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HISTOPHATHOLIC/CYTOLOGIC TECHNIQUESINTRODUCTION TO GENERALPATHOLOGYHISTOTECHNOLOGYIs the art and science performed by the histotechnologist to produce a tissue section of good quality that will enable the pathologist to diagnose the presence or absence of disease.Error in the laboratory is a serious...

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HISTOPHATHOLIC/CYTOLOGIC TECHNIQUES

INTRODUCTION TO GENERAL PATHOLOGY

 Structural changes in cells brought by the agent 4. CLINICAL SIGNIFICANCE/FUNCTIONAL CONSEQUENCES  Outcome or Endpoint at cellular level  Clinical Manifestations  Signs and Symptoms

HISTOTECHNOLOGY Is the art and science performed by the histotechnologist to produce a tissue section of good quality that will enable the pathologist to diagnose the presence or absence of disease. Error in the laboratory is a serious crime  Field of applied laboratory science  Deals with processing of specimen in anatomic pathology, provided by the doctor  Immediately to avoid deterioration of specimen  Raw material to quality slide to diagnosis to interpretation to treatment  Pathologist to perform microscopic examination and evaluation  Doctor for interpretation and possible intervention or treatment  Majority are cancer or suspected cancer patients PATHOLOGY/ PATHOBIOLOGY  Ancient Greek Pathos – Pain/Suffering/Disease Logos – Study of  Scientific study of Disease  Cause of illness or Etiology, how it develops, mechanism involved, effects or outcome RUDOLF VIRCHOW  Father of Modern and Cellular Pathology  Pioneered an assumption of pathological processes taking place in the course of disease through cell theory proposed by Theodore Schwann  Disease happen at cellular level, basic structural and functional unit of life because of it independent existence PATHOLOGIST  Expert in the field of pathology ASPECTS OF PATHOLOGY 1. ETIOLOGY  Causation or causative agent, reason why there is a disease 2. PATHOGENESIS  Mechanism or disease processes 3. MORPHOLOGIC CHANGES

HEALTH Is a state of complete physical, mental and social wellbeing and not merely the absence of disease or infirmity (WHO, 1948) DISEASE  Opposite of Health  Away from comfort (Dis and Ease)  Interchangeably with Infection but not the same brought by External Factors  Bacteria  Parasites  Fungi  Abnormal conditions that impairs body functions by Internal factors  Autoimmune disease – the body generates autoantibodies against the self (ex. Diabetes Mellitus, Rheumatoid Arthritis)  Hereditary disorders – transferred from one generation to another due to genetic make up  Congenital disease – poor development of the body part brought by certain drugs and chemicals

MANIFESTATION OF DISEASE  Syndrome – When both Signs and Symptoms happen 1.     2.  

SIGNS Objective Can be seen by the naked eye Measurable Ex. Jaundice, Fever SYMPTOMS Subjective Ex. Pain

HISTOLOGY  Is the branch of biology which studies the microscopic anatomy of biological tissues  Counterpart of gross anatomy TISSUE  Group of cells  Common point of embryonic origin 1.    

  

EPITHELIAL TISSUE Covers for external Lining for internal Highly cellular Avascular, without vessels

Ectoderm – Skin and Cornea Mesoderm – Reproductive system, hearth, kidney, lymphatic vessels Endoderm – Respiratory system, Digestive system except for mouth, anus. Pancreas, liver and gallbladder

BASED ON SHAPE OF CELL 1.   2.

Squamous Flat, scaly Ideal for protection Cuboidal

   3.  

Cube like structure Same height and width Secretion Columnar Length is 2x than the width Absorption BASED ON STRATIFICATION

1. 2.  3.   4.  

