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General Pathology > Exam # 1 > Flashcards

Exam # 1 Flashcards

1
Q

What are the 9 causes of cell injury?

A
  • Oxygen Deficiency
  • Physical Agents
  • Infectious Microbes
  • Nutritional Imbalances
  • Genetic Derangement
  • Workload Imbalance
  • Chemicals, Drugs, and Toxins
  • Immunologic Dysfunction
  • Aging
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2
Q

What is an example of reversible cell injury?

A

Acute Cell Swelling

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3
Q

What is an example of irreversible cell injury?

A
  • Oncotic Necrosis
  • Types of oncotic necrosis
  • Cell death by Apoptosis
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4
Q

What are the Chronic cell injuries and adaptation

A

Chronic injury: Autophagy
Adaptations:
- Atrophy
- Hypertrophy
- Hyperplasia
- Metaplasia
- Dysplasia
(An Animal Has Hefty Metabolic Demands )

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5
Q

What are the 6 final biochemical mechanisms?

A
  1. ATP depletion
  2. Permeabilization of cell membranes
  3. Mitochondrial damage
  4. Lost of Ca homeostasis
  5. Oxidative stress
  6. Damage to DNA
    (A Police Man Loses old Defendant)
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6
Q

What are 3 types of responses to cell injury?

A

1.) Degeneration
2.) Death
3.) Adaptation
(Acronym: DAD)

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7
Q

What are some examples of oxygen deficiency (Hypoxia)

A
  • Inadequate oxygenation of blood (cardiac or respiratory failure)
  • Reduction of vascular perfusion (ischemia) - Reduced 0 2
    transport by erythrocytes (anemia or carbon monoxide
    toxicosis)
  • Inhibition of respiratory enzymes of the cell (cyanide toxicosis)
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8
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Anemia ( Reduced O2 Transport by Erythrocyte)

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9
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Physical agents. This is Mechanical Trauma

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10
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Immersion Foot Syndrome in Horses (Trench Foot)

A Physical Agent.

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11
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Infectious Microbes

  • Exotoxins
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12
Q

What are the some infectious causes of cell injury?

A
  • Bacteria
  • Exotoxins
  • Endotoxins
  • Viruses
  • Fungi
  • Parasites
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13
Q

What are some examples of nutritional imbalances that lead to cell injury?

A
  • Imbalances
  • Deficiencies
  • Excesses
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14
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Rickets (Vitamin D Deficiency)

Nutritional Imbalances

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15
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Polycystic Kidney Disease (Persian Cats)

Genetic Derangement

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16
Q

What are some examples of genetic derangement

A

Mutation Results in:

  • Production of abnormal protien
  • Production of defective enzyme
  • Lack of Necessary enzyme
  • Inactovation of regulatory protien- cell death and/or Neoplasia, ect.
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17
Q

Bonus Question: Where is the mutation located that causes Persian Cats to have Polycystic Kidney Disease?

A
  • PDK-1 and PDK-2
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18
Q

What are some factors that result in cell injury from workload imbalance?

A
  • Overwork or overstimulation
    • Hypertrophy of muscle in weightlifters
    • Myocardial hypertrophy secondary to valvular stenosis, etc
  • Underwork or lack of stimulation
    • Disuse atrophy
    • Denervation atrophy
    • Lack of endocrine stimulation
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19
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Myocardial Hypertrophy Seconday to Valvular Stenosis

Workload Imbalance

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20
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A 
Denervation atrophy (secondary to equine protozoal myeloencephalitis)
Workload Imbalance
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21
Q

What are some examples chemicals, drugs, and toxins, causing cell injuries?

A

Binding receptors, inhibiting or inducing enzymes (altering metabolic pathways), producing free radicals…
• Various metals

  • Pesticides, herbicides, insecticides
  • Poisonous plants, mycotoxins, venom
  • Therapeutic drugs
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22
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Snake Bite

Toxins, Chemicals, Drugs

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23
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Pyrrolizidine alkaloid containing plants (Senecio sp., Echium plantagineum, Crotalaria sp.)

Chemicals, Drugs, Toxins

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24
Q

What are some examples of cell function caused by Immunological Dysfunction?

A
  • Immunologic deficiencies
  • Allergies or hypersensitivity
  • Autoimmune diseases
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25
Q

What is an autoimmune disease?

A

An autoimmune disease develops when an animal’s immune system produces antibodies against their own cells.

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26
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Allergy (Atopic Dermatitis)

Immunologic Dysfunction

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27
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Autoimmune (Pemphigus) - the animal’s immune system built antibodies against the epidermis —> bilateral, symmetrical distribution; This is a chronic condition that can be easily treated.

Immunologic Dysfunction

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28
Q

What is the process taking place in this image? How did this occur? Which of the 9 causes of cell injury is this related to?

A

Cerebral Cortical Atrophy due to neuronal damage

Aging

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29
Q

What happens as an animal ages?

A

As an animal ages, the mechanism of protection starts to fail, leading to tissue damage.

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30
Q

What are some causes of cell injury by aging?

A
  • Cumulative damage to cell proteins, lipids, nucleic acids
  • Attributed to Reactive Oxygen Species (ROS), DNA mutations
  • Cumulative damage to DNA predisposes to neoplasia
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31
Q

What is an alternative term for reactive oxygen species?

A

Free radicals

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32
Q

What is the process taking place in this image? Which of the 9 causes of cell injury is this related to?

A

Penile Squamous cell carcinoma.

Very common in old horses because there is cumulative DNA damage.

Aging

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33
Q

What is the initial response of the cell to pertubation of homeostasis in reversible cell injury?

A

Acute cell swelling

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34
Q

Reversible cell injury = ?

A

Acute cell swelling = degeneration

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35
Q

Cellular response to injury depends on what factors? What will these factors determine?

A
  1. The type of cell/tissue/organ
  2. Time of exposure
  3. Severity of the injury

These factors will determine the type of lesion or the morphology of the lesion.

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36
Q

True or False: Once a cell is injured, no matter the severity or duration, the cell will not be able to recover or return to normal.

A

FALSE

If the injury is not too severe or too prolonged, the cell can
recover and return to normal structure and function

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37
Q

What are some synonyms for acute cell swelling?

A

Hydropic degeneration, Ballooning degeneration (keratinocytes), cytotoxic edema (astrocytes)

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38
Q

What are the 3 ways in which ATP is produced by the cell?

A
  1. Glycolysis (Glucose —> Pyruvate) = 2 ATP
  2. Kreb’s Cycle = 2 ATP
  3. Oxidative Phosphorylation = 32 ATP
    1.
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39
Q

Where does the Kreb’s cycle take place?

A

In the mitochondria

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40
Q

Where does Oxidative Phosphorylation occur?

A

In the mitochondria

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41
Q

Where does Glycolysis take place?

A

In the cytosol

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42
Q

What is the most productive form of ATP production?

A

Oxidative phosphorylation

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43
Q

Of the three ways in which ATP can be produced, which ones are O2 dependent? O2 independent?

A

Glycolysis and Kreb’s Cycle are O2 independent.

Oxidative Phosphorylation is O2 dependent.

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44
Q

Why is ATP depletion so detrimental to the cell?

A
  • Reduction in function of cell membrane pumps (sodium-potassium

pump)

  • Sodium/potassium and calcium abnormalities
  • Alterations in cellular metabolism
  • Disruption of protein synthesis
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45
Q

After ATP depletion, what electrolyte abnormalities do you see in the cell? How do they change? This can lead to?

A

Sodium, Water, and Calcium will increase (causing acute cell swelling)

Potassium will decrease.

This can lead to Hydropic Degeneration —> Hypoxia, Ischemia

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46
Q

What happens when there is an increase in extracellular Ca?

A

When the Na/K pump stops working, extracellular Ca enters the cell. The mitochondria and ER will release their Ca contents into the cytoplasm of the cell. Increased levels of calcium in the cytoplasm activates 4 enzymes: ATPase, Endonuclease, Protease, Phospholipase.

