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Peds II Final > Peds Endocrine > Flashcards

Peds Endocrine Flashcards

1
Q

Most common endocrine cell type in the pancreas

A

Beta cells

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2
Q

Endocrine cell types

A 
Beta (60%)
Alpha (25%)
Delta (10%)
Gamma (4%)
Epsilon (1%)
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3
Q

Measurement of endogenous insulin

A

C-peptide

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4
Q

Most common etiology of DM1

A

Autoimmune (90%)

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5
Q

Etiologies of DM1

A

Autoimmune

Idiopathic

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6
Q

Age peaks of DM1

A 
Mid-childhood (4-6 YO)
Early puberty (10-14 YO)
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7
Q

Highest incidence of DM1 by location

A

Finland - Possible environmental factor: Farther from equator

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8
Q

Non-modifiable risk factors for DM1

A
  • Non-Hispanic white population = Highest risk***

- Genetic susceptibility: 1-8% increased risk w/ affected parent

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9
Q

Possible environmental risk factors for DM1

A 
Viral infections
Further from equator
Diet (early exposure to cows milk, intro of cereals)
Higher socioeconomic status
Obesity
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10
Q

Viral infections that may cause DM1

A

EBV
Coxsackie
CMV

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11
Q

Most common (classic) clinical presentation of DM1

A

Polyuria, Polydipsia, Polyphagia + weight loss/fatigue

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12
Q

Different presentations of DM1

A
  1. Classic (most common)
  2. DKA
  3. Silent (incidental) discovery
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13
Q

DKA presentation

A

Fruity-smelling breath

Drowsiness/lethargy

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14
Q

Treatment of DKA

A

Hospitalization!

Rehydration and insulin replacement therapy

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15
Q

DM1 Diagnosis Criteria

A

1 of the 4 signs of abnormal glucose metabolism:

  • Fasting glucose >126 mg/dL
  • Random glucose >200 mg/dL
  • Plasma glucose >200 mg/dL 2 hours after oral glucose tolerance test
  • Hemoglobin A1C >6.5%
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16
Q

Onset of Type 1 DM

A

Acute severe

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17
Q

Female:Male of Type 1 DM

A

1:1

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18
Q

Body habitus of Type 1 DM

A

20-25% overweight

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19
Q

Insulin sensitivity of Type 1 DM

A

Normal when controlled

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20
Q

Family Hx association with Type 1 DM

A

Infrequent (5-10%)

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21
Q

Pancreatic auto-antibodies

A

Type 1 DM

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22
Q

Onset of Type 2 DM

A

Insidious to severe

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23
Q

Age of onset for Type 2 DM

A

Puberty

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24
Q

Female:Male of Type 2 DM

A

2:1

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25
Q

Body habitus of Type 2 DM

A

> 80% OBESE

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26
Q

Insulin sensitivity of Type 2 DM

A

Decreased

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27
Q

Family hx association with Type 2 DM

A

Frequent (75-90%)

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28
Q

Hospitalization for DM1

A

Typically hospitalize at diagnosis

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29
Q

DM1 Education

A

Explain disease
Blood glucose testing (3-4 x per day initially)
Insulin administration
Recognizing hypoglycemia
Blood or urine ketone measurements if ill

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30
Q

DM1 Treatment goals

A

Achieve glucose control WITHOUT hypoglycemia

  • Start low, go slow!
  • Set realistic goals for child, family, and lifestyle
  • Goals become more aggressive as child ages
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31
Q

Hypoglycemia risk decreased with

A

Age

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32
Q

Ideal fasting glucose for <5

A

80-200

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33
Q

Ideal fasting glucose for 6-11 YO

A

70-180

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34
Q

Ideal fasting glucose for 12-19 YO

A

70-150

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35
Q

Target HbA1C for <5

A

7.5-8.5%

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36
Q

Target HbA1C for 6-11 YO

A

<8.0%

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37
Q

Target HbA1C for 12-19 YO

A

<7.5%

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38
Q

Types of insulin

A

Rapid-acting
Short-acting
Intermediate-acting
Long-acting

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39
Q

Rapid acting insulins

A

Lispro
Aspart
Glulisine

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40
Q

Short acting insulins

A

Regular insulin

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41
Q

Intermediate acting insulins

A

NPH insulin

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42
Q

Long acting insulins

A

Glargine

Detemir

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43
Q

Administration of short acting insulins

A

Pre-meal bolus 5-30 min before meal

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44
Q

Administration of intermediate acting insulins

A

Targeted manner in combo with long acting insulins

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45
Q

Administration of long acting insulins

A

1-2 times per day

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46
Q

Pediatric Insulin Dosing

A

“Physiologic Regimen” (most common):

  • Basal dose: Intermediate, long, or ultra-long
  • Bolus dose: Rapid or short at meals
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47
Q

Reason for a basal dose

A

Suppress endogenous hepatic glucose production throughout the day

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48
Q

Reason for bolus dose

A

Cover carb intake at meals

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49
Q

Types of insulin administration

A

Syringe
Pen
Pump

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50
Q

New DM1 patients are started on what type of insulin administration

A

Syringe

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51
Q

Advantages of syringe

A

Can mix different insulins (decreases # of injections)
Cheaper
Requires less training

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52
Q

Disadvantages of syringe

A

More prone to hypoglycemia

Frequent needle sticks

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53
Q

Advantages of the pen

A

Disposable/reusable

Ease of use and portability

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54
Q

Disadvantages of the pen

A

More expensive (than syringes)

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55
Q

Advantages of the pump

A

More accurate
Improves HbA1C
Allows you to exercise w/out increasing carbs
Less prone to hypoglycemia

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56
Q

Disadvantages of the pump

A

More training

Most expensive

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57
Q

Assessment of obesity in children

A

BMI Percentiles

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58
Q

Overweight BMI percentile

A

85th-95th percentile

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59
Q

Obese BMI percentile

A

> 95th percentile

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60
Q

Severely obese BMI percentile

A

> 120th percentile

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61
Q

How many children in US are overweight or obese

A

1/3

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62
Q

Ethnicity obesity is most common in…

A

American Indian
Black
Mexican Americans

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63
Q

Strong predictor of adult obesity

A

Childhood obesity

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64
Q

Non-modifiable risk factors for obesity

A

Ethnicity

Family hx of Type 2 DM, metabolic disorders, and CV disease

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65
Q

Modifiable risk factors for obesity

A 
Diet high in fat &amp; CHO
Sugared beverages
Lack of CV exercise
Sedentary lifestyle
Shortened sleep duration
Medications
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66
Q

Medications that can cause obesity

A

Glucocorticoids

Psychoactive drugs

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67
Q

Calorie intake recommendation for children 6-12

A

900-1200 kcal per day

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68
Q

General nutrition recommendations

A 
Stabilize weight or small weight loss if severely obese
Portion control
Avoid sugary drinks
Limit milk intake
900-1200 kcal per day (6-12 YO)
Eat meals at home
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69
Q

The diabetes plate method

A

1/2 Nonstarchy vegetables
1/4 Lean protein
1/4 Grains or starchy vegetables

70
Q

Exercise recommendations

A

30-60 min per day

71
Q

Non-academic screen time

A

Restricted to 2 hours per day

72
Q

Progression of Type 2 DM

A

Insulin resistance -> Beta cell hyperplasia -> Beta cell failure (early) -> Beta cell failure (late)

73
Q

Blood glucose with beta cell hyperplasia

A

Normoglycemia

74
Q

Result of early beta cell failure

A

Impaired glucose tolerance (Hyperglycemia)

75
Q

Result of late beta cell failure

A

Diabetes

76
Q

DM2 Risk factors

A

Obesity*
Family Hx*
Ethnicity
Conditions associated with insulin resistance

77
Q

Ethnic groups at higher risk for DM2

A 
Native American
African American
Latino
Asian American
Pacific Islander
78
Q

DM2 Clinical presentation (symptoms)

A

Often ASYMPTOMATIC*

  • Fatigue, irritability, difficulty concentrating
  • Polydipsia
  • Polyuria
  • Visual disturbances
  • Frequent infections
79
Q

DM2 Clinical presentation (signs)

A

Overweight/Obese
Acanthosis Nigricans
DKA (Rare)

80
Q

Acanthosis Nigricans

A

Thickened, velvety, hyperpigmented skin typically on the posterior neck, axilla, abdomen, thighs, and antecubital fossa

81
Q

When to screen children for DM2

A

> 10 YO if overweight/obese AND 2 of the following:

  1. Type 2 DM in a 1st or 2nd degree relative
  2. High-risk ethnic group
  3. Signs of insulin resistance or conditions associated with insulin resistance
  4. Maternal hx of DM or gestational DM when child was in utero
82
Q

When do you repeat DM screening for at risk kids

A

Every 3 years

83
Q

Diagnosis of DM2

A
  1. Fasting glucose >126 mg/dL
  2. Random glucose >200 mg/dL
  3. Plasma glucose >200 mg/dL 2 hours after oral glucose tolerance test
  4. HbA1C >6.5%
84
Q

Primary medications for DM2 management

A

Metformin and insulin

85
Q

First-line DM2 medication

A

Metformin

86
Q

What benefits does metformin have

A
  • Increased insulin-mediated glucose uptake in tissues
  • Decreased hepatic glucose production
  • Promotes modest weight loss
87
Q

When is insulin therapy considered in DM2

A 
Ketosis
Severe hyperglycemia
Mixed features of type 1 and type 2
Random glucose >250 OR
HbA1C >9%
88
Q

How often do you monitor A1C

A

Every 3 months

89
Q

Treatment monitoring for DM2 patients

A
  • Review weight, BMI, diet, and physical activity
  • Blood glucose (self-monitoring)
  • HbA1C
  • Monitor other comorbidities if applicable
90
Q

How often is blood glucose checked

A

3 times per day if on insulin

91
Q

First-line meds in treating HTN for DM2 pts

A

ACE or ARB

92
Q

Second-line meds in treating HTN for DM2 pts

A

Thiazide
CCBs
Beta-blockers - USE WITH CAUTION! (May mask hypoglycemia symptoms)

93
Q

Elevated BP for children >13 YO

A

120-129 Systolic AND

Diastolic <80

94
Q

Stage 1 HTN for children >13 YO

A

130/80 to 139/89

95
Q

Stage 2 HTN for children >13 YO

A

> 140/90

96
Q

Goals for lipid levels in children with DM2

A

LDL-C <100
HDL-C >35
Triglycerides <150

97
Q

Treatment recommendations for elevated lipids

A

6 months nonpharmacologic therapy first

HMG-CoA reductase inhibitors if criteria met

98
Q

Criteria for HMG-CoA drug therapy in children

A

LDL >130
>10 YO
Obesity/Other CV risk factors

99
Q

Definition of short stature

A

Height 2 standard deviations below mean

100
Q

Most widely used system to assess skeletal age

A

Greulich-Pyle Atlas method (GP method)

101
Q

GP method

A

Left-hand radiograph compared to atlas of radiographs for that age and gender

102
Q

Normal variants of growth etiologies

A

Familial short stature*
Constitutional delay of growth*
Idiopathic short stature
Small for gestational age

103
Q

Pathologic causes of growth failure

A

Systemic disease
Endocrine
Genetic syndromes

104
Q

Endocrine causes of short stature

A

Cushing’s
Hypothyroidism
GH Deficiency***
Sexual Precocity

105
Q

Genetic causes of short stature

A

Turner Syndrome
Prader-Willi Syndrome
Noonan Syndrome
Achondroplasia

106
Q

Familial short stature

A

Parents are short = Short offspring

-Check mean parental height

107
Q

How to check mean parental height

A

Girls: 5 inches subtracted from father’s height and averaged with the mother’s height.
Boys: 5 inches added to the mother’s height and averaged with the father’s height

108
Q

Bone age in familial short stature

A

NORMAL

109
Q

Most common cause of short stature

A

Constitutional delay of growth

110
Q

Bone age in constitutional delay of growth

A

DELAYED

111
Q

“Late-bloomers”

A

Constitutional delay of growth

112
Q

Parents’ puberty timing in constitutional delay of growth

A

Often delayed

113
Q

Adult height for familial short stature

A

Short

114
Q

Adult height for constitutional delay of growth

A

Normal

115
Q

Parent’s stature for constitutional delay of growth

A

Average

116
Q

Etiologies of GH deficiency

A 
Genetic mutations (rare)
Processes affecting hypothalamic/pituitary function
117
Q

Things to R/O before GH deficiency diagnosis

A

Hypothyroidism
Turner’s Syndrome
Skeletal disorders

118
Q

Labs for GH evaluation if no evidence of other cause

A

IGF-1
IGFBP-3
Bone Age
May consider GH stim test

119
Q

First-line treatment of GH deficiency

A

Recombinant Human Growth Hormone (rhGH)

120
Q

Monitoring rhGH therapy

A 
IGF-1 levels (age and gender specific)
Bone age (annually)
121
Q

SE of rhGH therapy

A

Pseudotumor cerebri
Hyperglycemia/insulin resistance
Gynecomastia
Increased conversion of T4 to T3

122
Q

Turner’s Syndrome features

A

45, X (loss of part or all of an X chromosome)

Short stature

123
Q

Noonan Syndrome features

A

Autosomal Dominant
Short stature
CHD (pulmonic stenosis most common)
Variable gene mutations

124
Q

Prader-Willi features

A

Defect on chromosome 15
Obesity
Short stature

125
Q

Most common cause of bone dysplasia in humans

A

Achondroplasia

126
Q

Achondroplasia genetics

A

Autosomal dominant

Mutations in fibroblast growth factor receptor 3 (FGFR3) gene

127
Q

Clinical features of achondroplasia

A
  • DISPROPORTIONATE short stature (rhizomelic shortening)
  • Macrocephaly
  • Normal cognition
128
Q

Rhizomelic shortening

A

Proximal limbs are shorter (humerus, femur)

129
Q

Medical complications of achondroplasia

A

Recurrent otitis media
Obesity
Obstructive sleep apnea
Leg bowing

130
Q

Other signs of achondroplasia

A

Brachydactyly
Short hand
Transverse palmar crease

131
Q

Excess pre-pubertal GH

A

Gigantism

132
Q

Excessive growth of long bones

A

Gigantism

133
Q

Evaluation of gigantism

A

Serum IGF-1*
GH suppression test*
MRI* (evaluate pituitary and hypothalamus)

134
Q

GH suppression test

A

Administer glucose and if GH fails to fall below 1 ng/mL = abnormal result

135
Q

Treatment of Gigantism

A

Surgery
Radiation
Octreotide***
Bromocriptine

136
Q

Normal age of puberty for boys

A

9-14 YO

137
Q

Normal age of adrenarche (girls)

A

After age 8

138
Q

Normal age of thelarche

A

8-14 YO

139
Q

Normal age of menarche

A

Two years following thelarche

140
Q

Benign premature thelarche

A

Onset prior to age 3

-If present after age 7 or 8, may progress to precocious puberty

141
Q

Premature adrenarche

A
  • Elevated DHEA
  • More common in girls
  • Absence of additional pubertal development
142
Q

Precocious puberty definition

A

Girls: <8 YO
Boys: <9 YO

143
Q

Central precocious puberty

A

Elevated GnRH and gonadotropins

144
Q

Peripheral precocious puberty

A

Elevated gonadal steroids with LOW gonadotropins

145
Q

Gonadotropin-dependent

A

Central precocious puberty

146
Q

Gonadotropin-independent

A

Peripheral precocious puberty

147
Q

Etiologies of central precocious puberty

A

Idiopathic (90%)

CNS tumors/abnormalities

148
Q

Serologic studies for central precocious puberty

A

LH
FSH
Estradiol or Testosterone

149
Q

LH:FSH suggestive of puberty

A

> 1

150
Q

Imaging for central precocious puberty

A

MRI (brain/pituitary)
Pelvic U/S
Bone age

151
Q

Pelvic U/S findings for central precocious puberty

A

Normal ovaries/uterus for pubertal stage, but premature for age

152
Q

Treatment of central precocious puberty

A

GnRH analogue

153
Q

Etiologies of peripheral precocious puberty

A
  • Exposure to gonadal steroids outside HPG axis (tumor, exogenous)
  • Congenital adrenal hyperplasia
  • McCune-Albright Syndrome
154
Q

Treatment of peripheral precocious puberty

A

Treat underlying cause

155
Q

Pubertal gynecomastia prognosis

A

Usually benign! - Should go away

156
Q

Most common cause of primary testicular failure

A

Klinefelter’s Syndrome

157
Q

Prepubertal gynecomastia etiologies

A

Klinefelter’s Syndrome
Aromatization due to obesity
Adrenal or testicular neoplasm

158
Q

Klinefelter’s Syndrome Genetics

A

XXY

159
Q

Primary cause of congenital adrenal hyperplasia

A

21-hydroxylase deficiency

160
Q

Gene responsible for 21-hydroxylase deficiency

A

CYP21A2

161
Q

Results of 21-hydroxylase deficiency

A

Aldosterone and Cortisol are not formed; Diverted to formation of sex hormones

162
Q

Sex hormones elevated in 21-hydroxylase deficiency

A

DHEA
Androstenedione
Testosterone

163
Q

When do sex hormones begin to elevated in someone with 21-hydroxylase deficiency

A

3rd month of life

164
Q

Salt losing 21-hydroxylase deficiency signs

A

Females: Genital atypia
Males: FTT, dehydration, hyponatremia, hyperkalemia at day 7-14 of life

165
Q

Non-salt losing 21-hydroxylase deficiency signs

A

Females: Genital atypia
Males: Early virilization at age 2-4 years (peripheral precocious puberty)

166
Q

Non-classic 21-hydroxylase deficiency signs

A

Females: Early pubarche, sexual precocity, hirsutism, menstrual irregularities, or ASYMPTOMATIC
Males: Early pubarche, sexual precocity

167
Q

Treating 21-hydroxylase deficiency

A 
GnRH analog (decrease sex hormone synthesis)
Hydrocortisone (replace cortisol)
Fludrocortisone (replace aldosterone)
168
Q

Clinical presentations of excess androgens

A

Acne
Clitoromegaly
Hirsutism

169
Q

Clinical presentations of deficient cortisol

A

Hypoglycemia

Decreased response to illness

170
Q

Clinical presentations of deficient aldosterone

A

Salt-wasting

Hypotension

Peds II Final (3 decks)

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