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Cardiology.CV.hemolymph > Smith.Ch.37.Diseasesofhematopoeitic and Hemolymph sys > Flashcards

Smith.Ch.37.Diseasesofhematopoeitic and Hemolymph sys Flashcards

1
Q

acute massive blood loss induces hypovolemic shock characterized by:

A

tachycardia
tachypnea
cold extremities
pale mucous membranes
muscle weakness
eventual death (resulting from CV collapse)

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2
Q

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

A

within 12 to 24 hours

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3
Q

Hypovolemic shock should be treated with administration of:

A

40 to 80 ml/kg of sodium containing crystalloid fluids

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4
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

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5
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

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6
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

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7
Q

Describe routine blood typing crossmatch:

A

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

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8
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

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9
Q

Severe anaphylactic reactions to blood transfusion should be treated with

A

epinphreine (0.01 to 0.02 mg/kg

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10
Q

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

A

w/in 5 days

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11
Q

Define hemoperitoneum

A

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

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12
Q

Causes of hemoperitoneum in the horse

A

trauma
postoperative abdomina lhemorrahge
neoplasia
complications from pregnancy an dfoaling (utero-ovarian, middl euterine, external ilaic artery rupture)
organ rupture
mesenteric injury
coagulopathies
ovarian hemoatoma
systemic mayloidosis
idiopathic hemoperitoneum

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13
Q

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

A

76%

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14
Q

What are the most common causes of hemoperitoneum in horses?

A

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

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15
Q

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

A

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

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16
Q

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

A

central venous pressure
blood lactate concentration

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17
Q

Primary goals of therapy in hemoperitoneum

A
  1. tx hypovolemic shock
  2. restore perfusion & O2 delivery to tissues
  3. correcting fluid deficits
  4. stopping further blood loss
  5. preventing complications
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18
Q

Which carries the worse prognosis pre or post partum hemorrhage?

A

prepartum: 100% vs
postpartum: 20% mortality

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19
Q

Causes of hemothorax in neonatal foals

A

lacerated lung or vessels from fractured ribs

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20
Q

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

A

no

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21
Q

Causes for chronic blood loss

A

bleeding GI lesions
certain renal diseases
hemostati cdysfunction
blood sucking external parasites
haemonchosis (esp goat sand sheep)

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22
Q

Causes of GI hemorrhage

A
  1. Neoplasia
    Horses: gastric SCC
    cattle: abomasal lymphoma
  2. parasitism
  3. mucosal ulceration
    NSAID tox in horses
    abomasal ulcers: cattle
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23
Q

Renal sources of chronic blood loss

A

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

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24
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

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25
Q

What is a good source of iron for patients?

A

good quality forages

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26
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

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27
Q

What 2 components are involved in hemostasis?

A
  1. coagulation
  2. fibrinolysis

function: arrest bleeding from damaged blood vessel and maintain nutrient blood flow

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28
Q

After a blood vessel is damaged, what occurs

A

vasoconstriction occurs
rapid adherence of plts to subednothelial collage

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29
Q

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

A

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

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30
Q

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

A

platelet factor 3

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31
Q

What are zymogens?

A

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

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32
Q

When is the extrinsic coagulation system activated?

A

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

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33
Q

Where is tissue factor located?

A

widely dsitirbuted in most tissues
(endothelial cells * monocytes

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34
Q

When is intrinsic coagulation system activated?

A

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

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35
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

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36
Q

What is thrombin generated from?

A

formation of activated factor X (Xa)

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37
Q

Function of thrombin

A

catalyzed the conversion of fibrinogen to fibrin
promotes plt aggregation
enhances cofactor activities of factor V and VIII
activates factor XIII & protein C

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38
Q

Examples of plasma anticoagulant proteins include:

A
  1. serpins: inhibit activate coagulation factors
  2. protein C system: directed against cofactors V and VIII
  3. Antithrombin III (AT III): main inhibitor of thrombin and Xa
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39
Q

heparin accelerates which anti-coagulant protien by 2000 fold?

A

AT III

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40
Q

Function of activated protein C

A

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

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41
Q

What is plasmin?

A

primarily responible for degradation of fibrin

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42
Q

Plasmin exists in plasma as the zymogen

A

plasminogen

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43
Q

What zymogen has a high affinity for fibrin?

A

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

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44
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

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45
Q

Why does a blodo clot not lyse spontaneously?

A

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

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46
Q

What is a potent stimulus for release of endothelial tpA

A

stasis of blood upstream fro teh occluded vessel

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47
Q

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

A

the rate of fibrin formation

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48
Q

Breeds that have prekallikrein deficiency?

A

miniature hroses in US
belgian horses in Canada

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49
Q

Abnormal blood parameters from horses with prekallkrein deficiency?

A

prolonged aPTTs
normal PTs

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50
Q

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

A

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

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51
Q

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

A

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

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52
Q

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

A

intrinsic pathway
** second step

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53
Q

Factor XI deficient Holsteins show what clotting time abnormalities?

A

normal PTs
prolonged aPTTs

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54
Q

How is Factor XI deficiency inherited?

A

autosomal recessive trate

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55
Q

What gene encodes factor XI?

A

F11

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56
Q

What spp & breeds have Factor VIII deficiency?

A
  1. horses: thoroughbreds, standardbreds, quarter horses, tennessee walking horses
  2. cattle: hereferods & japanese brown cattle
    sheep: alpine white sheep
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57
Q

Coagulation panel results in a patient with Factor VIII deficiency:

A

normal PT
prolonged aPTT

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58
Q

Clinical signs of factor VIII deficiency (hemophilia A)

A

inappropriate bleeding incidents: epsitaxis
petechial hemorrhage
formation of IM hematomas
hemoarthorsis
hemopericardium
hemoperitoneium
prolonged, life-threaning bleeding at sites of invasiv procedures, umbilical cords and castration

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59
Q

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

A

vWF

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60
Q

Factor VIII deficiency (Hemophilia A) inheritance

A

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

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61
Q

Treatment of factor VIII deficiency in humans

A

factor replacement therapy

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62
Q

Prognosis for animals with factor VIII deficiency (hemophilia A)

A

poor
**most owners choose euthanasia

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63
Q

Von willebrand factor function

A

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

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64
Q

Von willebrand factor deficiency reported in

A

-a QH filly
-simental cattle- 10 mo Heifer

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65
Q

What are the vitamin K dependent coagulation factors?

A

factor II, VII, IX and X

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66
Q

Deficiency of vitamin K dependent factors have been reported in?

A

5 lambs from a flock of rambouillet sheep

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67
Q

coagulation profile of vit K deficient coagulation factors:

A

prolonged aPPT and pT

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68
Q

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

A

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

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69
Q

Fibrinogen deficiency has been reported in what spp?

A

Saanen kid (goat)
border leicester lamb

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70
Q

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

A

fibrinogen deficiency

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71
Q

Describe the steps in the coagulation cascade:

A
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72
Q

Define Thrombasthenias

A

rare
inherited defectsin platelet function
result in spontaenous or excessive bleeding

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73
Q

Thrombastenias coagulation panel

A

normal aPTT, PT and plt count

**INC plt or buccal mucosal bleeding times

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74
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

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75
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

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76
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

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77
Q

Recommendations for owners of Glanzmann thrombasthenia horses?

A

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

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78
Q

Atypical equine thrombasthenia is a case report in

A

1 thoroughbred filly

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79
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

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80
Q

Simmental Hereditary Thrombopathy: blood has what:

A

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

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81
Q

Bovine Chediak Higashi Syndrome is characterized by

A

abnormal secretory granules in plts, leuks, & melanocytes

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82
Q

Bovine Chediak Higashi syndrome has been identified in what breeds?

A

Holstein
Brangus
Japanese Black cattle

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83
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

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84
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

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85
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

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86
Q

Define vasculitis

A

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

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87
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

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88
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

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89
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)

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90
Q

Definitive diagnosis of vasculitis involves:

A

histopathology of involved vessels
**full thickness punch biopsies

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91
Q

Define purpura hemorrahgic

A

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

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92
Q

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

A

Streptococcus equi (**Vaccination against S. equi)
Streptococcus zooepidemicus
Rhodococcus equi
Corynebacterium pseudotuberculosis

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93
Q

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

A

2 to 4 weeks

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94
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)

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95
Q

Predominant clinical signs of purpura hemorrhagica

A

subcutaneous edema of all four limbs
lethargy
anorexia
fever
hemorrhages on mucous membranes
tachycardia
(other C/S: tachypnea, reluctance to move, serum exudation from the skin, colic, epistaxis).

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96
Q

The predominant laboratory abnormalities seen with Equine purpura hemorrhagica?

A

anemia
neutrophilia
hyperproteinemia
hyperfibrinogenemia
hyperglobulinemia
elevated mm enzymes
thrombocytopenia–Rarely seen

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97
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

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98
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)

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99
Q

what are the 4 types of hypersensitivity reaction

A
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100
Q

Horses with infarctive purpura hemorrhagica present with clinical signs of:

A

colic
lameness
muscle swelling
stiffness

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101
Q

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

A

high CK values

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102
Q

What is the recommended treatment for purpura hemorrhagica?

A

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

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103
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)

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104
Q

Possible complications of purpura hemorrhagica

A

skin sloughing
laminitis
cellulitis
pneumonia
diarrhea

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105
Q

What is the prognosis for purpura hemorrhagica?

A

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

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106
Q

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

A

pan vasculitis
edema
hemorrhage
abortion in pregnant mares

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107
Q

Equine viral arteritis describe the infectious organism:

A

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

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108
Q

Equine viral arteritis virus epidemiology

A

order: nidovirales
family: ARterivridae

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109
Q

Equine viral arteritis clinical signs:

A

pyrexia
lethargy
anorexia
limb edema
stiffness
rhinorrhea
epiphora
conjunctivitis
rhinitis
abortion
edema (periorbital, supraorbital, ventrum, mammary gland, scrotum or limbs)
Other: urticarial rash, abortion, resp signs, ataxia, mucosal eruptions, submaxillary lymphadenopathy and intermandibular and shoulder edema

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110
Q

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

A

abortion rate: <10% to >60%

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111
Q

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

A

3 to 10 months

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112
Q

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

A

No

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113
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

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114
Q

How is EAV transmitted?

A

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

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115
Q

Does EAV remain viable in frozen semen?

A

Yes (fresh, chilled and frozen semen

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116
Q

Is transmission of EAV through fomites possible?

A

yes

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117
Q

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

A

Long-term immunity

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118
Q

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

A

w/in 60 days

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119
Q

What percentage of acutely infected stallions become persistently infected?

A

30 to 60%

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120
Q

In stallions where is the virus maintained?

A

w.in the accessory organs: ampullae, vasa deferentia

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121
Q

Seroprevalence for EAV is common is what breeds?

A

standardbred
warmblood breeds
** has been recently estab. in Quarter horses

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122
Q

How can EAV be diagnosed?

A

virus isolation
viral nucleic acid (PCR)
serology

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123
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)

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124
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

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125
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

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126
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)

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127
Q

Is there evidence that vaccinated stallions become carriers?

A

No

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128
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)

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129
Q

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

A

late fall
winter
spring

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130
Q

Is Anaplasma phagocytophila considered zoonotic?

A

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

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131
Q

What are the vectors of Anaplasma phagocytophila ?

A

Ixodes pacificus- California
Ixodes scapularis- eastern and midwestern US
Ixodes ricinus- Europe

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132
Q

What are potential/proposed reservoirs for Anaplasma phagocytophila?

A

white footed mice
chipmunks
white tailed deer
dusky footed wood rats
cervids
lizards
birds

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133
Q

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

A

cytolysis
induction inflammation
cell sequestration
consumption
desruction

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134
Q

Clinical signs of Anaplasma phagocytophila

A

early signs: FUO, partial anorexia
reluctance to move
fever (102.9-106.3F)
mild to mod tachycardia (50 to 60 bpm)
decreased appetite
limb edema
petechiation
icterus
weakness
ataxia
recumbency

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135
Q

What is the incubation period for Anaplasma phagocytophila?

A

Believed to be less than 14 days

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136
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 days
inoculation with infected blood: 3 to 10 days

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137
Q

Anaplasma phagocytophila clin path abnormalities:

A

anemia
leukopenia characterized by granulocytopenia and lymphopenia
thrombocytopenia

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138
Q

What is the definitive diagnosis of Anaplasma phagocytophila?

A

morulae w/in the cytoplasm of neutrophils and eosinphils
OR
positive PCR assay in peripheral blood

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139
Q

False positive Anaplasma phagocytophila morulae can occur with

A

Dohle bodies in toxic neutrophils

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140
Q

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

A

confirms recent exposure

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141
Q

Pathologic findings of Anaplasma phagocytophila

A

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

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142
Q

What is the treatment of choice for Anaplasma phagocytophila?

A

oxytetracyline: 7 mg/kg
or doxycycline

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143
Q

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

A

in 2 to 3 weeks if left untreated

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144
Q

Prevention for Anaplasma phagocytophila?

A

tick control

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145
Q

Mechanisms of thrombocytopenia

A
  1. decreased production
  2. abnormal sequestration (spleen)
  3. inc consumption or destruction
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146
Q

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

A

<10,000/uL

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147
Q

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

A

<40,000/uL

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148
Q

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

A

fresh whole blood
platelet rich plasma (preferable)

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149
Q

Causes of Immune mediated thrombocytopenia

A
  1. primary
  2. secondary
    drug administration, neoplasia or other immunologic disorders (EIA lymphoma, autoimmune hemolytic anemia)
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150
Q

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

A

DIC

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151
Q

Alloimmune thrombocytopenia of neonates include clinical signs of

A

depression
loss of suckle
a bleeding tendency
blood loss
rapidly developing anemia d/t profound thrombocytopenia

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152
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

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153
Q

Differentials for alloimmune thrombocytopenia in foals include

A

neonatal sepsis
neonatal maladjustment syndrome
neonatal isoerythrolysis

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154
Q

Laboratory abnormalities associated with alloimmune thrombocytopenia

A

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

155
Q

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

A

megakaryocytic hyperplasia

156
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)

157
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

158
Q

pathogenesis of IMTP

A

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

159
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

160
Q

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

A

weeks to years

161
Q

Why is the spleen the major site of plt phagocytosis?

A
  1. much antiplt antibody is secreted locally
  2. more than 30% of circulating plts are normally stored there
  3. stagnant splenic blood flow allows sensitized plts to pass slowly through a dense network fo phagocytic cells
162
Q

Effect of treatment with corticosteroids for IMTP?

A

improve capillary integrity
impair clearance by the MPS
decrease number and avidity of macro Fc receptors
impair antiplt ab production
impede plt ab interactions
inc thrombocytopoeisis

163
Q

Blood coagulation proceeds with what 3 key reactions:

A
  1. formation of activated factor X
  2. formation of thrombin
  3. formation of fibrin
164
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

165
Q

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

A

localized or systemic septic processes
neoplasia
Gi disorders
renal disease
hemolytic anemia

166
Q

what renal disease is caused by DIC

A

ischemic cortical necrosis followed by acute tubular necrosis

167
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)

168
Q

What diseases must be differentiated from DIC:

A

IMTP
wafarin toxicosis (horses)
moldy sweet clover toxicosis
inherited coagulation abnormalities

169
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
170
Q

Gram negative endotoxins stimulate DIC through

A

direct factor XII activation
cytokine production by mononuclear phagocytes

171
Q

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

A

exaggerated generation of systemic thrombin which causes widespread microcirculatory thrombosis

172
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

173
Q

In DIC plasmin contributes to factor consumption by destorying factors:

A

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

174
Q

Plasmin contributes to factor consumption in DIC by destroying factors

A

V, VIII, XIIa, IX and XI

175
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

176
Q

IV fluid administration in the treatment of DIC

A

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

177
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

178
Q

Corticosteroids int he tretmetn of DIC

A

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

179
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

180
Q

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

A

low molecualr weight heparin

181
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

182
Q

What are clinical signs of warfarin toxicosis in horses?

A

hematomas
ecchymosis of mucous membranes
epistaxis
hematuria

183
Q

How are horses potentially exposed to warfarin?

A

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

184
Q

Coagulation panel abnormalities with warfarin toxicosis

A

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

185
Q

The diagnosis of warfarin toxicosis is made by:

A

history of exposure
clinical signs of large vessel hemorrhagic dithesis
prlonged PT w/ or w/o APTT

186
Q

Mechanism of Warfarin toxicsosi

A

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

187
Q

Which clotting factors require the presence of vitamin K?

A

II, VII, IX and X

188
Q

What are drugs/factors that can enhance warfarin toxicosis/unbinding from protein?

A
  1. phenylbutazone– allowing greater proprotion of administered drug to be unabound and active
  2. hypoalbuminemia– “”
  3. corticosteroids and thyroxin– inc receptor affinity and clotting factor catabolism
  4. barbiturate, rifampin, chloramphenicol– induce hepatic microsomal enzyme activity that can accelerate warfarin metabolism & reduce
    therapeutic response to a given dose
  5. reduction of Vitamin K in diet
  6. liver disease
189
Q

Treatment of warfarin toxicosis

A

Vitamin K1 (0.5 to 1 mg/kg Sc or IM) every 6 hours until PT is normal and stable
fresh plasma (provide clotting factors)

190
Q

Which vitamin K drug should not be used in horses (in regards to treatment of warfarin toxicosis)?

A

Vitamin K3– b/c it has poor therapeutic action & highly nephrotoxic for hosres

191
Q

warfarin is what kind of anticoagulant

A

coumarin derivative

192
Q

What is a natural coumarin that horses can be exposed to that causes toxicosis?

A

moldy sweet clover (Meliltous spp) or silage containin dicoumarol

193
Q

Natural coumarins in sweet clover can be converted to

A

dicoumarol when hay or silage isi mproperly cured adn old forms

194
Q

Early signs of Sweet clover toxicosis

A

epistaxis
melena
subcu hematomas
periarticular swellings
***visible swelling at points of trauma

195
Q

Sweet clover toxicosis is most commonly seen which geographic location?

A

Northern Plains states

196
Q

Clinical pathology abnormalities associated with sweet clover toxicosis:

A

prolonged PT (earliest abnormalities)
plt count normal

197
Q

Pathogenesis of moldy sweet clover toxicosis

A

Identical to warfarin toxicosis:
Dicoumarol interferes with hepatic synthesis of clotting factors II, VII, IX and X by inhibiting vitamin K

198
Q

Moldy sweet clover toxicosis appears in cattle how many days after ingestion?

A

within 2 to 7 days
**lower levels of dicoumarol (<70 mg/kg) in feed may prolong the onset of signs for up to 3 months

199
Q

What si the toxic level of dicoumarol in sweet clover ?

A

10 mg//kg of feed

200
Q

Is grazing sweet clover dangerous?

A

No, b/c of its high forage yield, usually harvested as silage, which should carry less danger of molding when properly cured

201
Q

List infectious causes of Hemolytic Anemia:

A

Parasitic:
- Anaplasmosis
-Babesiosis
-Hemobartonellosis
-Eperythrozoonosis
-Theileriasis
-Trypanosomiasis
Bacterial:
-Leptospirosis
-bacillary hemoglobinuria
Viral:
-Equine infectious anemia (EIA)

202
Q

list causes of immune mediated hemolytic anemia

A

Autoimmune hemolytic anemia
neonatal isoertyrholysis (NI)
Drug induced: penicillin, trimethoprim-sulfamethoxazole

203
Q

list causes of heinz body hemolytic anemia

A

phenothiazine toxicity
wild onion poisoning
red maple leaf poisoning

204
Q

List less common causes of hemolytic anemia in large animals

A

severe cutaneous burns
L-tryptophan indole intoxication
water intoxication
post-parturient hemoglobinuria
copper poisoning hemolytic syndrome in horses with liver failure
erythropoietic porphyria in Holstein cattle

205
Q

Several common clinical signs are seen in animls with severe hemolytic anemia, regardless of teh cause, what are those:

A

mucous membrane pallor
fatique
depression
anorexia

206
Q

Icterus seen with hemolytic anemia is dependent on:

A

rate of red cell destruction
liver’s ability to exrete bilirubin

207
Q

What are signs of enhanced erythropoietic response:

A

anisocytosis
polychromasia
reticulocytosis
presence of nucleated red blood cells in circulation

208
Q

What is the life cycle of Anaplasma within a tick?

A

Enters the midgut epithelial cell, completes the first round of replication

– migrates to salivary epithelial cells & undergoes second round of replication

–enters saliva– where can be passed to another host

209
Q

In regards to Anaplasma, what does it mean that organisms can be transmitted transtadially?

A

from larvae to nymps and nymphs to adults

**indicating that ticks can becom infective and transfer anaplasma spp toa new host after only a single molt

210
Q

When are clinical signs of anaplasma seen (in regards to percentage of red cells infected)?

A

when >15% of rbcs are infected

211
Q

Bovine anaplasmosis:
anemia occurs because of:

A

splenic and hepatic macrophage mediated phagocytosis fo infected erythrocytes

212
Q

Anaplasma marginale expresses a variety of major surface proteins, which accounts for what immunologically?

A

allow sfor different bacterial surface strcutures leading to immune evasion and persistent infection in the animal

213
Q

Bovine anaplasmosis: protective immunity requires what?

A

induction of both antibody against ht eouter membrane proteins and macrophage activation for enhance pahcytosis and bacterial killing

214
Q

Bovine anaplasmosis: whlie the immune system controls the acute phase of infection– organisms are not complete cleared from blood due to

A

emergence of antigenic variants

215
Q

Bovine anaplasmosis: infected animals demonstrate cyclic subclinical peaks of rickettsemia and immune response every:

A

6 to 8 week period

216
Q

Bovine anaplasmosis, A. marginale: In the United State infection is endemic where:

A

West, Midwest and SE

217
Q

Bovine anaplasmosis: endemic regions are maintained by

A

prevalence of competent tick vectors and persistently infected carrier cattle

218
Q

What role do wild ruminants play in the transmission of anaplasma?

A

unkonwn role?

219
Q

Bovine anaplasmosis: incubation period

A

10 to 30 days (as long as 60 days)

220
Q

Bovine anaplasmosis: calf exposure clinical signs

A

lethargy
anorexia
24 to 48 hours

221
Q

Bovine anaplasmosis: adult acute disease

A

**highly susceptible
high fever (103 to 106)
tachycardia
tachypnea
anorexia
lethargy
dec milk production )9dairy cows)

222
Q

Bovine anaplasmosis: why do cattle stagger or become aggressive?

A

as a result of cerebral hypoxia associated with anemia

223
Q

Does hemoglobinuria occur with Bovine anaplasmosis?

A

No because hemolysis occurs extracellularly

224
Q

differential diagnosis for Bovine anaplasmosis:

A

**dzes produce anemia and or icterus
babesiosis, bacillary hemoglobinuria, leptospirosis
hepatotoxic plant poisonings (Senecio)
chemical
other causes of liver disease
copper poisoning in sheep

225
Q

Bovine anaplasmosis: what occurs if animal survies the acute crisis?

A

recovered animals remain carriers for life & serve as a reservoir for ongoing transmission

226
Q

Does Anaplasma ovis cause severe disease in sheep?

A

usually asymptomatic
** can cause anemia esp in immunosuppression

227
Q

Bovine anaplasmosis: On necropsy what is a common pathology seen?

A

splenomegaly

228
Q

Bovine anaplasmosis: what sample can be sumitted to confirm diagnosis?

A

detection of A marginal infected rbcs within capillaries of Giemsa stsianed histo sections

229
Q

Definitive diagnosis of acute anaplasmosis requires

A

Identification of A. marginale or A ovis infected rbcs by microscopic exam
OR
PCR of aniamls with severe anemia

230
Q

What is used for official testing of anaplasma by many regulatory agencies?

A

competitive enzyme linked immunosorbent assay
**high sensitivity and specificity

231
Q

Bovine anaplasmosis: what are the antibiotics of choice?

A

tetracyclines

232
Q

what are vaccine control measures for available Bovine anaplasmosis?

A

-endemic regions: beef cattle allowed to become infected at a young age

  • live vaccine licenses in Australaia, AFrica, Asia and central and south america (not USA)

-killed vaccines are less efficacious and reqmultiple immunizations (licenses in 14 states)

233
Q

Bovine anaplasmosis: control measures besides immunoprophylaxis

A

-quarantine and serologic screening using cELISA
-strategic use of pastures, insecticides and management of herd additions
-prevent iatrogenic transmission

234
Q

Acute babesiosis is characterized by

A

fever
hemolytic anemia
icterus
hemoglobinuria
death

235
Q

Babesia bigemina characteristics

A

appears in mature rbcs as nonpigmented, paired, pear shape bodies joined at an acute angle

irregularly shaped, round, or amoeboid forms also seen

236
Q

babesia bovis characteristics

A

small, pleomorphic
signle round body or paired pear shaped bodies joined at an obtuse angel within mature RBCs

237
Q

B. bovis vs B. bigemina

A

B. bovis is the most virulent

238
Q

Natural transmission of B. bovis and B. bigemina

A

ticks from the genus Boophilus

239
Q

Life cycle of Babesia within the tick

A

Ticks infected transovarially (vetrically)
-female infected by ingestion of parsaite during engorgement
-babesial orgnaisms reproduced /win tick- reproducign organsims incorporated withind eveloping tick embryos
-babesia transmittedt o new certebrate hosts by feedign of ensuing tick larvae nymphs or adults

240
Q

Larval ticks can trasmit what species of babesia?

A

B. bovis
**not B. bigemina– not transmitted until the larvae have molted into the nymphal or adult stages

241
Q

Can Babesia bovis and bigemina be transmitted iatrogenically?

A

yes

242
Q

Incubation period Babesia bovis and bigemina

A

less than 5 days to 3 weeks

243
Q

Babesia bovis and bigemina cause of anemia

A

IV dstruction of erythorcytes by escaping merozoites following intraerythorcytic reproduction of the babesia by binary fission

244
Q

With Babesia bovis and bigemina, why can massive lysis occur even though the parasitemia may be less than 1%?

A

because osmotic fragility of the whole RBC population increases terminally

immune mediated condition may result in the spleen removing adamged and healthy RBCS from circulation

245
Q

Babesia bovis and bigemina: what causes the clinical signs of emtabolic acidosis and anoxia?

A

parasite associated proteolytic enzymes are released into hte plasma– interact with bood components

246
Q

Clinical signs of cerebral babesiosis

A

hyperexcitability
convulsions
opisthotonos
coma
death

247
Q

what is the pathogenesis of cerebral babesiosis?

A

anoxia and or RBC blockage of cerebral capillaries

248
Q

All cattle breeds are susceptible to babesiosis, but what breeds exhibit a degree of resistance to Babesia bovis and bigemina?

A

bos indicus breeds

249
Q

Which spp have a natural immunity to babesiosis?

A

calves

250
Q

Why are calves resistant to babesiosis

A

-suspect maternal immunity
RBCS contain factors indepednet of ab that provide an innat eresistance to severe babesiosis

251
Q

What happens with calves infected with babesios under 9 months of age?

A

minimum reaction to dz and become asymptomatic carriers

252
Q

How long do carriers remain resistant to babesiosi clinical disease?

A

at least 4 years

253
Q

Babesia bovis and bigemina: carrier state can be over come by:

A

stress such as calving, malnutrition or concurrent disease

254
Q

What are other conditions that may exhibit some of the same signs as babesios

A

anaplasmosis
trypanosomiasis
theileriosis
leptospirosis
chronic copper toxicity
bacillary hemoglobinuria

255
Q

When can Babesia spp be detected in smears made from peirpheral blood?

A

in acute infection

256
Q

A positive diagnosis of Babesia requires?

A

Giemsa stined thin blood smears
positive serology (IFA, ELISA< CF)
PCR

257
Q

B bovis favors capillaries in what locations?

A

brain and kidney– b/c major energy producing pathway of Babesia is anaerobic glycolysis

258
Q

Postmortem findings on cattle that die peracutely of babesios

A

characteristic of acute hemolytic crisis

259
Q

Prognosis for babesios

A

Poor: hemoglobinuria or cerebral signs

PCV>12% respond well to treatment

260
Q

What are beneficial control measures for prevention of babesiosi

A

eradication of boophilus tick vectors effect control in USA
– reduce tick ifnestations: controlled range burning, cultivation, prolonged pasture rest, use of repellents

261
Q

Piroplasmosis of the horse is caused by what organism?

A

Babesia caballi and Theileria equi

262
Q

What is a unique characteristic of T. equi

A

intraerythrocytic parasites divide into four cells to forma Maltese cross

263
Q

Babesia caballi and Theileria equi are transmitted by

A

ticks of genera:
Dermacentor
Hyalomma
Rhipicephalus

264
Q

Life cycle of B caballi in tick?

A

passed transovarially (vertically) from one tick generation to the next

265
Q

Life cycle of T. equi in tick?

A

only transstadially (horizontally): one tick stage (larvae or numphs) becomes infected and dz agent is passed to the enxt certebrate host in the next tick stage (nymph or adult)

266
Q

What species is naturally infected with Theileria equi?

A

zebras in africa

267
Q

Babesia caballi and Theileria equi survivors become

A

chronic carriers

268
Q

Babesia caballi and Theileria equi incubation period

A

5 to 28 days

269
Q

Babesia caballi and Theileria equi clinical signs

A

hemolytic anemia
jaundice
hemoglobinuria
death

generalized signs: depression, anorexia, incoordination, lacrimation, mucous nasal discharge, welling of eyelids and freq lying down or are seen

270
Q

Difference in clinical disease between Babesia caballi and Theileria equi

A

Theileria equi: most pathogenis and responsible for greater incidence of hemoglobinuria and death

Babesia caballi: more persistent fever and anemia

271
Q

Differential diagnosis for Babesia caballi and Theileria equi

A

equine monocytic ehrlichiosis
EIA
liver fialure with hemolytic anemia
other hemolytic anemias of the horse

272
Q

What is the official tesing method for Babesia caballi and Theileria equ?

A

cELISA test
PCR available

273
Q

Babesia caballi and Theileria equi post mortem features:

A

similar to hemolytic crisis, jaundice is prominent

274
Q

What is the drug of choice for eliminating the carrier state of animals infected with Babesia caballi and Theileria equi

A

imidocarb

higher doses– cause colic in horses

275
Q

Control of Babesia caballi and Theileria equi?

A

control of tick infestation does much to reduce disease incidence
** no vaccines available

276
Q

Diagnosis of Babesia caballi and Theileria equi in the US

A

veterinarian can enroll the horse in the USDA controlled treatment program

277
Q

Haemobartonella bovis is located where on teh rbc?

A

epicellular organism that is closely associed with the surface of erythrocytes
**may appear as a rode shape, an ovoid or in chains wtih conventional stains

278
Q

Does haemobartonella bovis cause anemia?

A

Rarely

279
Q

Eperythrozoon wenyonii (mycoplasma weyonii) infection causes

A

in normal cattle– usually latent & not assoc with clinical signs

if C/s– causes mild depression ,fever and modest anemia

280
Q

Mycoplasma ovis (epertythrozoon ovi) can produce what clinical sigsin sheep?

A

profound depression anemia
significant death loss in young lambs

281
Q

Theileriasis is caused by?

A

a small hemoparasite of the genus Theileria tha tinfects lymphocyte and erythrocytes of ruminants

282
Q

Theileria is most common seen in what locations?

A

tropical and subtropical climates

283
Q

Theileria is spread by

A

blood sucking arthropods
**particularly Ixodidae family

284
Q

What is the cause of East coast fever?

A

Theileria parva
**highly fatal disease in Africa

285
Q

Describe trypanosomes

A

flagellated protozoal organism

286
Q

Trypanosoma congolensi causes what disease in cattle in africa?

A

Nagana

287
Q

Trypanosoma theileri (Trypanosoma americanum) is seen in north america, and is usually pathogen or nonpathogenic?

A

nonpathogenic

288
Q

Leptospira infections that produce hemolytic syndrome are seen with what species?

A

most commonly calves and lambs

289
Q

Bacillary hemoglobinuria is caused by

A

Clostridium haemolyticm (clostridium novyi type D)

290
Q

Where is bacillary hemoglobinuria endemic?

A

in poorly drained areas of the western United States

291
Q

Pathognesis of bacillary hemoglobinuria?

A

organism finds a favorable environment for development in areas of pre-existing liver damage most often have been produced by migrating liver flukes

–>bact produce a focal liver lesion

292
Q

Clinical manifestation of bacillary hemoglobinuria?

A

severe depression
anorexia
fever
hemoglobinemia
hemoglobinuria
**develop C/S rapidly
**death loss are often seen

293
Q

Equine infecitou sanemia virus (EIAV) epidemiology

A

family: Retroviridae
Genus: lentivirus

**RNA virus

294
Q

Pathogenesis of EIAV

A

–uses virally coded reverse transcriptase to convert RNA genome to a DNA intermediate that is integrated into the shot’s genome by another virally encoded enzyme integrase
-integrated DNA (provirus) usurps the host cell to replicate its genome, manufacture viral proteins and assemble the virally encoded proteins into virionsthat bud from the cell
**results in lifelong infection

295
Q

he test for identificaiton of EIAV equids that are seropositive?

A

the Coggins test AGID and ELISA

296
Q

Most horses with EIAV have what clinicals signs?

A

most are inapparent arriers and are healthy

297
Q

How can EIAV be transferred?

A

blood transfered from an inapparent to carrier: instruments, blood products or by insect vectors

298
Q

The clinical form of Equine infectious anemia is characterized by three defined temporal stages:

A
  1. acute
  2. chronic
  3. Inapparent
299
Q

Acute stage of Equine infectious anemia:

A

high fever
thrombocytopenia
nonspecific signs of malaise (lethargy and inappetence)
+/- ecchymoses or petechiae

300
Q

Chronic stage of Equine infectious anemia

A

C/s during episodes of viremia and clinical quiescnece & low viremia

301
Q

Inapparent stage of Equine infectious anemia

A

once levesl fo ciremia are immunologically contained and no c/s are detected

302
Q

What can precipitate clinical disease of Equine infectious anemia?

A

Episodes of stress
Corticosteroids

303
Q

Which horses pose the biggest risk of transmision to uninfected horses?

A

horses with high-titered viremia

304
Q

EIA: What mechanism of viral replicaiton allows for generation of viral variants that differ genetically from preexisting ones?

A

DNA dependent RNA polymerase (reverse transcriptase) that imisincroporates nucleotides, resulting in changes in teh viral genoma

305
Q

Pathogenesis of EIAV in DIC/thrombi formation

A

EIAV replication in endothelial cells may play role in DIC by viral damage to endothelial cells–> exposure of subendothelial–> plt aggregation and formation of thrombi

–> tissue edema by transudation of fluid from compromised small vessels

306
Q

EIA: clinpath during clinical disease

A

profoudn thrombocytopenia
– progression to DIC

307
Q

EIA in chronic infections: clin. path

A

anemia– d/t intravascular hemolysis, extravascular hemolysis and depression of bone marrow erythropoiesis

308
Q

Clin path during the inapparent stage of infection of EIA

A

inc plasma total solids and globulin concentrations
mild anemia
dec albumin concentrations

309
Q

What are high risk regions for EIA in teh US

A

Texas Oklahoma lousiana and Arkansas

310
Q

States are considered as low risk for EIA in the US

A

mid-Atlantic area, New England, Alaska, Hawaii

311
Q

Pathogenesis of autimmune hemolytic anemia

A

-antibodies combine with complement and antigens on red cell membrane–> lead to rapid removal of affected cells from circulation

312
Q

Clinical signs of severe hemolytic anemia (IMHA)

A

marked anemia (PCV<15%)
depression, pale mucous membranes, variable icterus, elevated heart and respiratory rate and variable to intermittent fever

313
Q

Secondary autoimmune hemolytic anemia in horses has been associated most often with what other primary problems:

A

purpura hemorrhagica
lymphoma
other neoplasms
protein losing enteropathy
chronic bacterial infections

314
Q

What drugs have been associated with IMHA in hroses?

A

procaine penicillin
trimethoprim sulfamethoxazole

315
Q

What does the direct Coombs test detect?

A

presence of antierythrocyte antibodies and/or complement on teh red cell memrbane

316
Q

False negative results to the Coombs test are possible and occur due to

A

low concentrations of antibody
low binding ot he red cell membrane
prior to treatmetn with corticosteroids

317
Q

Autoimmune hemolytic anemia has rarely been reported in alg animals but can is due to a secondary problem such as

A
  1. association with certain types of neoplasia
  2. with a variety of viral, bact, rickettsial and protozoal infections
  3. following exposure to certain drugs
  4. in assoc with other immune mediated disorders like systemic lupus erythematosus
318
Q

Initiating factors for autoimmune disorders are not completely understood but may related to

A

alterations in red cell membrane through direct or indirect injury–> elcits abnormal resposne by the immune system

319
Q

Most commonly affected red cells are removed form circulation at a rapid rate by what ?

A

reticuloendothelial system of the liver and spleen

320
Q

Spherocytes on blood smears are characteristic diagnostic feature of what disase?

A

autoimmune hemolytic anemia
**most commonly seen in human and canine patients

321
Q

What would ctreatment with corticosteroids contraindicated in horses with IMHA?

A

b/c therapy must be directed at the primary agent
**corticosteroids can cause recrudescnce of viremia in horses with EIA

322
Q

what blood factors are associated with NI in horse foals?

A

Qa Qb Qc Aa Pa and Dg and donkey factor in mule foals
**most ommon antigens are Qa and Aa

323
Q

Heinz body hemolytic anemia can develop following exposure to what oxidizing agents?

A

phenothiazine, methylene blue, acetylphelhydrazine or plants with wild or domestic onions, members of the Brassica family (rape or kale) and wilted or dried leaves of the red maple (acer rubrum)
-sheep- low in molybdenum diets= chronic copper tox
-cattle- grazing rye grass or selenium deficient pastures in Florida

324
Q

Clinical signs of heinz body hemolytic anemia

A

weakness
lethargy
anorexia exercise intolerance
death loss
mucpale mucous mebranes
INC HR and RR
Temp WNL

325
Q

Clinical signs of horses with red maple leaf tox

A

subclinical or
lethargy, muddy or cyanoti cmucous mebranes, tachycardia, inappetence, weakness, colic, icterus, brown discoloration fo the blood and pigmenturia
RARE: sudden death

326
Q

Clinical signs of horses with red maple leaf tox

A

subclinical or
lethargy, muddy or cyanoti cmucous mebranes, tachycardia, inappetence, weakness, colic, icterus, brown discoloration fo the blood and pigmenturia
RARE: sudden deathWhen do hroses develop clinical red mpale leaf toxicosis?

327
Q

Clinical signs of horses with red maple leaf tox

A

subclinical or
lethargy, muddy or cyanotic mucous membranes, tachycardia, inappetence, weakness, colic, icterus, brown discolorationof the blood and pigmenturia
RARE: sudden death

328
Q

When do horses develop clinical red maple leaf toxicosis?

A

during summer and fall
**high morality rate in comb of rapidly progressive hemolytic anemia and formation of methemoglobin

329
Q

What are heinz bodies?

A

round, oval to serrated, refractile granules located near the cell margin or protruding from the cell
***visualized best with vital stains like crystal violet or new methylene blue applied to unfixed blood smears

330
Q

Maple leaf tox clin path abnormalities

A

total plasma protein remains within normal limits
Coombs test negative
depletion of red cell mass
reduced glutathione
methemoglobinemia
INC osmotic fragility
modest elevations of liver derived serum enzyme activities

331
Q

What renal injury can occur d/t red maple leaf tox?

A

renal failrue secondary to hemoglobin nephrosis

332
Q

How common is renal insuffieicny in horses with red maple leaf toxicosis

A

40% of cases

333
Q

Inflammatory leukogram is present in what percentage of cases of red maple leaf toxicosis

A

75% of cases

334
Q

How are Heinz bodies formed?

A

by precipitation of oxidatively denatured hemoglobin

335
Q

Hemoglobin contains with rbc is constantly undergoing mild oxidative stress assoc with oxygen transport–> leads to generation of

A

superoxid radicals and hydrogen peroxide within teh cell

336
Q

What mecnaism cowithin the red cell counteract oxidative processes?

A

by production of the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH) and reduced glutathione

337
Q

How does selenium deficiency contribute to Heinz body anemia?

A

impeding the ability of the cells to repond to oxidative stress
__ selenium deficiency results in a derase in glutahtione peroxidase, a selenium containing enzyme

338
Q

What component of red maple leaves is ipmliatedin teh oxidation of hemoglobin, methhemoglobin formation and Heinz body anemia?

A

Gallic acid

339
Q

Methemoglobin formation in red maple leaf toxicosis results from

A

oxidative change of hemoglobin iron to nonfunctional ferric state

340
Q

Normally methemoglobin formation is usually prevented by

A

glutathione reductase
ascorbic acid
reduced glutathione

341
Q

What are the consequence of methemoglobinformation

A

cannot laod or transport oxygen
**gives blood brown color and mucous mebranes

342
Q

Why are IV fluids indciated in HEinz body anemia?

A

to prevent renal damage seondary to hemoglobinuria or azotemia

343
Q

Are corticosteroids beneficial in the treatment of heinz body anemia?

A

No, have an increased risk of death

344
Q

What is the mortality rate of experimental and naturally occurring red maple leaf toxicosis?

A

60 to 65%

345
Q

Intravascular hemolysis has been reported in horses following severe cutaneous burns affected what percentage of their body surface?

A

more than 25%

346
Q

What is the pathophysiology of hemolysis associated with intravascular hemolysis following cutaneous burns?

A

production of hydroxyl radicals by complement activated neutrophils

347
Q

What has been shown to be beneficial for burn treatment in humans?

A

early fluid therapy
free radical scavencers
supportive and wound care
control pain and inflammation
sepsis prophylaxis

348
Q

Water intoxication- what is it?

A

massive water intake may produce marked hypotonicity o fbody fluid with subseueetn IV hemolysis of RBCs

349
Q

When is water intoxication a problem?

A

when milk reared calves when they first given access to unlimited quantites of water

350
Q

Clinical signs of water intoxication

A

severe neuro signs: depression, convulsions, coma
respiraotry distress
hemoglobinuria
death

351
Q

What are clinicopathologic features of water intoxication?

A

hemolytic anemia
hypoproteinemia
hyponatremia
hypochloremia
hyposmolality
hemoglobinuria
hypothenuria

352
Q

Clinical signs of water intoxication

A

severe neuro signs: depression, convulsions, coma
respiratory distress
hemoglobinuria
death

353
Q

Treatment of water intoxication?

A

**restrict water
hypertonic saline (return sodium to 120 to 125 mmol/L)
mannitol
corticosteroids

354
Q

Postparturient hemoglobinuria: commonly affected animals

A

high-producing multiparous cows that develop C/S during the first month after calving

355
Q

Postparturient hemoglobinuria syndrome characterized by

A

intravascular hemolysis
hemoglobinuria
anemia

356
Q

C/S of Postparturient hemoglobinuria

A

depression
decreased feed consumption
decreased milk production
anemia (marked at 4 to 5 days)
hemoglobinuria
icterus

357
Q

Suspected pathogenesis of Postparturient hemoglobinuria

A

Hypophosphatemia– low intracellular phosphate may interfere with energy metabolism–> affects cell viability & ability of red cells to deal with potential hemolysis

358
Q

Treatment for Postparturient hemoglobinuria

A

1.blood transfusion & IV fluids– highly valuable animals

2.correct hypophosphatemia: sodium acid phosphate: 60 g/300 ml of water IV, followed by oral supplementation with 200 to 300 g sodium phosphate salts every 12 hours

359
Q

Which spp is most susceptible to the toxic effects of copper?

A

lambs
**sheep, goats and cattle

360
Q

Which breed of sheep is more resistant to copper toxicity?

A

meirno sheep> british breeds

361
Q

Ingestion of copper pathway

A

ingested salts of cooper absorbed through enterocytes by carrier proteins
2. transported to blood by in loose complexes with albumin and aa
3.ionic copper internalized by hepatocytes
4. redistributed in bile, packed in lysosomes in protein complexes or used for formation of ceruloplasmin

362
Q

Hemolysis caused by copper

A

Free inorganic copper is an oxidant– partticpiate in the FEnton rxn
–>cellular damage related to oxidative hydroxide and peroxides (not copper oxidation)–> leads to denaturation of proteins within RBCs

363
Q

Hemolysis caused by copper

A

Free inorganic copper is an oxidant– participate in the Fenton rxn
–>cellular damage related to oxidative hydroxide and peroxides (not copper oxidation)–> leads to denaturation of proteins within RBCs

364
Q

The hemolytic phase of copper poisoningis often initated by:

A

Noxious stimuli
-shipping, hierarchal change, admin of oxidative drugs, starvation or change of housing

365
Q

What diets have increased resistance to hemolytic crisis in sheep caused by copper toxicosis?

A

High protein diets

366
Q

What are sources of copper that have been responisble for copper accumulation in animals?

A

trace mineralized salt
inappropriately formulated cereal grain mixtures
forages from pastures that have been fertilized by swine or chicken manure
orchard pastures contam by copper containing fungicides
rations containing more than 20$5 chicken litter
diets that contain high concen of palm kernal oil

367
Q

What is the toxic dose of copper dependent upon?

A

Variable
Dependents on duration of exposure
animals genetic
amount of molybdenum being fed

368
Q

What two minerals inhibit the absorption of copper?

A

High dietary inc and Iron– these elements share a competitive affinity for metallothionein

369
Q

What reduce decreases the absorption of molybdenum from plants, thus increasing the potential for pathologic accumulation of copper in herbivores?

A

soil sulfates

370
Q

Which spp is resistent to high dietary conentrations of copper?

A

Horses

371
Q

Clinical signs of Copper toxicosis occur when and then see clinical signs fo what organs?

A

**asymptomatic until onset of hepatic necrosis
–> rapid onset: anemia, myopathy, neurologic, renal and hepatic disease

372
Q

Copper toxicosis clinical signs

A

inappetance
lethargy
weakeness
recumbency
cool extremities
pallor
grayish discoloration of the mucous membranes
+/- poor pulses qulaity, tachypnea, hypotension, hypothermia

373
Q

In copper toxicosis feces can be what color?

A

dark or yellowish discoloration– do not contain hemoglobin unless secondary abomasal ulceration occurred

374
Q

Necropsy findings of animals with copper tox

A

-pale/icteric in hemolyzing animals
-liver: pale, yellow
lungs: firm
-kidneys: black, metallic sheen d/t entrapped hemoglobin
-urinary bladder: serosanguineous urine filled

375
Q

How long is hepatic necrosis detectable in cases of copper toxicity on microscopic exam?

A

412 days post poisoning

376
Q

Can diagnosis of copper toxicosis be made on liver biopsy or plasma concentrations of copper?

A

Normal hepatic copper and plasma copper concentrations have been reported

**but may be diagnostic

377
Q

With cllin path abnormalities, when are consistent hematologic changes seen?

A

Not until 24 hours after hemolytic crisis

378
Q

What are clin path changes that occur during the acute hemolytic crisis caused by Copper tox?

A

Heinz body formation
intrascular hemolysis
methemoglobinemia (as much as 5%)
decrased PCV
increased concen of plasma bilirubin, AST, GGT, ALP, Tbili, CK crea, plasma urea nitrogen, plasma ceruloplasmin

379
Q

Describe urine in copper tox

A

color: dk brown to black
- high concen of protein, blood and hemoglobin casts

380
Q

Treatment of Copper tox with D-penicillamin causes

A

increases urinary copper excretion by 10 to 20 fold
**single dose therapy the effect is transient and insifignificant for reudcing total hepatic copper load. treat daily for 6 days

381
Q

Copper tox: animals with acute hemolytic syndrome should be treated with:

A

-insufflated oxygen
-VItamin E

382
Q

Treatment with ammonium tetrthiomolybdate has been recommended for treatmetn of acute hemolytic crises due to Copper tox, for what MOA?

A

reduces lyosomal and cytosolic opepr in hyepatocytes

383
Q

Prevention of copper toxicosis for pastures that are heavily contaminated with copper

A

top dress the pasture with molybdenum phosphate

Cardiology.CV.hemolymph (6 decks)

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