Brainscape's Knowledge GenomeTM

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


See full index

Medicine > Paediatrics 2 > Flashcards

Paediatrics 2 Flashcards

Rashes & infectious diseases Endocrine

1
Q

When does the rash associated with measles appear?

A

3-4 after symptom onset

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

School exclusion criteria for measles

A

4 days after rash onset

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

Measles causative organism

A

RNA paramyxovirus

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

Measles clinical manifestations

A

Maculopapular rash behind ears - spreads and becomes confluent
Koplik spots
Conjunctivitis
Irritable

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

Measles investigations

A

< 3 days: PCR for measles mRNA
> 3 days: IgM/IgG antibodies

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

Post-measles complications

A

Otitis media
Pneumonia
Myocarditis

Encephalitis

Subacute sclerosing panencephalitis - 5-10 years later

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

Dawson disease

A

Subacute sclerosing panencephalitis

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

School exclusion criteria for measles

A

4 days after rash onset

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

Rubella causative organism

A

Togavirus - rubivirus

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

School exclusion criteria for rubella

A

5 days after rash onset

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

Rubella clinical manifestations

A

Maculopapular rash on face - spreads to body
Lymphadenopathy
Forchheimer spots

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

Congenital rubella syndrome

A

Sensorineural deafness
Cataracts
PDA

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

Complications post-rubella

A

Thrombocytopaenia
Encephalitis
Myocarditis
Arthritis of small joints

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

When is rubella vaccinated against?

A

MMR:
12-13 months
2-3 years old

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

Rubella incubation period

A

14-21 days

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

Rubella investigations

A

PCR
IgM antibodies

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

Erythema infectiosum: alternative names

A

5th disease
Slapped cheek syndrome

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

Describe the rash associated with erythema infectiosum

A

On face (slapped cheeks)
Spreads to trunk and limbs (lacy)

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

Erythema infectiosum causative organism

A

Parvovirus B19

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

Erythema infectiosum school exclusion criteria

A

No school exclusion

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

Roseola infantum symptoms

A

Extremely high fever
to
Rash on trunk to extremities

Febrile convulsions

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

Roseola infantum epidemiology

A

6 months - 2 years

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

Roseola infantum causative organism

A

HHV6

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

Roseola infantum complications

A

Aseptic meningitis
Hepatitis

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

Roseola infantum school exclusion criteria

A

No school exclusion

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

Hand, foot and mouth disease causative organisms

A

Coxsackie A16 virus
Enterovirus 71

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

Hand, foot and mouth disease school exclusion

A

No school exclusion

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

Hand, foot and mouth disease complications

A

Viral meningitis
Encephalitis

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

Herpangina

A

Coxsackie A affecting mouth only

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

Why should ibuprofen be avoided in children with chickenpox?

A

Increase risk of necrotising enterocolitis

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

Chicken pox rash

A

Itchy, starting on head/trunk and spreads
Macular -> papular and vesicular

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

Congenital varicella syndrome

A

Limb atrophy
Ocular defects
Neurological defects

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

Chicken pox complications

A

Secondary bacterial infection of lesions – B-haemolytic Group A Strep
Encephalitis
Disseminated haemorrhagic chickenpox
Pneumonia

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

Chicken pox school exclusion criteria

A

Until lesions have crusted over

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

Meningitis investigations

A

Blood cultures
LP

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

Meningitis antibiotics

A

< 3 months: amoxicilln (listeria) + cefotaxime
> 3 months: cefotaxime / ceftriaxone

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

Meningitis prophylactic antibiotics

A

1st: Ciprofloxacin single dose
2nd: Rifampicin 2 days

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

Indication for benzylpenicllin for meningitis

A

Menogococcal meningitis
Non-blanching rash

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

Most common complication after meningitis

A

Sensorineural hearing loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Cause of purpura/petechiae

A

Dermal capillary micro thrombi that rapidly lead to haemorrhagic skin necrosis
Endotoxin released by bacteria which induced oedema formation and capillary thrombosis with extravasation of blood into interstitial space

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

Close contact

A

Same household during 7 days before onset of illness
Anyone in direct contact with patient’s oral secretions

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

Waterhouse-Friedrichsen syndrome

A

Adrenal gland failure which can occur after meningitis

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

HSP pathophysiology

A

IgA mediated small vessel vasculitis

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

HSP clinical manifestations

A

After viral URTI
Purpural rash
Abdominal pain
Joint pain
Haematuria +/- proteinuria (nephritis)

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

Describe the rash associated with HSP

A

Purpural, non-blanching
Buttocks, back, legs, trunk spared

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

HSP management

A

Usually self-limiting
NSAIDs can be given for arthalgia
Steroids can be used

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

2 causes of desquamating rash

A

Scarlet fever
Kawasaki disease

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

Diagnostic critieria for Kawasaki disease.

