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VET375 Pathology > Necrosis and Calcification > Flashcards

Necrosis and Calcification Flashcards

1
Q

What can cause Cell Injury?

A
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2
Q

There are 2 types of Cell injury what are they and what are their subtypes?

A

•Reversible injury

  • •Cell swelling (hydropic or vacuolar degeneration)
  • •Fatty change (lipidosis)

•Irreversible injury (=cell death)

  • •Necrosis
  • •Apoptosis
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3
Q

What is Cell Degeneration (Hydropic Change)?

A
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4
Q

WHat is Cell Degeneration (Fatty Change)?

A
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5
Q

Are Hydropic and fatty changes irreversible or reversible

A

Reversible if adequate oxygen is restored before the point of no return.

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6
Q

What are the 3 key events in Irreversible Cell Injury?

A
  1. High-Amplitude Mitochondrial swelling
  2. Cell membrane damage
  3. Nuclear breakdown
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7
Q
  • What is Necrosis?
  • Is it Passive or Active
  • Is it Pathologic or Physiologic?
A

Necrosis (oncotic necrosis)

  • Refers to the process of local cell death, with subsequent degradation, that occurs in living tissue
  • Passive process, always pathologic
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8
Q
  • What is Apoptosis?
  • Is it Passive or Active
  • Is it Pathologic or Physiologic?
A

Apoptosis

  • Refers to pathways of cell death that are regulated and programmed
  • Active process, can be pathologic or physiologic

Not mutually exclusive; both can occur at the same time

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9
Q

The two mechanisms of Cellular degradation are Autolysis and Hetrolysis, what are their differences?

A
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10
Q

Explain what the gross appearance of Necrosis would be.

A
  • As a general rule, affected tissue becomes soft and friable, usually develops pallor
  • Affected tissue sharply demarcated from viable tissue, often by a zone of inflammation
  • Timeline of appearance:
  • <6 hr: ultrastructurally
  • 6-12 hr: microscopically
  • 24-48 hr: grossly
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11
Q

Describe the patterns of Necrosis and their causes.

There are 3 of them and one is Multifocal Random

A
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12
Q

What are the Nuclear changes of necrosis that can be seen microscopicallyh?

A
  • Pkynosis - Condensation of Chromatin - Nucleus shrinks and becomes more basophilic (Blue)
  • Karyorrhexis - Nucleus fragments and chromatin fragments become distributed in cytoplasm
  • Karyolysis - Nuclear pallor due to dissolution fo chromatin
  • Absencs of Nucleus - Nucleus becomes completely dissolved
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13
Q

These are the diffent Nuclear changes of Necrosis, can you name them here?

A

nuclear pyknosis (arrows),

karyorrhexis (arrowheads),

karyolysis (arrowheads 1)

Cells eosinophilic, shrunken, lose adherence to BM (arrowheads 2)

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14
Q
  1. What are the 4 Major patterns of Necrosis?
  2. What are the 3 kinds of gangrene?
A

•Major patterns of necrosis:

  • Coagulative necrosis
  • Liquefactive necrosis
  • Caseous necrosis
  • Fat necrosis
  • Gangrene = advanced and grossly visible necrosis
  • Dry gangrene
  • Wet gangrene
  • Gas gangrene
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15
Q

What is Coagulative Necrosis?

What are some common causes?

Where is it commonly seen?

A
  • Basic Architecture of tissue is preserved
  • Common with ischaemia eg. Infaction and in some toxic/metabolic injuries
  • Common in Kidney, liver and Muscle
  • Gross appearance: Pallor of affected tissue
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16
Q

What type of necrosis is this?

Where is this type of necrosis common?

A

Liquefactive Necrosis

Overall Architecture of tissue is lost

  • Due to digestion of dead tissue by lytic enzymes eg. during heterolysis from neutrophil/bacterial enzymes
  • Gross appearance: Cavity containing thick fluid

Common in bacterial abscesses and in the brain

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17
Q

What is Caseous Necrosis

A
  • Mixture of coagulative and liquefactive necrosis
  • Much of tissue architecture lost and cell outlines often lost, but cells are NOT totally destroyed
  • Gross appearance: affected tissue becomes pale tan and friable with a caseous (cheese-like) texture
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18
Q

What is Fat Necrosis?

A

Occurs when adipose tissue is destroyed

  • E.g. trauma to fat and pancreatitis with fat necrosis
  • Pancreatitis: action of lipases on triglycerides FFAs + glycerol. FFAs complex with Ca2+ Ca2+ soaps precipitate
  • Grossly apparent as chalky white deposits
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19
Q

What is the clinical term for death of tissue within a living body?

What types are there?

A
  • Gangrene
    • Dry Gangrene
    • Wet Gangrene
    • Gas Gangrene
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20
Q

What would be the cause of Dry gangrene?

What does it look like?

A
  • Predominately coagulative necrosis
  • Usually due to gradual decrease blood supply (infarction followed by mummification (extremities only)
  • No significant bacterial decomposition
  • Tissues become cold, dry, brown-black and shrivelled
  • Underlying causes include peripheral artery disease, frostbite, ergot and fescue poisoning
21
Q

What is Wet Gangrene

What is it associated with

What does it look like?

A

Predominately liquefactive necrosis

  • Usually secondary to ¯decrease blood supply plus superimposed bacterial infection
  • Bacterial and leukocytic enzymes cause liquefaction
  • Grossly, tissues are soft, moist, red-black and malodourous
  • Usually occurs post ¯ blood supply due to heat, freezing thrombosis or tourniquet
22
Q

What does Gas Gangrene refer to?

A
23
Q

What is a free radical

A

A chemical that is highly reactive due to the presence of an unpaired electron in the outer orbit.

24
Q

What are some common Free Radicals?

A
25
Q

What can happen with an excess of Oxygen in preterm babies?

A

Hyperoxia, Cell Injury

Severe retinopathy and blindness due to pure oxygen inhalation (hyperoxia) in preterm babies

26
Q

What cellular components are at risk from Free Radicals

A

Protiens, Membrane lipids and nucleic acids (they become oxidized)

27
Q

What is an antioxidant?

A

a substance that when present in low concentrations relative to the oxizable substrate significantly delays or reduces oxidation of the substrate

28
Q

What are some free radical mediated diseases?

A

Reperfusion injury e.g. myocardial infarction and stroke

Selenium and vitamin E deficiency

  • •Myopathies (ruminants)
  • •Encephalomalacia, exudative diathesis (poultry)
  • •Hepatosis dietetica and mulberry heart disease (pigs)

Certain toxicities e.g. paracetamol, CCl4, chloroform paraquat, halothane, DDT, oxygen

Role in many other conditions including inflammation, carcinogenesis, atherosclerosis, alcoholic liver disease, Alzheimer’s disease, cataracts, and ageing

29
Q
  1. What causes Reperfusion injury
  2. What does it produce?
  3. What can be used to reduce injury in reperfusion?
A
30
Q

The free radical diease caused by Selenium/Vitamin E deficiency is called what?

And what kind of animal does it effect?

A

White Muscle Disease

Ruminants

Can also cause vascular damage with hemorrage/odema and muscle necrosis in Poultry (esp turkeys)

31
Q

What is Apoptosis

A

Programmed cell death = Metabolic pathway which leads to cell death without lysis or damage of neighbouring cells

  • Tightly regulated program where cells self-digest their own DNA and proteins
  • Can be normal (physiologic or developmental), protective (eliminate potentially harmful cells) or pathologic (when cell is damaged beyond repair
  • Has Distinct morphological features that distinguish it from necrosis.
32
Q

What are the diffences of Apoptosis vs Necrosis

A
33
Q

What are the 4 phases of Apoptosis?

A
  1. Initiation phase (signalling pathway which initiates process)
    • Two pathways: Receptor-Mediated of non-receptor mediated
  2. Control and intergration phase
    • Transmits the signal to the active protiens
  3. Execution Phase
    • Phase in which the cell destruction event occur
  4. Dead Cell Removal Phase
34
Q

Receptor-Mediated apoptosis (Extrinsic or Death Receptor pathway is triggered by what?

A
  • Binding of Tumour Necrosis Factor (TNF) to its receptor
  • Binding of the FAS-ligand to its receptor, Fas (CD95)

This Pushes cells into apoptosis.

35
Q

In Receptor-mediated apoptosis after the ligand binds to the death receptor (eg TNF receptor) what is the next steps?

A

The signal is transfered via intermediate adaptor protiens

  • TNF-receptor associated death domain (TRADD)
  • Fas-associated Death Domain (FADD)
  • This signal is then passed via the death-inducing signal complex (DISC) to activate CASPASE 8 and the execution pahse of apoptosis
36
Q

Explain the Execution phase of Apoptosis

A

Activated CASPASE 3 acts on many cellular substrates, leading to protien hydrolysis, and triggering endonucleases (which chop DNA in 200 base pair fragments)

37
Q
  • What pathway does Non-receptor-Mediated apoptosis belong to?
  • How can it be triggered?
  • What is the key event?
A
  • INtrinsic or mitochondrial pathway
  • Cell may also be triggered into apoptosis by withdrawal of trophic substance (eg hormone) or cell damage/injury (=pull)
  • Key event = increased mitochondrial permeability
38
Q
  1. What is Non-Receptor-Mediated apoptosis (mitochondrial pathway) regulated by?
  2. How is the mitochondrial membrain made to be more permeable?
  3. How does this increased mitochondrial premeability lead to the execution phase ?
A
  1. Regulated by anti-apoptotic (BCl-2) and pro-apoptotic (bax) proteins.
  2. Bax creates channels in mitochondria (increasing permeability) and can also bind to block BCl-2 (which is its protector). With the decreased BCl-2
  3. Increased mitochondrial permeability releases Cytochrome C into the cytoplasm, which activated caspase 9 which in conjunction with Apaf-1 activates Caspase 3 (executioner caspase)
39
Q

What is Autophagy

A

Another mechanism of cell degradation in which cells “eat themselves” to remove/ utilise unnecessary cellular components. All these steps happen inside the cell.

  • Formation of autophagosome
  • fusion with lysosome (enzymes) –> autolysosome
  • Breakdown of Cell Components
40
Q

What are the two main types of Pathologic Calcification?

A

Two main types:

  1. Dystrophic calcification
  • Localised calcification of injured or necrotic tissue
  • Injured/dead cells can’t regulate Ca2+ à Ca2+ influx into cell
  • Mitochondria act as foci of mineralisation
  • NORMAL blood calcium
  1. Metastatic calcification
  • Calcification of living tissue secondary to hypercalcaemia
  • INCREASED blood calcium
41
Q

What are some Examples of Dystrophic Calcification

A

•Fat necrosis

•insoluble calcium soaps

•Atheromatous plaques

•common in humans, some hypothyroid dogs

•Degenerate heart valves

•functional consequences!

•Caseous granulomas

•e.g. tuberculosis, often calcify (enables radiagraphic detection)

•Soft tissue injury

•e.g. calcification of scars, myositis ossificans

•Psammoma bodies

•whorls of calcification in some tumours e.g. meningioma

42
Q

How does Metastatic Calcification differ from Dystrophic?

A
43
Q

What are some causes of metastatic calcification

A

•Primary hyperparathyroidism

  • •Usually due to parathyroid adenoma

•Secondary hyperparaythroidism

  • •Renal failure

•Pseudohyperparathyroidism

  • •Aka hypercalcaemia of malignancy
  • •Parathyroid-like hormone (PTHrp) produced by tumours

•Destruction of bone

  • •Usually due to primary or metastatic neoplasia

•Vitamin D toxicosis

•Milk-alkali syndrome

REMEMBER HYPERCALCAEMIA

44
Q

What is the main hormone involved in Calcium Regulation?

Where in the body is low calcium serum levels detected?

How do we get more calcium into circulation?

A
45
Q

What is the result of Primary hyperparathyroidism?

What could a cause of it?

A
  • Means that no PTH can be released therefor serum calcium can not increase
  • Parathyroid Gland Tumour
46
Q

What is secondary hyperparathyroidism.

What is it secondary to?

What are some of the harmful side effects?

A
  • a disease outside of the parathyroids causes all of the parathyroid glands to become enlarged and hyperactive.
  • Secondary to Chronic Renal Failure
  • Bone demineralisation and Soft tissue metastatic calcification. Uraemic meneralisation “Rubber Jaw”
47
Q
  1. What is Algor Mortis?
  2. What is Rigor Mortis?
  3. What is hypostatic congestion(Livor Mortis)?
A
  1. the second stage of death, is the change in body temperature post mortem, until the ambient temperature is matched.
  2. the third stage of death, is one of the recognizable signs of death, caused by chemical changes in the muscles post mortem, which cause the limbs of the corpse to stiffen
  3. the settling of venous blood in the lower part of an organ or the body
48
Q
  • Why does Rigor Mortis occur?
  • When does it usually start?
  • How long before it disappears?
A
  • = the stiffening of a dead body
  • Accompanies depletion of ATP in muscle fibres
  • Variable onset & disappearance (depends on temperature & muscle activity before death); usual onset 3-8 hours and disappears by about 36 hours with advancing autolysis
49
Q

What causes Postmortem gas production?

What is this sometimes called?

What would it look like in the tissues?

A
  • Bacteria (Clostridia spp.) invasion from gut occurs
  • Bacteria often produce gas
  • Post mortem bloating (must distinguish from bloat)
  • Gas bubbles in tissue (crepitus, cavitations)

VET375 Pathology (6 decks)

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