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Heme Flashcards

1
Q

What is the only direct thrombin inhibitor?

A

Dabigatran (pradaxa)

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2
Q

How are factor Xa inhibitors cleared (renally/hepatically)? What is the significance of this?

A

Renall, thus dialysis patients or patients with renal disease will have altered clearance

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3
Q

How long does is take to clear the new Xa inhibitors?

A

12-24 hours

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4
Q

How do you reverse factor Xa inhibitors? (3)

A

TXA
4 factor PCC
IR consult if necessary

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5
Q

What is the reversal agent for dabigatran? What is the efficacy of this?

A
  • Idarucizumab

- Questionable efficacy

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6
Q

What is the reversal agent for apixaban and rivaroxaban? What is the efficacy of this?

A
  • Andexanet

- Questionable efficacy (rebound effect)

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7
Q

What is a febrile non-hemolytic transfusion reaction? Treatment?

A

Fever from blood products. Give tylenol and stop the transfusion temporarliy

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8
Q

What is the treatment for a simple allergic (urticarial) reaction to blood?

A

Benadryl. Continue to give product, but watch carefully.

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9
Q

What are the symptoms of a hemolytic transfusion reaction?

A

Fever
Flank pain/hematuria
Shock, DIC, death

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10
Q

What is the diagnostic test for a hemolytic transfusion reaction?

A

Coombs test

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11
Q

What is the treatment for a hemolytic transfusion reaction?

A
  • IVFs, and titrate to UOP of 100-200 cc/hr

- Treat hyperkalemia

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12
Q

What is in the differential for a patient presenting with shock and fever following a transfusion? Tests?

A

Sepsis vs hemolytic transfusion reaction

-Coombs test and blood cultures from pt and bag

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13
Q

What is the differential for a patient that presents with difficulty breathing following a transfusion?

A

Anaphylaxis
TRALI
TACO

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14
Q

What are the factors that lead to an increased risk for TRALI?

A
  • Massive transfusions
  • SIRS/Sepsis
  • Trauma pts
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15
Q

What is the role of lasix in the treatment of TRALI?

A

Do NOT give

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16
Q

What is the treatment for TACO?

A

Lasix, supoortive care (treat like CHF exacerbations)

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17
Q

What is the protein that is exposed on injured blood vessel walls that causes platelets to adhere?

A

vWF

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18
Q

What is the general role of the following:

  • Anti-thrombin III
  • Protein C
  • Protein S
A

All anticoagulants

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19
Q

What is the inheritance pattern of type A and B hemophilia respectively?

A

both AR

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20
Q

Which coag test will be elevated with hemophilias PT or PTT

A

PTT

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21
Q

What is the definitive test for a hemophilia?

A

Factor activity levels

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22
Q

What is the dosing of factor 8 and 9 for mild moderate and severe bleeding respectively?

A 
Mild = 12.5/25
Moderate = 25/50
Severe = 50/100
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23
Q

How does DDAVP work to improve clotting?

A

Releases extra vWF which carries factor 8

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24
Q

What is the alternative treatment for replacing lost factors?

A

DDAVP
Cryo
FFP

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25
Q

What are types I, II, and III vWF disease?

A 
I = decreased number of vWF
II = non-functional vWF
III = complete lack of vWF
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26
Q

Which type of vWF does DDAVP not work for?

A

III

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27
Q

What is the treatment for vWF?

A

DDAVP
Non-recombinant VIII
-cryo

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28
Q

What is the role of FFP in vWF?

A

Not used, since not much vWF in it

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29
Q

What is the antidote to heparin?

A

Protamine sulfate

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30
Q

What is the MOA of heparin?

A

Binds to and activates antithrombin III, which inhibits Xa

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31
Q

What is the MOA of protamine? Why is there a limit on the dose?

A

Binds heparin and prevents it from working, but it in itself is actually an anticoagulant

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32
Q

Why must protamine be given slowly?

A

Anaphylactoid rxn

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33
Q

What is the dosing scheme for protamine? Max dose?

A

1 mg for every 100 units of heparin over the last 4 hours with a max dose of 50 mg

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34
Q

What is the role of protamine in lovenox bleeding?

A

Reverses about 60% of lovenox

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35
Q

What are the three agents used to reverse coumadin?

A

FFP
Vit K
PCC

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36
Q

What is FFP?

A

All the coag factors and proteins in blood

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37
Q

What is PCC?

