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Y4 Paediatrics > Endo > Flashcards

Endo Flashcards

1
Q

what could cause dehydration in child?

A
  • Definition: Loss of body fluids exceeding intake, leading to imbalanced electrolytes and reduced hydration
  • Causes: Vomiting, diarrhea, fever, inadequate fluid intake
  • Symptoms: Thirst, dry mouth, decreased urine output, sunken eyes, lethargy, irritability
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2
Q

how is dehydration in a child managed?

A

Oral rehydration solution (ORS) for mild cases, intravenous fluids for moderate to severe dehydration
treat underlying cause - anti-diarrhoea meds
advice on hydration
anti-pyretics

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3
Q

what are some sources of electrolytes in a hospital for children?

A

oral: diet, breast milk, enteral, oral rehydration solution, electrolyte supplements, sports drink

parenteral: IVF, electrolyte infusions, medications, blood products

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4
Q

what defines short stature in a child?

A

height more than 2 standard deviations below the average for their age and sex

this is the same as being below the 2nd centile

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5
Q

what causes short stature in a child?

A

familial
constitutional delay
malnitrition
chronic disease
hypothyroidism
growth hormone deficiency
genetic syndromes

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6
Q

how would you investigate short stature?

A
  • hypothyroid - TSH and fT4
  • bone age studies - wrist XR
  • chronic diseases - U&E, faecal calprotectin, bNP, tTG and IgA
  • specific - IGF-1, (glucagon GH) (morning cortisol)
  • genetic testing
  • MRI brain
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7
Q

what is the prognosis for constitutional delay?

A
  • short stature in childhood when compared to peers
  • normal height in adulthood
  • puberty is delayed
  • growth spurt during puberty lasts longer
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8
Q

how is constitutional delay diagnosed?

A

history
examination
xray of hand and wrist

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9
Q

what is the pathophysiology of growth hormone deficiency?

A
  • congenital: disruption of hormone axis, genetic mutations
  • acquired: - secondary to infection, trauma or interventions such as surgery, can occur alongside hypopituitarism
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10
Q

how does growth hormone deficiency present in neonates?

A
  • micropenis (in males)
  • hypoglycaemia
  • severe jaundice
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11
Q

how does growth hormone deficiency present in older infants?

A
  • poor growth, usually stopping or severely slowing from age 2-3
  • short stature
  • slow development of movement and strength
  • delayed puberty
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12
Q

how is suspected growth hormone deficiency investigated?

A
  • GH stimulation test
  • TFT
  • adrenal deficiency
  • MRI brain
  • genetic testing
  • XR of wrist
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13
Q

how is GH deficiency managed?

A
  • follow up with a paediatric endocrinologist
    • daily subcutaneous injections of growth hormone (somatropin)
    • treatment of other associated hormone deficiencies
    • close monitoring of height and development
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14
Q

what could cause tall stature?

A
  • familial tall stature
  • marfan’s syndrome
  • hyperthyroidism
  • obesity
  • klinefelter syndrome
  • precocious puberty
  • GH excess → gigantism
  • homocystinuria
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15
Q

how do you investigate tall stature?

A
  • karyotype
  • T4, TSH
  • IGF-1
  • bone age assessment and prediction of final height
  • special investigations include:
    • serum LH, FSH and testosterone levels
    • glucose suppression test for GH
    • visual field examination
    • MRI of pituitary
    • serum cortisol
    • serum prolactin
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16
Q

how do you define obesity?

A

clinical intervention - BMI above 91st centile
assess for co-morbidities if BMI above 98th centile

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17
Q

how does obesity relate to stature?

A
  • obese children are often tall for their age and come from overweight families
  • if children are short and obese, consider investigating for endocrine causes e.g. hypothyroidism
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18
Q

what could cause polydipsia?

A
  • Inadequate fluid intake.
  • Excessive exercise; especially in hot environments.
  • Excessive water drinking, termed primary polydipsia is caused by an increase in fluid intake that results in large volumes of urine being excreted from the body.
  • Hyperglycaemia, for instance, in undiagnosed or uncontrolled diabetes mellitus (DM), can cause an osmotic diuresis leading to polydipsia and polyuria.
  • Diabetes insipidus
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19
Q

when does normal puberty start?

A
  • starts age 8-14 in girls
  • 9-15 in boys
  • takes about 4 years from start to finish
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20
Q

when does precocious puberty occur?

A

before 8 in females

before 9 in males

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21
Q

what are some investigations for female precious puberty?

A
  • TFT
  • LH, FSH, oestradiol
  • X-ray bone age
  • USS pelvis
  • LHRH test
  • MRI brain and pituitary
    • if before 6
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22
Q

what are some complications of early puberty?

A

short stature - closure of epiphyseal plates
psychological disturbance
early menarche - RF for gynae issues
safeguarding issues

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23
Q

how is female precocious puberty managed?

A

GnRH analogue (decapeptyl)

monthly

3 monthly

6 monthly

until 10-11 years

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24
Q

what are some causes of central precocious puberty?

A
  • idiopathic or constitutional (most common)
  • CNS lesions e.g. hydrocephalus
  • pituitary gonadotropin-secreting tumours (rare)
  • post-sepsis
  • radiotherapy
  • birth anoxia
  • tuberous sclerosis
  • neurofibromatosis
  • obesity
    • increased levels of leptin
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25
Q

what is the pathophysiology of central precocious puberty?

A

premature activation of the hypothalamo-hypophyseal axis → early initiation of pubertal changes → early development of secondary sexual characteristics and gonadarche

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26
Q

how do you investigate for central precocious puberty?

A
  • elevated GnRH levels
  • raised levels of basal LH and FSH
  • GnRH stimulation test (gold standard)
    • LH and FSH levels increase after IV administration of GnRH
  • sex hormones
    • increased serum testosterone in males
    • increased serum oestrogen in females
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27
Q

what are some causes of peripheral precocious puberty?

A

increased androgen production - cyst, congenital adrenal hyperplasia

increased oestrogen - hCG secreting germ cell

increased beta-HCG - primary hypothyroidism, obesity, hepatoblastoma

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28
Q

how is peripheral precocious puberty investigated?

A
  • normal levels of GnRH
    • levels suppressed by elevated gonadal hormones
  • increased oestrogen or testosterone
  • decreased LH and FSH
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29
Q

when does late puberty occur?

A
  • NO signs of secondary characteristics
    • after 13 in females
    • after 14 in males
  • or girls who have not had their period by 16
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30
Q

what causes late puberty?

A
  • maturational delay
  • gonadal failure
  • hypothalamic pituitary dysfunction
  • Chronic and severe disease
  • Chemo/radiotherapy
  • Metabolic: Glycogen storage disorders, galactosaemia
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31
Q

what are some girls specific causes of delayed puberty?

A
  • Turner’s Syndrome- the absence of one of the X chromosomes
  • Anorexia Nervosa
  • Low body weight/athletic lifestyle
  • Autoimmune failure- premature ovarian failure
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32
Q

how is delayed puberty investigated?

A

initial: FBC, ferritin, U&E, anti-TTG
hormonal: early morning FSH, LH, TFT, GH, prolactin
genetic: kleinfelters, turners
imaging: XR, Pelvic USS, MRI brain

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33
Q

how is late onset puberty managed?

A
  • treat underlying condition
  • if constitutional delay, reassurance and observation
  • replacement sex hormones can be used to induce puberty by specialists (oestrogen in girls and testosterone in boys)
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34
Q

what is type one diabetes?

A

the inability to produce/secrete insulin due to autoimmune destruction of the beta-cells (production site of insulin) in the pancreatic islets of Langerhan

*In patients with T1DM, thedestruction of beta-cells leads to the progressive reduction in insulin secretion

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35
Q

what can cause T1DM?

A
  • It may be triggered by certain viruses, such as theCoxsackie B virus andenterovirus
  • Vitamin D deficiency
  • Other autoimmune conditions
  • Genes
36
Q

what are some clinical features of T1DM?

A
  • Polyuria
  • Polydipsia
  • Weight loss
  • Weakness
  • Lethargy
  • vomiting
  • Dehydration
  • Tachycardia
  • Kussmauls
  • Confusion
37
Q

how is T1DM investigated?

A
  • HbA1c
  • Capillary blood glucose
  • Flash glucose monitoring
  • FBC, U&Es, CRP, LFT, ABG
38
Q

how is T1DM managed?

A
  • Subcutaneous insulin regimes (Insulin is usually prescribed as a combination of abackground, long acting insulin given once a day and ashort acting insulin injected 30 minutes before intake of carbohydrate (i.e.at meals).
  • Monitoring dietary carbohydrate intake
  • Monitoring blood sugar levels on waking, at each meal and before bed
  • Monitoring for and managing complications, both short and long term
39
Q

what are come complications of T1DM?

A
  • Hypoglycaemia
  • Hyperglycaemia(and DKA)
  • Coronary artery diseaseis a major cause of death in diabetics
  • Peripheral ischaemia causes poor healing, ulcers and “diabetic foot”
  • Stroke
  • Hypertension
  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularlyglomerulosclerosis
  • Urinary Tract Infections
  • Pneumonia
  • Skin and soft tissue infections, particularly in the feet
  • Fungal infections, particularly oral and vaginal candidiasis
40
Q

what is the progression of T1DM?

A
  • Without insulin replacement,people with type1 diabetes would die within days or weeks.
  • With insulin replacement,people with type1 diabetes can participate normally in the usual activities of daily life but are at risk of complications
41
Q

what is DKA?

A

Life threatening complication of diabetes mellitus, characterised by:

  • hyperglycemia (high blood sugar),
  • ketosis (accumulation of ketones), and
  • metabolic acidosis (acidic blood pH)
42
Q

what causes DKA?

A
  • Insufficient insulin levels, often due to missed insulin doses, illness, or undiagnosed diabetes.
  • Stressors such as infections, surgery, or trauma can trigger DKA
  • Specific microorganisms can include Streptococcus and Staphylococcus species.
43
Q

how is pathophysiology of DKA?

A

Low insulin initiates ketogenesis, leading to more ketones, which cause acidosis when bicarbonate is not enough to compensate

44
Q

what clinical features of DKA?

A
  • Polyuria
  • Polydipsia
  • Nausea and vomiting
  • Weight loss
  • Acetone smell to their breath
  • Dehydration and subsequent hypotension
  • Altered consciousness
  • Symptoms of an underlying trigger (i.e. sepsis)
  • Kussmaul breathing
  • Tachycardia
  • Hypotension
45
Q

what are the differentials for DKA?

A
  • Hyperosmolar hyperglycemic state (HHS): A severe hyperglycemic crisis more common in type 2 diabetes.
  • Other causes of metabolic acidosis: These include renal disease, toxic ingestions, and other metabolic disorders.
46
Q

how is DKA investigated?

A
  • Blood glucose
  • ABG - metabolic acidosis
  • Elevated serum ketones
  • Elevated potassium
  • FBC - may be leukocytosis
  • Urinalysis - ketones, glucose
47
Q

how is DKA managed?

A
  • correct dehydration over 48h not fast as risk of cerebral oedema
  • fixed rate insulin infusion
  • avoid fluid boluses
  • treat underlying triggers
  • prevent hypoglycaemia
  • add potassium
  • monitor for signs of oedema
  • monitor glucose, ketones and pH
48
Q

what are some complications of DKA?

A
  • Cerebral edema: A rare but serious complication, characterized by increased intracranial pressure.
  • Hypokalemia: Can occur during treatment due to shifts in potassium.
  • Other complications: Dehydration, thrombosis, respiratory distress, and electrolyte imbalances.
49
Q

what is the progression of DKA?

A
  • With prompt and appropriate treatment, DKA can be resolved within 24-48 hours.
  • Monitoring continues until acidosis is corrected, and the child can tolerate oral fluids and food.
50
Q

why are children with DKA at high risk of developing cerebral oedema?

A

Dehydrationandhigh blood sugar concentrationcause water to move from theintracellular spacein the brain to theextracellular space. This causes thebrain cellstoshrink and becomedehydrated. Rapid correction ofdehydrationandhyperglycaemia(with fluids and insulin) causes arapid shift in water from theextracellular spaceto theintracellular spacein thebrain cells. This causes the brain to swell and becomeoedematous,which can lead to brain cell destruction and death.

51
Q

how is cerebral oedema managed?

A

slowing IVfluids,IVmannitoland IVhypertonic saline

52
Q

what are some risk factors for T2DM?

A
  • overweight
  • inactive lifestyle
  • family history
  • asian, african and afro-caribbean ethnic groups
53
Q

what are some clinical features of T2DM?

A
  • urinary frequency
  • nocturnal enuresis
  • nocturia
  • polydipsia
  • fatigue
  • blurred vision
  • weight loss
  • getting more infections
  • impaired growth
  • reduced school performance
  • acanthosis nigricans
54
Q

how is T2DM investigated?

A

persistent hyperglycaemia is defined as:

  • fasting plasma glucose level of 7.0 mmol/L or more
  • random plasma glucose of 11.1 mmol/L or more in the presence of symptoms or signs of diabetes
  • do not usemeasurement of HbA1cto make a diagnosis of type 2 diabetes in children
55
Q

how would you advice a kid with T2DM?

A
  • diet: fruit and veg, high fibre, portion control, controlling fatty and sugary food, mealtime routines
  • exercise: minimise sedentary time, regular advice to lower glucose
  • alcohol and smoking cessation as can prolong hypoglycaemia effects of insulin etc
56
Q

how is T2DM holistically managed?

A

MDT
lifestyle changes
education programme
risk assessment
immunisations
measure growth
advise use of medicalert bracelet or diabetes identity card or wristband

57
Q

how is T2DM managed?

A
  • HbA1c target is 48mmol or 6.5% or lower
    • should be measured every 3 months
  • standard-release metformin
  • insulin therapy may be needed in some cases
58
Q

what are the sick day rules for T2DM?

A
  • ensure there are sick day foods and drinks supplies readily accessible at home:
    • easily digestible foods and sugary drinks (to provide energy and to prevent further ketosis)
    • over-the-counter oral rehydration therapy (ORT) sachets (to prevent dehydration)
    • glucose tablets or oral gel (to prevent hypoglycaemia)
    • equipment for monitoring blood glucose and ketones (if appropriate)
    • additional supplies of insulin (if appropriate)
    • glucagon kit (if appropriate)
  • do not stop insulin but dose may need to be altered during illness so seek advice from diabetes team
59
Q

why is there a deterioration of blood glucose control in older teens?

A
  • endocrine changes leading to increased insulin resistance
  • erratic meal and exercise patterns
  • poor adherence to treatment regimens
  • eating disorders
  • hazardous and risk taking behaviours
60
Q

what is the pathophysiology of diabetes insipidus?

A

condition characterised by either a decreased secretion of antidiuretic hormone (ADH) from the pituitary (cranial DI) or an insensitivity to antidiuretic hormone (nephrogenic DI)

61
Q

what are some causes of diabetes insipidus?

A

cranial: head injury, pituitary surgery, sarcoidosis, haemachromatosis

nephrogenic: genetic, electrolytes like hypercalcaemia, hypokalaemia, lithium

62
Q

how might diabetes insipidus present?

A

babies: crying, irritable, slower growth, hyperthermia, weight loss

child: excessive thirst, wetting bed, loss of appetite, fatigue

63
Q

how is diabetes insipidus investigated?

A
  • high plasma osmolality, low urine osmolality
  • a urine osmolality of >700 mOsm/kg excludes diabetes insipidus
  • water deprivation test
64
Q

how is diabetes insipidus managed?

A

nephrogenic: thiazides, low salt or protein
central: desmopressin

65
Q

what are some causes of obesity?

A
  • dietary
  • lack of physical activity
  • genetics
  • environmental factors
  • psychosocial factors
  • endocrine disorders and genetic syndromes: hypothyroidism, prader-willi
66
Q

how is obesity investigated?

A
  • BMI Assessment: Calculating BMI using a child’s height and weight to classify obesity severity.
  • Blood Tests: May include lipid profile, fasting glucose, and insulin levels to assess metabolic health.
  • Assessment of Obesity-Related Comorbidities: Monitoring for conditions like hypertension and fatty liver disease.
67
Q

how is obesity managed?

A

lifestyle modification
dietary counselling
physical activity
behavioural interventions
family based interventions
medical mx: orlistat, liraglutatide, bariatric surgery

68
Q

what is the pathophysiology of congenital hypothyroidism?

A
  • underdeveloped thyroid gland (dysgenesis)
  • fully developed gland that does not produce enough hormone (dyshormonogenesis)
  • rarely it can be due to pituitary or hypothalamus dysfunction

*picked up on new born blood spot

69
Q
A
70
Q

how does hypothyroidism investigated?

A
  • fatigue and low energy
  • poor growth
  • weight gain
  • poor school performance
  • constipation
  • dry skin and hair loss
71
Q

how is hypothyroidism investigated managed?

A
  • TFTs
    • TSH, T3 and T4
  • thyroid ultrasound
  • thyroid antibodies
  • by a paediatric endocrinologist
  • levothyroxine PO OD
72
Q

what is the pathophysiology of thyrotoxicosis?

A
  • Thyroid hormone (T3 and T4) regulates metabolism and affects nearly every system in the body.
  • In thyrotoxicosis, excessive thyroid hormone levels lead to increased metabolic rate, weight loss, and various systemic symptoms.
73
Q

what are some examinations thyrotoxicosis?

A
  • Elevated heart rate (tachycardia),
  • goitre (enlarged thyroid gland),
  • fine tremor,
  • warm and moist skin, and
  • lid lag (abnormal eye movement).
74
Q

how is thyrotoxicosis managed?

A
  • TFTs - TSH usually low, high T4 and T3
  • Thyroid antibodies
  • Thyroid imaging - US, radioactive iodine uptake
  • Options include antithyroid medications
    • carbimazole, propylthiouracil
  • radioactive iodine therapy
  • Beta-blockers may be used to manage symptoms such as tachycardia and tremor
  • thyroidectomy
75
Q

what are some types of adrenal insufficiency?

A
  • addison’s: adrenal glands have been damaged, resulting in reduced secretion of cortisol and aldosterone
  • secondary: congenital, surgery, infection, loss of blood flow, radiotherapy
  • tertiary: inadequate CRH from hypothalamus, long term steroid
76
Q

how might adrenal insufficiency present?

A

babies: lethargy, vomiting, poor feed, hypoglycaemia, jaundice, failure to thrive

child: N+V, poor weight gain, reduced appetite, abdo pain, development delay, broke hyperpigmentation to the skin

77
Q

how is adrenal insufficiency investigated?

A

U&E
glucose
serum cortisol, ACTH, aldosterone, renin
short synACTHen test

78
Q

how short synACTHen test done?

A
  • performed in the morning
  • give synthetic ACTH (synacthen)
  • blood cortisol measured at baseline, 30 and 60 minutes after administration
  • synthetic ACTH will stimulate healthy adrenal glands to produce cortisol
  • cortisol levels should at least double
  • failure to rise double the baseline indicates addisons disease
79
Q

how is adrenal insufficiency managed?

A
  • hydrocortisone: glucocorticoid that replaces cortisol
  • fludrocortisone: mineralocorticoid replaces aldosterone
  • steroid card and emergency ID tag
  • paeds endocrine: growth, development
80
Q

what are the sick day rules for adrenal insufficiency?

A
  • minor coughs, colds without fever
  • tempover 38: dose increased, blood sugar monitored closely, D+V, IM steroids
81
Q

what is an adrenal crisis?

A

acute presentation of severe addisons

absence of steroid hormones results in life threatening presentation

*- reduced consciousness
- hypotension
- hypoglycaemia
- hyponatraemia
- hyperkalaemia
- can be the first presentation of addisons disease
- can be triggered by infection, trauma or other acute illnesses
- can also occur if patient on long term steroids abruptly stops taking them

82
Q

how is an adrenal crisis managed?

A
  • do not wait for investigations before initiating treatment
  • intensive monitoringif they are acutely unwell
  • parenteral steroids (i.e.IV hydrocortisone)
  • IV fluidresuscitation
  • correcthypoglycaemia
  • careful monitoring of electrolytes and fluid balance
83
Q

what is congenital adrenal hyperplasia?

A
  • Congenital adrenal hyperplasia is caused by acongenital deficiencyof the21-hydroxylaseenzyme.
  • This causesunderproductionofcortisolandaldosterone andoverproductionofandrogensfrom birth
84
Q

what is the pathophysiology of congenital adrenal hyperplasia?

A
  • In 21-hydroxylase deficiency, impaired cortisol synthesis leads to elevated ACTH, causing adrenal hyperplasia and excess production of adrenal androgens (testosterone and androstenedione).
  • The lack of cortisol feedback results in increased ACTH secretion, which further stimulates adrenal androgen production.
85
Q

how does congenital adrenal hyperplasia presented?

A

Ambiguous genitalia, particularly in females due to in utero exposure to excessive androgens.
Hypotension.
Salt-wasting crises characterised by dehydration, low sodium, and high potassium levels leading to circulatory shock and metabolic acidosis.
Vomiting.
Virilisation, or the development of masculine secondary sexual characteristics.
Precocious puberty (males)

86
Q

how is congenital adrenal hyperplasia investigated?

A

Blood tests: Specific hormone assays such as 17-hydroxyprogesterone, cortisol, and ACTH levels. Elevated 17-hydroxyprogesterone and ACTH with low cortisol suggest CAH.
Genetic testing: Can confirm the diagnosis and identify the specific enzyme defect.
Imaging: In certain cases, imaging such as ultrasound can help in the assessment of internal sex organs in patients with ambiguous genitalia.

87
Q

how is congenital adrenal hyperplasia managed?

A

Acute treatment: Fluid and sodium replacement with intravenous saline (if salt-wasting) and administration of hydrocortisone for its glucocorticoid and mineralocorticoid effects.

Long-term treatment: Lifelong hormone replacement therapy, typically with hydrocortisone and fludrocortisone as needed.

Surgical intervention: In virilised females, genital surgery may be necessary to correct external genital abnormalities.

Patient education: Those dependent on steroids should be educated about the critical importance of adhering to their medication regimen and following ‘sick day’ rules.

Y4 Paediatrics (16 decks)

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