Cardiovascular

Question 1

What is NTpro-BNP? Where does it originate from? What does it do?

Answer 1

Natriuretic peptide - released from the atria and ventricular myocardium in response to stretch, hypoxia, sympathetic or RAAS activation. Aim is to control circulating blood volume and subsequently blood pressure. N-terminal pro-B type natriuretic peptide, is the inactive half that circulates in blood. The C (carboxyl) half is the active counter-part.

Question 2

What is the indications for measuring NT proBNP? What are the limitations?

By limitations, list the other differentials that could potentially incr

Answer 2

Useful as a functional test for cardiac disease e.g. determining whether a dyspneic cat has heart disease causing the dyspnea. It’s affected by renal dysfunction, pulmonary hypertension, and hyperthyroidism.

Question 3

What are the main differentials for sinus tachycardia in small animals?

Answer 3

Pain

Hyperthermia/ pyrexia

Excitement/ stress/ high arousal levels/ anxiety/ fear

Hypoxia/ anaemia

Hypovolaemia/ shock

Primary cardiac disease/ heart failure

Sepsis

Medications or toxins

Hyperthermia

Question 4

What are the main differentials for sinus bradycardia in small animals?

Answer 4

Hypothermia

Hypothyroidism

Medications or toxins

Increased intra-cranial pressures

Brainstem lesions

Vagal maneuvers - increased pressure on eyes or carotid sinus, or airway obstruction resulting in vaso-vagal reflex and increased parasympathetic tone

Severe metabolic dysfunction (hyperkalaemia, uraemia)

Question 5

Name the four different cardiac diseases that results in increased diastolic filling (preload)

Answer 5

MMVD

Tricuspid valve dysplasia

PDA - R->L shunting

Endocarditis

Question 6

Name four different cardiac diseases that results in increased afterload/ reduced ejection volume

Answer 6

Subaortic stenosis

Pulmonic valve stenosis

Major vessel thrombo-embolism

Pulmonary hypertension

Question 7

Name two different cardiac diseases that results in reduced elasticity/ impeded diastolic filling

Answer 7

HCM

Pericardial disease - restrictive, and cardiac tamponade

Question 8

Name two different cardiac diseases that results in reduced contractility/ reduced cardiac output

Answer 8

Arrhythmogenic cardiomyopathies

DCM

Question 9

Name the four neuro-hormonal mechanisms that manage blood pressure and blood volume.

According to Cunningham’s Veterinary Internal medicine textbook

Answer 9

Baroreceptor reflex

Atrial volume receptor reflex

Defense alarm system

Vasovagal syncope

Question 10

Describe the baroreceptor reflex - specifically where receptors are located, systems activated during response, aim of the reflex, as well as limitations of the reflex

Answer 10

Baroreceptor reflex is triggered by stretch receptors within the aortic arch and carotid branches. These are constantly firing - increased signaling occurs when there is increased arterial pressure, and decreased signaling occurs when there is decreased arterial pressure. When there is a change in blood pressure, activation of both sympathetic and parasympathetic to help change cardiac output and peripheral resistance. Main limitations is that the reflex only MINIMISES the change in blood pressure, and over time, it adapts to a new set point.

Question 11

Describe the atrial volume receptor reflex - specifically where receptors are located, systems activated during response and aim of the reflex

Answer 11

Reflex is triggered by specialized stretch receptors within the atria, as well as pulmonic veins. They work synergistically with the baroreceptor reflex - not only do they activate efferent sympathetic and parasympathetic nervous pathways, but they also act on the hypothalamus, pituitary gland to release ADH, and RAAS system.

Question 12

Describe briefly the two psychogenic reflexes for controlling blood pressure

Answer 12

Defense alarm system - fight or flight response to help increase sympathetic activation and decrease parasympathetic activation in response to emotional state. Whilst sleep and fighting may be extreme examples, can have a spectrum of activation of this system e.g. resting in a vet clinic vs. resting in own bed at home. It is important to note that the baroreceptor reflex’s set point gets elevated so it does not interfere with the changes attempted by the aroused emotional state

Vasovagal syncope - increased activation of the parasympathetic nervous system in response to emotional arousal

Question 13

Briefly describe the different sympathetic adrenergic receptors as well as effects when activated, and locations

Answer 13

alpha1 - vasoconstriction of arterioles, found in all organs

alpha2 - vasoconstriction of splanchnic organs

beta1 - increased stroke volume and heart rate, and activation of renin release from juxtaglomerular apparatus

beta2 - increased vasodilation in working skeletal muscles, coronary vessels

Question 14

Briefly describe the different parasympathetic nervous system muscarinic receptors, locations and effects when activated

Answer 14

M2 - reduces heart rate and stroke volume, as well as reduces effects of noradrenaline on ventricular myocardial cells

M3 - mediates vasodilation of arterioles generally through nitric oxide

Question 15

What is Starling’s mechanism? How does it help in relation to heart failure?

Answer 15

Starling’s mechanism occurs when there is decreased stroke volume of the left ventricle, there is still transient increased stroke volume of the right ventricle, which increases pressure of the left atria via increased volume in the left atria and pulmonary arteries. This increases end-diastolic volume of the left ventricle, which increases preload and helps to combat the sudden decrease in contractility of the left ventricle.

Question 16

What are the three main triggers for renin release? What inhibits renin release? Where is renin released? What inhibits its action?

Answer 16

Renin is released from the juxtaglomerular apparatus of the kidneys. It is activated by either decreased sodium concentration detected by the macula densa cells found within the distal convoluted tubules, or sympathetic activation, or reduced renal perfusion. It is inhibited by atrial natriuretic peptide released from atrial stretch receptors.

Question 17

What is the RAAS pathway?

Answer 17

Renin released from the kidneys -> cleaves angiotensiogen (from liver) into angiotensin I, where ACE (from lung vascular endothelium) converts into angiotensin II. Angiotensin II then acts on variety of tissues, such as hypothalamus, cardiovascular system, and adrenal glands to release aldosterone and help retain blood pressure and volume

Question 18

Describe the effects and tissues affected by angiotensin II.

Answer 18

-Cardiovascular - Gq coupled protein receptor AT1 in peripheral vasculature results in vasoconstriction

-Acts on hypothalamus to increase thirst, as well as release ADH from the posterior pituitary

-Acts on zona glomerulosa of the adrenal cortex to release aldosterone

-Stimulates release of noradrenaline from the sympathetic nervous sytem

-Acts on afferent and efferent arterioles of the juxtaglomerular apparatus to vasoconstrict

-Increases sodium re-absorption by the proximal convoluted tubules in the kidneys

Question 19

Describe the effects aldosterone, as well as where it is made

Answer 19

Zona glomerulosa of the adrenal cortex - acts on the principal cells and segment cells in the collecting ducts of the nephrons. Increases ENaC Na+ channels in the apical membrane of principal cells. Stimulates basolateral Na+/K+ ATPase activity.

Re-absorbs sodium via Na+/K+ ATPase pump, which results in retenion of sodium, but increased excretion of potassium

Question 20

Name the four main categories of anti-arrhythmic medications according to the Vaughan Williams system and broad mechanisms of action.

Answer 20

Class I - acts on sodium channels and of the myocardium and bundle of His and Purkinje fibres, which results in depression of depolarisation and prolonged repolarisation.

Class II - acts on adrenergic receptors, and generally antagonises sympathetic action (via beta1 receptors)

Class III - helps to prolong repolarisation by acting on potassium channels

Class IV - prolongs the depolarisation phase by acting on calcium channels

Question 21

The Vaughan Williams system for categorising anti-arrhythmics separates class I drugs into three separate sub-categories. Explain each sub-category, and give examples of each.

Answer 21

Class Ia - tends to moderately slow down myocardium (stage 0 depolarisation), and also increases repolarisation length. Quinidine

Class Ib - prefers less negative resting membrane potential myocardium (abnormal), and shortens repolarisation. Lidocaine, mexiletine

Class Ic - markedly suppresses depolarisation (phase 0), and little to no effect on repolarisation. Little clinical use in veterinary medicine at the moment.

Question 22

Describe lignocaine’s mechanism of action in relation to treatment of arrhythmias, as well as indications and side effects

Answer 22

Lignocaine - class Ib anti-arrhythmic, resulting in suppressing phase 0 of depolarisation of cells with lesser negative resting energy potential (making it more targeted towards diseased myocardium). It’s mainly used to treat ventricular tachyarrhythmias, and main side effects are neurotoxicity (depression, tremors, seizures), and gastrotoxicity (nausea, anorexia, vomiting, diarrhoea)

Question 23

Describe mexiletine’s mechanism of action, as well as indications and side effects

Answer 23

Mexiletine - class Ib anti-arrhythmic drug. Similar profile to lidocaine, but has reduced hepatic first pass metabolism, and lasts longer when given orally. Indicated in the chronic management of ventricular tachyarrhythmias, particularly if they have responded to lidocaine. Main side effects are gastrotoxic, so needs to be given with a full stomach.

Question 24

Describe diltiazem’s mechanism of action, as well as indications and side effects

Answer 24

Diltiazem - class IV anti-arrhythmic, or a non-dihydropyridine calcium channel blockers. Prolongs conduction through the AV node via inhibiting calcium channels, and prolongs the refractory period. Indicated for supraventricular tachyarrhythmias. Side effects related to hypotension from vasodilation, as well as bradycardia, and reduced cardiac contractility

Question 25

What are the roles of natriuretic peptides? Where are they synthesised?

Answer 25

Natriuretic peptides produced in brain, as well as atria and ventricles of the heart. They are released in response to stretch, and inhibits renin release from juxtaglomerular cells, as well as antagonises aldosterone at the adrenal cortex, and ADH.

Question 26

What is cardiac troponin I? Where is it synthesised, and what is its role as a diagnostic tool? What are its limitations?

Also half-life. And breed can affect its values too (which breed?)

Answer 26

Cardiac troponin I is a regulatory molecule that attaches to the thin filaments (actin) of myocardium. When there is myocardial injury, it is released into circulation, with half-life of 6hrs. It can be affected by renal dysfunction, GDV, exercise induction, age and breed (greyhounds). It can be measured to determine if there is possibility for cardiac disease causing clinical signs, but does NOT indicate underlying cardiac pathology.

Question 27

Describe the mechanisms of action of pimobendan

Make reference to biochemical reactions within the myocardium and vascul

Answer 27

Pimobendan belongs to the class inodilator. It exhibits its actions via two main mechanisms:
1. Phosphodiesterase III inhibitor - helps to reduce breakdown of cAMP, which increases intracellular Ca2+ concentrations. This means more calcium available to help bind with troponin C, and increased contractility.
2. Phosphodiesterase III and V inhibition also acts on smooth muscles within the vasculature - increased cAMP actually inhibits protein kinase C, which causes relaxation = vasodilation
3. Increased sensitivity of troponin C to binding to Ca2+ = increased contractility without proportional increase in oxygen consumption

Question 28

What are the indications, contra-indications and side effects of using pimobendan in small animals?

Answer 28

Indicated in valvular insufficiencies and dilated cardiomyopathies in dogs - can be used in cases where increased contractility would be beneficial. Contra-indicated in HCM in cats. Side effects include vomiting, diarrhoea, PU/PD, sinus tachycardia, increased risk of ventricular tachyarrhythmias.

Question 29

Describe the mechanism of action of benazepril, and it’s indications in veterinary medicine.

Answer 29

Benazepril is an ACE-inhibitor, and is primarily used in the treatment of cardiac disease, systemic hypertension, proteinuria, and idiopathic renal haematuria(1).

It works by inhibiting ACE, which stops the conversion of Angiotensin I into Angiotensin II. Works for proteinuria by decreasing glomerular transcapillary hydrostatic pressure and systemic blood pressure. It also reduces GFR (hence monitoring creatinine closely when initiating therapy).

