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Table 57–2. Control Mechanisms for Pituitary Hormones.

Hormone Control Antidiuretic hormone (ADH) Serum osmolality Oxytocin Neural Growth hormone Serum glucose; hypothalamic GHRH 1, GHIH 1 Prolactin Hypothalamic PRH 1, PIH 1 Thyrotropin Serum thyroxine; hypothalamic TRH 1 Gonadotropins Serum estrogen, progesterone, testosterone; hypothalamic GRH 1 (LHRH 1 and FRH 1) Corticotropin Serum cortisol; hypothalamic CRH 1
 Table 57–1. Cell Types and Hormones of the Pituitary.

Cell Type Anterior pituitary Somatotroph Lactotroph Corticotroph 1

Quantity

Hormone

Action

40–50% 15–20% 15–20%

Growth hormone (somatotropin) Prolactin Corticotropin (ACTH) Beta–lipotropic hormone Beta–endorphin Alpha–melanocyte stimulating hormone

Growth of all body tissues; antagonist to insulin Proliferation of ductal tissue in breast and initiation of milk secretion Stimulation of adrenocortical steroid synthesis and secretion ... Endogenous opiate Dispersion of melanin in skin Stimulation of thyroid hormone synthesis and secretion Preovulatory growth of graafian follicle and estrogen secretion; with LH, induces ovulation With FSH, induces ovulation, formation of corpus luteum, and progesterone secretion ...

Thyrotroph Gonadotroph 2

5% 5%

Thyrotropin (TSH) Follicle–stimulating hormone (FSH) Luteinizing hormone (LH)

Nonsecretory (null) cells Posterior pituitary Hypothalamic nuclei

15–20%

None

Antidiuretic hormone (ADH) Oxytocin

Water resorption in distal nephron; arteriolar constriction Contraction of smooth muscle of uterus and breast ducts

Table 58–3. Differential Features in Thyroid Disease. Thyroid Gland Thyroid Hormones 1 Thyroid–Stimulating Hormone Autoantibodies

Hyperthyroidism Primary Graves' disease Toxic nodular goiter Toxic adenoma Subacute thyroiditis Secondary Pituitary thyrotropic adenoma Hypothyroidism Primary Thyroid agenesis Enzyme deficiency Iodine deficiency Hashimoto's thyroiditis Secondary Pituitary failure Atrophy Decreased Decreased None Absent Diffuse enlargement Diffuse/nodular goiter Diffuse enlargement Absent Decreased Decreased Decreased Elevated Elevated Elevated Elevated None None None Antithyroglobulin, anti–microsomal, anticolloid Diffuse enlargement Elevated Elevated None Diffuse enlargement Multinodular goiter Solitary nodule Tender enlargement Elevated Elevated Elevated Elevated Decreased markedly Decreased Decreased Normal Thyroid–stimulating Ig; exophthalmos–producing factor None None None

Table 17–4 Biologic Roles of Glucagon-Related Peptides.

Target Tissue Islet

Glucagon Stimulates insulin secretion

GLP-1 Stimulates insulin and somatostatin secretion Inhibits glucagon secretion (indirectly)

GLP-2

GIP Stimulates insulin, somatostatin, and glucagon secretion Inhibits glucagon secretion (indirectly)

Increases inhibiting inducing proliferation

cell mass by Increases cell death and inhibiting cell inducing cell cell death and cell mass by

proliferation Liver Stimulates glycogenolysis, glucogenesis, fatty acid oxidation, and ketogenesis Inhibits glycogen synthesis and fatty acid synthesis Stomach Inhibits gastric acid secretion Inhibits gastric emptying Intestine Stimulates mucosal growth and nutrient absorption Inhibits motility Adipose tissue Stimulates adipogenesis, lipogenesis, and adipokine production Inhibits appetite Inhibits gastric acid secretion and gastric emptying

Brain (hypothalamus)

Table 17–7 Factors Reducing Response to Insulin.

Pre-receptor

Insulin autoantibodies Reduced transendothelial transit

Primary defect in insulin signaling

Insulin receptor mutations Leprechaunism (complete) Rabson-Mendenhall syndrome (partial) Type A (mild) Defects in other genes involved in insulin signaling Insulin receptor autoantibodies (Type B) Ataxia telangectasia syndrome

Secondary to other endocrine disorders Cushing syndrome Acromegaly Pheochromocytoma

Glucagonoma Hyperthyroidism Insulinoma Secondary to other disorders Visceral obesity Stress (infection, surgery, etc) Uremia Hyperglycemia (mild resistance seen in type 1 diabetes) Liver disease Cytogenetic disorders (Down, Turner, Klinefelter) Neuromuscular disorders (muscular dystrophies, ataxias, muscle inactivity) Congenital lipodystrophies/lipoatrophy Acquired lipodystrophy Secondary to normal physiologic states Puberty Pregnancy Starvation Secondary to medications Glucocorticoids Atypical antipsychotic drugs Antiretroviral protease inhibitors Nicotinic acid Thiazide diuretics Oral contraceptive Progesterone

Blockers

Table 17–1. Summary of Principal Hypothalamic Regulatory Mechanisms.

Function Temperature regulation

Afferents from Temperature receptors in the skin, deep tissues, spinal cord, hypothalamus, and other parts of the brain

Integrating Areas Anterior hypothalamus, response to heat; posterior hypothalamus, response to cold

Neuroendocrine control of: Catecholamines Vasopressin Oxytocin Thyroid-stimulating hormone (thyrotropin, TSH) via TRH Adrenocorticotropic hormone (ACTH) and -lipotropin ( Limbic areas concerned with emotion Osmoreceptors, "volume receptors," others Touch receptors in breast, uterus, genitalia Temperature receptors in infants, perhaps others Dorsal and posterior hypothalamus Supraoptic and paraventricular nuclei Supraoptic and paraventricular nuclei Paraventricular nuclei and neighboring areas

Limbic system (emotional stimuli); reticular formation Paraventricular nuclei ("systemic" stimuli); hypothalamic and anterior pituitary cells sensitive to circulating blood cortisol level; suprachiasmatic nuclei (diurnal rhythm)

-LPH) via CRH Follicle-stimulating hormone (FSH) and luteinizing hormone (LH) via GnRH Prolactin via PIH and PRH Hypothalamic cells sensitive to estrogens, eyes, touch receptors in skin and genitalia of reflex ovulating species Touch receptors in breasts, other unknown receptors Preoptic area; other areas

Arcuate nucleus; other areas (hypothalamus inhibits secretion) Periventricular nucleus, arcuate nucleus

Growth hormone via somatostatin and GRH "Appetitive" behavior Thirst

Unknown receptors

Osmoreceptors, probably located in the organum vasculosum of the lamina terminalis; angiotensin II uptake in the subfornical organ Glucostat cells sensitive to rate of glucose utilization; leptin receptors; receptors for other polypeptides Cells sensitive to circulating estrogen and androgen, others

Lateral superior hypothalamus

Hunger

Ventromedial, arcuate, and paraventricular nuclei; lateral hypothalamus Anterior ventral hypothalamus plus, in the male, piriform cortex Diffuse, in limbic system and hypothalamus Suprachiasmatic nuclei

Sexual behavior

Defensive reactions (fear, rage) Control of body rhythms

Sense organs and neocortex, paths unknown Retina via retinohypothalamic fibers

Table 219-16 Differential Diagnosis of Hypoglycemia

Stroke Transient ischemic attack Seizure disorder Traumatic head injury Brain tumor Narcolepsy

Multiple sclerosis Psychosis Sympathomimetic drug ingestion Hysteria Altered sleep patterns and nightmares Depression

Ill or medicated individual 1. Drugs Insulin or insulin secretagogue Alcohol Others (refer to UpToDate table on drugs that cause hypoglycemia) 2. Critical illnesses Hepatic, renal, or cardiac failure Sepsis (including malaria) Inanition 3. Hormone deficiency Cortisol Glucagon and epinephrine (in insulin-deficient diabetes mellitus) 4. Nonislet cell tumor Seemingly well individual 5. Endogenous hyperinsulinism Insulinoma Functional β-cell disorders (nesidioblastosis) Noninsulinoma pancreatogenous hypoglycemia Post gastric bypass hypoglycemia Insulin autoimmune hypoglycemia Antibody to insulin Antibody to insulin receptor Insulin secretagogue Other 6. Accidental, surreptitious, or malicious hypoglycemia

Features That Differentiate Hypoglycemia Due to Insulinoma from Factitious Hypoglycemia