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Endocrinology Flashcards

0
Q

What’s the purpose of the endocrine system?

A

Maintenance of the internal environment, integration and regulation of growth and development. Control and maintenance of and instigation of sexual reproduction.

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1
Q

What are the endocrine organs

A

Hypothalamus, adrenals, pituitary, pancreas, parathyroid a. Thyroid, ovaries, testes

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2
Q

What are peptide hormones?

A

Made up of amino acids. Start as a preprohormone, ER modification to Prohormone then becomes active and packaged in vesicles.

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3
Q

Amino acid hormones?

A

Thyroxine epinephrine

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4
Q

Steroid hormones

A

Derived from cholesterol and are lipid soluble. Therefore permeate membranes. Are synthesised in the adrenals, gonads and placenta.

Cholesterol – various p459s–> product

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5
Q

What do glucocorticoids?

A

Control carbohydrate metabolism and moderate the inflammatory response. Respond to stress.

E.g. Cortisol

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6
Q

Mineralocorticoid

A

Control salt balance and BP.

E.g. Aldosterone

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7
Q

Fatty acid derivatives- eicosanoids

A

Prostaglandins, leukotrienes and thromboxanes

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8
Q

What is neural control?

A

Neural input into the hypothalamus stimulates synthesis and secretion if releasing factors. This stimulates hormone secretion.

E.g. Stress –> ACTH –> cortisol

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9
Q

An example of positive feedback

A

LH stimulation of oestrogen which stimulates a surge of LH at ovulation

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10
Q

Why is pulsatile release of GnRH important?

A

Slower release = no gonad function

Faster = gonadotropin release inhibited therefore steroid production reduced

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11
Q

How are the thyroid hormones carried through the body?

A

They are hydrophobic and are therefore carried by thyroxine binding globulin

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12
Q

Where are t3 and t4 produced?

A

Follicular cells of the thyroid gland when iodides are available.

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13
Q

What does PTH do?

A

Increases blood Ca2+ and decreases Po4-. Ca released from bone and increases vitamin D production which increases dietary absorption of Ca.

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14
Q

What are the 3 layers of the adrenal cortex and what do they produce?

A

Zona glomerulosa- mineralocorticoids
Zona Fasiculata- glucocorticoids
Zona reticularis- sex hormones

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15
Q

What does the adrenal medulla produce?

A

It acts as part of the sympathetic NS producing Noradrenaline and adrenaline

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16
Q

What is aldosterone and what does it do?

A

It’s a mineralocorticoid that regulates mineral electrolyte levels in the blood. It’s controlled by blood plasma ion conc, renal secretion of renin and ACTH from the ant. Pituitary.

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17
Q

What is cortisol and what does it do?

A

It’s a glucocorticoid that helps to maintain blood glucose conc. it increase aa levels, promotes the use of fat for energy production and stimulates gluconeogenesis.

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18
Q

What does the pancreas produce?

A

α cells- glucagon
β cells- insulin
δ cells- somatostatin

These all regulate blood glucose

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19
Q

What does glucagon do?

A

Causes the liver to produce glucose via glycogen oldies and gluconeogenesis. It’s regulated by blood glucose directly

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20
Q

What does insulin do?

A

Decreases blood glucose levels by increasing glycogen formation, reducing gluconeogenesis and increases glucose transport into cells.

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21
Q

What is male Hypogonadism?

A

Androgen deficiency &/or decreased sperm production.
Primary- reduced testosterone with increased FSH & LH
Secondary- reduced test. With normal or low FSH & LH

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22
Q

What does the leydig cell do and what does it respond to?

A

It’s found adjacent to seminiferous tubules and produce testosterone in the presence of LH. Prolactin increase cell response to LH.

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23
Q

What is the serotoli cell and what does it do?

A

It’s part of the seminiferous tubule and is activated by FSH. It develops sp,srm through spermatogenesis.

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24
Q

What’s the presentation of male Hypogonadism?

A

Small or absent testes, gynaecomastia, infertility and sexual dysfunction, small prostate, reduced hair, osteoporosis.

25
Q

What are the investigations for Hypogonadism?

A

Morning testosterone x2, LH and FSH + semen analysis x2

26
Q

Causes of primary Hypogonadism

A

Kleinfeldters, orchitis, castration, androgen resistance, drugs/alcohol, chronic kidney/liver disease

27
Q

Causes of secondary hypogonadism

A

Cushings, constitutional delayed puberty, hypo pituitary, hyperprolactinaemia, anabolic steroids

28
Q

What is PCOS?

A

Androgen excess from the ovary

29
Q

Presentation and investigation of PCOS

A

Ovarian dysfunction, weight gain, hirsutism, acne.

Investigations: increased LH:FSH ratio, USS ovaries, increased test.

30
Q

What is turners syndrome?

A

Chromosome deficiency: XO in females.

31
Q

Signs of androgen excess

A

Hirsutism, virilisation, increased test, acne, aggression

32
Q

Presentation of Turners syndrome

A

Primary amenorrhea, lymphodoema of hands and feet, neck webbing, growth faltering cubits valgus

33
Q

Precocious puberty

A

Rare in boys. Is oestrogen secretion before 7-8y.o. = early onset of puberty. Treat with reducing LHRH

34
Q

What hormones are involved in calcium homeostasis?

A

PTH- stimulates bone resorption & renal tubular reabsorption of Ca2+
Calcitonin- minimal importance, decreases ca2+ and po4-
Vit D- increases calcium and phosphate

35
Q

What Are the main causes of Hypercalcaemia?

A

1’ hyperparathyroidism, malignancy

Milk-alkali syndrome, increased vit d intake, sarcoidosis, granulomatous disease, thiazides.

36
Q

What is primary hyperparathyroidism?

A

Excess PTH secretion–> Adenoma, hyperplasia, carcinoma.

Is generally asymptomatic–> stones! moan! groan! bones and psychiatric overtones.

37
Q

What is 2’ and 3’ hyperparathyroidism?

A

2’ is compensatory, increased PTH secondary to hypocalcaemia with parathyroid hyperplasia.

3’ is autonomous secretion of PTH following long term hypocalcaemia.

38
Q

What is malignant Hypercalcaemia?

A

Malignancy –> increased osteoclast bone resorption

Occurs at end stage disease.

39
Q

Causes of hypocalcaemia?

A

Hypoparathyroidism, impaired PTH secretion, target organ resistance, Vit related disorders, HIV, drugs, pancreatitis

40
Q

What is pseudo Hypoparathyroidism and how does it present?

A

Resistance to PTH rather than lack of it. Presents with Albright’s hereditary dystrophy.

41
Q

Hypomagnasaemia?

A

Reduced Mg levels which causes reduced PTH, PTH resistance and therefore reduced Ca and k.

Presents with NMJ excitability, tingling extremities, tetany, long QT.

42
Q

What is Phaeochromocytoma?

A

Increased catecholamine production from adrenal/extra adrenal tumour.

Presents with associated symptoms do adrenaline.

43
Q

Cushing’s disease and it’s causes?

A

Increased cortisol by the Zona fasciculata.

Caused by- adrenal Adenoma, adrenal carcinoma, pituitary cushings, ectopic ACTH

44
Q

Presentation of Cushing’s syndrome?

A

Central obesity, buffalo hump, fatigue, moon face, HTN, pigmentation, hyperglycaemia, hirsutism, depression, bruising

45
Q

What is Addison’s disease?

A

Primary adrenal insufficiency.

Causes: autoimmune, TB

Presentation: pigmentation, malaise, N&V, weight loss, hypoglycaemia, postural hypotension.

46
Q

What is Conn’s syndrome?

A

Endocrine HTN, caused by excess secretion of aldosterone from the Zona glomerulosa.

1’ hyperaldosteronism.

47
Q

Symptoms of hypocalcaemia?

A

Fasciculations, spasms, tingling, numbness, seizure and convulsions.

48
Q

What are the gonads controlled by?

A

Hypothalamic/pituitary axis.

LHRH & GnRH –> LH (leydig cells- test.) & FSH (sertoli cells- sperm)

49
Q

Causes of testicular failure?

A

1’ orchitis, radiation, trauma, tumour
2’ increased prolactin, pit/hypothalamic tumour

Leads to reduced sperm and test.
LH and FSH low in 2’, high in 1’

50
Q

What stimulates oestrogen?

A

FSH stimulates conversion of testosterone to oestrogen.

51
Q

What are the types of hormone?

A

Endocrine- hormones travel via bloodstream
Neuroendocrine- released by synapse into the bloodstream
Paracrine- act on adjacent cells
Autocrine- act on same cell that produced them
Intracrine- work within the source cell

52
Q

What systems are controlled by the hypothalamic- pituitary axis?

A

Thyroid, adrenal cortex, gonads

53
Q

What is HbA1c?

A

Glycocylated haemoglobin- indicates glycemic levels over the last 120 days.
50% formed in the 1month preceding.

54
Q

Symptoms of T2DM

A

Increased thirst, micrurition, headaches, blurred vision, difficulty concentrating and extreme tiredness.

55
Q

What receptor does glucose bind to in the β cells of the pancreas?

A

GLUT-2 receptor.

This stimulates insulin release.

56
Q

How does Gliclozide work and what sort of drug is it?

A

It stimulates insulin release in the same way as glucose but binds to the sulphonylurea receptor.

It is a sulphonylurea.

57
Q

Functions of insulin?

A

Enhances peripheral glucose uptake, inhibits breakdown of liver glycogen, enhances storage of glucose and glycogen, increases protein synthesis, increases TG storage

58
Q

What is an incretin?

A

Group of GI hormones that stimulate a decrease in blood glucose levels.

E.g. GLP-1

59
Q

Where is the most glucose reabsorbed in the kidneys and by what mechanism?

A

In the PCT, mainly through SGLT2, and some through SGLT1. Thighs gives minimal excretion in urine.

Inhibition of SGLT2 = increased excretion

60
Q

What is insulin resistance and what are its symptoms?

A

Cells do not respond to the presence of insulin - hyperglycaemia and hyperinsulinaemia.

Symptoms- reduced concentration, bloating, depression, lethargy, acanthosis nigricans, hunger, HTN, weight gain

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