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Cardiology.cv.hemolymph Flashcards

1
Q

Right atrium is made up of what two parts?

A

Sinus venarum cavarum: veins emptyAuricle: conical out pouching

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2
Q

What are the structures that drain into the right atrium?

A

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

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3
Q

What is the ova fossa?

A

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

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4
Q

Leaflets of the tricuspid valve

A
  1. Septal2. Parietal: lies on the right margin3. Angular: between the AV opening & right outflow tract
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5
Q

What the the pulmonary valve leaflets?

A

RightLeft Intermediate

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6
Q

What are the mitral valve leaflets?

A
  1. Septal2. Parietal
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7
Q

The interventricular septum is made up of what tissues?

A

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

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8
Q

Where is the location of the sinus of Valsalva?

A

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

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9
Q

Where do the 2 coronary arteries originate?

A

The sinus of valsalva

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10
Q

The ductus arteriosus connects what?

A

Joints the pulmonary artery to the descending aorta in the fetus

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11
Q

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

A

Vagal tone: reducingSympathetic tone: increasing

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12
Q

Systole is made up of:

A

Isovolumetric contraction phase & ventricular ejection

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13
Q

Diastole is made of:

A

Isovolumic relaxation phaseRapid filling phaseDiastasisAtrial contraction

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14
Q

What marks the beginning and ending of systole?

A

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

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15
Q

What makes up the phase of isovolumetric diastole?

A

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

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16
Q

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

A

Determined by the rate of active relaxation of the myofibers

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17
Q

When do mitral valve leaflets open?

A

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

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18
Q

Describe/define diastesis (of diastole)

A

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

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19
Q

The duration of diastesis is determined by?

A

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

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20
Q

S1 heart sounds

A

Closure of the AV valvesmechanical onset of systole

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21
Q

S2 heart sound

A

Closure of the semilunar valves**end of systole

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22
Q

S3 heart sound

A

Early ventricular filling **rapid filling phase of diastole

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23
Q

S4 heart sound

A

Atrial contraction

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24
Q

Systolic function refers to

A

Ability of the ventricles to contract and eject blood

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25
Q

Diastolic function refers to

A

The ability of the ventricles to adequately relax and fill

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26
Q

What are the major factors that affect ventricular systolic function

A

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

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27
Q

Events that cause an increase in pre-load?

A

ExerciseAnaemiaFeverPregnancy

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28
Q

Factors that affect myocardial contractility

A

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

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29
Q

Ventircular filling is affected primarily by:

A

Venous returnAtrioventricular valve functionAtrial functionPericardial compliance Heart rateMyocardial relaxationCompliance

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30
Q

Inadequate end-diastolic volume will result in:

A

Inadequate stroke volume**reduced coronary perfusion

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31
Q

What are the two major factors that affect ventricular diastolic performance

A

Chamber complianceMycoardial relaxation

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32
Q

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

A

A greater filling pressure

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33
Q

Examples of conditions that cause a decrease in ventricular compliance

A

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

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34
Q

Myocardial relaxation may change acutely in response to

A

HypoxiaIschaemiaAltered afterloadTachycardiaCatecholaminesVarious pharmacological agents

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35
Q

What are disease processes that produce diastolic dysfunction

A

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

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36
Q

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

A

Atrial fibrillationVentricular tachycardiaHigh degree AV conduction block

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37
Q

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

A

Atrial preloadImpedance to atrial emptyingInotropic state of atrial myocytesAtrial compliance

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38
Q

What are the 3 methods commonly used to determine cardiac output

A
  1. Fick method2. Thermodilutioon method (overestimates cardiacoutput)3. Lithium dilution method
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39
Q

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

A

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

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40
Q

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

A

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

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41
Q

Indexes of diastolic function on M-mode echocardiography?

A

-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

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42
Q

What is starlings law of the heart?

A

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

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43
Q

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

A

Heart rate (chronotropic effects)

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44
Q

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

A

Heart rateContractility (inotropic effects)

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45
Q

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

A

Integrated by the brain stem

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46
Q

Baroreceptors sense

A

Stretch — detect high pressure within the vascular system

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47
Q

Where are baroreceptors located? that detect high pressure

A

Within the aortic arch and carotid sinus

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48
Q

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

A

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

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49
Q

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

A

Glossopharyngeal and vagal nerves

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50
Q

Glossopharyngeal and vagal nerves terminate where

A

Nucleus tractus solitarius (NTS)

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51
Q

Alpha 2 adrenoreceptor agonists effect o nheart

A

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

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52
Q

Cardiac glycosides (digoxin) cause

A

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

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53
Q

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

A

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

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54
Q

Vasomotor nerves are controlled by which system and hormone?

A

Sympathetic nerves— Noradrenaline on alpha 1 adrenoreceptors

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55
Q

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

A

M2 muscarinic receptors

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56
Q

Renin is produced by what cells?

A

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

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57
Q

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

A

Angiotensin converting enzyme (ACE)Angiotensin II

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58
Q

Where is angiotenson converting enzyme located?

A

Endothelial cells— especiallly in the lung

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59
Q

What is synthesized in response to angiotensin II?

A

Aldosterone

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60
Q

Aldosterone MOA

A

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

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61
Q

Hormone: AdrenalineCV and Renal effects:

A

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)

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62
Q

Hormone: Angiotensin IICardiovascular and renal effects

A

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)

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63
Q

Hormone: Antidiuretic hormone (vasopressin)Cardiovascular and renal effects

A

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

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64
Q

Hormone: Aldosterone Natriuertic peptides (ANP & BNP)

A

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

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65
Q

Define Edema

A

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

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66
Q

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

A
  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
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67
Q

What are the most common causes of increased capillary permeability?

A

traumainfectionendotoxemiahypersensitivity (allergic) vasculitis

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68
Q

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

A

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

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69
Q

CHF cause of increased hydrostatic pressure?

A

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

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70
Q

Causes of hypoproteinemia?

A
  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
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71
Q

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

A

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

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72
Q

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

A

-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

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73
Q

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

A

-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

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74
Q

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

A

-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

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75
Q

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

A

-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

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76
Q

Common causes of cardiac arrythmias in horses

A

-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)

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77
Q

Uncommon causes of cardiac arrhythmias in horses

A

-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)

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78
Q

Common causes of cardiac arrythmias in ruminants

A

-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

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79
Q

Uncommon causes of cardiac arrythmias in ruminants

A

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

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80
Q

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

A

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

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81
Q

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

A

myocarditisvalvular diseaseconduction system abnormalitiespericarditis

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82
Q

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

A

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

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83
Q

Placement of base-apex lead for ecg

A

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

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84
Q

Common causes of cardiac murmurs in horses:

A

valvular regurgitationcongenital defectsanemiaexcitementfeverfunctional murmurexercise

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85
Q

Uncommon causes of cardiac murmurs in horses

A

aortic cardiac fistulaaortopulmonary fistulacardiomyopathypericarditiscranial mediastinal abscess

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86
Q

Common causes of cardiac murmurs in ruminants

A

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

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87
Q

Uncommon causes of cardiac murmurs in ruminants

A

-cardiomyopathy-myocarditis

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88
Q

What is the graded scale of cardiac murmurs?

A

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

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89
Q

The presence of a musical murmur indicates:

A

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

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90
Q

Diastolic murmurs occur between which heart sounds?

A

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

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91
Q

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

A

patent ductus arteriosus

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92
Q

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

A

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

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93
Q

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

A

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

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94
Q

Reasons for muffled heart sounds:

A
  1. pericardial effusion: displacement of the heart from the thoracic wall by fluid2. abscess or tumor: soft tissue mass3. pneumothorax, pneumomediastinum, or emphysema: air
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95
Q

Common causes of muffled heart sounds in horses

A

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

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96
Q

Uncommon causes of muffle heart sounds in horses

A

pulmonary emphysemapneumothoraxneoplasia: mesothelioma, squamous cell carcinoma, fibrosarcoma

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97
Q

Common causes of muffled heart sounds in ruminants

A

pneumothoraxidiopathic hemorrhagic pericardial effusion

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98
Q

Common causes of exercise intolerance, weakness and syncope in horses

A

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

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99
Q

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

A

myocardial diseasecardiac arrhythmiascongenital heart defectschronic heart failure

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100
Q

define syncope

A

sudden collapse and loss of consciousness (fainting)

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101
Q

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

A

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

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102
Q

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

A

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

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103
Q

heart rates greater than 240 bpm limit cardiac output by

A

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

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104
Q

What are the most common bradyarrythmias to cause clinical signs?

A

complete heart blockadvanced second degree heart block

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105
Q

Common causes of jugular venous distention and pulsation in horses

A

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

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106
Q

Uncommon causes of jugular venous distention and pulsation in horses

A

ionophore toxicitypericarditismyocarditisventricular tachycardiasquamous cell carcinomafibrosarcomacor pulmonalechronic obstructive pulmonary diseaseoverhydration

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107
Q

Common causes of jugular venous distention and pulsation in Ruminants

A

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

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108
Q

Uncommon causes of jugular venous distention and pulsation in ruminants

A

ionophore toxicityidiopathic hemorrhagic pericardial effusionoverhydrationcranial mediastinal mass

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109
Q

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

A

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

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110
Q

Common causes of painful peripheral swellings in horses

A

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

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111
Q

Uncommon causes of painful peripheral swellings in horses

A

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

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112
Q

Common causes of painful peripheral swellings in Ruminants

A

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

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113
Q

Uncommon causes of painful peripheral swellings in ruminants

A

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

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114
Q

Common causes of enlarged lymph nodes in horses

A

strangleslymphosarcomaupper respiratory infectionCorynebacterium pseudotuberculosis lymphadenitis

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115
Q

Uncommon causes of enlarged lymph nodes in horses

A

ulcerative lymphangitisepizootic lymphangitissporadic lymphangitisglandersmelioidosisgranulomatous lymphadenitisplasma cell myelomatuberculosishemolytic uremic syndrome

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116
Q

Common causes of enlarged lymph nodes in ruminants

A

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

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117
Q

Uncommon causes of enlarged lymph nodes in ruminants

A

tuberculosissporadic bovine encephalomyelitismalignant catarrhal fever

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118
Q

Describe when the arterial pressure occurs with heart contraction

A

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

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119
Q

Common causes of abnormal peripheral pulses in horses

A

dehydrationshocktoxemiacongestive heart failureelectrolyte imbalancesacid-base disordershypertensionhypotensionexercisefeverlaminitisaortic regurgitationcardiac arrhythmias

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120
Q

Uncommon causes of abnormal peripheral pulse in horses

A

aortic cardiac fistulaaortopulmonary fistulaperipheral arteriovenous shuntpatent ductus arteriosus

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121
Q

When do hyperkinetic arterial pulses occur in patients with:

A

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

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122
Q

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

A

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

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123
Q

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

A

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

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124
Q

Common causes of abnormal puerperal pulse in ruminants

A

dehydrationshocktoxemiacongestive heart failureelectrolyte imbalancesacid-base disordersfevercardiac arrythmias

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125
Q

Uncommon causes of abnormal peripheral pulse in ruminants

A

patent ductus arteriosusaortic regurgitationperipheral arteriovenous shunt

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126
Q

Cardiac output values in resting horse range from

A

32 to 40L/min

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127
Q

What are methods to determine cardiac output?

A

Fick methodDoppler echocardiographydye dilution/ thermodilution/ litium dilution

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128
Q

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

A

perimembranous

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129
Q

VSDs are more common in which equine breeds?

A

Welsh mountain poniesArabianStandardbredQuarterhorse

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130
Q

Why do ventricular septal defects occur?

A

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

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131
Q

Describe Eisenmenger complex

A

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

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132
Q

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

A

less than 0.3

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133
Q

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

A

-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

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134
Q

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

A

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

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135
Q

define patent ductus arteriosus

A

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

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136
Q

Why does the ductus arteriosus close?

A

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

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137
Q

Clinical signs of a PDA are dependent on:

A

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

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138
Q

Describe PDA murmur

A

continuous machinery murmurs

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139
Q

Direction of PDA shunt usually occurs?

A

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

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140
Q

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

A

When pulmonary resistance equal or exceeds the systemic vascular resistance

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141
Q

When is PDA closure expected in foals?

A

by 96 hours of age

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142
Q

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

A

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

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143
Q

Define tetrology of fallot vs pentalogy of fallot

A
  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
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144
Q

Pathogenesis of tetralogy/pentology of fallot

A

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

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145
Q

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

A

tetralogy of fallot

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146
Q

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

A

<5 g/dL (unoxygenated hemoglobin)

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147
Q

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

A

oxygen administration

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148
Q

What is the most common atrial septal defect?

A

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

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149
Q

Pathogenesis of persistent foramen ovale

A

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

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150
Q

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

A

persistent foramen ovale

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151
Q

atrial septal defect murmur

A

holosystolic crescendo-decrescendo murmur at the left heart base

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152
Q

triscupid valve atresia c/s

A

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

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153
Q

Define persistent truncus arteriosus

A

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

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154
Q

Pseudotruncus arteriosus definition

A

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

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155
Q

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

A

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

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156
Q

What is Eisenmenger complex?

A

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

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157
Q

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

A

cattle

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158
Q

What defects are associated with ectopia cordis cervicalis?

A

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

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159
Q

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

A

foot abscessesrumenitisreticular abscessother septic process lead to sustained or recurrent bacteria

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160
Q

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

A

streptococciPasturella or Acitnobacillus sppTruepuerella pyogenes (formerly Arcabobacterium pyognes)

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161
Q

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

A

systolicdiastolic (most common in lg animals)or Both

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162
Q

Aortic regurgitation in horses is most commonly associated with

A

degenerative valve disease

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163
Q

pulmonary regurgitation in cattle is most commonly associated with

A

bacterial endocarditis

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164
Q

Describe aortic valve lesion murmurs

A

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

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165
Q

Signs of congestive heart failure in cattle/horses

A

tachycardiacoughingrespiratory distressjugular venous distentionsubcutaneous edemaascitesmammary vein distention (cattle)

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166
Q

describe murmur of ruptured chordae tendinae?

A

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

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167
Q

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

A

ruptured chordae tendinae

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168
Q

Describe murmur of mitral valve prolapse

A

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

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169
Q

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

A

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

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170
Q

Echo evidence of mitral valve regurgitation

A

-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

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171
Q

Tricuspid regurgitation echocardiac evidence

A

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

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172
Q

aortic regurgitation echocardiographic evidence

A

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

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173
Q

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

A

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

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174
Q

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

A

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

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175
Q

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

A

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

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176
Q

Jet lesions occur due to

A

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

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177
Q

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

A

ruptured chordae tedinaeflail valve leafletsmarked valvular thickening

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178
Q

Treatment of endocarditis can ultimately result in?

A

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

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179
Q

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

A

antibiotic with gram positive coverage

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180
Q

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

A

to prevent platelet adhesion and increased size of the valvular mass

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181
Q

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

A

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

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182
Q

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?

A

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

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183
Q

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

A

trauma to heart valvesmicroembolisminfarction**in horses

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184
Q

Define cor pulmonale

A

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

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185
Q

Pathogenesis of cor pulmonale

A

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

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186
Q

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

A

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

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187
Q

Pathogenesis of High mountain disease?

A

hypoxic vasoconstriction from high-altitude dwelling

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188
Q

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

A

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

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189
Q

What are the primary presenting clinical signs of brisket disease?

A

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

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190
Q

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

A

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

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191
Q

Horses with clinical signs of cor pulmonale?

A

RAO–> leading to cor pulmonalelabored breathingcoughingexercise intolerancewheezes ausculted bilaterally

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192
Q

Differentials for clinical signs of right sided heart failure

A

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

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193
Q

The response to hypoxia in brisket disease is dependent on:

A

amount of smooth mm in the pulmonary arteries

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194
Q

Brisket disease path:Chronic pulmonary artery hypertension causes

A

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

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195
Q

Chronic right sided heart failure can lead to what?

A

diastolic dysfunction of the left ventricle

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196
Q

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

A

Swainsonine** causes toxic mycoardial damage

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197
Q

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

A

over 6000 feet

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198
Q

In what seasons is high mountain disease most commonly seen?

A

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

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199
Q

Is cor pulmonale reversible in HMD?

A

Yes–if animal is brought to lower altitudes

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200
Q

When do cattle not have reversible cor pulmonale?

A

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

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201
Q

Selection of breeding stock to prevent HMD?

A

low or normal PAPs at altitudes above 5000 feet

202
Q

Define myocarditis

A

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

203
Q

What are common causes of bacterial myocarditis?

A

Stpahylococcus aureusStreptococcus equiClostridium chauveoeiMycobacterium spp

204
Q

What are known viral causes of myocarditis?

A

foot and mouth diseaseequine infectious anemiaequine viral arteritisequine influenzaAfrican horse sickness

205
Q

What are known parasitic causes of myocarditis?

A

strongylosiscysticercosissarcocystic infection in ruminentas

206
Q

Define cardiomyopathy

A

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

207
Q

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

A

chronic renal diseasepain assoc with chronic laminitisponies with EMS

208
Q

Dilated cardiomyopathy is associated with:

A

-ventricular dilationincreased ventricular massdecreases systolic function

209
Q

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

A
  1. red holstein gene in Holstein Friesan cattle2. curly hair coat in polled herefords and in Japanese black calves
210
Q

What toxic components can cause cardiomyopathy?

A

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

211
Q

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

A

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

212
Q

Differentials for causes of dilated cardiomyopathy

A
  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
213
Q

Differential diagnosis for dilated cardiomyopathy?

A

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

214
Q

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

A

activation of renin-angiotensin aldosterone system & iNC arterial resistance

215
Q

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

A

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

216
Q

Microscopic abnormalities associated with cardiomyopathy

A
  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
217
Q

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

A

administration of Vit E

218
Q

Why are corticosteroids controversial in treatment of cardiomyopathy?

A

Possible viral recruidescence if the cause is viral

219
Q

What are therapeutic strategies used for treatment of dilated cardiomyopathy?

A
  1. positive inotropic agents (digoxin)2. diuretics3. vasodilators4. rest5 +/- removal of pleural or abdominal fluid
220
Q

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

A

monensin toxicosis

221
Q

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

A

1 to 2 ng/mL

222
Q

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

A

dehydrationacid-base balanceelectrolyte abnormalities

223
Q

When should the dose of digoxin be reduced in patietns?

A

with elevated creatinine or blood ure anitrogen levels

224
Q

What diuretic is most commonly used in large animals?

A

furosemide: 1 mg/kg

225
Q

Which ACE inhibitor is most effective in horses?

A

benazeprilOther ace inhibitors: quinapril, ramipril, enalapril

226
Q

Define pericarditis

A

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

227
Q

Causes of pericarditis in large animals

A

-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)

228
Q

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

A

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

229
Q

Contrast auscultation of pericarditis vs pleuritis?

A

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

230
Q

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

A
  • can be attributed to accumulation of gas and fluid in pericardium **indicative of presence of gas forming (anaerobic organisms) **grave prognosis
231
Q

Electrocardiogram abnormalities that are can be seen with pericarditis?

A
  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
232
Q

What is the safest site to perofrm a pericardiocentesis?

A

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

233
Q

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

A

Actinobacillus organisms

234
Q

What are the consequences of pericardial effusion to the heart?

A
  • 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
235
Q

Difference between effusive and constrictive pericarditis

A

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

236
Q

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

A

Eastern tent caterpillars

237
Q

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

A

less than10%

238
Q

Treatment of pericarditis in horses

A

– 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

239
Q

Why can diuretics results in worsening heart failure with pericarditis?

A

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

240
Q

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

A

black cherry trees

241
Q

What is the most common cardiac tumor in large animls?

A

lymphosarcoma

242
Q

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

A

mesotheliomasmelanomaslipomasfibrosarcomaadenocarcinomasother cacrinomassquamous cell carcinomas

243
Q

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

A

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

244
Q

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

A

1 to 4 %

245
Q

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

A

cattle younger than 30 months of age

246
Q

The prognosis for survival for cardiac neoplasia?

A

poor– death expected within 6 months

247
Q

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

A

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)

248
Q

Define aneurysms

A

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

249
Q

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

A

progression of intimal atherosclertoic lesions that has enlarged from hemorrhagecalcificationulcerationthrombus formation

250
Q

Causes of aneurysms in large animsl

A

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

251
Q

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

A

sinus of Valsalva

252
Q

Define thrombosis

A

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

253
Q

causes of thrombosis

A

traumavenous stasiscatheterization for adminsiterin gmedication or fluidsneedle penetrationindwelling acehtersthrombogenic solutionsbacterial contamination

254
Q

Secondary thrombosis causes:

A

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

255
Q

Examples of a hypercoagulable states:

A

dehydrationendotxemiaanemiahypotensionstress stasis

256
Q

Define mebolism

A

foreign material carried in the bloodstream

257
Q

In large animals, embolis most commonly occur with:

A

bacterial endocarditisthromboplhebitisomphalophlebitisparasitic arteritis

258
Q

Calves with aorto or aortoiliac thrombosis clinical signs?

A

weaknesslamenessknucklingparesisparalysis of the hindlimbsinability to risecold hindlimbslacking a femoral pulse

259
Q

Aortopulmonary rupture and fistulization occur in what breed?

A

Fresians

260
Q

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

A

thoughout to be rupture

261
Q

Unruptured aneurysms may have other complications such as

A

thrombosis or emoblization o fthe thrombus

262
Q

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

A

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

263
Q

Spontaneous thromboembolism is commonly associated with?

A

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

264
Q

What are risk factors for catehter associated thrombophlebitis

A

large intestinal diseasehypoproteinemiaendotoxemiasalmonellosisfeverdiarrhealocalled produced fluids

265
Q

Arteriosclerosis recognized in cattle is most frequently caused by:

A

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

266
Q

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

A

Strongylus vulgarus

267
Q

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

A

aorta

268
Q

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

A

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

269
Q

Atrial fibrillation is characterized by

A

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

270
Q

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

A

high resting vagal tone

271
Q

Causes of atrial fibrillation

A

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

272
Q

Define “lone Afib”

A

no undelrying cardiac disease can befound

273
Q

Cattle with atrial fibrillation usually have what undelrying disease?

A

gastrointesitnal disease

274
Q

Define paroxysmal atrial fribillation

A

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

275
Q

What is a common cause of paroxysmal atrial fibrillation inhorses?

A

transient potassium depletion associated with administration of furosemide

276
Q

What supplements are associated with atrial fibrillation in horses?

A

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

277
Q

Describe atrial fibrillation arrhythmias

A

irregularly irregular - absent 4th heart sound

278
Q

Differentiate 2nd degree AV block from atrial fibrillation

A

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

279
Q

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

A

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

280
Q

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

A

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

281
Q

What if cTnI remains elevated in horses with afib?

A

Activ emyocardial disease shoul dbe suspected

282
Q

electrocardiogram abnormalities in Afib

A

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

283
Q

Echocardiographic image that should be performed to indicate left atrial enlargement

A

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)

284
Q

Which breeds have the highest incidence of AF?

A

standardbredthoroughbreddraft horses

285
Q

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

A

mitral valve disease

286
Q

Quinidine in the treatment of atrial fibrillation:

A

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

287
Q

What are possible negative side effects of quinidine?

A

nasal edemacutaneous reactions (urticaria or wheals)laminitiscolicmarked diarrheaataxia

288
Q

Max number of consecutive doses of quinidine to administer?

A

4 doses

289
Q

When should therapy with quinidine be discontinued

A

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

290
Q

How often administer a dose of quinidine?

A

1 dose every 2 hours

291
Q

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

A

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

292
Q

Caveat to combination therapy of digoxin and quinidine?

A

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

293
Q

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

A

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

294
Q

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

A

KCL

295
Q

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

A

220 bpm

296
Q

Define ventricular tachycardia

A

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

297
Q

Clinical signs associated with ventricular tahycardia

A

exerciseintolerancesyncope episodesdepressionweaknesscolicresp distresscoughingventral edemapulmonary edema

298
Q

In cattle ventricular tachycardia occurs most frequently secondary to

A

sepsis and toxemia

299
Q

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

A

atrium and ventricle contract simultaenously

300
Q

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

A

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

301
Q

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

A

multiform VT

302
Q

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

A

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

303
Q

Diagnosis of VT is made how?

A

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

304
Q

Vtach: morphology of QRS complexes can be described as:

A

uniform (similar)vary in morphology (multiform)

305
Q

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

A

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

306
Q

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

A

rupture of the aortic root at the right sinus of valsalva

307
Q

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

A

sympathetic stimulation (increasing the amplitude of early afterdepolarizations)

308
Q

What is an important cause of sustained VT?

A

reetnry in the ventricle

309
Q

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?

A

Ventricular tachycardia leading to ventricular fibrillation

310
Q

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

A

males– usu. middle-aged at time of rupture

311
Q

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

A

GI diseasehorses– following severe hemorrhage

312
Q

Does slow, uniform VT require treatment?

A

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

313
Q

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

A

antiarrythmic therapy

314
Q

ECG findings associated with life threatening VT

A

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

315
Q

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

A

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

316
Q

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

A

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

317
Q

acute massive blood loss induces hypovolemic shock characterized by:

A

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

318
Q

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

A

within 12 to 24 hours

319
Q

Hypovolemic shock should be treated with administration of:

A

40 to 80 ml/kg of sodium containing crystalloid fluids

320
Q

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

A

2 to 4 ml/kg 7.2% sodium chloride

321
Q

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

A

crystalloid solutions distribute throughout the extracellular space

322
Q

Why is blood transfusion viewed as a temporary therapeutic procuedure?

A

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

323
Q

Describe routine blood typing crossmatch:

A

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

324
Q

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

A

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

325
Q

Severe anaphylactic reactions to blood transfusion should be treated with

A

epinphreine (0.01 to 0.02 mg/kg

326
Q

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

A

w/in 5 days

327
Q

Define hemoperitoneum

A

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

328
Q

Causes of hemoperitoneum in the horse

A

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

329
Q

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

A

76%

330
Q

What are the most common causes of hemoperitoneum in horses?

A

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

331
Q

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

A

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

332
Q

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

A

central venous pressureblood lactate concentration

333
Q

Primary goals of therapy in hemoperitoneum

A
  1. tx hypovolemic shock2. restore perfusion & O2 delivery to tissues3. correcting fluid deficits4. stopping further blood loss5. preventing complications
334
Q

Which carries the worse prognosis pre or post partum hemorrhage?

A

prepartum: 100% vspostpartum: 20% mortality

335
Q

Causes of hemothorax in neonatal foals

A

lacerated lung or vessels from fractured ribs

336
Q

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

A

no

337
Q

Causes for chronic blood loss

A

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

338
Q

Causes of GI hemorrhage

A
  1. Neoplasia Horses: gastric SCC cattle: abomasal lymphoma2. parasitism3. mucosal ulceration NSAID tox in horses abomasal ulcers: cattle
339
Q

Renal sources of chronic blood loss

A

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

340
Q

How does iron deficiency anemia develop?

A

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

341
Q

What is a good source of iron for patients?

A

good quality forages

342
Q

NSAID pathogenesis in right dorsal colitis

A

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

343
Q

What 2 components are involved in hemostasis?

A
  1. coagulation2. fibrinolysisfunction: arrest bleeding from damaged blood vessel and maintain nutrient blood flow
344
Q

After a blood vessel is damaged, what occurs

A

vasoconstriction occursrapid adherence of plts to subednothelial collage

345
Q

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

A

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

346
Q

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

A

platelet factor 3

347
Q

What are zymogens?

A

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

348
Q

When is the extrinsic coagulation system activated?

A

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

349
Q

Where is tissue factor located?

A

widely dsitirbuted in most tissues (endothelial cells * monocytes

350
Q

When is intrinsic coagulation system activated?

A

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

351
Q

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

A

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

352
Q

What is thrombin generated from?

A

formation of activated factor X (Xa)

353
Q

Function of thrombin

A

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

354
Q

Examples of plasma anticoagulant proteins include:

A
  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
355
Q

heparin accelerates which anti-coagulant protien by 2000 fold?

A

AT III

356
Q

Function of activated protein C

A

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

357
Q

What is plasmin?

A

primarily responible for degradation of fibrin

358
Q

Plasmin exists in plasma as the zymogen

A

plasminogen

359
Q

What zymogen has a high affinity for fibrin?

A

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

360
Q

What ist he main physiologic inhibitor of plasmin

A

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

361
Q

Why does a blodo clot not lyse spontaneously?

A

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

362
Q

What is a potent stimulus for release of endothelial tpA

A

stasis of blood upstream fro teh occluded vessel

363
Q

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

A

the rate of fibrin formation

364
Q

Breeds that have prekallikrein deficiency?

A

miniature hroses in USbelgian horses in Canada

365
Q

Abnormal blood parameters from horses with prekallkrein deficiency?

A

prolonged aPTTsnormal PTs

366
Q

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

A

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

367
Q

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

A

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

368
Q

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

A

intrinsic pathway ** second step

369
Q

Factor XI deficient Holsteins show what clotting time abnormalities?

A

normal PTsprolonged aPTTs

370
Q

How is Factor XI deficiency inherited?

A

autosomal recessive trate

371
Q

What gene encodes factor XI?

A

F11

372
Q

What spp & breeds have Factor VIII deficiency?

A
  1. horses: thoroughbreds, standardbreds, quarter horses, tennessee walking horses2. cattle: hereferods & japanese brown cattlesheep: alpine white sheep
373
Q

Coagulation panel results in a patient with Factor VIII deficiency:

A

normal PTprolonged aPTT

374
Q

Clinical signs of factor VIII deficiency (hemophilia A)

A

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

375
Q

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

A

vWF

376
Q

Factor VIII deficiency (Hemophilia A) inheritance

A

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

377
Q

Treatment of factor VIII deficiency in humans

A

factor replacement therapy

378
Q

Prognosis for animals with factor VIII deficiency (hemophilia A)

A

poor**most owners choose euthanasia

379
Q

Von willebrand factor function

A

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

380
Q

Von willebrand factor deficiency reported in

A

-a QH filly-simental cattle- 10 mo Heifer

381
Q

What are the vitamin K dependent coagulation factors?

A

factor II, VII, IX and X

382
Q

Deficiency of vitamin K dependent factors have been reported in?

A

5 lambs from a flock of rambouillet sheep

383
Q

coagulation profile of vit K deficient coagulation factors:

A

prolonged aPPT and pT

384
Q

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

A

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

385
Q

Fibrinogen deficiency has been reported in what spp?

A

Saanen kid (goat)border leicester lamb

386
Q

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

A

fibrinogen deficiency

387
Q

Define Thrombasthenias

A

rareinherited defectsin platelet functionresult in spontaenous or excessive bleeding

388
Q

Thrombastenias coagulation panel

A

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

389
Q

Glanzmann Thrombasthenia

A

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

390
Q

Glanzmann Thrombasthenia: platelet dysfunction

A

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

391
Q

Glanzmann Thombasthenia has been reported in what breeds?

A

-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

392
Q

Recommendations for owners of Glanzmann thrombasthenia horses?

A

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

393
Q

Atypical equine thrombasthenia is a case report in

A

1 thoroughbred filly

394
Q

What is atypical equine thrombasthenia?

A

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

395
Q

Simmental Hereditary Thrombopathy: blood has what:

A

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

396
Q

Bovine Chediak Higashi Syndrome is characterized by

A

abnormal secretory granules in plts, leuks, & melanocytes

397
Q

Bovine Chediak Higashi syndrome has been identified in what breeds?

A

HolsteinBrangusJapanese Black cattle

398
Q

Pathogenesis of Bovine Chediak Higashi syndrome that leads to bleeding

A

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

399
Q

Bovine Chediak Higashi syndrome gene mutation

A

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

400
Q

Clinical signs of Bovine Chediak Higashi Syndrome

A

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

401
Q

Define vasculitis

A

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

402
Q

Cause of vasculitis in large animals:

A

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

403
Q

Clinical manifestations of vasculitis

A

-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

404
Q

Name examples of vasculitis syndromes with predominant cutaneous involvement

A

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

405
Q

Definitive diagnosis of vasculitis involves:

A

histopathology of involved vessels**full thickness punch biopsies

406
Q

Define purpura hemorrahgic

A

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

407
Q

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

A

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

408
Q

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

A

2 to 4 weeks

409
Q

What age range are commonly affected by equine purpura hemorrhagica?

A

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

410
Q

Predominant clinical signs of purpura hemorrhagica

A

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

411
Q

The predominant laboratory abnormalities seen with Equine purpura hemorrhagica?

A

anemianeutrophiliahyperproteinemiahyperfibrinogenemiahyperglobulinemiaelevated mm enzymesthrombocytopenia–Rarely seen

412
Q

Skin biopsy of equine purpura hemorrhagica

A

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

413
Q

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

A

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

414
Q

Horses with infarctive purpura hemorrhagica present with clinical signs of:

A

colic lamenessmuscle swellingstiffness

415
Q

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

A

high CK values

416
Q

What is the recommended treatment for purpura hemorrhagica?

A

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

417
Q

Corticosteroid treatment regimen recommended for treatment of Purpura hemorrhagica?

A

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)

418
Q

Possible complications of purpura hemorrhagica

A

skin sloughinglaminitiscellulitispneumoniadiarrhea

419
Q

What is the prognosis for purpura hemorrhagica?

A

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

420
Q

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

A

pan vasculitisedemahemorrhageabortion in pregnant mares

421
Q

Equine viral arteritis describe the infectious organism:

A

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

422
Q

Equine viral arteritis virus epidemiology

A

order: nidoviralesfamily: ARterivridae

423
Q

Equine viral arteritis clinical signs:

A

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

424
Q

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

A

abortion rate: <10% to >60%

425
Q

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

A

3 to 10 months

426
Q

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

A

No

427
Q

What is the pathogenesis of EAV in blood vessels?

A

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

428
Q

How is EAV transmitted?

A

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

429
Q

Does EAV remain viable in frozen semen?

A

Yes (fresh, chilled and frozen semen

430
Q

Is transmission of EAV through fomites possible?

A

yes

431
Q

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

A

Long-term immunity

432
Q

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

A

w/in 60 days

433
Q

What percentage of acutely infected stallions become persistently infected?

A

30 to 60%

434
Q

In stallions where is the virus maintained?

A

w.in the accessory organs: ampullae, vasa deferentia

435
Q

Seroprevalence for EAV is common is what breeds?

A

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

436
Q

How can EAV be diagnosed?

A

virus isolationviral nucleic acid (PCR)serology

437
Q

How can a diagnosis of EVA be made on serology?

A

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

438
Q

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

A

sperm rich ejaculate

439
Q

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

A

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

440
Q

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

A

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

441
Q

Is there evidence that vaccinated stallions become carriers?

A

No

442
Q

Anaplasma phagocytophila describe appears within neutrophils/eosinophils

A

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

443
Q

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

A

late fallwinterspring

444
Q

Is Anaplasma phagocytophila considered zoonotic?

A

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

445
Q

What are the vectors of Anaplasma phagocytophila ?

A

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

446
Q

What are potential/proposed reservoirs for Anaplasma phagocytophila?

A

white footed micechipmunkswhite tailed deerdusky footed wood ratscervidslizardsbirds

447
Q

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

A

cytolysisinduction inflammationcell sequestrationconsumptiondesruction

448
Q

Clinical signs of Anaplasma phagocytophila

A

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

449
Q

What is the incubation period for Anaplasma phagocytophila?

A

Believed to be less than 14 days

450
Q

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

A

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

451
Q

Anaplasma phagocytophila clin path abnormalities:

A

anemialeukopenia characterized by granulocytopenia and lymphopeniathrombocytopenia

452
Q

What is the definitive diagnosis of Anaplasma phagocytophila?

A

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

453
Q

False positive Anaplasma phagocytophila morulae can occur with

A

Dohle bodies in toxic neutrophils

454
Q

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

A

confirms recent exposure

455
Q

Pathologic findings of Anaplasma phagocytophila

A

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

456
Q

What is the treatment of choice for Anaplasma phagocytophila?

A

oxytetracyline: 7 mg/kg or doxycycline

457
Q

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

A

in 2 to 3 weeks if left untreated

458
Q

Prevention for Anaplasma phagocytophila?

A

tick control

459
Q

Mechanisms of thrombocytopenia

A
  1. decreased production2. abnormal sequestration (spleen)3. inc consumption or destruction
460
Q

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

A

<10,000/uL

461
Q

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

A

<40,000/uL

462
Q

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

A

fresh whole bloodplatelet rich plasma (preferable)

463
Q

Causes of Immune mediated thrombocytopenia

A
  1. primary2. secondary drug administration, neoplasia or other immunologic disorders (EIA lymphoma, autoimmune hemolytic anemia)
464
Q

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

A

DIC

465
Q

Alloimmune thrombocytopenia of neonates include clinical signs of

A

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

466
Q

Alloimmune thromboctyopenia in foals results from what?

A

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

467
Q

Differentials for alloimmune thrombocytopenia in foals include

A

neonatal sepsisneonatal maladjustment syndromeneonatal isoerythrolysis

468
Q

Laboratory abnormalities associated with alloimmune thrombocytopenia

A

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

469
Q

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

A

megakaryocytic hyperplasia

470
Q

Definitive diagnosis of IMTP

A

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

471
Q

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

A

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

472
Q

pathogenesis of IMTP

A

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

473
Q

In secondary IMTP pathogenesis is

A

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

474
Q

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

A

weeks to years

475
Q

Why is the spleen the major site of plt phagocytosis?

A
  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
476
Q

Effect of treatment with corticosteroids for IMTP?

A

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

477
Q

Blood coagulation proceeds with what 3 key reactions:

A
  1. formation of activated factor X2. formation of thrombin3. formation of fibrin
478
Q

The pathologic process of DIC is described as

A

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

479
Q

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

A

localized or systemic septic processesneoplasiaGi disordersrenal diseasehemolytic anemia

480
Q

what renal disease is caused by DIC

A

ischemic cortical necrosis followed by acute tubular necrosis

481
Q

Negative effects of DIC can be seen in which organs?

A

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

482
Q

What diseases must be differentiated from DIC:

A

IMTPwafarin toxicosis (horses)moldy sweet clover toxicosisinherited coagulation abnormalities

483
Q

Diseases initiate DIC by what 2 major mechanisms?

A
  1. generation of excessive procoagulant activity within the blood 2. contact of blood with abnormal surfaces
484
Q

Gram negative endotoxins stimulate DIC through

A

direct factor XII activationcytokine production by mononuclear phagocytes

485
Q

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

A

exaggerated generation of systemic thrombin which causes widespread microcirculatory thrombosis

486
Q

What are the effects of thrombin in DIC:

A

-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

487
Q

In DIC plasmin contributes to factor consumption by destorying factors:

A

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

488
Q

Plasmin contributes to factor consumption in DIC by destroying factors

A

V, VIII, XIIa, IX and XI

489
Q

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

A

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

490
Q

IV fluid administration in the treatment of DIC

A

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

491
Q

Flunixin meglumine treatment in DIC

A

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

492
Q

Corticosteroids int he tretmetn of DIC

A

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

493
Q

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

A

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

494
Q

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

A

low molecualr weight heparin

495
Q

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

A

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

496
Q

What are clinical signs of warfarin toxicosis in horses?

A

hematomasecchymosis of mucous membranesepistaxishematuria

497
Q

How are horses potentially exposed to warfarin?

A

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

498
Q

Coagulation panel abnormalities with warfarin toxicosis

A

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

499
Q

The diagnosis of warfarin toxicosis is made by:

A

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

500
Q

Mechanism of Warfarin toxicsosi

A

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

RandomSmithChapters (15 decks)

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