Introduction to Pathology S. Pongsabutra

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Pre Test (10 )

Introduction to PathologyBy

1. ! 1.1 .....? 1.2 Anatomy & Physiology ? ? 1.3 ..? ? ..? ? 1.4 ? ?

S. Pongsabutra2 5 June. 09

.... .... .... .....

Introduction to Pathology : (Clinico-Pathological Correlation ) 5. 1. 2. 3. 4.

[-] = (disease= dis+ease)=

1.

= = (

?)

()

, ? . ... ? ...

(AP)

(CP) excreta, *Autopsy Path. *Surgical Path. *Molecular Path. *Forensic Path. (Medicine). *Cytopathology & papsmear Examination ...etc

? ?? ? ?

()

() ( 1. Autopsy Pathology () ) . . ? ? 2.Surgical Pathology (biopsy) biopsy) 3. Cyto-Pathology Cyto 4.Molecular Pathology Gene Gene Gene ? Gene ?........... ...........

2.

() (Internal Homiostasis) 4

Basic Groups of Diseases

3. 3Formation of Tumor ; * Non Neoplastic tumor * Neoplastic tumor

1Congenital Disorders

2Reaction of self defense mechanism * inflammation * Immune disorders

( )

() ( )

Hereditary Disease

Congenital anomaly

* Genetics * Abnormal Growth & diseases Development eg. harelip, cleft palate etc.

4

Unclassified Diseases: * most 0f unclassified diseases usually are complex in nature such as metabolic ,degeneratives , neuropsychic diseases etc

1. Etiology = * ? !! 2. Pathogenesis

:

*Etiology* Pathogenesis *Pathological change= lesion * Clinical manifestation * Complication * Prognosis

?3. Pathological changes ? (= Lesion) 4. Clinical manifestation

(Pathophysiologic changes) 5.. Complication (secondary changes of the other related organs) ? 6. Prognosis ?

.... cell organelles Histological character . .Immunohistochemistry .. . ..... .........

Normal squamous cell vs abnormal squamous cell? Structure Normal mucosal small bowel vs abnormal mucosal small bowel ?(tissue) Normal organ liver vs abnormal organ liver? Function(Islets cells)

Normal blood sugar vs abnormal blood sugar? eg. Blood sugar between non diabetes and diabetes patients..etc..

Liver

Abnormal surface liver characterized by brownish yellow color and diffuse small nodular lesions size1-2 mm,

Liver

Abnormal cut surface liver characterized by multiple nodules (masses) varying in size, up to 1 cm. grey white color

Abnormal cut surface liver show diffuse small white masses, size vary from~ 1-3 mm.

Section shows cells characterized by abnormal shape, size and nuclei, together with loss of organ Architecture

Liver show alternated diffuse small dark lines and spots in background yellow brown color cut surface

Liver lobule shows dilated Central vein and sinusoidal spaces accompanied with necrosis of liver cell cords around central vein

Cut surface Liver shows diffuse dark green spots and focal darkgreen liquefaction areas 0.2-1 cm. in size

4.

Fact .: .. (S&S = clinical symptom and sign) ? (=) ? ? ? ? ( = )

Section shows 0rganism( fluke?) in the space which lining by glandular structure.

4.1 () (S&S)

19 1 3-5 ? PE. - 20 / . ( = ?) - 115 / . ? ( = ? ) - Apex beat

Basic Medical Science & Clinical sci.

* : Anatomy * : Physiology

*

Systemic Pathology & Clinical skill ( )

* Clinical skill , , , ?

* , ? ......

5th I.C.S;?

Mid Clavicular line?(?)

- Apex beat Diastolic Murmur 4 (?) Crepitation (), . ( ? )

:Relation between Anatomy, Physiology of C.V.S

() Related to (& ?)(PE.)

and

RS.

Normal Function of organs Normal structure 0f organs Heart & Lung Site, size & shape of heart (wall , chambers) Character of valves; location, leaflets and chordae tendinae; Characters of Lungs; Gross and micro. Consistency; Anatomic relation between the heart and lungs? .etc Heart & Lung -Heart :Function of chambers?;valves? . Circulation blood between heart and lung; rate and

: 17 ( OPD ) 1 : 3- 5 *

rhythm of Heart beat, sound character and site of blood flow through valves? - Lung; sound and rate of breath, ---etc

*20/ *115/ *Apex beat 5 ICS lateral to MCL with Diastolic murmur gr.4 and thrill on touching. * * crepitation

basic medical sciences Anatomy, Physiology, Systemic Pathology, Clinical skills (Physical examination)

4.2 clinic( symptom & sign )Clinico Pathological CorrelationAnatomic changes Functional changes

Anatomic changes Mitral Valve stenosisIncrease work load to heart caused

Functional changes Diastolic Murmur gr.4Lt.Ventricle contain blood Volume less than normal H.R. 115 / min = Compensate for normal blood Volume [1st.. Step]

Mitral Valve stenosis [ Leaflets characterized by sclerosis, fused together, result in narrow opening ]

Diastolic Murmur

gr.4 ?Lt. Ventricular Hypertrophy for increase blood Volume [2st.. Step]

Flow of blood through stenosed Mitral Valve during lt. Atrium systole and Lt.ventricle-Diastole, genesis murmur(diastolic murmur at Apex) and the same time volume blood through LV chamber is lessen than normal

Overload

Lt.ventricular failure = Lt. sided Heart failure=

(pulmonary edema) RT. Atrium chamber

RR. 20/min (=)

O2

Chronic Endocarditis of Mitral valve with marked stenosis and sclerosis. Acute pulmonary edema, marked *

4.3 symptom & sign -# ; X - rays, EKG, , Immunology Antibody. Group A Streptococci () ?. .........

Anatomical Diagnosis

= (Clinical Diagnosis ) Chronic Rheumatic Heart With Congestive Heart Failure Etiologic Diagnosis

4. 4 ; - 1. (group A streptococci) -2. (immunnological mediated inflammatory)

Lt. atrium Rt.atrium bicuspid valve Tricuspid valve) Lt. ventricle

, ?

Chordae tendinae

Interventricular septum

Normal Heart

Pathological changes: Heart valve

Mitral valve and chordae tendinae show sclerotic changes in chronic Rheumatic endocarditis

Mitral valves show fusion of the sclerotic leaflets with

marKed narrowing the Openning in Rheumatic heart dis.

left Ventricular hypertrophy

Abnormal Cardiac muscles Fibres,(larger than normal) with fine brown pigments in cytoplasm beside the nucleus

5.

1.1. 2. 3.

1. () 2. (Autopsy Examination and others specialty branches) 3. 4. 5. 6.

Interalveolar vessels show congestion and containing large amout of acidophilic homogeneous material with vacuoles in alveolar spaces

Clinical problems(sign& symptom)

Pathology is the key to open the secret 0f Diseases= STUDY ABNORMAL STATE OF BODY PARTICULAR IN MORPHOLOGICAL & FUNCTIONAL CHANGES OF ORGAN, TISSUE CELLS.

Basic medical sciences

Introduction to Pathology.

Post test

**. Introduction to Pathology ? . . ......?

2

Cell Pathology

Cell Pathology=

: * Review cell biology * cell adaptation * cell Injury ( degeneration & necrosis) * Somatic death

Cell Biology

Review cell biologyDefinition : ( (homeostasis) Function (Physiology ) Structure (Anatomy) * :

Ingestion & Egestion [excitation] * * *

Cell wall (membrane) Mitochondria Endoplasmic reticulum Nucleus

Basic Cell Structure Organelles

Cell wall (membrane) structure (Molecular level) Phospholipids Proteins, glycoprotein

(rER, sER) Endoplasmic Reticulum Nucleus Nuclear membrane

Products Mitochondria Cytoplasm Cell wall (Plasma membrane)

Function1. Barrier () 2. Molecules ions 3

Receptors Nuclear PoresCell = Smallest unit of life which having ability to be free living by interaction with the environment -Transmembrane Proteins bind Molecules molecules

Active transport- Na+, K+, Ca++ H+ ion - internal homeostasis molecules Na+ Pump

Diffusible- aminoacid, glucose Proteins

MitochondriaStructure- 1 9 - Cristae Cytoplasm

Endoplasmic reticulum rER FunctionStructure Function

- , (powerhouse of cell) ATP - generate Oxidative phospholylationphosphate glucose, fatty acid glucose fatty Acid ADP ATP, Mitochondria ATP Mitochondria Cytoplasm ATP ADP + ADP Mitochondria ATP

Ribosome Organelle rough Endoplasmic Reticulum rER

Enzymes Proteins Ribosomes ER Cytoplasm Aminoacids Proteins (Polypeptides) mRNA Amino acid Proteins cell

NucleusDefinitionStructure Function

Cell Pathology

cellNuceolus Nuclear wall Chromosomes Cytoplasm Nucleus Chromosomes 46 23 genebearer / chromatin Genetic material chromosomes / chromosomes DNA Histone / gene Function unit (Locus) Chromosome

(Gene)-

- Enzymes, Proteins -

(adaptation) (cell injury) (cell necrosis)

Cell adaptation

Types of cell Pathology 1. Cell adaptation 2. Cell injury ()Type of injury: Degeneration & Death)

maintain internal homeostasis ;

3. Somatic death (The whole cells of body )

* Atrophy decrease in size * Hypertrophy increase in size * Hyperplasia increase in cell number * Metaplasia = normal original Cell transformation to another type cell (adult cell) * Dysplasia = abnormal tissuesforming (= abnormal orientation, size and shape of cells)

