Acquired and Congenital Bleeding Disorders Flashcards

1
Q

Bleeding Disorders

Conditions that alter the ability of blood vessels walls, platelets and coagulation factors to maintain hemostasis

Causes: Diseases (leukemia), drugs, radiation, chemo

supplements: fish oil, omega-3 fatty acids, vitamin E, ginkgo, garlic, bilberry, ginger, dong quai, Asian ginseng, tumeric, medaow sweeet, willow, coumarin-containing herbs, chamomile, horse chestnut, red clover, fenugreek

A

Phases of hemostasis

Primary

  1. Vascular: vasoconstriction, induce platelet adhesion (wVF), initiates extrinsic pathway coagulation
  2. Platelet has surface proteins that sticks to vWF of exposed subendothelial tissues. Forms platelet plug. Also converts fibrinogen to fibrin, forms fibrin mesh.

Secondary

Coagulation (fibrin formation): intrinsic/extrinsic

Injury to fibrin-stabilized clot = 9-18 min

Thrombin on platelet surface converts fibrinogen to fibrin.

Finbrinolysis

Plasminiogen >>>(tPA)>>>>> Plasmin

Plasmin binds to fibrin and causes it to break up

tPA = tissue-type plasminogen activator

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2
Q

Coagulation Pathways

A
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3
Q

Platelet and Aspirin

A

Platelet aggregation: needs thromboxane (platelet product) which is produced in the COX pathway. Aspirin inhibits COX, causing irreversible dmg to platelet (life 8-12 days). Takes 9 days to clear all old platelets from blood.

  • Aspirin: most common anti-platelet drug*
  • 81 mg can lead to excessive bleeding in surgery, ok to suspend.*
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4
Q

Lab Values

aPTT (activated partial thromboplastin time)

  • checks intrinsic (F8,9,11,12) + common pathways
  • thromboplastin = tissue factor (TF), which initiates intrinsic clotting cascade
  • normal 25-35 s, abnl > 35 s

PT (prothrombin time)

  • checks extrinsic (F7) + common pathway
  • normal 11-15 s
  • INR format: standardizes PT assays (for pt on coumadin)

Platelet count

  • checks for thrombocytopenia (# platelet, not platelet dysfunction)
  • normal 140 K - 400 K/uL
  • excess bleeding when severe trauma: 50-100 K
  • excess bleeding with minor trauma: < 50 K
  • spontaneous bleeding: < 20 k
A

Disorder of

  • intrinsic pathway: normal PT, abnormal aPTT
  • extrinsic pathway: abnormal PT, normal aPTT
  • common pathway: prolonged PT + aPTT
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5
Q

Types of Acquired Bleeding Disorders

Vascular Defects

Scurvy: vit C deficiency >> weakened collagen

Platelet Disorders (#1)

Defective Thromboxane production

  • aspirin/NSAIDs, penicillins, CCB, alcohol

Coagulation Disorders

Disseminated Intravascular Coagulation (DIC)

etio: snake bite (#1), infection, preg complic, cancer

Acute: excessive bleeding. Chronic: blood clots

DIC: small blood clots develop throughout the bloodstream, blocking small blood vessels. The increased clotting depletes the platelets and clotting factors needed to control bleeding, causing excessive bleeding.

A

Systemic Problems

Liver disease affect:

  • coagulation: synthesis of vit K dependent cofactors
  • platelets: thrombocytopienic due to sequestration of platelets in spleen (splenomegaly from portal hypertension)
  • alcohol use

Leukemia thrombocytopenia from marrow crowding

Malabsorption or Long-term Antibiotics

affect gut bacteria that produce vitamin K

Renal Disease platelet dysfunction due to plasma toxin

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6
Q

Anticoagulant Drugs

Heparin: monitored with aPTT. LMWHs

Direct factor Xa Inhibitor: Apixaban

Coumadin: inhib liver synthesis of vit K-dependent factors (2-prothrombin,7,9,10). Mostly for A-fib. Monitored by PT (measures 2,7,10 extrinsic) but INR better accuracy international normalized ratio.

