Instructions: Select the single best answer. Explanations appear immediately after each response. Your scores populate the Score Report tab in real time.
Question 1 of 5 — LO 1 · C21 vs C19 vs C18 Steroid Classes
A biochemist analyzes five endogenous steroids by mass spectrometry. Steroid I has 21 carbons and binds the progesterone receptor with high affinity. Steroid II has 19 carbons, a ketone at C17, and binds the androgen receptor with moderate affinity. Steroid III has 19 carbons, a hydroxyl at C17, and binds the androgen receptor with 2–3× the affinity of testosterone. Steroid IV has 18 carbons, an aromatic A ring, and binds the estrogen receptor with very high affinity. Steroid V has 21 carbons, 11β-hydroxyl and 17-hydroxyl, and binds the glucocorticoid receptor. Which set best matches I → V?
AI = progesterone · II = androstenedione · III = DHT · IV = estradiol · V = cortisol
BI = DHEA · II = testosterone · III = androstenedione · IV = estrone · V = aldosterone
CI = cortisol · II = DHEA · III = testosterone · IV = estriol · V = progesterone
DI = aldosterone · II = DHT · III = androstenedione · IV = estradiol · V = cortisol
EI = progesterone · II = DHEA · III = DHT · IV = estrone · V = cortisol
A. LO 1 nomenclature: C21 steroids include progestins (progesterone) and corticosteroids (cortisol, aldosterone). C19 steroids are the androgens — the two forms differ at C17: "-one" ending (ketone) = weaker androgens like androstenedione and DHEA; "-ol" ending (hydroxyl) = stronger androgens like testosterone and DHT. C18 steroids are the estrogens (aromatic A ring lost the C19 methyl via aromatase). DHT is ~2-3× more potent than testosterone at the androgen receptor.
Question 2 of 5 — LO 2 · Androgen Receptor Affinity Ranking
A pharmacology lab measures androgen receptor (AR) binding affinity for five circulating steroids and constructs a dose-response curve. One compound produces a maximal AR-mediated transcriptional response at roughly one-third the concentration required by testosterone, while another requires about 10× more substrate to achieve the same response as testosterone. A third compound is essentially an inactive reservoir form — sulfated and 10,000× less active than testosterone at the AR. Rank the following from HIGHEST to LOWEST AR affinity:
B. AR affinity rank (highest → lowest): DHT > testosterone > androstenedione > DHEA > DHEA-S. DHT is ~2–3× more potent than T because its 5α-reduced A-ring binds AR more tightly and dissociates more slowly. DHEA and androstenedione are weak androgens — they are precursors/reservoirs; the PERIPHERAL conversion of DHEA → testosterone → DHT is what actually drives masculinization in most tissues. DHEA-SULFATE is essentially inactive at AR (the sulfate blocks receptor interaction) — it serves as an abundant, slowly-cleared adrenal reservoir that local tissues can desulfate as needed.
Question 3 of 5 — LO 2 · Estrogen Rank & Pregnancy
A 30-year-old woman is at 32 weeks of a healthy pregnancy. Her 24-hour urine shows markedly elevated metabolites of three estrogen species. The three estrogens are present at very different concentrations and bind the estrogen receptor with very different affinities. Which statement best describes the relative ER affinity and physiologic relevance of the three estrogen species?
AEstradiol is strongest & the dominant form pre-menopause; estrone rises post-menopause; estriol is the weakest but is the dominant estrogen of pregnancy (made in placenta from fetal adrenal DHEA-S)
BEstriol is the strongest form and is dominant pre-menopause
CAll three estrogens bind ER with equal affinity
DEstrone binds ER ~10× more tightly than estradiol
EEstriol is dominant pre-menopause and estradiol dominant in pregnancy
A. LO 2 estrogen hierarchy: estradiol (E2) > estrone (E1) > estriol (E3) by ER affinity. Pre-menopause: ovarian granulosa cells make predominantly E2 (strongest). Post-menopause: ovaries stop making E2 → peripheral aromatization of adrenal androstenedione in fat produces predominantly E1 (which is why obesity in postmenopause is a risk factor for estrogen-dependent cancers). Pregnancy: a fetus cannot make estrogens directly because the fetal adrenal lacks 3β-HSD; instead the fetal adrenal makes DHEA-S, which the placenta aromatizes to E3 — making estriol the marker of fetal well-being. E3 is only weakly active at ER but overwhelms by sheer concentration in pregnancy.
Question 4 of 5 — LO 2/5 · SHBG & Free Testosterone
A 45-year-old man with BMI 40 and type 2 diabetes presents with loss of libido and erectile dysfunction. Labs: total testosterone 450 ng/dL (low-normal, reference 300–1000), SHBG 12 nmol/L (low, reference 15–50), calculated free testosterone 45 pg/mL (low, reference 70–160). His insulin resistance is pronounced. Which statement best explains why his free testosterone is disproportionately LOW given a relatively preserved total testosterone?
AObesity / hyperinsulinemia suppress hepatic SHBG synthesis, reducing the bound reservoir so the free fraction decreases even when total remains normal
BSHBG is upregulated by estrogen, which is low in obese men
CPeripheral aromatization increases free testosterone by displacing it from SHBG
DTestosterone is inactivated before it can be measured
ELow SHBG increases DHT conversion, which is measured instead
A. LO 2 + LO 5 integration. SHBG (sex hormone-binding globulin) binds testosterone (with highest affinity), DHT, and estradiol — about 60–70% of circulating testosterone is SHBG-bound (and ~30% weakly bound to albumin; only ~2% FREE). Insulin SUPPRESSES hepatic SHBG synthesis, so hyperinsulinemic states (obesity, T2DM, metabolic syndrome) have low SHBG. The direct effect: less bound testosterone reservoir + faster clearance → lower free testosterone and true hypogonadism symptoms, despite total testosterone sometimes measuring in the "low-normal" range. Conversely, ESTROGEN (pregnancy, OCP, liver disease) increases SHBG → high total, normal free T.
Question 5 of 5 — LO 1/2 · Testosterone → DHT Target Tissue Specificity
A 24-year-old genetic male raised as female presents at age 13 with spontaneous virilization at puberty (deepened voice, growth of the phallus, development of muscle mass). DNA shows 46,XY karyotype and homozygous 5α-reductase 2 deficiency. Testosterone level is high-normal for an adolescent male. Which feature is this individual most likely to LACK, despite normal pubertal virilization?
APubic hair
BDeepening voice
CProstate enlargement and male-pattern balding
DGrowth of the phallus at puberty
ESpermatogenesis
C — Prostate enlargement and male-pattern balding. LO 1/2 clinical integration. The androgens have tissue-specific receptor requirements: testosterone alone drives internal male genital structures (Wolffian duct → epididymis, vas, seminal vesicles), muscle, voice deepening, and spermatogenesis. DHT (5α-reduced) is required for external genitalia in utero (penis, scrotum), prostate growth, sebaceous gland activity, and male-pattern hair (both androgenic alopecia AND beard/body hair). Patients with 5α-reductase 2 deficiency are born phenotypically female (no DHT for external genitalia in utero), but virilize at puberty when testosterone rises enough to activate AR directly — yet they have life-long absent prostate growth and retain a full hairline. Finasteride/dutasteride clinically exploit this (5α-reductase inhibitors for BPH and alopecia).
Block 2 — Sources & Biosynthesis
5 questions · LOs 3, 4
⏱
07:30
Block Timer
Instructions: Select the single best answer. Block 2 focuses on the two-cell-two-gonadotropin model, the fetal-placental unit, aromatase, and 5α-reductase physiology + pharmacology.
Question 1 of 5 — LO 3 · Two-Cell Two-Gonadotropin Model
A medical student draws the follicular steroidogenesis diagram for her friend. She labels "Cell A, which receives LH stimulation, makes androstenedione because it has all the enzymes up to 17,20-lyase but LACKS aromatase." She labels "Cell B, which receives FSH stimulation, expresses aromatase and converts androstenedione into estradiol." What are Cell A and Cell B?
AA = ovarian theca interna · B = ovarian granulosa cells
BA = ovarian granulosa cells · B = ovarian theca interna
CA = Sertoli cells · B = Leydig cells
DA = corpus luteum · B = ovum
EA = adrenal ZR · B = ovarian theca interna
A.Two-cell, two-gonadotropin theory: Theca interna expresses LH receptor + 17α-hydroxylase + 17,20-lyase (CYP17) but lacks aromatase → makes and exports androstenedione. Androstenedione diffuses to adjacent granulosa cells, which express FSH receptor + aromatase (CYP19) but lack CYP17 → they convert androstenedione → testosterone → estradiol (E2). This cooperative architecture is the physiologic basis for the FSH + LH requirement for ovarian estrogen synthesis. In the MALE analog, Leydig cells are theca-equivalent (LH-driven androgen synthesis) and Sertoli cells are granulosa-equivalent (FSH-driven, aromatase-expressing, androgen-binding-protein-making).
Question 2 of 5 — LO 3/4 · Placental Estriol & Fetal-Placental Unit
A pregnant woman at 20 weeks gestation has routine quad-screen testing. Maternal serum estriol is very low, and quad-screen shows trisomy-21 risk elevated. A maternal-fetal medicine specialist explains that estriol synthesis requires a functional fetal adrenal cortex and a functional placenta in sequence. Which chain of events best explains why fetal adrenal aplasia or fetal anencephaly causes low maternal estriol?
AFetal adrenal makes DHEA-S → placenta desulfates and aromatizes DHEA-S → estriol (E3) → crosses back to mother
BPlacenta makes DHEA-S → fetal liver aromatizes → estriol crosses to mother
CMaternal adrenal makes DHEA-S → maternal liver aromatizes → estriol
DPlacenta makes cortisol → aromatization → estriol
EFetal liver makes cholesterol → fetal adrenal makes estriol directly
A — Fetal adrenal + placental enzymes cooperate. LO 3 placental unit detail. The placenta expresses aromatase (CYP19) but LACKS CYP17 — so it cannot make androgens from scratch. The fetal adrenal lacks 3β-HSD in its fetal zone — so it cannot make estrogens or cortisol from scratch but abundantly produces DHEA-S. DHEA-S travels to the placenta, which desulfates and aromatizes it to estriol (E3). That estriol crosses back to the maternal circulation. Anencephaly / fetal adrenal hypoplasia / Smith-Lemli-Opitz all cause low maternal estriol because no fetal precursor arrives at the placenta.
Question 3 of 5 — LO 4 · Aromatase Deficiency / Excess
A 46,XX newborn presents with ambiguous genitalia (clitoromegaly, partial fusion). Her mother developed progressive virilization during the pregnancy (deepening voice, acne, hirsutism) that resolved after delivery. Labs on the child: androstenedione and testosterone high; estradiol low; LH/FSH elevated when tested at puberty; tall stature with delayed epiphyseal closure; osteoporosis in adulthood. Which enzyme deficiency best explains this picture?
AAromatase (CYP19)
B5α-reductase
C17β-HSD
D21-hydroxylase
EP450c17 (17α-hydroxylase / 17,20-lyase)
A — Aromatase deficiency. Unique clinical footprint from LO 4: virilization of 46,XX infant (no conversion of maternal/fetal androgens to estrogens → androgen excess reaches the baby), virilization of the MOTHER in utero (same reason — fetal androgens cross placenta without being aromatized), tall stature, delayed epiphyseal fusion, and osteoporosis (estrogen is the PRIMARY closer of epiphyseal plates and the bone-protective sex steroid in BOTH sexes — recall the XY aromatase-deficient male phenotype of severe osteoporosis despite normal testosterone). Aromatase excess has the mirror picture: male gynecomastia and tall-then-short stature from premature closure. Clinically: aromatase inhibitors (anastrozole, letrozole) treat ER+ postmenopausal breast cancer by cutting off peripheral estrogen production.
Question 4 of 5 — LO 3/4 · DHEA-S as Adrenal Tag
A 32-year-old woman presents with 6 months of hirsutism, deepening voice, and clitoromegaly. Her menses have become irregular. Testosterone is 280 ng/dL (reference <70). DHEA-S is 1,200 µg/dL (markedly elevated; reference <400). Ovarian ultrasound is normal. Which source of androgen excess is most likely?
C — Adrenal tumor. Critical LO 3 source-of-origin test: DHEA-sulfate is produced almost exclusively by the adrenal zona reticularis. A markedly elevated DHEA-S localizes an androgen source to the ADRENAL, not the ovary. Ovarian androgen-secreting tumors (arrhenoblastoma, B) typically produce testosterone / androstenedione with normal/low DHEA-S. PCOS (A) usually has mildly elevated testosterone + mildly elevated DHEA-S but rarely this high. CAH non-classic (D) elevates 17-OHP, and can elevate DHEA-S but not dramatically without other features. DHEA-S is your fastest localizing test for hyperandrogenism source in a woman.
Question 5 of 5 — LO 4 · Steroid Biosynthesis Blockade (Finasteride)
A 60-year-old man with benign prostatic hyperplasia (BPH) is started on finasteride 5 mg daily. Over 6 months his prostate volume decreases, nocturia improves, and male-pattern hair loss slows. His serum testosterone is unchanged or slightly higher, but his serum DHT drops by ~70%. Which enzyme does finasteride block?
AAromatase
B5α-reductase (type II predominantly)
C17β-HSD
D3β-HSD
E17,20-lyase
B — 5α-reductase (type II). LO 4 pharmacology: 5α-reductase converts testosterone → DHT in the prostate, skin (hair follicles, sebaceous glands), and genital tissues. Type II is the dominant isoform in prostate and hair follicles. Finasteride (type II selective) and dutasteride (type I + II) block this conversion → shrinks the prostate and slows androgenic alopecia. Testosterone rises slightly because the DHT-mediated feedback on LH is reduced. Side effects track with DHT deficiency: decreased libido, erectile dysfunction in some men. Note that 5α-reductase deficiency as a natural gene defect was covered in Block 1 Q5 — finasteride pharmacologically mimics that phenotype.
Instructions: Select the single best answer. Block 3 integrates SHBG physiology, the nuclear-receptor mechanism for sex steroids, and clinical SERM / aromatase-inhibitor / clomiphene pharmacology.
Question 1 of 5 — LO 6 · Androgen Receptor Mechanism
A researcher treats prostate epithelial cells with radiolabeled DHT. Within 30 minutes, she observes: (1) DHT binds a cytoplasmic ~110 kDa receptor that is in complex with HSP90 before ligand binding. (2) DHT-receptor dimerizes and translocates to the nucleus. (3) The complex binds palindromic AREs on DNA upstream of prostate epithelial genes. (4) Transcription increases. This sequence matches which broad receptor class?
AMembrane G-protein coupled receptor
BReceptor tyrosine kinase
CCytoplasmic/nuclear steroid receptor family
DLigand-gated ion channel
ECytokine JAK-STAT receptor
C — Nuclear/cytoplasmic steroid receptor. LO 6 directly. The androgen receptor (AR) is a member of the steroid-nuclear-receptor superfamily, along with GR, MR, PR, ER, VDR, and TR. Its unliganded form sits in the cytoplasm in an HSP90 chaperone complex. Binding of DHT or testosterone → conformational change → HSP90 release → dimerization → nuclear translocation → binds androgen response elements (AREs) in target DNA → recruits coactivators + RNA polymerase → transcription. The mechanism is slow (30 min–hours) compared with GPCRs or RTKs, which is why sex-steroid effects unfold over days to weeks.
Question 2 of 5 — LO 6 · Complete Androgen Insensitivity Syndrome (CAIS)
A 16-year-old phenotypic female presents with primary amenorrhea. Examination: normal breast development, absent pubic and axillary hair, no uterus or ovaries on ultrasound, short blind-ending vagina, bilateral inguinal masses (found on imaging to be testes). Karyotype 46,XY. Labs: testosterone high for a male, LH high, estradiol appropriate for a female. Which molecular defect best explains the phenotype?
AAromatase deficiency
B5α-reductase deficiency
CLoss-of-function mutation of the androgen receptor
DAnti-Mullerian hormone receptor defect
ESRY deletion
C — Loss-of-function AR mutation (Complete Androgen Insensitivity Syndrome). Classic LO 6 disorder. Patients are 46,XY with functional testes making testosterone and AMH normally, but target tissues cannot respond to testosterone/DHT because AR is nonfunctional. Consequences: AMH is intact, so no uterus/fallopian tubes (Müllerian regression occurred). Testosterone can't virilize → external genitalia default to female phenotype. Aromatase peripherally converts the high testosterone into estradiol, which produces normal-appearing female breast development at puberty. No pubic/axillary hair is diagnostic — androgen-dependent hair requires functional AR. Gonads are intra-abdominal testes and need removal due to neoplastic risk.
Question 3 of 5 — LO 6 · SERMs & Tamoxifen Tissue Selectivity
A 55-year-old postmenopausal woman with ER+ invasive breast cancer is prescribed tamoxifen for adjuvant therapy. Tamoxifen blocks breast ER (desired), but the physician warns her that it STIMULATES endometrial ER and carries a ~2× risk of endometrial hyperplasia / carcinoma. Which best describes the mechanism of tamoxifen's tissue-selective behavior?
ATamoxifen is a pure antagonist in all tissues
BTamoxifen is a pure agonist in all tissues
CTamoxifen is a SERM — its ER-ligand complex recruits different coactivators/corepressors in different tissues, producing antagonist effect in breast but agonist effect in bone and endometrium
DTamoxifen irreversibly methylates ER
ETamoxifen is a membrane-receptor agonist
C — SERM (Selective Estrogen Receptor Modulator). LO 6 clinical extension. SERMs bind ER the same way in every tissue, but the ligand-induced conformation is intermediate, and the tissue-specific ratio of coactivators vs corepressors determines whether the final output is agonist or antagonist. Tamoxifen: antagonist in breast (treats ER+ breast cancer), agonist in bone (anti-osteoporotic), agonist in endometrium (risk of hyperplasia/cancer). Raloxifene: antagonist in breast AND endometrium, agonist in bone → no endometrial risk → used for postmenopausal osteoporosis. Clomiphene: antagonist at the hypothalamus → disinhibits GnRH/FSH/LH → induces ovulation. This is mechanism-based clinical choice.
Question 4 of 5 — LO 5 · Estrogen and Hepatic Protein Synthesis (OCP Effects)
A 24-year-old woman starts a combined oral contraceptive. After 3 months, repeat labs show: increased total T4, increased TBG, increased CBG, increased SHBG, mildly elevated factor levels (II, VII, IX, X, fibrinogen), and increased angiotensinogen. Her free T4, free cortisol, and free testosterone are all unchanged. Which of the following best explains the overall pattern?
AEstrogen directly upregulates hepatic synthesis of binding globulins and several coagulation factors, raising TOTAL but not FREE hormone levels and predisposing to clotting
BOCPs inhibit hepatic metabolism of TBG and coagulation factors
COCPs induce autoantibodies against binding proteins
DOCPs cross-react with the assays used
EProgesterone in the OCP downregulates binding globulins
A. LO 5 hepatic effects. Estrogen increases hepatic synthesis of binding proteins (TBG, CBG, SHBG) and procoagulant factors. Consequence: measured TOTAL levels of T4, cortisol, testosterone, estradiol all rise, while FREE (active) levels are physiologically unchanged because the binding reservoir expanded. This is the same mechanism as pregnancy. Clinically important: (1) Don't misinterpret high total T4 in a woman on OCP as hyperthyroid; check free T4 / TSH. (2) Increased clotting factors underpin the OCP-associated DVT / PE / stroke risk, especially with smoking, Factor V Leiden, or age >35. (3) Hepatic first-pass also relevant to why oral estrogens affect SHBG more than transdermal estrogens.
Question 5 of 5 — LO 5/6 · Clomiphene for Anovulatory Infertility
A 30-year-old woman with PCOS and anovulatory infertility is prescribed clomiphene citrate to induce ovulation. Clomiphene blocks ER in the hypothalamus; serum estradiol, normally providing negative feedback on the HPG axis, cannot signal effectively. Which downstream cascade best explains clomiphene's mechanism of ovulation induction?
BClomiphene blocks ER feedback at the hypothalamus → GnRH pulse frequency ↑ → FSH and LH ↑ → follicle recruitment and LH surge
CClomiphene is converted to testosterone → direct ovarian stimulation
DClomiphene is an aromatase inhibitor that raises intraovarian androgens
EClomiphene directly activates LH receptor on theca cells
B. LO 5 (hormone negative feedback) + LO 6 (ER signaling) combined into a classic reproductive pharmacology vignette. Clomiphene is a SERM: at the hypothalamus it acts as an ER antagonist, so physiologic estradiol feedback is blocked. The hypothalamus "thinks" estrogen is low → increases GnRH pulse frequency → pituitary secretes more FSH + LH → FSH drives follicle maturation → dominant follicle emerges → LH surge → ovulation. Letrozole (an aromatase inhibitor, D) is also used for ovulation induction now and may have slightly better live-birth rates in PCOS — it works differently by reducing peripheral E2 enough to disinhibit the HPG axis. Both exploit the estrogen-negative-feedback pathway therapeutically.
Source review. Every item below was pulled from your 3rd Party Biochem + Physio folders and hand-mapped to END05 Sex Steroid Synthesis & Action LOs — C21/C19/C18 classes, sources (gonad vs adrenal vs placenta), biosynthesis pathways, carrier proteins & half-life, and nuclear-receptor mechanisms of action. Grouped by LO to complement — not duplicate — the in-house exam Blocks 1-3 above.
Legend:BRS BiochemBRS PhysioWaite & Sheakley
Group A · Physiology & Source Mapping (LOs 2, 3, 4)
Ext Q1 — LO 3/4 · DHT and Male External Genitalia — BRS Physio Ch 32 Q23
During fetal development, the formation of male genitalia is directly stimulated by:
ATestosterone
BDihydrotestosterone
CDehydroepiandrosterone
DAndrostenedione
EEstrone
B — DHT. LO 3 source + LO 4 conversion. In utero, the testes produce testosterone, which is converted by 5α-reductase 2 to DHT in the primitive external genital tissue. DHT drives formation of the penis, scrotum, and prostate (external structures). Testosterone itself drives INTERNAL male structures (Wolffian duct derivatives — epididymis, vas deferens, seminal vesicles). 5α-reductase 2 deficiency = female external phenotype at birth with internal male structures, virilization at puberty when high testosterone activates AR directly.
The pubertal growth spurt is mainly stimulated by the hormone:
ACalcitonin
BVitamin D
CEstradiol
DTestosterone
EDihydrotestosterone
C — Estradiol. Counterintuitive but tested: estradiol is the primary driver of linear growth AND epiphyseal closure in BOTH sexes. In boys, the high testosterone at puberty is aromatized to estradiol, which acts at the growth plate to both stimulate growth AND ultimately close the epiphyses. Aromatase-deficient 46,XY males (from Block 2 Q3) are extremely tall with delayed epiphyseal fusion and severe osteoporosis — proving estrogen, not testosterone, is the bone hormone. Clinical aside: this is why aromatase inhibitors used in pediatric endocrinology can prolong growth and why estrogen-dependent cancers are rare in aromatase-deficient men.
Conversion of androgens to estradiol by the follicular granulosa cells is stimulated by which hormone?
ALuteinizing hormone
BFollicle-stimulating hormone
COxytocin
DGrowth hormone
EProlactin
B — FSH. Two-cell two-gonadotropin model. LH acts on theca cells → androstenedione synthesis via CYP17. FSH acts on granulosa cells → upregulates aromatase (CYP19) → converts theca-supplied androstenedione to testosterone → estradiol. The cooperative architecture is why both FSH AND LH are needed for ovarian estrogen synthesis, and why in menopause (ovary reserves exhausted) the LH and FSH rise dramatically as feedback is lost.
The hormone inhibin has direct negative feedback effects on the release of:
AProlactin
BFollicle-stimulating hormone
CLuteinizing hormone
DTestosterone
EGonadotropin-releasing hormone
B — FSH. LO 3 regulatory feedback. Inhibin is made by granulosa cells (ovary) and Sertoli cells (testis) and selectively suppresses FSH at the anterior pituitary (without affecting LH). This gives an elegant selective feedback: if spermatogenesis or folliculogenesis is proceeding well, inhibin is high → FSH falls, but LH (and testosterone or estradiol) remains intact. Conversely in primary gonadal failure, inhibin falls → FSH rises (early sensitive marker). Estradiol and testosterone provide the broader negative feedback on GnRH / LH / FSH together.
Group B · Gonadotropin-Driven Sex Steroid Synthesis (LO 3)
A hormone is described as "Binds to receptors on Leydig cells."Which of the following matches this description?
ALuteinizing hormone (LH)
BProlactin (PRL)
CThyroid-stimulating hormone (TSH)
DGrowth hormone (GH)
EFollicle-stimulating hormone (FSH)
A — LH. LO 3 source identification: LH binds Leydig cells → stimulates testosterone synthesis. This is the male analog of LH binding theca cells to drive androstenedione in females. FSH binds Sertoli cells (male) / granulosa (female). The two-hormone cooperative logic applies in both sexes.
Ext Q6 — LO 3 · LH and the Corpus Luteum — BRS Biochem Q5
A hormone is described as "Stimulates the production of progesterone by the corpus luteum."Which of the following matches this description?
ALuteinizing hormone (LH)
BProlactin (PRL)
CThyroid-stimulating hormone (TSH)
DGrowth hormone (GH)
EFollicle-stimulating hormone (FSH)
A — LH. After the LH surge triggers ovulation, the residual follicle luteinizes into the corpus luteum, which continues to receive tonic LH support during the luteal phase → produces progesterone (and estradiol). When pregnancy does not occur, LH falls → corpus luteum regresses → progesterone falls → menstruation. In early pregnancy, hCG (which structurally resembles LH at the LH/CG receptor) maintains the corpus luteum until ~week 8-10, when the placenta takes over progesterone production ("luteal-placental shift").
A hormone is described as "Stimulates the production of estradiol by the immature ovarian follicle."Which of the following matches this description?
ALuteinizing hormone (LH)
BProlactin (PRL)
CThyroid-stimulating hormone (TSH)
DGrowth hormone (GH)
EFollicle-stimulating hormone (FSH)
E — FSH. FSH drives granulosa cell aromatase, which converts androstenedione (theca-derived, LH-driven) into estradiol (E2). This is the cooperative two-cell-two-gonadotropin process in the developing follicle. As the dominant follicle matures, its own granulosa cells make enough estradiol to drive the positive feedback switch that produces the mid-cycle LH surge → ovulation.
Group C · Disorders of Sex Steroid Synthesis (LOs 4, 6)
Ext Q8 — LO 4/6 · CAH as Virilizing Syndrome — BRS Biochem Q29
A female patient presents to her primary care doctor with thinning scalp hair, excessive facial hair, and high ACTH and low cortisol. The physician should seriously consider which of the following problems?
AA tumor of the anterior pituitary that produces abnormally large amounts of POMC
BA tumor of the adrenal medulla
CA genetic deficiency of an enzyme in the pathway for cortisol synthesis
DA mutation in CRH that decreases its production
EAn insulinoma
C — CAH enzyme deficiency. LO 4 from the sex-steroid angle: when an adrenal enzyme blocks cortisol synthesis, ACTH rises (no feedback) and drives precursors into the still-intact androgen pathway. In women, excess adrenal androgens → hirsutism, male-pattern balding, acne, virilization. Common culprits: 21-OH deficiency (non-classic form in adults, very common), 11β-OH deficiency (adds hypertension), 3β-HSD deficiency. Contrast with a POMC tumor (A) which would have HIGH cortisol (Cushing disease). DHEA-S is typically moderately elevated here, confirming the adrenal origin.
A 69-year-old man has been feeling lethargic; blood work reveals testosterone 168 ng/dL (low). Which row best represents the properties of testosterone?
Precursor to Receptor Estradiol is Represses GC Stimulates more potent? location precursor? synthesis? GnRH release? A. No Cytoplasm Yes Yes No B. No Nucleus No Yes Yes C. Yes Nucleus No No Yes D. Yes Cytoplasm Yes No Yes E. Yes Nucleus No No No
ARow A
BRow B
CRow C
DRow D
ERow E
E. Covered in Block 1 Q5 and Block 3 Q1. Testosterone IS reduced to DHT (the more potent androgen → "Yes" for precursor). It binds the INTRACELLULAR AR (classic steroid-receptor family, cytoplasmic/nuclear — the chart considers the ACTIVATED location = nucleus). Testosterone is a PRECURSOR of estradiol (not the other way around → "No"). It does NOT repress glucocorticoid synthesis. It INHIBITS GnRH release (negative feedback → "No" for "stimulates"). Row E matches.
Ext Q10 — LO 4 · Anti-17α-Hydroxylase & Sex Steroid Loss — Waite & Sheakley Q38
A 15-year-old girl presents with primary amenorrhea, hypernatremia, hypokalemia, hypertension, and hyperpigmentation. Autoantibodies blocking the function of a key steroidogenic enzyme are identified. Which autoantibody explains the combined loss of cortisol + sex steroids with mineralocorticoid excess?
AAnti-thyroglobulin
BAnti-thyroid peroxidase
CAnti-TSH-receptor
DAnti-17α-hydroxylase (CYP17)
EAnti-21β-hydroxylase
D — Anti-17α-hydroxylase. LO 4 bridging with end04. CYP17 performs TWO functions: 17α-hydroxylation (needed for cortisol) and 17,20-lyase (needed for sex steroid precursors DHEA/androstenedione). Losing CYP17 simultaneously kills cortisol synthesis AND ALL sex steroid synthesis (estrogens and androgens). ACTH rises (no cortisol feedback) → drives the remaining intact mineralocorticoid path → DOC/corticosterone excess → HTN, hypokalemia, hypernatremia and MSH from POMC → hyperpigmentation. The sex-steroid loss explains primary amenorrhea and absent sexual development in females, and severe undermasculinization in 46,XY karyotypes. Classic "HTN + absent puberty" pattern.
Performance Dashboard
—
Total Score
—
Block 1 — Classes & Affinity
—
Block 2 — Sources & Biosynthesis
—
Block 3 — Transport & Action
—
3rd Party Bank
Question-by-Question Breakdown
Answer questions in the Exam Blocks to see your breakdown here.