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Small Animal Medicine > Bleeding Disorders > Flashcards

Bleeding Disorders Flashcards

1
Q

What is hemostasis?

A

process of clot formation and subsequent breakdown

  • balance between clotting and fibrinolysis
  • excess clotting = thrombosis
  • excess fibrinolysis = hemorrhage
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2
Q

What are the 4 steps in hemostasis?

A
  1. endothelial injury
  2. primary hemostasis - platelets and vWF form platelet plug
  3. secondary hemostasis - clotting factors form fibrin clot
  4. fibrinolysis once injury is no longer present
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3
Q

How does endothelial injury start off hemostasis?

A

injury to vascular endothelium results in localized vasoconstriction to reduce blood loss and tissue factor exposure to blood, initiating coagulation

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4
Q

What are the 4 steps to primary hemostasis?

A
  1. vWF at the site of endothelial injury and collagen exposr=ure causes platelet adhesion
  2. platelets undergo changes in their shape (activate!)
  3. platelets release granules of ADP and TxA2 to recruit more platelets
  4. more platelets aggregate and form the hemostatic plug (linked together with fibrinogen and vWF)
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5
Q

What are the 2 pathways of blood coagulation during secondary hemostasis? What coagulation factors take part in each? What tests evaluate each?

A

EXTRINSIC - factor VII activated by tissue factor release with blood exposure; PT

INTRINSIC - factors XII, XI, IX, VIII activated by direct collagen contact; PTT

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6
Q

What are the steps in the intrinsic, extrinsic, and common pathways of blood coagulation?

A

INTRINSIC - rollback special ($12 —> $11.98)

EXTRINSIC - 7 + 3 (TF) = 10

COMMON - 10/5 = 2

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7
Q

What does secondary hemostasis require? How does it occur?

A

clotting factors and fibrinogen produced by the liver

  • prothrombin is cleaved into thrombin
  • thrombin converts fibrinogen into fibrin
  • factor XIII is activated and crosslinks fibrin to stabilize the initial blood clot
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8
Q

What 2 things occur during fibrinolysis?

A
  1. plasminogen is converted into plasmin by tissue plasminogen activator (t-PA)
  2. fibrin monomer and x-linked fibrin are broken down into degradation products by plasmin, resulting in the production of FDPs and D-dimers and removal of the fibrin plug

(FDPs and D-dimers can be measured to analyze abnormal clot formation and fibrinolysis)

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9
Q

What coagulopathies are associated with primary and secondary hemostasis?

A

PRIMARY - thrombocytopenia, thrombocytopathia, endothelial disease

SECONDARY - congenital/acquired coagulopathies

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10
Q

What are 6 common presentations in patients with bleeding disorders?

A
  1. black stool (melena) - GI bleeding
  2. owner or groomer notices petechia and ecchymosis
  3. bloody urine
  4. known/possible ingestion of vitamin K rodenticides
  5. sudden collapse
  6. hemoabdomen
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11
Q

What clinical signs are associated with primary hemostasis?

A
  • petechia, ecchymosis
  • mucosal hemorrage
  • epistaxis
  • urinary hemorrhage
  • melena
  • hematemesis
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12
Q

What clinical signs are associated with secondary hemostasis?

A
  • ecchymosis
  • hemarthrosis
  • body cavity hemorrhage
  • melena
  • hematemesis
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13
Q

What should be avoided in patients with high probability of hemorrhage when trying to diagnose causes of coagulopathies?

A

jugular vein sampling

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14
Q

What testing is most commonly used for diagnosing primary vs secondary hemostasis?

A

PRIMARY - platelet counts, buccal mucosal bleeding times (should be around 4 mins), vWF concentration

SECONDARY - prothrombin time (extrinsic, common), partial thromboplastin time (intrinsic, common), D-dime (DIC, hypercoagulability)

  • park trucks (PT) outside
  • poker table tournament (PTT) inside
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15
Q

What are the most common tests for analyzing platelets taking part in primary hemostasis?

A

platelet coount - thrombocytopenia most common, does NOT assess platelet function

buccal mucosal bleeding time - assess function of platelets and endothelium —> should take about 4 mins

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16
Q

What are the major tests for secondary hemostasis?

A

prothrombin time (PT) = extrinsic, common

partial thromboplastin time (PTT) = intrinsic, common

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17
Q

What are the 2 major tests of overall hemostasis?

A
  1. fibrin degradation products (FDP) - increased due to fibrinolysis or excessive coagulation
  2. D-dimer - more accurate than FDP
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18
Q

When are clinical signs of thrombocytopenia seen? What signs are characteristic?

A

bleeding = <50 k/uL

(<30 k/uL)
- petechia
- mucosal hemorrhage
- epistaxis
- urinary hemorrhage
- melena

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19
Q

What is thrombocytopenia? What must also be done fora diagnosis? Why?

A

decreased platelet numbers

confirmation with a manual blood smear

pseudothrombocytopenia commonly seen with platelet clumping (cats!) and congenital macrothrombocytopenia where the machine do not recognize these platelets

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20
Q

What is congenital macrothombocytopenia? What breeds are predisposed?

A

inherited abnormality in platelet formation with a count ranging from 50000-100000/uL with many larger circulating platelets —> no bleeding tendencies

  • Cavalier King Charles Spaniels
  • Norfolk Terriers
  • Cairn Terriers
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21
Q

What are the 4 major causes of thrombocytopenia?

A
  1. destruction - immune-mediated, infection, vaccination
  2. consumption - DIC, neoplasia, vasculitis, hemorrhage
  3. sequestration - hypersplenism
  4. decreased production - immune-mediated, marrow neoplasia, Ehrlichiosis, FeLV, myelodysplasia, myelofibrosis
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22
Q

What is idiopathic immune-mediated thrombocytopenia (IMTP)? What breeds are predisposed? What clinical signs are associated?

A

abnormal immune response directed against platelets +/- megakaryocytes

  • Cocker Spaniels
  • Old English Sheepdog
  • Poodle

spontaneous hemorrhage without other signs of illness

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23
Q

What are the 3 most common laboratory findings associated with IMTP? What additional finding is less common?

A
  1. severe thrombocytopenia (0-20000/uL)
  2. regenerative anemia (blood loss)
  3. hemorrhage* - hypoalbuminemia, hypoglobulinemia, elevated BUN

hemolysis (Evan’s syndrome) - hyperbilirubinemia, spherocytosis, RBC agglutination

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24
Q

What is the most common cause of IMTP? What are 4 other possible causes?

A

PRIMARY = idiopathic, must rule out everything else

SECONDARY

  1. drugs - Cephalosporins, Penicillins, Sulfonamides
  2. vaccination
  3. infection - Rickettsial (Ehrlichiosis, Anaplasmosis, RMSF, Borreliosis), FeLV, focal infections
  4. neoplasia - lymphoma
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25
Q

What diagnostics are recommended for IMTP?

A
  • minimum database (CBC/Chem, UA) - r/o UTI, assess organ function
  • blood smear - confirmation, r/o hemolysis (Evan’s), evaluate for infection or neoplasoa
  • thoracic rads / abdominal ultrasound - evaluate for neoplasia or focal infection
  • infectious disease testing - 4DX Snap or SNAP FIV/FeLV +/- PCR and serology panels based on suspicion for Rickettsial disease
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26
Q

What are the 3 major treatment principles for IMTP? What is the initial goal?

A
  1. identify and treat any underlying causes
  2. suppress the abnormal immune response
  3. maintain tissue perfusion and oxygenation

increase platelet count above the threshold for spontaneous hemorrhage (30000/uL)

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27
Q

What immunosuppressive is recommended for IMTP treatment? What 4 can be added on if there is no response?

A

Prednisone - effective by itself in most cases

  1. Azathioprine
  2. Mycophenolate
  3. Cyclosporine
  4. Leflunomide
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28
Q

What 2 adjuvant treatments or IMTP are recommended?