(1) https://onlinelibrary.wiley.com/doi/full/10.1111/jsap.13352

Question 30

List side effects of using benazepril

Answer 30

1. Vomiting, diarrhoea, lethargy
2. Hypotension
3. Hyperkalaemia, increase in creatinine

Question 31

Describe the pathogenesis of development of atrioventricular valvular disease

Also known as endocardiosis/ myxomatous disease

Answer 31

There are many different mediators that contributes to the development of atrioventricular valvular disease. Essentially, the leaflets become more stiff. This is caused predominantly by activated valve interstitial cells, which promotes valve leaflet remodelling. Increased collagen and decreased elastin, as well as disruption to collagen fibril organisation. Mediators that increases matrix metalloproteases, collagenases and elastases are angiotension II, catecholamines, tumour necrosis factor, endothelin, interleukin, oxidative and mechanical stress. Initial mechanical injury to the valve leaflets is thought to be the initiating factor for development of MMVD.

Question 32

Describe the pathophysiology by which atroventricular valvular disease leads to heart failure

|No need to mention acute complications

Answer 32

Regurgitation of blood through valve due to valve leaflet edges no longer coapting -> gradual volume overload of affected atrium -> progressive atrial enlargement -> progressive ventricle enlargement -> gradual reduction in cardiac output (lack of atrial kick as well) -> activation of neuro-hormonal compensatory mechanisms -> progressive worsening of disease as mechanisms unable to completely compensate for changes -> increasing regurgitation and cardiac remodelling -> banking of blood in pulmonary veins -> increased pressure in pulmonary interstitial -> congestive heart failure

Question 33

List possible complications of chronic MMVD that may result in acute presentation

Answer 33

1. Arrhythmias, such as atrial fibrillation, or ventricular tachyarrythmias
2. Ruptured chordae tendinae
3. Ruptured atria (rare)
4. Iatrogenic volume overload (medications, IVFT)
5. Increased cardiac workload - e.g. exercise induction, sepsis, anaemia, hypertension

Question 34

Describe the pathogenesis and requirements of developing endocarditis.

And most common bacterial species isolated?

Answer 34

1. MUST have a bacteraemia to develop bacterial endocarditis, as route of infection is direct inoculation onot the leaflets of the valves
2. Usually also have endothelial damage, resulting in fibrin and platelet aggregations (which form vegetative lesions) which then can form a surface for bacteria to grow on
3. Vegetative lesions then reduces coaptation of the valve leaflets, resulting in valvular insufficiency (or if large enough, valvular stenosis)
4. Vegetations may break off and cause thromboembolism, or bacterial metastasis

Most common bacteria isolated are E.coli, Streptococcus spp, Staphylococcus spp., and Bartonella spp.

Question 35

According to ACVIM consensus guidelines 2019, what are the criteria for a dog to be in stage B2 MMVD?

Answer 35

1. Grade 3/6 heart murmur
2. La:Ao ratio >1.6
3. LVIDDN (left ventricle internal diameter in diastole normalised) >1.7 (when breed adjusted)
4. VHS >10.5 (when breed adjusted)

Ideally all the above criteria met

Question 36

What are the treatment recommendations for animals in stage B2 MMVD?

Answer 36

1. Commence on pimobendan 0.25-0.3 mg/kg BID (1)
2. Mild salt restricted diet
3. ACEI implementation - mixed results according to studies

Question 37

According to ACVIM consensus guidelines 2019, what are the criteria for a dog to be in stage C MMVD?

Answer 37

Any dog that has experienced clinical signs relating to heart failure, and is NOT refractory to standard treatment. Important to utilise appropriate diagnostic testing to rule out primary respiratory disease as cause for clinical signs.

Question 38

What are the long-term treatment recommendations after stabilisation for animals with heart failure due to MMVD?

Answer 38

1. Pimobendan 0.25-0.3 mg/kg BID
2. Furosemide 2 mg/kg q8-12hrs. Doses exceeding 8 mg/kg q24hrs moves patient to stage D
3. Can consider torsemide at 5-10% of furosemide dose for patients that do not respond to furosemide
4. ACEI - benazepril or enalepril 0.5 mg/kg PO BID
5. Spironolactone - 2 mg/kg PO SID to BID
6. Digoxin and dialitazem titrated to effect in animals with atrial fibrillation

Recheck renal parameters and electrolytes in 3-14 days after initiation of therapy

Question 39

What is the mechanism of action of furosemide? What are its indications and side effects?

Answer 39

Furosemide is a loop diuretic - it inhibits the Na/K/Cl co-transporter within the thick ascending loop of Henle. This means more sodium is excreted into the lumen, and hence more water. It is a high ceiling diuretic, and has quite high potency. Indicated for animals in congestive heart failure, or other conditions with fluid accumulation. Side effects are related to hypovolaemia, with associated azotaemia if dehydration occurs, as well as electrolyte imbalances (namely hyponatraemia, hypokalaemia, hypochloridaemia)

Question 40

What is the aetiopathogenesis of dilated cardiomyopathy in dogs?

Answer 40

There is no one causative aetiology for development of dilated cardiomyopathy in dogs.
1. Genetics - large breed to giant breed dogs tend to be affected - Dobermans, Great Danes, Irish Wolfhounds, Saint Bernards. Cocker Spaniels also affected more
2. Other factors that may contribute include biochemical defects, nutritional deficiencies, toxins, immunulogic mechanisms and infections

Dilated cardiomyopathy ultimately results in poor systolic function and poor myocardial contractility due to eccentric hypertrophy.

Question 41

What is the pathophysiology for developing heart failure subsequent to DCM?

Answer 41

Gradual poor systolic function/ myocardial contractility results in reduced ejection fraction, which causes volume overload -> this leads to gradual eccentric hypertrophy of the myocardium, and increased stiffness of the myocardium and papillary muscles, may cause valve leaflets to be stretched apart and cause valvular regurgitation -> changes in diastolic filling -> compensatory mechanisms such as RAAS and sympathetic activation try to compensate -> unable to compensate and development of congestive heart failure
-> may develop ischaemia leading to infarcts and arrhythmias

Question 42

Describe the aetiology for patent ductus arteriosus in dogs?

Answer 42

During birth, ductus arteriosus exists to divert blood away from the lungs, which have high vascular resistance. During birth, influx of oxygen into body results in constriction of smooth muscle within the ducts arteriosus and subsequent closure over the following weeks. In dogs with patent ductus arteriosus, have increased elastin, and decreased smooth muscle present. As such, get incomplete closure of the ductus arteriosus.
Genetics play a role (polygenic inheritance pattern likely, as seen with miniature poodles) as some breeds more prone - maltese, shetland sheepdogs, pomeranians, miniature poodles. Females 2.5 times more prevalent than males.

Question 43

Describe the pathogenesis of patent ductus arteriosus resulting in heart failure in left to right shunting.

Answer 43

Patent ductus arteriosus means blood diverted from the left side (increased resistance from systemic vasculature) to the right side (less vasculature resistance in pulmonary parenchyma). This results in volume overload to the LEFT side of the heart -> gradual eccentric hypertrophy of left atrium and ventricle due to increased strain -> activation of compensatory mechanisms -> gradual dilatation of mitral valve annulus and left atrium -> mitral valvular regurgitation -> left sided congestive heart failure

Question 44

Describe the development of RIGHT to LEFT shunting in animals with patent ductus arteriosus

Answer 44

R->L shunting occurs when the pulmonary vasculature resistance is GREATER than the resistance of systemic vasculature. This can be due to retained foetal vascular resistance (congenital pulmonary hypertension), or can be acquired depending on severity of the shunt from increased blood diverting into the pulmonary vasculature, which increases vascular resistance.

Question 45

What is the aetiopathogenesis of suboartic stenosis?

Which breeds most affected as well? And inheritance pattern?

Answer 45

Subaortic stenosis caused by genetic defect, resulting in a fibrous or fibromuscular ring located just under the mitral valve. Seen most often in Rottweilers, Newfoundlands and Golden Retrievers. Believed to be autosomal dominant trait with other genes overlying affecting phenotypic expression.
Animals affected are born with abnormal tissue arising from the sub-valvular region of the conotruncal septum, which retains its ability to undergo chodrogenic proliferation. Gradually, as the animal matures, the tissue becomes more fibrous/ fibromuscular, resulting in stenosis.

Question 46

What are the three severity grades of sub-aortic stenosis seen in Newfoundland dogs?

Answer 46

Grade I - no clinical signs, evidence of partial fibrous ring on post mortem
Grade II - mild clinical signs and haemodynamic changes with incomplete fibrous ring on post mortem
Grade III - severe clinical signs, and complete fibrous ring on post mortem

Some dogs may have mitral valve apparatus deformation, and some may have dynamic anterior motion of the mitral valve, which may cause clinical signs.

Question 47

Describe the pathophysiology for sub-aortic stenosis resulting in clinical signs seen?

Answer 47

Gradual stenosis of the sub-aortic valvular region -> reduction in cardiac output -> activation of compensatory mechanisms, as well as concentric hypertrophy of the left ventricle -> reduction in capillary density in myocardium due to hypertrophy -> increased systolic wall tension, as well as narrowing of coronary vessels -> increased risk of backflow of coronary blood -> increased risk of ischaemic damage and infarctions -> either get development of arrythmias and subsequent collapse or death, OR get fibrosis of the infarcts, and subsequent development of mitral or tricuspid valve regurgitation (from secondary changes)

Question 48

What is pulmonary hypertension? Describe the five different groups of pulmonary hypertension.

According to the classification system by the World Health Organisation

Answer 48

Pulmonary hypertension refers to increased systolic pulmonary arterial prssure >35mmHg, or mean pulmonary arterial pressure >25mmHg.

Mild = 35-55mmHg
Moderate = 55-80mmHg
Severe = >80mmHg

Group I = primary pulmonary hypertension, due to retained foetal pulmonary vascular resistance
Group II = secondary to chronic increased pulmonary venous pressure, usually due to left sided congestive heart failure
Group III = increased pulmonary vascular resistance secondary to hypoxia, such as fibrous bronchopulmonary disease, collapsing trachea, bronchomalacia, eosinophilic pneumopathy, idiopathic pulmonary fibrosis
Group IV = secondary to thromboembolism, such as PTE, or heartworm disease
Group V = idiopathic

Question 49

What is the mechanism of action of spironolactone? What are its indications and side effects?

Answer 49

Spironolactone is a competitive mineralocorticoid inhibitor. It competitively binds to the mineralocorticoid receptors of the principal cells in the collecting ducts. This REDUCES ENaC Na+ channel upregulation, and decreases stimulation of the Na+/K+ ATPase, which helps to REDUCE sodium retention and REDUCE potassium excretion. (weak diuretic, but mainly used to reduce risk of hypokalaemia) Mainly used as an adjunct to management of congestive heart failure in conjunction with other diuretics.

Main side effects are gastro-intestinal (anorexia, vomiting, diarrhoea), risk of hypotension and hyperkalaemia.

Question 50

What are the differentials for a bradyarrhythmia?

Answer 50

Sick sinus syndrome
AV blocks (1st, 2nd and 3rd degree blocks)

Question 51

Describe the different AV blocks.

Answer 51

• 1st degree AV block - there is a QRS complex for every p wave, but prolonged P-R interval
• 2nd degree AV block - Mobitz type I - there is gradual prolonging of P-R interval until eventuallly there is a P wave without QRS complex (Wenckebache phenomenon). After this dropped QRS complex, the cycle repeats
• 2nd degree AV block - Mobitz type II - there are P waves NOT associated with QRS complexes, but the P-R interval remains the same.
• 3rd degree AV block - complete dissociation between P waves and QRS complexes

Question 52

Outline 8 different common complications that may occur secondary to advanced acquired atrioventricular valve disease in dogs?

Answer 52

1. Heart failure refractory to medications (stage D according to ACVIM consensus guidelines 2019)
2. Pulmonary hypertension
3. Cardiac arrythmias - typically ventricular tachycardia, although may get intermittent bradyarrhythmias
4. Ruptured left atrium
5. Ruptured chordae tendinae
6. Development of systemic hypertension
7. Progressive renal failure
8. Chronic bronchitis/ airway disease

Question 53

List the 3 different points of Virchow’s triad, as well as examples of each

Answer 53

1. Blood stasis/ obstruction
   e.g. intra-luminal or extra-luminal obstructions, portal hypertension
2. Hypercoagulable state
   2a - systemic causes e.g. neoplasia, severe inflammatory conditions e.g. IMHA, SLE, pancreatitis, amyloidosis, sepsis, SIRS
   2b - polycthaemia e.g. polycythaemia vera, secondary to hypoxaemia, R-L shunting, EPO secretion, kidney disease
   2c - hypertriglyceridaemia - hyperadrenocorticism, hypothyroidism, diabetes mellitus, primary breed related (miniature schnauzers, shelties)
   2d - cardiovascular disease - heartworm, HCM, endocarditis
3. Endothelial damage to vessels
   e.g. DIC, vasculitis

Question 54

What clinical signs may be associated with heartworm disease in dogs?

Answer 54

70% of dogs positive for heartworm antigen are asymptomatic, about 25% will have signs associated with pulmonary hypertension or pneumonitis (such as exercise intolerance, syncope, coughing, respiratory difficulty), and 5% will have signs of caval syndrome

Question 55

Describe the pathophyisology of heartworm disease in dogs.

Answer 55

Migration of L5 to the peripheral pulmonary arteries of the caudal lung lobes. During migration and settlement in the pulmonary vasculature, will get reactive arteritis due to endothelial damage by the larvae and adult worms. Widening of the intercellular space from the worms results in peri-arterial oedema. Endothelial sloughing increases white cell adhesion and platelet aggregation. Will also get trophic factors from the endothelium causing smooth muscle in the intima proliferatin, collagen and endothelial deposition, resulting in narrower arteries.

Will also get endotoxin release from Wolbachia spp. and immune reaction to Wolbachia surface proteins (WSP) resulting in renal and pulmonary inflammation

Question 56

What pathophyisological factors increase risk of pulmonary thromboembolism in dogs with heartworm disease?

Answer 56

1. Endothelial damage, as well as endothelial sloughing can promote platelet aggregation and white cell adherence, increasing risk of thrombus formation
2. Dead worms circulating through pulmonary vasculature

Question 57

Describe the pathophysiology of heartworm disease leading to RSCHF, and eventually caval syndrome, in dogs

Answer 57

Pulmonary pneumonitis or eosinophilic penumonitis from the peri-arteritis can result in hypoxic vasoconstriction, leading to pulmonary hypertension. Increased pressures leading to pressure overload of the right ventricles, leading to gradual eccentric hypertrophy, and eventual dilatation of the right ventricle, and subsequent reduced cardiac output.

Caval syndrome occurs when the worm burden grows so large that the worms infiltrate through the right outflow tract and start going into the right ventricle. This can cause valvular insufficiency, as well as physical obstruction of the outflow tract. The mass of worms often causes schistocytosis, anaemia and haemoglobinaemia.

Question 58

What class of drug is amlodipine? What is its mechanism of action and indications, contra-indications and side effects?

Answer 58

Amlodipine is a second generation dihydropyridine calcium channel blocker. It acts on the L-type calcium channels on myocardial and vascular smooth muscle cells, and blocks the initial influx of calcium, which reduces muscle contraction due to reduced binding to calmodulin and subsequent cascade.

Main effects are on the peripheral arteriolar vasculature and results in vasodilation, causing decrease in blood pressure. Negligible negative inotropic and chronotropic effects at therapeutic doses.

Indications for management of systemic hypertension in small animals, as well as proteinuria in cats.