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47
Q

What is the function of the enzyme ATPase?

A

ATPase degrades ATP

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48
Q

What is the function of the enzyme Endonuclease?

A

Damages DNA

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49
Q

What is the function of the enzyme Protease?

A

Protease damages DNA

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50
Q

What is the function of Phospholipase?

A

Phospholipase causes cell membrane damage.

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51
Q

What can be used as protection against Reactive Oxygen Species? What does each one do?

A

Antioxidants:
• Block formation or scavenge (sacrifice themselves)
- Vit A, C, E, Selenium = without these, no protection from ROS —> cell & tissue injury

• Sequestration of inducing agents (transport proteins for copper and iron)
- Ferritin and Ceruloplasmin bind to iron to prevent formation of ROS.

  • Enzymes (decomposes H2O2, OH, O2-)
  • Catalase, Superoxide dismutases (SOD), Glutathione peroxidase = produced by the cell to protect it from ROS damage.
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52
Q

What are effects of ROS?

A
  1. Lipid peroxidation —> membrane damage
  2. Protein modifications —> Breakdown, misfolding
  3. DNA damage —> mutations
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53
Q

What is a reperfusion injury?

A

It’s the tissue damage caused when blood supply returns to tissue (re-perfusion)
after a period of ischemia or lack of oxygen (anoxia or hypoxia)

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54
Q

What is the 4 mechanisms of reperfusion injury?

A
  • Oxidative stress (ROS)
  • Intracellular calcium overload
  • Inflammation
  • Activation of complement system

Ros Came In Cab

(ROS, Calcium overload, Inflammation, Complement)

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55
Q

What are the Ultrastructural morphology of cell swelling?

A
  • Generalized swelling of the cell and its organelles (especially mitochondria)
  • Blebbing of the plasma membrane
  • Detachment of ribosomes from ER
  • Clumping of nuclear chromatin
  • Myelin figures (from damaged organelles membrane
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56
Q

What leads to the detachment of ribosomes from the ER?

A

Swelling of the ER.

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57
Q

Organelle membrane damage leads to?

A

Myelin formation

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58
Q

What is the main difference between reversible and irreversible cell injury?

A

Blebbing but no rupture.

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59
Q

What are the microscopic morphology of acute cell swelling?

A
  • Swollen
  • Pale eosinophilic, and finely vacuolated cytoplasm
  • Besides water (hydropic degeneration), lipids and glycogen also can accumulates in reversible cell injury (Discussed in more detail later in these lectures)
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60
Q

Explain what is going on in this image:

A

Diffused cell injury in organ on the left leads to an increased volume and weight of organ due to an increase in water.

Left Liver: Liver lobes are enlarged and rounded.

61
Q

What are the gross morphology of cell swelling?

A
  • Increases the volume and weight of organs (if diffuse)
  • Imparts pallor
  • Swollen and rounded edges (liver)
62
Q

What Generates Reactive Oxygen Species during cell injury?

A
  • Mitochondrial damage
  • Reperfusion injury
  • Ionizing radiation
  • Transition metals (iron, copper)
  • Leukocytes
63
Q

How do Leukocytes generate ROS?

A

Leukocytes destroy bacteria and microorganisms by producing ROS/free radicals.

64
Q

Name three situations in which an animal would have a decreased supply of Oxygen?

What is produced as a result?

A
  1. Radiation, Toxins, Reperfusion
  2. Leads to the production of ROS including: Superoxide, Hydrogen peroxide, and Hydroxyl radical
65
Q

What injurious agents can lead to mitochondrial damage?

A
  • Hypoxia
  • Toxic agents
  • Increased levels of cytosolic calcium
  • Oxidative stress
  • Phospholipid breakdown
66
Q

Define atrophy

A

Decreased size and/or number of cells after it reached its normal size (decrease in number and size of organelles).

67
Q

Define Hypoplasia

A

tissues or organs that are smaller than normal because they never developed completely.

68
Q

What are the mechanisms of atrophy?

A

Apoptosis and autophagy

69
Q

Define Autophagy

A

Autophagy: Cells consume their own damaged organelles, as a housekeeping function, to remain alive.

70
Q

What are the causes of atrophy?

A
  1. Nutrient deprivation (lack of adequate blood flow)
  2. Loss of hormonal stimulation,
  3. Decreased workload (disuse atrophy)
  4. Denervation (especially in skeletal muscle)
  5. Compression (adjacent to neoplasms or other masses)
71
Q

Define hypertrophy and give an example.

A
  • Increase in size and volume of a tissue or an organ due to increase in cell size
  • Increase in size or number of organelles
  • Ex: Heart and skeletal muscle (cells are postmitotic and incapable of replication)
72
Q

What are the causes of hypertrophy?

A

Increased workload.

73
Q

Define hyperplasia. How can this occur?

A
  • Increase in number of cells
  • This response can occur only in a cell population that is capable of mitosis (epithelial cells respond quickly)
74
Q

What is the difference between Hyperplasia and Neoplasia?

A

Differs from neoplasia because subsides if the stimulus is removed.

75
Q

What are the causes of Hyperplasia?

A
  • Hormonal stimulation (mammary glands and endometrium during lactation and gestation, respectively)
  • Iodine deficiency leading to thyroid hyperplasia (goiter)
  • Idiopathic: nodular hyperplasia in spleen, liver, adrenals in older dogs
76
Q

Define metaplasia. Give an example

A

Change of cell type of the same germ line.
Ex: Squamous epithelial → Columnar epithelial, translational epithelial —> squamous epithelial

77
Q

What can Metaplasia act as? Give examples.

A

Metaplasia can act as a protection mechanism in response to chronic injury.
Examples:
1. Squamous metaplasia of trachea and bronchi in smokers can lead to full neoplastic transformation
2. Vitamin A deficiency: Squamous metaplasia.
3. Chronic regurgitation can lead to intestinal (columnar) metaplasia of the esophagus and predispose to esophageal tumor. (Barrett’s esophagus) neoplastic.

78
Q

Define dysplasia. Give an example

A

Implies an abnormality in formation of a tissue.
E.g. renal and hip dysplasia

79
Q

What is the definition of dysplasia when it is applied to epithelium? What is it caused by?

A
  • When applied to epithelium, dysplasia implies a disorganized cells varying in size, shape, with nuclear pleomorphism and increased mitotic figures.
  • Always pre-neoplastic
  • Induced by chronic injury such as UV radiation, viruses
80
Q

List all of the types of intracellular accumulations.

A

• Intracellular
◦ Lipids
◦ Glycogen
◦ Proteins
◦ Viral inclusion bodies
◦ Lead inclusions

81
Q

List all of the types of extracellular accumulation

A
  1. Amyloid
  2. Fibrinoid change
  3. Cholesterol
  4. Urate trophi
82
Q 
# Define lipidosis. 
What is this process also called?
Where does this occur? What happens as a result?
A

Lipidosis is the accumulation of lipids within parenchymal cells.
It is also called steatosis.
Develops in many tissues, but because the liver is important to lipid metabolism, hepatic lipidosis is common.

83
Q

What are the causes of hepatic lipidosis?

A

Increased delivery of fatty acids to the hepatocyte
◦ Starvation in overweight animals
◦ High fat diet
◦ Diabetes mellitus (increased mobilization from fat stores)
Decreased mobilization of lipids from hepatocytes
◦ Suppression of fatty acid oxidation: Hypoxia, any other cell damage
◦ Suppression of apoprotein synthesis and impaired release of lipoproteins from hepatocytes: Toxins such as Aflatoxins

84
Q

In homeostasis, where is glycogen stored? In metabolic abnormalities?

A

Homeostasis: Glycogen is stored in hepatocytes and skeletal muscle.

