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Flashcards in 54-Breakdown of Homeostasis Deck (66)
1

What is homeostasis

normal steady state

2

What happens when cells encounter physiologic stress

They must adapt, get injured, or die

3

What is the most crucial event in evolution of disease

Cell death

4

What happens after prolonged or severe injury

Cell death-necrosis or apoptosis

5

What are the cellular adaptations to stress

Atrophy
Hypertrophy-physiologic or pathologic
Hyperplasia-physiologic or pathologic
metaplasia

6

What is atrophy

Shrinking of cell to preserve function and survive

7

What is hypertrophy

Cell enlarges, limited capacity to divide

8

What is hyperplasia

More cells are produced if they are capable of replication

9

What is metaplasia

Differentiation from one adult cell type to another

10

What happens to skeletal muscle when it loses its innervation

denervation-atrophy, become small and angular

11

What causes atrophy

Decreased workload
loss of innervation
Diminished blood supply
Inadequate nutrition
Loss of endocrine
aging

12

what is an example of pathologic hypertrophy

Hypertension and enlargement of heart
Muscular Dystrophy

13

What is an example of physiologic hypertrophy

Pregnancy from estrogen

14

What is an example of physiologic hyperplasia

Pregnancy and proliferation of breast tissue

15

What is the difference between hyperplasia and cancer

Hyperplasia is tightly controlled
Cancer has uncontrolled growth

16

What is an example of metaplasia

Chronic smokers
Change of epithelium in branches from columnar to squamous

Gain survival, but loss of protection like mucous secretion and cilia

17

Why does metaplasia occur

One cell type is sensitive to stress and is replaced by a type that can withstand the stress to try to survive

18

What causes cell injury

EVERYTHING
Intrinsic-genetic
Acquired-everything else

19

What does cell response to injurious stimuli depend on

Type, duration, severity

20

What are the consequences of injurious stimulus

Cell type, status, adaptability, genetic make up

21

Where are the sites of vulnerability for cell injury

Mitochondria, calcium, membrane, protein and DNA integrity

22

What are the morphologic changes from injury

Biochemical changes
They are time dependent

23

What does mitochondrial damage lead to

ATP depletion and increase ROS, necrosis and apoptosis

24

ATP depletion is due to what

Decreased oxygen, reduced nutrients, mitochondrial damage, toxins

25

If you have ATP depletion what can you test for

Lactic acidosis in serum blood test

26

Increase ROS leads to what

Damaged lipids, proteins, DNA

27

How does reduced ATP affect cells

Reduced ATP dependent sodium and calcium pumps, anaerobic glycolysis (lactic acid production and decreased pH), disruption of protein synthesis

28

How are ROS formed

Produced normally during redox reactions
Produced by phagocytic leukocytes (neutrophils and Macs) for destroying microbes

29

How does ROS contribute to disease

Cancer-mutation from free radicals
atherosclerosis-plaque formation
Aging-accumulative damage
Toxicology-acetaminophen toxicology
hypoxia

30

What are the sources of calcium

mitochondria, ER, extracellular space

31

What does increased calcium do

activate enzymes which leads to:
Membrane damage
Nuclear damage
Decreased ATP
trigger apoptosis

32

Most important sites of membrane damage are

Mitochondrial, lysosomal, plasma

33

What does damage to lysosomal membranes do

leak enzymes and digest cell components

34

What does damage to DNA and proteins lead to

Accumulation of damaged DNA, misfolded proteins.

35

What happens when damage exceeds repair mechanisms

apoptosis

36

What is ischemia

Decreased blood flow leading to loss of oxygen and nutrients

37

Does ischemic or hypoxic lead to faster injuries

ischemia

38

What is hypoxia

Decreased oxygen delivery, use anaerobic glycolysis as result

39

What happens to oxygen deprived cells

Decreased ATP, mitochondrial damage, accumulation of ROS, Ca influx

40

What happens during the sequence of changes in cell injury

Quickly lose cell function, but still reversible injury
Death and irreversible, biochemical alterations
ultrastructural changes (EM)
Light microscope changes (AP)
Gross morphological changes

41

How can you reverse cell injury

During early stages if damaging stimulus is removed

42

What are the 2 morphological correlates in reversible injury

Cell swelling
Fatty change

43

What causes cell swelling in reversible injuries

Failure of energy ion pumps, inability to maintain ionic and fluid homeostasis

44

What happens in reversible cell swelling

Loss of microvilli, swollen mitochondria, membrane blebbing

45

What happens in fatty change

Clear lipid vacuoles in cells participating in fat metabolism, caused from chronic alcohol use

46

What 2 characteristics cause irreversibility

Cannot correct mitochondria dysfunction
Profound disruption of membranes

47

What are the common early changes in necrosis

hypereosinophilia-really pink
vacuolization
Nuclear changes (pkynosis, karyorrhexis, karyolysis, disappearance)

48

What are the later changes in necrosis

Coagulation and liquefaction

49

What is coagulative necrosis

autolysis-intrinsic source
Preservation of cell outlines

50

What is a type of coagulative necrosis

Myocardial infarction, ischemic injury

51

What is liquefactive neccrosis

heterolysis-extrinsic source
Loss of cell outline

52

What is a type of liquefactive necrosis

Bacterial abscess

53

What is caseous necrosis

TB infection!!
Cheese like appearance
Aggregate of granular pink material
tissue architecture obliterated

54

What is fat necrosis

Fat destruction from release of pancreatic lipases, liquefy membranes of fat cells

Microscopically-shadowy outline with basophilic calcium deposits

55

What is fibrinoid necrosis

Immune reaction with antigens and antibodies in walls of arteries
Bright pink appearance

56

What is dystrophic calcification

Calcification in dead or dying tissues, seen in plaques

57

What causes intracellular accumulation

Abnormal metabolism
Abnormal protein folding and transport
enzyme defect
Incomplete lysosomal degradation

58

What are some intracellular accumulations

Lipids, proteins, glycogen, pigments

59

What accumulates in Alzheimer's

tau proteins

60

Is necrosis physiologic or non physiologic

ALWAYS PATHOLOGIC

61

What are the 2 ways to initiate apoptosis

Mitochondrial/intrinsic
Death receptor/extrinsic

62

nonmorphologic characteristics of necrosis

Pathologic, no gene transcription, unregulated, no energy, lysosome disruption, cell membrane leakage

63

Non morphologic characteristics of apoptosis

Physiologic and non physiologic
Gene transcription
Highly regulated
Needs energy
Cleave chromatic
Lysosome intact
cell membrane intact

64

Morphologic characteristics of necrosis

Death of groups
karyolysis and karyorrhexis
organelles destroyed
Swelling
Inflammatory response

65

Morphologic characteristics of apoptosis

Death in individual cells
Chromatic clumping
Organelles preserved
Cell shrinkage
No inflammation

66

Biochemical pathway that can be manipulated by pharmacology

Apoptosis-cancer