Cardiovascular Pathalogical Anatomy Flashcards

1
Q

Rigor morris of the myocard

A

Rigid ventricular walls and empty left ventricle

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2
Q

What is the difference between clots formed anti Mortem and post mortem

A

Post mortem clots are red, free from attachment to any surrounding structures and found in arteries, the right ventricle and large vessels at the base of the heart.

Anti - mortem clots may be free (blood clot) or attached = thrombus

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3
Q

The discovery of pale chicken fat clots is suggestive of

A

They have few erythrocytes = animal may have suffered from severe anemia, or prolonged agonal period (time between fatal event and death).

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4
Q

Macroscopic picture of Hb imbibition

A

Imbibition is the result of red blood cell lysis in tissues starting more than 12. Hours after death - Hb is liberated from erythrocytes and gives a diffuse red/pink staining to tissues.

In the heart there is a diffuse red colouration of the endocard and epicardium that imitates haemorrhage!

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5
Q

In myocardial cell necrosis we expect to see

A

Leukocytic invasion and phagocytosis of sarcoplasmic content - sarcolemma tubules and condensed interstium with vessels remain. Rarely see myocyte regeneration, unless in very young animals and avians.

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6
Q

Patent ductus arteriosus

A

A persistent channel between pulmonary artery and aorta in foetal life (allows blood to bypass lungs in uteri) should convert to ligamentum arteriosum post natally, however in k9 breeds such as poodle collie and Pomeranian this does not happen.

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7
Q

Describe a atrial septal defect

A

Foremen ovale connection between atria in foetus fails to close postnatal in breeds such as boxer, Doberman and Samoyed.

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8
Q

Describe Ventricular septal defect

A

Failure of the interventricular septum to form fully (usually upper membranous part rather than lower muscular part) as a result shunting of blood occurs between the cavities. Common in English bull dog, springer spaniel and westies.

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9
Q

What is a pulmonic stenosis

A

Narrowing of the pulmonary artery - leads to hypertrophy of the right ventricle due to increased intraventricular pressure. Common in beagles, chihuahuas and English bull dogs.

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10
Q

Valvular hameatomas or hemocyts are ??

A

Bulging blood filled lesions on the edge of atrioventricular valves commonly found in young ruminants. They usually regress after several months of age and don’t effect heart function.

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11
Q

What is a persistent right aortic arch

A

Right aortic arch fails to regress normally and therefor the oesophagus and trachea are trapped between it and the ligamentum arteriosum at the level of the base of the heart.

Animals suffer from oesophageal dilation, regurgitation, aspiration pneumonia. GSDs and red setters are susceptible.

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12
Q

What is ectopia cordis

A

Congenital development abnormality of the heart - heart sits outside the thoracic cavity.

Extra thoracic, pre eternal or intro abdominal

Dislocation within the thorax occur due to asymmetric pressure ie. in a congenital diaphragmatic hernia, or pleural effusion.

A congenital absence of a pericardium can occur in dogs

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13
Q

What is endocardial fibro-elastosis

A

Diffuse endocardial thickening when any of the heart chambers remain dilated for a long period of time

Primary - left ventricular hyper trophy & dilation and diffuse endocardial thickening by collagen and elastic fibres, without a associated cardiac malformation. ** Burmese cats

Secondary - heart disease in turkeys: cardiomyopathy left ventricular hypertrophy and dilation - heart has a round shape.

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14
Q

Non inflammatory fluid accumulated in the pericardial sac is associated with which kind or cardiovascular disturbance

A

Circulatory disturbances which causes findings such as hydropericardium, haemopericardium

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15
Q

Characterise hydro pericardium

A

Accumulation of clear to light yellow watery serous fluid in the pericardial sac.

Acute - pericardial surfaces and smooth and shiny
Chronic- epicardium opaque, Fibrinous thickening, rough granular

Causes: generalized anasarca, congestive heart failure, nutritional (low protein), neoplastic metaplasia to pericardium, lymphoma of myocardium.

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16
Q

Characterise haemopericardium

A

Accumulation of blood in pericardial sac.

Sudden death - cardiac tamponade

Causes: atrial rupture in dogs, intrapericardial aortic rupture in horses, complication of intracardiac injection

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17
Q

What is the cause of serous atrophy of fat in the heart

A

Rapid mobilisation of fat deposits occurs following anorexia, starvation and cachexia.

Normally animals have abundant white epicardia’s fat deposits particularly in the ateioventricular junction - this fat is lysed and fat vacuoles of lipocytes are small, replaced by protein rich fluid. At the same time as an increase in interstitial fluid the deposits are converted to grey gelatinous masses with small white foci of necrotic fat.

Lipocytes are atrophic and surrounded by oedema.

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18
Q

What affect may visceral gout of snakes and birds have on the pericardium

A

Urate deposits are found in pericardium - serosal surface appears thickened and white.

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19
Q

Name the different types of pericarditis

A

Fibrinous
Suppurative
Constrictive

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20
Q

Characterise fibrinous pericarditis

A

Rarely significant exudation of fluid = no distension of pericardial sac.

Fibrin exudation from damaged vessels or inflammatory response to haematogenous infection, starts at the base of the heart and spreads to cover pericardium and epicardium.

Both pericardial surfaces appear rough and are covered by yellowish fibrin deposits, the pericardium microscopically appears congested and has a layer of fibrin that is stained eosinophillically with NEU.

With time fibrous adhesions may form between the pericardial surfaces following fibrous organisation.

Causes:

Cattle: pasturellosis, black leg, coliform Septicaemia, SBE sporadic bovine encephalitis

Pigs: glassers disease, streptococcal infection, pasturellosis, enzootic mycoplasmal pneumonia, salmonellosis

Horses: streptococcal infection

Birds: psittacosis

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21
Q

Characterise suppurative pericarditis

A

Purulent/ suppurative exudate in the pericardial sac of cattle often due to traumatic reticuloperitonitis (HARDWARE DISEASE)

foreign bodies such as nails and wire penetrate the reticulum, diaphragm and pericardial sac introducing infection.

Cattle may survive for weeks or months before death from congestive heart failure and Septicaemia.

Pericardial surfaces are thickened and white rough shaggy masses of Fibrinous tissue with an accumulation of thick foul purulent exudate in the sac.

Also seen in horses and cats associated with empyema.

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22
Q

Characterise constrictive pericarditis

A

Chronic inflammatory lesions with extensive fibrous proliferation and adhesions in the pericardial space.

Advanced adhesions cause pericardial sac obliteration and constriction of the heart which interferes with cardiac filling. Compensatory mechanisms such as myocardial hypertrophy, chambers are lower in volume which also contributes to eventual heart failure.

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23
Q

Degenerative disorders of the endocardium

A

Endocardial Mineralisation
endocardial fibrosis
Valvular fibrosis / endocarditis

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24
Q

Mineralisation of the endocardium

A

Vit D toxicosis, carcinogenic plant intoxication (vit d analogs) ie. Enzootic calcinosis

Large firm white plaques on the endocardial surface of the heart and intima of large elastic arteries.

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25
Q

Endocardial fibrosis

A

Develops following chronic cardiac issues - chronic heart dilation in cattle with johns disease

Dogs that have had a previous uremic episode - lesions caused by ulcerative endocarditis in left atria, heal but fibrotic tissue remains.

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26
Q

Characterise valvular endocarditis / valvular fibrosis

A

Age related disease in K9s

MOST COMMON CAUSE OF CONGESTIVE HEART FAILURE IN OLD DOGS

Lesions are more frequent on mitral/ bicuspid valve (left atrium left ventrical two cusps) than tricuspid (right atrioventricular 3 cusps)

Valves are short and thick with diffuse or nodular and smooth appearance instead of rough

Histology: valves show fibroblastic proliferation and deposition of mucopolysacharides

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27
Q

Which type of lesions are seen in endocarditis and what do they look like

A

Mural

Valvular

Cause: bacterial infections that result in bacteremia or strongylus vulgaris/ mycotic infections in horses.

Acute ulcerative endocarditis of the left atrium - uremic syndrome in dogs.

Macroscopically: Adhering friable yellow to grey masses occlude valve orifices - they are made up of fribrous CT and look wart like.

Microscopically: there are layers of fibrin surrounding bacterial colonies, with NEU infiltration and granulation tissue in chronic lesions.

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28
Q

Characterise ulcerative endocarditis of canines

A

Acute condition of the left atria - distinctive lesion caused by acute renal insufficiency.

Swelling of interstitial spaces in subendocardium or tunica intima of arteries —> either heals with some fibrosis or progresses to necrosis of cells, collagen, elastic and reticular fibres. These ulcerations can perforate the wall of the atrium causing thrombi formation and heavy deposition of calcium salts.

If the renal insufficiency is re established then the lesion may heal leaving irregular patches of sclerosis - intact endothelium covers white plaques of mineralisation.

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29
Q

Myocardial growth disturbances

A

Hypertrophy - increase in muscle mass due to an increase in myocyte size. Usually a secondary compensatory response to increased workload of the heart.

ECCENTRIC hyper trophy = enlarged cardiac chambers (dilation) walls are normal to thinner than normal caused by increased blood volume load a result of valve insufficiencies and septal defects (shunting).

CONCENTRIC hypertrophy = small cardiac chambers with thickened walls caused by an increase in pressure/load due to valve stenosis, systemic hypertension, pulmonary disease (cor pulmonale).

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30
Q

Common causes of RIGHT ventricular hypertrophy

A
  1. Dirofilariasis (heart worm) K9
  2. Congenital pulmonary artery stenosis K9
  3. Brisket disease in cattle
  4. Chronic vesicular emphysema in equines
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31
Q

Causes of LEFT ventricular hypertrophy

A

Congenital sub aortic stenosis in K9’s

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32
Q

Define fatty infiltration of the heart

A

Associated with obesity, increased numbers of lipocytes are deposited between myocardial fibres.

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33
Q

Define fatty degeneration of the myocard

A

Accumulation of sarcoplasmic lipid droplets within cardiomyocytes. Heart is pale and flabby, this lesion occurs in systemic disorders such as anaemia, toxaemia and copper deficiency.

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34
Q

Define hydropic degeneration of the myocard

A

Associated with the use of ‘anthracyclines’ anti-neoplastic drugs that results in the degeneration of fibres of cardiomyocytes - they have extensive vacuolisation of their sarcoplasm which appears eosinophilic, eventually there is lysis of contractile material (myofibrils).

35
Q

What is lipofuscinosis?

A

Also called browns atrophy

Occurs in severe cachexia, or as a hereditary lesion in Ayrshire cattle.

Hearts are brown - nuclear poles of myocytes have clusters of yellow-brown granules

36
Q

Characterise myofibrilar degeneration

A

Sublethal injury of cardiac muscle cells

Fibres appear pale and have eosinophilic sarcoplasm that lacks cross striations, microscopically myofibrils have a varying extent of dissolution.

37
Q

Define myocardial necrosis and mineralisation

A

Myocardial cells are dystrophic, common occurrence when ever there is necrosis of cardiac fibres. Areas of the heart appear pale and become yellow to white dry and gritty.

Microscopically lesions are focal, multi focal or diffuse such as in white muscle disease, or fit E selenium deficiency.

Hyper eosinophilic, lack of strict Atkins, hyaline necrosis, shredded appearance, areas of ischemic necrosis.

Occurs 24-48hrs after injury

Causes: nutritional deficiency, ishemia, metabolic disorders, chemical and plant toxicosis, physical injury

38
Q

What is the outcome of myocardial necrosis

A

1.Death from acute heart failure
2.Death from cardiac dilation and scarring
3.Minimal damage, detectable only by MS

39
Q

Describe two circulatory disturbances of the myocardium

A
  1. Haemorrhage - areas appear red in a petechial to ecchymotic or suffusive extent
  2. Thrombosis - or embolism, of coronary arteries may result in a myocardial infarction and heart failure. (Uncommon)
40
Q

Characterise myocarditis

A

Inflammation of the myocardium as a result of various systemic diseases including haematogenous infections.

It is rarely a primary lesion!

Myocarditis can be suppurative, necrotising, haemorrhagic, lymphocytic or eosinophilic.

41
Q

Suppurative myocarditis

A

Pyogenic bacterial infection of the myocardium.

Cause: usually secondary to left sides lesions of valvular endocarditis.

Macro: pale disseminated lesions
Micro: NEU infiltration and myocyte necrosis, formation of abscesses.

42
Q

Necrotising myocarditis

A

Commonly seen in dogs and cats with TOXOPLASMOSIS

43
Q

Haemorrhagic myocarditis

A

Commonly occurs alongside haemorrhagic inflammation of skeletal muscles in cattle with BLACK LEG: CLOSTRIDIUM CHOVEIAE

44
Q

Lymphocytic myocarditis

A

Commonly associated with VIRAL infections

  • PARVOVIRUS PUPPIES

Affected k9s die suddenly from congestive heart failure - heart is pale and flabby with disseminated interstitial infiltration of lymphocytes

Myocytes have Intranuclear basophillic inclusion bodies

Older lesions - fibrosis

45
Q

Eosinophilic myocarditis

A

Occurs alone or alongside similar lesions in skeletal muscles.

Caused by various PARASITIC INFECTIONS

  • SARCOSPORIDIOSIS / ECHINOCOCCUS/ SARCOCYSTS

lesions are yellow to green without distinct margins

46
Q

What primary neoplasms of the myocardium do we know

A

Rhabdomyoma

Rhabdomyosarcoma

Neurofibroma

Haemangiosarcoma

47
Q

Secondary neoplasm of myocardium

A

Lymphosarcoma (malignant lymphoma)

Modular or diffuse lesions that are invasive and destructive, substitution of normal cells and tissues of ventricular walls by lymphoid cells.

ENZOOTIC BOVINE LEUKOSIS

48
Q

Characterise cardiac haemangiosarcoma

A

Primary - neoplasm arises in the heart
Secondary - metastatic lesion from a site elsewhere ie. Spleen.

Macro: protruding red to red black blood filled masses that are located on the epicardial surface.

Micro: composed of scattered, elongated and plump neoplasticism endothelial cells that may or may not form vascular spaces containing blood.

49
Q

Key cells involved in the reaction to vessel injuries are?

A

Endothelial cells - metabolically active barrier between blood and vessel wall. When damaged plasma proteins move into the sub endothelium - necrosis leads to exposure of collagen which results in the formation of a thrombus.

Endothelial cells at the edge of the damaged area begin to proliferate and re-endothelialise the vessel wall.

Smooth muscle cells - produce vascular tone of blood vessels, secrete extra cellular components collagen, elastin and proteoglycans. They are also involved in monocytes recruitment, lipoprotein metabolism and production of prostaglandins and free radicals.

Control of these functions is regulated by a variety of mediators eg. Growth factors, cytokines and inflammatory mediators.

50
Q

Describe haemoglobin imbibition of blood vessels

A

12-24 hours post mortem the intimate surface of blood vessels appears red instead of white. Cause is the lysis of erythrocytes and liberation of Hb into surrounding tissue.

51
Q

Post mortem clotting must always be differentiated from

A

Thrombosis

52
Q

Characterise aneurysm

A

A localised dilation of a part of a vessel where the wall has become thin and weakened.

Causes: copper deficiency (required for normal elastic tissue development)

Types: berry, sacular, fusiform, dissected.

True aneurysm involves all layers of vessel wall

False aneurysm - rupture of artery or aneurysm = haematoma that communicates with arterial lumen.

53
Q

Horses are susceptible to which type of arterial ruptures

A

Sudden rupture of the ascending aorta as a result of extreme exertion - during periods of excitement and activity ie. Racing or breeding stallions.

Increased aortic pressure leads to rupture.

54
Q

Arterial hypertrophy is a response to …

A

Sustained increase in pressure or volume of blood moving through the lumen.

55
Q

Characterise arterial hypertrophy

A

Thickening of the walls of muscular arteries in response to sustained increased pressure or volume. Hypertrophy of smooth muscle cells in the medial layer of the wall.

56
Q

Which arteries in which species are commonly affected by arterial hypertrophy

A

Cats - associated with TOXOCARA / DIROFILARIASIS parasite infections: muscular pulmonary arteries

cattle - pulmonary hypertension associated with high altitudes - muscular pulmonary arteries

Pregnant animals - uterine arteries

57
Q

Define arteriosclerosis

A

An age related lesion that rarely causes any clinical alterations.

Chronic degenerative and proliferation changes in arterial wall which results in hardening/loss of elasticity and luminal narrowing.

Abdominal aorta frequently affected where turbulent blood flow occurs.

Macro: slightly raised form white plaques
Micro: mucopolysacharide deposits cause thickening of intima, subsequent infiltration and proliferation of smooth muscle cells and fibrous tissue into the intima —-> splitting and fragmentation of internal elastic lamina.

58
Q

What is atherosclerosis

A

Rarely seen in animals. Deposits of lipid (atheromas), fibrous tissue and calcium in vessel walls lead to luminal narrowing.

May been sen in pigs, chickens or rabbits fed high cholesterol diet.

59
Q

Define arterial medial calcification

A

A disorder that occurs often in animals that involves both elastic and muscular arteries, often concurrently with endocardial mineralisation too.

Causes: calcinogenic plant toxicosis (enzootic calcinosis), vitamin D toxicosis, renal insufficiency, severe debilitation in cattle with johns disease.

Macro: calcification may be dystrophic or metastatic, arteries have an appearance as solid, dense pipe like or there are raised solid white plaques.

Micro: prominent basophilic staining granular deposits in elastic fibres of elastic arteries, or in complete rings on the medial musculature of muscular arteries.

60
Q

Hyaline degeneration, amyloidosis and fibrinoid necrosis are lesions of which vessel types

A

Small muscular arteries and arterioles

61
Q

Which stains are used for the differentiation between hyalin degradation, amyloidosis and fibrinoid necrosis

A

Amyloid - Congo red and methyl violet
Fibrinoid deposits - PAS periodic acid Schiff stain
Hyaline - does NOT stain

62
Q

Which important diagnostic feature is seen at necropsy in swine with deficiency of selenium and vitamin E, oedema disease, cerebrospinal angiopathy and organic mercury toxicosis

A

Fibrinoid necrosis of muscular arteries and arterioles - fibrin polymerisation is stained eosinophillic and obliterates cellular structure of walls.

63
Q

Some predisposing factors to the development of thrombosis

A

Endothelial damage, altered blood flow, hypercoagulative states /coagulopathies.

64
Q

Which type of emboli may originate from thrombotic lesions

A

Septic or bland emboli

Septic emboli originate from lesions caused by endocarditis

65
Q

Describe DIC disseminated intravascular coagulation

A

Not a disease! Just an intermediary mechanism.

Pathological activation of the coagulation system leading to generalized intravascular clotting particularly within the arterioles and capillaries.

Increased clotting results in the consumption of platelets and coagulation factors (thrombocytopenia and excessive clotting)

  • ischemia, impaired organ perfusion and organ damage.

Excess thrombin converts plasminogen to plasmin —-> fibrinolysis and fibrin degradation products

  • excessive bleeding hemorrhage = shock, hypotension and increased vascular permeability.

The process can be ACUTE / SUBACUTE / CHRONIC and may be LOCAL or GENERALIZED.

Causes: wide spread endothelial damage and exposure of subendothelial collagen, or direct activation of coagulation cascade by the extrinsic/intrinsic pathway (bacteria, parasites, virus, neoplasia, aflatoxins, immune complexes, GDV, heat stroke, red maple ingestion, snake bite enzymes, pancreatitis etc.)

66
Q

Typical findings at necropsy if an animal dies from DIC

A
  • petechial to Ecchymotic haemorrhages on mucosal surfaces and in skin
  • microthrombi cause congestion, edema, haemorrhage, and necrosis of organs
  • microthrombi are easily seen in capillaries of brain, glomeruli, adrenal glands, lungs and the heart

Microthrombi may consist of

  1. Hyaline thrombi - fibrin
  2. Granular thrombi - platelets
  3. Fibrin degradation products
67
Q

Arteritis is a common feature of which types of disease

A

Infectious and immune mediated. All vessel types can be affected - vasculitis, angiitis

68
Q

Typical findings in arteritis

A

Inflamed vessels have leukocytes present within and around their walls, damage is evident as fibrin deposits or necrosis of endothelial cells and smooth muscle cells.

69
Q

Causes of arteritis

A

Initial endothelial injury by infectious agents or immune mediated mechanisms

Focal extension of suppurstive or necrotising inflammatory processes adjacent to vessel walls ie. bacterial pneumonias, abscesses, purulent meningitis, aspergillosis, acute metritis.

Erteritis of hameatogenous origin - septicaemia or bacterial endocarditis.

Pigs: Salmonellosis, erysipelas, hog cholera - purple discoloration of skin, not, abdomen which become necrotic and slough.

Horses: infected by parasite strongylus vulgaris - larval stage migrates through intestinal arteries, most severe lesions in cranial mesenteric artery. Vessels are enlarged and walls are firm and fibrotic, containing adhered thrombi and larvae. Microscopically there is leukocyte infiltration and proliferation of fibroblasts.

70
Q

Neoplasms that arise from vessel walls

A

Haemangiomas - benign often involve skin in dogs
Haemangiosarcomas - malignant occurs frequently in the spleen and right side of the heart

Haemangiopericytoma - tumour of the skin in canines, distinctive laminated arrangement of elongated plump neoplastic pericytes surrounding the small blood vessels.

71
Q

What is a variscosity

A

Localised Dilation of the vein due to weakened walls caused by primary congenital defects ie. Venous diaghram, agenesis, hypoplasia or ectopia. Or secondary to trauma, neoplasia, surgery.

72
Q

What is phlebectasia

A

Generalized dilation of the veins due to weakened vessel walls

73
Q

Characterise phlebitis

A

Phlebitis is inflammation of the veins often causing thrombosis.

Causes: systemic infections (salmonellosis, FIP), local spread of infection (metritis or hepatitis) iatrogenic faulty IV injection procedures

74
Q

What is omphalophlebitis

A

Inflammation of the umbilical vein. Occurs in farm animals due to bacterial contamination of the umbilicus following birth.

Infection at this site can cause septicaemia, supurrative polyarthritis (joint Ill), hepatic abscesses, umbilical abscesses.

75
Q

Describe lymphangiectasis

A

Dilation of lymph vessels, caused by obstruction: invading neoplastic masses.

Intestinal lymphangiectasis is an important disease in dogs that leads to protein losing enteropathy

Diseases that cause severe acute inflammation and vascular damage often lead to lymphatic dilation ie. BIVINE PASTURELLOSIS - lung lesions.

76
Q

What is lymphangitis

A

A common feature of multiple diseases - inflammation of lymph vessels.

Often vessels are seen as thick cord like structures in the distal limbs. Nodular suppurative lesions can ulcerate and discharge pus onto the surface of the skin.

Granulomatous lymphangitis is seen in the mesenteric lymphatic vessels of cows with JOHNS DISEASE

77
Q

Which benign tumour of the lymph vessels do we know

A

Lymphangioma - benign tumour composed of lymphatic channels

78
Q

How can we differentiate between non inflammatory and inflammatory pericardial diseases

A

Non inflammatory disturbances include fluid accumulation ie. Hydropericardium or haemopericardium general causes of oedema or haemorrhage - pericardial sac distension may be seen.

Inflammatory diseases rarely have fluid exudation ie. Pasturellosis, blackleg, coliform septicaemia, streptococcal infections etc spread via the blood and distension of pericardium is rarely observed.

79
Q

Visceral gout in birds and reptiles causes which changes in the pericardium

A

Urate deposits - serous surface is thickened and white ( plaster of Paris )

80
Q

Common complication of hardware disease in cattle

A

Traumatic reticuloperitonitis - can cause suppurative or purulent pericarditis
FBs penetrate the reticulum wall, diaphragm next to the pericardial sac —> COR RUGOSUM thick pericardial surfaces with white shaggy masses of Fibrinous tissue and white to grey thick foul smelling purulent exudate.

81
Q

What term is used to describe chronic inflammatory lesions and adhesions of the pericardial space - pericardial sac obliteration and heart constriction.

A

Constrictive pericarditis - myocardial compensation = hypertrophy. Thicker walls result in a smaller volume of blood passing through ventricles —> congestive heart failure.

82
Q

When does endocardial mineralisation occur alone

A

In cases of vitamin d toxicosis

83
Q

What is the difference between endocarditis and valvular endocarditis (valvular fibrosis)

A
  1. Endocarditis is caused by bacterial infections or migrating parasites - mural or valvular lesions.

Valves have large adhering friable yellow masses that occlude the valve orifice. Chronic lesions have fibrin deposits / verruca wart like lesions - layers of fibrin and bacteria surrounded by granulation tissue. (Arcanobacterium, streptococcus, erysipelothrix)

  1. Valvular endocarditis is a disease of old dogs - common cause of congestive heart failure it most commonly affects bicuspid/mitral valve.

Valves are short and thick, with a diffuse or nodular appearance that is smooth (fibroblastic proliferation) acid mucopolysaccharide deposits.