Prof. Manal Maher Hussein Prof. Manal Maher Hussein 9/14/2015 Clinical Pathology.

Prof. Manal Maher Prof. Manal Maher HusseinHussein

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Clinical Pathology


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Overall Aims of Course

By the end of this course, the students should By the end of this course, the students should have a basic pathology knowledge of have a basic pathology knowledge of structural and functional changes in disease,structural and functional changes in disease, what causes disease,what causes disease, how disease starts, progresses & how disease starts, progresses & how patient signs and symptoms are related how patient signs and symptoms are related

to underlying pathology. to underlying pathology. This knowledge should provide the students a This knowledge should provide the students a

sound foundation for rational clinical care sound foundation for rational clinical care and therapy and to help student to and therapy and to help student to understand the patient and his disease.understand the patient and his disease.


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Course Contents Introduction and definitions, Introduction and definitions, Reversible cell injury, Irreversible cell injury,Reversible cell injury, Irreversible cell injury, Intracellular accumulations and extracellular Intracellular accumulations and extracellular

depositions depositions Growth disturbancesGrowth disturbances Neoplasia Neoplasia Circulatory disturbancesCirculatory disturbances Diseases of the heartDiseases of the heart Diseases of the respiratory systemDiseases of the respiratory system Diseases of the upper gastrointestinal tractDiseases of the upper gastrointestinal tract Diseases of lower gastrointestinal tractDiseases of lower gastrointestinal tract Diseases of the liverDiseases of the liver Diseases of bones and jointsDiseases of bones and joints


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Assessment Schedule Assessment 1… 2 Periodical sheet exams Assessment 1… 2 Periodical sheet exams

Week beginning from 4thWeek beginning from 4th Assessment 2 … 2 Practical exams Assessment 2 … 2 Practical exams

Weeks 5 & 10Weeks 5 & 10 Assessment 3… Final written exam Assessment 3… Final written exam

Week ?Week ? Assessment 4 … Oral examAssessment 4 … Oral exam


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Weighting of Assessments Mid-Term Examination Mid-Term Examination 10 % (10 10 % (10

Marks)Marks) Final-term Examination Final-term Examination 50% (50 50% (50

Marks) Marks) Oral Examination. Oral Examination. 15% (15 15% (15

Marks) Marks) Practical Examination 25% (25 Practical Examination 25% (25

Marks) Marks) Semester Work Semester Work Other types of assessmentOther types of assessment TotalTotal 100% (100 Marks) 100% (100 Marks)


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Recommended Books

Recommended BooksRecommended Books Pathologic Basis of Disease, Robbins Pathologic Basis of Disease, Robbins

and Cortran, Elsevier Saunders 8th and Cortran, Elsevier Saunders 8th Edition, 2010 Edition, 2010


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PATHOLOGY

Pathology of a disease is formally studied Pathology of a disease is formally studied under four subdivisions: under four subdivisions: AetiologyAetiology - Study of cause / causative - Study of cause / causative

agent of disease.agent of disease. PathogenesisPathogenesis- Study of disease - Study of disease

progression.progression. Morphology Morphology - Study of structural - Study of structural

changes in disease (gross & changes in disease (gross & microscopic).microscopic).

Clinical SignificanceClinical Significance - Study of how - Study of how clinical features are related to changes.clinical features are related to changes.


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PATHOLOGY Disease presents with many 'problems' Disease presents with many 'problems'

known as known as symptomssymptoms e.g. pain, and with e.g. pain, and with abnormalities noticed by physician abnormalities noticed by physician

known as known as signssigns e.g. abnormal heart e.g. abnormal heart sounds.sounds.

Finding the nature of disease is known Finding the nature of disease is known as as diagnosisdiagnosis..

Predicting the future course of disease Predicting the future course of disease is known as is known as prognosis.prognosis.

Taking precautions to prevent disease Taking precautions to prevent disease is known as is known as prophylaxisprophylaxis..


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Cellular Injury


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Response to Injury:

Adaptations Adaptations (reversible)(reversible) Hypertrophy/ increase size of cellsHypertrophy/ increase size of cells Hyperplasia/ increase no of cellsHyperplasia/ increase no of cells Atrophy/ decrease in size of cellsAtrophy/ decrease in size of cells Accumulations - protein, fat, etc.Accumulations - protein, fat, etc. Extracellular calcium depositionExtracellular calcium deposition

Necrosis Necrosis (irreversible)(irreversible) – cell death – cell death


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REVERSIBLE CELL INJURY REVERSIBLE CELL INJURY

(DEGENERATION) (DEGENERATION)

Functional and Functional and morphological changes that morphological changes that are are reversiblereversible


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REVERSIBLE CELL INJURY REVERSIBLE CELL INJURY (DEGENERATION)(DEGENERATION)

If the irritant persist, death, necrosis.If the irritant persist, death, necrosis. Affects Affects parenchymalparenchymal (metabolically (metabolically

active) cells, such as liver cells, renal active) cells, such as liver cells, renal tubules more than mesenchymal cells as tubules more than mesenchymal cells as cardiac muscle. cardiac muscle.

Causes: reduced Causes: reduced oxidative oxidative phosphorylation, ATP depletion phosphorylation, ATP depletion

cellular swellingcellular swelling caused by caused by changes in ion changes in ion concentrations and water influxconcentrations and water influx..

Degenerations are Degenerations are mainly due to mainly due to intracellular accumulation of water or fatintracellular accumulation of water or fat..


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Types of degeneration:

1.1. Cloudy swellingCloudy swelling Swelling of the cells (due to Swelling of the cells (due to water water

accumulationaccumulation) and granulation of the ) and granulation of the cytoplasm (due to cytoplasm (due to lipid depositionlipid deposition). ).

The injurious agents, mainlyThe injurious agents, mainly hypoxia, hypoxia, inhibit oxidative phosphorylation and ATP inhibit oxidative phosphorylation and ATP formationformation

FateFate:: reversible, reversible, if the injury continues, it proceeds to if the injury continues, it proceeds to

hydropic swellinghydropic swelling (reversible) or (reversible) or necrosisnecrosis..


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Normal liver/ Cloudy swelling


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2.2. Hydropic swelling (Hydropic or Hydropic swelling (Hydropic or vacuolar degeneration):vacuolar degeneration):

Excess water accumulationExcess water accumulation inside the inside the cells forming cells forming vacuolesvacuoles in the in the cytoplasm. The lesion is cytoplasm. The lesion is more more advancedadvanced than cloudy swelling. than cloudy swelling.


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Hydropic change in ischemic - kidney

Microvilli


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Types of degeneration:3. Fatty change (steatosis):3. Fatty change (steatosis):

Small or large Small or large lipid vacuoles (neutral lipid)lipid vacuoles (neutral lipid) in in

cyto.cyto. due to the due to the suppression of mitochondrial lipid suppression of mitochondrial lipid

metabolic enzymesmetabolic enzymes. . Common in liver, heart and kidneyCommon in liver, heart and kidney Causes:Causes:

hypoxiahypoxia bacterial toxins bacterial toxins chemical agents as alcohol, carbon chemical agents as alcohol, carbon

tetrachloridetetrachloride


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Fatty change (steatosis)

Fatty changes in the Fatty changes in the liver cellsliver cells are also are also

caused bycaused by:: intake of excess dietary fat or starvation.intake of excess dietary fat or starvation. Diseases / Diseases / viral hepatitisviral hepatitis.. DeficiencyDeficiency of lipotropic factors as of lipotropic factors as choline choline

and methionineand methionine accumulation of accumulation of

neutral fat inside the liver cells.neutral fat inside the liver cells.


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Normal liver/ fatty change Normal liver/ fatty change (Steatosis)(Steatosis)


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IRREVERSIBLE CELL INJURY IRREVERSIBLE CELL INJURY (NECROSIS)(NECROSIS)

Local death of cells or tissues Local death of cells or tissues within the living body (irritant)within the living body (irritant). .

Necrosis either occurs Necrosis either occurs directlydirectly or or follows reversible injuryfollows reversible injury..

Necrotic tissue Necrotic tissue appears appears opaque/ whitish opaque/ whitish / swollen/ swollen. .

The surrounding tissue appears The surrounding tissue appears red due to red due to inflammatory inflammatory hyperemiahyperemia..

Microscopic changes due to Microscopic changes due to lytic action of lytic action of lysosomal lysosomal enzymesenzymes


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IRREVERSIBLE CELL INJURY IRREVERSIBLE CELL INJURY (NECROSIS)(NECROSIS)

Nuclear changesNuclear changes:: Pyknosis:Pyknosis: The nucleus shrinks and stains The nucleus shrinks and stains

darkly.darkly. Karyorrhexis:Karyorrhexis: Nuclear fragmentation Nuclear fragmentation Karyolysis:Karyolysis: Faint dissolved nucleus. Faint dissolved nucleus.

Cytoplasmic changesCytoplasmic changes:: The cells appear The cells appear homogenous and homogenous and indistinct from each other.indistinct from each other.

