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BCS Flashcards

1
Q

What hormone do sertoli cells produce?

A

Anti-mullerian hormone

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2
Q

What hormone do leydig cells produce?

A

Testosterone

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3
Q

What is the key part of sex differentiation?

A

Y chromosome, SRY gene

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4
Q

What do the primoridal germ cells become?

A

Sperm in men, oocytes in women

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5
Q

What do the primitive sex cords become?

A

Sertoli cells (AMH) in men, Granulosa (estradiol) in women

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6
Q

What do the mesonephric cells become?

A

Leydig cells in men (testosterone), Theca cells in women (androsteriedione = substrate for estradiol)

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7
Q

What are the three ‘waves’ of cells that invade the genital ridge?

A

Primordial germ cells, primitive sex cords, mesonephric cells

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8
Q

Outline primordial germ cell migration

A
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9
Q

Outline primitve sex cord development - men and women

A
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10
Q

Outline roles and future development of mullerian and wolffian ducts

A

Men - wolffian - seminal vesicles and vas deferens Women - mullerian - uterine tubes, uterus, upper 1/3 of vagina

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11
Q

Outline the differentiation of the gonad in men and women, cells and hormones involved

A
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12
Q

What is the role of DHT in men?

A

Fusion of labial scrotal fold, growth of phallus and prostate

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13
Q

What does the lack of androgen in utero do in female development?

A

Leads to vagina, labia and clitoris

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14
Q

Define gonadal dysgenesis

A

Sex differentiation is incomplete or gonad development is abnormal

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15
Q

Describe partial and complete AIS - Int and external genitalia, role of hormones, effect at puberty

A

Puberty delayed in partial, absent if complete

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16
Q

What happens if XY,, makes testosterone, but it doesn’t work?

A

Androgen insensitivity syndrome

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17
Q

Whast happens if XY, testosterone is made but not DHT?

A

5 alpha reductase deficiency

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18
Q

Describe 5 alpha reductase deficiency - Int and external genitalia, role of hormones, effect at puberty

A
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19
Q

What happens if only 45 chromosomes XO

A

Turner syndrome (1:3000)

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20
Q

Describe Turner syndrome - Int and external genitalia, role of hormones, effect at puberty

A
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21
Q

What happens if XX exposed to high levels of androgens in utero?

A

Congenital adrenal hyperplasia (1:15,000)

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22
Q

Describe Congenital adrenal hyperplasia - Int and external genitalia, role of hormones, effect at puberty, difference between XX and XY

A

Pathway block so aldosterone and cortisol are not produced in sufficient quantities, more androgens produced - impact on XX genitalia

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23
Q

REVIEW events in sex differentiation with foetal ages

A
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24
Q

What is kisspeptin and how does it stimulate GnRH production? How many amino acids?

A
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25
Q

How many amino acids does GnRH have?

A

10

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26
Q

Describe the journey made by Kisspeptin and GnRH

A
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27
Q

Describe the importance of pulsaltile GnRH secretion - what is the significance of slow vs rapid frequency pulses?

A
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28
Q

What are the gonadotrophins and what are their structures?

A
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29
Q

What are the three sex steriods?

A

Estradiol (E2), Progesterone (P4), and Testosterone

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30
Q

Describe puberty changes in men and women

A
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31
Q

Describe process of adrenarche - what is happening? What is secreted? At what age is this occurring? Which adrenal steriods are involved? What triggers it?

A
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32
Q

What happens to DHEAS in the body?

A

Can be converted to testosterone / DHT

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33
Q

Describe pubarche - what is it? at what age is it considered early? What other changes are associated?

A
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34
Q

Review relationship between androgens and pilosebaceous units

A
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35
Q

Describe gonadarche - what is it? what is the relationship between gonadarche and foetal development? What triggers its start?

A
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36
Q

Describe epiphyseal fusion

A
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37
Q

What stimulates the onset of puberty? (3 theories)

A
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38
Q

Describe the biphasic effect of eastrogen on epiphyseal growth

A
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39
Q

Define consonance and outline normal progression for boys and girls

A
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40
Q

Review Tanner scale of pubertal development - outline stages 1-5 for boys and girls

A
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41
Q

What are the psychological changes that occur during puberty? (3)

A
  1. increasing need for independence 2. increasing sexual awareness / interest 3. development of sexual personality
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42
Q

How do you define a delay in puberty (what age in boys and girls?)

A

Absence of secondary signs in boys by 14yo and in girls at 13yo (or absence of menarche by 18)

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43
Q

Outline causes of pubertal delay

A
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44
Q

Describe McCune Albright syndrome - symptoms

A
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45
Q

Central precocious puberty - what causes it? is consonance maintained? How do you manage it?

A
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46
Q

What causes 33% of cases of central precocious puberty?

A
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47
Q

Peripheral precocious puberty - what causes it? is consonance maintained? How do you manage it?

A
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48
Q

What kind of cells become the egg and sperm?

A

Primordial germ cells

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49
Q

Describe the journey of germ cells to the gonad

A

First identifiable in yolk sac at 3 weeks, undergo many cycles of mitosis, migrate to genital ridge which becomes the gonads

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50
Q

What do germ cells become in the ovary? What are they called once mitosis stops?

A

Oogenia when in the ovary Primary oocytes once mitosis stops

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51
Q

How long does the primary oocyte remain in first phase of meiosis?

A

Until ovulated or it dies - so maybe 52 years

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52
Q

REVIEW mitosis

A
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53
Q

REVIEW meiosis

A
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54
Q

Describe the process of oogenisis and folliculogenesis

A
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55
Q

Where are the primary oocytes in the ovary?

A

Outer layer, cortex

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56
Q

What cells make up the primordial follicle?

A
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57
Q

What is the definition of folliculogenesis?

A

Growth and development of follicles from the early resting stages in foetus through ovulation

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58
Q

What layers are formed around the follicle as it grows? (2 more)

A

Zona pellucida (acellular) Theca cells

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59
Q

What stimulates the follicle growth process?

A
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60
Q

How are follicles generally classified?

A

Pre-antral (or primary), antral (or secondary), preovulatory / Graafian follicle, ovulatory

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61
Q

Are all follicles visible on ultrasound?

A

No, pre-antral follicles are not

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62
Q

Describe the processes of follicle initiation and recruitment

A
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63
Q

Outline the stages of follicle growth - how long does each phase take? how big are they? Is the process gonadotrophin-dependent?

A
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64
Q

Describe role of LH and FSH - what cells do they work on and what is the impact?

A
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65
Q

What is the feedback process of folliculogenesis? What hormones are involved?

A
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66
Q

REVIEW summary of follicle formation and growth

A
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67
Q

What should you consider if some is trying to get pregnant?

A

HIV / Hep B/STIs Haemoglobinopathy Folic acid - 400 mcg or 5mg Alcohol, smoking, drus Chronic disease management

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68
Q

REVIEW reliability stats on various contraceptives

A
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69
Q

Condoms - advantages and disadvantages

A
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70
Q

Caps - types, advantages and disadvantages

A
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71
Q

Fertility awareness - factors used, advantages and disadvantages

A
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72
Q

Combined oral contraception - types

A
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73
Q

Combined oral contraception - basic principles, roles of estrogen and progesterone

A
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74
Q

COCP - benefits

A

BENEFITS Reliable Safe Unrelated to coitus Woman in control Rapidly reversible Halve ca ovary Halve ca endometrium Helps endometriosis, premenstrual syndrome, dysmenorrhoea, menorrhagia Can stop periods if taken continuously

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75
Q

COCP - risks

A

Cardiovascular - Arterial – Progestogen , HBP, smoking (>15 and >35), Venous – Oestrogen-VTE-clotting disorders (DVT, PE, Migraine) Neoplastic - Breast, Cervix, Liver Gastrointestinal – COH/insulin metabolism, Weight gain, Crohn’s disease Hepatic – hormone metabolisms, congenital non-haemolytic jaundices, gall stones Dermatological – Chloasma, acne, erythema multiforme Psychological – Mood swings, depression, Libido

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76
Q

COCP contraindications - absolute (13) and relative (5)

A

Breast cancer; undiagnosed genital bleeding; pregnancy; <3 weeks post partum; breast feeding; hypertension; PH thrombosis; migraine with aura; active liver disease; thrombophilia; systemic lupus erythematosus; thrombotic thrombocytopenic purpura; smoking >15 and age >35 Relative contraindications: BMI>35;migraine without aura; hypertension; diabetes; hyperprolactinoma;

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77
Q

REVIEW COCP interactions and drug which reduce hormone levels

A

REDUCE Barbiturates Lamogitrine Topiramate Carbamazepine Oxcarbazepine Phenytoin Primidone Rifampicin Griseofulvin Certain antiretrovirals Modafinil INTERACTIONS Lamogitrine (levels reduced by cocp) Ciclosporin (levels reduced by cocp) Potassium sparing diuretics (in drosperidone containing cocp)

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78
Q

Monitoring for COCP

A

Annual BMI and BP

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79
Q

Combined vaginal contraceptive ring

A

Same as COCP except vaginal delivery (ring) for 21 days Remove for 7 days Adv – don’t have to take every day Disadv - don’t have to take every day!!

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80
Q

What are the progesterone only methods?

A
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81
Q

What are the principles of the progrogesterone only methods?

A
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82
Q

Describe copper IUD, benefits, disadvantages (not risks)

A
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83
Q

Copper IUD - Risks, absolute contraindications, relative contraindications

A
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84
Q

What is the best option for emergency contraception? How does it work? How far after sex can it be used?