Metabolic Abnormalities: Glycogen accumulates is a result of Diabetes mellitus and canine hyperadrenocorticism.

Also in glucocorticoid therapy (exogenous source)

85
Q

Histologically, proteins are?

A

Eosinophilic (pink to orange to red in an H&E

86
Q

When is the term “hyaline” used when referring to proteins? Give examples

A

• When it has a homogenous, eosinophilic and translucent appearance the term “hyaline” is used
Example:
◦ Hyaline droplets in the apical cytoplasm of proximal renal tubular epithelial cells in protein-losing nephropathy.
◦ Mott cells have cytoplasmic hyaline globules (Russell bodies): they are immunoglobulins. Mott cells are plasma cells containing immunoglobulins.

87
Q

Define viral inclusion bodies

A

Viral inclusion bodies are proteins produced by viral replication

88
Q

What is the difference between a DNA virus and an RNA virus? Give examples

A

◦ DNA virus: Intranuclear inclusion bodies (Herpesvirus, Adenovirus, Papilloma)
◦ RNA virus: Intracytoplasmic inclusion bodies (Rabies)

89
Q

What are the exceptions to the definition of viral inclusion bodies?

A

• Exceptions:
◦ Poxviruses are DNA and produce cytoplasmic inclusion bodies.
◦ Distemper virus (Morbillivirus, family Paramyxoviridae) produce both cytoplasmic and nuclear inclusion bodies.

90
Q

What happens in some cases of lead poisoning? What stains are ideal for this type of case?

A
  • In some cases of lead poisoning, intranuclear inclusion develop in renal tubular epithelial cells.
  • The inclusions are a mixture of lead and protein.
  • More easily observed with acid-fast stain (Ziehl–Neelsen) than H&E
91
Q

Define amyloid.

A

• Misfolding disorder of soluble and functional proteins, converting them into insoluble and nonfunctional aggregates

92
Q

Where can amyloids be deposited?

A

• It can be deposited in any tissue but is commonly found in the liver, kidney, and vessel’s wall

93
Q

What are the mechanisms of amyloidosis?

A
  • Propagation of misfolded proteins that serve as a template for self- replication
  • Accumulation of misfolded proteins due to failure to degrade them.
  • Genetic mutations that promote misfolding of proteins (Alzheimer’s and Huntington’s disease).
  • Protein overproduction because of abnormality or proliferation in the synthesizing cell (Plasma cell neoplasia).
94
Q

How is amyloidosis classified?

A
  • Amyloid can be classified by the biochemical identity of protein
  • AA (systemic, derived from serum amyloid A)
  • AL (localized, derived from immunoglobulin light chains)
  • Hereditary or familial AA
  • **Histologically similar**
95
Q

Describe AA Amyloidosis

A

• Serum amyloid A (AA) is produced by hepatocytes in cases of chronic inflammation
• Systemic deposition of serum AA (fibrillar protein)
• Commonly deposited in the kidney (renal glomeruli) and Liver (space of Disse)
• Hereditary or familial forms of AA Amyloidosis
◦ Shar-Pei dogs and Abyssinian cats
◦ Renal medullary interstiium +++, rather than renal glomeruli

96
Q

Describe AL Amyloidosis

A
  • Localized form of amyloidosis
  • Derived from immunoglobulin light chains
  • Commonly deposited adjacent to plasma cell tumors
  • Nasal amyloidosis in horses (conjunctiva might be affected)
97
Q

Define fibrinoid change

A
  • Leakage of plasma proteins into the wall of a blood vessel.
  • Septic or immune-mediated vasculitis.
98
Q

Where does cholesterol form?
What does it induce?

A
  • Form in tissue at sites of chronic hemorrhage and in atherosclerosis
  • Induce inflammatory response
99
Q 
# Define urate trophi.
In what species does this occur in?
What can it lead to?
A

• Deposition of crystals of uric acid in cases with hyperuricemia (renal disease or dehydration)
- Birds, primates, reptiles

100
Q

The cellular response to injury depends on?

