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Semester 2 > Cardiovascular 3 > Flashcards

Cardiovascular 3 Flashcards

1
Q

how to control vascular smooth muscle tone

A

vascular smooth muscle cells are bathed in microenvironment rich in vaso-active substances
tone is determined by balance of vasoconstrictive and vasodilatory influences

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2
Q

Where are voltage operated calcium channels found and the types

A 
are found in :
- Nerves
- Vascular smooth muscle
- Cardiac cells
Types 
1) L type 
• Vascular smooth muscle
• Cardiac muscle (won't effect nerves or skeletal muscle 
- nodal tissue
- Myocardium
2) N-type 
•  Effect nerves
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3
Q

What are the 2 main classes of drugs used as vasodilators and classes within

A

1) Venous dilators
- Nitrates
2) Arterial dilators
- Hydralazine
- Calcium channel blockers
- Alpha blockers
- Beta blockers
- Angiotensin converting enzyme inhibitors

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4
Q

Nitrates what class of drug what does it breakdown into, what does it do and how used in veterinary medicine and how given

A

venous dilator (venodilator)

  • reduces venous return, reduce EDV, reduce workload as reduce SV and CO
  • increases NO which increases cGMP inactivating myosin resulting in vasodilation
  • used in acute decompensated heart failure (animal collapsed)
  • not tablet as fist pass effect but onto the skin
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5
Q

Hydralazine what class of drug, how work, how strong, what problems and when used

A

arteriodilator

  • mechanism unknown
  • very potent
  • reflex tachycardia - problem as quick reduction in blood pressure but then restore of pressure
  • used in retinal detachment
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6
Q

calcium channel blocker what class of drug, what does it block, mechanism of action, what tissues and affect at those tissues

A

direct vasodilator
- block L type calcium channels (heart and vas smooth muscle)
- bind to channel from inside so requires a open channel to block - use dependence (vascular beds with higher resting tone will dilate more)
What tissues do they effect
• Nodal /conducting tissue–> decreased heart rate, & AV conduction
• Myocardium –> decreased force of contraction
• Vascular smooth muscle –> relaxation

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7
Q

vascular:myocardial selectivity for 3 different drugs of calcium channel blockers

A

– Verapamil 1:1 - equal effect on both
– Diltiazem 7:1
– Amlodipine 14:1 - 14 times more selective for vascular smooth muscle than myocardial

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8
Q

alpha blocker what class of drug, where does it act and machanism and what is benefit

A 
indirect vasodilator acts on arteriolar and venous 
mechanism -
less NA binding 
- less IP3 and DAG 
- decreased intracellular Ca2+
- relaxation - less contraction 
- less tachycardia then hydralazine
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9
Q

beta blocker what class of drug and what is it cardiac and renal effects

A

indirect vasodilator
Cardiac effect:
- Decrease HR (SA node)
- Decrease SV (contractility)
- Decrease cardiac output
- Reduce blood volume so reduce blood pressure
Renal effect
- Block B1 receptors on JG (juxtaglomerular) cells
- Decreased renin release
- Decreased angiotensin formation - most potent vasoconstrictor
- Decreased TPR

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10
Q

what are the 3 main side effects of beta blockers and what is the mechanism behind them

A

1) cold extremities
- alpha dominance without beta receptor activation more vasoconstriction
2) Fatigue - reduced cardiac output baroreflex cannot occur as blocking beta so cannot get increase in HR
3) bronchoconstriction - beta 2 antagonist effect causing bronchodilation - now blocked

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11
Q

what does chronic activation of the RAAS system result in

A

• Persistent vasoconstriction –> increased pre load and afterload (consistent)
• Increased blood volume–> increased preload
• Increased angiotensin–> decreased baroreceptor sensitivity and myocardial toxicity
- Baroreceptors get reset at a higher pressure
Myocardial toxin as damage blood vessels

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12
Q

what are the 2 drugs used that affect RAAS and what is used most commonly

A

1) Angiotensin converting enzyme inhibitors (ACE inhibitors) - most widely used
2) Angiotensin II receptor blockers - bind on receptors and prevent binding of angiotensin II

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13
Q

what are the main cardiorenal effects of ACE inhibitors

A

• Vasodilation (arterial & venous)
- reduce arterial & venous pressure - TPR
- reduce ventricular afterload & preload
• Decrease blood volume as decrease fluid retention
- natriuretic
- diuretic
• Depress sympathetic activity
Inhibit cardiac and vascular hypertrophy

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14
Q

how are ACE inhibitors administered and when used

A
  • as a prodrug - metabolised in liver to active form and dependent on kidney for clearnace therefore TEST RENAL FUNCTION FIRST
    used in congestive heart failure as reduce pre and afterload - generally lifelong drug
    also used in chronic renal insufficiency in cats where systemic hypertension leads to increased glomerular filtration pressure and glomerular damage (still requires clearnace through kidney need to be considered)
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15
Q

what are the 2 main effects of ACE inhibitors and why

A

1) ACE converts angiotensin to active form - ACE I to ACE II
therefore ACHEI decrease vasoconstriction and water retention as prevents ACE II being produced
2) ACE also breaks down bradykinin which causes vasodilation
ACHEI increases vasodilation and increase vascular permeability - generally occurs more in lungs resulting in dry cough (doesn’t occur as much in animals)

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16
Q

angiotensin II receptor antagonists

A
  • More selective than ACE inhibitors (no effect on BK metabolism)
  • More complete inhibition of Angiotensin
  • Drugs of the future
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17
Q

maximal oxygen consumption what is it, how relate to athletes

A

comes a point where you can run faster but oxygen consumption plateaus out
Above this point relying on anaerobic respiration
- better the athlete - thoroughbred racehorses higher then maximal oxygen consumption

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18
Q

what determine oxygen delivery

A

VO2 = Q X (Ca - Cv)

  • VO2 is rate of oxygen consumption (mls/min)
  • Q is the cardiac output (L/min)
  • Ca is the content of oxygen in the arterial blood (into the muscles/tissue)
  • Cv is the content of oxygen in the venous blood (out of the muscle/tissue)
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19
Q

What are the 3 ways in which you can increase oxygen delivery

A

1) increase cardiac output
2) increase Ca - content of oxygen within arterial blood
3) decrease Cv - content of oxygen in the venous blood

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20
Q

What are the ways in which you can increase cardiac output

A

1) increase HR - decrease parasymapthetic and increase sympathetic tone
2) increase SV - increase EDV - larger heart
increase ESV - increase contractility or decrease afterliad

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21
Q

what are the ways in which you can increase Ca and decrease Cv

A

Increase Ca
- increase Hb concentration in the blood, horse uses splenic contraction - increase RBCs
decrease Cv
- increase oxygen extraction, Bohr Effect

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22
Q

does heart size matter and what can affect this

A

heart size in terms of percetnage body weight does matter for elite athletes - athletic animals have relatively larger hearts
- excercise training can increase heart size - increase ventricular size increase EDV

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23
Q

steps in formation of sigmoid heart

A

establish ventricle and atrium sac via

1) elongation of pericardial sac
2) elongation folds up on itself and forms S shape
3) creation of inflow and outflow trunks

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24
Q

what are the 4 steps in the formation of the four-chambered heart

A

1) 2 projections
2) the interventircular spetum
3) formation of valves
4) formation of the inter-atrial septa

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25
Q

what is involved in the 2 projection stage of the formation of the four-chambered heart

A

cranial and caudal A-V endocardial cushions fuse - divides common A opening into L. and R. A-V canal
- Separates left and right sides of the heart

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26
Q

what are the steps in the formation of the interventricular septum

A
  1. Grows dorsally from ventral floor of primitive ventricle R. and L. ventricles
  2. Septum unites with A-V endocardial cushions and spiral septum
  3. Until union - opening connects 2 ventricles
  4. Small area - finally closes I-V gap - membranous part of the definitive I-V septum
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27
Q

what occurs with the formation of valves for the heart

A

the dense mesenchymal tissue breaks down forming fibrous flaps including the papillary muscle, chordae tendineae and atrioventricular valves

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28
Q

formation of the inter-atrial septa what are the 2 septa involved

A
  1. Interatrial septum I -
    ○ Descends from cranio-dorsal part of atrium towards CaVC
    ○ Is destined to become flap of foramen ovale
    ○ Doesn’t complete the seal
  2. Interatrial septum II
    ○ Descends on R. side of first septum
    ○ Thick, firm partition - will become definitive I-A septum
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29
Q

what are the 3 foramina formed during the inter-atrial septa formation and their functions

A

○ 1st formed by advancing crescentic free edge of I-A septum I
- gradually closes
○ 2nd opens as perforation in craniodorsal region of I-A septum I as first foramen is closing
- Progressively enlarges – channel of Foramen ovale
○ 3rd foramen - large oval opening in centre of I-A septum II - Foramen ovale
- Persists until birth
- One way valve
Used to divert blood away from lungs

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30
Q

what are the four-embryonic circulations

A

Extra-embryonic circulation -
1. Yolk Sac - Vitelline circulation - before placenta is fully developed
2. Allantoic/umbilical circulation to definitive placenta
Intraembryonic circulation -
3. Systemic circulation
4. Pulmonary circulation

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31
Q

formation of the spiral septum what does this achieve what occurs and evidence

A
  • divides the pulmonary trunk from the aorta - from one outflow tract to two
  • rotates 180 as it grows in cauda-cranial direction resulting in the position of the pulmonary trunk and aorta relative to each other
  • Ductus arteriosus (channel between aorta and pulmonary trunk) that is closed up to form ligamentum arteriosum I the adult
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32
Q

what creates the major arteries in the embryo, what forms what

A

aortic arches encircles pharynx and segment into:
3rd arch – forms carotid arteries
4th arch – forms aortic arch on the left
- (right part of the 4th arch forms R subclavian)
(5th arch is only transient - doesn’t become anything)
6th arch – pulmonary arch
- (and ductus arteriosus maintained on the left

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33
Q

vitelline venous system what does the intra-embryonic vein divide into

A

Proximal portion -
- R. proximal vitelline v. will form hepatic segment of CaVC
–Middle portion -
- Gives rise to hepatic sinusoids hepatic segment of CaVC
–Distal portion -
- Gives rise to many branches - form most of the portal system

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34
Q

what is the ductus venosus what is its function and when does it disappear

A
  • Large vascular channel between L. umbilical v. and hepatic part of caudal vena cava
  • Allows oxygenated blood from placenta to flow directly through liver to heart due to laminar flow
  • Persists until birth – (carnivores, ruminants, primates)
  • Disappears during gestation – (horse and pig)\
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35
Q

List the 3 important foetal shunts

A

1) ductus venosus
2) formen ovale
3) ductus arteriosus

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36
Q

what occurs to the umbilicus vein from umbilicus to liver after birth

A
  • vestiges may remain in falciform ligament
  • (neonatal carnivores - round ligament of liver)
  • Ductus venosus usually obliterated after birth -
  • Vestiges may remain ligamentum venosum
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37
Q

foramen ovale where situated what does it do

A

On entry into R. atrium: Right to left atrium

  • lamina of oxygenated blood faces crista dividens
  • Diverted stream through foramen ovale contains most of oxygenated blood from ductus venosus
  • Greater portion of CaVC flow is diverted to R. ventricle - mixes with deoxygenated flow from CrVC
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38
Q

what is the foetal cardiac output for the left and right ventricle and oxygen saturation and what enters and exits

A

Left ventricle 35% of foetal cardiac output:
- Higher oxygen saturation
- oxygenated placental blood flow foramen ovale
- In L. atrium: oxygenated placental blood joined by small volume of deoxygenated blood returned from lungs; mixture leaves L. ventricle via aorta
Right ventricle 65% of foetal cardiac output:
3 sources:
1) Caudal vena cava:
- Oxygenated flow (placenta), deoxygenated flow – (caudal embryo)
2) Cranial vena cava (deoxygenated blood from cranial embryo)
3) Venous drainage of heart

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39
Q

what is the resistance in the foetal circulation and what are the 3 differences from foetal to adult circulation

