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05 Endo > Obesity and DM > Flashcards

Obesity and DM Flashcards

1
Q

childhood obesity is more prevalent in

A

males
student in private schools
children in urban areas

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2
Q

how to measure obesity

A 
body weight for height
bmi
cdc bmi chart
who growth chart
waist and hip circumference
skinfold thickness
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3
Q

bmi chart results

A

bmi > 85th percentile: overweight

bmi > 95th percentile: obese

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4
Q

who growth chart 0-5 yo

A

above +2 sd: overweight

above +3 sd: obese

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5
Q

who growth chart 5-19 yo

A

above +1 sd: overweight
above +2 sd: obese
above +3 sd: morbidly obese

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6
Q

adult interpretation for skinfold thickness

A

lean: 6-12 mm
obese: 40-50 mm

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7
Q

cut offs for weight

A 
underweight bmi < 5th percentile
normal =5th to < 85th percentile
overweight >/= 84th to 95th percentile
obese >/= 95th percentile
severe obesity
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8
Q

causes of simple obesity

A

high caloric intake
low energy expenditure

with no demonstrable disease that accounts for excess adiposity

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9
Q

t/f pathologic (endogenous) obesity accounts for a great majority of obesity in children

A

false, simple (exogenous) obesity is more common

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10
Q

causes of pathologic obesity

A 
gh deficiency
congenital and acquired hypothyroidism
cushing syndrome
prader-willi syndrome
adrenal insufficiency due to medications
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11
Q

features of gh deficiency

A

morning headaches, vomiting, visual disturbances, excessive urination and drinking
cherubic facies
short stature
craniopharyngioma*

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12
Q

features of acquired hypothyroidism

A

dry skin, constipation, intolerance to cold, easy fatigability
manifests later

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13
Q

features of congenital hypothyroidism

A

macroglossia, periorbital puffiness, flat nasal bridge, dry skin, frontal bossing, distended abdomen, constipation

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14
Q

features of cushing syndrome

A

selective accumulation of fat in the neck and trunk, purple/violaceous striae
hypertrichosis, truncal obesity, prominent cheeks, acne, stunted growth

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15
Q

features of prader willi syndrome

A

hypotonia, hyperphagia, short stature, mental retardation, hypogonadism, likes to pick their skin

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16
Q

t/f pediatric obesity may signal to underlying pathology

A

true

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17
Q

t/f one of the most common consults is due to skin infections

A

false, due to high bp (headaches, loss of consciousness)

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18
Q

pathogenesis of nalfd from obesity

A

obesity > insulin resistance or hyperinsulinemia > steatosis > steatohepatitis > liver cirrhosis > HCC

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19
Q

signs of osa

A

patient prefers to sleep sitting down or needs cpap to sleep

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20
Q

orthopedic complications of childhood obesity

A

blout’s disease (bowing of legs)

slipped capital femoral epiphysis (fermoral head slips from epiphyseal plate)

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21
Q

causes of orthopedic complications in childhood obesity

A

compressive pressure on the proximal medial metaphyseal area of tibia

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22
Q

t/f medical consequences of childhood obesity is more prevalent

A

false, phsycosocial consequences are more prevalent

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23
Q

this is the most long-term complication of obesity

A

metabolic syndrome

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24
Q

components of successful weight loss plan

A

education, dietary management, exercise or physical activity, lifestyle and behavior modification, family involvement!!

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25
Q

recommended physical activity

A

30-60 minutes of moderate to vigorous play or physical activity daily

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26
Q

recommended time watching tv/playing games

A

max 2 hours per day

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27
Q

t/f medical treatment is not a first line treatment for childhood obesity

A

true

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28
Q

types of surgeries for childhood obesity

A

jejunoileal bypass
gastric bypass
gastric plication or gastroplasty by stapling
jaw wiring

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29
Q

a loss of ___ of total body weight can reduce many of the health risks associated with obesity

A

5-20%

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30
Q

5210 care approach to prevent CO

A

5 fruits and vegetables
cut screen time to 2 hours
1 hour physical activity
0 soda or sweetened drinks

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31
Q

t/f t1dm presents with acanthosis nigricans

A

false (2022 table 4)

32
Q

incidence of t1dm

A

minor peak at 4-6 years (infection)

major peak 10-14 years (puberty)

33
Q

usually a __ reduction in beta cell volume is required to induce symptomatic t1dm

A

80%

34
Q

main problem in t2dm

A

peripheral insulin resistance, relative insulin deficiency

NOT ABSOLUTE INSULIN DEFICIENCY!

35
Q

expected bmi in t2dm obesity

A

85th percentile for age and sex

mean bmi 27-38 kgm2

36
Q

mean age of diagnosis for t2dm puberty

A

12-16 yo

peak age of diagnosis of t2dm

37
Q

sign that presents in 90% of children and adolescents with t2dm

A

t2dm acanthosis nigricans

also associated with insulin resistance, hyperinsulinemia, and obesity

38
Q

perinatal factors in t2dm

A

high maternal bs during pregnancy
maternal or fetal undernutri
large or small for gestational aage

39
Q

t/f breast feeding has a protective effect against obesity and t2dm

A

true, encouraged until 2 yo

40
Q

who to screen for t2dm in children or adolescents

A

bmi 85th percentile
wfh > 85th percentile
weight > 120% of ideal for height

+ any 2 risk factors:
family history, ethnicity, signs of insulin resistance, maternal history of diabetes or gdm

41
Q

age of initiation of monitoring and frequency for t2dm

A

initiate: at risk age 10 or younger
screen: every 2 years

42
Q

preferred screening study for t2dm

A

fasting plasma glucose

43
Q

signs and symptoms for dm

A

polyuria, nocturia, polydipsia, polyphagia, mood changes and tiredness, blurring of vision, numbness of hands and feet (not necessarily diabetic retinopathy), candidiasis, non-healing wound

44
Q

t/f you can diagnose a child with diabetes if he has an rbs of 200

A

true

45
Q

t/f adults and pedia have different cut offs

A

false, they have the same

46
Q

when to request for ogtt

A

when patient’s fbg is not high but patient has signs and symptoms, family history, and high index of suspicion

47
Q

additional work up for dm

A

serum insulin (low in t1dm)
c-peptide (low in t1dm, high in t2dm)
ica and anti-gad (+ for t1dm, + or - in t2dm)

48
Q

preferred treatment for t2dm in children

A

ohas are not used, use insulin sensitizers

49
Q

daily sc injections for t1dm

A

rapid acting insulin + long acting insulin
intermediate insulin + short acting insulin
2-4 injections a day regimens

50
Q

__ injections a day mimics the normal physiologic insulin production of the body

A

4 injections a day

51
Q

mainstay treatment for t2dm

A

diet, exercise, healthy lifestyle

52
Q

the only drug fda approved for use in children

A

metformin

53
Q

progression of treatment for t2dm in children

A

lifestyle -> metformin for asymptomatic -> oha -> insulin

54
Q

indications to immediately start insulin therapy in t2dm

A

symptomatic
increased blood glucose levels
hba1c >8% (+ dka or hhs)

55
Q

glucose management for toddlers and preschool (0-6 yo)

A

a1c 7.5-8.5
fasting before a meal goal 100-180
bedtime or overnight goal 110-200

56
Q

glucose management in school age (6-12 yo)

A

a1c <8
fasting before a meal goal 90-180
bedtime or overnight goal 100-180

57
Q

adolescents/ya (13-19 yo)

A

a1c <7.5
fasting before a meal goal 90-130
bedtime or overnight goal 90-150

58
Q

why are values for toddlers’ glucose management higher

A

to avoid hypogly, seizures, or loss of consciousness because they don’t always report what they’re feeling

59
Q

main cause of morbidity/mortality in children with t1dm

A

dka

60
Q

pathophysiology of dka

A

low insulin, high counter-regulatory hormones -> inc glucose from liver/kidney, dec peripheral glucose use -> hypergly, proteolysis, lipolysis -> ketosis and met acid

61
Q

clinical manifestation of dka

A

glucosuria leading to dehydration
catabolic state leading to body weakness
ketonemia and met acid

62
Q

common misdiagnoses of dka

A

penumonia, bronchitis, asthma, uti, gastritis

if PE and tachypnea don’t match, do a cbg or rbs

63
Q

biochemical defintion of dka

A

hypergly (>200 mg/dl)
venous ph <7.3
serum hco3 <15 mmol/l

64
Q

severity of dka

A

mild ph <7.3 shco3 <15
moderate ph <7.2 shco3 <10
severe ph <7.1 shco3 <5

65
Q

risk factors for dka

A 
poor metabolic control
peri-pubertal girls
difficult family circumstances
psych disorders
insulin omission or treatment error*
inadequate insulin therapy during intercurrent illness
66
Q

dka management

A

hypergly + milk ketosis, no vomiting or severe dehydration: wards
moderately to severely dehydrated: icu admission (risk of cerebral edema)

67
Q

dka management: restoration of vascular volume

A

if in shock with poor peripheral perfusion or come give 10 cc/kg of plain 0.9 nss x 10-30 min until pulses are good

fluid requirements should include maintenance, deficit, and continuing losses

68
Q

other aspects of volume restoration

A

potassium supplementation at 3rd hour or as patient is voiding
shift to glucose containing soln when blood glucose is down to 200 mg/dl

69
Q

dka management: inhibition of lipolysis and correction of hyperglycemia

A

insulin therapy after reversal of shock and 1-2 hrs after fluid replacement

70
Q

t/f do not stop insulin infusion or decrease below 0.05 u/kg/hr

A

true, glucose and insulin are both needed to promote anabolism and reduce ketosis

71
Q

dka management: correction of acidosis

A

fluids to stop lactic acidosis

insulin to stop ketoacidosis

72
Q

holiday segar method

A

first 10 kg = 100 ml/kg/d , 4 ml/kg/h
second 10 kg = 50 mg/kd/d , 2 mg/kg/h
every kg after 20 ml/kg/d , 1 ml/kg/h

73
Q

complications of dka

A

cerebral edema before, during, or 4-12 hrs after treatment started

warning signs: headache, deterioration of consciousness, seizure, papilledema, slow pulse, inc bp

74
Q

associated conditions in t1dm

A

autoimmune (thyroiditis, celiac, adrenal insufficiency)

skin diseases and infections

75
Q

lab test frequencies

A 
bsm daily
hba1c every 3 mos
urinalysis and microalbuminuria every 12 mos
crea and liver function at diagnosis
lipid at diagnosis and every 12 mos

05 Endo (16 decks)

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