Hematology/Oncology Flashcards

1
Q

Main causes of microcytic hypochromic anemia (what is the most common?)

A
  1. MC is iron deficiency anemia
  2. Thalassemia minor/major
  3. Anemia of Chronic Disease/inflammatory diseases
  4. Sideroblastic Anemias and Pb Poisoning
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2
Q

Iron deficiency anemia accounts for ____% of anemias worldwide

A

50%

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3
Q

Normal lab values for the following:

  • -Serum Iron, Fe
  • -Total Iron Binding Capacity
  • -Fe/TIBC saturation
  • -Serum Ferritin
A

Serum Iron: 40-140 uG/dL

TIBC: 200-400 uG/dL

Fe/TIBC Saturation: 25-50%

Serum Ferritin: 30-250 ng/ml

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4
Q

Causes of Iron Deficiency Anemia

A
  1. GI Bleeding (ALWAYS BE SUSPICIOUS OF THIS!)
  2. Excessive menstruation
  3. Malnutrition & Dietary insufficiency
  4. Malabsorption (celiac sprue, crohn’s, subtotal gastrectomy)
  5. Increased demand (pregnancy, growth spurts in children)
  6. Blood donation, bllod loss in dialysis & Factious Auto-phlebotomy
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5
Q

Specific clinical manifestations of iron deficiency anemia

A
  • -Angular Cheilosis
  • -PICA
  • -Koilonychia
  • -Plummer-Vinson Syndrome (Fe def anemia, esophageal webs, dysphagia and atrophic glossitis)
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6
Q

What do Fe levels, TIBC, saturation, and ferritin look like in Iron Deficiency Anemia

A

Dec. Fe++

Increase TIBC

Dec. Saturation < 10%

Dec. Ferritin < 20 ng/dL

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7
Q

Tx of choice for iron deficiency anemia

A

Ferrous sulfate 325mg TID w/ meals for 6 months

Can give IV/IM doses if pt is not oral tolerant

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8
Q

Fe++ side effects

A
  • Constipation
  • Black stools
  • Nausea
  • Bloating
  • Abdominal Pain
  • Diarrhea
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9
Q

In which drugs does Fe bind to and decrease their activity?

A

Tetracyclines

Fluroquinolones (cipro, levofloxin)

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10
Q

______ increases Fe++ absorption

A

Vitamin C (orange juice)

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11
Q

Does AML typically appear in the older or younger population?

A

Older (>65)

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12
Q

Most common signs/symptoms in AML

A

< 3 month onset
Fever, bleeding, fatigue, SOB

Less common: retinal hemorrhages, gingival hyperplasia, solid tumors

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13
Q

Polys and blast cells with nothing inbetween is _______ and is a sign for _______.

A

Leukemic Hiatus

AML

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14
Q

Auer Rods are characteristic cells for what?

A

AML

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15
Q

How do you treat AML?

A

Induction therapy

  • -> 7 days of Cytarabine continuous IV
  • -> 3 days of anthracycline

If not entered CR then retreat or switch to salvage therapy

Older pts >70 do not tolerate standard therapy…need supportive therapy if they chose to go through this (abx, blood products, etc.)

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16
Q

A patient presents with a fever, fatigue, shortness of breath w/ bleeding and thrombosis. What is the likely diagnosis?

A

APL (Acute Promyelocytic Leukemia)

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17
Q

Name the 5 clotting factors and the 5 anti-clotting factors

A

Clotting: Platelets, soluble clotting factors, tissue factor, collagen, phospholipids

Anti-clotting: Nitric Oxide, protein C & S, Anti-thrombin III, fibrinolytics, prostacyclin

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18
Q

2 vWF functions

A
  1. Binds factor VIII and extends its life

2. Binds platelets to injured vessel endothelium

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19
Q

What does Protime (PT) measure and what is its usual length

A

Factors II, VII, IX, X

~12 seconds

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20
Q

Is a PT shortened or prolonged when a pt is taking Coumadin?

A

Prolonged

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21
Q

What does aPTT measure and what is its usual length?

A

Factors II (prothrombin), VIII, IX, X, XI & Fibrinogen

~32 seconds

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22
Q

Where is vWF stored?

A

Epithelial cells

Platelets

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23
Q

vWF’s production is stimulated by ______ & ______ and its release is stimulated by _____, _____, ______, & ______.

A

Production: estrogen & T4

Release: vasopressin, epinephrine, histamine, thrombin

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24
Q

Hemophilia A is a deficiency of factor ___ and Hemophilia B is a deficiency of factor ____.

A

A = Factor VIII

B = Factor IX

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25
Q

Which type of vWF Disease is more common? Type 1 or Type 2?

A

Type 1

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26
Q

How do you treat vWF disease type 1 vs. type 2?

A

Type 1 = DDAVP as nasal spray

Type 2 = DO NOT give DDAVP because it can cause thrombocytopenia

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27
Q

Describe the inheritence of vWF, Hemophilia A&B, and Factor XI Deficiency

A

vWF = autosomal co-dominant

Hemophilia A&B = x-linked recessive

Factor XI Deficiency = autosomal co-dominant

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28
Q

Which is more common? Hemophilia A or B?

A

A: 1 in 5000

B: 1 in 30,000

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29
Q

_____ affects 6% of Jewish population.

A

Factor XI Deficiency

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30
Q

Tx for Factor XI Deficiency

A

FFP

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31
Q

What is Vitamin K responsible for activating?

A
F II
F VII
F XI
F X
Proteins C & S
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32
Q

Half life of Factor VII is ____.
Half life of Prothrombin is ___.
Half life of Factor X is ____.

A
VII = 4 hrs
Prothrombin = 72 hours
X = 48 hrs
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33
Q

Therapeutic Coumadin level for PT and INR

A
PT = 17-25
INR = 1.5-3
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34
Q

1st line tx for coagulopathy of liver disease

A

FFP

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35
Q

1st line tx for coagulopathy of kidney disease

A

Restore renal function w/ dialysis

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36
Q

One pt has coagulopathy of the liver and the other has one of the kidney. Which will likely be more severe?

A

Liver

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37
Q

Where is DIC most commonly observed?

A

Septic shock

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38
Q

Underlying conditions of DIC

A
  • Snake or insect venom
  • Bacteremia/Sepsis
  • Neoplasms (adenocarcinomas, APL)
  • Brain Injury
  • Fat or Amniotic fluid emboli
  • Abrutio placentae
  • Severe pre-eclampsia
  • HELLP Syndrome
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39
Q

HELLP Syndrome

A

Hemolysis
Elevated LFTs
Low Platelets

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40
Q

Clinical Hallmark of DIC

A

Diffuse bleeding from mucosal sites, sites of previous surgery

Organ failure (kidney and liver most common)

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41
Q

Lab values for DIC:

  • -Blood work?
  • -PT & aPTT
A

Micro-angiopathic Hemolytic Anemia

Thrombocytopenia

Inc. PT and aPTT time

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42
Q

Tx for DIC

–first line and what to do after

A

Treat the underlying cause

Next think about replacing clotting and anti-clotting factors w/ FFP

No platelet tranfusions or anti-coagulants

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43
Q

How would you check to see if a patient has developed auto-antibodies to inhibit clotting factors?

A

1:1 Normal Plasma Mixing Study

  • -> Mix pt’s plasma w/ normal plasma and rechecking the abnormal clotting studies (PT & aPTT). If bleeding is d/t a factor deficiency then the normal plasma will correct the problem and the PT and aPTT will be normal.
  • -> If the bleeding is d/t an inhibitor then the inhibitor will anticoagulate the clotting factors in the normal plasma and the PT and aPTT will remain abnormal
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44
Q

How do you tx one who has acquired auto -antibodies inhibiting factor VIII?

A

High dose of Factor VIII replacement along w/ immune suppressive rx

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45
Q

The 3 types of drugs that inhibit platelet function

A
  1. ) Aspirin
  2. ) Clopidogrel
  3. ) GPIIb/GPIIIa Inhibitors (abciximab, eptifiatide)
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46
Q

Does Aspirin irreversibly bind or reversibly bind to platelets?

A

Irreversibly…so it lasts for the life of a platelet (7 days)

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47
Q

T/F: High does of platelets are effective to use as anti-platelet rx

A

False

Dose: 81-325mg

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48
Q

The most commonly inherited hypercoaguable state is:

A

Factor V Leiden

49
Q

Tx for Factor V Leiden

A

Asymptomatic carriers = education about increased risk situations

In high risk situations = rx w/ anti-coagulation until situation is resolved

If pt has > 1 previous DVT or PE = anticoagulation for life

50
Q

The 2nd most commonly inherited hypercoaguable state that increases plasma levels of prothrombin is _________.

A

Prothrombin Gene Mutation G20210A

51
Q

A hypercoaguable state that is often associated w/ SLE

A

The Anti-Phospholipid Antibody Syndrome

52
Q

Clotting problems are d/t these 5 reasons:

A
  1. Problems of vessel walls
  2. Problems w/ soluble clotting factors
  3. Problems w/ soluble anti-clotting factors
  4. Problem w/ platelets
  5. Problems w/ a mixture of components of the clotting system
53
Q

Classic Pentad of TTP and HUS

A
  1. Microangiopathic hemolytic anemia
  2. Thrombocytopenia
  3. Renal Failure
  4. Fluctuating Neuro s/s
  5. Fever
54
Q

If a pt presents w/ the TTP& HUS pentad of symptoms but renal failure is the dominating one is the diagnosis most likely TTP or HUS?

A

HUS

55
Q

Which is more common in children? TTP or HUS?

A

HUS

56
Q

Describe the following lab diagnosis for TTP:

  • -Type of anemia
  • -PT and aPTT
  • -LDH
  • -Indirect Bilirubin
  • -Haptoglobin
  • -Reticulocyte count
  • -Direct Coombs
A

Microangiopathic Hemolytic Anemia w/ thrombocytopenia

Normal PT and aPTT

Increased LDH
Inc. Indirect Bilirubin
Dec. Haptoglobin
Inc. retic's
Negative Direct Coombs
57
Q

Treatment for TTP and HUS

A

Urgent plasmapharesis

If offending agent is identified then discontinue it

Steroids may be of some benefit

58
Q

Before plasmaphoresis, TTP had an 80-90% mortality rate but now if prompt diagnosis and tx are initating it should be ____.

Relapses occur in _____% of cases so long term _____ may be used.

A
59
Q

Is DIC a syndrome or a disease?

A

A syndrome

60
Q

What must one exclude to diagnose someone w/ ITP?

A
Lymphomas
Medications
SLE
HIV
Hepatitis B or C
vWD
Antiphosphlipid Syndrome
61
Q

ITP w/ autoimmune hemolytic anemia is ______.

A

Evans Syndrome

62
Q

Myeloproliferative Syndromes:

  • -Too many RBC =
  • -Too many platelets =
  • -Too many neutrophils =
  • -Too many RBC, platelets, neutrophis =
A

Polycythemia Vera (PVC)

Essential thrombocytosis (ET)

CML

Myelofibrosis

63
Q

A pt presents w/ pruritis, fatigue, HA and upon examination has ruddy complexion and mild spenomegaly. What is the likely diagnosis and what mutation is associated with this?

A

Polycythemia vera

–> JAK 2 mutation

64
Q

How would you go about treating a pt w/ polycythemia vera?

A

Phlebotomy until they are Fe deficient

Tx associated symptoms (gout, pruritis, HA/Vertigo)

65
Q

A pt w/ polycythemia vera has an increased Hct. What is the diagnostic Hct and what is seen more commonly in males v. females?

A

Dx: >60% Hct

Usually see levels however of:
Males = 52-60%
Females = 48-60%

66
Q

What are the differential diagnosis for Polycythemia vera? (3)

A
  1. Gaisbock’s Syndrome
  2. Chronic Hypoxia
  3. Renal Cell CA
67
Q

Treatment for essential thrombocytosis if asymptomatic

A

Observation w/ routine follow up and pt education on worrisome symptoms

68
Q

Treatment for essential thrombocytosis if symptomatic or above a certain platelet count (which is…)?

A

Platelets > 1 million warrents tx

1st line = either anagrelide or hydroxyurea to lower platelet count

69
Q

____ is almost diagnostic of CML but the sine qua non of CML is _____.

A

Basophilia

Sine qua non- Philadelphia chromosome

70
Q

Which s/s of CML are worryisome and require urgent treatment?

A

Thrombocytosis of > 1million associated w/ wet purpura, GI bleeding, or thrombosis

71
Q

2 phases of CML

A

Chronic Phase

Accelerated Phase

Blast Crisis

72
Q

What is the treatment goal of CML and what does this mean?

A

Goal is complete molecular remission meaning no evidence of BCR-ABL1 transcripts by RT-PCR

73
Q

The tyrosine kinase inhibitor used to tx CML is called ______.

A

Imatinib (Gleevec)

74
Q

Leuko-erythroblasts (immature WBC and RBC that are tear dropped shaped) are indicative of what disease?

A

Myelofibrosis Myeloid Metaplasia (MMM)

75
Q

Poor prognosis factors of Myelofibrosis myeloid metaplasia (5) and what the risk/average survival rate that correlates with these risks

A

Risk:

  • Age > 65yo
  • Constitutional Sx
  • Hgb 10%
  • WBC > 25,000

Low Risk = 0 of these sx = 11year survival

Intermediate 1 = 1 sx = 8 yr survival

Intermediate 2 = 2 sx = 4 yr survival

High Risk = 3+ sx = 2 yr survival

76
Q

How are GI cancers staged?

A

TNM System (Tumors, Nodes, Mets)

77
Q

Using the TNM staging system for colon CA: what is stage 0, 1A, 1B, 2, 3A, 3B, 4

A
Stage 0: Tis N0
Stage 1A: T1, N0
Stage 1B: T2, N0
Stage 2: T1,T2 N1 or T3 N0
Stage 3A: T3 N1,2
Stage 3B: T4
Stage 4: Mets
78
Q

Most GI CA arises from _____ and the most common type is ______.

A

Arise from epithelial layer of mucosa

MC type = adenocarcinoma

79
Q

Upper and mid esophageal CAs are mostly _________ (type)

A

Squamous Cell

80
Q

Tx for Tis or high grade dysplasia or T1 =

A

Endoscopic ablation

Esophageal resection

81
Q

Although gastric cancer has declined world-wide, where in the world is it still a common problem?

A

Japan and some other areas of Asia

82
Q

Factors contributing to gastric CA

A
  • Diets low in vitamins A&C
  • Consumptin of smoked or cured foods
  • Untreated infection w/ H. pylori
  • Genetic Predispositions (Blood type A, Pernicious anemia)
83
Q

Most gastric CA are _______ (type)

A

Adenocarcinomas

84
Q

The 3rd most common and 3rd most lethal CA in the US is _____.

A

Colorectal CA

85
Q

Primary Prevention of GI Cancers: (4 things)

A
  1. High fiber and low fat diets
  2. NSAIDs
  3. Ca++
  4. HPV Vaccine (prevent anal CA)
86
Q

Colorectal CA screening

A

Start @ 50yo or 10 years before age that 1st degree relative was dx’d w/ CRC

87
Q

How often does fecal blood occult test miss colon cancer?

A

50% of the time (false negative)

88
Q

How often does flixble sigmoidoscopy miss colon CA?

A

50% of the time

89
Q

What drug is the backbone of Rx for almost all GI cancers?

A

5FU (5 Fluorouracil)

90
Q

Do GISTs respond well to chemo?

A

NO!

91
Q

Are soft tissue sarcomas cancers of children or adults?

A

Adults

92
Q

Most common CNS cancer is ______.

A

Metastatic (lung, breast, pancreas, melanoma)

93
Q

Most common bone cancer is _____.

A

Metastatic (prostate, breast, lung)

94
Q

Sickle cell deforms RBCs causing _______, ________, and _______.

A

Hemolysis
Splenic sequestration
Microvascular occlusion

95
Q

Splenic infarction causes overwhelming infection by encapsulated organisms. These organisms are?

A

Strep
Hemophilus
Klebsiella
Salmonella

96
Q

How to dx sickle cell anemia?

A

Hg Electrophoresis –> detects HbS (trait has 40% and disease has >95%)

Blood smear –> sickled cells, hemolysis, reticulocytosis, nucleated RBCs, target cells, hollow jolly bodies d/t autosplenectomy

97
Q

Tx of sickle cell anemia. How does this tx work?

A

Hydroxyurea

  • Increases HbF which decreases HbS and painful crisis
  • Also decreases WBCs and retics (could worsen sx)
98
Q

Warm autoimmune hemolytic anemia results in _______ hemolysis whereas cold autoimmune hemolytic anemia results in ______ hemolysis.

A

Warm = IgG = extravascular hemolysis

Cold = IgM = intravascular hemolysis

99
Q

Most common cause of B12 deficiency

A

Pernicious Anemia

–Lack of intrinsic factor

100
Q

How do you distinguish B12 and Folate deficiency?

A

B12 has increased homocysteine levels and increased MMA levels whereas Folate has increased homocysteine but NORMAL MMA levels.

B12 also involves peripheral neuropathy whereas folate does not

101
Q

Causes of Folate Deficiency Anemia

A
  1. Inadequate intake (alcoholics)
  2. Increased requirement (pregnancy)
  3. Defective absorption (celiacs)
  4. Exposure to folic acid antagonists (methotrexate, trimethoprim, anticonvulsants)
102
Q

What 3 drugs are folic acid antagonists?

A
  1. Methotrexate
  2. Phenytoin
  3. Trimethoprim
103
Q

EPO is secreted by the ______ and ___ is its main stimulus

A

Kidney

02

104
Q

What are 3 substrates needed for EPO to create new RBC

A

Folate
B12
Iron

105
Q

Life cycle length of RBC, platelet, WBC

A
RBC = 120 days
Platelet = 7 days
WBC = 1 day
106
Q

Which two populations usually have low RBC mass

A

Elderly

African Americans

107
Q

What are 4 instances in which there are changes in plasma volume that may decrease or increase RBC concentration and skew lab results

A
  1. Acute Bleeding (dec. volume may show nml Hgb and Hct levels)
  2. When nml volume is restored (pt might demonstrate anemia)
  3. Dehydration (when dydrated the Hgb & Hct fall)
  4. Pregnancy (plasma volume increases faster than RBC therefore pt may appear falsly anemic)
108
Q

In a pregnant women the plasma concentration increase by ____% whereas the RBC increase by ___%.

A

Plasma inc. 50%

RBC inc. 25%

109
Q

Heinz Bodies =

A

Thalassemia!

110
Q

Complications of Beta-Thalassemia Major (Cooley’s Anemia)

A
  1. Growth retardation
  2. Severe anemia
  3. Abnormal facial structures
  4. Fx & Osteopenia
  5. Hepatosplenomegaly
  6. Jaundice and bili gall stones
  7. High output CHF
  8. Short life span (<30yo)
111
Q

Target cells, Basophilic stippling, heinz bodies =

A

Beta thalassemia

112
Q

Transfusion complications of thalassemia:

A

Iron Overload –> heart failure, liver failure, pancreatic failure, skin pigmentation

113
Q

A 70 yo pt presents with fatigue, SOB, and angina. You order a CBC and results come back noting anemia, thrombocytopenia, and leukemia. Upon peripheral smear the lab techs notice ringed sideroblasts and increased number of blast cells. What is the diangosis? If a pt was older and had a high level of blasts (~15%) what would be your suspected treatment?

A

Myelodysplastic Syndrome

If a pt had increased blasts their average survival rate decreases and especially if the pt was older I would choose supportive tx and not put on chemo since this cancer is not curable

114
Q

Gingival hyperplasia is a tip off for what type of leukemia?

A

Monocytic Leukemia

115
Q

Which is more common: non-hodgkins lymphoma or Hodgkin’s Lymphoma?

A

NHL

116
Q

Are NHL mostly B cells or T cells

A

85% B cell

117
Q

The 2nd most common of all adult lymphomas is _______ which accounts for ____%

A

Follicular Lymphomas

30%

118
Q

Most non-hodgkins lymphomas, Waldenstrom’s Macroglobulinemia, and Multiple Myeloma are diseases of ___ cells

A

B cells

119
Q

MALT Lymphomas stand for what?

A

Mucosally Associated Lymphoid Tissue