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Cardiology (SP23) > Module 4: Cardiovascular Pathology - Schreeg (Week 6) > Flashcards

Module 4: Cardiovascular Pathology - Schreeg (Week 6) Flashcards

1
Q

Disturbance of Growth:
Uncontrolled and abnormal growth of cells that exhibits invasive behavior

A

Neoplasia
- Can be primary of metastatic

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2
Q

What does not occur as a ‘response’ to injury, BUT is a morphologic change?

A

Neoplasia

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3
Q
  • Malignant and aggressive neoplasm of endothelial cells that is common in aged large breed dogs
A

Hemangiosarcoma
- Predilection site: Right atrium/auricle
- Widespread metastasis common: Lungs, spleen, and liver
- rupture of the hemangiosarcomas that can lead to cavity hemorrhage and shock

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4
Q

What is the most common tumor out there?

A

Lymphoma

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5
Q
  • Malignant neoplasm of lymphocytes that can occur in the heart in any species -> most common in cattle infected with bovine leukosis virus (BLV)
A

Lymphoma
- RA most common
- arrhythmias, loss of functional myocardial mass

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6
Q
  • Neoplasm arising from chemoreceptor cells at the base of the aorta (aortic body) -> brachycephalic dogs predisposed
    - often slow-growing but can be malignant with distant metastasis
A

Chemodectoma
- red mottling mass arising from/attached to the base of the heart
- left side
- can be incidental finding

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7
Q

Cell Death and Associated Lesions:
- Sublethal, reversible cell injury
- No gross lesions, but key histologic changes

A

Cardiac Myofiber Degeneration

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8
Q

Cell Death and Associated Lesions:
- Lethal, irreversible cell injury

A

Cardiac Myofiber Necrosis
- Toxins: Ionophores
- Nutritional: Vitamin E/Selenium Deficiency
- Infectious: Blackleg

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9
Q

Cell Death and Associated Lesions: Grass appearance
- Tissue pallor progressing to prominent white-yellow foci that may be firm or mineralized; can have accompanying hemorrhage

A

Cardiac Myofiber Necrosis
- White muscle disease (young ruminants): Myofiber necrosis due to oxidative damage from Vitamin E/Se deficiency
- Hemorrhage: Mulberry heart Disease (Pigs): Myofiber AND vascular necrosis due to oxidative damage from Vitamin E/Se deficiency
- Acute Hemorrhage: Blackleg = Clostridial Myositis: Myofiber necrosis and hemorrhage due to toxin production by Clostridium chauvoei; minimal inflammation

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10
Q

Cell death and Associated Lesions:
- Non-specific response to chronic injury
- Collagen replaces or infiltrates between myofibers and/or on endocardial or epicardial surfaces

A

Cardiac Fibrosis
- Indicates chronicity

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11
Q

Cell death and Associated Lesions:
Gross appearance: Firm foci of tissue pallor

A

Cardiac Fibrosis
- Jet Lesions = Raised, linear, fibrotic endocardial/endothelial lesions secondary to high-pressure “jets” of blood flow caused by turbulence, regurgitation, etc

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12
Q

Cell death and Associated Lesions:
- Deposition of calcium salts into tissue
- Two flavors
- Metastatic: Secondary to systemic calcium and phosphorus imbalance
- Dystrophic: Secondary to local tissue necrosis and calcium release

A

Cardiac Mineralization
- Gross feature: White to tan foci that are HARD and Chalky
- Dystrophic mineralization should be associated with another underlying cardiac lesion (i.e. necrosis)
- Metastatic mineralization will NOT be associated with another cardiac lesion but will be associated with other lesions of Ca/P imbalance

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13
Q

What allows the cardiac muscle cells to contract in a coordinated fashion so that the heart can work as a pump?

A

Intercalated discs

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14
Q

Intercalated discs are part of the sarcolemma and contain two structures important in cardiac muscle contraction, which are:

A

Gap junctions and desmosomes

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15
Q

Definition:
Anchor the ends of cardiac muscle fibers together so the cells do not pull apart during individual fiber contraction

A

Desmosomes

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16
Q

What are the most important component of the tunica intima and form the primary barrier between blood and tissue?

A

Endothelial cells

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17
Q

Disturbance of Growth
Definition:
Increase in cell size

A

Hypertrophy

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18
Q

Definition:
Increase in number of cells

A

Hyperplasis

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19
Q

Definition:
Increase in the number of cells

A

Hyperplasia

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20
Q

Disturbances of Growth:
The heart has more mass than normal due to an increase in the size of cardiac myofibers

A

Hypertrophy

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21
Q

Disturbance of Growth: Cardiac Hypertrophy
- Response to increased afterload (increased pressure)
- Heart must ‘beef up’ to ‘push against’ increased pressure
- Myofibers have sarcomeres added in parallel = flatter myofibers
- Heart is thicker, chambers narrow

A

Concentric

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22
Q

Disturbance of Growth: Cardiac Hypertrophy
- Response to increased preload (increase volume)
- Heart must ‘stretch’ to ‘accommodate’ increased volume
- Myofibers have sarcomeres added in series = longer myofibers
- Heart is thinner, chambers dilated

A

Eccentric

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23
Q

Cardiac Hypertrophy:
Diastolic dysfunction = Heart can’t relax

A

Concentric

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24
Q

Cardiac Hypertrophy:
Systolic dysfunction = Heart can’t contract

A

Eccentric

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25
Q

Clinical Presentation:
- Old Cats with weight loss, thyroid slip, elevated
- Thyroid adenoma
- Increased metabolic demands of the body contributes to hypertension and concentric hypertrophy

A

Thyrotoxic Cardiomyopathy

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26
Q

Clinical presentation:
- Young to middle-aged cats, possibly purebred (Maine Coon, Sphynx, Ragdoll)
- Stasis of blood in left atrium can result in thrombus formation that can detach and become lodged in the distal aorta -> saddle thrombus

A

Hypertrophic Cardiomyopathy

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27
Q

Clinically Relevant Examples: Eccentric Hypertrophy
- Bi-ventricular eccentric hypertrophy

A

Canine Dilated Cardiomyopathy

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28
Q

Clinically Relevant Examples: Eccentric Hypertrophy
- Right ventricular eccentric hypertrophy

A

Boxer Cardiomyopathy

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29
Q

Disturbance of Growth:
Decrease in cardiac size/mass

A

Atrophy

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30
Q

Disturbance of Growth:
Small size that is present from birth

A

Hypoplasia

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31
Q

Clinically Relevant Example:
Myofiber atrophy can be seen with any _______________

A

End-stage cardiomyopathy

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32
Q

(T/F) eccentric hypertrophy and atrophy can be easily differentiated grossly

A

False, it may be impossible to differentiate grossly

33
Q

Definition:
Mechanisms involved in the formation of a thrombus in an injured vessel

A

Thrombosis

34
Q

Definition:
Coagulation of blood

A

Clot

35
Q

Definition:
Coagulation of blood in a vessel lumen

A

Thrombus

36
Q

Definition:
A fragment of SOMETHING is lodged in a vessel

A

Embolism (could be anything)

37
Q

Definition:
The fragment of a thrombus breaks and gets lodged further down the vessel

A

Thromboembolism

38
Q

Definition:
Ischemia and infarction

A

sequela of thrombosis

39
Q

Describe the Gross appearance of Thrombosis:

A
  • Motting red-tan
  • Dull surface
  • Firm texture
  • Endothelial adherence
40
Q
  • Feline saddle thrombus
  • Pulmonary thromboembolism (PTE)
  • Portal thrombosis
  • Caval thrombus
    These are clinically relevant examples of …
A

Thrombosis

41
Q

Definition:
Exudation of blood outside of a vessel due to injured endothelium or alterations in platelets or coagulation factors

A

Hemorrhage

42
Q

Describe the Gross features of Hemorrhage:

A

Red to dark red discoloration or fluid/gelatinous material where it doesn’t belong

43
Q

Hemorrhage vs. Congestion

Definition:
Engorged but intact vessels

A

Congestion

44
Q

Hemorrhage vs. Congestion

Definition:
Blood outside of vessels

A

Hemorrhage

45
Q
  • Can affect the heart wall (mural) or more commonly valves (valvular)
  • Almost always caused by bacterial agents – suppurative inflammation
  • Aortic and mitral valves most commonly affected except in cattle (tricuspid)
    This is describing …
A

Endocarditis

46
Q

List the Gross findings for Valvular Endocarditis:

A
  • Raised
  • Roughened
  • Friable
  • Yellow to tan to red material
    (so-called ‘vegetative’ lesions)
47
Q

Pericarditis: Clinically relevant example
- Primary traumatic puncture by sharp foreign bodies from the reticulum of cattle through the diaphragm and into the pericardial sac with secondary bacterial colonization/infection of the wound tract

A

Traumatic Reticulopericarditis
- AKA “Hardware Disease”
Prevention: Prophylactic ‘placement’ of magnets in the reticulum

48
Q

What are the gross findings for hardware disease?

A
  • Suppurative pericarditis
  • Foul odor
  • Acute: Fibrinosuppurative pericarditis (“bread and butter disease”)
  • Chronic: Fibrous adhesions (restrictive pericarditis)
49
Q

Definition:
- Presence of inflammatory cells infiltrating and disrupting the wall of the vessel
- Most often is a result of either infectious or immune-mediated diseases

A

Vasculitis

50
Q

Vasculitis: Clinically Relevant Examples

  • Cranial mesenteric arteritis (large vessel) in horses due to migration of L4 larvae of Strongylus vulgaris (large strongyle)
  • Gross findings: Thickened, roughened, fibrotic, tortuous vessel walls +/- aneurysms, occasional ruptures, formation of luminal thrombi
A

Equine Verminous Arteritis

51
Q

Vasculitis: Clinically Relevant Examples

  • Worms cause physical irritation, proliferation, and fibrosis of pulmonary vessels
  • Proliferative arteritis – thickened with markedly narrow lumen
  • Pulmonary hypertension, pulmonary thromboembolism
A

Heartworm Disease

52
Q

Definition:
- Process of ‘backing up’ of blood within the cardiovascular system and accumulation of extravascular/cavitary fluid (edema and effusions) due to failure of appropriate cardiac output
- Sequela of MANY heart diseases
- Can be divided into right and left-sided heart failure

A

Congestive Heart Failure

53
Q

Definition:
- Failure of the left heart to appropriately pump blood out to the body -> backup of fluid into the lungs
- Gross features: Pulmonary edema, Cavitary (pleural, pericardial, peritoneal) effusions in CATS
- In other species, USUALLY indicates right-sided heart failure

A

Left-sided Congestive Heart Failure

54
Q

Definition:
Wet, heavy lungs that exude abundant clear to red-tinged watery fluid on cut surface; can be brown-tinged with chronicity (macrophages eat RBCs and break down pigments)

A

Pulmonary edema

55
Q

Left-sided Congestive Heart Failure

Functional significance of pulmonary edema:
What does fluid in the air spaces lead to?

A

Impaired oxygen perfusion, tachypnea, dyspnea, and hypoxia

56
Q

Left-sided Congestive Heart Failure

List examples of common diseases for which left-sided heart failure is a consequence:

A
  • Feline HCM
  • Canine mitral valve disease
57
Q

Definition:
- Failure of the right heart to appropriately pump blood to the lungs -> backup of blood and fluid in the rest of the body
- Gross findings:
- Abdominal organ congestion, including passive hepatic congestion
- Cavitary effusions in animals other than cats
- Subcutaneous or dependent edema

A

Right-sided Congestive Heart Failure

58
Q

Passive hepatic congestion:
- Enlarged, dark red liver with rounded margins

A

Acute passive congestion

59
Q

Passive hepatic congestion:
- “nutmeg liver” due to centrilobular congestion contrasting with vacuolar change/swelling of portal hepatocytes

A

Chronic passive congestion

60
Q

What is the Functional significance of Right-sided congestive heart failure?

A

Effusiosns can impede lung (pleural) and heart (pericardial) function; significant passive congestion in the liver can lead to centrilobular hepatocyte necrosis

61
Q

Unique conditions leading to Right-sided Congestive Heart Failure
Pathogenesis: Interstitial lung diseases -> hypoxia and pulmonary hypertension -> right-sided heart failure
- Long-term interstitial pneumonia
- “High altitude disease” of cattle

A

Cor Pulmonale

62
Q

Unique conditions leading to Right-sided Congestive Heart Failure
- Compression of the heart due to severe pericardial effusion
- Hemopericardium most common: RA hemangiosarcoma rupture
- Gross findings: Fluid markedly distends pericardial sac; cavitary effusion or abdominal organ congestion due to right-sided heart failure

A

Cardiac Tamponade

63
Q

What is the Function significance of Cardiac Tamponade?

A

Cardiac compression by fluid in the pericardium -> compression of the right heart -> reduced cardiac output to the lungs, right-sided heart failure -> systemic hypoxia

64
Q

Definition:
Reduction of blood flow and oxygen to tissue that can result in cellular degeneration or necrosis

A

Ischemia

65
Q

Definition:
Tissue necrosis secondary to ischemia

A

Infarction

66
Q

List the possible causes for Ischemia and Infarction:

A
  • Thrombosis
  • Vasculitis
  • Vascular compression from external masses or inflammation
67
Q

Infarction:
- Red due to a combination of hemorrhage and congestion

A

Acute infarctions

68
Q

Infarction:
- Tan due to cell swelling and hemolysis/degradation of RBCs

A

Subacute infarctions (1-5 days)

69
Q

Infarction:
- Tan, firm and depressed due to loss of tissue architecture and replacement by fibrosis

A

Chronic infarctions

70
Q

Functional significance:
What will infarctions result in?

A

Coagulative necrosis and loss of functional organ mass

71
Q

Ischemia and Infarction: Organ Considerations
Brain and nervous tissue will undergo …

A

Liquefactive necrosis (malacia)

72
Q

Ischemia and Infarction: Organ Considerations
Liver and lung will undergo …

A

Infarction RARE due to the dual blood supply

73
Q

Ischemia and Infarction: Organ Considerations
Myocardial infarction (“heart attack”) is ….

A

uncommon in domestic animals, but can be associated with atherosclerosis in primates, pigs, and birds

74
Q

Ischemia and Infarction: Organ Considerations
Chronic renal infarctions are …

A

COMMON in aged cats: associated with “chronic kidney disease” in this species

75
Q

Ischemia and Infarction: Organ Considerations
Intestinal infarction is …

A

the sequela of strangulating lesions (e.g strangulating lipoma, volvulus) and “thromboembolic colic” in horses

76
Q

Definition:
- Clinicopathologic syndrome in which critical organs are under-perfused with blood

A

Shock

77
Q

What is the most common tumor out there?

A

Lymphoma

78
Q

(T/F) Neither hypertrophy nor atrophy has the appearance of distinct pale tan nodules in the heart

A

True

Cardiology (SP23) (8 decks)

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