Endocrine 2025 Flashcards

(87 cards)

1
Q

Q: What is the primary function of the endocrine system?

A

A: To secrete hormones into the bloodstream to regulate distant target cells, tissues, and organs.

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2
Q

Q: What is the core of endocrinology?

A

A: Cell-to-cell communication.

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3
Q

Q: What types of cells can release signaling molecules?

A

A: All cells in the body, not just those in endocrine glands.

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4
Q

Q: What are the types of cell signaling based on distance?

A

Juxtacrine (direct contact)
Autocrine (self)
Paracrine (local)
Endocrine (long-distance via hormones)
Neuroendocrine (neurons releasing hormones into blood)

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5
Q

Q: What is neuroendocrine signaling?

A

A: Neurons release hormones into the bloodstream to act on distant targets.

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6
Q

Q: What types of molecules can act as messengers?

A

A: Proteins/peptides, steroids, amines, lipids, DNA/RNA, metabolites.

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7
Q

Q: How are hydrophilic and hydrophobic messengers transported?

A

Hydrophilic: dissolved in plasma or in exosomes
Hydrophobic: bound to carrier proteins

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8
Q

Q: What regulates insulin secretion from pancreatic beta cells?

A

↑ Glucose (primary)
↑ Amino acids, fatty acids (augment)
PSNS (stimulates), SNS (inhibits)
Incretins (GLP-1, GIP), glucagon, somatostatin

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8
Q

Q: What determines the rate of hormone release?

A

A: The sum of stimulatory and inhibitory signals.

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9
Q

Q: What are the three steps in hormone action on target cells?

A

Molecular recognition (binding to receptor)
Activation (conformational change)
Intracellular response (signal transduction)

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10
Q

Q: What is signal amplification?

A

A: One hormone molecule can activate many intracellular molecules.

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11
Q

Q: Name four types of hormone receptors.

A

G-protein coupled receptors (e.g., oxytocin)
Tyrosine kinase receptors (e.g., insulin)
Cytokine receptors (e.g., prolactin)
Steroid receptors (e.g., estrogen)

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12
Q

Q: What are second messengers?

A

A: Intracellular molecules that amplify the signal from the first messenger.

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13
Q

Q: What is hormone insensitivity?

A

A: When target cells don’t respond to normal or high hormone levels due to receptor or signaling issues.

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14
Q

Q: Example of hormone resistance?

A

A: Type II diabetes (insulin resistance).

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15
Q

Q: What causes hypersecretion disorders?

A

Excess hormone production
Reduced clearance
Increased tissue response

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16
Q

Q: What causes hyposecretion disorders?

A

Low hormone production
Increased clearance
Tissue insensitivity

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17
Q

Q: What is the hypothalamus composed of?

A

A: Nuclei (neuronal cell bodies) and nerve tracts (axons).

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18
Q

Q: What are the main functions of the hypothalamus?

A

Regulates homeostasis (e.g., temperature, metabolism, water balance)
Controls behaviors (e.g., reproduction, feeding, rage)
Integrates neural and humoral inputs
Acts as both neural tissue and an endocrine gland

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19
Q

Q: What are humoral signals?

A

A: Fluid-borne messengers like hormones circulating in blood or lymph.

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20
Q

Q: What are the outputs of the hypothalamus?

A

A: Neural signals and neurohormones.

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21
Q

Q: What are the two main neurohormones secreted by the posterior pituitary?

A

A: Vasopressin (ADH) and Oxytocin.

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22
Q

Q: Where are vasopressin and oxytocin produced?

A

A: In the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus.

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23
Q

Q: What type of neurons produce these hormones?

A

A: Magnocellular neurons.

