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FHB IV- Endocrinology > Endocrinology 2 > Flashcards

Endocrinology 2 Flashcards

1
Q

Categorize and differentiate properties of hormones based on their chemical structure.

A

Amines (half life: 2-3 minutes)
Catecholamines: derived from single tyrosine
Indoleamines: derived from single tryptophan

Thyroid hormone (T4/T3): derived from 2 tyrosines
(very long half life – T4 = 8 days; T3 = 24 hours)

Peptides/Proteins (half life: 4-170 minutes)
most hormones are of this type

Steroids (half life: minutes to several hours)

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2
Q

What kind of hormone is derived from tryptophan?

A

indoleamine

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3
Q

What kind of hormone is derived from one tyrosine?

Derived from 2 tyrosines?

A

one tyrosine - catecholamines

2 tyrosines- thyroid hormone

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4
Q

Which hormone has the longest half life?

A

thyroid hormone (T4/T3)

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5
Q

Compare and contrast catecholamines and indoleamines. Describe their basic biosynthetic pathways and inactivation mechanisms.

Half life?
How they travel in blood?
How they activate?
Main difference?

A

Half-life is very short. These hormones act very fast and are rapidly degraded.

Travel freely in the blood

Always bind to a membrane receptor to activate second messenger signaling pathways.

  • *Main difference = synthesis
  • tyrosine or tryptophan
  • tyrosine hydroxylase or tryptophan hydroxylase
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6
Q

Give example of tyrosine-derived hormones.

What is the RLS?

A

Dopamine, Norepinephrine, Epinephrine (aka – adrenaline)

Tyrosine hydroxylase is rate limiting step. Often used as a marker for dopaminergic activity

Slide 10

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7
Q

Describe dopamine and its action.

Which 2 body organs is it made in?

A

Functions as a neurotransmitter and a hormone

Dopamine is made in 2 main body organs:

1. Brain: 
substantia nigra (Parkinson Disease), ventral tegmental area 
arcuate nucleus (for release to pituitary).

Regulates multiple brain functions as neurotransmitter – reward pathways, attention, mood

  1. Adrenal Gland: adrenal medulla where it is converted to norepinephrine.

Hormone action: inhibits prolactin release from the anterior pituitary.

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8
Q

How is norepinephrine synthesized?

A

from dopamine in adrenal medulla with dopamine Beta hydoxylase

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9
Q

Describe the role of dopamine.

From where do dopaminergic neurons arise?

Where is dopamine released?

How are DA concentrations maintained?

A

Tonic inhibitor of prolactin in the anterior pituitary

Dopamingergic neurons arise from arcuate nucleus

Dopamine is released into hypophysial capillary bed

Dopaminergic neurons in the arcuate are distinct from those in other parts of the brain – TH is constitutively active maintaining high DA concentrations in arcuate

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10
Q

Describe norepinephrine.

What does stimulation require?

Describe tissue concentrations. Where does conversion take place?

What catalyzes the reaction?

A

Functions as a neurotransmitter and hormone

Requires sympathetic nervous system stimulation

Most tissue concentrations equal that of the synapse – conversion takes place primarily in neurons

Dopamine beta-hydroxylase catalyzes reaction

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11
Q

What type of neurons release NE?

Describe the receptors through which NE acts.

What innervates the adrenal medulla where conversion to epi occurs?

Which cells release hormone into the blood?

A

Sympathetic post-ganglionic neurons release NE

NE acts through both alpha- and beta-adrenergic receptors

Splanchnic nerve innervates the adrenal medulla where conversion to epinephrine occurs

Chromaffin cells of adrenal medulla are homologous to postsympathetic neurons – release hormone into blood

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12
Q

Draw/write out the reaction for what can be synthesized from tryptophan.

What step is rate limiting?

A

Slide 15
Tryptophan to serotonin to melatonin

Tryptophan hydroxylase (TPH) is rate limiting

Serotonin – both a neurotransmitter and a hormone

Melatonin – hormone produced in pineal gland
(rate limiting enzyme = SNA)

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13
Q

Describe serotonin.

Name?
What type of cells (and where) is most serotonin produced?

A

Neurotransmitter in the brain
“the happiness hormone”

Most (95%) of the serotonin in the body is produced by enterochromaffin cells in gut

Vasoconstrictor
Stimulates smooth muscle contraction in intestine

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14
Q

Describe the two primary mechanisms of monoamine metabolism..

Describe the enzymes involved in these processes.

A

DEAMINATION AND METHYLATION

Monoamine Oxidase (MAO) = oxidative deamination

  • removes an amine group resulting in aldehyde and ammonia
  • inactivates catecholamines and indoleamines

Catechol-O-methyltransferase (COMT) = adds a methyl group
-metabolism of catecholamines

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15
Q

What does monoamine oxidase do?

A

Monoamine Oxidase (MAO) = oxidative deamination

  • removes an amine group resulting in aldehyde and ammonia
  • inactivates catecholamines and indoleamines

MAOIs = pharmaceutical drugs used to treat depression and anxiety disorders

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16
Q

What does Catechol-O-methyltransferase (COMT) do?

A

Catechol-O-methyltransferase (COMT) = adds a methyl group
-metabolism of catecholamines

Aldehyde dehydrogenase (AD) = oxidation of aldehydes

17
Q

Draw a graph/flow chart of catecholamine metabolism starting with epinephrine and norepinephrine.

A

Slide 18

18
Q

How do Selective serotonin reuptake inhibitors (SSRI) function? What are they used to treat?

What are some important clinical considerations to keep in mind?

A

Increases the concentration of serotonin at the synaptic cleft.

Used clinically to treat depression and other related mental health disorders

Clinical Considerations:
Physiological basis of depression is not well understood

Desensitization/downregulation of postsynaptic receptors

Negative feedback – less serotonin produced in presynaptic cells

(Slide 19)

19
Q

Explain the anatomical location of the pineal gland and the structure/function of melatonin.

What is rate limiting enzyme?

A

Converted from serotonin in the pineal gland

N-acetyltransferase is the rate limiting enzyme and is most active during the night.

Used therapeutically for variety of conditions including insomnia, jet lag, seasonal affective disorder, migrane, etc.

Potent inhibitor of reproduction – causes decreased spermatogenesis and testis size in males.

20
Q

Describe how light is conveyed to the SCN.

What does the SCN do?

When does melatonin peak?

A

Light information is conveyed to the SCN via the retinohypothalamic tract (RHT).

The SCN transmits the information to the pineal gland to regulate its circadian activity.

Melatonin is undetectable during daytime and peaks in the middle of the night.

21
Q

Describe the steps involved in the post-translational processing of peptide and protein hormones.

A

Slide 24

22
Q

For the following endocrine organs provide the hormone, basic structure and half life.

Hypothalamus
Pituitary
Thyroid
Parathyroid
Pancreas
Adipose Tissue
Kidney
Liver
Heart
A

Slide 25

23
Q

Describe the biosynthetic pathways of steroid hormones and recognize specific enzymes important for their conversion from precursor hormones.

A

Slide 28, 29

24
Q

From what precursor are steroids derived?

Describe the steroids that come from adrenal cortex, kidney, placenta, testis, ovary.

A

Steroids – all derived from cholesterol precursor.
Adrenal Cortex: Cortisol (human), mineralocorticoid, DHEA, androstenedione

Kidney: Vitamin D

Placenta: progesterone, estriol

Testis: testosterone

Ovary: 17β-estradiol, progesterone

25
Q

(Obj: Diagram hormone feedback pathways and provide an example of each type of feedback.)

Explain the components of an “endocrine axis”

What is short loop and long loop?

A

Three tiered biological system: hypothalamic neurons, anterior pituitary cells, peripheral endocrine gland

Hormones can exert feedback to regulate any part of the axis

Important for diagnosing cause of endocrine disorder

slide 32

“Short loop” – hormone feedback from pituitary to hypothalamus

“Long loop” – hormone feedback is at level of hypothalamus/ pituitary

26
Q

Describe negative feedback (general model and osmoregulation)

At what points can negative feedback from hormone occur?

A

slide 31, 34

at pituitary and hypothalamic

27
Q

Give four examples of positive feedback in the body.

A

Partuition – childbirth
Contractions stimulate oxytocin release from hypothalamus —more contractions stimulate more oxytocin – birth stops loop.

Lactation
Suckling stimulates oxytocin release from hypothalamus —more suckling stimulates more oxytocin – lack of suckling stops loop.

Ovulation
LH stimulates estradiol in developing follicle – estradiol stimulates more LH – release of oocyte stops loop

Blood clotting
Tissue injury activates platelets — platelets activate more platelets – clotting stops release of signals that activate platelets

28
Q

Look at the graph on p 37. What is the primary defect?

A

Primary defect = high baseline TSH due to loss of negative feedback (low T3), normal pit response to TRH.

29
Q

Compare/contrast failure at pituitary vs failure at hypothalamus.

A

Failure at pituitary (secondary)
No response to TRH
Undetectable TSH levels

Failure at hypothalamus
(tertiary)
Normal response or protracted return to baseline

teritiary lines are harder to diagnose… often looks like things in normal range
slightly higher than normal baseline. some lack of negative feedback. protracted response bc normally not making TRH which causes TSH receptors to down regulate over time. get some response, some receptors traffic to membrane and some return to baseline. normally tertiary conditions v hard to diagnose.

Low basal levels and delayed return to baseline following TRH
stimulation indicates tertiary defect.

30
Q

What is Euthyroid sick syndrome?

A

Euthyroid sick syndrome
Hypothyroid symptoms with low T4/T3
Normal TSH and thyroid

Primary defect = high baseline TSH due to loss of negative feedback (low T3), normal pit response to TRH.

31
Q

What are 5 factors affecting circulating hormone levels?

A 
AGE
BODY WEIGHT
TIME OF DAY
MALE/FEMALE
DIET

Important to recognize that “normal range” will change with age and sex.

32
Q

Describe ANP/BNP. Which has the longer half life? What is significance of this?

What can normal levels rule out?

What are higher levels associated with?

What are lower levels associated with?

How does this change with age?

Are levels higher in men or women?

A

ATRIAL AND BRAIN NATRIURETIC PEPTIDES (ANP, BNP)
-Made in heart; Regulates blood pressure

BNP – longer half-life than ANP making it a useful diagnostic tool

Normal levels can rule out congestive heart failure

Higher levels with heart and renal failure

Lower levels with obesity

Increases with age

Higher levels in women

33
Q

What would it look like if there was a primary or secondary failure?

A

Slides 37-39

34
Q

How do the following change with age (in terms/refernce of peripuberty and perimenopause)

catecholamines
glucocorticoids
testosterone
estradiol
andrenal androgens
interleukin 6
A

Slide 42

FHB IV- Endocrinology (17 decks)

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