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Clinical Pathology (VEM 5221) > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

How long do platelets last in circulation?

A

10 days

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2
Q

What does thrombocytosis mean?

A

increased platelets

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3
Q

What can cause a thrombocytosis

A

Inflammation
Iron deficiency anemia
Cushing’s disease
Steroid therapy

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4
Q

Can hemorrhage cause a thrombocytopenia

A

likely not. Unless you’ve lost all your blood volume or are in DIC

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5
Q

Why do we use a purple top when looking at platelets

A

Platelets have calcium in them and the clotting reactions need Ca+2. The purple tops have K/EDTA to inhibit Ca+2 in the blood so it won’t clot.
EDTA chelates the Ca+2 so it won’t clot

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6
Q

Calcium

A

positively charged and mediates the binding of the coagulation factor enzyme complexes via their negatively charged residues to the negatively charged phospholipid surfaces of platelets . allows the platelets to act as scaffolds for these reactions to occur

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7
Q

Most common breed to have Von Willebrand’s factor

A

Doberman

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8
Q

Cat platelets

A

Larger- with higher mean platelet volume.

Especially sensitive to activation during blood sample collection.

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9
Q

Hemostasis

A

the arrest of bleeding. Effective hemostasis requires an integrated response from the blood vessels, platelets, circulating clotting factors, and fibrinogen becoming fibrin

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10
Q

Primary hemostasis

A

peripheral vasoconstriction occurs.
Blood starts flowing again after momentary stoppage.
Platelets start degranulating and releasing Ca+2 to form a platelet plug.
Endothelial defect exposes subendothelial collagen.
End result= platelet plug

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11
Q

Secondary hemostasis

A

Stimulation of the coagulation system.
Thrombin converts fibrinogen to the active fibrin.
Fibrin is incorporated into the clot and the clot is stabilized

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12
Q

Coagulopathy

A

excessive bleeding due to abnormal function or lack of presence of a coagulation factor. Defect in secondary hemostasis. This is more of a problem than a platelet or a primary hemostasis problem. Lead to large amounts of bleeding not just petechiae or purpura.

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13
Q

Clot in the tube

A

Cannot trust the values from the hematology analyzer. She won’t even look at it.

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14
Q

Inherited asymptomatic thrombocytopenia

A

with macrocytic platelets. Seen in King Charles Spaniels and Greyhounds. 60-80,000 platelets can be normal; they are larger.

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15
Q

Mean platelet volume

A

Large platelets are younger platelets. Clumps will falsely decrease platelet count and increase MPV.

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16
Q

Thrombocytopenia

A

leads to petechiae, purpura or ecchymoses. Usually when they are less than 50,000, but usually even less than that. Worry about little hemorrhages that can occur in the brain, lungs, kidney, ect

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17
Q

Spontaneous hemorrhage

A

does not usually occur unless platelet counts are below 20,000

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18
Q

Blood draws for thrombocytopenic animals

A

veins far from the heart!! Also, you don’t wanna be sticking any organs for sample collection because you might not be able to stop the bleeding

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19
Q

Hallmark of tick borne disease

A

Thrombocytopenia

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20
Q

Evan’s syndrome

A

IMHA and immune-mediated thrombocytopenia (ITP) simultaneously

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21
Q

Thrombocytopenia differentials

A

Increased platelet destruction- most common.
Decreased platelet production.
Increased platelet consumption.

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22
Q

Decreased platelet production

A

do a bone marrow aspirate to see if you have enough platelet precursors (megakaryocytes). If you do not have enough it is perhaps do to myelophtisis (space occupying lesion of BM), myeloproliferative diseases or aplastic anemia.

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23
Q

Aplastic anemia

A

bone marrow not making anything! for example, estrogen knocks out bone marrow in ferrets and dogs

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24
Q

Increased platelet consumption

A

DIC, thrombosis, vasculitis and hemangiosarcoma in dogs. These animals would likely show changes in their PT/PTT since they are using a lot of platelets to make clots elsewhere (clotting factors too).

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25
Increased platelet destruction
Most common cause. Primarily autoimmune thrombocytopenia (ITP). Secondary immune-mediated thrombocytopenias (drugs, infectious, neoplasia)
26
Vitamin K dependent clotting factors
2, 7, 9, 10
27
Vitamin K
works by inhibiting the enzymes, vitamin K epoxide reductase, in the liver, making these factors hypofunctional. **If factor 7 disfunction animal with have prolonged PT on the test
28
Anticoagulant proteins
anti-thrombin and alpha 2 macroglobin. Anti-thrombin stops thrombin. Thrombin converts fibrinogen to fibrin. Heprin keeps thrombin and antithrombin together
29
Protein losing enteropathy (PLE)
low albumin and low globulin
30
Protein losing nephropathy (PLN)
Low albumin only
31
Low anti-thrombin
hypercoagulable state DIC PLN PLE
32
Phases of clotting
1) vascular phase- exposure of subendothelial matrix and exposure of tissue factor. 2) platelet phase- adhesion, activation, shape change, secretion, aggregation, platelet adhesion (Von Willebrand's factor)
33
Von Willebrand's factor
how platelets adhere to each other and the vasculature. | Deficiency in dobermans. Desmopressin stimulates transienty release of Von Willebrand factor from endothelial cells.
34
Platelet activating factor (PAF)
Major platelet agonists. Made by cells of immune system, this is one way that inflammation and coagulation are linked.
35
Hypercoagulable with inflammation
DIC
36
DIC
secondary to underlying cause, it is not primary disease. | Pancreatitis, IMHA (especially intravascular because schist flying around)
37
Clotting casccade
Tests are not very sensitive. Intrinsic: 12, 11, 9, 8 (PTT test) + common pathway. Extrinsic: VIIa, TF (PT test) + common pathway. Common pathway: 10+ 5, 2, 1
38
Buccal mucosal bleeding test
platelet function test. | If prolonged- probably von willebrand's factor defiency
39
Factor VIIa
has the shortest half life
40
Rodenticide
If an animal got into Vitamin K antagonist rodenticide it will have a prolonged PT (cause Vlla is in extrinsic pathway)
41
Fibrinogenolysis
Occurs from crotalase in Eastern Diamondback rattlesnake venom
42
cryoprecipitate
Contains von willebrand factor, fibrinogen, factors 8 and 13
43
Thrombocytosis
increased platelets. Inflammation is the most common reason (IL6 leads to increased thrombopoietin). Iron deficiency anemia. Prednisone (immunosuppressive and prevents macs from phagocytosing old platelets)
44
Hypercoagulable state
Most likely to have clot. Initial reactions that lead to thrombosis and DIC. Anti-thrombin deficiency
45
Mast cells in circulation in dogs
IMHA, inflammation, or parvo virus especially. | Likely not from a mast cell tumor.
46
Mast cells in circulation in cats
likely has a mast cell tumor in spleen, liver or intestines
47
Snake venoms
degrade fibrinogen (you'd see increased FDPs, but not increased D-dimers, may see spheroechinocytes)
48
Increased FDPs
it doesn't necessarily mean the activation of the clotting cascade with active lysis of cross-linked fibrin clot.
49
presence of D-dimers
means the active breakdown of convalently, crosslinked (via factor 13a) fibrin. Increased D-dimers means active coagulation and breakdown of clots. D-dimers are more specific for thrombus formation becuase it only occurs when soluble fibrin has been crosslinked by factor 13a and plasmin has cleaved this stable fibrin to form these unique D-dimers.
50
Fibrinogen is a positive acute phase protein
Increases with inflammation (might be only sign you see in large animals). See increased fibrinogen if an animal is inflammed- if you don't see it animal is in liver failure, cant make fibrinogen or its throwing clots (DIC?)
51
DIC signs
low fibrinogen increased D-dimers increased FDPs consumption of platelets (thrombocytopenia) fragmentation morphologies of RBC (acanthocytes, schistocytes, keratocytes) Animal need plasma now! or it will die. must find underlying cause.
52
Hemophilia A
factor 8 deficiency
53
Hemophilia B
factor 8 deficiency
54
Factor 12
deficiency does not cause bleeding disorders. it's missing in some cats and other species. It will increase PTT in vivo because the test is in a plastic tube.
55
PTT
assesses the intrinsic and common pathway
56
PT
Tissue factor, factor 7a and common pathway
57
If PT is normal but PTT is prolonged
only intrinsic pathway is affected. | can commonly be seen in cats since some don't have factor 12
58
If PT/PTT are both prolonged
think common pathway. factors 10, 5, 2 (pro-thrombin to thrombin), and 1 (fibrinogen to fibrin)
59
Leukemoid response
about 50,000 leukocytes/ul; indicates serious acute inflammation, is called leukemoid because it almost looks like leukemia. Infectious processes such as pyothorax and pneumonia. Immune-mediated disorders such as IMHA and polyarthritis. Differentiate from CML. Mostly seen in dogs because they have huge neutrophil reserves.
60
metarubicytes
nucleated RBCs | blood machines will count as leukocytes- beware
61
Where are neutrophils stored?
normal neutrophil storage pool in the bone marrow. | Dogs > cats >horses > cows and sheep
62
absolute numbers verse percentages
must look at absolute numbers of leukocytes!!
63
Hypersegmentation in neutrophils
five or more distinct nuclear lobes. endogenous or exogenous glucocorticoids (old neutrophils in circulation), old blood samples.
64
Granulocytes
basophils, eosinophils, neutrophils
65
Chediak-Higashi
neutrophil production problem. cannot form phagolysosome
66
Left shifting
more immature forms of neutrophils are coming out of bone marrow. Sign of inflammation. Normal: 0-300 bands Over 300 bands know you have an inflammation leukogram
67
Neutrophilic toxicity
toxic change refers to immaturity in neutrophils since theres an accelerated release from bone marrow and they haven't had time to clean up and basophilic RNA in their cytoplasm +1 = dohle bodies or basophilic cytoplasm +2 = dohle bodies and basophilic cytoplasm +3 = plus vacuolization of cytoplasm +4 = granulation brand "band neutrophil"
68
band
immature neutrophil
69
segmented neuts
mature neuts
70
infectious agents of neutrophils
thrombocytopenia and shifting leg lameness=tick borne disease
71
Regenerative left shift
mature neutrophils dominate. Mature (segs) >immature (bands, metamyelocytes, myelocytes). Better prognosis
72
Degenerative left shift
immature neutrophils dominate immature >mature Worse prognosis, bone marrow is not keeping up with demand.
73
Pelger-Huet Anomaly
in Australian Shepherd Dogs | Cannot segment neutrophils, eosinophils, basophils but they are still functional.
74
Horses
have hypersegmented neutrophils
75
Causes of neutrophilia
Epinephrine- causes BV and spleen to contract and neutrophils come out. Glucocorticoids- prednisone causes neutrophils not to egress from blood so there are a lot of old neutrophils in the blood. Inflammation.
76
Inflammatory Leukogram
more immature neutrophils and also usually accompanied by some neutrophil toxicity. Over 300 bands= inflammatory leukogram. Often see inflammatory leukogram with underlying stress leukogram
77
Physiologic leukogram
caused by stress- "excitement leukogram", mostly caused by vasoconstriction and splenic contraction. Mature neutrophilia with lymphocytosis. but mostly the lymphocytosis. Ex: took 30 minutes to draw blood. can see up to 20,000 lymphocytes in a scared cat just from splenic contraction
78
Stress leukogram
Mature neutrophilia, lymphopenia, eosinopenia, monocytosis. Lymphopenia may be the only salient feature because you could have an underlying inflammatory leukogram. Glucocorticoid effect- neutrophils cannot extravasate out of circulation and into the tissues, so they build up in the blood. Will have a mature neutrophilia.
79
Example of mixed leukogram
Bands over 300 Lymphopenia Inflammatory leukogram with underlying stress leukogram
80
neutropenia
``` increased utilization or destruction. acute infection before granulocytic hyperplasia has had time to occur. overwhelming sepsis or endotoxemia. look for an infection! mirgration into tissues is most common!! Decreased marrow production. Estrogen toxicity in dogs and ferrets. Viral infections (parvo). Severe chronic ehrlichiosis. ```
81
Eosinophilia
May be observed with certain cancers, such as a eosinophilic leukemia (super rare), mast cell tumors and T cell lymphomas.
82
Low TP in a baby animal
could indicate failure of passive transfer and put them at huge risk for infections because they don't have any maternal antibodies to protect them from pathogens and their immune systems are not fully developed.
83
Leukemia
Cancer arising from bone marrow. 2 main kinds- lymphoid and myeloid. Acute means you have a lot of blasts and immature forms in circulation. Chronic means the cells are well-differentiated.
84
Type of leukemia you'd rather have
Chronic lymphocytic leukemia> chronic myelogenous leukemia> acute lymphocytic leukemoa> acute myelogenous leukemia. You'd rather have well-differentiated cells in circulation and neutrophils. If you don't have neutrophils you need IV Abx
85
Moderate to severe lymphocytosis in a dog
usually raises suspicion for chronic lymphocytic leukemia (CLL) and I'd want to do a bone marrow or advance dx to make a diagnosis.

Clinical Pathology (VEM 5221) (1 decks)

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