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Clinical Pathology > Hemostasis > Flashcards

Hemostasis Flashcards

1
Q

Primary hemostasis

A

Platelets and platelet function

- vessels

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2
Q

Secondary

A

Coagulation

  • coagulation factors
  • vessel
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3
Q

Tertiary

A

Fibrinolysis

  • fibrinolytic molecules
  • vessel
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4
Q

_____ plays a role in all 3 parts of hemostasis

A

Vessel

  • no test to assess vessel function/viability
  • look for morphological presence via biopsy
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5
Q

If endothelial cells are quiescent, they will _____ primary and secondary and _____ tertiary

A

Inhibit; enhance

- once activated, they enhance primary and secondary and inhibit tertiary

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6
Q

Platelet - structure

A

Small fragments of megakaryocyte cytoplasm

  • phospholipid membrane w/ glycoproteins
  • open canalicular system of membrane invaginations
  • cytoskeleton
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7
Q

Platelet - granules

A
  • tubular system of ER: stores Ca (platelet activation and TBX production)
  • alpha granules: hemostasis and angiogenesis
  • dense granules: Ca, Mg, ADP, ATP
  • glycogen and mitochondria
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8
Q

Megakaryopoiesis and thrombopoiesis

A

Thrombopoietin and other cytokines

  • BM, spleen, lung (most important site of production)
  • platelets released directly into the blood
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9
Q

Thrombopoietin

A
  • hepatocytes (dogs), renal tubular epithelium, BM stromal cells
  • constitutively expressed
  • plasma concentration dependent on MPL receptor numbers (present in platelets and megakaryocytes)
  • inflammation: IL-6 –> TPO expression in BM
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10
Q

Reticulated platelets

A
  • young platelets
  • increased RNA
  • less than 24 hours in dogs
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11
Q

Platelet concentration

A
  • production
  • consumption
  • destruction
  • shift/sequestration
  • dilution
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12
Q

Blood smear

A
  • platelet estimation

- morphologic abnormalities

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13
Q

Platelet sample

A
  • EDTA
  • citrate, theopylline, dipyridamole, and adenosine (CTAD tubes) may be useful for cats
  • 8 hr at RT and 48 hr at 4C
  • check for platelet clumping
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14
Q

Platelet count

A
  • impedance counters
  • optical or laser flow cytometers
  • CBC
  • hemocytometer
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15
Q

Mean platelet volume

A

Varies between analyzer, anticoagulant and storage time

- presence of cell fragments and large platelets

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16
Q

Thrombocytopenia

A

Concentration is lower than the LRL

  • common in Greyhounds and Shiba Inus (lower than other dogs)
  • reflects a pathologic process (not a diagnosis)
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17
Q

Thrombocytopenia less than 30,000/uL

A
  • petechiae and ecchymosis

- mucosal bleeding (epistaxis, hematochezia, melena), hematuria, hyphema

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18
Q

Pseudo-thrombocytopenia

A
  • not all platelets were counted
  • in vitro platelet activation or aggregation
  • presence of large platelets (cats or CKCS) in impedance counters
  • cold agglutinins, or anticoagulant induced, antibody-mediated agglutination
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19
Q

Thrombocytopenia - shift/sequestration

A
  • reversibly distributed in vascular systems (spleen)
  • mild or moderate thrombocytopenia
  • splenomegaly
  • severe hypothermia (20 C, spleen and liver in dogs)
  • endotoxemia: lung pooling in dogs (may see increased consumption)
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20
Q

Thrombocytopenia - decreased production

A
  • generalized BM dz or MK specific process

- idiopathic thrombocytopenia of CKCS –> maybe due to lack of production

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21
Q

Thrombocytopenia - decreased production due to drugs

A
  • predictable, dose-dependent –> antineoplastic chemotherapeutic agents
  • idiosyncratic (sporadic)
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22
Q

Thrombocytopenia - decreased production due to infection

A

Multifactorial, often include decreased production

  • direct infection of MK (BVD, canine distemper)
  • myelosuppressive cytokines (EIA)
  • unclear (canine parvo, canine monocytic ehrlichiosis)
  • FeLV (due to neoplasia)
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23
Q

