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1. Cardiorespiratory > Cardiovascular Pathology > Flashcards

Cardiovascular Pathology Flashcards

1
Q

The wall of the heart has 3 layers, what are they?

A
  1. Epicardium = visceral pericardium (mesothelium with some CT underlying it)
  2. Myocardium = myocytes
  3. Endocardium = endothelium. Lines the chambers & covers the valves, chordae tendinae & papillary muscles.
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2
Q

Describe the post-natal growth of myocytes in the heart.

A

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.

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3
Q

Name the compensatory mechanisms that maintain cardiac output.

A
  1. 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.
  2. 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).
  3. Increase HR
  4. Increase peripheral resistance
  5. Increase blood volume
  6. Redistribution of blood flow
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4
Q

Reaction of muscle cells to injury

A

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

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5
Q

Describe the stages of myocardial infarct.

A

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.

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6
Q

Describe PM changes in the heart

A
  1. 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)
  2. Intracardiac euthanasia injection –> haemopericardium (bleeding in pericardial sac) or pallor (pale) & crystalline deposits
  3. Undiluted IV barbituate can discolour R atrium and ventricle myocardium = stick dark blood
  4. PM rigor results in expulsion of blood from L ventricle = often empty
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7
Q

What is CHF

A

Heart can’t pump sufficient blood relative to the venous return and metabolic needs of the body

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8
Q

Describe what happens in acute CHF & oedema.

A
  1. Renal blood flow is decreased –> renal hypoxia
  2. Renin released
  3. Aldosterone released from adrenal glands
  4. Acts on renal tubules –> Na+ & H20 retained
  5. increased plasma volume –> increased hydrostatic P
  6. Oedema
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9
Q

Describe what happens in chronic CHF & oedema.

A
  1. Decreased renal blood flow –> chronic renal hypoxia
  2. decreased erythropoietin produced in renal tubules
  3. decreased erythropoiesis in BM
  4. decreased PCV
  5. decreased blood viscosity
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10
Q

Describe left-sided CHF.

A
  • 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
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11
Q

What are the causes of left-sided CHF

A

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)

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12
Q

Describe right-sided CHF

A

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”
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13
Q

What are the causes of right-sided CHF

A
  • 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.
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14
Q

Describe pericardial disease.

A
  • Pericarditis
  • Circulatory disturbances
    • fluid accumulates in the pericardial sac: hydropericardium, haemorrhagic pericardial effusion, haemopericardium
  • Pericardial adhesion
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15
Q

Describe the types of pericarditis

A

(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

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16
Q

What is hydropericardium?

A
  • 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
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17
Q

What is haemopericardium?

A
  • 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
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18
Q

What is traumatic reticuloperitonits

A

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)
19
Q

Describe the types of endocarditis

A

(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

20
Q

Bacteria involved in valvular endocarditis (different species)

A

Cattle: actinomyces pyogenes

Pigs: strep, erisipelothrix rhusiopathae

Dogs & cats: strep, e coli, staph

Horse: strep equi, actinobacillus equuli

Cats: NOT COMMON

21
Q

What other sequelae follow valvular endocarditis?

A

Septic emboli can lodge in lungs, brain, spleen, joints, kidneys –> abscessation & infarction

22
Q

How would you diagnose valvular endocarditis?

A

Blood culture

Ultrasonography

23
Q

What is a type of non-infectious endocarditis

A

uraemic ulcerative endocarditis

  • complication of renal failure (dogs)
  • L atrium
  • oedema –> ulceration
    • might heal
    • might be replaced by white plaques of fibrous & mineralised tissue
24
Q

What is valvular endocardiosis?

A
  • 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
25
Q

What sequelae may follow valvular endocardiosis?

A

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

26
Q

How can you distinguish between endocarditis & endocardiosis?

A

Endocardiosis:

  • smooth
  • degenerative
  • old dogs

Endocarditis

  • rough vegetative/wart-like
  • inflammatory
  • any age
27
Q

List the myocardium cardiomyopathies

A
  1. Inflammation = myocarditis
  2. 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
  3. Circulatory disorders: infarction.
  4. DoG: congenital abnormalities, hypertrophy.
28
Q

What are the clinical signs of thromboembolism?

A
  • Hind limb pareses/paralysis
  • pain
  • pulse free
  • cold hind limbs & pads
29
Q

What is the gross pathology of idiopathic hypertrophic cardiomyopathy?

A
  • Enlarged heart
  • Small ventricular cavity (decreased CO)
  • Dilated atrium (increased end diastolic P –> increase pulmonary venous P –> left sided CHF)
30
Q

Describe idiopathic hypertrophic cardiomyopathy histology

A
  • Individual myocardial fibres are hypertrophied
  • Myocardial fibres in disarray rather than uniformly parallel
  • Interstitial fibrosis
  • Myocardial cells degenerate
31
Q

Describe dilated cardiomyopathies.

A
  • 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
32
Q

Gross & microscopic appearance of dilated cardiomyopathy

A

Grossly:

  • rounded hearts due to biventricular dilatation
  • diffusely white thickened endocardium

Microscopically:
- interstitial fibrosis & myocardial fibre degeneration.

33
Q

Describe myocarditis (inflammation)

A

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.
34
Q

What can cause myocardial necrosis?

A
  • Nutritional deficiencies
  • Plant & chemical toxicities
  • Ischaemia: infarcts secondary to coronary artery disease. Common in humans, rare in other animals
  • Metabolic disorders: uraemia
  • Physical injuries
35
Q

What are some congenital cardiac defects (DoG)?

A
  1. 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
  1. 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
  2. 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
  3. 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

  1. 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

  1. Tetralogy of Fallot:
    (1) IV septal defect
    (2) Aortic dextroposition
    (3) Pulmonary stenosis
    (4) R ventricular hypertrophy
  2. R AV valve fusion & stenosis
    - R ventricle fails to expand normally
    - R atrium enlarged
36
Q

What types of cardiac neoplasia can you get?

A

Primary:

  1. Rhabdomyoma & rhabdomyosarcoma
  2. Schwannomas involving cardiac nerves
  3. Haemangiosarcoma
  4. Lymphoma

Secondary
1. Haemangiosarcoma (usually RA, occasionally RV). Rupture –> haemopericardium & cardiac tamponade

Extracardiac tumours

  1. 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
37
Q

How does heartworm disease affect the CVS?

A
  • 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
38
Q

Other sequelae to heartworm disease

A

(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

39
Q

5 Pathological processes: inflammation of vessels

A

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

40
Q

5 Pathological processes: degeneration of vessels

A
  1. 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)

  1. Arteriosclerosis (hardening of arteries due to lost elasticity)
  2. Venous dilatation- varicosity
41
Q

5 Pathological processes: circulatory disturbances of vessels

A
  1. 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

42
Q

5 Pathological processes: DoG of vessels

A
  1. Hypertrophy
    - Aelurostrongylus abstrusus, heartworm, toxoplasmosis, non-parasitic infections
  2. 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
  3. Neoplasia: haemangioma, haemangiosarcoma, haemangiopericytoma
43
Q

5 Pathological processes: pigments/deposits of vessels

A

Atherosclerosis: buildup of lipid, calcium in artery wall which can restrict blood flow

1. Cardiorespiratory (4 decks)

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