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Module 10 > Cardiovascular Pathology 2 > Flashcards

Cardiovascular Pathology 2 Flashcards

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1
Q

what are primary arrhythmias

A

no morphological abnormality

may be normal in species/breed (often disappear with increased activity –> horses)

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2
Q

what are secondary arrhythmias

A

secondary to underlying disease

atrial fibrillation in cardiomyopathy

ventricular tachycardia in ventricular hypertrophy

heart block following myocardial damage

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3
Q

what are examples of inherited arrythmias in dogs

A
  1. boxers with arrhythmogenic right ventricular cardiomyopathy (ARVC) –> cardiomyocytes replaced by fatty plaques
  2. severe subvalvular aortic stenosis (SAS)
  3. doberman dilated cardiomyopathy (DCM)
  4. myocarditis (chagas) –> infectious causes (affects conduction system)
  5. german shepherds with inherited ventricular tachycardia (VT)
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4
Q

what is sick sinus syndrome (bradycardia-tachycardia syndrome)

A

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

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5
Q

what are the causes of sick sinus syndrome

A

usually idiopathic

may have ischemia or fibrosis of SA node

possibly inherited (min schnauzer)

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6
Q

what are first degree heart blocks

A

delay of impulse through AV node

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7
Q

what are second degree heart blocks

A

intermittent failure to conduct through AV node with dropped beat

considered normal in horse

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8
Q

what are third degree heart blocks

A

complete block

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9
Q

what are heart blocks associated with

A

areas of myocardial scarring in dogs and horses

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10
Q

what is the normal microanatomy of the heart (4)

A
  1. striated muscle with centrally located nuclei
  2. myofibres are branching
  3. purkinje fibres –> conduct electrical stimuli through heart
  4. intercalated discs –> connections between myofibres that allow for unified contraction of sarcomeres
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11
Q

what are the physiological changes to the myocardium

A
  1. atrophy: cardiomyocytes are smaller
  2. hypertrophy: cardiomyocytes are larger
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12
Q

how do alterations in heart size occur

A

due to increases in cell volume not number of cells

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13
Q

what is concentric hypertrophy

A

increase in myocyte width due to addition of sarcomeres in parallel

ex. pressure overload, valvular stenosis, systemic hypertension, lung disease

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14
Q

what is eccentric hypertrophy

A

increase in myocyte length due to addition of sarcomeres in series

ex. volume overload, valvular insufficiencies, septal defects

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15
Q

what are the stages in myocardial hypertrophy

A
  1. initiation
  2. stable hyperfunction (ex. athletes)
  3. deterioation of function (due to degeneration of hypertrophied fibres)
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16
Q

what are examples of physiological hypertrophy

A

pregnancy

exercise

postnatal growth

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17
Q

is the heart functioning normally in physiological hypertrophy

A

normal or increased

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18
Q

do the cardiomyocytes increase in size in physiological hypertrophy

A

yes but still functional

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19
Q

is there fibrosis, apoptosis and fetal gene activation in physiological hypertrophy

A

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

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20
Q

what are examples of pathological hypertrophy

A

high blood pressure

myocardial infarction

valvular heart disease

cardiomyopathy (diabetes, alcoholic/toxic, genetic/familial)

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21
Q

what occurs to heart function in pathological hypertrophy

A

initially heart size increases

then later decreased (depressed)

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22
Q

is there fibrosis, apoptosis and fetal gene activation in pathological hypertrophy

A

yes

fetel gene reactivation –> atrial natriuretic peptide (ANP), BNP

both regulate BP and volume

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23
Q

what is the cycle heart hypertrophy

A

heart develops depressed cardiac function –> fetal gene reactivation causes abnormal hypertrophy

once fibrosis occurs: doesn’t go away

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24
Q

what are examples of myocardial disease (4)

