1 cellular injury & death, adaptation

8/4/2019 1 Cellular Injury & Death, Adaptation

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Cellular Injury &Death, AdaptationRita Grace Marcon


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Myocardial Hypertrophy Myocyte hypertrophy

-increased size of both cytoplasm and

nucleus

Lipofuscin pigment (adjacent to nucleus)


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Myocardial Hypertrophy 10x


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40x

Lipofuscinpigments


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Chronic Pyelonephritis Dilated Tubules

Thyroidization (pink staining substances

look like thyroid follicles) Flattened lining epithelium (atrophy)


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Chronic Pyelonephritis 10x


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Flattenedliningepithelium

Thyroidization


8/50Atrophic Endometrium 10x


9/5040x


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Nodular/Benign ProstaticHyperplasia Glands vary widely in size and shape

Papillomatous folds of lining mucosa

Cystically dilated

Lined by columnar or cuboidal cells withsmall uniform nuclei


11/50Nodular/Benign Prostatic Hyperplasia 4x


12/5010x

Cystic dilation


13/5040x

Columnarepithelium


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Squamous metaplasia,Cervix (Chronic Cervicitis) Replacement of simple columnar

epithelium with mature stratified

squamous epithelium Mononuclear infiltrates composed of

lymphocytes, plasma cells, and

macrophages


15/50Chronic Cervicitis 10x


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Fatty Change, Liver Widespread cytoplasmic vacuolization of

hepatocytes

Nuclei pushed to one side


17/50Fatty Liver 10x


18/5040x


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Chronic PassiveCongestion of Lungs Intracellular accumulation of Hemosiderin

Yellow-brown granular pigment within

alveolar macrophages


20/50Chronic Passive Congestion of Lungs 10x


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40x

Hemosiderinaccumulations in

macrophages


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Anthracosis Benign deposition of coal dust in the

lungs from inhalation of sooty air

Black, granular pigment in CT,lymphatics, and alveolar septae


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Anthracosis 10x


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Coagulation Necrosis(Acute M.I.) Coagulation necrosis of myocardial cells

Abundant neutrophilic infiltrates between

necrotic cells Necrotic myocardial cells have opaque

and highly acidophilic cytoplasm

Nuclei are lost (karyolysis), pyknotic, orfragmented (karyorrhexis)


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Coagulation Necrosis (M.I.) 10x


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40x

Neutrophilicinfiltration

Karyolysis


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Caseation Necrosis (TB ofLungs) Granulomatous Lesions throughout lung

parenchyma

Caseation Necrosis- cheesy white grossappearance of the area of necrosis


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Caseation Necrosis (TB of Lungs) 10x


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Caseation Necrosis (TB ofLymphadenitis) Lymph Node architecture replaced by

coalescent granulomas

Amorphouse pinkish granular debris


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Caseation Necrosis (TBL m hadenitis 4x


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10x


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40x


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Enzymatic Fat Necrosis(Pancreatitis) Neutrophilic and monocytic infiltrates

Areas of enzymatic fat necrosis char. Bysemi-digested fat cells, basophilic calciumdeposits, and neutrophilic infiltrates


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Pancreatitis 4x


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Neutrophilic infiltration in

Pancreatitis 40x


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Enzymatic Fat Necrosis in

Pancreatitis 10x


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Gangrenous Necrosis (SoftTissue Gangrene, dorsalaspect of foot) Both Coagulation necrosis and liquefaction

necrosis are present

Striated muscles undergoing coagulationnecrosis are swollen, eosinophilic, arewithout striations and nuclei

Neutrophils as seen in between necrotic

cells In liquefaction necrosis, only cellular

debris and abundant neutrophilic inflitrates

observed


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Gangrenous Necrosis 4x

Area of coagulationnecrosis

Area of liquefactionnecrosis


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10x


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40x


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Side questionsVenus Eisha L. Barte


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Main components of the nucleus Nucleolous Chromatin

Nuclear membrane DNA and RNA are NOT visible by light

microscopy Atrophy can be pathologic and physiologic, and

example of physiologic atrophy would be theatrophic endometrium during menopause The organ which undergoes pure hypertrophy

is the skeletal muscles


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When the heart cells hypertrophy they enlarge but without increase in thenumber of cells, the nuclei of the heart enlarges but the lumen in the heartnarrows

Poor blood supply brought about by cholesterol / TAG accumulation in the

intima of the arteries causes the heart cells to pump more blood triggershypertrophy of heart cells Hyperplasia can be both pathologic and physiologic Hyperplasia can be combined with hypertrophy, example: pregnant uterus,

BPH Metaplasia is REVERSIBLE when the injurious agent is no longer causing it,

but when malignancy is suspected, theres a big chance that it wont reverseback.

Pathogenesis of fatty changes in the liver: TAG accumulation in liver transported to hepatocytes Esterified to TAGs, cholesterol, phospholipidsor oxidized to ketone bodies, also acetate. Due to chronic alcoholism orother factors, there is a disruption in the transport of TAG causing reduced

protein and increased fat accumulation Diseases that cause fatty liver:

DM Anoxia CHON malnutrition Obesity


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Hemosiderin accumulation is due to thelocal excess of Iron, where Ferritin forms

Hemosiderin granules, damaged cellswhich are taken up by macrophages, red-brown in color

Anthracotic pigments are black in color,and is usually associated with coal dustaccumulation, or CO2 accumulation


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Anthracosis: An example would be coal minerspneumocossis, wherein there is so much coal dust inthe lungs, and the lungs cannot accommodate norremove the particles inside it.

Development of anthracosis: This happens when thelungs capacity to accommodate and remove theparticles is exceeded. Coal miners

Urban people who smoke or are exposed to machinery(vehicular) fumes

Bargemen

Hypoxia causes cell injury by: When tissue hypoxia happens,


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yp j y y yp ppthe body undergoes glycolysis (anaerobic metabolism) to try toattempt generating ATP which is only 2 compared withoxidative metabolism which is 36 ATP. The end result is theformation of Lactic Acid which triggers a lot of factors like:Producing pain and injury to the cells.

ATP deficiency causes swelling by reduced oxidativephosphorylation in the mitochondria secondary to ischemia.This in turn reduces sodium pump which increases Calcium,

Sodium, and water while efflux of Potassium causes cellularswelling.

Water accumulates during hydropic change in between lamellarstacks of membranes.

Reversible injury becomes irreversible when ischemia persistsand when necrosis ensues which causes: Severe mitochondrial swelling

Extensive damage to the plasma membrane

Lysosomal swelling

Massive influx of Calcium


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Oxygen radicals are formed when there is a reduction-oxidation reaction like mitochondrial phosphorylationsuperoxide, H2O2, OH-

Free radicals damage cells by attaching to the foam

cells (Atherosclerotic plaque) and thereby narrowingblood entry

Histologic signs of necrosis High eosinophil count Loss of glycogen particles

Vacuolated and moth eaten cytoplasm Dead cell calcification Myelin figures

The most common form of necrosis is coagulation necrosis


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Features of coagulation necrosis Preservation of the basic outline of the coagulated cell for a span of at

least some days

The injury or the subsequent increasing intracellular acidosis denaturesnot only structural CHONS but also enzymes and so blocks proteolysisof the cell

Examples:

MI

Hypoxic death in all tissues except the brain

We usually find caseous necrosis in the lungs and lymph nodes

Apoptosis is programmed cell death A pathway of cell death induced by a tightly regulated intracellular

program in ehich cells destined to die activate enzymes that degrade thecells own nuclear DNA and nuclear cytoplasmic CHONS

Apoptosis differs from necrosis No inflammation, programmed

Necrosis: (+) Inflammation, injurious


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Ecclesiastes 3:11 GOD makes ALL things BEAUTIFUL inHIS time

God bless everyone

1 cellular injury & death, adaptation

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