Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

General Peds Boards > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Addison Disease signs and symptoms

A
  • Primary adrenal insufficiency
  • Fatigue, nausea, weight loss, hypotension, volume depletion, and diffuse hyperpigmentation (due to elevated ACTH)
  • Hyponatremia, hyperkalemia, hypoglycemia, metabolic acidosis, low serum cortisol, high adrenocorticotropic hormone level, and eosinophilia.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Treatment of Addison Disease (acute and long term)

A
  • Acute: fluid resuscitation, IV hydrocortisone (100 mg/m2 then 100 mg/m2/d)
  • Chronic: hydrocortisone and fludrocortisone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hyperthyroidism signs/symptoms

A

Fatigue, hair loss, tachycardia, hypertension, sweating

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Grave’s disease labs and treatment

A
  • Low TSH and high thyroid-stimulating immunoglobulin
  • Tx: methimazole is first line, radioactive iodine and surgery are used if meds aren’t effective, also often need a b-blocker initially d/t tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Type 2 diabetes screening labs

A
  • Fasting glucose > 125
  • 2 hr glucose level during OGTT > 200
  • Hgb A1c > 6.5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Indications for growth hormone

A
  • Born SGA and didn’t catch up to a height of at least 2 SDs below the mean by 2 years of age
  • Idiopathic short stature with height less than 2.25 SD below the mean
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Sex differentiation

A
  • Presence of androgens is responsible for formation of male external genitals
  • Presence of mullerian inhibiting factors results in regression of female internal duct structures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Causes of male gynecomastia

A
  • Ketoconazole, Klinefelter syndrome

- Galactorrhea can be due to marijuana use

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Order of male pubertal development

A

Testicular growth –> Pubarche –> Penile growth –> Peak height velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

First sign of pubertal development in males

A

Testicular enlargement (usually between ages 10-11)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Cause of pubic hair development and penis enlargement in the absence of testicular enlargement

A

Androgen stimulation from outside gonadal area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Order of female pubertal development

A

Breast budding –> pubarche –> peak height velocity –> menarche
- Can begin as young as age 8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Definition of delayed puberty

A
  • No pubertal signs by 14 in boys or 13 in girls
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Most common cause of delayed puberty in boys

A

Constitutional delay - benign, will have bone age 2 or more years delayed

Tx: IM testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes of delayed puberty in girls

A

Can have constitutional delay but also commonly have functional gonadotropin deficiency (anorexia) and primary ovarian failure (Turner)

Tx: oral estrogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Definition and causes of premature adrenarche

A

Presence of androgenic sexual characteristics (hair, acne, odor) without estrogenic sexual characteristics (breast development, menarche) and without growth spurt

  • Elevated DHEA and DHEA-S, low testosterone
  • Can also be caused by exogenous androgen, endogenous androgen secreting tumor, late onset congenital adrenal hyperplasia, or PCOS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes of premature thelarche

A
  • Breast development in girl younger than 8 with no other sex symptoms
  • Usually benign and due to premature activation of hypothalamic pituitary axis
  • Can be due to exogenous sex steroids or estrogen producing tumors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Benign premature thelarche age and future risks

A
  • Can happen in infants/toddlers and again in childhood but resolves by age 4
  • 10% go on to develop central precocious puberty
  • Also increased risk for PCOS
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Early development of puberty in addition to acceleration in linear growth or advanced bone age

A

Central precocious puberty

  • Before age 9 in boys or 8 in girls
  • Leads to short adult height
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Mccune Albright syndrome

A
  • Peripheral precocious pubery
  • Cafe au lait spots
  • Polyostotic fibrous dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Workup for central precocious puberty

A
  • Imaging (depending on symptoms may need brain MRI, ovarian/adrenal ultrasound)
  • Bone age xrays
  • Labs: LH, FSH, adrenal steroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Treatment for precocious puberty

A

GnRH agonist leuprolide to stop the progression

- Often used in males, age < 6, those with rapidly advancing symptoms, or those with psychosocial disturbances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Genetic males (XY) with external female genitalia but no uterus

A

Androgen insensitivity syndrome

  • Prenatal amnio shown XY but is born a girl
  • Teenage girl with primary amenorrhea –> workup shows no uterus or ovaries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Micropenis with hypogylcemia

A

Panhypopituitarism
- Need to check all pituitary hormones

  • Can be part of: Prader Willi, Kallmann, or septo-optic dysplasia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Newborn presenting with septic picture and male with excessive scrotal pigmentation or female with ambiguous genitalia (posterior labial adhesions and clitoral hypertrophy)

A

Congenital adrenal hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Presentation of CAH in an older kid

A
  • No medical care
  • Growth delay
  • Hirsuitism
  • Amenorrhea
  • -> autosomal recessive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Biologic cause of CAH

A
  • Deficiency of 21-hydroxylase

- Leads to lack of aldosterone and cortisol which leads to increased testosterone and virilization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Labs in CAH

A
  • Hyponatremia, hyperkalemia
  • 21-hydroxylase deficiency
  • 17-OH levels are high, high testosterone
  • Low cortisol
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Screening protocol for CAH

A
  • Newborn screen tests for levels of 17-OH, if high then need to repeat the test
  • If repeat test is high then need to measure serum electrolytes and urinary sodium/potassium excretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Electrolyte abnormalities associated with adrenal crisis

A

Hypoglycemia, hyponatremia, hyperkalemia

  • Treat initially with glucose containing fluids, then IV hydrocortisone, then glucocorticoid replacement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Primary adrenal deficiency symptoms

A
  • Increased ACTH levels but no production of aldosterone
  • Hyperpigmentation, salt wasting, hyperkalemia, hyponatremia, fatigue, weight loss

Tx with fludrocortisone and hydrocortisone

Addison disease is the autoimmune form

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Muscle weakness and decreased cardiac function following stopping adrenocorticoid or glucocorticoid medication

A

Secondary adrenal insufficiency - would not commonly see electrolyte imbalances

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Secondary adrenal deficiency has what abnormal levels

A
  • LOW ACTH (pituitary isn’t making it) but CRH is normal (made in the hypothalamus)
  • Normal electrolytes because aldosterone is normal and no hyperpigmentation because no excess ACTH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How does ACTH stimulation test work

A
  • Give ACTH to test the adrenals
  • If no cortisol rise happens, it’s primary adrenal deficiency
  • If cortisol rise happens, then it’s secondary adrenal insufficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Acne, purple striae, hirsutism, virilization, buffalo hump, increased BMP with growth arrest

A

Cushing syndrome (excess glucocorticoid)

  • Will also have delayed bone age
  • MCC is chronic use of topical, inhaled, or oral corticosteroids
  • Cushing in infants = MCCUNE ALBRIGHT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Lab tests to diagnose Cushing syndrome

A
  • 24 hr urinary free cortisol excretion is gold standard
  • Midnight sleeping plasma cortisol level
  • If midnight levels are undetectable –> CT/MRI to look for adrenal tumor
  • If midnight levels are elevated –> MRI to look at pituitary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Diabetes insipidus, exophthalmos, lytic bone lesions

A

Langerhans cell histiocytosis (posterior pituitary disease)

- Posterior part only makes ADH and oxytocin

38
Q

Growth rate before puberty

A

5-6 cm/year

39
Q

Peak growth age and SMR during puberty

A
  • SMR 3 in both boys and girls
  • Boys peak growth is about 2 years after girls
  • Peak growth for girls is about 1.5 years before menarche at SMR3
40
Q

Cranial irridation side effects with growth

A
  • Growth hormone deficiency due to damaging pituitary so can lead to short stature
41
Q

Micropenis, severe postnatal growth failure, hypoglycemia, short stature

A

Congenital growth hormone deficiency

  • Can be associated with septo-optic dysplasia, breech presentation, prolonged jaundice
  • Bone age will be delayed
42
Q

Normal bone age with low weight and low height

A

Chronic malnutrition

43
Q

Decrease in growth rate in early teen years, delayed onset of puberty, bone age below chronological age

A

Constitutional delay - more common in males

44
Q

Growth velocity decelerates around 6-18 months of age but then follow the curve, bone age is equal to chronological age

A

Familial short stature

45
Q

Delayed bone age, cold intolerance, constipation, dry skin

A

Hypothyroidism

46
Q

Tall kid and want to know the most important determinant for ultimate adult height

A

SMR (to know how much growing they have left to do)

