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Endocrine Flashcards

0
Q

What can PCB’s cause?

A

Polychlorinated biphenyl

It is an environmental endocrine disruptor.

Competes with Thyroid Hormone for its binding protein (TTR:TBG) and causes compensatory increase in thyroid hormone production –> Goiter

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1
Q

What is Cretinism caused by?

What are its symptoms?

A

Cretinism = Congenital Hypothyroidism.
Caused by iodine deficiency in utero.

Symptoms:
Impaired bone formation
Mental retardation
Motor deficits

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2
Q

What can DES cause?

A

Diethylstilbestrol = synthetic estrogen

It is an environmental endocrine disruptor. Was used to prevent pregnancy complications in the past. Increases chance of developing cervical/vaginal cancers by 40%.

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3
Q

What are catecholamines derived from?

A

Tyrosine

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4
Q

What are indolamines derived from?

A

Tryptophan

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5
Q

In what order are catecholamines produced in the catecholamine synthesis pathway?

A

Tyrosine –(Tyrosine Hydroxylase)–> L-DOPA —-> Dopamine –>
Norepinephrine —> Epinephrine

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6
Q

What is the rate-limiting step in catecholamine synthesis?

A

Tyrosine Hydroxylase

Tyrosine —> L-DOPA

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7
Q

Where is Dopamine primarily produced? What is its effect there?

A

In the brain (substantia nigra, VTA, arcuate nucleus).

It modulates reward pathways, attention, mood.

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8
Q

What is Dopamine’s hormone activity?

A

It is released into the hypophyseal portal system and inhibits prolactin release from the anterior pituitary.

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9
Q

What type of neurons tonically release dopamine? Where are they located?

A

TIDA neurons constantly release it. They have a constantly active Tyrosine Hydroxylase. They are located within the arcuate nucleus and release Dopamine into the hypophyseal portal blood.

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10
Q

What does meth do in the brain?

Cocaine?

A

Meth —> increases dopamine release from presynaptic vesicles
Coke —> inhibits reuptake into presynaptic neuron

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11
Q

What enzyme catalyzes Dopamine —> NE?

A

Dopamine beta-Hydroxylase

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12
Q

What type of cells in the adrenal gland release norepinephrine?

A

Chromaffin cells in the adrenal medulla. They are similar to sympathetic postganglionic neurons but release into the blood rather than a synaptic cleft.

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13
Q

What is the rate-limiting step in the synthesis of indolamines?

A

Tryptophan Hydroxylase (TPH)

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14
Q

Where is melatonin produced?

A

ONLY in the pineal gland.

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15
Q

What is another name for serotonin?

A

5-Hydroxytrypamine

5-HT

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16
Q

Where is most of the serotonin in the body produced?

What is its effect there?

A

95% produced in the gut

It contracts smooth muscle and acts as a vasoconstrictor.

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17
Q

What is the rate-limiting enzyme in melatonin synthesis?

When is it most active?

A

N-acetyltransferase

Melatonin produced from serotonin.

It is most active during the night.

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18
Q

How is melatonin secretion controlled?

A

Light –> retinohypothalamic tract –> SCN –> pineal gland –> melatonin release.

Peaks during the middle of the night.

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19
Q

How would dopamine be administered to the brain?

A

Only L-DOPA can cross the BBB. Drugs must be given to prevent its deamination and its conversion before it can be delivered to the neurons.

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20
Q

What does MAO do?

A

Monoamine Oxidase inactivates some neurotransmitters, including serotonin, melatonin, NE, and epinephrine. MAOI’s can be used to treat depression (not used anymore).

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21
Q

What are the hormones of the anterior pituitary?

A

LH, FSH, TSH, ACTH, GH, PRL, Somatostatin

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22
Q

What are the hormones of the posterior pituitary?

A

OXY, AVP, ADH

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23
Q

What is a preprohormone?

A prohormone?

A 
Preprohormone = signal peptide + copeptides + hormone
Prohormone = copeptides + hormone

**Copeptides are released in the same granule as hormone

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24
Q

What enzyme converts cholesterol to pregnenolone?

What is seen with deficiency?

A

P450scc (desmolase)

Deficiency is embryonic lethal because no steroid hormones can be produced.

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25
Q

What is responsible for transport of estrogens/androgens?

A

Sex Hormone Binding Protein (SHBP)

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26
Q

What is found to bind cortisol in the blood?
What percent of cortisol is typically free cortisol?
How is this affected by estrogen?

A

Corticosteroid Binding Globulin (CBG)

3-4% as free cortisol

Estrogen decreases CBG –> increased free cortisol

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27
Q

What are T3 and T4 typically bound to in the blood?
Which has a higher affinity?
Which has a higher concentration?

A

Thyroxine Binding Globulin (TBG)
Transthyretin (TTR)

TBG has higher affinity, but TTR has higher concentration.

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28
Q

Are water soluble or lipid soluble hormones usually faster acting?

A

Water soluble. They tend to bind to extracellular receptors and activate second messenger systems (IP3/DAG, cAMP, etc.).

Lipid soluble hormones tend to have intracellular receptors and often involve modulating protein expression.

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29
Q

What type of extracellular receptor do most proteins and peptide hormones bind?

A

G Protein-Coupled Receptors

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30
Q

How do intracellular receptors work?

A

They are bound by chaperones in the cytosol. Ligand binding causes translocation into the nucleus where they can bind Hormone Response Elements (HRE) –> activate or repress transcription.

**Almost all of these receptors bind DNA through 2 Zn fingers

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31
Q

Where are paracrine hormones secreted into?

A

The interstitial space

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32
Q

What is the difference between short loop feedback and long loop feedback?

A

Short loop feedback refers to the pituitary inhibiting the hypothalamus. Long loop feedback refers to the peripheral organ inhibiting either the pituitary or the hypothalamus.

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33
Q

In an endocrine axis, what would be seen on a diagnostic stimulation if the problem were a primary defect?
Secondary defect?
Tertiary defect?

Use TRH, TSH, as an example. TRH is injected.

A 
Primary = high baseline TSH, normal TSH response seen.
Secondary = No detectable TSH, no response seen.
Tertiary = Low baseline TSH, slow return to baseline after response.
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34
Q

What task does renin perform?

A

It cleaves angiotensinogen to angiotensin I.

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35
Q

What are ANP & BNP?
Where are they released from?
What are their effects?

A 
ANP = Atrial Natriuretic Peptide
BNP = Brain Natriuretic Peptide

ANP from atrial myocytes, BNP from ventricular myocytes in response to stretch.

They both decrease peripheral vascular resistance and promote natriuresis (excretion of sodium & therefore water) to reduce blood volume. Makes sense since cardiac stretch occurs with high blood volume/peripheral resistance.

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36
Q

How do ANP & BNP reduce blood pressure?

A

Decrease vascular tone
Decrease smooth muscle contraction
Increase capillary permeability

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37
Q

Does ANP or BNP have a longer half life?

Why is this important?

A

BNP does. It is useful as a clinical indicator of heart and renal status.

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38
Q

What do high BNP levels indicate?
How does obesity affect these levels?
How does age affect these levels?
Do males or females have higher levels?

A

High BNP = possible heart and/or renal failure.
Obesity decreases BNP levels.
Levels increase with age.
Women generally have higher BNP levels.

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39
Q

What defines a classical endocrine gland?

A

They are ductless.
Secrete hormones directly into extracellular space or bloodstream.
They must be primarily dedicated to endocrine function.

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40
Q

What causes Cushing Disease?

A

Excessive cortisol production due to pituitary adenoma.

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41
Q

What are the important parts of the hypothalamus to know?

A

PVN
Preoptic Area
Arcuate Nucleus
Median Eminence (where axons from all of these converge)

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42
Q

Where are GnRH-releasing neurons found?

A

Scattered throughout forebrain, mostly in Preoptic Area (POA) of the hypothalamus.

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43
Q

GnRH must be released in a pulsatile manner. How does the frequency affect what takes place downstream?

A

Faster pulses preferentially stimulate LH, slower pulses preferentially stimulate FSH.

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44
Q

What type of hormone is GnRH?

What type of receptor does it act on?

A

It is a peptide hormone (decapeptide).
It acts on a GCPR.

GPCR –> IP3/DAG –> Ca2+ signaling

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45
Q

What is Kallman Syndrome?
How is it inherited?
What are its symptoms?

A

It is a failure of GnRH-releasing neurons to migrate into the CNS during development.

It is rare, and can be X-linked (Kal1) or autosomal (Kal2)

Symptoms: Reproductive failure, anosmia.

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46
Q

What does GnRH target?

What do these release?

A

Targets gonadotropes.

They release LH & FSH.

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47
Q

Where is CRH released from?

What cells does it target?

A

Corticotropin-Releasing Hormone

Released mostly from the PVN (paraventricular nucleus) of the hypothalamus. Released in a PULSATILE manner.

It targets corticotropes in the anterior pituitary to release ACTH & POMC.

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48
Q

What is the central regulator of the HPA axis?

A

CRH

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49
Q

What type of receptor does CRH bind to?

A

CRH R1 & CRH R1

R1 is higher affinity for CRH.

They are both GPCR’s & can activate multiple G pathways.

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50
Q

What is TRH?
Where is it released from?
What type of hormone is it?

A

Thyrotropin-Releasing Hormone
It is released from the PVN (Parvocellular Nucleus)
It is a peptide hormone (Glu-His-Pro)

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51
Q

What is the target of TRH?

How is it released?

A

TRH targets thyrotropes in the anterior pituitary (TSH).

It is released in a PULSATILE manner. This is not required for TSH pulsatility but does affect it.

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52
Q

How do TRH receptors (anterior pituitary thyrotropes) respond to ligand binding?

A

They are quickly phosphorylated making them inactive. Arrestin facilitates their internalization, where they can be dephosphorylated and recycled back to the membrane.

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53
Q

Where is GHRH released from?

What cells does it act on?

A

The arcuate nucleus (hypothalamus).

Acts on somatotropes of the anterior pituitary to stimulate GH release.

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54
Q

Where is Somatostatin released from?

Where are its targets?

A

Released from the PeVN (Periventricular Nucleus).

It inhibits GHRH release from the hypothalamus and GH/TSH release from the anterior pituitary.

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55
Q

What enzyme processes prosomatostatin to Somatostatin 28?
Somatostatin 14?

Where are each of these found in the body?

A

Furin –> Somatostatin 28
PC1/PC2 –> Somatostatin 14

Somatostatin 28 is released from stomach & duodenal D cells. Somatostatin 14 is released in the brain (mostly) and pancreas.

Both have identical C-termini.

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56
Q

What are somatostatin’s effects on GHRH and GH?

A

Somatostatin decreases frequency of GHRH pulsatility and inhibits GH.

It does so by decreasing intracellular cAMP.

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57
Q

What is the tuberoinfundibular system?

A

It comprises all of the neurons that send axons to the median eminence. Hormones target the anterior pituitary through the capillary system,

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58
Q

What is the neurohypophysial tract?

A

It is comprised of neurons whose axons terminate in the posterior pituitary

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59
Q

What is the adenohypophysis composed of?

A

Adenohypophysis = Anterior Pituitary

It is composed of glandular tissue (epithelial cells).

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60
Q

What is the neurohypophysis composed of?

A

Neurohypophysis = Posterior Pituitary

It is composed of neural tissue (terminal axons and glial cells).

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61
Q

What are the hormones of the posterior pituitary?

A 
Arginine Vasporessin (AVP) (ADH)
Oxytocin (OXY)
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62
Q

What is the anterior pituitary composed of?

The Posterior?

A

Adenohypophysis:
Pars Distalis (90%)
Pars Intermedius
Pars Tuberalis (stalk)

Neurohypophysis:
Pars Nervosa
Infundibulum

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63
Q

What are Herring Bodies?

What do they contain?

A

They are dilations of unmyelinated axons in the neurohypophysis that contain granules of either OXY or ADH and Neurophysin (binding protein).

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64
Q

Which neurophysin is associated with each Post. Pituitary hormone?

A 
ADH = neurophysin II
OXY = neurophysin I
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65
Q

Where are the cell bodies of ADH-producing neurons located?

A

In the PVN and Supraoptic Nucleus (SON)

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66
Q

Do Parvocellular or Magnocellular ADH neurons project to the neurohypophysis?

A

Only magnocellular neurons do –> regulate fluid balance

Parvocellular neurons –> regulate anxiety/stress

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67
Q

How does AVP affect ACTH release?

A

AVP amplifies ACTH’s response to CRH.

ACTH and cortisol both feedback inhibit AVP.

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68
Q

What is the “monogamy gene”?

A

AVP is considered the monogamy gene because overexpression of it can induce monogamous behavior in rodents. This can then be blocked with V1aR antagonists.

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69
Q

What can cause Diabetes Insipidus?

A

Two possible causes:

1) Underproduction of AVP (trauma, tumor, etc.)
2) Renal unresponsiveness to AVP (X-linked mutation; lithium treatment, hypokalemia)

Underproduction is the most common cause.

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70
Q

What are the effects of Oxytocin (OXY)?

A

Milk Ejection (let-down effect)
Smooth muscle contraction for parturition
Stimulates maternal behaviors

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71
Q

What is the synthetic Oxytocin used to induce labor?

A

Pitocin

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72
Q

What is the path of the Hypophyseal Portal System?

A

Superior Hypophyseal Artery –> Primary Capillary Plexus (median eminence) –> Hypophyseal Portal Veins –> Secondary Capillary Plexus (pars distalis) –> Venous system

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73
Q

Does the Median Eminence lie inside or outside of the BBB?

A

Outside

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74
Q

What types of cells are Acidophils in the anterior pituitary?
What do they look like when stained?

A

Somatotrophs (GH)
Lactotrophs (PRL)

They stain lightly.

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75
Q

What types of cells are Basophils in the anterior pituitary?

What do they look like when stained?

A

Corticotrophs (ACTH)
Gonadotrophs (LH/FSH)
Thyrotrophs (TSH)

They stain darkly.

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76
Q

Are there more Acidophils or Basophils in the anterior pituitary?
Chromophobes?

A

Acidophils (40%)
Basophils (10%)

Chromophobes (50%) –> maintain hormone-secreting cells via paracrine action.

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77
Q

How is GH released?

A

It is released in a pulsatile manner, and highest at night.

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78
Q

What molecule does GH act through?

Where is this produced?

A

GH acts through IGF-I (Insulin-like Growth Factor I)

It is produced in the liver & release is dependent on insulin. You don’t want to be anabolic if in starvation.

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79
Q

What stimulates IGF-I?
What are its target tissues?
What is it dependent on?

A

GH stimulates IGF-I release from the liver.

It causes increased growth & protein turnover in muscle, organs, and connective tissue. It feedback inhibits GH.

Its release from the liver is dependent on insulin.

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80
Q

What are the effects of GH release?

A

GH –> Liver (IGF-I production) –> muscle, organ, & bone growth

GH (directly) —> decreases glucose uptake, ^adipose lipolysis, ^muscle anabolism —> promotes lean body mass & increases blood glucose.

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81
Q

Stimulators of GH release?

Inhibitors of GH release?

A

Stimulators: GHRH; catecholamines (exercise); AA’s; Thyroid Hormone

Inhibitors: Somatostatin; IGF-I; glucose (hyperglycemia; FFA (obesity)

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82
Q

What diseases are associated with excess GH?

A

Gigantism = excess GH before epiphyseal plates close –> larger long bones

Acromegaly = excess GH during middle age –> large hands & feet, large facial features, increased organ size.

Both are most often caused by a somatotrope tumor.

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83
Q

What is Laron Syndrome caused by?
What are its symptoms?
How is it treated?

A

Cause: A genetic defect in GH receptor –> no IGF-I release

Symptoms: Dwarfism

Can be treated with exogenous IGF-I.

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84
Q

What causes African Pygmy dwarfism?

A

Partial defect in GH receptor –> some IGF-I.

Normal blood GH levels. No IGF-I increase during puberty.

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85
Q

What are the symptoms of adult GH deficiency?

A

Increased fat deposition, muscle wasting, reduced bone density, higher TG’s/LDL.

Usually caused by pituitary surgery or treatment due to tumor.

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86
Q

How is Prolactin (PRL) regulated?

A

It is tonically inhibited by dopamine. It is not part of an endocrine axis. Suckling causes its release.

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87
Q

What are the effects of Prolactin?

A

Mammary gland development & differentiation

Milk production:
Synthesis of milk proteins (beta-Casein & alpha-Lactalbumin)
Synthesis of lactose
Synthesis of milk fats

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88
Q

What are the cause & symptoms of excess prolactin?

A

Prolactinoma = PRL-secreting adenoma (common pituitary adenoma)

Symptoms:
Hyperprolactinemia
Galactorrhea (milk production)
Reproductive dysfunction (PRL inhibits GnRH)

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89
Q

What is Sheehan’s Syndrome?

A

Pituitary insufficiency due to excessive blood loss/shock during childbirth and partial destruction of the pituitary.

It is often discovered due to lack of lactation (PRL deficiency) but affects other pituitary hormones & has associated symptoms.

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90
Q

What are the histological layers of the adrenal gland?

A

From outside in:

Zona Glomerulosa (dark)
Zona Fasciculata (light)
Zona Reticularis (dark)
Medulla
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91
Q

What hormones are produced in each of the adrenal cortex layers?

A

Zona Glomerulosa –> Mineralocorticoids (Aldosterone)
Zona Fasciculata –> Glucocorticoids (Cortisol)
Zona Reticularis –> Weak androgens (DHEA)

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92
Q

Why is the Zona Fasciculata lighter than the rest of the adrenal medulla?

A

It contains many fat droplets to supply cholesterol for glucocorticoid production.

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93
Q

Describe the bloodflow of the adrenal glands.

A

Suprarenal arteries –> Capsular arteries –> Subcapsular plexus –> medulla –> medullary veins –> central vein

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94
Q

What enzyme is present in the Zona Glomerulosa that is not present anywhere else in the body?

A

Aldosterone synthase

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95
Q

What precursor of aldosterone also has mineralocorticoid action?

A

11-Deoxycorticosterone

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96
Q

What are the effects of aldosterone in the kidney distal tubule?

A

Increased synthesis of ENaC’s (apical) and Na+/K+ ATPase (BL)

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97
Q

What receptor do mineralocorticoids bind to?
What else can bind to this receptor?
How does the kidney handle this?

A

Mineralocorticoids bind to the MR.

Glucocorticoids can also bind this. They are much higher in the blood but are bound up by CBG.

The kidney handles this using 11beta-HSD Type II. This causes Cortisol –> Cortisone (inactive) within the renal cell. Thus, the intracellular MR can preferentially bind mineralocorticoids.

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98
Q

Where is renin produced?
Angiotensinogen?
Aldosterone?
ACE?

A 
Renin = kidney (juxtaglomerular apparatus)
Angiotensinogen = liver
Aldosterone = adrenal cortex
ACE = lung
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99
Q

What are the effects of Angiotensin II?

A

Potent vasoconstriction

Release of Aldosterone from adrenal cortex.

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100
Q

What is the difference between aldosterone and AVP action?

A

Aldosterone = increased Na+ reabsorption and thus water reabsorption/blood volume.

AVP = increased free water reabsorption (aquaporin insertion in kidney)

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101
Q

What enzyme can convert cortisone –> cortisol in the peripheral tissue target cells?
Where does the cortisone come from?

A

11beta-HSD 1

Cortisone is generated through a side pathway in cortisol-producing cells. It is also converted from cortisol in renal cells (to preferentially bind aldosterone).

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102
Q

Is the glucocorticoid receptor ubiquitous? Is the MR?

A

GR is expressed in most tissues. MR is restricted (kidney, colon, sweat ducts, salivary ducts)

103
Q

How do glucocorticoids inhibit inflammation?

A

When bound to GR, they increase synthesis of IkB and directly inhibit NF-kB translocation to the nucleus. This prevents expression of proinflammatory cytokines.

104
Q

What are the metabolic effects of cortisol?

A

It antagonizes the effects of insulin. Causes gluconeogenesis, proteolysis, lipolysis, increases plasma glucose.

Fat redistribution occurs, leading to higher abdominal fat and lower subcutaneous fat.

105
Q

What 3 metabolic enzymes does cortisol upregulate?

A 
Tyrosine aminotransferase (amino acid degradation)
Phosphoenolpyruvate Carboxykinase (PEPCK; gluconeogenesis)
Glucose-6-Phosphatase (gluconeogenesis)
106
Q

How does Cortisol promote proteolysis?

A

Increased ubiquitination
Decreased GLUT4 at membrane –> decreased glucose uptake
Decreased protein synthesis

107
Q

What are the effects of cortisol on the cardiovascular system?

A

Stimulates RBC production
Maintains responsiveness to catecholamines:
Constriction of peripheral vessels (alpha adrenergic)
Dilation of coronary arteries (beta adrenergic)

Excess glucocorticoids = high blood pressure

108
Q

What are the effects of Cortisol on the immune system?

A

Inhibits inflammation

Increases neutrophils, platelets, & RBC’s

109
Q

What are the effects of Cortisol on bone?

A

Decreases Ca2+ absorption in intestine.
Stimulates osteoclasts
Inhibits bone formation

110
Q

What effect does Cortisol have on the CNS?

A

Feedback inhibits CRH & ACTH. Causes depression, anxiety, panic, rage.

111
Q

What type of pancreatic cell secretes insulin?
Somatostatin?
Glucagon?
Ghrelin?

A 
Insulin = beta
Somatostatin = delta
Glucagon = alpha
Ghrelin = epsilon
112
Q

What does Pancreatic Polypeptide do?

What type of cell secretes it?

A

Inhibits acinar (exocrine) cells via paracrine action.

Secreted by PP cells in pancreas.

113
Q

What is the half-life of Insulin?

What is a better indicator of pancreatic function?

A 
Insulin = 3-8 minutes
C-Peptide = 35 minutes, better indicator of function.
114
Q

Describe the release of Insulin beginning with high blood glucose.

A

Glucose outside beta cell –> GLUT2 transports it in –>
Glucokinase results in G-6-P –> Metabolism produces ATP –>
ATP causes K+ membrane channels to close –> Cell depolarizes –> Ca2+ channels open (voltage-gated) –>Insulin vesicle exocytosis

  • *GLUT2 = low affinity, so only when blood [glucose] is high will it transport
  • *AA’s & FA’s can do this too, not as effectively as Glucose.
115
Q

What is GLP-1?
What is its effect?
How does it do this?

A

GLP-1 = Glucagon-Like Peptide 1

It prevents glucose sequestering in beta cells, making it available for ATP production –> potentiates insulin release.

116
Q

How do catecholamines affect Insulin release?

A

They inhibit it via alpha-adrenergic receptors.

117
Q

What pattern defines Insulin release?

Why?

A

Insulin is released in a biphasic pattern, with a large initial spike then a gradual increase in the blood. This is because there are vesicles docked at the cell membrane for quick release, and then more insulin must be synthesized/retrieved.

118
Q

What type of receptor are insulin receptors?

What domain binds insulin?

A

Tyrosine Kinase receptors

The alpha subunit binds insulin, and the beta subunit is autophosphorylated.

119
Q

What is the most common cause of congenital adrenal hyperplasia (CAH)?

A

21-alpha Hydroxylase deficiency.

Causes excess DHEA since cortisol & aldosterone pathways are blocked. Can cause virilization.

