Cellular Adaptations, Injury and death Flashcards
What is gross pathology?
The recognition and description of macroscopic, morphological changes to tissues and organs at biopsy, surgical removal or post mortem examination.
What must you include in your description?
Organ/Tissue. Position. Number. Weight. Distribution. Contour. Size. Colour. Shape. Consistency. Other features.
Why is the description so important?
Ephemeral - when it’s over, it’s over as the animal/organ/tissue will be incinerated. Critical to describe findings and interpretations accurately, especially as notes are a legal document. Basis for a permaneant, historic and legal record. Definitive diagnosis of a disease is not always made at a microscopic level. Diagnosis requires integration of clinical signs, gross pathology, histopathology and other tests. If the description is insufficient then it may be hard to identify the site of origin.
What are the potential outcomes of a gross pathological examination?
Definitive diagnosis based on appearance alone. Determine potential problem(s) which may correlate with clinical signs and support a presumptive diagnosis. Suggest pathogenesis/mechanism of a disease. Changes not distinct enough to establish a diagnosis (further tests required).
What are the types of distribution?
Random. Symmetrical. Focal. Multifocal. Multifocal to coalescing. Miliary. Segmental. Diffuse.
Descibe random distribution.
Without relationship to the architecture of the organ or tissue.
Describe symmetrical distribution.
Highlights or outlines an anatomical or physiological subunit (e.g. groups of related cells in paired organs).
Describe focal distribution.
A single defined lesion on a normal background or background exhibiting a different process.
Descibe multifocal distribution.
More than one discrete lesion on a background.
Describe multifocal to coalescing distribution.
Many lesions which appear to be growing together or “fusing” suggesting an active process that is expanding or not to be contained.
Describe miliary distribution.
Numerous tiny foci which are too numerous to count.
Describe segmental distribution.
A well defined portion of the tissue is abnormal, usually defining a vascular bed.
Describe diffuse distribution.
The whole tissue is affected.
What types of contour are there? How would you describe them?
Raised, something added. Fluids (blood, transudate, exudate, effusion, oedema, urine). Cells (hyperplasia, hypertrophy, neoplasia, inflammation). Tissues (fat, cartilage, bone etc.) Depressed, something removed. Necrosis. Atrophy. Flat, neither raised or depressed. Has not had time to progress or does not cause expansion or necrosis.
What are the determinants of normal colour?
Innate colour and number of cells, special pigments, adipose tissue and the amount of blood in the vascular bed. Dark tissues - High pigment : Tissue ratio Light tissues - Low pigment : Tissue ratio
What may these colours of tissue suggest? Red - Red/Black White/grey/yellow Black Green-black Green
Red - Red/Black : Congestion or haemorrhage White/grey/yellow : Lack of blood, necrosis, icterus, fibrosis Black : Melanin (melanosis is flat, melanoma is raised) Green-black : Pseudomelanosis (H2S pigments) Green : bile and some fungi
What types of smells can be distinctive?
Foul and rotting smell : putrefactive necrosis or saprophytic bacteria. Ammonia : Uraemia. No odour : Aseptic process.
Suggest some distinctive sounds and describe them.
Crepitant (crackly) : emphysema, gas producing bacteria, normal lung (absence = atectasis, defined as the collapse or closure of the lung resulting in reduced or absent gas exchange). Sloshing : Fluid filled structure, ascites, effusions, diarrhoea.
Define algor mortis.
Cooling of the body after death. Consider the scenario as this may speed it up or slow it down.
Define rigour mortis.
Contraction of the muscles in the body, caused by chemical changes in the muscle cells and prevented in animals in which the muscles were previously depleted of energy (extreme malnutrition). Rigour will normally last for 1-2 days.
Describe bloating as a post mortem change.
Gaseous distension of the gastrointestinal tract due to the production of gas by bacteria.
Describe putrefaction as a post mortem change.
Softening of the tissues by bacteria and cellular breakdown (autolysis).
Describe livor mortis.
Pooling of the blood to the lowest parts of the animal at death. Also known as hypostatic congestion.
List and describe the clot types (post mortem).
Clotting : post mortem clots will not be adhered to vessel walls and they form casts of the vessels in which they are found. Ante mortem clots (thrombi) In artery : attached to the artery wall and often dry and taper off in the direction of blood flow before death, Lines of Zahn : are a characteristic of thrombi that appear particularly when formed in the heart or aorta. They have visible and microscopic alternating layers (laminations) of platelets mixed with fibrin, which appear lighter, and darker layers of red blood cells. In vein : may be attached to vessel but may resemble post mortem clots.
Describe imbibition.
Staining of tissues red by blood or green by bile (bile imbibition).
What causes pseudomelanosis.
Hydrogen sulphide produced by putrefying bacteria, stains the tissue blue-green.
Why perform a PME?
Confirm or refute the clinical diagnosis or refines the list of possible differential diagnoses. Provides a diagnosis where no clinical diagnosis was possible (sudden or apparent sudden death). Provides a reason why treatment may have failed. Aids diagnosis of group or herd problems. A record of findings for further use (disease surveys, legal action). Provides material for further examination (histopathology, bacteriology, virology and toxicology).
How to perform a PME?
Follow a standard procedure - be consistent. Examine all organs. Sample and fix all tissues in 10% formalin. Histological examination of all fixed tissues by a pathologist.
What initial information is required for a PME?
Permission from the owner to perform the PME (written or verbal, written is best as it cannot be backed out of). Description of the animal (then check this before you carry out the post mortem, things can get mixed up) Clinical history. Time and manner of death (this may explain the degree of autolysis and will help you to identify changes that you would expect to occur). Cadaver storage details (chilled or frozen, can explain tissue and cellular changes. Frozen tissues will be darker). Reason for the PM examination (in particular RSPCA cases need particularly careful attention and you must be careful to check and document everything).
What classifications of changes would you expect to find?
Lesions (clinically significant or incidental). Agonal changes (around the time of death). Post-mortem changes (usually autolysis).
Give an example of an agonal change.
Endocardial petechial haemorrhages. Heart wall streaking in animals and distended spleens in animals PTS with barbiturates.
What should be considered when looking at post mortem changes?
Timing - it may be hard to cool a body sufficiently, particularly in the horse so the core body temperature may remain higher than the cooling temperature for a long time after death. Blood pooling - how the body was laid at the time of death should be considered. Lungs will have a different colour if frozen (a deeper red).
Descibe some common post mortem changes.
Some congestion would be expected in the lungs, with imprints for where pressure would have been exerted by the ribs. Chicken fat clots within the heart chamber, with a clear differentiation between plasma and fat portions. It will not be adhered to the vessel walls. Distension of the abdomen is to be expected due to the autolysis that it will experience.
Describe the external examination of the animal to be PME’d.
It is similar to the examination of the live animal, but it is dead. Cadaver condition. Give a body condition score. Orifices, ears and mucous membranes. Inspect for discharges, visible lesions, colour changes (yellow = jaundice, pallor = anaemia, bleeding/reddening = septicaaemia or toxaemia)
Descibe the removal of the skin during a PME.
Dissect between the scapula and rib cage. Disarticulate the coxo-femoral joints. Incise the skin over the sternum. Extend from mandibular symphysis to anus.
What should the subcutis be examined for?
Solids - haematomas, enlarged lymph nodes, tumours (lipomas). Liquids - oedema, pus, blood. Gases - emphysema (bacterial or traumatic). Colour changes (haemorrhages, jaundice).
Describe PME procedure for the abdominal cavity.
Open at the xiphisternum and extend midline incision to the pelvic brim. Incise down the costal margins and lay peritoneum flat. Examine for adhesions (e.g. mesentery), ascites, normal positioning of organs, abnormalities (e.g. intestinal torsion). Check for negative pressure in the thorax (stab the diaphragm, it should “whoosh” towards you.
A lack of negative pressure in the thorax may suggest…
Pneumothorax. Autolysis.
Describe how you would gain access to the thoraxic cavity.
Cut along the costo-chondral junctions on one side. Fold the sternum over to expose the contents of the cavity. Break or dislocate the ribs at the costo-chondral junction on the opposite side. Remove the flesh, cut the ribs and remove the top of the ribcage.
How would you remove the pluck?
Make deep incision parallel and immediately medial to each mandibular ramus. Evert the tongue ventrally. Cut the hyoid bone each side. Strip the plug, incising the oesophagus, aorta and caudal vena cava near the diaphragm and remove the pluck. Use the scalpel to free away fascia.
How would you demonstrate gall bladder patency? What does this show?
Incise the anterior duodenum and squeeze the gall bladder, expressing bile into the duodenum. Nothing coming out demonstrates a post hepatic obstruction, if something does come out then you can’t rule out an obstruction.
Describe the examination of the abdominal cavity.
Locate and remove the adrenal glands. Remove the spleen and liver. Examine the mesenteric and ileocaecal lymph nodes. Cut through the mesentery close to the intestine and straighten the gut (you can do this in or ex situ). Incise through the distal oesophagus and colorectum to remove the alimentary tract. Examine kidneys, ureters and bladder before the removal (checking that they are following the normal pathway and are all connected). Examine the abdominal aorta and sublumbar lymph nodes.
Where should interal organs be placed for examination?
On a table.
How should the pluck be examined?
Examine and remove the throid (dark) and parathyroid (pale) glands. Use scissors with one blunt prong to open the oesophagus. Examine it for lesions (inflammation, tumours, presence of ingesta, foreign bodies). Open the trachea and cut into the major bronch. Examine and palpate the lungs, observing for evidence of distribution.
What should you examine the trachea and bronchi for?
Froth (due to pulmonary oedema). If oedema is full to the top there may be a pathology, or it may be an agonal change. Ingesta (aspiration, pneumonia). Inflammation.
Describe the distribution of broncho-, interstitial- and multifocal- pneumonias.
Bronchopneumonia - usually in the cranial lobes and caused by a virus. Interstitial - usually diffuse and caused by a bacteria. Multifocal - pinpoint across the lungs.
What must you do when you examine the heart?
Ensure you have examined all chambers and valves.
What should you check when examine the external heart?
Size. Weight (weigh it). Chamber sizes.
Describe the examination of the heart.
Initial transverse section 1/3 of the way between the apex and base (assess the chamber thickness and myocardial lesions). Place the heart with the caudal surface towards you. Cut up the right ventricle to the caudal coronary artery. Cut through the atrioventricular ring and expose the right atrium. Cut up close to the left coronary artery and expose the pulmonary artery. Similarly, exposure the left ventricle, left atrium and aortic valves.
What must you examine the heart for?
Possible defects. Heart valves (check them). Endocardiosis (mitral valve of older dogs). Bacterial endocarditis (less common in small animals, but common in farm. Fibrin adhesions or cauliflower appearance may be seen.)
Descibe the examination of the liver and spleen.
Examine the external surface for lesions. Slice into them at 1-2 cm intervals. Examine all cut surfaces for lesions.
Describe the appearance of the spleen of an animal PTS with barbiturates.
Distended with a blackberry appearance.
When is the brain examined?
In situ. Once removed. A minimum of 5 days after fixing.
Name some exogenous pigments and there colours?
Carbon (anthracosis)- black (darkened) Dust (pneumoconicosis)- heavy mucous surface Carotenoids (lipochrome)- soluble yellow (yolk) Iatrogenic- tattoos
Name some endogenous pigments and there colours?
Melanin- skin hair etc Blood/bile-
Haemosiderin, intracellular protein golden brown/yellow
Bilirubin- Yellow, remains of haeme, indicates icterus or jaundice
Haematin- Acid haematin- artefact!
Lipofuscin- wear and tear, golden brown granular!
Ceroid- Similar to lipofuscin- mainly kuppfer cells
Name the different classifications of icterus?
Pre hepatic icterus- excessive production of bilirubin due to haemolysis
Hepatic icterus- Hepatocyte damage, increase in unconjugated bilirubin.
Post hepatic icterus- Obstruction of bile excretion, increase in conjugated bilribun in the blood
Name the different examples of pre, hep, post, icterus?
- Pre hepatic icterus- Due to large haemorrhage into tissues (predominantly in the liver and kidney)
- Hepatic icterus- Liver damage by chemical or toxins also could be hepatocellular tumour
- Post hepatic icterus- Obstruction of bile outflow by gall stone, tumour, inflammation
Name the different types of mineralisation and their examples?
- Calcification, either dystrophic or metastatic. Due to dead or dying tissues accumulating Ca2+..Muscle cellular accumulation. (dystrophic)
- 1 Metastatic due to deposition of ca2+ salts in normal tissues leading to high blood press. Can lead to hyper parathryoidism- rubber jaw.
Gout- deposition of sodium urate crystals
Chloresterol- by product of haemorrage
Oxylate crystals- ethylene glycol
How can you distinguish antifreeze intoxication and the process which occurs? What animal is most prevalent to this?
Cats. antifreeze intoxication leads to oxylate crystal formation. Which can be distinguished by polarized light on the microscope. Absorption throught the GIT and the metabolism converts to a toxic product which causes acute tubular necrosis in the kidneys.
What are the two types of cellular degeneration?
Cellular swelling (hydropic degeneration)- can refer to the distention of endoplasmic reticulum
Fatty change- can be swollen, pale, friable, accumulation of variably sized vacuoles in the cytoplasm. Hepatic lipidosis
What is the process of cellular swelling?
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What is the main process that causes fatty change in the liver and the causes that intiate the main process?
Starvation, overeating, and metabolic disease
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What are the three main causes of necrosis?
- Loss of blodd supply- tissues need their blood supply to remain alive.
- Living agents- bacteria, viruses, fungi and parasites
- Non living agents- chemical or physical injuries.
Explain the process of loss of blood supply?
Hypoxia- Reduction in blood supply
Ischaemia- Loss of blood supply
Infarction- Necrosis of a portion of tissue due to an interruption usually sudden. Can occur in three ways:
- Compression of the blood vessels from outside
- Narrowing of the vessel lumen
- Blockage of the lumen
Give examples of how ischaemia can occur?
Intestinal torsion- venous outflow impeded leading to swelling of the arterials and the tissue finally undergoing ischaemic necrosis.
Arteriosclerosis- may occur in hypertension
Atherosclerosis- rare and may occur in hypoparathyroidism.
Blockage of the lumen- tumours or thrombosis/embolisms
What are the different types of necrosis?
- Coagulative necrosis: remains firm
- Liquefactive necrosis: becomes liquid
- Caseous necrosis: Looks like cottage cheese
- Fat necrosis: Hard soap- like appearence of affected body fat
- Gangrene- mostly a post necrotic change
What are the indicators of necrosis and can you show the events leading to necrosis?
Pyknosis
Karyorrhexis
karyolysis
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