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Module 10 > Cardiovascular Pathology 2 > Flashcards

Cardiovascular Pathology 2 Flashcards

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
Q

what is dilated cardiomyopathy

A

eccentric hypertrophy

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26
Q

what is hypertrophic cardiomyopathy

A

eccentric

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27
Q

what are examples of myocardial degeneration

A
  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
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28
Q

what are the PM findings of this hear

A

lipofuscinosis

brown colouration

29
Q

what are the stages in myocardial necrosis

A
  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
Q

what is an example of myocardial necrosis

A

white muscle disease (selenium/vit E deficiency)

31
Q

what pathology is shown here

A

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)

32
Q

what is an example of myocarditis

A

canine parvovirus

33
Q

how does canine parvovirus cause myocarditis

A

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
Q

what is shown here

A

canine parvovirus

35
Q

what is shown here

A

bacterial myocarditis

partially healed lesion (sectioned) following wire penetration in a case of traumatic reticuloperitonitis (hardware disease)

36
Q

what is shown here

A

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
Q

what is shown here

A

parasitic myocarditis

sheep heart with cycticercus ovis

tapeworm cysts in heart or skeletal muscle (check diaphragm too)

38
Q

what are the consequences of myocardial necrosis/myocarditis

A
  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
Q

what are examples of primary cardiomyopathies

A
  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
Q

what is feline hypertrophic cardiomyopathy

A

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
Q

what is shown here

A

myocyte disarray due to feline hypertrophic cardiomyopathy

42
Q

what does feline hypertrophic cardiomyopathy cause

A
  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
  4. hypertrophy and disarray of myocytes, interstitial fibrosis
43
Q

what is shown here

A

left: hypertrophic cardiomyopathy
right: dilated cardiomyopathy

44
Q

what occurs in dilated cardiomyopathy in canines

A

cardiac dilation and contractile dysfunction of the ventrciles

left heart failure: pulmonary edema

progression: CHF with dilation of all chambers

45
Q

what is the significance of dilated cardiomyopathy in the dog

A

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
Q

what is shown here

A

dilated cardiomyopathy

47
Q

what is restrictive cardiomyopathy

A

least common

increased ventricular stiffness –> abnormal fibrosis

loss of left ventricular diastolic function (restrictive filling & reduced diastolic volume)

48
Q

what is shown here

A

restrictive cardiomyopathy

fibrous connective tissue

ventricular stiffness

49
Q

what are secondary cardiomyopathies

A

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
Q

what are the 3 types of valvular disease

A
  1. developmental anomalies
  2. inflammation (valvular endocarditis)
  3. degeneration (valvular endocardiosis)
51
Q

what is the pathology of valvular endocardiosis

A
  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
Q

what types of dogs are affected by valvular endocardiosis

A

degenerative disease of older dogs (medium/small breeds esp. cavalier king charles spaniels)

53
Q

what is shown here

A

endocardiosis, smooth thickened atrio-ventricular valves

valve should be smooth, nodular looking, won’t function well

mucoid degeneration

54
Q

what are the possible consequences of endocardiosis

A

ruptured right atrium

massively dilated right atrium

55
Q

what is valvular endocarditis

A

bacterial infection of valves

56
Q

what occurs in valvular endocarditis in cattle

A

right AV valve

trueperella pyogens

57
Q

what occurs in valvular endocarditis in pigs, sheep and dogs

A

left AV

erysipelothrix rhusiopathiae, streps

58
Q

what occurs in valvular endocarditis in horses

A

less common in adult

aortic valve

strep equi, actinobaciluus equuli, e coli

59
Q

what is the pathology of endocarditis

A

friable, yellow and grey masses or vegetations

layers of fibrin with embedded bacterial colonies

septic embolism to lungs, heart, kidneys

60
Q

what is shown here

A

bovine endocarditis

early vegetative lesions on AV valves

61
Q

what is shown here

A

bovine endocarditis –> tricuspid valve

well established lesion on

dilated thin walled ventricle (right ventricle)

if embolized will go to lungs

62
Q

what is shown here

A

endocarditis on aortic valve

seen in horse

63
Q

what causes sudden death in pig

A

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
Q

suggest 2 causes of cardiac myocyte atrophy

A
  1. bed rest
  2. wasting disease (chronic metabolic disorders toxemia, anemias)
65
Q

give 2 causes of physiological hypertrophy

A
  1. increased workload (exercise, athletes)
  2. pregnancy
66
Q

give 2 causes of pathological hypertrophy

A
  1. valvular heart disease
  2. cardiomyopathy
67
Q

list the 3 differences between physiological and pathological hypertrophy

A
  1. pathological causes fibrosis
  2. apoptosis
  3. pathological initally increases heart function but then later decreases and becomes depressed
68
Q

what is the difference between endocarditis and endocardiosis

A

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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