Brainscape's Knowledge GenomeTM

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


See full index

Peds > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

short stature

A

2SD below mean ht
normal variant short stature- short but growing at norm velocity
pathologic short statue-short and suboptimal growth
if grow 2in/y btw 3-puberty= no endocrinopathy or underlying pathologic D

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

hypopituitarism

A

suspect when hx of hypoglycemia, prolong jaundice, cryptorchidism, microphallus

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

normal variant short stature

A

familiar short stature: below 2SD, normal bone age and onset of puberty
constitutional short stature- >2SD, delayed bone age and late onset of puberty

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

disproportionate short stature

A

rickets (frontal bossing, bowed legs, low serum phosphorus, high serum alkaline phosphatase) and skeletal dysplasias

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

proportionate short stature

A

in utero: enviro, chromo (down, turner), genetic (prayer will,), viral (CMV)
postnatal- malnutirtion,psych, organ system disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

evaluate short stature

A

Lab: cbc, ESR, T2, BMP, IGF-1 (indirect test for GH),, chromosome analysis for turner’s
radiographic study: bone age, pituitary gland - craniopharyngioma- distortion of sella truck and suprasellar ca

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

GH deficinecy

A

uncommon.
P: prolong neonatal jaundice, hypoglycemia, cherubic facies, central obesity, microphallus, crytorchidism, midline defects, growth curve show poor velocity
causes: craniopharyngioma if kid older than 5yo not growing 2in/y
bone age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

endocinopathies that cause growth stunt

A

all bone age

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

female puberty

A

onset btw 7-13yo

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

male puberty

A

9-14yo. first sign is testibular enlargement

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

precocious puberty

A

girls: breast dev or pubic hair bf 7yo or monarch bf 9yo. premature the larch at 2yo and adrenarch at 5 w/o the other needs no workup.
boy: testicular changes,penile enlarge, pubic/axillary hair bf 9yo

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

isosexual prevovious puberty = central precocious puberty (CCP

A

norm dev at hearier age. females tend to be idiopathic. males organic so need MRI head for all cases. Can be caused by hydrocephalus, CNS infections, hypothalamic hamartomas, atrocity, gliomas, head trauma, benign cerebral palsy, hypothyroidism
dx: FSH, LH, sex steroid elevated. GNRH sitmulation test(assess activation of HPGA axis. if cause incr LH, likely LH.

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

peripheral prevocious puberty (PPP)= heterosexual gonadotropin indep puberty

A

indeed of HPGA axis due to peripheral sex steroid (Not FSH or LH) production. flat response on GnRH stimulation bc HPGA axis not activated
boy- feminization, pubic hair, no testicular enlargement bc no incr in FSH
girls- variation or breast dev
etio: exogenous sex steroid, gonadal tumor, adrenal tumor, hyperplasia of adrenal gland
boys with testicular enlargment:
1) McCune -Albright syndrome- bony changes and coast of maine cafe au last spots. endocrinopathies
2) testotoxicosis- enlarge b/l
3) betal HCG secreting tumor- only in boys
same evils CPP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

delayed puberty

A 
boy: no testicular enlargement by 14
Girl- no breast tissue by 13 or monarch by 14
2 types
1) hypogonadotropic hypogonadism:
2) hypergonadotropic hypogonandism:
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

hypogonadotropic hypoganadism

A

inactivity of hypothalamus and pituitary. flat GnRH stimulation test
etio: constitutional delay of puberty: usually fx, associated with constitutional delay of growth. immature hypothalamus. chronic disease like anorexia, IBD, HF, RF. hypopituitarism, primary hypothyroidism, prolactinoma, genetic (klaxon, prader will)

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

hypergonadotorpic hypogonadism

A

end organ dysfunction. high FSH, LH, low testosterone estradiol
boys: klinefelter
girls- turner
AI- hashimotot thyroiditis, addison’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

ambiguous genitalia male

A

1) inborn error in testosterone synthesis:
2) gonadal intersex: internal structures of combo of M and F: mixed gonadal dysgenesis (mosaicism 45XO/46XY, vas def and fallopian tubes). true hermaphroditism
3) partial androgen insensitivity- defective binding- x linked. testicular feminization syndrome has complete insensitivity and present as normal phenotypic female with 46XY.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

ambiguous genitalia in virilized female

A

1) CAH caused by 21 hydroxyls deficiency is most common pseudohermaphroditism. suggested by incr BP
2) virilizing drug taken by mom in preg
3) virilizing tmor in mom while preg
decr BP suggest adrenal insuff.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

cortisol def sx

A

anorezia, weakness, hyponatremia, hypotension, incr pigmentation over healing scars

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

aldosterone def

A

FTT, salt craving, hyponatremia, hyperkalemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

primary adrenal insufficinecy

A

addison’s, CAH, adrenoleukodystrophy.

