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EndoRepro > Week 3 > Flashcards

Week 3 Flashcards

1
Q

How are hormones released (pathways) into the anterior pituitary and the posterior pituitary?

A
  • Anterior pituitary – releasing hormones released into blood supply from hypothalamus → travel to Ant. Pituitary → releases another hormone into the body
  • Posterior pituitary – nerves from hypothalamus release releasing hormone directly to central blood supply
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2
Q

What hormones go through the anterior and posterior? Diagram.

A
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3
Q

What are the 4 types of proteins?

A

AA derivatives, steroids, peptides, proteins

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4
Q

What are the two amino acids that hormones are derived from? What hormones are derived from each?

A
  • Amino Acid Derivatives
    • Tyrosine → catecholamines
    • Tryptophan → serotonin and melatonin
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5
Q

Name 6 steroid hormones and what they are dervied from?

A
  • Steroids
    • Derived from cholesterol → progesterone, androgens, testosterone, aldosterone, cortisol
    • Vitamin D: 7-dehyrocholesterol → cholecalciferol (Vitamin D3) via sunlight
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6
Q

What are three drug types that modulate steroids hormones? What are their MOAs?? What can these be used for?

A
  • Pharmacology
    • Tamoxifen/raloxifene – antiestrogens for ER-positive breast cancer
    • Aminoglutethimide/Anastrazole – aromatase inhibitor, blocks estrogen synthesis
      • Premenopausal women – estrogen synthesis in ovary
      • Postmenopausal women – estrogen synthesis in adipose tissue
    • Flutamide/Bicalutamide – antiandrogens useful for prostate cancer
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7
Q

Name some peptide hormones (4)

A
  • Peptides – less than 50 amino acids
    • TRH, oxytocin, ACTH, insulin
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8
Q

Name some protein hormones (4)

A
  • Proteins
    • FSH, LH, TSH, hCG – highly conserved 92 AA unit

Note that these 4 are VERY VERY SIMILAR

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9
Q

How are signals transduced from hormones? 3 pathways

A

Signal Transduction

  • 7TM-GPCRs, Tyrosine kinases, Nuclear receptors
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10
Q

Define negative feedback and what it does in terms of hormone regulation.

A

Negative Feedback

  • Tight regulation of “hormonal homeostasis” that maintains hormonal levels in a tight physiological range
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11
Q

Name two GnRH analogs and what they are used in. What are their MOAs?

A
  • GnRH analogs
    • Leuprolide/goserelin – used in prostate cancer
      • MOA: analog binds → constant stimulation of ant. pituitary → desensitization → decreased testosterone/estrogen
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12
Q

Name 2 antiestorgens, 2 aromatase inhibitors, 2 antiandrogens?

A
  • Tamoxifen/raloxifene – antiestrogens for ER-positive breast cancer
  • Aminoglutethimide/Anastrazole – aromatase inhibitor, blocks estrogen synthesis
    • Premenopausal women – estrogen synthesis in ovary
    • Postmenopausal women – estrogen synthesis in adipose tissue
  • Flutamide/Bicalutamide – antiandrogens useful for prostate cancer
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13
Q

Follicular phase

  • What hormone is dominant?
  • Is LH or FSH release more?
  • What occurs to the endoemetrium?
A
  • Follicular (Proliferation of the endometrial tissue) – estrogen dominant
    • Increased pulsatile frequency of GnRH release favors LH release, but in lower concentrations
      • Continuous release of a GnRH analogue → decreased release of LH, FSH
    • Changes in endometrium
      • Mitosis, thickening of stroma, growth of glands
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14
Q

Luteal phase

  • What hormone is dominant?
  • Is LH or FSH release more?
  • What occurs to the endoemetrium?
A
  • Luteal (Secretions by endometrial tissue) – progesterone dominant
    • Decreased pulsatile frequency of GnRH release favors FSH release, but in higher concentrations
    • Changes in endometrium
      • Secretion from glands, edematous stroma, growth of endometrium inhibited
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15
Q

What are the main steps in the ovarian cycle?

A

Primoridal follicles → recruitment → Follicular growth → selection of dominant follicle → ovulation → luteal phase → menstruation → pregnancy (if fertilized)

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16
Q

What happens to the primordial follicles at the beginning of the ovarian cycle?

A
  • Primordial follicles – goes through cycles of growth and apoptosis independent of FSH/LH
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17
Q

What happens in the recruitment phase of the ovarian cycle? How many follicles are recruited? What hormones are low and high?

A
  • Recruitment – FSH stimulates multiple (3 to 11) primordial follicles → primary follicles → antral (secondary) follicles
    • At luteal-to-follicular transition, steroids (estrogen) and inhibin are low → high levels of FSH (high estrogen inhibits FSH release)
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18
Q

What happens in the follicular growth phase of the ovarian cycle? What cells are stumulated? What hormones are high?

A
  • Follicular growth – Increasing FSH → stimulation of granulosa cells → increased estrogen (estradiol) → growth
    • LH stimulates Theca cells → production of androgens/testosterone from cholesterol → granulosa cells convert androgens to estrogen via aromatase (high estrogen increases LH release)
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19
Q

What happens in the selection of dominant follicle phase of the ovarian cycle? When does it occur? What cells are stumulated? What hormones are high?

A
  • Selection of the dominant follicle (cycle day 5 to 7) – estrogen/FSH induce FSH receptor expression on one of the developing follicle → granulosa proliferation → dominant follicle
    • Also induces activation of VEGF → capillary bed formation (more blood flow) → more FSH reaches dominant follicle
    • FSH also induces LH receptors on granulosa cells
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20
Q

What happens in the ovulation phase of the ovarian cycle? What is synthesized and what does this lead to? What happens to the follicle as a result?

A
  • Ovulation – due to LH surge (can also be seen as an increase in temperature due to progesterone release)
    • Synthesis of collagenases and prostaglandins → thinning of follicular wall and contraction of smooth muscle around follicle → dominant follicle ruptures and releases oocyte
    • Remaining follicle → corpus luteum → production of progesterone and drop in estrogen
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21
Q

What happens in the luteal phase of the ovaian cycle? What is inhibited/activated? What occurs if there is no fertilization?

A
  • Luteal phase (14 days)– the production of hormones (progesterone, estrogen, inhibin) by corpus luteum by LH stimulation
    • Inhibin inhibits both FSH and LH
    • If no fertilization, corpus luteum after 9 to 11 days → corpus albicans
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22
Q

What happens during the menstruation phase of the ovarian cycle? How long does it last? What are the hormone levels?

Does the follicular phase or luteal phase vary?

A
  • Menstruation – last about 3 to 5 days
    • Decrease in estrogen and progesterone levels → menstrual shedding of endometrium
    • Cycle lengths vary due to variation in length of follicular phase
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23
Q

What occurs during pregnancy? Why do you not get menses (what happens to the hormones)?

A
  • Pregnancy (fertilization of oocyte by sperm) – results in rescue of corpus luteum
    • Production of Human chorionic gonadotropin (hCG) – molecule similar to LH
      • Stimulates the corpus luteum to produce progesterone and estrogen
      • No fall in E + P → No menses
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24
Q

What is the cervix response to estrogen?

A
  • Mucous production
    • Estradiol
      • Thin, watery mucous
      • Glairy “raw egg white”
      • Facilitates sperm progression
      • Ferns on microscope slide
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25
Q

What is the cervix response to progesterone?

A
  • Mucous production
    • Progesterone
      • Thick, white, opaque mucous
      • Inhibits sperm penetration
      • Ac ts as barrier to pathogens
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26
Q

Enjoy this graph. Memorize it. Love it. Do whatever you want to it.

A
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27
Q

For cervical squamous cell carcinoma:

  • What is the epidemiology?
  • What is the etoiolgy (specify what types)?
  • What is the presentation?
A

Cervical Squamous Cell Carcinoma

  • Epidemiology:
    • Ages 40-50
    • Most pre-invasive lesions do not become invasive cancers → 30% of invasive cancers lead to mortality
    • Cervical cancer is the 4th most common cancer in the world
  • Etiology: HPV (dsDNA virus)
    • HPV types 6 and 11 (LR-HPV): associated with low oncogenic risk (genital warts/condyloma)
    • HPV types 16, 18, 31, and 33 (HR-HPV): associated with cancer and pre-invasive lesions
  • Presentation: vaginal bleeding, cervical discharge
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28
Q

For cervical squamous cell carcinoma:

  • What is the pathophys?
  • What is the natural history?
  • What are the risk factors?
A

Cervical Squamous Cell Carcinoma

  • Pathophysiology
    • HR-HPV → produces E6 and E7 → inhibition of tumor suppressor genes → uncontrolled cell proliferation
      • E6: inhibits p53
      • E7: inhibits RB-E2F, p53, p21
  • Natural History
    • Transient infection: usually clear within 1-3 years (self-limiting)
      • LSIL tends to be transient
    • Persistent infection: HR-HPV DNA integrates into host DNA → malignant transformation → 30% risk of developing high grade squamous intraepithelial lesion (HSIL) → untreated → invasive cancer
  • Risk Factors for Carcinogenesis: tobacco, immune suppression
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29
Q

What is this? Name it and describe it.

A
  • Squamous intraepithelial lesions (pre-invasive) of cervix
    • Low-grade squamous intraepithelial lesion (LSIL)
      • Micro: On top of epithelial layer, dysplasia is noted; however, normal N/C ratios at top (mature cells with lots of clear cytoplasm - koilocytes)
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30
Q

What is this? Name it, define it, and describe it.

A
  • Squamous intraepithelial lesions (pre-invasive) of cervix
    • High-grade squamous intraepithelial lesion (HSIL)
      • Definition: any moderate/sever dysplasia or in-situ carcinoma
      • Micro: On epithelial layer, dysplasia is noted widely (top to bottom); N/C ratios are high throughout
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31
Q

What is this? Name it and describe it?

A
  • Invasive carcinoma of cervix
    • Gross: tan mass
    • Micro: irregularly shaped nest of malignant squamous cells with keratinization infiltrating stromas (see pic)
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32
Q

What is this? Name it and describe it.

A
  • Gross: acetowhite lesions related to squamous intraepithelial lesions
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33
Q

How do you screen/prevent for cervical SCC? What is the gold standard?

A
  • Pap smear – gold standard (sample of most superficial layer of transformation zone)
  • Vaccinations: available for HPV, but not effective against established infections and duration of protection is unknown
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34
Q

What is this? Describe it and what does it show?

A
  • Normal pap smear: Normal N/C ratios with one nucleus (pic)
    • Most mature cells (pink cytoplasm), less mature cells (blue cytoplasm)
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35
Q

What is this? Describe it and what does it show?

A
  • LSIL pap smear: koilocytes with abnormal/multiple nuclei and still lots of cytoplasm (pic)
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36
Q

What is this? Describe it and what does it show?

A
  • HSIL pap smear: high N/C ratio with multiple nuclei per cell (pic)
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37
Q

Know the screening guidelines for cervical scc of all ages and of different histories!

A
  • Age < 21 y/o: No screening
  • Age 21 to 29: cytology (pap smear) alone every three years
  • Age 30 to 65: cytology and HPV co-testing every 5 years preferred
  • Age > 65 y/o: No screening after adequate prior negative screening
  • Hx of HSIL or CA: continue annual screening for 20 years in women with hx
  • After hysterectomy: no screening
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38
Q

What is the blood supply involved in penile erection? Two arteries.

A
  • Blood supply
    • Pudendal a. supplies the corpus cavernosum
    • Dorsal a. supplies the urethra
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39
Q

What is the innervation during a penile erection?

  • Peripheral
  • Sympathetic
    • Nerve roots
    • Pathway
    • Function
  • Parasympathetic
    • Nerve roots
    • Pathway
    • Function
A
  • Innervation
    • Peripheral Nerve: Dorsal nerve → sensation
    • Autonomic Nerves (**Point and Shoot)
      • Sympathetic: T11-L2
        • Lumbar splanchnic nerves → inferior mesenteric/superior hypogastric plexuses → pelvic plexuses
        • Function: detumescence (flaccidity), orgasm, and ejaculation
      • Parasympathetic: S2-3
        • Pelvic splanchnic nerves → pelvic plexus + superior hypogastric plexus → cavernous nerves
        • Function: tumescence (erection), orgasm, and ejaculation
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40
Q

Explain the physiology of an erection. Very detailed

A
  • Dilation of arterioles and arteries by increased blood flow
  • Trapping of incoming blood by expanding sinusoids
  • Compression of subtunical venous plexus between tunica albuginea and peripheral sinusoids reducing venous outflow
  • Stretching of the tunica which occludes emissary veins between the inner and outer layers
  • Increase PO2 and intracavernous pressure (full erection)
  • Contraction of ischiocavernosus muscle (rigid erection)
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41
Q

What neuro transmitters are involved in flaccidty/detumescence?

