Cardiovascular Pathology Flashcards
The wall of the heart has 3 layers, what are they?
- Epicardium = visceral pericardium (mesothelium with some CT underlying it)
- Myocardium = myocytes
- Endocardium = endothelium. Lines the chambers & covers the valves, chordae tendinae & papillary muscles.
Describe the post-natal growth of myocytes in the heart.
First few months post-natally = hyperplasia, then ceases. Then hypertrophy until myocytes reach size normal for the species.
Means when there is injury, scarring occurs as no hyperplasia.
Name the compensatory mechanisms that maintain cardiac output.
- Cardiac dilatation (increase in chamber size!)
- A compensatory response to increase cardiac output.
- Cardiac muscle cells stretch to increase contractile force –> increase stroke volume.
- However, stretching beyond certain limits results in lower contractile strength & wall becomes thinner. - Myocardial hypertrophy
- Increase in muscle mass.
- Compensates for disease that increases heart’s workload: increase P or volume overload
- Reverses when cause is removed (controlled DoG). - Increase HR
- Increase peripheral resistance
- Increase blood volume
- Redistribution of blood flow
Reaction of muscle cells to injury
Cell injury/degeneration
- sublethal cell injury: fatty degeneration, lipofuscinosis, vacuolar degeneration
- Lethal injury: necrosis or apoptosis (cardiac myocytes are not regenerated)
DoG (controlled)
- atrophy or hypertrophy
Describe the stages of myocardial infarct.
Day 1: coagulative necrosis (coagulation of muscle fibres)
Day 3-4: acute inflamm response (neutrophils)
> necrosis, calcification, fibrosis
> extensive healing, dense collagenous scar replaces necrotic myocardial fibres.
Describe PM changes in the heart
- Red clots in chambers & occasional “chicken fat” clots that contain few erythrocytes (PM clots not attached to endothelium and fall off easy. When attached we strongly suspect thrombosis/clotting prior to death)
- Intracardiac euthanasia injection –> haemopericardium (bleeding in pericardial sac) or pallor (pale) & crystalline deposits
- Undiluted IV barbituate can discolour R atrium and ventricle myocardium = stick dark blood
- PM rigor results in expulsion of blood from L ventricle = often empty
What is CHF
Heart can’t pump sufficient blood relative to the venous return and metabolic needs of the body
Describe what happens in acute CHF & oedema.
- Renal blood flow is decreased –> renal hypoxia
- Renin released
- Aldosterone released from adrenal glands
- Acts on renal tubules –> Na+ & H20 retained
- increased plasma volume –> increased hydrostatic P
- Oedema
Describe what happens in chronic CHF & oedema.
- Decreased renal blood flow –> chronic renal hypoxia
- decreased erythropoietin produced in renal tubules
- decreased erythropoiesis in BM
- decreased PCV
- decreased blood viscosity
Describe left-sided CHF.
- Causes pulmonary congestion & oedema (backward failure)
- Clinically animal often presents with a cough
Acute:
- alveolar capillaries become engorged, dilated & tortuous
- alveolar septal oedema
- dilated & tortuous vessels can –> focal intra-alveolar haemorrhages
Chronically:
- alveolar septae thicken & become fibrotic
- alveolar macrophages accumulate in alveoli
- > erythrophagy (due to RBC forced into alveolar spaces due to nature of vascular endothelium in pulmonary vessels)
- > haemosiderophages a.k.a heart failure cells
What are the causes of left-sided CHF
Myocardial contractility can be lost due to:
- myocarditis
- myocardial necrosis
- cardiomyopathy
Valvular insufficiency
- Left A-V valve
- Aortic valve
Congenital heart disease
- aortic stenosis (blood backs up through L atrium & pulmonary veins)
Describe right-sided CHF
Systemic congestion, esp liver, spleen & dependent parts (backward failure)
Acute:
- enlarged liver
- distended central veins and sinusoids
- centrilobular hepatocellular degeneration
Chronic
- red-brown congestion around central veins
- accentuated against the fatty but viable pale swollen periportal hepatocytes
- “NUTMEG liver”
What are the causes of right-sided CHF
- Pulmonary hypertension (increased pulmonary arterial P); secondary to:
- lung disease
- cardiac defects: L –> R shunts
- heartworm disease - Cardiomyopathy
- Pulmonic stenosis: insufficient emptying of the R ventricle, blood backs up in R atrium & vena cava –> liver engorgement.
Describe pericardial disease.
- Pericarditis
- Circulatory disturbances
- fluid accumulates in the pericardial sac: hydropericardium, haemorrhagic pericardial effusion, haemopericardium
- Pericardial adhesion
Describe the types of pericarditis
(a) Fibrinous pericarditis
- Haematogenous
- Cattle: pasteurellosis, black leg, coliform septicaemias
- Horse: strep
- Outcomes: rapid death due to septicaemia, fibrous adhesions & organisation of the exudate
(b) Granulomatous
- bovine tuberculosis
(c) Chronic suppurative
- traumatic reticulo-pericarditis
What is hydropericardium?
- Excess serous fluid accumulates in pericardial sac
- occurs in diseases causing generalised oedema (ascites, CHF, hypoproteinaemia due to renal/intestinal disease)
- Rapid onset + sufficient volume –> cardiac tamponade (compresses heart)–> interferes cardiac filling and venous return
- slow onset –> pericardium stretches - no cardiac tamponade
What is haemopericardium?
- Whole blood accumulates in the pericardial sac
- Death can occur from cardiac tamponade
CAUSED BY:
- spontaneous atrial rupture (dogs)
- Rupture of intrapericardial aorta (horse)
- Complication of cardiac injections
What is traumatic reticuloperitonits
The wall of reticulum is penetrated by an ingested foreign body.
AKA Hardware disease
CLINICAL SIGNS:
- anorexia
- fall in milk yeild
- abdominal pain/grunting
- rumenal stasis
- mild pyrexia
PATHOGENESIS
- Lodges and penetrates through reticulum
- If wall not perforated = no illness (FB is corroded away) OR illness later
- If perforated –> acute local peritonitis (spontaneous recovery if adhesions form)
- if diaphragm penetrated: penetrates pleural or pericardial sacs (pleuritis, pneumonia, pericarditis [cardiac tamponade/compresses heart > heart unable to pump, expand & fill > decr SV & CO > ACUTE CHF; chronic inflamm > fibrous adhesions between visceral & parietal pericardium> constricts heart> compensatory myocardial hyptertrophy > reduced ventricular chamber volumes, SV > CHF)
Describe the types of endocarditis
(a) Valvular endocarditis: lesions usually on valves:
- large, adhering, friable, yellow grey masses = “vegetations” (endo damage ->thrombosis-> fibrosis)
- Interferes with valve function/occlude valve orifice
- Most commonly effected: L AV > aortic > R AV > pulmonary
PATHOGENESIS
- extracardiac infection –> bacteraemia
- thrombi develops on endocardium
- endothelium disrupted
- bacteria prolif
- inflamm with fibrin deposition
Mural endocarditis: extension into adjacent wall
Bacteria involved in valvular endocarditis (different species)
Cattle: actinomyces pyogenes
Pigs: strep, erisipelothrix rhusiopathae
Dogs & cats: strep, e coli, staph
Horse: strep equi, actinobacillus equuli
Cats: NOT COMMON
What other sequelae follow valvular endocarditis?
Septic emboli can lodge in lungs, brain, spleen, joints, kidneys –> abscessation & infarction
How would you diagnose valvular endocarditis?
Blood culture
Ultrasonography
What is a type of non-infectious endocarditis
uraemic ulcerative endocarditis
- complication of renal failure (dogs)
- L atrium
- oedema –> ulceration
- might heal
- might be replaced by white plaques of fibrous & mineralised tissue
What is valvular endocardiosis?
- Associated with degeneration of valvular collagen.
- Common in old dogs (often incidental PM, but is the MOST common cause of L sided CHF in old dogs)
- Affected valves are shortened & thickened either diffusely or are nodular.
- Appear smooth
- L sided CHF most likely caused by: L AV> R AV > aortic & pulmonary
- Genetic predispositions: males, Cavalier King Charles spaniel
Microscopically:
- fibroblastic prolif
- deposition of acid mucopolysaccharides
What sequelae may follow valvular endocardiosis?
L CHF -> atrial dilatation -> atrial “jet lesions” [lesions of incr turbulence of blood flow back into atrium -> thrombosis] ->rupture of chordae tendinae -> splitting/rupture of L atrial wall
How can you distinguish between endocarditis & endocardiosis?
Endocardiosis:
- smooth
- degenerative
- old dogs
Endocarditis
- rough vegetative/wart-like
- inflammatory
- any age
List the myocardium cardiomyopathies
- Inflammation = myocarditis
- Degeneration =
- necrosis
- hypertrophy: primary (idiopathic- uncommon in dogs; common in cats, middle-aged, persians) & secondary (adaptive response to increased workload on the heart; volume or P overload; hyperthyroidism)
- dilatation - Circulatory disorders: infarction.
- DoG: congenital abnormalities, hypertrophy.
What are the clinical signs of thromboembolism?
- Hind limb pareses/paralysis
- pain
- pulse free
- cold hind limbs & pads
What is the gross pathology of idiopathic hypertrophic cardiomyopathy?
- Enlarged heart
- Small ventricular cavity (decreased CO)
- Dilated atrium (increased end diastolic P –> increase pulmonary venous P –> left sided CHF)
Describe idiopathic hypertrophic cardiomyopathy histology
- Individual myocardial fibres are hypertrophied
- Myocardial fibres in disarray rather than uniformly parallel
- Interstitial fibrosis
- Myocardial cells degenerate
Describe dilated cardiomyopathies.
- Idiopathic form in dogs (male large breed) & cats (middle age male)
- Taurine deficiency in cats (reversed by supplement)
- Peripartum form (dogs)
- Important cause of CHF (dogs, cats)
- Some cats develop aortic thromboembolism
Gross & microscopic appearance of dilated cardiomyopathy
Grossly:
- rounded hearts due to biventricular dilatation
- diffusely white thickened endocardium
Microscopically:
- interstitial fibrosis & myocardial fibre degeneration.
Describe myocarditis (inflammation)
can be
- a primary cardiac disease
- secondary to haematogenous spread of systemic diseases
- vegetative valvular endocarditis, TRP, bacteraemia
- Toxoplasmosis - dogs & cats
- Black leg - cattle: Clostridium chauvoei
- Viral - e.g. parvovirus
Eosinophilic myocarditis
- Idiopathic
- Parasitic myocarditis e.g. protozoa - Sarcoystis spp.
What can cause myocardial necrosis?
- Nutritional deficiencies
- Plant & chemical toxicities
- Ischaemia: infarcts secondary to coronary artery disease. Common in humans, rare in other animals
- Metabolic disorders: uraemia
- Physical injuries
What are some congenital cardiac defects (DoG)?
- Pulmonary stenosis: narrowing of the pulmonary outflow tract.
- Valvular pulmonary stenosis most common. Abnormal development of valve cusps.
- Infundibular pulmonary stenosis: hypertrophy of ventricular muscle wall beneath the pulmonary valve
- Subvalvular pulmonary stenosis: excessive fibrous tissue proliferation beneath the valve.
- Blood passes through a smaller orifice in the pulmonary valve during ventricular contraction
–> Post stenotic turbulence
–> Loud systolic murmur with ventricular contraction
–> Increased pressure dilates pulmonary trunk
Stenosis increases resistance to pulmonary outflow –> RV wall dilation & hypertrophy - Clinically signs of R CHF
- Aortic stenosis
- A fibromuscular ring proliferates around the aortic outlet just below the aortic valve.
- Loud systolic murmur on ventricular contraction
- Post stenotic dilation in ascending aorta distal to the valve.
EFFECTS
- increases resistance to outflow –> L ventricle dilates & hypertrophies –> L atrium dilates secondarily –> clinical signs of L CHF - Interventricular septal defect
- Opening at the dorsal part of the IV septum
- Faulty closure of the I-V foramen
- If small might not be clinically evident (common in cows)
EFFECTS:
- Turbulent forcing of blood through defect from L ventricle into pulmonary trunk OR into R ventricle during ventricular contraction –> heart murmur
- Clinically L CHF with pulmonary hyptertension
- R ventricular dilation & hypertrophy in severe cases - Interatrial Septal Defects
CAUSED BY:
- Failure of foramen ovale to close at birth.
- Faulty development of interatrial septum
–> higher L atrial pressure shunts blood L –> R
-> Increasd volume of blood to R heart –> overloaded & overworked –> dilation & hypertrophy of RA & RV
–> R CHF
Eventually all 4 chambers affected
- Left AV valve defects (AKA L AV valve insufficiency)
- Valve leaflet too short
- L AV orifice doesn’t fully close on ventricular contraction
- blood regurgitates to LA
- systolic heart murmur
- L CHF
- L ventricular & atrial dilation
SAME CAN OCCUR ON R SIDE WITH RIGHT A-V VALVE
- Tetralogy of Fallot:
(1) IV septal defect
(2) Aortic dextroposition
(3) Pulmonary stenosis
(4) R ventricular hypertrophy - R AV valve fusion & stenosis
- R ventricle fails to expand normally
- R atrium enlarged
What types of cardiac neoplasia can you get?
Primary:
- Rhabdomyoma & rhabdomyosarcoma
- Schwannomas involving cardiac nerves
- Haemangiosarcoma
- Lymphoma
Secondary
1. Haemangiosarcoma (usually RA, occasionally RV). Rupture –> haemopericardium & cardiac tamponade
Extracardiac tumours
- Heart base tumours
(a) Primary neoplasms of extracardiac tissues in dogs.
- -> vascular obstruction & cardiac failure
(b) Include aortic body tumour (chemodectoma).
- aortic body is a chemoreceptor organ
- brachycephalic breeds most affected
How does heartworm disease affect the CVS?
- Myointimal (smooth muscle cells of vessel wall) proliferation & thrombosis –> pulmonary hypertension (high BP).
- > R CHF (-> e.g. ascites)
- > R ventricular hypertrophy & R atrial enlargement
- > Enlarged pulmonary artery
Other sequelae to heartworm disease
(1) Postcaval syndrome/ vena caval syndrome
- Dogs with many adult worms in the vena cava + R heart & pulmonary artery
- -> DIC, intravascular haemolysis & liver failure.
- Blocked vena cava –> passive congestion –> hepatomegaly
- Many adults –> intravascular haemolysis
(2) Glomerulonephritis
- Deposition of immune complexes in glomerular capillary walls
5 Pathological processes: inflammation of vessels
Vasculitis:
- arteritis (arteries)
- phlebitis (veins)
- omphalophlebitis (navel ill/umbilical vein; secondary to bacterial contamination of umbilicus after parturition ; –>septicaemia, suppurative polyarthritis, hepatic & umbilical abscesses)
Often complicated by thrombosis.
Arises from:
- systemic infections & immune mediated disease e.g. parasites, viruses, drug reactions, purpura
- local extension of infection
- faulty IV injection (esp veins; irritants, catheter, injecting vascular wall)
FIP –> phlebitis (immune complexes deposit in vessels)
Strangles –> purpura (petachiae, ecchymosises & larger haemorrhages are scattered on many body surfaces)
- 2-4 wks after acute strangles or vaccination
- vasculitis
Type 3 hypersensitivity
5 Pathological processes: degeneration of vessels
- Aneurysms
- a localised outpouching of a thinned & weakened portion of a vessel.
- usually in arteries but also in veins
- Can rupture –> usually fatal if large arteries involved.
CAUSED BY: mostly idiopathic, Cu def (pigs), strongylus valgaris in wall of cranial mesenteric artery (horse)
- Arteriosclerosis (hardening of arteries due to lost elasticity)
- Venous dilatation- varicosity
5 Pathological processes: circulatory disturbances of vessels
- Haemorrhage: necrosis/destruction of wall.
- aortic rupture (trauma, spontaneous, cardiac tamponade, guttural pouch mycosis)
- petaechial & ecchymotic haemorrhages (due to either vascular defect [i.e. from sepsis] OR coagulation factor/platelet defect)
Thrombosis & embolism
5 Pathological processes: DoG of vessels
- Hypertrophy
- Aelurostrongylus abstrusus, heartworm, toxoplasmosis, non-parasitic infections - Congenital diseases
- portocaval shunts (dogs, cats): abnormal vessels directly link portal vein to systemic circulation –> blood bypasses liver –> failure of hepatic degradation of N (i.e. ammonia) –> CNS dysfunction = hepatic encephalopathy - Neoplasia: haemangioma, haemangiosarcoma, haemangiopericytoma
5 Pathological processes: pigments/deposits of vessels
Atherosclerosis: buildup of lipid, calcium in artery wall which can restrict blood flow
