Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Child Health > Oncology & Haematology > Flashcards

Oncology & Haematology Flashcards

(72 cards)

Start Studying
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
What are some of the causes of acute anaemia in sickle cell disease? (3)
Haemolytic (infection) Aplastic (parovirus) Sequestration (sudden hepatosplenomegaly, abdo pain + circ collapse)
26
List the long-term complications of sickle cell disease (9)
Short stature Gallstones ``` Heart failure (from uncorrected anaemia) Cardiomegaly (chronic anaemia) ``` ``` Adenotonsilalr hypertrophy Renal dysfunc Leg ulcers Stroke/cognitive probs Educational/behav probs ```
27
What are some of the triggers of a sickle cell crisis? (5)
``` Cold Stress XS exercise Infection Hypoxia ```
28
How is a sickle cell crisis managed? | What are the other aspects of management in sickle cell anaemia? (3)
Crises: analgesia + maintain good hydration + O2 ``` Prophylaxis: full imms + penicillin throughout childhood Folic acid (due to increased demand) Avoiding crises triggers ```
29
What ethnicity is a-thalassaemia major mostly seen in? | What are the features (of major)?
SE Asian Fetal hydrops in 2ndT (fetal anaemia → oedema + ascites) 3 deletions → mild/mod anaemia 2 deletions → asymp
30
What are the 2 main types of B-thalassaemia? What are their Hb status?
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
What biochemical signs would be seen in someone with B-thalassaemia trait? (3) What condition may it be confused with?
Hypochromic Microcytic Anaemia absent (→disproportionate with MCH/MCV) Can confuse with Fe defc (here Ferritin stores normal)
32
What are the clinical features of thalassaemia? (5)
Severe anaemia (transfusion dependant from 3-6m) Jaundice Failure to thrive Extramedullary haemopoiesis: Bone marrow expansion (maxillary overgrowth + skull bossing) Hepatosplenomegaly
33
What are the chances of a child being affected/carrier in heterozygous parents of thalassaemia?
Affected: 25% chance Carrier: 50% chance → therefore offer prenatal Dx
34
What are the management options in thalassaemia? (2)
``` Lifelong monthly transfusions (or else fatal) Marrow transplant (curative - from compatible sibling) ```
35
What are some complications of repeat transfusions in thalassaemia? + how these treated?
→ Chronic Fe overload: Cardiac failure, Cirrhosis, DM, Growth failure, infertility Treat with Iron chelation (removes XS Fe)
36
What are the main features of bleeding disorders? (5)
``` Bruising Petechiae Purpura Mucosal bleeding (epistaxis, gums etc) Major haemorrhage (GI bleed, intracranial - rare) ```
37
What is the bleeding risk in platelets: <20? 20-50? 50-150?
<20 → high spontaneous bleeding risk 20-50 → high risk excess bleeding in trauma/surgery 50-150 → low risk bleeding (unless major trauma/surg)
38
What happens in immune thrombocytopenia purpura? | What is the incidence?
ITP: anti-platelet IgG autoantibodies destroy circulating platelets (→ increased megakaryocytes) Incidence 1 in 25,000
39
How do children with ITP usually present? (age + features)
B/wn 2-10yrs Post-viral infection Features of bleeding disorders: Bruising/petechiae/purpura / mucosal bleeding / GI bleed
40
What are some atypical features of ITP? (4)
Anaemia Neutropenia Hepatosplenomegaly Marked lymphadenopathy
41
What are some DDx of ITP?
ALL (req. marrow biopsy if lymphadenopathy) Aplastic anaemia SLE
42
How is ITP managed?
80% self-limiting within 6-8wks | Only req admission if major haemorrhage/persistent minor
43
What is DIC
= disorder of coag pathway activation → diffuse fibrin deposition in microvasc + consumption of coag factors/platelets
44
What things could cause DIC in children (2)
Severe sepsis e.g. meningococcal septicaemia | Shock from circulatory collapse e.g. extensive tissue damage from trauma/burns
45
What are the clinical features of DIC (3) | What biochemical markers should you suspect DIC? (7)
