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Endo/Repro Flashcards

1
Q

DM1 w/ hypoglycemia (didn’t have anything to eat), what’s the main counterregulatory response to restore blood glucose?

A

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

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2
Q

What’s vaginal adenosis?

A

Squamous epi replaced w/ glandular epi. Happens when mom was exposed to DES (diethylstillbestrol) during pregnancy. Precursor of clear cell adenocarcinoma of the vagina

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3
Q

Delayed 2ndary sexual characteristics + anosmia. What’s the hormone defect?

A

GnRH
This is Kallmann syndrome, which is defective migration of GnRH cells (so get decreased GnRH synthesis in hypothalamus) and formation of olfactory bulb

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4
Q

What 2 ways do does beta blockers help with thyrotoxicosis (too much T4)?

A

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

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5
Q

2 drugs that actually reduce synthesis of thyroid hormones?

A

Propylthiouracil
Methimazole
(both inhibit thyroid peroxidase)

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6
Q

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?

A

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

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7
Q

What kind of insulin is used to prevent postprandial rise in blood sugar?

A

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)

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8
Q

What insulin med doesn’t have a peak?

A

Insulin glargine - long acting

another long acting one is detemir but this one has a peak and has a FA side chain

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9
Q

What kind of receptor does insulin bind to? What’s the effector in this signaling cascade?

A

Surface tyrosine kinase-coupled receptors
Activates protein phosphatase (which dephosphorylates glycogen synthase -> activates glycogen synthesis; and fructose 1,6-bisphosphatase -> inactivates gluconeogenesis)

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10
Q

What kind of receptor does GLP-1 bind to?

A

Surface adenylate cyclase-coupled receptors (G-protein coupled)

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11
Q

In healthy ppl, what’s the single most significant factor that is responsible for differences in bone mass/density?

A

Genetics!

Other factors like diet and exercise play smaller role

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12
Q

Female w/ infertility + acne + hirsutism + insulin resistance + central obesity + bilateral ovarian cysts

A

Polycystic ovarian syndrome

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13
Q

Mucopurulent cervicitis + cervical motion tenderness

A

PID assc w/ gonorrhea or chlamydia

increased risk of ectopic pregnancy, infertility (salpingitis -> fallopian tube scarring)

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14
Q

Components of OCP and what they do

A

Estrogen: suppress midcycle gonadotropin surge -> inhibits ovulation
Progesterone: counteract risk of endometrial cancer (if unopposed estrogen), decrease cervical mucus permeability to sperm

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15
Q

6 absolute CIs for OCP use

A
  1. Pregnancy
  2. Hx of stroke or thromboembolic events
  3. > 35 yo who smoke heavily
  4. HyperTG
  5. Decompensated/acute liver disease (can’t metab steroids)
  6. Hx of estrogen-dependent tumor
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16
Q

Macroglossia + floppy + umbilical hernia + jaundince in 1 mo. Dx?

A

Congenital hypothyroidism
Can also get mental retardation (T4 important to brain development and myelination), heart defects (ASD and VSD), constipation, myxedema, coarse facial features

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17
Q

What 2 things would you find on vaginal exam of a woman w/ endometriosis?

A

Nodularity of uterosacral ligaments
Fixed retroversion of uterus
Distortion of pelvic anatomy by adhesion, etc. is why endometriosis predisposes to infertility

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18
Q

3 sx of caudal regression syndrome and mother’s disease association

A

Sx: agenesis of sacrum (and sometimes lumbar spine) -> flaccid paralysis of legs, dorsiflexed contractures of feet, urinary incontinence
Assc. w/ poorly controlled maternal diabetes

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19
Q

4 things that can happen to fetus w/ maternal cocaine abuse

A

spontaneous abortion
intrauterine growth retardation
placental disruption
prematurity

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20
Q

4 sx in baby whose mother overuses vit A. What syndrome does this resemble?

A

Craniofacial abnormalities, pos. fossa CNS defects, auditory defects, abnormalities of great vessels
Similar defects to DiGeorge

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21
Q

Differences bet. Klinefelter and Kallmann besides anosmia

A

Klinefelter would have elevated FSH&LH whereas Kallmann’s FSH decreases

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22
Q

Histologic finding in testes of Klinefelter pts?

A

Tubules atrophied and replaced by pink, hyalinized tissue

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23
Q

Steps of insulin release

A
  1. Glucose enters via GLUT-2 (facilitated diffusion) -> glycolysis and TCA -> produces ATP
  2. ATP binds regulatory unit of KATP channel -> channel closes -> beta cell depolarized
  3. Voltage-dependent Ca2+ channels open
  4. High cellular Ca2+ -> insulin release
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24
Q

What cells secrete MIF?

A

Sertoli

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25
Q

What does urogenital fold transform into?

A

Fusion of folds -> urethra in both sexes
Ventral penis (so get hypospadias if incomplete fusion)
Labia minora

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26
Q

What does genital swelling transform into?

A

Scrotum (bifid scrotum if malunion of labioscrotal folds)

Labia majora

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27
Q

What does urogenital sinus transform into?

A

Bladder, urethra, prostate gland, bulbourethral glands

Lower vagina, Bartholin’s glands

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28
Q

What molec do you measure to guage how much vit D you have in your body?

A

25-hydroxy vitamin D -> accurately reflects status of dietary and skin production b/c this step of liver synthesis is not tightly regulated

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29
Q

Winter’s formula and example of use?

A

PaCO2 = [HCO3- x 1.5] + 8 -> range in plus minus 2
Used to gauge whether resp compensation is appropriate in metabolic acidosis
Example: pt w/ DKA -> calculate PaCO2 -> if the real PaCO2 is above this value (doesn’t matter if it’s the normal value of 40!), it means pt is not compensating well and has superimposed resp acidosis or is in resp failure (pt should have been in Kussmaul respiration to try to get the acids out!)

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30
Q

With high testosterone level & precocious puberty, how do you tell whether the problem is with adrenal gland (CAH) or leydig cells?

A

17-hydroxyprogesterone is elevated in CAH (this is a hormone of adrenal gland only - it’s one of the precursors to cortisol)

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31
Q

Tx of CAH?

A

Low-dose corticosteroid (suppresses ACTH activity)

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32
Q

What body parts do you measure to gauge insulin resistance?

A

Waist-to-hip ratio -> b/c goal is to see ratio of visceral fat deposition (waist) and subQ fat deposition (hip) -> insulin resistance state/metabolic syndrome/DM2 will have greater visceral fat

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33
Q

Main risk for cervical cancer?

A 
# of sexual partners -> b/c HPV is the main risk factor
Smoking is an independent risk (alcohol, diet, + fam hx DONT play a role)
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34
Q

2 main tx of BPH?

A

a1 ANTAgonist -> “-zosin” -> deals w/ dynamic component of bladder outlet obstruction by relaxing smooth muscle in bladder neck (takes only days-weeks to achieve effects)
5a-reductase inhibitor (so reduces DHT) -> deals w/ fixed component of bladder outlet obstruction by reducing prostate volume (takes 6-12 months)

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35
Q

Which inguinal hernia can carry content down to scrotum and more prone to incarceration?

A

Indirect inguinal hernia

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36
Q

What zone of adrenal gland do you get hyperplasia in Cushing disease?

A

Fasciculata and reticularis (glomerulosa is regulated mainly by Ang II and is hyperplastic in Conn’s syndrome)

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37
Q

In what disease do you see diffuse atrophy of adrenal cortex?

A

Addison disease -> autoimmune process

Medulla is spared

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38
Q

What other tumor can happen in adrenal medulla besides pheochromocytoma?

A

Neuroblastomas (highly malignant, childhood)

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39
Q

What does low-dose dexamethasone suppression test distinguish? What about high-dose?

A

USE THIS TEST WHEN YOU HAVE HIGH ACTH (so this won’t be beneficial in adrenal malignancy/exogenous intake where you have high cortisol and reflex low ACTH b/c you won’t need to do this in the first place)
Low-dose: suppression of ACTH and cortisol is seen in normal ppl -> so if not suppressed, consider Cushing syndrome (move on to high-dose to find etiology)
High-dose: suppression is seen in Cushing DISEASE (pituitary adenoma) -> so if not suppressed, consider ectopic ACTH production (Cushing syndrome) like small cell lung cancer

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40
Q

Hormone that marks ovulation? Hormones that peak before and after ovulation?

A

Marks ovulation: LH surge
Peaks before ovulation (proliferative phase): estrogen
Peaks after ovulation (luteal/secretory phase): progesterone

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41
Q

Which GLUT is inducible by insulin and in what tissues is it expressed?

A

GLUT-4 (stored in cytoplasmic vesicles and increased expression w/ insulin whereas other GLUTs are constitutively expressed)
Expressed in adipocytes and muscles

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42
Q

How long after ovulation do you expect to detect beta-hCG in blood if conception happens at ovulation? When does it peak?

A

Earliest is 6 days after ovulation (secretion from blastocyst begins), but might require up to 11 days (need successful implantation to detect in maternal blood)
Peak at 9 wk -> falls by mid pregnancy

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43
Q

What should you suspect in a woman who had a prompt tx of PID but is presenting now w/ infertility?

A

Antibiotic therapy might not have been inappropriate -> shouldn’t be treated ONLY w/ ceftriaxone or azithromycin/doxycycline but BOTH (gonorrhea and chlamydia usually co-infect)

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44
Q

When does advanced maternal age become a factor in the inability to conceive?

A

> 35 yo

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45
Q

Signs of hyperthyroidism + testicular mass. What’s going on?

A

Testicular mass (nonseminomatous germ cell tumor) that secretes B-hCG -> alpha subunit is identical to TSH, LH, FSH -> so get thyroid sx (paraneoplastic hyperthyroidism)

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46
Q

What tumor is assc. w/ elevated PLAP (placenta-like alkaline phosphatase)?

A

Testicular seminoma

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47
Q

What sx of hyperthyroidism can’t be fixed by beta blocker?

A

Exophthalmos -> but may respond to corticosteroid

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48
Q

What happens to FSH, LH, and estrogen in anorexia?

A

All go down

Anorexia causes HYPOTHALAMIC dysfx so everything downstream from there is affected

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49
Q

What’s a sick euthyroid syndrome and who’s susceptible?

A

Low T3 syndrome

Anorexic pts -> initially just low T3, later T4 also low as well

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50
Q

How does uremia affect thyroid hormone?

A

Decreases peripheral conversion of T4 to T3 -> functionally hypothyroid state

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51
Q

What organ is glucose pulled from during fasting in the initial phase and prolonged phase?

A

First 24 hr from liver: from glycogenolysis until hr 12-18; after that, gluconeogenesis predominates
Then from kidney

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52
Q

Glucagon affects gluconeogenesis exclusively in what organ?

A

Liver
Glucagon doesn’t have substantial effects in kidney, muscle, adipocytes (epinephrine does to muscle and adipocytes -> decrease glucose uptake and stimulates TG breakdown, respectively)

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53
Q

Male w/ only 1 testis. What happens to FSH and LH?

A

LH will be normal (compensation by the remaining Leydig cells) -> LH regulated by testosterone level
FSH will increase b/c it’s downregulated by inhibin B -> one testis means fewer Sertoli and less inhibin B

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54
Q

What does triple test test for? And when should it be performed?

A

Performed week 16-18 of gestation
AFP: elevation most commonly due to dating error! (confirm that before you think about neural tube defects, etc)
hCG: elevation from multiple gestation, mole, choriocarcinoma
Estriol: decreased from placental insufficiency (intrauterine growth retardation, placental abnormalities)

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55
Q

3 drugs that can be used for hirsutism?

A

Spironolactone
Flutamide
Finasteride

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56
Q

Where along the kidney tubule is most amount of water reabsorbed?

A

PCT! (> 60% of water absorbed here no matter what the state of body hydration is)
At late distal tubule and collecting duct -> water reabsorption can be modified by hormones, but the max amount reabsorbed is 20%

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57
Q

Dx of kidney enlargement/distortion + papillae compression + thinning of parenchyma around calyces + cortical atrophy? What’s the most common cause? And What do you see under microscope?

A

Urinary flow obstruction
Most common cause in older men is BPH
Under microscope see interstitial fibrosis w/ patches of mononuclear infiltration & tubular atrophy

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58
Q

Another name for IGF-1?

A

Somatomedin C

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59
Q

What 2 processes does TSH affect in thyroid hormone synthesis?

A

Na+/I- symporter (just bringing I- inside cell; the actual oxidization to I2 is done outside of cell in the colloid on the other side)
Synthesis of thyroGLOBULIN (by increasing gene transcription)

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60
Q

What are the 2 Ab against in Hashimoto’s thyroiditis?

A

Anti-thyroid peroxidase

Anti-thyroglobulin

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61
Q

Which cell in ovary does LH influence? FSH? What do they produce?

A

LH influences theca INTERNA cells (outside) -> make it convert cholesterol to androgen and progesterone
FSH influences granulosa cells (inside) -> aromatase activity -> make it convert androgen to estradiol
Theca EXTERNA doesn’t do anything, just an outermost layer of SMC and fibroblasts that provides support

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62
Q

2 causes of congenital torticollis? Assc. conditions?

A

Develops by 2-4 weeks of age, might be assc. w/ hip dysplasia, metatarsus adductus (adduction of forefoot), clubfoot. Soft tissue might be palpable on affected neck
Causes: breech delivery, malposition of head in utero

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63
Q

What is fetus most at risk of w/ maternal HTN?

A

Asymmetric intrauterine growth restriction -> normal head size w/ reduced abdominal circumference
Increased risk of placental abruption

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64
Q

Endocrine hormones that work thru cAMP

A

“FLAT ChAMP”: FSH, LH, ACTH, TSH CRH, hCG, ADH (V2), MSH, PTH
Also calcitonin, GHRH, glucagon

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65
Q

Endocrine hormones that work thru IP3

A

“GOAT HAG”: GnRH, Oxytocin, ADH (V1), TRH, Histamine (H1), Ang II, Gastrin

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66
Q

Molecules that work thru NON-RECEPTOR tyrosine kinase (meaning “receptor-assc.” b/c there’s NO intrinsic enzyme activity, uses JAK/STAT pathway)

A

“PIG”: Prolactin, Immunomodulators (cytokines), GH

Think acidophiles + cytokines

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67
Q

3 anions that inhibit I- uptake into follicular cells

A

Perchlorate
Pertechnetate
Thiocyanate

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68
Q

Types of epithelial lining from vagina to ovary

A

Non-keratinized stratified squamous: vagina - ectocervix
Simple columnar: endocervix - fallopian tube (+ciliated and peg cells in fallopian tube; pseudostratified in uterus)
Simple cuboidal: ovary

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69
Q

What’s in suspensory ligament of the ovary? When is it ligated?

A

Nerves, arteries, veins, lymphatics supplying ovary

Ligated when trying to remove ovarian mass

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70
Q

What’s in round ligament of uterus? What does it attach to?

A

Artery of Sampson
Attaches uterus to external genitalia (so this is the structure that can be found in inguinal canal)
It’s a / ovarian ligament

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71
Q

What does ovarian ligament attach to?

A

Uterine pole of ovary to body of uterus

It’s a vestige of gubernaculum (sup portion) along w/ round ligament of uterus

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72
Q

What’s in cardinal ligament? When is it ligated?

A

Cardinal ligament = transverse cervical ligament
Contains uterine artery
Ligated duringr radical hysterectomy

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73
Q

Where is IGF-1 synthesized and released?

A

Liver (after being stimulated by GH)

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74
Q

Where’s the defect in Laron dwarfism?

A

GH receptors

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75
Q

Why do you not get hypernatremia w/ mineralocorcicoid excess?

A

Aldosterone escape mechanism: high aldos causes increased renal Na+ and water absorption -> increases renal blood flow and GFR -> increase in rate of Na+ excretion from renal tubules

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76
Q

How does prolactin cause amenorrhea or decreased libido?

A

It suppresses GnRH (so work from top down)

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77
Q

1st aortic arch derivative?

A

Part of maxillary artery

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78
Q

2nd aortic arch derivatives (2)?

A

Stapedial artery

Hyoid artery

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79
Q

3rd aortic arch derivatives (2)?

A

Common carotid artery

Internal carotid artery (proximal part) -> so part of circle of Willis

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80
Q

4th aortic arch derivatives (2)?

A

Left: aortic arch -> so part of circle of Willis
Right: right subclavian (proximal part)

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81
Q

6th aortic arch derivatives (2)?

A 
Pulmonary arteries (proximal part)
Ductus arteriosus (left side only)
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82
Q

1st branchial/pharyngeal CLEFT derivative?

A

External auditory meatus

83
Q

2nd-4th branchial/pharyngeal CLEFT derivatives?

A

Temporary cervical sinues -> later obliterated by proliferation of 2nd arch mesenchyme (if not -> branchial cleft cysts on lateral neck)

84
Q

1st branchial/pharyngeal ARCH derivatives (2 nerves, 6 cartilages, 5 groups of muscles)?

A

Nerves: CN V2 and V3
Cartilages: Meckle cartilage (mandible, malleus, incus, sphenomandibular ligament), maxilla, zygoma, vomer, palatine, temporal bone
Muscles: muscles of mastication (temporalis, masseter, lateral&medial pterygoids), mylohyoid, digastric (ant belly), tensor tympani, tensor veli palatini

85
Q

Syndrome assc. w/ 1st branchial/pharyngeal ARCH derivatives?

A

Treacher Collins syndrome (1st arch neural crest fails to migrate) -> mandibular hypoplasia, facial abnormalities

86
Q

2nd branchial/pharyngeal ARCH derivatives (nerve, cartilage, 4 groups of muscles)?

A

Nerve: CN VII
Cartilage: Reichert cartilage (stapes, styloid process, lesser horn of hyoid, stylohyoid ligament)
Muscles: muscles of facial expression, stapedius, stylohyoid, platysma, digastric (belly)

87
Q

What happens in congenital pharyngo-cutaneous fistula?

A

Fistula bet. tonsillar area and lateral neck

From persistence of 2nd cleft and pouch

88
Q

3rd branchial/pharyngeal ARCH derivatives (nerve, cartilage, muscle)?

A

Nerve: CN IX
Cartilage: greater horn of hyoid
Muscle: stylopharyngeus

89
Q

4th branchial/pharyngeal ARCH derivatives (nerve, 5 cartilages, 3 groups of muscles)?

A

Nerve: superior laryngeal branch of CN X
Cartilages: same as 6th (thyroid, cricoid, arythenoids, corniculate, cuneiform)
Muscles: most pharyngeal constrictors, cricothyroid, levator veli palatini

90
Q

6th branchial/pharyngeal ARCH derivatives (nerve, 5 cartilages, 1 group of muscles)?

A

Nerve: recurrent laryngeal branch of CN X
Cartilages: same as 6th (thyroid, cricoid, arythenoids, corniculate, cuneiform)
Muscles: all intrinsic muscles of larynx except cricothyroid

91
Q

1st branchial/pharyngeal POUCH derivatives (3)?

A

Middle ear cavity
Eustachian tube
Mastoid air cells

92
Q

2nd branchial/pharyngeal POUCH derivative?

A

Palatine tonsil

93
Q

3rd branchial/pharyngeal POUCH derivatives (2)?

A

Inf. parathyroids (dorsal wings)

Thymus (ventral wings)

94
Q

4th branchial/pharyngeal POUCH derivatives (2)?

A

Sup. parathyroids (dorsal wings)

C cells of thyroid

95
Q

Tx of radioactive iodine poisoning?

A

Potassium iodide -> to competitively inhibit radioactive one from entering thyroid follicular cells
Large increase also inhibits iodine organification (Wolff-Chaikoff)

96
Q

What’s the word for accessory nipples?

A

Polythelia

97
Q

What do mesonephric ducts become in females? Males?

A

Females: Gartner’s duct
Males: epididymis, ductus deferens, seminal vesicles, ejaculatory ducts

98
Q

What accounts for amphotericin B’s side effects?

A

It’s meant to bind ergosterol in fungi but it also does bind human cholesterol to a degree

99
Q

What happens to endometrial cells after withdrawal of progesterone?

A

APOPTOSIS (not atrophy!)

Why get vaginal bleeding after progesterone therapy or w/ anti-progesterone abortifacient

100
Q

Most reliable test to confirm menopause?

A

Increased serum FSH!

LH rises later so less sensitive

101
Q

3 unique things that can happen to fetus in gestational diabetes?

A

Fetal macrosoma (high insulin produced by fetus -> increased fat deposition and enhanced fetal growth)
Caudal regression syndrome
Hypertrophic cardiomyopathy

102
Q

What is hPL (human placental lactogen) responsible for? What cells secrete this?

A

hPL increases maternal insulin resistance -> so mom gets shitty stuff like FAs and ketones while baby gets glucose
Secreted by syncytiotrophoblast

103
Q

What are Hurthle cells and what condition do you find these in?

A

Large eosinophilic thyroid follicular epithelial cell w/ granular cyto
See this in Hashimoto’s thyroiditis

104
Q

Dx of “follicular hyperplasia w/ tall cells forming intrafollicular papillary projections”?

A

Papillary thyroid cancer, tall cell variant -> seen in older ppl and carries worse prognosis

105
Q

Dx of “mixed, cellular infiltration w/ occasional mutinuclear giant cells” in thyroid gland?

