Path Cardiovascular Flashcards
- The four histological features of cardiac heart muscle ?
- intercalated discks
- branching
- central nucleus
- striations - What is the faint brown granular pigment depicted ?
Lipofuscin
Light brown pigment granules made up of lipid containing residues of lysosomal digestion. This is an incidental finding considered to indicate aging “wear and tear pigments”
Describe the ‘normal’ (non-pathological) cardiovascular changes that may be observed post mortem ?
Incidental post mortem changes of the heart
- Rigor mortis
- Contracted myocardium may lead to emptying of the left ventricle. - Post mortem clotting
- The clot is usually found in the right ventricle
- red current jelly clots atria, right ventricle and large vessels
- White chicken fat clots
- composed primarily of clotted plasma and fibrin
- reduced number of erythrocytes
- often occurs in horses (rapid ESR) erythrocte sedimentation rate
- may occur in anemia, leukaemia and systemic inflammation.
Describe the reversible and irreversable cardiac cell response to injury ?
Cardiac cell response to injury
1. Reversible / sublethal / degeneration
- inflammation
- haemorrhage
- adaptation (atrophy, haemorrhage)
- fatty degeneration or infiltration
- Lipofuscin build up
- Vacuolar degeneration
- Irreversible (lethal) damage
- necrosis (or apoptosis)
- leukocytes infiltration and phagocytosis
- repair by fibrosis (non specific to aetiology)
- peracute injury: may be no visable lesions
Cardiomyocytes have a limited ability to regenerate. This is partially due to the continual contraction of remaining healthy cells.
- hyperplasia only occurs over the first seven months of life
Describe the tissues seen here ?
Diffusely pale heart. No histological abnormalities.
Young animals have a lower haematocrit.
Disscuss why haemorrhage is often observed in the epicardium, myocardium and endocardium ?
Haemorrhage
Petechiae = smaller pin point haemorrhages 1-2 mm
Ecchymosis = larger haemorrhages 3-5mm
Injury to endothelium and increased pressure within in heart
- commonly due to septacaemia, endotoxaemia, electrocution or anoxia (total oxygen deprivation).
- usually observed coronary groove
Disscuss the five common compensatory mechanisms of the heart ?
The common compensatory mechanisms of the heart to injury
- Cardiac dilation; allows for more stretching to increase contractile force Frank Starling phenomenon.
- Hypertrophy; allows maintenance of outflow against sustained volume / pressure overload.
- increase heart rate
- increase blood volume (increase Na+)
- redistribution of blood volume
The peripheral circulation may feel cold
What factors could result in Eccentric hypertrophy ?
Eccentric hypertrophy
Is enlargement of the ventricular chamber (dilation)
- wall remains normal or decrreases in thickness
- this pathology is due to increased blood volume
eg valvular insufficiencies, septal defects
What factors could result in concentric hypertrophy ?
Concentric hypertrophy
A thicker wall resulting in a smaller ventricular chamber.
Hypertrophy = increase in cell size
This results from an increase in pressure load
eg valvular stenosis, systemic hypotension, pulmonary disease and aortic stenosis (common).
A = Dilation (Eccentric hypertrophy)
B= Concentric hypertrophy
Disscuss cardiac syncope and its causes ?
Cardiac syncope
Failure to get adequte blood supply to the brain (acute)
- acute collapse and loss of consiousness
- extreme changes in HR and blood pressure
- lesions may be or may not be present
The causes
- Arrhythmias - ventricular fibrillation, AV node heart block etc
- massive myocardial necrosis
Disscuss congestive heart failure and its causes ?
Congestive heart failure
Usually a chronic manifestation of cardiac disease
- CHF and CCF
- heart has 3-5 fold reserve capacity
Usually develops slowly due to chronic changes
- pressure overload, volume overload or cardiac disease
- pulmonary disease
- congenital abnormalities
- renal disease
- valvular disease
- myocardial disease
- vascular disease
Define backward heart failure, forward heart failure, systolic heart failure and distolic heart failure ?
Forward failure decreased blood flow forwards to peripheral tissues
Backward failure = accumulation of blood behind the failing chamber
Systolic failure = inadequate inability to eject blood adequately
Diastolic failure - inadequate ventricular filling
Why does cardiac failure lead into a visious cycle ?
The viscious cycle of cardiac failure
- reduced renal blood flow
- hypoxia of kidneys
This causes renin release of the juxtaglomerular apparatus - stimulates aldosterone from the adrenal cortex - angiotensin 2
This acts on the renal tubules causing Na+ and H2O retension
1. oedema especially body cavities
2. polycythaemia (abnormally high number of red blood cells) increased velocity of blood
3. hypovolaemia (increased plasma volume
4. increasing the workload on an already failing heart
Describe the appearance of acute and chronic left sideded heart failure ?
Left sided congestive heart failure
Acute
- pulmonary congestion and oedema
Chronic
- chronic passive pulmonary congestion and oedema (lung fails to collapse)
- haemosiderosis “heart failure cells”
- pulmonary fibrosis
These pathological changes appear grossly - red-purple tinge to the lungs, foamy fluid in airways and alveoli
Stable foam = surfactant mixed with arterial fuid
What factors could result in this pathology and discuss how it is caused?
Left sided congestive heart failure
The causes / factors
- loss of contractility
- severe congenital heart disease
- dysfunction of the mitral or aortic valves
Describe the depicted cell type ?
Heart failure cells
= alveolar macrophages containing haemosiderin
These erythrocytes are pushed into the alveolar interstiteum due to pulmonary congestion - where they are ingested by alveolar macrophages.
Describe the pathology of acute and chronic right sided heart failure?
Congestive right sided heart failure
Acute
- systemic congestion
- hepatomegaly
- splenomegaly
Chronic
- chronic systemic congestion (nutmeg liver)
- severe sodium and water retention
- ventral subcutaneous oedema horses and ruminants
- ascites or hydrothorax in cats
What factors could result in this type of congestive heart failure?
Right sided congestive heart failure
Caused by
- pulmonary hypertension
- cardiomyopathy
- dysfunction of the tricupsid or pulmonary valve
Describe the poisoning which occurs after pimelea simplex ingestion ?
Pimelea simplex ingestion - contains toxin simplexin
This toxin results in chronic right sided heart failure.
- Desert rice flower
- affects cardiopulmonary function and induces anaemia
- toxin constricts muscle of pulmonary venules
- increasing pulmonary vascular resistance
- right sided heart failure
The clinical signs
- severe diarrhoea and potential death
- muffled heart sounds
- prominent jugular pulse
- weight loss, rough coat
Left sided heart failure
acute pulmonary congestion seen in a dog
Answers
1. Alveoli macrophages which have consumed haemidersiderin
2. Chronic congestion and oedema of the lungs (not collapsed) + large numbers of heart failure cells in the lung = left sided congestive heart failure.
- mottled brownish appearance
Prussian blue reaction
Identify the six possible causes of congenital abnormalities ?
The six causes of congenital abnormalities
1. Spontaneous
2. Hereditory
3. Chemicals = drugs, toxins = thalidomide, griseofuluin
4. Nutritional deficiencys Vitamin A, Zinc and Copper
5. Irradiation
6. Foetal hypoxia
Define stenosis ?
Stenosis = The abnormal narrowing of a passage in the body.
Describe foetal circulation ?
Foetal circulation
Ductus venosus = liver shunts approximately 50% of blood from the umbilical vein to the vena cava
Foramen ovale = Blodd shunted from the right atrium to the left atrium
Ductus arteriosis = (bypasses the lungs) Moves from the right ventricle into the aorta through a patent duct ductus arteriosus
- vascular channel from the pulmonary artery and aorta
Identify and describe this underlying pathology ?
Patent ductus arteriousus
The ductus arteriosus becomes patent (unobstructed failure to close).
The blood is shunted from the aorta to pulmonary artery
- results in pulmonary hypotension
- blood usually shunts the lungs during foetal life but the ductus arteriosus becomes ligamentum arteriosum postnatally (closing around 7 - 10 days after birth in dogs)
- frequent in dogs and cats
- often inherited in poodles
- increased blood flow to the lungs.
What are the consequences of the following pathology ?
PDE Patent ductus arteriosus
The consequences of PDA
- continuous murmur
- volume overload affecting the pulmonary arteries, pulmonary veins, left atrium and ventricle (increased preload)
- dilation of left atrium and ventricle - eventually leading to left sided CHF
Identify this defect and describe its consequences ?
ASD = Atrial septal defect
Can be due to failure of closure of the foramen ovale or other septal defects (faulty development of the septum).
Consequences of ASD
- A large ASD >9mm may cause clinically remarkable left to right shunt.
- blood shunted left to right atrium (volume overload of the right arium and righht ventricle).
- if left untreated can result in enlargement (dilation / hypertrophy) of the right side of the heart and ultimately heart failure.
small restrictive defects may have little consequence
Cattle are more prone to right sided heart failure.
Identify this defect and describe its consequences ?
VSD Ventricular septal defect
Failure of a complete development of the IV septum, especially in the upper membranous portion.
Consequences
This allows blood to shunt between ventricles left to right.
- pressure gradient
- degree of shunting depends upon the size of defect
- blood recirculating through pulmonary vessels and left cardiac chambers - dilation
- right ventricle may dilate as well in animals with large septal defects
- MOST VSDS ARE SMALL
Cattle are more prone to develop right sided heart failure
Identify this pathology and its consequences ?
Tetralogy of Fallot
The consequences
- The consequences are dependant on the severity of stenosis, size of VSD and ratio of vascular resistance between pulmonary and systemic circulation.
- decreased blood flow to pulmonary circulation
- deoxygenated blood passing into the aorta
- animals suffer fatigue, generalised cyanosis and polycythemia (high red blood cells)
- eventually end up with a higher pressure system on the right hand side
Describe the four lesions of the Tetralogy of fallot
Tetralogy of fallot
There are four lesions
- pulmonic stenosis
- ventricular septal defect (high in septum)
- Dextraposition of the aorta (overides both L and R ventricles)
- secondary hypertrophy of RV myocardium
Identify this pathology and describe its consequences ?
Pulmonic stenosis
There are several types of lesions possible
Subvalvular stenosis = formation of a circumferential band of fibrous or muscular tissue beneath the valve.
(Observed in photo)
Valvular stenosis = malformation of the valve itself
small orifice in a dome of thickened tissue
Identify this pathology and describe its consequences ?
Subaortic stenosis
This is seen as a thick zone of endocardial fibrous tissue - which encircles the LV outflow tract below the valve
- frequently observed in pigs and dogs
- can be subclinical if mild
The consequences
- foci of myocardial necrosis
- fibrosis in inner LV wall
- visible dense white band
Identify this pathology and where it is most frequently observed ?
Failure of normal valvular development
Valvular Haematomas (haematocyst)
- blood filled cyst on the valve
- most frequently observed on the AV valaves in ruminant species
- usually regresses spontaneously
Identify this pathology ?
Valvular lymphocyst
- serum filled cyst on the AV valves
Identify this pathology ?
Mitral valve dysplasia
Dysplasia = abnormal development of an organ or tissue
- common in cats and dogs
Note = thickened fused mitral valve leaflets
Identify this pathology ?
Persistant right aortic arch
The right aortic arch (instead of left) develops and ascends on the right side of the midline (aortic arch is on the wrong side).
This causes the ligamentum arteriosum to form a vascular ring over the oesophagus and trachear (vascular ring anomaly)
- oesophageal obstruction
- proximal megaoesophagus
- especially prevalent in dogs
Identify this pathology ?
Endocardial fibroelastosis
Prominent white thickened endocardium
- frequent in Burmese and Siamese cats
Identify this pathology ?
Ectopic cordis
Development of the heart in abnormal locations outside the thoracic cavity
Answers
A. pulmonic stenosis = concentric hypertrophy of the right ventricle (thickening).
B. Aortic stenosis = concentric hypertrophy of the right ventricle.
C. Ventricular septal defect = right ventricle dilation (eccentric)
What could cause this pathology ? Identify the pathology ?
Hydropericardium
Excess accumulation of clear light yellow watery fluid
- may contain a small amount of fibrin
- non-inflammatory lesion
Potential causes of hydropericardium
- Generalised oedema (ascites, hydrothorax)
- Congestive heart failure
- pulmonary hypotension
- systemic vascular injury
- hypoproteinaemia
Describe the gross pathology of acute and chronic hydropericardium ?
Gross pathology
Acute hydropericardium
- smooth glistening
- may cause cardiac tamponade
Chronic hydropericardium
- epicardium and pericardium may be opaque (mild fibrous thickening).
Define cardiac tamponade
Cardiac tamponade = compression of the heart through the accumulation of fluid in the pericardial sac.
Identify this lesion and its cause?
Haemopericardium
This is the accumulation of whole blood in the pericardial sac (may cause cardiac tamponade).
Causes of haemopericardium
- spontaneous atrial rupture dog
- rupture of intrapericardial aorta horse
- cardiac neoplasms haemangiosarcomas, heart base tumors
- unknown cause especially large and giant dog breeds
Treatment may involve removal of the pericardial sac
Identify this pathology ?
Fibrinous pericarditis
adhere and easily pulled apart “bread and butter”
Identify this type of pericarditis and its causes?
Fibrinous pericarditis
Acute (fibrinous easily pulled apart like a bannana)
The parietal and visceral surface are covered in yellow fibrin
adhere and easily pulled apart “bread and butter pudding”
This is the most common form of pericarditis
- usually results from haematogenous infection
- pasteurellosis, Glasser’s disease
Identify this pathology and its causes ?
Suppurative pericarditis
The pericardial surfaces are thickened with white masses of fibrous tissue enclosing thick purulent exudate.
hardware disease
the animal may survive weeks to months, then die from CHF and septicaemia
three metabolic disorders of the pericardium
Identify the possible metabolic disorders of the pericardium ?
The three metabolic disorders of the pericardium
Serous atrophy of fat
- gelatinous pale epicardial fat
- anorexia, starvation, cachexia
Epicardial mineralisation “cardiac calcinosis”
- inherited in some inbred mice
- dystrophic calcification
Urate deposits
- birds and reptiles
- visceral gout
- reduced access to water
- uric acid crystals deposited
- gritty white appearance
What type of pericarditis usually follows suppurative pericarditis ?
Constrictive pericarditis
(chronic can not pull apart - extensive fibrin)
- fibrous adhesions between visceral and parietal surfaces
- constricts heart and interferes with filling
What is the difference between fibrous and fibrinous ?
There are two different types of adhesions
Fibrinous = the adhesions which form early composed of fibrin. These can be pulled apart (acute)
Fibrous lesions are more organised and can not be pulled apart (chronic)
Identify this pathology provide details ?
Epicardial minerlisation
“cardiac calcinosis”
- inherited in some inbred mice
- dystrophic calcification
Identify this pathology and its causes ?
Serous atrophy of fat in the pericardium
- gelatinous pale epicardial fat
- metabolic disorder
caused by anorexia, starvation and cachexia
Identify this pathology and its causes ?
Endocardial minerlisation
Minerlisation often occurs in conjuction with fibrosis or alone
Appears as firm white plaques of minerlised tissue in the endocardium and intima of large elastic arteris.
Causes
- especially common in cattle
- excessive dietary intake of vitamin D
- calcinogenic plants cestrum and solanum
Identify these two pathologies
Minerlisation and fibrosis of the endocardium
minerlisation and fibrosis may occur together or alone
This occurs in animals with
- chronically dilated hearts
- debilitated cattle with Johne’s disease
- dogs with healed endocarditis lesions
- jet lesions from vulvular insufficiencies
What is endocardiosis and under which circumstances dose it commonly occur ?
Endocardiosis
It is the degeneration of the valves of the heart - valve disease
Inside the heart there are four valves mitral, tricupsid, aortic and pulmonary
- important pathogenesis in middle age to old small dogs
- most common cause of CHF in these dogs
- esp. cavalier King Charles spaniels
Causes
- mucoid vulvular degeneration degeneration of vulvular collagen
- mitral valve disease shortened thick nodules appear smooth and shiny
- valvular insufficiency develop atrial ‘jet lesions’ rough firm streaks of fibrosis from trauma
Identify this pathology and discuss possible causes ?
Valvular endocardiosis
Define a jet lesion ?
Jet lesion = Blood forced through a narrow opening - causing blood to flow back causing corrugation of the surface.
Identify this pathology and its potential causes ?
Endocarditis (vegetative valvular endocarditis)
This has a complicated pathogenesis
- involves Virchows triad of Thrombogenesis
- endothelial damage, turbulance and hypercoagulability
- affected animals often have gingivitis, dermatitis etc
- causes bout of bacteraemia
The common bacteria involved - Streptococcus, E.coli, Arcanobacter pyogenes, Erysipelothrix rhusiopathiae
Death may occur due to
- cardiac failure due to valve dysfunction
- bacteraemia
- septic emboli in kidneys or coronary vessels
Describe the gross pathology of endocarditis and its causes ?
Endocarditis
Inflammatory endocardial disease -
- usually affects the valves “Valvular endocarditis
- large fibrile yellow grey masses of fibrin
- “vegetations” can occlude valve orifice
- Layers of fibrin and bacterial colonies lay over the top of inflammatory granulation tissue
- older lesions become less organised by fibrous tissue - appear wart like (verrucous)
Answer
1. Most likely a the valve is not working correctly allowing blood to mix and be forced back into the left atrium.
2. Eccentric hypertrophy
Answer
a. multi focal coalescing irregular yellow lesion within the endocardium
b. Endocarditis vegetative chronic severe
c. Sepsis and heart failure
List four main mechanisms of hydropericardium
Four main mechanisms of hydropericardium
1. Generalised oedema - often concurrently with ascites and hydrothorax
2. Congestive heart failure
3. Pulmonary hypotension
4. Hypoproteinaemia
5. Systemic vascular injury.
Describe the differences between endocardiosis and endocarditis, including pathogenesis and pathological consequences ?
The difference between endocardiosis and endocarditis
Endocardiosis = degeneration of the heart valves
congestive heart failure in dogs
Path = valvular insufficiency or degeneration of collagen
consequence = CHF dogs
Endocarditis = inflammatory endocardial disease
Path = Virchows triad of Thrombogenesis
consequences = sepsis, cardiac failure, septic emboli
Describe the pathological consequences of
A. Mitral valve insufficiency
B. Tricupsid valve insufficiency
Answer A consequences
A. Mitral valve insufficiency
- between left atrium and ventrical
- reduces blood flow to the periphery
B Tricupsid valve insufficiency
- between the right atrium and left ventricle
- reduced blood flow to the lungs = backward heart failure.
There are four types of myocardial degeneration
Describe the different types of myocardial degeneration ?
Myocardial degeneration
This is what is observed during myocardial degeneration
- Fatty change - lipid droplets in cardiomyocytes
- Hydropic degeneration - vacuolation
- Lipofuscinosis - age related
- Myofibril degeneration - pale eosinophilic lack striations
Desribe the gross pathology and identify the pathology?
Myocardial necrosis and minerlisation
The histological appearance depends on the age of the lesion
Acute necrosis
- Swollen hypereosinophilic fibres (hyaline degeneration)
- loss of striations
- basophillic granules of mineralisation
- pyknotic nucleis (condensation of chromatin)
- can sometimes appear shredded due to hypercontraction
- ischaemic necrosis will cause coagulative necrosis
By 24-48 hrs
- infiltration by macrophages and neutraphils
If animals survives healing occurs through fibrosis (fibroblast proliferation, collagen deposition)
Identify the many different causes of myocardial necrosis and minerlisation ?
Potential causes of necrosis and mineralisation
- Nutritional deficiencies (selenium, vitamin E young animals, potassium, copper, magnesium etc)
- Plant toxins (Cestrum = calcinogenic plants)
- Ischaemia = thrombosis
- Metabolic disorders ( uraemia)
- Physical injury (overexertion, defibrillation)
The histological appearance depends upon the age of the lesion.
Describe the different types of myocarditis ?
Myocarditis
There are many different forms of myocarditis