A
  • Placental circulation - low resistance pathway
  • Pulmonary circulation - high resistance pathway
    •High resistance in foetal lungs diversion of large volume of blood to placenta
    1) 2 ventricles pump simultaneously into same arterial network
  • Massive ductus arteriosus unites aorta and pulmonary trunk
    2) Foetus - R. ventricle does more work than L.
    3) Foetal heart operates close to full capacity - no reserve
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40
Q

what is the most common foetal stress and how relieved

A

Asphyxia - commonest cause of foetal stress - inability to get oxygen into animal as not breathing yet
- Uterine contractions - reduce uterine blood flow
- Foetus - born in state of physiological asphyxia
○ Relieved by first few breaths
○ Additional relief - intact umbilical cord
- Foetal heart works at full capacity
○ No reserve for dealing with asphyxia

41
Q

what are the neonate changes in vascular resistance

A

•Sudden great increase in blood flow through lungs
- Increase flow through pulmonary veins
- Increase venous return to L. atrium
•L. R. pressure gradient across foramen ovale flap closes
•Loss of placenta causes
- Increase resistance in systemic arterial system
•Creates pressure gradient from aorta to lungs so blood flow through ductus arteriosus is reversed and get functional closure (constriction smooth muscle) permanent closure may take months

42
Q

what are the changes in pulmonary circulation after birth

A

After first breath -

  • Decrease in pulmonary vascular resistance
  • Accompanied by increase in pulmonary blood flow
43
Q

how does closure of umbilical arteries occur

A

Birth - rupture of umbilical cord
- Natural point of rupture ~1.5cm outside body wall
•Intra-abdominal regions of the umbilical aa.
- Pulled partly out of the abdomen and rupture -
- Ends constrict and retract into abdomen as large amount of elastin preventing them for bleeding out

44
Q

how does closure of the ductus venosus occur and what can result

A

•Closure occurs passively
•Functional closure hours to days after birth
•Few weeks for permanent closure by c.t. (connective tissue)
•Patent ductus venosus after birth -
- Leads to portacaval shunts - anomalous connections between portal vein and CaVC

45
Q

when does closure of the foramen ovale occur

A

•Functional closure after first few breaths
•Not secure until permanent fusion of valvula with I-A septum
•Fusion occurs -
- Quickly in ungulate species - tube-like valvula
- Slower in carnivores and primates - sheet-like valvula

46
Q

what are the most common cardiovascular defects in dogs, cats, ruminants and horses and camelids

A 
–Dog -
•Patent ductus arteriosus
•Pulmonary stenosis
–Cat -
•Mitral valve insufficiency
•Patent ductus arteriosus
–Ruminants, horse and camelids -
•Interventricular septal defects
47
Q

what is the prevalence of cardiac anomalies in dogs, pigs, horses and cattle

A

dogs - 1% (mainly male purebred due to polygenic inheritence)
pigs - as high as 4% in some herds
0.2% in horses and cattle

48
Q

Where is the most common location for an ectopic heart (ectopic cordis)

A

abnormal site (e.g. intra abdominal or pre-sternal)

49
Q

the clinical significance of congenital absence of the parietal pericardium

A
  • has been recorded by dogs and cats

- asymptomatic

50
Q

What is a congenital peritoneopericardial diaphragmatic hernia and what is its clinical significance?

A
  • a triangular defect in the ventral diaphragm and in the parietal pericardium - herniation of abdominal viscera (especially small intestine and mesentery +/- liver lobes, omentum, spleen) into the pericardial sac
  • often clinically silent
51
Q

in what species is a patent ductus arteriosus most common and what is the consequences

A
  • common in dogs especially females
  • results in left-to-right shunt during systole and diastole, increase blood in pulmonary circulation increase vlume load LA (dilation) and LV (dilation or eccentric hypertrophy)
  • if pulmonary hypertension may get sustained pressure overload in RV - concentric hypertrophy
52
Q

what occurs in an complicated PDA

A

pulmonary artery pressure rises until exceeds aortic pressure resulting in shunt reversal right to left shunt, blood bypasses the lungs - peripheral cyanosis (not cranial as subclavian and brachiocephalic trunk branches off aorta before PDA

53
Q

in what species does a patent foramne ovale occur commonly and is it clinically significant

A
  • common in ruminants
  • there is functional closure of the foramen ovale due to pressure difference between RA and LA therefore there is no shunting of the blood as the flap remains closed
  • no clinical signs
54
Q

What are the potential post-natal consequences of an atrial septal defect

A

shunting of blood from the LA to RA - increased central venous pressure and a volume overload on RA (- dilation) and RV (- dilation - chronic eccentric hypertrophy)
○ there is also a volume overload on the LA due to return of the extra blood from the lungs (0 dilation)
- if sufficient pulmonary hypertension develops, the shunt may reverse (right-to-left) - generalised cyanosis

55
Q

What are the potential post-natal consequences of a ventricular septal defect

A
  • small may be clinically insignificant
  • left to right shunting of blood, pressure overload RV hypertrophy, increase blood from lungs to LA and LV eventually get eccentric hypertrophy
  • may get reversal as right to left shunt - generalised cyanosis
56
Q

why do some ventricular septal defects eventually close

A

reparative marginal fibrosis induced by blood turbulence

57
Q

what animals and at what age are animals more likely to develop a right to left shunt reversal

A
  • six months of post-natal life

- larger defect allowing left to right shunting of large volumes of blood into the pulmonary arterial system

58
Q

What are the possible defects associated with abnormal development of the endocardial cushions and in which species are endocardial cushion defects common

A
  • high VSD, low ASD (ostium primum), tricuspid or mitral valve dysplasia or a common atrioventricular canal
  • common in pigs and cats
59
Q

What is a persistent truncus arteriosus

A
  • due to incomplete separation of the truncus arteriosus into pulmonary artery and aorta by the spiral septum - generalised cyanosis
  • severe defect
60
Q

What is an overriding aorta (dextropositioned aorta)

A

the aorta straddles the ventricular septum (which has a high VSD) and hence receives blood from both the RV and LV; the pulmonary artery drains the RV as per normal

61
Q

What are the four components of a tetralogy of Fallot and what clinical signs would you expect to see in an animal with a tetralogy of Fallot?

A

1) VSD
2) pulmonic stenosis
3) overriding aorta
4) concentric hypertrophy of the RV due to systolic pressure overload
clinical signs - rapid fatigue during exercise, retarded growth rate and generalised cyanosis (“blue baby syndrome” in humans)
- affected animals often have polycythaemia (an absolute increase in the erythrocyte count

62
Q

What are the consequences of a pulmonic stenosis and in which species is this defect common?

A

narrowing of the RV outflow tract - systolic pressure overload on RV - chronic concentric hypertrophy of the RV
- common defect in dogs

63
Q

What are the typical consequences of mitral or tricuspid valve dysplasia

A

○ tricuspid insufficiency - volume overload on the RA and RV - RA dilation and RV dilation or chronic eccentric hypertrophy - right-sided heart failure in young animals (large breed dogs)
- mitral valve insufficiency - volume overload on the LA and LV - LA dilation and LV dilation or chronic eccentric hypertrophy - left-sided congestive heart failure in young animals (cats)

64
Q

What is the most common vascular ring anomaly in animals and which species is most commonly affected?

A
  • persistent right aortic arch (PRAA)

- sometimes seen in dogs and calves

65
Q

What are the potential consequences of a persistent right aortic arch and why?

A
  • with the aorta in this position, the ligamentum arteriosum traps the oesophagus at the level of the heart base and compresses it against the trachea
  • oesophageal obstruction - megaoesophagus cranial to the obstruction, regurgitation of solid food once affected animals are weaned, and risk of aspiration pneumonia
66
Q

What can excessive moderator bands in the left ventricle (false tendons) cause in cats? How old are most clinically affected cats?

A

decreased cardiac compliance with decreased diastolic filling of the LV - left-sided congestive heart failure in middle-aged or older cats

67
Q

What is endocardial fibroelastosis and what is the functional consequence of this condition?

