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  1. What are the actions of oestrogen on various parts of the reproductive tract?
    • Endometrium: Preovulatory, oestradiol stimulates mitotic proliferation and thickening of the glandular epithelium and the stroma.
    • Cervical mucus: Oestradiol stimulates the epithelium lining of the cypts of the cervix to secrete mucus.
    • Vagina: Oestrogen stimulates proliferation of vaginal epithelial cells (post puberty)
  2. Describe the role of cervical mucus and fertility. How does it change over time?
    • Secretory cells of the mucosa of the cervix produce a glycoprotein rich secretion, ~20-60 ml per day, called cervical mucus
    • This helps regulate fertility in humans as women are only fertile for 3-5 days ;
    • At ovulation, cervical mucus is more hospitable to sperm, less viscous and more alkaline
    • At other times, viscous mucus forms a cervical plug that physically impedes sperm penetration into the uterus/uterine tube prior to ovulation
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    • Day 0 = ovulation; chances of pregnancy greatly increased if you knew when this was
    • If intercourse was had exactly 2 days before ovulation, the probability of getting pregnancy is about 35%. If it is 4 days before ovulation it drops to 20%
    • And if you were poorly fertile the chances of fertilisation are minimal unless intercourse is on the right day- and day 0 happens the day after you are most fertile.
    • []
    • Where the 50th percentile is average
    • Progesterone appears after ovulation, and so we would see reduction in the volume of mucus, and reduced sperm penetration and a rise in body temperature
    • * Some women thought they could predict their fertility- and perhaps time intercourse in a contraceptive way by the rise in temperature- however the temperature rise occurs 2-3 days after ovulation and therefore was not a misleading gauge of fertility (as)
  3. Describe the actions of oestrogen and progestagen during the endometrial cycle
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    • They are important role of driving proliferation of the endometrium; oestrogen is a powerful mitogen of the endometrium and allows it to grow much thicker until ovulation and production of progestagen by the corpus luteum
  4. How can cervical mucus be used to gauge the fertility of a woman?
    Two fancy german words
    • Spinnbarkeit: This is the stretchiness of the cervical mucus. It should be almost elastic and may stretch 10 cm or more (Spinnbarkeit is German for viscosity, ability to form a thread). It can be used as a gauge of when a woman is most fertile through maximum “stretchiness”
    • Ferning: When the cervical mucus dries on a microscope slide, it should take on the appearance of ferns. This assures that the mucus has been exposed to adequate levels of estrogen without any exposure to progesterone
    • Mittelschmerz: The small amount of blood that sometimes leaks into the pelvic cavity from the ruptured follicle can cause pain, known as mittelschmerz (pain in the middle). 20% of women feel this
  5. What are progestagens and their functions?
    • Progesterone is the major steroidal hormone of the corpus luteum and of the placenta. The hormone of pregnancy; as the placenta once there is a pregnancy will start making enormous amounts of progesterone
    • This is the hormone which is most different between the sexes, as males don’t have any in circulation (- nitty gritty fact they produce some but it never leaves the cell), and women have high levels of progesterone but only post-ovulation or during pregnancy.
    • Functions; it prepares the reproductive tract for implantation and the maintenance of pregnancy
  6. *Describe the potency and abundance of progestagens; Including serum levels during the menstrual cycle
    • Outside of the post-ovulatory phase of the menstrual cycle and of pregnancy, only small amounts of progesterone (mainly originating from the adrenal cortex) are present in the circulation.
    • Potency: Progesterone (P)(100%) > 17α-Hydroxyprogesterone (17α-OHP) (40-70%) > 20α-Hydroxyprogesterone (20α-OHP) (5%)

    • Serum levels of progesterone during the menstrual cycle;
    • • Pre-ovulatory: < 4 nmol/L
    • • LH surge causing a rise: <4-10 nmol="" l="" br="">• Post-ovulation (mid luteal phase) which is the peak: 25-120 nmol/L
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  7. Outline the principle properties of progestagens (6)
    • Endometrial action (secretory phase)
    • Maintain thick endometrial layer of uterus during pregnancy-
    • Action on cervical mucus
    • Stimulate growth of mammary glands, but suppresses secretion of milk- and when the placenta is delivered the negative feedback is lost and lactation occurs
    • Regulate secretion of gonadotrophins
    • General mild catabolic effect/CNS and thermoregulation
  8. Give the actions of progesterone on the reproductive tract
    Progesterone appears after ovulation, and so we would see reduction in the volume of mucus, and reduced sperm penetration and a rise in body temperature. Different tissues → different functions

    • Endometrium:
    • • Reduces mitotic proliferation
    • • Increased water content and vascularity of the stroma
    • • The endometrium becomes more secretory and stable
    • I.e. it gives the best environment for the embryo to implant- thick and secretory

    • Cervical mucus:
    • • Inhibits cervical mucus secretion (a characteristic utilised by progesterone-only pills in low doses causing a thickening of cervical mucus and decreasing penetration- high doses inhibit ovulation)
  9. Name the labeled structures of the undifferentiated external genitalia
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    • Genital tubercle (red)
