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GSSE Phys > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Which hormone stimulates growth of breast ducts and alveoli?

A

oestrogens

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2
Q

Which hormone stimulates proliferation of breast lobules?

A

Progesterones

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3
Q

Which hormone stimulates milk production?

A

Prolactin

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4
Q

Which hormone stimulates milk let down?

A

Oxytocin

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5
Q

Where in the adrenal gland is aldosterone produced?

A

Zona glomerulosa

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6
Q

What is a summary of the effects of aldosterone?

A

Works to increase retention of sodium and water and therefore to increase intravascular volume

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7
Q

Where does aldosterone act in the kidneys?

A

Distal convoluted tubule and collecting ducts

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8
Q

How does aldosterone act on the kidney?

A

It acts on nuclear mineralocorticoid receptors to increase the number of basolateral sodium/potassium channels. More sodium is pumped out of the cells in exchange for potassium in the extracellular fluid, and this sets up a concentration gradient which causes the movement of sodium out of the tubular lumen and into the tubule cells across the apical membrane. Thus, sodium is retained.

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9
Q

Where else does aldosterone act apart from the kidneys?

A

Sweat glands, colon

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10
Q

What does aldosterone do in the collecting ducts and in the colon?

A

increases the number of epithelial sodium channels (ENaCs) in the collecting ducts and the colon, increasing the permeability of the apical membrane to sodium. Other effects include secretion of potassium and protons (H+) into the tubular fluid, increasing loss of these two ions

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11
Q

What stimulates aldosterone production?

A

Aldosterone secretion is stimulated by hyperkalaemia, a rise in angiotensin II or ACTH, or decreased blood pressure (detected by atrial stretch receptors).

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12
Q

What conditions lead to a rise in aldosterone levels?

A

Increased secretion is seen in pregnancy, trauma, burns and blood loss.

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13
Q

What are the effects of cortisol?

A

Cortisol causes mobilisation of protein, lipid and carbohydrate stores, and immunosuppression.

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14
Q

What are the effects of too much cortisol?

A

Excess levels cause muscle wasting, a characteristic fat deposition around the abdomen and between the scapulae, thin skin and striae, psychiatric disorders, hyperglycaemia and diabetes mellitus, poor healing, osteoporosis, oedema, and fluid retention.

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15
Q

What is Cushing’s syndrome?

A

An excess of glucocorticoids.
2 types ACTH dependent (i.e. from a secreting tumour in the pituitary) and ACTH independent (i.e. taking too much steroid, adrenal carcinoma)

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16
Q

What suppresses ACTH production?

A

Excess glucocorticoid has a negative feedback and suppresses production

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17
Q

How many amino acids does the mature form of PTH include?

A

84

6 amino acids are removed from the PTH precursor in the golgi apparatus

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18
Q

What effect does oestrogen have on GnRH?

A

Estrogen stimulates GnRH secretion by a positive feedback effect on the hypothalamus.

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19
Q

What happens to basal body temperature during the follicular phase of the menstrual cycle?

A

It gradually declines and then rises at the time of ovulation due to the effects of progesterone

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20
Q

At what stage of pregnancy does the placenta make enough hormones to support foetal life and development?

A

The placenta makes enough progesterones and oestrogens to support foetal development from around the sixth week of pregnancy. Prior to this, the ovaries produce these sex hormones, and removal of the ovaries will result in termination of the pregnancy. After six or more weeks, the pregnancy will survive even if the ovaries are removed.

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21
Q

How does thyroxine circulate in the blood?

A

Thyroxine is bound in the greatest amount to thyroid-binding globulin and in smaller amounts to thyroid binding albumin and prealbumin.

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22
Q

How do thyroid hormones effect erythrocytes?

A

Thyroid hormones stimulate erythrocyte production by causing the maturation of erythrocyte progenitors.

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23
Q

What effect do thyroid hormones have on the oxygen dissociation curve?

A

They increase oxygen dissociation from haemoglobin

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24
Q

What are oestrogens?

A

Oestrogens are C18 steroids, and include estriol, estrone and 17-beta estradiol.

