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VET 408: Cardio/Respiratory > Pathology of Valvular and Myocardial Diseases > Flashcards

Pathology of Valvular and Myocardial Diseases Flashcards

1
Q

what are two ways that the heart can compensate for changes in load

A

dilation and hypertrophy

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2
Q

how does dilation affect filling and ejection

A

increases chamber size to improve filling
increases amount ejected UP TO A POINT

if too much dilation –> decreased contraction ability

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3
Q

how does hypertrophy affect filling and contractility

A
  1. concentric: decreases filling, increases contractility
  2. eccentric: increases filling, decreases contractility
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4
Q

concentric hypertrophy

A

sarcomeres added in parallel to increase wall thickness

caused by increased pressure (afterload)

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5
Q

eccentric hypertrophy

A

sarcomeres added in series to increase wall length

caused by increased volume (preload)

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6
Q

pathologic hypertrophy

A

when hypertrophy exceeds physiologic state and becomes pathologic

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7
Q

concentric pathologic hypertrophy

A

causes diastolic dysfunction from decreased compliance

increases EDP and decreases conduction

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8
Q

eccentric pathologic hypertrophy

A

causes systolic dysfunction from decreased contractility

growth occurs in random directions = loss of coordinated contraction

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9
Q

intracardiac consequences of hypertrophy

A

reduced heart function

fibrosis, dysrhythmias, increased myocyte mass, decreased contractility and CO

if CO < demand –> heart failure

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10
Q

extra cardiac consequences of hypertrophy

A

fluid accumulation and ischemia

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11
Q

what is the most common cause of heart disease in animals

A

valvular disease

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12
Q

what is the most common cause of valve disease in animals

A

AV valve disease (MV, TV)

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13
Q

sign of AV valve disease

A

regurgitation

valve forms incomplete seal causing blood to back flow from ventricle to atrium

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14
Q

sequela to AV valve disease

A

atrial dilation + ventricular hypertrophy

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15
Q

AV valve dysplasia

A

congenital malformation of the valve

nodular: rounded, thickened tissue
imperforate: valve leaflets never separated

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16
Q

tricuspid valve dysplasia

A

causes regurgitation

common in labradors

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17
Q

mitral valve dysplasia

A

causes regurgitation

common in cats and cavalier King Charles spaniels

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18
Q

AV valve endocardiosis

A

degeneration of the valve at a faster than normal rate

usually myxomatous
usually mitral valve

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19
Q

myxomatous mitral valve endocardiosis

A

smooth, firm/rubbery, multi nodular tissue that blends into adjacent valve tissue

causes regurgitation and turbulent flow leading to jet lesions

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20
Q

jet lesions

A

endocardial thickening in response to turbulent flow

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21
Q

AV valve endocarditis

A

infectious inflammation of the valve

usually bacterial
usually mitral valve
(except cows: tricuspid valve)

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22
Q

bacterial MV endocarditis

A

proliferative, granular or friable (fibrin) material that adheres to the valve surface

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23
Q

what bacterial causes valvular endocarditis in pigs, horses, and cattle

A

pigs: strep. suis OR E. rhusiopathiae
horses: strep. equi OR actinobacillus equuli
cattle: trueperella pyogenes OR E. coli

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24
Q

what causes bacterial endocarditis

A
  • aseptic jugular catheter placement
  • sustained bacteremia that attaches to valve (endocardiosis predisposes)
  • immunosuppression
  • congenital valve defects
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25
Q

outcome of bacterial endocarditis

A

usually fatal due to significant vascular injury and remodeling

can cause embolisms when pieces of bacteria break off as flap closes/opens and gets trapped in next capillary bed

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26
Q

sign of semilunar valve disease

A

stenosis

narrowing of vessels leaving the heart –> increases vascular resistance –> increases afterload

27
Q

sequela to SL valve disease

A

concentric hypertrophy + post-stenotic vessel dilation

also causes jet lesions from turbulent flow

28
Q

primary myocardial disease

A

disease that is intrinsic to the myocardial fiber

usually idiopathic

progressive and irreversible

29
Q

dilated cardiomyopathy

A

enlargement and dilation of the ventricles and atria

causes eccentric hypertrophy and systolic dysfunction

30
Q

what species and which chamber is most commonly affected by DCM

A

dogs
left ventricle

31
Q

what kind of drugs would you want to use to treat DCM

A

positive inotropes
(increase contractility)

32
Q

arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

subset of DCM characterized by loss of myocytes with fatty infiltrate

causes eccentric hypertrophy with fatty infiltration (not fibrosis)

usually right ventricular

33
Q

hypertrophic cardiomyopathy

A

thickening of the ventricular wall from concentric hypertrophy leading to diastolic dysfunction