Architectural changesArchitectural changes:: Necrotic tissue Necrotic tissue structurelessstructureless due to due to cell lysiscell lysis.. Protein denaturation Protein denaturation (coagulation(coagulation)) may may

precede cell lysis. precede cell lysis. Necrotic cells Necrotic cells preserve the architectural preserve the architectural

outlinesoutlines of the original tissue of the original tissue


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22 - Normal cardiac muscle/ 22 - Normal cardiac muscle/ coagulative necrosis


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Types of Necrosis:1.1. Coagulative NecrosisCoagulative Necrosis::

Caused by Caused by sudden cut of the blood sudden cut of the blood supplysupply (ischemic necrosis) (ischemic necrosis)

Denaturation of cellular proteinsDenaturation of cellular proteins causing the tissue to appear causing the tissue to appear hardhard, , opaque whiteopaque white and and preserves its preserves its architecturearchitecture..

Heart, kidney & spleen Heart, kidney & spleen Splenic Infarction

Renal Infarction


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Types of Necrosis:

2.2. Liquefactive Necrosis:Liquefactive Necrosis: The necrotic tissue is rapidly liquefied. It The necrotic tissue is rapidly liquefied. It

occurs in:occurs in: Infarction of the Infarction of the brain and spinal cordbrain and spinal cord Pyogenic abscessPyogenic abscess: The necrotic core is : The necrotic core is

liquefied by the proteolytic enzymesliquefied by the proteolytic enzymes released from pus cells.released from pus cells.

Amoebic abscessAmoebic abscess

Stroke- Liquifactive necrosis


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TYPES OF NECROSISTYPES OF NECROSIS

3. Caseous Necrosis:3. Caseous Necrosis: Typical for Typical for tuberculoustuberculous

lesions. lesions. caseous because the caseous because the

necrotic tissue appears necrotic tissue appears yellowish-whiteyellowish-white and and ““cheesycheesy””

Necrosis is followed by Necrosis is followed by

slow partial liquefactslow partial liquefactiionon.. Architecture is completely Architecture is completely

obliteratedobliterated


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Caseous Necrosis


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4. Fat Necrosis: 4. Fat Necrosis: 1.1. Enzymatic fat necrosisEnzymatic fat necrosis: :

It occurs in acute It occurs in acute hemorrhagic pancreatitishemorrhagic pancreatitis..

The enzyme The enzyme lipaselipase,, digests fat cells with digests fat cells with

the production of the production of fatty acidsfatty acids. .

fatty acids +with calcium fatty acids +with calcium calcium calcium

soapssoaps,/dull ,/dull opaque white patchesopaque white patches. .


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4.4. Fat Necrosis: Fat Necrosis:

2. Traumatic fat necrosis2. Traumatic fat necrosis::

It occurs due to trauma of the adipose It occurs due to trauma of the adipose

tissue of tissue of breast and subcutaneous fat.breast and subcutaneous fat.

The fat cells rupture and The fat cells rupture and self-digestionself-digestion

takes place with takes place with release of fatty acidsrelease of fatty acids, ,

which combine with which combine with calcium. calcium.


Small areas

Regeneration/ fibrosis

Necrosis

Inflammation surrounds necrotic

area

Phagocytosis necrotic tissue

Large areasfibrous capsule

dystrophic calcification

Drainage of liquefied tissue by lymphatics


NecrosisNecrosis death of cells within the living death of cells within the living

body caused by body caused by an irritantan irritant. .

occurs directly or follows occurs directly or follows

reversible injury reversible injury

associated with release of associated with release of

chemical mediatorschemical mediators

InflammationInflammation surrounds the surrounds the

necrotic area.necrotic area.

accompanied by healing & accompanied by healing &

calcification.calcification.

accompanied by nucleus accompanied by nucleus

KaryolysisKaryolysis

ApoptosisApoptosis involves involves few or single cellsfew or single cells..

Occur without injury or mild Occur without injury or mild

injury not causing necrosisinjury not causing necrosis energy-dependent programmed cell energy-dependent programmed cell

death death RRemoval of unnecessary or emoval of unnecessary or

diseased cellsdiseased cells

Not associated with release of Not associated with release of

chemical mediators, chemical mediators,

it does not excite it does not excite

inflammation.inflammation.

It is not accompanied by It is not accompanied by

healing or calcification.healing or calcification.

Formation of apoptic bodies, Formation of apoptic bodies,


APOPTOSIAPOPTOSISS

Morphological Morphological changes:changes:

Cell shrinkageCell shrinkage Chromatin Chromatin

condensation condensation followed by followed by fragmentation of fragmentation of DNA. DNA.

Formation of apoptic Formation of apoptic bodies, composed of bodies, composed of cytoplasm cytoplasm with/without nuclear with/without nuclear fragments.fragments.

Phagocytosis of Phagocytosis of apoptic cells or apoptic cells or bodies by bodies by macrophages.macrophages.


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APOPTOSIS In physiological conditionsIn physiological conditions : :

Hormone dependentHormone dependent / regression of lactating / regression of lactating breast after stopping lactation.breast after stopping lactation.

Normal turnover of cells.Normal turnover of cells. Programmed cell destruction during Programmed cell destruction during

embryonic development.embryonic development. In pathological conditionsIn pathological conditions : :

Reduction of cell number in Reduction of cell number in atrophy.atrophy. In cases of mild In cases of mild radiation injuryradiation injury.. Cell death in Cell death in tumour regressiontumour regression Liver cells in Liver cells in viral hepatitis.viral hepatitis.


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INTRACELLULAR ACCUMULATIONS

The following substances may accumulate The following substances may accumulate inside the cells: inside the cells: waterwater as in cloudy and hydropic swelling, as in cloudy and hydropic swelling, fatfat as in fatty change, as in fatty change, mucinmucin as in mucoid change, as in mucoid change, glycogenglycogen as in glycogen storage disease as in glycogen storage disease proteinprotein as in hyaline change and as in hyaline change and pigmentspigments..


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Types of degeneration:Types of degeneration:

4. Mucoid change: (Mucoid Degeneration)4. Mucoid change: (Mucoid Degeneration) Accumulation of Accumulation of mucinmucin inside the inside the

epithelial cellsepithelial cells, which , which swelswelll Cells rupture release of mucin Cells rupture release of mucin

(catarrhal inflammation).(catarrhal inflammation). Extracellular accumulation of mucin is Extracellular accumulation of mucin is

called called MYXOMATOUS DEGENERATIONMYXOMATOUS DEGENERATION. .


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5.5. Hyaline change: (Hyalinosis)Hyaline change: (Hyalinosis) The The cellular or extracellularcellular or extracellular deposition deposition

of “hyaline” of “hyaline” ((proteinprotein material material) gives a ) gives a homogenous, structureless, glassy homogenous, structureless, glassy pink appearancepink appearance..

Connective tissue (extracellular)Connective tissue (extracellular) hyalinosis is commonly seen in hyalinosis is commonly seen in old old scars, blood vesselsscars, blood vessels

Cellular hyalinosisCellular hyalinosis : : in the islets of in the islets of Langerhan’sLangerhan’s in diabetes mellitus. in diabetes mellitus.


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Types of degeneration:6.6. Waxy degeneration: Waxy degeneration: (Zenker’s (Zenker’s

degeneration)degeneration) It is a special type of It is a special type of hyalinosis hyalinosis of the of the

skeletal musclesskeletal muscles. . The muscles The muscles loose its loose its

striationstriation and become and become

waxy, homogenous waxy, homogenous

and structurelessand structureless Causes:Causes: The The bacterial bacterial

toxins and the excesstoxins and the excess

lactic acid accumulatiolactic acid accumulationn


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Pigments Melanin:Melanin: Melanin normally exists in Melanin normally exists in skin, hair, skin, hair,

eyeseyes. . increased increased melanin pigmentation melanin pigmentation

(Hyperpigmentation):(Hyperpigmentation):

1.1. Prolonged exposure to Prolonged exposure to sunsun

2.2. ChloasmaChloasma:: Hyperpigmented Hyperpigmented brown patchesbrown patches affecting the affecting the face of women face of women during pregnancy,during pregnancy, the use of the use of oral contraceptives.oral contraceptives.

3.3. Pigmented Pigmented skin tumoursskin tumours: Benign and : Benign and malignant melanomas.malignant melanomas.


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Pigments Haemoglobin- derived pigments:Haemoglobin- derived pigments: bilirubin bilirubin

and haemosiderin.and haemosiderin. Bilirubin:Bilirubin: is an is an iron-free pigmentiron-free pigment, which , which

increases in liver in case of increases in liver in case of jaundicejaundice.. HaemosiderinHaemosiderin:: is is brownish iron brownish iron

containing pigment. containing pigment. Localized haemosiderosisLocalized haemosiderosis: In areas of: In areas of haemorrhagehaemorrhage, in cases of , in cases of lung lung congestion, around infarcts congestion, around infarcts

Generalized haemosiderosis:Generalized haemosiderosis: excess excess ironiron in blood. in blood.


