Path 2 - Midterm - Auburn Rounds 2

drraythe's version from 2015-04-18 22:35

Week 5

Question Answer
CASE 1: Labrador retriever, 10yo, F spayed. Presented with acute collapse, weakness, pale MM. UTD on vx. The PE revealed she was in shock *(temp 97.8F, HR 120, RR 44/min, CRT <2sec). Pale pink mm, distal pulse not palpable. There was a mid-abominal mass in capsule of spleen. Upon necropsy there was mult masses in the spleen, thoracic, and abd. cavities. The liver had variable masses throughout. Kidney had masses (focal), and poinpoint masses on omentum. the lungs also had pinpoint masses.There was also a mass on the R auricle of the heart--> metastisis to pericardial sac--> 100mL of fluid in there. Why was the animal pale and icteric? What do you think is going on?pale and icteric because liver masses (=liver probs), blood was being lost/going to other places so pale. This ended up being a hemangiosarcoma which has metastisized. Difficult to tell if started in heart or spleen, but they think spleen was the original site.
CASE 2: F spayed feline, 13yo presented for lethargy and anorexia. She was euthanized (owners had no money). Necropsy showed KIDNEYS had very thin cortices which were irreg and firm. Some pallor on kidney, right around brim of pelvis. Also bile duct is VERY tortuous and dilated and then there was a cholelith about a cm before it entered papilla of duodenium. On liver, lobular pattern! and the bile ducts were with rim of CT around them. What's the main problem with this cat?Well, most old cats have kidney problems-- the signs here are of chronic kidney dz. However, the liver stuff was NOT normal/common for older cats. The fibrosing bile canniculi and the tortuous/dilated bile duct go along with obstruction, which is explained by the cholelith. So, the problem was more likely to be a chronic inflammatory dz of the hepatic ducts due to cholelithiasis (rare!)
CASE 3: Golden retriever 7yo, M. a week prior to presentation, dog had sx for FB (resection/anastomosis). a week later, the dog deteriorated with hemorrhagic diarrhea, seizures, and hematemesis. Fluid in abdomen and fluid filled structure in Cr. ventral abdomen noted. Upon necropsy there was multiple intestinal adhesions, areas of hemorrhage and adhesions to surface of pancreas and inside pancreas (was very red). What happened?Hemorrhagic diarrhea, seizures, and hematemesis can all be explained by HEMORRHAGIC PANCREATITIS. This can occur as a complication to surgery if the pancreas is handled too much--> it sets off enzymes and and inflammatory processes within it
CASE 4: Siberian husky, 4mo. Presented for presumptive dx of a portosystemic shunt. The ultrasound revealed a intrahepatic shunt, and a laparatomy sx was performed (Placed catheter in the vessel coming from spleen, and put ligature around it). Shortly after the sx the abdomen became filled with a clear thin fluid. Liver is consistent with appearance of a very small pale liver (not surprising, already diagnosed PSS would cause this). In the Prox 1/3 of sm int there was a deep red discoloration and thickening of mucosa, contents pure red. What happened?Animal had a shunt, shunt was fixed (not completely occluded but made much smaller)... but the narrowing of the shunt caused severe hypertension, which caused ascites to leak into the abdomen. Also this hypertension could have caused leakage/forceage of RBCs into sm. int. Put it all together and you get “acute portal hypertensive syndrome” is a risk associated with the surgery. Usually happens with complete ligation but can happen with partial ligation like this situation. Liver is not well perfused enough to suddenly handle the higher load of fluid, and there is resuling portal hypertension leading to fluid leakage and pressure issues
CASE 5: Guinea fowl, F, mature. Presented weak and the sudden death (not really CSs), she was in active egg production, presented dead for necropsy. Necropsy showed she had lots of fat reserves. L liver lobe was partially circumscribed with a blood clot, and several smaller clots near liver lobe. Liver had pale tan to yellow discoloration. What happened?RUPTURE OF FATTY LIVER! Fatty liver is very common in commercial laying hens and It easily ruptures, which causes them to bleed and die. because of their high canola/rapeseed diets they get lots of fat stores, and then the constant laying of eggs requires the fat to be mobilized through the liver.
CASE 6: Layer hen, sure. Submitted for necropsy. Pale viscera...lots of fat. She had been laying. Obvious thing is a pale friable liver with a large blood clot attached. What do you think is going on?Condition called fatty liver hemorrhagic syndrome... usually fat hens in full production, often egg in oviduct, open up and find a huge blood clot in liver and maybe other small hemorrages in the liver. Pathogenesis is uknown, might be related to fat in liver strain reticular framework.. no tx, reduce energy in feed and give them some exercise. Other than that, speculation about hormonal issues and genetics. Only black hens were being affected so maybe genetic component?

Week 6

Question Answer
CASE 1: holstein-fresian bovin, 1yo. presented with progressive severe ataxia and hypermetria (exaggerated mvts) of 10 day duration. She has been kept on rye pasture with 10-15 other heifers. Clinical signs began after a bull attempted to mount her. Upon necropsy, it was seen that her T5-T6 vertebrae was double regular size. Spinal cord was lateral and dorsal to where it should have been, and was stenotic. What is up?spinal cord lesion in thoraco-lumbar area... she has abnormal vert. the damage probably started in utero then, and the mounting pushed the abnormal vert too far and caused damage, perhaps? DDX: spinal cord trauma, vert. body abscesses, microfracture or vert, listeriosis?
CASE 2: 5yo male boxer presented with neurological signs- ataxia, lateral recumbancy, possible seizures. Inguinal region with cluster of petchial brain, SC, there was cerebellar herniation though foramen magnum. Bisected brain, lesions were roughly symmetrical. What are some possible causes of this?Keep in mind ehrlichia stuff, maybe GME, maybe fungal shed keep on her list. No really CBC abnormalities so that's off. Hemorrhages in cerebrum and caudal brain stem. It was a vasculitis (necrosis of vessels of cerebellum) no bact or fungi found, no neospora or toxoplasma . Cause of vasculitis was not determined.
CASE 3: kitten with thoracolumbar paralysis, vertebral column abnormalities, fecal incontinence, respiratory distress. Xrays said there were sig abnormalities in vert. Column before being euthanized. what are some possible causes to think about?Dissected out the cord. Loss of vascular pattern, softening of cord, compression of cord. Don't know what caused problem, prolly genetic, or sthing dam was exposed to in utero. Had abnormalities of spine (lordosis, scoliosis and kyphosis)... misshapen spinal canal causing compression on cord causing secondary problems. Exact cause unknown. Seen in cats from time to time. Perhaps kitten was positioned abnormally in mom?--> myelomalasia
CASE 4: male castrated dog presented with acute onset of pain that was progressive. There was inappetance, tetraparesis, L hemiplegia, pain sensation. Mentation and cranial nerves were normal. The neuro lesion was determined to be between C1-6. Necropsy found at C4-5 there was a small deficit in the CT over the intervertebral disk space. Corresponding white lesion attached to the dura and impinging on the SC. What are you thinking?probably some sort of disk dz

Week 7

Question Answer
CASE 1: Red angus calf found dead in pasture. On necropsy, there were several places where there were black, wet muscles, and fibrin on the surface of the heart. What's going on?BLACKLEG! This is a clostridium chauvoei infection which is fairly common in food animals. There might also be crepitence. can be wet or dry black lesions. Classic case is "animal found dead"
CASE 2: Mastiff, 2yo F intact. She was bitten by a snake, collapsed, and presented to critical care-- ventral edema, died from cardiac arrest. Creatinine: 10, BUN: 200. Hyperphosphatemia, hyperkalemia. Explain what happens to certian organs in envenomationresult in mm necrosis, renal dz, and can also cause coagulopathies (hemorrhage resulting). KIDNEY: Hemorrhage and edema. L and R kidney the same-- capsule was hard to remove, with a mottled appearance. Pinpoint tan lesions, roughly 1 m throughout all capsule. On cortex, see more multicfocal regions of tan and red pinpoint. Found white streaks in the medulla. Pelvises of kidney dilated--> prolly hydronephrosis. Makes sense bc she was azotemic with BUN 200. hyperphosphatemia and hyperkalemia but urine output adequate. UB-> mucosal surface 1mm raised tan circular lesions surrounded by dark red rim. Most likely polypoid cystits.. also edema on v aspect of abdomen and vulva edema too...prolly had protein losing nephropathy, could have been to snake snake bite. (affect depend on snake, but some snakes have potent toxins which cause tissues necrosis. Very acute condition. Most probs from snake bite. Also had severe renal dz/damage to tubules bc of snake venom. Some hemorrhage could have been due to coagulopathies from venom.
CASE 3: Lab retriever, was a healthy hunting dog which was doing routine exercise and then collapsed and was dead within seconds. Necropsy found near thoracic index a geiser of blood. Blood in pericardial sac, so tamponade, but no hemangiosarcoma to be found. White foci on endocardial surface of ventricle...and then more white foci throughout wall of myocardium. On valve there was yellow nodular material. Granuloma in there, necrotic pinkish center. Histo revealed cellular infiltrate...predom cells are eosinophils and lymphocytes. What do you think the problem is, and the cause?probably Eosinophilic graunlomatous myocarditis. The exact cause was not determined, but most likely a fungus or some sort of protozoa (toxo, leish, chagas)
CASE 4: American paint horse, M castrated and 8yo. Hx of colon impaction which resolved after tx. A while later there was swelling in the laryngeal region with a RETROPHARYNGEAL abscess which developed after NG intubation. At necropsy, found a large area containing food and purulent exudate between eso and trach. Larynx prominent swelling on L epiglottic fold...and loss of continuity near where eso diverges... greenish brown discoloration of mm/fascia on both sides. Congestion and firinous exudate on gutteral pouch. Swelling of trachea...10-12mm thick swelling. On microscopy, lots of exudate, fibrin, neutrophils, and bact (cocci) prolly streptococcus. What do you think?NG intubation causes problems sometimes in horses