Week 8- Chronic Hematology and Endocrinology Interventions

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169 Terms

1

Hemoglobin/hematocrit lab looks for overall

health of RBCs

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2

Reticulocytes lab

young RBCs (looks for bone marrow activity)

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3

Iron lab

essential for hemoglobin and oxygen binding

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4

Transferrin lab

evaluates iron binding capacity, metabolism, and storage

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5

Ferritin lab

evaluates iron storage in the body

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6

Bilirubin lab

assesses rate of RBC breakdown

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7

Folate lab

measures component essential for RBC formation and maturation

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8

4 general anemia management strategies

identify/treat underlying cause, drug therapy, nutritional therapy, and RBC transfusions/or NS

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9

Nutritional therapy for patients with anemia should be focused on a diet high in

vitamin B12, iron, and folic acid

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10

Packed RBC transfusions are indicated when a patients hemoglobin level falls below ____ or they are ____

70, symptomatic

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11

Drugs for anemias include

iron therapy, cyanocobalamin (vitamin B12), and folic acid

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12

Patients on iron supplements should be encouraged to take them ____ and with ___

on an empty stomach, vitamin C/orange juice

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13

Common side affect of iron is

constipation

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14

In order to limit constipation on iron supplements, we can encourage patients to

drink water, increase their movement, and increase fibre intake

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15

Enteric coated iron is

ineffective (iron is absorbed in the deuodenum and small intestine, so enteric coating is pointless)

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16

Vitamin B12 injections are commonly indicated for what time of anemia?

pernicous anemia

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17

Folic acid is essential for

RBC production

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18

Hematopoietic agents help stimulate bone marrow to

make cells or stop making cells

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19

Erythropoiesis-stimulating agents (ESAs) have a high risk of serious

cardiovascular events (MI, stroke, thromboembolism)

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20

ESAs risk for cardiovascular events is increased when patients hemoglobin levels rise > ____ or when there is a rapid rise of hemoglobin >____ over ___ weeks

110 g/L, 10 g/L, 2 weeks

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21

Target hemoglobin for patients on ESAs is

100-110g/L

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22

When patients are receiving lots of blood products (including clotting factor replacements for hemophilia) they are at an increased risk of developing

antibodies

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23

When patients are on desmopressin (synthetic ADH) for hemophilia, it is important that we monitor for signs of

hyponatremia (caused by too much water reabsorption)

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24

First lime therapy for iron deficiency anemia is

oral iron therapy (ferrous sulfate, ferrous gluconate)

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25

IV iron is used for

malabsorption, severe anemia, or CKD (iron sucrose)

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26

Transfusions are used for

severe symptomatic anemia or acute blood loss

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27

Patients who are on iron supplements should avoid taking them with

calcium and antacids (reduce absorption)

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28

Educate patients for GI side effects of iron such as

constipation, nausea, and black stools

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29

IV iron has a risk for ___ and ____

anaphylaxis and hypotension

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30

Sickle cell disease is managed with both preventative and acute treatments to reduce ____, enhance ___, and alleviate ___

complications, quality of life, pain crises

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31

First line treatment for sickle cell disease is

hydroxyurea (myelosuppressive therapy)

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32

The only cure for sickle cell disease is

hematopoietic stem cell transplant (HSCT)

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33

3 main priorities for management of sickle cell crisis

pain control, hydration, and oxygen therapy

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34

Other priorities for sickle cell crisis are

blood transfusions and priapism treatment (if indicated)

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35

Sickle cell crisis moderate-severe pain control

opioids (morphine, hydromorphone)

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36

Sickle cell crisis mild-moderate pain control

NSAIDs (avoid in renal impairment)

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37

Sickle cell crisis pain non-pharmacologic therapies

heat therapy and relaxation tecniques

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38

Sickle cell crisis hydration is important to

increase RBC flexibility and decrease sickling

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39

Sickle cell crisis hydration first step is

IV fluids

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40

If there is a severe sickle cell crisis, it may be indicated to perform a

RBC exchange transfusion (take sickled RBC cells out of body and replace with new packed RBCs)

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41

Blood transfusions for sickle cell crisis are used for _____, _____, and _____

acute chest syndrome, stroke prevention, severe anemia

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42

Treatment for priapism includes

IV fluids, analgesics, vasodilators, and aspiration if severe (if lasting over 4 hrs)

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43

Chronic kidney disease (CKD) leads to reduced

erythropoietin

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44

Decreased levels of erythropoietin in CKD leads to

anemia

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45

Treatment for anemia in CKD is focused on correcting ____ and ____ while minimizing complications such as ___ and ____

low RBC production, iron deficiency, HTN, thrombosis

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46

Erythropoiesis-stimulating agents (ESAs) stimulate the

bone marrow to increase RBC production

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47

ESAs have a slower onset compared to

blood transfusions (2-6 weeks)

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48

If patients with CKD are on ESAs, we must monitor ___, ____, and _____ regularly

BP (risk for hypertension due to too many RBCs), hemoglobin (do not go >110 or >10 from baseline over 2 wks), iron stores

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49

ESAs are only effective if the body has enough

iron stores (monitor iron levels)

