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Clinical Pathology (VEM 5221) > Exam 2 > Flashcards

Exam 2 Flashcards

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
Q

Increased platelet destruction

A

Most common cause.
Primarily autoimmune thrombocytopenia (ITP).
Secondary immune-mediated thrombocytopenias (drugs, infectious, neoplasia)

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26
Q

Vitamin K dependent clotting factors

A

2, 7, 9, 10

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27
Q

Vitamin K

A

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

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28
Q

Anticoagulant proteins

A

anti-thrombin and alpha 2 macroglobin.
Anti-thrombin stops thrombin.
Thrombin converts fibrinogen to fibrin.
Heprin keeps thrombin and antithrombin together

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29
Q

Protein losing enteropathy (PLE)

A

low albumin and low globulin

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30
Q

Protein losing nephropathy (PLN)

A

Low albumin only

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31
Q

Low anti-thrombin

A

hypercoagulable state
DIC
PLN
PLE

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32
Q

Phases of clotting

A

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)

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33
Q

Von Willebrand’s factor

A

how platelets adhere to each other and the vasculature.

Deficiency in dobermans. Desmopressin stimulates transienty release of Von Willebrand factor from endothelial cells.

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34
Q

Platelet activating factor (PAF)

A

Major platelet agonists. Made by cells of immune system, this is one way that inflammation and coagulation are linked.

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35
Q

Hypercoagulable with inflammation

A

DIC

36
Q

DIC

A

secondary to underlying cause, it is not primary disease.

Pancreatitis, IMHA (especially intravascular because schist flying around)

37
Q

Clotting casccade

A

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
Q

Buccal mucosal bleeding test

A

platelet function test.

If prolonged- probably von willebrand’s factor defiency

39
Q

Factor VIIa

A

has the shortest half life

40
Q

Rodenticide

A

If an animal got into Vitamin K antagonist rodenticide it will have a prolonged PT (cause Vlla is in extrinsic pathway)

41
Q

Fibrinogenolysis

A

Occurs from crotalase in Eastern Diamondback rattlesnake venom

42
Q

cryoprecipitate

A

Contains von willebrand factor, fibrinogen, factors 8 and 13

43
Q

Thrombocytosis

A

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
Q

Hypercoagulable state

A

Most likely to have clot.
Initial reactions that lead to thrombosis and DIC.
Anti-thrombin deficiency

45
Q

Mast cells in circulation in dogs

A

IMHA, inflammation, or parvo virus especially.

Likely not from a mast cell tumor.

46
Q

Mast cells in circulation in cats

A

likely has a mast cell tumor in spleen, liver or intestines

47
Q

Snake venoms

A

degrade fibrinogen (you’d see increased FDPs, but not increased D-dimers, may see spheroechinocytes)

48
Q

Increased FDPs

A

it doesn’t necessarily mean the activation of the clotting cascade with active lysis of cross-linked fibrin clot.

49
Q

presence of D-dimers

A

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
Q

Fibrinogen is a positive acute phase protein

A

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
Q

DIC signs

A

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
Q

Hemophilia A

A

factor 8 deficiency

53
Q

Hemophilia B

A

factor 8 deficiency

54
Q

Factor 12

A

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
Q

PTT

A

assesses the intrinsic and common pathway

56
Q

PT

A

Tissue factor, factor 7a and common pathway

57
Q

If PT is normal but PTT is prolonged

A

only intrinsic pathway is affected.

can commonly be seen in cats since some don’t have factor 12

58
Q

If PT/PTT are both prolonged

A

think common pathway. factors 10, 5, 2 (pro-thrombin to thrombin), and 1 (fibrinogen to fibrin)

59
Q

Leukemoid response

A

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
Q

metarubicytes

A

nucleated RBCs

blood machines will count as leukocytes- beware

61
Q

Where are neutrophils stored?

A

normal neutrophil storage pool in the bone marrow.

Dogs > cats >horses > cows and sheep

62
Q

absolute numbers verse percentages

A

must look at absolute numbers of leukocytes!!

63
Q

Hypersegmentation in neutrophils

A

five or more distinct nuclear lobes. endogenous or exogenous glucocorticoids (old neutrophils in circulation), old blood samples.

64
Q

Granulocytes

A

basophils, eosinophils, neutrophils

65
Q

Chediak-Higashi

A

neutrophil production problem. cannot form phagolysosome

66
Q

Left shifting

A

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
Q

Neutrophilic toxicity

A

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
Q

band

A

immature neutrophil

69
Q

segmented neuts

A

mature neuts

70
Q

infectious agents of neutrophils

A

thrombocytopenia and shifting leg lameness=tick borne disease

71
Q

Regenerative left shift

A

mature neutrophils dominate.
Mature (segs) >immature (bands, metamyelocytes, myelocytes).
Better prognosis

72
Q

Degenerative left shift

A

immature neutrophils dominate
immature >mature
Worse prognosis, bone marrow is not keeping up with demand.

73
Q

Pelger-Huet Anomaly

A

in Australian Shepherd Dogs

Cannot segment neutrophils, eosinophils, basophils but they are still functional.

74
Q

Horses

A

have hypersegmented neutrophils

75
Q

Causes of neutrophilia

A

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
Q

Inflammatory Leukogram

A

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
Q

Physiologic leukogram

A

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
Q

Stress leukogram

A

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
Q

Example of mixed leukogram

A

Bands over 300
Lymphopenia
Inflammatory leukogram with underlying stress leukogram

80
Q

neutropenia

A 
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
Q

Eosinophilia

A

May be observed with certain cancers, such as a eosinophilic leukemia (super rare), mast cell tumors and T cell lymphomas.

82
Q

Low TP in a baby animal

A

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
Q

Leukemia

A

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
Q

Type of leukemia you’d rather have

A

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
Q

Moderate to severe lymphocytosis in a dog

A

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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