GU CM Flashcards

(418 cards)

1
Q

in women of child bearing age abnormal bleeding is attributed to what UNLESS proven otherwise?

A

PREGNANCY!!!

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2
Q

what test does every woman of child bearing age get when she is having abnormal bleeding?

A

PREGNANCY TEST!!!

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3
Q

what two tests should ever patient get when they have abnormal bleeding?

A
  1. pregnancy test
  2. CBC with platelets
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4
Q

when you think of dysmennorhhea and infertility in a 25 year old what should you think of?

A

endometriosis

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5
Q

dismennorreahh and increasing heavy periods in a 48 year old you should think about what two things?

A
  1. endometrial hyperplasia/cancer!!! NEED TO THINK OF THIS
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6
Q

regular periods but a uterus the size of a 10 week pregnancy in a 35 year old should make you think of?

A

a FIBROID!!!

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7
Q

new onset of bleeding in a 70 year old should make you think of?

A

cancer until otherwise!!

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8
Q

what is the predominat bacterial of the vaginal flora?

A

lactobacillis

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9
Q

explain the normal vaginal flora and ph of the vagina?

predominant flora?

vaginal wall cell type?

cells make?

pH?

A

predominant flora: lactobaciillis….produce lactic acid

vaginal wall: strafified squamous

cells make: glyconuitrient rich environment for microorganisms

pH: 3.5-4.5

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10
Q

what are 7 normal organisms in the vaginal canal other than lactobacillis?

A
  1. yeast
  2. e. coli and other fecal bacteria
  3. garnerella
  4. staph, strep
  5. anaerobes
  6. trichomonads
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11
Q

what should you watch out for if you see discharge in a young woman?

A

abuse!

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12
Q

where are bartholins glands? what are their function?

A

two glands located slightly posterior to the left and right of the opening of the vagina

secrete mucous to lubricate the vaginal opening

1 or 2 drops when sexually aroused

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13
Q

what might cause creamy white discharge in 10 year old girl?

A

early estrogen secretion

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14
Q

what shoud you think of with white vaginal discharge with intense vaginal itching?

A

yeast!

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15
Q

what should you think of if post coital spotting in a 70 year old woman?

A

atrophic vaginitis

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16
Q

what should you think about with intense vulvar itiching in a 60 year old?

A

lichen sclerosis

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17
Q

what should you think of with a asymptomatic mass at the introitus? 2

A
  1. bartholin cyst
  2. relaxation issue

dependent on age as to what to think about!

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18
Q

stress urinary incontinence

who is this common in?

why does it occur?

explain the pressure differences?

what actions might bring this on?

what are 3 things that could cause this in a person?

A

common problem in women of all ages and results from weakness or disruption in the pelvic floor muscles leading to poor support of the vesicourethral sphincters

usually: the i_ntraurethral pressure is greater than the intravesicular pressure_ which is called the urethral closure pressure

if i_ntra-abdominal pressure increases_ from things like coughing, laughing, or sneezing and the pressure isn’t equally distributed to the urethra then incontinence occurs

causes of decreased muscle tone: aging, child birth, surgical procedures

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19
Q

urge urinary incontinence

what does the pt feel?

what is this associated with?

what is the definition of this?

what are 2 contributing factors?

3 symptoms?

A

overactive, nocturia, urinary frequency, detrusor overactivity

loss of urine associated with strong desire to void URGENCY, often associated with overactive bladder

definition: urgency, frequency with or without incontinence in the absence of UTI or obvious pathology

Two contributing factors to overactive bladder:

  1. CNS and neural control of bladder sensation and emptying, ex: stroke, Parkinsons, MS
  2. smooth muscle of the bladder itself (myogenic)
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20
Q

incomplete emptying “overflow” urinary incontinence

what are 7 signs of this?

what are two causes?

what are 2 causes in women?

what are 2 causes in men?

A

intravesical pressure exceeds the maximal urethral pressure because of bladder distension

dribbling, weak urinary stream, frequency, and nocturia, hesitancy, frequency, nocturia, nocturnal enuresis (bedwetting), detrusor underactivity or bladder outlet obstruction

women causes: uterine prolapse, previous incontinence surgery

men: most common is enlarged prostate gland

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21
Q

what are the 3 PE tests you want to do with someone with urinary incontinence?

what are the 4 workup tests you would do?

A

PE:

  1. pelvic exam
  2. digital rectal exam (masses, prostate)
  3. neuro exam if sudden loss (think cauda equina)

Workup:

  1. urinalysis
  2. prostate specific antigen
  3. post void bladder scan
  4. urology consult
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22
Q

although urinary incontince tx is dependent on the type, what are 5 tx options you could consider?

A
  1. fluid management
  2. timed voiding
  3. bladder retraining
  4. keagle/pelvic floor exercises
  5. surgical intervention
  6. pessaries to hold uterus up
  7. decrease caffine/alchohol
  8. (urge) anticholinergics

(oxybutynin, possibly tricyclic antidepressant)

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23
Q

Nephrolithiasis

what are the two things you need for the formation of crystals?

what are four risk factors that allows this to happen?

what are the four types of stones?

A

formation is dependent on supersaturation and an environment that allows the stone to grow!

supersaturation risk:

heredity- cystinuria SLC3A1/SLC7A9

environmental

diet

obesity

four types of stones:

  1. calcium oxalate
  2. struvite
  3. uric acid
  4. cystine
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25
Q

nephrolathiasis

struvite stone

what 2 things is this associated with?

4 bacteria?

can you pass them?

when do they get bigger?

3 tx options?

A

“staghorn” stones that always associated with UTI and alkaline urine

  1. produced by UTI with urease producing bacteria
  2. proteus, klebsiella, pseudomonas, enterobacter
  3. made of magnesium ammonium
  4. usually too large to pass and require lithotripsy or surgical removal
  5. they enlarge as the bacterial count increases

Tx:

  1. prevent UTIs
  2. lithrotripsy
  3. surgical removal
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26
nephrolithiasis calcium oxalate stones can you see it on a xray? what is it usually associated with? what are 4 associated factors? 3 tx options in general?
MOST COMMON TYPE OF STONE 1. **_RADIOOPAQUE_** 2. usually associated with high calcium levels in the blood and urine 3. contributing factors: excessive bone reabsorption, bone disease, hyperparathyroidism and renal tubular acidosis predispose for these stones TX: treat underlying conditions increased fluid intake thiazide diuretics | (70-80%)
28
nephrolithiasis uric acid stone what is this caused by? can you see on xray? what are 2 RF? 2 tx options?
**_caused by low Ph (acidic) urine_** 1. **_radiolucent_** cant be seen on xray 2. caused by high levels of uric acid in the urine or gout 3. RF: obesity/diabetic or both Tx: 1. decrease uring PH below 6 (more alkaline) using _potassium citrate_ 2. allopurinol with decrease purine diet (fish, shellfish, and meats)
29
nephrolithiasis cystine stones what type of disorder is this and who is it common in? what is the appearance of the stones? what are the two treatement options?
**_autosomally recessive inherited abnormalities CYSTINURIA_** "childhood caliculi" 1.**_smooth-edged ground glass appearence_** TX: 1. increase urine volumes to 3 L a day and increase urine pH to greater than 7 2. occasionally chelating agents
30
what is the most important test when suspecting nephrolithiasis? what do you expect to see for each of the stones? 4 types of labs you should consider ordering?
1. non-contrast CT (gold standard) used to identify the size, location and type of stone ## Footnote - _low density_ (aka can't see): uric acid, cystine - _high density_: calcium oxalate, struvite - _struvite_: laminar, rugged apperance, full of casts with "stag horn apperance" \*\*\*\*\*do renal US for pregnant people who can't have the CT\*\*\*\* 2. labs 1. urinalysis (stone type/blood) 2. BMP (calcium and creatinine if worried about kidney function) 3. 24 hour urine for the amount excreted 4. thyroid function test
31
what are 6 RF for nephrolithiasis in general?
high humidity high temp sedentary high animal protein and high salt FH for calcium stones hyperthyroidism/hypothyroidism
32
what are the 4 most common symptoms with nephrolithiasis? and less common symtpoms? (4)
**Most common:** 1. unilateral flank pain 2. sudden onset 3. renal colic 4. hematuria **Less common:** 1. vague abdominal pain 2. acute abdominal/flank pain 3. difficulty urinating 4. penile or testicular pain
34
what are 6 things that would qualify for urologist referral in a patient with nephrolithiasis?
acute renal failure urosepsis urinary obstruction concomitant pyelonephritis \>10 cm haven’t passed for 4-6 weeks
35
what are the 5 tx options for nephrolithiasis?
**1. NSAIDS and opoids!!** **1.5. increased fluid intake key!** **2. shock wave lithotripsy (small renal caliculi)** **3. precutaneous nephrolithotomy** **4. rigid and flexible ureterscopy +/- stent placement** (tx of choice for maority of middle and distal urethral stones or those who failed shock wave lithrotripsy) **5. diet changes for Ca oxalate stones** (decrease spinach, animal protein, Na intake)
36
what is the most common cause of recurrent calcium stones?
most common abnormality elevated Ca excretion, decreased serum Ca
37
stone passage ## Footnote 1. explain how size and location effect the ability to pass the stone? 2. what are two meds you can give to help during the passage?
**size** 5-10 mm less likely to pass on their own \>10 mm won’t pass on their own **location** stones in proximal ureter less likely to pass ureterovesicular junction more likely to pass _Meds to help pass:_ alpha blocker (tramsulosin) CCB (nifedipine)
38
if you txing a pt with nephrolithiasis what are 3 things you want to do to help manage the pt? when do you consider hospitalization (2)?
1. most managed conservatively with pain management Nsaids and Opoids (BETTER USED TOGETHER!!) 2. hydration 3. strain urine **consider hospitalization:** uncontrolled pain/fever can’t tolerate oral intake
41
why is it important to educate your patient on recurrence for nephrolithiasis?
⅓ will experience stone recurrence within 5 years ½ experience stone reccurence within 10 years
42
explain what falls under the two categories of uncomplicated UTI (2) and complicated UTI? (6)
**uncomplicated UTI** - acute cysitits - acute pyelonephritis **complicated UTI** 1. something that makes the more likely to fail treatment - obstruction - anatomic abnormality urologic dysfunction - MDR uropathogen 2. pregnant 3. elderly 4. children 5. males 6. recurrent
43
Complicated UTI Pregnancy what are 3 things its assocaited with? do you screen? if positive what must you do (2)? what is one really key thing to remember about UTI and pregnant women?
associated with preterm birth, low birth weight, prenatal mortality screen in 1st trimester with UC **_admit them since dangerous with baby_** always check urine culture if asymptomatic because the bacteria in the urine can cause the things under A, if + treat with abx **_if they get 2+ positive tests with greater than 100,000 positive tests they they will be on suppressive abx for the remainder of the pregnancy_**
44
Complicated UTI eldery what are two groups of peopel that are esp susceptible? what are three things that contribute to the first?
**postmenopausal women** 1. bladder/uterine prolapse 2. loss of lactobacilli in vaginal flor allos for E. coli to take over 3. diabetes (sugar) **benign prostatic hypertrophy**
45
complicated UTI children who is this more common in? 3 symptoms? what is the DOC? how long do you treat for, two options?
white children more common than black children **fever, hematuria, abdominal pain** **DOC: 2nd-3rd line cephalosporin** _7-14 days_ if febrile _5 days_ if immune competent and afebrile
46
complicated UTI males what are two risk factors? urethra length?
unusual for men 15-50 RF: **uncircumcised, anal intercourse** antibacterial material in prostatic fluid **18-20 cm urethra**
47
who are UTIs most common in? what is the most common route of infection? what are most from? what isthe pathogenisis of this and what does it RARELY come from?
**30:1 ratio women to men** because women have a significantly short urethra route of infection: ascending from the urethra UTI most commonly from _uncomplifcated acute cystitis_ pathogenisis: 1. colonization of vaginal introitus by uropathogens from fecal flora ascend from urethra into bladder **CYSTITIS** 2. uropathogens ascend from bladder to kidney via ureters RARELY CAUSED BY SEEDING OF BACTERIA
48
what are 5 RF for UTI?
female sex frequent sexual intercourse diaphragm/spermicide use delayed post-coital micturition (not urinating after intercourse) hx of UTI
49
what are four bacteria that cause UTI and which is by far the most common? what percent?
**e.coli most common 75-95%** proteus mirabilis klebsiella pneumoniae enterococcus
50
what are the difference in symptoms for cystitis (6) vs pyelonephritis? (5)
cystitis: ## Footnote 1. dysuria or burning while urination 2. increased frequency/urgency 3. suprapubic pain/discomfort 4. hematuria 5. voiding small amounts 6. AFEBRILE pyelonephritis 1. FEBRILE 2. chils 3. flank pain 4. costovertebral tenderness 5. CBC with left shift
51
what 3 lab tests are important to do when diagnosiing a UTI? what do you find on each?
**1. UDIP** _+ leukocyte esterase (product of baceteria)_ _+ nitrites (conversion of nitrates to nitrites via bacteria)_ _+WBC_ _+WBC casts (**INDICATES KIDNEY ORIGIN!\*\*\***)_ **2. hematuria** **3. culture greater than 100,000**
52
what are the DOC fo acute cystitis (4) vs pyelonephritits (2)? what do you need to note?
**_acute cystitis_** _DOC1: TMP-SMX_ DOC2: CIPRO DOC3 if pregnant/allergic: Nitrofurantoin \*\*\*add _pyridium_\*\*\* **_acute pyelonephritis_** _DOC1: ciprofloxacin_ DOC2: TMP-SMX \*\*\*\*\*NOTE THE DOC FOR FOR THESE TWO ARE DIFFERENT!!!\*\*\*\*\*
53
what is the DOC for an inpatient with UTI/pyelonphritis?
CIPROFLOXACIN!! others: fluoroquinolone, amp+gentamycin, ceftriaxone
54
what is the most common nosocomial infection in the US? what is the tx protocol with this?
cathertized associated UTI ## Footnote _if asymptomatic don’t need to treat with abx_ screen urine 48 hours after removing catheter
55
recurrent UTIs ## Footnote what are the two definitions of this? what should you consider? what about in women with decrease in lactobacillis?
_3 or more episodes per year confirmed UC_ OR _2 UTIs in last 6 months_ ## Footnote consider self treatment at first sign (urine cup for UC) vaginal estrogen in women since they have a decrease in lactobacillus
56
in _asymptomatic bacteremia_ who do you treat (3) and who do you not treat (3)? \*key!\*
**_treat:_** 1. pregnant 2. before urologic procedures 3. after renal transplant **_DONT TREAT_** 1. diabetics 2. elderly 3. patients with spinal cord injury or indwelling urethral catheter
57
do you tx UTI empirically while waiting for culture?
YES! then adjust abx as appropriate! :)
58
thelarche pubarche menarche
thelarche: breast development in females pubarche: production of pubic/axillary hair menarche: menses
59
polymenorrhea
consistent menstrual cycle with a length of 21 days or FEWER!!!
60
oliomenorrhea
consistent menstrual cycle with a length of 35 days or GREATER
61
dysmenorrhea
painful menstruation
62
how to anticholingerics decrease URGE incontinence? 3 what are the four SE to be aware of?
1. increase bladder compactiy 2. decreased in bladder contractions 3. improve urgency sxs SE: NO PEE, NO SEE, NO SHIT, NO SPiT
63
what are keagles? how often should you do them? how long should you hold them?
contraction of the pelvic floor muscles hold 3-5 seconds 50-100 reps a day
64
dysfunctional uterine bleeding ## Footnote what is this? who do you most commonly find it in? what is the MC cause? what are the two dx tests you always do on eat pt?
dx of exclusion where abnromal bleeding without pathologic cause has been ruled out in very young or perimenopausal woman ## Footnote usually an issue with the _hypothalmic-pituitary-ovarian hormaone axis_ **MC: shortly after menarche or during perimenopause because of increased _anovulatory_ cycles (90%) since there is _unopposed estrogen_ it leads to _irregular, unpredictable sheeding/bleeding_**"think: when cycle changes" DX: **Always run:** **CBC and platelents** **PREGNANCY TEST** consider: all other testing needed to rule everything else out!!
65
how do you tx dysfunctional uterine bleeding with acute bleeding or long term bleeding? 2 4
1. MC: NSAIDS Acute: 1. oral progestins 2. IV estrogen for life threatening bleeding chronic: 1. cycle with low dose COP, patch, or vaginal ring 2. cycle with progestin 3. choice depends on sage, smoking hx, preference 4. endometrial ablation
66
what is the most common gynecological malignancy?
endometrial cancer
67
endometrial cancer ## Footnote who is this most common in? what is the most common sxs of this? dependent on what? explain the characteristics of the two types? 5 4 what are the 4 dx methods?
MC gynecological cancer ## Footnote **_most postmenopausal 75%, 50-60 years old_** **_estrogen dependent cancer_** _mc sxs, inappropriate uterine bleeding postmenopausal_ type 1: MC type unopposed estrogens stimulate the endometrium well differentiated starts as hyperplasia curable type 2: endometiral atrophy undifferentiated clear cell and papillary serous histology mor agressive and found at later stage DX: **_1. entometrial bx_** 2. transvaginal US **_\>4mm_** 3. hysterscopy with bx 4. **_dilation and cutterage_** GOLD STANDARD but not more effective, and not therapeutic
68
what are the tx methods for endometrial cancer? 3 what has a protective effect?
1. total hysterectomy 2. radiotherapy and chemo at advanced stages 3. reccurence is txed with high dose progestins OCP have protective effect?
69
what are 6 RF for type 1 endometrial cancer?
1. obesity-fat makes weak estrogen which are unopposed after menopause and causes cellular change in uterus 2. metabolic syndrome 3. diabetes 4. polycystic ovarian syndrome 5. exogenous unopposed estrogen 6. tamoxifen (breast cancer med)
70
explain the progession of type 1 endometrial cancer? explain the interventions throughout the process
1. high weight + unoppposed estrogen+low exercise +low isofalvones leads to _unhealthy endometrium_ 2. unhealthy endometrium leads to _endometrial hyperplasia_ (overgrowth of endometrial cells, **premalignant** and presents with heavy periods) \*\*\*intervene here with diet, exercise, weight loss program, hormone therapy 3. if no intervention leads to _endometrial hyperplasia with atypical cells_ \*\*intereven here with hormone therapy and surgery\*\* 4. if not intervention wil leads to _endometrial adenocarcinoma which is CANCER!!!_
71
explain tx options in: 1. endometrial hyperplasia without atypical cells 2. endometrial hyperplasia with atpical cells 3. endometrial adenocarcinoma
1. **endometrial hyperplasia without atypical cells:** diet, exercise, weight loss program, hormone therapy **(progestin pO or mirena so estrogen isn't unopposed and limits endometrial growth)** 2. **endometrial hyperplasia with atypical cells**: hormone therapy and surgery to remove effected areas **3. endometrial adenocarcinoma: HYSTERECTOMY with radiation and chemo for advanced stages**
72
endometriosis ## Footnote what is this? where is it most commonly found? who is it common it? what does it cause? classic sxs? find on PE? 1 2 dx methods? 6 tx options?
tissue histologically that r**_esembles endometrium_** found **_outside_** of the uterus, **_MC on ovary and pelvis_****_,_** that **_responds to cycical hormonal changes,_** at **_less than 35 years ol_****_d who is nullparous_** (not given birth to child) mc cause of infertility 25-35% classic triad: 1. cyclic prementrual pain, pelvic area 2. dysmennorhea (including spotting) 3. dyspareunia (with deep thrust) PE: tender nodularity of the _cul de sac_ and uterine ligs DX: 1. US 2. laproscopy Tx: (based on sxs and location, child bearing desire) 1. NSAIDS 2. OCP-relieve sxs 3. progestins- reduce flow, ovulation and cause less bleeding/discmfort 4. danazol 5. GnRH-block release of pituiatry hormoens governing menses 6. surgery-last resort if fertiliy is to be maintained
73
leiomyoma aka fibroids ## Footnote what is this? who is it MC in? 2 what is it dependent on so who is more likely to get this? 2 sxs? pe finding? dx? 3
benign uterus smooth muscle tumor, MC in african americans and those older than 40 ## Footnote small, to large, singe, multiple **_estrogen dependent_** and seen more comonly in those who have endometrial hyperplasia, anovulatory statees, and estrogen producing ovarian tumors SXS: **_bleeding is MC sxs_** **mennorrhagia** PE: **_firm, enlarged, irregular uterine mass_** DX: **_Pelvic US_** D&C laproscopy
74
how do you tx leomyoma or uterine fibroids? 6
depends on the age, parity, reproductive plans, general health, size and location 1_. observation-MC_ 2. GnRH agonist-shrink fibroid 6 months only 3. OCP/IUD progestin-inhibit estorgen 4. myomyectomy-high risk of reccurence so done close to when she wants to become pregnant 5. hysterectomy \*definitive\* 6. uterine fibroid embolization (UFE)
75
explain the 5 different types of leomyomas/fibroids and their location?
`1. **pedunculated**: bubble off uterus with stock 2. **intracavity**: within uterus 3. **intramural**: within the uterine muscle 4. **submucous**: directly under the endometrium, causes uterine bleeding 5. **subserous**: directly under the serous lining, outside of the muscle
76
what are two risks that are increased if a woman has leomyomas or fibroids?
1. endometrial cancer 4x 2. spontaneous abortion
77
pelvic organ prolapse ## Footnote what is this? what are the 2 RF? what are 2 key sxs? 3 PE? 1 5 tx options? 2 key
one organ protruding into another where it isn't supposed to be RF: **_weakness of pelivic floor muscles_** **_MC cause: childbirth_** SXS **_pelvic fullness, heaviness, and "falling out" sensation or "sitting on a ball"_** **_low back pain esp with prolonged standing that improves after laying down_** urinary frequency urgengy and stress PE: **_bulging mass est with increased intrabdominal pressure ie valsalva_** Tx: 1. **_DO NOTHING IS ASYMPTOMATIC!!!_** 2. pessaries 3. **_keagles_** 4. estrogen (improve atrophy) 5. surgery
78
pelvic organ prolapse: uterine prolapse what is this? what are the 3 types?
uterine herniation into the vagina Types: **anterior wall desent:** protrustion of the urethra into vaginal canal **posterior wall descent:** protrusion of the rectum into the vaginal canal **central prolapse**: protrusion of the uterus into the vaginal canal
79
pelvic organ prolapse: cystocele
posterior bladder herniating into anterior vagina
80
pelvic organ prolapse: rectocele
distal sigmoid colon (rectum) into the posterior distal vagina
81
what are the 5 RF or causes of pelvic organ prolapse?
1. age MC after menopause, risk increases to 50% post menopause 2. parity-vaginal delivery 3. _obesity_-increased intrabdominal pressure 4. chronic cough 5. chronic constipation
82
what is the grading for pelvic organ prolapse?
**grade 1:** dsecent into the upper 2/3 of the vagina **grade 2:** cervix approaches the introitus (vaginal canal) **grade 3:** outside introitus (seen outside body) **grade 4:** entire uterus outside of the vagina-complete prolapse
83
Cervical Cancer ## Footnote what is it? what 4 things most commonly cause it?
**_IT IS A STI!!!!_** ## Footnote HPV in 99.7% of cases HPV: **_16, 18_**, 31, and 33
84
Cervical cancer ## Footnote what are two important stats on this? where does this likely occur? what are the two most common histological types?
3rd most common GYN cancer in US and #2 of ALL CANCERS in women worldwide ## Footnote usually occurs at the **_transformation zone_** (at SJC junction between squamous epithelium and glandular epitelium) squamous cell 69% adenocarcinoma 25%
85
explain the progesson of cervical cancer and why this is considered a cancer that effects 40-50s and why we screen in younger women?
cervical dysplasia is a precursor for cervical cancer ## Footnote **Cervical intraepithelial neoplasia _CIN_ is the _preinvasive phases of cervical cancer_** (it isn't cancer yet!) **carcinoma in situ _CIS is the first cell change to cancer_** Ages: 20s: common occurance of CIN 25-35: CIS becomes more common in addition to continuation of CIN 40-50: Cervical cancer
86
explain the ranking of cervical intraepithelial neoplasia (CIN)?
CIN1: mild dysplasia CIN2: modterate dysplasia CIN3: severe dysplasia \*\*1/3 of patients will progress to carcinoma\*\* CIS: carcinoma in situ
87
how do you prevent cervical cancer?
gardisil vaccine protects: 6, 11, _16, 18_ reccomended ages for bots and girls 11-26 years old
88
why was the pap smear considered a epidemology succes?
decreased the insicidence and mortality from cervical cancer 75% in the last 50 years in developed countries, 95% according to hoffmans lecture?
89
what symptom and PE findings are found with cervical cancer? what do you use to dx? what are the tx options? 3
SXS: early cervical CA is **_asymptomatic_** irregular or heavy vaginal bleeding **_post coital bleeding and spotting MC sxs_** PE: **_possible lesions that are raised and friable_** DX: colpscopy with bx Tx: if early stage **_\<4 mm and confined to cervix can be cured via:_** 1. radical hysterectomy 2. fertility-sparing surgery 3. radiation and chemo **_if metastic of reccurent, media survival is less than 2 years_**
90
explain the process of performing a colposcopy? what is it used for? what are 2 management tecnniques?
used to follow up abnormal pap results ## Footnote magnifies cervix cervix stainged with **_acetic acid (vinegar) or iodine_** to identify the areas that need to be bxed tx/management options 1. loop-electrosurgical excision procedure (LEEP) 2. ablation of T-zone with cryrotherapy or laser
91
what are you intervention options based on the possible cervical bx results?
1. mild lesions may resolve spontaneously 2. preinvasive neoplasia can be txed with electrocautery, cryocautery, laser surgery, conization, large loop excesion of transitional zone, or LEEP procedure (Green book)
92
explain HPV 16 and 18 and what they are likely to cause?
responsible for 70% of cervical cancers **_16_:** higher rates of **_squamous cell cancers_** CIN3 **_18:**_ higher rates of _**adenocarcinomas_**
93
what percent of woman who get cervical cancer never got a pap?!
50%
94
what are the screening guidelines for a pap smear?
1. start at age 21 until 65 (don't check if under 21 and sexually active) ## Footnote 2. screen every _3 years_ from _21-29_ 3. _pap + HPV "co-test" every 5 years_ if between _30-65_ \*\*notice you don't screen for the actualy HPV virus if you are under 30
95
incompetent cervix or cervical insufficency what is this? what are 4 RF? what are 3 sxs? 2 tx options?
**_premature cervical dilation established in the 2nd trimester_** RFs: 1. previous cervical trauma/procedure 2. uterus defects 3. DES exposure in utero 4. multiple gestations SXS: 1. vaginal bleeding 2. vagininal discharge esp in 2nd trimester 3. _painless dilation and effacement of cervix_ **TX:** **1. bedrest** **2. cerclage (suturing of cervical OS)**
96
Vaginal and vulvar neoplasms ## Footnote what are these associated with? how common are each? who do you find them in? in the second...what is the MC precention? what do they look like?
premaligment and malignant lesions commonly associated with HPV **_vaginal intraepithelial neoplasia (VAIN)**_/_**vaginal cancer_** RARE less than 1% of all GYN cancers women over 50 **MC presentation is postmenopausal blleding or bloody discharge** **_vulvar intraepithelial neoplasia (VIN)/vulvar cancer_** 3-5% of all GYN cancers **MC are _squamous cell carcinoma in postmenopausal woment_** younger women with warty lesions assocaited with HPV older women less associated with HPV **_puritis MC precention or asymptomatic_** red/white ulcerative crusty lesions
97
vaginal and vulvar cancers ## Footnote how do you dx? 3 tx options?
DX: colopscope Tx: **excision** **laser** **tropical antineoplastic agents** 1. 5-FU 2. imiuimod
98
lichen sclerosis ## Footnote what is this? 2 sxs? what are the characterisitcs of acute and chronic lichen sclerosis? 3 2 what does chronic produce a higher risk of? tx goal? tx?
**MC vulvar dermatological disorder** benign chronic inflammatory process SXS - pain - dysuria from loss of elasticity **_ACUTE_** **_red/purple_** lesions on **_non-hair-bearing ares_** in the perineum and perianal area in a **_hourglass pattern_** - erythema and edema - white plaques (keratosis) - intense puritis **_Chronic_** skin becomes **thin, white, and shiny** **can lead to loss of genital landmarks** - labia fusion - introital stensosi Tx: STOP SCRATCH ITCH CYCLE -STEROIDS
99
what does lichen sclerosis put you at increase risk for?
squamous cell carcinoma
100
bartholin's cyst ## Footnote what is this? what are the 4 sxs? dx? 3 tx methods?
obstruction of the duct of bartholins gland causing retention of secretions and cystic dilation that can cause infection SXS non infected: minimal infected: pain, tenderness, erythema, dyspareunia with fluctulant mass DX: culture/cbc Tx: none if asymptomatic drain with ward catheter or marsupulize excisions if recurrent
101
bartholins glands ## Footnote what are they? what are their functions?
two glands located slightly posterior to the left an right of the opening of the vagina function: secrete mucous to lubricate the vaginal opening 1-2 drops when sexually aroused
102
Amenorrhea ## Footnote what is this? what are the two types? what are they qualifications for both? what is the most common cause of the last? what are 6 other causes?
the absense of a menses **primary: never had menses, younger girls** -absense of menstruation before age 16 **secondary: had menses and stopped _for 3 months if cycles are normal, or 6 months if the cycles are irregular_** **_most common cause is pregnany!!_** others: 1. drug use 2. stress 3. weight gain 4. excessive exercise 5. _Asherman's syndrome_-acquired endometiral scarring 6. _polycystic ovary syndrome_
103
Ammenorhea ## Footnote what are two tests you want to run for this? what are two tx options?
DX: 1. **_PREGNANCY TEST EVERYTIME!!!_** 2. progesterone challange idirectly determines if the ovary produces estrogen if endometrium is primed with estrogen (functioning ovaries) progestin will produce menses expect withdrawal bleeding within several days of completing progestin course Tx: 1. OC 2. cyclic progesterone for 5-12 days a month for smokers for over 35 year olds
104
dysmenorrhea ## Footnote what is this? what are the two types and their characteristics? what age group are they common in?
**_painful menstruation_** **_primary_** not due to pelvic pathology due to **_excess of prostaglandins and leukotrienes**_ leading to _**painful uterine contractions, N/V/D_** starts 1-2 years after the onset of menarche in **_teenagers_** **_secondary_** **_due to pelvic pathology_** so a identifiable condition **_25 years and older_** endometriosis, adenomyosis, uterine fibroids, PID, IUD
105
dysmenorrhea ## Footnote what are the sxs associated with primary and secondary dysmennohrea? what are the tx options for both?
sxs ## Footnote **primary:** 1. cramping, bloating, and lower abdominal pain that radiates to the back or thighs 2. begins before or during menses for 1-3 days **secondary:** the above PLUS 1. bloating 2. mennorrhagia/dyspareunia tx: primary: **NSAIDS** **heat, exercise, OCP** secondary: tx underlying condition
106
premenstrual sydrome ## Footnote what is this? when does it occur? what must be present? what percentage of women get this? what two tests shoudl you do? what are the 5 tx options?
**cluster of physical, behavioral, mood changes with cyclical occurence during luteal phase of the menstrual cycle** **occurs 1-2 weeks prior to mentstraion and ends 1-2 days after the onset of sxs** a symptom free period during the follicular phase, day 1 of menses must exist **_75%_** of women have some symtpms of this 5% have severe sxs and distress that limit their ability to participate in lfe basically DX: thryoid to rule out thyroid issues CBC to rule out anemia Tx: **1. limit caffine, alcohol, sodium** **2. frequent high-complex carb meals** **3. stress management/exercise** **4. SSRIs 14 days prior to the onset of menses** **5. NSAIDS**
107
menopause ## Footnote what wualifications does this have? what age does this occur around? what do the symptoms come from? 4 sxs? 3 3
**cessation of menses after 1 year** loss of ovarian activity at approximately 51 SXS: vaso motor sxs from decreased estrogen production **_1. HOT FLASHES_** upper body, face, chest, and neck - interfere with sleep - 75% have them - last 6 months -2 years depends on person **_2. atrophic vaginitis with discharge and itching and loss of elasticity_** -can lead to dyspareunia and sexual dysfunction making a low quality of life, self-esteem, and sexual intimacy **_3. sleep distrubances_** **_4. new onset depression_**
108
menopause ## Footnote what are the 3 tx options?
1. systemic hormone therapy most effective estrogen or progesterone with the lowest effective dose and shortest duration but _limited to 5 years or less of use_ ## Footnote 2. SSRIs 2nd 3. SNRIs
109
what must you consider when txing women for menopause with hormone replacement therapy?
**use progesterone and estrogen as hormone therapy for this** must consider if woman has uterus or not BEFORE giving hormone therapy 1. if no uterus: can use esterogen alone this is the most effective tx, however, it **_increases the risk for endometrial cancer so you ONLY use it patients WITHOUT a uterus_** 2. if uterus: must use estrogen AND progesterone **_NO icnreased risk for endometrial cancer so can be used in patients with a uterus_** slightly increases risk for breast cancer so must keep this in mind
110
how do you dx menopause in woman? what if you wanted to check labs? what are they at increased risk for?
typically a clincial dx in labs you would use FSH to dx because this would be high as well as LH while the estrogen levels are still low they are at increased risk for osteoporosis so may want to consider putting them on medicalion to prevent this
111
giving someone estrogen increases their risk for?
BREAST CANCER
112
giving someone unopposed estrogen increases their risk for what if they have a uterus?
endometrial cancer
113
estrogen has protective effects over what?
OSTEOPOROSIS
114
infertility ## Footnote what is this defined as for the different age groups? what are the 3 most common cuases? what are 4 RF?
**_failure to conceive past 1 year of unprotected regular intercourse**_ _**in women less than 35 and after 6 months in women older than 35_** 30% male, 30% female, 25% unknown RF: 1. cigarette smoking 2. radiation 3. chemo 4. autoimmune dxs
115
what is the oocyte aging process? numbers? degeneration accelerates quickly at? when do you see the largest population of people seeking fertility help?
**OOCYTE aging** _1. decrease in both the quality and quantity of oocytes_ 2. 1-2 million follciles at birht to 300,000 at the onset of puberty 3. loss acceralates quicky at 30s 35-39 is when you see the biggest population of couples seeking fertility help!!
116
female infertility ## Footnote what are 6 causes of female infertility and what are the two most common causes?
1. ovulatory disease MC 25% ## Footnote PCOS, eating disorders, CUshings, CAH, Turners, thyroid disease 2. endometriosis 15% damage or lining changes prevent ovulation fertiliation and implantation 3. pelvic adhesions 4. tubal blockage 5. uterine fiboirds 6. congenital defects
117
male infertility ## Footnote what are the 3 branches of male infertility causes? what is the MC cause? 4 3 1
1. testicular disease 30-40% MC ## Footnote Klinefelders syndrome varicocele Y chromosome deletions STIS 2. disorders of sperm transport 10-20% epididylmal dysfunction vas deferens dysfunction ejaculatory dysfunctions 3. hypothalamic pituitary disease (secondary hypogonadism) 1-2%
118
what are 7 test you would want to check in a woman who is infertil?
1. FSH-ovarian function at day three 2. TSH-thyroid function 3. menstrual hx 4. LH surge prior to ovulation or luteal progesterone 5. prolactin 6. pelvic US 7. hysterosalpingogram (HSG)
119
what four testing methods would you want to use in a male who is infertil? ## Footnote what does the first asses for? 5 things exaplin the collection requirements?
1. semen analysis ## Footnote volume and pH asses sperm: _motility, concentration, and morphology_ _leukocyte count_ _immature germ cells_ collect 2-7 days after abstinence, need at LEAST _2 samples collected 1-2 weeks apart_ 2. decrease alcohol, marijuana, tobacco use 3. endocrine levels 4. genetic testing
120
who do you asscess for infertiliy in these groups: 1. after 12 months of unprotectedand frequent sex 2. after 6 months of unprotected and frequent sex 3. upon presentaiton
1. under 35 y/o after 12 months 2. 35-40 y/o after 6 months 3. upon presentation - over 40 - amenorrhea - hx of chemo, radiation, end stage endometriosis - uterine or tubal dx - male with hx of groin, testicular surgery, chem, or radiation
121
what are the 5 tx objections for someone with infertility? 3 under female 3 under male
1. smoking cessation 2. decreased caffine, alcohol use 3. appropriate timing of sex around ovulation time using predictor kit 4. **therapeutic interventions** - **clomid** ovulation stimulator - interuterine insemination (IUI) - in vitro fertilization (IVF) 5. male tx hypogonadism from hyperprolactin: bromocriptine to lower prolacting - other hypogonadism: HcG injections - sperm disorders: retrograde ejaculation
122
if someone has unexplained infertility what should be the first and second step to try to tx it?
1. climpiphene + intrauterine insemination since low cost and low SE ## Footnote 2. gonadotropin injections and interuterine insemination
123
adenomyosis ## Footnote what is this who does it occur in what are 3 sxs what might you find one PE? 3 dx tactics 4 tx options
**uterine thickening that occurs when entometrial tissue invades the myometrium**, and can cause a mass in the uterus called a _adenomyoma_ unknown cause MC: women older than 30 who have had children, increases with age! SXS: **_tender and "boggg" uterus_** **_mennorrhagia_** (heavy menses) **_dysmenorrhea_** PE enlarged uterus uterine mass DX: US endometrial sample MRI Tx: 1. nothing 2. progestin containing IUD (supress bleeding and allows mass to shrink) 3. OC 4. surgery last chance
124
premenstrual dysphoric disorder ## Footnote what is this? what does it do? what must you have? and the many sxs?
basically PMS on steroids that **disrupts daily living** must have _5 or more of these symptoms_ and _occur the week before the onset of menses and start to improve within a few days after the onset of menses and not during other times_ 1. marked affective lability (mood swings, sensitivity) 2. marked irritability or anger or increased interpersonal conflicts 3. marked depressed mood, feelings of helplessness, self-depreciating thoughts 4. marked anxiety, tension, feeling of being on edge 5. decreased interest in usual activities 6. subjective sense of difficulty in concentration 7. lethargy, easily fatigued, marked lack of energy 8. marked change in appetite, overeating, or specific food cravings 9. hypersomnia or insomnia
125
vaginitis-candida ## Footnote what percent of women get this? what are the 3 causes? 3 sxs? 2 dx? 2 tx options?
75% of women have it at least once **_candida albicans MC and causes 90% of cases_** also candida glabrata and tropicalis SXS: cheesy white discharge intense itching inflammed vagina and vulva DX: clinical wet prep with KOH Tx: ***_imadazoles_ oral or topical*** recurrent: likely glabrata or tropicalis **_fluconazole for 2 weeks_**
126
do you tx the sexual partner of someone who has candidal vaginitis?
only if they are asymptomatic!
127
atrophic vaginitis ## Footnote what is this the combination of? when are 3 times this is more likely to happen? 4 sxs? tx?
caused by the combination of **_low estrogen_** - prepubertal - post menopausal - after childbirth esp if nursing **_and_** **_thinned vaginal epithelium_** SXS dryness, spotting, seroanginious discharge, dyspareunia Tx: intravaginal estrogen
128
women who are exposed to diethylstilbestrol (DES) are at increased risk for....
clear cell adenocarcinoma of the vagina
129
vulvodynia ## Footnote what is this? what are the 2 types? sxs? 8 tx options?
**vulvar pain in the absence of physical findings** **1. PROVOKED** 20-30 year olds comes after something like childbirth or infecion vestibular erythema tendernress introital pain **2. UNPROVOKED** over age 40-60 larger area of pain cause unknown SXS burning, irritation, hyperalgesia Tx 1. pelvic floor pT 2. lidocaine 3. tea tree 4. topical estrogen 5. tricyclic antidepressant 6. _gabapentin_ 7. vulvar vesticuloectomy 8. chronic pain referral
130
squamocolumnar junction (SCJ) ## Footnote what is this and what type of cells are involed? what happens as you age? what happens here? how much does it move?
