Path 2 - Hemolymphatic System 5

drraythe's version from 2016-02-09 00:59

Granulocytes/monocytes continued...

Question Answer
Monocytic Ehrlichiosis → (Not Granulocytic Ehrlichiosis). Explain the diffSome Ehrlichiae have a tropism for mononuclear cells, so Ehrlichiae morulae may be found in mononuclear cells of infected animals
Potomac horse fever is czd by what? What are the CS?It is an Equine Monocytic Ehrlichiosis czd by Neorickettsia risticii. The Rickettsia infects monocytes & enterocytes & czs a diarrheal dz
Ehrlichia canis czs what dz? What cells does it infect? What are the major effects 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 & subendothelial tissue infxn, which leads to platelet consumption, sequestration & destruction → thrombocytopenia, as well as leukopenia & anemia. (ONLY in DOG)
Ehrlichia canis czs what kind of anemia & has what CS associated w/ it?There is a NON-REGENERATIVE ANEMIA (the thrombocytopenia → bleeding tendencies → chronic blood loss → nonregen)
along w/ fever
LN enlargement
Bone marrow hypoplasia ±pancytopenia
Multifocal Nonsuppurative Meningoencephalitis
Interstitial pneumonia
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 & dogs. What happens is proliferation of nonneoplastic (i.e., polyclonal), well-differentiated but highly erythrophagocytic macrophages. Hemophagocytic syndrome occurs 2º to neoplasia, infxn, or other underlying dz (macrophage proliferation & hyperactivation in response to ↑ production of stimulatory cytokines in the 1º dz process)
What does the blood of an animal affected w/ hemophagocytic syndrome look like? What are the 4 big sequale?High numbers of macrophages in the bone marrow, LNs, spleen, liver & affected animals have cytopenias of 2 or more cell lines
The sequelae are:
Bleeding tendencies
Cytopenias of 2 or more cell lines.


Question Answer
Immune-Mediated Thrombocytopenia (IMT) → what czs this? What is the main result? What are some problems IMT could be 2° 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 2° to infxns (like Ehrlichia, EIA, or bacterial/fungal/protozoal) or drug administration (Cephalosporins, Sulfonamides), neoplasia, or other immune-mediated dzs
What is Evans syndrome?IMT + IMHA
Anaplasma platys is what kinda organism? Which cells does it infect? What is the main effect on the blood & what dz does it cz (& 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 czs is called Infectious Canine CYCLIC Thrombocytopenia. (Megakaryocytic hyperplasia & organism-associated antigen w/in 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 w/ impaired platelet fxn. Infxn of bone marrow megakaryocytes & circulating platelets
How does Feline leukemia virus (FeLV) relate to platelets?FeLV czs an infxn of hematopoietic cells, leading to platelet abnormalities (thrombocytopenia, thrombocytosis, ↑ platelet size & ↓ fxn)
Chédiak-Higashi Syndrome (CHS) → how does this relate to platelets? Explain the mechanismThis syndrome leads to platelet dysfxn (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).
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 & III of vWD(I) Low plasma [vWF], normal multimer 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?)


Question Answer
Know the diff btwn leukemia & lymphomaLeukemia originates in the BM, lymphoma originates in the lymphatic tissues
*What are the main types of lymphosarcoma for each species?EVERYONE IS MULTICENTRIC.....except for cats which are alimentary (Bc cat reasons)


Question Answer
**********WHICH COAG FACTORS ARE K-DEPENDENT? WHY IS THE K NEEDED?II, VII, IX & X!!!! (Also regulatory molecules Protein C & Protein S). They are K-dependent bc the factors must undergo carboxylation (catalyzed by γ-glutamyl carboxylase) to be fxnal & carboxylation requires vitamin K as a cofactor
Poisoning w/ coumarin-related molecules (e.g., warfarin) czs a coagulopathy how?(Condition associated w/ 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 & protein C & protein S)
How does fat malabsorption lead to a coagulopathy?K is a fat dependent vitamin. if there is a 1º intestinal dz or impaired biliary outflow (uncommon), the K cannot be co-absorbed w/ 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?Rare
How do ABx & coagulopathies relate?ABx can interfere w/ vitamin K absorption or usage
What lab findings will you see w/ avitaminosis K?↑ Clotting in PT, PTT & ACT
Disseminated Intravascular Coagulation (DIC); “consumptive coagulopathy" occurs when what happens? What usually czs this?Happens when there is continuous activation of both coagulation & fibrinolytic pathways. This is usually bc of a 2º complication of many underlying dzs → neoplasia, sepsis, endotoxemia, immune-mediated dz, IV hemolysis, shock, heat stroke, obstetric complications (e.g., premature placental separation in mares) (common in critically ill domestic animals)
Explain the PATHOGENESIS of DICRelease of tissue factor (thromboplastin) >> activation of coagulation pathways & platelets (also involves defective normal inhibition of coagulation or defective fibrinolysis). There is an INITIAL HYPERCOAG STAGE (thrombosis & infarction will occur), followed by a subsequent hypocoagulable phase (consumption of coagulation factors & platelets >> hemorrhage)
What is going on in hemophilia A? Who does this disorder affect?Deficiency of fxnal 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 fxnal coagulation factor IX (Nine B missing, bc I don't have a Nine) & it affects dogs & 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 & activity level of the affected individual. CARRIER FEMALES ARE USUALLY ASYMPTOMATIC