BCP Weeks 1 and 2 Flashcards

1
Q

Hematocrit constitutes what % of whole blood?

A

Hematocrit:

  • 40 - 50% in males
  • 36 - 44% in females
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2
Q

What makes up the “buffy coat?”

A

Leukocytes and platelets (

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3
Q

How much blood does an average person have?

A

~ 5L (7% of body weight)

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4
Q

Where does hematopoiesis take place?

A
  • In the bone marrow

- In lymphoid tissues (tonsils, peyer’s patches, thymus, etc.)

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5
Q

Where does hematopoiesis take place in the fetus?

A
  • first in the yolk sac
  • then the liver and spleen
  • late in development in the bone marrow
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6
Q

What do mature red blood cells lack in addition to nuclei?

A

Mitochondria and other organelles

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7
Q

What is the approximate life span of a red blood cell in circulation?

A

120 days

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8
Q

Where are red blood cells broken down?

A
  • Liver
  • Spleen
  • Macrophages
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9
Q

Type of anemia resulting from a hereditary hemoglobin deficiency:

A

Thalassemia

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10
Q

Universal red cell donor:

A

Type O negative

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11
Q

Universal plasma/platelet donor:

A

Type AB

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12
Q

What is the function of neutrophilic granules?

A

Specialized lysosomes to destroy invaders

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13
Q

How do lymphocytes appear under a microscope?

A

Single, dark nucleus with little cytoplasm

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14
Q

What % of leukocytes are lymphocytes?

A

~ 30% (20 - 40)

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15
Q

True or false: like red blood cells, platelets do not contain mitochondria and other organelles.

A

False. Platelets lack nuclei but contain mitochondria, ribosomes and other organelles

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16
Q

What is the average life span of platelets?

A

5 - 10 days

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17
Q

What is Jak/STAT signaling involved in?

A
  • Leukopoiesis

- Thrombopoiesis

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18
Q

The presence of a Reed-Sterberg cell indicates what type of cancer?

A

Hodgkin’s Lymphoma

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19
Q

What does a Reed-Sterberg cell look like under a microscope?

A

A large, eosin staining, multi-nucleated (owl’s eye nuclei) cell

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20
Q

What microscopic finding is diagnostic of acute myelogenous leukemia?

A

myeloblasts with Auer rods

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21
Q

What type of leukemia is associated with a mutation in the “Philadelphia chromosome?”

A

Chronic myelogenous leukemia

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22
Q

How is bcr-abl produced and what does it do?

A
  • translocation of chromosomes 9 and 22

- leads to constitutively active Abl kinase

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23
Q

Common condition resulting from chemotherapy (among other causes) where bone marrow does not make blood cells:

A

Aplastic anemia

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24
Q

What molecular marker is associated with hematopoietic stem cells (HSCs)?

A

CD34+

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25
Q

True or false: Cytokines trigger WBC formation via Jak/STAT signaling

A

True

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26
Q

CBC vs. CBC with differential:

A
  • CBC: WBCs, RBCs + indices, platelets

- CBC with differential: CBC + amount of each type of WBC

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27
Q

What do elevated basophils suggest?

A

Myeloproliferative disorder

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28
Q

What do elevated neutrophils indicate?

A

Bacterial infection

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29
Q

What do elevated lymphocytes indicate?

A

Viral infection

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30
Q

What do elevated monocytes indicate?

A

chronic infection or inflammation

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31
Q

What does the phrase “left shift” refer to?

A

Increase % of immature neutrophils in the blood. Normal response to infection, generally bacterial.

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32
Q

Which count is a measure of how well the bone marrow is making blood?

A

Reticulocyte count (corrected count = retic x hct/45)

33
Q

How is reticulocyte count used to classify anemias?

A
  • Low = bone marrow production problem
  • Normal = iron/folate/B12 deficiency
  • High = hemolysis or blood loss
34
Q

What is anemia of chronic disease?

A

Anemia characterized by:

  • iron sequestration
  • relative lack of EPO response
  • not due to any other cause
35
Q

3 reasons for a low platelet count:

A
  • low production
  • high clearance
  • sequestration (from a clot)
36
Q

What is the function of alpha granules in platelets?

A

Signal endothelial cells to start clot formation

37
Q

What is the function of dense granules in platelets?

A

Activate other platelets

38
Q

What is a common side effect of drugs that target kinases?

A

Bleeding

39
Q

GP1b dysfunction leads to what disease?

A

Bernard-Soulier Syndrome

40
Q

3 reasons why people get blood clots:

A
  • clotting activates improperly
  • clotting does not self-regulate properly
  • clotting resists breaking down properly
41
Q

2 vitamin K dependent natural antithrombotic factors produced in the liver.

A

Proteins C and S

42
Q

How does factor V Leiden leads to increased thrombosis?

A

Proteins C and S can only cleave factor V at a specific site. With factor V Leiden this site is altered.

43
Q

Antiphospholipid syndrome:

A
  • autoantibodies to phospholipids
  • antibodies: anticardiolipin, anti-beta-2-glycoprotein I, etc.
  • Lupus anticoagulant not a specific antibody, but an effect of the condition on lab assay.
44
Q

What is the “1 in 5” rule:

A

1 in 5 people that have a stroke will test + for antiphospholipid antibodies.

45
Q

Physiologic effects of warfarin (coumadin):

A
  • blocks vitamin K recycling

- decreases factors 10, 9, 7, and 2 (1972)

46
Q

What can you give to treat both von Willebrand’s disease and hemophilia A?

A

DDAVP: promotes the release of vWF, leading to both increased vWF and increased factor VIII.

47
Q

Important facts about TTP (thrombotic thrombocytopenic purpura):

A
  • Characterized by long vWF multimers

- PT and PTT not affected b/c doesn’t activate coag pathway

48
Q

Important facts about DIC (disseminated intravascular coagulation):

A
  • Shattered red blood cells

- activates and depletes coag pathways, so PT and PTT affected

49
Q

True or false: anticoagulants can be used to break down a clot.

A

False

50
Q

Schematic dosing for warfarin:

A

One size fits 1/3. Start everyone on 5 mg qd and adjust to target INR. 1/3 of patients will be good on 5 mg.

51
Q

2 major indications for warfarin therapy:

A
  • prevent embolic stroke in a fib

- treating or preventing a VTE or PE

52
Q

Clopidogrel:

A
  • ADP blocking leads to decreased platelet activation

- Used in combination with aspirin in coronary syndromes and stents

53
Q

Dipyridamole:

A
  • Increases level of cAMP leading to platelet activation

- Used with aspirin for stroke prevention

54
Q

Abciximab, tirofiban, eptifibatide:

A
  • IIa-IIIb blocking leads to decreased platelet-platelet binding
  • Used for acute MI
55
Q

5 Ps of hypercoagulation:

A
  • Pregnancy
  • Prothrombin 20210 mutation
  • Protein C, S deficiency
  • Polycythemia vera
  • Paroxysmal nocturnal hemoglobinuria
  • Smoking
56
Q

HAD of hypercoagulation:

A
  • HIT
  • Hyperhomocysteinemia
  • Antithrombin III deficiency
  • Dysfibrinogenemia
57
Q

CAUSED of hypercoagulation:

A
  • CHF
  • Antiphospholipid syndrome
  • Uremia
  • Surgery
  • Estrogen
  • Diabetes
58
Q

CLOTS of hypercoagulation:

A
  • Cancer
  • Factor V Leiden
  • Obesity
  • Travel, Thalassemia, Thyroid disease
  • Sepsis
59
Q

UFH:

A
  • Potentiates AIII
  • Used for immediate anticoagulant effect
  • Monitor aPTT, heparin levels and platelets
  • IV infusion (usually bolus + drip)
60
Q

LMWH:

A
  • Blocks only Factor Xa
  • Longer half life than UFH
  • SubQ injection
61
Q

Drugs used to break apart existing clots:

A

tPA’s

62
Q

Gold standard test for iron stores:

A

Bone marrow (serum ferritin most direct but not most reliable)

63
Q

Lab tests for B12 deficiency:

A

MMA or homocysteine

64
Q

Lab tests for folate deficiency

A

homocysteine

65
Q

causes of B12 deficiency:

A
  • achlorhydria
  • pernicious anemia
  • surgery
66
Q

3 facts about pernicious anemia:

A
  • Antibodies to parietal cells
  • Lack of intrinsic factor
  • Associated with other autoimmune diseases
67
Q

Uses for cryoprecipitate:

A
  • DIC
  • Hypofibrinogenemia
  • Bleeding from excessive anticoagulation
68
Q

Treatments for leukemia:

A

AML: anthracycline + cytarabine, BMT
ALL: chemo (daunorubicin, vincristine, prednisone, asparaginase)
CML: Leukapheresis + myelosuppression. Tyrosine kinase inhibitors.
CLL: Observe or combination chemo (fludarabine, cyclophosphamide, rituximab or bendamustine with rituximab)

69
Q

SSx of non-Hodgkin lymphoma:

A
  • In bone, trabecular infiltrate of monoclonal lymphoid aggregates
  • Lymph node involvement
  • Fever, weight loss, drenching night sweats
70
Q

Treatment for Burkitt Lymphoma:

A

Intense cyclic chemotherapy + intrathecal chemo

71
Q

SSx of myelofibrosis:

A
  • Extreme fatigue, anemia, splenomegaly
  • BMBx shows fibrosis, atypical megakaryocytic
  • Smear shows leukoerythroblastosis
72
Q

Tx for myelofibrosis:

A
  • Jak2 inhibitor (ruxolotinib)
  • BMT
  • Splenectomy/radiation
73
Q

Prototype for indolent NHL:

A

Follicular Lymphoma

74
Q

Prototype for aggressive NHL:

A

Diffuse Large B cell lymphoma

75
Q

Prototype for highly aggressive NHL:

A

Burkitt’s Lymphoma

76
Q

How is LDH used in the assessment of lymphoma?

A

Correlates with tumor burden, used for risk stratification.

77
Q

Tx for DLBCL:

A

R-CHOP

78
Q

SSx for multiple myeloma:

A

CRAB:

  • hyperCalcemia
  • Renal dysfunction
  • Anemia
  • Bone pain

Also, M protein in serum or urine