CV Pathology

Question 1

Define dilation

Answer 1

a response to an increased workload. This can be transient (e.g. when performing exercise) or persistent

Question 2

Define hypertrophy

Answer 2

the reversible increased in the mass of the heart cells without increasing in number.

Question 3

What are the two types of hypertrophy ?

Answer 3

concentric (pressure overload)
- no increased in ventricular volume
eccentric (volume overload)
- increase in ventricular volume

Question 4

Name the three arteriovenous connections present in embryology

Answer 4

ductus arteriosus
foramen ovale
ventricular holes

Question 5

What are the sequelae of left-to-right shunting

Answer 5

volume overload of the pulmonary circulation –> left sided eccentric hypertrophy

Question 6

Clinical signs of left-to-right shunting

Answer 6

exercise intolerance
syncope
dyspnoea
sudden death
murmur (“washing machine”)

Question 7

Define patent ductus arteriosus

Answer 7

a connection between the pulmonary artery and the aorta

Question 8

Define arterial septal defects

Answer 8

a connection between the two atria, allowing blood to pass between them

Question 9

Define ventricular septal defects

Answer 9

can happen anywhere along the septum, can be perimembranous or muscular. causes insufficiency

Question 10

Define stenotic diseases

Answer 10

diseases affecting the semilunar valves
may be pulmonic or aortic (or subaortic)
increases afterload

Question 11

Define dysplastic valvular diseases

Answer 11

involve the AV valves
increases preload

Question 12

What is a transposition complex and name the most common

Answer 12

malpositioning of arterial trunks
overriding aorta most common (aorta straddles septum and recieves blood from both ventricles)
may also see partial transposition, overriding pulmonary artery and complete transposition

Question 13

Define and give the characteristic features of primary myocardial disease

Answer 13

idiopathic diseases to the myocardial fibre.
characterized by cardiomegaly (increased %BW of heart), increased ventricular wall thickness and mural thrombosis

Question 14

Define DCM

Answer 14

dilated cardiomyopathy
leading to systolic dysfunction
grossly, atria and ventricle dilation and non-specific histo

Question 15

Define HCM

Answer 15

hypertrophic cardiomyopathy
–> diastolic dysfunction due to impaired ability to relax
leads to ventricular outflow tract obstruction, causing turbulence
grossly, asymmetrical hypertrophy of left ventricle, subtle histo

Question 16

Define RCM

Answer 16

restrictive cardiomyopathy
–> diastolic dysfunction due to restriction in the ability of the ventricles to fill
grossly, fibrosis, moderator bands and dilated atria with normal ventricles

Question 17

Define ARVC

Answer 17

arrhythmic right ventricular cardiomyopathy
–> ventricular arrhythmias due to a nerve block
grossly, hypertrophy of ventricle and dilation of atrium
distinctive histology of fibro-fatty replacements of cardiomyocytes

Question 18

Name some secondary causes of cardiomyopathies

Answer 18

hormone
nutritional
toxin
infectious agents
inflammation

Question 19

What are the sequelae of secondary cardiomyopathies ?

Answer 19

altered myocyte metabolism (most commonly hyperthyroidism in cats)

myocyte death (myocardial necrosis, white band visible in the muscle (sometimes “white muscle” disease), neurological disease/nutritional (Vit E/selenium)/toxins cause

myocarditis.
- necrotizing
- suppurative
- pyogranulomatous
- eosinophilic
- lymphoplasmacytic

Question 20

How do cardiomyocytes react to injury ?

Answer 20

regeneration is rare as the cells a post-mitotic
loss results in fibrosis
remaining myocytes have the ability to compensate via hypertrophy

Question 21

Clinical Signs of conduction disorders

Answer 21

ECG abnormalities, syncope, sudden death

Question 22

Define endocardiosis

Answer 22

the degenerative disease of the hearts mitral valve (left AV valve). responsible for 75% of all heart diseases in dogs

Myxomatous Valve Degeneration (MVD) :
- most common cause of Cv diseases in dogs
- genetic predisposition for small dogs
- grossly, thickened and shortened valves with a smooth endocardial surface.
- if clinically significant, will see “jet lesions” of fibrosis in the left atrium
- histologically, myofibroblastic proliferation and deposition of acid mucopolysaccharides within valvular stroma

Question 23

What is the sequelae of endocardiosis ?

Answer 23

valvular insufficiency (regurgitation)
occurs when there is a volume overload
eccentric hypertrophy, dilating the previous chamber and causing these “jet lesions”
mural thrombi may also form attached to the heart wall

Question 24

Define endocarditis

Answer 24

inflammation of the inner lining of the heart

Question 25

What is endocarditis commonly caused by ?

Answer 25

bacteria.
commonly, Strep. Staph. E. coli
often associated with extracardiac infections

Question 26

Gross appearance of endocarditis

Answer 26

friable, yellow-to-grey-to-red masses of fibrin with a roughened surface (“cauliflower-like”), may extend into the mural endocardium in the form of plaques

Question 27

Define hydropericardium

Answer 27

excess clear fluid within the pericardial cavity
may be caused by decreased oncotic pressure, decreased lymphatic drainage, increased hydrostatic pressure and increased vascular permeability

Question 28

Define hemopericardium

Answer 28

pure blood in the pericardial cavity
occurs with the rupture of BVs

Question 29

What are the sequelae for fluid in the pericardial cavity ?

Answer 29

cardiac tamponade (compression of the heart resulting in impaired atrial and ventricular filling)

Question 30

Define serous atrophy of fat in the heart

Answer 30

lipid is replaced by a proteinaceous fluid
grossly, what should be white fat becomes gelatinous and translucent
occurs with NEBAL

Question 31

Define pericarditis and give some causes

Answer 31

Inflammation of the pericardium

infectious, as an extension of pleuropneumonia
traumatic, i.e. from traumatic reticuloperitonitis

Question 32

Define congestive heart failure

Answer 32

the end-point of a number of conditions.
for whatever reason, the heart compensatory mechanisms are exhausted, resulting in a decreased CO

Question 33

What happens (generally) in congestive heart failure and how do we aim to treat this ?

Answer 33

the body becomes congested due to an inability of CO to match venous return

the RAAS system gets activated by low BP or BV, and aims to increase BP and BV. this adds to and worsens congestion

solution = diuretics (decrease venous return)

Question 34

Define the problems with LEFT sided congestive heart failure

Answer 34

back up into the pulmonary system
lung congestion and oedema
lungs will be wet, heavy and non-collapsible
will see haemosiderin-laden macrophages (heart failure cells)
CS : dyspnoea with exercise, increased resp effort, cough, crackles on inspiration, froth in airways, syncope, weakness

Question 35

Define the problems with RIGHT sided congestive heart failure

Answer 35

back up into the vena cava system
leading to increased systemic venous pressure and passive congestion
the big organs that are draining into the vena cava will have a back up of blood (splenomegaly, hepatomegaly and intestinal oedema)

Question 36

Name the most common primary cardiac neoplasms

Answer 36

Hemangiosarcoma (right auricle and atrium)
Heart base tumours (most common in paraganglioma, neuroendocrine cell tumours)

Question 37

Name the most common secondary heart neoplasms

Answer 37

Round cell neoplasms (most common)
lymphomas

Question 38

Define thrombosis

Answer 38

coagulation as a pathology

Question 39

Name the 3 components of Virchow’s triad

Answer 39

endothelial injury
hypercoagulability
abnormal blood flow

Question 40

Name the gross and histo appearance of a chronic thrombus

Answer 40

onion-like appearance of layers built up over time
alternating layers of platelets, fibrin and RBCs +/- mineralization and fibrosis

Question 41

Name the gross and histo appearance of an acute thrombus

Answer 41

dull red, more classic clot-like appearance
not that exiting on histo

Question 42

Define fibrinoid necrosis

Answer 42

endothelial damage, characterized by accumulation of serum proteins and fibrin in the vessel wall

Question 43

Define arteriosclerosis

Answer 43

“hardening of the arteries”
loss of artery elasticity
often insignificant but can promote thrombi due to blood flow disruptions

Question 44

Define atherosclerosis

Answer 44

fibrofatty plaques (atheromas) in the wall of the vessel

Question 45

Define an aneurysm

Answer 45

focal dilations of any vessel. tend to be idiopathic.
can be dissection, true or false

Question 46

Define vasculitis

Answer 46

inflammatory cells within and around the wall of vessels with concurrent damage to the wall

Question 47

name some common infectious aetiologies of vasculitis

Answer 47

EAV
orbiviruses
EIA
ASF
CSF
Rickettsia
Aspergillus
Heartworm

Question 48

name some common non-infectious aetiologies of vasculitis

Answer 48

autoimmune or drug hypersensitivit

Question 49

Define lymphoedema

Answer 49

defective transport OR abnormal vessel development OR blockage

leads to fibrosis, skin folds and ulceration

Question 50

Define an intestinal lymphangiectasia

Answer 50

impaired protein absorption in the GI leads to protein losing enteropathy

Question 51

Define lymphangitis

Answer 51

inflammation of lymph vessels