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Heme/Onc/Endo > Heme/Onc Exam 2 Cards > Flashcards

Heme/Onc Exam 2 Cards Flashcards

1
Q

Proportion of deaths in the US caused by cancer

A

1 in 4

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2
Q

Top three cancer causes

A

Breast or Prostate
Lung
Colon

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3
Q

Top three cancer deaths

A

Lung
Breast/Prostate
Colon

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4
Q

Why might there be more cancer cases but fewer deaths than in the past?

A

We are diagnosing more cancer, but those diagnosed are also living longer

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5
Q

In addition to physical morbidity, what two things may cancer also be associated with?

A

Emotional distress and reduction of quality of life

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6
Q

Primary prevention

A

Prevents a disease before it even starts - includes addressing risk factors and promoting health

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7
Q

Secondary Prevention

A

Screening for early detection and treatment for those at risk

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8
Q

Tertiary prevention

A

Rehabilitating, preventing complications and improving quality of life for those with illness

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9
Q

Percent of cancer risk that likely comes form your environment

A

90-95% (Most of that from diet)

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10
Q

2 cancers associated with lack of physical activity

A

Colon and Breast

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11
Q

4 cancers associated with high fat diets

A

Breast, Colon, Prostate, Endometrium

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12
Q

Cancer prevented by dietary fiber

A

Colon polyps, Colon cancer

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13
Q

4 Carcinogens to remember
3 viruses and 1 substance

A

Epstein Barr virus
Alcohol
H. Pylorii
Hepatitis B or C

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14
Q

Sensitivity

A

proportion of persons with the disease who test positive in the screen

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15
Q

Specificity

A

Proportion of persons who do not have the disease who test negative in the screen

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16
Q

Positive predictive value

A

Proportion of persons who test positive that actually have the disease

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17
Q

Negative predictive value

A

Proportion testing negative that do not have the disease

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18
Q

At what age should yearly mammograms begin

A

Age 40

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19
Q

What and what are the screening guidlines for colon cancer

A

After 45, a colonoscopy every ten years or something else every five years

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20
Q

Cervical cancer screening guidelines

A

Begin at age 21
Every 3 years from 21-29
Every 5 years from 30 to 65
Not recommended after 65

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21
Q

CAUTION warning signs of cancer

A

Change in bowel or bladder habits
A sore that does not heal
Unusual bleeding or discharge
Thickening lump in breasts, testes, or elsewhere
Indigestion of difficulty swallowing
Obvious change in a mole
Nagging cough or hoarseness

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22
Q

3 classic cancer warning signs

A

Nightsweats, Unexplained weight loss, Persistent low grade fever

Also chronic pain and persistent fatigue

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23
Q

Clinical vs. Pathalogical staging

A

Clinical is based on physical exam, pathological is based onsurgical findings

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24
Q

TNM system

A

Tumor, Node, Metastasis - localized to regional, to systemic

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25
Q

Stage IA lung cancer

A

Smaller than 3cm, no spread to lymph nodes

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26
Q

Stage IB lung cancer

A

3-4 cm not in lymph nodes or main bronchus

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27
Q

Difference between lung cancer stages IVA and IVB

A

IVA can be other lung OR site outside lungs
IVB is at least two sites outside lungs

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28
Q

Karnofsky performace index

A

Rates mobility and autonomy of cancer patients 0=Dead
100=Full independance

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29
Q

Tumor marker for gonadal germ cell tumor

A

Human chorionic gonadotropin (HCG)

Can also indicate pregnancy

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30
Q

Tumor marker for medullary thyroid cancer

A

Calcitonin

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31
Q

Tumor marker for hepatocellular carcinoma or germ cell cancer

A

a-fetoprotein

Can also be cirrosis

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32
Q

Tumor marker for colon, pancreas, lung, breast, and ovary

A

Carcinoembryonic antigen

Can also be pancreatitis, hepatitis, IBF, smoking

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33
Q

Lymphoma or Ewing’s sarcoma marker

A

Lactate dehydrogenase

Can also be hepatitis or hemolytic anemia

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34
Q

Marker for prostate cancer

A

Prostate specific antigen

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35
Q

Marker for ovarian cancer and some lymphomas

A

CA-125

Can also be menstruation, peritonitis, or pregnancy

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36
Q

Marker for COLON cancer as well as pancreatic and breast

A

CA-19-9
Can be pancreatitis or UC

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37
Q

Agranulocytosis

A

Absence of granulocytes - Neutrophils, Eosinophils, Basophils

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38
Q

Proliferation stage

A

WBCs can divide but don’t yet have special functions

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39
Q

Differentiation stage

A

WBCs have special functions but no longer multiply

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40
Q

Immature granulocytes that we should NEVER see in circulation

A

Metamyelocytes

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41
Q

Common progenitor of all non-lymphoid WBCs

A

Myeloblast

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42
Q

Absolute v. relative cell counts

A

Absolute = actual number of cells - more reliable
Relative = Percentage of total cells

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43
Q

3 places neutrophils might be hanging out

A

In the storage pool in the marrow (reserves)
Extramedullary either free in the bloodstream or attached to endothelial walls (marginal pool

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44
Q

Neutrophilic shift

A

Marginal pool neutrophils move to the general circulation
Can be due to stress

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45
Q

True neutrophilia

A

Release of neutrophils from the storage pool

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46
Q

3 types of true neutrophilia

A

Spurious - We counted wrong
Primary - inherent defect
Secondary - due to another problem like infection

