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Veterinary Pathology > Chapter 1 DEGENERATION : Reversible Injury > Flashcards

Chapter 1 DEGENERATION : Reversible Injury Flashcards

1
Q

CAUSES OF CELLULAR INJURY

A
  1. Hypoxia
  2. Physical agents including trauma, heat, cold, radiation and electric shock
  3. Chemical agents and drugs
  4. Infectious agents including bacteria, viruses, parasites, fungi etc.
  5. Immunologic reactions
  6. Genetic derangements
  7. Nutritional imbalances
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2
Q

A condition in which the body or a region of the body is deprived of adequate oxygen supply at the tissue level.

A

Hypoxia

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3
Q

Cutting object, blows, compression

A

Mechanical trauma

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4
Q

Lightning, high-frequency currents

A

Electrical trauma

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5
Q

Heatstroke, sunstroke, fever, burns

A

Heat

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6
Q

Local tissue freezing, cold shock

A

Cold

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7
Q

Ultraviolet light, x-irradiation

A

Radiant Energy

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8
Q

Increased, decreased

A

Pressure

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9
Q

Bacterial and fungal toxins, venoms

A

Biological toxins

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10
Q

Organophosphates (parathion)

A

Pesticides

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11
Q

Tetracycline, and many other drugs

A

Therapeutic toxins

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12
Q

Paraquat, 2,4-D, dinitrophenols

A

Herbicides

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13
Q

Metal, nitrates, PCB’s

A

Environmental toxins

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14
Q

Vitamin A and D

A

Dietary excess

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15
Q

Viruses, prions

A

Acellular agent

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16
Q

Bacteria

A

Prokaryotes

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17
Q

Fungi, protozoa, algae

A

Eukaryotes

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18
Q

Cestodes, nematodes, trematodes, insects

A

Metazoan parasites

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19
Q

Protein, vitamins, calories

A

Nutritional deficiency

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20
Q

water, oxygen, sunlight

A

Environmental Deficits

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21
Q

Natural aging, premature aging

A

Aging

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22
Q

Autoimmune disease

A

Immunologic defects

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23
Q

Single mutant gene to chromosomal breaks

A

Genetic defects

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24
Q

The gradual decline of a disease process or a process of disintegration or dissolution.

A

Lysis

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24
Q

A severe form of hypoxia that occurs when the body or brain does not get any oxygen.

A

Anoxia

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25
Q

A reversible form of injury

A

Degeneration

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25
Q

Literally may imply a “sick cell”

A

Degeneration

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26
Q

the most common and most important response to cellular injuries of all types, including mechanical, anoxic, toxic, lipid peroxidation, viral, bacterial and immune mechanisms.

A

Swelling of the cell

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27
Q

An adaptive change that may progress to cell death (necrosis)

A

Degeneration

28
Q

This occurs when excessive physiologic stresses, pathologic stimuli result in a new but altered state that preserves the viability of the cell.

A

Cellular adaptation

29
Q

Increase in tissue mass

A

Hypertrophy

29
Q

Decrease in
tissue mass

A

Atrophy

30
Q

Cells/tissues that accumulates substances in abnormal quantities.

A

Infiltrations

31
Q

This occurs when cell injury is sublethal and sustained.

A

Infiltrations

32
Q

Occur because of marked mitochondrial damage, cessation of ATP production and failure of sodium pump leading to increased osmotic pressure within cells. Thus, affecting the selective permeability of cellular membranes leading to increased entry of water inside the cell.

A

Hydropic degeneration (Acute cellular swelling, Cloudy swelling)

32
Q

Types of Intracellular accumulations

A
  • Water vacuolation
  • Fat vacuolation
  • Glycogen vacuolation
33
Q

usually associated with epithelial lesions but term should not be used for gross lesions.

A

Hydropic degeneration (Acute cellular swelling, Cloudy swelling)

34
Q

The presence of sodium
increases the osmotic pressure in the cell, water
moves in, and this results in swelling.

A

Water vacuolation

34
Q

Control mechanisms for the osmotic gradient at the
cell membrane. Pushes sodium out of the cell and pulls potassium into the cell, and this reaction requires energy produced in the cell membrane.

A

Sodium pump

35
Q

An old term for any swollen cell in which the cytoplasm has a uniformly swollen,
cloudy appearance.

A

Cloudy Swelling

36
Q

Term used to describe swelling of cells and is considered to have causes similar to those of cloudy swelling but to be a more advance lesion. - also called ballooning degeneration.