Thrombocytopenia - decreased production due to marrow replacement

A

Myelophthisis

  • bone marrow neoplasia: primary or metastatic, physical replacement, lysis of marrow cells, competition for nutrients, secretion of inhibitors, obstruction of blood supply
  • myelonecrosis: infections, neoplasia, toxicants
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24
Q

Thrombocytopenia - destruction

A

Immune mediated thrombocytopenia

  • platelet surface associated Ig (PSAIg)
  • Ab binds directly or indirectly
  • destruction by mononuclear phagocytic system
  • defective immune system –> defective platelets
  • absorbed antigens from neoplasm, drugs, infectious agents
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25
Q

IMT

A

Idiopathic or primary

  • not associated to a detected disease
  • could be autoimmune
  • common in dogs
  • Ab may target MKs
  • usually < 50 x 10^3/uL, often <10
  • anemia in 50%
  • usually MK hyperplasia (hypoplasia is possible)
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26
Q

Drug induced IMT

A

Drug independent Ab
- drug not necessary for binding
- Ag of drug cross-react with platelet Ag
Drug dependent Ab
- less common in animals
- Ab binds to drug that is associated to platelet
- suspected when IMT develops a few days after drug treatment was started

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27
Q

Drug induced IMT - criteria for diagnosis

A
  • PSAIg present
  • plasma Ab bind in vitro to platelets only in presence of drug
  • resolution after drug is discontinued
  • relapse after drug is reintroduced
  • gold salts, sulfonamides (dog)
  • methimazole and propylrhiocuracil (cats)
  • penicillin and TMS (horses)
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28
Q

IMT associated to infection - pathogenesis

A

Usually multifactorial

  • cross-reactive Ab
  • bacteria induced Ab production
  • exposure of hidden platelet Ag
  • binding of Ab to organism that is bound to platelets
  • immune complex formation that adhere to platelet membrane
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29
Q

IMT associated to infection - diseases

A
  • acute canine ehrlichiosis
  • Ehrlicia and Anaplasma
  • rocky mountain spotted fever
  • histoplasmosis, leishmaniasis
  • distemper or modified virus vaccination
  • equine infectious anemia
  • babesiosis
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30
Q

IMT - neonatal alloimmune thrombocytopenia

A

Maternal alloantibodies –> epitope on neonate’s platelets

  • horses, mule, foals, pigs
  • must be differentiated from other causes, especially sepsis
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31
Q

IMT - neoplasia

A

Multifactorial

  • may include immunologic mechanisms
  • lymphoma (dogs and horses)
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32
Q

IMT - systemic immune mediated diseases

A
  • SLE: evidence of increased PSAIg

- Evan’s syndrome: IMHA with IMT described in dogs (IMHA dogs prothrombotic, leading to platelet consumption)

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33
Q

Thrombocytopenia - dilution

A
  • blood loss (acute, severe): thrombocytopenia due to consumption, mild-moderate, self-limiting
  • hemodilution: crystalloids, colloids, plasma, packed erythrocytes
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34
Q

Thrombocytopenia - consumption

A
  • platelet activation w/ accelerated consumption or use: localized IV coagulation, consumption at the site, thrombin is a potent platelet activator
  • DIC
  • drugs or foreign materials
  • envenomation
  • vasculitis or endocarditis
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35
Q

Vasculitis/endocarditis

A

Activated endothelial cells or exposure of subendothelium

  • infections
  • bacterial endocarditis
  • endothelial cell damage and necrosis
  • Greyhounds cutaneous and glomerular vasculopathy associated with ingestion of Shiga toxin E. coli
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36
Q

Idiopathic thrombocytopenia of CKCS

A

Inherited giant platelet disorder

  • congenital (autosomal recessive)
  • common in the breed
  • macrothrombocytopenia (< 100,00/uL)
  • 50 - 100,00/uL is common, but platelet crit might be normal
  • no clinical bleeding problem
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37
Q

