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what are the two types of cell injury and what cell type undergoes both

1) sublethal and reversible (= cell degeneration)
2) irreversible and lethal (= cell death via oncotic necrosis or apoptosis)
- Liver cells generally undergo both frequently


what is hydropic degeneration how common, and what occurs, in health how is it normally controlled

acute cell swelling
most common expression of cell injury
affected cell can no longer maintain homeostasis and regulate entry and exit of water or ions so their cytoplasm swells with water
intra cellular water and ion concentration largely a function of Na+/K+ ATPase


what are the 2 main causes of hydropic degeneration what occurs and an example

1) physical damage to plasma membrane and/or organelle membranes
the damaged membranes are leaky, allowing entry of water and Na+ and Ca++ ions, and loss of intracellular K+ and Mg++ ions
- Causes cytoplasm swelling and sometimes swelling of the goli body and endoplasmic reticulum
eg - bacterial toxins
2) failure of cell energy production
- hypoxia decrease O2 so decrease aerobic respiration decrease ATP failure of Na+/K+ ATPase movement of Na+ into cell and consequent movement of water in


ultrastructural appearance of hydropic degeneration

- dilated cisternae of smooth and rough endoplasmic reticulum, the Golgi apparatus and the outer nuclear membrane
- swollen mitochondria
- detachment of ribosomes from rough endoplasmic reticulum
- +/- swollen, distorted or lost cilia and microvilli


microscopic appearance and gross appearance of hydropic degeneration

- affected cells appear swollen, with pale, cloudy or wispy to finely vacuolated cytoplasm
- the mildest form is often referred to as cloudy swelling
- extreme his referred to as ballooning degeneration, with marked cell enlargement and voluminous clear cytoplasm due to water accumulation and degradation of cytoplasmic proteins (e.g. virus-infected epithelial cells)
gross - heavy, pale, swollen. soft, friable


fate of affected cell that under hydropic degeneration

- however, the injury is still potentially reversible
- if the membrane damage can be repaired or the oxygen supply restored before the “point of
no return” is reached, affected cells can return to normal appearance and function


what is fatty change, what is it also called, what cells occur the most and what form of fat most involved

intracellular accumulation of excess lipid
- also called lipidosis, steatosis or fatty degeneration
(especially hepatocytes but also renal tubular epithelial cells and myocardial fibres)
- the lipid that accumulates is predominantly in the form of triglycerides (triacylglycerols)


hepatic lipidosis what occurs

most incoming fatty acids are esterified by the hepatocytes to form triglycerides, are then packaged by the hepatocytes with apoproteins to form VLDL exported into the circulation as a readily available energy source for other tissues
the packaging involved lots of energy so injured cells may not pack but may continue creating


causes of hepatic lipidosis and example

1) entry of excess fatty acids into the liver, exceeding its capacity for rapid processing
- e.g. high lipid diets (including milk in suckling animals)
2) inadequate supply of proteins or cofactors to permit synthesis of apoproteins
- e.g. chronic protein malnutrition
3) sublethal hypoxia
- diminished hepatocyte ATP (energy) stores available for synthesis of apoproteins and packaging of VLDL for export
4) sublethal toxic injury
eg - damage to rough endoplasmic reticulum of hepatocytes, decreased apoprotein


microscopic appearance and gross of fatty change

distended by a single large clear cytoplasmic vacuole that displaces the nucleus
gross - organs may be enlarged, slightly pale, soft, friable


fate of affected cells that have undergone to fatty change

may or may not be dysfunctional
- if the cause can be removed and the cell injury repaired, affected cells can return to normal appearance and function
however, severe and prolonged fatty change can lead to cell death and/or to tissue fibrosis (scarring) and architectural remodelling that can be irreversible


intracellular accumulation of glycogen where does storage normally occur, does it occur in health

stored in the cytoplasm of skeletal myocytes and hepatocytes
does occur in health so cell function not neccessarily compromised


List 3 examples of pathological accumulation of glycogen

1) steroid hepatopathy in dogs
2) glycogen storage in diabetes mellitus
3) glycogen storage disorders


steroid hepatopathy in dogs, common in dogs with what, how to confirm it is glycogen, is it responsible for dysfunction and is it reversible

- accumulation of excess glycogen in hepatocytes is common in dogs with hyperadrenocorticism and referred to as steroid hepatopathy
- due to a functional ACTH-producing pituitary tumour (most common) (caused by excessive use of corticosteroids - excess storage of glycogen in hepatocytes
- confirmed as being glycogen by performing histochemical stains (glycogen stains positively with periodic acid Schiff (PAS) stain and the positive staining is lost after addition of diastase)
not responsible for dysfunction of hepatocytes and is a reversible change


intracellular accumulation of proteins what sometimes called and 4 examples of how this occurs

hyaline droplets
1) absorbed colostrum proteins - neonatal - normal
2) resorbed protein droplets - within renal proximal tubular epithelial cells with damage leakage into urine
3) excess immunoglobulins (russell bodies) accumulate within aged plasma cells
4) cells may accumulate misfolded proteins


lysosomal storage disorders what occurs and the two types

- lysosomal storage disorders (LSD) are conditions in which substrates derived from normal cell catabolism accumulate within lysosomes rather than being degraded by lysosomal enzymes
1) inherited lysosomal storage disorders
2) acquired lysosomal storage disorders


inherited lysosomal storage disorders what pattern of inheritance, what occurs and clinical signs, what are the most vulnerable fibres

inherited in an autosomal recessive pattern, reduced lysosomal enzyme activity so reduced deregulation activity, substrate accumulation begins in utero and progressively gets worse, clinical signs depend on degree of compromise of enzymatic activity generally get signs after a few months of life
neurons and myocardial fibres


what is an example of an inherited LSD in animals

glycoproteinoses - defective catabolism of the carbohydrate component of N-linked glycoproteins - e.g. α-mannosidosis in Angus, Murray Grey and Galloway cattle and cats


acquired lysosomal storage disorders how acquired, clinical disease what like and how to tell difference between inherited

lyososomal enzymes may also be inhibited by exogenous toxins
alpha mannosidosis
clinical disease comparable to the inherited and inherited effects young animals


list 3 disorders of degeneration of extracellular tissues

1) amyloidosis
2) fibrinoid change
3) collagenolysis


what is amyloid, what is amyloidosis, what makes them permanent

amyloid = an insoluble, extracellular, fibrillar glycoprotein deposit
amyloidosis = disease resulting from localised or generalised (systemic) tissue deposition of amyloid
- the β-pleated conformation renders the deposits resistant to enzymatic degradation (e.g. by proteolytic enzymes of macrophages)


what are the 4 main types of amyloid what each derived from

1) AL Amyloid - humans most common type of amyloid derived from antibodies (light chains) - may develop domestic animals
2) AA amyloid - most common in domestic animals - insoluble fragment from serum amyloid A (SAA)
3) IAPP Amyloid - many cats with type 2 diabetes mellitus, develop deposits of amyloid in the pancreatic islets of Langerhans (islet amyloidosis)
4) Amyloid derived from misfolded prion proteins - transmissible spongiform encephalopathies (TSE), amyloid deposits composed of misfolded proteins may develop in the brain
eg - scrapie in sheep


describe AA Amyloid and how identified and causes

fragment from serum amyloid A (SAA) normally produced by liver in small concentrations. most with increase SAA blood concentrations don't develop amyloidosis
- identified by its loss of affinity for Congo red stain
cause - underlying disease or inherited or familial


how do transmissible spongiform encephalopathies work in terms of protein

- in these disorders, the amyloid is thought to be due to aberrant post-translational misfolding (β-pleating) of a normal α-helical host cell membrane sialoglycoprotein (PrPc), caused by exposure to a prion (a proteinaceous infectious particle) (PrPSc)
it is currently thought that PrPSc acts as a template on which PrPc is refolded, thereby progressively converting the host PrPc into a likeness of itself


microscopic appearance of amyloidosis in terms of staining and gross appearance

H&E stain eosinophilic
congo red stain - positive orange-red
it appears green and birefringent when stained with Congo red and viewed with polarised light (“apple-green fluorescence”)
gross - only apparent if severe will get enlarged, firm, pale tissues


effects of amyloid deposition
mild - moderate deposition
severe hepatic amyloidosis
renal amyloidosis

- may be asymptomatic
- however, can physical compression of adjacent cells and compromised vascular perfusion (Act as concrete and prevent capillary access, atrophy or cell degeneration (with decreased cell function) or cell death
- severe risk of spontaneous liver rupture, potentially fatal
- renal amyloidosis often succumb to renal failure and those with renal glomerular amyloidosis may suffer from hypoproteinaemia due to loss of circulating proteins through the damaged glomeruli into urine


fibrinoid change what is it, what occurs and when visible

• fibrinoid change = an extracellular degenerative phenomenon observed in damaged blood vessels, especially small arteries and arterioles
- accumulation of plasma proteins (including polymerised fibrin derived from circulating fibrinogen),
- +/- complement and/or immunoglobulins (antibodies) in the tunica intima
-only visible microscopically but may be accompanied by vascular thrombosis and/or haemorrhage and oedema that may be visible grossly
the extravasated plasma proteins (especially fibrin) appear deeply eosinophilic in H&E- stained sections


List 5 causes of fibrinoid change

1) e.g. renal failure - due to endothelial injury by circulating toxins
2) e.g. systemic hypertension - high systemic blood pressure - problem in older patients
3) e.g. vasculitis
4) e.g. selenium/vitamin E deficiency in pigs - due to endothelial injury by reactive oxygen species
e.g. oedema disease in pigs - due to endothelial injury by circulating E. coli toxins


collagenolysis what is it, how look under stain, what may be preceded by

collagenolysis = lysis (dissolution) of collagen fibrils
- a microscopic lesion caused by proteolytic enzymes released by such cells as eosinophils and neutrophils
- the affected collagen fibrils appear amorphous and lightly eosinophilic in H&E-stained sections
- may be preceded by a so-called collagen degeneration stage in which targeted collagen fibres are surrounded by brightly eosinophlilic, granular to amorphous material representing massed eosinophils and their released granules (“flame figures”)


give 3 examples of causes of collagenolysis

1) e.g. insect bite hypersensitivity reactions
2) e.g. mast cell tumours
3) e.g. eosinophilic collagenolytic granulomas in cats and horses