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GENERAL PATHOLOGY > TOPIC 1 (CHAPTER 1) > Flashcards

TOPIC 1 (CHAPTER 1) Flashcards

1
Q

It is the study of disease.

A

Pathology

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2
Q

It involves the investigation of the causes of disease and the associated changes at the levels of cells, tissues and organs that gives rise to the presenting signs and symptoms of the px.

A

Pathology

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3
Q

A term that refers to “study”

A

Logos

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4
Q

A term that refers to “suffering”

A

Patho

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5
Q

It is the origin of a disease.

A

Etiology

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6
Q

It includes the underlying causes and modifying factors.

A

Etiology

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7
Q

What are the common diseases?

A
  • Hypertension
  • Diabetes
  • Cancer
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8
Q

What is the cause of the common diseases such as hypertension, diabetes and cancer?

A

Inherited Genetic Susceptibility and Environmental Triggers

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9
Q

It refers as to why a disease arise.

A

Etiology

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10
Q

It refers to the steps in the development of disease.

A

Pathogenesis

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11
Q

It describes how etiologic factors trigger cellular and molecular changes that gives rise to the specific function and structural abnormalities that characterize the disease.

A

Pathogenesis

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12
Q

It also describes how a disease develop.

A

Pathogenesis

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13
Q

It provides the scientific foundation for the practice of medicine.

A

Pathology

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14
Q

What do you call to the person or people that identifies the changes in the gross microscopic appearance of cells, tissues and biochemical alterations in body fluids (such as blood and urine).

A

Pathologists

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15
Q

They also use a variety of morphologic, molecular, microbiologic, immunologic techniques to define the biochemical, structural and functional changes that occurs in cell, tissues & organs in response.

A

Pathologists

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16
Q

What techniques do pathologists uses to define the biochemical, structural and functional changes that occurs in cell, tissues and organs in response.

A
  • Morphologic
  • Molecular Technique
  • Microbiologic Technique
  • Immunologic Technique
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17
Q

It focuses on the cellular and tissue alteration caused by pathologic stimuli in most tissues.

A

Former

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18
Q

It examines the rx and abnormalities of different specialized organs.

A

Latter

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19
Q

Are active participants in their environment, constantly adjusting their structure and function to accommodate changing demands and extracellular stress.

A

Cells

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20
Q

It encounters physiologic stress or pathologic stimuli, they can undergo adaptation, achieving a new steady state and preserving viability and function.

A

Cells

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21
Q

When cells encounter physiologic stress or pathologic stimuli, they can undergo ____?

A

Adaptation

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22
Q

Cells undergo adaptation when encountered with ____?

A

Physiologic stress or Pathologic Stimuli

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23
Q

A steady state

A

Homeostasis

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24
Q

A new steady state and preserving viability and function.

A

Adaptation

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25
Q

What are the principal adaptive responses?

A
  • Hypertrophy
  • Hyperplasia
  • Atrophy
  • Metaplasia
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26
Q

It develops when the adaptive capability is exceeded or if the external stress is inherently harmful.

A

Cell Injury

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27
Q

Cells return to a stable state; within certain limits.

A

Reversible Injury

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28
Q

It is when stress is severe, persistent and rapid onset.

A

Irreversible Injury

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29
Q

Death of affected cells

A

Irreversible Injury

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30
Q

It is one of the most crucial events in the evolution of disease in any tissue or organ.

A

Cell Death

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31
Q

This results from a diverse cause like ischemia, ix, tx and immune rx.

A

Cell Death

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32
Q

Cell death results from a diverse cause like:

A
  • Ischemia
  • Infection
  • Toxin
  • Immune Reaction
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33
Q

It is also normal and essential process in Embryogenesis, the development of organs, and maintenance of homeostasis.

A

Cell Death

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34
Q

It is an increase size of the individual cells; Increase in load.

A

Hypertrophy

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35
Q

A lack or reduced of blood flow.

A

Ischemia

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36
Q

What are other variables that reversible and irreversible injury depends on?

A
  • Basal cellular metabolism
  • Blood
  • Nutrient supply
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37
Q

Are reversible changes in the number, size, phenotype, metabolic activity or functions of cells in response to changes in their environment.

A

Adaptation

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38
Q

It represents responses of cells to normal stimulation by hormones or endogenous chemical mediator.

A

Physiological Adaptations

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39
Q

It represents responses to stress that allow cells to modulate their structure and function and thus escape injury.

