Clin Path- Coagulopathies and Thrombogram 2

drraythe's version from 2016-03-10 15:37

Lecture 3

Question Answer
how common is a deficiency in vit K?second most common coagulopathy, way more common than intrinsic path probs
what might cause a vit K deficiency?Warfarin and its derivatives, Malabsorption, liver disease, AB treatment
what are the clin path abnormalities of a vit K deficiency? (4)(1) Markedly prolonged PT (2) Mildly prolonged PTT (3) Regenerative hemorrhagic anemia (4) Hypoproteinemia
what is OSPT? what does it measure?one stage prothrombin time. Examines extrinsic and common pathways.
what should be performed concurrently with a OSPT?and aPTT
what is PIVKA? what does it test?proteins induced by vitamin K antagonists. it tests for the Absence of or presence of VitK antagonists. (Inactive (non-functional) coagular-anticoagfactors basically---abnormalities in the vitamin-K dependent clotting factors)
what does a prolonged PIVKA mean?Strongly suggests warfarin
what is TCT/TT? what does it measure?Thrombin Clotting Time. measures the time it takes for a clot to form in a citrated plasma sample after an excess of thrombin has been added.
what does a prolonged TT/TCT mean?A prolonged TT or (delayed TCT) indicates an abnormality in the conversion of fibrinogen (soluble protein) to fibrin (insoluble protein) due to a quantitative (fibrinogen deficiency aka Hypofibrinogenemia) or qualitative (dysfunctional fibrinogen) defect.
what is Tertiary Hemostasis? (look at slide 6)enzymatic digestion of fibrin (fibrinolysis) after repair of blood vessels
what is happening in Hypercoagulation?Rate of activation of coagulation proteins >>rate Activation of anticoagulant factors. This leads to excessive blood clotting
what usually causes Hypercoagulation? what is a common Sequelae?Inflammation or infection usually cause this, and sequelae might be Thrombosis which precedes DIC
look at case studies in this lecturesigh
which tests are for checking the EXTRINSIC path?OSPT (one stage prothrombin time), PIVKA
which tests are for checking the INTRINSIC path?APTT ( Activated Partial Thromboplastin Time), ACT (activated coagulation time), CT (coagulation time)

