Cell Injury 1 Flashcards

1
Q

pathology

A

the nature, cause and development of diseases

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2
Q

study of pathology requires

A

tissue/biopsy to see cellular changes

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3
Q

homeostasis

A

maintenance of constant cellular environment. Volume regulation is critical, 25% of energy is needed to regulate. Plasma membrane is critical.

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4
Q

cellular adaptations

A

attempt to reach new steady state. can cause injury if unable to adapt.

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5
Q

reversible changes (5)

A

hypertrophy, hyperplasia, atrophy, metaplasia, dysplasia

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6
Q

hypertrophy

A

increase in cell size/max function. cells unable to replicate. Caused by increased demand or growth hormone. increased gene expression, survival

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7
Q

hyperplasia

A

increase in cell number/tissue. cells able to proliferate. does increase tissue size.

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8
Q

atrophy

A

reduction in cell size, ultimately reduction in tissue/organ size. Longterm, decreased number of cells. “disuse, denervation, ischemia”

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9
Q

metaplasia

A

cell type replacement, response to repeat stress. can become malignant.

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10
Q

dysplasia

A

disordered cell growth/maturation. Can improve if stimulus is removed.

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11
Q

what reversible changes often occur together, and what can they both be?

A

hyperplasia and hypertrophy, pathological or physiologic

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12
Q

example of hypertrophy

A

hypertension/myocyte or muscle cell from exercise, myometrial smooth muscle during pregnancy, cardiac mycoses

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13
Q

example of hyperplasia

A

prostatic hyperplasia, endometrial glands

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14
Q

examples of atrophy

A

muscle tissues, decreased blood supply, aging, hormone changes

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15
Q

examples of metaplasia

A

barettes esophagus, smoking squamous cell epithelium in smoking

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16
Q

example of dysplasia

A

cervical dysplasia

17
Q

ischemic vs hypoxic injury

A

hypoxic- decreased o2 level, ischemia- decreased o2 level and decreased substrate levels (low oxygen IN THE BLOOD)

18
Q

reversible cell injury- volume

A

temporary loss of control, swelling, leakage of small molecules, influx of h20/ions

19
Q

reversible cell injury- energy

A

alterations in metabolism, decreased aerobic

20
Q

reversible cell injury- morphology

A

ER dilation, condensed mitochondria, plasma blebbing

21
Q

irreversible cell injury- volume

A

permanent loss of permeability, large molecule leakage

22
Q

irreversible cell injury- morphology

A

cytoplasmic staining, pyknosis, karyolysis, karyohexis, mitochondria gets granules, swells and ruptures

23
Q

irreversible cell injury- energy

A

uncoupled phosphoralative oxidation. increased glycogen, decreased PH, mitochondria issues

24
Q

mechanisms of injury (5)

A

aerobic respiration, mitochondria, systolic calcium levels, ROS, cell membrane, protein synthesis, genetic apparatus integrity

25
ischemia/re perfusion paradox
some cells die after reestablished blood flow> new processes, new free radicals, calcium availability, leukocytes cause damage
26
autophagy
self devouring of certain cellular contents, controlled by ATG genes.
27
all diseases can be traced to
changes in normal cells
28
causes of cell injury
oxygen deprivation, physical agent, infection, immunologic reactions, genetic derangement, nutritional imbalance
29
domino effect
compromising one intracellular system leads to damage in the others
30
what comes first, biochemical or morphological changes?
biochemical!
31
aerobic respiration and cell injury
low ATP/ glyclytic depletion leads to loss of energy, can't maintain volume regulation
32
mitochondria damage and cell injury
MPTP pore stays open, city c leaks, triggers apoptosis
33
calcium homeostasis and cell injury
enzyme activation can lead to protease activation and cell damage
34
oxygen derived free radicals and cell injury
imbalance of generation vs scavanging> tissue and cell damage
35
pyknosis
nucleus shrivels
36
karyolysis
punctured nucleus> halo
37
karyorrhexis
nucleus fragmented
38
autophagy process
phagopore> autophagosome, fuse with lysosome. Degrade and reuse cellular materials