A
  • Flaccidity and detumescence:
    • Alpha adrenergic fibers releasing norepinephrine at the cavernous arteries
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42
Q

What neuro transmitters are involved in erection?

A
  • Erection
    • Nitric oxide (NO) released from nonadrenergic/noncholinergic (NANC) nerve endings as well as from vascular endothelium
    • Boosts cGMP which relaxes the cavernous smooth muscle (Viagra works here)
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43
Q

What NT are involved in modulation of an erection?

A
  • Modulation
    • Acetylcholine modulates response by inhibiting alpha adrenergics and promoting NO release
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44
Q

What are organic causes of erectile dysfunction (4 groups with different disease/injuries in each group)?

A
  • Organic
    • Vasculogenic: arteriogenic (trauma), cavernosal (venous leak)
    • Neurogenic: spinal cord injury
    • Anatomic: Peyronie’s disease
    • Endocrinologic: diabetes
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45
Q

What are psychogenic causes of erectile dysfunction?

A
  • Generalized (general depression/anxiety), situational (about the idea of having intercourse)
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46
Q

What are the hormonal reasons for having erectile dysfunction?

A
  • Hormone status
    • Hypogonadism (reduced testosterone)
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47
Q

What are risk factors for ED? include meds

A
  • Risk factors of ED: increasing age, psych disorders, CV dysfunction, diabetes, poor SES, smoking
    • Meds: antihypertensives, psych meds, antiandrogens, opiates, alcohol, tobacco
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48
Q

Split up causes of ED into CNS/PNS/vascular in terms of diagnosis

A
  • Diagnostic view of ED
    • CNS: issue with arousal
      • Situational anxiety, lack of interest, Parkinson’s, stroke, low testosterone
    • PNS: issue with transmission of message through nervous system
      • Diabetes, prostate surgery/pelvic fx (damages nerves)
    • Vascular: damaged vessels in perineum
      • PVD, diabetes, smoking, trauma, radiation, HTN, Peyronie’s, cycling
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49
Q

What are examples of PDE-5 inhibitors uded in ED. Know three drug names and their brand names.

A
  • Phosphodiesterase-5 inhibitors (amplifies the message)
    • Examples: sildenafil (Viagra), tadalafil (Cialis), vardenafil (Levitra)
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50
Q

What is the MOA of PDE-5 inhibitors

A
  • MOA: inhibits PDE5 → inhibits conversion of cGMP to 5 GMP → increases the levels of cGMP → smooth muscle relaxation → vasodilation
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51
Q

What are the SE of the PDE-5 inhibitors. Know SE for each one. Know if short acting or long acting.

A
  • SE (all contraindicated with nitrates due to risk for severe hypotension)
    • Sildenafil (short-acting): visual disturbances, headaches
    • Tadalafil (long-acting) headaches all day, myalgias
    • Vardenafil: contraindicated with antiarrhythmics
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52
Q

How do injectable prostaglandins work?

A
  • Injectable prostaglandins (bypasses message system → directly activates)
    • Inject prostaglandin into corpora cavernosa → direct vasodilation
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53
Q

What is the last resort treatment for ED

A
  • Implanted penile prosthesis (last resort)
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54
Q

What are normal and abnormal bleeding patterns in a woman?

  • Think length of cycle, length of menstruation, volume of blood
A
  • Normal bleeding patterns
    • Cycle length: 21-35 days, length of menstruation: ~7 days, Vol: 30-60 mL
  • Abnormal bleeding patterns
    • Vol: 80 mL (excessive)
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55
Q

What are the etiology groups of uterine bleeding?

A

PALM-COEIN

  • Structural
    • Polyp
    • Adenomyosis
    • Leiomyoma
    • Malignancy
  • Non-structural
    • Coagulopathy
    • Ovultory dysfunction
    • Endometrial (aka endometritis)
    • Iatrogenic
    • Not yet classified
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56
Q

What etiology of abnormal uterine bleeding is this? Descirbe the gross pathology of this? Describe what you see here.

A
  • Polyp (Endometrial polyp)
    • Pathology
      • Gross: sessile mass projecting into the endometrial cavity
      • ]Micro (see pic)
        • Thick walled blood vessels
        • Dilated “out of sync” endometrial glands
        • Neoplastic fibrous stroma
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57
Q

What do you see here? Decribe and name it. What would the gross pathology look like? What is the presenation of this disease?

A
  • Adenomyosis
    • Pathology
      • Gross: bulging mass in myometrium with trabecular cut surface
      • Micro: abnormal endometrial glands and stroma deep within the myometrium (see pic)
        • Surrounded my normal smooth muscle
    • Presentation: pelvic pain, menorrhagia, dyspareunia, bleeding
58
Q

What is this? Describe the gross pathology. What kind of person gets these lesions and what are they sensitive to?

A
  • Leiomyoma (aka fibroid)
    • Description: very common benign smooth muscle tumor sensitive to hormones (multiple lesions); common in pre-menopausal women
    • Pathology:
      • Gross: well-defined bulging white/tan mass (see right pic)
59
Q

What is this? Describe the micro pathology. What kind of person gets these lesions and what are they sensitive to?

A
  • Leiomyoma (aka fibroid)
    • Description: very common benign smooth muscle tumor sensitive to hormones (multiple lesions); common in pre-menopausal women
    • Pathology:
      • Micro: spindle cells (see left pic)
60
Q

What is this? Describe the micropathology? What would the gross pathology look like? Describe the disease.

A
  • Leiomyosarcomas
    • Description: rare, malignant single-lesion smooth muscle tumor in myometrium; seen in post-menopausal women
    • Pathology:
      • Gross: poorly-defined, invasive grey/yellow mass
      • Micro: atypia, hypercellularity, multiple mitotic figures (see left pic)
61
Q

Under Malignancy, is endometrial hyperplasia:

  • Describe it.
  • Risk factors?
  • Epidemiology?
A
  • Endometrial hyperplasia (precursor lesion to cancer)
    • Description: exaggerated proliferation of glands of irregular size and shape with an associated increased gland to stroma ratio due to unopposed estrogen stimulation
    • Risk Factors: obesity, PCOS, and diabetes (secondary to unopposed estrogen)
    • Epidemiology: post-menopause bleeding
62
Q

What is this? Describe the micro? What is the malignant potential

A
  • Endometrial Hyperplasia without atypia
    • Micro: crowded, irregular shaped glands made up normal N/C ratio; epithelium remain stratified columnar (see left pic)
    • Malignant potential: 3-4 fold increase risk
63
Q

What is this? Describe the micro? What is the malignant potential

A
  • Endometrial hyperplasia with atypia (aka Endometroid intraepithelial neoplasia/EIN)
    • Micro: high N/C ratio, prominent nuclei, crowded irregular gland (must compare to normal adjacent epithelium) (see left pic)
    • Malignant potential: 14-45 fold increase risk
64
Q

Under Malignancy, is endometrial carcinoma:

  • Describe it.
  • Epidemiology?
  • Two types?
A
  • Endometrial carcinoma
    • Description: most common malignant proliferation of endometrial glands
    • Epidemiology: post-menopausal bleeding
    • Types
      • Type I: Endometroid, mucinous, secretory
      • Type II: Serous, clear cell
65
Q

For type I endometrial carcinoma:

  • Types?
  • Epidemiology?
  • Etiology (genes)
  • Pathophys?
  • Prognosis?
A
  • Type I: Endometroid, mucinous, secretory
    • Epidemiology: younger, obese, unopposed estrogen, insulin resistance
    • Etiology: PTEN, MLH1, kras, MSI
    • Pathophysiology (classical pathway – estrogen excess): endometrial proliferation → non-atypical hyperplasia → EIN → endometroid carcinoma
    • Prognosis: good prognosis
66
Q

For type II endometrial carcinoma:

  • Types?
  • Epidemiology?
  • Etiology (genes)
  • Pathophys?
  • Prognosis?
A
  • Type II: Serous, clear cell
    • Epidemiology: older, black people, hx of breast CA
    • Etiology: p53, HER2, PIK3CA
    • Pathophysiology (alternative pathway – no estrogen excess): endometrial atrophy → intraepithelial carcinoma → serous invasive carcinoma
    • Prognosis: poor
67
Q

What is this? Describe the micropathology.

A
  • Type I: Endometroid, mucinous, secretory
    • Micropathology: hyperplasia with atypia that invades myometrium (looks similar to normal endometrium) (see left pic)
68
Q

What is this? Describe the micropathology.

A
  • Type II: Serous, clear cell
    • Micropathology: non-circular papillary glands with bumpy linings (see pic to the right)
69
Q

Explain some Coagulopathy causes of abnormal uterine bleeding.

A
  • Coagulopathy
    • Examples: Von Willebrand Disease, thrombocytopenia, coagulation factor deficiencies, hemophilia is rare (b/c x-linked)
70
Q

Explain some ovulatory dysfunction causes of abnormal uterine bleeding.

  • What are physiologic and pathologic states that you cang get anovulaton or oligo-ovulation?
A
  • Ovulatory Dysfunction
    • Description: anovolulation or oligo-ovulation caused by:
      • Physiologic: adolescence, perimenopause, pregnancy/lactation
      • Pathologic: thyroid disease, hyperandrogenic state (i.e. PCOD), hyperprolactinemia, hypothalamic dysfunction, premature ovarian failure
71
Q

What are some Iatrogenic causes of abnormal uterine bleeding?

A
  • Iatrogenic
    • Causes: IUDs, meds, radiation/chemotherapy
      • Meds: gonadal steroids (estrogen, androgens), steroid related therapy (SERMs, GnRH analog), anticoagulants
72
Q

What are some Not yet classified causes of abnormal uterine bleeding?

A
  • Not yet classified
    • Examples: arteriovenous malformation, Müllerian anomalies
73
Q

What do you do look for history, PE, labs, and imaging when abnormal uterine bleeding is ocurring

A
  • History: bleeding patterns, GynHx, SurgHx, meds, weight gain/loss, nipple d/c
  • PE: Look for bruises, hirsutism, acne, acanthosis, thyroid issues, pelvic mass, vaginal issues
  • Labs: pregnancy test, CBC, TSH, prolactin, pap smear, STD testing, coag studies
  • Imaging: US, sonohysterogram, MRI, hysteroscopy
74
Q

When do you get pathologic sampling/biopsy in abnormal uterine bleeding?

A
  • Pathologic sampling
    • Indicated in: women >45 or women with <45 with risk factors
75
Q

What are consequences of abnormal uterine bleeding?

A
  • Consequences: anemia, quality of life, hyperplasia, cancer
76
Q

Define endometrisis. What is the most common site? What is the inheritance?

A
  • Definition: presence of endometrial glands and stroma at extrauterine site
    • Ovaries are the most common site
  • Genetics: polygenic, multifactorial inheritance
77
Q

What are the 4 theories of endometriosis? What is the evidence for each?

A
  • Retrograde menstruation: endometrial cells enter peritoneal cavity via retrograde flow
    • Evidence: disease seen in ovaries (presents as painful nodules)
  • Vascular/lymphatic dissemination: transportation of endometrial cells via vessels/lymphatics
    • Evidence: disease seen in lymph system (distant sites)
  • Coelomic metaplasia: cells in the peritoneal cavity can change to functional endometrial tissue
    • Evidence: presence of endometriosis prior to menarche
  • Stem cells: stem cells from the endometrium differentiate into endometrial tissue
    • Evidence: presence of endometriosis after placing stem cells in animal
78
Q

What is the clinical presentation of endometriosis? What are some classical things?

A
  • Clinical presentation: may be asymptomatic, adhesions/pelvic scarring
    • Classic: progressive dysmenorrhea (starts 1-2 days before menses) with deep dyspareunia
    • Others: pelvic pain (chronic), bowel issues, infertility, urinary sx
79
Q

What can infertility in endometriosis be caused by in terms of disease progession?

A
  • Infertility can be caused by:
    • Extensive disease: distortion of fertile anatomy
    • Minimal disease: presence of cytokines/autoantibodies/ prostaglandins → hostile environment for pregnancy
80
Q

What is seen on pelvic exam of endometriosis?

A
  • Pelvic exam: uterosacral nodularity is classic (rare), ovarian mass, retroverted uterus
81
Q

When is expectant treatment for endometriosis indicated?

A
  • Expectant treatment
    • Indicated for: pregnant women, mild symptoms, older women awaiting menopause
82
Q

What are 4 hormonal treatments for endometriosis?

A

OCP + NSAID (1st line), Progestin, androgen, GnRH

83
Q

How does OCP treat endometriosis?

A
  • OCP (plus NSAID): causes decidualization (change in endometrial tissue) → atrophy of endometrial tissue → less bleeding
84
Q

How does Progestin treat endometriosis? Name some progestins

A
  • Progestins (Depo Provera, IUD, Nexplanon/arm contraceptive): causes decidualization → atrophy of endometrial tissue → less bleeding and pain relief
85
Q

How does androgens treat endometriosis? Name an androgen? Name some side effects

A
  • Androgens (Danazol): suppresses LH/FSH surges → no estrogen production → endometrial atrophy/amenorrhea
    • SE: acne, hot flashes, deepening of voice (not reversible)
86
Q

Ho do GnRH agonists treat endometriosis? Name one. What are SE?

A
  • GnRH agonist (Lupron): pituitary desensitization → downregulation of FSH/LH secretion
    • SE: hot flashes, night sweats, decrease in bone density (can add progestin to avoid these)
87
Q

What are surgical treatment for endometriosis?

A
  • Surgical treatment
    • Conservative: destruction/removal of visible lesions, normalization of anatomy
    • Definitive: hysterectomy
88
Q

Define the following:

  • Sexual orientation
  • Gender identity
  • Gender expression
  • Sexual development
  • Transgender
  • Non-binary
  • Difference of sexual dysfunction (DSD)
A
  • Sexual orientation: physical and emotional attraction to same/opposite gender
  • Gender identity: psychological identification as a man, woman, or other
  • Gender expression: external characteristics/behaviors that are defined as masculine or feminine
  • Sexual development: variations in sexual anatomy (aka intersex)
  • Transgender: umbrella term describing state of person’s gender that does not match birth gender
    • FTM: female to male (transgender male), MTF: male to female (transgender woman)
  • Non-binary: having a gender that does not meet concepts of “all male” or “all female”
  • Difference of sexual dysfunction (DSD): a person with sexual anatomy, reproductive organs, and/or chromosome patterns that do not fit the definition of male/female
89
Q

What are 5 types of difference of sexual function?

A
  • Difference of sexual dysfunction (DSD): a person with sexual anatomy, reproductive organs, and/or chromosome patterns that do not fit the definition of male/female
    • Congenital development of ambiguous genitalia (clitormegaly, micropenis),
    • Congenital disjunction of internal and external sex anatomy (5-alpha reductase deficiency),
    • Incomplete development of sex anatomy (vaginal agenesis; gonadal agenesis
    • Sex chromosome anomalies (Turner Syndrome; Klinefelter Syndrome)
    • Disorders of gonadal development (ovotestes)
90
Q

What are challenges associated with in the LGBT community?

A
  • Challenges of LGBT community
    • More likely to: commit suicide, be homeless, get HIV/STD, be obese, have mental health issues, abuse alcohol/tobacco/drugs
    • Less likely to: get preventative services for cancer, carry health insurance
91
Q

What are three diseases that the LGBT community is more likely to get? Why? And what group?

A
  • Cervical cancer
    • Lesbians get pap smears less frequently, but are still at risk for woman-woman transmission (WSW)
  • Breast cancer
    • Lesbians get mammograms less frequently, but have more risk factors
  • STIs:
    • WSW: bacterial vaginosis, chlamydia, HSV-1, HPV, Trichomonas, Syphilis, HIV
    • MSM (high risk): HIV, syphilis, gonorrhea, chlamydia, hepatitis A/B, HSV, HPV
92
Q

What are the 4 factors that demonstrate gender dysphoria?

A
  • Transgender health – physician role to help with transition
    • Gender dysphoria (DSM V criteria)
      • Strong and consistent cross-gender identification
      • Persistent discomfort with birth sex
      • Discomfort is not concurrent with intersex
      • Disturbance causes clinically significant distress in life
93
Q

What are treatment options for gender dysphoria?

A
  • Changes in gender expression and role
  • Psychotherapy
  • Hormone replacement therapy
  • Gender confirmation surgery
94
Q

What are hormone replacement therapies in MTF and FTM transitions? Explain effects of each.

A
  • MTF: anti-androgens, estrogens
    • Estrogens: decreased hair loss, risk of thromboembolic events, increased CV disease, hyperprolactinemia, HTN, infertility
  • FTM: androgens
    • Cessation of periods, increased muscle mass, facial hair, deepening of voice, clitoral enlargement
  • Others: spironolactone (testosterone antagonist), testosterone, estradiol, GnRH analog
95
Q

What can you do for gender confirmation surgery?

A
  • change breasts, external/internal genitalia, facial features,
96
Q
  • For vulvovaginitis:
    • Definition
    • Epidemiology
    • Pathophys
    • Symptoms
    • Diagnosis
    • Types
A

Vulvovaginitis

  • Definition: inflammation of the vulva and the vagina
  • Epidemiology: most frequent CC at PCP office for women
  • Pathophysiology: imbalance of the normal vaginal ecosystem
    • Normal: lactobacilli → produces lactic acid/H2O2 → maintains normal vaginal pH (3.8-4.2)
      • Normal vaginal discharge: clear to white without odor
  • Symptoms: abnormal vaginal discharge, itching, burning, odor, irritation
  • Diagnosis: Hx of symptoms, physical exam findings of pain/vaginal discharge, testing
    • Testing: vaginal pH, microscopical exam (KOH), amine/whiff test, NAAT, gram stain/culture
  • Types: bacterial vaginosis, trichomonas, vaginal candidiasis, atrophic vaginitis, viral infection (HPV/HSV)
97
Q

For bacterial vaginosis:

  • Pathogenesis
  • Risk factors
  • Complications
  • Diagnosis
A
  • Pathogenesis: non-inflammatory overgrowth of anaerobic bacteria in vagina and/or decreased protective lactobacilli
    • Microbiology: Gardnerella vaginalis, Mobiluncus species, Mycoplasma hominis
    • Lactobacillus growth: increases with estrogen
  • Risk factors: poverty, WSW, douching, smoking, lots of unprotected sex, abx
  • Complications: pre-term delivery, endometritis, salpingitis/PID, recurrent UTIs
  • Diagnosis: clue cells (epithelial cells with attached bacteria) on microscopy with few WBC
98
Q

What is Amsel’s criteria? What is it used for?

