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BIOM3200 > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

what is the homeostasis

A

Maintenance of a stable internal environment necessary for normal body functioning

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2
Q

is Stable ≠ static

A

Stable ≠ static
State of dynamic equilibrium
BALANCE of everyday physiological
processes

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3
Q

how is homeostasis in the internal enviornment

A

Our internal environment remains remarkably
consistent despite changes in the external
environment

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4
Q

does specialized organs allow moving the chemicals from the external enviornment to the internal enviornment in the body

A

Specialized organ systems allow movement
of chemicals from the external to the internal
or vice versa

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5
Q

what does homeostatic mechanism provide

A

• Homeostatic mechanisms provide the stable

conditions necessary for cell function

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6
Q

what fetures helps organs to mentain the homeostasis

A 
Every organ in your 
body helps to maintain 
homeostasis through 
neural and/or hormonal 
mechanisms
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7
Q

what are the enviornmental changes controlled by

A
  • Constant monitoring of the composition of blood (multiple sensory systems)
  • Responding to changes in blood composition (multiple response systems)
  • Most response systems operate in a negative feedback manner
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8
Q

what are the two factors in the enviornmental changes

A

Neurotransmitters + Hormones

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9
Q

body is the communication between …… and ……..

A

The body’s means of communication between cells and tissues

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10
Q

what is the homeostasis control mechanism

A

• SENSOR: Responsible for constant monitoring
• INTEGRATOR: Coordination of response(s)
• EFFECTOR: Response to effect change in
variable(s)

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11
Q

what are the sensor, integrator and affector in lyding&raquo_space;»>stanging up

A 
blood pressure falls: simulator 
blood pressure receptor responed: sensor 
brain: integrator center 
heart rate increase: affector 
4. rise blood pressure : affect
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12
Q

what is the 10th leading death in canada

A

Mellitus diabets

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13
Q

how many of the canadians have the thyroid disorders

A

1 in the 10 canadians

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14
Q

what are the distruption of the homeostasis that cause the disease in the body

A 
Overproduction: Hypersecretion
Underproduction: Hyposecretion
Hormone resistance
Transport or clearance problems
Hormone resistance
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15
Q

what is the endocrine physiology

A

Endocrine Physiology
The study of hormones and their actions
The study of how endocrine glands regulate
the physiology and behaviour of animals

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16
Q

what is the endocrine glands

A

Endocrine Glands
Any tissue which releases (secretes)
hormones into the bloodstream to effect
change in another tissue

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17
Q

what is the dicovery of pancreas involved in

A

Discovery of pancreas involvement in

diabetes

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18
Q

how Discovery of pancreas involvement in

diabetes

A

1.Surgically remove pancreas => dog
develops symptoms of diabetes
2. Implant pieces of pancreas under skin =>
prevents symptoms of diabetes

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19
Q

how the insulin is descovred

A

Discovery of insulin
(Banting and Best, 1921)
1. Identified anti-diabetic substance in
pancreatic extracts
2. Injected extracts prevented symptoms of
diabetes (prevents elevated blood
glucose)

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20
Q

how is the affect of the affect of the molecules secregation on the endocrine glands

A

Molecules secreted by endocrine
glands (organs) into the extracellular
the fluid that exerts their effects on the target
tissues some distance away

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21
Q

what are the level of the effcet

A

autocrine: secretory cell and the target cell are in the same tissue
paracrine: secretory cells affect target cells and other nearest tissue
endocrine : secretory cell segregate hormone in the blood stream and it goes through the target tissue via the circulatory system

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22
Q

what are the classes of the hormons

A

Amines
Peptides
Proteins
Steroids

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23
Q

what are the amins hormones

A

Norepinephrine
Epinephrine
Thyroxine
Melatonin

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24
Q

what are the peptid hormones

A

Hypothalamic
hormones
Insulin

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25
Q

what are the protein hormones

A

Growth hormone

Prolactin

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26
Q

what are the stroids hormones

A

Glucocorticoids
Mineralocorticoids
Gonadal steroids

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27
Q

what is the synthesis , storage , release from cell, transport in blood , half life, and example of the peptides/ proteins

A 
Synthesis> In advance
Storage >Secretory vesicles
Release from cell >Exocytosis
Release from cell > Exocytosis
Half life> Short
Example> Insulin
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28
Q

what is the synthesis , storage , release from cell, transport in blood , half life, and example of the Steroids

A 
Synthesis > On demand
Storage > --
Release 
from cell >Diffusion
Transport in blood> Bound to carrier proteins
Half life>Long
Example >Estrogen
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29
Q

what is the synthesis , storage , release from cell, transport in blood , half life, and example of the Amines
(Catecholamines)

A 
Synthesis>In advance
Synthesis > In advance
Release from cell> Exocytosis
Transport in blood> Dissolved in plasma
Half life > Short
Example > Epinephrine
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30
Q

what is the synthesis , storage , release from cell, transport in blood , half life, and example of the Amines
(Thyroid)

A 
Synthesis >In advance
Storage > Secretory vesicles
Release from cell > Diffusion
Transport in blood> >Bound to carrier proteins
Half-life > Long
Example > Thyroxine
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31
Q

how hormones binf tot the receptors in the target cell

A

Hormones bind non-covalently to

receptors in/on target cells

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32
Q

where are the receptors for most hormones

A

• The receptors for most hormones
are found in the plasma membrane
of target cells

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33
Q

where are the receptors for steroid and thyroid hormones

A

• The receptors for steroid and
thyroid hormones are found in the
cytoplasm/nucleus of the target
cells

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34
Q

are receptor very high specificly

A 
Receptors have very high 
specificity for a particular 
hormone (e.g., insulin receptors 
usually only bind insulin), but some 
non-specific binding does occur
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35
Q

• There is continuous turnover of
the receptor-hormone complex
(essential for any signaling system

A

• There is continuous turnover of
the receptor-hormone complex
(essential for any signaling system

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36
Q

what kind of the hormone receptor do we have in the body

A

transmembrane receptor&raquo_space; most hormones
cytoplasm ( majority )
nucleus( thyroid hormone recptor )

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37
Q

how does the Transmembrane receptor works

A

Use second messenger systems

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38
Q

what are the second Transmembrane receptor types

A

G-protein linked receptors

Tyrosine kinase receptors Cytokine receptors

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39
Q

what are the two types of the G-protein linked receptors

A

Two types:
Adenylate cyclase-cAMP
Phospholipase C-Ca2+

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40
Q

how does G-protein linked receptors work

A

Downstream effects promote
phosphorylation + activation of enzymes responsible
for carrying out hormone’s effect

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41
Q

how does Tyrosine kinase receptors

Cytokine receptors work

A

Directly phosphorylate + activate enzymes responsible for carrying out hormone’s effect

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42
Q

which hormones use the second messenger

A

All hormones EXCEPT for steroid/thyroid hormones use 2nd messenger systems

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43
Q

what are the examples for the Adenylate cyclase-cAMP 2nd messenger system

A

Example: Norepinephrine + epinephrine

(catecholamines) beta adrenergic receptors

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44
Q

what are the Adenylate cyclase-cAMP 2nd messenger system steps

A

Steps:
1. Hormone binds to receptor
2. Alpha subunit dissociates from G proteins
3. Alpha subunit activates adenylate cyclase
4. cAMP is formed
5. cAMP activates protein kinase
6. Protein kinase phosphorylates various
enzymes in the cell

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45
Q

what are the Phospholipase C-Ca2+ 2nd messenger system examples

A

Example: Norepinephrine + epinephrine (catecholamines) alpha 1 adrenergic receptors

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46
Q

what are the Phospholipase C-Ca2+ 2nd messenger system steps

A

Steps:

  1. Hormone binds to receptor
  2. Alpha subunit dissociates from G proteins
  3. Alpha subunit activates phospholipase C
  4. DAG and IP3 is formed
  5. IP3 enters endoplasmic reticulum
  6. Stored Ca2+ diffuses into cytoplasm
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47
Q

explain the insulin receptor

A
  1. two half receptors form dimer prior to insulin binding
  2. insulin binding causes autophosphorylation of receptor
  3. activate tyrosine kinase of receptor phosphorylate insulin receptor substrate
  4. activate signaling molecule causes cascade of the effect
  5. glucose uptake and anabolic reaction
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48
Q

what are the Cytokine 2nd messenger system examples

A

Example: Growth hormone receptor

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49
Q

what are the Cytokine 2nd messenger system steps

A

Steps:
1. Hormone binds to receptor
2. JAKs are activated
3. Activated JAK proteins then phosphorylate
STAT proteins
4. Activated STAT proteins translocate to
nucleus to influence gene expression

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50
Q

what is the Nuclear hormone receptors example

A

Example:

Thyroid hormones

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51
Q

what is the Steroid hormones’s receptors steps

A 
Steps:
1. Steroid hormone transported bound to 
a plasma carrier protein
2. Steroid hormone binds to a receptor in 
the cytoplasm
3. Translocates to the nucleus, binds to DNA (acts 
as a transcription factor)
4. Stimulates gene transcription
5. Protein products 
6. Hormone response
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52
Q

what are the Thyroid hormones Steps:

A 
Example: Thyroid hormones
Steps:
1. Thyroxine hormone (T4) usually bound to 
carrier protein 
2. T4 is converted into T3 (triiodothyroxine)
3. T3 enters nucleus
4. Hormone-receptor complex binds DNA 
5. New mRNA
6. Protein synthesis
7. Hormone response
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53
Q

what is the role of the hormones in the changes in tissues

A

To enact change in tissues, many hormones are controlled via negative feedback mechanisms through hormone producing structures

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54
Q

what are the hormone producing structures:

A
  1. Endocrine organs within the hypothalamus-pituitary glandtarget cell (HPTC) axes
  2. Endocrine cell groups/zones/layers
    • E.g. pancreatic islets, adrenal medulla
  3. Dispersed endocrine cells
    • E.g. gut hormones, thyroid parafollicular cells
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55
Q

what are the The biological relevance of HPTC axes

A

Links the endocrine system to the environment via the brain Step-wise increase in signal from
hypothalamus => pituitary gland => peripheral target tissues
Adjustments can be made at several different levels of each axis

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56
Q

HPTC axeis connect two things

A

Links the endocrine system to the environment via the brain

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57
Q

what does HPTC step-wise increase

A

Step-wise increase in signal from hypothalamus => pituitary gland => peripheral target tissues

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58
Q

can adjustment make at the HPTC

A

Adjustments can be made at several different levels of each axis

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59
Q

what does anterior pituitary control in the body

A

endocrine glands

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60
Q

what does posterior piturity control in the body

A

extension of neural tissues

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61
Q

what is the Hypothalamus and Pituitary Gland protected by

A

protected by bone

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62
Q

what are the two system that hypothalamus is master of

A

Hypothalamus is the master
controller of lower autonomic
functions AND the endocrine system

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63
Q

hypothalamus produce and secretes hormones into ……… and ………. lobe of the pituitary glands

A

Produces and secretes hormones
into the anterior and posterior lobe
of the pituitary gland

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64
Q

when does the hypothalamus produce or secrete hormones

A

Receives feedback from target
tissues to promote or inhibit
hormone production/release

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65
Q

what is the Pars distalis

A

Pars distalis: anterior lobe (endocrine part of pituitary gland)

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66
Q

what is the Pars tuberali

A

Pars tuberalis: wraps around

infundibulum

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67
Q

what is the Infundibulum

A

Infundibulum: funnel-shaped

structure

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68
Q

what is the Posterior lobe:

A 
Posterior lobe: neural part of the 
pituitary gland (pars nervosa)
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69
Q

what is the action of the ADH/ oxytocin with the axonal

A

Axonal projections from neurosecretory cells of the hypothalamus supply pars nervosa with ADH/oxytocin

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70
Q

what are the Supraoptic nucleus neurosecretory

cells

A

Supraoptic nucleus neurosecretory

cells: ADH/oxytocin

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71
Q

what is the Paraventricular nucleus

neurosecretory cells

A

Paraventricular nucleus
neurosecretory cells:
Other hypothalamic hormones

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72
Q

what does Paraventricular nucleus neurosecretory cells do

A

These cells produce hypothalamic hormones
that are secreted into blood capillaries to
reach the anterior pituitary

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73
Q

what are the Importance of the anterior lobe

A 
Function of target glands is dependent 
upon adequate stimulation by anterior 
pituitary (AP) hormones
Hypothalamic hormones are secreted 
into the portal venules that bring them 
to the AP
Endocrine cells respond to hypothalamic 
hormones and secrete OR inhibit 
release of AP hormones
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74
Q

function of the target glands is depends upon what ??

A

Function of target glands is dependent
upon adequate stimulation by anterior
pituitary (AP) hormones

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75
Q

Importance of the anterior lobe

A 
Function of target glands is dependent 
upon adequate stimulation by anterior 
pituitary (AP) hormones
Hypothalamic hormones are secreted 
into the portal venules that bring them 
to the AP
Endocrine cells respond to hypothalamic 
hormones and secrete OR inhibit 
release of AP hormones
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76
Q

what are the hormones of the hypothalamus

A

dopamine (PIH) inhibits secretion of prolactin
PRH ( prolactin-releasing hormones ) Stimulates the release of prolactin TARGET THE MAMMARY GLANDS
thyrotropin-releasing hormone ( TRH) Regulates the secretion of thyroid-stimulating
hormone (TSH) thyroid
Corticotropin-releasing hormone (CRH) Regulates secretion of adrenocorticotropic hormone (ACTH) & melanocyte-stimulating hormone (MSH) Adrenal cortex & skin and hair
Somatostatin (growth
hormone inhibiting hormone; GHIH) Inhibits secretion of growth hormone (GH) Growth hormone releasing hormone (GHRH) Stimulates secretion of GH target cells&raquo_space;>Many (liver, muscle, bone, etc.)
Gonadotropin-releasing hormone (GnRH) Regulates secretion of luteinizing hormone (LH) and follicle stimulating hormone (FSH) target gland/tissue is Gonads
Antidiuretic hormone (ADH) released by posterior pituitary) target tissue /cell&raquo_space;» Kidney

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77
Q

what is the CRH

A

CRH (Corticotropin releasing hormone)
Peptide hormone, G-protein-coupled
receptor (cAMP) on cells in anterior
pituitary

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78
Q

what is the ACTH

A

ACTH (Adrenocorticotropin hormone)
Peptide hormone, G-protein-coupled
receptor (cAMP) on cells in the adrenal
cortex

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79
Q

what is the ACTH

A

ACTH (Adrenocorticotropin hormone)
Peptide hormone, G-protein-coupled
receptor (cAMP) on cells in the adrenal
cortex

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80
Q

how does the CRH produced

A

CRH synthesis and release
Produced by neurosecretory cells within the
paraventricular nucleus of the hypothalamus
under noradrenergic stimulation

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81
Q

how does the CRH released

A

Released into blood vessels in the

hypothalamo-pituitary portal system

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82
Q

how does the capillaries bring CRH to simulate the G-protein

A

Capillaries bring CRH to stimulate G-proteincoupled receptors on cells in the anterior pituitary to produce POMC (prohormone)

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83
Q

what is the precursor molecule

A 
Many hormones are derived from a 
precursor molecule (prohormone)
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84
Q

where does the processing of prohormone > hormone happens

A

Processing of prohormone => hormone

usually occurs within the gland cell

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85
Q

what are the prehormones

A

Prehormones: Inactive hormones are
converted after secretion to become
active in their target cells

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86
Q

what are some example of the prehormones

A

Examples of prehormones:
• Vitamin D3 is converted to 1,25-
dihydroxyvitamin D3 in target tissue

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87
Q

where does T4 convert to T3

A

Thyroxine (T4) is converted into triiodothyronine

(T3) in target tissue

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88
Q

what is the Pro-opiomelanocortin:

A

Pro-opiomelanocortin: A prohormone for many hormones

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89
Q

POMC is a precursor of which hormones

A

POMC is a precursor for ACTH,

MSH, and other hormones

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90
Q

in AP what has happend to the POMC

A

In the AP, POMC is produced

and cleaved into ACTH and Blipotropin

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91
Q

what is ACTH released by

A

Active ACTH hormone is released by anterior

pituitary and travels to adrenal glands

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92
Q

what does ACTH binds to

A

binds to MC2R (melanocortin-2 receptor; Gprotein-coupled)

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93
Q

what are the primary and secondery actions of the ACTH

A

Primary action: Stimulates secretion of
glucocorticoids (cortisol)
Secondary action: Stimulates secretion of sex
steroids

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94
Q

what is the adrenal glands

A

The Adrenal Glands
Paired organs that cap the superior borders of
the kidneys
Consist of an outer cortex and inner medulla
(function as separate endocrine glands)

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95
Q

what does medulla produces

A

Medulla: Produces catecholamines

epinephrine

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96
Q

what is the cotex made of and what are the each layer responsibility

A

Cortex: A steroid factory (corticosteroids)

  1. Zona glomerulosa: mineralocorticoids
    (aldosterone) – regulates Na+ and K+ balance
  2. Zona fasciculata: glucocorticoids
    (cortisol) – regulates glucose balance
  3. Zona reticularis: sex steroids (adrenal
    androgens) – produced in small amounts
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97
Q

what is the starting material for the Steroidogenesis

A

Starting material: Cholesterol

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98
Q

what is common between steroid production

A

ALL steroid production begins with
the conversion of cholesterol to
pregnenolone

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99
Q

how to make cortisol

A

ACTH (through cAMP) stimulates insertion of StAR protein in the MB StAR protein helps cholesterol move to the inner membrane where it is then converted into pregnenolone Pregnenolone is then converted through a series of steps to become cortisol

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100
Q

what is the main glucocorticoid in the animals

A

Corticosterone is the
main glucocorticoid in
amphibians, reptiles,
rodents, and birds

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101
Q

what is the main glucocorticoid in the humans

A

Cortisol is the main

glucocorticoid in humans

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102
Q

how does cortisol is released

A

Cortisol Release triggered by:
• Chronic stress (trauma, starvation, exam season, etc.)
• Hypoglycemia

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103
Q

what are the immune system of the cortisol

A

Cortisol
Immune system:
• Decreases cytokine production
• Reduces the production of some immune cells and
cytokines
• Cortisol is a natural immunoregulatory hormone, but
can also be used clinically as an anti-inflammatory
agent

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104
Q

what are the glucose metabolism of the cortisol

A

Glucose metabolism:
• Primary regulator of glucose metabolism during
fasting/starvation
• REDUCES glucose uptake in tissue and
PROMOTES gluconeogenesis and glycogenolysis in
liver

105
Q

see lecture endocrine 2 page 19

A
106
Q

what cause the Cortisol Excess

A

Primary hyperadrenocorticism: adrenal tumour causes over-secretion of cortisol (Cushing’s syndrome)
• Secondary hyperadrenocorticism: Pituitary tumour causes over-secretion of ACTH leading to excess cortisol (Cushing’s disease) –MORE COMMON
• Endogenous incidence is rare, but can occur after prolonged exposure to exogenous glucocorticoids

107
Q

how does the cortisol affects the appearence of the body

A

Cortisol Excess
• Causes changes in metabolism; hyperglycemia;
hypertension; muscular weakness
• Metabolic problems give rise to puffy
appearance, CNS disorders (depression, decreased
learning, memory, etc.)

108
Q

what are the treatments for the hyperglycemia, anti-hypertensive

A

Treatment:
• Surgery
• Drugs to inhibit steroidogenesis
• Medical management of symptoms (insulin for
hyperglycemia, anti-hypertensives for BP)
• If not treated, overall health can deteriorate;
worsening diabetes, high BP can lead to strokes
or heart attack

109
Q

what cause the cortisal deficiency

A

Causes:
• Primary hypoadrenocorticism: Destruction of
adrenal cortex causes under-secretion of
adrenal cortex hormones (Addison’s disease)
– MORE COMMON
• Secondary hypoadrenocorticism: Destruction of
pituitary gland causes under-secretion of ACTH
• Treatment for Cushing’s can result in symptoms
of Addison’s disease

110
Q

what is a disorder caused by the cortisol secretion

A

Primary Hypoadrenocorticism

Addison’s Disease

111
Q

(Addison’s Disease) diagnosis

A 
Diagnosis:
• Weight loss, poor appetite, weakness, 
BP changes, hyperpigmentation*, 
hypoglycemia, low blood sodium (from 
↓ aldosterone)
• ACTH stimulation test
Treatment:
• Steroid preparations (aldosterone & 
cortisol analogs)
112
Q

how does the skin afftected by the secrecate of the ACTH

A

*Increased ACTH → POMC → increased MSH (melanocyte stimulating hormone) → more pigment in skin

113
Q

what is the result of the increase in basal metabolic rate

A

INCREASE basal metabolic rate!
• More ATP production
• More heat production

114
Q

what are the hormones in the thyroid axies

A 
TRH: Peptide hormone with a Gprotein coupled receptor (IP3/DAG)
TSH: Protein hormone with Gprotein coupled receptors (both 
cAMP & IP3/DAG)
Thyroxine (T4): Amine hormone, 
can freely cross the cell membrane 
and become T3
Triiodothyronine (T3): Amine 
hormone, nuclear receptor
115
Q

what is the anathomy of the thyroid gland

A

Anatomy
Situated below larynx (voice box) on either side of the trachea Two lobes and an isthmus connecting the two sides (prominent isthmus in humans, cows, horses; indistinct in dogs/cats) Largest purely endocrine gland (20-25 g in humans, 10-15 g in dogs)Also home to parathyroid glands

116
Q

where is the thyroid follicles

A

Thyroid follicles are where T4 (and

some T3) are produced

117
Q

what is the macroanathomy of the thyroid

A

Microanatomy
Thyroid follicles are where T4 (and some T3) are produced Follicular cells (thyrocytes) surround thyroid follicles and uptake iodide (I-) from surrounding blood vessels Follicles are filled with colloid, which contains thyroglobulin and enzymes to synthesize T4 and T3 Parafollicular cells dispersed throughout synthesize calcitonin (next lecture)

118
Q

what is the role of the thyrocyets

A

The role of thyrocytes Iodide (I-) from the blood is transported into the cell by a Na+/I- symport protein Production of thyroglobulin (TG): TSH-mediated gene transcription + protein translation occurs in thyrocytes TG is a long peptide chain with lots of tyrosine side chains on it; once produced it is exocytosed to the lumen (colloid space) Iodide channels pump I- into the colloid space

119
Q

How is thyroid hormone produced? ( first 3 steps )

A
  1. Iodide enters colloid and is converted from iodide to iodine by thyroid peroxidase (TPO)
  2. Once oxidized, iodine can bind, one at a time, to tyrosine residues on
    thyroglobulin (thanks to TPO)
  3. This makes: One iodine + one tyrosine = monoiodotyrosine (MIT; T1)
    Two iodines + one tyrosine = diiodotyrosine (DIT; T2)
120
Q

How is thyroid hormone produced? ( second 3 steps )

A
  1. Thyroglobulin brings bound MIT and DIT molecules together
  2. Enzymes in the colloid modify the structures of MIT and DIT to make thyroid hormones:
  3. T3 (TRIiodothyronine)
  4. T4 (TETRAiodothyronine or thyroxine)
  5. TSH stimulation induces thyrocytes to take up bound T3 and T4, hydrolyze them from thyroglobulin, and secrete hormone into the blood
121
Q

How is thyroid hormone produced and released?

A

TSH (released by anterior pituitary) stimulates production of TG and release of free T3/T4 from thyrocytes

122
Q

when the circadian secretion is highst in the humans

A

Circadian secretion of T3/T4 (highest between

10 AM and 2 PM in humans)

123
Q

is T3/T4 secretion higher in younger or older animals

A

• T3/T4 secretion higher in younger animals

124
Q

T3/T4 secretion higher under which conditions

A

T3/T4 secretion higher under stress/cold

conditions

125
Q

what are the effects of the physiological action of thyroid

A

MAIN EFFECTS:

1) Regulation of metabolic rate (glucose consumption + ATP production in cells) and thermogenesis (heat production)
2) Appropriate levels of thyroid hormone are essential for normal cardiac function
3) Essential for normal fetal development, particularly gonad and CNS development

126
Q

what is the Hypothyroidism

A

• Hypothyroidism is a condition in which
serum levels of T4/T3 are abnormally
low

127
Q

what are the clinical signs of the Hypothyroidism

A

Clinical signs: Lethargy, weight gain,
exercise intolerance, cold intolerance
(slowing of metabolic processes)

128
Q

what causes the Hypothyroidism

A

• Causes: Immune-mediated destruction
of thyroid gland (often); iodide
deficiency in diet

129
Q

secondary or tertiary disease mutant :

A

Less often: Secondary or tertiary disease,
mutant hormone receptors, mutant transport
proteins

130
Q

what is the Hypothyroidism in developing babies

A

Cretinism

131
Q

what is the Cretinism

A

Cretinism: Congenital deficiency of
thyroid hormone production usually due
to maternal hypothyroidism

132
Q

how does the cretinism happens

A

Lack of thyroid hormones from mother in utero (delivered through the placenta) leads to reduced physical growth AND severe mental disability

133
Q

how does thyroid helps in brain development

A

Brain development in utero is a complicated
process; thyroid hormone assists with
neuronal maturation, myelin formation, and
dendritic/axonal growth

134
Q

how many people are suffering from the iodine deficiency

A

approximately 2 billion people

135
Q

what is the Hyperthyroidism

A

• Hyperthyroidism is a condition in which
serum levels of T4/T3 are abnormally
high

136
Q

what are the signs of the hyperthriodism

A 
Clinical signs: Weight loss, heat 
intolerance, increased heart rate, 
increased appetite, diarrhea, vomiting, 
exophthalmia (associated with Graves’ 
disease)
137
Q

what cause hyperthrodism

A

• Causes: Auto-antibody stimulation of
TSH receptors (Graves’ disease);
thyroid tumour

138
Q

what is the Goiters

A 
Goiters
• Excess growth of
thyroid gland
• Associated with both
hypo- and hyperthyroidism
139
Q

see lecture 2 slide 47

A
140
Q

what kind of the hormon is growth hormon

A

Protein hormone

141
Q

what is the growth hormone receptor

A

• Binds to cytokine receptors

142
Q

how long is the growth hormon half life

A

Half-life: 6-20 mins

143
Q

how does the growth hormon mostly transported

A

• Mostly transported bound to a binding protein

GHBP

144
Q

where does growth hormone Synthesized, stored, and secreted?

A

Synthesized, stored, and secreted by somatotropes

in the anterior pituitary

145
Q

which tissues are affecetd by the growth hormon and what do they secrecate

A

growth hormon Signals tissues to produce IGF-1

146
Q

how is the GH secretion patterns

A

• Pulsatile secretion: GH is secreted as several large

pulses or peaks each day, 10-30 mins in duration

147
Q

when does the largest gh peak occurs

A 
The largest GH peak occurs about 1 hr after onset 
of sleep (circadian pattern)
148
Q

explain the lifetime of the growth hormone

A

Lifetime: Overall levels highest early in life; amplitude/frequency are greatest during pubertal growth spurt and then decline throughout adult life

149
Q

what is the result of the studies in the state about the youngsters sleeping and its relationship with the growth hormone

A

Results from the study in the U.S. showed youngsters bed down for 4.5 hours extra a day for two days just before a growth spurt, taking an average of three extra naps a day.

150
Q

what is the effect of the Sleep Increase, Exercise, Hypoglycemia, Hyperglycemia, High dietary protein,Excess cortisol, Endocrine disruptors, Ghrelin (hunger hormone), IGF-1 & Somatostatin o the growth hormone

A 
Sleep Increase
Exercise Increase
Hypoglycemia Increase
Hyperglycemia Decrease
High dietary protein Increase
Excess cortisol Decrease
Endocrine disruptors Decrease
Ghrelin (hunger hormone) Increase
IGF-1 & Somatostatin Decreas
151
Q

growth hormone affects the liver to produce which of the compounds

A

Several classes: IGF-1 through 7 (only discuss IGF-1 and -2)
• Protein/peptide hormone
• Binds to tyrosine kinase receptors
• Half-life: much longer, ~12 hrs

152
Q

where does the IGF-1 many produce and when human have the highest production of it and what it is needed for

A

Mainly produced in liver Low at birth, high at puberty, lower later
in life Needed for skeletal and extra-skeletal development, adipocyte differentiation

153
Q

where does the IGF-2 is produced

A

Produced in many developing tissues
Prominent during embryonic/fetal
growth

154
Q

what are the IGF actions

A

Autocrine
Paracrine
Endocrine

155
Q

what is the relationship between the GH and IGF-1

A

Take home message: GH stimulates IGF-1 synthesis and release in
many tissues, not just the liver! IGF-1 produced by tissues can act
on the same cell OR another cell within that tissue

156
Q

how does GH exert its effects via IGF-1

A

GH exerts many of its effects directly on tissues, but also

indirectly through IGF-1

157
Q

is it easy to differentiate between direct actions of GH and those of
IGF-1

A

Difficult to differentiate between direct actions of GH and those of
IGF-1

158
Q

do GH and IGF-1 have the same actions

A

• GH and IGF-1 appear to exert opposite actions in some tissues,
which suggests that they have independent roles

159
Q

what is the other name of the IGF

A

IGFs are also called

“somatomedins” – they mediate the effects of GH

160
Q

what is the function of the Liver glucose release on the GH and IGF-1 (SEE LECTURE 3 SLIDE 13 OF THE ENDOCRINOLOGY )

A

Liver glucose release Increase>GH Decrease> 1GF-1

161
Q

what are the direct act of the GH on the blood and its indirect effect on the musculoskeletal

A

GH acts directly on many tissues to increase blood levels of fatty acid + glucose
GH acts indirectly through IGF-1 to increase growth of musculoskeletal tissues

162
Q

see lecture 3 slide 15

A
163
Q

which organ of the body release the GHRH

A

GHRH is released from hypothalamus

after a stimulus

164
Q

which organ produces the gh and where does it act on

A

GH is released from anterior pituitary and acts

on liver, fat tissue, and other tissues

165
Q

does the igf-1 inhibits the release of the gh which hormone does it promote

A

IGF-1 produced from liver inhibits release of GH and promotes the production of somatostatin (SST; also called growth hormone inhibiting hormone [GHIH])

166
Q

what is the somatostain

A

somatostatin (SST; also called growth hormone inhibiting hormone [GHIH])

167
Q

what does IGF-1 increase in the blood and what does it inhibit

A

increased fatty acids and glucose in the blood will also inhibit GH release

168
Q

see slide 18 of the lecture 3

A
169
Q

body size increases thanks to what

A

Body size increases thanks to growth and elongation of the

skeleton + associated soft tissues (ligaments, tendons, muscles)

170
Q

bones are growth in which dimentions

A

Bone grows in DIAMETER and in LENGTH during growth phases

171
Q

what is the endochondral ossification process

A

LENGTH: During endochondral ossification (fetal stage) cartilage
cells “mineralize”, eventually giving way to osteoblasts (bone building
cells)
Some cartilage cells left at the epiphyseal plates continue to
proliferate and mineralize, either becoming bone or allowing nearby
osteoblasts to help build more bone (after birth)

172
Q

how does the bone growth in the diameter

A

DIAMETER: Osteoblasts lay down more minerals (calcium and

phosphate) and collagen on the outer surface of the bone

173
Q

what is the result of the GH action on the cartilage cells

A

GH acts directly on cartilage cells, maintaining a resting population
(resting zone) or helping them mineralize (hypertrophic zone)

174
Q

which organs are affected by the GH for the IGF-1 production

A

. GH stimulates production of IGF-1

in liver and in bone

175
Q

how does IGF-1 promote the bone formation

A

. IGF-1 (local and system) helps stimulate chondrocyte proliferation (proliferative zone), mineralization, and osteoblast activity to promote bone formation

176
Q

see slide 24 of the lecture 3

A
177
Q

what is the Acromegaly (post-pubertal disorder)

A
  • Hypersecretion of growth hormone after epiphyseal plate closure
  • Can result in severe disfigurement
  • In >90% of acromegaly patients, the overproduction of GH is caused by a benign pituitary tumour (pituitary adenoma)
178
Q

what is the Gigantism (pre-pubertal disorder)

A

Hypersecretion of growth hormone before epiphyseal plate closure
• Influences IGF release from the liver and therefore stimulates
extensive bone growth
• Usually caused by a tumour on the anterior pituitary gland

179
Q

what is Dwarfism (pre-pubertal disorder

A

Dwarfism (pre-pubertal disorder
• Hyposecretion of growth hormone before epiphyseal
plate closure
• Overall reduction in growth; normal body proportions
(limb:torso)
• Differs from achondrodysplasia (short limbs, normal
torso)

180
Q

what is the Dog breeds

A

Most toy breeds are pituitary (ateliotic) dwarfs (GH deficiency, small all over):
Chihuahuas, Boston Terriers, Italian Greyhounds, Maltese, Miniature Pinschers, Miniature Spaniels, Pomeranians, Toy Poodles, Yorkies, etc.

181
Q

what is the Brachycephalic

A

Brachycephalic: Boxers (shortened skull bones, short muzzle)

182
Q

what is the Micromelic

A

Micromelic (short legged) breeds include: Basset Hounds, Bulldogs, Corgis,
Dachshunds, Lhasa Apsos, Scottish Terriers, Shetland Sheepdogs, etc.

183
Q

what is the role of the calcium salt in the body

A 
Calcium salts (with phosphate) provide the 
structural integrity of bone
184
Q

how much calcium are in the body

A

Total body amount: ~1,200 g of Ca2+ in a

70kg human

185
Q

how does the calcium stored in the body

A

99% of calcium is stored in bones in the
form of hydroxyapatite (Ca10[PO4]6[OH]2)
The rest can be found intracellularly (0.9%)
or extracellularly (0.1%)

186
Q

what is the extracellular ca2+ regulated by

A

Extracellular Ca2+ is very tightly regulated:
• Ionized Ca2+ (“free”: 50%)
• Protein-bound Ca2+ (40%)
• Ca2+ with PO4 and citrate (10%)

187
Q

Intracellular is associated with :

A

Intracellular Ca2+ is also tightly regulated:
• Largely associated with membranes in
mitochondria, endoplasmic reticulum and
plasma membrane

188
Q

how we gat most of the calcium of the body and how does it absorbed

A

Intake: Entirely through diet
~1/3 of calcium is absorbed
through small intestine
Hormone regulated

189
Q

how does the calcium output works

A

Output: Kidneys

Our bodies cannot make calcium Lost through urine, so must be replaced through diet

190
Q

what is the Total body calcium

A

Total body calcium = intracellular + extracellular (ECF/blood + bone)

191
Q

see lecture 3 slide 37

A
192
Q

what is the Parathyroid hormone (PTH)

A 
Parathyroid hormone (PTH)
Peptide hormone produced and secreted by the parathyroid glands
193
Q

what are the chief cells in the parathyroid glands produce

A

Chief cells in parathyroid glands produce

and secrete PTH

194
Q

what is the relationship between the chief cells and ca2+

A

Chief cells respond to changes in Ca2+
serum concentration; PTH is secreted
when Ca2+ levels are low

195
Q

can people live without the thyroid

A

People can live
without a thyroid, but
parathyroid glands are
essential for life!

196
Q

what is the role of the PTH in regulation of Ca2+ levels

A
  1. PTH stimulates osteoclasts to resorb bone (primary mechanism)
  2. PTH stimulates kidneys to reabsorb Ca2+ but inhibits reabsorption of PO43-
  3. PTH stimulates kidneys to produce the enzyme needed to make 1,25 dihydroxyvitamin D3 to promote better absorption of Ca2+ from food across
    the intestinal epithelium
    All three mechanisms raise blood Ca2+ levels
197
Q

how does the PTH regulate the CA+2 level

A

Ca2+-sensitive receptors (CaSR) on
parathyroid cells activate cAMPmediated release of PTH when
Ca2+ signal is missing
PTH then binds to G-proteincoupled receptors on target tissue
(kidney cells, osteoclasts)
PTH is produced/released
continuously, NOT stored

198
Q

is Bone is constantly being formed and

resorbed (dynamic turnover)

A

Bone is constantly being formed and

resorbed (dynamic turnover)

199
Q

what does OsteoCLAST cells do

A 
OsteoCLAST cells dissolve 
hydroxyapatite (Ca10[PO4]6[OH]2) to 
allow free Ca2+ and PO4
3- to move to 
the bloodstream
200
Q

what do OsteoBLAST cells produce?

A

OsteoBLAST cells produce and
secrete collagen (part of bone matrix),
which hardens in the presence of
hydroxyapatite

201
Q

how does the CA2+ reabsorption happens

A

Ca2+ reabsorption primarily takes place in the distal tubules PTH regulates a calcium channel protein to facilitate Ca2+ reabsorption from tubular fluid into
the bloodstream PTH inhibits PO4 3- reabsorption to reduce bone formation

202
Q

how does pth use the vitamin d3 for the regulation

A

PTH also regulates conversion of a
prehormone (Vitamin D3) to active
hormone 1,25-dihydroxyvitamin D3

203
Q

how does the vitamin d3 synthesized

A

Vitamin D3 is either synthesized with
exposure to sunlight or ingested through
diet

204
Q

what happens to the vitamin d3 in the liver

A

Vitamin D3 is converted to 25-

hydroxyvitamin D3 in the liver

205
Q

what happens for the vitamin d3 in the kidneys

A

Converted to 1,25-dihydroxyvitamin D3
in kidneys thanks to 1α-hydroxylase
(stimulated by PTH)

206
Q

what are the primary and secondary mechanism of the d3

A 
Primary mechanism: Stimulates active 
transport of Ca2+ from intestine to 
bloodstream when [Ca2+] is low 
Secondary mechanism: Active 
reabsorption of Ca2+ AND PO43- from kidney
207
Q

does d3 provide ca2+ and po4-3

A

Provides Ca2+ and PO43- for bone deposition

208
Q

what happens when there is a ca2+ deficiency

A

When diet is Ca2+ deficient: Stimulates
the production of more osteoclasts
(primary goal ALWAYS is to raise blood Ca2+)

209
Q

how do the PTH and 1,25-dihydroxyvitamin D3 increase blood Ca2+

A

Together, PTH and 1,25-dihydroxyvitamin D3 increase blood Ca2+ by:

  1. Increasing intestinal absorption of Ca2+
  2. Promoting osteoclast activity
  3. Increasing Ca2+ reabsorption in kidney Increased Ca2+ levels leads to reduces PTH secretion
210
Q

what is the Calcitonin produced by

A

Calcitonin is released by parafollicular
cells of the thyroid (C cells) when Ca2+
levels are high

211
Q

what is the role of the calcitonin in the adult humans

A

Plays only a minor role in adult humans
Peptide hormone that is stored until
needed (hypercalcemic conditions)

212
Q

what is the emergency role of the calcitanin

A

May work as an “emergency” hormone

to maintain homeostasis

213
Q

what is the opposing effect of the calcitonin against pth

A

Opposes PTH effect in kidneys and bone

to lower blood Ca2+

214
Q

what is the Hyperparathyroidism

A

Hyperparathyroidism
Non-cancerous growth on the parathyroid
gland(s) causes hypersecretion of PTH

215
Q

what are the Clinical signs and characteristics of Hyperparathyroidism

A 
Clinical signs and characteristics:
• Hypercalcemia
• Increased bone reabsorption 
(increased risk of fractures; 
osteoporosis)
• Appetite loss/weight loss
• Mineralization of soft tissues
216
Q

what causes the Secondary hyperparathyroidism

A

Secondary hyperparathyroidism
can arise due to kidney failure or
vitamin D deficiency

217
Q

what is the Hypoparathyroidism

A

Causes: Idiopathic (ie. Unknown cause);
immune-mediated, or iatrogenic
(“physician-associated”; thyroid removal

218
Q

what are the clinical signs of the Hypoparathyroidism

A 
Clinical signs and characteristics:
• Hypocalcemia + hyperphosphatemia
• Muscular weakness
• Cardiac arrhythmias
• Seizures
219
Q

what is the Rickets

A 
Malnutrition resulting in severe 
calcium and vitamin D deficiency in 
young individuals
Bone malformations, enlarged 
weakened joints, soft skull
220
Q

what is the Osteomalacia

A

Osteomalacia
Vitamin D deficiency and low dietary calcium
in older individuals
Bone “softening” leading to increased fracture
risk, spinal deformation, bone changes

221
Q

what is the Osteoporosis

A

Most common bone disorder
• Bone matrix becomes thinner (less collagen +
hydroxyapatite) due to an imbalance between
bone formation and bone resorption
• Higher risk of bone fractures

222
Q

what are the risk factors for the Osteoporosis

A

Known RISK factors include:
• Age (risk doubles every 5 years between 40 and 60)
• Sex (females are more at risk after menopause)
• Calcium deficient diet or malabsorption
disorders
• Previous fractures

223
Q

how to prevent the osteoporosis

A

• Prevalence: Fractures from osteoporosis are more common than heart attack, stroke and breast cancer combined. More than 2 million Canadians have osteoporosis, 80% of which identify as women

224
Q

how much is the coast of the osteoporosis

A

• Costs: $1.9 billion/year, Canada alone

225
Q

how to prevent the osteoporosis

A

Osteoporosis
Treatment
• Diet modification: Adequate calcium and Vitamin D intake; bone mass begins to decline after 30 years old
• Hormone therapy: Exogenous PTH analogues (low, infrequent doses) and calcitonin can help limit improve bone mineral density (limiting osteoclast activity and/or promoting bone formation); estrogen replacement therapy can be helpful in menopausal women
• Estrogen plays a role in bone formation, and thus menopause presents an osteoporosis risk because of the decline in estrogen

226
Q

how to prevent the Osteoporosis

A

BEST TREATMENT IS PREVENTION!
• Calcium-rich foods, vitamin D supplementation
• Physical exercise (emphasis on resistance exercises

227
Q

what is the GnRH

A

Peptide hormone, G-protein coupled receptor

228
Q

how is the GnRH secretion

A

• Pulsatile secretion (not continuous secretion) results in release of LH/FSH from anterior pituitary (consistent pulses in males; differs in females)

229
Q

what is the FSH hormone

A

Peptide hormone, G-protein coupled receptor
• Acts on Sertoli cells within seminiferous tubules
to support spermatogenesis
• Sertoli cells also produce inhibin, a peptide hormone,
to inhibit FSH release from AP

230
Q

what is the LH (Luteinizing Hormone)

A

• Peptide hormone, G-protein coupled receptor
• Acts on Leydig cells (located between the tubules)
to stimulate them to secrete testosterone
• Testosterone subsequently inhibits release of LH and GnRH

231
Q

how does the gonadal axis affect the Embryonic stage of male

A

Gonadal axis ACTIVE, FSH/LH
promotes differentiation of
gonads/gametes into
testes/spermatogonia

232
Q

how does the gonadal axis affect the Pre-puberty stage of male

A

Gonadal axis SUPPRESSED

233
Q

how does the gonadal axis affect Puberty & onwards of male

A

Gonadal axis ACTIVE, FSH/LH promotes volume increase and final sperm maturation

234
Q

what kind of hormones is testosterone and what kind of the receptors does it have

A

Steroid hormone, intracellular receptor

235
Q

what is the • Major androgen produced in the body

A

testostron

236
Q

what is the testosterone produced by

A

• Produced by Leydig cells upon stimulation by LH

237
Q

what is the testosterone converted from

A 
Converted from pregnenolone in mitochondria of 
Leydig cells (see Steroid Production in Endo Lecture 2)
238
Q

what are the role of the testosterone in the body

A

Sex determination> Development of male primary sex characteristics
(gonads and accessory organs; see future Repro
lectures)
Spermatogenesis.At puberty: Complete maturation of sperm
After puberty: Maintenance of spermatogenesis
Secondary sex characteristics> Growth and maintenance of primary and
accessory sex organsGrowth of facial and axillary hair Body growth
Anabolic effects> Protein synthesis + muscle growthGrowth of bones Growth of other organs (like larynx)

239
Q

what are the Anabolic-androgenic steroids

A

• Synthetic derivatives of testosterone

240
Q

did canada approved the hypogonadism

A

FDA/Health Canada approved treatment for
hypogonadism, delayed puberty in boys, or other
gonadal axis dysfunction

241
Q

what is the Unapproved use of Anabolic-androgenic steroids

A

Unapproved use: Performance enhancement (gain

of muscle mass/strength for sports-related activities)

242
Q

are the derivatives of the Anabolic-androgenic steroids more anabolic or androgenic

A

• Derivatives are more anabolic than androgenic

243
Q

what are the side effects of the Anabolic Steroids

A

Hormonal effects (in males):
• Decreased sperm production
• Decreased size of testes
• Increase in breast tissue size

244
Q

why anabolic steroids have the side affect

A

Testosterone derivatives shut down gonadal axis
• ↓ FSH/LH = suppressed sperm development, ↓
production of endogenous testosterone

245
Q

what is the gynecomastia

A

Testosterone/estrogen imbalance in breast

tissue causes gynecomastia

246
Q

what is the conterception

A 
Contraception (or birth control) is any method 
used to prevent pregnancy 
Can be hormonal-based or non-hormonal 
(barrier)-based (condoms, diaphragms, 
vasectomy) to prevent fertilization
247
Q

what is the Goal of hormonal-based contraceptives:

A

Goal of hormonal-based contraceptives:
Pharmacological agents that prevent ovulation
(females) OR prevent spermatogenesis (males)

248
Q

what is the synthetic progesterone in the body

A

Progestin (synthetic
progesterone, an
ovarian steroid) also
inhibits the gonadal axi

249
Q

what is the progestron

A

Progesterone: Produced from
pregnenolone in theca cells and
granulosa cells of ovaries

250
Q

what is the estradiol

A

Estradiol (type of estrogen):
Produced from androgens
(androstenedione/testosterone) in
granulosa cells of ovaries

251
Q

what is the difference between men and female in terms of the estrogen and progesterone hormones

A

Females with ovaries have higher

estrogen:testosterone than males

252
Q

does fsh/lh act on the ovaries

A

FSH/LH act on ovaries

253
Q

does ovaries make estradiol

A

Ovaries make estradiol that influences egg (ovum)

release into the fallopian tube

254
Q

what are the progesterone and estradiol produce by

A

Estradiol and progesterone produced by ovaries act on

the uterus

255
Q

what is the role of the uteres

A

Uterus prepares for pregnancy; lining is shed if

implantation does not occur

256
Q

what does UTERINE/MENSTRUAL CYCLE: do

A

UTERINE/MENSTRUAL CYCLE:

Prepare uterus for implantation of fertilized ovum

257
Q

what does the OVARIAN CYCLE do

A 
OVARIAN CYCLE: 
Prepare egg (ovum) for ovulation
258
Q

what is the The Ovarian Cycle

A

Low frequency GnRH pulses stimulate FSH production and release from anterior pituitary
• Follicles containing immature ova respond to FSH and grow (follicular phase)
• Granulosa cells within follicles produce and secrete estradiol (a form of estrogen)
• Estradiol acts on hypothalamus to increase frequency GnRH pulses (POSITIVE FEEDBACK)
Increased frequency of GnRH pulses thanks to estradiol = more LH secretion (LH surge)
• LH surge triggers ovulation; remaining follicle becomes corpus luteum
• Corpus luteum produces and secretes progesterone (along with estradiol); luteal phase
• Combined, estradiol and progesterone inhibit LH/FSH secretion through NEGATIVE FEEDBACK

BIOM3200 (3 decks)

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