A

aid immune system temporarily

  1. Vincristine
  2. IVIg - Ig blocks Fc receptors on macrophages to block platelet consumption
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29
Q

What treatment is recommended for Rickettsial infections that may trigger IMTP? How is it started?

A

Doxycycline - Ehrlichia, Anaplasma, Borrelia, RMSF

start while waiting for infectious disease results (or if testing is not possible) and continue for 28 days

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30
Q

Why is Vincristine commonly indicated as an adjuvant for IMTP therapy?

A

increases platelet count quicker than Prednisone alone by poisoning platelets so macrophages undergo apoptosis when they try to eat the platelets

  • smaller than chemotherapy dose
31
Q

What are 3 potential side effects when using Vincristine for treating IMTP? What needs to be avoided?

A
  1. GI upset - anorexia, vomiting, diarrhea
  2. transient leukopenia
  3. vesicant

extravasation - place a new IVC dedicated to administering Vincristine and remove it once the drug is given

32
Q

When is blood transfusion indicated? What is most commonly transfused?

A

clinical signs related to blood loss anemia are present

  • fresh whole blood
  • packed red blood cells (pRBCs)
33
Q

What are 2 negative prognostic indicators for IMTP?

A
  1. GI hemorrhage
  2. increased BUN
34
Q

What is thrombocytopathia?

A

impaired platelet function when there is normal platelet counts and clotting times (PT, PTT), which predisposes to hemorrhage

35
Q

What are 4 acquired causes of thrombocytopathia?

A
  1. DRUGS: Aspirin, Clopridogrel, NSAIDs, calcium channel blockers, antibiotics
  2. INFECTION: Ehrlichiosis
  3. ORGAIN FAILURE: liver, kidney
  4. NEOPLASIA: multiple myeloma
36
Q

What is the most common congenital cause of thrombocytopathia? What are 2 other causes?

A

von Willebrand’s disease

  • Glanzmann’s thrombasthenia
  • Bassett Hound thrombopathia
37
Q

What is von Willebrand disease? What is it associated with?

A

congenital thrombocytopathia caused by a lack of vWF, which is responsible for adhering platelets to damaged endothelium

prolonged bleeding following trauma or elective surgeries +/- conpantous mucosal bleeding

38
Q

What are the 5 most common breeds affected by von Willebrand disease?

A
  1. Doberman Pinscher
  2. German Shorthaired/Wirehaired Pointer
  3. German Shepherd
  4. Scottish Terrier
  5. Shetland Sheepdog
39
Q

What crude test is used for diagnosing von Willebrand disease? Confirmatory test?

A

BMBT > 4 mins, consider performing in at-risk breeds

vWF assays (vWF:Ag)

40
Q

What affects BMBT results?

A

platelet count, platelet function, health of endothelium —> assesses endothelial and platelet function

  • only perform in patients with normal platelet counts
41
Q

What is the best option for treating von WIllebrand’s disease? What are 2 other options?

A

replace deficient vWF with cryoprecipitate, which has high concentrations

  • fresh frozen plasma
  • DDAVP can cause a release of preformed vWF, but it is not very effective in dogs with VWD
42
Q

What are 4 acquired causes of secondary hemostasis deficiencies?

A
  1. vitamin K antagonists - rodenticides!
  2. liver failure
  3. neoplasia
  4. DIC
43
Q

What is hemophilia A and B? What are they associated with?

A

X-linked, recessive traits commonly affecting males, resulting in Factor VIII and IX deficiencies

prolonged bleeding with trauma or elective surgeries, or spontaneous cavitary bleeding

44
Q

What patients will have the highest suspicions of hemophilia A or B? How are they diagnosed? How are each treated?

A

young animals with unexplained bleeding and prolonged PTT with normal PT

factor assays

  • A = cryoprecipitate
  • B = fresh frozen plasma
  • given for severe bleeding episodes or prophylactically before invasive procedures
45
Q

What is vitamin K? What is it required for?

A

fat-soluble vitamin that requires bile acids to facilitate GI absorption

production and activation of coagulation factors II, VII, IX, and X

46
Q

What are the 2 major causes of vitamin K deficiency?

