Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Child Health > Oncology & Haematology > Flashcards

Oncology & Haematology Flashcards

1
Q

List the possible features of Acute Lymphoblastic Leukaemia (regarding infiltration sites) (10)

A

General: Malaise + Anorexia

Marrow infiltration:
Thrombocytopenia (bruising, petechiae)
Neutropenia (infection)
Anaemia (lethargy)
Bone pain

Reticulo-endothelial infiltration:
Hepatosplenomegaly
Lymphadenopathy

Other organ infiltration:
Testes enlargement
CNS (palsies, headache, vomiting)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the peak age of ALL presentation?

A

Can occur all ages but peak age 2-5y/o

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What Ix can be done in ALL? (3)

A

FBC - abnormal
Bone marrow biopsy (confirm Dx + grade)
CXR (id mediastinal masses = T-cell disease)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the diff tumour cell types in ALL? (3)

How does the type affect Tx approach?

A

L1 - small uniform cells
L2 - large varied cells
L3 - large varied cells with vacuoles

T-cell → cyclophosphamide + intense asparaginase Tx
Mature B-cell → treat like lymphoma (short-term intensive + high dose MTX)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 5 general regimes / steps in treating ALL?

Ray Is the Crazy Cancer Teacher

A

Remission induction
Intensification (to consolidate remission)
CNS (intrathecal chemo)
Continuing therapy (PCP prophylaxis)
Treatment of relapse (high dose chemo, total body irradiation + marrow transplant)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the main prognostic factors in ALL (7)

A

Gender: male
Age: <1 or >10
Tumour load (measured by WBC)
Spread: CNS involvement worse
Cytogenetic abnormalities in tumour cells
Speed of response to initial chemo
Minimal residual disease assessment (high submicroscopic levels leukaemia on PCR)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the haematological differences b/wn fetal/neonatal and adult blood? (4)

A

Fetus haemopoiesis in liver → bone marrow
HbF (2a2y - higher O2 aft) → HbA (2a2B) by 1yr old
Hb: high (14-21 compensates for low O2 conc) → low (10 RBC production)
WCC in neonates higher than in older children
Platelet counts sim to adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the main complications of ALL treatment? (4)

A

Neutropenic sepsis
Hyperuricaemia (tumour lysis syndrome - give allopurinol)
Poor growth
CNS infiltration / relapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

In anaemia, what are some causes of:
Microcytic (2)
Macrocytic (3)
Normocytic (2)

A

MCV < 70 : Fe defc anaemia, Thalassaemia
MCV > 100 : Folate defc, B12 defc, Haemolysis
MCV 80-100 (normal): Haemolysis, Marrow failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the causes of Fe defc anaemia in children?

A

Inadequate intake
Malabsorption
(Common in infants as require more + more to accompany blood volume growth)
(Can develop due to delayed weaning >6m)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What dietary advice can be given to prevent Fe defc anaemia? (5)

A 
Avoid cow's milk if <1yr
If formula-fed - iron fortified
If breast fed - wean at 4-6m
Adequate Vit C intake
Iron supplements (if premature)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

At what Hb do symptoms of Fe defc anaemia appear?

What are the features of Fe defc anaemia? (4)

A

Tires easily
Feeds slower than usual
Pallor (conjunctiva / tongue/ palmar)
Pica (eating dirt)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What should be Ix if normal dietary changes / supplements don’t improve a child’s Fe defc anaemia? (2)

A

Malabsorption (coeliac)

Bleeding (oesophagitis, Meckel’s diverticulum)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is usually the cause of haemolysis in neonates?(1) + in children? (3)

A

Neonates - autoimmune haemolytic anaemia

Children - RBC membrane/enzyme disorders (hereditary spherocytosis, G6PD defc, PK defc), haemoglobinopathies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the features of haemolytic anaemia (5)

A 
Jaundice (raised unconj bili + urobili)
Gallstones (raised bill)
Anaemia
Hepatosplenomegaly (reticulo-endothelial hyperplasia)
May present with aplastic crisis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What Ix can be done for haemolytic anaemia?

