Blood/ Coagulopathy Flashcards

1
Q

What are the 2 functions of RBCs

A
  1. Transport O2 via Hgb

2. Store carbonic anhydrase (H2CO3) to be used in converting HCO3 to CO2 during exhalation

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2
Q

What is the equation for converting CO2 to HCO3 using carbonic anhydrase

A

CO2+H2O—>carbonic anhydrase—> >H2CO3–>carbonic anhydrase—>HCO3+H

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3
Q

Normal value of RBCs for men and women

A

Men: 5 million/mm3
Women: 4.5 million/mm3

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4
Q

Normal value for Hct

A

40-45% nominally

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5
Q

Normal value for Hgb

A

14-15g/100mL

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6
Q

Where does RBC production occur?

A

Bone marrow especially of long bones

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7
Q

Describe the chain reaction of RBC production (5 steps)

A
  1. Decreased O2 from anemia, blood loss, systemic hypoxia, infection or increased altitude
  2. Erythropoietin secretion triggered in kidneys (10% of excretion occurs in the liver)
  3. Erythropoietin secretion peaks within 24 hours
  4. Growth and differentiation inducers (also activated at low oxygen levels) mature and divide RBCs
  5. New RBCs formed within 5 days
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8
Q

What is an example of a growth and differentiation inducer in the formation of RBCs

A

Interleukin-3

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9
Q

What are 3 elements required for RBC formation (brought into the body via digestive tract)?

A
  1. Vitamin B-12 (cyanocobalamin)
  2. Folic acid
  3. Iron
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10
Q

What is the chemical formation of Hgb and why does iron play an important role in its formation?

A

Hgb make-up: 4 heme chains connected by 4 iron molecule

Without iron we cannot make Hgb

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11
Q

What is the main role of Hgb?

A

To carry oxygen

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12
Q

What is the lifespan of a RBC

A

120 days

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13
Q

Where are all the clotting factors contained?

A

Plasma

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14
Q

What are 3 indications for a HCP to give plasma?

A
  1. To increase the circulating volume
  2. For the treatment of angioedema
  3. To improve the function of clotting in pts with poor coagulation (low circulating clotting factor, on warfarin, ineffective heparin function)
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15
Q

What is a key component of cryoprecipitate?

A

Fibrinogen

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16
Q

What is the most influential factor in surgical coagulopathy?

A

Platelets

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17
Q

What is the lifespan of a platelet?

A

10 days

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18
Q

How many platelets are formed a day?

A

30,000 per day per mL of blood

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19
Q

Normal platelet value

A

150,000-450,000

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20
Q

What are the 3 reasons platelet loss can occur

A
  1. Deficiencies in production (due to nutritional deficiencies, sepsis, or bone marrow pathology)
  2. Antibody formation against plts
  3. Presence of extensive thrombi that is sequestering plts (think DIC)
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21
Q

What are the 2 roles of WBCs

A
  1. Phagocytes ingestion vis granulocytes and monocytes

2. Antibody formation to destroy substances

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22
Q

Where are WBCs formed

A

Bone marrow and lymphatic tissue

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23
Q

What is the life-span of a WBC

A

4-8 hours (NOTE: vast majority of WBCs are kept in storage in the bone marrow and lymph until the are needed

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24
Q

Normal value of WBCs

A

5,000-10,000/ mL

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25
Q

What are the most common type of WBC?

A

Neutrophils (60% of WBCs)

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26
Q

Which 2 types of WBCs are known for their flexible movement and thus are sent out to moved toward inflamed tissue and pathogens first?

A

Neutrophils and monocytes

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27
Q

What is a monocyte called after it envelopes a pathogen

A

Macrophage

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28
Q

What are pathogens attacked by WBCs?

A

Abnormal shape and no protein protectors—> if these are missing, antibodies will mark them to be destroyed

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29
Q

Liposomes

A

Intracellular organelle that digests and breaks down pathogens

30
Q

What are the methods of pathogen invasion?

A

Soft tissue, GI tract, lungs, and skin

31
Q

What are 3 systems in place to intercept pathogens?

A
  1. Lymphatic system
  2. Lung macrophages
  3. Liver via Kupffer cells
32
Q

What is the name of the cells in the liver that assist in intercepting pathogens

A

Kupffer cells

33
Q

Name the 6 steps in the inflammatory response

A
  1. Injury to tissue
  2. Vasodilation at site of injury—>increased blood flow
  3. Increased capillary permeability causing movement of fluid to interstitial space (WBCs and clotting factors moved out)
  4. Clotting largely due to fibrinogen
  5. WBCs encapsulate and eradicate pathogens
  6. Tissue edema occurs
34
Q

What is the trauma triad that can occur with substantial volume replacement

A
  1. Hypothermia
  2. Acidosis
  3. DIC
35
Q

7 components of fluid therapy

A
  1. Fluid movement between spaces
  2. Swelling
  3. Volume shifts
  4. Coagulation
  5. Circulation volume and pressure
  6. Electrolyte balance
  7. PH stasis
36
Q

The extrinsic clotting pathway

A

Injury—>tissue factor release—>conversion of VII to VIIa—>conversion of X to Xa—> prothrombin activator—>prothrombin to thrombin—> fibrinogen to fibrin

37
Q

What is another name for prothrombin

A

Factor II

38
Q

Intrinsic clotting pathway

A

Exposure of activator (usually via collagen)—>XII to XIIa—>XI to XIa—> IX to IXa—> converges with the extrinsic pathway at Xa

39
Q

Where in prothrombin produced and what element must be present for its production?

A

The liver and vitamin K must be present

40
Q

This part of the clotting cascade is the key to maintaining the clot from anti-clotting factors

A

Fibrin

41
Q

What is the role of thrombin

A

Form clots, activate platelets, and catalyze the formation of fibrin

42
Q

What is the most prevalent clotting factor in circulation

A

Fibrinogen

43
Q

What is the name of the receptor where fibrinogen and platelets bind

A

GP2b/3a

44
Q

What are 3 types of synthetic clotting factors we might give?

A

K-Centra
Factor VIII
VWF

45
Q

What 2 synthetic clotting factors might you give someone with hemophilia A

A

Factor VIII and VWF

46
Q

What factors are contained in K-Centra

A

II, VIII, IX, X, and Protein C and S

47
Q

What is found in the endothelium and inhibits the activation of factor VII by binding to tissue factor thus neutralizing factor X

A

Tissue factor pathway inhibitor

48
Q

Mast cells in the lungs secrete ___

A

Heparin

49
Q

Heparin doesn’t inhibit clotting but increases the action of anti thrombin III by _____%

A

1000%

50
Q

How do platelets adhere to the endothelium after an injury

A

They adhere to VWF via GP1b

51
Q

Platelet aggregation occurs via

A

Fibrinogen

52
Q

What anti-clotting factor lives in the vessel wall and bind to thrombin to prevent is action in uninjured places

A

Thrombulin

53
Q

This is created when thrombin and thrombulin bind together

A

Protein C

54
Q

Protein C can inhibit thrombin receptor and inactivate what 2 factors

A

V and VIII

55
Q

A C=Reactive Protein lab gives information about _____

A

Inflammation and clotting: increased C proteins—> increased inflammation and clotting

56
Q

This anti-clotting factor breaks down Xa and thrombin and is naturally circulating in the plasma

A

Anti-thrombin III

57
Q

This anti-clotting factor transforms plasminogen into plasmin to break down clots (may take a few days)

A

Tissue plasminogen activator (tPA)

58
Q

A prothrombin time evaluates what aspects of the clotting cascade

A

Vit K dependent factors: VII, X, V, and prothrombin

59
Q

Normal prothrombin time

A

12 seconds

60
Q

This evens the PT scale to account for the amount of tissue factor in the medium

A

International normalized ratio

61
Q

Normal value for INR

A

0.9-1.3

62
Q

What does a partial thromboplastin time evaluate

A

The function of heparin

63
Q

Normal value for PTT

A

30-40 seconds

64
Q

Normal value for an activate clotting time

A

110-130 seconds

65
Q

What coagulation evaluation lab is not appropriate in patients with multi factorial coagulopathy?

A

Activated clotting time

66
Q

This coagulation evaluation looks at clotting as a whole

A

Thromboelastograph

67
Q

What individual aspects of the cascade does a TEG assess

A

Fibrinogen, plt function, certain clotting factors, and heparin

68
Q

The coagulation evaluation represents fibrinogen that has been broken down

A

D-dimer

69
Q

This is used to diagnose VTE and DIC

A

D-dimer

70
Q

What are the clinical manifestations of DIC

A

Uncontrolled hemorrhage and lack of clotting

71
Q

Patho of DIC

A

Body’s control mechanism to restrain the action of thrombin to the site of injury stops working—> profound clotting causes all factors to be sequestered usually in distal perfusion sites and lungs and not at the sight of the injury leading to uncontrolled hemorrhaging