Cardiovascular Pathology 2 Flashcards
what are primary arrhythmias
no morphological abnormality
may be normal in species/breed (often disappear with increased activity –> horses)
what are secondary arrhythmias
secondary to underlying disease
atrial fibrillation in cardiomyopathy
ventricular tachycardia in ventricular hypertrophy
heart block following myocardial damage
what are examples of inherited arrythmias in dogs
- boxers with arrhythmogenic right ventricular cardiomyopathy (ARVC) –> cardiomyocytes replaced by fatty plaques
- severe subvalvular aortic stenosis (SAS)
- doberman dilated cardiomyopathy (DCM)
- myocarditis (chagas) –> infectious causes (affects conduction system)
- german shepherds with inherited ventricular tachycardia (VT)
what is sick sinus syndrome (bradycardia-tachycardia syndrome)
group of disorders involving sino-atrial node (+/- AV node, HIS bundle and/or bundle branches)
potentially life threatening –> periods of ventricular standstill –> syncope
paroxysms of supraventricular tachycardia –> syncope
what are the causes of sick sinus syndrome
usually idiopathic
may have ischemia or fibrosis of SA node
possibly inherited (min schnauzer)
what are first degree heart blocks
delay of impulse through AV node
what are second degree heart blocks
intermittent failure to conduct through AV node with dropped beat
considered normal in horse
what are third degree heart blocks
complete block
what are heart blocks associated with
areas of myocardial scarring in dogs and horses
what is the normal microanatomy of the heart (4)
- striated muscle with centrally located nuclei
- myofibres are branching
- purkinje fibres –> conduct electrical stimuli through heart
- intercalated discs –> connections between myofibres that allow for unified contraction of sarcomeres
what are the physiological changes to the myocardium
- atrophy: cardiomyocytes are smaller
- hypertrophy: cardiomyocytes are larger
how do alterations in heart size occur
due to increases in cell volume not number of cells
what is concentric hypertrophy
increase in myocyte width due to addition of sarcomeres in parallel
ex. pressure overload, valvular stenosis, systemic hypertension, lung disease
what is eccentric hypertrophy
increase in myocyte length due to addition of sarcomeres in series
ex. volume overload, valvular insufficiencies, septal defects
what are the stages in myocardial hypertrophy
- initiation
- stable hyperfunction (ex. athletes)
- deterioation of function (due to degeneration of hypertrophied fibres)
what are examples of physiological hypertrophy
pregnancy
exercise
postnatal growth
is the heart functioning normally in physiological hypertrophy
normal or increased
do the cardiomyocytes increase in size in physiological hypertrophy
yes but still functional
is there fibrosis, apoptosis and fetal gene activation in physiological hypertrophy
no
crucial for proper heart development
once you’re born you don’t want them to keep working
if reactivated later in life –> pathological hypertrophy
what are examples of pathological hypertrophy
high blood pressure
myocardial infarction
valvular heart disease
cardiomyopathy (diabetes, alcoholic/toxic, genetic/familial)
what occurs to heart function in pathological hypertrophy
initially heart size increases
then later decreased (depressed)
is there fibrosis, apoptosis and fetal gene activation in pathological hypertrophy
yes
fetel gene reactivation –> atrial natriuretic peptide (ANP), BNP
both regulate BP and volume
what is the cycle heart hypertrophy
heart develops depressed cardiac function –> fetal gene reactivation causes abnormal hypertrophy
once fibrosis occurs: doesn’t go away
what are examples of myocardial disease (4)
- degeneration (ageing, nutritional, toxic)
- necrosis (nutritional, toxic, traumatic)
- myocarditis (viral –> lymphocytic, bacterial –> suppurative, parasitic –> public health)
- cardiomyopathies (inherited, acquired)
what is dilated cardiomyopathy
eccentric hypertrophy
what is hypertrophic cardiomyopathy
eccentric
what are examples of myocardial degeneration
- lipofuscinosis: wear and tear, age
- fatty degeneration: systemic diseases, circular fatty inclusions
- myocytolysis: loss of cross striations, eosinophilic cardiac myocytes, sick cells
- vacuolar degeneration: fluid accumulations, some toxicities
what are the PM findings of this hear
lipofuscinosis
brown colouration
what are the stages in myocardial necrosis
- hyaline necrosis: hypereosinophilic fibres, pyknotic nuclei (very pink, no cross striations, nucleus shrinks)
- or apoptosis: membrane blebbing (shredded appearance), contraction band necrosis
- macrophage invasion: 24-48 hours post injury, immune response to clear up damaged cells
- healing with fibrosis: can’t move properly with scar tissue, can’t function properly
what is an example of myocardial necrosis
white muscle disease (selenium/vit E deficiency)
what pathology is shown here
myocardial necrosis due to selenium/vit. E deficiency (white muscle disease)
secondary to necrosis get mineralization –> metastatic calcification (if high circulating Ca) or dystrophic calcification (normal Ca levels, but Ca laid down on necrotic tissues)
what is an example of myocarditis
canine parvovirus
how does canine parvovirus cause myocarditis
bloody diarrhea
if they survive –> can develop myocarditis
viral inclusions in cardiac cells –> the cardiac myocytes are still dividing so the virus can get into these cells
causes lymphocytic myocarditis (degeneration of cardiac myocytes) –> pale heart with areas of necrosis
what is shown here
canine parvovirus
what is shown here
bacterial myocarditis
partially healed lesion (sectioned) following wire penetration in a case of traumatic reticuloperitonitis (hardware disease)
what is shown here
myocardial abscess
congestive cardiac failure in a cow
distended ventricle
valve function will be abnormal –> heart has to work harder to get blood out
what is shown here
parasitic myocarditis
sheep heart with cycticercus ovis
tapeworm cysts in heart or skeletal muscle (check diaphragm too)
what are the consequences of myocardial necrosis/myocarditis
- sudden death
- myocardial scarring (sudden death, chronic heart failure, clinically normal)
- various biochemical markers may be detectable from 1-3h to 10-14d after damage (creatine kinase, troponins)
what are examples of primary cardiomyopathies
- idiopathic, some are inherited/familial:
- hypertrophic (cat, dog, pig, hamsters)
- dilated (dog esp large breeds, cattle (cor pulmonale, brisket disease), cat)
- restrictive: fibrosis and scarring, movement of heart wall is restricted - cat:
- arrhythmogenic right ventricular (ARVC, ARVD)
- rare in horse, dog
what is feline hypertrophic cardiomyopathy
sarcomeric defects in cardiac myocytes
1-3 year old cats, many breeds affected (maine coon, ragdoll cats)
mutations in cardiac myosin-binding protein C (MYCPC) –> myocyte hypertrophy, fibrosis, myocyte dissarray
what is shown here
myocyte disarray due to feline hypertrophic cardiomyopathy
what does feline hypertrophic cardiomyopathy cause
- marked LV wall hypertrophy
- septal thickening –> diastolic failure
- left atrial enlargement: pulmonary edema and/or pleural effusion, progression to either congestive heart failure or sudden death
- hypertrophy and disarray of myocytes, interstitial fibrosis
what is shown here
left: hypertrophic cardiomyopathy
right: dilated cardiomyopathy
what occurs in dilated cardiomyopathy in canines
cardiac dilation and contractile dysfunction of the ventrciles
left heart failure: pulmonary edema
progression: CHF with dilation of all chambers
what is the significance of dilated cardiomyopathy in the dog
one of the most prevalent acquired (large breeds mainly –> doberman, portuguese water dog)
a major CVS cause of morbidity and mortality
only supprassed by degenerative valve disease and in some parts of the world heartworm disease
what is shown here
dilated cardiomyopathy
what is restrictive cardiomyopathy
least common
increased ventricular stiffness –> abnormal fibrosis
loss of left ventricular diastolic function (restrictive filling & reduced diastolic volume)
what is shown here
restrictive cardiomyopathy
fibrous connective tissue
ventricular stiffness
what are secondary cardiomyopathies
in cats
hyperthyroidism (HCM) –> no fibrosis or myofibril disarray, can return to normal, the heart should repair
taurine deficiency (DCM, TRCM)
drugs, toxins, nutritional disorder
what are the 3 types of valvular disease
- developmental anomalies
- inflammation (valvular endocarditis)
- degeneration (valvular endocardiosis)
what is the pathology of valvular endocardiosis
- myxomatous or mucoid degeneration of valve connective tissue matrix (slow progression, often subclinical)
- smooth, pearl-white round thickenings on valve leaflets +/- thickening of chordae tendinae
*most common on mitral valves (mitral insufficiency, regurgitation, commonest cause of congestive HF in adult dogs)
what types of dogs are affected by valvular endocardiosis
degenerative disease of older dogs (medium/small breeds esp. cavalier king charles spaniels)
what is shown here
endocardiosis, smooth thickened atrio-ventricular valves
valve should be smooth, nodular looking, won’t function well
mucoid degeneration
what are the possible consequences of endocardiosis
ruptured right atrium
massively dilated right atrium
what is valvular endocarditis
bacterial infection of valves
what occurs in valvular endocarditis in cattle
right AV valve
trueperella pyogens
what occurs in valvular endocarditis in pigs, sheep and dogs
left AV
erysipelothrix rhusiopathiae, streps
what occurs in valvular endocarditis in horses
less common in adult
aortic valve
strep equi, actinobaciluus equuli, e coli
what is the pathology of endocarditis
friable, yellow and grey masses or vegetations
layers of fibrin with embedded bacterial colonies
septic embolism to lungs, heart, kidneys
what is shown here
bovine endocarditis
early vegetative lesions on AV valves
what is shown here
bovine endocarditis –> tricuspid valve
well established lesion on
dilated thin walled ventricle (right ventricle)
if embolized will go to lungs
what is shown here
endocarditis on aortic valve
seen in horse
what causes sudden death in pig
valvular endocarditis (tricuspid and pulmonary)
erysipelothrix rhusiopathiae
streptococcus suis
septicemic pig with dark purple ear tips –> heart failure and pulmonary edema
as well the endocarditis had fibrous pericarditis
suggest 2 causes of cardiac myocyte atrophy
- bed rest
- wasting disease (chronic metabolic disorders toxemia, anemias)
give 2 causes of physiological hypertrophy
- increased workload (exercise, athletes)
- pregnancy
give 2 causes of pathological hypertrophy
- valvular heart disease
- cardiomyopathy
list the 3 differences between physiological and pathological hypertrophy
- pathological causes fibrosis
- apoptosis
- pathological initally increases heart function but then later decreases and becomes depressed
what is the difference between endocarditis and endocardiosis
endocardiosis: degenerative disease –> myxomatous or mucoid degeneration of valve connective tissue matrix, smooth pearl-white round thickenings on valve leaflets +/- thickening of chordae tendinae (most freq on mitral valves)
endocarditis: bacterial infection of valves –> friable, yellow and grey masses or vegetations