Simple Stratified Multi layered Pseudostratified False Variation of nuclei Transitional There is a change Stratified cuboidal and stratified columnar

2. MUSCLE TISSUE  From mesoderm except iris of the eye from ectoderm  Basic type of tissue that enables locomotion and transport of fluid and substances  High degree of contractility, ability to shorten  Myogenesis: Process of muscle formation, production during embryonic stage

1. Skeletal Tissue  Voluntary except pharynx and upper part of esophagus  Oval nucleus  Hundred nuclei per fiber  Nuclei are longitudinal oriented located at the peripheral portion  10 – 35 cm of fiber 2. Cardiac Tissue  Occurs in heart  Striated  Cylindrical but splits off to branches  1 – 2 nuclei 3. Smooth tissue  Slow and not forceful  Fisiform in shape

3.            

NERVOUS TISSUE Neural tissue Resembles epithelium From ectoderm/ gastrula Neurons – functional unit of nervous tissue Cell body, perikaryon, soma-containing the nucleus Dendrites determine the shape of cell, towards soma, shorter than axon Axon, away from soma, one per neuron Arborization, pulsing Irritability, reacts to stimuli Main tissue of nervous system that controls and regulates body function CNS, brain and spinal cord PNS, all other outside CNS

4.      

CONNECTIVE TISSUE From Mesoderm With high extracellular matrix Ground substance, composed of water Fiber Few and scattered cells Resident –Fibroblast, Fibrocyte, Adipose cells, Reticular cells  Wandering – Inflammatory cells  Special type of Connective Tissue  Cartilage  Bone  Blood  Connective tissue proper

 Associated with reversible change in size, number, appearance/phenotype, metabolic functions

1. Physiologic  Occurs to normal stressors 2. Pathologic  Abnormal stressors

ATROPHY/INVOLUTION/DIMINUTION         

A – Without Trophy – Nourishment Without nourishment Reduction in size and number of cells Small and Shrunk Cells are alive, just small in size Firmer consistence Prominent blood vessels Reduction in size because of reduction in organelles particularly mitochondria, myofilaments and ER  Increased autophagy vacuoles or organelle destroyers  Production of wear and tear pigment, lipofuscin, yellowish-brown pigment

PHYSIOLOGIC I. II.

CELLULAR ADAPTATION III.  Refers to changes made by a cell in response to adverse environmental changes

Atrophy of thymus. Atrophy of gonads after menopause. Atrophy of brain with aging (senile atrophy)

 If cells cannot adapt, they can die

PATHOLOGIC Vascular atrophy Pressure atrophy Starvation/ hunger atrophy Atrophy of disuse Endocrine atrophy

RETROGRESSIVE PROGRESSIVE DEGENERATIVE Abnormal growth patterns

Catabolism > Anabolism

Anabolism > Catabolism

Smaller than normal

Larger than normal

1. Atrophy 2. Developmenta l Defects

Hypertrophy

Metaplasia

Hyperplasia

Dysplasia

   

Hypoplasia Aplasia Agenesia Atresia

 Can make an entire organ collapse

PRESSURE ATROPHY

 

Anaplasia Neoplasia

 

 Tumor  Aneurysm – ballooning of structure or tissue  Causes persistent of constant pressure against other tissue  Leads to injury Erosion of spine by tumor in nerve root Erosion of skull by meningioma arising from pia-arachnoid Erosion of sternum by aneurysm of arch of aorta Vascular atrophy – Inhibit performance of blood vessels and vascular aspects affects the transport of nutrients and oxygen

STRAVATION/HUNGER ATROPHY  Wasting of tissue because of lack of nutritional supply necessary for normal growth  Marasmus – Caloric deficit and massive nutritional deficiency  Kwashiorkor/Edematous Malnutrition –Protein deficiency ATROPHY OF DISUSE    

Inactivity leading to dysfunction Immobilized Decreased workload = decreased size of muscle Atrophy of the pancreas in obstruction of pancreatic duct

ENDOCRINE ATROPHY  Reduced endocrine stimulation  Loss of endocrine regulatory mechanism results in reduced metabolic activity of tissues and hence atrophy • Hypopituitarism may lead to atrophy of thyroid, adrenal and gonads • Hypothyroidism may cause atrophy of the skin and its adnexal structures

 A reversible process thought to be caused by stem cell reprogramming.  Increases the cell survival than cellular protection  Related to malignancy or cancer 1. Epithelial  This is the more common type  The metaplastic change may be patchy or diffuse and usually results in replacement by stronger but less well specialized epithelium.  Occurs in epithelium, exposed in mechanical trauma, chronic irritation, prolonged inflammation  Ex. Chronic bronchitis, pseudostratified columnar, ciliated epithelium are changed into stratified, squamous cells brought smoking or pollution 2. Mesenchymal  Less often, there is transformation of one adult type of mesenchymal tissue to another  Undifferentiated and biological tissue  Occurs in connective tissues where fibroblast are transformed into osteoblast, fat cells and tissue macrophages. CELLULAR ADAPTATION  Independent existence which able to respond to injuries through changes for survival

RETROGRESSIVE CHANGES HYPERTHROPHY  Increased in size of cell = enlargement of tissue or organ without any change in number of cells  Response of a specific tissue or organ to increased demand to work  Enlarged and heavy  Increased DNA and RNA = Increased protein synthesis = Increased intracellular organelles like mitochondria  Affects muscles and non-dividing cells  Caused by increased functional demand or specific hormonal stimulation  Pathologic – Increased functional demand Ex. Systemic hypertension, increased size myocardial muscles weighing around 700-800 g compared to 350 g, enlargement of muscle fibers and nuclei  Psychologic – Enlargement of muscles among athletes and weightlifters along enlargement of reproductive organs METAPLASIA  Occurs when a differentiated cell of a certain type is a replaced by another cell type, which may be less differentiated.

HYPOPLASIA  Hypo – Under  Plasia – Plasis or Formation  Underdevelopment or incomplete development of a tissue or organ  Not opposite of Hyperplasia  Congenital condition  Enamel coating is thinner than normal, some chemical or structural units are missing but not absolute  Hypomineralization  Testes in klinefelter’s syndrome  Ovaries in Fanconi anemia, gonadal dysgenesis, trisomy X  Thymus in DiGeourge syndrome  Labia majora in popliteal pterygium syndrome  Cerebellum caused by mutation in Reelin gene  Tooth caused by oral pathology, such as Turner’s hypoplasia  Small bowel in coeliac disease.

APLASIA  More severe and extreme  Incomplete or defective development of tissue or organ  Usually affecting paired organs like kidneys, gonads and adrenal glands

2.     

Pathologic Stimulation of growth factors Excessive hormonal stimulation Hyperthyroidism – Increased Thyroid stimulating hormone Adrenal – Increased Adrenocorticotrophic hormone Parathyroid hyperplasia

AGENESIA/AGENESIS  Failure of an organ to develop during embryonic growth and development 1. Renal agenesis 2. Testicular agenesis 3. Ovarian agenesis 4. Lungs or Thyroid glands  Complete non-appearance of an organ  Has many causation but usually the exposure to toxic chemicals  Lethal or deadly  May also in limbs or extremities  Anencephaly (failure for the brain to develop)  Meromelia (failure of hand or feet to develop)  Phocomelia (failure of arms or legs develop)  Amelia (complete absence of limbs)  Penile agenesis (failure of penis to develop)  Mullerian agenesis (failure of the uterus or vagina to develop)

ATRESIA   1.  2.   3.

Failure of an organ to form an opening or closure Must be surgically corrected Anal atresia/Inperforate anus Malformation of intestinal tract Bile Duct atresia Accompanied by jaundice Unable to digest fatty foods Esophageal atresia

PROGRESSIVE CHANGES HYPERPLASIA   1. 

