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Big Ol' Patho. > PID, Breast + Ovarian + Uterine CA > Flashcards

PID, Breast + Ovarian + Uterine CA Flashcards

1
Q

PID - what is it?

A

• Infl of repod tract beyond the cervix (has moved past vagina into urterus + beyond)
o Uterus = endometritis
o Tubes = salpingitis
o Ovary = oophoritis

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2
Q

Et of PID?

A

• Polymicrobial eg
- Chlamydia, gonococci, staphylococci, streptococci –> Said to be “pyogenic” microbes – are pus producing
• Untreated bacterial infection → leads to PID
- 10% gonorrhea
- 20% Chlamydia

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3
Q

Patho of PID?

Common complication?

A

Fig 46-6 p. 1097
• Microbes enter cervix (dilated at menstruation) → endometrium → tubes
• Endocervix is where this infection manifests, then transitions up toward tubes (?)
• Rapid prolif as endometrium sloughs (as provides nutrition for bacteria)
• Ascending infection up toward infundibulum, ovaries, entering abdominal cavity

• Common complication: pelvic abscess (pockets of pus?) → followed by peritonitis….possible massive fluid shifts, ascites, etc.

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4
Q

Parametritis = ?

A

inflm of mesenteries that attach reproductive structures to abdominal wall (ligaments that support uterus = parametrium)

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5
Q

Manifestations of PID?

A

1) Lower abdominal pain (d/t extensive inflm) often first symptom
- Acute onset (as infection develops rapidly), often described as sharp, aching
2) heavy, purulent vaginal discharge (this is one of main defining manifestations of PID)
3) Dyspareunia (pain during sexual intercourse d/t inflm)
4) Adnexal tenderness: ad = toward; nexal = uterus…areas in vicinity of uterus present with pain upon palpation
5) Fever
6) Leukocytosis
7) Occasional vaginal bleeding

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6
Q

WHy do you see lots of purulent discharge in PID?

A

• In early stages otherwise asymptomatic (besides pain)..but shortly after bacteria are setting in defenses set in…producing lots of exudate

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7
Q

Long term complication of PID?

A

infertility – tissue damage + scarring d/t inflm… implantation, ovulation etc affected

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8
Q

Dx of PID?

A
  • Presentation
  • Inc CRP + ESR (erythrocyte sedimentation rate) – both nonspecific markers for inflm
  • Laproscopy – see internal structures, scoping body cavity and determining which parts of reprod system have been affected
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9
Q

What is ESR?

A

erythrocyte sedimentation rate

ESR: if leave RBC’s with anticoag in vessel, will eventually settle at bottom and fluids rise to top. When add proteins involved in inflm process, are inc level of protein content in the blood, which tends to cluster the RBC’s in the blood (NOT clotting) and they tend to settle to the bottom faster

CRP more often used than ESR now – is specific to inflm

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10
Q

Tx of PID?

A
  • Multiple broad spectrum Abx (90% success – if no significant damage, prognosis is very good)
  • Eval and treat partner
  • Sx? (May need to repair/remove abscesses, repair oviduct)
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11
Q

Why broad spectrum abx in PID?

A

Often multiple microorganisms involved…

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12
Q

What is the most common female CA?

A

Breast

  • Major cause of CA death
  • Rarely in men
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13
Q

Et + risks for breast CA?

A

• Basic CA et: Mutation of genes that control cell proliferation
• Inc age - cumulative exposure
• Genetic predisposition (no specific gene identified but are most susceptible to risk factors if have genetic makeup)
• Hereditary (5-10%) – is true etiology (next slide has details)
• Hormonal factors (these are risks…not true etiology)
1) Excessive exposure to estrogen for menopause
2) Early menarche
3) Late menopause
4) Nulliparity

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14
Q

Outline the hereditary kind of breast CA

Which specific genes are involved?

A

o Only 5-10% of these CAs are inherited (defective gene tranmitted from mom to child)…this is contrary to what the media wants to make us believe
o Over this 5-10%, 70-80% will have one of two genetic defects:
o BRCA1 gene on chr 17 + BRCA2 gene on Chr 13 (Breast Cancer Gene 1 and 2) – these are tumour suppressor “stop” genes
• Are autosomal dominant – 50% change of getting

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15
Q

Why are hormonal factors expected to be implicated in develop of breast CA?

