Endocrinology Flashcards
define DKA
pH <7.3 or plasma HCO3- <15
and
blood ketones >3mmol/l
- sometimes: blood glucose >11mmol/l
cause of death DKA children
cerebral oedema (maj)
hypokalaemia
aspiration pneumonia (ileus or gastric paresis)
risk of DKA in patient per year
1-10%
DKA pathophysiology
absolute deficiency of insulin…counter rise in glucagon, cortisol, catecholamines and GH…increased gluconeogenesis…raises blood glucose and breakdown of fatty tissue…increased ketones…hyperglycaemia causes an osmotic diuresis…polyuric and pt becomes dehydrated + vomiting = worsening acidosis and dehydration
DKA risk factors
non compliance with insulin
device failure
changing insulin requirement during puberty
increased ingestion of glucose
infection
clinical features DKA
mean duration of 16.5 days of sx
- generally unwell
- lethargic
- N+V
- abdo pain
- headache and irritability
- confusion
examination DKA
deep, sighing breathing (kussmaul breathing)
tachypnoea
subcostal and intercostal recession
shock
dehydration
abdo pain
ketotic breath
signs of neurological compromise (cerebral oedema) DKA
irritability
slowing pulse
hypertension
reduced conscious level
papilloedema
DKA ddx
hyperosmolar hyperglycaemic state (no ketone production nor acidosis)
new presentation of type 1 SM
sepsis
appendicitis
DKA severity
mild - venous pH 7.20-7.29 or HCO3 <15
mod - 7.10-7.19 or <10
severe - <7.10 or <5
DKA management
A-E assessment
children in shock :
initial bolus - 20ml/kg of 0.9% NaCl over 15 mins
ongoing fluids - up to 40ml/kg total
children not in shock:
initial - 10ml/kg over 1 hr
ongoing fluids - calculate fluid deficit based on % dehydration (subtract initial bolus from this and add maintenance)
DKA - not clinically dehyrdrated and not vomiting
oral fluids and subcut insulin
but most will require IV fluids and insulin infusion (insulin should be delayed for 1-2 hours after IV fluid therapy). Dose of 0.05-0.1 units/kg/hr of soluble insulin
DKA fluids
resus fluids - given as bolus when in shock
deficit fluids - calculated from assumed dehydration. if bolus given for pt who is NOT IN SHOCK (subtract from this), DONT if pt is in shock
maintenance - 100 ml/kg/d for first 10 kg, 50 ml/kg/d for next 10 kg, 20ml/kg/day thereafter up to 80 kg
IMPORTANT to give 0.9% NaCl with 20mmol K in each 500ml bag. however if in AKI - anuric, so may result in hyperkalaemia - not administer K until urine passed
DKA resolved
clinically well
drinking and tolerate fluids
blood ketones <1mmol/l or pH normal
…then stop tx one hour later
hyperthyroidism prevalence
higher in girls and increasing age
neonatal thyrotoxicosis with mothers who have autoimmune hyperthyroidism
causes of hyperthyroidism
Grave’s
toxic multinodular goitre
toxic adenoma
thyroid carcinoma
neonatal hyperthyroidism
hCG-secreting tumours
functioning pituitary adenoma
risk fx of hyperthyroidism
family hx
personal or fhx of autoimmune disease
increase iodine intake
smoking (thyroid eye disease!)
female
hyperthyroidism ddx
transient thyroiditis
hashimotos (hashitoxicosis)
eating disorder
DM
phaeochromocytoma
neonatal thyrotoxicosis
if mother has grave’s - baby has TFT done between day 5-14 to check TFT
grave’s management childreb
carbimazole as propylthiouracil as increased s/e
administer via titration or block with higher dose and then replacement levothyroxine is given
NICE - titrating for 2 years and stop to see if gone into remission
s/e of anti-thyroid drugs
rashes, nausea
agranulocytosis
hepatitis
acute pancreatitis
neonatal hyperthyroidism management
self limiting within 1-3 mths, may require tx with propranolol or carbimazole
radioactive iodine therapy
not recommended <6 yrs old or with active eye disease or severely uncontrolled hyperthyroidism
total thyroidectomy
indications - <6 yrs old, etc
complications of untreated hyperthyroidism
weight loss
hypercalcaemia
osteoporosis
CVS dysfunction, afib
hyperthyroidism prognosis
40-75% relapse within 2 years
congenital hypothyroidism epidemiology
1:2000 - 1:4000
congenital hypothyroidism pathophysiology
thyroid dysgenesis - developmental abnormality -> either agenesis or ectopic (dysgenesis)
thyroid dyshormogenesis - anatomically normal thyroid gland, enzymatic defect so can not produce thyroid hormone normally
congential hypoithyroidism risk
female
prematurity
low birth weight
twins
clinical features congenital hypothyroidism
asx - screening programme (between 5th and 8th day of life)
feeding difficulties
lethargy + increased sleeping
constipation
prolonged jaundice
hoarse cry
examination congenital hypothyroidism
poor growth
macroglossia
myxedema
large fontanelles
hypotonia
bradycardia
distended abdomen with umbilical hernia
goitre
most sensitive test for congential hypothyroidism
TSH
(NOTE: depends on child’s age)
long term tx of hypothyoridism
transient - may not require tx after 2 years
if permanent - trialled off levothyroxine at 2/3 years of age to decide if lifelong tx required
complications of delayed tx congenital hypothyroidism
impaired neurocognitive development and growth
ADRENAL CORTISOL INSUFFIENCIENCY RISK FACTORS
high doses of steroids for prolonged periods
surgery to adrenal gland
radiation therapy
any pituitary insult
children adrenal cortisol insufficiency
delayed puberty alongside other sx
adrenal cortisol insufficiency primary
congenital adrenal hyperplasia
congenital adrenal hypoplasia
familial glucocorticoid deficiency
selective mineralocorticoid deficiency
addison’s
autoimmune polyglandular syndromes 1,2,4
adrenal cortisol insufficiency secondary
steroid withdrawal
hypopituitarism
catastrophic infection/illness - waterhouse-friderichsen syndrome and adrenal necrosis
adrenal cortisol insufficiency management
fluid resus
IM hydrocortisone
other steroid replacmenet
babies in 1st year of life - NaCl supplements
sick day rules
medical alert bracelet and emergency hydrocortisone
adrenal cortisol insufficiency complciations
addisonian crisis
arrhythmias
neonatal - disorders of sexual development
baby - collapse and seizures
puberty begins in girls
10.5
puberty begins in boys
11.5
precocious puberty
pubertal changes before age of 8 in girls and 9 in boys
late onset puberty
physical changes (breast and testicular development) not begun before age of 13.5 in boys and 13 in girls. or girls not had period by 16
consonant puberty
the order of characteristics’ development typically follows a set sequence for both girls and boys
stages of sexual development
tanner scale
end of puberty linked
to fusion of epiphyseal growth plates
puberty in girls
adrenarche - increased sebaceous gland activity (acne), sweating, hair growth (axillary then pubic), body odour
thelarche - for 5/6 years
menarche - menstuation, coincides with stage 3 of breast development. average as is 12.9
growth - typically grow 5-10cm from date of menarche
puberty in boys
adrenarche - increased hair, deepened voice, ability to ejaculate
testicular development - measured using orchidometer, increased pigmentation, scrotal thickening, penile growth and thickening
growth - increased body size and muscle bulk, usually between 14-17
complications of puberty
acne
gynecomastia(imbalance of oestrogen and androgens at puberty onset)
types of precocious puberty
true - early activation of HPA axis
fale - gonadotrophin independent, isolated development of one characteristic
causes of true precocious puberty
hydrocephalus
post sepsis, surgery, trauma
brain tumour
causes of false precocious puberty
CAH
exogenous sex steroids
ovarian/testicular tumours
hypothyroidism
McCune albright syndrome
consequences of early puberty
short stature - loses 2/3 years of typical GH
psychological
early menarche
safeguarding concerns
late onset puberty causes boys
maturational delay
hypogonadotropic hypogonadism (high LH and FSH if gonadal failure or both low if pituitary failure)
kallman’s syndrome
tumours
infection
trauma
glycogen storage disorders
late onset puberty causes boys
tuner’s
anorexia
low birth weight
primary ovarian failure
