ENDOCRINE SYSTEM Flashcards

(46 cards)

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
Describe osteoporosis
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
Describe hypercalcemia
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
Describe hypocalcemia
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
What parts of the adrenal cortex make what steroid?
Zona glomerulosa: mineralocorticoid = aldosterone Zona fasciculata: glucocorticoid = cortisol Zona reticularis: sex steroids mainly androgens Adrenal medulla: catecholamines = adrenaline, noradrenaline
29
How to remember what the adrenal cortex secretes
Salt, sugar, sex regulate chemical balance, metabolism and other glands
30
What are the three main functions of cortisol release
protein catabolism lipolysis expression of enzymes
31
explain protein catabolism due to cortisol release
stimulates protein catabolism reduces uptake of glucose increased circulation of amino acids and lactate
32
explain lipolysis due to cortisol release
stimulates lipolysis in WAT, which provides reactants for gluconeogenesis
33
explain expression of enzymes due to cortisol release
stimulates expression of enzymes controlling protein catabolism and lipolysis
34
How does ACTh stimulate cortisol production
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
What is the hypothalamic pituitary adrenal axis
describes the interaction between the hypothalamus, pituitary and adrenal glands. Stress -> CRH release - > ACRH release - > Cortisol/Hormone production
36
Outline addisons disease
Loss of adrenocortical function, auto-immune disease aldosterone, cortisol decrease leads to hypotension treatment is daily oral administration of glucocorticoids and mineralocorticoids
37
Outline cushings syndrome
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
What is stress
experiences the are challenging, physically or emotionally
39
What is good and bad stress
experiences that are limited duration and can be mastered experiences where there is no sense of control, exhausting or dangerous
40
What are acute and chronic stressors
Acute: occur once (car crash, class question) Chronic: repeated, prolonged (arthritis, sleep deprivation)
41
What does stress activate
HPA axis (cortisol) sympathetic nervous system (adrenaline)
42
What is general adaption syndrome
A 3 step response the body has to stress
43
Step 1 of general adaption syndrome
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
Step 2 of general adaption syndrome
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
Step 3 of general adaption syndrome
Exhaustion (1-3 months) cortisol remains high and ANS again activated ``` muscle wasting hyperglycaemia gastric ulceration bone loss vascular damage ```
46
What are some mental health consequences due to long term stress
headaches lack of energy nervousness and despair anger and irritability trouble concentration