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Block 3; Week 6 Michelle > Adrenal Gland O'Driscoll > Flashcards

Adrenal Gland O'Driscoll Flashcards

1
Q

The adrenal glands help maintain homeostasis in the body by which 3 mechanisms?

A

stress response
water, Na+, K+ balance
BP control

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2
Q

What are the 2 main classes of steroids that the adrenal gland secretes? What are the specific hormone types?

A

Steroids: glucocorticoids, mineralcorticoids, androgens
Catecholamines: epinephrine, norepinephrine

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3
Q

90% of the anatomy of the adrenal gland is _____. 10% is ______.

A

90% is adrenal cortex.

10% is adrenal medulla.

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4
Q

Where is aldosterone secreted from in the adrenal gland? What makes aldosterone?

A

Zona glomerulosa

aldosterone synthase

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5
Q

If you lost all fcn of your adrenal glands…what would happen?

A

You would die w/i 2 weeks from either a hypoglycemic coma or circulatory collapse (shock)

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6
Q

What types of hormones are secreted from the zona glomerulosa? What controls this secretion?

A

mineralcorticoids

Controlled by ECF conc’n of Ang II & K+ & RAAS

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7
Q

What types of hormones are secreted from the zona fasciculata? What controls this secretion?

A

glucocorticoids

Hypothalamic-Pituitary Axis via ACTH

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8
Q

What types of hormones are secreted from the zona reticularis? What controls this secretion?

A

Androgens

Hypothalamic-Pituitary Axis via ACTH

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9
Q

In one word, what is secreted from the adrenal cortex?

A

Steroids

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10
Q

What type of hormone is aldosterone & where is it secreted from?

A

mineralcorticoid

secreted from the zona glomerulosa

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11
Q

What type of hormone is cortisol & where is it secreted from?

A

glucocorticoid

secreted from the zona fasciculata

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12
Q

What type of hormone is DHEA & where is it secreted from?

A

androgen

secreted from the zona reticularis

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13
Q

Small amounts of sex hormones are also secreted from the adrenal cortex. Where in the adrenal cortex?

A

the zona reticularis

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14
Q

What is the main mineral corticoid? What is another natural mineralocorticoid that does not have any glucocorticoid activity?

A

Aldosterone

Deoxycorticosterone

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15
Q

What is a synthetic mineralocorticoid that is more powerful than aldosterone & has no glucocorticoid activity?

A

9a-Fluorocortisol

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16
Q

What are the hormones that are mainly glucocorticoids, but have some mineralocorticoid activity? List them from most powerful to least.

A

cortisol
corticosterone
cortisone

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17
Q

What is the main glucocorticoid hormone?

What is a hormone that is natural & is only a glucocorticoid?

A

Cortisol

**there are none that fit that description

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18
Q

What are the synthetic hormones that are only glucocorticoids & are more powerful than cortisol? List them from most powerful to least.

A

Prednisone (4X powerful)
methylprednisone (5X powerful)
Dexamethasone (30X powerful)

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19
Q

What are 2 hormones, aside from cortisol, that are mainly glucocorticoids, but also have some mineralocorticoid activity? Which is more powerful?

A

Cortisone (more powerful)

Corticosterone

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20
Q

So…Cortisol, Cortisone, & Corticosterone all share both mineralocorticoid activity & glucocorticoid activity. Which one do they mainly exhibit, though?

A

Mainly glucocorticoid.

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21
Q

Do corticosteroids usu bind to transport proteins to travel in the blood? if so, which ones?

A

YES–>they are steroids, hydrophobic
Mainly CBG: corticosteroid binding globulins aka transcortin.
Note: they also bind albumin

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22
Q

Where are plasma binding proteins produced?

A

in the liver

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23
Q

Where are corticosteroids inactivated?

A

in the liver

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24
Q

Where are the conjugates of the corticosteroid excreted?

A

thru the urine

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25
Q 
Some questions about cortisol:
% bound to plasma protein
T1/2
blood conc'n
secretory rate per day
A

90-95% bound
T1/2=60-90 min
Blood conc’n: 6ng/dL
Secretory Rate: 0.15 mg/day

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26
Q 
Some questions about aldosterone:
% bound to plasma protein
T1/2
blood conc'n
secretory rate per day
A

60% bound
T1/2=20 min
Blood conc’n: 12microgram/dL
Secretory Rate: 15 mg/day

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27
Q

What are the main actions of aldosterone?

A

sodium retention
potassium excretion
**mainly accomplished in the kidney

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28
Q

What does aldosterone target in the kidney?

A

principal cells in DCT & collecting duct

intercalated cells in the collecting duct

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29
Q

Aldosterone also prevents sodium loss from other parts of the body (aside from the kidney). How does it accomplish this?

A

Sweat Glands: conserves salts in hot environment
Salivary Glands: conserves salts w/ excessive salivation
Intestinal Epithelial Cells: keeps salts from being lost in stools.

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30
Q

How long does it usu take for mineralocorticoids to have their effect? Why is this?

A

45-60 minutes

b/c it requires gene transcription

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31
Q

Explain how aldosterone has its effect?

A

Diffuses thru the plasma membrane & binds a mineralocorticoid receptor. This complex goes to the nucleus & has the DNA transcribe certain RNA–>mRNA–>proteins to carry out the desired effect.

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32
Q

What types of proteins does aldosterone encourage the transcription of? What is the overall effect?

A

Enzymes, like sodium potassium pump
Membrane transport proteins, like ENaC (epithelial sodium channel)
Overall: increased transepithelial sodium transport

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33
Q

The slower actions of aldosterone are the genomic effects. What are these?

A

transcription of genes involved in ion transport
increase Na+ reabsorption
increase K+ excretion

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34
Q

The faster actions of aldosterone are the non-genomic effects. What are these?

A

activation of a second messenger system, including activating PKA (thru increase in cAMP)
increase bicarb retention
increase H+ excretion

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35
Q

If you lack aldosterone, what will happen to the sodium?

A

It will be lost in the urine each day. 10-20 grams

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36
Q

If you have excess aldosterone, what will happen to the sodium?

A

increase in Na+ in the ECF

decrease in K+ in the body

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37
Q

Aldosterone helps to maintain BP. Which substance has the opposite effect of aldosterone on BP?

A

the anti-aldosterone is the atrial natriuretic peptide

This is secreted by the heart.

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38
Q

Describe in detail the process by which low BP can be controlled by aldosterone.

A

Kidney senses low BP.
Releases renin
Changes Angiotensinogen–>Ang I
This is changed to Ang II
Ang II causes secretion of aldosterone from the adrenal gland.
the genomic effects of the increased aldosterone are more renal sodium channels–>sodium reabsorption
this sodium retention also causes osmotic reabsorption (like of water)
This causes an increase in blood volume
This increases blood pressure
Now, the kidneys aren’t secreting renin & the heart is secreting ANP.

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39
Q

When there is excess aldosterone there is an increase in ECF, but not an increase in the Na+ conc’n. Why?

A
  • as Na+ is reabsorbed by the kidney, there is simultaneous osmotic reabsorption of water.
  • if the Na+ conc’n of the ECF increases at all–>it stimulates thirst
  • Overall: even tho the amount of sodium in the ECF will increase, the Na+ conc’n won’t really increase.
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40
Q

If aldosterone causes ECF volume to be elevated for more than 1 or 2 days, then there is another change. What is that?

A

an increase in arterial pressure b/c increased blood volume increases CO & increases BP

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41
Q

What is aldosterone escape? Why is it important?

A

this is when salt “escapes” from the reabsorption trap of aldosterone…
this happens b/c of the increase in GFR (from increased blood volume) & the decrease in proximal tubule Na+ reabsorption
it escapes!
Important to balance everything out & avoid formation of edema.

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42
Q

What are the main results of aldosterone falling to zero?

A 
lots of sodium is lost in the urine
less sodium in the ECF
less ECF volume
ECF dehydration
Low blood volume
Circulatory Shock
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43
Q

How would minimal aldosterone affect potassium levels in the body?

A

it would cause hyperkalemia

possible cardiac toxicity–>weakness of heart contraction & development of arrhythmia

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44
Q

How would excess aldosterone affect potassium levels in the body?

A

it would cause hypokalemia
muscle weakness & cramping
change in excitability of nerves & muscles

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45
Q

What is the relationship b/w Na+ & H+ in the collecting ducts?

A

Na+ is reabsorbed at the expense of H+, which is excreted.

this happens in the intercalated cells of the cortical collecting tubules

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46
Q

Why is it important that the body reabsorbs bicarb & excretes H+?

A

to maintain a healthy pH

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47
Q

What is the relationship b/w Na+ & K+ in the collecting ducts?

A

Na+ is also reabsorbed at the expense of K+, which is excreted. This happens in the principal cells of the collecting ducts

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48
Q

With respect to H+, what can be a negative consequence of excess aldosterone?

A

this greatly increases H+ secretion & excretion

this decreases H+ conc’n in ECF greatly & can cause metabolic alkalosis

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49
Q

T/F Cortisol can bind mineralocorticoid receptors with high affinity.

A

True.

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50
Q

Although cortisol isn’t as potent as aldosterone, ____________.

A

its plasma conc’n is much higher than aldosterone & it can still bind mineralocorticoid receptors with high affinity

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51
Q

T/F cortisone isn’t as good as cortisol at binding mineralocorticoid receptors.

A

True.

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52
Q

Where is the following enzyme found & what does it do?

11β-hydroxysteroid dehydrogenase type 2

A

It is found in renal epithelial cells

converts cortisol to cortisone

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53
Q

What is AME: apparent mineralocorticoid excess syndrome?

A

pseudohyperaldosteronism
seems like you have excess aldosterone…presents the exact same way except that your aldosterone levels are low
**this is caused by the inhibition of 11β-hydroxysteroid dehydrogenase type 2
This causes high levels of cortisol, which exhibit mineralocorticoid effects.
Licorice can cause AME b/c of the glycyrrhetic acid that blocks this enzyme.

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54
Q

What inhibits aldosterone secretion?

A

ANP (there b/c of high BP)

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55
Q

What role does ACTH play in regulating aldosterone secretion from the adrenal cortex?

A

It plays a passive role. ACTH is extremely important in stimulating release of other hormones from the adrenal cortex. Less so w/ aldosterone…
If it is absent, no aldosterone secretion.
If it is present, doors open to aldosterone secretion.

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56
Q

What does an increase in Na+ in the ECF do to aldosterone secretion?

A

decreases it slightly

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57
Q

What are the main regulators of aldosterone release?

A

High K+ in blood

High Angiotensin II (there b/c of low BP)

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58
Q

When there is an increase in Ang II what happens to the vasculature?

A

There is increased vasoconstriction in response to the low plasma volume & increase in Ang II.

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59
Q

When sodium is a little low, what happens to alderstone secretion? When sodium is really low, what happen?

A

A little low: inhibitory effect on aldosterone secretion

Really low: activates aldosterone secretion

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60
Q

What causes the release of ACTH in the first place? Where is it released from?

A

released from the anterior pituitary b/c of stress

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61
Q

What are the main effects of aldosterone in the body?

A

vasoconstriction
increased sodium reabsorption
increased potassium secretion
increased BP

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62
Q

Starting with low BP…describe how an increase in aldosterone secretion occurs.

A

LOW BP
sensed by kidney–>renin release
Renin converts angiotensinogen to Ang I in the bloodstream.
Ang I converted into Ang II by ACE.
Ang II goes to the adrenal cortex and causes the release of aldosterone.
This will increase Na+ reabsorption in the kidney & increase BP.

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63
Q

Which glucocorticoid is so potent that it is responsible for 95% of all glucocorticoid activity? What are its 2 names?

A

cortisol aka hydrocortisone

64
Q

Which glucocorticoid is responsible for 4% of glucocorticoid activity?

A

corticosterone. this is less potent than cortisol.

65
Q

What are the main effects of cortisol?

A

resisting stress & inflammation
main effect is to increase blood glucose
effects metabolism of proteins, carbs, fats
**affects most tissues b/c most tissues have glucocorticoid receptors

66
Q

What could your stress do to you if you had no cortisol?

A

it could be deadly!

67
Q

what is the cellular mechanism of normal levels of cortisol?

A

Note: most tissues have glucocortioid receptors.

  • steroid hormone diffuses thru the cell membrane
  • cortisol binds intracellular cytoplasmic glucocorticoid receptor
  • receptor-hormone complex diffuses thru the nuclear membrane.
  • hormone receptor complex binds a glucocorticoid response element to alter gene transcription
68
Q

What is the cellular mechanism of high levels of cortisol?

