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Paediatrics > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is the presentation of T1DM?

A

DKA
Polyuria and polydipsia
Weight loss and fatigue
Secondary enuresis
Recurrent infections

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2
Q

What are the ix into a new diagnosis of T1DM?

A

If fever = cultures.
FBC, U+E, BM, HbA1c, TFTs and TPO, anti TTG, insulin ab

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3
Q

What is needed for diagnosis of T1DM?

A

Random BM >11mmol/L or fasting glucose >7mmol/L w sx or x2 bloods over 2 weeks

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4
Q

What is the management of T1DM?

A

SC insulin - background, long or short acting, SC or admin by pump, basal bolus
Screen for complications.

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5
Q

What are the sx of hypoglycaemia?

A

Hunger, sweating, tremor, irritability, dizzy, pale
Severe - reduced conc, coma, death, seizure

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6
Q

What are some causes of hypoglycaemia?

A

Too much insulin
Not enough carbs or not processing carbs properly eg. malabsorption, diarrhoea, vom and sepsis
Not T1DM related - hypothyroidism, GH def, liver cirrhosis, fatty acid oxidation defects

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7
Q

What is the management on hypoglycaemia?

A

If conc - oral rapid acting glucose and slower acting carbs
Not conc - IV dextrose, IM glucagon

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8
Q

What are the long term complications of T1DM?

A

Macrovascular - coronary artery disease, diabetic foot, stroke HTN
Microvascular - neuropathy, retinopathy, nephropathy
Recurrent infection

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9
Q

What are some options for monitoring T1DM?

A
  • HbA1c - shows control over last 3 months
  • Cap blood glucose - immediate result
  • Freestyle libre - sensor
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10
Q

What is the presentation of congenital hypothyroidism?

A

Screened at birth in newborn blood spot screening test but:
- Prolonged neonatal jaundice
- Poor feeding
- Constipation
- Increased sleeping
- Reduced activity
- Slow growth and develop - undiagnosed can cause ID

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11
Q

What is the presentation of acquired hypothyroidism?

A

Hashimotos autoimmune thyroiditis, associated w anti TPO ab and T1DM and coeliacs:
- Fatigue and low energy
- Poor growth
- Weight gain
- Poor school performance
- Constipation
- Dry skin and hair loss

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12
Q

What is they management of hypothyroidism?

A

Ix - TFTs, thyroid US and thyroid ab
Levothyroxine every day

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13
Q

What is the pathophysiology of DKA?

A

No glucose in tissues so ketogenesis is started = ketone acids in the blood, kidneys produce bicarb to buffer but after a while = no bicarb and blood acidic = ketoacidosis.
Glucose in urine = osmotic diuresis = polyuria = dehydration.
K+ not added to cells as no insulin so is left in blood = hyperkalaemia

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14
Q

What are the features of DKA?

A
  1. Hyperglycaemic - >11mmol?l
  2. Ketoacidosis - acidic blood >3mmol/L ketones and pH <7.3
  3. Potassium imbalance - hyperkalaemia
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15
Q

What is the presentation of DKA?

A

Polyuria and polydipsia
N+V
Weight loss
Acetone breath
Dehydration and hypotension
Alt conc
Sx of underlying trigger

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16
Q

What are the principles of DKA management in children?

A
  1. Correcting dehydration over 48 hours - dilutes ketones and hyperglycaemia
  2. Fixed rate insulin infusion
    - Avoid fluid bolus to reduce risk cerebral oedema
    - Prevent hypoglyaemia if needed
    - Give K w fluids and insulin
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17
Q

What are some potential problems w treating DKA?

A
  • Hypokalaemia - insulin drives K+ into cells, could do this suddenly when give insulin = arrhythmia and death
  • Cerebral oedema - dehydration and high BM = water leaves cells in brain, rapid correction of dehydration and hyperglycaemia = rapid shift of water into brain cells = oedema
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18
Q

What are some warning signs of cerebral oedema in DKA?

A

Headache
Alt behaviour
Brady
Reduced conc

19
Q

What is adrenal insufficiency?

A

Adrenal glands don’t produce enough cortisol and aldosterone
Primary adrenal insufficiency = Addison’s, mainly autoimmune
Secondary adrenal insufficiency = not enough ACTH
Tertiary adrenal insufficiency = not enough CRH from hypothalamus = not enough ACTH = not enough cortisol, normally caused by long term steroid use

20
Q

What are the features of adrenal insufficiency in babies?

A

Lethargy
Vomiting
Poor feeding
Hypoglycaemia
Jaundice
Failure to thrive

21
Q

What are the features of adrenal insufficiency in older children?