    • Glans area
    • Urethral folds
    • Urethral groove
    • Labioscrotal swelling
    • Urogenital sinus
    • Perineum
    • Anus
  10. How does female external genitalia differentiation occur?
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    • The male and female external genitalia develop from a single bipotential precursor.
    • The urethral folds and labioscrotal swellings remain separate, thus forming the labia minora and majora. The genital tubercle (glans area) forms the clitoris.
  11. How does male external genitalia differentiation occur?
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    • The male and female external genitalia develop from a single bipotential precursor.
    • Fusion of the urethral folds enclosing the urethral tube forming the shaft of the penis. Labioscrotal swellings fuse in the midline forming the scrotum. The genital tubercle (glans area) expands forming the glans penis.
    • Androgens induce this differentiation
  12. What is the climacteric? What is the menopause? Why do they occur?
    • Menopause: Final cessation of menstruation – the last menstrual period, which on average is at 50 years. It is characterised by;
    • - Menstrual disturbance; associated with anovulatory cycles then amenorrhoea
    • - Vasomotor Symptoms; hot flushes, night sweats
    • - Genitourinary symptoms; vaginal and urethral dryness, atrophy
    • - Other possible symptoms; mood change, lower libido, joint pains, hirsutism

    • Climacteric or Perimenopause: Years around the menopause characterized by hormonal changes. Most women experience a variety of clinical symptoms of oestrogen deprivation during perimenopause;
    • - Bone metabolism: osteoporosis
    • - Behavioural/Psychological changes: depression, tension, anxiety, mental confusion loss of libido
    • The menopause is the consequence of the ovaries running out of follicles. There is a steady decline of follicles, with puberty (~400,000), through to menopause (<1000 follicles
    • - Decrease circulating oestrogens and increase FSH & LH
  13. What happens to circulating FSH, LH and oestrogen levels during and after the menopause?
    • The amount of oestrogen produced daily is less than one-tenth of what she produced in earlier years in the late preovulatory phase of her menstrual cycle.
    • - most is from extraglandular production, mainly from aromatisation in the stromal cells of adipose tissue of androstenedione secreted by the adrenal cortex.
    • - Oestrone is the product of this aromatisation. It is only weakly oestrogenic having approximately one-tenth the biological activity of oestradiol.
    • In response to this deficit, the hypothalamus produces gonadotrophin releasing hormones, and LH and FSH levels rise in attempt to promote oestragen production. But no ovaries.
  14. Most falls in older people result from multiple contributing factors.
    (a) Discuss the factors that may have contributed to Mrs Davies’ fall. (3 minutes)
    (b) What factors, in addition to age, may contribute to proximal leg weakness in older people? (3 minutes)
    • (a) 10% are related to loss of consciousness or dizziness
    • - Polypharmacy (the use of 5 or more medications) in elderly, can lead to drugs causing postural hypotension; sedation; arrhythmia, parkinsonism (e.g., tricyclics, neuroleptics, including metoclopramide and prochlorperazine, as well as alcohol).
    • - Cognitive impairment: delirium and dementia
    • - and many others along the lines of functionality; mobility, sensory impairment, strength and ability to grip etc.
    • (b) Exercise can ameliorate many of these losses substantially and help preserve function and independence. Exercise also helps treat and prevent and treat osteoporosis. Other factors include;
    • - Immobility
    • - Prolonged inpatient stay
    • - ICU stay
    • - Increasing age
    • - Nutritional status
    • - Muscular atrophy; through disuse and avoidance (for instance due to arthritis or general fatigue associated with ageing), demyelinisation
  15. What is Osteoporosis?
    What factors other than age and a family history could increase Jackie's risk of osteoporosis? (5 mins)
    • Osteoporosis: a loss of bone mass and/or microarchitecture associated with an increased risk of fracture
    • # Risk factors
    • Menopause: Increased bone resorption by osteoclasts with oestrogen deficiency
    • - On average women lose 2% of their bone mass each year for first 5 years after the menopause due to low oestrogen levels
    • Muscular atrophy through disuse and avoidance (for instance due to arthritis or general fatigue associated with ageing), demyelinisation
    • Calcium and vitamin D intakes are determinants because of their role in bone homeostasis (Their supplementation may help hinder osteoporotic development);
    • - calcium from the bones can be mobilized to maintain calcium plasma concentration, and
    • - vitamin D synthesis promotes intestinal calcium absorption and bone mineralization.
