4- Post Mortem Changes

what do post mortem changes result from

autolysis

post mortem changes vary based on

• tissue type

• animal

• cause of death

• temp

• body temp

• microbial flora

describe decompositions

dead organic substances broken down into simpler organic or inorganic matter via 2 diff mechanisms (putrefaction and autolysis)

putrefaction

state of decomp when microorganisms cause tissues to turn into gases, liquids, simple molecules

autolysis

destruction of cells or tissues by their own enzymes aka self digestion

rank how fast tissues die from fastest to slowest

1. neurons

2. cardiac m

3. parenchyma cells

4. chondrocytes

describe autolysis

occurs in dead body and involves whole body

no inflammation

begins w/in minutes of last heartbeat and causes unavoidable changes

describe necrosis

occurs in live tissues

localized or regional

inflammation present

whats the order of autolysis

heart beat stops, hypoxia, inc CO2 = pH decrease, cytosolic lysosome rupture and enzymes enter cytosol, autolysis

t or f: depending on autolysis severity nothing may be left to diagnose

true due to extensive tissue breakdown.

postmortem autolysis can mask what

antemortem lesions

how does autolysis look histologically

lack of cell architecture and cell detail

numerous saprophytic bacteria

what are the 5 post mortem changes

1. fresh

2. putrefaction/bloat

3. active decomp

4. advanced decay

5. skeletonization

whats rigor mortis

2-36 hrs post death - muscle stiffening

small muscles first

why does rigor mortis result in hyperextension

extensors stronger than flexors

• SR degrades which releases Ca and floods the sarcomere to bind actin and myosin

• no atp aka no relaxation

define livor mortis

tissue discoloration due to intravascular blood pooling (hypostatic congestion) (gravitational)

describe livor mortis

occurs in all body cavities, hypoxic capillaries dilate pooling blood

• develops in 30 min to 2 hrs

describe algor mortis

cooling of body to environment equilibrium

• thick fur = will autolyze more rapidly

describe hemoglobin inhibition

staining of tissues by free hemoglobin

• red discoloration

describe bile inhibition

staining by bile, yellow/green discoloration for the extrahepatic biliary system

what is Pseudomelanosis

putrefactive bacteria that diffuses thru tissues and reacts with iron creative iron sulfide

what is melanosis

normal dark melanin pigment of tissues

describe post mortem clots

occurs right after death but dissapers within 2 hours

• fibrinolysin released from the endothelial cells resulting in incoagulable blood in the vessels

describe antemortem clots

true clot from the elements of Virchow’s triad

(hypercoagulability, endothelial damage, turbulent blood flow)

describe and name this clot

rough, friable, difficult to remove

antemortem clot

describe and name this clot

smooth, shiny, easy to remove

“chicken fat clot”

postmortem clot

what type of clot

antemortem

name this

non lesion bile inhibition

non lesion or pathology?

non lesion- rigor mortis

non lesion or pathology

non lesion

hemoglobin inhibition

postmortem autolysis or pathology

hemoglobin inhibition that deposits in dentin

non lestion or path

non lesion- hydrogen sulfide from bacteria forming iron sulfide

ante or post mortem clot

antemortem