A

Pathological Adaptation

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40
Q

It is an increase in the size of cells resulting in increase in the size of organ.

A

Hypertrophy

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41
Q

There are no new cells, just bigger cells containing increased amounts of structural proteins and organelles.

A

Hypertrophy

42
Q

It takes place if the tissue contains cell populations and is an adaptive response in cells capable of replication.

A

Hyperplasia

43
Q

It occurs when cells have limited capacity to divide.

A

Hypertrophy

44
Q

Hypertrophy can be physiologic or pathologic and is caused either by increased functional demand or by ____?

A

Growth factor or hormonal stimulation/ functional demand

45
Q

Two types of hypertrophy signals.

A

Mechanical Triggers and Tropic Triggers

46
Q

Soluble mediators

A

Stimulate cell growth (growth factors and adrenergic hormones)

47
Q

It takes place if the tissue contains cell population capable of replication and it can also be physiologic or pathologic.

A

Hyperplasia

48
Q

What are the two types of physiologic hyperplasia:

A
  • Hormonal hyperplasia
  • Compensatory hyperplasia
49
Q

Exemplified by the proliferation of the glandular epithelium of the female breast at puberty and during pregnancy

A

Hormonal hyperplasia

50
Q

Residual tissue grows after removal or loss of part of an organ.

A

Compensatory hyperplasia

51
Q

Are caused by excessive hormonal or growth factor stimulation.

A

Pathologic hyperplasia

52
Q

Shrinkage in the size of the cell by the loss of cell substance; decreased workload

A

Atrophy

53
Q

Senile atrophy

A

Aging

54
Q

Atrophy is also accompanied by increased ____?

A

Autophagy

55
Q

Increased in the number of autophagic vacuoles

A

Autophagy

56
Q

(“self-eating”) is the process in which the starved cell eats its own components in an attempt to survive.

A

Autophagy

57
Q

It is a reversible change in which one adult cell type (epithelial or mesenchymal) is replaced by another adult cell type

A

Metaplasia

58
Q

Is thought to arise by reprogramming of stem cells to differentiate along a new pathway rather than a phenotypic change (transdifferentiation) of already differentiated cells.

A

Metaplasia

59
Q

Increased cell and organ size, often in response to increased workload; induced by growth factors produced in response to mechanical stress or other stimuli; occurs in tissues incapable of cell division.

A

Hypertrophy

60
Q

Increased cell numbers in response to hormones and other growth factors; occurs in tissues whose cells are able to divide or contain abundant tissue stem cells.

A

Hyperplasia

61
Q

Decreased cell and organ size, as a result of decreased nutrient supply or disuse; associated with decreased synthesis of cellular building blocks and increased breakdown of cellular organelles.

A

Atrophy

62
Q

Change in phenotype of differentiated cells, often in response to chronic irritation, that makes cells better able to withstand the stress; usually induced by altered differentiation pathway of tissue stem cells; may result in reduced functions or increased propensity for malignant transformation

A

Metaplasia

63
Q

In early stages or mild forms of injury the functional and morphologic changes are reversible if the damaging stimulus is removed; there may be significant structural and functional abnormalities, the injury has typically not progressed to severe membrane damage and nuclear dissolution.

A

Reversible cell injury

64
Q

Serves many normal functions and is not necessarily associated with pathologic injury.

A

Apoptosis

65
Q

It does not elicit an inflammatory response

A

Apoptosis

66
Q

With continuing damage, the injury becomes irreversible, at which time the cell cannot recover and it dies.

A

Cell death

67
Q

Two types of cell death

A

necrosis and apoptosis

68
Q

When damage to membranes is severe, enzymes leak out of lysosomes, enter the cytoplasm, and digest the cell.

A

Necrosis

69
Q

Which is characterized by nuclear dissolution without complete loss of membrane integrity. The cells kills itself by another type of death.

A

Apoptosis

70
Q

What are the causes of injury?

A
  • Oxygen Deprivation (hypoxia)
  • Chemical Agents
  • Infectious Agents
  • Immunologic Reactions
  • Genetic Factors
  • Nutritional Imbalances
  • Physical Agents
  • Aging
71
Q

A lack of oxygen, which can occur due to ischemia (reduced blood flow) or conditions like pneumonia or anemia.

