Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Heme Week 3 > Therapy and prevention of coagulopathy > Flashcards

Therapy and prevention of coagulopathy Flashcards

1
Q

Is ITP acquired or inherited?

A

acquired

women of childbearing age, MPV high, hemoglobin normal, thrombocytopenia is the only symptom

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

Below what level of platelets warrant treatment in ITP?

A

30-50K/ul (this is because even with only 30-50K platelets, the platelets in ITP are large and the bleeding time will be fairly normal at this level)

only observe if above 30-50K

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

What is the initial treatment for ITP?

A

prednisone and dexamethasome (take 3-4 days to work) +-

quick–IV/Ig (if platelets below 10K and bleeding) and anti-D +-

quick– platelets (if bleeding)

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

What does anti-D do?

A

hemolyzes RhD+ red cells which are taken up via the RES in the spleen in a way that “competitive inhibits” the spleens uptake of ITP platelets

but this is costly to the body

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

What does IVIg do?

A

saturates the Fc receptors in the RES and platelets are salvaged.

but this is costly to the body

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

How is relapses ITP treated?

A

prednisone/dexamethasome and

rituximab or anti-D or IVIg or TPO receptor (Mpl) agonist or splenectomy

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

What bacteria/viruses can cause ITP?

A

H. pylori, HIV, Hep C

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

T or F. Splenectomy can be done with only 30-50K platelets and no platelets are needed

A

T. No infusion necessary usually

this is effective for ITP

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

What is the differential for thrombotic microangiopathy?

A

1) TTP
2) HUS
3) HELLP syndrome
4) DIC
5) SLE
6) Malignant hypertension

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

What lab findings would indicate thrombotic microangiopathy?

A
  • hemolytic anemia
  • thrombocytopenia
  • microclots
  • elevated liver enzymes
  • renal dysfunction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the symptoms of TTP (Moscovitz’s pentad)?

A
  • MAHA
  • Thrombocytopenia
  • renal failure/abnormality
  • fever (from dead tissue creating cytokines)
  • CNS manifestations
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens in TTP?

A

Antibody against ADAMTS13 prevent cleaving of vMF which bind platelets and slice red cells (shistocytes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What binds Hb dimers after intravascular hemolysis?

A

haptoglobin, and then they are taken up by the liver so haptoglobin is reduced

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What happens to unbound Hb dimers?

A

it oxidizes to methemoglobin and is taken up by the kidneys and some leaks into urine (brown colored)

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

What is the treatment for TTP?

A

plasma exchange (not only adds ADAMST13 but also removes the antibodies so its better)

or infusion

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

Does TTP show abnormalities in PTT or PT?

A

No, neither. Even though micro thrombi occur, there really isn’t enough consumption of clotting proteins for that

17
Q

What happens in HUS?

A

Shiga toxin makes antibodies to Gb3 (acts similarly to ADAMTS13) on weibel-palade bodies that prevent cleaving, and thus activate micro-thrombi mostly in kidneys

and complement is activated against red cells

18
Q

How does DIC present?

A
  • PT AND PTT prolongation (clotting factors are used up)
  • fever
  • CNS changes
  • high LDH (mostly from anoxic damage- not hemolysis)
  • anemia
  • hypotension
  • rash from micro thrombi
  • cyanosis of digits
19
Q

What happens in DIC?

A

intravascular deposition of fibrin leading to overactive clotting and micro thrombi formation and eventually and organ failure from anoxia. Eventually, depletion of platelets and coagulation factors may result in bleeding

both PT and PTT prolonged and d-dimer increased

20
Q

What can trigger DIC?

A

the main thing is release of TF

  • bacterial sepsis
  • acidosis, shock, heat stroke
  • malignancies
  • obstetrical complications
21
Q

What is a main clinical site of DIC?

A

bleeding from 3 unrelated sites and platelets aren’t very low

22
Q

T or F. Schistocytes are seen in DIC

A

T.

23
Q

How is DIC treated?

A
  • stop trigger process
  • supportive therapy (only if bleeding)
  • no specific treatments

if not bleeding, only watch

treat if an invasive procedure is needed

prophylactic therapy has no proven benefit

24
Q

What is HIT?

A

Factor 4 (on platelets) IgG antibodies complex them and activate them in the presence of heparin which causes:

1) platelet aggregation and thrombosis (rare)
2) platelet removal by RES and thrombocytopenia (more common)

25
Q

What is the 4T pretest scoring system for HIT?

A

1) Thrombocytopenia
2) Timing
3) Thrombosis
4) oTher causes

26
Q

Describe the thrombocytopenia portion of the 4T system

A

2 pts- platelets drop 50+%
1pt- drop 30-50%
0 pts- drop less than 30%

everyone on heparin have at least 8% drop in platelets

27
Q

Describe the timing portion of the 4T system

A

2 pts- antibody in 5-10 days
1 pt- not clear if 5-10 days
0 pt- less than 4 days

28
Q

Describe the thrombosis portion of the 4T system

A

2 pts- new thrombosis; skin necrosis
1 pt- progressive or recurrent thrombosis; no skin necrosis
0 pt- none

29
Q

Describe the oTher causes portion of the 4T system

A

2 pts- none apparent
1 pt- possible
0 pt- definite

30
Q

How is the 4T test interpreted?

A

0-3- low (don’t test)
4-5 intermediate (testing indicated)
6-8 high

31
Q

What is the gold standard assay for HIT diagnosis?

A

Serotonin release assay (SRA) sensitive and specific

antibody test is very nonspecific

32
Q

What should you do if the 4T comes back intermediate or high?

A
  • discontinue heparin!!

- obtain anti-PF4/heparin ELISA

33
Q

What is the anti-PF4/heparin ELISA comes back strongly OD 1+) or weakly positive (OD 0.4-0.99)?

A

obtain functional assay- if +, HIT, if not, probably not HIT

34
Q

What is the treatment for HIT?

A
  • avoid platelet transfusion unless bleeding

- other anticoag (fondaparinux might not work)

35
Q

What is the target platelet level for prevention of spontaneous mucocutaneous bleeding?

A

10-20K+ (menorrhagia, gum bleeding)

36
Q

What is the target platelet level for insertion of central venous catheters?

A

20-50+

37
Q

What is the target platelet level for administration of therapeutic anticoagulation?

A

30-50K+

38
Q

What is the target platelet level for minor surgery and invasive procedures (endoscopy, etc.)?

A

50-80K+

39
Q

What is the target platelet level for major surgery (neuro, etc.)?

A

80-100K+

Heme Week 3 (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions