Exam 2 - chapter 22 Flashcards
where are clotting factors made
liver
warfarin/coumadin
blocks synthesis of vitamin k dependent clotting factors, doesn’t dissolve clot (requires weekly blood test)
what puts a patient at risk for developing a bleeding disorder
liver disease, leukemia, chemotherapy
treatments for bleeding disorders
Treat underlying cause
Replacement of clotting factor
Cryoprecipitate
Give platelets if teh pt is suffering from thrombocytopenia
cryoprecipitate
cool plasma down, plasma proteins will come out of solution. Spin down, get pellet at bottom, Resuspend the precipitate (all plasma proteins and clotting factors at high concentration) put it in physiological saline and give it to patient (The only time you administer - pt is bleeding out and you can’t figure out why)
Why pt with bleeding disorder shouldn’t take NSAID
inhibits platelet stickiness
platelet
- thrombocyte
- Stored in spleen and released when needed
- Live 8-9 days
- Large fragments of megakaryocytes in bone marrow
Thrombopoietin
(platelet production)
Made in liver, kidney, smooth muscle, bone marrow
Thrombocytosis
(increased platelet number)
- Iron deficient anemia, splenectomy, polycythemia
hypercoagulability causes
platelets are extra sticky
- endothelial damage (atherclerosis, smoking, diabetes)
- increased sensitivty to factors
thrombocytopenia
decreased platelets, increased bleeding
- DECREASED PRODUCTION → loss of bone marrow function (leukemia, aplastic anemia, chemotherapy, infection)
OR
- INCREASED DESTRUCTION –> antiplatelet antibodies (ITP), Sequestration and destruction in spleen, Platelets used up in forming clots (DIC TTP)
impaired platelet function cause
- NSAIDS - inhibit platelet stickiness
- Heart lung machines
- Uremia - decreased function due to build up of metabolic wastes
- Von willebrand disease - decreased platelet adhesion
ITP
immune/ideopathetic thrombocytopenia purpura (antiplatelet antibodies attach to platelets and are removed by spleen, causing decreased platelets levels and more bleeding)
TTP
thrombolytic thrombocytopenia purpura (platelets are used up forming clots, causing decreased platelet levels and increased bleeding)
s/s of a bleeding disorder
Persistent bleeting
Petechiae
Purpura
Ecchymosis
Excessive bleeding from minor tissue trauma
Hemophilia A
deficit in clotting factor VIII (administer factor 8 to treat) passed down x chromosome
Hemophilia B
deficit in clotting factor IX (administer factor 9 to treat)
Von willebrand disease
deficiency in von willebrand factor, most common hereditary bleeding disorder (takes longer to clot than normal, might not administer anything to treat)
hemostasis
vaso/vessel spasm
Platelet plug formation
Coagulation
Fibrinogen → fibrin (mesh like protein that holds the clot together)
Dissolving the clot
DIC
Acquired, disseminated intravascular coagulation
- Involves both excess clotting and excessive bleeding
- Stage 1: massive activation of the coagulation cascade (release of thromboplastin, activates extrinsic clotting pathway)
- Stage 2: clotting factors used up, so excess bleeding bc fibrinolysis has been stimulated
DIC causes
- Preeclampsia or eclampsia (hypertensive during pregnancy)
- Abruptio placentae (placenta pulls away from uterus wall and the damage releases thromboplastin
- Carcinomas release substances that trigger clotting
- Major trauma (dead tissues release thromboplastin)
- Blood transfusion reaction (has negative impact on endothelium, releases thromboplastin, blood vessels become blocked
s/s DIC
- Hemorrhage due to low plasma fibrinogen
- Thrombocytopenia (low platelets)
- Low BP, shock
- petechiae , ecchymoses, hematuria
Infarctions
treatment DIC
Treat underlying cause such as infection
Treat current problem (bleeding or clotting)
polycythemia
too many RBCs (hematocrit above 50%)
primary polycythemia
neoplastic
- Increased production of RBC and other cells in bone marrow
- Increase in RBC, granulocytes, thrombocytes
- Increased blood volume and viscosity (decreased blood flow)
- HTN - headaches, trouble concentrating, - dizziness
- Hemorrhage
- Thromboembolism
- Bone marrow = hypercellular
- Spleen and liver are congested and enlarged
- Itching, pain in figers/toes
secondary polycythemia
response to an increase in erythropoietin
- Chronic hypoxia
- Heart failure
- COPD
- High altitude
Diagnosis and treatment of polycythemia
- Blood cell count and hematocrit are markedly elevated
- Drugs and radiation - used to suppress bone marrow activity - hydroxyurea and interferon alpha)
- Phlebotomy
- Low does aspirin (reduces clotting)
