Endo Flashcards
initial fluid bolus in shock DKA
normal saline at 10ml/kg
more specific DKA fluid restoration
fluid should be replaced slowly over 36- 48 h
100ml/kg for weight <10kg
1050 for above 10kg
1520 for above 20 kg
first line of action in DKA
REHDRATE THEN SORT OUT INSULIN
why don’t we want to bring down the glucose too fast
brain edema
when should u give glucose in Dka
if glucose falls to less than 11 or 14
when is bicarbonate therapy indicated in ska
unless ph is very low <6.9 or is hyperkalemia is present
side effects of bicarbonate
brain edema
tissue hypoxia
paradoxical increase in CNS acidosis
osmotic changes
signs of cerebral edema to look out for in dka
headache detorriation in mental status opthalplegia anisocria bushings sign (bradycardia+hypertension)
when to switch from iv insulin to sc insulin (preparation for outpatient)
- when ph is normal
- when bicarb is >15
- patient is tolerating oral feeds
The first SC insulin dose should be given 30 to 45 minutes before discontinuation of the IV insulin infusion.
= Starting doses are approximately 1U/kg/24 hours
=» Using a mixed split-dosing regimen including short-acting
insulin in conjunction with long-acting insulin — basalbolus scheme.
acanthuses nigricans is
a sign of insulin resistance
neonatal diabetes
<6 months different to type 1 because autoimmune and has 2 forms transient and permanent
which genetic disorders increase the risk ofdibates
downs and tuners
Much do the beta cells have to be destroyed in order to have the clinical signs of diabetes
80-90%
which genes increase risk of diabetes
HLA DR3/DR4 found in 90% of children with DM 1
what other diseases are associated with diabetes
HASHMIMOTOS hypothyroidism celiac disease RA Addiosons
antibodies to celiac
Tissue transglutaminase antibodies
antibodies to Addisons
21-hydroxylase antibodies
ab for hashimotos
Antiperoxidase thyroid antibodies
diagnosis of diabetes
fasting >7 or 7.8 not sure lol
random >11.1
raised glycosylated
criteria so far (check book)
ph <7.25
hco3 <15
ketonemia/ketonuria
complications of DKA
brain edema due to treatment 1. intracrhail thrombus! pulmonary edema 2. kidney failure/acute tubular necrosis 3. arrthmias due to k 4. bowel ischemia 5. pancreatitis
treatment of cerebral edam
Treatment: iv mannitol and intubation and hyperventilation
‘honeymoon period
Starts in the first weeks of therapy and usually continues for a few months at most, but can last 2 years
Don’t stop insulin in DM1 patients if once started!!!
aim of hba1c
6.5 %
complications of diabetes
similar to the associations! Addisons, thyroid , celiac PEPTIC ULCER +IG A DEFICIENCY
reatment of hypoglycemia=
Rapidly absorbed oral glucose (glucose
gel or tablets, fruit juices, and nondiet
glucagon injection - seizures/at home
iv glucose- hospital
values for hypoglycaemia
neonate - <2.2.
preterm <1.1.
infants <3.5
Ketotic hypoglcemia of childhood
occurring in some children if they have not eaten over a long period of time or when ill. It almost always goes away when the children are a little older and almost never causes any permanent harm.
can have vomiting due to the ketones
dawn phenomenon
absence of insulin which usually will counterbalance gh so now gh is unopposed and it usually is secreted in early hours of morning but dx np hypoglcemia at 2/3am
causes of early morning hyperglycaemia
somogyi and dawn
sommogyi
too high insulin or too low food intake before bed- so you get hypoglycaemia at 2/3am and you wake up in the morning with rebound hyperglycaemia +headache and sweating and nightmares
how to dx between dawn and smoggy
check levels at 2/3 am
high/nomral - dawn
low - smoggy effect
which diabetes has a stronger FH
TYPE 2
HOMA INDEX
Fasting insulin x fasting glucose/22.5
when does cerebral edam typically begin
around 6-12 h after theary and usually after a period of clinical improvement
when to calculate urinary ketones
Urine ketones also should be tested during periods of intercurrent illness or when blood glucose levels >300mg (divide by 18 to get In mmol/l
CUSHINGS DISEAS VS SYNDTOME
diseases = caused by increase in ACTH
syndrome : iatrogenic causes so levels of acth are not always high!
prada willi syndrome
babies : hypotonia, weak sucking reflex , failure to thrive
children : never satiated and mental cognitive impariment
signs of hypothyroidism
pale cold mottled dry skin horse cry /face large cry prolonged jaundice -affects conjugation process large fontanelle bradycardia constipation large fontanelle (posterior) umbilical hernia distention of abdomen
treatment of congenital hypothyroidism
before baby is 2-3 weeks old to prevent neurological , levothyroxine 0.25-0.5 mg a day
odd signs of elevated cortisol in cushings
rubeosis hypernatremia myopathy psychosis brain shrinking hirtisuism
diagnosis of turners
often due to short stature
or congenital hear defect at birth
HIGH FSH AND LH
gonadtoropin is released by
pituitary by a feedback of hypothalamus
WHENS SHOULD U ADD GLUCOSE IN A DKA PATIENT
IF IT DECREASES BELOW 14 MML
another name for Addisons
autoimmune adrenalits
adrenal crisis Addisons
hypoglycaemia hyponatremia hyperkalemia circulatory collaps abdominal pain fever
emergency protocol at home for adrenal crisis
IM CORTISOL
waterhouse freidrickson
WFS is caused by severe infection with meningococcus bacteria or other bacteria, such as:
Group B streptococcus
Pseudomonas aeruginosa
Streptococcus pneumoniae
Staphylococcus aureus
true precocious puberty
early hypothalamic maturation - a central cause!
which babies present with hypglcemia
diabetic
gh deficiency
gh deficiency
small penis
delayed puberty
doll like face
in ska what do you care most about
fixing the electrolytes and ph the glucose is the least of your concern it will correct itself in the end and slowly
MAURIAC SYNDROME
Mauriac syndrome is a rare complication of type 1 diabetes characterized by extreme liver enlargement due to glycogen deposition, along with growth failure and delayed puberty. It occurs in some children and adolescents with type 1 diabetes irrespective of their glycemic control.
SYMPTOMSM: enlarged liver, obesity, delayed puberty
hypogonadtropic hypogonadism is an example of
kallman syndrome (affects both males and females)
kleinfelters labs
because its primary (glands) you’ll see a compensation so increased FSH + LH unlike in kallamans where it was all low
tuners labs
like kleinfelters high fish and lh
