First Pass Miss Flashcards
What type of receptors do TGFbeta, activin, and inhibin use?
They all use serine/threonine kinase receptors which traverse the transmembrane domain
What hormones stimulate and inhibit prolactin secretion in the posterior pituitary?
Prolactin is continuously secreted on a basal level unless it is inhibited. There is no dedicated releasing hormone, but are things which loosely stimulate it.
Stimulate: Estrogen, thyroid releasing hormone (TRH)
-> galactorrhea and infertility in primary and secondary hypothyroidism
Inhibit: Dopamine (PHIH)
Remember, many symptoms of prolactinoma are due to PRL decreasing GnRH
What structures are most likely to be directly affected by pituitary tumors?
Structures directly adjacent to the sella turcica
- Cavernous sinus - directly adjacent, includes distal portions of internal carotid arteries, cranial nerves 3, 4, V1/V2, and 6, with 6 most likely to be damaged.
- Optic chiasm -> sits directly above sella
- Sphenoid sinus
- Diaphragma sellae, sits above and prevents CSF access into the sellae -> damage = empty sellae
What hormones are produced more in the lateral vs medial portions of the anterior pituitary and why does this make sense?
Lateral - GH / PRL
Medial - TSH / ACTH
-> makes sense because stress hormones and metabolic hormones are more critical to life
What cell lines are derived from somatotroph stem cells?
Thyrotrophs, mammosomatrophs, and somatrophs
What is a functional vs nonfunctional pituitary adenoma? What nomenclature is used with the latter?
Functional - can secrete hormone and produces symptoms based on this
Nonfunctional - may or may not be producing hormone, but will have no symptoms caused by hormones. This could also be due to a loss in end-organ response.
These are described as “silent”. I.e. silent corticotroph adenoma.
What is Cushing’s syndrome vs Cushing’s disease?
Cushing’s syndrome - syndrome of features associated with prolonged exposure to cortisol
Cushing’s disease - Cushing’s syndrome due to ACTH oversecretion by anterior pituitary (may be due to pituitary or hypothalamic dysfunction)
What is an invasive adenoma? Why does this matter?
Tumors showing gross tumor invasion into the dura or bone
Increased likelihood of recurrence. But remember, these cannot metastasize (these are benign adenomas).
Atypical -> increased proliferation
Pituitary carcinoma -> very rare, characterized by presence of local or systemic metastasis.
What is lymphocytic hypophysitis and what causes it?
Autoimmune inflammation of adenohypophysis caused by infiltration of lymphocytes, leading to destruction of anterior pituitary with fibrosis.
Usually occurs in women during late pregnancy or shortly after delivery
What is primary vs secondary empty sella syndrome and who does it occur in? How does it present?
Primary - protrusion of a diverticulum of arachnoid membrane into sella. Occurs in middle-aged women, often with obesity and hypertension (same demographic as pseudotumor cerebri) -> presents as headache.
Secondary - pituitary fails to take up entire space of sella which allows CSF to seep in, follows surgical resection, apoplexy, or radiation treatment of sellar tumor
What is the most common sellar tumor in children and what might is be confused with?
Craniopharyngioma - a tumor derived from Rathke’s epithelium
May be confused with pituitary adenoma -> both present with headache, hypopituitarism, and bitemporal hemianopsia
What does the pathology of craniopharyngioma look like?
“Adamantinomatous” - squamous epithelium which appears cystic due to fluid accumulation between squamous epithelial cells.
Calcification is extremely common (remember pathoma’s mnemonic about this being derived from mouth and teeth have calcium).
“Wet keratin” - keratin pearls appear overly plump.
What is a chordoma? Where does it occur? Who tends to get it?
A moderately malignant tumor derived from embryonic notochord - type of sarcoma.
Arises in sacrum (nucleus pulposus) or spheno-occipital bones (typically around the clivus of the occipital bone) typically in middle-aged men.
Physaliphorous cells - prominent vacuolization of cells as they produce extracellular matrix resembling cartilage + myxoid stroma
Pituitary dysfunction, CN3 involvement, or headaches
How do men and women present differently with prolactinoma?
Women - present early when it is still a microadenoma (<1cm) with galactorrhea (not pathognomonic), amenorrhea, or oligomenorrhea (if you have irregular periods, should always check). Often presents with decreased bone density due to decreased estrogen.
Men - Present with macroadenoma (>1 cm), present very late because they do not seek medical attention for gonadal dysfunction. Typically present with visual field defects / headaches.
What are some causes of hyperprolactinemia which are not prolactinoma?
- Estrogens - i.e. pregnancy or birth control pills -> number one cause of lactotroph hyperplasia
- Primary hypothyroidism - Increased TRH levels stimulate PRL
- D2 antagonist antipsychotics
- Cocaine use -> depletion of central dopamine stores
What are the common causes of death in acromegaly / what important conditions are they at greater risk for?
Congestive heart failure -> most common cause of death
Patients also have increased relative risk of colon and breast cancer
-> IGF-1 has a permissive effect in tumorigenesis
Other symptoms you might not remember: arthritic joint complaints, hyperhidrosis
-> may present early as obstructive sleep apnea (large tongue) or carpal tunnel syndrome
What is the most common cause of congenital hypopituitarism? What hormones will be low?
Mutation in Pit-1, which causes failure of differentiation of somatotroph stem cells, and subsequent failure to deevelop lactotrophs, somatotrophs, and thyrotrophs (see Kupsky lecture)
-> PRL, GH, and TSH will be low, with relative preservation of ACTH and LH/FSH
What are the symptoms of pituitary apoplexy?
- Sudden onset severe headache
- Visual disturbance -> bitemporal hemianopia
- Diplopia due to CN3 palsy
- Features of hypopituitarism -> i.e. emergent cortisol insufficiency leading to hypotension
It is a medical emergency.
-> usually occurs in the setting of pre-existing pituitary adenoma
What are the presenting symptoms of Sheehan syndrome?
Failure to lactate -> loss of prolactin secretion
Absent menstruation / loss of pubic hair -> failure of LH / FSH secretion
Cold intolerance -> loss of TSH
What role does testosterone have in epiphyseal closure?
It leads to the closure of epiphyseal plates in puberty because estrogen is made from testosterone (requires aromatase).
Formation of estrogen closes epiphyseal plates. The estrogen is also what accounts for the bone-forming / massforming effect of testosterone.
How is testosterone transported and what form is readily bioavailable? How does this differ from males and females?
98% is transported via sex hormone binding globulin (SHBG) and albumin in both males and females
Only free and albumin-bound testosterone are bioavailable. Males have less SHBG binding and more albumin-binding relative to females -> higher circulating levels of bioavailable testosterone.
(Note: estrogen stimulates synthesis of SHBG to make this happen)
What are the physical features of Klinefelter syndrome and what is it?
Syndrome of extra X chromosome
Testicular atrophy / fibrosis -> small testes (pre-pubertal size) with seminiferous tubular sclerosis and rare Sertoli cell / sperm. -> infertility
Eunuchoid body shape + gynectomastia -> feminization of features (increased estrogen to testosterone ratio, leads to decreased testosterone availability)
Disproportionately long arms / legs.
Increased FSH and LH due to lack of feedback from inhibin B (sertoli) and testosterone (leydig). Estrogen magically increased due to increased relative sertoli cell function with aromatase.
What are some acquired causes of primary hypogonadism?
- Mump orchitis in adulthood
- Radiation / chemotherapy - germ cells are very sensitive
- Ketoconazole
- Testicular torsion
- Hemochromatosis - (secondary)
- Autoimmune damage
- Chronic systemic diseases i.e. cirrhosis, renal failure, aids
- Aging - decline in Leydig cell number / volume, blood supply, decreased testosterone and number of Sertoli cells
What is male gonadal dysgenesis and what causes it? What is the associated risk increase?
Mutation in SRY
Patient will have streak gonads and female type external genitalia, with Mullerian duct development
-> associated with high risk of malignant transformation of the gonads
Other than Kallman syndrome, what other congenital conditions are associated with lack of GnRH?
Prader-Willi
-> both are more associated with obesity
Laurence-Moon-Bardet-Biedl
-> associated with retinitis pigmentosa and polydactyly as well
What are the differential effects of primary vs secondary hypogonadism in the first trimester?
Primary - can lead to a spectrum of pathology, from development of female external genital to partial virilization with hypospadias (depend on degree of T deficiency)
Secondary (problem not at the level of the testes) - Differentiation of external genitalia will be completely normal because testosterone production is driven by placental HCG in the first trimester (HCG is homologous to LH)
What happens if androgen deficiency onsets prior to puberty?
Lack of virilization and Tanner development (lack of puberty), as well as development of Eunuchoid habitus (long arms / legs), poor muscle mass development / reduced peak bone mass
What are the side effects of using testosterone to treat hypogonadism? What is the contraindication?
- Acne
- Gynecomastia (increased estrogens)
- Testicular atrophy (from suppression of FSH/LH)
- Polycythemia / hyperviscosity syndrome -> testosterone increased RBC mass
Contraindicated in men with KNOWN prostate cancer
What will the lab values be for 5alpha reductase deficiency?
Normal estrogen/testosterone levels, LH may be normal or elevated.
-> testosterone is responsible for negative feedback in the pituitary
Main thing: Increased testosterone to DHT ratio. Testosterone levels are not high enough until puberty to stimulate the development of external genitalia (DHT has much higher affinity than T for same receptor which allows it to do dis early on)
What is balanoposthitis and how can it be prevented?
Infection of glans penis + prepuce
-> can be prevented with circumcision, since it is generally due to poor local hygiene in uncircumcised penis getting infected
What is Bowen disease vs erythroplasia of Queyrat?
Both are forms of squamous cell carcinoma in situ
Bowen disease - occurs on penile shaft or scrotum and appears as leukoplakia
erythroplasia of Queyrat - occurs on glands penis as shiny red or velvety plaques
What is Bowenoid papulosis and how is it different from Bowen disease?
Bowenoid papulosis is SqCC in situ which occurs in younger patients (<40 years) and presents as multiple pigmented reddish papules.
-> will NOT progress to invasive carcinoma
Bowen disease - happens in older patients, more frequently progresses to invasion
What controls the descent of the testes / what are the two phases? What happens if this fails and where does this usually occur?
- Transabdominal phase - controlled by Mullerian-inhibiting factor of Sertoli cells
- Inguinoscrotal phase - through inguinal canal, controlled by androgens
If this fails -> Cryptorchidism. Usually the testes are found in the inguinal canal.
What are the two age groups which get testicular torsions and why do they occur (defect?)?
- Neonates - in utero or shortly after birth, not associated with any developmental abnormality
- Adolescents - occur due to bell-clapper abnormality -> tunica vaginalis does not stop posteriorly but entirely wraps around testes, allowing for increase mobility of testicle.
Abnormality is often bilateral and needs to be fixed surgical when one presents
Acute severe pain and absent cremasteric reflex without inciting trauma
What tends to cause orchitis is young adults vs older adults?
Young adults - Chlamydia trachomatis, Neisseria gonorrhoeae
-> STDs
Older adults - E. coli and Pseudomonas -> as a result of ascending UTIs
These are the same as the causes for acute prostatitis
What is the most common category of all testicular tumors and how does this relate to how we tend to treat testicular tumors? Who tends to get them?
Germ cell tumors -> represent 95% of all testicular tumors. These are usually malignant and as a result we tend to resort to radical orchiectomy as empiric treatment
These commonly occur in young men (15-40)
What are the two subgroups of germ cell tumors and what does this mean?
- Germ cell neoplasia in situ (GCNIS)-derived
and - non-GCNIS
These are seminoma-like cells (germ cells) with large nuclei, clumped chromatin, and prominent nucleioli along the basememnt membrane of seminiferous tubules. These cells are positive for embryonic stem cell marker OCT3/4
What tumors fall into non-GCNIS derived?
- Spermatocytic tumor - >65 years, 3 distinct cell populations, looks like seminoma, rarely metastasizes
- Prepubertal Yolk sac tumor -> most common testicular tumor in boys <3 years
- Prepubertal teratoma -> will be mature, only type of benign teratoma in men
How does seminoma appear grossly? Who tends to get it?
Homogenous, lobulated gray-white mass with no hemorrhage or necrosis. Lobules are made via delicate fibrous stroma infiltrated by T cells.
Gotten by young men in their 30s. NEVER in infancy.
How does embryonal carcinoma differ from seminoma grossly and prognostically?
It is grossly much more poorly demarcated and punctuated by foci of hemorrhage and/or necrosis, more painful than seminoma.
It is composed of primitive epithelial cells forming glands and papillary structures
It has a much worse prognosis than seminoma because it can rapidly hematogenously disseminate
What marker do embryonal carcinoma stain positive for, and what are they commonly mixed with / how does this affect their markers which are elevated in serum?
EC is positive for CD30
Commonly mixed with yolk sac tumors, so can also cause elevated alpha-fetoprotein (AFP levels)
Also, like seminomas they can have syncytiotrophoblasts and have elevated hCG.
What are yolk sac tumors also called and who tends to get them? What is the prognosis in this group?
Also called endodermal sinus tumors
Tends to occur in children. It is the most common testicular tumor in children <3 years. In this age group, it is a pre-pubertal YST which is non-GCNIS derived and has an excellent prognosis (pure form of yolk sac tumor).
Schiller-Duval bodies - glomeruloid
Yellow, mucinous grossly
Are pure choriocarcinomas common? And what is their pattern of infiltration? What cell types make them up?
Made of syncytiotrophoblasts and cytotrophoblasts which produce beta-HCG.
Pattern of infiltration is formation of small tumors with rapid hematogenous spread around the body (since trophoblast cells have a tropism towards blood cells)
They are rare in their pure form, tend to be expressed in another form of germ cell tumor (i.e. seminoma, embryonal carcinoma)
What symptoms do patients with choriocarcinoma often have and why?
Often have symptoms of hyperthyroidism or gynecomastia
-> alpha subunit of hCG is structurally similar to LH, FSH, and TSH
How do testicular cancers tend to spread?
Seminomas tend to spread via para-aortic lymph nodes before hematogenous.
Non-seminoma GCNIS derived tend to present at a later stage via metastasis with hematogenous routes very early.
How does a Leydig cell tumor present?
Produces androgens so:
Prepubertal boys -> presents as precocious puberty
Adults -> Presents as gynecomastia (excess testosterone gets converted to estrogen)
Reinke crystals - rod-shaped eosinophilic cytoplasmic inclusions with unknown function
Appears very yellow with clear, vacuolated cytoplasm
What is a Sertoli cell tumor also called? What does it look like microscopically and what is its clinical behavior?
Androblastoma
- > looks like tall columnar cells forming cords -> immature seminiferous tubules
- > Usually benign and clinically silent (does not produce enough androgen to be significant)
What is the most common form of testicular tumor in men over the age of 60 and what is its behavior? Is it a primary tumor?
Testicular lymphoma - usually a diffuse B cell lymphoma
- > very aggressive with a poor prognosis
- > It is a secondary tumor arising elsewhere
What causes chronic prostatitis and how will the symptoms differ?
May or may not be UTI related, but often cultures of prostatic secretions are negative despite showing lymphocytic inflammatory infiltrate.
More likely to present with lower back pain.
What are the secondary complications which may occur due to BPH? What can be done to surgically correct this problem?
Distention and hypertrophy of bladder (Due to increased resistance), hydronephrosis (due to backflow of urine), recurrent UTIs
Surgically correct with TURP - transurethral resection of the prostate
BPH is caused by increased age-related conversion of testosterone to DHT
What is the growth pattern of prostate adenocarcinoma?
Small, invasive glands with prominent nucleoli. Basal cell layer is lost.
Tends to show perineural invasion
What is the most common site of metastasis for prostate cancer and how does this show up on labs?
Lumbar spine or pelvis -> osteoblastic metastasis which presents as lower back pain.
Serum alkaline phosphatase will go up (osteoblastic activity marker) as well as prostatic acid phosphatase (PAP)
What are Gleason groups and what are they used for? What is the most useful prognosticator?
Groups of Gleason scores to indicate prognosis. There are groups 1-5 (probs don’t memorize):
Group 1: Score 6 Group 2: Score 7 (3+4) Group 3: Score 7 (4+3) Group 4: Score 8 Group 5: Scores 9-10
Most useful prognosticator is the Gleason score associated with the stage
What are some anti-androgens used in prostate cancer?
Leuprolide - continuous GnRH analog
Flutamide - competitive inhibitor at the androgen receptor
-> Flutes are anti-manly
Place the following in the correct order, and define them:
Growth spurt, adrenarche, pubarche, thelarche, menarche
What is the definition of precocious vs delayed puberty in females?
Thelarche - breast bud / breast growth Pubarche - pubic hair growth Adrenarche - axillary hair growth (A = axillary) Growth spurt - follow hair growth Menarche - first menstrual bleed
Precocious - Tanner Stage 2 at <8 years
Delay - Tanner Stage 1 at age 13, or no menses by age 16.
What are the most common causes of precocious pseudopuberty in boys and girls? What is this also called?
GnRH-independent puberty (peripheral puberty)
this is opposed to “true precocity” which is due to central GnRH overaction
Boys - Testicular tumor (either Leydig cell or choriocarcinoma secreting hCG)
Girls - Ovarian tumor (i.e. granulosa cell making estrogen)
What marker do primary follicles express, and what stage of Meiosis are they found in? When do they move on?
They express **anti-Mullerian hormone **-> can be used to track the development of the primary follicles
They are stuck in Prophase I of Meiosis I, they will move on when the corona radiata (inner layer of granulosa cells) stops delivering cAMP thru the zona pellucida (distinct mucopolysaccharide band) during the Graafian follicle stage -> secondary oocyte will arrest at Metaphase II until fertilization.
Metaphase til they “met” a sperm
What is going wrong hormonally in PCOS which accounts for the symptoms?
Hyperinsulinemia / insulin resistance alter the hypothalamic hormonal balance and cause:
- Increased LH:FSH ratio, which stimulates increased androgen production from theca interna cells –> hirsutism.
- High circulating androgen levels are converted to estrone via adipose tissue (these women are obese with insulin resistance) -> feedback by estrone decreases FSH levels secreted by anterior pituitary.
- Since FSH is low, androgens are not rapidly turned into estrogen via granulosa cells -> slowed rate of follicular maturation. This leads to small follicular cysts and anovulation -> infertility.
What are the pharmacologic treatments for PCOS?
- Weight reduction
- OCPs -> prevent endometrial hyperplasia due to unopposed estrogen (provide hormones exogenously)
- Clomiphene - infertility treatment which blocks estrogen receptor negative feedback in hypothalamus
- Metformin - to combat insulin resistance
- Spironolactone / ketoconazole -> block androgen receptor as well as production
- Statins - for treatment of metabolic syndrome.
What is the approximate age of onset of normal menopause, and what marker is specific for it?
Approximately 51 years (can be earlier in smokers)
Increased FSH levels are specific (loss of negative feedback on FSH due to decreased estrogen levels. This is due to decreased granulosa cells responding to FSH)
What is the source of estrogen in menopause, and what are the general symptoms to remember?
Peripheral conversion of androgen to estrogen. (LH stimulates the theca cells). These increased androgens can lead to hirsutism.
Remember HAVOCS:
Hot Flashes
Atrophy of ->
Vagina
Osteoporosis (first three from decreased estrogen)
Coronary Artery Disease
Sleep Disturbances (from hot flashes and night sweats)
What is the question you have to ask yourself when evaluating primary amenorrhea?
Is there normal development of female secondary sexual characteristics.
If NO -> hypogonadism, hyper or hypogonadotropic (as explained before)
If YES -> Mullerian anomalies, outflow obstruction, androgen insensitivity, or weight/exercise issue
Why do patients with Mullerian agenesis have primary amenorrhea? How will their gonads look?
Mullerian ducts give rise to fallopian tubes, uterus, and upper vagina.
- > uterus and upper vagina + fallopian tubes will be hypoplastic
- > usually variable uterus development and blind / short upper vagina
- > lower 1/3 of vagina formed via urogenital sinus and develops normally
What genitalia will those with androgen insensitivity have?
They have normal female external genitalia, but blind vagina / absent uterus / upper vagina (MIF secreted by Sertoli cells to inhibit Mullerian duct).
Wolffian / mesonephric duct not formed properly due to lack of testosterone response.
-> testes will be present with normal high circulating levels of testosterone for a male, the only difference is end-organ response
What is the first step in the algorithm for secondary amenorrhea (amenorrhea which has started after menarche)? What does a positive test mean?
Progesterone / progestin challenge test
- > Withdrawal bleeding 2-7 days after giving progesterone (and levels have dropped) indicates that there is a presence of estrogen, but ovulation and thus formation of corpus luteum has not been occurring
- > endometrium stuck in proliferative phase, never reaches secretory phase to turn over
Basically, withdrawal bleed = ANOVULATION, where estrogen is present
What do you do if there is no withdrawal bleed after the progestin challenge? What are the possible results?
Estrogen + Progesterone challenge
If bleeding -> reason for amenorrhea is low estrogen. Check FSH levels to see if gonadal failure or CNS failure.
If no bleeding -> uterus / anatomical outflow tract problem
How is the diagnosis of functional hypothalamic amenorrhea made, and is it common?
Low estrogen levels, with no withdrawal bleed from progestin challenge
It is one of the most common causes of amenorrhea
- Low weight (eating disorders like anorexia / bulimia) -> we said these are causes of anovulation as well
- Endocrine conditions (hypothyroid, hyperprolactinemia, diabetes)
Stress and exercise also contribute
-> results in ultimately low GnRH
What are the symptoms of trichomoniasis and how is it transmitted? How is it visualized?
It is an anerobic, flagellated protozoan which does NOT form cysts so it is sexually transmitted
Symptoms:
Pruritis with foul-smelling greenish discharge
Inflamed cervix: “Strawberry cervix”
Visualize as MOTILE via wet mounts.
What is chronic atrophic dermatitis also called and who tends to get it?
Lichen sclerosis (et atrophicus) -> commonly seen in postmenopausal women, with possible autoimmune etiology
atrophy of epidermis with sclerosis and thickening of underlying dermis
Primary cause of non-HPV related squamous cell carcinoma of the vulva
What is the hallmark of invasive cervical carcinoma and a feared complication?
Invasion of the stroma.
Often, it can invade anteriorly into the bladder wall, leading to ureteral obstruction
-> post-renal azotemia is a common cause of death in advanced carcinoma
What is “inadequate luteal phase” and how does it present?
Inadequate corpus luteal progesterone output
- > presents as infertility (many miscarriages due to underdeveloped decidua) with early dysfunctional uterine bleeding
- > underdeveloped glands relative to where they should be in the cycle
What is the hallmark of chronic endometritis and what are some common causes?
Plasma cells in the stroma as part of chronic inflammation, as lympocytes and macrophages are often present in endmetrial stroma
Causes: Pelvic inflammatory disease Retained gestational products IUDs TB -> will show granulomatous inflammation
What is the most common cause of dysfunctional uterine bleeding? Who tends to get it?
Anovulatory cycle
-> lack of ovulation occurs, so there is excessive estrogen stimulation of proliferative phase, leading to unscheduled breakdown of stroma
Common at menarche and in perimenopausal women (ovulation never occurred, so no secretory phase)
What is an endometrial polyp?
Masses of endometrial tissue which protrude into the endometrial cavity
-> overgrowth of endometrium with crowded glands and multiple proliferating cells
Causes painless abnormal uterine bleeding, associated with tamoxifen use
What discharge will be seen in acute endometritis and how is the situation remedied?
Purulent BLOODY discharge with many PMNs
- > removal of retained product removes nidus for infection
- > this is an organic cause of uterine bleeding
What proliferates in endometrial hyperplasia and what is the general underlying cause? How does it present?
Caused by a hyperplasia of endometrial GLANDS relative to stroma
Excess estrogen stimulation, i.e. obesity, estrogen replacement, anovulatory cycles, or polycystic ovarian syndrome (increased circulating estrone)
Presents as postmenopausal uterine bleeding
What does endometrial hyperplasia increased your risk for and what gene is associated with it?
Associated with inactivation of PTEN tumor suppressor gene (increased risk with Lynch syndrome)
-> increased risk for endometrial carcinoma (endometroid type) -> which is the most common gynecologic malignancy
What are the two ways in which endometrial hyperplasia is histologically characterized based on its growth? Which is more important?
- Simple vs complex
- > simple = glands look nice
- > complex = glands look complicated with many outpouchings and loss of stroma - Presence of absence of cellular atypia
- > nuclear atypia is more important
What is the other type of endometrial cancer and who tends to get it?
Sporadic endometrial cancer -> Type 2, occurs in older (POST-menopausal women, i.e. 70s/80s), no associatd with estrogen
- > Occurs in the setting of atrophic endometrium with no precursor lesion
- > early p53 mutations and very aggressive behavior
What is the most common form of sporadic endometrial carcinoma (Type 2) and what is seen on histology?
Serous carcinoma. Forms papillary structures which can necrose around fibrovascular cores, leading to psammoma body formation.
To remember it forms psammoma bodies, alot of people remember it as “papillary-serous carcinoma”