A
  1. anticoagulant rodenticides
  2. hepatic disease, like extrahepatic bile duct obstruction or intrahepatic cholestasis, which causes decreased bile secretion and vit K absorption
47
Q

How do vitamin K antagonist rodenticides work? What does this result in?

A

inhibits vitamin K reductase, which causes rapid depletion of active vitamin K and an inability to produce active clotting factors

PT will prolong first, since VII has the shortest half-life and clinical signs will be observed 2-5 days after ingestion (cavitary bleeding!)

48
Q

How is vitamin K antagonist rodenticide toxicity diagnosed?

A
  • PT prolonged first within 36-72 hrs, later followed by PTT
  • anticoagulant rodenticide screening panels based on blood or liver —> determines type of anticoagulant ingested
49
Q

What are the 3 types of anticoagulants?

A
  1. FIRST GEN - shorter acting (7-14 days) Warfarin
  2. INTERMEDIATE - Chlorphacinone, Dipacinone
  3. SECOND GEN - longer acting (21-30 days) Brodifacoum, Bromadiolone, Difethiolone

identification of type affects duration of treatment

50
Q

How is asymptomatic anticoagulant toxicity treated?

A

remove toxin by inducing emesis if within 4 hr of ingestion + monitor PT —> baseline, 48 hr, 72 hr - if PT prolongs, start vit K1 therapy

OR

start vit K1 therapy initially WITH FOOD to aid in absorption —> recheck PT in 48 and 72 hr

51
Q

How is symptomatic anticoagulant toxicity treated?

A
  • blood component therapy
  • vit K1 therapy - oral (NEVER IV) with food and recheck PT within 48 and 72 hr
52
Q

What are the 2 transfusion therapies recommended for anticoagulant toxicity treatment?

A
  1. fresh frozen plasma - replaces depleting clotting factors while waiting for vit K1 to take effect, most commonly in patients with signs of significant bleeding
  2. fresh whole blood - replaces clotting factors and provides RBCs for patient with clinical anemia

if fresh whole blood is not available, give frozen plasma + pRBCs

53
Q

What primary hemostasis defects can liver disease cause?

A
  • THROMBOCYTOPENIA: decreased hepatic thrombopoietin, DIC
  • THROMBOCYTOPATHIA
54
Q

What secondary hemostasis defects can liver disease cause?

A
  • decreased clotting factor synthesis
  • hypofibrinogenemia
55
Q

What is the main therapy used with liver disease causing hemostasis deficiency? What other 2 treatments should be considered and when?

A

treating underlying hepatic disease (clinical bleeding associated with fulminant or end-stage failure)

  1. vitamin K1 therapy - cholestasis with prolonged PT or PTT and are undergoing a surgical procedure or are bleeding
  2. fresh frozen plasma - prolonged PT or PTT and undergoing surgery or are actively bleeding
56
Q

What are the 4 steps to the pathophysiology of disseminated intravascular coagulation?

A

systemic activation of coagulation

  1. proinflammatory cytokines and endotoxins cause the release of tissue factor
  2. excess TF leads to thrombin generation (coagulation!)
  3. intravascular fibrin deposition, platelet activation, thrombosis and organ damage begin to occur non-clinically
  4. consumption of clotting factors and platelets lead to a hypocoagulable state and clinical bleeding
57
Q

What are the 4 causes of hemorrhage due to DIC?

A
  1. coagulation factor deficiency due to consumption from excessive coagulation
  2. thrombocytopenia due to consumption
  3. thrombocytopathia due to FDP coating platelets
  4. excessive fibrinolysis due to the activation of plasmin, which breaks down fibrin clots (increased FDP nad D-dimers)
58
Q

What are the most common signs of chronic, compensated DIC?

A
  • often no signs
  • mild hemorrhage
  • may abruptly decompensate
  • clinical signs associated with underlying disease
59
Q

What are the most common signs of acute, uncompensated DIC?

A

SEVERE FORM

  • hemorrhage
  • hypotension due to endothelial damage, thrombi, and hemorrhage
  • multiple organ failure
  • thrombosis of large vessels, like pulmonary, aortic, portal, and vena cava
60
Q

What diseases are associated with DIC?

A
  • neoplasia
  • sepsis
  • immune-mediated hemolytic anemia
  • pancreatitis
  • liver disease
  • snake bite envenomation
  • heat stroke
  • major trauma
61
Q

What are the 2 major supportive evidences of DIC? What are 4 others?

A
  1. thrombocytopenia (mild to moderate)
  2. prolonged PTT +/- PT
  • schistocytes
  • increased FDPs or D-dimers
  • hypofibrinogenemia
  • viscoelastic testing to differentiate stages
62
Q

What is the main part of DIC therapy? What are 3 other aspects?

A

diagnose and treat underlying disorder

  1. fluid therapy - combats capillary obstruction and restores profusion
  2. prevent further thrombosis with platelet inhibitors (aspirin, clopidogrel) or clotting factor inhibitors (heparin) only if in the hypercoagulable state, NOT if clinical bleeding is susspected
  3. replenish clotting factors with fresh frozen plasma (no blood loss) or fresh whole blood (blood loss) if int he hypocoagulable state
63
Q

What is the prognosis of DIC like?

A
  • depends on underlying disease
  • chronic form is usually not life-threatening
  • acute, decompensated form is life-threatening
64
Q

What causes thrombosis?

A

disruption of hemostatic balance (Virchow’s triad)

  • endothelial damage
  • abnormal blood flow
  • hypercoagulable state
65
Q

What are some predisposing factors to endothelial damage?

A
  • promotion of coagulation
  • loss of anticoagulation
  • sepsis
  • vasculitis
  • neoplasia
  • heartworm disease
  • IV catheter
  • atherosclerosis
66
Q

What are some predisposing factors to blood stasis or turbulence?

A
  • heart disease: enlarged atria, valvular disease
  • increased viscosity
  • shock
  • prolonged recumbency
67
Q

What are some predisposing factors to hypercoagulability?

A
  • hemolytic anemia
  • hyperadrenocorticism
  • glomerular disease
  • DIC
  • sepsis
  • neoplasia
  • pancreatitis
68
Q

What is the most common sign of pulmonary thromboembolism? What are 3 radiographic signs?

A

acute onset of respiratory distress and hypoxemia

  1. interstitial or alveolar infiltrate
  2. hypolucency (hypoperfusion)
  3. pleural effusion
    (rads may be normal, may need CT to find smaller embolisms —> must be a good GA candidate)
69
Q

What are 3 signs of aortic thromboembolism? In what patients is this most common?

A
  1. acute onset of hind limb paresis
  2. painful, firm muscles
  3. cool distal hind limbs that lack femoral pulses

cats with cardiomyopathy and dilated LA

70
Q

How is thromboembolic disease diagnosed?

A
  • clinical presentation for specific locations
  • presence of underlying disease
  • imaging: radiographs, contrast studies, U/S
  • D-dimer to r/o hypercoagulation
71
Q

What 3 possible thromboprophylaxis is recommended in patients that could develop PTE?

A
  1. ultra-low-dose Aspirin
  2. Clopidogrel
  3. Heparin

prevents new clot formation and breaks down current ones

72
Q

How does aspirin and clopidogrel worl?

A

ASPIRIN - cyclooxygenase inhibition, which blocks thromboxane and prostaglandin formation

CLOPIDOGREL - P2Y12 receptor antagonist and glycoprotein IIa/IIIb inhibitor, which blocks platelet adhesion and aggregation

73
Q

What are the 2 options for heparin treatment?

A
  1. unfractionated - binds to anti-thrombin III, which stops the inhibition of factor Xa and thrombin = more risk of bleeding
  2. low molecular weight (Enoxaparin, Deltaparin) - not as effective at inhibiting thrombin because it binds to factor Xa only = less risk of bleeding
74
Q

What are 2 factor Xa inhibitors? What does their action result in?

A
  1. Rivaroxaban
  2. Apixaban

blocks clot formation

Small Animal Medicine (52 decks)

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