PATHOLOGY
Pathos : suffering
Logos : study
The study of suffering.
A discipline that bridges clinical practice
and basic science
PATHOLOGY
1. ETIOLOGY
2. PATHOGENESIS
3. MORPHOLOGIC CHANGES
4. FUNCTIONAL DEARANGEMENT AND
CLINICAL MANIFESTATION
RUDOLF VIRCHOW
A FATHER OF MODERN PATHOLOGY
( 19TH CENTURY)
NORMAL HOMEOSTASIS
CELLULAR ADAPTATIONS
1. HYPERPLASIA
- PHYSIOLOGIC H.
- PATHOLOGIC H.
2. HYPERTROPY
- PHYSIOLOGIC
- PATHOLOGIC
MECHANISM OF HYPERTROPHY.(Fig.1-4)
3. ATROPHY
MECHANISM OF ATROPHY
4. METAPLASIA
MECHANISM OF METAPLASIA
HYPERPLASIA
INCREASE IN NUMBER OF CELLS (ORGAN/TISSUE)
PHYSIOLOGIC HYPERPLASIA
1. HORMONAL HYP.
INCREASES FUNCTIONAL CAPACITY WHEN
NEEDED
(FEMALE BREAST AT PUBERTY ,PREGNANT
UTERUS)
2.COMPENSATORY HYP.
INCREASES TISSUE MASS AFTER
DAMAGE,OR PARTIAL RESECTION
(REGENERATION OF LIVER,AFTER
NEPHRECTOMY)
MECHANISMS OF HYPERPLASIA.
LOCAL PROD.OF GROWTH F GROWTH
F.RECEPTOR ACTIVATION INTRACELLULAR
SIGNALLING PATHWAY TRANSCRIPTION F.
TURN ON MANY CELLULAR GENES ( GENES
ENCODING G.F.,RECEPTOR FOR G.F.
AND CELLS CYCLE REGULATORS
CELLULER PROLIFERATION.
HYPERTROPHY : - PHYSIOLOGIC
- PATHOLOGIC
CAUSED BY :
- INCREASED FUNCTION DEMAND
- SPECIFIC HORMONAL STIMULATION
FOR EXAMPLE : INCREASED WORK LOAD
(-bulging muscles of bodybuilders)
(-chronic hemodynamic over load hypertensive heart)
MECHANISMS OF HYPERTROPHY
ATROPHY : 1. PHYSIOLOGIC A.
2. PATHOLOGIC A.
AD.1. - During early development (notochord, thyreoglossal duct)
- Uterus post partum
AD.2. Depends on underlying cause
- Disused atrophy
- Denervation atrophy
- Diminished blood supply
- Inadequate nutrition
- Aging (senile atrophy)
- Pressure
MECHANISMS ATROPHY
* PHYSIOLOGIC CONDITIONS
-THE PROGRAMMED DESTRUCTION OF CELLS
DURING EMBRYOGENESIS
-HORMON DEPENDENT INVOLUTION IN ADULT
-DEATH OF HOST CELLS
-ELIMINATION OF POTENTIALLY HARMFULL SELF-
REACTIVE LYMPHOCYTES
-CELL DEATH INDUCED BY CYTOTOXIC T CELLS
* PATHOLOGIC CONDITIONS
*PATHOLOGIC CONDITIONS
- CELL SHRINKAGE
- CHROMATIN CONDENSATION
- FORMATION OF CYTOPLASMIC
BLEBS AND APOPTOTIC BODIES
- PHAGOCYTOSIS OF APOPTOTIC
CELLS OR CELL BODIES, USUALLY BY
MACROPHAGES
BIOCHEMICAL FEATURES OF APOPTOSIS
1. PROTEIN CLEAVAGE
- ACTIVATION OF CYSTEINE PROTEASES
CLEAVE MANY VITAL CELLULAR PROTEIN,
LAMINS BREAK UP THE NUCLEAR
SCAFFOLD & CYTOSKELETON (ACTIVE
DNASES).
2. DNA BREAKDOWN
3. PHAGOCYTIC RECOGNITION
MECHANISMS OF APOPTOSIS
1.DYSTROPHIC CALCIFICATION
-CALCIFICATION IN AREAS OF
NECROSIS (COAGULATIVE,
CASEOUS, LIQUEFACTIVE TYPE, IN
ENZYMATIC NECROSIS OF FAT
2.METASTATIC CALCIFICATION
- IN NORMAL TISSUE, HIPERCALCEMIA
(+)
CAUSES OF HIPERCLACEMIA
1.INCREASED SECRETION OF
PARATHYROID HORMON
2.DESTRUCTION OF BONE TISSUE
(MULTIPLE MYOLOMA, LEUKEMIA,
DIFFUSE SKELETAL METASTASIS)
3.VITAMIN D RELATED DISORDERS
4.RENAL FAILURE
CELLULAR AGING
PROGRESIVE LOSS OF FUNCTION
CAPACITY
THE RESULT OF PROGRESIVE DECLINE IN
PROLIFERATIVE CAPACITY IN LIFE SPANS
OF CELLS AND THE EFFECTS OF
CONTINUOUS EXPOSURE TO EXOGENOUS
INFLUENCES THAT RESULT IN THE
PROGRESSIVE ACCUMULATION OF
CELLULAR AND MOLECULAR DAMAGE
(Fig.1-43)
July 2005