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Pathophysiology > W.11: Disturbances in Pituitary function > Flashcards

W.11: Disturbances in Pituitary function Flashcards

1
Q

Primary regulator/(-ors) of hormone synthesis?

A

Target glands such as thyroid, adrenal cortex, gonads.

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2
Q

Secondary regulator of hormone synthesis?

A

Anterior pituatary

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3
Q

Tertiary regulator of hormone synthesis?

A

Hypothalamus

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4
Q

Hormones have negative inhibition on what?

A

On the anterior pituitary.

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5
Q

Anterior pituitary have negative ihibition on what?

A

Hypothalamus

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6
Q

Pathway of hormone synthesis.

A

Hypothalamus –> Releasing hormones (TRH, CRH, GnRH) –> Ant. pituitary –> Tropic hormones (TSH, ACTH, FSH, LH) –> Target glands (thyriod, andrenal cortex, gonads) –> Hormones

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7
Q

Ant. pituitary hormones?

A
  • Corticotropin- releated peptides
    • ACTH, LPH, MSH, endorfins
  • Somatomammotrops (peptides)
    • GH, PRL
  • Glycoproteins (2alfa, 2beta)
    • LH, FSH, TSH
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8
Q

Defects that might cause a loss of pituitary function? (5)

A
  • Congenital
  • Pituitary tumors
    • Functional
    • Non- functional
  • Non- pituitary tumors
    • Craniopharyngioma
    • Metastases
  • Trauma
    • Surgical
    • Head trauma
  • Inflammation
    • Autoimmune hypophysitis
    • Granulomatous disease
      + Histiocytosis X
      + Sarcoid
      + Tuberculosis
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9
Q

Typical progression of hormone loss?

A

GH –> LH –> FSH –> ACTH –> TSH

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10
Q

Definition of dwarfism (Nanosomia)

A

Height <147 cm.

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11
Q

Possible reasons for developing dwarfism? (6)

A
  • Achondroplasia (70%)
  • GH associated diseases
  • Other endocrine diseases (hypothyreosis, Cushings- syndrome)
  • Connective tissue diseases (Osteogenesis imperfecta)
  • Genetic disorders, Turner syndrome
  • Stress- psychogen dwarfism
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12
Q

Achondroplasia

A

FGF R3 mutation. 75% of individuals with achondroplasia are born to parents of average size due to new mutation or genetic change.

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13
Q

What might GH deficiency lead to? (7)

A
  • Growth retardation (in children)
  • High fat content, increased waist/ hip
  • Decreased BMD 1-2 SD below age matched mean
  • Increased fracture 2x
  • Increased total cholesterol and LDL/ HDL
  • Increased insulin, insulin resistance
  • Fatigue, muscle weakness
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14
Q

Sporadic GH deficiency

A
  • Acquired

- Hypothalamic

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15
Q

Genetic GH deficiency

A
  • FSH and LH deficiency also present

- Monotropic GH defiencency (70% respond to GnRH)

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16
Q

Underlying cause of GH deficiency might be?

A

Pituitary or hypothalamic deficiency.

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17
Q

Clinical manifestations seen in GH receptor defect (Laron Dwarf)?

A
  • Extreme short statue <122 cm
  • Increased serum level of GH
  • Absence of GH receptor in tissues
  • GH secretion is not suppressible by glucose
  • IGF-I level is low - tumor, DM decrease
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18
Q

Manifestations seen in Somatomedin- C (SM-C, IGF-I) defects?

A
  • Total absence of IGF-I, IGF-II normal
    • Failure of IGF-I to increase at puberty (seen in African pygmy)
  • Absence of IGF-I receptors
  • Post IGF-I receptor defect (normal binding, but decreased uptake of amino acids)
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19
Q

Treatment of hypopituitarism?

A
  1. Remove cause

2. Replacement therapy (depends on hormone lost)

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20
Q

Treatment in secondary hypothyroidism?

A

Thyroxine

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21
Q

Treatment of secondary hypoadrenalism?

A

Hydrocortisone

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22
Q

Treatment for induction of ovulation?

A

FSH+LH

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23
Q

GH excess may cause…

A
  • Childhood
    • Gigantism
  • Adults
    • Acromegaly
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24
Q

Etiology of GH excess?

A
  • 98% GH- producing pituitary tumor
  • 2% ectopic GHRH secretion
    • SCC lung cancer
    • Bronchial or intestinal carcinoid tumors
    • Pancreatic islet cell tumor
    • Pheochromocytoma
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25
Q

Clinical signs of acromegaly?

A
  • Somatotropic adenoma of pituitary
  • Acromegalic facies
  • Cardiomegaly
  • Barrel chest
  • Abnormal glucose tolerance secondaty to insulin resistance
  • Degenerative arthritis
  • Thickened skin (hypertrophy of sebaceous and sweat glands)
  • Hyperostosis (thoracic vertebrae)
  • Carpal tunnel syndrome
  • Increased size (hands, feet)
  • Growth of long bonws (children)
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26
Q

Patophysiology of acromegaly? (6)

A
  • Increased GH secretion
  • The nocturnal sruge is absent
  • Glucose suppression is lost
  • Paradox dopamine stimulation test
  • Increased serum somatomedins
  • Insulin resistance
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27
Q

Treatment of acromegaly?

A
  1. Surgical removal of the tumor
  2. Additional therapy:
    • Somatostatin analouge
    • Radiation
    • GH- receptor antagonist
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28
Q

Frequency of pituitary tumors?

A
  • PRL- secreting 35%
  • Non- functioning 30%
  • GH- secretion 20%
  • Mixed GH- and PRL- secretion 7%
  • ACTH and Lipotropin sec. 7%
  • LH-, FSH-, or TSH- sec. 1%
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29
Q

Normal prolactin level?

A

<900 pmol/L

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30
Q

Main clinical manifestation seen in women/ men due to Hyperprolactinemia?

A

Women:

  • Amnorhea 57- 90%
  • Galactorrhea 30- 80%

Men:

  • Decreased libido 75- 100%
  • Impotence 68- 100%
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31
Q

Treatment of prolactinomas?

A

Dopamin agonist therapy will normalize prolactin and lead to timor regression in most patients with macro- and microprolactinomas.

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32
Q

ADH release is stimulated by?

A
  • Plasma osmolality >280 mosm/L
  • A fall in plasma volume
  • Emotional factors and stress
  • Sleep
  • Other factors:
    • Cholinergic stimulation, alfa- adrenergic stimulation
    • Angiotensin II, prostaglandin E
    • Opiates, Nicotine
    • Histamine, Ether, Phenobarbitate
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33
Q

Definition of Diabetes Insipidus

A

DI is a disorder resulting from deficiency of anti- diuretic hormone (ADH) or its action and is characterized by the passage of copious amounts of diluted urine.

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34
Q

Central DI

A

Failure of pituitary gland to secrete adequate ADH.

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35
Q

Causes of Central DI?

A
  • Idiopathic (30% of cases)
  • Suprasellar tumors (30% of cases)
  • Infections (encephaitis, TB, etc)
  • Non- infectious granuloma (sarcoid, etc.)
  • Trauma or skull srugery
  • Leukemia
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36
Q

Nephrogenic DI

A

Results when the renal tubules of the kidney fail to respond to circulating ADH.

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37
Q

What does the renal concentration defect seen in nephrogenic DI lead to?

A

Loss of large volumes of diluted urine. This causes cellular and extracellular dehydration and hypernatremia.

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38
Q

Causes of nephrogenic DI (primary and secondary)?

A
  • Primary familial:
    X- linked recessice that is severe in boys and mild in girls.
  • Secondary to:
    • Chronic pyelonephritis
    • Hypokalemia
    • Hypercalcemia
    • Sickel cell disease
    • Protein deprivation
    • Drugs (Li) etc.
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39
Q

SIADH

A

Syndrome of Inappropriate secretion of ADH

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40
Q

When is SIADH seen?

A

SIADH occurs when ADH is released in amounts far in excess of those indicated by plasma osmotic pressure.

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41
Q

SIADH is characterized by?

A
  • Fluid retention
  • Serum hypoosmolality
  • Dilutional hyponatermia
  • Hypochloremia
  • Concentrated urine in the presence of normal or increased intravascular volume
  • Normal renal function
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42
Q

SIADH may be caused due to…

A
  • Pulmonary conditions: pneumonia, TB, lung abscesses, positive pressure ventilation
  • Trauma (most frequently head related)
  • Meningitis, subarachnoid hemorrhage
  • AIDS, Addison’s disease
    Peripheral neuropathy, psychoses
  • Vomiting, stress and many medications
  • Symtoms may also be caused by ADH secreting tumors
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43
Q

Which hormones are secreted by the ovary?

A

Graafian follicle:
- Estrogens (estradiol): Steroid

Corpus Luteum:

  • Progestins (Progesterone): Steriod
  • Relaxin: Polypeptide
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44
Q

Which hormones are secreted by the testis?

A

Leydig cells:
- Androgens (Testosterone): Steriod

Sertoli cells:
- Inhibin: Protein

Seminal vesicles:
- Contain leutinizing hormone receptors, may be regulated by the ligand, luteinizing hormone.

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45
Q

Which hormone/ hormones are secreted by the adrenal cortex?

A

Glucocorticoids (cortisol): Steroid

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46
Q

Which hormone/ hormones are secreted byt the placenta?

A

Human Chorionic Gonadotropin (hCG): Glycoprotein

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47
Q

Which hormone/ hormones are secreted by the endometrial cups?

A
  • Equine Chorionic Gonadotropin (eCG): Glycoprotein
  • Estrogens/Progestins: Steroids
  • Realxin: Protein
  • Placental Lactogen: Glycoprotein
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48
Q

Pricipal function of Estrogens?

A

Mating behavior, secindary sex characteristics, maintenance of female duct system, mammary growth.

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49
Q

Pricipal function of Inhibin (Folliculostatin)?

A

Regulates release of FSH from ant. pituitary.

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50
Q

Pricipal function of Porgestins (Progesterone)?

A

Maintenance of mammary growth, pregnancy and secetion.

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51
Q

Pricipal function of Relaxin?

A

Expansion of pelvis, dilation of cervix.

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52
Q

Pricipal function of Androgens (Testosterone)?

A

Male mating behaviour, spermatocytogenesis, maintenance of male duct system and accessory glands.

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53
Q

Pricipal function of Inhibin?

A

Regulates release of FSH.

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54
Q

Pricipal function of Prostaglandin F2- alfa?

A

Regression of CL. Stimulate myometrial contracions, ovulation. Produced by uterus when stimulated by oxytocin.

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55
Q

Pricipal function of hCG?

A

LH- like. Involved with establishment of pregnancy in human. Support and maintain CL.

56
Q

Pricipal function of eCG?

A

FSH- like. Some LH activity, immunological protection of foal. Formation of accessory CL in mare.

57
Q

Pricipal function of estogens/ progestins?

A

Regulate placental blood flow. Maintenance of pregnancy.

58
Q

Pricipal function of Placental Lactogen?

A

Stimulates mammary growth and milk secretion.

59
Q

How are the sex steriods transported?

A

They are bound to plasma proteins.

60
Q

What does SHBG resp. DHT bind to?

A

SHBG binds to T and DTH: 66- 78%

and E: 37%.

61
Q

What does CBG bind to?

A

90% of cortisol

28% of progesterone

62
Q

What does albumin bind to?

A

60- 80% of E and P

20- 30% of T and DHT

85% of Androstenedione

63
Q

Where is SHBG synthesized?

A

In the liver. E increases its synthesis and T decreases it. Why female levels are much higher.

64
Q

Where are E and P metabolized?

A

In the liver.

65
Q

Half life of P?

A

Approx. 5 min.

66
Q

What stimulates the hepatic SHBG synthesis?

A
  • E2
  • T4
  • Anticonvulsants
  • Liver disease
  • Age
67
Q

What decreases tje hepatic SHBG synthesis?

A
  • Testosterone
  • Anabolic steriods
  • Insulin (eg. in obesity)
68
Q

How big amount of testoterone is excreted?

A

90%

69
Q

Effect of testosterone?

A
  • Wolffian duct
  • Bone formation
  • Muscle mass
  • Spermatogenesis
70
Q

Testosterone + 5alfa- reductase (6-8%) –>

A

DHT

71
Q

Testosterone + Aromatase (0,3%)

–>

A

Estradiol

72
Q

Effects of DHT?

A
  • External genitalia features
  • Prostate growth
  • Acne
  • Facial/ body hair
  • Scalp hair loss
73
Q

What does total testosterone include?

A
  • Biologically inactive SHBG- bound testosterone (60%)
  • Albumin- bound testosterone (38%)
  • Unbound free testosterone (2%)
74
Q

Testosterone deficinencies may cause? (4)

A
  • In utero: Female external phenotype
  • Post- natal: Micropenis/ crypotochid
  • Childhood: Failure to enter puberty
  • Adult- onset:
    • Sexual dysfunction
    • Osteopaenia/ sarcopaenia
    • Central obesity/ dyslopidaemia
    • Think skin and gynaecomastia
    • Diminished muscle mass
    • Absent/ reduced body hair
    • Small, soft tetes
    • Infertility
75
Q

Laboratory evaluation of male reproductive function?

A
  • Measure serum testosterone
  • Calculate free testosterone from total testosterone and SHBG
  • Stimulation test (hCG, clomiphene, GnRH)
  • Semen analysis
  • Testicular biopsy
76
Q

Disorders of sexual differentiation?

A
  • Seminiferous tubule dysgenesis: Klinefelter syndrome
  • Gonadal dysgenesis and its variants: Turner syndrome
  • Complete and incoplete form to XX and XY gonadal dysgenesis
  • True hermaphroditism
77
Q

Most common form of primary hypogonadism and infertility in male?

A

Seminiferous tubule dysgenesis (Klinefelter syndrome)

78
Q

Clinical symptomes seen in Seminiferous tubule dysgenesis?

A
  • Gynecomastia
  • Diminished facial and body hair
  • SMall phallu, poor muscular development
  • Eunochiod tall body habits
  • Increased incidence of:
    - Mild DM
    - Varicose veins
    - Chronic pulmonary disease
    - Carcinoma of breast
  • Progressive testicular lesion
79
Q

Clinical features seen in Syndrome of Gonadal Dysgenesis (Turner syndrome)?

A
  • Sexual infantilism
  • Short stature
  • Lymphedema of the extremities
  • Typical face
  • Short neck, shieldlike chest
  • Coarctation of the aorta
  • Hypertension, renal abnormalties
  • Obesity, DM, Hashimoto’s thyroiditis, rheumatoid arthiritis etc.
80
Q

Features of pseudohermaphroidism, female?

A
  • Normal ovaries
  • Extragonadal hypersecretion of androgen
  • Masculinization, clitoral hypertrophy
81
Q

Features of pseudohermaphroidism, male?

A
  • Teste, genital ducts or extragenitals are not completely masculinized
  • Deficient testosterone secretion
82
Q

What might deficient testosterone secretion seen in pseudohermaphroidism lead to?

A
  • Failure of testicular differentiation
  • Failure of secretion of tesosterone or Müllerian duct inhibitory factors
  • Failure of target tissue response to T or DHT
  • Failure of conversion of T to DHT
83
Q

Clinical features of true hermaphroditism?

A
  • Uterus
  • Ovotestis
  • Breast development
  • Menses (50%)
84
Q

Causes of true hermaphroditism?

A
  • Sexchromatin mosaicism or chimerism
  • Y to autosome; Y to X chromosome translocation or exchange
  • Autosomal mutant gene
85
Q

Disorders of puberst, causing Precocious puberty?

A
  • Central, Gondaotropin dependent
    • Idiopathic
    • Hypothalamic hamartoma or other lesions
    • CNS tumor or inflammatory state
  • Perfipheral, GnRH- independent (precocious pseudopuberty)
    • Isosexual sexual precocity
    • Heterosexual sexual precocity
  • -> gynecomastia
86
Q

Causes of Isosexual sexual precocity?

A
  • Congenital adrenal hyperplasia
  • hCG- secreting tumor
  • McCune- Albright syndrome
  • Activating LH receptor mutation
  • Exogenous androgens
87
Q

Causes of Heterosexual sexual precocity?

A
  • Estrogen producing tumor
  • Familial aromatase excess
  • Marijuana smoking
  • Germ cell tumors - secrete hCG
88
Q

Causes of delayed puberty, GnRH dependent?

A
  • Idiopathic
    • Sporadic or familial (associated with constitutional growth delay)
  • Chronic diseases
    • Malnutrition, anemia, acidosis, anorexia nervosa, cystic fibrosis, chronic renal insufficiency
  • Psychosocial deprivation
  • Hypothalamic- pituitary causes:
    • Congenital disorders: GnRH receptor mutation, adrenal hypoplasia, Kalmann syndrome.
    • Acquired with other pituitary hormone deficinecies: Pituitary tumors, cranial irradiation, granulomatous disease, hemosiderosis.
89
Q

Causes of delayed puberty, GnRH independent?

A
  • Congenital:
    • Anorchia
    • Chromosomal abnormalties: Klinefelter syndrome, Noonan’s syndrome
  • Acquired:
    • Autoimmune inflammation (APS)
    • Orchitis
    • Bilateral undescendent testes or anorchia
    • Radio- or chemotherapy
    • Trauma
    • Surgery
90
Q

Which are the primary congenital disorders of male reproductive functions during adulthood?

A
  • Klinefelter’s syndrome
  • Noonan’s syndrome
  • Inborn errors of testosterone biosynthesis
  • Androgen resistance states
91
Q

Primary acquired disorders of male reproductive functions during adulthood?

A
  • Undescended testes
  • Bilateral torsion of the testes
  • Bilateral orchitis
  • Orchidectomy
  • Gonadal toxins (radio- and chemotherapy)
  • Acute and chronic systemic disease
92
Q

Secondary congenital disorders of male reproductive functions during adulthood?

A
  • Isolated GnRH deficiency
  • Isolated LH deficiency
  • Prader- Willi syndrome
  • Laurence- Moon- Biedl syndrome
93
Q

Secondary acquired disorders of male reproductive functions during adulthood?

A
  • Piruitary tumors and infarct
  • Trauma
  • Craniopharyngioma
  • Hyperprolactinaemia (primary and secondary)
  • Haemochromatosis
  • Neurosarcoid
  • Ageing
94
Q

How much T do females produce in 24h?

A

300 mikrogram (25% in the ovary)

95
Q

Which androgens are produced by the ovary?

A

T, DTH and androstenedione

96
Q

Abnormalities associated with androgen excess seen in females?

A
  • Acne
  • Alopecia
  • Android obesity
  • Cardiovascular disease
  • Dyslipidemia
  • Glucose intolernace/ insulin resistance
  • Hirsutism
  • Hypertension
  • Infertility
  • Menstrual dysfunction
97
Q

Name three female reproductive disorders.

A
  • Premenstrual syndrome (PMS)
  • Dysmenorrhea (= painful menstruation)
  • Polycystic ovarian syndroma (PCOS)
98
Q

Definition PMS

A

Occurs prior to menstruation and is charachterized by irratibility, bloating, weight gain, breast tenderness and headaches.

99
Q

Primary dysmenorrhea

A

Is thought to resylt from periodic uterine contractions due to uterine PG. Pain can be accompanied by nausea and diarrhea.

100
Q

Secondary dysmenorrhea

A

Results from problems such as endometriosis or congenital anomalies.

101
Q

Polycystic ovrian syndrome (PCOS)

A

Characterized by anovulation and high circulating androgen, estrogen and LH. The ovaries are enlarged with many follicles undergoing atresia due to low FSH.

102
Q

What might PCOS result in?

A

Due to that high amount of estrogen is aromatized –> hirsutism and acne.

103
Q

Most common cause of hirsutism?

A

PCOS

104
Q

Clinical features PCOS?

A
  • Oligomenorrhoea
  • Anovulation
  • Hirstuism
  • Acne
  • Obesity
  • Hypertension
  • Glucose intolerance
  • Dyslipideamia
105
Q

Biochemical features seen in PCOS?

A
  • Increased LH:FSH in follicular phase
  • Increased prolactin
  • Increased testosterone
  • Low SHBG
  • Raised fasting insulin
  • Dyslipidaemia
    (- Increased DHEAS Androstenedione)
106
Q

Dynfunctions of which organs cause amenorrhea?

A

Dysfunctions of:

  • Hypothalamus
  • Pituitary
  • Ovaries
  • Uterus
  • Vagina
107
Q

Amenorrhea can be both primary and secondary. Give the definitions.

A

Primary: Absence of mearche by the age of 16.

Secondary: absence of menses from more than three cycle internals or six monthsin women who were previously menstruating.

108
Q

Cause of primary amenorrhea?

A
  • Chromosomal abnormalties : 45%
  • Physiologic delay of puberty : 25%
  • Müllerian agenesis : 15%
  • Transverse vaginal septum or imperforate hymen : 5%
  • Absent hypothalamic production of GnRH : 5%
  • Anorexia nervosa : 2%
  • Hypopituitarism : 2%
109
Q

Name the conditions where secondary amenorrhea can be seen?

A
  • Pregnancy
  • Anovulation
  • High PRL
  • Abnormality in the outflow tract
  • Destruction of uterine endometrium by curretage or chronic infections
110
Q

Definition of hirsutism.

A

The development of androgendependent terminal body hair in a woman in places in which terminal hair is normally not found.

111
Q

Definition hypertrichosis.

A

A diffuse increase in total body hair. It is not androgen dependent.

112
Q

Name the common causes of hypertrichosis.

A
  • Drugs
  • Systemic illness
    (hypothyroidsm, anorexia nervosa, malnutrition, porphyria, dermatomyositis)
  • Paraneoplastic syndrome in some cancers
113
Q

Common etiology of hirsutism.

A
  • Idiopathic hirsutism (47,7%)
  • PCOS (50%)
  • Ovarian testosterone producing tumour
  • Cushing’s syndrome
  • Congenital adrenal hyperplasia
114
Q

Clinical manifestation PCOS.

A
  • Hirsutism
  • Frontal balding
  • Acne
  • High serum androgen
  • Menstrual irregularity (oligo- or anovulation)
115
Q

Clinical manifestation idiopathic hirsutism.

A
  • Hirsutism
  • No other clinical abnormalties
  • No menstrual irregularity
  • May be a mild variant of PCOS
116
Q

Name the less common causes of hirsutism (2,3%).

A
  • Hyper- PRL
  • Drugs
  • CAH
  • Ovarian tumors
  • Adrenal tumors
  • Acromegaly
117
Q

How does obesity affect androgen production?

A

It causes and increase in the androgen production and clearance rates.

118
Q

Effect of hyperinsulinemia (female reproduction).

A

Hyperinsulinemia caises ovarian hyperandrogenism, by acting via theca- cell receptors for IGF-I.

Insulin also decreases serum SHBG.

119
Q

Diagnosis of hirsutism?

A
  • No labs. if long- standing mild to moderate hirsutism.
  • Testosterone: mild to moderate hirsutism.
  • DHEA-S in addition to T: if progressive hirsutism, irrgeular menses and any signs of virilization
  • Prolcatin, FSH, LH: if irregular menses
120
Q

Relation LH/ FSH in PCOS?

A

LH > FSH

121
Q

Level of prolactin in prolactinoma?

A

> 100- 200ng/ mL

122
Q

Definition of endometriosis.

A

Presence of endometrial tissue, including both endometrial glands and stoma outsde the lining of the uterine cavity.

123
Q

Most common sites of endometriosis?

A 
- Ovary: chocolate cyst
Peritoneum of the rectovaginal cul-de-sac of the Pouch of Douglas
- Uterosacral ligaments
- Sigmoid colon
- Broad ligament
124
Q

Less common sites of endometriosis?

A
  • Cervix
  • Round ligament
  • Urinary system: bladder, ureter
  • Umbilicus
  • Appendix
  • Laparotomy scars
  • Lung, brain etc.
125
Q

Name the signs and symptoms of endometriosis.

A
  • Chronic pelvic pain
  • Dysmenorrhea
  • Abnormal uterine bleeding
  • Dyspareunia
  • Infertility
  • Pelvic mass (endometrioma)
  • Misc: Tenesmus, hematuria, hemoptysis
126
Q

Name the risk factors of endometriosis.

A
  • Early menarche
  • Short menstrual cycle
  • Alcohol
  • Caffeine
127
Q

Name the protection factors of endometriosis.

A
  • Term pregnancy
  • Regular extercise
  • Smoking
128
Q

Mean age at time of diagnosis of endometriosis.

A

25- 30 years.

129
Q

Give a short description of the Implantation theory, retrograde menstruation.

A
  • Endometrial cells in menstrual fluid are capable of implating on peritoneal surfaces
  • Woman with endometriosis have higher volumes of reflux
  • Peritoneal endometrial cells recovered during menses can atach to and penetrate the peritoneum
  • Endometriosis is most commonly seen in dependent portions of pelvis.
  • Endometriosis occurs in patients with uterine outlet obstruction
  • Most woman have some degree of retrograde menstruation but only 6- 10% have endometriosis.
130
Q

Give a short description of the Coelemic metaplasia, transformation of embryonic tissue.

A
  • Peritoneal mesothelium, Müllerian epithelium and germinal epithelium may be derived from a common ambryonic tissue
  • Metaplastic change in the coelomic epithelium (peritoneum and pleura): spontaneous or induced.
131
Q

Supporting eviences of theory based on Coelemic metaplasia, transformation of embryonic tissue.

A
  • Endometriosis have been found in prepubertal girls
  • Pleural and pulmonary endometriosis
  • Endometriosis in men treated with high doses of estrogen
  • In vitro, ovarian surface epithelium can be induced by estradiol to form endometrial glands
  • Unusual sites such as knee, thumb, eye
132
Q

Name some theories in the pathogenesis of endometriosis.

A
  • Implantation theory, retrograd menstruation
  • Lymphatic and vascular dissemination theory
  • Coelomic metaplasia
  • Immune theory
  • Genetic theory
133
Q

Briefly describe the Lymphatic and vascular dissemination theory.

A

The theory may explain endometriosis in distant sites outside plevis eg. brain, colon.

134
Q

Briefly describe the Immune theory and mechanisms supporting the theory.

A
  • Not all women with seeding of menstrual debris into plevis develop endometriosis.
  • Evidence for decreased cellular immunity
  • Increased prevalence of humoral antibodies against endometrial tissue
  • INcreased number of macrophages –> promote disease by secreting a variety of cytokines and growth factors that stimulate endometriotic attachment, invation, proliferation and neovascularization.
135
Q

Briefly describe the Genetic theory.

A
  • First degree relatives have 6- 7 times higher risk.
  • Detoxification enzymes –> susceptibility to envionmental stimuli (dioxin)
  • Genes associated with malignant transformation (eg. tumor suppressor genes).
136
Q

Describe the molecular mechanism of endometriosis.

A

Estrogen production plays a key role in endometriosis.

  • Ovaries secrete estradiol
  • Aromatase in adipose tissue and skin
    - - Androstenedion –>Etrone –> Estradiol
  • Endometriotic tissue expresses a complete set of sterogenic genes, incl. aromatase-
    - - Cholesterol –> Estradiol

Pathophysiology (14 decks)

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