    • Other disorders: Primary hyperparathyroidism, T1DM, T2DM
    • - Smoking and alcohol abuse, immobilisation, drugs
  16. What ways can you manage people at risk of osteoporosis?
    • Nondrug strategies to reduce bone loss in postmenopausal women include;
    • - a diet adequate in calcium and vitamin D,
    • - weight-bearing exercise,
    • - cessation of smoking.
    • In addition, patients at risk for osteoporosis should avoid drugs that increase bone loss such as glucocorticoids (decrease Ca absorb from gut).
    • #
    • Drugs: Bisphosphonates are analogs of pyrophosphate. They decrease osteoclastic bone resorption via several mechanisms, including,
    • 1) decrease in osteoclastic formation/activation,
    • 2) increase in osteoclastic apoptosis (programmed cell death), and
    • 3) inhibition of the cholesterol biosynthetic pathway important for osteoclast function.
    • The decrease in osteoclastic bone resorption results in a small but significant net gain in bone mass in osteoporotic patients, because the bone-forming osteoblasts are not inhibited.
    • It also decreases the risk of bone fracture in patients with osteoporosis
  17. Loss of muscle strength is likely to have been a significant factor contributing to Jackie's mother's fall.
    (a) What changes occur in muscle with increasing age?
    (b) What factors other than age can lead to increasing muscle weakness in people 80 years and over?
    • Unless an active effort is made to sustain it, muscle mass and strength declines with age. This is called sarcopenia.
    • - also includes fatty infiltration within the sarcopenic muscle, a decrease in muscle protein synthesis, and impaired postprandial fate of amino acids.
    • #
    • Factors: malnutrition and weight loss in the elderly affects lean mass (mainly muscle) and water reserves more than fat mass.
    • - Aging is associated with a physiological anorexia , where food intake gradually diminishes with age. A decreased appetite is influenced by multiple physiological changes; perhaps decreased energy needs due to reduced physical activity, but consider decreased ability to recover/build muscle.
    • - Physiological causes for sarcopenia include; increase in the production of proinflammatory cytokines, leading to a hypercatabolic state, decrease in the synthesis of testosterone and oestrogen causing a decrease in muscle anabolic potential
    • - With aging, increased fat mass promotes insulin resistance and a decline in the anabolic effect of insulin, potentially predisposing to sarcopenia.
    • - early satiety develops with age, related to gastrointestinal changes (delayed gastric emptying and altered gastric distension), which can all contribute to anorexia.
    • - Physical activity has positive effects on osteoporosis and sarcopenia progression.
    • - psychosocial factors; financial difficulty in buying food, and loneliness, and psychiatric factors such as depression and dementia.
    • - Medication side-effects which may affect appetite regulation.
  18. List 2 effects of oestrogen and 2 effects of progestogen that are particularly relevant to HRT. (5 minutes)
    What kind of HRT will Jackie's GP probably prescribe, oestrogen alone, progestogen alone or oestrogen plus progestogen? Explain the reasons for your decision.
    • Estrogen: decreases the resorption of bone from osteoclasts, helping prevent osteoporosis
    • - treatment reestablishes feedback on hypothalamic control of norepinephrine secretion, leading to decreased frequency of “hot flushes.”
    • Progesterone: acts to reduce mitotic proliferation of the endometrium
    • - Inhibits cervical mucus secretion (thickening cervical mucus)
    • #
    • Most likely progesterone + oestrogen , as progesterone helps reduce the risk of endometrial carcinoma associated with unopposed estrogen.
    • - No uterus, you would go oestrogen only as progestins may unfavorably alter the beneficial effects of estrogen
  19. In 2003 the National Health Committee set out eight criteria it believed should be considered when deciding whether to introduce an organised population-based screening programme. Using these criteria, briefly explain why a national prostate screening programme is not currently recommended in New Zealand.
