POST MORTEM ARTIFACTS Flashcards

1
Q

removal of organs (esp eyes, tongue, rectum) of carcass by carrion eating animals (e.g., dogs, coyotes, ravens, vultures, etc).

A

postmortem scavenging

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2
Q

▪ is the rigidity or stiffening of muscles after death due to contraction of musclefibers as ATPs are depleted or exhausted.
▪ usually within 1-6

A

Rigor Mortis

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3
Q

gradual cooling of the body after death.

A

Algor Mortis

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4
Q

gravitational pooling/settling of blood to the dependant regions (“down side”) of the body. In this instance, you will know the position of the individual when it was dead.

A

Livor Mortis (hypostatic congestion)

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5
Q

▪ occurs in heart and vessels.
▪ rbc’s may separate from plasma (esp in animals with high fibrinogen levels, eg horses) = “chicken fat clot”

A

Postmortem Clotting

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6
Q

▪ HgB released by rbc breakdown (after death) → staining tissues.
▪ especially lining of heart and blood vessels; also common in tissues of aborted fetuses and frozen tissues.

A

Hemoglobin Imbition

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7
Q

leakage of bile from gall bladder and major bile ducts which stains adjacent tissues green to yellow.

A

Bile Imbibition

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8
Q

▪ term used to describe an artifactual black discoloration of tissues (similar in an appearance to melanosis).
▪ due to saprophytic/putrefactive bacterial production of hydrogen sulfide (H2S) + iron → iron sulfide (FeS).

A

Pseudomelanosis

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9
Q

after death, decomposition of tissues begins by progressive release of endogenous enzymes (autolysis) and more gradually by the action of saprophytic bacteria (especially from gut).

A

Postmortem autolysis / decomposition

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10
Q

putrefaction (rotting), refers to the enzymatic decomposition of organic material (tissue) with production of foul-smelling compounds (eg H2S, NH3, mercaptans), especially by saprophytic / putrefactive bacteria.

A

Putrefaction and Postmortem Emphysema (bloating)

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11
Q

2 FORMS OF PIGMENTATION:

A
  1. EXOGENOUS PIGMENTATION
  2. ENDOGENOUS PIGMENTATION
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12
Q

are usually caused by inhalation of compounds in mineral or organic dust and become visible in the respiratory tract and draining lymph nodes.

A

EXOGENOUS PIGMENTATION

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13
Q

occupational pathological pigmentations of the lung (as a group) are called

A

pneumoconiosis.

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14
Q

The only exogenous pigmentation of concern in animals is caused by anthracosis, which occurs as a result of inhalations of carbon compounds.

A

anthracosis

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15
Q

EXOGENOUS PIGMENTS
Comprise the following groups of materials:

A

a) Metals
b) Fungi
c) Colored substances
d) Coarse Materials

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16
Q

may be divided into groups of those related to melanin or those derived from lipids, hemoglobin or porphyrins.

A

ENDOGENOUS PIGMENTATION

17
Q

is a normal pigment made by melanoblasts and melanocytes and present in cells, which receive it from melanocytes

A

MELANIN PIGMENTS

18
Q

is the presence of melanin in abnormal location such as on the pleura, meninges or heart.

A

melanosis

19
Q

congenital complete absence of melanin in an individual.

A

albino

20
Q

Macrophages that pick up granules of melanin are called

A

melanophores

21
Q

ENDOGENOUS PIGMENTS:

A
  1. MELANIN PIGMENTS
  2. LIPID PIGMENTS
22
Q

is found as yellowish-brown granules in the cytoplasm of affected parechymal cells.

A

Lipofuscin

23
Q

is a condition in which the kidney or liver becomes discolored black because of excess accumulation of non-iron staining brown pigment in hepatocytes and renal
tubular epithelium.

A

hemachromatosis

24
Q

usually seen in association with jaundice

A

Bilirubin

25
Q

is formed from the tetrapyrrole ring structure of hemoglobin when iron and protein have been removed. It is a normal by-product of hemoglobin breakdown but may occur at times in
excess.

A

bilirubin

26
Q

occurs when bilirubin is presented in the plasma in excess
and all tissues are stained yellowish-brown.

A

jaundice

27
Q

Jaundice is of three types:

A

a. Prehepatic jaundice
b. Hepatic jaundice
c. Posthepatic jaundice

28
Q

occurs following acute hemolytic conditions whereby
bilirubin are brought to the liver in larger quantities to be conjugated with glucuronic acid.

A

prehepatic jaundice

29
Q

occurs from direct damage to liver cells and there is release of conjugated and unconjugated bilirubin into the blood.

A

hepatic jaundice

30
Q

the bilirubin has passed through the liver but is blocked from entry into the intestine.

A

posthepatic jaundice

31
Q

abnormal synthesis of hemoglobin lead to porphyrin accumulation

A

Porphyrins

32
Q

arises from phylloerythrin, a metabolite of chlorophyll that has photosensitizing properties.

A

hepatotoxic type

33
Q

is caused by plants that contain compounds directly
photosensitive by ingestion without hepatic injury.

A

primary type