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genitourinary Flashcards

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1
Q

describe anatomy of prostate

A 
it is encapsulated 
Close to the bladder
urethra goes through the prostate
seminal vessicle close
post surface in contact with rectum
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2
Q

does the prostate get bigger or smaller as you age?

A

bigger

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3
Q

what are the common ages and occurrences (%) for benign prostatic hyperplasia?

A

> 40 ~20%
60 years ~50%
80 ~90%

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4
Q

benign prostatic hyperplasia Et?

A 
unclear
ageing -risk
- are related changes in androgen levels
altered T:E
-genetics, race, diet
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5
Q

what is DHT

A

dihydrotestosterone: active metabolite of testosterone

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6
Q

what is the relation between T, DHT, and E with BPH?

A

testosterone enters the circulation and accessory organs of male reproductive system and as it enters the prostate, about 95% of it is converted to DHT. DHT supports growth and function of prostate and other accessory organs

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7
Q

what is T 5a-reductase

A

enzyme that converts T

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8
Q

what sensitizes the prostate to DHT?

A

Estrogen. it is responsible in facilitating the action of DHT on the cell (sensitizes the cell-makes it more responsive to it)

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9
Q

what happens to the hormones during BPH

A

testosterone declines, estrogen remains the same so it is a relative increase of E–> sensitizes prostate to DHT –> enlargement

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10
Q

what happens as a result of the hormone change of BPH

A

bc of the relative inc in E–> hyperplasia of periurtheral tissues–> compresses urethra
-also hypertrophy of smooth muscle
-impedes urine flow so..
more urine accumulates in the bladder bc of constriction of urethra causing urine to back up into bladder

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11
Q

what are the compensatory str changes due to hormone changes from BPH

A

bladder wall thickens because more urine assume

trabeculations and diverticula- inc capacity of the bladder (they are folds that open up)

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12
Q

what occurs bc of urine stasis in BPH?

A

-complication could be UTI and calculi (stones)
ureters distend with urine –> hydroureter (when bladder is full and remains full)
-ureters loop downward & fishhook
-urine backs up in the kidney causing hydronephrosis (distention of the renal pelvis and the calculi)

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13
Q

Muftis of BPH?

A

frequency (bladder is full, attempt to urinate but can’t completely void)

  • hesitancy (difficulty starting urine stream)
  • Weak urine stream
  • Post void dribbing or terminal dribbling
  • Complete ouster of urethra (urine retention)
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14
Q

Dx BPH

A

hx, mnfts, px
DRE (digital rectal exam)..this is a screen
PSA (prostate specific antigen)
BUN, creatinine
urinalysis (infect & hematuria- renal calculi)

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15
Q

what does the PSA for BPH

A

prostate specific antigen is a component of prostatic fluid and int enters the circulation
Total PSA (tPSA) is proportional to the mass of the prostate (the larger the gland, the more the cells, the greater the quantity of secretion)
PSAD (density) # of cells
PSAV (veolcity) speed at which cells form
need to do an US to get size

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16
Q

Tx BPH?

A

behavioral modifications: maybe avoid drinking fluid before bed
based on severity and complications
-A adrenergic antagonists (alpha blocking the binding- objective to relax the muscles)
..act on muscles (muscle in urethra)
…dec obstr –> improves urination
-5a-reductase inhibitor (long term) inhibits the enzyme
..dec DHt
TURP (transurethral) or laser prostatectomy (aim to remove the prostate)

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17
Q

is prostate CA 1,2,3,4,5 cause of CA death?

A

3

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18
Q

after what age does prostate cancer usually develop? why?

A

after age 65. d/t accumulative effect of carcinogens, enough damage to cause mutations.

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19
Q

what are the risks of prostate cancer?

A

age, diet, ethnicity, familial, androgens

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20
Q

what is the patho of prostate cancer?

A

adenocarcinomas in peripheral, multicentric origins

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21
Q

does the development of prostate cancer start near the urethra or the peripheral edge?

A

peripheral edge

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22
Q

where does the spread occur in prostate cancer?

A

extension to bladder and seminal vessicle

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23
Q

where are it met in prostate cancer?

A

bone (initially back, hip), liver and lungs

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24
Q

when do mnfts appear in prostate cancer?

A

after invasion or mets (through blood & lymph)

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25
mnfts of prostate cancer?
appear very different among people prostatitis common late hip and back pain (if mets to bone)
26
Dx of prostate cancer?
Hx, Px DRE, PSA biopsy (transurethral biopsy) US
27
Tx of prostate cancer?
stage, grade, and age based localized= low risk --> active surveillance -1st line: antiandrogen (prostate is supported by androgens so if you withdraw support- limit growth) -radical prostatectomy (remove prostate and seminal vessicle -radiation
28
what is PID?
inflm of reprod tract beyond cervix (usually d/t bact infect)
29
what are the words that describe inflame in uterus; tubes; ovary?
uterus: edmoetritis tubes: salpingitis ovary: oophoritis
30
Et of PID?
polymicrobial (bact) they are pyogenic- pus producing bacteria - chlamydia, gonocci, staphylococci, streptococci Untreated back infect 10% gonorrhea 20% chlamydia
31
Patho of PID?
microbes enter cervix and there is dilation at menstruation and bact get into endometrium, tubes (eventually infundibulum, and body cavity) - rapid proliferation and multiplication as endometrium sloughs - ascending infect (endocervix to uterus)
32
whats a common complication of PID?
``` pelvic abscess (containing pus and bacteria) parametritis (inflm of mesenteries) -entry into the circulation ```
33
mnfts of PID?
lower abide pain (acute onset, sharp, achy pain) - largely asymptomatic before inflm - dyspareunia (pain during intercourse) - adnexal tenderness (tender on palpation of uterus) - Heavy purulent vaginal discharge - Fever - Leukocytosis - Some vaginal bleeding - Infertility
34
Dx of PID?
presentation inc ESR (erythrocyte sedimentation rate- inc proteins in the blood will allow RBC to cluster and clump to the bottom of a tube) -Inc CRP -Laparoscopy (visualize the external organs see inside the body cavity)
35
Tx of PID?
multiple broad spectrum Abx (90% success) -evaluate and treat partner Sx (if pelvic abscess, obstr of ovary duct)
36
How common is breast cancer in females?
1 in 8
37
Et/ Risks of Breast cancer?
``` inc age (bc accumulative exposure) genetic predisposition hereditary (5-10%) hormonal factors early menarche late menopause nulliparty ```
38
how much of genetic predisposition of breast cancer is inherited and non inherited? how many genes in inherited?
5-10% is inherited 90% is non inherited 7-8 of the inherited have 1 or 2 genes
39
what are the genes that are hereditary for breast CA? | how are they acquired?
BRCA1 gene on chr 17 and BRCA gene on chr 13 (they are tumor suppressor genes) only count for 75% of inherited form. Autosomal dominant (50% chance)
40
what hormonal factors inc risk for breast CA?
excessive exposure to estrogen for menopause (at menopause the ovary seizes prod of sex hormones) and then abruptly the estrogen is gone. thats why they give E
41
what are the different types of tumors for breast CA? (patho)
ductal carcinoma in situ (glandular epithelial tissue) | -infilitrating ductal carcinoma
42
why is it more common to see tutors that are "carcinoma type" as opposed to muscle?
because epithelial tissue replicates easily and muscle does not.
43
what are the characteristics of ductal carcinoma in situ? in breast CA (prevalence, site, stage)
- 20% - intraductal (noninvasive) - stage 0 (saying no tutor is in place but that is not correct bc there has to be malignancy in place)
44
what are the characteristics of infiltrating ductal carcinoma (prevalence, site, mets)
most common - 75% ductal origin (solid, irreg mass) invasive (infilitrating) local at the site of origin proximal mets (lymph vessels and short distance like axillary lymph nodes) distal mes (liver, bone, brain) deposition of collagen fibres (solid mass)
45
mnfts of breast cancer?
fixed, irreg, painless mass - usually UOQ late: discharge, retraction & edema (in nipple)
46
Dx of breast CA?
mammography, biopsy (malignant or benign) E & P receptors (# of E and progesterone receptors) Tumor markers (eg. CEO - carcinoembroyonic antigen)
47
what is CEO (breast cancer)
carcinoembryonic antigen it is a tutor marker that is not exclusive to breast cancer. produced by breast tissue that gets into circulation. it helps with cell adhesion. found in high quantities in GI tissue in the fetus, the more cells you have, the more sec of this protein
48
Breast CA tx?
sx, chemo, radiation usually 2 or 3 of these are used if E/P receipts inc, Hx therapy (also considered chemo) -lumpectomy (mass and surrounding tissue) quadrantectomy (quadrant removal) -Mastectomy (breast) (radica- removing some muscle tissue in chest wall or removal of other breast)
49
explain hormone therapy in breast CA
if you have lots of receptors for E you want to remove E so - Tamoxifen (antiE) - Estrogen (high doses of estrogen down regulate the # of receptors and estrogen can't adequately bind so the cells die) - Androgen (antiE) - Progesterone
50
why is ovarian cancer difficult to diagnose?
75% mets at detection. | similar to growth of oocytes
51
Et/RIsks of ovarian cancer?
``` ageing (most between 64-84) ovulatory age autosomal dominant in some forms family hx other factors: nulliparity, infertility, dysmenorrhea ```
52
Patho of ovarian cancer?
diverse types -epith (90%), germ cell, or stream tutors (ground tissue, matrix) silent growth and spread -tubes, uterus, & ligaments, other ovary -bowel surfaces, livery & other organs (through seeding) -pressure on adj organs or abdm distension
53
mnfts of ovarian cancer and complications
early non specific GI disturbances: initially silent complications: abdm distension pain, urinary, and bowel obstr -ascites with dyspnea -Pelvic mass usually 1st finding (but late) US and exploratory Sx
54
Tx of ovarian cancer
determined by exploratory sx aggressive tx: excise uterus, tubes, ovaries, & omentum then chemo (intermediate & advanced disease laparotomy after 6-12 m some recover fully
55
what age is most common for uterine cancer?
55-65
56
what is uterine cancer most related to? (ET)
inc E (hyperestroginitin) could have exogenous or extraneous E (tx or body) - some unrelated to E - Family Hx
57
what are the risks of uterine cancer?
age, pelvic radiation, hx of other reproductive CA, diabets- low. metab disease so can involve synthesis of E, htn, estrogen and progesterone (balance each other out- one peaks and other drops)
58
patho of uterine cancer?
``` usually adenocarcinoma (~85%) glandular tissue -hyperplasia, dysplasia to anaplasia -E -> endometrial hyperplasia (physiologic) 2 types ```
59
patho of type 1 uterine cancer? | how prevalent is this type?
``` E sensitive (hyperestrogenitism) -endometrial hyperplasia better prognosis ```
60
patho of type 2 uterine cancer? | how prevalent is this?
non E dependent this type is associated with atrophy of the edmoetrium poor prognosis spreads to uterus
61
what is the cervix?
it is an aperture
62
where does cervical cancer occur specifically? is it avoidable?
wall surrounding the opening is where the malignancy develops. 100%
63
Et/ risks of cervical cancer?
HPV infect Early age sex, multiple sex partners Smoking (organ specific carcinogens), hx of STDs
64
how many strains of this virus are there? (cervical ca) what are they from?
>100. 40 are sexually transmitted 4 are of concern 6 and 11 cause is 90% genital warts
65
which strains of the virus cause cervical cancer?
16 and 18
66
what does the HPV vaccine do for cervical cancer?
invades cells and interferes with DNA of cell
67
what is the patho of cervical cancer?
mostly squamous cell origin initial dysplasia (preCA lesion) then carcinoma in situ (pith layer) later invasive (CA deeper layers)
68
what are the levels of cervical intraepithelial neoplasia (CIN)?
mild dysplasia (CIN 1) earliest pos change Moderate (CIN 2) Severe dysplasia & carcinoma (CIN 3)
69
how many years between the preCA and invasive stage? (Cervical cancer)
2 years
70
how does cervical cancer mets?
lymphatics
71
what is the paps smear?
papilicniow. it is a staining procedure where you collect exfoliating cells and take smear from the surface of the cells and put them on a slide and stain them and see if they go into dysplasia. if squamous cells-neg. if it nt normal then you have dysplasia and if they change further then you have anaplasia
72
how can you detect the different positive reports of paps smears?
CIN 1,2,3. looking at neoplasia in the cervis and inside epithelial tissue
73
Dx of Cevical CA?
PAP (repeat) | Colposopcy (looking at cervix through the vagina)
74
Manifestations of cervical CA
vaginal discharge and bleeding metorrhagia inc freq of menses pain
75
Tx of cervical ca?
``` early- excision invasive- radiatoin & sx cryosurgery (freezing the effected tissue and inducing necrosis to freeze it) conoization- taking out the cone shape laser- using heat to get rid of it radical hysterectomy ```
76
what the basic pattern of bleeding is changed, what is this due to? what if the pattern is normal but there are superimposed bleeding episodes or spotting
lack of ovulation and disturbances in the pattern of hormone secretion organic lesions or hematologic disorders
77
what is amenorrhea?
absence of menstruation
78
what is primary amenorrhea?
is failure to menstruate by 15yrs old or by 13yrs old if accompanied by absence of secondary sex characteristics. It is usually caused by gonadal dysgenesis, congenital mullerian agenesis, testicular feinization, or a hypothalamic-pituitary-axis disorder
79
what is secondary amenorrhea?
is the cessation of menses for at least 6 months in a woman with established normal menstrual cycles. Causes include: ovarian, pituitary or hypothalamic dysfunction; intrauterine adhesions; infections; pituitary tumor; anorexia nervosa; or strenuous physical exercise (that alters fat-muscle ratio which is necessary for menses to occur)
80
what is Dx of amenorrhea?
history with emphasis on bleeding pattern and physical exam, endocrine studies, pregnancy test, endometrium, endometrial biopsy, D&C with and without hysteroscopy, progesterone withdrawal tests, and CT scan or MRI to exclude pituitary tumor
81
Tx of amenorrhea?
cause induce menses with cyclic progesterone or combined E and P
82
what is dysmenorrhea?
pain or discomfort with menstratution that is generally not serious but can cause some monthly disability for certain women
83
what is the cause of dysmenorrhea?
could be excess prostaglandin production causing painful contraction of the uterus and arteriolar vasospasm
84
what is primary dysmenorrhea?
menstrual pain that isn’t associated with a pathologic process or physical abnormality. Treatment is directed at controlling symptoms. Aspirin and acetaminophen relieve minor cramps but prostaglandin synthetase inhibitors (eg ibuprofen, naproxen) are best if contraception isn’t desired. Ovulation suppression and symptomatic relief can be achieved with oral contraceptive.
85
what is secondary dysmenorrhea?
menstrual pain caused by specific organc conditions eg endometriosis, uterine fibroids, adenomyosis, pelvic adhesions, IUDs or PID. Medical or surgical intervention may be necessary.
86
what is menorrhagia? et?
prolonged or excessive bleeding during regular menstrual flow usually r/t endocrine disturbances in young woman later in life usually bc inflm disturbances, tumors of the uterus, or hormonal imbalances
87
what is metrorrhagia? et?
* Vaginal bleeding between regular menstrual periods. This is the most significant form of menstrual dysfunction as it may signal cancer, benign tumours of the uterus, or other gynaecologic problems and prompt evaluation is necessary * In women on oral contraceptives bleeding between periods is usually not serious but women taking HT (hormone therapy maybe??) should be evaluated

patho (12 decks)

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