hemodyamics Part 3

Question 1

describe the role that doses play in warfarin and heparin on PT and PTT

Answer 1

• low does of heparin = normal PT, but prolonged PTT
• High dose of heparin = prolonged PT and PTT
• Low dose of warfarin = prolonged PT and normal PTT
• High dose of warfarin = prolonged PT and PTT

Question 2

what are the special considerations in elderly

Answer 2

• increased age associated with increased sensitivity at usual doses
• comorbidity
• increased drug interactions
• increased bleeding risk independent of the above

Question 3

when is warfarin therapy contraindications

Answer 3

• Pregnancy
• situations where the risk of hemorrhage is greater than the potential clinical benefits of therapy like in alcohol/drug abuse or unsupervised dementia/psychosis

Question 4

what are the signs of warfarin overdosage

Answer 4

• any unusual bleeding
• blood in stools or urine
• excessive menstrual bleeding
• bruising
• excessive nose bleed/bleeding gums
• persistent ooxing from superficial injuries
• bleeding from tumor, ulcer or other lesion

Question 5

Describe Warfarin Necrosis

Answer 5

• patients have low levels of protein C which can cause a transient hypercoagulable state resulting in local thrombosis of dermal vessels
• normally involves thighs, breasts and buttocks
• lesions develop that present with localized pain followed by erythema progressing to blue-black lesion that blisters

Question 6

describe heparin-induced thrombocytopenia

Answer 6

• seen in 5% of population given unfractionated heparin
• platelet factor 4 is released by platelets and binds heparin, thus BLOCKING its action and promoting coagulation
• antibodies to heparin bind heparin/platelet factor 4 complex resulting in endothelial injury and platelet activation which induces PROTHROMBOTIC STATE

Question 7

define bernard-soulier disease

Answer 7

• hemorrhagic disorder - Platelet abnormalities

- defect of platelet adhesion due to lack of glycoprotein Ib

Question 8

define glanzmann’s thombasthenia

Answer 8

• hemorrhagic disorder - platelet abnormalites

- defect of platelet aggregation due to lack of Glycoprotein IIb/IIIa

Question 9

define thrombotic thrombocytopenic purpura (TTP)

Answer 9

• hemorrhagic disorder - platelet abnormalities
• antibodies directed against the von willebrand factor cleaving protease
• ADAMTS-13 breaks up platelet-von willebrand complex
• form small thrombi
• patients have low platelets

Question 10

define idiopathic thrombocytopenic purpura (ITP)

Answer 10

• have antibodies directly against their platelets

Question 11

define aplastic anemia

Answer 11

• pancytopenia
• all the cell lines are done
• marrow gets fibrosis so you can’t produce any red cells or white cells

Question 12

define von willebrands disease

Answer 12

• coagulopathies
• deficiency of von willebran’s antigen
• most common bleeding disorder
• presentation = easily bruised, nosebleeds, gingival bleeding, menorrhagia (heavy perioid)

Question 13

define hemophilia A

Answer 13

• factor VIII deficiency

- most common

Question 14

define hemophilia B

Answer 14

• factor IX deficiency

Question 15

define hemophila C

Answer 15

• factor XI deficiency
• milder form
• often found in Ashkenazic jewish
• very rare

Question 16

what are the clinical presentations of hemophilia

Answer 16

• severe bleeding episodes throughout from minor trauma for A and B
• deep internal bleeding
• joint damage (arthropathy)
• tranfusion transmitted infection from blood transfusions that are given as tx
• adverse reaction to clotting factor treatment
• intracranial haemorrhage (can cause disorientation, nausea, loss of consciousness)

Question 17

how is the presentation of a factor deficiency different than a paltelet deficiencyfrom

Answer 17

• deficiency of coagualtion factor presents as trouble stopping bleeding from any wound
• platelet deficiency or defect presents as purpura, petechiae, and ecchymoses

Question 18

What is Disseminated intravascular coagulation (DIC)

Answer 18

• acute, subacute, or chronic onset of widespread activation of coagulation system
• tiny fibrin thromi form throughout the body, primarily in capillaries and small vessels
• depletes the supply of platelets (thrombocytopenia) and coagulation factors such that the patient is now in danger of bleeding (consumptive coagulopathy)

Question 19

describe the underlying mechanisms of DIC

Answer 19

• Underlying disorder causes systemic activation of coagulation
• -> results in consumption of platelets and clotting factors leading to BLEEDING
• -> Results in enhanced fibrin formation leading to microvascular thrombosis resulting in ORGAN FAILURE

Question 20

what are the effects of DIC

Answer 20

• results from the release of any substance into the bloodstream that results in WIDESPREAD ACTIVATION OF THROMBIN
• strands of fibin may block capillaries or may bridge them so that RBC are cut in half when they pass through
• Thombi may also obstruct circulation and cause numerous small infarcts

Question 21

how do you diagnose and treat DIC

Answer 21

• D-dimer assay measure plasmin-cleaved insoluble cross-linked fibrin (WILL BE HIGH)
• D-Dimer INDIRECTLY measures plasmin and thombin activity and those are biochemical markers of DIC
• TREATMENT = treat underlying cause and use blood products and heparin as needed

Question 22

What are the 3 states that can lead to thrombosis (referred to as Virchow’s triad)

Answer 22

• endothelial injury
• abnormal blood flow (circulatory stasis)
• hypercoagulability

Question 23

describe the mechanism Factor V leiden

Answer 23

• glutamine substitutes for arginine at position 506 of Factor V proteins
  –> causes resistance to degradation by activated protein C
• thereby producing an increased probability of thombosis
  (often develop recurrent DVT)

Question 24

what are some secondary risks for hypercoagulable states

Answer 24

• PROLONGED BEDREST OR IMMOBILIZATION (long flights etc)
• mycardio infarction
• atrial fibrillation
• tissue injury

Question 25

describe antiphospholipid antibody syndrome

Answer 25

• serum antibodies directed against anionic phospholipids
• in vitro (in test tube): inhibit clotting tests due to interference with assembly of phospholipid complexes
• in vivo (in person): causes hypercoagulable state
• clinical manifestations include: recurrent venous or arterial thrombi, repeated miscarriages, cardiac valve vegetations, thombocytopenia