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Phase 3a - Arun&Erin > Paeds - Endocrine, Oncology, Neonatal > Flashcards

Paeds - Endocrine, Oncology, Neonatal Flashcards

1
Q

what is congenital hypothyroidism?

A

child is born with an underactive thyroid gland. This occurs in around 1 in 3000 newborns.

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2
Q

what two ways does congenital hypothyroidsm occur

A

dysgenesis - thyroid gland is underdeveloped

dyshormonogenesis - fully developed gland that does not produce enough hormone

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3
Q

how is congenital hypothyroidism picked up

A

newborn blood spot screening test

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4
Q

what is the presentation of congenital hypothyroidsm (6)

A

-poor feeding
-constipation
-increased sleeping
-reduced activity
-slow growth and development
-prolonged neonatal jaundice

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5
Q

what is hashimotos thyroiditis

A

an acquired autoimmune hypothyroidism leading to inflammation of the thyroid gland

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6
Q

what antibodies is hashimotos thyroiditis associated with (2)

A

-antithyroid peroxidase (anti-TPO)
-antithyroglobulin antibodies

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7
Q

Sx of hashimotos thyroditis

A

-Fatigue and low energy
-Poor growth
-Weight gain
-Poor school performance
-Constipation
-Dry skin and hair loss

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8
Q

Ix of hypothyroidism (3)

A

thyroid function blood tests (TSH, T3 and T4), thyroid ultrasound
thyroid antibodies

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9
Q

Mx of hypothyroidism

A

Levothyroxine once daily

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10
Q

risk factors for undescended testes (5)

A

Family history of undescended testes
Low birth weight
Small for gestational age
Prematurity
Maternal smoking during pregnancy

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11
Q

What is cryptorchidism

A

A congenital condition where the testis fail to reach the bottom of the scrotum by 3 months of age

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12
Q

Complications of cryptorchidism

A

-risk of infertility
-increased risk of testicular seminoma (cancer)
-testicular torsion

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13
Q

Tx of cryptorchidism (3)

A

Orchidopexy at 6- 18 months of age - mobilisation of testis into dartos pouch ( bottom of scrotum)

Intra-abdominal testis - evaluated laparoscopically and mobilised.

Past 2 years
Orchidectomy as decreased risk of malignancy

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14
Q

What is retractile testicles

A

Before puberty the testes move out the scrotum into the inguinal canal due to cremasteric reflex

Sometimes do not come back down and need orchidopexy

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15
Q

what is hypogonadotropic Hypogonadism

A

deficiency in LH and FSH (gonadotrophins)

leading to a deficiency in oestrogen and testosterone

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16
Q

what is the root cause of hypogonadotrophic hypogonadism

A

abnormal functioning of pituitary gland

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17
Q

give 5 causes of hypogonadotropic Hypogonadism

A

-damage to hypothalamus or pituitary
-tumours - astrocytomas, craniopharygiomas, prolactinomas
-GH deficiency
-Hypothyroidism
-Hyperprolactinameia (high prolactin)
-CF - delay puberty
-IBD - delay puberty
-kallmans syndrome
-excessive exercise or dieting -delays menstruation in girls
-bulimia

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18
Q

what is kallmans syndrome

A

-genetic condition resultig in the failure to start puberty and an impairment in smell

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19
Q

what is kallmans syndrome associated with

A

anosmia - absent smell

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20
Q

investigations for delay in puberty
categories
1. initial (3)
2. hormonal blood tests (4)
3.genetic tests (2)
4 imaging (3)

A

initial
-FBC + ferritin for anaemia
-U+E - for CKD
-Anti TTG/ anti EMA - coeliac

hormonal blood tests
-early morning LH + FSH - low in hypogonadotropic Hypogonadism
-TFTs
-GH tests - insulin like growth factor
-serum prolactin

Genetic testing
-kleinfelters
-turners
(can both cause delayed puberty

Imaging
-xray of the wrist to assess bone age
-pelvic ultrasound - assess ovaries
-MRI of the brain - pituitary pathology + assess olfactory bulbs (kallmans syndrome)

