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Flashcards in Pathology Deck (90)
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What are the four factors on which the degree of cellular injury depend?

1. Dose of injurious agent - eg.  the more virus or bacteria assaulting the cell, the worse the injury could be;

2. Duration of agent's action - the longer, the worse the effect, typically

3. Vascular flow & nutrient supply - eg., oxygen from blood. Typically, cells in tissue that are poorly supplied with blood tend to be more susceptible to infection, but in cases where the antigen/pathogen travels via blood, then those cells that reside in richly vasculated areas like lung, liver, heart, kidneys can be worse affected.

4. Cell Type - highly active/metabolic cells eg. hepatocytes, proximal convoluted tubular epithelium of kidney & cardiac myocytes most susceptible to injury, compared with less metabolically active cells like tenocytes of tendon.


What five stimuli cause cellular injury?

i/ ATP-depletion (ATP needed for cell function). This can occur with:
a/ damage to mitochondrial membrane, which would halt metabolism and thus deprive the cell of ATP & thus result in cell death;
b/ damage to lysosome membrane, so that cellular components would be lysed;
c/ damage to cell’s plasma membrane itself, leading to loss of cellular contents into interstitial fluid.

ii/ Accumulation of waste products like lactate

iii/ Increased cell metabolism - non-renal/cardiac/hepatic cells can also turn on their metabolism to meet demands 

iv/ hypoxia of cell

v/ Pressure changes on cellular organelles - eg., when organelles degenerate, ↑ pressure on the cell inside (basically the rotting/detritus of organelles jams up cell cytoplasm)


What are the five main types of cellular degeneration? 

Degeneration occurs when observable change can be detected within the individual cell.

1. Cellular swelling - mildest, earliest detectable degenerative change due to damage to cell membrane; first stage of cell injury; might be momentary or quickly becoming serious damage.

2. Hydropic - more severe/advanced form of cellular swelling. Cells might swell up like balloon prior to destruction OR vacuole/bleb of fluid develops inside cytoplasm. Looks progressively more swollen & irregular in shape.

3. Cellular fatty change - accumulation or increase of fatty substances within cyctoplasm of specific cells eg., liver, kidney, heart parenchyma, but DOES NOT include accumulation of fat in normal fatty stores.

4. Mucoid (myxoid or myxomatous) - Two types:
I. Extracellular - tend to show faint bluish tinge in H&E stains (check on this for examples)
II. Changes in ground substance aka matrix produced by fibroblasts in connective tissue or epithelial tissue (excessive secretion of mucin). 

5. Hyaline - always pathological, means “glassy”. 
Microscopically, degeneration appears amorphous, staining pinkish red with eosin in H&E.
Intracellular - Eg. degeneration of skeletal muscle
Extracellular - Eg. hyaline protein casts in urine


What are the causes and significance of cellular-swelling degeneration, and what does it look like grossly & microscopically?

CAUSED by influx of H20 into the cell, caused by anoxia & mild toxins (they cause plasma-membrane damage);

SIGNIFICANCE: leads to very subtle change, not so different from early post-mortem or agonal change.

GROSSLY, the tissue would appear paler than normal, and upon cutting, the tissue might bulge because the cells within are swollen.

MICROSCOPICALLY, you would see moderate swelling of cells.


What are the causes and significance of hydropic degeneration?

CAUSE: Excess fluid transferred to ER, which swells, fragments & leaves fluid vacuole in cytoplasm.
SIGNIFICANCE: might indicate viral infection, eg., FMD. Common in metabolically active cells, and those that have well-developed ion pumps.



ATP Production decreases
⬇(Cell membrane damage)

Na+ & H2O move into cell

K+ moves out of cell

Osmotic pressure ↑

More H2O moves into cell

Cisterae of ER distend, rupture & form vacuoles

Ruptured ER & vacuoles merge Extensive vacuolation



What are the causes of cellular fatty change?

I. Dietary & Metabolic:
i/ Starvation - liver is overwhelmed by ↑ mobilisation of fat, stored as neutral fat in liver.
ii/ Overeating - dietary intake is greater than energy expenditure, so fat is temporarily stored prior to movement to body-fat stores.
iii/ Lipotrope derangement - these are basically transporters of fats out of liver. They’re amino acids that help conjugate fat with proteins to form lipoprotein that’s excreted out of cell. Choline & methionine deficiency in diet can lead to fatty change.
(metabolic disease lead to DIFFUSE fatty change)

II. Anoxia:
i/ Anaemia - due to haemhorrage or haemolysis
ii/ Circulatory disorders - eg. ischaemia, chronic venous congestion (leads to ZONAL fatty change with “nutmeg” liver, in periportal areas & congestion in periacinar areas).

