Post Mortem Flashcards
Aetiology of Disease
- Infectious - viruses, bacteria, fungi and parasites
- Physical - trauma (e.g. foreign body in intestine perforated the wall of gut.
Released gut contents into abdomen), pressure, heat, cold, radiation
- Chemical - Toxic organic and inorganic substances, need to examine env’t as well for diagnosis
- Toxins produced by infectious organisms
- Nutritional - Deficiencies of vitamins and trace elements - Excess vitamins and trace elements
- Genetic - Range of defects: some are incompatible with life, others affect specific systems within body and ability to intervene through gene therapy
Pathogenesis
(Time Course)
Pathogenesis: temporal development of a disease
- Acute - of sudden onset & short duration. Possible outcomes (sequelae):
- Causes death of the animal
- Resolves due to host defence or clinical therapy
- Becomes chronic disease
- Chronic - of insidious onset and protracted course. Possible outcomes:
- Progressively destroys tissue compromising its function and endangering life (and in somecases ending life)
- Its course is halted and the tissue repairs by scarring
Post mortem exams become more informational with experience on whether the pathogenesis was chronic or acute
Pathogenesis
(Interplay of Factors Involved)
Way disease develops over time
- Animal: Age, Nutritional and immune status (immunosuppressed?), modified by recent or concurrent disease, Previous exposure to the agent(s) responsible
- Agent: Most don’t cause a uniform pattern of disease: host defences important.
- its capacity to produce disease depends upon the dose/virulence of the agent
- Several agents may be involved; usually one agent debilitates, allowing others to exert a greater effect
- Presence of an agent does not necessarily mean it’s the cause of disease
-Absence of a pathogenic agent may be due to clinical therapy and/or host defence systems
- *Environment:** Overcrowding of animals
- *Mixing** animals from differing origins allows ‘carriers’ to infect susceptible animals
Changes in management routine
Lesions
(and Descriptions)
What we recognise when an animal comes into the exam room. Or lesions that occur in a living animal or post mortem.
- Abnormalities or changes due to disease in living tissues that can be observed in the:
- live animal,
- biopsies from live animals
- & necropsy/ post-mortem examination in animals soon after death
Lesion Descriptions
- Size
- Shape
- Colour
- Weight - generally referred to body weight
- Texture and Consistency
- Appearance of the cut surface
- Contents of hollow organs
- Position, relationships and effects on adjacent tissues
Lesions do not occur in dead animals – major changes after death are due to autolysis and putrefaction
make sure to understand gross and microscopic lesions
Pathophysiology
(Renal Failure)
Functional Changes: E.g. diabetes mellitus (endocrine cells, islets, within the pancreas changes due to functional change of insulin lack)
- Failing kidney does not activate vitamin D –> ↓ Ca2+ resorption from intestinal tract
- Phosphate retention –> hyperplasia of parathyroid glands
- PTH secretion ↑ calcium resorption from skeleton, including from the bones of the face
- Demineralisation affecting bones of skull termed ‘rubber jaw’ or osteodystrophia fibrosa
- Retention of proteinaceous compounds (e.g. PTH)= toxic –> haemorrhagic necrosis of tongue & stomach
- Loss of erythropoietin –> anaemia
- ↓ blood flow in kidney –> ↑ contraction and size of heart fibres
- Excess Ca and P deposits minerals in damaged tissue
Pathophysiology
(Sertoli Cell Tumors)
Occur in testes of middle-aged dogs, larger tumours–> oestrogen:
- Causes feminisation
- Atrophy of other testis
- Squamous metaplasia of prostate
- Bilateral alopecia- These remote effects of the disease (affecting the skin) are more likely to be noticed by the animal’s owner than the primary tumour in the testis
Pathology
(Importance and Methods)
Importance
- Pathology= fundamental to disease diagnosis
- Accurate pathology enables accurate diagnosis, therapy and control
- Can get definitive diagnosis from histo, but the experience comes in where you can make a judgement call as soon as possible while waiting for other test results
Methods
- Biochemistry - blood, urine, discharges from orifices, etc..
- Cytology - cells in smears, aspirates and fluids. number and type of cell present in fluid indicates underlying process
- Necropsy - gross changes in the dead body (post mortem examination). POST MORTEM is beneficial to group animals or companion animals as it establishes why it died, use for future treatment
- Histopathology - microscopic examination of tissues selected from the dead body after necropsy, or biopsy/excision of lesions in the living animal
- Histochemistry - microscopic visualisation of enzymatic activity in tissues. Use of enzymes to detect different types of tissue- for example different fibre types by ATPase staining of skeletal muscle
- Immunological methods - detection of specific antibodies or antigens in tissues or fluids (e.g. To show prior exposure to an infectious agent)- Use of labelled antibodies to detect cell markers (e.g. in cancer diagnosis) or infectious agents in tissues - ex: CD3 immunohistochem. to diagnose T-cell tumor
- Electron microscopy - fine detail of the surfaces or internal structures of cells
- Bacteriology/Virology/Parasitology - isolation & identification of pathogenic bacteria/viruses/parasites
- Toxicology - analysis of tissues for particular poisons and toxins, NEED TO DO ENVIRONMENTAL ASSESSMENT(Need to know which toxin to let the lab to know to look for)
Examination of Bodily Fluids
(Urine Sediment and Cerebral Spinal Fluid)
Urine Sediment
- Useful for: Analysing renal function & identifying urinary infections & renal
protein loss, metabolic disease (e.g. diabetes)
Cerebral Spinal Fluid
- Produced by the choroid plexuses
- Flows through the ventricles of the brain & central canal of the spinal cord
- Provides a cushion around the brain and spinal cord in the meninges
- Is an efficient shock absorber
- Normally contains very few cells
- Can be very useful in diagnosing types of brain disease
Sequelae
(consequences of disease)
- Ex: Cataracts as a consequence of pancreatic problem.
- Often the reason an owner will bring an animal in due to noticing these sequelaes.
- Sequels to underlying cause
Post Mortem Changes
Three different types of changes can be identified in the cadaver:
- lesions (due to disease),
- agonal change (occurs prior to death)
- & post mortem changes (occur after death and before the cadaver is examined)
Post Mortem Clotting of Blood
- Blood separates post-mortem into:
- An upper plasma layer- paler & more translucent (chicken fat look)
- A lower red blood cell layer- intensely red (sedimented RBC’s, red current jelly look)
- There’s no damage to the inner surface of the vessel & can easily remove clot
- Whereas in ante-mortem clotting (thrombus formation)- A thrombus is firmly attached to the underlying vascular endothelium, has a white interior, and is layered
-If they die due to thrombosis (clotting), need to distinguish between thrombis and post mortem clot
-Post mortem clot: can be easily removed from the vessel, no damage to the organ observed
-Thrombus: majority of these cases are consequences of a damaged inner lining and cannot be easily removed from chamber. Usually white crumbly material and have layers of successive thrombosis (like tree rings)
Hypostatic Congestion: livor mortis
- Blood gravitates to the lower most portions of the body postmortem (the dependent portions)
- Process starts within an hour of death & stabilises in 12 to 24 hours
- May be apparent externally in animals with little hair cover (pigs)
- Best appreciated in the dependent lung and kidney during dissection (ex: Blue venous blood has seeped to the right lung and not the left)
Pig lying on slating floor after death, can see marks by gravitational pool of blood
-if Livor mortis is different than the position of the animal presented, IT HAS BEEN MOVED
Rigor Mortis
Rigor Mortis- the contraction of muscles occurring after death
- Commences 1 to 6 hours after death and lasts for 1 to 2 days
- Starts in the heart (blood pushed out of the left ventricle)
- Head and neck muscles affected first then the extremities
- Contraction reverses as the carcase autolyses
- Muscular animals often have stronger rigor whereas emaciated animals have weaker
- ↑ environmental temperature or activity before death accelerate rigor
- Mechanism:
- ↓ ATP availability after death –> Build-up of Ca2+ in cytoplasm –> muscle contraction that persists
- Subsequent muscle relaxation is due to enzymatic digestion of actin-myosin cross-links
- After animals dies, lack of ATP, relaxation process for muscle inhibited
Normal Muscle Contraction
- Calcium ions are sequesterd in the sarcoplasmic reticulum
- An AP results in calcium being released into the cytoplasm, binding to the troponin on the actin myofibril, which exposes the binding site for myosin and results in contraction of the sarcomere
- Exposing myosin and causing contraction
- ATP dependent process for relaxation!
Algor Mortis
Algor Mortis- the cooling of a carcase to the temperature of the environment
- Aids in estimating the time of death
- Practical importance in meat production: The rapid cooling of production animal carcasses in freezer for meat production is imp.
Timing of death- estimated based on a carcase held at 10-20°C: (Combine to estimate time of death)
- Warm & flaccid carcase – dead < than 3 hours
- Warm & stiff carcase – dead for 3-8 hours (stiffen first!)
- Cold & stiff carcase – dead for 8-36 hours
- Cold & flaccid carcase – dead for > than 36 hours
**These estimations were originally based on parameters of deceased beagles
Post Mortem Imbibition of Blood
Within hours of death, haemoglobin released by lysed erythrocytes stains blood vessel walls and adjacent tissues- Very red pigment (oxygen carrying content)
- Best appreciated on surface vessels of organs such as the intestine
- Autolysis is causing the cells to rupture in the first place, but is something that occurs throughout PM
- Aborted foetuses which have died a few days prior to expulsion are usually diffusely red with imbibition
- Blood in right ventricle diffusely stains the endocardium rather than left
- If there’s been haemolytic crisis, staining of tissues occurs early after death: Due to increased fragility of RBCs so if there are already RBC’s rupturing (i.e. trauma) during life, PM imbibition will occur much more quickly. But in life there are macrophages consuming these ruptured RBC’s so you see less of this effect until death
- See most easily on sites of the intestine and in pregnancy failures when the fetus is carried by the mother for a while after death
- becomes more black over time
- Can obscure lesions in PME (most common obscurer)- hence why PMs should be done ASAP: This effect can be the most difficult issue during PM exams due to the intense staining. This is why you want to them QUICKLY after death. Colder temperatures will slow this as well as all other PM changes
Post Mortem imbibition of bile pigment
- Within hours of death, bile penetrates the gall bladder’s wall & stains adjacent tissue (local liver, omentum & GIT) yellowish –> greenish brown
- Whereas jaundice (icterus) is a diffuse yellowish discolouration of normally pale tissues: mucous membranes, sclera & subcutis in non-pigmented skins during life–> should not be confused! Quite different from PM change of imbibition
- imbibition Will stain the lining overlaying the liver as well
- Imbibition is very localized to the liver, not to be confused with yellowish/greenish color of jaundice
Gaseous Distension of the Alimentary Tract
- ESPECIALLY IN RUMINANTS AND HINDGUT FERMENTERS
- Bacterial fermentation in alimentary tract continues after death–> gas build-up. Bacteria remain viable for a period of time and continue to produce gas that resides in alimentary tract
- Pressure of distension may squeeze blood from adjacent tissue –> surface pallor of these other organs (an unhealthy pale appearance). Pressure of gas on adjacent organs makes them become paled due to distension squeezing blood out of them
- Gas rises: distended loops –> pale & lower loops hypostatically congested. Some parts will be more blood distended and some gas distended
- Abdominal viscera may be pale in comparison to thoracic viscera or the musculature of the hind limbs
- Excessive distension may–> intestine tearing
- Do not confuse with inflammation!
- Whereas in Antemortem Rupture- signs of inflammation & matts of fibrin
- PM reaction, there is no host reaction (no hemorrhage, no inflammatory reaction)
- Sometimes animal will rupture before the PM exam can occur
- Caecum of a horse (gaseous distention)
Putrefaction
- Most putrefactive bacteria= anaerobes-e.g. Clostridia found in the large intestine- As commensals largely in the large intestine
- These putrefactive bacteria –> enzymes–> breakdown of proteins, fats and carbohydratesinto simpler substances –> proteoses, polypeptides and amino acids, also produce an unpleasant odour
- Hydrogen sulphide–> Responsible for the colour and smell of putrefying tissue (noticeable features)
- Pseudomelanosis- Greenish/ blackish discoloration of tissues due to ferrous sulphide
Putrefaction: breakdown is associated with bad odor (HS)
—> one big difference to autolysis
- sometimes Bubbly appearance due to accumulation of gas (can see some gas bubbles on x-section)
- Early putrefaction: very small bubbles
- Late: larger bubbles
Antemortem Intestinal Rupture
Can see intestinal content escaping (also in PM)
–> but really diff is:
-Hemorrhage
-can take sections near tear to look under microscope to look for hemorrhage
Puncture has caused intestinal contents to release
- see hemorrhage around the tear
- would not see this PM!
Animal can survive for a while after a puncture or tear
-would then see hemorrhage and fibrin accumulations
–> Yet again should not see this if this is a PM change!!
- Antemortem Gastric Rupture: Can see hemorrhage clearly around the tear
