PRELIM LEC: INTRODUCTION IN GENERAL PATHOLOGY Flashcards
- underlying cause of death
- structural and functional changes in cell, tissue and organ
- molecular basis of disease
HISTOPATHOLOGY
Only in tertiary laboratory available (Hospitals)
HISTOPATHOLOGY
4 DIVISIONS OF PATHOLOGY
GROSS PATHOLOGY
MICROSCOPIC PATHOLOGY
ANATOMICAL PATHOLOGY
CLINICAL PATHOLOGY
- physical changes (color, weight, size of organ)
- Macroscopic examination of tissues and organs
GROSS PATHOLOGY
- microscopic changes
MICROSCOPIC PATHOLOGY
- Surgical
- Biopsy (living), Autopsy (dead)
Histopathology
ANATOMICAL PATHOLOGY
ANTE-MORTEM EXAMINATION
BIOPSY
POST-MORTEM EXAMINATION
AUTOPSY
Stages of the Cellular Response to Stress and Injurious Stimuli
- NORMAL CELL
- ADAPTION
- CELL INJURY
Normal cells handle physiologic demand through______
Homeostasis
act of maintaining a steady state
Homeostasis
When there is a slightly severe stress, or some pathologic stimuli, cells undergo _______in order to survive and continue to function.
adaptation
reversible structural and functional response of cells to stress and stimuli
adaptation
But if the limits of adaptive response are exceeded, or when cells are exposed to injurious stimuli (agents or stress), or deprived of essential nutrients, _____ occurs.
cell injury
- altered cell structure or function due to exposed to injuries stimuli (agents or stress)
- reversible or irreversible
cell injury
If the stimulus is mild and transient, the injury is ______. The cell may go back to its normal state.
reversible
If it is severe and progressive, the injury is _________. Cells that undergo irreversible injury will ultimately suffer cell death, which may be pathological or physiological.
irreversible
Pathologic cell death
necrosis (Premature cell death)
Physiologic cell death
apoptosis (Programmed cell death)
Other types of stress can induce responses other than cellular
adaptation, injury and death. The responses are the following:
- Autophagy
- Intracellular accumulation of substances
- Pathologic calcification
- Cellular aging
starved cells eat its own components during nutrient deprivation (self-eating)
Autophagy
too much substances such as proteins, lipids, hyaline, glycogen, pigments
Intracellular accumulation of substances
abnormal tissue deposition of calcium salts
Pathologic calcification
progressive decline in the life span and functional capacity of cells
Cellular aging
- Changes made by a cell in response to stress or stimuli
- May be physiologic or pathologic
CELLULAR ADAPTATION
5 CELLULAR ADAPTION
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Dysplasia
- can be physiologic
- increase of functional demand
- specific hormone stimulation
- Increased Cell Size TO Increased Organ Size
- Due to increased protein synthesis
Hypertrophy
Most common stimulus of hypertrophy:
Increased Workload
3 TYPES OF HYPERTROPHY
TRUE
FALSE
COMPENSATORY
STIMULATED BY HORMONES
TRUE HYPERTROPHY
EXCESS OF ACCUMALATION OF MOLECULES
FALSE HYPERTROPHY
can take place only if some portion of the original structure is left to react to the loss
COMPENSATORY HYPERTROPHY
- Increased Cell Number TO Increased Organ Mass
- Due to proliferative actions of growth factor, and/or stem cells
Hyperplasia
- decreased workload
- loss of blood supply
- inadequete nutrition
- Decreased Cell Size & Number Reduce tissue/organ size
- Due to decreased protein synthesis, and increased protein degradation
Atrophy
- it cant cause disease
- Change in one cell type to another
- Due to reprogramming of existing stem cells in normal tissue, or of undifferentiated mesenchymal cells in order to withstand adverse environment
Metaplasia
- Abnormality of cell development
- “disordered growth”; presence of abnormal cells within a tissue (reversible)
Dysplasia
2 TYPES OF PHYSIOLOGIC HYPERPLASIA
HORMONAL HYPERPLASIA
COMPENSATORY HYPERPLASIA
Breast during puberty or
pregnancy
HORMONAL HYPERPLASIA
Liver cells regeneration
COMPENSATORY HYPERPLASIA
PATHOLOGIC HYPERPLASIA
- Excess Hormonal Stimulation
- Excess Growth Hormone Stimulation
Increased Estrogen TO Endometrial hyperplasia TO abnormal menstrual bleeding
Excess Hormonal Stimulation
Papillomavirus mucosal lesions
Excess Growth Hormone Stimulation
Any change from a state of health as a result of certain forms of stimuli and stress, which leads to impaired physiological functioning
Disease
father of modern pathology
Rudolf Virchow
Four Aspects of a Disease Process
ETIOLOGY
PATHOGENESIS
MORPHOLOGIC AND MOLECULAR CHANGES
CLINICAL MANIFESTIONS
Cause or origin of the disease; might be genetic factors or acquired factors
ETIOLOGY
- Mechanisms of the development of the disease
- Sequence of events from initial stimulus to ultimate expression of the disease
- How etiologic factors trigger cellular & molecular changes in a disease
PATHOGENESIS
Structural, biochemical and molecular alterations induced in the cells and organs of the body as a result of the disease
MORPHOLOGIC AND MOLECULAR CHANGES
Functional consequence of the changes
CLINICAL MANIFESTIONS
Effects that can be observed by others
SIGNS
Effects apparent only to the patient
SYMPTOMS
- decreased workloads
- loss of blood supply
- inadequate nutrition
ATROPHY
- Decreased Cell Size & Number Reduce tissue/organ size
- Due to decreased protein synthesis, and increased protein degradation
ATROPHY
- aging
- may be increased and complicated by the presence of arteriosclerosis.
SENILE ATROPHY
HYPERTROPHY CAN CO-EXIST WITH HYPERPLASIA BECAUSE THEY HAVE THE SAME STIMULUS. TRUE OR FALSE?
TRUE
- as in puberty when the thymus and the lymphoid organs decrease in size (e.g. Atrophy of uterus after pregnancy)
PHYSIOLOGIC ATROPHY
TYPES OF ATROPHY (PATHOLOGIC)
- Atrophy of disuse
- Vascular Atrophy
- Starvation Atrophy
- Loss of endocrine hormone stimulation
- Pressure Atrophy
- Exhaustion Atrophy
decreased workload, thus diminished function of organ
(e.g. skeletal muscle atrophy due to bedrest)
Atrophy of disuse
Diminished/loss blood supply (ischemia)
e.g. brain atrophy during atherosclerosis
Vascular Atrophy
- inadequate nutrition of cell
e.g. muscle wasting (or cachexia) due to use of skeletal muscle as source of energy during protein malnutrition
Starvation Atrophy
- due to decrease of regulating hormones
e.g. breast atrophy after menopause due to loss of
estrogen stimulation
Loss of endocrine hormone stimulation
as in growth of tumors, atrophy occurs when tumors suppress the blood supply or by directly putting
pressure to surrounding healthy cells
Pressure Atrophy
due to increase in metabolism resulting to increase of metabolites and loss of the actual cell space
Exhaustion Atrophy
- it cant cause a disease
- Change in one cell type to another
- Due to reprogramming of existing stem cells in normal tissue,
or of undifferentiated mesenchymal cells in order to withstand adverse environment
METAPLASIA
METAPLASIA 2 TYPES
EPITHELIAL METAPLASIA
MESENCHYMAL METAPLASIA
Habitual cigarette smokers - ciliated columnar cells of trachea and bronchi are replaced by stratified squamous cells
EPITHELIAL METAPLASIA
Barrett esophagus - squamous cells of esophagus are replaced by intestinal-like columnar cells in response to refluxed acid
MESENCHYMAL METAPLASIA
squamous cells of esophagus are replaced by intestinal-like columnar cells in response to refluxed acid
BARRETTE ESOPHAGUS/SYNDROME
- Abnormality of cell development
- “disordered growth”; presence of abnormal cells within a tissue (reversible)
DYSPLASIA
MICROSCOPIC CHANGES SEEN IN DYSPLASTIC CELL (dysplasia)
Anisocytosis
Poikilocytosis
Hyperchromatin
Presence of mitotic figures
ed blood cells that are of different SIZES
Anisocytosis
an increase in abnormal-SHAPED red blood cells
Poikilocytosis
darken color
Hyperchromatin
A measure of how fast cancer cells are dividing and growing
Presence of mitotic figures
Alteration in cell structure or function due to stress or pathologic stimuli
CELLULAR INJURY
CELLULAR INJURY CAUSES
Hypoxia
Physical Agents
Chemical Agents and Drugs
Infectious Agents
Immunologic Reactions
Genetic Abnormalities
Nutritional Imbalances
Morphological Alterations in Cell Injury
- Generalized swelling of cell and organelles - first manifestation
- Blebbing of plasma membrane
- Detachment of ribosome from ER
- Clumping of nuclear chromatin
Occurs after irreversible injury
CELL DEATH