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47
Q

When might we see pseudoneutropenia

A

In the morning

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48
Q

Low neutrophil count at which we should worry about serious infection and at which we should consult

A

Under 500 - Worry
Under 1000 - Consult

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49
Q

2 myeloid growth factors for neutropenia

A

Filgrastim (Neupogen) - Only stimulates granulocytes
Sargramostin (Leukine) - stimulates granulocytes and macrophages

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50
Q

Distinguishing factor of eosinophils

A

Bi-lobed nucleus

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51
Q

Complication of eosinophilia and level at which we should be concerned about it

A

Tissue damage
Most likely to occur at over 1500/microliter

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52
Q

Where do most eosinophils live

A

in the tissues

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53
Q

3 organs most commonly affected by eosinophilia

A

Skin, airway, GI tract

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54
Q

2 things released by basophils

A

Heparin and Histamine

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55
Q

Common cause of primary basophilia

A

Chronic myelogenous leukemia

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56
Q

Hallmark of basophils

A

Blue-black (dark) granules

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57
Q

Special property that makes B and T cells different than other WBCs

A

They can still divide after diffierentiating

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58
Q

3 types of t cells and their roles

A

Helper/CD4 - antibody production and activation of other T cells
Cytotoxic/CD8 - Attack and destroy foreign cells including cancer cells and infected cells
Regulatory T cells - Turn off immune response of other T cells

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59
Q

Function of B cells

A

Present antigens to T cells, can become memory or plasma cells

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60
Q

Natural Killer cells

A

Lymphocytes that do not need stimulation to kill infected cells. Can recognize between foreign and self cells

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61
Q

What ages correspond with increased lymphocytes

A

Younger ages

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62
Q

Monoclonal lymphocytosis

A

More likely a malignancy than polyclonal

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63
Q

Polyclonal lymphocytosis

A

More often due to stress an infection or even a splenectomy

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64
Q

3 work ups for lymphocytosis

A

Repeat CBC, Do a peripheral blood smear, Perform flow cytometry

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65
Q

2 common procedures you should NEVER do on an immune compromised patient

A

Digital rectal exam
Foley catheter placement

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66
Q

To nutritional causes of lymphocytopenia

A

Zinc deficiency and Alcohol abuse

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67
Q

Nucleus shape of Monocytes

A

Kidney shaped or notched nucleus

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68
Q

5 potential etiologies for monocytosis

A

Bacterial infection complicated by neutropenia
Monocytic leukemia or lymphoma
Asplenia
Inflammatory or autoimmune conditions
Treatment with corticosteroids or colony stimulating factors

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69
Q

2 pharmacotherapies used for leukopenia

A

Broad spectrum antibiotics
Granulocyte colony stimulating or granulocyte-macrophage colony stimulating factors

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70
Q

3 Additional treatment options for leukopenia

A

Corticosteroid therapy, Correction of nutritional deficiencies, Splenectomy if unresponsive to all other treatments

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71
Q

Left shift

A

an absolute increase in neutrophils with an increase in bands and sometimes increases in even less mature forms

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72
Q

Hypersegmentation

A

Nuclei with 5 or 6 lobes rather than 3 or 4

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73
Q

3 places we might see hypersegmented neutrophils

A

Megaloblastic anemia, chemotherapy, myeloproliferative disorders

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74
Q

Dohle body

A

Irregularly shaped blue staining area associated with infections

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75
Q

Smudge or basket cell

A

Ruptured WBC remnant from fragile lymphocytes - associated with CLL

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76
Q

Platelet satellitosis

A

Platelets seen adering to WBCs - this leads to an artificially low PLT count

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77
Q

Flow cytometry

A

cells flow past a detector that can detect surface antigens and abnormal cells

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78
Q

3 goals of cancer treatment if the cancer cannot be eradicated

A

Palliation
Treatment of symptoms
Preservation of quality of life

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79
Q

Four main subtypes of cancer treatment

A

Sugery
Radiation
Chemotherapy
Biologic therapy

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80
Q

Percent of cancer patients that can be cured by surgery

A

40%
Surgery may not cure but may be helpful in managing cancer by removing bulk to enhance efficacy and preserving organ function

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81
Q

One condition that is needed for successful cancer removal surgery

A

Clear tumor borders

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82
Q

3 types of radiation therapy

A

Teletherapy - beams at a distance aimed at patient
Brachytherapy - Sources of radiation implanted in or near tumor
Systemic therapy - radionuclides are designed to hone in on site of cancer such as radioactive iodine for thyroid cancer

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83
Q

Systemic effects of local radiation therapy (4)

A

Fatigue, anorexia, nausea, vomiting

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84
Q

3 other localized cancer therapies

A

Radiofrequency ablation - Uses microwaves to cook tumors
Cryosurgery - uses cold to kill lesions
Chemoembolization - Localized administration of chemotherapeutic agents

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85
Q

4 types of chemotherapeutic agents

A

Conventional cytotoxic agents
Targeted agents
Hormonal therapies
Biologic therapies

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86
Q

Antimetabolites for chemotherapy (2)

A

Methotrexate, 5-fluorouracil

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87
Q

3 toxic manefestations of antimetabolites

A

Stomatitis, Diarrhea, Myelosuppression

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88
Q

MOA and class of Methotrexate

A

Competes and counteracts folic acid - Antimetabolite

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89
Q

MOA and class of 5-fluorouracil

A

Prevents thymidine formation - Antimetabolite

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90
Q

MOA of antimetabolites

A

Direct prevention of DNA synthesis

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91
Q

3 mitotic spindle inhibitors used in chemotherapy

A

Vincristine
Vinblastine
Paclitaxel

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92
Q

3 common toxic manifestations of mitotic spindle inhibitors

A

Alopecia, neuropathy, myelosuppression

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93
Q

MOA of alkylating agents

A

Get broken down by cells or spontaneously to form metabolites that covalently modify DNA bases and cross link strands

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94
Q

3 Alkylating agents

A

Cyclophosphamide
Chlorambucil
Cisplatin

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95
Q

Class and 3 side effects of cisplatin

A

Alkylating agent - Neurotoxicity (stocking glove syndrome), hearing loss, renal failure

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96
Q

Doxyrubicin

A

Antitumor antibiotic, binds to DNA and then generates free radicals to damage it
Bright Red
Cardiotoxic

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97
Q

Etoposide

A

Chemo drug, topoisomerase inhibitor that binds to topoisomerase II and causes breaks in the DNA
Can lead to secondary leukemia

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98
Q

Treatment for Chemo induced nausea

A

Ondensetron (Zophran)

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99
Q

Treatment for chemo induced neutropenia

A

Colony stimulating factors like filgrastatin (has a lot of side effects)

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100
Q

Mucositis

A

Oral soreness and ulcerations caused by 5-FU, methotrexate, and cytarabine
Use magic mouthwash to treat

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101
Q

Drug that especially causes chemo induced diarrhea and what to give for it

A

5-FU
Give Loperamide (Immodium) can give octerotide if no response to loperomide

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102
Q

Alopecia

A

Hair loss - chemo cap a controversial treatment

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103
Q

Most common side effect of chemotherapy

A

anemia

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104
Q

3 routine blood tests for patients of Chemo

A

CBC, CMP, PT/aPTT

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105
Q

3 presentations of chemo induced nausea

A

Acute
Delayed
Anticipatory

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106
Q

Effect of cancer on coagulation

A

Causes a hypercoagulable state

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107
Q

Paraneoplastic syndrome

A

Conditions that come with tumors but are not related to the mass effect of the tumor

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108
Q

Three ways paraneoplastic syndromes can arise

A

Initiated by a tumor product
Effect of destruction of normal tissue
Effects due to unknown mechanisms

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109
Q

Tumor will often present with ______________ symptoms before being recognized

A

Endocrine

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110
Q

Lambert-Eaton syndrome

A

Immune mediated neurologic syndrome characterized by muscle weakness of the limbs

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111
Q

Subacute cerebellar syndrome

A

Immune mediated degeneration of the cerebellum - dizzyness nausea and vertigo

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112
Q

2 Neurologic paraneoplastic syndromes

A

Lambert Eaton Syndrome and Subacute cerebellar syndrome

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113
Q

Dermatomyositis

A

Seen with Small cell and Non-small cell lung cancers leads to systemic inflammation of muscles and skin

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114
Q

Acanthosis nigricans

A

Thickening of skin with brown discoloration, often see in T2DM, with cancer you will more likely see it on mucous membranes

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115
Q

Neutropenic fever

A

Recurrent temp above 38 or single temp over 38.3 with a neutrophil count under 500 - often a result of chemotherapy

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116
Q

Symptoms of neutropenic fever

A

vague and mild at first but can rapidly progress to sepsis and death

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117
Q

Etiology of neutropenic fever

A

May be from viral, bacterial or fungal agents

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118
Q

PE Workup for a neutropenic fever

A

Thorough physical exam including access sites but NO digital rectal exam

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119
Q

Tx for neutropenic fever
2 Labs
3 Drugs

A

Take cultures, CXR, Labs and start empiric antibiotic therapy
Ceftazidime for Pseudomonas
Aminoglycoside for gram neg
Vancomysin for MRSA

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5
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120
Q

Etiology of oncogenic spinal cord compression
Where does the tumor metastasize to and what are the three mechanisms by which it inflicts damage

A

Cancer metastasizes to the spinal cord resulting in trauma to the spinal cord from edema, hemorrhage, and pressure induced ischemia

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121
Q

Clinical presentation of oncogenic spinal cord compression and 4 things that make it worse

A

Back pain at the level of the tumor with some nerve root/spinal symptoms
Aggravated by lying down, weight bearing, sneezing or coughing

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122
Q

Progression of spinal cord compression symptoms(6)

A

LE weakness
Hyperreflexia
Motor/Sensory loss
Loss of reflexes
Loss of Bowel/Bladder function
Paraplegia

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123
Q

Diagnostic of choice and 3 treatments for oncogenic spinal cord compression

A

MRI to diagnose
High dose IV corticosteroids
Surgical decompression
Radiation

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124
Q

Hallmark of a malignant fracture is that it is _____________________

A

Atraumatic

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125
Q

Three mechanisms of oncogenic hypercalcemia

A

Tumors release osteolytic proteins
Tumors directly break down bone
Increased absorption of calcium from active vitamin D metabolite

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126
Q

MCC of hypercalcemia in cancer patients

A

Parathyroid hormone-related peptide secreted by cancer cells

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127
Q

Mnemonic for hypercalcemia symptoms

A

Bones - remodeling, fracture risk
Stones - Kidney stones
Groans - Abdominal cramping, nausea and constipation
Moans - Lethargy, depression, psychosis

