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CMT > Heme/Onc Pathophys > Flashcards

Heme/Onc Pathophys Flashcards

1
Q

RBC lifespan

A

120 days

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2
Q

what happens to RBC at end of life?

A

phagocytized in reticuloendothelial system

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3
Q

what does RBC destruction stimulate?

A

erythropoiesis

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4
Q

role of hemoglobin

A

transport vehicle for oxygen

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5
Q

definition of anemia

A

reduction in the volume (hematocrit) of or concentration (hemoglobin) of RBCs when compared to similar values from a reference population

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6
Q

what is hgb

A

expression of amount

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7
Q

what is hct

A

expression of volume

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8
Q

describe the mechanisms of anemia

5 general

A
  1. RBCs destroyed early
  2. ineffective erythropoiesis
  3. insufficient erythropoiesis
  4. blood loss
  5. hemolysis
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9
Q

4 things required for RBC production

A
  1. iron
  2. B12
  3. folic acid
  4. erythropoietin
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10
Q

what is the role of erythropoietin?

A

stimulates RBC production when O2 is low

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11
Q

compensatory response to severe bleeding (acute onset w/ massive volume loss)

A
  • immediate: peripheral vasoconstriction and central vasodilation
  • w/ time: systemic small vessel vasodilation
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12
Q

components of systemic small vessel vasodilation

A
  • increased blood flow to increase tissue oxygenation
  • decreased systemic vascular resistance
  • increase cardiac output, tachycardia, tachypnea
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13
Q

what way will Hgb-O2 dissociation curve shift w/ anemia? why?

A
  • right shift
  • enhances O2 release to tissues
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14
Q

2 other compensatory responses for anemia

A
  1. increase in plasma volume to enhance tissue perfusion
  2. stimulation of EPO production
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15
Q

causes of left shift on hgb-O2 curve

6

A
  1. low temp
  2. high pH
  3. low 2, 3-BPG
  4. fetal Hb
  5. methemoglobinemia
  6. carboxygemoglobinemia
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16
Q

describe the implications of a left shift on hgb-O2 curve

A
  1. increased oxygen affinity (stays w/ hgb)
  2. reduced oxygen delivery to tissues
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17
Q

causes of right shift on hgb-O2 curve

4

A
  1. low pH
  2. increased CO2
  3. high temp
  4. high 2,3-BPG
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18
Q

describe the implications of a right shift on hgb-O2 curve

A
  1. reduced oxygen affinity (leaves hgb easier)
  2. increased oxygen delivery to tissues
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19
Q

causes of decreased RBC production

5 primary causes

A
  1. marrow failure/suppression (decreased raw materials, RBC defects, blood cancers, chemo)
  2. renal failure (decreased EPO)
  3. lack of nutrients (iron, B12, folic acid)
  4. low levels of hormones which stimulate RBC production
  5. chronic disease/inflammation
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20
Q

differentials for anemia due to accelerated loss of RBCs

4 categories

A
  1. inherited hemolytic anemias (sickle cell, thalassemia major)
  2. acquired hemolytic anemias (autoimmuno, TTP/HUS, malaria)
  3. G6PD deficiency
  4. hereditary spherocytosis
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21
Q

screening recs

A
  1. infants at 9-12 mo
  2. pregnant women
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22
Q

key hx components

8

A
  1. hx of medical condition known to result in anemia
  2. onset of anemia
  3. ethnicity/country of origin
  4. mediations/supplements
  5. use of alcohol, aspirin, NSAIDs
  6. hx of blood transfusions
  7. exposure to toxic chemicals
  8. hx of liver disease
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23
Q

key sx of anemia

10

A
  1. DOE, SOB
  2. fatigue
  3. weakness
  4. palpitations
  5. dizziness
  6. poor concentration
  7. HA
  8. angina/a. fib
  9. neuropathy
  10. pica (craving ice)
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24
Q

key signs of anemia

8

A
  1. orthostatic vital signs
  2. jaundice
  3. lymphadenopathy
  4. bony tenderness
  5. petechiae
  6. pallor
  7. tachycardic
  8. melena (FOBT testing)
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25
Q

key labs for anemia

A
  1. CBC (Hgb, Hct, MCV, MCH, RDW)
  2. peripheral blood smear
  3. reticulocyte count
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26
Q

RBC Indices

what does MCV represent

A

cell volume (big vs small)

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27
Q

RBC Indices

what does MCHC represent

A

concentration of Hb in each RBC (pale vs deep red)

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28
Q

RBC Indices

what does MCH represent

A

Hb content in each RBC

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29
Q

which types of anemia are microcytic?

5

A
  1. iron deficiency
  2. thalassemia
  3. chronic disease/inflammation
  4. sideroblastic anemia
  5. lead posioning
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30
Q

which causes of anemia can be normocytic?

5

A
  1. acute blood loss
  2. chronic disease
  3. hypersplenism
  4. bone marrow failure
  5. hemolysis
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31
Q

which causes of anemia can be macrocytic?

5

A
  1. B12 or folic acid deficiency
  2. hemolysis with reticulocytosis
  3. chemotherapy
  4. hypothyroidism
  5. MDS
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32
Q

define reticulocyte count

A

the # of immature RBCS released from bone marrow into peripheral circulation

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33
Q

causes of increased reticulocyte count

3

A
  • hemolytic anemia
  • acute bleeding
  • response to anemia treatment
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34
Q

causes of decreased reticulocyte count

A
  • iron, B-12, folate deficiencies (will be decreased until the nutrient is replaced, then it will be increased)
  • decreased erythropoietin
  • bone marrow failure
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35
Q

additional labs to order

A
  • vitamin levels
  • LDH, bilirubin, haptoglobin
  • coomb’s test
  • hemoglobin electrophoresis
  • serum protein electropheresis (SPEP)
  • creatinine
  • TSH
  • urinalysis
  • stool guaiac
  • bone marrow biopsy
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36
Q

Iron Deficient Anemia Meds

Ferrous Sulfate

MOA, dosing, mode, adverse rxn

A
  • replaces iron, found in hemoglobin, myoglobic
  • dosing: 65mg PO QD
  • available as tablets or solutions
  • adverse rxns (nausea, darker stools, constipation)
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37
Q

Iron Deficient Anemia Meds

Iron Dextran (INFED)

indications, dosing, mode, adverse rxn

A
  • indications: lack of response to PO iron, chronic kidney disease, IBD
  • adverse rxns: anaphylactic rxns, infusion rxns, flushing, pruritis, injection site skin discoloration, arthralgia
  • IV
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38
Q

Iron Deficient Anemia Meds

Ferric Carboxymaltose (Injectafer)

MOA, dosing, mode, adverse rxn

A
  • MOA: non-dextran formulation that allows for iron uptake w/out release of free iron
  • used in pregnancy (2-3rd trimester)
  • dosing: 750mg IV 2x per week (if >50 kg wt); 15mg/kg IV 1x per week (if < 50 kg wt)
  • adverse rxns: hypersensitivity, hypertension, hypophosphatemia, skin discoloration
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39
Q

Iron Deficient Anemia Meds

Sodium Ferric Gluconate Complex

MOA, dosing, mode, adverse rxn

A
  • MOA: supplies a source to elemental iron necessary to the function of hemoglobin, myoglobin, and specific enzyme systems
  • indications: IDA (hemodialysis pts)
  • dosing: 125mg IV every 6 wks
  • adverse rxns: hypersensitivity, HTN, nausea, injection site discoloration, muscle cramps
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40
Q

Anemia of Inflammation/Chronic Disease

inflammation causes

A
  1. dysregulation of iron homeostasis
  2. impaired marrow RBC development
  3. blunted EPO response (CKD)
  4. increased phagocytosis of RBCs
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41
Q

Sickle Cell Anemia

hydroxyurea (hydrea)

indications, dosage, contraindications, side effects

A
  • unk MOA
  • indications: SCA, CML, polycythemia vera, essential thrombocythemia
  • 500mg PO
  • contraindications: pregnancy
  • side effects: myelosuppression, macrocytosis, secondary leukemia, skin cancer, rash, hepatotoxicity, n/v
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42
Q

Hemolytic Anemia

general

A

anemia due to increased destruction of RBCs to the point that destruction exceeds capacity of bone marrow production

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43
Q

Hemolytic Anemia

what does increased cell turnover result in?

3 things

A
  1. increased production response in the bone marrow
  2. increased requirement for erythropoietin
  3. increased cell waste products
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44
Q

Hemolytic Anemia

describe intravascular hemolysis

2 components

A
  • hgb released from lysed RBCs binds to haptoglobin which decreases haptoglobin levels
  • if lysed hgb does not bind, it will leak into the renal tubules (hemoglobinuria)
  • IN blood vessels
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45
Q

Hemolytic Anemia

describe extravascular hemolysis

3 components

A
  • **spleen and liver **macrophages phagocytize RBCs
  • no change in haptoglobin
  • excess hemolysis in speen leads to hypersplenism and then neutropenia/thrombocytopenia
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46
Q

Hemolytic Anemia

which hemolytic anemias are hereditary and intracorpuscular defects?

A
  1. hemoglobinopathies
  2. enzymopathies
  3. membrane-cytoskeletal defects
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47
Q

Hemolytic Anemia

which hemolytic anemias are acquired and intracorpuscular defects?

1

A
  • paroxysmal nocturnal hemoglobinuria
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48
Q

Hemolytic Anemia

which hemolytic anemias are hereditary and extracorpuscular defects?

1

A
  • familial HUS
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49
Q

Hemolytic Anemia

which hemolytic anemias are acquired and extracorpuscular?

5

A
  • mechanical destruction
  • toxic agents
  • drugs
  • infection
  • autoimmune
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50
Q

Hemolytic Anemia

causes of intravascular hemolysis

A
  • direct trauma
  • shear stress
  • heat damage
  • osmotic lysis following infusion of hypotonic solutions
  • lysis from bacterial toxins (clostridial sepsis)
  • G6PD deficiency, TTP, DIC
  • Transfusion rxn
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51
Q

Hemolytic Anemia

intrinsic causes of extravascular hemolysis

4

A
  • membrane defects
  • glycolytic defects
  • oxidation vulnerability
  • hemoglibinopathies
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52
Q

Hemolytic Anemia

extrinsic causes of extravascular hemolysis

A
  • immune (autoimmune/drug tox)
  • microangiopathic (TTP, DIC)
  • infection
  • hypersplenism
  • burns
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53
Q

Hemolytic Anemia

what does coombs positive mean?

A
  • autoimmune, Rh incompatibility
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54
Q

Hemolytic Anemia

what does neg coombs test mean?

A
  • intrinsic RBC disease (sickle cell, thalassemia, hereditary spherocytosis, G6PD deficiency)
  • extrinsic RBC disease (microangiopathic hemolytic anemia, TTP, DIC, prosthetic valve hemolysis, splenic sequestration)
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55
Q

Hemolytic Anemia

differentiate Indirect and direct coombs?

A
  • indirect: seeing if the plasma has the antibodies
  • direct: seeing if the blood has the antibodies (if abx clump together = pos test = they do have abx on RBCs)
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56
Q

Hemolytic Anemia

autoimmune hemolytic anemia acute tx? refractory?

3

A
  • prednisone
  • rituximab
  • immunoglobulin
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57
Q

Hemolytic Anemia

prednisone

MOA, class, dosing, pregnancy

A
  • MOA: decreases inflammation by suppression of leukocytes and decreased capillary permeability; suppresses the immune system
  • Class: corticosteroid
  • Dosing: by weight/disease; given PO
  • Pregnancy: crosses the placenta
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58
Q

Hemolytic Anemia

prednisone adverse reactions

6

A
  • facial erythema
  • flushing/diaphoresis
  • fluid retention
  • HA
  • impaired wound healing
  • increased LFTs
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59
Q

Hemolytic Anemia

any dosing greater than 1 wk requires?

A

tapering

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60
Q

Hemolytic Anemia

Rituximab

MOA, class, indications, dosing

A
  • MOA: eliminates B cells via apoptosis, antibody dependent cytotoxicity and complement mediated cytotoxicity
  • Class: monoclonal antibody
  • Indications: initiate therapy with glucocorticoids w/ no improvement
  • Dosing: 375 mg/m^2 IV weekly for 4 wks
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61
Q

Hemolytic Anemia

Rituximab- Adverse Effects

3

A
  • infusion reaction
  • long term immunosuppression
  • reactivation of Hep B
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62
Q

Hemolytic Anemia

what pre infusion meds should be given for Rituximab

3

A
  • acetaminophen
  • anti-histamines (benadryl)
  • methylprednisolone 100mg IV
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63
Q

Hemolytic Anemia

Immunoglobulin

MOA, dosing, pregnancy, adverse rxns

A
  • MOA: interferes with cell receptors within the reticuloendothelial system; provides passive immunity
  • Dosing: varies, can be subQ or IV
  • pregnancy: crosses placenta
  • Adverse: hypersensitivity rxns
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64
Q

G6PD Deficiency

which are oxidative meds to avoid?

7

A
  • dapsone
  • methylene blue
  • phenazopyridine
  • primathoprim/sulfamethoxazole
  • sulfadiazine
  • pegloticase
  • quinolones
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65
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH)

which meds to treat?

A

eculizumab

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66
Q

Paroxysmal Nocturnal Hemoglobinuria (PNH)

Eculizumab

MOA, Dosing, Adverse effects, pregnancy

A
  • MOA: IgG antibody that binds to complement proteins which blocks formation of membrace attack complex (MAC) to stabilize hemoglobin
  • Dosage: IV infusion Q2 wks for life
  • Adverse Effects: infusion rxn, HTN, HA, skin rash, renal insufficiency, fever, increased susceptibility to meningitis
  • Pregnancy: crosses placenta
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67
Q

Hereditary Hemochromatosis

describe effects of gene mutation on iron and hepcidin

3 components

A
  1. mutation of HFE gene causes dysregulation of hepcidin
  2. increased iron absorption (low hepcidin, high iron), up to 2-4mg daily
  3. increased iron deposition in different organs
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68
Q

Aplastic Anemia

meds to tx

3

A
  1. erythropoietic growth factors
  2. myeloid growth factors
  3. blood product transfusions
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69
Q

Aplastic Anemia

Erythropoietic Stimulating Agents

Med Names, MOA, BBB, Dosing

A
  • Epoetin or darbepoetin
  • MOA: induces erythropoiesis by stimulating progenitor cells; induces release of reticulocytes from the bone marrow into blood to mature to RBCs
  • BBB: increases risk of death, mI, strok, venous thromboembolism, thombosis of vascular access
  • Dosage: wt based; SubQ
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70
Q

Aplastic Anemia

erythropoietic stimulating agents

pregnancy, adverse effects, contraindications

A
  • Pregnancy: does not cross
  • Adverse: HTN, n/v, fever, thrombosis
  • contra: HF patients
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71
Q

Aplastic Anemia

how long until effect of erythropoietic stimulating agents ?

A

reticulocyte counts increase w/in 10 days

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72
Q

Aplastic Anemia

myeloid growth factors AKA

A

granulocyte colony stimulating factor

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73
Q

Aplastic Anemia

which meds are myeloid growth factors?

2

A
  1. filgastrim
  2. sargramostim
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74
Q

Aplastic Anemia

Myeloid Growth Factors

MOA, Dose, Adverse, Pregnancy

A
  • MOA: granulocyte colony stimulating factor activates neutrophils to increase migration and cytotoxicity
  • Dose: varies; IV or SubQ
  • Adverse Rxns: chest pains, splenic rupture, arthralgia, fever
  • Preg: crosses placenta
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75
Q

Aplastic Anemia

Antithymocyte Globulin

Drug Name, MOA, Dosing, Pregnancy, Adverse Rxns

A
  • Equine anti-thymocyte globulin (ATG)
  • MOA: suppresses killer T cells; induces hematologic response in aplastic anemia
  • Dosing: wt based
  • pregnancy: crosses placenta
  • Adverse: many, do test dose first
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76
Q

Aplastic Anemia

Cyclosporine

Drug Class, MOA, Dosing, Preg

A
  • Calcineurin Inhibitor
  • MOA: inhibits production and release of interleukin II
  • Dosing: wt; PO or IV
  • Preg: crosses placenta
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77
Q

Aplastic Anemia

Cyclosporine

adverse, notes

A
  • Adverse: HTN, nephrotoxicity, tremors
  • Notes: monitor cyclosporine levels, avoid grapefruit juice
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78
Q

Myelodysplastic Syndrome (MDS)

meds for MDS?

3 categories

A
  • lenalidomide
  • azacitidine or decitabine
  • growth factors
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79
Q

Myelodysplastic Syndrome (MDS)

Lenalidomide

Class, use w/ , Dose, side effects

A
  • Class: vascular endothelial growth factor (VEGF) inhibitor
  • Use w/ dexamethasone
  • Side effects: neutropenia, thrombocytopenia, venous thrombosis
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80
Q

Myelodysplastic Syndrome (MDS)

Azacitidine

MOA, Dosing, use w/, side effects, goal

A
  • MOA: anti-metabolite which inhibits DNA hypomethylation
  • Dosing: 75 mg/m
  • Use w/ dexamethasone
  • Side Effects: pancytopenia, renal failure, interstitial lung disease, rash
  • goal: improve overall survival, delay conversion to AML
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81
Q

what vaxxes must pts have before splenectomy?

A
  • Pneumococcus
  • H. flu B (HIB)
  • Meningococcal
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82
Q

Leukemia

general- what is leukemia

A

malignancy of the blood

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83
Q

Leukemia

what is the cell of origin for myelogenous leukemias?

A

granulocytes

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84
Q

Leukemia

which cells are granulocytes?

A
  • neutrophils
  • eosinophils
  • basophils
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85
Q

Leukemia

lymphocytic leukemias originate from which cells?

A

lymphocyte lineages

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86
Q

Leukemia

what type of cells dominate acute leukemias

A
  • high proportion of immature, nonfunctional cells
  • ex: blast cells
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87
Q

Leukemia

what type of cells dominate chronic leukemias

A
  • higher proportion of mature cells w/ reduced function
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88
Q

Leukemia

general pathophys of leukemia

2 components

A
  • uncontrolled/dysfunctional multiplication of 1+ types of leukocytes, resulting in undifferentiated, immature, nonfunctional cells in the bone marrow
  • this hyperproliferation reduces the space for other cell lineages which reduces their space
89
Q

Leukemias

which one is seen among children? which is most common form of adult leukemia?

A
  • ALL
  • CLL/SLL
90
Q

Chromic Lymphocytic Leukemia

AKA

A

small lymphocytic lymphoma (SLL)

91
Q

Chromic Lymphocytic Leukemia

which meds for tx?

A
  • Anti-CD20 agent (Rituximab or Obinutuzumab)
    PLUS
  • tyrosine kinase inhibitor (ibrutinib)
    or
  • BCL-2 targeted agent (venetoclax)
92
Q

Chromic Lymphocytic Leukemia

Ibrutinib

MOA, Class, Dosing, Caution, Adverse Effects

A
  • MOA: Inhibits BTK leading to inhibition of malignant B cell proliferation
  • Class: BTK inhibitor
  • Dose: 420mg PO QD
  • Caution: w/ CYP3A inhibitors
  • Adverse: lymphocytosis, HTN, cardiac arrhythmias, rash, infections, bleeding risk w/ Warfarin
93
Q

Chromic Lymphocytic Leukemia

Venetoclax

Class, MOA, Dosing, Adverse

A
  • Class: BCL-2 Inhibitor
  • MOA: inhibits B-cell lymphoma 2 protein leading to restoration of apoptosis
  • Dosing: 400mg PO QD
  • Side Effects: tumor lysis syndrome (may need to be hospitalized for first cycle), neutropenia, infection
94
Q

Chromic Lymphocytic Leukemia

Tumor Lysis Syndrome

risk, cause, complications, sx

A
  • risk in hematologic and rapidly proliferating solid tumor malignancies
  • caused by rapid release of cellular contents
  • w/ impaired breakdown: hyperuricemia (AKI), hyperkalemia, hyperphosphatemia
  • sx: n/v, seizures, arrhythmias, death
95
Q

Chromic Lymphocytic Leukemia

preventive for tumor lysis syndrome

A
  • order baseline uric acid
  • allopurinol to prevent increased uric acid
  • Rasburicase IV (converts uric acid to allatoin)
  • IV hydration
96
Q

Chronic Myeloid Leukemia

which meds?

A

TKI inhibitors (imatinib or nilotinib)

97
Q

Chronic Myeloid Leukemia

side effects of TKIs

5

A
  • drug rashes
  • QT prolongation
  • edema
  • cytopenia
  • diarrhea
98
Q

Chronic Myeloid Leukemia

when can TKIs be discontinued?

A

after prolonged response (> 2 yrs) has been achieved (2 yrs of no BCR-ABL on PCR); near 100% survival at 9 yrs

99
Q

Chronic Myeloid Leukemia

what to do if TKIs fail?

A

allogenic transplant

100
Q

Chronic Myeloid Leukemia

hyperleukocytosis

define, sx

A
  • total leukemia blood cell count > 500,000 to 1 mil
  • sx of decreased tissue perfusion
  • medical emergency!
101
Q

ALL/AML

phases of tx

3

A
  1. inducation (“hard hitting chemo”)
  2. consolidation (less harsh chemo)
  3. maintenance
102
Q

Acute Lymphocytic Leukemia

tx

A

CAR-T therapy

103
Q

Acute Lymphocytic Leukemia

CAR-T therapy

what does CAR-T stand for?, MOA, response rates

A
  • Chimeric antigen receptor T cells
  • MOA: pt’s own T cells are removed and genetically modified to express a receptor programmed to fight against specific cells (for ALL: those that express CD19) and then modified cells are infused back into the patient
  • Response rate: up to 90% but frequent relapses
104
Q

Review Question

where are these absorbed?
* B12
* Iron
* Folate

A
  • Iron: duodenum
  • Folate: jejunum
  • B12: ileum

Dow Jones is Frankly Bad

105
Q

Hemostasis/Coag Cascade

generally what is hemostasis

A
  • innate, stepwise processes within the body that occurs following blood vessel injury
  • leads to clot formation and cessation of bleeding
106
Q

Hemostasis/Coag Cascade

what are two steps of hemostasis

also describe

A
  • Primary: platelet adhesion, activation, and aggregation to the damaged vascular endothelium, forming a plug that stops the bleeding temporarily
  • Secondary: activation of the coagulation cascade resulting in the formation of a stable plug (strong fibrin clot)
107
Q

Hemostasis/Coag Cascade

what three things drive vasoconstriction?

A
  • neural stimulation reflex
  • endothelin
  • thromboxane A2
108
Q

Hemostasis/Coag Cascade

describe neural stimulation reflex

A
  • innate contraction of the vascular smooth muscles upon injury
109
Q

Hemostasis/Coag Cascade

describe endothelin

A

a vasoconstrictor secreted from the damaged endothelial cells

110
Q

Hemostasis/Coag Cascade

describe thromboxane A2

A

a vasoconstrictor released from activated platelets

111
Q

Hemostasis/Coag Cascade

what are the 4 components of primary hemostasis?

A
  1. adhesion
  2. activation
  3. aggregation
  4. secretion
112
Q

Hemostasis/Coag Cascade

what do platelets adhere to?

A

the site of injury w/ exposure to subendothelial components

113
Q

Hemostasis/Coag Cascade

what drives platelet adhesion?

A

when the subendothelial layer is broken, vonWillebrand factor is released and platelets will bind to them

114
Q

Hemostasis/Coag Cascade

describe potent platelet activators

2

A
  • thrombin: produced in coag cascade
  • collagen: interacts w/ platelets at site of injury
115
Q

Hemostasis/Coag Cascade

describe weak platelet activators

A
  • ADP (adenosine diphosphate): acts in an autocrine fashion because it gets released by platelets to activate more platelets
  • Epinephrine
116
Q

Hemostasis/Coag Cascade

describe what happens when platelets are activated

A
  • shape change: elongated to be more adherent
  • activate GpIIb/IIIa receptors
  • release granules (alpha or dense) which release different things to further the coag cascade
117
Q

Hemostasis/Coag Cascade

what do Gp IIb/IIIa receptors start to bind to?

