Week 2 Flashcards

Question

What are the 8 main types of etiologies?

Answer 1

Description of lesion: Squamous metaplasia of the esophagus of a parrot. The raised white plaques are keratin. Dx: Avitaminosis A (a type of disease of adaptation, degeneration and cell death)

Answer 2

Dx: Embolic nephritis (kidney of horse) (a type of disease of inflammation and repair) (Embolic means a descending type of infection coming from the blood stream. Initially goes in the cortex) Etiology: Caused by Actinobacillus equuli

Answer 3

MDx: Congenital porphyria of cow bone (a type of tissue deposit/pigmentation) Etiology: Defect in heme synthesis caused by a deficiency in uroporphyrinogen III cosynthetase

Answer 4

Dx: Chronic passive congestion (nutmeg liver) of liver of a cow (a type of circulatory disorder) Causes: right sided heart failure, ingestion of hepatotoxin (i.e. Wedelia glauca, etc.)

Answer 5

Dx: Globoid cell leukodystrophy of a dog (a type of Lysosomal storage disease, type of genetic disorder) Etiology: Defect in an enzyme (galactosylceraminidase)

Answer 6

MDx: Acute allergic rhinitis with secondary plant foreign body (disease of immunity, lupus is also an example of this) Etiology: Type I hypersensitivity reaction- plant allergen

Answer 7

Dx: Bovine abomasal lymphoma (type of neoplasia) Etiology: Bovine leukemia virus

Answer 8

Dx: Epithelial plaques, papular stomatitis of the hard palate mucosa of a calf (type of microbial infection) Etiology: Parapoxvirus

Answer 9

Diseases of unknown cause or spontaneous origin Epilepsy, hypertrophic cardiomyopathy, renal amyloidosis, canine polyarteritis, pulmonary fibrosis, laryngeal hemiplasia

Answer 10

Occurs when the cell homeostasis is distorted by stresses or pathologic stimuli. The cell is not dead, just morphologically different from the normal cell. Can return to normal morphology and homeostasis when the stress is removed. Cells preserve viability and function. Reversible change! Principles responses of adaptation are: atrophy, hypertrophy, hyperplasia, metaplasia

Answer 11

Tendency to stabilize the normal body states of the organism; it is the ability to maintain internal equilibrium by adjusting its physiological processes

Answer 12

Decrease in size and/or number of the cells and their metabolic activity after normal growth has been reached. Remember, cells are not dead. They are still functioning, just smaller. Decreases protein synthesis and increases protein degradation Causes: decreased workload, denervation (e.g. recurrent laryngeal nerve denervation --\> laryngeal atrophy), decreased blood supply or oxygen, inadequate nutrition, loss of endocrine stimulation, aging Examples: muscle disuse of limb in cast, sedentary atrophy, adrenal cortex atrophy by reduction of ACTH stimulation (steroid therapy), atrophy in tissues adjacent to a tumor due to pressure and compromised blood supply, physiologic atrophy (e.g. non-lactating mammary gland atrophy), serous atrophy of heart or bone marrow (lack of fat, dilated lymphatics)

Answer 13

Hydrocephalus with compression atrophy of a cat can be caused by intrauterine infection of panleukopenia.

Answer 14

Hypertrophy is increased size of cells and their functions. Synthesis of more organelles and structural proteins--\> bigger cells. More common in cell with little or no replication, stable or permanent cells such as cardiomyocytes and neurons.

Answer 15

Hypertrophic pregnant uterus Weightlifter with hypertrophic muscle cells

Answer 16

Cardiac hypertrophy beyond the limit that it can keep up with the burden can lead to regressive changes (lysis and loss of contractile elements) and ultimately cell death and cardiac failure in extreme cases. This is an example of how adaptation to stress can progress to functionally significant cell injury if the stress is not relieved. Concentric when walls grow inward (reduction of chamber size), eccentric when they grow outward. Haphazardly arranged cells on histopath, can even have fat or fiber replace muscle cells in extreme cases. Etiologies of cardiac hypertrophy: Aortic valve disease, hypertension, Genetic mutation (e.g. Main Coon cat)

Answer 17

Increase in number of cells of an organ. An enlarged organ can be differentiated as hyperplastic or hypertrophic by histology. Occurs in cells capable of replication, e.g. lymph tissue, skin, etc. Hyperplastic nodules are usually irreversible and have no proper function.

Answer 18

Physiologic hyperplasia- Hormonal (breast growth during pregnancy) or compensatory (post-hepatectomy liver growth) Pathologic hyperplasia- most commonly caused by excessive hormonal or growth factor stimulation, e.g. epidermal thickening (repeated irritation) or respiratory mucosa (in viral infections), fibrous hyperplasia (MDx) of gingiva

Answer 19

Change in phenotype of a differentiated cell. Response to chronic irritation --\> cell withstand stress. May result in decreased functions or increased propensity for malignant transformation (neoplasia). Reversible if cause is removed! Most often in epithelial cells.

Answer 20

Chronic irritation in lungs (smokers) Vitamin A deficiency Estrogen toxicity Mammary tumors

Answer 21

Refers to abnormal development, mostly of epithelial cells. Term is mostly used in neoplastic processes, near-synonym but not as advanced as "carcinoma in situ." It is in between metaplasia and neoplasia.

Answer 22

Nephrolith (xanthinuria) with hydronephrosis, cortical and medullary atrophy and medullary fibrosis, diffuse

Answer 23

MDx: Skin, hyperplasia on the right, dysplasia on the left Dx: Squamous cell carcinoma in situ of a female DSH cat

Answer 24

MDx: Gastric hypertrophy of a snake. (histology needed to differentiate it from hyperplasia) Etiology: Cryptosporidium

Answer 25

Lesion description: whitish, multifocal nodular areas of a feline stomach MDx: Gastric lymphoid hyperplasia

Answer 26

MDx: Hepatocellular carcinoma with nodular hyperplasia, dog

Answer 27

MDx 1: Hydronephrosis with secondary diffuse cortical atrophy MDx 2: Hydroureter Etiology: Ureteral obstruction

Answer 28

MDx: Cystic renal disease, aka Polycystic kidney disease Associated cell adaptation: atrophy

Answer 29

Reversible cell injury: cellular swelling, fatty changes (lipidosis) Irreversible cell injury: necrosis, apoptosis, other types of cell death

Answer 30

aka hydropic degeneration, hydropic change, cytotoxic edema (CNS), ballooning degeneration (epidermis) Definition: Early, reversible, sub-lethal manifestation of cell damage, characterized by increased cell size and volume due to water overload. Most common and fundamental expression of cell injury. Mitochondria and ER are the organelles that can dilate to hold extra water and when they can't hold any more is when it goes from reversible to irreversible.

Answer 31

Highly vulnerable: Cardiomyocytes, proximal renal tubule epithelium, hepatocytes, endothelium, CNS neurons, oligodendrocytes and astrocytes (cytotoxic edema) Not sensitive: adipose, bone, skeletal muscle, CT

Answer 32

Loss of ionic and fluid homeostasis. Loss of water and ion transport across the cell membrane, mainly sodium. Failure of cell energy production, cell membrane damage, injury to enzymes regulating ion channels of membranes. E.g. Mostly from hypoxia and toxic agents! Can also be due to physical mechanical injury, free radicals, viruses, bacteria or immune-mediated injury

Answer 33

Slightly swollen organ with rounded edges Pallor when compared to normal Cut surface: tissue bulges and cannot be easily put in correct position Slightly heavy ("wet organ")

Answer 34

H2O uptake dilutes the cytoplasm, so cells are enlarged with pale cytoplasm. May show increased cytoplasmic eosinophilia. Nucleus is in normal position with no morphological changes- this is important! It can be difficult to appreciate with the light microscope though.

Answer 35

Ballooning degeneration of epidermis resulting in vesicle formation (bullae/blister)- it is an extreme variation of hydropic degeneration. Histo is seen in picture on the right. On the left is its avian counterpart. Etiology: vesicular exanthema of swine virus, a calcivirus (vesivirus) on the snout of a pig

Answer 36

All changes start at the outside and move toward the center of the cell. 1. Plasma membrane alterations, such as blebbing, blunting and loss of microvilli. 2. Mitochondrial changes, including swelling and the appearance of small, amorphous densities 3. Dilation of the ER, with detachment of polysomes; intracytoplasmic myelin figures may be present. 4. Nuclear alterations, with disaggregation of granular and fibrillar elements.

Answer 37

Cell swelling- Hydropic change, fatty change. Due to increased uptake of H2O and then to diffuse disintegration of organelles and cytoplasmic proteins. Cell enlargement- Hypertrophy. Caused by increase of normal organelles.

Answer 38

It depends on the number of cells affected and importance of cells Good prognosis if oxygen is restored before the point of no return. Poor prognosis if the hypoxia progresses to irreversible cell injury.

Answer 39

Lipofuscin- aka wear and tear pigment Evidence of a previous injury (e.g. neuron)

Answer 40

Sub-lethal cell damage characterized by intracytoplasmic fatty vacuolation. It may be preceded or accompanied by cell swelling (difficult to differentiate the 2 by microscopy). All major classes of lipids can accumulate in cells (e.g. triglycerides, cholesterol (esters), phospholipids, abnormal lipid-carb complexes (lysosomal storage disease), etc.

Answer 41

Accumulation of triglycerides and other lipid metabolites (neutral fats and cholesterol) within parenchymal cells (e.g. liver, heart muscle, skeletal muscle, kidney) Hepatic lipidosis- prototype. Clinical manifestations are usually alterations in function (elevated liver enzymes, icterus) bc liver is central to lipid metabolism.

Answer 42

Main causes: chronic hypoxia (e.g. clot, pneumonia, high altitude, anemia, chronic heart failure), toxicity, metabolic disorders Seen in abnormalities of synthesis, utilization and/or mobilization of fat

Answer 43

Impaired metabolism of fatty acids --\> accumulation of triglycerides --\> formation of intracytoplasmic fat vacuoles

Answer 44

Hepatic lipidosis is aka fatty liver, fatty change, hepatic steatosis Diffuse yellow if all cells affected. Enhanced reticular pattern if only some cells affected. Edges are rounded and will bulge on section. Tissue is soft, often friable, greasy and cuts easily. Some sections may float in liquid if disease is severe.

Answer 45

In late pregnancy (pregnancy toxemia) and heavy early lactation (ketosis) in ruminants

Answer 46

Nutritional disorders- obesity, protein-calorie malnutrition (impaired apolipoprotein synthesis), starvation (increased mobilization of triglycerides) Endocrine diseases- diabetes mellitus (increased mobilization of triglycerides), feline fatty liver syndrome, fat cow syndrome (unknown cause) Neimann Pick disease (phospholipid sphingomyelin)- a lysosomal storage disease)

Answer 47

Well delineated, lipid-filled vacuoles in cytoplasm. Vacuoles vary in quantity or size and may displace the nucleus to the periphery of the cell.

Answer 48

Initially reversible, but can lead to irreversible hepatocyte death. ID and tx of 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. Most often seen in cats secondary to anorexia, can also be seen in mini horses, ruminants and camelids.

Answer 49

Severe swelling of mitochondria Extensive damage to plasma membranes (gives rise to myelin figures) Excessive swelling of lysosomes and vacuoles Happens to myocardium 30-40 mins after ischemia. Cell death mainly occurs by necrosis, but sometimes apoptosis. Necrotic change is seen ultrastructurally in less than 6 hours, histologically in 6-12 hours and grossly in 24-48 hours.

Answer 50

Pale, soft, friable and sharply demarcated from viable tissue by a zone of inflammation.

Answer 51

(Turkey) MDx: Hepatitis, multifocal to coalescing, subacute, severe necrosis. Reddish in center (non-functional, blood vessel dies resulting in leakage on the inside of the circles) and whitish around borders (functional and spreading) Etiology: Histomonas meleagridis Dx: Blackhead disease

Answer 52

Denatured proteins --\> increased binding of eosin (pink) Loss of RNA --\> Loss of basophilia Loss of glycogen particles --\> Glassy homogeneous Enzyme-digested cytoplasm organelles --\> Vacuolation and moth-eaten appearance Calcification can be seen

Answer 53

May provide clues about the underlying cause Do not reflect underlying mechanisms but are used by pathologists and clinicians.

Answer 54

e.g. infarcts, nutritional myopathy Common cause: ISCHEMIA (reduced blood perfusion) in all solid organs except the brain Architecture of dead tissue is preserved up to several days. Ultimately necrotic cells are removed by phagocytosis by WBCs and by digestion by lysosomal enzymes of WBCs. Infarcts shown in pictures. They are usually caused by obstruction or obliteration of blood vessel. Turn red, then white. Wedge/triangle shaped. Often acute necrosis.

Answer 55

Vitamin E/ selenium (antioxidant) deficiency causes Nutritional myopathy aka white muscle disease. Grossly, heart in picture has locally extensive nutritional muscular degeneration and (coagulative) necrosis. White streaks alternating with muscle color. Loses muscle striation, becomes large and fragmented. Cytologically, skeletal muscle shows degeneration and (coagulative) necrosis. The area in the highlighted circle has blood supply cut off so will appear white grossly.

Answer 56

Necrotic architecture is liquefied. Dead cells are digested --\> transformation of the tissue into a liquid viscous mass. Typically in CNS! Abscess is in this category bc under cytology, tissue is unrecognizable, you only see inflammatory cells, bacteria, etc. Occurs in: tissue with high neutrophil recruitment and enzymatic release with digestion of tissue, tissues with high lipid content, focal bacteria and occasionally fungal infections. Microbes stimulate the accumulation of WBCs (including neutrophils) and the liberation enzymes from these cells. Neutrophils cause collateral damage bc just attack whatever's there.

Answer 57

Bilateral symmetrical encephalomalacia Areas with arrows are affected. Matter is missing so necrosis. Necrosis in CNS is always called malacia, which is a type of liquefactive necrosis.

Answer 58

MDx: Multifocal necrohemorrhagic leukomyelitis Etiology: Sarcocystic neurona EDx: Sarcocystic leukomyelitis

Answer 59

(Horse) MDx: Multifocal hemorrhagic poliomyelitis EDx: Viral poliomyelitis DDx: Equine herpesvirus 1 Rabies (Lyssavirus) West Nile virus (Flavivirus)

Answer 60

(Sheep) Dx: Polioencephalomalacia

Answer 61

Goat Dx: Pituitary gland abscess Liquefactive necrosis (usually abscesses are surrounded by a CT membrane, but not in brain because brain doesn't have CT)

Answer 62

Gangrenous necrosis is not a specific pattern of cell death but begins mostly as coagulative necrosis (likely due to ischemia). Usually used in reference to distal extremities (toes, udder, ear, pinna) and involves multiple planed of tissue. Dry gangrene- no bacterial superinfection, appears dry. Wet gangrene- bacterial superinfection has occurred, tissue appears liquefactive by actions of degradative enzymes in the bacteria and attracted WBCs.

Answer 63

(Cottage) cheese-like. Friable (crumble) white. Necrotic debris represents dead WBCs. Possible causes include myco-, coryne-, fuso- bacterium and fungal infections.

Answer 64

Caseous necrosis