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3a > Paeds endo/Reproductive > Flashcards

Paeds endo/Reproductive Flashcards

1
Q

What is insulin and where is it produced ?

A

-Anabolic hormone produced by the beta cells in the islets of Langerhans. inthe pancreas

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2
Q

In what 2 ways does insulin reduced blood sugar ?

A
  • Causes cells to absorb glucose
  • Causes muscle and liver cells to absorb glucose and stored as glycogen
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3
Q

What is glucagon and where is it produced ?

A

-Catabolic hormone that increasedsblood glucose and is produced by alpha cells in the islets of langerhans of the pancreas

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4
Q

How does glucagon increase blood glucose ?

A
  • Glycogenolysis : tells the liver to break glycogen to glucose
  • Gluconeogenesis : tells the kiver to convert proteins and fats to glucose
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5
Q

What is ketogenesis and when does it occur

A
  • The liver converts fatty acids to ketones
  • Occurs when there is insufficient supply of glucose and glycogen stores are exhausted
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6
Q

How do children present with T1DM?

A

-DKA

OR

  • Polyuria
  • Polydipsia
  • Weight loss
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7
Q

What are the two methods of insulin injection for T1DM

A

-Insulin pump
OR
-Long acting inuslin + short acting injected 30 mins before carb intake -> Basal-Bolus

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8
Q

How is severe hypoglycaemia treated ?

A

-IV dextrose + intramuscular glucagon

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9
Q

Give 4 macrovascular complications of hyperglycaemia

A
  • Coronary artery disease
  • Peripheral ischaemia
  • Stoke
  • HTN
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10
Q

Give 3 microvascular complications of hyperglycaemia

A
  • Peripheral neuropathy
  • Retinopathy
  • Kidney disease, particularly glomerulosclerosis
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11
Q

What 3 problems arise in DKA ?

A
  • Ketoacidosis
  • Dehydation -> polyuria, polydipsi
  • Potassium imbalance -> low total body potassium
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12
Q

How is DKA diagnosed ?

A
  • Hyperglycaemia
  • Ketosis
  • Acidosis
  • Raised creatinine kinase
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13
Q

Why should someone in DKA have their GCS closely monitored ?

A
  • Risk of cerebral oedema
  • The rapid correction of dehydration and hyperglycaemia causes water to shift from extracellular to intracellular space cause the brain to swell
  • Tx : slow IV fluids, IV mannitol and IV hypertonic saline
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14
Q

How is DKA treated?

A
  1. Correct dehydration evenly over 48 hrs -> IV fluids (0/9% NaCl 10ml/kg)
  2. Get a fixed rate of insulin infusion : 0.1 units/kg/hr
  • Prevent hypoglycaemia with IV dextrose once blood glucose is below 14mmol/l
  • Add potassium and monitor
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15
Q

What is hypospadias?

A
  • > Congenital abnormality : ventral urethral meatus, hooded prepuce and chordee (curvature) in more severe forms
  • > management with surgery at 12 mnths, cicrumcision is CI
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16
Q

What is a cause of primary adrenal insufficiency ?

A

-Addison’s disease -> most commonly autoimmune and is damage to the adrenal glands resulting in reduced cortisol and aldosterone

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17
Q

What blood results are seen in primary adrenal failure ?

A
  • Low cortisol
  • Low aldosterone
  • High ACTH
  • High renin
18
Q

What is an addisonian crisis ?

A
  • Acute presentation of severe addisons
  • Reduced consciousness, hypotension, hypoglycaemia, hyponatraemia and hyperkalaemia
19
Q

How is an addisonian crisis managed ?

A
  • IV hydrocortisone (100mg)
  • IV fluid resus (1 litre saline over 30-60min)
  • Correct hypoglycaemia (dextrose in fluid)
20
Q

How is addisons disease managed ?