  • Low intensity therapy: INR 2-3 (2.5 target)
  • High intensity therapy: INR 2.5-3.5 (3 target)
  • normal = 1
A

Antiplatelet Drugs

Aspirin: irreversible inhibition of platelet cyclooxygenase, preventing synthesis of thromboxane A2.

NSAIDs: reversible COX inhibitors

Clopidogrel: irreversibly inhibit Platelet ADP receptor (usu for arterial stents)

Causes of Thrombosis

  • Venous thrombosis: age, h/o, immobilization, obesity, infec, hospitalization, major surgery, pregnancy*
  • Artierial thrombosis: atherosclerosis*
  • Venous+Arterial: malignancy, hormonal therapy, DIC*
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7
Q

Dental Management

INR 3.5 or below: OK for minor oral surgery without discontinuing drug (major surgery INR 3)

Extractions, dentoalvolar surgery OK if > 50 K/ul

Local Anesthesia: ok if platelet > 30 K/ul.

Drugs that will increase bleeding:

  • APAP, NSAIDs/aspirin, antibiotics,
  • Post op pain management: Low dose Tylenol + codeine
  • Avoid NSAIDs!
  • herbal meds

Drugs that increase clotting: steroids, barbiturates

Topical hemostatic agents: gauze, gelfoam, surgicel, colla-cote/tape/plug

INR adjustment:

  • 3-5 days needed for reduction of INR
  • confirm INR within 2 days before surgery
  • if no sig psot op complications, can resume warfarin
A

Oral manifestations

  • Spontaneous gingival bleeeding
  • Oral tissue petechiae, ecchymoses, jaundice, pallor, ulcers
  • Cancer patients: gingival hypeplasia, ulcers/tumors, osseous lesions, loose teeth, paresthesia
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8
Q

Congenital Bleeding Disorders

von Willebrand Disease: lack of vWF

  • #1 inherited platelet disorder
  • vWF allow platelet adhesion to damaged vascular wall >> lack of platelet adhesion
  • vWF carry factor 8 (hemophilia A) in circulation >> deficiency of factor 8 (unbound >> destroyed in circulation)
  • prolonged aPTT

Bernard-Soulier disease Platelet adhesion disorder: lack of glucoprotein 1b on platelet membrane (for binding of vWF)

Glanzmann’s thrombasthenia Platelet cannot bind to fibrinogen because of membrane glycoprotein dysfunc

HHT/Osler-Weber-Rendu syndrome: multiple telangiectasias with mechanical fragility of abnormal vessels (affect skin/mucous membranes/viscera). Telangiectasias in oral, face, nasal mucosa (nose bleeds), fingertips, toes, trunk.

Hemophilia A: #1 inherited coagulation disorder. Deficiency/defect in F-8 (carried by vWF in circulation). X-linked recessive. Spontaneous hemarthrosis. Prolonged aPTT.

Hemophilia B: deficiency/defect in F-9 (X’mas). X-linked recessive. Prolonged aPTT.

Hemophilia A and B: high risk for contaminated blood (HIV, Hep C)

Medical management:

mild: desmopressin, aminocaproic acid, tranexamic acid
severe: factor replacement therapy

A

Dental Management

Med consult and lab

Anesthesia: avoid blocks/lingual infiltration, FOM injection, IM (unless pt on desmopressin, aminocaproic acid, factor concentrates). OK to do infiltration and PDL.

Endodontic treatment: non vital teeth no precaution. Avoid over-instrum/filling. Vital teeth: Intrapulpal with EPI or 1:1000 epi on paperpoint for control of bleeding.

Analgesics: Tylenol +/- codeine only (no NSAIDS)

Antibiotics: not indicated unless acute infection present

Allergy: Factor replacement can cause allergic rxn

Trauma: Trauma to mand lingual tissue can cause airway obstruction. Splints for surgical procedures. Recall in 24-48 hr to check for bleeding.

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