WILL OF MED NINJA🥷🔥.
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🔹 Langhans giant cell:
Arranged in a horseshoe pattern
🔹 Foreign body giant cell:
Arranged in a scattered pattern
🔹 The mediator IL-8 is for:
Chemotaxis
🔹 Regeneration occurs:
▪️ All the time in labile tissues
▪️ Limited in stable tissues
▪️ Does not occur at all in permanent tissues
🔸️Tissue Repair:the restoration of tissue architecture and function after an injury.
🔸️Regeneration: full restoration of normal tissue structure and function.
🔸️Scarring: replacement by fibrous tissue when full regeneration is impossible.
🔹️Role of Stem Cells:
▪️Provide new cells for regeneration
▪️Essential for tissue repair
▪️Present in labile and stable tissues
🔹️Scarring involves :
▪️Creating new blood vessels
▪️laying down collagen
▪️remodeling the collagen
🔹️Three types of tissues:
▪️Labile → regenerate easily
▪️Stable → limited regeneration
▪️Permanent → no regeneration, scar only
🔹️First intention healing:
▪️Fast healing
▪️Minimal inflammation & scar
▪️Small wounds
🔹️Second intention healing:
▪️Large, open wounds
▪️Slow healing
▪️More inflammation & scarring
🔸️Keloid scar = excessive fibrosis beyond wound margin.
🔸️Proud flesh = excessive granulation tissue protrudes above wound surface.
🔹️Granulation Tissue ≠ Granuloma
🔸️Granulation tissue: normal healing process
🔸️Granuloma: chronic inflammatory lesion
🔸️Inflammation:
A protective physiological
response to cell injury
🔹️Involves:
▪️ vascular events
▪️cellular events
▪️chemical mediator events
🔹️Cardinal Signs of Inflammation:
▪️Redness (Rubor) → vasodilation & hyperemia
▪️Heat (Calor) → increased blood flow
▪️Swelling (Tumor) → exudate + inflammatory cells
▪️Pain (Dolor) → edema + bradykinin & prostaglandins
▪️Loss of function (Functio laesa) → pain + swelling
🔹️Purpose of Inflammation:
▪️Localize the injury
▪️Eliminate the cause
▪️Repair damaged tissue
🔸️Effects of Inflammation🔸️
🔹️Local:
▪️Killing microorganisms
▪️Swelling & loss of function
🔹️Systemic:
▪️Fever
▪️Malaise
▪️Leukocytosis
🔹️Leukocytosis:
▪️Neutrophils ↑ → acute bacterial infection
▪️Lymphocytes ↑ → viral or chronic inflammation
🔸️Fever🔸️
🔹️Caused by cytokines (IL-1, IL-6, TNF)
▪️Improves leukocyte killing
▪️Inhibits microbial replication
🔸️Acute Phase Reactants🔸️
▪️CRP & ESR ↑
▪️Produced by liver
Due to IL-1, IL-6, TNF
🔸️Classification of Inflammation🔸️
🔹️Acute inflammation:
▪️Short duration (days–weeks)
▪️Neutrophils
▪️Cardinal signs present
🔹️Chronic inflammation:
▪️Long duration (months–years)
▪️Lymphocytes, macrophages
▪️Fibrosis
🔸️Morphologic Patterns of Acute Inflammation🔸️
▪️Serous → protein-poor fluid (blister)
Suppurative (purulent) → pus
▪️Boils (Furuncle) →collection of abscess commonly in hair follicles
▪️Ulcerative → loss of epithelium
▪️Pseudomembranous → diphtheria
▪️Fibrinous → fibrin deposition (pericarditis, pleura)
🔸️ Acute Inflammatory Response🔸️
🔹️ Vascular events:
▪️Vasoconstriction (seconds)
▪️Vasodilation
▪️Increased vascular permeability
▪️Stasis of blood
🔹️Cellular events:
▪️Margination
▪️Rolling
▪️Adhesion
▪️Migration (diapedesis)
▪️Chemotaxis
▪️Phagocytosis
🔹️Humoral events:
▪️Chemical mediators
▪️The cornerstone of inflammation
▪️Control vascular & cellular responses
🔸️Exudate: high protein, inflammatory
🔸️Transudate: low protein, non-inflammatory
🔹️Outcomes of Acute Inflammation:
▪️Resolution
▪️Fibrosis
▪️Abscess formation
▪️Progression to chronic inflammation
⭕️طبعاً كلام الدكتور مهم جداً جداً
والذي كتبته هنا كله من كلام الدكتور وتقريباً شامل لكل ما قاله
سلايدات عملي لمادة علم الأمراض:
Including identify and features for Necrosis & Apoptosis
*Apoptosis*
🔹️One cell
🔹️Shrunken cell bodies
🔹️Fragmented nuclei with condensed chromatin
🔹️Some pieces of cells breaking off
Identify: Fibrinoid Necrosis in artery
🔹️Microscopic Features
*Bright pink, struckless area in the arterial wall
*Endothelial injury
*Fibrinoid necrosis of small arteries
*Formation of pink fibrin
*🔹️Dry Gangrene:*
*Black, dry, shrunken tissue
*Usually in distal extremities
*Minimal inflammation
*🔹️Wet Gangrene:*
*Red/black, swollen, moist tissue
*Usually in internal organs
*Associated with bacterial infection and tissue liquefaction
Identify:
Pancreatic fat necrosis
🔹️Gross Features:
*White, chalky deposits.
*Hard necrotic areas.
*saponification.
🔹️Microscopic Features:
*Necrotic fat cells with vague outlines
*Loss of nuclei.
*pink granular cytoplasm
macrophages, giant cells.
Identify: Lung – Caseous necrosis (Tuberculosis)
🔹️Gross Features:
*Large yellow-white cheesy necrotic area
*Friable (قابل للتفتت)
🔹️Microscopic Features:
*Acellular pink eosinophilic necrotic tissue.
*Surrounded by granulomatous inflammation: epithelioid cells, lymphocytes, fibroblasts, Langhans giant cells.
Identify: Liver – Liquefactive necrosis (Pyogenic abscess)
🔹️Gross Features:
*Multiple micro-abscesses.
*Pale/yellow soft areas.
🔹️Microscopic Features:
*Numerous neutrophils causing focal liquefactive necrosis.
*Beginning of organizing abscess wall.
*Pink fibrin deposition.
