Endocrine Flashcards

(46 cards)

1
Q

Endocrine glands

A

Pile o cells

Exception to exocrine glands

 - > goblet cells 
         - unicellular exocrine gland
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2
Q

Mechanisms of Hormonal Action

-see pic

A

Binding of hormone causes G protein to shift and activate inactive enzyme

Activates ATP -> AMP

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3
Q

Hypothalamus

A

The “master master gland”

  1. Controls the anterior pituitary via the release of Releasing Hormones
  2. Controls posterior pituitary gland via direct neural stimulation
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4
Q

Pituitary Gland

A

The “master gland” - anterior pituitary controls other endocrine glands via the secretion of Tropic Hormones

Tropic hormones -> secreted by anterior pituitary gland and controls other glands

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5
Q

Hypothalamus & Pituitary structure

A

Infundibulum

Anterior pituitary

 - epithelial cells 
 - aka -> adenohypophysis

Posterior pituitary

 - neurons 
 - aka -> neurohypophysis

Pars intermedia

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6
Q

Hypophyseal Portal System

A

The hypothalamus communicates with the anterior pituitary gland via a vascular* connection called the hypophyseal portal system

Artery -> primary plexus (in hypo)->
veins -> secondary plexus (in ant p) ->
veins

Plexus -> capillaries

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7
Q

Hypothalamic Hypophyseal Tract

A

The hypothalamus communicates with the posterior pituitary gland via the Hypothalamic Hypophyseal Tract -> neural connection*

Cell bodies (in hypo) -> AP’s -> post p
-> axon terminals (where secretion takes place)

Synaptic vesicles -> secrete

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8
Q

Posterior Pituitary hormones

A
  1. Synthesized in the hypothalamus
  2. Stored in the posterior pituitary
  3. Released from the posterior pituitary

a.) oxytocin
- comes from paraventricular cells in the
hypothalamus

b.) ADH
- antidiuretic hormone
- comes from cells called supraoptic
cells in the hypothalamus

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9
Q

Hypothalamic inhibiting hormones

Hypothalamic releasing hormones

Anterior pituitary hormones

A

Hypothalamic inhibiting hormones:

  • GHIH -> growth inhibiting hormone
  • PIH -> prolactin inhibiting hormone

Hypothalamic releasing hormones:

  • GNRH (gonadotropin releasing hormone)
  • TRH (thyroptropin releasing hormone)
  • CRH (corticotropin releasing hormone)
  • GHRH (growth hormone releasing hormone
  • PRH (prolactin releasing hormone)

Anterior pituitary hormones:

GNRH -> FSH* LH*

TRH -> TSH* (thyroid stim hormone)

CRH -> ACTH* (adrenocorticotropin hormone)

GHRH -> GH (growth hormone)

PRH -> PRL (prolactin)

  • ———> tropic hormone**
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10
Q

Growth hormone

A

Growth hormone -> somatotropin

Direct effects:
GH -> tissue effects

Indirect effects
GH -> skeletal muscle ->
liver -> somatomedins
bone -> -tissue effects
adipose ->

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11
Q

Growth hormone - direct effects

A
  • increase in cellular lipolysis (fat breakdown)
  • increase in lipoprotein transport in blood
  • increase in lipid burning (muscle + liver)
  • increases glycogen breakdown
    - > glucose into blood
    - > increased glucose blood concentration
    - diabetogenic effect
  • decrease glucose uptake + burning

GH -> adipose breakdown

         - > increased lipids in blood 
             - > increased fat burning
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12
Q

Growth Hormone - indirect effects

A

Anabolic *

Somatomedins
- increased amino acid uptake
- sulfur uptake
->
-> both required for production of
proteins -> increased protein
production

Those proteins:

  • increased cartilage production
  • increased bone growth production
  • increased skeletal muscle production
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13
Q

Control of Growth Hormone secretion

A

If there is:

  • decreased GH
  • decreased glucose
  • decreased lipids
  • increased amino acids
     -detected by-> hypothalamus 

Hypo -> increased release of GHRH on
anterior pituitary

anterior pituitary -> increased GH release

————————————————

If there is:

  • increased GH
  • increased somatomedins
  • increased lipids
  • increased glucose-detected by-> hypothalamus

Hypo -> GHIH (GH inhibiting hormone->
Anterior pituitary
-> decreased secretion of GH

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14
Q

Disorders of GH secretion

A

Hypersecretion

In children: giantism
- grow tall (> 7 feet)

In adulthood: acromegaly

Symptoms of acromegaly

  • progressive distortion of face features
    • overgrowth of:
      • frontal
      • nasal
      • tongue expands
      • mandible + maxilla
      • heart -> decreased lifespan

—————————
Hypo secretion

In children: pituitary dwarfism (< 4ft)

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15
Q

Posterior pituitary hormones

A

Oxytocin

  • child birth
  • lactation

ADH
- increased H2O retention by kidneys
(decreased urine output)

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16
Q

Control of secretion of ADH

A

If:

Increased solutes in blood plasma
(Dehydration)

-detected by ->

Hypothalamic Osmoreceptors (thirst*)

-impulses->

Posterior pituitary
-> increased output of ADH

————————

If: drink a lot of water

  • decreased solutes in blood plasma
    -detected by hypothalamus ->
    -> decreased ADH output
    (increased urination)
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17
Q

ADH and alcohol

A

Alcohol
—> decreases ADH output
—> this increases urination

Urination -> dilute urine

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18
Q

Secondary effect of ADH

A
  • vasoconstriction (makes BP go up)
  • vasopressin

Shock:
if you have a signification blood loss (> 10%)
this means decreased blood volume which
equals decreased blood pressure
-detected by->

   Hypothalamus 

      - stimulates thirst 
      - big blast of ADH
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19
Q

Disorders of ADH secretion (hyper)

A

Hypersecretion of ADH:
-> SI ADH
(syndrome if inappropriate ADH)

Causes:

  • hypothalamic damage
  • cancer -> tumor cells secrete ADH

Symptoms:

  • increased H2O retention
    - > increased blood pressure
    - > edema - hyponotremia
    - > H2O intoxication
20
Q

Disorders of ADH secretion (Hypo)

A

Hyposecretion
-> Diabetes Insipidus

  • no ADH production

Causes

  • hypothalamic damage
  • genetic

Symptoms
- excess production of dilute urine
(dilute-> mostly water little solutes)
-> causes increase in concentration of
solutes —> causes thirst

21
Q

Thyroid Gland

- pic in notes

A

Lumen
-> contains Thyroglobulin Colloid

 Thyroglobulin Colloid 
      -> large glycoprotein that stores 
            Thyroxine (t3, t4)

Follicle cells (simple cuboidal)

Parafollicular cells (C) 
     -> calcitonin
22
Q

The synthesis, storage, and release of t3 and t4

  • pic in notes
A

TSH, all amino acids (especially Tyrosine), and Iodine’s
-> enter follicle from capillary

Follicle cells synthesize colloid, release it into follicle via exocytosis
Colloid -> stored

TSH
-> enters follicle from capillary

TSH also stimulates follicle cells to absorb colloid, spilt off t3, t4 + release t3, t4 into the blood

t3, t4 in blood attach to Thyroid Binding Globulin
—> blood to tissues

23
Q

Control of secretion if t3, t4

A

If: t3, t4 decreases

-detected by-> hypothalamus 

Hypo -> releases TRH (Thyrotropin releasing hormone) on to ->

 Anterior P 
    -> increased TSH (thyroid stimulating 
         hormone on Thyroid 

         -> increased t3, t4 secretion 

*** vice versa
(increased t3, t4 -> decreased TRH output)

24
Q

t3, t4 effects

A

Stimulates an increase in oxidative respiration by cells
- controls BMR (basal metabolic rate)

** see formula in notes **

  • increased oxygen consumption
  • increased glucose consumption
  • increased CO2 production
  • increased heat production
    • > calorigenic effect
      - increased temp
      - increased heat
  • increased ATP production
25
Other t3, t4 effects
Required for proper: - CNS function - female reproduction function - GI function - skin hydration - skin sebum production Required for development of: - NS - skeletal system - muscular system
26
t3, t4 disorders (hyper)
Hyperthyroidism -> Graves’ disease Causes: - autoimmune - > immune system makes antibodies that mimic TSH Symptoms - increased temperature - flush - increased swearing - nervousness - weight loss - exopthalmos -> bulging eyes
27
t3, t4 disorders (hypo)
Hypothyroidism - decreased t3,t4 Causes: - goiter -> iodine deficiency - I131 poisoning - hashimitos thyroiditis -> autoimmune Symptoms In adults: myxedema - decreased BMR - decreased temperature - weight gain - mental sluggishness - dry skin - hair loss - constipation - edema -> tissue swelling In children: cretinism - severe mental impairment - retarded development of muscle and bone
28
Calcitonin
Secreted by parafollicular cells Overall effect: decrease calcium in blood * important in growing children Also.. - stimulates osteoblasts - inhibits osteoclasts - increased calcium loss in urine - inhibits secretion of PTH (parathyroid h)
29
Control of calcitonin secretion
If: Increased levels of calcium - detected by -> parafollicular cells - > increase calcitonin sec. * vice versa
30
Parathyroid glands secrete
Parathyroid hormone (PTH) Effect: increased calcium in blood PTH - - stimulates osteoclasts - increased calcium (destroys bone = more ca+ in blood) - inhibits osteoblasts - decreased calcium loss in urine - increased calcium concentration from GI
31
Control of PTH
If: Decreased levels of calcium in blood -detected by-> Parathyroid glands -> increased output of PTH (parathyroid h) ** vise versa
32
Parathyroid hormone disorders (hyper) | *chart in notes
Hyper secretion of PTH - > hypercalcemia - > high levels of calcium ``` - increased risk of developing nephrolothiasis (kidney stones) - CNS depression - bone leeching - Osteitis Fibrosa Cystica -> bone replaced by DFCT ```
33
Parathyroid hormone disorders
Hypo PTH - > hypocalcemia - decreased calcium - increased bleeding - > blood won’t clot as well - tetany - > skeletal muscles locking up - > can lead to respiratory arrest
34
Adrenal glands | *pic in notes
Help the body deal with stress Adrenal capsule -> DFCT Adrenal cortex - stratified cuboidal epithelial cells - produces steroid hormones Adrenal medulla - neurons (sympathetic) - catecholamines
35
Adrenal cortex zones
Outer zone -> zona glomerulosa Middle zone -> zona fasciculata Inner zone -> zona reticularis
36
Zona glomerulosa
Mineralcorticoids -> aldosterone Main effect of aldosterone is to increase sodium retention by the kidneys -> = retain more water Also stimulates a decrease in potassium retention by the kidneys
37
Control of secretion of aldosterone
1. If decreased sodium and/or increased potassium - detected by zona glomerulosa - > increased aldosterone secretion 2. Stress -> hypothalamus -> releases CRH (corticotropin RH) Anterior pituitary -> increases ACTH output on to-> (adrenocorticotropin hormone) Adrenal cortex - increases aldosterone sec. - increases cortisol sec. - increased androgens ** aldosterone causes increase in blood pressure 3. (most important) Renin - angiotensin mechanism If: - decreases BP, - decreased sodium, - increased potassium - decreased plasma osmorality - > juntaglomerulosa apparatus - > renin Angiotensinogen - does nothing until stimulates by the enzyme Renin, then becomes active protein —> turns into Angiotensinogen 2 - > stim zona glomerulosa - > increased aldosterone
38
Aldosterone disorders (hypo)
Hyposecretion - > primary adrenal insufficiency - > Addison’s disease Addison’s disease - decreased aldosterone - decreased cortisol Symptoms - decreased sodium - increased potassium - hypoglycemia - decreased BP - weight loss - wasting - bronzing -> tan appearance
39
Aldosterone disorders (hyper)
Hyper secretion - > aldosteronism - > increased sodium retention - > leads to increased H2O retention - > increased fluid volume - increased BP - edema (tissue swelling)
40
Zone fasciculata
``` Produces the hormone -> glucocorticoids -> cortisol -> maintains increased glucose in blood during times of stress ``` Control - stress - decreased glucose in blood - decreased cortisol Detected by hypothalamus -> released CRH on -> Anterior pituitary -> released ACTH on -> Zona fasciculata -> increased cortisol
41
Cortisol - specific effects
- stimulates fat breakdown -> released fatty acids into the blood - stimulates protein breakdown - > releases amino acids into the blood - stimulates gluconeogenesis -> creation of new glucose from non carbohydrate molecules * gluconeogenesis - > converts liberated fatty acids and amino acids into glucose
42
Cortisol - Other systematic effects
- stimulates vasoconstriction - > increases BP - enhances effects of catecholamines - anti inflammatory agent**
43
Cortisol disorders (hypo)
Addison’s disease
44
Cortisol disorders (hyper)
(Overdose) - cushing’s disease/syndrome Symptoms - fluid retention - increased BP - edema - weight gain (obesity) - redistribution of adipose deposition - “moon face” - pot belly - buffalo hump - immunosuppressive - loss or muscle and bone
45
Zona reticularis
Gonadocorticoids -> androgens Effects: Females -> libido Males -> no effect Control: - via ACTH, however, no androgen feedback
46
Zona reticularis disorders
Hypo: no effect Hyper secretion: a. ) female fetal pseudohermaphrodism - > generic female fetus whose mother produces excess androgens during gestational period -> children have male reproductive development in female b.) adrenogenital syndrome -> adult female - produces excess cortical androgens s -> causes Virilization Virilization -> development of male secondary characteristics c. ) precocious puberty - > in young boys - excess cortical androgens - early puberty (ages 5-6)