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adv princip II exam 2 (6/13) > hemostasis > Flashcards

hemostasis Flashcards

0
Q

what factor do intrinsic & extrinsic pathways converge on?

A

-factor X (10)

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1
Q

what is the deadly triad of blood transfusions?

A

-acidosis
-coagulopathy
-hypothermia
“A-C-H”

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2
Q

the factor comes from where?

1. von wildebrands

A
  1. endothelium
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3
Q

what does each lab test for?

  1. ptt
  2. pt
  3. bleeding time
  4. teg
  5. act
A
  1. PTT tests for intrinsic and common pathways
  2. PT tests for extrinsic and common pathways
  3. bleeding time tests for platelet dysfunctions, effects of asa and vWF disease
  4. TEG tests for all factors in the clotting cascade
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4
Q

what is the time frame and pressure needed to form a clot?

A

less than 60 MAP for 10 seconds

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5
Q

heomstasis is depends on what?

A

time and flow

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6
Q

hemostasis is termed as what?

A

“the combined activity of vascular, platelet and plasma factors counterbalanced by regulatory mechanisms to limit accumulation of fibrin and platelets in the area of injury”
or -
the arrest of bleeding from an injured vessel

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7
Q

what are the 4 processes that contribute to hemostasis?

A
  1. vasoconstriction from:local (thromboxane, ADP, serotonin) and systemic (epinephrine) vasocontrictors.
  2. Platelets (ADP & thromboxane and von willibrand combined with GP1b) make platelets sticky
  3. Fibrin (calcium joins fibrin monomers into polymers)
  4. factor XIII- forms a net/ mesh from fibrin polymers
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8
Q
  1. what is fibrinolysis?

2. what factores cause fibrinolysis?

A
  1. the break down of the clot
  2. a. presence of blood clot induces secretion of TPA
    b. TPA convertes plasmin”ogen” into plasmin
  3. plasmin (also containing antithrombin III and urokinase) works on the clot
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9
Q
  1. what is the intrinsic pathway?
  2. what triggers this pathway and what factors are involved?
  3. what do these factors activate?
A
  1. intrinsic is triggered from within
  2. damage to vessel wall stimulates activation of factors 8, 9,11 & 12
  3. those factors in turn activate factor X (which causes the actual clotting cascade)
    (intrinsic=inside cost -$11.98 is almost $12 (8,9,11,12))
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10
Q
  1. what is the extrinsic pathway?
  2. what factors trigger this pathway?
  3. what do these factors do?
A
  1. damage to tissue outside of the vessel ; clots blood that has escaped into tissues (extrinsic is external)
  2. factors III (thromboplsatin) and VII cause activation of factor X
  3. those factors in turn activate factor X (which causes the actual clotting cascade)
    (extrinsic is an extra $37)
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11
Q
  1. what factor does both extrinsic and intrinsic pathway converge on?
  2. what factors does this factor join up with to form a clot (name them all)?
A
  1. all converge on factor X

2. I,II,V,X, XIII (you can get it on the first and second day of the month at the “five & dime” for thirteen bucks)

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12
Q
  1. most coagulation factors are formed where?
  2. what factor is made from endothelial cells?
  3. what factor comes from diet?
  4. of the factors, which are dependent on vitamin K?
A
  1. the liver
  2. von willebrands factor is formed by endothelial cells
  3. calcium (is actually not a factor but a co-factor obtained by diet)
  4. vitamin K dependent factors are: II, VII, IX & X
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13
Q
  1. what is the best way to measure clotting including platelets?
  2. what does it measure?
  3. what is normal?
A
  1. bleeding time
  2. looks at first stage of clotting:
    - -aspirin inhibition of platelets
    - -platelet function
    - -lack of clotting factores (von willibrands disease etc).
  3. 3-9 minutes (>12 is abnormal)
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14
Q

what does a platelet count do?

A

identifies quantitative platelet disoeders (thrombocytopeina or thrombocytosis)

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15
Q
  1. aPTT: activated partial thromboplastin time measures what?
  2. what drug does the test monitor?
  3. what factors are monitored by PTT?
  4. what is a normal PTT?
A
  1. the intrinsic and common pathways
  2. monitors heparin therapy
  3. measures factors: I, II, V, VII, IX, X, XI, XII (1,2,5,8,10,11,12)
  4. normal: 5-32 seconds
16
Q
  1. what does PT measure?
  2. what drug does it monitor?
  3. what is the norm?
  4. what is abnormal
A
  1. extrinsic and common pathways
  2. coumadin
  3. the control (12-13 seconds)
  4. > 3 seconds above the control
17
Q
  1. what is the INR?

2. what is normal?

A
  1. INR is the ratio of the patient’s PT to a reference PT

2. the INR of < 1.5 means the patient has a normal PT (NOT anticoagulated)

18
Q
  1. What does an ACT measure?
  2. what is the activator in the tube?
  3. when is it used?
  4. what is a normal ACT?
A
  1. evaluates intrinsic and common coagulation pathways
  2. diatomaceous earth or kaolin
  3. evaluates heparin
  4. normal ACT=90-120 seconds
19
Q
  1. what is a TEG scan?

2. what is measured?

A
  1. evaluates clot formation and dissolving (dissolution) over time
  2. guide to giving blood components (most accurate test of all); measures
    - -fibrin-platelet bond
    - -platelet function
    - -coagulation cascade
    - -rate of fibrinolysis
20
Q
  1. what causes fibrinogen split products?

2. what is normal? abnormal?

A
  1. the presence of clot break down (seen in PE and DIC)

2. normal=40

21
Q
  1. What is von willebrands (vWF) disease?
  2. what tests would you use to test for it?
  3. what are 4 treatments and their actions?
  4. *what factor is given when there is no ____ or patient is resistant to ____?
A
  1. lack of von willebrands factor (which is a plasma carrier for factor VIII (8)) that causes platelets to adhere and released from the endothelium
  2. tested by: bleeding time
    3a. –recombinant factor VIII-vWF concentrate
    3b. —DDAVP (stimulates the release of vWF)
    3c. —cryoprecipitate (provides factor VIII and *)
    3d. FFP- provides all factors
  3. *cryoprecipitate is given when there is no recombinant factor VIII-vWF and the patient is resistant to DDAVP
22
Q
  1. what is hemophilia?
  2. what is factor 8 deficiency?
  3. what is factor 9 deficiency?
  4. how is it treated?
A
  1. X-linked defect which occures in males; can be A or B (christmas disease)
  2. Hemo A is factor VIII (8) deficiency;
  3. Hemo B is a factor IX (9) deficiency
  4. factor 8 concentrate, cryoprecipitate, desmopressin (increases factor 8 and vWF).
23
Q
  1. How do ASA and NSAIDS work in the body?
  2. asa and nsaids are best evaluated by what test?
  3. when should you NOT withold ASA?
A
  1. irreversibly inhibits throboxane A2 by inhibiting prostaglandins and arachadonic acid (blocks platelet action)
  2. bleeding time
  3. SECONDARY PREVENTION (of stroke, MI or with stents)
24
Q
  1. what is the action of plavix?
  2. how does that differ from ticlid?
  3. how do you reverse treat the action of plavix?
  4. what are the IV reversible drugs like plavix?
A
  1. plavix is an antiplatelet drug that irreversibly inhibit receptors on GPIIA/IIIB as well as ADP receptor
  2. ticlid is considered reversible
  3. platelets
  4. reversible IV GPIIA/IIIB such as integrilin and reapro
25
Q
  1. what is the action of heparin in anti clotting?
  2. how does it work in clotting?
  3. where is heparin produced naturally in body?
  4. what is the reversal for heparin?
A
  1. inhibits thrombin by binding to anti-thrombin III
  2. acts as a cofactor in clotting by accelerating antithrombin III activity
  3. produced by mast cells (mostly in lung)
  4. protamine sulfate or FFP
26
Q
  1. How does coumadin work?
  2. way to reverse mild coumadin od?
  3. best and fastest way (best for severe od)?
A
  1. inhibits vitamin K
  2. vitamin K 5-10 mg po or SQ;
  3. FFP 10-20 ml/kg (best way)
27
Q
  1. what is sickle cell disease?
  2. what lab should be checked?
  3. what causes sickling?
  4. management of sickle cell patient?
A
  1. sickling of blood d/t abnormal beta globin chain
  2. hgb S
  3. hypoxemia (pao2 of 20-40 mmHg)-causes P50 of 31 (right shift)
    acidosis, hypothermia, dehydration
  4. keep patient hydrated, keep sat >95%, keep patient warm, no tourniquets (if possible)
28
Q
  1. how do you calculate bicarb deficit?
  2. if patient’s bicarb is 17 and they weigh 70 kg; what is the deficit?
  3. how do you replace bicarb deficit?
  4. how much bicarb is in one amp of bicarb?
A
  1. 0.4 x weight (in kg) multiplied by (normal bicarb - patient’s bicarb)
  2. 0.4 x 70 (24-17)= 28 (24-17)=196 meq (so about 4 amps down)
  3. give 50% over first 4 hours; give the other over the next 8-24 hours.
  4. 1 amp of 8.4% bicarb is 50 meq
29
Q

what is the definition of massive transfusion

A

entire blood volume in a 24 hour period

30
Q

what is the 1st step of the clotting cascade?

A

vasoconstriction of the vessel vall

  1. from local controls: thromboxane, adp, serotonin release at site of injury
  2. from systemic controls: epinephrine released from adrenals causes general vasoconstriction
31
Q

a. what is the second step in the clotting cascade?

b. what is happening elsewhere (in the healthy vessels)

A

platelets clump together
1. thromboxane makes platelets sticky
2. von willibrand factor combines with GP1b to cause stickiness
Prostacycline starts to inhibit platelet aggregation in healthy vessels

32
Q

what is the 3rd step in the clotting cascade?

A
  1. intrinsic pathways are triggered from INSIDE the vessel:
    (factors 8,9,11 & 12 converge on factor 10)
  2. EXTRINSIC pathways are triggered from OUTSIDE the vessels (from a clot that has escaped into the tissues):
    (factors 3 & 7 converge on factor 10)
  3. convergence on factor 10 (common pathway)
    (factors 1,2,5,10,13 meet)
33
Q

A. what factor is the key to the clotting mechanism?

B. what 5 things does it do?

A

A. factor 10 (thrombin):
B….
1. activates factors 5,8 & 13
2. converts fibrinogen to fibrin
3. stimulates platelet aggregation
4. acts as an anticoagulant by releasing tPA
5. provides positive feed back to accelerate the clotting cascade

34
Q
  1. what is the 4th stage in the clotting cascade?

2. what does this factor do?

A
  1. factor 13 (XIII) is activated
  2. causes the cross cross polymerization of the loose fibrin polymers into a firm, insoluble, hemostatic net which attracts red blood cells and forms a clot
35
Q

what does calcium do to the fibrin monomers?

A

causes them to link into polymer strands (which will form the mesh for the clot)

adv princip II exam 2 (6/13) (5 decks)

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