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50

Polycythemia vera

myeloproliferative disordwe causing overproduction of RBCs, WBCs, and platelets

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51

Polycythemia vera increases patients risk for

thrombosis (DVT, PE, stroke)

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52

Treatment for polycythemia vera focuses on reducing ___ and preventing ___

RBC overproduction, blood clots

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53

First line therapy for polycythemia vera is

phlebotomy

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54

Phlebotomy

removing blood from the body

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55

Patients who are high risk with polycythemia vera may be put on

myelosuppressive therapy (hydroxyurea)

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56

If patient is resistant to hydroxyurea, patient can be put on

ruxolitinib (JAK2 inhibitor)

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57

Hydroxyurea reduces

RBC production in the bone marrow

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58

Adjuvant therapies for polycythemia vera include

low dose aspirin, encouraging hydration, and frequent mobility to prevent clots

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59

Hemophilia treatment focuses on ____ replacement, ____ prevention, and ______ management

factor, bleeding, emergency

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60

First line therapy for hemophilia is

clotting factor replacement therapy

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61

Adjunctive therapies for hemophilia include

desmopressin and tranexamic acid

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62

Desmopressin is used for hemophilia

A (NOT effective for hemophilia B)

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63

Desmopressin stimulates the release of stored

factor VIII

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64

Tranexamic (antifibrinolytic) acid is used for prevention of

mucosal bleeding (ex. nosebleeds, dental procedures)

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65

Tranexamic acid (antifibrinolytic) prevents the

breakdown of clots

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66

____ and ____ should be avoided in patients with hemophilia due to increased risk of bleeding

NSAIDs, aspirin

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67

Patients with hemophilia should be educated on bleeding

prevention strategies

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68

Hemophilia emergencies include

intracranial hemorrhage, GI bleed, joint bleed (COMMON), retroperitoneal bleeding, and major trauma/surgery

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69

Intracranial hemorrhage signs and symptoms

severe headache, N/V, vision changes, seizures, and altered LOC

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70

GI bleed signs and symptoms

black/tarry stools, hematemesis, abdominal pain, and pallor

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71

Joint bleed signs and symptoms

joint swelling, warmth, stiffness, and severe pain

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72

Retroperitoneal bleeding signs and symptoms

severe back/flank pain, hypotension, and abdominal distention

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73

Major trauma/surgery signs and symptoms

active uncontrolled bleeding, hypotension, and tachycardia

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74

Immediate management for all hemophilia emergencies is

administer factor replacement

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75

Immediate management for joint bleed

give factor replacement, immobilize joint, apply ice, and pain management

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76

Other management for other types of hemophilia emergencies

administer IV fluids (GI bleed/retroperitoneal bleed), rapid response/head CT (intracranial hemorrhage), and monitor for shock

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77

Diabetes insipidus (DI) is caused by deficient ____ or kidney _____

antidiuretic hormone, resistance to ADH

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78

Central DI

lack of ADH production from the hypothalmus/pituitary damage

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79

Nephrogenic DI

kidneys do not respond to ADH

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80

DI common symptoms

severe polyuria, polydipsia, dehydration (hypotension/tachycardia/dry mucous membranes), and dilue urine

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81

Goals of therapy for DI include restoring ____, preventing ____, correcting ____, and reducing ___

fluid balance, dehydration, underlying cause, excessive urination

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82

Central DI treatment

desmopressin

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83

Nephrogenic DI treatment

thiazide diuretics (hydrochlorothiazide) and NSAIDs (indomethacin)

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84

Thiazide diuretics and NSAIDs reduce

urine output by altering kidney response

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85

Patient with DI should adjust

fluid intake to ensure adequate hydration

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86

When giving desmopressin, what is the most important lab to monitor?

sodium

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87

Desmopressin has a high risk for

hyponatremia

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88

Desmopressin is preferred over vasopressin as it has lowered ____ and longer ____

side effects, duration

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89

Other nursing management for DI is

strict I/O monitoring, daily weights, monitor sodium/urine specific gravity/osmolarity, monitor for hypotension/hypertension, monitor for excessive thirst/urination/confusion

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90

Syndrome of inappropriate antidiuretic hormone is caused by excessive

secretion of antidiuretic hormone

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91

SIADH leads to fluid ____, dilutional ___, and low ____

retention, hyponatremia, serum osmolarity

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92

Causes of SIADH

CNS disorders, malignancies, medications, and pulmonary disorders

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93

What medications can cause SIADH?

SSRIs, opioids, antipsychotics, carbamazepine, NSAIDs, and some chemotherapy agents

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94

Symptoms of SIADH include symptoms of

fluid overload (weight gain, low urine output, HTN, tachycardia)

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95

Hyponatremia neurologic symptoms

confusion, seizures, and lethargy

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96

In SIADH, urine concentration will be ____ and blood osmolarity will be _____

high, low

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97

Major discrepancy for SIADH manifestations is that there will be no

peripheral edema (cerebral edema will kill them before signs of peripheral edema)

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98

Goal of therapy for SIADH is correct ____ and promote ____

hyponatremia, free water excretion/prevent dehydration

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99

First line treatment for SIADH is

fluid restriction (<1L/day)

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100

Medications for SIADH include

vasopressin receptor antagonists (tovaptan and conivaptan)

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