Hematology #2 Flashcards

(30 cards)

1
Q

DIC excessive clotting cascade and lysis cascade results in:

A
  • Exhausted factors and co-factors
  • partially developed and broken down clots
  • micro emboli caught in capillaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Organs with most capillaries

A

Heart, liver, spleen, brain, lungs,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MODS and death result from DIC why?

A

Entire system losing blood due to mass micro emboli occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

DIC lab values

A
  1. Positive D-Dimer (fibrin degradation products)
  2. Low fibrinogen and platelets (clotting factors)
  3. Hg PT, aPTT, INR, FSP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

PT

A

Prothrombin Time

-measurement of intrinsic coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

aPTT

A

Activated partial thromboplastin time

-measurement of extrinsic coagulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

INR

A

International Normalized Ratio

  • universalized rabbit serum to measure PT
  • normal 1.0
  • high INR suggest it is taking longer to clot
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

FSP or FDP

A

Fibrin Split / Degradation Product

-clot break down

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

DIC treatment #1 goal

A

Treat precipitating cause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

DIC traditional treatment

A

Give FFP, Cryo, platelets to create clots

-May add to the problem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

DIC and heparin treatment

A

Only studies to be beneficial when secondary yo neoplasms and CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Antithrombin III (ATIII) therapy

A

Interferes with fibrinogen converting to fibrin (normal process in body)

  • prevents coagulopathy
  • primarily inhibits factors IIa (thrombin) and X (Stuart factor)
  • in FFP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Chronic heparin therapy can cause what deficiency?

A

ATIII

  • body processes out heparin bound w/ ATIII
  • can cause DIC, tx w/ FFP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

PRBC indication

A

Increase O2 carry capacity of blood

-volume expander only secondary to this qualification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

PRBC HgB indications

A

Indicated for

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

RBC antigen that can cause a reaction

17
Q

Rh(-) female

A

Can reach sensitization with Rh (+) blood.

  • anaphylaxis possible
  • Rh (+) fetus can be aborted (rogan can prevent this)
18
Q

Rh(+) / Rh(-) blood to male or females

A

Females: Rh(-)
Males: Rh (+)
-can be sensitized, but does not have fetal complication for future.

19
Q

How many ml are in one unit of PRBCs?

20
Q

PRBC pediatric dose

21
Q

Citrate toxicity considerations

A

Multiple units: 4 units in less than 20 minutes

-citrate chelates ionized Ca- renders it useless in clotting cascade

22
Q

Administer Ca if giving PRBCs at what rate

A

One unit in less than 5 minutes or 1 ml/kg/min

General rule: 1 amp of Ca q 4 units PRBCs.

23
Q

Liver considerations with citrate

A

Liver processes citrate. Liver dysfunction can lead to citrate toxicity despite PRBC admin at slower rates.

24
Q

Universal donor

25
Universal recipient
AB(+) | Can take A, B, AB
26
1 unit of PRBCs increases the H&H by what?
1&3
27
Q unit of PRBCs at storage temp will decrease core temp by?
0.25 c
28
PRBC and acidosis considerations
Store blood continued metabolism = lactate = acidotic - citrate converts to HCO3 = self correcting - watch ABGs
29
PRBC and hyperkalemia considerations
RBCs die and release K in storage. Stored blood K levels can reach 17-24. -administration rates greater than 90-120 ml/min can result in hyperkalemia. Watch ECG for changes.
30
DIC cause and mechanism
Causes: sepsis, massive trauma, hypoxia Mechanism: systemic activation of clotting cascade by overwhelming release of thromboplastin factor. Lysis cascade goes into overdrive as a result to overwhelming clot formation. Clots broken down prematurely.