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25
Q

Where are oestrogens produced?

A

They are produced by the ovarian granulosa cells, placenta and corpus luteum.

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26
Q

What stimulates oestrogen production?

A

Oestrogen production is stimulated by LH and FSH

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27
Q

What are oestrogens derived from?

A

Oestrogens are derived from androgens such as testosterone and androstenedione, by a process called “aromatisation” (facilitated by the enzyme aromatase), in the granulosa cells of the ovary.
The androgens are supplied by the theca interna cells.

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28
Q

What does oestrogen do?

A
  • Protein anabolism
  • Increases uterine bloodflow and myometrial excitability
  • Ovarian follicle growth
  • Increased fallopian tube motility
  • Increased libido
  • Breast duct and alveolar growth
  • Reduction of plasma cholesterol
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29
Q

What role does prolactin have in calcium homeostasis?

A

Reduces calcium excretion in the urine

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30
Q

What role do growth hormone, thyroxine and cortisol have in calcium homeostasis?

A

Increase urinary calcium excretion

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31
Q

How does parathyroid hormone change from inactive to active?

A

It begins as a preprohormone, and is converted to a prohormone and then to an active peptide hormone within the parathyroid glands, before being secreted.

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32
Q

What is the primary effect of parathyroid hormone?

A

Increases calcium- does this by increasing resorption of bone and mobilising bony calcium stores

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33
Q

What effect does PTH have on the kidneys and intestine?

A

It increases phosphate excretion in the distal convoluted tubules and increases calcium reabsorption in the kidney and intestine

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34
Q

What is the effect of PTH on Vitamin D?

A

It also catalyses the conversion of vitamin D to its active form, 1,25-dihydroxycholecalciferol.

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35
Q

What is the effect of PTH on osteoclasts and osteoblasts?

A

It is stimulatory to both (in the long term)

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36
Q

What happens to PTH in chronic renal failure?

A

In chronic renal failure, calcium losses at the kidney rise and tertiary hyperparathyroidism results, as PTH tries to maintain serum calcium levels.

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37
Q

Is PTH necessary for life?

A

PTH is necessary for life—without it, profound hypocalcaemia and death will result.

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38
Q

What stimulates renin secretion?

A

Renin secretion is increased by increased sympathetic stimulation, catecholamines, and prostaglandins. Other stimuli include sodium depletion, haemorrhage, standing upright, cardiac failure, diuretics, cirrhosis, dehydration, renal artery stenosis, and hypotension.

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39
Q

What inhibits renin secretion?

A

It is decreased by increased sodium and chloride reabsorption in the macula densa, vasopressin, angiotensin II, and increased afferent arteriolar pressure.

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40
Q

What are the effects of thyroid hormones on the cardiovascular system?

A

Thyroid hormones increase cardiac output, heart rate, and pulse pressure (the difference between systolic and diastolic blood pressure). Thyroid hormones cause a decrease in peripheral vascular resistance, and mean arterial pressure falls

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41
Q

What are the effects of thyroid hormones on the basal meatbolic rate?

A

thyroid hormones increase the basal metabolic rate due to increased expression of Na+/K+ ATPase in tissues.

42
Q

What is gluco-corticoid remediable aldosteronism?

A

Glucocorticoid-remediable aldosteronism is an autosomal dominant inherited disorder due to the overactivity of the aldosterone synthase enzyme.
It is a primary hyperaldosteronism so renin levels are low

43
Q

How much of the bone in the body is compact bone?

A

80%

44
Q

How do the bone cells lie in compact bone?

A

In lacunae

45
Q

How does compact bone receive nutrients?

A

via Haversian canals

46
Q

Thyroid hormones increase BMR and oxygen consumption of many tissues except?

A

spleen, testes, adult brain, uterus, lymph nodes, and anterior pituitary gland.

47
Q

How much iodine do you need per day for normal thyroid function?

A

150 micrograms

48
Q

Which is more biologically active T3 or T4?

A

T3

49
Q

How is thyroid hormone synthesised?

A

During thyroid hormone synthesis, oxidation and reaction of iodide with a glycoprotein known as “thyroglobulin” is mediated by thyroid peroxidase.

50
Q

How is T3 formed?

A

T3 has a higher biological activity than T4 and is formed in peripheral tissue by deiodination of T4.

51
Q

Where and when is calcitonin produced?

A

Calcitonin is secreted by the parafollicular C cells in the thyroid when calcium levels are raised.

52
Q

What does calcitonin do?

A

It lowers serum calcium levels by decreasing osteoclastic resorption of bone and increasing excretion at the kidney.

53
Q

What stimulates calcitonin release?

A

Levels may be increased by dopamine, oestrogens, beta-agonists, glucagon and gastrin.

54
Q

How are iodides stored?

A

Iodides are stored in the thyroid follicles mainly in the form of thyroglobulin

55
Q

What stimulates prolactin secretion?

A

Exercise, stress, and nipple stimulation increase secretion as does TRH and TSH.

56
Q

What decreases prolactin secretion?

A

Dopamine, chlorpromazine

57
Q

How is prolactin produced?

A

Prolactin is produced by the anterior pituitary. Its secretion is routinely inhibited by the hypothalamus; thus dividing the pituitary stalk and removing this control will result in increased prolactin secretion.

58
Q

What increases the release of growth hormone?

A

Starvation and protein deficiency, increased blood amino acids such as L-arginine, low concentration of fatty acids in the blood, hypoglycemia, exercise, trauma, and excitement
Growth hormone-releasing hormone produced from the hypothalamus, testosterone, and estrogen also increase its levels. Growth hormone levels are also increased during the first two hours of deep sleep.

59
Q

What effect do plasma potassium levels have on aldosterone?

A

Potassium blood levels directly regulate aldosterone secretion. High potassium levels will stimulate aldosterone secretion. This negative feedback mechanism will avoid a hyperkalemia. A low potassium level with reduce aldosterone secretion.

60
Q

Where is glucagon produced?

A

Pancreatic alpha cells of the pancreatic islets of Langerhans synthesize and secrete glucagon.

61
Q

What is the function of glucagon?

A

Glucagon’s primary function is to increase blood glucose and fatty acids in the bloodstream (lipolysis)

62
Q

Where else in the body apart from in the plasma is glucose found?

A

Besides the plasma, glucagon is normally found in the brain and gastrointestinal tract. In the brain, glucagon plays a role in the regulation of appetite and satiety.

63
Q

Where in the adrenal gland is epinephrine produced?

A

Adrenal medulla. Also produces a small amount of norepinephrine.

64
Q

What does the adrenal zona fasiculata produce?

A

Glucocorticoids

65
Q

What effect does insulin have on lipoprotein lipase?

A

It activates it

66
Q

What does lipoprotein lipase do?

A

LPL splits the triglycerides into fatty acids, which are absorbed into the adipose cells, where they are reconverted to triglycerides and stored.

67
Q

How is testosterone produced in the testes?

A

Luteinizing hormone, secreted by the anterior pituitary gland, stimulates the Leydig cells to secrete testosterone. Testosterone is secreted by the Leydig cells located in the interstitium of the testis.

68
Q

How does testosterone travel in the plasma?

A

97% bound to albumin or sex-hormone binding globulin

69
Q

What is the role of FSH in sperm production?

A

Follicle-stimulating hormone, also secreted by the anterior pituitary gland, stimulates the Sertoli cells for conversion of spermatids to sperm.

70
Q

Where is most of the body’s phosphorous?

A

In the skeleton

71
Q

What happens to phosphorous in the kidney?

A

85-90% is reabsorbed, mostly in the proximal tubules

72
Q

What effect does growth hormone have on liver cells?

A

Growth hormone stimulates the production of somatomedins by hepatocytes which play their role in bone growth. Somatomedins are also called “insulin-like growth factors”.

73
Q

How are oestrogens excreted?

A

They are excreted by conversion to glucuronides and sulfate conjugates in the liver, and then secreted into bile to enter the gut.

