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ALS > Block 8 > Flashcards

Block 8 Flashcards

1
Q

what does sexual function depend on? (5)

A
  • intact genitals
  • intact vascular supply
  • appropriate sexual stimulations
  • intact nervous supply
  • intact endocrine functions
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2
Q

what is the sexual trichotomy? (3)

A
  • sexual identity
  • sexual behaviour
  • sexual orientation
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3
Q

what is the sexual response? (2)

A
  • interplay between the mind and the body
  • interpersonal, cultural, environmental and biological factors interact to modulate sexual experience
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4
Q

what are two models of sexual responding?

A
  • Basson’s circular model
  • Blended sex response cycle
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5
Q

what is desire?(2)

A
  • spontaneous sexual interest
  • provides motivation to be sexual
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6
Q

what are sexual cues dependant on?

A

neuroendocrine function

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7
Q

what is controlled by the brain?

A

sexual thoughts

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8
Q

what is libido?

A

desire for sexual activity

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9
Q

what are the triggers for libido? (8)

A
  • sight
  • sound
  • smell
  • dopamine
  • oxytocin
  • melatonin
  • seratonin
  • prolactin
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10
Q

what inhibits sexual response? (3)

A
  • endocannabinoids
  • prolactin
  • y-aminobutyric acid
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11
Q

what brain regions are involved in sexual arousal? (6)

A
  • anterior cingulate gyrus
  • temporo-occipital lobes
  • prefrontal cortex
  • hypothalamus
  • thalamus
  • amygdala
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12
Q

what are the reasons for difficulty with desire? (3)

A
  • distracted
  • concerned
  • a lot on the mind
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13
Q

what happens during arousal? (6)

A
  • genital vasocongestive responses are highly automated
  • both sexes:
  • raised BP, resp rate
  • flushing over chest, breasts, face
  • nipple erection
  • muscular contraction
  • pelvic engorgement
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14
Q

what happens in male arousal? (4)

A
  • penis erects
  • scrotum thickens
  • testes rise
  • can occur during sleep
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15
Q

what happens in female arousal? (6)

A
  • enlargement of breasts
  • erection of nipples
  • vaginal lubrication
  • vasocongestion of vaginal walls
  • erection of clitoris
  • elevation of cervix
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16
Q

what is plateau? (4)

A
  • period of sexual excitement prior to orgasm
  • can be lost or gained
  • sense of impending orgasm
  • can last up to 3 minutes
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17
Q

what happens in women’s plateau? (4)

A
  • ‘orgasmic platform’ - labia becomes more swollen, darker red
  • lower 1/3 vagine swells and thickens
  • bartholiths secretions increase
  • clitoris sensitive and withdraws
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18
Q

what happens in male plateau? (2)

A
  • urethral sphincter contract to prevent urine mixing with semen
  • pre-ejaculatory fluid (Cowper’s gland) - testes rise
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19
Q

what is an orgasm? (2)

A
  • release of sexual tension and endorphins at end of plateau phase
  • quick muscle contractions - euphoric sensations
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20
Q

what are the features of male orgasms? (3)

A
  • 3-5 contractions of urethra
  • ejaculation
  • single orgasm
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21
Q

what are the features of female orgasms? (3)

A
  • 5-12 contractions
  • increased vaginal secretions
  • can have multiple orgasms
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22
Q

what is resolution?

A
  • relaxation - PR, BP falls, drowsiness
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23
Q

what are the features of male resolution? (3)

A
  • nipples/penis soften
  • scrotum relaxes
  • testes drop
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24
Q

what are the features of females resolution? (3)

A
  • blood vessels dilate
  • pelvic organs drain
  • cervix opens
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25
Q

what are the factors that affect sexual response? (7)

A
  • mood
  • age
  • relationships
  • psychological factors
  • illness
  • fertility concerns
  • medications
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26
Q

what is NATSAL and what did they find? (3)

A
  • National Surveys of Sexual Attitudes and Lifestyles
  • found more men and women are engaging in same sex - more common in women
  • increased average age of loosing virginity under 16
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27
Q

what is Hypoactive Sexual Disease? (HSD) (3)

A
  • lack or absence of sexual fantasies and desire for sexual activity
  • more common in women
  • causes significant distress
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28
Q

what are the factors of hypoactive sexual desire? (6)

A
  • partners
  • relationship
  • individual vulnerability
  • cultural
  • medical
  • physical
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29
Q

what is vaginismus?

A

cannot achieve penetration due to muscle spasm

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30
Q

what is female anorgasmia?

A
  • persistent or recurrent delay in or absence of orgasm
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31
Q

what might be the cause of female anorgasmia? (4)

A
  • anger
  • fear
  • loss of control
  • poor technique
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32
Q

what is premature ejaculation? (3)

A
  • ejaculation before wished, recurrently
  • more common in younger men
  • ‘performance anxiety’
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33
Q

what is the management of premature ejaculation? (4)

A
  • SSRIs
  • anaesthetic creams
  • thick condoms
  • start/stop method
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34
Q

what is male orgasmic disorder?

A

delay or absence of orgasm/ejaculation persistently

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35
Q

what are the causes of male orgasmic disorder?

A
  • sexual trauma
  • hostility
  • overcontrol
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36
Q

how to manage male orgasmic disorders?

A

psychological intervention

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37
Q

what is erectile dysfunction?

A

inability to attain/retain an erection until completion of sexual activity

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38
Q

what are the types of causes of erectile dysfunction? (3)

A
  • physical
  • psychological
  • mixed reasons
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39
Q

what is the management for erectile dysfunction?

A
  • taking a sexual history
  • physical exam
  • injections
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40
Q

what are the effects of aging on sexual function in males? (5)

A
  • delayed erections
  • longer excitement stage
  • more direct stimulation needed
  • shorter plateau
  • longer refractory period
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41
Q

what are the effects of aging on sexual function in females? (4)

A
  • decreased lubrication
  • decreased engagement
  • decreased muscular tension
  • decreased libido
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42
Q

what is the most common medication linked to dysfunction? (2)

A
  • SSRIs
  • antihypertensives
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43
Q

what is male circumcision?

A

foreskin is removed

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44
Q

when is male circumcision performed?

A

1 or 2 days after birth

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45
Q

how long does the male circumcision take?

A

5-10 mins

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46
Q

why do males get circumcised?

A

religious reasons

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47
Q

what are some indications of male male circumcision? (4)

A
  • phimosis - tight foreskin
  • recurrent blanitisis
  • paraphimosis
  • cancer
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48
Q

what is Female Genital Mutilation? (2)

A
  • partial/total removal of external female genitalia
  • illegal some places, no health benefits
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49
Q

what age is what is Female Genital Mutilation performed at?

A

under 18

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50
Q

why do people undergo Female Genital Mutilation? (4)

A
  • good tradition
  • religious reasons
  • cleanliness
  • preserve virginity
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51
Q

what are the types of FGM? (4)

A
  • type 1 - clitoridectomy - removal of clit
  • type 2 - excision - remove of clit and inner labia
  • type 3 - infundibulation - sewing inner/outer labia
  • type 4 - other harmful procedures - stretching, cutting, burning
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52
Q

what are the laws against FGM? (2)

A
  • FGM Act 2003 - guilty of an offence if mutiliation is performed
  • Serious Crime 2015 - duty to notify police if discovered
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53
Q

what are the life stages of men and women?

A
  • female - premenarcheal - fertile - perimenopausal - postmenopausal
  • male - preadolescent - fertile -
    decline in between stages
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54
Q

what is adolescence?

A

puberty and associated psych development

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55
Q

what is puberty?

A

state of becoming capable of procreation

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56
Q

what is adrenarche?

A

adrenal development towards puberty

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57
Q

what is pubarche?

A

pubic hair development part of puberty

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58
Q

what is menarche?

A

time of first menstrual period

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59
Q

what is menopause?

A

last menstral bleed (12mths ago)

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60
Q

what is climacteric?

A

period of life leading up to last menstrual bleed (10yrs+)

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61
Q

what is perimenopause?

A

period of life prior to and 12 months after menopause

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62
Q

what is post menopause?

A

life after menopause

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63
Q

how is the preadolescent phase characterised? (3)

A
  • immature hypothalamus
  • slow pulses of GnRH
  • minimal FSH and LH from pituitary - no ovarian follicle development so no testorone or oestradiol production
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64
Q

what are the critical weights? (2)

A
  • initiation of adolescent spurt - 30kg
  • onset of menarche - 46kg
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65
Q

how has the age for menarche changed overtime? (2)

A
  • age has fallen as general health and nutrition has improved
  • 1860 to 1960, 17yrs to 13yrs
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66
Q

what are the clinical problems of menarche?

A
  • precocious puberty - menarchy - <9yrs
  • delayed puberty - menarchy - >16yrs
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67
Q

what is the optimal time for fertilisation?

