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59 Cards in this Set
- Front
- Back
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3 most common cardiac anomalies in dog
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PDA
pulmonic stenosis aortic stenosis |
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5 most common cardiac anomalies in cat
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AV septal defects
AV valve dysplasia endocardial fibroelastosis PDA aortic stenosis |
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PDA
a. lesions b. clinical signs |
a. PDA, cardiomegaly, L & R sided dilation
b. exercise intolerance, poor wt. gain & growth, machinery murmur, dyspnea, orthopnea, tachypnea, asymptomatic |
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PDA
a. signalment (dogs) b. px |
a. poodles (mini, toy), saluki, GSD, sheltie, collie, Pomeranian, F 2x > M
b. -excellent w/ early surgical correction of L --> R shunt - R --> L shunt --> hypoxia, cyanosis, polycythemia |
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PDA
a. direction of shunt b. result of shunt |
a. L --> R
b. L --> R shunt --> ↓ CO to general circulation, ↑ workload of L heart d/t ↑ flow to L side --> L atrial & ventricular dilation --> R ventricular dilation & hypertrophy may occur d/t back pressure caused by ↑ blood flow into pulmonary a. --> ↑ resistance to pumping by RV - may have an aneurismal dilation of aorta d/t turbulence at site of defect - can also have dilation of a segment of pulmonary a. |
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pulmonic stenosis
a. signalment b. locations c. px |
a. inherited in beagles; seen in other dogs & cats
b. subvalvular (pre), valvular (most common), supravalvular (post) c. varies w/ severity of defect |
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pulmonic stenosis
a. lesions b. clinical sign |
a. compensatory RV hypertrophy d/t ↑ workload of RV trying to pump blood thru stenotic opening
-congestion of liver (CPC: chronic passive congestion), hypertension in liver --> ascites --> R sided heart failure -aneurysm to saccular dilation of pulmonary a. distal to stenosis, jet lesion: d/t blood going thru narrow lumen under ↑ force --> moves faster --> crashes against opposite wall --> turbulence & trauma b. ↓ oxygenation of blood --> exercise intolerance |
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aortic stenosis
a. signalment b. locations c. px |
a. Newfies, golden retriever, GSD, rottie, boxer
- may be detected in older dogs w/o prior problems b. -supravalvular: rare in dogs, most common location in cats -valvular -subvalvular: most common location in dogs c. varies w/ severity of defect |
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aortic stenosis: lesions
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-LV hypertrophy d/t ↑ workload caused by ↓ outflow
-may get dilated sac distal to senosis, aortic aneurysm, jet lesion -pulmonary edema d/t L sided CHF -secondary endocarditis -sudden death sometimes occurs d/t infarction & myocardial necrosis |
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IVSD
a. signalment b. location c. lesions |
a. most common cardiac anomaly in horses & cattle
-dog: English bull dog, Keeshond b. most commonly, hole is subaortic: below aortic semilunar valves is a hole that exits just below right AV valve c. depends on size of defect & duration -L & R ventricular hypertrophy -jet lesion: R ventricle opposite defect -thickened, roughened L & R ventricular endocardium -endocardial fibrosis from turbulence in LV |
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interatrial septal defect (patent foramen ovale)
a. signalment b. lesions c. px |
a. common in pigs & cats
b. depends on size of defect -if open, flow is L --> R --> overworks R heart --> exercise intolerance d/t ↓ CO to general circulation -R atrial & ventricular hypertrophy & dilation c. small defect may be subclinical |
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tetralogy of Fallot: 4 lesions
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IVSD
pulmonic stenosis overriding aorta R ventricular hypertrophy |
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tetralogy of Fallot
a. signalment b. prevalence c. signs d. direction of shunt & effect |
a. keeshonds, horses (arabs) cattle
b. most common cyanotic anomaly in domestic animals (though not common overall) c. dyspnea, cyanosis d. shunt is R --> L (probably d/t pulmonic stenosis) --> RV hypertrophy --> severe cyanosis (little blood getting to lungs) --> 2º polycythemia |
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truncus arteriosus
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“aorta” overrides both ventricles & receives blood from both
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persistent right aortic arch (PRAA)
a. signalment b. signs c. px |
a. young animals post-weaning, esp. GSD, Irish Setters
b. GI signs d/t megaesophagus: wt. loss, regurgitation shortly after eating solid foods (see post-weaning), aspiration pneumonia c. guarded; esophageal malfunction may persist; aspiration pneumonia may occu |
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PRAA: 4 components of ring
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dorsally: ligamentum arteriosum
left: pulmonary a. right: aorta ventrally: base of heart |
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PRAA: pathogenesis
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-aorta normally arises from LEFT 4th aortic arch & thus is on LEFT of trachea & esophagus