    • 99% are adenocarcinomas, many are harmless and it is hard to detect cancers that won't cause death.
    • - e.g. About a third of men in their 4th and 5th decades have histologically evident prostate cancer – mainly well differentiated and microscopic. But clinically significant tumours are likely to be larger and higher grade
    • Screening can therefore detect many prostate cancers that won’t cause death
    • - means that there is opportunistic PSA (and DRE) screening, but recall this can lead to harm from unnesessary treatment; think the thyroid cancer surgeries which haven't decreased mortality

    • suitable condition worth screening
    • suitable test
    • intervention (subsequent)
    • Quality of evidence, RCTs
    • Benefit vs. harm
    • If a follow-up is required, is this possible
    • Social and ethical considerations
    • Cost of the screening intervention
  20. What are two potential fates of testosterone at the testis?
    • To Dihydrotestosterone (5α-DHT) via enzyme 5α-reductase
    • To Oestradiol via enzyme aromatase
  21. Distinguish between 1o and 2o hypogonadism
    • Primary hypogonadism: from direct dysfunctional testis. Low testosterone and LH and FSH likely high
    • - causes include surgery, radiation, autoimmunity etc.
    • - examples include Klinefelter's syndrome
    • Secondary hypogonadism: Pubertal delay/absence, where we expect low levels of GnRH, LH and FSH and Testosterone
    • - Loss of secondary sex characteristics
    • - causes include pituitary tumours, Kallmann syndrome
    • Therapy = GnRH or T depending on source of deficiency
  22. What is seen in PCOS? Give some potential treatments for PCOS
    • no large follicle selected for ovulation, hence no increase Oestragen or LH surge
    • follicle granulosa cell apoptosis decreased plus thecal tissue hypertrophy → increased androgens
    • #
    • Treatments include;
    • - clomiphene – blocks oestrogenR and may increase FSH; also used in ovulation induction
    • - Metformin - reduces insulin - may reduce androgens
    • - surgical sectioning or drilling of ovary
    • - IVF
    • - reduce obesity
  23. Outline the different fates of cells from the Morula/blastocyst
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    • The position of cells in the morula determines their cell fate i.e.;
    • - Cells of the inner cell mass (ICM) are destined to form the foetus
    • - Cellls of the outer typotrophic layer go on to form the placenta
    • #
    • Cells of the ICM are destined for;
    • → epiblast → embryo and amnionic membrane
    • → hypoblast → primitive yolk sav, and extraembryonic mesoderm
    • Cells of the trophoblast
    • → cytotrophoblast and syncitiotrophoblast → chorion = foetal part of placenta
  24. What methods can be used to screen the foetus for abnormalities?
    • * all methods guided by ultrasound so you don't stab the developing foetus
    • Amniocentesis: to remove amnionic fluid after 14 weeks with a big needle
    • - it is part of foetal tissue, so can do genetic testing on it
    • Chorionic villi sampling: a transabdominal/vaginal needle to remove villus tissue
    • - can be done earlier (10-12 weeks)
  25. * What are the maternal immune adaptations during pregnancy? Give two reasons
    • The placenta is genetically foreign to the mother’s immune system. It is in intimate contact with large amounts of maternal blood, and large numbers of immune cells in the decidua. Why then is it not rejected?
    • • The placenta hides itself from the immune system.
    • Trophoblasts alter the profile of cytokines secreted from immune cells in order to dampen down the mothers immune system.
  26. Changes in the function of T cells found within the uterine tissues at the fetal interface.
    • High levels of pregnancy hormones; Helper T cells decline relative to suppressor cells, and the classes of immunoglobulin produced change their balance.
    • A further possibility is that a more dramatic local immune regulation occurs in the close vicinity of the conceptus. Among the population of leucocytes in the uterus, natural killer (NK) cells predominate. By contrast, T cells are sparse in the decidua and it is uncertain whether these decidual T cells recognize the antigens expressed by invading trophoblast.
    • - Even if they do, they appear to be relatively anergic either because of specific tolerance or because of some unique property of the local environment. There is circumstantial evidence that high local levels of progesterone, corticosteroids and/or chorionic gonadotrophin might modulate local responsiveness
  27. How does the placenta hides itself from the immune system?
    • Trophoblasts do not express class I (HLA-A and B) and class II MHC, which ‘hides’ the placenta from the maternal immune system.
    • Trophoblast express a unique combination of HLA-C (class Ia), HLA-G and HLA-E (class Ib) MHC molecules, which actively help the placenta avoid immune attack.
    • HLA-G can interact with receptors on cytotoxic T lymphocytes and natural killer cells, inhibiting their ability to induce cell lysis.
  28. How does the fetus dampen down the mothers immune system?
    • The syncytiotrophoblast is an epithelial layer that constantly sheds into the mothers circulation.
    • This ‘trophoblast debris’ interacts with endothelial cells and macrophages in the maternal circulation.
    • This may play an important role in inducing maternal immunotolerance of the placenta/fetus.
  29. What are the foetal and parental components of the placenta?
    • Parental: The decidua underlying the implanatation site is called the decidua basalis
    • The decidua overlying the implantation site is called the decidua capsularis
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    • Foetal: Chorion frondosum & amnionic membrane
  30. Describe the blood vessels of the placenta, and the sub-divisions
    • There are 2 arteries and 1 vein
    • The 2 arteries going from the foetal heart carry deoxygenated blood
    • The vein carries oxygenated blood from the placenta to the systems
    • Subdivisions of the placenta = lobes
  31. What is the main component of the placenta? Function?
    • Wharton's jelly: containing mainly hyaluronic acid and proteoglycans
    • Protects from tieing up and occluding blood flow
  32. Describe the structure of the placenta.
    What is the function of these features?
    • Fetal, outer part of trophoblast cells called the chorion
    • Maternal, endometrium below the chorion is called decidua
    • Chorionic villi – extending from chorion into endometrium
    • Villi are the fetal component of the placenta. The villus is the site of gas exchange. It contains foetal blood vessels and is part of the foetal chorionic placenta
    • A single placenta is formed and is discoid in shape - approx 20cm across, 500gm
  33. What are some physical features of the placenta and the blood-oxygen interface? (3 major differences from adult lungs)
    • Haemochorial - fetal chorionic epithelium (villi) is bathed in maternal blood. Villi protrude into placental lacunae aka. intervillus spaces
    • 50-80 finger-like capillaries which project into maternal blood pools (lacunae), maternal arterial blood is ejected into the pool via spiral arteries and drained out via veins.
    • Compared to the adult lung, minimum diffusion distance is large 3.5 microns vs 0.5 microns, and gas permeability poor (incomplete equilibration between maternal and fetal blood in the placental exchange area)
    • Total surface area is 16m2 vs 50-60 m2
  34. What are the functions of the placenta (3)?
    • Transport of oxygen and nutrients, waste removal.
    • Endocrine organ for maintenance of pregnancy and fetal development.
    • Barrier to prevent immunologic attack by mum.
  35. Describe the structure of the umbilical vessels to and from the placenta
    • Two arteries take blood to the placenta from the heart (deoxygenated blood –artery)
    • One vein takes blood back to the heart from the placenta (oxygenated blood –vein)
    • It is surrounded by mesenchymal tissue (Wharton’s Jelly) which acts as a protective buffer
  36. Describe the structure of the amniotic sac
    • The amniotic sac is a tough but thin transparent pair of membranes (amnion and chorion), which hold a developing embryo (and later fetus – an embryo becomes a fetus after 12 weeks) until birth.
    • Amnion: The inner membrane which contains the amniotic fluid and the fetus.
    • Chorion: The outer membrane which contains the amnion and is part of the placenta.
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  37. What is the purpose of the amniotic fluid (5)?
    • Hydraulic brace – protective buffer.
    • Permits movements, fetal breathing movements.
    • Fluid reservoir – blood volume, electrolyte balance, fetal and maternal fluid balance
    • Helps maintain temperature
    • Nutrient reservoir – swallowing.
  38. What is the composition of amniotic fluid?
    • Fetal urine is the primary constituent which consists mainly of water (very hypotonic)
    • The remainder is; electrolytes, urea and bile pigments (fetal poo – meconium), glucose, paracrine products, fetal and placental cells.
  39. How is amniotic fluid formed?
    • Input: Urine, Lung liquid, Oral-nasal
    • Output: Swallowing, Absorption into fetus across skin and cord (intramembranous), Absorption into mum (transmembranous)
    • Volume peaks around 33 weeks at around 800-1000ml. It then decreases by 100-150ml per week
    • At term gestation volume is around 400-600ml. But 980-1000ml goes in and out.
  40. What is the term for excess amniotic fluid production? What are the consequences?
    • Polyhyramnios: Can cause mum to have cardio-respiratory problems, and to cause placental abruption, fetal hypoxia, and death.
