Exam 1: Ch 2 Flashcards Preview

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Flashcards in Exam 1: Ch 2 Deck (62):
1

atrophy

cells decrease in size and activity in response to decreased workload or poor environmental conditions

generally reversible

2

atrophy in muscle

decrease in oxygen consumption, # of mitochondria, and # of myofilaments

3

causes of atrophy

disease

denervation

poor nutrition

ischemia

decreased endocrine stimulation (IGF 1)

4

hypertrophy definition and 2 types

cells increase in size in response to increased workload

physiologic or pathologic

5

physiologic hypertrophy

increased muscle size with exercise

6

pathologic hypertrophy

response to disease

Hypertension

Valvular heart disease

7

excessive hypertrophy is _____

counterproductive

8

signals for hypertrophy

hormonal (IGF1, EGF, growth factors)

mechanical (HTN)

9

hyperplasia

increase in the number of cells (usually epithelial or connective tissue)

Tissues with cells capable of mitotic division

10

3 examples/types of hyperplasia

hormonal: breast enlargement with pregnancy

compensatory: liver cell division after partial hepatectomy

wound healing

11

metaplasia

change in cell type

results from chronic inflammation/irritation (if untreated can turn into dysplasia)

ex. cilliated columnar epithelium --> stratified squamous in airways of smokers

12

dysplasia

higher deranged cell growth (usually from inflammation)

precursor to cancer

ex. abnormal pap smear of cervix

13

intracellular accumulations

cells build up substances they cannot eliminate

14

categories of substances in intracellular accumulations

normal substances present in excess (jaundice, lipofuscin)

products of abnormal metabolism (lipids in brain --> Tay-Sachs, glycogen in liver ---> Von Gierke)

exogenous substances (blue line in gum tissue from lead poisoning)

15

dystrophic calcification

deposits of calcium phosphate crystals in injured tissue

calcium found in atheroscletotic lesions or heart valves

16

metastatic calcification

deposits of Ca in normal tissues when serum Ca is high

occurs in lungs, blood vessels, and kidneys

17

3 causes of metastatic calcification

Paget's disease (excessive osteoclast activity)

renal failure (phosphate retention)

cancer

Hyperparathyroidism

18

what can cause cell injury

physical agents

radiation

chemicals

biological agents

nutritional imbalances

19

cell injury: physical agents

mechanical trauma: damages tissues/blood vessels

temperature: burns, frostbite--destroy blood flow

electrical: disrupt cardiac and nervous system, burn

20

3 types of radiation

ionizing

nonionizing -- thermal damage

UV

21

ionizing radiation

kills immediately/causes genetic damage

endothelium most vulnerable --> blood vessel damage, burns, enteritis

chronic damage --> fibrosis/scarring

22

UV radiation

sunburn

increased skin cancer risk (DNA damage)

23

cell injury: chemicals

drugs: directly toxic/toxic metabolites

lead: paint, old pipes, air, industrial exposure

mercury: industrial/medical sources

24

lead toxicity

absorbed through GI & respiratory tract

stored in bones and teeth

blocks brain development (demyelization) and is toxic to RBS (anemia)

25

lead is particularly toxic to _______

children

CDC says blood lead [ ] > 5 micrograms/dL is dangerous

26

mercury toxicity

interferes with brain development

children/pregnant women at risk

predator fish contain mercury

27

cell injury: biological agents

viruses

bacteria

parasites

28

cell injury: nutritional imbalance

excesses or deficiencies

29

what is a free radical (ROS--reactive oxygen species)

chemical with unpaired electron in outer shell-- highly
unstable

product of normal metabolism (convert O2 to ROS)

product of increased reperfusion --> overwhelm protective mechanisms

30

free radical injury

damages organelles (mitochondria) and DNA

may contribute to ALS, aging, other diseases

31

which vitamins are free radical scavengers?

C & E

32

hypoxia

oxygen deprivation

induction of genes for hypoxia inducible factors (HIF) --> increased RBC & angiogenesis

if severe, ATP production is interrupted

33

hypoxic cell injury

time until damage depends on cell's energy requirement

permanent damage in 4-6 min for brain

pH falls, Na/K pump fails

34

hypoxia in rats

epithelial cells of kidney tubules can survive 20-30 min

anything greater than that decreases O2 delivery to tissues and produces hypoxic damage

35

_____ is important as a 2nd messenger

calcium

36

impaired calcium movement

levels must be kept very low

ischemia and toxins disrupt the ability of cells to exclude calcium

intracellular enzymes are released/activated and cell destroys itself

37

reversible cell injury

Na/K pump fails and causes swelling (hypoxic damage)

intracellular fat accumulations: associated with high serum fat

38

2 types of lethal cell injury

necrosis

apoptosis

39

apoptosis

programmed cell death

eliminates excess and damaged cells

eventually membrane is disrupted and debris consumed by phagocytes

40

apoptosis and cancer

important in normal development and destruction of cancer cells

cancer cells learn to escape apoptotic signals

p53 gene inactivated ---> cancer

41

diseases involving overstimulation of apoptosis

ALS

Parkinson's

Alzheimer's

42

2 types of apoptosis pathways

extrinsic

intrinsic

both activate endonucleases --> DNA fragments

43

extrinsic apoptosis

activation of death receptors like TNF or Fas ligand receptor

death domain activated

procaspases --> caspases (activated form) in cascade

44

intrinsic apoptosis

multiple inputs damage mitochondria

caspase cascade activated

45

necrosis

uncontrolled cell death that is not pre-programmed

46

types of necrosis

liquefaction

coagulation

caseous (form of coagulation)

47

liquefaction necrosis

cells die but enzymes remain active

dead tissue is soft

seen in infection

ex. flesh eating bacteria (meningococcemia)

48

coagulation necrosis

area becomes hard

acidosis destroys enzymes

seen in ischemia/infarction

ex. dry gangrene, avascular necrosis

49

caseous necrosis

fatty infiltrates

seen in interior of TB lesions

50

gangrene

large mass of necrotic tissue

51

3 types of gangrene

dry

wet

gas (type of wet)

52

dry gangrene

type of coagulation necrosis

caused by interruption of arterial blood flow

line of inflammation between healthy/dead tissue

can progress to wet gangrene with infection

53

wet gangrene

type of liquefaction necrosis from infection

caused by venous obstruction or infection

area cold, swollen, pulseless

rapid spread

54

gas gangrene

type of wet gangrene (which is a type of liquefaction necrosis)

wound infection from Clodtridium bacteria

commonly following dirty trauma, bowel obstruction/rupture

bacteria product hydrogen sulfide gas --> tissue death

debridement, antibiotics, maybe amputation

55

cellular aging

normal process that decreases organ system function over time

may reflect accumulation of environmental and genetic damage

56

replicative senescence

cells can divide a fixed number of times (Hayflick limit)

involves shortening of telomeres

telomerase is active in germ cells/cancer cells

57

genetic influences on cellular aging

some gene alleles protect against chronic disease (increases longevity)

58

progeria

genetic defect that causes premature aging

59

gene

DNA that codes for a protein

60

cellular adaptation

how cells respond to persistent stress by activating gene pathways

61

ARDS

acute respiratory distress syndrome

systemic infection

62

DIC

disseminated intravascular coagulation

systemic infection

clotting factors/platelets get used up -- excessive bleeding