cardiovascular path 3

Question 1

The most common congenital heart anomalies are:
- for dog, cat, cattle

Answer 1

• Dog: PDA, pulmonic stenosis, subaortic stenosis
• Cat: left AV valvular dysplasia
• Cattle: Ventricular septal defect, aortic transpositions

Question 2

Patent ductus arteriosus (PDA)
- what is it? origin?
- result?

Answer 2

• A duct connecting the ascending aorta and pulmonary artery, where they cross just proximal to the aortic arch
• In fetuses, the ductus arteriosus shunts blood from the pulmonary artery to the aorta, so that the blood bypasses the lungs. It usually closes soon after birth, but may remain open (patent) for a week or two in normal foals.
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• blood is shunted from the aorta (high pressure) to the pulmonary artery (low pressure), resulting in a volume overload on the left atrium and ventricle, with pressure overload on the pulmonary artery
• With time, some cases develop increased resistance to blood flow through the lung— the pulmonary arterioles hypertrophy and won’t let blood through easily
  > This leads to pulmonary hypertension.
  > Then, blood flow can reverse direction, i.e. from the pulmonary artery into the aorta.

Question 3

Atrial septal defects - significance

Answer 3

• usually of little functional importance
• normal within the first week or two of life

Question 4

Ventricular septal defect
- what is it?
- effects?
- progression?

Answer 4

• hole in the interventricular septum, usually up near the valves but occasionally down near the apex.
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• volume overload on the right ventricle, pulmonary circulation, and left atrium and ventricle
  > In addition, the right ventricle may have a pressure overload, depending on the size of the ventricular septal defect
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• Thus, we expect eccentric hypertrophy of the left ventricle, and either eccentric or concentric hypertrophy of the right ventricle
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• As for PDA, these begin as left-to-right shunts, VSD can rarely progress to right-to- left shunts if there is increased resistance to blood flow through the lung.

Question 5

Subaortic stenosis (SAS)
- who?
- why?
- effects
- significance
- secondary lesions

Answer 5

• Newfoundland, boxer, and German shepherd dogs
• developmental abnormality
• clinical signs or death at 6 months or older
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• white fibrous band thickening the endocardium of the left ventricle, just proximal to the aortic valve > stenosis of outflow > pressure overload > left ventricular concentric hypertrophy
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• one of the more frequent causes of sudden death in young dogs, and of anesthetic-associated death at the time of spay/ neuter
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• Turbulent blood flow after the stenosis can cause secondary lesions:
  > endocarditis of the aortic valve (turbulence and trauma to the endothelium predisposes to bacterial colonization)
  > post-stenotic dilation of the proximal aorta

Question 6

Pulmonic stenosis
- forms
- sequelae
- breeds

Answer 6

It can be:
* valvular, in which malformation of the valve causes narrowing of the pulmonic outflow tract, OR
* subvalvular, in which a white fibrous band or a band of muscle located in the ventricle (just proximal to the valve) causes narrowing of the outflow tract
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Sequelae:
- right ventricular concentric hypertrophy.
- There may be post-stenotic dilation of the pulmonary artery
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- Beagles, bulldogs or Chihuahuas are most frequently affected.

Question 7

hemangiosarcoma in dogs
- typical presentation
- effects

Answer 7

• red, white, or mottled masses, usually affecting the right auricle
• In a dog, any red mass on the right atrium or auricle is likely to be hemangio-arcoma
• Rupture causes hemopericardium and cardiac tamponade
• Rupture of lung metastases cause hemothorax.

Question 8

Heart base tumours
- what are they?
- most common?
- effects

Answer 8

• neoplasms in the soft tissue dorsal to the heart, in the neighbourhood of the aorta and pulmonary artery
• aortic body tumour is the most common
  > The normal aortic body is a mass of neuroendocrine tissue in the wall of the aorta, which regulates blood oxygen levels
  > more common in brachycephalics due to chrnoic hypoxemia
  > usually benign, but form an expansile mass that may cause heart failure because they obstruct filling of the atria.

Question 9

reaction of vessels to injury
Endothelial cells:

Answer 9

• Normally have anticoagulant action through production of prostacyclin, thrombomodulin, plasminogen activator
  > inflammation induces procoagulant (thrombus-inducing) activity by endothelial cells
• Secrete leukocyte chemoattractants, and express adhesion molecules important for leukocyte migration and platelet function

Question 10

Consequences of endothelial injury

Answer 10

• tissue edema > Water leaks out of damaged blood vessels
• thrombus formation > Plasma leaks into the damaged vessel wall where it contacts collagen in the subendothelial basement membrane
  > seen histologically as fibrinoid material, sign of vascular damage
• hemorrhage > leakage of erythrocytes from damaged vessels > typically petichiae or ecchymoses (as opposed to hematomas)

Question 11

arteritis vs phlebitis

Answer 11

inflammation that targets arteries (arteritis) or veins (phlebitis)

Question 12

Some diseases in which vasculitis is an important to the pathogenesis include:

Answer 12

• Equine viral arteritis
• Hemophilus somnus encephalitis and myocarditis: vasculitis causes infarcts and inflammation in brain and myocardium
• Erysipelas rhusiopathiae infection in pigs: infarcts + inflammation in skin, kidney
• Feline infectious peritonitis: vascular leakage → protein-rich exudates
• Malignant catarrhal fever
• Heartworm disease
• Strongylus vulgaris larval migration → cranial mesenteric arteritis with thickening and roughening of the intima, thrombosis, embolism→ intestinal ischemia causing colic
• Immune-mediated vasculitis
• Drug reactions

Question 13

Arteriosclerosis
- what is it
- effects and significance

Answer 13

• fibrosis (sclerosis, or hardening) of the tunica intima of arteries
• This may cause loss of elasticity, and narrowing of the lumen.
• However, it is often an incidental finding of no consequence

Question 14

Atherosclerosis
- what is it

Answer 14

• deposition of lipid in the wall of large arteries
• uncommon in domestic animals
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• deposition of lipid and lipid-laden macrophages in the arterial wall, which stimulates formation of fibrous tissue, smooth muscle proliferation, and mineralization of vessel walls
• can narrow arterial lumen, cause infarction
• seen occasionally in psittacines
• occasionally seen connected with hypothyroidism in dogs > hypercholesterolemia and altered lipid metabolism

Question 15

Arterial mineralization
- location, lesions
- sequelae
- casues

Answer 15

• calcification, typically in aorta
• Grossly, mineralized arteries are hard, brittle, and gritty; or contain gritty plaques. These are prone to rupture, which causes massive blood loss.
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  Causes:
• “Metastatic” mineralization due to hypercalcemia:
  > vitamin D toxicity
  > iatrogenic (“Downer D”, cows)
  > vitamin D-containing rodenticide toxicity in dogs
  > toxic plants that contain vitamin D-like substances
  > chronic debilitating &/or granulomatous diseases (Johne’s disease, rarely in blastomycosis).
• “Dystrophic mineralization” due to vascular damage; eg. damage to the cranial mesenteric artery of horses caused by Strongylus vulgaris larvae.

Question 16

Arterial Rupture
- seen mostly when?

Answer 16

• horses: aortic rupture > sudden death
  > often during races

Question 17

Aneurysm
- what is it?
- issues?
- causes?

Answer 17

• a localized dilatation or out-pouching of an artery due to thinning and weakening of the wall
• prone to rupture
• uncommon in domestic animals
  > may be caused by Strongylus vulgaris larval migration in horses, or Spirocirca lupi infection of dogs in tropical countries

Question 18

thrombosis
- causes

Answer 18

• A blood clot that forms inside one of your veins or arteries
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• Injury to endothelial cells: vasculitis and vascular necrosis (see above), turbulent blood flow (eg cardiac anomalies such as subaortic stenosis or ventricular septal defect), uremia, endotoxemia
• Stasis of blood flow: cardiogenic shock due to heart failure, immobility (eg. human geriatrics, or long air flights), polycythemia
• Hypercoagulable states:
  > severe inflammation (cytokines stimulate endothelial cells and platelets)
  > glomerular disease (loss of antithrombin)
  > corticosteroid therapy
  > malignant neoplasia (neoplastic cells express tissue factor)

Question 19

embolus
- causes

Answer 19

• A blood clot that forms in a blood vessel in one area of the body, breaks off, and travels to another area of the body in the blood
  > can lodge itself in a blood vessel
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• Bacterial endocarditis of cardiac valves
• Jugular thrombosis as a sequel to jugular catheters or administration of irritant drugs
• Liver abscesses (in feedlot cattle as a sequela to rumen acidosis)

Question 20

Disseminated Intravascular Coagulation (DIC)
- Inciting causes
- pathogenesis
- lesions
- sequelae
- lab indicators

Answer 20

Causes:
* Endotoxemia and sepsis
* Malignant neoplasia
* Glomerular diseases: thrombosis is due to loss of antithrombin from the blood
* Viral or immune-mediated injury to endothelium
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- widespread, unregulated activation of coagulation
> thrombus formation in small venules throughout the body, which depletes clotting factors and platelets (and over-activates the fibrinolytic system)
> The depletion of clotting factors and platelets causes a “consumptive coagulopathy” that results in widespread petechial or ecchymotic hemorrhages.
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Lesions:
* Fibrin thrombi in small venules in many organs, most easily seen in lung, occasionally kidney, and elsewhere
* Petechial or ecchymotic hemorrhages throughout the body.
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Sequelae:
* Ischemia and infarcts: microscopic thrombi form in multiple organs and obstruct the arterial supply or the venous drainage, leading to ischemic damage and/or edema. This most often affects the kidney, heart, brain and lung.
* Coagulopathy, leading to disseminated hemorrhages in skin, mucus membranes
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Laboratory indicators of DIC: thrombocytopenia, prolonged APTT and PTT, increased levels of fibrin degradation products.

Question 21

Hemangiosarcoma
- what animal, what is it
- primary sites
- lesions
- behaviour

Answer 21

• Very common malignant tumour of dogs, derived from endothelial cells
• Primary sites: right atrium, spleen, skin
• Lesions: masses are usually red and blood- filled, but can be solid and white or mottled
• Behaviour: hemangiosarcoma is often clinically silent until the atrial, splenic or lung mass ruptures to cause fatal hemorrhage. Visceral hemangiosarcoma metastases readily to liver, lung and omentum. Metastases often form red-black round “cannon ball” nodules.