TOPNOTCH MEDICAL BOARD PREP PATHO MAIN DIGITAL HANDOUT BY KEVIN ELOMINA, MD

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BENIGN PROSTATIC
HYPERPLASIA
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COMMON FORMS OF PROSTATITIDES

ACUTE BACTERIAL CHRONIC BACTERIAL CHRONIC ABACTERIAL
FEATURE
PROSTATITIS PROSTATITIS PROSTATITIS
Epidemiology - - • Most common
• E. coli, G(-) rods, enterococci, • Same as ABP, primarily E. coli • C. trachomatis, M. hominis,
Etiology
staphylococci Trichomonas, U. urealyticum
• Fever, chills, dysuria; • History of recurrent UTI; tender, • (-) History of recurrent UTI
Diagnostic clues tender, boggy prostate on boggy prostate on DRE • Painful ejaculation
DRE • May be asymptomatic • Same as CBP
WBC in prostatic • >10/HPF
• > 15/HPF; without pyuria
secretions
Bacterial culture • Positive • Negative

PROSTATIC
FEATURE ADENOCARCINOMA
PROSTATIC ADENOCARCINOMA
• Age: > 50 years STAGING (TNM)
• Race: Blacks • Nodal status: if positive, automatically associated with a fatal
• Environmental influences: high fat diet, obesity and alcohol outcome, regardless of T
Risk factors
• Androgens • Grade and stage: best prognostic factors
• Family history

(most common symptom) • Increased urinary frequency

Metastases
Dysuria
Clinical
Complete urinary retention
(in findings
decreasing PROSTATE CANCER
Back/hip pain (bone metastases) • Hematuria https://qrs.ly/r3bjbbv
frequency)
esicles and bladder
markers
Tumor
base 21. FEMALE GENITAL TRACT
Bone (most common site:
Morphology lumbar spine > proximal femur > pelvis > thoracic spine > ribs); predominantly BLASTIC lesions

nds without basal layer (single layer of cells) •• Inflammation/Infections

Fallopian tubes
•• Vulva
Ovary
tosis • PSA: elevated in non-neoplastic, benign, •• Vagina
Gestational and placental
• Cervix disorders
modalities • Body of Uterus
INFLAMMATION/INFECTIONS
& Endometrium
ssed in 95% of prostate CA (urine) TYPE CERVICITIS ENDOMETRITIS
normal biopsy
• Clinically significant • Etiology: bacterial
etiologic agents (can infections
cause both acute and postpartum or
chronic): abortion
1. Gonococcus • Clinically significant
Acute
2. Chlamydia etiologic agent:
3. Mycoplasma Chlamydia (can cause
4. HSV both acute & chronic)
• Histology: PMNs in • Histology: PMNs in
cervical stroma endometrial stroma
The one I’m discussing here is prostatic acinar adenocarcinoma, which • Usually, little clinical
is the most common. significance; some
degree of • Etiology: Chronic
inflammation is PID, IUDs, retained
Dr. Elomina present in virtually all gestational tissue TB
Chronic
PROSTATE-SPECIFIC ANTIGEN (PSA) women • Histology: Plasma
• Synthesized in the epithelial cells of the prostate gland • Histology: cells in endometrial
o High tissue specificity lymphocytes/ plasma stroma
• Normal reference range: 0-4 ng/mL cells in cervical
• Exists in complex with protease inhibitors or free stroma
o Free PSA (unbound): higher in BPH than in CA
o Complexed PSA: higher in CA than in BPH
Henry’s Clinical Diagnosis and Management by Laboratory Methods, 23th edition

GRADING PELVIC INFLAMMATORY DISEASE (PID)

• Gleason scoring system: based on glandular pattern and degree • Infection that begins in vulva/vagina, that ascends to involve the
of differentiation (LPO) upper reproductive tract
o 1-5 points: from well to poorly-differentiated • Most common etiologic agents: Gonococcus and Chlamydia
o Gleason score: Score of dominant pattern + score of next o Gonococcal: usually starts from endocervical mucosa, ascends
dominant pattern (e.g. 4+3 = 7) (order is important!) through mucosal involvement
• The
WHOorder
contemporary prostate
is important cancer
because grading
it has systemsignificance.
prognostic (2016) (5 o Nongonococcal: history of uterine manipulation, spreads
group grades,
Gleason 3+4 fallsbased
underon Gleason
WHO Gradescore)
Group 2, while Gleason 4+3 falls lymphohematogenously
under WHO Grade Group 3. The latter has worse prognosis than the • Clinically: Pelvic pain, adnexal tenderness, fever and vaginal
former. The two are so different, even though they’re both equal to 7. discharge

Dr. Elomina

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 DYSPLASIA/CIS CIN SIL
FEATURE LICHEN SCLEROSUS
Mild dysplasia CIN I LSIL
Gross • Leukoplakia Moderate dysplasia CIN II
• Thinning of the • Acanthosis Severe dysplasia HSIL
ORGAN MORPHOLOGY CIN III
epidermis • Mitosis Carcinoma in situ
• Intense acute inflammatory infiltrates
General • Basal cell • Hyperkeratosis
with intracellular Gram-negative
morphology degeneration • Dermal
diplococci
Histology • Hyperkeratosis lymphocytic
• Acutechanges
Cervix • Sclerotic and chronic
of cervicitis
infiltrate
• Usuallydermis
Endometrium superficial spared
• Acute
• Dermal suppurative salpingitis à
lymphocytic
Pyosalpinx (Pus in the lumen) à Chronic
infiltrate
Fallopian tube salpingitis (consequence
• Not premalignant, of repair) à
• Not premalignant,
Clinical Hydrosalpinx
but symptomatic LS (fimbrial fusion
but may be leads
seentoon
significance accumulation
has increased risk of secretions)
margins of vulvar
• Salpingo-oophoritis
of vulvar cancer àcancer
tubo-ovarian
Ovary
abscess
TOPNOTCH MEDICAL BOARD PREP PATHO MAIN DIGITAL HANDOUT BY KEVIN ELOMINA, MD
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VULVA
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GONOCOCCAL PID PREMALIGNANT AND MALIGNANT LESIONS
• Most common: Carcinoma spreading from the cervix
• Most common primary: Squamous cell carcinoma
o Premalignant lesion: Vaginal intraepithelial neoplasia (VaIN)
• SARCOMA BOTRYOIDES
SQUAMOUS o Disease of the young (<5 years)
HYPERPLASIA o Gross: grape-like clusters “botryoid”
o Malignant embryonal rhabdomyoblasts
§ Small, with oval nuclei and tennis racket like appearance with/without striations
§ Cambium layer: concentration of neoplastic cells beneath intact epithelium
o Can cause death by urinary tract obstruction (due to invasion)

ENDOCERVICAL POLYPS
BARTHOLIN CYST
• Can be a cause of irregular vaginal bleeding (post-coital)
• Cystic dilation of the Bartholin gland due to duct obstruction • • Fibromyxoid stroma, lined by endocervical type epithelium,
Lining: transitional or squamous epithelium usually with inflammation
• May be infected (adenitis); abscess formation
• Occurrence in >40 years old, biopsy to rule out malignancy NON- PREMALIGNANT AND MALIGNANT NEOPLASMS OF THE
CERVIX
NEOPLASTIC EPITHELIAL LESIONS
• High-risk HPVs: most important factor in the development of
BENIGN EXOPHYTIC LESIONS cervical cancer and squamous carcinomas in other sites
• Condyloma acuminata o Most common high-risk HPV: HPV 16 (60%), followed by 18
o Benign, genital warts (10%)
o HPV 6, 11 o HPV infects immature cells, but can replicate in mature cells §
o Exophytic papillary architecture E7 à Rb, p21 and p27 inactivation à cell proliferation § E6 à
o Acanthosis, Hyperkeratosis p53 inactivation and activation of telomerase à
o Koilocytic change cellular immortality
o NOT precancerous lesions
CERVICAL INTRAEPITHELIAL NEOPLASIA
SQUAMOUS NEOPLASTIC LESIONS • Cancer confined to the epithelium
• VULVAR SQUAMOUS CELL CARCINOMA • Premalignant lesion of cervical carcinoma (high-grade SIL) • Two-
Nuclear
tiered atypia isnowcharacterized
classification used: low- andbyhigh-grade
nuclear
o 30%: HPV-related (Basaloid and verrucous)
enlargement, hyperchromasia, coarse chromatin pattern, and
§ Premalignant lesion: vulvar intraepithelial neoplasia (VIN) squamous intraepithelial lesion (SIL)
§ Younger patients
SIL: Morphology
o 70%: Non-HPV-related (Keratinizing)
§ Occur in Lichen Sclerosus and squamous hyperplasia • Nuclear atypia
§ Premalignant lesion: differentiated vulvar intraepithelial • Koilocytic atypia: Nuclear atypia with cytoplasmic “halos”
neoplasia o E5: HPV-encoded protein
§ Older patients • Grade: expansion of immature cells from basal layer
o LSIL: confined to lower third of epithelium
LESION
o HSIL: expansion REGRESS PERSIST
to upper two-thirds PROGRESS*
of epithelium
GLANDULAR NEOPLASTIC LESIONS
Dr. Elomina

Natural history
• >80% of LSILs and 100% of HSILs: associated with high-risk
HPVs; HPV 16 being the most common type
VAGINA • LSIL is not treated as a premalignant lesion
and neuroendocrine
o Most (5%)
of LSILs regress
• SEPTATE VAGINA LSIL 60% 30% 10% to HSIL
i.e. Stage
HSIL III) 30% 60% 10% to CA
• EXTRAMAMMARY PAGET DISEASE * Adenocarcinoma in punch
- Progression within biopsy specimens is a diagnostic challenge,
2-10 years
because there are two possibilities:
o Similar to Paget Disease of breast clinically and histologically 1. Cervical primary,
o Not associated with underlying invasive cancer CERVICAL
2. ExtensionCANCER
from endometrium
• CIN + invasion beyond the basement membrane
The distinction is important because the stage will be different. We do this
• Squamous (80%); adenocarcinoma (15%); adenosquamous
by IHC.
DEVELOPMENTAL ANOMALIES
• Most common cause of death: uremia (extension to the kidneys
o Failure of Mü llerian duct fusion; accompanied by uterus
didelphys
o Associated with genetic syndromes and DES exposure in
utero
• VAGINAL ADENOSIS
 o Areas of columnar mucinous epithelium (endocervical-like)
o 35-90% of patients with in utero exposure to DES Dr.

Elomina § Associated with Clear cell CA of vagina

• GARTNER DUCT CYST

o Remnant of the Wolffian (mesonephric duct)
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 TOPNOTCH MEDICAL BOARD PREP PATHO MAIN DIGITAL HANDOUT BY KEVIN ELOMINA, MD
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BODY OF THE UTERUS AND ENDOMETRIUM
CERVICAL CANCER • Endometrial disorders
AND INTRAEPITHELIAL o Dysfunctional uterine bleeding
NEOPLASIA o Endometriosis and Adenomyosis
https://qrs.ly/aubjey0 o Endometrial polyps
o Endometrial hyperplasia
o Endometrial carcinoma
• Myometrial tumors

DYSFUNCTIONAL UTERINE BLEEDING (DUB)

• AUB without an organic (structural) cause
• Most common cause: Anovulatory cycle
o Unopposed estrogen stimulation due to failure of ovulation
i.e. no corpus luteum and progesterone à endometrial
proliferation à bleeding
o Histology: Menstrual endometrium (eosinophilic epithelial
metaplasia and stromal breakdown) without progesterone-
mediated change

ENDOMETRIOSIS AND ADENOMYOSIS

FEATURE ENDOMETRIOSIS ADENOMYOSIS
Definition • Ectopic endometrial glands and stroma • Endometrial glands and stroma in the myometrium
Clinical • Menometrorrhagia, colicky dysmenorrhea, dyspareunia,
• Infertility, dysmenorrhea, chronic pelvic pain
presentation premenstrual pelvic pain
• Subserosal red-blue to yellow brown nodules on sites
of involvement;
• Symmetrically enlarged corpus, with multiple blood lakes
Gross • Ovaries (most common site): maybe converted into a
within the myometrium
cyst containing chocolate brown material (chocolate
cysts); (+) fibrosis if long-standing
• Endometrial glands and stroma; cyst lining: • Presence of endometrial stroma, with or without glands,
Histology endometrial; (+) hemosiderin-laden macrophages in within the myometrium, separated from the decidual
old hemorrhage; fibrosis basalis by 2-3 mm

ENDOMTERIOSIS: PATHOGENESIS
• General: áPGE2 from endometrial tissue à áestrogen synthesis ENDOMETRIAL HYPERPLASIA
by stromal cells à survival of the endometriotic implants • Important cause of AUB, and precursor to endometrial carcinoma
• Theories: (Type I)
o Regurgitation theory (Retrograde menstruation) • Risk factors: Estrogen excess
§ Explains most of the anatomic locations o Obesity, menopause, PCOS, Functioning granulosa cell
o Benign metastases tumor, ovarian cortical stromal hyperplasia, ERT
o Metaplastic (Coelomic metaplasia) • PTEN inactivation in 20% of cases
o Extrauterine stem/progenitor stem cells • Non-atypical and atypical, by presence of nuclear atypia
• PTEN: tumor suppressor gene commonly mutated in atypical o Atypical (endometrial intraepithelial neoplasia): more
endometriosis, endometrial hyperplasia and endometrial associated with endometrial carcinoma (Type I)
carcinomas
o Also mutated in endometrioid and clear cell carcinomas of the ENDOMETRIAL CARCINOMA
ovary • Most common malignancy of the female genital tract
• Two major types:
o Type I (endometrioid) and Type II (serous)
ENDOMETRIOSIS § Type II is more aggressive than Type I
• Generally occurs in women 55-65 years
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o Clinically present with postmenopausal bleeding
• Stage: most important prognostic factor

ENDOMETRIAL POLYPS
• Exophytic masses that project into endometrial cavity
o Clinically silent or AUB
• Stroma: Neoplastic
• Glands: may be hyperplastic, atrophic or (+) secretory changes
if functional
o If associated with generalized endometrial hyperplasia,
hyperplastic; responsive to estrogen but little to no response
to progesterone
• Seen in patients on Tamoxifen
• Rarely give rise to carcinomas
Figure 22-24. Robbins and Cotran Pathologic Basis of Disease, 9th ed. 2015

The two types of endometrial carcinoma have different molecular

pathogenesis. Type I carcinomas proceed through a hyperplasia à
atypical hyperplasia à carcinoma sequence, and the most common
mutation is inactivation of PTEN, a TSG. Type II carcinomas occur in the
setting of atrophy. The most common mutation in p53 inactivation, and
the precursor lesion is serous endometrial intraepithelial carcinoma. In
gynecologic pathology, when you hear serous carcinoma, regardless of
the site, it’s bad.
Dr. Elomina

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 FEATURE
FEATURE
LEIOMYOMA LEIOMYOSARCOMA TOPNOTCH MEDICAL BOARD PREP PATHO MAIN DIGITAL
• Not(ENDOMETRIOID)
encapsulated, HANDOUT BY KEVIN ELOMINA, MD
• Localized polypoid •
well-circumscribed • Atrophic
Bulky, fleshyuterus
masses For inquiries visit
Gross tumor or
grayish-white that invade
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OVARY or
TYPE I
infiltrating
tumors; locations: uterine wall;
infiltrative or
masses
TYPE II (SEROUS)
intramural (most •
• Papillary
Polypoid masses
fronds that
or
common); project into the
• Glandular and solid
submucosal and uterine lumen
subserosal glandular, serous
Architecture
HISTOLOGY distinguished from
proportion of solid predominantly
•
Generally present, but
glandular nuclear
(if
• Three grades high-grade
(depending on the atypia)
types may show only
Cytologic • Mild to Moderate • Marked
minimal atypia
(high-
atypia (low-grade nuclei) • endometrioid
grade by
component) 10/HPF –nuclei)
if (+) atypia
Other • Scarce
• Squamous
to low (in and necrosis
histologic mitotically active (in •
differentiation 5/HPF – if (+)- atypia
clues leiomyoma)
20% of cases) and large
(epithelioid) cells
Necrosis • Absent • Usually present
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MORPHOLOGY
• Cysts
• Polycystic ovarian syndrome (Stein-Leventhal syndrome)
ENDOMETRIAL • Ovarian tumors
CARCINOMA
https://qrs.ly/ocbjbc1 CYSTS
• CYSTIC FOLLICLES (≤ 2 cm)/FOLLICLE CYST (> 2 cm)
o Lining: Granulosa cells, may be flattened due to pressure
atrophy
o Outer theca cells with pale cytoplasm (luteinization)
o If pronounced luteinization (hyperthecosis): hyperestrinism
and secondary endometrial abnormalities
• LUTEAL CYST (Corpus luteum cysts)
o Lining: Luteinized granulosa cells
o May rupture, and cause peritoneal reaction
o May be difficult to distinguish from endometriotic cyst, if
with hemorrhage and fibrosis
• POLYCYSTIC OVARIAN SYNDROME (PCOS) (Stein-
Leventhal syndrome)
o Complex endocrine disorder characterized by
hyperandrogenism, menstrual abnormalities, polycystic
Gross ovaries, chronic anovulation and decreased fertility
o Associated with obesity, Type 2 DM and
premature atherosclerosis
o Numerous cystic follicles or follicle cysts that enlarge the
ovaries
MYOMETRIAL TUMORS
• Generally absent,
• LEIOMYOMA
Atypia but some types may
well-differentiated OVARIAN TUMORS
o Most commonshowtumor
mild in women
atypia • Most are benign (80%)
o Malignant transformation is rare • Incidence of malignancy increases with age
• LEIOMYOSARCOMA • Major groups (4):
o Relatively uncommon
Mitotic o Mü llerian epithelium (most common); germ cell, sex cord-
o Commonly arise de novo
figures stromal, metastatic
• Common clinical symptoms:
MORPHOLOGY
o Attributed to mass effect, tumor invasion, vaginal bleeding
OTHER UTERINE TUMORS SURFACE EPITHELIAL TUMORS
• Malignant Mixed Müllerian Tumor à both glands and stroma are • Histologic types (3): serous (most common) mucinous and
malignant; atrophic uterus, bulky polypoid mass; may have endometrioid
heterologous elements • Benign, borderline and malignant forms:
• Adenosarcoma à glands are benign, stroma is malignant • General classification (2): Type I and II
• Endometrial stromal tumors à can be nodules (benign), low- o Type I (low-grade)
grade or high-grade sarcomas (malignant) § Arise from borderline tumors
§ Low-grade serous, Mucinous and Endometrioid
o Type II (high-grade)
FALLOPIAN TUBES § Arise from serous tubal intraepithelial carcinoma (STIC)
• Common lesions: Inflammation and cysts
§ High-grade serous
o Salpingitis: suppurative (most common: gonococcus);
• Most common symptoms: lower abdominal pain and abdominal
tuberculous
enlargement
o Cyst: paratubal cysts (tubal-like epithelial lining)
• Most women present with high-stage disease
• Rare lesions: Tumors
• CA-125: tumor marker to monitor recurrence/progression
• Fallopian tube epithelium related to high-grade serous carcinoma
of the ovary • General morphology
o Serous tubal intraepithelial carcinoma (STIC) o In serous and mucinous tumors:
§ Borderline tumors are distinguished from benign tumors by
presence of atypia and more complex architecture
The current concept is that high-grade serous carcinomas of the § Atypia and architectural complexity increase as you go from
Dr. Elomina
ovary arise from the fallopian tube (in the fimbriated part). borderline to carcinoma
§ Carcinomas are distinguished from borderline and benign tumors
by presence of stromal invasion

SEROUS TUMORS
• Tumors with tubal-like epithelium
 o Ciliated cuboidal to columnar epithelium • Type I à Low Grade Serous; or Mucinous
• Most are benign or borderline (70%) o Mutations: TP53, KRAS, BRAF
• Carcinomas are divided into low- and high-grade • Type II à High Grade Serous or Clear Cell
• Usually bilateral o Mutations: TP53, BRCA, PIK3CA
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TOPNOTCH MEDICAL BOARD PREP PATHO MAIN DIGITAL HANDOUT BY KEVIN ELOMINA, MD
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MUCINOUS TUMORS
TERATOMAS PARAMETER MATURE IMMATURE
• Tumors with non-ciliated, tall columnar epithelial lining with apical • Cystic, lined by
mucin Architecture skin-like structures • Solid
• Most are benign; primary mucinous carcinomas are uncommon (dermoid cyst)
• Usually
o Thinkunilateral
of metastatic mucinous adenoCA • Reproductive age • Young women and
Age group
women children
o If bilateral, exclude extraovarian origin first! • Tissues from
different origin
• May produce large masses • Neuroepithelium
Histologic (skin and adnexa),
• Associated with mucinous ascites (pseudomyxoma peritonei) o Most hallmarks cartilage, bone,
(small, round, blue
common site of mucinous tumor in PMP: Appendix cells)
thyroid and neural
tissues
ENDOMETRIOID TUMORS Biologic
• Benign and borderline tumors: uncommon • Benign • Malignant
behavior
o If it’s endometrioid, most likely it is a carcinoma • 1%
• 15-20% coexist with endometriosis Malignant
• (Most common: • N/A
transformation
• Hallmark: presence of tubular glands resembling benign or SCCA)
malignant endometrium
In the ovaries, the presence of a significant amount of
o Squamous differentiation: common clue that it is neuroepithelium warrants the diagnosis of an immature teratoma,
endometrioid which has a less favorable clinical behavior. Always remember the
• Bilateral in 40%, usually signifies extension beyond genital difference between testicular and ovarian teratomas.
tract
Dr. Elomina

GERM CELL TUMORS MONODERMAL/SPECIALIZED TERATOMAS

• 15-20% of ovarian tumors • Struma ovarii
• Most common: mature cystic teratomas o Thyroid tissue; may cause hyperthyroidism
• Carcinoid
o Serotonin; may cause carcinoid syndrome
o Always exclude metastatic intestinal carcinoid (bilateral
in most cases)

th

Figure 22-37. Robbins and Cotran Pathologic Basis of Disease, 9 ed. 2015

GERM CELL TUMORS

DYSGERMINOMA YOLK SAC TUMOR
FEATURE OVARIAN CHORIOCARCINOMA
(COUNTERPART OF SEMINOMA) (ENDODERMAL SINUS TUMOR)
• Most common malignant germ cell
Incidence • Second most common; albeit rare • Less common
tumor
• Schiller-Duval bodies/glomeruloid:
• Nests of large, vesicular cells with central blood vessel enveloped by
Histologic
clear cytoplasm, centrally located tumors cells within a space lined by • See “gestational choriocarcinoma”
pearls
nuclei + lymphocytic infiltration tumor cells
• AFP(+) hyaline globules
Tumor
• KIT • AFP • HCG
markers
Prognosis
In • Generally
prepubertal GrCTs, patients favorable • Generally
will present with precocious puberty. in the reproductive age group, patients•will
In GrCTsfavorable Generally unfavorable
present with AUB. In
postmenopausal GrCTs, patients will present with postmenopausal bleeding.

Dr. Elomina

GERM CELL SEX CORD-STROMAL

OVARIAN TUMORS OVARIAN CANCER
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SEX-CORD STROMAL TUMORS

FEATURE GRANULOSA CELL TUMOR SERTOLI-LEYDIG CELL TUMORS FIBROMA/THECOMA
• Mass effect; associated with Meigs
Clinical • Hypestrinism (depending on age
• Defeminization, virilization syndrome (Hydrothorax, Ascites,
syndrome group)
Ovarian tumor)
• Small, cuboidal to polygonal cells in
• Fibroblast-like cells (Fibroma) or
sheets, cords; may recapitulate
Histologic • Tubules formed by Sertoli cells or plump spindle cells with lipid
gland-like structures with central
pearls Leydig cells interspersed in stroma droplets (Thecoma) or mixed
acidophilic material (Call-Exner
(Fibrothecoma)
bodies)
Tumor • Estrogen • None (Fibroma)
• Androgens
markers • Inhibin • Functional (pure thecoma (rare))
Biological • All are potentially malignant; may • Generally favorable; recurrence • Generally benign (if
behavior behave as low-grade malignancy and metastases <5% Fibroma/Thecoma)
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TOPNOTCH MEDICAL BOARD PREP PATHO MAIN DIGITAL HANDOUT BY KEVIN ELOMINA, MD
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GESTATIONAL TROPHOBLASTIC DISEASES 22. BREAST

HYDATIDIFORM MOLE • Clinical presentations of breast disease
• Histologic hallmark: cystic swelling of the chorionic villi with • Inflammatory disorders
trophoblastic proliferation • Epithelial breast lesions
• Clinically important: • Carcinoma of the breast
o One of top differentials for bleeding in the first half of • Stromal tumors
pregnancy (together with abortion and ectopic) • Diseases of the male breast
o Precursor to persistent molar disease (invasive mole) and
gestational choriocarcinoma (complete mole) CLINICAL PRESENTATIONS OF BREAST DISEASE
• Complete or partial
• Pathogenesis
o Complete
§ Most common: chromosome duplication of paternal
chromosomes Diploid karyotype à (46XX)
o Partial
§ Dispermy and a haploid ovum à Triploid karyotype
(69XXX or 69XXY)

Figure 23-3a. Robbins and Cotran Pathologic Basis of Disease, 9th ed. 2015

• Pain
o Usually benign
• Palpable masses
o Most common: cysts, fibroadenomas, carcinomas
• Nipple discharge
o Suspect cancer if spontaneous and unilateral

INFLAMMATORY DISORDERS
ACUTE MASTITIS
• Most common cause: Staphylococcus aureus
o Suppurative inflammation; abscess formation
Figure 22-52. Robbins and Cotran Pathologic Basis of Disease, 9th ed. 2015
• Less common: Streptococcus pyogenes
FEATURE PARTIAL MOLE COMPLETE MOLE o Cellulitis
• 69 XXX
Karyotype • 46 XX
or 69 XXY FAT NECROSIS
• CLINICAL PRESENTATION May mimic cancer clinically
• Diagnosis • Missed abortion • Molar gestation History of breast trauma
• Uterine size • Smaller for dates • Larger for dates Histology
Theca-Lutein o Acute: hemorrhagic, liquefactive fat necrosis with
• Rare • Uncommon
cysts neutrophils and macrophages
Initial hCG • <100,000 o à Giant cells, calcifications, and hemosiderin à fibrosis
• >100,000 mIU/mL
levels mIU/mL
Medical
• Rare • Uncommon EPITHELIAL BREAST LESIONS
complications*
Rate of • Divided into three categories with respective risks of
subsequent • 1-5% of cases • 15-20% of cases developing invasive carcinoma
GTN**
PATHOLOGY CATEGORY RR* ALR (%)**
Embryo-Fetus • Often present • Absent Non-proliferative breast changes 1 3
Amnion, Fetal Proliferative breast disease 1.5-2.0 5-7
• Often present • Absent
erythrocytes without atypia
Villous edema • Focal • Widespread Proliferative breast disease with 4-5 13-17
Trophoblastic atypia
• Slight to severe • Marked
proliferation Carcinoma in situ 8-10 25-30
Trophoblastic * - Relative risk: Risk compared to women without any risk factors
• Mild • Marked
atypia ** - Absolute lifetime risk: Percentage of patients expected to
* - Anemia, hyperthyroidism, hyperemesis gravidarum, preeclampsia, and develop invasive carcinoma if untreated
infection
** - Gestational trophoblastic neoplasia
INVASIVE
CELL BENIGN DCIS
GESTATIONAL CHORIOCARCINOMA CA
Ductal cells Benign Malignant Malignant
Myoepithelial
Present Present Absent
cells
This is one
BENIGN VS.of MALIGNANT
the few things in pathology that I want you to remember. In
invasive malignant lesions, there is no myoepithelial layer. How do we
• Malignant neoplasm of trophoblastic cells derived from a assess the presence of myoepithelial cells in breast tissue, we do IHC using
Dr. Elomina

previous normal or abnormal pregnancy p63 (most commonly used). If a suspected lesion is negative for p63, then
• Histologic hallmark (same for both): proliferation of syncytio- it is invasive.
and cytotrophoblasts WITHOUT villi formation
Question: rapidly
• Behavior: What differentiates
invasive, invasive BUT
widely metastasizing, mole from
choriocarcinoma? Presence of villi in invasive mole.
responsive to chemotherapy
Choriocarcinoma does not form chorionic villi.
o Ovarian: generally unresponsive due to absence of tumoral
paternal antigens
 Dr. Elomina

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 TOPNOTCH MEDICAL BOARD PREP PATHO MAIN DIGITAL HANDOUT BY KEVIN ELOMINA, MD
For inquiries visit www.topnotchboardprep.com.ph or
https://www.facebook.com/topnotchmedicalboardprep/ This handout is only valid for the Sept 2020 PLE batch. This will be rendered obsolete for
the next batch since we update our handouts regularly. The breast has two main duct systems: the large duct system and the
NON-PROLIFERATIVE BREAST CHANGES terminal duct-lobular unit (TDLU). TDLU is hormonally responsive, and
that is why it is the site where invasive breast carcinomas arise.
FIBROCYSTIC CHANGES
• Cysts
Dr. Elomina
o Dilation of lobules; filled with brown or blue fluid;
calcifications common
CLINICAL PRESENTATION OF BREAST CARCINOMA
o Lining: flattened atrophic or (+) apocrine metaplasia
• Fibrosis
o Cyst rupture à inflammation à fibrosis
• Adenosis
o Increase in number of acini per lobule
o Lining: columnar; maybe with atypia (“flat epithelial atypia”)
PROLIFERATIVE DISEASE WITHOUT ATYPIA
EPITHELIAL HYPERPLASIA
• >2 layers of cells in a duct (normally, one luminal and one
myoepithelial)
• Distorted lumina at periphery
• Mimics ductal carcinoma in situ (DCIS)
• If mild, categorized under non-proliferative breast changes th

SCLEROSING ADENOSIS Figure 23-3b. Robbins and Cotran Pathologic Basis of Disease, 9 ed. 2015

• Stromal fibrosis compresses ducts at the center

• Solid cords or double strands of cells in a densely fibrotic stroma • • Abnormal mammographic findings:
Closely mimics carcinoma o Densities
Usually the inner ducts/acini are the ones compressed, while the
§ Rounded: Fibroadenomas, cysts
outer ducts/acini are dilated. The compressed ducts look like cords
of single cells in a background of fibrosis, and this lesion may be § Irregular: Carcinomas
mistaken for carcinoma. How to not fall into the trap? Sclerosing o Calcifications
adenosis should have a lobular architecture (meaning it looks like a § Small, irregular, numerous, clustered: Carcinomas
normal lobule). If it’s haphazard, that’s more likely a malignant
CARCINOMA IN SITU
• DUCTAL CARCINOMA IN SITU (DCIS)
Dr. Elomina

PAPILLOMA
• Malignant clonal proliferation of epithelial cells limited to ducts
• Papillary fronds with fibrovascular cores growing in a dilated
and lobules by the basement membrane
duct
• Two types:
• Myoepithelial layer present in fronds
• Comedo DCIS
• Clinically, bloodyofnipple
Papillary lesions discharge
the breast if stalk
can range goes
from infarction
benign (papilloma) to § High-grade nuclei
in situ (Papillary DCIS) to malignant (Encapsulated papillary Ca
§ Central necrosis
and Invasive papillary Ca). (Too advanced; that ’s why I didn’t include it
here. It will suffice for your to appreciate that myoepithelial cell • Non-comedo DCIS
assessment is most commonly done on these types of lesions to § Variable nuclear grade and architectural patterns
determine the true diagnosis. DCIS • Ducts filled with cells with high-grade
MORPHOLOGY
Comedo nuclear atypia
Dr. Elomina
• Central necrosis
COMPLEX SCLEROSING LESION (Radial scar)
• Combination of epithelial hyperplasia, sclerosing adenosis and
Non-comedo
papilloma Solid
• Ducts completely filled with cells, appearing as
• Central nidus of entrapped glands in a hyalinized stroma
solid nests
• Mimics cancer mammographically, grossly and histologically Cribriform
• Ducts filled with cells with secondary lumina
PROLIFERATIVE DISEASE WITH ATYPIA “cribriform pattern”
Micropapillary
ATYPICAL DUCTAL HYPERPLASIA (ADH) • Bulbous projections WITHOUT fibrovascular cores
• = DCIS - full duct involvement • Papillary fronds WITH fibrovascular cores BUT NO myoepithelial
Papillary
• Monomorphic cells (vs. heterogeneous in epithelial layer in fronds
hyperplasia) EPITHELIAL HYPERPLASIA VS. DCIS
• Cribriform pattern “cookie-cutter” appearance (sometimes) FEATURE
EPITHELIAL
DCIS
HYPERPLASIA
ATYPICAL LOBULAR HYPERPLASIA (ALH)
HISTOLOGY
• = LCIS, but <50% involvement of acini in a lobule Cellular
• Heterogeneous • Monomorphic
• Monomorphic, loosely cohesive cells appearance
o Similar with LCIS and ILC Cytoplasmic
• Indistinct • Distinct
• Loss of E-cadherin borders
o Observed in LCIS and ILC Cytoplasm • Eosinophilic • Pale
Nuclei • Oval • Round
CARCINOMA OF THE BREAST
Streaming • Present • Absent
IMMUNOSTAINS
• Most common non-skin malignancy in women • (+) • (-)
CK5/6
• Second to lung cancer in causing deaths in women • (+), Mosaic • (+), Diffuse
ER
• General Types:
o Carcinoma in situ This is too advanced, but I just want you to remember that when you see
ducts filled with super uniform-looking cells, think DCIS.
o Infiltrating (invasive) carcinoma
• Risk factors
Dr. Elomina

PAGET DISEASE OF THE NIPPLE

o Sex (Female)
• Rare manifestation of breast cancer
o Genetic
§ Germline mutations (BRCA1 (Ch17) and BRCA2 (Ch13), most • Unilateral eruption with a scale crust, pruritic (like eczema) •
common; 80-90% of familial Breast Ca) Malignant cells (Paget cells) reach ductal system without
§ History of Breast Ca in first-degree relatives violation of BM àà epidermis
o Hormonal (Estrogen excess) • Palpable mass in 50-60% of cases
§ OCPs, Obesity, Early menarche, Late menopause, o Most have invasive carcinoma
Nulliparity/Primiparity at age 35 § Poorly-differentiated, ER(-) and HER2(+)
o Environmental factors • Most of patients without mass have an underlying DCIS
§ Radiation and Toxins
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TOPNOTCH MEDICAL BOARD PREP PATHO MAIN DIGITAL HANDOUT BY KEVIN ELOMINA, MD
For inquiries visit www.topnotchboardprep.com.ph or https://www.facebook.com/topnotchmedicalboardprep/ This handout is only
valid for the Sept 2020 PLE batch. This will be rendered obsolete for the next batch since we update our handouts regularly.
In Paget, there are malignant cells in the nipple epidermis (They INFLAMMATORY CARCINOMA
• No
lookparticular
ugly). Now, what aresubtype
molecular the differentials for this? Melanoma and
Squamous
• Usually cell carcinoma are the common ones. But of course, if we
high-grade
see DCIS or invasive carcinoma in the breast, we lean more towards
Dr. Elomina • Extensive invasion and proliferation within lymphatic channels
LOBULAR CARCINOMA IN SITU (LCIS) o Clinically presents as swelling (“Peau d’orange”) that can
mimic non-neoplastic inflammatory disorders
• Clonal proliferation of cells within ducts and lobules that grow
in a dyscohesive fashion
o CDH1 (E-cadherin) loss MOLECULAR SUBTYPES OF BREAST CANCER
• Cytology • Based on estrogen and progesterone receptors (ER/PR), and
HER-2/Neu status
o Uniform population of cells with oval or round nuclei and
• Immunohistochemistry
small nucleoli (IHC)
• Fluorescence in situ
o Same with ALH hybridization
and ILC (FISH)
o Done to confirm positivity to HER-2 in cases of equivocal,
FEATURE DCIS LCIS or even strongly positive results (because Trastuzumab is
Basement expensive)
• Intact • Clinical importance
membrane
Disruption of o Determines amenability to hormonal or HER-2 targeted
• Yes • No therapy
lobules
Necrosis and • Usually absent, MOLECULAR SUBTYPES OF BREAST CANCER
• Present, thus (+)
secretory thus (-) o Pushing borders
calcifications
activity calcifications
• Yes, Paget • No Pagetoid • HER2(+)
• ER(-),
Involvement of
disease of the spread is • ER, PR (+/-)
the nipple skin
nipple observed
Bilaterality • 10-20% • 20-40% • 40-
• ER, PR(+);
Hormonal status • Variable
HER2(-)

INFILTRATING CARCINOMA • HER-2

INVASIVE BREAST CARCINOMA, NO SPECIAL TYPE (IBC NST) targeted • In
• Most common type therapy study
• Basically, in situ disease + absence of intact myoepithelial layer
• Haphazardly disposed cells with desmoplasia
• Nottingham histologic score:
o Tubule formation
o Nuclear pleomorphism
o Mitotic figures (/10 HPF)
§ Sum of three parameters determines grade (Elston score)
Important special types of infiltrating carcinoma:
INVASIVE LOBULAR CARCINOMA (ILC)
• CDH1 (E-cadherin) loss; ER/PR(+), HER2(-)
• Most common breast Ca to present as occult primary
o Little desmoplasia
• Dyscohesive infiltrating tumor cells in single file (“Indian file”) STROMAL TUMORS
o Mucin (+) signet ring cells may be seen

BREAST CANCER
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MUCINOUS (COLLOID) CARCINOMA

• Clusters and small islands of tumor cells floating in pools of
extracellular mucin
• Usually, cells have low atypia
• ER/PR(+), HER2(-)

MEDULLARY CARCINOMA
• Usually ER and HER2 (-)
• Morphology:
o Syncytium-like solid sheets of large cells with pleomorphic FEATURE BENIGN BORDERLINE MALIGNANT
nuclei and prominent nucleoli Tumor • Well- • Focally • Infiltrative
o Increased mitosis borders defined infiltrative
o Lymphoplasmacytic infiltrates Cellularity • Fibroblastic • Moderate • High
appearance
For the sake of board exams, please stick to the handout, but I just want Atypia • Little/Mild • Moderate • Marked
to share that Medullary carcinoma is now considered as a pattern of
poorly differentiated IBC NST. It’s now called IBC NST with medullary
Mitosis • <5 • 5-9 • ≥10
pattern. This is just nice-to-know okay. J (/10HPF)
Stromal • (-) • (-) or focal • (+)
overgrowth
 LUMINAL HER-2 o High-grade IMC NST
FEATURE BASAL
A B ENRICHED o High degree of aneuploidy
o High incidence of lung and brain metastases
Phenotype • ER(+), HER2(-) HER2
(-)
Frequency • ~10% • ~20% • ~15% FIBROADENOMA
55%
Proliferation • Most common benign tumor of the female breast
index • Low • High • Usually high • Intralobular stroma proliferates à surrounds (pericanalicular) or
(Ki-67) compresses (intracanalicular) proliferating epithelial component
• Hormonal • Complex fibroadenomas* have low risk of malignancy
Treatment therapies * Cysts larger than 0.3 cm, sclerosing adenosis,
(Tamoxifen) epithelial calcifications, or papillary apocrine change
(Trastuzumab)
• Luminal A and B tumors have lower grade than HER-2 PHYLLODES TUMOR
enriched and basal tumors • Proliferation of intralobular stroma covered by epithelium
o Luminal B tumors have higher grade than luminal A • Distinguishing features:
tumors • Luminal A tumors are more responsive to o Leaf-like projections
hormonal therapies o Stromal overgrowth
than Luminal B tumors o Infiltrative borders
• Triple-negative is NOT equal to Basal
o Gene profiling methods needed to classify tumors as o High cellularity, mitosis, and nuclear pleomorphism
basal • Triple-negative tumors PHYLLODES TUMOR TYPES

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 FEATURE FIBROADENOMA
PHYLLODES TOPNOTCH MEDICAL BOARD PREP PATHO MAIN
TUMOR DIGITAL HANDOUT BY KEVIN ELOMINA, MD
CLINICAL For inquiries visit
Age • Younger • Older www.topnotchboardprep.com.ph or
PITUITARY HORMONE
Size of lesion • Smaller • Larger CLINICAL MANIFESTATIONS
CELL TYPE PRODUCED
MICROSCOPIC
• Galactorrhea and
• Epithelial = • Stromal >
Proliferation amenorrhea (females)
Stromal (Balanced) Epithelial Lactotroph • Prolactin
• Sexual dysfunction,
Stromal
• Lower • Higher infertility
cellularity
• Gigantism (children)
Atypia • (-) • Variable Somatotroph • GH
• Acromegaly (adults)
Mitosis • Rare to absent • Variable
• Cushing syndrome
https://www.facebook.com/topnotchmedicalboardprep/ Corticotroph • ACTH
This handout is only valid for the Sept 2020 PLE batch. This will be rendered obsolete for
the next batch since we update our handouts regularly. • Nelson syndrome*
WORRISOME FEATURES IN PHYLLODES TUMORS CLINICAL
Thyrotroph • TSH
MANIFESTATIONS • Hyperthyroidism
• Stromal overgrowth • Hypogonadism
o 4 LPO fields show only stromal component Gonadotroph • FSH, LH • Mass effect
o Important criteria for malignancy • Hypopituitarism
• Metaplastic elements
o Cartilage, bone, skeletal muscle
o Aggressive; automatic malignant
• Tumor necrosis
o Poor prognosis

FIBROADENOMA VS. PHYLLODES TUMOR

Just remember the two clinical characteristics because they will make
you lean more on one diagnosis, when you ’re in doubt. Basically, PT is
more on the stroma, while FA is a balance of the glands and the stromal
Dr. Elomina
component. * - development of large, destructive pituitary adenomas post-
adrenalectomy for treatment of Cushing syndrome
PITUITARY ADENOMA
One of the most important things in endocrine physiology is the concept
DISORDERS OF THE MALE BREAST • of
Morphology
endocrine atypia i.e. cells of endocrine tissues may be a bit ugly, but it
o Uniform,
doesn ’t necessarily mean cells
polygonal that they’re malignant.
in sheets In pituitary carcinomas,
and cords
the requirement
o Sparse for diagnosis
reticulin networkis (vs.
METASTASIS.
normal pituitary parenchyma)
o Invasion and increased mitosis: atypical adenomas
o Immunohistochemistry required to determine specific type
PITUITARY CARCINOMAS
• Atypical adenomas + Metastases (CSF/systemic)
• Usually functional
o ACTH (42%)
o PRL (33%)
HYPERPITUITARISM
• Most common cause of hyperpituitarism: functional anterior
GYNECOMASTIA 23. ENDOCRINE SYSTEM pituitary adenoma
• Increase in dense collagenous connective tissue • 1 cm: limit size to determine micro/macroadenomas
• Epithelial hyperplasia of the duct lining with characteristic • More commonly diagnosed early (due to endocrine effects) •
tapering micropapillae Most common: Prolactin cell adenoma (30%)
• Rare lobule formation • Second most common: Somatotroph adenoma
MALE BREAST CANCER
• Rare
• Usually
This is one of the chapters in this handout that you really, really need
ER-positive
to master physiology in order to understand.
• Distant metastases are common at presentation

PITUITARY DISEASES
• Pituitary diseases
DEFICIENT
• Thyroid diseases HORMONE
CLINICAL MANIFESTATIONS
• Parathyroid diseases
• Diseases of the Endocrine pancreas GH
• Adrenal gland diseases
• Amenorrhea, infertility (females) •
• Multiple Endocrine Neoplasia (MEN) syndromes FSH and LH Decreased libido, impotence, loss of
pubic and axillary hair (males)
TSH • Hypothyroidism
• Hypoadrenalism
Dr. Elomina
ACTH
Prolactin • Failure of postpartum lactation
Because of the location of pituitary gland, its enlargement can
CLINICAL
impinge onMANIFESTATIONS OF PITUITARY
the optic chiasm leading DISEASE
to visual field defects, and it MSH • Pallor
• Hyperpituitarism
can cause increase –inHormone
ICP because it’s in the cranial vault. Pituitary
excess In primary empty sella, there is a sellar diaphragm defect where
apoplexy is a sudden onset of neurologic impairment because of a
o Elaboration of hormones the arachnoid and CSF herniate into the sella turcica, and impinge
rapidly enlarging adenoma (because of hemorrhage).
• Hypopituitarism – Hormone deficiency the pituitary. In secondary empty sella, either the contents of the
o Destructive processes and nonfunctional adenomas sella are removed iatrogenically or by a pathologic process e.g.
• Mass effect
o Sellar abnormalities
o Visual field defects
o Increased ICP
o Pituitary apoplexy

Dr. Elomina
 o Rathke cleft cyst
o Empty sella syndrome (Primary and secondary)
o Inflammatory/infection
o Genetic defects
Dr. Elomina

HYPOPITUITARISM CLINICAL MANIFESTATIONS

• Occurs at approximately 75% parenchymal loss
• Most cases are destructive processes directly involving the
anterior pituitary • Growth failure in children (pituitary
o Hypopituitarism + evidence of posterior pituitary dwarfism)
dysfunction: almost always hypothalamic in origin
• Loss of hormonal function proceeds in an ordered manner
o GH and gonadotropin (FSH and LH) (lost first) à TSH
and
ACTH à prolactin (lost last)
• Causes
o Tumors/mass lesions (pituitary and hypothalamus)
o TBI/SAH
o Pituitary surgery/radiation
o Pituitary apoplexy
o Ischemic pituitary necrosis and Sheehan
syndrome (postpartum) Dr. Elomina

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