Increased tissue mass = increased cells Cells capable of mitosis or division Physiologic Increased local production of growth factor receptors on the responding cells activating transcription factors and leading to cell proliferation  Hormonal (e.g., breast and uterus during pregnancy)  Compensatory - regeneration of liver following partial hepatectomy, taking almost 20 years

DEGENERATIVE CHANGES DYSPLASIA      

Irregularity in size Loss or increased size of nucleus Presence of mitotic figures Disruption of normal architectural patterns Chronic irritation leading to atypical hyperplasia Reversible Tissues prone to dysplasia

1. 2. 3.

Cervical Respiratory epithelia Vicinity of cancerous cells ANAPLASIA/Dedifferentiation

 With disorganized features leading formation of primitive cell type  Towards malignancy  Extremely dysplastic and irreversible

INFLAMMATION ANTIGEN/IMMUNOGEN  Foreign substance  Responsible to the activation of B-cells to transform into plasma cells to generate antibodies  Antibody generator  An antigen may be a substance from the environment, such as chemicals, bacteria, viruses, or pollen  An antigen may also form inside the body.

ANTIBODIES/IMMUNOGLOBULIN  Proteins with immune function  Produced by the immune system in response to antigen.

 Inflammation occurs in living organisms only.

Five types 1. 2. 3. 4. 5.

IgG – Most dominant IgA IgM IgE IgD

INFLAMMATION IS A DYNAMIC PROCESS  Dynamic means changes  Interconnected events that undergoes evolution through several phases

HOST DEFENSE MECHANISM/LINES OF DEFENSE  Provides various ways to protect the body from various substance 1. General Defense Mechanism (First Line & Second Line Defense)  Non-specific host defense  Innate/Natural/Inborn  No immunological memory 2. Specific Defense Mechanism (Third Line of Defense)  Acquired  Adaptive  Through encounters of specific microorganisms INFLAMMATION  Inflammatory response  Latin words: Inflammatio, Inflammare - To set on fire (burning)  Non-specific but predictable response of living, vascularized tissues  Part of second line of dense

CARDINAL SIGNS OF INFLAMMATION By Aulus Celsus  1. 2. 3. 4.

Roman Physician Rubor (Redness) Dolor (Pain) Calor (Heat) Tumor (Swelling)

By Rudolf Virchow  Father of modern pathology 1. Functio laesa (Diminished functions)

Acute - Sudden onset - Short duration - Exudative inflammation

Subacute/Subchronic - Transitional phase Chronic - Extension of acute phase - Slow and gradual onset - Long duration

Increased granulocytes particularly neutrophil because of their high mobility When neutrophils die they form pus or exudate IgM is first to arise

Increased agranulocytes particularly monocyte and lymphocyte Induces proliferation Increases fibroblast that causes damage and scarring of the tissue IgG is dominant

TYPES OF INFLAMMATION ACCORDING TO CHARACTER OF EXUDDATE 1.   2.  3.   4.  5. 

Serous Inflammation for watery type of secretions. With low protein content Pulmonary type of tuberculosis Fibrinous inflammation associated with high fibrin or fibrinogen Diphtheria Catarrhal Inflammation for mucoidal type of secretions Hypersecretion of goblet cells In Respiratory tract or Digestive tract Hemorrhagic Inflammation for bloody type of secretions. Found in bacterial types of infection Suppurative (Purulent) Inflammation. Large amount of pus or dead WBC

ELEMENTS OF INFLAMMATION  Inflammation is a dynamic process.  Inflammation occurs in multicellular organisms.  Inflammation has a protective role.

INFLAMMATION OCCURS IN MULTICELLULAR ORGANISMS

 Coordinated reactions, involving nerves, blood vessels, hematologic cells, soluble chemical mediators, normally released by damaged tissues or cells 1. Plasma derived mediator  Inactive state (zymogen) requires activators. 2. Cell derived mediator  Stored in granules of WBS  (+) Acute phase reactants – substances that increases during the course of inflammation (Immunoglobulins, transferrin, C-reactive protein)  (-) Acute phase reactants – substances that decreases (albumin, other plasma type protein) not responsible in restoring the tissue INFLAMMATION HAS PROTECTIVE ROLE

