04a: Growth, Gender Flashcards
Postnatal growth velocity (increases/declines) progressively until (X) years old, when it becomes constant at (Y)/year until onset of puberty.
Declines (25cm, 12 cm, 8 cm/y)
X = 3
Y = 4.5 cm
“Short stature” is defined by which characteristics?
- Height more than 2 SD below mean for age/sex OR
2. Below 3rd percentile for age/sex
Mid-parental height for F equation
(mom’s height + father’s height-13 cm)/2
Mid-parental height for M equation
(mom’s height+13 cm + father’s height)/2
T/F: Most conditions that cause poor linear growth also cause delay in skeletal maturation (retarded bone age).
True (malnutrition, hypothyroid, GH deficiency)
Your M patient has slow growth rates and a family Hx of delayed puberty/growth spurt. If you wanted to estimate his bone age, what chart/value might you use?
Height age - age at which the patient’s height would fall into 50th percentile
(patient likely has constitutional delay of growth)
Any (M/F) who presents with unexplained (X), esp (with/without) fam Hx of (X), should be tested for Turner syndrome.
F
X = short stature
Without
Preserved weight gain or frank obesity associated with poor linear growth suggests an (systemic illness/endocrine disorder).
Endocrine disorder;
decreased weight-to-height ratio generally indicates a systemic illness
GH receptor (GHR) has (intracellular/extracellular/transmembrane) domain(s) and exists as (monomer/dimer/pentamer).
All 3
Dimer
T/F: One GH molecule binds one GHR active site on extracellular domain.
False - one GH binds two GHR
T/F: GH binds GHR causes conformational change in receptor and autophosphorylation.
False - no intrinsic kinase activity in GHR; instead, recruit/transphosphorylate JAK2
GH binding GHR causes conformational change and (activation/inhibition) of (X), which then causes (activation/inhibition) of (Y).
Activation (via transphosphorylation)
X = JAK2 (tyrosine kinase)
Activation (phosphorylation)
Y = STAT5b (signal transducers and activators of transcription)
JAK2 phosphorylates tyrosines on intracellular domain of (X) receptor, which serves as docking site for STAT5b. What happens next?
X = GH
Phosphorylates STAT5b; STAT5b dissociate from R, dimerize, go to nucleus, bind DNA, initiate IGF-1 gene transcription
Assessing GH deficiency: levels of (X) are useful because their concentrations parallel (Y).
X = IGF-1 and IGF BP-3 (major carrier for IGF-1) Y = secretion of GH
T/F: GH levels are not used to assess GH deficiency because they cannot be measured in the serum.
False - can be, but not useful; secreted in pulsatile manner and serum levels are low between pulses
Your pre-pubertal male patient tells you he thinks he sometimes identifies as female. His uncertainty makes you reluctant to start hormone therapy. What step could you take at this point to help him/her?
Give him/her time;
GnRH analog will delay puberty in reversible fashion
F to M transgender hormone Rx:
Testosterone (doses similar to those used for hypogonadal males)
M to F transgender hormone Rx:
- Anti-androgen (spironolactone is drug of choice in US)
2. Estrogen supplementation
At (higher/lower) doses, (X) BP med is used as hormone Rx for (M/F) to (M/F) transition.
Higher (up to 200 mg/day);
X = spironolactone
M to F
Which estrogen supplementation options exist for M to F transgender patients?
- Permarin (conjugated estrogens)
2. Estradiol
Biggest concerns for F to M transgender hormone Rx
- Increased Hct (thrombosis risk)
- Decreased HDL (CAD risk)
- More aggressive?
- Sleep apnea
T/F: There are no real health concerns in M to F transition, compared to F to M transition.
True - maybe decreased libido? Be sure to screen prostate and developing breasts for cancer
