M4-ENDOCRINOLOGY TRANS Flashcards

(182 cards)

1
Q

What are the two primary feedback mechanisms in the endocrine system?

A

Feedback inhibition (negative feedback) and feedback stimulation (positive feedback)

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2
Q

How does feedback inhibition work?

A

An increase in a specific hormone inhibits its production to maintain balance

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3
Q

How does feedback stimulation work?

A

A decrease in a specific hormone stimulates its production to restore levels

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4
Q

What glands compose the hypothalamic-pituitary-target organ axis?

A

Hypothalamus

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5
Q

What is the role of the anterior pituitary gland?

A

Synthesizes hormones like TSH

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6
Q

What is the role of the posterior pituitary gland?

A

Stores and releases hormones produced by the hypothalamus (ADH and oxytocin)

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7
Q

What are hormones?

A

Chemical substances that transmit messages to target cells in the body

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8
Q

What are the four types of hormone communication?

A

Endocrine

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9
Q

How do endocrine hormones communicate?

A

Messages sent via the bloodstream to distant target cells

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10
Q

How do exocrine hormones communicate?

A

Messages sent via the gastrointestinal tract (e.g.

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11
Q

How do neurocrine hormones communicate?

A

Messages sent neurologically through synaptic transmission

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12
Q

How do paracrine hormones communicate?

A

Messages sent via interstitial fluid to nearby cells

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13
Q

What defines the hypothalamic-pituitary-target organ axis?

A

A feedback-regulated system where the hypothalamus releases hormones to stimulate the pituitary

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14
Q

What hormones does the hypothalamus produce to regulate the anterior pituitary?

A

TRH (TSH release)

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15
Q

What anterior pituitary hormones are synthesized (not stored)?

A

TSH

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16
Q

What hormones are stored (not synthesized) in the posterior pituitary?

A

Oxytocin and ADH (produced in hypothalamic nuclei

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17
Q

How does TRH regulate thyroid function?

A

TRH → anterior pituitary → TSH release → thyroid → T3/T4 synthesis (negative feedback suppresses TRH/TSH when T3/T4 levels rise)

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18
Q

What cells produce ACTH in the anterior pituitary?

A

Corticotrophs (stimulated by CRH

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19
Q

What clinical condition results from hypothalamic-pituitary stalk damage?

A

Diabetes insipidus (ADH deficiency) or hypopituitarism (e.g.

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20
Q

What is the role of the hypophyseal portal system?

A

Connects hypothalamus to anterior pituitary

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21
Q

Why is synthetic oxytocin (Pitocin) used during labor?

A

To induce/augment uterine contractions when natural oxytocin production is insufficient (e.g.

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22
Q

What defines Sheehan’s syndrome?

A

Postpartum pituitary necrosis due to severe hypotension

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23
Q

How is adrenal insufficiency (Addison’s) diagnosed?

A

Low cortisol + elevated ACTH (primary) or low ACTH (secondary)

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24
Q

What surgical intervention treats pheochromocytoma?

A

Adrenalectomy after α-blockade (phenoxybenzamine) to prevent catecholamine crisis

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25
What criteria warrant adrenal incidentaloma surgery?
Size ≥4 cm
26
What distinguishes Cushing’s disease from syndrome?
Disease: pituitary ACTH-secreting adenoma; Syndrome: any etiology causing hypercortisolism (e.g.
27
How does the renin-angiotensin system regulate aldosterone?
Renin (from kidneys) → Angiotensin II → aldosterone release (sodium retention
28
What genetic mutation causes congenital adrenal hyperplasia?
21-hydroxylase deficiency (95% of cases)
29
What is the first-line test for pheochromocytoma?
24-hour urine fractionated metanephrines (elevated normetanephrine/metanephrine)
30
What hormone imbalance causes acromegaly?
Chronic GH excess (pituitary adenoma) → elevated IGF-1 (somatomedin C)
31
What lab findings confirm primary hyperaldosteronism?
Elevated aldosterone + suppressed renin (aldosterone:renin ratio >30)
32
What is the function of ANP-like peptides in the adrenal medulla?
Counteract RAAS by promoting natriuresis and vasodilation (distinct from cardiac ANP)
33
What are the three hormones produced by the thyroid gland?
Thyroxine (T4) Triiodothyronine (T3) Calcitonin
34
What is the role of calcitonin?
Hypocalcemic agent released in response to hypercalcemia inhibiting PTH and vitamin D
35
What does parathyroid hormone (PTH) regulate?
Hypercalcemic agent released during hypocalcemia activating bone resorption renal calcium reabsorption vitamin D production
36
What are the layers of the adrenal cortex?
Outer layer producing aldosterone cortisol adrenal androgens and estrogen
37
What hormones does the adrenal medulla secrete?
Norepinephrine Epinephrine
38
What androgens do the ovaries produce?
Dehydroepiandrosterone (DHEA) Dehydroepiandrosterone Sulfate (DHEAS)
39
What hormones do the testes produce?
Testosterone Inhibin B
40
What is glucagon's function?
Hyperglycemic agent released by pancreatic alpha cells during hypoglycemia via glycogenolysis and gluconeogenesis
41
What is insulin's mechanism?
Hypoglycemic agent released by pancreatic beta cells promoting glucose uptake and glycogenesis
42
What hormone regulates sleep-wake cycles?
Melatonin produced by the pineal gland inhibited by light and released in darkness
43
How does light exposure affect melatonin?
Light inhibits melatonin production while darkness stimulates its release
44
What is the primary role of thyroxine (T4)?
Regulates metabolism by increasing basal metabolic rate and oxygen consumption
45
What converts T4 to active T3?
Deiodination in peripheral tissues (liver kidneys)
46
What triggers PTH release?
Hypocalcemia detected by parathyroid gland calcium-sensing receptors
47
How does PTH increase calcium levels?
Activates osteoclasts to resorb bone enhances renal calcium reabsorption stimulates renal vitamin D synthesis
48
What is aldosterone's primary action?
Sodium reabsorption in renal tubules to regulate blood pressure and electrolyte balance
49
What controls cortisol secretion?
ACTH from the anterior pituitary which is stimulated by CRH from the hypothalamus
50
What are adrenal androgens?
Sex hormones (DHEA DHEAS) produced by the adrenal cortex alongside gonadal hormones
51
What distinguishes pancreatic alpha and beta cells?
Alpha cells secrete glucagon (raises blood glucose) beta cells secrete insulin (lowers blood glucose)
52
What is the role of melatonin in circadian rhythm?
Synchronizes sleep-wake cycles with environmental light-dark patterns
53
What happens to melatonin production during nighttime light exposure?
Artificial light blocks melatonin release disrupting sleep patterns
54
What defines the hypothalamic-pituitary-target organ axis?
A feedback-regulated system where the hypothalamus releases hormones to stimulate the pituitary which then activates target glands (e.g. thyroid adrenals)
55
What hormones does the hypothalamus produce to regulate the anterior pituitary?
TRH (TSH release) CRH (ACTH release) GnRH (LH/FSH release) GHRH (GH release) somatostatin (GH/TSH inhibition)
56
What anterior pituitary hormones are synthesized (not stored)?
TSH ACTH FSH LH prolactin GH
57
What hormones are stored (not synthesized) in the posterior pituitary?
Oxytocin and ADH (produced in hypothalamic nuclei transported via hypothalamohypophyseal tract)
58
How does TRH regulate thyroid function?
TRH → anterior pituitary → TSH release → thyroid → T3/T4 synthesis (negative feedback suppresses TRH/TSH when T3/T4 levels rise)
59
What cells produce ACTH in the anterior pituitary?
Corticotrophs (stimulated by CRH suppressed by cortisol)
60
What clinical condition results from hypothalamic-pituitary stalk damage?
Diabetes insipidus (ADH deficiency) or hypopituitarism (e.g. Sheehan’s syndrome)
61
What is the role of the hypophyseal portal system?
Connects hypothalamus to anterior pituitary allowing direct hormone transport (e.g. CRH → ACTH release)
62
Why is synthetic oxytocin (Pitocin) used during labor?
To induce/augment uterine contractions when natural oxytocin production is insufficient (e.g. prolonged labor)
63
What defines Sheehan’s syndrome?
Postpartum pituitary necrosis due to severe hypotension causing panhypopituitarism (ACTH/TSH/LH/FSH deficiency)
64
How is adrenal insufficiency (Addison’s) diagnosed?
Low cortisol + elevated ACTH (primary) or low ACTH (secondary) confirmed by cosyntropin stimulation test
65
What surgical intervention treats pheochromocytoma?
Adrenalectomy after α-blockade (phenoxybenzamine) to prevent catecholamine crisis
66
What criteria warrant adrenal incidentaloma surgery?
Size ≥4 cm hormonal hypersecretion (cortisol/aldosterone/catecholamines) or malignant imaging features
67
What distinguishes Cushing’s disease from syndrome?
Disease: pituitary ACTH-secreting adenoma; Syndrome: any etiology causing hypercortisolism (e.g. adrenal tumor exogenous steroids)
68
How does the renin-angiotensin system regulate aldosterone?
Renin (from kidneys) → Angiotensin II → aldosterone release (sodium retention potassium excretion)
69
What genetic mutation causes congenital adrenal hyperplasia?
21-hydroxylase deficiency (95% of cases) leading to cortisol deficiency + androgen excess
70
What is the first-line test for pheochromocytoma?
24-hour urine fractionated metanephrines (elevated normetanephrine/metanephrine)
71
What hormone imbalance causes acromegaly?
Chronic GH excess (pituitary adenoma) → elevated IGF-1 (somatomedin C)
72
What lab findings confirm primary hyperaldosteronism?
Elevated aldosterone + suppressed renin (aldosterone:renin ratio >30)
73
What is the function of ANP-like peptides in the adrenal medulla?
Counteract RAAS by promoting natriuresis and vasodilation (distinct from cardiac ANP)
74
What are the main structural classifications of hormones?
Amine Peptide Protein Glycoprotein Steroid Fatty Acids
75
What defines amine hormones?
Derived from amino acids (tryptophan/tyrosine) with short half-lives (e.g. catecholamines thyroid hormones melatonin)
76
What are examples of amine hormones?
Epinephrine Norepinephrine Triiodothyronine Thyroxine Serotonin Melatonin
77
What characterizes peptide hormones?
Hydrophilic ≤50 amino acids (e.g. vasopressin oxytocin) requiring cell surface receptors
78
How do peptide hormones enter cells?
Bind surface receptors (cannot cross lipid bilayer) triggering secondary messengers
79
What distinguishes protein hormones?
>50 amino acids (e.g. ACTH calcitonin insulin glucagon)
80
What defines glycoprotein hormones?
Protein-carbohydrate conjugates (e.g. FSH LH TSH)
81
What are steroid hormones derived from?
Cholesterol (hydrophobic) crossing membranes easily (e.g. aldosterone cortisol sex hormones)
82
How are steroid hormones transported in blood?
Bound to carrier proteins (slow diffusion)
83
What are fatty acid-derived hormones?
Eicosanoids from arachidonic acid (e.g. prostaglandins leukotrienes thromboxane) with rapid degradation
84
What role do eicosanoids play?
Mediate inflammation blood clotting and cellular signaling
85
What determines hormone solubility?
Chemical structure: hydrophilic (peptides) vs hydrophobic (steroids)
86
How do amine hormone half-lives compare?
Short-lived (rapid degradation) due to amino acid structure
87
What differentiates T3/T4 from other amines?
Thyroid hormones have longer half-lives (days) due to protein binding
88
Why do peptide hormones act faster than steroids?
Water-soluble peptides circulate freely while steroids require carrier proteins
89
What are key examples of glycoprotein hormones?
FSH LH TSH (regulate reproductive/thyroid functions)
90
How do steroid hormones affect gene expression?
Bind intracellular receptors → DNA transcription (direct genomic effects)
91
What distinguishes prostaglandins from thromboxanes?
Prostaglandins regulate inflammation while thromboxanes promote platelet aggregation
92
Why are fatty acid hormones short-lived?
Degraded within seconds (localized signaling)
93
What is the precursor for eicosanoids?
Arachidonic acid (membrane phospholipid derivative)
94
How do hydrophilic vs hydrophobic hormones differ in receptor binding?
Hydrophilic bind surface receptors (peptides) hydrophobic bind intracellular receptors (steroids)
95
How are hormones metabolized?
Catabolism (breakdown) and anabolism (synthesis)
96
What organs eliminate most hormones?
Kidneys and liver
97
How are steroid hormones excreted?
Through urine or bile
98
What inactivates thyroid hormones (T3/T4)?
Intracellular deiodinases
99
How are catecholamines eliminated?
Via blood circulation
100
What happens to fatty acid-derived hormones?
Rapidly inactivated by metabolism
101
What are the two forms of hormone transport?
Free/unbound (physiologically active) and protein-bound
102
How do water-soluble hormones travel in blood?
Easily dissolved (hydrophilic nature)
103
Why do fat-soluble hormones need carrier proteins?
Hydrophobic nature prevents free circulation in blood
104
Can water-soluble hormones cross cell membranes?
No (require surface receptors due to lipid bilayer barrier)
105
Can fat-soluble hormones enter cells directly?
Yes (cross lipid bilayer easily)
106
What structural feature determines hormone solubility?
Peptides=hydrophilic steroids=hydrophobic
107
What is the most common hormonal feedback loop?
Negative feedback (maintains homeostasis)
108
How does thyroid hormone negative feedback work?
High T3/T4 → inhibits hypothalamic TRH and pituitary TSH
109
What is positive feedback's primary function?
Amplifies changes until endpoint (e.g. childbirth)
110
What triggers oxytocin release during labor?
Cervical stretch receptors (Ferguson reflex) stimulating hypothalamus
111
What happens if natural oxytocin production is insufficient during labor?
Synthetic Pitocin administered to sustain contractions
112
What defines amine hormones?
Derived from tyrosine/tryptophan (e.g. catecholamines thyroid hormones)
113
How do peptide hormones signal cells?
Bind surface receptors → activate cAMP/calcium second messengers
114
What is unique about steroid hormone receptors?
Located intracellularly (direct DNA binding after crossing membrane)
115
What enzyme activates cAMP in peptide signaling?
Adenylyl cyclase (converts ATP → cAMP)
116
How is cAMP deactivated?
Phosphodiesterase (PDE) breaks it down
117
What distinguishes glycoprotein hormones?
Protein-carbohydrate complexes (e.g. FSH LH TSH)
118
Why do steroid hormones act slower than peptides?
Require DNA transcription/translation (genomic effects)
119
What is the half-life of luteinizing hormone (LH)?
20 minutes (shorter than FSH 3-4 hours)
120
What degrades hypothalamic releasing hormones?
Specific peptidases at release/action sites
121
What is the hypothalamic-pituitary-thyroid axis?
TRH → TSH → T3/T4 → negative feedback
122
How does ADH regulate water balance?
Binds kidney tubule receptors → inserts aquaporins → water reabsorption
123
What activates the renin-angiotensin system?
Low blood pressure → renin → angiotensin II → aldosterone release
124
What is the mobile receptor mechanism?
Steroids bind intracellular receptors → DNA transcription → protein synthesis
125
What is the fixed membrane receptor mechanism?
Peptides bind surface receptors → secondary messengers (e.g. cAMP)
126
What causes diabetes insipidus?
ADH deficiency (posterior pituitary/hypothalamus damage)
127
How is primary hyperaldosteronism diagnosed?
Elevated aldosterone + suppressed renin (ratio >30)
128
What happens in Sheehan’s syndrome?
Postpartum pituitary necrosis → panhypopituitarism
129
Why are NSAIDs used for inflammation?
Block prostaglandin synthesis from arachidonic acid
130
What is the role of phosphodiesterase inhibitors?
Prevent cAMP breakdown (prolong hormone signaling)
131
What defines primary hypothyroidism?
Thyroid gland dysfunction causing ↓T4 with ↑TSH (normal pituitary/hypothalamus)123
132
What defines secondary hypothyroidism?
Pituitary dysfunction causing ↓T4 + ↓TSH (normal TRH)435
133
What defines tertiary hypothyroidism?
Hypothalamus dysfunction causing ↓T4 + ↓TSH + ↓TRH435
134
What hormone pattern confirms primary hypothyroidism?
↓T4 ↑TSH ↑TRH235
135
What hormone pattern confirms secondary hypothyroidism?
↓T4 ↓TSH ↑TRH435
136
What hormone pattern confirms tertiary hypothyroidism?
↓T4 ↓TSH ↓TRH435
137
What is the most common cause of primary hypothyroidism?
Hashimoto’s thyroiditis (autoimmune)163
138
What causes secondary hypothyroidism?
Pituitary tumors Sheehan’s syndrome radiation damage435
139
What causes tertiary hypothyroidism?
Hypothalamic tumors TRH deficiency/resistance435
140
What defines primary hyperthyroidism?
Thyroid overactivity causing ↑T4 + ↓TSH735
141
What defines secondary hyperthyroidism?
Pituitary overactivity causing ↑T4 + ↑TSH735
142
What defines tertiary hyperthyroidism?
Hypothalamic overactivity causing ↑T4 + ↑TSH + ↑TRH735
143
What hormone pattern confirms primary hyperthyroidism?
↑T4 ↓TSH ↓TRH735
144
What hormone pattern confirms secondary hyperthyroidism?
↑T4 ↑TSH ↓TRH735
145
What hormone pattern confirms tertiary hyperthyroidism?
↑T4 ↑TSH ↑TRH735
146
How does emotional stress affect hormone levels?
Increases cortisol catecholamines growth hormone prolactin89
147
When does cortisol peak?
8 AM (declines throughout day)89
148
When does ACTH peak?
6-9 AM (nadir at 11 PM-3 AM)89
149
What inhibits melatonin production?
Light exposure89
150
How does iodine deficiency affect thyroid function?
Reduces T3/T4 synthesis → compensatory TSH-driven goiter23
151
Why does primary hypothyroidism show high TSH?
Intact pituitary responds to low T4 by releasing more TSH123
152
Why does secondary hypothyroidism show low TSH?
Damaged pituitary fails to respond to low T4435
153
Why does tertiary hypothyroidism show low TRH?
Hypothalamus cannot stimulate TSH release due to TRH deficiency435
154
What distinguishes primary vs secondary hyperthyroidism TSH levels?
Primary: ↓TSH (feedback inhibition) Secondary: ↑TSH (pituitary defect)735
155
What lab findings indicate Hashimoto’s thyroiditis?
High TPO antibodies + hypothyroid pattern635
156
How is Sheehan’s syndrome diagnosed?
Postpartum panhypopituitarism with low ACTH TSH FSH/LH435
157
What causes drug-induced hypothyroidism?
Antithyroid medications (methimazole) or lithium235
158
Why does radioactive iodine cause hypothyroidism?
Thyroid gland destruction during hyperthyroidism treatment235
159
What hormone dominates the follicular phase?
FSH (stimulates follicle development)
160
What hormone surge triggers ovulation?
LH (mid-cycle luteinizing hormone spike)
161
What characterizes the proliferative endometrium phase?
Estrogen-driven thickening (parallels follicular phase)
162
What defines the secretory endometrium phase?
Progesterone-driven glandular maturation (post-ovulation)
163
How long does the luteal phase typically last?
14 days (fixed duration vs variable follicular phase)
164
What hormonal pattern confirms menopause?
↑FSH + ↓estrogen (cessation of ovarian function)
165
How is menopause clinically diagnosed?
12 consecutive months without menses (no other causes)
166
What is the primary benefit of HRT for menopausal women?
Relief of vasomotor symptoms (hot flashes/night sweats)1[^2][^6]
167
What cardiovascular risks accompany combined HRT (estrogen+progestin)?
↑Venous thromboembolism ↑stroke risk (oral > transdermal)12[^7]
168
Why is estrogen-only HRT restricted?
Increases endometrial cancer risk (requires hysterectomy for use)1[^5][^8]
169
What HRT formulation minimizes clotting risk?
Transdermal estrogen + micronized progesterone2[^6][^7]
170
How does HRT impact bone health?
Prevents osteoporosis (maintains bone density)[^2][^4][^6]
171
What reduces breast cancer risk with HRT?
Natural estradiol (vs synthetic CEE) + short-term use (<5 years)2[^5][^8]
172
Why is HRT timing critical?
Starting before age 60/within 10 years of menopause maximizes benefits[^6][^7][^8]
173
What non-hormonal alternative helps urogenital symptoms?
Vaginal moisturizers/lubricants (supplemental to low-dose topical estrogen)1[^5]
174
Who requires testosterone replacement?
Hypogonadal men (confirmed low levels + symptoms)3
175
What risks accompany non-prescription testosterone use?
↑Cardiovascular events ↑prostate cancer risk3
176
What endocrine effect causes testicular shrinkage?
Negative feedback suppressing LH/FSH (reduced spermatogenesis)3
177
How do corticosteroids disrupt glucose?
Induce insulin resistance → hyperglycemia3
178
Why do psychotropic drugs cause SIADH?
Enhance ADH secretion/action → hyponatremia3
179
What is methimazole's primary action?
Inhibits thyroid peroxidase (blocks T3/T4 synthesis)3
180
How do ACE inhibitors affect aldosterone?
Reduce angiotensin II → ↓aldosterone (risk of hyperkalemia)3
181
How does high-carb intake affect growth hormone?
Disrupts glucose-mediated GH suppression → potential acromegaly risk3
182
What dietary factor protects bone during menopause?
Adequate calcium/vitamin D intake (synergistic with HRT)