Cell injury for e-learning Dr. Faten Wagdi

Cell injury Morphological +/- functional changes Of individual cells in response to any stress.

PATHOLOGICAL STIMULI (Injurious agent/ stress) 1- Hypoxia 2- Chemical agents 3- Infectious agents 4- Physical agents 5- Immunological agents 6- Genetic agents

Effect of these stimuli on cells ADAPTATION REVERSIBLE INJURY IRREVERSIBLE INJURY

DEPENDING ON: Severity & Duration of stimulus AND Type of affected cell

Cellular adaptation -No cell injury -Reversible -Change in ??? number/ size/ type/ function of the cell in response to ??? physiological or pathological changes Why???

Forms of cell adaptation 1- Atrophy 2- Hypertrophy 3- Hyperplasia 4- Metaplasia

Forms of cell adaptation

A mother noticed empty right sided scrotal sac of her infant. Ultrasound revealed tiny right testicle few mms with normal sized left testicle. The right testicular condition is known: A- Atrophy B- Aplasia C- Agenesis

The myocardial fibers of right ventricular wall In the arrowed heart Displays: A- Increase in number B- Decrease in number C- Increase in size D- Decrease in size E- A+C

The increase in size Of this organ is Attributed to: A- Increase in number of its cells B- Increase in size of its cells C- A+B

True or false ?? The lining urothelium of the renal pelvis may be ossified due to prolonged irritation by oxalate stones.

Transformation of one cell type to another is known as: A- Hyperplasia B- Dysplasia C- Aplasia D- Metaplasia E- Neoplasia

How injurious agents lead to cell injury ????

Mechanisms of cell injury: 1- Depletion of ATP 2- Mitochondrial damage 3- Increased intracytoplasmic calcium 4- Accumulation of oxygen-derived free radicals 5- Membrane damage 6- Nuclear damage

Which of these may be used as clinical parameter of cell death? A- Serum Calcium level B- Serum Ph C- Oxygen-derived free radicals D- Serum lysosomal enzymes

Lowered intracellular p H in cell injury is attributed to: A- Calcium influx B- Accumulation of oxygen –derived free radicals C- Failure of Na pump D- Anaerobic glycolysis

Reversible cell injury A- Cellular swelling (hydropic change) OR B- Intracellular accumulations of: Fat Proteins Glycogen Glycoproteins (mucin)

REVERSIBLE CELL INJURY Cloudy swelling / Hydropic change/ vacuolar degeneration Accumulation of water within the cell cytoplasm. Represents the first manifestation of almost all forms of injury to the cell.

Small cytoplasmic vacuoles in hydropic change represents: A- Distended mitochondria B- Distended endoplasmic reticulum C- Distended lysosomes D- Distended ribosomes

NECROSIS -Definition -D.D. from autolysis -Pathogenesis -Morphology ( cytoplasm & nucleus) -Types - Assosiated pathological changes

Types of necrosis ?? Type of necrosis depends on Balance between Protein denaturation & Lysosomal digestion

Types of necrosis: 1- Coagulative 2- Liquefactive 3- Caseous 4- Fat 5- Fibrinoid

Cut of blood supply leads to liquefactive necrosis in: A- Heart B- Spleen C- Spinal cord D- Kidney E- Intestine

Case n= 1 A 40 yrs old female presents by a firm mass in the breast 2 weeks after she has been subjected to car accident. Needle biopsy reveals chronic inflammatory cellular infiltrate with granular basophilic deposits. A- What is your diagnosis? B- What is the clinical importance? C- Give another example to the same pathological condition.

Renal infarction is suspected grossly by: A- Thin walled cystic lesion B- Cheesy yellowish lesion C- Hard chalky white foci D- Firm pale area

APOPTOSIS -Definition -Morphology -Examples -Pathogenesis - D.D. from necrosis

FAS FasL Bak p53 ??? Bcl-x1???