Bruising / Petechiae / Purpura ``` D-dimers Reduced platelets Reduced fibrinogen (/raised products) Reduced antithrombin Reduced Protein C + S Prolonged PT/APTT Microangiopathic haemolytic anaemia ```
46
How is DIC managed? (2)
1. treat underlying causes e.g. sepsis (in ICU) | 2. Supportive care: FFP, platelets, coag factor transfusion
47
What is the factor defc in Haemophilia A + B? + their incidences
Haemophilia A: factor 8, 1 in 5000 | B: factor 9, 1 in 30,000
48
How does haemophilia present?
``` In neonatal: intracranial haemorrhage / oozing from heel prick In older (when walking starts): crippling arthritis (bleeding in joints/muscles) ```
49
How is Haemophilia managed? (4)
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
What are the indications for splenectomy? (4)
Hereditary spherocytosis IPT (Chronic) Lymphoma Spleen trauma + uncontrolled bleeding
51
What prophylactic measures must be done before/after a splenectomy?
Before: imms to pneumococcus, HiB, meningococcus, influenzae After: lifelong Abx + malaria precautions abroad
52
Which forms of lymphoma are commoner in young/older children | What is the cure rate in both types
Younger = NHL Older (adolescent) = Hodgkin's Both >80% survival rate
53
How does Non-Hodgkins lymphoma present?
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
What cells are involved in Hodgkin's lymphoma? | How does it present?
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
List the short term SEs of chemo (8)
Hair loss Sore mouth N + D + V Appetite/wt loss Anaemia Infection (neutropenia) Bruising Mood instability/irritability
56
List the long-term SEs of chemo (6)
Cancer recurrence Psychological effects Subfertility Reduced growth Delayed puberty Toxicity: neuro / hepato / renal / cardio / pulm
57
What tissue does neuroblastoma originate from?
Neural crest tissue in adrenal medulla + sympathetic nervous tissue
58
How does a primary tumour present in neuroblastoma? (4)
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
How does neuroblastoma present if metastatic? (4)
>2yrs old Bone pain Marrow suppression Wt loss / malaise (+ Limp + Hepatomegaly (neurblastoma progressed))
60
What syndromes is Wilm's tumour (nephroblastoma) associated with?
Overgrowth syndromes | T18
61
What are the presentational features of Wilm's tumour? (7)
<5yrs (>80% cases) ``` Abdo mass (incidental find) Abdo pain Anorexia ``` Haematuria Hypertension Anaemia
62
What will be shown on scan in Wilm's tumour What is the prognosis like
USS and/or CT/MRI → Shows intrinsic renal mass distorting normal structures >80% cured (60% if metastasised) However often recur so worse prognosis
63
Where does a rhabdomyosarcoma originate from? | What are some common sites?
Primitive mesenchymal tissue (various primary sites - each with diff presentation/prognosis) Head+neck (40%) GU (bladder/ female GU tract/ paratesticular)
64
How does a rhabdomyosarcoma present in head+neck? (3)
Proptosis Nasal obstrn Blood stain nasal discharge
65
How does rhabdomyosarcoma present in GU? (4)
Dysuria Urinary obstrn Blood stained vag discharge Scrotal mass
66
How does an osteosarcoma present?
Persistent localised bone pain Usually limbs Pain preceding detection of mass Pt otherwise well
67
What Ix should be done in osteosarcoma?
``` Bone X-Ray (shows destruction + new periosteal home formation) Chest CT (lung metastases) ```
68
What is the cause of retinoblastoma?
Hereditary (100% in bilateral, 20% in unilateral) | Susceptibility gene on csome13 (dominant)
69
How does retinoblastoma present? (3)
<3yrs old White pupillary reflex (not red) OR a squint
70
What is the incidence of childhood malignancy in <15s | What are the commonest cancers in children? (3)
1 in 500 <15s Leukaemias (32%) Brain/Spinal (24%) Lymphomas (10%)
71
``` What age do you see: Neuroblastoma Wilms Hodgkins Bone tumours ```
Neuro + Wilms <6yrs | Hodgkins + bone tumours → peak in adolescence
72
What type of anaemia will be seen on blood film in B12/Folate defc?
Macrocytic megaloblastic anaemia

Child Health (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions