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303 Cards in this Set
- Front
- Back
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gastrointestinal tract |
continuous tube from mouth to anus |
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accessory structure of GI |
teeth, tongue, salivary glands, liver, gall bladder |
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borborygmus |
gut sounds, gurgling noise |
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coprophagia |
eating poop |
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dyschezia |
straining to defecate |
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hematochezia |
bloody stool |
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pica |
eating none nutritive items |
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poikilocytosis |
abnormal shape of RBC |
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tenesmus |
cramping, painful straining |
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obstipation |
severe or complete constipation |
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what are some issues with the oral cavity |
- dental disease - oral trauma - salivary mucocele - oral neoplasia |
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what are common causes of oral trauma |
- falls (fractures) - fights - burns (electrical) - blunt trauma (HBC) - foreign objects (sticks, fish hooks, sewing needle) - lacerations |
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What disease? - hx of signs of head trauma - increased salivation - inability to close mouth - reluctance or inability to eat - presence of foreign object |
oral trauma |
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what is diagnosed via thorough exam of the oral cavity and radiographs |
oral trauma |
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what happens to persian cats commonly that involves the mouth
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yawn and pop out the TMJ causing mouth to be stuck open |
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what is this disease? - most common disease of salivary glands in dogs - dogs 2-4 years, G. sheps, mini poodles - hx of slowly enlarging, fluid filled swelling on the neck (many see fluid filled swelling on the tongue) |
salivary mucocele |
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mucocele |
excessive accumulation of saliva in subcutaneous tissue and resultant tissue reaction |
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what is the most common oral neoplasia |
malignant melanoma squamous cell carcinoma fibrosarcoma |
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what is the most common oral neoplasia in dogs and has a worse prognosis |
malignant melanoma |
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what oral neoplasia can look like eosinophilic plaque |
squamous cell carcinoma |
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what oral neoplasia is rapidly growing and involves the bone, metastasize to lungs and lymph nodes - brown, black or unpigmented - poor prognosis |
malignant melanoma |
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what oral neoplasia is the most common oral tumor in cats - ulcerative and erosive, invasive, involve gingiva and tongue |
squamous cell carcinoma |
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what oral neoplasia is locally invasive, second most common oral tumor in cats - involves gingiva and palate |
fibrosarcoma |
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how do you diagnose oral neoplasia |
biopsy and histopathology |
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how do you treat oral neoplasia |
surgical removal with wide excision - may involve removal of portion of mandible or maxilla - radiation, chemo - new vaccine for melanoma shows promise |
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what oral neoplasia has a developing vaccine |
malignant melanoma |
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what benign neoplasia has a DNA viral etiology in young patients - proliferative masses on mucous membranes anywhere in the oral cavity - transmission through fomites and direct contact - wart-like can cause dysphagia and may bleed - diagnosed on appearance - self-limiting: regress on own (or can pop) |
papillomas |
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what oral neoplasia is most common benign oral mass in dogs -pedunculated mass growing of gingiva - has 3 forms - may see pain, bleeding, hypersalivation - definitive dx via biopsy - treatment: surgical removal, radiation |
epulides |
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what epulides oral mass type is from margin of gums and smooth |
fibromatous |
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what epulides oral mass type involves bone |
ossifying |
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what epulides oral mass type is ulcerative, from periodontal ligament |
acanthomatous (can be malignant) |
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esophagitis |
inflammation of the esophagus |
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what disease is associated with contact of the mucosa with irritants (acids, alkalis, drugs, hot materials) - extent of damage depends upon type of material, length of contact, integrity of mucosal barrier - can also be caused by chronic vomiting and damage by foreign bodies |
esophagitis/ gastroesophageal reflux |
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what drug in cats can cause esophagitis |
doxycycline |
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what is a common cause of esophagitis |
GER (gastoesophageal reflux) |
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what are clinical signs of esophagitis |
-pain
-anorexia - dysphagia, salivation, regurgitation |
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how do you diagnose esophagitis |
endoscopy |
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how do you treat esophagitis |
-decrease inflammation, prevent further damage - can be long process, esophagus heals slowly |
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in what form of esophagitis do you treat by never inducing vomiting, administering neutralizing agents, bathing of flushing skin with water, rest esophagus, and sucralfate slurry |
esophagitis due to irratants |
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how do you treat GER |
- high protein, low fat diets to promote gastric emptying - sucralfate, H2 blockers, proton pump inhibitors - metoclopramide |
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what drug stimulates GI motility |
metoclopramide |
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when giving cats meds what must you always do after |
chase with water |
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how do you remove an esophageal obstruction |
- endoscopy - gastrotomy - risk of stricture, poor healing (scarring can cause stricture) |
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exaggerated swallowing movements, increased salivation, retching, restlessness, anorexia and hx of chewing foreign objects are all clinical signs of what |
esophageal obstruction |
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how to you diagnose esophageal obstruction |
endoscopy radiography |
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What disease: -persistant right aortic arch - ligamentum arteriusum persists and does not allow esophagus to expand in that area - creates megaesophagus |
vascular ring anomaly (congential from PRAA)
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what disease: -is caused by hypomotility of the esophagus -ingesta transported abnormally - ingesta accumulates and causes stretching and dilation of the esophagus - may be segmental or generalized and mild or severe - etiology may be from nerve, muscle or neuromuscular junction (myasthenia gravis) - idiopathic most common |
megsesophagus |
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when does congenital megaesophagus occur |
occur at weaning when starting to eat solid foods |
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when does aquired megaesophagus occur |
at any time |
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what is the number one symptom of megaesophagus |
1. regurgitation - increased risk for aspiration pneumonia due to this |
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how do you diagnose megaesophagus |
-hx of regurgitation after meals - thoracic radiographs - fluoroscopy, esophagoscopy - testing for primary disease: myasthenia gravis |
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how do you treat megaespophagus |
- treat primary cause if possible - elevated feeding (bailey chair) - small frequent meals - prevent aspiration |
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what is a common cause of vomiting in dogs and cats |
acute gastritis |
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what is the etiology of acute gastritis |
-diet: spoiled food, diet change, food allergies, food intolerance - infection: bacterial, viral, parasitic - toxins: chemicals, plants, drugs, organ failure - foreign object ingestion |
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what are clinical signs of acute gastritis |
-anorexia - acute onset vomiting - +/- painful abdomen, dehydration - history of above |
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how do you diagnose and treat acute gastritis |
diagnose: Hx, PE, CBC: stress leukogram, Chem: rule out metabolic or organ failure, rads Treat: treat underlying cause, NPO 24-36 hrs, fluids, bland diet, antiemetics (maropitant (cerenia), metoclopromide (reglan), odansetron |
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what is commonly a result of drug therapy in dogs and cats? (NSAIDs) |
GI ulcers |
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what do NSAIDs do that results in GI ulcers |
disrupts normal mucosal barrier |
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what causes GI ulcers |
- drug therapy - stress - renal failure, liver failure, hypoadrenocorticism |
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what are clinical signs of GI ulcers |
- can be asymptomatic - anemia - melena - anorexia - edema - abdominal pain - septicemia if ulcer perforates |
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how do you diagnose and treat GI ulcers? |
diagnose: rads (contrast studies), endoscopy (direct visualization) treat: oral antacids, H2 blocker (famotidine), proton pump inhibitors (omeprazole), sucralfate (binds and protects ulcer site), misoprostol (synthetic prostaglandin), supportive care |
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what should clients know about GI ulcers |
- no NSAIDs w/out supervision - never give Ibuprofen, naproxen, acetominophen, aspirin w/out vet consult - Give NSAID w/ meal - stop NSAID if vomiting - never give at same time as corticosteroid like prednisone |
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what is GDV |
gastric dilation volvulus - acute, life threatening condition (often called bloat but different) |
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what are clinical signs of GDV |
- non-productive retching/ vomiting attempts - hypersalivation - markedly distended abdomen - marked discomfort- pace, whine, stretch - depression, weakness, collapse - tachypnea, tachycardia |
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how do you diagnose GDV |
-hx and PE - depression, weak, slow CRT - RADS: right lateral, air filled stomach, pylorus located dorsal and cranial to the fundus (popeye arm) - CBC/ChemL electrolytes disturbances |
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what lateral do you want when looking for a GDV |
Right lateral
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how do you treat GDV |
-emergency - correct circulatory shock: fluids (cath both legs: bolus), corticosteroids - decompress (pass stomach tube, trocarization - correct volvulus ( surgery, gastroplexy) - antibiotics (for gram neg bacteria) - ECG monitor for VPC's - potassium and bicarb |
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What is gastric neoplasia |
-fairly uncommon - malignant more common - adenocarcinoma, lymphoma - weight loss, vomiting, obstruction - endoscopy, biopsy - surgical resection if possible, chemo and radiation not very successful |
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what is GI obstruction |
- usually by foreign body - clinical signs: based on duration, breed, type, degree, vomiting, anorexia, abdominal pain, anorexia, polydipsia, dehydration, systemic toxicity - diagnose: RADS, endoscopy, exploratory - tx: surgical or endoscopic removal, induced vomiting |
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what is IBD |
inflammatory bowel disease - chronic gastritis, enteritis or colitis |
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what is the etiology of IBD |
-inflammatory cells accumulate in the cells lining the GIT - Cats> dogs - abnormal immune tolerance to gut bacteria or dietary substances |
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how do you diagnose and treat IBD |
diagnose: biopsy and histopathy, CBC, Chem (maybe normal), GI panel (cobalamin and folate levels), ultrasound may measure thichened walls tx: meds (prednisolone (azathioprine), metro, sulfasalazine (not cats), tylosin, B12 |
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what are clinical signs of IBD |
- gastric as for acute gastritis - intestinal: chronic intermittent vomiting +/- diarrhea, weight loss, lethargy, pu/pd, borborygmus - colon: diarrhea, little weight loss, increased fecal volume and frequency, tenesmus, hematochezia, increased mucus |
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what must you rule out for IBD since symptoms are similar |
intestinal lymphoma |
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osmotic diarrhea |
increased solute load in bowel |
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secretory diarrhea |
hypersecretion of ions |
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exudative diarrhea |
increased permeability and loss of protein |
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dysmotile |
abnormal motility |
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what is acute diarrhea |
-common - etiology: disruption of normal bacteria flora, often from diet change, stress, drugs - signs: abrupt onset diarrhea, +/- vomiting -dx: rule out other causes, fecal float, hct -TX: supportive, fluids, NPO 24-48 hrs, bland diet, probiotics, antibiotics, anti-diarrhea if warrented |
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what is small intestinal diarrhea caused by? |
parasite: round, hook, whipworms, coccidia, giardia, cryptosporidium viral: parvo, distemper, panleuk bacterial: salmonella, shigella, campylobacter, e. coli, clostridium, staphylococcus |
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what are signs, dx, tx for small intestinal diarrhea |
signs: diarrhea +/- blood, +/- fever, anorexia dx: r/o parasite, fecal smear, cytotoxin assays tx: antibiotics, fluids, electrolytes prn client ed: good hygiene |
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what is lymphangiectasia |
chronic protein-losing intestinal disease of dogs |
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what is lymphangiectasia etiology? |
- impaired intestinal lymphatic drainage due to obstruction of normal flow - lymph back up releases fluid into the intestinal lumen and causes loss of fat, plasma proteins and lymphocytes |
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what is lymphangiectasia clinical signs? |
- edema, effusion - ascites - light colored diarrhea - weight loss, emaciation-progressive |
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how do you diagnose lymphangiectasia |
CBC/Chem: lumphopenia, hypocholesterolemia, hypoglobulinemia, hypoalbuminemia, hypocalcemia - intestinal biopsy: chyle-filled lacteals w/ ballooning of villi, mucosal edema - endoscopy: lipid droplets protruding into lumen |
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how do you treat lymphangiectasia and whats client ed |
tx: stop protein loss, prednisone and metro, low fat diet, quality protein diet, suppliment w/ fat soluble vitamins, B12 client ed: progressive disease, no cure |
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what are the fat soluble vitamins |
A, B, C, K |
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what is a linear foreign body? |
- caused by long object anchoring in the intestines causing them to bunch on each other -signs: anorexia, vomiting, lethargy, abdominal pain, diarrhea, look for string (under tongue) - DX: find string, plication on rads/ultrasound - TX: surgery, may need resecting and anastomosis of dead bowel - Client ed: no strings or like objects, do not pull on protruding strings |
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what are clinical signs that a linear foreign body has perforated? |
- pain - fever - vomiting - collapse |
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what are small intestinal neoplasia disease |
- adenocarcinoma: 25% of intestinal cancer in dogs, 52% in cats - lymphosarcoma: 10% of GI neoplasia in dogs, 21% in cats |
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what are clinical signs, DX and TX of small intestinal neoplasia? |
signs: progressive, related to location and growth rate of tumor, weight loss, anorexia, +/- vomiting, +/- melena, diarrhea DX: palpable mass or thickened bowel loops, enlarged mesenteric lymph nodes, Rads, biopsy, labs (maybe anemic, hypoproteinemic) TX: surgical removal, supportive care, chemo |
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Tenesmus |
cramping |
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how to tell is diarrhea is small or large bowel related? |
small: increased volume, melena, maybe vomiting, weight loss large: markedly increased frequency of defecation, decreased volume, fecal mucus present, hemotochezia, tenesmus, urgency, dyschezia, steotorrhea |
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what is intussusception defined as? |
when smaller, more proximal segment of intestine at the ileocolic junction invaginates into the larger, more distal segement of large bowel
- produces partial or complete obstruction and compromises blood supply ( necrosis) |
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what is intussusception etiology, signs, DX, TX |
etiology: idiopathic, parasites, foreign bodies, infection, neoplasia signs: vomiting, anorexia, depression, diarrhea +/- blood dx: palpate sausage-like mass in abdomen, untrasound (multilayered concentric rings) tx: surgical reduction/resection, supportive care, antibiotics, bland food |
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what is megacolon? |
etiology: 62% idiopathic, poss defect in neurostimulation mechanism promoting bowel emptying, other things disrupting motility (hypokalemia, hypothyroidism, pelvis deformity) signs: straining to defecate, vomiting, diarrhea, weakness, anorexia, passing small hard bm or liquid bm, +/- blood, mucus dx: palpate distended colon, Rads: colon wider then lumbar vertebrae, CBC (dehydration) tx: enemas, stool softeners, cisapride, dietary (increase fiber and water intake), surgical (subtotal colectomy), fluids, deobstipate |
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what are accessory GI structures |
Liver and exocrine pancreas |
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what is the role of the liver |
large functional reserve and regenerative capacity - injury must be severe before laboratory parameters show evidence of a disturbance |
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what are clinical signs of liver disease |
- initially vague - anorexia, weight loss, vomiting, diarrhea, pu/pd - bleeding tendencies (vit K, clotting factors) |
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what are classifications of liver disease |
drug or toxin induced infectious neoplastic congenital hepatic lipidosis |
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what are the liver chemistries |
- total protein - albumin - globulins - fibrinogen - alanine transaminase (ALT) - Aspartate transaminase (AST) - Alkaline phosphates (ALP) - Gamma glutamyltransferase (GGT) - bilirubin - bile acids - cholesterol - glucose - BUN |
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what is the #1 cause of acute hepatotoxicity? |
- ingested drugs (first pass effect): acetaminophen, phenobarbital, antifungals - some may cause chronic toxicity over time |
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what is the first pass effect |
the fact that the liver receives 100% of blood flow thru the portal vein from stomach and intestines before the rest of the body |
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what animal is most affected by cholangiohepatitis |
cats - especially persians |
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what complex of disorders is involved in cholangiohepatitis |
- cholangitis - cholangiohepatitis - biliary cirrhosis |
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what is cholangiohepatitis etiology adn clinical signs? |
-etiology: bile duct inflammation causes hepatocyte injury causing biliary cirrhosis, possible asceding bacterial infection from GI -signs: anorexia, depression, weight loss, vomiting, dehydration, fever, jaundice, ascites, hepatomegaly |
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what is cholangiohepatitis diagnosis and treatment? |
-dx: increase ALT, ALP, GGT, bile acids, hypoalbuminemia, low BUN, left shift neutrophil, mild regenerative anemia, rads (hepatomegaly), histopath (cellular infiltrates around bile ducts) - tx: antibiotics (ampicillin, metro), ursodial (prevents gall stones), prenisolone, fluids, vitamins, electrolyte support |
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what should clients know about cholangiohepatitis? |
- variable prognosis - tx may be prolonged - liver maybe permanently damaged |
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what is feline hepatic lipidosis etiology? |
idiopathic disease mostly in hepatopathy cats that are adults and obese etiology: unknown cause, triggered by stress, prolonged anorexia creates imbalance in lipid breakdown and clearance, excess accumulation of fat in hepatocytes results resulting in hormone impairment, decreased fatty acid oxidation, impaired VLDL formation and release |
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what are clinical signs, dx and tx of feline hepatic lipidosis? |
signs: anorexia, weight loss(>25%), depression, sporadic vomiting, icterus, mild hepatomegaly, +/- coagulopathy DX: CBC (non-regenerative anemia, stress neutrophillia, lymphopenia, poikilicytosis), Chem (elevated ALP, ALT, AST, bilirubin, bile acids and hypoalbuminemia, ultrasound (hyperechoic liver), biopsy (vacuolized hypatocytes, fat confirmed) TX: aggressive support, nutrition (high cal and protein), feeding tube, vitamins (B1, B12, thiamine, carnitine, taurine), electrolytes, fluids |
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what are intrahepatic portosystemic shunts (congenital) |
- most common in large breed dogs - failure of ductus venosus to close at birth |
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what should you avoid with hepatic lipidosis animals? |
valium, propofol, don't use jugular due to hemolysis potential |
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what is PSS |
portosystemic shunts (congenital) anomalous vessels that, allow normal portal blood draining from the stomach, intestines, pancreas and spleen to pass directly into systemic circulation without first passing through the liver (adnormal should pass through liver, this diverts the first pass affect, toxins go right into blood) |
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what is extrahepatic portosystemic shunts |
- most common in small breeds and cats - mini schnauzers and yorkies - extrahepatic shunts connect the portal vein or one of its tributaries to the caudal vena cava or the azygos vein (toxins normally filtered out by liver get into systemic circulation) |
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what are clinical signs of portosystemic shunts (PSS) |
- 6 months of age - CNS: anorexia, depression, lethargy, weakness, ataxia, head pressing, circling, pacing, blindness, seizures, coma - cats: hypersalivation, aggressive or bizarre behavior - GI: vomiting, diarrhea, pu/pd - Urinary: urate urolithiasis (non-dalmations since dalmations have this genetic defect) |
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when do PSS signs worsen? |
right after a meal, especially one with high protein |
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how to you diagnose PSS? |
dx: CBC (mild anemia, poikilocytosis, microcytosis, target cells) Chem (hypoprotenemia, hypoglycemia, hypoalbumonemia, decreased BUN, increase ALT, ALP, bile acids, hypoammonemia), UA (ammonium bilurate crystals, isosthenuria, hyposthenuria) rads (microhepatics), ultrasound (visualize shunt) |
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how do you treat PSS? |
medical tx: (won't do well without surgery) low protein diet, lactulose, neomycin, metro, fluids surgical tx: surgical ligation of the shunt (must ligate slowly so liver can adapt to handle new blood flow) |
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what can be used during PSS ligation to allow slow ligation of the shunt and let the liver adapt |
ameroid ring |
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what can happen in PSS animals especially cats, after surgery |
shunt can recanalize and relapse |
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what is the major function of the pancreas |
-secretion of digestive enzymes into the small intestine - secrete bicarbonate to neutralize stomach acid and inhibit bacterial overgrowth - absorption of vitamin B12 and other nutrients - close association w/ stomach, liver, duodenum |
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what is etiology of pancreatitis? |
- acute or chronic - unpredictable w/ varying degrees of severity - more prevalent in obese animals etiology: high fat diet, dietary indiscretions, associated w/ hepatic lipidosis cats, caused by drugs (azothioprine, sulfonamides, furosimide), parasites, edema, trauma, tumors, disruption of bacterial flora in small intestine |
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waht is pathophysiology and signs of pancreatitis |
path: activation of enzyme occurs w/in gland leading to autodigestion and inflammation, results in tissue damage and multisystemic involvement signs: hx of recent fatty meal (pork), depression, anorexia, vomiting, +/- diarrhea, fever, dehydration, +/- abdominal pain, shock collapse |
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how do you diagnose and treat pancreatitis
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dx: CBC (leukocytosis, high PCV) Chem (azotemia, increased ALT, low calcium, hyperlipemia), cPLI & fPLI (canine/feline pancreatic lipase immunoreactivity test), Rads, ultrasound TX: support fluids/lytes, NPO 24-48hrs, antibiotics, pain meds, antiemetics, plasma, albumin, bland diet |
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when are cases of pancreatitis more common? |
around the holidays when pets are fed fatty meals |
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what is the best diagnostic test for pancreatitis |
cPLI or fPLI test (canine/feline pancreatic lipase immunoreactivity test) |
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what is the etiology of exocrine pancreatic insufficiency (EPI) |
- pancreatic acinar atrophy ( young german sheps, cats w/ chronic pancreastitis - progressive loss of acinar cells and digestive enzymes (signs occur when 85-90% secretory ability is lost) - lack of normal enzyme secretions alters mucosal lining of intestines decreasing ability to absorb, causing bacterial overgrowth - can also affect insulin |
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what is EPI |
exocrine pancreatic insufficiency |
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what are clinical signs, diagnostics and treatment of EPI? |
signs: mild to marked weight loss, polyphagia, coprophagia, pica, diarrhea, light, fatty stool, flatulence DX: CBC (normal), Chem (elevated ALT), TLI test (decreased <2 mcg/L) TX: suppliment pancreatic enzymes (pancrezyme, viokase, pig pancreases), low fiber, highly digestible diet, vitamin suppliment, antibiotics for SIBO (metro, tylosin) |
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what is the best diagnosic for EPI? |
TLI test (trypsin-like immunoreacticity) |
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what should clients know about EPI? |
-lifelong, irreversible - clinical signs will resolve with supplimentation - must be given w/ every meal - do not touch or inhale enzyme powder |
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what does the thyroid gland do? |
produce thyroid hormones T3, T4, calcitonin (decreases blood calcium) |
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what does the adrenal gland do?
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salt, sugar, sex |
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what animal is hypothyroidism most common in? |
dogs -cats can get but usually as a result of over treating hyperthyroidism |
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what are the two etiologic agents that cause hypothyroidism? |
1. thyroid atrophy 2. lymphocytic thrtoiditis (tumor) |
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what are clinical signs, diagnostics and treatment for hypothyroidism? |
signs: weight gain, bilaterally symmetrical alopecia (rat tail), recurrent skin problems (dry coat, excessive shedding, skin hyperpigmentation), cold intolerance, repro problems dx: low T4 or free T4, high thyroid stimulating hormone (TSH), mild non-regenerative anemia, increased cholesterol tx: lifelong supplimentation with levothyroxine |
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in what animal is hyperthyroidism most common |
cats |
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what causes hyperthyroidism in cats? |
thyroid adenoma - 70% bilateral - 1-2% due to thyroid adenocarcinoma - benign but causes thyroid to oversecrete T3 and T4 |
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what are clinical signs of hypothyroidism? |
- signs: weight loss, polyphagia, vomiting, tachycardia +/- murmur, hyperactivity, palpable thyroid, increased BP, blindness (retinal detachment, engorged retinal vessels, hyphema) |
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what is hyphema |
blood in anterior chamber of the eye |
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what do you give to treat hyphema? |
amlodipine |
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how do you diagnose hyperthyroidism? |
DX: palpable thyroid, increased serum T4 or free T4, elevated ALT, ALKP, may be azotemic, hypertensive |
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how do you treat hyperthyroidism? |
1. anti-thyroid drugs: methimazole, disrupts synthesis of T4, treats, doesn't cure 2. radioactive iodine I-131 (treatment of choice, cure, specialized facility) 3. thyroidectomy (need stable patient, cure, can re-grow, danger to parathyroid glands and calcium regulation 4. Diet: hills Y/D (iodine restriction, no other food or treats allowed |
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what is the cure/ treatment of choice for hyperthyroidism |
radioactive iodine |
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what do beta cells produce |
insulin: insulin helps glucose get into cells to be used for energy |
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what do alpha cells produce |
they secrete glucagon - glucagone increases blood levels of glucose when levels are low (mobilize from storage cells) |
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what is the etiology of diabetes mellitus |
- beta cells stop producing insulin or cells stop responding to insulin - may be caused by chronic pancreatitis - "lipolysis causes increased fatty acid and ketone production, protein catabolism, hyperglycemia due to decreased glucose uptake and increased gluconeogenesis, and decreased tissue utilization of glucose, fatty acids and amino acids" |
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what is type one diabetes |
- insulin dependent (destruction of beta cells) - 100% of dogs - rare in cats - requires insulin therapy |
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what is type 2 diabetes |
- non-insulin dependent (impaired secretion of insulin) - 80% of cats - may need diet +/- insulin therapy |
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what are clinical signs of non-ketotic diabetes |
- pu/pd/pp - weight loss (cats) - sudden cataract formation - plantigrade stance (cats) |
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what are clinical signs of ketotic diabetes |
- depression, weakness - vomiting - tachycardia - acetone breath |
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how do you diagnose diabetes |
- elevated fasting BG >200 mg/dL (cats >250) - glycosuria - high fructosamine (cats) - if ketotic: electrolyte abnormalities, ketonuria, dehydration - may have concurrent disease: Uti, pancreatitis, hepatic lipidosis |
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how do you treat diabetes mellitus
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- diet: dogs-higher fiber and complex carbs, maintain optimum body weight, cats- high protein, low carb diets, maintain optimum body weight ( some cats will go into remission when diet changes) - insulin therapy |
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what is non complicated insulin therapy for diabetes in dogs and cats? |
dogs: intermediate acting insulin (vetsulin, humulin N) cats: glargine (lantus)- long acting (high protein diet=remission in 1-4 months, vetsulin, PZI |
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what is the best food for diabetic cats |
canned food |
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what is insulin therapy for complicated diabetic dogs and cats |
- short acting insulin - aggressive supportive care (IV fluids, correct electrolyte imbalances) |
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how should monitoring be done on a diabetic patient |
- BG curves: IH or at home to determine nadir and duration of action, adjust dose accordingly - fructosamine assay: higher w/ poor control, con;t determine nadir or duration - urine glucose sticks: determine is more in depth testing is needed |
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what are signs of hypoglycemia |
- weakness - lethargy - seizure - coma |
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what does the adrenal cortex produce |
1. mineralocorticoids (aldosterone- sodium and water) 2. glucocorticoids (suppress inflammation, suppress immune system) 3. sex hormones |
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what does the adrenal medulla produce |
1. epinephrine 2. norepinephrine (sympathetic nervous system: fight or flight) |
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what is hypoadrenocorticisms common name |
addison's |
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what animal is hypoadrenocorticism common in |
dogs -rare in cats - standard poodles, labs, westies |
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what is the etiology of hypoadrenocorticism? |
-etiology: idiopathic atrophy of adrenal cortex, decreases production of glucocorticoids and mineralocorticoids |
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what does decreased aldosterone due to hypoadrenocorticism lead to ? |
decreased aldosterone levels lead to abnormal sodium and potassium exchange as well decreased water conservation-hypotension |
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what are clinical signs of addison's (hypoaddrenocorticism) |
- female > males, middle aged - depression, lethargy, weakness- may wax and wane - anorexia, weight loss - vomiting, diarrhea (often hemorrhagic) - pu/pd - bradycardia, dehydration |
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how do you diagnose addison's (hypoaddrenocorticism) |
- Na:K ratio < 27:1 (atypical cases may have normal electrolytes) - non-regenerative anemia - azotemia, dilute urine - hypoglycemia, hypercalemia - ACTH Stimulation test definitive dx: expect rise in cotisol between pre and post sample but w/ addison's remains unchanged |
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what is the definitive diagnostic for addison's (hypoaddrenocorticism) |
ACTH stimulation |
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how do you treat acute addison's (hypoaddrenocorticism)(addisonian crisis) |
* emergency 1. fluid therapy: shock (stabilize electrolytes) 2. glucocorticoid replacement: (dex meth, pred) 3. treat GI hemorrhage (GI protectants) 4. mineralocorticoid replacement (DOCP) |
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what is the mineralocorticoid DOCP |
Desoxycorticosterone pivalate |
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how do you treat chronic addison's (hypoaddrenocorticism) |
-DOCP injection every 25-28 days - prednisolone - fludricortisone (oral mineralo and corticoid supplementation) |
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what is the common name for hyperadrenocorticism |
Cushing's |
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what animal commonly gets Cushing's (hyperadrenocorticism |
- common in dogs, rare in cats - poodles, dachshund, terriers (PDH) - majority of cases are females > 6 years |
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what is the etiology of Cushing's (hyperadrenocorticism |
- excessive secretion of cortisol 1. pituitary adenoma: excess ACTH- excess cortisol (pituitary dependent) 2. functional adrenal tumor: excess cortisole (leads to unilateral adrenal enlargement and atrophy of the other) 3. iatrogenic: overmedicating with exogenous steroids |
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what are clinical signs of Cushing's (hyperadrenocorticism |
- pu/pd/pp - excessive panting - abdominal enlargement (weakening of stomach muscles) - obesity - muscle weakness, lethargy, lameness - bilateral symmetrical alopecia, pyoderma (skin infections) - calcinosis cutis, abnormal gonads |
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calcinosis cutis |
calcified plaques on the skin |
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comidomes |
black heads
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how do you diagnose Cushing's (hyperadrenocorticism |
- Chem: elevated ALT, ALKP, cholesterol, glucose, decreased BUN, lipemia - increased urine cortisol: creatine ration (normal ratio rules out cushing's) - dilute urine, uti's - ACTH stimulation test (higher then normal cortisol levels after injection) - Low Dose Dex test (should suppress in normal pet, elevated cortisol in Cushing's) - Ultrasound : may show enlarged adrenal |
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what is the definative diagnostic for Cushing's (hyperadrenocorticism |
Low dose Dexamethasone suppression test |
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how do you treat Cushing's (hyperadrenocorticism |
- surgically remove adrenal tumor - w/ pituitary dependent: Mitotane, trilostane Other: ketoconazole, selegiline (anipryl) |
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what does primary hyperparathyroidism cause |
hypercalcemia |
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hypoparathyroidism causes what |
hypocalcemia |
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insulinoma causes what |
hypoglycemia |
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normal canine and feline gestation length |
62-65 days - fetuses palpable dogs: 25-36 days, cats: 21-28 days - skeletal mineralization on rads: 45 days |
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Ovarian remnant syndrome |
etiology: ovarian tissue not completely excised at time of spay or ovarian tissue is dropped into the abdominal cavity and revascularizes signs: estrus after OVH, false pregnancy DX: vaginal cytology w/ signs of estrus (cornified epithelium, LH testing, anti-mullerian hormone test, estrodiol levels after stimulation w/ gonadotropin, serum progesterone, exploratory TX: surgical removal of remnant |
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Eclampsia |
-2-3 weeks after parturition, small dogs Etiology: lactation and diet deficient in calcium signs: nervousness, salivation, stiff gait, ataxia, seizures DX: hx, clinical signs, hypocalcemia TX: slow IV infusion of calcium gluconate (monitor heart for bradycardia or arrhythmia), once stable, oral calcium supplement (TUMS) |
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what is the etiology of a pyometra |
- common in middle aged to older intact females - etiology: increasing progesterone results in hyperplasia of endometrial glands of uterus, becomes cystic and secretes fluid while cervix is closed and myometrial contractions are inhibited (cystic endometrial hyperplasia), fluid causes inflammation, good medium for bacteria, or caused by administration of progestins (megastrol acetate) |
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what bacteria is often associated with pyometras |
- e. coli (most common in dogs), staphylococcus, streptococcus, pasteurella, proteus, moraxella |
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what are clinical signs of a pyo |
- +/- vulvar discharge depending on open or closed - abdominal enlargement - vomiting - lethargy - pu/pd - dehydration, azotemia |
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how do you diagnose a pyo |
- HX of estrus or irregular estrus - rads (enlarged uterus) - ultrasound (fluid filled uterus) - CBC: neutrophilic leukocytosis with left shift, azotemia - Cytology: degenerate neutrophils, bacteria |
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how do you treat a pyo |
- #1 OVH (spay) - correct dehydration first - if pet needed for breeding: prostaglandin F2-alpha (lutalyse), should breed next cycle - antibiotics based on cult and sens |
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what is dystocia |
difficulty in delivery of fetuses through birth canal - fetal factor: large fetus, abnormal positioning (breech not a factor) - maternal factors: narrow canal, uterine inertia |
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what are clinical signs of dystocia |
- in labor > 4 hours w/out producing a fetus - green vaginal discharge during parturition - more than 1 hour between fetus |
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how do you diagnose and treat a dystocia? |
DX: PE, digital palpation of vagina, Rads (positioning and birth canal), ultrasound to assess fetal viability TX: manually dislodge w/ careful manipulation, oxytocin for inertia, C-section |
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how can you tell a neutered male cat from a cryptorchid cat? |
no spines on the penis - smell of tom cat urine |
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what is cryptorchidism and its etiology? |
- hereditary developmental defect - etiology: failure of one or both testicles to descend into the scrotum within 8 weeks of birth, maybe located subQ, inguinally, abdominally, produce testosterone but not sperm, Dogs>cats |
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how do you diagnose and treat cryptorchidism |
DX: PE, testosterone levels, gonadotropin stimulation tests, ultrasound, exploratory surgery TX: castration is treatment of choice, prevent torsion, neoplasia |
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what is benign prostatic hyperplasia (BPH) |
-aging change causing enlargement of the prostate in intact males - signs: maybe asymptomatic, tenesmus - DX: prostate palpates symmetrically enlarged, non-painful (normal), biopsy TX: castration (70% decrease in size within 7-14 days), DES (estrogen suppliment) |
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What is the etiology and clinical signs of prostatitis |
-etiology: infection w/ bacteria from urogenital tract or direct infection (e. coli typically, also proteus, klebsiella, pseudomonas, strep, staph, brucella canis), acute or chronic - Signs: acute (anorexia, fever, lethargy, stiff gait, caudal abdominal pain) Chronic ( asymptomatic, chronic, intermittent UTI) |
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what is the diagnosis and treatment of prostatitis |
DX: UA w/ pyuria, hematuria, bacteruria, PE, Culture TX: antibiotics 4-6 weeks, ideally based on cult, castration |
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prostatic abcesses |
more severe form of prostatitis |
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what is a mammary tumor and what are the risks? |
- represents 50% of all tumors in female dogs - hormone dependent in dogs >cats RISKS: 0.5% in OVH before 1st heat, 8% in OVH after 1 estrus, 26% OVH after 2 or more estrus, dogs 50/50 benign vs malignant, cats 80-90% malignant |
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what are clinical signs, diagnosis and treatment options for mammary gland tumors |
- Signs: firm nodule along mammary chain (local invasion, ulceration=malignant), regional lymph node enlargement - DX: exam, biopsy (adenocarcinoma) - TX: perform met check first, surgical removal #1, chemotherapy |
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priapism |
condition where penis remains erect for a prolonged period of time |
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paraphimosis |
inability of a dog to retract his penis back into his sheath |
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what are the top 5 transplacental parasitic infections in dogs |
- toxocara canis - neospora caninum - babesiosis - leishmaniasis - dirofilarial microfilariae |
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what are the abbreviations for feline idiopathic/interstitial cystitic |
-FIC - FUS - FLUTD |
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what is FIC and what are it's forms? |
- non- malignant inflammatory condition Forms: 1. Ulcerative, 2. non-ulcerative or 1. Obstructive 2. non-obstructive |
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what is the etiology and clinical signs of FIC |
- cause is unknown: viral, NOT bacterial, often stress related Signs: self-limiting in most cats w/ resolution in 1-10 days (therefore may appear any treatment is working), hematuria, dysuria, pollakiuria, inappropriate urination |
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how is FIC diagnosed and treated? |
DX: urinalysis (r/o bacterial cystitis or systemic disease), urine culture (negative), ultrasound (may have irregular, thickened bladder wall) TX: decrease stress (increase activity, climbing areas, hiding spaces), diet change (promote dilute urine, canned food, special new diets), analgesia to ease discomfort |
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what are the defense mechanisms of the urinary tract? |
- frequent voiding - urethral and ureteral peristalsis - glycosaminoglycan layer - pH and concentration of urine |
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what is the most common cause of cystitis in dogs |
canine bacterial cystitis (UTI) |
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what is the etiology and signs of canine bacterial cystitis? |
-etiology: most commonly from bacteria ascending from the urethra (e. coli, proteus), once in bladder adhere to biofilms, alteration of defense mechanisms due to other illness, immune suppression, etc (Cushings) - Signs: pollakiuria, hematuria, dysuria, cloudy urine, abnormal odor, frequent licking, urinary accidents |
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how do you diagnose and treat canine bacterial cystitis (UTI) |
DX: urinalysis (pyuria, bacteruria, hematuria), cult and sens (collect via cysto) TX: antibiotics based on cult, empiric antibiotics (ampicillin, clavamox, TMS, enrofloxacin, cephalexin), adequate duration (10-14 days for acute, 4-6 weeks for chronic) |
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what may be a source of recurrent canine bacterial cystitis (UTI) infection in male dogs |
prostate |
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urolith |
crystalline concretion composed of mineral with a small amount of matrix - found anywhere in urinary tract - may be radiodense (seen on rads) - may be radiolucent (not on rads, double contrast on ultrasound) - can damage bladder lining causing secondary infection or hematuria - can obstruct outflow tracts |
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urethral plug |
large amount of matrix with small amount of material |
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what are struvite uroliths and what is there etiology? |
-60% cat uroliths, 80% of dogs - etiology: cats- historically diets high in magnesium, dogs- most are associated with bacterial cystitis, form in alkaline urine |
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what urolith is associated with bacterial cystitis in dogs |
struvite |
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what are the clinical signs, diagnostics and treatment for struvites |
- signs: whether obstructed or not, asymptomatic, hematuria, dysuria, pollakiuria, inappropriate urination, straining, vomiting, collapse, death - DX: rads, ultrasound may show crystals, stone analysis (MN urolith lab( - TX: surgical removal, diet (acidifying or preventative), antibiotics, acidifying drugs (methionine) |
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What is the #1 rule out for FIC |
UTI |
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pylonephritis |
UTI that has ascended up to the kidney |
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what are flat sides on a urolith from |
rubbing on another stone in the bladder |
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what are calcium oxilate uroliths and what is their etiology? |
- cats: 27% of stones (Bermese, himalayan, persian) - dogs: males 5-12 yrs, small breeds - etiology: used to be "over correction" from struvites w/ acidifying diets new diets prevent this, hypercalcemia in some cases, form in acidic urine |
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what are clinical signs of calcium oxilate uroliths |
-dependent upon whether obstruction is present or not
- asymptomatic - hematuria, dysuria, pollakiuria - inappropriate urination - straining - vomiting, collapse, death (UO) |
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what is diagnostic, treatment and prevention for calcium oxyalate uroliths |
DX: rads (if radiopaque), ultrasound (acoustic shadowing), urinalysis may show crystal representation of stone type (not always), stone analysis (MN lab) TX: surgical removal, CaOx stones cannot be dissolved by diet or meds Prevention: control calcium levels, alkalinizing diets or drugs (potassium citrate) |
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what are ammonium urate crystals
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- uric acid is by-product of purine metabolism - with faulty metabolism uric acid builds up, urate salts - also liver disease such as shunts - dalmations** (bulldogs, shi tzu, yorkie, schnauzer), 3-6 yrs - radiolucent** (not seen on rads) - TX: diet (protein restriction), surgery, meds to alkinize urine |
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what are cystine crystals |
- inherited disorder of kidney tubular transport - acidic urine - *male dachshund 3-6 yrs - mostly radiolucent on rads (can't see), visualize w/ ultrasound |
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what is the etiology of urethral obstruction (UO) |
- uroliths or urethral plug blocks urine outflow - urine backs up (distended bladder, ureters, and into kidneys halting filtration, cuases pressue necrosis, mucosal injury, impaired Na and H2O resorption and excretion of Ph, K, BUN, Cr, H+ - uremia within 24-48 hrs (depression, vomiting, anorexia, metabolic acidosis, denaturing of proteins) - hyperkalemia is most life threatening- decreases depolarization of the heart |
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what is the most danger/ life threatening aspect of a UO |
hyperkalemia which can cease depolarization of the heart |
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how do you diagnose a UO |
- hx and pe (vocalizing, unproductive straining, vomiting, lethargy, anorexia, weak, recumbent, tachypneic, hypothermic, bradycardic, palpable firm distended bladder, pain - labs: azotemia, hyponatremia, hyperphosphatemia, hhyperkalemia, hyperglycemia, decreased bicard and pH - UA: hematuria, proteinuria, glucosuria, Sediment ( pyuria, bacteriuria, crystalluria, casts, dark red urine=worse) -rads: distended bladder, uroliths, mass, rupture (free abdominal fluid) |
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how do you treat a UO? |
- relieve onstruction by passing u-cath (retrograde hydropulsion, pushed stones into bladder), surgical removal of stones from bladder (cystotomy), utethrotomy, perineal urethrostomy, aggressive supportive care, indwelling catheter closed system |
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what 2 drugs help with UO's? |
- phenocybensamine, prazosin (relax smooth muscle of urethral sphincter) |
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how do you prevent a UO |
- rx diet, canned is preferred |
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what is acute renal failure and what is its etiology? |
Sudden decrease in glomerular filtration- azotemia - etiology: 1. hypoperfusion (decreased BP during anesthesia, shock, hypovolemia, dehydration), 2. nephrotoxic injury damages nephron (drugs: aminoglycosides, sulfonamides, antifungals, chemo drugs, NSAIDs. Toxins: ethylene glycol, plants, grapes, heavy metals. infection, hypercalemia |
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what are clinical signs of acute renal failure? |
- non-specific - may have hx of recent toxin exposure - enlarged, painful kidneys - anorexia, vomiting, diarrhea, weakness - pu/pd, oliguria - +/- fever |
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how do you diagnose acute renal failure and how do you treat it?
