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💉Paper 1 - Physiology: Endocrinology
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Paper 1 - Physiology: Endocrinology
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Table of Contents

  • Appetite regulation
  • Parathyroid hormone; Actions of PTH; Vitamin D; Calcitonin
  • Adrenal cortex; Cushing syndrome vs Cushing disease; Dexamethasone suppression test; Actions of glucocorticoids
  • Pancreatic hormones
 

High-yield / Revision Questions:

Tricky Q’s: 🌟
Q: Which of the following hormones acts on its target tissues by a steroid hormone mechanism of action? - Thyroid hormone; Parathyroid hormone; ADH on the collecting duct; alpha-1 adrenergic agonists; Glucagon
  • Ans: Thyroid hormone
Q: What is the most important step in the production of thyroid hormones? - Passive transport of iodine into the thyroid gland; Synthesis of thyroglobulin by follicular epithelial cells; Oxidation of iodine by lysosomal degradation; Organification of iodine by lysosomal degradation; Conversion of T3 into T4 by deiodinase
  • Ans: Synthesis of thyroglobulin by follicular epithelial cells
    • Thyroglobulin is synthesized in the follicular epithelial cells and secreted into follicular lumen. It is an essential step to produce thyroid hormones. Organification of iodine together with tyrosine produce T3 and T4.
Q: Recap anti-thyroid medications 🌟
 
Q: A 61yo woman with hyperthyroidism is treated with PTU (propylthiouracil). The drug reduces the synthesis of thyroid hormones as it inhibits the oxidation of~? - Triiodothyronine (T3); Thyroxine (T4); Diiodotyrosine (DIT); TSH; Iodide (I-)
  • Ans: Iodide (I-)
    • PTU inhibits TPO (thyroid peroxidase), an enzyme that oxidizes iodide → iodine (and also involves in organification, which is the incorporation of iodine into thyroglobulin)
 
Insulin causes uptake of glucose mostly in ~tissue:
  • Adipose tissue
Q re: function of ANP (Atrial natriuretic peptide) - it inhibits the release of ~hormones: (3)
  • Renin, aldosterone & ADH
  • Note: ANP is released from atrial muscle cells when the atria are stretched (from increased circulating blood volume). ANP functions to reduce blood volume by inhibiting the RAAS system → resulting in increased sodium and water excretion. ANP also promotes renal vasodilation.
Q: What drugs may cause SIADH? (4) 🌟
Mnemonic: "CTss"
  • Carbamazepine
  • Tricyclics (amitriptyline, clomipramine, imipramine, etc.)
  • SSRIs (citalopram, fluoxetine, sertraline, escitalopram)
  • Sulfonylureas (gliclazide, glipizide, tolbutamide, glimepiride)
Q: A 50yo man has gynecomastia - which of the following drugs is least likely the cause of his symptoms? - Spironolactone; Carbimazole; Chlorpromazine; Cimetidine; Methyldopa
  • Ans: Carbimazole
    • Drug to tx hyperthyroidism
  • Note that many drugs may cause gynecomastia - Mammary glandular tissue proliferation is physiologically stimulated by estrogens and inhibited by androgens.
    • Antiandrogens (bicalutamide, flutamide) = antagonize action on testosterone and dihydrotestosterone on mammary glands
    • H2 histamine receptor blockers - Cimetidine = most frequently causes gynecomastia
    • 5-alpha-reductase inhibitors (finasteride, dutasteride) = prevents conversion of testosterone to dihydrotestosterone → testosterone is then transformed into estradiol → increasing estrogen
    • Spironolactone - as an aldosterone antagonist and potassium-sparing diuretic = has anti-androgenic activities
    • Dopamine antagonist (risperidone, chlorpromazine domperidone)
    • Methyldopa = dopamine agonist = one of the older drugs associated with gynecomastia
    • More recent (in 2005) - Anti-hypertensives like CCBs (amlodipine, diltiazem, felodipine, nifedipine, verapamil)
 
 
[more high-yield Q’s and tips in our notes]

Pituitary gland

Memory aid: Hormones with the word "releasing" in them, are secreted by ~(structure): 🌟
  • Hypothalamus
      • Note that the hypothalamus also produces ADH, but it is stored in the posterior pituitary gland.
Posterior pituitary gland receives nerve innervation from hypothalamus, where the nerve cell bodies are located: (2) in the hypothalamus 🌟
  • Paraventricular and supraoptic nuclei in the hypothalamus
 
Anterior pituitary gland secretes (7) hormones: 🌠
  • GH
  • TSH
  • ACTH
  • Prolactin
  • LH & FSH
  • Melanocyte releasing hormone (Recap that the anterior pituitary gland receives hormonal stimuli from the hypothalamus via hypothalamo-pituitary axis)!
Posterior pituitary gland secretes (2) hormones: 🌠
  • Oxytocin
  • ADH
 

Growth hormone

also known as ~(name) & secreted by ~(structure): 🌟
  • Somatotropin
  • Secreted by anterior pituitary gland
What are the (3) factors in GH negative feedback loops? 🌟
  • Increased levels of GHRH
    • signals hypothalamus to stop making more
  • Muscles and liver releasing somatomedins
    • signals anterior pituitary to stop producing GH
  • Increased levels of GH (as well as somatomedins)
    • signals hypothalamus to produce somatostatin (aka. GH-inhibiting hormone) → in the pituitary, it blocks the GHRH from acting on somatotroph cells
 