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21
Q

what is HYPERgonadotropic hypogonadism

A
  • gonads dont respond to stimulation from the gonadotrophins (LH and FSH)
  • There is no negative feedback from the sex hormones (testosterone and oestrogen),

-so anterior pituitary produces increasing amounts of LH and FSH to try harder to stimulate the gonads

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22
Q

what are the potential causes of hypergonadtropic hypogoandism

A

is due to abnormal functioning gonads

genetic:
-kleinfelters
-turners syndrome

-congenital abscence of the ovaries or testes

-previous damage to the gonads e.g testicular torsion

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23
Q

Management for a delay in puberty

A

-treat the underlying condition e.g GH deficiency
-replacement of sex hormones to induce puberty

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24
Q

what inheritance pattern is kallmanns syndrome

A

x linked recessive

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25
Q

features of kallmanns sydnrome

A

-delayed puberty
-hypogonadism
-cryptorchidism
-anosmia
-sex hormone levels low
-low FSH and LH
-patients above average height
-cleft lip
-visual/ hearing defects

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26
Q

Mx of kallmanns syndrome

A

-testosterone supplementation
-Gonadatrophin (LH/FSH) supplementation

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27
Q

typical epidemiology of kallmanns syndrome

A

lack of smell in a boy with delayed puberty

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28
Q

what is androgen insensitivity syndrome

A

condition where cells are unable to respond to androgen hormones due to a lack of androgen receptors

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29
Q

what inheritance pattern is androgen insensitivity syndrome

A

X linked recessive

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30
Q

Sx of androgen insensitivity syndrome

A

-lack of pubic hair + facial hair
-taller in height - female
-infertility
-primary amenorrhoea - abscence of menstruation
-undescended testes
-breast developement

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31
Q

Why do males with androgen insensitivity syndrome develop external female characteristics

A

-the males produce testosterone but there is no response to it

-there is also conversion of additional androgens to oestrogen

-this leads to a female phenotype externally

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32
Q

Presentation of someone with androgen insensitivity syndrome

A

-inguinal hernias containing testes in infancy
-primary amennorrhoea at puberty

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33
Q

Mx of androgen insensitivity syndrome

A

Bilateral orchidectomy - to avoid testicular cancer

Oestrogen therapy

Vaginal dilators and vagina surgery to create adequate vaginal length

Counselling - understand how to live with condition socially and sexually - normally raised as female

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34
Q

How to diagnose androgen insensitivity syndrome (2)

A

-buccal smear/ chromosome analysis to reveal 46 XY chromosome

-post puberty testosterone levels will be higher than normal

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35
Q

What is congenital adrenal hyperplasia

A

Congenital deficiency of 21 hydroxylase enzyme causing underproduction: Cortisol + Aldosterone
Overproduction of androgens

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36
Q

Inheritance pattern of Congenital adrenal hyperplasia

A

Autosomal recessive

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37
Q

Give three examples of steroid hormones

A

Androgens - e.g Testosterone

Glucocorticoids- e.g Cortisol

Mineralcorticoids - e.g Aldosterone

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38
Q

Pathophysiology of congenital adrenal hyperplasia

A

-21 hydroxylase normally converts progesterone into aldosterone and cortisol

-progesterone is also used to create testosterone

-the defect in the 21 hydroxylase means extra progesterone circulates with less conversion to
Aldosterone and cortisol

-gets converted to testosterone

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39
Q

Levels in Congenital adrenal hyperplasia in
Aldosterone
Cortisol
testosterone

A

Aldosterone - low
Cortisol - low
testosterone -high

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40
Q

How to diagnosis Congenital adrenal hyperplasia

A

-ACTH simulation testing measures adrenal gland response to ACTH

-newborn screen - not offered in UK

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41
Q

Presentation in MILD cases of congenital adrenal hyperplasia

A

Female patients - virilization (more manly)
Tall for age
Deep voice
Early puberty
Hyperpigmentation

Facial hair
Absent periods

Male patients
Tall for age
Deep voice
Early puberty
Hyperpigmentation

Large penis
Small testicles

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42
Q

Presentation of severe cases of Congenital adrenal hyperplasia

A

-ambiguous genitalia in females
-enlarged clitroris (due to high testosterone)
-skin pigmentation -due to ACTH

-salt wasting crisis which can lead to: - too little aldosterone
Poor feeding
Arrhythmias
Dehydration
Vomiting

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43
Q

In CAH what is salt wasting crisis and what three conditions does this cause

A

LIFE THREATENING
-adrenal glands make too little aldosterone, causing the body to be unable to retain enough sodium

-leads to hyponatraemia, hypoglycaemia + hypokalemia

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44
Q

Why skin hyperpigmention in CAH

A

-anterior pituitary gland responds to the low levels of cortisol by producing increasing amounts of ACTH

-A byproduct of the production of ACTH is melanocyte simulating hormone.

-This hormone stimulates the production of melanin (pigment) within skin cells.

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45
Q

Mx of CAH (3)

A

See paediatric endocrinologist

-Cortisol replacement - hydrocortisone,

-Aldosterone replacement - fludrocortisone

-Female patients with ambiguous genitals may require corrective surgery

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46
Q

What are gliomas

A

Tumours of the brain and spinal cord

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47
Q

What are the three types of glial cells

A

astrocytes
oligodendrocytes
ependymal cells

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48
Q

Types of gliomas - which one is most malignant

A

Astrocytoma (the most common and aggressive form is glioblastoma)

Oligodendroglioma

Ependymoma

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49
Q

Tx of gliomas

A

Radiation and chemotherapy

-correct hormone imbalances if necessary

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50
Q

What condition may increase risk of hypothalamic tumours

A

Neurofibromatosis

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51
Q

Sx of hypothalamic tumours

A

-euphoric sensations
-failure to thrive
-headache - fluid can collect in brain
-hyperactive
-loss of appetite
-vision loss
-seizures

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52
Q

What is precocious puberty

A

onset of secondary sexual characteristics in children at an age that is two standard deviations younger than the mean age of pubertal onset

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53
Q

What are the two types of precocious puberty

A

central + Peripheral

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54
Q

What is central precocious puberty

A

-early maturation of hypothalamic+pituitary gonadal axis

-early release of LH+FSH

-increases sex hormones

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55
Q

Causes of central precocious puberty

A

-largely idiopathic
-infection/cyst
-radiation damage to brain (reduced -ve feedback)
-GnrH secreting tumour

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56
Q

What is peripheral precocious puberty

A

Overproduction of sex hormones by gonads (GnRH independent)

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57
Q

Causes of peripheral precocious puberty (5)

A

-cyst/tumour
-genetic condtions - mccune Albright syndrome
-thyroid/ adrenal dysfunction
-exogenous hormones e.g creams

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58
Q

How to diagnose precocious puberty

A

-Tanner scale
-GnRH levels - see if dependent (central) or independent (peripheral)
-ultrasound/MRI - to look for abnormalities

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59
Q

Tx of precocious puberty

A

GnRH analogues - reduce LH/FSH production

Surgery to remove cyst/ tumour

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60
Q

What is testicular torsion

A

Twisting of the spermatic cord with rotation of the testicle which can lead to ischemia and necrosis

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61
Q

Presentation of testicular torsion

A

-Sudden onset severe scrotal pain,
-Abdominal pain - in boys always rule out TT
-nausea + vomiting.
-Tender testis.
-Overlying scrotal skin may be reddened and oedematous.

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62
Q

What is bell clapper deformity

A

RISK FACTOR FOR TESTICULAR TORSION

where the fixation between the testicle and the tunica vaginalis is absent so the testicle hangs in the horizontal postion and is more able to twist

63
Q

Mx of testicular torsion

A

SEEN WITHIN 6 HOURS

-Nil by mouth, in preparation for surgery
-Analgesia as required
-Urgent senior urology assessment

-Surgical exploration of the scrotum

-Orchiopexy (correcting the position of the testicles and fixing them in place)

-Orchidectomy (removing the testicle) if the surgery is delayed or there is necrosis

64
Q

What is whirlpool sign in testicular torsion

A

-In an ultrasound scan used to confirm the diagnosis
- will see a spiral appearance of the spermatic cord and blood vessels

65
Q

What are the examination findings of testicular torsion

A

-absent cremasteric reflex
-elevated testicle
-firm swollen testicle
-abnormal lie (horizontal)
-epididymis in wrong place

66
Q

What is wilms tumour

A

Specific type of tumour affecting the kidney in children, typically under the age of 5 years.

67
Q

Presentation of wilms tumour

A

mass in abdomen
Abdominal pain
Haematuria
Lethargy
Fever
Hypertension
Weight loss

68
Q

Dx of wilms tumour

A

initial investigation
-ultrasound of the abdomen to visualise the kidneys.

-A CT or MRI scan used to stage the tumour.

-Biopsy to make a definitive diagnosis.

69
Q

Mx of Wilms tumour

A

-surgical excision of the tumour along with the affected kidney (nephrectomy).

Adjuvant therapy
-radiotherapy
-chemotherapy

70
Q

Which tumour most commonly spread to brain

A

lung (most common)
breast
bowel
skin (namely melanoma)
kidney

71
Q

Most common brain tumour in children

A

Pilocytic astrocytoma

72
Q

Tx of medullobalstoma

A

Treatment is surgical resection and chemotherapy.

73
Q

What is craniopharygioma

A

solid/cystic tumour of the sellar region that is derived from the remnants of Rathke’s pouch

74
Q

Presentation of craniopharyngioma

A

hormonal disturbance
symptoms of hydrocephalus
bitemporal hemianopia.

75
Q

What will you find on imaging on glioblastoma multiforme

A

solid tumours with central necrosis and a rim that enhances with contrast.

76
Q

Mx of pituitary tumours

A

-Trans-sphenoidal surgery (through the nose and sphenoid bone)

-Radiotherapy

-Bromocriptine to block excess prolactin

-Somatostatin analogues (e.g., octreotide) to block excess growth hormone

77
Q

Presentation of pituitary tumours

A

Bitemporal hemianopia

Cushings sx moon face, purple striae
Acromegaly sx big hands and jaw, headaches
Hyperprolactoinaemia sx galactorrhea, amenorrhea
Thyrotoxicosis sx palpitations, anxiety, fatigue

78
Q

What are acoustic neuromas

A

benign tumours of the Schwann cells that surround the vestibulocochlear nerve that innervates the inner ear

79
Q

What condition are acoustic neuromas associated with

A

neurofibromatosis type 2.

80
Q

Presentation of acoustic neuromas

A

Unilateral sensorineural hearing loss (often the first symptom)
Unilateral tinnitus
Dizziness or imbalance
Sensation of fullness in the ear
Facial nerve palsy (if the tumour grows large enough to compress the facial nerve)

81
Q

1st line investigation in patients with brain tumours

A

MRI scan

82
Q

Presentation of retinoblastoma

A

abnormal light reflex - White pupillary reflex
squint
visual deterioration

83
Q

What is a retinoblastoma?

A

A malignant tumour of retinal cells

84
Q

What secondary malignancy can occur in retinoblastoma?

A

Sarcomas (soft tissue cancer)
Osteosarcoma (bone)

85
Q

What is the treatment of retinoblastoma?

A

-Chemotherapy followed by local laser treatment to the retina

-Radiotherapy

-Enucleation of the eye - removal of eye from muscles and tissue

86
Q

What marker is raised in hepatoblastoma?

A

Serum Alpha feto protein

87
Q

Treatment of hepatoblastoma (3)

A

Chemotherapy, e.g. platinum drugs and anthracyclines

Surgical resection

Liver transplant

88
Q

What are the two types of bone cancer in children?

A

Ewing sarcoma
Osteogenic sarcoma - more common

89
Q

Which gender is more likely to get bone tumours?

A

Males

90
Q

Presentation of bone tumours

A

Persistent localised bone pain usually present in limbs

91
Q

Management of bone tumours

A

Chemotherapy before surgery

En block resection - removal of tumour without removal of its capsule

Radiotherapy – only in Ewing sarcoma

92
Q

What are neuroblastomas?

A

Tumours that arise from neural crest tissue in the adrenal medulla and sympathetic nervous system

93
Q

Presentation of neuroblastoma

A

Usually an abdominal mass present
Weight loss
Pallor
Hepatomegaly
Bone pain
Limp

Less common:
Paraplegia
Skin nodules
Raccoon eyes
Proptosis

94
Q

Investigations for neuroblastoma (4)

A

Bloods + urine - raised Catecholamines (hormones produced in adrenal glands

Biopsy

Ultrasound of abdomen

MIBG scan - neuroendocrine cells absorb so you can map and see abnormalities

95
Q

Management of neuroblastoma

A

Nonmetastatic
Surgery

Metastatic disease
Chemotherapy
Surgery
Radiotherapy
Retinoic acid - reduces recurrence

96
Q

Risk factors for hypoglycaemia in first 24 hours of life

A

-too small for gestational age - intrauterine growth restriction
-polycythaemia
-maternal diabetes mellitus
-prematurity
-hypothermia

97
Q

Mx of hypoglycaemia in newborns

A

Prevention - early and frequent milk feeding
Monitor blood glucose

Increased risk of hypoglyceamia - regularly monitor blood glucose

If blood glucose below 2.6/ symptomatic :
IV dextrose to maintain above 2.6
IM glucagon

98
Q

How should you administer high concentrations of glucose in someone with hypoglyceamia and why?

A

Central venous catheter

To avoid:
Reactive hypoglycemia - too much insulin produced in response causing reactive dip in BG

Extravasation(leakage) into the tissues - lead to skin necrosis

99
Q

Sx of hypoglycaemia in neonates

A

-Cyanosis
-apnoea
-seizures + tremors
-sweating
-irritability
-hypotonia
-difficulty feeding
-lethargy

100
Q

How is nocturnal hypoglycaemia treated

A

Bolus insulin regimes
Snacks at bedtime to regulate throughout the night

101
Q

What is respiratory distress syndrome

A

A disease affecting premature neonates born before the lungs start to produce enough surfactant

102
Q

Pathology of respiratory distress syndrome

A

-Inadequate surfactant leads to high surface tension within alveoli.

-This leads to atelectasis (lung collapse), as it is more difficult for the alveoli and the lungs to expand.

-This leads to inadequate gaseous exchange, resulting in hypoxia, hypercapnia (high CO2) and respiratory distress.

103
Q

Mx of respiratory distress syndrome

A

-dexamethasone - allows for maturation of lungs and increased surfactant production

Premature neonates may need:

Intubation and ventilation- fully assist breathing
Endotracheal surfactant- artificial surfactant
Continuous positive airway pressure (CPAP) - keep lungs open
Supplementary oxygen

104
Q

Complications of respiratory distress syndrome

Short term
Long term

A

Short term:
Pneumothorax
Infection
Apnoea
Intraventricular haemorrhage
Pulmonary haemorrhage
Necrotising enterocolitis

Long term:
Chronic lung disease of prematurity
Retinopathy of prematurity
Neurological, hearing and visual impairment

105
Q

What is the investigation for respiratory distress syndrome

A

Chest X- ray
* ground glass appearance of lungs
*Air bronchogram - heart borders become obscured due to lungs being more opaque

ABG- check blood oxygen

106
Q

Clinical signs of RDS

A

-tachypnoea - 60 breaths per minute +
-laboured breathing
-recessions
-tracheal tug
-nasal flaring
-expiratory grunting
-cyanosis - if severe

107
Q

What is bronchopulmonary dysplasia?

A

A breathing disorder in premature infants resulting from poor lung growth

108
Q

What is the prevention of bronchopulmonary dysplasia

A

-corticosteroids to mothers that show signs of pre term labour at less than 36 weeks

-Use of CPAP
-caffeine to stimulate respiratory effort
-not over oxygenating

109
Q

Mx of bronchopulmonary dysplasia (6)

A

Corticosteroids given to mothers showing signs of prematurity

CPAP for the neonate

Caffeine- stimulated respiratory effort

Not over oxygenating

Sleep study - assess o2 sats during sleep

Home low dose oxygen - slowly weaned off

RSV protection for bronchiolitis - monthly injection of palivizumab

110
Q

Clinical feature of bronchopulmonary dysplasia

A

-low oxygen saturations
-increased work of breathing
-poor weight gain
-poor feeding
-wheeze
-crackles
-increased susceptibility to infection

111
Q

What is meconium aspiration

A

Where the baby passes meconium in the womb and swallows it into the lungs

112
Q

Sx of meconium aspiration

A

-cyanosis
-breathing problems
-greenish amniotic fluid
-limpness of infant
-coarse crackles
-bradycardia

113
Q

Tx of meconium aspiration (5)

A

-large bore suction Catheter
-if bradycardic then CPAP
-Abx to treat any infection
-maintain body temperature
-chest tapping to loosen secretions

114
Q

Dx of aspiration Pneumonia (4)

A

-fetal monitor - shows bradycardia
-abnormal breath sounds - coarse crackles
-capillary blood gas - acidosis, decreased oxygen and increased CO2
-CXR- streaky areas on lungs

115
Q

What is hypoxic ischemic encephalopathy

A

A lack of oxygen during birth causing lack of oxygenated blood flow to the brain leading to brain damage (encephalopathy)

116
Q

Biggest complications of HIE

A

Cerebral palsy

117
Q

Causes of HIE

A

Intrapartum haemorrhage
Maternal shock
Prolapsed cord - compression of cord during birth
Nuchal cord - cord wrapped around the neck Of baby

118
Q

Mx of HIE

A

Supportive care
-neonatal resuc
-ventilation
-acid base balance
-circulatory support
-therapeutic hypothermia

119
Q

What is therapeutic hypothermia for HIE

A

Reduce inflammation and neurone loss after hypoxia by:
-actively cooling the core temperature of the baby
-using cooling blankets and hat
-between 33-34 degrees using a rectal probe
-gradually warmed to a normal temp

120
Q

What is sarnat staging of HIE

A

Mild:
Poor feeding, generally irritability and hyper-alert
Resolves within 24 hours
Normal prognosis

Moderate:
Poor feeding, lethargic, hypotonic and seizures
Can take weeks to resolve
Up to 40% develop cerebral palsy

Severe:

Reduced consciousness, apnoeas, flaccid and reduced or absent reflexes
Up to 50% mortality
Up to 90% develop cerebral palsy

121
Q

What are the TORCH infections

A

Toxoplasmosis gondii
Other - VSV, parvovirus B19, HIV, syphilis
Rubella
CMV
HSV

122
Q

What are torch infections

A

Infection of the developing fetus hat can occur IN UTERO, DURING DELIVERY or AFTER BIRTH

123
Q

Complications of TORCH infections

A

Preterm birth
Delayed development
Physical malformations
Loss of pregnancy

124
Q

How are torch infections passed to fetus (3)

A

-through placenta
-passing through birth canal
-breastfeeding

125
Q

How is toxoplasmosis gondii transmitted originally

A

Consumption of undercooked meats
Exposure to cat faeces

126
Q

Signs and symtoms of toxoplasmosis

A

Cory has a big head and likes stiff calcium jerky

Cory -Chorioretinitis
Big head - hydrocephalus
Stiff - rigidity
Calcium - intracranial calcifications
Jerky - seizures

127
Q

general TORCH infection signs and symptoms

A

Microcephaly
Low birth weight
Sleepiness
Cataracts
Hearing loss
Hepatosplenomegaly
Purpura or petechiae
Jaundice
Seizures
Deafness

128
Q

Classic triad of features on congential toxoplasmosis (CHI)

A
  1. Chorioretinitis (inflammation of the choroid and retina in the eye)
    Intracranial calcification
  2. Hydrocephalus
  3. Intracranial calcification
129
Q

How is CMV trasmitted

A

Direct contact with bodily fluids:
-Semen
-tears
-saliva
-mucus
-vaginal fluids

130
Q

Presentation of CMV in children (6)

A

Janice, peri, cory are pure death

-jaundice
-periventricular calcifications + microcephaly
-inflammation of eye (chorioretinitis)
-pinpoint petechial blueberry muffin type rash
-deafness (sensorineural)

131
Q

What is the common cellular presntation of CMV

A

Owls eye appearance of infected cells
-due to intranuclear inclusion bodies

132
Q

Tx for CMV

A

Gangciclovir - antiviral that can reduce risk of hearing loss and microcephaly

133
Q

Tx for congenital toxoplasmosis gondii (2)

A

Pyrimethamine - anti parasitic medication
&
Sulfadiazine - antibiotic

134
Q

How are the different types of HSV transmitted

A

HSV-1 trasmitted through oral secretions (cold sores)
HSV-2 trasmitted sexually

135
Q

Features of herpes simplex virus

A

Gingivostomatitis - inflammation of oral mucosa
Cold sores
Genital ulcerations

136
Q

Mx of HSV

A

gingivostomatitis: oral aciclovir/chlorhexidine mouthwash

cold sores: topical aciclovir

genital herpes: oral aciclovir

137
Q

When is spiramycin given in TORCH infections and what is it

A

Spiramycin - ABX and antiparastic

Given to mothers who have early detected toxoplasmosis during pregnancy to reduce transmission to fetus

138
Q

What is the management of HSV in pregnant mother

A

-elective caesarean at term
-women with recurrent herpes - suppressive therapy aka acyclovir

139
Q

Main investigation for HSV

A

Viral cultures + PCR

140
Q

CMV main investigations

A

-DNA detection on PCR
-viral culture
-CMV specific immunoglobulin M antibody measurements

141
Q

What is cleft lip and palate

A

Congenital malformation in the upper lip, oral cavity and roof of mouth due to improper fusion of facial bones and tissues

142
Q

Three types of cleft lip and palate

A

Cleft lip

Cleft palate -uvula commonly also split

Combination - split alveolar ridge and uvula

143
Q

Risk factors for cleft lip and palate

A

Genetic condtions- pataus, stickler syndrome

Folate deficiency during development

Hypoxia in uterus

Pesticide exposure

144
Q

Complications of cleft lip and palate (4)

A

Speech impediment

Hearing issues

Recurrent otitis media

Difficulty eating

145
Q

Signs and sx of cleft and palate

A

Dysphonia - hypernasal voice
Dysarthria
Nasal cavity infection - food gets trapped in nasal cavity
Velopharyngeal insufficiency - causes speech problems

146
Q

How to diagnose cleft lip and palate (3)

A

Prenatal ultrasound - helps evaluate the nares and upper lip

MRI

CT scan/ X-ray

147
Q

Tx of cleft lip and palate

A

Surgical closure by three months of age

Prostethic implants

Speech and language therapy

Prevention:
Folate supplementation during pregnancy

148
Q

Presntation of HSV encephalitis (6)

A

Altered consciousness
Altered cognition
Unusual behaviour
Acute onset of focal neurological symptoms
focal seizures
Fever

149
Q

Dx of HSV encephalitis (5)

A

-LP + PCR

-CT scan if a lumbar puncture is contraindicated

-MRI scan after the lumbar puncture to visualise the brain in detail

-EEG

-Swabs of other areas can help establish the causative organism, such as throat and vesicle swabs

-HIV testing is recommended in all patients with encephalitis

150
Q

Give some contraindications for LP (4)

A

-GCS below 9
-haemodynamically unstable,
-active seizures or post-ictal.
-meningococcal septicaemia

151
Q

Tx for HSV encephalitis

A
  • Aciclovir - started if encephalitis is suspected
  • Repeat LP to ensure success TX
152
Q

Complications for encephalitis

A

Seizures
Hormone imbalance
Learning disability
Changes to memory
Changes in mood
Lasting fatigue

153
Q

Osteosarcoma
Ewing sarcoma
Chondrosarcoma
X - ray finding

A

OsteoSarcoma= Sunburst pattern
Ewings sarcoma= OnEwin (onion skin)
Chondrosarcoma= PopChon (popcorn calcification

154
Q

3 clinical signs of syphilis in babies (5)

A

Hutchinsons triad
-Hutchinson teeth - small notched teeth
-CN8 nerve palsy
-interstitial keratitis

-also saber shins and saddle nose

Phase 3a - Arun&Erin (15 decks)

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