What Tx?

A

Ix - blood film, Coombs test (+ve in autoimmune)

Tx - folate supplements (mild), splenectomy (severe)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the incidence of hereditary spherocytosis?
What is the pathophysiology?
What can trigger severe anaemia due to HS?

A

1 in 5000 (3 dominant: 1 spontaneous)
Defective RBC skeletal prots → RBC loses some memb + becomes spheroidal as passes thru spleen + destroyed

Parovirus 19 can → severe anaemia (aplastic crisis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does G6PD defc present? (4)

A

Neonatal jaundice - 1st 3/7 OR precipitated by infection/drugs/broad beans

Fever
Malaise
Haemoglobinuria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is G6PD defc?

A

Common RBC disorder
X-linked
High prevalence in central Africa
G6PD stops oxidative damage to cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is Pyruvate Kinase (PK) defc?

A

2nd commonest cause haemolytic anaemia

Due to lack of glycolysis enzyme → decrease in ATP → cell becomes rigid → spleen destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What mutation has occurred in sickle cell anaemia?

What ethnicities is it commoner in?

A

Point mutation = glutamine → valine

Common in Afro-Caribbean / black

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the 4 types of sickle cell disease / trait? (+their Hb status)

A

Sickle cell anaemia - HbSS (homozygous) mutation in both B-globin genes → some HbF + no HbA

HbSC (HbB = diff point mutation in B-globin → no normal B-globin genes → no HbA)

Sickle B-thalassaemia → no normal B-globin (sim symps to HbSS)

Sickle trait → 60% blood HbA (40%HbS) → asymp (only ID by blood test)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How does HbS end up causing symptoms?

A

HbS → sickle shaped RBCs
→ Have reduced life span
→ Can trap in microcirculation → vessel occlusion + ischaemia in organ/bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the features of sickle cell disease (6)

A

Painful (vaso-occlusive) crises
Splenomegaly - in younger
Infection susceptibility to pnuemococci/HiB (hyposplenism from micro infarcts)
Priapism (erection) - treat asap or later erec dysfunc
Anaemia: moderate or acute (sudden drop)
Clinical jaundice (from haemolysis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are some of the causes of acute anaemia in sickle cell disease? (3)

A

Haemolytic (infection)
Aplastic (parovirus)
Sequestration (sudden hepatosplenomegaly, abdo pain + circ collapse)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

List the long-term complications of sickle cell disease (9)

A

Short stature
Gallstones

Heart failure (from uncorrected anaemia)
Cardiomegaly (chronic anaemia)
Adenotonsilalr hypertrophy
Renal dysfunc
Leg ulcers
Stroke/cognitive probs
Educational/behav probs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are some of the triggers of a sickle cell crisis? (5)

A 
Cold
Stress
XS exercise
Infection
Hypoxia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How is a sickle cell crisis managed?

What are the other aspects of management in sickle cell anaemia? (3)

A

Crises: analgesia + maintain good hydration + O2

Prophylaxis: full imms + penicillin throughout childhood
Folic acid (due to increased demand)
Avoiding crises triggers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What ethnicity is a-thalassaemia major mostly seen in?

What are the features (of major)?

A

SE Asian

Fetal hydrops in 2ndT (fetal anaemia → oedema + ascites)
3 deletions → mild/mod anaemia
2 deletions → asymp

30
Q

What are the 2 main types of B-thalassaemia? What are their Hb status?

A

B-thalassaemia major - abnorm B-globin gene/production
→ HbA not produced

B-thalassaemia intermedia - B-globin mutations
→ little HbA + lots HbF (milder/variable severity)

31
Q

What biochemical signs would be seen in someone with B-thalassaemia trait? (3)
What condition may it be confused with?

A

Hypochromic
Microcytic
Anaemia absent (→disproportionate with MCH/MCV)

Can confuse with Fe defc (here Ferritin stores normal)

32
Q

What are the clinical features of thalassaemia? (5)

A

Severe anaemia (transfusion dependant from 3-6m)
Jaundice
Failure to thrive

Extramedullary haemopoiesis:
Bone marrow expansion (maxillary overgrowth + skull bossing)
Hepatosplenomegaly

33
Q

What are the chances of a child being affected/carrier in heterozygous parents of thalassaemia?

A

Affected: 25% chance
Carrier: 50% chance
→ therefore offer prenatal Dx

34
Q

What are the management options in thalassaemia? (2)

A 
Lifelong monthly transfusions (or else fatal)
Marrow transplant (curative - from compatible sibling)
35
Q

What are some complications of repeat transfusions in thalassaemia?
+ how these treated?

A

→ Chronic Fe overload:
Cardiac failure, Cirrhosis, DM, Growth failure, infertility

Treat with Iron chelation (removes XS Fe)

36
Q

What are the main features of bleeding disorders? (5)

A 
Bruising
Petechiae
Purpura
Mucosal bleeding (epistaxis, gums etc)
Major haemorrhage (GI bleed, intracranial - rare)
37
Q

What is the bleeding risk in platelets:
<20?
20-50?
50-150?

A

<20 → high spontaneous bleeding risk
20-50 → high risk excess bleeding in trauma/surgery
50-150 → low risk bleeding (unless major trauma/surg)

38
Q

What happens in immune thrombocytopenia purpura?

What is the incidence?

A

ITP: anti-platelet IgG autoantibodies destroy circulating platelets (→ increased megakaryocytes)
Incidence 1 in 25,000

39
Q

How do children with ITP usually present? (age + features)

A

B/wn 2-10yrs
Post-viral infection

Features of bleeding disorders:
Bruising/petechiae/purpura / mucosal bleeding / GI bleed

40
Q

What are some atypical features of ITP? (4)

A

Anaemia
Neutropenia
Hepatosplenomegaly
Marked lymphadenopathy

41
Q

What are some DDx of ITP?

A

ALL (req. marrow biopsy if lymphadenopathy)
Aplastic anaemia
SLE

42
Q

How is ITP managed?

A

80% self-limiting within 6-8wks

Only req admission if major haemorrhage/persistent minor

43
Q

What is DIC

A

= disorder of coag pathway activation → diffuse fibrin deposition in microvasc + consumption of coag factors/platelets

44
Q

What things could cause DIC in children (2)

A

Severe sepsis e.g. meningococcal septicaemia

Shock from circulatory collapse e.g. extensive tissue damage from trauma/burns

45
Q

What are the clinical features of DIC (3)

What biochemical markers should you suspect DIC? (7)

A

Bruising / Petechiae / Purpura

D-dimers
Reduced platelets
Reduced fibrinogen (/raised products)
Reduced antithrombin
Reduced Protein C + S
Prolonged PT/APTT
Microangiopathic haemolytic anaemia
46
Q

How is DIC managed? (2)

A
  1. treat underlying causes e.g. sepsis (in ICU)

2. Supportive care: FFP, platelets, coag factor transfusion

47
Q

What is the factor defc in Haemophilia A + B? + their incidences

A

Haemophilia A: factor 8, 1 in 5000

B: factor 9, 1 in 30,000

48
Q

How does haemophilia present?

A 
In neonatal: intracranial haemorrhage / oozing from heel prick
In older (when walking starts): crippling arthritis (bleeding in joints/muscles)
49
Q

How is Haemophilia managed? (4)

A

Prophylactic factor 8
Recombinant factor 8/9 (IV, when bleeding)
Desmopressin (allows mild haemophilia w/o recombinant)
Physio - preserve muscle strength / avoid immob damage

50
Q

What are the indications for splenectomy? (4)

A

Hereditary spherocytosis
IPT (Chronic)
Lymphoma
Spleen trauma + uncontrolled bleeding

51
Q

What prophylactic measures must be done before/after a splenectomy?

A

Before: imms to pneumococcus, HiB, meningococcus, influenzae
After: lifelong Abx + malaria precautions abroad

52
Q

Which forms of lymphoma are commoner in young/older children

What is the cure rate in both types

A

Younger = NHL
Older (adolescent) = Hodgkin’s

Both >80% survival rate

53
Q

How does Non-Hodgkins lymphoma present?

A

Depends on T/B cell

T cell (same spectrum as ALL):
Mediastinal mass (poss → SVC obstrn)
Marrow infiltration

B cell:
Localised LN disease (head/neck/abdo (pain/intuss))

54
Q

What cells are involved in Hodgkin’s lymphoma?

How does it present?

A

Reed-Sternberg cells

Painless lymphadenopathy (hard/firmer than benign)
Starts in upper body (neck) + spreads down slowly
RARELY systemic symptoms (anorexia, wt loss) - even advanced
55
Q

List the short term SEs of chemo (8)

A

Hair loss
Sore mouth
N + D + V
Appetite/wt loss

Anaemia
Infection (neutropenia)
Bruising

Mood instability/irritability

56
Q

List the long-term SEs of chemo (6)

A

Cancer recurrence
Psychological effects
Subfertility

Reduced growth
Delayed puberty

Toxicity: neuro / hepato / renal / cardio / pulm

57
Q

What tissue does neuroblastoma originate from?

A

Neural crest tissue in adrenal medulla + sympathetic nervous tissue

58
Q

How does a primary tumour present in neuroblastoma? (4)

A

Abdo mass (can be along symp chain neck→pelvic, classically adrenals)
Mass often large/complex, crosses midline + major vessels/LNs
If invade adj intervert foramen → spinal cord compression
Limp
Hepatomegaly

59
Q

How does neuroblastoma present if metastatic? (4)

A

> 2yrs old
Bone pain
Marrow suppression
Wt loss / malaise

(+ Limp
+ Hepatomegaly (neurblastoma progressed))

60
Q

What syndromes is Wilm’s tumour (nephroblastoma) associated with?

A

Overgrowth syndromes

T18

61
Q

What are the presentational features of Wilm’s tumour? (7)

A

<5yrs (>80% cases)

Abdo mass (incidental find)
Abdo pain
Anorexia

Haematuria
Hypertension
Anaemia

62
Q

What will be shown on scan in Wilm’s tumour

What is the prognosis like

A

USS and/or CT/MRI
→ Shows intrinsic renal mass distorting normal structures

> 80% cured (60% if metastasised)
However often recur so worse prognosis

63
Q

Where does a rhabdomyosarcoma originate from?

What are some common sites?

A

Primitive mesenchymal tissue (various primary sites - each with diff presentation/prognosis)

Head+neck (40%)
GU (bladder/ female GU tract/ paratesticular)

64
Q

How does a rhabdomyosarcoma present in head+neck? (3)

A

Proptosis
Nasal obstrn
Blood stain nasal discharge

65
Q

How does rhabdomyosarcoma present in GU? (4)

A

Dysuria
Urinary obstrn
Blood stained vag discharge
Scrotal mass

66
Q

How does an osteosarcoma present?

A

Persistent localised bone pain
Usually limbs
Pain preceding detection of mass
Pt otherwise well

67
Q

What Ix should be done in osteosarcoma?

A 
Bone X-Ray (shows destruction + new periosteal home formation)
Chest CT (lung metastases)
68
Q

What is the cause of retinoblastoma?

A

Hereditary (100% in bilateral, 20% in unilateral)

Susceptibility gene on csome13 (dominant)

69
Q

How does retinoblastoma present? (3)

A

<3yrs old
White pupillary reflex (not red)
OR a squint

70
Q

What is the incidence of childhood malignancy in <15s

What are the commonest cancers in children? (3)

A

1 in 500 <15s

Leukaemias (32%)
Brain/Spinal (24%)
Lymphomas (10%)

71
Q 
What age do you see:
Neuroblastoma
Wilms
Hodgkins
Bone tumours
A

Neuro + Wilms <6yrs

Hodgkins + bone tumours → peak in adolescence

72
Q

What type of anaemia will be seen on blood film in B12/Folate defc?

A

Macrocytic megaloblastic anaemia

Child Health (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions