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Repro Midterm > Path > Flashcards

Path Flashcards

1
Q

What are the 6 most clinically relevant gram positive bacteria?

Hint: two cocci, four bacilli

A

Cocci
-Staph
-Strep
Bacilli (rods)
-Non-sporeformers: Corynebacterium diptheriae, Listeria monoctyogenes
-Spore-formers: Bacillus sp., Clostridium

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2
Q

What are the rest of medically relevant bacteria (not gram +)?

A

Gram -
Ex: Syphillus (Treponema palledum): Dark field microscopy, inclusion stains
E. coli

Special staining

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3
Q 
In terms of organisms, which of the following tend to cause the majority of salient diseases?
A) Bacteria
B) Viruses
C) Fungi
D) Parasites
E) Prions
A

A and B!

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4
Q

What are the most clinically relevant organisms as related to salient categories/types of infx, issues related to acquisition, and gender?

-Staph (TSS tampons)
-Bacterial UTIs (females): E. coli
-Non-specific urethritis (NGU): purulent Chlamydia, Ureaplasma urealyticum, S. saprophyticus
-Vaginitis:
Bacterial=Gardnerella vaginalis
Fungal=Candida
Parasitic protozoan=____________
-Prostatitis
-Gonorrhea in men=purulent d/c–>epididymus hurts…risk of septic arthritis
-Gonorrhea in women=purulent d/c or asympt–>fallopian tubes–>infertility or septic arthritis
-Common STDS:
MC chlamydia (NGU, PID)
Gonorrhea (PID)
Syphilis
HSV
HIV
-Uncommon STDS:
Hemophilus decreyi: chancroid
Chlamydia: lymphogranuloma venereum
Klebsiella granulomatis: granuloma inguinale
-Enterococcus: hospitals

A

Trichomoniasis

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5
Q

20 yo female presents w/ fever, high WBC w/ left shift, diffuse suprapubic pain, left lower back pain. Dysuria

Dx? Primary infection?

A

Bacterial infection of the bladder
MC E. Coli

(left shift=incr neuts=bacterial)

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6
Q

Microorganisms–>Dz

1) Microbial flora: coexist, may–>infx
2) Pathogenic, non-commensal (small or large dose–>dz)

Routes of Entry:

1) Epithelial surface
2) Inhalation
3) Ingestion
4) Sexual transmission

Respiratory, GI, GU infx caused by ______ mircoogranisms that can penetrate epithelium

A

virulent

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7
Q

Urine is sterile….anatomy=role in risk of UTI (women>men)…Obstruction or flow or reflux compromises normal defenses and increases susceptibility to urinary tract infxs…
Ex?

A
  • BPH

- Uterine prolapse

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8
Q
  • Antibiotics can kill the lactobacilli and allow overgrowth of yeast–>_________
  • Minor trauma (sex)–>expose immature prolif epithelial cells susceptible to infx by HPV
A

candidiasis

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9
Q

Host defense: urination
Breach: obstruction, microbial, attachment, local prolif

Ex?

A

E. coli

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10
Q

Host defense: normal vaginal flora
Breach: Antibiotic use

Ex?

A

Candida albicans

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11
Q

Host defense: normal vaginal flora
Breach: Microbial attachment and local prolif

Ex?

A

N. gonococcus

Chlamydia

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12
Q

Host defense: intact epidermal/epithelial barrier
Breach: direct infx/invasion

Ex?

A

Herpes (MC ulcerating dz in world)

Syphilis

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13
Q

Host defense: intact epidermal/epithelial barrier
Breach: Local trauma

Ex?

A

STIs including HPV, HIV

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14
Q

Dx?

  • Bacitracin resistant, B hemolytic, colonizes vagina, causes pneumonia, meningitis, and sepsis mostly in BABIES
  • screen preg women at 35-37 wks
  • if + give penicillin
A

Group B strep

B=babies

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15
Q

Meningitis/meningoencephalitis syndromes….setting/ages w/ organisms?

A
  • Listeria, E. Coli, Group B strep (neonates)
  • Consider N. meningococcemia (kids/young adults…petechial rash, waterhouse friderichsen syn)
  • H. influenza type B (+ epiglotittis)
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16
Q

Gonorrhea in infants? children?

A

Infants: conjunctivitis
Children: abuse!

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17
Q

Eye infx in infants and older children?

A

Chlamydia

risk–>blindness

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18
Q

Fetal calcifications in the brain?

A

Cytomegalovirus
Toxoplasma gondii

(vertical transmission mom–>baby)

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19
Q

Chanker not painful
Collapsed nose
Blind
Deaf

A

Congenital syphilis

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20
Q

Uveitis
Arthritis
Conjunctivitis

A

Reiter’s syndrome (youths male)

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21
Q

Monoarticular, septic arthritis in sexually-active young person?

A

Gonorrheal gram - diplococci

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22
Q

Aplastic anemia?

A

Parvovirus, B19

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23
Q
  • infx during 1st trimester
  • heart malformations
  • mental retardation
  • cataracts
  • deafness
A

Rubella
Placental-fetal transmission

(third tri little effect)

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24
Q

-Transmission during birth includes what key examples?

A

Herpes, gonococcal, chlamydia conjunctivitis

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25
Q

-Postnatal transmission in maternal milk includes…?

A

CMV, HIV, HBV

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26
Q

TQ

  • Cervical dysplasia and cancer (F)
  • Vulvar cancer (F)
  • Cancer of the penis (M)
  • Condyloma acuminatum (M/F)

Dx?

A

HPV

acuminatum (HPV 6 and 11….no SCC…see koilocytosis….16 and 18–>SCC)

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27
Q 
TQ
-Urethritis, cervicitis, salpingitis, PID (F)
-Urethritis, epididymitis, proctitis (M)
-Lymphogranuloma venerum (M/F)
Dx?
A

Chlamydia trachomatis

resurgence due to co-infx with HIV

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28
Q

TQ

  • Cervicitis, endometritis, salpingitis, infertility (F)
  • Epididymitis, prostatitis (M)

Dx?

A

Neisseria gonorrhea

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29
Q
  • Chanker not painful

- No inflamed inguinal LN

A

Syphilis (T. pallidum)

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30
Q
  • Painful chanker

- Inguinal LN swollen

A

Chancroid (H. ducreyi)

also painful in herpes!

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31
Q
  • Chanker not painful
  • Inguinal LN swollen
  • strictures/fibrosis
A

Granuloma inguinale (Klebsiella granulomatis)

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32
Q
  • Urethritis, balanitis (penis)
  • Vaginitis (F)
  • Greenish d/c, mobile protozoa
A

Trichomonas vaginalis

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33
Q
  • Causes skin infx in immunosupp–>endocarditis

- Can become resistant–>flesh eating

A

Staph

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34
Q
  • Causes pharyngitis–>PSGN

- MC community acquired pneumonia (esp in elderly)

A

Streptococcus

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35
Q

What is included in dx of ulcerating lesions of genital/inguinal region?

NOT limited to GI or STDs!! (Bubonic plague=Y. pestis), francisella tularensis

A

Herpes, syphilis (USA),

Chancroid, G. inguinale, L. venerum (non-USA)

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36
Q

What dxx includes…
Dysuria
Urgency
Frequency

A
  • Chlamydia
  • Gonorrhea
  • Ureaplasma urealyticum
  • S. saprophyticus
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37
Q

Dx of

Syphilius vs CMV vs HSV on slide

A

Syphilis: Dark-field micro, inclusion stains
CMV: intranuclear + cytoplasmic inclusions
HSV: Intranuclear, multinucleated

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38
Q

CMV transmission?

A
  • Transplancental
  • Neonatal (breastmilk)
  • Saliva (day care)
  • Genital route (15 yo)
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39
Q

HIV:

  • AIDS….who is at greatest risk of infx?
  • HIV is a non-transforming virus and is replicates via…

Notes:
Sex=dominant mode of HIV infx worldwide, semen–>abrasions in rectum/oral mucosa–>infx of CD4 cells….AIDS also infects B cells

Can also target CNS--enceph
Phases:
1) Acute retroviral syn
2) Asymptomatic/chronic
3) Clinical AIDS
A

Men having sex w/ men

Reverse transcriptase
Has subgroups and clades

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40
Q

What are some AIDS-defining opportunistic infections and neoplasms found in pts w/ HIV?

A

Protozoa/helminth:
Cyptosporidiosis, pneumocystosis, toxoplasmosis

Fungal: candida, cryptococcus, disseminated coccidioidomycosis and histoplasmosis

Bacterial: Mycobacterium, nocardia, salmonella)

Viral: CMV, HSV, Varicella

Neoplasms: Kaposi, primary lymphoma of brain, invasive cancer of cervix

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41
Q

32 yo male presents with sore throat, chronic diarrhea, and rt-sided painful rash….He thinks its the “flu that never went away”. Lost wt. Fever. Oral candidiasis. Lower CD4 counts 480.

Dx?

A

Chronic HIV infx

Not acute: diffuse lymphadenopathy
Not AIDS: multiple neoplasms with CD4 less than 200

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42
Q

37 yo white female complains of dyspareunia (pain with sex). Vulva/vagina ok but cervical erythema w/ focal, superficial erosions. Ki-67 positiove and p16.

Dx?

A

HPV (cervicitis, erosions)

NOT gardnerella b/c that would have vaginal pain

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43
Q

TQ
T/F
HPV is a transforming virus

A

TRUE–>SCC

HPV-16 and 18

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44
Q

TQ

37 yo female has a low grade lesion. This reflects HPV infx which cells of the cervix?

A

IMMATURE, BASILAR SC

(NOT mature!!)

Basil prolif=malignant….CIN III=carcinoma in situ
Cervical transition zone MC b/c immature basil prolif occurs here

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45
Q

What are the 2 routes for placental infections?

1) ascending through birth canal (MC)–>infx of membrane–>rupture–>preterm delivery
2) Hematogenous (transplancental)…ex?

A 
TORCH
Toxoplasmosis
Others (syphilis, TB, listeria)
Rubella
CMV
HSV
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46
Q

24 yo female complains of genital pain. Painful ulcerative lesino on left labia. Hx indicates sexual contact 4 days prior…
Dx?
What should it look like on smear?

A

HSV
Multinucleated syncytia w/ bluish intranuclear inclusions

Remember: granoluma inguinale and T. pallidum NOT painful

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47
Q

19 yo pregnant female. Distress. Cervix effaced/dilated. Membranes ruptured and amniotic fluid turbid w/ purulent exudates. SGA female infant 25 wks–>intubate. Cultures show TORCH…Which of the following is most likely

A. Toxo
B. CMV
C. Syphilis
D. Listeria
E. Rubella
A

D. Listeria!

A and B) mom–>pre-labor calcifications in brain

C) teeth, deaf, blind
E) early in pregnancy

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48
Q
  • pelvic pain + adnexal tenderness + fever + d/c

- Common causes?

A

PID

  • Chlamydia
  • Post-abortion/abnormal devliery (puerperal infx)
  • Gonococcus: 2 to 7 days after vaccination
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49
Q 
29 yo female seeks fertility consult. Been married 4 years and cannot conceive. Hx indicates sexual activity from early teens w/ multiple partners...Hysterosalpinogogram shows contrast media penetrating only a short distance laterally in both tubes...Most likely which of the following?
A) Antecedent ectopic preg
B) HPV 16, 18
C) Chlamydia
D) Neisseria
E) Herpes
A

C) chronic salpingitis (PID)–>infertility

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50
Q

MC cause of urethritis?

A

NGU! Chlamydia (also PID)

and ureaplasma urealyticum

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51
Q

17 yo female complains of significant vagina pain and itching…Insulin-dependent diabetes…vulvovaginal erythema w/ curd-like whitish discharge…
Dx?

A

Candida albicans (immunocomp.)

N. gonorrhea (purulent)
Trichomonas (green)
Chlamydia (asympt + serous d/c)

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52
Q

22 yo female in ED, shock, abd pain, diffuse lower abd pain w/ rebound (peritonitis). Purulent cervical d/c. Left knee swollen and red…Dx PID complicated by peritonitis/sepsis and suspect tubo-ovarian abscess…

Dx?

A

Neisseria

Septic arthritis!

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53
Q

A 17 G1P1 delivers male infant at 27 wks. SGA w/ desquamative rash of palms and soles…Vomer of nose flat and legs bowed. Hepatic transaminases elevated. Diffuse hepatocellular damage w lymphoplasmacytic infiltrates and focal obliterative endarteritis. Consult ophthalmology and audiology.

Dx?

A

Treponema pallidum

def/blind–>chronic hep

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54
Q
  • Inflammatory lesions of Bartholin glands may produce cysts.
  • They are tubuloalveolar glands that produce mucin
  • Contain watery or thick mucoid fluid, and / or become infected with what organism?
A

Gonorrhea! (gram-neg diplococci)

When they heal, expect a cyst

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55
Q
  • Chancroid of the vulva

- Gram-neg coccobacillus

A

Haemophilus ducreyi

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56
Q
  • Changes in inflammatory reaction
  • Intracytoplasmic diplococci
  • Background of lactobacilli
A

Gonorrhea

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57
Q
  • Purulent discharge of cervix

- Clear swollen cells

A

Chlamydia

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58
Q
  • small pearly papules with central depression of the vulva
  • white cheesy material
  • painless/itchy lesions that may become inflamed, red, and swollen
  • pox virus inclusions (cup shaped with glassy nuclei pushing the nuclei to periphery)
A

Molluscum contagiosum

Molluscum bodies=inclusions

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59
Q
  • Tzank prep w/ papanicolaou stain
  • Three M’s:
    1) moulding of nuclei
    2) margination of chromatin
    3) multi-nucleated giant cells w/ ground glass nuclei (central viral inclusions)
A

Herpes

Do a C section if preg

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60
Q

TQ

  • Histo: koilocyte (wrinkled nucleus)
  • Vulva: warts, intra-epithelial neoplasia, carcinoma
A

HPV
chondyloma accuminata

Low risk=6, 11
High risk=16, 18

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61
Q

TQ

  • most common lesion on the vulva
  • band of loose, pale-staning, collagen forms underneath the epidermis
  • Thinning of epidermis and fibrosis of dermis, hyperkeratosis, loss of rete ridges, dermal edema
  • **White scales, tissue paper appearance….gray and parchment-like or cigaret-paper-like and becomes itchy
  • Benign, but few percent turn malignant→SCC
  • Can cause leukoplakia (among other things)
A

Lichen Sclerosis (aka “chronic atrophic vulvitis”)

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62
Q
  • Fungal infection of the vulva?

- see hyphae

A

Candida

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63
Q
  • nonspecific condition resulting from rubbing and scratching of the skin.
  • Looks “like” leukoplakia. Vulva looks pink‐red like some one scratched it. Not premalignant.
  • Hyperplasia of the epidermis, thickening of the epidermis and hyperkeratosis
A

Squamous cell hyperplasia

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64
Q

TQ
What stage of syphilis?
-Separated, papular white lesions around vulva (wartlike)
-Rash on hands and feet
-Stromal fibrosis, squamous hyperplasia, chronic inflam., PLASMA CELL infiltrate

A

Secondary syphilis
(condyloma latum)

Reminder: syphilis=Treponema pallidum, a spirochete.

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65
Q

What stage of syphilis?
-Chancre on vulva

How do we visualize?

A

Primary syphilis

Dark field micro, warthin-starry silver stain, immunofluorescence

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66
Q

TQ

  • White raised papules on vulva (papillary)
  • branching fibrous stalk with a thickened epithelium
  • Hyperkaratosis
  • Parakaratosis
  • Koilocytic atypia→koilocytic cells with dark/hyperchromatic, wrinkled nuclei (from all those extra copies of the viral genome) and a perinuclear clear zone (halo)
A

Condyloma acuminatum (HPV 6, 11)

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67
Q
  • Most common BENIGN tumor of vulva
  • Presents as an ulcerated and bleeding nodule
  • Originates from exocrine sweat glands
  • Intraductal papilloma of the breast, only in the vulva along the embryonic milk line
A

Papillary Hidradenoma

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68
Q
  • mucin-rich clear cells in the epidermis of the vulva or perineum with prominent nuclei/nucleoli
  • Gross sharply demarcated red, itchy, moist, crusted/ulcerated skin lesion
  • usually no underlying cancer
  • Cells: PAS +, Keratin +
A

Extramammary Paget’s disease

pagets of vulva→ usually no underlying cancer

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69
Q

Differential dx of extramammary Paget’s disease?

A

Carcinoma vs melanoma

  • why melanoma? Malig population present in epidermis→ can also occur in vulva…make a distinction: is this carcinoma (pagets) or melanoma→ DO STAINS!
  • Paget cells: PAS +, Keratin +, and S100 –
  • Melanoma: PAS-, Keratin -, S100 +
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70
Q

TQ
-Presents as leukoplakia→ have to biopsy to distinguish

  • Basaloid and warty, caused by HPV 16→ preceded by dysplasia [VIN (vulvar intraepithelial neoplasia)] and carcinoma in situ. Young pts
  • not caused by HPV →arise in long standing lichen sclerosis or idiopathic hyperkeratosis (these are more aggressive). Older people usually
A

Squamous Cell carcinoma

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71
Q
  • residual glandular/columnar epithelium under the squamous epithelium in the upper vagina
  • Risk of adenocarcinoma
  • Assoc w/ hx of DES exposure
A

Vaginal adenosis

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72
Q
  • Inclusion cysts in wall of vagina

- Wolffian duct remnants

A

Gartner duct cysts

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73
Q
  • Nondysplastic
  • Noncondylomatous
  • No Koilocytic atypia
A

Squamous papilloma

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74
Q

-mature squamous epithelium overlying the benign appearing fibrovascular core

A

Fibroepithelial polyp

skin tags

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75
Q
  • Primary carcinoma of vagina
  • Invasive
  • Precursor lesion=vaginal intraepithelial neoplasia (VAIN) (low or high grade)

Ex: high grade vaginal intraepithelial neoplasia (incr epidermis and atypia)

A

Squamous cell Ca due to HPV 16, 18

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76
Q

TQ

  • MC vaginal sarcoma
  • Presents as bleeding and BUNCH OF grapes that protrude from vagina! Usually in girls
A

Embryonal Rhabdomyosarcoma (Sarcoma Botryoides)

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77
Q

What is the transformation zone?

A

Where the columnar epithelium of the endocervix meets the squamous epithelium of the ectocervix

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78
Q

What screen?

  • Endometrial cells in woman >40 yo
  • Epithelial cell abnormalities (atypical SC (ASC-US)), LSIL, HSIL, SCC
  • Glandular cell abnomralities (atypical endocervical cells)
  • Obtain the smear two weeks after the first day of the last menstrual periodo
A
  • PAP smear is gold standard for screening→ scrape away cells from transition zone→ look for dysplasia (high N:C ratio), dark, hyperchromatic nucleus
  • Pap smear is good to detect SCC and precursor lesions
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79
Q
  • Clue cells (fuzzy) in flora

- Vaginal pH is more alkaline (above 4.5)

A

-Bacterial vaginosis due to Garderella

  • Lactobacilli produce lactic acid which maintain the pH below 4.5. An alkaline pH is bad!!!
  • Infections may cause acute or chronic cervicitis causing reparative and reactive changes to appear in the PAP smear
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80
Q
  • bad-smelling, red (“strawberry”) inflammation with a thin discharge
  • wet mount: looks like a bouncing pear moving about with wiggly flagella (pears and whips)
  • On a pap smear, there is often a second micro-organism, a very long filamentous bacterium called “leptothrix”.
  • Often the result of illess or poor hygiene
A

Trichomonas

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81
Q
  • adenomatous, may cause bleeding
  • fibrous nubbins covered with epithelium, hanging out of the
  • They act as a wick, drawing bacteria into the endocervix and endometrial cavity.
A

Endocervical polyp

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82
Q
  • Results from progesterone stimulation of the endocervix (i.e., pregnancy, old-fashioned contraceptive pills).
  • The glands are abundant and have only a lacy stroma between them, along with many neutrophils.
A

Microglandular hyperplasia

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83
Q
  • superficial and intermediate squamous cells
  • mature squamous cells w/ production of large, resilient, cytoplasmic surface
  • endocervical cells have flat honeycomb cluster with clear cytoplasm. Irregular shaped nuclei with short protrusions
A

normal PAP

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84
Q
  • Dysplasia of the cervix (“cervical intraepithelial neoplasia”)
  • Due to PERSISTANT HPV infection
  • CIN I (LSIL) can regress (less likely with higher grades)→ can eventually become carcinoma in situ
  • L1 protein staining:
  • L1 staining still there→ maybe you can just watch
  • L1 staining lost→ likely to persist/get nasty

What stage are each of these?

1) Koilocytes only (halo + atypia). Perhaps a condyloma acuminatum or a flat wart. (mild dysplasia))
2) Plenty of atypical cells in the lower portions, normal maturation toward the surface (moderate dysplasia)
3) The cells no longer mature as they reach the surface (severe dysplasia)

A
  • CIN I: Koilocytes only (halo + atypia). Perhaps a condyloma acuminatum or a flat wart. (mild dysplasia))
  • CIN II: Plenty of atypical cells in the lower portions, normal maturation toward the surface (moderate dysplasia)
  • CIN III: The cells no longer mature as they reach the surface (severe dysplasia)
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85
Q

What type of Cancer?

  • arising from CIN III is usually squamous.
  • Carcinoma in situ becomes this
  • Presents as vaginal bleeding or post coital bleeding
  • New stain for p16 lights up the more aggressive intraepithelial lesions
A

INVASIVE CANCER

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86
Q
  • See koilocytic atypia on PAP
  • low grade or high grade (invasive)
  • Ki‐67 and p16 IHC
  • Recall the E6 (p53) and E7 (pRb) proteins prevent cell cycle arrest.
A

HPV

  • Low risk HPV, 6, 11, 42, 43
  • High risk HPV, 16, 18, 31, 33
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87
Q

Uterine defects:

  • prolapse
  • Bicornuate uterus
  • _______: variant of bicornuate. contains two cervixes
A

Didelphis

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88
Q

Which phase of the menstrual cycle?

  • contains small, quiet glands. -cells undergoing mitosis or stromal mitosis
  • some edema
A

Early proliferative stage

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89
Q

Which phase of the menstrual cycle?

  • glands start to get tortuous
  • some edema
A

Middle proliferative stage

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90
Q

Which phase of the menstrual cycle?

  • glands are now very tortuous
  • no edema
A

Late proliferative stage

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91
Q

Which phase of the menstrual cycle?

-Subnuclear vacuoles

A

Early secretory phase

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92
Q

Which phase of the menstrual cycle?

  • Exhaustion
  • disorganized
A

Late secretory phase

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93
Q

Which phase of the menstrual cycle?

  • Stromal break down
  • RBCS
A

Menstrual endometrium

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94
Q

Secretory Phase: Starts at ovulation (Day 14):

  • Day 14-16: glycogen vacuoles appear.
  • Day 19 or so: more secretion, and the glycogen and vacuoles are gone.
  • Day 20 or so: lots of secretion and begin to see stromal edema.
  • Day 22: maximal secretion, maximal sawtooth appearance of glands, but no decidualization.
  • Day 23-34: sawtoothing of glands, spiral arteries begin to nourish the fetus, predecidual reaction and lymphocytes
  • Day 24: great predecidua and lymphocytes.
  • Day 26: neutrophils, no pregnancy this month…..

What will the baby make to keep the endometrium growing?

A

hCG

note: Guf says wont ask days but just review anyways…

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95
Q

What does most “dysfunctional uterine bleeding” result from?

  • common around menarche and menopause
  • results in estrogen-driven proliferative phase without progesterone-driven secretory phase
  • Endocrine disorders, ovarian lesions, metabolic disturb
A

Anovulatory cycles (failure to ovulate)

Eventually get overgrowth of blood supply→ begin to degenerate and then there will be bleeding

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96
Q

What are some other causes of dysfunctional uterine bleeding?

A

Inadequate luteal phase

  • Infertility
  • Increased bleeding or amenorrhea
  • Decreased progesterone in the post ovulatory period
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97
Q

Age group related abnormal bleeding?
-Prepuberty: precocious puberty (hypothalamic, pituitary, or ovarian origin)
-Adolescence: Anovulatory cycle, coagulation disorders–>amemia
-Reproductive age:
–>Complications of pregnancy (abortion, trophoblastic disease, ectopic pregnancy)
–>Anatomic lesions (leiomyoma, adenomyosis, polyps, endometrial hyperplasia, carcinoma)
–>Dysfunctional uterine bleeding (anovulatory cycle, ovulatory dysfunctional bleeding (e.g.,
inadequate luteal phase)
-Perimenopausal: dysfunctional uterine bleeding due to anovulatory cycle or anatomic lesions (carcinoma, hyperplasia, polyps)
-Postmenopausal: Endometrial atrophy, anatomic lesions (carcinoma, hyperplasia, polyps)

A

Just look over…table from robins

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98
Q
  • secondary amenorrhea due to loss of basalis→ scarring
  • Result of overaggressive dilation and curettage (D & C) → scrape away too much of uterine wall (scrape away basalis so you cant regenerate endometrium)
A

Asherman syndrome

intrauterine adhesions/scarring can cause pain and/or infertility

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99
Q
  • Inflammation of the endometrium of the uterus

- Presence of microabscesses and / or neutrophils within the endometrial glands

A

Acute endometritis

may be staph or strep

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100
Q
  • Inflammation of the endometrium
  • Incr plasma cells within the endometrial stroma
  • Abnormal uterine bleeding
  • Pelvic pain
  • Infertility
A

Chronic endometritis

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101
Q

Common causes of chronic endometritis?

PLASMA CELLS

A

Chlamydia

Also:
TB, cancer

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102
Q
  • Exophytic mass projecting into the endometrial cavity
  • clonal overgrowths of endometrium that do not cycle with the rest of it (likely to bleed between cycles)
  • thick-walled blood vessels
  • risk of torsion

What can these arise as a side effect of ?

