Lecture 9: Hematology/Oncology Flashcards

1
Q

Difference b/t ALL and AML (acute leukemia)

- prevalaence + peak ages

A

ALL

  • MC (ALL kids have ALL)
  • peak 2-4 yrs

AML

  • less common
  • peak: < 2 yrs
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2
Q

What d/o incr your risk of acute leukemia

A
  1. imunodefic syndromes
  2. DNA repair/Repair Syn
  3. Down Syndrome
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3
Q

Lung, skin, and GI organ s/s of Acute Leukemia

A

Lung –> SOB

Skin –> easy bleeding/bruising, petechiae

GI organs enlarged (liver/spleen)

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4
Q

3 Main things seen on labs a/w Acute Leuknemia

What are these things d/t?
Which 2 most commonly seen on labs

A
  1. Anemia (Normocytic, normochromic)
  2. Neutropenia
  3. Thrombocytopenia
    - most have 2+3

blast cell proliferation in bone marrow –> decr production og RBCs, WBCs, Plts

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5
Q

What may be seen on PBS that is a/w Acute Leuknemia?

Seen on Tumor Lysis labs?

Seen on XR?

A

+/- circulating blast cells

incr K, Ca, P, LDH, Uric acid, Cr (d/t breakdown of leukemia cells)

+/- pleural effusions, mediastinal mass

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6
Q

What is used to determine type of leukemia/Tx? how?

A

Flow Cytometry determine type of leukemia/Tx by biological markers

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7
Q

Difference b/t Tx of ALL and AML (intensity, bone marrow transplant)

Which type is remission more common in? relapse?

A

ALL

  • less intensive induction
  • b. marrow transplant = rare
  • remission more common

AML

  • more intensive + toxic
  • b. marrow transplant = common
  • RELAPSE more common
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8
Q
  1. GH defic
  2. HL
  3. Heart damage
  4. 2nd CAs
  5. Abn bone/muscle growth
  6. infertility
  7. Cognitive defects
  8. Psych issues
  9. Low thyroid fxn
  10. Reduced lung fxn
  11. Obesity/metabolic Syn
A

Late effects of childhood CA

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9
Q

What type of lymphoma is MC?

Which is curable in most?

A

MC = NHL

Hodgkin’s Lymphoma = curable in most most

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10
Q

Difference in presentations b/t HL and NHL?

A

HL

  • central/mediastinal LNs
  • Reed Sternburg cells

NHL

  • peripheral LNs
  • Starry Sky histology
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11
Q

What is the MC S/s for brain tumors?

combo of what 2 Sxs together = more reliable for Brain tumor

Other s/s:

  1. N/V
  2. Visual Field defecit
  3. Endocrine dysfx
  4. seizure, gait abn
A

HA

HA + Neuro Sxs = more reliable for Brain tumor

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12
Q

Main imaging modality of choice for brain tumors

What would suggest marrow infiltration

Tx = surg, radiation, chemo

Do infants have good or poor prognosis?

A

MRI = best for brain tumors

bone pain or abn CBC suggests marrow infiltration

infancy = poor prognosis w/brain tumors

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13
Q

Where does neuroblastoma arise from

A

primitive neuroblasts in neural crest tissue

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14
Q

How does presentation of neuroblastoma differ before and after age 1?

A

< 1

  • tumors above diaphragm/localized
  • better prognosis

> 1

  • MC = tumor in abd
  • most has widespread dz
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15
Q

What can be seen on plain films w/neuroblastoma?

What labs are usu elevated in most pts?

A

Stripped calcifications on XR

Elevated urinary catecholamines in most pts

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16
Q

Tx of neuroblastoma:

  • low risk
  • intermed
  • high
A
  • low risk –> surgery
  • intermed –> surgery + chemo
  • high –> multimodal
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17
Q

Where is Wilm’s tumor located? MC age range? more commonly unilateral or bilateral?

A

tumor in kidneys

MC b/t 1-5 y/o

More commonly unilateral

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18
Q

MC presentation of Wilm’s tumor

Others:

  1. HTN
  2. Gross hematuria
  3. Fever
A

Asx (not painful) abd mass

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19
Q

describe constipation in Wilm’s tumor and whats seen on XR

Common lab finding?

Tx = multimodal
how long to f/u? why?

A

constipation

  • doesnt resolve w/tx
  • on XR = “shifting bowel”

Anemia

F/u for 8 yrs –> look for spread to other kidney

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20
Q

Where is osteosarcoma MC common? more specific?

age group most common in?

MC Sxs

Labs?

What is required for Dx?

A

MC at metaphysis of long bones (area of bone growth)
- distal femur = MC

MC in adolescence

Sx = Pain

HIGH AlkP + LDH

Need Bx for Dx

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21
Q

Imaging of Osetosarcoma:
- what is characteristically see on XR

  • what imaging is used for looking for METs? MC sites?
A

XR –> sunburst rxn

MRI –>look for METS
- MC in lungs, other bones

22
Q

Why is radation therapy not used for osteosarcoma?

What are the 2 surgical Tx options?

A

radiation wont work b/c osteosarcoma tumors are radioresistant

Surgery

  1. amputation
  2. limb sparing w/prosthesis
23
Q

What is cause of Retinoblastoma? result?

More commonly uni or bilateral?

MC before what age

A

Heritable mutation/deletion of RB1 tumor suppressor gene –> uncontrolled tissue growth in eye

More commonly bilateral

MC before age 2

24
Q

Main Sign of Retinoblastoma?
- meaning of sign?

3 other signs?

A

Main sign = leukocoria
- absent red reflex

  1. Strabismus
  2. Proptosis
  3. Neuro Sxs
25
Q

3 Tx option for Retinoblastoma?

A
  1. Radiation
  2. Chemo
  3. *Enucleation
26
Q

When is retic count high?

When is the retic count low?

A

High retics w/incr RBC destruction

Low retics w/RBC production problem

27
Q

MCV (mean cell/corpuscular volume) stands for?

How is MCV in newborns? why?

How to calculate norm MCV in young kids

A

MCV (mean cell/corpuscular volume) = avg size of the RBCs

MCV is high in newborns d/t fetal Hb –> decr over couple months

upper limit of norm MCV in kids = 70 + age

28
Q

incr RBC destruction:

  1. Hemoglobinopathies
  2. RBC membrane defects
  3. Enzyme Defects
  4. immune mediated

examples

A
  1. ..
  2. RBC membrane defects= Speherocytosis, Elliptocytosis, Pyropoikilocytosis
  3. Enzyme Defects = G6PD or Pyruvate Kinase Defic
29
Q

Pt has unconjugated hyperbilirubinemia, + DAT/coombs test and + maternal Ab screening and hemolysis on PBS (incr retics, macrocytosis, polychromasia) What is Dx?

A

Immune mediated Hemolytic Dz

30
Q

If D antigen is present on surface of RBCs what does that tell you about the pt?

A

Pt is Rh+

31
Q

in Anti-Rhesus (Rh) Dz what causes hemolytic anemia in the neonate/newborn

A

Maternal sensitization

32
Q

What occurs during maternal sensitization

Why is not a problem in the pregnancy that the sensitization occurs in?

When is most maternal sensitization? Other time can occur?

A

small amts of FETAL blood transferred to MOTHER across placenta during pregnancy –> mother forms IgM Abs
- not a problem b/c IgM Abs dont cross placenta –> baby not infected

most in 3rd trimester
- also during delivery (incr amt of fetal blood exposed to mother)

33
Q

Why are babies of subsequent pregnancies at risk for Rh-Dz? result?

A

IgG Abs produced by mother –> can cross placenta –> Hemolytic Dz of the Newborn

34
Q

What is the fetal response to maternal sensitization in susequent pregnancies? (3)

A
  1. Fetal RBC’s get coated w/maternal IgG –> erythroblastosis –> destruction of fetal RBCs
  2. Anemia –> stim erythropoiesis
  3. Extramed erythropoiesis–> HSM
35
Q

How to prevent Rh-Dz and immune mediated hemolytic dz of newborn?

A

GIVE ALL Rh (-) women Rhogam

- anti-D immunoglobulin

36
Q

When is Rhogam given to Rh (-) women? (2 instances)

How does it work to prevent immune mediated hemolytic dz?

A
  1. at 28 and 34 wks gestation
  2. Postpartum if baby is Rh+

Fetal blood crosses placenta to mother–> Ab attaches to infant blood
- mother’s body destroys Ab-coated RBCs before she creates Abs to it

37
Q

A women comes in who has had a previous maternal sensitization but not given rhogam during that pregnancy and now has Rh Abs. She is pregnant again, can you give her Rhogam? why y/n?

A

No

- Rhogam can only be given if mother doesnt have Abs

38
Q

What is the predominant feature of Hemolytic Dz of newborn/ABO compatability….?

A

Hyperbilirubinemia in first 12

to 24 hours of life

39
Q

How does ABO incompatibility differ from Rh-Dz?

A

No prior exposure is needed w/ABO incompatability

- body automatically makes Abs to what you dont have

40
Q

Two ways to manage hemolytic Dz of the Newborn, what are they aimed at preventing?

A
  1. Antepartum therapy
    - prevent Hydrops Fetalis
    ( > 2 abn fetal fluid collections)
  2. Postpartum therapy
    - prevent kernicterus
    (acute bilirubin encephalopathy)
41
Q

How to prevent Hydrops Fetalis w/ antepartum therapy (2)

A
  1. Intrauterine transfusion

2. Early delivery

42
Q

Elevated lab findings in Iron Deficiency Anemia?

A

TIBC, transferrin

everything else is LOW
Ferritin, MCV, Hb, MCH, MCHC, retics, RBCs

43
Q

MC cause of Fe defic in toddlers? what is this d/t?

A

inadequate dietary intake of iron

- d/t excessive cow’s milk intake

44
Q

2 Tx options for Iron deficiency anemia?

Other edu/Tx?

How long to treat?

A
  1. Liquid preps - elemental iron
  2. Polysaccharides prep - Niferex, Nu-Iron

Edu –> NO MILK, incr dietary iron

Tx til iron labs normalize then 2-3 mo after to replete stores

45
Q

3 main causes of bleeding d/o and their assoc tests?

A
  1. Vasoconstriction problems
    - no testing for
  2. Primary hemostasis problems
    - plt count/aggreg, vWF studies
  3. Secondary hemostasis problems
    - PT/PTT, fibrinogen
46
Q

4 common Sxs of Bleeding d/o?

Others:

  • hematemesis
  • melena
  • hematuria
  • hemoptysis
A
  1. Bruises
  2. Petechiae
  3. Bleeding
  4. Deep muscle + joint bleeding
47
Q

Pt presents w/ bleeding from large vessels, subQ hematoma, Hemarthosis, Intramuscular hematoma. What type of bleeding is this?

A

Secondary Hemostasis bleeding

48
Q

Presentation of Hemophilia in peds pts (5)?

A
  1. Bleeding from circumcision
  2. Prolonged bleeding w/heel stick
  3. multiple, raised palpable bruises
  4. Bleeding from IM inj
  5. Swollen tender jionts after minor injury
49
Q

What is peds palliative care

A

interdisciplinary approach w/with curative, restorative and life prolonging Tx

50
Q

What 3 things does peds palliatvie care focus

A
  1. relieve suffering
  2. slow dz progression
  3. Improve QoL