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
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
3
Q
90% of the anatomy of the adrenal gland is _____. 10% is ______.
A
90% is adrenal cortex.
10% is adrenal medulla.
4
Q
Where is aldosterone secreted from in the adrenal gland? What makes aldosterone?
A
Zona glomerulosa
aldosterone synthase
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)
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
7
Q
What types of hormones are secreted from the zona fasciculata? What controls this secretion?
A
glucocorticoids
Hypothalamic-Pituitary Axis via ACTH
8
Q
What types of hormones are secreted from the zona reticularis? What controls this secretion?
A
Androgens
Hypothalamic-Pituitary Axis via ACTH
9
Q
In one word, what is secreted from the adrenal cortex?
A
Steroids
10
Q
What type of hormone is aldosterone & where is it secreted from?
A
mineralcorticoid
secreted from the zona glomerulosa
11
Q
What type of hormone is cortisol & where is it secreted from?
A
glucocorticoid
secreted from the zona fasciculata
12
Q
What type of hormone is DHEA & where is it secreted from?
A
androgen
secreted from the zona reticularis
13
Q
Small amounts of sex hormones are also secreted from the adrenal cortex. Where in the adrenal cortex?
A
the zona reticularis
14
Q
What is the main mineral corticoid? What is another natural mineralocorticoid that does not have any glucocorticoid activity?
A
Aldosterone
Deoxycorticosterone
15
Q
What is a synthetic mineralocorticoid that is more powerful than aldosterone & has no glucocorticoid activity?
A
9a-Fluorocortisol
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
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
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)
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
20
Q
So…Cortisol, Cortisone, & Corticosterone all share both mineralocorticoid activity & glucocorticoid activity. Which one do they mainly exhibit, though?
A
Mainly glucocorticoid.
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
22
Q
Where are plasma binding proteins produced?
A
in the liver
23
Q
Where are corticosteroids inactivated?
A
in the liver
24
Q
Where are the conjugates of the corticosteroid excreted?
A
thru the urine
25
```
Some questions about cortisol:
% bound to plasma protein
T1/2
blood conc'n
secretory rate per day
```
90-95% bound
T1/2=60-90 min
Blood conc'n: 6ng/dL
Secretory Rate: 0.15 mg/day
26
```
Some questions about aldosterone:
% bound to plasma protein
T1/2
blood conc'n
secretory rate per day
```
60% bound
T1/2=20 min
Blood conc'n: 12microgram/dL
Secretory Rate: 15 mg/day
27
What are the main actions of aldosterone?
sodium retention
potassium excretion
**mainly accomplished in the kidney
28
What does aldosterone target in the kidney?
principal cells in DCT & collecting duct
| intercalated cells in the collecting duct
29
Aldosterone also prevents sodium loss from other parts of the body (aside from the kidney). How does it accomplish this?
Sweat Glands: conserves salts in hot environment
Salivary Glands: conserves salts w/ excessive salivation
Intestinal Epithelial Cells: keeps salts from being lost in stools.
30
How long does it usu take for mineralocorticoids to have their effect? Why is this?
45-60 minutes
| b/c it requires gene transcription
31
Explain how aldosterone has its effect?
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.
32
What types of proteins does aldosterone encourage the transcription of? What is the overall effect?
Enzymes, like sodium potassium pump
Membrane transport proteins, like ENaC (epithelial sodium channel)
Overall: increased transepithelial sodium transport
33
The slower actions of aldosterone are the genomic effects. What are these?
transcription of genes involved in ion transport
increase Na+ reabsorption
increase K+ excretion
34
The faster actions of aldosterone are the non-genomic effects. What are these?
activation of a second messenger system, including activating PKA (thru increase in cAMP)
increase bicarb retention
increase H+ excretion
35
If you lack aldosterone, what will happen to the sodium?
It will be lost in the urine each day. 10-20 grams
36
If you have excess aldosterone, what will happen to the sodium?
increase in Na+ in the ECF
| decrease in K+ in the body
37
Aldosterone helps to maintain BP. Which substance has the opposite effect of aldosterone on BP?
the anti-aldosterone is the atrial natriuretic peptide
| This is secreted by the heart.
38
Describe in detail the process by which low BP can be controlled by aldosterone.
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.
39
When there is excess aldosterone there is an increase in ECF, but not an increase in the Na+ conc'n. Why?
- 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.
40
If aldosterone causes ECF volume to be elevated for more than 1 or 2 days, then there is another change. What is that?
an increase in arterial pressure b/c increased blood volume increases CO & increases BP
41
What is aldosterone escape? Why is it important?
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.
42
What are the main results of aldosterone falling to zero?
```
lots of sodium is lost in the urine
less sodium in the ECF
less ECF volume
ECF dehydration
Low blood volume
Circulatory Shock
```
43
How would minimal aldosterone affect potassium levels in the body?
it would cause hyperkalemia
| possible cardiac toxicity-->weakness of heart contraction & development of arrhythmia
44
How would excess aldosterone affect potassium levels in the body?
it would cause hypokalemia
muscle weakness & cramping
change in excitability of nerves & muscles
45
What is the relationship b/w Na+ & H+ in the collecting ducts?
Na+ is reabsorbed at the expense of H+, which is excreted.
| this happens in the intercalated cells of the cortical collecting tubules
46
Why is it important that the body reabsorbs bicarb & excretes H+?
to maintain a healthy pH
47
What is the relationship b/w Na+ & K+ in the collecting ducts?
Na+ is also reabsorbed at the expense of K+, which is excreted. This happens in the principal cells of the collecting ducts
48
With respect to H+, what can be a negative consequence of excess aldosterone?
this greatly increases H+ secretion & excretion
| this decreases H+ conc'n in ECF greatly & can cause metabolic alkalosis
49
T/F Cortisol can bind mineralocorticoid receptors with high affinity.
True.
50
Although cortisol isn't as potent as aldosterone, ____________.
its plasma conc'n is much higher than aldosterone & it can still bind mineralocorticoid receptors with high affinity
51
T/F cortisone isn't as good as cortisol at binding mineralocorticoid receptors.
True.
52
Where is the following enzyme found & what does it do?
| 11β-hydroxysteroid dehydrogenase type 2
It is found in renal epithelial cells
| converts cortisol to cortisone
53
What is AME: apparent mineralocorticoid excess syndrome?
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.
54
What inhibits aldosterone secretion?
ANP (there b/c of high BP)
55
What role does ACTH play in regulating aldosterone secretion from the adrenal cortex?
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.
56
What does an increase in Na+ in the ECF do to aldosterone secretion?
decreases it slightly
57
What are the main regulators of aldosterone release?
High K+ in blood
| High Angiotensin II (there b/c of low BP)
58
When there is an increase in Ang II what happens to the vasculature?
There is increased vasoconstriction in response to the low plasma volume & increase in Ang II.
59
When sodium is a little low, what happens to alderstone secretion? When sodium is really low, what happen?
A little low: inhibitory effect on aldosterone secretion
| Really low: activates aldosterone secretion
60
What causes the release of ACTH in the first place? Where is it released from?
released from the anterior pituitary b/c of stress
61
What are the main effects of aldosterone in the body?
vasoconstriction
increased sodium reabsorption
increased potassium secretion
increased BP
62
Starting with low BP...describe how an increase in aldosterone secretion occurs.
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.
63
Which glucocorticoid is so potent that it is responsible for 95% of all glucocorticoid activity? What are its 2 names?
cortisol aka hydrocortisone
64
Which glucocorticoid is responsible for 4% of glucocorticoid activity?
corticosterone. this is less potent than cortisol.
65
What are the main effects of cortisol?
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
What could your stress do to you if you had no cortisol?
it could be deadly!
67
what is the cellular mechanism of normal levels of cortisol?
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
What is the cellular mechanism of high levels of cortisol?
have genomic effects intracellularly as described
| also have some rapid non-genomic effects that have something to do w/ cell membrane ion transport
69
What is the effect of cortisol on carbohydrate metabolism?
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
What is the effect of cortisol on protein metabolism?
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
What is the effect of cortisol on fat metabolism?
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
What types of stressful situations might glucocorticoid secretion increase in?
```
trauma
infection
surgery
intense cold
intense heat
```
73
How does cortisol help in resisting stress & inflammation?
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
In a simpler model, what are the 5 stages of inflammation?
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
In a more complex model, what are the 7 stages of inflammation?
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
In the simpler model of inflammation, which substances are released as activators of inflammation by the damaged cells in step 1?
```
histamine
bradykinin
proteolytic enzymes
prostaglandins
leukotrienes
```
77
What are the anti-inflammatory effects of Cortisol?
1. Blocks early stages of inflammation
* activates anti-inflammatory agents
* inhibits pro-inflammatory agents
2. Causes rapid resolution/healing
78
What are some of the anti-inflammatory agents that Cortisol activates?
```
Interleukin antagonists
Lipocortin 1
b2 adrenoreceptor
Secretory leukocyte-
inhibitory protein
```
79
What are some of the pro-inflammatory agents that Cortisol inhibits?
Cytokines eg. IL-1
Chemkines eg. IL-8
Endothelin 1
Adhesion molecules
80
B/c of the anti-inflammatory effects of cortisol & other glucocorticoids they are helpful in which 3 clinical cases?
1. allergies
2. autoimmune disease
3. transplantation
81
What are 6 more specific things that high levels of cortisol do to decrease the inflammation?
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
What is the significance of cortisol stabilizing the lysosomal membrane?
no release of proteases!
83
What is the significance of cortisol decreasing the permeability of capillaries?
not leaky, no loss of plasma into the tissues
84
What is the significance of cortisol decreasing WBC migration?
fewer WBCs get entrance into the inflamed area
85
What is the significance of cortisol decreasing the phagocytosis of damaged cells?
less release of prostaglandins & leukotrienes
86
What is the significance of cortisol suppressing the immune system?
**this means fewer T lymphocytes, T cells, & antibodies (a part of the inflammation response)
87
What is the significance of cortisol decreasing WBC cytokine release (such as interleukin-1)?
this decreases fever
88
T/F Cortisol increases the production of RBCs.
TRUE
89
Why is cortisol useful in allergic reactions?
b/c the inflammatory process of anaphylaxis is blocked by cortisol, saving people who might have otherwise died.
90
When Cortisol is too low/too high you see polycythemia, lymphocytopenia, eosinopenia.
TOO high--polycythemia, lymphocyteopenia, eosinopenia
91
When Cortisol is too low/too high you see anemia.
TOO low--anemia
92
What controls the release of Cortisol from the adrenal cortex?
ACTH secreted from the anterior pituitary
93
Aside from Cortisol & other glucocorticoids, what else does ACTH control the production of?
adrenal androgen production in the adrenal cortex
94
What controls ACTH release?
CRH from the hypothalamus
95
What pattern of release does Cortisol use?
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
Which hormones are secreted from the zona reticularis of the adrenal cortex? What is the function of these hormones?
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
What is hypoadrenalism? What is another name for it?
aka adrenal insufficiency
| **failure of the adrenal cortex to produce sufficient hormones
98
What are the 2 types of hypoadrenalism? Which one did JFK have?
1. Primary Adrenal Insufficiency: Addison's Disease
* JFK
2. Secondary Adrenal insufficiency: pituitary gland doesn't produce sufficient ACTH
99
Describe Addison's disease & its 4 potential causes.
```
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
Addison's disease causes mineral corticoid deficiency & glucocorticoid deficiency. What is the consequence of the mineral corticoid deficiency?
```
**think about the fcn of aldosterone
hyponatremia
hyperkalemia
mild acidosis
decreased plasma volume
decreased CO
decreased BP
circulatory shock
death
```
101
Addison's disease causes mineral corticoid deficiency & glucocorticoid deficiency. What are the consequences of glucocorticoid deficiency?
```
impaired fuel mobilization
decreased gluconeogenesis
hypoglycemia
weight loss
muscle weakness
extreme sensitivity to stress
death
```
102
Addison's disease causes pigmentation. Why?
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
What is another name for hyperadrenalism? What is it?
Cushing's syndrome
prolonged exposure to too much cortisol
**also associated w/ glucocorticoid & androgenic excess
104
What are the various causes of Cushing's syndrome?
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
What happens in a person with Cushing's syndrome as a result of glucocorticoid excess?
* *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
What happens in a person with Cushing's syndrome as a result of androgenic excess?
acne
| hirsutism (excess growth of facial hair)
107
Aside from the symptoms that have already been discussed, what are the results of Cushing's syndrome?
```
HTN-cardiac hypertrophy
buffalo hump
amenorrhea
purpura (skin thing)
skin ulcers b/c of decreased wound healing
```
108
Conn's Syndrome is also known as what? What is it?
primary aldosteronism
| too much aldosterone in the system
109
What are 2 causes of Conn's Syndrome?
1. tumor of zona glomerulosa cells in the adrenal cortex-->increase aldosterone secretion
2. hyperplastic adrenal cortex-->secretion of aldosterone instead of cortisol
110
What happens sometimes to patients w/ Conn's?
```
hypokalemia--muscle paralysis
hypervolemia--HTN
(low plasma renin levels)
alkalosis
Remember: aldosterone causes K+ & H+ excretion & Na+ reabsorption
```
111
What is adrenogenital syndrome? How is it diagnosed?
adrenocortical tumor that causes excessive androgen secretion
*diagnosed by looking at super high levels of 17-ketosteroids (breakdown products of androgens)
112
What does adrenogenital syndrome do in females?
Females-->masculinization: beard growth, voice deepening, body hair, growth of clitoris
113
What does adrenogenital syndrome do in males?
Males-->rapid sexual development in pre-puberty period
114
What is congenital adrenal hyperplasia?
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
What is the presentation in mild, moderate, & severe congenital adrenal hyperplasia?
```
Mild: infertility due to anovulation
Moderate: perpubertal virilization
Severe: ambiguous genitalia
prenatal virilization
life-threatening vomiting & dehydration @ beginning of life
```
116
Describe the organization of the adrenal gland & what is secreted from each section.
```
Adrenal Cortex:
zona glomerulosa: aldosterone
zona fasciculata: glucocorticoids
zona reticularis: androgens
Adrenal Medulla:
epi (mainly) & norepi (catecholamines) (a little dopamine too)
```
117
Rather than being an endocrine gland, the adrenal medulla is actually _______.
a modified sympathetic ganglion
118
What types of cells are found in the adrenal medulla? What is their innervation?
```
chromaffin cells (neuroendocrine cells-modified postganglionic neurons)
innervation: cholinergic preganglionic neurons (thoracolumbar spinal cord)
```
119
Epinephrine only comes from the adrenal medulla. Where else does NE come from?
sympathetic terminals
| extraadrenal chromaffin cells
120
What is found in chromaffin cells?
chromaffin granules (contain catecholamines, ATP, ADP, neuropeptides)
121
What type of molecule is an enkephalin? What is their function?
enkephalin: neuropeptide
| * *bind to opiod receptors & produce analgesic responses
122
What is the basic molecule that starts the synthesis of catecholamines?
tyrosine
123
Which AA can be converted into tyrosine for catecholamine synthesis?
phenylalanine
124
Starting from Tyrosine what are the steps for catecholamine synthesis?
```
Tyrosine
DOPA
Dopamine
NE
Epi
```
125
Tyrosine-->DOPA What is involved in this step?
tyrosine hydroxlase
hydroxylation
**happens in the cytosol
**inhibited by NE
126
DOPA--> Dopamine What is involved in this step?
DOPA decarboxylase
decarboxylation
**happens in the cytosol
127
Dopamine-->NE What is involved in this step?
Dopamine beta hydroxylase
hydroxylation
**happens in secretory vesicles
128
NE-->Epi What is involved in this step?
PNMT
methylation
**happens in the cytosol
**regulated by cortisol
129
What are the key stimuli that cause catecholamine secretion?
ACh released from preganglionic neurons
| stresses: exercise, hypoglycemia, extreme temp, trauma
130
Describe the details of the preganglionic innervation of the chromaffin cells.
```
Pregang neuron
ACh release
nicotinic receptors receive
sodium influx
depolarization
increased intracellular calcium
membrane fusion (exocytosis)
```
131
Once catecholamines are released into the blood, how do they get to their target? What is their half life?
transported bound to albumin
| t1/2 short: 10 sec-->1.7min
132
Describe the metabolism of catecholamines.
can be reuptaken by extra neuronal sites
can be degraded by target cells
can be excreted directly into the urine
133
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?
COMT & MAO
| Vanillylmandelic acid-->conjugated w/ glucuronic acid & sulfates
134
What is the main job of catecholamines & glucocorticoids?
Catecholamines--immediate fight or flight
| Glucocorticoids--to maintain that fight or flight vibe
135
What are the effects of catecholamines involved in the fight or flight response?
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
Which signaling mechanism is used by target cells when they bind to catecholamines?
G protein coupled receptors
137
Which receptors are found on vasculature? What is their signaling mechanism specifically? What is the results?
alpha 1 & alpha 2
IP3 increases
vasoconstriction
138
Which receptors are located on the presynaptic nerve terminal? What is their signaling mechanism specifically? What is the results?
alpha 2
cAMP decreases
**less NE release
139
Which receptors are located on the heart?
| What is their signaling mechanism specifically? What is the results?
beta 1 & beta 2
cAMP increases
**increases heart contractility, conduction, velocity
140
Which receptors are located on skeletal muscle blood vessels? What is their signaling mechanism specifically? What is the results?
beta 2
cAMP increases
vasodilation
141
Which receptors are located on the lungs (bronchial smooth muscle)? What is their signaling mechanism specifically? What is the results?
beta 2
cAMP increases
bronchodilation
142
Which receptors are located on the juxtaglomerular apparatus of the kidney? What is their signaling mechanism specifically? What is the results?
beta 1
cAMP increases
increased renin release
143
What is the signaling mechanism of alpha 1 receptors?
Gq
| increased IP3 & DAG
144
What is the signaling mechanism of alpha 2 receptors?
Gi
| decreased cAMP
145
What is the signaling mechanism of beta 1 & beta 2 receptors?
Gs
| increased cAMP
146
Does alpha adrenergic or beta adrenergic cause the following?
intestinal relaxation
alpha
147
Does alpha adrenergic or beta adrenergic cause the following?
bladder sphincter contraction
alpha
148
Does alpha adrenergic or beta adrenergic cause the following?
uterine smooth muscle contraction
alpha
149
Does alpha adrenergic or beta adrenergic cause the following?
Intestinal & bladder wall relaxation
beta
150
Does alpha adrenergic or beta adrenergic cause the following?
calorigenesis
beta
151
Does alpha adrenergic or beta adrenergic cause the following?
intestinal sphincter contraction
alpha
152
Does alpha adrenergic or beta adrenergic cause the following?
lipolysis
beta
153
Does alpha adrenergic or beta adrenergic cause the following?
glycogenolysis
beta
154
Does alpha adrenergic or beta adrenergic cause the following?
uterus relaxation
beta
155
What is a pheochromocytoma?
chromaffin cell tumor that causes over secretion of catecholamines
156
How do you diagnose a pheochromocytoma?
detect increased levels of catecholamines & their metabolites in the blood & urine
157
What are the dominant features of a pheochromocytoma?
```
elevated heart rate
systemic HTN
anxiety
pallor & sweating
hyperglycemia
```
