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Human Physiology 1 > Endocrinology Lectures 2021 > Flashcards

Endocrinology Lectures 2021 Flashcards

1
Q

Describe Endocrinology as a science

A

Homeostatic control mechanisms
–> Physiological systems need communication and coordination

eg: metabolism, salt and water balance, temperature,
reproduction, growth

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2
Q

When did Endocrinology begin?

A

Began in the early 20th century with two researchers William

Bayliss and Ernest Starling

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3
Q

Was the secretion of alkaline juice in the duodenum under

nervous or chemical control?

A
  • stomach would produce acidic chyme (semi-digested food from stomach that enters the intestine & its too acidic for the intestine to operate properly so the pancreas secretes alkaline fluid to neutralize that acidic chyme)
  • found that there were still alkaline secretion from the pancreas upon entry of acidic chyme into the duodenum
  • suggested there must be a blood borne agent that may be released from the lining of the duodenum targeting the pancreas & its stimulate (+) the pancreas to release the alkaline juice & neutralize that chyme
  • stimulus of that endocrine agent is the acidic chyme itself (feedback loop regulation)
  • that hormone subsequently was identified later as secretin (target pancreatic exocrine cells to promote alkaline juice secretion from those exocrine cells)
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4
Q

What did they used to define hormone as?

A

released from the endocrine gland into the circulation & acts at a target distinct from the site of circulation

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5
Q

7 points about hormones

A
  1. More than one produced in one endocrine gland
  2. More than one tissue secretes the same hormone
  3. More than one target cell type for a single hormone
  4. Secretion varies over time and will be affected by changes in
    the environment
  5. A single target cell can be influenced by more than one
    hormone
  6. Hormones can be blood borne or neuronally derived
  7. Some hormones are excreted from tissues that have other
    functions
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6
Q

Hormones are 1 part of a system…

A

Cell A secretes –> Hormone –> Cell B responds

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7
Q

What is the chemical classification of Peptides?

A

Structure: chains of amino acids (3 → 500+)

Solubility: hydrophilic

Secretion: exocytosis

Transport: free active peptide or precursor

Source: pituitary, pancreas, GI tract etc

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8
Q

What is the chemical classification of Amino acid derivatives?

A

Structure: catecholamines, thyroid hormone, melatonin

Solubility: hydrophilic, hydrophobic, hydrophilic

Secretion: exocytosis, Endo- & exocytosis, exocytosis

Transport: ~50% to carrier protein, most bound to carrier protein, ~50% to carrier protein

Source: adrenal medulla, thyroid gland, pineal gland

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9
Q

What is the chemical classification of Steroids?

A

Structure: cholesterol derivative

Solubility: hydrophobic

Secretion: diffusion

Transport: Most bound to carrier protein

Source: adrenal and sex steroids*

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10
Q

Describe Hormone processing

A
  1. Secretion
  2. binding of hormone to carrier protein
  3. Activation
  4. Inactivation
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11
Q

What are the 7 Post-translational modification of peptide hormones?

A
  1. Peptide cleavage
  2. Glycosylation
  3. Phosphorylation
  4. Sulfation
  5. Amidation
  6. Acetylation
  7. Subunit aggregation
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12
Q

ACTH

A

imp. hormone for cortisol
- regulates stress axis

(pituitary gland)

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13
Q

What is Feedback control?

A

this is predominantly (-), ie: output conteracts input, & is frequently seen in the TROPHIC hormones

  • can also be (+) (ex’s: let down reflex in nursing moms & oxytocin parturition)
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14
Q

Neuroendocrine reflexes

A

Combination of neural and hormonal processes. Not the same as neuromodulation

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15
Q

Estrogen

A

reset balance of these (neuromodulation)

  • can govern mood, appetite, depression, bipolar & anxiety
  • not same as neuroendo functions
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16
Q

Rhythms

A

Release of hormones is entrained to environmental

cycles which vary in interval length and duration

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17
Q

Melatonin secretion…

A

peaks at night

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18
Q

Cortisol secretion has…

A

2 prominent peaks

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19
Q

Carrier proteins

A

can be general or specific to the hormone in question, dictated by binding affinity

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20
Q

Specific carriers vs General carrier

A

Specific carriers:
Corticosteroid binding globulin (CBG) – CORTICOSTEROIDS

Thyroid hormone binding globulin and transthyretin (TBG) – THYROID HORMONES

General carrier:
Albumin - many hydrophilic hormones like epi will bind to albumin & typically affinity is low

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21
Q

Hormone Activation

A

Metabolism of the precursor or release from the carrier protein will activate the hormone that will then have a half life in the blood

The length of time for hormone half life follows the general
pattern:

  1. Single amino acid derivatives: minutes (short half life)
  2. Peptide hormones: minutes – hours
  3. Steroid hormones: hours (more energy to produce steroid hormone so we hold onto it for longer)
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22
Q

Hormone Inactivation

A

Enzyme degradation (Trypsin is common - breaks up) (ex: endopeptidase & exopeptidase)

Hormone receptor complex endocytosis

Conjugation (chemical group steroid sulfation)

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23
Q

What are 2 Endocrine dysfunctions?

A

Hyposecretion & Hypersecretion

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24
Q

Hyposecretion

A

primary or secondary, usually the result of atrophy of the endocrine gland and normally treated through replacement therapy

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25
Q

Hypersecretion

A

primary or secondary, usually the result of a benign tumour (adenoma), normally treated through inhibition

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26
Q

Target cell

A

– lack of receptors or biochemical machinery at the target cell
Eg: Hyperinsulinemia

*Target cell responsiveness is also altered naturally!

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27
Q

Response at target cell

A
  1. UP & DOWN REGULATION – Receptors at the target cell are themselves regulated in response to hormone levels influencing ABUNDANCE and AFFINITY
  2. PERMISSIVENESS – One hormone CANNOT fully exert its effect without the other being present
  3. SYNERGISM – The COMBINED effect is greater than the sum of the parts
  4. ANTAGONISM - The actions of one hormone REDUCES the effectiveness of the second – can be direct or indirect (happens naturally)

Measurement of binding kinetics for hormone/receptor complexes relies heavily on the chemical law of mass action:

Kd = [H] [R] / [HR]

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28
Q

So if Kd is high, binding affinity is?

A

LOW (easy for molecule to dissociate from receptor)

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29
Q

Do all hormone receptor complexes adhere to the law of mass action?

A

NON-COOPERATIVE = Law of mass action is upheld

POSITIVELY COOPERATIVE = ligand binding increases receptor affinity of vacant receptors

NEGATIVELY COOPERATIVE = ligand binding decreases receptor affinity of vacant receptors

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30
Q

Synergistic effects of hormones

A

glucagon + epinephrine + cortisol

combo is greater than parts

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31
Q

Hormone receptors

A
  1. MEMBRANE BOUND
    → Ligand gated, enzyme linked, guanylyl cyclase and Gprotein linked receptors
    → Second messenger systems include:
    adenylate cyclase
    guanylate cyclase
    inositol phosphate and diacyl glycerol
  2. NUCLEAR RECEPTORS
    Most lipophilic hormones act through nuclear receptors and
    many genes will have responsive elements
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32
Q

What are 4 main parts of the Pituitary & Hypothalamus?

A
  1. INFUNDIBULUM - is the stalk that connects the pituitary to the brain
  2. POSTERIOR PITUITARY - is an extension of the neural tissue (connected directly to hypothalamus)
  3. SPHENOID BONE
  4. ANTERIOR PITUITARY (is a true endocrine gland of epithelial origin)
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33
Q

Nomenclature of Anterior Pituitary & Posterior pituitary

A

Anterior Pituitary:

  • Pars distalis
  • Adenohypophysis

Posterior pituitary:

  • Pars nervosa
  • Neurohypophysis

Trophic hormones will typically stimulate production of hormones from anterior pituitary

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34
Q

3 points about the Posterior pituitary

A
  1. The hypothalamus and posterior pituitary form a neuroendocrine system with cell bodies based in the
    hypothalamus
  2. Posterior pituitary hormones synthesised in the hypothalamus
  3. Axons then extend down the INFUNDIBULUM and terminate in the posterior pituitary
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35
Q

A difference b/t Anterior & Posterior pituitary

A

Anterior pituitary: constitutive release –> constant

Posterior pituitary: these hormones are released on demand –> regulated (most hormone release is regulated)

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36
Q

Where is vasopressin & oxytocin mostly from?

A

Vasopressin –> supraoptic nucleus

Oxytocin –> paraventricular nucleus

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37
Q

Neurohypophysial peptides

A

Two nonapeptides (OT and AVP)

*Simple in structure but do diff things

Precursor peptides produced in the hypothalamus – neurophysins
Closely related but one can work without the other.

  • pos. pit is the storage & release site for 2 neurohormones: oxytocin & vassopressin
  • the neurons producing OT & AVP are clustered together in areas of the hypothalamus known as the paraventricular & supraoptic nuclei
  • these 2 pos. pit. neurohormones are composed of 9 AA’s each

eg: Brattleboro rats
- genetically diabetic (tasted urine)
diabetes –> running through (have to go to the bathroom a lot)
diabetes insipidus (insipid –> sour) –> vasopressin
diabetes mellitus (honey “sweet” - full of glucose) –> insulin

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38
Q

In the Posterior pituitary, AVP and OT neurophysins + PROTEOLYTIC ENZYMES are…

A

packaged in secretory granules and begin to migrate down the axon to the neurohypophysis where the nerve terminals are located

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39
Q

Vasopressin – Arginine Vasopressin – Anti-diuretic hormone

Release:

A

Reduced ECFV → ↑ plasma osmolality → ↑ osmoreceptor
activity → ↑ vasopressin release

Reduced ECFV → ↓ left atrial volume → ↓ arterial blood
pressure → ↑ vasopressin release

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40
Q

What are the 2 roots “reduced ECFV” can arise from?

A
  1. Loss of blood through hemorrging
  2. Loss of fluid through an INCREASE in plasma osmolarity as fluid moves from the EC space to IC space
    (ex: working out & sweating –> loose volume & you want to protect cellular fluid space so as a result that INCREASES concentration of salts & solutes in the ECF space we will get INCREASE in plasma osmolarity
    - that triggers osmoreceptor & that causes vasopressin release from posterior pituitary
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41
Q

Vasopressin – Arginine Vasopressin – Anti-diuretic hormone

ACTION:

How does the vasopressin address this reduced ECFV?

A

↑ H2O reabsorption in renal tubules –> 1 reason why its called ADH (diuresis –> increase in urine flow rate & anti-diuresis –> reduction)

Vasoconstriction of vascular smooth muscle

NET EFFORT:

  • CLOSED caridovas space
  • if you loose volume in that closed space, 1 way to maintain volume & same pressure is to make that space smaller
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42
Q

Oxytocin

RELEASE:

A

Birth canal distension → ↑ oxytocin release

Infant suckling → ↑ oxytocin release

BOTH (+) feedback

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43
Q

Oxytocin

ACTION:

A

↑ uterine muscle (myometrium) contraction during parturition

↑ milk ejection from mammary gland

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44
Q

Behavioural aspects of OT:

A

OT:
• INcreases maternal behaviour in rats but estrogens need to be present

  • Plasma OT levels INcrease during sexual arousal in both sexes
  • Act as neuromodulators in the brain to influence social recognition, memory and affiliative behaviours such as “pair bonding” (rodent research)
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45
Q

Behavioural aspects of AVP:

A

AVP:
• Stimulates release of ACTH that is synergistic with CRH

• Seems to play a greater role in MALES rather than females in regard to social recognition and consolidation of social memory (rodent research)

• Aggression, courtship, scent marking, and learning (rodent
research)

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46
Q

Anterior pituitary Portal

A

Portal

Capillary bed –> Capillary bed

Arteriole –> capillary –> venule

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47
Q

Adenohypophysial cells

A

Histological and cytological methods have provided definitive evidence on the cellular source for each hormone released from the adenohypophysis

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48
Q

Corticotroph

A

Hormone: ACTH

Staining characteristics: basophil

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49
Q

Thyrotroph

A

Hormone: TSH

Staining characteristics: basophil

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50
Q

Gonadotrophs

A

Hormone: FSH, LH

Staining characteristics: basophil, basophil

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51
Q

Lactotroph

A

Hormone: PRL

Staining characteristics: acidophil

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52
Q

Somatotroph

A

Hormone: Somatotroph

Staining characteristics: acidophil

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53
Q

Hypothalamic – Anterior pituitary axis

A

Hormones synthesized and released from the anterior pituitary are under the control of HYPOPHYSIOTROPIC hormones that can be stimulatory or inhibitory

ex: Corticotropin releasing hormone (CRH)
- pituitary hormone: adrenocorticotropic hormone
- “final” hormone: cortisol

The hypophysiotropic hormones:

  • TRH
  • CRH
  • GnRH
  • GHRH
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54
Q

In the hypothalamus, somatostain ______ & dopamine _____

A

inhibits control

stimulates control

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55
Q

Structural characterisation of adenohypophysial hormones

A

GROWTH HORMONE FAMILY:

  • Growth Hormone
  • Prolactin

Growth hormone is well conserved however there are many different variants of prolactin.

GLYCOPROTEIN FAMILY:
- Follicle stimulating hormone (FSH), leutinizing hormone (LH), thyroid stimulating hormone (TSH),
- So named due to the large percentage of carbohydrate moieties
– up to 33% by weight
- Each has an α and β subunit. The amino acid sequence of the α subunit is similar between the hormones but the β subunit varies

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56
Q

Pars intermedia

A

Many animals have an anatomically separate pars intermedia

The predominant endocrine product is αMSH (involved in regulating melanocytes –> melanocyte regulation - skin pigmentation (pleiotropic hormone - means many actions, anorexogenic factor - inhibit food intake)
In humans this is also the case during development

As adults these cells are not anatomically distinct but still synthesise and secrete αMSH

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57
Q

Precursor peptide Pro-opiomelanocortin (POMC)

A
  • happens INTRAcellularly also involved in regulating FOOD INTAKE
  • within ANTERIOR PITUITARY
  • diff cell types will express proconvertase enzymes (PC1, 2 & 3)
  • response for CHOPPING UP POMC in diff places depending on the signal response
  • no 1 precursor molecule of POMC can synthesize both ACTH & a-MSH & release both of those hormones
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58
Q

Normal growth means:

A
  1. Protein, fat and cartilage synthesis
  2. Cell proliferation - Hyperplasia and hypertrophy
  3. Bone lengthening - Increased extracellular matrix
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59
Q

Normal growth is influenced by:

A
  1. Genetic resolve
  2. Diet and nutrient transfer
  3. Disease and stress
  4. Multiple layers of hormonal control
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60
Q

Growth rate

A

Neonatal growth under the influence of placental hormones
Growth rate varies throughout life

  • GH levels increase during puberty
  • In males, testicular androgens are v. important and increase dramatically during puberty
  • Adrenal androgens also increase and may be more important in females (b/c males lack androgen in testes?)
  • Testosterone and estrogen both ultimately “put the brakes on”
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61
Q

Growth hormone (GH)

A

• GH production stimulated by GHRH and inhibited by
GHIH (somatostatin)

• GH is a 191 amino acid long polypeptide produced in
somatotrophs

• It is the most ABUNDANT adenohypophysial hormone (4-
10% of the wet weight of the gland ~ 5-10mg)

• Spontaneous secretion over a 24 h period usually peaks
in the first 90 minutes of sleep

• Transported in plasma attached to one or more binding
proteins

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62
Q

GHIH = somatostatin

A

inhib. factor that inhibits GH release from the anterior pituitary

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63
Q

GH = somatotropin

A

drives the axis

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64
Q

The Somatomedin hypothesis

A

“Growth hormone does not have a direct effect on growth of
any given tissue but rather acts indirectly through
somatomedins”

There are two main somatomedins – Insulin like growth
factors (IGF) I & II (predominantly synthesized & secreted by the liver)

They are 70 and 67 amino acids respectively and share many similarities with insulin

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65
Q

With The Somatomedin hypothesis, could they influence bone growth from blood samples? What was controlling?

A

indicated to researches that GH was stimulating something else (IGF) into the circulation that facilitated & directed growth in these samples

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66
Q

What are 2 similarities b/t Insulin & IGF receptors?

A
  1. Both SINGLE PASS (1 straight line through the membrane) receptors that are linked to these TKD’s on the intracellular side of the cell membrane
  2. Both exist as dimers
    - 2 monomers attached here by sulfate bridges
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67
Q

IGF’s

A

Circulating levels of IGF I increase massively during pubertal
growth spurt but GH increases moderately by comparison (long bone growth excellerates during puberty)

Tissue specific regulation of IGF I synthesis

GH does not regulate IGF II production to the same extent

IGF II is important during fetal development and plays a role in adult growth but not to the same extent as IGF I

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68
Q

Bone growth

A

Bone is LIVING TISSUE surrounded by an extracellular organinc matrix with a variety of cell types that have specific roles

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69
Q

Compact Bone vs Spongy bone

A

Compact bone: is dense & used for support

Spongy bone or trabecular bone: forms a calcified lattice

LOTS OF CARTILAGE IN BONE

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70
Q

Osteoblasts & Osteoclasts

A

Osteoblasts –> bone BUILDERS

Osteoclasts –> bone BREAKERS

these bone breakers/builders are critically imp. for the modulation & shaping of bone
- also play a very imp. role in Ca2+ balance

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71
Q

3 parts of the bone:

A

EPIPHYSIS: is the end of a long bone

EPIPHYSEAL PLATE: is the site of bone growth (imp. in long bone growth)

DIAPHYSIS: is the shaft of a long bone (lone part of bone)

*The DIAPHYSIS is the mature bone shaft with the EPIPHYSIS at either end. In a growing bone the epiphysis is separated from the diaphysis by the EPIPHYSEAL PLAYE

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72
Q

Osteoblasts produce…

A

enzymes (osteoid) collagen and proteins to provide a framework for hydroxyapatite crystals.

They deposit new bone on the outer edges of old bone to increase width. This is a dynamic process

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73
Q

Osteoblasts will ultimately turn into mature bone cells –>

A

osteocytes

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74
Q

Bone length growth…

A

is a different process and is regulated by cartilage cells, CHONDROCYTES, located in the epiphyseal plates

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75
Q

Chondrocytes

A

divide and multiply, lengthening the epiphysis with the older cartilage cells enlarging at the border of the diaphysis.

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76
Q

Hyperplasia vs. Hypertrophy

A

Hyperplasia - lots of cell division

Hypertrophy - INcrease cell size

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77
Q

The Dual-effector theory

A

Driven by: GH & IGF

  1. Development of IGF-I responsiveness
  2. Expression of IGF-I gene
  3. Local production of IGF-I
  4. Stimulation of clonal expansion by autocine/paracrine mechanisms

Cytoplasmic maturation

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78
Q

Abnormal growth

A
  1. Site of lesion in ANTERIOR pituitary
    - hypopituitary dwarfism - if inhibited
    - gigantism (infant) or acromegaly (adult) - if stimulated (hyperactivity)

Fezik –> Andre the giant

  • gigantism & acromegaly
  • hyperactive pituitary gland during infancancy & adulthood

Robert Wadlow

  • 2.7m or 8.9 feet tall
  • worlds tallest individual suffered from gigantism

Maurice Tillet

  • large forehead
  • big hands
  • big jaw
  • probably had problem in pituitary gland during puberty
  1. Laron dwarfism (IGF DEcrease production)
    - Site of lesion in LIVER
    - “Little women of Loja”
    - everyone in that village is short in height (especially women but also men to some extent)
    - can be lack of GH receptors on liver
    - lack IGF responsiveness
    - decrease GH BP (binding protein)
    - decrease IGF carrying capacity
  2. End organ resistance
    - site of lesion in somatic cells
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79
Q

Thyroid hormones

A

– involved in energy homeostasis.