A

fibrinogen

118
Q

Hemostasis/Coag Cascade

describe fibrinogen

A
  • symmetric molecule
  • can bind 2 platelets simultaneously forming bridges between platelets which results in platelet aggregation and formaion of a weak plug
119
Q

Hemostasis/Coag Cascade

functions of the released alpha/dense granules released

5

A
  • recruit and activate additional platelets
  • stimulate expression of GpIIb/IIIa on platelets enhancing aggregation
  • promote vasoconstriction
  • stimulates the process of vascular repair via fibroblast/smooth muscle cell recruitment
  • contribute to initiation of coag cascade
120
Q

Hemostasis/Coag Cascade

what does secondary hemostasis ultimately result in

A

a strong, cross linked fibrin clot

121
Q

Hemostasis/Coag Cascade

describe extrinsic pathway

A
  • primaryily responsible for initiation of cascade
  • activated by tissue factor (III)
  • evaluated by PT
  • factor 3 –> 7 –> 10 (common)
122
Q

Hemostasis/Coag Cascade

describe intrinsic pathway

A
  • primarily involved in amplification of cascade
  • activated by collagen (12)
  • evaluated by aPTT
  • 12 –> 11 –> 9 –> 8 –> 10 (common)
123
Q

Hemostasis/Coag Cascade

describe common pathways

A
  • starts when factor X is activated
  • formation of fibrin clot which occurs at end of common pathway
124
Q

Hemostasis/Coag Cascade

what is the inactive form of coagulation factors

A

zymogens (circulate bloodstream as this)

125
Q

Hemostasis/Coag Cascade

how to write out that an enzyme has been activated?

A

add an a (ex: XIIa)

126
Q

Hemostasis/Coag Cascade

what are majority of factors produced by? which are the exceptions?

A
  • most: the liver
  • Factor 3 & 8 originate from damaged endothelial cells
  • Factor 4: Ca2+ is freely circulating in the bloodstream
127
Q

Hemostasis/Coag Cascade

factors of:
* extrinsic
* intrinsic
* common

A
  • extrinsic: III and VII
  • intrinsic: XII, XI, IX, VIII
  • common: X, V, II, I, and XIII
128
Q

Hemostasis/Coag Cascade

what are many factors dependent on?

A

vitamin K

129
Q

Hemostasis/Coag Cascade

describe role of vitamin k

3 parts

A
  • lipid cofactor that is required for normal blood clotting
  • primarily synthesized in the colon as a byproduct of bacteria
  • activated by epoxidase reductase in the liver
130
Q

Hemostasis/Coag Cascade

which factors are vitamin K dependent?

A

factors II, VII, IX, X (undergo carboxylation to become functional)

131
Q

Hemostasis/Coag Cascade

how soon after birth should babies receive vit K?

A

6 hrs

132
Q

Hemostasis/Coag Cascade

what are 4 things that inhibit coagulation?

A
  • tissue factor pathway inhibitor (TFPI)
  • antithrombin III
  • protein C
  • protein S
133
Q

Hemostasis/Coag Cascade

describe role of tissue factor pathway inhibitor

2

A
  • inhibits activation of factor X
  • located primarily on the surface of microvascular endothelial cells
134
Q

Hemostasis/Coag Cascade

describe role of anti-thrombin III

2

A
  • natural circulating anti-coagulant produced by the liver
  • inhibits activated forms of factors II, IX, and X
135
Q

Hemostasis/Coag Cascade

describe role of protein C

2

A
  • vitamin K dependent factors produced by the liver
  • protein C cleaves and inactivates factors V and VIII
136
Q

Hemostasis/Coag Cascade

describe role of protein S

A
  • vitamin K dependent factors produced by the liver
  • augments the activity of protein C
137
Q

Hemostasis/Coag Cascade

describe the fibrinolytic phase

3

A
  • functions to remove the clot after the vasculature is repaired
  • prevents excessive fibrin deposition
  • accomplished primarily by plasmin
138
Q

Hemostasis/Coag Cascade

describe role of plasmin

2

A
  • cleaves fibrin fibers (fibrinolysis) to form fibrin degradation products
  • cleaves other clottin factors (V, VIII, IX, X)
139
Q

Hemostasis/Coag Cascade

how is plasminogen activated?

A

activates to plasmin by:
* tPA and uPA which are both secreted by endothelial cells

140
Q

Hemostasis/Coag Cascade

generally what is tPA

A

clot buster!

141
Q

Hemostasis/Coag Cascade

who should not get tPA

14

A
  • significant head trauma or stroke w/in last 3 mo
  • sx which suggest SAH
  • arterial puncture at non-compressible site w/in 7d
  • hx of previous intracranial hemorrhage
  • intracranial neoplasms, AVM, or aneurysm
  • seizure w/ postical neuro impairments
  • recent intracranial surgery
  • BP > 185/110
  • active internal bleeding, low platelet counts
  • use of heparin in preceeding 48 hrs & prolonged aPTT
  • INR >1.7
  • use of direct thormbin inhibitors or direct factor Xa
  • hypoglycemia (< 50)
  • non-contrast CT shows multi-lobar infarction
142
Q

Hemostasis/Coag Cascade

what are coagulation studies? (general not test types)

A

studes that reflect the funtion of blood vessels, platelets, and coag factors

143
Q

Hemostasis/Coag Cascade

describe Prothrombin time (PT)

A
  • evaluates extrinsic and common pathways
  • time taken for the plasma to clot when exposed to tissue factor
  • normal range: 11 to 13s
144
Q

Hemostasis/Coag Cascade

why might PT be elevated?

A
  • warfarin therapy
  • vitamin K deficiency
  • deficiency of factors II, V, VII, X
  • liver disease
  • disseminated intravascular coagulation (DIC)
145
Q

Hemostasis/Coag Cascade

what is INR?

A
  • ratio comparing the patient’s PT to reference PT
  • measures function of the extrinsic and common pathways
  • normally: 0.8-1.1
146
Q

Hemostasis/Coag Cascade

describe activated partial thromboplastin time (aPTT)

3

A
  • measures the intrinsic and common pathway
  • time taken for plasma to clot when exposed to negatively charged substance
  • normal: 25-40s
147
Q

Hemostasis/Coag Cascade

when would aPTT be elevated

5

A
  • heparin therapy
  • hemophilia
  • von Willebrand disease
  • liver disease
  • disseminated intravascular coagulation
148
Q

Hemostasis/Coag Cascade

describe bleeding time test

A
  • archaic
  • measures time for bleeding to stop after incision (indirect measure of platelet function)
  • normal range: 2-7 min
149
Q

Hemostasis/Coag Cascade

what might elevate bleeding time?

A
  • thrombocytopenia
  • disseminated intravascular coagulation (DIC)
  • von willebrand disease
  • renal failure
  • NSAID/aspirin use
150
Q

Hemostasis/Coag Cascade

describe fibrinogen testing

A
  • precursor to fibrin
  • levels < 100 mg/dL increase bleeding risk
151
Q

Hemostasis/Coag Cascade

describe use of d-dimer

A
  • d-dimer is a product of fibrin degradation which is released upon cleavage of cross linked fibrin
  • this indicates recent or ongoing coagulation and fibrinolysis
  • normal: < 500
152
Q

Hemostasis/Coag Cascade

what can elevate d-dimer (related to COAG things)

4

A
  • DVT/PE
  • stroke
  • disseminated intravascular coagulation (DIC)
  • COVID-19 infection
153
Q

Myeloproliferative Neoplasms

generally describe

A
  • clonal myeloid conditions in which blood production is deregulated and independent of growth factors
  • caused by acquired genetic defects in myeloid stem cells
  • chronic phase that can advance to an acute leukemia
154
Q

Myeloproliferative Neoplasms

general presentation

3

A
  • unusual thromboses
  • splenomegaly
  • constitutional
155
Q

Polycythemia Vera

tx options for primary

5

A
  1. avoid iron supplements
  2. phlebotomy
  3. ASA 81mg PO QD
  4. Hydroxyurea 500-1500 mg PO QD
  5. Ruxolitinib (PO JAK2 inhibitor, for those who are intolerant to hydroxyurea)
156
Q

Lymphomas

generally describe

A
  • aberrant proliferations of WBC in lymphatic tissue
157
Q

Lymphomas

WHO classifications

3 categories

A
  • Non-Hodgkin Lymphoma: B-cell neoplasms
  • Non-Hodgkin Lymphoma: T and NK cell neoplasms
  • Hodgkin Lymphoma
158
Q

Hodgkin Lymphoma

types (include subtypes)

4 total

A
  • Classical Hodgkin’s: nodular sclerosis, mixed cellularity, lymphocyte rich/depleted
  • Nodular lymphocyte predominant
159
Q

Multiple Myeloma

describe lytic lesions

A
  • bony destruction caused by accumulation of plasma cells
  • plasma cells increase bone absorption which results in bony destruction
  • tx is IVZ bisphosphonates (inhibit osteoclasts)
160
Q

Hemostasis

how to assess for primary hemostasis?

A
  • bleeding time (tests quality and quantity of platelet function)
  • platelet count

(BRUISING)

161
Q

Hemostasis

how to assess for secondary hemostasis

A
  • PT (Prothrombin time; assesses function of extrinsic pathway)
  • aPTT (activated partial thromboplastin time; assesses function of intrinsic pathway)

BLEEDING

162
Q

Platelet Disorders

sx associated w/ platelet disorders

4 components

A
  • easy bruising
  • slow, minor bleeding (bleeding brushing teeth; menorrhagia)
  • epistaxis
  • petechial rash
163
Q

Hemostasis

what are brusing disorders associated with? what are bleeding disorders associated with?

A
  • bruising: platelet problems
  • bleeding: coag problems
164
Q

Platelet Disorders

causes of low platelet counts

A
  • Decreased production in bone marrow
  • Decreased survival (increased destruction)
  • Splenic sequestration
165
Q

Platelet Disorders

describe thrombocytopenia of sequestration

A
  • splenomegaly causes an increase in splenic platelet pool and corresponding decrease in peripheral platelet count
166
Q

ANTICOAGULATION DISORDERS

Warfarin MOA

A
  • inhibits the synthesis of vitamin K dependent clotting factors which are II, VII, IX, X and Proteins C/S
167
Q

ANTICOAGULATION DISORDERS

Warfarin

Contraindications, Dosing, labs

A
  • Contraindications: pregnancy, avoid in liver disease
  • Dosing: begins at 5mg PO QD
  • Monitor PT/INR levels, target 2.0 to 3.0
168
Q

ANTICOAGULATION DISORDERS

what does warfarin inhibit? timing?

A
  • the synthesis of all vitamin K dependent proteins (including C/S)
  • initially decreases protein C fastest
169
Q

ANTICOAGULATION DISORDERS

complication of warfarin in pts w/ protein C/S deficiency

A

warfarin necrosis (blood will coagulate with treatment begins, so we should administer w/ anti-coag)

170
Q

ANTICOAGULATION DISORDERS

what things can interact w/ vitamin K antagonists?

7 categories

A
  • drugs
  • febrile illness
  • gastroenteritis
  • liver disease
  • vitamin K containing foods
  • enteral feeds
  • Foods: mango, avocado, fish oil, soy milk, grapefruit
171
Q

ANTICOAGULATION DISORDERS

how to reverse warfarin?

3 options

A
  • vitamin K 2-5mg PO, SQ, or IV (slow infusion)
  • fresh frozen plasma
  • prothrombin complex concentrates
172
Q

ANTICOAGULATION DISORDERS

infusion/injection anticoagulants

A
  • unfractionated heparin infusion/injection
  • LMWH
  • fondaparinux IM
173
Q

ANTICOAGULATION DISORDERS

Unfractionated Heparin

MOA, dosing, testing, monitor

A
  • binds reversibly to antithrombin to inhibit thrombin + factor Xa
  • Dosing: bolus + continuous infusion
  • Testing: PTT (target range 65-80sec or 1.5-2.5x baseline)
  • Monitoring: Q 4-6 hrs after dose change
174
Q

ANTICOAGULATION DISORDERS

differentiate low and high dose heparin

A
  • low dose: inactivates factor Xa and inhibits conversion of prothrombin to thrombin
  • high dose: inactivates factors IX, X, XI, and XII, and inhibits conversion of fibrinogen to fibrin
175
Q

ANTICOAGULATION DISORDERS

LMWH

MOA, Dosing, monitoring, peak activity

A
  • MOA: binds to and accelerates the activity of antithrombin, but w/ preferential effect on Xa
  • Dosing: 1 mg/kg SC BID or 1/5 mg/kg SC QD
  • Monitoring: none needed
  • Peak: anti-Xa level is 2-6 hrs post dose
176
Q

ANTICOAGULATION DISORDERS

Fondaparinux

MOA, Dosing, monitoring

A
  • MOA: binds & enhances activity of AT by 300-fold (does not bind other plasma proteins) no effect on thrombin
  • Dosing: wt based (7.5 mg SC QD)
  • Monitoring: none needed, but can look at anti-Xa activity
177
Q

ANTICOAGULATION DISORDERS

Argatroban

Class, MOA, onset, indications, dosing, adverse effects, caution in?

A
  • Class: Direct Thrombin Inhibitor
  • MOA: reversibly binds to the active thrombin site of free and clot-associated thrombin. Inhibits fibrin formation and activation of factors V, VIIi, XIII, protein C, and platelet aggregation
  • Onset: immediate
  • Use: HIT, heart cath
  • Dosing: wt based
  • Adverse: hypotension, bleeding, fever
  • Caution: hepatic impairment
178
Q

ANTICOAGULATION DISORDERS

Dabigatran

Class, use, dosing, adverse, caution in?

A
  • Class: Direct Thrombin Inhibitor
  • Use: VTE, afib
  • Dosing: 150mg BID
  • Adverse: hemorrhage, abd pain, dyspepsia
  • Caution In: renal impairment
179
Q

ANTICOAGULATION DISORDERS

DOACs: Factor Xa inhibitors

MOA, monitoring

A
  • inhibits platelet activation and fibrin clot formation via inhibition of free and clot bound factor Xa
  • Compareable efficacy to VKA in adults w/ lower risk of bleeding
  • anti-factor Xa should be ordered to monitor activity
180
Q

ANTICOAGULATION DISORDERS

DOACs- Factor Xa Inhibitors

Pregnancy, Monitoring, Caution in, Adverse

A
  • Pregnancy: insufficient data
  • Monitoring: CBC, aPTT, PT, serum creatinine, LFT
  • Caution: surgeries which raise gastric pH can decrease absorption of edoxaban; not rec for pts with triple positive antiphospholipid syndromes
  • Adverse: increased rates of recurrent thrombotic events compared to VKA therapy; avoid removal of epidural or intrathecal catheter due to risk of spinal/epidural hematoma
181
Q

ANTICOAGULATION DISORDERS

Edoxaban

Use, dosage, caution in, adverse

A
  • Use: DVT, PE, a fib, cancer pts
  • Dosage: wt based
  • Caution: severe hepatic or renal impairment
  • Adverse: hemorrhage
182
Q

ANTICOAGULATION DISORDERS

Apixaban

Target, sse, dosage, Caution, adverse

A
  • Target: factor Xa
  • Use: VTE, a fib, prophylaxis, cancer pts
  • Dose: 10mg BID for 7d then 5mg BID
  • Caution: mod to severe hepatic impairment
  • Adverse: hemorrhage
183
Q

ANTICOAGULATION DISORDERS

Rivaroxaban

Target, use, dosing, caution, adverse

A
  • Target: factor Xa
  • Use: DVT, PE, a fib, CAD, PAD, SVT, cancer pts
  • Dosing: 15mg BID w/ food for 21d then 20mg QD w/ food
  • Caution: severe hepatic or renal impairment; dairy allergy/lactose intolerance (contains lactose)
  • Adverse: hemorrhage, gastroenteritis, vomiting
184
Q

ANTICOAGULATION DISORDERS

when are DOACs fully “out of the system”?

A

5 half lives

185
Q

ANTICOAGULATION DISORDERS

generally describe thrombolytic therapy

A
  • activates plasminogen to form plasmin which accelerates the lysis of thrombi
186
Q

ANTICOAGULATION DISORDERS

Thrombolytic Therapy- tPA

dose, what to use w/?, what to assess for, adverse effects

A
  • Dose: 0.5 to 1mg/hr
  • use w/ DOACs
  • Assess clinically for PE or neuro sx
  • Adverse: bleeding
187
Q

ANTICOAGULATION DISORDERS

contraindications to tPA

8

A
  • active major bleeding or potential for bleeding
  • surgery w/in 10d
  • neurosurgery w/in 60d
  • seizures w/in 2d
  • sepsis
  • elevated serum creatinine
  • uncontrolled HTN
  • contrast allergy
188
Q

ANTICOAGULATION DISORDERS

types of thrombolysis

A
  • tPA (tissue plasminogen activator)
  • Catheter-Directed Thrombolysis
  • Systemic Thrombolysis
189
Q

ANTICOAGULATION DISORDERS

what is hirudotherapy

A
  • medial leaches
190
Q

ANTICOAGULATION DISORDERS

Hemophilia Tx- Desmopressin

MOA, Use, Avoid In, Adverse

A
  • MOA: synthetic analouge of vasopressin
  • Use: DI, hypernatremia, hemophilia A, ICH 2’ to anti-platelet agents, vWD
  • Avoid: mod to severe renal impairment
  • Adverse: hyponatremia, xerostomia, fluid retention
191
Q

ANTICOAGULATION DISORDERS

Hemophilia Tx- Emicizumab

MOA, Use, Adverse, Caution

A
  • MOA: humanized monoclonal modified immunoglobulin G4 antibody w/ specific factor IXa and factor X directed antibody; bridges activated factor Ix and X to restore function of missing factor VIIIa
  • Use: hemophilia A
  • Adverse: injection site rxn, HA, arthralgia
  • Caution: pregnancy
192
Q

Hematopoietic Stem Cell Transplants (HSCT)

what is being transplanted?

A

bone marrow

193
Q

Hematopoietic Stem Cell Transplants (HSCT)

how do SCTs work?

A

pt receives healthy (unaffected) stem cells to replace their own

194
Q

Hematopoietic Stem Cell Transplants (HSCT)

types of transplants?

A
  • Autologous (patient’s own cells)
  • Allogenic (cells from someone else)
195
Q

Hematopoietic Stem Cell Transplants (HSCT)

when to do autologous SCT?

5

A
  • non-Hodgkin lymphoma
  • Hodgkin’s lymphoma
  • AML
  • MM
  • Solid Tumors
196
Q

Hematopoietic Stem Cell Transplants (HSCT)

indications for allogenic SCT?

