1. All Rights Reserved 2017/Aliraqia
University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 1
2. All Rights Reserved 2017/Aliraqia
University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 2 Dedication To my students of the third stage in
Dentistry faculty at Aliraqia university with best wishes. Prof.Dr.
Khalil HassanAljeboori The admonstrator
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 3 Topics of Lectures First Term Lectures 1-Introduction
2-Degenerative changes and cellular injury 3- Necrosis and
apoptosis (Irreversible cell injury). 4- Disturbances of
Pigmentation. 5- Inflammation. 6- Tissue repair healing and
regeneration. 7- Cellular adaptation and disturbances of growth. 8-
The Infectious Disease I 9- The Infectious Disease II 10-
Disturbances of body fluids and electrolytes I 11- Disturbances of
body fluids and electrolytes II 12- Immunopathology. 13-Neoplasia
(tumors). 14-Ionizing radiation. 15-Genetic diseases Second Term
Lectures 16- Cardiovascular system I 17- Cardiovascular system II
18- Cardiovascular system III 19- Diseases of respiratory system I
20- Diseases of respiratory system II 21- Diseases of respiratory
system III 22- Diseases of Alimentary system I 23- Diseases of
Alimentary system II 24- Diseases of Alimentary system III 25-
Diseases of liver and pancreas I 26- Diseases of liver and pancreas
II 27- Pathology of Lymphoid System I 28- Pathology of Lymphoid
System II 29-Hematopathology I 30-Hematopathology II
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 4 Contents Lecture 1: Introduction 13 -Normal cell
composition -Definitions -Fields of pathology Lecture 2:
Degenerative changes and cellular injury 15 1.Gloudy swelling
2-Hydropic degeneration 3- Fatty change or steotosis 4- Hyaline
degeneration A. Connective tissue hyaline B. Epithelial hyaline 5-
Glycogen infiltration A. metabolic disease diabetes mellitus B.
glycogen storage disease Lecture 3: Necrosis and
apoptosis(Irreversible cell injury) 19 *Apoptosis *Necrosis:
1.coagulative necrosis 2. Liquefactive necrosis 3. Caseous necrosis
4. Fat necrosis 5. Gangrenous necrosis 6. Fibrinoid necrosis * Fate
of necrosis Lecture 4: Disturbances of Pigmentation 22 *Exogenous
pigments *Endogenous pigment *Disturbances of minerals 1.
Dystrophic calcification 2. Metastatic calcification *Gout Lecture
5: Inflammation 24 Purpose of inflammation and the inflammatory
exudates. Clinical signs or hallmarks of inflammation Exudates or
exudation Transludate (non inflammatory edema)
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 5 Major important mediator of inflammation Types of
inflammation 1- According to duration 2- According to exudates A)
Acute inflammation 1-Serous inflammation 2-fibrinous inflammation
3-Hemorrhagic inflammation 4-Purulent (supportive) inflammation 5-
Necrotizing or pseudo membranous inflammation 6-Allergic
inflammation B) Chronic inflammation Granuloma Systemic effects of
inflammation Consequence of excessive inflammation action Lecture
6: Tissue repair healing and regeneration 29 Regeneration Repair
A)Healing by first intention Stages of wound healing by first
intention B) Healing by second intention Factors affecting wound
healing 1-Local 2-systemic Lecture 7: Cellular adaptation and
disturbances of growth 31 Adaptation 1. Hypertrophy 2. Atrophy 3.
Hyperplasia 4. Metaplasia Dysplasia Anaplasia Lecture 8: The
Infectious Disease I 33 Infection Defenses mechanism 1-Nonspecific
defense mechanism 2- Specific defense mechanism Mechanism of virus
damage to cells Mechanism of bacterial injury, and damage to tissue
Lecture 9: The Infectious Disease II 36 -Some human infectious
diseases.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 6 Viral diseases Bacterial infections Parasitic infection
Mycotic infection Lecture 10: Disturbances of body fluids and
electrolytes I 43 Extra cellular fluid Intracellular fluid Fluid
and electrolyte balance 1. Sodium 2. Potassium 3. Chloride Causes
of edema (transudate) Pathological features of edema:
1-Subcutaneous edema 2-Pulmonary edema 3-Brain edema Clinical
significance of edema Hyperemia and congestion Hemorrhage Types of
hemorrhage Lecture 11: Disturbances of body fluids and electrolytes
II 49 Ischemia Thrombosis Fate of thrombosis Embolism Infarction 1-
Red infarction 2- White infarction 3- Septic infarction Shock
Categories of shock Pathological changes in shock Lecture 12:
Immunopathology 55 1) In adequate immune response a. Primary
immunodeficiency b. Secondary immunodeficiency Acquired
immunodeficiency syndrome (AIDS) 2) In appropriate immune response.
Autoimmune diseases Immunological tolerance Classification of
autoimmune diseases 3) Hypersensitivity or immunological injuries
1- Type I hypersensitivity reaction or anaphylaxis 2- Type II
hypersensitivity, cellular cytotoxicity or cellular lysis 3- Type
III hypersensitivity
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 7 4- Type IV hypersensitivity Cell mediated cytotoxicity
4)Amyloidosis Lecture 13: Neoplasia (tumors) 71 Nomenclature of
neoplasms Biology of tumor growth 1. Malignant transformation 2.
Growth rates of tumor cells 3. Local invasion 4. Metastasis
Precancerous condition Cellular effector mechanism against the
tumor Effect of tumor on the host Grading and staging Tumor markers
Carcinogenesis Lecture 14: Ionizing radiation 81 Ionizing radiation
1. Electromagnetic radiation 2. Particulate radiation Irradiation
effects Tissue changes Result of irradiation Lecture 15: Genetic
diseases 83 Types of genetic diseases - Chromosomal abnormalities
A. Abnormalities of Chromosome number B. Abnormalities of
Chromosome structure C. Chromosomal mosaicism - Inherited disorders
(gene abnormalities) A. Pattern of inheritance B. Inherited
metabolic disorders 1-disorder of carbohydrate metabolism
2-disorder of carbohydrate metabolism 3-disease of amino acid
metabolism 4- Disorders of lipid metabolism 5 -lipid storage
disease Lecture 16: Cardiovascular system I 90 -Diseases of
Arteries Arteriosclerosis Medial sclerosis Endoarteritis oblitrans
Arteriosclerosis
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 8 Arteritis Thromboangitis oblitrans Aneurysm - Diseases
of vein Varicose veins (varicosities) Phlebitis Venous thrombosis
Neoplasms Lecture 17: Cardiovascular system II 94 - Diseases of
lymph Lymphangitis Tumors of blood and lymphatic vessels - Diseases
of heart Coronary heart disease. Hypertensive cardiopathy.
Rheumatic heart disease. Congenital heart disease. - Diseases of
endocardium Endocarditis Valvular deformities Carcinoid
cardio-vascular disease Lecture 18: Cardiovascular system III 98 -
Diseases of myocardium Coronary sclerosis. Coronary occlusion.
Coronary thrombosis. Myocardial infraction Hypertrophy of heart.
Hypertensive heart disease. Myocarditis. Metabolic disease. Heart
block. - Diseases of pericardium Pericarditis. Tuberculous
pericarditis Constrictive pericarditis (picks disease)
Polyserositis (Concatos disease) Hydropericardium Hemopericardium
Lecture 19: Respiratory system I 103 -The nose and nasal sinuses
-Diseases of larynx -Diseases of bronchi 1. Chronic bronchitis
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 9 2. Bronchial asthma 3. Bronchiectasis - Diseases of
lungs 1. Chronic venous congestion 2. Edema 3. Thrombosis and
embolism 4. Infarction Lecture 20: Respiratory system II 107
-Pneumonia 1. Labor pneumonia 2. Lobular pneumonia
(bronchopneumonia) 3. Interstitial pneumonia -Rheumatic pneumonia
-Lung abscess -Pulmonary tuberculosis (granulomatous pneumonia)
-Pulmonary bilharziasis -Pulmonary hypertension -Obstruction
-Atelactasis Lecture 21: Respiratory system III 111 -Emphysema 1.
Obstructive emphysema 2. Senile emphysema occur in small lung 3.
Pulmonary interstitial emphysema -Pneumoconiosis 1.Anthracosis
2.Silicosis 3. Asbestosis 4. Silicosiderosis 5. Berylliosis
6.Byssinosis 7.Bagassosis 8. Farmer lungs 9. Alveolar pronteinosis
- Tumors of the lungs 1. Benign tumors 2. Malignant tumors -
Diseases of pleura 1. Pleurisy, pleuritis 2. Empyema 3. Pleural
effusion a. Hydrothorax b. Hemothrax c. Pneumothorax - Hemoptysis -
Coin lesions
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 11 Lecture 22: Diseases of Alimentary system I 116 -
Lesion of oral cavity - Ulcers of stomach - Tumors Lecture 23:
Diseases of Alimentary system II 121 - Intestinal tract diseases
1.Congenital malformations 2.Diverticula of intestine
3.Inflammation and ulcerations 4.Tumors of intestine 5.Intestinal
obstruction Lecture 24: Diseases of Alimentary system III 127 -
Diseases of periton 1. Ascites 2. Intraperitoneal hemorrhage 3.
Peritonitis - Tumors - Hemorrhoids (piles) - Anal vistula -
Pilonidal sinus - Celiac diseases and sprue 1. Celiac diseases 2.
Tropical sprue 3.Protein losing-enteropathy (exudative enteropathy)
4. Whipples disease (intestinal lipodystroply) Lecture 25: Diseases
of liver and pancreas I 132 - Circulatory disturbances - Infections
of liver 1. Pyogenic abscesses 2. Pylephlebitis 3. Tuberculosis 4.
Visceral leishmaniasis (kala-azar) 5. Amebic abscess 6. Weils
disease 7. Syphilis 8.Viral hepatitis 9.Yellow fever 10.Hydatid
cyts 11.Schistosomiasis (bilharziasis) 12.Actionomycosis abscesses
-Cirrhosis of liver Distinctive patterns of cirrhosis
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 11 Cirrhosis in infancy and childhood Liver Neoplasms
Lecture 26: Diseases of liver and pancreas II 138 - Diseases of
Gallbladder and bile ducts Cholecystctis Cholesterolosis
Cholelithiasis Jaundice - Disease of pancreas Acute hemorrhagic
pancreatitis Acute interstitial pancreatitis Chronic pancreatitis
Cysts Fibrocystic disease Lesions Calculi Diabetes mellitus -
Lesions in kidneys - Lesions in cardiovascular system
Hematochromatosis Tumors Lecture 27: Pathology of Lymphoid System I
144 -Diseases of spleen Infectious splenomegaly Non-infectious
splenomegaly - Diseases of the thymus Thymic hyperplasia Tumors
Lecture 28: Pathology of Lymphoid System II 147 - Diseases of lymph
nodes Reactive hyperplasia Acute nonspecific lymphadenitis Chronic
nonspecific lymphadenitis Granulomatous lymphadenitis Lymphoid
tumors Lecture 29: Hematopathology I 151 -Diseases of
erythropoietic system Anemia 1. Deficiency anemia 2. Hypopoietic
anemia
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 12 Acute hemolytic anemia Acquired and congenital icterus
Sickle cell anemia Mediterranean anemia: (thalassemia)
Erythroblastosis fetalis. Polycythemia. Polycythemia vera Purpura
Lecture 30: Hematopathology II 169 - Diseases of leukopoietic
system Neutrophilic leukocytosis Eosinophilic leukocytosis
(eosinophilia) Basophils leukocytosis Monocytosis Lymphocytosis
Agranulocytosis Leukemia
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Aljeboori 13 Lecture 1 Prof.Dr. Khalil Hassan Zenad Aljeboori
Introduction Compositions: The normal cell: composed mainly 1.
Nucleus 2. Cytoplasm 3. Cell membrane. The nucleus: contain
chromosomes a carriers for genes and nucleolus. It is the heart of
cell maintaining the genetic constitution of cell, namely
chromosome network responsible for hereditary characters cell
production and proliferation. The cytoplasm: contain organelles
mitochondria, endoplasmic reticulum, Golgi apparatus. The dominant
constituents of nucleus and cytoplasm the ribose nucleic acid (RNA)
in the mitochondria and in nucleolus and deoxyribose nucleic acid
in nucleus particular in chromosomes. The cell membrane: regulate
internal environment of cells determine what is goes in and what is
come out it is surface structure consisted of lipid,
polysaccharides and small amount of protein. Mitochondria: main
power plant of cell have different enzymes utilize molecular oxygen
and distribute energy yielding component to other organelles and
responsible for cell respiration. Endoplasmic reticulum: series of
vesicles, canals responsible for protein synthesis. Golgi
apparatus: remove cell products to outside. Pathology: is the
science which deal with disease causes, nature of disease together
with anatomical and functional changes induced by disease. Disease:
is any departure of a state of health. Etiology of disease:
bacteria and parasite, fungi, viruses, chemical, toxins, heat,
cold, light, electricity, irradiation, foreign body, trauma,
immunological, disorders.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 14 Nature of disease: 1. Congenital 2. Inflammation 3.
Degeneration 4. Physical disturbances circulatory, trauma,
obstruction of hollow organs foreign body, hernia, thermal
disturbances, light electricity, irradiation, chemical) 5. Tumors
Pathogenesis: the development of disease. Prognosis: result of an
attack of disease. Complication of disease, new disorders occurred
after usual course of disease. Symptoms: functional evidence of the
disease. Example pain. Signs: objective evidence of the disease.
Syndrome: a set of symptoms occur together. Field of pathology: 1.
Histopathology: concerned with investigation and diagnosis of
disease by tissue examination. 2. Gross pathology: refers to
changes in organs or tissue in disease by naked eye (morbid
anatomy) or (post mortem pathology) 3. Clinical pathology: is
concerned with analysis of disease itself using laboratory methods
or techniques. 4. Cytopathology: concerned with examination of
cells to reach diagnosis of disease. 5. Hematology study: the blood
and blood forming tissue. 6. Comparative pathology: is the study
disease of lower animal comparable to human disease. 7.
Physiological pathology: study changes in physiology in disease. 8.
Experimental pathology: study the disease experimentally in animal
model. 9. Immunopathology: study the disturbances affecting
defenses mechanism of body related of disease process. 10. Chemical
pathology: study the disease and diagnosis from chemical changes.
11. Toxicology: study the effects of poisons in the body. 12.
Genetics: study abnormal chromosomal alteration and genes related
to disease process. 13. Forensic pathology: application of
pathology to legal purposes i.e. investigation of death in
suspected circumstances. End Of Lecture 1
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 15 Lecture 2 Prof.Dr. Khalil Hassan Zenad Aljeboori
Degenerative changes and cellular injury 1- Cloudy swelling :
reaction of cells to injury by swelling and accumulation of the
water in their organelles or albumin so called albuminous or
parenchymatous degeneration it usually reversible type of cell
injury , most of acute infection or toxic condition are accompanied
by cloudy swelling , mostly seen in liver , kidney . Grossly:
Affected area in organ was swollen, capsule is tense and bulging
during cut section, organ opaque. Microscopically: The affected
cell are swollen, granular cytoplasm due to aggregate protein or
albumin and water in cells organelles such as mitochondria,
endoplasmic reticulum so the cell cytoplasm as ground glass
appearance. Causes: 1- Hypoxia. A. O2 in blood,decrease. B.
Ischemia I.e. No oxygenated blood reach tissue due to thrombus. C.
Reduce oxygen capacity of RBCS due to anemia and CCl4 toxicity. 2-
Chemical agents, ethanol,CO2. 3- Infections. 4- Genetic defects. 5-
Nutritional imbalances. 6- Immunological reactions Ag- Ab
complexes. 7- Aging. 8- Physical agents, radiation and electric
shock. * All these agents cause disturbances in oxidation-
phosphorylation process (energy, ATP) in cell membrane and plasma
membrane so Na+ and water or albumin pumped inside cell cytoplasm
or cell organelles resulted to cell swelling. The pumping of these
materials are through pores in the cell membrane or plasma
membrane. 2-Hydropic degeneration : Hydrops or vacuolar
degeneration While in cloudy swelling there is too little amount of
water in cell organelles, in hydropic degeneration too much amount
of water in the cell cytoplasm is related to severity of the
etiological agents, So the organ;
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 16 Grossly: Swollen but more degree than in cloudy
swelling. Microscopically: Clear spaces (water or albumin) these
removed during tissue processing so appear clear spaces irregular
or hazy borders in liver, kidney. Cause: Similar to cloudy swelling
but extensive degree. Blisters: Specific defect of hydropic
degeneration in which cystic swelling filled with water or albumin
surrounded by thin membrane. Causes: A. hot metallic materials. B.
Hot oil &water. C. Hard materials. D. Virus herpes virus. 3-
Fatty change or steotosis Abnormal accumulation of fat droplets in
cell cytoplasm of the parenchymal cells, kidney, heart and liver.
Grossly: Seen mostly in liver, kidney and heart target organs for
fat metabolism (triglycerides mainly) so the affected organs are
yellow, fatty in nature, greasy inconsistency. Microscopically: Fat
droplets appear as clear spaces with regular borders in the
cytoplasm, these vacuoles or clear spaces coalesce together to form
large vacuole displace the nucleus to the periphery. The clear
space originally was fat droplets removed during the tissue
processing under the effect of alcohol or xylole in (H&E) by
special stain: Fat droplets: staining Sudan iii orange Sudan IV
pink Osmic acid black Causes: 1- Toxins,alcohol, ethanol. 2-
Metabolic disease diabetes mellitus. 3- Obesity (normally extra
cellular fat). 4- Protein malnutrition lipoproteins. 5- Anoxia. 6-
Starvation release fatty acids from adipose tissue.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 17 Disturbances in metabolism of cholesterol: abnormal
level of cholesterol termed hyper cholesterolemia occur in; A.
hypothyroidism. B. some renal disease. C. lipoid nephrosis. D.
biliary obstruction. *so deposition of cholesterol in tissue occur
such as in atherosclerosis, in gall bladder, old hemorrhage,
necrotic tissue, the macrophages in contact with these lipid debris
and engulf the lipid appear as a foamy appearance of their
cytoplasm so called foam cells . In atherosclerosis both the smooth
muscle and macrophages are filled with these lipid. *Similarly in
the hereditary hyperlipidemia and in acquired hyperlipidemia the
macrophage filled with these lipid form masses in the dermis and
tendon called: A. Xanthomas. B. Gauchers disease in which lipid in
spleen, brain, skin. C. Neimann pick disease in all tissues. 4-
Hyaline degeneration: after line degeneration translucent,
homogenous, structure less, materials, protein in nature and stain
eosinophilic. Types: A. Connective tissue hyaline: occur in pleura,
spleen capsule, corpus albicans C.T hyaline in arteriosclerosis in
both the fibroblast lose their nuclei and old age tissue injury. B.
Epithelial hyaline which occur: In the kidney when more albumin
excrete and accumulated in PCT epithelial hyaline droplet, occur in
case of nephrotic syndrome in which combine albumin with lysosomes
in PCT epithelium by pinocytosis . in kidney hyaline casts when
albumin or protein aggregated renal tubules. Or in liver in case of
alcoholic hepatitis Mallory bodies. Immunoglobulin proteins
aggregated in plasma cells Russel bodies. In prostate corpora
amylacea also aggregation of protein hyaline, Onion like
appearances in prostatic acini protein. in brain Alzheimer disease
a Neurofibrillary tangle (NFTs) protein in neuron cells
aggregated.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 18 C. Keratohyaline: in skin which indicate extensive
thickening of stratum corneum, keratin without nuclei for examples
hand calluses and foot corns. Causes: 1. Prolonged irritation and
friction. 2. Warts viral disease papilloma virus and pox virus. 3.
Ichthyosis fish scaly skin congenital disease. Specific type Zinker
degeneration is a hyaline degeneration occur in skeletal muscles
fibers described by zinker occur due to extensive bacterial toxins
or excessive accumulation of lactic acid, so muscles pale friable
and loss of striation due to lack of vitamin E . 5- Glycogen
infiltration: normally in liver, SK. muscles excessive
intracellular deposits of glycogen are associated with the
abnormalities in the metabolism of either glucose or glycogen.