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128
Q

2 EKG signs of hypercalcemia

A

QT and ST depression

129
Q

4 treatments for hypercalcemia

A

Hydration and diuresis
Bisphosphonates
Calcitonin
Hemodialysis

130
Q

Tumor lysis syndrome occurrence and most commonly associated cancer

A

Occurs 1-3 days after radiochemotherapy
Most common in hematologic malignancies, especially Burkitt lymphoma

131
Q

Effects of tumor lysis sundrome

A

Releases large amounts of cell contents such as phosphorus and potassium into the bloodstream, can cause AKI, cardiac arrhythmias or hyperkalemia

132
Q

2 treatments for tumor lysis syndrome

A

IV hydration and electrolyte abnormality correction may require emergency hemodialysis

133
Q

Effect of hyperkalemia on EKG

A

Causes peaked T waves

134
Q

Why do cancer related effusions most often develop

A

Direct involvement of the serous surface with the tumor

135
Q

2 MCC of malignant pericardial of pleural effusions

A

Lung or breast cancer

136
Q

4 MCC of malignant ascites

A

Ovarian, Colorectal, Stomach and Pancreatic cancers

137
Q

3 signs of cardiac tamponade

A

Narrowed pulse pressure, distended neck veins, muffled heart sounds

138
Q

Diagnostic tool of choice and treatment of choice for cardiac tamponade

A

Use a transthoracic echocardiogram to diagnose
Use an echo guided percutaneous pericardiocentesis to treat

139
Q

Superior Vena Cava Syndrome - with MCC

A

Results from direct obstruction of the superior vena cava by malignancies - most commonly caused by bronchogenic carcinoma

140
Q

Physical exam findings for SVC syndrome (3)

A

Nonpitting edema of the neck, tongue and facial swelling, distended neck arm and chest veins

141
Q

Diagnostic tool of choice and 2 treatments for SVC syndrome

A

Chest CT with contrast for diagnosis
Glucocorticoids to decrease inflammatory response to tumor
Stenting chemo and radiation alse effective

142
Q

3 elements of Virchow’s triad

A

Stasis, Vessel Wall Injury, HYpercoagulability

143
Q

How can cancer cause each of the virchow’s triad elements

A

Malignancy causes a hypercoagulable state
Neoplastic cells can cause intimal injury
Obstructive tumors can cause venous stasis

144
Q

5 signs of a cancer related thromboembolic event

A

Low grade fever, tachypnea, tachycardia, pleural rub, unilateral LE swelling

145
Q

2 tools to diagnose thromboembolic events in cancer patients

A

Ventilation perfusion scan
Spiral chest CT with contrast

146
Q

3 therapy options from first line to last resort for cancer related thromboembolic events

A

Anticoagulation with LMW Heparin
Rivaroxaban for 21 days PO
Thrombolytic therapy if there is hemodynamic compromise and RV failure

147
Q

What cancer complication may be the initial finding/complaint in a cancer patient

A

Development of an effusion

148
Q

3 indications for bone marrow aspiration or biopsy

A

Potential for cancer, blood, or bone
marrow disorder, fever of unknown origin, unexplained splenomegaly

149
Q

Contraindication for bone marrow aspiration/biopsy

A

Severe bleeding disorders but NOT low PLT count

150
Q

3 sites to avoid when taking a bone marrow biopsy

A

Infection, injury, excess adipose tissue

151
Q

Preferred and alternate bone marrow biopsy sites

A

Preferred - posterior iliac crest
Alternate - Anterior iliac crest

152
Q

Sites for aspiration only and indications for use

A

Tibia - commonly used for infants under 12 months
Sternum only for 12+ years old and morbidly obese patients

153
Q

Etiology of Acute Lymphoblastic Leukemia (ALL)

A

Originates in a single lymphoblast (lymphocyte progenitor) and often results from a chromosomal translocation

154
Q

4 qualities of A.L.L. mutant lymphoblasts

A

Rapid proliferation
Reduce normal cell proliferation
Don’t differentiate
Resist apoptosis

155
Q

4 places where ALL lymphoblasts accumulate

A

liver, spleen, meninges, and lymph nodes

156
Q

5 risk factors for ALL

A

5% genetic
In utero radiation exposure
Chemicals
High birth weight
Lack of exposure to infections - immune system needs to be activated

157
Q

Epidemiology of ALL

A

Most common ages are under 5 or over 60
More common in caucasians that african americans

158
Q

5 symptoms of ALL

A

Fever of unknown origin, Pancytopenia, Lymphadenopathy, Bone pain (deep and difficult), Painless testicular swelling

159
Q

Leukostasis of ALL with three associated symptoms

A

Too many WBCs cause circulation issues leading to HA, altered mental staus, priapism, etc.

