GP 04 - Cellular Adaptation and Inflammation Flashcards

1
Q

In general, what is cellular adaptation? Is it physiological or pathological?

A

Cellular adaptations are reversible changes in the number, size, phenotype, metabolism, or functions of cells in response to changes in their environment. These adaptations can be either physiological (e.g. - in response to hormonal stimuli) or pathological (e.g. - in response to stress in order to avoid injury).

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2
Q

List the patterns of cellular adaptation

A
  1. Atrophy
  2. Hypertrophy
  3. Hyperplasia
    1. Metaplasia
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3
Q

What is a premalignant condition?

A

A premalignant (aka - precancerous) condition is a term used to describe certain conditions of lesions involving abnormal cells which are at an increased risk of becoming cancerous

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4
Q

Describe what atrophy is and what its most common causes are.

A

It is a decrease in size and function of cells (not a decrease in #). It is usually caused by:

  • Decreased blood supply
  • Loss of innervation
  • Loss of trophic signals
  • Decreased workload
  • Aging
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5
Q

Describe what hypertrophy is and what usually causes it.

A

Hypertrophy is the increase in size (not #) of cells due to increased functional demands. It can be either physiological (e.g. - enlargement of uterus during pregnancy) or pathological (e.g. - cardiac muscle during hypertension)

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6
Q

Why would a cell hypertrophy when it could just divide?

A

Hypertrophy occurs mainly when the cell has limited capacity to divide

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7
Q

What is hyperplasia and how does it relate to hypertrophy?

A

Hyperplasia is an increase in the number of cells, stimulated by growth factors. Hyperplasia and hypertrophy are distinctly different but they can occur at the same time

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8
Q

Describe the types of hyperplasia.

A
  • Physiologic Hyperplasia
    • In response to hormones (e.g. - mammary epithelium druing puberty/pregnancy)
    • Compensatory (e.g. - residual tissue grows after removal of part of an organ)
  • Pathologic Hyperplasia
    • Occurs when there is disturbance in the balance of the hormonal stimuli (e.g. - excessive TSH causing thyroid enlargement)
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9
Q

What distinguishes hyperplasia from cancer?

A

If the growth factor that initiated the hyperplasi is removed, the growth stops. In cancer, growth continues

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10
Q

Describe what metaplasia is and what causes it.

A

Metaplasia is a reversible change in which one adult cell type is replaced by another adult cell type. This occurs in response to stress because the new cell type is more able to withstand the stress. There is stem cell reprogramming and not just a phenotypic change of already differentiated cells.

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11
Q

What is dysplasia?

A

If the insult causing metaplasia presists, the metaplastic population begins to grow and mature in an increasingly disordered manner. This is still reversible if the insult is removed but can develop into a neoplasm if it is not.

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12
Q

Out of the following, which are considered to be premalignant:

  • Atrophy
  • Hyperplasia
  • Metaplasia
  • Dysplasia
A

Dysplasia

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13
Q

What are the primary factors that lead to cellular aging?

A
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14
Q

What is the arrow pointing to in this image?

A

Lipofuscin accumulations in aging cells

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15
Q

What has happened to this tissue?

A

Hypertrophy

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16
Q

What is this a photo of?

A

Squamous metaplasia of the respiratory epithelium

17
Q

What is this an example of?

A

Hypertrophy

18
Q

What is happening with the tissue here?

A

Hyperplasia

19
Q

What is happening in this image?

A

Atrophy

20
Q

What is this a photo of?

A

Columnar metaplasia of the esophagus

21
Q

What is the purpose of inflammation?

A
  • Removal of the injurious agent and necrotic tissue through a series of vascular and cellular changes
  • Setting the base for the tissue healing and repair process
  • Setting the bases of the long lived, more specific, adaptive immune response
22
Q

What are the major drawbacks of inflammation?

A
  • Inflammatory reaction may cause or exacerbate tissue injury
  • Can cause pain
  • Can fail to resolve leading to complication (e.g. - abscess)
  • Can occur at inapropriate times (e.g. - allergic reactions and autoimmunity)
23
Q

List the general sequence of events to inflammation

A
  1. The offending agent, which is located in extravascular tissues, is recognized by host cells and molecules
  2. Leukocytes and plasma proteins are recruited from the circulation to the site
  3. The leukocytes and plasma proteins become activated and work together to destroy and eliminate the offending agent
  4. The above reaction is terminated
  5. The damaged tissue is repaired
24
Q

What basic information do we need to know about acute inflammation.

A
  • It is the initial rapid response to tissue injury
  • It develops within minutes to hours
  • It lasts for several hours or days
  • Characterized by the presnece of exudate
  • Predominant leukocyte is the neutrophil
25
Q

What basic information do we need to know about Chronic inflammation?

A
  • It develops slowly and is of longer duration
  • It is associated with more tissue destruction
  • Its predominant leukocytes are lymphocytes and macrophages
26
Q

What are the cardinal signs of inflammation?

A
  • Heat (calor)
  • Redness (rubor)
  • Swelling
  • Pain (dolor)
  • Loss of function
27
Q

How does the body recognize microbes and damaged cells?

A
  • Cellular receptors (most notably toll-like receptors) recognize microbes
  • Upon introduction to the body, some microbes can be coated by antibodies (IgG), complement proteins (C3), and collectins (opsonization) which can be recognized by leukocytes, leading to the release of cytokines and initiation of the inflammatory process
  • Certain circulating proteins like mannose-binding lectin and collectins can recognize microbial sugars or proteins and then activate the complement system
  • All cells have cytosolic receptors that recognize a diverse set of molecules that are only liberated or altered when the cell is damaged. Once stimulated, these receptors activate a multiprotein cytosolic complex called the inflammasome, which induces the production of cytokines