22
Q

secondary adrenal insuf

A

ACTH or CRH lvl problem. since minerocorticoids not reg by them, no aldosterone def and normal seem K.
etio- most common is iatrogenic- glucocorticoids >2wk suppress hypothalamus

23
Q

congenital adrenal hyperplasia (CAH)

A

AR. most common cause of ambiguous genitalia with unpalpable gonads.
enzyme def lead to less cortisol or aldosterone and build up of precursors that is shunted into androgen production.
3 types of 21-H hydroxyls def
1) classic salt wasting: cortisol and aldo def= FFT, vomit, electrolyte abn
2) simple virilizing CAH, only cortisol def. tall, adv bone age, pubic hair, penile enlargement, girl virile. no electrolyte ab
3) nonclassic CAH: late onset with mild cortisol def no aldo def.
111 beta hydroxylase def- hypertensive, and hypokalemic
3beta hydroxyteroid deH def: salt wasting crises, cotisol def, ambiguous genitalia and early black in all three adrenal steroid pthwy.

24
Q

CAH workup

A

1) incr 17- hydroxyprotestone (17OHP) in 21 hydroxylase def
2) incr specific compound S in 11 beta hydroxylase def
3) incr DHEA and 17 hydroxypregnenolone in 3 beta hydroxysteroid deH def
4) low Na, high K

25
Q

CAH management

A

cortisone admin to suppress ACTH so less excess androgen production = don’t interfere with proper growth
mineralcorticoid replacement- fluorocortisol
f/u

26
Q

glucocorticoid excess

A

poor growth with delay bone age, central obesity, moon facies, nuchal fat pad, easy bruising, purple striae, HTN, glu intolerance
hypercortisolism etio: iatrogenic -most common, cushings syndrome (adrenal tumor), cushing disease (excessive ACTH production -pituitary tumor,)
labs: 24hr urine cortisol elevated, dex supression test- no suppression,

27
Q

DMI

A

95% have HLA hypolotype DR3 or DR4
viral infection,
AI: islet cell ab in 85%.
clinical: girsl have protracted monilial vulvovagininitis
adolescent present in puberty when GH and sex steroid antagonize insulin action
dx- hyperglycemia >200 with polyuria/dipsia, wt loss, or nocturne

28
Q

somogyi phenomenon

A

evening dose too high so body make epi and glucagon to counter in morning resulting in hyperglycemia induced by insulin. tx by lowering insulin

29
Q

DKA

A

mild in DM2. can be severe in DM1. hyperglycemia >300 with coterie and serum bicarb

30
Q

acanthosis nigricans

A

hyper pig skin at neck and ancillary folds. in DM2

31
Q

congenital hypothyroidism etio

A

most common metabolic D
etio
1) thyroid dysgenesis: 90%. 2/3 aplasia or hypoplasia. 1/3 exctopic- base of tongue to mid chest
2) thyroid dyshormogenesis- inborn errorAR> often goiter and sensorineural hearing loss
3) PTU use in mom cause transit hypothyroidism in newborn
4) materal Ai thyroid disease- transit hypothyroidism

32
Q

congenital hypothyroidism P

A 
asx initially
hx: of jaundice and poor feeding
lthargy and constipation
PE: large anterior and posterior fontanelle, protruding tongue, umbilical hernia, myxedema, mottled skin, hypothermia, delay neurodev (TH is essenial for 1st 2y of brain dev), poor growth
Labs: normal NH3, normal glu
33
Q

hashimoto’s disease

A

chronic lymphocytic thyroiditis (CLT) that cause follicular fibrosis and atrophy and follicular hyperplasia.
most common acquired hypothyroidism w/wo goiter
more in girls
P: variable. asx, goiter, short, transient hyperthyroidism-hashitoxicosis,