A

Endometrial polyps

Tamoxifen (anti-estrogenic on breast BUT pro-estrogenic effects on endometrium)

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103
Q
  • Endometrium (glands and stroma) outside the uterus (MC ovary)
  • Sx: dysmenorrhea, pelvic pain, infertility
  • Risk of malignant transformation (assoc w/ ovarian ca=endometrioid and clear cell type)
  • Release pro-inflam factors
  • PGE-2 incr estrogen locally
A

Endometriosis

  • Minor lesions look like powder burns under the serosal surface→ gun powder appearance if involves soft tissue
  • Large lesions: blood has organized & w/ extensive fibrosis (fallopian tube lesions=scarring→ increases risk of infertility/ectopic pregnancy]

note: oral contraceptive pill seems to prevent endometriosis from forming.

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104
Q

-present as “chocolate cysts” →full of old blood

A

Longstanding endometrial lesion (endometriosis)

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105
Q

-Endometrial tissue extends deep into the wall of the uterus (myometrium)

A

Adenomyosis

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106
Q

-Common cause of abnormal bleeding and serves as a precursor to endometrial cancer
-Toooo….many glands, toooo….little stroma.
-Due to too much estrogen (endogenous, exogenous)
-Assoc. conditions:
obesity (adipose tissue–>estrogen), menopause, PCOS, drugs
-Inactivation of the tumor suppressor gene PTEN.
-The world health organization, describes two types: Non‐atypical and atypical

A

Endometrial hyperplasia

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107
Q

Which type of endometrial hyperplasia?

  • no atypia
  • crowded glands
  • decr stroma
  • dilated glands
A

Non‐atypical

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108
Q

Which type of endometrial hyperplasia?

  • atypical nuclei w/ anaplasia
  • prominent nucleoli
  • incr mitosis
  • incr # glands
  • decr stroma
A

Atypical

109
Q

Which type of endometrial carcinoma?
-Age: 55‐65 yr
-Presents w/: unopposed estrogen, obesity, hypertension, diabetes
-Endometrioid morphology
-Precursor: Hyperplasia
-Genetic abnormalities:
PTEN, ARID1A (regulator of chromatin), PIK3CA (PI3K), KRAS, FGF2 (growth factor), MSI *, CTNNB1 (Wnt signaling), TP53
-Behavior: Indolent, spreads via lymphatics

A

Type I endometrial carcinoma

endometrial hyperplasia→ carcinoma→ endometriod appearance (looks like endometrium BUT it is piled up on histo

110
Q

Which type of endometrial carcinoma?
-Age: 65‐75 yr
Presents w/: atrophy, thin physique,
-Serous, clear cell mixed müllerian tumor morphology
-Precursor: serous endometrial intraepithelial carcinoma
-Genetic abnormalities: TP53*, aneuploidy, PIK3CA (PI3K), FBXW7 (regulator of MYC, cyclin E), CHD4 (regulator of chromatin), PPP2R1A (PP2A)
-Behavior: aggressive, intraperitoneal and lymphatic spread

A

Type II endometrial carcinoma

  • sporadic (get it from an atrophic endometrium)→ histo: serous (often has papillary structures) so sometimes call it papillary serous
  • resembles oviduct. Look for “hobnail cells” and psamomma bodies
111
Q
  • Gross sharply circumscribed firm gray‐white tumors w/ “whorled silk/white whorled masses”
  • may have areas of degeneration, hemorrhage and calcification.
  • Benign proliferation of smooth muscle cells arising in myometrium (oval nucleus and long slender bipolar cytoplasmic processes)
  • more common in blacks
  • tumors with rearrangements of chromosomes 12q14 and 6p involving the HMGIC and HMGIY genes, respectively
A

Leiomyomas (fibroids)

  • MC tumor of women
  • Related to estrogen exposure→ size increases with pregnancy and decreases with menopause therefore premenopausal women usually
112
Q

T/F

Leiomyomas do not become leiosarcomas

A

TRUE

113
Q
  • mesenchymal uterine tumors classified between benign leiomyomas and leiomyosarcomas
  • usually dont metastasize
A

Smooth muscle tumors of uncertain malignant potential (STUMP)

114
Q
  • bulky, fleshy masses that invade the uterine wall or polypoid masses that project into the uterine lumen
  • nuclear atypia, mitotic index, and zonal necrosis.
  • usually single and in older pop
  • de novo
  • hemorrhage and necrosis in mass
A

Leiomyosarcoma

  • Must distinguish from STUMP.
  • A subset contains MED12 mutations, a genetic aberration that appears to be virtually unique to uterine smooth muscle tumors.
115
Q

-arise from the endometrium and contain both malignant glands and malignant mesenchymal elements.
-epithelial and stromal components derived from the same founding cell.
• Mutations involve the same genes that are mutated in endometrial carcinoma, such as PTEN , TP53, and PIK3CA , while alterations typical of those found in sarcomas are absent

A

Malignant Mixed Müllerian Tumors

note: In addition to bizarre spindle cells, there may be muscle, bone, fat, endometrial stromal sarcoma, and/or cartilage…often a previous history of radiation…aggresive

Example: Chondrosarcoma with mixed müllerian cancer
Example: Rhabdomyoblasts with mixed müllerian cancer
You can stain with myoglobin, and can see cells with z-bands on electron microscopy.

116
Q

TQ

  • caused by cancerous cells (mucinous adenocarcinoma) that produce abundant mucin or gelatinous ascites.
  • Most often from the appendix or ovary
A

Pseudomyxoma peritonei

117
Q

-benign condition were leiomyomas are found disseminated in the peritoneal cavity

A

Disseminated peritoneal leiomyomatosis

118
Q

Well differentiate papillary mesothelioma vs diffuse malignant mesothelioma?

A
  • Well-diff: low malignant potential

- diffuse: atypia + malig

119
Q

-Purulent access in distal part of the fallopian tubes and ovaries

A 
Suppurative salpingitis
(suppurative=purulent=bacterial)

Other PID:

  • Chronic
  • Tuberculous (SE Asia)
120
Q

-cysts in the fallopian tubes that arise from embryonic structures (müllerian duct remnants)

A 
Hyatids of Morgagni  (distal)
Paratubal cysts (midportion)

Also:

  • Adenomatoid tumor (assoc w/ mesothelioma)
  • Primary malignancy
121
Q

-Graafian follicle remnants that did not regress…possess luteinized theca cell tissue–>hyper-estrogenism

A

Follicular cysts

122
Q
  • Oversized ovarian cyst filled with blood and fatty debris

- Under estrogen effects

A

Luteal cyst (corpus luteum cyst)

123
Q
  • hyperplasia and luteinization of the theca cells–>
  • overproduce androstenedione.
  • Big & yellow ovaries
  • Most pts are post-menopausal
A

stromal hyperthecosis

124
Q
  • Contains both endometrial glands and stroma
  • Chocolate cyst (hemorrhagic)
  • Hemoptysis w/ menstrations
A 
Endometriotic cysts
(of the lung)

Can be large cystic masses

125
Q
  • serous
  • mucinous, endocervical-like and intestinal type
  • endometrioid
  • clear cell
  • transitional cell/Brenner
  • epithelial-stromal tumors
A

Epithelial surface-stromal tumors

MC and most impt!!

126
Q
  • granulosa tumors
  • fibromas
  • fibrothecomas
  • thecomas
  • Sertoli-Leydig tumors
  • Steroid (lipid) cell tumors
A

Sex-cord stromal tumors

127
Q
  • Teratoma
  • dysgerminoma
  • yolk sac tumor
  • mixed
A

Germ cell tumors

  • MC solid tumor of the male
  • Rare in women except benign teratoma
  • Worse prognosis in kids and older adults
128
Q

MC mets to ovary?

A

Gastric and breast

129
Q 
Ovarian tumors:
What age group is assoc with each type?
-Benign
-Borderline
-Malignant
A

Benign: young women (20-45 yo)

Borderline: slightly older ages

Malignant: older women (45-65 yo) + familial cases younger women

130
Q

What are the the three ovarian components that most tumors of the ovary arise ultimately from ?

A
  • surface/fallopian tube epithelium and endometriosis (MC)
  • germ cells (migrate to the ovary from the yolk sac, pluripotent, benign cystic teratomas)
  • stromal cells (sex cords)
131
Q
  • Abdominal pain and distention
  • urinary and GI symptoms
  • vaginal bleeding
A

ovarian tumor

132
Q

Which type of ovarian tumors are generally considered to be epithelial?
What forms do they appear as?

A

Serous, Mucinous, Endometrioid

Benign, borderline, malignant

133
Q

Which ovarian tumor most often arises in a malignant form?

A

Serous borderline tumor

MC metastatic tumor of ovary derived form mullerian origin

134
Q

Which ovarian tumors most often arise bilaterally?

A
  • Serous malignant tumor (MC)
  • Endometrioid carcinoma
  • Clear cell carcinoma
  • Metastatic
135
Q
  • associated with inclusion cysts
  • may arise from distal fallopian tube
  • serous type
A

Serous Tubal Intraepithelial Carcinoma (STIC)

136
Q

MC type of ovarian malignancy?

A

serous tumors

137
Q
  • present b/t ages 20-45 yo
  • tubal-like epithelium
  • bilateral
  • incr risk if no children, FH, KRAS mut, TP53 mut)
  • decr risk if b/t 40-59 yo and hx of oral contraceptives or tubal ligation
  • may be on ovarian surface or be primary tumors
A

Serous tumors

138
Q
  • middle adult life
  • KRAS mutation
  • unilteral
  • primary tumors uncommon
  • ovarian surface rarely involved
  • form larger multilocular, cystic masses containing gelatinous fluid
A

Mucinous tumors

139
Q

-intraperitoneal accum of mucinous material from ovarian or appendiceal tumor

A

pseudomyxoma peritoneii

140
Q

If diagnose a young pt with ovarian endometrial cancer, what should you also look out for?

note endometrioid tumors have KRAS and TP53 mutations as well

A

Endometrial carcinoma

Endometrial malignancy of the ovary w/ endometrial ca present earlier than those without concomitant endometrial ca

141
Q
  • lower abdominal pain and abdominal enlargement
  • GI complaints, frequency/dysuria
  • Benign forms easily resected
  • Malignant: progressive weakness, weight loss and cachexia
  • extend through the capsule to seed the peritoneum, massive ascites (with exfoliated tumor cells or fragments)…peritoneal seeding pattern
  • Regional nodes frequently involved as well as mets to liver, lungs, GI tract and other sites (NOT breast/bone)
  • Mets across the midline to the contralateral ovary in @ 50% of cases
  • Most women with ovarian cancer present with high stage disease/late, therefore poor prognosis
  • CA-125 useful only to monitor recurrence or progression
  • Screening of women with BRAC mutations or strong family history is necessary
A

ovarian epithelial tumors

142
Q

Germ cell tumor presenting as a cystic mass containing mature well-differiated elements from all 3 germ layers

A

Mature (Benign) Teratomas AKA CYSTIC TERATOMA

143
Q

Germ cell tumor presenting as an aggressive mass with immature/embryonic neural tissue (glial tissue)

A

immature teratoma

If malignant, may have SCC or adenoCa inside it..otherwise still aggressive)

144
Q
  • MC in adolescents
  • Counterpart to seminomas of the testis
  • Good prog w/ chemo and radiation
  • Incr LDH, clear cytoplasm w/ central nuclei=fried egg
A

Dysgerminoma

145
Q
  • Intermediately differentiated aggressive germ cell tumor
  • AFP
  • Male infants
  • Yellow hemorrhagic solid mass
  • Schiller duval bodies=glomerulus-like structure
A

Yolk sac tumor (endodermal sinus tumor)

146
Q
  • Rare intermediately differentiated germ cell tumor
  • emulate chorionic villi so –>
  • hCG+
A

Choriocarcinoma

147
Q

-Poorly differentiated, anaplastic germ cell tumor

A

Embryonal carcinoma

148
Q
  • derived from ovarian stroma
  • granulosa and theca cells may secrete estrogens so can be feminizing
  • Leydig cells secrete androgens so may be masculinizing
A

Sex Cord-Stromal Tumors

149
Q
  • Fluid associations
  • basal cell nevus syndrome (multiple basal cells ca–>melanoma)
  • Meigs syndrome
A

Fibroma, thecoma, fibrothecoma

150
Q

Triad of:

  • ovarian fibroma
  • ascites
  • hydrothorax
A

Meigs syndrome

151
Q
  • Assoc w/ breast dz, endometrial hyperplasia and ca in adults
  • sexual precocity if pre-adolescent
  • produces estrogen
  • behave like low grade malignancies
A

Granulosa cell tumors

152
Q

TQ

Common cause of ruptured fallopian tube other than ectopic pregnancy?

A

Granulosa cell tumor

153
Q

TQ

Bilateral metastases composed of mucin-producing, signet-ring cancer cells, most often of gastric origin.

A

Krukenberg tumor

154
Q 
A 27 year old female presents with profound lower abdominal pain and fever of 102.4F. Upon PE she has vaginal erythema and a slight purulent cervical discharge. Imaging is most consistent with bilateral tubo-ovarian abscesses. A loculated area under the right diaphragm suggests perihepatitis. 
Most likely of the following?
A) Hydatids of Morgagni
B) suppurative salpingitis 
C) tuberculous salpingitis 
D) STIC
E) hepatitis B
A

B) suppurative salpingitis (purulent, PID)

 NOT
A) peritubal @ fimbriae end, large
C) Chronic w/necrotizing granulomas, indolent
D) serous ca
E) salpingitis not viral!
155
Q 
A 27 year old female presents with profound lower abdominal pain and fever of 102.4F. Upon PE she has vaginal erythema and a slight purulent cervical discharge. Imaging indicates bilateral tubo-ovarian abscesses. A loculated area under the right diaphragm suggests perihepatitis. Most likely etiology?
A) chlamydia
B) granuloma inguinale
C) gram positive spore former 
D) gram negative diplococcus 
E) gram positive diplococcus
A

D) Gonorrhea!

NOT
A) chlamydia asymp (tubo-lumenal destruction–>infertility)
B) fibrosis/strictures
C) clostridium (puncture wounds), bacillis anthracis (soil)
E) strep pneumo

156
Q

A 25 year old G0P0 female complains of night sweats and increasingly, excess facial and lower extremity hair. She is muscular with a BMI

A

D) Stromal hyperthecosis (low change of preg, solid, thecal cells=stromal hypercellulity and luteinization)

NOT
A) cystic, high BMI (obesity T2DM), follicle cysts w/ serous fluid through stroma
B) young, bilat, cystic
C) cystic thecal-luteal
E) sex cord stromal tumors may not be functional

157
Q 
A 47 year old G3P3 presents with pelvic pain and a serosanguinous (serous/bloodY) vaginal discharge. Imaging shows a 9.5cm right ovarian mass. It is multicystic with areas of mural nodularity (wall of cyst thick). Biopsies show tubal-type epithelium arranged in papillae with stratification and anaplasia of invasive epithelial cells. Serum AFP and HCG are negative. Molecular studies indicate TP53+, KRAS-, BRAC1/2-Most likely of the following?
A) Primary epithelial lesion of the ovary
B) STIC
C) Sex cord-stromal tumor
D) Metastatic carcinoma
E) Malignant teratocarcinoma
F) Mucinous cystadenocarcinoma 
G) Familial serous cystadenofibroma 
H) Endometrioid cysadenofibroma
I) Sporadic serous cystadenocarcinoma
A

I) Sporadic serous cystadenocarcinoma (TP53+, KRAS-)

NOT
A) Primary epithelial lesion of the ovary
B) STIC (not a big mass, not invasive, intrapeithelial)
C) Sex cord-stromal tumor (not cystic/large, of epith tumors of ovary)
D) Metastatic carcinoma (unliateral, tubal type from breast/GI…mucinous and cell anaplasia…Bilateral!!)
E) Malignant teratocarcinoma F) Mucinous cystadenocarcinoma (KRAS +)
G) Familial serous cystadenofibroma
H) Endometrioid cystadenofibroma (not malig., glands/fibrosis)

158
Q

Serous tumor vs. mucinous tumor?

A

Serous=tubal-type epithelium

Mucinous=endocervical/intestinal like epith

159
Q

Tx of malignant serous cyst?

A

Bilateral salpingoophorectomies

160
Q 
A 35 year old G2P2 female complains of deep pelvic pain, primarily on the right. She is short of breath and states she is unable to work out anymore. She attributes weight gain (approximately 10 lbs in recent weeks) to her now sedentary lifestyle. PE in noteworthy for an abdominal fluid wave. Workup ultimately reveals a left-side, solid ovarian mass measuring 7.2cm in greatest dimension and a right pleural effusion. Ovarian biopsies show fibroblastic proliferation and aggregates of plump cells that are Oil red O positive. Her pleural effusion is most likely
A) Chylothorax
B) Hemothorax
C) Malignant
D) Hydrothorax
E) Due to alcoholic liver disease
What is her ovarian lesion best characterized as? 
A) Retroperitoneal fibrosis
B. Germ cell tumor - embryonal 
C) Benign solid teratoma
D) Sex-cord, stromal tumor
E) Dysgerminoma
A

D) Hydrothorax (serous fluid)

NOT
A) Chylothorax (lipids..thoracic duct)
B) Hemothorax (blood)
C) Malignant (mets-->pleural effusion)
E) Due to alcoholic liver disease (ascites but not thorax)

D) Sex-cord, stromal tumor
(fibroma-thecoma…meigs syn)

NOT
A) surrounds ureters
B) malig, lung mets and chorios
C) cystic

161
Q

What are some factors in the development of cancer?

A
  • Infection w/ HPV
  • Obesity (post-meno)
  • Reproductive hx: estrogen stimulation, timing, and number of pregnancies
162
Q

T/F nongenetic factors, such as birthdate, can influence the risk of developing a breast cancer

A

TRUE:
For instance, breast cancer risk in females who inherit mutated copies of the BRCA1 or BRCA2 tumor suppressor genes is almost threefold higher for women born after 1940 than for women born before that year, perhaps because of changes in reproductive history.

163
Q

Why do we have so much breast cancer in modern, industrialized society?

A
  • organ undergoes marked periodic changes during adulthood, particularly during pregnancy, before involuting with age.
  • old times: puberty–>multiple pregnancy at a young age and didn’t live long
  • now: decr # pregancies, incr age of preg=incr # periods, live longer
164
Q

The ducts and lobules of the breast have two types of epithelial cells and type types of stroma. What are they?

A
  • epithelial cells: luminal and myoepithelial

- stroma: interlobular and intralobular

165
Q

Structure of the breast:

  • 6-10 major duct orifices open onto the skin surface at the nipple
  • superficial portions are lined by keratinizing squamous cells that change to the double-layered epithelium (luminal and myoepithelial cells) of the remainder of the duct/lobular system.
  • Successive branching of the large ducts eventually leads to what important unit?
A

terminal duct lobular unit

166
Q

supernumary nipples can develop anywhere along the what?

A

milk line=milk line remnants

other development:

  • axillary breast tissue
  • congenital nipple inversion
167
Q

Benign or malignant?

-pain

A

benign, not malignant

168
Q

Benign or malignant?

-nipple discharge <60 yo, bilateral

A

benign

worry if unilateral, spontaneous in women >60 yo

169
Q

Benign or malignant?

-older women with palpable mass

A

maybe malignant…

if bilateral and multiple think benign

170
Q

abnormal mammogram:

-small irregular clusters

A

malignant calicfications

171
Q
  • Usually occurs during early lactation
  • In a non-lactating woman, the usual problem is a pre-existing dermatitis, smoking, and/or a piercing
  • Usually staph aureus (abscess maker)
  • Less often, it is strep (spreading cellulitis)
  • Almost NEVER a sign of cancer
A

acute mastitis

cracks in epith–>infx

172
Q
  • older women w/ erythematous swollen breast
  • maybe b/l
  • emboli blocking dermal lymphatics
A

inflammatory breast carcinoma

173
Q
  • keratin plug–>
  • ruptured skin due to keratin debris inflam–>
  • fistula opening at edge of areola
A

keratinizing squamous metaplasia (lactiferous ducts)

174
Q
  • benign, usually painless lump from trauma–>necrotic fat, giant cells
  • Necrotic fat cells surrounded by a mixed inflammatory infiltrate, later with calcification, foreign body reaction, scarring
A

Fat necrosis

175
Q
  • Autoimmune disease that runs with Hashimotos, Type I DM, scleroderma
  • dense lymphocytic infiltrate around some of the lobules, perhaps with fibrosis;
  • Can produce HARD LUMPS
A

Lymphocytic mastopathy (SLL)

176
Q
  • Confined to breast lobules
  • All these women have been pregnant
  • autoimmune reaction against the secretory units
  • r/o TB, sarcoid, fungal, chronic inflam, and a reaction to implant
A

Granulomatous mastitis

177
Q
  • likely to be tender before menses and after drinking coffee
  • dilated ducts containing cloudy serous fluid (sometimes bloody or infected)
  • All breasts during childbearing years contain microscopic form
  • Gross: blue dome
  • Surrounding stroma likely to be fibrous
  • Epithelium may be flattened, cuboidal, columnar, piled up, and/or show apocrine metaplasia.
  • very pink mitochondrion filled cells resemble real apocrine cell
A

Cysts

fibrocystic change/nonproliferative

178
Q
  • dense collagenization/stroma distorting and compressing the epithelial structures
  • most common in upper outer quadrants, patients in 30’s
  • can sometimes see calcium buildup, but means nothing
A

Fibrosis

fibrocystic change/nonproliferative

179
Q
  • extra, crowded acini in some of the lobules
  • Calcification is common
  • can be lactational (during preg)
  • can be flat epithelial atypia (2 layers)
A

Adenosis

180
Q
  • more than the usual two layers of cells in ducts and/or lobules. -at least one layer will be myoepithelial cells.
  • does NOT produce a mass
  • Between the heaps of cells, you will see cracks and crevices
A

Epithelial hyperplasia

181
Q
  • proliferation of small ductules and acini in a fibrous stroma (but the basic architecture is intact)
  • Contains easy to see admixture of myoepithelial cells
  • CK5/6 stain of a needle biopsy will show you the myoepithelial cells
  • tender lump in the upper outer quadrant.
  • Patient is usually around age 30-40.
  • Presence=3 x future breast CA risk
A

Sclerosing adenosis

182
Q
  • possess fibrovascular cores, with epithelial hyperplasia-type lesions on the top. Seldom produce masses
  • myoepithelial cells within the lesion demonstrate it is a papilloma rather than carcinoma in situ.
  • Risk of breast CA→ these benign lesions are probably caused by mutations of genes other than BRCA1, BRCA2, and p53.
A

Papilloma

183
Q
  • architectural features suggesting progression toward malignancy
  • swiss cheese (cribiform)
  • myoepithelium only on the bottom layer
  • nuclei run streaming along the glands and the lumen isn’t filled
  • atypia
A

-Atypical ductal hyperplasia

184
Q
  • parts of lobules are partially filled with abnormal cells

- atypia

A

-Atypical lobular hyperplasia

185
Q

T/F:

carcinoma in situ (lobular and ductal) has a high risk of malignancy and high risk overall

A

True

186
Q

Almost all breast malignancies are adenocarcinomas and can be based on the expression of what two genes?

A

Estrogen Receptor
HER2

(ER)-positive, HER2-negative (50% to 65% of tumors)

HER2-positive (10% to 20% of tumors, which may either be ER- positive or ER-negative); and

ER-negative, HER2-negative (10% to 20% of tumors).

187
Q

An increase in age is highly associated with which group of breast cancer?

A

Estrogen receptor positive

HER2 negative

188
Q

Which form of breast cancer is more common in non-whites (AA, hispanics)

A

HER- ER- tumors

(basal-like…BRAC1)

(ER + more common in whites, ER-HER2+ same)

189
Q

Risk factors for breast cancer:

  • Germline mutations (BRAC)
  • 1st degree relatives with breast cancer
  • Race/ethnicity (AA, hisp. worse)
  • Age (incr w/ age)
  • Menarche (age of pub???)
  • Age at first live birth (before 20 decr risk)
  • Benign breast disease (prolif w/ atypia incr risk)
  • Estrogen exposure
  • Breast density (>60 incr risk)
  • Radiation exposure (HL pts)
  • Carcinoma of contralateral breast or endometrium (lobular lesions more b/l)
  • Diet
  • Obesity (decr
A

Puberty before 11 incr risk

After 14 decr risk

190
Q

What is the single gene mutation assoc?

  • half of all breast cancers
  • mutations rare
  • subtypes of medually and metaplastic)
  • Poorly differentiated and basal like (triple neg) + p53 mut
A

BRAC1 (chr 17)

familial breast and ovarian

191
Q

What is the single gene mutation assoc?

-Male breast cancer assoc

A

BRAC2

192
Q

What is the single gene mutation assoc?

  • Triple negative cancer
  • mutated in sporadic form
  • half are ER- HER2+
A

TP53

193
Q

What is the single gene mutation assoc?

-incr risk of breast cancer after radiation exposure

A

CHEK2

194
Q

T/F:

Evidence suggests all breast carcinomas actually arise from cells in the terminal duct lobular unit.

A

true!

ductal=of the breast

195
Q
  • crusty scale on nipple surface
  • Intraepithelial growth of large, pale, mostly-single cancer cells in the nipple. It looks inflamed
  • Large cells with clear halo
  • This is an underlying cancer (DCIS) invading the epidermis. DON’T MISS IT!
  • Do NOT treat “eczema of the nipple” with cortisone; biopsy it.
  • Any DCIS extending in the ducts may produce cancerization of lobules (ie: filling the terminal ductules in a lobular unit)
  • Women may choose mastectomy and breast reconstruction for ductal carcinoma in situ
A

Paget’s disease of the breast

(DCIS, invasive)

196
Q
  • MC DCIS
  • resembles blackheads on gross exam, and the necrotic cores can be squeezed out.
  • Central necrosis→ tends to calcify
  • Sign that this DCIS is likely to turn invasive
A

Comedocarcinoma (DCIS)

197
Q
  • Fills ducts.
  • Solid, seen as early microcalcifications
  • Cells are monomorphic and monotonous
A

Solid DCIS/non-comedo

198
Q
  • proliferation of tame-looking cells, slightly larger than normal, filling the ductules of one or more lobules.
  • CADHERIN NEGATIVE
  • may be bilateral
  • lobules are expanded but not distorted.
  • Often there are signet-ring cells
  • Tend to feature “non-cohesiveness”
A

LCIS

199
Q

Firm fibrous, rock hard mass with sharp margins and small, glandular, duct-like cells

A

Invasive ductal carcionma

Special subtypes:

  • Mucinous/colloid: clumps of cells floating in lakes of mucus, gelatinous
  • Tubular: single-layer tube, star shaped
  • Medullary: big, bulky, soft, polygonal cells w/ lymphocytes, HLA-DR
  • Metaplastic–>SC
  • Inflammatory–>tumor emboli
200
Q

ER/HER2?