A

de Quervain’s thyroiditis

Will also see markedly reduced radioactive iodine uptake

106
Q

Where does fluid collect in hydrocele?

A

Tunica vaginalis

107
Q

What layer is external spermatic fascia and where is it derived from?

A

Outermost layer, just deep to dartos muscle and scrotal fascia
Derived from aponeurosis of external oblique abd muscle

108
Q

What is cremasteric fascia derived from?

A

Internal oblique abdominal muscle and aponeurosis

109
Q

What layer is internal spermatic fascia and where is it derived from?

A

Immediately overlies spermatic cord and tunica vaginalis

Derived from transversalis fascia

110
Q

What 3 things decrease the risk of ovarian cancer?

A

OCPs!
Multiparity
Breast-feeding

111
Q

Why are pregnant women & ppl on OCPs at risk of gallstones?

A 
Estrogen = cholesterol hypersecretion
Progesterone = gallbladder hypomotility
112
Q

2 most common causes of eugonadotropic (normal 2ndary sexual characteristics) amenorrhea?

A

Mullerian duct anomalies
Incomplete canalization/imperforate hymen -> hematocolpos/accumulation of blood in vaginal canal felt w/ ant rectum palpation -> might accumulate enough to distend vagina and cause back pain + difficulties defecation and urination

113
Q

Common meds causing impotence?

A 
SSRIs
Sympathetic blockers (clonidine, methyldopa, beta-blockers)
114
Q

What kind of Ab is anti-Rh(D) and when is it administered?

A

IgG -> to catch fetal RBC in MATERNAL circulation (doesn’t cause transplacental fetal hemolysis b/c administer really low quantity)
Give at 28 wks gestation and in the immediate postpartum period

115
Q

What should you think about in a pt who presents w/ fever and soar throat w/ hx of hypothyroidism?

A

Agranulocytosis induced by thionamides (methimazole and propylthiouracil) -> so get WBC count w/ differential, don’t just send them home w/ ibuprofen!

116
Q

When would you prefer propylthiouracil over methimazole?

A

Life-threatening thyroid storm (b/c it also has the added effect of decreasing peripheral conversion of T4 to T3 on top of being thyroid peroxidase inhibitor)
Also use during 1st trimester of pregnancy (b/c methimazole is teratogenic during that trimester)
Otherwise, usually doesn’t prefer propylthiouracil b/c of hepatotoxicity

117
Q

Important cause of hypoglycemia in diabetics?

A

Exercise -> they don’t have normal mechanism in healthy ppl where drop in blood glucose stops insulin release b/c they’re on exogenous insulin or other meds -> so their blood sugar gets really low really fast

118
Q

2 things that are elevated in maternal serum in neural tube defects?

A

AChE and AFP

119
Q

Dx of pt hospitalized for recurrent renal colic w/ peptic ulcers who has high serum Ca2+, low phosphorus, high Ca2+ excretion?

A

Primary hyperparathyroidism

120
Q

What’s the difference bet. responses to GnRH analog administered continuously vs. GnRH antagonist?

A

GnRH analog administered continuously (ie leuprolide): will see initial stimulation (concordant increase in both testosterone and DHT) followed by concordant decrease in testosterone and DHT
GnRH antagonist: no initial flare -> just suppress testosterone and DHT immediately

121
Q

Differences bet. androgen-binding protein and sex hormone-binding globulin?

A

Androgen-binding protein: secreted by Sertoli cells to ensure high LOCAL testosterone conc
SHBG: blood hormone

122
Q

Med of choice in gestational DM?

A

Insulin, but only after diet and exercise has failed

123
Q

Different kinds of receptors acted on by thyroid hormones? TSH? TRH?

A

Thyroid hormones: nuclear receptors
TSH: cAMP
TRH: IP3

124
Q

Lab dx of PCOS? What are they at high risk for?

A

LH/FSH ratio > 3

High risk for DM2 and endometrial adenocarcinoma

125
Q

Molecules that work thru INTRINSIC tyrosine kinase (meaning thru MAPk pathway)?

A

Think growth factors (NOT GH): insulin, IGF-1, FGF, PDGF, EGF

126
Q

Differences bet. BRCA1&2 and HER2 mutations as far as breast cancer is concerned?

A

HER2 mutations are acquired

BRCA1&2 mutations are inherited

127
Q

What does insulin depletion do to K+ inside and outside cell? What does this mean to DKA management?

A

Think of insulin effect as being like aldosterone
Intracellular K+: DECREASE
Extracellular K+: normal or increase
So ALWAYS give K+ in DKA even if you see normal or elevated serum K+

128
Q

What’s amylin and what condition do you see this in?

A

Amylin = islet amyloid polypeptide

See this in DM2

129
Q

What group of conditions do you have to look out for as they may affect HbA1C measurements? What time period of glucose level does HbA1C represent?

A

Any changes affected RBC survival -> anemia, chronic kidney disease, hemoglobinopathies
Avg blood glucose level over previous 10-12 wks

130
Q

What are you looking for when you measure amniotic fluid bilirubin?

A

Erythroblastosis fetalis

131
Q

What kind of transporter takes up iodide at thyroid gland?

A

Na+/I- symporter (energy dependent; against conc gradient)

132
Q

Diff in what you see on endometrial curettage of ectopic pregnancy vs. successful pregnancy?

A

Ectopic pregnancy: decidualized endometrium WITHOUT chorionic villi
Successful pregnancy: decidualized endometrium WITH chorionic villi & embryonic tissue

133
Q

What happens in Sheehan’s syndrome exactly?

A

Ischemic necrosis of pituitary

NOT apoplexy

134
Q

What are sx of autoimmune hypophysitis and how do you distinguish it from Sheehan’s syndrome? When does it usually occur?

A

Sx: headachesm cortisol deficiency, VISUAL FIELD DEFICITS & ACUTE PRESENTATION (vs. Sheehan’s)
Usually occurs late pregnancy or early postpartum

135
Q

What electrolyte abnormalities occur in addison’s disease?

A

Decreased aldos means hyperkalemia, non-anion gap metabolic acidosis -> also get compensatory hyperchloremia for this!
And don’t forget hyponatremia from decreased Na+ reabsorption (and compensatory increase in ADH from lacking aldos)

136
Q

What does normal serum sodium + hypokalemia + hyperchloremic metabolic acidosis suggest?

A

Proximal renal tubular acidosis

137
Q

How do you distinguish bet. aromatase deficiency and 21a-hydroxylase deficiency?

A

There’ll be maternal virilization (hirsutism) in aromatase deficiency b/c androgens can cross to maternal circulation
No maternal virilization in 21a-hydroxylase b/c of intact placental aromatase activity

138
Q

How does adrenergic agent (like epinephrine) regulate insulin secretion?

A

Thru both b2 and a2 receptors!
b2 receptors: promotes insulin release
a2 receptors: decreases insulin release
But the effect that’s predominant is a2 -> so sympa stimulation will result in inhibition of insulin secretion -> unless you block the a2 response w/ something!

139
Q

What groups of condition should you be thinking about w/ someone w/ untreated prolactinoma who just had a pathological fracture?

A

DONT think about MEN1 -> fracture is most likely from prolactin-induced hypogonadism and fall in estrogen -> so bone loss is most likely from decreased estrogen not hyperparathyroidism assc. w/ MEN1
So the conditions you should think about are anything related to low estrogen -> like vaginal dryness

140
Q

Dx of hypertension + low renin + weakness and paresthesias?

A

Primary mineralocorticoid excess (hyperaldosteronism) -> don’t see edema or hypernatremia b/c of aldosterone escape
Hypokalemia is what causes weakness and paresthesias

141
Q

Pt on long-term prednisone is now in adrenal crisis after surgery. What happened?

A

Long-term glucocorticoids suppress HPA axis -> gets low CORTISOL, ACTH, CRH -> suppression might remain even after withdrawal
During stressful times (like surgery), this means you need higher dosage or the pt will risk adrenal insufficiency (n/v, abd pain, hypotension, tachycardia)

142
Q

How does sex steroids (like estrogen) impact long bones?

A

Encourages closure of epiphyseal growth plate
So initially will increase linear growth at first (puberty) -> why precocious puberty will result in shorter stature after initial growth spurt

143
Q

How do TNF-a, catecholamines, glucocorticoids, and glucagon induce insulin resistance?

A

Aberrant phosphorylations of serine kinases & threonine residues -> phosphorylation of IRS-1 and inhibition of IRS-1 phosphorylation by insulin

144
Q

What congenital condition increases risk for testicular torsion?

A

Horizontal positioning of testes (Bell clapper deformity)

145
Q

Ulcerative/vesicular lesion on external genitalia + painful regional LAD + proctitis w/ tenesmus and bloody dischange?

A

Chlamydia - LGV (lymphogranuloma venerum)

Painful LAD is a cardinal feature

146
Q

Glucocorticoids increase protein synthesis in what organ?

A

Liver - b/c increase synthesis of enzymes used in gluconeogenesis and glycogenesis
Everywhere else it break things down: muscles (why get increased BUN w/ glucocorticoid), skin (why get striae and impaired wound healing), lymphoid tissue, bones

147
Q

How does gonadotroph adenoma usually present?

A

Mass effects and hypogonadism (b/c they usually don’t produce intact FSH or LH, but overproduce alpha subunits)

148
Q

What do most nonsecretory adenomas of pituitary arise from?

A

Gonadotrophs

149
Q

What is the most common cell type in normal pituitary?

A

Somatotrophs (GH)

150
Q

What is the feared complication of pituitary apoplexy?

A

Cardiovascular collapse from ACTH deficiency -> adrenocortical insufficiency -> so give glucocorticoids

151
Q

What’s the main way catecholamines increase blood glucose?

A

Increasing glycogenolysis

152
Q

What does metyrapone administration do?

A

It inhibits 11-B-hydroxylase -> decreased cortisol synthesis -> pt w/ intact HPA will have reactive increase in ACTH, 11-deoxycortisol, and urinary 17-hydroxycorticosteroids

153
Q

Where’s the damage when you have permanent central DI vs. transient central DI?

A

Permanent central DI: damage to hypothalamic nuclei

Transient central DI: damage to pos. pituitary

154
Q

What’s the point of giving menotropin followed by hCG for fertility tx?

A

Menotropin: acts like FSH -> formation of dominant ovarian follicle
hCG: stimulates LH surge -> ovulation

155
Q

What is beta hydroxybutyrate a marker of?

A

Insulin deficiency

So present ONLY in DM 1 (not 2)

156
Q

What are 2 molecs that increase insulin resistance in overweight ppl?

A

FFA and TG

NOT LDL or other things

157
Q

Most common cause of death in DM pts?

A

Coronary heart disease (MI)

158
Q

What structure secretes neuropeptide Y? What does it do? It’s under influence of what molec?

A

Arcuate nucleus of hypothalamus
Appetite stimulant
Leptin decreases its production

159
Q

What structure secretes alpha-MSH? What does it do? It’s under influence of what molec?

A

Arcuate nucleus of hypothalamus (POMC)
Inhibits food intake
Leptin stimulates its production

160
Q

3 infections that cause genital lesions that initially are NOT painful?

A
  1. Klebsiella inguinale (donovanosis): painless then eventually ulcerates -> DON’T see LAD, see intracytoplasmic Donovan bodies -> elephantitis if untreated
  2. Syphilis
  3. Chlamydia (LVG): painless then painful ulceration & inguinal LAD -> see chlamydial inclusion bodies in cyto
161
Q

Diff stages of monozygotic twinning?

A

Day 0-4: dichor/diam
Day 4-8: monochor/diam
Day 8-12: monochor/monoam
Day 13: conjoined

162
Q

Dx of thyroid bx that shows “uniform polygonal or spindle-shaped cells w/ extracellular amyloid deposits”?

A

Medullary thyroid cancer

163
Q

What happens to a 46,XY w/ no Sertoli cells but normal Leydig?

A

Internal genitalia: BOTH male and female (because there’s testosterone for male internal genitalia development and there’s no MIF to inhibit internal female development)
External genitalia: male (DHT intact)

164
Q

3 meds that decrease peripheral conversion of T4 to T3 besides propylthiouracil and nonselective beta blockers?

A

Glucocorticoids
Amiodarone
Iopanoic acid

165
Q

What does tocolysis mean?

A

Suppression of premature labor

B2 stimulation does this

166
Q

What condition should you think about if a pt has normal hormonal profile but lacks sperm?

A

Obstruction along path from tests to seminal fluid -> so think congenital absence of vas deferens in CF

167
Q

Dx of “large cells w/ overlapping nuclei containing finely dispersed chromatin and numerous intranuclear inclusions and grooves”?

A

Papillary carcinoma of the thyroid
finely dispersed chromatin = ground-glass appearance = Orphan Annie eye
intranuclear inclusions and grooves = invagination of nuclear membrane

168
Q

What is colloid nodules?

A

Focal hyperplasia of normal thyroid follicular cells -> benign
See variable-sized thyroid follicles, colloid, macrophages

169
Q

What is excessive hCG (such as in hydatidiform moles) put you at risk for?

A

Theca-lutein cysts (b/c it stimulates ovarian growth)

170
Q

What’s the marker of yolk sac tumors of ovaries and testes?

A

Elevated AFP

171
Q

In what conditions is DHEA elevated?

A

Excess production of ADRENAL androgens -> like in adrenal neoplasia

172
Q

Signs of urethral injury? What is CI?

A

High-riding, boggy prostate (hematome below gland), can’t void despite sensation of full bladder, blood at urethral meatus

173
Q

Diff parts of male urethra? Which part is susceptible to injury from trauma to the pelvis?

A

Pos. urethra -> prostatic and membranous
Ant. urethra -> bulbous (supported by corpus spongiosum) and penile
Injury to pelvis usually disrupts pos. urethra at the bulbomembranous jx (membranous is the weakest point of pos. urethra)

174
Q

When do you use oral glucose tolerance test vs. fasting blood sugar?

A

Fasting blood sugar: to dx DM 1 & 2

Oral glucose tolerance: screening pregnant women for gestational DM

175
Q

What is carcinosarcomas and what do you see under the microscope?

A

Malignant mixed mullerian tumors of uterus

See endometroid glands (epithelial component) and sarcomatous stroma (mesenchymal component)

176
Q

Sx that are only seen w/ hyperthyroidism from Graves’ as opposed to other things?

A

Pretibial myxedema (lower-leg skin thickening and induration), exophthalmos, periorbital edema, eye-movement limitations -> these sx are caused by autoimmune response not just increased hormone levels -> increased fibroblast proliferaton and GAG secretion

177
Q

In what condition do you see myxedema coma?

A

Decreased mental status in severe hypothyroidism (don’t confuse this w/ pretibial myxedema seen in Graves’)

178
Q

Diff LNs that drain diff parts of male organ?

A

Testes -> para-aortic (retroperitoneal) LNs
Scrotum (& anus up to pectinate line) -> superficial inguinal LNs
Glans penis (and clitoris and cutaneous portion of pos. calf) -> deep inguinal LNs

179
Q

What is the most sensitive screening test for primary hypothyroidism?

A

Serum TSH! (rises before fall in hormones is seen)

This doesn’t apply to central hypothyroidism, but that’s uncommon anyway

180
Q

What does hyponatremia, hyperkalemia, and hypoglycemia suggest w/ hx of vomiting, abd pain, weight loss, and hyperpigmentation?

A

Adrenal crisis -> give corticosteroids immediately

Might be component of N. meningitidis if there’s shock too

181
Q

Pt w/ metabolic acidosis was tx w/ something and now has increased bicarb and sodium, decreased serum osmolality, and decreased serum K+. How do you tell what condition is this acidosis related to?

A

This is DKA and pt was given insulin and normal saline -> b/c insulin pushes K+ into cells, cause decrease in ketone production (so increased bicarb) and normal saline fixes Na+ and decrease osmolality
Other conditions like hypoaldosteronism (type 4 renal tubular acidosis) and loop diuretics use will also be assc. w/ metabolic acidosis, but both aldosterone and loop diuretics will cause INCREASED serum osmolality

182
Q

What cells mediate destruction of beta cells? How much needs to be destroyed before DM1 clinical sx?

A

Cell-mediated immunity (T cells; see Ab on site too but these play permissive role only)
Clinical sx once > 90% of cells are destroyed

183
Q

What createss the appearance of skin retraction in breast cancer?

A

Cancer infiltrates suspensory Cooper ligaments

dermal lymphatic OBSTRUCTION is assc. w/ peau d’orange when cancer infiltrates lymphatic drainage

184
Q

Endometrial hyperplasia + adnexal mass. What’s the mass? And what do you see under the microscope?

A

Granulosa cell tumor -> b/c it probably secretes estrogen leading to endometrial hyperplasia
See Call-Exer bodies -> follicle-like structures filled w/ eosinophilic secretions

185
Q

What ovarian tumor progresses to pseuomyxoma peritonei?

A

Mucinous cystadenocarcinoma

186
Q

Why is response to vasopressor blunted when pt is in adrenal crisis?

A

B/c glucocorticoids have permissive effect on vasoconstriction (so infusion w/ vasopressor substance won’t do anything until treated w/ corticosteroids first)

187
Q

Dx of breast tumor w/ solid sheets of pleomorphic cells w/ central necrosis + chronic inflammation + periductal concentric fibrosis?

A

Comedocarcinoma -> subset of DCIS

Might calcify as membranes become necrotic

188
Q

What does sclerosing adenosis look like?

A

Central acinar compression and distortion by fibrotic tissues + peripheral ductal dilation
Common finding in fibrocystic change

189
Q

Dx of inspissated breast secretions + chronic granulomatous inflammation in periductal & interstitial areas?

A

Mammary duct ectasia

190
Q

How often do you test neurological fx in diabetic pts?

A

Yearly (not monthly)

Foot care on the other hand is what you recommend the pt do every day

191
Q

Fever + foul-smelling discharge + tender uterus a couple of days after delivery. What do you have to think about?

A

Endometritis -> mixed flora but Bacteriodes species most commonly isolated

192
Q

How do you identify corpus cavernosa and corpus spongiosum on penis transverse section?

A

2 caves and 1 sponge
Corpora cavernosa: paired structure on dorsum (top) side -> PDE inhibitors work in this area
Corpus spongiosum: surrounds urethral lumen on ventral (bottom) side

193
Q

What happens to serum Na+ and ammonia in DKA?

A

Hyponatremia: glycosuria encourages osmotic diuresis and sodium loss
Hyperammonemia: counterregulatory hormones encourage protein degradation

194
Q

Mullerian agenesis vs. androgen insensitivity syndrome?

A

Both will have rudimentary vagina (blind pouch) w/ no internal sexual organs (uterus, upper vagina, etc), both will have breast
BUT mullerian agenesis will have normal hormone profiles (HPA axis normal), whereas androgen sensitivity syndrome will have elevated testosterone and LH, and you can palpate testes in androgen sensitivity syndrome

195
Q

What’s a cephalhematoma and what conditions is it assc. w/?

A

Hemorrhage w/in the circular region of scalp that enters the lower uterus during birth -> you can see it as a big bump on baby’s head
Assc. w/ sudden delivery, disproportion bet. diameter of head and birth canal, inappropriate forceps use

196
Q

Hypocalcemia + hyperPTH in young person w/ skeletal abnormalities. What do you have to consider?

A

Albright hereditary osteodystrophy -> pseudohyperparathyroidism from end-organ resistance to PTH
Skeletal abnormalities = short statues, short fingers, round face

197
Q

Heavy menses & passing clots occasionally + heaviness and palpable mass in abdomen + signs of anemia but no WBC elevation. Dx?

A

Leiomyoma (suspect this esp if African American)
Heavy menses = menorrhagia -> don’t confuse this w/ dysmenorrhea (pain during period like in endometriosis)
Ovarian cysts only rarely cause menorrhagia

198
Q

Diff in mutations causing MEN1 and MEN2?

A

MEN1: MEN1 gene is a tumor suppressor so mutation is needed on both genes
MEN2: RET is an oncogene so only need one mutation
Both are AD tho

199
Q

Dx of scrotal mass that doesn’t transilluminated, palpable when standing up and disappears when lying down?

A

Varicocele
Relieved when lying down b/c there’s less pressure on gonadal vein (left renal vein is normally compressed in bet. SMA and aorta)

200
Q

What effect does continuous leuprolide have exactly (in treating prostate cancer)?

A

Reducing circulating testosterone

NOT impairing steroid synthesis (that’s the job of ketoconazole)

201
Q

What’s a general rule to decide whether a drug can cross placenta or not?

A

Lipophilic: can cross (think warfarin, unconj bilirubin)
Hydrophilic: can’t cross (thin heparin which is charged, conj bilirubin)

202
Q

Ovaries contain multiple white bodies representing atretic follicles. What’s the mechanism?

A 
Apoptosis of oocyte and graulosa cells
NOT differentiation (don't confuse follicular atresia w/ corpus luteum)
203
Q

5-yo girl w/ precocious puberty and 9-yo bone age. Giving her GnRH induces increase in LH. What’s the tx?

A

Precocious puberty can be central or peripheral. The fact that giving GnRH can induce increase in LH means it’s central.
So fix centrally -> give CONTINUOUS leuprolide (so anti-GnRH)

204
Q

Drug for difficulty attaining/sustaining erection? For premature ejaculation?

A

Attaining/sustaining: sidelnafil (PDEi)

Premature ejaculation: SSRIs

Question Bank (10 decks)

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