Complete set of notes for this element in the Bristol A100 Pre-clinical course. This is everything you need to know to achieve 90% marks. It is presented in a simple question, simple answer layout. If you have any questions or if anything doesn’t make sense, email me at mh14782@my.bristol.ac.uk....
Endocrine and Reproductive Systems 2
Lecture 1: Introduction to the Endocrine System 2
Lecture 2 & 12: Endocrinology of Obesity and Diabetes 2
Lecture 3: Hypothalamo-pituitary Axis 5
General Anatomy of the Hypothalamus 5
Embryological Development and Anatomy of the Pituitary Gland 7
Blood Supply 7
Nerve Supply 8
Cell types in Anterior Pituitary 8
Lecture 4: Hypothalamo-pituitary Axis 2 9
Lecture 5: Thyroid Function 12
Lecture 6: Growth Hormone 16
Lecture 7: Adrenal Glands 16
Lecture 8: Parathyroid & Calcium Regulation 20
Lecture 9: Introduction to Reproduction 23
Lecture 10: Male 1 23
Lecture 11: Male 2 26
Lecture 13: Drug Control of the Thyroid, Adrenal Gland & Growth Hormone Secretion 29
Clinical Case Studies 31
Lecture 14: Embryology 32
Lecture 15: Female 1 34
Lecture 16: Female 2 38
Lecture 17: Disorders of Ovulation 40
Lecture 18: Female 3 40
Lecture 19: Perspectives on HIV 41
Lecture 20: Menopause & Gonadal Failure 42
Lecture 21: Gametes, Conception and Early Pregnancy 43
Lecture 22: The Placenta 47
Lecture 23: STIs 51
Chlymydia 51
Gonorrhea 51
Genital Warts 51
Syphilis 52
Epidiemiology 52
Lecture 24: Foetus 1 52
Lecture 25: Genetics of Obesity 55
Lecture 26: Foetus 2 56
Lecture 27: Puberty 58
Lecture 28: Labour & Lactation 60
Lecture 29: Contraception 62
, Endocrine and Reproductive Systems
Lecture 1: Introduction to the Endocrine System
• What is the endocrine system? A system of hormone glands secreting substances into the blood
stream that influences remote tissues
• What are circadian rhythms? An endogenously created physiological cycle that is close to 24 hours.
This cycle is present without external light stimuli
• What is a diurnal rhythm? The rhythm of the body in time with daylight. The circadian rhythm is
fine-tuned to the amount of sunlight in the day to make the body’s diurnal rhythm
• What are ultradian rhythms? Hour to hour fluctuations in level of wakefulness
• Briefly, what do the following hormones do and where are they made?
Hormone Action Made by
Atrial natriuretic peptide Natriuresis Atria
Leptin Signals you’ve had enough to Made by adipose cells, in
eat (in greek, leptos = thin) proportion to today body fat
Adiponectin Stimulates fatty acid oxidation Made by adipose cells, in
when you are starved inverse proportion to body fat
% (very weird)
Incretins Enhances effects of insulin Gut
Growth hormone ⇑height in children Anterior pituitary
⇑calcium retention to aid bone
mineralisation
⇑lipolysis and GNG
⇑protein synthesis
• How does renal failure lead to hyperparathyroidism? Renal failure à failure of vitamin D being
hydroxylated à Low calcium absorption from gut à hypocalcaemia à hyperparathyroidism to try
and ⇑[Ca2+]
• A lot of content was covered about thyroid hormones and various diseases but they’re covered
later on in greater detail – this was just an introduction
Lecture 2 & 12: Endocrinology of Obesity and Diabetes
• What % of type II diabetics are obese? Around 80%
• What goes wrong with type II diabetes? Your body doesn’t respond to insulin
• What is the BMI? Weight (kg)/height2 (m)
• What is ‘healthy’ BMI? 20-25
• Is obesity multifactorial? Yes, the obese phenotype arises from exposing individuals with a
predisposing phenotype to an inappropriate environment. People can be genetically wired to want
to eat. The genetics for obesity is polygenic (in rare cases monogenic – see later)
• What happens to someone if they don’t produce leptin? The body never thinks it’s had enough to
eat so you have a veracious appetite à severe obesity
• What is a ‘monogenic’ cause for obesity? A single gene that if you have, will make you obese. This
accounts for a tiny minority of obese people
• What are 2 monogenic causes of obesity for mice? Ob/Ob and Db/Db genotypes
• What is the parabiosis experiments? When you take Ob, Db and normal mice and surgically attach
them to each other so that they share blood supply. This allowed the researchers to identify the
cause of the mutations. The results from the attachments were:
Marc Huttman 2
, 1. Ob mouse + normal mouse à Ob mouse weight
⇓, normal mouse weight –
2. Db mouse + normal mouse à Db mouse weight –,
normal mouse weight ⇓
3. Ob mouse + Db mouse à Ob mouse weight ⇓, Db
mouse weight –
The conclusions were that:
Ø Ob = blood borne hormone
Ø Db = receptor to that hormone
• What is the Ob gene? It’s the gene that makes leptin!
• Why can’t you inject leptin into obese people, which will
suppress their appetite and make them thin? Because most people who are obese will also be
leptin resistant
• How does [leptin] vary in fasting and feeding? Since it’s the hormone that tells you you’ve had
enough o eat, it would make sense if [leptin] ⇑ in feeding. So:
o [leptin] is ⇓ in fasted state
o [leptin] is ⇑ in fed state
• What is leptin made by? Adipose tissue
• What is [leptin]plasma proportional to? Fat mass. So the more fat mass you have, the higher the levels
of leptin will be in your blood plasma
• What does the Db gene code for? The leptin receptor
• What stimulates leptin production? Insulin. This makes sense as insulin is released in the fed state
to store away food, which is when you want leptin levels to be high too to suppress your appetite.
• Where does leptin act? In the hypothalamus
• What, apart from suppressing appetite, does leptin do? Stimulates thermogenesis
• How does leptin cause the hypothalamus to suppress appetite? It changes the expression of
orexigenic and anorexigenic genes which code for orexigenic and anorexigenic hormones. Orexigenic
= stimulates appetite; anorexigenic = suppresses appetite. Leptin will therefore suppress orexigenic
hormones and stimulate anorexigenic hormones.
• What are the key orexigenic and anorexigenic hormones?
Orexigenic hormones (⇓ by leptin) Anorexigenic (⇑ by leptin)
Neuropeptide Y (NPY) Melanocyte stimulating hormone (αMSH)
Agouti-related peptide (AgRP) Cocaine and amphetamine-related transcript
(CART)
• What is αMSH made from? Pro-opiomelanocortin (POMC) which is cleaved into ACTH, which is then
cleaved again into αMSH. This occurs in the hypothalamus.
• What are the functions of the hormones above?
o NPY à ⇑ feeding
o AGRP à antagonist at melanocortin 4 receptor (MC4R) à ⇑ feeding
o CART à ⇓ feeding
o αMSH à agonist at melanocortin 4 receptor (MC4R) à ⇓ feeding
• What are the hormones produced by? Neurones in the arcuate nucleus of the hypothalamus
• So, overall, what happens when you’ve eaten enough?
1. Insulin is released
2. This triggers leptin release by the adipose tissue
3. This leptin travels to the hypothalamus
4. Leptin inhibits AGRP/NPY neurones meaning:
(i) Less NPY produced (which normally ⇑ feeding) à feeding ⇓
(ii) Less AgRP produced (which normally ⇑ feeding by antagonising MC4R) à feeding ⇓
5. Leptin activates the POMC/CART neurones meaning:
Marc Huttman 3
, (i) More CART produced à feeding ⇓
(ii) More αMSH produced à agonises MC4R à feeding ⇓
6. Hence, appetite is suppressed and feeding stops
• What is the enzyme prohormone convertase-1? The enzyme that cleaves ACTH to make αMSH
• What are the monogenic disorders leading to obesity? Incredibly rare:
1. Frameshift mutation in leptin à no leptin produced à no appetite suppression
2. Truncated leptin receptor à no appetite suppression
3. Frameshift mutation in prohormone convertase-1 à it gets stuck in ER à can’t process
ACTH to make αMSH à no agonizing MC4R à no ⇓feeding
4. Frameshift mutation in MC4R à can’t respond to ⇑αMSH and ⇓AgRP which are meant to
suppress feeding
Ø Note that the above mutations represent all the steps of leptin produced à act on
receptor à αMSH made à act on MC4R à ⇓feeding
• What are the risk factors for these diseases? Consanguineous relationships (siblings/cousins)
• Why isn’t the appetite of obese people suppressed? Because the neurones in the hypothalamus are
resistant to leptin à overeat
• What are the common mutations leading to polygenic obesity? Unlike the monogenic disorders
which are mutations in coding regions of DNA, the mutations leading to polygenic obesity are in
non-coding regions (introns/SNPs):
1. There are 13 convincing SNPs that ⇑⇑risk of obesity including:
- A SNP for the non-coding bit of the MC4R gene
- The FTO gene (if you have it, you’ll be 3kg heavier)
- Each loci may account for a 0.05-0.24 BMI unit increase
2. There are 100 other quite convincing SNPs that ⇑risk of obesity
• What is the link between leptin and fertility? Since the Ob/Ob mouse is infertile, and patients with
a leptin deficiency show delayed puberty, we can infer a link between the two that leptin triggers
fertility. The thinking behind it is that you can’t reproduce until you have sufficient energy stores to
release leptin
• What drugs are good at triggering weight loss?
o Reductil and Acomplia which have been withdrawn
o Xenical = a pancreatic lipase inhibitor à reduces triglyceride uptake. This induces a 3%
weight loss but includes side effects of diarrhoea and steatorrhoea
• What drugs would be good at reducing obesity?
o MC4R agonist à ⇓feeding
o Mitochondrial uncoupling proteins (allows H+ gradient built up by electron transport chain to
relieve itself as H+ enter the cell, generating heat instead of ATP) – dinitrophenol did this and
was very effective at weight loss, but kills you
o β3 agonists that regulate the uncoupling proteins
o Activating things that induce satiety (feeling of fullness) including GLP1, PYY and CCK
o Inhibiting things that induce hunger including Ghrelin and orexins
Marc Huttman 4
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