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

Cell Injury, Death, and Adaptation Flashcards

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

A

the contraction of muscles after death

25
Q

algor mortis

A

the gradual cooling of the cadaver

26
Q

livor mortis

A

hypostatic congestion or gravitational pooling of blood

27
Q

postmortem blood clotting

A

shiny and can be pulled out easily

28
Q

hemoglobin inhibition postmortem

A

postmortem staining of tissues with blood pigment

29
Q

bile imbibition (postmortem)

A

postmortem staining of tissues with bile

30
Q

pseudomelanosis postmortem

A

postmortem staining of tissues with blood pigment digested by bacteria

31
Q

atrophy

A

decrease in mass or size of tissue

32
Q

causes of atrophy

A

nutrient depravation, chronic decrease in blood supply (not severe ischemia, loss of innervation, disuse, pressure/compression, loss of hormonal stimulation, physiological, idiopathic

33
Q

hypoplasia

A

failure to grow to normal size; congenital/developmental
*** need hx to diagnose

34
Q

hypertrophy

A

increase in size of cells; happens in cells that do not proliferate well (neurons, skeletal muscle, cardiac muscle, smooth muscle)

35
Q

hyperplasia

A

increase in the number of cells; happens ONLY in cells capable of mitosis (glandular tissue/epithelial cells)

36
Q

causes of hypertrophy

A

compensatory (smooth muscle of bladder, skeletal muscle due to workload, cardiac muscle due to workload)

hormonal

37
Q

causes of hyperplasia

A

hormonal, compensatory (hepatocytes proliferating due to loss of other hepatocytes), idiopathic

38
Q

metaplasia

A

change of one mature cell type to one of another of the same germline

39
Q

aplasia

A

complete absence/failure of a tissue to grow

40
Q

dysplasia

A

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
Q

neoplasia

A

abnormal, uncontrolled, and clonal proliferation of cells

42
Q

calcification

A

abnormal deposition of calcium; seen as dark blue (basophilic) granular material and sometimes black sharp fragments

43
Q

dystrophic calcification

A

calcification of necrotic tissue with normal serum calcium

44
Q

metastatic calcification

A

occurs in living tissues as a result of hypercalcemia

45
Q

causes of hypercalcemia

A

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
Q

pigments derived from hemoglobin

A

hemosiderin and bilirubin

47
Q

hemosiderin

A

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
Q

bilirubin

A

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
Q

three causes of jaundice

A

pre-hepatic (hemolytic), hepatic, and post-hepatic

50
Q

contusions

A

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
Q

melanin

A

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
Q

disorders of melanin pigmentation

A

albinism (partial or patchy loss of melanin)
hyperpigmentation (sevelops secondary to almost any cutaneous insult)
neoplasia

53
Q

lipofuscin

A

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
Q

amyloidosis

A

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
Q

characteristics of all amyloid

A

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
Q

light chain amyloid (primary)

A

made up of monoclonal immunoglobulin light chains. seen with plasma cell (mature lymphocytes) tumors and dyscrasias, NOT related to inflammation

57
Q

reactive amyloid (secondary)

A

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
Q

islet amyloid

A

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
Q
A

FTK III- Gen Path (5 decks)

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