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DX: UA- "active" sediment w/ casts, CBC/Chem- increased PCV, BUN, CR, Increased K+, Phos, acidosis TX:IV fluids (restore perfusion, hydration, restore electrolytes), D/C nephrotoxic drug, adjunct (H2 blockers, PPI's, anti-emetics, phosphate binders, sodium bicarb), diet (low protein, low phos) |
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what is chronic renal failure and what is its etiology? |
- CRD: chronic renal disease, common in older pets - etiology: congenital, familial, acquired, cats> dogs, progressive decline in renal function caused by destruction of the nephrons- decreased GFR- uremia, abnormal excretion/retention of electrolytes, water, solutes, impaired renal hormone synthesis, systemic hypertension, GI abnormalities |
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GRF |
Glomerular filtration rate |
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what are ways to acquire chronic renal failure through disease
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- amyloidosis, polycystic kidneys, neoplasia, pyelonephritis, obstruction |
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what happens with decreased erythropoietin in CRF |
non-regenerative anemia |
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happens with decreased calcitriol in CRF |
secondary hyperparathyroidism (abnormal calcium and phosphorous regulation) |
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what are clinical signs of CRF |
- pu/pd (often earliest sign) - weight loss, poor body condition - anorexia, dehydration, lethargy - vomiting, diarrhea, halitosis - oral ulcers, dysphagia, gingivitis - constipation - signs of hypertension ( retinal hemorrhage, hyphema, retinal detachment) - seizure, CNS signs, hypothermia |
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how do you diagnose CRF? |
- HX, PE: dehydration, palpate small, lumpy kidneys - CBC: normocytic, normochromic, non-regenerative anemia - Chem: azotemia, hyperphosphatemia, hypokalemia, hypermagnesemia, hyper- or hypo- calcemia, metabolic acidosis - UA: Dilute urine (sosthenuria), proteinuria, hematuria, pyuria, bacteriuria, cult to r/o concurrent UTI - elevated UPC (urine protein: creat ratio) - SDMA elevated |
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what is the best test for CRF |
SDMA |
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why is the SDMA a better CRF test |
- more sensitive than Cr - detects at ~24% damage vs. 75% |
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how do your treat CRF |
- diet: lower protein, phosphorous, sodium - fluids: SQ fluids aid in maintaining hydration and increases elimination of BUN - phosphate binders: AIOH - potassium supplementation - pro- crit or darbopoeitin for anemia - anti-hypertensive agents: calcium channel blockers (amlodipine) - ACE inhibitors for proteinuria (lowers glomerular BP) - GI support |
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what is urinary incontinence and what is its etiology? |
- loss of voluntary control of micturition - all about pressure (bladder pressure > urethral pressure, urine leaks) - etiology: neurogenic (spinal cord disease of trauma), non-neurogenic (congenital abnormalities [ectopic ureters], estrogen deficiency [spay incontinence], urethral sphincter incompetence [degenerative], hypercontractile [urge incontinence] |
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what are clinical signs and how do you diagnose urine incontinence |
-signs: leakage when pet is sleeping/relaxed or exercising, perineal area wet or soiled, may have concurrent UTI - DX: UA, rads, r/o uti, metabolic disease |
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how do you treat urinary incontinence? |
- treat underlying cause - PPA: phenylopropanolamine (increases urethral sphincter tone, proin) - estrogens: DES, estriol (incurin), help improve sphincter tone - propantheline: relaxes bladder detrusor muscle, helps urge incontinence |
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what is idiopathic vestribular disease, whats its etiology and clinical signs? |
-"old vestibular disease" - common cause of peripheral vestibular signs in dogs & cats - etiology: unknown, no lesions or inflammation can be found - signs: acute onset ataxia, disorientation, nystagmus, head tilt, nausea vomiting, NO weakness or conscious proprioception deficits |
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how do you diagnose and treat idiopathic vestibular disease |
DX: clinical signs, rule out central disease (weakness, neuro deficits), otitis media/externa, trauma, signs do not progress after first 24 hours TX: resolve spontaneously over days to weeks (may have residual head tilt or ataxia), supportive care only ( dramamine, meclizine for motion sickness, maropitant for vomiting, no evidence steroids help) |
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what is idiopathic epilepsy |
- repeated episodes of seizure for which no cause exists - exclude other causes of seizures - breed predispositions: G. Shep, G. retrievers, poodles, St. Bernards, cocker, beagle - onset 1-3 yrs - may occur singly or in clusters - grand mal= general seizure lasting 1-2 min - brought on by stress, estrus, excitement |
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what are clinical signs of idiopathic epilepsy |
-pre-ictal/prodromal/aura phase: may act abnormally (hide, vocalize, seek companionship) - ictal phase: active seizuring (sudden unconsiousness, limb motions, loss of bowel and bladder control, salivation, dilated pupils, vocalization - post-ictal: recovery period (subtle or may have dementia, blindness, pacing, aggression |
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what are generalized seizures
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general seizure involving both sides of the brain and are bilateral |
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simple partial seizure |
involves one side of the cerebral cortex with abnormal movement on one side of the body |
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complex partial seizure |
manifest as a change in the level of consciousness |
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focal seizures |
abnormal electrical signals in a focal part of the brain causing a localized or unilateral seizure |
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limbic seizure |
manifest as intermittent vomiting, diarrhea, salivation episodes that last a few days - similar to GI disease but resolve with antiepileptic drugs |
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reactive seizure |
occur secondary to other systemic disease |
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cluster seizures |
multiple seizure episodes in a row in a short period of time |
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how do you diagnose and treat idiopathic epilepsy |
DX: CBC, Chem, UA, BP, CT/MRI, CSF (based on history) TX: treat underlying cause if possible, with chronic (phenobard, potassium bromide, keppra, zonisamide, monitoring) If having current seizure treat with: diazepam/midazolam IV, CRI, rectal, propofol boluses or CRI, levetiracetam, phenobarb, pentobarbital |
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when do you start treatment for idiopathic epilepsy |
-large breed: after 2-3 episodes - others: seizures increase in length and severity and if occur < 30-45 days apart |
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what is the kindling phenomenon |
-worsening/uncontrolled seizures damage control mechanisms of the brain- the more frequent the neurons are exposed to abnormal electrical impulses, the quicker and easier it becomes to trigger - can lean to cluster seizures, status epilepticus, death |
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what can cause secondary (acquired) epilepsy |
- structural brain disease: storage disease, malformations, neoplasia, trauma, infection, vasular accidents - metabolic disease: hepatoencephalopathy, hypoglycemia - toxins |
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what is status epilepticus |
- emergency!! - prolong period of seizure >5-10 mins (can lead to irreversible coma and death - body temperature can rise > 105F=cool patient - cerebral edema: give mannitol - IV pentobarbital, diazepam |
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what is intervertebral disk disease (IVDD) |
-common - occurs in all breeds of dog, occationally cats - most chondrodystrophic dogs have degeneration of their disks by 1 yr -etiology: degeneration within the disk results in herniation and spinal cord injury |
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what are the 2 types of intervertebral disk disease (IVDD) |
- Type 1: younger dogs (acute rupture of the annulus fibrosis w/ extrusion of nucleus pulposis into the spinal canal - Type 2: Older >5yr, large breed (extrusion occurs more gradually, less acute and less severe signs, often lateralize |
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what are clinical signs of intervertebral disk disease (IVDD) |
-depends upon location, speed at which disk material is deposed, degree and duration of compression - locations= cervical, caudal thoracic, lumbar - pain, acute onset (type 1) - paresis or paralysis - motor or sensory deficits - altered deep pain - decreased panniculus reflex caudal to the lesion |
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With intervertebral disk disease (IVDD) how could you use the limbs to determine where the injury is? |
limbs caudal to the injury are affected |
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what is the most important clinical signs in intervertebral disk disease (IVDD) diagnosis? |
-depends upon location, speed at which disk material is deposed, degree and duration of compression |
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what are clinical signs of cervical intervertebral disk disease (IVDD)
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- often cry out suddenly for no apparent reason - carry head low - reluctant to move head: follow w/ eyes or by turning their whole body - changes in forelimbs and hindlimbs |
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what are clinical signs of thoracolumbar intervertebral disk disease (IVDD) |
- may cry our suddenly - reluctant or unable to jump up onto furniture - pain w/ pressure over area - changes in hind limbs - may appear as if having abdominal pain - hunched - very tense abdomen |
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how do you diagnose intervertebral disk disease (IVDD) |
-PE, HX - neuro exam - Rads w/ anesthesia (narrow disk spaces, myelogram definitive) - CT/MRI |
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how do you treat intervertebral disk disease (IVDD) |
- Medical: those w/ pain and no or mild deficits: REST!, strict care, minimum 2 wks, steroids to decrease inflammation, +/- pain meds or NSAIDs (not w/ steroid), supportive care (express bladder, carry) - Surgical: those w/ neuro deficits or unrelenting pain/recurring episodes: remove expelled disk material, fenestration, hemilaminectomy, can worsen w/ surgery |
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why should a painful patient never receive steroid/pain meds and NOT be restricted |
because they could injure themselves further due to the fact they can not tell when they are painful and can worsen the initial injury |
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what is the common name of cervical spondylomyelopathy |
Wobbler's |
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what is cervical spondylomyelopathy |
- C5-C7 malformation - great danes, dobermans - signs at young age - progressive hindlimb ataxia - abnormal proprioception - DX: rads, CT/MRI - poor prognosis w/out TX - Surgery: decompression and stabilization (disk replacement) |
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what is degenerative myelopathy |
- German Shepards, > 5 yrs - diffuse degeneration of white matter in ascending and decending spinal cord tracts - progressive ataxia and rear limb paresis, loss of proprioception - muscle wasting, scuffed tops of feet - no treatment |
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what is a cruciate ligament injury |
- cranial and caudal cruciate ligaments are within the stifle joint and help stabilize the stifle joint (anterior and posterior are the human equivalents) - often in middle ages, overweight animals |
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what is the etiology of a cruciate ligament injury |
- very common injury in the dog - major cause of degenerative joint disease (DJD) - ruture or tear occurs due to: trauma, degenerative process (atraumatic process) - often rupture of the contralateral ligament occurs within 1 year - tear: leads to painful inflammation - rupture: pain, inflammation, swelling, instability |
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what are clinical signs of a cruciate ligament injury |
- acute onset - non-weight bearing on affected leg, or classic "toe touch" - inward tibial rotation when weight bearing - joint effusion |
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how do you diagnose cruciate ligament injury |
- positive cranial drawer movement (tibia slides forward excessively, beyond femoral condyles) - tibial compression test: flex hock, tibia presses forward beyond femoral condyles - rads: cranial displacement of tibial plateau, bone avulsion at attachment sight, effusion |
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how do you treat cruciate ligament injury |
- surgery is treatment of choice - extracapsular (extra-articular) stabilization (best in dogs < 15kg, suture in placed around fabella and through hole in tibial crest to stabilize joint - intraarticular stabilization: patellar tendon graft, tibial plateau leveling osteotomy (TPLO), tibial tuberosity advancement (TTA), achive stability by changing the biomechanics of knee |
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what is medial patellar luxation |
- toy, miniature, large breeds- congenital - traumatic - 75-80% of time |
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what is lateral patellar luxation |
- toy, miniature, large, giant breeds - often goes along with hip dysplasia in large breeds |
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what is etiology of patellar luxation |
- occur early in life, congenital - anatomic abnormalities: changes in femoral angle causes medial displacement of the quadriceps muscle (in young animals w/ open growth plates, this causes the tibial tuberosity to be "pulled" more medially- bowing of the legs) - shallow femoral trochlear groove |
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what are clinical signs of patellar luxation |
- abnormal gait - unilateral or bilateral - intermittent lameness, waxing and waning - persistent lameness, crouched gait - discomfort when stifle is manipulated |
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how do you diagnose patellar luxation |
- PE and HX - maybe seen on Rads |
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what are the grades of patellar luxation |
grade 1: manually luxated but immediately returns to normal position grade 2: patella luxates and returns to normal position spontaneously grade 3: patella permanently luxated but can be manually reduced grade 4: patella permanently luxated and can not be replaced into groove |
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how do you treat patellar luxation |
- depends upon severity and clinical signs - mild= rest and NSAID's - moderate-severe: surgery - supportive care: NSAID's, PSGAGs, glucosamine, chondroitin, optimal body weight |
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what are the 3 surgery options for patellar luxation |
1. Trochleoplasty: remove wedge of sulcus, then replace cartilage 2. Tibial tuberosity transposition: moves the insertion of the patellar ligament laterally to cause the quadriceps to pull over the center of the trochlear groove 3. combination of both |
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what is canine hip dysplasia (CHD) |
- malformation and degeneration of coxofemoral joints - most common in large breed dogs |
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what is the etiology of canine hip dysplasia (CHD) |
- secondary to shallow acetabulum or congenital malformation of the femoral head - results in coxofemoral instability - body tries to counteract the instability creating arthritis, osteophytes, microfractures in the cartilage |
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what are the clinical signs of canine hip dysplasia (CHD) |
- may be as early as 5-8 months of age - depends upon degree of laxity and osteoarthritis - decreased activity - reluctance to run, jump, climb stairs - lameness worse after exercise - difficulty rising |
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how do you diagnose canine hip dysplasia (CHD) |
- PE: abnormal gait (swaying or bunny hop, decreased flexion and extension of hip during ambulation), variable lameness, muscle atrophy, palpation (pain, crepitus, decreased range of motion), positive ortolani sign: laxity - Rads: VD hip extended, subluxation of hip joint, incongruent head of femur and acetabulum, flattened femoral head, thickening of femoral neck |
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what is Morgan's line |
osteophyte on neck of femur |
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how do you treat canine hip dysplasia (CHD) |
-medical: NSAIDs, chondroprotective agents, O3FA's, physical therapy, weight reduction, acupuncture - surgical: total hip replacement (large dogs), femoral head and neck ostectomy ( small-medium dogs), juvenile pubic symphysiodesis (cauterize growth plate to close it, acetabulum is rotated dorsally, then all is reattached via bone plates), triple pelvic osterotomy (TPO) |
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what is Legg-Calve- Perthes |
- avascular necrosis of the femoral head - small breed dogs (toys and terriers) - pain and muscle atrophy - surgically remove femoral heads |
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what is Osteochondrosis Dissecans (OCD) |
- degeneration of bone and cartilage w/ reossification (failure of endochondral ossification) - results in cartilage flap (inflammation, pain, lameness) - shoulder, stifle, hock, elbow - large breed 3-18 months |
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what is Panosteitis |
- medium- large breed dogs, 6-8 months old (male german shepherds) - intermittent lameness - acute, shifting leg lameness, hx of trauma - viral? - thickening of endosteal bone, long bones - self limiting by 1 yr - TX: rest, NSAIDs |
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what is neoplasia in regards to the musculoskeletol system?
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- 85-95% osteosarcoma (shoulder/carpus, distal femur/proximal tibia) - high metastasis rate - TX: amputation and chemo - not good long term prognosis |
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what is degenerative joint disease/ osteroarthritis |
- degenerative, progressive, irreversible - loss of articular cartilage, osteophyte formation, periarticular fibrosis - primary arthritis due to aging or secondary trauma, conformation, surgery |
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