Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Block 3 Week 6 > Adrenal Glands- Driscoll > Flashcards

Adrenal Glands- Driscoll Flashcards

1
Q

What contribute to maintaining homeostasis through salt/ water/ potassium balance, stress responses, and control of BP?

A

Adrenal Gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 2 families of hormones that adrenal gland produces and which family is the chief secretory product?

A 
steroid hormones (Chief product)
catecholamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are secreted by the adrenal gland and correspond to the steroid hormone category?

A

glucocorticoids, mineralcorticoids, and androgens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are secreted by the adrenal gland and correspond to the catecholamine category?

A

norepinephrine and epinephrine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where are the majority of hormones produced in the adrenal glands?

A

the cortex (90%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the four functional zones of the adrenal gland?

A

the Zona glomerulus
The zona fasciculata
The zona reticularis
Medulaa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Do we really need our adrenal glands?

A

yes, if you dont have one you will die within 2 weeks and go into hypovolemic shock (i.e you dot have any blood volume) or hypoglycemic coma (cuz cortisol can help you out to increase glucose)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What does the zona glomerulosa produce and what effects the rate of secretion?

A

Aldosterone (mineralcorticoids)

ECF volume and the kidneys (via Renin angiotensin system)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What does the zona fasciculata produce and what effects the rate of secretion?

A

Coritsol (glucocorticoids)
cortisol is a glucocorticoid because it affects the rate of glucose secretion*
ACTH effects the release of cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is a mineralcorticoid?

A

Affects the electrolytes (minerals) of the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a glucorticoid?

A

affects the level of glucose in the body ( and protein and fat metabolism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are androgens?

A

sex hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does the zona reticularis secrete and what controls this rate of secretion?

A

androgens and DHEA

ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does the medulla secrete and what controls this rate of secretion?

A

catecholamines (norepi and epi (majority))

Sympathetic nervous system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is DHEA?

A

a metabolic intermediate in the biosynthesis of the androgen and estrogen sex steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cortisol is special because it has a dual property, i.e it is a glucocorticoid as well as a (blank)

A

mineralcorticoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the most potent mineralocorticoid?

Glucocorticoid?

A

aldosterone

cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q 
What are these?
Deoxycorticosterone
corticosterone
flurocortisol****
cortisol
cortisome
A

Mineralcorticoids

flurocortisol is more potent than aldosterone*

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are these and put them in order of potency?

A

glucocorticoids

dexamethasone>methylprednisone>prednisone>cortisol>cortisone>corticosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How are adrenocortical hormones transported throuh the blood?

A

free and bound to albumin or CBG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Is most cortisol bound or free?

Aldosterone?

A

95% is bound

60% is bound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

If a hormone is bound to a protein does it have a longer or shorter half life? Considering that more cortisol is bound then aldosterone what can you expect the half life of cortisol to be, longer or shorter than aldosterone?

A

longer half life

longer than aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Which is found in larger concentrations in the blood, aldosterone or cortisol?

A

cortisol (and it is secreted in much higher quantities than aldosterone)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where are plasma binding proteins for adrencorticol hormones produced?

A

in the liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where does inactivation of hormones occur?

A

liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Where are conjugates excreted?

A

in the urine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What does aldosterone do?

A

increases Na absorption and K excretion (i.e. increaeses EFV)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What does aldosterone target in the kidney?

A

principle cells of distal tubule and intercalated cells of collecting duct

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What does other places does aldosterone target other than the kidney?

A

sweat glands
salivary glands
intestinal epithelial cells
(all about conservation of salt)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Are steroid hormones lipid soluble, what does this mean for them?

A

yes, than can diffuse through cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Explain the cellular mechanism of aldosterone action

A

Aldosterone is a steroid so it diffuses into the cell and meets up with a cytoplasmic mineralcorticoid receptor, the complex then enters the nucleus and promotes gene transcription of proteins that aid in Na transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What does aldosterone promote the gene transcription of?

A

Enzymes (Na/K atpase)

membrane transport proteins (Na Channels)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

(blank) cause a change in gene transcription so these effects take a while to see (about an hour)

A

mineralcorticoids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Aldosterone has two major effects what are they?

A

Regulates blood pressure through:

genomic effects-> create proteins to aid in Na transport
Non-genomic effects-> second messanger cascade with H,HCO3 transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Which effect of aldosterone is faster, the non genomic or genomic effects?

A

non genomic are faster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Explain how aldosterone works as a nongenomic effector?

A

aldosterone binds to receptor which causes increase in PK which phosphorylates things and activates target proteins to allow for H secretion and HCO3 absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What happens if you dont have aldosterone?