Actions of GH and homeostasis: 🌠
 
[more high-yield details in our notes]
 

Prolactin 🌟

Prolactin is constantly inhibited by ~(hormone): 🌟
  • Dopamine (which is secreted by the hypothalamus)
~(hormone) increases the release of prolactin: 🌟
  • TRH (Thyrotropin-releasing hormone)
~(type of drug) increases the release of prolactin:
  • Dopamine antagonist - since dopamine causes prolactin release, the opposite will result in inhibition
    • i.e., Metoclopramide, Chlorpromazine, Risperidone, Quetiapine, Clozepine
Prolactin inhibits ~(hormone): 🌟
  • GnRH (Gonadotrophin-releasing hormone) → if inhibited, it inhibits ovulation and spermatogenesis!
 
  • Actions of prolactin:
      • Stimulates (2):
      • Milk production in the breast
      • Breast development (with estrogen)
      Inhibits (2):
      • Ovulation
 
Factors that affect prolactin secretion: 🌠
Recap that: Injury to the hypothalamic-pituitary tract (i.e., from head trauma)→ increased prolactin release due to absence of dopamine secretion!
 

ADH - Antidiuretic hormone

Produced by ~(structure):🌟
Hypothalamus (and stored in posterior pituitary) - produced specifically by ~(nuclei) of the hypothalamus: 🌟
  • Specifically by supraoptic nuclei of hypothalamus
ADH acts on (2) structures in the kidney tubule:
  • Distal Convoluted Tubule & Collecting Duct
    • ADH increases water permeability → water retention
It also causes ~(action) of blood vessels:
  • Causes vasoconstriction
 
The following factors regulate ADH - do they Stimulate OR Inhibit ADH release? 🌟
Ethanol
  • Inhibits ADH release
  • That's why drinking alcohol makes you pee!
High serum osmolarity
  • Stimulates ADH release
ANP (Atrial natriuretic peptide)
  • Inhibits ADH release
  • ANP is a hormone secreted by the cardiac atria - it functions to lower BP and control electrolyte hemostasis (Hypervolemia stretches the atria → releases ANP → which inhibits release of ADH, renin and aldosterone → causes more water excretion, lowering BP)
Hypovolemia
  • Stimulates ADH release
  • To retain water in blood vessels.
Opiates
  • Stimulates ADH release
Low serum osmolarity
  • Inhibits ADH release
Nausea
  • Stimulates ADH release
Alpha-agonist (e.g., Norepinephrine)
  • Inhibits ADH release
Hypoglycemia
  • Stimulates ADH release
Pain
  • Stimulates ADH release
 

Thyroid gland

~(which thyroid hormone) is more active while ~(which thyroid hormone) is being synthesized more? 🌟
  • T3 is more active
  • More T4 is synthesized
Toggle for summary:
Observe that TSH increases activity of thyroid peroxidase enzyme^
Further details re: Synthesis of T3 & T4 hormones: (in Part B) 📖
Uptake of iodide (I-) by thyroid follicular cells (thru active pump) → 3 processes occur, catalyzed by thyroid peroxidase enzyme:
  1. Oxidation of iodide → iodine
  1. Organification: Iodine + tyrosine (which is carried by thyroglobulin) → MIT (mono-iodotyrosine) and DIT (di-iodotyrosine)
  1. Coupling:
      • MIT + DIT → T3
      • DIT + DIT → T4
  • T3 and T4 released from follicular cells into the blood
  • Recycling of iodide - catalyzed by deiodinase from MIT and DIT → which is added back into intracellular iodide pool
 

Actions of thyroid hormones

The net result of thyroid hormones is ~(catabolic or anabolic) → hence, resulting in a ~metabolic state:
  • Catabolic (in terms of protein synthesis and catabolism) = breaking down complex substances
  • Diabetogenic (elevated glucose level)
    • Since it induces gluconeogenesis, glycogenolysis (as well as glucose absorption and utilization)
Mandatory screens for neonatal hypothyroidism is essential to prevent ~(condition): 🌟
  • Irreversible mental retardation
In the autonomic system, it functions as a ~agent: 🌟
Sympathetic agent - by upregulating ~receptors in the heart:
  • Beta-1 adrenergic receptors
 
[more high-yield details in our notes]
 

Anti-thyroid medications 🌟

~medication inhibits peroxidase and blocks the formation (coupling) of T3 and T4:
  • Thionamides - i.e., Carbimazole and Propylthiouracil
    • Note Carbimazole given in 2nd-3rd trimester of pregnant mom w/ hyperthyroidism
    • PTU given in 1st trimester of pregnant mom w/ hyperthyroidism
~medication inhibits peripheral de-iodination of T4 (aka. Inhibits the oxidation of Iodide I-):
  • PTU (propylthiouracil)
    • Note that PTU can cause liver damage
~medication is capable of inhibiting organification + inhibits hormone release + decreases the size and vascularity of thyroid gland (esp. in thyrotoxicosis patients prior to surgery)
  • Lugol's solution (iodide)
 
 
[more high-yield details in our notes]
 
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