    • Causes are generally unknown, but can include maternal diabetes which increases fetal glucose which in turn increases fetal urination.
  41. What is the term for reduced urine production? What are the consequences?
    • Oligohydramnios: Can cause fetal hypoxia through cord compression which can cause injury and death, and tightening of amniotic membranes across fetal tissues
    • This can result in loss of tissue or reduced or malformed limb growth. Causes are variable, but include diseases such as bilateral renal agenesis (a.k.a; Potter’s syndrome).
  42. Bioethically, when should you consider when in a situation to withhold or withdraw life-sustaining treatment in the newborn?
    • #
    • Futility: how pointless is the treatment? What is the chance that it works and is the cost worth the risk (considering sustainability of healthcare system)?
    • Awaiting certainty: Are we at a point where we can determine the chances? Is this point a reality?
    • Individualised prognosis: What is the present quality of life? What is the future quality of life?
    • Blanket prohibitions: Limits on how much we will spend and how long we'll wait before the plug is pulled
    • #
    • Consider the bioethical principles;
    • - Distributive Justice
    • - Non-malificence
    • - Beneficience
    • - Autonomy: Consider who needs to be included in the discussion. Parents, GP, others??
    • #
    • Consider how the information is communicated;
    • - when
    • - language; layperson? moral strangers?
    • - to who, and what state they're in
    • - honesty, respect, thorough and considerate. As opposed to confusing, incomplete, evasive, hurried or dismissive
  43. What are some tells for Paediatric Developmental Red Flags?
    Give some key examples of disorders you should look out for
    • Developmental Assessment: functionality of the different modalities; visual and sensory
    • General Observations: Dysmorphic Features i.e. what does the child look like.
    • #For these conditions, consider what clues there would be
    • Down syndrome
    • Hydrocephalus
    • Achondroplasia
    • Cyanotic baby with congenital heart defect
  44. Describe the development of the mammary gland pre-puberty, at puberty, Menstrual cycle, pregnancy and with lactation
    Also give the hormones which contribute to gland development at each stage
    • Prepubertal: early duct growth, limited branching
    • – occasional perinatal (i.e. in foetus) activation by maternal hormones
    • Puberty: branching of ducts, deposition of adipose tissue, development of two layered epithelium (secretory cells
    • and myoepithelium)
    • – sex steroid (particularly estrogen) induction of branching
    • - Menstrual cycle; there are cyclical changes in breast tissue in response to hormones, growth and regression. Also increase in breast size from fat deposition. Changes include; cyclical changes in estrogen and progesterone, increased blood flow and lobular oedaema during luteal phase
    • Pregnancy: duct sprouting and branching, loss of adipose tissue, lobule formation, little/no secretion
    • – estrogen, progesterone, and prolactin/placental lactogen; lactogenic hormones required for lobular development
    • Lactation: full alveolar development, copious milk secretion
    • – prolactin required for continued milk secretion
  45. Outline the hormonal changes associated with pregnancy and lactation
    • Although the breasts are able to begin milk secretion by month 4 of pregnancy, copious milk secretion characterizing full lactation does not occur until after parturition. Why?
    • - The disappearance of oestrogen and progesterone,
    • - and perhaps also of human placental lactogen (hPL),
    • from the maternal circulation occurring at or soon after parturition holds the key to the initiation of lactation (lactogenesis).
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    • Although prolactin increases in plasma concentration throughout pregnancy and reaches a maximum at term, the breast is simply not responsive to it until after steroid levels, particularly progesterone, fall. The steroids, helped perhaps by hPL, appear to inhibit milk secretion by acting directly on mammary tissue, probably on the alveolar cells.
  46. Describe how lactogenesis (i.e. initiation of milk secretion) starts and is sustained
    • After parturition, prolactin levels also fall but more slowly. In the absence of suckling, the newly initiated milk secretion will last for only 3 or 4 weeks (as prolactin levels come down from elevation).
    • However, if prolactin levels are to remain elevated and full lactation is to continue with copious milk secretion (lactopoiesis), nipple stimulation by suckling is essential.
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    • Suckling achieves this release of prolactin from the anterior lobe of the pituitary via a neuroendocrine reflex (i.e. reduction in dopamine → increase prolactin).
    • Furthermore, this reflex causes increased release of oxytocin → contraction of myoepithelial cells of the lactiniferous glands
  47. How does weaning and the cessation of lactation occur?
    • Reduced stimulation of milk synthesis (suckling stimulus)
    • Distention and engorgement of mammary gland
    • Compression of blood vessels, hypoxia
    • Resorption of secreted material, and collapse of alveoli
    • Loss of glandular elements, increase in fat deposition
    • Full regression of the gland may take 2-3 months
  48. Give the steps, stages and symptoms of labour
    • The process of labour is divided into three stages.
    • The first stage: begins with its onset (regular painful contractions, and dilation and shortening of the cervix) and ends when the uterine cervix is fully dilated to become one continuous birth canal.
    • - Spontaneous Rupture of Membranes (SROM); i.e. ‘breaking of the waters’, happens when the amniotic sac (which surrounds the baby) ruptures, resulting in amniotic fluid trickling or gushing from your vagina.
    • - increase prostaglandin synthesis, myometrial gap junction (strengthen muscle?) and oxytocin receptor formation
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    • The second stage of labour: begins at full dilation of the cervix and ends with complete delivery of the fetus.
    • The third stage: begins with completion of fetal expulsion and ends with delivery of the placenta.
  49. What are some psychosocial take-home messages for menopause?
    • Negative attitudes towards menopause = more symptoms
    • Stressful vs. Non-Stressful Conditions: Under stress, more hot flushes objectively (electrodermal changes) + subjectively
    • - i.e. The way that a woman enters menopause affects her experience
    • Despression: there is an increased risk of developing in the peri- and early postmenopausal stages.
    • - A life-stage perspective (i.e. menopause is a natural life course) is useful for understanding mood disorders as well as hormonal changes.
    • Sexual function: deteriorates with the menopausal transition and aging.
    • - can be painful plus physiological issues
  50. Describe the stages of the PLISSIT model, state examples of how you would use this model at each stage, and describe why you would use this model
    • The PLISSIT model, also known as the PLISSIT model of sex therapy, is a modeling system used in the field of sexology to determine the different levels of intervention for individual clients.
    • Importance: Sexual well being is important for physical and mental health.
    • - A minority of patients will seek help – if you don’t ask, they won’t tell.
    • - Patients may be embarrassed and uncertain about whether sexual concerns are legitimate.
    • - Importance of gaining comprehensive healthcare from physician e.g. PDE5s are available on the internet → sideeffects.
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    • The letters of the name refer to the four different levels of intervention that a sexologist can apply;
    • Permission (P): many clients only require the permission to speak and voice their concerns about sexual issues in order to understand and move past them, often without needing the other levels of the model.
    • Limited information (LI): client is supplied with limited and specific information on the topics of discussion, so that organizations, and support groups for those specific subjects can be provided
    • Specific suggestions (SS): suggestions related to the specific situations and assignments to do in order to help the client fix the mental or health problem. This can include;
    • - suggestions on how to deal with sex related diseases or
    • - information on how to better achieve sexual satisfaction by the client changing their sexual behavior.
    • The suggestions may be as simple as recommending exercise or can involve specific regimens of activity or medications
    • Intensive therapy (IT): refer the client to other mental and medical health professionals that can help the client deal with the deeper, underlying issues and concerns being expressed.
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  51. Describe typical sexual behaviour during Primary School (6-10 years)
    • • Secrecy
    • • Sexual talk, giggling
    • • Exhibitionist and intrusive behaviours tended to decrease
    • • Retrospective recall suggests mutual sexual experiences – showing and touching genitals, sexual games
  52. Describe changes in sexuality during older age.
    • Social expectations/sexual culture
    • Lack of education, knowledge
    • Medical and surgical interventions
    • Physiological changes
    • Illness, disability, pain
    • Medications
    • Tiredness
    • Loss of partner
    • Residential care
    • #
    • Older Age: Women
    • • Slowness and reduction in vaginal lubrication and vasocongestion
    • • Less erotic response to vulvar, clitoral, breast, and nipple stimulation
    • • Diminished sex drive
    • • Fewer sexual fantasies and preoccupations
    • • Sensations of genital stimulation changes
    • • Orgasms may take longer, feel less intense
    • • Ovarian production of hormones diminishes: estradiol 85%, estrone 58%, testosterone 29%.
    • • Labia and clitoris shrink
    • • Vaginal tissue thins
    • • Changes to pelvic floor
    • #
    • Older Age: Men
    • • Decrease in sex drive and changes in erections
    • • Fewer spontaneous erection, less firm, less certain, longer refractory period.
    • • Changes in ejaculation – less sense of imminence, intensity, changes in sensation, volume.
    • • No dramatic decrease in testosterone, part of a larger physiological process involving endocrine changes, loss of cellular receptors for androgen, loss of enzymatic activity that converts testosterone into usable form + unknown factors.
    • • Risk factors for erectile difficulties: smoking, hypertension, obesity, abnormal lipids, diabetes.
    • • More direct stimulation of penis needed
  53. What stages of the sexual response model exist, from which is referred to in the DSM 5? Give criticisms
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    • Criticism of the sexual response cycle:
    • - Biologically based
    • - Linear
    • - Neglects psychosocial factors and life stages such as parenting and menopause
    • - Male-centric?
    • - Sexual satisfaction ≠ orgasm
    • - Coital based
    • - Subjective arousal ≠ objective arousal
    • - Neglects multiple motivations for sex
  54. Recognise the disorders of each stage of the sexual response model as contained in the DSM 5 for males.
    • Male hypoactive sexual desire disorder: Persistently or recurrently deficient (or absent) sexual/erotic thoughts or fantasies and desire for sexual activity. The judgement of deficiency is made by the clinician, taking into account factors that affect sexual functioning, such as age and general and socio-cultural contexts of the individual’s life.
    • Delayed ejaculation
    • Erectile disorder
    • Premature (early) ejaculation
    • Substance / medication induced sexual dysfunction
  55. Recognise the disorders of each stage of the sexual response model as contained in the DSM 5 for females.
    • Female sexual interest / arousal disorder: Absent/reduced interest in sexual activity, erotic thoughts or fantasies
    • - unresponsive to partner’s attempts to initiate
    • Female orgasmic disorder: Marked delay in, marked infrequency of, or absence of orgasm. Markedly reduced intensity of orgasmic sensations.
    • - Distress is a necessary criterion.
    • Genito-pelvic pain /penetration disorder
    • Substance / medication induced sexual dysfunction
  56. State the five “additional criteria” stated in the DSM-5 and give examples.
    • Partner factors (e.g., partner’s sexual problems; partner’s health status)
    • Relationship factors (e.g. communication)
    • Individual vulnerability factors, psychiatric comorbidity, or stressors (e.g. depression, job loss, poor body image, abuse hx)
    • Cultural or religious factors
    • Medical factors relevant to prognosis, course, or treatment
  57. Understand the biopsychosocial sexual response model.
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    • Signal: Signal Presence (external or internal) and Reception Capacity (Psychological or Biological)
    • #
    • Evaluation:
    • - Present (switch): do I have a partner, setting/other obligations, time, energy etc
    • - Proximate (switch): ongoing life issues (health, family, work)
    • - Past (circuit breakers): Knowledge about sex, Personal beliefs and values, Past sexual experiences, Attitudes and expectations about sex and relationships
    • #
    • Interest: Drive + Wish + Motivation
    • - Drive = Sexual desire (spontaneous and responsive), Wish = For closeness, affection, sensual touch and Motivation = A deliberate choice to be sexual
    • #
    • Response: Physical capacity to respond (anatomical, neurological, physiological, vascular), no pain, no medication impediment.
    • #
    • Outcome: Physical and Emotional
    • #
    • Feedback Loop: Negative = Avoidance and Positive = Repetition
  58. Describe and give examples of general etiological mechanisms whereby sexual difficulties are associated with physical and mental health problems.
    • Direct effects of vascular, neurological (including pain), hormonal, anatomical, or other damage to an area functionally connected to sexual response.
    • Indirect effects of a medical or psychiatric condition, such as changes to perception or judgement, mood or behavioural volatility, sensory or motor alterations, bladder and bowel incontinence, spasticity, tremor, fatigue, anxiety, depression, chronic pain, and so on.
    • Iatrogenic effects of treatment e.g. radiation, surgery, medication
    • Contextual effects i.e. due to biopsychosocial complexity and situational components
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RDA Content
2015-10-16 02:02:11

Identify and evaluate the ethical issues that may arise in reproduction, development and aging. Describe the structure and function of the reproductive system. Describe the physiological and psychological changes that occur during pregnancy, parturition and lactation. Describe the normal human development from fertilisation to birth and identify points of vulnerability. Describe normal growth and development from birth through adolescence to adulthood. Describe common patterns of sexual development behaviours and how these impact on sexual health. Develop skills of communication to be able to comfortably and appropriately discuss issues relating to reproduction, development and aging, including sexual health. To describe the process of aging and its impact on health and disease.
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