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Vertebrate Endocrinology > Exam 1 (not all there) > Flashcards

Exam 1 (not all there) Flashcards

1
Q

Central nervous system

A
  • contains the brain and the spinal chord
  • very quick system, immediate response but short effect
  • use chemicals to get response (neurotransmitters)
  • neurotransmitters are produced in massive amounts in direct travel along neurons
  • neurotransmitters bind to receptor with low affinity bc so many are produced
    Ex: put hand on hot burner, immediately rip off
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2
Q

Thalamus

A
  • in the brain, above the hypothalamus

- relay station to send motor and sensory signals

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3
Q

Hypothalamus

A
  • endocrine organ/gland in the brain
  • right under the thalamus
  • highly involved in endocrine function
  • works with pituitary gland to maintain homeostasis
  • it is the regulator of the body*
  • information center, coordinate physiological responses, maintains homeostasis, takes sensory input from environment and creates neuroendocrine response
    Ex: controls body temp, thirst, hunger, and other homeostatic systems
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4
Q

What is the difference between male and female endocrine organs

A
  • only the testicles and ovaries/vagina
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5
Q

Endocrinology

A
  • biology dealing with the endocrine system
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6
Q

Function of endocrine glands/organs

A
  • to secrete hormones and trigger a response in the body
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7
Q

Endocrine

A
  • where a gland produces a hormone, releases it into the blood stream and exerts its effect on a DISTANT organ
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8
Q

Paracrine

A
  • where a gland produces a hormone and exerts its effect on a NEARBY target organ
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9
Q

Autocrine

A
  • where an endocrine organ releases a hormone and binds to a receptor back on ITSELF
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10
Q

Intracrine

A
  • when a hormone is produced and never released, it binds to a receptor INSIDE its own organ/gland
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11
Q

4 ways hormones exerted affect target organs

A
  • in order for a hormone to exert an effect it must target an organ and bind to a receptor
  1. Endocrine
  2. Paracrine
  3. Autocrine
  4. Intracrine
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12
Q

Where can receptors be located

A
  1. Cell membrane
  2. Nuclear membrane
  3. Inside the nucleus
  4. Inside the cytoplasm
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13
Q

What can receptors do

A
  • receptors are specific for a hormone, so they bind to a receptor and exert an effect
  • much like a switch
  • can turn on or off the system
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14
Q

Conditions that can change the effect of a hormone/receptor

A
  1. The number of hormones and receptors
    - it will affect the result
  2. Antagonists- will reduce an effect and do the opposite of its regular function
  3. Protagonists- will make the effect larger
  4. Mutations - varying effects
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15
Q

Half life

A
  • how long does it take for 50% of whatever measure to be taken up by an animal
  • hormone half life effects the efficiency of the animal
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16
Q

Are receptors monogamous to one hormone

A
  • no, different hormones have different effects by binding to diff types of receptors
  • different subclasses of the same receptor will create a varying effect

Ex: if you give a patient with diabetes insulin it is supposed to lower the sugar levels, but if the receptor is mutated it can have a varying effect

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17
Q

Affinity

A
  • how tightly the hormone binds to its receptor
  • aka how easy is the molecule dissociated from the receptor

Ex: carbon monoxide has a high affinity
- it will bind so strongly to the receptor that it will kill you because it wont let go

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18
Q

Specificity

A
  • some hormones will bind to multiple receptors, while others will only bind to a specific one
  1. Low specificity- hormone will bind to many receptors
  2. High specificity- hormone will bind to one receptor
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19
Q

Endocrine system responses

A
  • not fast, but response lasts longer
  • use chemicals to get response (neurotransmitters)
  • indirect travel bc travels along the blood stream
  • neurotransmitters bind with high affinity to receptors
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20
Q

Endocrine system and CNS relationship

A
  • compliment to each other

- work together to maintain homeostasis

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21
Q

How do hormones become active

A
  • hormones are synthesized as prohormones or preprohormones
  • in order to become active must get rid of the pre and pro part
  • the pre and pro keep the hormone in check until it is needed
  • when pre/prohormone is released it can run into an enzyme that removes the pre/pro and it will become a bioactive hormone
  • if it is missing a matching enzyme it may never become bioactive
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22
Q

Hormones as steroids

A
  • they are lipid soluble (able to pass through the membrane)
  • membrane of cells is a phospholipid bilayer with a polar or hydrophilic heads and hydrophobic tails
  • cell is selectively permeable and only lipid soluble things can pass through aka steroids
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23
Q

Where is a steroids receptor

A
  • it is intracellular

- therefore, the steroid can fuse through and bind to the hormone inside of the cell

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24
Q

Forms of hormones

A
  • can be dimerized, a heterodimer, a homodimer, homotrimer, heterotrimer
  • can be made up of different components
  • the receptors can also be made up of dimerization
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25
Q

Ways hormones can remain inactive

A
  • if they do not have a matching enzyme to activate them by losing the pre or pro in the hormone
  • some will produce a secretory granule(capsule) to carry the hormone to distant locations and the capsule will inhibit bioactivity
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26
Q

Hormone metabolism

A
  • associated with half life (how long it takes 50% of hormone to be removed by the body)
  • metabolic clearance rate (MCR)
  • the half life of a hormone is how fast it moves through the plasma and is broken down
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27
Q

What does the half life of a hormone determine

A
  • determines how bioactive the hormone is in the body

- the longer the half life and MCR, means it has a longer bioactive length

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28
Q

Regulation of hormones

A
  • KD -> refers to receptors and dissociation of hormone from the receptor (measure of affinity)
  • it is the equilibrium dissociation constant
  • the concentration of hormone at which 50% of available receptors are bound to a hormone
  • inversely proportional with affinity
  • lower KD = higher the affinity of the receptor for the hormone
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29
Q

Negative Feedback

A
  • most common way feedback occurs

- releases hormone that binds to a receptor and shuts something off

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30
Q

Positive Feedback

A
  • less common way feedback occurs
  • hormone is released, binds to a receptor and turns something on

Ex: oxytocin and contractions in child birth
- fetus reaches the birth canal, oxytocin triggers contractions and increases its levels until birth occurs
Ex 2: profuse bleeding
- positive stimulus on arteries to have major vasoconstriction
- temporary response and then signal stops

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31
Q

Homeostasis

A
  • body constantly regulates back and forth in flux
  • never perfectly level
  • feedback and homeostasis work together to maintain levels
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32
Q

Agonist Receptor

A
  • hormone binds and elicits a biological response
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33
Q

Antagonist receptor

A
  • hormone binds and shuts down a response

Ex: beta blocker is an antagonist that blocks a receptor

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34
Q

Ligand gated receptor

A
  • hormone binds to a receptor and a channel opens in the membrane
  • allows certain molecules to diffuse through
  • ligand is a generic word for something that binds to a receptor, can be a hormone
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35
Q

Intracellular Receptor

A
  • can have a receptor in the cytoplasm, on the nuclear membrane, or on a promoter region inside the nucleus
  • cytoplasm is the most common intracellular receptor
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36
Q

G-Protein Linked Receptor Structure

A
  • a class of proteins
  • a 7 transmembrane receptor associated with 3 subunits that are heterotrimeric g-proteins
  • receptor crosses the membrane 7 times and has a N and C terminal end
  • the N terminal is on the outside of the cell and the C terminal is intracellular
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37
Q

G-Protein linked receptor Function

A
  • 3 subunits= alpha, beta and gamma
  • hormone binds extracellularly, can not diffuse across the membrane, based on the KD will eventually dissociate
  • if the hormone is an agonist it will trigger a rxn inside the cell
  • if the hormone is an antagonist it will suppress a rxn inside with a receptor
38
Q

G-Protein linked receptor

- GDP/GTP and subunit functions

A
  • GDP becomes GTP inside the cell
  • GTP exerts an affect on the alpha subunit, causing it to break off and beta/gamma become a heterodimer
  • beta and gamma then create a downstream affect
  • downstream effect is based on varying alpha subunit
39
Q

Gprotein linked receptor

- alpha subunit function and types

A
  • acts as an activation, responsible for determining the signal through the beta/gamma heterodimer to decide which event to trigger
  • beta and gamma activation is based on alpha subunit
  • when GTP binds to it, beta and gamma become a heterodimer and create a downstream affect

3 types of alpha subunit

  1. G alpha s
    - ultimate target is to activate adenylate cyclase enzyme
  2. G alpha i
    - when activated it is inhibitory, dec adenylate cyclase
  3. G alpha q
    - when activated, inc levels of phospholipase C (PLC)
40
Q

G alpha s subunit

A
  1. Inc cAMP
  2. Inc pKA
  3. Inc proteins
  4. Inc adenylate cyclase
  • if G alpha s is activated, but pKA levels are bad for example, adenylate cyclase will not be triggered
  • entire downstream effect must occur, 1 malfunction will shut down entire system
41
Q

G alpha i subunit

A
  1. Dec cAMP
  2. Pka - no change
  3. Proteins- no change
  4. Dec adenylate cyckase
  • inhibitory of production
42
Q

G alpha q subunit

A
  1. PLC activates through the G alpha q subunit
  2. PLC hydrolyzes PIP2 and cleaves(cuts) it in half into DAG and IP3
  3. DAG(stays in the membrane) activates PKC which activates IP3 and allows it to bind to parts of the cell
  4. IP3 binds to the endoplasmic reticulum’s receptor and calcium is released
  5. To increase calcium production, calcium binds to calmodulin
  6. Downstream effects increase
  • if mutation occurs at PLC, calcium will never be secreted
43
Q

Which G alpha subunit would you choose to cause an increase in intracellular effect?

A
  • G alpha q subunit
44
Q

G alpha 12 subunit

A
  • not well understood
45
Q

Endocrine Organs

A
  1. Hypothalamus
  2. Pineal Gland
  3. Anterior or Posterior Pituitary Glands
  4. Thyroid gland
  5. Parathyroid Gland
  6. Adrenal Glands
  7. Kidneys
  8. Pancreas
  9. Ovaries or Testes
46
Q

Hormone Receptor Regulation

A
  • changes based on the hormones themselves
  • a cell can detect the amount of hormones in blood stream and will regulate the amount of receptors created for those hormones
  • if there are more hormones than receptors cell will up-regulate the amount of receptors and vice versa (down-regulation)
  • desensitization will occur, the signal is still there, but neurons become desensitized and used to it
  • receptors can become desensitized to the level of circulating hormones
  • it is a dynamic process, varying levels of hormones and receptors
47
Q

Hormone Release

A
  1. Neural Control
    - sympathetic(fight/flight) and parasympathetic nervous system(rest/digest)
  2. Hormonal Control
    - the hormone released travels to a different site and goes to the target organ which will affect which hormones are released
  3. Nutrient or Ion Control
    - how cell regulates calcium balance and water balance (aquaporins in kidney)
48
Q

Experiment involving mice and pituitary glands

A
  • cut the pituitary glands off of rodents and discovered that it stopped relay of info between the hypothalamus and pituitary glands
49
Q

Hormones produced in Hypothalamus

A
  1. GHRH (growth hormone releasing hormone)
  2. CRH (corticotropin releasing hormone)
  3. TRH (thyrotropin releasing hormone)
  4. GnRH (gonadotropin releasing hormone)
  5. GHIH (growth hormone inhibiting hormone)
  6. Dopamine
  7. Oxytocin
  8. ADH (Antidiuretic hormone)
50
Q

Hormones PRODUCED AND RELEASED from Anterior Pituitary Gland

A
  1. GH (growth hormone)
  2. PRL (prolactin)
  3. TSH (thyroid stimulating hormone)
  4. FSH (follicle stimulating hormone)
  5. LH (Luteinizing Hormone)
  6. ACTH (adrenocorticotropic hormone)
51
Q

Thyroid Gland Hormones

A
  • make thyroid hormone from the thyroid gland
  • intermediates:
    1. T3 (triiodothyronine)
    2. T4 (thyroxine)
    3. Calcitonin (regulate calcium levels in blood stream)
52
Q

Parathyroid Gland Hormones

A
  1. PTH (parathyroid hormone)
53
Q

Adrenal Gland Hormones

A
  1. cortisol
  2. aldosterone
  3. adrenal androgens
  4. epinephrine
  5. norepinephrine
54
Q

Pancreas Hormones

A
  1. Insulin

2. Glucagon

55
Q

Ovaries Hormones

A
  1. E2 (Estrogen)

2. P4 (Progesterone)

56
Q

Testes Hormones

A
  1. Testosterone
57
Q

Hypophyseal Portal System

A
  • hypothalamus needs major blood supply to support feedback mechanisms (neg feedback regulatory system)
  • > connects what happens at the level of the hypothalamus to the pituitary gland
  • major blood supply in the endocrine system
  • region between hypothalamus and pituitary gland is the infundibular stalk
  • structure diffusely located within the hypothalamus is the median eminence
  • hypophyseal portal vein (from hypothalamus to anterior pituitary gland)
  • inferior hypophyseal arteries (under pit glands) and superior hypophyseal artery (goes into infundibular stalk)
  • hypothalamic artery (goes into hypothalamus)
  • nerves go from hypothalamus into Post Pit Gland
  • > regulatory hormones go into the median eminence and then an activation will be released in the anterior pituitary
58
Q

What pituitary gland both produces and releases hormones? Which pituitary gland only releases hormones?

A
  • anterior pituitary gland both produces and releases hormones
  • posterior pituitary gland only releases hormones
59
Q

What is the other names for the anterior pituitary and posterior pituitary glands?

A
  1. Anterior Pituitary
    - pars distalis, adenohypophysis, anterior lobe
  2. Posterior Pituitary
    - pars nervosa, neurohypophysis, posterior lobe
60
Q

Posterior Pituitary Gland

A
  • only releases hormones
  • neural origin, from ventral hypothalamus where it was derived from
  • 3 neurons in the hypothalamus with nerve ends in post pit
  • the neurohypophysis (post pit gland) consists of axons and nerve endings with their cell bodies residing in the hypothalamus
61
Q

When inside the CNS a collection of cell bodies is referred to as?

A
  • nuclei
62
Q

Outside the CNS a collection of cell bodies is called?

A
  • ganglia

- inside the PNS

63
Q

What is the name for nerves in the hypothalamus? (CNS)

A
  • hypothalamic neuropophyseal nerves

- have neurons and axons

64
Q

Nuclei in the hypothalamus

A
  1. PVN
    - contains magnocellular and parvocellular neurons
    - paraventricular nuclei
  2. SON
    - only contains magnocellular neurons
    - supraoptic nuclei
  • nuclei contain A LOT of NERVE CELL BODIES
  • IF SAYS parvocellular or magnocellular NEURONS, it does not go into these structures, on its own in hypothalamus
  • IF SAYS parvocellular cell goes inside the structures
65
Q

Development of Anterior Pituitary Gland

A
  • originates from Rathke’s Pouch
  • 4 to 5 weeks of human gestation ant pit becomes visible
  • functionally mature at 20 weeks gestation
  • roof of mouth depression creates an intermediate lobe and then regresses
  • intermediate lobe can be called pars intermedia
  • > will continue to function in monkeys, rodents and dogs
  • intermediate lobe produces hormone POMC (proopiomelanocortin)
  • > is cleaved into two substances: alpha-MSH and a little ACTH
  • > in humans since regressed gives function to anterior pituitary
66
Q

Magnocellular Neurons

A
  • originate in the hypothalamus and end in posterior pituitary
67
Q

Parvocellular Neurons

A
  • originate in hypothalamus and end in median eminence
68
Q

What pituitary gland is larger?

A
  • the anterior pituitary gland is larger
  • 2/3 Anterior: 1/3 Posterior
  • when female is pregnant entire gland size doubles because hormone stimulation
69
Q

Afferent and Efferent signals to the hypothalamus

A
  • accompanies massive blood supply and nerves
    1. hypothalamus receives afferent signals
  • sensory signals coming in = input
  • stomach, liver, intestines
    2. Efferent signals are going out of the hypothalamus
  • motor signals = output
  • neurotransmitters, peptides
70
Q

Oxytocin in Females

A
  • once activated for 1-5 minutes deactivated by blood flow through the liver
  • in female is located in the uterus and mammary gland
  • when activated contractions begin and oxytocin signals up-regulate the receptors until birth (pos feedback)
  • plays a role in milk letdown, works with prolactin during breast stimulation
  • during lactation there are receptors in the breast and levels of oxytocin increase
71
Q

Oxytocin in males

A
  • binds in males at the level of the leydig cells in the testicles (cuddle hormone)
  • study where men received nasal spray of oxytocin or placebo
  • ones who got oxytocin were more inclined to play with their children
  • also a study where they found that men with increased levels of oxytocin were monogomous
    • if had a non function G-alpha-q receptor nothing would happen when received oxytocin
72
Q

What receptor does oxytocin bind to?

A
  • G-alpha-q
  • second activation of phospholipase C (PLC)
  • release calcium eventually
73
Q

What will happen if there is an oxytocin deficiency in nursing females?

A
  • will not have milk letdown
  • after childbirth oxytocin levels will tank and it is hard to come back up (very hard to produce milk)
  • to induce labor give oxytocin
  • altered fertility has no affect
74
Q

ADH, AVP, or Vasopressin

A
  • produced by hypothalamus
  • increases water reabsorption at the level of the kidney
  • increase of ADH, increase of water uptake
  • volume of urine decreases because takes up water
  • Alcohol is an inhibitor of ADH
  • prevents water uptake and electrolytes
  • Urine output increases due to this
  • ADH targets the KIDNEYS
75
Q

Kidney Structure

A
  • comprised of a million nephrons
  • nephrons are the functional unit of the kidney
  • Kidney has a medulla (inner portion) and cortex (outer portion)
  • Nephrons that go from the cortex to the medulla are called cortical medullary nephrons
  • Nephrons that stay only in the cortex are called cortical nephrons
  • the longer the Loop of Henle, the better the ability to reabsorb water
76
Q

Nephron

A
  • Bowman’s Capsule
  • PCT (proximal convoluted tubule)
  • dLOH (descending loop of henle)
  • aLOH (ascending loop of henle)
  • DCT (distal convoluted tubule)
  • nephron ends here and connects to the collecting duct
  • main target for ADH (kidneys receptor for ADH is on the nephrons)
  • collecting duct are the last chance to reabsorb water before excreted from the body
77
Q

If we have a patient that is not absorbing water, but is not drinking alcohol what could be the issue?

A
  • can be a problem with the brain or with the kidneys
    1. Brain
  • ADH is produced in the hypothalamus, therefore it can be a problem with the hypothalamus or the ADH hormone itself
    2. Kidneys
  • there can be a deficiency of nephrons, or a problem with the ADH receptors on the nephrons
78
Q

Why is it necessary for molecules to filter through a nephron before being secreted?

A
  • because molecules are pressed out using pressure only
  • a glomerulus is a ball of blood vessels
  • it goes in afferent and leave efferent
  • glomerulus pressure causes molecules to be pushed out
  • > water, ions and nutrients
  • > Glomerulus uses pressure to push molecules into Bowman’s Capsule using just force, not selective
  • nephron determines regulates what is reabsorbed and what is secreted, determines what the body needs
79
Q

2 Types of Cells in the Glomerulus

A
  1. Macula Densa Cells
  2. Juxtaglomerular Cells (afferent mainly)
    - together they form the juxtaglomerular apparatus
    - contains cells that detect chemicals and pressure
    - measure afferent and efferent flow
80
Q

Blood pressure

A
  • exerts affect on blood vessels
  • we have stretch receptors that let us know what type of blood vessels we have
  • if increase water reabsorption, sodium follows(uptake), inc blood pressure (and vice versa)
  • if increase sodium, water follows(uptake), and blood pressure increases
  • Hormones can also play a role in the inc of blood pressure
  • > if inc ADH levels, inc water reabsorption, inc sodium uptake and as a result blood pressure will increase
81
Q

Epithelial Cells on Nephron

A
  • very stable/organized in a group setting
  • form apical (top) or basal (bottom)
  • basal side adheres to the basement membrane/extracellular matrix and has a blood vessel underneath
  • form a sheath and attach to each other via proteins
  • selectively permeable (channels->aquaporins)
  • if did not function properly anything in Bowman’s capsule would be secreted through urine
82
Q

Where absorption occurs in nephron and what type

A
  1. DCT = permeable to H2O and solutes
  2. dLOH = permeable to H2O only
  3. aLOH = permeable to solutes only
  4. PCT = permeable H2O and solutes
  5. Collecting Duct = permeable to H2O only
    - at top near DCT and PCT it is diluted
    - at bottom of loop of henle it is concentrated bc reabsorbed water in dLOH
    - reabsorption is coming out of nephron into blood vessel
83
Q

Primary effect of ADH

A
  1. to increase the permeability of water in the collecting duct and DCT
    - > will result in smaller volume of urine that is more concentrated
    - without ADH we would urinate constantly!!!
  2. ADH has an effect on vascularizing blood vessels
    - if an animal has a major wound, increase ADH to vascularize the blood vessels
84
Q

Glomerulus Filtrate

A
  • what is filtered out of glomerulus into Bowman’s capsule

- H2O and solvents(nutrients and ions)

85
Q

Where does the majority of water reabsorption occur?

A
  • 10% of water reabsorption occurs in the collection duct

- the majority, 90% of water reabsorption occurs in LOH, DCT and PCT

86
Q

Aquaporins in Nephron

A
  • aquaporins are channels specifically for water
  • CD is under influence of ADH and that is how we adjust the last 10% of water reabsorption for our needs
  • AQP 1, AQP 2, and AQP 3/4
    1. AQP 1 inserts itself on basal and apical sides of epithelial cells in the DCT, PCT and LOH
  • not under hormonal control, constitutively expressed (allows reabsorption of water in these areas)
    2. ADH binds to G-alpha-s receptor on basolateral side of epithelial cell in collecting duct, causes activation of G-alpha-q
    3. G-alpha-q causes downstream effects that result in the phosphorylation of another water channel
    4. AQP2 is inserted on apical side of epithelial cell in CD and is under hormonal influence
  • causes presence of AQP 3/4 through phosphorylating events
    5. AQP 3/4 is inserted on basal side of epithelial cell in CD and is not under hormonal influence
87
Q

Plasma(blood) Osmolality

A
  • the amount of water and solutes in a blood vessel
    Ex 1:
  • if a patient is dehydrated, will have low water and high solutes in blood vessel (high plasma osmolality)
  • signals hypothalamus to produce ADH so patient can increase water absorption and set stretch receptors back to a steady state
    Ex 2:
  • if a patient is hypotonic (too much water reabsorption), lots of signals to the hypothalamus to decrease production of ADH
88
Q

Macula Densa Cells and Juxtaglomerular in Vasoconstriction

A
  1. Macula Densa Cells are chemoreceptors and determine levels of solvents in a blood vessel (primarily sodium)
  2. Juxtaglomerular Cells are osmoreceptors and determine stretch coming in and out of the the glomerulus
    - very sensitive
89
Q

What happens when blood volume decreases by 10% or more? What happens when blood pressure decreases by 10% or more?

A
  1. When blood volume decreases by 10% or more, will release ADH
  2. When blood pressure decreases by 10% or more, juxtaglomerular cells will produce renin
    - liver will produce angiotensinogen
    - renin will convert angiotensinogen to angiotensin 1
    - liver will produce its own enzyme to convernt angiotensin 1 to angiotensin 2
    - angiotensin 2 binds to osmoreceptors and communicates need to regulate water uptake
90
Q

Disorders of ADH production

A
  1. If have dec in ADH release can be due to a tumor in the hypothalamus or the posterior pituitary gland
  2. If have Excessive inc in ADH release can have same problem as 1
  3. Diabetes insipidus
    - always thirsty, can not quench thirst
    - can be a mutation in ADH
  4. Mutation in AQP3/4 will allow them to absorb water through AQP1
    - can be a defect in the CD or a problem with the brain
    - will alter ability to regulate the last 10% of water uptake
91
Q

SON

A
  • only contains magnocellular cell bodies

- releases ADH and oxytocin

92
Q

PVN

A
  • contains magnocellular and parvocellular cell bodies

- releases TRH(thyrotropin RH) and CRH(corticotropin RH)

Vertebrate Endocrinology (4 decks)

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