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GI/Endo/Repro > Assessment 5 > Flashcards

Assessment 5 Flashcards

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1
Q

Boundaries of Pelvic inlet: Pelvic Brim

A

Pubic crest
Pectineal line
Arcuate line
Ala and promontory of sacrum

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2
Q

Boundaries of pelvic outlet

A 
Inferior end of pubic symphysis
Ischiopubic ramus
Ischial tuberosity
Sacrotuberous ligament
Tip of coccyx
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3
Q

Pelvis Major

A

False pelvis, above pelvic aperture

Part of abdominal cavity, abdominal viscera

Lateral: Iliac fossa
Posterior: L5 and S1
Anterior: Abdominal wall

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4
Q

Pelvis Minor

A

True pelvis, inferior to pelvic inlet

Inferior limit: inferior pelvic aperture/Pelvic brim

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5
Q

Conjugate diameter

A

Distance between sacral promontory and thickest portion of pubic symphysis

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6
Q

Greater sciatic foramen

A

Created by greater sciatic notch and sacrospinous ligament

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7
Q

Lesser sciatic foramen

A

Lesser sciatic notch
Sacrospinous ligament
Sacrotuberous ligament

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8
Q

Anterolateral wall of pelvis

A

Pubic bones
Portion of ischia
Obturator internus muscle
Lesser sciatic foramina

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9
Q

Posterolateral wall of pelvis

A

Pelvic surface of sacrum
Grater sciatic foramina
Priformis muscle

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10
Q

Structures originating from posterolateral wall exit…

A

Greater sciatic foramen

Piriformis muscle
Nerves of lumbosacral plexus
Arteris

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11
Q

Structures originating from anterolateral wall exit…

A

Lesser sciatic foramen

Obturator internus tendon

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12
Q

Pelvic diaphragm components

A

Levator ani

Coccygeus

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13
Q

Levator ani components

A

Pubocorectalis
Pubococcygeus
Iliococcygeus

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14
Q

Pubocorectalis

A

Puborectal swing, involved with incontinence

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15
Q

Origin of iliococcygeus

A

Arises from tendinous arch which comes from fascia of obturator internus

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16
Q

Coccygeus origin and insertion

A

Ischial spine to coccyx

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17
Q

Pelvic diaphragm - male

A

Urogenital diaphragm

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18
Q

Ureters: 3 constrictions

A

Ureteropelvic junction

Pelvic brim

Ureterovesical junction (bladder)

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19
Q

Parts of bladder

A

Detrusor muscle
Internal sphincter
Ureteric orifices
Interureteric fold

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20
Q

Rectosigmoid junction

A

Level of S3

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21
Q

Rectal ampulla

A

Dilation superior to pelvic diaphragm - stores feces before expulsion

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22
Q

Anorectal ring - pectinate line

A

Termination of puborectalis muscle

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23
Q

Blood supply to rectum: 3

A

Superior rectal artery
Middle rectal artery
Inferior rectal artery

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24
Q

Superior rectal artery origin

A

IMA

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25
Middle rectal artery origin
Internal iliac artery
26
Inferior rectal artery origin
Internal pudendal artery
27
Superior rectal vein drains into..
IMV - portal system
28
Middle rectal vein drains into..
Internal iliac vein - caval
29
Inferior rectal vein drains into..
Internal pudendal then internal iliac - caval
30
Internal/External hemorrhoids
Internal: Dilation of veins of internal rectal plexus External: Dilation of external veins of rectal plexus
31
Superior gluteal artery
Passes between lumbosacral trunk and S1 Exits greater sciatic foramen superior to piriformis muscle
32
Posterior division of male pelvis
Superior gluteal artery Iliolumbar artery Lateral sacral artery
33
Anterior division of male pelvic blood supply
``` Umbilical artery Obturator Middle rectal Inferior gluteal Internal pudendal Inferior vesical ```
34
Endopelvic fascia and spaces (ligaments)
Transverse cervical - cardinal Uterosacral Uterovesical
35
Rectouterine pouch
Adjacent to posterior fornix of vagina Between vagina and rectum
36
Corpora cavernosa
Ventral portion of erectile tissue Deep penile artery central within each tissue mass
37
Corpus spongiosum
Central tissue, attaches to glans
38
Crura of penis
Continuation of corpora cavernosa Covered by ischiocavernosus muscle
39
Bulb of penis
Expanded portion at base of spongiosum Covered by bulbospongiosus
40
Parts of urethra
Spongy Intermediate (membranous) Prostatic urethra Intramural urethra
41
Parts of vagina
``` Mons pubis Glans clitoris Labium majus Labium minus Vestibule - space between labia minora ```
42
Scrotum female equivalent
Labia majora
43
Ventral surface of penis female equivalent
Labia minora
44
Main innervation of perineum
Pudendal nerve and branches: Inferior rectal Perineal nerve Dorsal nerve of penis/clitoris
45
Perineal nerve branches
Superficial perineal - posterior scrotal/labial Deep perineal - muscles of superficial and deep pouches
46
Ilioinguinal nerve
Anterior scrotal/labial
47
Genitofemoral nerve
Genital branch - overlap anterior scrotal/labial
48
Inferior cluneal nerve
Inferior buttock and gluteal fold
49
Path of pudendal nerve
From S2-S4 --> through greater sciatic foramina and lesser sciatic foramina
50
Superficial perineal pouch boundaries
Superior: Perineal membrane Inferior: Perineal fascia Lateral: Ischiopubic rami
51
Deep perineal pouch boundaries
Superior: Inferior fascia of pelvic diaphragm Inferior: Perineal membrane Lateral : Obturator fascia
52
Epistiotomy
Controlled incision of perineum to aid passage of infant: Median and mediolateral incision
53
Primordial germ cells
Arise in yolk sack, migrate through umbilical cord to GI tract Lie in intermediate mesoderm Epithelial cells proliferate and surround PMG's --> sex cords
54
Sex cords: Male and female
Early gonad has both so it is called indifferent gonad Male sex cords develop first = primary. Located in inner region = medullary sex cords Female sex cords develop second = secondary. Located in outer region = cortical sex cords
55
Medullary sex cords + TDF
Pre Sertoli cells --> Sertoli cells
56
Sertoli cells
Produce Anti Mullerian hormone
57
Leydig cells
Produce Testosterone when stimulated by LH
58
Anti mullerian hormone
Produced by Sertoli cells Degenerate Mullerian duct = no uterus, cervix, superior vagina
59
Testes determining factor
Encoded by SRY
60
Female cortical sex cords development
Develop into follicle cells
61
Testosterone and development
Protect Wolffian duct = vas deferens, epididymis
62
Female development of Mullerian/Wolffian ducts
No TDF or AMH = no degeneration of Mullerian duct No testosterone = Degeneration of Wolffian duct
63
Remodeling of female anatomy: Paramesonephric ducts
Paramesonephric ducts fuse caudally at pelvic urethra and thicken = Uterus, uterine tubes, cervix, fornix, superior vagina
64
Remodeling of female anatomy: Pelvic urethra
Endoderm, proliferates to form sinovaginal bulb Elongates to form hymen and inferior portion of vagina
65
Incomplete fusion of paramesonephric ducts
Uterus bicornis: 2 uterine horns Uterus didelphys: Double uterus Uterus didelphys with double vagina
66
Incomplete formation of urorectal septum
Rectocloacal canal: Common outlet for urethra, vagina, rectum Rectovaginal fistula: Common outlet for rectum and vagina
67
Androgen insensitivity sundrome
XY male with mutation of testosterone receptor Testosterone normal/high --> converted to estrogen Testes but no sperm, no male accessory organs Anti mullerian hormone present = no internal female genitalia Estrogen = female external genitalia, blind ended vagina, breasts
68
Formation of broad ligament
Fusion of mullerian ducts and break away from mesenchyme Pouches anterior and posterior to broad ligament
69
Gubernaculum
Connects ovaries to labia majora, passes behind uterine tubes When paramesonephric ducts fold, pulled medially Superior: ovarian ligament Inferior: round ligament of uterus
70
Kiss1 neurons
Part of HPG axis Positive feedbak to GnRH neurons Sex steroids inhibit Kiss1 = inhibition of GnRH
71
Excess and minimal GnRH and LH/FSH
Both can cause reduced LH/FSH release
72
HyperPRL and HPG
Decrease activity of entire axis
73
HyperTSH and HPG
Can activate FSH
74
Leptin and HPG axis
Lack of body fat can decrease HPG axis
75
HPG for males
FSH - sertoli cell function and spermatogenesis LH - Leydig cell function --> testosterone
76
Inhibin
Released by sertoli cell, can inhibit FSH
77
Testicular Androgen binding protein
Need local androgen for spermatogenesis ABP binds androgens from leydig cell to increase concentration of androgens Exogenous androgen thus does not help with spermatogenesis
78
Developmental actions of testosterone
Differentiation of Wolffian ducts (DHT) Descent of testes Male brain
79
Adolescent and testosterone
Secondary sex characteristics: Voice, hair, penis size | Aggression
80
HP(ovarian) Axis
Requires pulsating GnRH
81
Developmental actions of estrogen/progesterone
Female sexual differentiation (no need for hormones)
82
Adolescent and estrogen/progesterone
E: Secondary sex characteristics - ovary/vagina/uterus/breast size increase
83
Overall process of male gonadal development Gonads --> penis
Gonad + SRY = Testes Mullerian ducts + AMH = degeneration Wolffian ducts + Testosterone = Vas deferens, epidiymis, seminal vesical DHT androgenizes external male genitalia
84
Critical in utero time for sex development
7-13 weeks
85
3 categories of DSD
1. Sex chromosome DSD 2. 46, XY DSD 3. 46, XX DSD
86
Sex chromosome DSD (3)
1. Turners - 45 X 2. Klinefelters - 47 XXY 3. Mixed gonadal dysgenesis - 45,X/46,XY
87
46, XY DSD etiology
Disorders of gonadal development Disorders of androgen synthesis/action
88
46, XX DSD etiology
Disorders of gonadal development Androgen excess - maternal and fetal
89
Palpable gonads in child = ?
Testicles = Y chromosome
90
Uterus present/absent
``` Absent = AMH = testicles Present = No AMH = no testes = ovaries/abnormal testes ```
91
Normal puberty - males First and second occurrences
1. Testicular enlargement - 11.5yrs 2. Pubic/axillary hair Testicular enlargement before 9 is early
92
Spermarche
~13.5 yrs Tanner 3-4 gonads
93
Growth spurt - males
Later than females Tanner 3-4
94
Normal puberty females - first and second sign
1. Thelarche - 10.7yrs, can be pubarche though 2. Pubarche ~12yrs Breast development before 8yrs is early
95
Menarche
Usually 2-2.5yrs after thelarche Mean age - 12.7
96
Central precocious puberty
Gonadotropin dependent Sexual development before: 9 in boys, 8 in girls - testes/breasts Pubertal levels of FSH/LH More in females
97
Central precocious puberty causes
Harmatomas (GnRH) Pineal masses Optic glioma Abcess, encepalitis, trauma MOST cases idiopathic
98
How does puberty start?
Mean LH/FSH rise - larger LH rise Enhanced GnRH episodic secretion Kiss1 and leptin = positve regulation
99
Mini puberty
Peak at 2-3 months, gone by 1yr Males: Elevated testosterone = genitalia, sperm for later Females: Still not sure, follicle development? Understand HPG axis
100
Peripheral puberty
Gonadotropin independent Estrogen/testosterone elevated but LH/FHS low Gonadal causes: ovarian tumor, leydig tumor, familial testotoxicosis Adrenal causes: CAH, tumor HCG tumor (boys) Exogenous exposure
101
Severe hypothyroidism
Precocious puberty (increase in GnRH release) Spillover effect of TSH on FSH receptor maybe?
102
McCune Albright Syndrome clinical presentation
Triad of: 1. Precocious puberty 2. Cafe au lait pigmentation (coast of Maine 3. Polyostotic fibrous dysplasia
103
McCune Albright Syndrome cause
Somatic activating mutation of Galpha protein Pituitary adenomas with excess LH, FSH, GH, PRL
104
Bone age
Sex steroids determine ossification within epiphyses Bone age = True physical development age
105
Estrogen recetor and aromatase enzyme mutations and bones?
Growth plates don't fuse, become very tall
106
Constitutional delay of puberty
Delayed growth spurt but normal pre pubertal growth Genetic Bone age will be delayed
107
Hypogonadotropin hypogonadism
Isolated or part of other pituitary deficiency Complete pituitary workup, head MRI
108
Kallman syndrome
Kallman 1 codes anosmin (other genes can be involved) Gene mutation affect migration of GnRH neurons and creation/migration of olfactory neurons
109
Hypogonadotropin hypogonadism examples
``` Functional Anorexia (leptin) Prader-Willi HyperPRL Hypothyroid Cushings ```
110
Gonadal failure (boys) - common causes
Testicular failure (high gonadotropins) Klinefelter syndrome Mumps orchitis Trauma/radiation Vanishing testes Noonan syndrome
111
Klinefelter syndrome
47, XXY Most common cause of gonadal failure Small testes, talls tature, gynecomastia, developmental delay
112
Noonan syndrome
Normal karyotype Short stature, cubitis valgus, triangular fascies, mild MR Cardiac defects 1/2 have testosterone/sperm production dysfunctions - delayed puberty