A

Factors 2, 7, 9, 10

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38
Q

What is the treatment for a supratherapeutic INR but less than 5 without bleeding?

A

Skip next dose of coumadin

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39
Q

What is the treatment for a supratherapeutic INR between 5 and 9 without bleeding?

A

Omit 1-2 warfarin doses, 5 mg vit K PO

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40
Q

What is the treatment for a supratherapeutic INR over 9 without bleeding?

A

Withhold warfarin, vit K 5-10 mg PO

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41
Q

What is the antidote to tPA?

A

Aminocaproic acid

TXA

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42
Q

What is the reversal agent for plavix?

A

Give platelets

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43
Q

What happens with anion gap with multiple myeloma?

A

Lower

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44
Q

What is the monoclonal protein that is found with multiple myeloma?

A

Bence Jones protein

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45
Q

What test is diagnostic of multiple myeloma?

A

SPEP/ UPEP

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46
Q

Why is ESR elevated with multiple myeloma?

A

Slow sedimentation rate due to rouleaux formation

47
Q

Who is typically affected with follicular lymphoma? What is the natural history of the disease?

A
  • Older adults

- Widespread and incurable, but pts live years

48
Q

Who is typically affected with Diffuse large B-cell lymphoma? What is the natural history of the disease?

A
  • Older adults

- Aggressive, 50% curable

49
Q

How does Hodgkin’s lymph nodes present?

A

Contiguous pattern of LAD

50
Q

REed-sternberg cell = ?

51
Q

What are the two classes of lymphoid cells?

A

B cells and T cells

52
Q

What are the classes of myeloid cells?

53
Q

What are the s/sx of ALL?

A
  • LAD
  • Fatigue/anemia
  • Bleeding/petechiae
  • Infxs
54
Q

What are the s/sx of AML?

A
  • NO LAD
  • fatigue/anemia
  • Infiltration of gums
55
Q

Auer rods = ?

56
Q

How can you differentiate CLL vs CML on a CBC?

A

CML has increased platelets

57
Q

How many WBCs are present with leukostasis?

A

over 100,000

58
Q

What are the s/sx of leukostasis?

A
  • Hypoxia

- HA/visual changes

59
Q

What is the treatment for leukostasis? (4)

A
  • Induction chemotherapy
  • Allopurinol
  • Hydroxyurea
  • Leukapheresis
60
Q

What are the four major metabolic derangements with tumor lysis syndrome?

A
  • Hyperuricemia
  • Hyperkalemia
  • Hypocalcemia
  • Hyperphosphatemia
61
Q

What is the most important test to diagnose tumor lysis syndrome?

62
Q

What are the two medications to treat tumor lysis syndrome?

A

Allopurinol

Rasburicase

63
Q

What causes the hypocalcemia with tumor lysis syndrome?

A

hyperphosphatemia–phosphate binds to calcium

64
Q

What is the difference in prognosis for ITP in kids vs adults?

A

Kids is self limiting disease, adults is usually chronic

65
Q

What are the two major/broad pathophysiologic processes that lead to ITP?

A
  • Immune mediated destruction of platelets

- Decreased production

66
Q

What is the first line treatment for ITP? Second line?

A

Corticosteroids

IVIG

67
Q

What are the components of the pentad of s/sx that make up TTP?

A
  • AMS
  • Thrombocytopenia
  • Fever
  • Anemia
  • ARF
68
Q

What is the role of platelets in the treatment of TTP?

A

Will make worse, do NOT give

69
Q

What enzyme is deficient in TTP?

70
Q

What is the pathophysiology of TTP?

A

vWF untangles from intima, platelets bind. No ADAMTS-13 to cleave, so leave large sheets of platelets in blood vessels. RBC get sheared

71
Q

What happens to bili with TTP? LDH? Fibrinogen?

A
  • Unconjugated Bili increases
  • LDH increases
  • Normal fibrin
72
Q

What is the treatment for TTP?

A
  • FFP
  • IVIG
  • PET (plasma exchange trans)
73
Q

Why does FFP work to treat TTP?

A

Replaces ADAMTS-13

74
Q

What is the classic triad of HUS?

A
  • MAHA
  • Thrombocytopenia
  • ARF
75
Q

How do you diagnose HUS?

A

Send stool/urine for shiga toxin

76
Q

Should you give platelets to HUS?