Causes: A. metabolic disease diabetes mellitus in which abnormal
glucose metabolism, so glycogen accumulates in kidney and cardiac
muscles. B. glycogen storage disease in which defect in enzyme
synthesis or breakdown of glycogen resulted into massive
accumulation and death of cells or cell injury grossly cells
swollen. Microscopically: glycogen particles appear in the
cytoplasm solitary or coalesce together a (alpha) particles
(150-300 A) or (beta) particles in electronic microscope). )
Special stain: PAS stain +ve Best carmine stain pink 6- Mucinous
degeneration: Mucin is a structure less material pale in H&E
secreted from epithelium of intestine. Causes: (Catarrhal
inflammation) or in some ovarian tumor when present in more amount
termed epithelial mucinous degeneration. Mucoid degeneration or
myxomatous degeneration formed by connective tissue fibroblast
normally in umbilical cord or in subcutaneous tissue in case of
thyroid deficiency (myxedema) and in C.T tumor myxoma stain pale
basophilic sky appearance with criss cross arrangement of fibrils
and pleomorphic fibroblast nuclei. mucoid degeneration of fat
tissue, serous atrophy, gelatin material in fat tissue, stain pink
due to fatty acid react with k+. End Of Lecture 2
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 19 Lecture 3 Prof.Dr. Khalil Hassan Zenad Aljeboori
Necrosis and apoptosis (Irreversible cell injury) Apoptosis: It is
programmed cell death in which the relevant cell activate enzyme
capable to degrading the cell own nuclear DNA and other cytoplasmic
and nuclear proteins, the apoptic cell (dead) is rapidly cleared
before its content have leaked out and therefore the cell death by
this path way does not elicit inflammatory reaction in the host the
apoptosis differ from necrosis that in: ApoptosisNecrosis 1- No
still intact.1- Loss of membrane integrity. 2- No leakage.2-
Leakage of cell contents. 3- No inflammatory.3- Inflammatory host
reaction. Causes of apoptosis: It is physiological in nature so it
is important in physiological conditions: 1. during embryogenesis
(organogenesis and involution). 2. Involution of hormone dependent
tissue example damage of endometrium during menstrual cycle and
regression of lactating breast. 3. In proliferating cells
(intestinal epithelium) maintain a constant number. 4. In the cell
served their function like neutrophils in inflammation. 5. in
self-reactive lymphocytes to prevent tissue destruction. 6.
Cytotoxic T cells against viral infected cells or tumor cell.
Microscopically: Apoptic cell appear round or oval intense
cytoplasm eosinophilic condensed chromatin, fragmented
(karyorrhexis) shrinkage of cells with cytoplasmic buds and
fragment into apoptic bodies composed of membrane bound vesicles of
cytoplasm and organells, these fragment are phagocytosed without
eliciting inflammatory reaction. Necrosis: Is a local death of
tissue in the living body, the process of degeneration that lead to
death termed necrobiosis.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 21 Types of necrosis: 1.coagulative necrosis : Occur by
cut blood supply(infarction) in Such necrosis the general
architecture of tissue are preserved and loss of cellular details,
firm in texture , pale. Microscopically: homogeneous cytoplasm,
eosinophilic and nuclear changes, pyknosis, karyolysis and
karyorrhexis, coagulative necrosis or ischemic necrosis termed. The
necrotic cell either removed by leukocytes or digested by
leukocytes lysosomal enzymes. 2. Liquefactive necrosis: In which
complete digestion of dead cells and tissue leaving liquid mass
enclosed within cystic cavity. Liquefaction necrosis occur by two
ways: A.Focal pyogenic bacterial infection with pus production
(abscess). B.Ischemic destruction of brain tissue leaving a cavity
filled with fluid, edema. 3. Caseous necrosis: Occur in
tuberculosis with production cheesy like material in the center of
tubercles. Microscopically :The caseation appear as amorphous
granular mass, complete loss of tissue structure and cellular
details, the necrotic area surrounded by inflammatory cellular
reaction forming granuloma . 4. Fat necrosis : This occur in acute
pancreatitis in which pancreatic lipase lysis fat cells of pancreas
and peritoneum, then the triglycerides split into fatty acids
combine with Ca++ give violet colour, with K+pink colour,with
Na+blue colour Microscopically: Grossly white chalky material, it
occur also in female breast following trauma (traumatic fat
necrosis), the dead fatty tissue become soapy material like in the
necrotic fatty area. 5. Gangrenous necrosis : It is not a
distinctive pattern of cell death , the term still use clinically,
it occur in limbs , lower legs following cut blood supply , under
going into coagulative necrosis (dry gangrene )when infected by
bacteria modify into liquefactive action of bacteria and attract
leukocytes become wet gangrene with gas bubbles production . Moist
gangreneDry gangrene 1. In enriched blood supply organs lung and
intestine. 1. In ill blood supply organs limb, hands. 2. Not
prominent inflammation zone.2. Prominent inflammatory zone. 3.
Putrefied odor more3. Less putrefied odor. 4. Too much gas
bubbles.4. Less gas bubbles.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 21 6. Fibrinoid necrosis: Seen in the immune response
involving blood vessels, deposition of immune complexes with fibrin
leakage from B.V. result in bright pink of amorphous material this
type appear in polyarteritis nodosa. The leakage of proteins from
dead cells result into for examples cardiac muscles fibers give
creatinine kinase, troponine, liver cells give GOT, GPT and ALK
phosphatase. Fate of necrosis: A. Liquefaction, removed by blood,
lymph. B. Liquefaction, cyst formation. C. Liquefaction abscess
formation. D. Sloughing, desquamation. E. Replacement by scar
tissue. F. Calcification. G. gangrene, necrosis invaded by
saprophytic bacteria (Dry and moist gangrene). End Of Lecture 3
AutolysisNecrosis 1. All dead tissue.1. Presence of dead tissue and
living tissue. 2. Only dead tissue.2. Dead tissue accompanied by
inflammatory reaction. 3. All RBCs lysed.3. Congestion and RBCs
living.
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Aljeboori 22 Lecture 4 Prof.Dr. Khalil Hassan Zenad Aljeboori
Disturbances of Pigmentation Pigment are colored substance either
Exogenous or Endogenous. Exogenous pigments: 1. Carbon in coal
dust, air pollutant when inhaled by phagocytes (macrophages)
(alveolar macrophages) to regional lymph node and in pulmonary
parenchyma (anthracosis) in excessive amount cause coal workers
pneumoconiosis. 2. Tattooing: form of pigment (tattoos pigment) in
skin by needle or by sharp instrument. Endogenous pigments: 1.
Lipofuscin or wear tear pigment: brown yellow granules
intracellularly accumulated in heart, liver and brain, this pigment
composed of lipid and protein derived peroxidation of unsaturated
lipid of body during starvation , malnutrition = brown atrophy. 2.
Melanin :Endogenous pigment brown black induced by catalyzed
oxidation of tyrosine to dihyroxyphenylalnine, it form in
melanocytes located in epidermis protect the body against
ultraviolet radiation, absence of melamine termed albinism, in
melanoma , nevus and freckles the melanine deposited due to focal
melanoblasts proliferation . 3- Hemosiderin :Is brown pigment of
red cells in which hemoglobin break down in too much amount the
pigment contain iron either free or phagocytosed macrophages, also
appear in case hemorrhagic anemia , blood transfusion and passive
congestion, the pigment occur in different organs , in case of
increase absorption of high iron diet . ( when excessive
hemosiderin which more extensive accumulation of iron are seen in
hereditary hematochromatosis in skin and viscera in which tissue
injury, fibrosis, heart failure and diabetes mellitus occur) .
Ochronosis: Melanine pigment affected the cartilage, of ear, nose,
and may be congenitally. Bilirubin: Is the pigment of bile derived
from Hb but unlike hemosiderin contains No iron. In hepatocytes
changed into bilirubin, jaundice occur when too much bilirubin
resulted from extensive lysis of RBCs or damage of hepatocytes or
obstruction of bile ducts.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 23 Hematoidin: Is close to bilirubin formed in tissue
from Hb like hemosiderin its formation is intracellular but need
several days to occur in lacking O2 tissue, in dead tissue usually
occur. Hematin: When break down of blood red cells is formed by
direct action of acids or alkalies on Hb, is not precursor for
hemosiderin or bilirubin . Malarial of pigment: Like hematin effect
parasite on RBcs, Hb. Disturbances of minerals Calcification:
Characterized by abnormal deposition of calcium salts mainly in the
dead tissue it is present in 2 type: 1. Dystrophic calcification:
occur in dead tissues, grossly chalky like materials and gritty
sound during cutting. Microscopically: intra and extra cellular
basophilic deposits, plates like 2. Metastatic calcification: Seen
in cases of hypercalcemia due to: A. Increase level of parathyroid
hormone. B. Destruction of bone example in Paget's disease in which
bone turnover occurred. C. Vitamin D disorders or intoxication. D.
Renal failure. Metastatic calcification occur through all body
organs. Gout: Is the deposition of crystals ofuric acid and urates
in cartilaginous, ligament about joints, synovial membrane and
viscera. Such as heart valves, kidney, the uric acid and urates may
deposited in kidney collecting tubules or in renal cortex form
granuloma. Uric acid derived from nucleoproteins of food, when the
disturbance of purine metabolism uric and urates were deposited.
End Of Lecture 4
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 24 Lecture 5 Prof.Dr.Khalil Hassan Zenad Aljeboori
Inflammation Is a local tissue reaction, changes against injury or
irritation.ie is progressive reaction followed by healing and
repair. Causes: 1- Microbial infections. Bacteria..etc. 2- Physical
against. Radiations, trauma. 3- chemicals, drugs, toxins. 4-
Immunological reaction. Purpose of inflammation and the
inflammatory exudates. 1- destroy injurious agents. 2- wall off
injurious agents. 3- stimulate the immune response. 4- promote
healing. Clinical signs or hallmarks of inflammation: 1- Redness
(rubor). 2- Heat (calor). 3- Pain (dolor). 4- Swelling (Tumor). 5-
Loss of function. Exudates or exudation: Is escape of fluid,
protein, blood, cells from blood vessels into tissue surrounded.
Transludate (non inflammatory edema): Escape of fluid only from the
blood such us in case of heart failure. Exudates Transudate 1- 1-
Protein ,RBCS, WBCS ,fibrin. 1-watery fluid. 2- 2- Acidic PH.
2-Alkaline PH. 3- 3- Putrefied odor. 3-odourless. 4- 4- associated
with inflammatory process. 4-without inflammation occurs. 5- 5-
protein 4% more 5-protein 4% less 6- 6- specific gravity 1.017 more
6- 1.017 less
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Aljeboori 25 Inflammation has 4 major mechanism components or
vascular reactions, changes: 1- Vasodilation of B.V and increase
blood flow. 2- Increase vascular permeability and reduce blood
flow. 3- emigration and activation of leukocytes and increase their
phagocytic activity. 4- Chemotaxis. Attract leukocytes to site of
inflammation. Major important mediator of inflammation: 1-
Vasoactive amines. Such as A) Histamine. B) Serotonin (5-hydroxy
tryptamine). 2- Plasma proteins. a) Complement system protein C3a,
C5a, enhance vascular permeability and chemotaxis respectively. b)
Kinine system in which prekallikrein changed into kallikrein,
converts C5 into C5a and C5b (chemotactic mediator). c) Clotting
system in which thrombin generate insoluble fibrin clot bind to
platelets RBCS, WBCS form clot then followed by plasmin lysis the
clot and increase vascular permeability. 3- Phospholipids derived
mediators: a) Arachidonic acid metabolites: prostaglandin,
leukotriene and lipases mediate all steps of inflammation. b)
Platelets activating factors cause vasoconstriction and increase
leukocytes adhesions. 4- Cytokines and chemokines, tumor necrosis
factor (TNF) and interleukin1(IL1). Their role in inflammation
during the a) Enhance cell adhesions (endothelia). b) Enhance the
thrombogenicity of endothelia. c) Enhance acute phase protein. d)
1L8 interleukin 8 important for chemotaxis of neutrophils. 5-
Nitric oxide (NO) is a potent vasodilator for B.V. 6-lysosomes of
leukocytes those enzyme activity to degrade bacteria and tissue
debris with in phagocytes and other extracellular components
collagen, fibrin, elastin. 7-oxygen derived free radicals (H2O2,
O2, HO) to destroy phagocytosed microbe, damage tissue, fluid,
Serum, host cells possess anti-oxidant activity against these free
radicals.
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Aljeboori 26 8- Neuropeptides: play a role in initiation and
propagation of inflammatory response during the increase vascular
permeability and regulation blood pressure. Types of inflammation:
Classify: 1- According to duration: a) Per acute infl. occur within
18 hrs. b) Acute infl. occur within few days c) Subacute infl.
occur within 7_14th days d) Chronic inflammation occur within
14days to months, years. 2- According to exudates Type of
inflammatory cells and protein exudate. 1-Serous inflammation: in
which fluid enriched with protein containing few inflammatory cells
mainly neutrophils, these serous fluid appear directly in early
influenza infection. 2-fibrinous inflammation: Abundant fibrin in
the exudate together with neutrophils and RBCS in this type of
inflammation damage to B.V. occur by toxins of bacteria such as in
diphtheria. 3-Hemorrhagic inflammation: in with large amount of
RBCS with inflammatory cells (neutrophils) such as in anthrax,
plague. 4-Purulent (suppurtive) inflammation: in which exudate
composed of pus (consisting of the neutrophils (dead and living)
and necrotic tissue debris with RBCS. This type caused by pyogenic
bacteria (staph, strept. Corynebacterium, pseudomonas). Supportive
inflammation may be occur on the surface of tissue lead to: 1.
Ulcer in which loss of continuity of the surface of skin, or
mucosa, due to surrounding suppurative exudate. 2. Abscess
localized pus accumulated in solid tissue encapsulated by fibrous
tissue if become chronic. Or may be spread the pus into blood
vessels with bacteria cause pyemia or small abscess in skin called
boil or furuncles or wide abscessation in skin (carbuncles) giving
discharge at several points. *phlegmonous inflammation (cellulitis)
diffuse abscessation spread through subcutaneous tissue.
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Aljeboori 27 5- Catarrhal inflammation: superficial inflammation of
mucous membrane it is commonly in infection of upper respiratory
tract and intestine (in case food poisoning, parasitic infection).
6- Necrotizing or pseudo membranous inflammation: occur by powerful
necrotizing agent such as diphtheria, irritant gasses, bacillary
dysentery in which the necrotic pseudodiphtheric membrane occur in
intestinal mucosa. 7- Allergic inflammation: in which eosinophils
and much fluid and necrosis such as arthus reaction occur by when
antigen injected into skin of previously sensitized individual to
the same antigen or microbial agent. Prognosis or results of acute
inflammation: 1- Resolution, or healing by fibrosis. 2- Spread and
generalization of inflammation. 3- Become chronic. B) Chronic
inflammation: May be the result of acute inflammation or may start
with low virulence organism early and divided into; 1- Chronic
nonspecific inflammation in which mixture of mononuclear cells seen
(lymphocytes, macrophage and plasma cells) is the predominant cells
type with fibroblasts. 2- Chronic specific inflammation in which
mixture of cells present(occur in T.B. or syphilis), the cells
include; 1) Lymphocytes. 2) Macrophages. 3) Plasma cells. 4)
Basophils (become mast cells). 5) Eosinophils (when parasitic or
allergic infection). *Macrophages or Histiocytes when fusion
together formed giant cells against foreign body, foreign body
giant cells or langhans giant cells against T.B (tubercle bacilli)
in which nuclei arranged at the periphery and centrally located
cytoplasm giving picture like horse shoe appearance. 6) Fibroblasts
is connective tissue cells proliferated gradually and replace the
inflammatory cellular reaction also enclosing the chronic state of
inflammation such as pus or tubercle granuloma.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 28 Granuloma: A variety of chronic specific infection in
a sort of mass consisting of mononuclear cells aggregation, giant
epithelipoid cells and outside fibrous tissue encapsulation with
the central caseous necrosis in advance stage granuloma divided
into either; 1- infective granuloma caused by (Immune granuloma)
Bacteria such as T.B, fungi. Spirochete. viruses, protozoa,
Helminths components egg, larvae. 2- Non infective granuloma due to
regional ileitis (Chrons disease) or sarcoidosis or foreign bodies.
Systemic effects of inflammation: Include clinical and pathological
changes. 1-Fever in response to pyrogens that act by prostaglandin.
2- Acute phase proteins. a) C-reactive protein (CRP). b)
Fibrinogen. c) Serum amyloid A protein (SAA) both CRP and SAA act
as opsonins around bacterial cells and fix complement.
3-Leukocytosis may reach into 40,000 IuL or even 100,000 IUL with
leukemoid like reaction such Leukocytosis may be due to
neutrophilia with bacterial Infection, lymphocytosis with viral
infection and eosinophilia with allergic or parasitic
manifestation. Certain infections such as typhoid fever, viruses,
rickettsia and protozoa associated with leucopenia. 4-other
manifestation of infection. Increase pulse and blood pressure
5-Disseminated intravascular coagulation and septic shock due to
too much microbial agent their lipopolysaccharides enhance tumor
necrosis factor and interleukin-1 both responsible for endothelial
damage and intra vascular coagulation C inhibition of natural
anticoagulant activity and shock resulted. Consequence of excessive
inflammation action: 1- Cancer example chronic uncreative colitis.
2- Atherosclerosis. 3- Ischemic heart disease 4- Some
neurodegenerative disease such as Alzheimer disease. End Of Lecture
5
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Aljeboori 29 Lecture 6 Prof.Dr.Khalil Hassan Zenad Aljeboori Tissue
repair, healing and regeneration Regeneration : complete
reinstitution of damage component of the affected tissue i.e.
tissue return to a normal state ,the most specialized tissue such
as neurons of central nervous system and myocardium not
regenerated, whereas ,liver , connective tissue surface epith of
skin regenerate easily. Physiological regeneration that occurs in
RBCS and skin surface epithelia. Repair : restoration of tissue
structure and function after injury this occur by regeneration
andor healing which proliferation of various cells and close
intercellular spaces by matrix Healing: a reparative process in
which laying down connective tissue (fibrous tissue) that result in
scar tissue formation this occur when: 1- Injured area are in
capable for complete regeneration(wound is much wide). 2- The
supporting structures are severely damaged. Healing of cutaneous
wound can occur by first intention and second intention. A)Healing
by first intention : In which healing of a clean uninfected
surgical wound focal disruption of epithelial basement membrane
continuity and death of few cells (epithelia) and fibroblasts.
Epithelial regeneration predominates over fibrosis from edges, a
small scar is formed and mild wound contraction, such type of wound
healing united within 2 weeks and dense scar tissue laid down
within 1 month. Stages of wound healing by first intention 1-
Fibrin clotted blood fill narrow wound incision. 2- Within 24 hrs.
Neutrophils migrate to word the fibrin clot. 3- Within 24-48 hrs.
epithelial migration from edges along the dermis. 4- By day 3
neutrophils replaced by macrophages and granulation tissue invade
the incision space granulation tissue composed of new capillaries
and proliferated fibroblasts. 5- By 5th day neovascularization
reach its peak as granulation tissue fill the incisional space. 6-
During 2nd week collagen accumulation, fibrosis proliferation that
bridge the incision.
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Aljeboori 31 7- Processes of blanching begins accomplished by
collagen deposition and regress of vascular channels. 8- By the end
of first month the connective tissue scar devoid inflammatory
cells, covered by normal epidermis. B) Healing by second intention:
This occur when wound edges are widely separated, the gab cannot
bridged directly. Here is extensive loss of epithelia, sever wound
contamination and sub epithelial tissue damage so healing occur by
granulation tissue from the bottom to the surface of wound .the
larger defect is greater mass of scar tissue than healing by first
intention, such scarring result too much wound contraction, the
mode of healing in 2nd intention occur in large wound, abscess
ulcerations, and after infarction. Secondary healing differs from
primary by 1- Large clot enriched in fibrin and fibronectin form at
the surface of wound. 2- Inflammation more intense because more
tissue defects occurred. 3- Much larger amount of granulation
tissue result in greater scar formation. 4- Associated with wound
contraction. Factors affecting wound healing 1-Local: 1- Wound
sepsis. 2- Poor blood supply. 3- Wound tension. 4- Foreign bodies.
5- Previous irradiation. 6- Poor technique. 2-systemic: 1-
Nutritional deficiencies 2- Systemic diseases , D.M 3- Therapeutic
agents 4- Age. End Of Lecture 6
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Aljeboori 31 Lecture 7 Prof.Dr.Khalil Hassan Zenad Aljeboori
Cellular adaptation and disturbances of growth Adaptation: Are
reversible change in tissue either physiological like enlargement
of uterus or breast during pregnancy or due disease conditions. 1.
Hypertrophy: increase in size of cells resulted into increase in
the size of the whole organ maybe: A. Physiological: like
hypertrophy of skeletal muscle in athletes or workers, or uterus
during pregnancy. B. Pathological like cardiomegaly secondary to
hypertension. The adaption can progress to dysfunction if the
stress or cause is not relieved. 2. Atrophy: shrinkage of cell size
by loss of cell substance this opposite to hypertrophy, when more
cells involved lead to reduce the size of organ. Causes: A.
