Glossary of Cardiovascular Pathology
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- 3 most common cardiac anomalies in dog
- PDA
pulmonic stenosis
aortic stenosis
- 5 most common cardiac anomalies in cat
- AV septal defects
AV valve dysplasia
endocardial fibroelastosis
PDA
aortic stenosis
- 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
- 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
- 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.
- 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
- 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
- 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
- aortic stenosis: lesions
- -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
- 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
- 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
- tetralogy of Fallot: 4 lesions
- IVSD
pulmonic stenosis
overriding aorta
R ventricular hypertrophy
- 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
- truncus arteriosus
- “aorta” overrides both ventricles & receives blood from both
- 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
- PRAA: 4 components of ring
- dorsally: ligamentum arteriosum
left: pulmonary a.
right: aorta
ventrally: base of heart
- PRAA: pathogenesis
- -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
- portacaval shunts: pathogenesis
- 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
- congenital portacaval shunts: locations (large vs. small breed dogs)
- 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
- congenital portacaval shunts: lesions
- hypoplastic liver (small; mild lesion)
collateral vessels widely dilated
may have ammonium biurate crystals in urine
- acquired portacaval shunts: location
- more than 1 vessel involved --> multiple shunts around liver
- acquired portacaval shunts: pathogenesis
- 2º to marked hepatic vascular resistance (ex. cirrhosis, hepatic neoplasia)
severe liver lesion --> marked hypertension --> development of collateral paths around liver
- 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. ↑
- 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. ↑
- portacaval shunts: clinical signs
- -weight loss/↓ weight gain
-hepatoencephalopathy: head pressing, snapping, biting, circling, lethargy, etc. d/t ↑ ammonia, hypoglycemia
- Why is BUN decreased with portacaval shunts?
- ammonia not entering liver --> not being converted to BUN
- Absence of hyperbilirubinemia w/ concurrent evidence of liver dz in young animal is VERY suggestive of what?
- portacaval anomaly
- 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?)
- valvular dysplasias
a. signalment
b. lesions - a. pigs, also dogs, cats, horses
b. abnormal valves: missing or partially missing, thick (defective)
- 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
- causes of petechiae
- -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)
- etiologies for hemopericardium
- Neoplasia, Cu def., HBC, HSA
- etiologies for hydropericardium
- Neoplasia, CHF, liver dz, glomerular dz
- ddx for hemopericardium
- -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)
- Transudate
a. SG
b. protein
c. color
d. cells - a. < 1.018
b. < 2.5 mg/dl
c. clear
d. few
- 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
- 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
- 4 main causes of edema
- dec. colloidal osmotic pressure
inc. hydrostatic pressure
inc. vascular permeability
lymphatic obstruction
- 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
- causes of inc. hydrostatic pressure
- CHF
neoplasia of pericardium or heart
- causes of lymphatic obstruction
- neoplasia, lymphangitis
- causes of inc. vascular permeability
- toxic, infectious
- dx of HSA
- Clin Path: regenerative anemia, acanthocytes, schistocytes, nRBCs
episodes of weakness
DON'T see sarcoma cells exfoliate into body cavity effusions (only lymphomas, carcinomas exfoliate)
- 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)
- What are some etiologies of cardiac mineralization?
- 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
- 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
- endocarditis: 2 locations
- valvular (common)
mural (uncommon)
- What are the most common valves affected by endocarditis & what are the effects?
- L AV valve most common (emboli --> aorta --> various organs)
R AV or R semilunar most common in cows (pulmonary emboli)
- valvular endocarditis: pathogenesis
- 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
- 2 major problems assoc. w/ valvular endocarditis
- valvular insufficiency
source of emboli (septic or bland)
- what is mural endocarditis?
- inflammation of endocardium lining the walls of heart chambers
- What are some etiologies of mural endocarditis?
- jugular catheter, esp. if it enters R atrium
atrial thrombosis: CATS, dogs, cattle
-cats: saddle thrombi as part of CM
dog: uremia, mucoarteritis, vasculitis
- Endocarditis
a. 2 clinical findings
b. 2 clin path findings - a. fever (of unknown origin), murmur
b. monocytosis, leukocytosis
- possible causes of myocardial infarct in dogs
- endocarditis: emboli lodge in coronary a.
CM
atherosclerosis (d/t hypothyroidism)
GDV
anomalies that may have thrombi shed
- what are the lesions assoc. w/
a. hypertrophic CM
b. dilated CM - a. thick walls, rigid structure, cats primarily
b. thin walls, flabby structure
- What non-cardiac lesions are assoc. w/ feline hypertrophic CM?
- aortic thromboemboli (saddle)
renal infarcts
pulmonary congestion + edema
- What can cause dilated CM in cats?
- taurine deficiency
- What type of CM is most common in dogs?
- dilated
- signalment for dilated CM in dogs
- common in dogs < 5 yo (Doberman, giant breeds, Boxer, Cocker, M > F)