Westminster Slade Hemostasis

Front 1

4 stages of hemostasis

Back 1

Vasoconstriction
Primary hemostasis
Secondary hemostasis
Resolution

Front 2

__________, released by activated endothelium, and neurohumoral factors induce vasoconstriction

Back 2

Endothelin

Front 3

Endothelin is a potent ________

Back 3

vasoconstrictor

Front 4

Injury-induced exposure of the subendothelial matrix provides a substrate for _____________

Back 4

platelet adhesion and activation

Front 5

_______ is a large protein secreted by both activated platelets and injured endothelium

Back 5

Von Willebrand factor (vWF)

Front 6

serves as a bridge molecule of adhesion by binding one end to platetets and the other to the injured endothelium

Back 6

Von Willebrand factor (vWF)

Front 7

________ is the most common coagulation disorder

Back 7

Von Willebrand disease

Front 8

3 types of Von Willebrand disease

Back 8

Type 1 is a quantitative defect
Type 2 is a qualitative defect and there are 4 subtypes
Type 3 is the most severe

Front 9

_________ release granule contents including ADP and TXA2

meds that block this?

Back 9

Activated platelets

ticlid

Front 10

released ADP is important in platelet aggregation because ________-

Back 10

it causes platelets to become sticky and adhere to each other

Front 11

released ADP is important in platelet aggregation because it causes platelets to become sticky and adhere to each other stickiness involves exposing receptors on platelets and allowing _______ to link platelets

Back 11

fibrinogen

fibrinogen (Factor I)

Front 12

Thrombin proteolytically activates _______ (soluble) to form _______ (insoluble)

Back 12

fibrinogen


fibrin

Front 13

fibrin is soluble/insoluble

Back 13

insolube

Front 14

fibrinogen is soluble/insoluble

Back 14

soluble

Front 15

_________ polymerizes around the site of injury forming a secondary (definitive) hemostatic plug

Back 15

fibrin

Front 16

________ also induces more platelet recruitment and activation

Back 16

Thrombin

Front 17

________ and ________ factors limit the hemostatic process to the site of vascular injury.

Back 17

Natural anticoagulant and thrombolytic factors

t-PA (tissue plasminogen activator)
Thrombomodulin that activates inhibitors of the coagulation cascade
Prostacyclin that inhibits platelet coagulation and vasoconstriction
Surface heparin-like molecules

Front 18

The accumulation of ______ at the site of injury form the platelet plug

Back 18

platelets

Front 19

________ on activated endothelial cells and leukocyte microparticles together with platelet acidic phospholipids initiate the steps of the coagulation cascade (extrinsic Pathway)

The cascade ultimately results in the formation of _______

Back 19

Tissue factor

fibrin

Front 20

All Factors Except _____ are made in the Liver

Back 20

VIII

Front 21

Vit K dependent factors?

Back 21

2,7,9,10

Front 22

PTT prolonged in...

Back 22

Hemophilia A
Hemophilia B
vW dz (XIII plus protein moiety)

Front 23

Heparin prolongs ___ and ____ as both pathways are affected

Back 23

PTT and PT

Front 24

Hemophilia A (X)

Back 24

Found on the X chromosome
A paucity (low level) of factor VIII
30% of normal levels of VIII needed for coagulation function
Replaced with Factor VIII concentrate

Front 25

treatment for Hemophilia A

Back 25

Replaced with Factor VIII concentrate

Front 26

A paucity (low level) of factor VIII is _____

Back 26

Hemophilia A

Front 27

Factor IX deficiency is...

treatment?

Back 27

Hemophilia B

FFP

Front 28

treatment for Hemophilia B?

Back 28

FFP

Front 29

____ is caused by decreased VIII levels AND a protein moiety important for the function of VIII and platelets

Back 29

von Willebrand’s Disease

Front 30

treatment of choice for von Willebrand’s Disease?

Back 30

DDAVP
Humate P
Cryo can be used but is less effective

VIII is ineffective. Why? Platelets are also ineffective.

Front 31

von Willebrand’s Disease

Back 31

Autosomal dominant
Prolonged bleeding time (poor test). Be careful with regional techniques.
Caused by decreased VIII levels AND a protein moiety important for the function of VIII and platelets
Treatment options
DDAVP
Humate P
Cryo can be used but is less effective

Front 32

Humate P

Back 32

While FFP, Cryo, and DDAVP can all be used to treat bleeding from vW dz, but Humate P is the most effective choice.
Humate P is a derivative of plasma that contains VIII and vWF. Viral deactivated.
Most hospitals do not have this but since most vW dz is type 1 and most of these are DDAVP responsive then DDAVP is a good choice.

Front 33

vW dz that is quantitative?

Back 33

type 1

Front 34

Fibrinolytic System

Back 34

There is an intricate system of checks and balances that maintains blood in fluid state
A number of protease inhibitors are present in blood keeping the coagulation process localized
Antithrombin III is the most important
Inhibits thrombin but also several other activated coagulation factors
Heparin enhances antithrombins effects several hundred fold

Front 35

___ is the most important protease inhibitor present in blood keeping the coagulation process localized

Back 35

Antithrombin III

Front 36

Heparin enhances -______ effects several hundred fold

Back 36

antithrombin III

Front 37

Fibrinolytic System-Other inhibitors of clotting

Back 37

Protein C is converted by thrombin to and active protease that inhibits factors V and VII

Another limiting mechanism of clotting the removal of fibrin via enzymatic destruction by Plasmin

Front 38

Fibrinolytic System

Back 38

Factor XII‡Plasminogen‡Plasmin‡Fibrin‡Fibrin Split Products

Front 39

Plasmin can be formed from ________ by factor _____ and other tissue activator substances

Back 39

plasminogen


XIIa

Front 40

Tissue Plasminogen activator is produced by ______

Back 40

endothelial cells and is released

Front 41

________ are used to convert plasminogen to plasmin to enhance fibrin breakdown

Back 41

Urokinase, streptokinase,

Front 42

Platelet inhibitors

Back 42

Abciximab
aspirin
clopidogrel,
Dipyridamole
ticlopidine
tirofiban

Front 43

Anticoagulants

Back 43

Warfarin
heparin
enoxaprin
Danaparoid
lepirudin

Front 44

neuroaxial blockade with low-molecular weight heparin???

Back 44

NO NO NO

Front 45

Vitamin K defeciency causes what lab changes?

Back 45

prologed PT

Front 46

___ is responsible for production of gamma carboxyglutamic acid (essential for proper factor function)

Back 46

vit K

Front 47

vit K Deficiency can be due to

treatment?

Back 47

loss of gut flora and malnutrition

Deficiency can be treated with parental Vit. K(3-6 hours to work) or emergently with FFP

Front 48

Inhibit ADP mediated platelet aggregation [2]

Back 48

Ticlopidine & clopidogrel (plavix)

Front 49

Antibody that blocks binding of fibrinogen and von Willebrand factor

Back 49

Abiciximab

Front 50

Blocks binding of fibrinogen

Back 50

Tirofiban

Front 51

Inhibits TXA2 synthesis/must be used in combo with aspirin

Back 51

Dipyridamole

Front 52

Accelerates the activity of antithrombin III

Back 52

Heparin and low molecular weight heparins

Front 53

what Rapidly inactivation of several coagulation factors most importantly thrombin and Factor Xa?

Back 53

Heparin and low molecular weight heparins

Front 54

Direct thrombin inhibitor from the leech

Back 54

Lepirudin

Front 55

Anti-Factor Xa

Back 55

Danaparoid

Front 56

Uses co-factor anti-thrombin III to work on neutralizing (IX,X,XI) which inactivates thrombin which prevents it’s action on fibrinogen

Back 56

heparin

Front 57

heparin reversal?

Back 57

Strong acid and reversal, protamine is a strong base which form a _____?

Front 58

prolonged effects of heparing wiht ____ syndrone

Back 58

hepato-renal

Front 59

Vitamin K antagonists

Back 59

Warfarin and dicumarol
Vitamin K is a co-factor important in the final carboxylation of several coagulation factors
Warfarin and dicumarol impairs Vitamin K’s ability to work as a co-factor

Front 60

Interferes with synthesis of Vit K dependent procoagulants.

Back 60

coumadin

Front 61

coumadin can prolong __ and ___

reversed with...

Back 61

Can prolong both PT PTT

vit K or FFP or both

Front 62

what thrombolytic agent rapidly activates plasminogen bound to fibrin? (fibrin selective)

Back 62

Alteplase

Front 63

What thrombolytic agents bind to an active complex with plasminogen which then converts uncomplexed plasminogen to plasmin?

Disadvantages?

reversal?

Back 63

Streptokinase/Urokinase

is that it catalyzes fibrinogen and Factors V and VII

Whole blood (preferably fresh), PBRC’s and cryo, or FFP

Front 64

Treatment of bleeding?

Back 64

Blood products
Aprotinin (now being pulled from the market) And now for some editorializing on stupid people.
Drugs for bleeding
Protamine sulfate directly binds and inactivates heparin
Aminocaproic acid and tranexamic acid inhibit plasminogen activation (They protect the clot.)

amicar

Front 65

________ opposes those actions produced by warfarin and dicumarol but requires about 24 hours for effects

Back 65

Vitamin K

Front 66

_______ inhibits trypsin which in turn inhibits plasmin and it’s fibrinolytic activity (now being pulled from the market)

Back 66

Aprotinin

Front 67

Causes an increase in the VIII:vWF moieties by causing their release from endothelial cells?

Back 67

DDAVP

If a patients has a history of being a poor responder to DDAVP then give Humate P (viral deactivated VIII and vWF concentrate)

Front 68

Protamine

Back 68

Be careful with this drug and not just because it is made from fish sperm!
Can be anticoagulant as well if too much reversal is used
Can have severe reactions during infusion
Hypotension
Pulmonary hypertension
Anaphylactic and anaphylactoid reactions can occur
Flushing, bronchospasm, edema

Front 69

protamine dose?

if reaction, give what?

