Path Terms Flashcards
Fibrous Osteodystrophy
Bone Change due to prolonged PTH stimulation (hyperparathyroidism)
- Nutritional
- Renal due to decreased tgfr increasing the P concentration
Hyperostosis
Increased bone production
Caused by trauma
Chronic inflammation
Idiopathic
Osteosclerosis
Abnormally dense bone due to the failure of osteoclasts activity
Osteonecrosis
Death of bone cells
Osteomyelitis
Bone and medullary tissue is inflamed
Periostieitis
Periosteal surface inflamed
Benign bone tumor
Osteoma, chondroma, ossifying fibroma, osteochondroma
Metastatic bone tumor
Osteosarcoma
Pannus
Growth of fibrovascular tissue with subsequent destruction of cartilage
Fibro consistent with fibrous
Chronic
Necrosuppurative
Necrosis with neutrophils
Pyogranulomatous
Neutrophils and macrophages
Chondromalacia
Thinning and fibrillation of cartilage due to matrix loss
Subchondral bone hyperostosis (eburnation)
Increased focal compression on subchondral plate due to loss of cartilage or abnormal joint loading
Osteosarcoma
Malignant tumornthat has a characteristic loss of cortical bone (thinned). Will not cross the bone surface
Periarticular osteophyte formation
Focal hyperostosis at attachment points of joint capsule; edges of articular surface. Due to abnormal joint loading and instability.
- this is a feature of chronic changes around the joint. The abnormal joint loading will cause hyperostosis at the periphery of the joint.
Osteoarthritis pathogenesis
Draw it out and review the sheet
Osteochondrosis dessecans pathogenesis
Draw it out and review the sheet
Glomerulosclerosis
Reaction to long term glomerular injury
Amyloidosis
manifestation of systemic AA deposition
Glomerulonephritis: Immune complex disease
this is the #1 glomerular disease we encounter caused by antigens, Ag-ab complex accumulation
Membranous pattern of Glomerulonephritis
supepithelial plus thickened Glomerular basement membrane
Proliferative pattern of glomerulonephritis
mesangela + mesangeal cell proliferation
Membranoproliferative Pattern of glomerulonephritis
subendothelial + thickened glomerular basement membrane. This pattern can be seen in a Lyme disease case
Clinical features of nephrotic syndrome
proteinuria
Hypoalbuminemia
Subcutaneous edem
Hypercholesterolemia
Phelitis
inflammation of the renal pelvis
Pyelonephritis
pelvis + renal parenchyma are inflammed
hydronephrous
dilation of the renal pelvis, can result in renal crest necrosis
Nephroliths
massive stones found wiithin the renal pelvis
Cystomegally
distended bladder
hydroureter
distended ureter
ureteritis
inflammation of the ureter
cystitis
inflammation of the bladder
urethritis
inflammation of the urethra
Urolithiasis
stone formation around nidus
- usually a mineral precipitate
- predisposing factors : alkaline urine, dehydration, bacterial infection, diet
- Obstruction at narrow points such as the sigmoid flexure
Common neoplasms of the lower urinary tract
Transitional cell carcinoma
Leiomyoma
Leiomyosarcoma (along the smooth muscle)
Leptospirosis in the Urinary tract
Acute- hemoglobinuric nephrosis
Chronic- renal disease
- enlarged nodular kidneys
- lymphogranulomatous and purulent tubulointerstitial nephritis
What is the apperance of the kidney when there is chronic glomerular nephritis
The kidney is smaller than it should be. Tend to maintain a normal shape, but have blebbed apperance with white flecks to it.
Renal dysplasia
-congenital/neonatal defects
Inherited in several breedds
-CRF by 3 years of age
Small segmentally fibrotic kidneys
When a sheep liver is presented to you and it is diffusely black brown in color
Copper toxicosis
- Cu accumulates in the liver
- Massive release of Cu from liver -> acute hemolysis
- hemaglobinuric nephropathy
Erosion
loss of epithelium down to the basement membrane
Ulcer
defect in cornea through the basement membrane
Keratitis
The inflammation of the cornea
Leukocytosis
Increased white blood cell count
Myelophthisis
replacement of bone marrow by non-native tissue/cells
SCID in foals
hyoplasia of the thyus
splenic histocytic sarcoma
splenic mass of macrophage lineage
Pathogenesis for cushings in a horse
Equine chromophobe adenoma fo pars intermedia causes pituitary pars intermedia dysfunction.
- A fnctional tumor increases ACTH-> as this expands into the hypothalamus, there is impaired ADH production leading to hirsutism and hyperhidrosis, PU/PD
Canine “cushing’s like syndrome
Due to a functional chromaphobe adenoma. This increases the ACTH secreation and causes diffuse adrenal cortical hyperplasia.
What is the sequella to pituitary adenoma that is non-functional
there will by bilaterally symmetrical atrophy of the adrenal cortex
What is the sequella to a pituitary adenoma in a canine that is functional
bilaterally symetrical hypertrophy of the adrenal glands
An increase in calcitonin will do what to serum calcium levels
Decrease serum calcium (This is antagonistic with PTH)
What clinical signs will you see in a dog with hypothyroidism
bilaterally symetrical alopecia, epidermal atrophy, hypercholesterolemia
In concentric hypertrophy of the heart what happens to the volume of fluid the heart can hold?
it decreases. The lumen size is smaller
What are the 3 zones of the adrenal cortex?
zona glomerulosa, Zona fasiculata, Zona REticularis
What is the function of the adrenal gland?
release of epinephrine and norepinephrine
Pheochromocytoma
neoplasm of the adrenal medulla
If you have hyperadrenocorticism in ferrets, what do you expect to see as changes in the ferret
Increased estrogenic production, so feminization ; persistant estrus
If you increase PTH, what will happen to calcitonin and calcium levels?
decreased calcitonin and increased calcium
If you have a functional parathyroid adenoma, what else will you see?
Fibrous osteodystrophy with hypercalcemia
Anal sac adenocarcinomas in dogs secrete what?
PTH related peptide causing a hyperparathyroidism, and FOD.
What are soem clinical signs you would see with a pheochromacytoma
anorexia, vomiting, diarrhea etc.