Apoptosis vs Necrosis

Apoptosis is characterised by being : A- Surrounded by inflammatory cells B- Always pathological C- Affect group of contiguous cells D- Active process E- Reversible cell injury

Gangrene = Necrosis + putrefaction Necrosis : Ischaemia…… Putrefaction: Saprophytic organisms in soil & air/ in colon

Types of gangrene I- Dry gangrene II- Wet gangrene III- Gaz gangrene

Gangrene may affect all these sites except: A- Brain B- Vulva C- Lung D- Hand E- Intestine

Complete: In dry gangrene …………………. Represents a zone of acute inflammation separating the …….. Part from the …… part.

INTRACELLULAR ACCUMULATIONS A- Normal constituents: Lipids Proteins Carbohydrates B- Abnormal metabolic products C- Pigment: Endogenous or exogenous.

Intracellular accumulation of fat: 1- Triglycerides in parenchymatous cells: Fatty change ( steatosis ) 2- Cholesterol in macrophages: Hges, cholesterolosis, xanthomas 3- Stromal fatty infiltration: Obesity (fat cells in stroma) 4- Abnormal lipids in reticulo endothelial cells : Lipid storage diseases

Fatty change of liver occurs in the following conditions except: A- D.M. B- Cholesterolosis C- CHF D- Chronic alcoholism E- Starvation

To stain intracellular fat the tissue must be: A- Formaline fixed B- Alcohol fixed C- Saline fixed D- Frozen E- Bouin’ s fixed

Intracellular accumulation of proteins: Homogenous eosinophilic intracytoplasmic

Russel bodies represent intracellular accumulation of: A- Proteins in lymphocytes B- Proteins in macrophages C- Proteins in plasma cells D- Glycogen in plasma cells E- Glycogen in macrophages

Hyaline change ??? -Hyalos ??? -Descriptive non specific term??? -Protein or Not protein(secretion, degenerated collagen……) -Different pathological conditions -Intracellular (renal tubules/ russel bodies) or Extracellular (Wall of arterioles in hypertension)

Intracellular accumulation of ( GLYCOGEN ) 1- D.M.?? : (renal tubules, cardiac myocytes, islets of langerhans) 2- Glycogen storage diseases?? ( cardiac and skeletal myocytes, hepatocytes) Hx & E VACUOLATED CYTOPLASM

Cell with vacuolated cytoplasm: -Fat frozen, Sudan III or oil red -Glycogen alcohol fixed, PAS before& after diastase - Water No staining

Mucoid (myxomatous)change: Glycoprotein (mucin) Produced normally by epithelial and mesenchymal cells?? Deposited under certain pathological conditions ?? Epithelial form---- mucoid Mesenchymal form---myxoid

P.A.S. is used to stain: A- Fat B- Calcium C- Haemosiderin D- Proteins E- Glycogen

Pathological pigmentation Endogenous Exogenous Melanin Skin Haemosiderin Inhalation Lipofuscin Ingestion Parasitic

Pregnancy associated hyperpigmentation is known as: A- Freckles B- Vitiligo C- Chloasma D- Naevi

Abnormal deposition of haemosiderin: A- Haemosiderosis: Deposition in phagocytes with no tissue damage. B- Haemochromatosis: Extensive deposition in parenchymatous cells with tissue damage.

Some special stains -Fat : Sudan III and oil red on frozen -Glycogen : PAS before & after diastase -Mucin : PAS before & mucicarmine -Iron : Prussian blue reaction(Perl’s)

All these conditions may result in secondary haemochromatosis except: 1- Repeated blood transfusion 2- Prolonged administration of iron 3- Fe deficiency anaemia 4- Chronic haemolytic anaemia

All these are endogenous pigment except: 1- Melanin 2- Haemosiderin 3- Lipochrome 4- Lipofuscin 5- Porphyrin

Pathological calcification Deposition of Ca salts in abnormal sites ??usually extracellular Where is the defect ?? Serum Ca level= Metastatic OR Site of deposition= Dystrophic

The following are examples of dystrophic calcification except: A- Calcified bilharzial ova B- Calcified atheroma C- Renal stones D- Wall of chronic abscess E- Uterine fibroid

Cellular aging Senescence

Cellular aging

Progressive shortening of telomeres leads to: A- Activation of apoptosis B- Initiation of necrosis C- Metaplastic changes D- Neoplastic changes E- Cell senescence