Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
68 Cards in this Set
- Front
- Back
|
What is Endocardiosis?
|
Myxomatous degeneration of the heart valves.
The most common cardiovascular lesion and the most common cause of heart failure in dogs. |
|
|
Endocardiosis has polygenic inheritance in which two dog breeds?
|
CKC Spaniels, Dachshunds
|
|
|
What is the prevalence of endocardiosis?
|
Male>Female
Increases with age. Especially toy breeds, but also seen in Dobermans VERY high onset in CKC |
|
|
What is Myxomatous Degeneration?
|
Pathological weakness of connective tissue
|
|
|
Which valves are most commonly affected by endocardiosis?
|
The mitral valve, and to a lesser extent, the tricuspid valve. Occasionally the aortic and pulmonic valves affected.
|
|
|
In endocardiosis, the earliest lesions develop where?
|
The margins of the valve leaflets.
|
|
|
What are some of the lesions of endocardiosis?
|
See small discrete nodules at the margins of the valve leaflets or more uniform valve thickening-> large nodules and plaquelike deformities +/- fixed upward displacement of the free valve margins into the atrium (valve prolapse)
|
|
|
What happens to the chordae tendineae in endocardiosis?
|
They become thickened where they insert into the valves.
|
|
|
What is the main consequence of endocardiosis?
|
Valvular insufficiency-> regurgitation of blood during systole->volume overload on the atrium and ventricle--> atrial dilation and ventricular dilation/eccentric hypertrophy
|
|
|
What is endocarditis?
|
Inflammation of the endocardium.
A serious condition, usually characterized by intra-cardiac thrombosis and risk of thromboembolism. |
|
|
What is the most common type of endocarditis?
|
Valvular...but can involve the heart chamber (mural)
|
|
|
Valvular endocarditis is usually caused by?
|
Recurrent or persistent bacteraemia.
|
|
|
The earliest lesions of valvular endocarditis tend to develop on which part of the leaflets?
|
The side exposed to forward blood flow. The atrial side of the tricuspid and mitral valves.
|
|
|
Valvular endocarditis is most often seen in which animals?
|
LARGE animals (especially pigs) and seldom seen in dogs and cats.
|
|
|
What are some clinical signs of valvular endocarditis?
|
Pyrexia, shifting lameness (due to deposition of immune complexes in synovial membranes) and cardiac murmur.
|
|
|
Give two uncommon causes of valvular endocarditis?
|
Fungi (Aspergilla) or Parasites (Strongylus vulgaris larvae in horses)
|
|
|
Which side of heart does valvular endocarditis usually affect? And in what order are valves affected?
|
Most common in the heart in LEFT Mitral> Aortic > Tricuspid > Pulmonic Valve
Tricuspid most common in cattle Aortic most common in horses |
|
|
The most common lesions of valvular endocarditis are?
|
Early: valve leaflet swelling with irregular ulceration of the valvular endocardium
Older Lesions: Large, friable, rough surface, yellow/grey/red vegetations largely composed of thrombis (usually containing deeply buried bacterial colonies) |
|
|
What is the sequelae of valvular endocarditis?
|
Commonly fatal.
Valves may become stenotic or insufficient and eventually lead to heart failure Also risk of bland or septic thromboembolism. Tricuspid or Pulmonary valve-> Lungs Mitral or Aortic-> myocardium, kidneys, spleen, liver.... |
|
|
Why might mural endocarditis develop?
|
Could be an extension of severe valvular endocarditis (especially in cattle with Arcanobacterium Pyogenes infection.
Extension of infection in underlying myocardium. |
|
|
What is the most common cause of heart failure in dogs?
|
Endocardiosis...in the mitral valve.
|
|
|
What is the most common cardiovascular lesion?
|
Endocardiosis.
|
|
|
Name three distinct forms of mural endocarditis?
|
Parasitic endocarditis in horses, blackleg in ruminants and uraemic ulcerative endocarditis in dogs
|
|
|
What causes parasitic endocarditis in horses?
|
Strongylus vulgaris larvae. Now rarely seen due to anthelminthic therapy.
|
|
|
What is Blackleg in Ruminants? Describe it...
|
Rapidly fatal gangrenous myositis caused by Clostridium chauvoei.
In cattle and sometimes in sheep Skeletal muscle->activation of latent bacterial spores --> local proliferation of bacteria and absorption of endotoxins +- bacteria into circulation Affected animals usually have acute fibrinohaemorrhagic pleuritis and pericarditis and acute diffuse pulmonary oedema |
|
|
What is the most common mural endocarditis?
|
Uraemic Ulcerative endocarditis in dogs.