A

Copper IUD Up to 120 hours after presumed ovulation or 120 hours after one single episode of UPSI at any time of the cycle Failure extremely rare Copper kills sperm in 1st part of the cycle Device prevents implantation in 2nd part of the cycle

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85
Q

What pills are available for emergency contraception? How do they differ?

A
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86
Q

Describe the symptoms (7) of the menstrual transition and relate them to the physiology of the menopause.

A

Reduced cycle length - due to reduced length of follicular phase

Reduced fertility - fewer eggs, cycles may become anovulatory

Heavier periods and breast tenderness - due to high oestrogen

Hot flashes, dry vagina and disturbed sleep - due to decling oestrogen levels

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87
Q

Describe treatment options for menopausal symptoms - hot flashes, vaginal dryness, irregular menstrual cycle

A

Can give low dose HRT (needs to be oestrogen with opposition from prospesterone unless the woman has had a hysterectomy

Can give combo of progesterone and estrogen in form of mirena IUS (or oral) and estrogen patch

SSRIs are sometimes indicated

Topical for vaginal dryness

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88
Q

Outline the changes in the hypothalmic axis leading up to menopause

A
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89
Q

What are the physiological (or pathological) changes observed in the lead up to menopause? (4)

A

Reduced number of follicles

Reduced number of granulosa cells

Loss of granulosa cell function

Increased chromosomal abnormalities of oocytes

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90
Q

At age do you have the most eggs in the ovary? How many do you have in menstrual transition?

A

20-24 weeks - 6-7 million

Puberty - 300,000-400,000

Menstrual transition - 100s

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91
Q

What factors contribute to follicular depletion?

A

Increased apoptosis (which can be increased by smoking)

Accleratied follicular loss (because AMH declines, FSH increases, more follicular recruitment)

Decline in graulosa cell numbers (by about 30%)

Loss of granulosa cell function

Decline in oocyte function and development

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92
Q

What is the role of the granulosa cell in menstrual transition?

A

The produce less inhibin B in follicular phase which allows higher FSH

Anovulatory cycles lead to drop in inhibin A (as no luteal phase) which allows higher FSH

Decrease in FSH receptors prevents recruitment of dominant follicle

Less secretion - GFs, signalling, oestrogen and progesterone

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93
Q

What are the symptoms of granulosa cell dysfunction?

A
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94
Q

What is the first hormonal sign of declining ovarian function? What are the other hormonal changes and when do they occur?

A
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95
Q

What factors can affect the age of menopause?

A

Smoking, ethnicity, geography, mother’s age of menopause, several candidate genes, surgery / chemotherapy

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96
Q

Describe considerations when prescribing HRT - dosage, risks, contraception, progesterone

A

Hyperplasia found in 56% of women who take unopposed estrogen, 3% will develop carcinoma (so give 10-13 days progesterone)

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97
Q

Describe the different modes of prescribing estrogen and progesterone - risks and benefits of each

A
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98
Q

Discuss the long term risks and possible benefits of HRT in terms of other illnesses

A

More than 5 years, BC risk goes up (but not as bad as alcohol, obesity_

May have benefits in alzheimer’s - unknown

Improves osteoporosis BUT not if only on for 5 years (give bisphosphonates instead)

No benefits in incontinence

May help with sleep disturbance (by addressing hot flashes)

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99
Q

What is menopause?

What is peri-menopause / transition?

A

Menopause - 1 year without menstruation (retrospective diagnosis) - if woman are under 40, its ‘premature ovarian failure’

Perimenopause - 2-8 years pre-menopause

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100
Q
A
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101
Q

Outline the HPG axis in terms of the control of the mnstrual cycle

A
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102
Q

What does GnRh have to be pulsaltile? What happens if it’s continous? What do slow or fast pulses do?

A

If continuous, production of LH/FSH stops

Slow - FSH

Fast LH

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103
Q

What is happening on day 1 of the menstrual cycle?

A

Bleeding

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104
Q

What is happening in day 1-14 of menstrual cycle? Which hormone is key?

A

Follicular phase, growth of follicles to prepare for ovulation

Dominated by estrogen (which is produced by follicles)

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105
Q

What is happening in day 14-18 of menstrual cycle? Which hormone is key?

A

Luteal phase, formation of corpus luteum from empty follicle which produces progesterone

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106
Q

Outline the HPG feedback through the menstrual cycle - at late luteral/early follicular, mid follicular, mid cycle and mid luteal

When does it change from negative to positive feedback?

A

At end of follicular phase, E2 levels are raised for long enough (48hr) and at high enough levels (more than 300pM) to switch feedback from negative to positive

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107
Q

What is important about the inter-cycle rise and fall of FSH?

A

Selection of a single follicle - the early rise (during menses) allows one follicle to be selected to grow. The fall in FSH prevents other follicles from growing unnecessarily (fall caused by rise in oestrogen levels which reinstated negative feedback)

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108
Q

Once selected, how is the dominant follicle maintained despite the drop in FSH levels?

A

The dominant follicle gains LH receptors on the granulosa cells - as the LH levels rise, this keeps this dominant follicle stimulated

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109
Q

REVIEW cells nad receptors of dominant follicle

A
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110
Q

Outline which steroids are produced by theca and granulosa cells (1 each) and which ones are created by both (3)

A
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111
Q

Describe what triggers the LH surge - what triggers it and what does it cause?

A
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112
Q

Describe process of ovulation - what are the ‘cascade of events’ occurring?

A
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113
Q

When / why does the follicle complete the first meiotic division? What does it become?

A
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114
Q

Describe corpus luteum formation and its hormone production - how does it differ during pregnancy?

A
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115
Q

Role of corpus luteum secretions, what is its lifespan?

A

Progesterione supports oocyte in journey, maintains CL, prepares endometrium, controls cells in fallopian tubes, alters cervical secretions

Estrogen - for endometrium

Life span is 14 days (fixed)

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116
Q

Potential treatments if issues with mentstrual irregularity

A
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117
Q

What is ‘normal’ in terms of length of menstrual cycle?

A

menses - 3-8 days

cycle can vary in length (27-32) but there should not be 4+ day variability month to month

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118
Q

What are clinical signs of ovulation?

A
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119
Q

In what part of your cycle are you fertile?

A

Generally 6 day span - egg lives from 24 hr post ovulation, sperm can live up to 5 days (median is 1.5 days)

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120
Q

REVIEW basic anatomy of uterus

A
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121
Q

REVIEW anatomy of uterus, cervix, ovary

A
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122
Q

Why is a newborn uterus larger than 4 year old?

A

Because newborn female has been effected by maternal steroids

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123
Q

Where does fertilisation occur?

A

Ampulla of uterine tubes

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124
Q

What makes the myometrium grow?

A

Estradiol

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125
Q

What layer of the myometrium grows during childhood?

A

Outer layer

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126
Q

What are the layers of the myometrium (3)? and what shape are their fibres?

What are the other layers of the uterine wall (2)?

A

Inner - circular

Middle - Figure 8 / spiral

Outer - longitudinal

Other layers are endometrium and perimetrium

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127
Q

REVIEW layers of endometrium, blood supply

A
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128
Q

What is the amount of endometrium a good indicator for?

A

Good ‘bioassay’ of estradiol levels

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129
Q

Which endometrial cells are changing throughout the menstrual cycle?

A

Changes in glandular and epithelial cells through cycle.

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130
Q

What does the endometrium look like after menstruation - cell type, thickness

A

After menstruation - stromal matrix with small columnar cells with glandular extensions 2-3mm thick

glands are simple and straight.

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131
Q

Describe the endometrial proliferative phase - what is it stimulated by (and where is this made?)

What occurs to the cells / glands / blood supply (and when are these changes at max levels)

A

Proliferative phase Stimulated by estradiol from the dominant follicle.

Stromal cell division, ciliated surface. Glands expand and become tortuous, increased vascularity, neoangiogenesis

maximal cell division by days 12-14.

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132
Q

At what thickness of endometrium do progesterone receptors develop? And what other process starts?

A

When endometrium >4mm induction of progesterone receptors and small muscular contractions of the myometrium.

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133
Q

REVIEW overview of follicular and endometrial phases - what are the phases called, which hormones are peaking when?

A
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134
Q

When does the secretory phase of the endometrium start? What stimulates it? What happens to the glands, blood supply, muscle cells?

A

Secretory phase (luteal phase of ovary) 2-3 days after ovulation, the gradual rise in progesterone (secreted by CL) causes a reduction in cell division.

Glands increase in tortuosity and distend…secretion of glycoproteins and lipids commences.

Oedema, increased vascular permeability arterioles contract and grow tightly wound.

Myometrial cells enlarge and movement is suppressed

blood supply increases.

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135
Q

Describe regression of corpus luteum? What keeps it alive? What is its lifespan?

What saves it during pregnancy? What happens if it isn’t saved?

A

Corpus luteum stimulated by LH from pituitary during luteal phase.

The fertilised oocyte becomes a blastocyst and produces human chorionic gonadotrophin (hCG) which acts like LH ie on LH receptor, and ‘rescues’ the CL.

In the absence of this, falling levels of steroid from the CL results in menstruation.

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136
Q

Describe menstruation - what day of cycle? What stimulates prostaglandins? What do the prostaglandins do?

How long does bleeding last? How much? What layers remain? What start the next cycle?

A

Prostaglandin release (caused by drop in progesterone, as CL has died) causes constriction of spiral arterioles. Hypoxia causes necrosis.

Vessels then dilate and bleeding ensues.

Proteolytic enzymes released from the dying tissue.

Outer layer of endometrium shed, 50% lost in 24hrs, up to 80ml is considered normal. Bleeding normally lasts 4+ days.

Basal layer remains and is then covered by extension of glandular epithelium.

