure when portion of tissue removed or diseased. e.g➡compensatory hyperplasia of remaining liver after hepatectomy.
🖇pathological
🔸️.adenomatous hyperplasia of endometrium after normal M.C d/t increased esreogen /progesterone ratio.
🔸️hyperplasia of thyroid follicle in 1ry hyperthyroidism.
🔸️hyperplasia associated with viral infection(HPV)
🔸️benign prostatic hyperplasia.
🔸️ important in wound healing.

🚫Estrogen:
Hyperplasia and hypertrophy _▪︎ Normal : pregnancy (uterus and breast)
🏷Metaplasia:reversible changes ;ons cell type replaced by another cell type.
💭metaplasia fertile soil for malignant transformation
التغير ح نسميه حسب نوع الcell الي طلعلي '!

⛔ types of metaplasia:
1-epithelial(reversible)
🔸️Seq.metaplasia.
(replacement of columnar epith by st.seq.epith).
.
🔸️columnar metaplasia
barrett esophagus..(normal st.seq.epith.of lower esophagus replaced by gastric or intestinal type columnar epith
2-mesenchymal (irreversible)
🔸️fibroblast to chondroblast to produce cartilage.
🔸️fibroblast into osteoblast to produce bone.(myositis ossificans)
كل ال adaptation ح تكون reversible إلا النوع هذا.


🚩 barrett esophagus: metaplasia >>>
✔adaptation
✔dysplasia >>precancer >> cancer.
#pathology
Adaptation

#pathology
#endocrine