Brainscape's Knowledge GenomeTM

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


See full index

Paediatrics > Cardiology and Haematology > Flashcards

Cardiology and Haematology Flashcards

1
Q

L-R shunts

A

Breathless
VSD
PDA
ASD

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

R-L Shunts

A

Blue
Tetralogy of Fallot
Transposition of the great arteries

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

Common mixing

A

Breathless and blue

Complete atrioventricular septal defect

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

Outflow obstruction in well child

A

Pulm stenosis

Aortic stenosis

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

Outflow obstruction in sick neonate

A

Coarctation of the aorta

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

Ductus arteriosus

A

Ligamentum arteriosum

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

Ductus venosus

A

Ligamentum venosum

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

Foramen ovale

A

Fossa ovalis

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

Umbilical arteries and abdo ligaments

A

Medial umbilical ligaments

Superior vesicular artery to bladder

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

Umbilical vein

A

Ligamentum teres

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

Rubella and CnHD

A

Peripheral pulmonary stenosis

PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Warfarin

A

Pulmonary valve stenosis

PDA

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

Foetal alcohol syndrome

A

ASD
VSD
Tetralogy of Fallot

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

Down’s syndrome

A

AVSD

VSD

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

Turner’s syndrome

A

Aortic valve stenosis

Aortic coarctation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Characteristics innocent murmur

A 
4S
aSymptomatic pt
Soft blowing murmur 
Systolic only
left Sternal edge
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Still’s murmur

A

Early-mid systolic murmur
Best heard between left sternal edge and apex
Louder on lying down

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

Venous hum

A

Continuous systolic and diastolic murmur
Best heard below clavicles
Abolished by compression of the jugular vein
Abolished by child lying down

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

Neck bruits

A

Systolic murmur
Maximal above clavicle
Need to distinguish from mild aortic stenosis

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

Symptoms HF

A

Breathlessness
Sweating
Poor feeding
Recurrent chest infections

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

Signs HF

A 
Poor wt gain/ faltering growth
Tachypnoea
Tachycardia
Heart murmur, gallop rhythm
Cardiomegaly
Hepatomegaly
Cool peripheries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Causes HF Neonates

A

Hypoplastic LH syndrome
Critical aortic valve stenosis
Severe aortic coarctation
Interruption of the aortic arch

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

Causes HF infants

A

VSD
AVSD
Large PDA

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

Causes HF Older children/ adolescents

A

Eisenmenger syndrome
Rheumatic HD
Cardiomyopathy

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

Eisenmenger syndrome

A

Irreversibly raised pulmonary vascular resistance due to chronically increased pulmonary arterial pressure and flow

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

Peripheral cyanosis

A

Blue hands and feet
Child cold or unwell from any cause
Polycythaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Central cyanosis

A

Slate blue tongue

? CnHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Ix for ?CnHD

A

CXR, ECG: rarely diagnostic but can help establish that abnormality is present, baseline for future changes
Echo and Doppler US: diagnostic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ASD Classification

A

Partial (primum) ASD: defect in anteroinferior aspect of septum, a form of AVSD
Secondum ASD: (80%) defect in the fossa ovalis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Sx ASD

A

Commonly ASYMPTOMATIC
Recurrent chest infections/ wheeze
Arrythmias (4th decade onwards)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Signs ASD

A

ESM (best heard at upper left sternal edge - increased flow across pulmonary valve)
Fixed split S2
Apical pansystolic murmur (primum only)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Ix ASD

A

CXR: cardiomegaly, enlarged pulmonary arteries, increased pulmonary vascular markings
ECG primum: superior QRS axis
ECG secundum: partial RBBB, R axis deviation
ECHO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Mx ASD

A

If ASD large enough to cause RV dilatation, it requires treatment
Secundum: catheterisation with insertion of occlusion device
Primum: surgical correction
Tx usually done age 3-5 (prevent RHF and arrhythmias later in life) ++++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

VSD Classification

A

Small: smaller than aortic valve in diameter (=3mm)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Small VSD Sx and signs

A

Asymptomatic
Loud pansystolic murmur LLSE
Quiet pulmonary second sound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Ix Small VSDs

A

ECG + CXR: normal

ECHO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Mx small VSDs

A

Lesions often close spontaneously (ass w disappearance of murmur, normal ECG + echo)
While VSD present, need good dental hygiene to prevent endocarditis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Sx large VSDs

A

HF (R+L) with breathlessness
Failure to thrive after 1 wk
Recurrent chest infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Signs large VSDs

A 
Active precordium
Tachypnoea, tachycardia, enlarged liver from HF
Soft pansystolic/ no murmur 
Apical mid-diastolic murmur
Loud P2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

ECG large VSD

A

Biventricular hypertrophy from age 2

Upright T wave in V1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

CXR Large VSD

A

Cardiomegaly
Enlarged pulmonary arteries
Pulmonary oedema
Increased pulmonary vascular markings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Mx Large VSD

A

Med: Diuretics +/- captopril (ACEi)
Additional calorie input
Surgical: surgery at 3-6 months to prevent HF and permanent lung damage
Usually intra-cardiac (while under cardiopulm bypass), can be transcatheter
Slowed growth should catch up after 1-2 years, excellent LT prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Definition PDA

A

DA that has failed to close 1 month after EXPECTED DATE of delivery (flow across PDA is from aorta to pulmonary artery). In preterm infant PDA from CnHD but prematurity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Sx PDA

A

Usually asymptomatic

If duct v large –> pulmonary blood flow –> pulm HTN and HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Signs PDA

A

Continuous murmur behind L clavicle

Bounding pulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Ix PDA

A

ECG + CXR: usually normal
If v large, as for VSD
Echo: distinguish btwn PDA and VSD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Mx PDA

A

Surgical closure recommended (abolish lifelong risk bac endocarditis and pulm vasc disease). Closure via coil/ occlusion device introduced via cardiac catheter at 1 yr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Cyanotic CnHD

A 
5Ts 
Truncus arteriosus
Transposition great arteries
Tricuspid atresia
Tetralogy of Fallot
Total anomalous pulm venous return
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Hyperoxia (N2 washout) test

A

Determine presence HD in cyanosed infant
Put infant in 100% O2 for 10 mins
If R radial pAO2 still low ( dx Cyanotic CnHD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Mx Cyanotic CnHD

A 
ABC
Prostagladin Infusion (PGE, 5ng/kg/min) to maintain PDA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Tetralogy of Fallot defects

A

(Most common cause cyanotic CnHD)

1) Large VSD
2) Overriding aorta
3) Sub pulm art stenosis
4) RV hypertrophy as a result

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

TOF Sx

A

Some dx antenatally
Some dx after identifying murmur in 1st 2 months (+/- cyanosis)
Classical triad: severe cyanosis, hypercyanotic spells, squatting on exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

TOF Signs

A

Clubbing fingers/ toes

Loud, harsh ESM at L sternal edge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

TOF CXR

A

Small heart, ‘boot-shaped’ (RV hypertrophy)
Pulm artery ‘bay’ (concavity on L heart border
Reduced pulm vascular markings

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Mx TOF

A

Initially med mx, definitive surgery 6 months (close VSD, relieve RV outflow tract obstruction)
V cyanosed neonates may require shunt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Transposition great arteries definition

A

Aorta -> RV, pulm artery -> LV
Deoxy blood returned to body, oxy blood returned to lungs
Often co-morbid abnormalities -> mixing, e.g. ASD, VSD, PDA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Sx transposition great arteries

A

Cyanosis (profound and life-threatening)

Usually day 2 when duct closes)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Signs transposition great arteries

A

Cyanosis (always present)
Loud and single S2
Usually no murmur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Transposition great arteries Ix

A 
CXR: Classically narrow upper mediastinum
'Egg on side' appearance cardiac shadow
Increased pulm vascular markings 
ECG: normal 
ECHO
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Mx transposition great arteries

A 
Sick cyanosed infant, key = improve mixing
Prostaglandin infusion (keep PDA open) 
Balloon atrial septostomy (tears fossa ovalis to enable mixing) 
Arterial switch surgery during neonatal period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Aortic Stenosis Comorbidities

A

Mitral valve stenosis

Aortic coarctation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Aortic stenosis symptoms

A

Most ASYMPTOMATIC
Severe: reduced exercise tolerance
Chest pain on exertion/ syncope
Critical: severe HF -> shock

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Aortic stenosis signs

A 
Slow rising pulse 
Carotid thrill
ESM 
Delayed, soft S2
Apical ejection click
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Aortic stenosis Ix

A

CXR: normal or
Prominent LV with post-stenotic dilatation of asc aorta
ECG: LV hypertrophy

65
Q

Mx aortic stenosis

A 
Reg clin + echo assessment (assess when to intervene)
Balloon valvotomy (children w sx on exercise, resting pressure gradient >64mmHg)
66
Q

Pulm stenosis sx

A

Most ASYMPTOMATIC

Critical: present in 1st few days life w cyanosis

67
Q

Pulm stenosis signs

A

ESM
Ejection click
RV heave

68
Q

Pulm stenosis Ix

A

CXR: normal or post-stenotic dilatation of pulm artery
ECG: RV hypertrophy

69
Q

Pulm stenosis mx

A

Pressure gradient >64mmHg -> intervene

Transcatheter balloon dilatation

70
Q

Adult-type aortic coarctation definition

A

Constricted aortic segment DISTAL to ductus arteriosus

71
Q

Infantile aortic coarctation definition

A

Constricted segment proximal to ductus arteriosus

72
Q

Adult-type aortic coarctation sx and signs

A 
ASYMPTOMATIC 
Systemic HTN in R arn
ESM at upper sternal edge 
Collaterals heard w continuous murmur at back
Radiofemoral delay
73
Q

Adult-type aortic coarctation Ix

A

CXR: ‘Rib-notching’
‘3 sign’ visible notch in desc aorta
ECG: LV hypertrophy

74
Q

Mx

A

Severe (as assessed by echo): stent via catheter

75
Q

Infantile-type coarctation of aorta clin features

A 
Normal on 1st day life 
Acute circulatory collapse at 2 days
Sick baby with severe HF
Absent femoral pulses
Severe metabolic acidosis
76
Q

Infantile-type coarctation of aorta Ix

A

CXR: cardiomeg from HF and shock
ECG: normal

77
Q

Mx Infantile-type coarctation of aorta

A

ABC
Prostaglandin ASAP
Surgical repair soon after dx

78
Q

Rheumatic fever definition

A

Abnormal immune response to preceding infection with group A strep mainly in children aged 5-15

79
Q

Rheumatic fever major manifestations

A 
Pancarditis (endocarditis, myocarditis, pericarditis)
Polyarthritis
Syndenham chorea
Erythema marginatum 
Subcut nodules
80
Q

Rheumatic fever clin features

A

Pharyngeal infection -> latent interval 2-6 weeks -> polyarthritis, mild fever, malaise

81
Q

Rheumatic fever minor manifestations

A 
Fever
Polyarthralgia
Hx RF
Raised inflammatory markers
Prolonged PR interval on ECG
82
Q

Jones criteria for the diagnosis of RF

A

2 major OR 1 major and 2 minor criteria and supportive evidence of preceding group A strep infection
(Markedly increased ASO titre/ other strep Abs/ group A strep on throat culture)

83
Q

Chronic RF complications

A

Mitral stenosis

84
Q

Mx acute Rheumatic fever

A

Bed-rest and NSAIDs
Steroids if fever and inflamm don’t resolve quickly
Symptomatic HF -> diuretics and ACEis
Monthly injections BENZATHINE PENICILLIN for 18-21 yrs, possibly life to prevent recurrence

85
Q

RFs infective endocarditis

A 
Usually occurs w CnHD 
- small VSDs
- PDAs
- mitral regurg
- aortic regurg 
- severely restricted outflow tract obstruction
- aorto-pulmonary shunts 
Prosthetic valves
Risk NOT increased in isolated secondum ASD
86
Q

Microorganisms causing infective endocarditis

A

Commonest = viridans strep

87
Q

Symptoms infective endocarditis

A

Recurrent fever, arthralgia, malaise
Splenomegaly
Uncommon signs: splinter haemorrhages, petechial haemorrhagic Janeway lesions, Osler nodes, retinal Roth’s spots

88
Q

Dx infective endocarditis

A

multiple blood cultures before giving abx

echo can confirm but not exclude dx

89
Q

Tx infective endocarditis

A

High dose penicillin + an aminoglycoside

6 wks high-dose therapy

90
Q

Prevention infective endocarditis

A

Good dental hygiene - encourage in all pts w CnHD
Dental/ surgical interventions non-infected areas -> no abx
Procedure in actively infected area -> prophylactic abx

91
Q

Embryonic Hb production

A

4-8 weeks gestation

92
Q

Foetal Hb structure

A

2 alpha chains 2 gamma chains

Increased affinity for O2

93
Q

Foetal Hb production

A

After 8 wks gestation

Main hb during foetal life

94
Q

Hb types at birth

A

HbF
HbA (adult Hb)
HbA2 (normal variant HbA, may be increased in beta-thalassaemia)

95
Q

Hb types at 1 yr

A

V low percentage HbF

Increased HbF sensitive indicator haemoglobinopathies

96
Q

Hb values at birth

A

Term infants: 14-21.5 g/dl

High as low O2 conc in foetus

97
Q

Hb values 2 weeks

A

13.4-19.8 g/dl

98
Q

Hb values 2 months

A

9.4-13 g/dl

99
Q

Hb values 1yr

A

11.3- 14.1

100
Q

Hb values 2-6yrs

A

11.5-13.5

101
Q

Hb values 6-12yrs

A

11.5-15.5

102
Q

Hb values males 12-18

A

13-16

103
Q

Hb values females 12-18

A

12-16

104
Q

Anaemia values (neonate/ 1-12 months/ 1-12yrs)

A

Neonate:

105
Q

Commonest cause anaemia

A

Iron deficiency

106
Q

Causes anaemia

A

Impaired red cell production
Increased red cell destruction (haemolysis)
Blood loss

107
Q

Causes impaired red cell production

A

1) Red cell aplasia (no red cell production)
- parovirus infection
- Diamond-Blackfan anaemia
- Transient erythroblastopenia of childhood
2) Ineffective erythropoiesis (RC production at normal rate but differentiation/ survival of cells defective)
- iron deficiency
- folic acid deficiency
- chronic inflamm (e.g. JIA)
- chronic RF

108
Q

Causes increased haemolysis

A

1) Red cell memb disorders
- Hereditary spherocytosis
2) Red cell enzyme disorders
- G6PD def
3) Haemoglobinopathies
- thalaessaemias
- sickle cell disease
4) Immune
- Haemolytic disease of the newborn
- Autoimmune haemolytic anaemia

109
Q

Causes blood loss

A

1) Fetomaternal bleeding
2) Chronic GI blood loss
- Meckel diverticulum
3) Inherited bleeding disorders
- von Willebrand disease

110
Q

Blood results ineffective erythropoiesis

A

Normal reticulocyte count

Abnormal MCV

111
Q

Causes iron deficiency

A

Inadequate intake (common)
Malabsorption
Blood loss

112
Q

Elemental iron requirements

A

1mg/kg/day

113
Q

Sources iron

A

Breast milk (low iron content but 50% absorbed)
Infant formula (supplemented with iron)
Cow’s milk (higher content vs breast milk but only 10% absorbed)
Solids at weaning

114
Q

Causes inadequate iron intake

A

Delay in introduction mixed feeding beyond 6 months
Diet with insufficient iron-rich foods
Iron intake much increased when taken w vitamin C

115
Q

Clin features iron-def anaemia

A

Children asymptomatic until

116
Q

Dx iron-def anaemia

A

Microcytic, hypochromic anaemia

Low serum ferritin

117
Q

Causes microcytic anaemia

A

Iron def
b-thalassaemia trait
a-thalassaemia trait
anaemia chronic disease

118
Q

Complications iron-def anaemia

A

Detrimental to behavioural and intellectual function

119
Q

Mx iron def anaemia

A

Dietary advice
Oral iron supplementation (e.g. sytron or niferex - don’t stain teeth)
Continue until Hb normal, and then another 3 months to replenish iron stores
Blood transfusion NEVER needed for iron def
If fail to respond, ix for malabsorption/ chronic blood loss

120
Q

Tx iron def with normal Hb

A

Dietary advice to increase oral iron

Offer parents oral iron supplements

121
Q

Blood values red cell aplasia

A

Low reticulocyte count despite low Hb
Normal bilirubin
Negative direct antiglobulin test (Coombs test)
Absent red cell precursors on bone marrow exam

122
Q

Diamond-Blackfan anaemia

A

FHx 20%, 80% sporadic
Mutations in ribosomal protein
Most cases present 2-3 months
Some sx anaemia, some congen abnormalities, e.g. short stature, abnormal thumbs
Tx: oral steroids, monthly blood transfusions if unresponsive

123
Q

Transient erythroblastopenia of childhood

A

Triggered viral infections
Same haem features as diamond-blackfan anaemia (DBA)
Unlike DBA, TEC always recovers, usually within several weeks

124
Q

Commonest severe inherited coagulation disorders

A

Haemophilia A
Haemophilia B
Both X-linked recessive

125
Q

Haemophilia A factor deficiency

A

Factor 8

126
Q

Inheritance haemophilia A and B

A

XLR

B: 2/3 FHx, 1/3 sporadic

127
Q

Freq Haemophilia A and B

A

1/5,000 male births (A)

1/30,000 male births (B)

128
Q

Definition haemophilia

A

Group of hereditary blood disorders that impair the body’s ability to clot blood normally

129
Q

Haemophilia B deficiency

A

Factor 9

130
Q

Von Willebrand Disease deficiency

A

Absence of VWFactor -> rapid degradation of factor 8

131
Q

Grading of haemophilias

A

Mild/ moderate/ severe depending on Factor 8 or 9 level
Mild: >5-40%
Moderate: 1-5%
Severe:

132
Q

Sx mild haemophilia

A

Bleeding after surgery

133
Q

Sx moderate haemophilia

A

Bleed after minor trauma (intracranial haemorrhage, bleeding post-circumcision, oozing from heel-rpick/ venepucture sites)

134
Q

Sx severe haemophilia

A

Recurrent, spontaneous joint/ muscle bleeds
Can lead to crippling arthritis if not properly treated
Present towards end of 1st year

135
Q

Age of onset of bleeding disorders

A

Neonate: 20% haemophilias present now
Toddlers: haemophilias may present when starting to walk
Adolescent: vWF disease may present with menorrhagia

136
Q

Mucous membrane bleeding and skin haemorrhage

A

Platelet disorders/ vWF disease

137
Q

Bleeding into muscles/ joints

A

Haemophilias

138
Q

Scarring and delayed haemorrhage

A

Disorders of connective tissue, e.g. Marfan syndrome, osteogenesis imperfecta, factor 8 deficiency

139
Q

PT/ APTT/ Factor8:c Haemophilia A

A

PT: Normal
APTT: Increased (++)
Factor 8:c : Reduced (–)

140
Q

PT/ APTT/ Factor8:c vWF disease

A

PT: Normal
APTT: Increased/ normal
Factor 8:c : Reduced or normal

141
Q

Mx haemophilia

A

A: recombinant factor 8 concentrate
B: recombinant factor 9 concentrate
Both via IV infusion whenever there is any bleeding
Minor bleed/ simple joint bleed: raise circulating level to 30% normal
Home tx encouraged to avoid delay in tx
Major surgery/ life-threatening bleed: raise to 100%, maintain at 30-50% for up to 2 weeks to prevent 2y haemorrhage
Desmopressin can be given for mild haemophilia A to prevent use blood products.
AVOID IM injections, aspirin and NSAIDs

142
Q

Complications of tx of haemophilia

A

Inhibitors (antibodies to factor 8/9): 5-20%, reduce or completely inhibit effect of tx
Transfusion-transmitted infections (e.g, HIV, Hep A/B/C)
Periph veins may be difficult to cannulate, central lines may become infected/ thrombosed

143
Q

Prophylactic tx haemophilia

A

All children with severe haemophilia A/B to prevent severe joint damage. Begins age 2-3, given 2-3x week

144
Q

Functions vWF

A

1) Facilitates platelet adhesion to damaged endothelium
2) Acts as carrier protein for factor 8:c, protecting it from inactivation and clearance
vWF disease: defective platelet plug formation, factor 8:c deficiency

145
Q

Inheritance and subtypes vWF

A

Usually AD
But many mutations in gene/ types vWD
Commonest subtype = type 1, (60%), fairly mild, often not dx until puberty/ adulthood

146
Q

Clinical features vWD

A

Bruising
Excessive, prolonged bleeding after surgery
Mucosal bleeding e.g. epistaxis, menorrhagia
Spont soft tissue bleeding, e.g. haematomas, haemarthroses uncommon

147
Q

Mx vWD

A

Type 1: DDVAP (Desmopressin), increases both F8 and vWF secretion into plasma
DDVAP: use with caution in

148
Q

Vitamin K deficiency symptoms

A

Increased risk of bleeding

Prolonged PT

149
Q

Causes vitamin K def

A

1) Inadequate intake
- Neonates
- LT chronic illness w inadequate intake
2) Malabsorption
- Coeliac disease
- Cystic fibrosis
- Obstructive jaundice
3) Vitamin K antagonists
- Warfarin

150
Q

Thrombocytopaenia definition

A

Platelet count

151
Q

Sx thrombocytopaenia

A

Bruising
Petechiae
Purpura
Mucosal bleeding (epistaxis, gums bleed when brushing teeth)
Less common: severe GI bleeding, intracranial haemorrhage, haematuria

152
Q

Immune thrombocytopaenia

A

Commonest cause thrombocytopaenia of childhood
Destruction circulating platelets by anti-platelet IgG antibodies
Often after viral illness

153
Q

Immune thrombocytopaenia mx

A

Most children treated at home
Usually remits spont in 6-8 weeks
If severe, tx options: oral prednisolone, IV anti-D, IVIg

154
Q

DIC definition

A

Coagulation pathway activation leading to diffuse fibrin deposition in the microvasculature and consumption of coagulation factors and platelets

155
Q

Causes DIC

A

Severe sepsis
Shock due to circulatory collapse
- meningococcal septicaemia
- extensive tissue damage from trauma/ burns

156
Q

Clin features DIC

A

Bruising
Purpura
Haemorrhage

157
Q

Dx DIC

A 
No single diagnostic test 
Thrombocytopaenia
Prolonged PT
Prolonged APTT 
Low fibrinogen
Raised fibrinogen degradation products, D-dimers
158
Q

Mx DIC

A

Tx underlying cause

Supportive care: fresh frozen plasma, cryoprecipitate, platelets

Paediatrics (7 decks)

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