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59 Cards in this Set

  • Front
  • Back
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)