Unit 6.6

Question 1

1. What can high levels of glucose in the blood cause?
2. Two antagonistic hormones responsible for regulating blood glucose concentrations?
3. Where are these hormones released from?
4. Where do they principally act on?
5. What occurs when glucose levels are high?
6. What occurs when glucose levels are low?

Answer 1

1. Damage cells (creates hypertonicity).
2. Insulin and Glucagon.
3. Pancreatic pits called Islets of Langerhans.
4. The liver.
5. Insulin released from beta cells of the pancreas, cause a decrease in blood glucose concentration. May involve stimulating glycogen synthesis in liver (glycogenesis), promoting glucose uptake by liver and adipose tissue or increase rate of glucose breakdown via cell respiration.
6. Glucagon released from alpha cells of pancreas, cause increase in blood glucose concentration. May involve stimulating glycogen breakdown in liver (glycogenolysis), promoting glucose release by liver and adipose tissue or decreasing rate of glucose breakdown via reduced cell respiration rates.

Question 2

1. What is diabetes mellitus?
2. Describe type 1 diabetes?
3. Describe type 2 diabetes?
4. What is diabetes insipidus?
5. How is type 1 diabetes caused?
6. How is type 2 diabetes caused?

Answer 2

1. A metabolic disorder that results from a high blood glucose concentration over a prolonged period.
2. Early onset in life, you don’t produce enough insulin, it’s genetic and treated by insulin patches and injections.
3. Later onset in life, the cells don’t respond to insulin, it is caused by poor diet, ethnicity, age and lifestyle and is treated by a healthier diet and exercise.
4. A brain issue that causes over urination.
5. Insulin is not produced by beta cells in the pancreas and hence glucose is not removed from the bloodstream, causing diabetes.
6. Prolonged overproduction of insulin leads to desensitisation of the insulin receptors and hence glucose is not removed from the bloodstream, causing diabetes.

Question 4

1. Explain what thyroxine is and what stimulates it.
2. Why is thyroxine important?
3. What is its primary role?
4. How can this be achieved?
5. Consequence of metabolic activity?
6. What is is partially composed of and what will a deficiency of this lead to?
7. What does an iodine deficiency cause?

Answer 4

1. A hormone secreted by thyroid gland in response to hypothalamus signals, is released in response to decreased body temp.
2. Acts on nearly every tissue in the body and is essential to the proper development and differentiation of cells.
3. Increase basal metabolic rate (amount of energy used by body at rest).
4. By stimulating carbohydrate and lipid metabolism via oxidation of glucose and fatty acids.
5. Production of heat - hence thyroxine helps control body temp.
6. Partial composed of iodine so deficiency of iodine in diet causes decreased thyroxine production.
7. Iodine deficiency will cause thyroid glands to become enlarged, causes a disease called goitre as the thyroid tries to make as much thyroxine as possible.

Question 5

1. What is leptin?
2. How does it carry out its function?
3. What does overeating cause?
4. What does undereating cause?
5. What happens to obese people?
6. How else can leptin resistance develop?
7. How was leptin used to treat clinical obesity?

Answer 5

1. A hormone produced by adipose cells, regulates fat stores in the body by suppressing appetite.
2. Binds to receptors in hypothalamus to inhibit appetite and reduce food intake.
3. Causes more adipose cells to form so more leptin produces, further suppressing appetite.
4. Periods of starvation lead to reduced adipose tissue so less leptin is released, causing hunger.
5. Obese people constantly produce higher levels of leptin, their body becomes progressively desensitised to the hormone. Thus, less likely to feel hungry or recognise when they are full so more likely to overeat.
6. Also develop with age, increasing the potential for weight gain later in life.
7. Suppresses appetite so theoretically leptin injections would reduce hunger and limit food intake leading to weight loss.

Question 6

1. How were leptin trials conducted?
2. What occurred when the obese mouse with no leptin was parabiotically fused to a healthy mouse?
3. What occurred when the obese mouse with defective leptin receptors was parabiotically fused to a healthy mouse?
4. What are most cases of obesity caused by?
5. Why are leptin treatments not considered to be effective in controlling obseity?

Answer 6

1. Surgically fusing the blood circulation of obese and health mice through parabiosis.
2. Leptin in healthy mouse blood transferred to obese mouse, obese mouse responded to leptin and began to lose weight. This demonstrated the potential viability of leptin treatment.
3. Leptin transferred to healthy mouse (the obese mouse overproduced leptin to compensate for low receptor sensitivity). Obese mouse remained obese as its body couldn’t respond to leptin, healthy mouse became emaciated bc of abnormal leptin levels transferred to its bloodstream.
4. Unresponsiveness to leptin.
5. Few participants in human trials experienced significant weight loss in response to leptin injections, however many did experience side effects from the injections such as skin irritations.

Question 7

1. Melatonin function?
2. What are circadian rhythms and what are they driven by?
3. What is melatonin secretion suppressed by?
4. What occurs to melatonin levels with age?
5. What is jet lag?
6. What is it caused by?
7. How does it affect the body?

Answer 7

1. A hormone secreted by pineal gland in brain, responsible for synchronising circadian rhythms and regulates body’s sleep schedule.
2. body’s physiological responses to the 24 hour day-night cycle, are driven by an internal (endogenous) circadian clock, although they can be modulated by external factors.
3. bright light (principally blue wavelengths) and hence levels increase during the night.
4. naturally decrease with age, leading to changes in sleeping patterns in the elderly
5. a physiological condition resulting from a change to the body’s normal circadian rhythm.
6. caused by the body’s inability to rapidly adjust to a new time zone following extended air travel.
7. pineal gland continues to secrete melatonin according to old time zone so that sleep schedule isn’t synchronised to the new time zone.

Question 8

1. Jet lag symptoms?
2. How can it be combated?
3. How many chromosomes does a human body cell have?
4. How many chromosomes does a sex cell have?
5. What is a haploid cell?
6. What was the historically soil and seed theory proposed by aristotle?
7. Who theory did William Harvey propose?

Answer 8

1. headaches, lethargy, increased irritability and reduced cognitive function.
2. Taking melatonin near sleep time or new time zone to recalibrate the body. Artificially increasing melatonin levels at right time can allow body to respond quicker to new time zone.
3. 46
4. 23
5. Contains half the number of chromosomes.
6. Male produces a ‘seed’ which forms an ‘egg’ when mixed with menstrual blood the ‘soil’. The egg develops into a foetus inside the mother according to the information contained within the male ‘seed’ alone.
7. He studied the sexual organs of female deer after mating in an effort to identify the developing embryo. He was unable to detect a growing embryo until approximately 6-7 weeks after mating had occurred. He concluded that Aristotle’s theory was incorrect and that menstrual blood didn’t contribute to fetal development. However, he incorrectly asserted that the foetus didn’t develop from a mixture of male and female ‘seeds’.

Question 9

1. Explain the modern theory of sexual reproduction.
2. What chromosomes for females possess?
3. What chromosomes do males possess?
4. What does the SRY gene code for?
5. In the absence of what, do ovaries form?
6. What is testosterone responsible for? (3)

Answer 9

1. A foetus forms by the fertilisation of a female egg cell by the burrowing of a sperm cell into this egg cell.
2. XX
3. XY
4. Codes for a testis-determining factor (TDF) that causes embryonic gonads to form into testes.
5. Absence of the TDF protein.
6. the pre-natal development of male genitalia.
   * involved in sperm production following the onset of puberty
   * aids development of secondary sex characteristics for example:
   It helps to maintain the male sex drive (libido)

Question 10

1. Role of female progesterone and oestrogen? (2)
2. Role of tesis?
3. Role of epididymis?
4. role of vas deferens.
5. role of Seminal vesicle?
6. Role of prostate gland?
7. Role of urethra?

Answer 10

1. promote the pre-natal development of the female reproductive organs
   * responsible for the development of secondary sex characteristics for example:
   * They are involved in monthly preparation of egg release following puberty (via the menstrual cycle)
2. Responsible for the production of sperm and testosterone (male sex hormone
3. Site where sperm matures and develops the ability to be motile (i.e. ‘swim’) – mature sperm is stored here until ejaculatio
4. Long tube which conducts sperm from the testes to the prostate gland (which connects to the urethra) during ejaculation
5. Secretes fluid containing fructose (to nourish sperm), mucus (to protect sperm) and prostaglandin (triggers uterine contractions)
6. Conducts sperm / semen from the prostate gland to the outside of the body via the penis (also used to convey urine)
7. Conducts sperm / semen from the prostate gland to the outside of the body via the penis (also used to convey.

