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M2 Reproduction > repro pathology > Flashcards

repro pathology Flashcards

1
Q

what is the triple test for breast cancer diagnosis?

A
  1. clinical examination
  2. radiology/imaging: ultrasound, mammogram
  3. pathology: fine needle aspiration, core biopsy, excision biopsy
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2
Q

acute mastitis pathogenesis and presentation

A

pathogenesis: cracked or inflamed nipple permits entry of microbe (s. aureus or other staphylococci) during nursing –> microbe proliferates in stagnant milk –> acute inflammation results in abscess formation

presentation: acute inflammation of the breast, erythematous red breast with concurrent fever

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3
Q

idiopathic granulomatous mastitis pathogenesis and presentation

A

pathogenesis: autoimmune disease targets secretory products of the breast - best controlled by steroids and immunosuppressants

presentation: lobulocentric granulomatous inflammation, ddx is TB

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4
Q

paraffinoma pathogenesis and presentation

A

pathogenesis: fibrosis around paraffin breast implant with foreign body-type inflammation

presentation: radiodense empty spaces surrounded by multinucleate giant cells and histiocytes

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5
Q

classical presentation of fibrocystic changes of the breast

A

• in women during reproduction decades (esp premenopausal decade)
• due to normal cyclic breast changes
• bilateral, multifocal soft lump

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6
Q

prognosis of fibrocystic changes of the breast

A

depends on the level of epithelial hyperplasia!
low: fibrosis, cystic changes, apocrine metaplasia
moderate: moderate hyperplasia, sclerosing adenosis (scar-like fibrous tissue in breast lobules)
high: atypical hyperplasia

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7
Q

changes involved in fibrocystic changes of the breast

A

non-proliferative:
cysts and apocrine metaplasia (cells have eosinophilic cytoplasm and round nuclei)

proliferative:
epithelial hyperplasia, fibrosis, (sclerosing) adenosis –> hard rubbery lump may be mistaken for breast cancer

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8
Q

fibroadenoma pathogenesis and presentation

A

pathogenesis: pleomorphic lesion of fibrous and glandular tissue

presentation:
- young women (25yo)
- MOUSE IN THE BREAST!!! firm well-defined slow-growing mobile tumour (1-6cm)
- tan white colour with yellowish specks
- glandular and stromal elements
- circumscribed and uniform

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9
Q

phyllodes tumour pathogenesis and presentation

A

pathogenesis: fibroepithelial tumour from intralobular stroma

presentation:
- presents in young women (25yo)
- risk of malignancy due to proliferating stromal elements (EXCISE A LARGE MARGIN)
- leaf like pattern = benign, stromal proliferation = malignant
- haematogenous metastasis to the lungs
- possible necrosis and/or haemorrhage

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10
Q

papilloma pathogenesis and presentation

A

pathogenesis: benign neoplastic papillary growth

presentation:
- premenopausal women
- commonly causes bloody nipple discharge
- solitary lesions/lumps but too small to see on mammogram
- necrosis of tips of papillae may cause haemorrhage, bloody nipple discharge, nipple retraction

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11
Q

risk factors for breast carcinoma

A

rich, obese, premenopausal woman who is Caucasian, Jew or Parsi with previous breast disease, who has never had children and doesn’t breastfeed, takes hormones, loves radioactive material, has positive family history (BRCA1, BRCA2, p53, PTEN genes) who had early menarche and will have late menopause

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12
Q

presentation of breast carcinoma

A
  • palpable mass that is scirrhous, encephaloid or mucinous
  • most commonly in upper outer quadrant > subareolar > others
  • nipple discharge and retraction or Paget’s disease (erosion and redness)
  • mammographic density and calcifications
  • peau d’ orange appearance (tethered skin due to Cooper ligaments)
  • lymph node metastases (esp palpable axillary nodes)
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13
Q

ductal carcinoma in situ presentation

A
  • mammographic density, nipple discharge, Paget’s disease, palpable mass
  • found in ducts (duh)
  • medium or large sized cells with varied histological types (comedo, cribriform, solid, papillary, micropapillary)
  • higher chance of malignant change and E-cadherin expression
  • possible necrosis
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14
Q

lobular carcinoma in situ presentation

A
  • incidental finding, not really any symptoms
  • found in lobules (duh)
  • small cells with solid histology
  • low chance of malignant change
  • may express ER, PR or HER2 receptors
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15
Q