2

A
  • Malignant Disorders (any)
  • Non-Malignant Disorders (aplastic anemia, thalassemia, sickle cell)
197
Q

Hematopoietic Stem Cell Transplants (HSCT)

HSCT process

5 steps

A
  1. conditioning
  2. stem cell infusion
  3. neutropenic phase
  4. engraftment phase
  5. post-engraftment period
198
Q

Hematopoietic Stem Cell Transplants (HSCT)

describe graft versus host disease (GVHD)

A
  • if donor cells see the host cells as foreign, they attack the host
  • Acute: < 100d post transplant
  • Chronic: > 100d post transplant
199
Q

Blood Transfusions

universal donor? universal recipient?

A
  • donor: O negative
  • recipient: AB pos
200
Q

Blood Transfusions

Rh Factor in blood

A
  • found on surface of RBC
  • negatives can donate to neg and pos; pos can only donate to pos
201
Q

Blood Transfusions

Rh incompatability in Pregnancy

A
  • only occurs when mother is Rh- and baby is Rh +
  • give RhoGAM shots to all Rh- mothers
202
Q

Blood Transfusions

indications of RBC Transfusion

A
  • acute blood loss
  • symptomatic anemia
203
Q

Blood Transfusions

RCB transfusion- what constitutes one unit of blood?

A
  • 300 mL
  • will increase Hgb 1 g/dL
204
Q

Blood Transfusions

which preparations contain RBCs?

A
  1. whole blood
  2. packed RBCs
  3. Autologous RBCs
205
Q

Blood Transfusions

Different Preparations?

A
  1. Washed/Leukoreduced (remove residual plasma, for severe allergic rxns/immunodeficient)
  2. Frozen (rare blood phenotype/multiple antibodies)
  3. Volume reduced
  4. Irradiated (for immunodeficient)
  5. CMV negative (for immunodeficient/neonates)
  6. Autologous (scheduled surgery)
206
Q

Blood Transfusions

screenings for blood transfusion?

A
  • type & screen (don’t need transfusion right now, but anticipate you might)
  • type & cross match (need it now)
  • informed consent
  • maybe: acetaminophen or benadryl
207
Q

Plasma

platelet transfusion recommendations:
* < 10,000
* < 20,000
* < 50,000

A
  • 10: always
  • 20: if minor bleeding, coagulopathy or minor procedure
  • 50: if major bleed or invasive procedure
208
Q

Plasma

describe fresh frozen plasma

A
  • 200-250 mL of plasma which contains all clotting factors, AT-III, and Proteins C/S
  • Indications: correct factor deficiencies, thrombotic microangiopathies (TTP), correct/prevent coagulopathy
209
Q

Plasma

describe cryoprecipitate

A
  • cryoprecipitated antihemophilic factor (AHF) (thaw FFP and precipitate refrozen)
  • 15-20 mL per unit (fibrinogen >150 mg; Factor VIII >80; Factor XIII 50-75; vWF 100-150)
  • Indications: acute DIC, low fibrinogen
  • 1 unit will increase fibrinogen 8 mg/dL
210
Q

Transfusions

complications

5

A
  • volume overload
  • transfusion rxn
  • iron overload
  • infections
  • hyperkalemia
211
Q

Transfusions

describe acute transfusion rxns

A
  • complication that occurs during or after a blood produce transfusion
  • Minor: urticarial transfusion rxn, febrile non-hemolytic transfusion rxn
  • Major: TACO, RALI, AHTR, sepsis, anaphylaxis
212
Q

Transfusions

Describe Urticarial Transfusion Rxn

A
  • common rxn
  • occurs during or within 2 hrs of transfusion
  • commonly due to antigen-antibody interaction between the patient and the product
  • Clinical Features: hives, pruritus
  • Management: mild rxns can continue the transfusion, antihistamines
213
Q

Transfusions

describe febrile non-hemolytic transfusion rxns (FNHTR)

A
  • occurs within 4 hrs of transfusion
  • Type II hypersensitivity rxn where the hsot antibodies target donor leukocytes
  • Prevent: by giving leukoreduced blood produts
  • Manage: hold transfusion for 30min, acetaminophen for fever, CBC + bilirubin
214
Q

Transfusions

Transfusion Associated Circulatory Overload (TACO)

A
  • occurs within 6 hrs of transfusion
  • pt develops pulmonary edema due to volume or circulatory overload
  • At Risk Pts: receive multiple units, hx renal/cardiovasc disease
  • Clinical Features: sudden tachycardia, HTN, overload sx (JVP)
  • CXR: bilateral infiltrates
  • Management: stop transfusion
  • Diuresis (furosemide)
  • supplement oxygen
215
Q

Transfusions

Transfusion-related acute lung injury (TRALI)

A
  • occurs w/in 6 hrs of transfusion
  • Acute lung injury occurs due to HLA antibodies in donor blood triggering the neutrophils and pulmonary endothelial cells of recipient
  • Sx: fever, chills, resp distress, hypotension
  • CXR: bilat infiltrates
  • Management: stop transfusion, maintain oxygenation, IV steroids
  • NO DIURETICS
216
Q

Transfusions

Acute hemolytic transfusion reaction (AHTR)

A
  • EMERGENCY
  • occurs within 1 hr of transfusion
  • acute intravascular hemolysis of transfused RBCs usually due to wrong blood type
  • sx: high grade fever, flank pain, hematuria, tachycardia/pnea, hypotension, oozing from IV site (DIC), HA, anxiety, cardiovascular collapse
  • Management: stop transfusion; aggressive IV hydration; confirm tranfusion details; retype/match; coombs test (POSITIVE); coag studies
217
Q

Transfusions

Transfusion-associated sepsis

A
  • rare rxn, occurs w/in 1 hr of transfusion
  • bacterial infection from a transfusion product that is contaminated
  • Sx: fever, chills, hypotension
  • Management: stop infusion, culture recipient’s & donor’s blood, broad spectrum abx
218
Q

Transfusions

Anaphylactic transfusion reaction

A
  • occurs within 4 hrs of transfusion
  • Sx: angioedema, wheezing, resp distress, hypotension, nausea/vomiting, cardiac arrest/shock
  • Management: stop transfusion, hemodynamic stabilization (IV fluids, vasopressors), airway management, epinephrine/steroids/antihistamines

CMT (78 decks)

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