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Normal liver/- Bilirubin in liver


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- Hemosiderin in pulmonary macrophage


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EXTRACELLULAR DEPOSITIONS

These include These include amyloid, cholesterol, uric amyloid, cholesterol, uric acid, calciumacid, calcium..

Amyloid:Amyloid: Amyloidosis is the extracellular Amyloidosis is the extracellular

deposition of amyloid, an deposition of amyloid, an abnormal abnormal proteinprotein usually resulting from usually resulting from antigen-antigen-antibody reactionantibody reaction..

Amyloid deposits in the Amyloid deposits in the walls of blood vessels and walls of blood vessels and basement membranes.basement membranes.


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Amyloid proteins are of two types:

ImmunoglobulinsImmunoglobulins secreted by plasma cells. secreted by plasma cells.

Amyloid associated proteinAmyloid associated protein present as a present as a

Precursor proteinPrecursor protein in serum. in serum.

Markedly increased in Markedly increased in chronic chronic

inflammatory and destructive diseasesinflammatory and destructive diseases,,

as in as in tuberculosis.tuberculosis.

Amyloidosis

Localized Amyloidosis

Generalized Amyloidosis

Senile Amyloidosis of brain: Alzheimer disease,

Tumours of endocrine gland: thyroid, pancreas.

Larynx, tongue, heart, urinary bladder, muscles

Primary AmyloidosisMalignant neoplasm of plasma cell abnormalities of B lymphocytes

Secondary Amyloidosis

Generalized Amyloidosis

Secondary Amyloidosis

ChChronic suppurations//

chronic lung abscesschronic lung abscess

Granulomas as tuberculosis

Autoimmune disease as

rheumatoid arthritis.

malignant tumours as Hodgkin’s disease

Haemodialysis-associated Amyloidosis

Hereditary Amyloidosis:familial Mediterranean

fever


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Cholesterol The normal cholesterol level The normal cholesterol level in bloodin blood is is 150-250 mg/100150-250 mg/100 HypercholesterolemiaHypercholesterolemia may be: may be:

PhysiologicalPhysiological as in as in pregnancy and lactationpregnancy and lactation.. PathologicalPathological hypercholesterolemia hypercholesterolemia results in the results in the

deposition of cholesterol in the intima of the arteries deposition of cholesterol in the intima of the arteries ((atherosclerosis)atherosclerosis) or in skin ( or in skin (xanthoma)xanthoma)..


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Xanthomas


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Uric acid Normal Normal end product of the metabolism of the end product of the metabolism of the

nucleic acid purinenucleic acid purine.. Causes: Causes:

Primary goutPrimary gout with known or unknown with known or unknown enzyme defectenzyme defect, it may be , it may be hereditaryhereditary or or

secondary goutsecondary gout due to increase due to increase nucleoproteinnucleoprotein breakdown, breakdown, as in chronic as in chronic leukemias.leukemias.

increase of serum uricincrease of serum uric acid to above 6 mg% acid to above 6 mg% (normal= 3-6mg %), known as (normal= 3-6mg %), known as hyperuricemiahyperuricemia

the deposition of sodium the deposition of sodium urate crystals in urate crystals in tissuestissues, known as , known as goutgout. .

The deposit forms small masses called The deposit forms small masses called tophi.tophi.


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Tophus on the elbow of a middle aged man with chronic gout.

gouty tophi of the gouty tophi of the helix of the ear.helix of the ear.


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Uric acid

The urate crystals deposit in The urate crystals deposit in jjointsoints

(particularly the big toe, ankle), (particularly the big toe, ankle),

cartilagecartilage of the eye, ear and nose, of the eye, ear and nose,

in in cardiac valvescardiac valves and in and in

the interstitial tissue ofthe interstitial tissue of kidneykidney

leading to leading to urate stonesurate stones in the in the

kidney and renal failurekidney and renal failure


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Calcium

Pathological calcificationPathological calcification is the is the

deposition of calcium saltsdeposition of calcium salts

(phosphate and carbonate) (phosphate and carbonate) in in sites sites

other than bone and teethother than bone and teeth. .

The calcified tissue appears The calcified tissue appears chalky chalky

white and hard.white and hard.


