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Physiology > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Describe the affects of hypo and hypercalcaemia:

A

Hypocalcaemia: nervous system becomes more excitable as intracellular stores of Ca2+ are released in an attempt to increases blood Ca2+ levels. Muscles may also become tetanic.
Hypercalcaemia: leads to depression of nervous system and muscular activity. Ca2+ may precipitate out of blood as calcium oxalate kidney stones

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2
Q

Suggest when there may be a change to Ca2+ homeostasis?

A
  • During pregnancy and lactation: huge loss of Ca2+ into milk (can lead to eclampsia)
  • Egg-laying: Ca2+ deposited in spongy medullary bone to allow fast calcium mobilisation
  • Poor absorption: due to low D3 or foods high in phylates which bind Ca2+ and prevent its absorption.
  • Oxalate poisoning: Ca2+/oxalate compounds are excreted or crystallise to form kidney stones.
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3
Q

How is parathyroid release controlled?

A
  1. Low extracellular Ca2+ around chief cells in the PT gland leads to a reduction in binding of Ca2+ to Gq receptors
  2. Causes decreased intracellular calcium (opposite to normal)
  3. Increased PTH vesicle release (due to specialised SNARE proteins which are calcium inhibited)
    - Also innervated by autonomic nerves so has a slight circadian rhythm.
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4
Q

How are Ca2+ bone stores controlled by PTH?

A

Balance between growth (by osteoblasts) and destruction (by osteoclasts)
- PTH promotes osteocytic osteolysis (erosion) of bone and inhibits osteoblasts from laying down new bone.
- Progenitor cells differentiate into osteoclasts.
- Positive feedback of osteoblasts on osteoclasts to cause further erosion.

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5
Q

Detail the effects of PTH on the kidneys

A

Fast response:
- Causes increased active reabsorption in the DCT of the kidney (insertion of TRVP5 and calbindin).
- Powerfully inhibits reabsorption of Pi ions in PCT to lower extracellular concentration.
- Loss of Pi from kidneys offsets increase from bone dissolution
Slower response:
- Activates vit D3 for intestinal absorption of Ca2+ (from 25-OHD to calcitriol)

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6
Q

How is vitamin D3 obtained and what are its roles?

A
  • Obtained via synthesis from cholesterol in keratinocytes (when exposed to UVB) or in diet and stored in liver.
  • Increases calcium absorption in gut: 25-OHD (calcitriol) acts as a nuclear receptor to upregulate the expression of apical Ca2+ channels; upregulate calbindin protein and upregulate Ca2+/ATPase and Ca2+/Na+ exchange pumps
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7
Q

What is calcitonin and what are its functions?

A
  • Produced by C-cells in thyroid
  • Works antagonistically against PTH (less powerful) to inhibit the absorption of bone
  • Better to reduce PTH levels than increase calcitonin massively.
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8
Q

What are the consequences of low vitamin D levels?

A
  • Poor Ca2+ absorption, leading to
    weakened bones
  • Rickets results in children, osteomalacia (distorted bones) in adults. Osteoporosis also common.
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9
Q

Describe the general structure of the pituitary gland and how each section is controlled.

A

Anterior pituitary (adenohypophysis) = hormonally controlled:
- Hypothalamus (median eminence) secretes into the hypothalamic-hypophyseal portal vein to pituitary.
- Tertiary organ often involved to create axis of control (e.g. hypothalamus-pituitary-thyroid axis)

Posterior pituitary (neurohypophysis) = nervous control:
- Nervous control from hypothalamus

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10
Q

What are sommatomamotropins?

A

Body-breast-change

  • Secreted by somatotrophs and inhibited by somatostatins (produced by δ-cells in pancreas)
  • Mainly for metabolic control in pregnancy
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11
Q

What controls growth hormone release?

A

Primary control:
- Growth hormone releasing hormone (GHRH) from hypothalamus
- Ghrelin from stomach

Feedback Loops:
- Short-loop: GH promotes somatostatin release
- Ultra-short loop: GHRH inhibits its own release

Other factors:
- Sex: males release spike in early sleep; females more erratic
- Metabolism: fasting causes GH resistance as fibroblast growth factor (FGF21) levels high

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12
Q

How is growth hormone (GH) transported? How does it cause a response?

A
  • Bound to binding protein with a 20min half life (even though water soluble)
  • Binds to membrane based receptors. Tyrosine kinase linked and activated Janus kinase (JAK-2) enzymes to phosphorylate proteins.
  • E.g. responsive cells produce insulin-like growth factors (IGFs)
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13
Q

What are some permissive factors required for growth hormone effect?

A
  • High amino acid levels (particularly arginine)
  • High insulin levels (hypoglycemic even)
  • Low fibroblast growth factor (FGF-21)
  • High thyroid hormone
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14
Q

What effects does growth hormone have on a) muscle growth b) bone growth?

A

Muscle growth:
- Promotes amino acid uptake into muscle cells
- Increases protein synthesis rate
- Results in insulin-like growth factor release (IGF-1)

Bone growth:
- Promotes amino acid uptake into chondrocytes (cartilage cells): opposes closing of growth plate.

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15
Q

Describe the zones of a growing bone:

A
  • Resting zone (chondrocyte stem cells present)
  • Proliferative zone (division)
  • Hypertrophy zone (increase in size)
  • Calcifying zone (cells die and calcify into crystalline structure)
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16
Q

What role do oestrogen and testosterone have in bone growth?

A
  • Oestrogen induces closure of growth plate
  • Testosterone locally converted to oestrogen for same purpose.
17
Q

What role does GH have in metabolic control?

