Path Cal Review

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Path Cal Review
2010-11-13 17:49:02
CAL Pathology

VPTH 602 exam 3
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  1. What are the four cell types that normally reside in the epidermis
    Merkel Cells, langerhans cells, melanocytes, keratinocytes
  2. Describe the process of cornification, which allows for the normal barrier function of skin.
    1. Lipid-laden lamellar granules migrate from the stratum spinosum to the junction of the stratum granulosum and stratum corneum. 2. Granules are released into the intercellular space, creating a hydrophobic seal. 3. Proteases, DNAases, and RNAases are released, which denature the keratinocyte nucleus and organelles4. Filaggrin causes the polymerization of intermediate filaments forming a keratin core of the corneocyte. Transglutaminase converts the plasma membrane into a hard protein shell5. Desquamation
  3. Define parakeratosis
    persistence of the nuclei of keratinocytes as they rise into the stratum corneum of the epidermis.
  4. What cornification process is abnormal in parakeratotic skin?
    Improper cell maturation can occur with an increased epithelial cell turnover. The decreased transepidermal migration time does not allow for nuclear degredation.
  5. Perivascular dermatitis with severe parakeratosis is seen in the following conditions. Name the condition, and prognosis. A Siberian Husky with hyperkeratotic plaques on the face and pressure points.
    Zinc-responsive dermatosis, good prognosis with zinc supplementation
  6. Perivascular dermatitis with severe parakeratosis is seen in the following conditions. Name the condition, and prognosis. A dog presenting with lameness due to hyperkeratosis of footpads and blood chemistry indicating liver disease
    Necrolytic Migratory Erythema (Hepatocutaneous Syndrome), poor prognosis
  7. Perivascular dermatitis with severe parakeratosis is seen in the following conditions. Name the condition, and prognosis. A Bull Terrier puppy with hyperkeratotic plaques on the muzzle that is having trouble suckling
    Lethal acrodermatitis of Bull Terriers, poor prognosis
  8. Differentiate acanthosis from acantholysis
    Acanthosis is hyperplasia of the stratum spinosum while acantholysis is the loss of cohesion between keratinocytes (loss of desmosomes) resulting in the formation of clefts, vesicles, and bullae.
  9. In what conditions can acantholytic cells be found?
    Acantholytic cells can commonly be seen in pemphigus foliaceus, superficial bacterial infections (due to proteolytic enzyme release), ballooning degeneration in viral diseases, and severe spongiosis.
  10. Pemphigus vulgari. Autoantibodies to what protein? Histologic Pattern? Affected skin layer? Type of skin?
    1. desmoglein 3 (a cadherin) 2.Intraepidermal vesicular dermatitis 3. Between S. basale and S. spinosum. 4. mucous membranes & mucocutaneous junctions
  11. Pemphigus foliaceus. Autoantibodies to what protein? Histologic Pattern? Affected skin layer? Type of skin?
    1.Desmogelin 1 ( a cadherin) 2.Intraepidermal pustular dermatitis 3. All but S. basale (Suprabasilar)4. Haired skin
  12. Bullous pemphigoid. Autoantibodies to what protein? Histologic Pattern? Affected skin layer? Type of skin?
    1. Hemidesmosomes2. Subepidermal vesicular 3.No layers affected. (Subbasilar bulla) 4.mucous membranes & mucocutaneous junction
  13. What are the three most common causes of folliculitis?
    Bacterial: staphylococcus intermedius Fungal: dermatphytosis (Ringworm) Parasitic: demodecosis (Demodectic Mange)
  14. Define Anagen What hormones favor this phase?
    stage of active growth. Thyroid hormone, androgens
  15. Define Catagen.
    transitional stage
  16. Define Telogen. What hormones favor this phase?
    Resting stage/no growth. Glucocorticoids, estrogen.
  17. To what family of viruses does Feline Infectious Peritonitis Virus belong?
  18. What are the two ways in which a cat can be infected with a virulent feline infectious peritonitis virus?
    Cats can be infected by exposure to exogenous virus, probably by the oro-nasal route, or infection may arise from mutation of an endogenous enteric coronavirus.
  19. Describe the pathogenesis of the wet form of feline infectious peritonitis (FIP)
    Viral infection → no cell-mediated immune response → antibody production → macrophages producing virus accumulate around vessels and in the interstitium of the serous surfaces and tissues throughout the body → virus enters these tissues → virus complexes with antibodies → complexes deposit on vessel walls and attract complement → damage to vessel walls → leakage of protein rich fluid into body cavities → effusive or wet form of FIP which may lead to dyspnea and/or cardiac tamponade.
  20. Describe the pathogenesis of the dry form of FIP and describe its appearance
    Viral infection → Weak or ineffective cell-mediated immune response → less florid macrophage response in tissue and poorer virus production → The noneffusive or dry form of FIP ensues.
  21. When ingesta is found in the peritoneal cavity at postmortem examination; how can you tell whether the gastrointestinal tract was ruptured premortem or postmortem?
    Rupture of the gastrointestinal tract is common in horses, cattle, and rabbits. When seen on post mortem exam it is important to determine whether the rupture occured antemortem or postmortem. If this occured postmortem the margins of the defect of the gastrointestinal wall are not hemorrhagic, and the peritoneal surfaces show no indication of inflammation.
  22. What is glaucoma?
    A group of diseases characterized by a persistent increase in intraoccular pressure, which causes pathological changes in the eye.
  23. What is the pathogenesis of glaucoma?
    Physical or functional obstruction of the filtration angle → decreased outflow of aqueous humor → increased intraocular pressure
  24. List five (5) sequelae of glaucoma
    Optic disc cupping, Corneal edema- striate keratopathy, BuphthalmosCataract (lens malnutrition),Exposure keratitis secondary to buphthalmos, Iris and ciliary body atrophy, Retinal atrophy (inner layers first), Retinal separation following buphthalmos,Scleral thinning
  25. What structures are inflammed in panuveitis?
    The iris, ciliary body, and choroid (all structures within the sclera) are inflammed in panuveitis, a combination of anterior and posterior uveitis
  26. List five (5) Sequelae of uveitis.
    Corneal opacity (edema, inflammation, fibrosis)Anterior and/or posterior synechiaeGlaucomaRetinal degeneration or separation, Cataracts, Preiridial fibrovascular membrane (PIFMs) with intraocular hemorrhage (also caused by retinal separation/detachment), Phthisis bulbi
  27. Define: Descemetocele.
    herniation of Descemet's membrane (usually outward through the corneal stroma and epithelium).
  28. Define: Anterior synechia
    adhesion of the iris to the cornea.
  29. What is the pathogenesis of corneal rupture beginning with corneal injury
    Corneal Injury (chemical, physical trauma, microbial, immune mediated, glaucoma, or genetic)→ Erosion: loss of epithelium→ Edema: due to increased stromal fluid from the aqueous humor via damaged endothelium and from tears through damaged epithelium→ Inflammation: keratitis (The eye can return to normal if successful healing occurs at this point)→ Ulceration: loss of epithelium through the basement membrane→ Neovascularization→ Deep corneal stromal ulcer → Descemetocele→ Corneal rupture
  30. What is the pathogenesis of cataract formation in a diabetic patient?
    Blood glucose >90mg/dl → hexokinase saturated in glycolysis pathway in lens fibers → glucose is shunted to sorbital pathway → sorbital accumulates → sorbital osmotically attracts water → hydropic degeneration (vacuolization) and rupture of lens fibers → opacification
  31. What conditions increase the likelihood of cataract development?
    • Diabetes mellitus
    • Trauma
    • Inflammation
    • Glaucoma
    • Interferences with lens nutrition
  32. What are the gross, histologic, and urinalysis findings in an acutely inflammed bladder?
    Gross findings: The mucosa is reddened, possibly bleeding.Histologic findings: Erosions and ulcers accompanied by a neutrophil infiltrate and edema of the lamina propria.Urinalysis findings: Blood, abundant sloughed epithelial cells and leukocytes.
  33. What additional features might one find with chronic cystitis?
    Prolonged cystitis results in proliferative changes such as urothelial hyperplasia, urothelial metaplasia to squamous cells, and abundant inflammatory cells that include lymphocytes, plasma cells, and probably macrophages and eosinophils. These inflammatory cell aggregates might be grossly visisble as gray or red foci. A chronic, yet active cystitis will still have numerous neutrophils.
  34. Systemic effects of chronic renal failure are known as uremia. List some morphologic diagnoses for uremic lesions.Clinical signs (polydipsia, polyuria, malaise, halitosis, vomiting, and diarrhea) are NOT lesions.
    alimentary tract ulcersuremic mineralization of various tissuesfibrous osteodystrophyanemiaedema
  35. What generalities can be made regarding the analysis of urine from CRF animals?
    specific gravity: isosthenuric (1.008 to 1.012)sediment cellularity: variable; cellular and hyaline castsdip stick findings: albumin +++
  36. What generalities can be made regarding the analysis of blood from CRF animals?
    creatinine: elevated; usually well above 2.0 mg/dLphosphorus: elevated, usually above 7mg/dL for nonruminantsprotein: diminshed total protein due to low albumin fraction <2g/dL
  37. What portion of the nephron is damaged in ARF?
    convoluted tubules of the cortex
  38. Why does oliguria and anuria develop with ARF?
    Acute tubular necrosis results in shedding of tubular epithelial cells, which occludes the lumen of the tubule and form casts.
  39. Describe the pathogenesis that leads to this kind of renal injury.
    his is the death by "poison" or death by "suffocation" story. There are numerous causes.
  40. What are the three most common causes of skeletal muscle atrophy?
    • disuse
    • denervation
    • malnutrition/starvation/cachexia/metabolic
  41. What are the 4 molecular events that occur in denervation atrophy within the skeletal muscle?
    1. Synthesis of contractile proteins is reduced 2. Expression of muscle regulatory proteins is increased (MyoD, Myogenin) 3. Acetylcholine receptors increase in number and become extrajunctional spreading over the surface of the muscle 4. Neural cell adhesion molecule (NCAM) expression increases and NCAMs spread over the entire surface of the denervated muscle
  42. uring the response to denervation atrophy, what happens to axons in the proximity of the atrophied muscle fiber?
    Schwann cell proliferation at the motor end plate of the denervated fiber cause collateral sprouting of neighboring neurons. With increased numbers of NCAMs on their processes, the Schwann cells guide the new branch of the axon to the motor end plate of the atrophied muscle fiber.
  43. Explain the effect that this process has on fiber-type and the histological appearance of the muscle bundle?
    Normally, motor unit types (nerve and associated muscle fiber) are intermingled, giving the muscle bundle a checkerboard appearance of both fast and slow muscle fibers. With renervation a single neuron may innervate more adjacent myofibers, changing their phenotype, producing the histological appearance of type grouping.
  44. Describe the sequence of events that follows focal mild skeletal muscle necrosis assuming complete regeneration occurs.
    Insult (trauma) Loss of muscle striation and cytoplasm becomes hypereosinophilic Influx of macrophages and inflammatory cells, which begin to clear necrotic debris Cell nuclei move from the periphery to the center of the myofiber, and the necrotic area is walled off from the rest of the intact muscle Satellite cells within the injured area begin to proliferate and join, forming a syncitium in the basal lamina of the damaged fiber. The muscle fiber is regenerated.
  45. Etiology of myositis
    Immune-mediated, infectious agents (bacteria, such as Clostridium spp. and protozoa, such as Sarcocystis spp, Neospora.)
  46. Etiology of endocrine myopathy
    hypothyroidism, hyperadrenocorticism (iatrogenic and spontaneous)
  47. Etiology of nutritional myopathy
    vitamin E and/or selenium deficiency
  48. Explain the pathogenesis and final outcome of white muscle disease
    Deficiency in vitamin E and/or Selenium → peroxidation of membrane lipids (sometimes exacerbated by stress) → Ca 2+ enters cytoplasm and mitochondria, damaging respiratory mechanisms → cell death → symmetrical necrosis of the most active skeletal muscle (like postural muscles)
  49. What four lesion characteristics determine the clinical signs associated with a brain tumor?
    • location of lesion
    • size of lesion
    • rate of growth
    • secondary vascular lesions (edema and hemorrhage)
  50. What are the two main characteristics of the nervous system that determine clinical signs seen with lesions or trauma?
    Localization or distribution of function.Unique anatomic and physiological features
  51. What are four unique principles that relate to the localization and distribution of nervous system function which influence the clinical and pathologic manifestations of neurologic disease:
    1. The nervous system is vulnerable to focal lesions, which is compounded by the limited ability of the nervous system to regenerate following inury.2. Because there is localization of function in the nervous system, the same pathologic process can present clinically different when a different part of the system is affected. Conversely, different diseases affecting the same area of the nervous system will present clinically similar. A meningioma at the base of the brain may compress the optic nerve and lead to blindness.Yet, a meningioma in the lateral cortex may lead to seizures and a meningioma in the medulla may cause a head tilt.A choroid plexus tumor, infarct, or inflammation affecting the medulla may also lead to a head tilt.3. Groups of neurons are selectively vulnerable to different diseases.Because the nervous system is comprised of different types of cells, different toxins will affect different groups of neurons, which results in a specific pattern of pathologic changes.4. The response of the nervous system to injury is limited and non-specific, so the diagnosis often depends on the location of the injury rather than the microscopic appearance of the lesion.
  52. Small focal injuries anywhere in the nervous system (inflammation, trauma, neoplasms) can lead to death. Explain how a small focal lesion in the frontal cortex leads to death:
    focal lesion → secondary edema and hemorrhage → occupies space due to limited and fixed volume of the calvaria → increased intracranial pressure → herniation of the brain caudally → compression of medullary respiratory and cardiocascular centers → death
  53. What is the difference between herniation and protrusion?
    Herniation of the nucleus pulposus = extrusion of the nucleus pulposus through a tear in the annulus fibrosis(a.k.a. Hansen's Type I)Protrusion of the annulus fibrosis = bulging of the annulus fibrosis - usually into the spinal canal(a.k.a. Hansen's Type II)
  54. What is the pathogenesis of intervertebral disc disease?
    degeneration of the nucleous pulposus (earliest lesion in chondrodystrophic dogs)protrusion or herniation through the damaged annulus fibrosus (earliest lesion in non-chondrodystrophic dogs)direct compression of the spinal cord and/or nerve roots and spinal vessels when disc material hits spinal corddemyelination (least severe)leukomyelomalacia (more severe)edema and hemorrhage (more severe)poliomyelomalacia (most severe)occasionally ascending myelomalacia occurs following severe disc disease due to an unknown pathogenesis
  55. Identify four routes infectious agents can use to enter the central nervous system.
    • blood (most common route)
    • local extension (occurs from established infections)
    • direct penetration
    • retrograde axonal flow
  56. What do you call....a. inflammation of brain white matterb. necrosis of the spinal cordc. necrosis of brain grey matterd. inflammation of meninges and brain
    a. leukoencephalitisb. myelomalaciac. polioencephalomalaciad. meningoencephalitis
  57. a cat with cerebellar hypoplasia due to panleukopenia virus.9. List three general mechanisms by which this or other congenital malformations could occur. Give examples of each.
    Inhibition of cell mitosis examples: microencephaly, cerebellar agenesis or hypoplasia, optic nerve hypoplasiadestruction of cells before complete maturationexamples: porencephaly/hydraencephaly, cerebellar hypoplasia/degeneration, like from feline panleukopenia viruscell migration disordersexamples: lissencephaly, microgyri, macrogyri, porencephaly
  58. List three types of injury to axons and their myelin sheaths.
    axonal injury (transection of an axon leading to Wallerian degeneration) segmental demyelination (destruction of the myelin sheath, composed of Schwann cells in the PNS and oligodendrocytes in the CNS, leaving bare axon) axonal degeneration (axonodystrophy)
  59. Describe what happens to an axon in the PNS following transection of the axon (axonal injury).Remember that successful regeneration in the PNS depends on three physical factors:site of injury (more distal = better recovery)distance between severed ends (less distance = better recovery)amount of damage and debris at injury site (less damage/debris = better )
    After transection of the axon with separation of the distal and proximal portions, the adjacent axonal membranes self-sealAnterograde and retrograde axonal flow are both halted and there is swelling of the severed ends due to accumulation of neurofilaments, mitochondria, and debris within 24 hours of the injuryThe distal segments undergoes Wallerian degeneration (axon and myelin sheath degenerates and is removed by macrophages and glial or Schwann cells)Chromatolysis of cell body occurs (cell body swells, cytoplasm becomes homogenous & glassy, nucleus moves to eccentric position)Presynaptic terminals move out of synaptic contact while affected neuron is attempting to repairIf the site of axonal injury is close to the cell body, the neuron may die.Anterograde and retrograde transneuronal atrophy may occur because of the trophic relationship between the neurons of assemblies. Schwann cell proliferation occurs distally inside the tubes of the basement membrane of the original Schwann cells.Axonal sprouts appear proximally at the site of transection.Axonal sprouts follow Schwann cells to the site of the former synapse.Schwann cells remylinate the axon.
  60. Describe what happens to an axon following segmental demyelination in the PNS.Note: Segmental demyelination is usually associated with inflammatory or toxic diseases.
    Destruction of myelin sheaths leaving intact axon bare (internode or segment of myelin is lost)Conduction block or slowing of nerve impulseSchwann cells proliferate and remyelination is often complete
  61. Describe what happens to an axon following axonodystrophy (axonal degeneration).Remember: axonal degeneration is a metabolic derangement of the entire neuron associated with toxic, inherited, and metabolic diseases.
    Distal portion of the axon dies back and the myelin sheath breaks down at the same time.Axonal regeneration is very poor, and there is little Schwann cell proliferation.
  62. Describe what happens to an axon following semental demyelination in the CNS. Remember: Demyelination in the CNS is caused by damage to oligodendrocytes, which each may myelinate up to 50 internodes on one or multiple axons.
    Oligodendroglial cells do not proliferate readily and therefore there is very poor remyelination in the CNS.Loss of myelin sheath is detected by a lack of staining using stains specific for myelin (ex., Luxol-blue).