34
Q

incr TSH

A

first sign of thyroid failure

35
Q

hyperthyroidism

A

lid lag and exophthalmos, enlarge thyroid gland that is smooth, tachycardia, palpitations, warm and flushed skin. if see vitiligo or alopecia there may be other AI polyendocrinopathis like addison and DM. nervousness, fine tremors, fatigue, delay monarch and gynescomastia in boys

36
Q

grave’s

A

incr T3, T4 with suppressed TSH bc TSI

tx: PTU and methimazole

37
Q

PTH

A

releases ca and phosphorus from bone. excrete phosphorus through kidney. reabsorption of ca and bicarb

38
Q

25 OH vit D

A

converted into 1,25 OH D in kidney which stimulate Ca absorption in GI

39
Q

hypocalcemia: etio, labs

A

serum Ca 4yo: hypoPTH, digeorge, hyperphosphatemia (from excessive phosphate intake or uremia)

3) childhood hypocalcemia: hypoPTH, pseudohypoPTH (PTH resistance, AD D, short, dev delay, incr PTH), hypomagnesemia (malabsorptive disease), it D def (low phosphorus dev)
labs: serum Ca, phosphorus, mg, ECG (prolong QT), PTH, Vit D, radiograph of wrist of knee to eval for rickets

40
Q

tetany

A

1) carpopedal spasm- hypocalcemia cause peripheral MN excitement, painful spasm of wrist and ankles
2) laryngospasm
3) paresthesias

41
Q

pseudohypocalcemia

A

de to low albumin lvl. in nephrotic syndrome

42
Q

hypocalcemia tx

A

mild asx don’t need tx.

newborn with lvl

43
Q

Rickets etio

A

cause by VitD def. def mineralization of growing bone w/ normal bone matrix
predisposed by: exclusive breast fed, fad diet, anticonvulsants, renal/hepatic failure
etio: vit D def, GI D- fat malabsorption, nutritional, defective vit D metabolism,
1) vit D dep rickets -rare= enzume def 1 alpha hydroxylase vita D results in no 1,25 OH D. present with incr PTH, low it D, low Ca, low P, incr alkaline phosphatase
2) vit D résistent rickets- familial hpophosphatemia: most common type of rickets. x-linked dom. renal tubular phosphorus leak. low serum P lvl. normal ca. bowl legs no tetany. tx with P sup and 1,25 D analogs
3) ocogenous rickets- in pt with bone pain or myopathy

44
Q

rickets P

A

occu

45
Q

diabetes insipidus

A

inability to maximally conc urine bc low ADH (central DI) or unresponsive to ADH (nephrogenic DI
P: nocturia, enuresis, poort wt gain, polydipsisa/uria
dx: if thirst intact +access to water then electrolytes normal. otherwise hyponatremic dehydration with inappropriately dilute urine in face of incr serum Na and incr serum osmolarity. early morning urine SG >1.018 ro DI. water deprivation test - rise serum osmolarity despite urine output, low osmo, MRI head, bone scan- langerhans

46
Q

central DI

A

AI (ab target ADH producing cells), trauma and hypoxic ischemic brain injury, hypothalamic tumor, langerhans cell histiocytosis (25%), granulomatous disease (tb, sarcoidosis), vascular (aneurysm), genetic (AD)
tx: DDAVP (synthetic ADH)

47
Q

nephrogenic DI

A

x linked R. non-responsive to ADH

48
Q

hypoglycemia

A

definition:

49
Q

persistent neonatal hypoglycemia

A

last >3d.

1) hyperinsulinism due to islet cell hyperplasia (nesidioblastosis), beck with-wiedemann syndrome. LGA and present with visceromegaly, hemihypertorphy, macroglossia, umbilical hernia, distinctive ear crease
2) hereditary defect in carbohydrate meta- glycogen storage disase type I, aa meta (maple syrup)
3) hormone def: GH def or cortisol def. suspect congeital hypopituitarism in neonate who present with hypoglycemia, microphallus, midline defect ~ cleft palate

50
Q

hypoglycemia in infancy and kids

A

uncommon. DD
1) ketotic hypoglycemia- 1-6yo. in late morning with coterie and low insulin bc can’t adapt to fasting state. thin and hypoglycemic after infection
2) ingestions-alcohol, oral hypoglycemic agents
3) inborn erros of metabosim
4) hyperinsulinism

Peds (21 decks)

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