III. Toxins: more severe form of cellular swelling when toxins cause fatty change in liver.
i/ bacterial & fungal toxins - produced in bloodstream from circulating bacteria or produced elsewhere & absorbed into bloodstream;
ii/ chemical toxins - CCl4, phosphorous, arsenic, lead
iii/ some plant & fungal toxins - cause fatty change in v. early stages of poisoning.


What are the different types of hyaline degeneration?

Intracellular - Eg. degeneration of skeletal muscle
Extracellular - Eg. hyaline protein casts in urine
Eg. hyaline membranes in lung - protein escaping into
alveoli, impairing gas exchange.


What is fibrinoid degeneration?

Partly degenerated muscles & elastic fibres; partly increased amount of protein ground substance around degenerated fibres; appears fibrin-like red smudging - suggests either local hypersensitivity reaction or hypertension in the blood vessels.


What is amyloid degeneration?

Polymerisation of abnormal peptides into fibrillar proteins from wide variety of sources including albumin, immunoglobin, acute phase proteins & hormones.

β-pleated fibrils (sheets) make up 95% of amyloid - they’re insoluble and can’t be removed from tissues once formed. Remaining 5% derived from connective tissue & include serum amyloid P component, glycosaminoglycans & proteoglycans.

i/ chronic inflammatory process elsewhere in the body (in most cases);

ii/ tumours as in plasma cell & thyroid tumours

iii/ prion disease eg. BSE



What is the difference between primary amyloidosis & secondary amyloidosis?

Give examples of each.

Primary amyloidosis is seen in neoplasia/neoplastic diseases. AL =  amyloid light chain - made up of complete immunoglobulin light chains secreted by plasma-cell tumours. Ie., too much antibody proteins
Eg.,  affected animals have monoclonal gammopathy with abnormal protein in urine (Bence-Jones proteinuria)
- many cases in humans not associated with plasma cell tumours but with increase of normal plasma cells in bone marrow (may produce more immunoglobulin) - sometimes called Dyscrasia

Secondary amyloidosis - amyloid protein deposited in the renal glomeruli of dog & ox - AA = amyloid associated protein
- also called Reactive Systemic Amyloidosis
- secondary to inflammatory reactions, particularly chronic infections


What is renal amyloidosis and what are its effects?

Renal amyloidosis is a secondary amyloidosis, as a reaction secondary to inflammatory reaction esp to chronic infection, as opposed to primary, which is due to neoplastic disease.

Aka Reactive Systemic Amyloidosis & Nephrotic Syndrome

AA (amyloid-associated) protein deposited in the renal glomeruli of dog & ox. 


- failure of normal renal function, sustained loss of protein (mainly albumin) into urine
- reduces osmotic potential of blood to attract fluid back into the blood at the venous end of the capillary bed
- results in oedema of the subcutis and abdominal cavity


What are three types of secondary amyloidosis that can effect the body's organs as a result of a inflammatory reaction to a chronic infection? 

Renal amyloidosis - aka Nephrotic Syndrome or Reactive Systemic Amyloidosis; amyloid deposition in renal glomeruli

Hepatic amyloidosis - Amyloid deposition in the liver causes hepatomegaly with a high risk of haemorrhage

Endocrine amyloidosis - Amyloid deposition can occur in endocrine organs (e.g. the islets of Langerhans in the pancreas)


What is infiltration in terms of pathology?

When something accumulates in the individual cell or surrounding tissue:

1. Glycogen

2. Viral inclusion bodies

3. Abnormal storage products


What is necrosis? 

Death of substantial numbers of cells within the living body, or attached to the living body, resulting in either:

a/ further changes in tissue itself and/or

b/ surrounding unaffected living tissue reacting against necrotic tissue.


What are the causes of necrosis?

Ischaemia / Infarction

Non-living agents: Physical injury, Chemical injury

Living agents: bacteria, parasites, viruses



What is ischaemia and how does it lead to necrosis? 

Ischaemia is reduced blood supply to tissue. 

It can lead to necrosis (ischaemic necrosis) if blood supply is severely reduced due to:




of blood vessel


Give examples of how COMPRESSION of a blood vessel can lead to ischaemic necrosis.

