CV 5 (2) Flashcards
A person is Rh-positive if they have the
Rh Antigen on RBCs
– No Rh-antibodies in the plasma
A person is Rh-negative if they lack the
Rh Antigen on RBCs
– No Rh-antibodies (IgGs) in the plasma
– No Rh-antibodies (IgGs) in the plasma IF the person
has never been exposed to Rh+ blood (2)
• May see a mild agglutination response 2-4 weeks
after Rh-negative person receives Rh+ RBCs
• Usually the first response, if it occurs, is mild
Erythroblastosis Fetalis
Rh-negative mother, Rh-positive fetus.
Erythroblastosis Fetalis
First pregnancy: (3)
fetal red cells leak into maternal circulation.
– Mother develops anti-Rh antibodies.
– Low risk to fetus because this occurs late in
pregnancy.
Erythroblastosis Fetalis
Second pregnancy:
maternal IgG crosses placenta, destroys fetal RBC’s.
Erythroblastosis Fetalis
Treatment:
administration of anti-RhD immunoglobulin (RhoGAM) after delivery.
Platelets
Cytoplasmic fragments derived from megakaryocytes (thrombocytes).
Platelets concentration in blood
150,000 – 300,000/μl of blood
platelet lifespan
10 days
platelet primary role in
hemostasis
platelet content
no nuclei, cannot divide
platelets contain (5)
- Actin and myosin
- Enzymes and organelles for aerobic CR
- Enzymes for Prostaglandin synthesis
- Fibrin – stabilizing factor (important for hemostasis)
- Growth factors that stimulate endothelial cell, VSM, and fibroblasts to divide and grow
Recent evidence that platelets can act as (2)
immune cells and contribute to
the inflammatory process of atherosclerosis
Hemostasis
The physiological mechanisms that stops bleeding
Hemostasis is a 4-step process:
- Vasoconstriction of damaged vessel to decrease blood flow and pressure
- Formation of platelet plug to block hole in damaged vessel
- Clot formation (requires Fibrin)
- Clot dissolution
Steps Leading to Platelet Plug and Vasoconstriction
Platelets stick to damaged Endothelial cell surface (Von Willebrand Factor (vWF))
- Platelets release contents of secretory vesicles
- Stimulate production of Thromboxane A2 from platelet plasma membrane
Causes of platelet plug/vasoconstriction (2)
- Vasoconstriction of damaged vessel
2. Platelet plug formation (+ feedback Platelet activation)
Clotting =
coagulation
– Blood converted into solid gel called clot or thrombus
Blood Clot occurs around
platelet plug
Blood Clot fxn
to support and reinforce platelet plug
Blood Clot defense mechanism
dominant hemostatic defense mechanism
Clotting Factors =
Zymogens
ntrinsic Pathway
Activated when there is: (2)
- trauma to blood
- blood comes in contact with collagen from traumatized blood vessel wall
All required factors found within the blood
Extrinsic Pathway
Activated when there is: (2)
Requires:
- trauma to vascular wall
- trauma to surrounding extravascular tissue.
Tissue Factor (Thromboplastin) produced by cells located outside of endothelial cells
Normally, thrombus formation begins with
extrinsic pathway followed by intrinsic
activation by Thrombin
Step 4: Fibrinolysis (4)
The plasma protein plasminogen is trapped in a clot just like other plasma proteins Over time, injured tissues and endothelial cells slowly release tissue plasminogen factor (t- PA) t-PA converts plasminogen to plasmin a few days after clot is formed Plasmin digests fibrin fibers, fibrinogen, prothrombin, and Factors V, VIII, and XII
A thrombus is a
clot that forms and persists in an
unbroken blood vessel.
Thrombus can block the vessel; leads to
ischemia and tissue death
downstream from the clot (i.e., cause of fatal heart
attacks).
Embolus is a
free floating object in the blood stream; can
wedge and occlude a vessel (referred to as an embolism).
Pulmonary embolism impair
oxygenation
cerebral embolism cause
strokes
Anticoagulants (6)
Aspirin Heparin Recombinant t-PA Warfarin Dabigatrin etexilate (Pradaxa) Clopidogrel (Plavix)
Aspirin
‒ Low doses - Inhibit formation of
‒ High doses - Inhibit formation of
thromboxane A2 by platelets but not prostacyclin by endothelium
prostacyclin
Heparin
‒ Binds to Antithrombin III and increases its activity by 100-1000x
Recombinant t-PA
– Dissolve intravascular clots if given immediately
Warfarin
‒ Blocks vitamin K
Dabigatrin etexilate (Pradaxa)
‒ Blocks active site of thrombin
Clopidogrel (Plavix)
‒ Blocks platelet activation
Thrombocytopenia
what is it?
what causes it? (2)
treatment?
is characterized by a lack of platelets, causes
spontaneous bleeding in small blood vessels.
Even normal movement causes internal
hemorrhaging (petechiae) in the skin.
Anything that affects bone marrow can cause this
(chemotherapy, irradiation etc.).
The only treatment is platelet transfusion.
Liver Disease
what is it?
Severe cases like total impairment of liver function associated with
Impaired liver function causes a lack of zymogens
cirrhosis and hepatitis can require transfusions.
Hemophilia
– Genetic disorder caused by deficiency of gene
for specific coagulation factor (Factor VIII is most common form)
Von Willebrand’s disease (2)
– Reduced levels of vWf
– Decreases platelet plug formation
Vitamin K deficiencies (2)
– Decreased synthesis of clotting factors
– Newborns (Vitamin K shots)
activated partial thromboplastin time (PTT/aPTT)
assessment of intrinsic pathway
prothrombin time (PT)
assessment of extrinsic pathway
Citrate is added to prevent blood from clotting as it will
bind to calcium ions. Except for the first two steps in the intrinsic pathway, calcium ions are required for all blood-clotting reactions.
INR=International Normalized Ratio. (6)
PT times Tissue factor is isolated from human tissue (like placenta) Can have a wide range of activities between batches. INR allows individual tests to be normalized. Each batch comes with a normal PT time Patient values compared to normalized PT time provided (INR = PTpatient/PTnormal)
If INR:
< 1.1
~ 2 - 4 (3)
> 4 (2)
– normal blood clotting
‒Blood clots 2-4x slower than normal
‒Effective therapeutic range
‒OK for Dental work
‒Risk of bleeding too great
‒Work with physician