A

Used to diagnose bacterial vaginosis:

  • Amsel’s criteria (3/4): grayish discharge, clue cells, + Whiff test, pH > 4.5
99
Q

What are the two treatments for bacterial vaginosis?

  • For each, provide MOA, SOA, SE
A
  • Tx (both cause NVD)
    • Metronidazole (po, topical)
      • MOA: inhibits nucleic acid synthesis → disrupts bacterial DNA → bacteriostatic
      • SOA: anaerobes, protozoa, and microaerophilic bacteria
      • SE: disulfiram reaction (no alcohol), metallic taste, CYP2C9 inhibitor (increases warfarin levels)
    • Clindamycin (topical)
      • MOA: binds 50s rRNA → inhibits translocation → bactericidal
      • SOA: gram positive bacteria and anaerobes
      • SE: pseudomembranous colitis (C. Diff)
100
Q

For trichomoniasis:

  • Definition
  • Signs
  • Complications
  • Diagnosis
  • tx
A

Trichomoniasis

  • Definition: motile (flagellated) anaerobic protozoan causing a vaginitis/STI
  • Signs: frothy, green-yellow discharge with odor, pH >4.5, strawberry cervix
  • Complications: preterm birth
  • Diagnosis: microscopic exam (motile trichomonas), copious WBC, NAAT
  • Treatment: oral metronidazole (treat partners too), oral tinidazole
101
Q

For vaginal candiadisis:

  • Definition
  • Sx
  • Risk factors
  • Diagnosis
  • tx
A

Vaginal Candidiasis

  • Definition: vaginal infection by C. albicans (90% of the time)
  • Symptoms: odorless white discharge, burning sensation, pH <4.5
  • Risk factors: pregnancy, OCPs, abx, DM, HIV, steroids, cancer, thyroid disease
  • Diagnosis: KOH (reveals pseudo-hyphae)
  • Tx: OTC meds (miconazole, clotrimazole, tioconazole), prescription meds (fluconazole, butoconazole/terconazole)
    • Self-treaters must come back if symptoms persist >3 days
102
Q

For atrophic vaginitis:

  • Definition
  • Sx
  • Risk factors
  • Diagnosis
  • tx
A
  • Description: lack of estrogen → thinning of vaginal tissue → inflammation
  • Risk factors: menopause, lactation, oophorectomy, radiation therapy, chemotherapy, immunologic disorders, endocrine disorders, antiestrogen medications
  • Symptoms: watery yellow discharge
  • pH > 6.0
    • Absence of lactobacilli
    • Wet Prep: numerous PMN’s; parabasal epithelial cells; background bacteria are cocci
  • Treatment: vaginal lubricants and moisturizers; local or systemic estrogen
103
Q

For desuqamative inflammatory vaginitis:

  • Description
  • sx
  • tx
A

Desquamative Inflammatory Vaginitis

  • Description: inflammation of the lining of the vagina (mucositis due to aerobic overgrowth)
  • Symptoms: similar to atrophic vaginitis, but with: copious green-yellow frothy discharge, abundant WBCs, parabasal cells
  • Treatment: clindamycin, topical hydrocortisone
104
Q

For HSV STD

  • Etiology
  • signs/sx
  • complications
  • dx
  • tx
A
  • Herpes Simplex Virus
    • Etiology: HSV 1 (oral), HSV 2 (genital) → live in dorsal root ganglion
    • Signs/symptoms: painful multiple blisters, tingling pain, tender lymphadenopathy
    • Complications: vertical transmission to fetus (can be prevented with C-section)
    • Diagnosis: PCR, viral culture
    • Treatment: acyclovir/valacyclovir/famciclovir
      • Acyclovir MOA: acyclovir is converted to monophosphate and triphosphate by viral thymidine kinase → inhibits HSV DNA polymerase
105
Q

For chancroid STD

  • Etiology
  • signs/sx
  • dx
  • tx
A
  • Chancroid
    • Etiology: Hamophilus ducreyi (a fastidious gram-negative coccobacillus)
    • Signs/symptoms: painful single ulcer with gray necrotic base
    • Diagnosis: chocolate agar
    • Treatment: IM ceftriaxone, Azithromycin
106
Q

For syphilis, generally explain:

  • Etology
  • Transmission
  • Three stages
  • Diagnosis
  • Screening
  • Tx:
A
  • Syphilis
    • General:
      • Etiology: systemic disease caused by a motile anaerobic spirochete Treponema pallidum
      • Transmission: direct contact of mucosa with lesion/transplancetally
      • Three stages: Primary → Secondary → Latent → Tertiary
      • Diagnosis: direct fluorescent antibody microscopy of lesion
      • Screening:
        • Non-treponemal tests: RPR (rapid plasma regain), VDRL (venereal disease research laboratory)
          • Must confirm positive with treponemal tests: FTA-ABS, TP-PA, MHTA-TP (antibody tests to virus)
      • Treatment: Penicillin G
107
Q

Primary syphilis

  • Description
  • Sx
A
  • Primary Syphilis
    • Description: painless papule that ulcerates
    • Symptoms (resolve in 3-6 weeks): mild lymphadenopathy
108
Q

Secondary syphilis

  • description
  • sx
A
  • Secondary Syphilis
    • Description: popular eruption → condyloma lata
    • Symptoms (resolves in 2-6 weeks): fever, sore throat, malaise, myalgia, weight loss, patchy alopecia, uveitis, lymphadenopathy
109
Q

Latent syphilis

  • Decsription
  • Types
A
  • Latent Syphilis
    • Description: seroactivity without evidence of disease
    • Types
      • Early latent (within a year of symptoms)
      • Late latent (greater than a year since symptoms)
110
Q

Tertiary syphilis

  • Types?
A
  • Tertiary Syphilis
    • Gummatous syphilis: soft tumor-like inflammatory balls affect skin, bone, liver
    • Cardiovascular syphilis: aortitis
    • Neurosyphilis: involves CNS → meningitis, menigovascular syphilis
      • Seizures, Argyll Robertson pupils (non-reactive to light and does focus)
111
Q

Chlamydia trachomatis

  • Epidemiology
  • Etiology
  • Sx for each serotype
  • Diagnosis
  • tx
A

Chlamydia trachomatis

  • Epidemiology: most frequently reported infectious disease in the US
  • Etiology: gram negative obligate intracellular bacteria forms
  • Symptoms:
    • Sertoypes A-K: cervicitis, urethritis, trachoma (conjunctivitis from corneal abrasion), salpingitis/PID in untreated women
    • Serotypes L1-L3 (Lymphogranuloma venereum): induce
      • Primary: painless papule/ulcer
      • Secondary: lymphoproliferative reactions → necrosis
      • Tertiary stage: rectovaginal fistulas
  • Diagnosis: NAAT or urinalysis (include Gonorrhea testing)
  • Treatment: azithromycin, erythromycin, doxycycline
112
Q

Gonorrhea

  • Epidemiology
  • Sx
  • Diagnosis
  • tx
A

Gonorrhea

  • Epidemiology: second most reported infectious disease in the US
  • Symptoms: green-yellow discharge, vaginal burning, dysuria, PID
  • Diagnosis: NAAT, urinalysis, cervix swab (include Chlamydia testing)
  • Treatment (aggressive): ceftriaxone plus azithromycin
113
Q

For HPV STD:

  • Description
  • Etiology
  • Tx (3 drugs)
    • Explain MOAs
A
  • Description: condyloma acuminata/genital warts
  • Etiology: HPV 6 and 11
  • Treatment:
    • Warts are treated with cytosurgery, lase ablation, trichloacetic acid
    • Infection is treated with:
      • Cephalosporins (bactericidal): beta-lactam inhibiting transpeptidase → peptidoglycan cannot form
      • Macrolides (bacteriostatic): binds to 50s ribosomal unit
      • Tetracyclines (bacteriostatic): binds to 30s ribosomal unit
114
Q

Physiology of control of testicular function (3 main hormones and functions)

A
  • GnRH binds to a membrane receptor on pituitary gonadotrophs, and stimulates synthesis and secretion of FSH and LH
    • Pulsatility of GnRH release is required for precision of signaling to pituitary
  • FSH: Required for determination of the testicular Sertoli cell number and for induction and maintenance of spermatogenesis
  • LH: stimulates the secretion of gonadal steroids through Leydig cell activity
115
Q

Spermatogenesis

  • Definition/location/length
  • Phases and what occurs in each?
A
  • Definition: process in which spermatozoa are produced from germ cells via mitosis/meiosis in seminiferous tubules (~ 2 months)
  • Phases (periphery to inside)
    • Proliferative phase – spermatogonia divide to
      • replace their number (self-renewal)
      • differentiate into daughter cells that become mature gametes
    • Meiotic phase
      • germ cells undergo a reduction division
      • results in haploid spermatids
    • Spermiogenesis phase
      • spermatids undergo profound metamorphosis
      • become mature spermatozoa
116
Q

Pathway of ejaculation

A
  • Seminiferous tubules → rete testis → efferent ducts → epididymal tubules → vas deferens → ejaculatory ducts → prostatic urethra
117
Q

Failed spermatogensiss: Failure of GnRH secretion can be caused by what?

A
  • Pituitary disorders (secondary hypogonadism) – decreased secretion of either LH or FSH
  • Hypothalamic disorders (tertiary hypogonadism)
  • Other
118
Q

Name 2 pituitary disorders that cause failure of GnRH secretion leading to failed spermatogenesis

A
  • Failure of GnRH secretion
    • Pituitary disorders (secondary hypogonadism) – decreased secretion of either LH or FSH
      • Isolated LH deficiency (fertile eunuch syndrome) – hypoandrogenism but production of viable sperm due to normal FSH
      • Isolated FSH deficiency – normal androgenization (b/c normal LH) but no spermatogenesis
119
Q

Name 1 hypothalamic disorder that causes failure of GnRH secretion leading to failed spermatogenesis

A
  • Failure of GnRH secretion
    • Hypothalamic disorders (tertiary hypogonadism)
      • Kallman’s syndrome – anosmia (can’t smell) and possible undescended testes
120
Q

What are three other causes of failure of GnRH secretion leading to failed spermatogensis?

A
  • Failure of GnRH secretion
    • Other
      • Space-occupying lesion in the sella turcica – tumors in the anterior pituitary (prolactinoma – most common causes on infertility associated with decreased libido and headaches)
      • Infection: granulomata infection, sarcoidosis, histiocytosis, hemochromatosis
      • Systemic disease: obesity, malnutrition, diabetes
121
Q

What are extrapituitary reasons for failed spermatogensis?

A
  • Extra-pituitary endocrine modulators
    • Exogenous androgen – testosterone negatively inhibits GnRH secretion
    • Drugs: cannabis (decrease plasma testosterone), antipsychotics (dopamine antagonism), opioids (suppress LH release)
122
Q

What are primary hypogonadism reasons for failed spermatogensis? What are the labs and give an example

A
  • Primary hypogonadism – impaired testosterone synthesis caused by Leydig cell dysfunction
    • Labs: elevated LH w/ decreased T (testosterone)
    • Ex: Klinefelter syndrome (XXY) – most common cause of male hypogonadism
123
Q

Testicular torsion:

  • Clinical presenation
  • PE
  • Dx
  • Tx
A
  • Testicular torsion – twisting of the spermatic cords
    • Clinical presentation: severe scrotal pain with rest, activity of trauma, N/V
      • If presenting in neonates: perinatal testicular torsion
    • PE: scrotal edema and erythema, absent cremasteric reflex
    • Dx: Doppler US shows no blood flow
    • Tx: orchiectomy, orchiopexy (w/in 6 hrs), contralateral orchiopexy
124
Q

Torsion of appndages of testicles

  • Epidemiology
  • Dx
A
  • Torsion of appendages – appendages on the testes or epididymis lose blood flow
    • Epidemiology: most common cause of acute scrotum in ages 7-12
    • Dx: Doppler US, blue dot sign
125
Q

Epididymitis, epididymo-orchitis, orchitis

  • Epidemiology
  • Presentation
  • PE
  • Labs
  • Dx
  • Tx
A
  • Epididymitis, epididymo-orchitis, orchitis – inflammation due to infection
    • Epidemiology: men < 35 – STI (Chlamydia/Gonorrhea); older men – BPH, UTI
    • Presentation: gradual progressive onset of posterior testicular pain +/- fever
    • PE: cremasteric reflex present, loss of rugae
    • Labs: elevated WBC, UA shows bacteria
    • Dx: Doppler US (normal to increased blood flow)
    • Tx: abx, NSAIDS
126
Q

Testicular tumor

  • Epidemiology
  • Labs
  • Dx
  • Tx
A
  • Testicular tumor – painless testicular mass
    • Epidemiology: most common solid malignancy among men 20-40
    • Dx: US,
    • Labs: AFP, hCG, LDH
    • Tx: radical orchiectomy
127
Q

For scrotal trauma, how do you diagnose it?

A
  • Scrotal trauma – rupture due to laceration of tunica albuginea of testicle
    • Dx: penetrating injury (exploration in OR), blunt force injury (work up via US)
128
Q

Inguinal hernia

  • Presentation
  • Tyes and describe each
A
  • Inguinal hernia – herniation of peritoneal structures into scrotum through inguinal canal
    • Presentation: pain and swelling of scrotum and groin
    • Types
      • Incarcerated: irreducible hernia
      • Strangulated: incarcerated hernia w/ no blood supply → pain → surgical emergency
129
Q

For fournier’s gangrene

  • Epidemiology
  • Preseantion
  • PE
  • Diagnosis
  • Tx
A
  • Fournier’s gangrene – acute necrotizing fasciitis of scrotum and groin
    • Epidemiology: often seen in immunocompromised/diabetic patients
    • Presentation: associated with cellulitis/abscess, pain and fever
    • PE: diffuse enlargement, necrosis, crepitus
    • Dx: US, CT-scan
    • Tx: immediate debridement, broad spectrum abx
130
Q

What is the optimal time for breast exam?

What do you do during PE?

When is a mammogram indicated?

What do you if palpable breast mass?

A

Breast Examination

  • In pre-menopausal women – optimal time for exam is 7-9 days after onset of menses (lowered estrogen)
  • PE: inspection → palpation of breasts → palpation of regional lymph nodes
  • Mammograms: yearly screening after age 40, highly indicated for dense breasts
  • If palpable breast mass: ultrasound for all ages with biopsy plus mammogram for 30+
131
Q

Define carcinoma-in-situ

A
  • Carcinoma in-situ: malignant proliferation of cells that has not breached the basement membrane
132
Q

What are the risk factors for malignnt breast disease

A
  • Risk factors for breast cancer: gender, age, genetic factors (BRCA1/2), menstrual period, post-menopausal hormonal therapy, non-breast feeding, obesity, alcohol, fat diet, smoking, lack of exercise
133
Q

For intraductal papilloma

  • Presentation
  • Type of nipple discharge - compare to normal!
A
  • Intraductal Papilloma – epithelial proliferation characterized by finger-like structures within ducts
    • Presentation: 30-50 y/o with mass or nipple discharge, moderate increased risk for cancer
    • Nipple Discharge
      • Normal: green, yellow, white, grey, brown discharge (due to duct ectasia) or milky (lactation)
      • Pathologic: clear or bloody
134
Q

For fibroadenoma of breast

  • Presentation
  • Dx
  • Complication
A
  • Fibroadenoma – mobile/rubbery unilateral solid tumor that is hormone sensitive
    • Presentation: younger women with nontender mass
    • Dx: US hypoechoic, core biopsy
    • Complications: may mask Phyllodes tumor
135
Q

For breast abscess

  • Presentation
  • Dx
  • Tx
  • Types (what bugs cause each)
  • Complication
A
  • Breast abscess
    • Presentation: pain, erythema, low-grade fever
    • Tx: I&D, abx
    • Dx: anechoic (black) with posterior enhancement on US
    • Types:
      • Sub-areolar abscess (most common) – caused by aerobes (Staph) and anaerobes
      • Peripheral abscess – caused by aerobes (staph/group A strep)
    • Complications: fistulas
136
Q

For fibrocystic changes in breast

  • Presentation
  • Dx
  • Complications
A
  • Fibrocystic changes – dilated ducts
    • Clinical presentation: 20-40 y/o woman with bilateral, lumpy-bumpy with blue domed cysts
      • Responds to menstrual hormones (rare after menopause)
    • Dx: spongy appearance on ultrasound
    • Complications: may mask cancer
137
Q

For invasive breast cancer:

  • Clinical
    • receptor types
  • Dx of metastasis
  • Tx (for each receptor type)
A
  • Invasive carcinoma (ductal of lobular): invasion of basement membrane
    • Clinical: tend to be multifocal, hard to detect by palpation or mammography
      • Receptor types: ER+, PR+, HER2+ (poor prognosis)
    • Dx: to check for metastasis, perform sentinel node biopsy
      • Preferred over axial node biopsy because high rates of lymphedema
    • Tx:
      • Breasts: Lumpectomy + radiation OR mastectomy
      • Systemic:
        • SERM/Aromatase inhibitor (ER+)
        • Chemo: Adriamycin/Cytoxan/taxane (ER-)
        • Chemo + Trastuzumab (HER2+)
138
Q

For ductal carcinoma in situ:

  • Describe
  • Presentation
  • Types
  • Labs
  • Tx
A
  • Ductal carcinoma in-situ
    • Presentation: clusters of microcalcifications on mammogram
    • Types: solid, cribriform, micropapillary, papillary
    • Labs: usually ER+, PR+ possibly
    • Tx:
      • Breast conversing therapy: lumpectomy + breast radiation
      • Mastectomy: if extensive disease
      • Adjuvant therapy: SERM (selective estrogen receptor modulator) or aromatase inhibitor if ER+
139
Q

For lobular carcinoma in situ:

  • Describe
  • Natural history
  • Tx
A
  • Lobular carcinoma in-situ: filling an expanding lobules by small uniform tumor cells
    • Natural history: increased risk for invasive carcinoma
    • Tx: observation OR observation + tamoxifen OR bilateral mastectomies
140
Q

Trastuzamab

  • MOA?
  • SE?
A
  • Trastuzumab (Herceptin) – MAB that binds to the extracellular domain of HER2 → inhibiting HER1 and HER2 dimerization → blocking cellular proliferation and angiogenesis
    • SE: LV dysfunction → CHF, hypersensitivity, pulmonary toxicity
141
Q

Aromatase inhibitor

  • MOA?
  • SE?
A
  • Aromatase inhibitors – blocks conversion of androgens to estrogen
    • SE: decreased bone density, joint pains, vaginal atrophy, hyperlipidemia
142
Q

SERMS

  • MOA?
  • 2 examples?
  • SE?
A
  • SERMs – competitive inhibitors of estrogen binding to estrogen receptors on tumor tissue
    • i.e. Tamoxifen, Raloxifene
    • SE: hot flashes, endometrial hyperplasia/cancer, DVT, cataracts (due to agonist effects)

EndoRepro (8 decks)

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