Estrogen from follicle in next follicular phase starts cycle off again.

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137
Q

What are the sections (4) and cellular levels of the uterine tubes (3)?

A
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138
Q

What changes do the cells in the uterine tubes undergo during the cycle? (2 types of cells)

When in cycle are changes occurring? Role of hormones

A

Estrodiol before

Progesterone after

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139
Q

How long does the fertilied embryo remain in uterine tube?

A

5-6 days

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140
Q

What can cause damage to the uterine tubes? And resulting symptoms?

A

Damage to lining of the tube by infection, endometriosis, surgery or adhesions may cause blockage or damage to ciliated epithelia, resulting in…

pain

infertility

ectopic pregnancy

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141
Q

Describe investiagetions to determine if uterine tube blockage?

A

Laparoscopy better if you suspect endometriosis or PID as you have view inside

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142
Q

What are the parts of the cervix? What is its role? What cells are present (and their role?)?

A
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143
Q

What is happening to the cervix in the follicular phase? What causes this?

A

Estrogen in the follicular phase causes…

change in vascularity of cervix and oedema

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144
Q

What happens to the cervix mid cycle? Why?

A

Mid-cycle estrogen levels cause change in mucous to become less viscous.

change in mucous composition, contains glycoproteins which become aligned and form microscopic channels and sperm swim up the channels!

145
Q

What happens to the cervix in the luteal phase? Which hormone causes it? What happens to mucus?

A

Progesterone in luteal phase causes…

Reduced secretion and viscous mucous (reduced water content)

Glycoproteins now form mesh like structure: acts as barrier

One mechanism of action of oral contraceptives.

146
Q

Describe vagina - length / cell types?

A

Thick-walled tube approx 10cm

Lined by specialised ‘squamous epithelial’ cells

147
Q

Vagina - why is it susceptible to infection AND how does it prevent infection (3)?

A

Warm damp environment containing glycoprotein…

Susceptible to infection, which is prevented by…

layers of epithelial cells shed constantly and ‘flow’ downwards with the secretions

secretions are from cervix and transudation from vaginal epithelium

secretions change with cycle and are generally acidic providing anti-microbial protection

148
Q

Vagina - Which glands are present - where? and what do they do? what is the equivalent in men?

A

Bartholins glands located slightly posterior and to the left and right of the opening of the vagina secrete mucus to lubricate the vagina and are homologous to bulbourethral glands in males.

149
Q

What are the layers of the endometrium? (4) Which are shed during menstruation? (2)

A
  • Compactum (SHED)
  • Spongiosum (SHED)
  • Basalis
  • Junctional zone

And then muscle

150
Q

Ouline the stages of menstruation - what initiates it? What are the local mediators involved?

A
  • Initiated by withdrawal of E and P
  • Local mediators PG’s (F2a and Tx), PAF (platelet activating factor)
  1. Vasoconstriction
  2. Ischaemia and tissue damage
  3. Relaxation
  4. Shedding of functional endometrium
  5. And then fibrinolysis / coagulation balance

Menstruation occurs as a consequence of intense vasoconstriction and coagulation in the spiral arteries leading to intense inflammation and partial necrosis, after which the functionalis layer of the endometrium separates from the underlying basalis and is shed with blood

151
Q

What are the different types of prostaglandins? Which is most involved in menstruation?

A

Pro-bleeding (E+I) - anti-platelet, dilate blood vessels

Anti - bleeding (Tx and F2a) - pro-platelet, constrict blood vessels (this one is most involved)

152
Q

What interleukins are most involved in menstruation? (3)

A

8, 13, 16

153
Q

What cause the issues with menstruation? Three factors that can be thrown out of balance

A

Inflammation, coagulation, fibrinolysis

154
Q

What are the most cimmon causes of abnormal vaginal bleeding?

A

‘Pathological causes’

  • Fibroids – submucous
  • Adenomyosis
  • Endometrial pathology – benign adenomas or polyps
  • hyperplasia
  • carcinoma

•Cervical pathology – polyps

  • carcinoma
  • Cervical Infection - Chlamydia
  • Pregnancy

DUB - diagnosis of exclusion

155
Q

How much do submucosal fibroids increase the risk of abnormal peri-menopausal bleeding?

A

threefold increased risk

156
Q

What are the aims for investigations of abnromal uterine bleeding - what do we need to EXCLUDE first? (4) which methods should be used?

A
  • Exclude pregnancy
  • Exclude cervical pathology
  • Exclude focal intracavity pathology (polyps, submucous fibroids)
  • Consider endometrial pathology (> 40)
  • Use the least invasive method to achieve this
157
Q

Key points in abnormal bleeding history (4) and exam (4)?

A

HISTORY

  • –LMP - was it normal?
  • –Regular or irregular periods
    • •with bleeding between?
    • •heavy- clots, flooding?
    • •post coital bleeding?
    • •Pain
  • –Medication, smoker, smear, operations
  • –Contraception - is family complete?

EXAM

  • –BMI
  • –Abdomen
    • •Distension, scars, pain, masses
  • –Bimanual
    • •Uterine size, adnexal masses, pain
  • –Cervix
    • •polyps, suspect lesions
158
Q
A
159
Q

Potential investigations for abnormal bleeding (7) - what do you do, what are you looking for?

A
  • Pregnancy test where appropriate
  • Hb if heavy bleeding
  • Swabs – endocervical (Chlamydia)
  • Cervical smear – only if due
  • Transvaginal ultrasound
  • Endometrial sampling
  • Hysteroscopy - in-patient or OPD
160
Q

Transvaginal ultrasound - what is it good for seeing?

What do you do next if it’s abnormal?

A
  • Can assess the relationship of fibroids to the cavity
  • Has a high detection rate for polyps
  • Assess function – anovulatory cycles
  • Can reliably assess structures outside the uterus (tubal and ovarian pathology)
161
Q

What are the ‘cut-off’ values for endometrial thickness? pre / post menopausal

A

•Cut-off values for ET are arbitrary in premenopausal women - @ 6 mm post menstrual or 12 mm anytime in cycle

162
Q

Why would you do a hysteroscopy? (3)

A
  • If TVS abnormal
  • Non-response to medical therapy
  • Multiple risk factors for endometrial pathology
163
Q

What are the types of endometrial hyperplasia? What is the most common cause?

A

Simple and atypical, usually caused by unopposed estrogen

If atypical, need to investigate further

If simple, give progesterone

164
Q

Treating polyps - 1

A

Surgery -transcervical resection / polypectomy

165
Q

Treating fibroids - 3

A
  • –Medical Mirena IUS (if only symptom is heavy bleeding)
  • –Surgery TCRF/Myomectomy (if many fibroids)
  • –Hysterectomy
    • •total/subtotal abdominal
    • •vaginal
166
Q

Treating DUB - do you need to? what are the options (hormonal 4, non-hormonal 2, surgery 3)

A
  • •Nothing
  • •Medical
    • –Non Hormonal
      • •Anti fibrinolytics 40-50% reduction in blood loss
      • •Mefenamic acid 30% reduction in blood loss
    • –Hormonal
      • •COCP – 20 - 30% reduction in blood loss
      • •Progestagens NOT beneficial for loss
      • •Use to control cycle length in anovulatory DUB
      • •Mirena IUS – 90% reduction
    • Surgery
      • Endometrial resection / ablation - with radiofrequency
      • Hysterectomy
      • Remove ovaries?
167
Q

REVIEW treatment algorithm for menorrhagia

A
168
Q

What is the defition of labour? How can it be diagnosed?

A

DEFINITION: The process of _uterine contraction_s and cervical dilatation that enables the uterus to deliver the viable fetus (>24 weeks), placenta and membranes.

DIAGNOSIS: When there are regular & increasing painful uterine contractions that brings about progressive cervical effacement and/or dilatation

169
Q

What are the theories regarding the iniation of labour?

A

PROGESTERONE WITHDRAWAL?

NEURONAL STIMULATION FROM CERVICAL PRESSURE

CRH (corticotrophin releasing hormone) PLACENTAL CLOCK

INFLAMMATORY PROCESS IN CERVIX

170
Q

What are the stages of labour?

A

FIRST STAGE - THE PERIOD BETWEEN ONSET OF REGULAR PAINFUL UTERINE CONTRACTIONS TO FULL CERVICAL DILATATION (this is difficult to quantify and scientific studies are based on observed first stage of labour)

SECOND STAGE - FROM FULL CERVICAL DILATATION TO DELIVERY OF THE FETUS (usually one hour in the nulliparous & half an hour in the multiparous woman)

THIRD STAGE - FROM DELIVERY OF THE FETUS TO DELIVERY OF THE PLACENTA & MEMBRANES (usually <15 mins with active management of the third stage of labour)

171
Q

What are the two phases of the 1st stage of labour? Cervical signs, how fast does it usually progress?

A

LATENT PHASE - THE DURATION FOR THE CERVIX TO BECOME EFFACED (FROM 3 CM LONG TO <0.5 CM) AND DILATED TO 3 CM. WITH REGULAR UTERINE CONTRACTIONS IT COULD TAKE 6-8 HRS IN A NULLIPARA AND 4-6 HRS IN A MULTIPARA

ACTIVE PHASE - THE DURATION FOR THE CERVIX TO DILATE FROM 3 TO 10 CM (FULLY DILATED). THE RATE OF CERVICAL DILATATION IS ON THE AVERAGE ABOUT 1 CM/HR

172
Q

What does a partogram do? What factors does it look at?

A

A graphic representation of the process of labour

  • Rate of cervical dilatation
  • Descent of head
  • Contraction frequency / duration
  • FHR
  • Liquor colour and quantity
  • Caput and moulding fetal head
  • Maternal parameters (T, P BP, UO, Urine dip)
173
Q

What is the sinciput and occiput? How to measure descent of head?

