Endocrine System Flashcards

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1
Q

What is the endocrine system?

A

Cell to cell communication

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2
Q

What is exocrine system?

A

Cell to environment communication

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2
Q

Classical Definition of Hormones

A

A chemical released by specialized cells into the blood stream to elicit a specific response at tissues throughout the body

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3
Q

Broad definition of hormones

A

A chemical released by a cell which signals another cell

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3
Q

Direct Cell Signaling

A

Done by gap junctions between cells

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4
Q

Autocrine/Paracrine Cell Signaling

A

A cell sends a chemical messenger out and that messenger goes across a space in between cells and signals a receptor on the target cell (or itself). Happens with cells near each other

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5
Q

Endocrine Cell Signaling

A

Message is a hormone that travels through the blood stream throughout the body, targeting different cells. Different cells may give different responses to the same hormone as well

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6
Q

Neural Cell Signaling

A

Dendrites receive message, travels down the axon, fires through the axon terminal to another neuron’s receptors (dendrites)

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7
Q

Exocrine glands

A

Have cuts, poorly vascularized; release things to the external environment, ex: sweat, milt, saliva, etc. (gut is part of external environment)

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8
Q

Endocrine Glands

A

Highly vascularized, no ducts; release things into the internal environment (usually the blood stream). Ex: Hypothalamus, testes, ovaries, etc.

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8
Q

Peptide/Protein Hormones

A
  • Often end in “-in”
    • Large
    • Tend to act quickly
    • Hydrophilic
    • Between 20-120 amino acids long
    • Travels to target cell dissolved in extracellular fluid
    • Binds to transmembrane receptors (ligand binding domain) and changes their shape
    • Rapid effects on target cells
    • Leaves cell via exocytosis
    • Ex: Oxytocin, human growth hormone, etc.
    • Production and release:
      ○ Created in the rough ER via ribosomes
      ○ Is made as a preprohormone
      § Pre portion: Signal sequence, gets cleaved off in the rough ER
      § Pro portion: Transports through vesicles to the Golgi apparatus which modifies it
      □ Is stored in secretory vesicle until it needs to be released
      ® While in this vesicle the hormone is cleaved from the pro portion, producing peptide fragments
    • Synthesis and Secretion of Vasopressin
      ○ Follows the above mechanism
      ○ Works to control blood pressure by increasing H20 reabsorption and constricts arterioles which increase BP
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9
Q

Amine Hormones

A
  • Often end in “-ine”
    • Small
    • Have and amine (NH2) portion
    • Some are endocrine hormones, some neurotransmitters, some both
    • Mostly hydrophilic (except thyroid hormones)
    • Have diverse effects
    • Ex. Melatonin, histamine, thyroid hormones, norepinephrine, etc.
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10
Q

Steroid Hormones

A
  • Often end in “-one_
    • Lipids derived from cholesterol
    • Synthesized by the smooth ER or mitochondria
    • Three classes:
      ○ Mineralocorticoids for electrolyte balance (water ion balance)
      ○ Glucocorticoids are stress hormones
      ○ Reproductive hormones with regulated sex-specific characteristics
    • Ex. Cortisol, testosterone, progesterone, etc.
    • Hydrophobic
    • Made on demand; cannot be stored
    • Need a carrier protein (usually albumin)
    • Bind to intracellular (sometimes transmembrane) receptors
    • Effects the target cell slowly (except cortisol)
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11
Q

Receptors

A

○ Hydrophilic messengers bind to transmembrane receptors
○ Hydrophobic messengers bind to intracellular receptors
○ Receptors change shape/confirmation when bound by the ligand
○ Receptors become saturated at a certain amount (saturation) of ligand, you would need more receptors to go beyond this point
- A high-affinity receptor will reach saturation faster than a low-affinity one

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12
Q

Ligand

A

○ Chemical that binds to receptor
○ Agonist: Binds to and activate receptors, not necessarily the natural ligand
- Antagonist: Binds to and does not activate the receptor, prevents ligand binding

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13
Q

Inactivation of Ligand-Receptor Complex

A

○ Can happen by removal/destruction of receptor
§ Ex. For insulin receptors to not have too low of blood sugar

