Endo/Repro Flashcards
DM1 w/ hypoglycemia (didn’t have anything to eat), what’s the main counterregulatory response to restore blood glucose?
Epinephrine
NOT glucagon b/c its response to blood sugar is blunted in diabetics
The answer would be cortisol if this happened in a more chronic setting
What’s vaginal adenosis?
Squamous epi replaced w/ glandular epi. Happens when mom was exposed to DES (diethylstillbestrol) during pregnancy. Precursor of clear cell adenocarcinoma of the vagina
Delayed 2ndary sexual characteristics + anosmia. What’s the hormone defect?
GnRH
This is Kallmann syndrome, which is defective migration of GnRH cells (so get decreased GnRH synthesis in hypothalamus) and formation of olfactory bulb
What 2 ways do does beta blockers help with thyrotoxicosis (too much T4)?
1) Thyroid hormone causes hyperadrenergic actions by upregulating beta receptors at target tissues. B-blockers help block this effects
2) Decreases conversion of T4 to T3 at peripheral tissues by inhibiting iodothyronine deiodinase
2 drugs that actually reduce synthesis of thyroid hormones?
Propylthiouracil
Methimazole
(both inhibit thyroid peroxidase)
How do you treat severe hypoglycemia w/ loss of consciousness in a non-medical setting? Medical setting? How about when it’s only mild-moderate hypoglycemia w/ consciousness?
IM glucagon for severe hypoglycemia in non-medical setting
IV glucose (50 dextrose solution) for severe hypoglycemia in medical setting
Oral quick glucose like fruit juice in mild-moderate hypoglycemia that’s caught early enough
What kind of insulin is used to prevent postprandial rise in blood sugar?
RAPID-ACTING: lispro, aspart, glulisine (peaks in 45-75 min)
The regular insulin takes too long (2-4) and is best for IV use like DKA)
What insulin med doesn’t have a peak?
Insulin glargine - long acting
another long acting one is detemir but this one has a peak and has a FA side chain
What kind of receptor does insulin bind to? What’s the effector in this signaling cascade?
Surface tyrosine kinase-coupled receptors
Activates protein phosphatase (which dephosphorylates glycogen synthase -> activates glycogen synthesis; and fructose 1,6-bisphosphatase -> inactivates gluconeogenesis)
What kind of receptor does GLP-1 bind to?
Surface adenylate cyclase-coupled receptors (G-protein coupled)
In healthy ppl, what’s the single most significant factor that is responsible for differences in bone mass/density?
Genetics!
Other factors like diet and exercise play smaller role
Female w/ infertility + acne + hirsutism + insulin resistance + central obesity + bilateral ovarian cysts
Polycystic ovarian syndrome
Mucopurulent cervicitis + cervical motion tenderness
PID assc w/ gonorrhea or chlamydia
increased risk of ectopic pregnancy, infertility (salpingitis -> fallopian tube scarring)
Components of OCP and what they do
Estrogen: suppress midcycle gonadotropin surge -> inhibits ovulation
Progesterone: counteract risk of endometrial cancer (if unopposed estrogen), decrease cervical mucus permeability to sperm
6 absolute CIs for OCP use
- Pregnancy
- Hx of stroke or thromboembolic events
- > 35 yo who smoke heavily
- HyperTG
- Decompensated/acute liver disease (can’t metab steroids)
- Hx of estrogen-dependent tumor
Macroglossia + floppy + umbilical hernia + jaundince in 1 mo. Dx?
Congenital hypothyroidism
Can also get mental retardation (T4 important to brain development and myelination), heart defects (ASD and VSD), constipation, myxedema, coarse facial features
What 2 things would you find on vaginal exam of a woman w/ endometriosis?
Nodularity of uterosacral ligaments
Fixed retroversion of uterus
Distortion of pelvic anatomy by adhesion, etc. is why endometriosis predisposes to infertility
3 sx of caudal regression syndrome and mother’s disease association
Sx: agenesis of sacrum (and sometimes lumbar spine) -> flaccid paralysis of legs, dorsiflexed contractures of feet, urinary incontinence
Assc. w/ poorly controlled maternal diabetes
4 things that can happen to fetus w/ maternal cocaine abuse
spontaneous abortion
intrauterine growth retardation
placental disruption
prematurity
4 sx in baby whose mother overuses vit A. What syndrome does this resemble?
Craniofacial abnormalities, pos. fossa CNS defects, auditory defects, abnormalities of great vessels
Similar defects to DiGeorge
Differences bet. Klinefelter and Kallmann besides anosmia
Klinefelter would have elevated FSH&LH whereas Kallmann’s FSH decreases
Histologic finding in testes of Klinefelter pts?
Tubules atrophied and replaced by pink, hyalinized tissue
Steps of insulin release
- Glucose enters via GLUT-2 (facilitated diffusion) -> glycolysis and TCA -> produces ATP
- ATP binds regulatory unit of KATP channel -> channel closes -> beta cell depolarized
- Voltage-dependent Ca2+ channels open
- High cellular Ca2+ -> insulin release
What cells secrete MIF?
Sertoli