A
  1. The type of cell
  2. The severity
  3. The duration
101
Q

Susceptibility of cells to Hypoxia

A

‣ High
• Neurons: (3-5 min)
‣ Intermediate
• Myocardium, hepatocytes, renal epithelium (30 min - 2 hr)
‣ Low
• Fibroblasts, epidermis, skeletal muscle (many hrs)

102
Q

What happens in the case of severe and persistent injury?

A

Severe and persistent injury —> point of no return.

  1. Inability to reverse mitochondrial dysfunction
  2. Severe dysfunction of cell membranes (Lysosomal membranes → Lysosomal enzymes)
  3. Increased intracellular calcium levels
103
Q

What can necrosis lead to?

A

• Necrosis —> Pathological (point of no return) —> Oncotic necrosis (oncosis [derived from onkos, meaning swelling).

104
Q

What does apoptosis lead to?

A

Physiologic cell death/Programmed cell death.

105
Q

Name and explain three situations in which the body has reached the point of no return?

A

◦ Ultrastructural
‣ Swelling
‣ Rupture of plasma membrane and organelles (leakage of contents)
‣ Rupture of nucleus
‣ Mitochondria are swollen and develop amorphous densities
◦ Microscopic
‣ Hypereosinophilic cytoplasm (due to denatured proteins and loss of ribosomes)
‣ Nuclear changes:
‣ Pyknosis (nuclear condensation with shrinkage and intense basophilia)
‣ Karyorrhexis (nuclear fragmentation)
‣ Karyolysis (nuclear dissolution or loss)
◦ Gross (macroscopic)
‣ In general:
• Swelling and pallor (soon after cell death)
• Loss of structural detail and demarcation from adjacent viable tissue
• Discolored (usually white)
• Soft
‣ It varies a lot; it depends of: tissue involved, the nature of the injurious agent, and the time elapsed after cell death.
‣ Necrosis has been classified as coagulative, caseous, liquefactive or lytic, and gangrenous

106
Q

What are the types of oncotic necrosis?

A
  1. Coagulative necrosis
  2. Caseous necrosis
  3. Liquefactive necrosis
  4. Gangrenous necrosis
  5. Fat necrosis
  6. Necrosis of epithelium
  7. Sequelae to oncotic necrosis
  8. Cell death by apoptosis
107
Q

What is Coagulative necrosis typically caused by?

A

Hypoxia, ischemia, or toxic injury

108
Q

What are the three types of fat necrosis?

A

• Enzymatic:
◦ Occurs secondary to leakage of pancreatic enzymes (lipases) in cases of pancreatitis
• Traumatic:
◦ Blunt trauma or chronic pressure against bony prominences (subcutaneous adipose tissue in recumbent animals)
• Idiopathic (unknown cause): ◦ Necrosis of abdominal fat in overconditioned cattle

109
Q

Necrosis of epithelium can occur in?

A

Any epithelial surface

110
Q

Necrosis of epithelium can occur in?

A

Any epithelial surface

111
Q

What are the two types of necrosis epithelium?

A
  • Erosion: Superficial sloughing or exfoliation of dead cells (without rupture of basement membrane)
  • Ulcer: Full-thickness necrosis of the epithelium (with rupture of basement membrane)
112
Q

What does sequelae to Oncotic necrosis elicit?

A

An inflammatory reaction

113
Q

What does sequelae to Oncotic necrosis elicit?

A

An inflammatory reaction

114
Q

What happens as a result of sequelae oncotic necrosis?

A
  • Formation of a sequestrum (foreign material and bone fragments)
  • Inflammation with regeneration
  • Inflammation with scar formation
115
Q

What is physiologic apoptosis?

A

◦ Programmed cell destruction during embryogenesis
◦ Involution of organs or tissues deprived of hormonal stimulation (endometrial and uterine involution)
◦ Cell deletion in proliferating cell populations (to keep homeostasis). Epithelial cells of the skin, gut, etc..

116
Q

What causes pathological apoptosis?

