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Physiology > CV 5 (2) > Flashcards

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 =

A

Zymogens

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
Q

Extrinsic Pathway
 Activated when there is: (2)
 Requires:

A
  • trauma to vascular wall
  • trauma to surrounding extravascular tissue.

Tissue Factor (Thromboplastin) produced by cells located outside of endothelial cells

26
Q

Normally, thrombus formation begins with

A

extrinsic pathway followed by intrinsic

activation by Thrombin

27
Q

Step 4: Fibrinolysis (4)

A 
 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
Q

A thrombus is a

A

clot that forms and persists in an

unbroken blood vessel.

29
Q

Thrombus can block the vessel; leads to

A

ischemia and tissue death
downstream from the clot (i.e., cause of fatal heart
attacks).

30
Q

Embolus is a

A

free floating object in the blood stream; can

wedge and occlude a vessel (referred to as an embolism).

31
Q

Pulmonary embolism impair

A

oxygenation

32
Q

cerebral embolism cause

A

strokes

33
Q

Anticoagulants (6)

A 
Aspirin
Heparin
Recombinant t-PA
Warfarin
Dabigatrin etexilate (Pradaxa)
Clopidogrel (Plavix)
34
Q

Aspirin
‒ Low doses - Inhibit formation of
‒ High doses - Inhibit formation of

A

thromboxane A2 by platelets but not prostacyclin by endothelium

prostacyclin

35
Q

Heparin

A

‒ Binds to Antithrombin III and increases its activity by 100-1000x

36
Q

Recombinant t-PA

A

– Dissolve intravascular clots if given immediately

37
Q

Warfarin

A

‒ Blocks vitamin K

38
Q

Dabigatrin etexilate (Pradaxa)

A

‒ Blocks active site of thrombin

39
Q

Clopidogrel (Plavix)

A

‒ Blocks platelet activation

40
Q

Thrombocytopenia
what is it?
what causes it? (2)
treatment?

A

 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
Q

Liver Disease
what is it?
 Severe cases like total impairment of liver function associated with

A

 Impaired liver function causes a lack of zymogens

cirrhosis and hepatitis can require transfusions.

42
Q

Hemophilia

A

– Genetic disorder caused by deficiency of gene

for specific coagulation factor (Factor VIII is most common form)

43
Q

Von Willebrand’s disease (2)

A

– Reduced levels of vWf

– Decreases platelet plug formation

44
Q

Vitamin K deficiencies (2)

A

– Decreased synthesis of clotting factors

– Newborns (Vitamin K shots)

45
Q

activated partial thromboplastin time (PTT/aPTT)

A

assessment of intrinsic pathway

46
Q

prothrombin time (PT)

A

assessment of extrinsic pathway

47
Q

Citrate is added to prevent blood from clotting as it will

A

bind to calcium ions. Except for the first two steps in the intrinsic pathway, calcium ions are required for all blood-clotting reactions.

48
Q

INR=International Normalized Ratio. (6)

A 
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
Q

If INR:
< 1.1
~ 2 - 4 (3)
> 4 (2)

A

– 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

Physiology (53 decks)

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