Hypothyroidism = reduced growth, TH is largely permissive (neuronal development)

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80
Q

Insulin

A

involved in carbohydrate metabolism. Deficiency can

block growth and excess can promote growth, potential cross reactivity with IGF receptors

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81
Q

Androgens & estrogens

A

Arrest “long-bone” length increase by closure of the epiphyseal plate (causes ossification of the epiphyseal plate)

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82
Q

Prolactin

A

belongs to the GH family and influences mammary gland growth as well as aspects of the immune system (influences lymphocytes)

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83
Q

Placental lactogen

A

belongs to the GH family and influences neonatal development, maternal glucose and amino acid supply.
Peaks around mid pregnancy until full term
- can play a role in gestational diabetes (don’t be a diabetic after birth)

84
Q

Neurotropic factors

A

nerve growth factors (NGF’s)

  • used in early treatment of neurodegenerative disorder
85
Q

Erythropoietin

A

red blood cell growth factor

  • EPO doping (to remote blood cell growth)
86
Q

Platelet derived growth factors

A

vascular injury repair but also involved in the development of artherosclerosis

87
Q

Epidermal growth factors

A

enhanced proliferation of epidermis, gut lining, pulmonary lining

  • herbivores grazing (will leave saliva on plant that will use it to grow the plant)
88
Q

Tumour derived growth factors

A

angiogenesis (growth of blood vessels)
– Fibroblast growth factors
– Transforming growth factors

89
Q

Where is the vast majority of calcium?

A

in bone tissue

90
Q

~99% of out bodies Ca2+ is…

A

locked = bone

91
Q

Why regulate calcium?

A

Calcium is perhaps the most tightly regulated ion in circulation
– 99% of the bodies calcium is in calcified structures
– 0.9% is intracellular
– 0.1% exists in the ECF, half of this is bound to proteins or negatively charged ions and the rest is in free form Ca2+
(0.05% is in free form)

  1. Neuromuscular excitability – reduced calcium leads to tetanic muscle contraction and high levels lead to reduced muscular contraction
  2. Stimulus-secretion coupling: many cells will require calcium to enter the cell to stimulate the secretion of a given substance
  3. Cell–Cell integrity of tight junctions
  4. Cofactor for clotting blood
  5. Required for structural form of bone and teeth
92
Q

Where do we get calcium from?

A

balance (input vs output in terms of diet) vs. homeostasis (internal regulation)

93
Q

To maintain calcium balance, dietary intake should _____ Ca2+ loss in the urine & feces

94
Q

Calcium vs phosphate

A

Bone is a living tissue that is packed with hydroxyapatite crystals between a collagen matrix

3Ca2+ + 2PO43- –> Ks –> precipitation (can lead to kidney stones - precipate out in wrong place) (happens in bone - crystals precipate out)
[Ca2+] X [PO43-] < Ks –> solution

So regulation of calcium ALWAYS impacts phosphate concentrations

95
Q

Bone remodeling

A

Remodelling requires deposition and resorbtion.
– Osteocytes = mature bone cells
– Osteoblasts = bone builders responsible for depositing the collagen matrix (derived by stromal cells - connective tissue)
– Osteoclasts = bone breakers (desolve hydroxyapatite crystals within the bone matrix) (derived by haematopoeitic cells, macrophages & blood cells ex platelets)

96
Q

Important: # of key characteristics within osteoclasts that make them beneficial as bone breakers

A
  1. Rough jaggedy edge to the membrane of the cell in its interface for this bone solid space
    - INcreases the SA; allowing greater int. of any chemicals released from the osteoclasts
97
Q

Osteoclast

A
  • release hydrogen ions (decrease pH - more acidic)
  • release cathepsin (enzyme that will degrade collagen)
    (breaks down structure to free up hydroxyapatite crystals by creating an acidic pH (lower solubility coefficient, makes crystals go into solution faster)
98
Q

Osteocyte

A

start shape

99
Q

Bone matrix

A
  • solid
  • explains why its slow
  • hydroxyapatite crystals in here
  • where Ca2+ phosphate has exceeded the solubility coefficient & have participated out (it is solid)
100
Q

Slow & fast route

A

slow: taking it from the bone matrix
fast: taking Ca2+ & phosphate from the bone fluid space

101
Q

Osteoblast

A

imp. in context of the role of osteocysts & osteoblasts play:
- movement of ions that are liberated from the boney matrix or within this bone fluid space into the blood (requires specific Ca2+ transporters) & in particular Ca2+ ATPase (will allow cell to draw Ca2+ in or pump it out & then influence solubility coefficient in this bone fluid space & allow for movement of Ca2+ from bone fluid space into glut

102
Q

What are the hormones involved in bone remodeling?

A
  1. PARATHYROID HORMONE (PTH) – negative relationship
    between plasma [PTH] concentration and plasma [Ca2+] that
    is EXTREMELY sensitive
    - as plasma Ca2+ concen. falls, PTH concen. INcreases, such that PTH is a hypercalcemic hormone (INcreases Ca2+ concen. in the circulation)
    - parathyroid glands synthesize & release thyroid hormone
  2. VITAMIN D3 (cholecalciferol) – needs to be converted to 1,25 – (OH2) – vitamin D3 (calcitriol)
  3. CALCITONIN – the ONLY hypocalcaemic hormone (works to reduce the circulating levels of Ca2+ in your blood stream)
103
Q

Parathyroid hormone in BONE

A

Bone (stimulate osteoclast activity to promote the dissolution of hydroxyapatite crystals within that mineralized bone area)

  1. Fast homeostatic regulation of Ca2+ from bone fluid space (plasma)
  2. Slower balancing of total body calcium from resorptive processes

*body might call on that Ca2+ reserve to maintain Ca2+ homeostasis in the ECF space

104
Q

Parathyroid hormone in KIDNEY

A

PTH increases calcium and decreases phosphate reabsorption

INCREASE PO43- loss DECREASE Blood PO43- INCREASE Solubilisation of bone INCREASE Ca2+ release

105
Q

Parathyroid hormone in INTESTINE

A

Actions are INdirect through stimulation of vitamin D3 production

106
Q

Vitamin D

A

• Considered by many as a hormone as it can be produced in the skin from 7-dehydrocholesterol
- lipid soluble

• Two important enzymatic steps that involve the sequential addition of hydroxyl groups
- VD AKA seco-steroid (similar structure as normally steroids that have 4 aromatic ring structures but 1 of the aromatic rings is broken)

• Activation of 1α hydroxylase is the most important step and this enzyme is regulated by PTH

107
Q

NB vitamin D is often considered a steroid therefore

where does it act in the target cell?

A

Typically, influences gene expression (genomic effect tends to take a little while)

108
Q

Target sites for Vitamin D3

A

• The gut is probably the best documented area of vitamin D3 action.
Where both fast and slow components are initiated.
- bind to receptors on cell mem. & cause a rapid response

rickets - brittle bones would be result

Rapid component –> mainly facilitated by VD binding to cell membrane receptors (Na+ Ca2+ exchanger - NCX)
Longer lasting component –> mainly facilitated by VD binding to nuclear receptors (PM - plasma membrane Ca2+ ATPase (pump req’s energy)

109
Q

Regulation of vitamin D with PTH (Hypocalcaemic

event)

A

act as hypercalcaemic hormones
- job is to increase Ca2+ concen. in response to hypercalcaemic events

slide 79

110
Q

Calcitonin

A

Not involved in day to day regulation but may be involved during the absorptive state (post meal) and also during pregnancy (newborn req’s lots of Ca2+ during new growth)

Calcitonin has both hypocalcaemic and hypophosphatemic effects

slide 81

satiety hormone - that’s enough (baby sucking milk)

111
Q

Osteoblast – Osteclast communication

A

For the most part bone resorption and bone deposition balance each other out but there are times when this is not the case

Osteoblasts are derived from STROMAL CELLS in the bone marrow and osteoclasts are derived from MACROPHAGES in the bone marrow
– Osteoblasts and its precursor cells produce two main messengers RANKL (receptor activator of NFκB ligand) and OSTEOPROTEGERIN
– Estradiol stimulates the production of osteoprotegerin

112
Q

Osteoporosis

A

Reduced bone mineral density

Prevalent in pre and postmenopausal women

Onset of osteoporosis and ~1% of bone mass is lost every year

Therapy includes:
– Exercise
– Ca2+ supplements
– HRT
– Calcitonin
– SERMS (selective estrogen receptor modulator) and ANGELS (activators of non-genomic estrogen like signalling)
  • men don’t have increase’s in estrogens & don’t have same levels so as a conseq. there is disconnect
  • males produce testosterone –> aromatase –> estrogens
113
Q

Thyroid gland

A
  • vascularized

- next to imp. blood vessels (cardiac artery - red)

114
Q

Thyroid hormones

A

Tetraiodothyronine (T4) and triiodothyronine (T3) are both derived from THYROGLOGULIN and synthesized in the follicular cells and the colloid of the thyroid gland
- insufficient way to syn. & release

115
Q

T4 and T3…

A

are collectively referred to as the thyroid hormones (TH) and
are involved in the regulation of metabolic rate and are key during development

116
Q

The basic ingredients are the amino acid tyrosine and the element iodine…

A

Tyrosine can be made in the body whereas iodine is an

essential component of our diet

117
Q

Thyroid hormone classification

A
  • Thyroxine T4 (most relevent)
  • Triiodothyronine T3 (primarily biological active comp. of this active pathway)
  • Reverse T3 (T2 & T1 - loss of I on INNER RING)
  • functionally, is conferred by a loss of 1 I molecule on OUTER phenol ring
118
Q

Thyroid hormone synthesis, storage and release

A

slide 90

TRH –> TSH –> T3/T4 HPT

Thyroglobulin

  • has 2 identical subunits, both 330 kDa
  • maybe ~4-6 typosine residues (inefficient)
  • get limited # of synthesized

monoiodotyrosine
diiodotyrosine
–> go to make T3 or T4
- still attached to TG

  1. A Na+-I- symporter brings I- into the cell. The pendrin transporter moves I- into the colloid.
  2. Follicular cell synthesizes enzymes & thyroglobulin for colloid.
  3. Thyroid peroxidase adds iodine to tyrosine to make T3 & T4.
  4. Thyroglobulin is taken back into the cell in vesicles.
  5. Intracellular enzymes separate T3 & T4 from the protein.
  6. Free T3 & T4 enter the circulation.
119
Q

Thyroid hormone deiodination

A

• Deiodinases can have a strong preference for specific TH’s

  • Type I has a strong preference for reverse T3
  • Type II deiodinates ONLY the outer ring (highly expressed in the liver)
  • Type III deiodinates ONLY the inner ring

• These enzymes can be tissue specific

120
Q

Actions of thyroid hormones

A

CALORIGENIC – TH is the most important regulator of basal metabolic rate (brown adipose tissue will generate heat through futile cycles (imp. for generating heat)

SYMPATHOMIMETIC EFFECT – action is similar to the sympathetic nervous system (increases target response to catecholamines - in the heart, NE & E INcrease heart rate - chronotropic effect - time rate, & INcrease stroke volume - ionotropic - INcrease contraction force)

CARDIOVASCULAR – largely as a result of the increase in catecholamine receptors and calorigenic effects

GROWTH – synergistic actions with both GH and IGF’s. TH is essential for normal growth and neural development

121
Q

Thyroid hormone abnormalities

A
  • This is one of the more common endocrine disorders and is very prevalent in young adult women
  • Includes both hypothyroidism and hyperthyroidism either of which are characterised by GOITER
122
Q

Goiter

A

is an over stimulation of the thyroid gland and not necessarily related to the capacity of the gland to synthesize and release TH

123
Q

Graves disease

A

Exophthalmos is a common feature of Graves disease

which is an autoimmune disease

124
Q

Hypothyroidism

CAUSE: Primary failure of the thyroid gland

A

↓T3 & T4, ↑TSH

Goiter

125
Q

Hypothyroidism

CAUSE: Secondary to hypothalamic or anterior
pituitary failure

A

↓T3 & T4, ↓TRH and/or ↓TSH

NO

126
Q

Hypothyroidism

CAUSE: Lack of dietary iodine

A

↓T3 & T4, ↑TSH

GOITER

127
Q

Hyperthyroidism

CAUSE: Abnormal presence of long acting thyroid
stimulator (LATS) (Grave’s disease)

A

↑T3 & T4, ↓TSH

GOITER

128
Q

Hyperthyroidism

CAUSE: Secondary to excess hypothalamic or
anterior pituitary secretion

A

↑T3 & T4, ↑TRH and/or ↑TSH

GOITER

129
Q

Hyperthyroidism

CAUSE: Hypersecreting thyroid tumour

A

↑T3 & T4, ↓TSH

NO

130
Q

Hypothyroidism Symptoms

A 
Low BMR
Decreased perspiration
Slow pulse
Lowered body temperature
Cold intolerance
Lethargy, tiredness
Weight gain
Loss of hair
Edema of face and eyelids
Menstrual irregularities
Goiter (may or may not be present)
131
Q

Hyperthyroidism symptoms

A 
Elevated BMR
Increased perspiration
Rapid pulse
Increased body temp
Heat intolerance
Nervousness and anxiety
Weight loss
Muscle wasting
Increase appetite
Exophthalmos (sometimes)
Goiter (primary or secondary in origin)
132
Q

Melatonin definition

A

is the primary hormone released from the pineal gland and is

synthesized from the amino acid tryptophan

133
Q

Melatonin

A

Synthesised and released in a rhythmical fashion that is closely related to circadian rhythms – SCOTOPHASE (dark) and PHOTOPHASE (light)

Darkness is a universal stimulus for the synthesis and release of melatonin from the pineal gland suggesting a strong link between the pineal and the optic tract

The link comes in the form of the SUPRACHIASMATIC NUCLEUS (SCN) which is our major biological clock where the interaction between PER genes and CLOCK proteins cycle at a remarkably constant rate that shifts depending on light cues

134
Q

Melatonin synthesized from…

A

the pineal gland

  • individuals maintain a daily rhythm of melatonin & synthesis release if they live where it is dark all day
135
Q

Inhibition of pineal gland during photophase

A

sunlight DEcreases NE release

136
Q

Melatonin more facts

A

Melatonin release peaks in humans usually in the MIDDLE of the night

Enzymes involved in melatonin synthesis also follow a RYTHYM

Reproduction follows cycles so there is a link between melatonin - sex hormones and reproduction (antigonadotrophic actions of melatonin = long day breechers)

Melatonin supplements go in and out of favour. It is evident that the actions of melatonin are far reaching (like TH). (pleiotrophic)

137
Q

We will die without…

A

aldosterone

138
Q

The Adrenal gland

A

Zona glomerulosa – Mineralocorticoids (aldosterone)
- balance minerals

Zona fasiculata – Glucocorticoids (cortisol)
- glucose/energy

Zona reticularis – Adrenal androgens (DHEA)
- adrenal sex steroids

139
Q

Adrenal steroids released from the adrenal cortex:

A

– Mineralocorticoids: Aldosterone

– Glucocorticoids: Cortisol

– Sex hormones: Dehydroepiandrosterone androstenedione (androgens) & estrogens

140
Q

Catecholamines released from the adrenal medulla:

A

– Epinephrine ~ 80%
– Norepinephrine ~ 20%

often considered an extension of the sympathetic NS

141
Q

Cholesterol is…

A

imp. in our diet

- and a precursor

142
Q

1 of the primary enzymes that is req. for steroid synthesis is:

A

P450 side chain cleavage enzyme (P450 SCC)

  • 1st step in pathway
  • cleaves side chain off to provide the backbone
  • takes off the side chain here for cholesterol to provide precursors for steroid synthesis
  • we can lump these precursors based on the # of C atoms they have
143
Q

Three main “parent” molecules

A

C21 - Pregnane –> pregnenolone or progesterone

C19 - Androstane –> androgens

C18 - Estrane –> estrogens

144
Q

Adrenocorticosteroids

A

Glucocorticoids

Mineralocorticoids

145
Q

Sex steroids

A

Androgens

Estrogens

146
Q

Aromatase

A
  • very imp. enzyme in conversion of androgens –> estrogens
  • creates an aromatic ring structure 1st in ring A that confers estrogen activity
  • therefore, location of that enzyme is imp. in terms of optimal function within the tissue
147
Q

DHT (dihydrotestosterone)

A

very imp. enzyme in conversion of androgens to estrogens & action of aromatase

148
Q

Why don’t men have osteoporosis?

A

b/c they don’t have as much of a decline in androgen as women

149
Q

Mineralocorticoid

A

Aldosterone acts on the distal and collecting tubules of the nephron in the kidney (Goal: promote Na+ reabsorption)

Regulates body fluid volume which has implications on the renal and cardiovascular systems

The steroid is essential for life. It promotes Na+ retention and K+ excretion in the kidney

Secretion is regulated by the renin angiotensin system (angiotension II) and also directly by circulating K+ concentrations (as K+ increases, aldosterone syn & release is promoted). *Aldosterone regulation is largely independent of the pituitary gland (if there is a primary dysfunction with aldosterone synthesis, if there is not enough made the organism will die)

Hyperaldosteronism can be either primary dysfunction (site of syn of the hormone itself) (Conn’s syndrome - in adrenal gland, increasing aldosterone syn & release from the adrenal gland)) or secondary. Symptoms present as hypernatremia, hypokalemia and usually hypertension

150
Q

Hypernatremia

A

too much aldosterone & is responsible for Na+ retension

151
Q

Hypokalemia

A

too little K+

152
Q

Hypertension

A

INcrease Na+ in ECF, normally water follows

INcrease Volume –> INcrease pressure

153
Q

Why is hypernatremia & hypertension usually hand in hand?

A

b/c we have a fixed cardiovascular space (fluid volume)

  • we pull in Na+ into that space, water will follow
  • INcrease volume in that fixed space
  • water gonna have pressure & so we get hypertension
154
Q

Dehydroepiandrosterone (DHEA)

Why are estrogens considered female sex steroids and androgens considered male sex steroids?

A

b/c estrogens are predominantly produced in female gonads & androgens predominant in male gonad tissue

The adrenal gland produces small amounts of both as DHEA is an adrenal androgen

In males Testosterone overpowers the actions of DHEA. However as females otherwise lack androgens DHEA plays a role in the pubertal growth spurt, hair growth and the female sex drive

Adrenogenital syndrome – symptoms are dependent on sex and age of hyperactivity onset
– Adult females – masculinisation, facial hair, deepening of voice etc
– Newborn females – psuedohermaphrodism
– Adult males – no effect
– Pubertal males – precocious pseudopuberty

155
Q

Adrenarche

A

unique to humans & old world monkeys

156
Q

Glucocorticoid release

A

↑ Blood glucose
(by stimulating gluconeogenesis and inhibiting glucose uptake)

↑ Blood amino acids
(by stimulating protein degradation)

↑ Blood fatty acids
(by stimulating lipolysis)

157
Q

Glucocorticoids

Direct actions:

A

– Stimulates gluconeogenesis – generation of glucose from non-carbohydrate substrates (amino acids, pyruvates, glycerol)
– Inhibits glucose uptake by many peripheral tissues
– Stimulates protein degradation in muscle
– Stimulates lipolysis, mobilising fatty acids as an alternative energy source

158
Q

Glucocorticoids

Permissive actions:

A

– vascular collapse during acute stressful events in the absence of glucocorticoids

159
Q

Glucocorticoids

Anti-inflammatory and immunosuppressive:

A

– The anti-inflammatory effects are seen following administration of supra physiologic or pharmacologic levels
– Prevention of leucocyte infiltration into the wound site
– Atrophy of lymphatic system (chronic stress)

160
Q

Cortisol hyper/hypo-secretion

Cushings syndrome (hypersecretion):

A
  • Increased amounts of CRH or ACTH (caused by anemias in hypothalamus or pituitary, get excess production of these signals that will promote cortisol synthesis)
  • Adrenal tumours (primary dysfunction where we get excess cortisol being syn or released at the adrenal gland)
  • Ectopic ACTH release (being made of released from a site not typical)
161
Q

Cortisol hyper/hypo-secretion

Symptoms include:

A
  • Excess glucose (coining the term adrenal diabetes)
  • Fat deposition in the face and abdomen, thin legs and arms
  • Facial hair excess
162
Q

Cortisol hyper/hypo-secretion

Addisons disease (hyposecretion):

A
  • General name for bilateral damage to the adrenals

* Can also be primary or secondary in nature

163
Q

Cortisol hyper/hypo-secretion

Addisons disease (hyposecretion):

Symptoms include:

A
  • Increased integument pigmentation

* Weakness, weight loss, hypotension, salt craving and hypoglycemia

164
Q

General Adaptation to stress

A

Developed from Canon’s ideas on “ Fight or flight” and Hans Seyle’s “General adaptation syndrome”

  1. Primary alarm response:
    • catecholamine surge into the system
    • ↑ in BMR
    • ↑ in blood flow to required organs (brain in particular) (blood flow tends to go away from intestine & towards skeletal muscle to power)
    • hepatic glycogenolysis (breakdown of glycogen into glucose to provide that energy)
  2. Secondary resistance response
    • described actions of cortisol on metabolism
    • continued mobilisation of glucose for central organs
    • continued breakdown of alternative energy stores (lipids and proteins)
  3. Tertiary exhaustion response
    • muscle wasting, hyperglycemia (diabetes mellitus)
    • atrophy of the immune system, gastric ulcers
    • vascular derangements
165
Q

The adrenal medulla

A

The adrenal medulla essentially acts as an extension of the sympathetic nervous system

Catecholamine release from the adrenal medulla is largely under the control of the SNS

Both catecholamines are stored in chromaffin granule

vast maj. of catecholamine released from adrenal medulla during acute stressful event is: 80% epinephrine and 20% nor-epinephrine

Both are the active ligands in the adrenergic system and they will bind to adrenergic receptors: α1, α2, β1, β2, β3 (also lots of isoforms)

166
Q

Epinephrine

A

Rapid mobilisation of the bodies energy reserves
Increase cardiac output and total peripheral resistance
Increase coronary and skeletal muscle arteriolar dilation
Reduce gut motility
Increases glycogenolysis in liver and muscle
Increased CNS alertness
Dilates pupils and flattens the lens
Increases sweating

ex: almost stepping in front of bus

167
Q

Adrenoceptors

A

slide 119

β1 Heart & kidney NE = E ↑ cAMP Inotropic and chronotropic actions

if someone is on B blockers they will target this & red impact of NE & E on cardiac function

  • are 7-transmembrane receptors which mediate the central & peripheral actions of the n.t., NE & E
168
Q

Epinephrine reversal

A

Numerous agonists/antagonists for adrenoreceptors Phenylephrine is an antagonist specific for α adrenoceptors

can constrict or dilate –> multiple diff receptors will confer multiple diff physiological responses, to the extent where they could actually reverse that response

169
Q

The integrated stress response

170
Q

Exocrine (out)

A

acinar cells secrete pancreatic enzymes into pancreatic duct

171
Q

Endocrine (in)

A

islets of Langerhan cells secrete hormones into blood vessels

172
Q

Insulin & amylin:

A

Released from B or β cells

10:1

hypoglycaemic hormone

173
Q

Glucagon:

A

Released from α cells

hyperglycaemic hormone

174
Q

Somatostatin:

A

Released from D or δ cells

inhibiting GH

175
Q

Pancreatic polypeptide:

A

Released from PP or F cells

176
Q

Islets of Langerhans & pancreatic hormones

A

All these hormones are involved in regulating fuel metabolism and all act at multiple levels

177
Q

Amylin:

A

– Released with insulin following a meal
*– Slows down the appearance of glucose in the blood

  • while insulin does a very good job in moving that glucose to where it needs to be
  • it cannot handle a huge influx at 1 time so amylin (go to 2nd point)
178
Q

Somatostatin:

A

– Released in response to increased glucose and amino acid
levels
– D cells are always found in close association with α and β
cells
– Inhibits digestive and absorptive processes
(inhibits the mobilization of energy reserves, plays an integral role in regulating locally insulin & amylin release from the a & b cells)

179
Q

Pancreatic polypeptide:

A

– Dramatic postprandial increase in plasma PP
– PP levels suppress SST levels and vice versa (antagonist role b/t pancreatic polypeptide & SST within the pancreas)
– D and F cells may be regulating each other (as well as α
and β cells)

  • results in an overall balance of glucose within the circulation
180
Q

Glucose activation of insulin secretion from

pancreatic β cells

A

glucose enters B cell, increase ATP/ADP, inhibits KATPchannel, ALLOWING L-type Ca2+ channel, and insulin secretion into the blood

181
Q

Fuel metabolism

A

Fuel – Carbohydrates, Fats and Proteins

Metabolism – A generalist term for the chemical reactions that occur in the body

Anabolism – this requires energy input (ATP) and is the synthesis of larger macromolecules either for function or energy storage

Catabolism – breakdown of macromolecules eg:
– hydrolysis: glycogen → glucose
– oxidation: glucose → ATP

The balance between anabolism and catabolism is not always straightforward
– Growth periods
– Short and long term “gaps” in food intake
– Absorptive (fed) and post-absorptive (fasted) states

182
Q

↑ blood glucose

A
  • glucose absorption from digestive tract
  • *Hepatic glucose production
    a. glycongenolysis - breakdown of glycogen into glucose
    b. gluconeogenesis - conversion of fats or proteins into carbs & ultimately glucose

lead to increase in blood glucose concentration

183
Q

↓ blood glucose

A
    • Transport of glucose into the cells
      a. Energy production
      b. Energy storage
  • Urinary excretion of glucose
184
Q

1 of the key things about glucose:

A

it’s osmotically active
- if you have a INcrease conc. of glucose on 1 side of a semi-permeable membrane & a low conc. on the other, then the glucose will balance but water may follow to balance the osmotic pressure on the side of that semi-permeable membrane

  • a key symptom of a diabetic
  • a INcrease urine flow rate that is a very INcrease conc. of glucose
185
Q

Human insulin

A

syn. as a pro molecule

  • cleaved to become mature peptide
  • cysteine residues create disulfide bonds
186
Q

Insulin – carbohydrates

Facilitates glucose transports:

A

– Glucose cannot simply diffuse into cells it is transported by
a family of proteins known as GLUT or by Na+ glucose cotransport SGLT’s
– GLUT-4 transports most of the circulating glucose during
the absorptive state into skeletal muscle and adipose
tissue
– GLUT-4 are housed in intracellular vesicles and are
recruited onto the cell membrane in response to insulin
– In the post absorptive state glucose is transported out of
the hepatocyte by GLUT 2 transporters
– In the absorptive state insulin facilitates conversion of
glucose into glucose 6-phosphate to keep intracellular
concentrations low
– Glucose uptake in the brain is by GLUT-1 & 3 and is largely independent of insulin

187
Q

Fasted state vs. fed state

- adipose & resting skeletal muscle

A

Fasted state:

a) in the absence of insulin, there are no GLUT4 transporters in the membrane
- rather sitting waiting in these secreted vesicles, ready to be inserted when the appropriate signal comes along

Fed state:
b) insulin signals the cell to insert GLUT4 transporters into the membrane, allowing glucose to enter cell

188
Q

Diabetes Type II

A
  • more in older ppl
  • exercise can help
  • b/c imp. remedy to aleviate symptoms
  • 2 pathways:
    1. insulin indep.
    2. insulin dep.
  • exercise may increase GLUT4 insertion into cell membrane
  • exercise may increase insulin receptors
  • 1 of the main issues with type II diabetes is insulin insensitivity & so cells don’t respond to insulin the way they should in a type II diabetic
  • with exercise you’re promoting insulin receptors
  • resulting in an INcrease in insulin sensitivity at the target site
  • therefore as a consequence, that glucose challenge when there is an increase in blood glucose conc. not as much insulin is req. to initiate this response that we see, so less work is done by the pancreas to syn that insulin
189
Q

Fasted state vs. fed state

- liver hepatocytes

A

fasted state:
c) the hepatocyte makes glucose & transports it out into the blood, using GLUT2 transporters

fed state:
d) the glucose concen. gradient reverses, & glucose enters the hepatocyte (just at a meal)

190
Q

Insulin – carbohydrates

Inhibits glycogenolysis in the liver:

A

– Favoring carbohydrate storage

191
Q

Insulin – carbohydrates

Inhibits gluconeogenesis

A

– Reduces circulating amino acids

192
Q

Insulin – fats & proteins

Actions on fat:

A

– Inhibits lipolysis
– Stimulates fatty acid uptake in adipose tissue
– Stimulates glucose uptake and conversion to triglycerides

193
Q

Insulin – fats & proteins

Actions on protein:

A

– Promotes amino acid uptake
– Stimulates protein synthesis
– Inhibits protein degradation

all about energy storage in terms of the action insulin might play

194
Q

Insulin as the only hypoglycemic hormone

A

There is a positive relationship between blood glucose and amino acid concentrations and insulin concentration

Feed forward regulation by glucagon-like peptide-1 and gastric inhibitory peptide (Balis & Stalling were looking for these peptides when they were doing their original experiments)

195
Q

Transport Maxima for glucose

A
  • all the transporters for glucose to be reabsorbed by the kidney are occupied (no more room for glucose to be transported so it stays in the primary urine)
  • you will get increase come of glucose in that primary urine, that pulls water into that primary urine as well as you get a lot of urine with increase conc. of glucose in it
  • b/c glucose is osmotically active
196
Q

Diabetes mellitus

A

is likely the most common endocrine disorder in the

western world, literally means “honey running through”

197
Q

Type I or insulin-dependent diabetes:

A

lack of insulin secretion

– Normally seen in children and represents a small proportion of diabetics

198
Q

Type II or non-insulin-dependent diabetes:

A

lack of insulin sensitivity

– The most common form and invariably seen alongside obesity (80-90%)

199
Q

Insulin shock in type 1 diabetics

A

typically related to T1 diabetics that are early on with dealing with their meds & what levels & understanding the level of their meds & etc.

  • may administer too much med so too much insulin
  • so cells have to use alternate energy source (ketosis)
  • emergency response that is short lived
200
Q

Glucagon

A

Hyperglycemic hormone

There is a negative relationship between blood glucose levels and glucagon

• Carbohydrates:
– Stimulates hepatic glycogenolysis and gluconeogenesis

• Fats:
– Promotes fat breakdown (lipolysis) increases release of TG, DG and MG lipase’s from fats
– Inhibits hepatic ketogenesis reducing FFA conversion to ketone bodies.

• Proteins:
– Promotes hepatic protein catabolism

201
Q

Feasting and fasting actions of insulin and glucagon

A

Pancreatic α and β cells respond in the opposite direction to sugars and fats in the blood but in the same direction in response to amino acids

202
Q

With Na+ retention, water will come…

A

secondarily

203
Q

ANG II stimulates…

A

an increase in growth of the zona glomerulosa much like TSH on the thyroid gland

204
Q

The primary form of hyperaldosteronism is also known as…

A

Conn’s syndrome

205
Q

Why are estrogens considered female sex steroids & androgens considered male sex steroids?

A

b/c estrogens are predominantly produced in female gonads & androgens predominant in male gonad tissue

206
Q

Female Pseudohermaphrodism

A

Predominantly ovarian gonads but the phenotype presents itself with male genitalia

  • extreme cases are not uncommon
  • it is often accompanied by a lack of cortisol production - not -ve feedback on ACTH production that targets the adrenal cortex
  • stimulating steroid synthesis
  • however, the metabolics that accumulate due to enzymatic failure to convert them to cortisol are shunted over to other steroidogenic pathways & the net result is an increase in adrenal androgens

Human Physiology 1 (32 decks)

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