A

one day before ovulation

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68
Q

what factors reduce cumulative pregnancy rates? (3)

A
  • increasing age
  • smoking
  • pathology
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69
Q

what is the mean volume lost in one period?

A

30mL

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70
Q

what is the average length of a cycle?

A

28 days

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71
Q

what % of oestrogen are made from thecal cells?

A

95%

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72
Q

what happens in the absence of granulose cells? (2)

A
  • androgens cannot be converted into oestrogen
  • therefore no negative feedback on FSH and LH
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73
Q

where is GnRH produced?

A

hypothalamus

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74
Q

what is FSH and LH produced?

A

anterior pituitary

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75
Q

what are the features of older oocytes? (3)

A
  • less likely to fertilise
  • less likely for embryo to implant
  • more likely to miscarriage a genetically abnormal child
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76
Q

what is Premature Ovarian Failure?

A
  • amenorrhea (absence of period) for more than 6 months before 40
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77
Q

what % of women suffer from Premature Ovarian Failure?

A

1%

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78
Q

what is Premature Ovarian Failure characterised by? (3)

A
  • increased FSH
  • anovulation
  • hypoestrogenism
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79
Q

what are the causes of Premature Ovarian Failure?

A
  • apoptosis defects
  • unresponsive to hormone stimulation
  • X-linked sex gene
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80
Q

what % of fertility treatment is for women >35?

A

50%

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81
Q

what are climacteric (menopausal) symptoms? (8)

A
  • hot flushes
  • menstrual irregularity
  • mood swings
  • tiredness
  • inability to concentrate
  • depression
  • sleep disturbances
  • forgetfulness
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82
Q

what is HRT?

A
  • Hormone Replacement Therapy
  • given in pills, patches and implants
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83
Q

what could happen as a side effect of HRT? (2)

A
  • oestrogen could stimulate endometriosis, hyperplasia and carcinoma
  • prescribed alongside progestogens
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84
Q

what are the benefits and risks of HRT? (9)

A
  • relief of symptoms
  • osteoporosis prevention
  • general wellbeing
  • cardiac disease
  • thrombosis
  • uterine cancer
  • breast cancer
  • altzheimers
  • cardiac disease
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85
Q

How many steps are there to determine sex?

A

3

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86
Q

What are the three stages of sex determination?

A
  1. Development of bipotential gonad
  2. Sex determination
  3. Sex differentiation
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87
Q

What type of sex are determined in each stage?

A
  1. Genetic sex - determined by fertilisation
  2. Phenotypic sex - determined by gonad
  3. Secondary sex - driven by hormones
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88
Q

What determines sex?

A

Prescence of a Y chromosome

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89
Q

Which chromosome is shorter?

A

Y

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90
Q

What does Y chromosome do?

A

Starts the process of making a testis

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91
Q

When is sex determined?

A

At fertilisation

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92
Q

How many chromosomes do autosomes carry?

A

22

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93
Q

What can oocytes and sperm carry?

A
  • Oocytes - X
  • Sperm - X or Y
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94
Q

What is the golden rule?

A

If Y chromosome is present, then genetic sex is male

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95
Q

What are the exceptions to the golden rule?(2)

A
  • XXsxr = sex reversal - SRY region is translocated onto an X chromosome
  • XY females - absence of SRY
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96
Q

How does the gonad determine sex? (3)

A
  • Mesenchymal knots form behind dorsal aorta
  • Migration of cells from hindgut - sex indetermined
  • Expansion of these cells migrate to the developing kidney
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97
Q

Where do the PGCs colonise in each sex? (2)

A
  • In males, the pgc colonise the medulla
  • in females the cortex
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98
Q

What do the coelomic epithelia migrate to form?

A

Primitive sex cords

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99
Q

Where is SRY gene expressed?

A

Germinal epithelium

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100
Q

What does the fetal gonad form?

A

Bipotenital primordia

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101
Q

What does the cortex develop into in both sexes?

A
  • In females, the cortex develops into an ovary and the medulla degenerates
  • In males, the medulla develops into a testis and the cortex degenerates
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102
Q

What are the features of SRY expression in males? (4)

A
  • Expressed in cells of developing sex cords.
  • Proliferate and penetrate medullary mesenchyme
  • Surround PGCs [prospermatogonia]
  • Testis cords
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103
Q

What are the features of no SRY expression in females? (4)

A
  • Expressed in cells of developing sex cords.
  • Proliferate and penetrate medullary mesenchyme
  • Surround PGCs [prospermatogonia]
  • Testis cords
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104
Q

What are the features of no SRY expression in females? (3)

A
  • Sex cords lack defined structure
  • Do not penetrate into ridge
  • Condense and cluster around PGCs [oogonia]
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105
Q

How does SRY act? (2)

A
  • SOX9
  • Releases prostaglandin D2
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106
Q

What is the role of PGD2? (2)

A
  • sustains expression of SOX9
  • induces production of fibroblast growth factor 9 –which also drives expression of SOX9
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107
Q

What does SOX9 inhibit?

A

Foxl2

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108
Q

What hormone does SOX9 produce?

A

AMH - anti-malarian hormone

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109
Q

What triggers migration of mesonephric cells?

A

FG9

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110
Q

Where do the mesonephric cells migrate to?

A

Mullerian duct

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111
Q

What cells migrate to the mesonephric primordia in females?

A
  • Theca cells
  • Vascular tissue
  • Do not express SRY gene
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112
Q

What happens when there is no SRY gene?

A
  • Foxl2 not inhibited
  • Drives expression of Wnt4
  • Wnt4 signals to make granulose cell
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113
Q

What do PGCs do NOT express?

A

SRY

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114
Q

What are the features of PGC in males?

A

PGCs encased in sex cords and cease mitosis

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115
Q

What are the features of primordial germ cells (PGC) in females? (2)

A
  • are surrounded by granulosa
  • they enter meiosis, forming primary oocytes
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116
Q

What are essential for male development? (2)

A
  • AMH
  • Androgen
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117
Q

What happens in the absence of AMH and androgen?

A

Feminisation development

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118
Q

What are the two ducts?

A
  • Wolffian Duct [Mesonephric]
  • Müllerian Duct [Paramesonephric]
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119
Q

What happens to the ducts in female? (2)

A
  • Wolffian Duct regresses
  • Müllerian Duct produces female reproductive tract
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120
Q

What does the wolffian duct develop into? (2)

A
  • Epididymis
  • Vas deferens
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121
Q

what does the Mullerian duct develop into? (2)

A
  • oviducts
  • uterus
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122
Q

What happens when there is no androgen?

A

Wolffian duct regression

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123
Q

What happens to female exposure to androgen?

A

Male internal genitalia persist

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124
Q

What is the wolffian duct maintained by?

A

Androgens from Leydig cells

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125
Q

How do males and females differ? (7)

A
  • Breast development
  • Voice
  • Growth of genitalia
  • Musculature
  • Voice
  • Androgenous hair patterning
  • Baldness
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126
Q

When does observable puberty begin at?

A

‘Gonadarche’

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127
Q

Who updated nomenclature for Disorder of Sex Development (2)?

A

Chiacago consensus

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128
Q

What is DSD?

A

Differences in sex development

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129
Q

What is Turners syndrome? (3)

A
  • Xo
  • Unpaired X chromosome
  • Has ovaries but infertile
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130
Q

What is Klinefelters syndrome?

A
  • XXY
  • Extra sex chromosome
  • Has testes but infertile
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131
Q

What is androgen action?

A
  • Testi produces androgen
  • Acts on target tissue
  • androgen acts only on tissues with intracellular androgen receptors
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132
Q

What is AIS?

A
  • Androgen insensitivity syndrome
  • androgen is secreted by the testes, but target tissues fail to respond
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133
Q

what are the sex chromosomes in AIS?

A
  • XY sex chromosomes (male) but phenotypically female, and infertile
  • AMH acts on Mullerian Duct; no internal genitalia
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134
Q

What are the features of AIS?

A
  • Testes are present
  • Testosterone is produced
  • Target tissues fail to respond - androgen receptors are absent
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135
Q

What is Guevedoces?

A

Penis at 12

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136
Q

Who and what % of the population is affected by Guevedoces?

A
  • 2%
  • Dominican Republic
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137
Q

What are the features of Guevedoces? (4)

A
  • develop as girls until puberty – but are XY and have testes
  • then ‘clit’ expands into penis, testes descend
  • thereafter function as normal males
  • deficient in enzyme 5-α reductase
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138
Q

Why does Guevedoces occur?

A

at puberty rising androgen levels overcome tissue insensitivity

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139
Q

What is Congential Adrenal Hyperplasia? (5)

A
  • XX
  • Genetic basis – not linked to sex chromosomes.
  • Fetal adrenals hyperactive to overcome low production of corticosteroids.
  • Wolffian duct AND Mullerian duct retained.
  • External male genitalia
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140
Q

Who has menstral cycles? (6)

A

of post-pubertal age
* …of pre-menopausal age
* …who haven’t suffered POF
* …who are not severely under or overweight
* …who are not pregnant
* …who are not breast feeding*

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141
Q

How many amino acids make ip GnRH?

A

10

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142
Q

What are the three glycoproteins?

A
  • Luteinizing Hormone (LH)
  • Follicle Stimulating Hormone (FSH)
  • Chorionic Gonadotropin (CG)
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143
Q

What cannot cross the cell membrane?

A

Decapeptides

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144
Q

What does GnRH bind to?

A

GnRH receptors

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145
Q

What are the four classes of steroids?

A
  • Progestogens (21 C)
  • Androgens (19C)
  • Oestragens (18C)
  • Corticosteroids
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146
Q

What is the common biochemical precursor?

A

Cholesterol

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147
Q

What do all 4 steroids share?

A

The common synthetic pathway

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148
Q

What are estrogens aromatized forms of?

A

Androgen substances

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149
Q

What are steroids derived from?

A

Acetate/lipids

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150
Q

What is the clearance rate for each hormone? (5)

A
  • Steroid - 2-3 min
  • Prostaglandins – 3-10 min
  • LH – 30 min
  • FSH - 3-4h
  • CG – 24h
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151
Q

What are hormones regulated by? (4)

A
  • Receptor levels
  • Hormone production rate
  • Clearance rate
  • Binding proteins
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152
Q

Where is the location of the menstrual cycle?

A

Head
Ovary

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153
Q

How often do pulses of GnRH occur?

A

Every hour

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154
Q

When is endocrine function released?

A

At puberty

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155
Q

When is gametogenic potential established?

A

In the fetus

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156
Q

When are the mitotic stages of oogenesis all completed by?

A

Birth

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157
Q

Where do oocytes ride?

A

Primordial follicle

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158
Q

What do you call oocytes that reside in a primordial follicle?

A

Primary oocytes

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159
Q

What are primary oocytes surrounded by?

A

Granulosa cells

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160
Q

What happens at gamete production?

A
  • Proliferation by mitosis - all completed in females before birth.
  • Genetic ‘shuffling’ by meiosis - starts in fetal ovary, arrests, and restarts at puberty.
  • Cytodifferentiation - during ovarian cycle
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161
Q

What is folliculogenesis?

A
  • Follicles grow and mature.
  • Pre antral development sees oocyte growth.
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162
Q

How long does folliculogenesis take?

A

70 days

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163
Q

When is it referred to as a primary follicle?

A

When the egg is fully grown

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164
Q

What is a follicular trickle?

A

Primordial to primary to secondary (antral) to tertiary (pre-ovulatory)

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165
Q

What is the process called where an egg is lost?

A

Atresia

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166
Q

How often is an egg lost?

A

1 every 90 minutes

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167
Q

What is an antral?

A

Follicle with a gap full of fluid

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168
Q

What cells surround the antrum? (2)

A

Theca cells
Granulosa cells

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169
Q

When does the follicular phase start and end?

A

Day of menses and ends with ovulation

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170
Q

What is the first stage of ovulation?

A

Follicular phase

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171
Q

What receptors do theca cells express?

A

LH receptors

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172
Q

What receptors do granulosa cells express?

A

FSH receptors

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173
Q

What do the thecal cells produce?

A

Androgens

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174
Q

What do granulosa cells produce?

A

Androgen aromatase

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175
Q

What does an increase in androgen aromatase produce?

A

Increase in oestrogen

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176
Q

What do androgens cause granulosa cells to do?

A

Proliferate

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177
Q

What does proliferation of granulosa cells cause?

A

Follicular growth

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178
Q

What happens when there is an increase in granulosa cells?

A

Increase in oestrogen

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179
Q

What does an increase in oestrogen have on granulosa cells?

A

Cause granulosa cells to express both LH and FSH receptors

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180
Q

How much of an increase is there in oestrogen surge?

A

200x more in blood

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181
Q

What does an increase in oestrogen cause?

A

LH surge

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182
Q

What does an LH surge cause? (2)

A
  • Granulosa cells to produce progesterone
  • This triggers ovulation
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183
Q

When does second meiosis begin?

A

Metaphase
Oocyte arrests

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184
Q

What is nuclear maturation?

A

Oocyte resumes meiosis and undergoes ‘division.’

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185
Q

What is cytoplasmic maturation?

A
  • Cytoplasm reorganized.
  • Mitochondria relocate to periphery
  • Cortical granules migrate to periphery
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186
Q

What are cumulus cells?

A

Associated granulosa cells under expansion

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187
Q

When does ovulation occur?

A

Day 14/28

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188
Q

What happens in the luteal phase? (3)

A
  • Ruptured follicle forms - corpus luteum
  • Secretes oestragen and progesterone.
  • Theca cells now have LH receptors.
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189
Q

What do luteal cells produce?

A

increases - progesterone
decreases - oestrogen

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190
Q

what happens in the menstrual phase?

A

Shedding of the uterine lining

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191
Q

What are the phases of the uterine phase (3)

A
  • Menstrual phase
  • Proliferative Phase
  • Secretory Phase
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192
Q

What happens in the proliferative phase? (3)

A
  • Endometrium and myometrium begin to regrow.
  • Preparing for possible pregnancy
  • Cervical mucal secretions change.
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193
Q

What happens in the secretory phase? (3)

A
  • Blood supply to endometrial tissues remodeled.
  • Cervical secretions change again.
  • Supported by progesterone.
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194
Q

When is the endometrium re-epithelized after menstruation?

A

4-7 days

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195
Q

What hormones are produced in the secretory phase? (2)

A
  • Estrogen - cellular proliferation
  • Progesterone - swelling and secretory development
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196
Q

What are the two types of contraceptives?

A
  • Combined oral contraceptive
  • Progestin - High dose progestin, Lower dose progestin
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197
Q

how long does sperm survive?

A

up to 7 days

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198
Q

how long does oocytes survive?

A

up to 24 hours

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199
Q

how long is the fertile window?

A

8/9 days in each cycle

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200
Q

when is conception most likely to occur? (2)

A

following unprotected sexual intercourse…
- on day of ovulation OR
- proceeding 24 hours

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201
Q

what are the three natural methods of contraception?

A
  • Fertility Awareness Method (FAM)
  • Lactational Amenorrhoea Method (LAM)
  • Coitus interruptus (withdrawl)
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202
Q

what is the Fertility Awareness Method?

A

awareness of fertility indicators enabling women to know where they are in their cycle are most fertile

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203
Q

what are some fertility indicators? (4)

A
  • temperature
  • cervical secretions
  • calendar
  • standard days method
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204
Q

what is the best efficacy for the Fertility Awareness Method?

A

symptothermal method - plotting the changes in mucus, body temp and secretions

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205
Q

what is the mucus secreted as a result of the menstrual cycle called?

A

Spinnbarkeit mucus

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206
Q

which hormone changes the consistency of cervical mucus?

A

progesterone - forms plug

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207
Q

what are the advantages of the Fertility Awareness Method? (2)

A
  • no hormones involved
  • no alterations to cycle
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208
Q

what are the disadvantages of the Fertility Awareness Method?

A
  • unreliable
  • user dependant
  • no protection against STIs
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209
Q

what does breastfeeding delay in the Lactational Amenorrhoea Method (FAM)?

A

the resumption of ovulation after birth

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210
Q

what does the suckling stimulus disrupt?

A

release of GnRH

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211
Q

how long is the Lactational Amenorrhoea Method effective for?

A

up to 6 months after childbirth

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212
Q

what are some restrictions to FAM and LAM? (6)

A
  • irregular menstral cycles
  • postpartum
  • recent use of hormonal contraceptives
  • medications
  • medical conditions
  • teratogenic drugs
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213
Q

what is coitus interruptus also referred to as?

A

withdrawal

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214
Q

what % of women use withdrawal?

A

4-6%

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215
Q

what does pre-ejaculate contain?

A

sperm

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216
Q

what is the % effectiveness of ‘perfect’ use of withdrawal?

A

96%

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217
Q

what is the % effectiveness of ‘typical use’ of withdrawal?

A

78%

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218
Q

what is the mechanism of action of combined contraception? (2)

A
  • inhibition of ovulation
  • alterations to cervical mucus and endometrium
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219
Q

what are the advantages of combined contraception? (2)

A
  • relieve menstrual disorders
  • reduce risk of ovarian cancer
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220
Q

what are the adverse effects of combined contraception? (2)

A
  • increase risk of stroke/VTE
  • increase risk of breast and cervical cancer - decreases after stopping
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221
Q

what are the disadvantages of combined contraception? (4)

A
  • reliant on user
  • no STI protection
  • contraindications
  • side effects
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222
Q

what is the risk of thromboembolism when taking combined contraception?

A

15/100,000 per year

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223
Q

what increases the risk of thromboembolism? (2)

A
  • smoking
  • long term use in women over 35
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224
Q

what is POP?

A

progestogen only pill

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225
Q

what is the mechanism of POP? (2)

A
  • increases volume andviscosity of cervical mucus
  • variable effect on ovulation depending on progesterone used
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226
Q

what are the adverse effects of POP? (2)

A
  • menstral disturbances are common
  • hormonal side effects
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227
Q

what are the advantages of POP? (4)

A
  • highly effective
  • can help dysmenorrhoea
  • 12 hour window for desogestrel
  • quickly reversible
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228
Q

what are the disadvantages of POP? (2)

A
  • user dependant
  • no STI proteion
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229
Q

where is oestrogen absorbed?

A
  • in the GI tract
  • skin and mucous membranes
230
Q

where is oestrogen metabolised?

A

liver

231
Q

where is oestrogen excreted?

A

urine as glucronides and sulphates

232
Q

what are both COCP and POP metabolised by?

A

CYP 450 enzymes in the liver

233
Q

what is oral contraceptive efficacy reduced by?

A

enzyme inducing drugs

234
Q

what do enzyme inducing drugs increase?

A

the production of hepatic CYP450

235
Q

what effect does soya protein products have on oestrogen? (2)

A
  • enhance oestrogen absorption
  • reduce its storage in adipose and muscle
236
Q

by how much time do soya products reduce the life of contraceptives?

A

15 hours to 7 hours

237
Q

what does LARC stand for?

A

long acting reversible contraception

238
Q

what are some examples of long acting reversible contraception?

A
  • injectable progesterone
  • implant
  • intrauterine device
  • intrauterine system
239
Q

what is intrauterine system called a system?

A

because it releases progesterone overtime

240
Q

what is the mechanism of action of INJECTED progestogen only? (2)

A
  • inhibits ovulation
  • thickens cervical mucus and prevents endometrial proliferation
241
Q

what are the advantages of INJECTED progestogen only? (4)

A
  • reliable - eliminates user failure risk
  • suitable where COCP contraindicated
  • reduced bleeding - amenorrhoea by 12 months
  • self-administration increasing acceptability and convenience
242
Q

what are the adverse effects of INJECTED progestogen only? (3)

A
  • weak associations with breast and cervical cancer
  • weight gain
    small loss of BMD - recovers after stopping
243
Q

what are the disadvantages of INJECTED progestogen only? (4)

A
  • not possible to remove once given
  • clinical appointment needed every 12 weeks for IM option
  • delay in return to fertility up to 1 year
  • no protection from STIs
244
Q

what is the mechanism of action for the progestogen only IMPLANT? (2)

A
  • inhibits ovulation
  • thickens cervical mucus and prevents endometrial proliferation
245
Q

what are the advantages of the progestogen only IMPLANT? (4)

A
  • reliable
  • suitable when COCP contraindicated
  • lasts for 3 years
  • rapid return to fertility after removal
246
Q

what are the adverse effects of the progestogen only IMPLANT? (2)

A
  • altered bleeding patterns - likely to remain irregular
  • risk of fitting
247
Q

what are the disadvantages of the progestogen only IMPLANT? (2)

A
  • minor to insert
  • no protection from STIs
248
Q

what is an intrauterine system (IUS)?

A

progestogen releasing plastic device

249
Q

how long does the intrauterine system work for?

A

3-5 years

250
Q

what is the mechanism of action of the intrauterine system? (3)

A
  • reduces endometrial proliferation
  • preventing implantation
  • thickens cervical mucus
251
Q

what is the intrauterine device (IUD)?

A

plastic device with added copper

252
Q

how long does the intrauterine device (IUD) work for?

A

5-10 years

253
Q

what is the mechanism of action for the intrauterine device (IUD)

A
  • copper is toxic to sperm and ovum
  • prevents fertilisation
  • inflammatory reaction affecting endometrium preventing implantation
254
Q

what can be used to guide patient preference with patient safety?

A

UKMEC Summary Table - Hormonal & Intrauterine Contraception

255
Q

what does 1 on the UKMEC Summary Table represent?

A

a condition for which there is no restriction for the use of the method

256
Q

what does 4 on the UKMEC Summary Table represent?

A

a condition which represents an unacceptable health risk if the method is used

257
Q

what are the three types of emergency contraception?

A
  • intrauterine device
  • levonorgestrel
  • ulipristal acetate (UPA)
258
Q

when is the effectiveness of UPA reduced? (2)

A
  • if progesterone is taken in the following 5 days
  • OR previous 7 days
259
Q

what are the contraindications of emergency contraception?

A
  • IUD - same as routine insertion
  • UPA - severe asthma
260
Q

what are the cautions of emergency contraception? (3)

A
  • breast feeding
  • higher risk of perforation with IUD
  • express or discard milk after UPA for 7 days
261
Q

what is the mechanism of action of IUD? (2)

A
  • toxic to gametes therefore can prevent fertilisation
  • prevents implantation through the inflammatory reaction caused by the copper
262
Q

what is the mechanism of action of ulipristal acetate?

A

delays ovulation through disruption of the HPO axis

263
Q

what is the mechanism of action of levonorgestrel?

A

delays ovulation through disruption of HPO axis

264
Q

what is the mechanism of action of barrier methods? (4)

A
  • condoms
  • diaphragm/cap
  • all represent physical barrier preventing entrance of sperm into cervix
  • can be used with spermicide for additional barriers
265
Q

what are the advantages of the barrier method? (3)

A
  • reliable - average 80%
  • provides STI protection
  • male condom widely available
266
Q

what are the disadvantages of the barrier method? (3)

A
  • not as effective as other methods
  • diaphragm/cap requires healthcare professional to fit
  • latex sensitivity
267
Q

what is the mechanism of action of male surgical sterilisation? (2)

A
  • division of the vas deferens
  • done under anaesthesia
268
Q

what are adverse effects of male surgical sterilisation? (2)

A
  • immediate and post op bleeding, pain, infection, vasovagal, failure
  • long term - late failure, chronic pain
269
Q

name the types of female sterilisation? (3)

A
  • tubal occlusion
  • partial salpingectomy
  • laparoscopy
270
Q

what is the mechanism of action of tubal occlusion?

A

occlusion of the uterine (fallopian) tube using a ring or clip

271
Q

what is the mechanism of action of partial salpingectomy?

A

removal of a section of the uterine (fallopian) tube

272
Q

what are the adverse effects of female surgical sterilisation? (6)

A
  • bowel perforation
  • bleeding
  • infection
  • failure
  • ectopic pregnancy
  • post op pain
273
Q

what is the inner layer of the uterus called?

A

endometrium

274
Q

what is the middle layer of the uterus called?

A

myometrium

275
Q

what is the outside layer of the uterus called?

A

perimetrium (peritoneum)

276
Q

what are the subdivisions of the endometrium? (2)

A
  • stratum functionale
  • stratum basale
277
Q

which layer is involved in the shedding and building of the uterine wall?

A

stratum functionale

278
Q

what is the epithelium of the cervical canal?

A

simple columnar epithelium

279
Q

what is the epithelium of the ectocervix?

A

stratified squamous epithelium

280
Q

what is the epithelium of the vagina?

A

stratified squamous epithelium

281
Q

what main artery supplies the uterus?

A

internal iliac artery

282
Q

which structures are inferior to the pelvic diaphragm muscles? (4)

A
  • anal canal
  • distal urethra
  • external genitalia
  • spaces inbetween containing av & n
283
Q

what structures are contained in the superficial perineal pouch? (2)

A
  • corpus cavernous
  • bulb of vestibule
284
Q

what structure are contained in the deep perineal pouch?

A

greater vestibule glands

285
Q

what muscles are contained in the superficial perineal pouch? 4

A
  • bulbospongiosus
  • ischiocavernous
  • superficial transverse perineal
  • perineal body
286
Q

which nerve innervates the perineum?

A

pudendal nerve

287
Q

which nerves does the pudenal nerve branch off to in females? (2)

A
  • dorsal nerve of clitoris
  • posterior labial nerve
288
Q

which arteries supply the perineum in females? (5)

A
  • internal pudenal artery
  • deep artery of clitoris
  • dorsal artery of clitoris
  • artery of vestibular bulb
  • posterior labial artery
289
Q

which veins supply the perineum in females? (4)

A
  • internal pudendal vein
  • vesicle plexus
  • deep dorsal vein of clitoris
  • posterior labial vein
290
Q

what is a convenient index of weight?

A

BMI

291
Q

how do you calculate BMI?

A

weight (kg) / hight (m2)

292
Q

what is healthy BMI?

A

18.5-24.9

293
Q

what is overweight BMI?

A

25-29.9

294
Q

what is overweight BMI?

A

30-39.9

295
Q

what is BMI of obesity class 1?

A

30-35

296
Q

what is BMI of obesity class 2?

A

35-40

297
Q

what is BMI of obesity class 3?

A

40-45

298
Q

what does BMI not account for? (4)

A
  • sex
  • age
  • pregnancy
  • muscle mass/athletes
299
Q

What % increase was there for obesity in 2016?

A

18%

300
Q

What % of adults are classified as obese in the UK?

A

63%

301
Q

What is the universal guidance to diet? (4)

A
  • Eat sensible amount of calories
  • Eat variety of foods
  • Eat plenty of food rich in fibre/starch
  • Eat plenty of fruit and veg
302
Q

What is the Mediterranean diet? (2)

A
  • High in fruit, veg, whole grain, olive oil
  • High micronutrients, fibre, unsaturated fat
303
Q

Mediterranean diet is associated with lower…? (4)

A
  • CVD
  • Mortality
  • Obesity
  • Type 2 diabetes
304
Q

What are the impacts of unhealthy weight? (6)

A
  • Increase blood pressure
  • Increase LDLs, decrease HDLs
  • Insulin resistance
  • Increased diabetes risk
  • Increased CVD risk
  • Increased fasting glucose
305
Q

Who is the most common for central abdomen obesity?

A

Men

306
Q

Who is the most common with pear-shaped obesity?

A

Women

307
Q

What are the risks of having central/abdominal obesity? (3)

A
  • Increased heart disease
  • Increase insulin resistance
  • Increase diabetes
308
Q

How many inches must your waist be to be recommended to lose weight? (2)

A
  • Women - 37 inches
  • Men - 31.5 inches
309
Q

What does visceral fat secrete? (2)

A
  • Adipokines
  • Free fatty acids
310
Q

What is the equation for energy balance?

A
  • Energy intake - energy output
311
Q

What happens in a negative energy balance?

A

Loss of energy store, body weight, carbs, fat or protein

312
Q

What happens in a positive energy balance?

A

Gain in of energy store, body weight, carbs, fat or protein

313
Q

What are the key hormones in in appetite control? (4)

A
  • Leptin
  • Ghrelin
  • Insulin
  • Cortisol
314
Q

What regulates food intake and body weight?

A

Negative feedback loop

315
Q

What is ghrelin involved in? (3)

A
  • Appetite
  • Food intake
  • Energy balance
316
Q

What does ghrelin stimulate? (2)

A
  • Appetite
  • Lipid storage
317
Q

Before eating what are the levels of ghrelin and leptin?

A
  • Ghrelin is high
  • Leptin is low
318
Q

After eating what are the levels of ghrelin and leptin?

A
  • Ghrelin is low
  • Leptin is high
319
Q

Which hormone is significantly higher in patients with anorexia?

A

Ghrelin

320
Q

What does insulin stimulate? (3)

A
  • Glucose uptake by GLUT4
  • Glycogen synthesis
  • Fatty acid synthesis
321
Q

Whose responsibility is it to reduce obesity? (3)

A
  • Individual
  • Food industry
  • Government
322
Q

How can individuals reduce obesity? (6)

A
  • Make conscious choices
  • Avoid dieting
  • Get more active
  • Non-judgemental
  • Be supportive
323
Q

How can the food industry reduce obesity? (3)

A
  • Enable people to make the right choices
  • Advertise variety
  • Clarity in packing labels
324
Q

How can governments reduce obesity?

A

Regulate food industry

325
Q

How do we measure food intake? (3)

A
  • Food diary
  • Nutritionist interview
  • Weigh food
326
Q

How do we measure expenditure? (4)

A
  • Double-labelled water
  • Dominant wrist accelerator
  • Digital photography of food
  • Wearable tech
327
Q

What is evolutionary medicine?

A

Interface between evolutionary biology and medicine

328
Q

What is the purpose of evolutionary medicine?

A

Tries to find evolutionary explanations for vulnerabilities to disease

329
Q

What are examples of evolutionary medicine? (2)

A
  • Covid-19
  • Sickle cell anaemia
330
Q

What are proximate causes of ill health?

A

Causal factors, the way an individual behaves in their lifetime

331
Q

What are the evolutionary causes of ill health?

A

Factors influencing survival, inheritable traits

332
Q

Where has there been an increase in prevalence of obesity?

A

Populations undergoing ‘modernization’

333
Q

What is a western lifestyle?

A

Less energy expenditure and energy dense food with lower fibre

334
Q

What trait reduces obesity? (2)

A
  • Promote adipose tissue may have been adaptive
  • Better survival chances and greater reproductive success
335
Q

What cultural factors affect obesity? (2)

A
  • Different cultures have specific preferences for body shape
  • i.e. larger body mass may be favoured/avoided
336
Q

What is the link between obesity & diabetes? (2)

A
  • Obesity does not cause diabetes
  • Obese individuals are at higher risk of getting diabetes and many people with diabetes are obese
337
Q

What is diabetes?

A

Disease of glucose metabolism defined by elevated blood sugar

338
Q

What is type 1 diabetes? (2)

A
  • Insulin dependant
  • Occurs due to damage of insulin-producing cells in the pancreas
339
Q

What is type 2 diabetes?

A

Efficacy of insulin is reduced, therefore glucose not taken up by muscles and organs

340
Q

What are the complications of type 2 diabetes? (6)

A
  • Heart disease
  • Stroke
  • High BP
  • Circulatory problems
  • Nerve damage
  • Thrifty genotype
341
Q

What are the proximate causes of type 2 diabetes? (3)

A
  • High levels of obesity
  • Poor nutrition
  • Lack of exercise
342
Q

What are the evolutionary causes of type 2 diabetes? (2)

A
  • Genetic pre-disposition
  • Thrifty genotype
343
Q

What are the environmental causes of type 2 diabetes? (2)

A
  • Poor maternal nutrition
  • Thrifty phenotype
344
Q

Why do population differences affect diabetes diagnosis? (2)

A
  • Different distributions of adipose tissue
  • Higher body % at given BMI
345
Q

What is a genotype?

A

DNA sequence of an organism

346
Q

What is a phenotype?

A

Observable characteristics

347
Q

What is thrifty genotype hypothesis?

A

Genes related to type 2 diabetes enabled people in feast/famine environments to survive

348
Q

What is thrift?

A

Efficiency with energy is used

349
Q

How does the thrifty genotype work?

A

Prevents muscle breakdown by minimising glucose consumption for other organs

350
Q

What are the issues with thrifty genotype? (4)

A
  • Difficult to test hypothesis
  • Traits that run-in families may be environmental, not genetic
  • Based on short-term evolutionary environment
  • Too simplistic
351
Q

What is the thrifty phenotype?

A

Type 2 diabetes has an environmental rather than genetic basis

352
Q

How does thrifty phenotype work?

A

If maternal nutrition is inadequate, the growing fetus diverts nutrients to the brain at the expense of other organs i.e. pancreas

353
Q

What is semen a mix of fluid from? (3)

A
  • Testis
  • bulbourethral glands
  • Seminal vesicles
354
Q

What contents make up a sperm cell? (6)

A
  • Acrosome
  • Nucleus
  • Centrioles
  • Mitochondria
  • Head
  • Midpiece
355
Q

What are the testes organised into?

A

lobes

356
Q

What does each lobe contain?

A

Seminiferous tubules

357
Q

Where do the seminiferous tubules terminate?

A

Rete testis

358
Q

What the spaces in-between the seminiferous tubules called?

A

Septa of testis

359
Q

Where are the spermatozoa released?

A

Lumen of the seminiferous tubules

360
Q

What is in the clefts of the Sertoli cells?

A

Spermatozoa

361
Q

What do spermatogonium do?

A

Support spermatogenesis

362
Q

What are processes of mitosis? (4)

A
  • begins diploid (2n)
  • replicates DNA - 2n to 4n
  • divides (cytokinesis) - 2 x 2n
  • result = 2 diploid cells
363
Q

what is the process of meiosis? (6)

A
  • begins diploid (2n)
  • replicates DNA - 2n to 4n
  • Chiasmata forms
  • Cell divides to yield 2 x 2n
  • No second round of DNA replication
  • Cell divides - 2n to 1n
364
Q

Where does spermatozoa formation occur?

A

Basolateral side of tight junctions

365
Q

What is the process of spermatogonium? (5)

A
  1. Spermatogonial stem cells divides by mitosis, forming spermatogonium type 1
  2. Undergo 5 mitotic divisions to increase number, forms A2 A3 A4 and intermediate
  3. Intermediate spermatogonium goes through mitosis goes to type B
  4. Intermediate spermatogonium forms resting primary spermatocyte
  5. Mitosis STOPS
366
Q

How do we dictate the number of clones of the original spermatogonia stem cell?

A

Number of mitotic divisions from SSC to type B spermatogonium

367
Q

How many A1 cells can SSC generate?

A

16

368
Q

Where do the mitotic divisions occur?

A

lumen region of seminiferous tubules

369
Q

what does the first part of meiosis 1 create in spermatogenesis?

A

Primary spermatocyte

370
Q

what does completed meiosis 1 create in spermatogenesis?

A

secondary spermatocyte

371
Q

what does meiosis 2 create in spermatogenesis?

A

Early spermatids

372
Q

How do early spermatids convert to late spermatids?

A

Cytodifferentiation

373
Q

What does GO-TO-MA-TOZ tell us? (4)

A
  • SpermatoGOnia – mitotic
  • SpermaTOcytes – meiotic
  • SperMAtids – cytodifferentiation
  • SpermaTOZoa – the final product
374
Q

How many clones do we end up from 1 A1 spermatogonia?

A

512

375
Q

What is spermiogenesis? (2)

A
  • Site of differentiation
  • Spermatid to sperm cell
376
Q

How does the spermatid form into sperm cells? (4)

A
  • Nucleus moves to head region
  • Centrioles migrate to tail region
  • Microtubules form flagella
  • Cytoplasm becomes pinched around nucleus, forms mitochondria
377
Q

What does the sperm cell contribute to the egg in fertilisation? (2)

A
  • Nucleus
  • Centrioles
378
Q

In any section of seminiferous tubules what happens?

A

Only 1 SSC begins to differentiate

379
Q

How long is the spermatocyte cycle? (2)

A
  • Cycle interval - 16 days
  • Total length - 64 days
380
Q

How are men always fertile?

A

Spermatogenic waves - there are always cells in the cycle

381
Q

What is the role of the epididymis? (3)

A
  • Sperm concentration
  • Sperm maturation
  • Sperm storage
382
Q

How many couples require help with fertilisation?

A

1 in 7

383
Q

What is in a healthy sample of semen? (7)

A
  • Volume - 1.4ml
  • Total count - 39 million
  • Sperm concentration - 16 million/ml
  • Progressive motility - 30%
  • Morphology 4%
  • Vitality - 54%
  • pH > 7.2
384
Q

what is oligozoospermia?

A

Low sperm count

385
Q

what is aspermia?

A

Complete absence of semen

386
Q

what is azoospermia?

A

Complete absence of sperm

387
Q

what is asthenozoospermia?

A

low motility of sperm

388
Q

what is teratospermia?

A

Abnormal morphology

389
Q

What temperature does testi work at?

A

2 degrees below body temperature

390
Q

What do LH stimulates in males?

A

Leydig cells

391
Q

How does testosterone influence LH?

A

Negative feedback acts on hypothalamus

392
Q

What do Leydig cells do?

A

Form the blood teste barrier

393
Q

How much mg of testosterone is produced per day?

A

4-10mg

394
Q

What does FSH bind to in males?

A

Receptors on Sertoli cells

395
Q

What do Sertoli cells do once binded to LH? (3)

A
  • Stimulate production of androgen receptors
  • Inhibin also produced  inhibits FSH
  • Negative feedback on FSH receptor
396
Q

How do FSH and testosterone support spermatogenesis?

A

Oscillate synergistically

397
Q

What does the Sertoli cells do?

A

Converts testosterone to dihydrotestostermine

398
Q

What is responsible for the volume of semen?

A

Seminal vesicle

399
Q

What does seminal vesicles secrete? (3)

A
  • Fructose
  • Ascorbic acid (Vit C)
  • Prostaglandins
400
Q

What do elevated levels of PSA indicate?

A

Prostate hyperplasia

401
Q

What is the normal volume of semen?

A

2-5mls

402
Q

What % of semen does each structure contribute? (4)

A
  • Seminal vesicle 60%
  • Prostate 20-30%
  • Cowper’s gland 5%
  • Vas deferens 5%
403
Q

What does the prostate secrete?

A

PSA - protease, citric acid

404
Q

What is the prostate’s role?

A

Prevents sperm from sticking together

405
Q

What are the phases of arousal?

A
  • E- excitement
  • P - plateau
  • O -orgasm
  • R - resolution
406
Q

Where is fat stored?

A

Adipocytes

407
Q

Where is insulin made?

A

Beta cells by pancreas

408
Q

What are beta cells sensitive to?

A

Glucose is blood steam

409
Q

How does insulin store extra glucose?

A

Insulin converts glucose into glycogen

410
Q

Where is glycogen stored?

A

Liver and muscles

411
Q

What are the five different ways energy is stored?

A
  • ATP (adenosine triphosphate)
  • CP (creatine phosphate)
  • Glycogen
  • Fat
  • Protein
412
Q

What is creatine phosphate’s function?

A

Repair the used ATP by replacing it with carbohydrates

413
Q

How long does muscle glycogen provide energy for?

A

2-3 hours

414
Q

Why is the world weight issue a big problem?

A
  • Humans have excess food for the first time ever
  • Extra food metabolised is stored as fat for future requirement
415
Q

what is metabolic syndrome?

A

A cluster of conditions that occur together, increasing the risk of heart disease, stroke and type 2 diabetes

416
Q

When are you more likely to get metabolic syndrome? (5)

A
  • Are living with obesity
  • Eat a high-saturated-fat diet
  • Do not exercise much
  • Smoke
  • Drink lots of alcohol
417
Q

You have metabolic syndrome if you have 3+ of which conditions? (5)

A
  • High blood pressure
  • Large waistline
  • High blood sugar levels
  • High blood triglycerides
  • Low HDL cholesterol
418
Q

What are the treatments for metabolic syndrome? (3)

A
  • Losing weight
  • Changing diet
  • More exercise
419
Q

how does Orlistat work for weight loss? (2)

A
  • Works by preventing 1/3 of fat from food being absorbed
  • Undigested fat is not absorbed, instead passed out through faeces
420
Q

how does liraglutide work for weight loss? (2)

A
  • Helps the pancreas to release the right amount of insulin when blood sugar levels are high.
  • Slows the emptying of the stomach, decreasing appetite and cause weight loss
421
Q

what are the surgical options for managing obesity? (5)

A
  • bariatric surgery
  • sleeve gastrectomy
  • gastric imbrication
  • Gastric Band
  • Gastric Bypass
422
Q

What are the types of genetic obesity? (3)

A
  1. Monogenic obesity - excessive weight caused by a mutation in a single gene (MC4R)
  2. Polygenic obesity - variations in multiple genes contribute to the susceptibility of obesity
  3. Syndromic obesity - genetic changes in specific diseases
423
Q

What are the most common environmental factors that lead to obesity? (4)

A
  • Sedentary lifestyle
  • Regular consumption of high calorie foods
  • Poor sleep habits
  • Chronic stress
424
Q

What is the most common obesity gene variant?

A

MC4R gene

425
Q

What happens when there is a MC4R deficiency? (2)

A
  • Involved in hypothalamus controlling appetite regulation
  • Demonstrates stronger desire for food
426
Q

What makes up the pancreas? (4)

A
  • Tail
  • Head
  • Neck
  • Body
427
Q

What is the head end of the pancreas attached to?

A

Duodenum

428
Q

What is the head end of the pancreas attached to?

A

Spleen

429
Q

What regions are the pancreas divided into? (2)

A
  • Exocrine
  • Endocrine
430
Q

What are the features of the exocrine region? (3)

A
  • Bicarbonates
  • Zymosans
  • Enzymes
431
Q

What are the features of the endocrine region? (4)

A
  • Insulin
  • Glucagon
  • Somatostatin
  • Pancreatic polypeptide
432
Q

What are the functions of the endocrine pancreas? (2)

A
  • Produce hormones regulating blood sugar levels
  • Initiates hunger
433
Q

What is the exocrine pancreas composed of? (2)

A
  • Intercalated duct
  • Acinus
434
Q

What is the acinus?

A

A cluster of cells that resembles a many lobed berry

435
Q

What are the intercalated ducts?

A

The portion of the exocrine gland the drains from the acinus into larger ducts and eventually the intralobular duct.

436
Q

What is the function of intercalated ducts?

A

Produce an alkalic solution that ‘buffers’ the acidic environment to a pH optimal for enzymes to work.

437
Q

What is bicarbonate secreted by in the pancreas?

A

Intercalated ducts

438
Q

How is bicarbonate secretion stimulated from a duct cell in the pancreas? (5)

A
  1. Apical end bicarbonate secretion by interaction of Cl- and K+ channels and apical Cl-/HCO3- exchange
  2. The basal membrane contains the Na+/K+ pump that establishes an out to in Na+ concentration gradient that serves as a driving force for intracellular accumulation HCO3- via Na+/H+ exchange
  3. Secretin activates K+ and Cl- channels via generation of intracellular cAMP
  4. Activation of basolateral K+ channel hyperpolarises the cells favouring apical Cl- efflux through cAMP-activated Cl- channels (CFTR).
  5. Favour recycling of Cl- that is taken into the cell by Cl-/HCO3- exchange.
439
Q

What is cholecystokinin (CKK) responsible for?