A

N+V
Poor weight gain or weight loss
Reduced appetite
Abdo pain, muscle weakness, cramps
Develop delay
Bronze hyperpigmentation to skin caused by high ACTH levels which stim melanocytes

22
Q

What are the ix into adrenal insufficiency? What are the biochemical features?

A

Addisons - low cortisol, high ACTH, low aldosterone, high renin
Secondary adrenal insufficiency - low cortisol and ACTH, normal aldosterone and renin
Check U+E, BM
ACTH stim test

23
Q

What is the ACTH stim test?

A

Performed in the morning, give synthetic ACTH, if adrenal glands are normal the synthetic ACTH will increase cortisol, should at least double.
If doesn’t rise = Addison’s

24
Q

What is the management of adrenal insufficiency?

A

Cortisol = hydrocortisone
Aldosterone = fludrocortisone
Steroid card and emergency ID tag - can’t stop steroids suddenly and need to increase steroids during illness

25
Q

What are sick day rules w steroids?

A
  • Increase dose of steroid and give more regularly
  • BM closely monitored
  • D+V = IM steroid and admitted for IV steroids
26
Q

What is an Addisonian crisis?

A

Acute absence of steroid hormones:
Reduced conc, hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia
Is life threatening condition!!

27
Q

What is the management of Addisonian crisis?

A
  • Monitoring
  • IV hydrocortisone
  • IV fluid resus
  • Correct hypoglycaemia
  • Carefully monitor U+E
28
Q

What is the normal GH pathway?

A

Hypothalamus = GnRH to ant pit
Ant pit = GH which stim IGF-1 from liver = growth in children and adolescents

29
Q

What are the different types of GH def?

A

Congenital GH def - genetic mutation, hypopituitism
Acquired GH def - secondary to infection, trauma or surgical intervention

30
Q

What is the presentation of GH at birth?

A

Micropenis
Hypoglycaemia
Severe jaundice

31
Q

What is the presentation of GH in older children?

A

Poor growth, stops or slows from 2-3 years old
Short stature
Slow develop of movement and strength
Delayed puberty

32
Q

What are the ix into poor growth/short stature?

A

GH stim test - assess response to meds that normally increase GH eg. insulin or glucagon, in def there will be poor response to stim
- MRI brain to see if pit or hypothalamus structural probs
- Genetic testing eg. Turner’s or Prader Willi
- Test for associated hormone def eg. thyroid or adrenal probs

33
Q

What is the treatment of GH def?

A
  • Daily SC GH infections = somatropin
  • Treat associated hormone def
  • Closely monitor height and develop
34
Q

What is congenital adrenal hyperplasia?

A

Underproduction of cortisol and aldosterone and the overproduction of testosterone from birth - autosomal recessive.
Def of 21 hydroxylase enzyme - normally converts progesterone into aldosterone and cortisol, extra progesterone converted into testosterone instead

35
Q

What is the presentation of congenital adrenal hyperplasia?

A

Severe - female = virilised/ambiguous genitalia, enlarged clitoris, hyponatraemia, hyperkalaemia, hypoglycaemia, poor feeding, vom, dehydration, arrhythmia
Mild - sx normally related to high testosterone
- Female - tall, facial hair, no period, deep voice, early puberty
- Male - tall, deep voice, large penis, small testicles, early puberty

36
Q

What is the management of congenital adrenal hyperplasia?

A
  • Cortisol replacement w hydrocortisone
  • Aldosterone replacement w fludrocortisone
  • Corrective surgery if ambiguous genitalia in women
37
Q

What are the RF of T2DM in children?

A
  • Overweight
  • Inactivity
  • Poor diet
  • FH
  • Black, Hispanic, Carribean
  • Maternal gestational diabetes while mother was pregnant
  • Low birth weight
  • PCOS
38
Q

What is involved in the prevention of T2DM in children?

A

Healthier diet
Increase activity

39
Q

What is rickets?

A

Vit D deficiency = unable to absorb Ca and PO4- from food = skeletal disorder. Normally develop in childhood due to poor nutrition, lack of sun exposure or malabsorption syndromes.

40
Q

What are the sx of rickets?

A
  • Bowed legs
  • Bone pain
  • Stunted growth
  • Can have easily fractured bones
  • Hypocalcaemia = seizures and ID
41
Q

What are the types of diabetes insipidus and their causes?

A
  1. Cranial diabetes insipidus = not enough ADH - head trauma, inflam, meningitis, sickle cell
  2. Nephrogenic diabetes insipidus = ADH resistance
42
Q

What are the CF of diabetes insipidus?

A

Large volumes of dilute urine of low osmolality
Nocturia and excessive thirst
Enuresis
Failure to thrive

43
Q

What is the management of diabetes insipidus?

A

Cranial - desmopressin
Nephrogenic - stop offending drugs, diuretics?

Paediatrics (15 decks)

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