Endocrinology Flashcards

(64 cards)

1
Q

Endocrine portion of pancreas

A

Islet of Langerhans (mostly full of B cells that secrete insulin)

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2
Q

Normal physiology of glucose

A

High glucose stimulate insulin release from B cells

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3
Q

Pathophysiology of DM1

A

Destruction of pancreatic B cells (mostly autoimmune and rest are idiopathic) leads to decreased insulin secretion and hyperglycemia

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4
Q

2 peaks of type 1 DM

A

Mid childhood (age 4-6) and early puberty (10-14)

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5
Q

Incidence of DM in the world

A

Colder population and further from the equator has an increased incidence

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6
Q

Non-modifiable risk factors of type 1 DM

A

White population is highest

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7
Q

Possible environmental risk factors of type 1 DM

A

Viral infections (EBV, Coxsackier, CMV)
Diet
Higher socioeconomic status
Obesity

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8
Q

Diet risk factors for type 1 DM

A

Increased risk with exposure to cows milk and early cereal introduction
Decreased risk with breastfeeding and solid food at later ages

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9
Q

3 presentations of type 1 DM

A

Classic (3 Ps and weight loss/fatigue)
DKA (fruit smelling, drowsy)-hospitalize, hydrate, insulin
Silent (incidental) discovery

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10
Q

Diagnostic criteria of type 1 DM

A

Fasting plasma glucose >126
Random plasma glucose >200 mg/dL
(Plasma glucose >200 2 hrs after oral glucose tolerance test
HbA1C >6.5)

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11
Q

What to do when kid presents with type 1 for first time or DKA?

A

Hospitalize

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12
Q

Common sxs of hypoglycemia

A

Irritability, shaking, dizziness, sweating, nausea

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13
Q

Goals of type 1 tx

A

Achieve glucose control without hypoglycemia (higher risk when 4,5 and 6)–decreased risk when get older
Set goals

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14
Q

Target for ideal fasting blood glucose and HbA1C based on age

A

<5: 80-200 and 7.5-8.5%
6-11: 70-180 and <8%
12-19: 70-150 and <7.5%

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15
Q

Types of insulin

A
Rapid acting (lispro, aspart)
Short acting (regular insulin)- pre meal bolus 5-30 min before meal
Intermediate acting (NPH insulin)-combo with long
Long-acting (glargine, detemir) administer 1-2x/day
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16
Q

Which insulins are used to combat a significant increase in blood glucose?

A

Rapid and short acting

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17
Q

Physiologic regimen for insulin dosing

A

Basal: intermediate or long acting to suppress hepatic glucose production
Bolus: rapid or short acting to cover carb intake at meals
1 unit per kilo over 24 hrs (half and half)

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18
Q

Definition of obesity

A

Normal is 5th-85th percentile
Overweight is 85-95th percentile
Obese is >95th percentile
Severe obesity is >120th

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19
Q

When is obesity more common ethnically?

A

American Indian, black and Mexican Americans

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20
Q

What is a strong predictor of adult obesity?

A

Childhood obesity

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21
Q

General nutrition recommendations

A
Stabilize weight or small weight loss is obese
Portion control
Avoid sugary drinks
Limit milk intake (after 1)
900-1200 kcal/day when 6-12
Eat at home
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22
Q

Exercise recommendations

A

30-60 min of activity per day

Non-academic screen time to 2 hrs per day

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23
Q

Risk factors of type 2 DM

A

Obesity
Family hx
Native American, African American, Latino, Asian American or Pacific Islander
Conditions associated with insulin resistance

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24
Q

Sxs of type 2

A
Polydipsia and polyuria
Visual disturbances
Infections
Most are asymptomatic
Fatigue, irritable, can't concentrate
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25
Acanthosis nigricans
Risk factor for type 2 (excess keratin makes skin thicker due to receptors for insulin)
26
When do you screen for type 2 DM in kids?
Screen kids >10 YO if overweight/obese AND have 2 or more of following: type 2 DM in first or second degree high risk ethnic group signs of insulin resistance maternal hx of DM or gestational diabetes when kid in utero *every 3 yrs
27
Tx for type 2 overview
``` Lifestyle Treat psychosocial aspects Metformin and insulin Prevent macro and microvascular complications Comorbidities ```
28
First line tx type 2
Metformin
29
When is insulin recommended along with metformin and lifestyle changes?
Random plasma glucose >250 or HbA1C>9%
30
Monitoring for type 2
Review weight, DMI, diet and activity Blood glucose monitoring 3/day on insulin Monitor A1c every 3 mos Lab tests for HTN and hyperlipidemia
31
First line tx for HTN with type 2 DM
ACE-i or ARBs | second is thiazides, CCBs or BBs
32
Why do we not like BB for DM?
Masks sxs of hypoglycemia
33
Stages of HTN
Stage 1 is 130/80-139/89 | Stage 2 is >140/90
34
Goals for lipid levels in adolescents in DM
LDL<100 HDL>35 TAGs<150
35
Tx recommendation for hyperlipidemia
6 mos no meds first and then HMG CoA reductase inhibitors if LDL>130 if over 10 and obese
36
What is short stature?
Height 2 standard deviations below mean (<2.3 percentile)
37
Most widely used system to measure skeletal age
Greulich-Pyle Atlas method
38
Normal variants of growth leading to short stature
Familial short stature Constitutional delay of growth (most common) Idiopathic short stature Small for age
39
Pathologic Causes of growth failure
``` Systemic disease Endocrine (Cushings, hypothyroidism, GH deficiency, sexual precocity) Genetic syndromes (turner, PWS, noonans, achondroplasia) ```
40
What is familial short stature?
Kid is small b/c parents are short | Bone age is normal
41
How to check mean parental height to consider familial short stature
Girls: 5 in taken off fathers height and avg with mom Boys: 5 in added to mom and avg with dad
42
What is constitutional delay of growth?
Later bloomers b/c late growth spurt Bone is delayed and corresponds with height Usually parents were delayed too
43
How to diagnose GH deficiency
R/o hypothyroidism, turners and skeletal disorders | If none of them then do IGF-1, IGFBP-3, bone age (and maybe GH stimulation test)
44
First line treatment for GH deficiency
Recombinant human growth hormone therapy (must be before growth plate closes) Daily SC injections
45
Side effects of rhGH
Psuedotumor cerebri Hyperglycemia or insulin resistance Gynecomastia Increase T4 conversion without hypothyroidism
46
What is Noonan syndrome?
Autosomal dominant Short stature CHD (pulmonic stenosis) Variable genetic mutations
47
Most common cause of pathologic obesity and short stature
PWS (chromosome 15)
48
What is achondroplasia?
Autosomal dominant caused by mutations in FGFR3 gene (fibroblast growth factor)
49
Features of achondroplasia
Disproportionate short stature with rhizomelic shortening-proximal bones shortened like humerus and femur Macrocephaly Normal cognition Brachydactylyl and single transverse palmar crease
50
Gigantism
GH excess prior to closure of epiphyses so excessive growth of long bones (rare compared to acromegaly)
51
Diagnostics for GH excess
Increased serum IGF-1 GH suppression test (administer glucose and if GH fails to fall below 1 ng/mL then abnormal) MRI to look at pituitary and hypo
52
Tx for GH excess
Surgery, radiation, | Octreotide, bromocriptine
53
Normal age of puberty
Boys 9-14 YO | Girls 8-14 YO
54
Definition of precocious puberty
Onset of secondary sex characteristics before 8 in girls and before 9 in boys
55
Central precocious puberty
Gonadotropin dependent to elevated GnRH and gonadotropins | Short stature
56
Peripheral precocious puberty
Gonadotropin independent so elevated gonadal steroids with low gonadotropins
57
Causes of central precocious puberty
Idiopathic mostly or CNS tumors or abnormalities | Girls
58
Studies for central precocious puberty
LH and FSH high | Also do estradiol and testosterone
59
Tx of central precocious puberty
GnRH analogue
60
Causes of peripheral precocious puberty
Exposure to gonadal steroids outside of HPG axis Congenital adrenal hyperplasia McCune albright Syndrome (females) *normal LH, FSH levels
61
What is pubertal gynecomastic?
Benign
62
Causes of prepubertal gynecomastia
Klinefelters Aromatization due to obesity Adrenal or testicular neoplasm
63
Most common cause of contra sexual development
Congenital adrenal hyperplasia
64
Most common reason for congenital adrenal hyperplasia
21 hydroxylase deficiency