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Types of pathological calcification

1.1.Dystrophic calcificationDystrophic calcification:: Calcification of Calcification of injured injured or or necroticnecrotic tissues tissues

despite the despite the normalnormal serum calcium level. serum calcium level. It It occurs occurs in: in:

degenerated tissuesdegenerated tissues as as old scarsold scars, , degenerated degenerated heart valvesheart valves

necrotic tissuesnecrotic tissues as as old thrombi, old infarcts, old thrombi, old infarcts, fat necrosis, liquefactive necrosis, caseous fat necrosis, liquefactive necrosis, caseous tuberculous lesions and dead parasites and tuberculous lesions and dead parasites and ova of ova of bilharziasisbilharziasis


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1.1. Dystrophic calcificationDystrophic calcification:: TheThe causecause of calcium deposition and the of calcium deposition and the

formation of formation of calcium phosphatecalcium phosphate crystals is crystals is breakdown of organic phosphatebreakdown of organic phosphate leading to leading to

local local alkalinityalkalinity in the necrotic tissue, in the necrotic tissue, increased increased phosphatasephosphatase activity or activity or release of phosphate from release of phosphate from nucleoprotein nucleoprotein

breakdownbreakdown..


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Metastatic calcification: This is the calcification of This is the calcification of normal living tissuesnormal living tissues

due to due to hypercalcaemiahypercalcaemia. . Causes:Causes: of hypercalcaemia of hypercalcaemia include include

IIncreasedncreased calciumcalcium mobilizationmobilization from bone from bone BoneBone destructiondestruction by malignant tumours by malignant tumours

andand Prolonged immobilizationProlonged immobilization.. HyperparathyroidHyperparathyroid

IncreasedIncreased calciumcalcium absorptionabsorption from intestine from intestine as in hypervitaminosis D and excess milk as in hypervitaminosis D and excess milk intakeintake

Chronic renal diseaseChronic renal disease


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Metastatic calcification: Acid secretions or rapid changes in pH Acid secretions or rapid changes in pH

contribute to calcium salt formationcontribute to calcium salt formation It occurs in It occurs in

1. 1. Mucosa of stomachMucosa of stomach. . 2. 2. Renal tubulesRenal tubules. . 3. 3. Walls of the lung alveoli.Walls of the lung alveoli.

NB Hypercalcaemia accentuate dystrophic NB Hypercalcaemia accentuate dystrophic calcificationcalcification


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Metastastic calcification in the lung, Metastastic calcification in the lung, with hypercalcaemia with hypercalcaemia


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Idiopathic calcinosis:Idiopathic calcinosis:

This is calcification of unknown This is calcification of unknown

cause that may cause that may affect skin and affect skin and

other soft tissues, despite other soft tissues, despite normalnormal

tissue and calcium leveltissue and calcium level.. Stones:Stones:

Urinary stone, biliary stones Urinary stone, biliary stones

and and salivary duct stones.salivary duct stones.


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The decrease in calcium level in bones:The decrease in calcium level in bones:

In childrenIn children leads to leads to ricketsrickets,, mainly mainly

due to vitamin D deficiencydue to vitamin D deficiency

In womenIn women leads to low bone density leads to low bone density

(Osteomalacia(Osteomalacia)) at the menopause at the menopause

due to hormonal imbalance.due to hormonal imbalance.

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GROWTH DISTURBANCES


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Disorders of Growth: Decreased growthDecreased growth

Atrophy, Hypoplasia, AplasiaAtrophy, Hypoplasia, Aplasia

Increased growthIncreased growth Non NeoplasticNon Neoplastic – Normal DNA – Normal DNA

Due to a need.. Controlled.Due to a need.. Controlled. NeoplasticNeoplastic – – Abnormal DNAAbnormal DNA

not needed, auto, uncontrolled.not needed, auto, uncontrolled.


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Congenital Congenital

AnomaliesAnomalies

•AgnesiaAgnesia •HypoplasiaHypoplasia •AplasiaAplasia

Absence Absence of an of an

organ (kidney)organ (kidney)

Failure of an organ Failure of an organ

to achieve the to achieve the

full full adult sizeadult size

( infantile uterus)( infantile uterus)

Complete Complete failure of failure of

organ to developorgan to develop. .

severe hypoplasia severe hypoplasia

(rudimentary kidney) (rudimentary kidney)


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ACQUIRED

GROWTH

DISTURBANCES

Atrophy Hypertrophy Hyperplasia Metaplasia Dysplasia Neoplasia


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ATROPHY Atrophy is the Atrophy is the decrease in size and decrease in size and

weight weight of a tissue or organ after of a tissue or organ after it it has reached its full developmenthas reached its full development. .

Atrophy may be due to Atrophy may be due to reduction in reduction in number or size of component cells,number or size of component cells, or or both. both.


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Types of atrophy: A- Physiological atrophy:A- Physiological atrophy:

Some Some embryonic structuresembryonic structures undergo undergo atrophy during fetal development.atrophy during fetal development.

Atrophy of uterus, ovaries and Atrophy of uterus, ovaries and breast after menopause due to breast after menopause due to diminished hormone stimulation.diminished hormone stimulation.


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PATHOLOGICAL ATROPHY

Localized atrophy Generalized Atrophy

Disuse atrophy

Prolonged immobilization

Hormonal Atrophy/ of breast following resection of ovaries.

Loss of innervations/

atrophy of muscles

Diminished blood supply/

brain atrophy

Decreased anabolism

malnutrition &starvation

Increased catabolism

as in malignancy

Senile

Pressure (benign tumour

Compressing the surrounding tissue)


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Muscle ischemic atrophy:


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Kidneys, normal (left) and ischemic atrophy

(right)


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HYPERTROPHY Hypertrophy is the Hypertrophy is the increase in sizeincrease in size

and weightand weight of a tissue or organ due to of a tissue or organ due to increase in the size of cellsincrease in the size of cells, , to meet to meet increased functional demand. increased functional demand.

Types of hypertrophy:Types of hypertrophy: A- Physiological hypertrophyA- Physiological hypertrophy

Pregnant uterusPregnant uterus due to hormone due to hormone stimulation.stimulation.

Hypertrophy of striated muscles in Hypertrophy of striated muscles in muscle buildersmuscle builders..


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Pathological hypertrophy

Adaptive hypertrophyCompensatory hypertrophy

(one kidney is surgically removed)

Ventricular hypertrophy due to

hypertension or aortic valve stenosis

Hypertrophy of stomach in

pyloric stenosis.

Hypertrophy of intestinal wall

in chronic intestinal obstruction


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ventricular hypertrophy due to



pyloric stenosis.



LVH in Chronic Hypertension:

Left Ventricular HypertrophyLeft Ventricular Hypertrophy


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Thyroid gland, normal / hypertrophy and

hyperplasia


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HYPERPLASIA Hyperplasia is the Hyperplasia is the increase in sizeincrease in size and and

weight of a tissue or organ due to weight of a tissue or organ due to increase in the number of cellsincrease in the number of cells. .

Hyperplasia can occur Hyperplasia can occur only in cells only in cells capable of divisioncapable of division i.e. all cells except i.e. all cells except nerve cells, skeletal and cardiac nerve cells, skeletal and cardiac muscle cells.muscle cells.


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Types of hyperplasia:

A- Physiological hyperplasia:A- Physiological hyperplasia: Occurs in the breast and genital Occurs in the breast and genital

organs at puberty.organs at puberty. B- Pathological hyperplasia:B- Pathological hyperplasia: 1. Hormonal hyperplasia:1. Hormonal hyperplasia: e.g. e.g.

endometrial and mammary endometrial and mammary hyperplasia due to excessive hyperplasia due to excessive oestrogenoestrogen stimulation.stimulation.


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B- Pathological hyperplasia:

2. Compensatory hyperplasia2. Compensatory hyperplasia (may be (may be considered physiological or pathological):considered physiological or pathological): Bone marrowBone marrow hyperplasia following hyperplasia following

haemorrhage or haemolysishaemorrhage or haemolysis and in some and in some anemia.anemia.

Hyperplasia of Hyperplasia of the the liverliver after partial after partial hepatectomy, restoring the normal liver hepatectomy, restoring the normal liver weight within two weeks.weight within two weeks.

3. Irritation hyperplasia3. Irritation hyperplasia of of lymphoid tissuelymphoid tissue in response to in response to antigenic stimulation.antigenic stimulation.


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Sequels of Necrosis:

Cell DeathCell Death NecrosisNecrosis AutolysisAutolysis PhagocytosisPhagocytosis Organization & fibrous repair.Organization & fibrous repair.


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APOPTOSIS Apoptosis/ cell death /involves Apoptosis/ cell death /involves few or few or

single cellssingle cells.. It is an energy-It is an energy-dependentdependent programmed cellprogrammed cell

deathdeath RRemoval of unnecessary or diseased cellsemoval of unnecessary or diseased cells.. Occur Occur without tissue injurywithout tissue injury or or with mild with mild

injury not causing necrosis. injury not causing necrosis. Not associated with release of chemical Not associated with release of chemical

mediators, thus mediators, thus it does not excite it does not excite inflammation.inflammation.

It is not accompanied by healing or calcification.It is not accompanied by healing or calcification.


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Heart hypertrophy

in hypertensio

n:

Left VentricleLeft Ventricle


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Types of Amyloidosis:1.1. LocalizedLocalized AmyloidosisAmyloidosis::

a. a. Senile Amyloidosis of brainSenile Amyloidosis of brain: as in case of : as in case of

Alzheimer diseaseAlzheimer disease, ,

b. b. Tumours of endocrine glandTumours of endocrine gland: : thyroid,thyroid,

pancreaspancreas..

c. c. Localized idiopathicLocalized idiopathic: Larynx, tongue, heart, : Larynx, tongue, heart,

urinary bladder, muscles…etcurinary bladder, muscles…etc


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Infarction - Adrenal gland:

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GROWTH DISTURBANCES


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Disorders of Growth: Decreased growthDecreased growth

Atrophy, Hypoplasia, AplasiaAtrophy, Hypoplasia, Aplasia

Increased growthIncreased growth Non NeoplasticNon Neoplastic – Normal DNA – Normal DNA

Due to a need.. Controlled.Due to a need.. Controlled. NeoplasticNeoplastic – – Abnormal DNAAbnormal DNA

not needed, auto, uncontrolled.not needed, auto, uncontrolled.

Congenital Congenital

AnomaliesAnomalies

•AgnesiaAgnesia •HypoplasiaHypoplasia •AplasiaAplasia

Absence Absence of an of an

organ (kidney)organ (kidney)

Failure of an organ Failure of an organ

to achieve the to achieve the

full full adult sizeadult size

( infantile uterus)( infantile uterus)

Complete Complete failure of failure of

organ to developorgan to develop. .

severe hypoplasia severe hypoplasia

(rudimentary kidney) (rudimentary kidney)


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ACQUIRED

GROWTH

DISTURBANCES

Atrophy Hypertrophy Hyperplasia Metaplasia Dysplasia Neoplasia


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ATROPHY Atrophy is the Atrophy is the decrease in size and weightdecrease in size and weight

of a tissue or organ after of a tissue or organ after it has reached its it has reached its full developmentfull development. .

Atrophy may be due to Atrophy may be due to reduction in reduction in number or size of component cells,number or size of component cells, or or both. both.


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Types of atrophy: A- Physiological atrophy:A- Physiological atrophy:

Some Some embryonic structuresembryonic structures undergo atrophy undergo atrophy during fetal development.during fetal development.

Atrophy of uterus, ovaries and breast after Atrophy of uterus, ovaries and breast after menopause due to menopause due to diminished hormone diminished hormone stimulation.stimulation.

PATHOLOGICAL ATROPHY

Localized atrophyLocalized atrophy Generalized AtrophyGeneralized Atrophy

Disuse atrophyDisuse atrophy

Prolonged immobilizationProlonged immobilization

HormonalHormonal Atrophy/ of breast Atrophy/ of breast following resection of ovaries. following resection of ovaries.

Loss of innervations/Loss of innervations/

atrophy of musclesatrophy of muscles

Diminished blood supply/Diminished blood supply/

brain atrophybrain atrophy

Decreased anabolismDecreased anabolism

malnutrition &malnutrition &starvationstarvation

Increased catabolismIncreased catabolism

as in as in malignancymalignancy

SenileSenile

Pressure (benign tumour

Compressing the surrounding tissue)


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Kidneys, normal (left) and ischemic atrophy

(right)


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HYPERTROPHY Hypertrophy is the Hypertrophy is the increase in sizeincrease in size and and

weightweight of a tissue or organ due to of a tissue or organ due to increase increase in the size of cellsin the size of cells, , to meet increased to meet increased functional demand.functional demand.

Types of hypertrophy:Types of hypertrophy: A- A- PhysiologicalPhysiological hypertrophyhypertrophy

Pregnant uterusPregnant uterus due to hormone due to hormone stimulation.stimulation.

Hypertrophy of striated muscles in Hypertrophy of striated muscles in muscle muscle buildersbuilders..


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Ventricular hypertrophy due to



pyloric stenosis.




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Renal Infarction - Coagulative


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Splenic Infarction - Coagulative necrosis

Prof. Manal Maher Hussein Prof. Manal Maher Hussein 9/14/2015 Clinical Pathology.

Documents

manal maher husseinlvh

physiological hyperplasia

types of hyperplasia

size of cells

mammary hyperplasia

hormonal hyperplasia

compensatory hyperplasia

physiological atrophy