A

Digestion of fat and protein

440
Q

What is Secretin?

A

A hormone that regulates water homeostasis and secretions in stomach and duodenum.

441
Q

What are the two functions of secretin? (3)

A
  • Act on potassium channels
  • Act on the chlorine channels
  • Creates cAMP
442
Q

Which nerve innovates the control of bicarbonate secretion?

A

Parasympathetic vagus nerve

443
Q

What does CCK act on?

A

Enzymes in the acinus

444
Q

What is affected in a cystic fibrosis pancreas?

A

Abnormal transport of chloride and sodium across the epithelium

445
Q

What happens in a cystic fibrosis pancreas?

A

Produces thick viscous secretions that block exocrine movement of digestive enzymes

446
Q

What causes cystic fibrotic pancreas?

A

Frameshift mutation in the cystic fibrosis conductance regulator (CFTR) gene

447
Q

What does an Alpha cell produce?

A

glucagon

448
Q

what does a beta cell produce?

A

insulin

449
Q

what does a Delta cell produce?

A

somatostatin

450
Q

what does an Epsilon cell produce?

A

ghrelin

451
Q

what % of cells in the endocrine pancreas are insulin secreting b cells?

A

70%-75%

452
Q

What cells are involved in glucose homeostasis? (3)

A
  • Glucagon secreting a cells
  • Insulin secreting b cells
  • Somatostatin- secreting delta cells
453
Q

What cells are involved in regulation of appetite? (2)

A
  • Ghrelin secreting epsilon cells
  • Pancreatic polypeptide- secreting PP cells
454
Q

What is insulin involved in?

A

storage and controlled release within the body of the chemical energy stored in food

455
Q

what gene is insulin encoded on?

A

Chromosome 11

456
Q

Insulin that is not broken down is degraded where?

A

Kidneys

457
Q

Where is insulin carried?

A

Liver

458
Q

What are the features of the hexameric form of insulin? (4)

A
  • Inactive form
  • Storage
  • 6 insulin molecules
  • Arranged in 3 folds
459
Q

What are the features of the monomeric form of insulin? (2)

A
  • Active form
  • Half-life is 6 minutes
460
Q

What is the monomeric form of insulin composed of?

A

Alpha and beta chains linked by disulphide bridges

461
Q

How was the 3D structure of insulin discovered?

A
  • X-ray crystallography
  • Dorothy Hodgson (1969)
462
Q

What is the process of insulin synthesis? (7)

A
  • Synthesised a single polypeptide chain called preproinsul
  • 24aa signal peptide targets polypeptide chain to RER.
  • Signal peptide cleaved, forming proinsulin.
  • Proinsulin folds and 3 disulphide bonds form
  • Proinsulin moves to trans Golgi network.
  • Matures into active form due to endopeptidases releasing the central C-peptide fragment.
  • Mature insulin packaged into granules awaiting metabolic and vagal nerve stimulation to trigger release from cell into circulation
463
Q

How do you test for diabetes? (2)

A
  • Blood test
  • Low levels of C-peptide
464
Q

What are the steps of secreting insulin? (5)

A
  1. Glucose sensing
  2. ATP rise
  3. Depolarisation
  4. Calcium influx
  5. Exocytosis
465
Q

What gene is insulin receptor encoded on?

A

Chromosome 19

466
Q

What are the different types of insulin receptors?

A

IRS-1,2,3,4

467
Q

What does IRS-1 phosphorylation trigger?

A

Movement of GLUT-4- the high affinity receptor for glucose- to the cell surface facilitating uptake of glucose into the cell.

468
Q

What happens in people in type 2 diabetes in the insulin action?

A

Problem moving GLUT4 to the cell surface so cannot open channels to allow glucose release

469
Q

What % of insulin is oxidised to CO2 and H2O?

A

35%

470
Q

What % of insulin is stored?

A

65%

471
Q

How much (g) of glucose is produced each day?

A

200g

472
Q

What % of glucose is derived from liver glycogen and hepatic gluconeogenesis?

A

90%

473
Q

Which organ is the biggest consumer of glucose?

A

Brain

474
Q

What is glycogen breakdown called?

A

Glycogenolysis

475
Q

What is glucose breakdown called?

A

Glycolysis

476
Q

What happens in glycolysis?

A

Conversion of glucose into pyruvate for production of ATP

477
Q

What happens in glycogenolysis?

A

Liver glycogen converted to glucose and utilised by tissue throughout the body, including CNS.

478
Q

What is the other term used for muscles using insulin?

A

Facultative glucose consumers

479
Q

How long is the glucagon chain?

A

29 aa

480
Q

Where is glucagon produced?

A

Alpha cells in pancreas

481
Q

How is glucagon generated?

A

Proprotein convertase 2 cleaving proglucagon in alpha cells

482
Q

What happens to proglucagon in intestinal L cells?

A

Cleaves to alternative products e.g. GLP-1, GLP-2 and IP-2

483
Q

What effect does GLP-1 have on the body? (5)

A
  • Reduces appetite
  • Slows gastric emptying
  • Reduces hepatic glucose output
  • Suppresses a cell glucagon production
  • Stimulates insulin secretion
484
Q

How do you perform the blood glucose tolerance test? (3)

A
  1. Given isoglycaemic intravenous glucose
  2. Give oral glucose
  3. Measure how much insulin is produced
485
Q

Which cell produces somatostatin?

A

Delta cell

486
Q

What is the role of somatostatin?

A

Inhibits release of insulin and glucagon as well as exocrine pancreatic secretions

487
Q

Somatostatin is what two types of peptide?

A
  • Neuropeptide
  • Gastric peptide
488
Q

What is the definition of diabetes?

A

The body’s ability to produce or respond to the hormone insulin is impaired, resulting in abnormal metabolism of carbohydrates and elevated levels of glucose in the blood.

489
Q

What are the symptoms of diabetes? (4)

A
  • Thirst (polydipsia)
  • Excessive passing of urine (polyuria)
  • Fatigue
  • Increased risk of life-threatening illness with collapse, coma and death
490
Q

How rare is diabetes insipidus?

A

1 in 25,000

491
Q

What are the two major forms of diabetes insipidus?

A
  • Neurological linked to anti-diuretic hormone deficiency
  • Kidney or nephron dysfunction
492
Q

How many people live with diabetes?

A

442 million

493
Q

What is diabetes the major cause of? (5)

A
  • Blindless
  • Kidney failure
  • Heart attacks
  • Stroke
  • Lower limb amputation
494
Q

How many deaths were estimated to be directly caused by diabetes?

A

1.5 million

495
Q

Centre for disease control lists diabetes as the __th leading cause of death in the world?

A

7th

496
Q

Where is diabetes most prevalent?

A

Countries where the populace are living an increasingly ‘western’ lifestyle

497
Q

What is the annual cost of diabetes to the NHS?

A

£14 billion

498
Q

What % of cases does type 2 diabetes make up all diabetic causes?

A

90%

499
Q

What % of cases does type 1 diabetes make up all diabetic causes?

A

10%

500
Q

What is type 2 diabetes mostly associated with?

A

Insulin-resistance

501
Q

Who is type 2 diabetes normally detected in?

A

Obese adults

502
Q

What is type 1 diabetes mostly associated with?

A

Autoimmune condition

503
Q

Who is type 2 diabetes normally detected in?

A

Children and young adults (5-25)

504
Q

Who is gestational diabetes normally detected in?

A

Pregnant women

505
Q

What is the cause of gestational diabetes? (2)

A
  • hormone changes resulting in insulin-resistance.
  • Resolves upon birth of baby.
506
Q

What is the definition of type 1 diabetes?

A

An autoimmune condition where the immune system targets the insulin secreting beta cells in the Islets of Langerhans in the pancreas for destruction

507
Q

What is the definition of autoimmunity?

A

the inability of the immune system to recognise tissues as belonging to host and mounts an immune attack

508
Q

What is type 1 diabetes characterised by?

A

Anti-islet T and B cell responses

509
Q

Which countries is type 1 diabetes more prevalent in?

A

Countries of the Northern Hemisphere

510
Q

Which type of cells are the main killers of beta cells?

A

CD8+ T cells

511
Q

What is required for type 1 diabetes? (2)

A
  • Environmental triggers
  • Genetic predisposition
512
Q

What are the phases of type 1 diabetes?

A
  1. Beta cell death
  2. Priming of autoreactive B and T cells
  3. Destruction of beta cells
513
Q

How is beta cell death induced?

A

By infection

514
Q

What happens in the 2nd phase of type 1 diabetes?

A

Movement of differentiated B and T cells to islets in pancreas

515
Q

Movement of differentiated B and T cells to islets in pancreas
What happens in the 3rd phase of type 1 diabetes? (4)

A
  1. Period of regulation after initial influx of activated immune cells
  2. Loss of regulation, activated T cell release cytokines
  3. CD8+ T cells increase CTL potential and kill beta cells by apoptosis
  4. Innate cells-NK and macrophage potentiate this destruction
516
Q

What is the strongest genetic association for type 1 diabetes?

A

Human Leukocyte Antigen (HLA)

517
Q

Which genes, when expressed, gives a higher risk of developing type 1 diabetes? (2)

A
  • Expressing HLA class II molecule DQ8,
  • Expressing HLA class I molecule A2
518
Q

What is the second greater risk factor for type 1 diabetes?

A

Altered bases in genes encoding immunoregulatory proteins

519
Q

Give an example of an altered encoded immunoregulatory protein? (2)

A

Cytotoxic T cell Associated Antigen (CTLA)-4
* Involved in switching off T cells
* Allelic variant of CTLA-4 in T1D, poor ability to control T cell activity

520
Q

What is bystander activation?

A

immune response to infection causes damage to healthy tissue leading to release of islet antigens

521
Q

what is molecular mimicry? (2)

A
  • viral proteins resemble beta cell proteins
  • immune system attacks both as a consequence
522
Q

Where is type 2 diabetes prevalent?

A

Asian and African descendants

523
Q

What body shape is type 2 diabetes associated with?

A

The apple shape

524
Q

The number of antibodies to islet antigens correlates with what?

A

Increased risk of disease in genetically susceptible individuals

525
Q

What do free fatty acid signalling result in?

A

Fat oxidation in the mitochondria and cellular stress (ROS)

526
Q

What does ceramide synthesis act on? (2)

A
  • kinase pathway PKB/Akt
  • impeding effective responses to insulin and as a consequence movement of GLUT4 to plasma membrane and glycogen synthesis
527
Q

What are the endotypes of type 1 diabetes? (3)

A
  • > 15 CD45+ cells
  • Many CD20+ B cells
  • Many CD8+ T cells
528
Q

What are the endotypes of type 2 diabetes? (3)

A
  • Few CD45+ cells
  • Few CD20+ B cells
  • Few CD8+ T cells
529
Q

What do insulin sensitive adipocytes release?

A

Anti-inflammatory mediators e.g. IL-4, IL-13

530
Q

What do insulin resistance adipocytes release?

A

Pro-inflammatory cytokines and adipokines e.g. IL-6, IL-10

531
Q

What do pro-inflammatory cytokines increase?

A

Gluconeogenesis in liver and skeletal muscle

532
Q

What is the link between obesity and type 2 diabetes? (4)

A
  1. Increased free fatty acids put mitochondria under stress
  2. Activates ceramide
  3. These target kinases central to move GLUT4 to the cell surface
  4. Induce glycoensynthesis, so makes more glucose
533
Q

What is the commonality between type 1 and type 2 diabetes?

A

Type 2 diabetic therapies modulating beta cell function should be given to type 1 diabetics to enhance secretion from the microsecretors

534
Q

What is type 1.5 diabetes called?

A

Latent Autoimmune Diabetes in Adults (LADA)

535
Q

What 3 factors contribute of LADA?

A
  • Lifestyle factors
  • Islet autoimmunity
  • Genetic susceptibility
536
Q

What two systems does diabetes complicate?

A
  • Macrovascular
  • Microvascular
537
Q

What is the normal kidney function? (4)

A
  1. Large blood vessels divide into small blood vessels throughout kidney
  2. At outer sections, these form glomeruli
  3. Glomeruli and tubules form the nephron
  4. The job of the nephron is to filter blood; allows waste, water and some salt to be secreted in urine, keep blood cells and proteins in bloodstream
538
Q

How does raised glucose levels affect the kidney? (4)

A
  • alters chemical composition of kidney (↑ROS) causing cellular stress in the glomerulus
  • leading to malfunction and resultant leakage of protein into urine
  • proteins in kidney cross-link resulting in scar formation
  • Extensive scar formation replaces normal kidney tissue resulting in kidney failure
539
Q

What is diabetic neuropathy?

A

Family of nerve disorders caused by diabetes

540
Q

What are the symptoms of diabetic neuropathy?

A

‘tingling’, pain, loss of feeling in hands and feet

541
Q

What does Large Fibre Neuropathy affect?

A

affects ability to sense vibrations

542
Q

What does Small Fibre Neuropathy affect?

A

ability to feel pain, temperature, control of body functions.

543
Q

What does Proximal motor neuropathy affect? (3)

A
  • hip, buttock and thigh.
  • Typically one sided and rare.
  • Muscle weakness and pain.
544
Q

What does Entrapment Neuropathy affect?

A

chronic compression of nerve.

545
Q

What are the features of diabetic foot syndrome? (3)

A
  • Infection
  • Ulceration (poor wound healing)
  • Increased risk of amputation due to failure to deal with common infection e.g. fungus
546
Q

What is the leading cause of blindness in the world?

A

Diabetic retinopathy

547
Q

How many diabetics have diabetic retinopathy?

A

1/3 diabetics

548
Q

What are the three types of retinopathies?

A
  • Background
  • Pre-proliferative
  • Proliferative
549
Q

What is used to monitor how well people are controlling blood sugar levels?

A

Measurement of HbA1c

550
Q

What does metformin improve?

A

Insulin resistance in skeletal muscles and liver through cAMP mediated mechanism

551
Q

How does metformin work? (6)

A
  1. Inhibition of mitochondrial respiratory chain complex 1
  2. Reduced cellular energy status
  3. Activation of hepatic 5′-AMP-activated protein kinase (AMPK)
  4. Phosphorylation of key synthetic enzymes
  5. Shuts down pathways that consume ATP
  6. Switches hepatocytes from an anabolic to a catabolic state
552
Q

What are the adverse effects of metformin? (6)

A
  • Gastrointestinal upset
  • anorexia
  • nausea
  • taste disturbance
  • abdominal discomfort
  • diarrhoea.
553
Q

What is the benefits of metformin?

A

HbA1c reduction of ~ 11 mmol/mol

554
Q

What is the role of sulfonylureas?

A

Increases both first- and second-phase insulin secretion in response to a rise in plasma glucose.

555
Q

What is the benefit of sulfonylureas?

A

HbA1c reduction of ~ 11 to 15 mmol/mol

556
Q

What is the pharmokinetics of sulfonylureas? (3)

A
  • Rapidly absorbed orally.
  • Highly protein bound.
  • Metabolised by the liver.
557
Q

What are the adverse effects of sulfonylureas? (3)

A
  • Hypoglycaemia
  • Weight gain.
  • Hypersensitivity reactions
558
Q

What is the role of thiazolidinediones?

A

Modulates the transcription of insulin sensitising genes

559
Q

What are glitazones?

A

PPAR y agonists

560
Q

Where is pioglitazone metabolised?

A

In the liver

561
Q

What are the adverse effects of pioglitazone? (4)

A
  • Gastrointestinal disturbances.
  • Headache, dizziness, visual disturbances.
  • Anaemia.
  • Hypoglycaemia (with sulfonylureas).
562
Q

What are the two incretin hormones?

A
  • Glucagon-like peptide-1 (GLP-1)
  • Glucose-Dependent Insulinotropic Peptide (GIP)
563
Q

Where is Glucagon-like peptide-1 (GLP-1) derived from?

A

Intestinal L cells

564
Q

Where is Glucose-Dependent Insulinotropic Peptide (GIP) derived from?

A

Intestinal K cells

565
Q

What are the types of insulin? (4)

A
  • Short acting
  • Intermediate acting
  • Biphasic
  • Analogues
566
Q

What are the features of short acting insulin? (4)

A
  • Soluble e.g. Humulin S
  • Onset - 30 minutes
  • Peak - 1-3 hours
  • Duration of action up to 8 hours
567
Q

What are the features of intermediate-acting insulin? (3)

A
  • Onset - 1 1/2 hours
  • Peak - 4-12 hours
  • Duration of action up to 24 hours
568
Q

What are the features of premixed insulin? (3)

A
  • Onset - 30 minutes
  • Peak - 2-8 hours
  • Duration of action up to 14 hours
569
Q

What are the methods of insulin delivery? (2)

A
  • Insulin devices e.g. pens
  • Insulin vials and syringes
570
Q

What are the advantages of insulin devices? (7)

A
  • Improved dose accuracy
  • More convenient
  • Easy to use
  • Portable
  • Quick and What are the features of insulin pumps? (6)discreet
  • May reduce barriers to patient self-management
  • Preferred to syringes by patients
571
Q

What are the features of insulin pumps? (6)

A
  • Continuous subcutaneous insulin infusion (CSII)
  • Battery operated
  • Programmable computer
  • Basal insulin throughout day
  • Bolus insulin before meals
  • Needles/catheters changed every 2-3 days
572
Q

What are the side effects of insulin? (3)

A
  • Hypoglycaemia
  • Allergic reactions / lipoatrophy of subcutaneous fat
  • Injection site problems

ALS (9 decks)

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