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REPRODUCTIVE > REPRODUCTIVE- Pathology > Flashcards

REPRODUCTIVE- Pathology Flashcards

1
Q

What is the problem in Klinefelter syndrome?

A

XXY

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2
Q

Klinefelter syndrome is a male or female disease?

A

Male

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3
Q

Incidence of Klinefelter syndrome

A

1:850

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4
Q

Findings of Klinefelter syndrome

A

Testicular atrophy, eunuchoid body shape, tall, long extremities, gynecomastia, female hair distribution

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5
Q

How is the developmental function of Klinefelter syndrome?

A

May present with developmental delay

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6
Q

What is affected in Klinefelter syndrome?

A

Presence of inactivated X chromosome (Barr body)

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7
Q

What is Barr body?

A

Presence of inactivated X chromosome

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8
Q

Common cause of hypogonadism seen in infertility work up

A

Klinefelter syndrome

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9
Q

How is FSH affected in Klinefelter syndrome?

A

Dysgenesis of seminiferous tubules → ↓ inhibin → ↑ FSH

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10
Q

How is estrogen affected in Klinefelter syndrome?

A

Abnormal Leydig cell function → ↓ testosterone → ↑ LH → ↑ Estrogen

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11
Q

What is the main problem in Turner syndrome?

A

XO

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12
Q

Most common karyotype of Klinefelter disease

A

47 XXY (75%)

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13
Q

Turner syndrome is a male or female disease?

A

Female

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14
Q

Findings of Turner syndrome

A

Short stature (if untreated), ovarian dysgenesis (streak ovary), shield chest, bicuspid aortic valve, preductal coarctation (femoral

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15
Q

Most common cause of primary amenorrhea

A

Turner syndrome

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16
Q

How are Barr bodies in Turner syndrome?

A

No Barr bodies

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17
Q

How is the menarche in Turner syndrome?

A

Menopause before menarche

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18
Q

How are the hormones affected in Turner syndrome?

A

↓ estrogen leads to ↑ LH, FSH

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19
Q

Turner syndrome is the result of…

A

From mitotic or meiotic error

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20
Q

Which is the complete monosomy of Turner syndrome?

A

45 X0

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21
Q

Mosaicism of Turner syndrome

A

eg. 45 X0/ 46 XX

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22
Q

Which Turner syndrome cases is possible the pregancy?

A

OOcyte donation, exogenous estradiol 17 β and progesterone

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23
Q

XYY

A

Double Y males

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24
Q

Incidence of Double Y males

A

1: 1000

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25
Q

Findings of Double Y males

A

Phenotypically normal, very tall, severe acne, antisocial behavior (seen in 1-2% of XYY males)

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26
Q

How is the fertility in Double Y males?

A

Normal

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27
Q

Which psychiatric disorder may Double Y males have?

A

Small percentage diagnosed with autism spectrum disorders

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28
Q

Karyotypes for True hermaphroditism

A

46, XX or 47 XXY

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29
Q

How else are True hermaphroditism known?

A

Ovotesticular disorder of sex development

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30
Q

Sexual characters of True hermaphroditism

A

Both ovary and testicular tissue present (ovotestis) ambiguous genitalia

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31
Q

How common is True hermaphroditism?

A

Very rare

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32
Q

↑ Testosterone ↑ LH

A

Defective androgen receptor

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33
Q

↑ Testosterone ↓ LH

A

Testosterone-secreting tumor, exogenous steroids

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34
Q

↓ Testosterone ↑ LH

A

Primary hypogonadism

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35
Q

↓ Testosterone ↓ LH

A

Hypogonadotropic hypogonadism

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36
Q

Other disorders of sex development

A

Include terms pseudohermaphrodite, hermaphrodite and intersex. Disagreement between the phenotypic (external genitalia) and gonadal (testes vs ovaries) sex

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37
Q

Karyotype of Female psudohermaphrodite

A

XX

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38
Q

Findings of Female psudohermaphrodite

A

Ovaries present, but external genitalia are virilized or ambiguous

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39
Q

What explains Female psudohermaphrodite?

A

Due to excessive and inappropiate exposure to androgenic steroids during early gestation

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40
Q

Pathologies with excessive and inappropiate exposure to androgenic steroids during early gestation

A

Congenital adrenal hyperplasia or exogenous adminsitration of androgens during pregnancy

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41
Q

Karyotype of Male psudohermaphrodite

A

XY

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42
Q

Findings of Male psudohermaphrodite

A

Testes present, but external genitalia are female or ambiguous

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43
Q

Which is the most common form of Male psudohermaphrodite?

A

Is androgen insensitivity syndrome (testicular feminization)

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44
Q

Inability to synthesize estrogens form androgens

A

Aromatase deficiency

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45
Q

What is the effect of Aromatase deficiency?

A

Masculinization of female (46 XX) infants (ambiguous genitalia) and ↑ serum testosterone and androstenedione

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46
Q

How can Aromatase deficiency present?

A

With maternal virilization during pregnancy (fetal androgens cross the placenta)

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47
Q

karyotype of Androgen insensitivity syndrome

A

46 XY

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48
Q

Defect in androgen receptor

A

Androgen insensitivity syndrome

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49
Q

What could be the results of Androgen insensitivity syndrome?

A

Resulting in normal appearing female; female external genitalia with rudimentary vagina; uterus and fallopian tubes generally absent

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50
Q

How can Androgen insensitivity syndrome present?

A

With scant sexual hair; develops testes (often found in labia majora; surgically removed to prevent malignancy)

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51
Q

How are the hormones in Androgen insensitivity syndrome?

A

↑ testosterone, estrogen, LH (vs sex chromosome disorders)

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52
Q

Mode of inheritance of 5α reductase deficiency

A

Autosomal recessive; sex limited to genetic males (46 XY)

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53
Q

Inability to convert testosterone to DHT

A

5α Reductase

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54
Q

Characteristics of 5α Reductase deficiency

A

Ambiguous genitalia until puberty, when ↑ testosterone cuases masculinization/↑ growth of external genitalia

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55
Q

Hormonal levels in 5α Reductase deficiency

A

Testosterone/estrogen levels are normal; LH is normal or ↑

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56
Q

How are internal genitalia in 5α Reductase deficiency?

A

Normal

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57
Q

What is Kallmann syndrome?

A

Failure to complete puberty; a form of hypogonadotropic hypogonadism

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58
Q

What is the problem in Kallmann syndrome?

A

Defective migration of GnRH cells and formation of ollfactory bulb

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59
Q

What is affected in Kallmann syndrome?

A

Decrease synthesis of GnRH in the hypothalamus

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60
Q

Which sense is affected in Kallmann syndrome?

A

Anosmia

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61
Q

How are hormones affected in Kallmann syndrome?

A

↓ GnRH, FSH, LH, testosterone, and infertility

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62
Q

How is Kallmann syndrome manifested in males?

A

Low sperm count

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63
Q

How is Kallmann syndrome manifested in females?

