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Endocrine System > Endocrine > Flashcards

Endocrine Flashcards

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
Q

Other t3, t4 effects

A

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
Q

t3, t4 disorders (hyper)

A

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
Q

t3, t4 disorders (hypo)

A

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
Q

Calcitonin

A

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
Q

Control of calcitonin secretion

A

If:

Increased levels of calcium

  • detected by -> parafollicular cells
    • > increase calcitonin sec.
  • vice versa
30
Q

Parathyroid glands secrete

A

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
Q

Control of PTH

A

If:

Decreased levels of calcium in blood

-detected by->

Parathyroid glands

-> increased output of PTH (parathyroid h)

** vise versa

32
Q

Parathyroid hormone disorders (hyper)

*chart in notes

A

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
Q

Parathyroid hormone disorders

A

Hypo PTH

  • > hypocalcemia
    • decreased calcium
  • increased bleeding
    • > blood won’t clot as well
  • tetany
    • > skeletal muscles locking up
    • > can lead to respiratory arrest
34
Q

Adrenal glands

*pic in notes

A

Help the body deal with stress

Adrenal capsule -> DFCT

Adrenal cortex

 - stratified cuboidal epithelial cells 
 - produces steroid hormones

Adrenal medulla

 - neurons (sympathetic)
 - catecholamines
35
Q

Adrenal cortex zones

A

Outer zone -> zona glomerulosa

Middle zone -> zona fasciculata

Inner zone -> zona reticularis

36
Q

Zona glomerulosa

A

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
Q

Control of secretion of aldosterone

A
  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

  1. (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
Q

Aldosterone disorders (hypo)

A

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
Q

Aldosterone disorders (hyper)

A

Hyper secretion

  • > aldosteronism
    • > increased sodium retention
      - > leads to increased H2O retention
      - > increased fluid volume
      - increased BP
      - edema (tissue swelling)
40
Q

Zone fasciculata

A 
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
Q

Cortisol - specific effects

A
  • 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
Q

Cortisol - Other systematic effects

A
  • stimulates vasoconstriction
    • > increases BP
  • enhances effects of catecholamines
  • anti inflammatory agent**
43
Q

Cortisol disorders (hypo)

A

Addison’s disease

44
Q

Cortisol disorders (hyper)

A

(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
Q

Zona reticularis

A

Gonadocorticoids
-> androgens

Effects:
Females -> libido
Males -> no effect

Control:
- via ACTH, however, no androgen feedback

46
Q

Zona reticularis disorders

A

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)

Endocrine System (2 decks)

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