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Heme/Onc/Endo > Heme/Onc Exam 1 Cards > Flashcards

Heme/Onc Exam 1 Cards Flashcards

1
Q

Polycythemia

A

Increase in the total amount of Red Blood Cells, amount of Hb and RBC mass in circulation

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1
Q

Anemia

A

Reduction in the total number of red blood cells, Amount of Hb or RBC mass in circulation

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2
Q

Anisocytosis as defined by RDW

A

Variation in RBC size indicated by an RDW > 14.5

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3
Q

Poikilocytosis

A

Variation in RBC shape

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4
Q

Poikilocytosis

A

Variation in RBC shape

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5
Q

Polychromasia

A

Increase in blood reticulocyte count due to their premature release

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6
Q

Hypochromia

A

Central pallor greater than 1/3rd of the RBC

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7
Q

Microcytosis

A

Abnormally small RBCs

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8
Q

Macrocytosis

A

Abnormally large RBCs

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9
Q

Acanthocyte

A

Irregularly Spiculated RBC

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10
Q

Echinocyte

A

RBCs with short regular spicules such as in uremia

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11
Q

Spherocyte

A

RBC without central pallor

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12
Q

Spherocyte

A

RBC without central pallor

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13
Q

Ovalocyte

A

Elliptical RBC

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14
Q

Schistocyte

A

Fragmented bi or tri polar spiculated cell

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15
Q

Sickle cell

A

Bipolar spiculated RBC

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16
Q

Stomatocyte

A

Mouth like deformity

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17
Q

Target cell

A

RBC with concentric circles such as in thalassemia

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18
Q

Tear Drop

A

Unipolar spiculated RBC such as in myelofibrosis

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19
Q

Amount of blood in a healthy male/female

A

12 pints male, 9 pints female

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20
Q

Amount of blood in a healthy male/female

A

12 pints male, 9 pints female

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21
Q

5 Functions of Blood

A

Transport for Oxygen and nutrients
Blood Loss prevention
Immune response to fight infection
Carries waste to Kidney and Liver
Body temperature regulation

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22
Q

Lifespan of a RBC

A

120 days

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23
Q

5 types of WBCs

A

Neutrophil, Lymphocyte, Monocyte, Eosinophil, Basophil

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24
Q

Most abundant White Blood Cell

A

Neutrophill

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25
Q

What stimulates platelet production and where is it released from?

A

Thrombopoietin from the liver and kidney

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26
Q

Where are extra platelets stored

A

In the spleen

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27
Q

Platelet lifespan

A

7-10 days

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28
Q

Fishbone documentation for CBC from top clockwise

A

Hgb, PLT, HCT, WBC

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29
Q

Normal RBC range for Males and Females

A

4-6 x 10^6 for males
3.5-5 x 10^6 for females

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30
Q

Erythrocytosis

A

Increased RBCs

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31
Q

Erythrocytopenia

A

Decreased RBCs

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32
Q

Normal Hgb for males and females

A

14-17.5 for Males
12-16 for females

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33
Q

Equation for calculating hematocrit

A

(RBCxMCV)/10

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34
Q

Normal hct ranges for males and females

A

39-49% for males
35-45% for females

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35
Q

Equation for calculating hematocrit based on hemoglobin

A

Hgbx3

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36
Q

Mean corpuscular volume

A

Reflects the individual size of red blood cells

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37
Q

Normal MCV

A

80-100 fL

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38
Q

Mean corpuscular hemoglobin

A

Weight of hemoglobin per RBC

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39
Q

Normal range for MCH

A

27-33 pg

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40
Q

Low, normal and high MCH

A

Hypochromia, normochromia, Hyperchromia

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41
Q

Calculation for MCH

A

(Hgb/RBC) x 10

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42
Q

Mean corpuscular hemoglobin concentration

A

Average hgb concentration per RBC

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43
Q

Normal MCHC level

A

31-36%

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44
Q

Equation for MCHC

A

Hgb/Hct

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45
Q

Red Cell Distribution Width (RDW)

A

Measures percent of RBCs that fall outside of the normal distribution range

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46
Q

Normal RDW range

A

11.5-14.5

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47
Q

Normal platelet range

A

150-450 x 10^3 mcL

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48
Q

3 variables to adjust for in hematocrit

A

Age, Altitude, Ethnicity

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49
Q

Normal Mean Platelet Volume Range (MPV)

A

7.5-11.5

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50
Q

Relation of MPV and platelet production

A

Young platelets are larger than older platelets so a higher MPV indicates increase in the production of platelets

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51
Q

When can a peripheral blood smear be better than a machine blood count

A

When coagulation of a sample and clumping of platelets leads to false thrombocytopenia

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52
Q

4 Steps in erythropoiesis

A

Low oxygen delivery -> EPO stimulation -> RBC proliferation and maturation -> Reticulocyte release

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53
Q

Role of EPO in RBC maturation

A

Binds to proerythroblasts inducing cell maturation

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54
Q

Roles of folate and B12 in RBC maturation

A

Assist in proliferation of early to late erythroblasts

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55
Q

Role of Iron in RBC maturation

A

Assists in the accumulation of hemoglobin leading to the normoblast and then reticulocyte stages

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56
Q

3 defining characteristics of a reticulocyte

A

Not biconcave, Blue in color, May contain RNA

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57
Q

Lifespan of reticulocytes

A

Total of 4-5 days
3 days in Bone marrow
1-2 days in the blood

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58
Q

Normal reticulocyte count range

A

.5-1.5%

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59
Q

Technical definition of anemia

A

Reduction in one or more of the major RBC measurements Hgb, HCT, or RBC

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60
Q

Kinetic approach to anemia

A

Addresses the mechanism responsible for the fall in hemoglobin concentration

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61
Q

Morphologic approach to anemia

A

Categorizes anemias based on alterations in RBC characteristics and the reticulocyte response

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62
Q

3 mechanistic causes of anemia

A

Decreased RBC production
Increased RBC destruction
Blood Loss

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63
Q

Daily average RBC turnover

A

1% per day

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64
Q

5 common causes of reduced RBC production

A

Lack of nutrients
Bone marrow disorders
Bone marrow suppression
Low levels of trophic hormones
Acute/chronic inflammation

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65
Q

3 Causes of increased RBC destruction

A

Inherited hemolytic anemias
Acquired hemolytic anemias (ie. autoimmune)
Hypersplenism

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66
Q

4 types of blood loss

A

Gross blood loss
Occult blood loss
Iatrogenic blood loss
Underappreciated menstrual blood loss

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67
Q

Anemia is a _____________________ not a ____________________

A

Anemia is a symptom not a disease

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68
Q

How does blood loss compound anemia issues

A

Because blood loss leads to a lack of iron which makes it hard to then form replacement RBCs

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69
Q

Size of reticulocytes compared with normal RBCs

A

Reticulocytes are larger than normal RBCs

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70
Q

4 Causes of Macrocytic anemia

A

Folate or B12 deficiency, Drugs that interfere with nucleic acid synthesis, Abnormal RBC maturation, Alcohol abuse or liver disease

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71
Q

2 Causes of Microcytic anemia

A

Iron deficiency or Thalassemia

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72
Q

3 causes of normocytic anemia

A

CKD, Anemia of inflammation, Mild iatrogenic anemia (ie. too many blood draws

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73
Q

Symptoms of anemia are generally related to what?

A

Decrease in oxygen delivery to the tissues, and hypovolemia secondary to blood loss

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74
Q

Oxygen extraction compensation for anemia

A

Adequate when Hgb is greater than 8-9g/dL percent of O2 extracted from hemoglobin can rise from 25% to 60%

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75
Q

Heart compensation for anemia
How low can it go?

A

Increase in SV and HR adequate until Hgb falls below 5 g/dL

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76
Q

4 Questions to ask when presented with an anemic patient

A

Is the patient bleeding?
Is there evidence of RBC destruction?
Is there bone marrow destruction?
Is there a nutritional deficiency of Iron, Folate, or B12?

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77
Q

DD for new versus life-long anemia

A

New is likely acquired while life-long is more likely genetic

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78
Q

6 associated symptoms of anemia

A

Melena, Hematochezia, Menorrhagia, Renal failure, Rheumatoid arthritis, CHF

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79
Q

4 Skin signs that are relevant to anemia

A

Pallor, Jaundice, Petechiae, Bruising

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80
Q

2 non-blood sources of tarry stools`

A

Pepto Bismol and Iron supplements

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81
Q

4 places to check in an anemia related physical exam

A

Lymph nodes, Abdomen for Hepatosplenomegaly, Bony tenderness, Stool for occult blood

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82
Q

Two things that could make RBC and H&H low

A

Decreased RCM (Red Cell Mass) or Increased Plasma Volume

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83
Q

One thing that could make RBC and H&H elevated

A

Decreased plasma volume

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84
Q

Affect of blood loss on CBC readings - early vs. late stages

A

Does not show initially because equal amount of RBCs and plasma are lost, shows later when fluid is regained and dilutes blood

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85
Q

Problem with reticulocyte count in anemic patient

A

Lack of RBCs may falsely increase percentage of reticulocytes

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86
Q

Reticulocyte index calculation

A

%Reticulocytes x (Pt HCT/Normal HCT)

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87
Q

What does haptoglobin do?

A

Binds free hemoglobin that is released from RBCs

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88
Q

3 Markers of hemolytic anemia

A

Increased serum Lactate dehydrogenase (LDH) Increased unconjugated bilirubin, Decreased serum haptoglobin

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89
Q

Coombs test

A

Test for presence of antibodies of RBCs, a positive test indicates an autoimmune hemolytic anemia

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90
Q

Why is an automatic blood counting mechanism preffered?

A

A larger volume of blood can be sampled

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91
Q

3 Ways the body looses iron

A

Perspiration, Loss of epithelial cells, Menstruation

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92
Q

Distribution of iron in the body

A

65% in hemoglobin, 30% stored in the spleen or bone bone marrow, 4% in myoglobin

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93
Q

Normal serum iron values for Men and Women

A

65-175 mg/dL for men, 50-170 mg/dL for women

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94
Q

Normal percentage of bound transferrin

A

10-50%

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95
Q

Ferroportin, Transferin, Ferritin, Hepcidin functions

A

Ferroportin helps iron LEAVE cells, Transferrin transports Iron AROUND the body, Ferritin STORES iron in the body, Hepcidin BLOCKS ferroportin to decrease iron uptake

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96
Q

What 2 lab values make men or women anemic

A

Hemoglobin less than 12 for females and less than 13.6 for males
Hematocrit less than 36% for females and less than 41% for males

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97
Q

Intravascular hemolytic anemia

A

RBCs lyse within blood vessels

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98
Q

Consequences of intravascular hemolytic anemia (3)

A

Hgb is released into circulation decreasing haptoglobin, Total body iron decreases, Schistocytes form

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99
Q

Extravascular hemolytic anemia

A

RBCs are destroyed within the spleen and liver

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100
Q

Consequences of extravascular hemolytic anemia

A

Iron DOES NOT decrease, Sphereocytes are formed, Haptoglobin may not increase

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101
Q

Cause and epidemiology of Hereditary spherocytosis

A

Genetic defect that is often Autosomal dominant and results in the malformation of RBC proteins. Affects 1 in 5000 northern europeans

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102
Q

Pathology or hereditary spherocytosis

A

RBCs are round rather than biconcave, they become stuck in red pulp of the spleen and get destroyed

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103
Q

Presentation of hereditary spherocytosis

A

Jaundice, enlarged spleen, possible gallstones, RBCs with a lack of central pallor

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104
Q

Lab values for hereditary spherocytosis
H/H
Reticulocytes
MCHC
MCV
Haptoglobin
Peripheral smear
Coombs

A

H/H - Decreased
Reticulocytes - Increased
MCHC - May be elevated
MCV - Normal or Low
Haptoglobin - Normal or mildly decreased
Peripheral smear - Shows sphereocytes
Coombs - Negative

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105
Q

Transfusion recommendations for extravascular hemolytic anemias

A

NOT recommended unless anemia is very severe because it will lead to excessive iron in the body, EPO is a better option

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106
Q

3 Non definitive treatments for Hereditary spherocytosis

A

Folic acid, Transfusion or EPO for SEVERE cases

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107
Q

Definitive treatment for Hereditary Spherocytosis

A

Splenectomy preferably after 5 years of age or puberty in moderate cases
May observe if mild
Ant pneumococcal vaccination

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108
Q

Composition and abundance of the three hemoglobins

A

Hemoglobin A:
2 alphas 2 betas 97-99%
Hemoglobin A2:
2 alphas 2 deltas 1-3%
Hemoglobin F: - Fetal Hemoglobin
2 alphas 2 gammas less than 1%

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109
Q

Location and copies of the alpha globulin gene

A

Chromosome 16, 2 copies for 4 total genes

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110
Q

Location and copies of the beta globulin gene

A

Chromosome 11, 1 copy for 2 total genes

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111
Q

Cause of Alpha Thalassemia

A

Gene deletions result in reduced alpha chain synthesis

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112
Q

Pathology of alpha thalassemia (4)

A

Increase in small, pale RBCs, excess beta chains precipitate, RBC membranes are damaged, hemolysis occurs in the spleen and bone marrow

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113
Q

Common demographic for alpha thalassemia

A

Southeast Asian and Chinese descent, may be seen in mediterranean or African patients

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114
Q

The five degrees of alpha Thalassemia

A

4 working genes = Normal
3 working genes = Minima/Silent carrier, normal levels
2 working genes = Alpha thalassemia minor, HCT 28-40% MCV 60-75
1 working gene = Hemoglobin H disease, hemoglobin H is made of 4 beta chains and is barely useful HCT 22-32% MCV 60-70
0 working genes = Hydrops fetalis, die in utero late second to early third trimester

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115
Q

Alpha thalassemia lab findings
H/H
RBC
MCV
Reticulocytes
MCH
Hemoglobin Electrophoresis
Peripheral Smear

A

H/H - Normal or decreased
RBC - Increased
MCV - Markedly decreased
Reticulocytes - Normal or Increased
MCH - Decreased
Hemoglobin Electrophoresis - Normal in silent carriers and thalassemia minor, HbH bands with HbH disease
Peripheral Smear - Inclusion bodies in HbH disease, hypochromic, microcytic with target cells

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116
Q

Hemoglobin H disease smear presentation (3)

A

Hypochromic microcytic cells, Target cells, Poikilocytosis

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117
Q

Treatment for Alpha thalassemia Minima and Alpha thalassemia Minor

A

Genetic counseling only for Minima
Genetic counseling and possible transfusions or iron chelation in Minor

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118
Q

Treatment for Hemoglobin H disease
Two things to avoid
1 thing to monitor
And two potential treatments

A

Avoid iron and oxidative drugs, Monitor for iron overload and transfuse when necessary. May consider splenectomy in severe conditions

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119
Q

Treatment for hydrops fetalis

A

In utero transfusions are not recommended, Termination of pregnancy often recommended due to maternal morbidity

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120
Q

3 beta chain alleles

A

Beta - Normal production
Beta+ - reduced production
Beta0 - Absent production

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121
Q

Hb electrophoresis of beta thalassemia

A

Increased proportions of HbA2 and HbF

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122
Q

Demographics of beta thalassemia

A

Most common in Mediterranean descent patients may be seen in African or Asian patients as well

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123
Q

Pathology of beta thalassemia (4)

A

Many small pale RBCs (microcytic, hypochromic anemia), hemolysis in marrow spleen and liver, alpha chain inclusion bodies damaged erythroid precursors and surviving RBCs have a shortened lifespan

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124
Q

Intra and extra medullary fates of RBCs in beta thalassemia

A

Intra - Premature death via apoptosis
Extra - Shortened RBC survival

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125
Q

Genotypes for beta thalassemia minor

A

beta/beta+
beta/beta0

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126
Q

Needs of beta thalassemia minor

A

No transfusions needed

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127
Q

Hematocrit of beta thalassemia minor

A

28-40% 80-95% HbA 4-8%HbA2 1-5%HbF

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128
Q

Allele of beta thalassemia intermedia

A

beta+/beta+

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129
Q

Needs of beta thalassemia intermedia

A

Occasional blood transfusion

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130
Q

Hematocrit of beta thalassemia intermedia
Overall, A2, A, F

A

17-33% 0-30%HbA 0-10%HbA2 6-100% HbF

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131
Q

Alleles of severe beta thalassemia (major)

A

Beta0/beta+
beta0/beta0

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132
Q

Hematocrit of beta thalassemia major

A

may be less than 10%

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133
Q

Lab findings for beta thalassemia
H/H
RBC
MCV
Reticulocytes
MCH
Electrophoresis

A

H/H - decreased
RBC - increased
MCV - markedly decreased
Reticulocytes - normal or increased
MCH - decreased
Hemoglobin electrophoresis - Abnormal proportions (less HbA)

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134
Q

What would I observe in a beta thalassemia minor smear?

A

Hypochromic microcytic cells and target cells

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135
Q

What would I observe in a beta thalassemia intermedia smear?

A

Hypochromic microcytic cells and target cells, Poikilocytosis

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136
Q

What would I observe in a beta thalassemia major smear?

A

Hypochromic microcytic cells and target cells, Poikilocytosis, Nucleated RBCs

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137
Q

Facial phenotype of beta thalassemia

A

Chipmunk Facies

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138
Q

Treatment for beta thalassemia minor

A

Mostly just genetic counseling, monitor for iron overload

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139
Q

Treatment for beta thalassemia intermedia

A

Genetic counseling, transfusions or splenectomy may be needed. monitor for iron overload

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140
Q

Treatment of beta thalassemia major (4)

A

Monitor for iron overload and avoid iron supplements
Splenectomy of frequent transfusions
Luspatercept indicated fortransfusion dependant adults
Bone marrow transplant - definitive

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141
Q

MOA for Luspatercept

A

Promotes production of RBCs in beta thalassemia patients by interfering with TGF-beta signaling

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142
Q

Sickle cell and its cause

A

Autosomal recessive inherited disease
Hb-S composed of two alpha chains and 2 beta-s chains

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143
Q

Demographics of sickle cell anemia

A

1 in 400 black children in the US

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144
Q

Pathology of sickle cell disease

A

Polymerized HbS causes sickle shapes which gets stuck in capillaries causing ischemia and pain
Episodes can be triggered by various stressors like acidosis or anxiety

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145
Q

Hematocrit of sickle cell disease

A

20-30%

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146
Q

Lab findings for sickle cell disease
H/H
MCV
Reticulocytes
WBC
Electrophoresis

A

H/H - Normal with trait, low with anemia
MCV - normal
Reticulocytes - increased 10-25%
WBC - Elevated12000-15000
Electrophoresis - HbS band present

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147
Q

Peripheral smear findings for Sickle cell anemia (3)

A

Target cells, Sickled RBCs, Howell Jolly inclusion bodies

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148
Q

5 symptoms of Sickle Cell Anemia

A

Poorly healing ulcers of LE, Sausage fingers and toes, Retinopathy, Splenomegaly, Cardiomegaly

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149
Q

Clinical manifestation of a sickle cell crisis

A

Sudden pain, hand/feet pain less than 18 months, long bone pain children/teens, vertebral pain adults, Fever and tenderness

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150
Q

Items of note in a sickle cell retinal exam

A

hemorrhages, white cotton spots, tortuous veins

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151
Q

Splenic size in sickle cell anemia

A

grows until about 3 years old and then shrivels

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152
Q

Onset of sickle cell anemia

A

about 6 months

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153
Q

3 suggestions for sickle cell treatment

A

Low impact exercise, Medicate ANY fever, avoid stress

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154
Q

Common medication for sickle cell anemia treatment

A

Hydroxyurea - increases HbF levels and suppresses immune system, teratogenic!

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155
Q

Sickle cell alternative to hydroxyurea

A

L-glutamine (pharm grade)

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156
Q

Other potential drug for sickle cell disease

A

Crizanlizumab - reduces interaction of RBCs with the endothelium also used in patients who cannot tolerate hydroxyurea

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157
Q

Definitive treatment for sickle cell anemia

A

Stem cell transplantation

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158
Q

HOP treatment for acute sickle cell crisis

A

Hydration, Oxygenation, Pain control

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159
Q

Splenic sequestration crisis

A

Disproportionate amount of blood sequestered in spleen, HgB drop of 2 g/dL below baseline

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160
Q

Inheritance/MOA of G6PD deficiency

A

X-linked recessive genetic defect resulting in a deficit of the glucose-6-phosphate dehydrogenase enzyme

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161
Q

Demographic for G6PD deficiency

A

Most common in African american males although it can also be seen in patients of Asian and mediterranean descent

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162
Q

Pathology of G6PD deficiency (how it works)

A

Makes RBCs especially vulnerable to oxidative stress causing Hb to denature and form precipitate (Heinz bodies). Cells are destroyed by the spleen or rupture spontaneously

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163
Q

Presentation of G6PD deficiency

A

Usually asymptomatic with episodes of hemolytic anemia, no splenomegaly and potential prolonged jaundice in newborns

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164
Q

3 major triggers for G6PD deficiency

A

Antibiotics (sulfas, quinolones, nitrofurantoin); Aspirin or Phenazopyridine; Food (FAVA BEANS, soy, red wine, blueberries)

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165
Q

Lab findings for G6PD deficiency
H/H
MCV
Reticulocytes
MCH
G6PD Assay

A

H/H - Normal between episodes; low during episodes
MCV - Normal
Reticulocytes - Increased during episodes
MCH - Normal
G6PD Assay - Decreased, may be normal during episodes

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166
Q

Presentation of G6PD patient during an episode - 5 symptoms

A

Malaise, Weakness, Abdominal or Lumbar pain, Jaundice, Dark urine

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167
Q

4 peripheral smear findings for G6PD deficiency

A

Bite cells, Blister cells, Polychromatophils/reticulocytes, Heinz bodies seen when stained

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168
Q

3 Preventative measures and 2 therapeutic measures for G6PD deficiency

A

Preventative:
Avoidance of oxidant drugs
Avoidance of trigger foods
Genetic counseling

Therapeutic measures:
Removal of offending agent
Folic acid supplementation

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169
Q

Presentation of autoimmune hemolytic anemia

A

Abrupt, rapid onset, life threatening anemia - may be confused with drug induced hemolytic anemia

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170
Q

Pathology of autoimmune hemolytic anemia

A

RBCs are tagged for destruction, become spherecytes in the spleen and are stuck. RBCs are also destroyed by Complement and MAC in the liver and intravascular setting

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171
Q

Warm autoimmune hemolytic anemia

A

Autoimmune hemolytic anemia that happens at regular temperatures and is more common

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172
Q

Cold autoimmune hemolytic anemia

A

Autoimmune hemolytic anemia that is activated at colder temperatures, invloves cold agglutinins

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173
Q

Lab findings for Autoimmune hemolytic anemia
H/H
RBC
MCV
Reticulocytes
MCH
Platelets

A

H/H - Decreased (can drop fast)
RBC - Decreased
MCV - normal
Reticulocytes - increased
MCH - normal
Platelets - 10% have thrombocytopenia

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174
Q

Direct and Indirect Coomb’s test method and meaning

A

Direct - Reagent mixed with pt RBCs agglutination means that Ig and complement are on the RBC surface
Indirect - Pt serum is mixed with Type O or donor RBCs and reagent is added. Agglutination means that Ig is in the serum

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175
Q

2 findings on a peripheral smear for autoimmune hemolytic anemia

A

Marked microspherocytosis, Polychromatophils/reticulocytes

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176
Q

3 treatments for autoimmune hemolytic anemia

A

Immunosuppression - Prednisone 1-2 mg/kg/day, possible splenectomy
Treatment of comorbidities (ie. cold avoidance)
Transfusions depending on severity

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177
Q

Cause of hemolytic disease of the newborn or erythroblastis fetalis

A

Maternal IgG antigens attach to the surface of fetal RBCs caused by Placental abruption, maternal transfusion, pre existing maternal antibodies

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178
Q

Demographics for hemolytic disease of the new born

A

Rh- mother with Rh+ fetus, Most commonly ABO antibody issue, Most severe with Rh antibodies

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179
Q

Presentation of infant and mother in cases of hemolytic disease of the newborn

A

Newborn: Jaundice, Anemia, Positive direct coombs test, hepatosplenomegaly, Edema, Heart failure

Mother: Positive indirect coombs test

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180
Q

Before, After, and Preventative Care for Hemolytic disease of the newborn

A

Before:
Intrauterine fetal transfusion
Early induction of labor
Maternal Plasma exchange

After:
Transfusion
Supportive care

Prevantative
RhoGAM prevents Rh+/- immune response

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181
Q

What does RhoGAM do

A

Prevents Rh antibody formation, give it just after birth of Rh+ baby to Rh- mother

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182
Q

Cause of paroxysmal nocturnal hemoglobinuria

A

Acquired genetic defect leads to lysis of RBCs, deficit in complement regulating cell membrane proteins CD55 and CD59

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183
Q

Demographics of paroxysmal nocturnal hemoglobinuria

A

Most common in young adults
Can occur in patients of any age, equal in both genders and no evidence of heritability

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184
Q

Pathology of Paroxysmal Nocturnal Hemoglobinuria

A

RBCs are vulnerable to lysis by complement, MAC formation causes RBC destruction, free hemoglobin depletes nitric oxide

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185
Q

Presentation of Paroxysmal nocturnal hemoglobinuria

A

Episodic, heavier in the AM because of nightly drop in blood pH, venous constriction including ED and esophageal spasms, s/s of thrombosis

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186
Q

Life expectancy for significant Paroxysmal Nocturnal Hemoglobinuria

A

10-15 years

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187
Q

2 diagnostic tests for Paroxysmal nocturnal hemoglobinuria

A

Urine hemosiderin and Flow cytometry

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188
Q

Labs for paroxysmal nocturnal hemoglobinuria

A

everything decreased except for possibly reticulocytes and MCV

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189
Q

Treatments for Paroxysmal Nocturnal Hemoglobinuria

A

Mild - Observation only

Severe or aplastic anemia - Stem cell transplant

Severe hemolysis - Eculizumab

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190
Q

Supportive care for paroxysmal nocturnal hemoglobinuria (3)

A

Transfusion, Iron replacement, COrticosteroids

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191
Q

Acute Blood Loss Anemia

A

From external or internal hemorrhages trauma, GI bleed, etc

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192
Q

Chronic blood loss anemia

A

Anemia due to depletion of iron stores

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193
Q

3 Stages of blood loss anemia

A

Hypovolemia (CBC appears normal), Anemia (Hypovolemia is corrected and CBC is abnormal), Recovery (transient reticulocytosis)

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194
Q

Treatment for blood loss anemia

A

Consider investigative studies to find bleed
Transfusion
Fluid replacement
Supplemental iron

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195
Q

Most common cause of aplastic anemia

A

Idiopathic autoimmune suppresion of hematopoiesis

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196
Q

Diseases the can cause Aplastic Anemia (3)

A

Lupus, Paroxysmal nocturnal hemoglobinuria, transfusion related graft versus host disease

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197
Q

4 toxins that can cause aplastic anemia

A

benzene, toluene, insecticides, mercury

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198
Q

Medications that cause aplastic anemia (3)

A

Chemo, anticonvulsants, Sulfa drugs

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199
Q

Infections that cause Aplastic anemia (4)

A

hepatitis, Epstein barr, cytomegalovirus, Parvovirus B19

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200
Q

2 Other factors that can cause Aplastic anemia

A

radiation exposure, pregnancy

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201
Q

Presentation of aplastic anemia

A

Infections from decreased WBCs
Anemia from decreased RBCs
Bruising, bleeding, purpura/petechiae from decreased platelets

No hepato or splenomegaly

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202
Q

Labs of aplastic anemia
WBC
Platelets
Reticulocytes
MCV
MCH

A

WBC - decreased
Platelets - decreased
Reticulocytes - decreased or absent
MCV - normal or increased
MCH - normal

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203
Q

First line aplastic anemia treatment

A

Remove underlying factors

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204
Q

3 pharmacotherapies for aplastic anemia

A

Multilineage - Eltrombopag - Boosts all three

Erythropoietic - Epoetin, darbepoetin

Myeloid - Filgrastin, sargramostim

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205
Q

2 treatments for severe aplastic anemia

A

Bone marrow transplant or immunosuppression

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206
Q

3 options for immunosuppression in severe aplastic anemia

A

Equine ATG and cyclosporine
Steroids with ATG
Eltrombopag

207
Q

Criteria for severe aplastic anemia (PLT, NEU, RTC)

A

Neutrophils below 500/mcL, Platelets below 20,000/mcL reticulocytes below 60,000/mcL

208
Q

Difference between darbopoietin and epoetin

A

half life of darbepoetin is 3x longer

209
Q

Black box warnings of EPO or DARBY (4)

A

Stroke or thrombosis, Cardiovasular issues in CKD, Tumor progressing, DVT

210
Q

3 things to monitor for EPO or DARBY use

A

Iron status, Hb, BP

211
Q

Sideroblastic anemia description

A

Mixed group of disorders that share abnormalities in heme synthesis and mitochondrial function - ring sideroblasts seen in bone marrow aspirate

212
Q

MOA of sideroblastic anemia

A

Decreased Hb synthesis because of impaired ability to incorporate iron into protoporphyrin IX

213
Q

Most common and two other causes of sideroblastic anemia

A

Most common - X linked

Can also be Autosomal recessive or mitochondrial

214
Q

Ways sideroblastic anemia can be acquired (more common than inherited) (6)

A

General myelodysplastic syndrome
Chronic alcoholism
Lead poisoning
Copper deficiency
Chronic inflammation
Medications (isoniazid, linezolid, chloramphenicol)

215
Q

5 common signs of ANY anemia

A

Fatigue, Tachycardia, Dizziness, Dyspnea on Exertion, Palpitations

216
Q

Unique symptoms of sideroblastic anemia

A

Pallor of conjunctiva and palmar creases. May see s/s associated with myelodysplastic syndrome

217
Q

Sideroblastic anemia labs
H/H
MCV
RDW
Reticulocytes
Total iron binding capacity
Transferrin saturation
Increased Ferritin

A

H/H - Decreased 20-30%
MCV - Often decreased but can be elevated in acquired
RDW - Usually increased
Reticulocytes - Normal or decreased
Total iron binding capacity - Normal or decreased
Transferrin saturation - Increased
Iron - Increased
Increased Ferritin - Increased

218
Q

4 findings of a sideroblastic anemia peripheral smear

A

Basophilic stippling, Poikilocytosis, Anisocytosis, Polychromasia

219
Q

What test must be done to make a sideroblastic anemia diagnosis and what should you see?

A

Erythroid hyperplasia
Ringed sideroblasts with a Prussian blue stain (erythroid cells with iron deposits in the mitochondria

220
Q

Treatment for Sideroblastic anemia (5)

A

Correct underlying cause
Transfusions with severe anemia
Congenital may need B6 or B1 vitamins
Stopping medications
Genetic couseling

221
Q

Most common cause of anemia world wide

A

Iron deficiency anemia

222
Q

Percent of dietary iron that is usually absorbed

A

10%

223
Q

Amount of iron normally lost from the body per day

A

About 1 mg per day

224
Q

Effect of antacids on iron absorption

A

Decrease iron absorption

225
Q

Role of hepcidin in iron absorption

A

Breaks down ferroportin to prevent iron release to the blood stream from GI tract cells

226
Q

5 causes of iron deficiency due to iron loss

A

Deficient diet
Increased requirements (pregnancy, growth spurt)
Chronic blood loss (menstruation GI ulcers)
Decreased absorption
Iron sequestration

227
Q

4 Signs of iron deficiency anemia

A

Classic anemic symptoms
Smooth tongue and Brittle nails, Koilonycha, Cheilosis in severe cases
Pica
Neuro - restless leg syndrome and developmental delay

228
Q

Cheilosis

A

Inflammatory condition seem with anemia that causes scaling at the corners of the mouth

229
Q

Plummer-Vinson syndrome

A

Seen in severe iron deficiency anemia - esophageal webs leading to dysphagia

230
Q

Iron deficiency anemia Labs
H/H
MCV
MCH
Reticulocytes
Total iron binding capacity
Transferrin saturation
Iron
Ferritin

A

H/H - decreased
MCV - Normal early, dereased later
MCH - decreased
Reticulocytes - normal or decreased
Total iron binding capacity - increased
Transferrin saturation - decreased
Iron - decreased
Ferritin - decreased

231
Q

3 stages of iron deficiency

A

Low iron without anemia, normocytic anemia, microcytic anemia

232
Q

5 Peripheral smear findings for iron deficiency anemia

A

Hypochromic microcytic cells
Target cells
Poikilocytosis
Anisocytosis
Increased platelets

233
Q

Oral supplementation for iron deficiency anemia

A

Ferrous sulfate 325 mg orally 3x per day on an empty stomach

234
Q

How long should iron supplement therapy be continued after anemia resolution

A

6 months of longer

235
Q

Effect on iron supplementation of taking with food or ascorbic acid

A

Food decreases absorption
Ascorbic acid increases absorption

236
Q

How fast will hematocrit and reticulocytes rise with iron supplementation?

A

Hct halfway to normal in 3 weeks baseline in 2 months
Reticulocytes rise in 4-7 days peak in 1-1.5 weeks

237
Q

3 contraindications to iron supplementation

A

Allergy, hemochromatosis, hemolytic anemia

238
Q

Side effects of iron supplementation (5)

A

Constipation, N/V, dark stools, GI cramps, gray teeth or urine

239
Q

Cutaneous siderosis

A

Skin staining from IM iron injections

240
Q

4 Newer better parenteral iron treatments

A

Ferric carboxymaltose, ferumoxytol, iron sucrose, sodium ferric gluconate

241
Q

MOA of anemia of infection

A

Proinflammatory cytokines lead to increased hepcidin which leads to decreased iron absorption and availability

242
Q

Presentation of anemia of chronic inflammation

A

75% normocytic 25% microcytic
Decreased Iron
Increased or normal ferritin
Inflammatory process also present

243
Q

Cause of anemia of CKD

A

Failure to secrete adequate EPO by the kidneys

244
Q

Presentation of anemia of CKD

A

Known history of CKD with anemic symptoms
Normocytic, normochromic with normal iron studies

245
Q

3 anemias of hypometabolic states

A

Endocrine anemia - normocytic normochromic anemia caused by decreased EPO secretion d/t endocrine undersecretion

Anemia of chronic liver disease - Cholesterol deposits on RBCs make them look bigger and last less time. More succeptible to hemorrhage

Anemia of starvation - Decreased protein to decreased metabolism to decreased EPO

246
Q

Anemia of the Elderly - 3 causes and one diagnostic tip

A

Anemia caused by resistance to EPO, decrease in EPO secretion, and chronic low level inflammation. Anemic elderly patients with a negative work up for other etiologies

247
Q

When is EPO useful in treating anemia?

A

In situations where EPO secretion is diminished

248
Q

Daily utilization and absorption of B12

A

5mcg per day absorbed, 3-5 mcg per day used

249
Q

Absorption and storage of B12

A

Absorbed in the ilieum and stored in the liver (2-5 mg)

250
Q

5 causes of B12 deficiency

A

Dietary deficiency
Decreased intrinsic factor from pernicious anemia or gastric surgery
Pancreatic insufficiency
Transcobalamin II deficiency
Medications (PPI, Metformin, Colchicine)

251
Q

Blind loop syndrome

A

Overgrowth of bacteria in the bowel compete for B12 use with the body

252
Q

Presentation of B12 deficiency

A

GI - Nausea, anorexia, glossitis, angular cheilitis
Neuropathy

253
Q

Neuropathy progression of B12 deficiency

A

Peripheral parasthesias, then difficulty with balance and proprioception, then cerebral function issues

254
Q

Labs of B12 deficiency
H/H
MCV
MCH
MCHC
Serum B12
Homocysteine
Methylmalonic acid
Reticulocytes
WBC and platelets
LDH and Bilirubin

A

H/H - Decreased
MCV - Elevated
MCH - Elevates
MCHC - Normal
Serum B12 - Decreased (<200 deficiency, 200-300 equivocal)
Homocysteine - increased
Methylmalonic acid - increased
Reticulocytes - normal or decreased
WBC and platelets - normal or decreased
LDH and Bilirubin - increased due to intramedullary destruction by abnormal RBCs

255
Q

4 findings for B12 deficiency on a peripheral smear

A

Hypersegmented neutrophils
Macro-ovalocytes
Bizarre RBC shapes
Basophillic stippling

256
Q

2 labs used to detect pernicious anemia

A

Antiparietal cell antibodies
Gastrin levels

Neither test is highly specific, gastric biopsy also an option

257
Q

Recommended B12 and folic acid therapy for B12 deficiency

A

1 mg of each per day, any route

258
Q

Expected response to B12 deficiency treatment

A

Reticulocytosis in one week, Normal CBC in two months

259
Q

4 side effects of PO B12

A

Headache, Parasthesias, GI upset, Glossitis

260
Q

Maintenance monitoring for chronic B12 supplementation

A

CBC and B12 level every 3-6 months

261
Q

Routine monitoring for B12 supplemetation (5)

A

B12 level, H/H, RBCs, Reticulocytes, iron and folate

262
Q

Daily absorption, utilization and storage of folate

A

Absorbed 125 mcg/day Used 50-100 mcg per day we can store 5-10 mg

263
Q

5 causes of folate deficiency

A

Dietary deficiency, Increased need (pregnancy, hemolytic anemia), Inhibition of reduction to active form (methotrexate), Excess loss (hemodialysis), Decreased absorption

264
Q

Mnemonic to remember metabolic absorption sites

A

Dude is Just feeling Ill bro

Duodenum Iron, Jejunum Folate, Illeum B12

265
Q

Presentation of folate deficiency
4 pertinent positives and 1 pertinent negative

A

Anorexia, nausea, glossitis, angular chelitis

NO NEUROPATHY

266
Q

Folate deficiency labs
H/H
MCV
MCH
MCHC
Serum B12
Homocysteine
Methylmalonic acid
Reticulocytes
WBC and platelets
RBC folate and serum folic acid

A

H/H - decreased
MCV - elevated
MCH - elevated
MCHC - normal
Serum B12 - normal
Homocysteine - increased
Methylmalonic acid - normal
Reticulocytes - normal or decreased
WBC and platelets - normal or decreased
RBC folate and serum folic acid - decreased

267
Q

Difference between RBC folate and serum folic acid

A

RBC folate is long term
Serum folic acid is recent intake

268
Q

2 findings of Peripheral Smear for folate deficiency

A

Hypersegmented neutrophils, Macro ovalocytes

269
Q

Recommended Folate Treatments

A

1-5 mg daily PO for 4 months
Levomethylfolate if the patient cannot metabolize folate to its active form

270
Q

Response to folate deficiency Tx

A

Begin to see reticulocytosis in 1 week
CBC should normalize in 2 months

271
Q

Side effects and monitoring for folic acid treatment

A

Malaise and nausea, monitor Hb

272
Q

Polycythemia Vera

A

Excessive production of hematopoietic cells, especially RBCs

273
Q

Essential thrombocytosis

A

Excessive platelet production

274
Q

Myelofibrosis

A

Excessive production of collagen or fibrous tissue in the marrow

275
Q

Chronic myelogenous leukemia

A

Excessive production of granulocytes

276
Q

Presentation of myeloproliferative disorders (4)

A

Fatigue, Weight loss, Splenomegaly, Easy bruising

277
Q

Why do myeloproliferative disorders cause anemias

A

Abnormal cell growth competes with and suppresses erythroid precursors

278
Q

Lab work up to detect myeloproliferative disorders

A

CBC for anemia and WBC and PLT count
Bone marrow biopsy

279
Q

Treatment for myeloproliferative disorders

A

Myelosuppression or bone marrow transplant for CML or myelofibrosis. Observe if asymptomatic

280
Q

4 phases of hemostasis

A

Platelet plug
Clotting cascade
Termination of cascade
Fibrinolytic clot removal

281
Q

Lifespan of a platelet

A

10 days

282
Q

Fraction of platelets sequestered in the spleen

A

One Third

283
Q

Normal Platelet Count

A

150,000-450,000

284
Q

Contents of Platelet Dense Granules (4)

A

Serotonin, ADP, ATP, Calcium

285
Q

6 Alpha granule contents

A

Platelet derived growth factor, Transforming growth factor, Fibrinogen, VW factor, Platelet factor 4, Factor V

286
Q

What do platelets release to activate other platelets

A

Thromboxane

287
Q

3 functions of Von Willebrand factor

A

Binds to endothelium and promotes platelet adhesion
Plasma carrier for factor VIII
Binds to exposed collagen

288
Q

Source of activation for intrinsic and extrinsic clotting cascades

A

Intrinsic - Found in Blood
Extrinsic - Tissue factor

289
Q

Common joining point of extrinsic and intrinsic clotting cascades

A

Factor X

290
Q

Factors involved in the extrinsic, Intrinsic, and common Pathways

A

Extrinsic - 3 and 7
Intrinsic - 12, 11, 9, 8
Common - 10, 2, 1

291
Q

4 Things cleaved by Thrombin (Factor II)

A

Factors 5 and 8, Fibrinogen, Thrombomodulin

292
Q

Vitamin K dependent factors

A

2,7,9,10, Proteins C and S

293
Q

2 Factors not made in the liver only

A

3 and 5

294
Q

Three things that join to cleave factor 10

A

9a, 8a, and Calcium

295
Q

Action of proteins C and S

A

Inhibit the conversion of prothrombin to thrombin by inhibiting factors V and VII

296
Q

Antithrombin (III)

A

Inactivates factors of the intrinsic pathway, especially 10
Accelerated 1000x with heparin

297
Q

Fibrinolysis Cascade

A

Plasminogen is activated to Plasmin by t-PA which breaks down fibrin

298
Q

What does a D dimer test look for

A

Fibrin degradation products

299
Q

Universal donor for Blood

A

O negative - give in an emergency

300
Q

Transfusion recommendations for hemodynamically stable patients without active bleeding

A

Hgb<6 - recommended
Hgb 6-7 - likely indicated
Hgb 7-8 Consider depending on clinical status
Hgb 8-10 Generally not indicated but should be considered for active bleeding, ischemia, etc.
Hgb >10 Not indicated

301
Q

How much does one unit of PRBCs increase patient hemoglobin

A

about 1g/dL

302
Q

How long do you need to wait after a transfusion to assess patient hemoglobin

A

15 minutes

303
Q

4 most frequent transfusion reactions

A

Fever, chills, pruritis, urticaria (hives)

304
Q

MCC of death in transfusion patients and treatment

A

Circulatory overload - use diuretics

305
Q

Transfusion reaction common in smokers and alcoholics

A

Transfusion related acute lung injury

306
Q

Whole blood

A

Only used in cases of massive hemorrhage - hard to preserve

307
Q

Volume of 1 unit PRBCs

A

200mL

308
Q

3 flavors of Packed Red Blood Cells

A

Leukocyte reduced (performed on most blood products
Irradiated - Avoid graft versus host disease
Washed - gets rid of protein remnants that may cause a reaction

309
Q

Universal plasma donor and universal plasma recipient

A

UD - AB+
UR - O-

310
Q

Fresh Frozen Plasma

A

Used to replace deficient clotting factors, must be used within 24 hours of being thawed or factors 5 and 8 begin to decline

311
Q

Cryoprecipitate

A

Collected by thawing plasma at 4 degrees Celsius and collecting the white precipitate which is rich in VWF, 8, 13, and Fibrinogen

Allows for the same amount of replacement at a lower volume

312
Q

Indication for clotting factor concentrates

A

Specific factor deficiencies such as hemophilia A or B

313
Q

4 indications for platelet transfusion based on platelet counts (4)

A
  1. Platelet count under 10,000 to prevent spontaneous hemorrhage
  2. Platelet count under 50,000 who are actively bleeding, scheduled for an invasive procedure, or have an intrinsic platelet disorder
  3. Count under 100,000 who have a CNS injury, multisystem trauma, or scheduled neurosurgery
  4. Patients with normal levels and ongoing active bleeding or a reason for platelet dysfunction such as aspirin therapy or uremia
314
Q

How much should a unit of platelets increase the platelet count?

A

5,000-10,000

315
Q

4 Hemostasis promoting agents

A

Protamine sulfate
Vitamin K
Desmopressin
Thrombin

316
Q

Protamine sulfate
MOA, Use, Concerns

A

Neutralizes heparin and is used for that purpose during surgery or dialysis procedures. May result in severe hypotensive or anaphylactoid like reactions

317
Q

Vitamin K (Phytonadione)
MOA, Uses, Concerns

A

Reverses Warfarinused to treat vitamin K deficiency hepatic metabolism and renal and fecal excretion

318
Q

Desmopressin MOA, use, and route
3 factors it targets
Test it effects
1 Adverse effect
2 Routes

A

Increases plasma VW factor, factor 8, and t-PA contributing to a lower aPTT and bleeding time, used for hemostasis and may lead to hyponatremia. IV or Intranasal

319
Q

Topical thrombin MOA, use, and contraindications

A

Converts fibrin to fibrinogen and is applied directly at site of bleeding. Used in surgery for minor bleeding. Contraindicated in large vessels or sensitivity to bovine products

320
Q

3 types of antithrombotic drugs

A

Antiplatelet drugs, Anticoagulants, Fibrinolytic agents

321
Q

General MOA, Indication, and Contraindication for anticoagulants

A

MOA varies for each drug
Most commonly for venous thrombosis although can be for any clotting situation
Contraindicated in bleeding, renal problems, allergies

322
Q

4 Parenteral anticoagulants

A

Unfractionated heparin, Low-molecular weight heparin, Bivalirudin, Argatroban

323
Q

MOA of unfractionated heparin and cautions

A

Binds to antithrombin III, no adjustments needed in renal patients, pregnancy category C

324
Q

Monitoring for Unfractionated heparin

A

Use the PTT or factor Xa level for monitoring

325
Q

4 adverse effects of unfractionated heparin

A

Bleeding, Thrombocytopenia, Osteoporosis, Elevated LFTs

326
Q

7 Contraindications of unfractionated heparin

A

HIT, hypersensitivity, Active bleeding, hemophilia, PLT less than 50k, purpura, severe hypertension

327
Q

Heparin Induced THrombocytopenia

A

HIT - affects 3% of those exposed to heparin. Heparin and PF4 form a neoantigen on the PLT surface which induces immune response, splenic platelet clearance and platelet activation. Patients who have had HIT can never have heparin again

328
Q

HIT risk factors and monitoring

A

Patients new to heparin or on long term heparin, watch CBC for a drop in PLT count over 50% as well as necrosis, bruising or lesions at the injection sites

329
Q

4 Ts of HIT scoring and score interpretation

A

Thrombocytopenia, Timing of platelet count fall, Thrombosis or other sequelae, Other causes of thrombocytopenia
4-5 is intermediate

330
Q

3 confirmatory tests for HIT

A

HIPA, Serotonin release assay, Heparin-PF4 Ab ELISA

331
Q

4 substitutes for heparin in the case of HIT

A

Argatroban, danaparoid, fondaparinux, bivalirudin

332
Q

What should we use for long term anticoagulation after HIT and how long should it be used?

A

Warfarin 2-3 months if no thrombosis occured

3-6 months if thrombosis did occur

333
Q

How should HIT be listed in a patients chart

A

As a “heparin allergy”

334
Q

MOA route and half life of Low molecular weight heparin

A

Enhance inhibition of Antithrombin III, SC injection allowing for outpatient and 4 hour half life but not compatible with dialysis

335
Q

3 Indications and 1 contraindication of Low molecular weight heparin

A

Prophylaxis of venous thromboembolism, DVT or PE, Acute coronary syndrome

336
Q

Mechanistic difference between heparin types

A

Unfractionated heparin causes AT III to bind both Xa and THrombin Low molecular weight heparin only binds Xa

337
Q

When is monitoring for LMW Heparin recommended (3 things) and what should one monitor (1 thing)?

A

Pregnancy, CrCl 30 or under, Morbid obesity

Monitor anti Xa levels

338
Q

Adverse effects, Pregnancy category, and contraindications for LMW heparin

A

Bleeding, HIT, and osteoporosis (but less common than with unfractionated)
Pregnancy category C
Contraindicated in active bleeding or HIT hx

339
Q

5 advantages of LMW Heparin over Unfractionated heparin

A

Better bioavailability and longer half life, Dose independent clearance, More predictable anticoagulation response, Lower HIT risk, Lower osteoporosis list

340
Q

When should we “bridge” a patient from Warfarin to Lovenox before or after elective surgery or invasive procedures (4)

A

Embolic stroke within the past 3 months
Previous embolic stroke during interruption of anticoagulation
Mechanical heart valve
Atrial fibrillation in pt with high stroke risk

341
Q

MOA of argatroban (Acova)

A

Directly and selectively binds to the thrombin active site of free and clot associated thrombin
Inhibits fibrin formation, activation of coagulation factors V, VIII, and XIII, activation of protein C and platelet aggregation

342
Q

Metabolism of argatroban

A

Hepatic - caution with liver impairment

343
Q

2 indications, 1 adverse effect, and pregnancy category of Argatroban

A

Ind: HIT and Percutaneous coronary intervention
SE: bleeding
Pregnancy category B

344
Q

MOA and half life of bivalirudin

A

Direct highly sensitive thrombin inhibitor, reversibly binds to thrombin active site and has a 25 min half life

345
Q

Indications and clearance for Bivalirudin

A

Renal clearance

Alternative to heparin in percutaneous coronary intervention especially in those with hx of HIT - Used a lot in Cath labs

346
Q

MOA and monitoring for Warfarin

A

Inhibits vit K and therefore factors II, VII, IX, X. Hepatic metabolism with 36 hour half life and takes 5-7 days for full effect. Monitor PT and INR

347
Q

Pregnancy category for warfarin

A

Pregnancy D for heart valve, X for all others - don’t use
Does not pass into breast milk

348
Q

Indications (3) and Adverse reactions (2) for Warfarin

A

DVT or PE prophylaxis, embolic complications from A fib and cardiac valve replacement - adjust dose according to INR starting w/ 5mg per day

Adverse effects: Bleeding - variable. Necrosis due to paradoxical thrombosis in limbs, breast or penis occurs when started w/o LMW Heparin

349
Q

Effect of ethanol on warfarin

A

Acute binges increase PT/INR

Chronic use decreases PT/INR

350
Q

3 random facts about HIT

A

More common in females

More often involves Venous thrombosis

More common in surgical patients

351
Q

4 direct oral anticoagulants and what they inhibit

A

Dibigatran (Pradaxa) - Thrombin

Rivaroxaban (Xarelto) - Xa

Apixaban (Eliquis) - Xa

Edoxaban (Savaysa) - Xa

352
Q

Indications for dabigatran (3)

A

Stroke prevention in nonvalvular atrial fibrilation, DVT/PE, DVT/PE prophylaxis after hip or knee arthroplasty

353
Q

Contraindications, Adverse events, Antidote, and metabolism of dabigatran

A

ESRD or HD contrindicated, Can lead to bleeding especially GI bleeds, Reversed by Praxbind (idarucizumab), renal metabolism

354
Q

3 drug interactions for dabigatran (KTC)

A

Ketoconazole, Cyclosporine, Tacrolimus

355
Q

3 Indications for Ravaroxaban (Same as dabigatran)

A

Stroke prevention in nonvalvular atrial fibrilation, DVT/PE, DVT/PE prophylaxis after hip or knee arthroplasty

356
Q

Metabolism of Rivaroxaban and 2 contraindications

A

Hepatic CYP 3A4 avoid combination with CYP inhibitors
Contraindicated in ESRD, reduce dose if CrCl less than 50
Contraindicated in active pathologic bleeding

357
Q

Antidote for Rivaroxaban

A

AndexXa (andexanet alpha)

358
Q

MOA of apixaban (Eliquis)

A

Inhibits platelet activation and clot formation via direct selective and reversible inhibition of free and bound active factor X

359
Q

Indications of apixaban (Same as dagatroban and rivaroxaban)

A

Stroke prevention in nonvalvular atrial fibrilation, DVT/PE, DVT/PE prophylaxis after hip or knee arthroplasty

360
Q

Metabolism and Half life of apixaban (Eliquis)

A

Renal and hepatic including CYP3A4, 12 hour half life

361
Q

Adverse event, antidote and Contrindication of apixaban (Eliquis) same as rivaroxaban

A

Bleeding is the most severe adverse event, contraindicated in active pathologic bleeding. AndexXa (andexanet alfa) is the antidote

362
Q

MOA and indications of Edoxaban with renal dosing

A

Factor 10 inhibitor that does not require antithrombin 3 for activity. Used for stroke prevention in nonvalvular atrial fibrilation, DVT/PE Cannot use if CrCl over 95

363
Q

Metabolism of edoxaban (Savaysa) and time to peak plasma conc.

A

Hepatic primarily with CYP 3A4, peak reached in 1-2 hours with a 10-14 hr half life

NO ANTIDOTE

364
Q

Direct oral anticoagulant with the highest bioavailability

A

Rivaroxaban (80%)

365
Q

Lab tests needed with DOACs

A

No lab tests needed - less burden on patients than Warfarin

366
Q

MOA of aspirin

A

Irreversibly binds to COX enzymes and prevents the production of thromboxane A2, take 20-45 minutes to take effect

367
Q

Dose range for aspirin

A

75-325mg daily

368
Q

Indication for aspirin (3)

A

Primary prophylaxis of MI, Secondary prevention in patients with a history of vascular events, other vascular diseases

369
Q

When should aspirin be given in relation to NSAIDS and why?

A

60 minutes prior or 8 hours after

Because NSAIDs and ASA will compete at the COX-1 catalytic site

370
Q

3 adverse events related to aspirin

A

GI bleeding, Dyspepsia, ASA allergy

371
Q

MOA of clopidogrel (Plavix)
Time to take effect

A

Irreversibly inhibits ADP pathway of platelets but requires metabolic activation and takes 3-5 days for full effect

372
Q

2 indications for clopidogrel (Plavix)

A

Primary MI prophylaxis, standard prevention in patients with history of vascular events

373
Q

Adverse events, dosage adjustment, drug interaction and note about clopidogrel(plavix)

A

Bleeding is most serious complication
No hepatic or renal adjustment is necessary
Interacts with Omeprazole or Esomeprazole (effectiveness is decreased)
Genetic mutation may confer Plavix resistance

374
Q

MOA of Prasugrel (effient)

A

The active metabolite actively blocks P2Y12 component of ADP receptors on the platelet

375
Q

Duration of action of Prasugrel (effient)

A

5-9 days; takes effect in 2-4 hours

376
Q

Dose adjustment and contraindications for Prasugrel (Effient)

A

No does adjustment needed for hepatic or renal

Contraindicated in patients with a hx of TIA(Transient Ischemic Attack) or CVA (Cerebrovascular Accident)

377
Q

MOA of ticlodipine (Ticlid)

A

Irreversibly blocks P2Y12 component of ADP recenptors which prevents activation of GPIIb/IIIa receptor complex, thereby reducing platelet aggregation

378
Q

Hepatic/Renal Dose adjustments for ticlodipine (Ticlid)

A

No hepatic or renal dose adjustment

379
Q

4 dangerous potentials adverse effects associated with Ticlodipine (Ticlid)

A

Neutropenia
Agranulocytosis
Thrombotic thrombocytopenic purpura
Aplastic anemia

380
Q

Monitoring of Ticlodipine (Ticlid) and timing of TTP, neutropenia, and aplastic anemia

A

CBC w/ diff every 2 weeks

TPP most common 3-4 weeks
Neutropenia most common at 4-6 weeks
Aplastic anemia most common after 4-8 weeks

381
Q

MOA of ticagrelor (Brilinta)

A

REVERSIBLY and noncompetitively binds the Adenosine phosphate receptor on the platelet surface which prevents ADP mediated activation of the GPIIb/IIIa receptor complex thereby reducing platelet aggregation

NO metabolic activation

382
Q

Duration of Ticagrelor (Brilinta) effect and route

A

About 3 days, PO

383
Q

Contraindication and Black box warning for ticagrelor (Brilinta)

A

Contraindicated with severe liver disease (but no hepatic or renal dosing. Also contraindicated in active bleeding

Reduced effectiveness when taken with ASA over 100mg per day

384
Q

MOA of Kengrelor (Kengreal)

A

REVERSIBLY and noncompetitively binds the Adenosine phosphate receptor on the platelet surface which prevents ADP mediated activation of the GPIIb/IIIa receptor complex thereby reducing platelet aggregation

IMMEDIATE ONSET!!

385
Q

Indication for Cangrelor and route

A

IV only, for patients undergoing percutaneous coronary intervention

Contrindicated for bleeding patients

386
Q

Transition from IV Cangrelor to Oral ticagrelor, clopidogrel or prasugrel

A

for ticagrelor give loading dose immediately after or during infusion

For Clopidogrel and Prasugrel only AFTER the IV infusion is complete

387
Q

3 irreversible P2Y12 inhibitors

A

Ticlodipine, Clopidogrel, Prasugrel

388
Q

2 Reversible P2Y12 inhibitors

A

Ticagrelor, Cangrelor

389
Q

MOA of Epitifibatide (Integrilin) and Abciximab (Reopro)

A

Gp IIB/IIIA inhibitors, block receptors and inhibit platelet aggregation and activation

390
Q

Route of Epitifibatide (Integrilin) and Abciximab (Reopro) as well as peak time and length of duration

A

IV only, can be given with a bolus dose

Peak reached at 30 minutes after administration lasts from 24-48 hours

391
Q

Tow indications for Epitifibatide (Integrilin) and Abciximab (Reopro)

A

Patients undergoing PCI, high risk with stable angina

392
Q

Side effects of Epitifibatide (Integrilin) and Abciximab (Reopro)

A

Bleeding and thrombocytopenia

393
Q

Usage and MOA of fibrinolytics

A

Rapid dissolution of thrombi in life threatening situations - converts plasminogen to plasmin which breaks fibrin into fibrin degradation products

394
Q

Administrative route of fibrinolytics

A

Systemic for acute MI, stroke and massive PE

Peripheral for DVTs and arterial thrombosis can be delivered directly into the thrombus

395
Q

MOA of Alteplase (tPA)

A

Preferentially activates plasminogen that is bound to fibrin - in theory this results in clot dissolution

396
Q

4 indications of Alteplase (tPA)

A

PE with hemodynamic instability, acute STEMI, Severe DVT, asending thombophlebitis

397
Q

How soon does tPA or Alteplase need to be givien for a stroke?

A

Within 3 hours of onset

398
Q

MOA of streptokinase

A

A streptococcal protein; Catalyzes the conversion of inactive plasminogen to active plasmin

399
Q

Administration and indications (4) of streptokinase

A

IV for PE with hemodynamic instability, Acute STEMI, severe DVT and ascending thrombophlebitis
Contraindicated in those with antistreptococcal antibodies

NOT recommended for Ischemic stroke

400
Q

A few meds that can cause thrombocytopenia (4)

A

NSAIDs, Fish oil, anticoagulants/antiplatelets, some herals

401
Q

How might you distinguish a bleeding/bruising disorder from abuse?

A

Abuse will show bruises in various stages of healing

402
Q

4 initial tests to run for a diagnostic evaluation on a bleeding patient

A

CBC, Peripheral blood smear, Coagulation Panel (PT, PTT, INR), CMP (includes LIVER function)

403
Q

2 additional tests that you MIGHT want to run for a bleeding patient

A

Bleeding Time, Platelet aggregation study

404
Q

Bleeding Time Test

A

1-2 Standard incisions made on arm

BP Cuff put on and inflated to 140 mmHg

Measure by blotting blood with filter paper every 30 seconds

Normal 3-8.5 seconds

405
Q

Why might we want a CMP rather than a BMP on a patient with a bleeding disorder?

A

It will tell us about the patient’s LIVER function

406
Q

Platelet function analyzer

A

Puts whole blood through a capillary lined with platelet agonists and measures the time to the occulsion of the membrane

407
Q

Coagulation Panel elements (3)

A

PT/PTT/INR

408
Q

PTT (Partial thromboplastin time)

A

Measures intrinsic pathway by adding factor XIIa used to monitor HEPARIN

409
Q

Normal PTT value

A

21-35 seconds

410
Q

PT (Prothrombin time)

A

Measures extrinsic pathway by adding factor VIIa used to monitor WARFARIN

411
Q

Normal PT value

A

11-13 seconds

412
Q

INR

A

International Normalized Ratio

Ratio of a patients prothrombin time (PT) to a control sample raised to the ISI value of the tissue factor used for the test

413
Q

INR interpretation

A

Normally .8-1.2

2-3 on Warfarin

Higher INR=Higher bleed risk

414
Q

Hemophilia A

A

Congenital deficiency resulting in deficiency of coagulation factor VIII - X linked recessive

415
Q

Hemophilia B

A

Congenital deficiency of coagulation factor IX - X linked recessive

416
Q

Initial presentation of hemophilia

A

Presents in infancy or early childhood with joint and soft tissue bleeding
In patients with more mild hemophilia, patients present with more bellding than usual in SOME circumstances (ie. surgery)

417
Q

Common complication in hemophilia

A

Patients develop inhibitors to the clotting factors that they are missing

418
Q

Lab findings of hemophilia

A

Normal CBC
Normal PT/INR
Prolonged aPTT

419
Q

Severity determination for hemophilia

A

Use factor assays showing activity levels (50-150 % is normal for factor VIII)
Mild 5-40% of normal
Moderate 1-5% of normal
Severe Less than 1% of normal

420
Q

Treatment of hemophilia

A

A - DDAVP (Desmopressin) for mild, Factor VIII concentrate for bleeding episodes or severe condition

B - Factor IX concentrate for all severity levels

Treat for 3-10 days after surgery

421
Q

Treatment for hemophilia related arthritis

A

Celecoxib - a COX2 selective NSAID (do not use aspirin)

422
Q

Prognosis for hemophilia

A

Moat will live full, normal lives with proper treatment - causes of death include hepatitis, transfusion related HIV/AIDS and intercranial bleeding

423
Q

Patient education for hemophilia

A

Avoid contact sports, home infuse if needed and watch for signs of bleeding

424
Q

Role of Von Willebrand factor

A

Tethers platelets to the site of vascular injury

425
Q

Type 1 VWD

A

Autosomal dominant with no to severe bleeding. Quantatative defect

426
Q

Type 2 VWD

A

Usually autosomal dominant but can be recessive. Qualitative defect with moderate to severe bleeding

427
Q

Type 3 VWD

A

Autosomal recessive profound quantitative defect that presents with severe bleeding

428
Q

Clinical Features of vWD

A

Nosebleeds and hematomas
Prolonged bleeding from trivial wounds
GI bleeding is NOT common
Women are five times as likely to have menorrhagia

429
Q

Laboratory findings for vWD

A

Prolonged bleeding time (not specific) may be normal
Mildly prolonged aPTT (depends of severity)
NORMAL PT
Can measure vWF but may need multiple tests to confirm diagnosis

430
Q

2 treatments for vWF

A

DDAVP (Desmopressin) for milder bleeding
vWF or Factor VIII concentrates in more severe situations
Refer to hematology

431
Q

Factor XI deficiency

A

Sometimes referred to as hemophilia C
Autosomal recessive and common among Ashkenazi jews
Treat with Factor XI or FFP if factor is not available

432
Q

Thrombocytopenia

A

Too few platelets results in mucous membrane, gum, and GI bleeds or even cerebral hemorrhage - can result from increased destruction and decreased production

433
Q

Normal Platelet count and risks at:
Less than 100,000
Less than 50,000
Less than 10,000

A

150k-400k per microliter

At less that 100k - increased bleeding/complication during invasive procedures in enclosed spaces
At less than 50k - increased bleeding during invasive procedures and in trauma
At 10k - Risk of spontaneous hemmorhage

434
Q

One way to be sure the spleen is enlarges

A

If you can see or feel it

435
Q

5 potential causes of Destructive/Consumption thrombocytopenia

A

Splenomegaly
Antibody mediated destruction
Drug related destruction
Massive bleeding
Diffuse thrombi

436
Q

Mechanism of Splenomegaly/Hyperspleen

A

Splenic clearance is upregulated - treatment may require a splenectomy

437
Q

Immune thrombocytopenic purpura

A

Form auto-antibodies against antigens on the PLT surface which results in their destruction - Diagnosis of exclusion

438
Q

Presentation of ITP

A

sudden purpuric rash, may also have bleeding (ie. gums) - 3% need blood transfusions

439
Q

Diagnostic criteria for ITP

A

PLT count under 100k with all else normal
No other clinically apparent reason

440
Q

Treatment for ITP (5)

A

Watchful waiting - intervene in the case of life-threatening circumstances. Avoid anticoagulants.

Corticosteroids are first line pharmacotherapy
IVIG, PLT transfusions and Splenectomy may be needed

441
Q

Drug related PLT destruction MOA and Presentation

A

Usually immune mediated. Presents with mucocutaneous bleeding 7-14 days after exposure to a new drug

442
Q

10 drugs that can lead to thrombocytopenia

(KNOW 3)

A

ANTIBIOTICS ESP. KNOWN FOR THIS

Abciximab, Vancomycin, Amiodarone, Cimetidine, Carbamazepine, Ibuprofen, Heparin, Rituximab, Tacrolimus, Immunizations

443
Q

Treatment of Drug-Related PLT destruction

A

Stop problem medication, corticosteroids MAY be needed to reduce antibody titer

444
Q

Bleeding associated platelet consumption

A

Bleeding patient looses platelets faster than they can make them

445
Q

Hyperproliferative Thrombocytopenia - 4 potential causes

A

Leukemia/Aplasia, Metastasis to the bone marrow, Severe viral infections, Radiation of chemotherapy

446
Q

Usual etiology of Qualitative platelet disorders

A

Usually Iatrogenic or acquired - not usually congenital

447
Q

Good tool for picking up a qualitative platelet disorder

A

Peripheral blood smear

448
Q

General presentation of qualitative PLT disorder

A

Bleeding of mucous membrane that can be corrected by transfusion of platelets

449
Q

How soon should a reversible vs. Irreversible platelet drug be stopped before surgery

A

Irreversible needs to be stopped a week before (5-10 days)

Reversible needs to be stopped a couple of days before (1-2 days)

450
Q

2 irreversible and 1 reversible platelet inhibitor

A

Irreversible - Aspirin and Clopidogrel

Reversible - NSAIDs

451
Q

2 thrombotic microangiopathies

A

Thrombocytic thrombotic purpura

Hemolytic uremic syndrome

452
Q

Thrombocytic thrombotic purpura mechanism

A

Rare disease

Idiopathically, large multimers of vWF are formed in the blood stream and the body does not have ADAMTS13 to break them down

453
Q

Clinical presentation of thrombotic thrombocytopenic purpura

A

Acute or subactue symptoms related to neurologic dysfunction, anemia or thrombocytopenia
Fever
Dark urine

454
Q

4 diagnostics for thrombotic thrombocytopenic purpura diagnostics

A

Normal or slight elevation in WBC cunt
Depressed hemoglobin 8-9 g/dL
20k to 50k platelet count
Moderate to sever schistocytosis

455
Q

Four lab results for thrombotic thrombocytopenic purpura

A

D dimer - for clots
High LDH About 1k
High fibrinogen
Negative direct coombs test

456
Q

Therapy for TTP

A

Plasma exchange or transfusion if exchange is not possible - DO NOT GIVE PLATELETS

457
Q

6 possible second line treatments for TTP

A

Corticosteroids, rituximab, IVIG, vincristine, cyclophosphamide, splenectomy

458
Q

Hemolytic Uremic Syndrome pathology

A

Clinical syndrome of progressive renal failure cause by microangiopathic hemolytic anemia and thrombocytopenia - most common cause of acute renal failure in children

459
Q

Clinical features of HUS -5

A

Prodromal gastroenteritis
Lethargy
Seizures
Renal failure
Anuria

460
Q

Common cause of HUS

A

Secondary to E. coli 0157:H7 Shiga like toxin production 70-85 % of patients recover renal function

Can also be familial

461
Q

Labs for HUS (3)

A

Elevated BUN/CR
Thrombocytopenia with schistocytes
Check stool for E. coli and shigella

462
Q

Treatment for typical and atypical HUS

A

Typical - supportive care NO plasma exchange
Atypical - Plasma exchange

463
Q

Disseminated intravascular coagulopathy

A

Many clots form around the body
aPTT and PT are increased
Fibrinogen and PLT are decreased
The body is forming clots faster than it can break them down

464
Q

Etiologies of DIC (Stop Making New Thrombi)

A

Sepsis
Trauma
Obstetric complications
Pancreatitis
Malignancy
Nephrotic syndrome
Transfusion

465
Q

Clinical features of DIC

A

Bleeding at multiple sites including intravenous catheters or incisions. Purpura and petechiae

466
Q

Lab findings for DIC

A

Progressive thrombocytopenia
Pronged aPTT and PT
Low fibrinogen
Elevated D-dimer
Schistocytes due to shearing of RBCs in accluded vessels

467
Q

Goals for DIC patient levels of:
PLT
Fibrinogen
PT and aPTT
Hgb

A

PLT - over 20,000
Fibrinogen - over 80-100 mg/dL
PT and aPTT - under 1.5xNormal
Hgb - over 8 g/dL

468
Q

6 steps in DIC treatments

A

Assess for underlying cause
Establish baseline for PT, aPTT, d-Dimer, fibrinogen
Transfuse blood products but only when needed
Follow PLT, aPTT/PT, fibrinogen every 4-6 hours
Consider using heparin if the patient is bleeding (counterintuitive)
Monitor until resolved

469
Q

4 presentations of arterial thrombosis

A

MI, CVA, Limb ischemia, mesenteric ischemia

470
Q

5 presentations of venous thrombosis

A

DVT and PE

471
Q

Virchow’s triad of thrombosis

A

Stasis, Vessel wall injury, Hypercoagulability

472
Q

Two factors that can lead to vessel wall abnormalities that can lead to thrombosis

A

Infection and inflammation

473
Q

2 most common causes of a DVT

A

Stasis and hypercoagulability

474
Q

Do thrombophillic disorders increase the risk of a venous thrombosis, and arterial thrombosis or both?

A

Venous thrombosis only

475
Q

6 Vitamin K dependent factors

A

2,7,9,10, S, C

476
Q

Prevalence of factor V Leiden

A

5% (1-15% of white people)

477
Q

2 Mechanisms of Factor V Leiden

A

Factor V Leiden is inactivated more slowly by APC
There is a missing cleavage product of factor V that prevents it from stimulating protein C

478
Q

How would the addition of protein C effect the PTT of a person with factor V leiden

A

It would stay the same

479
Q

Treatment for Factor V leiden

A

Heparin for clots, only prophylax in cases of high risk surgery, pregnancy, and additional thrombophillic mutations

480
Q

How can pregnancy cause a DVT

A

Uterine compression of the Left iliac atery

481
Q

Prothrombin gene mutation

A

Causes a 30% higher plasma prothrombin load in heterozygous carriers

482
Q

Protein Clot Stoppers

A

Protein C and S

483
Q

Protein C deficiency inheritance pattern and prevalence

A

Autosomal dominant
1-9% of patients with venous thrombosis
1 in 200k to 300k newborns

484
Q

Homozygous protein C deficiency causes…

A

Purpura fulminans neonatalis (widespread venous thrombosis and skin necrosis)

485
Q

Risk factor for Warfarin induced skin necrosis

A

Protein C deficiency

486
Q

Two factors regulated by protein C

A

Factors VIII and V

487
Q

Inheritance pattern for protein S deficiency

A

Autosomal dominant

488
Q

6 mechanisms of acquired protein S deficiency

A

Pregnancy, Oral contraceptive use, sickle cell anemia, inflammation, nephrotic syndrome, coumadin theraoy

489
Q

4 factors inactivated by antithrombin III

A

IXa, Xa, XIa, XIIa

490
Q

Inheritance of antithrombin III

A

Autosomal dominant

491
Q

Prevalence and common clot sites for ATIII deficiency

A

Risk of thrombosis increases with age, most common sites are deep leg veins and mesenteric veins

492
Q

When is pregnancy related thrombosis most likely to occur?

A

The six weeks following delivery (puerperium)

493
Q

Antiphospholipid syndrome

A

Acquired hypercoagulable condition in which antiphospholipid antibody is found in the blood. Exact mechanism is not understood fully and results from a variety of effects of aPL upon coagulation

494
Q

4 conditions caused by APS with prevalence rang

A

9-14% of patients with pregnancy losses, CVA, MI, DVT

495
Q

2 conditions for which anti-phospholipid syndrome should be considered as a DDx

A

Young strokes, multiple pregnancy losses

496
Q

2 hallmarks of APS

A

Pregnancy losses and thrombotic events

497
Q

Percentage of untreated DVTs that progress to PE

A

50%

498
Q

Two congenital defects that can cause a DVT to relocated to systemic arterial circulation

A

Patent foramen ovale
Atrial septal defect

499
Q

4 symptoms of a DVT

A

Swelling, pain, discoloration, warmth in affected extremity

500
Q

5 symptoms of a pulmonary embolism

A

SOB, Tachypnea, Pleuritic chest pain, cough/hemoptysis, hypotension

501
Q

8 Wells criteria for DVT probability and interpretation

A

Active cancer
Paralysis
Bedridden 3 days within 4 weeks
Localized tenderness
Entire leg swollen
3 cm difference in calf size
Pitting edema
Collateral veins

0 - low probabilit
1-2 Moderate
3+ High

502
Q

Approach of choice for DVT testing

A

Venous doppler ultrasonography

503
Q

What is a D-dimer test best for

A

Ruling OUT rather than ruling IN a DVT

504
Q

4 diagnostic tests for a PE workup

A

Angiography
Ventilation perfusion scan
CT scan with contrast
D-dimer

505
Q

3 objectives in DVT treatment

A

Prevent further clot extension, prevent acute PE, reduce the risk of recurrence

506
Q

Combination treatment for an acute DVT

A

Heparin AND Warfarin PO

507
Q

Monotherapy for acute DVT/PE (4 options)

A

Pradaxa, Xarelto, Eliquis, Savaysa

DOACs

508
Q

Target INR for DVT therapy w/ heparin and warfarin

A

2.5 (2-3 is acceptable)

509
Q

When might you consider thrombolytics for a PE/DVT (3)

A

Unstable patient, Massive iliofemoral thrombosis, low bleed risk

510
Q

When might you use and IVC filter (2 reasons) and what is one?

A

Inferior Vena Cava Filter

Contraindication for anticoagulant therapy/ high PE risk
Recurrent DVT despite anticoagulation therapy

511
Q

4 initial tests and 2 follow up tests when you suspect a clotting disorder

A

Antithrombin, Protein C, Protein S, Factor V Leiden

Prothrombin gene, Antiphospholipid antibodies

512
Q

How to confirm thromboembolic related tests

A

Repeat them in 2-3 months

513
Q

Effect of Warfarin, Heparin and acute illness on thrombophilia workup

A

Warfarin - reduces protein C&S levels
Heparin reduces Antithrombin levels
Acute illness can effect levels of ANY anticoagulant

514
Q

Duration of heparin therapy for DVT/PE

A

5 days or until ideal reange INR is reached

515
Q

4 indicators for long term anticoagulation therapy

A

2 or more spontaneous events for all high-risk patients
1 spontaneous life-threatening thrombosis
1 spontaneous thrombosis at an unusual site (cerebral or mesenteric)
1 Spontaneous thrombosis in association with another clotting abnormality

Heme/Onc/Endo (5 decks)

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