Test 4: questions Flashcards
You perform a physical exam and you find dimpling of the skin overlying the lumbar region of the spinal column (image), an easily expressed bladder, absent anal sphincter tone, and analgesia to the skin of the perineum.
Given the signalment of the patient and the location of the lesion, what do you think is the most likely disease process —
, most likely specific type of disease —?
congenital
neural tube defect
On histologic examination of the spinal cord you see the changes depicted below:
What area of the spinal cord does this represent —?
What characteristic pathologic change to neurons are the arrows pointing to?
white matter
axonal swelling (spheroids)
What is the pathogenesis of this lesion?
Degeneration of the nucleus pulposus, annulus fibrosis and/or dorsal longitudinal ligament —> extrusion or herniation of disc material into spinal canal –> trauma to spinal cord and occlusion of blood vessels –> demyelination –> leukomalacia, hemorrhage (and poliomalacia if severe enough)
What is the name of this disease?
IVDD
Intervertebral disc disease
What serologic test(s) will you submit with the serum sample you collected antemortem, given the nature and distribution of the gross lesions in the spinal cord?
Equine herpes virus 1 and 4
Sarcocytis neurona
Equine Eastern Encephalitis virus
West Nile virus
Equine herpes virus 1 and 4
Sarcocytis neurona
On histologic examination of the spinal cord you find the changes below:
What etiologic agent is responsible for this disease?
What is the disease called?
Sarcocystis neurona
Equine protozoal myeloencephalitis (EPM)
What disease process do you suspect this represents?
what neoplasm does this most likely represent?
neoplasia
Peripheral nerve sheath tumor
Anatomic location and Gross: Multiple masses arising at the spinal nerve roots
Histology: Slender, fusiform cells arranged in bundles and plexiform nodules with bland oval nuclei.
Glaucoma is a diverse group of pressure dependent neurodegenerative disorders that all result in loss of normal function of the retinal ganglion cells and their axons in the optic nerve and ultimately lead to loss of vision. What is the single most consistently recognized feature of all glaucomas in veterinary patients?
Elevation in intraocular pressure (IOP)
While causes of glaucoma may vary (including causes of secondary glaucoma, covered below), sequelae of glaucoma may be consistently seen, and depend on the duration and severity of the disease. List the common sequelae of glaucoma and be able to describe why you would see these lesions.
Buphthalmia
Scleral thinning
Corneal edema
Corneal striae (breaks in Descemet’s membrane)
Exposure keratitis (secondary to buphthalmos)
Lens luxation or subluxation due to zonule damage
Cataract (lens malnutrition?)
Atrophy of iris and ciliary body
Retinal atrophy (inner layers first)
Retinal separation (after buphthalmos)
Optic disc cupping
What layers are missing in glaucoma related atrophy? What about PRA?
All cases of retinal atrophy (except glaucoma) begin in outer layer and progress inward: photoreceptors -> outer nuclear -> inner nuclear -> ganglion cell layer.
Can you list the reactions of the cornea to injury? Why do we see corneal opacities in a damaged cornea?
Damage to the corneal epithelium includes erosion or ulcers; healing can lead to cutaneous metaplasia (“squamitization”) and melanosis. The corneal stroma can become edematous (both due to loss of epithelium and loss of corneal endothelium which regulates water regulation in the stroma), neovascularization (from the limbus), necrosis, fibrosis, and inflammation (keratitis).
Opacities occur anytime there is loss of clarity and are caused by these responses to injury, usually a combination of these. One can also see a focal corneal opacity with anterior synechia (adherence of iris tissue to the cornea/corneal endothelium).
what do you see?
There is a focal corneal ulcer (fluorescein test; ulcer is green) and the surrounding cornea is grey-white (opacity), likely due to regional edema and keratitis.
what do you see?
Diffuse corneal opacity with metaplasia, neovascularization, possible melanosis. This dog has chronic corneal injury due to KCS.
What are the sequelae of uveitis?
Corneal opacities due to edema, keratitis, etc.
Anterior or posterior synechia
Retinal atrophy; possible separation
Cataracts
PIFM - may lead to intraocular hemorrhage
Secondary glaucoma
Eventual phthisis bulbi
Oh boy. Lots happening here. There is a diffuse corneal opacity, both anterior and posterior synechia, cataract, intraocular hemorrhage, complete retinal separation.
Define secondary glaucoma. List causes and be able to reason out why each of these causes leads to glaucoma (hint: how does it disrupt aqueous flow)?
Uveitis (inflammatory cells fill filtration angle, and/or leads to other lesions listed below).
Anterior and/or posterior synechiae (possible iris bombe)
PIFM
Lens luxation
Intraocular hemorrhage
Neoplasia
What is the most likely diagnosis in this cat? What is the clinical behavior?
Cat: Feline Diffuse Iris Melanoma most common; prediction of clinical behavior is difficult but there is a risk of distant metastasis.
- Diffuse iris melanoma more common than solitary masses
- May obstruct filtration angle and cause glaucoma
- Greater risk for distant metastasis with longer latency (3-5 years)
What is the most likely diagnosis dog? What is the clinical behavior?
Dog: Anterior uveal melanocytoma or malignant melanoma; diagnosis depends on histologic features but melanocytomas are more common.
- Prognosis based on histologic criteria (anaplasia, mitoses, invasion)
- Sites: iris - common - 90% benign; choroid - rare - usually benign
what kind of cancer spreads to these places
histiocytic
label
what do the arrows point to ?
what is their function?
Epiphysis- 1
Metaphysis- 2
Diaphysis- 3
Metaphyseal growth plates
Provide length to the bone
1) Identify this cell, provide its general lineage and primary function.
OsteobBLASTS (OBs): Mesenchymal lineage. Build bone (secrete the majority of osteoid and hydroxyapatite crystals during bone new formation (ie growth, remodeling/modeling, repair).
2) Identify this cell, provide its general lineage and primary function.
OsteoCYTES (OCs): Mesenchymal lineage. Maintains bone (can resorb and secrete small amounts bone matrix in their immediately surrounding lacunae.
3) Identify this cell, provide its general lineage and primary function
OsteoCLASTS (OCLs): Monocyte lineage. Breakdown bone. Differentiation & activation is stimulated by OB production of RANKL
Designated by the asterisk, name the extracellular matrix components (organic and inorganic)
Osteoid (organic) Hydroxyapatite (inorganic)
Name the extracellular matrix designated by “1”and the cells that create and maintain this matrix:
Hyaline cartilage produced by chondrocytes
Name the anatomic region designated by “2”:
Subchondral bone plate
From a molecular and functional standpoint, briefly list the key differences between the extracellular matrix in 1 versus 2 and the inherent response of these tissues to injury
ECM of hyaline cartilage is hydrophilic and acts as a shock absorber, distributing compressive forces to the subchondral bone. It also provides a smooth, gliding surface for moving articulations. Remember hyaline cartilage of the growth plates serves as a template for ECO. Subchondral bone serves to anchor the overlying hyaline articular cartilage to bone via the Articular-Epiphyseal complex (junction of mineralized cartilage & subchondral bone plate). Interconnecting trabeculae serve to transfer forces sustained during movement to the really strong compact (ie osteonal) bone that forms the diaphyseal cortices.
Identify the type of bone response featured in this image.
woven
Name the type of bone response featured in this image.
Lamellar bone (it also happens to be trabecular)
Briefly list the architectural and functional differences between the two types woven vs lamellar
Woven bone is hypercellular, disorganized and weaker in comparison to lamellar bone. WB forms during rapid growth & repair.
Describe how bone responds to injury
Excellent healing/regenerative response if vascular supply is adequate. Can form lamellar or woven (band-aid) bone depending on stimulus. Complete bone healing can produce bone as strong or stronger than original bone.
Describe how cartilage responds to injury
Poor healing or regenerative response. Can heal small defects with fibrocartilage. Often default pathway is degeneration with loss of proteoglycan matrix decreased water binding & shock absorption loss of cells & matrix, chondrones advanced lesions result in cartilage erosions & ulcers
List the 4 zones of EO
1) Resting
2) Proliferative
3) Hypertrophy
4) Ossification
What cells remove hypertrophied (dying) chondrocytes so that capillaries and osteoblasts can follow and line longitudinal spicules of mineralized cartilage with woven bone?
Osteoclasts
What cells remodel primary trabeculae into fewer trabeculae that are thinner and stronger (eg secondary & tertiary trabeculae)?
Osteoclasts
What cells secrete RANKL (osteoclast differentiation and activation factor)?
Osteoblasts
6-month-old Saanen goat ”rescue” presented for obstructive urolithiasis
Given the history and clinical findings, the skeletal lesion is characteristic of what general etiology/ies?
Degeneration
Genetic
Infectious
Nutritional
Neoplastic
Toxic
genetic
infectious
toxic
This malformation (missing or severely shortened humerus) is termed phocomelia and is characterized by aplasia or severe dysplasia of one or more segments of the appendicular skeleton. It often results from a genetic defect (in humans this can be autosomal recessive syndrome that also includes other congenital defects involving urogenital, cardiac, and nervous system), but especially in large animals we need to think of Teratogenic viruses and potential exposure to teratogenic toxins. The take home point is that any time you identify one congenital malformation, you should keep your eyes out for additional ones! Although this is an important concept, contents from this case (ie this slide and the previous one) will not be exam material.
Provide the general medical term for the disease that results in disproportionate dwarfism; where is the primary anatomic location of the lesion (eg cells, cartilage template, bone matrix)?
Chondrodysplasia
Briefly describe the clinical manifestation of Chondrodysplasia
Chondrodysplasia results in abnormally shortened and misshapen bones of the appendicular skeleton and can predispose to early DJD from the incongruency.
Osteogenesis imperfecta is an autosomal recessive heritable osteodysplasia that produces a defect in which important organic component of bone?
Type 1 collagen
Briefly describe the clinical manifestation of OI.
Osteopenia with poor quality bone & pathologic fractures. Also affects dentin of the teeth & collective tissues → joint laxity.
These are the distal femurs from a 2-year-old gelding Thoroughbred is presented for progressive bilateral 2-3/5 degrees hind limb lameness localized to the stifle joints. There was moderate effusion within both femoropatellar joints, but the swelling was not hot. Synoviocentesis yielded slightly watery, clear yellow synovial fluid that contains moderate increases in macrophages and lymphocytes.
How would you describe the lesions?
There are bilaterally symmetrical wedge-shaped depressions in the articular cartilage surface that partially extend to the subchondral bone and are partially filled with roughened white-tan cartilaginous tissue. There is mild generalized cartilage thinning over both trochlear ridges and intertrochlear groove.
These are the distal femurs from a 2-year-old gelding Thoroughbred is presented for progressive bilateral 2-3/5 degrees hind limb lameness localized to the stifle joints. There was moderate effusion within both femoropatellar joints, but the swelling was not hot. Synoviocentesis yielded slightly watery, clear yellow synovial fluid that contains moderate increases in macrophages and lymphocytes
Given the gross appearance and clinical history, what is your diagnosis?
Name the disease process that would eventually result from these lesions (hint- it’s the reason the horse was euthanized)?
Bilaterally severe osteochondritis dissecans.
DJD
These lesions represent a defect in which developmental process in bone formation
EO: Endochondral ossification
This is a pelvic radiograph from a 9-year-old miniature horse mare who was severely (grade 5/5) lame right hind and euthanized for a severely displaced femoral neck fracture with luxation of the coxofemoral joint.
fed high phos diet
Are the fractures traumatic or pathologic?
Which historical and histologic features support this diagnosis?
pathologic
Numerous activated OCLs bone lysis with fibrous replacement and paucity of osteoblasts. This is likely caused by the high phosphorous diet resulting in bilateral parathyroid gland hyperplasia and PTH-activation of OCLs and differentiation of FBs over OBs bone resorption with fibrous replacement and pathologic fractures
Based on location, what general classification of fracture is this?
traumatic Salter Harris (growth plate fracture)
The owner elects conservative management (external coaptation & cage rest). Based on fracture configuration, which 2 complications of fracture healing are most likely if internal fixation is not performed?
What other complication could this dog develop based on trauma to the growth plate cartilage?
Fibrous non-union/malunion & DJD
This dog could also develop limb shortening or angular limb deformity associated with the growth plate trauma.
Cartilage has a good repair response to injury (circle): TRUE OR FALSE
false
List 4 common etiologies of joint injury
- Congenital instability/incongruency
- Traumatic instability/incongruency
- Overuse
- Infectious/inflammatory arthritis
A 5-year-old German Shephard dog (see images next slide) is presented with severe bilateral hindlimb lameness. Physical exam localizes decreased range of motion and pain to the coxofemoral joints. Based on signalment and physical exam findings, which specific underlying disease do you most suspect?
Canine Hip Dysplasia