MATERI KULIAH

PATOLOGI ANATOMI
dr.Tengku Kemala Intan M.Pd
HP. 0815 3384 1903

 PENDAHULUAN
 IMMUNOLOGI
 RADANG
 INFEKSI
 DEGENERASI
 NECROSIS
PATHOLOGY, HEALTH AND
DISEASE

CAUSES DISEASES

PREVENTION
CLASSIFICATION
 STRUCTURAL
FUNCTIONAL
CHANGE

PATHOLOGY

CELLS
CONCEQUEN
AND
ORGANISM
TISSUES

•PATHOLOGY IS THE STUDY OF DISEASE PROCESSES

•EPIDEMIOLOGY PROVIDES A BROAD CONTEXT FOR UNDERSTANDING

PATHOLOGY

•BOTH PROVIDE A USEFUL FRAMEWORK FOR CLASSIFYING AND UNDER

STANDING MECHANISM OF DISEASE
 HEALTH, ILLNESS AND
DISEASE
 DISCUSS THE NATURE OF HEALTH AND
DISEASE

 DISCUSS WHY AND HOW DISEASE IS

CLASSIFIED

 DEFINE AETIOLOGY, PATHOGENESIS

CONGENITAL AND ACQUIRED
HEALTH DISEASE

WORLD HEALTH ORGANIZATION

HEALTH AS A STATE OF COMPLETE PHYSICAL
MENTAL AND SOCIAL WELLBEING AND NOT
MERELY THE ABSENCE OF DISEASE OR INFIRMITY

DISEASE AS A STATE OF PHYSIOLOGICAL OR PSYCHOLOGICAL

DYSFUNCTION, OR AN ABNORMAL VARIATION IN THE STRUCTURE
OR FUNCTION OF PART OF THE BODY
 PHYSICAL

AETIOLOGY INJURY CHEMICAL

LIVING AGENTS
CLASSIFICATION
OF
DISEASE GENETIC

INFLAMMATION
DEGENERATION
PATHOGENESIS ONCOGENESIS
IMMUNE REACTIONS
 WAYS OF THINKING ABOUT
DISEASES
 DEFINITION : CLINICAL – PATHOLOGICAL
 EPIDEMIOLOGY: INCIDENCE,
AGE/GENDER,GEOGRAPHY,RACE
 AETIOLOGY
 UNDERLYING PATHOLOGY
 CLINICAL PRESENTATION
 TREATMENT
 COMPLICATIONS
 PROGNOSIS
 12 Februari 2007
The Inflammatory Response
INFLAMMATION ?
Mechanism : neutralized, to limit spread, to
eradicated tissue injury caused by physical,
chemical or biological agent

CIRCULATORY SYSTEM
 CARDINAL SIGNS:
RUBOR / REDNESS
CALOR/HEAT MICROVASCULATURE
TUMOUR/SWELLING CELLULAR MEDIATORS
DOLOR/PAIN CHEMICAL MEDIATORS
LAESIO FUNCTAE /
LOSS OF FUNCTION
 Lymphoid series
STEM CELL

T – lym Thymus
phocyte

B-lym Plasma
phocyte Cell

Granulocyte series
Megakaryocyte
Red blood Basophil
Platelets
cells Mast cell
Monocyte / Eosinophil
Macrophage Neutophil

ORIGINS OF HAEMAPOIETIC AND LYMPHOID CELLS

 WHAT IS THE DIFFERENCE
BETWEEN ACUTE AND CHRONIC
INFLAMMATION
TISSUE INJURY

Cell-derived Plasma-derived
Inflammatory Inflammatory
mediators mediators

Platelets Mast cells Inflammatory Hageman factor Plasmin

(XII)
basophils cells (XI)
Arachidonic Platelet Kallikrein Clotting Fibrinolytic Co
acid activating system system system
mp
Metabolites factor
Serotonin Histamine
sys Lymphokines& Klinins Fibrin degr Com
monokines prdt com
INFLAMMATORY PROCESS :
* CAUSE OF THE DAMAGE
* NUTRITIONAL STATUS OF THE PATIENCE
* IMMUNE SYSTEMS
* ANTIBIOTICS, ANTIINFLAMMATORY
DRUGS
* SURGERY
External Factors

Structural changes
Cell Functional changes Symptoms
Tissue Adaptation and respoons Signs
Organ From cellular to whole
Person Person level

Internal Factors

THE DISEASE PROCESS

 LOBAR PNEUMONIA:ADDITIONAL SECONDARY
Streptococcus pyogenes MECHANISM
(extrinsic factor)

Reduced gas
Lung Transfer in alveolii
(functional change)

Improved gas
Transfer with
Hypoxia New equilibrium
(internal factor) achieved

Response=
Heart tachiradia
 KASUS
 LAKI – LAKI / 60 TAHUN
 ANAMNESE: NYERI DADA SEJAK 2 JAM
YANG LALU, NYERI MENJALAR
KELENGAN KIRI BAWAH, TD 90/50
mmHg, ECG : ANTERIOR MYOCARDIAC
INFARC (+),BILATERAL PULMONARY
OEDEMA
 •SEVERITY
•DURATUION
•VOLUME OF HEART MUSCLE
•COLLATERAL CIRCULATION
•METABOLIC DEMANDS

Macroscopic appearance
6 – 12 hours : normal
18 hours : pale – red blue
hyperaemia
Microscopic appearance
4-12hours : mild oedema
Vacuolar degeneration
24 jam:neutrophyl ,necrosis
Day 3: debris
FEATURES OF REVERSIBLE AND IRREVERSIBLE
CELL DAMAGE
 REVERSIBLE
Cell Swelling
Mitochondria swelling
Endoplasmic reticulum
swelling
Detachment of ribosomes
“Myelin” figures
Loss of microvilli
Surface blebs
Clumping of nuclear chromatin
Lipid deposition
 IRREVERSIBLE
Release of lysosomal enzymes
Protein digestion
Loss of basophilia
Membrane disruption
Leakage of cell enzymes and
proteins
Nuclear changes: pyknosis,
karyorrhexis, karyolysis
 THE IMMUNE RESPONSE
 ROLE OF THE LYMPHATIC SYSTEM IN
INFLAMMATION
Sistem lymphatik organisasi lymphoid tissue
dan pembuluh darah disebut lymphatic.
Mucosa –associated lymphoid tissue -MALT
 NECROSIS
 Necrosis is cell death dui to lethal injury
 Unlike apoptosis
 Is not an energy-dependent active process
 A consequence of sudden changes in the
microenvironment abolishing cell functions
 Denaturation of proteins
 Release of gigestive enzymes destroy
tissue
 Morphological patterns of necrosis
 Necrosis coagulative
 Necrosis colliquative or liquefactive
 Necrosis caseous
 Fat necrosis
 Gangrene
 Calcification in necrotic tissue
COAGULATIVE NECROSIS KIDNEY , MYOCARDIAL INFARCT

COLIIQUATIVE OR LIQUEFACTIVE NECROSIS HYDROLITIC

ENZYMES DEGRADE CELLULEAR COMPONENTS &
EXTRACELLULAR MATERIAL PROTEINACEOUS SOUP

CASEOUS NECROSIS TUBERCULOSIS / CRUMBLY CHEESE

INFLAMMATORY RESPONSE MULTINUCLEATED GIANT CELLS

MACROPJAGEE , LYMPHOCYTES
 FAT NECROSIS TRAUMA OF THE BREAST , PANREATITIS

RUPTURE OF ADIPOCYTES & RELEASE OF FATTY ACIDS

SCARRING , PALPABLE LUMP

GANGRENE TO DESCRIBE BLACK , DEAD TISSUE

ATHEROSCLEROSIS IRREVERSIBLE ISCHAEMIC DAMAGE

DRY GANGRENE COAGULATIVE TYPE

WET GANGRENE INFECTION WITH GRAM-NEGATIVE

GAS GANGRENE COMPLICATION – CLOSTRIDIUM WELC

FIBRINOID GANGRENE OCCURS IN ARTERIES

ATOLYTIC CHANGE LYSIS OF THE DEAD BODY

 COAGULATIVE AND
LIQUEFACTIVE NECROSIS
 COAGULATIVE  LIQUEFACTIVE
 MECHANISM

Severe ischaemia destroying Strong proteolytic enzyme

proteolytic ezymes action destroying tissue
APPEARANCE
Initial preservation of cell
outlines and tissue Loss of cell outlines. Tissue
architecture becomes cystic of fluid
OCCURRENCE
Kidney , heart
Brain , bacterial infections