Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology > Adaptation > Flashcards

Adaptation Flashcards

1
Q

Cellular adaptation types

A

Hypertrophy, hyperplasia, atrophy, metaplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Signals of hypertrophy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Atrophy

A

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

Physiologic or pathologic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Atrophy is caused by

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Autophagy

A

Starved cell eats its own components to find nutrients & survive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Dysplasia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Lysosomal Catabolism

A

Lysosomal digestion of proteins & carbohydrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Heterophagy

A

lysosomal digestion of materials from extracellular environment taken up through endocytosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Autophagy

A

lysosomal digestion of cell’s own components

Common in removal of damaged organelles & cellular remodeling; atrophy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Induction of smooth ER

A

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

20
Q

Mitochondrial alterations

A

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

21
Q

Cytoskeletal abnormalities

A

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

22
Q

Intracellular accumulations

A

Storage of some product by individual cell; metabolic derangement

23
Q

Mechanisms of intracellular accumulations

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)

A

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

25
Q

Most common cause of Steatosis

A

Alcohol & diabetes associated with obesity

26
Q

Atherosclerosis

A

plaques, smooth muscle, & macrophages within intimal layer of aorta & large arteries fill with lipid vacuoles (cholesterol) - foam cells
Aggregates produce yellow atheromas

27
Q

Xanthoma

A

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
Q

Cholesterolosis

A

Cholesterol causes gallstones to form in gallbladder

Eventually yellow foam cells turn gallbladder strawberry colored

29
Q

Protein accumulations

A

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
Q

Mallory bodies

A

alcoholic hyaline seen in alcoholic liver disease

Eosinophilic intracytoplasmic inclusions composed of cytoskeletal filaments

31
Q

Chaperones (Heat shock proteins)

A

aid in proper protein folding & transport
Repair misfolded proteins
Degrade damaged protein

32
Q

Ubiquitin

A

Marks abnormal protein for degradation by proteosomal complex

33
Q

Response to accumulation of misfolded proteins due to mutation or stress

A

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
Q

Hyaline change

A

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
Q

Glycogen deposits

A

appear as clear cytoplasmic vacuoles
due to abnormalities in metabolism of glucose or glycogen
Ex: diabetes mellitus & glycogen storage diseases (Pompe disease)

36
Q

Most common exogenous pigment

A

carbon

37
Q

Carbon stored in

A

macrophages & transported through lymphatics to regional lymph nodes

38
Q

Anthracosis

A

darkened lymph nodes & lung tissue from carbon accumulation

Heavy accumulation may be toxic

39
Q

Lipofuscin

A

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
Q

Melanin

A

Endogenous, non-hemoglobin-derived brown-black pigment formed in melanocytes from tyrosine in epidermis
Screen against UV-radiation

41
Q

Hemosiderin

A

Hemoglobin derived, golden-yellow-brown granular pigment

During excess of iron, ferritin forms hemosiderin granules

42
Q

Hemosiderosis

A

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
Q

Bilirubin

A

Major pigment found in bile; hemoglobin-derived but contains no iron
Excess bilirubin causes jaundice

44
Q

Pathologic calcification

A

abnormal deposition of calcium salts, mixed with smaller amounts of other mineral salts

45
Q

Dystrophic calcification

A

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
Q

Metastatic calcification

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions