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VMS2004 > CV Pathology > Flashcards

CV Pathology Flashcards

I, II, III, IV and V

1
Q

Define dilation

A

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

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2
Q

Define hypertrophy

A

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

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3
Q

What are the two types of hypertrophy ?

A

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

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4
Q

Name the three arteriovenous connections present in embryology

A

ductus arteriosus
foramen ovale
ventricular holes

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5
Q

What are the sequelae of left-to-right shunting

A

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

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6
Q

Clinical signs of left-to-right shunting

A

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

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7
Q

Define patent ductus arteriosus

A

a connection between the pulmonary artery and the aorta

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8
Q

Define arterial septal defects

A

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

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9
Q

Define ventricular septal defects

A

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

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10
Q

Define stenotic diseases

A

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

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11
Q

Define dysplastic valvular diseases

A

involve the AV valves
increases preload

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12
Q

What is a transposition complex and name the most common

A

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

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13
Q

Define and give the characteristic features of primary myocardial disease

A

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

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14
Q

Define DCM

A

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

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15
Q

Define HCM

A

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

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16
Q

Define RCM

A

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

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17
Q

Define ARVC

A

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

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18
Q

Name some secondary causes of cardiomyopathies

A

hormone
nutritional
toxin
infectious agents
inflammation

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19
Q

What are the sequelae of secondary cardiomyopathies ?

A

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

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20
Q

How do cardiomyocytes react to injury ?

A

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

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21
Q

Clinical Signs of conduction disorders

A

ECG abnormalities, syncope, sudden death

22
Q

Define endocardiosis

A

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

23
Q

What is the sequelae of endocardiosis ?

A

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

24
Q

Define endocarditis

A

inflammation of the inner lining of the heart

25
Q

What is endocarditis commonly caused by ?

A

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

26
Q

Gross appearance of endocarditis

A

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

27
Q

Define hydropericardium

A

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

28
Q

Define hemopericardium

A

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

29
Q

What are the sequelae for fluid in the pericardial cavity ?

A

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

30
Q

Define serous atrophy of fat in the heart

A

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

31
Q

Define pericarditis and give some causes

A

Inflammation of the pericardium

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

32
Q

Define congestive heart failure

A

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

33
Q

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

A

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)

34
Q

Define the problems with LEFT sided congestive heart failure

A

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

35
Q

Define the problems with RIGHT sided congestive heart failure

A

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)

36
Q

Name the most common primary cardiac neoplasms

A

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

37
Q

Name the most common secondary heart neoplasms

A

Round cell neoplasms (most common)
lymphomas

38
Q

Define thrombosis

A

coagulation as a pathology

39
Q

Name the 3 components of Virchow’s triad

A

endothelial injury
hypercoagulability
abnormal blood flow

40
Q

Name the gross and histo appearance of a chronic thrombus

A

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

41
Q

Name the gross and histo appearance of an acute thrombus

A

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

42
Q

Define fibrinoid necrosis

A

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

43
Q

Define arteriosclerosis

A

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

44
Q

Define atherosclerosis

A

fibrofatty plaques (atheromas) in the wall of the vessel

45
Q

Define an aneurysm

A

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

46
Q

Define vasculitis

A

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

47
Q

name some common infectious aetiologies of vasculitis

A

EAV
orbiviruses
EIA
ASF
CSF
Rickettsia
Aspergillus
Heartworm

48
Q

name some common non-infectious aetiologies of vasculitis

A

autoimmune or drug hypersensitivit

49
Q

Define lymphoedema

A

defective transport OR abnormal vessel development OR blockage

leads to fibrosis, skin folds and ulceration

50
Q

Define an intestinal lymphangiectasia

A

impaired protein absorption in the GI leads to protein losing enteropathy

51
Q

Define lymphangitis

A

inflammation of lymph vessels

VMS2004 (18 decks)

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