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A&P 2 > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What are endocrine glands?

A

Ductless glands that secrete blood borne messengers (secreted directly into blood) to act on target cells located a long distance away

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2
Q

What is the key function of the endocrine system?

A

To maintain homeostasis & regulate long-term processes
- Growth, metabolism, development, reproduction

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3
Q

What are hormones?

A

Chemical messengers to relay information & instructions to cells (signalling)

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4
Q

What are the mechanisms of intercellular communication?

A
  1. Direct communication
  2. Paracrine communication
  3. Autocrine communication
  4. Endocrine communication
  5. Synaptic communication
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5
Q

Where does transmission occur and what are the chemical mediators for direct communication?

A

Transmission: through gap junctions
Chemical mediators: ions, small solutes, lipid-soluble materials

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6
Q

What are the distribution effects of direct communication?

A

Usually limited to adjacent cells of the same type that are interconnected by connexons (protein that forms channels to connect cytoplasm of adj cells)

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7
Q

Where does transmission occur and what are the chemical mediators for paracrine communication?

A

Transmission: Through extracellular fluid
Chemical mediators: Paracrines

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8
Q

What are the distribution effects of paracrine communication?

A

Primarily limited to a local area
- where paracrine conc. are relatively high
- target cells must have appropriate receptors

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9
Q

Where does transmission occur and what are the chemical mediators for autocrine communication?

A

Transmission: Through extracellular fluid
Chemical mediators: Autocrines

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10
Q

What are the distribution effects of autocrine communication?

A

Limited to the cell that secretes the hormone
- Secretes chemical messenger that binds to receptor on same cell
- purpose is to dec. prod./secretion of particular chemical

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11
Q

Where does transmission occur and what are the chemical mediators for endocrine communication?

A

Transmission: Through the bloodstream
Chemical mediators: Hormones

Same as paracrine communication but dist. travelled is diff (endocrine comm. travels to cells/systems located far away

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12
Q

What are the distribution effects of endocrine communication?

A

Target cells are primarily in other tissues & organs and must have appropriate receptors

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13
Q

Where does transmission occur and what are the chemical mediators for synaptic communication?

A

Transmission: Across synapses
Chemical mediators: Neurotransmitters

Specifically targets NS = binds to neurons while hormones can bind to a range of diff cells & tissues

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14
Q

What are the distribution of effects of synaptic communication?

A

Limited to very specific area
- target cells must have appropriate receptors

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15
Q

What are the classes of hormones?

A

Hydrophilic (attracted to water)
Lipophilic (attracted to lipids)

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16
Q

What are the hydrophilic hormones?

A
  1. Peptide hormones (most abundant)
  2. Catecholamines
  3. Indoleamines
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17
Q

What are peptide hormones derived from?

A

Derived from diverse types of a.a.
- Slower response but longer lasting effect
- e.g. insulin/growth hormone

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18
Q

What are catecholamines derived from?

A

A.a. tyrosine
- Faster effect but shorter life
- e.g. dopamine

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19
Q

What are indoleamines derived from?

A

a.a. tryptophan

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20
Q

Can lipophilic hormones travel freely within bld. circulation?

A

NO!
- Requires carrier protein to help with tpt.

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21
Q

What are the lipophilic hormones?

A

Steroid hormones
Thyroid hormones

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22
Q

What are steroid hormones derived from?

A

cholesterol

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23
Q

What are thyroid hormones derived from?

A

a.a. tyrosine & iodine

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24
Q

Difference between functions of steroid hormones & thyroid hormones

A

Steroid hormones = more functions (diverse) = reproduction, metabolism, regulate stress resp

Thyroid hormones = more limited functions = regulating metabolism, growth, development

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25
Q

What are tropic hormones?

A

Tropic hormones target endocrine glands to regulate the activity of specific glands/release of certain hormones from those glands

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26
Q

Features of the endocrine system (complexity)

A
  1. One endocrine gland may secrete > 1 hormone (e.g. ant. pituitary)
  2. One hormone may be secreted by > 1 endocrine gland (e.g. somatostatin)
  3. One hormone may have > 1 target cell = >1 type of action (e.g. vasopressin = aka ADH)
  4. One target cell may be influenced by >1 hormone
  5. Some have non-endocrine functions
  6. Rate of secretion of hormones may vary over time in a cyclic pattern (melatonin)
  7. Some may be hormones AND neurotransmitters (noradrenaline)
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27
Q

What affects effective plasma concentration?

A
  • Rate of hormone secretion = more availability of hormones in bld circulation
  • Rate of metabolic conversion/activation (broken down/converted to other forms)
  • Transportation (extent of binding to plasma proteins) = X affect hydrophilic hormones bc can travel in blood
  • Rate of removal by excretion/metabolic inactivation
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28
Q

What is hormone secretion triggered by?

A
  • Humoral (change in extracellular fluid)
  • Hormonal (arrival/removal of hormone)
  • Neural stimuli (neurotransmitters)
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29
Q

What affects hormone secretion?

A
  • -ve feedback control = “turning off” (output of system counteracts a change in inputs)
  • Neuroendocrine reflexes (fight/flight)
  • Circadian/Diurnal rhythm (24 oscillation) or Time-based (menstrual)
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30
Q

How long do free hormones remain functional?

A

less than 1 hour

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31
Q

How long do thyroid & steroid hormones remain in circulation?

A

Remain in circulation much longer bc most are “bound” (usually lipophilic hormones)
- Involved long-term changes (e.g. growth/development)

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32
Q

How does hormone receptors affect hormone secretion?

A
  • Different receptors for different hormones (specificity)
  • One target organ can have multiple hormone receptors (e.g. liver)
  • Presence/absence = receptor expression determines hormonal sensitivity (amt of receptors on surface can be controlled = if need more, more receptors will be avail)
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33
Q

What alters hormonal response?

A

Upregulation/downregulation (increasing/decreasing no. of receptors)

Locally-acting -ve feedback loop = desensitization (e.g. insulin hypersecretion = reduced sensitivity over time)

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34
Q

Antagonistic hormone interaction

A

opposite effect = one hormone may lead to the loss of another hormone receptor = binding of one hormone to receptor leads to disappearance of another hormone: suppress

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35
Q

Synergistic hormone interaction

A

Additive effect = encourage binding of 2 or more hormones to same target cells

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36
Q

Permissive hormone interaction

A

One is needed for another to produce effect
- For hormone B to bind to receptor, hormone A has to be present (in adequate amt)

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37
Q

Integrative hormone interaction

A

Different but complementary results

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38
Q

What are the types of hormone interaction?

A
  1. Antagonistic
  2. Synergistic
  3. Permissive
  4. Integrative
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39
Q

Types of endocrine disorders

A
  1. Hyposecretion
  2. Hypersecretion
  3. Abnormal target cell responsiveness
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40
Q

What is hyposecretion (endocrine disorders)?

A

Primary or secondary (tropic hormone)
Genetic, dietary, toxins, immunologic, dz, iatrogenic, idiopathic

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41
Q

What is hypersecretion (endocrine disorders)?

A

Tumours, immunologic (antibody), substance abuse

  • Receiving wrong info = give impression that need to secrete more
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42
Q

What is abnormal target cell responsiveness (endocrine disorders)?

A

Genetic = e.g. testicular feminization syndrome
- testosterone receptors somehow reduced (even if there is enough hormones, not enough receptors = less availability of hormone receptor)

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43
Q

What are the central endocrine glands?

A
  1. Hypothalamus
  2. Anterior pituitary (Adenohypophysis)
  3. Posterior pituitary (Neurohypophysis)
  4. Pineal gland
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44
Q

Most anterior pituitary hormones are _________

A

Most anterior pituitary hormones are tropic

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45
Q

What is the role of the hypothalamus?

A
  1. Work with post. pituitary to secrete vasopressin & oxytocin
  2. Secrete hypothalamic releasing/inhibiting hormones to act on ANTERIOR pituitary gland
  3. Control of sympathetic output = neuroendocrine reflex
  • Connects nervous system & endocrine system
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46
Q

What are vasopressin (ADH) & oxytocin produced by?

A

Neurosecretory neurons in hypothalamus
- Made in hypothalamus but secreted by posterior pituitary gland

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47
Q

What is the supraoptic nucleus (SON) involved in?

A

Involved in systemic hormone release
- basically making & secreting

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48
Q

What does the paraventricular nucleus (PVN) regulate?

A
  • Regulate how much ADH & oxytocin being secreted
  • Regulates how much can be released by SON
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49
Q

Where do the axons between the hypothalamus & anterior pituitary terminate?

A

Axons crosses the pituitary stalk to terminate on capillaries in posterior pituitary

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50
Q

What is transported along the axon?

A

Secretory granules transport the hormones along axon, stored at neuronal terminals

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51
Q

Functions of vasopressin (ADH)

A
  • Inc. permeability of distal & collecting tubules to H2O (in nephrons in kidneys)
  • Causes vasoconstriction (arterioles throughout body)

Aka “water conserving” hormone

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52
Q

Functions of oxytocin

A
  • Stimulates uterine contractions (in uterus)
  • Stimulates milk ejection during breast-feeding (mammary glands)
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53
Q

What hormones does the anterior pituitary gland produce?

A
  1. Growth hormone (GH)
  2. Thyroid stimulating hormone (TSH)
  3. Adrenocorticotropic hormone (ACTH)
  4. Follicle-stimulating hormone (FSH)
  5. Luteinizing hormone (LH)
  6. Prolactin (PRL)
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54
Q

What type of cell produces the growth hormone (GH)?

A

Somatotropes

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55
Q

What type of cell produces the thyroid stimulating hormone (TSH)?

A

Thyrotropes

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56
Q

What type of cell produces adrenocorticotropic hormone (ACTH)?

A

Corticotropes

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57
Q

What type of cell produces FSH & LH?

A

Gonadotropes

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58
Q

What type of cell produces prolactin?

A

Lactotropes

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59
Q

Function of growth hormone?

A

Overall body growth
- Acts on liver = stimulates release of IGF-I which acts on bone & soft tissue = growth
- Acts on adipose tissue, muscle, liver (can inc./dec. stimulation) = metabolic actions

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60
Q

Function of TSH

A

Stimulate secretion of thyroid hormone & growth of thyroid gland
- Stimulates the thyroid gland = release of thyroid hormone (T3 & T4) = inc. metabolic rate

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61
Q

Function of ACTH

A

Stimulates secretion of cortisol & growth of adrenal cortex
- Stimulates the Adrenal cortex = release cortisol = metabolic actions, stress response

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62
Q

Function of FSH, LH

A

Regulates gonad function

FSH - gametes production (ova, sperm)
LH - regulate sex hormones’ secretion, ovulation, luteinization

LH & FSH stimulates gonads (ovaries in females & testes in males) = sex hormone secretion (estrogen & progesterone in females, testosterone in males) & gamete production (ova in females & sperm in males)

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63
Q

Function of PRL?

A

Lactation
- Prolactin stimulates mammary glands = breast growth & milk secretion

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64
Q

What hormones does the hypothalamus produce?

A
  1. Growth hormone releasing hormone (GHRH)
  2. Somatostatin (GH-inhibiting hormone) (GHIH)
  3. Corticotropin-releasing hormone (CRH)
  4. Gonadotropin-releasing hormone (GnRH)
  5. Prolactin-releasing peptide (PrRP)
  6. Dopamine (PRL-inhibiting hormone (PIH)
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65
Q

Actions of growth hormone releasing hormone (GHRH)

A

Stimulates release of GH (growth hormone)

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66
Q

Actions of Thyrotropin-releasing hormone (TRH)

A

Stimulates release of TSH (Thyroid stimulating hormone), PRL (Prolactin)

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67
Q

Action of Corticotropin-releasing hormone (CRH)

A

Stimulates release of ACTH (Adrenocorticotropic hormone)

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68
Q

Action of Somatostatin (GH-inhibiting hormone) (GHIH)

A

Inhibits release of GH, TSH
Inhibits secretion of insulin & glucagon
Dec. utilization of absorbed nutrients by tissues

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69
Q

Action of Gonadotropin-releasing hormone (GnRH)

A

Stimulates release of FSH & LH

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70
Q

Action of Prolactin-releasing peptide (PrRP)

A

Stimulates release of PRL

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71
Q

Action of Dopamine (PRL-inhibiting hormone)

A

Inhibits release of PRL

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72
Q

What does the unique vascular link between the hypothalamus & anterior pituitary gland help with?

A

Makes communication b/w these 2 structures more efficient
- bc. hormones come from hypothalamus can directly signal & regulate how much hormone is being released from the pituitary gland itself
- More rapid speed of communication faster bc. structurally connected

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73
Q

How are hormones transported from hypothalamus to anterior pituitary gland?

A
  1. Hypophysiotropic hormones (releaing hormones & inhibiting hormones) produced by neurosecretory neurons in the hypothalamus enter the hypothalamic capillaries
  2. Hypothalamic capillaries rejoin to form the hypothalamic-hypophyseal portal system = a vascular link to anterior pituitary
  3. The portal system branches into the capillaries of the anterior pituitary
  4. The hypophysiotropic hormones = leave blood across ant. pituitary capillaries = control release of ant. pituitary hormones
  5. When stimulated by appropriate hypothalamic releasing hormone, ant. pituitary secretes a given hormone into these capillaries
  6. The ant. pituitary capillaries rejoin to form a vein, through which ant. pituitary hormones leave for ultimate distribution throughout the body by systemic circulation
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74
Q

How do hormones travel from hypothalamus to target cells?

A
  1. Neural input/hormonal input stimulate/inhibit hypothalamic neurosecretory neuron
  2. Hypothalamic neurosecretory neuron secretes hormone 1
  3. Hormone 1 travels through the special short portal system to the anterior pituitary gland
  4. Stimulates/inhibits anterior pituitary gland to secrete hormone 2
  5. Hormone 2 enters systemic circulation
  6. Hormone 2 reaches target endocrine gland and secretes hormone 3
  7. Hormone 3 travels to target cells = physiological effect
  • negative feedback to anterior pituitary (signal to dec. prod of hormone 2 if too much & vice versa)
  • negative feedback to hypothalamic neurosecretory neuron (stimulate inhibiting hormone for hormone 2)
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75
Q

Pathway of cortisol secretion

A
  1. Hypothalamus secretes hypophysiotropic hormone (CRH)
  2. CRH acts on anterior pituitary
  3. Anterior pituitary secretes tropic hormone: ACTH
  4. ACTH acts on adrenal cortex
  5. Adrenal cortex releases cortisol
  • cortisol negatively feedbacks anterior pituitary & hypothalamus
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76
Q

What does growth depend on?

A
  1. Growth hormone
  2. Genes
  3. Diet
  4. State of health/other env. stressors
  5. other hormones (e.g. Thyroid hormone)
77
Q

How does growth hormone affect growth?

A
  • Exerts metabolic effects by binding directly to adipose tissue, skeletal muscles & liver = fat mobilisation
  • Indirect effects to aid growth = stimulate IGFs (Insulin growth factor) = hypertrophy (cell size) & hyperplasia (cell numbers)
  • Stimulates bone growth = thickness & length
78
Q

What are the factors that influence growth hormone secretion?

A

Diurnal rhythm, exercise, stress, food

79
Q

What happens with growth hormone deficiency?

A

Hyposecretion = Dwarfism

80
Q

What happens with growth hormone excess?

A

Hypersecretion = Gigantism, Acromegaly

81
Q

What stimulates growth hormone secretion?

A
  1. Exercise, stress, dec. bld. glucose, diurnal rhythm + inc. bld a.a., dec. bld. fatty acids, ghrelin stimulates the hypothalamus
  2. Stimulates somatostatin (growth hormone-inhibiting hormone, GHIH) or Growth hormone-releasing hormone (GHRH)
  3. Stimualtes ant. pituitary somatotrope
  4. releases GH
82
Q

What is the effect growth hormone secretion?

A

Stimulates liver to produce IGF-I = growth-promoting actions:
- inc. protein synthesis (dec. bld a.a.)
- cell division
- bone growth

Metabolic actions unrelated to growth:
- inc. fat breakdown (inc. blood fatty acids)
- Dec. glucose uptake by muscles (inc. bld glucose)
- Inc glucose output by liver (inc. bld. glucose)

83
Q

What hormones (other than GH) are essential for normal growth?

A
  • Thyroid hormone
  • Insulin
  • Sex steroids (e.g. androgens & estrogen)
84
Q

What is the master biological clock?

A

Suprachiasmatic nucleus (SCN)

85
Q

Where is the suprachiasmatic nucleus (SCN) located?

A

In hypothalamus above optic chiasm (where the optic nerve crosses)

86
Q

When does the SCN fire?

A

Self-induced rhythmic firing = fluctuating levels of clock proteins
- Synchronisation of biological clock w env. cues (e.g. light-dark cycle)

87
Q

What senses daylight/darkness?

A

Melanopsin
- helps to regulate SCN (Suprachiasmatic nucleus)

88
Q

Pathway to reset circadian rhythms to match light-dark cycle?

A
  1. Melanopsin-containing retina ganglion cells detect light/dark
  2. Stimulates the suprachiasmatic nucleus
  3. SCN stimulates the pineal gland
  4. Pineal gland dec. melatonin in the light or inc. melatonin in the dark
  5. Cyclic changes in melatonin
  6. Resets circadian rhythms to match light-dark cycle
89
Q

What is the hypophyseal portal system?

A

Network of blood vessels that connects the hypothalamus to the pituitary gland

90
Q

Where is the thyroid gland located?

A

Lies inferior to thyroid cartilage of larynx

91
Q

How many lobes does the thyroid gland consist of?

A

Two lobes
Connected by narrow isthmus

92
Q

How are the major cells that secrete thyroid hormone organised?

A

Organised into colloid-filled follicles
- Interspersed in the interstitial spaces b/w follicles are C cells (aka parafollicular cell), which secrete calcitonin (lower bld Ca2+)

93
Q

Where is thyroid hormone stored?

A

On the thyroglobulin molecule = functions more like a carrier protein = bc. thyroid hormone is lipophilic
- Most steps of thyroid hormone synthesis take place on the thyroglobulin molecules within the colloid

94
Q

Difference between Thyroxine (T4) and Triiodothyronine (T3)?

A

Almost the same functionality =
only diff is how fast they react & potency

95
Q

What is the thyroid gland stimulated by?

A

Thyroid stimulating hormone secreted by the ant. pituitary gland

96
Q

Where is the thyroid hormone synthesized?

A

Within the follicles

97
Q

What is the inactive form of Triiodothyronine (T3)?

A

T4 (thyroxine)
When T3 is needed, T4 will be converted to active T3

98
Q

Percentage of Thyroxine (T4) and Triiodothyronine (T3)

A

Thyroxine (T4) = 93%
Triiodothyronine (T3) = <7%

99
Q

Which has a higher potency: Triiodothyronine (T3) vs Thyroxine (T4)

A

T3 more potent than T4

100
Q

Which has a longer shelf life:
Triiodothyronine (T3) vs Thyroxine (T4)

A

T4 longer half life (inversely proportionate to potency)

101
Q

What happens if there is no thyroid-stimulating hormone (TSH)?

A

Follicle will be inactive = X synthesize & secrete thyroid hormones

102
Q

Function of thyroid hormones?

A

Activates genes involved in glycolysis & ATP production
- Results in calorigenic effect = inc. energy consumption & heat generation of cells + resp. for strong, immediate, short-lived inc. in rate of cellular metabolism

103
Q

How many iodine molecules are there in Triiodothyronine (T3) and Thyroxine (T4)?

A

T3 = 3 iodine molecules
T4 = 4 iodine molecules

104
Q

Steps in the synthesis, storage & secretion of thyroid hormone

A
  1. Thyroglobulin synthesized (ferry thyroid hormone into circulation)
  2. Iodide move from blood to colloid
  3. Iodide is oxidized by TPO (thyroid peroxidase)
  4. Monoiodotyrosine + Di-iodotyrosine = T3
  5. Di-iodotyrosine + Di-iodotyrosine = T4
  6. Follicular engulf Thyroglobulin-containing colloid
  7. Iodide products split from Tg
  8. Monoiodotyrosine & Di-iodotyrosine are deiondinated
  9. Thyroxine-binding globulin (TBG) binds T3 and T4
105
Q

Thyroid hormones have _____________ onset and _____________ duration of action

A

Thyroid hormones have slow onset and long duration of action

  • bc. lipophilic
106
Q

What are the effects of thyroid hormone?

A

Thyroid hormones inc. metabolism in almost all cells of the body
- Excessive quantities of thyroid hormone can (occasionally) inc. basal metabolic rate by 60% to 100% above normal
- When X thyroid hormone produced = basal metabolic rate falls to almost one-half of normal

107
Q

What are the physiological functions of the thyroid hormones?

A

Synthesis of new proteins =
- Many other systems
- Growth (stimulates secretion of growth hormone)
- CNS development (sympathomimetic effect)
- Cardiovascular
- Metabolism

Net result = generalized inc. in functional activity throughout body

108
Q

What are the physiological functions - Cardiovascular - of the thyroid hormones?

A
  • inc. cardiac output
  • inc. tissue bld. flow
  • inc. heart rate
  • inc. heart strength
  • inc. resp.
  • inc. force of contraction
109
Q

What are the physiological functions - Metabolism - of the thyroid hormones?

A
  • Inc. mitochondria
  • Inc. Na+-K+-ATPase
  • Inc. O2 consumption
  • Inc. glucose absorption
  • Inc. Gluconeogenesis
  • Inc. Glycogenolysis
  • Inc. Lipolysis
  • Inc. Protein synthesis
  • Inc. Basal Metabolic Rate
110
Q

Pathway of regulation of thyroid secretion

A

Inc. thyroid hormone in body fluids dec. TSH secretion by ant. pituitary

  1. If too much TSH secreted = -ve feedback = signal to anterior loop to dec. secretion of TSH = thyroid gland less stimulated = less thyroid hormone synthesized
  2. direct -ve feedback to hypothalamus = dec. thyrotropin-releasing hormone (TRH) = dec. TSH secreted = thyroid hormone X stimulated
111
Q

What are the types of thyroid dysfunction?

A
  1. Hypothyroidism
  2. Hyperthyroidism
112
Q

What are the causes of hypothyroidism?

A
  • Primary failure of the thyroid gland
  • Secondary to hypothalamic/ant. pituitary failure
  • Lack of dietary iodine
113
Q

Primary failure of thyroid gland:

Plasma conc. of relevant hormones &
Presence of goiter

A

Plasma conc. =
- Dec T3 & T4 (bc. thyroid gland X functioning = dec. thyroid hormone stimulated = stimulate ant loop to prod more TSH =
- Inc. TSH

Goiter present (bc. Inc. TSH leads to goiter)

114
Q

Secondary to hypothalamic/anterior pituitary failure:

Plasma conc. of relevant hormones &
Presence of goiter

A

Plasma conc. =
- Dec. T3 & T4
- Dec. TRH and/or dec TSH

Goiter not present (bc. thyroid gland not stimulated

115
Q

Lack of dietary iodine:

Plasma conc. of relevant hormones &
Presence of goiter

A

Plasma conc. =
- Dec. T3 & T4 (bc. building block –> iodine absent)
- Inc. TSH

Goiter present

116
Q

Abnormal presence of thyroid-stimulating immunoglobulin (TSI) (aka Graves’ dz)

Plasma conc. of relevant hormones &
Presence of goiter

A

Plasma conc. =
- Inc. T3 & T4
- dec. TSH (thyroid gland stimulated by TSI –> similar to TSH)

Goiter present

117
Q

Secondary to excess hypothalamic/ant. pituitary secretion

Plasma conc. of relevant hormones &
Presence of goiter

A

Plasma conc. =
- Inc. T3 & T4
- Inc TRH and/or Inc TSH

Goiter present

118
Q

Hypersecreting thyroid tumour

Plasma conc. of relevant hormones &
Presence of goiter

A

Plasma conc. =

  • Inc. T3 & T4
  • Dec. TSH (therefore no goiter)

No goiter

119
Q

What causes the presence of goiter?

A

Develops when thyroid gland is overstimulated

so no overstimulation = no goiter

120
Q

What is the adrenal glands composed of?

A

Adrenal cortex
Adrenal medulla

121
Q

What are the three layers of the adrenal cortex?

A
  1. Zona glomerulosa
  2. Zone fasciculata
  3. Zona reticularis
122
Q

Where is aldosterone secreted from?

A

Adrenal cortex (zona glomerulosa)

123
Q

Where is cortisol secreted from?

A

Adrenal cortex (zona fasciculata)

124
Q

Where is adrenal androgens such as Dehydroepiandrosterone (DHEA) secreted from?

A

Adrenal cortex (zona reticularis)

125
Q

Where is adrenaline/noradrenaline secreted from?

A

Adrenal medulla

126
Q

Action of aldosterone

A
  • Sodium & Potassium balance
  • Blood pressure homeostasis
127
Q

What is the action of cortisol?

A
  • Adaptation to stress
  • Metabolic regulation
  • Anti-inflammatory effects
128
Q

Action of DHEA

A

Early development of sex organs

129
Q

Action of adrenaline/noradrenaline

A
  • Reinforces the sympathetic nervous system
  • Inc. HR
130
Q

What is cortisol secretion regulated by?

A

Hypothalamus-pituitary-adrenal cortex axis

131
Q

Pathway for the secretion of cortisol

A
  1. Stress excites hypothalamus
  2. Hypothalamus stimulates the anterior pituitary gland
  3. ACTH secreted and acts on adrenal cortex
  4. Adrenal cortex secretes cortisol
  5. Cortisol physiological effects:
    - Gluconeogenesis
    - Protein mobilization
    - Fat mobilization
    - Stabilize lysosomes
  • If too much cortisol = -ve feedback to ant. pituitary gland & hypothalamus
132
Q

What physiological effects does cortisol have to reduce stress?

A
  • Inc. bld. glucose = by stimulating gluconeogenesis & inhibit glucose uptake
  • Inc. bld. a.a. = by stimulating protein degradation
  • Inc. bld. fatty acids = by stimulating lipolysis
133
Q

What does the adrenal medulla consist of?

A

Modified sympathetic postganglionic neurons

134
Q

How do adrenaline (epinephrine) and noradrenaline (norepinephrine) differ?

A

Adrenaline = relatively non-specific = bind to both alpha & beta receptor types almost equally well

Noradrenaline = binds to mostly alpha receptor but can bind to beta receptors to a certain degree

  • Functions similar!
135
Q

When is adrenaline released and what does it reinforce?

A

Released only on sympathetic stimulation of adrenal medulla
Reinforces the sympathetic NS & exerts metabolic effects

136
Q

Percentage of adrenaline & noradrenaline produced by adrenal medulla?

A

~75% of adrenaline
<25% of noradrenaline

137
Q

Are adrenaline or noradrenaline produced in greater amounts by neurons?

A

Mostly noradrenaline
Small amts of adrenaline

138
Q

How are adrenaline/noradrenaline transported when made in adrenal medulla?

A

Hormone = travel longer dist. to diff parts of the body

139
Q

How are adrenaline/noradrenaline transported when made in neurons?

A

Neurotransmitter = interact w next neuron (shorter dist)

140
Q

What are some adrenal gland disorders?

A
  • Aldosterone hypersecretion (E.g. Conn’s syndrome)
  • Cortisol hypersecretion (e.g. Cushing’s dz/syndrome)
  • Adrenal androgen hypersecretion (e.g. Polycystic ovary syndrome = PCOS)
  • Adrenocortical insufficiency (e.g. Addison’s dz)
141
Q

What is aldosterone hypersecretion associated with?

A
  • Hypokalemia
  • Inc. bld. vol
  • Inc. plasma Na+
  • Inc. BP
142
Q

Pathway of epinephrine secretion

A
  • Stressor stimulates the hypothalamus
  • Hypothalamus stimulates the sympathetic nervous system
  • Sympathetic nervous system stimulates the adrenal medulla which increases the secretion of epinephrine
  • epinephrine prepares body for “fight/flight”, mobilize energy stores & metabolic building blocks for use as needed, stimulates arteriolar smooth muscle to vasoconstrict = dec. bld flow through kidneys
143
Q

What tissues is the pancreas made up of?

A
  • Acini
  • Islets of Langerhans
144
Q

Which is the endocrine portion of the pancreas?

A

Islets of Langerhands

145
Q

Which is the exocrine portion of the pancreas?

A

Acinar & Duct cells
- Acinar cells secrete digestive enzymes
- Duct cells secrete aqueous NaHCO3 solution

146
Q

Which pancreatic hormones are the most important in regulating fuel metabolism?

A

Insulin & Glucagon
(secreted by islets of Langerhans)

147
Q

What is human insulin composed of?

A

Two a.a. chains
- Connected to e/o by disulfide linkages
- When the two a.a. split apart, insulin’s functional activity is lost (to be functional = must be connected in the right place)

148
Q

Pathway for insulin secretion

A
  • Food intake causes inc. in blood glucose conc. (major control)
  • Stimulates islet beta cells to secrete insulin
  • Inc. bld. a.a. conc. & inc. gastrointestinal hormones (incretins) stimulate islet beta cells to secrete insulin too
  • Dec. bld. glucose, dec. bld. fatty acids, dec. bld. a.a., inc. protein synthesis, inc fuel storage
149
Q

slide 24

150
Q

What is hyperglycemia?

A

Abnormally high glucose levels in bld.

151
Q

What is diabetes mellitus characterized by?

A

High glucose conc. that overwhelms reabsorption capabilities of kidneys
- Glucose appears in urine
- Polyuria = urine vol. becomes excessive
- Type I and II

152
Q

What does an excess of insulin cause?

A

Brain-starving hypoglycemia

153
Q

When is glucagon secretion increased?

A

Postabsorptive state (fasting state)

154
Q

Pathway of glucagon secretion

A
  • Dec. blood glucose stimulates alpha cells to release glucagon
  • Increase in glucagon
  • Inc. bld. glucose to normal

Vice versa for high bld. glucose level

155
Q

What does an elevation in blood glucose levels?

A

Elevated blood glucose stimulates insulin secretion, but inhibits glucagon secretion

156
Q

Where is somatostatin produced?

A
  • pancreas
  • hypothalamus
157
Q

What do the parathyroid glands do?

A
  • Regulate calcium levels in blood
158
Q

Calcium homeostasis is closely associated with ________ homeostasis

A

Calcium homeostasis is closely associated with phosphate homeostasis

159
Q

Why must plasma Ca2+ be closely regulated?

A

Prevent changes in neuromuscular excitability
Control of Ca2+ metabolism incl. regulation of Ca2+ homeostasis & Ca2+ balance

160
Q

What raises free plasma Ca2+?

A

Parathyroid hormone (PTH)

161
Q

What increases & decreases blood calcium levels?

A

PTH acts to inc. bld Ca2+ levels
Calcitonin acts to dec. bld. Ca2+ levels

162
Q

Bone is continually being deposited by ___________ and it is continually being reabsorbed where ___________ are active

A

Bone is continually being deposited by osteoblasts and it is continually being reabsorbed where osteoclasts are active

163
Q

What are osteoblasts responsible for?

A

Synthesis & mineralization of bone
- lead to dec. availability of free Ca2+

164
Q

What do osteoclasts do?

A

Break down bone tissue
- lead to inc. availability of free Ca2+

165
Q

Where are osteoblasts derived from?

A

Precursor cells in bone marrow

166
Q

What can affect osteoclast development?

A

Osteoblasts & their precursor products:
- RANK ligand (RANKL)
- Osteoprotegerin (OPG)

^ these two are proteins = will determine whether it will lead to inc./dec. bone mass

167
Q

Pathway to decrease bone mass

A
  • Osteoblasts & their precursors secrete RANK ligand (RANKL) (& OPG)
  • RANKL will bind to macrophages/osteoclasts (RANK receptor)
  • Binding triggers: differentiation of macrophages into osteoclasts & suppression of osteosclasts apoptosis
  • Both of these ^ increase osteoclast action
  • Osteoclast action outpaces osteoblast action (basically, osteoclast break down the bones faster than osteoblast can create)
  • dec. bone mass
168
Q

Pathway to increase bone mass

A
  • Osteoblasts & their precursors secrete osteoprotegerin (OPG) & RANKL
  • RANKL binds to OPG (RANKL bound to OPG not available to bind with RANK)
  • Blocks the action of RANK
  • Dec. osteoclast action
  • Osteoblast action outpaces osteoclast action (basically, osteoblasts make bone faster than osteoclast breakdown)
  • inc. bone mass

Basically, limit the RANKL = cannot bind to RANK receptor = osteoclast cannot breakdown bones = osteoblast can work faster than osteoclast breaks down

169
Q

What does mechanical stress favours?

A

Bone deposition

170
Q

What does increased PTH (Parathyroid hormone) do?

A

Increase osteoclast activity
= Increased blood calcium level

171
Q

What does increased calcitonin do?

A
  • Increase osteoblast activity
    = Reduced bld. calcium level
172
Q

What does PTH (parathyroid hormone) do?

A
  • Raises plasma Ca2+
  • promote localized dissolution of bone = release Ca2+ into plasma
  • Act on kidneys
173
Q

What does activation of vitamin D3 form?

A

1,25-dihydroxycholecalciferol (calcitrol)
- Activation needs 2 enzymes

174
Q

What does vitamin D increase?

A

Increases Ca2+ absorption in the intestine

175
Q

Vitamin D vs PTH

A

Vitamin D primarily focus on increasing Ca2+ ability by promoting the Ca2+ absorption

PTH = more rapid respondent = if need to inc. Ca2+ = stimulate their release from the bone

176
Q

What is the indirect effect of PTH?

A

Promotes absorption of Ca2+ & PO4^3- (phosphate)

177
Q

Pathway to increase plasma PO4^3- (phosphate)?

A
  1. (PTH)
    - Plasma Ca2+ will increase (bc of inverse r/s b/w plasma PO4^3- & Ca2+ conc. caused by solubility characteristics of calcium phosphate salt
    - Plasma Ca2+ will inhibit parathyroid glands
    - Decrease in PTH
    - Inc. PO4^3- reabsorption by kidneys = dec. urinary excretion of PO4^3- = inc. plasma PO4^3-
    - Dec. Ca2+ reabsorption by kidneys = inc. urinary excretion of Ca2+ = (counteract with inc. Ca2+ absorption in intestine) = no change in plasma Ca2+
  2. (kidney)
    - Kidneys stimulated to secrete more activated vitamin D
    - Inc Ca2+ absorption in intestine = Counteracts with inc. urinary excretion of Ca2+ = no change in plasma Ca2+
    - inc. activated vitamin D = inc. PO4^3- absorption in intestine = inc. plasma PO4^3-
178
Q

Where is the parathyroid hormone secreted from?

A

Parathyroid gland

179
Q

What is the action of the parathyroid gland?

A

Increased plasma calcium level

180
Q

Where is calcitonin secreted from?

A

Thyroid gland

181
Q

Where is vitamin D (calcitriol) secreted from?

A

Kidneys (turning vit D to its active form)

182
Q

What is the action of parathyroid hormone?

A

Increased plasma calcium level

183
Q

What is the action of calcitonin?

A

Reduced plasma calcium level

184
Q

What is the action of vitamin D (aka calcitriol)?

A

Increased calcium absorption (intestine)

185
Q

What may cause disorders in Ca2+ metabolism to arise?

A

Abnormal levels of PTH/Vitamin D

186
Q

What is PTH hypersecretion?

A

Excess PTH secretion = primary/secondary

187
Q

What is PTH hyposecretion?

A

Deficient PTH secretion = hypoparathyroidism

188
Q

What is the major consequence of vitamin D deficiency?

A

Impaired intestinal absorption of Ca2+
- may lead to rickets (inadequate mineralization of bones)

189
Q

What cell secretes somatostatin?

A

Delta cell

A&P 2 (5 decks)

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