RA18 Endocrine Flashcards

(37 cards)

1
Q

Endocrine

Phys 35 Endocrine System General Concepts

A

Hormome travels through the blood circulation to act on distant target cells

Distant-signalling

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2
Q

Paracrine

Phys 35 Endocrine System General Concepts

A

Hormone is secreted into the interstital fluid to act locally on nearby target cells

Nearby-signalling

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3
Q

Autocrine

Phys 35 Endocrine System General Concepts

A

Hormone is secreted into interstitial fluid to act on the cell that produced it

Self-signalling

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4
Q

How are hormones regulated? (3 ways)

Phys 35 Endocrine System General Concepts

A
  • Rate of hormone production (+ve/-ve feedback)
  • Rate of hormone delivery (perfusion, mass action law)
  • Rate of hormone excretion/degredation (half-life)
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5
Q

Peptide hormones
- Consists of/derived from?
- Synthesis
- Storage
- Solubility in plasma
- Carrier
- Receptors
- Response time
- Half life (effect time)
- Examples

Phys 35 Endocrine System General Concepts

A
  • Consists of 3 or more amino acids
  • Pre-prohormone in RER -> cleave signal sequence -> prohormone in Golgi aparratus -> packaged and trimmed -> active hormone in secretory vesicle
  • Stored in secretory vesicles
  • Soluble
  • Not bound to carrier
  • Bind cell surface receptors -> activate second messenger cascade
  • Fast acting
  • Short half life
  • E.g. glucagon, insulin
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6
Q

Steroid hormones
- Consists of/derived from?
- Synthesis
- Storage
- Solubility in plasma
- Carrier
- Receptors
- Response time
- Half life (effect time)
- Examples

Phys 35 Endocrine System General Concepts

A
  • Derived from cholesterol
  • Cholesterol -> pregnenolone (rate limiting step)
  • Synthesised on demand (by adrenal cortex, gonads, placenta), NOT stored
  • Insoluble
  • Bound to carrier
  • Bind intracellular receptors -> activate gene transcription
  • Slow acting
  • Long half life
  • E.g. estrogen, cortisol
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7
Q

Amino acid derivatives: thryoid hormones
- Consists of/derived from?
- Solubility in plasma
- Carrier
- Receptors
- Response time
- Half life (effect time)
- Examples

Phys 35 Endocrine System General Concepts

A
  • Derived from amino acids (tyrosine)
  • Insoluble
  • Bound to carrier
  • Bind intracellular receptors -> activate gene expression
  • Slow acting
  • Long half life
  • E.g. T3, T4
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8
Q

Amino acid derivatives: catecholamines
- Consists of/derived from?
- Solubility in plasma
- Carrier
- Receptors
- Response time
- Half life (effect time)
- Examples

Phys 35 Endocrine System General Concepts

A
  • Derived from amino acids (tyrosine)
  • Soluble
  • Not bound to carrier
  • Bind cell surface receptors -> activate second messenger pathway (signal cascade)
  • Fast acting
  • Short half life
  • E.g. epinephrine, norepinephrine
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9
Q

Where are carrier proteins synthesised?

Phys 35 Endocrine System General Concepts

A

Liver

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10
Q

Function of carrier proteins

Phys 35 Endocrine System General Concepts

A
  • Extend half life of hormones in circulation (protect hormones from degredation/excretion)
  • Sequester hormones from target cell receptor (i.e. hormones bound to carrier cannot bind to receptor; only free hormones are active)
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11
Q

Total hormone concentration in the blood

Phys 35 Endocrine System General Concepts

A

Bound (to carrier) + free

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12
Q

Plasma insoluble hormones bind to (…) receptors. Plasma soluble hormones bind to (…) receptors.

Phys 35 Endocrine System General Concepts

A

Plasma insoluble hormones bind to intracellular receptors. Plasma soluble hormones bind to cell surface receptors.

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13
Q

Adaptation/desensitisation of receptors

Phys 35 Endocrine System General Concepts

A

Chronically elevated level of hormone -> diminished cell response

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14
Q

Rebound of receptors

Phys 35 Endocrine System General Concepts

A

Prolonged absence of hormone -> increased receptor numbers -> hyperactive with return of hormone

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15
Q

Inactivation of hormonal response (3 ways)

Phys 35 Endocrine System General Concepts

A
  • Removal of hormone from circulation
  • Down regulation of hormone (sequestration i.e. endocytosis of receptor, uncoupling of receptor from donwstream signalling)
  • Removal of stimulus (negative feedback)
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16
Q

Hypothalamic-Pituitary-Adrenal (HPA) axis

Phys 35 Endocrine System General Concepts

A

Hypothalamus secrete CRH -> anterior pituitary secrete ACTH -> adrenal cortex secrete cortisol -> inhibit CRS and ACTH

CRH: corticotropin-releasing hormone
ACTH: adrenocorticotropic hormone

17
Q

Hyposecretion vs hypersecretion vs resistance

Disorder/dysregulation in endocrine system

Phys 35 Endocrine System General Concepts

A
  • Hyposecretion: secrete insufficient hormone
  • Hypersecretion: secrete excess hormone
  • Resistance: unresponsive to hormone (can lead to hyposecretion)
18
Q

Primary vs secondary vs tertiary endocrine pathology/deficiency

Phys 35 Endocrine System General Concepts

A
  • Primary: defect in target endocrine gland (adrenal cortex)
  • Secondary: defect in proximal regulator (pituitary) of target gland
  • Tertiary: defect in distal regulator (hypothalamus) of target gland
19
Q

Hormone levels in primary vs secondary vs tertiary endocrine pathology

Phys 35 Endocrine System General Concepts

A

Primary:
- Defect in adrenal cortex
- Low cortisol, high ACTH and CRH

Secondary:
- Defect in pituitary
- Low cortisol and ACTH, high CRH

Tertiary:
- Defect in hypothalamus
- Low cortisol, ACTH, CRH

20
Q

Bioassay test for cortisol hyposecretion

Phys 35 Endocrine System General Concepts

A
  • Stimulation test
  • Give ACTH to promote cortisol secretion
  • If cortisol increases -> HPA axis is intact
  • If cortisol remains low -> adrenal cortex or pituitary (loss of trophic effect of ACTH on adrenal cortex) is dysfunctional
21
Q

Bioassay test for cortisol hypersecretion

Phys 35 Endocrine System General Concepts

A
  • Suppression test
  • Give dexamethasone at midnight to suppress ACTH secretion -> prevents increase in cortisol in the morning
  • If cortisol is suppressed -> HPA axis is intact
  • If cortisol remains high -> adrenal cortex or pituitary is dysfunctional
22
Q

What are the regions of the adrenal gland? (2)

Phys 36 Adrenal Gland

A
  1. Adrenal cortex (outer region)
  2. Adrenal medulla (inner region)
23
Q

What are the layers of the adrenal cortex, from outer to inner layer? (3)

Phys 36 Adrenal Gland

A
  1. Zona glomerulosa
  2. Zona fasciculata
  3. Zona reticularis
24
Q

What hormones does each layer of the adrenal cortex secrete?

Phys 36 Adrenal Gland

A

Zona glomerulosa: mineralocorticoids (salt)
- Aldosterone

Zona fasciculata: glucocorticoids (sugar)
- Cortisol

Zona reitcularis: androgens (sex)
- Estrogen
- Testosterone

Sugar, salt, sex

25
Aldosterone - Site of synthesis - Action - Regulation
- Made in zona glomerulosa of adrenal cortex - Increase blood vol/pressure by increasing reabsorption of sodium + excretion of potassium by kidney - Regulated by Renin-Angiotensin-Aldosterone system (RAAS)
26
Hyperaldosteronism - Cause - Effects - Example
Cause: - Hypersecretion of aldosterone Effects: - Hypertension (reabsorption of Na+ -> increased blood vol + pressure) - Hypokalemia (excretion of K+) Example: - Primary hyperaldosteronism (Conn's syndrome)
27
Cortisol - Site of synthesis - Action - Regulation
- Made in zona fasciculata of adrenal cortex - Increase blood glucose (by increasing insulin resistance and mobilising fuel), anti-inflammatory (decrease immune system function) - Regulated by hypothalamic-pituitary-adrenal (HPA) axis
28
Metabolic effects of cortisol in: - Liver - Skeletal muscle - Adipose tissue
Liver: - Increase gluconeogenesis - Increase glycogenolysis Skeletal muscle: - Decrease protein synthesis - Increase protein degradation - Decrease glucose uptake Adipose tissue: - Increase lipid degradation Net result: mobilise fuel stores to increase plasma glucose
29
Cortisol levels are (...) in the morning and (...) at night
Cortisol levels are highest in the morning and lowest at night
30
Issues with excess use of cortisol
- Bone breakdown: osteoporosis, avascular necrosis of joints, osteoarthritis - Insulin resistance: type 2 diabetes - Immune suppresion: increased risk of infections
31
Cushing's syndrome - Cause - Clinical features
- Caused by excess cortisol (hypercortisolism) - Thinning of hair, facial plethora, dorsocervical and supraclavicular fat pads, weight gain, thin limbs with muscle atrophy, purple striae on abdomen due to thinning of skin | Cushing's disease: dysfunction in pituitary gland (ACTH) specficially
32
What are the levels of cortisol and ACTH in primary vs secondary Cushing's syndrome?
Primary: - High cortisol (due to overactive adrenal gland) - Low ACTH (due to -ve feedback from cortisol) Secondary: - High cortisol - High ACTH (due to overactive pituitary gland that does not respond to -ve feedback)
33
Addison's disease - Cause - Cortisol vs ACTH levels - Clinical manifestations
- AKA adrenal insufficency - Deficiency in all adrenal cortex hormones, especially glucocorticoids and mineralcorticoids (main source of androgens = gonads) - Low cortisol, high ACTH - Excess ACTH -> excess α MSH -> hyperpigmentation of skin - Deficient aldosterone + cortisol -> low Na+ and high K+ -> hyponatremia, hyperkalemia, hypotension, salt craving
34
Catecholamines (epinephrine, norepinephrine, dopamine): - Site of synthesis - Action/metabolic effects
- Made in adrenal **medulla** - Activate **sympathetic system** (fight or flight response) -> **increase cardiac output** -> **constrict blood vessels** to peripheral tissues and gut to increase oxygen delivery to muscles -> **dilate smooth muscle in bronchi/bronchioles** to increase oxygenation of blood -> **inhibit insulin release** to maintain blood glucose levels -> **increase lipolysis** in adipose tissue to raise blood glucose
35
Pheochromocytoma - Cause - Clinical features
- Caused by excess catecholamines - Five Ps: pain, pallor, palpitations, pressure (hypertension), perspiration
36
What kind of cells comprise the thyroid gland?
Thyroid follicles - Epithelium = single layer of cuboidal follicular cells - Fluid filled space = colloid -> contains thyroglobulin
37