Cardiology.cv.hemolymph

Question 1

Right atrium is made up of what two parts?

Answer 1

Sinus venarum cavarum: veins emptyAuricle: conical out pouching

Question 2

What are the structures that drain into the right atrium?

Answer 2

Cranial vena cava: draining structures of head and neckCoronary sinus: draining coronary circulationCaudal vena cava: drianing abdominal structures into the azygous vein

Question 3

What is the ova fossa?

Answer 3

Diverticulum at the point of entrance of the caudal vena cava** remnant of the foramen ovale— the communicaiton between the 2 stria of the

Question 4

Leaflets of the tricuspid valve

Answer 4

1. Septal2. Parietal: lies on the right margin3. Angular: between the AV opening & right outflow tract

Question 5

What the the pulmonary valve leaflets?

Answer 5

RightLeft Intermediate

Question 6

What are the mitral valve leaflets?

Answer 6

1. Septal2. Parietal

Question 7

The interventricular septum is made up of what tissues?

Answer 7

Muscular tissue (primarily)Fibrous tissue: at its most dorsal extennt (membranous/nonmuscular)

Question 8

Where is the location of the sinus of Valsalva?

Answer 8

At the base of the Aorta **boulbous in shape—- is hte sinus of valsalva

Question 9

Where do the 2 coronary arteries originate?

Answer 9

The sinus of valsalva

Question 10

The ductus arteriosus connects what?

Answer 10

Joints the pulmonary artery to the descending aorta in the fetus

Question 11

The degree of AV conduction delay is influenced by autonomic tone. With what causing increase/decrease in rate of conduction

Answer 11

Vagal tone: reducingSympathetic tone: increasing

Question 12

Systole is made up of:

Answer 12

Isovolumetric contraction phase & ventricular ejection

Question 13

Diastole is made of:

Answer 13

Isovolumic relaxation phaseRapid filling phaseDiastasisAtrial contraction

Question 14

What marks the beginning and ending of systole?

Answer 14

Beginning: onset of the QRS complexEnding: closure of the aortic valve

Question 15

What makes up the phase of isovolumetric diastole?

Answer 15

Start when AV closes Ventricular pressure continues to rapidly decline **all cardiac valves are closed

Question 16

The rate of intraventricular pressure decline during the isovolumic relaxation of diastole?

Answer 16

Determined by the rate of active relaxation of the myofibers

Question 17

When do mitral valve leaflets open?

Answer 17

When when left ventricular pressure drops below left atrial pressure** onset of rapid filling phase of diastole

Question 18

Describe/define diastesis (of diastole)

Answer 18

The atriovetnricular pressure difference approaches zeroVentricular volume reaches a plateua**minimal changes in intraventricular pressure and volume

Question 19

The duration of diastesis is determined by?

Answer 19

Inversely related to heart rate**resting heart rate— diastesis is longest phase of diastole

Question 20

S1 heart sounds

Answer 20

Closure of the AV valvesmechanical onset of systole

Question 21

S2 heart sound

Answer 21

Closure of the semilunar valves**end of systole

Question 22

S3 heart sound

Answer 22

Early ventricular filling **rapid filling phase of diastole

Question 23

S4 heart sound

Answer 23

Atrial contraction

Question 24

Systolic function refers to

Answer 24

Ability of the ventricles to contract and eject blood

Question 25

Diastolic function refers to

Answer 25

The ability of the ventricles to adequately relax and fill

Question 26

What are the major factors that affect ventricular systolic function

Answer 26

Preload (ventricular end-diastolic volume)Inotropic/contractiel state of myocardiumAfterload: impedence to ventricular outflowHeart Rate

Question 27

Events that cause an increase in pre-load?

Answer 27

ExerciseAnaemiaFeverPregnancy

Question 28

Factors that affect myocardial contractility

Answer 28

Autonomic outputCirculating substances (hormones, pharmacologic agents, endogenous & exogenous toxins, etc)Locally produced metabolitesPathologic processes (ischemia, acidosis, infarction, etc.)

Question 29

Ventircular filling is affected primarily by:

Answer 29

Venous returnAtrioventricular valve functionAtrial functionPericardial compliance Heart rateMyocardial relaxationCompliance

Question 30

Inadequate end-diastolic volume will result in:

Answer 30

Inadequate stroke volume**reduced coronary perfusion

Question 31

What are the two major factors that affect ventricular diastolic performance

Answer 31

Chamber complianceMycoardial relaxation

Question 32

If ventricular compliance is reduced what is required to achieve a given diastolic volume?

Answer 32

A greater filling pressure

Question 33

Examples of conditions that cause a decrease in ventricular compliance

Answer 33

**chronic conditionsReduction in LV lumen sizePathological hypertrophyFibrosisInfiltrative diseasesPericardial tamponade or constrictionDz or dilatation fo the opposite ventricle

Question 34

Myocardial relaxation may change acutely in response to

Answer 34

HypoxiaIschaemiaAltered afterloadTachycardiaCatecholaminesVarious pharmacological agents

Question 35

What are disease processes that produce diastolic dysfunction

Answer 35

Pressure overload states— myocardial hypertrophy or fibrosis (aortic and pulmonic stenosis,, systemic or pulmonary hypertension)

Question 36

What are examples of dysrhythmias that produce a loss of effective atrial systole resulting in poor exercise tolerance, wekaness or syncope

Answer 36

Atrial fibrillationVentricular tachycardiaHigh degree AV conduction block

Question 37

What are factors that affect systolic & diastolic function of the atria?

Answer 37

Atrial preloadImpedance to atrial emptyingInotropic state of atrial myocytesAtrial compliance

Question 38

What are the 3 methods commonly used to determine cardiac output

Answer 38

1. Fick method2. Thermodilutioon method (overestimates cardiacoutput)3. Lithium dilution method

Question 39

What are the parameters measured on echocardiogram to determine LV systolic function?

Answer 39

Fractional shortening: percent decrease of LV minor axisEjection fraction: percent decrease in end-diastolic volumeMean VCF: veloicty of circumferential fiber shortening

Question 40

Used pulsed doppler on echocardiogram, what measurements can estimate LV systolic function/indexes

Answer 40

Peak and mean velocityAccelerationEjection time**aortic root or pulmonary artery

Question 41

Indexes of diastolic function on M-mode echocardiography?

Answer 41

-peak and mean velocites of early (passive) ventricular filling (peak and mean E-wave velociteies)Peak and mean velocities of late (atrial systolic) ventricular filling (peak and Mean A wave velocites)-E/a ratio

Question 42

What is starlings law of the heart?

Answer 42

The more blood which returns to the heart (venous return) and stretches the heart in diastole, the large the stroke volume ejected per beat

Question 43

Parasympathetic nervous system controls what (in regards to the heart)

Answer 43

Heart rate (chronotropic effects)

Question 44

Sympathetic nervous system controls what (in regards to the heart)?

Answer 44

Heart rateContractility (inotropic effects)

Question 45

The sympathetic and parasympathetic control of the heart is controlled by what part of the brain?

Answer 45

Integrated by the brain stem

Question 46

Baroreceptors sense

Answer 46

Stretch — detect high pressure within the vascular system

Question 47

Where are baroreceptors located? that detect high pressure

Answer 47

Within the aortic arch and carotid sinus

Question 48

Baroreceptors that detect low pressure are located (central volume receptors) where?

Answer 48

Atrial tissue (primarily at junction with the great veins)Pulmonary arteries & ventricles

Question 49

Affarent input to the CNS from the heart are transmitted via the

Answer 49

Glossopharyngeal and vagal nerves

Question 50

Glossopharyngeal and vagal nerves terminate where

Answer 50

Nucleus tractus solitarius (NTS)

Question 51

Alpha 2 adrenoreceptor agonists effect o nheart

Answer 51

Increase vagal tone to heartReduce sympathetic tone to blood vessels**bradycardia, hypotension

Question 52

Cardiac glycosides (digoxin) cause

Answer 52

Increase in parasympathetic tone to heartIncreased baroreceptor stimulation** reflec reduction in sympathetic vasoconstrictor nerve activity**variable depending on physiological state of animal

Question 53

Why is the effect of cardiac glycosides (digoxin) dependent on

Answer 53

Degree of activation of the natural hormone: endogenous digitalis-like substance— which binds to these receptors

Question 54

Vasomotor nerves are controlled by which system and hormone?

Answer 54

Sympathetic nerves— Noradrenaline on alpha 1 adrenoreceptors

Question 55

Acetylcholine is the neurotransmitter that acts on what receptors of the SA and AV nodes

Answer 55

M2 muscarinic receptors

Question 56

Renin is produced by what cells?

Answer 56

Modified smooth mm cells o the afferent arterioles in the juxtaglomerular apparatus

Question 57

Renin then acts on angiotensin 1 which is then converted via (BLANK ) to (BLANK)

Answer 57

Angiotensin converting enzyme (ACE)Angiotensin II

Question 58

Where is angiotenson converting enzyme located?

Answer 58

Endothelial cells— especiallly in the lung

Question 59

What is synthesized in response to angiotensin II?

Answer 59

Aldosterone

Question 60

Aldosterone MOA

Answer 60

Mineralocorticoid receptors — to preserve Na reabsorption from teh distal nephrome**results= INC in circulating volume

Question 61

Hormone: AdrenalineCV and Renal effects:

Answer 61

INC HR and force of contraction (beta 1)Increase vascular resistance, decrease venous capacitance (alpha 1 on vascular smooth mm, beta 2 on sympathetic nerve terminals)Increase in blood flow to skeletal & cardiac mm (Beta2)

Question 62

Hormone: Angiotensin IICardiovascular and renal effects

Answer 62

Inc vascular resistance, decrease venous capcitance (receptors on vascular smooth mm and on sympathetic nerve termianl which in rease noradrenaline release)Increase in heart rate and force of contraction and sitmualte cardiac mm cell hyeprtrophyEnhance sodium retention by the kidney 9direct effect in proximal tubule and mediated via aldosterone in distal tubule)Increase thirst and possible salt appetite, enhance ADH secretion (effects on brain)

Question 63

Hormone: Antidiuretic hormone (vasopressin)Cardiovascular and renal effects

Answer 63

Increase water retention at the kidney (V2 receptors)Vasoconstriction (V1 receptors on vascular smooth mm) seen at higher ADH concentrations

Question 64

Hormone: Aldosterone Natriuertic peptides (ANP & BNP)

Answer 64

Increase sodium retention and potassium excretion by kidneyIncrease salt and water excretion by kidney (direct effects and inhibition of aldosterone)Inhibit renin and ADH secretionInhibit the peripheral and central actions of angiotensin IIVasodilatation (modest) of resistance of blood vesselsIncrease in capillary permeability— reduction in circulating volume

Question 65

Define Edema

Answer 65

abnormal accumulation of extracellular fluid in the interstitial spaces of the tissues or in body cavities that can be generalized or localized

Question 66

What are the forces that govern fluid movements at the capillary level?

Answer 66

1. intravascular hydrostatic pressure2. interstitial fluid hydrostatic pressure (keep fluid in capillary)3. Intravascular colloid oncotic pressure exerted by plasma proteins4. interstitial fluid colloid osmotic pressure5. vascular surface area capable of fluid transport6. vascular permeability to proteins and water

Question 67

What are the most common causes of increased capillary permeability?

Answer 67

traumainfectionendotoxemiahypersensitivity (allergic) vasculitis

Question 68

In horses and ruminants, what is the most common causes of increased hydrostatic pressure?

Answer 68

-CHF-venous thrombosis-liver dz causing obstruction of portal venous thrombosis-lymphadneopathy-cranial mediastinal mass-compression bandage-limb immbolizationtopica administraiton of counterirritants

Question 69

CHF cause of increased hydrostatic pressure?

Answer 69

pulmonary & vascular systemic congestion--compensatory salt and water retention increases ventricular diastolic, venous and capillary pressure= formation of generalized edema

Question 70

Causes of hypoproteinemia?

Answer 70

1. decreased production of plasma proteins: starvation, liver dz, severe heart failure2. augmented loss of plasma proteins resulting form kidney disease, PLE, (johnes disease, chronic inflammatory bowel disease), peritonitis, or pleuritis

Question 71

lymphedema occurs when lymphatics are absent or obstructed, what are causes of this edema in horses/cattle?

Answer 71

-congenital absence-- rare-tumor-local inflammation (lymphangitis or lymphadenitis)-elevated ventral venous pressure (ie: heart failure)

Question 72

Common causes of peripheral edema, pleural effusion, and ascites in horses

Answer 72

-chronic right sided or biventricular heart failure-pericarditis-pleuritis/pleuropneumonia-peritonitis-pregnancy-neoplasia: lymphosarcoma-cranial mediastinal mass-hypoproteinemia-liver dz-GI malabsorption: infalmmatoyr bowel dz, neoplasia, parasitism-vasculitis-equine infectious anemia-purpura hemorrhagica-Anaplasma phagocytophilum-equine viral arteritis-thrombophlebitis-lymphatic obstruction-ulcerative lymphantiis-lymphadenitis (corynebacterium pseudotuberculosis abscesses)Trauma-Equine viral arteritis-Thrombophlebitis

Question 73

Uncommon causes of peripheral edema, pleural effusion and ascites in horses

Answer 73

-aortic cardiac fistula-aortopulmonary fistulaheart base tumor other than lymphosarcoma-neoplasia: mesothelioma, melanoma, plasma cell myeloma, squamous cell carcinoma, fibrosarcoma-starvation-kidney dz, glomerulonephritis, amyloidosis-ionophore toxicity-copper deficiency-counterirritant application-hemodilution-ruptured bladder-Cassia occidentalis toxicity

Question 74

Common causes of peripheral edema, pleural effusion and ascites in ruminants

Answer 74

-chronic right sided heart failure-high altitude disease (brisket disease)-cor pulmonale-pericarditis (traumatic reticulopericarditis)-pleuritis-pregnancy (udder edema in heifers)-cr mediastinal mass: lymphosarcoma-hypoproteinemia-liver disease-kidney disease: amyloidosis, glomerulonephritis-Gi malabsorption, lymphosaromca, Johnne's dz, parasitism-lymphatic obstruction (corynebacterium pseudotuberculosis, lymphosarcoma)-thrombophlebitis-urolithiasis ruptured urethra or bladder

Question 75

Uncommon causes of peripheral edema, pleural effusion, and ascites in ruminants

Answer 75

-mycoplasma wenyoni-idiopathic hemorrhagic pericardial effusion-chronic right sides heart failure d/t cardiomyopathy, infectious myocarditis, ionophore toxicity-starvation-hemodilution-copper deficiency-vasculitistrauma-caudal vena caval thrombosis-anaplasmosis-gossypol toxicity-cassia occidentalis-phalaris spp toxicity-oxytropis (locoweed) toxicity

Question 76

Common causes of cardiac arrythmias in horses

Answer 76

-excitement-autonomic imbalance-fever-sepsis-toxemia-hypoxemia-colic-disorders of acid base or electrolyte homeostasis-congenital defects-myocarditis-valvular disease-idiopathic (presumptive myocardial fibrosis or fibrofatty infiltrate)

Question 77

Uncommon causes of cardiac arrhythmias in horses

Answer 77

-ionophore toxicity-ziplatrerol toxicty-anesthesia-other drugs-pericarditis-cardiomyopathy-cardiac or heart base tumor-aortic root rupture-aortopulmonary rupture-atypical myopathy-aortic regurgitation-severe hemorrhage-dynamic upper airway obstruction-rattlesnake envenomation-cardiotoxic plants-hyperthyroidism (iatrogenic)

Question 78

Common causes of cardiac arrythmias in ruminants

Answer 78

-GI disease-Lymphosarcoma-valvular heart disease-myocardial diseases-brisket dz-pericarditis-cor pulmonale-excitement-foot rot-fever-sepsis-toxemia-disorders of acid-base or electrolyte homeostasis-myocarditis

Question 79

Uncommon causes of cardiac arrythmias in ruminants

Answer 79

-ionophore toxicity-Beta-adrenergic agonist (zilpaterol) toxicity- anesthesia-hypoxemia-cardiomyopathy-autonomic imbalance-cardiotoxic plants (Rhododendron and Taxus spp.)

Question 80

Automaticity/ the ability to initiate action potentials spontaneously is a property of cells located where?

Answer 80

-sinus note-part of atria-AV junction-His-purkinje system

Question 81

Primary arrhythmias can be caused by pathologic conditions of the heart, such as:

Answer 81

myocarditisvalvular diseaseconduction system abnormalitiespericarditis

Question 82

Secondary arrhythmias develop in the absence of heart disease, such as those caused by:

Answer 82

-excitement-fever-sepsis-hypoxemia-acid-base disorders-electrolyte abnormalities-Gi disturbances-anemia-severe hemorrhage-anesthesia-ionophores-other drugs-toxemia

Question 83

Placement of base-apex lead for ecg

Answer 83

negative lead-- 2/3 rigth jugular furrow from the ramus of the mandible to the thoracic inletlead 1 or II: right armlead III: left arm

Question 84

Common causes of cardiac murmurs in horses:

Answer 84

valvular regurgitationcongenital defectsanemiaexcitementfeverfunctional murmurexercise

Question 85

Uncommon causes of cardiac murmurs in horses

Answer 85

aortic cardiac fistulaaortopulmonary fistulacardiomyopathypericarditiscranial mediastinal abscess

Question 86

Common causes of cardiac murmurs in ruminants

Answer 86

-anemia-excitement-fever-functional murmur-valvular regurgitation-congenital defects-lymphosarcoma-pericarditis (usually traumatic reticulopericarditis)

Question 87

Uncommon causes of cardiac murmurs in ruminants

Answer 87

-cardiomyopathy-myocarditis

Question 88

What is the graded scale of cardiac murmurs?

Answer 88

Grade 1: softGrade 2: soft murmur heard immediatelyGrade 3: murmur of moderate intensityGrade 4: loud murmur, with faint palpable thrillGrade 5: loud murmur with palpable thrillGrade 6: loud murmur, audible with stethoscope held away form the chest

Question 89

The presence of a musical murmur indicates:

Answer 89

vibration of a cardiac structure such as rupture of one of the chordae tendinea or torn valve leaflet

Question 90

Diastolic murmurs occur between which heart sounds?

Answer 90

S2 and S3(ventricular filling murmurs)ORS2 and S1(aortic regurge or rarely, pulmonic)

Question 91

Which lesion is described as a continuous washing machine murmur?**heard in a foal

Answer 91

patent ductus arteriosus

Question 92

Which lesion is described as a continuous washing machine murmur?**heard in an adult

Answer 92

aortic cardiac fistula secondary to rupture of the aortic root or of a sinus Valsalva aneurysmaorticopulmonary fistula--Fresian horses

Question 93

A continuous washing machine murmur in cattle is heard over the left cardiac areas is associated with what lesion?

Answer 93

traumatic pericarditis --d/t accumulation of fluid, gas, fibrin within the pericardium

Question 94

Reasons for muffled heart sounds:

Answer 94

1. pericardial effusion: displacement of the heart from the thoracic wall by fluid2. abscess or tumor: soft tissue mass3. pneumothorax, pneumomediastinum, or emphysema: air

Question 95

Common causes of muffled heart sounds in horses

Answer 95

obesitylarge or thick chest wallpericarditis or pericardial effusionneoplasia lymphosarcomapleural abscesschronic heart failure

Question 96

Uncommon causes of muffle heart sounds in horses

Answer 96

pulmonary emphysemapneumothoraxneoplasia: mesothelioma, squamous cell carcinoma, fibrosarcoma

Question 97

Common causes of muffled heart sounds in ruminants

Answer 97

pneumothoraxidiopathic hemorrhagic pericardial effusion

Question 98

Common causes of exercise intolerance, weakness and syncope in horses

Answer 98

myocardial diseasecardiac arrhythmiasaortic or pulmonary artery ruptureaortoiliac femoral thrombosiscongenital heart defectschronic heart failurepericardial diseasehyperkalemic periodic paralysis

Question 99

Common causes of exercise intolerance, weakness or syncope in ruminants:

Answer 99

myocardial diseasecardiac arrhythmiascongenital heart defectschronic heart failure

Question 100

define syncope

Answer 100

sudden collapse and loss of consciousness (fainting)

Question 101

The clinical signs of exercise tolerance, weakness or collapse that is caused by cardiovascular disease results from

Answer 101

failure to maintain cardiac output-- inability to regulate heart rate or stroke volume

Question 102

At what heart rates and mechanism do horses maintain cardiac output?

Answer 102

INC cardiac output HR <210 beats/min: tachycardia HR 210-240: INC stroke volume

Question 103

heart rates greater than 240 bpm limit cardiac output by

Answer 103

decreasing the time for diastolic perfusion of the myocardium or by limit in stroke volume because of the short diastolic intervals leave inadequate time for ventricular filling

Question 104

What are the most common bradyarrythmias to cause clinical signs?

Answer 104

complete heart blockadvanced second degree heart block

Question 105

Common causes of jugular venous distention and pulsation in horses

Answer 105

right sided heart failureleft-sided heart failure with pulmonary hypertensioncardiomyopathyatrial fibrillationtricuspid regurgitationcranial mediastinal masslymphosarcomaabscessjugular venous phlebitis and thrombosis

Question 106

Uncommon causes of jugular venous distention and pulsation in horses

Answer 106

ionophore toxicitypericarditismyocarditisventricular tachycardiasquamous cell carcinomafibrosarcomacor pulmonalechronic obstructive pulmonary diseaseoverhydration

Question 107

Common causes of jugular venous distention and pulsation in Ruminants

Answer 107

right sided heart failureleft sided heart failure with pulmonary hypertensionVitamin E and selenium defiiciency (white muscle disease)cardiomyopathytricuspid regurgitationpericarditisjugular venous phlebitis and thrombosisheart base abscessheart base tumor lymphosarcomacor pulmonale caused by chronic pneumoniabrisket disease

Question 108

Uncommon causes of jugular venous distention and pulsation in ruminants

Answer 108

ionophore toxicityidiopathic hemorrhagic pericardial effusionoverhydrationcranial mediastinal mass

Question 109

Abnormal jugular pulsation are associated with what side of the heart disease?

Answer 109

right sided--R-CHF--constrictive pericarditis-cardiomyopathy-tricuspid regurgitation

Question 110

Common causes of painful peripheral swellings in horses

Answer 110

thrombophlebitisabscess (Corynebacterium pseudotuberculosis)cellulitishypersensitivity vasculitis (complicated by skin necrosis and secondary infection)Equine viral arteritisEquine granulocytic ehrlichiosis (Anaplasma phagocytophilum)equine infectious anemiapurpura hemorrhagicclostridium spp myositisseptic tenosynovitisbursitismm disruption/hematomafractureinsect biteapplication of topical counter irritants, firing or soring

Question 111

Uncommon causes of painful peripheral swellings in horses

Answer 111

frostbite piroplasmosisulcerative lymphangitisepizootic lymphangitisglandersmelioidosissporotrichosisimmune vasculitisaortoiliac thrombosissporadic lymphangitiscongenital lymph node and lymphati cdysgenesishemangiosarcomasnakebite

Question 112

Common causes of painful peripheral swellings in Ruminants

Answer 112

thrombophelbitisabscessclostridial myositismalignant edemablacklegmm disurption/trauma/hematomacarpal hygromafescue footergotismcellulitis (inj site or wound)fracture insect bitefrostbite

Question 113

Uncommon causes of painful peripheral swellings in ruminants

Answer 113

disseminated hemangiosarcomaheartwater disease (Ehrlichia rumination, exotic)snake biteseptic tenosynovitisbursitis

Question 114

Common causes of enlarged lymph nodes in horses

Answer 114

strangleslymphosarcomaupper respiratory infectionCorynebacterium pseudotuberculosis lymphadenitis

Question 115

Uncommon causes of enlarged lymph nodes in horses

Answer 115

ulcerative lymphangitisepizootic lymphangitissporadic lymphangitisglandersmelioidosisgranulomatous lymphadenitisplasma cell myelomatuberculosishemolytic uremic syndrome

Question 116

Common causes of enlarged lymph nodes in ruminants

Answer 116

caseous lymphadenitis (Corynebacterium pseudotuberculosis)lymphosarcoma (including bovine leukosis virus)abscess or cellulitis of area drained

Question 117

Uncommon causes of enlarged lymph nodes in ruminants

Answer 117

tuberculosissporadic bovine encephalomyelitismalignant catarrhal fever

Question 118

Describe when the arterial pressure occurs with heart contraction

Answer 118

-opening of the aortic valve & ventricular ejection-rises rapidly in early systole-pulse pressure reach peak and declines as ventiruclar ejection slows

Question 119

Common causes of abnormal peripheral pulses in horses

Answer 119

dehydrationshocktoxemiacongestive heart failureelectrolyte imbalancesacid-base disordershypertensionhypotensionexercisefeverlaminitisaortic regurgitationcardiac arrhythmias

Question 120

Uncommon causes of abnormal peripheral pulse in horses

Answer 120

aortic cardiac fistulaaortopulmonary fistulaperipheral arteriovenous shuntpatent ductus arteriosus

Question 121

When do hyperkinetic arterial pulses occur in patients with:

Answer 121

-INC cardiac output (fever, exercise, excitement)-INC stroke volume -bradycardia-aortic valave regurgitation-patent ductus arteriosis-aortic cardiac fistulas-aortopulmonary fistulas

Question 122

In aortic valve regurgitation, the hyperdynamic pulses is caused by:

Answer 122

increased stroke volume (regurgitated blood int he left ventricle)-followed by rapid runoff of pressure later in systole (as a result of regurgitation)

Question 123

Hypokinetic pulses are present in patients with diminished stroke volume, as seen in what conditions?

Answer 123

hypovolemialeft ventricular failuremitral or aortic valve stenosis (RARE in lg animals)

Question 124

Common causes of abnormal puerperal pulse in ruminants

Answer 124

dehydrationshocktoxemiacongestive heart failureelectrolyte imbalancesacid-base disordersfevercardiac arrythmias

Question 125

Uncommon causes of abnormal peripheral pulse in ruminants

Answer 125

patent ductus arteriosusaortic regurgitationperipheral arteriovenous shunt

Question 126

Cardiac output values in resting horse range from

Answer 126

32 to 40L/min

Question 127

What are methods to determine cardiac output?

Answer 127

Fick methodDoppler echocardiographydye dilution/ thermodilution/ litium dilution

Question 128

Where is the most common location of ventricular septal defect in large animals?

Answer 128

perimembranous

Question 129

VSDs are more common in which equine breeds?

Answer 129

Welsh mountain poniesArabianStandardbredQuarterhorse

Question 130

Why do ventricular septal defects occur?

Answer 130

failure of fusion of part of the endocardial cushion and the muscular ventricular septum or failure of fusion of the truncal and conal septa

Question 131

Describe Eisenmenger complex

Answer 131

defect in which right-sided heart resistance to blood flow causes the shunt associated with VSD to become right to left (rare)**cyanosis is a distinguishing feature

Question 132

What size is a VSD (VSD to aortic root ratio) that is unlike to be hemodynamically significant?

Answer 132

less than 0.3

Question 133

With moderate to large VSDs, horses are at greater risk for developing congestive heart failure sooner. Why?

Answer 133

-simultaneous heart dz or Left sided heart failure d/t chronic volume overload can increase pulmonary vascular resistance-right ventricle-- chronic pressure overload**comb of pressure and volume overload= greater risk for developing CHF

Question 134

Which horses with VSDs are at risk for development of CHF early in life and have a shortened life expectancy?

Answer 134

Large defects: >3.5 cm or VSD/aortic ratio of 0.64peak shunt velocities: <3.5m/s

Question 135

define patent ductus arteriosus

Answer 135

persistent patency of the vessel that connects pulmonary arterial system to the aorta(pulmonary artery to aorta)

Question 136

Why does the ductus arteriosus close?

Answer 136

In response to:-lowered pulmonary vascular resistance-increased systemic vascular resistance-increased blood volume-increased left ventricular pressure when breathing begins-placental circulation removed

Question 137

Clinical signs of a PDA are dependent on:

Answer 137

-length and diameter of the ductus arteriosusdirection of the shunted bloodpresence of other cardiac defects

Question 138

Describe PDA murmur

Answer 138

continuous machinery murmurs

Question 139

Direction of PDA shunt usually occurs?

Answer 139

left to right--produces left ventricular volume overload-pulmonary hypertension & congestion+/- right sided ventricular hypertrophy

Question 140

When does switch of PDA shunt occur, to right to left?

Answer 140

When pulmonary resistance equal or exceeds the systemic vascular resistance

Question 141

When is PDA closure expected in foals?

Answer 141

by 96 hours of age

Question 142

In a foal with PDA, what is risk for future riding?

Answer 142

b/c of marked dilation of the pulmonary artery-- rupture of pulmonary artery is possible

Question 143

Define tetrology of fallot vs pentalogy of fallot

Answer 143

1. biventricular origin (overriding) of aorta)2. Ventricular septal defect3. obstruction of pulmonary arterial flow (pulmonary stenosis)4. secondary right ventricular hypertrophy (d/t obstruction of pulmonary arterial flow)5. atrial septal defect or persistent ductus arteriosus

Question 144

Pathogenesis of tetralogy/pentology of fallot

Answer 144

abnormal development of the conal septum in the embryonic heart-- leads to narrowing of the right ventricular infundibulum (pulmonic stenosis), an inability of the conal septum to participate in closure of the interventricular foramen (VSD) and overriding of the aorta

Question 145

What is the more common congenital cardiac defects that cause cyanosis in large animals?

Answer 145

tetralogy of fallot

Question 146

C/s of cyanosis is observed when unoxygenated hemoglobin is reduced to:

Answer 146

<5 g/dL (unoxygenated hemoglobin)

Question 147

Cyanosis resulting from heart failure or respiratory disease improves with what treatment?

Answer 147

oxygen administration

Question 148

What is the most common atrial septal defect?

Answer 148

ostium secundum defect-- patent foramen ovale PFO) is most frequent

Question 149

Pathogenesis of persistent foramen ovale

Answer 149

failure of septum primum (valve of foramen ovale)- to become adherent to the crista dividens after birth, when changes in left and right atrial pressures produce functional closure of the formen ovale

Question 150

In calves, what is the most common defect associated with PDA?

Answer 150

persistent foramen ovale

Question 151

atrial septal defect murmur

Answer 151

holosystolic crescendo-decrescendo murmur at the left heart base

Question 152

triscupid valve atresia c/s

Answer 152

cyanosiscrescendo-decrescendo or bandshape holosystolic murmur or pansystolic murmur audible over the rigth and left heart basetachycardiatachypneaweak peripheral pulsespolycythemia (common)

Question 153

Define persistent truncus arteriosus

Answer 153

one arterial vessel leaves the heart above a VSD**coronary and pulmonary arteries and aorta arise from this vessel

Question 154

Pseudotruncus arteriosus definition

Answer 154

presence of a remnant of an atretic pulmonary trunk**congenital cardiac disease

Question 155

What are the most common aortic anomalies seen in foals and calves?

Answer 155

dextropositioning or transposition of the aorta**other anomalies: persistence of the right aortic arch and double aortic arch (may cause esophageal compression)

Question 156

What is Eisenmenger complex?

Answer 156

Switch in blood flow from right to left side of the heart, to the left to right (results in decreased oxygenation of blood)

Question 157

Ectopia cordis cervicalis is a relatively common defect in which species?

Answer 157

cattle

Question 158

What defects are associated with ectopia cordis cervicalis?

Answer 158

defects of the heart, great vessels, neck (torticollis), ribs and sternebrae

Question 159

Chronic active infection such as what, can predispose animals to the development of bacterial endocarditis or nonvegetative valvulitis?

Answer 159

foot abscessesrumenitisreticular abscessother septic process lead to sustained or recurrent bacteria

Question 160

What are the most common bacterial isolates from equine and bovine endocarditis cases are:

Answer 160

streptococciPasturella or Acitnobacillus sppTruepuerella pyogenes (formerly Arcabobacterium pyognes)

Question 161

Lesions of aortic and pulmonic valves can produce what kind of murmurs?

Answer 161

systolicdiastolic (most common in lg animals)or Both

Question 162

Aortic regurgitation in horses is most commonly associated with

Answer 162

degenerative valve disease

Question 163

pulmonary regurgitation in cattle is most commonly associated with

Answer 163

bacterial endocarditis

Question 164

Describe aortic valve lesion murmurs

Answer 164

holodiastolicdescrescendomusical murmurs**can be descrescendo, soft & blowingwater hammer or bounding arterial pulse (assoc w/ sig L ventricular overload

Question 165

Signs of congestive heart failure in cattle/horses

Answer 165

tachycardiacoughingrespiratory distressjugular venous distentionsubcutaneous edemaascitesmammary vein distention (cattle)

Question 166

describe murmur of ruptured chordae tendinae?

Answer 166

radiating musical murmur-- distinctive honking quality*may have band shaped pansystolic murmur

Question 167

acute onset of respiratory distress with coughing and expectorating foamy pulmonary edema fluid is a relatively consistent feature of what cardiac abnormality?

Answer 167

ruptured chordae tendinae

Question 168

Describe murmur of mitral valve prolapse

Answer 168

crescendo midsystolic to late systolic or holosystolic murmur with PMI over the mitral valve area(similar with tricuspid valve prolapse)

Question 169

Triscupid valve lesions in horses vs cattle are most commonly due to:

Answer 169

cattle: bacterial endocarditis, neoplasia of the right atriumhorse: bacterial endocarditis from septic jugular vein thrombosis

Question 170

Echo evidence of mitral valve regurgitation

Answer 170

-INC left atrial and left ventircular dimensions-rounding of left ventricular apex- pattern of left sided volume overload+/- INC fractional shortening-bulging of interatrial septum toward the right-larger than nomral pulmonary artery (>aortic root)-- severe pulmonary hypertension

Question 171

Tricuspid regurgitation echocardiac evidence

Answer 171

right atrial and right ventricular enlargement with paradoxical septal motion--> visualizing lesions of endocarditis or neoplasia

Question 172

aortic regurgitation echocardiographic evidence

Answer 172

left ventricular dilationincreased aortic root diameter decreased aortic root diameter during diastole evidence of inc severity of aortic regurgitationINC left ventricular fractional shorteningdiastolic fluttering of the septal mitral valve leaflethigh frequency vibrations of the interventricular septum or aortic valve in diastole-->visualization of valve prolapse, fenestration, healing endocarditis lesions or tears

Question 173

Besides echocardiographic evidence of bacterial endocarditis, what are other C/s and diagnostics that indicate endocarditis

Answer 173

anemianeutrophilia (a left shift may be present)increases serum globulin concenINC SAAhyperfibrinogenemialiver enzymes INCurinalysis (+/- pyuria or hematuria)positive blood culture w/ febrile episodes other lab abnormalities of sepsis

Question 174

Most horses with mitral valve regurgitation do not develop fulminant pulmonary edema, instead they develop

Answer 174

chronic pulmonary hypertension leading to subtle respiratory signs associated with interstitial pulmonary edema and subsequent development of right-sided CHF

Question 175

In regards to valvular heart disease in horses, what is the most common valves involved?

Answer 175

Aortic is most commonly effected with degenerative valve changes**followed by mitral valve, tricuspid valve and pulmonic valve

Question 176

Jet lesions occur due to

Answer 176

asosciated with high -velocity turbulent regurgitant blood flow**usually found in the receiving chamber

Question 177

What lesions can cause moderate to severe valvular regurgitation and are more likely to progress rapidly and warrant a guarded to poor prognosis?

Answer 177

ruptured chordae tedinaeflail valve leafletsmarked valvular thickening

Question 178

Treatment of endocarditis can ultimately result in?

Answer 178

scarring of the valve leaflet, that leads to progression fo regurgitation and death of animal

Question 179

When treating cattle for bacterial endocarditis, the antibiotic of choise is?

Answer 179

antibiotic with gram positive coverage

Question 180

Indication of clopidogrel in treatment of bacterial endocarditis? (in horses)

Answer 180

to prevent platelet adhesion and increased size of the valvular mass

Question 181

Use of what medicatiosn can be used in cattle to prevent platelet adhesion and increased size of the valvular mass?

Answer 181

aspirin (100 mg/kg/day)low-dose sodium heparin (subcu 30 to 40 units/kg twice daily)

Question 182

Horses benefit (as do other spp) from the use of vasodilators in treatment of heart failure, what drug has been shown to be beneficial in horses with treatment of moderate MR or AR?

Answer 182

angiotensin converting enzyme (ACE inhibitors)**benazepril: 0.5 mg/kg PO once daily

Question 183

How do effective parasite control measures prevent predisposing causes of valvular heart disease?

Answer 183

trauma to heart valvesmicroembolisminfarction**in horses

Question 184

Define cor pulmonale

Answer 184

refer to the effect of the lung dysfunction on the heart and therefore a secondary form of heart idsease

Question 185

Pathogenesis of cor pulmonale

Answer 185

pulmonary hypertension that leads to right ventricular hypertrophy--> dilation or failure

Question 186

What is the primary cause of the cor pulmonale in cattle?

Answer 186

High mountain disease (brisket disease, high-altitude disease)

Question 187

Pathogenesis of High mountain disease?

Answer 187

hypoxic vasoconstriction from high-altitude dwelling

Question 188

What disease or factors contribute to the development of High Mountain disease?

Answer 188

pneumonialungwormingestion of locoweed (Oxytropis and Astragalus spp)chronic pulmonary disease

Question 189

What are the primary presenting clinical signs of brisket disease?

Answer 189

subcutaneous edema of the brisket, ventral thorax, submandibular area and occasionally limbslethargy weaknessbulging eyesdiarrheacollapsedeath may occurtachycardia (with a gallop rhythm, +/- splitting of S2 heart sound

Question 190

Why would there be splitting of the S2 heart sound in brisket disease?

Answer 190

because pulmonary hypertension may accentuate the separation of the aortic and pulmonic valve closures, producing an audible splitting of the S2 **most notable on inspiration

Question 191

Horses with clinical signs of cor pulmonale?

Answer 191

RAO--> leading to cor pulmonalelabored breathingcoughingexercise intolerancewheezes ausculted bilaterally

Question 192

Differentials for clinical signs of right sided heart failure

Answer 192

bacterial endocarditis or TRcardiomyopathycardiac lymphosarcoma/ other thoracic neoplasmstraumatic reticulopericarditisleft sided heart fialurepleuritis or pleural effusioncongenital pulmonic valve stenosis (rare)

Question 193

The response to hypoxia in brisket disease is dependent on:

Answer 193

amount of smooth mm in the pulmonary arteries

Question 194

Brisket disease path:Chronic pulmonary artery hypertension causes

Answer 194

pressure overload in the right ventricle-- responds with increased workload with hypertrophy, dilation or failure (dep on speed of which the condition develops)

Question 195

Chronic right sided heart failure can lead to what?

Answer 195

diastolic dysfunction of the left ventricle

Question 196

Why does ingestion of locoweed (oxytropis and Astragulus spp) predispose cattle to right sided heart failure?

Answer 196

Swainsonine** causes toxic mycoardial damage

Question 197

Brisket disease is common in cattle, kept over what altittude?

Answer 197

over 6000 feet

Question 198

In what seasons is high mountain disease most commonly seen?

Answer 198

fall and winter** due to cold weather exacerbating pulmonary hypertension

Question 199

Is cor pulmonale reversible in HMD?

Answer 199

Yes--if animal is brought to lower altitudes

Question 200

When do cattle not have reversible cor pulmonale?

Answer 200

-other lugn disease- mean PAP of 50 to 55 mm HG **rare- once heart failure develops

Question 201

Selection of breeding stock to prevent HMD?

Answer 201

low or normal PAPs at altitudes above 5000 feet

Question 202

Define myocarditis

Answer 202

inflammation of the myocardium caused by bacterial, viral or parasitic organism or thromboembolic disease

Question 203

What are common causes of bacterial myocarditis?

Answer 203

Stpahylococcus aureusStreptococcus equiClostridium chauveoeiMycobacterium spp

Question 204

What are known viral causes of myocarditis?

Answer 204

foot and mouth diseaseequine infectious anemiaequine viral arteritisequine influenzaAfrican horse sickness

Question 205

What are known parasitic causes of myocarditis?

Answer 205

strongylosiscysticercosissarcocystic infection in ruminentas

Question 206

Define cardiomyopathy

Answer 206

subacute or chronic disease of the ventricular myocardium that occurs without anatomic valvular disease, congenital malformations of the heart or vessels or pulmonary disease

Question 207

Hypertensive cardiomyopathy ahs been detected in horses associated with what diseases?

Answer 207

chronic renal diseasepain assoc with chronic laminitisponies with EMS

Question 208

Dilated cardiomyopathy is associated with:

Answer 208

-ventricular dilationincreased ventricular massdecreases systolic function

Question 209

What known genetic predispositions exist for the development of inherited/genetic cardiomyopathy

Answer 209

1. red holstein gene in Holstein Friesan cattle2. curly hair coat in polled herefords and in Japanese black calves

Question 210

What toxic components can cause cardiomyopathy?

Answer 210

monensinlasalocidsalinomycingossypolCassia occidentalisphalris sppvit E and selenium deficiencycopper deficiencyexcessive molybdenum high sulfatestes (secondary copper deficiency)Acer family (plant tox)rattle snake envenomation

Question 211

It is difficult to distinguish C/s of myocarditis from what diseases?

Answer 211

colicrespiratory diseaselamenesssepticemia--C/s of myalgia, reluctance to move exercise intolerance

Question 212

Differentials for causes of dilated cardiomyopathy

Answer 212

1. nutritional (Vit E, selenium, copper deficiency)2. toxic: monensin, gossypol, salinomycin, lasalocid, hypoglycin A, Cassia spp., or Phalaris)3. Infectious (viral, bacterial, or parasitic)4. Drug induced

Question 213

Differential diagnosis for dilated cardiomyopathy?

Answer 213

young-- congenital heart defects, cor pulmonale, nutritional myodegenerationAdults-- bacterial endocarditis, cardiac neoplasia, thoracic abscess, pericarditis, pleuritis, diaphragmatic hernia

Question 214

In an attempt to compensate for the reduced cardiac output, how is circulating fluid volume increased in cardiomyopathy

Answer 214

activation of renin-angiotensin aldosterone system & iNC arterial resistance

Question 215

What leads to the development of pulmonary edea in heart failure?

Answer 215

reduced cardiac output--> stim renin-angiotensin-aldosterone system-- INC arterial resistance-- INC ventricular preload (venous return)-- INC afterload (arterial resistance)--> causes pulmonary edema & reduced cardiac contractility

Question 216

Microscopic abnormalities associated with cardiomyopathy

Answer 216

1. INC fibrous tissue in interstitium in absence of inflammation (or foci of inflammation2. variation in cross-section of cardiomyocytes3. degeneration of adjacent myocardial fibers4. myocardial vacuolation and degeneration with necrosis and fibrosis

Question 217

Prompt administration of what drug can be beneficial to survivors of ionphore toxicosis?

Answer 217

administration of Vit E

Question 218

Why are corticosteroids controversial in treatment of cardiomyopathy?

Answer 218

Possible viral recruidescence if the cause is viral

Question 219

What are therapeutic strategies used for treatment of dilated cardiomyopathy?

Answer 219

1. positive inotropic agents (digoxin)2. diuretics3. vasodilators4. rest5 +/- removal of pleural or abdominal fluid

Question 220

When is the use of digoxin contraindicated in the treatment of dilated cardiomyopathy?

Answer 220

monensin toxicosis

Question 221

Ideally the peak and trough concentration of digoxin should be between:

Answer 221

1 to 2 ng/mL

Question 222

Before treatment of digoxin therapy what should be addressed int eh patient?

Answer 222

dehydrationacid-base balanceelectrolyte abnormalities

Question 223

When should the dose of digoxin be reduced in patietns?

Answer 223

with elevated creatinine or blood ure anitrogen levels

Question 224

What diuretic is most commonly used in large animals?

Answer 224

furosemide: 1 mg/kg

Question 225

Which ACE inhibitor is most effective in horses?

Answer 225

benazeprilOther ace inhibitors: quinapril, ramipril, enalapril

Question 226

Define pericarditis

Answer 226

inflammation of the pericardium that results in accumulation of fluid or exudate between the visceral and parietal pericardium

Question 227

Causes of pericarditis in large animals

Answer 227

-penetration of ingested foreign objects or external wounds -hematogenous spread (septicemia) of infection-extension of infection from the lung or pleura-viral infections (equine viral arteritis or equine influenza)-neoplasia-Mare reproductive loss syndrome (MRLS) (Actinobacillus spp)

Question 228

What are the most consistent clinical signs on auscultation with pericarditis?

Answer 228

tachycardiamuffling of heart soundsabsence of lung sounds in ventral thoraxdorsally lung ounds are louder thn normal

Question 229

Contrast auscultation of pericarditis vs pleuritis?

Answer 229

lung sounds are muffled ventrally (heart sounds are not0radiation fo heart sounds over a wider aea than normal

Question 230

Cattle: When auscultated with splashing sounds sometimes referred to as "washing machine murmur or rub", what does this mean clinically?

Answer 230

- can be attributed to accumulation of gas and fluid in pericardium **indicative of presence of gas forming (anaerobic organisms) **grave prognosis

Question 231

Electrocardiogram abnormalities that are can be seen with pericarditis?

Answer 231

1. decreased amplitude of the QRS complexes (<1.5 mV in the base apex lead)2. electrical alternans (altered congifuration fo the P, WRS or T complexes on a regular basis)3. ST segment elevation or slurring+/- right -axis deviation int eh stanard limb leads

Question 232

What is the safest site to perofrm a pericardiocentesis?

Answer 232

left fifth (fourth in cattle) intercotal space 2.5 to 10 cm dorsal to teh olecranon, above the level of the lateral thoracic vein

Question 233

What bacteria is commonly associated with pericarditis and mare reproductive loss syndrome?

Answer 233

Actinobacillus organisms

Question 234

What are the consequences of pericardial effusion to the heart?

Answer 234

- decreased distensibility (increased ventricular end-diastolic pressure) of the heart-- impairs the hearts ability to fill in diastole--INC atrial pressure- reduce venous flow or venous return to the heart and diastolic perfusion of the myocardium--> decreased ventricular contractility, stroke volume and cardiac output

Question 235

Difference between effusive and constrictive pericarditis

Answer 235

effusive: presence of pericardial fluid causes hemodynamic consequences**removal of fluid beneficialconstrictive: reduction in ventricular compliance d/t fibrinous or fibrotic involvement of pericardium and epicardium**removal of fluid not beneficial

Question 236

Exposure to what was the greatest risk factor for the development of fibrinous pericarditis during the mare reproductive and loss syndrome epidemic?

Answer 236

Eastern tent caterpillars

Question 237

Traumatic pericarditis is not uncommon in cattle, but occurs in less than what percentage of cattle with traumatic reticuloperitonitis?

Answer 237

less than10%

Question 238

Treatment of pericarditis in horses

Answer 238

-- placement of a large bore indwelling chest tube into the pericardial sac under echocardiographic guidance and drainage and lavage of the pericardial sac --> with local infusion of antibiotics

Question 239

Why can diuretics results in worsening heart failure with pericarditis?

Answer 239

Reduce venous return and preload in animals with pericarditis= compromise to cardiac output & worsening heart failure

Question 240

Removal of what trees can be beneficial in prevention of exposure to Eastern tent caterpillar?

Answer 240

black cherry trees

Question 241

What is the most common cardiac tumor in large animls?

Answer 241

lymphosarcoma

Question 242

Examples of neoplasias that may involve structures adjacent to the heart and may extend to the heart or heart base in horses,

Answer 242

mesotheliomasmelanomaslipomasfibrosarcomaadenocarcinomasother cacrinomassquamous cell carcinomas

Question 243

Lymphosarcoma is the most common cause of cardiac tumors in cattle, which has a predilection site for?

Answer 243

right atrial myocardium**RV not uncommon, rare: LA or LV

Question 244

Although more than 50% of cattle in some parts of the United State are infected with BLV, what percentage develop lymphosarcoma?

Answer 244

1 to 4 %

Question 245

Thymic lympohosarcoma, which is not associated with BLV infections, also involving the heart can occur in what age of cattle?

Answer 245

cattle younger than 30 months of age

Question 246

The prognosis for survival for cardiac neoplasia?

Answer 246

poor-- death expected within 6 months

Question 247

Control/prevention of cardiac tumors can only be performed for which tumors?

Answer 247

BLV--> isolation of BLV pos and BLV neg animals--> use of individual or serialized supplies-->feeding colostrum from serologically negative cows only--> frequent testing (at least every 6 months) & isolation of serologically positive animals over 6 months of age)

Question 248

Define aneurysms

Answer 248

vascular dilations, develop from weakening of the medial elastic coat of blood vessels

Question 249

Medial weakness of blood vessels seen in aneurysms can be caused by:

Answer 249

progression of intimal atherosclertoic lesions that has enlarged from hemorrhagecalcificationulcerationthrombus formation

Question 250

Causes of aneurysms in large animsl

Answer 250

**unknowntrauma (internal or external)sepsisparasite migrationdegenerative vascular diseaseatherosclerosisaging changes (dilation, elongation and loss of elasticity of blood vessels)

Question 251

Congenital aneurysms of what structure of the heart have been reported in horses?

Answer 251

sinus of Valsalva

Question 252

Define thrombosis

Answer 252

formation of a clot that obstructs blood flow in the circulatory system

Question 253

causes of thrombosis

Answer 253

traumavenous stasiscatheterization for adminsiterin gmedication or fluidsneedle penetrationindwelling acehtersthrombogenic solutionsbacterial contamination

Question 254

Secondary thrombosis causes:

Answer 254

perivascular inflammation caused by cellulitis, lymphangitis or other source so fbacterial invasion round the blood vessel

Question 255

Examples of a hypercoagulable states:

Answer 255

dehydrationendotxemiaanemiahypotensionstress stasis

Question 256

Define mebolism

Answer 256

foreign material carried in the bloodstream

Question 257

In large animals, embolis most commonly occur with:

Answer 257

bacterial endocarditisthromboplhebitisomphalophlebitisparasitic arteritis

Question 258

Calves with aorto or aortoiliac thrombosis clinical signs?

Answer 258

weaknesslamenessknucklingparesisparalysis of the hindlimbsinability to risecold hindlimbslacking a femoral pulse

Question 259

Aortopulmonary rupture and fistulization occur in what breed?

Answer 259

Fresians

Question 260

What is the most common outcome of aneurysm of a major vessel?

Answer 260

thoughout to be rupture

Question 261

Unruptured aneurysms may have other complications such as

Answer 261

thrombosis or emoblization o fthe thrombus

Question 262

In Friesians, rupture of the aorta occurs into the pulmonary artery at what location?

Answer 262

at the level of th eligamentum arteriosum and into the surrounding perivascular stuctures

Question 263

Spontaneous thromboembolism is commonly associated with?

Answer 263

parasitism in horses**aorta and cranial mesenteric arteries are the most common sites frequently involved

Question 264

What are risk factors for catehter associated thrombophlebitis

Answer 264

large intestinal diseasehypoproteinemiaendotoxemiasalmonellosisfeverdiarrhealocalled produced fluids

Question 265

Arteriosclerosis recognized in cattle is most frequently caused by:

Answer 265

excessive vitamin D3 supplementationingestion of calcinogenic plans: Soamum malaxocylon, estrum dirunum or Trisetum flavescens

Question 266

In horses arteriosclerotic lesions were caused by lesions induced by what organism?

Answer 266

Strongylus vulgarus

Question 267

Ingestion of calcinogenic plants in horses, results in lesion in what locations?

Answer 267

aorta

Question 268

Examples of anticoagulant therapy that may be effective in preventing the thrombus formation

Answer 268

clopidogrel: 2 mg/kg PO twice dailyaspirin; 100 mg/kg PO once daily ruminantssodium heparin: 20 to 40 units/kg SC twice daily

Question 269

Atrial fibrillation is characterized by

Answer 269

lack of coordinated atrial electrical activity-- caused by an abnormality of impulse conduction that results from multiple small rapid and random reentrant activation of the atria or by one or more discrete rotors

Question 270

What shortens the action potential duration in atrial myocardial cells, making atrial fibrilation more likely to occur in horses?

Answer 270

high resting vagal tone

Question 271

Causes of atrial fibrillation

Answer 271

atrial enlargement from atrial myocardial diseaseatrioventricular valvular regurgitationventricular failuremyocarditisendocarditisautnomic nervous system imbalanceelectrolyte or acid base distrubancesanesthetic drugs or tranquilzier adminitstration

Question 272

Define "lone Afib"

Answer 272

no undelrying cardiac disease can befound

Question 273

Cattle with atrial fibrillation usually have what undelrying disease?

Answer 273

gastrointesitnal disease

Question 274

Define paroxysmal atrial fribillation

Answer 274

usually lasts no more than 24 to 48 hours abefore spontaneous conversion to sinus thythm occurs

Question 275

What is a common cause of paroxysmal atrial fibrillation inhorses?

Answer 275

transient potassium depletion associated with administration of furosemide

Question 276

What supplements are associated with atrial fibrillation in horses?

Answer 276

bicarbonate "milk shakes"- paroxysmal AF-iatrogenic hyperthyroidism-- admin of Thyro L-supplements containing kelp or ground up shell fish

Question 277

Describe atrial fibrillation arrhythmias

Answer 277

irregularly irregular - absent 4th heart sound

Question 278

Differentiate 2nd degree AV block from atrial fibrillation

Answer 278

Second degree AV block-- regularly irregular rhythm, audible fourth heart soundAtrial fibrillation-- regularly irregular, absent 4th heart sound

Question 279

Most cattle with atrial fibrillation of what underlying acid-base distrubance?

Answer 279

metabolic alkalosis**experimentally metabolic alkalosis with hypokalemia have results in devleopmetn of Afib

Question 280

When is cardiac troponin (cTnI) elevated in horses with afib?

Answer 280

acute AF: w/in 4 to 6 hours after onset of Afib

Question 281

What if cTnI remains elevated in horses with afib?

Answer 281

Activ emyocardial disease shoul dbe suspected

Question 282

electrocardiogram abnormalities in Afib

Answer 282

irregular R-R intervalQT interval and appaearnce of T wave may varypwaves absent (replaced by fibrillation waves)

Question 283

Echocardiographic image that should be performed to indicate left atrial enlargement

Answer 283

2 chamber: measure in peak systole **stbd, thgbd: 13.5cm or lessLA to AO ratio in 2D short axis view (provides mroe info on LA enlargement)

Question 284

Which breeds have the highest incidence of AF?

Answer 284

standardbredthoroughbreddraft horses

Question 285

In horses with atrial fibrillation what is the most common valvular lesions?

Answer 285

mitral valve disease

Question 286

Quinidine in the treatment of atrial fibrillation:

Answer 286

negative inotrope at high dosages-causes systemic hypotension-increases ventricular reponse rate

Question 287

What are possible negative side effects of quinidine?

Answer 287

nasal edemacutaneous reactions (urticaria or wheals)laminitiscolicmarked diarrheaataxia

Question 288

Max number of consecutive doses of quinidine to administer?

Answer 288

4 doses

Question 289

When should therapy with quinidine be discontinued

Answer 289

QRS complex prolongation ( more than 25% of pretreatment value)fast (>80 to 100 bpm) sustained supraventricular arrhythmiaventricular rhythmcolicmarked diarrheaataxianasal edema laminitis

Question 290

How often administer a dose of quinidine?

Answer 290

1 dose every 2 hours

Question 291

What medication can be administered in addition to quinidine to assist in cardioversion from afib to normal sinus rythm?

Answer 291

digoxin (11 microg/kgPO twice daily)**can be helpful in cases, if conversion has not occurred in 24 to 48 hours

Question 292

Caveat to combination therapy of digoxin and quinidine?

Answer 292

concurrent admin of digoxin and quinidine results in an increased plasma digoxin concentration

Question 293

Digoxin can be indicated prior to pretreatment of atrial fibrillation in what circumstance?

Answer 293

When high heart hearts (want < 60 bpm in horses, <100 bpm in cattle before quinidine treatment)very low FS (<24%) indicative of underlying myocardial disease

Question 294

If furosemide cannot be removed from therapeutic tx regimen in a horse, what can be added to teh diet to prevent potassium depletion ?

Answer 294

KCL

Question 295

At exercise, horses with atrial fibrillation heart rate should not exceed?

Answer 295

220 bpm

Question 296

Define ventricular tachycardia

Answer 296

cardiac arrhythmia characterized by a rapid rhythm originating in teh ventricle**originates below hte bundle of HIS in specilized conduction system surround the ventircular myocardium or both

Question 297

Clinical signs associated with ventricular tahycardia

Answer 297

exerciseintolerancesyncope episodesdepressionweaknesscolicresp distresscoughingventral edemapulmonary edema

Question 298

In cattle ventricular tachycardia occurs most frequently secondary to

Answer 298

sepsis and toxemia

Question 299

Large pulse waves seen in teh jugular vein are called cannon "a" waves that occur when?

Answer 299

atrium and ventricle contract simultaenously

Question 300

When are signs of right sided CHF (ventral edema, venous distention) with ventricular tachycardia?

Answer 300

sustained uniform VT and increase in servity the longer duration and mroe rapid the rate of arrhthmias

Question 301

When are signs of left sided CHF (coughing, expectoration of foamy fluid, respiratory distress) seen in ventricular tachycardia

Answer 301

multiform VT

Question 302

What clinical signs help distinguish VT from sinus or supraventricular tachycardia?

Answer 302

presence of jugular pulsesbruit de cannon in an animal with rapid rhythm

Question 303

Diagnosis of VT is made how?

Answer 303

ECG: series of 4 or mor ventricular premature complexes**VPC may be widened and bizarre or WRS duration and apparent normal

Question 304

Vtach: morphology of QRS complexes can be described as:

Answer 304

uniform (similar)vary in morphology (multiform)

Question 305

What is commonly seen with ventricular tachycardia in association with the atrium?

Answer 305

atrioventricular dissociation-- atrial rate slower than the ventricular rate-- may see fusion and/or capture beats-- VT can be sustained or paroxysmal

Question 306

What should be considered in horses with acute onset of uniform VT and colic?

Answer 306

rupture of the aortic root at the right sinus of valsalva

Question 307

What is a mechanism described in exercise induced VT in horses?

Answer 307

sympathetic stimulation (increasing the amplitude of early afterdepolarizations)

Question 308

What is an important cause of sustained VT?

Answer 308

reetnry in the ventricle

Question 309

What is though tot be one of the leading causes of sudden cardiac death in horses when other causes of death cannot be found on postmortem examination?

Answer 309

Ventricular tachycardia leading to ventricular fibrillation

Question 310

Which gender is at increased risk for aortic root and sinus of Valsalva rupture?

Answer 310

males-- usu. middle-aged at time of rupture

Question 311

VT is more likely seen in large animals of any age with what diseases?

Answer 311

GI diseasehorses-- following severe hemorrhage

Question 312

Does slow, uniform VT require treatment?

Answer 312

often resolves or improves significantly with correction of underlying electrolyte or metabolic imbalances w/o requiring antiarrhythmic therapy

Question 313

Horses with sustained heart rate >120 bpm, uniform VT treatment

Answer 313

antiarrythmic therapy

Question 314

ECG findings associated with life threatening VT

Answer 314

multiform origin for the ventricula rpremature depolarizations-torsades de pointes (wdie VT)-presence of an R wave superimposedon preceding T wave (R on T)

Question 315

large animal with following C/S treatment recommendation?-C/S of CHF & hemodynamic collapse-Heart rate <120 bpm-Multiform VT (+/- R on T)

Answer 315

treat as cardiovascular emergecy-- death from ventricular fibrillation is likely w/o antiarrythmic therapy

Question 316

What drugs can be used to tx life-threatning VT:

Answer 316

lidocainequinidine gluconatemagnesium sulfateIV procainamide, IV and oral propafenone (refractory VT), IV flecainidesotalol

Question 317

acute massive blood loss induces hypovolemic shock characterized by:

Answer 317

tachycardiatachypneacold extremitiespale mucous membranesmuscle weaknesseventual death (resulting from CV collapse)

Question 318

When do you see changes in PCV or total protein with acute blood loss?

Answer 318

within 12 to 24 hours

Question 319

Hypovolemic shock should be treated with administration of:

Answer 319

40 to 80 ml/kg of sodium containing crystalloid fluids

Question 320

Hypertonic saline can be administered at what dose, to temporarily reverse the pathophysiologic sequelae of severe hemorrhagic shock?

Answer 320

2 to 4 ml/kg 7.2% sodium chloride

Question 321

Why is the total volume of crystalloid solution required is much greater than the volume of blood lost because

Answer 321

crystalloid solutions distribute throughout the extracellular space

Question 322

Why is blood transfusion viewed as a temporary therapeutic procuedure?

Answer 322

because crossmatch- compatible allogeneic RBCs are removed from circulation by mononuclear phagocyte system (MPS) w/in 2 to 4 days of transfusion

Question 323

Describe routine blood typing crossmatch:

Answer 323

incubating wash RBCs from donor (major) and recipient (minor) with serum from the other

Question 324

Why is the first blood transfusion of whole blood to a horse or ruminant, not previously transfused or senstized by immunization or pregnancy usually well tolerated

Answer 324

b/c natural alloantibodies are o flow concentration adn weak activity

Question 325

Severe anaphylactic reactions to blood transfusion should be treated with

Answer 325

epinphreine (0.01 to 0.02 mg/kg

Question 326

When does normal bone marrow start to replace cells, in cases of acute hemorrhage?

Answer 326

w/in 5 days

Question 327

Define hemoperitoneum

Answer 327

accumulation of blood in the abdominal cavity**can be life threatening

Question 328

Causes of hemoperitoneum in the horse

Answer 328

traumapostoperative abdomina lhemorrahgeneoplasiacomplications from pregnancy an dfoaling (utero-ovarian, middl euterine, external ilaic artery rupture)organ rupturemesenteric injurycoagulopathiesovarian hemoatomasystemic mayloidosisidiopathic hemoperitoneum

Question 329

The underlying cause of hemoperitoneum is identified in what percentage of cases?

Answer 329

76%

Question 330

What are the most common causes of hemoperitoneum in horses?

Answer 330

trauma (spleen and in mares, repro tract & assoc vessels)neoplasia

Question 331

Hemorrhagic abdominal effusion is characterized by high red cell count of:

Answer 331

RBC> 2, 400, 0000 RBC/microLPCV >18%total protein >3.2 g/dL*normal t high luek count

Question 332

What are early indicators of hypovolemia d/t acute blood loss?

Answer 332

central venous pressureblood lactate concentration

Question 333

Primary goals of therapy in hemoperitoneum

Answer 333

1. tx hypovolemic shock2. restore perfusion & O2 delivery to tissues3. correcting fluid deficits4. stopping further blood loss5. preventing complications

Question 334

Which carries the worse prognosis pre or post partum hemorrhage?

Answer 334

prepartum: 100% vspostpartum: 20% mortality

Question 335

Causes of hemothorax in neonatal foals

Answer 335

lacerated lung or vessels from fractured ribs

Question 336

Is exercise induced pulmonary hemorrhage a recognized caused of major blood loss in horses?

Answer 336

no

Question 337

Causes for chronic blood loss

Answer 337

bleeding GI lesionscertain renal diseaseshemostati cdysfunctionblood sucking external parasiteshaemonchosis (esp goat sand sheep)

Question 338

Causes of GI hemorrhage

Answer 338

1. Neoplasia Horses: gastric SCC cattle: abomasal lymphoma2. parasitism3. mucosal ulceration NSAID tox in horses abomasal ulcers: cattle

Question 339

Renal sources of chronic blood loss

Answer 339

renal neoplasia (Rare)congenital renal vascular anomalies (RARE)idiopathic hematuriaidiopathic recurrent hematuria of Arabian horses

Question 340

How does iron deficiency anemia develop?

Answer 340

With loss of erythrocyte iron secondary to chronic severe blood loss** hypoferremia or reduce serum ferritin develops with INC total Fe binding capacity and reduction in marrow iron

Question 341

What is a good source of iron for patients?

Answer 341

good quality forages

Question 342

NSAID pathogenesis in right dorsal colitis

Answer 342

inhibit cycolooxygenase -- (COX1 than inducible CO2 expressing during state of inflammation--> causes inhibition of prostaglandin E production--> hypoxic or ischemic GI mucosal damage and delayed mucosal healing

Question 343

What 2 components are involved in hemostasis?

Answer 343

1. coagulation2. fibrinolysisfunction: arrest bleeding from damaged blood vessel and maintain nutrient blood flow

Question 344

After a blood vessel is damaged, what occurs

Answer 344

vasoconstriction occursrapid adherence of plts to subednothelial collage

Question 345

after rapid adherence of platelets to a damaged blood vessel, then

Answer 345

triggeres aggregation, contraction and granule secretion (basic plaetlet reaction)

Question 346

What platelet phospholipoprotein provides the necessary surface to catalyze interactions among activate coagulation proteins that result in thrombin formation?

Answer 346

platelet factor 3

Question 347

What are zymogens?

Answer 347

precursor forms of procoagulant proteins that circulate in the blood **must be altered during coagulation to become active

Question 348

When is the extrinsic coagulation system activated?

Answer 348

When lipoprotein tissue factor (TF) gains access tohte bloo stream

Question 349

Where is tissue factor located?

Answer 349

widely dsitirbuted in most tissues (endothelial cells * monocytes

Question 350

When is intrinsic coagulation system activated?

Answer 350

When blood is exposed to a negatively charged surface (e.g. activated platelets)

Question 351

When factor XII and prekallikrein in the intrinsic coagulation pathway have reciprocal activation, then

Answer 351

the intinstric pathway stimulats formation of numerous inflammatory mediators such as kinins and complement

Question 352

What is thrombin generated from?

Answer 352

formation of activated factor X (Xa)

Question 353

Function of thrombin

Answer 353

catalyzed the conversion of fibrinogen to fibrinpromotes plt aggregationenhances cofactor activities of factor V and VIIIactivates factor XIII & protein C

Question 354

Examples of plasma anticoagulant proteins include:

Answer 354

1. serpins: inhibit activate coagulation factors 2. protein C system: directed against cofactors V and VIII3. Antithrombin III (AT III): main inhibitor of thrombin and Xa

Question 355

heparin accelerates which anti-coagulant protien by 2000 fold?

Answer 355

AT III

Question 356

Function of activated protein C

Answer 356

destroys factors V and VII** limiting its own activation** depn on thrombin and entohelial cofactor, thrombomodulin

Question 357

What is plasmin?

Answer 357

primarily responible for degradation of fibrin

Question 358

Plasmin exists in plasma as the zymogen

Answer 358

plasminogen

Question 359

What zymogen has a high affinity for fibrin?

Answer 359

plasminogen**as well as tissue plaminogen activator (tPA)

Question 360

What ist he main physiologic inhibitor of plasmin

Answer 360

alpha 2 antiplasmin (alpha 2-AP)**competes with the binding of plasminogen to fibrin and clot contains equal amounts of both glycoproteins

Question 361

Why does a blodo clot not lyse spontaneously?

Answer 361

b/c of molar balance betwen alpha 2- antiplasmin and plaminogen

Question 362

What is a potent stimulus for release of endothelial tpA

Answer 362

stasis of blood upstream fro teh occluded vessel

Question 363

What is the most important factor that determines the rate of fibrinolysis?

Answer 363

the rate of fibrin formation

Question 364

Breeds that have prekallikrein deficiency?

Answer 364

miniature hroses in USbelgian horses in Canada

Question 365

Abnormal blood parameters from horses with prekallkrein deficiency?

Answer 365

prolonged aPTTsnormal PTs

Question 366

What is the mode of inheritance of prekallikrein deficiency in horses?

Answer 366

likely autosomal recessive**underlying genetic mutation has not been determined

Question 367

Measurable deficiencies in factor XI activity have been reported in what breeds?

Answer 367

Holstein cattle (US, Canada & UK)Japanese Black cattle

Question 368

Activation of factor XI occurs in what step of coagulation pathway?

Answer 368

intrinsic pathway ** second step

Question 369

Factor XI deficient Holsteins show what clotting time abnormalities?

Answer 369

normal PTsprolonged aPTTs

Question 370

How is Factor XI deficiency inherited?

Answer 370

autosomal recessive trate

Question 371

What gene encodes factor XI?

Answer 371

F11

Question 372

What spp & breeds have Factor VIII deficiency?

Answer 372

1. horses: thoroughbreds, standardbreds, quarter horses, tennessee walking horses2. cattle: hereferods & japanese brown cattlesheep: alpine white sheep

Question 373

Coagulation panel results in a patient with Factor VIII deficiency:

Answer 373

normal PTprolonged aPTT

Question 374

Clinical signs of factor VIII deficiency (hemophilia A)

Answer 374

inappropriate bleeding incidents: epsitaxispetechial hemorrhageformation of IM hematomashemoarthorsishemopericardiumhemoperitoneiumprolonged, life-threaning bleeding at sites of invasiv procedures, umbilical cords and castration

Question 375

Animals with true Factor VIII deficiency should also have normal levels of what other factor?

Answer 375

vWF

Question 376

Factor VIII deficiency (Hemophilia A) inheritance

Answer 376

X linked and recessive** clinical dz reportedin male horses and cattle

Question 377

Treatment of factor VIII deficiency in humans

Answer 377

factor replacement therapy

Question 378

Prognosis for animals with factor VIII deficiency (hemophilia A)

Answer 378

poor**most owners choose euthanasia

Question 379

Von willebrand factor function

Answer 379

stablizes factor VIII in circulationpromotes plt endothelial adhesion at site sof vascular injury

Question 380

Von willebrand factor deficiency reported in

Answer 380

-a QH filly-simental cattle- 10 mo Heifer

Question 381

What are the vitamin K dependent coagulation factors?

Answer 381

factor II, VII, IX and X

Question 382

Deficiency of vitamin K dependent factors have been reported in?

Answer 382

5 lambs from a flock of rambouillet sheep

Question 383

coagulation profile of vit K deficient coagulation factors:

Answer 383

prolonged aPPT and pT

Question 384

Suggested genetic mutation results in vit K deficient coagulation factors in sheep?

Answer 384

autosomal recessive**single nucleotide polymorphism exon 4 of the gene encoding y-glutamyl carboxylase (GGCX)**mutation creates a STOP codon leading to premature termination of the protein

Question 385

Fibrinogen deficiency has been reported in what spp?

Answer 385

Saanen kid (goat)border leicester lamb

Question 386

Clinical coagulation tests for vitamin K dependent coagulation factors cannot be differentiated from what other deficiency in the coagulation cascade?

Answer 386

fibrinogen deficiency

Question 387

Define Thrombasthenias

Answer 387

rareinherited defectsin platelet functionresult in spontaenous or excessive bleeding

Question 388

Thrombastenias coagulation panel

Answer 388

normal aPTT, PT and plt count**INC plt or buccal mucosal bleeding times

Question 389

Glanzmann Thrombasthenia

Answer 389

quantitative or qualitative deficiencies of the plt membrane integrin alphaIIbBEta3 (glycoprotein IIb-IIIa)-alpha11b and Beta3 proteins: expressed by separate genes & form heterodimers that bind fibrinogen and mediate plt aggregation

Question 390

Glanzmann Thrombasthenia: platelet dysfunction

Answer 390

unable to aggregate in response to collagen or ADP ** blood forms loose clots with limited serum separation & decreased tensile strength

Question 391

Glanzmann Thombasthenia has been reported in what breeds?

Answer 391

-thoroughbred cross gelding-- homozygous mutation in exon2-Quarter horse filly- heterozygous or exon 2 missense mutation & 10 base pair deletion in second ITGA2B allele-Peruvian Paso horse-Oldenburg filly: homozygous for distinct missense mutation in exon 2

Question 392

Recommendations for owners of Glanzmann thrombasthenia horses?

Answer 392

-alert for signs of bleeding requiring supportive care-regularly monitor for anemia

Question 393

Atypical equine thrombasthenia is a case report in

Answer 393

1 thoroughbred filly

Question 394

What is atypical equine thrombasthenia?

Answer 394

AET plts have significantly reduced fibrinogen binding & limited prothrombinase activity & reduced factor V released from AET plt alpha grnaules

Question 395

Simmental Hereditary Thrombopathy: blood has what:

Answer 395

diminished clot retractionreduced aggregation in response to ADP or collagen**SHT platelets fail to aggregate in response to the calcium ionophore A23187

Question 396

Bovine Chediak Higashi Syndrome is characterized by

Answer 396

abnormal secretory granules in plts, leuks, & melanocytes

Question 397

Bovine Chediak Higashi syndrome has been identified in what breeds?

Answer 397

HolsteinBrangusJapanese Black cattle

Question 398

Pathogenesis of Bovine Chediak Higashi syndrome that leads to bleeding

Answer 398

Dense granules have markedly reduced the ADP content & release disproportionately less ADP-- plts aggregate normally in reponse to ADP**CHS plts have slow & transient aggregation in response to collagen

Question 399

Bovine Chediak Higashi syndrome gene mutation

Answer 399

Missense mutation in gene encoding protein lysosomal trafficking regulator LYST**autosomal recessive- 8.8% Japanese Black cattle were carriers

Question 400

Clinical signs of Bovine Chediak Higashi Syndrome

Answer 400

-hypopigmentation of skin, hair & eyes-photophobia-increased susceptibility to infection**present with infections or inapprorpiate bleeding

Question 401

Define vasculitis

Answer 401

inflammation and necrosis of blood vessel walls, regardless of size, location or cause

Question 402

Cause of vasculitis in large animals:

Answer 402

secondary to manifestation of a primary infectious, toxic or neoplastic disorder**has characteristics of the hypersensitivity vasculitis in humans

Question 403

Clinical manifestations of vasculitis

Answer 403

-demarcated areas of dermal or subcutaneous edema- infarction, necrosis and exudation-hyperemia, petechial and ecchymotic hemorrhages-ulceration of mucous membranes-->besides skin can occur in any organ system: lameness, colic, dyspnea, and/or ataxia

Question 404

Name examples of vasculitis syndromes with predominant cutaneous involvement

Answer 404

equine purpura hemorrhagica (EPH)equine viral arteritis (EVA)equine infectious anemia (EIA)equine granulocytic anaplasmosis (EGA)

Question 405

Definitive diagnosis of vasculitis involves:

Answer 405

histopathology of involved vessels**full thickness punch biopsies

Question 406

Define purpura hemorrahgic

Answer 406

noncontagious disease of horses characterized by vasculitis leading to extensive edema and hemorrhage of the mucosa and subcutaneous tissues

Question 407

What bacterial organisms have been known to cause/lead to purpura hemorrhagica?

Answer 407

Streptococcus equi (**Vaccination against S. equi)Streptococcus zooepidemicusRhodococcus equiCorynebacterium pseudotuberculosis

Question 408

Clinical signs of equine purpura hemorrhagic usually occur within what time frame of development of respiratory infection?

Answer 408

2 to 4 weeks

Question 409

What age range are commonly affected by equine purpura hemorrhagica?

Answer 409

young to middle aged horses (mean 8.4 years, range 6m to 19 yrs)

Question 410

Predominant clinical signs of purpura hemorrhagica

Answer 410

subcutaneous edema of all four limbslethargyanorexiafever hemorrhages on mucous membranestachycardia(**other C/S: tachypnea, reluctance to move, serum exudation from the skin, colic, epistaxis**).

Question 411

The predominant laboratory abnormalities seen with Equine purpura hemorrhagica?

Answer 411

anemianeutrophiliahyperproteinemiahyperfibrinogenemiahyperglobulinemiaelevated mm enzymesthrombocytopenia--Rarely seen

Question 412

Skin biopsy of equine purpura hemorrhagica

Answer 412

acute luekocytoclastic or nonluekocytoclastic vasculitis with necrosis of blood vessels-marked dermal and subcu hemorrhage, protein rich edema, multifocal areas of dermal infarction

Question 413

What immune complex deposition on blood vessel walls have been identified in Equine purpura hemorrhagica?

Answer 413

IgM or IgA ,strep M protein (type III hypersensitivity rxn)

Question 414

Horses with infarctive purpura hemorrhagica present with clinical signs of:

Answer 414

colic lamenessmuscle swellingstiffness

Question 415

Horses with infarctive purpura hemorrhagica may have what changes on bloodwork?

Answer 415

high CK values

Question 416

What is the recommended treatment for purpura hemorrhagica?

Answer 416

Antibiotics (penicillin)hydrotherapy/limb bandages/light exercise (handwalks)IV fluidsProlonged treatment with corticosteroids (2-4 weeks)

Question 417

Corticosteroid treatment regimen recommended for treatment of Purpura hemorrhagica?

Answer 417

**minimum of 2 to 4 weeks* dexamethasone: 0.04 to 0.2 mg/kg IV q24 (morning)*prednisolone: 0.5 to 1 mg/kg PO q24 (morning)

Question 418

Possible complications of purpura hemorrhagica

Answer 418

skin sloughinglaminitiscellulitispneumoniadiarrhea

Question 419

What is the prognosis for purpura hemorrhagica?

Answer 419

fair with early aggressive therapy & supportive care-retrospective: 53 horses: mortality rate of 7.5%

Question 420

Equine viral arteritis (EVA) is an infectious disease characterized by:

Answer 420

pan vasculitisedemahemorrhageabortion in pregnant mares

Question 421

Equine viral arteritis describe the infectious organism:

Answer 421

enveloped, spherical, postive stranded RNA virus (diamter 50 to 70 nm)-nonarthropod borne virus

Question 422

Equine viral arteritis virus epidemiology

Answer 422

order: nidoviralesfamily: ARterivridae

Question 423

Equine viral arteritis clinical signs:

Answer 423

pyrexialethargyanorexialimb edemastiffnessrhinorrheaepiphoraconjunctivitisrhinitisabortionedema (periorbital, supraorbital, ventrum, mammary gland, scrotum or limbs)Other: urticarial rash, abortion, resp signs, ataxia, mucosal eruptions, submaxillary lymphadenopathy and intermandibular and shoulder edema

Question 424

With natural exposure to Equine viral arteritis (EAV) , what is theepidemic abortions rate?

Answer 424

abortion rate: <10% to >60%

Question 425

Abortion due to Equine viral arteritis occurs in what months of gestation?

Answer 425

3 to 10 months

Question 426

Do mares infected with Equine viral arteritis become chronic shedders and have fertility problems?

Answer 426

No

Question 427

What is the pathogenesis of EAV in blood vessels?

Answer 427

localized in endothelium, medial myocytes and pericytes-- virus causes vasculitis with necrosis of the tunica media, abundant vascular and perivascular lymphocyte & lesser granulocytic infiltration with karyorrhexis, loss of endothelium and formation of large fibrinocellular stratified thrombi

Question 428

How is EAV transmitted?

Answer 428

aerosols from respiratory, urinary, or reproductive tract secretions of acutely affected animsl**semen from persistent infected stallions

Question 429

Does EAV remain viable in frozen semen?

Answer 429

Yes (fresh, chilled and frozen semen

Question 430

Is transmission of EAV through fomites possible?

Answer 430

yes

Question 431

With natural exposure to EAV does it cause short or long term immunity?

Answer 431

Long-term immunity

Question 432

How long does it take for mares/geldings to eliminate the infection?

Answer 432

w/in 60 days

Question 433

What percentage of acutely infected stallions become persistently infected?

Answer 433

30 to 60%

Question 434

In stallions where is the virus maintained?

Answer 434

w.in the accessory organs: ampullae, vasa deferentia

Question 435

Seroprevalence for EAV is common is what breeds?

Answer 435

standardbredwarmblood breeds** has been recently estab. in Quarter horses

Question 436

How can EAV be diagnosed?

Answer 436

virus isolationviral nucleic acid (PCR)serology

Question 437

How can a diagnosis of EVA be made on serology?

Answer 437

fourfold or more increase din serum neutralizing antibodies between acute and convalescent samples (3 weeks apart)

Question 438

Stallions that test with a positive titer of 1:4 should be tested for persistent infection by virus isolation from what sample?

Answer 438

sperm rich ejaculate

Question 439

Prior to vaccination of stallions for EAV, what should be performed?

Answer 439

Should have serum submitted to a US department of Agriculture (USDA) approved laboratory to confirm seronegative status

Question 440

After a stallion is vaccinated for EAV, what should then be performed?

Answer 440

Horses should be isolated for 28 days **can potentially shed the virus (MLV vaccine)

Question 441

Is there evidence that vaccinated stallions become carriers?

Answer 441

No

Question 442

Anaplasma phagocytophila describe appears within neutrophils/eosinophils

Answer 442

vacuoles/ inclusion bodies (1.5 to 5 miccrom in diameter) in cytoplasm-pleomorphic-contain one or more coccobacillus or large granular aggregates (morulae)

Question 443

Anaplasma phagoctyophila cases in horses most commonly occur during which season (s)

Answer 443

late fallwinterspring

Question 444

Is Anaplasma phagocytophila considered zoonotic?

Answer 444

Yes- human infection can occur via tick bite or transmission of infected blood

Question 445

What are the vectors of Anaplasma phagocytophila ?

Answer 445

Ixodes pacificus- CaliforniaIxodes scapularis- eastern and midwestern USIxodes ricinus- Europe

Question 446

What are potential/proposed reservoirs for Anaplasma phagocytophila?

Answer 446

white footed micechipmunkswhite tailed deerdusky footed wood ratscervidslizardsbirds

Question 447

Anaplasma phagocytophila: observed pancytopenia is thought to be caused by:

Answer 447

cytolysisinduction inflammationcell sequestrationconsumptiondesruction

Question 448

Clinical signs of Anaplasma phagocytophila

Answer 448

early signs: FUO, partial anorexiareluctance to movefever (102.9-106.3F)mild to mod tachycardia (50 to 60 bpm)decreased appetitelimb edemapetechiationicterusweaknessataxiarecumbency

Question 449

What is the incubation period for Anaplasma phagocytophila?

Answer 449

Believed to be less than 14 days

Question 450

What is the prepatent period for Anaplasma phagocytophila in experimental exposure to infected ticks or inoculation with infected blood?

Answer 450

experimental exposure to infected ticks: 8 to 12 daysinoculation with infected blood: 3 to 10 days

Question 451

Anaplasma phagocytophila clin path abnormalities:

Answer 451

anemialeukopenia characterized by granulocytopenia and lymphopeniathrombocytopenia

Question 452

What is the definitive diagnosis of Anaplasma phagocytophila?

Answer 452

morulae w/in the cytoplasm of neutrophils and eosinphilsORpositive PCR assay in peripheral blood

Question 453

False positive Anaplasma phagocytophila morulae can occur with

Answer 453

Dohle bodies in toxic neutrophils

Question 454

What does a four fold increase in IFA titer for Anaplasma phagocytophila mean?

Answer 454

confirms recent exposure

Question 455

Pathologic findings of Anaplasma phagocytophila

Answer 455

petechiae and ecchymosis of subcu tissueedema of ventral abdomen, limbs and prepuceproliferative and necrotizing vasculitis, thromboses and perivascular cuffing in sucu tissue, fascia, kidneys, heart, brain, lungs, ovaries and testes

Question 456

What is the treatment of choice for Anaplasma phagocytophila?

Answer 456

oxytetracyline: 7 mg/kg or doxycycline

Question 457

Anaplasma phagocytophila if left untreated, resolves in what time frame?

Answer 457

in 2 to 3 weeks if left untreated

Question 458

Prevention for Anaplasma phagocytophila?

Answer 458

tick control

Question 459

Mechanisms of thrombocytopenia

Answer 459

1. decreased production2. abnormal sequestration (spleen)3. inc consumption or destruction

Question 460

At what level of thromboctyopenia can spontaneous hemorrhage start to occur?

Answer 460

<10,000/uL

Question 461

When is prolonged bleeding from wounds, injections, or surgical procedures and propensity to form hematomas after minor trauma seen?

Answer 461

<40,000/uL

Question 462

Persistent life-threatening hemorrhage due to thrombocytopenia can be treated with transfusion of what biologic products?

Answer 462

fresh whole bloodplatelet rich plasma (preferable)

Question 463

Causes of Immune mediated thrombocytopenia

Answer 463

1. primary2. secondary drug administration, neoplasia or other immunologic disorders (EIA lymphoma, autoimmune hemolytic anemia)

Question 464

Thrombocytopenia in a horse, with obvious primary disease should the prompt a workup to rule out what disease process?

Answer 464

DIC

Question 465

Alloimmune thrombocytopenia of neonates include clinical signs of

Answer 465

depressionloss of sucklea bleeding tendencyblood lossrapidly developing anemia d/t profound thrombocytopenia

Question 466

Alloimmune thromboctyopenia in foals results from what?

Answer 466

*multiparous dams* immunoglobulins form mare, found in her plasma, serum and milk bind to the foal's platelets

Question 467

Differentials for alloimmune thrombocytopenia in foals include

Answer 467

neonatal sepsisneonatal maladjustment syndromeneonatal isoerythrolysis

Question 468

Laboratory abnormalities associated with alloimmune thrombocytopenia

Answer 468

severe thrombocytopenia (<40,000/L)prolonged bleeding timeabnormal clot retractionnormal thrombin time, PT, APTT, plasma fibrinogen+/- INC FDPs (fibrin degradation products)

Question 469

In IMTP what is seen on bone marrow aspirate or biopsy?

Answer 469

megakaryocytic hyperplasia

Question 470

Definitive diagnosis of IMTP

Answer 470

demonstration of INC quantities of plt assoc IgG or C3 or anti-plt activity in serum**flow cytometry (detect plt surface assoc IgG (PSAIgG)

Question 471

Without PSAIgG testing, the diagnosis of IMTP can be made based on:

Answer 471

small vessel hemorrhagic diathesis and severe thrombocytopenia in a horse with normal coagulation times & no other evidence of DIC**response to therapy-- supports diagnosis

Question 472

pathogenesis of IMTP

Answer 472

plt destruction mediated by antibodies coating the plt surface that cause premature plt removal from circulation by MPS

Question 473

In secondary IMTP pathogenesis is

Answer 473

Ig bound to plt surface is part of an immune complex composed of antibody that directed against a drug, microbe or neplastic ag**nonspecifically attached to plt Fc receptor

Question 474

Thromboctypenia caused by the chrysotherapy (gold therapy) may persist for how long after discontinuation of therapy?

Answer 474

weeks to years

Question 475

Why is the spleen the major site of plt phagocytosis?

Answer 475

1. much antiplt antibody is secreted locally2. more than 30% of circulating plts are normally stored there3. stagnant splenic blood flow allows sensitized plts to pass slowly through a dense network fo phagocytic cells

Question 476

Effect of treatment with corticosteroids for IMTP?

Answer 476

improve capillary integrityimpair clearance by the MPSdecrease number and avidity of macro Fc receptorsimpair antiplt ab productionimpede plt ab interactionsinc thrombocytopoeisis

Question 477

Blood coagulation proceeds with what 3 key reactions:

Answer 477

1. formation of activated factor X2. formation of thrombin3. formation of fibrin

Question 478

The pathologic process of DIC is described as

Answer 478

widespread fibrin deposition in the microcirculation and development ofhemorrhagic diathesis caused by the consumption of procoagulants and hyperactivity of fibrinolysis

Question 479

DIC in large animals is described in association with what other disease processes:

Answer 479

localized or systemic septic processesneoplasiaGi disordersrenal diseasehemolytic anemia

Question 480

what renal disease is caused by DIC

Answer 480

ischemic cortical necrosis followed by acute tubular necrosis

Question 481

Negative effects of DIC can be seen in which organs?

Answer 481

GIT (microvascular thrombosis)Renal (acute tubular necrosis)Pulmonary (micorvascular thombrosis, uncommon in lg animals)CNS (neurologic signs, uncommon in lg naimals)Lamina (digital ischemia)

Question 482

What diseases must be differentiated from DIC:

Answer 482

IMTPwafarin toxicosis (horses)moldy sweet clover toxicosisinherited coagulation abnormalities

Question 483

Diseases initiate DIC by what 2 major mechanisms?

Answer 483

1. generation of excessive procoagulant activity within the blood 2. contact of blood with abnormal surfaces

Question 484

Gram negative endotoxins stimulate DIC through

Answer 484

direct factor XII activationcytokine production by mononuclear phagocytes

Question 485

What is the net result of any triggering mechanism for DIC is

Answer 485

exaggerated generation of systemic thrombin which causes widespread microcirculatory thrombosis

Question 486

What are the effects of thrombin in DIC:

Answer 486

-activates factor XIII to render fibrin more resistant to fibrinolysis-enhances cofactor actiity of factors V and VIII-induces plt aggregation and exposure of plt phospholipid

Question 487

In DIC plasmin contributes to factor consumption by destorying factors:

Answer 487

V, VIII, XIIa, IX, XI**in addition to fibin and fibrinogen

Question 488

Plasmin contributes to factor consumption in DIC by destroying factors

Answer 488

V, VIII, XIIa, IX and XI

Question 489

The macrophage system in the liver and spleen play a vital role in pathogenesis of DIC, how?

Answer 489

Tissue fixed macro normally remove FDPs & activated clotting factors, until their rate of formation exceeds the ability of ht eMPS to clear them

Question 490

IV fluid administration in the treatment of DIC

Answer 490

helps prevent organ dysfunction after microvascular thrombosis & correct existing acid-base or electrolyte imbalances

Question 491

Flunixin meglumine treatment in DIC

Answer 491

mitigates the effects of endotoxin caused by eicosanoids an dused at dose of 0.25 mg/kg IV q8h

Question 492

Corticosteroids int he tretmetn of DIC

Answer 492

reduce phagocytic action of the MPS and potetniate hte vasoconstrito effects of catechoalmines

Question 493

What can be administered if DIC is causing life threatening hemorrhage (rare in lg animals)?

Answer 493

fresh plasma (15 to 30 ml/kg) to replace used coagulant and anticoagulant proteins

Question 494

What can be administered to stall disseminated microvascular thrombosis that precipitates organ failure in DIC?

Answer 494

low molecualr weight heparin

Question 495

For heparin to work in the treatment of DIC, what must be true?

Answer 495

appropriate ammounts of ATII, which is necessary for heparin to work and is often depleted by DIC

Question 496

What are clinical signs of warfarin toxicosis in horses?

Answer 496

hematomasecchymosis of mucous membranesepistaxishematuria

Question 497

How are horses potentially exposed to warfarin?

Answer 497

rodenticides ** used to be a tx for horses with navicular dz

Question 498

Coagulation panel abnormalities with warfarin toxicosis

Answer 498

prolongation of PT (earliest sign)APTT becomes prolonged eventually+/- blood loss anemia and hypoproteinemia

Question 499

The diagnosis of warfarin toxicosis is made by:

Answer 499

history of exposureclinical signs of large vessel hemorrhagic dithesisprlonged PT w/ or w/o APTT

Question 500

Mechanism of Warfarin toxicsosi

Answer 500

-competitive inhibition of vitamin K-- necessary for liver production of clotting factors II, VII, IX and X