Blood Disorders Flashcards
Test 3
vWF =
Von Williebrand factor
What is vWF?
A glycoprotein that plays a critical role in platelet adherence
How does vWF disorder present?
-Easily bruising
-Recurrent epistaxis (nosebleeds)
-Menorrhagia (heavy/long periods)
What is the most common hereditary bleeding disorder?
vWF disorder
vWF disorder has a strong _____ component
genetic
if parents have it –> child probably has it
Some types vWF disease will respond to ________. Which types?
DDAVP = Deamino-8-D-arginine Vasopressin
Type 1
Type 2A
Type 2M
Type 2B
(the less severe types)
what is the most mild type of vWF disease?
Type 1
What is the most rare/severe type of vWF disease?
Type 3
Which vWF disease types don’t respond to DDAVP?
Type 2N
Type 3
(the more severe types)
vWF disease will most likely require specific factor ____ concentrates
VIII (factor 8)
what do we need to do if a patient has vWF disease before taking them to the OR?
Consult hematology
How do labs look with vWF disease?
PT/aPTT normal
BT prolonged (bleeding time)
What is the Tx of vWF disease? (3)
- Desmopressin
- Specific factors
- Cryoprecipitate
What is the dosage for desmopressin? How is it given?
0.3 - 0.8 mcg/kg
In 50 ml of NS
Give over 15 - 20 mins (slowly)
What exactly is DDAVP? What does it do?
Synthetic analogue of vasopressin
Stimulates release of vWF by endothelial cells
You see the max affects of DDAVP in ______ mins and it last up to ______ hours.
30 mins
6-8 hrs
What are the main SE of DDAVP administration?
-HA
-Tachycardia
-Hyponatremia
-Water intoxication
Water intoxication –> _________
seizures
or
hyponatremia –> seizures
PO and IV hydration should be restricted for ______ after the use of DDAVP
4-6 hrs
What will pts taking DDAVP crave? What considerations should we have?
To drink water
They will even drink from the sink and toilet bc they are desperate for water. watch them closely.
CNS/ECG changes: Na+ 120
CNS: confusion; restlessness
ECG: widening of QRS
CNS/ECG changes: Na+ 115
CNS: Somnolence; Nausea
ECG: elevated ST; widen QRS
CNS/ECG changes: Na+ 110
CNS: seizures; coma
ECG: vtach; vfib
Chronic hyponatremic patient do ______ than acute hyponatremic patients
better
DDAVP is _______ hyponatremia
acute
Cryoprecipitate has an increased risk of ________. Why?
Infection
pooled together from multiple donors & Not submitted to viral attenuation/testing
Cryo is the ______ Tx for vWF disease.
secondary
1 unit of cryoprecipitate raises _______ levels by ________.
fibrinogen
50mg/dL
What does factor VIII concentrate consist of?
Factor 8
vWF
T/F: factor VIII concentrate doesn’t go through viral attenuation
F
It does –> decreases risk for infection
pulled from multiple donors
When do you give factor VIII?
Preop
Periop
When should DDAVP be administered?
60 Mins before Sx
What should you do if you find out your pt has vWF disease the morning of Sx? Why?
Cancel –> need to consult hematology
Normalized BT & FVIII before Sx
What type of anesthesia do you do with vWF disease? Why?
GA
Don’t want to poke –> increase risk of bleeding –> hematoma/hemorrhage
What anesthesia considerations should we have with vWF disease?
-avoid trauma (including traumatic intubations)
-arterial/CVC puncture not recommended –> use ultrasound if really needed
-avoid IM
what is acquired bleeding? What causes this? What is the most common cause?
Bleeding that is caused by medications:
Heparin/ lovenox (most common)
Warfarin
Fibrinolytics
Antiplatelets
Heparin is ______ charged
Negatively
Describe heparin structure
CHO containing glucuronic acid residue
What is heparin’s MOA?
Activates antithrombin III –> inhibits thrombin –> prevents conversion of fibrinogen to fibrin
T/F: heparin will work if you don’t have antithrombin III
F
Need antithrombin III to work
What lab should you monitor with heparin? How does it affect them?
PTT and ACT
Increases
what is ACT? What are normal ranges? Therapeutic ranges?
Seconds it takes to clot from the time the blood is pulled
Normal: <150 seconds
Therapeutic: 350-400 secs
The reversal for heparin is ______
Protamine
LMWH is _______ effective at VTE prophylaxis than UFH
more
(Lovenox)
Why is LMWH more predictable than UFH?
-fewer effects on platelet function
-reduced risk for HIT
How often do we monitor for systemic heparin?
PTT/ACT q8-12 hrs
What is Coumadin’s MOA?
Interferes with hepatic synthesis of vit K coag factors –> II, VII, IX, X
what are the vitamin K dependent coagulation factors?
II, VII, IX, X
What are the reversals for Coumadin? What are the differences between them?
Vitamin K: takes 6-8 hrs to work
Prothrombin complex concentrates (PCC), recombinant factor VIIa, FFP: works faster than vitamin K –> used in acute situations to stop bleeding fast
Fibrinolytics work on _______ clots
Existing
What medications are Fibrinolytics?
tPA (tissue plasminogen activator)
SK (streptokinase)
UK (urokinase)
What is the MOA of Fibrinolytics?
Convert plasminogen to plasmin –> cleves fribrin –> dissolves clot
What drugs are antifibrinolytics?
-TXA
-aminocaproic acid (cardiac Sx)
-aprotinin (renal pts)
How does anti-fibrinolytic affect clots?
Stops the breakdown of clots
What was TXA originally designed for?
Prolonged/heavy periods
Epitaxis with nose surgery
What is an AE of TXA toxicity?
Color vision loss
What consideration should I have with anti-platelets?
-DC drug on time
-I can transfuse platelets
-get platelet function panel
What is DIC?
Disseminated intravascular coagulopathy
Systemic activation of coagulation system –> consumption of platelets –> thrombus formation and bleeding simultaneously
What causes DIC?
Trauma
Amniotic fluid embolus
Malignancy
Sepsis
Incompatible blood transfusions
Tumors
T/F: DIC has an extremely high mortality
T
How does DIC affect your labs?
Increased pT/ptt/TT/concentration of soluble fibrin degradation products
Decreased platelets
How is DIC treated?
1st treat the underlying condition
-Replace coagulation factors/platelets
-Plasmapheresis
-exchange transfusion
Antifibrinolytic therapy is ________ in DIC. Why?
Contraindicated
Potential catastrophic from thrombotic complications
What are two prothrombic disorders?
F V Leiden
HIT
What is Factor V Leiden?
Mutations in factor V –> resistant to activation of protein C –> factor V continues to clot –> widespread clotting
what does protein C do in the clotting cascade?
Inactivates factor V when enough fibrin has been made to stop clots from growing larger than necessary
What is Factor V Leiden puts patient at an increased risk for?
DVT (w or w/o PE)
Factor V Leiden is normally silent until _______. How will this present?
Pregnancy
DVT
repeated missed abortions
recurrent late fetal losses
How is Factor V Leiden treated?
Prophylactic anticoagulants:
Warfarin
UFH
LMWH (lovenox)
T/F: Lovenox is heparin
T
Lovenox is a type of LMWH
What type of anesthesia is used for pts w/ Factor V Leiden?
GA
What is HIT?
Heparin induced thrombocytopenia
Autoimmune mediated drug reaction to any type of heparin.
HIT occurs in as many as ____% of pts getting heparin
5%
Thrombocytopenia in HIT occurs ______ after initial therapy
5-14 days
What is the Hallmark AE in HIT?
Decrease in platelets <100,000
What is the pathophysiology for HIT?
Platelet activation –> Decrease in platelets (thrombocytopenia) & widespread thromboses (hypercoaguable state)
What immune complexes is HIT mediated by?
IgG antibody
platelet factor 4 (PF4)
heparin
What is Tx for HIT?
1. D/C ALL HEPARIN
- Administer an alternative: direct thrombin inhibitor –> bivalirudin, lepirudin, argatroban
What medication are direct thrombin inhibitor? (3)
Bivalirudin
Lepirudin
Argatroban
With HIT, what medication is commonly given for VTE?
Fondaparinaux (synthetic Factor Xa inhibitor)
Has a similar structure to heparin
The immune complexes mediated during HIT clear within _____ months
3 months
T/F: HIT pts should avoid UFH
T
But idk I think I would just avoid heparin in general including LMWH
What should you consider giving if administration of heparin in uneffective?
FFP –> has antithrombin III
heparin cant work w/o antithrombin III