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14
Q

Intracellular Receptors

A
  • Hydrophobic ligand diffuses across cell membrane
    • Binds to receptor in cytoplasm or nucleus
      ○ Shape changes
    • L-R complex binds to specific DNA sequences
    • Regulates the transcription of target genes
      ○ Increases or decreases production of specific mRNA
    • Transcriptional Cascades:
      ○ Receptor is activated by hormone, causes transcription of mRNA, and that mRNA can split, with the different parts effecting multiple pathways
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14
Q
  • Basic/Hypothetical Receptor Enzyme
A

○ Has a ligand binding domain, trans-membrane domain, and catalytic domain in that order from top to bottom

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14
Q

Amplification

A

○ One hormone can bind to the receptor causing A to happen, which causes more things to happen, which causes more things to happen, etc.

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15
Q

Guanylate Cyclase

A

○ Receptor Enzyme
○ Uses GTP, converts it to cGMP
○ Steps:
1. Ligand binds to receptor guanylate cyclase, changing its conformation
2. The activated receptor catalyzes the conversion of GTP to GMP
3. The cGMP acts as a second messenger, and binds to PKG (phosphokinase G)
4. The activated G-kinase phosphorylates proteins on serine or threonine residue

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16
Q

Tyrosine Kinase

A

○ Receptor enzyme
○ Phosphorylates tyrosine
○ Steps:
1. Ligand binds to receptor
2. Receptors dimerize and auto-phosphorylate
3. Phosphorylated receptors interact with protein kinases
4. Protein kinases signal to Ras protein
Ras switches between the active and inactive forms

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16
Q
  • Serine/Threonine Kinase
A

○ Receptor enzyme
○ Serine or threonine get phosphorylated, different enzymes but basically the same
○ Steps:
1. Ligand binds to receptors
2. The bound receptor dimerizes with the type II receptor
3. The type II receptor phosphorylates the type I receptor, activating it
4. The activated receptor phosphorylates a SMAD protein
5. The activated SMAD enter the nucleus and regulates gene expression

17
Q

G-coupled protein receptors

A
  • Are either activating or inhibiting
    • Steps:
      1. Ligand binds to a G(subunit)-protein-coupled receptor, causing a conformational change
      2. The alpha(subunit) releases GDP, binds GTP, moves through the membrane, and activates adenylate cyclase
      3. Activated adenylate cyclase catalyzes the conversion of ATP to cAMP
      4. cAMP binds to the regulatory subunit of protein kinase A (PKA) which dissociates from the catalytic subunit, activating it
      5. The activated catalytic subunit phosphorylates proteins, causing a response
      6. The phosphorylated proteins are rapidly dephosphorylated by serine/threonine phosphates, terminating the response
      7. When ligand binds to a G(subunit)-protein-coupled receptor, the alpha(subunit) inhibits adenylate cyclase, inhibiting the signal transduction pathway
18
Q

Hypothalamus

A
  • Synthesizes and secretes neurohormones ex. Acetylcholine and GABA
19
Q

Tropic/Trophic Hormones

A

Hormones which target other endocrine glands and cause the release of other hormones

20
Q
  • Hypothalamic pituitary portal system
A

○ Anterior pituitary receives blood with neurohormones and releases them
Third order pathway

21
Q

GHRH and GHIH/Somatostatin

A

Lobe: Anterior
Associated Hormone: GH
Target/Effect/Hormone: Many tissues/promotes growth

22
Q

PRH, PIH/dopamine, and TRH

A

Lobe: Anterior
Associated Hormone: Prolactin (PL)
Target/Effect/Hormone: Breast tissue/promotes milk production

22
Q

TRH

A

Lobe: Anterior
Associated Hormone: Thyroid stimulating hormone
Target/Effect/Hormone: Stimulates release of T3 and T4

23
Q

CRH and GHIH

A

Lobe: Anterior
Associated Hormone: Adrenocorticotropic hormone (ACTH)
Target/Effect/Hormone: Stimulates cortisone release in the adrenal cortex

24
Q

Posterior pituitary

A
  • A part of the hypothalamus
    • Secretes oxytocin and vasopressin
    • Separate blood supply, not part of the portal vein system
24
Q

Vasopressin

A

§ Increases cell permeability to water which controls BP (water and salt raises BP)
1. Vasopressin binds G-protein-linked receptor
2. Receptor activates adenylate cyclase, increasing cAMP and activating protein kinase A
3. Phosphorylation of cytoskeletal and vesicle proteins occurs
4. The triggers translocation of vesicle to the cell membrane, with insertion of aquaporins

25
Q

GH

A

Growth Hormone

* Over secretion of GH early in life leads to gigantism, when late in life it leads to acromegaly
* GH deficiency and insensitivity lead to dwarfism
* IGF's mediate GH actions in postnatal vertebrates 
	○ Somatomedin hypothesis
* Important for growing as well as repairing
25
Q

IGF

A

Insulin-like Growth Factors

* Insulin-like in shape not function
* Fit broad definition of hormone
* Made by liver when GH targets the liver 
* Somatic tissues make IGF and cause themselves to grow
26
Q

PRL

A

Prolactin

* Causes human mammary gland to produce milk
* Promotes maternal behavior through effects on the brain
* Is found in all vertebrates, even those without mammary glands
* Prolactin does not cause the release of milk, that is oxytocin 
* Actions of PRL in vertebrates:
	○ Osmoregulation- PRL is a fresh-water adapting hormone in fishes, and plays a role in osmoregulation of embryos in amniotic fluid
	○ Reproduction- Deals with the consequences of reproduction; development of mammary, development of crop sac in pigeons. Inhibits GH secretion 
	○ Development- Studied most in amphibians, it is considered to be a GH in tadpoles; lack of prolactin is antimetamorphic
	○ Metabolism- Affects lipid and glycogen metabolism
	○ Integument (skin)- Affects (negatively) on hair growth, sebaceous glands, feather patterns in birds, pigmentation
	○ Behavioral Effects- Maternal behavior
27
Q

ACTH

A
  • Adrenocoricotropic hormone (ACTH)
    • Regulates the secretion of corticosteroids by the adrenal cortex. Is part of the stress response system
    • HPA Axis
      1. After a stressor, the hypothalamus releases CRH (coricotropic releasing hormone)
      2. Sends message to posterior pituitary and releases ACTH
      3. Targets adrenal gland, which releases cortisol
      4. Cortisol reduces stress
28
Q

GnRH

A

Gonadotropin Releasing Hormone

  • Synthesized and released from hypothalamus
    • Delivered to the anterior pituitary gland
    • Regulates FSH and LH release
29
Q

TSH

A

Thyroid Stimulating Hormone

* Controls the secretion of thyroxine by the thyroid
	○ Thyroxine is involved in:
		§ Digestion
		§ Heart and muscle function
		§ Brain development
		§ Maintenance of bone
* Produces T3 and T4 as well 
	○ Named based on number of iodine in each 
* Cretinism (short stature and the like) is caused by insufficient thyroid hormone during fetal and neonatal development. It is a condition of severe mental retardation and growth defects
* Thyroid gland has metabolic and thermogenic roles
	1. Hypothalamus secretes thyrotropin-releasing hormone (TRH)
	2. Anterior pituitary secretes thyroid-stimulating hormone (TSH or thyrotropin e)
	3. Thyroid gland secretes thyroid hormone (T3 and T4)
	4. Hormones are sent to body tissues leading to increased cellular metabolism
30
Q

Gonadotropins

A
  • Examples: FSH, LH
    • Peptide hormone from anterior pituitary
    • Controls steroid hormone synthesis in vertebrates
31
Q

Pancreas

A
  • Located near small intestine
    • Exocrine gland: Produces pancreatic enzymes and sodium bicarbonate
    • Endocrine gland: Produces insulin and glucagon (for glucose regulation)
32
Q

Insulin/Glucagon

A

Lowers blood glucose level (ß cells) under hyperglycemia
§ Regulates the metabolisms of carbs, fats, and proteins
§ Promotes absorption of glucose from the blood
§ Promotes glycogenesis and lipogenesis
§ Triggered by high blood glucose
§ Produced in pancreas
1. Stimulus: blood glucose rises from the normal 90/100 mg/mL
2. Glucose receptors and stretch receptors signal the pancreas (feed forward)
3. Beta cells release insulin into blood
4. Body cells take up more glucose, and the liver stores glucose as glycogen
5. Blood glucose level declines (stimulus)
6. Alpha cells of pancreas release glucagon
7. Liver breaks down glycogen and releases glucose
8. Blood glucose levels rise
○ Glucagon raises blood glucose levels (∂ cells) under hypoglycemia
§ Regulates metabolism of carbohydrates
§ Promotes glycogenolysis, lipolysis, and gluconeogenesis
§ Triggered by low blood glucose

32
Q

Somatostatin

A

§ Great inhibitor
□ Inhibits GH, TSH, adenylyl cyclase, prolactin, insulin, glucagon, and exocrine secretions of the pancreas

33
Q

Gastrin

A

Triggers stomach cells to produce HCl

34
Q

VIP

A

Vasoactive intestinal peptide

Stimulates the intestine to release water and salts back into the intestinal track

35
Q

Additivity

A

When two hormones work in the same way on the same target

36
Q

Synergy

A

When two or more hormones work together to increase target cell response much more than expected by additivity

37
Q

Type 1 Diabetes

A

○ Endocrine defect: A loss of beta cells in the pancreas, little to no insulin being produced
○ Is caused by autoimmunity, any trauma or substance that could cause a detriment to the cells of the pancreas like radiation for cancer, surgery on the pancreas, toxins that cause damage to islets
○ Consequences: Affects the whole body
§ Hyperglycemia
□ Heavy breathing, low pH
□ Usually results from not taking insulin
§ Hypoglycemia
□ Normal breathing, hypothermia
□ Taking too much insulin
§ Chronic vascular diseases
○ Treatment
§ Diet
§ Insulin replacement therapy
§ Insulin agonists
§ No cure available

38
Q

Type 2 Diabetes

A

○ Accounts for 80-90% of all cases of diabetes in the US
○ Is correlated to obesity
○ Caused by insulin resistance, which is caused by the insulin receptor getting exposed to too much glucose and then tiring out; a deficiency in response of beta cells to glucose results
○ Characteristics:
§ Insenstiive to endogenous insulin
§ Correlates with excess abdominal fat
□ Abnormally high waist-to-hip ratio
§ Inflated fat cells and over-nourished liver-muscle ceells
□ Resists deposit of glycogen
§ Hyperplasia of pancreatic beta cells
□ Normal/increased insulin in mild forms of T2D
○ Complications:
§ Heart disease
§ Stroke
§ Kidney disease
§ Eye problems
§ Diabetic neuropathy and nerve damage, especially in the feet
§ Depression
○ Treatment
§ Excersise
§ Diet
§ Metformin increases insulin sensitivity

38
Q

Isoreceptor Concept

A

○ Different receptors sometimes cause constriction and sometimes dilation but respond to the same ligand

39
Q

Long Term Stress Response

A

○ Glucocorticoid levels rise after stress
§ Proteins and fats break down and covert into glucose which is released into the blood
§ Possible suppression of immune system

40
Q

Fight or Flight Response

A
  1. Glycogen broken down to glucose
    2. Increase blood pressure/glucose
    3. Increased breathing rate
    4. Increases metabolic rate
    5. Change in blood flow patterns, leading to increased alertness and decreased digestive, excratory, and reproductive system activity
40
Q

Short Term Stress Response

A

○ Corticosteroids causes alarm and resistance after stress
§ Hydrocortisone for itches or example
§ Spraining and ankle would go:
□ Chronic stress –> corticosteroids –> suppress immune system –> inflammatory disease

41
Q

Addisons Disease

A

Primary adrenocortical insufficiency
○ Results in weakness, fatigue, weight loss, nausea, hypotension, hypoglycemia, vomiting
○ Associated with high ACTH

42
Q

Crushings Disease

A

○ Opposite of Addison’s disease
* Obesity, skin changes, increased hair growth, hypertension, etc.
Understand the HPA axis including the function of the adrenal glands hormones/structure/function