A

Injury from toxins, ROS

117
Q

What happens as a result of pathological apoptosis?

A

◦ Mitochondria and DNA damage (radiation, anticancer drugs)
◦ Mediated by cytotoxic T lymphocytes and NK cells
◦ Nutrient deprivation

118
Q

What is pathological apoptosis regulated by?

A

◦ *** regulated by pro-apoptic and anti-apoptotic intracellular proteins*** **** that activate gene and enzymes leading to cell death****

119
Q

What is the purpose of pathological apoptosis?

A

***Purpose: Eliminates unwanted, potentially harmful, useless, damaged cells***

120
Q

What is pathological apoptosis morphological characterized by?

A

Condensation and shrinkage of the cell

121
Q

What is the area circled in yellow called? In green?

A

Yellow: Chicken Fat Clot

Green: Jelly Clot

123
Q

How do you tell the difference between a blood clot that forms antemortem and one that forms postmortem?

A

Antimortem clot: Dry, friable, and attached to the lumen of the vein.

Postmortem clot: Pale in spots due to livor mortis. Clot is easily detached from and is wet and shiny.

124
Q

What can cause fluid leakage in patients post mortem?

A

If patient is frozen and then thawed, fluid leakage is evident

125
Q

What is occuring in this picture? Is it a post mortem or antimortem change? Why?

A

This is rumen mucosal sloughing, this is an postmortem change and as you can see in the image their are no signs of hemorrhage or inflammation so this has occured after death.

Common post mortem change that gets misinterpreted as lesion is rumen mucosal sloughing. Lining peels off easily. Tissue reaction not present= post mortem change.

126
Q

What is occuring in this picture? What causes it? Post mortem vs. Antimortem?

A

Pseudomelanosis

• Iron sulfide accumulation due to contact with the gut. Bacteria from the gut continues to proliferate and produce iron sulfide.

127
Q

What is an important characteristic for pseudomelanosis?

A

Only superficial area is black because it was the only area in contact with the gut.

128
Q

What is occuring in this image? Is this post mortem change or antimortem change? What causes it?

A

• Gas distention is a normal Post mortem process. It is due to the
growth of gut bacteria flora. Usually clostridium causes it.
Can be confused with ruminal tympany but this is a post mortem change because there are no signs of inflammatory response or any hemmorhage.

129
Q

What is occuring in this picture? Is it post mortem or antemortem? Why?

A

Post Mortem. Rectal prolapse

This is because of the build up of pressure in the abdomen due to the bacterial growth.

130
Q

How can you tell an antemortem intussception vs. a post mortem intususseption?

A

Antemortem: Gut is dark red due to congestion and is thickened/ wet due to edema. The cause of this is increased peristalsis. which can be.

Postmortem: Intestinal invagination of wall that leads to edema/ necrosis due to compression of the wall in antemortem change. Can occur post mortem due to peristalsis continues post mortem for a while, as long as there is no hemorrhage, edema, inflammation ect then it is a post mortem change.

131
Q

What can cause bloody nasal discharge in patients post mortem?

A

Secondary to swelling there is also degradation of vessel walls, which allows for bloody fluid to leak. This comes from nose, mouth ears, ect.

133
Q

What are the differences between post mortem and antemortem gastric rupture?

A

Post mortem: After death, bacteria keeps proliferating and form gas which can cause rupture of the stomach. The edges are discrete and thin. Postmortem digestion by acidic gastric juice also will contribute to it.

Antemortem: Antemortem gastric rupture shows signs of hemorrhage, inflammation, ect. Can lead to peritonitis and death. Serosa has pinpoint redness and other secondary tissue reactions.

134
Q

What is occuring in this image? Did it occur post mortem or antemortem ?

A

Example of Antimortem blood clot. Dry, friable, and attached to lumen of the vein.

135
Q

What is occuring in this image? Why?

A

• Tissues surrounding gallbladder will become stained yellow due to degradation of gall bladder wall.

136
Q

What is occuring in this image? Why?

A

• Lysis of erythrocytes will cause the hemaglobin to stain the vessel wall/ arteries. Not hemolysis. Important to know Time of death because if you see this and patient died < 30 minutes prior this could be a sign of intravascular hemolysis (ie antemortem change)

137
Q

What can Hemoglobin Imbibition indicate when seen on the external side of organs?

A

• When you see this hemoglobin imbibition on the external side of organs it can indicate rupture that caused hemorrhage. CPR can also cause hemorrhages in the liver and leakage of blood, so know the patients history thoroughly to rule out interventional causes.

138
Q

What is this change associated with, is it post mortem or antimortem? Is this common practice anymore?

A

• Intracardiac euthanasia used to be common with pentobarbitol. Solution can cause the solution to precipitate and look like mineralization. Know how euthanasia was administered.

139
Q

What can indicate improper euthanasia technique when a cardiac stick has been prefomed to administer the euthanasia solution?

A

Coagulative Necrosis of Myocardium

  • Intracardiac sticks into the myocardium ( inappropriate) instead of the lumen of the ventricles, can cause necrosis of myocardial cells which needs to be noted. Route of euthanasia solution administration can indicate if this was related to administration of euthanasia solution or not.
  • This image indicates coagulative necrosis. Tissue is solid and architecture remains. No evidince of neutraphils.
140
Q

What causes the spleen to look like this postmortem?

A

• Irregular distribution in spleen is common, during death spleen contracts and pulls blood to the periphery. The blood gets distributed irregularly in the paranchyma of the spleen.

141
Q

What is occuring in this image? Is this a post mortem or antimortem change?

A

• abdominal distension causes organs to press against rib cage so you may see these rib impressions.

142
Q

What is occuring to the organ in this image? Is this post mortem/ antimortem? What pathogen is usually the cause for this?

A
  • pale central area is due to intestinal distension being in contact with that focal area and causes blood to move to the periphery of the intestines. Poorly demarcated, rib impressions usually indicates postmortem changes. Do not confuse with necrosis that is normally clearly demarcated.
  • Softening of liver/ areas rich of enzymes, and feel for normal organ density. But know softening is normal in these organs.
  • The gas bubbles and discoloring is all due to proliferation of bacteria post mortem.

CLOSTRIDIUM IS THE BACTERIA THAT CAUSES THIS.

144
Q

What can be seen in advance stages of decomposition like in this picture?

A

• advances stage of decomposition will show dark green discoloration, large gas bubbles and very clear softening.

146
Q

Where can clostridium effect post mortem? How does it travel?

A

• Clostridium will go into the circulatory system and will effect all organs. This will cause gas bubbles to appear in organs like the brain due to clostridium proliferation.

147
Q

What can lens clouding indicate? Is it a postmortem or an antimortem change? How can you tell if it is because of cataracts vs. typical?

A

• Lens clouding can occur post mortem. Not a cataract. Occurs due to cold temperature. Lens is frozen in this picture. Lens clouds very easily in cold temperature. Recheck lens after finishing to see if the lens has returned to normal (i.e.: Thawed)

150
Q

What are 2 things that can happen to skin post mortem and why?

A
  1. ) Livor Mortis : Due to blood pooling. This can occur within organs also. The blood will pool based on gravity
  2. ) Color change of skin due to acids produced by bacteria.
152
Q

What allows for ruminal reflux, and what can it be confused with? Why is it not that? Hint: it is an antemortem finding?

A

Post mortem: Rumen dilates which allows for ruminal reflux.

Do not confuse reflux with aspiration pneumonia. If there is not any tissue reaction in the lungs, then it is not aspiration pneumonia. Tissue reaction is inflammation, ect,

163
Q

What is another word for gas bubble accumulation?

A

Emphysema

165
Q

What can cause rapid decomposition?

A
  • Overweight animals ( which insulate the body cavity and allow quicker decomposition)
  • Animals left in the heat/ sun
168
Q
A

General Pathology (18 decks)

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