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peds > Endo > Flashcards

Endo Flashcards

1
Q

initial fluid bolus in shock DKA

A

normal saline at 10ml/kg

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2
Q

more specific DKA fluid restoration

A

fluid should be replaced slowly over 36- 48 h
100ml/kg for weight <10kg
1050 for above 10kg
1520 for above 20 kg

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3
Q

first line of action in DKA

A

REHDRATE THEN SORT OUT INSULIN

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4
Q

why don’t we want to bring down the glucose too fast

A

brain edema

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5
Q

when should u give glucose in Dka

A

if glucose falls to less than 11 or 14

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6
Q

when is bicarbonate therapy indicated in ska

A

unless ph is very low <6.9 or is hyperkalemia is present

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7
Q

side effects of bicarbonate

A

brain edema
tissue hypoxia
paradoxical increase in CNS acidosis
osmotic changes

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8
Q

signs of cerebral edema to look out for in dka

A 
headache 
detorriation in mental status
opthalplegia 
anisocria 
bushings sign (bradycardia+hypertension)
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9
Q

when to switch from iv insulin to sc insulin (preparation for outpatient)

A
  1. when ph is normal
  2. when bicarb is >15
  3. 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.

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10
Q

acanthuses nigricans is

A

a sign of insulin resistance

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11
Q

neonatal diabetes

A

<6 months different to type 1 because autoimmune and has 2 forms transient and permanent

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12
Q

which genetic disorders increase the risk ofdibates

A

downs and tuners

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13
Q

Much do the beta cells have to be destroyed in order to have the clinical signs of diabetes

A

80-90%

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14
Q

which genes increase risk of diabetes

A

HLA DR3/DR4 found in 90% of children with DM 1

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15
Q

what other diseases are associated with diabetes

A 
HASHMIMOTOS 
hypothyroidism 
celiac disease
RA 
Addiosons
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16
Q

antibodies to celiac

A

Tissue transglutaminase antibodies

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17
Q

antibodies to Addisons

A

21-hydroxylase antibodies

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18
Q

ab for hashimotos

A

Antiperoxidase thyroid antibodies

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19
Q

diagnosis of diabetes

A

fasting >7 or 7.8 not sure lol
random >11.1
raised glycosylated

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20
Q

criteria so far (check book)

A

ph <7.25
hco3 <15
ketonemia/ketonuria

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21
Q

complications of DKA

A 
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
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22
Q

treatment of cerebral edam

A

Treatment: iv mannitol and intubation and hyperventilation

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23
Q

‘honeymoon period

A

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!!!

24
Q

aim of hba1c

A

6.5 %

25
Q

complications of diabetes

A

similar to the associations! Addisons, thyroid , celiac PEPTIC ULCER +IG A DEFICIENCY

26
Q

reatment of hypoglycemia=

A

Rapidly absorbed oral glucose (glucose
gel or tablets, fruit juices, and nondiet

glucagon injection - seizures/at home

iv glucose- hospital

27
Q

values for hypoglycaemia

A

neonate - <2.2.
preterm <1.1.
infants <3.5

28
Q

Ketotic hypoglcemia of childhood

A

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

29
Q

dawn phenomenon

A

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

30
Q

causes of early morning hyperglycaemia

A

somogyi and dawn

31
Q

sommogyi

A

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

32
Q

how to dx between dawn and smoggy

A

check levels at 2/3 am

high/nomral - dawn
low - smoggy effect

33
Q

which diabetes has a stronger FH

A

TYPE 2

34
Q

HOMA INDEX

A

Fasting insulin x fasting glucose/22.5

35
Q

when does cerebral edam typically begin

A

around 6-12 h after theary and usually after a period of clinical improvement

36
Q

when to calculate urinary ketones

A

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

37
Q

CUSHINGS DISEAS VS SYNDTOME

A

diseases = caused by increase in ACTH

syndrome : iatrogenic causes so levels of acth are not always high!

38
Q

prada willi syndrome

A

babies : hypotonia, weak sucking reflex , failure to thrive

children : never satiated and mental cognitive impariment

39
Q

signs of hypothyroidism

A 
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
40
Q

treatment of congenital hypothyroidism

A

before baby is 2-3 weeks old to prevent neurological , levothyroxine 0.25-0.5 mg a day

41
Q

odd signs of elevated cortisol in cushings

A 
rubeosis 
hypernatremia
myopathy 
psychosis
brain shrinking 
hirtisuism
42
Q

diagnosis of turners

A

often due to short stature
or congenital hear defect at birth
HIGH FSH AND LH

43
Q

gonadtoropin is released by

A

pituitary by a feedback of hypothalamus

44
Q

WHENS SHOULD U ADD GLUCOSE IN A DKA PATIENT

A

IF IT DECREASES BELOW 14 MML

45
Q

another name for Addisons

A

autoimmune adrenalits

46
Q

adrenal crisis Addisons

A 
hypoglycaemia 
hyponatremia 
hyperkalemia 
circulatory collaps 
abdominal pain 
fever
47
Q

emergency protocol at home for adrenal crisis

A

IM CORTISOL

48
Q

waterhouse freidrickson

A

WFS is caused by severe infection with meningococcus bacteria or other bacteria, such as:

Group B streptococcus
Pseudomonas aeruginosa
Streptococcus pneumoniae
Staphylococcus aureus

49
Q

true precocious puberty

A

early hypothalamic maturation - a central cause!

50
Q

which babies present with hypglcemia

A

diabetic

gh deficiency

51
Q

gh deficiency

A

small penis
delayed puberty
doll like face

52
Q

in ska what do you care most about

A

fixing the electrolytes and ph the glucose is the least of your concern it will correct itself in the end and slowly

53
Q

MAURIAC SYNDROME

A

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

54
Q

hypogonadtropic hypogonadism is an example of

A

kallman syndrome (affects both males and females)

55
Q

kleinfelters labs

A

because its primary (glands) you’ll see a compensation so increased FSH + LH unlike in kallamans where it was all low

56
Q

tuners labs

A

like kleinfelters high fish and lh

peds (26 decks)

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