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FTK III- Gen Path > Cell Injury, Death, and Adaptation > Flashcards

Cell Injury, Death, and Adaptation Flashcards

(59 cards)

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1
Q

What are the causes of cell injury

A

Oxygen and energy deprivation
Physical agents
Infectious Agents
Immunologic dysfunctions
Genetic derangements
Nutritional imbalances
Workload imbalance
Chemicals, drugs, and toxins
Aging

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2
Q

How long before you see microscopic changes in tissue?

A

6-12 hours

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3
Q

How long before you see gross changes in tissue?

A

hours-days

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4
Q

What are the mechanisms of cell injury? (explain in diagram)

A

Depletion of ATP or decreased ATP synthesis (lack of O2)
Mitochondrial damage
Influx of intracellular Ca2+ and loss of Ca2+ homeostasis
Accumulation of oxygen-derived free radicals
Defects in membrane permeability/membrane injury

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5
Q

Examples of reversible cell injury

A

Cell swelling
Fatty change (accumulation of fat in vacuoles in the cytoplasm of non-adipose cells)
Glycogen accumulation (increased levels of steriods)

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6
Q

What is a way cells may retain evidence of previous cell injury?

A

Lipofuscin accumulation after autophagocytosis of damaged organelles

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7
Q

What is the difference between necrosis and apoptosis?

A

with necrosis there is inflammation

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8
Q

Morphology of necrosis

A

hypereosinophilic cytoplasm; possible calcification
pyknosis
karyorrhexis
karyolysis

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9
Q

pyknosis

A

nuclear shrinkage and increased basophilia

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10
Q

karyorrhexis

A

nucleus fragments (can follow pyknosis)

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11
Q

karyolysis

A

fading or disappearing nucleus

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12
Q

patterns of necrosis (tissue level)

A

multifocal random, massive, zonal/regional

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13
Q

Causes of multifocal random necrosis

A

infectious causes

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14
Q

causes of massive necrosis

A

toxic or nutritional causes

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15
Q

causes of zonal/regional necrosis

A

toxic, hypoxic, or metabolic

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16
Q

types of necrosis (cellular level)

A

coagulative, liquefactive, fat, and caseous

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17
Q

Coagulative Necrosis

A

cells maintain their basic outline; seen with ischemia or toxins

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18
Q

Liquefactive Necrosis

A

no cell outline maintained; cells replaced with neutrophils and macrophages; focal collections of WBCs (pus) form abcesses; seen with infectious causes

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19
Q

Fat necrosis

A

enzymatic destruction of fat with subsequent mineralization (saponification)

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20
Q

caseous necrosis

A

cheese-like gross appearance of coagulative necrosis with subsequent inflammation and calcification

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21
Q

morphology of apoptosis

A

cell shrinkage, chromatin condensation, cytoplasmic blebs and apoptotic bodies *NO INFLAMMATION

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22
Q

causes of apoptosis

A

radiation, toxins, free radicals, withdrawl of growth factors or hormones, receptor ligand interaction (FAS, TNF- extrinsic pathways), cytotoxic T lymphocytes, DNA damage (p53)

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23
Q

postmortem autolysis

A

autolysis is the degradation of a cell by its own enzymes postmortem

leads to friable/soft tissues, involves entire tissue, no inflammatory response associated, RBCs in adjacent blood vessels are also autolysed (seen histologically)

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24
Q

rigor mortis

Study These Flashcards
A

the contraction of muscles after death

25
algor mortis
the gradual cooling of the cadaver
26
livor mortis
hypostatic congestion or gravitational pooling of blood
27
postmortem blood clotting
shiny and can be pulled out easily
28
hemoglobin inhibition postmortem
postmortem staining of tissues with blood pigment
29
bile imbibition (postmortem)
postmortem staining of tissues with bile
30
pseudomelanosis postmortem
postmortem staining of tissues with blood pigment digested by bacteria
31
atrophy
decrease in mass or size of tissue
32
causes of atrophy
nutrient depravation, chronic decrease in blood supply (not severe ischemia, loss of innervation, disuse, pressure/compression, loss of hormonal stimulation, physiological, idiopathic
33
hypoplasia
failure to grow to normal size; congenital/developmental *** need hx to diagnose
34
hypertrophy
increase in size of cells; happens in cells that do not proliferate well (neurons, skeletal muscle, cardiac muscle, smooth muscle)
35
hyperplasia
increase in the number of cells; happens ONLY in cells capable of mitosis (glandular tissue/epithelial cells)
36
causes of hypertrophy
compensatory (smooth muscle of bladder, skeletal muscle due to workload, cardiac muscle due to workload) hormonal
37
causes of hyperplasia
hormonal, compensatory (hepatocytes proliferating due to loss of other hepatocytes), idiopathic
38
metaplasia
change of one mature cell type to one of another of the same germline
39
aplasia
complete absence/failure of a tissue to grow
40
dysplasia
not a causative adaptation- unsure of advantage disordered growth; abnormal tissue development with disorientation of cells or tissue hyperplasia with atypical cell shape/size/orientation in fully developed tissues
41
neoplasia
abnormal, uncontrolled, and clonal proliferation of cells
42
calcification
abnormal deposition of calcium; seen as dark blue (basophilic) granular material and sometimes black sharp fragments
43
dystrophic calcification
calcification of necrotic tissue with normal serum calcium
44
metastatic calcification
occurs in living tissues as a result of hypercalcemia
45
causes of hypercalcemia
hypercalcemia of malignancy: when tumors produce parathyroid-like hormone primary hyperparathyroidism: produces parathyroid hormone vitamin toxicity uremic mineralization: renal failure; * may be with hypocalcemia, normocalcemia, or hypercalcemia; deposits on tongue, parietal pleura, pulm. interstitium, L atrium, kidney, and gastric mucosa destruction of bone from neoplasia
46
pigments derived from hemoglobin
hemosiderin and bilirubin
47
hemosiderin
comes from iron portion of hemoglobin; is a golden-yellow or yellow-brown pigment; indicates RBC turnover (hemmorahge or hemolysis), uses prussian blue staining
48
bilirubin
hyperbilirubinemia clinically manifests as jaundice; results in yellow staining of integument with bile pigments resulting fromm increased levels of bilirubin in plasma; formed by RBC breakdwon (heme portion of hemoglobin --> biliverdin --> bilirubin)
49
three causes of jaundice
pre-hepatic (hemolytic), hepatic, and post-hepatic
50
contusions
blunt trauma cuases damgae to local BV and hemorrhage--> lysis of erythrocytes--> macrophages phagocytize RBC debris --> lysosomes degrade hemoglobin --> bruise turns red- blue (hemoglobin) --> green-blue (biliverdin and bilirubin) --> golden-yellow (hemosiderin)
51
melanin
dark brown pigment produced by melanocytes in skin, hair, mucous membranes, eye, inner ear and meninges. melanocytes protect agains solar waves and absorb UV radiation
52
disorders of melanin pigmentation
albinism (partial or patchy loss of melanin) hyperpigmentation (sevelops secondary to almost any cutaneous insult) neoplasia
53
lipofuscin
brownish-yellow pigment that increases with age and atrophy; "wear and tear" or aging pigment; not harmful to the cell but marker of past free radical injury
54
amyloidosis
diverse group of extracellular proteinaceous substance that appear histologically and ultrastructurally similar; deposited in the interstitium and causes disease by either atrophy of adjacent cells or interferes with function of membranes; occurs in liver and kidneys
55
characteristics of all amyloid
smooth to fibrillar and eosinophilic using H&E stains, stains red with Congo Red stain and has an apple-green birefringence when viewed with polarized light, molecular structure is a beta-pleated sheet (resistant to enzymatic degradation)
56
light chain amyloid (primary)
made up of monoclonal immunoglobulin light chains. seen with plasma cell (mature lymphocytes) tumors and dyscrasias, NOT related to inflammation
57
reactive amyloid (secondary)
most commone, made up of serum amyloid-associated protein (acute phase protein produced by liver during inflammation), seen after chronic antigenic stimulation and chronic inflammation, common in shar peis and abyssinians
58
islet amyloid
precursor polypeptide is co-secreted with insulin by the beta cells in the pancreatic islets; deposited in pancreatic islets of aged cats; has been associated with diabetes mellitus and others not
59

FTK III- Gen Path (5 decks)

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