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 (“leakyâ€) --> ↓ 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)