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Clinical Chemistry > Intro to Endocrinology > Flashcards

Intro to Endocrinology Flashcards

Spring 2024

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1
Q

Hormone

A

Chemical substance that sends a message to another cell in the body

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2
Q

Give example of endocrine, exocrine, neurocrine, and paracrine cellular messaging

A

Endocrine: bloodstream
Exocrine: GI tract
Neurocrine: neurologically
Paracrine: interstitial fluid

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3
Q

List the glands that we cover

A
  • Hypothalamus
  • Pituitary
  • Thyroid
  • Parathyroid
  • Adrenal gland
  • Pancreas
  • Ovaries
  • Testes
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4
Q

List the 6 hormone classifications

A
  1. Amine
  2. Peptide
  3. Protein
  4. Glycoprotein
  5. Steroid
  6. Fatty acid
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5
Q

Amine hormones

A
  • Trp or Tyr are modified to create amine hormones
  • Epinephrine, triiodothyronine, thyroxine, serotonin
  • Very short half-lives
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6
Q

Peptide hormones

A
  • Chain < 50 aa
  • Water soluble, don’t cross membranes easily
  • Must first bind to membrane-bound receptors
  • Vasopressin and oxytocin
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7
Q

Protein hormones

A
  • Chain > 50 aa
  • ACTH, calcitonin, insulin, glucagon, oxytocin
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8
Q

Glycoprotein hormones

A
  • Conjugated to carbs
  • FSH, LH, and TSH
  • Solubility and half-life similar to protein hormones
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9
Q

Steroid hormones

A
  • Derived from lipid, usually cholesterol
  • Hydrophobic, must be transported in blood bound to carrier proteins
  • Can cross membranes due to lipids
  • Aldosterone, cortisol, estrogen, progesterone, testosterone, other androgens (DHEA)
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10
Q

Fatty acid hormones

A
  • Derivatives of arachidonic acid
  • Eicosanoids, leukotrienes, prostaglandins, thromboxanes
  • Rapidly degraded, effective for only seconds
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11
Q

Metabolism

A

The sum of chemical processes that occur within a living organism to maintain life (catabolism + anabolism)

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12
Q

Anabolism

A

Creating substances

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13
Q

Catabolism

A

Breaking down substances

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14
Q

Hormone metabolism

A

The speed of anabolism or catabolism determines the extent to which hormones are capable of binding to receptors and eliciting effects

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15
Q

Conditions that modify hormone metabolism/levels

A
  • Speed of production or breakdown affects blood hormone levels
  • Amount of carrier protein affects protein-bound hormone levels
  • Disease states (e.g., cirrhosis) affect enzymatic hormone breakdown
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16
Q

Effects of alcohol consumption on hormone metabolism

A
  • Increase testosterone degradation
  • Leads to cirrhosis, which can cause less albumin and other binding proteins
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17
Q

Adrenal steroid hormone synthesis

A

Many hormones are produced in the adrenal gland by a cascade of enzymatic reactions

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18
Q

Which two organs predominantly eliminate hormones?

A

Kidney and liver

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19
Q

General mechanism for hormone elimination

A

Blood -> Liver tags certain hormones for destruction or creation of different substances (or kidney)

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20
Q

Steroid hormone elimination mechanism

A

Inactivating metabolic pathways and excretion in urine or bile

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21
Q

Thyroid hormone excretion mechanism

A

Inactivated by intracellular deiodinases

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22
Q

Catecholamine hormone excretion mechanism

A

Rapidly degraded within blood circulation

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23
Q

Fatty acid derivative hormone excretion mechanism

A

Rapidly inactivated by metabolism and typically active for a short time period (seconds)

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24
Q

Negative feedback

A

A stimulus will feedback upstream and decrease production of itself (e.g., thyroid)

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25
Q

Positive feedback

A

Increase the stimulus received until a distinct endpoint is achieved (e.g., coagulation cascade)

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26
Q

Thyroid negative feedback mechanism

A

:)

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27
Q

Primary endocrine disorder

A

Thyroid main problem because lack thyroid hormones (T3, T4)

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28
Q

Secondary endocrine disorder

A

Pituitary is the problem. Lack TSH

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29
Q

Tertiary endocrine disorder

A

Hypothalamus is the problem. Lack TRH

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30
Q

List factors that affect hormone levels

I would review slide details for these

A
  • emotional stress
  • time of day
  • menstrual cycle
  • menopause
  • diet
  • drugs
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31
Q

List the 3 distinct parts of the pituitary

A
  • anterior pituitary
  • intermediate lobe
  • posterior pituitary
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32
Q

Posterior pituitary

A
  • Arises from diencephalon
  • Responsible for storage/release of oxytocin and AVP/ADH
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33
Q

Anterior pituitary

A

Receives 80%-90% of blood supply and many hypothalamic factors via the hypothalamic-hypophyseal portal system

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34
Q

When can pituitary function be gestationally detected?

A

Between 7th and 9th week

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35
Q

Lactotrophs

A

Prolactin-secreting cells

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36
Q

Somatotrophs

A

GH-secreting cells

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37
Q

Thyrotrophs

A

TSH-secreting cells

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38
Q

Corticotrophs

A

ACTH-secreting cells

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39
Q

Gonadotrophs

A

LH- and FSH-secreting cells

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40
Q

Afferent pathways (inputs) to the hypothalamus

A

Integrated in various specialized nuclei and then resolved into specific responses

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41
Q

Relate the hypothalamus’ many efferent (output) neural connections to higher brain centers to responses for each specific pituitary hormone

A

The responses are similar for each hormone and characterized by negative feedback mechanisms, pulsatility, and diurnal variation

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42
Q

Give example of endocrine feedback loop

A

Hypothalamic-pituitary-thyroidal axis

Thyroid secretes thyroxine to act on hypothalamus

43
Q

How are all anterior pituitary hormones secreted? Examples?

A

Pulsatile fashion, such as LH and FSH

44
Q

How is pulse frequency of secretion regulated?

A

Neural modulation and is specific for each hypothalamus-pituitary-end organ unit

45
Q

Which hormone’s secretion profile does GnRH pulse frequency affect?

A

LH

46
Q

Hormones with diurnal variation

A
  • ACTH (trough 11pm-3am, peak 6am-9am
  • TSH nocturnal levels 2x daytime levels
47
Q

T/F
According to autopsy studies, up to 50% of people harbor clinically silent pituitary adenomas

A

False, 20%

48
Q

T/F
Pituitary tumors are found in 10-30% of normal individuals undergoing MRI exams

A

True

49
Q

T/F
Pituitary tumors account for 78% of lesions from patients who have undergone transsphenoidal surgery

A

False, 91%

50
Q

When can pituitary enlargement be seen?

A

Puberty and pregnancy

51
Q

List tumors in order of clinical significance

A
  1. Prolactin-secreting
  2. “null cell”
  3. TSH, GH, ACTH, or gonadotropin-secreting
52
Q

List anterior pituitary hormones plus functions

A
  • GH = tissue growth
  • TSH = thyroid hormones
  • ACTH = cortical hormones
  • FSH = testes/ovaries
  • LH = testes/ovaries
  • PRL (prolactin) = breast glandular tissue
53
Q

List posterior pituitary hormones

A
  • oxytocin = uterine contraction/lactation
  • ADH/AVP/vasopressin = kidney water reabsorption
54
Q

Compare hormones secreted from anterior pituitary (AP) to those secreted from hypothalamus

A
  • AP hormones are larger and more complex
  • May be tropic or direct effectors
55
Q

Tropic hormones

A

Actions are specific for another endocrine gland

56
Q

Direct effectors

A

Directly act on peripheral tissue

57
Q

Hypothalamic-pituitary target organ axis

A

:)

58
Q

Role of pituitary gland and why

A

Vital for normal growth because it secretes somatotropin aka growth hormone

59
Q

Effect or removing the pituitary

A

Growth ceases
Also ceases if hormonal products from other endocrine glands acted on by anterior pituitary are replaced

60
Q

How do you restore growth?

A

Administer GH

61
Q

Somatotropin

A

Same as growth hormone, which is pulsatile

62
Q

Why is GH amphibolic?

A

Bc it directly influences both anabolic and catabolic processes

63
Q

How does GH affect fasting/fast states?

A
  • Allows person to transition from fed to fasting state
  • No shortage of normal intracellular oxidation substrates
64
Q

How does GH affect insulin/glucose metabolism?

A
  • Inhibits insulin effects
  • Promotes hepatic gluconeogenesis and lipolysis
  • Lipolysis enhanced by providing oxidative substrates for peripheral tissue and conserves glucose for CNS by stimulating hepatic delivery of glucose/inhibiting insulin-mediated glucose metabolism
65
Q

Is GH a tropic hormone or direct effector?

A

Direct effector on many peripheral tissues

66
Q

Insulin-like growth factor (IGF)

A
  • Growth factor induced by GH in liver
  • Cell surface receptors distinct from insulin, but IGF-2 can cross-react with insulin receptor and cause hypoglycemia
  • Mediates indirect effects of GH
67
Q

T/F
Single random GH measurement is diagnostic

A

False, it’s rarely diagnostic
GH measurement has limited value

68
Q

GH testing

A
  • Baseline measurements helpful
  • Interpret in conjunction with glucose suppression tests to diagnose acromegaly
  • Interpret in conjunction with GH stimulation test to diagnose GH deficiency
69
Q

How to diagnose acromegaly in childhood/adolescence

A
  • Glucose tolerance test and measuring IGF-1 (preferred)
  • IGF-1 useful in eval excess/deficient growth disorders in both adults and children
  • IGF-1 can monitor recombinant GH treatment and follow-up
70
Q

Strategies to stimulate GH

A
  • Insulin-induced hypoglycemia (outdated)
  • Combo infusions of GHRH and L-arginine
  • Infusion of L-arginine coupled with oral L-DOPA
71
Q

Acromegaly

A
  • Pathologic or autonomous GH excess, usually result of tumor
  • If GH-producing tumor occurs before epiphyseal closure of long bones, then gigantism results
72
Q

What happens if GH-producing tumor happens after puberty?

A
  • Classical/insidious features: bony and soft tissue overgrowth
  • Progressive enlargement of hands and feet, growth of facial bones (mandible/skull), teeth gaps, arthritis, sleep apnea, excess sweating/heat intolerance
73
Q

Acromegaly treatment

A
  • Tumor ablation with continued function of remaining pituitary
  • Transsphenoidal adenctomy procedure of choice
  • External beam/focused irrradiation may take several years to take full effect
  • Treatment does NOT reverse bone growth effects
74
Q

How does GH deficiency manifest in children

A

Growth failure
Not all short pts have GH deficiency

75
Q

How does GH deficiency manifest in adults?

A
  • Complete or partial anterior pituitary failure
  • Vague symptoms: social withdrawal, fatigue, loss of motivation, diminished feeling of well-being
  • Osteoporosis and body composition alterations
76
Q

Prolactin

A
  • Structurally related to GH and human placental lactogen
  • Stress hormone
  • Vital functions in reproduction
  • Unique due to tonic inhibition as mode of hypothalamic regulation instead of intermittent stimulation
77
Q

Prolactinoma

A
  • Pituitary tumor that secretes prolactin, most common functional pituitary tumor
  • Clinical presentation depends on pt age/gender, tumor size
78
Q

Prolactin-inhibitor factor

A

Dopamine
Only neuroendocrine signal that inhibits prolactin

79
Q

Management of prolactinoma

A
  • Reducing tumor mass
  • Restoring normal gonadal function/fertility
  • Preventing osteoporosis
  • Preserving normal anterior/posterior pituitary function
  • Therapeutic options: simple observation, surgery, radiotherapy, medical management with dopamine agonists
80
Q

Prolactin > 150ng/mL indicates what cause?

A
  • Prolactinoma
  • Degree of elevation correlates with tumor size
81
Q

Prolactin 25-100 ng/mL indicates what causes?

A
  • Pituitary stalk interruption
  • Dopaminergic antagonist meds
  • Primary thryoidal failure
  • Renal failure
  • Polycystic ovary syndrome
82
Q

Clinical eval of hyperprolactinemia

A
  • History/physical exam usually enough to exclude most common non-endocrine causes
  • Essential to obtain TSH and free T4 to eliminate primary hypothyroidism as a cause for the elevated prolactin
  • If pituitary tumor sus, assess other anterior pituitary function: ACTH/cortisol, LH, FSH, gender-specific gonadal steroids, MRI
83
Q

Idiopathic galactorrhea

A
  • Lactation in women with normal prolactin levels
  • Usually seen in women who have gotten pregnant several times and no pathological implication
84
Q

Hyperprolactinemia associated with…?

A
  • Renal failure
  • Cirrhosis
  • Hypothyroidism
  • Trauma
  • Inflammation
  • Drugs (TCS, phenothiazine’s, reserpine)
  • Adrenal insufficiency
  • Prolactinoma
85
Q

Clinical manifestation of prolactinoma in non-postpartum women and women with amenorrhea

A
  • Galactorrhea 30-%0&
  • Menstrual irregularity
  • Infertility
86
Q

Clinical manifestation of prolactinoma in men

A
  • Hypogonadism
  • Erectile dysfunction
  • Galactorrhea < 30%
  • Visual abnormalities
  • Extra-ocular muscle weakness
  • Headache
87
Q

Panhypopituitarism

A

Complete loss of anterior pituitary function due to failure of either pituitary or hypothalamus

88
Q

Monotropic hormone deficiency

A

Loss of single pituitary hormone

89
Q

Lab diagnosis of hypopituitarism

A
  • Straight-forward
  • Primary failure of endocrine gland accompanied by dramatic increases in circulating levels of corresponding pituitary tropic hormone
  • Secondary failure (hypopituitarism) associated with low or normal levels of tropic hormone
90
Q

Etiology of hypopituitarism

A
  • Various types of tumors
  • Postpartum ischemic necrosis of pituitary
  • Infiltrative diseases such as hemochromatosis, sarcoidosis, histiocytosis
  • Fungal infections, TB, syphilis
  • Lymphocytic hypophysitis
  • Severe head trauma, pituitary surgery, radiotherapy
91
Q

Panhypopituitarism treatment

A
  • Thyroxine, glucocorticoids, gender-specific sex steroids
  • Replacement therapy tricker in patients who desire fertility
92
Q

Posterior pituitary

A

Extension of forebrain and represents the storage region for AVP and oxytocin

93
Q

Where are AVP and oxytocin synthesized?

A
  • Supraoptic and paraventricular nuclei of the hypothalamus and transported to the neurohypophysis via axons in the hypothalamoneurohypophyseal tract
  • Also made outside of hypothalamus in various tissues
94
Q

Synthesis of AVP and oxytocin tightly linked to production of ______

A

Neurophysin

95
Q

Oxytocin

A
  • Critical role in lactation, labor, and parturition (childbirth)
  • Secretion responds to positive feedback loop
  • Uterine contractions propagate oxytocin release, causing more contractions
  • Maternal nurturing and mother-infant bonding
  • Effects on pituitary, renal, cardiac, metabolic, and immune function
96
Q

Pitocin

A

Synthetic oxytocin

97
Q

AVP major action

A

Regulate renal free water excretion

98
Q

Where are vasopressin receptors in kidney concentrated?

A

Renal collecting tubules and ascending limb of loop of Henle

99
Q

Other AVP functions

A
  • Potent pressor agent (elevates BP)
  • Affects blood clotting by promoting Factor VII release from hepatocytes
  • Von willebrand factor release from endothelium
100
Q

How dos plasma osmolality increase affect AVP secretion?

A

Increases vasopressin secretion
Osmoreceptors very sensitive to even small changes

101
Q

What happens to AVP release if blood pressure or volume fall?

A

Vascular baroreceptors initiate AVP release

102
Q

How is AVP regulated?

A

By hypothalamic osmoreceptors and vascular baroreceptors

103
Q

Diabetes insipidus

A

AVP deficiency or resistance

104
Q

AVP excess

A
  • Much more difficult to treat than deficiency due to free water retention
  • Restricting free water intake to small amounts each day has been main treatment

Clinical Chemistry (21 decks)

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