- Next would be bone age

47
Q

Tall stature, learning disabilities, small testicles, gynecomastia, delayed puberty

A

Klinefelter syndrome (47 XXY)

48
Q

Tall stature, macrocephaly, cognitive deficits

A

Soto’s syndrome

49
Q

Tall, overweight, normal to advanced bone age

A

High caloric intake (exogenous obesity)

50
Q

MCC preventable intellectual disability worldwide

A

Congenital hypothyroidism

51
Q

Poor feeding, jaundice, constipation, hypotonia, hoarse cry, large tongue, umbilical hernia, large anterior fontanelle

A

Congenital hypothyroidism - although 95% are asymptomatic at birth

52
Q

Newborn screening for congenital hypothyroidism

A
  • Initial total TSH followed by T4 if needed
  • If failed need test of free T4 and TSH
  • 85% of cases are sporadic and due to thyroid dysgenesis
53
Q

Boys with low total T4 but normal free T4 and TSH

A

Thyroxine binding globulin deficiency (X linked)

  • T3/T4 are bound to TBG but it’s the free hormone that is metabolically active
  • Dx confirmed by measuring aTBG level
54
Q

Low TSH, low free T4

A

Secondary hypothyroidism due to pituitary or hypothalamic disease

55
Q

Hypothyroidism symptoms or asymptomatic with presence of a goiter

A

Hashimoto thyroiditis

  • Autoimmune (chronic lymphocytic thyroiditis)
  • MC in females
56
Q

Labs in hashimoto

A
  • T4 can be normal if compensated but they have a high TSH
  • Also have anti-thyroglobulin and anti-thyroid peroxidase antibodies
  • Can be transiently hyperthyroid (hashitoxicosis)
57
Q

Difference with radioactive iodine uptake in Graves vs Hashimotos

A
  • High in Graves, normal/low in Hashimotos
58
Q

Bulging eyes, emotional lability, weight loss, sleep disturbance, lid lag

A
  • Graves

- Can also have itching, tremors, sweating, increased urination at night, decreased menstrual flow

59
Q

Antibody involved in Graves disease

A
  • IgG antibody (thyroid stimulating immunoglobulin)
  • Tx with methimazole (blocks organification of iodide and decreases thyroid synthesis)
  • PTU not preferred d/t risk of hepatitis and neutropenia
60
Q

Newborn with irritability, tremors, tachycardia in immediate newborn period

A

Neonatal thyrotoxicosis (have low TSH and high free T4)

  • Due to maternal antibodies crossing placenta (can happen even if mom had thyroid ablation in the past)
  • Tx methimazole
61
Q

Management of a thyroid nodule

A
  • FNA
  • Most are benign but higher risk of malignancy in teenager than adult
  • Can have normal or abnormal TFTs
62
Q

Four diagnostic criteria for diabetes

A
  • Hgb A1c > 6.5%
  • Random glucose > 200
  • Fasting glucose > 126
  • 2hr glucose > 200
  • Need 1/4 criteria with symptoms or 1/4 criteria on 2 separate occasions
63
Q

Physiology of type 1 DM

A
  • Destruction of ilet cells so can’t make insulin

- Symptoms and diagnosis happen when islet function is down to about 20%

64
Q

Acute DKA management and rationale why

A
  • Fluid replacement (10-20 cc/kg normal saline over 1-2 hours) –> assume 5-10% dehydration
  • Hyponatremia is dilutional (hyperglycemia pulls water into the cell) and should rise as glucose comes down, if it doesn’t be worried about cerebral edema
  • Total body potassium is low
  • Add insulin after initial fluid bolus
  • Start adding dextrose when glucose is < 300
  • Give insulin until acidosis has resolved and patient can tolerate oral intake
65
Q

Type 2 DM with elevated serum osmolality and serum glucose

A

Hyperosmolar non-ketotic coma

- Manage like hypernatremic dehydration

66
Q

Definition of metabolic syndrome

A

Hyperinsulinemia
Dyslipidemia
Hypertension
Obesity

67
Q

Causes of hypercalcemia

A

Williams syndrome, vitamin D intoxication, vitamin A intoxication, thiazide diuretics, skeletal dysplasias, immobility, hyperparathyroidism

