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HISTOPATHOLOGY > PRELIM LEC: INTRODUCTION IN GENERAL PATHOLOGY > Flashcards

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
Q
  • Changes made by a cell in response to stress or stimuli
  • May be physiologic or pathologic
A

CELLULAR ADAPTATION

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26
Q

5 CELLULAR ADAPTION

A

Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Dysplasia

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27
Q
  • can be physiologic
  • increase of functional demand
  • specific hormone stimulation
  • Increased Cell Size TO Increased Organ Size
  • Due to increased protein synthesis
A

Hypertrophy

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28
Q

Most common stimulus of hypertrophy:

A

Increased Workload

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29
Q

3 TYPES OF HYPERTROPHY

A

TRUE
FALSE
COMPENSATORY

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30
Q

STIMULATED BY HORMONES

A

TRUE HYPERTROPHY

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31
Q

EXCESS OF ACCUMALATION OF MOLECULES

A

FALSE HYPERTROPHY

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32
Q

can take place only if some portion of the original structure is left to react to the loss

A

COMPENSATORY HYPERTROPHY

33
Q
  • Increased Cell Number TO Increased Organ Mass
  • Due to proliferative actions of growth factor, and/or stem cells
A

Hyperplasia

34
Q
  • 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
A

Atrophy

35
Q
  • 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
A

Metaplasia

36
Q
  • Abnormality of cell development
  • “disordered growth”; presence of abnormal cells within a tissue (reversible)
A

Dysplasia

37
Q

2 TYPES OF PHYSIOLOGIC HYPERPLASIA

A

HORMONAL HYPERPLASIA
COMPENSATORY HYPERPLASIA

38
Q

Breast during puberty or
pregnancy

A

HORMONAL HYPERPLASIA

39
Q

Liver cells regeneration

A

COMPENSATORY HYPERPLASIA

40
Q

PATHOLOGIC HYPERPLASIA

A
  • Excess Hormonal Stimulation
  • Excess Growth Hormone Stimulation
41
Q

Increased Estrogen TO Endometrial hyperplasia TO abnormal menstrual bleeding

A

Excess Hormonal Stimulation

42
Q

Papillomavirus mucosal lesions

A

Excess Growth Hormone Stimulation

43
Q

Any change from a state of health as a result of certain forms of stimuli and stress, which leads to impaired physiological functioning

A

Disease

44
Q

father of modern pathology

A

Rudolf Virchow

45
Q

Four Aspects of a Disease Process

A

ETIOLOGY
PATHOGENESIS
MORPHOLOGIC AND MOLECULAR CHANGES
CLINICAL MANIFESTIONS

46
Q

Cause or origin of the disease; might be genetic factors or acquired factors

A

ETIOLOGY

47
Q
  • 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
A

PATHOGENESIS

48
Q

Structural, biochemical and molecular alterations induced in the cells and organs of the body as a result of the disease

A

MORPHOLOGIC AND MOLECULAR CHANGES

49
Q

Functional consequence of the changes

A

CLINICAL MANIFESTIONS

50
Q

Effects that can be observed by others

A

SIGNS

51
Q

Effects apparent only to the patient

A

SYMPTOMS

52
Q
  • decreased workloads
  • loss of blood supply
  • inadequate nutrition
A

ATROPHY

53
Q
  • Decreased Cell Size & Number  Reduce tissue/organ size
  • Due to decreased protein synthesis, and increased protein degradation
A

ATROPHY

54
Q
  • aging
  • may be increased and complicated by the presence of arteriosclerosis.
A

SENILE ATROPHY

55
Q

HYPERTROPHY CAN CO-EXIST WITH HYPERPLASIA BECAUSE THEY HAVE THE SAME STIMULUS. TRUE OR FALSE?

A

TRUE

56
Q
  • as in puberty when the thymus and the lymphoid organs decrease in size (e.g. Atrophy of uterus after pregnancy)
A

PHYSIOLOGIC ATROPHY

57
Q

TYPES OF ATROPHY (PATHOLOGIC)

A
  1. Atrophy of disuse
  2. Vascular Atrophy
  3. Starvation Atrophy
  4. Loss of endocrine hormone stimulation
  5. Pressure Atrophy
  6. Exhaustion Atrophy
58
Q

decreased workload, thus diminished function of organ
(e.g. skeletal muscle atrophy due to bedrest)

A

Atrophy of disuse

59
Q

Diminished/loss blood supply (ischemia)
e.g. brain atrophy during atherosclerosis

A

Vascular Atrophy

60
Q
  • inadequate nutrition of cell
    e.g. muscle wasting (or cachexia) due to use of skeletal muscle as source of energy during protein malnutrition
A

Starvation Atrophy

61
Q
  • due to decrease of regulating hormones
    e.g. breast atrophy after menopause due to loss of
    estrogen stimulation
A

Loss of endocrine hormone stimulation

62
Q

as in growth of tumors, atrophy occurs when tumors suppress the blood supply or by directly putting
pressure to surrounding healthy cells

A

Pressure Atrophy

63
Q

due to increase in metabolism resulting to increase of metabolites and loss of the actual cell space

A

Exhaustion Atrophy

64
Q
  • 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
A

METAPLASIA

65
Q

METAPLASIA 2 TYPES

A

EPITHELIAL METAPLASIA
MESENCHYMAL METAPLASIA

66
Q

Habitual cigarette smokers - ciliated columnar cells of trachea and bronchi are replaced by stratified squamous cells

A

EPITHELIAL METAPLASIA

67
Q

Barrett esophagus - squamous cells of esophagus are replaced by intestinal-like columnar cells in response to refluxed acid

A

MESENCHYMAL METAPLASIA

68
Q

squamous cells of esophagus are replaced by intestinal-like columnar cells in response to refluxed acid

A

BARRETTE ESOPHAGUS/SYNDROME

69
Q
  • Abnormality of cell development
  • “disordered growth”; presence of abnormal cells within a tissue (reversible)
A

DYSPLASIA

70
Q

MICROSCOPIC CHANGES SEEN IN DYSPLASTIC CELL (dysplasia)

A

Anisocytosis
Poikilocytosis
Hyperchromatin
Presence of mitotic figures

71
Q

ed blood cells that are of different SIZES

A

Anisocytosis

72
Q

an increase in abnormal-SHAPED red blood cells

A

Poikilocytosis

73
Q

darken color

A

Hyperchromatin

74
Q

A measure of how fast cancer cells are dividing and growing

A

Presence of mitotic figures

75
Q

Alteration in cell structure or function due to stress or pathologic stimuli

A

CELLULAR INJURY

76
Q

CELLULAR INJURY CAUSES

A

Hypoxia
Physical Agents
Chemical Agents and Drugs
Infectious Agents
Immunologic Reactions
Genetic Abnormalities
Nutritional Imbalances

77
Q

Morphological Alterations in Cell Injury

A
  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
78
Q

Occurs after irreversible injury

A

CELL DEATH

HISTOPATHOLOGY (8 decks)

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