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24
Q: What are the main actions of vasopressin?
Decreases water excretion by kidneys (anti-diuretic effect) Causes vasoconstriction of blood vessels
25
Q: What regulates vasopressin secretion?
Osmoreceptors (detect solute concentration in ECF) Stretch receptors (detect blood volume)
26
Q: What are the main actions of oxytocin?
Stimulates uterine contractions during labor Stimulates milk ejection during lactation
27
Q: What stimulates oxytocin secretion?
Cervical distension during childbirth Suckling of the nipple (Both are positive feedback loops)
28
Q: What are other roles of oxytocin?
Acts as a neurotransmitter in the CNS Involved in emotional bonding, trust, and possibly orgasm
29
Q: What receptor and pathway does oxytocin use in myoepithelial cells?
Oxytocin receptor (OT-R) coupled to Gαq Activates PLC → PIP2 → IP3 + DAG IP3 triggers Ca²⁺ release → myosin phosphorylation → contraction
30
Q: What are the five types of endocrine cells in the anterior pituitary and their hormones?
Somatotrophs → GH (Growth Hormone) Lactotrophs → PRL (Prolactin) Gonadotrophs → LH & FSH Thyrotrophs → TSH Corticotrophs → ACTH
31
Q: What is the difference between tropic and trophic hormones?
Tropic: Control activity of other endocrine glands Trophic: Promote growth of target tissues
32
Q: How are anterior pituitary hormones regulated?
By hypothalamic neurohormones (releasing/inhibiting factors) via the hypothalamo-hypophyseal portal system.
33
Q: What happens when the pituitary stalk is severed?
Secretion of most anterior pituitary hormones decreases, except prolactin, which increases due to loss of dopamine inhibition.
34
Q: What are the hypothalamic regulators for each hormone?
GH: GHRH (+), Somatostatin (−) Prolactin: Dopamine (−) FSH & LH: GnRH (+), GnIH (−) TSH: TRH (+) ACTH: CRH (+)
35
Q: Where is GH produced and what is its structure?
A: Produced by somatotrophs; it's a 191 amino acid single-chain polypeptide.
36
Q: When is GH secretion highest?
A: During slow-wave sleep in pulsatile bursts.
37
Q: What regulates GH secretion?
GHRH (stimulates) Somatostatin (inhibits) Negative feedback from GH and IGF-1
38
Q: What receptor family does the GH receptor belong to?
A: Class I cytokine receptor family.
39
Q: What is the main GH signaling pathway?
Jak-STAT pathway GH binds GH-R → activates Jak2 Jak2 phosphorylates STAT5 STAT5 dimerizes and translocates to nucleus Activates gene transcription (e.g., IGF-1)
40
Q: What is the somatomedin hypothesis?
A: GH stimulates the liver to produce IGF-1 (somatomedin C), which then promotes tissue growth.
41
Q: What are the actions of IGF-1?
Stimulates cell proliferation and survival Acts via PI3K/AKT and MAPK pathways Promotes hypertrophy and hyperplasia
42
Q: What signaling pathway does GH primarily use?
A: The Jak-STAT pathway.
43
Q: What are the key molecules in GH signaling?
Jak2 (Janus kinase 2) STAT5 (Signal Transducer and Activator of Transcription 5)
44
Q: What is the sequence of GH receptor signaling?
GH binds GH-R GH-R changes shape Jak2 is activated and phosphorylates GH-R STATs dock and are phosphorylated STATs dimerize and enter nucleus STATs activate gene transcription (e.g., IGF-1)
45
Q: What is the somatomedin hypothesis?
A: GH stimulates the liver to produce IGF-1 (somatomedin C), which promotes tissue growth.
46
Q: What are the actions of IGF-1?
Stimulates cell proliferation and survival Acts via PI3K/AKT and MAPK pathways Promotes hypertrophy and hyperplasia
47
Q: What are the two major postnatal growth spurts?
Infancy (birth to ~2–3 years) Puberty (girls: 8–13 yrs, boys: 10–15 yrs)
48
Q: What regulates long bone growth?
A: GH and IGF-1 at the epiphyseal plate.
49
Q: What causes growth plate closure?
A: Oestrogen after puberty.
50
Q: What are GH’s direct metabolic effects?
Muscle: ↑ amino acid uptake, ↓ glucose uptake, ↓ protein breakdown Adipose: ↑ lipolysis, ↓ glucose uptake Liver: ↑ gluconeogenesis, ↑ protein synthesis Overall: ↑ blood glucose (anti-insulin effect)
51
Q: What regulates GH secretion?
GHRH (stimulates) Somatostatin (inhibits) IGF-1 (negative feedback)
52
Q: What is Pit1?
A: A transcription factor essential for pituitary development and GH expression.
53
Q: What factors influence GH secretion?
Metabolic: High amino acids, low fatty acids, hypoglycemia Neural: Exercise, slow-wave sleep, malnutrition Hormonal: Sex steroids
54
Q: What are the effects of GH deficiency in children?
Short stature (max ~1.2 m) Normal proportions Poor muscle development Excess fat Treatable with recombinant GH if diagnosed early
55
Q: What is gigantism?
A: GH excess before epiphyseal closure → abnormally tall stature with normal proportions.
56
Q: What is acromegaly?
A: GH excess after epiphyseal closure → enlarged hands, feet, face, thickened soft tissues.
57
Q: How is acromegaly treated?
Somatostatin analogues Surgery (e.g., for pituitary tumors)
58
Q: What is the structure of prolactin?
A: A polypeptide hormone with 199 amino acids.
59
Q: Where is prolactin synthesized and secreted?
A: From lactotrophs in the anterior pituitary.
60
Q: What stimulates and inhibits prolactin secretion?
Stimulated by an unknown Prolactin Releasing Factor (PRF) Inhibited by dopamine (Prolactin Inhibiting Factor, PIF)
61
Q: How does dopamine inhibit prolactin?
Binds to D2 receptors (Gi-coupled) on lactotrophs Inhibits adenylyl cyclase, ↓ cAMP Prevents Ca²⁺ influx and PRL exocytosis
62
Q: What are the effects of dopamine on prolactin?
Short-term: inhibits secretion Medium-term: inhibits synthesis Long-term: inhibits lactotroph proliferation
63
Q: What receptor does prolactin use?
A: Cytokine receptor (tyrosine kinase-associated)
64
Q: What is the main signaling pathway for PRL?
JAK2-STAT5 pathway PRL binds → activates JAK2 → phosphorylates STAT5 → STAT5 dimerizes → enters nucleus → gene transcription
65
Q: What are the main actions of prolactin?
Stimulates milk synthesis and secretion Promotes mammary epithelial cell (MEC) differentiation Involved in immune function and behavior
66
Q: What does prolactin do during pregnancy?
Induces alveologenesis (formation of milk-producing alveoli) Works with oestrogens and progesterone
67
Q: What does prolactin do during lactation?
Regulates lactopoiesis (milk production) Increases expression of milk proteins (e.g., β-casein, WAP, α-lactalbumin) Stimulates lactose production (main osmotic driver of milk volume)
68
Q: What type of feedback regulates prolactin in non-lactating individuals?
A: Short-loop negative feedback via dopamine.
69
Q: Why is there no long-loop feedback for prolactin?
A: The mammary gland does not produce a hormone to feedback to the hypothalamus.
70
Q: What causes increased PRL during lactation?
Reduced dopamine (PIF) Increased PRF (identity unknown) Oestrogens upregulate PRL mRNA
71
Q: What hormones are involved in the suckling response?
Oxytocin: triggers milk ejection (immediate) Prolactin: stimulates milk production for the next feed (feed-forward)
72
Q: What is the main signaling pathway for prolactin?
A: JAK2–STAT5 pathway.
73
Q: What happens after PRL binds to its receptor?
JAK2 phosphorylates STAT5 STAT5 dimerizes and translocates to the nucleus Activates transcription of target genes (e.g., milk proteins)
74
Q: What other STATs may be involved in PRL signaling?
A: STAT1 and STAT3 in some cells.
75
Q: What are PRL’s key actions in MECs during lactation?
Stimulates milk protein synthesis (β-casein, WAP, α-lactalbumin) Enhances milk fat secretion Regulates lactose production via lactose synthase Maintains tight junction integrity
76
Q: What neurons mediate PRL’s short-loop negative feedback?
A: Tuberoinfundibular dopamine (TIDA) neurons in the arcuate nucleus.
77
Q: How does PRL regulate dopamine?
PRL binds to PRL-R on TIDA neurons Activates JAK2–STAT5 Increases tyrosine hydroxylase expression → ↑ dopamine synthesis Dopamine inhibits PRL secretion
78
Q: What happens to PRL regulation during lactation?
Suckling reduces dopamine output TIDA neurons become insensitive to PRL Leads to hyperprolactinemia, which is normal in lactation
79
Q: What causes TIDA neuron insensitivity to PRL?
Upregulation of CIS (Cytokine-Inducible SH2-containing protein), a SOCS protein CIS blocks JAK-STAT signaling in TIDA neurons
80
Q: What is hormone insensitivity?
A: When hormone levels are normal or high, but target cells fail to respond due to receptor or signaling defects.
81
Q: What causes PRL insensitivity in TIDA neurons during lactation?
Not due to reduced PRL-R expression Due to increased CIS expression, which inhibits STAT5 activation
82
Q: What are symptoms of prolactin hypersecretion (e.g., prolactinomas)?
Females: Galactorrhea, amenorrhea Males: Gynecomastia, low libido
83
Q: What is the effect of high PRL on reproduction?
A: Inhibits the hypothalamic-pituitary-gonadal axis, reducing fertility.
84
Q: What causes the increase in PRL during suckling?
Reduced dopamine (PIF) → disinhibition of lactotrophs Increased PRF (identity unknown)
85
Q: What is the role of PRL in lactation?
Maintains milk production Supports alveolar cell differentiation Regulated by short-loop feedback that is suppressed during suckling
86