A
  1. degeneration (ageing, nutritional, toxic)
  2. necrosis (nutritional, toxic, traumatic)
  3. myocarditis (viral –> lymphocytic, bacterial –> suppurative, parasitic –> public health)
  4. cardiomyopathies (inherited, acquired)
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25
what is dilated cardiomyopathy
eccentric hypertrophy
26
what is hypertrophic cardiomyopathy
eccentric
27
what are examples of myocardial degeneration
1. lipofuscinosis: wear and tear, age 2. fatty degeneration: systemic diseases, circular fatty inclusions 3. myocytolysis: loss of cross striations, eosinophilic cardiac myocytes, sick cells 4. vacuolar degeneration: fluid accumulations, some toxicities
28
what are the PM findings of this hear
lipofuscinosis brown colouration
29
what are the stages in myocardial necrosis
1. hyaline necrosis: hypereosinophilic fibres, pyknotic nuclei (very pink, no cross striations, nucleus shrinks) 2. or apoptosis: membrane blebbing (shredded appearance), contraction band necrosis 3. macrophage invasion: 24-48 hours post injury, immune response to clear up damaged cells 4. healing with fibrosis: can't move properly with scar tissue, can't function properly
30
what is an example of myocardial necrosis
white muscle disease (selenium/vit E deficiency)
31
what pathology is shown here
myocardial necrosis due to selenium/vit. E deficiency (white muscle disease) ## Footnote secondary to necrosis get mineralization --\> metastatic calcification (if high circulating Ca) or dystrophic calcification (normal Ca levels, but Ca laid down on necrotic tissues)
32
what is an example of myocarditis
canine parvovirus
33
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
34
what is shown here
canine parvovirus
35
what is shown here
bacterial myocarditis partially healed lesion (sectioned) following wire penetration in a case of traumatic reticuloperitonitis (hardware disease)
36
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
37
what is shown here
parasitic myocarditis sheep heart with cycticercus ovis tapeworm cysts in heart or skeletal muscle (check diaphragm too)
38
what are the consequences of myocardial necrosis/myocarditis
1. sudden death 2. myocardial scarring (sudden death, chronic heart failure, clinically normal) 3. various biochemical markers may be detectable from 1-3h to 10-14d after damage (creatine kinase, troponins)
39
what are examples of primary cardiomyopathies
1. 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 2. cat: - arrhythmogenic right ventricular (ARVC, ARVD) - rare in horse, dog
40
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
41
what is shown here
myocyte disarray due to feline hypertrophic cardiomyopathy
42
what does feline hypertrophic cardiomyopathy cause
1. marked LV wall hypertrophy 2. septal thickening --\> diastolic failure 3. left atrial enlargement: pulmonary edema and/or pleural effusion, progression to either congestive heart failure or sudden death 3. hypertrophy and disarray of myocytes, interstitial fibrosis
43
what is shown here
left: hypertrophic cardiomyopathy right: dilated cardiomyopathy
44
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
45
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
46
what is shown here
dilated cardiomyopathy
47
what is restrictive cardiomyopathy
least common increased ventricular stiffness --\> abnormal fibrosis loss of left ventricular diastolic function (restrictive filling & reduced diastolic volume)
48
what is shown here
restrictive cardiomyopathy fibrous connective tissue ventricular stiffness
49
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
50
what are the 3 types of valvular disease
1. developmental anomalies 2. inflammation (valvular endocarditis) 3. degeneration (valvular endocardiosis)
51
what is the pathology of valvular endocardiosis
1. myxomatous or mucoid degeneration of valve connective tissue matrix (slow progression, often subclinical) 2. 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)
52
what types of dogs are affected by valvular endocardiosis
degenerative disease of older dogs (medium/small breeds esp. cavalier king charles spaniels)
53
what is shown here
endocardiosis, smooth thickened atrio-ventricular valves valve should be smooth, nodular looking, won't function well mucoid degeneration
54
what are the possible consequences of endocardiosis
ruptured right atrium massively dilated right atrium
55
what is valvular endocarditis
bacterial infection of valves
56
what occurs in valvular endocarditis in cattle
right AV valve trueperella pyogens
57
what occurs in valvular endocarditis in pigs, sheep and dogs
left AV erysipelothrix rhusiopathiae, streps
58
what occurs in valvular endocarditis in horses
less common in adult aortic valve strep equi, actinobaciluus equuli, e coli
59
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
60
what is shown here
bovine endocarditis early vegetative lesions on AV valves
61
what is shown here
bovine endocarditis --\> tricuspid valve well established lesion on dilated thin walled ventricle (right ventricle) if embolized will go to lungs
62
what is shown here
endocarditis on aortic valve seen in horse
63
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
64
suggest 2 causes of cardiac myocyte atrophy
1. bed rest 2. wasting disease (chronic metabolic disorders toxemia, anemias)
65
give 2 causes of physiological hypertrophy
1. increased workload (exercise, athletes) 2. pregnancy
66
give 2 causes of pathological hypertrophy
1. valvular heart disease 2. cardiomyopathy
67
list the 3 differences between physiological and pathological hypertrophy
1. pathological causes fibrosis 2. apoptosis 3. pathological initally increases heart function but then later decreases and becomes depressed
68
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

Module 10 (27 decks)

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