160
Q

4 tests in an initial workup of ALL

A

CBC, CMP, Blood culture if infection is suspected
Imaging depending on symptoms (CXR if pulmonary, MRI/CT if neuro)

161
Q

CBC results suggestive of ALL

A

High percentages of large unstained cells and lymphocytes - all counts and other percentages are low

162
Q

3 items for further workup in ALL

A

Peripheral smear, LDH levels (evidence of tissue destruction), CT Chest with contrast

163
Q

Biggest concern in patients with leukostaisis

A

Brain bleed

164
Q

Why do we want a lumbar puncture in ALL

A

Spinal infiltration of disease will require different chemotherapy

165
Q

2 antigens expressed by ALL cells

A

CD19 and CD10 antigens

166
Q

Definitive diagnosis for ALL

A

Bone marrow aspiration and biopsy with greater than 20% lymphoblasts

167
Q

4 initial treatment steps for an ALL patient

A

Refer to Heme/Onc
Screen for infection if febrile
Induction chemotherapy
CNS prophylaxis

168
Q

Induction chemotherapy

A

Multidrug therapy over the course of 4-6 weeks, goal is to induce remission at 65-85%

169
Q

ALL CNS prophylaxis

A

Intrathecal chemotherapy given through a spinal tap to prevent remission

170
Q

Consolidation/Intensification therapy for ALL

A

For young patients who respond well
Readminister induction regimen or higher after hematopoiesis is restored
4-8 months to increase remission time

171
Q

Maintenance therapy for ALL

A

For young patients who tolerate chemo
Less intensive regimen daily or weekly for 2-3 years

172
Q

ALL therapy for older patients who tolerate chemo less well

A

Allogenic stem cell transplant (from a donor). Once given IV cells with find their way to the bone marrow

173
Q

Apheresis

A

Removal and replacement of blood that includes removing an element of it along the way
Plasmapheresis removes plasma
Leukopheresis removes WBCs

174
Q

Cure rate and recurrence of ALL

A

Cure: 90% in children 50% in adults
Recurrence is usually within the first two years

175
Q

4 criteria for poor ALL prognosis

A

Chromosomal abnormalities
Age over 60
WBC count over 100,000
Failure to achieve remission in 2 weeks of therapy

176
Q

Normal WBC count

A

4,500-11,000 per microliter

177
Q

Chronic Lymphocytic Leukemia

A

Malignant lymphoid neoplasm characterized by the accumulation of long lived, functionally incompetent, mature B cells

178
Q

Epidemiology of CLL

A

Most common form of leukemia, 90% of cases occur after age 50

179
Q

4 clinical symptoms of CLL

A

Lymphadenopathy, recurrent infections, hepatosplenomegaly, anemia/thrombocytopenia

180
Q

CBC findings for CLL

A

WBC over 20,000 with isolated absolute lymphocytosis may have decreased RBC and platelets

181
Q

Peripheral smear findings for CLL

A

Many lymphocytes with some smudge cells and possibly prolymphocytes

182
Q

5 stages of CLL

A

Low Risk
0 - Lymphocytes over 15,000 and 40%
Intermediate Risk
I - Enlarged nodes in any site
II - Hepatomegaly or splenomegaly
High Risk
III - Anemia
IV - Thrombocytopenia

183
Q

Treatment for low risk CLL

A

Observe and treat when symptoms appear

184
Q

Treatment for high or intermediate risk CLL (3 options)

A

Chemo and growth factors to decrease post-chemo neutropenia
Allogenic stem cell transplant - reserved for chemo failure and not suited to elderly patients
Splenectomy for refractory splenomegaly and ppancytopenia

185
Q

Obstructive lymphadenopathy

A

Enlarged lymph nodes compress internal organs

186
Q

4 complications of CLL

A

Obstructive lymphadenopathy
Transformation into aggressive large cell lymphoma
Autoimmune hemolytic anemia
Thrombocytopenia

187
Q

Prognosis for CLL

A

Low risk - 10-15 years
Intermediate/High risk - 90% survive 2 years 70% survive 5 years

188
Q

Acute myelogenous leukemia

A

Results from an arrest in the early development of myeloid precursors
Rapid proliferation of myeloblasts with no differentiation

189
Q

Progeny of a myeloblast

A

Non-lymphocyte WBCs
(Granulocytes and Monocytes)

190
Q

Pathogenesis of AML

A

Chromosomal translocation and other genetic mutations

191
Q

Most common risk factor for AML and 3 other risk factors

A

Myelodysplastic syndrome

Down’s syndrome
Environmental exposure
Chemotherapeutic agents

192
Q

Median age of onset for AML

A

70 years

193
Q

Auer rod

A

Eosinophilic, needle like inclusion in the cytoplasm of myeloblasts - confirmatory for AML

194
Q

CBC findings for AML

A

Decreased RBC, Platelet, Neutrophil - WBC may be normal, high, or low

195
Q

If you don’t see any Auer rods in a peripheral smear, how else can you confirm AML

A

Using flow cytometry to differentiate between myeloid and lymphoid antigens on cell surfaces

196
Q

How might a CMP be useful for cancer assessment

A

Look at Liver and Kidney function

197
Q

How might blood cultures be useful in a cancer workup

A

look for signs of infection

198
Q

How might a lactate dehydrogenase level be useful in a cancer workup

A

Shows increase in tissue destruction

199
Q

What are we looking for in a bone marrow biopsy for AML

A

Predominant blasts

200
Q

Lumbar puncture for AML

A

Only if there are symptoms - CNS infiltration is rare

201
Q

Autologous stem cell transplant

A

Uses patients own cells removed and then replaced after therapy

202
Q

Treatment for AML

A

Induction chemotherapy (induces remission in 80-90% of patients under 60 and 50-60% of patients over 60)
Post remission chemo or stem cell replacement (allogenic preferred)

203
Q

Chronic Myeloid Leukemia (CML)

A

Dysregulated production and uncontrolled proliferation of mature and maturing granulocytes

204
Q

Hallmark of CML

A

Translocation between 9 and 22 known as the philadelphia chromosome

205
Q

Average age of onset for CML

A

55 years old, may be brought on by ionizing radiation exposure

206
Q

3 phases of CML

A

Chronic phase (3-5 years) - WBCs differentiate (usually detected in this stage
Accelerated Phase
Terminal phase - Fatal blast crisis

207
Q

5 clinical presentations of CML

A

Fatigue/weight loss
Low grade fever/night sweats
Hepatosplenomegaly
Bone tenderness
Allergy-like symptoms due to basophil overproduction (flushing, pruritis, etc.)

