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HSF Block 1 > Physio - Endocrinology > Flashcards

Physio - Endocrinology Flashcards

1
Q

What is endocrinology?

A

Basics:

  • cellular chemical communication system & information transfer

Maintain Internal Homeostasis:

  • Support Cell Growth
  • Coordinate Development
  • Facilitate Responses to External Stimuli

Communication:

  • Signal is received
  • Signal is amplified
  • Response –> change in protein levels/assocations
  • Specificity = possible at all levels
  • Feedback = possible
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2
Q

What are tropic hormones?

A

Basics:

  • derived from the pituitary
    • regulate synthesis/secretion of other hormones

Anterior Pituitary

  • Thyroid
    • TSH
  • Adrenal Cortex
    • ACTH
  • Bone/Muscle
    • GH
  • Testes/Ovaries
    • LH/FSH
  • Mammary
    • Prolactin (PRL)
  • Melanocyte-stimulating hormone (MSH)

Posterior Pituitary

  • Kidney = ADH
  • Uterus = Oxytocin
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3
Q

Endocrine vs Exocrine

A

Endocrine Glands “ductless”

  • thyroid, pineal, pituitary, pancreas, hypothalamus, adrenal
    • release chemicals directly into cells/surrounding tissue
    • regulate/maintain events
      • metabolism, menstruation, uterine, reproductive
  • PTH, Calcitonin, etc

Exocrine Glands “ducts”

  • salivary, sweat, mammary, digestive
    • release secretions thru duct –> directly to external or internal surface
    • regulate events:
      • temp via sweat glands; eye via lacrimal glands
  • Sebacous/Eccrine/Apocrine
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4
Q

What are the 5 Methods of Communication?

A
  1. Classic endocrine
    • hormones travel –> bloodstream to target
  2. Paracrine
    • hormones –> act on adjacent cells
  3. Autocrine
    • hormones –> release & act on same cell
  4. Synaptic Signal
    • synapse, neurons secrete neurotransmitters short distance
  5. Neuroendocrine Signaling
    • secrete neurohormones –> target cells via bloodstream
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5
Q

A simple endocrine pathway

A

Hypothalamus —> Adenohypophysis —> Target Organ

  • Ex: GHRH –> GH –> Liver (and all body)

Hypothalamus —> Neurohypophysis —> Target Organ

  • Ex: Oxytocin —> Mammary gland
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6
Q

Control Pathway of Cortisol

A
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7
Q

What are the 2 Types of Hormones?

A
  1. Water soluble
    • synthesized in endocrine cells
    • packaged into secretory vesicles
    • exocytosis
      • freely soluble in blood
  2. Lipid soluble
    • synthesized in endocrine cells
    • NOT packaged
    • passively diffuse out of endocrine cell
      • get complexed w/ blood proteins (globulins)

Note:

  • The solubility of a hormone = correlates w/ the location of their receptors inside/on surface of target cell
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8
Q

What are the 3 Major Classes of Hormones?

A
  1. Polypeptides
    • proteins/peptides
  2. Amines
    • derived from AAs
    • Water soluble = Surface receptor
  3. Steroids
    • ​Vitamin D
    • Lipid = Intracellular receptor
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9
Q

What messanger system do Cell-surface receptors activate?

A

Second messenger systems

  • Cell surface receptors = couple w/ 2nd messanger systems
    • lead to QUICK reaction from cell

Second messanger systems include:

  • Adenylate cyclase = ATP –> cyclic AMP
  • Guanylate cyclase = GTP –> cyclic GMP
  • Ca & Calmodulin; Phospholipase C –> catalyzes phosphoinositide turnover —> inositol phosphates (IP) + diacylglycerol (DAG)

Each 2nd messanger system activates a specific protein kinase enzyme:

  • protein kinases
  • Ca/Calmodulin-dependent protein kinase
  • leads to cascade
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10
Q

How do hormone levels vary?

A
  • Rise/fall due to synthesis of hormone & degradation
    • target cell binding = small fraction of removal of hormone from circulation
  • Target cell receptors, transducers, effector levels can change
    • age, sex, physiological or dev. states can affect this

Note:

  • Cells can make more than one hormone
  • Same hormone –> affect target cells differently because:
    1. different receptors for hormone
    2. different signal transduction pathways

Example: Epinephrine

  • Liver = break down glucose
  • Skeletal muscle = dilate vessels
  • GI = constrict vessels
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11
Q
A
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12
Q
A
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13
Q

Mechanisms of Endocrine Disease

A
  • Hormone Deficiency
  • Hormone Excess
    • Usually = Disease
  • Hormone Resistance
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14
Q

What is the relationship btw Steroid Hormones and Cancers?

A
  • Steroids/hormones = act in cell-type/gene specific manner
    • regulate metabolism, inflammation, cancer, immunity, etc

Estrogen

  • Hormone =
    • necessary for dev. and growth of breast/organs
    • helps maintain heart & healthy bones
  • Over-expression = can lead to breast cancer
    • blocking synthesis of estrogen = effective at preventing breast cancer
      • via aromastase inhibitors
      • BAD PART: leads to other cancers

Cancer

  • Selective estrogen receptor modulators (SERMs)
    • Ex: Tamoxifen
      • regulate a subset of normal gene fxn
      • clinically used but can be 100% –> 0% efficacy
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15
Q

What are Spare receptors and how are they involved with dosing?

A

Spare receptors:

  • based on relationship that max biological activity = 5%-10% of receptors are bound
  • GREATER # of receptors = GREATER sensitivity for hormone

Dosing:

  • Increase Potency (lower Km) = more receptors
  • Decreased Potency (higher Km) = less receptors

Therapeutic Index:

  • Larger TI = Safer the drug
  • Smaller TI = Higher potential for toxicity
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16
Q

What is Growth Hormone?

A

Growth Hormone (GH) & Somatotropin

  • Growth Hormone
    • hormone regulating growth
    • produced by anterior pituitary
      1. Uses IGF-1 to I_NCREASE chondrocyte proliferation & osteoblast activity in bone_
      2. Increases rate of muscle synthesis
      3. Increases lipolysis of FAs
  • Somatotropin
    • produced by hypothalamus & delta cells of pancreas
    • decreases GH secretion
  • Liver synthesizes Insulin-like growth factor-1 (IGF-1)
    • helps regulate growth
    • acts as mediator

Notes:

  • A number of hormones also influence specific target tissues:
    • FSH = ovary
    • ACTH = adrenal
    • Estrogen = breast, uterus
    • TSH = Thyroid
    • Testosterone = prostate
17
Q

Regulation of GH secretion

A

Regulation of GH secretion

  • Water soluble hormone
    • 2nd messanger pathway
    • Somatostatin = slows pathway
  • Strenuous exercise
  • Sleep
    • both = increase GH

Other factors that affect GH secretion:

  • Starvation (severe protein def)
  • AGE
  • Hypoglycemia
  • Exercise
  • Excitement
  • Trauma
18
Q

How are GH Effects Diabetogenic?

A

Basics:

  • GH causes insulin resistance
    • decreased glucose utilization by the cells
  • Raising blood levels of FAs above normal = decreased sensitivty of liver & skeletal muscles to insulin effects

Insulin + Carbs = necessary for growth hormone

  • insulin = protein anabolic effect
  • GH = increase ability of pancreas to respond to insulinogenic stimuli, such as glucose

Stimulate GH

  • DECREASE blood glucose, FAs
  • Starvation
  • Trauma, stress, excitment
  • Exercise
  • Testosterone/Estrogen

Inhibit GH

  • INCREASE blood glucose, FAs
  • Aging
  • Obesity
  • GHIH (Somatostatin)
19
Q

What causes Dwarfism & African Pygmy?

A

Panhypopituitarism (dwarfism)

  • during childhood
  • body parts dev normally, but dev = slow
  • DOES NOT pass pubert
  • Sexual maturity can occur if only GH is deficient

African Pygmy

  • Rate of GH = normal/high
  • GH insensitivity & hereditary inability to form IGF-1
  • GH is not affected; just IGF-1
20
Q

What is the differenct between Gigantism & Acromegaly?

A
  • Gigantism (linear growth)
    • Acidophilic tumors of Anterior Pituitary BEFORE puberty
      • body tissue grows rapidly
      • dev before epiphysis & shaft unite
    • hyperglycemia
  • Acromegaly (lateral growth)
    • Acidophilic tumor AFTER puberty
      • bones continue to get thicker
      • soft tissue = thicker
      • Enlargment of organs
      • Kyphosis
21
Q

What is WOLFF‐CHAIKOFF EFFECT ?

A
  • Plasma Iodide levels = EXTREMELY HIGH
    • inhibition of iodide organification
22
Q

What are the Actions of Thyroid Hormones?

A

Basics:

  • TSH = thyroid stimulating hormone
  • TRH = thyrotropin-releasing hormone

Functions:

  • Increase basal metabolic rate
  • Stimulate synthesis of Na/K ATPase
  • Increase body temp
    • calorigenic effect
  • Stimulate protein synthsis, lipolysis, use of glucose & FA
  • Enhance some actions of catecholamines
  • regulate dev of growth of nervous tissue/bones
23
Q

How does the CONTROL OF TSH release occur?

A

Basics:

  • TRH stimulates release of TSH
  • Classic multiple loop-feedback
    • T3 = predominant NEG feedback control
    • Free T4 –> converted to T3 (peripheral tissue)

TSH:

  • Lipid soluble
  • Acts at 2nd messanger
    • both cAMP & DAG/IP3 pathways
  • Regulate thyroid gene expression thru transcription factors

Converstion of T4–>T3

  • T3 = much greater biological activity than T4
  • thyroid gland capable of sotring many WEEKS worth of thyroid hormone
    • if no iodine availbale , secretion is still maintained

Regulation of Thyroid Hormone Levels

  • low iodide levels = INCREASE iodine transport into follicular cells
  • high iodide levels = LOW iodine transport into follicular cells
    • NEGATIVE feedback by hypothalamus & anterior pituitary
24
Q

Hypothyroidism

A

Basics:

  • Early onset = delayed/incomplete physical/mental dev.
  • Later onset = Impaired physical growth
  • Adult onset (Myxedema) = gradual changes
    • tiredness, lethargy, et gain, hair loss, low mental fxn

Primary:

  • Disease of the gland
    • autoimmune = Hashimoto throiditis
      • lack of iodine
      • decrease T3 & T4
      • increase TSH

Secondary:

  • Disease higher up (hypothalamus…)
    • Follicular cells = less active
      • decrease T3 & T4 & TSH

Goiter Relation:

  • Insufficient iodine = DECREASE thyroid hormone production
    • leads to increased TSH release (neg feedback)
25
Q

Hyperthyroidism

A

Basics:

  • Emotional symptoms, fatigue, heat intolerance, elevated metabolic rate, wt loss, goiter

Graves Disease:

  • excress production of thyroid hormone
  • enlarged thyroid gland
  • TSI to TSHR in B cells can mimick TSH

Primary:

  • Disease in gland (Graves)
    • increase T3 & T4 –> decrease TSH
    • NOT affeceted by neg feedback

Secondary:

  • Disease is higher up (Hypothalamus)
    • increased TRH = increase TSH & T3 & T4

HSF Block 1 (19 decks)

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