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eBMS2031 > ENDOCRINE SYSTEM > Flashcards

ENDOCRINE SYSTEM Flashcards

1
Q

What are some of the functions of Ca in the body

A

Bone formation

Muscle contraction

Neurotransmission

Sinus rhythm

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2
Q

How much of the Ca in the body is ionised, free and biologically active?

A

50%

The part of body Ca that can be regulated

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3
Q

Outline the process of resorption

A

osteoclasts break down the tissue in bones and release the minerals

resulting in a transfer of calcium from bone tissue to the blood

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4
Q

How to osteoclasts perform resorption

A

Osteoclasts originate from hematopoietic stem cells

secrete hydrogen ions and hydrolytic enzymes which digest osteoid

release Ca and PO4 back into blood

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5
Q

How do osteoblasts perform bone formation

A

Osteoblasts originate from mesenchymal stem cells and synthesis the collagen organic matrix of bone

Use Ca and PO4 from the blood to produce hydroxyapatite that is deposited into the matrix

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6
Q

What are osteocytes

A

Osteoblasts that become surrounded by calcified matrix.

Have long cytoplasmic processes that extend through bone forming tight junctions with other osteocytes

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7
Q

Explain how bone resorption is stimulated

A

Osteoblasts produce RANKL which binds to RANK proteins of osteoclasts triggering bone resorption

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8
Q

What hormones stimulate RANKL production and therefore bone resorption

A

PTH

1,25-dihydroxy Vitamin D

Cortisol

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9
Q

Explain how bone resorption is inhibited

A

Osteoblasts also produce OPG, a decoy receptor that binds to RANKL preventing activation of RANK on osteoclasts.

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10
Q

What hormones stimulate OPG production and therefore inhibit bone resorption

A

Testosterone

Estrogen

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11
Q

What are the body responses to secreted parathyroid hormone

A

Increases bone resorption (therefore Ca and PO4 in blood)

Stimulates formation of 1,25D (increases Ca GI absorption)

Increases Ca reabsorption in kidneys

Decreases PO4 reabsorption in kidneys (to cancel out PO4 release from bone)

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12
Q

Where is parathyroid hormone produced

A

the parathyroid glands (embedded into posterior surface of thyroid gland)

secreted by chief cells as an 84 amino acid protein

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13
Q

Describe how PTH release is inhibited/stimulated

A

High extracellular Ca activates Ca sensing receptor on chief cells

signalling cascade inhibits PTH transcription and release from vesicles

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14
Q

Ultimately, PTH…

A

increases Ca

decreases PO4

in extracellular fluid and blood

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15
Q

How is vitamins D3 usually produced

A

UV radiation from sunlight on a cholesterol derivative in the skin

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16
Q

Explain the production pathway for 1,25D

A

In liver, dietary vitamin D has OH group added by 25-hydroxylase

In kidney OH group added by 1-hydroxylase (rate limiting step)

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17
Q

How does PTH increase production of 1,25D

A

Stimulates activity of 1-hydroxylase (the rate limiting step)

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18
Q

What is the main action of 1,25D

A

stimulate intestinal absorption of Ca and PO4

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19
Q

How does 1,25D stimulate intestinal absorption of Ca and PO4

A

Binds to intracellular VDR receptor increasing expression of Ca transporters and binding proteins.

20
Q

Ultimately, 1,25-dihydroxy Vitamin D….

A

increases Ca levels in extracellular fluid and blood

21
Q

How is calcitonin synthesis stimulated

A

parafollicular cells of the thyroid have Ca sensing receptors

when they detect low Ca synthesis of Calcitonin is activated

22
Q

What does calcitonin due in fish and rodents

A

Counteracts the actions of PTH

inhibits bone resorption and renal reabsorption of Ca and PO4

23
Q

Outline calcitonin in humans

A

No physiological action

does inhibit bone resorption

used to clinically treat Pagets disease, hypercalcemia and osteoporosis

24
Q

Describe Rickets disease

A

Deficiency in mineralisation of bone matrix due to insufficient vitamin D (so Ca GI absorption cannot occur)

soft bones, growth issue

treatment by daily doses of vitamin D (sometimes CA salts needed or surgery to correct bones)

25
Q

Describe osteoporosis

A

Bone matrix is lost due excess bone resorption stimulation (due to high bone resorption hormones levels or low bone formation hormones)

decreased bone mass and strength

Observed with age and in postmenopausal women

Treatment: Ca and vitamin D throughout life, estrogen for recent post menopause, bisphosphonates, SERMs, calcitonin

26
Q

Describe hypercalcemia

A

High Ca levels due to primary hyperparathyroidism (benign tumour in 1 of parathyroid glands), no negative feedback of PTH and 1,25D

tiredness and nausea

Treatment is Surgical removal of tumour

27
Q

Describe hypocalcemia

A

Low Ca levels due to loss of parathyroid gland function

decreased bone resorption, excitability of nerves, muscle seizures

Treatment includes Ca salts and 1,25D

28
Q

What parts of the adrenal cortex make what steroid?

A

Zona glomerulosa: mineralocorticoid = aldosterone

Zona fasciculata: glucocorticoid = cortisol

Zona reticularis: sex steroids mainly androgens

Adrenal medulla: catecholamines = adrenaline, noradrenaline

29
Q

How to remember what the adrenal cortex secretes

A

Salt, sugar, sex

regulate chemical balance, metabolism and other glands

30
Q

What are the three main functions of cortisol release

A

protein catabolism

lipolysis

expression of enzymes

31
Q

explain protein catabolism due to cortisol release

A

stimulates protein catabolism

reduces uptake of glucose

increased circulation of amino acids and lactate

32
Q

explain lipolysis due to cortisol release

A

stimulates lipolysis in WAT, which provides reactants for gluconeogenesis

33
Q

explain expression of enzymes due to cortisol release

A

stimulates expression of enzymes controlling protein catabolism and lipolysis

34
Q

How does ACTh stimulate cortisol production

A

Increases concentration of cholesterol at inner mitochondrial membrane via regulation of an acute steroidogenic protein

increases production of CYP11A1 which regulates rate limiting step of cortisol production

35
Q

What is the hypothalamic pituitary adrenal axis

A

describes the interaction between the hypothalamus, pituitary and adrenal glands.

Stress -> CRH release

  • > ACRH release
  • > Cortisol/Hormone production
36
Q

Outline addisons disease

A

Loss of adrenocortical function, auto-immune disease

aldosterone, cortisol decrease leads to hypotension

treatment is daily oral administration of glucocorticoids and mineralocorticoids

37
Q

Outline cushings syndrome

A

Excess cortisol due to tumour in adrenal gland of anterior pituitary or exogenous corticosteroids

increased cortisol = catabolism of bone. muscle, skin, fat redistributed to trunk, face and back, hypertension

38
Q

What is stress

A

experiences the are challenging, physically or emotionally

39
Q

What is good and bad stress

A

experiences that are limited duration and can be mastered

experiences where there is no sense of control, exhausting or dangerous

40
Q

What are acute and chronic stressors

A

Acute: occur once (car crash, class question)

Chronic: repeated, prolonged (arthritis, sleep deprivation)

41
Q

What does stress activate

A

HPA axis (cortisol)

sympathetic nervous system (adrenaline)

42
Q

What is general adaption syndrome

A

A 3 step response the body has to stress

43
Q

Step 1 of general adaption syndrome

A

Alarm reaction/ short term response (6-48 hours)

adrenaline and noradrenaline released

increase HR, BP, gluconeogenesis, metabolic rate

dilation of bronchioles

decreased digestive activity and urine

44
Q

Step 2 of general adaption syndrome

A

Resistance/ long term (>48 hours)

CRH and ACTH release for actions of cortisol

protein and fat catabolism to produce glucose

increases blood glucose, BV, BP

suppressed immune system

retention of sodium and water

45
Q

Step 3 of general adaption syndrome

A

Exhaustion (1-3 months)

cortisol remains high and ANS again activated

muscle wasting
hyperglycaemia
gastric ulceration
bone loss
vascular damage
46
Q

What are some mental health consequences due to long term stress

A

headaches

lack of energy

nervousness and despair

anger and irritability

trouble concentration

eBMS2031 (6 decks)

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