hemodyamics Part 3 Flashcards
1
Q
describe the role that doses play in warfarin and heparin on PT and PTT
A
- 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
2
Q
what are the special considerations in elderly
A
- increased age associated with increased sensitivity at usual doses
- comorbidity
- increased drug interactions
- increased bleeding risk independent of the above
3
Q
when is warfarin therapy contraindications
A
- 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
4
Q
what are the signs of warfarin overdosage
A
- 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
5
Q
Describe Warfarin Necrosis
A
- 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
6
Q
describe heparin-induced thrombocytopenia
A
- 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
7
Q
define bernard-soulier disease
A
- hemorrhagic disorder - Platelet abnormalities
- defect of platelet adhesion due to lack of glycoprotein Ib
8
Q
define glanzmann’s thombasthenia
A
- hemorrhagic disorder - platelet abnormalites
- defect of platelet aggregation due to lack of Glycoprotein IIb/IIIa
9
Q
define thrombotic thrombocytopenic purpura (TTP)
A
- 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
10
Q
define idiopathic thrombocytopenic purpura (ITP)
A
- have antibodies directly against their platelets
11
Q
define aplastic anemia
A
- pancytopenia
- all the cell lines are done
- marrow gets fibrosis so you can’t produce any red cells or white cells
12
Q
define von willebrands disease
A
- coagulopathies
- deficiency of von willebran’s antigen
- most common bleeding disorder
- presentation = easily bruised, nosebleeds, gingival bleeding, menorrhagia (heavy perioid)
13
Q
define hemophilia A
A
- factor VIII deficiency
- most common
14
Q
define hemophilia B
A
- factor IX deficiency
15
Q
define hemophila C
A
- factor XI deficiency
- milder form
- often found in Ashkenazic jewish
- very rare
16
Q
what are the clinical presentations of hemophilia
A
- 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)
17
Q
how is the presentation of a factor deficiency different than a paltelet deficiencyfrom
A
- deficiency of coagualtion factor presents as trouble stopping bleeding from any wound
- platelet deficiency or defect presents as purpura, petechiae, and ecchymoses
18
Q
What is Disseminated intravascular coagulation (DIC)
A
- 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)
19
Q
describe the underlying mechanisms of DIC
A
- 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
20
Q
what are the effects of DIC
A
- 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
21
Q
how do you diagnose and treat DIC
A
- 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
22
Q
What are the 3 states that can lead to thrombosis (referred to as Virchow’s triad)
A
- endothelial injury
- abnormal blood flow (circulatory stasis)
- hypercoagulability
23
Q
describe the mechanism Factor V leiden
A
- 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)
24
Q
what are some secondary risks for hypercoagulable states
A
- PROLONGED BEDREST OR IMMOBILIZATION (long flights etc)
- mycardio infarction
- atrial fibrillation
- tissue injury
25
describe antiphospholipid antibody syndrome
- 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