68
Q

Treatment for hypercalcemia

A
  • Calcium > 11

- Fluid, lasix, EKG monitoring

69
Q

Function of parathyroid hormone

A
  • Acts on the kidney, skin, and bone to increase calcium and decrease phosphate
  • Primary hyperPTH causes hypercalcemia
  • Secondary hyperPTH is reactive and due to low calcium
70
Q

Symptoms of hypocalcemia

A
  • Painful muscle spasms
  • Generalized seizures
  • Vomiting
  • Prolonged QT interval
71
Q

Chvostek sign

A

Tapping just anterior to the ear lobe below the cheek bone, contraction of the distal muscles is a positive finding

72
Q

Trousseau sign

A

Inflate the blood pressure cuff above systolic pressure and leave it there for 2 minutes –> positive is carpal muscle spasm

73
Q

Causes of hypocalcemia

A
  • Pseudohypoparathyroidism
  • Nutritional deficiency
  • DiGeorge syndrome
  • Nephrotic syndrome
  • Renal insufficiency
74
Q

Relationship of magnesium and calcium

A

Elevated magnesium decreases PTH secretion so hypomagnesemia can result in intractable hypocalcemia that won’t respond to calcium until you correct the magnesium

75
Q

Labs in pseudohypoparathyroidism

A
  • High PTH
  • Hypocalcemia
  • End organ kidney resistance to the hormone
76
Q

Bone pain, anorexia, decreased growth rate, widening of the wrist and knees, delayed tooth eruption, bowed legs

A

Symptoms of rickets

  • Look for enlarged costochondral junctions (rachitic rosary) and softening of skull bones (craniotabes)
  • Serum alkaline phosphatase levels will be elevated in all forms
77
Q

Calcipenic rickets

A
  • Parathyroid hormone is always elevated

- Three types: vitamin D deficienct, vitamin D dependent, hereditary vitamin D resistants

78
Q

Risk factors for vitamin d deficient rickets

A
  • Breast feeding without vitamin D supplementation
  • Poor exposure to natural sunlight
  • Low birth weight
  • Infants on strict vegan diets
  • Lactose intolerant/avoiding dairy
79
Q

Difference in vitamin D levels (types)

A
  • 25 hydroxy is the storage form (25 added by the liver)
  • 1,25 hydroxy is the active form (1 added by the kidney)
  • 25 will be low in vitamin D deficient rickets but normal in the others
80
Q

Labs and treatment of vitamin D deficient rickets

A
  • Low 25-hydroxy and 1,25-hydroxy vitamin D
  • Low/normal calcium and phosphorus
  • Elevated serum alkaline phosphatase

Tx with vitamin D and calcium

81
Q

Why dose liver disease cause rickets

A

Reduced availability of bile salts in the gut and decreased absorption of vitamin D

82
Q

Vitamin D dependent rickets cause and labs

A
  • Autosomal recessive
  • Inadequate renal production of 1,25 vitamin D
  • Low calcium
  • Tx with vitamin D and 1,25 vitamin D
83
Q

Cause of phosphopenic rickets

A
  • Renal wasting, can be X-linked if congenital

- Tx with phosphate supplementation and 1,25 vitamin D

84
Q

Type 1 diabetes health maintenance

A
  • Dilated eye exam if > 10
  • Lipid panels
  • Celiac screening
  • TSH screening
85
Q

Causes of ketotic hypoglycemia

A
  • Benign ketotic hypoglycemia
  • Hormonal deficiencies
  • Glycogen storage diseases
  • Abnormalities of gluconeogenesis
86
Q

Causes of non-ketotic hypoglycemia

A
  • Hyperinsulinism (can be commonly transient in neonates)

- Fatty acid oxidation disorders

87
Q

First sign of puberty in girls and age

A

Breast development age 10.5-11

- Then 2 years before menarche

88
Q

First sign of puberty in boys and age

A

Testicular growth age 11.5

89
Q

Labs for central precocious puberty

A
  • High LH, FSH
  • High estradiol/testosterone
  • Advanced bone age
  • MRI brain to look at hypothalamus/pituitary
90
Q

Labs for peripheral precocious puberty

A
  • Low LH, FSH

- High estradiol/testosterone

91
Q

Ages for delayed puberty

A

No signs by age 13 for girls or 14 for boys

General Peds Boards (24 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions