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Y2 LCRS 1 - Pharm, Endo, Reproduction > ENDO; Lecture 12, 13 and 14 - Endocrinology of pregnancy, Endocrine and metabolic bone disorders, Obesity and the endocrine control of food intake > Flashcards

ENDO; Lecture 12, 13 and 14 - Endocrinology of pregnancy, Endocrine and metabolic bone disorders, Obesity and the endocrine control of food intake Flashcards

1
Q

What is bone formed from?

A
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2
Q

What are the cells present in the bone?

A

Osteoblasts and osteoclasts

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3
Q

What is the function of the osteoblasts?

A

Synthesise osteoid and participate in mineralisation/calcification of osteoid (bone deposition)

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4
Q

What is the function of osteoclasts?

A

Release lysosomal enzymes which break down bone (bone resorption)

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5
Q

How does bone remodelling occur?

A
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6
Q

How do you differentiate between osteoclasts?

A

RANKL is expressed on osteoblast surface which binds to RANK-R to stimulate osteoclast formation and activity

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7
Q

What is Osteoprotegerin?

A

Decoy receptor for RANKL -> inhibits osteoclast differentiation

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8
Q

How is bone remodelling regulated?

A

Osteoblasts synthesise new bone, expressing receptors for PTH and calcitriol which regulate bone remodelling and Ca balance

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9
Q

How does Ca homeostasis work?

A
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10
Q

How do changes in EC Ca affect nerve and skeletal muscle excitability?

A

Hypercalcaemia = Ca blacks Na influx so less membrane excitability. Hypocalcaemia = enables greater Na influx so MORE membrane excitability

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11
Q

What is the normal range of serum Ca?

A

2.2-2.6 mmol/L

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12
Q

What are the signs and symptoms of hypocalcaemia? [CATs go numb]

A

Sensitises excitable tissues leading to muscle cramps/tetany, tingling; parasthesia (hands/mouth/feet/lips), convulsions, arrhythmias, tetany

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13
Q

What is Chvostek’s sign?

A

Tap facial nerve just below zygomatic arch -> twitching of facial muscles indicates neuromuscular irritability due to hypocalcaemia

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14
Q

What is Trousseau’s sign?

A

Inflation of BP cuff for several minutes induces carpopedal spasm indicating NM irritability due to hypocalcaemia

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15
Q

What are the causes of hypocalcaemia?

A
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16
Q

What are the signs and symptoms of hypercalcaemia? [Stones, abdominal moans and psychic groan]

A

Stones (renal effects) -> polyuria/thirst, nephrocalcinosis, renal colic, chronic renal failure; Abdominal moans (GI effects) -> anorexia, nausea, dyspepsia, constipation, pancreatitis; psychic groans (CNS effects) -> fatigue, depression, impaired concentration, altered mentation, coma (usually >3mmol/L)

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17
Q

What are the causes of hypercalcaemia?

A
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18
Q

How do you approach diagnostically hypercalcaemia - 1ry hyperparathyroidism?

A

Raised Ca and Raised (unsuppressed) PTH

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19
Q

How do you approach diagnostically hypercalcaemia - hypercalcaemia of malignancy?

A
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20
Q

What is a vitamin D metabolite?

A

Calcitriol (bioactive form)

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21
Q

What is the principal effect of calcitriol?

A

Stimulates intestinal absorption of Ca and PO4^3-, providing necessary ions for normal bone mineralisation

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22
Q

What are the other effects of calcitriol?

A

Regulates osteoblast differentiation; renal effects -> increased Ca reabsorption, decreased PO4 reabsorption via FGF23 (hormone produced by bone whihc increases urine PO4 excretion)

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23
Q

What is a Vit D deficiency state?

A

Lack of mineralisation in bone -> results in softening of bone, bone deformities, bone pin, severe proximal myopathy

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24
Q

What is the name of Vit D deficiency in adults and children?

A

Children = Rickets, Adults = osteomalacia

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25
Q

How are Vit D metabolites and calcium metabolism related?

A
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26
Q

What are the causes of Vit D deficiency?

A

Diet, lack of sunlight, GI malabsorption (coeliac, IBD), renal/liver failure, Vit D receptor defects

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27
Q

What is primary hyperparathyroidism?

A

Problem with parathyroid gland causing the increase in PTH

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28
Q

What is secondary hyperparathyroidism?

A

PTH goes up SECONDARY to increase of Ca

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29
Q

How do you diagnose Vit D deficiency?

A
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30
Q

How does impaired renal function (renal failure) lead to bone disease?

A

PO4 rises, accentuating hypocalcaemia, stimulating PTH due to low Ca levels; increase in PO4 leads to calcification/calcium deposition in vessels (coronary)

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31
Q

What are brown tumours?

A

Radiolucent bone lesions which reflect excessive osteoclastic bone resoprtion secondary to high PTH

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32
Q

How would you treat Vit D deficiency in normal renal function and renal failure?

A
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33
Q

What occurs in vit D excess?

A

LEads to hypercalcaemia, hypercaliuria due to increased intestinal absorption of Ca

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34
Q

How can vit D excess occur?

A

Excessive treatment with active metabolites of Vit D (Alfacalcidol); granulomatous diseases (sarcoidosis, leprosy, TB)

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35
Q

What is osteoporosis?

A

Condition of reduced bone mass and a distortion of bone microarchitecture which predisposes to fracture after minimal trauma

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36
Q

How do you define osteoporosis?

A

BMD that is 2.5 SD or more below average for young healthy adults -> measured by Dual Energy X-ray Absorption

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37
Q

What are the predisposing conditions for osteoporosis?

A

Postmenopausal oestrogen deficiency (leads to loss of bone matrix, so increased risk of fracture), Age-related deficiency in bone homeostasis (osteoblast senescence), hypogonadism in young women and men, endocrine conditions (cushing’sS, hyperthyroidism, 1ry hyperparathyroidism), iatrogenic (prolonged use of glucocorticoids, heparin)

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38
Q

What are the treatment options for osteoporosis?

A

Oestrogen/selective oestrogen receptor modulators, bisphosphates, denosumab, teriparatide

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39
Q

How does oestrogen treat osteoporosis and what are the concerns related to it?

A
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40
Q

How do SERMS treat osteoporosis and what are the concerns related to it?

A
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41
Q

What are the 2 types of SERM?

A

Tissue selective ER antagonists = tamoxifen; tissue selective ER agonists = raloxifene

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42
Q

How do bisphosphonates treat osteoporosis?

A
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43
Q

When would you use bisphosphonates?

A
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44
Q

What are the pharmacokinetics of bisphosphonates?

A
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45
Q

What are the unwanted actions of bisphosphonates?

A
46
Q

What is denosumab?

A

Human monoclonal antibody, whihc binds RANKL, inhibiting osteoclast formation and cativity, inhibiting osteoclast-mediated bone resorption; SC injection every 6 months (2nd to bisphosphonates)

47
Q

How does teriparatide treat osteoporosis and what are the concerns related to it?

A
48
Q

What is Paget’s disease of bone and what does it result in?

A

Characterised by abnormal, large osteoclasts -> excessive in number

49
Q

Who does Paget’s disease affect?

A

Positive family history, evidence for viral origin, men and women affected = , not apparent under 50y, most patients asymptomatic, orevalent in UK, N.America, Australia, NZ; lowest in Asia and Scandinavia

50
Q

What are the clinical features of Paget’s disease?

A
51
Q

How do you diagnose Paget’s disease?

A
52
Q

What are the treatment options for Paget’s disease?

A

Bisphosphonates (helpful for reducing bony pain and disease activity; simple analgesia

53
Q

How is food intake controlled?

A
54
Q

How does the hypothalamus control body weight homeostasis?

A
55
Q

Which part of the hypothalamus controls food intake?

A

Arcuate nucelus

56
Q

What is the arcuate nucleus?

A

Involved in regulation of food intake, has incomplete BBB, allowing access to peripheral hormones

57
Q

What is the function of the arcuate nucleus and what are the 2 neuronal popn present?

A

Integrates peripheral and central feeding signals -> Stimulatory (NPY/Agrp neuron) and inhibitory (POMC neuron)

58
Q

What are the functions of the 2 types of neuronal popn?

A

NPY/Agrp neurons INCREASE APPETITE; POMC neurons DECREASE APPETITE. Both sets of neurons extend to other hypothalamic and extra-hypothalamic regions.

59
Q

What is the melanocortin system?

A
60
Q

What are the different human CNs mutations that occur which affect appetite?

A

No NPY/Agrp mutations discovered; POMC deficiency and MC4-R mutations cause morbid obesity

61
Q

What are the other brain regions involved in food intake?

A
62
Q

What is the ob/ob mouse?

A

Recessive mutation, profoundly obese, diabetic, infertile, stunted linear growth, decreased body temp/energy expenditure/immune function -> NB: similar to starved animals; lacks leptin

63
Q

What is leptin?

A

Amino acid hormone -> high wen high body fat and low when low body fat -> central/peripheral admin decreases food intake and increases thermogenesis

64
Q

What is the function of leptin?

A

Activates POMC and inhibits NPY/Agrp neurones

65
Q

What is leptin resistance?

A

Leptinc circulates in plasma in conc proportional to fat mass which means most fat hummans have high leptin -.> obesity due to leptin resistance means it is ineffective as a weight control drug

66
Q

What occurs in the absence of leptin?

A

Hyperphagia, lowered energy expenditure, sterility -> anti-starvation hormone rather than anti-obesity hormone

67
Q

What does the presence of leptin tell the brain?

A

Sufficient fat reserves for normal functioning but high leptin has little effect

68
Q

What is the role of insulin in food intake?

A

Insulin circulates at levels proportional to body fat, with receptors in the hypothalamus, with central administration reducing food intake

69
Q

What do gut hormones influence?

A

Processes including gut motility, secretion of other hormones, appetite; release regulated by gut nutrient content

70
Q

Which gut hormones exist and what is their function?

A
71
Q

What is ghrelin?

A

Gastric hormone and ghrelin O-acetyltransferase adds an ester linkage forming ghrelin

72
Q

What is the function of ghrelin?

A

Stimulates NPY/Agrp neurones, inhibits POMC neurones, increases appetite

73
Q

What do L-cells secrete?

A

Peptide YY and GLP-1

74
Q

What is the function of PYY?

A

Inhibits NPY release, stimulates POMC neurons, decreases appetite

75
Q

What is GLP-1?

A

Gut hormone coded for by preproglucagon gene and released post prandially

76
Q

What is the function of GLP-1?

A

well-characterised incretin role in stimulating glucose-stimulated nsulin release and also reduces food intake

77
Q

What is Saxenda?

A

Long-acting GLP-1 receptor agonist (liraglutide) which has a longer half-life

78
Q

How should Saxenda be given?

A

T2DM needs double dose and given for obesity

79
Q

How is PYY used as a drug?

A

Has very narrow therapeutic window; with different people reacting differently to same dose

80
Q

How can you manipulate diet?

A

Synthetic nutrients to stimulate nutrient receptors, delivery nutrients to specific regions of the gut

81
Q

Which comorbidities are associated with obesity?

A
82
Q

What is the thrifty gene hypothesis?

A

Specific genes selected for to increase metabolic efficiency and fat storage, evolutionarily sensible to put on weight as thin humans didn’t survive famines, so didn’t pass their genes on to modern humans

83
Q

What is the adaptive drift hypothesis?

A

Normal distribution of body weight -> fat eaten and thin starve; but then humans learned to defend against predators which means that obesity is not selected against and in current context, inheritors of genes become obese

84
Q

Which cells produce oestrogen in the male reproductive tract?

A

Germ cells, Leydig cells and ?Sertoli cells

85
Q

What is the function of secretory products in the epididymal fluid?

A

Provide energy for impending journey, coat surface of spermatozoa

86
Q

What causes the secretory products to move into the epididymis?

A

Androgens move the nutrients and glycoproteins into the epididymis

87
Q

What is present in the ejaculate of the male?

A

Semen: spermatozoa (15-120x10^6/ml), seminal fuid (2-5ml), leucocytes, potentially viruses

88
Q

How many spermatozoa in ejaculate actually reach the cervix?

A

1%

89
Q

Which parts of the male reproductive tract produce seminal fluid?

A

Small contribution from epididymis/testis; mainly from accessory sex glands: seminal vesicle, prostate and bulbourethral glands

90
Q

What are the components of the seminal fluid?

A

Epididymis/testis: Inositol carnitine, glycerylphosphorylcholine. Accessory sex glands: fructose, fibrinogen, citric acid (Ca chelator), acid phosphatase, fibrinogenase

91
Q

How does the sperm adapt to achieve fertilisation in the female reproductive tract?

A

Loses glycoprotein ‘coat’, changes in surface membrane characteristics, whiplash movements of the tail

92
Q

What causes the capacitation of sperm?

A

Oestrogen-dependent, takes place in ionic and proteolytic environment of Fallopian tube, Ca dependent

93
Q

What is the reaction that occurs with the acrosomal cap and the ovum?

A

Sperm binds to ZP3, Ca influx into sperm stimulated by progesterone, release of hyaluronidase and proteolytic enzymes, spermatozoon penetrates the zona pellucida

94
Q

What is the zona pellucida?

A

Glycoprotein layer surrounding the plasma membrane of the oocyte

95
Q

Where does fertilisation occur?

A

Within the Fallopian tube

96
Q

What occurs when fertilisation happens?

A

Triggers cortical reaction, where cortical granules release molecules which degrade the zona pellucida so prevent binding of other sperm hence stopping diploidy -> results in expulsion of second polar body

97
Q

How does conceptus develop?

A

Continues to divide as it moves down the Fallopian tube to uterus (3-4d), receiving nutrients from uterine secretions -> free-living phase can last for 9-10d

98
Q

How does the fertilised egg become a blastocyst?

A
99
Q

How does a blastocyst become a foetus?

A

Inner cell mass becomes the embryo and outer trophoblast becomes chorion

100
Q

How does transfer to uterus occur?

A

Increasing progesterone to oestrogen ratio (luteal phase)

101
Q

How does the blastocyst implant in the uterus?

A

Attachment phase: outer trophoblast cells contact uterine surface epithelium; decidualisation of underlying uterine stromal tissue -> requires progesterone domination in presence of ostrogen

102
Q

Which molecules are involved in stimulating LIF and IL11 during blastocyst attachment?

A

LIF: TGF, TNF, HB-EGF, IL1, Leptin, Progesterone. IL11: IL1, TNF, TGF, Relaxin, PGE2

103
Q

What is LIF?

A

Leukaemia inhibitory factor from endometrial secretory glands stimulating adhesion of blastocyst to endometrial cells

104
Q

What is IL-11?

A

Also from endometrial cells and is released into uterine fluid

105
Q

How does decidualisation occur?

A

Endometrial changes due to progesterone, glandular epithelial secretion, glycogen accumulation in stromal cytoplasm, growth of capillaries, increased vascular permeability

106
Q

Which factors are involved in decidualisation?

A

IL11, histamin, certain prostaglandins, TGFbeta which promotes angiogenesis

107
Q

How do hormones change during pregnancy?

A
108
Q

When are progesterone and oestrogen produced during pregnancy?

A

First 5-6wks: in corpus luteum (maternal ovaries), stimulated by hCG (by trophoblasts), essential for developing fetoplacental unit, inhibit maternal LH/FSH; from day 40 the placenta starts to take over

109
Q

How are oestrogen and progesterone produced/controlled during pregnancy?

A
110
Q

How do the maternal hormones change?

A
111
Q

How are contractions caused during parturition?

A
112
Q

How is lactation controlled after childbirth?

A

Y2 LCRS 1 - Pharm, Endo, Reproduction (19 decks)

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