A

Preserves glucose for brain. When FFA and glucose levels low:
- Stimulates adipose tissue to release free fatty acids
- Stimulates hepatic gluconeogenesis and glucose release
- Diabetogenic effect: inhibits glucose uptake by muscles and adipocytes (insulin sensitive target cells)

18
Q

What are IGFs and what are their roles?

A

IGF = insulin-like growth factor

  • GH stimulates IGF production and differentiation of chondrocytes (diabetogenic effect and increased FFA to allow for growth - shifts body from storage to release state)
  • IGF stimulates growth of chondrocytes (growth, proliferation and hypertrophy).
  • In utero IGF-1 and 2 control growth (not GH)
19
Q

What is the evidence for the GH/IGF system and its control of growth?

A

Theory: GH stimulates differentiation of chondrocytes and IGF production (must be present to prepare the growth plate).

  • Original theory was that hepatic GH receptors lead to IGF production (evenly distributed in blood)
  • However; GH injection into growth plate stimulated growth only in that area –> liver not directly involved.
  • Further: if IGF-1 gene in liver knocked out, growth is normal.
20
Q

What is dwarfism and how can it caused?

A

Small size but normal proportions (not the same as acondroplasia which is IGF-1 deficiency and results in stunted (non-proportional) growth).

  • Pituitary dwarfism: failure to produce functional GH
  • Dwarfism of Sindh: defection of GHRH receptor (GH not stimulated)
  • Laron syndrome: GH receptor mutations (failure of IGF-1 production and preparation of growth plate)
21
Q

How can gigantism occur?

A

Child: overstimulation of growth plates in long bones from high GH levels
Adult: acromegaly (after fusion of long bones) results in large extremities/brow-bone.

22
Q

Describe the structure of the adrenal gland and which hormones are produced.

A

Medulla: catecholamine production (e.g. adrenaline)
Cortex: corticosteroid production (travels bound to bp causing longer-lasting effects)
- Outer = zona glomerulosa: aldosterone production
- Middle = zona fasciculata: corticosteroids like cortisol
- Inner = zona reticularis: androgens such as DHEA

Blood flows from cortex to medulla

23
Q

What is DHEA? What does it control?

A
  • DHEA is an androgen
  • Controls pubic hair and libido in females (overwhelmed by testosterone in males)
24
Q

How is ACTH released? What does it stimulate?

A

ACTH = adrenocorticotropic hormone

  • Hypothalamus releases corticotropin releasing hormone (CRH)
  • CRH stimulates corticotrophs (20% of anterior pituitary cells) to cleave POMC into ACTH and release it
    (- MSH and β-endorphin also released this way).
  • General stimulating effect on kidneys including cortisol production
25
Q

How is ACTH release controlled?

A
  • Long-loop -ve feedback: ACTH stimulates adrenal glands to produce cortisol which inhibits ACTH production – shown by injection of exogenous cortisol causing atrophy of adrenal cortex (ACTH not produced)
  • Simulated by corticotropin releasing hormone (CRH)
  • Circadian rhythm evident (surge before waking). The increase in cortisol resulting protects glycogen stores for later use.
26
Q

How is adrenaline release stimulated?

A
  • Sympathetic pre-ganglionic fibres release ACh
  • Acts on nicotinic receptors on chromaffin cells (Cr stain affinity) in the medulla of adrenal gland
  • Stimulates PNMT enzyme to convert noradrenaline to adrenaline
  • Adrenaline released into bloodstream
27
Q

What stimulates aldosterone production?

A
  • Angiotensin II binds to angiotensin type I receptors in the cortex promoting aldosterone release.
  • High [K+]
  • ACTH does not directly stimulate aldosterone but is a permissive factor.
28
Q

Give three examples of hormones released by the adrenal gland and their primary stimulus:

A

Adrenaline: nervous stimulation causing ACh release to chromaffin cells in medulla

Aldosterone: high [K+] and angiotensin II causes zona glomerulosa to produce aldosterone

Cortisol: released in response to hypoglycaemia and ACTH stimulation

29
Q

What was Hans Selye’s 3 stage theory of stress?

A

‘Alarm reaction’ : sympathetic nervous response and glucocorticoid release (minutes)

‘Stage of resistance’ : a new dynamic homeostasis reached with new set points

‘Stage of exhaustion’ : detrimental effects of long-term elevated glucocorticoids due to chronic stress

30
Q

Why do steroids take longer to be released?

A
  • Cannot be contained in vesicles since lipid soluble
  • Therefore must be synthesised on command
  • Takes more time
31
Q

What effects does cortisol have on metabolism?

A

Released in response to hypoglycemia:
- Promotes muscle and plasma protein breakdown for gluconeogenesis
- Stimulates liver enzymes to perform gluconeogenesis
- Inhibits glucose uptake by muscle and adipose tissue (diabetogenic effect)
- Promotes FFA release from adipose tissue (both direct effect and permissive factor for GH and adrenaline)

32
Q

How does cortisol travel through the body?

A
  • Steroid hormone so travels in blood, diffuses into cells and alters gene expression.
  • Travels bound to transcortin with long half-life (> 60mins)
33
Q

What effects does cortisol have on the immune system and brain?

A

Immune system effects: brings immune system back under control after alarm response
- Normal cortisol levels result in early activation of immune system
- Inhibits many components of inflammatory response (inhibits NO, cyclooxygenase (like aspirin), leukotrienes, TNF-α).

Can cross BBB so affects mood/sensory acuity.

34
Q

What effects does cortisol have on the kidneys?

A
  • Can bind to aldosterone receptor (lower affinity but higher quantities) therefore can cause Na+ reabsorption
  • Locally broken down to avoid this (and hypertension). This enzyme is inhibited by glycyrrhetinic acid in liquorice.
  • Also allows smooth muscle to respond to noradrenaline and angiotensin II (BP control).

Physiology (8 decks)

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