where the **_inner lining of columnar cells**_ meets the _**exterior sruface of squamous cells_** "eversion of the columnar epithelium onto the ectocervix" however this moves **inward** over time which is why you cant see it transformation zone: 1. where metaplasia and hyerplasia occur 2. neoplastic changes occur here 3. can be visualized in younger people (pic) but not in older peopel ebcause it moves into the cervical canal **_approximately 3cm_** from original location
131
nabothian cyst
yellowish translucent pear-like shaped cyst on the ecto cervix
132
cervical polyps ## Footnote what are characteristic of these? 6 who are they common in? how do you dx?
small, pedunculated neoplasms, _red_, _FRIABLE_ that originate from the endocervix and protrude _2-3 cm_ ## Footnote very common esp if older than 20, most are BENIGN DX: remove by grasping with forceps and twisting to send to pathology to r/o malignant changes
133
cervical stenosis ## Footnote wat is this? what are 4 causes of this?
**narrowing of the endocervical canal, usually at the OS, with partial to completely occlusion of the OS** causes: 1. congenital 2. hypoestrogenic 3. neoplastic 4. post surgical
134
what percent of pregnancies are unintended?
49%
135
what are 6 things you need to ask a patient before prescribing BC?
1. blood clots DVT/PE 2. pregnancy hx (rule out w/test) 3. clotting disorders (factor V lieden) 4. medications/allergies 5. smoking status 6. weight/BP
136
what are two things you must rule out before prescribing BC?
COC: BP (no HTN) IUD: pelvic exam, rule out STIs
137
long acting reversible contraception (LARC) ## Footnote what is the pregnancy rate? who can the be used in? 2 worse SE? what are the 4 options for this?
MOST EFFECTIVE, pregnany rate less than 1% can be used in all women _including adolescence_ bad things: longer bleeding and worse cramps OPTIONS: **1. Nexplanon implant** **2. paraguard COPPER IUD** **3. Levonorgestrel release IUD** **-mirena** **-liletta** **-Skyla** **4.methdroxyprogesterone acetate depo-provera shot**
138
LARCs: Nexplanon-estronogestrel implant what hormone is used? how long? menses effect? wouldn't want to use in somoene....
**Hormone: progestin** **duration: 3 years** **menses: lighter, irregular with unscheduled bleeding** Don't use: in someone who poor tolerance to amennorhea or unscheduled bleeding
139
LARC: paraguard IUD hormones? duration? menses effect? 3 risks? 6 epeopl you don't use it in?
**hormone: NONE!!! COPPER ONLY!!** **duration: 10 years** **menses: may get heavier with more cramping and unscheduled bleeding** risks: uterine perforation, expulsion, infection don't use: 1. heavy ir painful menses 2. iron deficiency 3. anemia 4. uterine abnormality 5. copper allergy 6. wilsons disase foreign body rxn and chemical changes may be toxic to sperm and ova
140
LARC: levnorgestril release IUD 3 options? hormone? duration? menses effect? poor choice for 2? 3 risks?
mirena liletta skyla **hormone: progestin** **duration: 3-5 years depending on type** **menses: lighter and irregular with unscheduled bleeding** risks: uterine perforation, expulsion, infection poor choice: lower tolerance to amennorhea or unscheduled bleeding
141
LARC: medroxyprogesterone acetate depo-provera pregnancy rate? hormone? administration timing? menses effect? 2 risks? poor choice for?
**pregnancy rate 6% first year of use** **hormone: progestin** **injection: every 12 weeks (3 months)** **menses: lighter and irregular with unscheduled bleeding** risks: weight gain and mood swings poor choice: for quick return of fertility
142
combination hormonal contraception (pill/patch/ring) ## Footnote pregnancy rate: hormone: 3 options and duration menses effect
**pregnancy rate: 9%** **hormone: progestin and estrogen** **pill: many combinations- _28 day, 21 day, extended cycle_** **ortho evra patch-** **Nuvaring-_monthly_** **menses: lightr, regular predictable withdrawal bleeding with cyclic use**
143
combined contraceptive options pill, patch, ring 11 contraindications you should know!
RISKS/Contras: 1. breast cancer 2. estrogen/progestin dependent neoplasms 3. hepatic tumors 4. stroke 5. DM with vascular 6. DVT/PE 7. hypercoagabilities (factor V) 8. migraines with aura 9. HTN uncontrolled 10. rythmn dxs lik afib 11. women older than 35 smoke
144
potential noncontraceptive benefits of cyclic estrogen-progestin contraceptive? 7
1. reduction in dysmennorhea with more regular cycles 2. reduce risk of etopic pregnancy 3. reduce PMS PMDD 4. decrease ovarian cancer 5. reduced endometrial cancer 6. reduction in acne 7. reduced hirsutism
145
what are two increased risks when taking BC that contains estrogen?
1. increase risk of breast cancer 2. increase vascular thrombolytic event from increased lipids (DVT/PE, AMI/CAD)
146
what are the 3 processes for steralization and what does each process entail?
1. Essure ## Footnote hyteroscopic steralization-metal coil inserted into the distal portion of each fallopian tube office based procedure under anastesia 2. bilateral tubal ligation laparoscoptic vs mini-lapro samoe day surgery 3. vasectomy non-scapel vasectomy-puncture is made through the scrtom skin overlying the vase defference and widened only enough to externalize the vas deference for transection officed based under local anastesia _need 20 ejaculates to get the left over sperm out_
147
barrier methods including male condoms, effective?
greater for STIs, not great for pregnacy 18% failure rate
148
how long can a pulse of GnRH last?
anywhere from 15 mins to 2 hours
149
explain how hormonal contraception works? 3
**1. inhibits secretion of pituitary gonadotropins via NEGATIVE feedback mechanism which prevent follicular follicle development and ovulation** **2. alters endometirum (thinning) which may effect implantation by producing unfavorable environment for fertilization** **3. thickens cerivcal mucous which inhibits sperm passage/penetration**
150
what are the two most common emergency contraception options?
1. levonorgestrel OTC (so convient) "plan B" 50-94% efficacy ## Footnote 2. ulipristal Rx "Ella" 98-99% effective \*\*MOST EFFECTIVE oral\*\* 3. paraguard \*MOST EFFECTIVE METHOD\*
151
how many menstrual cyles does a woman experience on average in her lifetime
about 400
152
explain the link between estrogen and breast cancer?
nullparity (not having children) increases the risk for breast cancer because it increases the number of menses the woman has thus **increasing the amount of unopposed estrogen she is exposed to** **this stimulation of cell proliferation during every cycle increases the risk for development of breast cancer** **those who have early menarch and late menopause are also at increased risk because it increases the number of menses they have and ultimately exposes them to more estrogen** **_first pregnancy_ appears to have a protective effect** **COOL FACT: THIS IS WHY NUNS HAVE A HIGH RISK FOR BREAST CANCER!!!**
153
Why is it important that GnRH is released in pulses rather than continuously?
**Pulsatile release:** maintains normal FSH, LH levels in the blood as GnRH is released it binds to gonadotrophs and causes released of **STORED** LH and FSH \*\*allowing a period of rest between pulses allows the gonadotroph to increase stores aka *priiming effect\*\** **continuous release**: results in a **REDUCTION** of the pituitary contens of FSH and LH and their release (since trying to replenish stores) clinical implications **GnRH agonists and antagonists:** down regulate LH and FSH release since it continiously sitmulates receptors and doesn't allow for the gonadotrophs to replemsih stores these can be used in certain cancers to lmit the amount of estrogen/progesterone they are exposed to since this is the ultimate product of this process. \*\*may cause an intial flare in sxs and then down regulate\*\* - breast cancer - endometriosis - prostatic cancer
154
what are seroids made from? explain their carbon and conversion properities?
steroids are made from cholesterol which comes from acetate ## Footnote **progesterones: 21 carbons** **androgens: 19 carbons** **estrogens: 18 carbons** **converstion of one steroid to another can be accomplished by enzymes that are a part of the cells _biosynthetic package_ where _carbons can be taken away but NOT added_** aka a progesterone can become an estrogen but an estrogen can't become a progesterone
155
what are most steroids produced from?
most likely acetate with the intermediate as cholesterol, however, direct synethesis also occurs with cholesterol that is produced by the liver or supplied by the diet
156
what is the first step of ALL steroid synthesis? what is this catalyzed by? explain the feedback between this and HMG coA reductase?
FRIST STEP: converstion of **cholesterol to pregnenolone "MOTHER OF ALL STEROIDS"** since all steroids stem rom this and process which occurs in the mitochondria of ther steroid producinc cell this process is **_cataliyzed by mitochondrial cytochrome P450 side chain cleaving also referred to as desmolase 20-22_** **_cholesterol is a negative feedback regulator of HMG CoA reductase_**....so when cholesterol is high this enzyme decreases, when cholesterol is low this enzyme increases \*\*\*THINK ABOUT IT: this is why HMG CoA reductase inhibits work for someone with high cholesterol, it prevents further synthesis!\*\*\*
157
explain the solubility of steroids? what consequences does this have? 3 options? explain the difference in affinities?
structually similar to cholesterol since that is what they are derived from so they are highly fat soluble and poorly water soluable....this means you find them bound to plasma proteins in the blood. MC albumin, sex steroid hormone, and cortisol binding globulin **_albumin_**: low affinity for bound steroids, weak bond **_sex hormone binding globulin (SHBG):_** high affinity for androgens (testosterone) and estrogens but low affinity for progestens and cortisol, strong bond
158
explain what is meant by bioavaliable steroid?
when you ask for a the lab to quantify the serum steroids it is a **combination of BOTH 'free" unbound steroids and bound steroids** (how most are) bioavaliable steroid referrs to both the bound and unbound steroid present
159
what is the free angrogen index?
meaures the amoutn of bioavaliable testosterone in a person this can help to explain a pt who presents with hirsuitism or features suggesting androgen excess
160
explain the relationship between sex binding hormone globulin and testosterone levels between males and females?
the majority of steroids are bound with proteins in the blood. many are bound with albumin, but many are **bound with sex hormone binding globulin (SHBG)** when bound with SHBG **the steroid becomes _inactivated_**. In men, more percent of testosterone is bound to ALBUMIN and therefore dissociates quickly, where in women is bound to SHBG and therefore is inactivated! This explains the higher **_andronization_** of males than females because the testosterone is more bioavaliable
161
do changes is steroid levels greatly effect the serume concentrations/steroid effects?
not usually.....the carrier proteins like abumin and sex hormon binding globulin are always in excess of steroids, so if there are massive increases they can accound for this and it will have little effect on the body the problem arises when there isn't enough binding proteins like ablumin or SHBG where the slight changes in hormones show their effects more readily and is seen in conditions like **liver diseases**
162
are sex steroids like progesterone, testosterone, and estrogen kept at high or low plasma levels? why?
_very low_ (much lower than cholesterol) with binding proteins like albumin and sex hormone binding globulins ## Footnote want to keep these low because they are like cholesterol and are lipid soluble, this means that they _can readily enter the cell_ if these were present in high concentrations in the plamsa, they could readily enter the cell and disrupt the membrane integrity! this is why _even small levels of plasma steroids are present in the bound protein form_
163
where are steroid hormone receptors found? and what are they bound to? what happens once they are stimulated?
found intracellular in both the nucleus and the cytoplasm often bound to _heat shock proteins_, that when stimulated by a steroid disocciate and bind to non steroid ligands like Thyroid hormones or vitamins once stimulated: they undergo _conformational change_ that allows them to recognize _hormone-resonse elements (HREs)_ in the DNA which then allows for protein transcription/production
164
where are most sex steroids produced? exception? role of target organs? what enzyme?
most sex steroid hormones **_(progesterone, estrogen, and testosterone)**_ are made in the _**gonads**_ with the exception of a _**pregnant female_** however it has been made clear the **_target organs have the ability to**_ _**participate in INTERCONVERSION of one steroid to another_** thus they can take a ciculating hormone and transform it enzymatically into another steroid to use LOCALLY **via its biosynthetic package of enzymes** EX: 5alpha-reductase converts testosterone to 5alpha-dihydrotestosterone "DHT" which is stronger!
165
what is the clinical correlation between 5alpha-reducatase and DHT levels? what percent of tesosterone is involved in this?
**5alpha reducatse** converts **testosterone** to **DHT** which is a stronger vesion of testosterone _5-8 % of total testosterone is converted to this_ **5alpha-reductase inhibitors, AKA FINASTRIDE, PREVENT the conversion of testosterone to DHT which can _support the development of benign prostatic hypertrophy_** so reducing this enzyme in men helps to shrink enlarged prostates, can also help with baldness since DHT also contributes to this
166
hypothalamo-pituitary-gonadal axis ## Footnote what is the pathway for production of steroids? how are they released?
**HYPOTHALAMUS: RELEASES GnRH** TRAVELS VIA HYPOPHYSEAL PORTAL VEINS TO **ANTERIOR PITUITARY RELEASE FSH AND LH** TRAVELS VIA BLOOD TO **THECAL/GRANULOSA CELLS** **RELEASE ESTROGEN, PROGESTERONE, TESTOSTERONE** keep in mind GnRH and FSH/LH released in CHICORDIAL PULSES!!
167
hypothalmic gonadotrophic releasing hormone ## Footnote what is this? where is it encoded? why is it difficult to measure?
**neurohormone** encoded on chromosome 8 on single gene serum levels: difficult to obtain since its release is confined to the hypophyseal portal blood supply and it has a short halflife 2-4 mins
168
FSH/LH ## Footnote what is anothe rname for these? what are they made of? which is cleared fast which is cleared slow?
"gonadotrophins" since they effect gonad steroid synthesis in BOTH sexes ## Footnote both contain alpha (identical) and beta subunits (different) gylcosylated with sugar **FSH is cleared more slowly since it has more carbohydrates and this explains why when looking at infertility you check this because it provides more of a picture while LH is cleared fast and only provides a snapshot**
169
inhibins activins
effect FSH release from anterior pituitary ## Footnote inhibins: allows only one follicle to be selected as graafian activin: allows for developement
170
why is it important to consider CNS injury/damage in infertility?
GnRH is considered the most important final common mediator of ovulation ## Footnote because the hypothalmus is the first step in the hypothalamo-pituitary-gonadal axis process to **release GnRH** OVULATION is needed for PREGNANCY so must have these pieces working if you want to get pregnant!! CNS can lead to infetility issues
171
follicular phase ## Footnote what does this refer to? when does it occur? 2 key points?
**_OVARY_** from **_first day of menses to ovulation_** ~10-16 days Key points: 1. new _antra follicles_ are recruited to proliferate 2. one of these will be selected as the _graafian follicle_
172
proliferative phase ## Footnote where does this occur? when does this occur? what are the 2 main things that occur?
**_UTERUS_** from the **_first day of menses to ovulation_** 1. the uterus is under the influence of increase **estrogen** and the **stratum functionalis** of the endometrium proliferates from **1-2 mm to 8-10 mm** in thickness 2. increase in estrogen **promotes the formation of progesterone receptors in the uterus so it can respond to progesterone in the post ovulatory phase of the cycle**
173
ovulation ## Footnote what is this marked by? what causes this? where does fertilization occur?
the **Graafian follicle** during the follicular phases **ruptures in response to _midcycle FSH/LH surge_ causing the occyte to be expelled from the follicle into the fallopiian tube** viable for ~24 hours where if sperm enter the oocyte can be fertilized at the ampullary-isthmus junction
174
luteal phase ## Footnote when/where does this occur? what are the 2 things that occur?
**OVARY after ovulation** until **onset of next menses** (assuming pregnancy doesn't occur 1. corpus luteum (formerly graafian follicle) is functional unit of the luteal phase and **_produces increased levels of progesterone_** 2. occurs 13-15 post ovulation
175
secretory phase ## Footnote where does this occur? when? what is it marked by? goal? if no implantation?
**UTERUS after ovulation until next menses** 1. high levels of **prosterone secreted from corpus luteum** have a "_quieting_' effect on the unterine endometrium and facilitate - secretions from the uterine endometrial glands to make condusive for implantation of a **blastocyst** - if no implantation: the **corpus luteum dies and the endometrial tissue looses its blood supply since loss of progesterone production and causes necrosis of linging and sloughing!! MENSES** and the begining of a new cycle
176
embryonic ovary ## Footnote what is the final goal of this step? explain the 4 phases of this developement?
1. oogonia undergo _MITOSIS for 3-4 months_ 2. _Enter meiosis I_ and are called _OOCYTES_ 3. they become **_arrested in PROPHASE of the first meiotic division_** 4. start to be surrounded with **_PRE-granulosa cells_** and is termed primordial follicle
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folliculogensis ## Footnote explain folliculogensis up until the formation of the graafian follicle? explain gonadotropin dependent and indepent phases? 5 steps
1. pulsatile LH and FSH released at **puberty**"awaken" the **primordial follicles** 2. primoridial follicles become **primary follicles with zona pellucida** that serves as attachment for the granulosa cells 3. primary follicles become **secondary occytes or "pre-antral follicles"** where the _granulosa cells increase in size and the thecal layer forms_ \*\*\*up until this point the the development has occured INDEPENDENT OF GONADOTROPINS\*\*\* 4. LH and FSH increase in response to decreasing estrogen and progesterone from the previous cycle stimulating the pre-antral follicle to tern into a **tertiary follicle** 5. one of these is _selected as the **graafian follicle**_
178
summary of the follicular phase ## Footnote explain all the steps of this
Increasing **FSH and LH** cause **an increase of estradiol 17B** which initially has a _NEGATIVE FEEDBACK_ of FSH and LH causing the storage of FSH and LH via decreased GnRH release as the **follicle develops** from early follicular phase to late follicular phase, the **LH receptors** that were originally present on only the thecal cells **become present on the granulosa cells where the FSH receptors are.** during this time the number of _granulosa cells size and number are increasing_ and _thecal membrane formation_ the **increase in LH binding** to these receptors (as stated above) causes the production of _andosteridione,_ which is **convered to estrogen via aromatase enzyme** this process increases the NET ESTROGEN to an extent that it causes **_POSTIVIE FEEDBACK_** on **GnRH in the hypothalamus and rlease of FHS and LH** and a **_LH SURGE_** that is a PARADOX (FSH doesn't surge because of the increase of **inhibin A levels rise as estogen rise)** **LUTEAL surge** causes the **estrusion of the oocyte from the follicle and completion of meiosis I.** OVULATION!
179
explain the postive and negative feedback cycles that are seen in the menstrual cycle?
low levels of estradiol 17 B feedback NEGATIVELY on FSH and LH release at both the level of both the pituitary and the hypothalamus in the early follicular phase and in the luteal phase HOWEVER, in the late follicular phase very high plasma levels of estradiol 17 B promote a POSITIVE feedback on both the pituitary and hypothalamus which is necessary to facilitate the midcycle surge of FSH/LH just prior to ovulation
180
explain how hormonal contraception methods play into the negative and postivie feedback mechanisms of the menstrual cycle?
if you use low levels of estrogen “low estrogen pill” it is inhibitory on FSH and LH and so you never get the LH surge which prompts ovulation! this means the ooccyte is never released into the fallopian tube also prevents the lining of the endometrium from proliferating since this also suppresses progesterone
181
given the menstrual cycle--what could you do if the patient was having a hard time getting pregnant from natually low levels of estrogen?
the low levels inhibit FSH and LH release with halts the whole process give pt **_clophene citrate**_ that is a _**estrogen antagonist**_ that increases these levels by _**knocking out the low estrogen levels_** this plays of the feeback mechanisms
182
explains what happens to the LH and FSH receptors during the mentrual cycle?
early to mid follicularp phase: ## Footnote **1. LH receptors are only found on the thecal cells** (outer layer) of the dominant follicle 2. FSH only found on granulosa cells mid to late follilcular phase: 1. **_LH receptos begin to appear along with FSH receptors on the granulosa cells of the selected follicle_** \*\*\*\*\*\*MAKES IT MORE RESPONSICE TO THE LH SURGE WHICH STIMULATES OVULATION AND THE DEVELOPMENT OF THE CORPUS LUTEUM POST OVULATION\*\*\*\*
183
luteal phase summary ## Footnote describe all the aspects of this
the increase from the **LH surge "lutinizes" (give the ability to make progesterone** to the corpus luteum **through stimulation of the LH receptors on the thecal and granulosa cells** causes **_massive**_ _**progesterone release and some estrogen_** which **prepares the endometrium for implantation by** **quieting it and**: - increasing blood flow - increasing nuitrient secretions - decreasing contractions of uterus massive release of progesterone and some estrogen **inhibits the FSH and LH release via GnRH inhibition** via _NEGATIVE FEEDBACK_ if no pregnancy the CL begins to die *(Cl needs FSH to LH to live and you have suppressed it so much through negative feedback there isn't enough to support it)* and the plasma estrogen and progesterone decrease, causes _NECROSIS OF ENDOMETRIAL LINING AND NECROSIS_ **starting the cycle over with the increase if estrogen and progsterone in follicular phase**
184
explain what happens in the luteal phase if fertilization occurs?
the **blastocyst implants on the endometrial wall** and forms _placental membranes_ that secrete **_human choronic gonadotropin_** HCG has a **very similar structure to LH** so it can therefore **_rescue the corpus luteum by binding with LH receptors_** this means the **PROGESTERONE PRODUCTION CONTINUES UNTIL WEEK 9-10 WHERE THE STEROID SYNTHESIS SWTICHES OVER TO THE PLACENTA** aka luteal-placental transition period
185
luteal phase defects ## Footnote what does this cause? 2 things it can cause? how does this happen?
**inadequate secretory transformation of the endometrium** **resulting from deficient progesterone production-\>_contributes to both infertility and recurrent pregnancy loss_** Causes: 1. abnormal follicular development from inadequate FSH and LH - causes inadequate growth of granulosa cells - causes lower estrogen levels - lower estrogen levels promote **suboptimal LH surge at ovulation resulting in deficient progesterone in the luteal phase**
186
exposure to estrogen can cause what?
increased risk of developing breast or uterine cancer since they stimulate proliferation of cells in both these tissue types
187
polycystic ovarian syndrome ## Footnote what does this cause? who is it common in? what is the triad? two additional considerations?
MC cause of infertility in women!! ## Footnote often in adolescents **_endrocine syndrome with triad of_** (must have 2/3) **1. oligo (infrequent) or ammenorhea (chronic anovulation)** **2. hyerandrodenism (obesity/hirsuitism)** **3. evidecent of polycystic ovaries** (not everyone) thought to be caused or involved with **_increased insulin resistance**_ (increases the androgens) and _**unopposed estrogen which increases risk for endometrial cancer since the person isn't ovulating and there is no progesterone production_**h
188
explain the hormonal interaction seen in polycystic ovarian syndrome? 7 steps explain how this factors into exposure to unopposed estrogen exposure?
caused by an abnormal hypothalamus-pituitary ovarian axis **1. increased LH realeased compared to FSH** **2. increase androstenedione and testosterone by the thecal cells of the ovary** **3. androstienedione is converted to estrogen in the tissues, and is a weak estrogen** **4. this STIMULATES LH release and inhibits FSH release** **5. the low levels of FSH prevent the follciles from fully developing and ovulation doesn't occur** **6. the androstienedione that accumulates from the LH binding to the thecal cells continues to increase the androgen present cause HIRSUITISM and ACNE** **7.this is a viscious cycle that cause anovulation and also the cystic formation of the ovaries** **\*\*\*INSULIN PLAYS ROLE BECAUSE IT IS THOUGHT TO CONTRIBUTE TO HIGH ANDROGEN LEVELS AND MAKE THE SITUATION WORSE!!!\*\*\*\*** this explains why they are at risk for unopposed estrogens because since there is no ovulation (or corpus luteum development) there is no increase in progesterone which leaves the estrogen unopposed and increased risk for endometrial cancer!
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polycystic ovarian syndrome ## Footnote 2 dx? 3 tx options?
DX: 1. increased testosterone levels 2. **_US_** TX: 1. **OCP** **first COC if contra then POP** treats hirsuitism and unopposed estrogen 2. **metformin for insulin resistance** 3. **clompihene citrate** for infertility-ovulation inducer
190
ovarian cysts general ## Footnote what is it? dx? 3 tx options? how to prevent?
**cystic enlargement of ovarian structures** DX: **_US_** Tx: 1. fluid filled **_monitor with periodic US_** because most resolve on their own and ovary still functional 2. if not fluid filled remove with **_laproscopic MC, remove is greater than 6 cm because increase risk of torsion_** **_3.NSAIDS_** prevention: OCPS
191
follicular cyst ## Footnote what is buz word? sxs? tx?
**mc cyst type** **"strawberry filled"** usually not sxs resolve spontaneous result from failure of ovulation so it doens't produce a functional egg
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corpus luteum cyst ## Footnote when does this occur? 2 characteristics? where does it develope
occurs **_after ovulation_** ## Footnote **thin walled and unilocular** **_developes withing the corpeus luteum_**
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theca-lutein cysts in pregnancy or molar gestation ## Footnote how large? at risk for? what does it often occur with?
**_3cm_** at risk for multiple gestations _coinsides with molar gestation_ molar gestation: there's not true DNA developing but enough it develops like a fetus but it will never be viable and has **_teratomas_** and can develop outside of the uterus
194
hemmorrhagic cyst ## Footnote what is the nickname for this? why does this occur?
"chocolate cyst" ## Footnote piece of endometriosis goes to the ovary and called this because of the accululation of blood and is messier if itruptures
195
what is the most LETHAL GYN cancer? what the nickname?
Ovarian cancer! "silent killer" by the time we dx it it is already really progressed and metastisizes!
196
if you find an enlarging ovarian mass with a solid component or change in character _esp in post menopausal woman_, what should you do?
REMOVE IT!! ASAP!!!
197
is it reccomended to screen for ovarian cancer?
no because it does not appeare to reduce mortality
198
what are the genetic markers associated with ovarian cancer?
CA-125 BRCA1 and 2
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what is the most common type of ovarian cancer?
_epithelial carcinomas_ 85-90% of all ovarian cancers
200
what are the 3 types of ovariance cancer classifications? ## Footnote include caracteristics of each 5 4 4
**1. _epithelial_** ## Footnote **MC TYPE** **most are benign** - epithelial carcinomas 85-90% of all ovarian cancers - clear cell-rarely benign - transitional **_2.**_ _**germ cell_** occurs in cells that produce eggs young women teenage-20s 5-10% _teratomes or dermoid cysts are in 40-50% and can contian hair and teeth_ _3. stomal carcinoma_ in connective tissues of the ovaries that produce estrogen and progesterone rare low grade _produce hormones_
201
what are 4 protective factors of ovarian cancer?
OCP more than 1 full term pregnancy before age 35 breast feeding tubal ligation
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what percent of women experienced at least one sxs of ovarian cancer during the year prior to dx?
83% of women...so pay attention!
203
if ovarian cancer only accounts for 2.4% of cancer, why do we worry about it so much?
it is dx in late prognosis! so it kills a lot of people "silent killer"
204
how much does have the BRCA1 and BRCA2 genes increase womens chance of ovarian cancer? what should they consider?
increase lifetime risk by 25-50% ## Footnote \*\*\*consider **_prophylactic billateral salpino-oophorectomy (BSO) by age 35 or as SOON as childbearing is complete for familial ovariance cancer syndrome!!!!!\*\*\*\*_**
205
what are 6 RF for ovarian cancer?
1. BRCA1 BRCA2 2. 65-75 years 3. early menarch, late menopause 4. _french canadians_ 5. never being pregnant 6. obesity
206
ovarian cancer ## Footnote what are the 3 sxs that are likely to present in late dxs? what do you need to keep in mind? 2 dx?
**usually asymptomatic until late disease** **_late stage sxs usually when person presents_** **1. abdominal pain/bloating** **2. early satiety (feeling full)** **3. urinary urgency/frequency** palpable ovary needs evaluation!!! dx: 1. transvaginal US 2. laparoscopic evaluation
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what is the 4 tx options for ovarian cancer?
1. surgery-removal of tumor (may be total hysterectomy) ## Footnote 2. oophorectomy 3. chemotherapy 4. sometimes radiation
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what is the 5 year survival rate for all stages of ovarian cancer? depends on? whats the key?
45% 5 year survival rate ## Footnote highly dependent on stage of dx \*\*EARLY DETECTION IS KEY: survival increases to 75% if detected before leaving ovary!!\*\*
209
low risk HPV causes: high risk HPV causes:
low=genital warts ## Footnote hight=cervical cancer/genital cancers
210
pap interpretation: abnormal pap: atypical sqaumous cell of undetermiens significance ASC-US 2 age brackets and their perferred method of intervention
_women over 25_: do HPV testing, if + go to colposcopy if - repeat cotesting in 3 years _21-24 year olds_ repeat in 1 year
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pap smear results: abnormal pap: low grade squamous intraepithelium lesion LSIL 2 tx groups!
_over 25_ perform HPV cotest if positive do colposcopy, if negative restest in 1 year _age 21-24_ repeat pape in 1 year, if above LSIL then colposcopy, if not continue guidelines
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pap results: abnormal: acute squamous carcinoma-can't exclude high grade (ASC-H)
high risk of carcinoma colposcopy for _ALL_ no matter HPV status
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pap smear results: abnormal pap: High grade squamous intraepithelium lesion (HSIL) 2 age groups? intervention for each?
correlates with CIN II or III at least ## Footnote _25 and over_ colposcopy OR immediate loop electrosurgical excision LEEP _12-24 year olds_ colposcopy ONLY
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pap results: abnormal pap: atypical glandular cells (AGC) 2 tx? correlates to?
colposcopy PLUS endometrial sampling if over 35 or at high risk for endometrial cancer
215
for your reading pleasure
216
breast pain "mastalgia" what is this? when is it more common? what are the two differnt types and their characteristics? 3 3 what tests do you do for each?
**MOST COMMON BREAST COMPLAINT IN PRIMARY CARE** premenopausal more common than post menopausal since _often cyclic, and increases in women taking OCP or hormonr replacement_ Non-cyclic women 40-50 sharp burning pain unrelated to mestruation _brest exam AND US **ADD MAMMO if over 30**_ cyclic heaviness soreness billaterall, MC in _upper outer quadrant_ _associated with hormone chages, usually 1 week prior to menstration_ (because the breast tissue proliferates _breast exam, US, add mammo if over 30_
217
what are the 6 tx options for mastalgia?
1. usually self limited 2. support garments 3. compresses 4. analgesics 5. evening primrose 6. danazol _only Rx for mastalgia but lots of SE_
218
T or F: breast pain is rarely cancer?
TRUE!
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nipple discharge ## Footnote what are 3 causes? characteristics? 2 1 2
usually benign 1. normal milk production a. normal secretory milk b. occurs 6 months after cessation of breast feeding 2. galactorrhea a. caused by _hyperprolactinemia, causing bilateral milky nipple discharge_ 3. pathologic (suspicious) a. secretion of other fluids other than milk **b. most common cause is papilloma (papilloma tumor growing from the lining of the breast**
220
if someone has pathologic nipple discharge what 5 sxs might they have?
1. spontaneous 2. unilateral 3. bloddy, clear, yellow, white, dark green (LOTS OF COLORS) 4. associated with mass _5. women over 40_
221
if someone has benign nipple discharge, what are 3 potenital sxs?
1. _discharge with compression only_ 2. often bilateral 3. clear, yellow, dark green
222
what must you do for ANY breast lump?
exclude cancer!!!!!!!!! ## Footnote this is 2nd most common breast complain in primary care, 90% are benign but still need to rule out cancer!!!
223
what is the triple test used when a breast lump is identified?
1. breast exam 2. mammorgram (often with US) 3. needle BX **A. fine need aspiration (FNA)** **B. core needle Bx (CNB)**
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how do you make a definitive dx of breast cancer? (3)
bx via... 1. fine needle aspiration 2. core needle bx 3. open bx
225
what is the most common cancer in women?
breast cancer!
226
where are the 7 MC mestastasis placed for breast cancer?
1. lymph node 2. muscle, fatty tissue, skin 3. bone 4. bone marrow 5. liver 6. lungs 7. brain
227
what are 7 potenital sxs of breast cancer?
1. lumps 2. bumps 3. skin changes 4. dimpling 5. red, hot 6. pain/no pain 7. regional node enlargement
228
what predominates in premenopausal women with bumps/lumps
benign conditions predominate
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what predominates in post menopausal women with lumps and bumps? what do you need to remeber?
malignant lesions ## Footnote in postmenopausal women, any dominant mass or assymetry should be presumed cancerous until proven otherwise
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how do you determine between a mass and a cyst?
US!!! sometimes simplest is to aspirate the mass
231
what should any solid mass, wheter or not it is imageable, warrants...
a definitive dx...bx it!!!
232
what is the GOLD STANDARD for dx breast cancer?
Biopsy!!! superior to even the most advanced imaging
233
when in doubt when it comes to a mass...
assume nothing! aspirate or refer to surgeon
234
Malignant neoplasm: Pagets disease what is this? common? what are two other things to look for? 5 sxs?
cells collect around the nipple causing eczematous appearance Rare-5% 97% also have **_ductal carcinoma in situ OR invasiver cancer elsewhere in the breast_** sxs: **_ITCHING_** **_TINGLING_** **_BURNING_** **_scaling and thickening of the skin_** **_yellow or bloody discharge from the nipple_**
235
non-invasive breast cancer: ## Footnote _ductal carinoma in situ_ what is this? common? life-threatening? how are they found? 2 tx options?
_MOST COMMON TYPE OF NON-INSIVE BREAST CANCER_ _1 in 5, 25% of all BC is this_ non-lifethreatening, typically without signs and symptoms **increases risk of developing invasive BC** **80% found on mammorgram** tx: 1. lumpectomy alone 25-30% recurrence 2. lumpectomy and radiation 15% recurreny
236
non-invasive breast cancer: _lobular carcinoma in situ_ what is this? what does it increase risk of? when/how is it dxed? receptor positive?
collection of abnormal cells, not true cancer ## Footnote **_increases risk of invasive cancer later in life_** dxed before menopause, usually dxed becuase bx performed for some other reason **hormonal receptor positive**
237
Breast Cancer: _invasive ductal carcinoma_ what is this? what percent? 6 sxs? 5 tx options?
most common invasive breast cancer!!! 70-80% of BC SXS: **_1. swelling of all or part of the breast_** **_2. skin irritation or dippling_** **_3. breast pain_** **_4. nipple pain/nipple turing inwards_** **_5. nipple discharge other than milk_** **_6. enlarged lymph nodes in the axilla_** TX: 1. lumpectomy less than 2 cm 2. mastectomy (partial, total, radical) 3. sentinel lymph node bx 4. axillary lymph node bx 5. post surgical radiation
238
what is involved in pt follow up for invasive ductal carinoma breast cancer? 4
1. provider visit with exam every 3-6 months for first 3 years 2. every 6-12 months for 4-5 years 3. every year post 5 years 4. yearly mammogram
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what are 5 additional tx options for a patient with with invasive ductal carcinoma post lumpectomy?
**1. chemotherapy** **2. hormonal therapy** **3. estrogen receptor down regulatiors-tamoxifen** **4. oviaran shut down or removal** **5. HER2 therapies-block HER2 that allows for rapid cancer growth**
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breast cancer: _invasive lobular carcinoma_ common? where does it occur? age?
**2ND MOST COMMON TYPE 10% OF CA** **BEGINS IN THE MILK PRODUCING LOBULES** occurs later in life around 60s
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invasive breast cancer: ## Footnote _inflammatory breast cancer_ what does this look like? how to dx? 4 staging options? 2 tx options?
rare, average age in 55s **_looks like eczema on the breast (not confined to nipple), breast enlarged_** DX: 1. **_skin punch bx_** Staging: **_1. CXR_** **_2. CT of chest/abdomen_** **3. bone scan** **4.LFT** TX: _1. chemotherapy prior to surgery_ _2. targeted therapy: if HER2 receptor postivie **also treat prior to surgery HECEPTIN**_
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invasive breast cancer: _inflammatory breast cancer_ how does your response to pre-surgical chemo effect the next step in tx?
if cancer response to first dose chemo before surgery: _modified radical mastectomy_ ## Footnote if no response to first dose chemo before surgery: _another round chemo + radiation and likely radiation AFTER surgery_
243
what are 7 RF in developing breast cancer?
1. female 2. greater to 55 3. no children, no breastfeeding 4. exogenous exposure to estroen 5. family hx postive for BC 1st degree relative 6. BRCA1 and 2 7. obesity
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BRCA1 and BRCA2 ## Footnote risk? age? where?
60% increase in risk of BC 1. develope breast cancer earlier 2. have bilaterally breast more often
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do malignant breast conditions tend to have more or less discharge?
less
246
how do you dx breast cancer? 4
1. yearly breast exam by provider 2. US 3. _aspiration/bx=gold standard_ 4. mammogram-controversial time frame
247
mammogram guidelines: ## Footnote (2 main guidelines)
very controversial ## Footnote 2 main: - start at 40, Q 1 or 2 years - start at 50, Q1 or 2 years
248
how is Breast cancer staged? 3
1. size 2. spread to lymph node 3. metastasis
249
when are 6 instances it is appropriate to test a patient for BRCA1 and BRCA2?
1. eastern european 2. AA before dx before 35 3. in all family of man dx 4. women with BC in both breasts 5. multiple family with breast or ovarian cancer 6. blood relative before 50
250
_benign brest lump:_ fibroadenoma 6 descriptive characteristics? who common in? from? dx?1 tx? 1
solid round, firm, notender, mobile mass "rolled to and edge" **TYPICALLY IN YOUNG woman 15-35** **likely from hormones** **DX:** _core needle bx_ TX: _excision_
251
fibrocystic disease ## Footnote 4 descriptive words? who common in? pain type? asspcoated with what? 2 presenting complaints? 2 dx? 1 follow up?
diffuse/ill-defined, **_TENDER_** fluid filled mass MC in premenopausal, cyclic breast pain **OFTEN ASSOCITED WITH HORMONAL CHANGES**, AND CAN CHANGE IN SIZE WITH MENSTRUATION presenting complaint: **_pain/palpable mass_** DX: 1. _US_ _2. fine need aspiration for confirmation_ **3. _CBE or US in 2-4 months following aspiration to document stability_**
252
galactorrhea cause?
billateral, milky nipple discharged caused by hyperprolactinemia
253
gynecomastica ## Footnote what is this? ages? 3 things found on PE? tx?
**benign proliferation of glandular tissue in male breast** neonatal, pubertal, older males due to **_increased estrogen and decreased androgen_** PE: _palpable mass over .5 cm (usually under the nipple)_ _NONTENDER_, _FIXED_ TX: usually self limited
254
what are 5 pathologic causes of gyncomastica?
1. drugs 2. cirrhosis 3. hypogonadism 4. tumors 5. CKD
255
mastitis ## Footnote what is this? when is it likely to occur causaitive agent? 4 PE? tx? 2
**inflammation and pain of the breast, most frequently occuring _during breastfeed from infection with staph aureus or strep_** **_MC: staph!!!_** if left untreated can become an abcess!! PE: 1. hard, red 2. inflammed tender area of breast \*\*\*since infection blocks off the duct and it becomes backed up, and at increased risk from breastfeeding since there are more cracks from suckling\*\*\* tx: **_DICLOXACILLIN or CLINDAMYCIN (MRSA)_**
256
breast abcess ## Footnote from? tx?
can be a complication of mastitis and required incision, drainage, and abx
257
what STI has the highest prevalence?
HSV
258
what STI has the highest incidence?
HPV
259
how many new STDs are there annually in the US?
19 million
260
what are 6 complications you see with STIs?
1. infertility 2. ectopic pregnancy 3. low fetal birth weight 4. chronic pelvic pain 5. cervical and angogenital cancer 6. HIV transmission
261
who is at greatest risk for STIs?
youth 50% are in those 15-25 year olds
262
what do you need to do if a patient has either gonnorhrea or chlamydia?
tx as if they have both
263
how much greater is the risk of HIV if you have a STI? why?
2-5x greater risk!! ## Footnote STIs attract CD4 cells to the genital area, so when infected with HIV they are already there. some STIs cause ulcers and therefore also create a portal of entry by treating the STI you _reduce risk 40%_
264
gonorrhea ## Footnote what bacteria? 4 things it effects? hallmark? Men 2 sxs women 2 locations, 4 sxs ANOTHER OPTION FOR INFECTION
neisseria gonorrhoae ## Footnote **_effects cervix, urethra, rectum, pharynx_** "Mucous membrane dxs" of men, women, babies **_antibiotic restisance is hallmark_** men **_1. urethral discharge (thick, milky white, yellowish, or greenish)_** **_2. swollen or tender testicles (epididymitis)_** women **_endocervical or urethra_** 1. **majory asymptomatic** **2. vaginal discharge, dysuria, labial pain/swelling** **3. pain during sex** \*\*\*\*DISSEMINATED GONOCOCCAL INFECTION\*\*\* SXS 1. arthritis-tenosynovitis 2. cutaneous and along tendon sheeths
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gonorrhea in infants ## Footnote 2 causes
mother can trasmit during child birth caues: sepsis opthalmia neonatorum
266
what are 6 RF for gonorrhea?
1. \<25 years 2. previous C/other STDS 3. commercial sex work 4. mew or multiple partners 5. inconsistent condom use 6. drug us
267
what testing do you use to dx gonnorhea in men and women? collection method?
NAAT \*make sure to monitor abx susceptibility\* collection method WOMEN: vaginal swab MEN: dirty urine sample
268
what is the tx for gonorrhea? 2 3 drugs each
DOC1: ceftriaxone 250 mg IM single dose + (azithromycin OR Doxy) DOC2: only if ceftraixone not avaliable cefixime + (azithromycin or doxy)
269
what are 3 complications a woman can get from gonorrhea?
**1. bartholins cysts** **2. pelvic inflammatory disease** **3. disseminated gonnocooccal infection**
270
what do you need to make sure you do when txing for gonorreah?
restest woman/men in 3 months after tx
271
chlamydia ## Footnote what bacteria causes this? what can it cause? 4 sxs in women? 4 sxs in men? 4
chlamydia trachomatis ## Footnote **_cervicitis, urethris, proctitis, PID_** men, women, children women _usually asymptomatic_ _mucopurlulent cervicitis, red and hot_ abnormal vaginal discharge pain during sex men _usually asymptomatic_ discharge from the penis, may be _running, whiteish, thin_ burning on urination swollen testicles, epididymitis
272
chlamydia ## Footnote how do you dx and collect in M/F? what si the DOC1? DOC2?
DX: NAAT urine test: men vaginal swab: women TX: DOC1: azithromycin 1 g once DOC2: doxy 100 mg BID x 7 days
273
do you need to bring people back in to be rested after tx for chlamydia?
ONLY IN PREGNANCY ## Footnote \*\*wait 3-4 weeks to restest so the DNA from the dead bacteria doesn't produce a a false positivie\*\*
274
expidited partner therapy ## Footnote what is it?
txing sex partners without a visit...rules still being written in maine. ## Footnote \*\*can legally write prescription for partner if they aren't youre pt so tx increases\*\*
275
herpes simplex ## Footnote what is a hint that an outbreak is going to occur? what is the important description of these? what are the two different types; where are they found and what percent of the population has them? how do you dx it and what do you see? what are the four treatment options?
**prodromal phases:** 24 hours before outbreak, get burning and tingling "painful grouped vesicles on erythmatous base!" HSV1: oral lesions **85%** population infected; transmitted via saliva, **outbreak triggered by random things** HSV2: genital herpes (more common and detrimental in women! more likely to have complications like ulcers and necrotic tissue), **25%** population infected DX: 1. clinical for the most part _2. tzank smear, geimsa stain shows **GIANT MULTINUCLEATED CELLS**_, can also check for antibodies for this​ via PCR TX: supportive therapy suppressive therapy **Acyclovir, valacyclovir, famcyclovir**
276
acute hepetic gingivostomatits ## Footnote what virus causes this? where does this tend to effect? how often are the outbreaks and who are they common in? what are three things you might find in this patient? explain the maturation of the vesicles?
HSV-1-trigeminal nerve predilection, eruptions 2x a year common in 6 months-5 years CHILDREN abrupt onset **fever, anorexia, red mucosa** **vesicles appear on gums, lip, tongue** **_vesicles colase to form ulcers or plaques_**
277
acute herpetic pharyngotonsillitis ## Footnote what virus causes this? who is it the most common in? what are four symptoms you see with this? what do the lesions look like?
more common in HSV1 than HSV2 primarily in ADULTS **fever, malaise, headache, sore throat** _vesicles on posterior pharynx and tonsils that RUPTURE to form ulcers_ (may have grayish exudate)
280
what are the _5_ complications you worry about from herpes simplex virus?
**1. herpetic withlow** (vesicles on the fingers) **2. herpes gladiatorum** (disseminated cutaneous infections common ing wrestlers) **3. keratoconjunctivitis** (dendritic corneal ulcers) **4. HSV or CNS ENCEPHALOPATHY!!** YIKES!! causes change in mental status and headache **5. infection during pregnancy** can infect the child
281
what is herpetic whithlow?
herpes lesion on the FINGERS
283
_Herpes Simplex-2_ what does this cause? what percent of the population is infected with this? where does this typically have predilection for? what do the lesions start and finish as? what percent of people will have reactivation in the first 12 months? how many reactivations will they have in their lifetime?
causes **genital lesions** 25% of the population infected with this **asymptomatic shedding and painful eruptions can occur** _sacral root ganglion predilection_ _VESICLES_ rupture to form _ULCERS_ reactivation in 90% occur in the first 12 months!! 30% have 6 episodes in their lifetime!!
284
where does Herpes simplex virus tend to hide?
dorsal root ganglion ## Footnote this is why it reactivates
285
acute cervicitis ## Footnote 4 characteristics 5 potenital pathogens
**_purluent vaginal discharge_** **_usually infectious_** **_risk of PID if not treated_** **_sometimes post-coital bleeding_** comon pathogens; 1. gonorrhea 2. chlamydia 3. candida 4. bacterial vaginosis 5. trichomonis "strawberry cervix"
286
chronic cervicitis ## Footnote main sxs? infectious? 4 sxs? 3 tx?
**leukorrhea main sxs** **noninfectious** dyspareunia dysmennoreah low back pain urinary sxs Tx: 1. cryrosurgery 2. laser 3. electrocautery
287
syphilis ## Footnote bacteria? transmission requirements? more common populations? when does most transmission occur? explain progression phases? 6
treponema pallidum ## Footnote spirochete bacterium transmission: vaginal, anal, oral through contact with _syphilis chancre, and requires contact with open lesions to spread_ More common in MSM and AA 30% occurs during the early or secondary phases early primary secondary early latent late latent tertiary neurosyphilis
288
early: primary syphilis what is the hallmark of this? 2 where does it go next? fast?
1. chancre at site of innoculation thats _NOT PAINFUL_ 2. heals spontaneously 3. quickly becomes systemic 4. spreads to local lymph nodes 5. dividing time of 30 hours
289
early: secondary syphilis when does this occur? in what percent? 4 findings? 2 additional related findings?
weeks to months after initial infection (25% of untreated) SXS: **_1. RASH MOST COMMON (can be on palps, and soles!!!!)_** 2. fever/malaise 3. annorexia 4. diffuse LAD Additional findings: **_1. condyloma lata_** -war like lessions in the genital area **_2. patchy alopecia_** -_"moth eaten appearance_
290
late: latent syphilis what is this marked by? infectious? tx?
totally asymptomatic past 1 year, marks this time ## Footnote **_1. slower metbolism of bacteria and prolonged dividing time_** 2. **_thought to be non infectious_** 3. requires longer tx
291
early: early latent syphilis what is important about this stage? S&S time frame? infectious?
infection demonstrateble by serologic testing with Treponema pallidum ## Footnote NO SIGNS OR SYMPTOMS _1 year or less_ _potentially infectious_
292
late: tertiary syphilis what are 2 things that mark this? 1 3 when does this occur?
1. gummas!! (nodular tumor like growths) 2. cardiovascular - aortitis MC - aortic aneurysm - aortic regurg **_1-30 years after initial exposure_** **_may never have had clinicallly apparent primary or secondary_**
293
late: neurosyphilis what are 9 presentations of this?
general paresis of the insane **_1. personality change_** **_2. hyperactive reflex_** **_3. argll-robertson pupils_** **_4. sensory deficits_** **_5. tabes dorsalis_** shuffling gate **_6. opthalmic involvement_** - uveitis - neuroretinits - optic neurtis **_7.auditory sxs_** **_8. cranial nerve palsies_** **_9. meningitis sxs_**
294
congenital syphilis
transmission to stillborn 90% result in stillborne **HUTCHINGSON TEETH**
295
How do you dx primary/secondary syphilis? ## Footnote 4
1. nontreponemal test ## Footnote **_screening for reactivity to cardiolipin-cholesterole-lecithin_** **_RAPID PLASMA REAGIN with titer_** 2. treponemal test **_CONFIRMATORY_** detects antibodies against treponemal cellular components, QUALITATIVE 3. multiplex PCR \*\*neurosyphilis must do CSF analysis\*\*
296
penile cancer ## Footnote what type of cells? tx?
**_squamous cell origin_** "something doesn't look right" TX: surgical
297
how do you tx early stages of syphilis? includes primary, secondary, and early latent
DOC1: penicillin G benzathine 2.4 million units IM DOC2: doxycycline
298
how do you tx late latent syphilis?
DOC1: 3 shots of 2.4 million penicillin G beenzathin IM over 3 weeks ## Footnote DOC2: doxy PO for 4 weeks
299
how do you tx tertiary syphilis?
Penicillin G 2.4 million units IM weekly for 3 weeks
300
how do you tx neurosyphilis?
penicillin G 3-4 million units IV Q4 OR 24 million units IV over 10-14 days
301
treating sex partners of those dxed with syphilis? 3 options
1. if patient in early stages ## Footnote **A. partner exsposure within 90 days TREAT PRESUMPTIVELY** **B. partner exposure over 90 days TREAT PRESUMPTIVELY if no test avaliable or partner followup unlikely, otherwise ok to tx by evaluation** 2. if patient in late stages **evaluate partner clinically** 3. if pt stage unknown approach same as early
302
what is a strange rxn you should know can occur when txing a patient for syphilis
jarish herxherime rxn ## Footnote occurs within 24 hours fever, HA, myalgia can cause early labor or fetal distress
303
\*\*\*\*\*what do you need to test patients with syphilis for???\*\*\*\*
NEED TO TEST ALL PATIENTS WITH SYPHILIS FOR HIV!!!!!! ## Footnote MUST ALSO RETEST IN 3 MONTHS in high prevalence areas!!!!
304
bacterial vaginosis ## Footnote what is this? 3 sxs? how dx? 1 tx?
controversy if it is an STD or not because it is an overgrowth of the patients own flora, however it rarely occurs in women who aren't sexually active **sxs:** **1. malordorous white/grey discharge** **2. pH greater than 4.5** **3. absence of dyspareunia** **DX:** **_CLUE CELLS-cells covered in coccibacilli_** \*\*don't do culture of this, just a wet moutn because it ths the womans own flora so the lab will just show that TX: **METRONIDAZOLE 500 mg BID x 7 days!!**
305
why do we care about txing bacterial vaginosis? 8
1. increased risk of preterm birth/rupture of membranes 2. amniotic fluid infection 3. postpartum endometriosis 4. PID 5. postsurgical infection 6. cervical intraepithelial neoplasia 7. mucopuruloent cervicitis 8. acquisition of HIV infection
306
blantitis ## Footnote who do you find this in? what is the typically cause? 2 tx?
"acorn infection that is like vaginal yeast in women" infection of the head of the penis usually _fungal_ often seen in _uncircumsized men_ TX: 1. OTC antifungals like monistat or oral fluconazole
307
trichomoniasis ## Footnote what is this? 5 sxs? 3 dx methods tx1?
**flagellated protozoan** **SXS:** **1. pruritis** **2. malordorous, froththy, yellowgreen discharge** **3. could have erythema around vagina** **4. dyspareunia** **5. post coital bleeding** dx: _1. wet mount show motile flagellates_ 1. amine test positive 2. pH 5-6 Tx: **METRONIDAZOLE in single 2 gram dose**
308
trichomoniasis: what do you need to do for all sex partners?
treat them!
309
hydrocele ## Footnote what is this? 2 ways to dx? 2 tx options?
**_water on the testicle from congenital remnants of the tunica vaginalis_** a soft, nontender fullness of the hemiscrotum that transillumates **_dx:_** **_1. us_** **_2. transillumination_** **_tx:_** **_1. usually reassurance_** **_2. hydrocoelectomy_**
310
explain how the parasympathetic and sympathetic system control and erection?
parasympathetic: engorgement of the copora cavernosa ## Footnote sympathetic control: contraction of SM and ejaculation
311
hypospadius ## Footnote what is this? what are two adaptations this person might have 3 locations? tx?
urethral meatus is no present at the tip of the glans a midline defect male may need to sit for urination and may cause issues with ejaculation optioins: 1. subcoronal (beneath glans 2. midshaft 3. penoscrotal Tx: sometimes requires correction
312
peronies disease ## Footnote what is this? 4 tx options?
**rigid scarring of the penis resulting in a crooked, painful erection** unknow etiology TX: 1. injection verapamil 2. radiotherapy 3. surgery 4. shock wave therapy
313
prostadynia
pain without infection....tx with NSAIDS
314
what is the name of the new drug that is used to tx overactive bladder?
beta-3 adrenergic MIrabegron that relaxes the SM
315
if a person has both BPH and ED...what drug do you want to give them?
tadalafil (cialis)
316
how often should DRE be preformed?
begin at age 50 if life expectancy is 10+ years
317
compare the curability of testicular cancer and prostate cancer?
testicular cancer is very curable where prostate cancer isn't
318
epididymitis/orchitis (testes) ## Footnote what are the two MC causes of this for the different age groups? how does this present? what sign is pos? 2 dx? 2 tx options?
younger less than 35: MC chlamyida ## Footnote older than 35: MC gram neg bacilli, E.coli **_sudden onset of unilateral top of the testicle pain and swelling often caused by secondary infection from reflux of urine_** \*\*\*Prehn sign positive: relief of sxs with elevation of the scrotum\*\*\* DX: US UA TX: 1**. E. coli: ciprofloxacin** 2. **chlamydia/gonnoreah: azithromycin + ceftriaxone**
319
prostatitis ## Footnote what is the difference between acute and chronic? SXS? 5 2 dx? 2 tx?
**ACUTE:** ## Footnote often in _young_, with _sudden onset_ often **_e.coli, klebsiella (poop bugs)_** **CHRONIC:** prostate normal on exam can be from reccurent infection or inflammation SXS: 1. **FEVER CHILLS** **2. PROSTATE TENDERNESS** **3. DYSURIA (SINCE INFECTION!)** **4. URINARY FREQUENCY** **5. LOW BACK PAIN!** DX: 1. consider prostate massage if first culture negative 2. clinical and UA Tx: 1. ciprofloxacin 2. alpha blockers
320
testicular torsion ## Footnote what is this and what are you at risk for? who is most likely to get this? esp? emergency? 3 sxs?
testes is anormally twisted in the spermatic cord thus comprimising arterial blood flow and venous drainage which leads to **testicular ischemia** most common in _prepubertal and post pubertal 12-18 year old males_, esp with those who had _crytorchidism_ or late decent of the testes UROLOCIAL EMERGENCY!! SXS: 1. **_negative prehns sign-no relief with elevation of the scrotiom_** **_2. unilateral, swollen, retracted testicle_** **_3. absent cremaster reflex_**
321
testicular torsion ## Footnote 2 dx? 3 tx?
DX: 1. clinically 2. doppler US shows decreased blood flow TX: 1. NSAIDS 2. surgical detorsion and orchiopexy (make teste descended) \*\*\*GOAL: GET THIS ALL DONE WITHIN 6 hours!!!\*\*\*
322
phimosis/paraphimosis ## Footnote what are these? who are they common in? tx?
**phimosis: can't readily retract the foreskin to the corona or the glans "turtle stuck inside"** **paraphomosis: tight forskin around the base of the glans so "turtle head can't go back in"** common in uncircumsized men TX: circumcision!! TOC
323
benign prostatic hyperplasia ## Footnote who does this happen in? where does it start in response to what? what does it cause? 7 sxs!!!
increased incidence in nearly ALL MEN!! 80 and up 90% incidence!!! begins around the **_urethra in response to increase dihydrotestosterone production and estrogen causing_** **_urinary obstruction leading to SXS_** SXS: **1. decrease in stream quality** **_a. hesitancy_** **_b. dribbling_** **_c. takes longer to pee, don't pee as far_** **2. incomplete emptying/frequency** **3. retention** **4. nocturia**
324
how are symptoms for BPH scored? 2
international prostate symptom score (IPSS) American system (AUA)
325
what are the 3 general tx options for BPH?
1. watchful waiting 2. medications 3. surgery \*\*depends on severtiy of sxs!!\*\*\*
326
what are 3 tx options for BPH? how do they work? any cautions? 3
1. alpha 1 adrenergic blockers "flow" ## Footnote **"TAMULOSIN"** **relax bladder to improve sxs** \*\*\*watch for decreased libido, dizziness, floppy iris syndrome\*\*\* 2. 5 alpha reductase inhibitors "shrink" **"FINASTERIDE"** inhibit enzyme that convert testosterone to 5 alpha dihydrotestosterone (DHT) which decreases testosterone stimulation of the gland 3. combination-increase flow and shrink 1. dutasteride/tamulosin 2. tadalafil
327
what is a strange non pharmaseutical that works for BPH?
phytotherapy with saw paletto (palm tree extract)
328
what are the 4 surigcal options for BPH?
1. transurethral resection of prostate (TURP) 2. transurethral microwave therapy (TUMT) 3. transurethral needle ablation (TUNA) 4. transurethral US guided laser induced prostaectomy (TULIP)
329
do you always tx BPH?
no! only if pt is symptomatic
330
varicocele ## Footnote what is this? where? what does it feel like? P&P? DX? TX?
dilation or vericose spermatic veins usually on the _left_ with _bag of worms feeling_ ## Footnote sxs: 1. non tender mass without transillumination 2. **_increases in size with valsalva_** **_3. decreases in size with scotal elevation_** DX: 1. doppler US TX: surgical repair via vein ligation only if paiful or preventing fertility
331
testicular cancer ## Footnote who is this most common in? what are the two types? 3 1 2 main presentations?
**typically in younger men 20-40 years old** 1. seminoma tumors a. less aggressive b. radiosensitive (get radiation tx) c. normal levels \*\*\*\*\*\*seminoma are Simple and Sensitive\*\*\*\*\* 2 ​non-seminomatous tumors a. screte AFP but not HCG (green book says both sxs: _painless testicular nodule_, solid mass, or enlargement "_heavy testicle_"
332
what puts a person at higher risk for testicular cancer?
cryptochidism (undescended testicle)
333
what is the cure rate for testicular cancer?
90%
334
testicular cancer ## Footnote 3 dx 3 tx
dx: ## Footnote **1. US** **2. Self exam/physical exam** **3. tumor markers** **_beta human gonadotrophic hormone_** (beta HCG) **_alpha feto protein (AFP)_** tx: 1. orchioplexy-CUT IT OUT 2. chemotherapy etoposide +cisplatin+/-bleomycin 3. fix cryptochidism before puberty
335
if someone is dx with testicular cancer, what MUST you do?!
you must get a chest xray because testicular cancer metastasizes here!
336
prostate cancer ## Footnote where does this occur? invasive? sizes of prostate? screening?
occurs in the secretory gland below the bladder that contributes to seminal fluid **_common, slow growing cancer that leads to urinary obstruction_**"you die with it not from it!! Prostate usually 20 ml (chesetnut or walnut) prostate cancer: 40 ml enlarged golf ball Need to make sure to screeen since hereditary!!!!
337
prostate cancer staging!\*\* ## Footnote what do you use to stage? explain the rating system
gleason scoring ## Footnote 1= well differentiated (favorable) 5=poorly differentiated (unfavorable) THEN add the two bx together for a score between 2-10, 10 is the worst oucome
338
what are the sxs with prostate cancer? 2 ## Footnote how do you dx? 3
sxs: _usually asymptomatic_ untill metastsizes to _bone_ causing _bone_ pain might cause urinary sxs if gotten into uretha and cause dx 1. DRE: hard irregularity/nodule, usually posterior 2. transrectal bx or US guided bx 3. if positive _get erdionucleotide bone scane to look for metastasis_
339
where are the 4 places prostate cancer likes to metastasize?
1. _bone_ 2. blood 3. lymph 4. local
340
how can you screen for prostate cancer? 3
controversial 1. DRE 2. PSA 3. prostate cancer antigen 3
341
who has the highest incidence for prostate cancer? general lifetime risk?
african americans general lifetime risk: 16%
342
what are the 4 tx options for prostate cancer? what is the gold standard?
1. surgery-radical prostatectomy or robotically ## Footnote a. can cure b. high incidence of impotence and incontinence 2. radiation with external beam or implantable seeds a. not curative b. palliation of bone mets c. less impotence and incontinence than surgery 3. hormone-androgen deprevation a. suppressive, not curative 4. chemo? not effective as much
343
what are you options when using hormone therapy for prostate cancer and androgen deprivation? what drugs can you use for each method?
1. remove testosterone production via orchiectomy (remove teste) ## Footnote 2. inhibit ACTH and estrogen (leuprolide) 3. inhibit testicular synthesis of testosterone (aminoglutethimide) 4. inhibit binding of androgen (flutamide)
344
prostate specific antigen ## Footnote what is this? 1 pro 2 cons controversial?
serine protease that is involved in liquefaction ## Footnote **pros:** **elevated in 65% of cases** **Cons:** **35% false negative rate** **non specific since also raised in prostate enlargement and prostatis** leads to more dx but doesn't decrease mortality so controversial...why look for a problem?
345
psychogenic causes of erectile dysfunction ## Footnote what percent of cases? what is this? 2 common causes? 3 problems seen
20% of cases ## Footnote common cause and occurs because the _mood must br right_, commonly effected by _depression and anxiety_ Problems seen: **1. can't initiate** **2. can't fill (encgorge) usually arterial proble** **-diabetes** **-HTN** **-ASHD** **3. can't store veno occlusive** **dysfunction**
346
organic causes of erectile dysfunction ## Footnote what perecent of cases is this? 4 causes 3 2 1 1
80% of cases ## Footnote causes: **1. hormonal** **-loss of testosterone in testicular failure** **-pituitary tumor producing prolactin** **-pituitary failue** **2. drugs** **-antihypertensives** **-psychological** **3. vascular disease** **4. peyronies disease**
347
what is premature ejaculation in origin? what can be used to help this?
psychological in origin ## Footnote SSRis like fluoxetine might help
348
priaspism ## Footnote what is it what do you do?
persistent painful erection ## Footnote emergent urology consult
349
what is the difference between primary and secondary hypogonadism?
_primary_ low testosterone, high LH or FSH (north works, south doesn't _secondary_ low testosterone, low to normal LH/FSH, so therefor north not working well too
350
what testing sequence should you do to evaluate for hypogonadism?
1. AM total testosterone level 2. if low, repeat morning testosterone x2 Interpreation: A. if low testosterone, with LH and FSH not elevated then it is **secondary hypogonadism** B. if low testosterone, with increased LH and FSH than **primary hypogonadism**
351
what are 5 test you want to do for erectile dysfunction?
**1. testosterone level** **2. prolactin levels** \*\*if this is high, it causes low levels of testosterone\*\* **3. LH** **4. US** **5. nocturnal penile tumescence testing "tape testing"**
352
if prolactin levels are high what do you want to do?
get MRI because it likely has CNS origin, possibly tumor
353
what are 5 tx options for erectile dysfunction? ## Footnote what does the medication do? what can it cause? effected by? 2 names?
1. replace testosterone if low 2. phosphodiesterase 5 inhibitor - relaxes SM allowing for filling - can cause headaches and flushing and when combined with nitrates can cause massive dip in BP - effected by high fat meanls SILDENAFIL/TADALAFIL 3. prostaglandin E1 - alprostadil - intra-penile injection or intraurethral 4. vaccum device 5. surgery-penile prosthesis
354
what is hypogonadism caused by? how to you give testosterone?
1. testicular failure 2. problems from hypothalamic/pituary axis \*\*give depo-testosterone _IM_ 1-2x a month!!\*\*
355
cryptochidism ## Footnote who does this occur in? what is this? 2 RF? consequences if not fixed? 1 PE finding? 1 Tx option
**one or more undescended testes that don't move into the scrotal sac, which remain in the _abdomen or stuck in the inguinal canal_** \*\*those born prematurely or are small for gestational age have he highest risk of effect\*\* **consequences:** **1. infertility** **2. testicular torsion** **3. maligancy** PE: 1. absence of palpable testicle, or palpable within the inguinal canal TX: 1. **_SURGERY! by age 1 to prevent risk of infertility_**
356
what does having cryptorchidism increase your risk for?
increases risk of malignancy in undescending testis is 4-10 times greater than gerneral population
357
what is parturition?
encompasses everything having to do with birth birthing, prelude to labor, prep for labor, actualy labor process, initial recovery from childbirth
358
what are the 4 things that initiate labor?
1. progesterone withdrawal 2. fetal lung maturity 3. fetal adrenal glands 4. oxytocin release
359
what are the 9 hormones that play a role in parturition?
estrogen progesterone oxytocin HCG prostaglandins LH relaxin corticotropin-releasing hormone parathyroid hormone related protein
360
FIRST STAGE what are 5 things this stage is marked by? body changes? how long? stages? 5 things youre doing?
1. cervical dilation 0-10 cm 2. longest stage 3. 7-14 hours 4. early/late, active transition 5. normal first stages eval a. monitoring mother b. monitoring fetus c. body care of woman d. supportive care for family e. screening for complications
361
second stage of labor ## Footnote dilation of what? how long? what are you doing? what to be concious of during this phase?
1. 10 cm to birth of baby 2. 1-3 hours avg 3. this is when your _push_ 4. fetal and maternal adverse outcomes occur during the second pahse of birth!!
362
how long does it take to push out the baby during the second phase of birth?
_nulliparious woman_ 1.1-2.9 hours, 3.6 hours with epidural _multiparous woman_ .39-1 hour, 2 hour with epidural \*\*\*hence women who are multiparous take less time to have a child\*\*\*
363
third stage of labor ## Footnote how long does this take? what happens here? what are 4 things that occur?
1. birth and delivery of placenta 2. 10-15 minutes on avg, up to 30 3. uterine contractions 4. uterine fundus at level of umbilicus 5. "folding of placenta at implantation site 6. formation of hematoma between placenta and decidua
364
what does the bishop score tell you?
the bishop score tells you how likely it is for succesful induction or compense spontaneously ## Footnote score of 8+ is relatibly predictive of succesful induction
365
what are the four phases of uterine contraction? ## Footnote 1 1 0 4
**_phase 1:_****_myometrium quiescence (rest)_** occurs for 95% of the pregnancy **_phase 2: uterine awakening_** contractions and cervical softening via collagen fibers **_phase 3: active labor_** **_phase 4: maternal recovery_** a. uterine involution b. cerical repair c. breast feeding d. restoration of fertility
366
uterine contractions ## Footnote what are the 5 anatomical changes that are occuring?
1. compression of nerve ganglia in cervix 2. stretching of the cervix 3. hypoxia of contracted myometrium 4. stretching of the perioneum overlying the fundus 5. uterine actitive - actively contracting upper segement becomes thicker and firm and doesn't relax so it continually pushes baby out - lower uterine segment and cervix become softer distended and mroe passive as labor occurs
367
what can the initiation of labor be marked by?
increase in vaginal discharge that is blood tinged
368
what are two changes to the cervix you see to prepare for labor?
1. cervical dilation 2. effacement (shortening and thinning)
369
what are 6 things that might mark the begining or getting closer to labor?
1. lightening 2 weeks before-breathe easier 2. cervical changes yielding ripeness 3. false labor (can go on for days) 4. permature rupture of membranes 80% of women will begin labor within 24 hours 5. bloody show 24-48 hours before onset of labor 6. gastrointestinal upset ie vomiting diarreah
370
what cervix dilation is marked as usually the begining of the active phase of labor?
6 cm appeares to be the landmark for the start of the active phase
371
what are 3 tests you use to determine if T/F labor, or postion of baby? what are 4 things you use to classify this?
1. sterile vaginal exam ## Footnote **EFFACEMENT** **DILATION** **STATION** distance between fetal presenting part and ischial spine 2. leopolds maneuvers 3. US use this to determine lie, presentation, position and variety
372
Baby: lie
transverse, longitudal
373
baby: presentation 3
cephalic (head down) breech (butt down) shoulder
374
baby: ## Footnote position and variety
occiput/vertex (want) siniput/military brow face
375
at what point is it pivitol the baby is cephalic?
34 weeks because before them babies move around a lot so not as worried about it
376
if breeched, what is the most succesful vaginal delivery that some placed will allow?
frank breech
377
what are the 3 P's that determine if the birth is going slower than expected?
1. passanger (size/position) 2. pelvis or passage 3. power (uterine contraction) maternal dehydration maternal exhaustion uterine insuffieciency
378
what are 7 options for pain mangement for labor?
1. stadol 2. nubain 3. demerol 4. fentanyl 5. nitrous oxide 6. epidural 7. morphine: long labor lasting longer than 2 days
379
where does a epidural block? what must you consider? 3 risks
_L4 to toes_ 1. reduced mobility 2. longer labor 3. must weigh with risks **_-epidural fever_** **_-maternal hypotension_** **_-fetal distress_**
380
what are the 7 cardinal movements of labor?
1. decent, flexion, and engagement (all together) 2. internal rotation 3. extension of the head 4. external rotation of fetal head 5. expulsion
381
placental separation timing? normal blood loss? abnormal blood loss? 4 traditional signs?
15-20 mins, sometimes 30 Normal blood loss: less 500 **post partum hemm: over 500** **four traditional signs:** **1. lengthening of umbilical cord** **2. uterus changes to more globular shape and becomes firm** **3. uterus rises in abdomen-placenta descends** **4. GUSH OF BLOOD OCCURS**
382
what is the physiologica or active management of: 1. uterotonic 2. uterus 3. cord traction 4. cord clamping
383
what is the most common cause of maternal mortality in developed countries? percentage?
postpartum hemmorage 18%
384
what are the 3 options for fetal monitoring?
**1. auscultation: fetoscope or dopple** **2. external fetal heart monitor-continuous or intermittent** **3. internal fetal heart rate monitor-fetal scalp electrode**
385
what is the gold standard to make sure the membranes are intact?
ferning method
386
how often should you monitor the fetal HR in the first and second stage of labor?
every 30 minutes in active labor ## Footnote every 5-15 minutes in second stage
387
is continuous external fetal moniting suggested?
NO! not according to the US task for! they say it increases the risk of c-section and unnessary use of forcepts and suction on children! increasing risk!
388
placental abruption ## Footnote what is this? what are 2 sxs? dx tx 2
life threatening for the fetus where placenta seperates from the uterus prior to delivery and blood pools behind the placenta ## Footnote MC cause of late pregnancy bleeding SXS: vagina bleeding abdominal pain DX: 1.. US TX: **if less than 36 weeks w/o distress**: monitor in hospital **if fetal or maternal distress:** deliver!! c-section!
389
what are risk factors for placental abruption? 8
1. previous placental abruption 2. HTN 3. abdominal trauma 4. substance abuse 5. premature rupture of membranes 6. blood clotting disorders 7. multiple pregnancy 8. maternal age-especially after 40
390
cesarean section ## Footnote what percent of births occur this way? what are the 5 most common causes of this?
**birth of the fetus through an insision in the abdominal and uterine wall** **1/3 of total births** **Causes:** 1. repeat cesarean 2. fetal intolerance to labor 3. fetal position 4. maternal emergency 5. CPD
391
dystocia ## Footnote wat is this? 3 causes to take into consideration? 4 tx options? when do yo uconsider them?
abnormal labor when the cervix fails to dilate progressively over time and the fetus fails to descend causes **1. pelvis:** passage through pelvis impaired **2. powers**: inadequate contractions to dilate cervix and expel baby -active upper portion with passive lower segement **3. passenger**: cephalopelivc disproportion, malpresentations and malpositions TX: **1. oxytoxin/pitocin to induce contraction** **2. amiotomy** **3. cessarian section** - indicated in _active_ stage measured for at least 4 hours without progress - point of maternal exhaustion **4. forcepts or vaccume options**
392
ectopic pregnancy ## Footnote what is this? where does it likel occur? viable? 4 sxs 2 dx 2 tx
**pregnancy that implants outside of the uterus 95% occur in the fallopian tube** **ALWAYS NON VIABLE** **needs immediate attention because is _life threatening_** SXS light bleeding nausea and vomiting dizziness abdominal plain DX: **_slow raising HCG (less than doubling every 48 hrs)_** **_US_** TX: 1. methotrexate 2. laproscopic surgery
393
what are the four most common RF for ectopic pregnancy?
1. recent IUD 2. hx PID 3. interfility txs 4. hx of previous ectopic
394
RH incompatability what appens in this? 2 tings it can cause in baby? what does it attack? 2 tests? tx option?
when the mother is **Rh negative and the baby is Rh positive** the mothers immune system can attach the baby, typically an issue in second pregnancy when IgG passes through the placenta and enters the + baby causeing in second child **_hemoyltic anemia and fetal hydrops (death)_** attack rhesus D antigen on baby RBC DX: **_1. KLEIHAUER-BETKE TEST_**-measures occurence and degree of fetomaternal hemmorage **_2. COOMBS test_**-test for antibodies TX: **_rhogam to destroy anti-fetal-rhesus D antibodies at 28-29 weeks_**
395
what are 4 complications of Rh incompatability?
1. anemia 2. hemolytic disease 3. fetal hydrops 4. still birth
396
premature rupture of membrane ## Footnote what is this? what are the two types and when do they occure? when are they expected to give birht ? at risk for?2 Dx 2? tx
premature rupture of membrane PROM: rupture of the amniotic membrane before the onset of labor at or _beyond 37 week gestation_ **if less than 37 weeks called _preterm premature rupture of membranes PPROM_** 90% of women with PROM will begin labor within _48 hours_ RISK with these: **_INFECTION_ aka endometritis and chorioamnionitis** DX: 1. sterile speculum examination 2. fern testing Tx: 1. deliver the baby if over 34 weeks!! prevents infection
397
what is the leading cause of maternal mortality worldwide? percent?
postpartum hemorrhage 6%
398
postpartum hemmorhage ## Footnote what is this? 2 qualifications? 3 tx options? first line?
blood loss requiring transfusion between admission and the postpartum period estimated loss: vaginal: over 500 c-section: over 1000 TX: 1. compression 2. blood 3. **_oxytocin first line tx!!_**
399
just 11 RF for postpartum hemmorhage?
placental issues baby over 4500 gm grand multiparity prolonged labor medications obesity induction precipitous birth first baby instrumental delivery general anesthesia
400
uterine rupture ## Footnote what is this? fetal mortality? 3 risks? warning sign?
**abnormal thinning of the lower uterine segment** EMERGENCY SITUATION with fetal mortality 50-75% RISKS: 1. high parity 2. previous c-section or subsequent long labor 3. over stimulation with oxytocin warning sign: retraction ring across the uterus between symphisis and umbilicus \*differentiation of uterine activity during active labor\*
401
placenta previa ## Footnote what is this? what should you avoid? 1 sxs? dx? 2 tx?
when placenta completely/partially covers the OS ## Footnote DON'T DO VAGINAL EXAMS BECAUSE CAN CAUSE BLEEDING, _significant risk of hemmorage_ SXS: 1. _painless bleeding of the vagina hallmark_ DX: US TX: 1. watchful waiting 2. **_cesaran section_**
402
multiple gestations ## Footnote occurence rate of twin, triplet? why happens more? best birthing position? 2 MC birth complications? 4 complications for fetus?
**twins: 1 in 100** **triplets: 1 in 1000** \*\*increased frequency from advanced reproductive technologies\*\* **vertex/vertex allows for vaginal birth** most common complications: 1. preterm birth 2. spontaneous abortion complications with twins: 1. intrauterine growth restriction 2. cord acidents 3. death of one twin 4. placental previa/ abruptio
403
preclampsia ## Footnote what is this a disease of? 2 requirements? when do you tx? 4 sxs? 1 dx? 2 tx options?
\*\*disease of placental vasculature\*\* ## Footnote **preeclampsia requirements:** **1. over 140/90 on 2 occasions 4 hours apart of over 160/110 _AFTER_ 20 weeks gestation in previous normotensive woman PLUS** **2. proteinuria over 0.3 gm in 24 hr urine** don't routinely tx unless BP unless: SBP over 150 DBP over 100 SXS 1. severe headache 2. chest discomfort 3. SOB 4. confusion DX: **_24 hour urine!!!_** tx: labetalol or hydralazine
404
what is HELLP syndrome?
preeclampsia with 1. H-hemoysis 2. E-elevated L-iver enzymes 3. Low platelets this is a complication
405
eclampsia ## Footnote what is this? 2 tx options 3 1
severe preeclampia _with the addition of seizures after 20 weeks gestation_ ## Footnote _leading cause of maternal and infant illness and death_ TX: **_1. magnesium sulfate_** tx for seizures neuroprotection for fetus can prolong pregancy up to 48 hours **_2. PREFERRED TX IS DELIVERY!!!_**
406
chronic HTN ## Footnote what is this classified by? when does this occur? when to watch? 5 tx for baseline? 2 tx options?
**SBP: over 140** **DBP: over 90** \*\*occurs prior to pregnancy\*\* and is **_present BEFORE 20 weeks gestation or persists longer than 12 weeks postpartum_** if less than 150/100 WATCH dx: get baseline 1. 24 hr urine 2. UR 3. LEFT 4. thyroid 5. EKG tx: 1. methyldopa 2. labetalol
407
what are 5 complications that can occur from chronic HTN?
1. preterm birth 2. c-section 3. superimposed preeclampsia 4. low birth weight 5. perinatal death
408
what percent of women with chronic HTN will have preterm birth? when?
2/3 have preterm delivery ## Footnote usually at 36-37 weeks instead of 38-40 weeks
409
preeclampsia superimposed on chronic HTN what is this? 2 labs? what percent of women get this?
when a woman with chronic HTN develops **_proteinuria_** after 20 weeks gestation **_elevated liver enzymes_** **_low platelets_** 25% of women with chronic HTN will get preeclampsia
410
gestational HTN ## Footnote what is this? when does it occur? 2 PE 2 dx?
HTN DETECTED _after 20 weeks gestation **without** proteinuria_ ## Footnote **PE** **increased BP** **no proteinuria** **TX:** **labetalol** **methlydopa**
411
gestational trophoblastic disease ## Footnote what is this? what type is most common and of this what are the two types? what happens in each? 1 2 which one is more common?
spectrum of diseases that arise fom the **_placenta_** and include: 1. hydatidiform moles (molar pregnancy)-MC and benign 2. trophoblastic tumors 3. choriocarcinomas two types of molar preg: 1. partial mole **_a. egg is fertilized by 1-2 sperm which redulicates itself_** **_b. fetus developes but is NONVIABLE and the placent develops into mass of cysts_** 2. complete mole-MC!!! grape like vessicles or snowstorm pattern **_a. 1-2 sperm combine with egg that has no DNA_** **_b. 20% can develope into malignant tumor (choriocarcinoma)_**
412
gestational trophoblastic disease ## Footnote 4 sxs? 2 dx? 2 tx?
SXS: 1. abnormal vaginal bleeding 2. larger uterine sizes 3. hyperemesis gravidum (excessive vomiting) 4. preeclampsia DX: **_US_** **_HCG, persistently elevated_** TX: 1. CHEMOTHERAPY 2. SURGERY
413
gestation diabetes ## Footnote what is this? what percent? target fasting? postprandial? how to dx?
**glucose intolderance that begins or is recognized in pregnancy** gestational diabetes MC in pregnancy (opposed to pregestational Diabetes)-90% gestational! target range: 90 fasting, 120 post prandial DX: 1. glucose on all pregnany women during first prenatal visit **_2. repeat screening at_** _24-28 weeks_
414
gestational diabetes ## Footnote explain the pathophys of why this occurs?
1. levels of **diabetogenic placental steroid and peptic hormones rise linearly through 2nd and 3rd trimester** 2. lead to increase of glucose levels in blood **3. progressive increase in tissue resistance to maternal insulin,** body dose this intentionally because if the mothers tissues are resistant to insulin, she won't take up the glucose and it will pass through the placenta to nourish the baby, mechanism to make sure the fetus gets nuitrients **3. resistance leads to increase of insulin levels** which doesn't help because the tissues are resistant **4. insulin contributes to post prandial hyperglycemia** since it isn't functioning and can't take up the sugar!! **5. when post prandial maternal glucose levels rise excessively it causes _fetal hyperglycemia**_ (since it has all passed through placent to fetus) _**and fetal hyperinsulinemia_** (since increases production to deal with massive glucose infux) **6.hyper insulinemia promotes storage excess** (since the amount avalible from mom is almost never ending compared to volume of blood avaliable in baby) **7.** increased nuitrients lead to macrosomia in baby (_enlargement and delayed pulmonary maturation_)
415
how/when do you screen for gestational diabetes? what are the results? 2 times
1.screen **24-28 weeks** via two step dx approach of **_1 hour screen 135-140_ _AND_ 2 abnormal values on _3 hour oral glucose tolerance test_ that includes 1 of 2 fasting value** ## Footnote 2. same screening at **_6 weeks postpartum!!_** \*\*if after being administred the glucose, if elevated, then you know she has DM because she is insulin resistant and it couldnt be taken up in the tissues\*\*
416
when talking about gestational diabetes what do you need to keep in mind about these populations; ## Footnote hispanic, native american, african, s outh east asian, pacific islander, indigenous australia BMI over 30, first degree relative, hx of GDM in pas
need to screen earlier because they are like to devlope disease sooner
417
what are the tx options for gestational diabetes?
_1. glyburide or insulin_ in uncontrolled diabetes with diet modification/exercise 2. ADA diet
418
if mother is on insulin and other meds for gestational diabetes...when do you want themto deliver? what should you offer?
39 weeks, might need induction ## Footnote offer c-section if weight over 4500
419
what are mothers with gestational diabetes at increased risk for?
T2DM in 5-10 years so screen annually 10-50% risk
420
what is the chance of spontaneous abortion if less than 20 weeks gestation?
20% aka 1:5 important to let mothers know this is common!
421
when is HCG first detected? doubling time?
first detected 11 days after conception ## Footnote 48 hour doubling time!
422
what are 5 additionaly considerations to be mindful of in a new mom who is going to be going through the birhting process? ## Footnote 2
1. thyroid function-test ## Footnote 2. maternal infection a. HERPES-always inspect before labor b. **_group B_** **_culuture at 36 weeks since transient on skin and can cause major problems, if pos tx with Peniciilin G_** 3. obesity 4. asthma control can change during pregnancy by 1/3s so just be concious 5. UTI
423
prolonged rupture of membranes ## Footnote risk? tx?
risk of infectioun ## Footnote tx: ampicillin and gentamycin _if fever add clindamycin_
424
pelvic inflammatory disease ## Footnote what is this? 2 ways to get it? 5 RF! 4 sxs, 1 buzz word 3 dx 1 tx
polymicrobial infection of the **upper reproductive tract** (**uterus, fallopian tubes, and ovaries) that can be either from _sexually transmitted_ or _exogenous_ bacterial** **\*\*the bacteria ascent!\*\*** **RF:** **_1. younger than 25_** **_2. nonbarrier contrception_** **_3. hx of new or symptomatic sex partners_** **_4. previous PID_** **_5. STI_** SXS **_1. lower abdominal/back pain_** **_2. fever_** **_3. esquisitly tender cervix on bimanual exam_** **_chandelier sign!_** **_4. purluent discharge_** DX: 1. test for gonnorhea/chlamydia (since most common) 2. transvaginal US 3. diagnostic laproscopy may be needed TX: ABX!!!!
425
what are the four most common cause of PID?
1. gonnoreah 2. chlamydia 3. staph 4. strep
426
metritis what is this?
inflammation of the wall of the uterus