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Pathology > Cell Injury - Reversible and Irreversible > Flashcards

Cell Injury - Reversible and Irreversible Flashcards

1
Q

What are the two options an injured cell has?

A
  1. Reverse the Injury

2. Die!

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2
Q

Reversible cell injury results in…

A

A decrease in cell function.

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3
Q

Acute cell swelling is AKA…(4)

A 
Hydropic degeneration
Hydropic changes
Cytotoxic edema (in the CNS)
Ballooning Degeneration (in the epidermis)
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4
Q

What cells are highly prone to hypoxia and cell swelling? (7)

A
  1. cardiomyocytes
  2. Proximal renal tubule epithelium
  3. Hepatocytes
  4. Endothelium
  5. CNS neurons
  6. Oligodendrocytes
  7. Astrocytes
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5
Q

What is acute cell swelling?

A

early, sub-lethal manifestation of cell damage, characterized by increased cell size and vol. due to water overload

-most common and fundamental expression of cell injury**

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6
Q

What is the Etiology of Acute Cell Swelling?

A

A. loss of ionic and fluid homeostasis

  • failure of ATP production
  • damage to cell membrane (inner and outer)
  • enzyme injury regulating ion channels of membranes
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7
Q

Examples of causes of Acute Cell Swelling…

A 
Physical, mechanical injury
HYPOXIA**
TOXIC AGENTS**
free radicals
viral organisms
bacterial organisms
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8
Q

What is the PATHOGENESIS of acute cell swelling? (9 steps!)

A

Injury, hypoxia, decreased ATP production, Na and H20 move into cell, K moves out of cell, increase in osmotic pressure, increase of H20 moving into cell, cistern of ER distend, rupture, and forms a vacuole, extensive vacuolation, HYDROPIC DEGENERATION

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9
Q

Describe the GROSS APPEARANCE of acute cell swelling?

A

slightly swollen organ with rounded edges
pallor when compared to normal
cut surface: tissue will budge and cannot be easily put in correct position

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10
Q

What is Vesicular Exanthema of Swine Virus, a Calicivirus (vesivirus)?

A

ballooning degeneration resulting in formation of a vesicle (bullae/blister)

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11
Q

What is the HISTOLOGICAL APPEARANCE of cellular swelling?

A 
H20 uptake dilutes cytoplasm
cells enlarge with pale cytoplasm
increased cytoplasmic eosinophilia
normal nucleus positioning with no morphological changes
**see hepatocyte slide from lecture**
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12
Q

What are the ULTRASTRUCTURAL CHANGES of cellular swelling? (4)

A
  1. PLASMA MEMBRANE alterations, such as BLEBBING, BLUNTING, and
    loss of microvilli
  2. MITOCHONDRIAL changes, including SWELLING and the appearance
    of small amorphous densities
  3. DILATION OF ER, with detachment of polysomes; intracytoplasmic myelin figures may be present (see later)
  4. NUCLEAR ALTERATIONS, with disaggregation of granular and fibrillar elements
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13
Q

Fatty Changes - Hydropic Change = Cell Swelling…what is this due to and what does it do to the organelles and cytoplasmic proteins?

A

due to ↑uptake of H2O & then to diffuse disintegration of organelles and cytoplasmic proteins

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14
Q

What is the PROGNOSIS of cellular swelling? Briefly explain.

A

GOOD - if oxygen is restored before the “point of no return”

BAD/POOR - if progression to irreversible cell injury occurs

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15
Q

What does the presence of Lipofuscin in a cell imply?

A

Evidence of Previous Injury

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16
Q

What is the definition of “Fatty Change”?

A

SUB_LETHAL cell damage characterized by intracytoplasmic fatty vacuolation
**may be preceded or accompanied by cell swelling

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17
Q

What classes of lipids can accumulate in cells?

A

ALL LIPIDS!

  • Triglycerides
  • Cholesterol/cholesterol esters
  • Phospholipids
  • Abnormal complexes of lipids and carbohydrates (lysosomal storage diseases)
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18
Q

What is Lipidosis? Where does it tend to occur? (4)

A

accumulation of triglycerides and other lipid metabolites (neutral fats and cholesterol) within parenchymal cells
ex: heart muscle, skeletal muscle, kidney and liver

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19
Q

Hepatic Lipidosis…

A

clinical manifestations are most commonly detected as alterations in function (elevated liver enzymes, icterus) because the liver is the organ most central to lipid metabolism

20
Q

What is the ETIOLOGY of fatty change?

A
  • Main causes: hypoxia, toxicity, metabolic disorders

* Seen in abnormalities of synthesis, utilization and/or mobilization of fat

21
Q

What is the PATHOGENESIS of fatty change? (2 steps)

A
  1. impaired metabolism of fatty acids resulting in triglyceride accumulation
  2. formation of intracytoplasmic vacuoles within the cell
22
Q

What are the possible mechanisms resulting in lipid accumulation - hepatic lipid metabolism?

A
  1. Excessive delivery of free fatty acids (FFA) from fat stores or diet.
  2. Decreased oxidation or use of FFAs.
  3. Impaired synthesis of apoprotein.
  4. Impaired combination of protein and triglycerides to form lipoproteins.
  5. Impaired release of lipoproteins from hepatocytes.
23
Q

What is the ONLY form in which triglycerides can be transported out of hepatocytes?

A

Lipoprotein

24
Q

What is the GROSS APPEARANCE of fatty change?

A

• Liver: Diffuse yellow (if all cells are affected)
• Enhanced reticular pattern if specific zones of hepatocytes are affected
• Edges are rounded & will bulge on section
• Tissue is soft, often friable, cuts easily and has a greasy texture
• If condition is severe small Cat liver sections may float in
fixative or water
See Cat Liver Image from Lecture

25
Q

What are some key cues for Hepatic Lipidosis AKA Fatty Liver?

A

clinically - alterations in liver function

  1. ↑liver enzymes (biochemical change)
  2. icterus
26
Q

Describe the PHYSIOLOGY of Hepatic Lipidosis in LATE PREGNANCY in ruminants…

A

Physiologic: in late pregnancy (PREGNANCY TOXEMIA) and heavy early lactation (KETOSIS) in ruminants

27
Q

What other disease/disorders are associated with Hepatic Lipidosis for the following categories:

  1. Nutritional Disorders
  2. Endocrine Diseases
A

Nutritional disorders:
• obesity
• protein-calorie malnutrition (impaired apolipoprotein synthesis)
• starvation (↑mobilization of triglycerides)
Endocrine diseases,
• diabetes mellitus (↑mobilization of triglycerides);
• feline fatty liver syndrome, fat cow syndrome (unknown cause)
**Niemann Pick disease (phospholipid sphingomyelin) – a **Lysosomal Storage Disease
the bottom 2 are other disease examples for Hepatic Lipidosis

28
Q

What is the HISTOLOGIC APPEARANCE of fatty change? (3)

A
  1. Well delineated, lipid-filled
    vacuoles in the cytoplasm
  2. Vacuoles are single to multiple, either small or large
  3. Vacuoles may displace the cell nucleus to the periphery
    **see image from Lecture
29
Q

What is the PROGNOSIS of fatty change?

A

Initially reversible – can lead to hepatocyte death (irreversible)

30
Q

How often is hepatic lipidosis seen in canines?

A

RARELY

31
Q

What is required for therapy of hepatic lipidosis?

A

ID and treatment of any predisposing diseases and aggressive nutritional support!!

32
Q

Are oral appetite stimulants adequate or inadequate for hepatic lipidosis treatment?

A

INADEQUATE!

33
Q

What are the 3 important morphological features associated with IRREVERSIBLE cell injury?

A

associated morphologically with:
– 1. severe swelling of mitochondria
– 2.extensive damage to plasma membranes (giving rise to myelin figures)
–3. swelling of lysosomes

34
Q

What contributes to Cell Death from Irreversible Cell Injury?

A

Cell Death:
– MAINLY BY NECROSIS!!
– apoptosis also contributes

35
Q

Necrosis is usually accompanied by….

A

INFLAMMATION!!!

36
Q

What are the 3 stages of Necrotic change and what timeline is associated with those changes?

A

Necrotic change:
Ultrastructurally – less than 6 hours
Histologically – 6 to 12 hours
Grossly – 24 to 48 hours

37
Q

What is Necrosis? (AKA Oncosis, Oncotic Necrosis)

A

cell death after irreversible cell injury by hypoxia, ischemia,
and direct cell membrane injury

38
Q

What are the 2 concurrent processes that contribute to the MORPHOLOGIC ASPECT of Necrosis?

A

– Denaturation of proteins
– Enzymaticdigestionofthecell
• byendogenousenzymesderivedfromthelysosomesofthedying cells=autolysis (self digestion)
• By release of lysosome’s content from infiltrating WBCs

39
Q

What is the most common outcome of necrosis?

A

INFLAMMATION!!! Apoptosis will NEVER be accompanied by inflammation!!! NEVER EVER EVER FORGET THIS!!!

40
Q

What are the light microscopy nuclear changes of Necrosis?

A
  1. Karyolysis - undergoing dissolution
  2. Pyknosis - nuclear shrinkage
  3. Kayorrhexis - nucelar fragmentation
41
Q

What is the GROSS APPEARANCE of Necrosis?

A

Pale, soft, friable and SHARPLY DEMARCATED from viable tissue by a ZONE OF INFLAMMATION.
**See Image of Turkey Liver from Lecture - - Hepatitis “Blackhead”

42
Q

Bonus Point…What PARASITE causes Blackhead in Turkey?

A

Histomonas! - - “EVERYTHING is connected!” - Dr. Reich

43
Q

What light microscopy changes in the CYTOPLASM of necrotic cells can be seen?

A

Denatured proteins: - ↑ binding of eosin (pink)
Loss of RNA - Loosing basophilia
Loss of glycogen particles - Glassy homogeneous
Enzyme-digested cytoplasm organelles - Vacuolation and moth eaten appearance

Calcification may also be seen.

44
Q

What are the patterns of Tissue Necrosis? (6)

A
  1. Coagulative Necrosis
  2. Liquefactive necrosis - “melting”
  3. Gangrenous necrosis - sever, highly necrotizing
  4. Caseous necrosis - ex: Tuberculosis - “cheesy” appearance
  5. Fat necrosis
  6. Fibrinoid necrosis - specific type seen in the walls of blood vessels
45
Q

Why are the patterns of tissue necrosis useful to us?

A

Does not reflect underlying mechanisms but are used by
pathologists and clinicians…
May provide clues about the underlying cause!

Pathology (14 decks)

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