Paget’s disease pathogenesis and presentation

A

pathogenesis: extension of DCIS along ducts in the epithelial layer to the nipple skin

presentation: eczematous scaly crusting/erosion/redness on the nipple unilaterally, causing ulceration of the nipple also

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16
Q

invasive ductal carcinoma presentation

A

desmoplastic change replacing normal breast fat and forming a firm palpable mass with an irregular border

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17
Q

invasive lobular carcinoma presentation

A

tumour cells invade stroma in a linear pattern forming strands (single file) with a loss of cellular adhesion, cells are E-cadherin negative

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18
Q

mucinous carcinoma presentation

A

rubbery soft tumour on a mucinous background, low grade and good prognosis tumour

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19
Q

medullary carcinoma presentation

A

high grade, poorly differentiated and well circumscribed tumour that initiates extensive lymphoplasmacytic/immune response and responds well to chemotherapy

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20
Q

no special type carcinoma presentation

A

indistinct tumour morphology but the most common type of breast carcinoma, basically for any tumour that doesn’t fit the others

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21
Q

causes of gynaecomastia

A

drug-induced, testicular atrophy, liver cirrhosis, estrogen-secreting tumours (testis, adrenal gland etc), hyperprolactinemia, hormonal imbalances from puberty

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22
Q

TNM staging of breast cancer

A

T: primary tumour (1-4)
N: lymphatic spread (0-3)
M: distant metastases (x, 0-1)

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23
Q

grading factors of breast cancer

A

histological grades (1-3) based on:
1. tubule formation
2. nuclear pleomorphism
3. mitotic count

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24
Q

benign prostatic hyperplasia pathogenesis

A

testosterone is converted into DHT by 5α-reductase and binds to androgen receptors on prostatic cells to produce growth factors (growth rate>death rate), leading to progressive hyperplasia of stromal and epithelial prostate cells especially in transitional zone

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25
Q

diagnosis of benign prostatic hyperplasia

A
  1. digital rectal examination for enlarged prostate
  2. ultrasound of testicles, prostate, kidney, bladder for associated pathologies
  3. prostate-specific antigen amt elevation
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26
Q

presentation of benign prostatic hyperplasia

A
  • storage: increased frequency and urgency of urination, nocturia
  • voiding: hesitancy or intermittent interruption of urine stream
  • urinary tract obstruction: bladder distention and hypertrophy, hydronephrosis, urinary tract infections –> pyelonephritis
  • urolithiasis and CKD
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27
Q

treatment for benign prostatic hyperplasia

A
  • transurethral resection of the prostate
  • α-blockers (Prazosin, Tamulosin) to relax the smooth muscle in the prostate and bladder neck
  • lower fluid, alcohol and caffeine intake
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28
Q

prostatic cancer presentation

A
  • asymptomatic
  • urinary symptoms, similar to BPH
  • back pain and other symptoms of metastases
  • constitutional symptoms
  • enlarged, hard, bumpy prostate gland on DRE
  • elevated serum prostate specific antigen levels
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29
Q

pathogenesis of prostatic carcinoma

A
  • usually found in acinar cells (95%) but may also be found in ductal cells
  • in the peripheral zone of the prostate
  • infiltrative malignant glands with nuclear atypia and absent basal cell layers
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30
Q

what is the Gleason grading?

A

grading for prostate cancer based on architecture of the two most undifferentiated/malignant looking parts of the prostate, can go up to 12

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31
Q

treatment for prostatic carcinoma

A
  • radical prostatectomy for localised disease
  • radiotherapy for localised/locally advanced disease
  • androgen deprivation therapy for advanced/metastatic disease
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32
Q

condyloma acuminatum pathology and presentation

A

pathology: sexually transmitted via HPV 6/8

presentation: benign tumour on the inner surface of the prepuce, can be sessile/pedunculated

histologically: branching papillary stroma, covered by epithelium with superficial hyperkeratosis and acanthosis, enlarged and irregular hyperchromatic nuclei with perinuclear haloes

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33
Q

squamous cell carcinoma of the penis risk factors

A

uncircumcised, HPV 16 and 18, poor genital hygiene, smoking

34
Q

features of squamous cell carcinoma of the penis

A
  • slow growing locally invasive tumour, only painful after secondary ulceration and infection
  • metastases to inguinal and iliac lymph nodes
  • may be preceded by penile intraepithelial neoplasia (PeIN)
35
Q

presentation of squamous cell carcinoma of the penis

A
  • lesion on the glans of the inner surface of the prepuce near the coronal sulcus
  • either papillary (like condyloma acuminatum) or flat (epithelial thickening with graying, fissuring mucosal surface)
36
Q

pathogenesis of squamous cell carcinoma of the penis

A
  • HPV genome E6 and E7 regions code for multiplication of viral genome and target tumour suppressor genes
  • E6 –> p53, E7 –> Rb protein
  • leads to nests of malignant squamous cells with nuclear pleomorphism and mitotic figures
37
Q

infections that typically cause orchitis and epididymitis

A

tuberculosis, mumps, gonorrhea, syphilis

38
Q

pathogenesis and presentation of cryptorchidism

A

pathogenesis: failure of intra-abdominal testis to descend into scrotal sac, usually found in high scrotum but may also be found in abdomen or inguinal canal

presentation: empty scrotal sac, possibly testicular dysfunction/decreased fertility/ testicular cancer

39
Q

hydrocele pathogenesis and presentation

A

pathogenesis: accumulation of serous fluid between the visceral and parietal layers of tunica vaginalis, due to excessive production/impaired absorption of serous fluid + obstruction of lymphatic drainage

presentation: enlarged, painless testicle illuminated by the transillumination test

40
Q

testicular torsion pathogenesis and presentation

A

pathogenesis: twisting of spermatic cord cutting off venous drainage to testis

presentation: sudden onset testicular pain –> testicular infarction and eventual infertility

41
Q

testicular torsion risk factors

A
  • congenital: bell clapper abnormality, horizontal testis, spermatic cord with long intrascrotal component
  • larger testis
  • cryptorchidism
  • trauma or exercise
42
Q

types of male sex-cord stromal tumours

A
  1. Leydig cell tumours: may secrete androgens causing hormonal effects as clinical presentation
  2. Sertoli cell tumours: presents as usually (90%) benign testicular mass that is hormonally silent
43
Q

lymphoma presentation in the male reproductive system

A
  • in older patients
  • non-Hodgkin B cell lymphomas
  • in genitourinary tract as secondary involvement, or primary lymphoma of the urinary tract
  • elevated serum LDH
44
Q

testicular neoplasm risk factors

A
  • youth (95% are germ cell tumours which are seen in young men)
  • cryptorchidism
  • genetic factors
  • testicular dysgenesis syndrome
45
Q

presentation of testicular neoplasms

A
  • painless testis enlargement
  • elevated markers: LDH, AFP (yolk sac tumours), β-HCG (choriocarcinoma)
46
Q

presentation and types of seminomatous germ cell tumours

A
  • localised for a long time (slow growing with good prognosis)
  • very radiosensitive
  • spread by lymphatics to para-aortic nodes
  • usually seminoma (elevated serum LDH and β-HCG, sometimes OCT4 positive) or mixed tumour
    –> histologically: polygonal tumour cells with clear cytoplasm and lymphocytic infiltrates, homogenous fleshy lobulated and tan-coloured tumour
47
Q

presentation and types of non-seminomatous germ cell tumours (NSGCT)

A
  • metastasize relatively earlier (more aggressive with poorer prognosis)
  • radioresistant
  • spreads via haematogenous route
  • can be yolk sac tumour (common in infants, Schiller-Duval bodies on histology), choriocarcinoma (from trophoblastic tissue - nests of multinucleated syncytiotrophoblasts and mononucleated trophoblasts with early mets), teratoma (tissue from multiple cell layers), embryonic carcinoma (15-34yo)
48
Q

developmental pathologies of the uterus

A

didelphys, arcuate, unicornate, bicornate, septate uteri

49
Q

common gynaecological pathogens

A

Herpes virus, Molluscum contagiosum, Human Papilloma virus, Chlamydia trachomatis, Neisseria gonorrhoeae, Candida, Trichomonas

50
Q

presentation of pathogen-infected uterus

A

bacterial vaginosis (thick, purulent exudate), protozoa (thin, greenish-yellow, bubbly discharge), fungus (patchy white adherent exudate)

51
Q

pathogenesis and presentation of pelvic inflammatory disease

A

pathogenesis: an infection of the female reproductive organs when STD spreads from vagina to uterus/fallopian tube/ovaries

presentation: pelvic pain, adnexal tenderness, fever and vaginal discharge and COMPLICATIONS (peritonitis, adhesions, bacteremia, tubal pregnancy and infertility)

52
Q

non-neoplastuc vulval pathologies (3)

A

Bartholin cyst, Lichen sclerosus (thin, whitened epidermis), Lichen simplex chronicus (hyperkeratosis secondary to pruritis)

53
Q

Paget’s disease of the vulva presentation

A

reddish “weeping” lesions visible on CK7 dye, neoplasm formed from squamous stratified epithelium

54
Q

vulvar malignancy pathology

A

usually secondary to HPV, starts as vulva intraepithelial neoplasia and can become invasive –> squamous cell carcinoma (keratinisation and cell junctions)

55
Q

clear cell adenocarcinoma of the vagina pathogenesis and presentation

A

pathogenesis: usually in-utero exposure of young women to diethylstilbestrol (DES) leading to vaginal adenosis

presentation: vacuolated tumour cells in clusters and gland-like structures

56
Q

sarcoma botryoides (embryonal rhabdomyosarcoma) presentation

A

grapelike tumour clusters, normal stratified squamous epithelium with undifferentiated sarcoma underneath

57
Q

histological changes in cervical intraepithelial neoplasia

A

higher N:C ratio, increased mitosis, nuclear irregularity (multinucleation, perinuclear haloes, crinkled nuclei) –> ranked mild/moderate/severe dysplasia as CIN1/2/3

58
Q

risk factors for cervical intraepithelial neoplasia

A
  1. HPV: HPV16 (assoc with amplification of 3q) and 18 especially
  2. early age intercourse
  3. multiple sexual partners
  4. increased parity
  5. exposure to oral contraceptives and nicotine
  6. genital infections
59
Q

3 steps to cervical cancer development

A
  1. HPV infection
  2. progression to cervical intraepithelial neoplasia
  3. invasion and mets (locally: uterus, vagina, bladder, rectum, lymphatic, haematogenously: lung, liver, bone, brain)
60
Q

gross presentation of cervical carcinoma

A

intermenstrual bleed, post coital bleed, post menopausal bleed, dyspareunia, fungating/ulcerative/infiltrative tumour

61
Q

histological presentation of cervical carcinoma

A

75-90%: squamous cell carcinoma aka keratin pearls, intercellular bridges, eosinophilic cells with intracellular keratin, polygonal cells
rest: adenocarcinoma (gland formation invading underlying stroma), adenosquamous, undifferentiated

62
Q

endometrial hyperplasia pathogenesis and presentation

A

pathogenesis: increase in the number of glands relative to the stroma, due to unopposed estrogen secretion

presentation: abnormal vaginal bleeding, may progress from simple hyperplasia to complex hyperplasia (loss of PTEN, glandular overcrowding, irregular shape)

63
Q

endometrial carcinoma types

A

1: caused by prolonged estrogen stimulation –> endometrial hyperplasia, ovarian estrogen-secreting tumours, estrogen replacement therapy

2: p53 mutation with no preexisting hyperplasia, poorly differentiated serous type, poor prognosis

64
Q

endometriosis pathogenesis and presentation

A

pathogenesis: endometrial glands and stroma found outside of the uterus (usually abdominal cavity)

presentation: dysmenorrhea, pelvic pain, infertility

65
Q

leiomyoma risk factors and presentation

A

risk factors: VERY COMMON!! IN >30yo woman (but regresses after menopause), high amounts of estrogen and progestins / being pregnant (causes rapid size increase and haemorrhagic degeneration)

presentation: beefy red tumour located subserosal/intramural/uterine cavity/pedunculated/submucosal, histologically bundles of spindle cells with elongated blunt-ended nuclei and cigar-shaped bland appearance

66
Q

adenomyosis pathogenesis and presentation

A

pathogenesis: ectopic endometrial deposits in the myometrium with accompanying overgrowth of muscle and connective tissue

presentation:
1. diffuse: deposits are confined to inner part of myometrium, foci of endometrium is brownish
2. localised: resembles fibroid with brownish foci

67
Q

causes to exclude in dysfunctional uterine bleeding:

A
  • uterine lesions
  • pelvic inflammatory disease
  • adenomyosis
  • ectopic pregnancy
  • hydatid mole
  • uterine leiomyoma
  • endometriosis
  • trauma and sexual abuse
  • medication
  • foreign bodies
68
Q

causes (by age group) of uterine bleeding

A

prepuberty: precocious puberty
adolescence: anovulatory cycle, coagulation disorders
reproductive age: complications of pregnancy, anatomic lesions
postmenopausal: endometrial atrophy, anatomic lesions

69
Q

types of fallopian tube inflammation

A
  • paratubal cyst (hydatids of Morgagni)
  • hydrosalpinx
  • pyosalpinx
  • actinomycotic salpingitis: eosinophilic structures with peripheral radiation aka Hippelis syndrome
70
Q

fallopian tube benign neoplasms

A

adenomatoid tumour: asymptomatic invagination of visceral mesothelium
salpingitis isthmica nodosa: diverticulum enters fallopian tube wall and causes swelling

71
Q

types of ovarian cysts

A

follicular cysts (physiologic), corpus luteal cyst (formed from corpus luteum), polycystic ovary syndrome

72
Q

polycystic ovary syndrome (PCOS) presentation

A
  • obesity, hirsutism, acne due to hormonal irregularities (way too much estrogen)
  • amenorrhoea
  • multiple cysts and stromal hyperplasia
  • persisten anovulatory state
73
Q

types of germ cell neoplasms

A

dysgerminoma (monotonous tumour cells with clear glycogen-filled cytoplasm), teratoma (2-3 germ layers of cells), endodermal sinus tumour (forms sac-like structures/Schiller-Duval bodies and rich in α-fetoprotein)

74
Q

types of ovarian surface epithelial tumours

A

mucinous cystadenoma/cystadenocarcinoma, serous cystadenoma, endometroid ovarian tumours (mimics endometrium), clear cell ovarian adenocarcinoma (large sheets of epithelial cells with clear cytoplasm and tubules with hobnail nuclei), Brenner tumour (nests of urothelial cells in a dense fibrous stroma with coffee bean nuclei)

75
Q

types of sex cord/stromal tumours in women

A
  • fibrothecomas: stromal tumours with fibroblasts and plump spindle cells with lipid droplets (thecomas)
  • granulosa cell tumour: large, focally cystic with lipid-filled luteinised cells, coffee bean nuclei and inhibin positive
  • Sertoli - Leydig cell tumour: resembles embryonic testes and secretes androgens
76
Q

Krukenberg tumour presentation

A
  • usually bilateral
  • friable and necrotic with vascular invasion
  • ovarian surface involvement
  • due to metastasis from a different site
77
Q

causes of spontaneous abortion (loss of pregnancy before 20 weeks of gestation without outside intervention)

A
  • uterine defects (fibroids, polyps)
  • endocrine factors
  • hypertension, diabetes
  • fetal chromosomal anomalies
  • TORCH infections
78
Q

predisposing factors for ectopic pregnancy

A
  • chronic salpingitis
  • peritubal adhesions
  • leiomyomas
  • previous surgery
  • benign cysts and tube tumours
  • intrauterine device (IUD)
79
Q

presentation of ectopic pregnancy

A
  • amenorrhea
  • abdominal pain
  • vaginal bleeding
  • rupture of fallopian tube
  • haemorrhage (haematosalpinx, haematoperitoneum) –> haemorrhagic shock
  • spontaneous regression of pregnancy
  • tubal abortion
80
Q

placental abnormalities

A
  1. placenta previa: implantation of placenta over/near internal os
  2. abruptio placentae: premature separation of normally positioned placenta from uterine wall before delivery
  3. placenta accreta/increta/percreta: adhesion of normal placental villi to uterine wall (aka no decidual plate between villi and myometrium)
81
Q

preeclampsia triad

A
  1. hypertension
  2. proteinuria
  3. oedema
82
Q

eclampsia sequentae

A

decreased uteroplacental perfusion –> arterial vasoconstriction (–> systemic hypertension) + endothelial injury + activation of intravascular coagulation –> disseminated intravascular coagulation –> proteinuria in the kidneys, seizures and coma in the CNS, abnormal liver function test, ischaemia and fibrin thrombosis

M2 Reproduction (5 decks)

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