34
Q

how does HCM cause arrhythmias

A

myocytes are laid down irregularly w/ fibrosis –> poor conduction –> arrhythmias

35
Q

what species and chamber is most commonly affected

A

cats
left ventricular > IVS > right ventricle

36
Q

what kind of drugs would you use to treat HCM

A

drugs that decrease HR
(allows for more time to relax/fill during diastole)

37
Q

what is a common sequela of HCM in cats

A

saddle thrombus

caused by blood stasis and congestion in lungs

signs: 5 Ps (pain, paresis/paralysis, pulselessness, poikilothermia, pallor)

38
Q

restrictive cardiomyopathy

A

fibrous tissue deposition within the endocardium and sub endothelium surrounding the ventricular lumen

causes a diastolic dysfunction due to NO compliance

usually idiopathic

39
Q

what species and chamber are most commonly affected by restrictive cardiomyopathy

A

cats (also dogs, cattle, pigs)
left ventricular

40
Q

secondary myocardial disease

A

myocardial disease that occurs as a result of an exogenous force (hypertension, nutrition, etc)

most are REVERSIBLE by removing primary disease

41
Q

feline hyperthyroidism

A

thyroid tumors leading to thyrotoxic heart disease

specific to CATS only - dogs do not get clinical thyroid tumors (but if they do then most are malignant)

42
Q

are cat thyroid tumors more often benign or malignant

A

benign but release free T4

follicular adenomas, multi nodular hyperplasia

43
Q

what lesions is seen with feline thyrotoxic heart disease

A

concentric hypertrophy WITHOUT fibrosis

similar to HCM grossly and clinically but NO collagen deposits on histology

44
Q

vitamin E/selenium deficiency causing secondary myocardial disease

A

low vit E/Se causes decreased protection from oxidative damage –> lipid peroxidation –> dec energy available for heart

45
Q

what lesion does vitamin E/Se deficiency cause in pigs

A

mulberry heart disease

fibrinoid vascular necrosis leading to hemorrhage
(hemorrhage + pallor)

46
Q

taurine deficiency causing secondary myocardial disease

A

taurine = essential AA in cats

without taurine –> “feline DCM”

eccentric hypertrophy

reversible w/ taurine supplementation

47
Q

toxic myocardial necrosis

A

toxins leading to death and necrosis of cardiomyocytes

  • cardiac glycosides
  • ionophores
  • blister beetles
  • doxorubicin
48
Q

cardiac glycoside toxicity

A

causes direct damage to cardiomyocytes

species: horses

ex. oleander

49
Q

ionophore toxicity

A

increases Ca uptake in cells –> increased sensitivity causes myocardial necrosis

species: horses

ex. monensin

50
Q

blister beetle toxicity

A

causes myocarditis, hemorrhagic enteritis, cystitis

species: horses

51
Q

doxorubicin toxicity

A

antibiotic that has cumulative dose related toxicity - once max dose is given, patient can not have this medication again in its life

species: small animals

52
Q

myocarditis

A

inflammation of the myocardium; many infectious etiologies (bacterial, viral, fungal, protozoal, parasitic)

53
Q

parvoviral myocarditis

A

rare complication of parvovirus resulting in infection of the myocardium

affects puppies 3-8 weeks old

presents as sudden death months after Parvo recovery

54
Q

what is the heart’s responses to injury

A

LIMITED regenerative capacity
- myocyte loss –> fibrosis
- remaining myocytes –> hypertrophy

55
Q

effect of fibrosis on heart function

A

decreases compliance and conduction

(dec. contractility and arrhythmias)

56
Q

what is heart failure

A

end point for many diseases; occurs when compensatory mechanisms are not enough to meet demand

57
Q

forward failure

A

decreased cardiac output

58
Q

backward failure

A

increased vascular stasis and congestion

59
Q

left sided heart failure

A

pulmonary edema

blood congests from LA –> PV –> lungs

starling forces (inc. hydrostatic pressure) drives effusion out of vessels

60
Q

gross lesion of L-HF

A

brown, enlarged, fluid filled lungs

brown b/c of alveolar macrophages that infiltrate to consume fluid and RBCs –> converts HgB into hemosiderin –> brown color

61
Q

clinical signs of L-HF

A

exercise intolerance
increased respiratory effort at rest
cough
crackles
syncope

62
Q

right sided heart failure

A

hepatomegaly, ascites or pleural effusion, peripheral edema, jugular distention

blood congests from RA –> cranial and caudal vena cava –> jugular vein and liver

causes species specific fluid accumulation

63
Q

R-HF fluid accumulation in dogs, cats, and LA

A

dogs: ascites
cats: pleural effusion
LA: subcutis (SQ edema)

64
Q

nutmeg liver disease

A

chronic hepatic congestion from R sided heart failure

VET 408: Cardio/Respiratory (38 decks)

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