A

you get hyponatremic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What has the opposite effect of aldosterone?

A

ANP released from cardiac cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

When you have a lot of aldosterone does your sodium plasma CONCENTRATION increase a lot?

A

no it doesnt because as more salt is absorbed, more water is so there is still the same ratio of salt to water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Aldosterone secretion leads to increased sodium and fluid retention which leads to increased blood volume which leads to increased (blank) which leads to elevation of blood pressure

A

cardiac output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

If you have increased levels of aldosterone you will eventually have increased levels of ECF which, if lasting more than 2 days can result in what?

A

increased arterial pressur

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

When you have increased arterial pressure, how does your body lower this pressure?

A

Distal tubule in kidney starts excreting sodium and water

this is called aldosterone escape

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

If you have too much aldosterone you can get hypokalemia, where did all your potassium go?
What can this cause?

A

moved into urine and into cells

muscle cramping and weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

If you have too little aldosterone you can get hyperkalemic which can cause what?

A

severe cardiac toxicity (arrhythmias and weak heart contractions)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Aldosterone causes potassium to be secreted into the tubules in exchange for sodium reabsorption in the (blank)

A

principle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Aldosterone causes secretion of hydrogen ions for sodium in the (blank)

A

intercalated cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Since cortisol is not very potent as a mineralcorticoid how come it still has a pretty good effect on the body?

A

because it is in such high concentration in the body and has really high affinity for mineralcorticoid receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Renal epithelial cells can converts cortisol to cortisone via what enzyme?
Why would you want cortisone?

A

11B hydoxysteroid dehydrogenase type 2

cuz cortisone wont bind to mineralcorticoid receptors so you wont have mineralcorticoid effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What does IIb-HSD1 do?

A

converts cortisone to cortisol to be used as a mineralcorticoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is psuedohyperaldosteronism (apparent mineralocorticoid excess syndrome (AME)?

A

it is when you are exhibiting symptoms of having too much aldosterone but really you just have too much cortisol (acting like a mineralcorticoid) due to a defect in cortisol converting to cortisone via 11BHD2 (can occur via a mutation or eating too much licorice)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Why would licorice lead to AME (pseudohyperaldosteronism)?

How can you tell you have pseduo and not real?

A

it makes glycyrrhetinic acid which blocks 11BHD2

in pseudo you will have low aldosterone levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is aldosterone secretion regulated by?

A

potassium and angiotensin levels in the ECF, YES it is totally surprising that Na Levels have almost no effect on aldosterone. ACTH levels just tell the adrenal glands that they can secrete aldosterone but they dont really regulate aldosterone levels.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What kind of role does ACTH play in aldosterone regulation?

What if you dont have ACTH?

A

just a permissive role, says yes you can be secreted but doesnt say hmmm you should be secreting a little more or a little less. It is more like a light switch rather than a dimmer :)
Huge problemo

54
Q

which is more portent, corticosterone or cortisol?

A

cortisol :)

55
Q

What do glucocorticoids do?

A

increase blood glucose

56
Q

What is cortisol important in?

A

resisting stress and inflammation

57
Q

What happens if you dont have cortisol?

A

physical and mental problems or death

58
Q

What are effected by cortisol?

A

all tissues and cells (most cells have glucocorticoid receptors ***thats why you can get inflammation everywhere)

59
Q

Explain the cellular mechanism of cortisol?

A

goes through membrane, binds to glucocorticoid receptors, complex binds to DNA, induces or represses gene transcription of proteins :)
(also has some non genomic effects but we dont know what they are)

60
Q

What does cortisol do?

A

decreases glucose utilization, increases protein breakdown except in liver (so we can used the amino acids to make glucose) and increase fat mobilization i.e increases gluconeogenesis and glycogen and thus increases insulin

61
Q

What happens if you have really high levels of cortisol?

A

you have a lot of insulin which leads to insulin desensitization and you become hyperglycemic

62
Q

Explain the effects of cortisol on proteins?

A

decreases synthesis of proteins and increases breakdown which increases A.A’s in plasma. These are all sent to the liver and increases proteins and AAs IN LIVER ONLY so we can use these to make glucose :)

63
Q

How come when we have cortisol we increase lipid mobilization and fatty acid oxidation?

A

because cortisol loves to hold onto glucose and not use it but we still need energy so we use fatty acids instead

64
Q

Explain the effects of cortisol on proteins?

A

decreases synthesis of proteins and increases breakdown which increases A.A’s in plasma. These are all sent to the liver and increases proteins and AAs IN LIVER ONLY so we can use these to make glucose :)

65
Q

How come when we have cortisol we increase lipid mobilization and fatty acid oxidation?

A

because cortisol loves to hold onto glucose and not use it but we still need energy so we use fatty acids instead

66
Q

What does aldosterone and angiotensin do to your blood vessels?

A

you have vasoconstriction

67
Q

Sometimes the inflammation associated with a disease or trauma can be more damaging than the condition itself such as (blank)

A

rheumatoid arthritis

68
Q

What are the five stages of inflammation?

A

1) Damaged tissues release susbtances that initiate inflammatory process (bradykinins, proteolytic enzymes, prostaglands, leukotrines)
2) Increased blood flow (mast cells release vasoconstricter/vasodilators)
3) increased capillary permeability resulting in 4)increased plasma to injured tissue area
5) tissue clots (platelets release clotting factors)
6) infiltration of leukocytes (neutrophils and macrophages)
7) get ingrowth of fibrous tissue

69
Q

What are the two basic anti-inflammatory effects of high levels of cortisol?

A

1) block early stages of inflammation (before inflammation begins)
2) if inflammation has already begun it causes rapid resolution of the inflammation and increased rapidity of healing.
i. e.it reduces inflammation

70
Q

Glucocorticoids inhibit proinflammatory genes and stimulate antiinflammatory genes. What are the proinflammatory genes?
What are the antinflammatory genes?

A

1) cytokines, chemkines, endothelin, adhesion molecules
2) Interleukin antagonists (interleukins are cytokines), lipocortin (suppresses phospholipase A2 so you cant make prostaglandins), B2 adrenoreceptor (inhibits histamine release from mast cells), secretory leuocyte inhibitory protein

71
Q

What are the anti-inflammatory effects of high levels of cortisol?

A

makes it difficult for proteolytic enzymes to escape lysosomes by reinforcing lysosomes membranes.
Decreases capillary permeability so factors and plasma cannot escape from the blood into damaged tissue
It blocks white blood cells from going to the damaged area so you wont have as many inflammatory signals and wont be phagocytising damaged cells
Suppresses the immune system and decreases the ability to synthesize T cells and antibodies
Reduces fever so you wont release interleukin and therefore wont release cytokines

72
Q

What are cortisol shots used for?

A

allergies, autoimmune disease and transplants

This is because it will all in all suppress the immune system :)

73
Q

What happens to your blood cells when you have a shot of cortisol?

A

you will lower your eosinophils and lymophocytes (remember cortisol is not a fan of white blood cells) but will increase your RBCs so you will get polycythemia if you have too much cortisol and you will become anemic if you have too little cortisol

74
Q

If you have lymphocytopenia or eosinopenia (lack of lymphocytes and eosinophils) as well as an polycythemia, what can you expect to be occuring?

A

increased levels of cortisol (hypercortisolemia)

75
Q

Give me the overall effects of high cortisol

A

you will increase your RBC
you will decrease your WBC (lymphocytes and eosinophils)
you will decrease immune response
you will decrease CRH and ACTH (negative feedback)
You will increase plasma glucose levels
increase beta oxidation
decrease proteins syhthesis and increase protein breakdown (except for in the liver)
Decrease insulin sensitivity (my result in hyperglycemia)

76
Q

Explain ACTH

A

Hypothalamus releases CRH which stimlates ACTH release and synthesis from anterior pituitary, ACTH stimulates adrenal androgens (sex hormones) and cortisol

77
Q

When you have a kept rhythm in a 24 hour cycle with peaks high in the morning and tapering off at night and then building again towards the peak in the morning, what do you call this?

A

diurnal or circaddian rhythm

78
Q

What exhibits cricadian/diurnal rhythm?

Why is this important clinically to know?

A

CRH, ACTH, and cortisol
Think of it like waking up in the morning is stressful
It is important because you must know what the average measurement for cortisol is at a certain time of day to compare the results of a patients cortisol levels because clearly the normal cortisol levels in the morning are very differnt than cortisol levels at mid day

79
Q

Several male sex hormones are released from the (blank) of the adrenal gland

A

zona reticularis

80
Q

What are the main actions of androgens?

A

weak effect on humans
contributes to early development of male sex organs
growth of pubic and armpit hair in females
converted to testosterone in testes
progesterone and estrogen are secreted a tiny bit

81
Q

What are the primary causes of hypoaldrenalism? (adrenal insufficiency)

A 
Primary->addisons disease (addison destroys adrenal cortex), caused by
antibodies
TB
fungus
adrenal hemorrhage
82
Q

What are the secondary causes of hypoaldrenalism?

A

pituitary gland problems

83
Q

What happens when you have addisons and what are the effects due to the mineralcorticoid deficiency?

A

in addisons disease the andrenal cortex is destroyed so is unable to produce cortisol, aldosterone and DHEA. The mineralcorticoid effect will be primarily from the lack of aldosterone. This results in reduced aldosterone which means you will have reduced Na absorption and K secretion which results in hyperkalemia, metabolic acidosis, hyponatremia and decreased ECF. Your CO and BP will go down and you can go into circulatory shock and then die.

84
Q

In addison’s disease what are the effects on glucocorticoids?

A

The adrenal gland will be unable to produce cortisol, aldosterone and DHEA. The effect on glucocorticoids will be primarily due to the lack of cortisol. If you dont have cortisol you will become hypoglycemia due to lack of glucose and you will have increased inflammation and anemia and extreme sensitivity to stress which may result in death

85
Q

In addison’s disease, what does your physical appearance look like?

A

You will get hyperpigmentation since cortisol is not being produced, CRH and ACTH are going to increase signif to try and compensate, this results in increased stimulation of MSH release and thus melanin formation

86
Q

Melatonin is released by the (blank)

While melanin is released by the (blank)

A

pineal gland

Intermediate lobe of pituitary gland and from POMC molecule

87
Q

What is the addisonian crisis?

A

it is when you lose your cortisol and aldosterone resulting in lack of digestive enzymes (vomiting, diarrea) and liver function, then you become hyperkalemia resulitng in cardiac issues, you have really low ECF and PV due to the hyponatremia and vomitting, and then you get really low blood pressure and you body goes into shock and you die or go into a coma :(

88
Q

What is Cushings syndrome?

A

too much cortisol caused by oversecretion of CRH or ACTH or a tumor in the adrenal cortex, ectopic secretion of ACTH (like in lung cancer) or treatment with too much cortisol

89
Q

When cushings syndrome is caused by too much secretion of ACTH by the pituitary it is no longer called cushings syndrome but (blank)

A

cushings disease

90
Q

What happens to your body when you have cushings syndrome?

A

too much cortisol results in hyperglycemia, decreased sensitivity to glucose, increased fat mobilization resulting in weird distribution of fat and a buffalo torso and a puffy moon face. You wil have so much protein loss that you will become weak in your bones and muscle and your skin will have striations. You will become susceptible to infections due to the suppression of your immune system and you will get a lot of androgens making acne and excess growth of facial hair (hirsuitism) prevalent

91
Q

What is the name for primary aldosteronism (too much aldosterone) and what causes it?

A

Conn’s syndrome
tumor in zona glomerulosa cells
or hyperplastic adrenal cortices secrete aldosterone instead of cortisol

92
Q

When you have too much aldosterone or conn’s syndrome what happens to your body?

A

hypernatremia, hypokalemic, metabolic alkalosis, muscle paralysis, hypertension, low renin levels (due to negative feedback)

93
Q

What is adrenogenital syndrome and how will it effect your body?

A

when you secrete too much androgens due to a tumor in your adrenal cortex.
females become masculine, males under rapid development of sex organs before puberty.

94
Q

How do you detect adrenogenital syndrome?

A

high levels of 17-ketosteroids (androgen metabolite) in the urine (10 to 15 times higher than normal)

95
Q

What is congenital adrenal hyperplasia?

A

An autosomal recessive disorder which makes you NOT secrete cortisol or aldosterone BUT makes you secrete TOOO MUCH androgen!

96
Q

What is congential adrenal hyperplasia caused by and what does it do the body?

A

deficiency in 21 hydroxylase (this converts progesterone into cortisol or aldosterone)

mild: infertility in women (due to inability to ovulate)
moderate: prepubescent virilization (getting sex organs early)
severe: death due to dehydration and vomitting and ambigious genitalia

97
Q

How do catecholamines get released?

A

sympathetic stimulation releases ACh to make the adrenal medulla release catecholamines

98
Q

How do catecholamines get released?

A

sympathetic stimulation releases ACh to make the adrenal medulla release catecholamines

99
Q

What secretes epinephrine and norepinephrine (but mainly large amounts of epinephrine)?

A

chromaffin cells

100
Q

What exactly are chromaffin cells?

A

they are found in the adrenal medulla and are modified postganglionic neurons that interact with ach preganglionics
(they release epinephrine mainly and, norepinephrine)

101
Q

What is the sole source of epinephrine?

What is the source of norepinephrine?

A

adrenals

adrenals and extradrenal sources

102
Q

What all does the adrenal medulla secrete?

A

Major amounts of epi, small amounts of norepi and tiny amounts of dopamine

103
Q

Is the adrenal medulla essential for life?

A

no just the sympathetic nervous system is

104
Q

THe (blank) is richly innervated by preganglionic sympathetic fibers and is in essence an extension of the sympathetic nervous system.

A

medulla

105
Q

What are the 2 sources of catecholamines?

A

sympathetic pathway and the adrenal sympathetic pathway

106
Q

Where are catecholamines synthesized and stored?

A

synthesized in the adrenal medulla in chromaffin cells and stored in chromaffin granules at high concentrations with ATp and ADP and some neuropeptides

107
Q

What bind to opoid receptors and produce analgesic responses?

A

enkephalins

108
Q

Explain catecholamine biosynthesis

A

phenylalinine is converted to tyrosine which is then hydroxylated to DOPA, which is converted to Dopamine via decarboxylase and then converted to norepinephrine via hydroxylation. Norepinephrine can further be converted to epinephrine via methylation

109
Q

How do you inhibit catecholamine biosynthesis?

A

the step to convert tyrosine to DOPA is tyrosine hydroxylase. This step is inhibited by norepinephrine thus you have negative feedback

110
Q

What steps of catecholamine biosynthesis take place in the cytosol?

A

the hydroxylation of tyrosine, the decarboxylation of DOPA and the methylatin of Norepinephrine
(hydroxylation of dopamine is down in secretory vesicles i.e. dopamine is in secretory vesicles)

111
Q

Catecholamines are amino acid derived hormones synthesized from (blank) and undergoes (blank) enzymatic reactions to be converted into epinephrine

A

tyrosine

4

112
Q

What converts norepinephrine to epinephrine?

A

phenylethanolamine N methyltransferase (PNMT)

113
Q

The way you get chromaffin cells to make epinephrine and norepinephrin is via sympathetic preganglionics stimulating them. What stimulates the sympathetics?

A

stress, excercise, hypoglycemia, extreme temps, emotional disturbances, and trauma

114
Q

How does ACh stimulate chromaffin cells?

A

it binds to nicotinic receptors to depolarize the chromaffin cell membranes via Na and Calcium

115
Q

How do adrenal medullary hormones transport through the blood?

A

mostly bound to albumin with low affinity

116
Q

Do catecholamines have a long half life?

A

nope super short (less than 2 min)

117
Q

How do we get rid (metabolize) catecholamines?

A

can undergo reuptake by tissues, degrade via COMT or MAO, or go into the urine

118
Q

What is the major end product of norepinephrine or epinephrine metabolism?

A

vanillymandelic acid

119
Q

What do you do with inactive catecholamines if you want to excrete them?

A

you conjugate them with glucuronic acid and sulfates and then pee them out

120
Q

What is the main function of adrenal medullary hormones?

A

rapid short term adjustments to threatening situations

long term actions are done via glucocorticoids

121
Q

What exactly do medullary hormones do?

A 
increase all the things that could help you with survival such as :
increasd CO
blood supply to brain and muscles
fuel
pulmonary ventilation
visual acuity
muscular performance
calming of gut
122
Q

How come catecholamines work in different ways on so many different tissues?

A

because they work on a bunch of G proteins coupled receptors and alpha and beta adrenergic receptors.

123
Q

What are the alpha adrenergic mediated effects of catecholamines?

A 
vasoconstriction
iris dilation
intestinal relaxation
intestinal sphincter contraction
pilomotor contraction
bladder sphincter contraction
bronchoconstriction
uterine smooth muscle contractions
cardiac contractility
124
Q

What are the beta adrenergic mediate effects catecholamine?

A 
vasodilation
cardio-acceleartion
increased myocardial strength
intestinal and bladder wall relaxation
uterus relaxation
bronchodilation
calorigenesis
glycogenolysis
lipolysis
125
Q

What are a1 receptors coupled to?

A

Gq receptors to make IP3 and DAG

126
Q

What are B1 and B2 receptors coupled to ?

A

Gs -> increase cAMP

127
Q

What are a2 receptors coupled to?

A

G1-> leads to decreased cAMP

128
Q

What is it called when you have an oversecretion of catecholamines?

A

pheochromocytoma

129
Q

What is pheochromocytoma?

A

it is when you have tumor on your chromaffin cells making you secrete too many catecholamines which will result in hypertension, anxiety, increased HR, sweating, and hyperglycemia.

130
Q

Explain the main response to stress

A

short term-> mediated by catecholamines, increases plasma glucose, decreases GI function and Kidney activity, increasd breathing rate, blood pressure
Long term-> retention of sodium and water by kidneys, increased blood pressure, increased glucose levels, immune system suppressed

Block 3 Week 6 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions