Diseases Of The Hematopoietic And Hemolymphatic Systems p1044-1083 Flashcards
Platelet adhesion to a damaged blood vessel from trauma causes membrane conformational changes that trigger a basic platelet reaction. List 3 responses.
- Platelet aggregation
- Platelet contraction
- Platelet granule secretion
What initiates the extrinsic pathway of coagulation and where is this found?
Lipoprotein tissue factor (TF), found in endothelial cells and monocytes, when released into the bloodstream, begins a pathway of the coagulation cascade. TF may also be secreted in response to pathological stimuli such as bacterial endotoxins.
Which factor do both the intrinsic and extrinsic pathway culminate in the formation of? And what does this ultimately lead to?
Factor X is activated to FXa, which then generates thrombin. Thrombin is then used in the conversion of fibrinogen to fibrin.
Fletcher factor deficiency, causing a coagulation disorder, has been found in miniature and Belgian horses. Most animals are asymptomatic, but bleeding in response to trauma can occur. The inheritance is unknown.
A) Prekallikrein
B) Factor XI
C) Factor VIII
D) Vitamin K-dependent
A) Prekallikrein
This factor is important in the beginning of the intrinsic pathway of coagulation. It is responsible for the activation of Factor XII.
The deficiency of this factor has been reported in Holstein, Holstein-Friesian, and Japanese Black cattle. Considered an autosomal recessive trait, resulting from an insertional mutation in exon 12 of the F22 gene. Cattle with this disease may be assymptomatic or have a range of signs. These can be prolonged bleeding, reduced resistance to infection and increased prevalence of repeat breeding, possibly due to a slower estrus cycle.
A) Prekallikrein
B) Factor XI
C) Factor VIII
D) Vitamin K-dependent
B) Factor XI deficient
Factor XI is activated by XIIa. Genetic analysis is needed to diagnose.
Hemophilia A has been reported in QHs, Japanese Brown cattle and Herefords. This deficiency is X-linked and recessive, with clinical disease occurring predominantly in males. A leucine-to-histidine mutation has been found in the F8 gene of Japanese Brown cattle. When this factor drops below 5%, these patients are moderate to severe hemophiliacs, with spontaneous hemorrhage occurring.
A) Prekallikrein
B) Factor XI
C) Factor VIII
D) Vitamin K-dependent
C) Factor VIII
This factor is stabilized in circulation with von Willebrand factor, which promotes platelet-endothelial adhesion at sites of vascular injury.
What are differential diagnoses for coagulation factor deficiencies?
DIC, warfarin toxicity, moldy sweet clover toxicosis, and acute hepatic disease.
A horse is presented to the hospital for epistaxis that is unrelated to exercise. Petechiations are also noted in the nasopharynx. Bloodwork shows normal for the following: platelet count, activated coagulation time, partial thromboplastin time, prothrombin, thrombin time, fibrin degredation products and plasma concentraiton of vWF. The gingival bleeding time is prolonged (> 60 minutes), clot retraction is markedly reduced and platelet aggregation is impaired.
No treatment is available for this horse with what disease?
A) Hemophilia A
B) Glanzmann thrombasthenia
C) Fletcher factor deficiency
D) Equine purpura hemorrhagica
B) Glanzmann thrombasthenia
This is a rare, inherited disease causing a qualitative or quantitiative defect in the platelet glycoprotein complex IIb-IIIa. This complex is responsible for binding fibrinogen and mediates platelet aggregation. The mutations have only been found in the alpha IIb subunit, which destabilizes the protein structure.
If a biopsy was performed on a horse with predominant cutaneous involvement of vasculitis, what would be the most common inflammatory pattern be found?
Neutrophilic infiltration of venules in the dermis and SQ with nuclear debris in and around involved vessels and fibrinoid necrosis.
What are some adverse sequelae of vasculitis?
Cellulitis, thrombophlebitis, laminitis, and pneumonia
Describe the pathogenic mechanism involved with vasculitis?
Immune complex deposition in vessel walls, with subsequent complement activation and chemoattractant production. Proteolytic enzymes, released by neutrophils and macrophages, cause vessel wall necrosis with subsequent edema, hemorrhagic and infarction of supplied tissues.
Equine purpura hemorrhagic is a noncontagious disease of horses characterized by vasculitis leading to extensive edema and hemorrhage of the mucosa and SQ tissue. This disease has been recognized as a sequela to infection or exposure to what?
Strep. equi, Strep zooepidemicus, R. equi, Corynebacterium pseudotuberculosis, and vaccination against S. equi.
A horse presents with panvasculitis, and abortion around 6 months of gestation. She will most likely clear this virus in 60 days, but 30-60% of acutely infected stallions will become PIs. In this mare, what does long term immunity look like?
Infected mares infected with this disease, equine viral arteritis, will not become EAV carriers or chronic shedders, nor do they appear to have infertility problems. Naturally exposed animals have long-term immunity.
EAV is maintained mainly in which portion of the male reproductive system?
A) Testicles
B) Epididymis
C) Bulbourethral gland
D) Ampulla
D) Ampulla
Anaplasma phagocytophilia is found in which equine blood cells?
A) RBCs
B) Monocytes
C) Neutrophils
D) Platelets
C) Neutrophils
This organism can also be found in equine eosinophils. The organism is found withing the vacuoles of these infected granulocytes.
