CR1 KCP1 Cellular Adaptation

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25 Terms

1
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What are the three cell types based on their proliferative capacity?

Labile cells (continuously dividing), Stable cells (quiescent, can divide upon injury), and Permanent cells (unable to divide).

2
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Give two examples of Labile cells.

Keratinocytes and intestinal epithelial cells.

3
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Give two examples of Stable cells.

Hepatocytes and renal tubular epithelial cells.

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Give two examples of Permanent cells.

Neurons and cardiac myocytes.

5
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What molecules regulate transitions through cell cycle phases?

Cyclins and Cyclin-Dependent Kinases (CDKs).

6
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What is checked at the G1/S cell cycle checkpoint?

Checks for DNA damage before allowing chromosome duplication in the S phase.

7
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What is checked at the G2/M cell cycle checkpoint?

Checks for damaged or unduplicated DNA before the cell enters mitosis (M phase).

8
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What causes reversible cell injury vs. irreversible cell injury?

Reversible injury is caused by mild, transient stimuli; Irreversible injury is caused by severe, progressive stimuli (including DNA damage).

9
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What are two classic morphological signs of reversible cell injury?

Cellular swelling and fatty change.

10
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What are the two forms of cell death resulting from irreversible injury?

Necrosis and Apoptosis.

11
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Define Hypertrophy and state its cellular mechanism.

An increase in cell size (and organ size) due to increased production of cellular proteins and organelles without changing cell division rates.

12
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Give one physiologic and one pathologic example of Hypertrophy.

Physiologic: Skeletal muscle enlargement in bodybuilders or pregnant uterus. Pathologic: Left ventricular hypertrophy from chronic hypertension or aortic stenosis.

13
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Define Hyperplasia and state its cellular requirement.

An increase in the number of cells in an organ/tissue. Requirement: The cell population must be capable of dividing (labile or stable cells).

14
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Give one physiologic and two pathologic examples of Hyperplasia.

Physiologic: Female breast at puberty/pregnancy or liver regeneration. Pathologic: Endometrial hyperplasia, Benign Prostatic Hyperplasia (BPH), or ductal epithelial hyperplasia.

15
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Why is pathologic hyperplasia clinically significant?

It constitutes a fertile soil in which cancerous mutations may eventually arise.

16
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Define Atrophy and name its two main molecular degradation pathways.

Reduction in cell size and number. Pathways: 1. Ubiquitin-proteasome pathway (protein degradation); 2. Autophagy (cell digests its own organelles).

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List 6 causes of pathologic atrophy.

Decreased workload (disuse), loss of innervation, diminished blood supply, inadequate nutrition, loss of endocrine stimulation, and pressure/aging.

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Define Metaplasia and state its mechanism.

Replacement of one adult cell type with another adult cell type. Mechanism: Reprogramming of tissue stem cells.

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Describe respiratory tract metaplasia in smokers.

Ciliated columnar epithelium is replaced by stratified squamous epithelium to resist chronic smoke irritation.

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Describe esophageal metaplasia in Barrett esophagus.

Stratified squamous epithelium is replaced by intestinal columnar epithelium due to chronic acid reflux.

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Define Dysplasia and state its key histological features.

Disordered growth characterized by loss of cellular uniformity and loss of architectural orientation (principally in epithelia).

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Is Dysplasia reversible or irreversible?

Mild to moderate dysplasia may be completely reversible if the stimulus is removed.

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What is Carcinoma-in-situ?

Severe dysplastic changes involving the full thickness of the epithelium while remaining strictly confined by the basement membrane.

24
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Define Dystrophy vs. Anaplasia.

Dystrophy: Degeneration/breakdown of tissue or organ. Anaplasia: Total loss of cellular differentiation (hallmark of cancer).

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A 45-year-old woman with hypertension has a shrunken right kidney due to renal artery stenosis. What is the adaptive mechanism?

Atrophy caused by diminished blood supply (reduced oxygen and nutrients).