More common in acute renal failure, than in chronic. |
|
|
Uraemic ulcerative endocarditis of dogs mainly involves which part of the heart?
|
The wall of the left atrium +- initial pulmonary artery and aorta
|
|
|
What is the appearance of uraemic ulcerative endocarditis of the dog?
|
Lesions commence as sub endothelial swelling with gyclosaminoglycan deposition >fibrosis or progression to necrosis with endothelial ulceration and local thrombosis
A perforating ulceration can lead to fatal hemopericardium |
|
|
What are some effects of barbiturate euthanasia?
|
Gritty, cream-white barbituate crystals may be found on endocardium of particularly the right ventricle
Post morem blood clots within the right heart chambers of euthanized animals may also be discolored brown or dark green and are friable. |
|
|
What is hyperemia?
|
Increased volume within a blood tissue.
|
|
|
What is Active Hyperemia?
|
Increased blood volume due to arteriolar dilation and expansion of the perfused capillary bed.
All capillaries in the affected area are distended and perfused. |
|
|
Is active hyperemia localized, generalized, or both?
|
ALWAYS localized
|
|
|
Active hyperemia is mediated by?
|
Vasoactive molecules--bradykinin, prostoglandins, lactic acid
|
|
|
What is meant by the terms active hyperaemia, passive congestion, pulmonary
hypertension and systemic hypertension? |
-active hyperaemia= increased blood volume due to arteriolar dilation and expansion of the perfused capillary bed.
-passive congestion= a passive process in which increased blood volume within a tissue results from impairment of venous outflow. -pulmonary hypertension=increased blood pressure within the pulmonary artery -systemic hypertension= abnormally high systemic arterial blood pressure. |
|
|
In what circumstances does active hyperaemia develop?
|
Increased tissue metabolism and oxygen consumption; e.g. inc. blood flow to GI tract following ingestion of food; inc. flow to skeletal muscles during exercise; inflammation
|
|
|
In what circumstances does localised passive congestion develop?
|
Blood pooling within venous channels and capillaries; e.g. luminal obstruction of veins eg by thrombi; intestinal strangulation from torsion; gravitational pooling of venous blood in inactive/recumbent animals.
|
|
|
In what circumstances does generalised passive congestion develop?
|
HEART FAILURE!!! Left sided: pools in pulmonary veins and alveolar capillaries of the lungs; Right sided: pools in vena cava and liver, spleen, etc.
|
|
|
• How would you grossly distinguish between active hyperaemia and passive congestion of an organ or tissue in a live animal?
|
Active= warm and red; passive= no change in temp, blue-red to blue-black.
|
|
|
What are the potential consequences of passive congestion of tissues or organs?
|
Increased hydrostatic pressure within engorged veins and capillaries promotes oedema formation, capillary rupture with haemorrhage etc., local tissue hypoxia due to chronic stagnation of poorly oxygenated blood->parenchymal cell degeneration or necrosis and reparative fibrosis. If obstruction develops slowly, may develop collateral channels to provide alt. routes of drainage e.g. blood may be shunted away from portal vein and liver into the caudal vena cava etc.
|
|
|
What is the renin-angiotensin-aldosterone system (RAAS)? What triggers its
activation and what are the consequences of its activation? |
Plays important role in blood pressure regulation. KIDNEYS. Following a drop in BP, renin released from renal juxtaglomerular cells and cleaves Ag->agI which is then cleaved to agII & agIII. Ag2+3 cause increase in ciculating blood vol. (via stimulating aldosterone secretion and hence renal sodium and water resorption) and TPR (via causing vasoconstriction). AgII also stimulates release of ADH to promote water resorption by kidneys. All of this causes an increase in blood volume and hence increases the blood pressure.
|
|
|
What is a potential consequence of sustained pulmonary hypertension?
|
May lead to cor pulmonale (pulmonary hypertensive heart disease), characterized by RIGHT ventricular dilation or hypertrophy and potentially right-sided heart failure.
|
|
|
What are some causes of pulmonary hypertension in domestic animals?
|
Congenital cardiac anomalies causing L->R blood shunts; pulmonary thromboembolism; heartworm disease (most common cause in DOGS); major airway obstruction leading to pulm. a. constriction.
|
|
|
What are common causes of systemic hypertension in cats and dogs?