A

Fever (>38.5) for > 5 days and at least 4 of:
- Conjunctivitis – bilateral (spares limbus)
- Rash – non-vesicular
- Cervical lymphadenopathy
- Strawberry tongue / cracked lips
- Hands & feet – swollen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Kawasaki disease management

A

High dose oral aspirin
IV immunoglobulin

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

Investigation of complications after Kawasaki disease

A

Echocardiogram for coronary artery aneurysm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Describe the conjunctivitis seen in Kawasaki disease

A

Bilateral
Spared limbus

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

Kawasaki disease complications

A

Coronary artery aneurysm
Reye syndrome

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

Pathophysiology of coronary artery aneurysm after Kawasaki disease

A

Fibrin deposited on blood vessel wall
Can’t gently stress
Bulges form ->
Coronary aneurysm

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

Reye syndrome aetiology + pathophysiology

A

Associated with aspirin use in children

Due to mitochondrial dysfunction

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

Reye syndrome features

A

After a viral infection / aspirin use

Non-inflammatory encephalopathy - slurred speech, lethargy
Fatty degeneration of liver - abnormal LFTs
Cerebral oedema - raised ICP

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

Reye syndrome diagnosis

A

Liver biopsy

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

Scarlet fever causative organism

A

Group A streptococci
Usually strep pyogenes

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

Scarlet fever school exclusion criteria

A

Return 24 hours after starting antibiotics

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

Scarlet fever: describe the rash

A

Neck to trunk & limbs
Fine punctuate erythema surrounding area around mouth
Sandpaper texture
Desquamation after 1 week

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Scarlet fever clinical manifestations

A

Fever
Malaise
Strawberry tongue - red with white bits
Tonsilitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Scarlet fever investigations

A

Throat swab
Increased anti streptolysin O (ASO)

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

Scarlet fever management

A

Give Abx before results of throat swab
Oral penicillin 10 days
Alternative azithromycin

Notifiable disease
Return to school 24 hours after Abx

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

Peak age of presentation of scarlet fever

A

4 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Scarlet fever complications

A

Rheumatic fever - 20 days later
Otitis media
Acute glomerulonephritis
PANDAS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Mumps causative organism

A

RNA paramyxovirus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Mumps clinical manifestations

A

Parotitis (unilateral then bilateral in 70%)
Fever, malaise, muscular pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Mumps school exclusion criteria

A

5 days after onset of swollen glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Mumps complications

A

Orchitis 1 in 3
Viral meningitis 1 in 4
Hearing loss 1 in 25
Pancreatitis 1 in 25
Encephalitis 1 in 1000

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Vaccines in the 6-in-1 vaccine

A

Polio
Whooping cough
Influenzae (HiB)
Tetanus
Hep B
Diphtheria

[DT, double P, double HB]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Whooping cough causative organism

A

Gram -ve Bordetella pertussis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Whooping cough school exclusion criteria

A

48 hours after starting antibiotics
Or 3 weeks from symptom onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Whooping cough management

A

Azithromycin or clarithromycin
Only if cough within 3 weeks of start (otherwise supportive)
Also for household contacts

Vaccine for women 16-32 weeks pregnant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Whooping cough diagnostic criteria

A

Cough > 14 days and 1 of:
Paroxysmal cough
Inspiratory whoop
Post-tussive vomiting
Apnoeic attacks in young infants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Why is erythromycin not used for whooping cough?

A

Associated with hypertrophic pyloric stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Threadworms causative organism

A

Enterobius vermicularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Threadworms infection symptoms

A

Anal & vulval itching
Visible white worms in faeces
90% are asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Threadworms investigation

A

Microscopy - sellotape to perianal area
Usually treated empirically

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Threadworms school exclusion criteria

A

No school exclusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Threadworms management

A

Single dose oral mebendazole for entire household > 6 months + hygiene advice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Contraindication to mebendazole for threadworms

A

< 6 months old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Contraindication to mebendazole for threadworms

A

< 6 months old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Steroids escalation

A

Hydrocortisone
Clobetasone
Betamethasone
Mometasone
Clobetasol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Eczema presentation in different ages

A

Infants: trunk and face
Younger children: extensor surfaces
Older children: flexor surfaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Eczema management

A

1st: Simple emollients
2nd: Topical steroids
3rd: Immunosuppressants, topical calcineurin inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Eczema herpeticum

A

Dermatological emergency
Eczema infected with HSV
Acyclovir

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Pityriasis rosea features

A

Herald patch - single pink scaly patch
Self-limiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Head lice organism + management + diagnosis

A

Pediculus capitum

1st line: wet combing / malathion
No school exclusion

Fine tooth combing of wet / dry hair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Management of urticaria

A

Hives
Antihistamines +/- steroids
Usually self limiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Impetigo appearance + management (treatment and school exclusion)

A

‘Golden crusted’ lesions arouns mouth

If well: benzoyl/hydrogen peroxide 1% cream
If signs of infection: fusidic acid or mupirocin
If systemically unwell: oral flucloxacillin (or erythromycin)

School exclusion:
Until lesions are crusted and healed, or 48 hours
after commencing antibiotic treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Impetigo causative organism

A

Staph aureus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Infective mononucleosis causative organism + diagnosis

A

EBV

FBC or Paul Bunnell/Monospot test +ve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Pityriasis versicolor causative organism

A

Malassezia furfur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Pityriasis versicolor appearance + treatment

A

Hypopigmentation patches (more noticeable after suntan)

Antifungals e.g. ketoconazole shampoo
2nd: itraconazole + send scrapings for diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Scabies causative organism + appearance

A

Sarcoptes scabei

Tracks and burrowing between finger webs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Scabies management

A

Whole family

1st: Permethrin cream 8-12 hours
Repeat 1 week later

2nd: malathion

Ivermectin for crusted scabies

School exclusion until treatment complete

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Molluscum contagiosum management

A

Self-limiting + emollients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

DKA investigations

A

Acidosis: pH < 7.3 & bicarbonate < 15mmol/L
Hyperglycaemia > 11mmol/L (unless known diabetic)
Ketonaemia - blood ketones > 3 mmol/L

Electrolytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

DKA severity by pH

A

pH < 7.1 – severe DKA (10% dehydration)
pH < 7.2 – moderate DKA (5% dehydration)
pH < 7.3 – mild DKA (5% dehydration)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

DKA management

A

Fluid resuscitation – 0.9% NaCl – over 48 hours (+ bolus - do not subtract if shocked)
Insulin infusion – 0.1 units/kg/h
Potassium replacement and cardiac monitoring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

DKA complications

A

Cerebral oedema
Hypokalaemia
Hypoglycaemia
Aspiration pneumonia
Death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

DKA: how does cerebral oedema present?

A

Headache
Agitation
Low HR + higher BP
Decreased consciousness
Pupillary inequality or dilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

DKA: management of cerebral oedema

A

Hypertonic saline
Or mannitol
Restrict fluid to half of maintenance rates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Guthrie test: which conditions are screened for?

A

Congenital hypothyroidism
Sickle cell anaemia
Cystic fibrosis
Glutaric aciduria
Homocystinuria
Isovaleric aciduria
Phenylketonuria
Maple syrup urine disease
MCAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Congenital hypothyroidism clinical manifestations

A

Puffy face
Macroglossia
Goitre
Hypotonia
Constipation
Prolonged jaundice
Feeding problems
Umbilical hernia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Congenital hypothyroidism - which type of bilirubinaemia is seen?

A

Unconjugated hyperbilirubinaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

3 sub types of CAH in order of prevalence

A

21-hydroxylase deficiency
11-beta hydroxylase deficiency
17-hydroxylase deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Mode of inheritance of CAH

A

Autosomal recessive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Action of 21-hydroxylase enzyme

A

Converts 17α-hydroxyprogesterone to 11-deoxycortisol in glucocorticoid pathway

Converts progesterone to 11-deoxycorticosterone in the mineralocorticoid pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

% chance of 2 homozygous recessive parents for CAH 21-hydroxylase deficiency having a child with ambiguous genitalia?

A

1/8

Breakdown:
1/4 chance of CAH
1/2 chance of XX child
1/4 x 1/2 = 1/8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Clinical manifestations of 21-hydroxylase deficiency + gene affected

A

Ambiguous genitalia (XX) or precocious puberty (XY)
Salt-wasting

CY212A2 gene mutation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Clinical manifestations of 11-beta hydroxylase deficiency

A

Ambiguous genitalia (XX) or precocious puberty (XY)
Hypertension

112
Q

Clinical manifestations of 17-hydroxylase deficiency

A

Abscence of secondary sex characteristic, amenorrhoea, infertility (XX) or inter-sex (XY)
Hypertension

113
Q

Biochemical abnormalities seen in salt-wasting CAH

A

Lack of aldosterone production
Low Na and high K

Metabolic acidosis on ABG

Hypoglycaemia

114
Q

Management of salt-wasting CAH

A

Hydrocortisone (double dose in illness)
Fludrocortisone

Monitor growth, skeletal maturity and plasma androgens

115
Q

Pathological causes of obesity in children

A

Growth hormone deficiency
Hypothyroidism
Down’s syndrome
Cushing’s syndrome
Prader-Willi syndrome

116
Q

Measuring obesity in children

A

< 2 years: weight to length ratio
> 2 years: BMI to age

117
Q

First sign of onset of puberty in boys

A

Testicular growth: > 4ml

118
Q

First sign of onset of puberty in girls

A

Breast budding

119
Q

Tanner staging: female

A

I - none
II - breast buds form being areolas
III - breast buds elevate beyond areola
IV - areola mounds form and project
V - mounds reduce, adult breasts form

120
Q

Tanner staging: male

A

I - testicular volume < 4ml
II - testicular volume ≥ 4ml, scrotum - enlarges, redens and change in texture
III - penis lengthens, testicular volume ≥ 10ml
IV - penis size increases (length and breadth), development of glans, testicular volume ≥ 16ml, scrotal skin darker
V - adult genitalia

121
Q

Precocious puberty age for diagnosis

A

Before 8 in females
Before 9 in males

122
Q

Classification of precocious puberty

A

Gonadotrophin dependent (central/true)
Due to premature activation of hypothalamic-pituitary-gonadal axis
Increase FSH and LH

Gonadotrophin independent (pseudo/false)
Due to excess sex hormones
Increase FSH and LH

123
Q

Precocious puberty: different testes appearance in males

A

Bilateral enlargement – gonadotrophin release from intracranial lesion
Unilateral enlargement – gonadal tumour
Small testes – adrenal cause

124
Q

Androgen insensitivity syndrome karyotype + mode of inheritance

A

46XY
X-linked recessive

125
Q

Androgen insensitivity syndrome: why can breast development still occur?

A

Testosterone can be converted to oestradiol

126
Q

Management of undescended testes

A

Unilateral
Re-examine 6-8 weeks
Re-examine at 4-5 months
Referral to paed surgery or urology and seen by 6 months

Bilateral
Review within 24 hours by senior paediatrician
If no DSD present – see in 6-8 weeks then urgent surgery 2ww

127
Q

Undescended testes: increased risk of what conditions?

A

Infertility
Testicular torsion
Testicular cancer

128
Q

Undescended testes: what % of cases are bilateral?

A

25%

129
Q

Undescended testes: types

A

Rectractile: testis is not present in scrotum but can be manipulated into scrotum before retracting again
Palpable: testis can be palpated in groin but cannot be manipulated into scrotum
Impalpable: no testis can be felt, and may lie in the inguinal canal, intra-abdominally, or be absent

130
Q

Predisposing factors for undescended testes

A

Prematurity
LBW
SGA
Family history
Maternal smoking during pregnancy

131
Q

Surgical correction for undescended testes

A

Orchidoplexy

132
Q

Neonatal resuscitation steps

A

Dry baby
5 inflation breaths
Re-assess
Recheck head position
Repeat inflation breaths
Chest compressions 3:1 if HR < 60

133
Q

Drugs used in neonatal resuscitation

A

Adrenaline 1:10000
Glucose
Sodium bicarbonate
IV fluids

134
Q

Antibiotics used in necrotising enterocolitis

A

Broad spectrum e.g. cefotaxime and vancomycin

135
Q

Necrotising enterocolitis presentation

A

Bilious vomiting
Blood in stools
Neonatal age
Distended abdomen
Shock
Food intolerance

136
Q

Risk factors for developing necrotising enterocolitis

A

SGA/IUGR/LBW
Prematurity
Formula feeds
Sepsis
PDA and other CHD
Co-amoxiclav use in pregnancy

137
Q

Necrotising enterocolitis diagnostic investigation + findings

A

Abdominal Xray

Dilated bowel loops
Pneumatosis intestinalis
Pneumoperitoneum

138
Q

Complications of necrotising enterocolitis

A

Perforation
Peritonitis
Stoma
Short bowel syndrome

139
Q

APGAR scoring

A

Activity
Pulse
Grimace
Appearance
Respiration

140
Q

Management of respiratory distress syndrome

A
  1. O2
  2. Intubate
  3. CO2 monitoring
  4. Surfactant therapy – intratracheal instillation
  5. Nasal CPAP and mechanical ventilation
  6. Fluids if indicated
141
Q

Management of transient tachypnoea of the newborn

A

Supportive management

142
Q

Xray findings seen in transient tachypnoea of the newborn

A

Fluid in horizontal fissure
Hyperinflation of lungs

143
Q

Meconium aspiration syndrome presentation

A

Meconium stained liquor
Respiratory distress

144
Q

Meconium aspiration syndrome Xray findings

A

Patch infiltrations
Atelectasis

145
Q

Meconium aspiration complications

A

Pneumothorax / pneumomediastinum from air leak
Persistent pulmonary hypertension of newborn
Respiratory tract infection

146
Q

Causative organisms of early onset (< 72 h) neonatal sepsis

A

GBS
E. Coli
P. Aeruginosa

147
Q

Causative organisms of late onset (> 72 h) neonatal sepsis

A

S. Aureus
S. Epidermis
Pseudomonas

148
Q

Sepsis 6

A

Blood culture
FBC
CRP
Blood gases
Urine MCS
LP

149
Q

Indications for fluid bolus for neonatal sepsis

A

Shock
Lactate > 2mmol/L

150
Q

Neonatal jaundice < 24 hours old

A

Always pathological

151
Q

Neonatal jaundice investigations

A

SBR > 80 µmol/L
FBC and film
Direct Coomb’s test

152
Q

3 causes of neonatal jaundice < 24 hours

A

Sepsis
Haemolytic cause
Congenital infection
Cephalohaematoma

153
Q

Mechanism of phototherapy

A

Light converts unconjugated bilirubin into water soluble pigment

154
Q

Which type of bilirubinaemia can cause kernicterus?

A

Unconjugated bilirubinaemia
Fat soluble so can cross BBB

155
Q

Kernicterus: which part of the brain is affected?

A

Basal ganglia

156
Q

Most common cause of SIDS

A

Hypoxia

157
Q

4 risk factors for SIDS

A

Prone sleeping
Parental smoking
Bed sharing
Hyperthermia and head covering
Prematurity

158
Q

Management of asymptomatic neonatal hypoglycaemia

A

Encourage normal feeding
Monitor blood glucose

159
Q

Management of symptomatic neonatal hypoglycaemia

A

Admit to neonatal unit
IV 10% dextrose

160
Q

Symptoms of neonatal hypoglycaemia

A

Jitteriness
Seizures

161
Q

Management of asymptomatic neonatal hypoglycaemia < 1mmol/L

A

Admit to neonatal unit
IV 10% dextrose

162
Q

Risk factors for neonatal hypoglycaemia

A

Preterm
Maternal DM
IUGR
Hypothermia
Neonatal sepsis

163
Q

Cleft lip pathophysiology

A

Failure of fronto-nasal and maxillary processes to fuse

164
Q

Cleft palate pathophysiology

A

Failure of palatine processes and nasal septum to fuse

165
Q

Blueberry muffin rash association

A

TORCH infection
Mum with recent flu

166
Q

Management of ITP

A

Depends on symptoms. Doesn’t need to be treated.
Otherwise:
1st: Steroids
2nd: IV IG
3rd: Rituximab

167
Q

Pathophysiology of HbS formation

A

Substitution of Glu with Val in B chain
HbS polymerises to form sickle shaped cells

168
Q

FBC findings for sickle cell anaemia

A

Low Hb
High reticulocyte count

169
Q

Sickle cell anaemia management

A

Folic acid supplementation

Prophylactic hydroxyurea/hydroxycarbamide - increased HbF levels - prevents painful episodes or blood transfusion

Bone marrow transplant - if severe disease

170
Q

Mechanism of hydroxycarbamide

A

Increases HbF levels

171
Q

Management of vaso-occlusive crisis in SCD

A

IV fluids and analgesia

172
Q

Acute complications seen in SCD

A

Acute chest syndrome
Splenic sequestration crisis
Vaso-occlusive/thrombotic/painful crisis
Aplastic crisis
Haemolytic

173
Q

Features of vaso-occlusive crisis

A

Precipitated by infection, dehydration, deoxygenation

174
Q

Features of sequestration crisis

A

Sickling within organs - splenomegaly
Increased reticulocyte count

175
Q

Presentation of acute chest syndrome

A

Dyspnoea
Chest pain
Pulmonary infiltrate on CXR

176
Q

Features of aplastic crisis

A

Parvovirus infection

Fall in Hb
Reduced reticulocyte count - bone marrow suppression

177
Q

Blood film appearance in sickle cell trait

A

Normal

178
Q

Blood film appearance in SCD

A

Sickled cells
Howell-Jolly bodies

179
Q

Diagnostic investigation SCD

A

Haemoglobin electrophoresis

180
Q

% chance of 2 carriers of sickle cell gene having unaffected offspring

A

75%=
25% unaffected
+
50% sickle cell trait

181
Q

Most common bleeding disorder

A

Von Willebrand disease

182
Q

Most common clotting disorder

A

Factor V Leiden

183
Q

Haemophilia clotting results

A

Prolonged PTT
Low factor 8/9 and normal vWF
Normal PT and platelet
Normal bleeding time

184
Q

Haemophilia mode of inheritance

A

X-linked recessive

185
Q

Von Willeband disease mode of inheritance

A

Autosomal dominant

186
Q

Fanconi anaemia mode of inheritance

A

Autosomal recessive

187
Q

Fanconi anaemia features

A

Most common cause of inherited aplastic anaemia

Café au lait spots
Short stature
Thumb/radius abnormalities

188
Q

Non-immune causes of hydrops foetalis

A

Severe anaemia e.g. parvovirus B19, alpha thalassaemia major, haemorrhage
Twin-to-twin transfusion syndrome
Infections e.g. CMV, rubella, VZV
Chorioangioma
Cardiac abnormalities

189
Q

Immune causes of hydrops foetalis

A

Blood group incompatility - haemolytic disease of newborn

190
Q

Beta thalassaemia mode of inheritance

A

Autosomal recessive

191
Q

3 subtypes of beta thalassaemia

A

Beta thalassaemia minor – 1 gene inherited of reduced/absent beta chains – heterozygote

Beta thalassaemia intermedia – 2 genes inherited of reduced beta chains

Beta thalassaemia major – 2 genes inherited for absent beta chains (beta 0) – homozygote

192
Q

Medical management options for constipation

A

1st: Osmotic laxative e.g. Movicol/macrogol
2nd: Stimulant laxative e.g. Senna
3rd: Alternative osmotic laxative e.g. Lactulose

193
Q

Management of gastroenteritis

A

Oral rehydration solution
Admit if severely dehydrated

194
Q

Management of gastro-oesophageal reflux

A

Advice regarding feeds

Trial thickened formula

2 week trial alginate therapy e.g. Gaviscon

4 week trial omeprazole suspension if:
Unexplained feeding difficulties
Distressed behaviour
Faltering growth

195
Q

Surgical procedure for GORD

A

Nissen fundoplication

196
Q

Meckel’s diverticulum presentation

A

Usually asymptomatic

Severe rectal bleeding
Intestinal obstruction: volvulus/intussusception

197
Q

Meckel’s diverticulum: investigation if haemodynamically stable

A

Technetium scan

198
Q

Meckel’s diverticulum: investigation if haemodynamically unstable

A

Mesenteric arteriography

199
Q

Meckel’s diverticulum surgical procedure

A

Wedge excision or small bowel resection

200
Q

Cow’s milk protein allergy management

A

Specialised formula feeds - extensively hydrolysed

201
Q

Cow’s milk protein allergy: differentiating IgE and non-IgE mediated

A

IgE mediated can be tested immediately with skin prick test as reacts immediately
Non-IgE is delayed

202
Q

Why is it advised that infants do not drink cow milk before age 1?

A

Risk of iron deficiency anaemia

203
Q

CMPA prognosis

A

55% with IgE mediated can drink cow’s milk by 5 years old

204
Q

Which type of hyperbilirubinaemia is seen in biliary atresia?

A

Conjugated bilirubinaemia

205
Q

Biliary atresia management

A

Surgery: Kasai procedure (hepatoportoeterostomy)

Nutrition and vitamin supplementation

Liver transplant if surgery fails or late presentation

206
Q

Diagnostic investigation for biliary atresia

A

Cholangiography/ERCP

207
Q

Biliary atresia presentation

A

Neonatal jaundice
Hepatomegaly and splenomegaly
Dark urine and pale stools

208
Q

First line imaging for biliary atresia

A

Ultrasound visualises fibrosis of biliary system

209
Q

Duodenal atresia presentation

A

Bilious vomiting from birth

210
Q

Definitive treatment of duodenal atresia

A

Duodenoduodenostomy

211
Q

Duodnela atresia Xray findings

A

‘Double bubble’ sign

212
Q

Duodenal atresia associated conditions

A

Down syndrome

213
Q

Pathophysiology of duodenal atresia

A

During 5th and 6th week of foetal development, duodenum is a solid cord

Apoptosis of cells in the centre of the solid cord leads to formation of normal cavity (lumen) of the duodenum - failure of process leads to duodenal atresia

214
Q

Blind-ending oesophagus epidemiology

A

Oesophageal atresia alone - 10%

85% have blind proximal oesophagus with distal oesophagus having fistula with trachea

5% have fistulae in both proximal and distal oesophagus

215
Q

Oesophageal atresia presentation

A

Polyhydramnios

Postnatal:
Respiratory distress
Drooling
Choking/swallowing problems
Distended abdomen

216
Q

Oesophageal atresia investigation

A

NG tube + CXR - NG tube inserted until it can’t go further and Xray is taken

217
Q

Management of oesophageal atresia

A

Surgical correction

218
Q

Most common site of intussusception

A

Ileocecal site

219
Q

Intussusception presentation

A

Sausage-shaped mass in abdomen
Redcurrant jelly stool
Abdominal distension
Shock

220
Q

Intussusception management

A

IV fluids
1st: Rectal air insufflation
2nd: Surgical reduction

221
Q

Intussusception investigations

A

USS: target sign
Concentric echogenic and hypogenic bands

222
Q

% of children requiring surgical reduction of intussusception

A

25%

223
Q

Giardiasis mangement

A

3 days metronidazole

224
Q

Giardiasis diagnostic criteria

A

Cysts in stool and motile forms in small intestine

225
Q

Coeliac disease presentation

A

Wasting of buttocks
Steatorrhoea (difficult to flush)
Dermatitis herpetiformis

226
Q

Coeliac disease investigations

A

TTG
Anti-endomysial and anti-gliadin antibodies

Gold: Small bowel biopsy from duodenum/jejunum

227
Q

Hirschsprung’s disease presentation

A

Neonates
Constipation
Delayed passage of meconium (after 48 hours)
Bilious vomiting
Lethargy & dehydration
Distended abdomen

228
Q

Hirschsprung’s disease investigations

A

AXR – dilated colon
Gold standard: rectal suction biopsy – shows lack of ganglionic nerves

229
Q

Hirschsprung’s disease management

A

1st line: Rectal washouts/bowel irrigation
Gold standard: surgery to affected segment of colon

230
Q

Hirschsprung’s disease surgical procedure

A

Swenson procedure

231
Q

Hirschsprung’s disease associated disorders

A

Down’s syndrome
Multiple endocrine neoplasia type IIa

232
Q

Meconium ileus management

A

“Drip and suck” - IV fluids and stomach drainage
Surgery if severe

233
Q

Meconium ileus investigation findings

A

AXR: bubbly appearance of intestines & lack of air-fluid levels

234
Q

Pyloric stenosis metabolic + electrolyte abnormality

A

Metabolic alkalosis
Hyponatraemia, hypokalaemia & hypochloraemia

235
Q

Pyloric stenosis management

A

NBM
IV fluids

Ramstedt pylorotomy

236
Q

Pyloric stenosis presentation

A

Non-bilious, projectile vomiting after feeds
Visible gastric peristalsis
Weight loss
Palpable, olive shaped mass on abdomen

237
Q

Pyloric stenosis investigations

A

Ultrasound - hypertrophy of pyloric sphincter

238
Q

Antibiotic use associated with pyloric stenosis

A

Macrolides e.g. erythromycin

239
Q

Malrotation presentation

A

Bilious vomiting
Abdominal pain

240
Q

Malrotation associated conditions

A

Exomphalos
Diaphragmatic herniae

241
Q

Malrotation management

A

Ladd’s procedure - division of Ladd bands and widening base of mesentery

242
Q

Congenital diaphragmatic herniae epidemiology

A

1 in 2000 newborns
50% survival rate
85% on left side

243
Q

Congenital diaphragmatic hernia manifestations

A

Respiratory distress
Bowel sounds in respiratory exam
Scaphoid abdomen (concave)
Reduced breath sounds

244
Q

Poor prognostic factor for congenital diaphragmatic hernia

A

Liver in thoracic cavity

245
Q

Management of umbilical hernia

A

Large or symptomatic – repair at 2-3 years
Small and asymptomatic – repair at 4-5 years

246
Q

Umbilical granuloma presentation

A

Overgrowth of red tissue – occurs during healing of umbilicus
Wet umbilicus, leaks clear/yellow fluid

247
Q

Umbilical granuloma management

A

Add salt to wound – osmosis occurs – tissue necroses

248
Q

Management of omphalitis

A

Topical + systemic steroids

249
Q

Mesenteric adenitis presentation

A

Enlarged mesenteric lymph nodes with normal appendix

250
Q

Risk associated with corticosteroid use in neonates < 8 days

A

Gastrointestinal perforation

251
Q

Prematurity + developmental milestones

A

Adjust for gestational age until age 2 (40 weeks**)

252
Q

Prematurity + immunisation schedule

A

Do not adjust for gestational age

253
Q

Suckling reflex

A

Develops at 35 weeks
NG tube feeds before this

254
Q

Surfactant production

A

Occurs between 24 - 28 weeks

255
Q

Prematurity: management of apnoea and bradycardia

A

Nasal CPAP
Stimulation with caffeine

256
Q

Why is there an increased risk of infection in premature infants?

A

Active IgG transfer occurs in last 3 months of pregnancy

257
Q

Medical management of neonatal abstinence syndrome

A

Opiate: Oral morphine sulphate
Non-opiate: Oral phenobarbitone

258
Q

Antibiotics given in preterm infants

A

IV BenPen + gentamicin

259
Q

6 in 1 vaccine contents

A

DT, double P, double Hb

Diphtheria
Tetanus
Pertussis
Polio
HiB
Hep B

260
Q

4 in 1 vaccine contents

A

Pre-school booster

Diptheria
Tetanus
Pertussis
Polio

261
Q

3 in 1 vaccine contents

A

Teenage booster:

Tetanus
Diphtheria
Polio

262
Q

3 inactivated vaccines

A

Rabies
Influenza
Polio

263
Q

2 conjugated vaccines

A

HiB
PCV

264
Q

Live attenuated vaccines

A

MMR
Rotavirus
Polio (inactivated in schedule)
BCG
Influenza (nasal) IM is inactivated
Typhoid
Yellow fever

265
Q

Toixoid vaccines

A

Diphtheria
Tetanus
Pertussis

266
Q

mRNA vaccines

A

Moderna
Pfizer

Encode spike protein

267
Q

Vaccines given at 2 months

A

6 in 1
Men B
Rotavirus

268
Q

Vaccines given at 3 months

A

6 in 1
PCV
Rotavirus

269
Q

Vaccines given at 4 months

A

6 in 1
Men B

270
Q

Vaccines given at 12-13 months

A

MMR
PCV
Men B
HiB / Men C

271
Q

Vaccines given at 2-8 years old

A

Annual flu vaccine

272
Q

Vaccines given at 3-4 years old

A

4 in 1 booster: diphtheria, tetanus, pertussis, polio
MMR

273
Q

Vaccines given at 12-13 years old

A

HPV vaccination

274
Q

Vaccines given at 13-18 years old

A

Men ACWY
3 in 1 booster: tetanus, diphtheria, polio

275
Q

First sign of onset of puberty in boys

A

Testicular growth: > 4ml

Medicine (13 decks)

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