Lecture 4 Flashcards

1
Q
A
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2
Q

What are the five main types of necrosis?

A
  1. Coagulative necrosis
  2. Liquefactive necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis (both wet and dry)
  5. Fat necrosis
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3
Q

What will the cytoplasm of a necrotic tissue look like?

A
  • Hypereosinophilic (or, more pink)
  • Homogenous
  • Smudged (really hard to see cell detail)
  • Swollen, then shrunken (depending on the phase of necrosis)
  • Pale/ghost-like
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4
Q

What are the gross indications of necrosis?

A
  • Pale, unless there are vascular changes, hemmorhage, or inflammation
  • Sharp line of demarcation
  • Friable - loss of tensile strength
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5
Q

What happens to tissue once it’s necrotic?

There are 4 main fates…

A

Fates of necrotic areas:

  1. Liquefied (drains into lymphatics)
  2. Calcified (dystrophic calcification)
  3. Phagocytosis (thanks macrophages!)
  4. Encapsulated (fibrous encapsulation as protection)
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6
Q

The _______ is a good indicator of necrosis.

A

The nucleus is a good indicator of necrosis.

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7
Q

The appearance of necrosis depends on….?

A

The appearance of necrosis depends on the type of cell, the cause of the lesion, and the duration

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8
Q

What is pyknosis?

A

Pyknosis is the irreversible condensation of chromatin in the nucleus of a cell undergoing necrosis or apoptosis. It is followed by karyorrhexis, or fragmentation of the nucleus.

The nucleus has shrunken to a small, dark structure

Extra, from Wikipedia: Pyknosis is also observed in the maturation of erythrocytes (a red blood cell) and the neutrophil (a type of white blood cell). The maturing metarubricyte (a stage in RBC maturation) will condense its nucleus before expelling it to become a reticulocyte. The maturing neutrophil will condense its nucleus into several connected lobes that stay in the cell until the end of its cell life.

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9
Q

What is karyorrhexis?

A

Karyorrhexis is the destructive fragmentation of the nucleus of a dying cell, whereby its chromatin is distributed irregularly throughout the cytoplasm. It is usually preceded by pyknosis and can occur as a result of either programmed cell death (apoptosis), senescence, or necrosis.

Dr. F-W stated in the review that she views Kayorrhexis and Karyolysis as essentially synonyms.

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10
Q

What is karyolysis?

A

Karyolysis is the complete dissolution of the chromatin of a dying cell due to the enzymatic degradation by endonucleases. The whole cell will eventually stain uniformly with eosin after karyolysis. It is usually preceded by karyorrhexis and occurs mainly as a result of necrosis, while in apoptosis after karyorrhexis the nucleus usually dissolves into apoptotic bodies.

Again, synonymous with karyorrhexis.

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11
Q

What does the absence of a nuclei mean for an RBC?

A

Nothing, that’s the RBC’s normal state of affairs.

RBC are long-lived, but as they don’t have a nucleus, they can’t replicate

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12
Q

Coagulation necrosis:

  1. Most typically occurs in the CNS
  2. Appears as dry, layered exudate
  3. Features preservation of cell outlines
A

Coagulation necrosis:

  1. Features preservation of cell outlines
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13
Q

Liquefactive necrosis:

  1. Most typically occurs in the CNS
  2. Appears as dry, layered exudate
  3. Features preservation of cell outlines
A

Liquefactive necrosis:

  1. Most typically occurs in the CNS
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14
Q

Caseation necrosis:

  1. Most typically occurs in the CNS
  2. Appears as dry, layered exudate
  3. Features preservation of cell outlines
A

Caseation necrosis:

  1. Appears as dry, layered exudate
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15
Q

Define anisocytosis

This is from her “unknowns” word cloud, from Lab 2 CCAs. Not sure if we need to know these for this class, but better safe than sorry.

A

Anisocytosis means that cells are of unequal size. Typically used in reference to RBC’s

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16
Q

Define hemosiderosis

This is from her “unknowns” word cloud, from Lab 2 CCAs. Not sure if we need to know these for this class, but better safe than sorry.

A

Hemosiderosis is a form of iron overload disorder resulting in the accumulation of hemosiderin.

Hemosiderin is an iron-storage complex. It is always found within cells (as opposed to circulating in blood) and appears to be a complex of ferritin, denatured ferritin and other material. The iron within deposits of hemosiderin is very poorly available to supply iron when needed. Hemosiderin can be identified histologically with “Perls’ Prussian-blue” stain. In normal animals, hemosiderin deposits are small and commonly inapparent without special stains. Excessive accumulation of hemosiderin is usually detected within cells of the mononuclear phagocyte system (MPS) or occasionally within epithelial cells of liver and kidney.

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17
Q

Define cholestasis

This is from her “unknowns” word cloud, from Lab 2 CCAs. Not sure if we need to know these for this class, but better safe than sorry.

A

Cholestasis is a condition where bile cannot flow from the liver to the duodenum. The two basic distinctions are an obstructive type of cholestasis where there is a mechanical blockage in the duct system that can occur from a gallstone or malignancy, and metabolic types of cholestasis which are disturbances in bile formation that can occur because of genetic defects or acquired as a side effect of many medications.

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18
Q

Define petechial

This is from her “unknowns” word cloud, from Lab 2 CCAs. Not sure if we need to know these for this class, but better safe than sorry.

A

A petechia is a small (1 - 2 mm) red or purple spot on the skin, caused by a minor hemorrhage (broken capillary blood vessels).

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19
Q

Are the circled cells in good health? If not, what’s going on?

A

If the blue line were an epithelial surface, the epi cells are attached to a basement membrane in health.

But if those cells undergo acute cell swelling and/or die, they tend to round up; there’s a change to the cytoskeleton. They may eventually detach from the basement membrane, and you may see them floating off into space like we see here.

So, another indicator that epithelial cells are dead or dying, is that they detach from the basement membrane

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20
Q

What is a zone of hyperemia?

A

A zone of hyperemia is a bright red zone around an area of necrosis. It’s a vascular change in response to that necrosis, and is an indication that the body has responded/reacted to it.

21
Q

What you see, histologically, on a cell undergoing coagulation necrosis?

A

Coagulation necrosis:

  • Cell and tissue are still identifiable
  • Delayed autolysis, due to decreased pH
  • Nuclear change: There probably won’t be a nucleus, but if there is, it’s pyknotic
  • Cytoplasm: Homogenous hypereosinophilic
22
Q

What are the main causes of coagulation necrosis?

A

The main causes of coagulation necrosis are:

  • Hypoxia
  • Cell membrane injury
  • Toxins
23
Q

What tissues are most commonly affected by coagulation necrosis?

A

Most commonly affected tissues from coagulation necrosis:

  • Liver
  • Kidney
  • Muscle
  • Neurons
24
Q

What do you see here? (circled in blue)

A

The circled area is an example of dystrophic calcification.

Not uncommon, even early on in coagulation necrosis

This would not be why the dog died, but it’s important to recognize it as a feature of coagulation necrosis

25
Q

Zenker’s necrosis is synonymous with…?

A

Zenker’s necrosis is synonymous with coagulation necrosis (of skeletal or cardiac muscle, not really smooth)

26
Q

What do you see, histologically, with caseation necrosis?

A

With caseation necrosis, you see:

  • The cell and tissue are unidentifiable
  • Will see a coagulum of debris, in more chronic situations. (and a solidifation of that material)
27
Q

What are the main causes of caseation necrosis?

A

Main causes of caseation necrosis:

  • TB granuloma
  • Mycobacteria sp.
  • Rhodococcus equi
28
Q

What tissues are most commonly affected by caseation necrosis?

A

Most commonly affected tissues of caseation necrosis:

  • Any site possible. Hooray!
  • Lymph nodes
  • Deep skin wounds
29
Q

What is this image a classic example of?

A

This is a classic “onion skin” or layered caseous necrosis lesion.

The center may be somewhat soft. The center may pour out once cut, but the wall is very thick.

30
Q

What would you see, histologically, in a cell/tissue undergoing liquefactive necrosis?

A

In liquefactive necrosis:

  • The cell/tissue is unidentifiable
  • Cavitation or focal loss of structure
  • Liquid debris and fluid
31
Q

What are the most common causes of liquefactive necrosis?

A

Causes of liquefactive necrosis:

  • Hypoxia
  • Bacteria
32
Q

What tissues are most commonly affected by liquefactive necrosis?

A

Commonly affected tissues, due to liquefactive necrosis?

The CNS, big time.

  • Enzymatic destruction
  • High lipid content

Abscesses - early on

  • Neutrophils
  • Hydrolytic enzymes
33
Q

There is large overlap between which two types of necrosis?

A

There is overlap between liquefactive necrosis and caseation necrosis.

Liquefactive necrosis will happen early, when it’s a bacterial cause.

Depending on the type of bacteria (whether it’s long-living or not), the longer they stay there and recruit neutrophils, the more likely you are to have that solid wall that looks like an onion skin (caseation necrosis)

34
Q

Gangrenous necrosis is….?

A

Gangrenous necrosis is coagulative necrosis in the presence of saprophytic bacteria.

Extra, from Wiki: A saprophyte or saprotroph is an organism which gets its energy from dead organic matter.

35
Q

When does wet gangrenous necrosis occur?

A

Wet gangrenous necrosis happens when you have a really good blood supply to a tissue, with or without bacteria

Large muscle area, mammary tissue

Gangrenous pneumonia, for example

36
Q

When does dry gangrenous necrosis occur?

A

You see dry gangrenous necrosis in the distal extremities

Mummification is a form of dry gangrenous necrosis. This is the big thing to think about, with dry gangrenous

Typically no bacteria present

Think Saddle thrombi in cats

Distal extremities may appear dry, shrunken, black tissue where they should have had feet and paw pads, and skin. May also see it at the tip of the tail

37
Q

What is this image an example of?

A

This is a mammary gland undergoing wet gangrene.

Very vascular structure

Bacteria can find their way in on a routine basis

Dark red, almost purple area

If you were to cut down into this, would see anything from dark green to dark red to black mammary gland tissue, instead of normal pink

38
Q

What is this an example of?

A

This is a sow’s ear, undergoing dry gangrene.

Distal tip has become almost mummified.

Dry, leathery, thick

Can see the zone of hyperemia, the bright red zone in between the normal skin and the dead skin. Still viable tissue there.

It will spread as far as the infarcted area

39
Q

What is the enzymatic necrosis of fat?

A

From Wiki: Fat necrosis is a form of necrosis characterized by the action upon fat by digestive enzymes.

In fat necrosis the enzyme lipase releases fatty acids from triglycerides. The fatty acids then complex with calcium to form soaps. These soaps appear as white chalky deposits.

It is usually associated with trauma of the pancreas or acute pancreatitis.

It can also occur in the breast, the salivary glands and neonates after a traumatic delivery.

40
Q

What happens grossly with enzymatic necrosis of fat?

A

Grossly, you’ll see saponification of fat. White, chalky appearance

Extra, from Wiki:

Saponification is a process that produces soap, usually from fats and lye.

41
Q

What is the difference between an ulcer and an erosion?

A

Ulcer: No longer have an intact basement membrane

Once you no longer have an intact basement membrane, all sorts of bad things can come through. An ulcer can go just to the submucosa, but can also go deeper.

Erosion: Occurs when there’s a focal loss of epithelial cells, but the basement membrane is still intact. As long as the basement membrane is still intact, the epithelial cells can spread across it and regenerate. Can heal, in a fairly rapid amount of time.

In an erosion, you may lose some serum, but it will keep out larger structures because the basement membrane is still intact

42
Q

What is a perforating ulcer?

A

A perforating ulcer is when an ulcer goes through the luminal side to the serosal side. This is a bad deal. You have an open communication from the GI lumen into the peritoneal space, and this is not typically survivable

43
Q

Describe the distribution of these lesions:

A

Distribution of lesions could be described as:

Multi-focal

Widely disseminated

44
Q

Describe somatic death

A

Somatic death is death of the body

45
Q

Describe clinical death

A

Clinical death is the absence of blood flow, breathing

46
Q

Describe brain death

A

Brain death is when there is no activity in the neocortex

Legal ramifications associated with this term

47
Q

Why are we intererested in the different kinds of death?

A

Death is a process, not a singular event.

48
Q

From the Pathology review session:

Brainstorm some things that could cause ulcerations.

A

Potential causes of ulcerations:

  • Helicobacter
  • Foreign body
  • Vet school (hee hee)
  • Goblet cell dysfunction (Hypoplasia or somehow inactivated)
  • Fecal impaction (i.e. mechanical obstructions)
  • GI lymphoma (especially in cat and cattle. Goes through all layers of the GI tract)
  • Less than stellar vascular supply to the epithelium
  • Inflammatory infiltrate
  • Infarction (Transmural necrosis)
  • Intussusception
  • Urinary bladder: Stones, multiple or one big one
  • Also see ulcerations in the cornea, trachea, laryneal area