1. Intestinal torsion
2. Intestinal intussusception (portion of sm. intestine becomes enveloped in another)


Venous flow impeded
Organ swells due to congestion
Swelling impedes arterial flow
Arterial flow stops
Tissue undergoes ischaemic necrosis
Intestinal blood barrier compromised - ie., breakdown of villus structure in lining
Bacterial toxins absorbed; prone to rupture with peritonitis ∴
Toxaemia & death


Give examples of how NARROWING of blood vessel can lead to ischaemic necrosis.

1. Arteriosclerosis - vessel wall becomes thickened, not due to any deposition of material; may occur in hypertension, age-related

2. Atheriosclerosis - deposition of lipid, cholesterol & inflammatory macrophages can cause thickening & narrowing of arteries & ischaemia; rare in animals, occasionally dogs with hyperthyroidism


Give examples of how BLOCKAGE of a blood vessels can lead to ischaemic necrosis.

1. Thombosis - Aortic thrombus in cat with hyperthyroidism; embolism

2. Valvular endocarditis (bacterial infection of valve leaflets)

3. Erysipeloxthrix rhusiopathiae in pigs (diamond-skin disease) - Bacterial infection of skin, occlusion of vessels supplying skin, which becomes ischaemic

4. Ingestion of ergot (fungus) - Ischaemic necrosis of extremities, especially ears, digits. Can cause abortion due to ischaemia of placenta.


Give an example of how an infarction can lead to necrosis?

Acute renal infarct - arterial vascular event -- sudden drop in blood supply -- that may cause irreversible damage to kidney tissues. It is often a sign of systemic illness.

Renal infarction can result from an embolus arising in a distant location or from thrombosis of the renal artery. Renal artery thrombosis can be secondary to a diseased artery, systemic hypercoagulability or trauma. Treatment of renal infarction will usually begin with anticoagulation. 


What are some examples of physical injuries that can lead to ischaemic necrosis?

- Burns
- Cold
- Frostbite
- X-rays
- Pressure - eg., recumbent horses can develop ischaemia due to weight of organs pressing down on back & hindlimbs
- Pinching or crushing of tissue - eg. Burdizzo castration


What are some examples of chemical injuries that can lead to ischaemic necrosis?

Oak poisoning (tannins) of foal


Give an example of how living agents -- bacteria, fungi, parasites, viruses -- can cause ischaemic necrosis?

Black Disease 

 aka Infectious Necrotic Hepatitis

A sheep infected with Fasciola hepatica trematode(liver fluke) suffers liver-parenchyma necrosis as the parasite triple in size, blocking blood supply to the liver.  The liver is haemhorragic & necrotic.

The necrotic, anaerobic/hypoxic conditions enable secondary infection by Clostridium novyii Type B, the spore-forming Gram (+) bacillus bacteria that produces toxins.


What are the three zones of necrosis, when microscopically observed, in histological sample?

1/ Sphere of necrosis - where the effect of the causal agent is maximal
2/ Zone of degeneration - a little further away, where the tissue will be damaged but not yet dead
3/ Zone of inflammation - still further away, where effect of agent is insufficient to cause death or degeneration of cells


What are the cellular events of necrosis that can be observed microscopically?

1/ Pyknosis 
2/ Karyorrhexis
3/ Karyolysis 
4/ Cytoplasm sometimes stains brighter pink (more eosinophilic due to lower pH)


What is pyknosis? 

It's a cellular event in necrosis that can be seen histologically: chromatin condenses & becomes small, dark & shrunken



What is karyorrhexis?

It's a cellular event in necrosis that is more advanced than pyknosis. Histologically, the nucleus can be seen to have broken up into several dense pieces.


What is karyolysis?

It's a cellular event in necrosis that is more advanced than pyknosis and karyorrhexis.

It's dissolution of the cell's nucleus. Staining of nucleus with haematoxylin becomes faint & only ghost outline remains.


What happens to the colour of cytoplasm in a cell that is undergoing necrosis when viewed with hematoxalin stain?

It stains brighter pink ie., more eosinophilic due to lower pH. 

(Eosinophilic is more acidic = pink

Basophilic is more basic/alkaline = blue)


What are the five different types of necrosis?

1. Coagulative

2. Liquefactive - Malacia (CNS)

3. Liquefactive - Abscesses

4. Caseous

5. Fat

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