Test 1: lab 2 Flashcards
Description:
The right cranial lung lobe is completely twisted (360 degrees) around its hilus. The affected lobe is diffusely swollen, dark red, and firm.
How does a torsion lead to injury of an organ?
Torsion leads to compression of the pulmonary veins. The more muscular arteries typically allow for blood to continue to flow into the affected lung lobe, which then becomes congested as blood pools in the vasculature behind the obstructed vein(s). The retained blood becomes depleted of oxygen, and the cells may undergo ischemia and necrosis (infarct).
Potential causes of the torsion in this case?
Fluid within the thoracic cavity may lead to lung lobe torsion. The air in the lungs makes them buoyant, and so lung lobes in fluid may float and rotate around their blood supply.
Other associated factors are trauma, pulmonary or pleural space disease (including neoplasia), or prior thoracic surgery. Many cases of lung lobe torsion are of unknown cause. Large, deep-chested dogs are predisposed.
Edema may also be seen with this lesion. What are the four causes of edema, and which one is the likely cause of edema in this case of lung torsion?
Causes of edema:
- ↑ vascular permeability
- ↑ intravascular hydrostatic pressure
- ↓ plasma colloid osmotic pressure
- ↓ lymphatic drainage
Lung lobe torsion → blockage of venous outflow → increased blood volume in vasculature behind obstruction → increased hydrostatic pressure → edema
describe and morphological
Description: There is a sharply demarcated zone of the left cerebral hemisphere that is cream-colored centrally with a dark red-brown rim. This area measures approximately 3 X 4 cm on the cut surface of the more caudal of the two sections, and approximately 1.5 X 4 cm on the more rostral of the sections.
Morphologic diagnosis: Severe locally extensive acute to subacute infarct of the cerebral hemisphere.
Why is the brain especially susceptible to ischemia of all types?
The brain has high oxygen and nutrient requirements and poor collateral circulation.
What type of necrosis is commonly associated with infarcts?
Infarcts lead to coagulative necrosis in most tissues, although it often results in liquefactive necrosis in the brain.
What is a clinical term for infarcts of the brain?
A cerebrovascular accident, or stroke (more common in humans than in animals)
Morphologic diagnosis:
Severe multifocal acute, subacute, and chronic renal infarcts.
Note: infarction is the pathological process of tissues dying due to ischemia, while an infarct is an area of ischemic necrosis in a tissue. Thus, the lesion is an infarct as a result of infarction.
What are the four phases of wound/tissue repair?
- Hemostasis 2. Acute inflammation 3. Proliferation 4. Tissue remodeling/maturation.
How do the gross appearances between acute and chronic infarcts correlate with the physiologic processes of tissue repair?
Hemorrhage gives acute infarcts a red appearance as blood escapes from the damaged vessel into the surrounding tissue until hemostasis is achieved. The tissue becomes swollen due to blood as well as acute inflammation (neutrophils and macrophages that infiltrate the tissue to remove dead cells and debris). With time, the erythrocytes are lysed, and their hemoglobin (and other pigment derivatives from the breakdown of hemoglobin) is removed from the tissue, giving a progressively paler appearance. As the lesion progresses, there is proliferation of blood vessels and fibroblasts to restore blood flow and the integrity of the tissue. Over time, tissue remodeling continues with the areas of necrosis and parenchymal loss being replaced by firm, tan, fibrous connective tissue. The final lesion is depressed and contracted.
In summary, acute renal infarcts are dark red to tan and level with the adjacent capsular surface. Chronic infarcts are depressed, pale tan, and firm. Both acute and chronic infarcts in the kidney are typically wedge-shaped. How deeply the infarct extends depends on what vessel is blocked.
diagnosis
jugular vein thrombosis
How would you differentiate the lesion within the jugular vein from a postmortem clot?
Antemortem thrombi appear as rough, dull red to tan masses of platelets and fibrin. They may have a laminated appearance as layers of platelets and fibrin adhere to the surface over time.
Postmortem clots are glistening, smooth, red to yellow masses of blood with a jelly-like consistency. They form from blood that has settled and clotted after death.
What are the three components of Virchow’s Triad?
Three causes of thrombosis (Virchow’s Triad) are:
- Endothelial injury
- Abnormal blood flow (stasis or turbulence)
- Hypercoagulability (inherited or acquired)
The jugular vein is a common site for intravenous injection for horses. How might this contribute to the lesion in this case?
Repeated injections into the same jugular vein may cause sufficient damage to the endothelium to initiate thrombosis. The type or volume of injected substances can be irritating or damaging to the endothelium as well. Intravenous catheters left in place for extended time have also been associated with thrombosis at this site. Of course, systemic issues (e.g., coagulopathies, sepsis) can also increase the risk of thrombus formation.
This dog was febrile and had a noticeable heart murmur.
What is the difference between a thrombus and a thromboembolus?
A thrombus is an aggregate of platelets, fibrin, and blood cells that forms on a vessel/heart wall in a living animal.
A thromboembolus is a piece of a thrombus that has broken off and traveled through the bloodstream until getting lodged in a vessel at a distant site. Grossly, a thrombus is attached to a vessel wall, and a thromboembolus, at least initially, will be detached and free in the vessel lumen.
Remember: not all emboli are thromboemboli. Any material (including thrombi, fat, air, fibrocartilaginous material from intervertebral discs, etc.) that enters the circulatory system can be carried by the blood from its point of origin to a distant site (an embolus), where it may obstruct blood flow and cause tissue dysfunction or necrosis.
How might the heart murmur be associated with the lesion in the pulmonary artery?
Cardiac disease can lead to alterations in blood flow and subsequent thrombosis. Given the history of fever, the murmur may be due to vegetative valvular endocarditis, a condition in which accumulations of bacteria, fibrin, and inflammatory cells form masses (thrombi) on the heart valves that can break off and travel in the bloodstream to a distant site.
If thrombosis first occurred in the heart, in which side of the heart would the thrombus have formed in this case?
A thrombus that forms in the right side of the heart can enter directly into pulmonary circulation, leading to a thromboembolus in the pulmonary arteries. Thrombi that form in the left side of the heart can enter directly into systemic circulation and lodge at distant sites, such as at the aortic bifurcation into the two external iliac arteries, which sometimes is seen in cases of heart disease in cats. In cases of vegetative valvular endocarditis, the kidneys are common sites for thromboemboli.
What are some non-cardiac causes of thrombus formation in multiple organs?
Many causes, including severe bacterial infections, inflammation of blood vessels (vasculitis), dysfunction of organs involved in production of clotting factors, some metabolic diseases, or immune-mediated diseases.
describe and morphologic
Describe the lesion: The featherless areas of skin around both eyes are covered by raised, brown, soft to firm, friable tissue with an irregular verrucous surface.
Morphologic diagnosis: Severe regionally extensive and bilateral proliferative and necrotizing dermatitis (eyelids and periocular area). A multifocal to coalescing distribution may also be considered.
Speculate on possible etiologies (remember “MINI VAN DITTI”):
The roughly bilaterally symmetric nature of the lesion would be highly unusual for neoplasia at this location. The changes to the tissue and distribution are most consistent with an inflammatory process with epidermal hyperplasia and necrosis, in this specific case caused by an infectious disease (an avian pox virus). The virus is transmitted by arthropod vectors (e.g., mosquitoes), direct contact through breaks in the skin, inhalation of air-borne particles contaminated with virus (e.g., feathers or crusts), and other ways. Histologic images are here as a supplement to demonstrate the different processes occurring in the lesion to create the gross appearance. The epidermis is severely thickened by increased numbers of squamous epithelial cells (hyperplasia), which are swollen from hydropic degeneration and contain prominent eosinophilic intracytoplasmic inclusion bodies (aggregates of viral DNA synthesis within the cytoplasm). The epidermis also has foci of necrosis, and inflammatory cells are present in the dermis.
describe and morphologic
Describe the lung (fresh specimen shown in the preceding photo): The fresh lungs seen in the photo can be described as follows: The cranioventral portion of the lung is consolidated, firm, and red with multiple tan foci. There are areas of fibrin on the pleural surface. The caudodorsal portion of the lung is pink and soft. Some interlobular edema is visible dorsally in the more normal pink portion of the lung adjacent to the more affected areas.
Morphologic diagnosis: Severe regionally extensive acute pneumonia. You can also add qualifiers like “necrosuppurative and fibrinous.” This case is a bronchopneumonia, but you will be taught specific patterns of pneumonia later in the semester. Thus, later in the course, your more specific morphologic diagnosis might be “severe regionally extensive acute necrosuppurative and fibrinous bronchopneumonia.”
Speculate on possible etiologies (remember “MINI VAN DITTI”):
The redness, swelling, and presence of fibrin and purulent material (pus) is consistent with acute inflammation and infection. Note the severity of the inflammation that can develop in a short time!
pneumonia
Two kidneys from dogs both with severe azotemia (elevated blood urea nitrogen (BUN) and creatinine), lethargy, weight loss, and polyuria (increased urination). A normal kidney has been provided as a reference for size and color.
describe and morphologic
Describe the affected kidneys: The kidneys are diffusely pale tan and firm with irregular cortical surfaces varying from numerous pinpoint depressions to more extensive areas of parenchymal loss, with one kidney in particular significantly smaller than normal.
Morphologic diagnosis: Severe diffuse chronic nephritis. To be more precise, this is a tubulointerstitial nephritis, but you will be taught specific patterns of kidney inflammation later in the semester.