77
Q

What is the treatment for HUS? What is not?

A
  • Supportive care

- No Abx, causes release of toxins

78
Q

Can you get HIT from lovenox?

79
Q

What is the definition of HIT?

A

platelets less than 150 K OR 50% drop from baseline

80
Q

What factor(s) does heparin vs lovenox work against?

A
  • Heparin inhibits Xa and thrombin

- Lovenox only against Xa

81
Q

What is the presentation of HIT?

A

clots everywhere

82
Q

What are the 4 T’s of HIT?

A
  • Thrombocytopenia
  • Thrombosis
  • Timing (5-14 days)
  • no oTher cause
83
Q

What is the treatment for HIT?

A

Stop heparin

Give Dabigatran

84
Q

What is the role of platelets for the treatment of HIT?

A

Do NOT give

85
Q

What happens to the following lab values with DIC:

  • platelet count
  • D-Dimer
  • PT
  • Fibrinogen
A
  • Platelet goes down
  • Dimer elevated
  • PT prolonged
  • Fibrinogen decreases
86
Q

Can you give DIC pts platelets?

A

Yes, but of variable efficacy

87
Q

When is dialysis indicated for the treatment of HUS?

A

If patient becomes anuric.

88
Q

What are the three major disease entities that you should not give platelets to?

89
Q

Which of the following have decreased platelets:

  • ITP
  • TTP
  • HUS
  • HIT
  • DIC
90
Q

Which of the following have increased PT/INR:

  • ITP
  • TTP
  • HUS
  • HIT
  • DIC
A

DIC

HIT +/-

91
Q

Which of the following have microangiopathic hemolytic anemia:

  • ITP
  • TTP
  • HUS
  • HIT
  • DIC
92
Q

Which of the following have low fibrinogen levels:

  • ITP
  • TTP
  • HUS
  • HIT
  • DIC
93
Q

Which of the following are associated with splenomegaly:

  • ITP
  • TTP
  • HUS
  • HIT
  • DIC
94
Q

Which of the following diseases cause the patient to look “sick”:

  • ITP
  • TTP
  • HUS
  • HIT
  • DIC
95
Q

Which of the following diseases is it okay to give platelets to:

  • ITP
  • TTP
  • HUS
  • HIT
  • DIC
96
Q

Which of the following diseases commonly have clots:

  • ITP
  • TTP
  • HUS
  • HIT
  • DIC
97
Q

What are the three major general etiologies of pancytopenia?

A
  • Infections (HIV)
  • Medications
  • Leukemia
98
Q

Microcytic or macrocytic: B12/folate deficiency?

99
Q

Microcytic or macrocytic: Fe deficiency?

100
Q

Microcytic or macrocytic: EtOH use

101
Q

Microcytic or macrocytic: blood loss

A

normocytic

102
Q

Microcytic or macrocytic: thalassemias

A

Microcytic

103
Q

Microcytic or macrocytic: anemia of chronic disease

A

Microcytic

104
Q

Microcytic or macrocytic: sideroblastic anemia?

A

Microcytic

105
Q

What are the characteristics of iron deficiency anemia in terms of:

  • Reticulocytes
  • ferritin
  • Total Fe
  • TIBC
A
  • Reticulocytes = low
  • ferritin = low
  • Total Fe = low
  • TIBC = high
106
Q

What are the characteristics of thalassemias in terms of:

  • Reticulocytes
  • ferritin
  • Total Fe
  • TIBC
A
  • Reticulocytes =high
  • ferritin = normal/high
  • Total Fe = normal/high
  • TIBC = normal
107
Q

Target cells are usually associated with which anemia type?

A

Target cells

108
Q

Pb poisoning has what characteristic microscopic appearance?

A

Basophilic stippling

109
Q

What are the characteristics of anemia of chronic disease in terms of:

  • Reticulocytes
  • ferritin
  • Total Fe
  • TIBC
A
  • Reticulocytes =low
  • ferritin = low
  • Total Fe = low
  • TIBC = low
110
Q

Hypersegmented PMNs are seen with which anemia(s)?

A

Vit B12 and folate deficiency

111
Q

Which causes neurologic changes: B12 or folate deficiency?

112
Q

What causes acute dactylitis?

A

Painful infarction of bone

113
Q

Which virus causes an acute aplastic crisis with SCC?

A

Parvovirus B19

Hippos (23 decks)

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