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Pathology > Adaptation > Flashcards

Adaptation Flashcards

(46 cards)

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1
Q

Cellular adaptation types

A

Hypertrophy, hyperplasia, atrophy, metaplasia

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2
Q

Hypertrophy

A

Increase in cell size due to increased synthesis of structural proteins causing increase in size of organ
No new cells
Physiologic or pathologic

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3
Q

Boxcar nuclei

A

Seen in hypertrophy

Nuclei become large & square because they have to create more proteins to keep up with increased work

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4
Q

Signals of hypertrophy

A

Mechanical triggers - stretch from increased workload
Vasoactive agents - alpha-adrenergic agonist
Growth factors - TGF-beta

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5
Q

Hypertrophy limited by

A

muscle enlargement no longer compensating for increased burden
Causes degeneration & fragmentation
(Cardiac failure & loss of heart cells if in heart)

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6
Q

Hyperplasia

A

Increase in number of cells in response to stimulus or persistent cell injury, usually results in increase size & weight of organ or tissue
Often occurs with hypertrophy
Can be physiologic or pathologic
Cells must be capable of replication

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7
Q

Pathologic hyperplasia

A

Most due to excessive hormones or growth factors acting on target cells
Ex: Endometrial hyperplasia, Benign prostatic hyperplasia, thyroid during Graves Disease

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8
Q

Atrophy

A

Reduced size of organ/tissue due to decrease in cell size

Physiologic or pathologic

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9
Q

Atrophy is caused by

A

Decreased workload, loss of innervation, decreased blood supply, inadequate nutrition, loss of endocrine stimulation, pressure

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10
Q

Autophagy

A

Starved cell eats its own components to find nutrients & survive

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11
Q

Metaplasia

A

Reversible change in which one differentiated cell type is replaced by another cell type
Done to better withstand stress; arise from stem cells through genetic reprogramming

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12
Q

Most common form of metaplasia

A

columnar to squamous cell type
Ex: bronchi ciliated columnar cells replaced with stratified squamous in smokers - loose important protective function & transformation can induce cancer

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13
Q

Connective tissue metaplasia

A

formation of cartilage, bone, or adipose tissue in tissue that doesn’t usually contain these
Result of cell or tissue injury

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14
Q

Dysplasia

A

Disordered growth
Most common in squamous epithelial cells following chronic injury
Variations in size & shape, disordered arrangement, nuclear changes

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15
Q

Subcellular responses to injury

A

Distinctive alterations involving only subcellular organelles & cytosolic proteins:
Lysosomal catabolism, Induction of smooth ER, Mitochondrial alterations, Cytoskeletal abnormalities

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16
Q

Lysosomal Catabolism

A

Lysosomal digestion of proteins & carbohydrates

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17
Q

Heterophagy

A

lysosomal digestion of materials from extracellular environment taken up through endocytosis

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18
Q

Autophagy

A

lysosomal digestion of cell’s own components

Common in removal of damaged organelles & cellular remodeling; atrophy

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19
Q

Induction of smooth ER

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A

Smooth ER undergoes hypertrophy as adaptive response to become more efficient at metabolising chemicals/synthesizing phospholipids

20
Q

Mitochondrial alterations

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A

Changes in number, size, & shape
Number increases in hypertrophy & decreases in atrophy
Enlarged during ETOH liver disease & nutritional deficiencies

21
Q

Cytoskeletal abnormalities

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A

Defects in cell function (locomotion, organelle movement); intracellular accumulations of fibrillar material

22
Q

Intracellular accumulations

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A

Storage of some product by individual cell; metabolic derangement

23
Q

Mechanisms of intracellular accumulations

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A
  1. Abnormal metabolism
  2. Alterations in protein folding & transport
  3. Deficiency of critical enzymes
  4. Inability to degrade phagocytosed (exogenous) particles
24
Q

Steatosis (fatty change)

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A

Abnormal accumulations of triglycerides within parenchymal cells - often liver, heart, muscle, kidney

25
Most common cause of Steatosis
Alcohol & diabetes associated with obesity
26
Atherosclerosis
plaques, smooth muscle, & macrophages within intimal layer of aorta & large arteries fill with lipid vacuoles (cholesterol) - foam cells Aggregates produce yellow atheromas
27
Xanthoma
Pts with hereditary hypolipidemia Macrophages in skin take up lipid & form mass under skin - foam cells Have high cholesterol levels Happens around eyes, knees, & Achilles tendon
28
Cholesterolosis
Cholesterol causes gallstones to form in gallbladder | Eventually yellow foam cells turn gallbladder strawberry colored
29
Protein accumulations
Proteins fold wrong & get stuck; reabsorption droplets in proteinuria; synthesis of excessive amounts of normal secretory protein (Russell bodies); cell injury Pink hyaline material in cytoplasm
30
Mallory bodies
alcoholic hyaline seen in alcoholic liver disease | Eosinophilic intracytoplasmic inclusions composed of cytoskeletal filaments
31
Chaperones (Heat shock proteins)
aid in proper protein folding & transport Repair misfolded proteins Degrade damaged protein
32
Ubiquitin
Marks abnormal protein for degradation by proteosomal complex
33
Response to accumulation of misfolded proteins due to mutation or stress
Increased synthesis of chaperones to help folding Decreased translation of proteins to reduce misfolded protein accumulation Activation of ubiquitin to mark proteins for degradation If not solved, will lead to apoptosis
34
Hyaline change
Non-specific morphologic change - glassy, pink homogenous appearance Intracellular: protein droplets in tubules, Russell bodies, Mallory bodies, viral inclusions Extracellular: collagenized scar, damaged glomeruli, amyloid
35
Glycogen deposits
appear as clear cytoplasmic vacuoles due to abnormalities in metabolism of glucose or glycogen Ex: diabetes mellitus & glycogen storage diseases (Pompe disease)
36
Most common exogenous pigment
carbon
37
Carbon stored in
macrophages & transported through lymphatics to regional lymph nodes
38
Anthracosis
darkened lymph nodes & lung tissue from carbon accumulation | Heavy accumulation may be toxic
39
Lipofuscin
insoluble, brownish-yellow granular intracellular material Accumulate in heart, liver, brain, & other tissue Non-injurious (marker of past free radical injury); associated with aging
40
Melanin
Endogenous, non-hemoglobin-derived brown-black pigment formed in melanocytes from tyrosine in epidermis Screen against UV-radiation
41
Hemosiderin
Hemoglobin derived, golden-yellow-brown granular pigment | During excess of iron, ferritin forms hemosiderin granules
42
Hemosiderosis
systemic overload of iron in many organs & tissues Caused by increased absorption of dietary iron, impaired use of iron, hemolytic anemias, transfusions Can cause liver fibrosis, heart failure, & diabetes
43
Bilirubin
Major pigment found in bile; hemoglobin-derived but contains no iron Excess bilirubin causes jaundice
44
Pathologic calcification
abnormal deposition of calcium salts, mixed with smaller amounts of other mineral salts
45
Dystrophic calcification
local process; occurs in injured or dying tissues, can cause organ dysfunction; seen in atherosclerotic plaques, aging or damaged heart valves, areas of necrosis
46
Metastatic calcification
reflects increased serum calcium; can happen anywhere (mainly interstitial tissue of blood vessels, kidneys, lungs, & gastric mucosa); characterized by hypercalcemia, usually no dysfunction unless severe

Pathology (6 decks)

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