Pathomorphology - postemortem changes, dystrophies, necrosis Flashcards

(86 cards)

1
Q

what is hypostasis or lividity

A

also referred to as Livor mortis, is the pooling of blood because of gravity in dependent body sites after the heart stops beating.

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2
Q

Algor Mortis

A

refers to the cooling of the body after death

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3
Q

conduction

A

the loss of heat through transfer to objects in contact with the body

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4
Q

convection

A

is the movement of air over the body causing cooling; and radiation, which is the loss of heat from the body through infrared heat rays

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5
Q

Autolysis

A

is a chemical process by the intracellular enzymes that causes the breakdown of tissue and organs.

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6
Q

hemosiderin

A

is an iron-storage complex that is composed of partially digested ferritin and lysosomes. The breakdown of heme gives rise to biliverdin and iron.

The body then traps the released iron and stores it as hemosiderin in tissues. Hemosiderin is also generated from the abnormal metabolic pathway of ferritin.

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7
Q

imbibition

A

is a special type of diffusion that takes place when liquid is absorbed by solids-colloids causing an increase in volume.

“Decomposition causes hemolyzed blood to leak out of the broken down blood vessels into the surrounding tissue (imbibition) usually within 12–24 hours after death.”

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8
Q

Adipocere

A

is a grayish-white to brown, firm, wax-like material made up of the fatty acids oleic, palmitic, and stearic acids. It is found primarily in the subcutaneous tissue and other fatty deposit areas.

Adipocere formation can take weeks to several months to develop and is resistant to chemical bacterial destruction. When a body is found immersed in water or in a damp, warm environment, adipocere formation may occur.

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9
Q

Entomology

A

the scientific study of insects

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10
Q

what term refers to the colonization by maggots of a live body.

A

Myiasis

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11
Q

define instar

A

is a developmental stage of arthropods, such as insects, between each moult (ecdysis), until sexual maturity is reached.

identifying the presence of instars during necropsy can aid in determining time of death

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12
Q

define degeneration

A

Defined as deterioration of live cells following injury, but with the potential to revert back to normal

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12
Q

how is Deterioration of cells is evaluated

A

in terms of morphological changes that occur inside or outside the cells

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13
Q

Cell injuries are classified according to (2)

A
  1. Magnitude/Severity
  2. Nature of injury
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14
Q

how does radiant energy cause injury to cells?

A

Radiant energy e.g. X-rays, UV light

induce formation of free radicals,
damage the genetic material causing genetic defects and neoplasia

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15
Q

Morphological changes that occur inside the cells following injury involve

A

accumulation of metabolites in the endoplasmic reticulum

One of these metabolites is water following injury of cells by hypoxia
Other metabolites known to accumulate inside cells following injury are:
– Protein
– Carbohydrates
– Lipids

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16
Q

Parenchymatous protein degenerations occur where vs mesenchymal

A

Parenchymatous protein degenerations are intracellular
&
Mesenchymal are extracellular

(mesenchymal = refers to cells that develop into connective tissue, blood vessels, and lymphatic tissue)

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17
Q

Parenchymatous protein degenerations can be (4)

A

Granular
Hyalin-drop
Vacuolar
Keratinous

Parenchymatous degenerations are intracellular and granular dystrophy is most frequent.

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18
Q

Mesenchymal protein degenerations can be (4)

A

Mucoid swelling
Fibrinoid changes
(= Fibrinoid necrosis is the death of cells in small blood vessels. )

Hyalinosis (= hyaline degeneration)
Amyloidosis (abnormal protein called amyloid, deposition)

mesenchcymal degenerations are extracellular

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19
Q

another term for Mixed protein degenerations

A

mixed dysproteinosis

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20
Q

name 3 types of hemoglobinogenic protein degenerations

A

Hemoglobinogenic pigments: hemosiderin, hematoidin, bilirubin

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21
Q

name a type of Proteinogenic protein degenerations

A

Proteinogenic pigment: melanin

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22
Q

name 2 types of lipid protein degenerations

A

Lipid pigments: lipofuscin, lipocromes

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23
Q

what is Uric acid diathesis

A

diathesis = a constitutional predisposition toward a particular state or condition

so an increased level of uric acid leads to (urate) gout
(diathesis urica = uric acid diathesis)
can also be called hyperuricemia

Gout occurs when urate crystals accumulate in your joints.

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24
lipidosis
or Fatty degeneration abnormal deposition of lipids in organs or tissues of the body, often resulting from genetic disorders of lipid metabolism Parenchymal fatty degenerations Mesenchymal fatty degenerations
25
name 3 types of Mineral degenerations
Metastatic calcification (= is deposition of calcium salts in otherwise normal tissue) Dystrophic calcification (= is deposition of calcium salt in degenerated tissues with the absence of a systemic mineral imbalance) Concrements or stones (= excess mineral forming crystals/stone)
26
macroscopic changes from cellular degeneration? (2)
Decolorization of tissues or organs. Changes of the consistency; tissue is softer, fragile and friable (= easily crumbled)
27
Chromatolysis
chromatolysis is the dissolution of the Nissl bodies in the cell body of a neuron.
28
Pyknosis (or karyopyknosis)
the reduction in size and increase in staining of a cell or its nucleus the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is followed by karyorrhexis, or fragmentation of the nucleus. Pyknosis is also observed in the maturation of erythrocytes and the neutrophil.
29
karyorrhexis
a degenerative cellular process involving fragmentation of the nucleus and the breakup of the chromatin into unstructured granules
30
Acantholysis
Acantholysis means loss of coherence between epidermal cells due to the breakdown of intercellular bridges. It is an important pathogenetic mechanism underlying various bullous disorders, particularly the pemphigus group, as well as many non-blistering disorders.
31
Steatosis
steatosis is abnormal retention of lipids within a cell or organ word commonly used for fatty liver disease
32
According to the triggering factors the following etiological forms of necrosis are specified: (5)
traumatic necrosis toxic necrosis angiogenic or circulatory necrosis allergic necrosis trophoneurotic necrosis (= due to defective nerve action in a part of an organ which results in failure of nutrition)
33
karyolysis
is the complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases
34
necrotic cytoplasm changes: (3)
coagulation plasmorrhexis (= rupture of a cell with loss of its contents) plasmolysis (involves contraction or shrinkage)
35
necrosis sicca s. coagulativa
Dry or coagulative necrosis
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necrosis humida s. colliquativa
Wet or liquefactive necrosis
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describe Coagulative necrosis (2)
Proteins denature and aggregate rather than degrade Dry gangrene
38
describe Liquefactive necrosis (2)
Enzymatic digestion of cellular components Wet gangrene
39
describe Fatty necrosis
End result of pancreatic lipases digesting fat cells resulting in calcium soaps
40
describe Caseous necrosis
End result of tuberculous infections, granuloma
41
describe Fibrinoid necrosis
Ag-Ab complexes and fibrin accumulate in arteries or other vessels
42
what is Zenker´s degeneration
necrosis of skeletal muscles
43
cyto steatonecrosis
Fat necrosis e.g. pancreatic cyto steatonecrosis or bacterial lipolytic enzymes Macroscopically: White spots in fat tissue. Calcification of necrotosed tissue and inflammation.
44
Cicatrization
is the contraction of fibrous tissue formed at a wound site by fibroblasts, reducing the size of the wound while distorting tissue. Cicatrization may refer to: The process of a wound healing to produce scar tissue.
45
Phlegmon
is a localized area of acute inflammation of the soft tissues Most commonly, it is used in contrast to a "walled-off" pus-filled collection (abscess), although a phlegmon may progress to an abscess if untreated.
46
Degeneration or dystrophy
denotes any disorder due to defective or faulty nutrition or metabolism of an organism, organ or tissue.
47
describe (dystrophia granularis)
In granular degeneration granules or grains accumulate in the cytoplasm of the cell, which makes the cytoplasm cloudy and the nucleus not so well visible. The cell expands in the process. The dystrophy-affected organs enlarge, swell, become brittle and of lighter colour than normal, often with irregular patches of colouring. Granular degeneration is the least severe form of degenerations.
48
describe (dystrophia hyalinoguttatica)
Hyalin-drop degeneration mainly affects kidneys (renal convoluted tubule epithelial cells); and liver more rarely. semi-transparent hyaline homogenous protein drops of various sizes appear in the cytoplasm of cells and can fill the entire cytoplasm by joining (destruction of the ultrastructure of the cell). This form of degeneration lacks characteristic external features and therefore a diagnosis is not possible without microscopic studies.
49
describe (dystrophia hydropica, dystrophia vacuolaris)
Hydropic or vacuolar degeneration fluid-filled vacuoles form in the cytoplasm (or nucleus, but that is more rare) of a cell. Hydropic dystrophy is caused by protein-water-electrolytes imbalance. progressed, the vacuoles grow and sometimes merge, filling the whole cell with liquid. the organs and tissues show little changes externally, except for their swelling. This type of degeneration can be identified only by histological examination.
50
describe (dystrophia keratinosa)
In keratinous degeneration the keratinizing epithelium develops either excessive keratin of normal consistency (hyperkeratosis) or keratin appears in regions where it normally does not exist (on mucosa – leucokeratosis, leucoplakia). The developing keratin may be of altered consistency (parakeratosis).
51
ichthyosis
is a group of skin disorders that lead to dry, itchy skin that appears scaly, rough, and red. The skin looks as if covered by fish scales with thin fur or hairs.
52
Extracellular dysproteinemias are
protein metabolism disturbances in fascia (stroma of organs and walls of blood vessels). Extracellular dysproteinemias include mucoid degeneration, fibroid degeneration, hyalin degeneration and amyloidosis.
53
what exactly is hyalin
Hyalin is a large fibrous protein, made up of plasma cells mostly. The protein has strong adhesive properties
54
Fibrinoid degeneration causes
the connective tissue of organs and vessels disintegrate; the collagen fibres swell and break down and the fibres and the ground substance of connective tissue soak in cells of blood plasma, fibrin mainly, and the result is a complicated compound – fibrinoid.
55
sclerosis
a pathological condition in which a tissue has become hard and which is produced by overgrowth of fibrous tissue or by increase in interstitial tissue.
56
General hyalinosis of blood vessels and connective tissue is
noted with arteriosclerosis The result is that the walls of the blood vessels are saturated with plasma proteins, precipitation of plasma proteins and hyalin. Due to hyaline production, the walls of the vessels harden and lose their elasticity, their lumen narrows or closes.
57
another term for sclerosis
Focal hyalinosis appears with chronic focal inflammations, where the connective tissue may become hyalinized.
58
Amyloidosis is
extracellular protein degeneration, characterised by amyloid deposit in tissues between cells.
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One of the most distinctive features of amyloid is
metachromasia with anil dye, i.e. amyloid will take a colour different from that of the dye solution. metachromatic: having the capacity to stain different elements of a cell or tissue in different colors or shades.
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another term for Chromoprotein metabolism disturbances
pathologic endogenous pigmentations A chromoprotein is a conjugated protein that contains a pigmented prosthetic group (or cofactor). A common example is haemoglobin, which contains a heme cofactor
61
Hemoglobinogenics pigments are the result of either physiological or pathological
erythrocyte hemolysis.
62
The result of physiological degradation of erythrocytes and hemoglobin in reticuloendothelial or macrophagic cells are the pigments (3)
hemosiderin, ferritin & bilirubin.
63
If the hemolytic process is pathological, aside from the usual pigments produced, what 3 compounds may be produced as well?
hematoidin, hematins, porphyrins.
64
histiocyte
is a tissue macrophage or dendritic cell, that is found in many parts of the body especially in the bone marrow, the blood stream, the skin, the liver, the lungs, the lymph glands and the spleen. is part of the mononuclear phagocyte system (also known as the reticuloendothelial system or lymphoreticular system). In histiocytosis, the histiocytes move into tissues where they are not normally found and cause damage to those tissues.
65
Bilirubin
is the most important bile pigment, a yellow-red haemoglobin-breakdown product derived from catabolised RBCs in the reticuloendothelial cells Bilirubin deposits in the liver, is present in bile
66
There are three main pathological forms of jaundice:
1) parenchymal 2) hemolytic 3) obstructive yellow due to higher levels of bilirubin
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Parenchymal (hepatocellular) jaundice occurs with
liver diseases, when the damaged hepatocytes have reduced ability to secrete bilirubin to hepato-biliary system (for example diseases like infectious hepatitis, toxic degeneration of liver, sepsis, leptospirosis etc.).
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Hemolytic (pre-hepatic) jaundice occurs with
intensive hemolysis (great quantities of bilirubin are produced). For example with some blood diseases, some infectious diseases and blood parasitic diseases and sepsis.
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Obstructive (post-hepatic) jaundice is caused by
an interruption to the drainage of bile (constricted or obstructed bile duct lumen, which may be the result of bile duct inflammation, gallstones, parasites; also external causes like tumors, scar tissue and some other factors). obstructive jaundice liver has yellow discoloration If bile is obstructed for a longer period, it causes necrotic changes in the liver and necrotic tissue will be replaced by connective tissue, which leads to biliary cirrhosis.
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Name 3 Proteinogenic pigments
Melanin, adrenochrome and pigment of enterochromafin cells
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melanosis
or melanism Excessive production of melanin and its depositing in skin and internal organs
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leucoderma
An acquired condition with localized loss of pigmentation of the skin after inflammations and other damage
73
Lipofuscin
is a lipid protein and lipid pigement, and appears as little yellowish brown granules in the cells Due to pigment build-up the organ becomes brownish.
74
Lipochromes
are pigments that give the yellow colouring to fatty tissue, adrenal cortex, egg yolk, blood plasma etc. Lipochromes are pigments that have dissolved in lipids
75
Lipochromes
are pigments that give the yellow colouring to fatty tissue, adrenal cortex, egg yolk, blood plasma etc. Lipochromes are pigments that have dissolved in lipids most widespread member of the group is carotene, therefore lipochromes are also called carotenoids. Carotenoids are of herbal origin. They enter animal organism via feed. Carotenoids are also a source of vitamin A.
76
Glycoproteins are
complex protein compounds with polysaccharides. The group includes mucous substances (mucins) and mucinoid substances (mucoids).
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The metabolic disturbance of glycoproteins is
mucoid degeneration.
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Mucoid degeneration
is the degeneration of connective tissue into a gelatinous or mucoid substance. Mucoid degeneration can be intracellular (parenchymal) and extracellular (mesenchymal).
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catarrh
is a build-up of mucus in an airway or cavity of the body.
80
Colloid dystrophy is a special form of
mucoid degeneration. In that case colloid pseudo-mucin is produced and deposited in the glandular organs (thyroid gland, adrenals, pituitary gland etc.). This form of degeneration occurs mostly in thyroid glands in the form of colloid struma (goiter) (struma colloidea) and is caused by iodine deficiency.
81
Disturbances in nucleoprotein change are
uric acid diathesis and uric acid infarct.
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uric acid diathesis
excessive amounts of uric acid and its salts are produced, which deposit in blood and cause hyperuricemia Uric acid and its salts deposit as uric acid crystals and amorphous sodium salt to tissues and organs, causing degenerative and inflammatory changes and necrosis. joint form is gout
83
There are two variations of uric acid diathesis:
1) visceral and 2) joint form.
84
Uric acid infarct mainly affects
newborns due to their more intensive metabolism during the first days. Uric acid and the salts deposit in convoluted renal tubules. It is a physiological process that will disappear after a while.
85
The fat that deposits in connective tissues under the skin, around kidneys etc. is called
neutral fat.