Thrombocytopenia - infectious

A

Decreased production

  • direct infection
  • immune suppression
  • BM inflammation
  • altered distribution
  • consumption
  • destruction (immune-mediated and nonimmune)
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38
Q

Thrombocytopenia - Anaplasma platys

A
  • infect platelets
  • clinical or subclinical
  • mild parasitemia (may be severe)
  • PCR diagnosis
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39
Q

Thrombocytopenia - neoplasms

A

Carcinomas, sarcomas, lymphomas, leukemias

  • 10% of dogs had thrombocytopenia
  • decreased production –> myelophthisis, myelodysplasia, estrogen secretion, chemotherapy
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40
Q

Thrombocytopenia - neoplasms (consumption)

A
  • DIC

- vasculitis or thrombosis

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41
Q

Thrombocytopenia - neoplasms (destruction)

A
  • secondary IMT

- hemorrhage, sepsis (due to immunosuppression), destruction (malignant histiocytic sarcoma)

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42
Q

Neoplasms - sequestration

A

Platelets being pooled into infected organs

  • splenomegaly or hepatomegaly (hemangiosarcoma)
  • organ congestion (sequestration)
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43
Q

Hypophosphatemia

A

Thrombocytopenia

  • hyperalimentation (dogs)
  • decreased platelet survival: decreased platelet ATP (decreased glycolysis)
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44
Q

Cats receiving parenteral nutrition do not have _____

A

Hypophosphatemia

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45
Q

Anaphylaxis

A

Thrombocytopenia

  • mechanism incompletely characterized
  • inflammatory mediators
  • DIC
  • immune complex interaction with platelets
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46
Q

Thrombocytosis

A

Platelet concentration greater than URL

  • redistribution
  • increased neoplasm: hemic neoplasm, reaction to other conditions
  • high altitudes: RI shifted upwards
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47
Q

Hemic neoplasia - primary

A

Essential thrombocytosis

  • chronic myeloproliferative condition
  • rare in dogs and cats
  • 1,000 to 5,000 x 10^3/uL
  • large, pleomorphic, hypogranular
  • increased numbers of MKs
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48
Q

Other chronic myeloproliferative diseases

A
  • polycythemia vera, primary erythrocytosis, chronic myeloid leukemia
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49
Q

Acute megakaryoblastic leukemia (M7)

A
  • subtype of myeloid leukemia
  • rare dogs and cats
  • > 30 of cells in BM are megakaryoblasts
  • thrombocytosis or thrombocytopenia
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50
Q

Thrombocytosis - reactive

A

Secondary

  • frequently mild to moderate
  • redistribution: physiologic thrombocytosis, dogs and cats, release from spleen or lungs
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51
Q

Reactive thrombocytosis leads to ______

A

Increased production

  • inflammation (IL-6 induced TPO production)
  • nonhemic malignant neoplasia (inflammation, thrombopoietic cytokines)
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52
Q

Iron defficiency

A

Common, but inconsistent in dogs

  • not cross reactivity with EPO
  • not increased TPO or IL-6
53
Q

Vinca alkaloids

A

Reactive thrombocytosis

  • vincristine and vimblastine
  • stimulation of thrombopoiesis
54
Q

Recovery from thrombocytopenia

A

Rebound

  • production exceeds destruction consumption
  • withdrawal of myelosuppression
  • recovery from IMT
  • after blood loss
55
Q

Thrombocytosis - increased production due to reactive

A

Postsplenectomy

  • occasionally marked thrombocytosis
  • increased TPO
  • transient (weeks)
  • decreased destruction
  • decreased sequestration
56
Q

Increased production due to blood loss

A

Chronic

  • several species
  • iron deficiency, inflammation, rebound, neoplasia
57
Q

Increased production due to hypercortisolemia

A

Hyperadrenocorticism and exogenous

58
Q

Function of the primary hemostatic plug

A

Adhesion –> perturbed endothelium or exposed subendothelium (collagen) via vWF binding to GPlb
Aggregation –> agonists (ADP, collage, PAF, thrombin), GPallbB3 via fibrinogen and vWF

59
Q

Release

A

Degranulation

  • fibrinogen, factor V, ADP, ATP, plasminogen
  • TXA2 adn arachidonic acid
60
Q

Facilitation of coagulation

A

Flipping of inner negatively charged phospholipids to outer cytoplasmic membrane

  • include phosphatidilserine (PF3)
  • high affinity sites for coagulation enzymes, cofactors, zymogen
61
Q

Clot retraction

A

Contractile process

  • activated platelets
  • GPallbB3 via fibrinogen
  • actin and myosin
62
Q

BMBT

A

Standardized primary hemostasis test

  • dogs and cats
  • interobserver and intraobserver variability
  • insensitive: only moderate to marked primary hemostasis defects
63
Q

BMBT procedure

A

Small cut 5 mm x 1mm upper lip

  • start timing when cut is made
  • remove excess blood from cut with filter paper w/o disturbing the cut
  • end point: when no blood is transferred to the paper filter
64
Q

Prolonged BMBT

A

> 4-5 min in dogs

  • thrombocytopenia
  • thrombopathia (platelet dysfunction): platelets, Htc, vWF WRI –> hereditary (uncommon), acquired: secondary
  • vWF: dobermans, prolonged BMBT, vWF:Ag <20%
  • anemia: centrally circulating platelets
  • vascular disease
  • antiplatelet drugs
  • afibrinogenemia
65
Q

vWF - physiologic process

A

Large multimeric protein –> large molecules are more functional

  • platelet adhesion
  • platelet aggregation
  • mostly produced by endothelial cells
  • forms noncovalent complexes with factor Vlll (protective and stabilizes)
66
Q

_____ is the most common hereditary bleeding disorder of dogs

A

vWF

  • 1: all vWF multimers are present, in decreased concentration
  • 2: deficiency of vWF with disproportionate decrease of large multimers
  • 3: absence of all multimers
67
Q

vWD - clinical and lab findings

A
  • mild to severe mucosal bleeding
  • hemarthrosis and hematomas in horses
  • absence of petechiae
  • prolonged BMBT
  • possibly decreased PTT due to decrease of factor Vlll (in humans, not dogs)
68
Q

Use ____ or ____ tubes for vWD

A

Sodium citrate or EDTA

- vWF:Ag is stable for 8 hours at RT

69
Q

vWD - interpretative considerations

A
  • intraindividual variation
  • exercise: increased after strenuous exercise
  • pregnancy: substantial increase (dogs)
  • epinephrine, endotoxin, azotemia, liver disease
70
Q

Coagulation

A

Forms thrombin –> converts soluble fibrinogen into insoluble fibrin

  • enzyme
  • substrate: fibrinogen, proenzyme
  • cofactors
  • on a phospholipid surface
  • presence of Ca –> mediates binding of factors onto platelet surface
71
Q

Coagulation eynzymatic factors are mostly ____

A

Proteases

  • primarily produced by hepatocytes
  • ll, Vll, lX and X are vit K dependent
  • factor lX is sex-linked (X chromosome)
72
Q

Coagulation - nonenzymatic factors

A
  • TF: cofactor for FVll, major activator of coagulation in vivo
  • fibrinogen: positive acute-phase protein produced by hepatocytes
  • FV and FVlll: markedly accelerate coagulation, facilitates surface attachment of other factors
73
Q

___ and ____ consumed during coagulation

A

FV and FVlll

- not in serum

74
Q

Extrinsic pathway

A

Initiated by TF that activates factor Vlll

  • initiates common pathway (factor X)
  • initiates intrinsic pathway (factor IX)
  • important in initiating thrombin generation
75
Q

Intrinsic pathway

A

Initiated by HMWK, PK and factor Xlll contacting negatively charged surfaces (collagen)

  • starts common pathway activating factor X
  • inhibited by ATlll
  • activated by factor Vllla –> activates factor IX
  • thrombin activates factor V, Xi and Vlll (propagates and amplifies thrombin generation)
76
Q

Common pathway

A

Initiated by activation of factor X

  • leads to formation of thrombin from prothrombin
  • thrombin forms fibrin monomers and multimers cross linked by factor Xllla
  • inhibited by ATlll
77
Q