A

Oxygen Deprivation (Hypoxia)

72
Q

Substances that disrupt cellular functions, ranging from common poisons to therapeutic drugs; An increasing number of chemical substances that can injure cells are being recognized; even innocuous sub- stances such as glucose, salt, or even water, if absorbed or administered in excess, can so derange the osmotic environment that cell injury or death results.

A

Chemical Agents

73
Q

Pathogens like viruses, bacteria, fungi, and parasites that cause disease.

A

Infectious Agents

74
Q

Autoimmune diseases and allergic reactions can damage cells and tissues.

A

Immunologic Reactions

75
Q

Mutations and genetic abnormalities can lead to diseases, such as sickle cell anemia or Down syndrome.

A

Genetic Factors

76
Q

Cause significant cell injury, with protein-calorie deficiencies being common among underprivileged populations.

A

Nutritional Imbalances

77
Q

Such as trauma, extreme temperatures, radiation, electric shock, and sudden atmospheric pressure changes can cause various effects on cells.

A

Physical Agents

78
Q

Causes cellular senescence, leading to changes in the replicative and repair capabilities of cells and tissues. This reduces the ability to respond to damage, ultimately resulting in cell death and the organism’s eventual death. The mechanisms of cellular aging are discussed in detail later in the chapter.

A

Aging

79
Q

In reversible and irreversible injury, it does not only depends on the nature and severity of the stress but also on several other variables such as:

A

Basal cellular metabolism, blood, nutrient supply

80
Q

What are two main morphologic of reversible cell injury?

A

Cellular Swelling and Fatty Change

81
Q

Is a result of failure of energy-dependent ion pumps in the plasma membrane, leading to an inability to maintain ionic and fluid homeostasis.

A

Cellular Swelling

82
Q

Occurs in hypoxic injury and in various forms of toxic or metabolic injury and it is manifested by the appearance of small on large lipid vacuoles in the cytoplasm.

A

Fatty Change

83
Q

It is the first sign of cell injury

A

Cellular Swelling

84
Q

Characterized lipid vacuoles in the cytoplasm , usually in cells involved fat metabolism.

A

Fatty Change

85
Q

A cell death marked by membrane rapture and leakage of cellular contents, leading to dissolution. This triggers inflammation to remove dead cells and begin repair.

A

Necrosis

86
Q

What are the nuclear changes:

A
  • Karyolysis
  • Pyknosis
  • Karryohexis
87
Q

Fading of chromatin basophilia due to Dnase activity.

A

Karyolysis

88
Q

Nuclear shrinkage and increased basophilia

A

Pyknosis

89
Q

Fragmentation of the pyknotic nucleus, leading to its disappearance within 1-2 days.

A

Karryohexis

90
Q

What are the types of Necrosis:

A
  • Coagulative Necrosis
  • Liquefactive Necrosis
  • Gangrenous Necrosis
  • Caseous Necrosis
  • Fat Necrosis
  • Fibrinoid Necrosis
91
Q

The tissue architecture remains intact for several days, giving affected areas a firm texture; characteristics in solid organs except brain.

A

Coagulative Necrosis

92
Q

Occurs in bacterial or fungal infection, where leukocyte enzymes digest the tissue; common in CNS due to hypoxia, leading to tissue transforming into liquid mass; it can result in pus, incases of acute inflammation, especially in bacterial infections.

A

Liquefactive Necrosis

93
Q

It refers to coagulative necrosis in limbs (usually lower legs) due to loss of blood supply. When bacterial infection occurs it leads to wet gangrene (a mix of coagulative and liquefactive necrosis).

A

Gangrenous Necrosis

94
Q

Seen in tuberculosis infection, with cheese like, yellow white appearance.

A

Caseous Necrosis

95
Q

Results from fat destruction due to pancreatic lipases, typically seen in acute pancreatitis. (chalky white appearance/area)

A

Fatty Necrosis

96
Q

Seen in immune reaction where antigen-antibody complexes and leaked fibrin deposit in artery walls.

A

Fibrinoid Necrosis

97
Q

What are the Fate Necrosis:

A
  • Persistence
  • Phagocystosis
  • Calcification
98
Q

Necrotic cells may remain in the tissue for sometime before being removed.

A

Persistence

99
Q

Dead cells may be engulfed and digested by neighboring cells or immune cells.

A

Phagocytosis

100
Q

Dead cells can accumulate calcium salts, leading to calcification, where the cell’s remnants turn into hard, chalky deposits.

A

Calcification

GENERAL PATHOLOGY (3 decks)

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