Decrease work load examples: immobilization of limbs. B.
Denervation as in poliomyelitis. C. Decrease blood supply. D.
inadequate nutrition. E. Loss of endocrine stimulation, example:
post-menopausal endometrial atrophy. 3. Hyperplasia: Increase in
the number of cells, randomly proliferation of cells under
different stimuli. A. Physiological hyperplasia proliferation of
glandular epithelial of breast during pregnancy and enlargement of
uterus during pregnancy. B. Compensatory hyperplasia occur when
part of tissue is removed, the other part of tissue proliferate to
restore the normal size of the organ like liver. Most of
pathological hyperplasia caused by excessive hormonal and growth
factor, example excessive estrogen stimulation lead to endometrial
hyperplasia and papilloma virus in skin cause squamous cells
hyperplasia, if the cause hormone or growth factor or virus are
subsided the hyperplasia disappear if the cause not subsided and
continued the hyperplasia develop into cancer .
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Aljeboori 32 4. Metaplasia: Reversible change in which the mature
adult cell (epith or mesenchymal cell) replaced by another relative
cell type, example: ciliated columnar epithelium of trachea,
bronchi replaced squamous epithelium in smoking. The metaplastic
epithelium still survive the protective mechanism such as cilia and
mucus production. Also if the cause example smoking is persisting
the metaplasia predispose into malignant transformation such
squamous cell carcinoma in bronchi in heavy smokers, also in
urinary bladder in schistosomiasis squamous metaplasia occur,if
persists may develop to cancer. Closely related topic to metaplasia
is the process of dysplasia which is the definite step in cancer
evolution. Dysplasia: A disordered growth in mucus membrane like
cervix, does not progress to cancer, dysplastic cells showed
pleomorphic, hyperchromatic and show abundant mitotic figure, mild
or moderate dysplasia is reversible but diffuse dysplasia become
cancer. Anaplasia: Loss of normal cellular differentiation or
organization i.e. cells become primitive, embryonic and
undifferentiated type, this important feature of tumor cell.
Anaplasia = Malignant Neoplasia = tumor End Of Lecture 7
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Aljeboori 33 Lecture 8 Prof.Dr.Khalil Hassan Zenad Aljeboori The
Infectious Disease I Commensals: microorganism live on expense of
the host without harm like: a- Bacteria of skin b- VIT K producing
bacteria. Pathogens: microorganism that injure the host, cause
disease. Pathogenicity: ability of microbe to cause disease.
Virulence: degree of Pathogenicity. Opportunistic infection :
microbe live in the body, but cause disease and become pathogenic
when depressed immunity in aids or microbe present in abnormal site
in body like E .coli normal flora in intestine but become
pathogenic when introduced in urinary tract other example
streptococcus viridians in mouth during tooth extraction may reach
valves of heart and cause endocarditis . Infection : Presence of
microbe in a part of body (normally absent). The microbe multiply,
stimulate the host response and cause the disease. Defenses
mechanism : 1- Nonspecific defense mechanism a- Mechanical barriers
example skin, mucosal layer of respiratory and GIT mucosa,
conjunctive. b- Glandular secretion : Acidity of sweat, gastric
acid, lysozyme enzymes secreted by mucous membrane, secretory IgA
(antiseptic paint). c- Secretions currents Continuous secretions of
tears, ciliated epith. Of respiratory system, obstruction of urine
flow, lacrimal gland, saliva .etc. d- Phagocytosis by neutrophils
and macrophages both migrate to microbial agent and ingulf it.
*inflammation and complement system are nonspecific defense.
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Aljeboori 34 2- Specific defense mechanism: Immunity: a- Humoral
immunity in which production of antibodies against microbial agents
when extracellular appearance in body tissue. b- Cell mediated
immunity:In which production of Lymphokines, Monokines, chemokines
against intracellular microbial agent such as T.B, viral infected
cell and cancer cell. How infections agents cause disease 1-
Microbe can contact or enter the host cell like T.B , cause cell
damage 2- Pathogens can release a- Endotoxins by Gram negative
bacteria or exotoxin by Gram positive bacteria that kill the host
cells. b- Release enzymes that cause tissue damage. c- Damage of
tissue by ischemia. 3- Pathogens induce cell response that mediated
tissue damage by immune mediated mechanisms. Mechanism of virus
damage to cells 1- Inhibit the host cell DNA ,RNA or proteins
synthesis like polio virus 2- Virus proteins inserted in host cells
and cause damage the cell or promote cell fusion like in measles ,
HIV ,herpes virus 3- Virus replicate in cells cause cell lysis like
polio virus. 4- Virus protein on the surface of host cells enhance
immune response against virus infected cell, cause liver failure
such as in hepatitis virus. 5- Virus damage defense mechanism lead
to secondary infections by bacteria (Strept. Pneumoniae) like in
influenza virus. 6- Virus kill one type of cells and cause damage
to other cells poliovirus lead to muscular atrophy. 7- Virus cause
cell proliferation transformation lead to cancer hepatitis virus,
EB virus. Mechanism of bacterial injury, and damage to tissue 1-
Adhere and enter the cells cause lysis such as T.B 2- Release
endotoxin polysaccharide produced by Gram negative bacteria
include; a- Include fever. b- Septic shock c- Respiratory distress
syndrome. 3- Release of exotoxin protein induced by Gram positive
bacteria such as; a- Diphtheria toxin by coryn. diphtheria cause
heart failure and neural defects. b- Tetanospasmin by clostridium
tetani cause tetanus.
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Aljeboori 35 Immune evasion by microbes: Microbe escape HI and CMI
BY 1- Kept and residing in host cells. 2- Cleave antibodies such as
gonococcus cleave IgA. 3- Resist complement mediated lysis. 4-
Survive in phagocytic cells such as T.B 5- Varying or shedding
antigen, continuously each time specific Ag. 6- Cause immune
suppression. End Of Lecture 8
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Aljeboori 36 Lecture 9 Prof.Dr.Khalil Hassan Zenad Aljeboori The
Infectious Disease II Some human infectious diseases. Viral
diseases: Rhinoviruses and influenza viruses: Responsible for
common cold , both RNA viruses type A,B,C, both types caused
pandemic infection 1918, it contain both hemagglutinin and
neuraminidase mutation of these protein resulted in to escape of
virus from the antibodies (antigenic drift) Avian influenza (bird
flu) H5N1 cause massive outbreak in poultry and jump to human and
cause outbreak. An outbreak at 2009 in virus H1N1 an epidemic of a
new strain referred to as swine flu.The resulted mutation of (4)
strains of influenza virus A H1N1 an endemic in human and endemic
in birds and two endemic in pigs in both the rhinitis , sinusitis ,
otitis media , Pharyngitis, tonsillitis , tracheitis , bronchitis ,
bronchiolitis , and secondary bacterial infection by strept.
Pneumonia. Herpes viruses infections Herpes virus DNA, HSV-1, HSV2
neurotropic virus , replicate in skin and mucous membranes at the
site of entrance of virus ( oropharynx or genitalia ) cause
vesicular lesions and infect neuron of the location . The virus
remain in nerve cells latent and reactivate and infect skin and
mucous membrane. Cells form multinucleated syncytia containing
inclusion of virus particles diagnostic in smear of the blisters
fluid .so the viral infection clinically show fever blisters (cold
sore). Intraepithelial vesicle (hydropic degeneration) of skin
around the lips, nose, burst, crust formation at the vesicles. The
forms of viral infection include; 1- Gingivostomatitis. Vesicles in
mouth, tongue, pharynx. (HSV-1). 2- Genital herpes vesicles seen at
genital mucosal layer and external genitalia, associated with
ulceration and rimmed by inflammation (HSV-1,2) neonates will
affected during delivery in neonates , splenomegaly liver lesion ,
lymphadenopathy, CNS lesion . 3- Herpetic eye infection: A-Herpes
epithelial keratitis lysis of corneal epith. B- Herpes stromal
keratitis due to immunological reaction to viral infection. 4-other
herpetic infections:Herpes encephalitis, Kaposi sarcoma, eczema
Herpeticum, herpes Esophagitis, Bronchopneumonia and
hepatitis.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 37 Bacterial infections: Hemophilus influenza : Gram
negative bacteria cause lower respiratory tract infection and
meningitis. So there is pharyngitis sinusitis, laryngitis, otitis
media. Bronchitis especially complicate viral respiratory tract
infection obstruction of air ways by fibrin rich exudate similar to
strept. Pneumonia infection. H. influenza also produce suppurative
meningitis in children. Tuberculosis : Mycobacterium tuberculosis
and M. bovis kill 3million patient each year M. tuberculosis
transmitted by inhalation mainly, M.bovis is transmitted by milk as
for M. avium and M.intracellurar cause infecting in aids patients.
M. leprae is the cause of leprosy. Pathogenesis of T.B. depend on
1- Virulence of bacteria. 2- Relationship of hypersensitivity to
immunity. 3- Infection degree. So T.B give no toxins ,no endotoxin
and no histolytic enzymes but enter macrophages and cause delayed
type of hypersensitivity in which macrophages secrete TNF- which
cause tissue damage and fever. DTH reaction cause destruction of
tissue initially nonspecific reaction by mononuclear cells
(lymphocytes macrophages . plasma cells )and few neutrophils then
by 2-3 weeks developed in to granuloma with caseous necrosis at the
center forming typical tubercle .the host response depend on either
the primary infection (first exposure to T.B or 2nd exposure
(previous infection ) the role of interferon gamma (INF-) secreted
by sensitized lymphocytes (CD4+ ), and activate the macrophages for
phagocytic activity to kill T.B and cause tissue damage . Primary
T.B When inhaled T.B in to the lung phagocytosis by alveolar
macrophages the T.B still multiply and lyse macrophages and enter
new cells which transport T.B to hilar lymph node during few weeks,
the granuloma developed with central necrosis . this under effect
of (INF-) released by CD4+ cells and granuloma developed under
effect of (INF-) and TNF- which cause activation of macrophages
,and later on tissue damage .(caseation) followed by calcification
in lung and hilar lymph node termed Ghon complex. Secondary and
disseminated T.B this occur when reinfection or reactivation of
dormant bacilli from primary infection when too much virulence of
bacilli or patient susceptible to infection (low immunity ) also
disseminated T.B in blood circulation , lymphatic and cause
caseation and granuloma in kindly lungs , meninges, bone marrow and
other organs. The caseation may followed by cavitation and T.B
reach blood circulation and cause military T.B in various
organs.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 38 Leprosy (Hansen disease) Caused by M. leprae infect
skin and peripheral nerve it transmitted through inhalation taken
by alveolar macrophage, through blood reach skin and peripheral
organs. Pathological features : 1- Tuberculosis leprosy when high
cellular immunity tuberculuid leprosy and epithelioid granuloma in
skin localized flat red in colour with induration ,depressed center
, Nerve when affected lead to atrophy in skin and muscles when
trauma , this part were ulcerated ,contraction , microscopically,
epithelioid granuloma , giant cells. Lymphocytes (CD4, CD8)
aggregation. 2- Lepromatous leprosy Involve skin, nerves, eye,
testes, hand, feet no infection in vital organ brain. Because high
temp. More than in peripheral organs. The lesions began macules
papules or nodular lesion, coalesce of lesion give a lion facies
.in nerve lead to loss of sensation in feet, hand. Microscopically
Macrophages laden with bacilli (AFB) some time in liver, lymph
node, spleen. In advanced cases in testes cause destruction and
erythema nudosumvasculitis. Lepromin test like T.B by injection of
lepromin Ag M.leprae Pyogenic bacteria. Staph epidermidis : cause
opportunistic infection in catheterized patients, prosthetic valves
, drug addicts Staph aureus : Causes: boil, carbuncles in skin,
pharyngitis, pneumonia, endocarditis, food poisoning, infections of
burn, surgical wound infections, toxic shock syndrome. virulence
factors include 1- Protein surface protein help bacteria to attach
to tissue. 2- Lytic enzymes , proteases ,lipase. 3- Toxins include
hemolytic, leucocidin enterotoxin, hemolytic toxins, exfoliation
toxin associated with scaled skin syndrome. Toxic shock syndrome
toxin. Streptococcal infection : Associated with pharyngitis,
scarlet fever, erysipelas, impetigo (infection of superficial
epidermis) rheumatic fever, and glomerulonephritis. In mouth
strept. Viridanse endocarditis In mouth strept.Mutans dental caries
Strep. Faecalis (enterococcus faecalis) UTI and endocarditis Strep.
Agalactiae UTI, neonatal sepsis, meningitis.
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Aljeboori 39 Virulence: 1- M protein prevent phagocytosis 2- C5a
peptidase (degrade C5a ) 3- Surface molecules (protein ) to attach
to host extracellular matrix 4- Polysaccharides inhibit
phagocytosis 5- Pneumolysin activate classical pathway lysis target
cells 6- Pyogenic exotoxin cause fever rash 7- Metabolism of
sucrose in to lactic acid by Strept.Mutans cause demineralization
of tooth, plaque, caries formation. 8- Anti strept M protein
antibodies cause cross react with cardiac myosin lead to rheumatic
fever. Gastrointestinal infection : occurred when host defenses
were weakened 1- Low gastric acidity. 2- Antibiotic. 3- Decrease
peristalsis movement. 4- Mechanical obstruction. Enteropathogenic
bacteria cause disease by: 1- Production of enterotoxins it cause
food poisoning e.g. S. typhimurium. 2- Exotoxin by E.coli , vibrio
cholera cause intestinal damage , secrete too much water. 3-
Invasion of mucosal layer by shigella, dysentria , salmonella cause
hemorrhage ,ulceration. 4- S. typhi cause damage mucosal layer to
peyer, s patches and to blood stream causing enteric fever. Normal
defense in GIT: 1- Acidic ph. gastric juice. 2- Mucus layer
covering the gut epith. 3- Pancreatic and bile salts lyse microbial
agents. 4- IgA (Anti septic paint) and M cells modified epith.
Cover mucosal associate lymphoid tissue take the pathogen to MAIT
area to destroy bacteria. 5- Bacterial flora inhibit pathogens
establishment. Helicobacter pylori : Causes: 1) Chronic superficial
gastritis. 2) Chronic atrophic gastritis. 3) Carcinoma of the
stomach, and sometimes lymphoma when reactive, invasion of B and T
cells clones.
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University/Dentistry/Pathology /Prof.Dr. Khalil Hassan Zenad
Aljeboori 41 Clostridial infection : Anaerobic bacteria produce the
following disease: 1) Anaerobic cellulites and gas gangrene by Cl.
per fringes (welchii) 2)Tetanus by Cl. tetani all these infection
occurred by contaminated wound, the toxins of these bacteria
(neurotoxin) potent toxin cause skeletal muscle contraction. 3)
Botulism caused by Cl. botulinum in contaminated canned food, also
neurotoxin released and block acetylcholine release so paralysis of
muscles fibers occur. 4) Pseudo membranous colitis by Cl. difficile
also release multiple toxins. Syphilis: Caused by Treponema
pallidum detected by: 1- Silver stain. 2- Dark filed examination.
3- Immunofluorescence. The infection occur in 3 stages: 1) Primary
stage: occur within 3 weeks, the infection in the form of firm
non-tender red raised lesion (chancre), located in external
genitalia composed of plasma cells, macrophages infiltrate, with
obliterative endarteritis. 2) Secondary stage: occur within 2-10
weeks as a diffuse rash in palms and soles, with white oral lesion,
fever, arthritis, and lymphadenopathy. 3) Tertiary stage : occur
later on in years after the primary the inflammatory lesions in
aorta, heart, CNS, liver, bone, skin, called gummas composed of
granuloma with central necrosis surrounded by macrophage palisading
with fibroblasts and outer plasma cells. Genital syphilis : The
Treponema transmitted from infected mother to placenta and cause:
1) Late abortion. 2) Still birth. 3) Death of newborn. 4) Persist a
latent in child life. Gonorrhea: caused by Neisseria gonorrhoeae,
gram negative diplococcus their pathogenesis occur when bacteria
invade epithelial cells and facultative intracellular bacteria
depends on host cell actins filaments, their capsule inhibit
phagocytosis, secrete protease cleave IgA and release endotoxin
which give TNF- cause shock and multisystem failure.the infection
by this microbe begin purulent exudates, granulation tissue
formation, fibrosis in urethra with mucopurulent exudates and
spread to epididymis, prostate, seminal vesicles and in chronic
cases sterility occur.
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Aljeboori 41 Chlamydial infection : Obligate intracellular
organisms in 2 forms either elementary bodies or reticulate bodies
both cause: 1-Lymphogranuloma venereum with epidermal vesicles on
the genitalia then ulcerate and oozes fluid, the ulcer base,
granuloma formation with stellate abscesses in the center of
granuloma. 2-Inclusion conjunctivitis: in infants from mother with
cervical infection caused by C.trachomatis. 3-Reiter syndrome: a
combination of conjunctivitis, genital infection and polyarthritis.
4-Trachoma: kerato conjunctivitis cause blindness in poor societies
and transmitted by hand contacts, flies. 5-Ornithosis: pneumonia by
C. psittaci secreted from infected birds inhaled with dust
particles. Diagnosis; by fluorescent antibody reaction, culture on
cell culture and by PCR. Parasitic infection : Schistosomiasis,
bilharziasis : Caused S. mansoni, S. hematobium and S. japonicum.
Larvae penetrate skin, migrate by B. circulate to traverse the
lung, reaching pelvic or portal vein. In pelvis develop into adult
with egg production and granuloma develop around the egg in pelvis,
bladder. Some eggs from portal vein to intestine wall depend on
type of parasite with granuloma. (S.mansoni) in pelvis. Granuloma
develop into carcinoma when in bladder occurred.(S.hematobium),egg
in stool or urine. S.mansoni in liver when present in portal vein
cause : 1- Hepatotoxic effect by egg toxin 2- Granuloma in liver
mediated by TNF, H1, H2, cells. 3- TH2 secret IL, 3, 4stimulate
mast cells level. 4- TH2 secrete IL5 important for eosinophils and
give basic protein kill the larvae. 5- Egg stimulate the lymphocyte
to give fibroblasts growth factor to form fibrosis in portal area
or in other site. Complication of schistosomiasis include :
1-granuloma in liver, gut, pelvis, in the center ova present,
portal fibrosis pipe stem fibrosis. 2-granulomatous pulmonary
arteritis, and 3-glomerulonephritis due to Ag- Ab complexes
deposition. *S.hematobium in urinary bladder cause hematuria,
calcified granuloma, later on develop to carcinoma (transitional
cell carcinoma) or (squamous cell carcinoma).
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Aljeboori 42 Hydatid cyst : Caused by Echinococcus granulosus and
sometime Echinococcus multicularis. The hexacanth embryo (larvae)
hatch in intestine of intermediate host (taken contaminated food
with egg). The larvae migrate to liver mainly and to the lung and
other organs cause hydatid cyst enlarged gradually and cause space
equipying lesion. The wall of cyst composed of germinal layer with
protosolices surrounded by laminated hyalinized layer and fibrous
capsule outside infiltrated with mononuclear cells, giant cells and
eosinophils. Trichomoniasis : Sexually transmitted disease,
protozoa flagellated, cause superficial infection in genital tract
of male and female with watery fluid in vagina and itching,
urethritis with mononuclear cells and neutrophils infiltration.
MYCOTIC INFECTION : Aspergillosis: Associated with allergic
lesions, sinusitis, pneumonia, the fungus appear branching
filaments hyphae and budding spores. The fungus surface had 1)
sialic acid to bind with protein matrix laminin, fibronectin. 2)
Produce aflatoxins (carcinogenic). 3) had restriction and
mitogillin both ribotoxin inhibit protein synthesis. 4) Allergic
reaction through IgE mediated hypersensitivity, allergic alveolitis
and bronchopneumonia with asthma mediated by mitogillin. 5)
aspergilloma colonization of the pre-existing cavity caused by T.B
,bronchiectasia. 6) Massive aspergillosis in immunodeficient
individuals with infection of all organs. Candidiasis: associated
with superficial infection of oral cavity (thrush), valvovaginitis
or systemic infection associated with Bronchopulmonary disease and
esophagitis. Candidiasis caused by candida albicans.