|
Renal disease (esp. glomerular dis.), hyperadrenocorticism, hypo/hyper-thyroidism, functional phaeochromocytoma (tumour of adrenal medulla producing excess A/NA).
|
|
|
What are the potential consequences of sustained systemic hypertension?
|
Damage delicate capillaries; persistent arteriolar constriction in response to hypertension->smooth m. hypertrophy of tunica media of arterioles->arteriosclerosis with narrowing of vessel lumen->further increase in vascular resistance exacerbating hypertension. These structural changes and vascular spasm can->capillary hypoxia, tissue damage, haemorrhage and tissue infarction with organ dysfunction. Also causes increased pressure load (afterload) on the heart->left ventricular concentric hypertrophy. Capillary damage from chronic hypertension->glomerulosclerosis (scarring of the glomerulus)->contributes to deterioration of renal function and further increases peripheral vascular resistance (i.e. chronic hypertension tends to perpetuate itself).
|
|
|
What is meant by the term oedema?
|
Accumulation of excess extracellular fluid in the interstitium and/or body cavities.
|
|
|
• What are the major factors that control the movement of water (and electrolytes and other small solutes) between the interstitium and the microvasculature and normally prevent the development of oedema?
|
Movement is carefully controlled by haemostatic mechanisms. Interstitial fluid pressure- influences whether fluid will move from blood vessels into the interstitium or from the interstitium into interstitial lymphatics. Osmotic and hydrostatic pressures control the movement of water, electrolytes and solutes across vessel walls in the microcirculation. Interstitial lymphatic’s remove the excess from the slight differences in pressure between plasma hydrostatic P and plasma colloid osmotic P.
|
|
|
What is meant by the terms ascites, hydrothorax, hydropericardium, hydrocoele and anasarca?
|
Ascites= accumulation of oedema fluid within peritoneal cavity
Hydrothorax= accum. of oedema fluid within pleural cavity Hydrocoele= accum. of oedema fluid within the cavity of the tunica vaginalis of the scrotum. Anasarca= severe, generalized oedema (often most prominently in the subcutis but with accompanying body cavity effusions) |
|
|
What are the five main mechanisms that can lead to oedema development?
|
1. decreased plasma colloid osmotic pressure
2. increased plasma hydrostatic pressure 3. lymphatic obstruction 4. increased vascular permeability 5. sodium retention |
|
|
Which of the five mechanisms of oedema provoke localised oedema?
|
plasma hydrostatic pressure
lymphatic obstruction increased vascular permeability |
|
|
Which of the mechanisms of oedema can lead to generalised oedema and why?
|
lymphatic obstruction- - due to severe congenital malformations of the lymphatic system
increased vascular permeability-in conditions with generalized vasculitis, oedema disease of pigs etc Sodium Retention- activation of the renin-angiotenison-aldosterone system and renal retention of sodium and water contribute to generalised oedema development in such conditions as hypoalbuminaemia, right sided congestive heart failure, and ascites caused by portal osmotic pressure by dilution of albumin Sodium Retention |
|
|
What gross features would allow you to recognise oedematous tissues or organs in the live or dead animal?
|
Excess watery, colourless-pale yellow, clear, non-viscous fluid within tissues or body cavities, swollen, heavy, ooze fluid, pitting oedema
|
|
|
What are the potential consequences of oedema?
|
Can impair wound healing, susceptible to secondary bacterial infection with impaired clearance of infection, cerebral oedema may cause seizures, pulmonary oedema can cause drowning from within via flooding alveoli and terminal bronchioles preventing ventilation and gas exchange.
|
|
|
What is meant by the term haemostasis?
|
The sequence of events that follows vascular injury to rapidly produce a localized plug to prevent blood loss.
|
|
|
What are the key events in formation of the primary haemostatic plug following injury to a blood vessel?
|
to a blood vessel?
1. vasoconstriction- immediately after injury, due to reflex neurogenic mechanisms and endothelin released by endothelium. 2. Endothelial injury exposes the highly thrombogenic (procoagulant) subendothelial extracellular matrix, causing platelets to adhere within seconds of vessel injury. 3. Adherent platelets become activated and release products that cause recruitment of additional platelets. 4. The platelets form a primary haemostatic plug at the site of vessel injury, which is unstable and short-lived but is sufficient to control bleeding from tiny injuries to small vessels. |
|
|
What is meant by the term hydropericardium?
|
Accumulation of non-inflammatory fluid (transudate or modified transudate) in the pericardial sac.
|
|
|
What are the possible mechanisms by which hydropericardium develops?
|
Right sided congestive heart failure, hypoalbuminaemia, local venous or lymphatic obstruction, increased vascular permeability.
|
|
|
What are the typical gross features of hydropericardium?
|
Clear colourless or pale yellow fluid, may form gel on exposure to air if rich in protein, serosal surfaces remain smooth and glistening.
|
|
|
What is meant by the term cardiac tamponade?
|
Compression of the heart leading to impaired atrial and ventricular filling.
|
|
|
What are the potential consequences of passive congestion of tissues or organs?
|
Increased hydrostatic pressure within engorged veins and capillaries promotes oedema formation, capillary rupture with haemorrhage etc., local tissue hypoxia due to chronic stagnation of poorly oxygenated blood->parenchymal cell degeneration or necrosis and reparative fibrosis. If obstruction develops slowly, may develop collateral channels to provide alt. routes of drainage e.g. blood may be shunted away from portal vein and liver into the caudal vena cava etc.
|
|
|
What is the renin-angiotensin-aldosterone system (RAAS)? What triggers its
activation and what are the consequences of its activation? |
Plays important role in blood pressure regulation. KIDNEYS. Following a drop in BP, renin released from renal juxtaglomerular cells and cleaves Ag->agI which is then cleaved to agII & agIII. Ag2+3 cause increase in ciculating blood vol. (via stimulating aldosterone secretion and hence renal sodium and water resorption) and TPR (via causing vasoconstriction). AgII also stimulates release of ADH to promote water resorption by kidneys. All of this causes an increase in blood volume and hence increases the blood pressure.
|
|
|
What is a potential consequence of sustained pulmonary hypertension?
|
May lead to cor pulmonale (pulmonary hypertensive heart disease), characterized by RIGHT ventricular dilation or hypertrophy and potentially right-sided heart failure.
|
|
|
What are some causes of pulmonary hypertension in domestic animals?
|
Congenital cardiac anomalies causing L->R blood shunts; pulmonary thromboembolism; heartworm disease (most common cause in DOGS); major airway obstruction leading to pulm. a. constriction.
|
|
|
What are common causes of systemic hypertension in cats and dogs?
|
Renal disease (esp. glomerular dis.), hyperadrenocorticism, hypo/hyper-thyroidism, functional phaeochromocytoma (tumour of adrenal medulla producing excess A/NA).
|
|
|
What are the potential consequences of sustained systemic hypertension?
|
Damage delicate capillaries; persistent arteriolar constriction in response to hypertension->smooth m. hypertrophy of tunica media of arterioles->arteriosclerosis with narrowing of vessel lumen->further increase in vascular resistance exacerbating hypertension. These structural changes and vascular spasm can->capillary hypoxia, tissue damage, haemorrhage and tissue infarction with organ dysfunction. Also causes increased pressure load (afterload) on the heart->left ventricular concentric hypertrophy. Capillary damage from chronic hypertension->glomerulosclerosis (scarring of the glomerulus)->contributes to deterioration of renal function and further increases peripheral vascular resistance (i.e. chronic hypertension tends to perpetuate itself).
|
|
|
What is meant by the term oedema?
|
Accumulation of excess extracellular fluid in the interstitium and/or body cavities.
|
|
|
• What are the major factors that control the movement of water (and electrolytes and other small solutes) between the interstitium and the microvasculature and normally prevent the development of oedema?
|
Movement is carefully controlled by haemostatic mechanisms. Interstitial fluid pressure- influences whether fluid will move from blood vessels into the interstitium or from the interstitium into interstitial lymphatics. Osmotic and hydrostatic pressures control the movement of water, electrolytes and solutes across vessel walls in the microcirculation. Interstitial lymphatic’s remove the excess from the slight differences in pressure between plasma hydrostatic P and plasma colloid osmotic P.
|
|
|
What is meant by the terms ascites, hydrothorax, hydropericardium, hydrocoele and anasarca?
|
Ascites= accumulation of oedema fluid within peritoneal cavity
Hydrothorax= accum. of oedema fluid within pleural cavity Hydrocoele= accum. of oedema fluid within the cavity of the tunica vaginalis of the scrotum. Anasarca= severe, generalized oedema (often most prominently in the subcutis but with accompanying body cavity effusions) |
|
|
What are the five main mechanisms that can lead to oedema development?
|
1. decreased plasma colloid osmotic pressure
2. increased plasma hydrostatic pressure 3. lymphatic obstruction 4. increased vascular permeability 5. sodium retention |