  • older women
  • Mets to bone
  • low prolif
  • may include BRAC2 mut
  • late relapse pattern
A

ER+, HER2-

201
Q

ER/HER2?

  • young women
  • Mets to bone and brain!
A

HER2 +

ER-/+

202
Q

ER/HER2?

  • triple negative cancer
  • young women BRAC1 mut, AA, hispanics,
  • mets to bone and brain
  • usually short relapse with rare survival when have mets
A

ER- HER2-

203
Q

Male breast cancer can metastasize where?

older, superficial and palpable

A

LLBB

204
Q

-ulceration of entire breast

A

Carcinoma en cuirasse

205
Q

Stages 0-IV (5 stages) of breast cancer….

A 
0=non-invasive
1=breaking through
2=spread to axillary LN
3=spread to sternal LN/chest
4=spread to body
206
Q
  • most common benign tumor of the female breast
  • young women
  • older women
  • polyclonal hyperplasias of lobular stroma
A

Fibroadenoma

intralobular stroma

207
Q
  • much less common than fibroadenomas
  • usually in older age group (50’s)
  • range in size from small to huge (“leaflike”)
  • some can be locally aggressive
A

Phyllodes tumor

intralobular stroma

208
Q

Interlobular stroma tumors include fat necrosis, lipoma, fibromatosis

Are these benign or malig?

A

benign

malig: angiosarcomas, lymphomas, epidermal/dermal tumors, mets

209
Q 
17 yo white female complains of bilateral nipple discharge and pain in her breasts prior to her period each month. Her menstrual cycle is regular and lasts 5 days each month. Menarche at 12 yo. Dense breasts with slight serous discharge bilaterally and multiple firm nodules bilaterally. PMH is notable for mom who died of breast cancer...
Most like which of the following?
A) BRAC1 positive
B) TP53 positive
C) ER- HER2-
D) ER + HER2-
E) none of the above
A

E! Probably bilaterally fibroadenomas…

FH :(
but young, b/l, painful, menarche after age 11, multiple nodules all point to :)

210
Q

Chorionic villi are intended to invade the:

A

Decidua

211
Q

Thin placenta. Think:

A

Intrauterine growth retardation from placental insufficiency

212
Q

Thick/big placenta. Think: (3)

A

Diabetes
Hydrops fetalis
Infection

213
Q

Big blood clot in placental. Suspect that there was an:

A

Abruption

214
Q

A few cotyledons on the placenta that are fibrotic. Think:

A

Old infarcts

215
Q

A few cotyledons on the placenta that are overly red:

A

New infarcts

216
Q

TQ

  • Benign hemangioma
  • no consequence unless it’s huge, in which case it acts like a shunt
  • consumes baby’s platelets and can causes CHF
  • looks like a fleshy, dark, red blob
A

Chorangioma

217
Q
  • Deep maroon
  • looks complete
  • No cotyledons

Which surface of the placenta?

A

Maternal

218
Q

-membranes are gray, glistening, and translucent, showing the maroon villi through them

which surface of the placenta?

A

fetal

219
Q

fetal surface of placenta is green in color. think:

A

meconium

pus (more yellow – chorioamnionitis)

220
Q

peculiar odor to fetal surface of placenta. think:

A

Infection.

listeria smells sweet, others malodorous

221
Q
  • an accessory lobe that is separated from the main placenta by vasculature
  • if it overlies cervix → likely to be bleeding
A

succenturiate lobe

222
Q
  • basal plate (mom’s side) is quite a bit bigger than the chorionic plate (baby’s side)
  • will appear as a ring around the edge on the fetal surface
  • can cause various problems as you’d expect, since the baby’s wrapped up inside
A

circumvallate placenta

223
Q
  • vernix caseosa embedded in the amnion
  • ERF: granulomatized sloughed baby skin cells
  • Usually there’s oligohydramnios
A

amnion nodosum

224
Q

-cord attached to the membrane but away from the placenta.

A

velamentous insertion

225
Q
  • results from the healing of tiny leaks in the amnion
  • it is a common cause of miscarriage
  • can result in damage to body parts in a baby that makes it to term.
A

amniotic band syndrome

226
Q
  • features a good placenta and membranes but no baby
  • due to a known or unknown genetic defect – some of these are triploid and this fades into moles
  • pathologist will eventually see the villi; unlike hydatidiform mole
  • trophoblast atrophy rather than proliferation
  • the edema of the villi isn’t impressive
A

blighted ovum / anembryonic pregnancy

227
Q
  • Child and placenta are enormous
  • Usually death is due to CHF, most often from severe anemia
  • problems with the cord cause the child’s death
A

hydrops fetalis

228
Q

-a twin who died and whose body was flattened by the other child’s

A

fetus papyraceous

229
Q

baby calcifies in utero

A

lithopedion

230
Q
  • Most often in ampulla of fallopian tube
  • suspect with hx of amenorrhea, lower-than-expected rise in hCG based on dates, and sudden lower abdom pain
  • confirm with U/S
  • often mistaken for appendicitis

risk factors:

  • hx of infertility
  • salpingitis (PID)
  • ruptured appendix
  • prior tubal surgery
A

ectopic pregnancy

231
Q

-Premature separation of placenta from uterine wall before delivery of infant

Risk factors:
-trauma (motor vehicle accident), smoking, HTN, preeclampsia, cocaine abuse

  • abrupt, painful bleeding in 3rd trimester
  • possible DIC, maternal shock, fetal distress
  • Life threatening for mother and fetus
A

Placental abruption

232
Q

Defective decidual layer ->
abnormal attachment and separation after delivery

Risk factors:

  • prior C-section (old scar*)
  • inflammation
  • placenta previa

describe each of the three types:

  • placenta accreta
  • placenta increta
  • placenta percreta
A

placenta Accreta – placenta Attaches to myometrium without penetrating it; MC type

placenta INcreta – placenta penetrates INto myometrium

placenta PERcreta – placenta penetrates (“PERforates”) through myopetrium and into uterine serosa (invades entire uterine wall); can result in placental attachment to rectum or bladder

233
Q

attachment of placents to lower uterine segment over (or < 2 cm from) internal cervical os

risk factors:

  • multiparity
  • prior C-section

assoc with painless 3rd trimester bleeding.

A

placenta previa

234
Q

one chorion = ?

two chorions = ?

A

one chorion = monozygotic

two chorions = dizygotic

235
Q

-Caused by a “one way valve in the placenta” [ie one-way channel between the twins’ umbilical cords]

ONE BIG TWIN AND ONE SMALL TWIN

  • The twin who gets the blood will be big and can die of circulatory overload.
  • The twin who loses the blood will be small and can die of anemia.
A

Chronic twin-twin transfusion syndrome

236
Q

amnion on both sides, chorion in the middle, so it must be:

A

dichorionic

237
Q
  • very malformed fetus with no heart

- go to term bc the healthy twin provides blood and beating hear

A

Acardius

238
Q

-new-onset HTN with either proteinuria or end-organ dysfxn after 20th week of gestation (
endothelial dysfxn*, vasoconstriction, ischemia

presents as:

  • BP ≥ 140/90
  • > 300 mg/day proteinuria
  • edema
A

preeclampsia

may also have to do with lack of tolerance to dad’s antigens

239
Q

preeclampsia + maternal seizures = ?

A

eclampsia

240
Q

vascular changes of eclampsia:

A

fibrinoids and clear fatty “atherosis”

241
Q

where is the necrosis located in the liver in eclampsia?

A

periportal necrosis

242
Q
  • presence of excess fluid in two or more fetal body parts, thorax, abdomen, skin
  • causes heart failure, profound anemia, hypoxia, extramedullary hematopoiesis, liver dysfxn
  • immune causes: erythroblastosis fetalis – hemolytic anemia due to maternal antibodies
A

hydrops fetalis

243
Q
  • large placenta
  • macrosomia
  • congenital malformations
  • increased risk of thrombosis
  • due to increased levels of maternal blood
A

gestational diabetes

244
Q
  • triploid (69,XXX/XXY/XYY)
  • 2 sperm + 1 egg
  • slight increase in hCG
  • contains fetal parts
  • sx: vaginal bleeding, abdominal pain
  • unevenly swollen villi
A

partial mole

245
Q
  • diploid (46,XX/XY)
  • marked increase in hCG
  • increased uterine size
  • 2% convert to choriocarcinoma
  • NO fetal parts
  • enucleated egg + single sperm (subsequently duplicated paternal DNA – “daddy’s girl”)
  • 15-20% malignant trophoblastic dz
  • sx: 1st trimester bleeding, enlarged uterus, hyperemesis, pre-eclampsia, hyperthyroidism
  • imaging: “honeycombed” uterus or “clusters of grapes,” “snowstorm” on U/S
  • uniformly swollen villi
A

complete mole

246
Q
  • hypertrophic trophoblast with at least some villi, penetrating deep into, and maybe through, the uterine and/or vaginal walls, following a hydatidiform mole
  • Villi may embolize to the lungs but not truly metastasize
A

invasive mole

247
Q
  • rare; can develop during or after pregnancy in mother or baby
  • malignancy of trophoblastic tissue (cytotrophoblasts, syncytiotrophoblasts
  • NO chorionic villi present
  • increased frequency of bilateral/multiple theca-lutein cysts
  • presents with abnormal increased hCG, shortness of breath, hemoptysis
  • hematogenous spread to the lungs
  • responsive to chemo
A

choriocarcinoma

248
Q

TQ
protein malnutrition resulting in:
-skin lesions (flaking rash similar to pellagra, no niacin made from tryptophan)
-edema (due to decreased plasma oncotic pressure – hypoalbuminemia)
-liver malfunction (fatty change due to decreased apolipoprotein synthesis)
-small child with swollen abdomen
-“flag sign” (without tyrosine to make melanin, the hair cannot pigment) – ERF

“MEALS” acronym:

  • Malnutrition
  • Edema
  • Anemia
  • Liver malfunction
  • Skin lesions
A

Kwashiokor

249
Q

total calorie malnutrition resulting in:

  • tissue and muscle wasting
  • loss of subcutaneous fat
  • variable edema
A

Marasmus

  • anorexia nervosa
  • child abuse / neglect (USA)
  • prisoners
250
Q
  • pain, paresthesias, blind spots, blindness…

- undernutrition + tobacco + something else

A

Strachen syndrome / Cuban epidemic neuropathy

251
Q

TQ

  • night blindness***
  • dry, scaly skin (xerosis cutis)*
  • corneal degeneration (keratomalacia)*
  • Bitot spots on conjunctiva*
  • Squamous metaplasia of the eye’s normal lubricant glands -> xerophthalmia (dry eyes)
  • immunosuppression
A

Vitamin A deficiency

252
Q

TQ

  • rickets in children
  • osteomalacia in adults
  • hypocalcemic tetany
  • high PTH
  • frayed costochondral junctions seen on x-rays – ERF
  • seen in exclusively breastfed infants
  • exacerbated by low sun exposure, pigmented skin, prematurity
  • veiling of women
A

Vitamin D deficiency

253
Q

TQ

  • hemolytic anemia
  • acantholysis
  • muscle weakness
  • posterior column and spinocerebellar tract demyelination
A

Vitamin E deficiency

aka tocopherol / tocotrienol

254
Q

TQ

  • neonatal hemorrhage with increased PT and increased aPTT but normal bleeding time (neonates have sterile intestines and are unable to synthesize this vitamin)
  • can also occur after prolonged used of antibiotics
  • preemies, “only milk” babies, fat malabsorption, liver failure, Coumadin Rx – ERF

-complication = brain hemorrhage in babies

A

Vitamin K deficiency

(vitamin K allows gamma-carboxylation of glutamic acid to make clotting factors II, VII, IX, X, C, and S)

“CS 1972”

255
Q

TQ
Deficiency results in impaired glucose breakdown -> ATP depletion worsened by glucose infusion; highly aerobic tissues (e.g., brain and heart) affected first
-causes Wernicke-Korsakoff syndrome and berberi
-seen in malnutrition and alcoholism
-dx made by increase in RBC transketolase activity following the deficient vitamin’s administration

Wernicke-Korsakoff syndrome:

  • confusion, ophthalmoplegia, ataxia (classic triad) + confabulation, personality change, memory loss (permanent)
  • damage to medial dorsal nucleus of thalamus and mammillary bodies

Wet beriberi:

  • high-output cardiac failure (dilated cardiomyopathy)
  • edema

Dry beriberi:

  • polyneuritis
  • symmetrical muscle wasting
A

Vitamin B1 deficiency
(aka thiamine)

Think “ATP”:

  • a-ketoglutarate dehydrogenase
  • Transketolase
  • Pyruvate dehydrogenase

“Ber1Ber1”

256
Q

TQ

  • Cheilosis*** (inflammation of lips, scaling and fissures at the corners of the mouth)
  • Corneal vascularization**
  • Glossitis***
  • first problem is impaired intestinal absorption of iron – ERF
A

Vitamin B2 deficiency
(aka riboflavin)

“2 C’s”

257
Q

TQ

  • glossitis
  • pellagra – can be caused by Hartnup dz (decreased tryptophan absorption), malignant carcinoid syndrome (increased tryptophan metabolism), and isoniazid (decreased vitamin B6)

pellagra (3 D’s):

  • Diarrhea
  • Dementia (also hallucinations)
  • Dermatitis (C3/C4 dermatome “broad collar” rash, hyperpigmentation of sun-exposed areas)
A

Vitamin B3 deficiency

aka niacin

258
Q
  • dermatitis
  • enteritis
  • alopecia
  • adrenal insufficiency
  • painful paresthesias in the lower legs (“burning feet”) – ERF
  • needed to make CoA! – ERF
A

Vitamin B5 deficiency

aka pantothenic acid

259
Q
  • convulsions
  • hyperirritability
  • peripheral neuropathy** (deficiency inducible by isoniazid and oral contraceptives)
  • sideroblastic anemias due to impaired synthesis and iron excess

-“may simply cause elevated homocysteine levels (like folate or B12 deficiency)”

A

Vitamin B6 deficiency

aka pyridoxine

260
Q

TQ

  • macrocytic, megaloblastic anemia
  • hypersegmented PMNs
  • glossitis
  • NO neurologic symptoms (as opposed to B12 deficiency)
  • increased homocysteine levels
  • normal methylmalonic acid levels
  • neural tube defects** / cleft palate
  • MC vitamin B12 deficiency in the USA
  • seen in alcoholism and pregnancy
  • “phenytoin users” – ERF
A

Vitamin B9 deficiency

aka folate

261
Q

TQ

  • macrocytic, megaloblastic anemia
  • hypersegmented PMNs
  • paresthesias** and subacute combined degeneration (degeneration of dorsal columns, lateral corticospinal tracts, and spinocerebellar tracts) due to abnormal myelin
  • associated with increased serum homocysteine and methylmalonic acid levels
  • prolonged deficiency -> irreversible nerve damage
  • pernicious anemia due to anti-intrinsic factor antibodies
A

Vitamin B12 deficiency

aka cobalamin

262
Q
  • exfoliative dermatitis
  • alopecia
  • enteritis

caused by antibiotic use or excessive ingestion of raw egg whites.

A

Vitamin B7 deficiency

aka biotin

263
Q 
TQ
Scurvy
-swollen gums**
-bruising*
-petechiae around hair follicles***
-hemarthrosis
-anemia
-poor wound healing**
-perifollicular and subperiosteal hemorrhages***
-"corkscrew hair"

-weakened immune response

A

Vitamin C deficiency
(aka ascorbic acid)
-Collagen synthesis defect

264
Q

TQ

  • hypochromic, microcytic anemia
  • koilonychia
  • cracks at side of mouth
A

iron deficiency

265
Q

TQ

  • delayed wound healing**
  • hypogonadism
  • decreased adult hair
  • dysgeusia (distorted taste)
  • anosmia
  • acrodermatitis enteropathica** (well-demarcated, scaly plaques in intertriginous areas – dermatitis around the mouth and anus)
  • may predispose to alcoholic cirrhosis

Triad:

  • alopecia
  • dermatitis
  • diarrhea
A

Zinc deficiency

acrodermatitis enteropathica – AR inability to take up zinc [SLC39A4]

266
Q

Deficiency known in preemies, starvation, old protocols for total parenteral nutrition, zinc enthusiasts.

Anemia, bony deformities (if longstanding in kids), and depigmentation.

A

Copper deficiency

267
Q

TQ

  • China’s Kashen dz
  • Central Asia’s “Kashin-Beck” dz
  • Deficiency within soil
  • makes hearts more vulnerable to Coxsackievirus ***
  • Mutilates growing bones and joints
A

Selenium deficiency

268
Q

TQ

  • pot-bellied
  • pale
  • puffy-faced child
  • protruding umbilicus
  • protuberant tongue
  • poor brain development
A

Iodine deficiency -> cretinism

“6 P’s”

Repro Midterm (8 decks)

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