A

Amenorrhea

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64
Q

Cystic swelling of chronic villi and proliferation of chorionic epithelium (only trophoblast)

A

Hydatidiform mole

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65
Q

Which is the treatment for Hydatidiform mole?

A

Dilation and curettage and methotrexate

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66
Q

What must be monitor in Hydatidiform mole?

A

β hCG

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67
Q

Types of Hydatidiform mole

A

Complete mole

Partial mole

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68
Q

Karyotype of Complete mole

A

46 XX; 46 XY

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69
Q

Karyotype of partial mole

A

69 XXX; 69 XXY; 69 XYY

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70
Q

Levels of hCG in complete mole

A

↑↑↑↑

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71
Q

In which type of Hydatidiform mole is the uterine size increased?

A

Complete mole

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72
Q

Percentage of Complete mole that converts to Choriocarcinoma

A

2%

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73
Q

In which type of Hydatidiform mole can we find fetal parts?

A

Partial Mole (partial= fetal part)

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74
Q

Components of Complete mole

A

Enucleated egg + single sperm (subsequently duplicates paternal DNA); empty egg + 2 sperm is rare

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75
Q

Risk complications of complete mole

A

15-20 % malignant trophoblastic disease

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76
Q

Symptoms of complete mole

A

Vaginal bleeding, enlarged uterus, hyperemesis, preeclampsia, hyperthyroidism

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77
Q

What is found on imaging studies for complete mole?

A

Honeycombed uterus or “clusters of grapes”, “snowstorm on ultrasound

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78
Q

How is hCG in Partial mole?

A

↑

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79
Q

How common does Partial mole converts to Choriocarcinoma?

A

Rare

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80
Q

Components of Partial mole

A

2 sperm + 1 egg

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81
Q

Risk of complications of Partial mole

A

Low risk of malignancy (

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82
Q

Symptoms of Hydatidiform mole

A

Vaginal bleeding

Abdominal pain

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83
Q

What do Imaging studies show on Partial mole?

A

Fetal parts

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84
Q

Alternative name for Gestational hypertension

A

Pregnancy induced hypertension

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85
Q

What defines Gestational hypertension?

A

BP > 140/90 mmHg after the 20th week of gestation
No pre existing hypertension
No proteinuria or end organ damage

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86
Q

What is the treatment for Gestational hypertension?

A

Antihypertensives (α methyldopa, labetalol, hydralazine, nifedipine)

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87
Q

When can delivery be done in Gestational hypertension?

A

At 39 weeks

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88
Q

How is Preeclampsia defined?

A

As hypertension (>140/90 mmHg) and proteinuria (> 300 mg/ 24 hr) after 20th week of gestation to 6 weeks postpartum

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89
Q

Hypertension and proteinuria,

A

Molar pregnancy

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90
Q

Severe features of Preeclampsia

A

BP > 160/110 mmHg with or without end organ damage, eg. headache , scotoma, oliguria, ↑ AST/ALT, thrombocytopenia

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91
Q

What causes preclampsia?

A

By abnormal placental spiral arteries, results in maternal endothelial dysfunction, vasoconstriction, or hyperreflexia

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92
Q

In which patients is preclampsia incidence increased?

A

In patients with preexisting hypertension, diabetes, chronic renal disease, or autoimmune disorders

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93
Q

Complications of Preeclampsia

A

Placental abruption, coagulopathy, renal failure, uteroplacental insufficiency, or eclampsia

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94
Q

What is the treatment for preclampsia?

A

Antihypertensives, deliver at 34 weeks (severe) or 37 week (mild), IV magnesium sulfate to prevent seizures

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95
Q

How is Eclampsia defined?

A

Preeclampsia+ maternal seizures

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96
Q

What causes maternal death in eclampsia?

A

Due to stroke → intracranial hemorrhage or ARDS (Acute respiratory distress syndrome)

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97
Q

What is the treatment for eclampsia?

A

Antihypertensives, IV magnesium sulfate immediate delivery

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98
Q

When is recommended the delivery in preeclamptic patients?

A

At 34 weeks (severe) or 37 week (mild)

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99
Q

When is recommended the delivery in eclamptic patients?

A

Immediate delivery

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100
Q

What is HELLP syndrome?

A

Hemolysis, Elevated Liver enzymes, Low Platelets

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101
Q

How is HELLP syndrome related to preeclampsia?

A

HELLP can be a manifestation of severe preeclampsia, although may occur without hypertension

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102
Q

Which is the treatment for HELLP syndrome?

A

Immediate delivery

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103
Q

Premature separation of placenta from uterine wall before delivery of infant

A

Placental Abrution (Abruptio placentae)

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104
Q

Types of Placental Abruption

A

Complete or partial

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105
Q

Risk factors to develop placental abruption

A

Trauma, smookung, hypertension, preeclampsia, cocaine abuse

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106
Q

Presentation of placental abruption

A

Abrupt, painful bleeding (concealed or apparent) in third trimester

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107
Q

Possible complications of placental abruption

A

DIC, maternal shock, fetal distress

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108
Q

Prognosis of Placental abruption

A

Life threatening for mother and fetus

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109
Q

Type of bleeding of Placental abruption

A

Concealed

Apparent

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110
Q

What explains Placenta accreta/ increta/ percreta?

A

Defective decidual layer → abnormal attachment and separation after delivery

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111
Q

Risk factor for Placenta accreta/ increta/ percreta

A

Prior C section, inflammation, placenta previa

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112
Q

What defines the types of Placenta accreta/ increta/ percreta?

A

By the depth of penetration

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113
Q

Which is the most common type between Placenta accreta/ increta/ percreta?

A

Placenta accreta

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114
Q

Placenta attaches to myometrium without penetrating it

A

Placenta accreta

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115
Q

Placenta penetrates into myometrium

A

Placenta increta

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116
Q

Placenta penetrates through the myometrium and into uterine serosa (invades entire uterine wall)

A

Placenta percreta

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117
Q

What could be the complications of Placenta percreta?

A

Can result in placental attachment to rectum or bladder

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118
Q

Presentation of Placenta accreta/ increta/ percreta

A

No separation of placenta after → massive bleeding

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119
Q

Who is at risk in Placenta accreta/ increta/ percreta?

A

Life threatening for mother

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120
Q

Attachment of placenta to lower uterine segment

A

Placenta previa

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121
Q

Types of Placenta previa

A 
Lies near (Marginal)
Partial covers (Partial)
Completely covers internal cervical os
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122
Q

Risk factors to develop Placenta previa

A

Multiparity

Prior C section

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123
Q

What may retained placental tissues cause?

A

Postpartum hemorrhage, ↑ risk of infection

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124
Q

Which is the most often site of Ectopic pregnancy?

A

In ampulla of fallopian tube

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125
Q

When should Ectopic pregnancy be suspected?

A

With history of amenorrhea, lower than expected rise in hCG based on dates, and sudden lower abdominal pain

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126
Q

How is Ectopic pregnancy confirmed?

A

With ultrasound

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127
Q

With what is often clinically mistaken Ectopic pregnancy?

A

With appendicitis

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128
Q

Clinical Characteristics of Ectopic pregnancy

A

Pain with or without bleeding

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129
Q

Risk factos for Ectopic pregnancy

A

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

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130
Q

When is consider polyhydramnios?

A

> 1.5- 2 L of amniotic fluid

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131
Q

What is associated to polyhydramnios?

A

With fetal malformations, maternal diabetes, fetal anemia, multiple gestations

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132
Q

Malformations associated to Polyhydramnios

A

Esophageal/duodenal atresia, anencephaly; both result in inability to swallow amniotic fluid

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133
Q

How is Oligohydramnios diagnose?

A
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134
Q

What is associated to Oligohydramnios?

A

Placental insufficiency, bilateral renal agenesis or posterior urethral valves (in males) and resultant inability to excrete urine

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135
Q

What can any profound oligohydramnios cause?

A

Potter sequence

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136
Q

What does dysplasia and carcinoma in situ of cervix means?

A

Disordered epithelial growth

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137
Q

Where does dysplasia and carcinoma in situ of cervix begin?

A

At basal layer of squamocolumnar junction (transition zone) and extends outwards

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138
Q

How is dysplasia of cervix classified?

A

CIN 1, CIN 2, CIN 3 depending on extent of dysplasia

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139
Q

What does CIN 3 mean?

A

Severe dysplasia or carcinoma in situ

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140
Q

What is associtated to dysplasia and carcinoma in situ of cervix ?

A

With HPV 16 and HPV 18

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141
Q

What do HPV 16 and HPV 18 produce?

A

The E6 gene product (inhibits p53 suppressor gene) and E7 gene product (inhibits RB supressor gene)

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142
Q

What is the function of E6 gene?

A

Inhibits p53 suppressor gene

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143
Q

What is the function of E7 gene?

A

Inhibits RB supressor gene

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144
Q

How is the progression of dysplasia and carcinoma in situ of cervix?

A

May progress slowly to invasive carcinoma if left untreated

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145
Q

How do you suspect of dysplasia and carcinoma in situ of cervix?

A

Typically asymptomatic (detected with pap smear) or presents as abnormal vaginal bleeding (often postcoital)

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146
Q

Risk factors for dysplasia and carcinoma in situ of cervix

A

Multiple sexual partners (#1), smooking, early sexual intercourse, HIV infection

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147
Q

Which is the most common type of invasive carcinoma of cervix?

A

Squamous cell carcinoma

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148
Q

What is the function of Pap smear?

A

Can catch cervical dysplasia (koilocytes) before it progresses to invasive carcinoma

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149
Q

What is tje risk of Invasive carcinoma?

A

Lateral invasion can block ureters, causing renal failure

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150
Q

Histological findings in endometritis

A

Inflammation of the endometrium (with plasma cells and lymphocytes)

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151
Q

What is associated to Endometritis?

A

Products of conception following delivery (vaginal/C section)/miscarriage/ abortion of foreign body such as an IUD

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152
Q

What does Retained material in uterus promotes?

A

Infection by bacterial flora from vagina or instestinal tract

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153
Q

What is the treatment for Endometritis?

A

Gentamincin + clindamycin with or without ampicillin

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154
Q

Hystological findings of Endometriosis

A

Non neoplastic endometrial glands/ stroma outside of the endometrial cavity

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155
Q

Where can Endometriosis be found?

A

Anywhere

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156
Q

Most common sites of endometriosis

A

Ovary, pelvis, and peritoneum

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157
Q

How does Endometriosis appears in the ovary?

A

As endometrioma

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158
Q

What is an Endometrioma?

A

Blood filled chocolate cyst

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159
Q

Causes of endometriosis

A

Can be due to retrograde flow, metaplastic transformation of multipotent cells, or transportation of endometrial tissue via the lymphatic system

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160
Q

Clinical findings of Endometriosis

A

Chracterized by cyclic pelvic pain, bleeding, dysmenorrhea, dyspareunia, dyschezia, infertility

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161
Q

What is dyschezia?

A

Pain with defecation

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162
Q

How is the size of the uterus in Endometriosis?

A

Normal size

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163
Q

Treatments for Endometriosis

A

NSAIDs, OCPs, progestins, GnRH agonists, surgery

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164
Q

Extension of endometrial tissue (glandular) into the uterine myometrium

A

Adenomyosis

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165
Q

What causes adenomyosis?

A

By hyperplasia of the basalis layer of the myometrium

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166
Q

Clinical findings of Adenomyosis

A

Dysmenorrhea, menorrhagia

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167
Q

Characteristics of the uterus in adenomyosis

A

Uniformly enlarged, soft, globular uterus

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168
Q

Treatment for Adenomyosis

A

Hysterectomy

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169
Q

What is an Adenomyoma (polyp)?

A

Well circumscribed collection of endometrial tissue within the uterine cavity. May contain smooth muscle cells

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170
Q

How much can an adenomyoma extend?

A

Can extend onto the endometrial cavity in the form of a polyp

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171
Q

What is Endometrial hyperplasia? What causes it?

A

Abnormal endometrial gland proliferation usually caused by excess estrogen stimulation

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172
Q

What risk is increased with Endometrial hyperplasia?

A

Endometrial Carcinoma

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173
Q

How does endometrial hyperplasia manifest?

A

As postmenopausal vaginal bleeding

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174
Q

Risk factors to develop Endometrial hyperplasia

A

Anovulatory cycles, hormone replacement thearpy, polycystic ovarian syndrome, and granulosa cell tumor

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175
Q

Most common gynecologi malignancy

A

Encometrial carcinoma

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176
Q

Peak occurrence of Endometrial carcinoma

A

55-65 years old

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177
Q

How does Endometrial carcinoma manifest?

A

With vaginal bleeding

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178
Q

What typically precedes Endometrial carcinoma?

A

Endometrial hyperplasia

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179
Q

Risk factors to develop Endometrial carcinoma

A

Prolonged use of estrogen without progestins, obesity, diabetes, hypertension, nulliparity, hypertension, nulliparity and late menopause

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180
Q

What decreases the prognosis of Encometrial carcinoma?

A

↑ myometrial invasion

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181
Q

Alternative name for Leiomyoma?

A

Fibroid

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182
Q

Most common tumor in females

A

Leiomyoma

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183
Q

How is often presented the leimyoma?

A

With multiple discrete tumors

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184
Q

Which patients have an increased incidence for fibroids?

A

In blacks

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185
Q

Hystological features of leimyoma

A

Benign smooth muscle tumor

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186
Q

How often is the malignant transformation of Fibriod?

A

Rare

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187
Q

For what is Leimyoma sensitive?

A

Estrogen sensitive- tumor size ↑ with pregnancy and ↓ with menopause

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188
Q

Peak occurence of Leimyoma

A

at 20-40 years old

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189
Q

Clinical findings of Fibroids

A

May be asymptomatic, cause abnormal uterine bleeding or result in miscarriage

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190
Q

What does severe bleeding in leiomyoma lead to?

A

To iron deficiency anemia

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191
Q

Can Leimoyma progress to leiomyosarcoma?

A

No

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192
Q

Gross findings of Fibroids

A

Whorled pattern of smooth muscle bundles with well demarcated borders

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193
Q

Gynecologic tumor epidemiology incidence

A

Endometrial> ovarian> cevical

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194
Q

Gynecologic tumor epidemiology worst prognosis

A

Ovarian > Cervical > Endometrial

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195
Q

What is Premature ovarian failure?

A

Premature atresia of ovarian follicles in women of reproductive age

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196
Q

Findings of Premature ovarian failure

A

Patients present with signs of menopause after puberty but before age 40

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197
Q

Hormonal levels in Premature ovarian failure

A

↓estrogen, ↑ LH, FSH

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198
Q

Most common causes of anovulation

A

Pregnanacy, polycystic ovarian syndrome, obesity, HPO axis abnormalitis, premature ovarian failure, hyperprolactinemia, thyroid disorders, eating disorders, female athletes, Cushing syndrome, adrenal insufficiency

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199
Q

Which is the Stein Leventhal syndrome?

A

Polycystic Ovarian syndrome

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200
Q

What is seen in Polycystic Ovarian syndrome?

A

Hyperandrogenism due to deranged steroid synthesis by theca cells, hyperinsulinemia

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201
Q

Pathophysiology of Polycystic Ovarian syndrome

A

Estrogen ↑ steroid hormone- binding globulin (SHBG) and ↓ LH, ultimately resulting in ↓ free testosterone; insulin and testosterone ↓ SHBG → ↑ free testosterone

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202
Q

What explains ↑ LH in Stein Leventhal syndrome?

A

Due to pituitary/ hypothalamus dysfunction

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203
Q

What is the result of Stein Leventhal syndrome?

A

In enlarged, bilateral cystic ovaries

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204
Q

How is Stein Leventhal syndrome presented?

A

With amenorrhea/ oligomenorrhea, hirsutism, acne, infertility

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205
Q

What is associated to Stein Leventhal syndrome?

A

With obesity

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206
Q

What risk is increased with Polycystic Ovarian syndrome?

A

Of endometrial cancer

207
Q

What explains the increased risk of Endometrial cancer in Polycystic Ovarina syndrome?

A

Secondary to increased estrogen from the aromatization of testosterone and absence of progesterone

208
Q

What is the treatment for Hirsutism, acne in Polycystic Ovarian syndrome?

A

Weight reduction, OCPs, antiandrogens

209
Q

Mechanism of action of OCPs in Polycystic Ovarian syndrome?

A

Estrogen ↑ SHBG and ↓ LH → ↓ free testosterone

210
Q

For infertility in Polycystic Ovarian syndrome, what is recommended?

A

Clomiphene citrate, metformin

211
Q

How does Clomiphene citrate helps for infertility in Polycystic Ovarian syndrome?

A

Block negative feedback of circulating estrogen, ↓ FH, LH

212
Q

How does metformin help patients with infertility in Polycystic Ovarian syndrome?

A

↑ insulin sensitivity, ↓ insulin level, results in ↓ testosterone; enables LH surge

213
Q

For endometrial protection what is recommended in Polycystic Ovarian syndrome?

A

Cyclic progesterones

214
Q

What is the benefit of cyclic progesterones in patients with Polycystic Ovarian syndrome?

A

Antagonizes endometrial proliferation

215
Q

How are hormones affected in Polycystic Ovarian syndrome?

A

↑ LH, ↑ FSH (LH: FSH, 3:1), ↑ testosterone, ↑ estrogen (from aromatization)

216
Q

Which is the most common cause of infertility in women?

A

Polycystic Ovarian syndrome

217
Q

How is Follicular cyst formed?

A

Distention of unruptured graafian follicle

218
Q

What may be associated to Follicular cyst?

A

With hyperestrogenism and endometrial hyperplasia

219
Q

Most common ovarian mass in young women

A

Follicular cyst

220
Q

How is Corpus luteum cyst formed?

A

Hemorrhage into persistent corpus luteum

221
Q

How is the common evolution of Corpus luteum

A

Commonly regresses spontaneously

222
Q

How is Theca-lutein cyst often presented?

A

Bilateral/multiple

223
Q

How are Theca-lutein cyst formed?

A

Due to gonadotropin stimulation

224
Q

Pathologies associated to Tstheca-lutein cyst

A

Choriocarcinoma and moles

225
Q

What causes hemorrhagic cyst?

A

Blood vessel rupture in cyst wall

226
Q

How does hemorrhagic cyst grows?

A

With ↑ blood retention

227
Q

Evolution of hemorrhagic cyst

A

Self resolves

228
Q

Also known as Mature teratoma

A

Dermoid cyst

229
Q

Characteristics of Dermoid cyst

A

Cystic growhts filled with various types of tissue such as fat, hair, teeth, bits of bone and cartilage

230
Q

Endometriosis within ovary with cyst formation

A

Endometrioid cyst

231
Q

How does Endometrioid cyst varies?

A

With menstrual cycle

232
Q

When is endometrioid cyst called “chocolate cyst”?

A

When filled with dark, reddish brown blood

233
Q

Ovarian cysts

A 
Follicular cyst
Corpus luteum cyst
Theca lutein cyst
Hemorrhagic cyst
Dermoid cyst
Endometriod cyst
234
Q

Most common adnexal mass in women > 55 years old

A

Ovarian neoplasms

235
Q

How are ovarian neoplasm classified?

A

Benign and malignant

236
Q

From where do ovarin neoplasms arise?

A

From surface epithelium, germ cells and sex cord stromal tissue

237
Q

From where do majority of malignant ovarian neoplasms arise?

A

From epithelial cells

238
Q

Which is the most common malignant ovarian neoplasm?

A

Majority (95%) are epithelial (serous adenocarcinoma most common)

239
Q

What increases the risk of ovarian malignant neoplasm?

A

Advanced age, infertility, endometriosis, Polycystic Ovary Syndrome, genetic predisposition

240
Q

Genetic predisponents for Malignant ovarian cancer?

A

BRCA 1 or BRCA 2 mutation, HNPCC (Hereditary nonpolyposis colorectal cancer), strong family history

241
Q

What decreases the possibility of ovarian cancer?

A

Previous pregnancy, history of breastfeeding, OCPs, tubal ligation

242
Q

How does Ovarian neoplasm present?

A

With adnexal mass, abdominal distention, bowel obstruction, pleural effusion

243
Q

How is Ovarian cancer diagnose?

A

Surgically

244
Q

How is monitor progression of ovarian cancer done?

A

By measuring CA-125 levels

245
Q

Is CA 125 good for screening of ovarian cancer?

A

NO

246
Q

Most common ovarian neoplasm

A

Serous cystadenoma

247
Q

Gross characeteristics of Serous cystadenoma

A

Thin walled, uni or multilocular

248
Q

Histological apperance of Serous cystadenoma

A

Lined with fallopian like epithelium

249
Q

Is Serous cystadenoma more often unilateral or bilateral?

