171. Intro to Endo Flashcards

1
Q

What are the 3 classes of hormones?
How are they synthesized?
Give examples of each

A
  1. Polypeptides: produced as HMW precursors cleaved to active form, water soluble (bind membrane receptors), largest # hormones in this class (ex: insulin)
  2. Steroids: derived from cholesterol + differ only in ring structure/side chain, lipid soluble (bind cytoplasmic receptors), (ex: GCs - cortisol, MCs - aldosterone, androgens - testosterone, estrogens - estradiol, progesterone, vitamin D)
  3. Amines: derived from tyrosine, bind membrane receptors (ex: thyroxine - lipid soluble, epinephrine - water soluble)
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2
Q

Anterior Pituitary

  • how does it connect to hypothalamus?
  • what hormones does it produce?
  • sx of oversecretion and hypopituitary syndromes
A

Connects via H-P portal vessels
hormones: TSH, ACTH, FSH/LH, PRL, GH

Oversecretion Syndrome
PRL - prolactinoma (galactorrhea, amenorrhea, infertility, less libido, erectile dysfx)
GH - acromegaly (gigantism, facial changes, large hands/feet)
ACTH - cushing’s disease (centripetal obesity, purple striae, thin skin, bruising, DM, HTN)
TSH - hyperthyroidism (weight loss, weakness, tremor, sleepless)
FSH/LH - no syndrome, just mass effect

Hypopituitary Syndrome
PRL - cannot lactate after delivering baby
GH - growth failure, fatigue, muscle loss, fat gain, bone loss, heart risk
ACTH - fatigue, dizziness, weight loss
TSH - hypothyroidism: fatigue, weight gain, constipation, dry skin, sleepiness
LH/FSH - hypogonadism: amenorrhea, infertility, loss of libido, erectile dysfx

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3
Q

Neurohypophysis

  • communication to hypothalamus?
  • how is it regulated
  • hormones secreted
  • syndrome of hormone secretion
A

magnocellular neurons originate from supraoptic and paraventricular nuclei - project through stalk and diaphragm sella
regulated by neurons from osmoreceptors, baroreceptors, emetic center
Secretes: Oxytocin, AVP (ADH)

Diabetes Insipidus: decreased AVP, kidneys cannot concentrate urine = polyuria, polydipsia

High AVP secretion: increased kidney water retention = hyponatremia and water intoxication

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4
Q

Adrenal Glands

  • parts of gland
  • hormones and their function
  • 3 primary adrenal diseases
A

Adrenal Cortex
- secretes lipid-based steroid hormones (CS)
MC: aldosterone: secreted due to low BP/blood volume (terminal RAAS hormone), prompts distal/collecting tubule to reabsorb more Na, water follows, increase BV
GC: cortisol: keeps BG high enough to support brain activity, catabolic (breaks down protein), redirects circulating lymphocytes to peripheral tissues where pathogens are, in large doses = suppress immune/inflammatory response
Androgens: androstenedione, DHEA-S

Adrenal Medulla - secretes EPI and NE

  1. Adrenal Insufficiency: Addison’s Disease (atrophy, hypocortisolism)
  2. Adrenal Excess: Cushing’s Syndrome (adenoma or ca)
  3. Congenital Hyperplasia: mutations in enzymes for cortisol synthesis (loss of cortisol, loss/excess MC/androgens)
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5
Q

Thyroid Gland

  • location
  • hormones produced
  • composition
  • function of each hormone
  • two groups of thyroid diseases
  • what is goiter?
A

Location: ant neck, inf to larynx; 2 lat lobes and isthmus
Hormones: Thyroid Hormone, Calcitonin
Spherical follicles: follicle cells (produce thyroglobulin - precursor of thyroid hormone), colloid lumen contains thyroglobulin, parafollicular C cells produce calcitonin

T3/T4: increase BMR, affects protein synthesis, bone growth, neuronal maturation, cell differentiation

Calcitonin: secreted when serum Ca too HIGH - lowers serum Ca by slowing oclast activity and increasing kidney Ca excretion; acts during childhood (minor in adults), produced in excess by MTC

Hyperthyroidism: HIGH T3/T4, LOW TSH - high BMR due to thyroid stimulating IgG
Hypothyroidism: LOW T3/T4, HIGH TSH - low BMR due to autoimmune

Goiters: enlarged thyroid, either diffuse or nodular, can be cancerous

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6
Q

Parathyroid Glands

  • location
  • hormone
  • structure
  • two broad disease classes
  • effects of hormone
A

4 glands imbedded/behind thyroid gland
Chief Cells: produce PTH (+ Oxyphil cells: unknown fx)
PTH: stimulated by low serum Ca
effect of PTH: stim oclasts to resorb Ca from bone, decrease Ca excretion by kidney, activate vitamin D from kidney
Vit D: activated by PTH to 1,25 diOH vit D: increases gut Ca absorption, increases Ca bone resorption, decreases PTH secretion (negative feedback)

Hyperparathyroidism: excess PTH from adenoma/hyperplasia = hyperCa

Hypoparathyroidism: hypoCa due to removal of parathyroid, congenital, autoimmune cause

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7
Q

Pancreatic Islet Cells of Langerhans

  • 3 cell types, their hormones, their fx
  • 1 key disease, subtypes, pathogenesis for each
  • other disease instance opposite of disease
A

Alpha cells: glucagon, increase BG, in periphery of islet
Beta cells: insulin, decrease BG, central of islet
Delta cells: SS, inhibit glucagon and insulin

Diabetes Mellitus
T1: Immune dysregulation + enviro triggers = beta cell injury = auto-antibodies = loss of ins response = glu intolerance = loss of C-peptide [B-cell destruction w/ lack of insulin]
T2: insulin receptors become resistant = impaired ins secretion w/ genes/lifestyle interaction b-cells cannot compensate [insulin resistance w/ insulin deficiency]

Hypoglycemia: due to high ins + nutrient intake during DM tx, or rare pancreas tumor (insulinoma), or reactive hypoglycemia due to timing problems of ins release and food absorption early in T2DM

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