Sporotrichosis: caused by sporotrichiumschenkii ulceration with
abscess formation in skin and subcutaneous tissue. Disease of
trichophytonrubrum include Tineacorporis (Ring worm) tineapedis (
Athlet's foot). Disease include histoplasmosis, Histoplasma
capsulatum and coccidiodomycosis (Coccidiodesimmitis)
cryptococcusis (Cryptococcus neoformans) both associated with
pneumonia and meningitis. End Of Lecture 9
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Aljeboori 43 Lecture 10 Prof.Dr.Khalil Hassan Zenad Aljeboori
Disturbances of body fluids and electrolytes I Fluid present in
extra cellular and in intra cellular compartment the extra cellular
compartment divided in to intra vascular (plasma) and in
interstitial tissue. Extra cellular fluid: Chemical composition are
similar for the extra cellular fluid mainly sodium, chloride,
bicarbonates and low concentration of potassium, magnesium,
calcium, phosphate, and sulphate ions together with few protein,
glucose and urea. Blood plasma contain large amount of protein
comparable to low amount in intracellular fluid. Intracellular
fluid: Contain high concentration of potassium and low
concentration of sodium and chloride, also it contain more
phosphates, sulphate, magnesium, and protein and less bicarbonates
than in extracellular fluid. Extracellular fluid Intracellular
fluid More Less Na Na Bicarbonates Bicarbonates Chloride Chloride
Less More Mg++, k+, Ca++ k, PO4, SO4 PO4 +++ , SO4 ++ . Protein
Protein, glucose, urea Mg Fluid and electrolyte balance: In healthy
individual there is balance between the amounts of water taken in
to the body and that eliminated as well as normal distribution and
balance of body fluid and their electrolytes. The water intake by
food and drinking and leave body from kidney, skin, lung, glandular
secretion A constant exchange between fluid compartments keep the
water in dynamic state, depending on electrolytes and protein
concentration (active osmotic particles) in fluid compartment.
While exchange of substances between the plasma and interstitial
fluid occurred by filtration and diffusion across the capillary
endothelia, whereas water passes freely
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Aljeboori 44 between the intra and extra cellular compartment in
accordance with osmotic pressure relationship whereas, electrolytes
do not cross the cell members. Kidney: considered important factor
regulate water and electrolytes balance. Both conserve or excrete
from kidney in maintaining normal volume, concentration, PH of body
fluid this regulation in kidney occur by antidiuretic hormone (ADH)
and adrenal cortical hormone. Dehydration : Disturbances in water
balance in which output exceed the intake causing water below the
normal level. As in disorder in swallowing, comatose patients.
Mental patient, sweating that is in primary dehydration. Second
dehydration cause by loss of sodium, and electrolytes from body
during, vomiting, diarrhea, urinary loss of Na+ in Addison disease,
chronic renal disease or by both from of dehydration (primary and
secondary). Electrolytes disturbances: The role of electrolytes in
the maintaining of osmotic pressure and preservation of acid base
balance and normal neuromuscular irritability. Electrolytes also
had a role in balance and distribution of body fluid among these
electrolyte: Sodium: is extra cellular fluid important for
extracellular fluid osmotic equilibrium, it origin from food and
water and salts. Urinary output of sodium equal to the intake. The
retention of sodium and water resulted in edema, this occur in
congestive heart failure, hepatic cirrhosis and in nephrotic
syndrome. Decrease sodium level in plasma hyponatremia: occur when
retention of water more than sodium retention, so there is muscle
twitching nausea, fatigability. Hypernatremia: occur when
dehydration, diabetic coma, in which output of water in excess of
sodium or sever restriction of water (in dehydration) also occur in
case of aldosteronism. Potassium: main intracellular, important for
cell metabolism and conduction of nerve impulses and for
contraction of cardiac and skeletal muscles, help equilibrium
between cells water and extracellular fluid. Hypokalemia occur when
less K+ taken in starvation or excess loss in vomiting, diarrhea,
surgical trauma, administration of adrenocortical hormone and
adrenocortical activity. Pathological effects of K+ decrease in
heart (foci of hyaline change) on myocardium, vacuolization of
proximal convoluted tubules (PCT) in kidney and muscle
paralysis.
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Aljeboori 45 Hyperkalemia K+ increase rarely occur, because kidney
excrete K+ when in high level. Chloride: follow the change of
sodium concentration in plasma. Magnesium: intracellular concerned
with carbohydrate and protein metabolism and neuromuscular
conduction. Hypomagnesemia mg++ decrease occur in starvation,
alcoholic, diuresis and associated with muscular twitching, coma
and convulsion. Hypermagnesemia when mg++ increase occur in sever
dehydration. Diabetic acidosis so there is coma, lethargy and
respiratory failure. Disturbances of circulation (blood flow)
Edema: excessive accumulation of fluid in tissue spaces such as in
pleura termed hydrothorax, in periton (ascites) in pericardial sac
(hydro pericardium). Anasarca is a generalized subcutaneous edema.
Edema non inflammatory = transudate Inflammatory edema= exudate
Causes of edema (transudate): 1- Increase hydrostatic pressure
either localized or generalized (systemic) Localized increase in
vascular pressure can result from impaired venous return example
lower extremity, deep venous thrombosis can result in edema
restricted to distal portion of the affected leg. Generalized
increased venous pressure with resulted systemic edema occur in
congestive failure with involvement of right ventricular cardiac
function together with reduced renal perfusion resulted in renal
fluid retention and edema with increase venous pressure heart. 2-
Reduced plasma osmotic pressure: This occurred when loss of albumin
and plasma protein form circulation in case of nephrotic syndrome
so decrease colloidal osmotic pressure which mainly depend on
albumin also decrease albumin synthesis in liver disease (cirrhosis
) and malnutrition (poor protein) , in all these cases (reduced
osmotic pressure) lead to movement of fluid in to interstitial
spaces accompanied by renal hypo perfusion together with trigger
the renin-angiotensin aldosterone axis induced to much water and
salt retention by secondary aldosteronism similar in heart failure
.
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Aljeboori 46 3- Lymphatic obstruction: Impaired lymphatic drainage
result in localized edema like elephantiasis (caused by
wucheriabancrofti-their filarial close the lymphatic system of
lower limbs and genitalia resulted in edema (lymphedema) . cancer
of breast cause loss of lymphatic drainage so upper limb edema
similarly in breast carcinoma obstruction of the superficial
lymphatics cause edema of overlying skin (lymphedema). 4- Sodium
and water retention. Increase of salts with water obligate cause
increase hydrostatic pressure due to expansion of intravascular
volume with reduced vascular osmotic pressure. Salt retention occur
with impairment renal function such as in post streptococcal
glomerulonephritis and acute renal failure. Pathological features
of edema: 1) Subcutaneous edema: This can be diffuse in regions
with high hydrostatic pressure such as 1-In gravity termed
dependent edema with gravity. Distribution involving the leg when
standing for long time, sacrum when recumbancy, dependent edema is
a feature of cardiac failure of right side. 2-Edema due to renal
dysfunction or nephrotic syndrome, affect all parts in body equally
it is more sever than cardiac edema, all organs affected such as in
eyelid periorbital edema. In any part of body finger pressure leave
finger shaped depression so called pitting edema. 2) Pulmonary
edema : Occur with the following: 1- Left ventricular failure. 2-
Renal failure. 3- Acute respiratory distress syndrome. 4- Pulmonary
infection. 5- Hypersensitivity reaction. Gross lung, heavy, frothy
fluid blood tinged. Microscopically alveolar spaces fluid with
fluid (pale pink), congestion of alveolar capillaries. 3) Brain
edema: Localized with infarction, abscesses, tumor Generalized in
encephalitis or with obstruction of brain venous out flow, trauma
cause localized or generalized depend on extent of injury brain
appear swollen, flattened gyri.
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Aljeboori 47 Clinical significance of edema Subcutaneous edema
indicate renal and cardiac failure it is harmful effect. Pulmonary
edema: death due to abnormal respiration function. Brain edema:
fatal rapidly. Hyperemia and congestion: Local increased volume of
blood in particular tissue. Hyperemia: is active process resulted
from augmented blood flow due to arterial dilation example in
skeletal muscle during Practice or flushing Physiological hyperemia
in which affected part more red because engorgement of arterial
oxygenated blood, also with acute inflammation . Congestion:
passive process resulted from low venous return out of tissue it
may occur systemically as in cardiac failure or locally resulted
from local venous obstruction. The affected organ blue red colour
(cyanosis) due to deoxygenated blood in affected tissue. Congestion
of capillary closely related to edema so both occur together long
standing congestion called chronic passive congestion which due to
deoxygenated blood cause hypoxia and degeneration and death of
parenchymal cells. Subsequent fibrosis capillary rupture at this
site cause lysis of RBCS and hemosiderin engulfing by macrophages
(hemosiderin laden macrophages). Grossly- cut section oozing blood,
red of affected site. Microscopically: In acute pulmonary edema
congestion of alveolar capillaries with alveolar edema and
hemorrhage In chronic cases septae, alveolar wall thickened,
fibrotic and alveolar spaces filled with hemosiderin laden
macrophages (heart failure cells) with edema. C.V.C in lung termed
brown induration. In liver : In acute congestion: central vein and
sinusoids distended with blood. With degeneration of central
hepatocytes the peripheral hepatocytes better oxygenated because
still receive oxygenated blood from arterioles. In chronic venous
congestion (CVC) : Grossly: liver enlarged oozing blood in cut
section, the central region of liver red, congested, the
surrounding region in hepatic lobule uncongested, tan, sometime
fatty liver (nutmeg liver).
