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PANCE review > Hematology > Flashcards

Hematology Flashcards

1
Q

Three basic pathophysiological causes of anemia

A
  1. Decreased RBC production - bone marrow, renal failure, low B12 or folate
  2. RBC loss - hemorrhage, hemolysis
  3. Production of defective RBCs
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2
Q

Clinical definition of anemia

A

Hemoglobin less than 12 in women and 13 in men

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3
Q

Symptoms of anemia

A

fatigue, dizziness, tachycardia, pallor, orthostatic HTN, exertional dyspnea

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4
Q

What are reticulocytes?

A

immature RBCs

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5
Q

What is MVC measure?

A

volume of average RBC in sample

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6
Q

MCV of microcytic and macrocytic anemia?

A 
Microcytosis = MCV less than 80 (small cells)
Macrocytosis = MCV +100 (big cells)
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7
Q

How to determine blood cell morphology?

A

peripheral blood smear

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8
Q

What measures are included in CBC?

A

WBC, RBC, hematocrit, platelet count, retic count, MCV, RDW, MCHC

basophil, eosinophil, lymphocyte, monocyte, neutrophil %s

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9
Q

What is the significance of low reticulocyte count?

A

means poor RBC production

seen in all microcytic anemias

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10
Q

Most common cause of microcytic anemia

A

iron deficiency

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11
Q

Causes of iron deficiency

A 
GI bleeds (think NSAIDs)
Decreased iron intake
Decreased iron absorption
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12
Q

Signs of iron deficiency anemia

A 
fatigue
mouth ulcers
palpitations
pallor
brittle nails
angular cheilitis
dysphagia
pica
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13
Q

What is ferritin and transferrin?

A

Ferritin = iron stores

Transferrin = transport protein for iron or iron binding capacity

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14
Q

What lab is diagnostic of iron deficiency anemia?

A

plasma ferritin < 10 in women and < 30 in men

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15
Q

Treatment of iron deficiency anemia

A

ferrous sulfate 325 TID x 6 months

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16
Q

Side effects of iron supplementation

A

lots of GI issues

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17
Q

Epidemiology of alpha and beta thalassemia

A

alpha - Southeast Asia, Middle East, African

beta - Mediterranean

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18
Q

minor vs major thalassemia

A

Minor = gene inherited from one parent; few or no symptoms

Major = gene inherited from both parents
- Alpha major = Bart’s Hgb
Still born or death soon after birth (hydrops fetalis typical outcome)
- Beta major = Cooley’s anemia
Born without a problem, but develop severe anemia over the first year and typically don’t survive past 30 yo

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19
Q

Symptoms of thalassemia

A

bone issues, splenomegaly, jaundice, severe anemia, osteopenia, fatigue

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20
Q

How to definitively dx thalassemia

A

HgB electrophoresis

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21
Q

Treatment of thalassemia

A

Folic acid

Serial blood transfusions but watch for iron overload

Genetic counseling

Splenectomy

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22
Q

Basophilic stippling on peripheral blood smear seen in what 3 hematologic diseases?

A

beta thalassemia

lead poisoning and sideroblastic anemia

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23
Q

Diagnostic test of choice for sideroblastic anemia

A

Prussian blue staining of bone marrow - shows ringed sideroblasts

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24
Q

How can sideroblastic anemia be acquired?

A

alcoholism
lead poisoning
myelodysplasia

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25
Q

Heinz bodies seen in what anemia?

A

alpha thalassemia

G6PD deficiency anemia

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26
Q

What are Howell-Jolly bodies? in what diseases?

A

DNA remnants seen with macrocytic anemia or damaged spleen

B12 or folate deficiency anemia, sickle cell anemia, celiac disease

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27
Q

Hemolysis of macrocytic anemia can progress to ______ dysfuction.

A

spleen

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28
Q

Microcytic anemias

A

iron deficiency
thalassemia
lead poisoning

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29
Q

Macrocytic anemias

A

folic acid deficiency
B12 deficiency
Sickle cell
G6PD deficiency

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30
Q

hypersegmentation of PMN nuclei on peripheral blood smear =

A

folic acid or B12 deficiency

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31
Q

stocking glove paresthesias =

A

B12 deficiency or diabetic neuropathy

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32
Q

bite cells =

A

G6PD deficiency

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33
Q

Clinical presentation of folic acid deficiency

A

sore/swollen tongue
GI issues - diarrhea
mouth and peptic ulcers

anemia sx’s

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34
Q

Pathophysiology of pernicious anemia

A

inability of GI tract to absorb B12 due to missing transport protein called intrinsic factor

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35
Q

Causes of B12 deficiency

A
  • Pernicious anemia (#1 cause)
  • Vegan diet
  • Bowel surgery
  • Crohn’s disease
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36
Q

B12 absorbed where in body?

A

terminal ileum

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37
Q

Clinical presentation of B12 deficiency

A

neuro sx’s: stocking glove paresthesias, ataxia, dementia, depression

anemia sx’s

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38
Q

How is B12 deficiency differentiated from folic acid deficiency?

A

Neurologic sx’s
Low LDH
Low indirect bilirubin

  • Low serum B12 is NOT diagnostic
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39
Q

Schilling test

A

Determines cause of B12 deficiency; pernicious anemia or terminal ileum disease (bacteria Crohns, sprue)

  1. IM B12 injection to saturate B12 receptors in ileum
  2. Patient given oral radioactive B12

Normal = B12 in urine; B12 binds to intrinsic factor and absorbed into bloodstream

Pernicious anemia = B12 in urine only if patient also given intrinsic factor

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40
Q

B12 deficiency treatment

A

Treat underlying cause if possible

Intramuscular B12

High dose of oral B12 will allow some to pass through small intestine by passive diffusion without intrinsic factor

Oral intrinsic factor may be given, but if patient has intrinsic factor antibodies this method will not be effective.

Neurological symptoms which are treated within the first 6 months do well. Starting treatment after 6 months of symptoms may result in permanent damage.

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41
Q

Etiology and Epidemiology of Sickle cell anemia

A

autosomal recessive

predominantly African American

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42
Q

What is a sickle cell crisis?

A

Life-threatening; acute painful episode due to ischemia somewhere in body

Increased risk associated with dehydration, acidosis, and hypoxemia

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43
Q

How do carriers of sickle cell trait present?

A

Asymptomatic unless under stress (dehydration, acidosis, hypoxia)

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44
Q

Sickle cell anemia makes patients at increased risk for what other conditions?

A

splenomegaly (pneumococcal infections), non-healing ulcers, strokes, retinopathies, osteomyelitis, necrosis of femoral head

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45
Q

Elevated retic count anemia

A 
Sickle Cell
G6PD deficiency (during hemolytic episode)
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46
Q

Definitive diagnosis method for Sickle cell anemia

A

electrophoresis - HbS in red blood cells

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47
Q

Sickle cell treatment

A

No specific treatment
Folic acid supplement and pneumococcal vaccination
Acute painful episode – fluids, pain meds, and oxygen
Exchange transfusion may be necessary in severe crisis

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48
Q

Drugs that increase risk of hemolytic episode

A 
Antimalarials
Sulfonamides
Methylene blue
Aspirin
Fava beans
Menthol
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49
Q

I came in to see my physician assistant because of…

Prolonged jaundice
Hemolytic crises secondary to illness, certain medications or foods.

A

G6PD deficiency anemia

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50
Q

Treatment of G6PD deficiency anemia

A

Supportive; episodes are self-limiting

Prevention is key

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51
Q

Inheritance of G6PD deficiency anemia

A

X-linked recessive

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52
Q

Signs of anemia + thrombocytopenia + decreased WBCs =

A

Normocytic anemia

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53
Q

Normocytic anemia treatment

A 
Treatment of underlying disease
Bone marrow transplant
Immunosuppression
Erythropoietin
Blood transfusions
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54
Q

Define hemophilia

A

a clotting factor deficiency

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55
Q

Utility of measuring PTT and aPTT

A
  • Assess intrinsic (12, 11, 9, 8) and common coagulation pathways (10, 5, 2, 1)
  • Monitor Heparin therapy

*PTT longer name than PT, and intrinsic pathway more coagulation factors

56
Q

Causes of delayed PTT include…

A

Heparin use, hemophilia, sepsis secondary to coagulation factor consumption

57
Q

Utility of measuring PT and INR

A
  • Assess extrinsic pathway of coagulation (VII = tissue factor)
  • Monitor Warfarin therapy
  • Check for liver damage
58
Q

Causes of delayed PT/INR

A

Warfarin use, liver damage

59
Q

Bleeding time used to assess _______.

A

platelet function

60
Q

Most common inherited clotting disorder

A

von Willebrand disease

61
Q

Functions of von Willebrand’s factor (vWF)

A

Helps platelets stick to blood vessel wall and bind to factor VIII
Increases half-life of circulating factor VII

62
Q

Symptoms of bleeding disorders

A

easy bruising/bleeding
frequent bloody noses
bleeding gums
heavy menses

63
Q

Results of following tests for von Willebrand disease:
PT/INR
PTT

A

PT/INR normal

PTT usually prolonged

64
Q

von Willebrand disease treatment

A

Desmopressin

Factor VII concentrate

Platelet concentrates may be given in severe cases

65
Q

Hemophilia A is deficiency in factor ____ and Hemophilia B is deficiency in factor ____.

A

VIII

IX

66
Q

Inheritance of hemophilia A and B

A

X-linked recessive

67
Q

Results of following tests for Hemophilia A and B:
PT/INR
Bleeding time
PTT

A

PT/INR are normal

Bleeding time is normal

PTT is prolonged

68
Q

What type of hemophilia primarily occurs in Ashkenazi Jews?

A

Hemophilia C

69
Q

Hemophilia C is deficiency in what?

A

coagulation factor XI

70
Q

Treatment of Hemophilia A, B, and C

A

Mild cases of A and B: Desmopressin to encourage factor VII release

Severe cases of A and B: factor concentrate 2-3x/week; patients may develop antibody to factor VIII and IX with treatment

C: tx usually unnecessary unless severe trauma or surgery; fresh frozen plasma, platelets, Desmopressin

71
Q

Congenital cause of hypercoagulable states

A

Factor V Leiden

72
Q

Acquired causes of hypercoagulable states

A 
Antiphospholipid syndrome (autoimmune disease where antibodies against cell membranes)
Poor blood flow (sedentary, Afib, Sickle cell disease, Polycythemia vera) 
Cancer 
Pregnancy
Nephrotic
Inflammatory bowel diseases
Estrogen/birth control
Obesity
Recent surgery
73
Q

What is Polycythemia vera?

A

excess production of red blood cells

74
Q

type of clots

A

DVT
Pulmonary embolism
Superficial vein thrombosis (SVT)

75
Q

How to manage a hypercoaguble state?

A

Treat underlying cause if possible

Long term warfarin – risk of major bleed is 3% per year

76
Q

How should pregnant woman with hypercoaguability be treated?

A

Warfarin is teratogenic so women who may become pregnant should use low molecular weight heparin

77
Q

________ defined as platelet count less than 50,000.

A

thrombocytopenia

78
Q

What distinguishes petechia and purpura from other rashes?

A

do not blanch

79
Q

Megathrombocytes

A

immature platelets recently released from bone marrow

80
Q

Petechiae and purpura are found on the skin and mucous membranes

Low platelet count with no apparent cause

A

ITP

81
Q

ITP treatment

A

Avoid aspirin and NSAIDS

Typically no treatment is necessary for either acute or chronic disease

Steroids

Splenectomy

Platelet transfusion in cases of severe trauma

82
Q

Petechiae and purpura
Low platelets
Labs tests showing less than 5% normal ADAMTS13 protein

DX?

A

TTP

83
Q

Symptoms of TTP

A 
Petechiae and purpura
Malaise
Fever
Bleeding from the nose and gums
Neuro sx's including hallucinations and altered mental status
Kidney failure
84
Q

TTP treatment

A

Plasma exchange

Steroids

Without treatment 95% of patients will not survive. With treatment this number drops to around 10%

85
Q

Similarities and differences between TTP and DIC

A

Both have hemolysis and thrombocytopenia

TTP has abnormal renal function but normal PT/PTT

DIC has normal renal function but prolonged PT /PTT causing increased clotting

86
Q

DIC treatment and prognosis

A

Platelet transfusion

Fresh frozen plasma

Anticoagulation may be necessary??

10-50% of patients will not survive

87
Q

Disease characterized by overproduction of WBCs

A

leukemia

88
Q

What are PE findings of leukemia?

A

swollen lymph glands, enlarged spleen

89
Q

How is chronic and acute leukemia differentiated in lab?

A

acute - cells immature from fast increase in WBC production

chronic - slower buildup of WBC so mature cells; cells still abnormal and non-functioning

90
Q

Myelogenous vs lymphocytic leukemia

A

Lymphocytic - overproduction of lymphocytes

Myelogenous- overproduction of RBCs as well as some WBCs and platelets

91
Q

Symptoms of leukemia

A 
Symptoms of anemia
Weakness
Fatigue
Fever/infection
Decrease in appetite
Bone and joint pain
Enlarged lymph nodes
Petechia
92
Q

Leukemia in ages 2-5 with excessive lymphoblasts

A

ALL

93
Q

Bone marrow biopsy of ALL and AML

A

hypercellular

94
Q

Most common type of leukemia, majority of men over 50 yo

A

CLL

95
Q

Auer rods are pathonomonic for ______.

A

ALL

96
Q

Leukemia treatment

A

Chemotherapy
Radiation
Steroids
Bone marrow transplant

97
Q

Which leukemias can present as asymptomatic?

A

CLL, CML

98
Q

Which leukemia can be managed with tyrosine kinase inhibitors?

A

CML

99
Q

Unlike leukemia, __________ is a solid tumor.

A

Hodgkins lymphoma

100
Q

Staging 1-4 for lymphoma

A

Stage 1: single site

Stage 2: two or more lymph nodes on same side of diaphragm

Or one extralymphatic site and one lymph node on same side

Stage 3: Affected lymph nodes on both sides of diaphragm and involvement of spleen or another extralymphatic site

Stage 4: Presence of B symptoms (fever, weight loss, night sweats) or diffuse extra lymphatic involvement

101
Q

Lymph node biopsy showing ________ is diagnostic for Hodgkins lymphoma.

A

Reed-Sternberg cells

102
Q

Differences between Hodgkins and non-Hodgkins lymphoma?

A
  • Both cancer of WBCs (lymphomas)
  • Non Hodgkins more common
  • Hodgkins has Reed-Sternberg cell on microscopy
103
Q

Build up of plasma cells in the bone marrow interfering with normal production

A

Multiple Myeloma

104
Q

Findings of Multiple Myeloma on skeletal survey

A

XR of skull shows punched on lesions

Lytic lesions

105
Q

Why is hypercalcemia seen in multiple myeloma?

A

excessive bone resorption

106
Q

Multiple Myeloma treatment and prognosis

A

No treatment other than treating end organ damage

Chemo with stem cell transplant

5 yr survival rate 35%

107
Q

Philadelphia Chromosome is pathognomonic for _____.

A

CML

108
Q

Bence-Jones proteins and rouleaux formation on peripheral smear

A

multiple myeloma

109
Q

hematopoiesis

A

development of blood cells

110
Q

How is fetal hemoglobin different than adult?

A

greater affinity for oxygen

111
Q

What is hematocrit measure?

A

percent of blood volume composed of RBC

112
Q

Normal range for WBC

A

4.5K to 11K

113
Q

Normal range for platelets

A

150K to 400K

114
Q

What is the spleens role in hematologic system?

A
  • filters out malformed, damaged, or old RBCs

- hematopoiesis in fetal period

115
Q

Site of hematopoiesis

A

bone marrow in adults

spleen in fetus

116
Q

What is aplastic anemia?

A

loss of hematopoietic cells leading to pancytopenia (decrease in all blood cell types)

117
Q

Pathologies of the hemoglobin

A

Sickle cell

Thalassemias

118
Q

Lab findings of hemolysis

A 
increased indirect bilirubin
increased LDH
increased reticulocytes
decreased free haptoglobin
schistocytes
119
Q

Type I hypersensitivity reaction

A

Anaphylaxis
IgE mediated
Allergies (food, dust, insects)

120
Q

Type II hypersensitivity reaction

A

Cytotoxic

mediated by IgG, IgM antibodies

121
Q

Hypersensitivity reaction with antigen-antibody complexes

A

Type III

122
Q

Cell mediated or delayed hypersensitivity reaction

A

Type IV

123
Q

What cells produce antibodies?

A

lymphocytes

124
Q

_________ is proliferation of WBCs in bone marrow and _________ is proliferation in lymphatic tissue.

A

Leukemia

Lymphoma

125
Q

Where is lymphatic tissue?

A

lymph nodes and spleen

126
Q

Causes of elevated WBC

A 
infection or inflammation
autoimmune disease
hematologic malignancy (leukemia, lymphoma)
127
Q

Cells that arrive at site of inflammation first

A

neutrophils

128
Q

Coagulation factors that need Vitamin K for synthesis?

A

Mneumonic: 1972

X, IX, VII, II

129
Q

What does abnormal PT and normal PTT mean?

A

problem with extrinsic pathway of clotting cascade

130
Q

MOA of Coumdadin and how is it monitored

A

anticoagulation; interferes with Vit K-dependent clotting factors (10, 9, 7, 2)

monitored by PT

131
Q

MOA of Heparin and how is it monitored

A

anticoagulation; increases antithrombin III activity and decreases amount of fibrin

monitored by PTT (intrinsic)

132
Q

What helps platelets stick together when forming a clot?

A

fibrinogen (factor I)

133
Q

Pathologies that cause platelet loss or destruction?

A

ITP
TTP
HUS
DIC

134
Q

Byproduct of RBC breakdown

A

Bilirubin, iron, and amino acids

135
Q

When _____ is negative, this rules out PE in a low risk patient.

A

D-dimer

PANCE review (18 decks)

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