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FD1 > Chronic cell injury and adaptations > Flashcards

Chronic cell injury and adaptations Flashcards

1
Q

If the injury is sublethal and chronic the cells may:

A
  • adapt
  • accumulate normal or abnormal substances
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2
Q

What is autophagy?

A
  • self eating
  • survival mechanism
  • consume damaged organelles
  • consume own proteins and carbs as a source of nutrition
  • protects cell from death
  • limits inflammation if cell dies
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3
Q

What is heterophagy?

A
  • where a cell phagocytosis another cell or part of another cell
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4
Q

What epithelium is this showing?

A
  • normal ep
  • simple columnar of mammary gland
  • purple shows nuclei
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5
Q

What is shown here?

A
  • atrophy = decrease in tissue mass due to decreased size and/ or number of cells after it has reached normal size
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6
Q

What are the causes of atrophy?

A
  • nutrient deprivation
  • loss of hormonal stimulation
  • decreased workload
  • loss of innervation
  • compression
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7
Q

What is hypoplasia?

A
  • tissues decreased in size because they never developed completely
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8
Q

What is this showing?

A
  • Hypertrophy = increase in tissue mass due to increased size of cells (parenchymal cells, not stroma or leukocytes)
  • increased size and number of organelles within cells (not water)
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9
Q

Causes of hypertrophy?

A
  • increased workload
  • increased hormonal stimulation
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10
Q

What is this showing?

A
  • Hyperplasia = increase tissue mass due to increased number of cells
  • subsides if stimulus removed
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11
Q

Causes of hyperplasia?

A
  • increased workload
  • increased hormonal stimulation
  • inflammation
  • physical trauma

(can be precursor to neoplastic transformation)

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12
Q

What is this showing?

A
  • Metaplasia = change from 1 differentiated cell type to another
  • e.g. squamous metaplasia (replacement of glandular with stratified squamous ep)
  • can be seen in healing after mastitis
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13
Q

Purpose of metaplasia?

A
  • protective mechanism
  • can have negative consequences
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14
Q

What is this showing?

A
  • Dysplasia = abnormality in formation of a tissue
  • in ep it implies:
    • increase in number of poorly differentiated cells
    • disorganised arrangment
    • variable appearance
    • can be precursor to neoplasia
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15
Q

Why do injured cells accumulate exogenous and endogenous substances?

A
  • altered metabolism
  • genetic mutations
  • exposure to indigestable exogenous substances
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16
Q

What is Lipidosis?

A
  • accumulation of lipid within parenchymal cells e..g. hepatocytes
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17
Q

Causes of lipidosis?

A
  • increased fatty acid metabolism
  • abnormal cell metabolism
  • impaired release of lipoproteins
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18
Q

What is the appearance of lipidosis?

A
  • swollen, yellowed liver
  • greasy texture
  • may float in water
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19
Q

What is the micro appearance of lipidosis?

A
  • sharply defined large lipid vacuoles
  • distend the cytoplasm
  • displace the nucleus peripherally
  • can see spaces where fat would be (washes out)
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20
Q

Where is glycogen normally stored?

A
  • hepatocytes
  • skeletal muscle cells
21
Q

In what situations is glycogen depleted?

A
  • starvation
  • sick animals
22
Q

When does glycogen accumulated intracellularly?

A
  • excessive in glycogen storage disease
  • in the liver with diabetes mellitus and canine hyperadrenocorticism
23
Q

What is the gross appearance of glycogen hepatopathy?

A
  • mottled
  • brown
  • swollen liver
  • if cut with a knife would not be greasy - not lipidosis
24
Q

What is the micro appearance of glycogen hepatopathy?

A
  • poorly defined
  • small
  • irreguarly shaped vacuoles (feathery)
25
Q

What colour does protein stain with H&E?

A
  • pink
26
Q

What colour do nucleic acid stain?

A
  • blue
27
Q

What would you observe with the accumulation of protein in cells?

A
  • Hylaine = glassy appearance
28
Q

When can protein accumulation be normal?

A
  • Russell bodies of plasma cells
29
Q

What is this showing?

A
  • kidney
  • purple is nucleus
  • pink is cytoplasm
  • granular and dark pink cytoplasm = protein that shouldnt be there
30
Q

What are viral inclusion bodies?

A
  • feature of some viruses
  • can be intranuclear, intracytoplasmic or both
  • can be eosinophilic, basophilic or amphophilic
31
Q

What is this showing?

A
  • virus (pink blobs in the nucleus and cytoplasm)
32
Q

Name the examples of extracellular accumulations

A
  • hyaline (protein) substances
  • pathological calcification
33
Q

What is this showing?

A
  • hyaline substance accumulation (extracellular)
  • stain homogenously eosinophilic on H&E stains
  • not indicative of a single protein
  • (kidney)
34
Q

What is this showing?

A
  • hyaline protein accumulation in kidney
    • protein casts in the lumen of renal tubules (albumin, haemoglobin, myoglobin)
    • serum or plasma in blood vessels
    • serum proteins in vessel walls
    • collagen fibres in some scare
    • collegaen encusted with proteins from eosinophils
    • thickened basement membranes
    • fibrin thrombi
    • amyloid
35
Q

What is this showing?

A
  • Pathological calcification
    • deposition of calcium salts in soft tissues
36
Q

What is Metastatic calcification?

A
  • calcification of soft tissues due to elevated serum calcium e.g.
    • renal failure
    • PTHrp in some neoplasms
    • bone invasion and lysis in some neoplasms
    • Vit D toxicity
37
Q

What is dystrophic calcification?

A
  • calcification of dead tissue (soft tissue necrosis)
  • body is trying to make the tissue more inert
  • calcium does not react with anything
38
Q

What is Calcinosis cutis?

A
  • calcification of the ep and collagen of the skin
    • canine hyperglucocortioidism (Cushings)
39
Q

What is Calcinosis circumscripta?

A
  • localised calcification of the dermis or subcutis
    • tends to happen on pressure points/ often bony prominences
    • a form of dystrophic calcification
40
Q

Name the exogenous pigmented substances

A
  • carbon and dust
    • anthracosis (black carbon pigment)
    • pneumoconiosis (lung disease due to dust)
  • tattoos
    • pigmentation of lymph nodes
  • carotenoid pigments
    • yellow colouration to plasam and lipid laden cells
  • tetracycline
    • yellow to brown discolouration of teeth if present during tooth development + bone
41
Q

What are the nonhaematogenous pigments?

A
  1. melanin
  2. lipofuscin
  3. ceroid
42
Q

What is this showing?

A
  • Melanosis = localised deposits of melanin (not a lesion)
43
Q

What does copper deficiency cause?

A
  • fading coat colour (copper required in production of melanin)
44
Q

What is vitiligo?

A
  • autoimmune attack of melanocytes
45
Q

What is lipofuscin?

A
  • yellow-brown lipoprotein that accumulates as residual bodies in secondary lysosomes
46
Q

What is ceroid?

A

= lipofuscin-like but accumulates in disease states (particularly oxidative stress)

47
Q

What are the haematogenous pigments?

A
  • haemoglobin
  • haematin
  • haemosiderin
  • haematoidin
  • bilirubin
  • porhyria
48
Q
A

FD1 (31 decks)

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