Chapter 1 DEGENERATION : Reversible Injury Flashcards
1
Q
CAUSES OF CELLULAR INJURY
A
- Hypoxia
- Physical agents including trauma, heat, cold, radiation and electric shock
- Chemical agents and drugs
- Infectious agents including bacteria, viruses, parasites, fungi etc.
- Immunologic reactions
- Genetic derangements
- Nutritional imbalances
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
3
Q
Cutting object, blows, compression
A
Mechanical trauma
4
Q
Lightning, high-frequency currents
A
Electrical trauma
5
Q
Heatstroke, sunstroke, fever, burns
A
Heat
6
Q
Local tissue freezing, cold shock
A
Cold
7
Q
Ultraviolet light, x-irradiation
A
Radiant Energy
8
Q
Increased, decreased
A
Pressure
9
Q
Bacterial and fungal toxins, venoms
A
Biological toxins
10
Q
Organophosphates (parathion)
A
Pesticides
11
Q
Tetracycline, and many other drugs
A
Therapeutic toxins
12
Q
Paraquat, 2,4-D, dinitrophenols
A
Herbicides
13
Q
Metal, nitrates, PCB’s
A
Environmental toxins
14
Q
Vitamin A and D
A
Dietary excess
15
Q
Viruses, prions
A
Acellular agent
16
Q
Bacteria
A
Prokaryotes
17
Q
Fungi, protozoa, algae
A
Eukaryotes
18
Q
Cestodes, nematodes, trematodes, insects
A
Metazoan parasites
19
Q
Protein, vitamins, calories
A
Nutritional deficiency
20
Q
water, oxygen, sunlight
A
Environmental Deficits
21
Q
Natural aging, premature aging
A
Aging
22
Q
Autoimmune disease
A
Immunologic defects
23
Q
Single mutant gene to chromosomal breaks
A
Genetic defects
24
Q
The gradual decline of a disease process or a process of disintegration or dissolution.
A
Lysis
24
A severe form of hypoxia that occurs when the body or brain does not get any oxygen.
Anoxia
25
A reversible form of injury
Degeneration
25
Literally may imply a “sick cell”
Degeneration
26
the most common and most important response to cellular injuries of all types, including mechanical, anoxic, toxic, lipid peroxidation, viral, bacterial and immune mechanisms.
Swelling of the cell
27
An adaptive change that may progress to cell death (necrosis)
Degeneration
28
This occurs when excessive physiologic stresses, pathologic stimuli result in a new but altered state that preserves the viability of the cell.
Cellular adaptation
29
Increase in tissue mass
Hypertrophy
29
Decrease in
tissue mass
Atrophy
30
Cells/tissues that accumulates substances in abnormal quantities.
Infiltrations
31
This occurs when cell injury is sublethal and sustained.
Infiltrations
32
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.
Hydropic degeneration (Acute cellular swelling, Cloudy swelling)
32
Types of Intracellular accumulations
- Water vacuolation
- Fat vacuolation
- Glycogen vacuolation
33
usually associated with epithelial lesions but term should not be used for gross lesions.
Hydropic degeneration (Acute cellular swelling, Cloudy swelling)
34
The presence of sodium
increases the osmotic pressure in the cell, water
moves in, and this results in swelling.
Water vacuolation
34
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.
Sodium pump
35
An old term for any swollen cell in which the cytoplasm has a uniformly swollen,
cloudy appearance.
Cloudy Swelling
36
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.
Hydropic degeneration
37
The gross appearance is yellow, with the degree of yellow corresponding to the extent of fat accumulation in hepatocytes.
Fatty liver
37
Lipoproteins cannot be formed and, as a result, the lipid cannot be secreted from the cell and therefore accumulates.
| Effect
Specific or nonspecific damage to the hepatocyte and certain nutritional deficiencies may interfere with protein production in the endoplasmic reticulum
| Cause
37
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”.
Fatty degeneration (Fatty change, Fat phanerosis)
38
Reversible if cause is removed.
Fatty degeneration
38
the abnormal accumulation of fat in the cytoplasm of parenchymal cells
Fatty degeneration (Fatty change, Fat phanerosis)
39
Have large amounts of fat in their renal tubular epithelium and therefore have pale-appearing kidneys.
Cats
40
The lesion is the presence of fat in adipose cells that accumulate in tissue in which they are not normally present.
Fatty infiltration
41
Abnormal accumulation of glycogen in cytoplasm of parenchymal cells. This occurs following a defect in glycogen metabolism as in diabetes mellitus.
Glycogen degeneration
42
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.
Mucoid degeneration
43
Previously noted as overproduction of mucinous secretion by cells.
Mucoid degeneration
43
Also previously known as jelly-like transformation of tissues.
Myxomatous degeneration
44
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.
Glycogen
44
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).
Hyaline
44
A term used to describe the change from normal to variable
degrees of smooth eosinophilic appearance in the microscopic examination of tissue.
Hyalinization or hyalinized
45
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.
Hyaline droplets
46
Fibrin is the major component along with
serum proteins, particularly immunoglobulins or antibodies.
Fibrinoid
46
An amorphous, bright,
eosinophilic material found particularly in
the walls of the blood vessels of various sizes.
Fibrinoid
47
A disease when amyloid deposition lead to functional and morphological lesions.
Amyloidosis
48
glycoprotein accumulation/deposition
Amyloidosis
49
An amorphous eosinophilic material that accumulates in tissues, particularly on basement membranes, and often causes clinically significant lesions.
Amyloid
49
Most prominent in renal glomeruli, liver simusoids, around lymph follicles and in and around walls of blood vessels in many tissues.
Amyloid
49
A space-occupying lesion particularly when it interferes with the functions of blood vessels when it collects on basement membranes.
Amyloid
50
2 types of amyloidosis
Primary Amyloidosis and Secondary Amyloidosis
51
Plasma cell tumor
Myeloma
51
Results from the production of immunoglobulin-amyloid precursors by abnormal
plasma cells.
Primary Amyloidosis
52
Occurs in chronic infectious diseases in which the immune system has been very active for a long period making immunoglobulins.
Secondary Amyloidosis
53
May also occur in hyperimmunized animals.
Secondary Amyloidosis
54
Disease that occurs when uric acid and urate crystals are deposited in
tissue owing to defects in purine metabolism.
Gout
55
May collect as crystals in tissue after severe damage or hemorrhage.
Cholesterol (Cholesterol clefts)
56
This is a similar to cholesterol in
avian species that in results from massive
accumulation of lipids in
macrophages.
Xanthomatosis
57
Circular, laminated concretions found in glandular tissue or free in secretions.
Corpora amylacea