74
Q

In which tissues does thyroid hormone increase the basal metabolic rate and oxygen consumption?

A

All except spleen, testes, adult brain, uterus, lymph nodes, and anterior pituitary gland

75
Q

Does cortisol travel unbound or bound in the plasma?

A

90-95% bound

76
Q

What is cAMP not a second messenger for?

A

Insulin

77
Q

What decreases the secretion of aldosterone?

A

Decreased renal nerve stimulation, fall in angiotensin II, increased blood pressure, hypokalaemia

78
Q

In what conditions would you expect to see an increased level of aldosterone?

A

Pregnancy, trauma, burns and blood loss

79
Q

What are the two most abundant minerals in the body?

A
  1. Calcium
  2. Phosphorous
    (3rd most abundant is sulphur)
80
Q

Which organ is the primary regulator of phosphorous?

A

The kidney

81
Q

What is the role of the theca interna?

A

Theca interna cells in the ovary express receptors for luteinizing hormone (LH) and produce androstenedione, an androgen. Through a process of aromatization, androgens are converted to estrogen by the granulosa cells. So strictly speaking, the Theca does not release oestrogens directly, but LH does stimulate androgen release that can then be converted to oestrogen.

82
Q

What causes a rise in plasma cholesterol?

A

Biliary obstruction (particularly primary biliary cirrhosis), diabetes mellitus, moderate to high intake of dietary amounts of cholesterol, and hypothyroidism can increase plasma cholesterol.

83
Q

What effect does adrenaline have?

A

Adrenaline causes lipolysis, which results in free fatty acid mobilisation from the adipocytes
widens pulse pressure and increases the basal metabolic rate.
It has a very weak vasoconstrictive effect on the vasculature of skeletal muscles and the liver, thus leading to a decreased total peripheral resistance and an increased cardiac output. 
Adrenaline increases the basal metabolic rate.

84
Q

What stimulates CRH release?

A

Fever, hypoglycaemia, stress

85
Q

What stimulates TRH release?

A

Cold temp, pregnancy

86
Q

What stimulates growth hormone releasing hormone?

A

Hypoglycaemia, high levels of amino acids in the blood, low fatty acids in the blood, exercise, healthy stressors

87
Q

Which nucleus in the hypothalamus produces oxytocin?

A

Paraventricular nucleus

88
Q

What stimulates oxytocin release?

A

Birthing process (stretch receptors in the uterus specifically), suckling (mechanoreceptors on nipple)

89
Q

What does oxytocin do to the uterus?

A

Increases intracellular calcium levels in myometrial smooth muscle cell to increase contraction of uterus

90
Q

Where is ADH produced?

A

Secreted from posterior pituitary, produced in supraoptic nucleus

91
Q

What stimulates ADH release primarily?

A

Low blood pressure, high plasma osmolality (hypertonic)

92
Q

How does the hypothalamus detect change in osmolality of blood?

A

Osmoreceptors at hypothalamus

93
Q

Where does ADH work in the kidney?

A

Binds to V2 receptor in collecting duct

94
Q

What does ADH do in the kidney?

A

Inserts aquaporin II channels into the collecting duct. This brings water into the bloodstream, therefore increasing plasma volume and blood pressure.

95
Q

In what condition is there low or no ADH secretion?

A

Diabetes insipidus

96
Q

Where ois growth hormone secreted?

A

Somatotrophes in anterior pituitary

97
Q

What does growth hormone do in the liver?

A

Produces IGF-1, gluconeogenesis

98
Q

What does IGF-1 do (produced due to growth hormone)?

A

Uptake of amino acids into muscle cells links them and make proteins in muscles = increase muscle size
Increases osteoblast and osteoclast activity, increases endochondral ossification, increases collagen type 1 and proteoglycan production, increases interstitial growth in cartilage/ bone

99
Q

What does growth hormone do to adipocytes?

A

Breaks down triglycerides into glycerol and triglycerides (lipolysis)

100
Q

The intestinal hormone thought to produce the greatest amount of insulin release in response to an oral glucose bolus is:

A

GIP

GSSE Phys (6 decks)

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