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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

25
complications of diabetes
similar to the associations! Addisons, thyroid , celiac PEPTIC ULCER +IG A DEFICIENCY
26
reatment of hypoglycemia=
Rapidly absorbed oral glucose (glucose gel or tablets, fruit juices, and nondiet glucagon injection - seizures/at home iv glucose- hospital
27
values for hypoglycaemia
neonate - <2.2. preterm <1.1. infants <3.5
28
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
29
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
30
causes of early morning hyperglycaemia
somogyi and dawn
31
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
32
how to dx between dawn and smoggy
check levels at 2/3 am high/nomral - dawn low - smoggy effect
33
which diabetes has a stronger FH
TYPE 2
34
HOMA INDEX
Fasting insulin x fasting glucose/22.5
35
when does cerebral edam typically begin
around 6-12 h after theary and usually after a period of clinical improvement
36
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
37
CUSHINGS DISEAS VS SYNDTOME
diseases = caused by increase in ACTH syndrome : iatrogenic causes so levels of acth are not always high!
38
prada willi syndrome
babies : hypotonia, weak sucking reflex , failure to thrive children : never satiated and mental cognitive impariment
39
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 ```
40
treatment of congenital hypothyroidism
before baby is 2-3 weeks old to prevent neurological , levothyroxine 0.25-0.5 mg a day
41
odd signs of elevated cortisol in cushings
``` rubeosis hypernatremia myopathy psychosis brain shrinking hirtisuism ```
42
diagnosis of turners
often due to short stature or congenital hear defect at birth HIGH FSH AND LH
43
gonadtoropin is released by
pituitary by a feedback of hypothalamus
44
WHENS SHOULD U ADD GLUCOSE IN A DKA PATIENT
IF IT DECREASES BELOW 14 MML
45
another name for Addisons
autoimmune adrenalits
46
adrenal crisis Addisons
``` hypoglycaemia hyponatremia hyperkalemia circulatory collaps abdominal pain fever ```
47
emergency protocol at home for adrenal crisis
IM CORTISOL
48
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
49
true precocious puberty
early hypothalamic maturation - a central cause!
50
which babies present with hypglcemia
diabetic | gh deficiency
51
gh deficiency
small penis delayed puberty doll like face
52
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
53
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
54
hypogonadtropic hypogonadism is an example of
kallman syndrome (affects both males and females)
55
kleinfelters labs
because its primary (glands) you'll see a compensation so increased FSH + LH unlike in kallamans where it was all low
56
tuners labs
like kleinfelters high fish and lh

peds (26 decks)

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