Senile Atrophy Brain (brain change in old age)

Atrophy (adaptation of endometrium)

Hyperplasia (adaptation of endometrium)

Hypertrophy heart ( adaptation of heart muscle ) Squamous metaplasia (adaptation of endocervix mucosa)

Normal epidermis

Hyperplasia (adaptation of epidermis)

Cell Injury (Structural Damage and Functional Disorders)

Dysplasia (squamous epithelium of uterine cervix)

Type of cell InjuryReversible injuryDegeneration Structure changes Histologic picture Ultrastructure organellesFunctional changesDefect in chemical changes Cellular Accumulation eg.water, glycogen, fat, protiens, pigmentation

Injurious Agents: Extracellular Agents Physical agents eg. Heat, Cold, radiation, Trauma. Chemical agents eg. Organic & inorganic compounds, Toxins, enzymes. Hormonal disorders Intracellular Agents

Irreversible Injury=Necrosis (cell death) Structure changesNuclear changes Pyknosis karyorrhexis kariolysis Cytoplasmic changes

O2 deprivation Loss of intracellular Ca++ homeostasis Intracellular accumulation free radicals

Diagram 0f cell injury Cell membrane Mitochondria Loss of Essential Function More or Less depend on type And severity of Injurious agents Reversible or nonlethal injury Withdraw Causes Return to normal Irreversible or Lethal injury Cell death [necrosis] Endoplasmic reticulum Nucleus

Cell Biochemical defects Cell Oxygen ischemia ca++ homeostasis ---- - - --

Cells ischemia Mitochondria Biochemical changes Emergency pathway Cell Damage energy dependentloss Na+,Ca+Pump

Loss of intracellular Ca++ homeostasis (lack of energy)Hypoxia = aerobic metabolism stop

Extra Cellular Ca++ ( 1.06-1.32 mm. Mol.) Cell membrane-----------------------------------------------------------------Intracellular Ca++ ( < 0.1 Mol.) Mitochondria Endoplasmic reticulum Release Ca++ Cytosolic Ca++ Activate Enzymes Activity

Anaerobic glycolysis ATP

Ribosomes ER

Release Ca++

Ca++,Na+ K+ - - ER

Glycogen glucose Glycogen

glucose + Lactic acid () pH

Proteins

AT Pase

Phospholipase

Protease

Endonuclease

Chromatin (Nuclear changes)

ATP decrease

Lipid * cell membrane damage

* disruption protein of cell membrane * Cytoxkeleton damage

Nuclear chromatin damage

3. [Free radicals ]Intracellular normal MetabolismBy oxidative process

Morphological Changes in reversible injury ultra structure Changes Cell wall; bleb Mitochondria swelling ER. swelling detach ribosomes

Histological changesCell * cloudy swelling * Vacuolar changes in cytoplasm * Hyaline changes in cytoplasm * Pyknotic Nuclei : * Accumulation of endogenous Substances

+ [=free electron unstable molecules ](catalist) , ActivatedAutocatalytic reaction protein fat..

releaseFree radicals Again Damage to cell wall, Organelles

Cell DeathNecrosis Apoptosis * Programmed cell death = Gene , characterized by cell shrinkage intracytoplasmic debris (Apoptotic bodies) follow by nuclear pyknosis and removed by phagocytic cell

Pathological cell death occur follow irreversible degeneration or direct lethal injuryReversible injuly ( Intracellular Fat Deposition)

Type of Necrosis (Classify by Gross changes)Coagulative necrosis Liquefactive necrosis Fat necrosis Caseous necrosis

Morphological changes in cell death (Microscopic Necrosis)Nuclear changes Pyknotic nuclear deeply basophilic mass Karyorrhexis Karyolysis Cytoplasmic changes Homogeneous deeply acidophillic staining Vacuolation Autolysis

Special type necrosis

*Fibrinoid necrosis (micro change) *Gangrene : Dry or Wet type (grosschange)

Somatic Death = [dead of Body] * Vital organs Eg. R.S - CVS - CNS Brain death , reflex ( EEG )

Sequences of Dead Body temperature drop down to environmental temperature Rivor Mortis=body blood fall down by gravitation and accumulate in lower part of body Rigor Mortis= rigidity of body (first start on mandible) Putrefaction [Autolysis]

Post test Cell pathology

1. Organelle Mitochondria ? A. B. C. D. E. 2. @ Metaplasia A. B. 3. 4. 5.

Pathogenesis: O2

Cell Anoxia

mitochondria Anoxia

Defined technical terms

Mitochondria ATP ATP Anaerobic Metabolism glycolysis ( glycogen Glucose) + Lactic acid () ADP ATP ( cell) PH ( Cytoplasm) Enzymes

Glucose

Na+pump +, K+, H O cell, mitochondria, ER Na 2 Ribosomes , Clumping chromatin Proteins