cardiovascular pathology 1

Question 0

how do you assess with regards to primary/secondary heart disease?

Answer 0

primary - may results in effects on other body organ systems eg. congestion of the liver
secondary - systemic organ disease may result in cardiac problems eg. hypertension due to renal disease.

Question 1

4 ways to assess heart disease?

Answer 1

1. primary/secondary
2. clinically apparent
3. maybe asymptomatic
4. malfunction of left/right side of heart

Question 2

how do you assess with regards to if it is clinically apparent?

Answer 2

1. clinical signs are predominantly cardiac

2. may be related to changes in other organs eg. resp distress.

Question 3

how do you assess if asymptomatic?

Answer 3

1. depends on duration, siting, extent of of lesion

2. cardiac compensation may hide symtoms - chronic may suddenly manifest as acute!!

Question 4

what is the difference between malfunction of the left/right side of the heart?

Answer 4

1. left - pulmonary congestion/oedema and decreased CO due to back up of blood to lungs.
2. right - excessive RA pressure and systemic venous congestion

Question 5

heart anatomy: name the valves?
explain where blood comes in and goes out. which ventricle extends to the apex of the heart. name the nodes? other features?

Answer 5

see notes.

Question 6

what could go wrong with the heart? (6)

Answer 6

pump failure
obstructed blood flow
regurgitant blood flow
shunted blood flow
rupture of heart or a bv
cardia conduction disorders.

Question 7

what adaptions can be made by the heart?

Answer 7

heart can only hypertrophy not hyperplasia as cardiomyocytes cannot divide.

hypertrophy is due to either increased exercise or due to pathological changes relating to increased preload/afterload.

Question 8

explain preload and afterload and what they may lead to?

Answer 8

preload - causes hypertrophy in the heart. increased blood entering heart during diastole ‘volume overload’ (contraction = systole)
afterload- increased resistance that the heart must pump against during systole ‘pressure overload’.

Question 9

give 5 compensatory mechanisms of the heart?

Answer 9

cardiac dilation (eecentric hypertrophy)
cardiac hypertrophy (concentric)

increased rate
blood redistribution (perihperal vasoconstriction)
incread blood volume (kidney etc)

Question 10

2 types of cardiac hypertrophy? what should ratio be of right ventricle:septum/left ventricle?

Answer 10

1. concentric - increased mass of ventricle and walls become thicker. no change in EDV. (might reduce) due to afterload!!
2. eccentric - increased mass but wall = longer and chamber dilates causing and increase in EDV. (PRELOAD) wall may appear thinner.

ratio - left ventricle should be 3:1 of right ventricle (septum same as left ventricle)

Question 11

how would hypertrophy progress?

Answer 11

may eventually fail as during prolonged hypertrophy, capillary density cannot keep up, cardiomyocytes become further away from their blood supply - hypoxia of cells and degenration leads to chronic fibrosis and scar tissue. -cardiac failure.

Question 12

what is a double apex heart?

Answer 12

when right ventricle also extends down to the apex due to RV hypertrophy/dilation.

Question 13

explain the embryogenesis of the heart? normal development. (congenital cardia defects)

Answer 13

1. starts from simples tubes (primordial) these then begin to fold.
2. the anterior portion will form the truncus arteriosus and the ventricles (aorta and pulmonary trunk) the caudal portion will form the omphalomesenteric veins + sinus venosus and atria.
3. looping then occurs and division of the L&R.
4. septums form - endocardial cusions come towards each other - defects are dorsal in the ventricular septum as it develops ventral-dorsal. foramen ovale can cause defects in the atrial septum as it should be closed at birth or not long after.
5. heart completely formed at 1st 3rd of preg and is function very soon.
6. spiral septum between the major vessels forms (aorta/pulmonic)

Question 14

aetiology of congenital cardiac defects? what is a teratogen?

Answer 14

genetic - inherited (from sperm/ova)
acquired - defect in fertilised zygote.

environmental - infections (bluetongue), physical - hypoxia,radiation, - nutritional (vit A ), chemical

anything causing congenital defects = teratogen!!

Question 15

4 ways to classify congenital defects?

Answer 15

1. septal defects (results in shunts)
2. abnormal great vessels and origins
3. valvular - dysplasias
4. other

Question 16

explain types of septal defects resulting in congenital cardiac defects?

Answer 16

1. atrial defects - ASD. persistent foramen ovale between atria. (late closure in calf, sheep, horse is not uncommon and is normal) blood flows from left to right due to higher pressure on the systemic side. -right atria-roght ventricle- high RV preload = atrial dilation = eccentric hypertrophy of the RV. also high pulmonary return = LA dilation
2. ventricular septal defect - VSD)
   Occurs on its own or associated with other defects (fallot) common in cattle sheep, pigs
   majority are located high up the septum as it develops from ventral to dorsal. (below aortic valve) blood is again shuted from left-right (relsuts in mixing of o2 and non-o2 blood. increased RV preload and pulmonary overperfusion. RV hypertrophy (preload- eccentric) and high pulmonary return - LA dilation and high LV preload = eccentric hypertrophy (LV)

Question 17

explain what can happen to result in abnormalities of the great vessels? 3 ways?

Answer 17

defect sin the truncus arteriosus (aorta and pulmonic vessel develop from this) - means spiral partition may not be formed - this and the valves may not develop properly if not aligned properly.

1. transposition defect at the root of the vessels - aorta displaced to lie over the right ventricle (dextrorotation)
2. persistent truncus arteriosus - failure to partition the great vessels and so one large vessel seen.
3. semilunar valve stenosis (narrowing) - formation of band of fibrous tissue at valve. associated ventricle is concentrically hypertropied due to the increased afterload. 9pressure during systole) + aortic poststenotic dilation and pulmonic too!!

Question 18

what is tetralogy of fallot?

Answer 18

various congenital diseases occur together with other abnormal features = complex malformations.

1. ventricular septal defect
2. pulmonary stenosis
3. RV hypertrophy
4. dextro-rotated aorta (transposition defect at root)

Question 19

explain a patent ductus arteriosus? what results form this and what is it?

Answer 19

may be a normal temporary feature of post natal life (calf). if small may not spresent clinical signs unless exercise. it is a vessel branch between the aorta and the PA. RESULTS IN A SHUNT FROM AORTA TO PULMONIC ARTERIES. high RV afterload. = concentric hypertrophy. plumonary overperfusion - high pulmonary return LA dilation and LV preload - eecentric LV hypertrophy.

Question 20

explain shunt reversal? ‘eisenmengers syndrome’

Answer 20

normally blood will shunt from left-right. (ue to high pressure in left)

this results in pulmonary hyperperfusion - vadcular changes in the lung occur over time and result in high resistance in the lung vessels. shunt reversal may happen - so goes now from right-left. this leads to less blood going to the lungs - cyanosis and less O2 blood in the body. eisenmengers syndrome is systemic hypoxia due to this.

Question 21

what occurs with a persistent right aortic arch? what is the normal development of this from a foetus?

Answer 21

normally - 6 foetal arches and only 4 develops into the aorta. abnormal development of these can results in an arch over the oesophagus and so it is constricted. (vascular rings cross it). results in megaoesophagus with reguritation of food undigested (not vomiting as not from stomach)

Question 22

3 types of persistent aortic arch syndrome?

Answer 22

1. persostent right aortic arch - ring betweenL6 AND L4.
2. double aortic arch.
3. anomalous subclavian arches - no brachiocephalic trunk but the subclavians come straight off the aortic arch.

Question 23

explain AV valve displasia? could be congenital or degenerative. 2 types?

Answer 23

AV valves fail to form properly. causes AV valve reguritation at systole. cardiac dilation. left AV is most common (mitral) results in cant fully prevent backflow of blood and so increased afterload.

1. web like valve formation (no clear leaflets)
2. short chordae with small papillary mm. - coomon in dog left AV valve.

Question 24

explain coartation of the aorta? -

Answer 24

narrowing of aorta (rare and in bovine only)

Question 25

explain ectopica cordis?

Answer 25

heart normal but situated outside the body or in the abdominal cavity. common in cattle/pigs

Question 26

explain endocardial fibro-elastosis?

Answer 26

dog/pig/calf/cat
affected animals found dead in 2-3 months
no prev clinical signs
left ventricle endocardium is thickened with fibroelastic tissue (valves and cords may be affected) right side may/ may not be affected too.

Question 27

explain congenital abnormalities of pericardium? common in? what else may also happen at same time?

Answer 27

absence /incomplete pericardial sac. may also have a diaphragmatic hernia in puppies. ‘peritoneopericardial diaphragmatic hernia’ - intestines in the pericardium.