Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

22 spring: Physiology > Test 3: lecture 8 adrenal gland > Flashcards

Test 3: lecture 8 adrenal gland Flashcards

(72 cards)

Start Studying
1
Q

layers of the adrenal cortex

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

___ are made by adrenal cortex

A

corticosteroids such as

mineralocorticoid – aldosterone (by zona glomerulosa)

glucocorticoids (by zona fasciculata and zona reticularis)

cortisol

corticosterone

androgens (by zona fasciculata and zona reticularis)

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

___ are made in the zona glomerulosa

A

Corticosteroids by adrenal cortex

mineralocorticoid – aldosterone (by zona glomerulosa)

glucocorticoids (by zona fasciculata and zona reticularis)

cortisol

corticosterone

androgens (by zona fasciculata and zona reticularis)

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

___ are made by the zona fasciculata

A

Corticosteroids by adrenal cortex

mineralocorticoid – aldosterone (by zona glomerulosa)

most of the glucocorticoids (by zona fasciculata and zona reticularis)

cortisol, corticosterone

some of the androgens (by zona fasciculata and zona reticularis)

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

___ are made in the zona reticularis

A

Corticosteroids by adrenal cortex

some of the glucocorticoids (by zona fasciculata and zona reticularis)

cortisol

corticosterone

most of the androgens (by zona fasciculata and zona reticularis)

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

___ are made in the adrenal medulla

A

catecholamines

epinephrine

norepinephrine

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

___ are catecholamines made in the adrenal medulla

A

epinephrine

norepinephrine

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

cortisol and corticosterone are ___made where?

A

glucocorticoids (corticosteroids by the adrenal cortex) made in the zona reticularis and zona fasciculata

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

corticosteroids are made from ___ in the __

A

cholesterol

mitrochondria and ER

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

rate limiting step of synthesis of corticosteroids

A

cholesterol → pregnenolone

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

aldosterone formation does not use what enzyme

A

hydroxylase (this is used to make cortisol and androgen)

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

Cholesterol desmolase

A

also known as

P450scc CYP11A1

1st step and rate limiting step of cholesterol into catecholamines

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

17a-hydroxylase/17,20 lyase

A

also known as P450c17 CYP17

used to make cortisol and androgen

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

Aldosterone synthase

A

P450c11AS CYP11B2

used to make aldosterone

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

synthesis of corticosteroids occurs in

A

mitochondria and ER

results in release of cortisol

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

transport of cortisol hormone

A

75% bound to cortisol-binding globulin (transcortin)

15% to albumin,

10% free.

Half-life: 60-90 minutes

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

___: 50% bound to albumin. half life is 20 mins

A

aldosterone

50% bound to albumin,

10% to transcortin,

40% free.

Short half-life: 20 minutes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

___ 75% is bound to transcortin with a 60-90 min half life

A

Cortisol

75% bound to cortisol-binding globulin (transcortin)

15% to albumin,

10% free.

Half-life: 60-90 minutes

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

why does aldosterone have a shorter half life then cortisol

A

40% of aldosterone is free (not bounded to protein)

can be broken down faster

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

___ is the most potent mineralcorticoid

A

aldosterone (90%)( made in the zona glomerulosa of the adrenal cortex)

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

what are some things other than aldosterone that can act as a mineralcorticoid?

A

Deoxycorticosterone (1/30 as potent, limited amount)

9a-fluorocortisol (synthetic, more potent)

Corticosterone (slight mineralocorticoid activity)- (type of glucocorticoid made mostly in the zona fasciculata)

Cortisol (slight, 10%)

Cortisone (synthetic, slight)

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

what is the major glucocorticoid

A

Cortisol (very potent, 95%)

Corticosterone (4%)

(type of glucocorticoid made mostly in the zona fasciculata, some made in the zona reticularis)

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

what are some synthetic glucocorticoids

A

Cortisone (as potent)

Prednisone (four times as potent)

Methylprednisone (five times as potent)

Dexamethasone (30 times as potent, specific)

