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Reversible Alterations of the Myocardium? (2)
Atrophy or Hypertrophy
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Sublethal injury/degeneration (3)
- Fatty Degeneration
- Lipofuscinosis
- Vacuolar Degeneration
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Lethal Injury
Apoptosis - little to zero inflamm/fibrosis
Necrosis - typically inflames and becomes fibrotic because myocardial cells cannot regenerate(*can regenerate in amphibian, fish, some birds, lab strain mice, and neonates)
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Compensatory Mechanisms of the CV System in order to maintain adequate CO(6)
- 1. Cardiac Dilation
- 2. Myocardial Hypertrophy
- 3. Increase HR
- 4. Increase peripheral resistance
- 5. Increase Blood Volume
- 6. Redistribute Blood Flow
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What is Congestive Heart Failure? What causes it?What does it cause?
- Gradual loss of Cardiac Pumping Efficiency
- -Increase workload (pressure/volume
- - pulmonary/renal/vasc dz)
- -Myocardial damage (heart dz)
Result:Decrease Blood Flow to peripheral tissues (forward failure)Accumulation of Blood behind the failing chamber (backward failure)
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Results of :Left-Sided Heart Failure? Right-Sided Heart Failure?
Left - Pulmonary Edema manifesting as cough
- Right - Hepatic Congestion
- Horses/Rums = Ventral SubQ Edema
- Dogs = AscitesCats = Hydrothorax
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What causes myocardial hypertrophy?
- Primary - idiopathic and irreversible
- Secondary (more common) - Compensatory to increase workload; Reversible
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What are the 3 stages of myocardial hypertrophy?
- 1. Initiation
- 2. Stable hyperfnxn
- 3. Deterioration of fnxn assoc w/ degeneration of hypertrophied myocytes
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Compare-Contrast:Concentric and Eccentric Hypertrophy
- Concentric
- small ventricular chambers w/thick walls and papillary mmdue to increased PRESSURE load (valvular stenosis, hypertension)
- Eccentric
- enlarged chambers with walls of normal to decreased thicknessdue to increased BLOOD VOLUME (mitral insuff., ventricular septal defect)
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Compare-Contrast Right and Left Ventricular Hypertrophy
- Left
- due to Left outflow problems OR systemic hypertension
- Right
- due to Right outflow problems OR pulmonary hypertension OR severe pulmonary dz-Heartworm, Pulmonic stenosis, High Altitude Dz in cattle, Chronic alveolar emphysema (heaves
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What are some common causes of systemic hypertension in cats and dogs?
Both - Chronic Renal Failure / Idiopathic
- Cats - Hypertension
- Dogs - Hyperadrenocorticism
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List 5 Primary (ie idiopathic) Cardiomyopathies
- 1. Hypertrophic
- 2. Dilated (congestive)
- 3. Feline - Left Ventricular Endocardial Fibrosis (a restrictive cardiomyopathy)
- 4. Other Restrictive Cardiomyopathies
- 5. Arrythmogenic Right Ventricular Cardiomyopathy
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Details on Primary Cardiomyopathies1. Hypertrophic2. Dilated (congestive)
1. Hypertrophy of L-Vent, InVent Septum, L-Vent cavity is small, L-Atr is dilated*Male Cats 1-3yrs oldsome cats have posterior paresis due to concurrent 'saddle embolus'
- 2. Cardiac dilation, contractile dysfunctionHeart is Rounded due to biventricular dilation*Cats and Dogs
- Cat - Taurine def. and 1-3yr old Males
- Dog - Large breed Males (Dobes, Dalmations, Boxers, Juvenile Portuguese Water Dogs)
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Details on Primary Cardiomyopathies3. Feline L-Vetn Endocardial Fibrosis4. Other Restrictive Cardiomyopathies5. Arrythmogenic R-Vent Cardiomyopathy
3. Cats - extensive endocardial fibrosis of L-Vent impairing filling; a sequela of endomyocarditis
- 4. Heart w/ inadequate compliance and diastolic ventricular volumeExcessive L-vent Moderator Bands, Fibrosis in Rats, Fibroelastosis in Burmese Cats
- 5. Replacement of R-Vent myocardium with Adipose and Fibrosis
- *Boxers - sudden death
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List 5 Secondary Cardiomyopathies
- 1. Hereditary (X-linked musc.dystrophy - goldies and other dogs)
- 2. Nutritional Def (Taurine in cats)
- 3. Toxic (doxorubicin)
- 4. Endocrine (thyrotoxic cardiomyopathy in Cats)
- 5. Neoplastic infiltration (lymphoma)
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Myocardial Necrosis
- Pale Yellow - Gray +/- gritty mineralized regions.
- Acute - hypereosinophilic swollen myocardia - Mphage and Neutro infiltrate
- Healing - fibroblasts and fibrosis
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What is the outcome of Myocardial Necrosis?
- Depends on Extent of Damage:
- Death of acute cardiac failure
- Early death from arrythmiaDevelop 2o Chronic Congestive heart failure...or just fibrosis in animals that die of something else entirely
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What are some causes of Myocardial Necrosis? (6)
- 1. Nutritional Def(Vit E Def - White m Dz in rums; Mulberry Hrt Dz in pigs)
- 2. Toxins(Ionophores - monensin - coccidiostat for birds and growth for cattles, cardiotoxic to horse and pig)
- 3. CNS lesions and trauma(Heart-Brain Syndrome - catecholamines, likewise pheochromocytoma, iatrogenic)
- 4. Gossypol in Pigs
- 5. Doxorubicin in Dogs
- 6. Poisonous Plants (foxglove, oleander)
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Myocardial Mineralization
- 2o to some necroses (vit E def)
- also Vit D tox -> spontaneous myocardial calcification in older rats and guinea pigs
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Myocarditis(4 General Causes)
- 1. Bacteria
- 2. Protozoa
- 3. Parasites
- 4. Viruses (*CPV-2 - pups under 10wks - no intestinal lesions, but intranuclear bodies in cardiomyocytes)
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Endocarditis
1. Cause?
2. Gross/Histo Lesions?
3. Where does it hit?
4. Secondary Fx?
5. Clinical Signs?
- 1. Bacterial (rarely parasitic/fungal)
- 2. Friable, irregular, yellow-gray raised 'vegetative' lesions.Abundant fibrin, necrotic leukocytes, granulation tissue, and bacteria
- 3. Valves - may extend to Mural region.1o M>A>T>P **Cattle T is most common above M4. Bacterial Emboli
- 5. Only detected late in Dz - Fever, Murmurs, Death from valvular dysfnxn OR bacteremia.
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What 2 factors are important in the Pathogenesis of Endocarditis?
- 1. Sustained/Recurrent Bacteremia(Cattle - A.pyogenes, Dog/Pig - Strep)
- 2. Tendency for lesion to occur at Lines of Apposition of Valve surfaces exposed to the Fwd Flow(minor damage allows adherence of bacteria)
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Valvular Endocardiosis (or myxomatous valvular degeneration)
Dogs older than 5yrsIdiopathic degen of valve collagenM>>T>>>>>>Semilunars
Smooth glistening nodules and thicker valve marginsProliferation of loose fibroblastic tissue, No Inflamm.
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Valvular Endocardiosis leads to??
- Valvular Insufficiency --> Congestive Heart Failure
- thickening > incompetent valves > improper closure > L-Atr regurg > jet lesions of L-AtrRupture of Chordae TendinaeL-Atr Thrombi (to Thromboemboli)Rarely - L-Atr rupture > tamponade
- All leading to Congestive Heart Failure (not enough blood pumped for body's demands)
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Endocardial Mineralization
- Vit D intoxication
- Calcinogenic plants (Cestrum, Trisetum) have Vit D analogs
- Johne's
- Dogs with Uremia 2o to Renal F --> Ulcerative Endocarditis
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Endocardial Fibrosis
Jet Lesions (atria, intima of large vessels)Restrictive Cardiomyopathies
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Acute Rupture of Chordae Tendinae
Traumatic, Spontaneous, or Assoc w/Chronic Valvular Degen or Endocarditis
Causes valve insuff and heart failure
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Hematocysts and Lymphocysts
Blood or Lymph filled cysts on margins of AV valves (common in Cattle)
Incidental Finding
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When does shit happen to the Pericardium?
Frequently involved by Direct Extension from myocardial, pleural, pulmonary, or systemic dz
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What are the 4 big pericardial issues? (One of which has a subset of 3)
- 1. Hydropericardium
- 2. Hemopericardium
- 3. Miscellaneous
- 4. Pericarditis
- A. Acute Fibrinous, B. Suppurative, C. Chronic
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Hydropericardium
- Clear-Yellow, watery, serous fluid
- occurs w/generalized edema (hrt fail, renal fail, vascular injury, etc..)
- acute can cause tamponade
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Hemopericardium
- Blood in pericardium
- usually results in Rapid Death
caused by Hemangiosarcoma, Heart Base Tumor, Atrial RuptureHorse - intrapericardial aortic ruptureLarge Dogs - idiopathic, slow onset
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Miscellaneous
- Serous Atrophy of Fat
- Urate Deposits (gout in birds/snakes)
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Acute Fibrinous Pericarditis
Hematogenous spread of infxn (Pasturella, Strep, Salmonella)
Yellow fibrin deposits on pericardiaFibrin w/neutrophils and vessel congestion
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Suppurative Pericarditis
- Pyogenic Bacteria
- Thick, malodorous exudate in pericardium(Hardware Dz)
- Congestive Failure and Septicemia
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Chronic Pericarditis
chronic inflamm of pericardia resulting in Fibroblast prolif w/collagen depot and fibrous adhesions bw visceral/parietal pericardium
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Congenital Anomalies
What are the 3 Left to Right Shunts?
- 1. PDA (aorta to pulmonary a.)
- 2. Atrial Septal Defect (foramen ovale or a true defect) (L to R atrium)
- 3. Ventricular Septal Defect (L to R Ventricle, overload on R ventricle)
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Congenital Anomalies
What are 3 congenital valve issues?
- 1. Pulmonic stenosis (esp Dogs - concentric hypertrophy of R-vent)
- 2. Subvalvular aortic stenosis (concentric hypertrophy of L-vent, possibly aortic dilation)
- 3. Mitral and Tricuspid Dysplasia (esp cats, esp mitral)
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Congenital Anomalies
How can the great vessels be displaced?
- 1. Persistent R.Aortic Arch - forms a vascular ring around esophagus and trachea, causing Proximal Megaesophagus
- 2. Transposition of aorta and pulmonary artery
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Congenital Anomalies
What is Ectopia cordis?
- Heart is outside of the thoracic cavity.
- Most frequent in Cattle
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Congenital Anomalies
What is the condition in cats/dogs in which the intestine and/or liver enter the pericardial sac?
Peritoneal-pericardial diaphragmatic hernia
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Congenital Anomalies
What are the 4 lesions of Tetralogy of Fallot?
- 1. Pulmonic Stenosis
- 2. Ventricular Septal Defect
- 3. Dextroposition of Aorta
- 4. R-Vent Hypertrophy (secondary)
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Congenital Anomalies
What happens in Tetralogy of Fallot?
Pulmonic Stenosis -> increase R pressure -> R-vent Hypertrophy -> Blood shunting R to L through Ventricular Septal Defect -> venous blood enters systemic circulation (due to great dextropositioning) -> Cyanosis
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Define: 1. Arteritis2. Polyarteritis3. Phlebitis
4. Vasculitis
- 1. inflammation of a.a.
- 2. inflammation of many a.a.
- 3. inflammation of v.v.
- 4. inflammation of vessels (a.a. and v.v.)
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Vasculitis is characterized by the presence of __A__ found ___B___with __C__. __C__ is indicated by _____D_____.___E___ results from endothelial damage; ischemia and infarction may follow.
- A. Inflammatory cells
- B. in/around blood vessel wall
- C. concomitant vessel wall damage
- D. fibrin depot, collagen degen, necrosis of endothelia and smooth m.
- E. Thrombosis
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What are some general causes of vascular inflammation?(6 categories, 1 with 2 specific examples to know)
- 1. Virus
- 2. Bacteria
- 3. Rickettsia
- 4. Fungi
- 5. Immune Mediated
- 6. Parasites
- A. S. vulgaris (cr. mes. artery -> thromboembolism of intestinal aa. -> colic)
- B. D. immitis (more to come)
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D. immitis
1. Adult parasites are found where?
2. What lesions happen in this area?
3. What are secondary effects?
4. What are clinical signs?
5. What's the worst that could happen?
- 1. Pulmonary a, "R-vent, R-atr"
- 2. Proliferative Endarteritis (irregular fibromuscular proliferation of the intima - Gross as Rough, Granular/Shaggy intimal surface)
- 3. Thromboemboli, R-vent Hypertrophy (possibly R-failure)
- 4. Cough, exercise intolerance
- 5. Caval Syndrome (shock, intravascular hemolysis, hepatic/renal failure)
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What are 3 degenerative diseases of the vascular system?
- 1. Arteriosclerosis
- 2. Atherosclerosis
- 3. Arterial medial calcifcation
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Arteriosclerosis
intimal fibrosis of large elastic arteries
-loss of elasticity and luminal narrowing = "hardening of the arteries"(rarely clinically significant)
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Atherosclerosis
- a subset of arteriosclerosis*Important in Humans... infrequent in animals
- -lipid, fibrous, and Ca deposits in vessel walls = luminal narrowing
- Arteries are thick, firm, and yellow-white. See Lipid Globules in cytoplasm of smooth m. and Mphages (Foamy cells)
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What animals get Atherosclerosis?
Pig, Rabbit, Chicken -- with high cholesterol diet
Dogs with Hypothyroidism and Diabetes Mellitus (w/assoc hypercholesterolemia)
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Arterial Medial Calcification
- often occurs w/concurrent Endocardial Mineralization
- caused by Calcinogenic Plant Tox, Renal inusuff, Johne's, etc...
Arteries appear as Solid, Dense, Pipelike structures w/raised White Intimal Plaques
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What is Omphalophlebitis?
Inflammation of Umbilical Vein
(bacterial -- can lead to septicemia, polyarthritis, hepatic abscesses, umbilical abscesses)
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What is an Aneurysm?
Localized abnormal dilation or outpouching of a thin/weak portion of a vessel
Often in large arteries - rupture is fatal
Causes - Cu def, S.lupi or S.vulgaris damage in dog, horse.
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Hemangiosarcoma
What is it?
Who does it hit and where?
What does it look like?
- Malig neo of Enothelial Cells (fusiform neoplastic endo. cells)
- Dogs - R-atr/aur (liver, spleen, heart, subcutis, adipose around urinary bladder)
- Red/Black - rupture lead to fatal hemopericardium, tamponade, and hemoabdomen
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Lymphosarcoma
White soft nodules or diffusely spread
Cattle Hearts predominantly, but any animal w/multiorgan lymphoma may have it at the heart
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Heart Base Tumors
usually Aortic Body (chemodectoma) in Brachycephalic dogs (Boxer, Boston)
May compress great vessels and atria
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Congenital Rhabdomyomatosis
Pigs and Guinea Pigs
actually a malformation, not a true neoplasm --- a Hamartoma of myocytes
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Rhabdomyoma . Rhabdomyosarcoma
rare
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Schwannoma (neurofibroma)
Involve cardiac nerves in Cattle
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Hemangioma
Benign neoplasm of endothelia, well circumscribed
in dermis and subcutis of dogs
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Vascular Hamartoma
Redundant proliferation of vessels ranging from large arteries to small capillary buds
Dog/Cat subcutis (rarely other sites)
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Hemangioperictyoma
originates from the Pericytes which surround the vessels
Subcutis and Dermis in Dogs - rarely metastasize
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Feline Ventral Abdominal Angiosarcoma
Ventral Abdomen - dermis and subcutis of Cats
Tissue is edematous and bruised.
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Backwards -- you just went through lots of neoplasms...
Name the 10 Neoplasias assoc with the cardiovascular system
- 1. Hemangiosarcoma
- 2. Lymphoma
- 3. Heart Base Tumor
- 4. Congenital Rhabdomyomatosis
- 5. Rhabdomyo(sarco)ma
- 6. Schwannoma (neurofibroma)
- 7. Hemangioma8. Vascular Hamartoma
- 9. Hemangioperictyoma
- 10. Feline Ventral Abdominal Angiosarcoma
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