A

Sinciput - front

Occiput - back

174
Q

What are the alert and action lines?

A

Using partogram to determine if labour is progressing at normal speed

ALERT LINE - A LINE DRAWN AT A RATE OF 1CM/HR FROM ADMISSION CERVICAL DILATATION IN THE ACTIVE PHASE

ACTION LINE - A LINE DRAWN 2 OR 3 CM TO THE RIGHT AND PARALLEL TO THE ALERT LINE

LABOUR PROGRESS TO THE RIGHT OF THE ACTION LINE IS DEEMED TO BE SLOW NEEDING SOME INTERVENTION

175
Q

What are the 3 factors that can slow down labour? Which is commonest?

A

Passage - is the space big enough?

Passenger - too big? wrong position?

Power - COMMONEST - issue with contractions

176
Q

What issues can slow labour in first stage lead to?

A

Dehydration / exhaustion

Infection

Fetal distress

Instrumental delivery

Uterine rupture

Postpartum haemorrhage

Maternal / fetal morbitity

Fistula

177
Q

What are the key things in the first stage of labour?

A

GET THE DIAGNOSIS OF LABOUR CORRECT!

PROVIDE SUPPORT, PAIN RELIEF & HYDRATION

EMOTIONAL SUPPORT IS ESSENTIAL

MIDWIFERY-LED CARE IF NORMAL

BE PREPARED FOR ANY EMERGENCY

CONSULT WHEN REQUIRED

178
Q

What factors may cause a prolonged second stage of labour?

A

–Nullip vs multip

–Epidural vs no epidural

–Active pushing vs not

–Maternal exhaustion vs distress

–Failure to descend / rotate

179
Q

Management in third stage of labour (6)

A

IM Syntometrine given to mum with delivery of baby’s anterior shoulder.

Left hand placed above symphysis pubis to guard anterior wall of uterus

Controlled cord traction until placenta is delivered

Placenta and membranes checked for completeness

Estimate blood loss

Check for tears and suture under local anaesthetic if required

180
Q

Issues with third stage of labour (5)

A

Retained placenta

Postpartum haemorrhage

Perineal trauma: 2nd / 3rd / 4th degree tear

Perineal / pelvic haematoma

Uterine inversion

181
Q

Descirbe the mechanism of labour - what position is the head in?

A
  1. occipito-transverse as it enters pelvis
  2. descent with head flexion (looking down)
  3. internal rotation to occipito-anterior
  4. Extension back (looking up)
  5. Restitution - external rotation to align head with the shoulders)
  6. shoulders delivered AP
182
Q

What is the ideal number of contractions per 10 mns? How can you speed up or slow down?

A

4-5 every 10 mins, lasting over 40seconds

If too often, give turbutiline (because cord compressed during contraction, need breaks for nutrients)

If not progressing, can give oxytocin to increase contractions (start with 2-4 and increase in units of 2-4)

183
Q

What time perod is the puerperium? Which systems are changing?

A

Delivery to Day 42 post-natal

Changes are multifactorial

  • –Physical
  • –Endocrine
  • –Immunological
  • –Psychological
  • –Social
184
Q

What is the biggest cause of maternal death in the UK?

A

Thrombo-embolism (others are Pre-eclampsia / eclampsia, Haemorrhage, Sepsis - GAS)

Highest INDIRECT cause of death is CVD

WORLDWIDE 600,000 deaths per year- Haemorrhage by far biggest cause (and then others above)

185
Q

What is the purpose of post-natal care? (5)

A
  • Facilitate and reassure normality for mother and baby including bonding and establishing feeding
  • Identify, investigate and manage abnormality
  • Consideration during lactation e.g. prescribing
  • Provide contraceptive advice
  • Make plans for next time!
186
Q

Outline the physical and endocrine shifts post birth? Which hormones are key (4) and what are 4 of the changes?

A

Involution means pregnant uterus returning to normal

187
Q

Outline the changes to the uterus, CVS, coagulation and metabolism post pregnancy

A

Uterine involution - autolysis

  • pelvis by D10
  • bleeding stops (lochia)
  • resumption menstruation (HPO axis)

CV changes - CO / TPR / BP

  • normal by 2 weeks

Coagulation - fibrinolysis normal within 30 minutes!

  • pro-coagulant state remains

(clotting factors increased)

Metabolic - insulin resistance goes immediately

188
Q

What inhibits prolactin pre-delivery?

A

High estrogen

189
Q

What are the factors involved in lactation post-delivery?

A
190
Q

What are the components of colostrum (3)? When does the normal milk come in and what are its components (3)?

A

First 48 hours = colostrum

Major source IgA (mucosal type Ig)

Lysosyme / macrophages

Moderate CHO / FAT (protein)

Day 3-4 = milk

Increased CHO / FAT (protein)

Lactose (glu/galactose)

Lactalbumin / Casein

191
Q

REVIEW pros and cons of breast feeding

A
192
Q

Outline some issues invovled with lactation - what most commonly causes mastitis? what happens if mastitis goes untreated?

A
  • Failure of lactation - rare
  • Cracked nipples and pain - common
  • Acute Mastitis
    • •usually following cracked nipple
    • •Key pathogen = Staph. Aureus
    • •Presentation - pain / red, hot breast / fever
    • •Mx - maintain feeding or expressing + antibiotics (flucloxacillin)
  • Breast abscess
    • •sequelae of ignored / untreated mastitis
    • •Mx - as above BUT also needs I+D
193
Q

Outline the types of PPH (3) and definition

A

Blood loss > 500ml from genital tract

5% - subjective and underestimated

Primary - first 24 hours

Secondary - >24 hours to 42 days

Tertiary - > 42 days

Causes significant maternal morbidity (anaemia / Tx)

and mortality

194
Q

Outline the causes (4) and management plans for primary PPH

4Ts and 4Rs

A

Causes Management

  • Tone Remedy the cause
  • Tissue Replace volume
  • Trauma Replace O2 carry cap.
  • Thrombin Replace clotting factors
195
Q

What are the risk factors for secondary PPH, how does it present, how do you manage it?

A

Secondary PPH - endometritis +/- RPOC

Presentation - Excessive lochia / pain / fever

Mx Antibiotics

Analgesia

If no improvement 48 hrs ERPC (evacuation of retained products of conception)

196
Q

When are women at thehighest risk of VTE / PE

A

Pro-coagulant state continues throughout the puerperium

Highest risk - 10-14 days

Majority - post-partum

Majority - multiple risk factors

VTE BIGGEST CAUSE OF MATERNAL MORTALITY

197
Q

Risk factors for VTE (8)

Prophylaxis options (5)

And management option

A

RISK

  • Obesity
  • Older
  • Intercurrent illness e.g. infection / PET
  • Immobility
  • Operative delivery - CS
  • Previous TED
  • FH TED
  • Known thrombophilia

PROPHYLAXIS

Stocking

S/C heparin

Early mobilisation

Adequate hydration

Education

MANAGEMENT

LMWH

198
Q

What is the most common cause of purperal pyrexia?

A

Infection - but need to find out where

Can be physiological within first 24-48 hrs

BUT if any fever, check for sepsis

ALWAYS CHECK LEGS AND CHEST

199
Q

Outline the three things you give, three things you take out in suspected sepsis

A

GIVE O2, fluids, broad spectrum antibiotics

TAKE bloods, lactate, urine

200
Q
A
201
Q

Outline the difference between baby blues, PND, puerperal psychosis

A

Baby Blues - very common (60 - 70%)

  • first 3-4 days
  • weepy, labile, helpless
  • support and reassurance only needed for most
  • short lived and self-limiting

PND - 10% (underestimated!)

  • from 4 weeks onwards (“after the event!”)
  • spectrum: mild mood disorder to severe clinical depression
  • most have risk factors - most common is previous PND or psych history

Puerperal psychosis - rare BUT severe

  • usually first 2 weeks
  • severe psychotic episodes
  • delusions and hallucinations
  • serious suicide / infanticide risk

Mx - URGENT PSYCHIATRIC HELP

  • Mother-baby units (try + keep together)
  • usually self limiting with good outcome
202
Q

What is a ‘trophoblast’? What do they secrete?

A

cells of blastocyst that invade endometrium and myometrium (D 5-6)

secrete ßHCG (Human Chorionic Gonadotrophin)

203
Q

What is the ‘chorion’? What is the ‘amnion’?

A

Chorion - becomes placenta

Amnion - becomes amniotic sac

204
Q

Describe the first 5-6 days for a fertilised egg

A
205
Q

REVIEW hormones of menstrual cycle

A
206
Q

Which two layers does the trophoblast invade?

A

Decidua and myometrium

207
Q

When is the ‘window of implantation’? When must the trophoblast start producing hCG?

A

Day 5-6, Day 10

208
Q

What is the significance of βHCG. When does it peak?

A
  • “maternal recognition of pregnancy”
  • Maintenance of the corpus luteum – Progesterone production
  • Decidualisation under progesterone
  • Vital until placental steroidogenesis established
  • Maximal by 9 – 11 weeks
209
Q

Difference between urine and serum pregnancy tests

A

Both BhCG - urine is just qualititative - it is either there or it’s not

Serum is quantitative to see if the preganancy is progressing normally

210
Q

What are the functions of the placenta? (4)

A
  • Steroidogenesis – oestrogens, Progesterone, HPL, cortisol
  • Provision of maternal O2, CHO, Fats, AA’s, Vitamins, Minerals, Antibodies
  • Removal of CO2, urea, NH4, Minerals
  • Barrier - e.g. bacteria, viruses, drugs, etc
211
Q

What makes the placenta so effective? (4)

A
  • Huge maternal uterine blood supply - low pressure
  • Huge reserve in function
  • Huge surface area in contact with maternal blood
  • Highly adapted + efficient transfer system
212
Q

Describe the layers of trophoblast that invade wall - which layer is first, second, third?