Question 11

1. role of ovary?
2. role of fimbria?
3. role of oviduct?
4. role of uterus?
5. role of endometrium?
6. role of vagina?

Answer 11

1. The mucous membrane lining of the uterus, it thickens in preparation for implantation or is otherwise lost (via menstruation).
2. a fringe of tissue adjacent to an ovary that sweep an oocyte into the oviduct.
3. transports the oocyte to the uterus – it is also typically where fertilisation occurs.
4. Where a fertilised egg will implant and develop (becoming an embryo).
5. where oocytes mature prior to release (ovulation) – it also responsible for oestrogen and progesterone secretion.
6. Passage leading to the uterus by which the penis can enter (uterus protected by a muscular opening called the cervix)

Question 12

1. Average menopause age?
2. Day menstrual cycle begins?
3. What menstrual hormones do the pituitary gland release?
4. What menstrual hormones do the ovaries release?
5. what does fsh do?
6. what does LH do?
7. what does oestrogen do?
8. what does progesterone do?

Answer 12

1. 45-55
2. 1
3. FSH and LH
4. Oestrogen and progesterone.
5. stimulates follicular growth in ovaries, stimulates oestrogen secretion.
6. Causes ovulation
   results in formation of corpus luteum.
7. Thickens uterine lining (endometrium), inhibits FSH and LH, stimulates their release pre-ovulation.
8. Maintains uterine lining

Question 13

1. 4 key events in the menstrual cycle?
2. what changes distinguish these events?
3. explain follicular phase?
4. explain ovulation.
5. explain luteal phase?
6. Explain menstruation?

Answer 13

1. Follicular phase, ovulation, luteal phase, menstruation.
2. hormonal levels, follicular development, status of the endometrium.
3. FSH released, stimulates growth of ovarian follicles, dominant follicle produces oestrogen which inhibits FSH. Oestrogen acts on uterus lining to stimulate thickening of endometrial layer.
4. Day 12 - oestrogen stimulates pituitary to secrete hormones. Positive feedback results in more LH and less FSH, LH causes dominant follicle to rupture and release an egg, ovulation.
5. Ruptured follicle develops into a slowly degrading corpus luteum, this secretes lots of progesterone and low levels of oestrogen, these both act on uterus to thicken endometrial lining for preggo preparation. O and P also inhibit LH and FSH.
6. If fertilisation occurs, developing embryo implants in endometrium, releases hormones to sustain corpus luteum. If no fertilisation, luteum degenerates, oestrogen and progesterone levels drop and endometrium can’t be maintained. It is sloughed away and eliminated as menstrual blood. Oestrogen and progesterone levels are to low to inhibit the anterior pituitary, cycle can begin again.

Question 14

1. What is IVF?
2. Name its 4 stages?
3. What is down regulation?
4. What is superovulation?
5. What is fertilisation?
6. What is implantation?
7. How is down regulation treatment administered?

Answer 14

1. External fertilisation using drugs to suspend normal ovulation before using hormone treatments to collect multiple eggs.
2. Down regulation, superovulation, fertilisation, implantation.
3. (suspension of normal ovulation) - drugs halt FSH and LH secretion to control timing and quantity of egg production.
4. Artificial doses of hormones to develop multiple eggs, patient injected with FSH to stimulate development of follicles. Follicles are treated with human chorionic gonadotrophin which stimulates the follicles to mature and the egg is then collected.
5. extracted eggs are then incubated in the presence of a sperm sample from the male donor.
6. two weeks prior to implantation, the woman begins to take progesterone treatments to develop the endometrium, healthy embryos selected and transferred into female uterus, many embryos transferred to improve chances of successful implantation. Pregnancy test is typically taken 2 weeks after.
7. In the form of nasal spray.