Coagulation Cascade Flashcards
two main components of blood
plasma (55%) and formed elements (45%)
composition of plasma
proteins, water, other solutes
- 92% water
- electrolytes
composition of formed elements
platelets, WBC, RBC
- majority is RBC
plasma proteins
- albumin and globulins (albumin 57%)
- clotting proteins (fibrinogen most plentiful clotting factor)
function of albumin in blood
regulates how much water is in cellular vs vascular space
regulates oncotic pressure
serum
plasma without the clotting factors
erythrocyte
RBC, most abundant cell in the blood
- transports O2 to and from the lungs and tissue cells
leukocytes
WBC whose main role is defense
neutrophils
type of WBC who is the first responder to site of injury
- also plays a role in phagocytosis
eosinophils
WBC who plays a role in allergic rxn and parasitic infections
basophil
type of WBC who plays a smaller role in allergic rxn
monoyte/macrophages
type of WBC whose role is phagocytosis
- eats debris and waste
lymphocyte
types of WBC who is responsible for defending and remembering pathogens
- b and t immunity cells
natural killer cells
type of WBC whose is the primary defense against tumors and viruses
platelet
irregularly shaped, anuclear cell w cytoplasmic properties that are essential for clotting
- contain cytoplasmic granules that can release adhesive proteins, coagulation, and growth factors when they sense vessel injury
normal platelet count
150,000-400,000
thrombocytopenia
less than 100,000 platelets
high risk for bleeding bc you cant clot
where are additional platelets stored
spleen
platelets circulate in a [blank] state
unactivated
what happens to platelets when bv is damaged
1) inc platelet adhesion (become sticky/dendritic)
2) activation leads to platelet aggregation
3) platelet/platelet and platelet-vascular wall adhesion inc
4) activation of clotting system forming immobilizing meshwork
clotting cascade
group of proteins that will form blood clot when activated
blood clot
meshwork of fibrin strands and platelets
- protein strands stabilize platelet plug and trap other cells
primary activator of clotting cascade
platelet
hemostasis
the stopping of blood flow
- clot plugs damage vessel to stop the bleeding
fibrin is made up of
protein strands
ways to stop the clot
anti thrombin and tissue factor pathway inhibitor
antithrombin
inhibits thrombin to stop clotting process
tissue factor pathway inhibitor
inhibits factor Xa
natural removal of clot
breakdown carried out by fibrinlytic system
- tissue plasminogen activator turns plasminogen into plasmin
- plasmin degrades fibrin to breakdown clot
coagulation therapy goals
- prevent clot formation
- break apart existing clots
- can help inc circulation and perfusion
- dec pain
- prevent further tissue damage
drugs that inhibit coag
- heparin, low wt molecular heparin
- warfarin
- apixaban
- aspirin
- clopidogrel
biggest concern for anti coags
bleeding
- internal or external
- know why pt is taking, and area of most risk for bleeding
- monitor h&h and vs
what happens to vs if pt is bleeding
HR inc
RR inc
inc pallor
BP dec
types of drugs used for clotting
anticoagulants
anti-platelet
anticoagulants
inhibit the action or formation of clotting factors
PREVENT CLOTS
anti platelet
prevent platelet plugs form forming by inhibiting platelet aggregation (dec sticky platelets)
- best for prevent stroke/heart attacks
thrombus
blood clot that remains attached to bv
- most common in veins due to flow and pressure
thromboembolism
detached blood clot
deep vein thrombosis
thrombus occurring in the lower extremity
- typically veins and more specifically around valves
triad of virchow
there are three factors that promote the formation of a clot
1) venous stasis
2) venous endothelial damage
3) hyper coagulation
high risk of triad of virchow
- ortho surgeries
- spinal cord injuries
- obstetric/gynecologic conditions
venous stasis
slow flow of the venous system
- typical in older adults, dec mobility, heart failure
venous endothelial damage
injury typically related to trauma, surgery or some types of IV meds
hyper coagulable states
high clotting state
- caused by malignancy, pregnancy, oral contraceptives, genetics
thrombus typically occur near
venous valves
patho of DVT/VTE
inflammation around the thrombus promotes inappropriate platelet aggregation and thrombus grows
- cause pain and redness but also no symptoms
thrombus can cause
significant obstruction to venous blood flow and can cause pressure buildup and cause edema of extremity
risk of DVT/VTE
- clotting disorders
- immobility
- injury/surgery
- pregnancy
- oral contraceptive/hormone replacement therapy
- overwt/obese
- smoking
- cancer/chemo
- heart failure
- inflammatory bowel diseases
- hx of DVT or fam hx
- over age 60
- varicose veins/spider veins
serious complication of DVT/VTE
- PE (prevents gas exchange in the lungs)
- chronic thromboembolic pulmonary HTN (caused by repeated clots, inc pressure in lungs, rare)
- post thrombotic syndrome (related to chronic te pulm HTN, pain, achy, fatigue, nerve issue, spider veins, inc pigmentation)
- phlegmesia cerula dolens (rlly rare, clots in major veins causing total occlusion, deep pain, intense cyanosis, can lead to gangrene and amputation)
treatment for DVT/VTE
- anti coag
- prevention of risk factors
- IVC filters
- embolectomy