A

o Have tissue that is highly hormone dependent (for both structure and fx)…as such, excessive exposure to the hormones (mainly estrogen), then likely that will bring about more proliferation = possible malignancy

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16
Q

outline excessive exposure to estrogen after menopause - why is this a used in women?

A

(exogenous estrogens) – ovary ceases exposure to sex hormones as menstrual cycle ceases – almost overnight, estrogen is withdrawn, which causes hot flashes, etc. → HR tx is providing estrogens here in absence of progesterone (this is important)

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17
Q

Why is early menarche factor in breast CA development? Late menopause?

A

Both inc breast exposure to E over lifetime

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18
Q

Nullparity as risk factor for breast CA?

A

no offspring; breaking menstrual cycle seems to dec risk; contrceptive pill also breaks up this cycle

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19
Q

Most common area for tumour in breast CA?

A

Most occurs at upper outer quadrant (near axilla) incl Tail of Spence; next highest around areola and then upper inner quadrant

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20
Q

What are the names of the kinds of breast CA?

A

Various forms (day pg 1577) - Look at the names of the other types + pick up ones that are most prevalent (don’t need to know all details!)
In notes:
1) Ductal carcinoma in situ
2) Infiltrating ductal carcinoma

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21
Q

What does “in situ” mean and what does it say about cancer prognosis?

A

“in situation” suggests is restricted to site of origin (good in terms of prognosis) – arises and remains in ductal epithelium

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22
Q

Ductal carcinoma in situ

  • How common?
  • Origin?
  • Invasive?
  • How is this staged?
A
  • ~20%
  • Intraductal – site of origin in ducts
  • Non-invasive
  • Stage 0 (sometimes categorized in this way….this is problematic because suggests that there is no tumour in place ) – cancer is in place but is very early stage of CA (but will progress if not dealt with)
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23
Q

Infiltrating Ductal Carcinoma

  • Does this always go through in situ stage?
  • How common?
  • Origin?
  • Invasive?
  • Mets?
  • What do you see deposited in breast?
A

• Doesn’t’ have to go through earlier stage
• Most common (~75% of breast CA)
• Ductal origin (therefore epithelial cells) (solid, irreg mass)
• Invasive
• 2 types of mets: proximal + distal
o Metastases means spread through lymph or blood
o Proximal mets spread into axillary lymph nodes
o Distal mets (eg: liver, bone, brain)
• See deposition of collagen fibres in the breast

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24
Q

Manifestations of breast CA?

A
  • Usually woman is one to detect it…which means mass is large enough to palpate, and is therefore in later stage
  • Fixed, irreg, painless mass – usually UOQ
  • Late: discharge (from nipple) retraction (of nipple) edema(in breast)??? → occurs in SOME types
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25
Q

Dx of breast cancer

A

1) Screen: mammography
2) Biopsy - will say if malignant or benign, stage + grade + type
3) Estrogen + Progesterone receptors (in biopsy)
4) Tumor markers eg: CEA = carcinoembryonic antigen

Most detected by pt (not good for early detection)

26
Q

What is mammography

A

sophisticated xray; detect tumours in the breast early – issues that arise: is this really a useful screen? As with other tests, can end up with false positive or false negative;
o Used as both screening + diagnostic test

27
Q

How is a biopsy often done with breast CA?

A

• Will remove whole mass + surrounding tissue to serve purposes of both biopsy and tx

28
Q

Why are you looking at E and P receptors in breast CA biopsy?

A

seeing how dependent this tissue is on these hormones → if see very high number of receptors on malignant cell, says to you that the cell is far more dependent on the hormones than it used to be
(look up significance of this?)

29
Q

carcinoembryonic antigen?

A

not exclusive to breast CA, is protein normally produced by breast tissue (is NOT marker of cellular breakdown from damage to cells) and involved in cellular adhesion, found in high quantities of GI tract of fetus; the more cells you have, the more secretion of this protein – this is how it serves as a marker

30
Q

Tx of breast CA?

names of surgeries?

A

• Quite varied, depending on type
• Sx, radiation, chemo, hormone therapy – usually 2 or 3 of these used
• If E/P receptors are seen to be inc, will deal with this with hormone therapy (remove the hormones)
- Tamoxifen (antiE)
- Estrogen
- Androgens
- Progestins (if high P receptor content)
SURGERY:
• Lumpectomy – tumour + surrounding tissue
• Quadrantectomy – remove quadrant
• Mastectomy – breast removal
• Radiation – irradiate entire breast + axilla
• Chemo – HT is also considered to be chemo; pre + post sx

31
Q

Use of Tamoxifen + Estrogen as hormone tx in breast CA?

A

o Tamoxifen = non-steroidal, antiE – good to treat malignant cells that have shown high E receptor content

o Estrogen - is reducing or increasing the number of receptors for that hormone (to dec or inc response to hormone); here is giving high doses of E (w/o progresterone) to DECREASE number of estrogen receptors as is causing damage to those receptors (destroys them)

32
Q

What is an important sign of prognosis in breast CA?

A

Prognosis is more based on whether axillary lymph nodes are involved, rather than how much breast tissue is involved.

33
Q

What is considered the most lethal form of reproductive cancer and why?

A

Ovarian
d/t silent growth (advances quickly + silently)…allowing progression before dx
• Difficult to dx → ~75% mets at detection

34
Q

Why is ovarian CA particularly hard to detect?

A

No shortage of space
• What occurs during ovulation (maturation of oocytes and oogenesis, englarging) and occurs normally is similar to what will occur if malignancy is arising – therefore difficult to detect if becoming pathologic!

35
Q

Et/risk factors for ovarian CA?

A

• Aging – most between 65-84 (post-menopausal disease) –> has to do with ovulatory age
• Autosomal dominant in some forms (has an inherited form)
• Family hx in others
• Woman who has had breast cancer has higher risk of developing both cancers
• Other factors
o Nulliparity, infertility, dysmenorrhea?? – not cause and effect, just some correlation

36
Q

How is ovulatory age a factor in ovarian CA?

A

Ovulatory cycle ongoing cycle…like breast CA and menstrual cycle: the longer the period without interruption, the greater the risk
• At birth, full number of eggs is in place – the later batches of eggs have greater exposure

37
Q

Patho of ovarian CA
What types are there?
How does spread occur?

A

• Diverse types: Epithelial (90%), germ cells or stromal tumors
• Silent growth and spread – spread (invasion + extension) into surrounding tissues, seeding into body cavities:
- Spread to Tubes, uterus & ligaments, other ovary (all of these are in contact with the site or origin)
o Seeding to Bowel surfaces, liver & other organs?? (this is spread to the body cavity) –> causes P on adj organs or abdm distension
o Mets via lymph + blood

38
Q

What is characteristic of primary tumours in ovary?

A

“papillations”

looked like yellow knobby things..

39
Q

What is usually the first finding in ovarian CA?

A

Pelvic mass…this is a LATE symptom

40
Q

Manifestations of ovarian CA?

A
  • Early stages have non=specific GI disturbances (abdm discomfort, gas) – will look at IBS, acute infection, IBD….not going to go to ovarian CA – therefore difficult to detect
    • Abdm distension – at this point know something is quite wrong but still not specific to O CA
    • Pain, urinary + bowel obstruction d/t P on bowel from original mass or seeding to the bowel itself
    • Ascites with dyspnea –> Ascites: massive inflammatory changes d/t progression of the tumour, seeding, etc
    • Pelvic mass usually 1st finding (but late)
    –> use U/S & exploratory sx (need to get in and confirm have mass, see involvement of other structures
41
Q

Tx of ovarian CA

A

• Determined by exploratory sx
• Aggressive tx
o Excise uterus, tubes, ovaries + omentum (maybe even into bowels…is very extensive sx)
• Then chemo (intermediate + advanced disease)
• Laparotomy after 6-24m to determine if further tx needed
• Some fully recover (but not good prognosis usually)

42
Q

What occurs during the menstrual cycle with regard to endometrium? Which hormone supports these changes?

A

• Endometrium thickens + has nutritive material stored here during menstrual cycle → on monthly basis, you are undergoing hyperplasia…need support to do this (hormones, esp E drives this) – this is physiologic hyperplasia…

43
Q

How common is uterine cancer?

In what age group?

A
  • Most common pelvic CA in women

* Usually 55-65yrs

44
Q

Uterine aka ___ Ca?

A

Endometrial

45
Q

Et of uterine CA?

A 
•	Mostly related to hyperestrogenism (excessive levels of estrogen)
• Some unrelated to E 
• Family hx 
RISKS:
- Obesity --> inc E prod + storage 
- Age
- Frequent pelvic radiation
- Hx of other reproductive CA
- DM – risk d/t metabolic defects
46
Q

How is obesity an important risk factor for uterine CA?

A

Entails excessive adipose tissue → estrogen is produced almost exclusively in ovary normally, however adipose tissue also has ability to synthesize estrogen (from an androgen precursor); adipose also has ability to STORE E (whatever is not utilized)…adding to supply of E

47
Q

How do E and P tend to fluctuate in relation to one another?

A

o Progesterone + E rise tend to “balance each other out”…when E high, P low – high E means have lower amounts of P

48
Q

Patho of uterine CA?

A
  • Usually adenocarcinoma (~85%)
  • E → endometrial hyperplasia (no longer physiologic - gone from dysplasia to anaplasia)
  • 2 TYPES (details to come)
  • Slow progression
  • Spreads to uterus (into deeper layers) & vagina – extension NOT mets
  • Late mets via lymph + blood
49
Q

Is uterine CA the same as cervical CA?

A

No

50
Q

Describe Types 1 and 2 of uterine CA based on:

  • Prevalence
  • E sensitivity
  • Relative prognosis
A 
TYPE 1 (~90%)
• E sensitive – is type in which hyperestrogenism is implicated  → endometrial hyperplasia
•	Better prognosis

TYPE 2 (~10%)
• Non E dependent – not driven by estrogen
• Linked to endometrial atrophy…women who have this atrophy are likely to develop the CA
• Poor prognosis

51
Q

Manifestations of uterine CA?

A
  • Painless vaginal bleeding (in between the menses)

* Others relate to invasion + mets

52
Q

Tx of uterine CA?

A
  • Based on stage
  • Sx w radiation – most successful approach
  • Hormone therapies also may be useful – E or anti-E like above
53
Q

What are the “positive” features of cervial CA?

A
  • Can be avoided almost all together
  • If caught in in situ stage, have 100% treatable
  • Goes through pre-CA state
  • Have very good screen
54
Q

Et + risks of cervical CA

A

HPV infection
• Early age sex, multiple sex partners (inc risk of transmission of HPV viruses)
• Smoking – organ specific carcinogens
• Hx of STD’s

55
Q

Describe relationship between HPV and cervical CA

What strains of HPV are particularly important here?

A

virus invades cells, interferes with DNA → > 100 strains of this virus, of which 40 are sexually transmitted; 4 of these of particular concern here:
o Strains 6 + 11 cause ~90% of warts
o Strains 16 + 18 account for ~70% of cervical CA

We have a reliable vaccine

56
Q

Patho of cervical CA

A
  • Mostly squamous cell origin (epithelial origin)
  • Initial dysplasia (preCA lesion)
  • Then carcinoma in situ (in epithelial layer) –lots of warning here!
  • Later invasive CA (deeper layers) → with progression into deeper layers, area of involvement becomes wider (forms V)
  • Several years between preCA & invasive stage
  • Mets via lymphatic’s (this will only occur if not dealt with for quite a long time)
57
Q

WHat are the levels of cervical intraepithelial neoplasia (CIN):

A

o Mild dysplasia = CIN 1
o Moderate dysplasia = CIN 2
o Severe dysplasia + carcinoma in situ (CIN 3)

58
Q

Dx of cervical CA

A

PAP screen
• Colposcopy – looking at cervix through vagina
• Diagnosis not difficult – looking at cellular changes

59
Q

How does PAP test work? Named after? If positive what will result show?

A

o Using pap stain, named after Papanicolaou
o Collect exfoliating epithelial cells to look for dysplasia
o If positive will see CIN with #

60
Q

Manifestations of cervical CA?

A
  • Vaginal discharge + bleeding
  • Metrorrhagia
  • Inc freq of menses
  • Pain assoc with menses (in late phases)
61
Q

Tx of cervical CA?

A
  • Early – excision
  • If later…Invasive – radiation & sx
  • Cryosurgery = freezing the affected tissue (inducing necrosis)
  • Conization = excise the cone-shaped area of affected tissue
  • Laser – induce necrosis
  • Radical hysterectomy (maybe in more advances stages)

Big Ol' Patho. (17 decks)

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