Endocrinology Flashcards

(43 cards)

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
What are sick day rules w steroids?
- Increase dose of steroid and give more regularly - BM closely monitored - D+V = IM steroid and admitted for IV steroids
26
What is an Addisonian crisis?
Acute absence of steroid hormones: Reduced conc, hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia Is life threatening condition!!
27
What is the management of Addisonian crisis?
- Monitoring - IV hydrocortisone - IV fluid resus - Correct hypoglycaemia - Carefully monitor U+E
28
What is the normal GH pathway?
Hypothalamus = GnRH to ant pit Ant pit = GH which stim IGF-1 from liver = growth in children and adolescents
29
What are the different types of GH def?
Congenital GH def - genetic mutation, hypopituitism Acquired GH def - secondary to infection, trauma or surgical intervention
30
What is the presentation of GH at birth?
Micropenis Hypoglycaemia Severe jaundice
31
What is the presentation of GH in older children?
Poor growth, stops or slows from 2-3 years old Short stature Slow develop of movement and strength Delayed puberty
32
What are the ix into poor growth/short stature?
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
What is the treatment of GH def?
- Daily SC GH infections = somatropin - Treat associated hormone def - Closely monitor height and develop
34
What is congenital adrenal hyperplasia?
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
What is the presentation of congenital adrenal hyperplasia?
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
What is the management of congenital adrenal hyperplasia?
- Cortisol replacement w hydrocortisone - Aldosterone replacement w fludrocortisone - Corrective surgery if ambiguous genitalia in women
37
What are the RF of T2DM in children?
- Overweight - Inactivity - Poor diet - FH - Black, Hispanic, Carribean - Maternal gestational diabetes while mother was pregnant - Low birth weight - PCOS
38
What is involved in the prevention of T2DM in children?
Healthier diet Increase activity
39
What is rickets?
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
What are the sx of rickets?
- Bowed legs - Bone pain - Stunted growth - Can have easily fractured bones - Hypocalcaemia = seizures and ID
41
What are the types of diabetes insipidus and their causes?
1. Cranial diabetes insipidus = not enough ADH - head trauma, inflam, meningitis, sickle cell 2. Nephrogenic diabetes insipidus = ADH resistance
42
What are the CF of diabetes insipidus?
Large volumes of dilute urine of low osmolality Nocturia and excessive thirst Enuresis Failure to thrive
43
What is the management of diabetes insipidus?
Cranial - desmopressin Nephrogenic - stop offending drugs, diuretics?