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Aljeboori 48 Microscopically: Center lobular necrosis, hemorrhage,
hemosiderin laden macrophages and hepatic fibrosis with long
standing heart failure. Causes of CVC: 1) Cardiac valves defect. 2)
Cirrhosis. 3) Obstruction of large blood vessel. 4) Age. 5)
Pregnancy. Hemorrhage: Extravasation of blood from vessels into
extravascular space. Capillary bleeding and hemorrhagic diathesis
occur in chronic congestion and wide variety of clinical disorders
both two cases hemorrhage by diapedesis. Hemorrhage by rhexis when
damage of artery by trauma, atherosclerosis, aneurysmal dilation,
inflammatory or neoplastic- erosion of vessel wall. Types of
hemorrhage: 1- Petechial H. with 1-2 mm pin point, in skin, mucosal
surface, serosa occur with: 1. Increase intravascular pressure
locally. 2. Low platelets count (thrombocytopenia). 3. Defect in
platelets function. 4. Clotting factor deficiency. 2- Purpura: H.
with 3-5mm width similar to petechial H. causes and with trauma,
vasculitis (infl. Of B.V). 3- Ecchymosis. H. with 1-2cm. wide area
of hemorrhage, associated with hemosiderosis. 4- Hematoma: wide
localized area of blood accumulation in body following trauma,
similar to ecchymosis lysis of red cells, hemosiderin in engulfed
macrophages appear. Large accumulation of blood in the thorax =
hemothrax, in pericardium= hemopericardium , in periton
=hemoperitoneum . End of Lecture 10
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Aljeboori 49 Lecture 11 Prof.Dr. Khalil Hassan Zenad Aljeboori
Disturbances of body fluids and electrolytes II Ischemia Decrease
of oxygenated blood flow in tissue due to contraction or
constriction of vessels (arterioles) due to: 1- Spasm of small
blood vessels. 2- Arterial wall defect (arteriosclerosis). 3-
External pressure on vessels (tumor, abscess,). 4- Blockage of
lumen by thrombus or emboli. Sudden ischemia cause coagulative
necrosis and infarction, and gangrene. Thrombosis: Coagulation of
blood within blood vessels during life. The pathological form of
hemostasis is thrombosis. Both hemostasis and thrombosis involve
three component. 1- Vascular wall. 2- Platelets. 3- Coagulation
cascade. Pathogenesis: 3 predisposing factor include: 1-
Endothelial injury. 2- Stasis or turbulence of blood flow. 3-Blood
hypercoagulability. 1- Endothelial injury: Endothelial loss can
lead to thrombosis during exposing of sub endothelial extracellular
matrix, adhesion of platelets. Release of tissue factor and local
depletion PGL2 and plasminogen activator. Similarly the
dysfunctional of pro coagulating factors platelets adhesion
molecules, tissue factor, plasminogen activator inhibitors or may
reduce anticoagulant effectors. Endothelial dysfunction occur in
through; 1- Hypertension. 2- Turbulent flow. 3- Bacterial
endotoxins. 4- Homocystinuria. 5- Hypercholesterolemia. 6-
Radiations. 7- Products absorbed from cigarette smoke.
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Aljeboori 51 2- Stasis and turbulence of blood flow : By both
mechanisms there is: 1- Disruption luminar flow and bring platelets
into contact with endothelia. 2- Prevent dilution of activating
clotting factor by fresh flow blood. 3- Retard the inflow of
clotting factor inhibitors and permit build up of thrombus. 4-
Promote endothelial cells activation resulting in local thrombosis
and leukocytes adhesions. Both mechanism (stasis and turbulence) of
blood flow occur in several clinical conditions: 1- Ulcerative
atherosclerotic plaque. 2- Aneurysm (local dilation) of aorta and
arteries. 3- Acute myocardial infarction. 4- Mitral valve stenosis
(after rheumatic heart disease). 5- Hyperviscosity syndrome,
(polycythemia). 6- Deformed red cells in sickle cell anemia. 3-
Hypercoagulability: (change in physical and chemical) component of
blood i.e. indicate alteration of coagulation pathway that
predispose to thrombosis primary (inherited) when mutation in
factor V gene and prothrombin gene. The pathogenesis of secondary
(acquired) hypercoagulability include: 1- Cardiac failure or trauma
associated with vascular injury. 2- Oral contraceptive and
pregnancy in which increase clotting factor by liver. 3-
Disseminated cancer. 4- Advance age. 5- Smoking and obesity.
Pathological features: 1- Thrombi can develop anywhere in
cardiovascular system in cardiac chamber, valves, arteries, veins
and in capillaries. 2- The size and shape of thrombi depend on site
or origin and the cause. Cardiac and arterial thrombi at the site
of endothelial injury whereas venous thrombi at site of flow
stasis. Thrombi in the heart valves may occur following bacterial
and fungal born infection cause valve damage and thrombus
formation, vegetation like in infective endocarditis, also
vegetation occur in non-infections state it develop in hyper
coagulable state (nonbacterial thrombotic endocarditis) .
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Aljeboori 51 Fate of thrombosis: 1. Propagation, additional
accumulation of fibrin and platelets cause vessel obstruction. 2.
Embolism when fragments of thrombus circulate in blood. 3.
Dissolution of thrombus by fibrinolytic activation which lead to
thrombus shrinkage and lysis of recent thrombi. 4. Organization and
canalization, organization of old thrombus by endothelia,
fibroblasts and smooth muscle proliferation. Occasionally instead
of organization the center of thrombus may under goes enzymatic
digestion by lysosomal enzymes of trapped leukocytes and platelets,
this recanalization convert the thrombus into vascularized mas of
connective tissue, these channels may not restore significant flow
to many obstructed vessels. Embolism An emboli is some a solid or
other foreign material carried in the circulation to a point
different from the origin. Emboli may be composed from portions of
thrombus, tumor cells, fat, air, masses of bacteria, mass of
parasites. Emboli that originated in the right side of heart or in
venous system it arrested in lungs if originated in portal vein it
arrested in liver whereas emboli originated at the left side of
heart and arteries it arrested in peripheral parts of arterial
system. Veins are easily penetrated by tumor cells so tumor emboli
arrested in liver and lungs. Forms of emboli: 1. Thrombo emboli: -
fragmental thrombi form 99% of emboli. 2. Fat emboli: - fat
droplets, injured fat tissue. 3. Air emboli: - bubbles of air
during surgery, pneumothorax. 4. Atherosclerotic emboli: -
(cholesterol emboli). 5. Tumor emboli-metastatic tumor cells. 6.
Foreign body emboli: - as bullets or shrapnel. 7. Bone marrow
emboli: - bits of bone marrow when bone fracture. Embolism from
thrombus this common type 99% of emboli, their effects depend on;
1. Emboli is septic or non-infected. 2. The size of embolus. 3. The
vessels in which become arrested. Pulmonary emboli which arrested
in lungs and originated in venous blood and right side of heart are
fatal whereas emboli that originated in cardiac chambers i.e. mural
endocardial thrombosis is a complication of cardiac
infarction.
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Aljeboori 52 Anticoagulant drugs, heparin and dicumarol are
important in management of thrombus or emboli. Septic emboli_ which
contain infective microorganisms causes pyogenic or abscess in new
arrested part in the body. Infected emboli from infected
endocarditis, valvitis spread infection to other parts of body,
infection of vein in appendicitis give septic emboli arrested in
liver, with multiple abscesses formation. Infarction or gangrene
may be originated from thrombus and emboli when cut oxygenated
blood supply occur in these areas in internal organs or
extremities. Infarction Localized area of ischemic necrosis in
living tissue or organ at an end artery area so triangular in shape
mostly. Infarction rarely occur in venous drainage area. Causes: 1.
99% of infarcts caused by thrombosis or emboli causing arterial
obstruction. 2. Expansion of atheromatous plaque by hemorrhage. 3.
Spasm of coronary artery. 4. Pressure on vessels from outside by
tumor, fibrous adhesion abscess. 5. Twisting (torsion) of the loop
of small intestine (volvulus), ovary testis, hernia in which
viscera protruded outside the cavity. 1-Red infarction: occur with
1. With venous occlusions such as in ovarian tumor. 2. In loose
tissue such as lung, intestine. 3. In tissue that had dual
circulation such as lung, small intestine rare in liver because
abundant circulation in liver. 4. In tissue with previous
congestion, slow flow 5. When flow is reestablished to a site of
previous arterial occlusion. 2-White infarction: occur with: 1.
Arterial occlusions or in solid organs heart, spleen, kidney. 2.
Infarct areas are wedge shape at the apex of end artery. 3. Infarct
area well defined by narrow rim of congestion with inflammatory
zone at the edge of lesion (line of demarcation), whereas line of
demarcation non- prominent in red infarct. 4. In solid organs few
extravasated RBCS lysis with releasing Hb in the form of
hemosiderin, thus infarct caused by arterial occlusion become pale
and depressed whereas in red infarct too much hemorrhage,
congestion and edema so infarct area still red protruded and in
with few days hemosiderin formed from lysis of RBCS to become red
brown and protruded. 5. Infarction in brain may be pale or
hemorrhagic, break of emboli give reopening of already closed
artery that pour blood into infarct area (pale infarction) and
become red due to this hemorrhage by reopened artery.
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Aljeboori 53 Microscopically: 1. Area of ischemic coagulative
necrosis except in brain may associated with liquefaction. 2.
Inflammatory zone around rim of infarction within 1-2days. 3.
Parenchymal regeneration begin at the periphery, all infarct area
replaced by scar (fibrous tissue formation). 3-Septic infarction:
when bacterial vegetation from heart cause emboli or microbe infect
the infarct area or infarction occur in already infected area.
Factors developing of infarcts: 1. Nature of blood supply 2. Rate
of development of the occlusion 3. Vulnerability to hypoxia. 4. The
oxygen content of blood. Clinical significance of infarction, 1.
Myocardial and brain infarct are fatal 2. Pulmonary infarction are
fatal 3. Bowel infarction are fatal 4. Ischemic necrosis of
extremities (gangrene) in D.M. Shock: Is the peripheral circulatory
deficiency due to decrease blood volume decrease cardiac output,
increase blood concentration, lowering blood pressure and
hyperkalemia. Categories of shock: 1. Cardiogenic shock this occur
in cardiac failure in the following: a) Myocardial infarction b)
Ventricular rupture c) Arrhythmia d) Cardiac tamponade e) Pulmonary
embolism 2. Hypovolemic shock: hemorrhage, injury. fluid loss,
vomiting, diarrhea. 3. Septic shock due to peripheral vasodilation
and pooling of blood, endothelium Damage, disseminated
intravascular coagulation in cases of; 1) Microbial infection,
diffuse. Endotoxic shock. Septicemia. Fungal sepsis. 2) Super
antigen toxic shock syndrome.
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Aljeboori 54 4. Neurogenic shock: Loss of vascular tone and
peripheral pooling of blood in the Anesthesia accidents. spinal
cord injury. 5. Anaphylactic shock: systemic vasodilation and
increase vascular permeability caused by IgE (type-1)
hypersensitivity reaction (anaphylaxis), so vasodilation of B.V and
pooling of blood in tissue result in tissue anoxia. Pathological
changes in shock: 1. Congestion of viscera and edema in tissue of
lungs are prominent findings. 2. Hyperemia and hemorrhage in
gastrointestinal mucosa, adrenal gland and in any part of body. 3.
Hyperemia and edema in the meninges are common. 4. Parcnethymatous
degeneration in kidney, liver, myocardium and the adrenal gland.
End Of Lecture 11
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Aljeboori 55 Lecture 12 Prof.Dr.Khalil Hassan Zenad Aljeboori
Immunopathology Body immune responses are normal defense mechanism
designed to protect the body from various environments factors, but
the diseases may result from: 1- Inadequate immune
response.(immunodeficiency). 2- Inappropriate immune
response.(autoimmune diseases ,Graft rejection). 3- Ex