Monocytic ehrlichiosis--> (not granulocytic ehrlichiosis). explain the diff
some ehrlichiae have a tropism for mononuclearcells, so ehrlichiae morulae may be found in mononuclearcellsof infected animals
Potomac horse fever is caused by what? What are the clinical signs?
It is a equine monocyticehrlichiosis caused by Neorickettsia risticii. The rickettsia infects monocytes and enterocytes and causes a diarrheal dz
Ehrlichia canis causes what dz? What cells does it infect? What are the major affects on the blood?
canine monocytic ehrlichiosis, which means the monocytes are infected. These infected monocytes then adhere to the vascular endothelium, which leads to vasculitis and subendothelial tissue infection, which leads to platelet consumption, sequestration, and destruction --> thrombocytopenia, as well as leukopenia and anemia. (ONLY ONE DOG)
Ehrlichia canis causes what kind of anemia, and has what clinical signs associated with it?
there is a NON-REGENERATIVE ANEMIA (the thrombocytopenia--> bleeding tendancies--> chronic blood loss--> nonregen), along with fever, LN enlargement, splenomegaly, thrombocytopenia, AND bone marrow hypoplasia ±pancytopenia, and multifocal nonsuppurative meningoencephalitis, interstitial pneumonia, and glomerulonephritis
how can you dx ehrlichia canis?
examination of Wright-Giemsa-stained impression smears of lung, liver, LNs, spleen, which will detect the morulae in the macrophages
Hemophagocytic syndrome occurs in who? what is happening? WHY is it happening?
This occurs in cats and dogs. What happens is proliferation of nonneoplastic (i.e., polyclonal), well-differentiated but highly erythrophagocytic macrophages. hemophagocytic syndrome occurs 2º to neoplasia, infection, or other underlying disease (macrophage proliferation and hyperactivation in response to ↑production of stimulatory cytokines in the 1º disease process)
what does the blood of an animal affected with hemophagocytic syndrome look like? what are the 4 big sequale?
high numbers of macrophages in the bone marrow, LNs, spleen, liver, and affected animals have cytopeniasof two or more cell lines. The sequelae are: splenomegaly, lymphadenopathy, bleeding tendencies, and cytopenias of two or more cell lines.
Immune-mediated thrombocytopenia (IMT)--> what causes this? what is the main result? what are some problems IMT could be secondary to?
idiopathic immune-mediated destruction of platelets, which results in a severe thrombocytopenia: (<10,000 platelets/μL), which obv leads to some bleeding tendencies! IT can be secondary to infections (like ehrlichia, EIA, or bacteral/fungal/protozoal), or drug administration (cephalosporins, sulfonamides), neoplasia, or other immune-mediated diseases
what is evans syndrome?
IMT + IMHA
Anaplasma platys is what kinda organism? which cells does it infect? What is the main affect on the blood, and what dz does it cause (and who does it affect?)
It is a rickettsial organism which infects platelets, which results in a recurrent marked thrombocytopenia! Hence, the name of the dz it causes is called infectious canine CYCLIC!! thrombocytopenia. (megakaryocytic hyperplasia and organism-associated antigen within macrophages). Dx by finding MORULAE in the platelets
Bovine viral diarrhea virus (type II BVDV) affects platelets how? what is the mechanism?
thrombocytopenic hemorrhagic syndrome with impaired platelet function. infection of bone marrow megakaryocytes and circulating platelets
how does Feline leukemia virus (FeLV) relate to platelets?
FeLV causes an infection of hematopeoitc cells, leading to platelet abnormalities (thrombocytopenia, thrombocytosis, ↑ platelet size, and ↓function)
Chédiak-Higashi syndrome (CHS)--> how does this relate to platelets? explain the mechanism
this syndrome leads to platelet dysfunction (thus bleeding tendencies). the mechanism behind this is that in the syndrome, platelets lack the dense granules that normally contain key bioactive molecules involved in hemostasis (ADP, serotonin).
**Q: WHAT IS THE MOST COMMON CANINE BLEEDING DISORDER?
von Willebrand disease (vWD)
****how severe is the thrombocytopenia caused by vWD?
TRICK QUESTION--- NO THROMBOCYTOPENIA CAUSED. THIS IS A DISORDER OF THE CLOTTING FACTORS, NOT PLATELETS
what does wVF actually do, which is why the lack of it is a problem?
vWF stabilizes coagulation Factor-8, which mediates binding of platelets to subendothelial collagen
explain type I, II, and III of vWD
(I) low plasma [vWF], normalmultimer proportions, mild to moderate bleeding tendency (II) low plasma [vWF], absence of large multimers, moderate to severe bleeding tendency (III) absence of vWF, severe bleeding tendency (THREE IS JUST THE WORST, ISN'T HE?)
**********WHICH COAG FACTORS ARE K-DEPENDENT? WHY IS THE K NEEDED?
II, VII, IX, and X!!!! (Also regulatory molecules Protein C and Protein S). They are K-dependent because the factors must undergo carboxylation (catalyzed by γ-glutamyl carboxylase) to be functional, and carboxylation requires vitamin K as a cofactor
poisoning with coumarin-related molecules (e.g., warfarin) causes a coagulopathy how?
(condition associated with avitaminosis K) inhibiting vitamin K epoxide reductase >> absence of vitamin K in its active reduced form (so it can't activate the K-dependent factors, 2,7,9,10, and protein C and protein S)
how does fat malabsorption lead to a coagulopathy?
K is a fat dependent vitamin. if there is a 1º intestinal disease or impaired biliary outflow (uncommon), the K cannot be co-absorbed with the fat, so it is not absorbed, leading to an avitaminosis K (which means clotting factors 2,7,9,10 can't be activated via K-dependent carboxylation)
how common is a dietary deficiency of K, leading to a coagulopathy?
how do antibiotics and coagulopathies relate?
Abx can interfere with vitamin K absorption or usage
(what lab findings will you see with avitaminosis K?)
inc clotting in PT, PTT, and ACT
Disseminated intravascular coagulation (DIC); “consumptive coagulopathy" occurs when what happens? What usually causes this?
happens when there is continuous activation of both coagulation and fibrinolytic pathways. This is usually because of a 2º complication of many underlying diseases---> neoplasia, sepsis, endotoxemia, immune-mediated disease, IV hemolysis, shock, heat stroke, obstetric complications (e.g., premature placental separation in mares) (common in critically ill domestic animals)
explain the PATHOGENESIS of DIC
release of tissue factor(thromboplastin) >> activation of coagulation pathways and platelets (also involves defective normal inhibition of coagulation or defective fibrinolysis). There is an INITIAL HYPERCOAG STAGE (thrombosis and infarction will occur), followed by a subsequent hypocoagulable phase (consumption of coagulation factors and platelets >> hemorrhage)
what is the triad of laboratory findings associated with DIC?
(1) MODERATE thrombocytopenia (2) prolonged coagulation times(PT and/or PTT) (3) ↓fibrinogen, or ↑[plasma fibrin degradation products] or D-dimers (you will also see dec plasma conc of antithrombin III, and schistocytes!!)
What is going on in hemophilia A? Who does this disorder affect?
deficiency of functional coagulation factor VIII (Eight was a real type-A kinda gal). Affects horses, cattle, dogs, cats
what is going on in hemophilia B? Who does this disorder affect? (aka?)
aka "Christmas dz". This is a deficiency of functional coagulation factor IX (Nine B missing, because I don't have a Nine) and it affects dogs and cats
how does an animal get hemophilia A or B?
X-LINKED recessive mode of inheritance
The bleeding tendencies (severity of) in hemophilia A/B depend on...
severity of the deficiency, exposure to trauma, size and activity level of the affected individual. CARRIER FEMALES ARE USUALLY ASYMPTOMATIC
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