Blood vessel constriction to conserve heat that continues until it matches the blood supply Fever is responsible for increased heart rate, metabolic rate, caloric demand, sever or mild form of dehydration 7. Pyrexia INFLAMMATION OCCURS IN LIVING TISSUES 1. Necrotic tissue are no longer functional, must be removed INFLAMMATION ACCORDING TO CAUSATION

 To neutralize microbial virulence factors  To get rid of the microorganisms and its possible consequences  To localize infection  To contain the microorganism in one area 1. Localized – confined to a specific region (carbuncles or folliculitis) 2. Systemic – affects various parts of body  Systemic Inflammatory Response Syndrome (SIRS) by septicemia

FEVER PHYSIOLOGY  36.2 – 37.5C  > 37.8 is considered as fever  Pyrogen stimulates fever reaction, originates outside (bacteria, toxins, virus and virulence factors) and inside (Interleukin 1/Endogenous pyrogen)  Non specific and 2nd line of defense  Increases WBC at the site of injury  Reduce available of iron needed by the microorganism to replicate  Interleukin 1 is needed for proliferation and maturation of WBC  Elevated temperature slows down the growth of microorganism

1. Patient with septicemia caused gram negative bacteria, gram negative sepsis or bacteremia that is characterized by fever, chills, exhaustion 2. The bacteria release endotoxin (part of cell wall, particularly the lipid component) into the bloodstream 3. Phagocytes ingest the endotoxin 4. The ingested endotoxin stimulated the phagocytes to produce IL-1 from macrophages 5. IL-1 stimulates the hypothalamus (body’s thermostat) to produce prostaglandins 6. Prostaglandins is metabolized, cause temp to go up

PATHOGENESIS OF INFLAMMATION

Systematic processes associated with disorder 1.    

Hemodynamic Changes Circulatory changes Vasomotor responses Hemo = Blood, Dynamic = Changes First response is changes in blood flow

1. Abraded tissues 2. Nerves are stimulated

3. Nerves transmit signals to arterioles 4. Vasocontraction mediated by endothelial factors to limit bleeding, lasts for several seconds 5. Vasodilation, increased blood flow or Hyperemia, allow the arterial blood to flood the capillary network Warm blood = Calor and Rubor To deploy WBC To supply nutrients and oxygen To dilute toxins to minimize damage 6. Blood is not actively regulated in the smaller vessels 7. Plasma filtration Not balanced 2. Vascular Changes 3. Cellular Changes

INFLAMMATION ACCORDING TO CAUSATION 1.  2. 

Endogenous Inside the body Exogenous Outside the body

CELLULAR CHANGES Extravasation Movement of leukocytes Through, Margination – Movement to endothelial lining Pigmenting – Allows WBS to layer Adhesion – Attachment of inflammatory cells Affected by adhesion molecules Diapedesis Clotting factor 12 – Hageman factor 1. 2. 3. 4.  

Activation of coagulation Fibrinolysis Kinin system Complement system Classical – Antibody dependent Alternative – Antibody independent Acts on cell wall permits permeability or leakage Acts on inflammatory cells

C3b – Opsonin, coats the bacteria for easy phagocytosis C4a – Anaphylatoxin C3a C5a – Chemotaxin that attracts WBC

Chemotaxis

LESSON 4; CELLULAR INJURY, CELL DEATH AND AUTOPSY CELLS  Basic unit that forms tissues and organs  Diseases occur at cellular level  Cells constantly react with the environment to maintain homeostasis

1. Cell digestion By lytic enzymes Change in cell aspect with intense eosinophilic cytoplasm It may show cytoplasmic vacuolization 2. Denaturing of protein Nuclear changes  Pyknosis – Condensation of nuclear chromatin  Karyolysis - Dissolution  Karyorrhexis – Fragmentation to many granular clumps  Depends on the type of causation, degree of severity and duration

CELLULAR INJURY  Consequent loss of cell function...