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Introduction
1. Anatomy
2. Microbiology
3. Physiology
3.1 Nervous system and special senses
3.2 Cardiovascular system
3.3 Respiratory system
3.4 Gastrointestinal system
3.5 Renal and urinary system
3.6 Endocrine system
3.6.1 Overview
3.6.2 Pituitary hormones
3.6.3 Thyroid hormones (TH)
3.6.4 Pancreatic hormones
3.6.5 Adrenal hormones
3.6.6 Calcium homeostasis
3.6.7 Erythropoietin
3.6.8 Additional information
3.7 Reproductive system
4. Pathology
5. Pharmacology
6. Immunology
7. Biochemistry
8. Cell and molecular biology
9. Biostatistics and epidemiology
10. Genetics
11. Behavioral science
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3.6.8 Additional information
Achievable USMLE/1
3. Physiology
3.6. Endocrine system

Additional information

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  1. Table showing common interpretations for TBG and T3 resin uptake*
Primary condition Test result
Hyperthyroidism High T4, high T3 resin uptake, low TBG
Hypothyroidism Low T4, low T3 resin uptake, high TBG
High TBG High T4, low T3 resin uptake
Low TBG Low T4, high T3 resin uptake

*T3 resin uptake is used to indirectly measure TBG levels.

  1. Somatostatin: It is secreted by the delta cells of the pancreas. It inhibits the secretion of both insulin and glucagon.

  2. Renin - angiotensin - aldosterone system (RAA): Renin is an enzyme that cleaves angiotensinogen to angiotensin I. Angiotensin I is then cleaved by angiotensin-converting enzyme (ACE) to angiotensin II. ACE is present in the vascular endothelium of the lungs, brain, heart, etc. Further breakdown produces angiotensins III and IV. Angiotensin II, III, and IV stimulate aldosterone secretion and vasoconstriction, with angiotensin II being the most potent vasoconstrictor.

Angiotensin II functions

  • Angiotensin II acts on AT1 receptors on blood vessels
  • Vasoconstriction and increased peripheral resistance and blood pressure
  • Stimulates Na+ reabsorption by the kidney
  • Stimulates the adrenal cortex to release aldosterone
  • Stimulates the release of ADH from the posterior pituitary
  • Stimulates thirst
  • Facilitates the release of norepinephrine from the sympathetic nerve endings

Renin release is stimulated by beta 1 stimulation, renal artery hypotension due to any cause, and decreased Na+ delivery to the distal renal tubules. Renin is produced and secreted by juxtaglomerular (JG) cells of the afferent arteriole in the renal glomerulus.

Specialized cells of the distal tubules, called the macula densa, lie adjacent to the JG cells. The macula densa senses the concentration of Na+ and Cl- reaching the distal renal tubule:

  • When NaCl is elevated in the tubular fluid, renin release is inhibited.
  • When tubular NaCl is reduced, renin release by the JG cells is stimulated.

Afferent arteriole pressure also regulates renin release:

  • Reduced afferent arteriole pressure causes the release of renin from the JG cells.
  • Increased pressure inhibits renin release.

PG E2 and PGI2 stimulate renin release in response to reduced NaCl.

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