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Gen Path > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Origin of a disease; understanding this can lead to prevention

A

Etiology

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2
Q

mechanism of a disease (from normal to abnormal); can develop disruptions in this process to treat disease.

A

Pathogenesis

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3
Q

Cellular injury results from _____

A

a disruption of one or more cellular components that maintain cellular viability.

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4
Q

When do the first clinical signs/symptoms of disease show up?

A

Far removed from the start of the morphologic and biochemical changes associated with cell injury.

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5
Q

Injury in one part of the cell can ____.

A

induce a cascade of effects.

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6
Q

Cell injury results in?

A

cell adaptation
cell death
or can be reversed

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7
Q

What are some causes of cell injury?

A

oxygen deprivation
infectious agents - bacteria, viruses, fungi, and parasites
physical agents - trauma, electricity, pollutants, burns, UV light, radiation
chemical agents and drugs - tobacco, alcohol, poisons, Rx/OTC drugs
immunologic reactions - allergies and autoimmune disease
genetic derangement - genetic mutations, chromosome abnormalities
nutritional imbalance - obesity, malnutrition, vitamin defeciency

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8
Q

Cellular structures that maintain cell viability -

A

plasma membrane
mitochondria
nucleus
macromolecular synthesis (proteins, nucleotides, carbs, lipids)

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9
Q

What biochemical mechanisms can be disrupted during cell injury? (hint: think about the cellular structures that maintain cell viability)

A 
ATP depletion
generation of ROS (oxidative stress)
loss of calcium homeostasis
altered plasma membrane permeability
mitochondrial damage
DNA/protein damage
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10
Q

Cell injury by reduced energy production is caused by ___?

A

decreased oxygen or no oxygen

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11
Q

Decreased Oxygen

A

hypoxia

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12
Q

No oxygen

A

anoxia

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13
Q

What causes reduced oxygen levels?

A

impaired absorption of oxygen
decreased blood flow
disease of blood or blood vessels
inadequate oxygenation of the blood

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14
Q

decreased blood flow

A

ischemia

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15
Q

Decreased oxygen impairs ___ ____ in the mitochondria

A

oxidative phosphorylation

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16
Q

What is a side effect in the cell of a decrease in ATP?

A

plasma membrane’s ability to maintain homeostasis reduces –> increased net gain of solute and isosmotic gain in cytoplasmic water

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17
Q

If the cell has an isosmotic gain (influx in sodium, thus influx of water) what does that lead to?

A

cell swelling w/ formation of cell surface blebs
swelling of mitochondria
dilation of ER

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18
Q

What happens if the ER dilates?

A

detachment of ribosomes from the RER. —> decrease in protein synthesis so you get increased lipid deposition

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19
Q

If oxidative phosphorylation is reduced, what other energy producing pathway kicks in?

A

glycolysis

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20
Q

What happens if glycolysis is increased?

A

lactic acid and inorganic phosphates produced which decreases intracellular pH leading to chromatin clumping

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21
Q

reduced substrate for ATP production

A

hyperglycemia

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22
Q

How are ROS generated in the body?

A

via normal endogenous oxidative reactions in the plasma membrane, mitochondria, cytoplasm, and peroxisomes

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23
Q

If ROS are generated in the body, what is associated with it?

A 
inflammation
oxygen toxicity
chemicals
irradiation
aging
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24
Q

What is considered an ROS?

A

superoxide
hydrogen peroxide
hydroxyl radicals

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25
Q

How does ROS damage cells?

A

lipid peroxidation
protein cross-linking
react with thymidine and guanine to induce single strand DNA breaks

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26
Q

You can reduce the effects of ROS by blocking their initiation or inactivating them.

A

True

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27
Q

How do you inactivate/prevent ROS intracellularly?

A

superoxide dismutase
catalase
glutathione peroxidase

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28
Q

How do you inactivate/prevent ROS extracellularly?

A

vitamins E, A, C and serum proteins that bind free iron and copper

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29
Q

How is cytoplasmic calcium maintained?

A

protein sequestration in the cytoplasm, mitochondria, and ER

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30
Q

What is a final common pathway of cell injury?

A

increased cytoplasmic calcium

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31
Q

What degradative enzymes are activated from high levels of calcium?

A

phospholipases
proteases
endonucleases
ATPase

32
Q

What are other causes of cell membrane injury?

A 
complement - C5 - C9 membrane attack complex
cytotoxic T-cells - perforin
viral
bacterial endotoxins and exotoxins
chemicals
33
Q

Degree of cell injury depends on ______.

A

cell type and its physiologic state

34
Q

Etiologies of reversible cell injury?

A

toxins
infectious agents
hypoxia
thermal injury

35
Q

characteristics of reversible cell injury?

A

acute in nature

cell injury is of short duration and minimal intensity

36
Q

What two types of morphology are associated with reversible cell injury?

A

hydropic (water retention) and fatty (steatosis- organelles retain fat)

37
Q

What are the two morphologic forms of cell death?

A

necrosis

apoptosis

38
Q

___ ____ leads to the release of cellular components into the extracellular environment.

A

cell death

39
Q

ROS cause ___ - ____ breaks in DNA.

A

Single-stranded, cause >30 different base modifications in both purines and pyrimidines. Thymidine and guanine are major sites

40
Q

What are some morphological changes that occur during necrosis?

A

Cell swells
protein denaturation yielding a glassy homogenous pink staining cytoplasm
organelle breakdown –> vacuolated cytoplasm
nuclei changes: karyolysis, pyknosis/karyorrhexis/total loss
inflammation - acute or granulomatous

41
Q

Type of necrosis present depends on….?

A

the patterns of enzymatic degradation and bacterial products present

42
Q

Most common form of necrosis (cytoplasmic proteins are coagulated)
nucleus is lost, but the eosinophilic outline of the cell is retained for a short time prior to the inflammatory response

A

Coagulative Necrosis

43
Q

Tissue is totally digested via lysosomal enzymes during acute inflammation
associated w/ focal bacterial or fungal infections
seen in the central nervous system
pus/purulence

A

Liquefactive Necrosis

44
Q

Associated w/ M. tuberculosis
tissue has white, cheesy appearance
microscopically - amorphous pink granular material w/in a ring of granulomatous inflammation
loss of tissue aritecture

A

Caseous Necrosis

45
Q

Common in trauma to the breast or in pancreatitis
adipose tissue has chalky white-yellow appearance
dead adipocytes give a “soap-bubble” appearance histologically

A

Fat Necrosis

46
Q

Programed cell death

A

apoptosis

47
Q

Morphologic features of apoptosis

A

cell shrinks
chromatin condensation followed by framentation
apoptotic bodies form
phagocytosis of the apoptotic bodies w/o significant inflammatory response

48
Q

Mechanism of apoptosis

A 
intrinsic program
death signals - Fas ligand binds to Fas receptor
removal of trophic signals (hormones)
ROS, radiation, and toxins
effect of cytotoxic T-cells
49
Q

What are the 2 pathways of apoptosis?

A

direct signaling - Fas lignad, TNF binding

regulation of mitochondrial permeability

50
Q

What serves as an on off switch that regulates mitochondria permeability?

A

Bcl 2 gene family

  • Bcl-2 and bcl-x inhibit apoptosis
  • Bax and bak stimulate apoptosis
51
Q

What disrupts the inhibitory effect of Bcl-2 function, favoring apoptosis?

A

Cytochrome-c

52
Q

Mitochondria release ___ which activates certain enzymes to execute apoptosis.

A

calcium

53
Q

What is caused by transgutaminases in response to calcium release?

A

cross-link cytoplasmic proteins

54
Q

What is caused by endonucleases in response to calcium release?

A

cleavage of DNA at the linker regions between nucleosomes

55
Q

How are dead cells removed?

A

phagocytosis by neighboring cells and macrophages

56
Q

How do cells adapt in response to injury?

A

change in size (atrophy or hypertrophy), number (hyperplasia) or differentiation (metaplasia), intracellular accumulations

57
Q

What leads to cellular adaptations?

A

chronic cell injury

58
Q

decrease in cell size and function

A

atrophy

59
Q

What causes cellular atrophy?

A 
decrease in workload
loss of innervation
decreased blood supply (ischemia)
inadequate nutrition
decreased trophic signals
aging
local pressure
60
Q

What do atrophic cells look like?

A

shrunken and reduced in structural components

61
Q

an increase in cell size associated with increase in functional capacity

A

hypertrophy

62
Q

Can hypertrophy be accompanied with hyperplasia?

A

yes organ size may increase too.

63
Q

What causes cellular hypertrophy?

A

responses to trophic signals
normal hormone stimulation - for smooth muscle hypertrophy in pregnant uterus
abnormal hormone stimulation - anabolic steroids to increase muscle size or overproduction of TSH due to iodine deficiency (goiter)
response to increased function - increased skeletal muscle use; increased workload of cardiac muscle

64
Q

increase in the number of cells in a tissue or organ

A

hyperplasia

65
Q

What cells proliferated during hyperplasia?

A

epithelial or stromal cells

66
Q

What stimulates cell proliferation?

A

hormones or cytokines (trophic factors)

67
Q

Hyperplasia may increase the risk for neoplasmic transformation.

A

true

68
Q

What causes hyperplasia?

A

hormones

growth factors

69
Q

What hormones stimulate hyperplasia?

A

endometrial glandular cells during menstrual cycle
gynecomastia
erythrocyte hyperplasia following ectopic production of renal cell carcinoma

70
Q

hyperplasia of the breast in men

A

gynecomastia

71
Q

How does wound healing display hyperplasia?

A

connective tissues and epithelial cells divide

72
Q

What causes lymph node hyperplasia?

A

lymphocyte hyperplasia from chronic inflammation and immune response

73
Q

Are calluses due to hyperplasia?

A

yes, epidermal hyperplasia

74
Q

Can chronic inflammation cause hyperplaisa?

A

yes

75
Q

one adult cell type is replaced by another adult cell type in response to chronic stress

A

metaplasia

Gen Path (7 decks)

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