A
  • Hydrocortisone to replace cortisol
  • Fludrocortisone to replace aldosterone
  • Sick day rules : increase steroid, monitor blood sugar and IM steroid if D&V
21
Q

Explain the short synacthen test

A
  • Synthetic ACTH is given
  • In healthy adrenal glands, cortisol will increase
  • Less than double the baseline rise in cortisol suggests addisons
22
Q

Congenital adrenal hyperplasia : what, inheritance

A
  • Congenital deficiency in 21-hydroxylase enzyme leading to underproduction of cortisol and aldosterone and overproduction of androgens from birth
  • Autosomal recessive
23
Q

What are the blood results in someone with CAH

A
  • Low cortisol
  • Low aldosterone
  • High testosterone
  • Raised ACTH

->21-hydroxylase is used to convert progesterone to cortisol and aldosterone, without it, the excess is converted to testosterone

24
Q

How does severe CAH present ?

A
  • At birth with ‘ambiguous genitalia’ and enlarged clitorus
  • Shortly after birth : Hyponatraemia, hyperkalaemia and hypoglycaemia + metabolic acidosis = poor feeding, vomiting, dehydration and arrhythmias
25
Q

How does milder CAH present in women ?

A
  • Tall for age
  • Facial hair
  • Absent periods
  • Deep voice
  • Early puberty
26
Q

How does milder CAH present in males ?

A
  • Tall for age
  • Deep voice
  • Large penis
  • Small testicles
  • Early puberty
27
Q

How does growth hormone deficiency present?

A
  • Neonates : micropenis, hypoglycaemia, severe jaundice
  • Older infants : poor growth, short stature, slow development of movement and strength and delayed puberty
28
Q

How is growth hormone deficiency managed ?

A

-Daily subcutaneous injections of GH (somatropin)

29
Q

If not picked up at birth, how can congenital hypothyroidism present ? (7)

A
  • Prolonged neonatal jaundice
  • Poor feeding
  • Constipation
  • Increased sleeping
  • Reduced activity
  • Slow growth and development
  • Puffy face, macroglossia
30
Q

What is the most common cause of hypothyroidism in children

A
  • Autoimmune thyroiditis (Hashimoto’s)
  • Anti-TPO antibodies
31
Q

Give 4 complications of undescended testis

A
  • Infertility
  • Torsion
  • Testicular cancer
  • Psychological
32
Q

when will a baby with undescended testis be referred and when with orchidopexy be carried out

A
  • Unilateral : referral from 3-6 mnths, surgery at 1 yr
  • Bilateral : review by paediatrician within 24 hrs
33
Q
  • Sudden onset severe testicular pain
  • Referred to lower abdo
  • N&V
  • Swollen, tender testis
A

Testicular torsion

34
Q

what are 3 signs of testicular torsion

A
  • Testis retracted upwards
  • Cremasteric reflex lost
  • Elevation of testis doesn’t ease pain (Prehn’s sign)
35
Q

what antibodies are seen in autoimmune thyroiditis

A

Antithyroid peroxidase (anti-TPO)
Antithyroglobulin

36
Q

give 5 causes of obesity in children

A
  • GH deficiency
  • Hypothyroid
  • Down’s
  • Cushing’s
  • Prader-Willi syndrome
37
Q

what are the features of DKA

A
  • Abdo pain
  • Polyuria, polydipsia, dehydration
  • Kussmal respiration
  • Acetone smelling breath
38
Q

what 3 abx are seen in T1DM

A
  • IAA (90% of young children - insulin autoantibodies )
  • Anti-GAD (glutamic acid antibodies)
  • ICA (islet cell Antibodies)
39
Q

when is T1DM diagnosed

A
  • Symptoms +
  • Fasting glucose >7.0mmol/l
  • Random 11.1 or greater
40
Q

What are the features of addison’s

A
  • Lethargy, weaknes, anorexia, N&V, weight loss, ‘salt craving’
  • Hyperpigmentation
  • Loss of pubic hair in women
41
Q

what bloods are seen in addisons

A
  • Hypoglycaemia
  • Hyponatraemia
  • Hyperkalaemia
  • Metabolic acidosis

3a (45 decks)

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