Symptoms get worse in accelerated phase

208
Q

CBC findings for CML

A

Average white count with granulocytosis in the chronic phase and decrease in PLT and RBC with myeloblasts in the accelerated phase

209
Q

Leukocyte Alkaline Phosphatase

A

Marker for WBC destruction

210
Q

Leukocyte alkaline phosphatase level in CML

A

Low due to granulocyte resistance to Apoptosis

211
Q

Symptoms of leukostasis

A

Usually neurologic symptoms

212
Q

Percentage of blasts in the blast stage of CML

A

Over 20%

213
Q

3 tissues that secrete alkaline phosphatase

A

Liver, Stomach and Bone

214
Q

Test to identify philadelphia chromosome

A

PCR for bcr/abl DNA segment

215
Q

Therapy for chronic phase CML

A

Single drug chemotherapy using a tyrosine kinase inhibitor - cancer cells are often “addicted” to this gene

216
Q

Hematologic remission of CML

A

Often within 3 months
Normal CBC

217
Q

Cytogenic remission of CML

A

Seen in 3-6 months, normal fromosome returns with less than 10% of cells testing positive for Philadelphia chromosome

218
Q

Molecular remission of CML

A

Negative PCR for the bcr/abl mRNA

219
Q

How long should therapy be continued for CML after molecular remission

A

2 years

220
Q

Therapy for CML accelerated or blast phase

A

Tyrosine kinase inhibitor AND multidrug chemotherapy
Stem cell transplant may also be considered, especially if resistant to TKI

221
Q

Multiple myeloma

A

A neoplastic proliferation of plasma cells that produce nonfunctional immunoglobulins

222
Q

Preceding condition to multiple myeloma

A

MGUS - Monoclonal Gammopathy of Undetermined Significance - results from abnormal plasma cell response to antigenic stimulation

223
Q

Epidemiology of Multiple Myeloma

A

Median onset is 65 years
Occurs more in men
occurs most in african americans

224
Q

5 pathophysiologic aspects of Multiple Myeloma

A

Diminished hematopoiesis due to overgrowth of plasma cells
Lack of adequate response to infection because neoplastic plasma cells are monoclonal
Increase in Osteoclastic activity, bone tumor formation and hypercalcemia
Myeloma proteins are an antibody secreted by plasma cells that harms organs
Infiltration of tissues leads to plasmocytomas

225
Q

3 skeletal presentations of multiple myeloma starting with MC

A

Bone pain in weight bearing back hips and ribs
Spinal cord compression
Pathologic fracture

226
Q

RBC rouleaux formation

A

RBCs form into strings - a result of increased fibrin from multiple myeloma

227
Q

4 Proteins we look for in MM and their significance

A

Paraprotein (M-protein) found via serum protein electrophoresis
Bence Jones protein found via 24 hout urine collection with urine protein electrophoresis
Low levels of non-myelomatous Ig
Beta-2 microglobulin DIRECTLY related to tumor burden

228
Q

Imaging for MM (3)
X ray CT MRI

A

X-rays for pathologic fracture (Skull, spine, and long bones)
CT for neoplastic bone disease
Spine MRI for spinal nerve compression

229
Q

Treatment for MM

A

Disease is uncurable but we can prolong life and improve symptoms
Triple agent chemotherapy
Stem cell transplant for young patients
Palliative, localized radtiation

230
Q

Treatment for MM pathologic fractures

A

Stabilize the bone and irradiate the lesion

231
Q

Treatment for MM vertebral body collapse

A

Vertebroplasty or Kyphoplasty - consult orthopedics

232
Q

3 treatments for spinal cord compression in MM

A

IV steroids, Radiation, Consult neurosurgery

233
Q

Prognosis for MM

A

median is 3 years to live - better for younger patients

234
Q

What happens to lymph nodes as we age?

A

They grow until about 12 years and then begin to atrophy

235
Q

Normal lymph node sizes in children for 3 nodes

A

Anterior cervical less than 2 cm
Axillary less than 1 cm
Inguinal less than 1.5 cm

236
Q

Normal lymph node size in adults

A

Less than 1 cm at any location

237
Q

5 characteristics of a lymph node that need to be documented

A

Size: 2 numbers (ie. 1.5x1)
Location: Examine all locations
Consistency: Hard, firm, rubbery, soft
Tenderness
Fixation: Is it mobile

238
Q

What does a swollen NON tender lymph node indicate

A

Malignancy instead of infection

239
Q

What do we mean if we say that lymph nodes are “matted”

A

They are stuck to each other

240
Q

What do hard nodes indicate?

A

Fibrotic cancers

241
Q

What do firm/rubbery nodes indicate?

A

Lymphomas/ chronic leukemia

242
Q

What do softer nodes indicate

A

Acute leukemia or inflammation

243
Q

Lymphadenopathy management in children

A

Clindamycin in high MRSA areas
Cefalexin or Augmentin in low MRSA areas
Add azithromycin for cat scratches

244
Q

Lymphadenopathy management in children

A

Workup to rule out malignancy and refer for node biopsy if needed

245
Q

Non-hodgkin lymphoma

A

Overgrowth of lymphocytes or their precursor in the lymphatic tissue - MC B cells 85%

246
Q

5 Etiologies for Non-hodgkin lymphoma

A

Chromosomal translocations, Infection, Environmental factors, Immunodeficiency status, Chronic inflammation

247
Q

Epidemiology of Non-Hodgkin lymphoma

A

Average age of onset 50 to 60 years old
Caucasians are most likely to get
Slightly more common in males

248
Q

Two types of non-hodgkin clinical presentation

A

Indolent - Slow gorwing
Aggressive - Fast growing

249
Q

Clinical presentation of indolent non-hodgkin lymphoma

A

Painless and slow growing lymphadenopathy, nodes may grow and then regress. Hepatosplenomegaly and cytopenias

250
Q

B symptoms

A

Systemic symptoms seen with a cancer (A symptoms indicates a lack of systemic symptoms)

251
Q

Clinical presentation of aggressive non-hodgkin lymphadenopathy (3)

A

Fast gowing and painless but may compress other structures such as the SVC. Systemic “B” symptoms also occur. Hepatosplenomegaly

252
Q

CBC and peripheral smear findings for non hodgkin lymphoma

A

CBC normal until infiltration of the bone marrow causes pancytopenia
Smear normal

253
Q

CMP and LDH levels with non-hodgkin lymphoma

A

Increased BUN/Creatinine with hydronephrosis
Increased LFT with hepatic involvement
Increased alkaline phosphatase with bone/liver involvement
Increased LDH with serious disease

254
Q

Imaging for non-hodgkin lymphoma

A

CXR for mediastinal mass/nodes
CT with contrast to evaluate lymph node involvement

255
Q

Diagnostic test for non-hodgkin lymphoma and its indication

A

Excisional lymph nod biopsy indicated by a node greater than 2.25cm squared or 2 cm in a single diameter
Biopsy of a peripheral node is preferred

256
Q

Bone marrow biopsy for non-hodgkin lymphoma

A

Must be bilateral due to patchy nature of the disease

257
Q

Three viruses we want to check for in non-hodgkin lymphoma

A

HIV, HCV, HBV

258
Q

Where do we need to CT scan for non-hodgkin lymphoma

A

Neck to Peolvis so that we can see what areas are involved

259
Q

Tests required to make an Ann arbor stage determination for non-hodgkin lymphoma

A

PET or CT of chest abdomen and pelvis and bilateral bone marrow biopsy

260
Q

Ann arbor staging for Lymphoma

A

I - Only one tumor
II - More than one tumopr but all on the same side of the diaphragm
III - Tumors on both sides of the diaphragm
IV Disseminated tumors - an extralymphatic organ without the associated node

261
Q

Letters used in ann arbor stage classifications

A

Represent organs and areas of the body - ie. E for extralymphatic site
B is for systemic symptoms

262
Q

Treatment for indolent Non-hodgkin lymphoma

A

Incurable if disseminated at time of diagnosis, treatment consists of chemotherapy and is only recommended for symptomatic patients

263
Q

Prognosis for indolent non-hodgkin lymphoma

A

10-15 years after diagnosis

264
Q

Treatment for aggressive non-hodgkin lymphoma

A

Chemotherapy with or without local radiation therapy, stem cell transplant

265
Q

4 poor prognostic factors for aggressive non-hodgkin lymphoma

A

Age over 60
Increased LDH
Poor response to standard therapy
Ann arbor stages 3 or 4

266
Q

Hodgkin Lymphoma

A

A malignancy of B lymphocytes within the lymph tissue characterized by the presence of Reed-Sternberg cells

267
Q

Reed Sternberg cells

A

Large abnormal lymphocytes that may contain more than one nucleus

268
Q

Two viral triggers for Hodgkin Lymphoma

A

Epstein Barr Virus
HIV

269
Q

2 Peaks for occurrence of hodgkin lymphoma
Gender and racial tendencies

A

Around 20 and around 50
More common in males, caucasians, and African Americans

270
Q

Presentation of Hodgkin lymphoma

A

Painless swollen lymph node with migration to other nodes in a contiguous pattern
B symptoms - fever, night sweats, etc.

271
Q

4 potential signs of Hodgkin lymphoma (not always present

A

Generalized pruritis
HSM
Mediastinal mass
Pain in swollen nodes with alcohol consumption

272
Q

Diagnostic test for Hodgkin lymphoma

A

Lymph node excisional biopsy - look for Reed-Sternberg cells

273
Q

Bulk

A

Lymph node over 10cm or mediastinal mass over 1/3 thoracic diameter

274
Q

Treatment for hodgkin lymphoma

A

Multidrug chemotherapy with possible radiation for stages 1 and non-bulky 2
Consider high dose chemo and stem cell transplant for relapse

275
Q

Prognosis and age risk factor cuttoff for Hodgkin lymphoma

A

Poor prognostics after age 45
90% survive ten years with I or non-bulky II
50-60% for later stages

276
Q

Gene mutation leading to polycythemia vera

A

JAK2

277
Q

Peak incidence age for polycythemia vera

A

50-70

278
Q

Three main consequences of Polycythemia Vera

A

Increased blood viscosity
Pruritis from basophilia that gets worse after a warm shower of bath
Bleeding from platelet dyfunction

279
Q

3 symptoms caused by increased blood viscosity

A

HA
Vertigo
Intermittent claudication

280
Q

One thing thought to trigger polycythemia vera

A

ionizing radiation

281
Q

Plethora

A

Reddish uneven complexion of the face, palms, nail beds and mucosa due to an excess of blood

282
Q

Confirmatory tests for polycythemia vera

A

Erythropoietin level - should be low
Genetic testing for JAK2 mutation

283
Q

Normal HCT for men and women with Polycythemia Vera

A

54% for males
51% for females
HCT will be high with very low EPO

284
Q

mL in 1 unit of blood

A

500mL

285
Q

Goal of therapeutic phlebotomy in polycythemia vera

A

Reduce HCT to under 45

286
Q

How much does removal of 1 unit of blood reduce a patient’s hematocrit

A

By 3%

287
Q

3 lifestyle modifications for polycythemia vera patients

A

Stop smoking
Manage CV risk factors
Manage hypoxic conditions such as COPD

288
Q

Treatment plan for polycythemia vera

A

Remove 1 unit of blood per week until the patient’s HCT is below 45%
Administer aspirin if not contrindicated by blood loss

289
Q

Iron replacement for polycythemia vera patients

A

DO NOT GIVE IRON

290
Q

2 medications for polycythemia vera

A

Hydroxyurea - suppresses bone marrow contraindicated in pregnancy
Ruxolitinib - Suppresses JAK1/JAK2 - Indicated for failure of phlebotomy can cause myelofibrosis and splenomegaly

291
Q

Low risk PV patients

A

Under 60 with no known hx of thromboembolism

292
Q

Therapy for low risk PV patients

A

Phlebotomy, ASA, and lifestyle modifications - only use cytoreductive therapy if treatment is not successful or tolerated

293
Q

Therapy for high risk PV patients

A

Phlebotomy, ASA, Lifestyle modifications, and Hydroxyurea

294
Q

MC cause of death and 1 other potential complication from polycythemia vera

A

MCC of death = Thrombosis
Myelofibrosis is also a complication

295
Q

Essential Thrombocytosis

A

Disorder of increased megakaryocyte production

296
Q

3 genetic mutations that cause essential thrombocytosis

A

MC is JAK2
CALR - Calrectulin
MPL - Myoproliferative Leukemia virus oncogene

297
Q

Average age for dx of essential thrombocytosis

A

50-60

298
Q

5 symptoms of essential thrombocytosis

A

Thrombosis (DVT or Mesenteric)
Headache
Transient Ischemic attacks (dizziness etc.
Bleeding
Microvascular occlusion leading to pain

299
Q

CBC and peripheral smear for ET

A

elevated PLT can be as much as 2million with large platelets

300
Q

3 factors the increase the risk of thrombosis in ET

A

Over 60 years old
hx of thrombosis
JAK2 mutation

301
Q

High risk ET

A

Hx of thrombosis and or over 60 with JAK2 mutation

302
Q

Intermediate risk ET

A

Over 60 w/o JAK2 or Hx of thrombosis

303
Q

Low risk ET

A

Under 60 with JAK2 and no thrombosis hx

304
Q

Very low risk ET

A

Under sixty, no JAK2 and no hx of thrombosis

305
Q

Management of low risk or very low risk ET

A

Observation and ASA 81mg daily - NO NSAIDs

306
Q

Management of Intermediate and High risk ET

A

Administer Hydroxyurea with a target PLT of 100-400k

307
Q

Prognosis for ET

A

Over 15 years with adequate treatment

308
Q

4 potential etiologies for secondary erythrocytosis

A

Tissue hypoxia
Decreased renal perfusion
EPO secreting tumors
Testosterone administration

309
Q

One symptom that differentiate secondary erythrocytosis from PV

A

No splenomegaly is present in SE

310
Q

4 symptoms of potential secondary erythrocytosis

A

Low arterial oxygen
HA and lethargy
Clubbing of fingers
Ruddy complexion

311
Q

Acrocyanosis

A

Hypoxia of the extremities turning them blue

312
Q

Reactive thrombocytosis

A

An elevated PLT that is secondary to another disorder

313
Q

2 main causes of increased megakaryocyte proliferation and maturation

A

Inflammatory cytokines or stimulation of RBC progenitors

314
Q

3 conditions that can cause inflammatory cytokine release and therefore RT

A

Infection
Chronic inflammation
Malignancy

315
Q

3 conditions that can cause stimulation of RBC progenitors

A

Hemorrhage, iron deficiency, hemolysis

316
Q

3 main causes of RT

A

Increased megakaryocyte proliferation and maturation
Accelerated PLT release
Reduced platelet turnover from asplenia

317
Q

3 symptoms each associated with a malignancy, inflammation, and bleeding

A

Inflammation - Pain, Swelling, Redness
Malignancy - Fever and weight loss, night sweats
Bleeding - Anemia, Fatigue, Visible blood

318
Q

4 Lab workups for ET if you suspect an inflammatory condition

A

Erythrocyte sed rate
C reactive protein
Antinuclear antibody
Rheumatoid factor

Heme/Onc/Endo (5 decks)

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