A

have genomic effects intracellularly as described

also have some rapid non-genomic effects that have something to do w/ cell membrane ion transport

69
Q

What is the effect of cortisol on carbohydrate metabolism?

A

increases gluconeogenesis in the liver from AA.
increases enzyme in the liver required to convert AA to glucose.
AA mobilized from muscle
Glucose utilization in other tissues is decreased
Storage of liver glycogen increases
Blood glucose increases (can cause hyperglycemia if too many glucocorticoids)
Insulin secretion increases
**if too much glucocorticoid secretion–>insulin resistance possible

70
Q

What is the effect of cortisol on protein metabolism?

A

protein stores decrease everywhere except the liver
protein synthesis decreases
protein catabolism increases
All free AA directed to the liver
Liver converts extra AA into glucose
there is also an increase in liver protein synthesis enzymes for some reason…

71
Q

What is the effect of cortisol on fat metabolism?

A

fatty acids are freed from adipose tissue
there are more fatty acids free in the blood
beta oxidation increases in cells
when you are starved or stressed you switch from using glucose for energy to using fatty acids

72
Q

What types of stressful situations might glucocorticoid secretion increase in?

A 
trauma
infection
surgery
intense cold
intense heat
73
Q

How does cortisol help in resisting stress & inflammation?

A

mobilizes fats & AA–>available for energy & synthesis of new compounds
anti-inflammatory effects especially important b/c inflammation can be one of the most damaging effects of a disease

74
Q

In a simpler model, what are the 5 stages of inflammation?

A
  1. Damaged Cells release activators of inflammation.
  2. Blood flow increases to that area
  3. Capillary permeability increases @ that area (plasma leaks out of capillaries into surrounding tissues & tissue fluid clots)
  4. Infiltration by leukocytes
  5. Fibrous tissue grows–>helps w/ long-term healing.
75
Q

In a more complex model, what are the 7 stages of inflammation?

A
  1. Bacteria enter wound.
  2. Platelets release clotting factors @ site.
  3. Mast cells release stuff that causes specific vasoconstriction & vasodilation such that there is an increase in delivery of blood, plasma, cells.
  4. Neutrophils secrete stuff to kill pathogens.
  5. Neutrophils & macrophages phagocytose pathogens.
  6. Macrophages release cytokines. this increases the immune response for tissue repair.
  7. This process continues until the wound is healed.
76
Q

In the simpler model of inflammation, which substances are released as activators of inflammation by the damaged cells in step 1?

A 
histamine
bradykinin
proteolytic enzymes
prostaglandins
leukotrienes
77
Q

What are the anti-inflammatory effects of Cortisol?

A
  1. Blocks early stages of inflammation
    * activates anti-inflammatory agents
    * inhibits pro-inflammatory agents
  2. Causes rapid resolution/healing
78
Q

What are some of the anti-inflammatory agents that Cortisol activates?

A 
Interleukin antagonists
Lipocortin 1
b2 adrenoreceptor
Secretory leukocyte- 
inhibitory protein
79
Q

What are some of the pro-inflammatory agents that Cortisol inhibits?

A

Cytokines eg. IL-1
Chemkines eg. IL-8
Endothelin 1
Adhesion molecules

80
Q

B/c of the anti-inflammatory effects of cortisol & other glucocorticoids they are helpful in which 3 clinical cases?

A
  1. allergies
  2. autoimmune disease
  3. transplantation
81
Q

What are 6 more specific things that high levels of cortisol do to decrease the inflammation?

A
  1. stabilizes lysosomal membrane
  2. decreases permeability of capillaries
  3. decreases WBC migration
  4. decreases phagocytosis of damaged cells
  5. suppresses immune system
  6. decreases WBC cytokine release (like of interleukin-1)
82
Q

What is the significance of cortisol stabilizing the lysosomal membrane?

A

no release of proteases!

83
Q

What is the significance of cortisol decreasing the permeability of capillaries?

A

not leaky, no loss of plasma into the tissues

84
Q

What is the significance of cortisol decreasing WBC migration?

A

fewer WBCs get entrance into the inflamed area

85
Q

What is the significance of cortisol decreasing the phagocytosis of damaged cells?

A

less release of prostaglandins & leukotrienes

86
Q

What is the significance of cortisol suppressing the immune system?

A

**this means fewer T lymphocytes, T cells, & antibodies (a part of the inflammation response)

87
Q

What is the significance of cortisol decreasing WBC cytokine release (such as interleukin-1)?

A

this decreases fever

88
Q

T/F Cortisol increases the production of RBCs.

A

TRUE

89
Q

Why is cortisol useful in allergic reactions?

A

b/c the inflammatory process of anaphylaxis is blocked by cortisol, saving people who might have otherwise died.

90
Q

When Cortisol is too low/too high you see polycythemia, lymphocytopenia, eosinopenia.

A

TOO high–polycythemia, lymphocyteopenia, eosinopenia

91
Q

When Cortisol is too low/too high you see anemia.

A

TOO low–anemia

92
Q

What controls the release of Cortisol from the adrenal cortex?

A

ACTH secreted from the anterior pituitary

93
Q

Aside from Cortisol & other glucocorticoids, what else does ACTH control the production of?

A

adrenal androgen production in the adrenal cortex

94
Q

What controls ACTH release?

A

CRH from the hypothalamus

95
Q

What pattern of release does Cortisol use?

A

Cortisol/Glucocorticoids & ACTH & CRH are all released in a pulsatile manner, based on the circadian rhythm. Called diurnal rhythm. Highest in the morning & lowest in the evening.

96
Q

Which hormones are secreted from the zona reticularis of the adrenal cortex? What is the function of these hormones?

A

DHEA
DHEA-S
androstenedione
**contributes to early development of male sex organs
**growth of pubic & axillary hair in females
**in the testes, these hormones are converted to testosterone

97
Q

What is hypoadrenalism? What is another name for it?

A

aka adrenal insufficiency

**failure of the adrenal cortex to produce sufficient hormones

98
Q

What are the 2 types of hypoadrenalism? Which one did JFK have?

A
  1. Primary Adrenal Insufficiency: Addison’s Disease
    * JFK
  2. Secondary Adrenal insufficiency: pituitary gland doesn’t produce sufficient ACTH
99
Q

Describe Addison’s disease & its 4 potential causes.

A 
adrenal cortex is destroyed
4 causes
1. autoimmunity: antibodies react w/ steroidgenic enzymes (80% of cases)
2. tuberculosis
3. fungal infections
4. adrenal hemorrhage following trauma
100
Q

Addison’s disease causes mineral corticoid deficiency & glucocorticoid deficiency. What is the consequence of the mineral corticoid deficiency?

A 
**think about the fcn of aldosterone
hyponatremia
hyperkalemia
mild acidosis
decreased plasma volume
decreased CO
decreased BP
circulatory shock
death
101
Q

Addison’s disease causes mineral corticoid deficiency & glucocorticoid deficiency. What are the consequences of glucocorticoid deficiency?

A 
impaired fuel mobilization
decreased gluconeogenesis
hypoglycemia
weight loss
muscle weakness
extreme sensitivity to stress
death
102
Q

Addison’s disease causes pigmentation. Why?

A

b/c the adrenal cortex doesn’t produce enough cortisol…no negative feedback to stop ACTH.
With a lot of ACTH release you get a lot of MSH (more melanin) release b/c they both come from the precursor molecule: POMC

103
Q

What is another name for hyperadrenalism? What is it?

A

Cushing’s syndrome
prolonged exposure to too much cortisol
**also associated w/ glucocorticoid & androgenic excess

104
Q

What are the various causes of Cushing’s syndrome?

A
  1. hyper secretion of CRH or ACTH (this is a secondary problem–called Cushing’s disease)
  2. adrenal cortex adenomas
  3. ectopic secretion of ACTH
  4. hypercortisolism (too many glucocorticoids)
105
Q

What happens in a person with Cushing’s syndrome as a result of glucocorticoid excess?

A
  • *gluconeogenesis increases–>hyperglycemia–>insulin sensitivity decreases
  • *fat mobilization from lower body to thorax & abdomen (buffalo torso)
  • *Round puffy face (moon facies)
  • *protein loss (not in liver)–>weakness, osteoporosis, striae on skin
  • *easier to get infections
106
Q

What happens in a person with Cushing’s syndrome as a result of androgenic excess?

A

acne

hirsutism (excess growth of facial hair)

107
Q

Aside from the symptoms that have already been discussed, what are the results of Cushing’s syndrome?

A 
HTN-cardiac hypertrophy
buffalo hump
amenorrhea
purpura (skin thing)
skin ulcers b/c of decreased wound healing
108
Q

Conn’s Syndrome is also known as what? What is it?

A

primary aldosteronism

too much aldosterone in the system

109
Q

What are 2 causes of Conn’s Syndrome?

A
  1. tumor of zona glomerulosa cells in the adrenal cortex–>increase aldosterone secretion
  2. hyperplastic adrenal cortex–>secretion of aldosterone instead of cortisol
110
Q

What happens sometimes to patients w/ Conn’s?

A 
hypokalemia--muscle paralysis
hypervolemia--HTN
(low plasma renin levels)
alkalosis
Remember: aldosterone causes K+ & H+ excretion & Na+ reabsorption
111
Q

What is adrenogenital syndrome? How is it diagnosed?

A

adrenocortical tumor that causes excessive androgen secretion
*diagnosed by looking at super high levels of 17-ketosteroids (breakdown products of androgens)

112
Q

What does adrenogenital syndrome do in females?

A

Females–>masculinization: beard growth, voice deepening, body hair, growth of clitoris

113
Q

What does adrenogenital syndrome do in males?

A

Males–>rapid sexual development in pre-puberty period

114
Q

What is congenital adrenal hyperplasia?

A

aut rec disorder caused 95% of the time by a 21 hydroxylase deficiency.
This prevents progesterone from being converted into cortisol or aldosterone, only allows for androgens! too many androgens & too few cortisol & aldosterone molecules

115
Q

What is the presentation in mild, moderate, & severe congenital adrenal hyperplasia?

A 
Mild: infertility due to anovulation
Moderate: perpubertal virilization
Severe: ambiguous genitalia
prenatal virilization
life-threatening vomiting & dehydration @ beginning of life
116
Q

Describe the organization of the adrenal gland & what is secreted from each section.

A 
Adrenal Cortex:
zona glomerulosa: aldosterone
zona fasciculata: glucocorticoids
zona reticularis: androgens
Adrenal Medulla:
epi (mainly) & norepi (catecholamines) (a little dopamine too)
117
Q

Rather than being an endocrine gland, the adrenal medulla is actually _______.

A

a modified sympathetic ganglion

118
Q

What types of cells are found in the adrenal medulla? What is their innervation?

A 
chromaffin cells (neuroendocrine cells-modified postganglionic neurons)
innervation: cholinergic preganglionic neurons (thoracolumbar spinal cord)
119
Q

Epinephrine only comes from the adrenal medulla. Where else does NE come from?

A

sympathetic terminals

extraadrenal chromaffin cells

120
Q

What is found in chromaffin cells?

A

chromaffin granules (contain catecholamines, ATP, ADP, neuropeptides)

121
Q

What type of molecule is an enkephalin? What is their function?

A

enkephalin: neuropeptide

* *bind to opiod receptors & produce analgesic responses

122
Q

What is the basic molecule that starts the synthesis of catecholamines?

A

tyrosine

123
Q

Which AA can be converted into tyrosine for catecholamine synthesis?

A

phenylalanine

124
Q

Starting from Tyrosine what are the steps for catecholamine synthesis?

A 
Tyrosine
DOPA
Dopamine
NE
Epi
125
Q

Tyrosine–>DOPA What is involved in this step?

A

tyrosine hydroxlase
hydroxylation
**happens in the cytosol
**inhibited by NE

126
Q

DOPA–> Dopamine What is involved in this step?

A

DOPA decarboxylase
decarboxylation
**happens in the cytosol

127
Q

Dopamine–>NE What is involved in this step?

A

Dopamine beta hydroxylase
hydroxylation
**happens in secretory vesicles

128
Q

NE–>Epi What is involved in this step?

A

PNMT
methylation
**happens in the cytosol
**regulated by cortisol

129
Q

What are the key stimuli that cause catecholamine secretion?

A

ACh released from preganglionic neurons

stresses: exercise, hypoglycemia, extreme temp, trauma

130
Q

Describe the details of the preganglionic innervation of the chromaffin cells.

A 
Pregang neuron
ACh release
nicotinic receptors receive
sodium influx
depolarization
increased intracellular calcium
membrane fusion (exocytosis)
131
Q

Once catecholamines are released into the blood, how do they get to their target? What is their half life?

A

transported bound to albumin

t1/2 short: 10 sec–>1.7min

132
Q

Describe the metabolism of catecholamines.

A

can be reuptaken by extra neuronal sites
can be degraded by target cells
can be excreted directly into the urine

133
Q

What are the 2 main enzymes that target cells use to break down catecholamines? What is the major end product of this metabolism? What do you conjugate the breakdown products w/ to excrete them in the urine?

A

COMT & MAO

Vanillylmandelic acid–>conjugated w/ glucuronic acid & sulfates

134
Q

What is the main job of catecholamines & glucocorticoids?

A

Catecholamines–immediate fight or flight

Glucocorticoids–to maintain that fight or flight vibe

135
Q

What are the effects of catecholamines involved in the fight or flight response?

A

increased visual acuity (pupil dilation)
increased HR (increased CO)
increased BP (b/c of arteriolar vasoconstriction)
Constriction of gut blood vessels (digestion slowed)
Vasodilation of arterioles in lungs (increased ventilation)
Increased perfusion of muscles (better muscle performance)
Increased perfusion in brain
Mobilization of glucose—more energy
increased sweating

136
Q

Which signaling mechanism is used by target cells when they bind to catecholamines?

A

G protein coupled receptors

137
Q

Which receptors are found on vasculature? What is their signaling mechanism specifically? What is the results?

A

alpha 1 & alpha 2
IP3 increases
vasoconstriction

138
Q

Which receptors are located on the presynaptic nerve terminal? What is their signaling mechanism specifically? What is the results?

A

alpha 2
cAMP decreases
**less NE release

139
Q

Which receptors are located on the heart?

What is their signaling mechanism specifically? What is the results?

A

beta 1 & beta 2
cAMP increases
**increases heart contractility, conduction, velocity

140
Q

Which receptors are located on skeletal muscle blood vessels? What is their signaling mechanism specifically? What is the results?

A

beta 2
cAMP increases
vasodilation

141
Q

Which receptors are located on the lungs (bronchial smooth muscle)? What is their signaling mechanism specifically? What is the results?

A

beta 2
cAMP increases
bronchodilation

142
Q

Which receptors are located on the juxtaglomerular apparatus of the kidney? What is their signaling mechanism specifically? What is the results?

A

beta 1
cAMP increases
increased renin release

143
Q

What is the signaling mechanism of alpha 1 receptors?

A

Gq

increased IP3 & DAG

144
Q

What is the signaling mechanism of alpha 2 receptors?

A

Gi

decreased cAMP

145
Q

What is the signaling mechanism of beta 1 & beta 2 receptors?

A

Gs

increased cAMP

146
Q

Does alpha adrenergic or beta adrenergic cause the following?
intestinal relaxation

A

alpha

147
Q

Does alpha adrenergic or beta adrenergic cause the following?
bladder sphincter contraction

A

alpha

148
Q

Does alpha adrenergic or beta adrenergic cause the following?
uterine smooth muscle contraction

A

alpha

149
Q

Does alpha adrenergic or beta adrenergic cause the following?
Intestinal & bladder wall relaxation

A

beta

150
Q

Does alpha adrenergic or beta adrenergic cause the following?
calorigenesis

A

beta

151
Q

Does alpha adrenergic or beta adrenergic cause the following?
intestinal sphincter contraction

A

alpha

152
Q

Does alpha adrenergic or beta adrenergic cause the following?
lipolysis

A

beta

153
Q

Does alpha adrenergic or beta adrenergic cause the following?
glycogenolysis

A

beta

154
Q

Does alpha adrenergic or beta adrenergic cause the following?
uterus relaxation

A

beta

155
Q

What is a pheochromocytoma?

A

chromaffin cell tumor that causes over secretion of catecholamines

156
Q

How do you diagnose a pheochromocytoma?

A

detect increased levels of catecholamines & their metabolites in the blood & urine

157
Q

What are the dominant features of a pheochromocytoma?

A 
elevated heart rate
systemic HTN
anxiety
pallor & sweating
hyperglycemia

Block 3; Week 6 Michelle (5 decks)

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