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Y3 Cardiovascular pathology > Cardiovascular pathology 2 > Flashcards

Cardiovascular pathology 2 Flashcards

1
Q

Describe the appearance of normal pericardial fluid.

What is the normal volume in horses and dogs/cats?

A
  • Clear, viscous fluid
  • Horse/cow 100 ml
  • Dog/cat: 10 ml
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2
Q

Describe a hydropericardium

A

Accumulation of clear to light yellow, watery, serous fluid (transudate: specific gravity < 1.015) in the pericardial sac

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3
Q

In which disease is a hydropericardium associated with vascular injury?

A

Mulberry heart disease in pigs
- a few fibrin strands are present, and the fluid could clot following exposure to air (exudate: specific gravity >1.015).

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4
Q

Describe the gross appearance of a hydropericardium in acute and chronic cases

A

Acute - pericardial surfaces are smooth and glistening

Chronic - pericardial surfaces are opaque with mild fibrous thickening due to villous proliferation of fibrous tissue

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5
Q

A hydropericardium is associated with diseases that have…?

A

Generalised oedema

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6
Q

Hydropericardium: Associated with those diseases that have generalized oedema - give examples

A
  • Increased vascular permeability: viruses, bacteria, type III hypersensitivity, toxins
  • Increased intravascular hydrostatic pressure: pulmonary hypertension, iatrogenic fluid overload
  • Decreased intravascular osmotic pressure: decreased albumin production, protein loss
  • Decreased lymphatic drainage: inflammation, obstruction
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7
Q

What is a cardiac tamponade?

A

Compression caused by fluid surrounding the heart which impairs cardiac filling and venous return to the heart

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8
Q

What is a haemorrhagic pericardial effusion?

A

Deposition of small amounts of blood, chronically - unknown aeitiology

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9
Q

What is a haemopericardium?

A

Accumulation of large amounts of blood in the pericardium

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10
Q

What are the consequences of a haemopericardium?

A

Cardiac tamponade, leading to compression and interfering with cardiac filling and emptying

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11
Q

What are 3 possible causes of a haemopericardium?

A
  • Atrial rupture due to a haemangiosarcoma of the right atrium in dogs
  • Rupture of the intrapericardial aorta in horses
  • Complications with intracardiac injections
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12
Q

What is the name given to a pericardial sac filled with air, how might this occur?

A

Pneumopericardium

- perforations in the oesophagus/stomach pass through the mediastinum near the pericardium

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13
Q

How does a chylopericardium occur?

A

Rupture of the thoracic duct which releases chyle - often white and gelatinous

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14
Q

Why would serous atrophy of epicardial adipose tissue occur?

A

Anorexia, starvation, cachexia, as fat is catabolised to maintain energy balance
- cases of emaciation

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15
Q

How does atrophy of epicardial adipose tissue appear grossly?

A

Transformation of the white or yellow epicardial fat deposits e.g. coronary groove, into grey gelatinous material

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16
Q

How does atrophy of epicardial adipose tissue appear microscopically?

A

Lipocytes are atrophic and oedema fluid is present in the interstitial tissue

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17
Q

Peri- / Epicarditis is?

A

Inflammation of peri/ epicardium

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18
Q

What are the portals of entry for inflammatory processes to get to the heart?

A
  • Foreign body penetration: From reticulum (cattle)
  • Local extension of severe inflammatory processes from adjacent structures (thoracic cavity / lungs / oesophagus)
  • Haematogenous spread of viruses / bacteria
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19
Q

Describe the different types of exudate

A
  • Serous = watery, low in protein and inflammatory cells
  • Fibrinous = acute
  • Purulent = dominated by neutrophils
  • Sero-fibrinous
  • Fibrino–purulent
  • Proliferative fibrosing = chronic inflammation
  • Granulomatous = chronic, macrophage dominated
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20
Q

Which of the following is acute and which is chronic:

  • Fibrous
  • Fibrinous
A
  • Fibrinous = acute

- Fibrous = chronic

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21
Q

How is the specific gravity of transudate and exudate different?

A

Transudate SG less than 1.015
- metabolic disorders
Exudate SG more than 1.015
- inflammatory

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22
Q

How does fibrinous pericarditis appear grossly?

A
  • Pericardial surfaces are covered by variable amounts of yellow fibrin deposits, adherence between the parietal and visceral layers.
  • When the pericardial sac is opened upon necropsy, these attachments are torn away
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23
Q

How does fibrinous pericarditis appear microscopically?

A

An eosinophilic layer of fibrin admixed with few neutrophils lies over a congested pericardium.

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24
Q

What are the two outcomes of fibrinous pericarditis?

A
  1. Early death by septicaemia

2. Constrictive pericarditis (proliferative fibrosing) - becomes thickened and scarred

25
Q

Describe constrictive pericarditis as an outcome of fibrinous pericarditis

A
  • Survival is prolonged => fibrous organization of the exudate forming fibrous adhesions between the surfaces
  • This obliterates the pericardial sac constricting the heart with fibrous tissue interfering with cardiac filling and output
  • Compensatory myocardial hypertrophy develops diminishing ventricular chamber volumes and contributing to eventual congestive cardiac failure
26
Q

What are some diseases in different species that causes fibrinous pericarditis?

A
  • Cats: FIP
  • Cattle: Pasteurellosis
  • Pigs: Glasser’s disease, pasteurellosis, Mycoplasma hyopneumoniae
  • Horses: Streptococcus spp
27
Q

What causes Glasser’s disease in pigs?

A

Haemophilus parasuis

28
Q

Describe the features (subacute and chronic) and cause of Glasser’s disease in pigs

A

Subacute lesions - pleuritis, pericarditis, peritonitis with or without bronchopneumonia
Chronic lesions - proliferating fibrosing
Cause - stress (weaning, transport)

29
Q

A horse with a streptococcal infection will have what changes to their heart?

A

Proliferative fibrosing - fibrin covering of the heart

Muscular hypertrophy

30
Q

What is the difference between fibrinous and Fibrino-suppurative?

A

Increased numbers of neutrophils in Fibrino-suppurative

31
Q

How does Fibrino-suppurative pericarditis appear grossly?

A

Pericardial surfaces are thickened by white, often rough, shaggy-appearing masses of fibrin with purulent exudate i.e .neutrophils

32
Q

What are the two outcomes of Fibrino-suppurative pericarditis ?

A
  1. Early death by septicaemia.
  2. Constrictive pericarditis: When survival is prolonged, there is a fibrous organization of the exudate forming fibrous adhesions between the surfaces => obliterates the pericardial sac and constricts the heart with fibrous tissue interfering with cardiac filling and output => myocardial hypertrophy develops diminishing ventricular chamber volumes and contributing to the eventual congestive cardiac failure
33
Q

Which disease in cattle is an example of Fibrino-suppurative pericarditis?

A

Traumatic reticulopericarditis “Wire” or “Hardware disease” in cattle

34
Q

Describe traumatic reticulopericarditis “Wire” or “Hardware disease” in cattle

A
  • Due to foreign bodies, often sharp / pointed that accumulate in the reticulum
  • Contraction of the reticulorumen caused the foreign body to penetrate the reticular wall and diaphragm enters the adjacent pericardial sac.
  • Bacteria are transferred with the foreign body to establish infection
35
Q

What is visceral gout, what are 3 causes of it?

A

Imbalance between production and excretion of uric acid

  • Congenital enzymatic deficiencies
  • Dietary: animal protein to herbivorous species in reptiles
  • Increased catabolism (debilitating diseases, tumours)
36
Q

What are some other causes of visceral gout?

A
  • Renal diseases: nephritis, tubular damages, Urolithiasis (kidney stones)
  • Dehydration
37
Q

In which species is visceral gout seen?

A

Reptiles and birds

38
Q

Describe the gross lesions seen in pericardial gout (uric pericarditis)

A
  • Uric acid deposition (urate crystals) in peri- and epicardium elicit a peripheral mixed cellular inflammatory response (macrophages and heterophils)
  • Grossly: white, gritty deposits (tophi)
39
Q

Describe the histological appearance of pericardial gout (uric pericarditis)

A

Urate crystals and mixed cell inflammation (macrophages and heterophils - avian granulocyte)

40
Q

What are the causes of endocardial mineralisation?

A
  • Excess vitamin D intake
  • Intoxication by carcinogenic plants
  • Hyperparathyroidism
  • Renal failure
  • Johne’s disease
41
Q

How does endocardial mineralisation appear grossly?

A

Multiple, large, white, rough, firm plaques of mineralised fibroelastic tissue within endocardium and intima of large elastic arteries

42
Q

When does endocardial fibrosis occur (2 examples)?

A
  • chronically dilated hearts
  • healed ulcerative endocarditis
  • jet lesions e.g. valvular stenosis/regurgitation
43
Q

Describe valvular endocardiosis

A

Myxomatous degeneration

  • Age-related cardiac disease of small and toy breeds (Cavalier King Charles Spaniel)
  • Associated with degeneration of valvular collagen
44
Q

How does valvular endocardiosis appear grossly?

A

Affected valves are shortened and thickened (nodular) appearing smooth and shiny

45
Q

What are the consequences of valvular endocardiosis?

A

Results in valvular insufficiency and congestive heart failure
- Development of jet lesions and rupture of chordae tendineae are common.

46
Q

What is the order of likeliness for each valve being affected by valvular endocardiosis?

A

mitral > tricuspid > aortic > pulmonary

47
Q

Describe left ventricular endocardial fibroelastosis

A
  • Defect in myocardial lymph drainage leads to chronic oedema and fibroelastic tissue proliferation
  • Restricted myocardial motion produces a reduction in output and can cause failure
48
Q

What can cause endocarditis?

A

Haematogenous spread of infectious agents (bacteria>parasites>fungi)

  • Pigs: Strep and E.rhusiopathiae
  • Cattle: Arcanobacterium pyogenes
  • Dogs/cats: Strep and E.coli
49
Q

How does endocarditis appear grossly?

A

The surface is rough and granular, with large, adhering, friable, yellow to grey masses “vegetations”

50
Q

How does endocarditis appear microscopically - cells and chronic lesions?

A
  • Fibrin, platelets, bacteria, leukocytes and erythrocytes.
  • In chronic lesions, the fibrin deposits are organized by fibrous connective tissue to produce irregular nodular masses that can become mineralised
51
Q

Describe the pathogenesis of endocarditis

A

Extracardiac infection - one or more bouts of bacteraemia

Injured valves - bacteria adhere, proliferate and initiate an inflammatory reaction

52
Q

Death due to endocarditis is a result of?

A
  • Cardiac failure from valvular dysfunction
  • Bacteraemia
  • Septic emboli leading to infarction or abscess formation in other organs (lungs, kidneys).
53
Q

Describe right cardiac endocarditis

A

Stenosis of right valve, chronic hepatic congestion and pulmonary embolism

54
Q

Describe left cardiac endocarditis

A

Stenosis of left valve, chronic pulmonary congestion and systemic embolism (kidney)

55
Q

Endocarditis is seen most commonly on which side of the heart?

A

Left - except in cows

56
Q

What is sequela to endocarditis?

A
  • Septic emboli disseminate throughout the body: “Embloic showers”, multifocal purulent lesions scattered randomly throughout an organ e.g. kidney
57
Q

Endocarditis is rare in which species?

A

Cats

58
Q

Describe ulcerative endocarditis and its gross appearance

A
  • Uraemia (acute renal insufficency) induce endocardial ulceration in dogs.
  • Grossly after the initial ulcer heals, the area is replaced by raised, white plaques of fibrous and mineralised tissue.

Y3 Cardiovascular pathology (4 decks)

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