-w/ this anomaly, aorta is on RIGHT side of trachea & esophagus & is connected to pulmonary a. by a long fibrous stalk (ligamentum arteriosum) --> complete circle around trachea & esophagus --> esophageal stricture forms --> megaesophagus cranial to stricture |
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portacaval shunts: pathogenesis
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portal v. drains GI tract & contains lots of ammonia which was to be delivered to liver for detox & conversion to urea
w/ anomaly, ammonia dumped into caudal vena cava & directly to heart & pumped out into general circulation |
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congenital portacaval shunts: locations (large vs. small breed dogs)
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large breed dogs: intrahepatic shunts more common (patent ductus venosus: most common)
small breed dogs: extrahepatic shunts more common can have atresia of portal vv. w/ collateral portosystemic shunts |
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congenital portacaval shunts: lesions
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hypoplastic liver (small; mild lesion)
collateral vessels widely dilated may have ammonium biurate crystals in urine |
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acquired portacaval shunts: location
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more than 1 vessel involved --> multiple shunts around liver
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acquired portacaval shunts: pathogenesis
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2º to marked hepatic vascular resistance (ex. cirrhosis, hepatic neoplasia)
severe liver lesion --> marked hypertension --> development of collateral paths around liver |
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acquired portacaval shunts: Clin Path data
a. liver enzymes b. ammonia c. BSP excretion time d. bilirubin e. BUN f. bile acids |
a. ↑
b. ↑ c. ↑ d. ↑ (icterus) e. ↓ f. ↑ |
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congenital portacaval shunts: Clin Path data
a. liver enzymes b. ammonia c. BSP excretion time d. bilirubin e. BUN f. bile acids |
a. N
b. ↑ c. ↑ d. N (no icterus) e. ↓ f. ↑ |
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portacaval shunts: clinical signs
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-weight loss/↓ weight gain
-hepatoencephalopathy: head pressing, snapping, biting, circling, lethargy, etc. d/t ↑ ammonia, hypoglycemia |
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Why is BUN decreased with portacaval shunts?
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ammonia not entering liver --> not being converted to BUN
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Absence of hyperbilirubinemia w/ concurrent evidence of liver dz in young animal is VERY suggestive of what?
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portacaval anomaly
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endocardial fibroelastosis
a. signalment b. prevalence c. lesions d. cause |
a. cats (Burmese), dogs, pigs, cattle, turkeys
b. rare c. thick white glistening endocardium, esp. LV, d/t ↑ fibrous & elastic tissue (late lesion) d. unknown (congenital defect in lymphatics?) |
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valvular dysplasias
a. signalment b. lesions |
a. pigs, also dogs, cats, horses
b. abnormal valves: missing or partially missing, thick (defective) |
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serous atrophy of epicardial fat
a. lesions b. causes c. why is it not seen w/ cancer cachexia? |
a. gelatinous, grayish, shiny translucent: thru this semiclear mucinous degeneration you should be able to see blood vessels that aren’t normally visible
b.malnutrition: fat mobilized from all over body -malnutrition comes from variety of causes: poor quality nutrition, lack of food, parasites, ↑ demands w/ inadequate intake (pregnancy, lactation, work) c. NOT seen w/ cancer cachexia b/c MUSCLE, not fat, is mobilized 1st |
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causes of petechiae
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-blood vessel problem (vasculitis)
-systemic infections (blackleg dz) -vasculitis (RMSF, MCF) -uremia: vascular lesion + platelet defect -pigs: mulberry heart dz, gut edema dz (d/t E. coli toxin) -platelet problem: thrombocytopenia or qualitative defect -DIC -bleeding defect: platelet or vessel problems (ITP, tick borne) |
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etiologies for hemopericardium
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Neoplasia, Cu def., HBC, HSA
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etiologies for hydropericardium
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Neoplasia, CHF, liver dz, glomerular dz
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ddx for hemopericardium
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-RA tears or ruptures: idiopathic (dogs)
-aortic rupture: idiopathic (horses) -trauma: neoplasia, HBC, cardiac puncture, foreign body -HSA: RA is common location in dogs -CM (cats) |
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Transudate
a. SG b. protein c. color d. cells |
a. < 1.018
b. < 2.5 mg/dl c. clear d. few |
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Modified Transudate
a. SG b. protein c. color d. cells |
a. > 1.018
b. > 2.5 mg/dl c. amber or pink, clear to slightly turbid d. few |
