CV 5 (2) Flashcards

1
Q

A person is Rh-positive if they have the

A

Rh Antigen on RBCs

– No Rh-antibodies in the plasma

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2
Q

A person is Rh-negative if they lack the

A

Rh Antigen on RBCs

– No Rh-antibodies (IgGs) in the plasma

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3
Q

– No Rh-antibodies (IgGs) in the plasma IF the person

has never been exposed to Rh+ blood (2)

A

• 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

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4
Q

Erythroblastosis Fetalis

A

Rh-negative mother, Rh-positive fetus.

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5
Q

Erythroblastosis Fetalis

First pregnancy: (3)

A

fetal red cells leak into maternal circulation.
– Mother develops anti-Rh antibodies.
– Low risk to fetus because this occurs late in
pregnancy.

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6
Q

Erythroblastosis Fetalis

Second pregnancy:

A

maternal IgG crosses placenta, destroys fetal RBC’s.

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7
Q

Erythroblastosis Fetalis

Treatment:

A

administration of anti-RhD immunoglobulin (RhoGAM) after delivery.

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8
Q

Platelets

A

Cytoplasmic fragments derived from megakaryocytes (thrombocytes).

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9
Q

Platelets concentration in blood

A

150,000 – 300,000/μl of blood

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10
Q

platelet lifespan

A

10 days

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11
Q

platelet primary role in

A

hemostasis

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12
Q

platelet content

A

no nuclei, cannot divide

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13
Q

platelets contain (5)

A
  • 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
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14
Q

Recent evidence that platelets can act as (2)

A

immune cells and contribute to

the inflammatory process of atherosclerosis

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15
Q

Hemostasis

A

The physiological mechanisms that stops bleeding

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16
Q

Hemostasis is a 4-step process:

A
  1. Vasoconstriction of damaged vessel to decrease blood flow and pressure
  2. Formation of platelet plug to block hole in damaged vessel
  3. Clot formation (requires Fibrin)
  4. Clot dissolution
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17
Q

Steps Leading to Platelet Plug and Vasoconstriction

A

 Platelets stick to damaged Endothelial cell surface (Von Willebrand Factor (vWF))

  1. Platelets release contents of secretory vesicles
  2. Stimulate production of Thromboxane A2 from platelet plasma membrane
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18
Q

Causes of platelet plug/vasoconstriction (2)

A
  1. Vasoconstriction of damaged vessel

2. Platelet plug formation (+ feedback Platelet activation)

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19
Q

Clotting =

A

coagulation

– Blood converted into solid gel called clot or thrombus

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20
Q

Blood Clot occurs around

A

platelet plug

21
Q

Blood Clot fxn

A

to support and reinforce platelet plug

22
Q

Blood Clot defense mechanism

A

dominant hemostatic defense mechanism

23
Q

Clotting Factors =

24
Q

ntrinsic Pathway

 Activated when there is: (2)

A
  • trauma to blood
  • blood comes in contact with collagen from traumatized blood vessel wall

 All required factors found within the blood

25
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
26
Normally, thrombus formation begins with
extrinsic pathway followed by intrinsic | activation by Thrombin
27
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 ```
28
A thrombus is a
clot that forms and persists in an | unbroken blood vessel.
29
Thrombus can block the vessel; leads to
ischemia and tissue death downstream from the clot (i.e., cause of fatal heart attacks).
30
Embolus is a
free floating object in the blood stream; can | wedge and occlude a vessel (referred to as an embolism).
31
Pulmonary embolism impair
oxygenation
32
cerebral embolism cause
strokes
33
Anticoagulants (6)
``` Aspirin Heparin Recombinant t-PA Warfarin Dabigatrin etexilate (Pradaxa) Clopidogrel (Plavix) ```
34
Aspirin ‒ Low doses - Inhibit formation of ‒ High doses - Inhibit formation of
thromboxane A2 by platelets but not prostacyclin by endothelium prostacyclin
35
Heparin
‒ Binds to Antithrombin III and increases its activity by 100-1000x
36
Recombinant t-PA
– Dissolve intravascular clots if given immediately
37
Warfarin
‒ Blocks vitamin K
38
Dabigatrin etexilate (Pradaxa)
‒ Blocks active site of thrombin
39
Clopidogrel (Plavix)
‒ Blocks platelet activation
40
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.
41
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.
42
Hemophilia
– Genetic disorder caused by deficiency of gene | for specific coagulation factor (Factor VIII is most common form)
43
Von Willebrand’s disease (2)
– Reduced levels of vWf | – Decreases platelet plug formation
44
Vitamin K deficiencies (2)
– Decreased synthesis of clotting factors | – Newborns (Vitamin K shots)
45
activated partial thromboplastin time (PTT/aPTT)
assessment of intrinsic pathway
46
prothrombin time (PT)
assessment of extrinsic pathway
47
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.
48
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) ```
49
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