Coagulation Study Guide

Question 1

What is thrombocytopenia

Answer 1

when you have a reduction in your platelet count

Question 2

What level of platelets is a patients considered thrombocytopenic

Answer 2

platelet count of below 150,000

Question 3

Spontaneous bleeding platelet count

Answer 3

less than 20,000

Question 4

prolonged bleeding platelet count

Answer 4

less than 50,000

Question 5

clinical manifestations of thrombocytopenia

Answer 5

Bruising, petechia, purpura, gingival bleeding, epitaxies (nose bleeds), pain/tenderness

Question 6

assessment of a thrombocytopenia patient

Answer 6

Assess skin, patient tolerance, signs and symptoms of bleeding

Question 7

DX studies for Thrombocytopenia

Answer 7

• Platelet count: less than 150,000
• ITP antigen specific assay to rule out
• PF4 heparin complex to rule out TTP
• increased LDH for TTP
• bone marrow examination: to rule out leukemias or anemais

Question 8

plan of care for thorombocytopenic patient

Answer 8

• Avoid aspirin or other thrombocytopenia drugs
• educate on signs of bleeding
• call provider if nosebleed is longer than 10 minutes
• avoid IM injections – use SQ since it is a smaller needle and hold pressure for 5-10 minutes after
• women: menstrual loss: count the sanitary pads

Question 9

what is ITP

Answer 9

ITP is immune thrombocytopenic purpura which is an autoimmune disease where the antibodies coat the platelets causing the spleen to recognize them as foreign and then destroy them with macrophages.
contributors: H. Pylori or viral infection

Question 10

how to treat ITP

Answer 10

• ITP is treated with corticosteroids like prednisone to help suppress the phagocytic response and to help depress the autoimmune antibodies.
• You can do IVIG if the patients are unresponsive to Option one.
• A splenectomy may be beneficial but if its chronic
• if they are unable to get one then they can take a thrombopoietin receptor a (romiplostim) to help increase platelet production.
• you can also have a platelet transfusion if less than 10,000 or there is anticipated bleeding before a procedure.

Question 11

what is TTP

Answer 11

• Combination of thrombocytopenia and anemia.
• normally cells release Vwf which will stick to exposed fibers in the torn tissue and become glue like allowing the platelets to stick to the site.
• as the platelets pile on top of each-other they link together and form a clot
• In TTP there is a deficiency in the enzyme ADAMTS13 which would normally break down Vwf when it is no longer needed.
• without this regulation by ADAMST13, small clots can form more frequently in the body.
• These small clots formed block normal BF through arteries= decreased platelets and increased rbc destruction

-Bleeding and clotting at the same time

Question 12

what is TTP

Answer 12

• Combination of thrombocytopenia and anemia.
• normally cells release Vwf which will stick to exposed fibers in the torn tissue and become glue like allowing the platelets to stick to the site.
• as the platelets pile on top of each-other they link together and form a clot
• In TTP there is a deficiency in the enzyme ADAMTS13 which would normally break down Vwf when it is no longer needed.
• without this regulation by ADAMST13, small clots can form more frequently in the body.
• These small clots formed block normal BF through arteries= decreased platelets and increased rbc destruction

-Bleeding and clotting at the same time because As the platelets clump together, fewer platelets are available in the blood in other parts of the body to help with clotting.

Question 13

How is TTP treated

Answer 13

• treating the underlying cause or infection.
• Plasmapheresis
• corticosteroids
• immunosuppressive therapy (rituximab for refractory plasma exchange to block the inhibitory ADAMTS13 IgG antibodies
• administering platelets is contraindicated because they will just continue to clot together.

Question 14

what is plasmapheresis

Answer 14

• a procedure in which blood is removed from the body, filtered through a device, and separated into its individual components.
• Some of the filtered blood components are removed, and the rest of the blood returns to the patient.
• It removes antibodies and cleans the blood.

Question 15

What is HIT

Answer 15

• complication of heparin that causes Decreased platelets in the blood
• antibodies are created against Heparin because its binding to PF4
• Heparin binding to PF4 creates positive feedback loop encouraging other PF4 heparin complexes to form
• antibodies attach to PF4 + heparin complex which activates the platelets
• small clots form and deplete platelet count
• Antibodies will attack these complexes and remove the platelets prematurely
• all this leads to more and more platelets getting activated and they start making clots. but also remaining platelets will get consumed = low platelet count.
• widespread abnormal clots= risk for thrombotic events

Question 16

when is HIT dx

Answer 16

when there is 50 % less platelets or less than 150,000 when given heparin within 5-10 days.

Question 17

Why is inclusion of HIT on a patient’s history so important?