A

Syn first, then cyto, then extraembryonic mesoderm

213
Q

Describe the structure of the placenta. What is the functional unit?

A

Functional unit - cotyledon

214
Q

What is the function of the amniotic cavity? (3)

A
  • Homeostasis - temp, fluid, ions,
  • Vital for development of certain structures e.g. limbs, lungs
  • Protection - physical and barrier e.g. ascending infection
215
Q

Describe how the amniotic sac develops

A
216
Q

What are some disorders of the placenta (5)

A
  • •Miscarriage - 15% (40%!?) pregnancies!
  • •Pre-eclampsia - 10% pregnancies!
  • •Hydatidiform mole
  • •Placental Insufficiency
  • •Transfer of other substances - drugs, toxins, infections
217
Q

What are some exampels of disorder of the amnion? (3)

A
  • •Polyhydramnios
  • •Oligohydramnios
  • •Premature Rupture of Membranes
218
Q

What is the role of progesterone in pregnancy? (4)

A
  • •Decidualisation (CL)
  • •Smooth muscle relaxation – uterine quiescence
  • •Mineralocorticoid effect – cardiovascular changes
  • •Breast development
219
Q

What is the role of oestrogens in pregnancy? (4) Which estrogen is strongest? Where are they made?

A
  • E3 > E2 > E1
  • WHERE? Rely on androgens from fetus and maternal adrenals
  • •Development of uterine hypertrophy
  • •Metabolic changes (insulin resistance)
  • •Cardiovascular changes
  • •Breast development
220
Q

REVIEW steroidogenesis - what is the precursor to testotsterone? What starts the whole process?

A
221
Q

What are the roles of CRH and cortisol? When do they increase? Where are they produced?

A
  • Placental
  • Both increase from T2 onwards
  • Cortisol
    • Metabolic changes (insulin resistance)
    • Fetal lung maturity
  • CRH
    • possibly involved in labour initiation (“placental biological clock”)
222
Q

What are the roles of HPL and Prolactin? What is HPL structurally similar to?

A
  • •Human placental lactogen (HPL)
    • •Similar to GH
    • •Metabolic changes – insulin resistance
    • •Possibly some role in lactation
  • •Prolactin
    • •Increases throughout pregnancy
    • •Breast development for lactation
223
Q

What are the objectives of antenatal care? (3)

A
  • Promote and maintain the physical, mental and social health of mother and baby by providing education on nutrition, personal hygiene and birthing process
  • Detect and manage complications during pregnancy, whether medical, surgical or obstetric
  • Develop birth preparedness and ‘complication readiness’
    • Help prepare mother to breastfeed successfully, experience normal puerperium, and take good care of the child physically, psychologically and socially
224
Q

Potential drawbacks on antenatal care (6)

A
  • •‘Medicalisation’ of a normal pregnancy
  • •Maternal anxiety
  • •Unnecessary interventions
  • •Doubtful benefit – many ‘age old’ practices
  • •Cost – resources, social costs
  • •Risk approach is not always an efficient or effective strategy for predicting complications
225
Q

How many antenatal visits?

A

Low risk - as few as 6

Higher risk may be more than 14

Where depends on what care is needed

226
Q

What is the main objective of the early antenatal ultrasound? When can it be performed? What issues does it help to prevent?

A
  • Detect gestational age - crown rump length
  • Between 10-13 weeks
  • •Ensures consistency of gestational age assessments
  • •Improves the performance of mid-trimester serum screening for Down’s syndrome
  • Reduces the need for induction of labour after 41 weeks
227
Q

What test can be used to measure gestational age after 14 weeks?

A

Pregnant women who present at or beyond 14 weeks’ gestation should be offered an ultrasound scan to estimate gestational age using head circumference or bi-parietal diameter

228
Q

What exams should be done on the women during pregnancy? When and how often? Which exams are not necessary?

A

Maternal weight and height should be measured at the first antenatal appointment, and the woman’s BMI calculated (weight [kg]/height[m]2) - Repeated weighing during pregnancy should be confined to circumstances where clinical management is likely to be influenced.

Screen for anaemia - early and at 28 weeks

Routine breast examination during antenatal care is NOT recommended for the promotion of postnatal breastfeeding

Routine antenatal pelvic examination is NOT recommended

229
Q

What blood screening should be offered in pregnancy?

A

Blood group and RhD status

If a pregnant woman is RhD-negative, her partner should be offered testing to determine whether the administration of anti-D prophylaxis is necessary

It is recommended that routine antenatal anti-D prophylaxis is offered to all non-sensitized pregnant women who are RhD negative

230
Q

What is the purpose of the second routine ultrasound scan?

A

Pregnant women should be offered an ultrasound scan to screen for structural anomalies, ideally between 18 and 20 weeks’ gestation

231
Q

Which infections are screened during pregnancy?

A

Rubella, HIV, Hep B, Syphilis

UTI check at every appointment

NO SCREENING for Hep C, Chlamydia and GBS

232
Q

What are the tests needed to confirm pre-eclampsia?

A

Proteinuria and high BP

233
Q

What dietary supplements should be given during pregnancy? For how long?

A

Folic acid (400mcg)

Vitamin D

Only the first 12 weeks ideally, and 3 months before

234
Q

REVIEW schedule of prenatal visits

A
235
Q

How do you determine the likely due date?

A

Last menstrual period - LMP – Add 7 days and 9 months (Naegle’s rule) - (The periods have to be 28 days – if not allowance should be given for irregular cycles, long cycles, lactation, use of contraceptives, early bleeding etc.)

236
Q

How do you determine the age of the fetus during the second trimester?

A

Fetal biometry - head circumfrence, femur length, bipareital diameter (but has 2-3 week margin of error)

237
Q

What causes maternal changes during pregnancy - general (3)

A
  • »High levels of steroids
  • »Mechanical displacement
  • »Fetal requirements
238
Q

Which hormones cause most of the maternal changesduring pregnancy? (4 types, 10 hormones)

A
  • placental peptides
    • hCG, hPL, GH
  • maternal steroids
    • placenta takes over ovarian (CL) production around wk 7
  • placental and fetal steroids
    • progesterone, oestradiol, oestriol
  • Maternal and fetal pituitary hormones
    • GH, thyroid hormones, prolactin, CRF
239
Q

During which week does the placenta take over maternal steriod production?

A

Week 7

240
Q

Outline the gain in weight during pregnancy

Recommended maximum weight gain?

A
  • Fetus plus placenta 5 kg
  • Fat and protein 4.5 kg
  • Body Water (this is excluding that in other listed structures) 1.5 kg (intravascular, interstitial, intracellular)
  • Breasts 1 kg
  • Uterus 0.5- 1kg
  • Ideally keep to less than 13kg: failure to gain or sudden change needs monitoring
241
Q

Where is the majority of the fat and protein gained stored?

A

Anterior abdominal wall

242
Q

What is the recommended increase in calorie consumption during pregnancy? What percent is for the fetus/uterus?

A
  • »350 kcal/day mid gestation
  • »250 kcal/day late gestation
  • 75% fetus and uterus, 25% respiration(H&L)
243
Q

When does the fetus need increased availability of glucose during pregnancy? Where does the fetus store some of the glucose?

A

2nd trimester, liver

244
Q

What changes occur to glucose production in the mother during prgnancy? When?

A
  • 1st Trimester
  • Maternal reserves
  • pancreatic b cells increase in number
  • plasma insulin increases
  • fasting serum glucose decreases (laid down as stores and used by muscle)
245
Q

What changes occur to the fetal reserves of glucose during the 2nd trimester? What can go wrong?

A
  • hPL causes insulin resistance ie less glucose into stores =increased availability in serum glucose (more crosses placenta)
  • BUT can cause diabetes
246
Q

What acts on RAAS system to increase water retention?

A

E2 and Progesterone

247
Q

What causes water gain during pregnancy (4)? What is the average amount gained?

A

Sodium retention,

resetting of the osmostat,

decrease thirst threshold,

decrease in plasma oncotic pressure (albumin)

8.5L

248
Q

Why and how does oxygen consumption increase during pregnancy?

A
249
Q

What happens to maternal blood during pregnancy?

A
  • Plasma volume increases (so do RBCs, but by less of a proportion so concentration of Hb falls)
  • Increased efficiency of iron absoprtion from gut
  • White cells go UP but immunocompromised
  • Clotting factors increase so hypercoaguable (there is increased fibrinogen for placental separation but increased risk of thrombosis)
250
Q

What are the CVS (HEART) changes the occur during pregnancy? (5)

A
  • expanding uterus
    • »pushes heart round
    • »changes ECG and heart sounds
  • increased cardiac output
    • »increased heart rate and stroke volume
    • »begins as early as 3 weeks to max 40% at 28 weeks
    • »for maternal muscle and fetal supply
251
Q

What are the CVS (VESSELS) changes the occur during pregnancy? (4)

A

Increased cardiac output and vasodilation by steroids= Reduced peripheral resistance.

Increased flow to :

  • • uterus
  • • placenta
  • • muscle
  • • kidney and
  • • skin

Neoangiogenesis….including extra capillaries in skin (spider naevi) to assist in heat loss

252
Q

Outline the changes to the GI tract during pregnancy?

A
  • appetite and thirst
  • reduced GIT motility (leading to constipation)
  • relax lower oesophageal sphincter (leading to acid refleux, which is made worse by the large uterus)
253
Q

How doees the urinary system change during pregnancy?

A
254
Q

When do pregnant women have to pee more (which trimester)

A

First and Third, during second the uterus is lifted out of the pelvis

255
Q

What are the changes to the uterus during pregnancy?

A
256
Q

What are the changes to the cervix during pregnancy? (4)

A
  • primary function is to retain the pregnancy
  • increase in vascularity
  • tissue softens from 8 weeks
    • »changes in connective tissue
    • »begins gradual preparation for expansion
  • proliferation of glands
    • »mucosal layer becomes half of mass
    • »great increase in mucus production
    • »protective..ie anti-infective
257
Q

Describe the process of everything returning to normal post pregnancy

A
  • Dramatic and rapid fall in steroids on delivery of the placenta
  • Most endocrine-driven changes return to normal rapidly
  • Uterine muscle rapidly looses oedema but contracts slowly: never returns to pre-pregnancy size
  • Removal of steroids permits action of raised prolactin on breast
258
Q

REVIEW the structure of chromosomes - how many chromosomes do humans have?

A

Histones are highly positively charged proteins that are attracted to the negative charge of DNA. Imagine this like coiling a garden hose up; in takes up less room to store than if you leave the garden hose out stretched. But it requires energy to coil that hose up and essentially that is what histones supply. They give the DNA a support to wrap around
A chromosome is an organized package of DNA found in the nucleus of the cell. Humans have 23 pairs of chromosomes–22 pairs of numbered chromosomes, called autosomes, and one pair of sex chromosomes, X and Y. Each parent contributes one chromosome to each pair so that offspring get half of their chromosomes from their mother and half from their father.

259
Q

What do chromosomes usually exist as?

A

Chromatin (DNA wrapped around histones)

260
Q

What is a nucleosome?

A

fundamental unit of DNA – eight histones and two turns of DNA

261
Q

REVIEW structure of histone

A
262
Q

What is euchromatin vs heterochromatin?

A
  • •Euchromatin
    • Extended state, dispersed through nucleus
    • Allows gene expression
  • •Heterochormatin
    • Highly condensed, genes not expressed

Significance for staining

263
Q

REVIEW what occurs to the chromome during s phase - how many chromosomes present?

A
264
Q

What are the definitions of metacentric, submetacentric and acrocentric chromosomes? What is the clinical significance?

A
  • •Metacentric
    • •p & q arms even length
    • •1-3, 16-18
  • •Submetacentric
    • •p arm shorter than q
    • •4-12, 19-20, X
  • •Acrocentric
    • •Long q, small p
    • •p contains no unique DNA
    • •13-15, 21-22, Y
    • TRISOMY MORE COMMON OF ACROCENTRIC
265
Q

Define haploid, diploid, polyploid, aneuploid - what types of cells?

A
  • •Haploid
    • •Single copy of each chromosome (n=23) e.g. gamete
  • •Diploid
    • •Two copies of each chromosome (2n=46) e.g. somatic cell
  • •Polyploid
    • •Multiple complete sets of chromosomes e.g. triploidy (3n=69)
  • •Aneuploid
    • •Extra or missing chromosomes, not exact multiple of haploid number e.g. trisomy 21 (2n+1 = 47)
266
Q

At what stage in the cell cycle are cells used for karyotyping?

A

Metaphase

267
Q

What is the goal of MITOSIS? Describe the process

A

To form two identical cells, with 46 chromosomes

268
Q

What is the goal of MEIOSIS? Describe the process

A

Meiosis is the formation of egg and sperm cells. In sexually reproducing organisms, body cells are diploid, meaning they contain two sets of chromosomes (one set from each parent). To maintain this state, the egg and sperm that unite during fertilization must be haploid, meaning they each contain a single set of chromosomes. During meiosis, diploid cells undergo DNA replication, followed by two rounds of cell division, producing four haploid sex cells.

STARTING CELL IS GERM CELL, END CELL IS SPERM OR EGG

269
Q

REVIEW mitosis and meiosis - side by side

A
270
Q

When does ‘crossing over’ occur? What are its other names?

A

Meiosis 1, Metaphase

chiasma formation, crossing over, recombination

271
Q

What is being pulled apart in meiosis 1? What is being pulled apart in meiosis 2?

A

1: Homologues
2. Sister chromatids

272
Q

What are the two types of chromosomal abnormalities that can occur? How can they be detected?

A

Numerical (traditional karyotyping, FISH, QF-PCR) or structural (traditional karyotyping, FISH)

273
Q

Possibly autosomal aneuploidy conditions (3)

A
  • Trisomy 13 - Patau Syndrome
  • Trisomy 18 - Edward Syndrome
  • Trisomy 21 - Down Syndrome
274
Q

Possibly sex xhromosome aneuploidy conditions

A
  • •47 XXY - Klinefelter
  • •45 XO - Turner Syndrome
  • •47 XYY
  • •47 XXX – Triple X syndrome
275
Q

Why do aneuploidies occur?

A

Non-disjunction during Meiosis 1 or 2

276
Q

Describe G-banding - which enzyme is used? Which stain is used? What can it show? Significance of the bands?

A
  • •Controlled digestion of chromosomes with trypsin
  • •Stain with Giemsa, a DNA binding chemical dye
  • Takes several days
  • Need metaphase chromosomes
  • Can detect aneuploidies, translocations & very large deletions but NOT small changes
  • •Produces alternating light (GC rich) and dark (AT rich) bands
  • •Banding pattern allows chromosome identification
    • •2 different sorts: euchromatin & heterochromatin
    • •Euchromatin = GC-rich; loosely packed; genes active
    • •Heterochromatin = AT-rich; tightly packed; genes inactive
    • •Stain differently
277
Q

What is FISH testing? When is it used? How long does it take

A

Fluorescence in situ Hybridization: FISH

  • •Requires probe specific to desired DNA sequence e.g. specific locus
  • •Probe labelled with fluorescent dye
  • •Probe hybridized to metaphase spread
  • •Expose to UV to visualize fluorescence
  • Often used in cancer diagnosis
  • Takes several days
  • Need to know what you are looking for! (in traditional kind)
278
Q
A
279
Q

What are the 4 areas of assessment of child development

A

Gross motor

Fine motor and vision

Communication and hearing

Social and interactive / play

280
Q

REVIEW progression of gross motor skills (image 0-12 months)

A
281
Q

What is normal gross motor progression for a 3month old? 6month old? 9 month? 12 month? 2 years?

A
  • 4m- lifts head and shoulders, weight on forearms, can turn to sides
  • 6m - arms extended, chest off couch,rolling front to back
  • 9m - crawling position, roll from both ways
282
Q

Describe a physical sign of DMD?

A

Gower sign

283
Q

What are RED FLAGS for gross motor delay? examinations to rule things out?

A

Red flags

  • Regression – neurological / neuro-degenerative
  • Motor delay with visual/hearing and balance problems
  • Other possibilities: Low muscle tone , severe Hypermobility of Joints, Hip , Nutritional Rickets, Hypothyroidism, systemic illness
  • Poor motor coordination- Ataxia, neurological , muscular problems
  • Autism- posturing, tip toe gait; repetitive climbing , spinning or body movement
  • Atypical pattern – DMD , CP

Examine Hips, CNS-gait, muscle tone and reflexes

Check CPK (for DMD)TFT (for hypothyroid) and other test as indicated

284
Q

What factor can affect fine motor development?

A

Visual impairment

285
Q

When is abnormal to see hand preference BEFORE?

A

18 months

286
Q

What is Developmental Co-ordination Disorder (DCD)?

A

Isolated difficulties in motor planning, balance and co-ordination

287
Q

Describe the progression of fine motor skills? When should they transfer object between hands? Have a mature pincer grasp? Build a three block tower? Draw a cross?

A
288
Q

When do babies spontaneously open hands? Regard their hands, play with feet?

A

3, 5, 5 months

289
Q

When do children start casting? When can they draw a circle, cross, triangle?

A

1 year

3,4,5 years

290
Q

Describe the progression of languages milestones - what are they doing at 3m, 6 months, 12 months? When do they ask questions? Tells stories?

A
291
Q

What are some examples of atyplical speech and language development (6)

A
  • Regression –, (transient or permanent?)
    • <3 years -commonly seen ? SCD; - Neurodegenerative disorders
    • >3 years ; Rare seizure Landau Kleffner syndrome
    • Rett’s syndrome
  • Echolalia – normal part of development but if it is persistent excessive - ?ASD
  • Phonological disorder / Unclear speech – Check for ? High frequency HL / Glue ears? / cleft palate / bifid uvula
  • Speech and motor difficulties – muscular problems / DCD
  • No speech at 3 years – severe autism / hearing loss
  • Selective mutism
292
Q

Provide examples of social and adaptive milestones - what is normal at 3months, 6 moths, 12 months, 18 months, 4 years?

A
293
Q

Examples of social behavious in a 6month old

A
  • •Smiles at mirror image
  • •Stretches arms to be lifted
  • •Shows displeasure on removal of a toy
  • •Fear of strangers
  • •Object permanence
294
Q

Examples of behaviours in a 9 month baby?

A
  • •Plays peek a boo
  • •Shows interest in picture books
  • •Understands ‘no’
  • •Anticipated actions in nursery rhymes
  • •Repeats performance being laughed at
  • •Waves bye-bye
  • •Responds to word Eg “Where’s daddy?”
295
Q

What 2 types of play are occurring by 2 years old? By 3-4 years? By 5?

A
  • parallel and pretend play
  • role-playing and interactive play
  • Complex interactive games by 5
296
Q

Overview - what are the developmental warning signs at each age?

A
  • At any age – Parental concerns, discordant development, asymmetry, regression
  • At 10 weeks – No social smile
  • At 6 months – Persistent primitive reflexes , no interest in people, noise, hand preference
  • At 8 months – Not sitting
  • At 12 months – No pincer grasp
  • At 18 months – Not walking, no words, drooling, mouthing
  • At 2 years –No phrases, not interactive
  • At 4 years – Unintelligible speech
297
Q

Components of a developmental asessment history?

A
  • Parental concerns
  • Birth history
    • Prenatal – AN scans, drugs, alcohol, maternal infections
      • Perinatal – Prematurity, HIE, NICU admission, meningitis, sepsis, jaundice
  • Past Medical History
    • CNS infections, injuries, epilepsy, co-morbidity
  • Developmental history
  • Family/Social History
298
Q

How common are developmental delays? What is a ‘global’ delay?

A
  • Developmental difficulties occur in approximately 5–10% of the childhood population
  • Specific/Global
  • Global developmental delay - significant delay in two or more developmental domains
  • Global delay prevalence - 1–3% of children < 5 year
299
Q

What does a GDD become after the age of 5yo? What are the three criteria of this diagnosis?

A

Intellectual disability

  1. Deficits of intellectual functions (reasoning, planning, judgment, learning, etc.)
  2. Deficits in adaptive functioning (not as independent / responsible as you ould expect for their age)
  3. Onset during the developmental period

NOT DETERMINED BY IQ, but by levels of adaptive functioning

300
Q

What are the assessments and investigations of GDD?

A

Assessment:

  • Clinical history
  • Family history
  • Developmental history - Reports from nursery, speech therapist
  • Developmental examination
  • Full Physical examination including Dysmorphologic examination
  • Neurologic examination
  • Growth including head circumference

Investigations:

  • Genetics – Array CGH/Fragile X
  • Thyroid functions
  • Creatinine kinase (all musclular dystrophies)
  • Metabolic investigations (if indicated)
  • MRI (if indicated)
301
Q

What are the physical characteristics of Down’s syndrome?

A
  • —Hypotonia
  • —Small nose and flat nasal bridge
  • —Small mouth with a tongue that may stick out
  • —Upward slanting palpebral fissures
  • —Epicanthl folds
  • —A flat back of the head
  • —Broad hands with short fingers
  • —Single palmar crease
  • —Below-average weight and height
302
Q

Descrive QF-PCR - what is it good for finding?

A

Quantitative Floresence PCR uses microsatellites (varying lengths of CA dinucleotide repeats with specific ends) to locate how many chromosomes there are - used in trisomies 13, 18, 21 (and other aneuploidies)

QUICKER than other methods

BUT you need to know what you are looking for (to use the right microsattelite)

Total length of the microsatellie varies so you can see if peope are heterozygous or homocygous based on results

303
Q

Describe the different causes / types of Down Syndrome (3)

A

Trisomy due to non-disjunction in meiosis (PICTURE) (95%)

Translocation - Robertsonian (4%) - generally translocation with chromosome 14 resulting in 2 and a bit chromosome 21

Mosiacism (1%) - mixed cell liknes, happens post-zygotically (forms a mosiac blastocyst), milder

304
Q

Describe monsomic conditions - sex and sutosomal - are they common? Which conditions? How do they happen?

A
  • •Autosomal are very very rare, found one case report from 1967
  • •Relatively common sex chromosome monosomy = Turner’s
  • •Full monosomy arise by non-disjunction in meiosis I or II
  • •Mosaic arises by non-disjunction in mitosis
  • •Partial monosomy (microdeletion syndromes) far more common – mechanism different (not non-disjunction)
    • –One full copy of X chromosome, one missing a chunk!
305
Q

Summary of numerical abnormalities - autosomal, sex-linked

How do they happen?

A
  • •Types (all can be mosaic)
    • –Autosomal
      • •Trisomy 13, 18, 21
    • –Sex chromosomes
      • •XO, XXY, XXX, XYY
  • •Mechanism
    • –Nondisjunction
    • –Robertsonian translocation – what’s this?
306
Q

What is a translocation? What are the two types? How common are they and what is the implication for offspring?

A
  • •Two chromosomes sustain break and are incorrectly joined
  • •Translocations may be:
    • •Reciprocal (between two non-homologous chromosomes)
    • •Robertsonian (between any two acrocentric chromosomes)
  • •About 1 in 500 of us has a translocation
  • •Carriers of balanced translocations generally ok BUT can produce unbalanced gametes
307
Q

What is a balanced vs unbalanced translocation?

A
  • •Balanced = have the right amount of each chromosome just maybe not in the expected place!
  • •Unbalanced = too much or too little of a particular chromosome

EXCEPTION to balanced being okay - WHEN THE NEW CHROMOSOME NOW HAS TWO PROTO-ONCOGENES. the Philadelphia chromosome arises due to a translocation between chromosomes 9 and 22. On chromosome 9 is a gene called ABL1 which is a proto-oncogene. When positioned correctly on chromosome 9, it is not harmful. On chromosome 22 is a gene called BCR (which stands for breakpoint cluster region). There is a relatively high frequency of translocation events between these two chromosomes which result in a new fusion gene being formed on the derivative chromosome which is mainly chromosome 22 plus the terminal chunk of chromosome 9 which contains ABL1. This fusion gene, BCR-ABL1, is oncogenic and is the cause of many cases of chronic myeloid leukaemia.

308
Q

Describe the possible outcomes of children of balanced translocation carriers (when partner has normal gametes)

A
309
Q

What is the chromosomal result of robertsonian translocation

A

45 rather than 46 because you have lost the small tops of two and the longer bottom bits have fused (losing top bit often okay, because this genetic material is superfluous)

310
Q

Describe the three types of chromsome shape - which are the acrocentric chromosomes? What is the significance of these? What is the significance of a ‘centromere’?

A
311
Q

Outline how a Robertsonian translocation may result in Trisomy 21 in thier children (so parent is balanced carrier)

A
312
Q

What are the possible outcomes of translocations? (3) Can you predict them?

A
  • •Very difficult to predict
    • –Only have approximate probability of producing possible gametes
  • •Some unbalanced outcomes may lead to spontaneous abortion of conceptus so early that not seen as problem
  • •Some unbalanced outcomes may lead to miscarriage later on and present clinically
  • •Some may result in live-born baby with various problems
313
Q

Provide examples of other types of structural changes that can occur (4)

A
  • The first two are deletions, either from the end of the chromosome or from within a chromosome
    • If the end of the chromosome is lost then the only way the chromosome can be made stable is if a new telomere is added; without the telomere the cell will die
  • Inversions and duplications are literally as they’re described:
    • An inversion is where there are two breakpoints within the same chromosome and when these are repaired the middle section is “upside down”
    • A duplication is where you get a region of the chromosome repeated – you’ll probably be familiar with this in terms of the globin gene family
  • A ring chromosome is where you get two breaks in the same chromosome and then the non-homologous end joining mechanism (technical term for when broken ends of the same or two different chromosomes get stuck together) joins the two ends of the large chunk together, resulting in a ring.
314
Q

How common are chromosomal deletions? What are the two types? What is the result? What tests can you use to see them?

A
  • 1:7000 live births
  • Deletion may be terminal or interstitial
  • Causes a region of monosomy
    • Haploinsufficiency of some genes
    • Monosomic region has phenotypic consequences
    • Phenotype is specific for size and place on deletion
  • Gross deletions seen on metaphase spread on G-banded karyotype

EXAMPLE: Di George syndrom (22q deletion)

315
Q

Describe what you would see on a FISH analysis of Cri-du-chat syndrome. How does FISH work?

A

5p-minus syndrome

(Left pic is G-banding, right is FISH)

YOU WOUD SEE NO FLUORESENCE ON ONE OF THE CHROMOSOMES

HOW FISH WORKS: A probe (a strand of DNA) is designed specifically to be complementary to part of the region deleted in 5p minus syndrome. The probe has a fluorophore attached which will glow under UV light. The probe will only anneal (bind to it’s complementary sequence) if that specific bit of sequence is present; otherwise it will be washed away. This shows the probe glowing yellow under UV on one copy of chromosome 5 but not on the other copy. And that is because that region simply isn’t there. So this shows that that region has been deleted.

316
Q

What tools should you use to visualise large structural abnormalities (translocations, inversions, rings, large deletions / duplications)

A

G-banding (metaphase spread) and FISH

317
Q

What is a microdeletion? What causes it? Three common examples

A
  • Small deletions not seen on standard karyotype, use array comparative genomic hybridisation
  • Unequal cross-over in meiosis I causes a gain or loss of a few genes
  • Common deletion syndromes (typically developmentally delayed)
    • Wolf-Hirschhorn, 4p16
    • Williams, 7q11
    • Di George, 22q11
318
Q

What test should you use to check for microdeletions? How does it work?

A

Array-CGH is how we can detect microdeletions and microduplications.

319
Q

Explain briefly how abnormal karyotypes may be detected using stained metaphase chromosomes, FISH and qfPCR

A

G-banding relies on differential staining of eu- and hetero-chromatin; FISH uses specific fluorescent probes; QFPCR is a quick molecular technique which amplifies specific chromosomal regions

320
Q

Outline how abnormal chromosome numbers or structures arise and state the karyotypic consequences

A

meiotic non-disjunction, mitotic non-disjunction, chromosomal breaks and incorrect repair, unequal crossing over in meiosis

321
Q

Outline the clinical application of array CGH in the diagnosis of developmental delay and microdeletion syndromes

A

dosage-based analysis comparing patient with healthy control genome using fluorescent probes

322
Q

Describe the structures / components of an early fertilised zygote (pre-cleavage)

A
323
Q

How many polar bodies are in the fertilised zygote? When did these form?

A
324
Q

Describe cell fate and give overview of how cells receive their fate. Consider what else can change cell fate

A
  • By the progressive, sequential, restriction of cell fate
    • A cell’s fate is determined by its gene expression
  • Cell fate in embryos is specified by signals from surrounding cells
  • Signals® receptors® transduction pathways® transcription factors® gene expression® switch in cell fate
  • Long-term changes are fixed by epigenetic modification (but can be reversed!)
325
Q

REVIEW restriction of cell fate - what does the inner cell mass develop into (2)

A
326
Q

How many cell fate decisions are made pre-implantation?

A

In mammalian embryos, two cell fate decisions are taken before implantation.

Trophoectoderm, Inner cell mass, Primitive endoderm and epiblast

327
Q

Provide a simple overview of jounrey - ovulation, fertilisation and cleavage. What cell types are in the blastocyst?

A
  • •At ovulation, a single (usually) oocyte is released
    • –Guided by the fimbriated infundibulum into the ovarian tube
  • •Fertilisation usually takes place in the ampulla region
    • –Reductive/cleavage divisions (~16-24h) occur within the rigid, zona pellucida
  • •Early blastomeres (cells) are totipotent (can give rise to ALL tissue) and the embryo can regulate (eg baby born from 5-cell embryo)
    • –Blastomeres become progressively restricted in fate – pluripotent, multipotent etc
  • •Morula (~12-16 cells) undergoes compaction and a cavity forms (blastocyst)
  • •Blastocyst consists of TE and ICM
    • –The blastocyst must hatch from the zona pellucida before implantation, TE forms trophoblast
328
Q

What is the clincial significance of pre-implantation development? (4)

A

IVF

Pre-implantation diagnostics

Stem cell - research and therapeutic

Cloning

329
Q

What is the role of the zona peullcida in ectopic pregnancy?

A

It should prevent it from occurring as it provides a barrier to implantation pre-hatching (which should occur as zygote enters uterus. Early partial or full hatching may result in ectopic pregnancy

330
Q

Describe the relationship between the epiblast, hypoblast, blastocoele and amniotic cavity during implantation

A
331
Q

What does the blastocoele become? When? What is also developing at this time?

A

Yolk sac, day 14

Extraembryonic coelom around the outside (chorionic cavity)

332
Q

Describe the process of implantation - cell layers, differentiation of cell types, which cavities form

A
  • •The syncytiotrophoblast surrounds the embryo
    • –Invasion into uterine wall similar to metastasis
    • –Trophoblast synthesises hCG (chorionic gonadotrophin)
    • –Circulating hCG maintains the corpus luteum to secrete progesterone, maintain pregnancy
  • •The ICM divides to generate epiblast (ectoderm) and hypoblast (extra-embryonic endoderm/primitive endoderm)
    • –Two cavities are formed – amniotic and chorionic
333
Q

Once implantation has occurred what is the embryo ready to start?

A

Gastrulation

334
Q

What is imprinting?

A

Differential regulation of maternal/paternal genes

335
Q

What is the clinical significance of implantation? How many implant successfully? Where does it usually occur?

A
  • Implantation usually in posterior uterine wall
  • Morning-after pills (RU486) & IUDs interfere with implantation
  • 70% of blastocysts implant
    • –40% abort over week 2
    • –15% abort over week 3
  • •About 50% of spontaneously aborted embryos are chromosomally abnormal
336
Q

What is a hydaditiform mole?

A

•Expression of paternal genes only results in hydaditiform mole

–Contains trophoblast cells only, no embryo (but can be partial)

337
Q

Describe the early steps of gastrulation - what do the epi and hypoblast become? What transformation does the epiblast undergo?

A
  • Primitive groove forms, then streak (thickening of epiblast/ectoderm) in mid line of embryonic disk
  • Epiblast undergoes epithelial-mesenchymal transformation and cells migrate between epiblast/hypoblast to generate mesoderm and endoderm
338
Q

What is formed by the ecto, endo and mesoderm?

A
  • Endoderm (inside)
    • –Linings: epithelium of GI, urinary and respiratory tracts, epithelial parts of liver, pancreas, thyroid
  • Ectoderm (outside)
    • –Neurectoderm
      • •Neural tube (CNS & spinal cord)
      • •Neural crest
    • –Surface ectoderm
      • •Epidermis, hair, nails, internal ear, lens, enamel
  • Mesoderm (middle)
    • –Paraxial: somites – muscle, skeleton
    • –Intermediate: urogenital
    • –Lateral: Heart, spleen, blood
    • –Head: skull, dentine
339
Q

Describe different ways monozygotic twins can develop (4) - how common is each type? approx which day does the split occur?

A
340
Q

Describe the process of neuralation - what is being formed? when does this occur?

A
  • •The whole brain, spinal cord, cranial and spinal nerves all form from the neural tube
  • •The cranial and spinal ganglia form from the neural crest (part of the neural tube)
  • •This takes place at the end of week 3 and all of week 4
  • –Often prior to detection of pregnancy

This forms in the sequence: neural plate > neural groove > neural folds > neural tube (and neural crest migration)

341
Q

REVIEW first steps in neurulation - what is the role of the notochord?

A
342
Q

What day should the neural tube start to close? What covers the tube?

A
343
Q

What is occurring at the same time as neuralation?

A

Gut formation, body folding (‘silk purse’ model)

344
Q

What are the 3 types of error that can occur from improper neural tube closure?

A
  • Anencephaly
  • Craniorachischisis
  • Spina bfida
345
Q

Which closures are associated with each condition? Which days are these closures occuring?

A
346
Q

What are the four variations of spina bfida?

A
  • –Occulta (unfused vertebral arches)
  • –Meningocoele – meninges protrude
  • –Meningomyelocoele – meninges and nervous tissue protrude
  • –Myeloschisis aperta – open spinal cord
347
Q

What causes neural tube defects? How common are they? How can you test for them in pregnancy?

A
  • CAUSE:
    • Genetic - single or polygenic
    • Environmental - drugs, geography?
      • FOLATE, malnutrition
    • Multifactorial likely
  • Most common CNS malformation (between 0.5-2/1000 pregnancies)
  • TEST: Leakage of Alpha Fetoprotein (AFP) associated with NTDs
    • –Measure serum levels ~15 weeks
348
Q

Describe the closure of neural tube in respect to the notocord - what does it induce?

A

median hinge points

BETTER GENETIC UNDERSTANDING WOULD HELP US FIGURE OUT WHY THIS PROCESS SOMETIMES GOES WRONG

349
Q

Outline the cell types, structures and organs developed from ECTODERM

A
350
Q

Describe the process of convergence - extension: why does it happen? Which days?

A

A process of lengthening by narrowing, which requires cells to become polarized, in the plane of the cell layer

Lengthening of the neural plate is required for neural tube folding

351
Q

How effective is folate in preventing NTds? What else does it help prevent? Why does it have these effects? One other supplement that may have this effect

A
  • •Up to ~70% of NTDs can be prevented by folate
  • •Only known intervention preventive for any congenital anomaly
  • •Probably no adverse effects
  • •Also reduces palate & heart defects
  • •Folate is involved in one-carbon (1C) metabolism
    • Human mutations of genes in this pathway lead to increased NTD risk
  • •Other supplements?
  • –Inositol shows promise
352
Q

Describe somitogenesis - what is it? What layer does this process originate from?

A

Mesoderm

Skeleton, muscle and •relationships of bone to muscle to nerve to blood vessels along the trunk AND skin to nerve

353
Q

Where does the somite originate from (which layer)? What are the four types of somite?

A

+ syndetome

354
Q

What are the FOUR things that the epithelial somites differentiate into?

A
  • –Sclerotome: vertebrae and ribs
  • –Myotome: epimere, hypomere, limb muscle
  • –Dermatome: dorsal dermis
  • –Syndetome: tendons
355
Q

Describe the origin of the vertebra, muscle, nerve relationship

A

& then with skin (dermatome on top and tendons between vertebra and muscle

356
Q

REVIEW origins of the dermatome - what is an example of clinical significance (condition that presents along a dermatome)

A

Shingles

357
Q

Define Teratogenesis - what is the most common type of anamoly? What is the most common cause? How many classes of known human teratogens? What is most potent? second?

A
  • •The causes of congenital malformation
    • –From teratos – Greek: “monster”
  • •2-3% births have a structural anomaly
    • –Cardiovascular most common
    • –Functional and late onset disease - % unknown
  • •Structural: ~50% genetic, ~10% environmental, ~40% unknown – polygenic and/or gene-environmental interactions
  • •~20 classes of known human teratogen
    • –Some receptor mediated
    • –Of all toxicants, relatively few are teratogens
  • Most potent: Thalidomide
    • SECOND: Retinoids
358
Q

REVEIW: When is it most dangerous to be exposed to a teratogen? What defects are most common at each stage?

A
359
Q

What are the 10 questions that make up the Abbreviated mental test score (AMTS) test? What is the purpose? and what is the significance of a high or low score?

A
  1. How old are you?
  2. WHat time is it (to nearest hour)?

REMEMBER ADDRESS - 42 West Street, have them repeat it

  1. Who is that perosn (indicating to nurse or doctor)? What do they do?
  2. What year is it?
  3. What is the name of this place?
  4. What is your date of birth?
  5. What year did WW1 start?
  6. Who is the present monarch?
  7. Please count backwards from 20 to 1
  8. Could you please tell me the address I told you early

Life Cycle (1 decks)

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