120
Q

What stimulates the conversion of NE to Epinephrine?

A

Cortisol

Only takes place in adrenal medulla

121
Q

What is the major cell type in the adrenal medulla?

A

Chromaffin Cells

122
Q

What type of adrenergic receptors are typically found on the heart?
Peripheral vessels?
Bronchial muscles?

A

Heart = beta1 –> vasodilation, increased CO

Peripheral vessels = alpha(1) –> vasoconstriction

Bronchial airways/vessels = beta2 –> bronchodilation/vasodilation

123
Q

What is the half life of catecholamines?

A

Very short. 10 seconds-1.5 minutes.

124
Q

What enzymes can degrade catecholamines?

A

Catechol-O-methyltransferase (COMT)

or

Monoamine Oxidase (MAO)

125
Q

What are catecholamines excreted as?

What can this be diagnostic for?

A

Vanillymandelic Acid (VMA)

Excreted in urine.

High levels in urine can indicate a tumor that is expressing NE or E.

126
Q

What are tumors from Chromaffin cells called?

What are the symptoms of catecholamine overproduction?

A

Pheochromocytomas (the 10% tumor)

Symptoms: Hypertension, tachycardias, headaches, high urinary metanephrines (NE/Epi metabolic byproducts)

127
Q

What class of drug interacts with the K+ channels found on pancreatic beta cells?

A

Sulfonylurea drugs (Glipizide) can bypass the glucose requirement to close K+ channels in beta cells –> membrane depolarization –> Ca2+ channels open –> Insulin release.

128
Q

What glucose transporters are found in the brain?

A

GLUT1 & GLUT3

129
Q

What other signaling molecules are transcribed with glucagon?
What cells release active glucagon?
What cells release inactive glucagon?
What do they release instead?

A

GLP-1 & GLP-2 (incretins) located on same gene.

Pancreatic alpha cells release active glucagon & inactive incretins.

L cells in intestine release active GLP-1 & GLP-2 but inactive glucagon (as Glicentin)

130
Q

What type of meal can stimulate Glucagon release?

What else can stimulate it?

A

Protein meals can stimulate glucagon.

Catecholamines can also stimulate it (exercise).

131
Q

What causes Somatostatin release?
What inhibits it?
What are its effects?

A

High fat, high carb meals –> SS28

Insulin inhibits its release

It slows gastric emptying.

132
Q

What is amylin?

What pathology might it be implicated in?

A

It is released along with insulin to help regulate blood glucose.

It may be a cause of beta cell destruction in T2DM

133
Q

What are the effects of Ghrelin?

What is its correlation to obesity?

A

It stimulates food intake (hypothalamus). It also inhibits insulin release from beta cells.

Ghrelin has an inverse correlation to obesity.

134
Q

What hormones are counter-regulatory to insulin?

A

Glucagon & Epinephrine

GH & Cortisol = secondary (6 hours later)
GH kicks in to preserve muscle mass after several hours of hypoglycemia. IGF-1 cannot be induced (no insulin), so glucose mobilization occurs but not proliferation that would occur due to IGF.

135
Q

What transporter can transport Fructose?

A

GLUT5

136
Q

How much glucose is needed by the brain per day?

A

180 grams

137
Q

What are the qualifiers for metabolic syndrome?

A

Visceral obesity (waist)
Insulin resistance
Dyslipidemia (high TG’s low HDL)
Hypertension

138
Q

What are the TF’s important for adipose storage regulation?

A

Sterol Regulatory Binding Protein 1C (SREBP-1C)
Promotes TG synthesis, traps Glucose in cells (glucokinase).
Activated by lipids & insulin.

PPAR-gamma
Nuclear steroid hormone receptor. Regulated TG storage & adipocyte differentiation.

139
Q

What are Thiazolidinediones used for?

How do they work?

A

TZD’s are used to treat mild T2DM.

They are PPAR-gamma agonists, which cause adipocyte differentiation and storage of TG’s. They can increase insulin sensitivity but often cause weight gain.

Avandia is a common TZD

140
Q

What are the stimulators of appetite?

A

Neuropeptide Y

Agouti-Related Peptide (AGRP)

Leptin inhibits these.

141
Q

What are the suppressors of appetite?

A

alpha-MSH

Cocaine-Amphetamine Regulate Transcript (CART)

Leptin stimulates these.

142
Q

What HbA1C levels are considered T2DM?
Fasting blood glucose levels?
Glucose tolerance levels?

A

HbA1C > 6.5%

126+ mg/dL fasting blood glucose

200+ mg/dL at any time is T2DM

143
Q

What are the symptoms of T2DM?

A

Polyphagia = eating a lot

Polyuria = peeing a lot
**Glucose in blood –> ^ blood osmolarity –> pulls water into blood –> increased urine volume

Polydipsia = thirst (due to excessive urine output)

144
Q

How do Biguanides work?

A

Metformin; used to treat T2DM

Inhibits liver gluconeogenesis & increases peripheral insulin sensitivity.

145
Q

What are alpha-glucosidase inhibitors used for?

A

To treat T2DM.

They slow down intestinal absorption of carbohydrates.

146
Q

What causes diabetic ketoacidosis?

A

Decreased insulin –> Increased FFA release/metabolism –> ketone bodies utilized –> lowers blood pH

Dehydration + acidosis –> coma; death.

147
Q

What are follicular cells in the thyroid?

What do they surround?

A

They are the epithelial cells found in the thyroid.

They surround a colloid (T3/T4/Thyroglobulin).

148
Q

What are parafollicular cells?
Where are they located?
What do they do?

A

They are in the thyroid gland. Also called C cells.

They produce calcitonin and maintain follicle.

149
Q

Thyroid gland histology:
What type of epithelium are follicular cells?
What surrounds a follicle?
What do parafollicular cells look like?

A

Follicular cells = cuboidal (squamous when inactive)

Follicle surrounded by basement membrane

Parafollicular cells = granular, do not touch colloid.

150
Q

How is iodide uptake regulated in the thyroid?

A

It is autoregulated, and so is hormone production. High iodide levels inhibit iodide uptake and hormone synthesis.

This can be used clinically to rapidly shut down thyroid hormone production in hyperthyroid patients.

151
Q

What transporter is responsible for iodide uptake in the thyroid?
What test can be done to analyze its function?

A

Sodium-Iodide Symporter (NIS)

Radioactive Iodide Uptake Scans can be done to assess the gland’s functioning.

152
Q

What are Hot Nodules and Cold Nodules?

Which is worse?

A

When reading a radioactive iodide uptake scan of a thyroid, hot nodules = lots of uptake, cold nodules = little/no uptake.

Cold nodules are worse because these nodules are nonfunctional and are often found to be malignant.

153
Q

What is perchlorate used for?

A

It blocks the NIS (sodium-iodide symporter) in the thyroid gland.

Can be used to test for organification (conjugation) defects. If NIS is blocked, iodide content should stay level normally, if organification can’t occur, it will decrease again as iodide leaves.

154
Q

What is the active form of thyroid hormone?

What is the form that is primarily secreted?

A

Active form = T3
Primary secreted form = T4

T4 has a longer half life and is converted to T3 within peripheral tissues.

155
Q

What is the only step in thyroid hormone synthesis that is not TSH-dependent?

A

Transport of iodide into lumen & oxidation by Thyroid Peroxidase (TPO).

156
Q

Describe the synthesis of thyroid hormones.

A

Iodide trapping –> transport/oxidation –> iodination of thyroglobulin –> conjugation –> endocytosis –> proteolysis –> secretion.

157
Q

What does Carbimazole do?

A

It inhibits Thyroid Peroxidase.

Used as a treatment for hyperthyroidism.

158
Q

What are the precursors of T4?
T3?
rT3?

A 
T4 = DIT + DIT
T3 = MIT (outer ring) + DIT (inner ring)
rT3 = DIT (outer ring) + MIT (inner ring)
159
Q

What is a normal 24h iodide uptake on a radioactive iodide uptake scan?
Hyperthyroid?
Hypothyroid?

A

Normal = 25%

Hyperthyroid >60%

Hypothyroid <5%

160
Q

What can each of the three types of deiodinases do?

A

All of them remove iodines from rings.

Type 1 = can make T3 or rT3
Type 2 = makes active T3 (acts on outer ring)
Type 3 = makes rT3 (acts on inner ring)

161
Q

What acts as the thyroid hormone sensor in the pituitary?

A

Type II deiodinase

Can only make T3.

162
Q

Does T4 or T3 have a longer half-life?

How long are they?

A

T4 = 7 days

T3 = 1 day

T4 is more tightly bound by transport proteins.

163
Q

What type of receptor is the thyroid hormone receptor?

A

THR is a nuclear receptor (like the steroid hormones).

It is expressed in almost all tissues.

164
Q

What are T3’s effects on metabolism?

A

It increases BMR by stimulating mitochondria.

Increased O2 consumption, heat production.

Increases carbohydrate mobilization, protein turnover, lipid turnover.

165
Q

What are the effects of T3 on the heart?

A

Increases beta-adrenergic receptors on the heart –> increased cardiac output

Hyperthyroidism can cause arrhythmias due to this.

166
Q

How is the HPT axis regulated?

A

T3 regulates it through a short loop & long loop feedback inhibition.

Somatostatin & Dopamine tonically inhibit pituitary release of TSH.

167
Q

What is the cause of Grave’s Disease?

What are its symptoms?

A

Autoantibodies stimulate TSH receptor. Long-Acting Thyroid Stimulator (LATS).

Symptoms:
Diffuse, symmetrical goiters
tachycardia
nervousness
heat intolerance
weight loss
168
Q

What causes Hashimoto’s Thyroiditis?

What are the symptoms?

A

Autoantibodies that destroy thyroid follicles. Directed against TG or TPO.

Symptoms:
Diffuse goiter
Hypothyroid symptoms: fatigue, hair loss, cold intolerance, weight gain

169
Q

What is Thyroid Storm?
What are the symptoms?
How is it treated?

A

Thyroid storm = hyperthyroidism coupled with severe acute illness.

Symptoms:
High fever
Tachycardia
Nausea/vomiting/diarrhea
Altered mental status
Circulatory collapse --> death

Treatment:
PTU
Carbimazole
Beta blockers to restore normal heart function

170
Q

What type of cells secrete PTH?

A

Chief cells

171
Q

What must be probed to determine PTH levels?

A

The entire hormone (1-84) since the C-terminal fragment lasts longer than the biologically active peptide.

172
Q

What is the primary PTH receptor?

What can it bind?

A

PTH 1R

Can bind 1-34, 1-84, PTHrP.

173
Q

What does PTH 2R bind?

A

Binds 1-34 only. No PTHrP

174
Q

What are the net effects of PTH?

A

To increase plasma [Ca2+] and decrease plasma Phosphate

175
Q

How does PTH stimulate osteoclast activity?

A

PTH –> PTH 1R on osteoblasts –> M-CSF secretion –> osteoclast precursors differentiate into osteoclasts

Also, PTH stimulates release of RANK ligand –> osteoclast maturation & bone resorption

176
Q

What is Osteoprotegerin?

How is it regulated?

A

OPG is a RANK ligand antagonist (prevents RANK ligand from inducing osteoclast maturation & bone resorption).

Estrogens stimulate OPG and Cortisol inhibits OPG.

This is why postmenopausal women get osteoporosis and why Cushing Disease causes brittle bones.

177
Q

What are PTH’s effects in the kidney?

A

It stimulates CYP1a, which encodes 1-alpha Hydroxylase.

1-alpha Hydroxylase converts Vit. D3 to Calcitriol.

PTH also causes insertion of Ca2+ channels in the apical membrane of the distal tubule.

178
Q

How is PTH regulated?

A

Calcium Sensing Receptor (CaSR) binds ionized Ca2+. When bound, it represses PTH transcription and promotes its degradation.

Calcitriol binds VDR (nuclear receptor) and inhibits PTH transcription, while activating CaSR transcription.

179
Q

Where does Calcitriol exert effects?

What are they?

A

Bone: stimulates osteoclast proliferation/differentiation

Intestine: stimulates Transcellular absorption of Ca2+ in Duodenum & absorption of Phosphate.

180
Q

What is a common cause of Hyperparathyroidism?

A

Chronic renal failure –> no Vit. D3 –> PTH not supressed

181
Q

What causes Ricket’s?

A

Called osteomalacia in adults.

It is caused by a Vit. D3 deficiency.

182
Q

What is the effect of Vit. D in the intestine?

A

Increased apical Ca2+ channels, increased calbindin, increased phosphate reabsorption.

183
Q

What is PTHrP?

What is its significance?

A

PTH-related Peptide

It is not usually physiologically significant. High levels are seen released by some tumors –> hypercalcemia.

184
Q

What are the effects of Calcitonin?

A

It inhibits bone resorption –> decreases blood Ca2+ levels

Excess/deficiency in humans –> no complications, so it is not involved in human Ca2+ homeostasis.

185
Q

What are the causes of hyperparathyroidism?

A

Primary: hyperplasia; carcinoma of the PT gland

Secondary: Renal failure –> Vit. D deficiency –> more PTH synthesis

186
Q

What is the Chvostek sign?

A

Twitching of facial muscles due to tapping on the facial nerve. It can demonstrate hypocalcemia

187
Q

What is the normal range of serum calcium levels?

A
  1. 8-10.3 mg/dL

2. 2-2.6 mM

188
Q

What is the normal range of serum phospate?

A
  1. 4-4.1 mg/dL

0. 8-1.45 mM

189
Q

What does hydroxyproline in the urine indicate?

A

Bone resorption/turnover

190
Q

Where is calcitonin released from?

A

C cells of thyroid gland

191
Q

What is Paget’s disease?

How is it treated?

A

High localized bone resorption & turnover.

Can be treated with Calcitonin.

Escape phenomenon is seen with Calcitonin. Receptors are downregulated within hours, making treatment difficult.

192
Q

What is the active form of DOPA?

A

L-DOPA

D-DOPA is inactive

193
Q

What is the common precursor of all steroid hormones?

A

Pregnenolone

Synthesized from cholesterol by desmolase.

194
Q

What hormones bind receptor kinase receptors?

A

Insulin and ANP

195
Q

What hormones bind Receptor-linked Kinases?

A

GH, PRL, & EPO

196
Q

What systems are positive feedback systems?

A

Parturition
Lactation
Ovulation
Blood Clotting

197
Q

Where is EPO produced?

A

Liver and kidney.

Liver as a fetus/infant, and kidney as an adult.

198
Q

Where is Renin produced?

A

Juxtoglomerular apparatus of the afferent arteriole.

199
Q

What frequency of GnRH pulsing will yield FSH?

LH?

A 
FSH = 2-3 hour pulses
LH = 30-60 minute pulses
200
Q

What are the major hypothalamic-releasing hormones? (6)

A 
GnRH
CRH
TRH
GHRH
Somatostatin
Dopamine
201
Q

What artery supplies the posterior pituitary?

A

Inferior hypophyseal artery

202
Q

What are distinctive about TRH & GnRH from the other hypothalamic hormones?

A

They activate IP3/DAG/Ca2+ systems as second messengers, rather than affect cAMP concentrations.

203
Q

Which hypothalamic hormones are not pulsatile?

A

Somatostatin & Dopamine

204
Q

Which Hypothalamic hormones have cell bodies in the PVN?

A

CRH & TRH

205
Q

Where is somatostatin produced within the hypothalamus?

A

Periventricular Nucleus (PeVN)

206
Q

What is the secondary effect of AVP?

Which neurons are used?

A

It increases the amplitude of ACTH release in response to CRH.
Parvocellular AVP neurons are involved in this.

207
Q

What is dexamethasone?

A

It is a potent synthetic glucocorticoid.

Can be used to suppress ACTH/CRH or as an immunosuppressant.

208
Q

What are they unique enzymes in the production of Aldosterone?
Cortisol?
What enzymes do they share?

A

Aldosterone:
3-beta-HSD
Aldosterone Synthase

Cortisol:
17-alpha hydroxylase

Shared:
21-alpha hydroxylase
11-beta hydroxylase
desmolase

209
Q

What enzymes are required for DHEA production in the adrenals?

A

Desmolase & 17-alpha hydroxylase

210
Q

What reaction does 11-beta HSD1 catalyze?

A

Cortisone –> cortisol

211
Q

What is hyperpigmentation of the skin indicative of?

How does this occur?

A

High ACTH levels.

ACTH normally binds MC2R in the adrenal, but high levels can bind (with low affinity) MC1R in the skin –> skin darkening.

212
Q

What are the effects of ACTH on the adrenal glands?

A

Zona Fasciculata & Reticularis hypertrophy
Cortisol & DHEA are synthesized

Dopamine –> NE in medulla

213
Q

What can cause CAH?

A

Congenital Adrenal Hyperplasia

Most commonly caused by a 21-alpha hydroxylase deficiency. Also caused by 11-beta hydroxylase deficiency.

214
Q

What is the difference between an 11-beta hydroxylase and a 21-alpha hydroxylase deficiency?

A

11-beta hydroxylase —-> Salt & water retention
21-alpha hydroxylase —-> Na+ loss

Both include masculinization from excess DHEA.

215
Q

With regard to pancreatic islet structure, what type of cell has a signaling advantage?

A

Beta cells do. They are in the center of the islets and blood flows from the center outward, giving them the first opportunity to release insulin and suppress glucagon production.

216
Q

What is packaged with OXY?
AVP?

When are they cleaved from the prohormone?

A 
OXY = neurophysin 1
AVP = neurophysin 2

Both are carrier proteins. Both are cleaved during axonal transport.

217
Q

What are the two types of AVP-producing neurons and where do they project?

A

Magnocellular –> Posterior pituitary (fluid balance)

Parvocellular –> median eminence (mood/stress)

219
Q

What is the major transporter of Glucose in the brain?

A

GLUT-3

220
Q

What does parvocellular AVP serve to do?

A

Acts synergistically with CRH to stimulate ACTH release.

221
Q

Which transporter transports fructose?

A

GLUT-5

It is located in the small intestine and spermatozoa.

222
Q

What are the symptoms of metabolic syndrome?

A

Visceral obesity
Insulin resistance
Dyslipidemia
Hypertension

223
Q

What are the important transcription factors associated with white adipose tissue?

A

SREBP-1C
and
PPAR-gamma

224
Q

How is SREBP-1C activated?

What does it promote?

A

SREBP-1C is activated by lipids and insulin.

It promotes TG synthesis within adipocytes.

225
Q

What hypothalamic-acting hormones does Leptin stimulate?

What is the effect?

A

alpha-MSH
CART

Leptin –> CART & a-MSH –> satiety

226
Q

What hypothalamus-acting hormones does Leptin inhibit?

What is the effect?

A

Neuropeptide Y
AGRP

Leptin –> less Neuropeptide Y & AGRP –> satiety

227
Q

What HbA1C value would constitute T2DM?

A

> 6.5%
aka
48 mMol

228
Q

What lab values for fasting glucose would constitute a diagnosis of pre-diabetes?
T2DM?

A

Pre-diabetes = 100-125 mg/dL

T2DM > 125 mg/dL

229
Q

What lab values would constitute a diagnosis of pre-diabetes on an oral glucose tolerance test?
T2DM?

A

Pre-diabetes = 140-199 mg/dL

T2DM > 200 mg/dL

230
Q

What are the symptoms of T2DM?

A

Polyphagia
Polyuria
Polydipsia

231
Q

How do physicians quickly shut down T3/T4 production clinically?

A

They give a large iodine dose.

Autoregulation of the thyroid gland prevents uptake and hormone synthesis in the face of high iodine levels.

232
Q

What intake of iodine would be considered deficient?

A

Under 20 ug/day

233
Q

What is required for NE –> EPI

A

Cortisol

234
Q

What are the Ig’s against in Grave’s Disease?

Hashimoto’s Thyroiditis?

A

Graves: FSH Receptor

Hashimoto’s: TPO

235
Q

What hormone can stimulate PRL?

A

High levels of TRH can stimulate PRL.

Otherwise it is tonically inhibited by Dopamine and is not part of an axis.

236
Q

What does SS14 do in the pancreas?

A

Suppresses insulin & is suppressed by insulin.

It is used in treating insulin-secreting tumors.

237
Q

What hormone is released alongside insulin to act synergistically with it?

A

Amylin

238
Q

Where is Ghrelin released from?

What does it do?

A

Stimulates food intake at the hypothalamus & inhibits insulin release.

Secreted from the stomach and pancreatic epsilon cells.

239
Q

What is GH’s effect on adipocytes?

Muscle cells?

A

Adipocytes: increased lipolysis (HSTL)
Muscle: increased protein synthesis

It inhibits glucose uptake (antagonizes insulin) in both of these tissues as well.

240
Q

What can be used as a clinical indicator of pancreatic function?

A

C peptide levels.

C peptide is released with insulin and has a 35 in half-life. Insulin’s is only 3-8 mins.

241
Q

Describe the iodination pattern of T3 & rT3

A

T3 = 2 iodides on inside ring

rT3 = 2 iodides on outside ring

242
Q

Why does a change in TBG or TTR not affect thyroid hormone functioning very much?

A

Over 99% of T3/T4 are bound in the blood, so a change in the concentration of their binding proteins will be easily buffered by what remains.

243
Q

What % of T3/T4 is bound in the blood?

To what?

A

99%+ is bound in the blood.
TBG = 70%
TTR = 10%
Albumin = 15-25%

244
Q

What type of receptor is the T3 receptor?
What does it dimerize with?
Does T4 bind it?

A

It is a nuclear receptor.

THR heterodimerizes with RXR (retinoic acid receptor).

T4 has low affinity for it and thus low biological activity. It is usually converted to T3 in the peripheral tissues.

245
Q

What tonically inhibits thyrotropes?

A

Somatostatin & Dopamine

247
Q

How much Ca2+ is typically ingested per day?

What is the net absorption seen?

A

1000 mg ingested per day

Net absorption is 200 mg. This equals excretion by the kidneys.

248
Q

What is RANK found on?

A

Osteoclasts.

It interacts with RankL on PTH-stimulated osteoblasts –> osteoclast maturation & bone resorption.

249
Q

What causes the osteoporosis seen in postmenopausal women?

A

Less estrogen –> less OPG –> Rank-RankL –> osteoclasts resorb bone.

250
Q

What does CYP1a encode?

A

1alpha-hydroxylase

251
Q

What are C cells?

Where are they located?

A

C cells secrete calcitonin.

They are parafollicular cells of the thyroid gland.

252
Q

What does the CaSR do?

A

Calcium-sensing receptor

It responds to free Ca2+ and represses synthesis of PTH in response. It also promotes degradation of preformed PTH.

253
Q

How does Vit. D affect PTH levels?

A

Directly: Inhibits PTH synthesis at the promoter level?

Indirectly: Stimulates CaSR transcription.

254
Q

How is Calcitriol produced?

A

Skin:
7-dehydrocholesterol –(UV)–> Cholecalciferol

Liver:
Cholecalciferol —-> Calcidiol

Kidney:
Calcidiol –(1alpha-hydroxylase)–> Calcitriol

255
Q

What is Calcitonin used to treat?

A

Paget’s Disease

Extremely high local bone turnover. Cause is unknown.

“Escape” phenomenon is seen with Calcitonin.

256
Q

What are the effects of GH on the liver?

A

Increased gluconeogenesis

Release of IGF-I (insulin-dependent)

FHB (8 decks)

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