Freeman Flashcards
(47 cards)
What is the incidence of Factor 5 Leiden? HOw does this affect your risk if you are heterozygous or homozygous for it?
hyper coagulability risk
Incidence: 3-8%
Hetero: 8X risk
Homo: 20X risk
What are some of the things that affect your mechanical flow dynamics?
prior sites of thrombus compression due to obesity chemical *nicotine *vasoconstricting agents
What are some modifiable risk factors for coagulation?
Obesity
Sedentary life-style
Travel
OCP
Pregnancy
Surgery
*elective, particularly
ortho
Smoking
Prior DVTWhat are som unmodifiable risk factors for coagulation?
Factor V Leiden
Prothrombin Gene Mutation
Malignancy
Surgery
*emergent
Chronic Illness
Lupus AnticoagulantWhat is the treatment for acute thrombogenesis?
Warfarin + Heparin
Heparin for 7-10 days
Which factors are Vit K dependent?
2, 7, 9, 10
Proteins C& S
**Vit K carboxylates the N terminus of these factors to activate
What is the half life of Factor X?
48 H
Note: this is a coagulant.
What is the half life of Protein C?
6 hours
Note: this is an anticoagulant
Why is it that you have to treat patients struggling with coagulation with heparin for a full 7-10 days?
b/c the factors that are alive & active take some time to die.
4-5 half lives.
This equals out to 7-10 days. Otherwise: just get a blood clot a few days later.
What affects the course of Warfarin?
based on the etiology of the thrombogenic event
When do you sometimes see lupus anticoagulants?
may be seen at the time of acute thrombotic events (acute phase reactants)
How is a lupus anticoagulant identified in lab? In vitro & in vivo?
In vitro: prolongs PTT
in vivo: procoagulant.
When a patient is taking both heparin & warfarin…when should the warfarin be instituted?
it can be initiated at the same time as heparin
66yo male admitted to Med Center w/hypotension, tachycardia, & fever.
W/U reveals gram(+) septicemia 2/2 staph aureus. Echocardiogram reveals mass in ‘upper’ R-ventricle. Nurses report patient ‘oozing’ from all iv sites.
EXAM: b/L foot amputations
No obvious source of skin
breakdown/infections
LABS: PT 13.3 secs (nl: 11-12.2 secs)
1:1 mixing study: PT normalizes
PMHx: DMII; no h/o cardiac dz.
D/C’ed 3 weeks earlier for gram(+) sepsis @ that time.
What’s going on?
the normalizing with the mixing study shows that this person probably has a factor deficiency
seems to be suffering from heparin inducted thrombocytopenia
**seems to have endocarditis after a staph aureus septicemia that induced DIC
Same pt
On admit, platelet count 175K (Nl: 150-400K)
Started on LMWH (Lovenox) prophylactically on admit; next day, platelets are 45K.
The ICU team requests Heme consult regarding recommendations for anticoagulant agent of choice; they suspect HIT. Cardiology suggests treatment of thrombus.
Your recommendations?
What should be done for this patient?
stop the heparin!
treat the endocarditis
DIC will go away…
Explain what happens in type I HIT.
- *Modest, transient decrease in platelets 2/2 heparin-induced platelet agglutination.
- *Self-limited; plt counts can return to normal while heparin is continued.
Explain what happens in Type II HIT.
A drug-induced, immune-mediated response 2/2 abs directed against heparin-plt factor 4 complete that results in a 50% or greater drop in platelet counts
**Severe thrombocytopenia w/bleeding is rare!
HIT is less likely with which type of heparin? When is HIT usu seen?
usu seen after major surgery where large volumes of heparin are required
less likely with low molecular weight heparin
What Should be considered in all recently hospitalized patients returning w/acute thrombosis w/in 1-2 weeks of their hospital stay?
HIT
shows thrombocytopenia & thrombosis!
What is the testing done for HIT? What is the treatment?
Testing: radiolabeled platelet-serotonin release assay
Rx: direct thrombin inhibitors
Why is there both thrombosis & thrombocytopenia in HIT?
blood clots being made
consumption of platelets
also autoimmune destruction of heparin-platelet 4 complex
How do you measure the effectiveness of 10a inhibitors?
measure 10a
measure D-dimer
What is the pathophysiology of DIC?
Widespread activation of the clotting cascade causing a consumption of clotting factors and platelets w/resultant bleeding.
Microvascular compromise 2/2 to thrombin formation results in tissue ischemia w/resultant end-organ damage, particularly of liver & kidneys.
DIC is triggered by diseases that promote the expression of tissue factor (transmembrane glycoprotein). Give some examples.
- Gram(-) septicemia
- damaged cerebral tissue
- APL (promyelocytic leukemia) awa other liquid/solid malignancies.
- Placental tissue from obstetric catastrophes
- Snake venoms
- Acute hemolytic transfusion rxns
- Hypotension from any cause can result in endothelial cell damage(CABG, etc.
- Massive Tissue Injury: trauma;burns; hypothermia
