Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pathology choefsho > Wound healing, necropsy, cell injury part II, circulatory, neoplasia > Flashcards

Wound healing, necropsy, cell injury part II, circulatory, neoplasia Flashcards

1
Q

What are the 5 main pathological processes?

A
  1. Degeneration and necrosis
  2. Inflammation and repair
  3. Circulatory disorders
  4. Disorders of growth (cell adaptiations, neoplasia, developmental anomalies)
  5. Pigments and tissue deposits

(can have more than 1; which happened first?)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is injured tissue called?

  1. Plaque
  2. Scar
  3. Hemorrhage
  4. Wound
A
  1. Wound
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is replacement of injured tissue called?

  1. Repair
  2. Damage
  3. Hyperplasia
  4. Metaplasia
A
  1. Repair
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When does healing of a wound begin?

  1. Immediately after the hemostasis phase
  2. Immediately after the inflammation phase
  3. Immediately after a wound develops
  4. Immediately after the proliferation phase
A
  1. Immediately after a wound develops
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 4 phases of cutaneous wound healing?

A
  1. Hemostasis
  2. Inflammation
  3. Proliferation
  4. Maturation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How many days after wound healing does proliferation occur?

  1. 1-2 days
  2. 3-7 days
  3. 21 days
  4. 1 month
A
  1. 3-7 days
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How long does the maturation phase of wound healing last?

A

Begins a few weeks in and can last for months to years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What happens during the hemostasis phase of wound healing?

A
  • Immediate
  • Vasospasm -> relaxation
  • Platelets aggregate to exposed collagen and a network of fibrin forms
    • Reduces blood loss
    • Binds edges of the wound together
    • Initiates angiogenesis (PDGF, TGF beta)
    • Releases chemotactic factors to initiate inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What happens during the inflammation phase of wound healing?

A
  • Begins 24-96 hours in(usually 1 day in)
  • Cardinal signs of inflammation seen
  • Some ECM components are chemotactic
  • Degradation: leukocytes “clean up” cell debris from the injury (main job)
  • Leukocytes secrete chemotactic and growth factors to initiate the proliferation phase
  • If excessive, can reduce healing (leads to excessive fibrosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What happens during the proliferation phase of wound healing?

A
  • Begins 3-7 days in, lasting up to 3-4 weeks
  • Regeneration of tissues
    • Endothelium (angiogenesis)
    • Epithelium (epithelialization)
    • Connective tissue (fibrosis)
  • Granulation tissue forms
    • Stem cells in a quiescent stage are influenced by cytokines/growth factors
    • Limited by proliferative potential of cell types involved
    • Fibroblasts proliferate to fortify the wound -> collagen deposition
    • Decreases with age and disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens during the maturation phase of wound healing?

A
  • Begins 3-4 weeks after injury, after proliferation, can last years
  • Remodeling of granulation tissue, maturation of fibrosis, and wound contraction
  • Required for return of tensile strength (increased tensile strength)
  • Re-establishment of cell interactions (epithelial cells)
  • Vascular regression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Wounds with opposed edges are associated with wound healing by __________ intention.

  1. Primary
  2. Secondary
  3. Tertiary
A
  1. Primary

(it is a clean wound with clean edges, easy to suture up)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Gaping wounds, septic wounds, foreign bodies, and wounds with delayed healing processes are associated with wound healing by ___________ intention.

  1. Primary
  2. Secondary
  3. Tertiary
A
  1. Secondary

(can’t bring the edges back together)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which type of wound has a larger blood clot, more granulation tissue, and more necrotic slough?

  1. Primary intention
  2. Secondary intention
  3. Same amount for both
A
  1. Secondary intention

  • (bigger defect to fill)*
  • (img: left primary, right secondary intention)*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Before epithelialization can occur in secondary intention wound healing, what needs to be present?

  1. Healthy bed of fibrous granulation tissue
  2. Healthy bed of fibrinous tissue
  3. Healthy bed of keratinized tissued
A
  1. Healthy bed of fibrous granulation tissue for the epithelium to grow on top

(granulation tissue maturation and wound contraction phase (3-6 weeks)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

During the phase of rapid proliferation in secondary intention wound healing (at 2-3 days), what starts to form beneath the epithelial proliferation?

  1. Necrotic tissue
  2. Vascular granulation tissue
  3. Scab
  4. Abscess
A
  1. Vascular granulation tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Secondary intention will cause a ___________ in tensile strength after the wound is healed.

  1. Increase
  2. Decrease
  3. No change
A
  1. Decrease

(tensile strength will eventually increase over time)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What phase of wound healing is this?

  1. Hemostasis
  2. Inflammation
  3. Proliferation
  4. Maturation
A
  1. Inflammation

(degradation: neutrophils remove junk before healing can occur; dead cells, leukocytes, cytokines, serum/clotting proteins, ECM substances)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do leukocytes degrade the “junk” during the inflammation phase of wound healing?

A
  • Phagocytosis and lysosomal degradation
  • Degranulation and release of digestive enzymes
  • Matrix metalloproteinases secreted- very important for degrading the ECM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Is this primary or secondary intention?

A

Secondary intention

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Regenerative epithelial cells are going to be

  1. Hypertrophic
  2. Atrophic
  3. Hyperplastic
A
  1. Hypertrophic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What phase of wound healing is this?

  1. Hemostasis
  2. Inflammation
  3. Proliferation
  4. Maturation
A
  1. Proliferation

(hypertrophic regenerative cells [stained basophilic] can be seen sneaking in beneath the necrotic tissue on the top left)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

A tissues ability to return to normal depends on:

A

(after the removal of necrotic tissue)

  • Retention of ECM structural framework
  • Regenerative capacity of cells
    • Labile/continuously dividing cells
    • Quiescent/stable cells
    • Permanent cell/non-dividing cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which type of cells proliferate throughout life, replacing those cells that are destroyed (ex. epithelial cells of liver, kidney, lung, pancreas, skin, mucous membrane)?

  1. Labile cells
  2. Quiescent cells
  3. Permanent cells
A
  1. Labile cells = continuously dividing cells
    * (Quiescent cells = stable cells*
    * Permanent cell = non-dividing cells)*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Which type of cells have a low level of replication, undergo rapid division in response to stimuli, and are capable of reconstituting the tissue of origin (ex. smooth muscle, fibrocytes, vascular endothelial cells, chondrocytes, osteocytes [mesenchymal cells])?

  1. Labile/continuously dividing cells
  2. Quiescent/stable cells
  3. Permanent cell/non-dividing cells
A
  1. Quiescent/stable cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Which type of cells have left the cell cycle and cannot undergo mitotic division in postnatal life (ex. neurons, cardiac, and skeletal muscle)?

  1. Labile/continuously dividing cells
  2. Quiescent/stable cells
  3. Permanent cell/non-dividing cells
A
  1. Permanent cell/non-dividing cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

T or F. If a wound does not go deep enough to damage the basement membrane, epithelial cells can just replicate on top of it without other phases.

A

True

(epithelialization)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What occurs during the regeneration of epithelium (epithelialization)?

A
  • Proliferate immediately at denuded surfaces
  • Must disassemble connections to the basement membrane and junctional complexes with neighboring cells
  • Must express surface receptors that bind ECM (if basement membrane is damaged)
  • Intact basement membrane greatly facilitates
  • Regulated by contact inhibition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the role of extracellular matrix (ECM) in regeneration and repair?

A
  • Liver regeneration with restoration of normal tissue after injury requires an intact cellular matrix
  • If the matrix is damaged the injury is repaired by fibrous tissue deposition and scar formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What happens during regeneration when there is no structural ECM framework of the tissue?

A

Fibrosis fills the defect = repair by scarring

(loss of function)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Why are growth factors needed for regeneration?

A
  • Needed for epithelialization, angiogenesis, and fibrosis
  • Needed for cellular proliferation and differentiation
  • Epidermal growth factor- bind receptors on epithelial cells > activates MAPK > induces G0 phase cell cycle
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

T or F. Stem cells are an important source for epithelial regeneration.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What are the 2 types of stem cells?

A
  1. Embryonic
    • Pluripotent; isolated from blastocytes (not from fetus!)
  2. Tissue stem cells
    • Not pluripotent; restricted lineage-specific differentiation capacity
    • Bone marrow (bone marrow, umbilical cord)- hematopoietic and mesenchymal cells (greater capacity for differentiation)
    • Skeletal muscle “satellite cells”
    • Ex. epidermal stem cells of hair follicles, intestinal stem cells at the base of a colon crypt
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What phase of wound healing is this?

  1. Hemostasis
  2. Inflammation
  3. Proliferation
  4. Maturation
A
  1. Proliferation

(neutrophils on the top right, new blood vessles in the middle, fibroblasts on the bottom left)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is angiogenesis?

A
  • A step in regeneration where new blood vessels are formed from existing ones
  • PDGF, FGF, VEGF-A bind GF-R’s on endothelial cells > induce vascular formation by
    • Endothelial proliferation
    • Recruitment of pericytes (cells that support the wall of a blood vessel)
    • Deposition of ECM proteins
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the steps in angiogenesis?

A
  1. Proteolysis of ECM (basal lamina must be broken down)
  2. Migration and chemotaxis to ECM
  3. Proliferation
  4. Lumen formation, maturation, and inhibition of growth
  5. Increased permeability through gaps and transcytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What phase of wound healing is this?

  1. Hemostasis
  2. Inflammation
  3. Proliferation
  4. Maturation
A
  1. Maturation (also the end of proliferation)

(can see fewer small blood vessesls, pink fibrillar material [collagen], more spindle cells [fibroblast])

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the migration and proliferation of fibroblasts?

  1. Fibroplasia
  2. Fibrosis
  3. Fibrinous
  4. Fibrogenesis
A
  1. Fibroplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is scar formation by connective tissue remodeling?

  1. Fibroplasia
  2. Fibrosis
  3. Fibrinous
  4. Fibrogenesis
A
  1. Fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Which of the following are not factors that favor fibrosis?

  1. Severe and prolonged tissue injury
  2. Loss of tissue framework (basement membranes)
  3. Large amounts of exudate/inflammation
  4. Extensive ECM structural framework
  5. Lack of renewable cell populations
A
  1. Extensive ECM structural framework
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is fibrous connective tissue?

A
  • Dense accumulations of fibroblasts and collagen
  • With time, the collagen becomes more densely packed
  • Persists for years (life)

(img: trichrome stain stains collagen blue and cytoplasm red)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How is ECM (extracellular matrix) synthesized

A
  • Collagen (mostly), elastin, fibronectin, laminin
  • Growth factors induces fibroblasts to synthesize collagen
  • Collagen = triple helices with lots of cross-linkage providing tensile strength
  • TGF-beta (cytokines)
    • Produced by platelets and leukocytes
    • Is important for fibroblast migration and proliferation and collagen/ECM protein synthesis

(ex. chronic interstitial nephritis and hypertrophic cardiomyopathy we do NOT want fibrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Microscopically, what are fibrillar substances that stains blue with Trichrome stain?

A

Collagen

(know this)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What are the consequences of fibrosis?

A
  • Loss of functional parenchymal tissue (atrophy)
  • Alteration of physical properties of tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What type of tissue is pictured?

  1. Fibrinous tissue
  2. Necrotic tissue
  3. Granulation tissue
A
  1. Granulation tissue

(different from granulomatous inflammation!!!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is granulation tissue?

A
  • Distinctive arrangement of connective tissue fibers, fibroblasts, and blood vessels
    • Fibroblasts and connective tissue grow parallel to wound surfaces
    • Blood vessels arranged perpendicular to fibrosis (to provide strength)
  • Fragile capillaries- bleeds easily
  • Granular surface
  • Can be excessive, a type of hypertrophic scar termed proud flesh
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

What happens when good granulation tissue goes bad?

A

Proud flesh/hypertrophic scar (exuberant granulation tissue); called hypertrophic because the scar is bigger than it should be, but it is hyperplasia

(caused by too much movement, too much tension, genetics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Why does wound contraction occur during the maturation phase of wound healing?

A
  • It is a normal part of maturation, but can be bad when connective tissue contracts and place tension on surrounding tissues
  • May immobilize or deform the tissue (ex. burns)
  • Mediated by myofibroblasts
    • Form within wounds in response to TGF-beta
    • Increase with time and severity

(ex. lungs, when things go bad: if the tissue contracts, and stays contracted, it can cause respiratory problems)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What are the conditions with impaired wound healing?

A
  • Tension on a tissue
  • Prolonged inflammation
    • Local infection, foreign material
    • Abundant necrotic tissue
  • Disorders in collagen synthesis
    • Protein malnutrition
    • Hyperadrenocorticism- antagonistic effect of steroids
    • Inherited defects- osteogenesis imperfecta, Ehlers-Danlos syndroms
    • Scurvy (vitamin C deficiency)
  • Poor blood supply
    • Diabetes mellitus- impaired angiogenesis
  • Impaired ability of cellular regeneration
    • Chemotherapy
    • Old age
    • Denervated tissue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What are the 6 steps to a successful necropsy?

A
  1. Get the history
  2. Do an external examination
  3. Open the body
  4. Remove the organs
  5. Examine and sample the organs
  6. Write the report

(determine the cause of death or the changes produced by disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

What is the point of biosafety considerations for necropsy areas?

A

to prevent zoonotic infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

At a minimum, necropsy must be conducted in accordance with __________ containment principles and practices.

  1. BSL-1
  2. BSL-2
  3. BSL-3
  4. BSL-4
A
  1. BSL-2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are a few containment considerations for necropsy?

A
  • At a minimum, necropsy should be conducted in accordance to BSL-2 containment principles
  • Review the animal’s history to see if BSL-2 practices are recommended based on the likelihood of zoonotic agents
  • Necropsy of small animals should be conducted within biosafety cabinet
  • Unessential personnel and others should not be allowed in the necropsy area
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Can you name some zoonotic animal diseases?

A

Yersinia pestis (plague; re-emerging), Leishmania donovani, Chlamydia psittaci, Venezuelan equine encephalitis virus, Eastern equine encephalitis virus, several species of Brucella (genital tracts, abortion), Rabies virus, Yellow fever, virus, Francisella, tularensis, Mycobacterium tuberculosis, SARS coronavirus, Coxiella burnetii, Rift Valley fever virus, Rickettsia rickettsii, Chikungunya, West Nile virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Why do necropsy procedures pose the greatest risk of disseminating infectious agents to humans?

A

Because of the large amounts of tissues and body fluids exposed during dissection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Which of the following are not part of the Personal Protective Equipment?

  1. Boots
  2. Gloves
  3. Glasses
  4. Apron
  5. None of the above
A
  1. Glasses

(for some diseases a respirator mask is recommended as well; double gloving is recommended)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Which of the following are not procedural considerations for necropsy?

  1. Rabies vaccination
  2. Tools should be used to the extent feasible to manipulate tissues to avoid cut hazards (forceps)
  3. No eating, drinking, grooming are permitted in necropsy areas
  4. All necropsies should be viewed as “universal precautions” (all specimens handled as if they had zoonotic diseases)
  5. Power tools are preferred to hand tools
  6. None of the above
A
  1. Power tools are preferred to hand tools

(HAND TOOLS are preferred to power tools)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Which of the following are not methods of carcass disposal?

  1. Composting (poultry, sheep and goats)
  2. Burial
  3. Biohazard dumpster
  4. Incineration
A
  1. Biohazard dumpster

(dispose of carcasses appropriately, away from scavengers that might drag parts to other locations and inadvertently expose people)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Where can you obtain blood from a carcass with suspected anthrax?

  1. Jugular vein
  2. Peripheral blood vessels
  3. Percutaneous cardiac puncture
  4. All of the above
A
  1. All of the above

(using both a red-top and a purple top (EDTA) blood collection tube for blood smear and blood culture [ear])

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

What are the methods for dissection of the heart?

A

Via right ventricle, left ventricle, aortic outflow (see image)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

What are the methods for removal of the brain?

A

Frontal incision, sagittal incision, or an incision from the external orbit to the occipital foramen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

What are the methods for removal of the spinal cord?

A

Via cervical, thoracic, or lumbar vertebrae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

How do you obtain blood from a carcass for necropsy?

A
  • Obtain heart blood using a 12 mL syringe with an 18G 1.5in needle, attempt to secure 3-10mL of heart blood (or from jugular vein)
  • It may be necessary to incise the left ventricle and aspirate blood from the surface (pleural and peritoneal fluids may be used if blood is not available)
  • Express blood into a green-topped (heparinized) blood collection tube)
  • If possible, obtain a second 10mL of blood and fill a red-topped blood collection tube
  • If heart blood is clotted and no body cavity fluid is available, a blood clot can also be collected and placed into one of the zipper lock tissue bags
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

How do you obtain urine from a carcass for necropsy?

A

Using a 12mL syringe with an 18G 1.5in needle, aspirate up to 10mL of urine from the urinary bladder and put the urine into a red-top blood collection tube

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

How do you obtain brain samples from a carcass for necropsy?

A
  • Collect appropriate specimens for the state rabies lab BEFORE taking any other samples or dividing brain (send to state rabies lab)
  • Place 1”x1” portions of cerebellum, brainstem and cerebrum into each of 2 different labeled zipper lock bags for microbiology and toxicology
  • The remainder of the brain needs to be placed in the largest formalin jar
  • For livestock, it may be necessary to split the brain between the 2 largest containers
  • The best fixation will be achieved if the brain is sliced every 0.5cm (no bigger) most of the way through (“bread-loafed”), leaving about 0.5-1cm of tissue unsliced along the ventral portion to keep the parts together
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

What are some anicillary tests for necropsy?

A
  • Skin (bovine): 0.25-0.5” piece of ear skin, place into plastic snap-top vial containing phosphate buffered saline
  • Adipose tissue (fat): obtain a sample 2”x3”, if possible, place in labeled zipper lock bag
  • Liver: submit a large portion (1”x2”), place in labeled zipper lock bag
  • Kidney: submit a large portion (1”x2”), place in labeled zipper lock bag, usually it will be tripped in triangular shape
  • Eyeball: submit intact eyeball, place in labeled zipper lock bag
  • Colon contents: collect approximately 2 teaspoons of colon (not small intestine) contents for parasitology, place in labeled fecal cup (do not fill more than 1/3 full
  • Stomach contents: collect approximately 2 tablespoons of simple stomach or rumen contents, place in labeled zipper lock bag, if possible, freeze stomach contents ASAP prior to packaging for shipment

Additional samples:

  • Depending on disease presentation
  • Lung for respiratory disease
  • Small intestine, cecum and large intestine for diseases that affect different parts of the same organ system (multiple samples)
  • Small lymph nodes submitted whole, larger lymph nodes sampled for microbiology (retropharyngeal, bronchial, mesenteric or peripheral lymph nodes) by collecting 0.5-1” pieces
  • Place all fresh tissues in labeled zipper lock bags
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

When should you inoculate microbiological transport media?

A
  • Whenever anaerobic cultures are indicated, to avoid bacterial contamination and overgrowth when samples cannot be shipped promptly, or when the prosector wants to direct the exact site of sampling for culture (ex. intestine or muscle when Clostridial infection is suspected)
  • This media will also support aerobic and fungal culture
  • When sampling from solid tissues, the surface of the tissue sample should be decontaminated by searing with a heated blade or flaming with alcohol, and then a stab incision is made with a sterile scalpel blade before inserting a sterile swab
  • When sampling hollow organs such as loops of bowel, it may be necessary to open a segment with a clean scalpel or scissors and swab the interior
  • Septicemias are best defined by culturing the same organism from more than one site (ex. GI tract and liver or lymph nodes)
  • If the carcass is noted to be severely autolysed, culture may not be worthwhile (because of bacterial overgrowth)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

What are examples of how to assemble fresh specimens?

A
  • Label and place anaerobic transport media, if used, in its own Styrofoam mailer to protect from breakage and temperature extremes
    • Place this inside a pouch and place in a shipping box (DO NOT CHILL OR PACK IN CONTACT WITH FREEZER PACKS)
  • Place labeled blood tubes, and urine and skin sample vials, into slots in absorbent pouch
    • Roll up, place it, with any inoculated and labeled transport media, into a labeled zipper lock bag
  • Place all fresh tissue bags and the fecal cup into the second, labeled zipper lock bag, place these packets inside the largest 95kPa-rated specimen pouch, seal, place pouch inside the insulated foil pouch with 2 frozen ice packs, and zip shut
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What are the classic necropsy fresh/frozen sample sets for toxicological investigation?

A
  • Brain, liver (no gall bladder; most toxins get metabolized here), kidney, fat (toxins get accumulated here), urine, aqueous humor or intact eyeball, skin, heart blood (collected into heparinzed tube/green top vacuum blood collection tube)
  • Collect stomach/rumen and intestinal/ feces contents last
  • Each tissue type should be placed in a separate container
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

If a particular toxin or class of toxins is suspected of being involved in animal morbidity or mortality, you may also want to collect various other samples, depending on possible routes of exposure such as:

A
  • Environmental samples
  • Feed samples
  • Water samples
  • Heparinized whole blood (20mL or more, green-topped blood collection tubes) from live animals

In most cases, toxicology samples should be stored frozen until tested

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Rabies submission information

A
  • Rabies virus may only be detected unilaterally > if submissions include only half the brain, on a longitudinal section, the diagnosis of rabies could be missed
  • Notify your County Public Health Department and submit the rabies exposure history form with the specimen
  • Small animals and wildlife- whole head (cerebellum and brainstem are vital; virus has higher affinity to these specific neurons)
  • Livestock- if the only testing is to rule out rabies and BSE/Scrapie, the brain stem and cerebellum can be removed through the foramen magnum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

How do you collect samples for necropsy from the nervous system?

A
  • Brain: put the remainder of the brain, into the formalin jar if not already done (see previous slides about “bread-loaf”; do not slice too thick because formalin cannot penetrate); it may be necessary to divide it for fixation and shipping into 2 jars (large livestock)
  • Peripheral nerves: collect a segment 1” of a peripheral nerve, such as the sciatic
  • Spinal cord: collect one or more sections, from cervical, thoracis, and lumbar areas, by disarticulating or sawing through the spinal column at various levels
  • Order of collection is based on autolysis: brain > pancreas > GI > liver > others
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

T or F. Where lesions are recognized, include sections that incorporate both normal and abnormal appearing tissue, when available.

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

What are the basic components of a necropsy kit?

A
  • Jars with 10% buffered formalin
  • Specimen labels
  • Zipper lock bags
  • Fecal cup
  • String (for tying off loops of bowel)
  • Absorbent material
  • Red-top blood collection tubes
  • Green-top (heparinized) blood collection tube
  • Scalpels/knife/scissors/forceps
  • Microbiology transport media (without charcoal) with swabs
  • Anaerobic transport medium tube with swab
  • Necropsy Kit Submission Form
  • NYS Rabies Laboratory instructions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

How do you describe a lesion?

A
  • Number
  • Size
  • Location
  • Distribution
  • Shape
  • Color
  • Consistency
  • Margins/Surface

“No SLo DiSCo CoMas”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Describe what is morphologically abnormal about this lung from a cow?

A

1cm in from the pleural surface, discrete triangular shape 4 cm in diameter, fleshy nodular mass, locally extensive, yellow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

What is the MDx of this lung from a young cow?

A

Severe, locally extensive, chronic granulomatous pneumonia

(if something is added: inflammation and repair OR disorders of growth)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

What is the etiology for this lung from a young cow?

A

Higher bacteria, Mycobacteria bovis (granulomas in any organ) > Tuberculosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Describe this mass from the mesentary of a horse.

A

Protruding from the serosal surface of the mesesntary is a 4-5cm in diameter smooth surface nodular mass

On cut surface, the mass exudes a thick opaque yellow exudate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

What is the MDx for this mass on the mesentary of a horse?

A

Focal, chronic, suppurative, mesenteric peritonitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Describe what is morphologically abnormal from this small intestine of a calf.

A

Diffusely, the mucosal surface of the small intestine is covered in thin mats or strands of friable white material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

What is the morphological Dx of this small intestine from a calf?

A

Diffuse, acute, severe fibrinous enteritis

(when you see fibrin > acute)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

What is the etiology of this small intestine from a calf?

A

Salmonella (zoonotic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

What is the etiology of this dog?

A

Congestive heart failure

(pressure from abdominal vasculature was so high that it pushed out fibrin from endothelial cells; NOT fibrinous peritonitis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

What is morpholgically abnormal about this pluck from a cow?

A

Pluck = lung, heart, trachea, esophagus all together

Diffusely the internal surface of the pericardium and epicardial surface are thickened with a shaggy surface, tan-green in color, about 3x its thickness; pericardium is opened

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

What is the MDx of this pluck from a cow?

A

Severe, chronic (fibrous CT), fibrinopurulent pleuropneumonia and epicarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

What is the etiology of this pluck from a cow?

A

Hardware disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

What is the pathogenesis of this pluck from a cow

A

Ingested foreign body (hardware) > through reticulum > through diaphragm > into pericardium and lungs > introduced bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

What are the potential consequences of Hardware disease?

A

Death (usually from hypoxia not necrosis), ascites, fluid in the thoracic cavity, fibrotic liver (from poor venous return), bottle jaw (from poor venous return)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Describe this opened thorax from a cat.

A

Fluid in the thoracic cavity, volume x mL, yellow, opaque (cellular debris), fibrin on the pericardial and pleural surface, collapsed lungs (only occupying 1/4th of the thoracic cavity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is the MDx of this opened thoracic cavity from a cat?

A

Fibrino-suppurative pleuritis OR pyothorax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

What is the etiology for this opened thorax of a cat?

A

Nocardia or Actinomyces bacteria

(img: high protein and high leukocyte counts)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

What is morphologically abnormal about this small intestine of a pig?

A

Diffusely the mucosa is thickened, cerebral form appearance, 10x normal thickness, blood on mucosal surface, thin white friable material with a green tinge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What is the morphological Dx and etiology of this small intestine from a pig?

A

Proliferative enteritis from a virus

(img: cellular enterocyte proliferation, inflammation, leukocytes [neutorphils filling crypts] no macrophages)

Common in pigs!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

What is the morphological Dx from this abdomen of a calf?

A

Suppurative omphalophlebitis (inflammation of the umbilical vein)

Common in young animals that die early in life!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

What is the MDx of this kidney from a cow?

A

Suppurative pyelonephritis

(img: pus in renal pelvis from bacteria)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

What is the outcome of irreversible cell injury? (put it in order)

  1. Ultrastructural changes
  2. Gross morphologic changes
  3. Biochemical alterations/cell death
  4. Light microscopic changes
A

3, 1, 4, 2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

What are the morphologic correlates to reversible cell injury?

A

Cellular swelling and fatty change (lipidosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Which of the following is not acute cell swelling?

  1. Ballooning degeneration (epidermis)
  2. Hydropic degeneration
  3. Hydropic change
  4. Hyperplastic edema
  5. Cytotoxic edema (CNS)
A
  1. Hyperplastic edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

All of the following cells are highly vulnerable to hypoxia and cell swelling, except:

  1. CNS neurons, oligodendrocytes, astrocytes
  2. Cardiomyocytes
  3. Hepatocytes
  4. Endothelium
  5. Epidermis
  6. Proximal renal tubule epithelium
A
  1. Epidermis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Define acute cell swelling

A

Early, sub-lethal manifestation of cell damage, characterized by increased cell size and volume due to H2O overload; most common and fundamental expression of cell injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

What causes acute cell swelling (etiology)?

A
  • Loss of ionic and fluid homeostasis
    • Failure of cell energy production
    • Cell membrane damage
    • Injury to enzymes regulating ion channels of membranes
  • Examples: physical, mechanical injury, hypoxia, toxic agents, free radicals, viral organisms, bacterial organisms, immune-mediated injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Explain the pathogenesis of acute cell swelling

A

Hypoxia > less ATP > Na+ into cell > water into cell > water in organelles first (first step) > osmotic pressure increases > K+ moves out of cell > more Na+ and water into cells > cell overloaded > ER ruptures > vacuoles formed in cell > cytoplasmic swelling > hydropic degeneration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

What is the gross appearance of acute cell swelling?

A
  • Slightly swollen organ with rounded edges
  • Pallor when compared to normal
  • Cut surface: tissue bulges and can not be easily put in correct apposition
  • Slightly heavy (“wet organ”)

(img: liver from a rodent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Which is the correct term used for this acute cell swelling in the picture?

A

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

  • Cutaneous vesicles, vesicular exanthema, snout, pig
  • Etiology: vesicular exanthema of swine virus, a calicivirus (vesivirus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

How does acute cell swelling look histologically?

A
  • Water uptake dilutes the cytoplasm (slightly vacuolated)
  • Cells are enlarged with pale cytoplasm
  • May show increased cytoplasmic eosinophilia
  • Nucleus in normal position, with no morphological changes
  • Difficult morphologic change to appreciate with the light microscope

(img: hepatocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Which cells are undergoing acute cell swelling in the picture?

  1. Epidermis
  2. Liver
  3. CNS
  4. Renal tubule cells
A
  1. Epidermis, ballooning degeneration

(extreme variant of hydropic degeneration; etiology: Swinepox virus)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Which of the following is not an ultrastructural change of cellular swelling?

  1. Dilation of the ER
  2. Plasma membrane alterations
  3. Nuclear alterations
  4. Mitochondrial changes
  5. All of the above are ultrastructural changes of cellular swelling
A
  1. All of the above are ultrastructural changes of cellular swelling
  • Plasma membrane alterations (blebbing, blunting, loss of microvilli)
  • Mitochondrial changes (swelling and the appearance of small amorphous densities
  • Dilation of the ER, with detachment of polysomes; intracytoplasmic myelin figures may be present (lipids)
  • Nuclear alterations, with disaggregation of granular and fibrillar elements
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

How does the size of a cell increase in acute cell swelling?

A
  • Hydropic change, fatty change (cell swelling)
    • Due to increased uptake of water and then to diffuse disintegration of organelles and cytoplasmic proteins
  • Hypertrophy (cell enlargement)
    • The cell enlargement is caused by increase of normal organelles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

What is the prognosis of cellular swelling?

A

Depends on the number of cells affected and importance of cells

  • Good if oxygen is restored before the “point of no return”
  • Poor if there is progression to irreversible cell injury

Example: accumulation of lipofuscin in a cell (evidence of previous injury) seen under a microscope can be helpful

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Define a fatty change (reversible cell injury)

A

Sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation; may be preceded or accompanied by cell swelling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

All major classes of lipids can accumulate in cells, such as:

A

Triglycerides, cholesterol/cholesterol esters, phospholipids, abnormal complexes of lipids and carbohydrates (lysosomal storage diseases)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

___________ is the accumulation of triglycerides and other lipid metabolites (neutral fats and cholesterol) within parenchymal cells.

A

Lipidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

In which organs do lipidosis occur?

A

Liver (most common; elevated liver enzymes, icterus) , heart muscles, skeletal muscle, kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

What are the main causes of fatty change (etiology)?

A

Hypoxia, toxicity, metabolic disorders

(seen in abnormalities of synthesis, utilization and/or mobilization of fat)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

What is the pathogenesis of fatty change?

A

Impaired metabolism of fatty acids > accumulation of triglycerides > formation of intracytoplasmic fat vacuoles (white, clear space)

Hepatic lipid metabolism and possible mechanisms resulting in lipid accumulation:

  1. Excessive delivery of FFA from fat stores or diet
  2. Decreased oxidation or use of FFAs
  3. Impaired synthesis of apoprotein (helps in the formation of lipoprotein)
  4. Impaired combination of protein and triglycerides to form lipoproteins
  5. Impaired release of lipoproteins from hepatocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

What is the gross appearance of fatty change in a liver?

A
  • Diffuse yellow (if all cells are affected)
  • Enhanced reticular pattern if specific zones of hepatocytes are affected
  • Edges are rounded and will bulge on section
  • Tissue is soft, often friable, cuts easily and has a greasy texture
  • If condition is severe small liver sections may float in fixative or water
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

The image is a gross appearance of what type of reversible cell injury?

  1. Acute cell swelling
  2. Fatty change
A
  1. Fatty change

  • (MDx: hepatic lipidosis, fatty liver, hepatic steatosis; increased liver enzymes, icterus)*
  • (img: pony liver, cut section)*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What are the 2 physiologic cases in which hepatic lipidosis can be seen?

A
  • Pregnancy toxemia: in late pregnancy, especially in cows and goats with 2 offspring
  • Ketosis: heavy early lactation in ruminants
    • Ketone bodies are alternative fuel for cells
    • Produced in the liver by mitochondria
    • Convertion of acetyl CoA from fatty acid oxidation = LIPOLYSIS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

In which nutritional disorders can you see hepatic lipidosis?

A
  • Obesity
  • Protein-calorie malnutrition (impaired apolipoprotein synthesis)
  • Starvation (increased mobilization of triglycerides)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

In which endocrine disease can you see hepatic lipidosis?

A
  • Diabetes mellitus (increased mobilization of triglycerides)
  • Feline fatty liver syndrome, fat cow syndrome (unknown cause)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

What type of disease is Niemann Pick disease?

A

Lysosomal storage disease (phospholipid, sphingomyelin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

What is the histologic appearance of fatty change?

A
  • Well delineated, lipid-filled vacuoles in the cytoplasm
  • Vacuoles are single to multiple, either small or large
  • Vacuoles may displace the cell nucleus to the periphery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

What is the prognosis of fatty change?

A
  • Initially reversible- can lead to hepatocyte death (irreversible)
  • Identification and treatment of any predisposing diseases and aggressive nutritional support is required for therapy of hepatic lipidosis
  • Oral appetite stimulants can be given but are usually inadequate alone
  • Mortality is high without treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

What animal species is hepatic lipidosis most commonly seen in?

A

Cats (obese, or secondary to anorexia of any cause), ruminants, camelids, and miniature equines

(rarely seen in dogs and horses)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Irreversible cell injury is associated morphologically with which of the following, except:

  1. Severe swelling of mitochondria
  2. Extensive damage to plasma membranes (giving rise to myelin figures)
  3. Genome alteration
  4. Swelling of lysosomes
A
  1. Genome alteration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

How does cell death usually occur?

A

Necrosis, but apoptosis also contributes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Irreversible cell injury to myocardium can take _______ minutes after ischemia.

A

30-40 minutes, very quick!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Necrotic change ultrastructurally takes _______ hours, histologically takes ________ hours, and grossly takes _________ hours

A

Ultrastructurally less than 6 hours

Histologically 6-12 hours

Grossly 24-48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

What are other names used for necrosis?

A

Oncosis, oncotic necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

What is necrosis?

A

Cell death after irreversible cell injury by hypoxia, ischemia, and direct cell membrane injury (etiology)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

The morphologic aspect of necrosis is due to which 2 processes?

A
  • Denaturation of proteins
  • Enzymatic digestion of the cell
    • By endogenous enzymes derived from the lysosomes of the dying cells = autolysis (self digestion)
    • By release of lysosome’s content from infiltrating WBCs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

What is a frequent outcome of cell death by necrosis?

A

Inflammation

(you will never see inflammation with apoptosis!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are nuclear changes due to necrosis as seen under the light microscope?

A
  • Karyolysis- nuclear fading, dissolution
  • Pyknosis- nuclear shrinkage, compacted (most common)
  • Karyorrhexis- nuclear fragmentation, ruptured
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

What are ultrastructural changes for necrosis?

A

Rupture of lysosomes and autolysis, nuclear pyknosis, nuclear karyolysis, or nuclear karyorrhexis, lysis of the ER, defects in the cell membrane, large densities, mitochondrial sweling, myelin figures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

What is the gross appearance of necrosis?

A

Pale, soft, friable and sharply demarcated from viable tissue by a zone of inflammation (white rim surrounding necrosis)

(img: turkey; MDx: hepatitis, multifocal to coalescing, subacute, severe, necrotizing; Et: histomonas meleagridis; Blackhead disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Light microscopy changes of necrotic cells in cytoplasm are: (cause and appearance)

A

Cause:

  • Denatured proteins: loss of RNA, loss of glycogen particles, enzyme-digested cytoplasm organelles

Appearance:

  • Increased binding of eosin (pink)
  • Losing basophilia
  • Glassy homogeneous
  • Vacuolation and moth eaten appearance
  • Calcification may be seen

(img: right side is necrotic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

All of the following are patterns/types of tissue necrosis, except:

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Purulent necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

What is coagulative necrosis?

A
  • Always acute
  • Architecture of dead tissues is preserved (days)
  • Ultimately the necrotic cells are removed:
    • Phagocytosis by WBCs
    • Digestion by the action of lysosomal enzymes of the WBCs

(img: left: subacute, edge bulges, center is red (hemorrhage), margin is paler because cells are being removed)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

What is an infarct?

A

Localized area of coagulative necrosis; obstruction of blood supply > tissue dies

(usually wedge shaped)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

A common cause of coagulative necrosis is:

A

Ischemia in all solid organs except the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Which number refers to coagulation necrosis? (1-4)

A

4

(1-normal tissue, 2-congestion and hemorrhage, 3-leukocyte barrier, 4- coagulation necrosis)

(img: dog, kidney, infart)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

The image shows a heart with nutritional myopathy/ white muscle disease (affects heart and skeletal muscle) due to vitamin E/ selenium deficiency. What type of necrosis is associated with this?

A

Coagulative necrosis

  • (img: heart, locally extensive nutritional muscular degeneration and necrosis)*
  • (img: skeletal muscle, degeneration and necrosis)*
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

What is liquefactive necrosis?

A

Necrotic architecture is “liquefied” = liquid; dead cells are ‘digested’ > transformation (“melt”) of the tissue into a liquid viscous mass; typically see in CNS (abscess)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Where does liquefactive necrosis usually occur?

A
  • Tissue with high neutrophil recruitment and enzymatic release with digestion of tissue
  • Tissues with high lipid content
  • Focal bacterial and occasionally, fungal infections
    • Microbes stimulate the accumulation of WBCs and the liberation of enzymes from these cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

What type of necrosis is pictured?

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Liquefactive necrosis (grossly)

(img: sheep, brain stem, areas of depression or “melted” off; MDx: bilateral symmetrical encephalomalacia)

147
Q

The image is an example of:

  1. Leukoencephalomalacia
  2. Leukomyelomalacia
  3. Polioencephalomalacia
  4. Poliomyelomalacia
A
  1. Poliomyelomalacia (spinal cord)
148
Q

The image is an example of:

  1. Leukoencephalomalacia
  2. Leukomyelomalacia
  3. Polioencephalomalacia
  4. Poliomyelomalacia
A
  1. Leukoencephalomalacia
  2. Leukomyelomalacia

(necrosis of white matter of cerebral hemispheres, brain stem and cerebellum)

149
Q

What is the pathogenesis of leukoencephalomalacia?

A

Ingestion of Fusarium moniliforme containing Fumonisin B1 toxin-producing moldy corn > sphingolipid (lipid precursor = toxic) synthesis inhibition > direct cellular toxicity > leukoencephalomalacia

150
Q

Which animal species are affected by leukoencephalomalacia?

A

Horse, chicken, pig (pulmonary edema)

151
Q

What is the MDx and etiology of the image from a horse with Equine Leukomyelitis?

A

MDx: multifocal necrohemorrhagic (leuko) myelitis

Etiology: Sarcocystis neurona (protozoan)

EDx: Protozoal leukomyelitis

152
Q

What is the DDx and EDx of a horse which shows multifocal hemorrhagic polyomyelitis?

A
  • Equine herpes virus 1
  • Rabies (Lyssavirus)
  • West Nile virus (Flavivirus)

EDx: Viral polyomyelitis

153
Q

What are some causes for polioencephalomalacia in sheep?

A
  • Thiamine (vit B1) deficiency diet (particularly in young animals)
  • Increased ruminal thiaminase activty
  • Administration of thiamine analogs Amprolium
  • High levels of sulfur in diet or water
  • Lead toxicity
  • Thiaminase containing plants: Bracken fern (Pteridium spp.)
154
Q

What type of necrosis is pictured?

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Liquefactive necrosis, necrotic material is frequently creamy yellow because of the presence of dead WBCs = pus

(img: goat, pituitary gland abscess)

155
Q

A localized collection of pus (liquefied tissue) in a cavity formed by disintegration of tissues surrounded by fibrous connective tissue (NOT IN CNS) is called a(n) _______________.

A

Abscess

(it is the result of the body’s defensive reaction to foreign material)

156
Q

What are the 2 types of abscesses?

A
  1. Septic (majority): infection, release of enzymes from WBCs and infectious agent (pyogenic bacteria, e.g. S. aureus)
  2. Sterile: process caused by nonliving irritants such as drugs or foreign bodies

(likely to turn into firm, solid lumps as they scar, rather than remaining pockets of pus)

157
Q

What will you be able to see histologically from liquefactive necrosis (e.g. abscess)?

A
  • Clear area of demarcation
  • Loss of cellular detail
  • Cells are granular
  • Eosinophilic and basophilic debris
  • Neutrophil nuclei may dominate nuclear debris
  • No tissue architecture is preserved (because everything is destroyed, even enzymes)
158
Q

What is gangrenous necrosis?

A

Not a specific pattern of cell death but begins mostly as coagulative necrosis (likely due to ischemia); usually applied to distal extremities (also toes, ear, udder, pinna) and involves multiple planes of tissue (extreme temperatures/cold)

  • Dry gangrene- no bacterial superinfection, tissue appears dry (image)
  • Wet gangrene- bacterial (anaerobes) superinfection has occurred, tissue appears wet and liquefactive; by actions of degradative enzymes in bacteria and the attracted WBCs
159
Q

What type of necrosis is pictured (udder)?

A

Wet gangrenous necrosis (black areas due to degradative enzymes of bacteria)

160
Q

What is caseous necrosis?

A
  • Caseous = cheese-like
  • Friable (crumble) white = area of necrosis
  • Necrotic debris represents dead WBCs
  • Chronic, compared with coagulation necrosis
  • Often associated with poorly degradable lipids of bacterial origin
161
Q

What are possible causes of caseous necrosis?

A

Mycobacterium, Corynebacterium, Fusobacterium, fungal infections

162
Q

What type of necrosis is pictured?

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Caseous necrosis

(img: Corynebacterium pseudotuberculosis, Caseous lymphadenitis)

163
Q

What type of necrosis is pictured?

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Caseous necrosis (abscesses)
164
Q

What type of necrosis is pictured?

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Caseous necrosis

  • (img: cow lung; MDx: multifocal caseous pneumonia; Tuberculosis)*
  • (compare to Johne’s disease > paratuburculosis > diffuse granulomatous)*
165
Q

What is the histopathology of caseous necrosis?

A
  • Necrotic area of eosinophilic granular cell debris with a rim of inflammatory cells (MQ, ~MNGC)
  • Obliterated tissue architecture
  • Dystrophic calcification > commonly to occur in center of lesion
166
Q

What are the 3 types of fat necrosis?

A
  1. Enzymatic necrosis (pancreatic necrosis of fat)
  2. Traumatic necrosis of fat
  3. Necrosis of abdominal fat
167
Q

What is the pathogenesis of enzymatic necrosis (pancreatic necrosis of fat)?

A
  • Action of activated pancreatic lipases in ‘escaped’ pancreatic fluid (escape duodenum) > destroy tissues; neutral fat (lipase > triglycerides)
  • Free fatty acids + Ca+ > calcium soaps (saponification)
168
Q

What type of necrosis is pictured?

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Fat necrosis (enzymatic necrosis of fat)

Dog with previous bouts of pancreatitis. Necrotic fat often becomes saponified and so grossly the lesion is chalky to gritty and pale white

169
Q

What type of necrosis is pictured?

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Fat necrosis

Pancreas, dog. Note the large area of fat necrosis with acute inflammation and saponification (basophilic areas); nucleus pushed to the side

170
Q

What are possible causes of traumatic necrosis of fat?

A
  • Dystocia
  • Subcutaneously in inter-muscular fat at sternum of recumbent cattle
171
Q

What are possible causes of necrosis of abdominal fat (cattle)?

A

Uknown cause (mesentery, omentum, retroperitoneum, extreme cases intestinal stenosis); Channel island breeds (Hereford, Jersey)

172
Q

What type of necrosis is pictured?

  1. Fibrinoid necrosis
  2. Fat necrosis
  3. Caseous necrosis
  4. Gangrenous necrosis
  5. Liquefactive necrosis
  6. Coagulative necrosis
  7. Purulent necrosis
A
  1. Fat necrosis

(img: cow, abdominal cavity)

173
Q

What is fibrinoid necrosis?

A
  • Special form of necrosis usually seen in immune reactions involving blood vessels
  • Occurs when Ag-Ab complexes are deposited in the walls of arteries
  • Deposits of these “immune complexes”, together with fibrin that has leaked out of vessels, result in a bright pink and amorphous appearance in H&E stains, called “fibrinoid” (fibrin-like, NOT FIBRIN) by pathologists
174
Q

T or F. Inflammation is a common outcome of apoptosis.

A

False!!! You will NEVER see inflammation with apoptosis, only with necrosis.

175
Q

A pathway of cell death induced by a tightly regulated suicide program is called ____________.

A

Apoptosis, sometimes referred to as programmed cell death.

Cells destined to die activate intrinsic enzymes that degrade the cells’ own nuclear DNA and nuclear and cytoplasmic proteins

  • Apoptotic cells break up into fragments, called apoptotic bodies, which contain portions of the cytoplasm and nucleus
  • Plasma membrane:
    • Remains intact
    • Its structure is altered > becomes ‘tasty’ targets for phagocytes
176
Q

What are some physiologic processes where apoptosis occurs?

A
  • Programmed cell death during embryogenesis
  • Hormone-dependent involution of organs in the adult (e.g. thymus, uterus post-parturition)
  • Cell deletion in proliferating cell populations (intestinal epith. turnover)
  • Deletion of auto-reactive T cells in the thymus (by cytotoxic T cells)
177
Q

What are some pathologic processes where apoptosis occurs?

A
  • Tumor necrosis factor or Fas ligand induction of apoptosis in many cells
  • DNA damage (UV light)
  • Accumulation of misfolded proteins
  • Cell injury in certain infections (viral)
  • Pathological atrophy in parenchymal organs after duct obstruction
178
Q

All of the following are cell morphologies during apoptosis, except:

  1. Chromatin condensation (pyknosis)
  2. Phagocytosis of apoptotic cells by adjacent healthy cells
  3. Formation of cytoplasmic blebs and apoptotic bodies (fragmentation)
  4. Cell shrinkage with increased cytoplasmic density
  5. Cell swelling with decreased cytoplasmic density
A
  1. Cell swelling with decreased cytoplasmic density
179
Q

What process can be seen in the image?

  1. Apoptosis
  2. Necrosis
  3. Acute cell swelling
A
  1. Apoptosis

(img: can see fragmentatin of nucleus)

180
Q

What are the mechanims of apoptosis?

A

Activation of caspases (cyteine proteases family)

  • Initiator caspases: 9 (intrinsic) & 8 (extrinsic)
  • Executioner caspases: 3 & 6

Via intrinsic pathway = mitochondrial pathway

Via extrinsic pathway = death receptor-initiated pathway

(img: different triggers than can induce apoptosis)

181
Q

Explain the intrinsic pathway of apoptosis.

A
  • Major mechanism of apoptosis in all mammalian cells
  • Result of increased mitochondrial permeability and release of pro-apoptotic molecules (death inducers) into the cytoplasm
  • Cytochrome-C: essential for life; released into cytoplasm from mitochondria > initiates suicide program of apoptosis
  • Controlled of release by: pro- and anti-apoptotic members of the Bcl family of proteins
182
Q

Bcl-2, Bcl-X, and Mcl-1 are _____-apoptotic proteins.

  1. Pro
  2. Anti
A
  1. Anti

FYI:

  • They can directly inhibit Apaf-1 (apoptotic protease activating factor 1) activation
  • Loss from cells may permit activation of Apaf-1
  • Apaf-1 binds to apoptosome to activate Caspae-9
  • Present within the mitochondria membranes and the cytoplasm
183
Q

Bak and Bax are ________-apoptotic proteins.

  1. Pro
  2. Anti
A
  1. Pro

Effectors

184
Q

Bim, Bid, and Bad are _______-apoptotic proteins.

  1. Pro
  2. Anti
A
  1. Pro (BH3-only proteins)

Sensors of damage and stress

185
Q

Explain the extrinsic pathway of apoptosis.

A
  • Initiated by death receptors (members of the TNF receptor family)
    • Death domain
    • Best known types: TNFR1 and Fas (CD95)
      • Fas-L is expressed on T cells that identify self Ag and some cytotoxic T cells (perforin, granzymes)
  • Forming a binding site for an adapter protein, that also contains a death domain: FADD (Fas associated death domain)
    • FADD in turn binds an inactive Caspase 8 > active caspase 8
  • Activation of execution phase of apoptosis
  • Can be inhibited by protein FLIP
186
Q

How are apoptotic bodies removed?

A
  • Edible for phagocytes (macrophages recognize several phospholipids)
  • Expressed phospholipids in the outer layer of the membrane (instead inner leaflet) to be ID by MQ receptors
  • May become coated with natural Ab and proteins of the complement system (C1q)
187
Q

How are apoptotic cells removed?

A
  • Secrete soluble factors that recruit phagocytes
  • Some express thrombospondin (adhesin glycoprotein that is ID by phagocytes)
  • MQ may produce proteins that bind to apoptotic cells (not to live cells) for engulfment
188
Q

What are disorders associated with defective apoptosis (too little) and increased cell survival (abnormal cells survive)?

A
  • Cells with mutations in p53 are subjected to DNA damage, not only fail to die but are susceptible to the accumulation of mutations because of defective DNA repair, these can give rise to neoplasia
  • Lymphocytes that react against self-antigens (autoimmune disorder)
  • Failure to eliminate dead cells (potential source of self-antigen; autoimmune disorder)
189
Q

What are disorders associated with increased apoptosis (too much) and excessive cell death?

A
  • Neurodegenerative disease: manifested by loss of specific sets of neurons (apoptosis caused by mutations and misfolded proteins); ex. Alzheimer’s disease
  • Ischemic injury, as in myocardial infarction and stroke
  • Death of virus-infected cells
190
Q

What are the difference between necrosis and apoptosis?

A

See image

(IMPORTANT, KNOW THESE!)

191
Q

Do the cells in the image represent reversible or irreversible cell injury (kidney tubules)?

A

Irrevesible

(loss of nuclei, loss of microvilli, pyknotic nuclei, fragmentation of cells, coagulative necrosis because architecture is more or less preserved)

(img: compare to normal cells, kidney tubules)

192
Q

Do the cells in the image represent reversible or irreversible cell injury?

A

Reversible

(cells enlarged (hydropic chage), microvilli not very clear, more eosinophilic, nucleus still okay)

(img: compare to normal cells, kidney tubules)

193
Q

Do the cells in the image represent reversible or irreversible cell injury?

A

Reversible

(img: compare to normal cells)

194
Q

Do the cells in the image represent reversible or irreversible cell injury?

A

Irreversible

(swelling of mitochondria, loss of microvilli, cytoplasmic blebs)

(img: compare to normal cells)

195
Q

What are the 2 types of encephalomalacia (liquefactive necrosis) and how are they different?

A
  1. Leukoencephalomalacia (brain- white matter inside)/ Leukomyelomalacia (spinal cord- white matter outside): white matter
  2. Polioencephalomalacia (brain- gray matter outside)/ Poliomyelomalacia (spinal cord- gray matter inside): gray matter
196
Q

What is necroptosis?

A

Programmed necrosis; same triggers as apoptosis, but causes inflammation

197
Q

T or F. The circulatory system consists of the heart, arteries, veins, capillaries, and lymphatics.

A

True

(the lymphatics parallel the veins and contribute to circulation by draining fluid from the extravascular spaces into the blood vascular system)

198
Q

What is the difference between veins and arteries?

A
  • Both have: tunica intima, tunica media, tunica externa
  • Wall of the arteries are thicker (tunica media) than the veins

See image

199
Q

All of the following are functions of vascular endothelium, except:

  1. Modulates perfusion
  2. Role in inflammation
  3. Role in hemostasis
  4. All of the above are functions of the endothelium
A
  1. All of the above are functions of the endothelium
  • Role in hemostasis:
    • Anti-thrombotic and pro-fibrinolytic in the normal state
    • Pro-thrombotic and anti-fibrinolytic during injury
  • Modulates perfusion:
    • NO relaxes and causes vasodilation
    • Endothelin causes vasoconstriction
  • Role in inflammation:
    • Regulates the traffic of inflammatory cells
    • Produces pro-inflammatory cytokines
    • Control angiogenesis and tissue repair
200
Q

___________ is the process of arresting bleeding by the physiological properties of vasoconstriction and coagulation or by surgical means.

A

Hemostasis

201
Q

What is the fluid distribution of the body?

(plasma, interstitial fluid, intracellular fluid, transcelluar fluid)

A

Total body water: 60-65% body weight

Plasma: 4-5%

Interstitial fluid: 15-16%

Intracellular fluid: 40%

Transcellular fluid: 5% (ex. peritoneum)

(the younger the animal, the more water content they have)

202
Q

What is interstitium?

A
  • The space between tissue compartments (microcirculation and cells)
  • The medium through which all metabolic products must pass between the microcirculation and the cells
  • Composed of the extracellular matrix (ECM) and supporting cells
203
Q

What is extracellular matrix?

A

It is composed of structural molecules (collagen, reticulin, elastic fibers) and ground substance (glycoproteins like fibronectin and laminin, plus glycosaminoglycans, proteoglycans, etc)

204
Q

Water distribution between plasma and the interstitium is primarily determined by ____________ pressure differences between the 2 compartments.

  1. Hydrostatic
  2. Osmotic
  3. Atmospheric
  4. A and B only
  5. A, B, and C
A
  1. A and B only

(hydrostatic pressure moves fluid out of the capillaries and the osmotic pressure of plasma proteins move fluid into the vasculature)

205
Q

If hydrostatic pressure is increased or plasma osmotic pressure is diminished, and the capacity for lymphatic drainage is exceeded, this will cause:

  1. Tissue edema
  2. Swollen vasculature
  3. No changes
A
  1. Tissue edema
206
Q

What are possible circulatory disturbances?

A
  • Edema
  • Hyperemia and congestion
  • Hemostasis
  • Hemorrhage
  • Thrombosis, embolism and DIC
  • Infacrction
  • Shock
207
Q

____________ is an abnormal accumulation of excess extracellular water in interstitial spaces or in body cavities.

A

Edema

(fluid is outside both the vascular fluid compartment and cellular fluid compartment [i.e. interstitium])

208
Q

Which of the following are not pathomechanisms of edema?

  1. Increased vascular permability
  2. Decreased plasma colloidal osmotic pressure
  3. Lymphatic obstruction
  4. Increased blood hydrostatic pressure
  5. Increased plasma colloidal osmotic pressure
A
  1. Increased plasma colloidal osmotic pressure
209
Q

What are ways to get increased blood hydrostatic pressure?

A
  • Generalized: right-sided congestive heart failure
  • Localized: tightly bandaged limb resulting in venous occulsion
210
Q

What are ways to get decreased plasma colloidal osmotic pressure?

A
  • Proteins not absorbed from diet (starvation, GI malabsorption)
  • Proteins not produced (liver disease)
  • Protein loss (glomerular disease, intestinal mucosal damage)
211
Q

What are ways to get lymphatic obstruction?

A
  • Surgery
  • Neoplasms
  • Inflammation
212
Q

What is a way to get increased vascular permeability?

A

Inflammation

213
Q

This type of edema has increased vascular permeability and is referred to as “exudate”.

  1. Inflammatory edema
  2. Non-inflammatory edema
A
  1. Inflammatory edema

(edema fluid in these cases is protein rich [>30g/L], specific gravity of > 1.025, total nucleated cells <7 x 10^9L, and less than 7,000 cells per microliter)

214
Q

This type of edema is referred to as “transudate” and is usually from congestive heart failure or liver failure.

  1. Inflammatory
  2. Non-inflammatory
A
  1. Non-inflammatory

(edema fluid in these cases are protein poor [<30g/L], low specific gravity <1.025, low cellularity <1.5x10^9L, and less than 1,500 cells per microliter)

215
Q

What is the gross appearance of edema?

A

Wet, gelatinous and heavy, swollen organs, fluid weeps from cut surfaces, may be yellow

216
Q

What is the histological appearance of edema?

A

Clear or pale eosinophilic staining depending on whether is non-inflammatory or inflammatory edema, spaces are distended, blood vessels may be filled with RBCs, lymphatics are dilated, collagen bundles are separated

217
Q

______________ is when pressure is applied to an area of edema and a depression or dent results as excessive interstitial fluid is forced to adjacent areas.

A

Pitting edema

(img: horse with congestive heart failure, prepuce)

218
Q

Fluid in the thoracic cavity is called ___________.

A

Hydrothorax

(usually associated with generalized edema, congestive heart failure, renal or hepatic disease)

219
Q

_______________ is also called “mulberry heart disease” which is a type of inflammatory edema in the pericardial sac.

A

Pericardial effusion

(a type of inflammatory edema because you see an increase in vascular permeability and leakage of proteins, NOT transudative edema [NOT hydropericadrium])

*Mulberry heart disease from vitamin E/selenium deficiency (muscle degeneration and necrosis)*

(img: fibrin strands and cloudy appearance (exudate) of the pericardial fluid can be seen)

220
Q

Fluid (transudate) within the peritoneal cavity is called ___________ or _____________.

A

Ascites or hydroperitoneum

(img: dog with congestive heart failure; can also result from hepatic or renal disease; NO FIBRIN)

221
Q

What condition is pictured in this horse with congestive heart failure?

A

Ascites (pitting edema)

222
Q

Very severe, generalized edema with profuse accumulation of fluid within the subcutaneous tissue is called ___________.

A

Anasarca

(img: puppies with anasarca from congenital disease)

223
Q

Submandibular edema is also called _______________ and is associated with severe GI parasitism and hypoproteinemia in sheep.

A

Bottle jaw (can also be from heart failure; parasite: Haemonchus contortus)

*Upon opening: classic gelatinous appearance, very wet*

224
Q

This horse forelimb had ________________ edema due to chronic protein-losing enteropathy.

  1. Generalized
  2. Localized
A
  1. Generalized

(img: gelatinous tissue with yellow-tinge)

225
Q

What is the clinical significance of edema?

A
  • It is dependent upon extent, location and duration
  • Tissue may become firm and distorted due to an increase in fibrous connective tissue after prolonged edema
226
Q

Non-inflammatory pulmonary edema is associated with what disease?

A

Left-sided congestive heart failure

(ex. congenital aortic stenosis; aorta cannot distribute blood > blood accumulates in the left side of the heart > blood accumulates in the lungs > increased hydrostatic pressure in the lungs > leakage of fluid into alveoli)

227
Q

Inflammatory pulmonary edema is due to damage to the pulmonary capillary endothelium and is associated with which disease?

A

Pneumonia (Acute respiratory distress syndrome, ARDS)

  • Sudden, diffuse, and direct- increase in vascular permeability (viral or bacterial condition): high fatality rate > followed by pneumonia if the animal survives
  • (another example: trauma to brain > inflammatory edema > ischemic injury > fatal)*
228
Q

What condition is pictured from this pig lung?

A

Pulmonary edema

(img: lungs slightly enlarged and heavy, rib impressions, froth from trachea and bronchi, interlobular connective tissue septa expanded [ruminants and pigs]) with yellow/gelatinous substance)

229
Q

What condition is pictured from this horse lung?

A

Pulmonary edema

(img: rupture on the right AV valve; many animals die, but some can survive and develop right-sided congestive heart failure [fluid in abdominal cavity and fluid in SQ tissues])

230
Q

What condition is pictured from this rat lung?

A

Pulmonary edema

(img: red/pink = eosinophilic fluid [protein] due to inflammatory edema; transudative edema = NO stain)

231
Q

Chronic pulmonary edema is most commonly associated with _______________.

A

Cardiac failure

(congestion of pulmonary blood vessels > hypoxic damage to alveoli > alveolar walls become thickened > may lead to fibrosis; congestion, micro-hemorrhages [due to hypoxic damage to endothelium] > and accumulation of heart failure cells [alveolar macrophages that phagocytize RBCs; hemosidirin produced])

232
Q

What condition is pictured from this lung tissue?

A

Chronic pulmonary edema

(img: heart failure cells present)

233
Q

What condition does the animal have from looking at this slide of lung tissue?

A

Chronic pulmonary edema

(H&E stain, dark brown pigment within the cytoplasm of alveolar macrophages [heart failure cells])

234
Q

What condition does the animal have from looking at this slide of lung tissue?

A

Chronic pulmonary edema

(Iron [Perl’s] stain, hemosiderin-laden macrophages [heart failure cells = siderophages] within alveoli)

235
Q

_____________ indicates passive venous engorgement; blood is not oxygenated (blue).

A

Congestion; congestion usually goes hand-in-hand with edema

(indicates a local increase in blood volume and flow within the vascular bed; ex. right-sided congestive heart failure)

236
Q

______________ indicates increase of arteriole-mediated engorgement of the vascular bed; blood is oxygenated (red).

A

Hyperemia

(indicates a local increase in blood volume and flow within the vascular bed; ex. inflammation from injury, physiologic)

237
Q

This refers to the increase in blood flow to the GI tract during digestion, increase in blood flow to muscles during exercise, increase in blood flow to the skin to dissipate heat (cool down), and involuntary increase in blood flow to the face (facial hyperemia) as a result of embarrassment or emotional distress (social anxiety).

  1. Physiological hyperemia
  2. Pathological hyperemia
  3. Physiological congestion
  4. Patholgocial congestion
A
  1. Physiological hyperemia
238
Q

This is usually caused by inflammation; arteriolar dilation occurs secondary to the inflammatory mediators, reddending can be seen (one of the cardinal signs), and is often associated with edema

  1. Physiological hyperemia
  2. Pathological hyperemia
  3. Physiological congestion
  4. Pathological congestion
A
  1. Pathological hyperemia
239
Q

The image shows an example of:

  1. Physiological hyperemia
  2. Pathological hyperemia
  3. Physiological congestion
  4. Pathological congestion
A
  1. Pathological hyperemia

(img: gingiv_itis_, dog)

240
Q

The image shows an example of:

  1. Physiological hyperemia
  2. Pathological hyperemia
  3. Physiological congestion
  4. Pathological congestion
A
  1. Pathological hyperemia

(bulbar and palpebral conjunctivitis, prominent blood vessels, human)

241
Q

What are ways that congestion can be classified?

A

Acute, chronic, localized (isolated area of venous obstruction), and generalized (systemic change like in congestive heart failure)

242
Q

What type of congestion is pictured?

A

Acute, local congestion

(Gastric volvulus [torsion] in a dog (pigs are also susceptible; after a meal, too much water, etc); twisting of vessels obstructs gastric veins > severe venous congestion > ischemia [necrosis] > loss of endothelial integrity > hemorrhage > septic shock [bacteria in feed] > death)

243
Q

What type of congestion is pictured?

A

Acute, local congestion

(intestinal volvulus [colic]; loop of intestine wraps around mesenteric axis > compression of veins > hemorrhage and necrosis > peritonitis from leakage [horses very susceptible] > venous infarction of the intestine; horse)

244
Q

What type of congestion is pictured?

A

Acute, local congestion and edema

(colonic torsion; torsion- piece of gut twists along its OWN axis, wall thickened (edema) > venous infarction > friable, necrotic mucosa > septis > death; left colon of the horse)

Pre-Mortem (veins prominent, bluish discoloration of serosal surface)

245
Q

Pulmonary congestion is usually the result of:

A

Left-sided heart failure > back up of blood in the left atrium > back up of blood in the lung > diffuse pulmonary congestion > increased hydrostatic pressure in the lungs > pulmonary edema

(img: acute pulmonary congestion, red = due to congestion, dog)

246
Q

What type of congestion is pictured (dog lungs)?

A

Chronic pulmonary edema

(img: not fixed; diffuse brownish discoloration (presence of many heart failure cells), chronic pulmonary edema and congestion secondary to left-sided congestive heart failure)

247
Q

The presence of heart failure cells in the lungs is called:

A

Pulmonary hemosiderosis

248
Q

Subacute to chronic ________________ is usually the result of right-sided congestive heart failure.

A

Hepatic congestion

(img: liver of horse with right-sided congestive heart failure; livers are enlarged (from increased venous blood), exhibit rounded edges, and fibrosis)

249
Q

What is the name of the disease for subacute/chronic hepatic congestion?

A

Nutmeg liver (lobules are enlarged, have rounded edges, and have nodular surfaces [from hypoxic injury])

Right-sided congestive heart failure > backing up of blood in the venous system > increased venous blood in liver (hypoxic injury)

250
Q

What type of congestion is pictured (liver)?

A

Subacute hepatic congestion, “Nutmeg liver”

(chronically, there is low-grade hypoxia and increase pressure of centrolobular hepatocytes leading to atrophy and necrosis)

251
Q

Explain the zones of hepatocytes in the liver. Which one is associated with immune-mediated anemia in dogs?

A

Zone 3- hepatocytes around central vein, furthest from arterial blood (most susceptible to ischemic injury!) > ex. dogs with immune mediated anemia

Zone 2- middle of hepatic lobule

Zone 1- around portal triad (most oxygenated blood here)

252
Q

What makes up the portal triad in the liver?

A

Hepatic vein, hepatic artery, and bile duct

Oxygenated blood comes in through the hepatic artery > blood runs through sinusoids > reaches central vein > drains into the caudal vena cava

253
Q

What do the dark red and pale/yellow areas respresent in Nutmeg liver?

A

Red in nutmeg liver: hepatocytes around central vein = atrophic > dilitation of sinusoids, centrilobular hepatocellular atrophy = hemorrhage

Pale/yellowish in nutmeg liver: hepatocytes in the middle zone = sinusoids swollen, vacuolated, fatty degeneration

254
Q

This is defined as the escape of blood from the blood vessels (extravasation). It can be external or internal (within tissues or body cavities)

A

Hemorrhage

255
Q

What are the causes of hemorrhage?

A
  • Trauma (damage to endothelium)
  • Sepsis, viremia, bacteremia or toxic conditions
  • Abdominal neoplasia may lead to hemoperitoneum (hemangiosarcoma)
  • Coagulation abnormalities (platelet and coagulation factor defects or deficiencies [congenital])
256
Q

What is the difference between hemorrhage, hyperemia, and congestion?

A

Hemorrhage is when the blood is outside the vessel wall; hyperemia is the increase of arterial blood within the blood vessel; congestion is the increase of venous blood within the blood vessel

257
Q

What determines the clinical significance of hemorrhage?

A

Location and severity (e.g. profuse blood loss is the most common cause of hypovolemic shock; hemorrhage in the brain or heart can be fatal)

(img: hemopericardium [seen in many HBC cases and right atrial hemangiosarcoma] > leads to fatal cardiac tamponade)

258
Q

What do you call hemorrhage due to a substantial rent/tear in the vascular wall (or heart)?

A

Hemorrhage by rhexis (ex. cutting yourself with a knife)

259
Q

What do you call hemorrhage due to a small defect in the vessel wall or RBC’s passing through the vessel wall in cases of inflammation or congestion?

A

Hemorrhage by diapedesis (ex. microhemorrhage of alveoli in a patient with left-sided heart failure)

260
Q

Copper deficiency and dissecting aneurysm is associated with what type of hemorrhage?

  1. Hemorrhage by rhexis
  2. Hemorrhage by diapedesis
A
  1. Hemorrhage by rhexis
    * (copper is needed to maintain the health of arterial walls; in addition to racing horses, dissecting aneurysms are also reported in the coronary and renal arteries of young male racing greyhounds which can lead to arterial rupture (aorta) and fatal hemorrhage)*
261
Q

A focal dilitation of an artery is called a(n) ________________.

A

Aneurysm

(dissecting aneurysm: the high pressure in the artery causes blood to penetrate/dissect the tunica intima, tunica media, and ultimately the tunica adventitia > rupture > fatal; ex. susceptible in turkeys’ abdomen)

262
Q

An increased tendency/susceptibility to hemorrhage from usually insignificant injuries (seen in a wide variety of clotting disorders) is called _____________________.

A

Hemorrhagic diathesis

(congenital anomalies from lack of clotting factors)

263
Q

What do you call blood in the thoracic cavity?

A

Hemothorax

264
Q

What do you call blood in the peritoneal cavity?

A

Hemoperitoneum

265
Q

What do you call blood within a joint space?

A

Hemarthrosis

266
Q

This is defined as the coughing up of blood or blood-stained sputum from the lungs or airways.

A

Hemoptysis

(in patients with respiratory infections or neoplastic lesions)

267
Q

What’s the fancy, doctor word for bleeding from the nose?

A

Epistaxis

(can be due to trauma, tumor, fungal infection, or exercise induced pulmonary hemorrhage [horses])

268
Q

Hemorrhage within tissues can be classified by size; which one is up to 1-2 mm and is usually found on skin, mucosal, and serosal surfaces?

A

Petechia; petechiae is plural

(can be due to sepsis or severe hypoxia)

269
Q

Hemorrhage within tissues can be classified by size; which one is up to 1-2 cm and is seen as in bruise (contusion) or small hematomas.

A

Ecchymosis, ecchymoses is plural

270
Q

_______________ hemorrhages are when petechiae and ecchymoses are associated with terminal hypoxia; they are usually seen in healthy animals at the slaughterhouse.

A

Agonal/hemorrhage

(like an artifact; sometimes seen along the coronary groove)

271
Q

Hemorrhage within tissues can be classified by size; which one is larger than ecchymosis, locally extensive/multifocal to coalescing, and contiguous?

A

Suffussive hemorrhage

(img: serosal surface of the stomach, dog)

272
Q

What type of hemorrhage looks like if red paint was hastily applied with a paint brush and is most common on mucosal and serosal surfaces?

A

Paint-brush hemorrhage

273
Q

What do you call a localized area of hemorrhage?

A

Hematoma

274
Q

What do you call a central mass of fibrin and RBCs surrounded by supportive vascular connective tissue? (macrophages will eventually phagocytize this lesion)

A

Organizing hematoma

275
Q

How are hemorrhages resolved?

A
  • Small amounts can be reabsorbed with time
  • Larger amounts require significant phagocytosis and degradation by macrophages
  • Organizing hematomas can form
276
Q

Trauma > damage to endothelium > hemorrhage > hematoma > ______________ > _______________ > _______________

Put the resolution of hematomas in order:

  1. Bilirubin (blue, green)
  2. Hemoglobin (red-blue)
  3. Hemosiderin (yellow-brown)
A
  1. Hemoglobin (red from extravasation) enzymatically converted to > 1. Bilibrubin and eventually to > 3. Hemosiderin
    * (you don’t really see this in animals because of their fur)*
277
Q

Which of the following is not a circulatory disturbance?

  1. Hemostasis
  2. Lymphangitis
  3. Thrombosis, Embolis
  4. Disseminated Intravascular Coagulation
  5. Hemorrhage
  6. Infarction
  7. Shock
  8. Hyperemia and congestion
  9. Edema
A
  1. Lymphangitis
278
Q

_____________ is the arrest in bleeding by PHYSIOLOGICAL or surgical means.

A

Hemostasis

  • Normal hemostasis is a physiological response to vascular damage
  • It provides a mechanism to seal an injured vessel to prevent blood loss
  • It is the result of a complex and well-regulated process which maintains blood as a flowing fluid within the cardiovascular system
279
Q

What is the PATHOLOGICAL form of hemostasis, where a clot forms within a vessel that is not injured or only mildly injured?

A

Thrombosis; thrombus = clot

  • Thrombosis can be viewed as an inappropriate activation of the normal hemostatic process
  • Can also be viewed as an “overreaction” of normal hemostasis (when hemostasis goes bad)
280
Q

All of the following are general components necessary for normal hemostasis or thrombosis to occur, except:

  1. Platelets
  2. Coagulation cascade
  3. Vascular wall (vascular endothelium)
  4. Macrophages
A
  1. Macrophages
281
Q

Which of the following is an endothelium-derived vasoconstrictor that is secreted after an initial injury?

  1. Endothelin
  2. von Willebrand factor
  3. Tissue factor
  4. Glycoprotein Ib
A
  1. Endothelin
282
Q

After endothelial injury and exposure of the extracellular matrix, platelets adhere to __________________ which results in the activation of platelets.

  1. Endothelin
  2. von Willebrand factor
  3. Tissue factor
  4. Glycoprotein Ib
A
  1. von Willebrand factor
283
Q

Primary hemostasis is the method in which aggregated platelets form a ____________________ within minutes of endothelial injury.

  1. Primary hemostatic plug
  2. Collagen bundle
  3. Fibrin plug
  4. Abcess
A
  1. Primary hemostatic plug
284
Q

_____________________ is a membrane-bound procoagulant glycoprotein made in the endothelium (upon endothelial damage) which activates the coagulation cascade.

  1. Glycoprotein Ib
  2. von Willbrand factor
  3. Tissue factor (factor III-thromboplastin)
  4. Endothelin
A
  1. Tissue factor (factor III-thromboplastin)

Tissue factor works with factor VII to activate the coagulation cascade which eventually generates thrombin (factor II)

285
Q

What cleaves circulating soluble fibrinogen into insoluble fibrin, creating a fibrin meshwork (secondary hemostatic plug)?

  1. Fibrinogenase
  2. Tissue factor
  3. von Willbrand factor
  4. Thrombin
A
  1. Thrombin

(thrombin also induces further platelet recruitment and granule release)

286
Q

T or F. The initial plate plug during hemostasis lasts longer than the secondary hemostatic plug.

A

False

(the secondary hemostasis sequence lasts longer and is more effective and stable than the initial platelet plug; in secondary hemostasis, fibrin wraps around platelets and forms the secondary hemostatic plug)

287
Q

Which of the following are part of the solid permanent plug to prevent any additional hemorrhage after hemostasis. (2 answers)

  1. Tissue factor
  2. Polymerized fibrin
  3. Aggregated platelets
  4. Endothelin
  5. Macrophages
  6. von Willbrand factor
  7. Collagen
A
  1. Polymerized fibrin
  2. Aggregated platelets
288
Q

Which 2 are involved in the interference of the coagulation cascade and limits the hemostatic plug to the site of injury?

  1. Tissue plasminogen activator (t-PA)
  2. Neutrophils
  3. Thrombomodulin
  4. Macrophages
  5. von Willbrand factor
  6. Collagen bundles
A
  1. Tissue plasminogen activator (t-PA)- a fibrinolytic product
  2. Thrombomodulin- interferes with the coagulation cascade
    * (without these, a thrombus can form)*
289
Q

Matching! Which of the following are anticoagulative and procoagulative?

A. Anticoagulation factors

B. Procoagulation factors

  1. von Willebrand factor
  2. Nitric oxide
  3. Tissue plasminogen activator (t-PA)
  4. Prostacyclin
  5. Thrombomodulin
  6. Thromboplastin
  7. Platelet activating factor (PAF)
A

A. Anticoagulation factors

  1. Nitric oxide
  2. Tissue plasminogen activator (t-PA)
  3. Prostacyclin
  4. Thrombomodulin

B. Procoagulation factors

  1. von Willebrand factor
  2. Thromboplastin
  3. Platelet activating factor (PAF)
290
Q

Thrombin converts _____________ to _______________.

A

Soluble plasma protein fibrinogen into insoluble fibrin

291
Q

Where in the body are coagulation factors made?

(Hint: they are plasma proteins)

A

Mainly in the liver

292
Q

This is an aggregate of platelets, fibrin and entrapped blood cells which can result in occlusion of the vascular lumen and embolism.

A

Thrombus, thrombi is plural

They are adhered to the vascular wall as opposite a blood clot

(img: arterial thrombus; RBCs, fibrin, platelets, and eosinophils in the middle)

293
Q

Put the pathogenesis of thrombosis (Virchow triad) in order:

  1. Endothelial injury
  2. Alterations in blood flow (turbulence or stasis)
  3. Increase in coagulation factors (or increase sensitivity to) and decrease in coagulation inhibitors (hypercoagulability)
A

See image of the Virchow triad

(need at least 2 from the Virchow triad to induce thrombosis)

294
Q

What condition is pictured (cat)?

A

Mural (in endocardium) thrombus, left ventricle

(common in cats with cardiomyopathy; from bacterermia > bacterial myocarditis >turbulence of blood flow > thrombosis)

295
Q

What condition is pictured (cat)?

A

Atrial thrombus, left atrium; cat with Hypertrophic Cardiomyopathy (HCM)

(10-20% of cats with a thrombus get it in the left atrium of the heart)

Reduced size of left ventricle >blood backs up in lungs > hypoxic damage to those tissues > endothelial injury > thrombosis

296
Q

What condition is pictured (dog)?

A

Pulmonary thrombosis

(seen in dogs with severe renal glomerular disease > protein losing nephropathy > significant loss of Antithrombin III, a major inhibitor of thrombin ALSO heart worm disease > D. immitis in right heart and pulmonary arteries > endarteritis > thrombus)

*Identify post-mortem vs. pre-mortem clot

  • Thrombus (pre-mortem clot)- blood is attached to the vessel
297
Q

What condition is pictured (horse)?

A

Verminous thrombosis

A thrombus formation in the cranial mesenteric artery of a horse with Strongylus vulgaris infection > damage to the vessel walls ALSO thrombus may form in the cecal and colonic arteries > ischemia to large intestine > infarction of cecum and colon > peritonitis > death

(img: left, larvae in mesenteric artery; right, complete obstruction of the vessel; bottom img: thrombus with larvae, septic shock from severe peritonitis)

298
Q

What is a major inhibitor of thrombin?

A

Antithrombin III

(too much antithrombin III > will not be able to make fibrin for clots)

299
Q

What condition is pictured (horse)?

A

Verminous thrombosis in the cranial mesenteric artery (Strongylus vulgaris)

(bottom img: Strongylosis in a horse colon)

300
Q

What condition is pictured (cat)?

A

Saddle thrombosis with hypertrophic cardiomyopathy (REMEMBER 10-20% of cats/dogs with HCM develop a thrombus in the left atrium), thrombus is located in the trifurcation of the abdominal aorta (external iliac a. and sacrococcygeal a.)

(cats and dogs with HCM > thrombus breaks off > saddle thrombosis > posterior paralysis)

301
Q

Which of the following is not an outcome of thrombi?

  1. Organization/recanalization
  2. Lysis
  3. Apoptosis
  4. Propagation
  5. Embolization
A
  1. Apoptosis
  • Organization/recanalization- neovascularization
  • Lysis- cells are phagocytized
  • Propagation- becomes bigger and bigger with time
  • Embolization- a piece of the thrombus breaks off

(cerebral thrombosis > stroke can develop > death)

302
Q

This is when a piece of thrombus breaks off from the original mass and sails downstream to lodge at a distant site.

A

Embolism, the mass that breaks off is called an embolus (solid, liquid, or gas)

Too much carbohydrates in feed (feedlot cattle) > ruminal acidosis > can recover, but damages the mucosa of rumen > bacteria reach systemic circulation (via portal vein) > abscess in liver (close to caudal vena cava) > rupture > septic shock

303
Q

What condition is pictured (spinal cord of a dog)?

A

Fibrocartilaginous embolism in a spinal cord > results in spinal cord infarcts (post-mortem; common in dogs)

(dogs play > sudden pain > posterior paralysis > prognosis not good )

304
Q

Fat embolism could be due to a complication of _____________________.

A

Long bone fractures

  • (rupture of vessels in bone marrow > fat and hematopoeitic tissue reaches systemic circulation > emboli > stuck in certain areas)*
  • (img: bone marrow emboli in pulmonary artery (human), secondary to CPR resuscitation efforts)*
305
Q

What condition is pictured (heart and lungs of cattle)?

A

Embolic pneumonia, an infectious cause of thrombosis/ thromboembolism

(bacterial valvular endocarditis in cattle often involve the right AV valve [septic thrombi attached to valve] and can give rise to septic emboli that will lodge in the pulmonary arteries > inflammation/ abscess formation)

306
Q

What condition is pictured?

A

Thrombotic Meningoencephalitis (TME)- acute neurological disease, death without clinical signs

  • (Histophilus somni [bacteria common in feedlots] infection > results in vasculitis and thrombosis)*
  • (img: focal areas of hemorrhage, necrosis, enlarged vessels)*
307
Q

What is a potentially catastrophic systemic reaction (thrombo-hemorrhagic disorder) in which there is generalized activation of the blood coagulation system?

A

Disseminated Intravascular Coagulation (DIC), not a primary disease; signs of tissue hypoxia, infarction and/or hemorrhage are seen; commonly seen in ICU

(img: fibrin thrombi within glomerular capillaries; PTAH stain, bluish green in glomeruli)

308
Q

What are possible etiologies for DIC?

A
  • Extensive tissue injury (car injury,etc)
  • Neoplasia
  • Systemic immunologic reactions (anaphylaxis)
  • Sepsis

Leads to a widespread activation of the coagulation cascade > hypoxia > multi-organ failure > death

These can lead to consumptive coagulopathy and hemorrhage diathesis = all of the coagulation factors for thrombus formation used up which leads to hemorraghic diathesis (lots of blood seen during necropsy)

309
Q

What is a localized area of ischemic necrosis in a tissue or organ caused by occlusion of either the arterial supply or the venous drainage?

A

Infarction

Venous infarcts are usually intensely hemorrhagic as blood backs up into the affected tissue behind the obstruction

Arterial infarcts are often initially hemorrhagic but become pale as the area of coagulation necrosis becomes evident (more common in humans)

Renal infarct

(img: venous infarction, small intestinal volvulus, pig)

310
Q

What condition is pictured (kidney of a rabbit)?

A

Renal infarct, acute pale infart, kidney

(multiple, pale white to tan pyramidal-shaped infartcs extend from the renal cortex to the medulla; the infarcts bulge above the capsular surface (center top, left image), indicative of acute cell swelling)

311
Q

T or F. Microscopically, an infarct is a focal area of coagulation necrosis.

A

True (coagulative necrosis associated with ischemia)

Loss of cellular structure, but preservation of the general structure of the organ (coagulative necrosis)

(img: triangular in shape due to the architecture of arteries; rim of inflammatory cells surrounding an infarct > if animal survives, it is replaced with connective tissue)

312
Q

What is the final common pathway for a number of potentially lethal clinical eventss, including severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis?

A

Shock

Shock gives rise to systemic hypoperfusion; it can be caused either by reduced cardiac output or by reduced effective circulating blood volume; the end results are hypotension, impaired tissue perfusion and cellular hypoxia

313
Q

T or F. Shock can lead to DIC and multi-organ system failure.

A

True

314
Q

Which of the following is not a type of shock?

  1. Anaphylactic shock
  2. Neurogenic shock
  3. Hypovolemic shock
  4. Cardiogenic shock
  5. Somatic shock
  6. Septic shock
A
  1. Somatic shock
  • Cardiogenic shock- failure of the heart to maintain normal cardiac output (ex. due to idopathic cardiomyopathy, toxicity (feed in cattle and poultry)
  • Hypovolemic shock- fluid loss due to hemorrhage, vomiting, diarrhea (ex. from trauma, HBC)
  • Blood maldistribution
    • Anaphylactic shock- type I hypersensitivity (ex. peanut allergy)
    • Neurogenic shock- neurological injury leading to loss of vascular tone and peripheral pooling of blood
    • Septic shock- results from the host innate immune response to infectious organisms that may be blood borne or localized to a particular site (ex. colonic torsion, rupture of stomach, Parvovirus, etc)
315
Q

How well do you know the pathogenesis of septic shock?

A

Seen commonly with infection of gram-negative bacteria > LPS > WBCs release cytokines (TNF, IL-1) > triggers the coagulation cascade

SEE IMAGE

316
Q

10-20% of cats/dogs with hypertrophic cardiomyopathy develop a thrombus in the ________________.

A

Left atrium

317
Q

Several goat kids presented with chronic diarrhea, weight loss, weakness, and decreased appetite. They also had submandibular swelling, ascites, and anemia. During necropsy, you noted pulmonary edema (froth), hydropericardium (transudate in pericardial sac), and infectious (hyperplastic) lesions in the jejunum (image). What is the MDx, etiology, etiologic diagnosis and the name of the disease?

A

MDx: chronic multifocal proliferative (hyperplastic) enteritis

Etiology: Eimeria spp.

Etiologica diagnosis: Protozoal enteritis, Enteric coccidiosis, or Coccidial enteritis

Name of the disease: Coccidiosis

(bottom img: schizonts and sexual stages of Eimeria spp.; pink = female stages, blue = male stages)

318
Q

You found a dead 6-month-old pig with the lesions circled in red. Upon opening, the intestines were diffusely friable, the walls were thickened and edematous. The mesenteric vessels were also very enlarged. What is the Dx and MDx?

A

Dx: umbilical hernia (common in pigs)

MDx: segmental venous infarction, jejunum

(obliteration of the vein walls = venous infarction; the animal developed peritonitis, DIC and died from sepsis)

319
Q

This horse’s stomach ruptured due to gastric dilatation (colic) from grain overload. You see hemorrhaging around the margins of the rupture, was this lesion pre-mortem or post-mortem?

A

Pre-mortem

(will not see hemorrhaging in the margins of the rupture for post-mortem)

320
Q

What is invading the ileum and ileo-cecal valve from this horse?

A

Anoplocephala perfoliata (tapeworms)

321
Q

A horse came in with severe pain that could not be managed and upon doing blood work, you noticed sepsis so it was euthanized. During necropsy, the right ventral colon was opened and this is what you saw (image). What is the Dx and MDx?

A

Dx: Cecocolonic intussusception

MDx: Venous infarction of the cecum secondary to cecocolonic intussusception

322
Q

You found these poor cows lined up along a fence and found burn lesions (serpentine lesions) on the skin. What do you suspect happened?

A

Death by lightening.

(multiple fractures may also be seen due to the acute/severe contraction of the muscles)

323
Q

______________ is the process of tumor formation.

A

Neoplasia

324
Q

______________ is a “new growth” composed of cells originally derived from normal tissues that have undergone heritable genetic changes that allows them to become relatively unresponsive to normal growth controls and expand beyond their normal anatomic boundary.

A

Neoplasm

(aka tumor)

325
Q

What is the study of tumors or neoplasm?

A

Oncology

326
Q

What are the 2 basic components of a neoplasm?

A
  1. Parenchyma (formed by neoplastic cells themselves)
  2. Stroma (in order to proliferate, connective tissue and blood vessels support the neoplastic cells)
    1. Some tumors induce prominent desmoplasia (the formation and development of collagen-rich fibrous CT stroma, such as scirrhous carcinomas (“stony hard consistency”); mammary, GI
327
Q

What are considered pre-neoplastic changes?

A

Hyperplasia, metaplasia, dysplasia

328
Q

An example of mammary gland cells (simple cuboidal) continuously proliferating during the normal menstruation cycle is

  1. Hyperplasia
  2. Metaplasia
  3. Dysplasia
A
  1. Hyperplasia
329
Q

An example of ciliated pseudostratified epithelium in the respiratory airways of a smoker being replaced by stratified squamous epithelium is

  1. Hyperplasia
  2. Metaplasia
  3. Dysplasia
A
  1. Metaplasia
330
Q

________________ are more susceptible to injury to the tip of their ears by UV light, causing hyperplasia and dysplasia of the epidermis. This can eventually develop into carcinoma in situ (confined to the basement membrane) and even squamous cell carcinoma (invasive).

A

White cats

331
Q

What are the 4 classifications of tumors?

A
  1. Mesenchymal tumors
  2. Epithelial tumors
  3. Undifferentiated tumors
  4. Mixed tumors

(usually 1 and 2)

332
Q

Out of the 4 classifications of tumors, which one arises from cells of mesodermal origin?

A

Mesenchymal tumors

  • If it is bengin: suffix “oma” (ex. osteoma)
    • ​Muscle: myoma
    • Smooth muscle: leiomyoma
    • Striated muscle: rhabomyoma
    • Cartilage: chondroma
    • Adipose tissue: lipoma
  • If it is malignant: suffix “sarcoma” (ex. osteosarcoma)**​​
    • ​Muscle: myosarcoma
    • Smooth muscle: leiomyosarcoma
    • Striated muscle: rhabomyosarcoma
    • Cartilage: chondrosarcoma
    • Adipose tissue: liposarcoma
333
Q

Out of the 4 classifications of tumors, which one primarily arises from cells of endodermal and ectodermal origin?

A

Epithelial tumors

334
Q

What is a benign epithelial tumor that projects from a mucosal surface?

A

Polyp

(nasal cavity, GI tract)

335
Q

What is a benign epithelial tumor that is an exophytic growth from an epithelial surface?

A

Papilloma

(skin surface)

336
Q

What do you call a malignant epithelial tumor?

A

Carcinoma

[add organ of origin; add whether arises from glandular epithelium or form glandular structures microscopically (“adeno”); add whether induces desmoplasia (scirrhous) or produces mucin (mucinus)]

  • Liver: hepatocarcinoma or adenocarcinoma (glandular)
  • Thyroid gland: thyroid carcinoma or thyroid adenocarcinoma
  • Boobs: scirrous mammary carcinoma when it is hard and filled with a lot of collagen (desmoplasia)
  • GI tract: mucinus adenocarcinoma of the stomach
337
Q

What do you call an epithelial tumor that is contained within the basement membrane?

A

Carcinoma in situ

338
Q

What are undifferentiated tumors?

A

When looking at the cells microscopically, can’t tell the cell of origin; have to do IHC testing (poor prognosis, usually malignant)

339
Q

What are mixed tumors?

A

When looking at the cells microscopically, there are multiple cell types derived from a single or multiple germ cell layers- pluripotential or totipotential cell

  • Mixed mammary tumors in dogs (areas of cartilage, epithelium, bone; benign or malignant, but usually benign 60-70%)
  • Teratomas
  • Nephroblastoma (embryonal nephroma, Wilm’s tumor)
340
Q

What type of mixed tumor arises from totipotent germ cells and contain tissues derived from all embryonic cell layers and consist of a bizarre mixture of adult and embryonic tissue types?

A

Teratomas [usually found in the gonads (testes), horses, or younger animals]

(img: horse, testicular teratoma with teeth, hair, bone, glandular tissue!)

341
Q

What type of mixed tumor contains both epithelial and mesenchymal components?

A

Nephroblastoma (aka embryonic nephromas or Wilm’s tumors) [common in children or pigs, usually unilateral; malignant in dogs]

(img: pig, kidney; forms a glomerular-like structure)

342
Q

This is a kidney from a young pig, what type of tumor is most likely?

A

Nephroblastoma (mixed tumor common in young pigs)

(there is a unique tumor reported in thoracolumbar junction of the spinal cord of young dogs, mainly German Shepards that is now believed to be a nephroblastoma)

343
Q

How can you differentiate a benign tumor from a malignant tumor?

A
  • Degree of differentiation/anaplasia
    • Benign tumors are well differentiated (parenchymal cells closely resembles cell of origin)
    • Malignant tumors can be well differentiated or anaplastic
  • Rate of growth
    • Most malignant tumors grow rapidly (high mitotic rate)
    • Benign tumors grow at a slower pace
  • Local invasion (expansile vs. infiltrative growth)
    • Benign tumors grow by expansion (compression atrophy of neighboring tissues)
    • Malignant tumors are infiltrative and grow into neighboring tissues
    • Moveable (benign) vs. attached tumors (malignant)
  • Presence or absence of metastasis (secondary growth of a tumor)
    • Benign tumors do not metastasize
344
Q

T or F. Benign tumors are undifferentiated and malignant tumors can be both undifferentiated and well-differentiated.

A

False, benign tumors are well-differentiated and malignant tumors can be both undifferentiated and well-differentiated.

345
Q

Anaplasia (‘cellular atypia’) is characterized by all of the following except:

  1. Loss of polarity (disorganization)
  2. Pleomorphism
  3. Abnormal nuclear morphology
  4. Low mitotic rate
  5. Lack of differentiation (“to form backwards”)
  6. More malignant
  7. All of the above are characteristic of anaplasia
A
  1. Low mitotic rate

Analplasia is characterized by a HIGH mitotic rate

(img: rhabdomyosarcoma, pleomorphic muscle cells, some nuclei are very large, some nuclei are very small, prominent nucleoli)

346
Q

What are the 2 main mechanisms that regulate tissue growth?

A
  1. Rate of cell proliferation (fraction of cells in the replicative pool > cells undergoing mitotic activity)
  2. Rate of programed cell death (apoptosis)
    • Genes for apoptosis can be compromised
347
Q

What is a non-lethal genetic damage that lies at the heart of carcinogenesis?

A

Apoptosis

(genetic damage per se does not constitute mutation, mutation occurs during DNA replication > the alteration in DNA sequence caused by genetic damage needs to be imprinted in the genome; many neoplasms may present alterations in apoptotic pathways leading to further genomic instability, one of the hallmarks of malignant transformation > cells that may have suffered significant DNA damage are allowed to replicate, eventually this may lead to the formation of increasingly aggressive subclones)

348
Q

T or F. Expansile growth : benign tumors and infiltrative growth : malignant tumors.

A

True

(img: horse, thyroid adenoma expansile growth; normal color is on the outside; localized, very well demarcated, sometimes encapsulated; common in old horses)

  • Hyperthyroidism common in cats
  • Hypothyroidism common in dogs
349
Q

This is a mammary tumor in a dog that has metastasized. Is it benign, malignant, or cannot be determined with the given information?

A

Malignant (metastasis = malignant)

(img: mammary carcinoma; margins not very clear; ulceration, necrosis due to the growth outpacing its blood supply, and hemorrhage seen)

350
Q

Is this mammary tumor from a cat benign or malignant?

A

Malignant carcinoma or malignant adenocarcinoma, 85% of mammary tumors in cats are malignant

(difficult to recognize the lumen of the alveoli, necrosis on the right side, alveoli lined by more than 1 epithelial cell layer, high degree of pleomorphism, large nuclei, prominent nucleoli; does not look close to normal, bottom image)

351
Q

Is this tumor from the intestine of a horse benign or malignant?

A

Benign lipoma (aka pedunculated peritoneal (mesenteric) lipoma; common in the mesentery of horses)

(bottom img: these lipomas can become necrotic from torsion of the peduncle [cut blood supply] and then mineralized > heavy > peduncle can twist around a piece of gut and cause volvulus)

352
Q

Is this tumor from the pancreas of a dog bengin or malignant?

A

Necrosis, uneven surface, cavitation and hemorrage seen, but it is a BENIGN adenoma (histologically)

(islet tumors that produce insulin = insulinomas, can cause hypoglycemia > hypoglycemic seizures > death)

353
Q

Is this tumor from a cat’s pituitary gland benign or malignant? (brain removed)

A

Benign pituitary adenoma (well circumscribed, not attached to brain)

(severe compression atrophy of the brain > severe neurological disease)

354
Q

Is this proliferative lesion on the brain of a cat benign or malignant?

A

Benign meningioma (surface of left cerebral hemisphere; compression atrophy all around; common in cats and dogs)

(bottom img: meningioma, occipital lobe; if it is on the surface, most likely a meningioma)

355
Q

What kind of tumor is this on the brain of a cat?

A

Meningioma (severe compression atrophy of cerebral hemisphere, hemorrhage, necrosis because the brain [bone] restricts its growth leading to hypoxia)

(bottom img: dog meningioma between 4th ventricle, cerebellum and brainstem > fatal)

356
Q

What type of tumor is this on the brain of a dog (ventral view)?

A

Malignant meningioma (lesion not very well demarcated, invades underlying tissues, cannot distinguish cranial nerves; in theory, nomeclature-wise, it should be malignant (meningi_oma_ vs. meningio_carcinoma_) but it is an exception to the rule)

357
Q

What type of tumor is this on the brain of a cat?

A

Meningioma (well demarcated, on the surface of the cerebral hemisphere, growth by expansion, compression atrophy [damage to cardiorespiratory centers > death], severe edema, necrosis in diencephalon, lateral ventricles collapsed)

358
Q

How are malignant tumors spread (metastasis)?

A
  • Transcoelomic spread (seeding/invading of body cavities and surfaces) > characteristic of carcinomas (epithelium)
    • Ex. ovarian carcinomas > cytokines increase perm. > ascites
  • Lymphatic spread
    • ​Mostly carcinomas; metastasize first to regional lymph nodes
  • Hematogenous spread
    • ​Mostly sarcomas

(img: metastatic cascade)

359
Q

What happens during the metastatic cascade?

A

Malignant tumor (carcinoma) > detached from each other (down regulation of genes and loss of production of adhesion molecules cadherin and catenin) > break through basement membrane > upregulation of integrins that attach to ECM > induce degradation of ECM (proteolytic enzymes, etc.) to get to blood vessel > most tumor emboli do not survive > those that survive attach to endothelium and migrate to ECM somewhere else > produce secondary tumor

360
Q

T or F. Tumor-parenchymal interactions play an important role in carcinogenesis

A

False, tumor-STROMAL interactions play an important role in carcinogenesis (tumor cells will produce certain things that will change how the stroma works and vice versa)

361
Q

Tumors are usually monoclonal in origin, but as they progress, they have more heterogeneity by:

A
  • Generated during tumor growth
    • By progressive accumulation of heritable changes in tumor cells
  • Generation of sublcones and successful subclones
362
Q

What are characteristics of a successful subclone (metastasis)?

A
  • Highly proliferative rate
  • Evasion of host immune response
  • Can stimulate development of independent blood supply
  • Are independent of exogenous growth factors (can produce their own GF to proliferate)
  • Can spread to distant sites
363
Q

Why is this cat’s histology sample diagnosed as a mammary CARCINOMA instead of a benign tumor?

A

Hypercellularity, borders not well demarcated, pleomorphism, clusters of neoplastic cells within the lumen of a lymphatic vessel (emboli = metastasis; in red circles)

(bottom img: metastasis to superficial inguinal lymph nodes)

364
Q

This mammary carcinoma in a cat has metastasized, even to the lymph nodes; which pathway of spread is circled in red?

  1. Transcoelomic
  2. Lymphatic
  3. Hematogenous
A

1. Transcoelomic spread (carcinomas can exfoliate and seed the pleural cavity [pleural carcinomatous])

Pathology choefsho (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions