PRELIM LEC: INTRODUCTION IN GENERAL PATHOLOGY Flashcards

1
Q
  • underlying cause of death
  • structural and functional changes in cell, tissue and organ
  • molecular basis of disease
A

HISTOPATHOLOGY

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2
Q

Only in tertiary laboratory available (Hospitals)

A

HISTOPATHOLOGY

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3
Q

4 DIVISIONS OF PATHOLOGY

A

GROSS PATHOLOGY
MICROSCOPIC PATHOLOGY
ANATOMICAL PATHOLOGY
CLINICAL PATHOLOGY

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4
Q
  • physical changes (color, weight, size of organ)
  • Macroscopic examination of tissues and organs
A

GROSS PATHOLOGY

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5
Q
  • microscopic changes
A

MICROSCOPIC PATHOLOGY

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6
Q
  • Surgical
  • Biopsy (living), Autopsy (dead)
     Histopathology
A

ANATOMICAL PATHOLOGY

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7
Q

ANTE-MORTEM EXAMINATION

A

BIOPSY

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8
Q

POST-MORTEM EXAMINATION

A

AUTOPSY

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9
Q

Stages of the Cellular Response to Stress and Injurious Stimuli

A
  • NORMAL CELL
  • ADAPTION
  • CELL INJURY
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10
Q

Normal cells handle physiologic demand through______

A

Homeostasis

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11
Q

act of maintaining a steady state

A

Homeostasis

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12
Q

When there is a slightly severe stress, or some pathologic stimuli, cells undergo _______in order to survive and continue to function.

A

adaptation

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13
Q

reversible structural and functional response of cells to stress and stimuli

A

adaptation

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14
Q

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.

A

cell injury

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15
Q
  • altered cell structure or function due to exposed to injuries stimuli (agents or stress)
  • reversible or irreversible
A

cell injury

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16
Q

If the stimulus is mild and transient, the injury is ______. The cell may go back to its normal state.

A

reversible

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17
Q

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.

A

irreversible

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18
Q

Pathologic cell death

A

necrosis (Premature cell death)

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19
Q

Physiologic cell death

A

apoptosis (Programmed cell death)

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20
Q

Other types of stress can induce responses other than cellular
adaptation, injury and death. The responses are the following:

A
  • Autophagy
  • Intracellular accumulation of substances
  • Pathologic calcification
  • Cellular aging
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21
Q

starved cells eat its own components during nutrient deprivation (self-eating)

A

Autophagy

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22
Q

too much substances such as proteins, lipids, hyaline, glycogen, pigments

A

Intracellular accumulation of substances

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23
Q

abnormal tissue deposition of calcium salts

A

Pathologic calcification

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24
Q

progressive decline in the life span and functional capacity of cells

A

Cellular aging

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25
- Changes made by a cell in response to stress or stimuli - May be physiologic or pathologic
CELLULAR ADAPTATION
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5 CELLULAR ADAPTION
Hypertrophy Hyperplasia Atrophy Metaplasia Dysplasia
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- can be physiologic - increase of functional demand - specific hormone stimulation - Increased Cell Size TO Increased Organ Size - Due to increased protein synthesis
Hypertrophy
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Most common stimulus of hypertrophy:
Increased Workload
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3 TYPES OF HYPERTROPHY
TRUE FALSE COMPENSATORY
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STIMULATED BY HORMONES
TRUE HYPERTROPHY
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EXCESS OF ACCUMALATION OF MOLECULES
FALSE HYPERTROPHY
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can take place only if some portion of the original structure is left to react to the loss
COMPENSATORY HYPERTROPHY
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- Increased Cell Number TO Increased Organ Mass - Due to proliferative actions of growth factor, and/or stem cells
Hyperplasia
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- 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
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- 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
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- Abnormality of cell development - “disordered growth”; presence of abnormal cells within a tissue (reversible)
Dysplasia
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2 TYPES OF PHYSIOLOGIC HYPERPLASIA
HORMONAL HYPERPLASIA COMPENSATORY HYPERPLASIA
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Breast during puberty or pregnancy
HORMONAL HYPERPLASIA
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Liver cells regeneration
COMPENSATORY HYPERPLASIA
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PATHOLOGIC HYPERPLASIA
- Excess Hormonal Stimulation - Excess Growth Hormone Stimulation
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Increased Estrogen TO Endometrial hyperplasia TO abnormal menstrual bleeding
Excess Hormonal Stimulation
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Papillomavirus mucosal lesions
Excess Growth Hormone Stimulation
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Any change from a state of health as a result of certain forms of stimuli and stress, which leads to impaired physiological functioning
Disease
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father of modern pathology
Rudolf Virchow
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Four Aspects of a Disease Process
ETIOLOGY PATHOGENESIS MORPHOLOGIC AND MOLECULAR CHANGES CLINICAL MANIFESTIONS
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Cause or origin of the disease; might be genetic factors or acquired factors
ETIOLOGY
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- 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
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Structural, biochemical and molecular alterations induced in the cells and organs of the body as a result of the disease
MORPHOLOGIC AND MOLECULAR CHANGES
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Functional consequence of the changes
CLINICAL MANIFESTIONS
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Effects that can be observed by others
SIGNS
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Effects apparent only to the patient
SYMPTOMS
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- decreased workloads - loss of blood supply - inadequate nutrition
ATROPHY
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- Decreased Cell Size & Number  Reduce tissue/organ size - Due to decreased protein synthesis, and increased protein degradation
ATROPHY
54
- aging - may be increased and complicated by the presence of arteriosclerosis.
SENILE ATROPHY
55
HYPERTROPHY CAN CO-EXIST WITH HYPERPLASIA BECAUSE THEY HAVE THE SAME STIMULUS. TRUE OR FALSE?
TRUE
56
- as in puberty when the thymus and the lymphoid organs decrease in size (e.g. Atrophy of uterus after pregnancy)
PHYSIOLOGIC ATROPHY
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TYPES OF ATROPHY (PATHOLOGIC)
1. Atrophy of disuse 2. Vascular Atrophy 3. Starvation Atrophy 4. Loss of endocrine hormone stimulation 5. Pressure Atrophy 6. Exhaustion Atrophy
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decreased workload, thus diminished function of organ (e.g. skeletal muscle atrophy due to bedrest)
Atrophy of disuse
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Diminished/loss blood supply (ischemia) e.g. brain atrophy during atherosclerosis
Vascular Atrophy
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- 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
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- due to decrease of regulating hormones e.g. breast atrophy after menopause due to loss of estrogen stimulation
Loss of endocrine hormone stimulation
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as in growth of tumors, atrophy occurs when tumors suppress the blood supply or by directly putting pressure to surrounding healthy cells
Pressure Atrophy
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due to increase in metabolism resulting to increase of metabolites and loss of the actual cell space
Exhaustion Atrophy
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- 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
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METAPLASIA 2 TYPES
EPITHELIAL METAPLASIA MESENCHYMAL METAPLASIA
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Habitual cigarette smokers - ciliated columnar cells of trachea and bronchi are replaced by stratified squamous cells
EPITHELIAL METAPLASIA
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Barrett esophagus - squamous cells of esophagus are replaced by intestinal-like columnar cells in response to refluxed acid
MESENCHYMAL METAPLASIA
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squamous cells of esophagus are replaced by intestinal-like columnar cells in response to refluxed acid
BARRETTE ESOPHAGUS/SYNDROME
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- Abnormality of cell development - “disordered growth”; presence of abnormal cells within a tissue (reversible)
DYSPLASIA
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MICROSCOPIC CHANGES SEEN IN DYSPLASTIC CELL (dysplasia)
Anisocytosis Poikilocytosis Hyperchromatin Presence of mitotic figures
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ed blood cells that are of different SIZES
Anisocytosis
72
an increase in abnormal-SHAPED red blood cells
Poikilocytosis
73
darken color
Hyperchromatin
74
A measure of how fast cancer cells are dividing and growing
Presence of mitotic figures
75
Alteration in cell structure or function due to stress or pathologic stimuli
CELLULAR INJURY
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CELLULAR INJURY CAUSES
Hypoxia Physical Agents Chemical Agents and Drugs Infectious Agents Immunologic Reactions Genetic Abnormalities Nutritional Imbalances
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Morphological Alterations in Cell Injury
1. Generalized swelling of cell and organelles - first manifestation 2. Blebbing of plasma membrane 3. Detachment of ribosome from ER 4. Clumping of nuclear chromatin
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Occurs after irreversible injury
CELL DEATH