Lecture 4

Question Answer
reversible BM abnormalities usually present as what first, and why?neutropenia, because neutrophils usually only live a few hours so they are depleted quickest (so, ddx of a neutropenia is a BM abnormality)
a reversible BM abnormality initially presents as a _________, what does it THEN present as?(neutropenia) a non-regen anemia, and a thrombocytopenia (all three are a aplastic pancytopenia)
what are two mechanisms by which you get reversible bone marrow abnormalities?BM suppression, destruction of stem cells(viruses, toxins, estrogens)
name some endogenous and exogenous situations where estrogen is causing the bone marrow abnormality. Is this treatable?ENDOGENOUS: (Genetic susceptibility in ferrets, Males dogs with sertoli cell tumor, Female dogs with cystic ovaries). EXOGENOUS: estrogen is used to treat Mismating, Pseudopregnancy, and Urinary incontinence. Early detection and tx restores normal BM function
what are the two ways a irreversible BM abnormality can present as?as a cytopenia or as unregulated proliferation(NEOPLASIA) (wide range of clinical signs happen from these)
what are some mechanisms of cytopenias/neoplasias which might be causing the irreversible BM abnormality? what is the possible etiology behind these?Lack of differentiation/ maturation of stem cells for cytopenias and in neoplasta, unregulated proliferation of stem cells. Viruses, toxins, radiation, idiopathic. (IRREVERSIBLE, so tx doesnt restore fx)
what is "atrophy" when referring to the BM? how rapidly do the clinical signs develop?Non-selective irreversible BM abnormality. clinical signs slow to develop
what is it called if only the erythrocytes are affected by the BM atrophy?pure red blood cell aplasia
which is more likely to occur, hypoplasia or atrophy?hypoplasia <<< atrophy (atrophy much more likely)
what is hypoplasia (in terms of BM)partial atrophy of the BM (according to the long notes)
Leukopenia+ Anemia+Thrombocytopenia= ?aplastic pancytopenia
what is hyperplasia of BM? and is a type of what response, to what causes?Increased cellularity of bone marrow (usually a selective process). form of bone marrow response, to things like inflammation, hemolysis, or acute hemmorhage.
describe the change in appearance of BM in a hyperplasiayellow(fatty, inactive) BM changes to red (Active)
how does hypertrophy relate to BM stuff?Hypertrophy=Increased organ size. This relates to Extramedullary hematopoiesis--> Hypertrophy of liver or spleen
**what happens in Myelodysplastic Syndrome (MDS)?Maturation of precursor cell stops at a certain point--> ****LEADS TO PENIAS***** (few mature cells in blood is why there is a penia)
what are the sequale (results) of a SELECTIVE MDS (myelodysplastic syndrome)? how about a NON-selective?selective: Anemia, or Leukopenia, or Thrombocytopenia. NON-selective: aplastic pancytopenia
what can be some causes of a myelodysplastic syndrome?usual suspects (virus, toxins, estrogens)
myelodysplastic syndrome (MDS) is a precursor to what?MPD-- myeloproliferative disease
WHAT IS A BLAST CRISIS?OVER the normal amount of blast(immature) cells (normal is up to 20, so, 21) but UNDER the amount required to be considered a leukemia (leukemia is 30, so, 29) thus, a blast crisis is when blast cells in the bone marrow are between 21-29%
what is a healthy ratio of blast cell:mature cell in healthy bone marrow?20:80
how does MDS and leukemia relate?it is a "pre" leukemia, as in, it is working up from the healthy normal of 20, up to the 30% definition of leukemia (it's 21-29%). MDS usually LEADS to leukemia
in what two situations might you get a blast crisis?atypical/still developing MPD or rpeleukemia (developing leukemia)
which specie is extremely susceptible to MDS?cats
what is Myelophthsis? what is it aka? what are the Sequelae(results) of it?aka-- panmyelophthisis. BM failure due to replacement of “normal” hemopoietic tissue with “abnormal” tissue (such a fibrous tissue, or neoplastic tissue) Sequelae can include anemia, thrombocytopenia, leukopenia (all together= aplastic pancytopenia)
what is Myeloproliferative Disease (MPD)? what is the mechanism (basic cause of this)Neoplasticclonal proliferation of one or more myeloid cells. Mechanism= Unregulated proliferation and differentiation
when does proliferation occur in MPD (myeloproliferative disease)?Proliferation may occur at any stage of the production line (blast-maturation-cyte)
what are the characteristics of myeloproliferative dz? (general) (3)(1) hypercellular BM (2) Distorted or disorderly maturation sequence (3) precursors May or may not spill into blood
what are some things that might cause MPD?Retroviruses, radiation, toxins (can cause selective or non-selective damage)
what are three most common reasons for high leukocytes?pyometria, peritonitis and acute MPD are most common reasons for high levels leukocytes
3 characteristics of an ACUTE myeloproliferative disease (MPD)?(1) undifferentiated cells in blood (2) >30% blast cells in BM (3) short survival time
6 characteristics of CHRONIC myeloproliferative disease (MPD)(1) lots of MATURE cells in blood (undiff in acute) (2) lots of MATURE cells in BM (blasts in acute) (3) longer survival time of cells (compared to the immature cells in acute) (4) infiltration of soft organs (5) splenomegaly (6) hepatomegaly
the clinical effects of MPD is dependent on the types of cells effected. list/name. what's important to note?note: there can be an initial period where there is no change in blood parameters! RBC precursors-->anemia. WBC precursors-->leukopenia(recurring infections). Megakaryocytes-->thrombocytopenia(bleeding). Aplastic pancytopenia.
the clinical effects of MPD is dependent on which cells spill into blood. list/name. what are some complications that might arise?RBC precursors-->Erythrocytosis. WBC precursors -->Leukocytosis=(leukemia). Megakaryocytes-->Thrombocytosis. Poor immune function: recurrent infection, bleeding etc...
3 acute characteristics of LEUKEMA?(1) undiff. cells in blood (2) >30% blast cells in BM (3) short survival time
3 chronic characteristics of leukemia?Lots of mature cells in bld, Lots of mature cells in BM, Longer survival time, Infiltration of soft organs, Splenomegaly, Hepatomegaly
Erythrocytic Sarcoma--> IN DOGS! what is going on? aka? how common is this dz? when in the production line does it occur, and what are some clinical signs?Neoplastic clonal proliferation of RBCs. AKA polycythemia vera. RARE dz. occurs late in production line-->mature RBC. The high primary RBC values means ---> erythrocytosis
Erythrocytic Sarcoma IN DOGS--> characteristics? (clin path abnormalities)Absence of heart or lung or kidney disease, EPO is WRI, Plasma proteins and albumin are WRI, High blood viscosity , Cyanosis, depression, thrombosis
Erythrocytic Sarcoma--> IN CATS! how common is this? what is the outcome dependent on? when in the production line does it occur? what kinda condition does it lead to?RARE. Outcome depends on RBC stage affected. occurs early in the production line-->Immature cells(these disintegrate easily and this leads to a non-regen anemia)
Erythrocytic Sarcoma IN CATS--> characteristics? (clin path abnormalities)Severe anemia, Many nRBCsin blood smear, Atypical cells in blood smear, Hepatomegaly?, Splenomegaly? (?=possibly)
what is Myelomonocytic Sarcoma?Neoplastic clonal proliferation of Granulocytoid or monocytoid cells or both.
how does myelomonocytic sarcoma present in the BM? (any abnormal blood parameters? which type of cell is most affected?)the WBCs are WRI to Low. The early precursor cells are affected.
how does myelomonocytic sarcoma present in the circulation? (what cells affected/seen? common in who? difference between acute and chronic? what is a DDX?)Mostly atypical cells (blast forms) in blood. it is common in DOGS. acute--> high numbers of blast cells. Chronic--> bands, metamyelocytes, myelocytes. DDX= leukemoid reaction
what is Megakaryocytic Sarcoma? describe early occurrence vs late occurrenceNeoplastic clonal proliferation of megakaryocytes. Early occurrence= thrombocytopenia, Neoplastic megakaryocytes--> (these can cause Myelophthisis (replacement of normal tissue with other, non fxn tissue) and Aplastic pancytopenia). Late occurrence= thrombosis and megaplatelets