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Endo/Repro > Puberty and Disorders of Development and Menstrual Disorders > Flashcards

Puberty and Disorders of Development and Menstrual Disorders Flashcards

1
Q

How does the menstrual cycle occur?

A
  • GnRH from the hypothalamus stimulates the follicle stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary, which stimulates estrogen and progesterone from the ovarian follicle
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2
Q

Where is the pituitary gland located?

A
  • Below the hypothalamus at the base of the brain within a bony cavity and is separated from the cranial cavity by a condensation of dura matter covering the sella turcica
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3
Q

What are the two divisions of the pituitary? What does each produce?

A
  • Anterior lobe: FSH, LH, TSH, prolactin, growth hormone, and ACTH
  • Posterior lobe: Vasopressin and Oxytocin
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4
Q

What are the phases of the normal ovarian cycle?

A
  • Follicular phase: begins with the onset of menstruation and culminates in the preovulatory surge of LH
  • Luteal phase: begins with the onset of the preovulatory LH surge and ends with the first day of menses
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5
Q

What do decreasing levels of estradiol and progesterone from the regressing corpus luteum of the preceding cycle do?

A
  • Initiate an increase in FSH by a negative feedback mechanism, which stimulates follicular growth and estradiol secretion
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6
Q

What is a major characteristic of follicular growth and estradiol secretion?

A
  • Is explained by the 2 gonadotropin (LH and FSH)

- 2 cell theory of ovarian follicular development

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7
Q

What is the 2 cell theory of ovarian follicular development and estrogen production?

A
  • Separate ovarian functions in the ovarian follicle
  • LH stimulates the theca cells to produce androgens
  • FSH stimulates the granulosa cells to convert these androgens into estrogen
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8
Q

What happens during the luteal phase?

A
  • LH and FSH are significantly suppressed at the start of the phase through the negative feedback effect of the elevated circulating estradiol and progesterone
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9
Q

What happens if conception does not occur during the luteal phase?

A
  • Progesterone and estradiol levels decline near the end of the luteal phase as a result of corpus luteal regression
  • Then FSH will rise which initiates new follicular growth for the next cycle
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10
Q

What are the 5 peptides that affect the reproductive cycle that are isolated from the hypothalamus?

A
  • GnRH
  • TRH
  • SRIF or somatostatin
  • CRF
  • PIF
  • All exert specific effects on the hormonal secretion of the anterior pituitary gland
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11
Q

What is GnRH responsible for?

A
  • Synthesis and release of LH and FSH

- Reaches the anterior pituitary and stimulates the synthesis and release of FSH and LH into the circulation

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12
Q

What does estradiol do in regards to GnRH and LH?

A
  • Enhance the hypothalamic release of GnRH and induce the midcycle LH surge
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13
Q

What do gonadotropins do on GnRH release?

A
  • Inhibitory effect
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14
Q

When do estradiol levels begin to rise?

A
  • Approximately 1 week before ovulation, they begin to rise

- Rise to a maximum 5 to 7 days after ovulation and returns to baseline before menstruation

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15
Q

When are estrogen levels at a maximum?

A
  • 1 day before the midcycle LH peak
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16
Q

What happens with progestin during follicular development?

A
  • Ovary secretes only a very small amount of progesterone

- Prior to ovulation the unruptured luteinizing graafian follicle begins to produce increasing amounts of progesterone

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17
Q

Where does a bulk of progesterone come from during follicular development?

A
  • The peripheral conversion of the adrenal pregnenolone and pregnenolone sulfate
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18
Q

When does secretion of progesterone reach a maximum?

A
  • Reaches a maximum 5-7 days after ovulation and returns to baseline before menstruation
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19
Q

What happens to primordial follicles during follicular development?

A
  • Undergoes sequential development, differentiation and maturation until a mature graafian follicle is produced
  • Follicle then ruptures and releases an ovum
  • Subsequent luteinization of the ruptured follicle produces the corpus luteum
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20
Q

What happens about 8 to 10 weeks of fetal development?

A
  • Oocytes become surrounded by precursor granulosa cells

- This complex is called the primordial follicle

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21
Q

What is the cumulus oophorus?

A
  • The innermost 3 to 4 layers of multiplying granulosa cells become cuboidal and adherent to the ovum
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22
Q

How does the antrum and corona radiata form among the granulosa cells?

A
  • Antrum enlarges and centrally located primary oocyte migrates to the wall of the follicle
  • Innermost layer of the granulosa cells of the cumulus become elongated and form the corona radiata
  • Corona radiata is release with the ootyce at ovulation
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23
Q

How does ovulation start?

A
  • Preovulatory LH surge initiates a sequence of biochemical and structural changes that result in ovulation
  • Cells on the follicular wall surface degenerate and a stigma forms, follicular basement membrane bulges through the stigma
  • When this ruptures, the oocyte is expelled into the peritoneal cavity
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24
Q

What makes of the corpus luteum?

A
  • Luteinized granulosa cells, theca cells, capillaries, and connective tissue
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25
Q

What does the corpus luteum do?

A
  • Produced copious amounts of progesterone and some estradiol
  • If pregnancy doesn’t occur, menses does causing the corpus luteum to be replaced by avascular scar tissue called corpus albicans
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26
Q

What is the normal life span of the corpus luteum?

A
  • 9 to 10 days
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27
Q

What is the endometrium responsive to?

A
  • Circulating progestins, androgens, and estrogens
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28
Q

What are the two zones of the endometrium?

A
  1. Outer portion or functionalis

2. Inner portion or basalis

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29
Q

What does the functionalis zone of the endometrium do?

A
  • Undergoes cyclic changes in morphology during the menstrual cycle and is sloughed off at menstruation
  • Contains spiral arteries
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30
Q

What does the basalis zone of the endometrium do?

A
  • Remains relatively unchanged during each cycle and after menstruation provides stem cells for the renewal of the functionalis
  • Contains basal arteries
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31
Q

What are the three stages of histopathology of the endometirum?

A
  1. Menstrual phase
  2. Proliferative or estrogenic phase
  3. Secretory or progestional phase
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32
Q

What occurs during the menstrual phase?

A
  • First day of menstruation is known as day 1
  • Disruption and disintegration of the endothelial glands and stroma, leukocyte infiltration, and red blood cell extravasation
  • Sloughing of the functionalis layer and compression of the basalis layer
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33
Q

What occurs during the proliferative phase?

A
  • Endometrial growth secondary to estrogenic stimulation

- Increase in length of spiral arteries and numerous mitoses can be seen in these tissues

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34
Q

What occurs during the secretory phase?

A
  • Following ovulation, progesterone secretion by the corpus luteum stimulates the glandular cells to secrete mucus, glycogen and other substances
  • Glands become tortuous and lumens are dilated and filled with these substances
  • Stroma become edematous
  • Spiral arteries extend into superficial layer of the endometrium and become convoluted
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35
Q

What happens if conception does not happen by day 23?

A
  • Corpus luteum begins to regress, secretion of progesterone and estradiol decline, and endometrium undergoes involution
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36
Q

What happens the day before menstruation during the secretory phase?

A
  • Marked constriction of the spiral arteries occurs resulting in ischemia of the endometrium, leukocyte infiltration and RBC extravasation
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37
Q

What is important in regulating menstruation?

A
  • Intact coagulation pathway
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38
Q

How does coagulation affect menstruation?

A
  • Menstruation disrupts blood vessels, but with normal hemostasis, they are repaired
  • Restoration of the vessels requires successful interaction of platelets and clotting factors
  • Anticoagulants impair the coagulation system and are associated with heavy bleeding
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39
Q

When does menarche occur?

A
  • 12.43 is median age
  • Occurs within 2-3 years after thelarche at Tanner stage IV, rare before tanner stage III
  • By age 15, 98% of females have had menarche
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40
Q

What is primary amenorrhea?

A
  • No menstruation by 13 without secondary sexual development OR by the age of 15 with secondary sexual characteristics
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41
Q

What is the average length of the first cycle and how many days do they bleed?

A
  • Length is 34 days

- Bleed for 2-7 days

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42
Q

What is the mean blood loss per menstrual period?

A
  • 30cc

- Most report changing a pad 3 to 6 times a day

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43
Q

What is blood loss of greater than 80cc associated with?

A
  • Anemia

- Changing a pad every 1-2 hours is considered excessive especially if bleeding is lasting >7 days

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44
Q

What is the usual age of puberty?

A
  • 10-16 years old
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45
Q

What is the onset of puberty determined by?

A
  • Genetic factors including race
  • Geographic location (metro areas and near sea level begin puberty early)
  • Obese children have earlier puberty
  • Malnourished, chronically ill with weight loss will have later onset
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46
Q

What mean weight is essential to start menarche?

A
  • 106 lbs
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47
Q

When do females have the peak number of oocytes?

A
  • 6-7 million by mid-gestation (16-20 weeks)
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48
Q

What happens during ages 4-10?

A
  • Hypothalamic-pituitary-ovary axis is suppressed
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49
Q

What 2 mechanisms do low levels of gonadotropins and sex steroids affect?

A
  • Gonadostat sensitivity to the negative feedback of low circulating estradiol
  • Intrinsic central nervous system inhibition of the hypothalamic GnRH secretion
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50
Q

What happens during ages 8-11?

A
  • Is an increase in serum concentration of DHEA, DHEA-S, and androstenedione
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51
Q

What are the initial endocrine changes associated with puberty?

A
  • Adrenal androgen production and differentiation by the zona reticularis of the adrenal cortex
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52
Q

What happens a result to a rise in adrenal androgens?

A
  • Growth of axillary and pubic hair
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53
Q

How does puberty start?

A
  • Around 11, there is a gradual loss of sensitivity by the gonadostat to the negative feedback of sex steroids. In combo with the intrinsic loss of central nervous system inhibition of hypothalamic GnRH release
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54
Q

What does an increase in GnRH promote?

A
  • Ovarian follicular maturation and sex steroid production, which leads to the development of secondary characteristics
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55
Q

What happens by mid to late puberty?

A
  • Positive feedback mechanism of estradiol on LH release from the anterior pituitary gland is complete and ovulatory cycles are established
56
Q

What is thelarche? What is required?

A
  • First physical sign of puberty
  • Unilateral development in first 6 months is not uncommon
  • Requires estrogen
57
Q

What is pubarche and adrenarche? What is required?

A
  • Pubic hair and axillary hair development

- Requires androgens

58
Q

When does maximal growth or peak height velocity occur?

A
  • Occurs 2 years earlier in girls

- Occurs about 1 year before onset on menses

59
Q

What is required for menarche?

A
  • Pulsatile GnRH from the hypothalamus, FSH and LH from the pituitary, estrogen and progesterone from the ovaries, normal outflow tract
60
Q

What happens during Tanner stage 1 for breast development?

A
  • Preadolescent

- Elevation of papilla only

61
Q

What happens during Tanner stage 2 for breast development?

A
  • Breast bud stage

- Elevation of breast and papilla as a small mound with enlargement of the areolar region

62
Q

What happens during Tanner stage 3 for breast development?

A
  • Further enlargement of breast and areola without separation of their contours
63
Q

What happens during Tanner stage 4 for breast development?

A
  • Projection of areola and papilla to form a secondary mound above the level of the breast
64
Q

What happens during Tanner stage 5 for breast development?

A
  • Mature stage

- Projection of papilla only, resulting from recession of the areola to the general contour of the breast

65
Q

What happens during Tanner stage 1 for pubic hair devleopment?

A
  • Preadolescent

- Absence of pubic hair

66
Q

What happens during Tanner stage 2 for pubic hair development?

A
  • Sparse hair along the labia

- Hair downy with slight pigment

67
Q

What happens during Tanner stage 3 for pubic hair development?

A
  • Hair spreads sparsely over the junction of the pubes

- Hair is darker and coarser

68
Q

What happens during Tanner stage 4 for pubic hair development?

A
  • Adult type hair

- There is no spread to medial thigh

69
Q

What happens during Tanner stage 5 for pubic hair development?

A
  • Adult type hair with spread to the medial thighs assuming an inverted triangle pattern
70
Q

What is precocious puberty?

A
  • Starting puberty two standard deviations before expected age
  • 8 years old for girls
  • 9 years old for boys
71
Q

What is needed to be done in precocious puberty?

A
  • Thorough evaluation to eliminate a serious disease and to arrest potential osseous maturation that can affect normal growth patterns
72
Q

What are the two types of precocious puberty?

A
  1. Heterosexual precocious puberty

2. Isosexual precocious puberty

73
Q

What is heterosexual precocious puberty?

A
  • Development of secondary sexual characteristics opposite of those anticipated
  • Think about: Virulizing neoplasms (sertoli leydig tumor), congenital adrenal hyperplasia, or exposure to exogenous androgens
74
Q

What is isosexual precocious puberty?

A
  • Premature sexual maturation that is appropriate for the phenotype of the affected individual
  • Constitutional and organic brain disease (tumors, trauma, infectious process)
75
Q

What is the most common cause of congenital adrenal hyperplasia (CAD)?

A
  • Defect of the adrenal cortex enzyme 21-hydroxylase leading to excessive androgen production
76
Q

What is classical CAD?

A
  • Most severe forms cause cause birth of female with ambiguous genitalia
  • If untreated progressive virilization and short adult status will result
77
Q

What is unclassical CAD?

A
  • Late onset adrenal hyperplasia can cause premature pubarche and an adult disorder resembling PCOS
78
Q

How does true isosexual precocity arise?

A
  • Premature activation of the normal process of pubertal development involving the HPO axis
79
Q

How does pseudoisosexual precocity arise?

A
  • Exposure to estrogens independent of HPO axis like estrogen producing tumors
80
Q

How is isosexual precocious puberty diagnosed?

A
  • Administration of exogenous GnRH and see a resultant rise of LH levels consistent with older girls who are undergoing normal puberty
81
Q

What are some CNS disorders that could cause isosexual precocious puberty?

A
  • Tumors
  • Obstructive lesions (hydrocephalus)
  • Granulomatous disease (sarcoidosis, TB)
  • Infective processes (meningitis, encephalitis, or brain abscess)
  • Neurofibromas
  • Head trauma
82
Q

How could a CNS disorder cause precocious puberty?

A
  • May interfere with normal inhibition of hypothalamic GnRH release
  • May often exhibit neural deficits before puberty development
83
Q

What is the treatment for isosexual precocious puberty?

A
  • GnRH agonist which suppresses pituitary release of LH and FSH, resulting in the decline of gonadotropins to prepubertal levels and arrest of gonadal sex steroid secretion
84
Q

What can occur of isosexual precocious puberty is not treated?

A
  • Half of girls will not reach 5 feet
85
Q

What are two syndromes that may cause pseduoisosexual precocious puberty?

A
  • McCune-Albright syndrome

- Peutz-Jehgars syndrome

86
Q

How could McCune-Albright syndrome cause pseudoisosexual precocious puberty?

A
  • Somatic mutation during embryogenesis which causes them to function independent of their normal stimulation hormones
  • Will have multiple cystic bone defects, cafe au lait spots
  • Adrenal hypercortisolism
87
Q

How could Peutz-Jehgars syndrome cause pseudoisosexual precocious puberty?

A
  • Associated with a sex cord tumor that secretes estrogen

- GI polyposis and mucocutaneous pigmentation

88
Q

When is puberty considered delayed?

A
  • Secondary sexual characteristics have not appeared by the age of 13
  • If thelarche has not occurred by 14
  • No menarche by age 15-16
  • When menses has not begun 5 years after the onset of thelarche
89
Q

What is a cause of hypergonadotropic hypogonadism/

A
  • Gonadal dysgenesis (Turner)
90
Q

What are some causes of hypogonadotropic hypogonadism?

A
  • Constitutional (physiologic) delay
  • Kallmann syndrome
  • Anorexia/extreme exercise
  • Pituitary tumors/disorders
  • Hyperprolactinemia
  • Drug use
91
Q

What are some anatomic causes of delayed puberty?

A
  • Mullerian agenesis
  • Imperforate hymen
  • Transverse vaginal septum
92
Q

What is amenorrhea?

A
  • Absence of menses
93
Q

What is primary amenorrhea?

A
  • No spontaneous uterine bleeding by age of 13 without secondary sexual characteristics
  • No menstruation by 15 years old with secondary sexual development
94
Q

What is secondary amenorrhea?

A
  • Patient with prior menses has absent menses for 6 months or more
95
Q

What are the diagnostic findings of primary amenorrhea with absence of secondary sexual characteristics?

A
  • FSH, LH
96
Q

What is Kallmann syndrome?

A
  • Mutation of the KAL gene on the x chromosome that prevents the migration of the GnRH neurons into the hypothalamus
  • Patients with often have anosmia or hyposmia (no or little smell)
97
Q

What tests can be done to evaluate for primary amenorrhea with absence of secondary sexual characteristics?

A
  • MRI of brain
  • FSH
  • Karyotype
  • Progesterone
  • Prolactin
98
Q

What is the physical presentation of someone with Turner’s syndrome?

A
  • Webbing of the neck
  • Broad flat chest like a shield with widely spaced nipples
  • Short stature
  • Rudimentary streaked ovaries
  • Absent or incomplete development of puberty
  • Coarctation of the aorta
99
Q

What are the two categories of primary amenorrhea with breast development and mullerian anomalies?

A
  1. Androgen insensitivity syndrome

2. Mullerian agenesis

100
Q

What are some characteristics of androgen insensitivity syndrome (AIS)?

A
  • Male levels of testosterone
  • 46XY
  • Defect in androgen receptor
  • Testes are in abdominal wall and secrete normal amounts of anti mullerian hormones meaning no uterus
101
Q

What does the external genitalia look like in AIS?

A
  • External female genitalia with absent to sparse pubic hair
  • Breast development with smaller than normal areola and nipples due to estrogen secretion in testes and conversion of androgens to estrogen in the liver
102
Q

What is mullerian agenesis (MRKH syndrome)?

A
  • Failure of mullerian ducts to fuse distally and to form the upper genital tract
  • Absent uterus but may have a unilateral or bilateral rudimentary uterine tissue, tubes, and ovaries
  • May have renal abnormalities
103
Q

What are some characteristics of mullerian agenesis?

A
  • Normal secondary development and external female genitalia
  • Normal female range of testosterone
  • Absent uterus and upper vagina
  • Normal ovaries
  • 46XX
104
Q

What does history and physical reveal for secondary amenorrhea?

A
  • Significant changes in weight
  • Strenuous exercise
  • Dietary habits
  • Concomitant illes
  • Abnormal facial hair
  • Galactorrhea
  • Dysparenuia
  • Presence of hot flashes or night sweats
105
Q

What labs are done for secondary amenorrhea?

A
  • Urine hCG
  • TSH
  • Prolactin
  • FSH
106
Q

What will thyroid disease show in the labs?

A
  • Normal prolactin

- Abnormal TSH

107
Q

What will be seen in hypothyroidism?

A
  • Hypermenorrhea or oligomenorrhea

- Treatment should restore menses

108
Q

What is seen in abnormal prolactin levels?

A
  • Normal TSH

- Galactorrhea is the most common symptom of hyperprolactinemia

109
Q

What is done for really high prolactin (≥100ng/ml)?

A
  • Evaluate for prolactinemia with head MRI to check for empty sella syndrome or pituitary adenoma
110
Q

What is done for high prolactin (<100ng/ml)?

A
  • If MRI is negative, consider other causes
111
Q

What is done for microadenomas found on MRI?

A
  • Monitored with repeat prolactin measurements and imaging
  • Typically slow growing and rarely malignant
  • Treatment should focus on management of infertility, galactorrhea, and breast discomfort
  • Consideration for dopamin agonist
112
Q

What is done for macroadenomas found on MRI?

A
  • May be treated with dopamine agonists

- Transphenoidal resection or craniotomy

113
Q

What are some causes of prolactin <100ng/ml?

A
  • Ectopic production
  • Breast feeding and stimulation
  • Excessive exercise
  • Severe head trauma
  • Hypothyroidism
  • Liver or renal failure
  • Meds like OCPs, antipsychotics, antidepressants, antihypertensives, H2 blockers, opiates, cocaine
114
Q

What is done if there is normal TSH and prolactin in secondary amenorrhea?

A
  • Progesterone challenge test
115
Q

What is a positive progesterone challenge test?

A
  • Positive bleeding

- Normogonadotropic hypogonadism (PCOS is most common)

116
Q

What is a negative progesterone challenge test?

A
  • No withdrawal bleeding

- Indicates inadequate estrogenization or an outflow tract abnormality

117
Q

What is done after a progesterone challenge test?

A
  • Do an estrogen/progesterone challenge test
118
Q

What does a negative estrogen/progesterone challenge test indicate?

A
  • Outflow tract obstruction
119
Q

What does a positive estrogen/progesterone challenge test indicate?

A
  • Abnormality with the hypothalamic pituitary axis or ovaries
120
Q

What is seen in a positive estrogen/progesterone challenge test?

A
  • Elevated FSH and LH would indicate ovarian abnormality

- Normal FSH and LH would indicate pituitary or hypothalamic abnormality

121
Q

What is nonclassic congenital adrenal hyperplasia?

A
  • Elevated 17-hydroxyprogesterone
  • Does not present with genital abnormalities
  • Associated with hirsutism, acne, and menstrual irregularities around puberty
122
Q

What are some causes of normogonadotropic amenorrhea with hyperandrogenism following a positive PCT?

A
  • Nonclassic congenital adrenal hyperplasia
  • Cushing’s syndrome
  • Adrenal androgen secreting tumor
  • PCOS
  • Sertoli leydig cell tumor
123
Q

What does PCOS cause?

A
  • Leading cause of female anovulatory infertility
  • 60-70% of patients have decreased insulin sensitivity causing to insulin hypersecretion
  • Elevated insulin and androgen levels reduce the hepatic production of sex hormone binding globulins leading to increase circulating testosterone
124
Q

How is the diagnosis for PCOS made?

A
  • Oligomenorrhea or amenorrhea
  • Biochemical or clinical signs of hyperandrogenism (LH to FSH 2:1)
  • U/S revealing multiple small cysts beneath the cortex of the ovary
125
Q

What are some features of PCOS?

A
  • Anovulation
  • Hyperandrogenism
  • Hirsutism
  • Acne
  • Menstrual dysfunction
  • Hyperinsulinemia
  • LH hypersecretion
  • Elevated testosterone
  • Acyclic estrogen production
  • Obesity
  • Sleep disorders
  • Acanthosis nigricans
  • Lipid abnormalities
126
Q

What are some treatment options for PCOS?

A
  • Weight loss
  • OCPs to suppress gonadotropins
  • Clomiphene citrate which can induce ovulation
  • Ovarian diathermy/laser treatment
  • Spironolactone
  • Insulin sensitizing agents
127
Q

What are some causes of hypergonadotropic hypogonadism (FSH >20 IU and LH >40 IU) in secondary amenorrhea?

A
  • Postmenopausal ovarian failure (ave age of menopause is 51)
  • Premature ovarian failure (before 40)
  • Ovarian injury from surgery
  • Pelvic radiation
  • Autoimmune and mumps
128
Q

What are some causes of hypogonadotropic hypogonadism (FSH and LH <5) in secondary amenorrhea?

A
  • Anorexia or bulimia
  • Chronic illness
  • Cranial radiation
  • Excessive exercise
  • Malnutrition and weight loss
  • Sheehan’s syndrome
129
Q

What labs are done during evaluation of hyperandrogenism?

A
  • 17-hydroxyprogesterone to exclude CAH
  • 24 hour free cortisol to rule out Cushing’s
  • Prolactin and TSH for hyperprolactinemia and thyroid dysfunction
  • Glucose and lipid levels
  • Testosterone and DHEA-S
130
Q

What does PALM stand for in AUB?

A
  • Polyp
  • Adenomyosis
  • Leiomyoma
  • Malignancy and hyperplasia
131
Q

What does COEIN stand for in AUB?

A
  • Coagulopathies (Von willebrand disease)
  • Ovulatory dysfunction (PCOS)
  • Endometrial causes (infection)
  • Iatrogenic (IUD, IUS, exogenous hormones )
  • Not yet classified (AVM)
132
Q

What medical history is needed of AUB?

A
  • Age of menarche and menopause
  • Menstrual bleeding patterns
  • Severity of bleeding
  • Pain
  • Medical conditions
  • Surgical history
  • Use of medications
  • Symptoms and signs of possible hemostatic disorders
133
Q

What laboratory tests are done for AUB?

A
  • Pregnancy test
  • CBC
  • Targeted screening for bleeding disorders
  • TSH
  • Chlamydia trachomatis
134
Q

What is the treatment for massive bleeding in AUB?

A
  • Hospitalization and transfusions if hemodynamically unstable
  • 25 mg IV conjugated estrogens then hormonal treatment
135
Q

What is the treatment for moderate bleeding in AUB?

A
  • Combination OCPs, Mirena
136
Q

What is done if treatment is unresponsive in AUB?

A
  • D&C, polypectomy, myomectomy, endometrial ablation, hysterectomy

Endo/Repro (31 decks)

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