Chapter 2 Part 1 Flashcards

1
Q

What are the four aspects of disease that form the core of pathology?

A

Etiology, pathogenesis, morphologic changes, and clinical manifestations

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2
Q

Definition of disease

A

Deviation from the normal structure or function of a part of an organ or system as manifested by symptoms and signs

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3
Q

Definition of disorder

A

Abnormality of function, morbid physical or mental state

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4
Q

Definition of neoplasm

A

New and abnormal growth, uncontrolled and progressive

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5
Q

Definition of Syndrome

A

A set of symptoms that occur together

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6
Q

Definition of cellular adaptations

A

Reversible functional and structural responses to changes in physiologic and sometime pathologic stimuli, results in a new but altered steady state

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7
Q

Definition of cell injury

A

Sequence of events following a cells exposure to injurious agent, deprivation of nutrients, or excessive mutation beyond which the cell can adapt to

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8
Q

What is a cell’s response to an injurious stimulant that causes increased demand and stimulation?

A

Hypertrophy and hyperplasia

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9
Q

What is a cell’s response to decreased nutrients and stimulation?

A

Atrophy

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10
Q

What is a cell’s response to chronic irritation?

A

Metaplasia

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11
Q

Definition of hypertrophy

A

increase in size of a cell resulting in the overall increase of the organ

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12
Q

What is the most common stimulus for hypertrophy?

A

increased workload

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13
Q

Hypertrophy is the result of what cellular process?

A

Increased protein production

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14
Q

What are the three stimulants that trigger cardiac hypertrophy?

A

Mechanical sensors, growth factors, vasoactive agents

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15
Q

What are the signal transduction pathways involved in muscular hypertrophy

A

PI3K/AKT pathway and GPCR downstream

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16
Q

What transcription factors are activated by the signal transduction pathways involved in muscular hypertrophy?

A

GATA4, NFAT, MEF2; work together to increase proteins responsible for hypertrophy

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17
Q

What protein switches are associated with contractile proteins in hypertrophy?

A

alpha isoform being replaced by the beta isoform (neonate form)

18
Q

What is one change in gene expression seen in cardiac hypertrophy?

A

Gene for ANF is expressed in atrium and ventricle in embryo heart and will be downregulated after birth. However, it may be increased as a result of cardiac hypertrophy in order to reduce load

19
Q

Definition of hyperplasia

A

increase in number of cells in response to a stimulus

20
Q

What causes physiologic hyperplasia?

A

hormones or growth factors released in excess due to an increase in functional capacity of hormone sensitive organs or if there is a need for a compensatory change

21
Q

What is an example of hormonal hyperplasia?

A

Growth of breast tissue in response to pregnancy?

22
Q

What is an example of compensatory hyperplasia?

A

Liver regeneration after a partial hepatectomy

23
Q

What causes pathologic hyperplasia?

A

excess or inappropriate actions of hormones or growth factors

24
Q

What is the pathogenesis of endometrial hyperplasia?

A

A disruption of estrogen and progesterone balance can result in an increase of Estrogen. This increase causes hyperplasia of the endometrial glands leading to abnormal menstrual bleeding.

25
What is one characteristic response to certain viral infections in cells?
Viruses interfere with host proteins that regulate cell proliferation and cause HYPERTROPHY
26
What are the two main mechanisms involved in hyperplasia?
growth factor-driven proliferation of mature cells, increased output of new cells from tissue stem cells
27
Definition of atrophy
reduction in size of an organ or tissue due to a decrease in cell size and number
28
Describe atrophy as it correlates to decreased workload
when a fractured bone is placed in a cast, skeletal muscle atrophy quickly begins, initially cell shrinking then apoptosis
29
Describe atrophy as it correlates to loss of innervation
Damage to nerves that contribute to metabolism and function of skeletal muscle results in atrophy
30
Describe atrophy as it correlates to diminished blood supply
a gradual in decrease in blood flow as a result of an arterial occlusion will cause tissues to atrophy
31
Describe atrophy as it corelates to inadequate nutrition
After glucose and adipose stores have been depleted, the body utilizes proteins of skeletal muscle causing the breakdown and damage of these cells
32
Describe atrophy as it correlates to loss of endocrine stimulation
Loss of a hormone (such as estrogen) can result in loss of stimulation and growth (breast tissue)
33
Describe atrophy as it correlates to pressure
Ischemic changes caused by a compromise of blood supply by pressure causing agent may lead to tissue destruction
34
What is the main mechanism of atrophy?
Protein degradation by the ubiquitin-proteasome pathway, may also be accompanied by autophagy
35
Definition of metaplasia
a reversible change where one differentiated cell type is replaced by another (cell replaced by another cell that can better withstand and adapt to the ongoing stress)
36
What is the most common type of epithelial metaplasia and what are some causes?
columnar to squamous, especially in respiratory tissue due to chronic irritation; also caused by stones in excretory ducts, vitamin A deficiency
37
What type of metaplasia is seen in Barrett esophagus?
squamous to columnar
38
What is the main mechanism of metaplasia?
Reprogramming of stem cells that exist in tissues, a dysregulation of proteins involved in cell differentiation and growth is commonly seen in metaplasia
39
What are some hallmarks of reversible cell injury?
Reduced oxidative phosphorylation and subsequent ATP reduction and cell swelling due to changes in ion concentrations and water influx
40
What are the seven common causes of cell injury?
Oxygen deprivation, physical agents, chemical agents, infectious agents, immunologic reactions, genetic derangements and nutritional imbalances
41
What are some morphologic features seen in reversible cell injury?
cellular swelling and fatty change
42
What are the ultrastructural changes seen in reversible cell injury?
Plasma membrane alterations, mitochondrial changes, dilation of ER, nuclear alterations