Answer 17

We have to know this because they can never have heparin again because the same thing will happen again.

Question 18

how is HIT dx

Answer 18

• normal PT and aPTT
• test for p4f antibodies (ELISA METHOD)
• individuals who recently started heparin therapy and experience a decrease in platelet count either within 1-2 weeks or within a day suggests HIT.

Question 19

Hemophilia A MOA

Answer 19

deficient in factor VIII (8)- cannot clot = prolonged, delayed, uncontrolled bleeding

Question 20

Hemophilia B MOA

Answer 20

deficient in factor IX (9) and generally in males- cannot clot = prolonged, delayed, uncontrolled bleeding

Question 21

Interventions for Hemophilia A and B

Answer 21

• replace clotting factor
• DDVAP for A to stimulate factor VIII and vWF
• antifibrinolytic which inhibits fibrinolysis by inhibiting plasminogen activations in the fibrin clot

Question 22

what is DIC

Answer 22

-where you are clotting out of control and lots and lots of blood clots will start to form in the body
-all of this clotting consumes platelets and clotting factors = not enough platelets circulating in the blood so other parts of the body start to bleed with the slightest damage.
-basically they have too much and too little clotting
-

Question 23

what is DIC

Answer 23

• where you are clotting out of control and lots and lots of blood clots will start to form in the body
• all of this clotting consumes platelets and clotting factors = not enough platelets circulating in the blood so other parts of the body start to bleed with the slightest damage.
• basically they have too much and too little clotting
• you have clots forming and thrombosis (clots obstructing the blood vessel) + bleeding from difficulty forming new clots

Question 24

what can trigger DIC

Answer 24

• underlying trigger like sepsis, pregnancy, trauma
• in these there could be an imbalance between clot formation and clot breakdown (more formation than breakdown)
• widespread clot formation is plugging up the medium and small vessels causing ischemia, necrosis, and damage
• this massive formation of clots depletes platelets and clotting factors and then you also have a hard time with clot formation
• ALL this = clots forming and thrombosis (clots obstructing the blood vessel) + bleeding from difficulty forming new clots

Question 25

5 things that can contribute to DIC

Answer 25

1. increased thrombin generation (increased clots)
2. platelet activation
3. consumption (using all cuz clotting too much) of coagulation factors
4. impaired fibrinolysis (process where you break down clot so it doesn’t get bigger than what is needed and dissolves when no longer needed)
5. inflammatory activation

Question 26

What are the mechanisms in DIC that explain the presenting s/s? What are precipitating factors for DIC?

Answer 26

Bleeding and clotting at the same time

could be caused by underlying trigger like sepsis, pregnancy, trauma

Question 27

Lab values for DIC

Answer 27

• decreased fibrinogen and platelets
• increased (prolonged) PT, PTT (both relate to low circulating coagulation factors)
• increased D-Dimer

Question 28

Thrombotic DIC mani

Answer 28

neuro: delirium, coma
	Integ: ischemia, gangrene
	renal: oliguria, azotemia
	pulmonary: ARDS- acute respiratory syndrome
	GI: paralytic ilieus

Question 29

Hemorrhagic DIC mani

Answer 29

neuro: intracerebral bleeding
integ: petechiae, ecchymosis
renal: hematuria (blood in urine)
Pul: dyspnea, hemoptysis
GI: massive bleeding
Mucus membranes: epistaxis (nose bleed), gingival hyperplasia (gum swelling)

Question 30

how is DIC managed

Answer 30

• treat prior disorder first
• monitor for bleeding (no bleeding no therapy)
• thrombosis: (heparin which depends on the risks and benefits) or antithrombin III (severe or sudden DIC),
• replace blood products (serious bleeding, surgeries, invasive procedures)

Question 31

when would someone with thrombocytopenia get a transfusion

Answer 31

when platelets are below 10,000 or they are actively bleeding

Question 32

what to monitor with heparin and antidote

Answer 32

monitor aPTT levels

-antidote: protamine

Question 33

what to monitor with warfarin and antidote

Answer 33

monitor PT and INR

• eat consistant amount of green leafy veggies
• antidote: Vitamin K

Question 34

Comparison of ITP and TTP

Answer 34

ITP:
-failure of blood to clot

-causes bruises and bleeding
-oral steroid treatment
-cause is autoimmune destruction of platelets
TTP:
-forming too many clots
-causes bruising and bleeding
-blood replacement therapy treatment
-cause-clumping of plt

Question 35

acute interventions for hemophilia

Answer 35

• stop bleeding
• manage life threatening complications
• admin any specific coagulation factors
• rest any involved joint (ROM when bleeding stops, weight bearing avoided until swelling is resolved)