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Year 3 Pathology > Cardiovascular 1, 2 and 3 > Flashcards

Cardiovascular 1, 2 and 3 Flashcards

1
Q

Describe CV embyrology?

A
  • Heart develops from splanchnic mesenchyme in cardiogenic area
  • Single heart tube- surrounding mesenchyme thickens to from myoepicardial mantle- dilations and constrictions forms 4 chambers
  • Cardiac looping- heart converted from tube to C-shaped structure
  • Cardiac septation- atrial septum primordia and ventricular septum primordia divide left and right
  • Atria partitioned by septum primum and secundum (incomplete until afer birth)
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2
Q

What is the foramen ovale?

A

Incomplete septum secundum allows blood to pass from left to right

After birth forms the fossa ovalis

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3
Q

What do the left and right 4th aortic arches form?

A

Left- proximal part of arch or aorta

Right- proximal part of subclavian artery

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4
Q

Describe foetal circulation from the placenta to the placenta?

A
  • Placenta to umbilical veins- liver/ductus venosus
  • Liver to vena cava to the right atrium
  • Right atrium through foramen ovale to left atrium
  • Left atrium to aorta- systemic arteries
  • Systemic arteries to umbilical arteries to placenta
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5
Q

What is the pericardium, epicardium, endocardium and myocardium?

A

Pericardium (sack)- one layer of the mesothelium with central layer of connective and adipose tissue

Epicardium- one layer of mesothelium on connective tissue and adipose tissue fused to the myocardium

Endocardium- endothelium identical to arterial with connective tissue and purkinje fibres in ventricle

Myocardium- muscle layer

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6
Q

Describe the histology of the myocardium

A

Centrally placed nuclei

Sarcomeric cross-striations

Ratio muscle fibre : capillaries 1:1

Purkinje fibres

Arranged in bundles

Connective tissue

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7
Q

What are the PM alterations of the the heart?

A

Blood clotting- red clots- atria, RV

Rigor mortis- occurs in left myocardium
Animals with prolonged heart disease may lack aquate glycogen for rigor mortis

Chicken fat clots- sedimentation of erythrocytes, closts of colourless fibrin

Haemoglobin imbibition- PM lysis of erythrocytes released Hb- red staining

Barbituate crystals- from phenobarbitone injection

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8
Q

What are the different pathological mechanisms of cardiovascular dysfunction?

A

Pump failure- weak contractility, myocardial disease

Obstruction of flow- valvular stenosis, vascular narrowing

Regurgitant flow- valvular dysfunction

Shunted flow- congenital defects

Ruptures- heart wall/ major vessels

Conduction disorders

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9
Q

What is cardiac syncope?

How is is characterised?

What can cause it?

A

Fainting/loss of conscious

Characterised clinically by collapse, loss of consciousness and extreme changes in HR and blood pressure

Myocardial necrosis, ventricular fibrillation, arrythmias, cardiac inhibition

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10
Q

What is congestive heart failure and the responses?

A

CHF- slow or gradual loss of puming efficiency, associated with pressure overload, volume overload, progressive myocardial damage
Reduced renal blood stimulated RAAS- sodium and water retention causing hypertension and increased workload on heart

Responses-
Cardiac dilation
Hypertrophy
Decompensation
Death

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11
Q

What does subacute and chronic Left/Right sided heart failure cause?

What are the causes of Right/Left sided heart failure?

A

Left-
Subacute- pulmonary congestion and oedema
Chronic- pulmonary congestion and oedema, fibrosis and hemosiderosis (iron deposits from erythropoesis)
Causes- left sided cardiomyopathies, dysfunction of aortic/mitral valve

Right-
Subacute- passive systemic congestion, hepatomegaly and splenomegaly
Chronic- systemic oedema (ascites), nutmeg liver
Causes- right sided cardiomyopathy, pulmonary hypertension, dysfunction of tricupsid and pulmonary valves

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12
Q

How can congenital defects of the heart present differently?

A

Extreme defects- animals do not survive in utero

Mildest defects- could have no clinical signs

Defects with immediate severity
Clinical signs- cardiac failure- cyanosis, excercise intolerance

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13
Q

What can cause congenital defects of the heart and pericardium?

A

Single or multiple gene defects

Toxins- thalidomide

Physical agents

Nutritional deficiencies

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14
Q

What does this image show?

What is acardia?

A

Amorphus globosus- acardiac monster attached to placenta

Acardia- agenesis of the heart

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15
Q

What is ectopia cordis?

A

Congenital development of the heart outside the thoracic cavity

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16
Q

What is patent ductus arteriosus?

A

Vascular channel between the pulmonary artery and aorta- allows blood to bypass the lung during foetal life- should convert to ligamentum ateriosum

Remains and therefore blood shunted from left to right causing:
Pulmonary hypertension therefore RV pressure overload, concentric hypertrophy, volume overload then eccentric hypertrophy

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17
Q

What are the two types of atrial septal defects?

A

Failure of foramen ovale to close

True septal defect- faulty development of interatrial septum

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18
Q

What does a ventricular septal defect cause?

A

Failure of inteventricular septum- bull dog, springer, Westie

Shunts blood left to right- equal pressures, pressure hypertrophy of right ventricle, volume hypertrophy of left

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19
Q

What are the three types of semilunar valve stenoses?

A

Supravalvular

Valvular

Subvalvular

Circumferential band of fibrous or musculat tissue of the valvular tissue- above or at level of tissue

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20
Q

What is a pulmonic stenosis?

What does it cause?

What species are affected?

A

Narrowing of pulmonart artery- usually valvular lesions

Causes pressure overload- right concentric hypertrophy- leads to roughening, deformatino and dilation of the surface of the pulmonary artery

Species- beagle, bulldog, Chihuahua

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21
Q

What causes subaortic stenosis?

What does it lead to?

A

Subvalvular lesions- thick zone of endocardial fibrous tissue that encircles the left ventricular outflow below the valve

Microscopically- endocardial mesenchymal necrosis and fibrosis

Pressure overload in LV- concentric hypertrophy

Pigs, dogs- boxer/GSH

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22
Q

What tetralogy of fallot?

A

Anomaly of four lesions

Ventricular septal defect

Pulmonic stenosis

Dextroposition of the Aorta

Secondarily- hypertrophy of the RV

Bulldogs and Keeshond

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23
Q

What are valvular haemotomas?

A

Haematocyst or lymphocysts frequently observes on the atrioventricular valves in ruminants

Generally regress spontaneously

Haematocyst- bulging, blood filled cysts
Lymphocyts- bulging, ywlloe serum-filled cyst

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24
Q

How does a persistent right aortic arch cause megaoesophagus?

A

Right 4th aortic arch- not left- develops and ascends in the right midline

Ligamentum arteriosum forms a vascular ring over the oesophagus and trachea

Oesophageal obstruction and dilation- megaoeosphagus

GSH, irish setter, great dane

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25
Q

What is valvular agenesis/hypoplasia?

A

Failure of valves to develop

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26
Q

What causes peritoneopericardial diaphragmatic hernia?

A

Dogs- with incomplete development of diaphragm

Abdominal viscera can be located in pericardial sac

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27
Q

What circulatory disturbances can there be of CV?

A

Haemorrhages

Frequent lesion in endocardium, myocardium, pericardium

Petechiae, ecchymoses- septicaemia
Mulberry heart disease

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28
Q

What is the normal appearance and ammount of pericardial fluid?

A

Clear, viscous fluid

Horse/cow- 100ml

Dog/cat- 10ml

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29
Q

What is hydropericardium?

What are the different causes of it and associated agents?

How do acute and chronic cases appear differently?

What are the consequences?

A

Hydropericardium- accumulation of clear to light yellow, watery serous fluid in the pericardial sac

Associated with vascular injury- generalised oedema:

  • Increased vascular permeability- virus (influenza) , bacteria (clostridium), III hypersensitivity, toxins (paraquat)
  • Increased IV hydrostatic pressure- pulmonary hypertension (LCHF, high altitude disease)
  • Decreased IV osmosotic pressure- decreases albumin (malnutrition)
  • Decreased lymphatic drainage- obstruction

Consequences- cardiac tamponade or compression, which impairs cardiac filling and venous return

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30
Q

What is haemorrhagic pericardial effusion?

What breed of dog does it affect?

A

Deposits of small amounts of blood, chronically

Great Dane, St Bernard, GSH

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31
Q

What is haemopericardium?

What can cause it?

A

Accumulation of large amount of blood in pericardium causing cardiac tamponade, leading to compression and interfereing with cardiac filling and empyting

Atrial rupture due to haemagiosarcoma of right atrium in dogs

Rupture of intrapericardial aorta in horses

Complications of intracardiac injection

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32
Q

What is a pneumopericardium and a cyclopericardium and what can cause them?

A

Pneumopericardium- air filled
Pulmonary ruptures, perforations of oesophagus/stomach

Cyclopericardium- specific gravity >1.015
Rupture of thoracic duct, often gelatinous and white

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33
Q

What can be found incidentally with the pericardium in sheep?

What can cause serous atrophy of epicardial adipose tissue?

A

Pigmentations- melanosis

Anorexia, starvation, cachexia- fat catabolised to maintain energy
Important for cases of emaciation (neglect)
Grossly- white/yellow fat to grey gellatinous material
Microscopically- lipocytes are atrophic and oedema present in interstitial tissue

34
Q

What is the name for inflammation of pericardium/epicardium?

What are the different portals of entry for inflammation?

A

Pericarditis and epicarditis

Foreign body penetration- reticulum cattle

Local extension- local extension of severe inflammatory processes for adjactent structures

Haematogenous- virus/bacteria

35
Q

What are the different categories of inflammation based of exudate?

A

Serous

Fibrinous

Purulent

Sero-purulent

Fibrino-purulent

Proliferative fibrosing

Granulomatous

36
Q

What is the normal specific gravity of transudate and exudate?

A

Transudate < 1.015

Exudate >1.015

37
Q

What causes mineralisation of the endocardium?

How does it appear grossly and histologically?

A

Intake of excessibe amounts of vitamin D and intoxication by calcinogenic plants in cows

or

Hyperparathyroidism, Renal failure, Johne’s disease

Gross- multiple, large, white, rough, firm plaques or mineralised fibroelastic tissue within the endocardium and intima or large elastic arteries

Histology- deep purple angular appearance

38
Q

What causes endocardium fibrosis?

What causes pigmentation of the endocardium in sheep?

A

Fibrosis-

Occurs in chronically dilated hearts
Healed ulcerative endocarditis in dog (uraemia)
jet lesions (valvular stenosis/regurgitation)

Pigmentation-

Melanosis, aortic valves, no clinical significance

39
Q

What is valvular endocarditis?

What happens to the affected valves?

How does it appear microscopically?

A

Age-related cardiac disease of small and toy breeds (CKCS)
Associated with degeneration of valvular collagen
Polygenic basis

Affected valves are shortened and thickened and appear smooth and shiny
These lesions results in vulvar insufficiency and CHF
Development of jet lesions and rupture of chordae tendinae are common

Microscopically- increased fibroblastic proliferation and deposition of mucopolysaccharides

40
Q

What is left ventricular endocardial fibroelastic disease?

What breed of cat does it affect?

How can it lead to CHF, left bundle branch block?

A

Defect in myocardial lymph drainage, leading to chronic oedema and fibroelastic proliferation

Siamese and Burmese cats

Restricted myocardial motion produces a reduction in output and may lead to CHF

May incarcerate subendocardial purkinje fibres which leading to left bundle branch block

41
Q

What can cause endocarditis?

How does it appear grossly and microcropically?

A

Often endothelial injury and other elements of Virchow’s triad involved
Prexisiting extracardiac infections leading to Haematogenous disseminations- bacteria> parasites>fungi

Grossly- the surface is rough and granular with large, adhering, friable, yellow to grey masses

Microscopically- Fibrin, platelets, bacteria, leukocytes, erythrocytes
In chronic lesions- fibrin deposits are organised by fibrous connective tissue (nodules) which can become mineralised

42
Q

Describe the pathogenesis of endocarditis

What results in death from endocarditis?

What differs between left and right?

A

Extracardiac infection, injured valve, bacteria adhere, proliferate and initiate inflammatory reaction
More often in cows right, left usually every other

Death- cardiac failure from valvular dysfunction, bacteraemia, septic emboli leading to infacrction or abscess formation in other organs
Septic emboli disseminate- ‘embolic showers’

Right- chronic hepatic congesion and pulmonary embolism

Left- Chronic pulmonary congestion, systemic embolism (kidney)

43
Q

What causes ulcerative endocarditis?

How does it appear after healing?

A

Uraemia induce endocardial ulceration in dogs

The area is replaced by raised, white plaques of fibrous and mineralised tissue

44
Q

How does fibrinous pericarditis appear grossly?

How does it appear microscopically?

A

Grossly- pericardial surfaces are covered by variable amounts of yellow fibrin deposits, adherence between parietal and visceral layers
When pericardial sac is opened upon necropsy attachments are torn away

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

45
Q

What are the 2 outcomes of fibrinous pericarditis?

A

Early death by septicaemia

Constrictuve pericarditis- proliferative fibrosing

  • When survival ir prolonged, there is a fibrinous organization of the exudate forming fibrous adhesions between the surfaces
  • This constricts the heart with fibrous tissue interfering with filling and output
  • Hypertrophy- CHF
46
Q

What diseases casue fibrinous pericarditis in the following species?:

Cats

Cattle

Pigs

Horses

Birds

A

Cats- FIP

Cattle- pasturella, blackleg

Pigs- glassers disease, streptococcus sp, salmonella

Horses- step

Birds- clamydia psittaci

47
Q

What is the common name for porcine polyserositis?

What is its aetiology?

What age of pigs does it affect?

What are the subacute/chronic lesions?

What are the predisposing factors?

A

Glassers disease

Aet- Haemophilus parasuis

Young pigs- weaning to 4mo

Acute- pleuritis, pericarditis, peritonitis, polyarthritis, meningoencephalitis

Chronic- proliferating fibrosing- CHF

Predisposing factors- stress (weaning/transport)

48
Q

How does fibrinosuppurative pericarditis grossly appear?

What are the outcomes?

A

Pericardial surfaces are thickened by white often rough appearing masses of fibrin with purulent exudate- neutrophils

Outcomes
Early death by septicaemia
Constrictive pericarditis- when the survival is prolonged, there is a fibrous organization of the exudate forming fibrosis adhesions between the surface- affects output- hypertrophy- CHF

49
Q

What is the pathologically correct term for wire of hardware disease in cattle?

What causes this disease?

Describe is pathology?

A

Traumatic reticuloperitonitis

Due to foreign bodies, oftensharp/pointed that accumulat in the reticulum

Contraction of the reticulorumen caused the foreign body to penetrate the reticular wall and diaphragm and enters the adjactent pericardial sac
Bacteria are transferred with foreign body to establish infection

50
Q

What is viceral gout?

What can cause visceral gout?

How does it appear histologically?

A

Catabolism of nucleic acids which is usually converted to uric acid and excreted through the kidney
Imbalence between production and excretions causes increased levels and deposits to form

Renal diseases- nephritis, tubular damages, urolithiasis
Dehydration
Enzyme defiencies
Diet
Increased catabolism- diseases, tumours

Histo- has a star appearance

51
Q

What are the two types of myocardium ruptures and what can cause them?

A

Traumatic- shot/RTA

Spontaneous- weakness, dilation, necrosis, neoplasm

52
Q

What are the three types of cardiomegaly causes?

A

Hypertrophy

Dilation

Cardiomyopathy

53
Q

What causes ventriculat hypertrophy?

What are the different types of ventricular hypertrophy and whar can cause them?

A

Compensatory mechanism- physiological response to maintain adequate cardiac output
Secondary- reversible to increased workload, Primary- irreversible idiopathic

Eccentric- heary with normal but enlarged ventricles, normal/decreased thickness- volume overload (valve/septal defects)

Concentric- increased wall thickness- pressure overload- valvular stenosis, hypertension, pulmonary disease
Cor pulmonae- an alteration in RV structure and function from primary disorder of respiratory system

54
Q

What are the DDXs of cor pulmonae?

A

Dirofilaris and congenital pulmonic stenosis in dogs

High altitude disease

Chronic alveolar emphysema in horses (heaves)

55
Q

What can cause ventricular dilation and why does it occur?

Why not hypertrophy?

A

Same causes as hypertrophy- compensatory response to achieve cardiac output- dilation allows stretching of cardiac muscle cells to increase contractile force

Myocardium cannot undergo hypertrophy due to insufficient time, inadequate nutrition or diseases

56
Q

What is a cardiomyopathy?

What are the classifications?

A

Disease of the heart

If pathogenesis unknown effect is described- ‘Primary’
Dilated cardiomyopthy
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy

Known pathogenesis-
Toxic, Nutritional, Genetic

57
Q

What species can be affected by hypertrophic cardiomyopathy?

How does it grossly and histologically appear?

A

Common in young adult to middle aged cats
Cats die from left atrial thrombosis and caudal aorta thromboembolism- saddle thrombosis
Uncommon in dogs

Grossly- heart enlarged, prominent hypertrophy of LV, ventricular septum, dilation of LA

Histologically- Prominent disarrays of hypertrophic degenerated myocytes, interweaving arrangment of fibres and interstitial fibrosis

58
Q

What animals can develop DCM- dilated cardiomyopathy?

How does it appear grossly?

How does it appear histologically?

A

Middle aged dogs- idiopathic or autosomal inheritance
Cats with low tissue concentrations of taurine

Grossly- biventricular dilation, white thickened endocardium, increased heart weight >1%- big round heart

Histo- may see no lesion, alternatively- interstitial fibrosis, fatty infiltration and myocyte degeneration

59
Q

What breed is affected by bovine DCM?

What are the symptoms?

How does it appear PM?

A

Well grown 2-3 yo Holstein cattle- genetic component

Peripheral oedema, jugular distension, fluid accumulation in body cavities

Enlargment of heart with a ‘globose’ shape- globe

60
Q

What is restrictive cardiomyopathy?

Why can it be difficult to diagnose?

What can cause it?

A

Walls are rigid and the heart is restricted from stretching and filling with blood properly

Rhythmicity and contractility may be normal

  • Cats with endocrdial lesions that impair ventricular flow
  • Short/irregular chordae tendinae
  • Abnormal crossbar like muscle/connective tissue in LV- ‘crista saliens’ dog, pig, cat
61
Q

What is myocardial necrosis?- come on if you don’t get that…

What can be the different causes?

A

Necrosis of the myocardium- acute cardiac failure, necrosis related arrythmias from condution disruption, CHF, dilation

  • Nutritional deficiencies- Vit E/selenium deficiencies, mulberry heart disease (seem to love this one)
  • Ischaemia- hypoxia
  • Ionophore toxicity- monensin intoxication
  • Plant intoxication- heart glycosides (avocado)
  • Doxirubin- treatment of lymphosarcoma in dogs
  • Secondary to myocarditis
62
Q

How does myocardial necrosis appear grossly- what is the most affected area?

How does it appear microscopically initially and after 24-48 houts, then weeks?

A

Grossly- affected areas are pale, yellow to white and dry- can become gritty due to dystrophic calcification
Most affeted areas are the papillary muscles and subendocardial myocardium

Microscopically initially-
Fibres swollen, hypereosinophilic, striations are indistinct, nuclei are pyknotic, scattered basophilic granules
Shredded appearance because of hypercontraction and formation of multiple transverse oriented bars of disrupted material (contraction band necrosis)

24-48h- infiltrationby inflammatory cells (macrophages, neutrophils) to phagocytose and lyse

Weeks- persistent stromal tissue (fibroblast, collagen and capillaries)

Pyknotic- irriversible condensation of DNA

63
Q

Using the following images which shows Myocardial necrosis histologically after the following periods?

Initially

24-48h

Weeks

another of one of the above

A

A- Weeks

B- Intially

C- 24-48h

D- Initially

64
Q

What is the aetiology and pathology of mulberry heart disease in pigs?

What does it cause primarily and secondarily?

A

Vitamin E/ Selenium deficiency (antioxidant deficiency)
Leads to peroxidation of cell membranes

Primarily- Vascular fibrinous necrosis, endothelial damage, fibrin thrombi

Secondary- Necrosis, hypdropericardium, haemorrhages

65
Q

What causes equine myocardial degeneration?
Horses with chickens

How does it present actuely?

How does it appear PM?

A

Monensin intoxication- coccidiostat for poultry

Acute- arrythmic heart beat, ventricular fibrillation

Petechial pericoronal haemorrhages, necrosis/hyalinosis of myocytes

66
Q

Can you grossly describe this histological picture of myocytes?

What could have caused this?

A

Chronic cardiotoxicity characterized pale myocardium, hyaline necrosis, hydropic degeneration of the myocytes

Chemotherapeutic agents- Doxorubicin- prevents synthesis of DNA, RNA and proteins

67
Q

What is myocarditis?

What are the portals of entry and therefore potential aetiologies?

What are the types?

A

Inflammation of the myocardium

Portal of entry- haematogenous dissemination, embolic dissemination from vegetative endocarditis

Aet- infectious agents- Virus/Bacteria/Fungi/parasitic

  • Purulent- vegetative endocarditis
  • Necrotising- toxoplasmosis
  • Haemorrhagic- black leg
  • lymphocytic- parvoviral
  • Eosinophilic- sarcocystosis
  • Granulomatous- fungi
68
Q

What viruses can produce acute necrosis with little of moderate lymphocytic inflammatory response?

A
  • Canine parvovirus
  • West nile
  • FMD
  • Distemper in young puppies
  • Blue tongue in sheep
  • Newcastle disease
  • Avian encephalomyelitis
69
Q

How does myocarditis septicaemic grossly appear?

What causes purulent myocarditis?

What inflammatory cell dominates it?

A

Multi focal or focal, purulent necrotizing

Bacterial causes-

  • Direct extension of pericarditis (hardware disease)
  • Direct extension of endocarditis
  • Any septicaemia:
    Lyme disease/ Listeria monocytogenes/ Black leg- clostridium chauvei

Dominated by neutrophils

70
Q

This image shows a horse heart

Give a morphological diagnosis?

What is a likely aetiology?

A

Equine disseminated granulomatous myocarditis
Macrophages!

Mycosis/aspergillosis

71
Q

What parasites can effect the heart?

Give the families and genuses

A

Protozoan-

Sarcocystis sp
Toxoplasma sp
Neospora sp

Metazoan-

Cestodes- cysts
Nematodes- Dirofilaria immitis, Angiostrongylus vasorum

72
Q

What cardiac parasite is this

What is the significance of this finding?

A

Protozoan- sarcocystis sp

Incidental finding- harmless

Host specific

73
Q

How are more likely to develop toxoplasmosis?

Describe its pathogenesis?

A

Immunosupressed and young animals

Tachyzoites spread systemically and cause intersitial pneumonia, myocarditis, hepatic necrosis
Heart- casues necrosis and chronic pyogranulomatous myocarditis

Causes abortion and still birth in sheep and goats

74
Q

What are the problems of Neospora caninum?

A

Dogs-
Puppies- CNS/neuronal symtom, dermatitis, hepatitis, pneumonia and myocarditis can occur
Adult dogs- sporadically develop neosporosis

Cattle- oral or transplacental- causes abortion in cattle, adults asymptomatic

75
Q

What parasites would cause the following presentations?

A

Left- cysticercus

Right- Hyatid cyst- Ecinococcus granulosus

76
Q

What parasite is this?

Where are the adults and larvae found?

A

Dirofilaria immitis

Adults- RV/ pulmonary arteries

Larvae- microfilariae in peripheral circulation

77
Q

Describe the pathology of Angiostrongylus vasorum

A
  • Adults live in pulmonary artery and RV- larvae in lung parenchyma
  • Enlarged RV, rounded cardiac silhouette
  • Right sided heart failure
  • Eosinophilic vasculitis
  • Multifocal granulomatous and eosinophilic pneumonia
  • Bleeding disorder
78
Q

What are the different neoplasms of endothelial cells of the heart and pericardium?

How do they appear grossly and histologically?

A

Haemangioma- benign- arising from the endothelial cells in vessels
Grossly- red-black blood containing masses that protrude into lumen or epicardial surface
Histologically- well differentiated vascular spaces lined by endothelial cells

Haemangiosarcoma- malignant- RA/spleen in dogs- metastastic
Gross- similar to haemangioma
Histologically- scattered, elongaget plumb endothelial cells

79
Q

What neoplasms can arise from the myocardium, Intersitium and Epi/pericardium?

A

Myocardium- rare- rhabdomyoma (dog, sheep, cattle, pig), rhabdomyosarcoma (dog)

Intersitium- fibroma, myxoma

Epi/pericardium- mesothelioma- focally invasive

80
Q

What are the three types of heart base tumours and what are their neoplastic names?

A

Aortic body tumours- Chemodectoma (chemoreceptor)
Carotid body tumour- chemodectoma, paranglioma
Arise and produce vascular obstruction and failure- surround and compress great vessels and atria

Ectopic thyroid- adenoma/carcinoma

Metastases- sarcoma, carcinoma, melanoma

Year 3 Pathology (21 decks)

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