Back 69

1 mg per 100 units of heparin

give epi for reaction to offset (Pulm vasoconstrictin in the face of systemic vasodialation)

Front 70

Platelets

Back 70

Platelets- One blood volume of transfusions will result in 65% loss of platelets. If two blood volumes are transfused 85% are lost. 10 day life.
Pre-surgical platelet count should be at least 50-100k
For epidurals pick a reasonable cutoff and defend it
Thrombocytopenia
Hypersplenism: cirrhosis, lymphoma,
ITP: 90% recover
Dilutional
DIC
Inhibited function
ASA, Ticlid, Plavix. Etc.
VW dz

Front 71

Thrombocytopenia can be from ....[4]

Back 71

Hypersplenism: cirrhosis, lymphoma,
ITP: 90% recover
Dilutional
DIC

Front 72

what can be the cause of bleesing after major transfusion?

Back 72

low factors (give FFP)
low platelets (give plts)
low Ca (citrate) give Ca

no LR with blood (ca in LR forms microclots)

Front 73

Massive Blood TransfusionProblems (PATCH)

Back 73

Platlets decrease, Potassium increased
ARDS, acid base changes: major tendency is acidosis based upon volume
Temp decreased or hypothermia
Citrate intoxification leading to hypocalcemia(hypotension, QT, coagulation)
Hepatitis (and other forms of infection)
Bonus: What is the most commonly transmitted disease in banked blood: CMV

Front 74

Transfusion Coagulopathies

Back 74

Coag factors less than 75% only slightly prolong PT/PTT.
Spontaneous bleeding generally occurs in the 10-20% factor range and oozing in the 20-30% range

Front 75

The most common transfusion reaction..

Back 75

Urticarial-Puritic: If these are the only signs then probably okay to continue the transfusion but watch closely.

Front 76

If temp rises 1 degree centigrade or more this must be suspected. Explore cause of fever and give antipyretics and benedryl. Usually leukocytes are the cause (washed cells)

Back 76

Febrile non-hemolytic reaction

Front 77

Can occur after only a few CC’s after exhaustion of haptoglobin binding capacity and cell lysis. Other signs and symptoms include increase in body temp, hypotension, hemoglobinuria, and DIC.

Back 77

Febrile-Hemolytic reaction:

Front 78

usually associated with wheezing and hypotension. Hemolysis can also occur.

Back 78

anaphylactic reactions

Front 79

transfusion reactino treatment...

Back 79

Stop the transfusion, support oxygenation, ventilation and circulation.
Maintain Urine output.
Send blood to lab to check free hemoglobin and for re-crossmatch. If blood is absolutely needed then give O neg
Send other labs (PT, PTT, Platelets, Fibrinogen)

Front 80

Order of transfusion in emergency

Back 80

Type specific full crossmatch
Type specific partial crossmatch
Type specific uncrossmatched
Type O, RH negative

If you go to o neg, stick with o neg

Front 81

Matches ABO and Rh and screens even low incident antigens (risk of reaction is 1:10,000)

Back 81

t and C

Front 82

Banked Blood Cells

Back 82

Normal red cell life is 120 days
Blood bank survival measured on 70% red cell survival at 24 hours post transfusion
CPD-A preserved blood has 35 day hl and ACD blood has 21 hl.

Front 83

what replaces all factor deficiencies to some degree as well as anti-thrombin III

Back 83

FFP

Front 84

FFP replaces all except?

Back 84

plts

Front 85

FFP

Back 85

Has all factors necessary for clotting except what?
Can it be used for volume expansion? NO!!
Replaces all factor deficiencies to some degree as well as anti-thrombin III
Reverses coumadin and heparin effects
Documented V and VIII deficiencies of if these are thought to exist i.e. massive blood loss.
TTP

Front 86

Causes of DIC [4]

Back 86

Sepsis (esp with gram neg)
Amniotic Fluid Embolism
Trauma
Transfusion reactions

Front 87

Consumptive coagulopathy presenting as exsessive bleeding or intravascular thrombosis?

Back 87

DIC

Front 88

DIC consumes: [4]

Back 88

Platelets
Fibrinogen
Clotting factors (which are most commonly exhausted?) 5 and 8

Front 89

Suggestive of DIC? (PT, fibrinogen, Platelets)??

Back 89

PT>15 seconds
Fibrinogen < 150 mg% (Fibrinogen levels in pregnancy should be at least 300mg%)
Platelet count <150,000

Front 90

Cryoprecipitate

Back 90

Used to replace factor VIII, fibrinogen, fibronectin, and vWF
Commercial preparations have high incidence associated with Hepatitis
FFP and Cryo can be given regardless of RH status but ABO compatibility should be maintained.

Front 91

tx fpr hyperthyroid?

Back 91

PTU 6-8 wks

10 day radioactive iodine/beta blocker

Only emergencies should be taken to OR prior to euthyroidism.
Give antithyroid drugs: PTU, sodium iodide, cortisol