A

Hydropic degeneration

37
Q

The gross appearance is yellow, with the degree of yellow corresponding to the extent of fat accumulation in hepatocytes.

A

Fatty liver

37
Q

Lipoproteins cannot be formed and, as a result, the lipid cannot be secreted from the cell and therefore accumulates.

Effect

A

Specific or nonspecific damage to the hepatocyte and certain nutritional deficiencies may interfere with protein production in the endoplasmic reticulum

Cause

37
Q

Implies the presence of fat globules within the cytoplasm of cells. Fat accumulates due to inability of the cell to metabolize fat. Sometimes displacing the nucleus at the cytoplasmic periphery giving a characteristic “ring appearance”.

A

Fatty degeneration (Fatty change, Fat phanerosis)

38
Q

Reversible if cause is removed.

A

Fatty degeneration

38
Q

the abnormal accumulation of fat in the cytoplasm of parenchymal cells

A

Fatty degeneration (Fatty change, Fat phanerosis)

39
Q

Have large amounts of fat in their renal tubular epithelium and therefore have pale-appearing kidneys.

A

Cats

40
Q

The lesion is the presence of fat in adipose cells that accumulate in tissue in which they are not normally present.

A

Fatty infiltration

41
Q

Abnormal accumulation of glycogen in cytoplasm of parenchymal cells. This occurs following a defect in glycogen metabolism as in diabetes mellitus.

A

Glycogen degeneration

42
Q

conjugates of protein and carbohydrates (mucopolysaccharides) normally found in secretions of epithelial cells and as ground substances of connective tissues and cartilage. Excessive accumulation of these substances is called now as mucopolysaccharidosis.

A

Mucoid degeneration

43
Q

Previously noted as overproduction of mucinous secretion by cells.

A

Mucoid degeneration

43
Q

Also previously known as jelly-like transformation of tissues.

A

Myxomatous degeneration

44
Q

May occur in abnormal amounts in the cytoplasm of cells and appear as clear vacuoles. This is not common but occurs in prolonged hyperglycemia, particularly in diabetes.

A

Glycogen

44
Q

Any alternation within cells or in the extracellular spaces or structure that gives a homogeneous, glassy-pink appearance in routine histologic sections stained with hematoxylin and eosin (H & E).

A

Hyaline

44
Q

A term used to describe the change from normal to variable
degrees of smooth eosinophilic appearance in the microscopic examination of tissue.

A

Hyalinization or hyalinized

45
Q

Are small eosinophilic structures in the cytoplasm of cells. This is more likely a compensatory functional change caused by accumulation of secretion or increased intake of compounds by esotropy.

A

Hyaline droplets

46
Q

Fibrin is the major component along with
serum proteins, particularly immunoglobulins or antibodies.

A

Fibrinoid

46
Q

An amorphous, bright,
eosinophilic material found particularly in
the walls of the blood vessels of various sizes.

A

Fibrinoid

47
Q

A disease when amyloid deposition lead to functional and morphological lesions.

A

Amyloidosis

48
Q

glycoprotein accumulation/deposition

A

Amyloidosis

49
Q

An amorphous eosinophilic material that accumulates in tissues, particularly on basement membranes, and often causes clinically significant lesions.

A

Amyloid

49
Q

Most prominent in renal glomeruli, liver simusoids, around lymph follicles and in and around walls of blood vessels in many tissues.

A

Amyloid

49
Q

A space-occupying lesion particularly when it interferes with the functions of blood vessels when it collects on basement membranes.

A

Amyloid

50
Q

2 types of amyloidosis

A

Primary Amyloidosis and Secondary Amyloidosis

51
Q

Plasma cell tumor

A

Myeloma

51
Q

Results from the production of immunoglobulin-amyloid precursors by abnormal
plasma cells.

A

Primary Amyloidosis

52
Q

Occurs in chronic infectious diseases in which the immune system has been very active for a long period making immunoglobulins.

A

Secondary Amyloidosis

53
Q

May also occur in hyperimmunized animals.

A

Secondary Amyloidosis

54
Q

Disease that occurs when uric acid and urate crystals are deposited in
tissue owing to defects in purine metabolism.

A

Gout

55
Q

May collect as crystals in tissue after severe damage or hemorrhage.

A

Cholesterol (Cholesterol clefts)

56
Q

This is a similar to cholesterol in
avian species that in results from massive
accumulation of lipids in
macrophages.

A

Xanthomatosis

57
Q

Circular, laminated concretions found in glandular tissue or free in secretions.

A

Corpora amylacea

Veterinary Pathology (7 decks)

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