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Exudate
a. SG b. protein c. color d. cells |
a. > 1.018
b. > 2.5 mg/dl c. turbid to opaque d. many inflammatory cells |
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4 main causes of edema
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dec. colloidal osmotic pressure
inc. hydrostatic pressure inc. vascular permeability lymphatic obstruction |
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causes of dec. colloidal osmotic pressure
fluid type? |
pure transudate
severe glomerular dz (or amyloidosis) --> low serum protein cachexia: low protein GI dz: malabsorption, parasitism --> PLE liver dz: ↓ synthesis of albumin |
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causes of inc. hydrostatic pressure
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CHF
neoplasia of pericardium or heart |
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causes of lymphatic obstruction
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neoplasia, lymphangitis
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causes of inc. vascular permeability
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toxic, infectious
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dx of HSA
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Clin Path: regenerative anemia, acanthocytes, schistocytes, nRBCs
episodes of weakness DON'T see sarcoma cells exfoliate into body cavity effusions (only lymphomas, carcinomas exfoliate) |
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What is the significance of
a. hemosiderin b. platelets in pericardial fluid? |
a. indicates hemorrhage has been there for a while
b. indicates blood contamination (should be NO platelets w/ hemoabdomen or hemothorax) |
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What are some etiologies of cardiac mineralization?
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white muscle dz: look for lesion in other (active) muscles
uremia: ↑ Ca x P vitamin D toxicity hypercalcemia: hypercalcemia of malignancy, renal failure brain-heart syndrome CNS lesion or massive trauma elsewhere in body --> mineralization in myocardium idiopathic |
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endocardiosis
a. species b. lesion c. functional effect |
a. dog
b. glistening, thick AV valves (rarely semilunar), nodular, white c. valves become incompetent (“leaky”) --> ↓ volume of blood pumped into next chamber --> ↓ CO --> heart failure |
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endocarditis: 2 locations
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valvular (common)
mural (uncommon) |
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What are the most common valves affected by endocarditis & what are the effects?
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L AV valve most common (emboli --> aorta --> various organs)
R AV or R semilunar most common in cows (pulmonary emboli) |
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valvular endocarditis: pathogenesis
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endothelial injury: parasites, IV catheter (jugular), anomaly (ex. IVSD)
platelets & fibrin adhere to endothelium --> growth of clot (expansion of fibrinous exudate into a wartlike lesion) septicemia: inoculation of bacteria into this mat of fibrin & platelets |
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2 major problems assoc. w/ valvular endocarditis
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valvular insufficiency
source of emboli (septic or bland) |
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what is mural endocarditis?
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inflammation of endocardium lining the walls of heart chambers
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What are some etiologies of mural endocarditis?
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jugular catheter, esp. if it enters R atrium
atrial thrombosis: CATS, dogs, cattle -cats: saddle thrombi as part of CM dog: uremia, mucoarteritis, vasculitis |
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Endocarditis
a. 2 clinical findings b. 2 clin path findings |
a. fever (of unknown origin), murmur
b. monocytosis, leukocytosis |
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possible causes of myocardial infarct in dogs
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endocarditis: emboli lodge in coronary a.
CM atherosclerosis (d/t hypothyroidism) GDV anomalies that may have thrombi shed |
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what are the lesions assoc. w/
a. hypertrophic CM b. dilated CM |
a. thick walls, rigid structure, cats primarily
b. thin walls, flabby structure |
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What non-cardiac lesions are assoc. w/ feline hypertrophic CM?
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aortic thromboemboli (saddle)
renal infarcts pulmonary congestion + edema |
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What can cause dilated CM in cats?
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taurine deficiency
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What type of CM is most common in dogs?
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dilated
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signalment for dilated CM in dogs
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common in dogs < 5 yo (Doberman, giant breeds, Boxer, Cocker, M > F)
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