113
Gonadal failure (girls)
Ovarian failure (high gonadotropins) Turners syndrome Trisomy 21 Physical/medical injury Autoimmune oophoritis
114
PCOS
Polycystic Ovarian hyperandrogenism Amenorrhea/chronic anovulation Elevated LH Numerous antral follicles - LH/FSH increases resulting in immature follicles Insulin resistance - hyperpigmentation Overweight/obese, metabolic syndrome Elevated androgen levels - hirsutism
115
Menstrual cycle overall
Ovarian cycle: Follicular genesis, Oogenesis Uterine (endometrial cycle)
116
Ovarian cycle overall
Day 0-14: Follicular phase Day 14-28: Luteal phase
117
Endometrial cycle overall
Day 0-4: Menses Day 4-14: Proliferative phase Day 14-28: Secretory phase
118
Atresia
Degeneration of follicles Can happen at any stage of development
119
Peak oogenia
~20 weeks fetal development 6-7 million follicles
120
Oogonia to primary oocyte
20 weeks fetus --> birth Oogonia enters Meiosis I and arrests at Prophase I Many become atretic but ~400k survive to puberty and surrounded by pregranulosa cells = primordial follicles
121
Folliculogenesis overall
``` Primary oocyte Primordial follicle Primary follicle Secondary follicle Tertiary follicle ```
122
Primordial --> Primary follicle
Granulosa cells develop and connected via gap junctions Enlarges
123
Primary --> Secondary follicle
Granulosa divides to form layers Stromal cells differentiate into theca cells Vascular supply forms
124
Early tertiary follicles
Granulosa cells increase Mucopolysaccharides secreted = zona pelucida Antrum appears
125
Graafian follicles
Dominant follicle Second antral stage, much larger antrum Antrum surrounds oocyte
126
Pre antral stages of folliclulogenesis
Primordial Primary Secondary
127
Antral stages of folliculogenesis
Early tertiary Late tertiary
128
Follicular phase dominant hormone
FSH
129
Later follicular phase and luteal phase hormone
LH
130
Domination of dominant (Graafian follicle)
Follicle with most FSH receptors and best blood supply will supply Low FSH means others will die out - atresia Dominant follicle will release oocyte during ovulation
131
LH surge
Primary signal to rupture follicle (induce ovulation) Proteolytic enzymes weaken follicular wall Contraction of theca externa + prostaglandins = total rupture Primary oocyte completes meiosis I, arrested in metaphase II 1st polar body formed
132
Significance of 1st polar body
Can be used for genetic screening Disease alleles can completely segregate into first polar body
133
Corpus luteum
Non dominant follicle cells form corpus luteum after ovulation Secrete mainly progesterone and some estrogen
134
Corpus luteum and fertilization
If corpus luteum interacts with hCG due to implantation, remains No hCG = degeneration to corpus albicans
135
Endometrium layers
Functionalis - shed during menstruation Basalis - not shed, regenerates functionalis layer
136
Menstrual stages and hormone dominance
Menses Proliferative - Unopposed estrogen driven Secretory - Progesterone + estrogen driven (opposed estrogen)
137
Time and location of fertilization
Usually in ampulla of uterine tube Within 24hrs of ovulation
138
Initiation of menstruation?
Degeneration of corpus luteum = lack of progesterone = hemorrhage of endometrium and menses
139
Bartholin glands
Produce lubrication during sexual arousal Not all lubrication
140
Female sexual innervation
Parasympathetic: Sexual response Sympathetic: Muscle contraction S2-4 innervate clitoris erectile tissue Very sensitive
141
Female sexual response and sperm transport
Sperm do not travel all the way only by swimming Oxytocin release during orgasm initates muscle contraction Contraction drives sperm to uterine ampulla
142
Two cell two gonadotropin model
Model by which androstedione and estradiol are produces Theca cell produces androstedione from cholesterol --> travels to granulosa cell Granulosa cell converts androstedione to estradiol (aromatase) - stimulated by FSH
143
Total Menstrual cycle
1. No fertilization = no hCG so progesterone decreases and endometrium hemorrhages 2. End of luteal phase and decrease in hormones = no negative GnRH feedback --> FSH increases 3. FSH rise = antral follicle growth, some estrogen produced 4. Decrease FSH and increase estrogen = increase GnRH pulsation and LH rise 5. Declining FSH means dominant follicle arises 6. Dominant follicle increases estrogen levels over 200pg/mL for 36-48hrs --> positive feedback to GnRH and subsequent LH surge, increased sensitivity to GnRH receptors 7. LH surge results in meiotic maturation, ovulation, corpus luteum formation 8. Rise of progesterone and estrogen (opposed) results in negative feedback to GnRH, FSH/LH decline 9. Basal LH required for corpus luteum function but becomes insensitive unless there is hCG. No hCG = luteolysis and menses
144
Orally active steroidal estrogens
17 beta estradiol conjugated equine estrogens Ethinyl estradiol Mestranol DES
145
17 B estradiol
Low bioavailability but most potent Requires high doses but thats risky, only use low dose therapy
146
Conjugated equine estrogens
From horse urine Higher bioavailability but less potent Estrone and estrone sulfate
147
Ethinyl estrogen
Synthetic steroidal estrogen Decreased first pass metabolism because of ethinyl group, higher bioavailability Can be administered in low doses but still get good therapeutic effect Administer with progestin as contraceptive
148
Mestranol
First gen used in OCP Combined with norethynodrel
149
Diethylstilbestrol (DES)
Synthetic estrogen Increased breast cancer risk for mother and cervical cancer in fetus
150
Uses of therapeutic estrogens
Hormonal replacement Contraception combined with progestin Primary hypogonadism treatment
151
Estrogen adverse effects
``` Breast tenderness Edema Nausea/vomiting Hyperpigmentation Migration Mid cycle breakthrough bleeding ```
152
Estrogen SAE
Cancer risk: Decrease colorectal, uterine, ovarion Increase benign hepatic adenomas, cervical, CNS Increase gall stones Increase cardiovascular risks: DVT, HTN, MI
153
Estrogen Contraindications
Estrogen dependent neoplasm Vaginal bleeding Thromboembolic disorder Cerebrovascular or CAD Heavy smoking Congenital hyperlididemia, liver disease PREGNANCY
154
Progestin physiological action
Thickened mucus Decrease estrogen receptor, promote cell differentiation in endometrium Decrease fallopian tube motility Contraceptive actions
155
Synthetic progestin ADME
Good absorption and distribution CYP3A4
156
Oral Progestin categories
C21 progestins - progesterone derivatives C19 progestins - 19 nortestosterone derivatives C17 progestin: Spironolactone analog
157
C21 progestins
Progesterone derivative MPA DMPA
158
C19 progestins
19-nortestosterone derivatives 1st gen: Northindrone acetate 2nd gen: Levonorgestrel 3rd gen: Desogestrel, Norgestimate
159
C17 progestin
Spironolactone analog Drospirenone (Yaz, Yasmin) PR activity, Anti AR activity, Anti MR activity Increased DVT
160
Clinical use of progestins
Contraception: Alone or combination Menstrual disorders Hormone therapy
161
Clomiphene
1st line drug for inducing ovulation Partial agonist of estrogen receptor Blocks ER --> Body senses as low estrogen --> increase GnRH --> Large rise in LH/FSH --> Follicle maturation and ovulation Ovarian enlargement and risk of multiple births
162
Raloxifine
2nd line for prevention of post menopausal osteoporosis Estrogen agonist in bone - Prevents bone resorption Estrogen antagonist in breast - Can reduce breast cancer risk Hot flashes/DVT
163
Tamoxifen
Use for prevention of breast cancer Estrogen receptor competative antagonist in breast - prevent estrogen driven genetic transcription Estrogen agonist in endometrium so risk for uterine neoplasia DVT
164
hMGs
Human Menopausal Gonadotropins Ovulation induction when unresponsive to clomiphene IVF Hypothalmic/Pituitary amenorrhea Ovarian enlargement/hyperactivity
165
Mifepristone
Progesterone antagonist - Morning after pill Prevents blastocyst implantation Induces luteolysis of early pregnancy Vaginal bleeding, infections, ectopic pregnancy rupture
166
Leuprolide
GnRH analog - treatment of endometriosis, uterine fibrosis Down regulation of GnRH receptors and reduction of hormones - LH/FSH/estrogen/Progesterone Reversible osteoporosis
167
Premature ovarian failure/primary ovarian insufficiency
Amenorrhea, hypoestrogen, elevated gonadotropins Menopause like symptoms Issue with ovaries, do not produce necessary hormones for proper uterine function Low inhibin = higher FSH Can be autoimmune, chromosome issue, genetic condition, damage to ovaries
168
Causes of missed periods
``` Secondary amenorrhea Eating disorder Pregnancy Hypothyroidism Medication Exercise Stress ```
169
Functional cysts: Cystic follicle vs follicular cyst
Originate in graafian follicle Pelvic pain >3cm - Follicular cyst
170
Luteal cyst
Form in corpus luteum Bright yellow on gross exam Due to preovulatory LH surge or ovulatory stimulus May rupture and cause peritoneal reaction
171
Non functional cyst types and difference from functional cysts
Non functional cysts DO NOT resolve over time 1. Endometriotic cyst 2. Teratoma (younger) 3. Cystadenoma (older)
172
Pathophysiology of androgen excess in PCOD
Androstedione produced in adipocytes and converted to estrone --> Estrone stimulates LH release --> LH stimulates more androstedione production --> Can travel to adipocytes OR converted to testosterone
173
Types of ovarian tumors
Surface epithelial tumors Germ cell Sex cord stroma Metastatic (other)
174
Types of surface epithelial tumors
Each has benign, borderline, malignant Serous Mucinous Endometroid Clear cell Transition cell
175
Types of germ cell tumors
Teratoma - Mature, immature, monodermal Dysgerminoma - rapid growth, good prognosis Yolk sac tumor - Elevated AFP
176
Sex cord tumors
Granulosa cell tumor Sertoli-Leydig tumor
177
Metastatic tumors
Krukenberg Psuedomyoxma peritonei
178
Atresia in aging woman
Atresia accelerates around 35-38yrs
179
Menopause
12 months without menses Loss of follicular function Mean age 51-52yo
180
Premature menopause
Loss of menses before 40 yrs old 1% POI Usually because of medication/therapy
181
Perimenopause
Transitionary period between normal function and menopause Mid/late 40s for 4-6yrs
182
Ovarian function in perimenopause
Decrease ovary size Decrease in # of follicles Inhibin decrease --> FSH increase Poor response to LH/FSH elevation Erratic ovulation and irregular menses
183
Perimenopause treatment
Oral contraceptives Improve menstrual irregularities Decrease ovarian cancer risk, no breast cancer risk
184
Menopause vasomotor symptoms
Hot flashes and night sweats Due to altered thermoregulatory function via estrogen withdrawal Vasodilation --> increase blood flow --> Sweating --> Shivering
185
Vasomotor symptom treatments
Lifestyle changes: Relaxation, cool down activity Non hormonal: SSRI, SNRI, anti-epileptic, antiHTN Soy isoflavanoids Hormone therapy: Estrogen (no uterus), E+P (uterus) - Low breast cancer risk in younger women
186
Menopause urogenital symptoms
Vaginal atrophy Dryness/itchiness Pain during sex UTI's and incontinence
187
Menopause urogential pathophysiology and treatment
Lack of estrogen Loss of glycogen rich superficial cells = No lactobacillus = alkaline vagina More pathogen colonization Treatment: Behavioral, moisturizers/lubrication Local estrogen therapy
188
HSDD
Hypoactive sexual desire disorder Decreased libido Low testosterone
189
HSDD treatment
Filabanserin Premenopausal women only Dopamine and serotonin levels
190
Where do tumors arise from in cervix?
Transition zone between endocervix and ectocervix
191
Cancer associated with ectocervix
Squamous cell carcinoma
192
Cancer associated with endocervix
Adenocarcinoma
193
Lower genital tract infectious agents
``` HSV Candida Trichomonas vaginalis Gardnerella vaginalis HPV ```
194
Lower and upper genital tract infectious agents
Neisseria gonorrhea Chlamydia
195
Herpes Simplex Virus
DNA STD virus Can be asymptomatic Latent phase - trigger is immunosuppression or stress
196
Active HSV presentation/test
TEst: TZank test Vesicles and punched out ulcers - Require C section
197
Congenital herpes
Baby born to active HSV mother transvaginally Conjunctivitis, GI bleeds, jaundice, seizures 67% mortality
198
Candida
Fungus 10% females are carriers White curd like discharge Pseudohyphae and yeast No fetus damage/sequelae
199
Trichomonas vaginalis
Purulent vaginal discharge Strawberry cervix - petechial hemorrhages Pear shaped flagellate organisms
200
Gardnerella Vaginalis
Most common bacterial vaginosis Fishy oder, low viscosity discharge Bacteria adhere to "clue cells"
201
Actinomyces
Associated with intrauterine device (IUD)
202
HPV
Human papilloma virus Benign and malignant lesions
203
Low risk HPV serotypes
6/11 Most common Spontaneously regress Koliocytosis - Nuclear enlargement, darker nuclear stain
204
High risk HPV serotypes
16, 18, 31-33, 35 Kolicytosis and dysplastic changes in epithelium starting at basal layer
205
High Risk HPV pathogenesis
Increase E6 activity = Decrease p53 Increase E7 = Decrease RB
206
Pelvic Inflammatory disease
Ab pain, fever, vaginal discharge, adnexal mass Major cause of infertility and ectopic pregnancy
207
Neisseria gonorrhea
Most common cause of PID and ascending bacterial infection Acute infections: Cervicitis, urethritis, scarring of tubes NO dysplasia or carcinoma risk Neutrophilic disease, organisms in neutrophils
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Chlamydia trachomatis
Most common STD worldwide Follicular cervicitis No dysplasia/carcinoma
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Vulvar disease
Vulvar intraepithelial neoplasia Invasive squamous cell carcinoma Extramammary paget disease
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VIN
Vulvar intraepithelial neoplasia Abnormal maturation confined to epithelium HPV 16/18 (90%) - younger, multicentric leasions, VAIN/CIN HPV negative (10%) - Older women, p53 mutation
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VIN staging
VIN I - Mild dysplasia, bottom 1/3 squamous epithelium VIN II - Moderate, bottom 2/3 epithelium VIN III - Severe, Full thickness abnormality Invasion of basal layer - Squamous cell carcinoma Non invasive can spontanouesly regress in YOUNGER WOMEN
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Vulvar squamous cell carcinoma
Association with HPV Most common vulvar malignancy Invasion through basement membrane
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Squamous cell carcinoma prognosis
Depends on: Tumor size, tumor invasion depth, lymphatic invasion Less than 2cm = good prognosis with vulvectomy and lymphadectomy
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Extramammary paget disease of vulva
Occurs in late reproductive age group White over black Pruritis, ulcerated skin lesions in labia majora/minora Affect epidermis layer NOT associated with carcinoma
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Rhabdomyosarcoma
Sarcoma Botryoides Malignant tumor of skeletal muscle cells Grape like growths and hemorrhages Under 5yrs old Surgery + adjuvant chemo
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Cervical Intraepithelial Neoplasia
Disease of young women Sex early and often is risk factor Pap smear diagnosis Koliocytes, multinucleated cells
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CIN staging
Same as VIN Mild, moderate, severe
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Cervical squamous cell carcinoma
Most common cervical cancer, 8th highest mortality Treat with partial hysterectomy, remove cervix
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Uterus layers
Endometrium - Glands & Stroma Myometrium - Smooth muscle
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Menstrual phase and spiral arteries
Spiral arteries become ischemic and rupture Functionalis shed
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Secretory phase histology
Piano key like structures | Glands irregularly shaped with subnuclear vacuoles
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Ch5ronic endometritis
Etiology - PID, IUD, TB, idiopathic, post partum Symptoms - Bleeding, pain, infertility Histology - 1 or more plasma cells Endometrial scarring
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Endometriosis
Functioning endometrial tissue growing in places that aren't endometrium: Ovary, uterine ligaments, fallopian tubes, lungs, pelvic peritoneum Dysmenorrhea, infertility, ab pain Hemisodern
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Ovarian endometriosis
Ovarian Chocolate cyst
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Pathogenesis of endometriosis
Congenital Endometrial tissue travels back towards ovary Shed tissue reaches blood supply and travels to other areas
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Adenomyosis
Endometrial glands within myometrium Menorrhagia, colicky dysmenorrhea, pelvic pain, bleeding Symmetrically enlarged, boggy uterus FUNCTIONAL ENDOMETRIAL TISSUE
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Endometrial hyperplasia
Proliferation of glands Increase gland/stroma Precursor to endometrial carcinoma Risk: Nulliparous, obesity, ovarian and stromal PTEN mutation because of excess estrogen
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Simple hyperplasia
No atypia: Proliferative endometrium, increase in glands, bland morphology, less than 5% carcinoma Atypia: Proliferative endometrium + loss of polarity/prominent nuclei, 8% carcinoma
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Complex hyperplasia
No atypia - Gland crowding no morphological change, 3% carcinoma Atypia: Above with nuclear hyperchromasia, stratification, nucleoli, mitosis
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Endometrial adenocarcinoma
Most common malignancy of uterus Most common female genital tract cancer PM women Risk: Nulliparity, obesity, diabetes, unopposed estrogen stimulation
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Two types of endometrial carcinoma
1. Excess unopposed estrogen stimulation and endometrial hyperplasia 2. Older individuals, p53 mutation, poor prognosis, poorly differentiated
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Grading system for adenocarcinoma
Grade I: Well differentiated, Less than 5% solid growth pattern Grade II: Moderate differentiation, 6-50% of solid growth pattern Grade III: Poor differentiation, >50% solid growth pattern Atypia raises grade by 1 level
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Myometrium neoplasm types
Benign Uncertain malignant potential Malignant
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Diagnosis/behavior of smooth muscle neoplasms
Necrosis MItotic count Borders
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Leiomyoma
Most common benign smooth muscle tumor Usually in uterine corpus Pelvis GI tract Round whorled lesions, non infiltrating borders, fascicles Cigar shaped nuclei
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Leiomyosarcoma
Rare malignant smooth muscle tumor Peri/Post menopausal woman Enlarged pelvic mass, vaginal bleeding Infiltrative borders, increased mitotic activity, cellular atypia Recurring 10-40% 5 yr survival Hysterectomy CHEMO DOES NOTHING
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Malignant neoplasms of fallopian tubes
Usually come from metastatic source from other area: Ovary, uterus, GI Primary tumors very rare
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Serous/mucinous tumors
Most common types of surface epithelial cells tumors Cystic Benign, borderline, malignant
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Benign vs malignant serous/mucinous tumors
Benign: Cystadenoma Single cyst, simple/flat lining, premenopasal women Malignant: cystadenocarcinoma, multiple, large with complex lining, post menopausal women
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BRCA mutation and ovary
Risk of breast and ovarian cancer Risk of serous malignant carcinoma or ovary and fallopian tube
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Endometrioid tumor
Endometrial tissue tumor, associated with endometriosis Usually malignant Check for endometrium endometrioid carcinoma
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Brenner tumor
Transitional cell tumor Usually benign Urothelial cells
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Germ cell tumors
2nd most common Occur at reproductive age Teratoma Dysgerminoma Endodermal sinus
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Cystic Teratoma
Cystic, bilateral, tissue from 2+ embryological tissues Cysts contain numerous tissue types: Teeth, hair, bone, gut, skin etc Mature = benign Immature = malignant
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Immature cystic teratoma
Mainly contains neuroectodermal tissue Malignant
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Somatic malignancy
Teratomal tissue has squamous cell carcinoma within Bad
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Dysgerminoma
Germ cell mass Increase LDH Good prognosis
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Yolk sac tumor
Endodermal sinus tumor Form from yolk sac Elevated AFP Schiller Duval bodies
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Granulosa cell tumors
Excess estrogen production
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Sertoli leydig cell tumor
Androgen production
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Choriosarcoma
Placental tumor Elevated bhCG Highly aggressive, no chemo response
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Meigs syndrome
Ovarian tumor Right sided pleural effusion Ascites
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Pseudomyoxma peritonei
Mucin deposition in peritoneum Associated with appendix
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Krukenberg tumor
Metastatic tumor usually from GI tract Signet ring Bilateral
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Inflammatory conditions of breast
Acute mastitis Periductal mastitis Fat necrosis Ductal ectasia
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Acute mastitis
Infection of breast usually via S. Aureus Associated with breast feeding Inflammation, warm erythematous breast Treat with drainage and doxicilin
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Periductal mastitis
Associate with smoking - lack of Vit D so metaplasia of columnar epithelium to squamous Subsequent block of subareolar duct and inflammation Subareolar mass and nipple retraction
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Fat necrosis
Associated with trauma Necrotic fat cells and giant cells Presents as mass or calcification on mammogram
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Ductal Ectasia
Inflammation of subareolar ductal wall and dilation of duct Inflammation Multiparous post menopausal women Green brown discharge
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Fibocystic breast changes
Cystic growth of fibrous tissue in breast Hormone sensitive BENIGN
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Fibrosis + cyst + Apocrine metaplasia
No increased risk for invasive carcinoma even though metaplasia
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Ductal hyperplasia
Increase in cells of duct 2x risk for invasive carcinoma
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Atypical hyperplasia
Atypical cells in duct or lobule 5x increase risk for invasive carcinoma
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Sclerosing adenosis
Development of mass due to glandular increase and stretching of tissue - associated fibrosis 2x increase risk invasive carcinoma
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Granulomatous mastitis
Rare Sarcoidosis Infections: Mycobacteria, fungal Dense granulomatous infection Scattered lymphocytes, giant cells
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Intraductal papilloma
Papillary finger like ductal growth surrounded by both types of epithelium Bloody nipple discharge
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Fibroadenoma
Most common benign growth in pre menopausal women Fibrous and glands Estrogen sensitive No invasive cancer risk
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Ductal vs Lobular carcinoma in situ
Ductal: 70-90% incidence, E cadherin (+), calcification, less frequently bilateral Lobular: 10-30% incidence, e cadherin (-), less common calcifications, bilateral, no paget's disease
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DCIS grading
Nuclear grading Grade 1 - nucleus same size as normal ductal epithelial cell Grade 2: Neither NG 1 or NG3 Grade 3: Pleomorphic nuclei, 2-3x size of normal ductal epithelial cells
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Invasive ductal carcinoma NOS - Luminal A
40-55% incidence Post menopausal ER+ Her2/Neu - Negative
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Invasive ductal carcinoma NOS - Luminal B
15-20% Non specific pt characteristics ER/PR + Her2+
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Invasive ductal carcinoma NOS - Basal Like
13-25% Young women, BRCA-1 Triple negative Very bad
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Invasive ductal carcinoma NOS - Her 2 positive
7-12% Brain metastases ER/PR negative Her 2 + high proliferation and 3/3 tumor grade
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Axillary node management
Positive nodes: Axillary dissection Negative: Sentinal lymph node biopsy - Positive = axillary dissection - Negative = No dissection
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Aromatase inhibitors
Anastrazole Letrozole Exemestane Post menopausal women only Inhibit androgen conversion to estrogen
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Trastuzumab
Targeted therapy Monoclonal antibody that binds to extracellular Her 2 domain
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Pertuzumab
Monoclonal antibody that prevent Her2/3 dimerization
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Lapatinib
Intracellular domain action Inhibits tyrosine kinase of Her2
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Denosumab
RANK ligand inhibitor Prevents bone destruction Use if metastatic at presentation
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Everolimus
mTOR inhibitor Reverses endocrine resistance

GI/Endo/Repro (8 decks)

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