A

Bilateral

250
Q

Gross findings of Mucinous cystadenoma

A

Multiloculated, large

251
Q

Histological features of Mucinous cystadenoma

A

Lined by mucus secreting epitheliu

252
Q

Mass arising form growth of ectopic endometrial tissue

A

Endometrioma

253
Q

Characteristics of Endometrioma in Ultrasound

A

Complex mass

254
Q

Clinical presentation of endometrioma

A

Pelvic pain, dysmenorrhea, dyspareunia

255
Q

Alternative name for Mature cystic teratoma

A

Dermoid cyst

256
Q

How is Dermoid cyst classified?

A

Germ cell tumor

257
Q

Most common ovarian tumor in women 20-30 years old

A

Mature cystic teratoma

258
Q

What can a Teratoma contain?

A

Elements form all 3 germ layers; teeth, hair, sebum are common components

259
Q

What explains the possible pain in Mature cystic teratoma?

A

Secondary to ovarian enlargement or torsion

260
Q

What is Struma ovari?

A

When a Dermoid cyst contain functional thyroid tissue and present as hyperthyroidism

261
Q

What apperance do Brenner tumor have?

A

Looks like bladder

262
Q

Gross apperance of Brenner tumor

A

Solid tumor that is pale yellow tan in color and appears encapsulated

263
Q

Hisological features of Brenner tumor on H&E

A

“Coffee bean” nuclei

264
Q

Histological characteristics of Fibromas

A

Bundles of spindle- shapped fibroblasts

265
Q

What does Meigs syndrome contain?

A

Triad of ovarian fibroma, ascities and hydrothorax

266
Q

Symptom caused by fibroma

A

Pulling sensation in groin

267
Q

How is Thecoma classified?

A

Like granulosa tumors

268
Q

What do Thecomas may produce?

A

Estrogen

269
Q

How does Thecomas usually present?

A

As abnormal uterine bleeding in a postmenopausal woman

270
Q

Malignant ovarina neoplasms

A 
Immature teratoma
Granulosa cell tumor
Serous cystadenomcarcinoma
Mucinous cystadenocarcinoma
Dysgerminoma
Choriocarcinoma
Yolk sac tumor
Krukenberg tumor
271
Q

Characteristics of immature teratoma

A

Aggressive, contains fetal tissue, neuroectoderm

272
Q

How is Immature teratoma most typically represented?

A

By immature/embryonic like neural tissue

273
Q

What do mature teratoma more likely contain?

A

Thyroid tissue

274
Q

Most common sex cord stromal tumor

A

Granulosa cell tumor

275
Q

In which patients is Granullosa cell tumor predominantly?

A

Women in their 50s

276
Q

What do Granullosa cell tumor produce?

A

Often produce estrogen and/ or progesterone

277
Q

How are Granullosa cell tumor presented?

A

With abnormal uterine bleeding, sexual preocity (in pre-adolescents), breast tenderness

278
Q

Main histologica characteristic of Granullosa cell tumor

A

Call Exner bodies

279
Q

What do Call Exner bodies resemble?

A

Primordial follicles

280
Q

Most common ovarian neoplasm

A

Serous cystadenocarcinoma

281
Q

Frequently how are Serous cystadenocarcinoma presented?

A

Bilateral

282
Q

Main histologiccal finding of Serous Cystadenocarcinoma

A

Psammoma bodies

283
Q

Which ovarian neoplasm is related to pseudomyxoma peritoni?

A

Mucinous cystadenocarcinoma

284
Q

What is pseudomyxoma peritoni?

A

Intraperitoneal accumulation of mucinous material from ovarian or appendiceal tumor

285
Q

In which group of age is Dysgerminoma more common?

A

In adolescents

286
Q

Which ovarian malignancy is equivalent to male Seminoma?

A

Dysgerminoma, but is rarer

287
Q

Which percentage of all ovarian cancer is Dysgerminoma?

A

1%

288
Q

Which Percentage of germ cell tumors is Dysgerminoma?

A

30%

289
Q

Histological characteristics of Dysgerminoma?

A

Sheet of uniform “fried egg” cells

290
Q

Tumor markers of Dysgerminoma

A

hCG, LDH

291
Q

How common is Choriocarcinoma?

A

Rare

292
Q

When can choriocarcinoma develop?

A

During or after pregnancy in mother or baby

293
Q

How is Choriocarcinoma classified?

A

Malignancy of trophobalstic tissue (cytotrophoblast, syncytiotrophoblasts); no chorionic villi present

294
Q

What other ovarian neoplasm is increased in frequency with Choriocarcinoma?

A

Theca-lutein cysts

295
Q

How is Choriocarcinoma presented?

A

With abnormal β hCG, shortness of breath, hemoptysis

296
Q

What complication can Choriocarcinoma has?

A

Hematogenous spread to lungs

297
Q

How is the response of Choriocarcinoma to chemotherapy?

A

Very responsive

298
Q

Alternative name for Yolk salc tumor

A

Endodermal sinus

299
Q

How is Yolk salc tumor consider?

A

Aggressive

300
Q

How is Yolk salc tumor presented?

A

In ovaries or testes (boys) and sacrococcygeal area in young children

301
Q

Most common tumor in male infants

A

Yolk salc tumor (Endodermal sinus)

302
Q

Gross findings of Yolk salc tumor (Endodermal sinus)

A

Yellow, friable (hemorrhagic), solid mass

303
Q

Histological findings in Yolk salc tumor (Endodermal sinus)

A

50% have Schiller Duval bodies

304
Q

What do Schiller Duval bodies resemble?

A

Glomeruli

305
Q

Tumor marker for Yolk salc tumor (Endodermal sinus)

A

AFP

306
Q

GI malignancy that metastasizes to the ovaries

A

Krukenberg tumor

307
Q

Histological features of Krukenberg tumor

A

Mucin secreting signet cell adenocarcinoma

308
Q

Vaginal tumors

A

Squamous cell carcinoma
Clear cell adenocarcinoma
Sarcoma botryoides

309
Q

Primary vaginal carcinoma but is rare

A

Squamous cell carcinoma

310
Q

What is related to Squamous cell carcinoma of vagina?

A

Usually secondary to cervical Squamous cell carcinoma

311
Q

Who is affected by Clear cell carcinoma?

A

Affects women who had exposeure to DES in utero

312
Q

What kind of variant is Sarcoma botryoides of vagina?

A

Rhabdomyosarcoma variant

313
Q

Who is affected by Sarcoma botryoides of vagina?

A

Girls

314
Q

Histological characteristic of Sarcoma botryoides of vagina?

A

Spindle shaped tumor cells that are desmin +

315
Q

Pathologies that develop in nipple

A

Paget disease

Breast abscess

316
Q

Pathologies that develop in lactiferous sinus

A

Intraductal pailloma, abscess/mastitis

317
Q

Pathologies that develop in Major duct

A

Fibrocystic change, DCIS, invasive ductal carcinoma

318
Q

Pathologies that develop in Terminal duct

A

Tubular carcinoma

319
Q

Pathologies that develop in Lobules

A

Lobular carcinoma

320
Q

Pathologies that develop in Breast stroma

A

Fibroadenoma

Phyllodes tumor

321
Q

Benign breast tumors

A

Fibroadenoma
Intraductal papilloma
Phyllodes tumor

322
Q

Clinical characteristics of Fibrodenoma of breast

A

Small, mobile, form mass with sharp edges

323
Q

Most common tumor in those

A

Fibroadenoma

324
Q

What increases the size and tenderness of Fibroadenoma?

A

↑ size and tenderness with ↑ estrogen (eg. pregnancy, prior to menstruation)

325
Q

Is Fibroadenoma precursor to breast cancer?

A

No

326
Q

Where does Intraductal papilloma grows?

A

Small tumor that grows in lactiferous ducts

327
Q

Where is typically located intraductal papilloma?

A

Typically beneath areola

328
Q

Type of nipple discharge of Intraductal papilloma

A

Serollodes tumorus or bloody nipple discharge

329
Q

Is intraductal papilloma precursor to breast cancer?

A

Slight (1.5- 2 x) in creases risk for carcinoma

330
Q

Clinical characterisitcs of Phyllodes tumor

A

Large bulky mass of connective tissue and cyst

331
Q

“Leaf like” projections

A

Phyllodes tumor

332
Q

When is more common to see Phyllodes tumor?

A

In 6th decade

333
Q

Is Phyllodes tumor precursor to breast cancer?

A

Some may become malignant

334
Q

When are more common the malignant breast tumors?

A

Postmenopausal

335
Q

From where do Malignant breast tumor usually arise?

A

From terminal duct lobular unit

336
Q

What do Malignant breast tumor express?

A

Overexpression of estrogen/progesterone receptors or c-erbB2 is common

337
Q

What is c-erbB2?

A

HER-2, an EGF receptor

338
Q

When do we consider to be agressive a Malignant breast tumor?

A

Triple negative (ER-, PR-, and HER2/Neu -)

339
Q

What is the importance of ER, PR, and/or HER2/Neu expression in Malignant breast tumor?

A

Type affects therapy and prognosis

340
Q

Which is the single most important prognostic factor of Malignant breast tumor?

A

Axillary lymph node involvement indicating metastasis

341
Q

Where are more often located the Malignant breast tumor?

A

In upper outer quadrant of breast

342
Q

Risk factors to develop Malignant breast tumor

A

↑ Estrogen exposure, ↑ total number of menstrual cycles, older age at 1st live birth, obesity, BRCA1 and BRCA2 gene mutations, African American ethnicity

343
Q

How does obesity increases the risk for Breast cancer?

A

↑ Estrogen exposure as adipose tissue converts androstenedione to estrone

344
Q

What risk is increased for African American patients with Malignant breast tumor?

A

↑ risk for triple - breast cancer

345
Q

How are Malignant breast tumor classified?

A

Noninvasive

Invasive

346
Q

Which Malignant breast tumor are Noninvasive?

A

Ductal carcinoma in situ (DCIS)
Comedocarcinoma
Paget disease

347
Q

Wat is affected in Ductal carcinoma in situ (DCIS)?

A

Fills ductal lumen

348
Q

From where do Ductal carcinoma in situ (DCIS) arise?

A

From ductal Atypia

349
Q

How is Ductal carcinoma in situ (DCIS) often seen in mammography?

A

As microcalcifications

350
Q

How is Ductal carcinoma in situ (DCIS) consider?

A

Early malignancy without basement membrane penetration

351
Q

Histological features of Comedocarcinoma

A

Ductal, caseous necrosis

352
Q

How is Comedocarcinoma classified?

A

As subtype of Ductal carcinoma in situ (DCIS)

353
Q

When do we see Paget disease?

A

Results from underlying Ductal carcinoma in situ (DCIS)

354
Q

Clinical findings of Paget disease

A

Eczematous patches on nipple

355
Q

Characteristics of Paget cells

A

Large cells in epidermis with clear halo

356
Q

What does Paget disease sugest?

A

Undelying Ductal carcinoma in situ (DCIS)

357
Q

Where else is Paget disease seen?

A

On vulva, though does not sugest underlying malignancy

358
Q

Who are invasive Malignant breast tumors?

A

Invasive ductal
Invasive lobular
Medullary
Inflammatory

359
Q

Clinical findings of Invasive ductal carcinoma

A

Firm, fibrous, “rock hard” mass with sharp margins

360
Q

Histologic apperance of Invasive Ductal carcinoma

A

Small, glandular, duct cells

361
Q

When invasive Ductal carcinoma is grossly, what is seen?

A

See classic “stellate” infiltration

362
Q

Which is the worst and most invasive malignant breast tumor?

A

Invasive Ductal carcinoma

363
Q

Most common type of breast cancer

A

Invasive Ductal carcinoma (76% of all breast cancers)

364
Q

Histologic features of Invasive lobulillar carcinoma

A

Orderly row of cells (“Indian file”)

365
Q

How is the presentation of invasive lobulillar carcinoma of breast?

A

Often bilateral with multiple lesions in the same location

366
Q

Histologic characteristics of Medullary carcinoma of breast

A

Fleshy, cellular, lymphocytic infiltrate

367
Q

How is the prognosis of Medullary carcinoma of breast

A

Good prognosis

368
Q

How is the invasion of Inflammatory breast cancer?

A

Dermal lymphatic invasion by breast carcinoma

369
Q

Presentation of Inflammatory breast cancer

A

Peau d’ orange (breast skin resembles orange peel)

370
Q

What could be seen in Inflammatory breast cancer?

A

Neoplastic cells block lymphatic drainage

371
Q

How is the prognosis of Inflammatory breast cancer?

A

50% survival at 5 years

372
Q

Most common cause of “breast lumps” from age 25 to menopause

A

Proliferative breast disease

373
Q

How does Proliferative breast disease manifest?

A

With premenstrual breast pain and multiple lesions, often bilateral

374
Q

What fluctates in Proliferative breast disease?

A

In size of mass

375
Q

Does Proliferative breast disease indicate increased risk of carcinoma?

A

No

376
Q

Histologic types of Proliferative breast disease

A

Fibrosis
Cystic
Sclerosing adenosis
Epithelial hyperplasia

377
Q

Hyperplasia of breast stroma in Proliferative breast disease

A

Fibrosis

378
Q

What are the characteritics of Cystic Proliferative breast disease

A

Fluid filled, blue dome. Ductal dilation

379
Q

Proliferative breast disease Characterized by ↑ acini and intralobular fibrosis

A

Sclerosing adenosis

380
Q

What is associated to Sclerosing adenosis?

A

With calcifications

381
Q

Which Proliferative breast disease is often confused with cancer?

A

Sclerosing adenosis. Because may present with calcifications

382
Q

Does Sclerosing adenosis increase the risk of cancer?

A

↑ risk (1.5-2x) of developing cancer

383
Q

↑ in number of epithelial cell layers in terminal duct lobule

A

Epithelial hyperplasia

384
Q

What risk is increased with Epithelial hyperplasia of breast?

A

Of carcinoma with atypical cells

385
Q

In which patients does Epithelial hyperplasia of breast occur?

A

In women > 30 years old

386
Q

What is acute mastitis?

A

Breast abscess

387
Q

When can we see acute mastitis?

A

During breast feeding, ↑ risk of bacterial infection through cracks in the nipple

388
Q

Most common patogen in Acute mastitis

A

S. aureus

389
Q

How is actue mastitis treated?

A

With dicloxacillin and continued breast feeding

390
Q

How is Fat necrosis consider?

A

A benign, usually painless lump

391
Q

How does Fat necrosis is formed?

A

As a result of injury to breast tissue

392
Q

What is seen in mammography in patients with Fat necrosis?

A

Abnormal calcifications

393
Q

What does biopsy show in Fat necrosis?

A

Necrotic fat , giant cells

394
Q

Which percentage of patients may not report trauma in Fat necrosis?

A

Up to 50% of patients

395
Q

Ginecomastia in males is the result of…

A

From hyperestrogenism, Klinefelter syndrome, or drugs

396
Q

Which hyperestrogenism situations may cause Ginecomastia?

A

Cirrhosis, testicular tumor, puberty, old age

397
Q

Which drugs may cause Gynecomastia?

A

Spironolactone, marijuana, Digitalis, Estrogen, Cimetidine, Alcohol, Heroin, Dopamine D2 antagonists, Ketoconazole

398
Q

Clinical findings of Prostatitis

A

Dysuria, frequency , urgency, low back pain

399
Q

Acute cause of Prostatitis

A

Bacterial (eg. E. coli)

400
Q

Chronic cause of Prostatitis

A

Bacterial or abacterial (most common)

401
Q

In which patients is Benign prostatic hyperplasia?

A

In men > 50 years old

402
Q

Characteristics of Benign Prostatic hyperplasia

A

By smooth, elastic, firm nodular enlargement of the periurethral (lateral and middle) lobes which compress the urethra into a vertical slit

403
Q

Is Benign Prostatic hyperplasia consider a malignant hyperplasia?

A

NO

404
Q

How is Benign Prostatic hyperplasia presented?

A

With frequency of urination, nocturia, difficulty starting abd stoping the stream of urine and dysuria

405
Q

What can Benign Prostatic hyperplasia lead to?

A

May lead to distention and hyperthrophy of the bladder, hydronephrosis, and UTIs

406
Q

How is prostate specific antigen (PSA) in Benign Prostatic hyperplasia?

A

Increased

407
Q

Which is the treatment for Benign Prostatic hyperplasia?

A

α1 antagonists (terazosin, tamsulosin)

Finasteride

408
Q

α1 antagonists

A

terazosin, tamsulosin

409
Q

What is the effect of α1 antagonists in Benign Prostatic hyperplasia?

A

Cause relaxation of smooth muscle

410
Q

In which patients is more common Prostatic adenocarcinoma?

A

In men > 50 years old

411
Q

From where does Prostatic adenocarcinoma arise more often?

A

From the posterior lobe (peripheral zone) of the prostate gland

412
Q

How is Prostatic adenocarcinoma most frequently diagnosed?

A

By increased PSA and subsequent needle core biopsies

413
Q

Which are useful tumor markers of Prostatic adenocarcinoma?

A

Protatic acid phosphate (PAP) and PSA are useful tumor markers (↑ total PSA, with ↓ fraction of free PSA)

414
Q

Which metastasis is the most common from Prostatic adenocarcinoma?

A

Osteoblastic metastasis in bone may develop in late stages

415
Q

What makes you suspect of Osteoblastic metastasis of Prostatic adenocarcinoma?

A

Indicated by lower back pain and an ↑ in serum ALP and PSA

416
Q

Undescended testis (one or both)

A

Cryptorchidism

417
Q

How is the spermatogenensis in Cryptorchidism?

A

Impaired spermatogenesis

418
Q

At which temperature do sperm develop best?

A
419
Q

How are testosterone levels in Cryptorchidism?

A

Normal levels (Leydig cells are unaffected by temperature)

420
Q

What risk is increased with Cryptorchidism?

A

Of Germ cell tumors

421
Q

What increases the risk to develop Cryptorchidism?

A

Prematurity

422
Q

What is affected in Cryptorchidism?

A

↓ inhibin, ↑ FSH, and ↑ LH

423
Q

When is testosterone affected by Cryptorchidism?

A

↓ in bilateral Cryptorchidism, normal in unilateral

424
Q

What is Varicocele?

A

Dilated veins in pampiniform plexus as a result of ↑ venous pressure

425
Q

Most common cause of scrotal enlargement in adult males

A

Varicocele

426
Q

Which side is more common to see Varicocele? Why?

A

Most often on the left side because of ↑ resistance of flow from gonadal vein drainage into the left renal vein

427
Q

What could be the consequences of Varicocele?

A

Can cause infertility because of ↑ temperature

428
Q

What apperance do varicocele has?

A

“Bag of worms”

429
Q

How is Varicocele diagnosed?

A

By ultrasound with doppler

430
Q

Which is the treatment for Varicocele?

A

Varicocelectomy, embolization by interventional radiologist

431
Q

95% of all testicular tumors

A

Testicular germ cell tumors

432
Q

Testicular germ cell tumors

A 
Seminoma
Yolk salc tumor
Chiriocarcinoma
Teratoma
Embryonal carcinoma
433
Q

Whe do Testicular germ cell tumors most often occur?

A

In young men

434
Q

Risk factors to develop Testicular germ cell tumors?

A

Cryotorchidism

Klinefelter syndrome

435
Q

How can Testicular germ cell tumors present?

A

As mixed cell tumor

436
Q

How is Seminoma consider?

A

Malignant

437
Q

Clinical findings of Seminoma

A

Painless, homogneous testicular enlargment

438
Q

Most common testicular tumor

A

Seminoma

439
Q

When is Seminoma more common?

A

In 3rd decade

440
Q

Can Seminoma appear during infancy?

A

NEVER

441
Q

Histologic characteristics of Seminoma

A

Large cells in lobules with watery cytoplasm abd a “fried egg apperance”

442
Q

Which lab is altered in Seminoma?

A

↑ Placental ALP

443
Q

For what treatment in Seminoma sensitive?

A

To Radiation

444
Q

How are the metastasis of Seminoma?

A

Late Metastasis

445
Q

Prognosis of Seminoma

A

Excelent

446
Q

In men which is Gross apperance of Yolk sac (endodermal sinus) tumor?

A

Yellow, mucinous

447
Q

How is Yolk sac (endodermal sinus) tumor consider?

A

Aggressive malignancy

448
Q

In which pathology do we see Schiller Duval bodies?

A

Yolk sac (endodermal sinus) tumor

449
Q

What do Schiller Duval bodies ressemble?

A

Primitive glomeruli

450
Q

Most common testicular tumor in boys

A

Yolk sac (endodermal sinus) tumor

451
Q

How is Choriocarcinoma consider?

A

Malignant

452
Q

What lab is altered in Choriocarcinoma?

A

Increased hCG

453
Q

What is the problem in Choriocarcinoma?

A

Disordered syncytiotrophoblastic and cytotrophoblastic elements

454
Q

How are the metastasis in Choriocarcinoma?

A

Hematogenous metastases to lungs and brain

455
Q

When do you suspect of brain metastasis of Choriocarcinoma?

A

When see a “hemorrhagic stroke” due to bleeding into the metastasis

456
Q

How else can Choriocarcinoma manifest?

A

May produce gynecomastia or symptoms of hyperthyroidism

457
Q

What explains that Choriocarcinoma may produce gynecomastia or symptoms of hyperthyroidism?

A

hCG is an LH and TSH analog

458
Q

How is Teratoma consider in males?

A

Unlike in females, mature teratoma in adult males may be malignant

459
Q

How is Teratoma consider in children?

A

Benign

460
Q

Which labs are altered in Teratoma?

A

↑ hCG and/or AFP in 50% of cases

461
Q

How is Embryonal carcinoma consider?

A

Maliginant

462
Q

Gross Characteristics of Embryonal carcinoma

A

Hemorrhagic mass with necrosis

463
Q

Clinical chracteristics of Embryonal carcinoma

A

Painful

464
Q

Which Testicular germ cell tumor has worst prognosis between Seminoma and Embryonal carcinoma?

A

Embryonal carcinoma

465
Q

Embryonal carcinoma histologic morphology

A

Often glandular/ papillary morphology

466
Q

How frequent is pure Embryonal carcinoma?

A

Rare, most commonly mixed with other tumor types

467
Q

Which labs could be found in Embryonal carcinoma?

A

May be associated to ↑ hCG and normal AFP levels when pure (↑ AFP when mixed)

468
Q

5% of all testicular tumors

A

Testicular non germ cell tumors

469
Q

Testicular non germ cell tumors

A

Leydig cell
Sertoli cell
Testicular lymphoma

470
Q

How are Testicular non germ cell tumors consider?

A

Mostly benign

471
Q

What does Leydig cell tumor contain?

A

Reinke crystals

472
Q

What does Leydig cell tumor produce?

A

Androgen

473
Q

Clinical effects if Leydig cell tumor

A

Gynecomastia in men

Precocious puberty in boys

474
Q

Gross apperance of Leydig cell tumor

A

Golden brown color

475
Q

Androblastoma from sex cord stroma

A

Sertoli cell tumor

476
Q

Most common testicular cancer in older men

A

Testicular lymphoma

477
Q

How does Testicular lymphoma arrise?

A

Not a primary cancer, arises from lymphoma metastases to testes

478
Q

How is Testicular lymphoma consider?

A

Aggressive

479
Q

Which lesion is the differential diagnosis from testicular cancer?

A

Tunica vaginalis lesions

480
Q

How is Tunica vaginalis lesions differentiated from testicular cancer?

A

Tunica vaginalis lesions can be transilluminated, and Testicular cancer don’t

481
Q

Characteristics of Tunica vaginalis lesions

A

Lesions in the serous covering of testis present as testicular masses

482
Q

Types of Tunica vaginalis lesions

A

Hydrocele

Spermatocele

483
Q

What causes hydrocele?

A

↑ fluid secondary to incomplete obliteration of processus vaginalis

484
Q

Dilated epidymal duct

A

Spermatocele

485
Q

Where is Squamous cell carcinoma of penis more common?

A

In Asia, Africa and South America

486
Q

Which is the precursor of Squamous cell carcinoma of penis?

A

In situ lesions:
Bowen disease
Erythropasia of Queyrat
Bowenoid papulosis

487
Q

How is Bowen disease presented?

A

In penile shaft, presents as leukoplakia

488
Q

What is Erythroplasia of Queyrat?

A

Cancer of glans

489
Q

How is Erythroplasia of Queyrat presented?

A

Presents as Erythroplakia

490
Q

How are Bowenoid papulosis presented?

A

As reddish papules

491
Q

What is associated to Squamous cell carcinoma of penis?

A

With HPV, lack of circumcision

492
Q

Painful sustained erection not associated with sexual stimulation or desire

A

Priapism

493
Q

What is associated to Priapism?

A

Trauma
Sickle cell disease
Medications

494
Q

How does Sickle cell diasea produces Priapism?

A

Sickled RBCs get trapped in vascular channels

495
Q

Which drugs can produce Priapism?

A 
Anticouagulants
PDE-5 inhibitors
Antidepressants
α blockers
cocaine
496
Q

Which drug has inhibitory effects on Hypothalamus?

A

Clomiphene

497
Q

Which drugs act in GnRH?

A 
GnRH antagonists (inhibition)
GnRH agonists (+/-)
498
Q

In female patients which drugs have Inhibitory effects in Anterior pituitary?

A

Oral contraceptives

Danazol

499
Q

Which enzyme helps in the synthesis of Androstenedione and Testosterine in the ovary?

A

P-450c17

500
Q

Whi inhibits P-450c17?

A

Ketoconazole

Danazol

501
Q

What is the importance of testosterone and androstenedione in women?

A

They become Estrogens by the effect of aromatase

502
Q

By the action of aromatase, what is the final product of Testosterone?

A

Estradiol

503
Q

By the action of aromatase, what is the final product of Androstenedione?

A

Estrone

504
Q

Which drugs inhibit aromatase?

A

Anastrozole, others

505
Q

How is the physiology of estrogens?

A

Estradiol ↔ Estrone → Estriol

506
Q

Which drugs work at Estrogen response elements?

A

Fulvestrant (-)

SERMs (+/-)

507
Q

Which drugs inhibits synthesis of testosterone by Testis?

A

Ketoconazole

Spironolactone

508
Q

Which enzyme makes the converison of Testosterone to Dihydrotestosterone?

A

5α reductase

509
Q

Which drug inhibits 5α reductase?

A

Finasteride

510
Q

Which drugs inhibits Androgen Receptor Complex?

A

Flutamide
Cyproterone
Spironolactone

511
Q

Mechanism of action of Leuprolide

A

GnRH analog with agonist properties when used in pulsatile fashion
Antagonist properties when used in continous fashion

512
Q

Down regulates GnRH receptor in pituitary → ↓ FSH/ LH

A

Leuprolide

513
Q

Clinical use for Leuprolide

A 
Infertility (pulsatile), prostate cancer continous use with flutamide)
Uterine fibroids (continous use)
Precocious puberty (continous)
514
Q

Toxic effects of Leuprolide

A

Antiandrogen, nausea, vomiting

REPRODUCTIVE (5 decks)

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