Brainscape's Knowledge GenomeTM

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


See full index

pediatrics > endocrinology > Flashcards

endocrinology Flashcards

1
Q

the only organ that is not enlarged in macrosomia

A

brain

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

congenital cardiac defect associations - diabetic mother

A

trans of great vessels

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

findings in infants of diabetic mothers

A
  1. Macrosomia (2nd and 3rd trimester) –> branchial plexopathy, clavicle fracture, perinatal asphyxia
  2. Small left colon syndrome (1st trimester)
  3. Cardiac anomalies (1st trimester)
  4. renal vein thrombosis (1st trimester)
  5. metabolic findings and effects (2nd or 3rd trimester)
  6. spontaneous abortion (1st trimester)
  7. polycythemia (2nd and 3rd trimester)
  8. neural tube defects (1st)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

macrosomia - blood

A

increased output from bone morrow –> polycythemia + hyperviscosity

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

infants of diabetic mothers - small left colon syndrome

A

congenitally smaller descending colon leads to distention from constipation
diagnosis by barium
treatment siwth smaller + more frequent feeds

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

infants of diabetic mothers - renal vein thrombosis

A
  • Flank mass + possible bruit

- hematuria + thrombocytopenia

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

infants of diabetic mothers - Metabolic findings + effects

A

hypglycemia: seizures
hypocalcemia: tetany
hypomagnesia: hypocalcemia + low PTH
hyperbilirubinemia: icterus = kernictuerus

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

infants of diabetic mothers - Cardiac anomalies

A
  1. asymmetric septal hypertrophy due to obliteration of LV lumen –> low CO (treated with b-blockers and IV fluids)
  2. trans of great vessels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

child’s RF for vit D deficient rickets

A
  • sunless environment

- low milk intake

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

Rickets is caused by lack of

A

Vit D, Ca2+, Phosphorus

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

children of which age are highest risk for rickets

A

6-24 months because their bones are rapidly growing

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

Rickets - types

A
  1. Vit D deficinet (low D)
  2. Vit D dependent: inability to convert 25 to 1,25
  3. X-linked hypophosph: innate kidney defect –> inability to retain P
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Rickets - presentation

A

child with ulnar/radial bowing and a waddling gait due to tibial femoral bowing

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

Rickets - diagnostic tests

A
  1. Rachitic rosary-like appearance on CXR of the costochondral joints with cupping and fraying of the epiphyesis
  2. Bowlegs is a characteristic sign
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Rickets - types and calcium/phosphate levels

A

Vit D def: normal/low Ca2+, low P
Vit D dep: low Ca2+, normal P
X-linked hypophosph: normal Ca+, low P

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

Rickets - types and levels of vit D 25 + 1,25

A

Vit D def: both decreased
Vit D dep: normal 25, low 1,25
X-linked: both normal

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

vit D in milk

A

no

recommended to given Vit D supplements beginning at 2 months if exclusively breastfed

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

how to diagnose 21 hydroxylase def

A

elevated 17-hydroxyprogesterone

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

evaluation of precocious puberty

A

bone age (normal or advanced)
A. normal: isolated breast development (premature thelarche or isolated pubic hair delop (premature adrenache –> reassurance
B. adanced: measure basal LH
- high: central
- low: GnRH stimulation test –> If high is central, if still low is peripheral

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

premature adrenarche is caused by

A

early activation of adrenal androgens and is more common in obese children (mildy elevated dihydroepiandrosterone, normal estrogen + testosterone)
NORMAL BONE AGE

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

common pathologucal causes of gynecomastia - categories

A
  1. androgen deficiency

2. increased estrogen prodction or peripheral conversion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Common pathological causes of gynecomastia - androgen def

A

Primary or 2ry male hypogonadism, hyperprolactinemia, Renal failure

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

common pathological causes of gynecomastia - increased estrogen production or peripheral conversion

A
  1. HCG producing tumors
  2. cirrhosis or malnutrition
  3. thyrotoxicosis
    androgen use
  4. Drugs (spironolactone, cimetidine etx)
  5. congenital excessive aromatase activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Von Gierke disease (type 1) pathophysiology

A

Glucose-6-phosphatase deficiency –> impaired gluconeogenesis and glycogenolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Von Gierke disease (type 1) findings

A
  1. Severe fasting hypoglycemia
  2. Increased glycogen in liver
  3. Increased blood lactate
  4. Hepatomegaly
  5. incdreased TG
  6. increased Uric acid (Gout)
    DOLL LIKE FACE, SHORT STATURE
26
Q

Pompe disease (type 2) pathophysiology

A

lysosomal a-1,4-glucosidase with α-1,4-glycosidase activity (Acid maltase) deficiency

27
Q

Pompe disease (type 2) findings

A
  1. Cardiomyopathy
  2. hypertrophic cardiomyopathy
  3. exercise intolerance
  4. Systemic findings leading to early death
28
Q

Cori disease (type 3) pathophysiology

A

a-1,6-glucosidase deficiency

29
Q

Cori disease (type 3) findings

A
  • Milder form of type 1 with normal blood lactate (and gluconeogenesis is intact)
  • Accumulation of limit dextrin-like structures in cytosol
30
Q

McArdle disease (type 4) pathophysiology

A

Skeletal muscle phosphorylase (myophosphorylase deficiency)

31
Q

McArdle disease (type 4) findings / mechanism

A
  1. Increased glycogen in muscle, but cannot break it down leading to painful muscle cramps
  2. Myoglobinuria (red urine) with strenuous exercise
  3. Arrythmia from electrolyte abnormalities
  4. 2nd wind phenomenon noted during exercise due to increased muscular blood flow
32
Q

MCC of congenital hypothyroidism worldwide

A

thyroid dysgenesis

33
Q

Refeeding syndrome

A

nutritional rehabilitation in anorexia nervosa –> carbohydrate intake –>insulin secretion –> cellular uptake of P, K+ Mg+ –> arrhythmia and cardiopulmonary failure

34
Q

precocious uberty?

A

onset of 2ry sexual characteristics in girls younger than 8 and boys younger than 9

35
Q

McCune-Albright syndrome

A

Gonadotropin-independet precocious puberty that presents with irregular cafe-au-lait macules and fibrous dyspasia of bone

36
Q

MCC of central precocious puberty

A

idiopathic (negative MRI)

37
Q

congenital adrenal hyperplasia - enzyme deficiency

A
  1. 17α-hydroxylase
  2. 21-hydroxylase
  3. 11β-hydroxylase
38
Q

17a hydroxylase deficiency - presentation

A

XY: psuedohermaphroditism (ambiguous genitalia, undescended testes
XX: lack secondary sexual development
- low cortisol, low sex hormones, high aldosterone

39
Q

21 hydroxylase deficiency - presentation

A
  1. present in infancy (salt wasting) or
  2. childhood (precosious puberty)
  3. XX: virilization
    - low cortisol, high sex hormones, low mineralcorticoids
40
Q

21 hydroxylase deficiency - labs

A
  1. increased renin activity

2. increased 17-hydroxyprogesterone

41
Q

11β-hydroxylase deficiency - presentation

A

XX virilization

  • low aldosterone but hugh deoxycorticosteone)
  • low cortisone
42
Q

congenital hypothyroidism presebts with

A
  1. constipation
  2. prolonged jaundice
  3. failure to thrive
  4. open fontanels
    MC asymptomatic
43
Q
  1. ….. is frequtnely the 1st sign of cretinism

2. radiology of cretinism

A
  1. prolonged jaundice
  2. radiology: X-rays shows poor bone development, thyroid scan shows decreased uptake with malformed thyroids and increased with iodide def
44
Q

short stature - ddx

A

A. bone age smaller than chronological age:
1. normal growth velocity: constitutional delay
2. abnormal GV: chronic illness, nutritional, endocrine
B. Bone age = chronological age
1. normal GV: familiar short stature
2. abnormal GV: genetic,

45
Q

tall stature - ddx

A

Bone age bigger than chronological age

  • normal GV: familial tall stature, obesity
  • abnormal GV: genetic, endocrine, CNS lesions
46
Q

constitutional delay - manifestation

A

short stature, delay puberty, delayed bone age

schedule follow up

47
Q

RF for infant butilism

A

honey or canned food

48
Q

CAH with increased androgen - bone age?

A

increased

49
Q

granulosa cell tumors secrete …

A

estrogen/progesterone

50
Q

Obese children are at high risk for precocious development as

A

adiposity can trigger excess insulin production, which then stimulates the adrenal glands to produce hormones

51
Q

precosious puberty - CAH?

A

peripheral

52
Q

inadequate total body glycogen stores?

A

newborns as a results of prematurity or intrauterine growth restriction –> low glucose
at first 24 hours

53
Q

macrosomic infant weight?

A

more than 4

54
Q

ketoacidosis in children - glucose?/ management

A

more than 200

- 10ml/kg isotonic fluid / h AND insulin infusion + K+

55
Q

clinical manifestation of refeeding sydnrome - clinical manifestation

A
  1. arrhythmia
  2. CHF
  3. pulm edema
  4. seizures
  5. wernicke enc
56
Q

hypothyroidism - precocious puberty

A

severe untreated hyothyroidism can cause gonadotropin DEPENDED precocious puberty

57
Q

constitutional age - at born?

A

normal delay between 6 months - 3 years

58
Q

isolated pubarche is more common in

A

obese (early activation of adrenal androgen)

59
Q

increased risk for male breast cancer

A

Klinefelter

60
Q

normal gynecomastia of puberty - uni or blateral ?

A

both

pediatrics (16 decks)

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