Pathology of the Cardiovascular System Flashcards

1
Q

What are the 4 normal functions of the heart?

A
  1. maintain adequate blood flow (cardiac output)
  2. delivery oxygen, nutrients, and hormones to peripheral tissues
  3. remove carbon dioxide and other metabolic waste products
  4. maintain normal thermoregulation and glomerular filtration rates —> urine output
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2
Q

What are 5 common compensatory mechanisms available to maintain cardiac function?

A
  1. cardiac dilatation - stretching of cardiac muscle to increase contractile force and stroke volume, necessary to maintain normal cardiac output
  2. myocardial hypertrophy - caused by increased workload
  3. increased heart rate
  4. increase in peripheral resistance - shunts blood from periphery to necessary organs
  5. blood flow redistribution
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3
Q

Normal heart:

A

(thick left ventricle to pump blood to organs and periphery)

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4
Q

Myocardium:

A
  • striated
  • central nucleus
  • intercalated discs
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5
Q

What are the 4 reversible changes in cardiac muscle in response to injury? 2 irreversible?

A

REVERSIBLE
1. vacuolar degeneration
2. fatty degeneration
3. fatty infiltrations (causing atrophy)
4. myocytolysis (partial loss of proteins)

IRREVERSIBLE
1. lipofuscinosis (wear and tear —> common in older animals or cachexic)
2. neoplasia

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6
Q

What are the 4 steps to the general response of cardiomyocytes to injury? What is another possible (but rare) outcome?

A
  1. normal cardiac muscle cells are injured (toxic insult, nutritional deficiency, physical insult, infection)
  2. hyaline necrosis
  3. macrophage invasion
  4. healing with fibrosis, where fibroblasts proliferate, causing scar (connective tissue) formation

regeneration is not common - BM is commonly ruptured, not allowing satellite cells to differentiate into myoblasts, and since connective tissue replaces cardiomyocytes, the heart is left more susceptible to subsequent injury

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7
Q

What is the normal ventricle thickness ratio?

A

1:3 ratio of RV and LV thickness

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8
Q

How does blood flow from the placenta through the fetus?

A

umbilical vein carries oxygenated blood to the fetus and umbilical arteries carry deoxygenated blood to the placenta

  • lungs are developing and do not need as much blood, so the foramen ovale allows atria to communicate and mix blood, and the ductus arteriosus is the only blood supply to the lungs
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9
Q

What does serous atrophy of the heart look like grossly? What is the most common cause?

A

yellow and gelatinous due to fat mobilization
- remember: the coronary groove is usually fatty to protect vessels!

poor nutrition
- dental disease
- insufficient/unbalanced diet
- GI disturbance

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10
Q

Epicardial hemorrhage, cow:

A
  • endotoxemia
  • anoxic/hypoxic
  • terminal hypoxia (stunning, hanging)

(petechia/ecchymosis)

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11
Q

What causes cardiac failure/decompensation?

A

the heart cannot keep up with increased physiological needs and compensatory mechanisms fail

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12
Q

What’s the difference between cardiac syncope and congestive heart failure?

A

CARDIAC SYNCOPE: acute onset of cardiac failure causing collapse and unconscious, commonly caused by abnormal heart rhythm, defective heart valves, etc.

CHF: develops slowly from gradual loss of cardiac output due to pressure or volume overload or myocardial injury

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13
Q

How does congestive heart failure typically manifest in bulls? What is the most common cause?

A

brisket edema, swelling near sternum

increased altitude results in less oxygen in the air, making the heart have to compensate by pumping blood to the lungs —> pulmonary hypertension

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14
Q

Idiopathic pulmonary hypertension leading to CHF, heifer:

A

recovered from severe pneumonia, causing connective tissue to replace and compress pulmonary veins which leads to pulmonary edema and hydrothorax
- blood pools on pulmonary side in the caudal vena cava, which can also cause hepatic congestion (nutmeg liver)

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15
Q

Ascites (hydroperitoneum), dog:

A
  • right-sided CHF
  • hypoproteinemia from renal disease or protein-losing enteropathy
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16
Q

What 4 things are we looking for during a postmortem examination of the heart?

A
  1. shape change - bigger, rounded, ventricle thickness
  2. valves - inflammation
  3. ventricular/atrial communication defects
  4. size of aorta and pulmonary veins
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17
Q

Normal tricuspid valve:

A

(right AV valve)
- thin and transleucent

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18
Q

Mitral valve, chordae tendineae:

A

can rupture with increased pressure due to chest trauma

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19
Q

What do congenital anomalies in the cardiovascular system involve? How does this tend to affect the animal?

A

heart or blood vessels

  • die in utero (stillborn, aborted)
  • present clinical signs after birth, like exercise intolerance, cyanosis, and stunted body growth
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20
Q

What are valvular hematocysts?

A

congenital valvular anomaly that manifests as a nodule filled with blood on/near valves (typically no vessels on valve in adults, since they get nutrition from osmosis)

  • (typically no clinical signs and will disappear with age)
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21
Q

What is the tetralogy of Fallot? In what dogs is it most common? How does it present in humans?

A
  1. ventricular septal defect (opening between RV and LV)
  2. overriding aorta (dextroposition over the septal defect)
  3. pulmonic stenosis
  4. right ventricle hypertrophy
  • Keeshonds
  • English Bulldogs
  • “blue babies” (blood on right side will be pushed to the periphery before it is oxygenated)
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22
Q

What is right ventricular hypertrophy commonly secondary to?

A

pulmonic stenosis - compensatory for pressure overload and to ensure the lungs still get proper blood supply

(prominent RV makes heart seem round)

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23
Q

What does subvalvular aortic stenosis result in?

A

compensatory concentric hypertrophy of the left ventricle and post-stenotic dilation of the aorta (fibrous band constricts aorta)

BLUE = aortic valve
GREEN = fibrous band

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24
Q

In what species is tricuspid dysplasia most common? What does this lead to?

A

cats

valvular insufficiency —> animals usually born dead

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25
Q

What are ventricular septal defects? What does this cause?

A

communication between RV and LV - LV is more powerful, so it pushes blood from LV to RV, causing the RV to overload and undergo hypertrophy which can then push deoxygenated blood into the LV —> cyanosis

  • exercise intolerance
  • heart failure
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26
Q

Ventricular septal defect, calf:

A
  • stunted growth
  • murmur

(view from right ventricle - tricuspid valve)

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27
Q

How can ventricular septal defects affect the endocardium?

A

increased turbulence causes the development of a fibrotic and thickened endocardium —> jet lesions, typically on the right ventricular free wall

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28
Q

Ventricular septal defect, jet lesion, right ventricular free wall:

A

(endocardial fibrosis)

29
Q

What is a patent ductus arteriosus?

A

the fetal ductus arteriosus responsible for bypassing blood flow to the non-functional lungs does not become the ligamentum arteriosus within 1-2 weeks of birth

  • results in blood from the aorta moving into the pulmonary artery which causes right-sided pressure overload and pulmonary hypertension —> issues getting blood into lungs (right sided CHF)
30
Q

How is the aortic arch typically situated with respect to the esophagus? What condition is related to an alteration in the position of the aorta? What does this result in?

A

normally on the left side of the esophagus and trachea

persistent right aortic arch (PRAA) - right aortic arch forms a ring around the esophagus with the ligamentum arteriosus
- dysphagia and megaesophagus, causing affected animals to die of aspiration pneumonia when introduced to solid food

31
Q

Persistent right aortic arch (PRAA), calf:

A
  • megaesophagus
  • aspiration pneumonia
32
Q

What dogs are predisposed to persistent right aortic arch (PRAA)?

A
  • German Shepherds
  • Irish Setters
  • Great Danes
33
Q

What are 3 possible causes of hemopericardium? What does this cause?

A

(blood in pericardial sac)
1. ruptured hemangiosarcoma (common in RA)
2. thoracic cavity trauma (HBC)
3. idiopathic

restricts heart contraction —> improper pumping/filling of blood

34
Q

Hemopericardium, ruptured atrial hemangiosarcoma:

A
35
Q

What is pericardial effusion? What is a common cause of this in pigs?

A

distension of pericardial sac with fibrin-filled fluid

mulberry heart disease (mottled with hemorrhage and palor) caused by malnutrition, specifically vitamin E and selenium deficiencies that allow oxidative damage to cause vasculitis and fluid escape

36
Q

Myocardial degeneration/necrosis and hemorrhage, pericardial effusion, pulmonary edema:

A

vitamin E and selenium deficiency

37
Q

What does fibrinous pericarditis look like grossly?

A
  • roughened, granular epicardium
  • necrotizing emphysema when associated with bacterial infection, like black leg (C. chauvei)
38
Q

Fibrinous pericarditis, steer:

A

black leg

39
Q

How can hardware disease affect the heart? How can this be diagnosed postmortem without opening up the reticulum?

A

cow eats metal, which goes straight to the reticulum and can puncture it and reach the pericardial sac and puncture the diaphragm

feel for adhesion between reticulum and diaphragm

40
Q

Hardware disease, cow

A

thick pericardium —> chronic inflammation

41
Q

What is a common way farmers prevent cows from developing hardware disease?

A

have cows swallow magnets that can collect hardware together and keep it from perforating the reticulum

42
Q

What happens when hardware penetrates both the reticulum and the diaphragm?

A

leakage of ingesta from into the peritoneum, causing fibrin admixed with suppurative exudate in the body cavity

  • if vagus nerve is involved, ruminal atrophy can result
43
Q

Chronic pericarditis, cow:

A

chronic cardiac tamponade
- CT restricts heart movement

44
Q

What are 2 common causes of endocardial mineralization?

A
  1. excessive intake of vitamin D or calcinogenic plants (Cestrum, Trisetum, Solanum) containing vitamin D analogs
  2. occurs in debilitated cattle with Johne’s disease (LA)

(fibrosis and mineralization of endocardium)

45
Q

What is valvular endocardiosis? What is suspected to be the cause? What dogs are most susceptible?

A
  • age-related disease in middle-aged to old dogs (males!) characterized by degeneration of valvular collagen
  • genetically-influenced degeneration of connective tissue
  • Cavalier King Charles Spaniel with 100% prevalence by 10 years of age

(valvular fibrosis, myxomatous/mucoid valvular degeneration)

46
Q

How does valvular endocardiosis look grossly? What does this cause?

A

shorter, nodular cusps (valvular hooding) cause increased pressure and evential rupture of chordae tendineae —> valve flapping (insufficiency)

47
Q

What is the most common cause of congestive heart failure in older dogs?

A

valvular endocardiosis
(thickened cusp/leaflet)

48
Q

Valvular endocardiosis, dog:

A

endocardial fibroelastosis within atrium (jet lesions due to increased turbulence!)

49
Q

What is the most common cause of valvular and mural endocarditis? What 3 things are involved in its pathogenesis?

A

inflammation caused by bacterial infections

  1. endothelial injury
  2. blood turbulence
  3. hypercoagulability
50
Q

What are the 2 causes of death resulting from endocarditis?

A
  1. heart failure secondary to valve dysfunction
  2. bacteremia (septic thrombi formation —> infarcts)
51
Q

How can endocarditis be differentiated from endocardiosis grossly?

A

friable and detachable material on valves (septic thrombi) that cause valvular insufficiency and increased turbulence

(endocardiosis = short, nodular valves)

52
Q

Endocarditis, dog aortic valve:

A

septic thrombi!

53
Q

What are chronic lesions due to endocarditis commonly referred to as? Which valves are most commonly affected?

A

vegetative or verrucous (wart-like) valvular endocarditis

right AV (tricuspid) and aortic valves

54
Q

Valvular bacterial endocarditis, histology:

A
55
Q

What is a common cause of valvular endocarditis in pigs?

A

Erysipelothrix rhusiopathiae infection (diamond skin disease)

-acute heart failure —> sudden death

56
Q

Verrucous valvular endocarditis, pig aortic valve:

A

dry, friable septic thrombi
- can break off into emboli and reach kidney, which causes focal infarction

(Etiology: Erysipelothrix rhusiopathiae)

57
Q

What is characteristic of ulcerative mural endocarditis caused by renal failure?

A

raised plaques of fibrous and mineralized tissue (uremic)

  • nodular, tan to reddish, gritty
58
Q

Uremic (ulcerative) endocarditis, dog:

A

renal failure

59
Q

What is dirofilariasis?

A

Dirofilaria immitis (heartworm) proliferation within the pulmonary arteries and right ventricle (+ RA and cranial/caudal vena cava in heavy infestations) that can lead to CHF and result in endocarditis, endarteritis, and pulmonary thrombosis

60
Q

What are 6 possible causes of myocardial necrosis and mineralization?

A
  1. nutritional deficiencies
  2. chemical and plant toxicities
  3. ischemia
  4. metabolic disorders
  5. inherited disease
  6. physical trauma
61
Q

What are the 4 most common causes of myocardial necrosis and mineralization in veterinary medicine?

A
  1. vitamin E and selenium deficiency (cattle, sheep, pigs)
  2. ionophore toxicity (horses, ruminants) - monesin, lasalocid, etc. antibiotics given to promote feed efficiency and prevent coccidiosis
  3. gossypol toxicity - cotton seed oil (pigs)
  4. uremia (dogs, cats)
62
Q

White muscle disease, calf:

A

vitamin E/selenium deficiency

  • lesions are chalky and have a gritty consistency
  • calf = left side of the heart
63
Q

Nutritional myopathy, lamb:

A

vitamin E/selenium. deficiency

  • white paint brush strokes
  • lamb = right side of the heart
64
Q

How can nutritional myopathy/white muscle disease be visualized microscopically?

A

Von Kossa stains mineralized calcium in degenerated/necrotic cardiac muscle fibers

65
Q

What nutritional myopathy causes myocardial necrosis/mineralization in pigs? What will the heart look like grossly? What can be seen histologically?

A

Mulberry heart disease - vitamin E/selenium deficiency

mottled red and palor

vasculitis - enlarged tunica media makes it difficult to see muscle cells of the artery

66
Q

How does monensin toxicity typically present?

A

(ionophore antibiotic, growth promoter)

  • respiratory signs
  • exercise intolerance
  • CHF: ascites, hydrothorax, nutmeg liver
67
Q

What are cardiomyopathies? What are the 2 types?

A

structural or functional abnormalities of the myocardium

  1. PRIMARY - idiopathic
  2. SECONDARY - clear etiology, specific heart muscle disease
68
Q

What are 3 types of primary cardiomyopathies and in which animals are they most common?

A
  1. dilated - DOG, cat, hamster, turkey, pig, cow
  2. hypertrophic - CAT, dog, rat, pig
  3. restrictive - cat (more rare)
69
Q

What are 8 possible causes of secondary cardiomyopathies?

A
  1. heritable disease - Duchenne-type muscular dystrophy in Golden Retrievers
  2. nutritional deficiencies - taurine deficiency in cats
  3. toxic - doxorubicin (chemo), monensin
  4. ischemic
  5. endocrine disorders - hyper/hypothyroidism, DM
  6. inflammatory
  7. neoplastic infiltration
  8. systmemic hypertension (cats)