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first aid chs part 2 > Repro > Flashcards

Repro Flashcards

1
Q

Unilateral, painful cystic lesion in the lower vestibule adjacent to the vaginal canal.

A

Bartholin’s cyst

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2
Q

What HPV types cause condyloma?

A

6 & 11

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3
Q

What HPV types cause cancer?

A

16, 18. 31, 33

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4
Q

Cells with raisin-like nucleus appearance is descriptive of…

A

Koilocytic change - HPV infection

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5
Q

HPV infection produces what type of change on histology?

A

Koilocytic change - raisin-like appearance of nucleus

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6
Q

What is koilocytic change?

A

Raisin-like appearance of nucleus in HPV

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7
Q

<p>Thin, parchment-like vulvar skin</p>

A

<p>Lichen sclerosis - will see leukoplakia</p>

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8
Q

Thinning of vulvar epidermis with thickening of dermis and leukoplakia.

A

Lichen sclerosis

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9
Q

What is lichen sclerosis?

A

Thin, parchment like vulvar skin with thinning of epidermis and fibrosis of dermis and leukoplakia.

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10
Q

What is the prognosis of lichen sclerosis?

A

Benign, but associated with a slightly increased risk of SCC

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11
Q

Thickened, leather-like vulvar skin

A

Lichen simplex chronicus - due to chronic irritation/scratching.

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12
Q

Hyperplasia of vulvar squamous epithelium with leukoplakia.

A

Lichen simplex chronicus - due to chronic irritation/scratching.

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13
Q

What is lichen simplex chronicus?

A

Thickening of vulvar skin due to hyperplasia of vulvar squamous epithelium caused by chronic irritation/scratching.

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14
Q

What causes lichen simplex chronicus?

A

Chronic irritation/scratching.

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15
Q

What is the prognosis of lichen simplex chronicus?

A

Benign - no increased risk of SCC like with lichen sclerosis.

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16
Q

A patient with vulvar leukoplakia can have which 3 disorders?

A

Lichen sclerosis (thinning of skin); Lichen simplex chronicus (hyperplasia of skin due to chronic scratching); Vulvar carcinoma (HPV or non-HPV related due to chronic lichen sclerosis)

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17
Q

What are the two pathways to development of vulvar carcinoma?

A

HPV related (16, 18, 31, 33); Non-HPV related (usually due to long-standing lichen sclerosis).

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18
Q

Malignant epithelial cell in the epidermis of the vulva

A

Extramammary Paget’s disease

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19
Q

Erythematous pruritic, ulcerated vulvar skin

A

Extramammary Paget’s disease

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20
Q

How does extramammary Paget’s disease present?

A

Erythematous pruritic, ulcerated vulvar skin

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21
Q

What does extramammary Paget’s disease represent?

A

Carcinoma in situ- usually no underlying CA

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22
Q

What is seen on biopsy of extramammary Paget’s disease?

A

Malignant epithelial cell in the epidermis of the vulva

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23
Q

Biopsy of vulvar cells show PAS + , keratin +, and S100 - cells. Dx?

A

Extramammary Paget’s disease (keratin + because it is a carcinoma, PAS + = cells are secreting mucus, so it must be a carcinoma).

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24
Q

Biopsy of vulvar cells show PAS - , keratin -, and S100 + cells. Dx?

A

Melanoma

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25
Q

How do you distinguish extramammary Paget’s disease from melanoma?

A

Extramammary Paget’s disease: PAS + , keratin +, and S100 - cells; Melanoma : PAS - , keratin -, and S100 + cells

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26
Q

Where is the underlying cancer usually located in extramammary Paget’s disease?

A

There is NO underlying cancer. There is only underlying cancer in Paget’s disease of the nipple.

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27
Q

Persistence of columnar epithelium in the upper 1/3 of vagina

A

Adenosis - precursor to clear cell adenocarcinoma

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28
Q

What is vaginal adenosis?

A

Persistance of columnar epithelium (from Mullerian duct) in the upper 1/3 of vagina. Precursor to clear cell adenoacarcinoma.

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29
Q

What causes vaginal adenosis?

A

Exposure to DES in utero

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30
Q

What lesion is considered a precursor to clear cell adenocarcinoma of the vagina?

A

Adenosis

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31
Q

Malignant vaginal proliferation of glands with clear cytoplasm.

A

Clear cell adenoarcinoma.

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32
Q

Exposure to DES in utero leads to increased risk for what two disorders?

A

Adenosis - persistence of columnar epithelium in upper 1/3 of vagina. Clear cell adenocarcinoma - malignant vaginal proliferation of glands with clear cytoplasm.

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33
Q

Malignant mesenchymal proliferation of immature skeletal muscle

A

Embryonal rhabdomyosarcoma

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34
Q

Bleeding with a grape-like mass protruding from vagina in a young girl

A

Embryonal rhabdomyosarcoma (Sarcoma botyroides).

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35
Q

<p>What is seen on histological examination of sarcoma botryiodes?</p>

A

<p>Cells with cytoplasmic cross-striations (spindle shaped cells) This is the description of a rhabdomyoblast.</p>

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36
Q

Rhabdomyosarcoma (sarcomam botryoides) stains for what IHC marker?

A

Desmin (IF for a muscle cell)

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37
Q

Tumor biopsy shows immature cells with cytoplasmic cross-striations. What cell is seen?

A

Rhabdomyoblast (also desmin positive)

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38
Q

What causes vaginal SCC?

A

HPV 16, 18, 31, 33

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39
Q

Cancer from the lower 2/3 of the vagina drains to which nodes?

A

Inguinal nodes

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40
Q

Cancer from the upper 1/3 of the vagina drains to which nodes?

A

Regional iliac nodes

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41
Q

Anatomically, HPV infects what part of the cervix?

A

The transformation zone (where columnar and squamous epithelia meet).

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42
Q

How does HPV cause cancer?

A

Produces: E6, which destroys p53 (G1—->S); E7, which destroys Rb (Free E2F allows G1 —> S)

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43
Q

Cervical dysplasia involving only the lowest 1/3 of cells.

A

CIN I (reversible)

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44
Q

Cervical dysplasia involving the lowest 2/3 of cells.

A

CIN II (reversible)

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45
Q

Cervical dysplasia involving most of the epithelium, but not all of it.

A

CIN III (reversible)

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46
Q

Cervical dysplasia involving the entire epithelium.

A

CIS (irreversible)

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47
Q

What is the #1 risk factor for cervical cancer?

A

Multiple sexual partners (others include smoking, immunodeficiency).

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48
Q

Why are HIV patients at a higher risk for cervical cancer?

A

Immune system can’t remove HPV virus (cervical cancer is an AIDS-defining illness)..

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49
Q

HPV can cause which type(s) of cervical carcinoma?

A

BOTH squamous (much more common) and adenocarcinoma (pap smear doesn’t screen for adenoCA well)..

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50
Q

Typically, how does cervical cancer spread?

A

Locally - invades anterior uterine wall into bladder, leading to hydronephrosis and post-renal failure.

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51
Q

What subtypes are included in the HPV vaccine?

A

6, 11, 16, 18

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52
Q

<p>What is Asherman syndrome?</p>

A

<p>Secondary amenorrhea due to loss of basalis (regenerative layer) and scarring or due to intrauterine adhesions. Result of overaggressive D & C.</p>

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53
Q

What layer of the endometrium is considered the stem cell layer?

A

Basalis (lost in Asherman syndrome due to overaggressive D&C).

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54
Q

What causes Asherman syndrome?

A

Overaggressive D & C

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55
Q

<p>What is the #1 cause of acute endometritis?</p>

A

<p>Retained products of conception. Retained products in uterus promotes infection by bacterial flora from vagina or intestinal tract</p>

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56
Q

What is the treatment for acute endometritis?

A

Gentamycin + clindamycin with or without ampicillin.

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57
Q

What must be seen on biopsy in order to diagnose chronic endometritis?

A

Plasma cells

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58
Q

<p>What is a main cause of endometrial polyps?</p>

A

<p>Tamoxifen</p>

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59
Q

<p>What is endometriosis?</p>

A

<p>Non-neoplastic Endometrial glands AND stroma misplaced outside the uterine endometrial lining</p>

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60
Q

What is the most common site of involvement of endometriosis?

A

Ovary (causing chocolate cyst)

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61
Q

What is a chocolate cyst?

A

Cystic lesion of the ovary filled with menstrual products as a result of chronic endometriosis.

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62
Q

How can endometriosis cause infertility?

A

Chronic endometriosis of the Fallopian tube can cause scarring.

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63
Q

<p>What is adenomyosis?</p>

A

<p>Endometriosis (presence of glands/stroma) in the myometrium
Treat with hysterectomy</p>

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64
Q

Endometriosis in the myometrium is called..

A

Adenomyosis

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65
Q

How does andenomyosis typically present?

A

Menorrhagia, dysmenorrhea, and uterine enlargement.

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66
Q

What is endometrial hyperplasia?

A

Hyperplasia of the endometrial glands relative to stroma

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67
Q

<p>What causes endometrial hyperplasia?</p>

A

<p>excess Estrogen</p>

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68
Q

What is the most common cause of postmenopausal uterine bleeding?

A

Endometrial hyperplasia

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69
Q

What is the most important predictor for progression of endometrial hyperplasia to carcinoma?

A

Cellular atypia

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70
Q

What are the 2 pathways leading to endometrial carcinoma?

A

Hyperplasia pathway - unopposed estrogen leads to cancer with endometrioid appearance. Sporadic pathway - no hyperplasia. Cancer arises from atrophic endometrium. Caused by p53 mutations, shows serous histology with papillae and psammoma bodies.

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71
Q

Sporadic (non-hyperplastic) endometrial cancer is driven by…

A

p53 mutations (papillary serous cancer with psammoma bodies, caused by atrophy)

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72
Q

Endometrioid appearance of endometrial biopsy…

A

Endometrial cancer caused by estrogen (hyperplasia pathway).

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73
Q

Serous (papillary) appearance of endometrial biopsy with psammoma bodies…

A

Endometrial cancer caused by atrophy. Caused by p53 mutations.

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74
Q

Name 5 cancers that show psammoma bodies on histology.

A

Papillary thyroid cancer; Mesothelioma; Papillary (serous) ovarian/endometrial cancer; Meningioma

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75
Q

Multiple, well-defined white whorled uterine masses.

A

Leiomyoma (no progression to leiomyosarcoma, driven by estrogen, completely benign).

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76
Q

Do leiomyomas become leiomyosarcomas?

A

NO! Leiomyosarcomas arise de novo.

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77
Q

Describe the gross findings of a leiomyoma vs. a leiomyosarcoma.

A

Leiomyoma - MULTIPLE, well-defined, white whorled masses. Leiomyosarcoma - SINGLE lesion with necrosis and hemorrhage

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78
Q

What is a follicular cyst?

A

Distension of unruptured Graffian follicle. Multiple follicular cysts are seen in PCOS.

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79
Q

What type of cysts are seen in PCOS?

A

Follicular (unruptured Graffian follicles).

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80
Q

LH:FSH >2

A

PCOS

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81
Q

What happens to LH and FSH levels in PCOS?

A

LH:FSH >2 (LH increases, FSH decreases)

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82
Q

What is the underlying cause of PCOS?

A

Increased LH causes increased production of androgens, which is converted into estrone in adipose tissue. Estrone feeds back to decrease production of FSH. Decreased FSH leads to degeneration of the follicle, causing it to become a cyst.

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83
Q

Obese young woman presenting with infertility, oligomenorrhea, and hirsuitism.

A

PCOS

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84
Q

What estrogen is made by adipose tissue?

A

Estrone (from T by aromatase)

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85
Q

What happens to estrogen levels in PCOS?

A

They increase due to increased testosterone production (secondary to increased LH), which is aromatized in adipose to estrone. Estrone feeds back to inhibit FSH release, which causes degeneration of follicles and formation of cysts.

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86
Q

Why are obese women at higher risk for PCOS?

A

Because adipose aromatizes the excess androgens into estrone, which feeds back to inhibit FSH release, which causes degeneration of follicles and formation of cysts.

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87
Q

Patients with PCOS are at a higher risk for what metabolic disorder?

A

Type II DM

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88
Q

Patients with PCOS are at a higher risk for what gynecologic cancer?

A

Endometrial (secondary to increased estrone)

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89
Q

What are the two most common subtypes of ovarian surface epithelial tumors and how are they differentiated?

A

Serous and mucinous. Both are cystic. Serous tumors are filled with a watery fluid, mucous tumors are filled with a mucinous fluid.

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90
Q

BRCA1 mutation increases risk for what non-breast tumors (2)?

A

Serous cystadenocarcinoma of the ovary and fallopian tube

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91
Q

Genetic association with serous cystadenocarcinoma of the ovary

A

BRCA1

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92
Q

CA-125

A

Ovarian cancer tumor marker. Good for monitoring progression, but not for screening.

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93
Q

Ovarian cancer tumor marker

A

CA-125

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94
Q

Ovarian tumor containing urothelium

A

Brenner tumor

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95
Q

What is a Brenner tumor?

A

Benign tumor of ovary that looks like bladder. H&E shows “coffee bean” nuclei.

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96
Q

What are the B’s of Brenner tumor?

A

looks like Bladder, coffee Bean shape nuclei, Benign.

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97
Q

What is pseudomyxoma peritonei?

A

Intraperitoneal accumulation of mucinous material from a mucinous cystadenocarcinmoa of the ovary or an appendiceal tumor. “Full belly of jelly”

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98
Q

Patient presents with massive intraperitoneal accumulation of mucous material. What 2 things are at the top of your ddx?

A

This is pseudomyxoma peritonei. Caused by: Mucinous cystadenocarcinmoa of the ovary or an appendiceal tumor.

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99
Q

What is a cystic teratoma?

A

Cystic ovarian tumor composed of fetal tissue derived from 2 or 3 embryologic layers

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100
Q

What is the most common form of immature tissue in an immature teratoma?

A

Neuroectoderm - highly malignant

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101
Q

Teratoma containing functioning thyroid tissue

A

Struma ovarii

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102
Q

What is struma ovarii?

A

Teratoma containing functioning thyroid tissue (causes hyperthyroidism).

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103
Q

What is somatic malignancy and what is the most common one?

A

Tissue in a teratoma having cancer. #1 cause = skin squamous cell carcinoma of skin in a teratoma.

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104
Q

Dysgerminoma is a neoplasm of what cells?

A

Germ cells (eggs)

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105
Q

What is the most common malignant germ cell tumor in females?

A

Dysgerminoma

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106
Q

How is a dysgerminoma treated?

A

Radiotherapy (responds well).

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107
Q

Tumor marker for dysgerminoma

A

LDH

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108
Q

Patient with ovarian mass and increased serum LDH

A

Dysgerminoma

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109
Q

Tumor marker for yolk sac (endodermal sinus) tumor

A

AFP

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110
Q

Patient with testicular/ovarian mass and elevated serum AFP

A

Yolk sac (endodermal sinus) tumor

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111
Q

Yolk sac tumor is AKA…

A

Endodermal sinus tumor

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112
Q

What is the most common germ cell tumor in children?

A

Yolk sac tumor

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113
Q

Child with ovarian/testicular mass - biopsy shows glomerulus-like (glomeruloid) tissue. Dx?

A

Yolk sac tumor (glomerulus-like tissue = Schiller-Duval bodies).

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114
Q

What is a Schiller-Duval body?

A

Glomerulus-like structure seen in ovarian/testicular yolk sac (endodermal sinus) tumor in kids.

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115
Q

Tumor marker for choriocarcinoma

A

B-hCG

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116
Q

Ovarian tumor with large primitive cells

A

Embryonal

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117
Q

<p>Name the 5 ovarian germ cell tumors and some characteristics about each.</p>

A

<p>Dysgerminoma - most common, formed from eggs. LDH is tumor marker.

Yolk sac tumor - most common in kids. Schiller-Duval bodies (primitive glomeruli). AFP is marker.

Choriocarcinoma- tumor of trophoblastic tissue with no villi. Very aggressive, spreads hematogenously, poor response to chemo if spontaneous mutation. Responds well if it is a result of pregnancy B-HCG is marker.

Teratoma- tumor made of 2 or 3 layers of epithelium. Can contain thyroid tissue (struma ovarii). Usually benign.

Embryonal carcinoma- contains large primitive cells, aggressive with early mets.</p>

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118
Q

<p>Name the 3 ovarian surface epithelial tumors and some characteristics of each.</p>

A

<p>Mucinous cystadenocarcinoma - cystic, produces mucin. Can cause pseudomyxoma peritonei (full belly of jelly).

Serous cystadenocarcinoma - cystic, produces serous fluid. Increased risk with BRCA-1 mutations. Psammoma bodies on histo.

Brunner tumor - looks like bladder, benign, coffee-bean shaped nuclei on histo.</p>

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119
Q

Ovarian tumor with psammoma bodies.

A

Serous cystadenocarcinoma

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120
Q

Ovarian tumor presenting with signs of estrogen excess (precocious puberty, abnormal bleeding).

A

Granulosa-theca cell tumor (produces estrogen).

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121
Q

Reinke crystals

A

Leydig cell tumor

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122
Q

Ovarian tumor showing tubules and Reinke crystals

A

Sertoli (tubes) Leydig (Reinke crystals) cell tumor

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123
Q

Ovarian fibroma, pleural effusion, ascites

A

Meig’s syndrome

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124
Q

Triad seen with Meig’s syndrome

A

Ovarian fibroma; Ascites; pleural effusion

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125
Q

<p>Name 3 sex-cord stromal tumors of the ovary and some characteristics of each.</p>

A

<p>Granulosa-Theca cell tumor - secretes high estrogen. Call-Exner bodies (small follicles filled with eosinophilic secretions).

Sertoli-Leydig cell tumor - secretes androgen, contains tubules (Sertoli) and Reinke crystals (Leydig);

Fibroma - fibrous tissue. Produce Meig's syndrome: fibroma + pleural effusion + ascites</p>

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126
Q

What are Call-Exner bodies?

A

Small follicles filled with eosinophilic secretions. Seen in Granulosa-Theca cell tumors.

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127
Q

Ovarian tumor biopsy shows small follicles filled with eosinophilic secretions. Dx?

A

Granulosa-Theca cell tumor. This is a description of a Call-Exner body.

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128
Q

What is a Krukenburg tumor?

A

Metastasis of a gastric signet-ring cell (diffuse type) carcinoma to the ovaries. Produces mucous.

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129
Q

What is a signet ring cell and what gynecological tumor is it associated with?

A

A cell with its nucleus pushed off to the side due to mucous accumulation. Associated with Krukenburg tumor (metastasis of diffuse-type signet ring cell gastric CA to the ovaries).

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130
Q

What GI cancer metastasizes to ovaries?

A

Diffuse type gastric cancer (signet-ring cell) - Krukenberg tumor.

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131
Q

What is placenta previa?

A

Placenta overlying the cervical os. Presents as bright red painless bleeding.

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132
Q

Placenta overlying the cervical os.

A

Placenta previa

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133
Q

Separation of placenta from decidua prior to delivery of fetus.

A

Placental abruption. Present with dark red, painful bleeding in the 3rd trimester.

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134
Q

<p>What is placenta accreta?</p>

A

<p>Placenta implantation into the myometrium. Presents with difficult delivery of placenta and massive post-partum bleeding. (increta is into the wall of uterus, all the way through the myometrium, percreta perforates through the uterus).</p>

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135
Q

What will be seen in the vessels of the placenta in pre-eclampsia?

A

Fibrinoid necrosis

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136
Q

What is pre-eclampsia?

A

HTN + proteinuria + edema

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137
Q

What is eclampsia?

A

HTN + proteinuria + edema (pre-eclampsia) + seizures

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138
Q

How do you treat pre-eclampsia?

A

Magnesium sulfate, deliver ASAP

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139
Q

What is HELLP?

A

Hemolysis, elevated liver enzymes, low platelets. Seen in pregnancy. Schistocytes are seen on peripheral smear.

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140
Q

What causes HELLP?

A

Platelet thrombus in a small vessel in the liver causes hemolysis and production of schistocytes with elevation of liver enzymes.

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141
Q

Name 3 risk factors for SIDS.

A

Sleeping on stomach, smoking in household, prematurity.

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142
Q

Uterus larger than gestational age

A

Molar pregnancy

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143
Q

What are the “grape-like” masses in a molar pregnancy?

A

Edematous villi

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144
Q

Snow storm appearance on US

A

Molar pregnancy

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145
Q

Karyotype of a complete mole

A

46 XX or XY

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146
Q

What causes a complete mole?

A

2 sperm fertilizing an empty ovum (46 XX or XY)

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147
Q

What causes a partial mole?

A

2 sperm fertilizing an egg (69 XXY, XXX or XYY)

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148
Q

What type of mole has fetal parts?

A

PARTial mole

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149
Q

Which mole has a greater risk of choriocarcinoma?

A

Complete mole

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150
Q

69 XXY

A

Partial mole

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151
Q

What is measured to ensure complete removal of a molar pregnancy?

A

B-hCG

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152
Q

What are the 2 ways to get a choriocarcinoma and how are they differentiated?

A

Spontaneous germ cell mutation - does NOT respond to chemotherapy; Result of pregnancy (molar) - responds WELL to chemotherapy

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153
Q

Under what circumstances does a choriocarcinoma respond to chemotherapy?

A

If it arises as a result of a pregnancy. If it arises de novo, it does not respond well to chemo.

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154
Q

What causes hypospadias?

A

Failure of the urethral folds to close

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155
Q

<p>Opening of the urethra on the inferior (ventral)

| surface of the penis.</p>

A

<p>Hypospadias</p>

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156
Q

<p>Is hypospadias or epispadias more common?</p>

A

<p>Hypospadias</p>

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157
Q

<p>Opening of the urethra on the superior (dorsal) surface of the penis.</p>

A

<p>Epispadias</p>

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158
Q

What causes epispadias?

A

Abnormal positioning of the genital tubercle

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159
Q

<p>Bladder exstrophy is associated with what penile malformation?</p>

A

<p>Epispadias</p>

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160
Q

What serotypes of C. trachomatis causes LGV?

A

L1-L3

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161
Q

What causes SCC of the penis?

A

High risk HPV - 16, 18, 31, 33; Lack of circumcision

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162
Q

In situ carcinoma presenting as leukoplakia of the shaft of the penis

A

Bowen disease (can invade as SCC)

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163
Q

In situ carcinoma presenting as erythroplasia of the glans of the penis

A

Erythroplasia of Queyrat

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164
Q

In situ carcinoma presenting as red papules on the shaft of the penis

A

Bowenoid papulosis

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165
Q

Cryptorchidism increases the risk for…

A

Seminoma and infertility

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166
Q

Painful testicle with absent cremasteric reflex

A

Testicular torsion

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167
Q

What causes infarction in testicular torsion?

A

The vein is blocked but the artery keeps pumping

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168
Q

What causes hydrocele?

A

Incomplete closure of processus vaginalis (infants) or blockage of lymphatic drainage (adults)

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169
Q

What are the two general categories of testicular tumors?

A

Germ cell or sex cord stromal tumors (no surface epithelial tumors like in ovary)

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170
Q

How do you biopsy a testicular tumor?

A

NEVER biopsy a testicular tumor due to risk of seeding scrotum.

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171
Q

How is a seminoma treated?

A

Radiotherapy. Responds very well.

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172
Q

Grossly, what is the appearance of a seminoma?

A

Homogenous mass with no hemorrhage or necrosis.

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173
Q

What happens to testicular embryonal carcinoma when it is treated with chemo?

A

It can differentiate into a teratoma

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174
Q

What is the #1 testicular tumor in children?

A

Yolk sac tumor

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175
Q

In choriocarcinoma, what cells make B-HCG?

A

Syncytiotrophoblasts (mimics TSH and can cause hyperthyroidism!)

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176
Q

Patient with testicular mass and hyperthyroidism. Dx?

A

Choriocarcinoma. Excess B-HCG produced by tumor mimics TSH.

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177
Q

Describe the appearance of the villi in a choriocarcinoma.

A

Villi are ABSENT. The tumor is only cytotrophoblasts and syncytiotrophoblasts.

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178
Q

Describe the behavior of testicular teratomas vs. ovarian teratomas

A

Malignant in males, benign in females

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179
Q

Leydig cell tumors produce…

A

Androgen

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180
Q

How does a Leydig cell tumor present in adults? Kids?

A

Kids - precosious puberty; Adults - gynecomastia

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181
Q

How does a male Sertoli cell tumor usually present?

A

Usually clinically silent

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182
Q

What is the most common cause of testicular mass in males > 60?

A

Lymphoma - metastasis. Usually DLBCL.

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183
Q

What is the #1 and 2 causes of acute prostatitis in young adults?

A

C. trachomatis and N. gonorrhea

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184
Q

What is the #1 and 2 causes of acute prostatitis in older adults?

A

E. coli and pseudomonas

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185
Q

What causes BPH?

A

DHT (T converted by 5 alpha reductase)

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186
Q

Where in the prostate does BPH occur?

A

The peri-urethral (lateral and middle) zone of the prostate

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187
Q

What happens to PSA in BPH?

A

Elevates slightly (4-10, normal is 0-4).

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188
Q

Name 3 treatments for BPH.

A

Alpha 1 antagonist (terazosin) to relax smooth muscle in hypertensive pts.; Seletive alpha 1A antagonists (tamsulosin) in normotensive patients; 5-alpha reductase inhibitors (finasteride) to reduce DHT

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189
Q

What is the gross hallmark of BPH?

A

Nodularity

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190
Q

Where in the prostate does prostatic adenocarcinoma occur and what is the significance of this?

A

Posterior zone. It is therefore clinically silent, because it occurs away from the urinary zone of the prostate. It is also picked up on DRE because DRE involves palpating the posterior zone.

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191
Q

Describe the appearance of the nuclei of prostate cancer cells.

A

They contain dark nucleoli - characteristic.

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192
Q

The Gleason grading system for prostate cancer uses what parameters?

A

Architecture, not nuclear atypia

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193
Q

What type of lesions does prostate cancer produce when metastasizing to spine?

A

Osteoblastic - causes increased increased alkaline phosphatase, which is indicative of increased osteoblastic activity.

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194
Q

What is flutamide?

A

Androgen receptor blocker used in prostate cancer

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195
Q

What is leuprolide?

A

Continuous GnRH analog used in prostate cancer.

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196
Q

What is finasteride?

A

5 alpha reductase inhibitor used in BPH

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197
Q

Describe the genital lesions seen in primary, secondary, and tertiary syphilis.

A

Primary - painless chancre; Secondary - condyloma lata; tertiary - gumma

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198
Q

Describe the changes seen in the uterus with an ectopic pregnancy.

A

Deciduilization of the uterus (just like in a normal pregnancy), with no embryonic tissue or villi.

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199
Q

<p>Karyotype, SSX of Klinefelter syndrome</p>

A

<p>47 XXY. Testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair distribution, Barr body, low T. Increased FSH due to dysgenesis of seminiferous tubules and decreased inhibin. Increased LH due to abnormal Leydig cell function causing increased LH and increased Estrogen. Note that the estrogen:Testosterone ratio determines the extent feminization</p>

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200
Q

<p>Karyotype, SSX of Turner syndrome.</p>

A

<p>45 XO. Short stature, ovarian dysgenesis (streak ovary with infertility), shield chest, bicuspid aortic valve, webbed neck (defects in lymphatics - cystic hygroma), horseshoe kidney, preductal coarctation of the aorta, NO Barr body. Decreased E leads to increased LH and FSH.</p>

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201
Q

Phenotypically female newborn with testes located in the labia majora and normal female genitalia.

A

Androgen insensitivity syndrome (46 XY)

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202
Q

Newborn male presents with decreased development of the penis, prostate, and scrotum.

A

5 alpha reductase deficiency

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203
Q

What causes Kallman syndrome?

A

Defective migration of GnRH cells and formation of olfactory bulb.

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204
Q

SSX of Kallman syndrome?

A

Anosmia, lack of secondary sex characteristics, decreased GnRH, FSH, LH, testosterone, and sperm count. Due to defective migration of GnRH cells and formation of olfactory bulb

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205
Q

Male presents with inability to smell and lack of secondary sex characteristics.

A

Kallman syndrome. Defective migration of GnRH cells and formation of olfactory bulb.

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206
Q

<p>Bent penis due to acquired fibrous tissue formation.</p>

A

<p>Peryione disease</p>

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207
Q

Describe the actions of the sonic hedgehog gene

A

Produced at the base of limbs in zone of polarizing activity. Involved in patterning along anterior posterior axis. Involved in CNS development

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208
Q

What can occur with mutation in the sonic hedgehog gene?

A

holoprosencephaly

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209
Q

Describe the actions of the WNT-7 gene

A

Produced at apical ectodermal ridge (thickened ectoderm at distal end of each developing limb)
necessary for proper organization along dorsal-ventral axis (so that feet and nose point in the same direction)

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210
Q

Describe the FGF gene

A

Produced at apical ectodermal ridge. Stimulates mitosis of underlying mesoderm, providing for lengthening of limbs

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211
Q

What occurs with mutation in FGF receptor 3?

A

Achondroplasia (short limbs)

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212
Q

Describe the Homeobox (HOX) genes

A

Involved in segmental organization of embryo in a craniosacral direction.

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213
Q

What occurs with a HOX mutation?

A

Appendages in wrong places

Note that retinoic acid can alter HOX gene expression

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214
Q

When does hCG secretion begin?

A

After implantation of the blastocyst.

Causes the corpus luteum to continue to secrete progesterone to maintain the uterine lining

215
Q

When does the embryo develop into a bilaminar disc?

A

Within 2 weeks you get the 2 layered disc

composed of epiblast and hypoblast (yolk sac)

216
Q

What occurs at 3 weeks of fetal development?

A

Trilaminar disc (3 weeks = 3 layers)
Ectoderm, mesoderm and endoderm
Gastrulation occurs.
The primitive streak, notochord, mesoderm and its organization and neural plate begin to form

217
Q

When does the neural tube close by?

A

By week 4

218
Q

When is the fetus extremely susceptible to teratogens?

A

During organogenesis (weeks 3-8)

219
Q

What special thing starts in week 4 of early fetal development?

A

Heart begins to beat.

Upper and lower limb buds begin to form (4 weeks = 4 limbs and 4 chamber heart)

220
Q

What occurs in week 8 of the early fetal development?

A

Fetal movement (Eight = Gait), fetus looks like a baby

221
Q

What occurs in week 10 of early fetal development?

A

Genitalia have male/female characteristics

222
Q

What is gastrulation?

A

Process that forms the trilaminar embryonic disc. Establishes the ectoderm, mesoderm and endoderm germ layers. Starts with the epiblast invaginating to form the primitive streak

223
Q

List a bunch of things that develops from surface ectoderm

A 
Adenohypophysis (AP)
Lens of eye
Epithelial linings of oral cavity
sensory organs of ear
olfactory epithelium
epidermis 
anal canal below the pectinate line
parotid, sweat and mammary glands
224
Q

List a bunch of things that develop from the neuroectoderm

A

Brain (plus PP, CNS neurons, oligodendrocytes, astrocytes, ependymal cells, pineal gland)
retina
optic nerve
spinal cord

225
Q

List a bunch of things that develop from the neural crest

A 
PNS (dorsal root ganglia, cranial nerves, celiac ganglion, Schwann cells, ANS)
melanocytes
chromaffin cells of adrenal medulla
Parafollicular C cells of the thyroid
Schwann cells
pia and arachnoid
bones of the skull
odontoblasts
aorticopulmonary septum
cornea
226
Q

What is the neural crest derived from?

A

Ectoderm

227
Q

List a bunch of things that develop from mesoderm

A 
Muscle
bone
connective tissue
serous linings of body cavities (peritoneum)
spleen (derived from foregut mesentery)
cardiovascular structures
lymphatics
blood 
wall of gut tube
wall of bladder
upper 1/3 vagina
kidneys
adrenal cortex
dermis
testes
ovaries
Notochord induces ectoderm to form neuroectoderm (neural plate). It's only postnatal derivative is the nucleus pulposus of the intervertebral disc
228
Q

What is the mnemonic for mesodermal defects?

A 
VACTERL
Vertebral defects
Anal atresia
Cardiac defects
Tracheo-Esophageal fistula
Renal defects
Limb defects (bone and muscle)
229
Q

List a bunch of things that come from endoderm

A

Gut tube epithelium (including anal canal above the pectinate line)
luminal epithelial derivatives - lungs, liver, gallbladder, pancreas, Eustachian tube, thymus, parathyroid, thyroid follicular cells
urethra
epithelium of bladder/urethra and lower 2/3 of vagina

230
Q

What is the difference between deformation and malformation?

A

Deformation: extrinsic disruption; occurs after the embryonic period

Malformation: Intrinsic disruption; occurs during the embryonic period (wks 3-8)

231
Q

What is fetal hydantoin syndrome and what drug can cause it?

A

Caused by phenytoin

Microcephaly, dysmorphic craniofacial features, hypoplastic nails and distal phalanges, cardiac defects, IUGR, mental retardation

232
Q

What are the teratogenic effects of thalidomide and cyclophosphamide?

A

Limb defects, limb hypoplasia

233
Q

What are the teratogenic effects of warfarin?

A

Bone deformities, fetal hemorrhage, abortion, ophthalmologic abnormalities

234
Q

What are the teratogenic effects of aminoglycosides?

A

CNVIII toxicity (ototoxicity)

235
Q

What are the teratogenic effects of Carbamazepine?

A

Neural tube defects, craniofacial defects, fingernail hypoplasia, developmental delay, IUGR

236
Q

What are the teratogenic effects of lithium?

A

Ebstein’s anomaly (atrialized right ventricle)

237
Q

What are the teratogenic effects of alcohol?

A

Alcohol is the leading cause of birth defects and mental retardation, causes fetal alcohol syndrome

238
Q

What are the teratogenic effects of cocaine?

A

Abnormal fetal development and fetal addiction; placental abruption

cocaine interferes with blood flow to the fetus

239
Q

What are the teratogenic effects of smoking?

A

Preterm labor, placental problems, IUGR, ADHD

Smoking interferes with blood flow to the fetus

240
Q

What are the teratogenic effects of Maternal diabetes?

A

Caudal regression syndrome (anal atresia to sirenomelia), congenital heart defects, neural tube defects

241
Q

What are the teratogenic effects of X rays?

A

Microcephaly, mental retardation

242
Q

What is the possibility with twinning if cleavage occurred on day 4-8?

A

Monochroionic diamniotic

243
Q

What is the possibility with twinning if cleavage occurred on day 8-12?

A

Monochorionic monoamniotic

244
Q

What is the possibility with twinning if cleavage occurred on day 13 or after?

A

Monochorionic monoamniotic, conjoined twins

245
Q

How does twin-twin transfusion syndrome occur?

A

Only with monochorionicity
can be mono/mono or mono/di twins

Anastamoses leads to shunting of blood

246
Q

What are the stem cells of the fetal component of the placenta?

A

Cytotrophoblasts

247
Q

What is the outer layer of the chorionic villi called which are multinucleated?

A

Synciotrophoblasts

248
Q

What do Synciotrophoblasts do?

A

Secrete hCG which stimulates the corpus luteum to secrete progesterone during the first trimester

249
Q

What happens to the sacrum because of childbirth?

A

Bilateral sacral flexion

250
Q

What is the decidua basalis?

A

Derived from the endometrium - maternal component of the placenta.
The maternal blood is located in the lacunae

251
Q

How does the umbilical vein drain?

A

Drains via ductus venosus into the IVC

252
Q

What are the umbilical arteries and umbilical vein derived from?

A

Allantois

253
Q

What would you think if you saw a single umbilical artery?

A

Uh-oh.

a single umbilical artery is associated with congenital (esp renal) and chromosomal anomalies

254
Q

What are the two things that can occur with failure of the urachus to obliterate?

A

Patent urachus - urine discharges from umbilicus

Vesicourachal diverticulum - outpouching of the bladder

255
Q

What are the two things that can occur with failure of the vitelline duct to close?

A

Vitelline fistula - meconium discharge from the umbilicus

Meckel’s diverticulum - partial closure, with patent portion attached to ileum. May have ectopic gastric mucosa –> melena, periumbilical pain, and ulcer

256
Q

What develops from the first aortic arch?

A

Part of maxillary artery (branch of external carotid) - 1st arch is maximal

257
Q

What develops from the 2nd aortic arch?

A

Stapedial artery and hyoid artery

Second=Stapedial

258
Q

What develops from the 3rd aortic arch?

A

Common Carotid artery and proximal part of internal Carotid artery

C=3rd letter in the alphabet

259
Q

What develops from the 4th aortic arch?

A

On left: aortic arch
on right: proximal part of right subclavian artery

4th arch = 4 limbs (systemic circulation)

260
Q

What develops from the 6th aortic arch?

A

Proximal part of pulmonary arteries and (on left only) ductus arteriosus

6th arch = pulmomonary and the pulmonary-to-systemic shunt (ductus arteriosus)

261
Q

What does the left recurrent laryngeal nerve get stuck on?

A

Ligamentum arteriosum

262
Q

What is the branchial apparatus?

A

Same thing as the pharyngeal apparatus

Composed of branchial clefts, arches and pouches

CAP covers outside from inside
Clefts = ectoderm
Arches = mesoderm
Pouches = endoderm

263
Q

What are the branchial clefts?

A

Derived from ectoderm. Also called branchial grooves

264
Q

What are the branchial arches?

A

Derived from mesoderm (muscles, arteries) and neural crest (bones, cartilages)

265
Q

What are the bronchial pouches?

A

Derived from endoderm

266
Q

What is derived from the first branchial cleft?

A

external auditory meatus

267
Q

What is derived from the 2-4th branchial clefts?

A

temporary cervical sinuses, which are obliterated by proliferation of 2nd arch mesenchyme

Persistence of cervical sinus = branchial cleft cyst within lateral neck

268
Q

What is the difference between a branchial cleft cyst an a thyroglossal duct cyst?

A

Branchial cleft cyst: lateral neck, doesn’t move with swallowing

Thyroglossal duct cyst: midline neck, moves with swallowing - gets pushed around due to its association with the thyroid cartilage

269
Q

List the cartilage, muscles, and nerves that are derived from the first branchial arch

A

1st arch = M’s and T’s

Cartilage: Meckel’s cartilage: Mandible, Malleus, incus, sphenoMandibular ligament

Muscles: Muscles of Mastication (Temporalis, Masseter, lateral and Medial pterygoid), Myelohyoid, anterior belly of digastric, Tensor Tympani, Tensor veli palatini

Nerves: CN V2 and V3 - chew

270
Q

What abnormality is seen with development of the first branchial arch?

A

Treacher Collins syndrome - first arch neural crest fails to migrate leading to mandibular hypoplasia and facial abnormalities

271
Q

List the cartilage, muscles, and nerves that are derived from the second branchial arch

A

2nd arch = S’s

Cartilage: Reichert’s cartilages: Stapes, Styloid process, lesser horn of hyoid, Stylohyoid ligament

Muscles: Muscles of facial expression, Stapedisu, Stylohyoid, posterior belly of digastric

Nerves: CN Seven Smile

272
Q

List the cartilage, muscles, and nerves that are derived from the third branchial arch

A

3rd arch = pharyngeal

Cartilage: greater horn of hyoid

Muscles: stylopharyngeus (think of stylopharyngeus innervated by glossopharyngeal nerve)

Nerve: CN IX (stylopharyngeus) swallow stylishly Glossopharyngeal nerve

273
Q

What is the abnormality seen with poor development of the 3rd branchial arch?

A

Congenital pharyngocutaneous fistula - persistence of cleft and pouch leading to fistula between tonsillar area, cleft in lateral neck (branchial cleft cyst)

274
Q

List the cartilage, muscles, and nerves that are derived from the 4th - 6th branchial arch

A

4th and 6th arches = cricothyroid and larynx

Cartilage: thyroid, cricoid, arytenoids, corniculate, cuneiform

Muscles:
4th arch - most pharyngeal constrictors; cricothyroid, levator veli palatini
6th arch - all intrinsic muscles of larynx except cricothyroid

Nerves:
4th arch - CN X (superior laryngeal branch)
6th arch - CN X (recurrent laryngeal branch)

275
Q

What is derived from the 1st branchial pouch?

A

Develops into the middle ear cavity, Eustachian tube, mastoid air cells

first pouch contributes to endoderm lined structures of the ear

276
Q

What is derived from the 2nd branchial pouch?

A

Develops into epithelial lining of palatine tonsil

277
Q

What is derived from the 3rd branchial pouch?

A

Dorsal wings - develops into inferior parathyroids
ventral wings - develops into thymus

The 3rd pouch contributes to 3 structures (thymus, left and right inferior parathyroids)

Note that 3rd pouch structures end up below the 4th pouch structures

278
Q

What is derived from the 4th branchial pouch?

A

Dorsal wings - develops into superior parathyroids

279
Q

What is the problem in DiGeorge syndrome?

A

Aberrant development of the 3rd and 4th branchial pouches (no thymus and no parathyroids)

280
Q

What is the mutation in MEN2A and what does it cause?

A

Mutation of germline RET (neural crest cells)

  • Adrenal medulla (pheochromocytoma)
  • Parathyroid tumor - 3rd and 4th pharyngeal pouch
  • Parafollicular cells (medullary thyroid cancer): derived from neural crest cells; associated with the 4th/5th pharyngeal pouches
281
Q

What has failed that leads to a cleft lip?

A

Failure of fusion of the maxillary and medial nasal processes (formation of primary palate)

282
Q

What has failed that leads to a cleft palate?

A

Failuer of fusion of the lateral palatine processes, the nasal septum, and/or the median palatine process (formation of secondary palate)

283
Q

What occurs in female embryology?

A

Default development - mesonephric duct degenerates and paramesonephric duct develops

284
Q

What 3 things occur in a male to allow for male development?

A
  • SRY gene on Y chromosome produces testis-determining factor
  • Sertoli cells secrete Mullerian inhibitory factor that suppresses the development of the paramesonephric duct
  • Leydig cells secrete androgens that stimulate the development of mesonephric ducts
285
Q

What develops from the paramesonephric (mullerian) duct?

A

female internal structures:
fallopian tubes
uterus
upper portion of vagina (lower portion comes from the urogenital sinus)

286
Q

What can the presentation be in a female patient with Mullerian duct abnormalities?

A

anatomical defects that may present as primary amenorrhea in female with fully developed secondary sexual characteristics (indicator of functional ovaries)

287
Q

What develops from the mesonephric (Wolffian) duct?

A 
male internal structures EXCEPT the prostate!
Seminal vesicles
Epididymis
Ejaculatory duct
Ductus deferens
288
Q

What causes a Bocornuate uterus?

A

Incomplete fusion of the paramesonephric ducts.

Can lead to urinary tract abnormalities and miscarriages

289
Q

What would occur if a patient had no sertoli cells or lacked mullerian inhibitory factor?

A

Development of both male and female internal genitalia and male external genitalia

290
Q

What would occur with a 5 alpha reductase deficiency?

A

Male internal genitalia, ambiguous external genitalia until puberty

291
Q

Why is it important to fix hypospadias?

A

To prevent UTIs

292
Q

What is the male and female remnant of the Gubernaculum (band of fibrous tissue)?

A

Male - anchors testes within the scrotum

Female - Ovarian ligament + round ligament of the uterus

293
Q

What is the male and female remnant of the processus vaginalis (evagination of peritoneum)?

A

Male - forms tunica vaginalis

Female - Obliterated

294
Q

What is the gonadal venous drainage?

A

Left ovary/testis drains to the left gonadal vein then drains to the left renal vein which drains to the IVC

Right ovary/testis drains to the right gonadal vein which drains to the IVC

295
Q

What is the gonadal Lymphatic drainage?

A

Ovaries/testes drain to the para-aortic lymph nodes

Distal 1/3 of vagina/vulva/scrotum drains to the superficial inguinal nodes

Proximal 2/3 of vagina/uterus drains to the obturator, external iliac and hypogastric ndoes

296
Q

Which testes has higher venous pressure?

A

Left venous pressure is higher than right venous pressure
this means that varicocele is more common on the left
(Left hands lower)

297
Q

What is the suspensory ligament of the ovaries?

A

Infundibulopelvic ligament

connects the ovaries tot he pelvic wall and contains the ovarian vessels

298
Q

What is the cardinal ligament?

A

Cervix to side wall of pelvis

contains the uterine vessels

299
Q

What is the round ligament of the uterus?

A

Uterine fundus to labia majora
contains artery of Sampson
travels through the round inguinal canal

300
Q

What is the broad ligament?

A

Connects the uterus, fallopian tubes, and ovaries to pelvic side wall
contains the ovaries, fallopian tubes and round ligaments of the uterus

301
Q

What is the ligament of the ovary?

A

Connects the medial pole of ovary to lateral uterus

302
Q

What is the normal histology of the vagina and ectocervix?

A

Stratified squamous epithelium, nonkeratinized

303
Q

What is the normal histology of the endocervix?

A

Simple columnar epithelium

304
Q

What is the normal histology of the uterus?

A

Simple columnar epithelium, pseudostratified tubular glands

305
Q

What is the normal histology of the fallopian tube?

A

Simple columnar epithelium, pseudostratified tubular glands

306
Q

What is the normal histology of the fallopian tube?

A

Simple columnar epithelium, ciliated (to swoop eggs)

307
Q

What is the normal histology of the ovary?

A

Simple cuboidal epithelium

308
Q

What is the pathway of sperm during ejaculation?

A 
SEVEN UP
Seminiferous tubules
Epididymis
Vas deferens
Ejaculatory ducts
nothing
Urethra
Penis
309
Q

What is the biochemical pathway that allows for an erection?

A

Parasympathetics
NO leads to increased cGMP leading to smooth muscle relaxation and vasodilation allowing for the penis to fill with blood and have an erection

310
Q

What is the biochemical pathway that is antierectile?

A

Sympathetics
Norepinephrine increases intracellular calcium leading to smooth muscle contraction and vasoconstriction and decreased erection

311
Q

What nerves allow for erection, emission and ejaculation?

A

Erection: Parasympathetic via the pelvic nerve

Emission: Sympathetic via the hypogastric nerve

Ejaculation: visveral and somatic nerves via the pudendal nerves

312
Q

What is the function of spermatogonia?

A

These are the germ cells, they maintain the germ pool and produce primary spermatocytes
They line the seminiferous tubules

313
Q

Are sertoli germ cells?

A

NO

314
Q

What is the function of sertoli cells? (6)

A
  • Secrete inhibin which inhibits FSH
  • Secrete androgen binding protein to maintain local levels of testosterone
  • maintain tight junctions between adjacent sertoli cells to form blood testis barrier which isolates the gametes from autoimmune attack
  • Support and nourish developing spermatozoa
  • regulate spermatogenesis
  • produce anti-mullerian hormone
315
Q

Which cells in the testes are temperature sensitive?

A

Sertoli cells are temperature sensitive,

leads to decreased sperm production and decreased inhibin with increased temperature

316
Q

What are leydig cells?

A

Endocrine cells
Secrete testosterone
Note that testosterone production is not affected by temperature
located in the interstitum

317
Q

When does spermatogenesis occur in men and how long does full development of the sperm take?

A

Beings at puberty
takes 2 months

“gonium is going to be a sperm, Zoon is Zooming to the egg”

318
Q

What is spermiogenesis?

A

Loss of cytoplasmic contents and gain of acrosomal cap in order to form a mature spermatozoan

319
Q

What is the function of LH in males?

A

Stimulates synthesis of testosterone in leydig cells

320
Q

What is the function of FSH in males?

A

Stimulates sertoli cells to make androgen binding protein and inhibin
and sperm

321
Q

List the order of potency of the male androgens?

A

DHT > Testosterone > Androstenedione

322
Q

What does aromatase do to Androstenedione and testosterone in a male?

A

converts andostenedione to estrone

converts testosterone to estradiol

323
Q

List the functions of Testosterone (5)

A
  • Differentiation od epididymis, vas deferens, seminal vesicles (internal genitalia except prostate)
  • Growth spurt (penis, seminal vesicles, sperm, muscle, RBCs)
  • Deepening of the voice
  • Closing of epiphyseal plates (via estrogen converted from testosterone)
  • Libido
324
Q

List the functions of DHT

A

Early - differentiation of penis, scrotum and prostate (works on urogenital sinus)

late - prostate growth, balding, sebaceous gland activity

325
Q

What is the function of 5 alpha reductase?

A

Converts Testosterone to DHT

Note that Finasteride INHIBITS 5 alpha reductase!

326
Q

What does exogenous testosterone do to a male?

A

Exogenous testosterone inhibits the hypothalamic pituitary gonadal axis leading to decreased intratesticular testosterone which leads to decreased testicular size and azoospermia

327
Q

What are the sources and potency of the different types of estrogen?

A

Estradiol > estrone > estriol

Ovary - 17Beta estradiol
placenta - estriol
adipose tissue - estrone

328
Q

What happens to estrogen during pregnancy?

A

50-fold increased in estradiol and estrone

1000 fold increased in estriol (indicator of fetal well being)

329
Q

List the functions of estrogen (4)

A
  • development of genitalia and breast, female fat distribution
  • Growth of follicle, endometrial proliferation, increased myometrial excitability
  • Upregulation of estrogen, LH and progesterone receptors; feedback inhibition of FSH and LH then LH surge; stimulation of prolactin secretion (but blocks its action at the breast)
  • Increased transport proteins, SHBG; Increased HDL decreased LDL
330
Q

What are the sources of progesterone?

A

Corpus luteum, placenta, adrenal cortex, testes

331
Q

List the functions of Progesterone (8)

A
  • Stimulation of endometrial glandular secretions and spiral artery development
  • Maintenance of pregnancy
  • decreased myometrial excitability
  • Production of thick cervical mucus, which inhibits sperm entry into the uterus
  • Increased body temperature
  • inhibition of gonadotropins (LH, FSH)
  • Uterine smooth muscle relaxation (preventing contractions)
  • decreased estrogen receptor expressivity
332
Q

What happens with the corpus luteum?

A

Formed after ovulation; produces progesterone and estrogen in the luteal phase; lasts 14 d (luteal phase) - if beta hCG from the placeta is present, the lifespan of the CL will extend to 6-7 weeks until the placenta is able to make its own progesterone

333
Q

List the 5 tanner stages of sexual development

A
  1. Childhood
  2. Pubic hair appears (pubarche); breast bud forms (thelarche)
  3. Pubic hair darkens and becomes curly; penis size/length increases; breast enlarges
  4. Penis width increases, darker scrotal skin, development of glans, raised areolae
  5. Adult; areolae are no longer raised
334
Q

How long is the menstrual cycle?

A

Follicular phase can vary; Luteal phase is always 14 days

Ovulation + 14 days = menstruation

335
Q 
Define:
Oligomenorrhea
Polymenorrhea
Metorrhagia
Menometorrhagia
A

Oligomenorrhea: > 35 day cycle

Polymenorrhea: < 21 day cycle

Metorrhagia: Frequent but irregular menstruation

Menometrorrhagia: heavy irregular menstruation at irregular intervals

336
Q

what happens when progesterone levels fall during the menstrual cycle?

A

Falls in progesterone lead to menstruation (via apoptosis of endometrial cells)

337
Q

List the endometrial layers - which is shed during menses?

A

Layers are stratum basalis, stratum spongiosum, stratum compactum

Shed during menses: stratum spongiosum and stratum compactum

338
Q

What causes increased temperature during ovulation?

A

Progesterone

339
Q

What is Mittelschmez?

A

mid cycle pain associated with ovulation; blood from ruptured follicle or follicular enlargement causes peritoneal irritation that can mimic appendicitis

340
Q

Describe oogenesis

A
  • Primary oocytes being meiosis I during fetal life and complete meiosis I just prior to ovulation
  • Meiosis I is arrested in prOphase I for years until Ovulation (primary oocytes)
  • Meiosis II is arrested in METaphase II until fertilization (secondary oocytes) “an egg MET a sperm”

If fertilization does no occur within 1 day, the secondary oocyte degenerates

341
Q

What allows for lactation after giving birth?

A

After labor, the decreased in progesterone disinhibits lactation. Suckling is required to maintain milk production, since increased nerve stimulation increases oxytocin and prolactin

342
Q

What is the function of prolactin?

A

Induces and maintains lactation and decreases reproductive function

343
Q

What is the function of oxytocin?

A

Appears to help with milk letdown and may be involved with uterine contractions

344
Q

What needs to be supplemented with breast milk?

A

Vitamin D

345
Q

Why are LH levels low during pregnancy?

A

LH levels are low during pregnancy due to progesterone feedback inhibition on the anterior pituitary

346
Q

What is the function of hCG?

A

Maintains the corpus luteum and therefore progesterone, for the first trimester by acting like LH - otherwise there’s no luteal cell stimulation and abortion results

347
Q

What does this mean: Menopause causes HHAVOC

A 
Hirsutism
Hot flashes
Atrophy of the Vagina
Osteoporosis
Coronary artery disease
348
Q

What is menopause

A

Decreased estrogen production due to age-linked decline in the number of ovarian follicles. Average age at onset is 51 years (earlier in smokers)

1 year without menses

349
Q

What is the best test to confirm menopause?

A

INCREASED FSH is the best test to confirm menopause (loss of negative feedback for FSH due to decreased estrogen)

350
Q

What are the lab hormonal changes seen in menopause?

A

Decreased estrogen, wayy Increased FSH, increased LH (no surge), increased GnRH

351
Q

What is Gravidity? Parity?

A

Gravidity - # of pregnancies
Parity - # of deliveries over 20 weeks (including stillbirths)
A = abortions; # of deliveries before 20 weeks (medical/spontaneous)

352
Q

What is seen on triple screen with trisomy 21?

A

Decreased AFP and estriol, increased hCG

353
Q

What is seen on triple screen with trisomy 18?

A

Decreased AFP, Estriol and hCG

354
Q

What is double Y males?

A

XYY; phenotypically normal, very tall, severe acne, antisocial behavior
Normal fertility. small percentage diagnosed with autism spectrum disorders

355
Q

What is the diagnosis: Increased Testosterone and increased LH

A

Defective androgen receptor

356
Q

What is the diagnosis: Increased testosterone and decreased LH

A

Testosterone secreting tumor, exogenous steroids

357
Q

What is the diagnosis: Decreased testosterone and increased LH

A

Primary hypogonadism

358
Q

What is the diagnosis: Decreased Testosterone and decreased LH

A

Hypogonadotropic hypogonadism (kallmann syndrome)

359
Q

What is pseudohermarphroditism?

A

Disagreement between the phenotypic (external genitalia) and gonadal (ovaries vs testes) sex

360
Q

Describe Female psudohermaphrodite (XX)

A

Ovaries are present but external genitalia are virilized or ambiguous. Due to excessive and inappropriate exposure to androgenic steroids during early gestation (e.g. congenital adrenal hyperplasia or exogenous administration of androgens during pregnancy)

361
Q

Describe Male pseudohermaphrodite (XY)

A

Testes present, but external genitalia are female or ambiguous. Most common form is androgen insensitivity syndrome (testicular feminization)

362
Q

Describe True hermaphroditism (46XX or 47XXY)

A

Both ovary and testicular tissue present (ovotestis); ambiguous genitalia. very rare

363
Q

What is androgen insensitivity syndrome (46, XY)?

A

Defect in androgen receptor resulting in normal appearing female; female external genitalia with rudimentary vagina; uterus and fallopian tubes generally absent; presents with scant sexual hair; develops testes (often found in labia majora; surgically removed to prevent malignancy)
increased testosterone, estrogen, LH (vs sex chromosome disorders)

364
Q

Describe 5 alpha reductase deficiency?

A

AR, sex limited to genetic males.
Inability to convert T to DHT
Ambiguous genitalia until puberty, when increased testosterone causes masculinization/increased growth of external genitalia.
Testosterone/estrogen levels are normal; LH is normal or increased.
Internal genitalia are normal

365
Q

Describe Kallmann syndrome

A

Defective migration of GnRH cells and formation of olfactory bulb; decreased synthesis of GnRH in the hypothalamus; anosmia; lack of secondary sexual characteristics
Decreased GnRH, FSH, LH, testosterone and sperm count

366
Q

How do you treat Kallmann syndrome?

A

Hormone replacement
testosterone in M and estrogen-progesterone in F

If patient desires fertility you can give them hCG and FSH to be used to stimulate production of gonadal steroid hormone

367
Q

What is seen with a hydatidiform mole?

A

Cystic swelling of hydropic/chorionic villi and proliferation of chorionic epithelium (trophoblast) that presents with abnormal vaginal bleeding

368
Q

What is the most common precursor of choriocarcinoma?

A

Hydatidiform mole (esp complete mole)

369
Q

Honeycombed uterus or cluster of grapes appearance, abnormally enlarged uterus.

A

Hydatidiform mole

370
Q

Complete moles classically have…

A

Snowstorm appearance with no fetus during 1st sonogram - “central heterogenous mass with numerous discrete anechoic spaces” = snowstorm

371
Q

What does preeclampsia before 20 weeks gestation suggest?

A

molar pregnancy

372
Q

When does preeclampsia normally occur?

A

20 weeks gestation to 6 weeks postpartum

373
Q

What causes preeclampsia?

A

Placental ischemia due to impaired vasodilation of spiral arteries, resulting in increased vascular tone

374
Q

What can preeclampsia be associated with?

A

HELLP syndrome

375
Q

What is HELLP syndrome?

A

Hemolysis, elevated liver enzymes, Low platelets

376
Q

What causes morality from preeclampsia?

A

cerebral hemorrhage and ARDS

377
Q

What are the clinical features of a patient with preeclampsia?

A

headache, blurred vision, abdominal pain, edema of face and extremities, altered mentation, hyperreflexia, lab findings may include thrombocytopenia and hyperuricemia

378
Q

What is the treatment for a patient with preeclampsia?

A

Delivery of fetus as soon as viable.
Otherwise bed rest, monitoring and treatment of hypertension

Treatment: IV magnesium sulfate to prevent and treat seizures of eclampsia
Methyldopa for hypertension

379
Q

What can increase the risk of abruption placentae?

A

Increased risk with smoking, hypertension and cocaine use

380
Q

What is the immediate cause of Abruptio placentae?

A

Rupture of maternal vessels in the decidua basalis leading to premature detachment of the placenta from the implantation site

381
Q

What is the Kleihauer Betke test?

A

Look for fetal red blood cells in moms blood

382
Q

List 3 things that can increase the risk of placenta accreta?

A

Prior C-section, inflammation, placenta previa

383
Q

What should you start to think if a patient fails to deliver the placenta within 30 minutes of birth?

A

Placenta accreta

384
Q

What is the pelvic diameter that must be adequate to ensure a safe delivery?

A

Obstetric conjugate

This is the shortest diameter through which the detal head must pass

385
Q

List 2 things that can increase the risk for placenta previa?

A

Multiparity and prior C section

386
Q

How does placenta previa present?

A

Painless bleeding in any trimester

Note that there will be no signs of fetal distress

387
Q

What is the concern with retained placental tissue after delivery?

A

May cause postpartum hemorrhage. Increased risk of infection

388
Q

What is seen with ectopic pregnancy?

A

Pain with or without bleeding - often mimics appendicitis.

Endometrial biopsy shows decidualized endometrium but no chorionic villi (develop only in intra-uterine pregnancy)

389
Q

What are the risk factors for ectopic pregnancy? (4)

A

History of infertility
Salpingitis (PID)
Ruptured appendix
Prior tubal surgery

390
Q

What is considered Polyhydraminos? Oligohydraminos?

A

Polyhydraminos: >1.5-2L
Oligohydraminos: <0.5 L

391
Q

List 4 conditions that are associated with increased fetal urination and therefore polyhydraminos?

A

High cardiac output due to anemia or twin-twin transfusion syndrome
esophageal/duodenal atresia
anencephaly

392
Q

List 3 conditions that are associated with oligohydraminos

A

placental insufficiency
bilateral renal agenesis
posterior urethral valves (in males)

393
Q

Where does cervical dysplasia being?

A

Begins at basal layer of squamo-columnar junction and extends outward

394
Q

What are the 4 risk factors for cervical dysplasia and carcinoma in situ?

A

due to HPV infection

  1. multiple sexual partners is #1
  2. smoking
  3. early sexual intercourse
  4. HIV infection
395
Q

What is invasive carcinoma manifest as?

A

often as squamous cell carcinoma

396
Q

How does endometriosis clinically manifest?

A

Severe menstrual related pain, painful intercourse and infertility, menorrhagia, dysmenorrhea, dyspareunia, infertility.
Note that the uterus is NORMAL sized

397
Q

How does Adenomyosis present?

A

Menorrhagia, dysmenorrhea, pelvic pain

Note that the uterus is ENLARGED

398
Q

What is the treatment for endometriosis?

A

Oral contraceptives, NSAIDs, leuprolide (like a chemical menopause), danazol

399
Q

What can endometrial hyperplasia progress into?

A

Endometrial carcinoma

400
Q

How does endometrial hyperplasia manifest clinically?

A

postmenopausal vaginal bleeding

401
Q

What are the risk factors for endometrial hyperplasia?

A 
XS estrogen....
anovulatory cycles
hormone replacement therapy
polycystic ovarian syndrome
granulosa cell turnover
402
Q

What is the most common gynecological malignancy?

A

Endometrial carcinoma

typically occurs at 55-65 yo

403
Q

What are the risk factors for endometrial carcinoma?

A 
HHONDA
Hyperplasia (endometrial)
HTN
Obesity
Nulliparity
Diabetes
Anovulatory state

note that Tamoxifen is also a risk factor!

404
Q

What are the two myometrial tumors?

A

Leiomyoma (fibroid)

Leiomyosarcoma

405
Q

What is the most common of all tumors in females?

A

Leiomyoma (20-40 yo)

406
Q

Are Leiomyomas sensitive to estrogen?

A

Yes - they increased in size with pregnancy and decreased in size with menopause

407
Q

Ultrasound shows concentric, solid, hypoechoic mass with acoustic shadowing consistent with hypertrophy of myometrial tissue

A

Leiomyoma

408
Q

What is a Leiomyosarcoma?

A

Bulky, irregular shaped tumor with areas of necrosis and hemorrhage
Highly aggressive tumor with tendency to recur
- desmin +, contains spindle cells with mitotic figures

409
Q

What is the incidence of Gynecological tumors in the US? worldwide?

A

US: endometrial> ovarian> cervical
worldwide: cervical is most common

410
Q

What is the worst prognosis of gynecological tumors?

A

Ovarian >cervical>endometrial

411
Q

What is premature ovarian failure and what are the commonly found lab findings?

A

Premature atresia of ovarian follicles in women of reproductive age. Patients present with signs of menopause after puberty but before age 40.

Labs: decreased estrogen, increased LH and FSH

412
Q

Describe Polycystic ovarian syndrome?

A

Increased LH production leads to anovulation and therefore no progesterone, hyperandrogenism due to deranged steroid synthesis by theca cells

413
Q

A patient presents with amenorrhea, infertility, obesity and hirsutism - what is the most likely cause?

A

Polycystic ovarian syndrome

414
Q

what are patients with PCOS at increased risk for?

A

Endometrial cancer, secondary to increased in estrogens from the aromatization of testosterone in fat cells without progesterone to oppose

415
Q

List 5 possible treatments for PCOS?

A
  1. weight reduction
  2. low dose OCPs or medroxyprogesterone (decreases LH and androgenesis)
  3. comiphene (for women who want to get pregnant)
  4. metformin (for patients with features of diabetes or metabolic syndrome)
  5. spironolactone (treats acne and hirsutism)
416
Q

PCOS patients can be insulin resistant - what is the problem with this?

A

Increaesd insulin levels and insulin stimulates androgen production in theca cells (theca cells make androstenedione) which is turned into estrogen by granulosa cells
estrogen will then feedback to further decrease FSH levels

417
Q

What are the lab values in PCOS?

A

Increased LH, decreased FSH, increased testosterone, increased estrogen (from testosterone aromatization)

418
Q

What is the most common ovarian mass in young women and what may it be associated with?

A

Follicular cyst.

May be associated with hyperestrinism and endometrial hyperplasia

419
Q

What is a corpus luteum cyst?

A

Hemorrhage into persistent corpus luteum. Commonly regresses spontaneously

420
Q

What is a theca-lutein ovaria cyst?

A

Often bilateral/multiple. Due to gonadotropin stimulation (from increased hCG). associated with crhoiocarcinoma and moles
Caused by luteinization and hypertrophy of theca interna layer of ovary

421
Q

What is a hemorrhagic ovarian cyst?

A

Blood vessel rupture in cyst wall. Cyst grows with increased blood retention. usually self-ersolves

422
Q

What is a dermoid ovarian cyst?

A

Mature teratoma. Cystic growths filled with various types of tissue such as fat, hair, teeth, bits of bone and cartilage

423
Q

What is an endometrioid ovarian cyst?

A

Endometriosis within ovary with cyst formation. Varies with menstrual cycle. When filled with dark, reddish brown blood it’s called a chocolate cyst

424
Q

Describe the difference between hirsutism and virilization?

A

Hirsutism: male pattern hair growth, acne, muscle mass, seen in PCOS!

Virilization: male pattern balding, deepening of the voice, clitoromegaly, seen with exogenous testosterone or androgens or androgen tumors!

425
Q

What is the female equivalent to a seminoma?

A

Dysgerminoma

426
Q

Ovarian germ cell tumor with sheets of uniform cells associated with Turner syndrome

A

Dysgerminoma

427
Q

Malignancy of trophoblastic tissue and chorionic villi are not present

A

Choriocarcinoma

428
Q

Rare but malignant ovarian germ cell tumor that can develop during or after pregnancy in mother or baby but it will contain only maternal DNA

A

Choriocarcinoma

429
Q

A patient has a choriocarcinoma ovarian germ cell tumor, what so they have increased frequency of?

A

Theca-lutein cysts

430
Q

Where can choriocarcinoma metastasize to?

A

Early hematogenous spread to lungs

431
Q

Yellow, friable, solid mass that may or may not have Schiller-Duval bodies (resembles glomeruli)

A

Yolk sac (endodermal) tumor

432
Q

Who can get yolk sac tumors?

A

Ovaries, testes, and sacrococcygeal area of young children

433
Q

What is the tumor marker for yolk sac (endodermal) tumors?

A

AFP

434
Q

What is the most common of ovarian germ cell tumors?

A

Teratoma

435
Q

Describe the difference between Mature teratoma and Immature teratoma in a ovarian germ cell tumor?

A

Mature teratoma: dermoid cyst; most common ovarian germ cell tumor, mostly benign

Immature teratoma - aggressively malignant

436
Q

What is a struma ovarii?

A

Teratoma that contains functional thyroid tissue. Can present as hyperthyroidism

437
Q

What is a serous cystadenoma ovarian non germ cell tumor?

A

Frequently bilateral, lined with fallopian tube-like epithelium. Benign

438
Q

What is a Serous cystadenocarcinoma ovarian non germ cell tumor?

A

malignant and frequently bilateral. Psammoma bodies seen on histology

439
Q

What is a mucinous cystadenoma ovarian non germ cell tumor?

A

Multilocular cyst lined by mucus secreting epithelium. Benign. Intestine-like tissue

440
Q

What is a mucinous cystadenocarcinoma ovarian non germ cell tumor?

A

Malignant.

Pseudomyxoma peritonei - intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor

441
Q

What is a Brenner tumor ovarian non germ cell tumor?

A

Benign and unilateral.
Looks like bladder.
Solid tumor that is pale yellow-tan in color and appears encapsulated
“Coffee bean” nuclei on H+E

442
Q

What is a Fibroma ovarian non germ cell tumor?

A

Bundles of spindle shaped fibroblasts
Presents with Meigs’ syndrome: ovarian fibroma, ascities, hydrothorax

Sometimes patients will have a pulling sensation in the groin

443
Q

What is a Granulosa cell tumor ovarian non germ cell tumor?

A

Secretes estrogen leading to precocious puberty in kids
Can cause endometrial hyperplasia or carcinoma in adults.
Call-Exner bodies - small follicles filled with eosinophilic secretions
May presents with abnormal uterine bleeding

444
Q

What is a Krukenberg tumor ovarian non germ cell tumor?

A

GI malignancy that metastasizes to ovaries causing a mucin-secreting signet cell adenocarcinoma

445
Q

Describe 3 vaginal tumors

A

Squamous cell carcinoma - usually secondary to cervical squamous cell carcinoma, Primary vginal carcinoma is rare

Clear cell adenocarcinoma -affects women who had exposure to DES in utero

Sarcoma botryoides - rhabdomyosarcoma variant; affects girls <4yo; spindle shaped tumor cells that are desmin positive

446
Q

Describe the 3 benign breast tumors

A

Fibroadenoma: small, mobile firm mass with sharp edges. Most common tumor in W projections. Most common in 60 yo, some may become malignant

447
Q

Where do malignant breast tumors commonly arise from?

A

Terminal duct lobular unit

448
Q

What is the single most important prognostic factor for malignant breast cancer?

A

involvement of the axillary lymph node

449
Q

Describe comedocarcinoma subtype of ductal carcinoma in situ

A

Malignant but noninvasive.

Ductal, caseous necrosis

450
Q

What is the most common breast cancer, and is the worst and most invasive?

A

Invasive ductal carcinoma

451
Q

Describe invasive ductal carcinoma

A

Firm, fibrous “rock hard” mass with sharp margins and small, glandular, duct-like cells. Classic stellate morphology

452
Q

Describe Invasive lobular breast cancer

A

Orderly row of cells (indian file) often bilateral with multiple lesions in the same location.
Due to inactivation of E-cadherin genes

453
Q

Describe medullary invasive breast cancer

A

Fleshy, cellular, lymphocytic infiltrate. Good prognosis

454
Q

Describe inflammatory invasive breast cancer

A

Dermal lymphatic invasion by breast carcinoma
Peau d’orange appearance
Neoplastic cells block lymphatic drainage

455
Q

Describe Paget’s disease invasive breast cancer

A

Eczematous patches on nipple . Paget cells = large cells in epidermis with clear halo.
Suggests underlying DCIS

456
Q

What is the pathologic hallmark of Paget’s disease?

A

Presence of malignant, intraepithelial adenocarcinoma cells (paget cells) within the epidermis of the nipple

457
Q

What is fibrocystic disease of the breast?

A

Most common cause of “breast lumps” from age 25-menopause. Presents with premenstrual breast pain and multiple lesions, often bilateral. Fluctuating in size of mass. Usually does not indicate increased risk of carcinoma.

458
Q

List the 4 histologic types of fibrocystic disease in the breast

A

Fibrosis - hyperplasia of breast stroma

cystic - fluid filled, blue dome. Ductal dilation

sclerosing adenosis - Increased acini and intralobular fibrosis. Associated with calcifications. Often confused with breast cancer

Epithelial hyperplasia - Increase in number of epithelial cell layers in terminal duct lobule. Increased risk of carcinoma with atypical cells. Occurs in W >30yo

459
Q

What is gynecomastia?

A

Occurs in males, results from hyperestrogenism (cirrhosis, testicular tumor, puberty, old age), Klinefelters syndrome, or drugs

460
Q

List Drugs that can cause gynecomastia?

A

Some Drugs Cause Awesome Knockers

Spironolactone
Digitalis
Cimetidine
Alcohol
Ketoconazole

Others - estrogen, marijuana, heroin, psychoactive drugs

461
Q

How should you treat prostatitis?

A

Fluoroquinoline like a UTI

or levofloxacin, TMP-SMX, Ciprofloxacin, doxycycline

462
Q

What is BPH?

A

Hyperplasia of the prostate gland characterized by a nodular enlargement of the periurethral (lateral and middle) lobes which compress the urethra into a vertical slit

463
Q

What can BPH cause?

A

distension and hypertrophy of the bladder
hydronephrosis
UTIs
increased free PSA

464
Q

List the 3 treatments you can use for BPH

A

Terazosin - alpha 1 antagonist

Tamsulosin - alpha 1A,D antagonist - no antihypertensive effects (note that alpha IB is found on blood vessels)

Finasteride - 5 alpha reductase inhibitor which slowly reduces DHT levels which will decreased the prostate volume

465
Q

How is prostatic adenocarcinoma diagnosed?

A

Increased PSA and subsequent needle core biopsies.
Prostatic acid phosphatase (PAP) and PSA are useful tumor markers (Increased total PSA with decreased fraction of free PSA)

466
Q

What can be seen in prostatic adenocarcinoma?

A

Osteoblastic metastases in bone may develop in late stages as indicated by lower back pain and an increased in serum alkaline phosphatase and PSA

467
Q

How can you treat prostatic adenocarcinoma?

A

Flutamide - blocks testosterone at receptor level

resection

468
Q

Can you have normal testosterone levels with cryptorchidism?

A

Yes, leydig cells are not affected by increased temperature. But T levels may be decreased in bilateral cryptorchidism but normal in unilateral
Will have decreased sperm because sertoli cells are effected by temperature
Also at risk of germ cell tumors

469
Q

What is the treatment for cryptorchidism?

A

Prepubertal - orchiplexy (bring down and sew it into the scrotum)

Post-pubertal - may be orchiectomy (removal)

470
Q

What is varicocele?

A

Dilated veins in pampiniform plexus as a result of increased venous pressure
(usually on the Left side)
bag of worms appearance, DX with US

471
Q

How do you treat varicocele?

A

Varicocelectomy, embolization by interventional radiologist

472
Q

Are testicular germ cell tumors usually benign or malignant?

A

Malignant most often

473
Q

Name the testicular germ cell tumor: Malignant, painless, homogenous testicular enlargement; most common testicular tumor mostly affecting males 15-35 yo

A

Seminoma

474
Q

Name the testicular germ cell tumor: Large cells in lobules with watery cytoplasm and a “fried egg” appearance. Increased placental alkaline phosphatase (PLA). Is radiosensitive, late metastasis and has an excellent prognosis

A

Seminoma

475
Q

Name the testicular germ cell tumor: Yellow, mucinous. Schiller-Duval bodies resemble primitive glomeruli. Will have increased AFP and can have a honeycomb appearance

A

Yolk sac (endodermal) tumor

476
Q

Name the testicular germ cell tumor: Malignant, Increased hCG. Disordered synciotrophoblastic and cytotrophoblastic elements. Hematogenous metastasis to lung.

A

Choriocarcinoma

477
Q

Name the testicular germ cell tumor: May produce gynecomastia as hCG is an LH analog. Or impotence, decreased libido or precocious puberty

A

Choriocarcinoma

478
Q

Name the testicular germ cell tumor: Malignant, painful, worse prognosis than seminoma

A

Embryonal carcinoma

479
Q

Name the testicular germ cell tumor: Often glandular/papillary morphology. most commonly mixed with other tumor types. May be associated with increased hCG and normal AFP levels when pure and increased AFP when mixed

A

Embryonal carcinoma

480
Q

Describe a teratoma in males

A

Unlike in females, mature teratoma in adult males if more often malignant. Benign in children.
Can have increased hCG and/or AFP in 50% of cases

481
Q

List the testicular non-germ cell tumors

A

Leydig cell tumor
Sertoli cell tumor
Testicular lymphoma

482
Q

Name the testicular non-germ cell tumor: Contains Reinke crystals

A

Leydig cell tumor

483
Q

Name the testicular non-germ cell tumor: usually androgen producing, gynecomastia in men, precocious puberty in boys. Golden brown color

A

Leydig cell tumor

484
Q

Name the testicular non-germ cell tumor: Androblastoma from sex cord stroma.

A

Sertoli cell tumor

485
Q

Name the testicular non-germ cell tumor: Most common testicular cancer in older men

A

Testicular lymphoma

486
Q

Name the testicular non-germ cell tumor: Not a primary cancer, arises from lymphoma metastases to testes. Aggressive. will present with fever, night sweats and weight loss

A

Testicular lymphoma

487
Q

What is a spermatocele?

A

Tunica vaginalis lesion due to a dilated epididymal duct

488
Q

Describe squamous cell carcinoma of the penis

A

More common in Asia, Africa, and south America

Commonly associated with HPV and lack of circumcision

489
Q

Describe Peyroni’s disease

A

Bent penis due to acquired fibrous tissue formation will have pain with erection
inflammation and fibrous tissue of tunica albuginea

490
Q

Describe priapism

A

Painful sustained erection not associated with sexual stimulation or desire.
Associated with trauma, sickle cell disease, medications (anticoagulants, PDE5 inhibitors, antidepressants, alpha blockers and cocaine)

can lead to ischemia and clotting of blood in the penis

491
Q

What can cause and how do you treat Epididymis?

A

35 yo: e.coli, pseudomonas, proteus, Klebsiella, TX with fluoroquinolone

492
Q

What is the MOA of leuprolide?

A

GnRH analog with agonist properties when used in pulsatile fashion; antagonist properties when used in continuous fashion (downregulates GnRH receptor in pituitary leading to decreased FSH/LH)

493
Q

What is the clinical use of leuprolide?

A 
Infertility (pulsatile), 
prostate cancer (continuous - use with flutamide), 
uterine fibroids (continuous), 
precocious puberty (continuous)
494
Q

What is the toxicity seen with leuprolide?

A

Antiandrogen, nausea, vomiting

495
Q

What is the MOA of testosterone and methyltestosterone?

A

Agonist at androgen receptors

496
Q

What is the clinical use of testosterone and methyltestosterone?

A

Treats hypogonadism and promotes development of secondary sex characteristics;
stimulation of anabolism to promote recovery after burn or injury

497
Q

What is the toxicity seen with testosterone and methyltestosterone?

A

Causes masculinization in females
reduces intratesticular testosterone in males by inhibiting release of LH (via NF) leading to gonadal atrophy
premature closure of epiphyseal plates
Increased LDL and decreased HDL

498
Q

List 4 anti androgens

A

Finasteride, Flutamide, Ketoconazole, Spironolactone

499
Q

What is the MOA of Finasteride?

A

A 5 alpha reductase inhibitor that decrases conversion of T to DHT.
Useful in BPH.
Also promotes hair growth used to treat male pattern baldness

“to prevent male-pattern hair loss, give a drug that will encourage female breast growth”

500
Q

What is the MOA of flutamide?

A

Nonsteroidal competitive inhibitor of androgens at the testosterone receptor.
Used in prostate carcinoma

501
Q

What is the MOA of ketoconazole?

A

Inhibits steroid synthesis (inhibits 17,20 desmolase)
used to treat PCOS
side effects include gynecomastia and amennorhea

502
Q

What is the MOA of Spironolactone?

A

Inhibits steroid binding
used to treat PCOS
side effects include gynecomastia and amennorhea

503
Q

Name 3 estrogen drugs

A

Ethinyl estradiol, DES, mestranol

504
Q

What is the MOA of estrogens?

A

Bind estrogen receptors

505
Q

What is the clinical use of estrogen drugs?

A

Hypogonadism or ovarian failure,
menstrual abnormalities,
HRT in postmenopausal women;
use in men with androgen-dependent prostate cancer

506
Q

What is the toxicity seen with estrogen use?

A

Increased risk of endometrial cancer
bleeding in postmenopausal women
clear cell adenocarcinoma of vagina in females exposed to DES in utero
increased risk of thrombi
Contraindications are ER positive breast cancer and a history of DVTs

507
Q

How are estrogens protective against osteoporosis?

A

Decreased osteoclast activity

508
Q

Name 3 Selective estrogen receptor modulators

A

Clomiphene, Tamoxifen, Raloxifene

509
Q

What is the MOA of clomiphene?

A

Partial agonist at estrogen receptors in hypothalamus. Prevents normal feedback inhibition and increases release of LH and FSH from anterior pituitary which stimulates ovulation

510
Q

What is the clinical use of clomiphene?

A

Used to treat infertility and PCOS

511
Q

What are the side effects that can be seen with clomiphene use?

A

Hot flashes, ovarian enlargement, multiple simultaneous pregnancies, visual disturbances

512
Q

What is the MOA of Tamoxifen?

A

Antagonist on breast tissue; used to treat and prevent recurrence of ER positive breast cancer

513
Q

What is the problem with Tamoxifen?

A

Has an agonist effect in the endometrium which can increase the risk of endometrial cancer

514
Q

What is the MOA of Raloxifene?

A

Agonist on bone; reduces resoprtion of bone; used to treat osteoporosis

Antagonist in breast and has no effect in the endometrium

515
Q

What is Anastrozole, exemestane, and letrozole?

A

Aromatase inhibitors used in postmenopausal women with breast cancer.
Inhibits estrogen production but can increase risk of osteoporosis and fractures

516
Q

What is the MOA of progestins?

A

Bind progesterone receptors, reduce growth and increased vascularization of endometrium
Ovulation suppression, stabilization of endometrium

517
Q

What is the clinical use of progestins?

A

Used in oral contraceptives and in the treatment of endometrial cancer and abnormal uterine bleeding

518
Q

What is the MOA of Mifepristone (RU-486)?

A

Competitive inhibitor of progestins at progesterone receptors

519
Q

what is the clinical use of Mifepristone (RU-486)?

A

Termination of pregnancy, administered with misoprostol (PGE1)

520
Q

What is the toxicity seen with Mifepristone (RU-486)?

A

Heavy bleeding, GI effects (nausea, vomiting, anorexia), abdominal pain

521
Q

How do oral contraceptives work?

A

Estrogen and progestins inhibit LH/FSH and thus prevent estrogen surge. No estrogen surge leads to no LH surge which leads to no ovulation

Progestins cause thickening of the cervical mucus, thereby limiting access of sperm to uterus. Progestins also inhibit endometrial proliferation, thus making endometrium less suitable for the implantation of an embryo

522
Q

Why do you have decreased acne with oral contraceptive use?

A

Decreased acne due to increased SHBG made in the liver which binds up the free testosterone

523
Q

What are the contraindications for oral contraceptive use?

A

smokers >35 yo due to increased risk of cardiovascular events

Patients with history of thromboembolism and stroke or history of estrogen dependent tumor

524
Q

What is terbutaline?

A

Beta 2 agonist that relaxes the uterus; reduces premature uterine contraction

525
Q

What is tamsulosin

A

Alpha 1 antagonist used to treat BPH by inhibiting smooth muscle contraction.
Selective for alpha1A,D receptors found on the prostate instead of alpha 1B receptors on the vvasculature

526
Q

What is the MOA of sildenafil and vardenafil?

A

Inhibit phosphodiesterase 5 causing increased cGMP

which leads to smooth muscle relaxation in the corpus cavernosum, increased blood flow and penile erection

527
Q

What is the clinical use of sildenafil and vardenafil?

A

erectile dysfunction

528
Q

What is the toxicity associated with sildenafil and vardenafil?

A

Headache, flushing, dyspepsia, impaired blue-green color vision.
Risk of life-threatening hypotension in patients taking nitrates

blue tint to vision field is due to sildenafil also inhibiting PDE6 which normally transforms light into electrical signals

529
Q

What is the MOA of Danazol?

A

Synthetic androgen that acts as partial agonist at androgen receptors. (counteracts estrogen)

530
Q

What is the clinical use of danazol?

A

endometriosis and hereditary angioedema

531
Q

What is the toxicity of danazol?

A

weight gain, edema, acne, hirsutism, masculinization, decreased HDL levels and hepatotoxicity

532
Q

What do tocolytics do?

A

stop contractions

Indomethacin, nifedipine, terbutaline, ridadrine

533
Q

Name some drugs that can be used to induce labor

A

Dinoprostone (PGE2 analog)
Misprostol (PGE1 analog)
Oxytocin

534
Q

A 28-year-old-male presents with acute onset of pain in his scrotum while playing baseball. Physical examination reveals an absent rise of his scrotum in response to light stroking of his proximal inner thigh. The most likely affected structure is the?

A

Spermatic cord.

This is a testicular torsion

first aid chs part 2 (6 decks)

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