ATlll

A

Produced by hepatocytes

  • same size of albumin
  • binds, inactivates, remove coagulation factor (lla, lXa, Xa)
  • ATll:enzyme complex is cleared by hepatocytes
  • markedly enhanced heparin (ex and endogenous)
78
Q

Activated coagulation or clotting time

A
  • sample: whole blood
  • screening coagulation test evaluates surface activation (intrinsic and common)
  • similar to PTT, but less sensitive
  • severe thrombocytopenia can increase ACT
  • standard protocol
  • used to monitor heparin therapy
79
Q

Activated partial thromboplastin time (aPTT)

A

Screen for intrinsic adn common

  • sample: citrated blood (plasma)
  • procoagulant phospholipids (partial thromboplastin), Ca
  • lab RI should be used
  • see changes with 70% or more decrease in activity of a factor
  • decreased FXll or PK (no hemorrhage) but prolonged aPTT
80
Q

Prothrombin time (PT)

A

Screening of extrinsic and common pathways

  • sample: citrated blood (plasma)
  • test: Ca, phospholipids, TF
  • use lab RI
81
Q

Thrombin time (TT)

A

Assesses transformation of fibrinogen in fibrin without the interference of thrombin generation

  • sample: citrated blood (plasma)
  • test: thrombin added to sample
  • lab specific RI
82
Q

Prolonged TT

A

Decreased fibrinogen

  • hypofibrinogenemia or afibrinogenemia
  • increased consumption localized coagulation or DIC
  • hereditary deficiency (rare)
  • dysfibrinogenemia (abnormal fibrinogen), hereditary or acquired (liver dz)
  • heparinized sample (due ATlll)
  • increased FDPs
  • paraproteinemia (abnormal Ig due to multiple myeloma)
83
Q

Proteins induced by vit K antagonism

A

Incompletely carboxylated vit K dependent factors

  • due to antagonism, deficiency, absence of vit K –> normal carboxylated factors are decreased
  • test: thrombotest PT, modified PT with added FV and fibrinogen added –> detects decreased activity of Fll, FVll, and X
  • can be decreased due to PIVKA presence since they compete with normally carboxylated factors
84
Q

Prolonged thrombotest PT

A
  • vit K antagonism or deficiency
  • other acquired and hereditary coagulopathies for PT excluding of FV and fibrinogen
  • cats with hepatic, biliary, or inflammatory bowel disease
  • heparin (endogenous or exogenous)
85
Q

ATlll (inhibitors)

A

Functional test: measure ATlll function not concentration

  • reported as % of either species-specific or human plasma pool
  • foals have decreased activity when compared with adult horses
86
Q

Decreased ATlll activity

A
  • hypercoagulable (prothrombotic) states
  • decreased production: liver dz, inherited dz, inflammation (decreased activity in baboons, and positive acute-phase protein in rabbits and cats), estrogens: decreased synthesis
  • loss: protein-loosing nephropathy or severe hemorrhage
87
Q

Decreased ATlll activity due to consumption

A

Increased hepatic clearance of complexes ATlll:F

  • localized coagulation or DIC
  • sepsis
  • heparin therapy (LMWH): accelerates use and thus hepatic clearance of ATlll
  • increased ATlll activity (unknown diagnostic utility)
88
Q

Decreased production

A
  • hepatic dz
  • inflammation
  • hyperestrogenism
89
Q

Loss

A

Protein losing nephropathy

90
Q

FIbrinolysis - process

A

Enzymatic degradation of fibrin

  • counteracts coagulation
  • initiated at the same time of coagulation
  • happens on hemostatic plug
  • plasmin
91
Q

Plasmin

A

Degrades: fibin, fibrinogen, FVa, FVllla, vWF, HMWK

  • rapidly inhibited by plasmin inhibitor
  • cleared by the liver
  • activated by t-PA
  • fibrin and fibrinogen degradation products: used to assess fibrinolysis, cleared by liver, phagocytes and kidneys
92
Q

Effects of increased FDPs

A
  • prolonged PT, aPTT, TT, ACT
  • impairs platelet function
  • compete with fibrinogen for thrombin
  • compete with fibrinogen for platelet binding sites
  • associate with fibrin monomers and may disrupt polymerization
93
Q

______ detects increased fibrinolysis due to excessive coagulation

A

FDPs

- may also detect increased fibrinogenolysis

94
Q

FDP sample

A

Serum

  • special tubes with thrombin or botox atrax venom
  • plasma: citrated plasma (24 hrs at 4 C)
95
Q

False results

A
  • serum samples: FDPs incorporated into the clots
  • generation of FDPs during blood collection
  • unspecificity of the test
96
Q

Increased FDPs

A
  • higher conenctration in equine neonates
  • localized intravascular coagulation
  • DIC
  • sepsis and inflammatory conditions
  • hemorrhagic fluid from body cavities
  • hyperplasminemia –> increased fibrinolysis: envenomations, administration of plasminogen activators, hypotensive shock/surgical trauma/heatstroke, increased endothelial production of t-PA
97
Q

D-dimer

A

Detect increased fibrinolysis due to excessive coagulation

  • should not detect fibrinogen
  • detects FXllla cross-linked fibrin
  • sample: citrated plasma (24 hrs at 4 C)
98
Q

Increased D-dimers

A

Similar for increased FDPs

  • except increased fibrinogenolysis
  • thromboembolic disease: specificity 80% - 94% (> 1,000 ng/mL)
99
Q

Blood vessel biopsy

A

Vasculitis and thrombosis

  • diseases involving small vessels
  • RMSF and equine purpura hemorrhagica
  • petechiae and ecchymosis
100
Q

Vessel disorders

A

Gross exam, serology, imaging, biopsy

  • large vessels: surgical and nonsurgical traumas, invasion, aneurysms, anomalies
  • small vessels: vasculitis (infections, immune-mediated and chemical), vasculopathies (rare)
101
Q

Blood disorders

A
  • impaired primary hemostasis
  • impaired secondary hemostasis
  • excessive fibrinolysis: DIC adn some envenomations
102
Q

Bleeding patterns

A
  • petechiae and ecchymosis: primary hemostasis problem or small vessels
  • subq hematomas and hemorrhage into blood cavities: secondary hemostasis (esp if petechiae and ecchymosis are absent)
  • hemorrhages thru mucosal surface: primary or secondary hemostasis problem
103
Q

Breed and age

A
  • breed: helps diagnose inherited dz

- age: young, inherited

104
Q

Gender

A

Hemophilia A FVlll deficiency and hemophilia B FlX deficiency

  • males are not carriers, only affected
  • females can be carriers or affected (rare) –> X linked
105
Q

Functional platelet problem: vWD or thrombopathia

A
  • PT = WRI
  • PTT = WRI
  • FDPs = WRI
  • TT = WRI
  • platelets = WRI
  • BMBT = prolonged
106
Q

Thrombocytopenia with or without platelet functional problems

A
  • PT = WRI
  • PTT = WRI
  • FDPs = WRI
  • TT = WRI
  • platelets = decreased
  • BMBT = prolonged
107
Q

Hepatic disease

A
  • PT = prolonged
  • PTT = prolonged
  • FDPs = WRI
  • TT = prolonged
  • platelets = WRI
  • BMBT = WRI or prolonged
108
Q

Hepatic disease

A

Defects in production and clearing of procoagulants, anticoagulants, profibrinolytics and antifibrinolytics
- bleeding is uncommon

109
Q

Hepatic disease - tests

A
  • PT, aPTT, TT, ACT: decreased production
  • FDPs and D-dimers: decreased clearance, intravascular coagulation
  • thrombocytopenia due to sequestration or decreased production
  • BMBT: thrombocytopenia, thrombopathia
  • fibrinogen: decreased production, consumption (DIC)
  • ATlll: decreased production, consumption
  • thrombopathia: FDPs or unknown
110
Q

Acquired or inherited

A
  • PT = WRI
  • PTT = prolonged
  • FDPs = WRI
  • TT = WRI
  • platelets = WRI
  • BMBT = WRI
111
Q

Hepatic or hepatobiliary disease, vit K antagonism (increased PT before aPTT)

A
  • PT = prolonged
  • PTT = WRI
  • FDPs = WRI
  • TT = WRI
  • platelets = WRI
  • BMBT: WRI
112
Q

Vit K antagonism (may see thrombocytopenia), hepatic disease (low normal fibrinogen)

A
  • PT = prolonged
  • PTT = prolonged
  • FDPs = WRI
  • TT = WRI
  • platelets = WRI
  • BMBT = WRI
113
Q

Vitamin K antagonism

A

Bleeding is common, 3-7 days after exposure

  • ingestion: hydroxycoumarins or indanediones, sweet clover or sweet grass, therapeutic coumadins, excessive coccidiostatis
  • inhibit recycling of oxidized vit K
  • absorbed in intestine
114
Q

Vit K antagonism - causes

A

Prolonged anorexia or abnormal diet

  • gut sterilization by antimicrobials
  • malabsorption (intra or extrahepatic cholestasis, intestinal malabsorption disease, exocrine pancreatic insufficiency
115
Q

Vit K tests

A
  • PT, aPTT, ACT: decreased vit K dependent factors

- thrombocytopenia: consumption

116
Q

Fulminant consumptive coagulopathy (DIC)

A
  • PT = prolonged
  • PTT = prolonged
  • FDPs = increased
  • TT = prolonged
  • platelets = decreased
  • BMBT = prolonged
117
Q

Consumptive coagulopathy

A

Process of accelerated or unbalanced coagulation that leads to destruction or removal of procoagulant molecules
- DIC: when this process happens throughout the vasculature (disseminated)

118
Q

Causes of consumptive coagulopathy

A
  • infection
  • tissue injury
  • malignant neoplasia
  • liver failure
  • heatstroke
  • pancreatitis
  • vascular disorders
  • toxins
  • immune mediated disorders
119
Q

CC - acute fulminant

A

Bleeding from multiple sites

120
Q

CC - chronic constipated

A

Not overly bleeding, but in fragile state

- may decompensate –> bleeding

121
Q

CC - diagnosis

A

Expect 3 or more:

  • thrombocytopenia
  • prolonged PT and/or PTT
  • increase FDP and/or D-dimer
  • decrease fibrinogen concentration
  • decrease ATlll
  • RBC fragments (schistocytes) on blood smear
122
Q

Causes of abnormal hemostatic test results

A
  • prolonged TT
  • thrombocytopenia
  • prolonged PTT, PT, ACT
  • decreased ATlll activity
  • increased FDP and D-dimers
  • prolonged BMBT
  • erythrocyte fragmentation
123
Q

Dilutional coagulopathy

A

Dilution of blood components by colloid fluids, crystalloid fluids, plasma poor packed erythrocytes or oxyglobin solution

124
Q

Inhibition of functional factors

A

Heparin administration or release from mast cells

  • prolongs PTT and ACT
  • PT usually has a heparin inactivator
  • FDPs –> increases TT, PTT, PT, ACT, BMBT
125
Q

Thrombosis

A

Formation of thrombi within vascular system

- shift of equilibrium between prothrombotic factors and antithrombotic factors

126
Q

Thrombosis causes

A
  • endothelial cell activation or damage
  • platelet activation
  • activation of coagulation
  • blood stasis
  • inhibition of fibrinolysis
  • deficiency or abnormalities of inhibitors
127
Q

Thrombosis - acquired conditions

A
  • vasculitis, endocarditis
  • CHF, feline cardiomyopathy, vascular defects
  • trauma
  • malignant neoplasia
  • sepsis, endotoxemia, equine colic and colitis
  • IMHA
  • hypothyroidism, hyperadrenocorticism
  • ATlll deficiency
128
Q

Thrombosis - hemostatic abnormalities

A
  • increased D-dimers
  • increased FDPs
  • decreased ATlll
  • thrombocytopenia
  • increased TT: decreased fibrinogen

Clinical Pathology (9 decks)

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