Coagulation Disorders Flashcards
What things are needed to clot
- Liver
- Calcium
- Phospholipids
- Tissue Factor
- Platelets
Intrinsic System
Most common. Uses elements only found in vessels
Extrinsic System
Requires tissue factor which is extrinsic to vessels and released when vessels rupture
What does a PT measure?
- Measures the time it takes for plasma to clot when exposed to tissue factor (extrinsic pathway)
- Measures effectiveness of warfarin
What does warfarin effect?
Extrinsic pathway
What is the purpose of an INR?
Normalizes the variance in PT values
What is the therapeutic value of INR on Warfarin?
2-3
Medications that increase the PT?
- Abx
- Cimetidine
- Salicylates
What is a normal PT value?
11-13 seconds
Activated Partial Thromboplastin Time (aPTT) measures..
- The time it takes to clot using the intrinsic clotting system
- Heparin therapy
aPTT levels can shift due to…
Variables such as disease, medications, physiological states
Why are heparin Anti-Xa labs sometimes preferred?
aPTT can shift so some hospitals prefer to use Anti-Xa lab tests for heparin
Normal aPTT times
25-38 seconds OR 21-35 seconds
What does an Anti-Xa measure?
Measure the intrinsic clotting system
Platelets are produced in… removed by….
Platelets are produced in the bone marrow and removed by the spleen
Normal platelet count is
150,000-400,000
Thrombocytopenia is
LOW PLATELETS
Platelet count below 150,000
Prolonged bleeding occurs when..
When platelets are less than 50,000
Spontaneous bleeding occurs when..
Platelets are below 20,000
This number is not definite… Could start much lower
Manifestations of thrombocytopenia
Epistaxis and gingival bleeding, petechiae, purpura, superficial echymosis, pain/tenderness
Why petechiae?
RBC are leaking out of the blood vessels and into the skin
Complications of thrombocytopenia
hemorrhage or thrombosis
Thrombocytopenia bleeding precautions
Prolonged bleeding after injection just as IM or venipuncture
Diagnostic studied of thrombocytopenia
Platelets: less than 150,000
Platelets: less than 50,000 prolonged bleeding
Platelets: less than 20,000 spontaneous bleeding
PT/aPTT: could be normal
Bone marrow examination: megakarycytes on bone marrow biopsy –> thrombocytopenia due to decrease bone marrow production
Diagnostic studies for thrombocytopenia to rule out other diseases
ITP antigen specific assay PF4 heparin complex (HIT) Increase lactate dehydrogenase (TTP) Anemia (TTP) Bone marrow aspiration (leukemia and anemia)
Heparin MOA
inactivates thrombin and factor Xa
Heparin route, onset, duration
IV or SubQ
Rapid
Brief
Heparin labs and antidote
aPTT
Protamine
Warfarin MOA
prevent synthesis of clotting before the vessels
Warfarin route, onset and duration
PO
Slow
Prolonged (days)
Warfarin labs and antidote
PT(INR)
Vitamin K
Which of the following patients should not take rivaroxaban?
Liver failure patient - can lead to further liver injury
Rivarixaban
Xa inhibitor
Uses: stroke, PE, VTE
NO testing
Dabigatran
Direct thrombin inhibitor
Uses: prevent and manage DVT, stroke, afib
NO testing
Dabigatran antidote
Idarucizumab
Rivaroxaban (-xaban) antidote
Andexanet
Neuro s/s with coag disorders
change in LOC, aphasia, decrease strength
Respiratory s/s with coag disorders
SOB, tachypnea, chest pain
GI s/s with coag disorders
occult bleeding, gastric pain
Skin s/s with coag disorders
color changes, decrease temp, decrease sensation, decrease pulse
Immune Thrombocytopenic Purpura (ITP)
Most common aired thrombocytopenia
Autoimmune: antibodies coat platlets –> spleen marks them as foreign –> macrophages destroy
Can platelets function with an antibody on them?
Yes, they can still function normally but they have a shortened survival rate which leads to low platelets
ITP diagnostics
ITP antigen assay
What causes ITP?
H. pylori or viral infection
ITP treatment: 1. corticosteroids
Used first
Supresses spleen from destroying platelets by suppressing phagocytes and autoimmune antibodies
ITP treatment: 2. IVIG
Second
For patients that are unresponsive to corticosteroids
ITP treatment: 3. Spleenectomy
- Spleen contains macrophages
- Structure enhances the attraction between macrophages and antibody coated platelets
- Some antibody synthesis occurs in spleen
- Spleen stores 1/3 –> increase circulating platelets
ITP treatment: 4. Thrombopoietin Receptor Agonists
Romiplostim
increases platelet production
ITP treatment: 5. Platelet transfusion
if 10,000 or less OR anticipated bleeding before procedure
Thrombotic Thrombocytopenia Purpura (TTP)
Uncommon
Combination of anemia and thrombocytopenia
ADAMTS13 enzyme breaks down von willebrand factor
Bleeding and clotting at the same time
TTP diagnostics
ADAMTS13 enzyme activity: low or undetectable
Increase in LDH
Normal Pt/aPTT
Blood smear: schistocytes
TTP treatment
- Treat underlying infection or cause
- Plasmapheresis
- Corticosteroids
- Immunosuppressive therapy (Rituximab)
How does Rituximab help with TTP
blocks inhibitory ADAMTS13 IgG antibodies
Why is administration of platelets contraindicated in patients with TTP?
platelets will continue to close and increase the problem
What happens if TTP is left untreated?
Irreversible renal failure and death
When does HIT appear?
5-10 days after heparin is started
Can by up to 14
HIT
immune mediated response where PF4 binds to heparin and creates a positive feedback loop that leads to increased clotting
This decrease the circulating platelets and causes clots
Platelets either drop by 50% or less than 150,000
Is bleeding common in patients with HIT?
No, because platelets don’t usually drop below 20,000
Major complications of HIT
venous thrombosis or arterial thrombosis
HIT diagnostics
Normal PT, aPTT (concerning because a person on heparin should have an increase PTT)
PF4 antibodies
Thrombocytopenia
HIT treatment
- STOP heparin
- Give direct thrombin inhibitor
- Protamine sulfate to interrupt heparin
- Plasmapheresis in severe
- Surgically remove clots if needed
Disseminated Intravascular Coagulation (DIC)
Bleeding and clotting
Exaggerated clotting response –> decreased clotting factors –> hemorrhage
Is DIC a disease?
DIC is NOT a disease, it is a RESPONSE to a disease
Commonly sepsis
Other: pregnancy, trauma, malignant
What is the manifestation for acute DIC?
bleeding
DIC can be..
Acute, subacute, chronic
Signs of thrombosis:
Neuro: delirium, coma Skin: Ischemia, gangrene Renal: oliguria, azotemia Resp: ARDS GI: paralytic ileus
Signs of hemorrhage:
Neuro: intracranial bleeding Skin: petechiae, ecchymosis Renal: hematuria Resp: dyspnea, hemoptysis GI: massive bleeding Mucous membranes: epistaxis, gingival bleeding
DIC patho: Clotting
Clotting activated via release of clotting factor
- increase intravascular clots
- platelet aggregation increased
- fibrin and platelets in capillaries and arterioles
DIC patho: Bleeding
- Fibrin split product accumulate
- clotting factors depleted
- increased consumption of platelets
DIC diagnostics
- Elevated fibrin split products (FSP)
- Decreased fibrinogen and platelets
- Prolonged PT, PTT, D-Dimer
DIC treatment
- Treat prior disorder
- Monitor for bleeding (no bleeding, no therapy)
- Thrombosis (heparin or antithrombin III to prevent clots)
- Replacement of blood products (FFP, platelet)
- Clot removal
Why would you use oral anticoagulants for chronic DIC?
Heparin doesn’t work well for chronic DIC
When do you use Heparin and Antithrombin III in DIC?
Heparin: when the benefits outweigh the risks
Antithrombin III: severe of sudden DIC
When do you use replacement blood product in DIC?
Serious bleeding, surgery, invasive procedures
Teaching for thrombocytopenia
- Avoid aspirin or other thrombocytopenia meds
- Teach s/s of bleeding
- Any injections hold pressure for 5-10 minutes
- Call doc if nose bleeds longer than 10 mins
- AVOID IM injections
- Women measure menstrual loss
Hemophilia in general is..
X-linked recessive disorder
Deficient coag factors leading to prolonged, delay or uncontrolled bleeding because they can’t clot
3 types: A, B, Von Williebrand disease
Hemophilia A
deficient in factor VIII
Most common
Hemophilia B
deficient in factor IX
usually males
Hemophilia diagnostics
Normal PT and platelets
Prolonged PTT
Factor assay-reduction factor VIII, factor IX, vWF
Treatment of hemophilia
- Replacement of deficient clotting factors prophylactically or on demand
- DDAVP for mild hemophilia A to stimulate VIII or vWF
- Antifibrinolytic - inhibits breaking down of clot by inhibiting plasminogen
Complications of replacing clotting factors
- Development of inhibitor factor VIII and IX
- Transfusion transmitted infectious disease
- allergic reaction
- thrombotic complications
Acute interventions for hemophilia
- Stop bleeding and manage life threatening complications like airway, compartment syndrome or intracranial bleeding
- Administer deficient factor
- Rest the involved joint, ROM when bleeding stops and weight bearing when swelling is gone
Why don’t you want to jump right into weight bearing exercises after acute hemophilia?
They should only be after the swelling is gone and as tolerated because it could cause permanent damage to the joint if it is too soon
What are some ways to stop bleeding with acute hemophilia?
Pressure, ice, gel foam or fibrin foam, topical hemostatic agents (thrombin)
Home care for hemophilia
- Educate on when to come to hospital and when to stay home
- Daily oral hygiene
- Noncontact sports
- Medic alert bracelet
What are thing a patient with hemophilia should come to the hospital for?
- Serve pain in joint that prevents mobility or sleep
- head injury
- swollen neck or mouth
- Abdominal pain
- Hematuria
- Melena
- Skin wounds that need stitches