A

collagen and elastin deposition - prominent gross white thickening of the endocardium (especially of the LV) by day 20 - decreased cardiac compliance
- ultimately, subendocardial fibrosis may entrap Purkinje fibres - degeneration - impaired electrical conductivity

68
Q

In which species are congenital valvular cysts common? What is the typical gross appearance of these lesions and consequence

A

common in the interior of the tricuspid and mitral valves at the leaflet margins, cysts contain watery fluid or blood

  • 0.5-1cm diameter
  • usually no valvular dysfunction unless very large
69
Q

What is a myocardial rhabdomyoma

A

neoplastic but rather anomalous malformations of myocardial fibres

70
Q

what lines the pericardial sac and the functions of these cells

A

mesothelial cells

1) capable of phagocytosis
2) produce plasminogen activator
3) secretes polysaccharide that acts as a low viscoisty lubricant

71
Q

what are the functions of a pericardial sac and is it needed

A
  1. maintenance of cardiac alignment and streamlining of the intra-cardiac blood flow
  2. provision of hydrostatic compensation for gravity and inertial forces
  3. maintenance of an even, low, external, transmural hydrostatic pressure on the right and left ventricles at the end of diastole
  4. prevention of sudden dilation of heart chambers
  5. prevention of spread of an infectious agent from the pleural cavity to the pericardial sac
    - however, the pericardium is not essential for life
72
Q

and what pericardial diseases lead constrictive heart disease

A

1) rapid pericardial effusion

2) chronic pericardial fibrosis

73
Q

what conditions are likely to cause cardiac tamponade

A
  1. non-inflammatory oedema of the sac (hydropericardium)
  2. haemorrhage into the sac (haemopericardium)
    3) inflammation of the epicardium and parietal pericardium (pericarditis
74
Q

what are possible mechanisms by which hydropericardium may develop

A
  1. right-sided congestive heart failure - venous drainage to right side
  2. hypoalbuminaemia - e.g. protein-losing enteropathy, protein-losing nephropathy, chronic liver disease, chronic starvation
  3. local venous or lymphatic obstruction - e.g. tumours located at the heart base or in the cranial mediastinum
  4. increased vascular permeability - e.g. pigs with oedema disease (with endothelial damage caused by circulating toxins derived from intestinal E. coli bacteria)
75
Q

what is the typical gross appearance of hydropericadium

A
  • clear to faintly cloudy to pale yello
  • remain smooth and glistening unless chronic effusion
  • in that case thickening and cream-white opacity due to subserold fibrosis
76
Q

why is haemopericardium usually fatal

A

due to cardiac tamponade

77
Q

what are some causes of haemopericardium in domestic animals

A

1) penetrating trauma with puncture of heart chamber of coronary vessel
2) bleeding haemangiosarcoma
3) coagulation factor deficiency - rodenticide anticoagulant poisoning
4) idiopathic pericardial haemorrrgae
5) hardwire disease - cattle

78
Q

what are the two most common pericarditis seen in domestic animals and which is more common

A

1) fibrinous - most common

2) suppurative

79
Q

what is the most common cause of fribinous pericarditis in domestic animals

A

haematogenous localisation of an infectious agent (especially a bacterium

80
Q

what is the typical gross appearance of fibrinous pericarditis

A
  • only small volume of exudate present
  • inflamed serosal membrane are hyperaemia and may have multiple small haemorrhages
  • fibrin sticks to pericardial membrane resultsin in bread-and-butter pericarditis
81
Q

In what species is suppurative pericarditis most commonly seen and why

A

cattle due to traumatic reticulopericarditis (“hardware disease”)
- injection of pyogenic (pus-forming) bacteria

82
Q

what are the different effects of fibrinous and suppurative pericarditis in terms of their effects on cardiac function

A

Fibrinous
- fibrin exudate can be removed and may cause bridging however usually no compromise on cardiac function
suppurative
- never completely resolves, granulation tissue - deep scar tissue - constrictive pericarditis - imparied filling of right ventricle - right sided congestive heart failure

83
Q

what does serous atrophy of epicardial fat indicate

A

recent rapid mobilisation of epicardial fat depots in anorexia, starvation and cachectic illnesses (e.g. malignancy)

84
Q

What are common causes of haemorrhage over the epicardium and/or parietal pericardium in domestic animals

A

1) hypoxia/anoxia or shock
2) acute infections - bacteraemia, septicaemia
3) disorders of primary haemostasis - platelet deficiency

85
Q

What are the post mortem artifactual lesions that you might find in the pericardial sac of animals
during a necropsy examination

A
  • after death, blood-stained watery (serosanguineous) fluid that does not clot accumulates within the pericardial sac (and in the pleural and peritoneal cavities)
  • imbibition of haemoglobin from lysing red blood cells -> red discolouration of the pericardial membranes
86
Q

what is the gross change that suggests subendocardial fibrosis and what is the most often cause of diffuse subendocardial fibrosis

A

remains smooth and shiny but appears milky white and opaque (obscuring the colour of the underlying myocardium)
- chronically dilated heart chambers

87
Q

what is the most common cause of jet lesions and where generally found

A

atria due to insufficiency of the atrioventricular valves (regurgitation)

88
Q

in what circumstances can mineral be deposited in the endocardium and cause of each

A
  • dystrophic mineralisation (i.e. mineral deposition in necrotic tissues) is more common than metastatic mineralisation (i.e. mineral deposition in healthy tissues due to an increased blood concentration of calcium or phosphate)
89
Q

how prevalent is endocartitis in dogs and what breeds are most likely to be affected at what age

A
  • most common cardiovascular lesion in dogs
  • prevalence increases with age (e.g. 5% of dogs under 1 year of age to > 75% at 16 years)
  • especially toy, small and medium dog breeds
  • high incidence and early onset in cavalier King Charles spaniel
90
Q

what is currently the aetiology of endocardiosis

A

an inherited degenerative disease of connective tissues - polygenic inheritance in Cavalier King Charles Spaniels

91
Q

which heart valves are commonly affected by endocardisosis in dogs and what gross lesions would suggest this

A
  • mitral valve and, to a lesser extent, the tricuspid valve
  • thickened by loose fibroblastic tissue and deposits of proteoglycans
  • affected valve leaflets become short and thick
  • small discrete nodules at the margins of the valve leaflets or more uniform valve thickening
92
Q

what are the potenial consequences of mitral or tricuspid endocarditis in a dog

A
  • valvular insufficiency -> regurgitation of blood during systole -> volume overload on the atrium and diastolic volume overload on the ventricle -> atrial dilation and ventricular dilation and chronic eccentric hypertrophy
  • jet lesions in the atrium
  • infrequently, may see rupture of chordae tendineae -> eversion of a valve leaflet into the atrium (“flail leaflet”) -> acute heart failure
93
Q

What is the most common cause of endocarditis in domestic animals and which species most
commonly develop endocarditis

A

most common is valvular endocarditis - persistent bacteraemia
- cattle and horses

94
Q

what do the lesions on endocarditis look like and composed of

A

vulvular

  • mitral > aortic > tricuspid > pulmonic valve)
  • large, friable, rough-surfaced, yellow-grey-red vegetations largely composed of thrombus
95
Q

what are the potential consequences of valvular endocarditis

A
  • often fatal
  • leukocyte phagocytosis and ingrowth of granulation tissue -> fibrosis +/- dystrophic mineralisation
  • valve become stenotic or insufficient
  • risk of thromboembolism
96
Q

what are some possible causes of mural endocarditis in domestic animals

A

1) extension of severe valvular endocarditis
2) parasitic endocarditis in horses - larvae
2) blackleg ruminants - clostridium cause, endotoxin release
3) uraemic ulcerative endocarditis in dogs - most common form, acute renal failure

97
Q

what can cause haemoorhages over the endocardium in domestic animals

A

same circumstances as epicardial haemorrhages

98
Q

What are the post mortem artifactual lesions that you might find in the endocardium of animals
during a necropsy examination

A
  • after death, the endocardium imbibes haemoglobin from lysing erythrocytes -> diffuse red discolouration

Semester 2 (17 decks)

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