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

what type of synthetic glucocorticoid does not have mineralocorticoid activity

A

Dexamethasone (30 times as potent, specific

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
aldosterone
mineralocorticoid – aldosterone (by zona glomerulosa)- adrenal cortex responsible for Na+/K+ balance **sodium-retention hormone** stimulates excretion of **K+ in the principal cells** stimulates excretion of **H+ in the intercalated cells** most effect in the **collecting tubules**, less effect in the distal tubule and collecting duct causes Na+ to be conserved and K+/H+ to be excreted responsible for 90% of the **mineralocorticoid** effects
26
\_\_\_ causes Na+ to be conserved and K+/H+ to be excreted
aldosterone **mineralocorticoid** – aldosterone (by zona glomerulosa)- adrenal cortex
27
aldosterone stimulates the reabsorption of ___ in the \_\_\_\_
Na kidneys, salivary and sweat glands
28
aldosterone stimulates the excretion of ___ in \_\_\_
K in the kidney, salivary and sweat glands H in the kidney
29
mechanism of aldosterone
**receptor in cytoplasm** leads to increase in Na/K ATPase (Na in/K out) Na/H antiporters (Na in/H out) sodium channels ( Na in)
30
increased \_\_\_in extracellular fluid → increases aldosterone secretion
K+
31
increased activity of the \_\_\_\_system → angiotensin II → increases aldosterone
renin-angiotensin
32
breakdown of aldosterone
conjugated to form **glucuronic acid and sulfates** excreted in bile (25%), feces and urine (75%) present in nanogram (10-9) levels (1000 times less than cortisol) **(present in very low levels- but very potent)**
33
**_Hypersecretion of aldosterone_**
Hypokalemia (low K+) –\> muscle weakness Alkalosis (more basic pH of blood, cause H are excreted) Hypertension (increase in Na causes increased BP)
34
**_Hyposecretion of aldosterone_**
Hyperkalemia (too much K)–\> cardiac toxicity Acidosis (pH decreases, more H in the blood) hypovolemia (sodium loss→ low BP → shock) -\> death
35
\_\_\_\_ is the stress hormone
cortisol ## Footnote type of glucocorticoids (by **zona fasciculata** and zona reticularis) which is a corticosteroid made in the adrenal cortex)
36
\_\_\_ is necessary to resist stress and inflammation
cortisol ## Footnote type of glucocorticoids (by **zona fasciculata** and zona reticularis) which is a corticosteroid made in the adrenal cortex)
37
cortisol stimulates ___ by liver
gluconeogenesis * Cortisol mobilizes amino acids from the extrahepatic tissues mainly from **muscle** * Cortisol increases the enzymes required to convert amino acids into glucose in the liver
38
•Cortisol mobilizes ____ from the extrahepatic tissues mainly from muscle
amino acids
39
•Cortisol increases the enzymes required to convert amino acids into ___ in the liver
glucose ## Footnote **stimulation of gluconeogenesis by liver**
40
cortisol has anti-\_\_\_ effects causing a decrease in the use of cellular glucose
insulin
41
cortisol increases blood ___ and can lead to \_\_\_\_
glucose adrenal diabetes
42
cortisol will cause the increase of proteins\_\_\_ and the reduction of proteins \_\_\_
in the liver in the muscles increased blood amino acids (aa), increased aa transport into hepatic cells, but decreased aa transport into extrahepatic tissues reduction in cellular proteins in all tissues except liver increased liver and plasma proteins enhanced mobilization of fatty acids from adipose tissue and utilization of free fatty acids for energy
43
cortisol enhanced mobilization of fatty acids from ___ and utilization of free fatty acids for energy
adipose tissue
44
cortisol will increase blood \_\_\_
glucose, amino acids and fatty acids
45
Inflammation Processes ## Footnote \_\_\_\_: release of chemical substances by damaged tissue. •Red (erythema): increased blood flow. \_\_\_\_: leakage of capillaries. •Fever \_\_\_ by leukocytes. •Scar: ingrowth of fibrous tissue.
pain * Edema * Infiltration
46
anti-inflammatory effect of cortisol
* stabilizes lysosomal membranes- **reduces tissue damage** * decreases permeability of capillaries- **reduces edema** * decreases migration of white blood cells (WBCs) to inflamed areas * **suppresses the immune system**, especially T lymphocytes * l**owers fever** – reduces release of IL-1 from WBCs * also causes resolution of inflammation **keeps inflammatory process under control**
47
large doses of cortisol will have a ___ effect
**immunosuppressive** * decreases the number of lymphocytes * decreases the output of both T cells and antibodies * prevents rejection of transplanted organs
48
why use large dose cortisol for transplanted organs
will suppress the immune system- suppress rejection
49
receptor for cortisol is \_\_\_
in the plasma
50
what is the DNA element that cortisol binds to
cortisol binds to receptor in the plasma, then the cortisol-receptor complex will go into nucleus and bind with the **GRE (glucocorticoid response element)**
51
regulation of cortisol secretion is by \_\_\_
Adrenocorticotropic hormone **(ACTH)** made by the anterior pituitary gland (peptide hormone) also called corticotropin
52
how does ACTH work
ACTH binds to melanocortin 2 receptor activation of adenylyl cyclase increased **intracellular cAMP** conversion of **free cholesterol to pregnenolone (1st step of coricosteroid production)** will eventually **stimulate adrenal gland to make cortisol**
53
\_\_\_\_ is the receptor for ACTH
melanocortin 2 receptor
54
\_\_\_ is the precursor to MSH and ACTH
POMC (proopiomelanocortin)
55
increased ACTH also means there is more ___ which leads to \_\_\_
MSH skin pigmentation **both ACTH and MSH come form POMC**
56
injection of angiotensin II will cause the expansion of \_\_\_
zona glomerulosa
57
an injection of ACTH would cause the expansion of \_\_\_
zona fasciculata zona reticularis
58
HPA
59
cortisol deficiency would result in
high ACTH and increase in skin pigmentation cause there is more MSH (from same precursor -POMC) cortisol not there to inhibit the production of ACTH
60
hyperadrenalism
cushing's disease * Pituitary tumor- * Ectopic ACTH-secreting tumors- increased amount of ACTH Adrenocortical tumors- decreased amount of cortisol **•****Mitotane is used to treat adrenocortical tumors**
61
hypoadrenaliam
addison's disease ## Footnote Mineralocorticoid deficiency Glucocorticoid deficiency _Causes_ **idiopathic:** autoimunne destruction of adrenal cortex. **sponataneous:** infections, tumors, trauma **iatrogenic:**(adrenal suppressive therapeutic agents)→Cytotoxic (mitotane)•Ketoconazole (blocks ACTH actions)
62
3 causes of addisons
hypoadrenalism ## Footnote _Causes_ **idiopathic:** autoimunne destruction of adrenal cortex. **sponataneous**: infections, tumors, trauma **iatrogenic:**(adrenal suppressive therapeutic agents)→ •Cytotoxic (mitotane)•Ketoconazole (blocks ACTH actions) mitotane is used to treat hyperadrenalsim- can go to far and cause hypo
63
what are made in the adrenal medulla
catecholamines → norepinephrine and epinephrine
64
catecholamines come from \_\_\_
tyrosine
65
sympathetic nervous system produces what type of catecholamines?
norephinephrine
66
why is the adrenal medulla redundant?
produces catecholamine- 80%epinephrine• 20% norepinephrine. the **sympathetic nervous system** also creates **norepinephrine**, which can be used to make epinephrine
67
physiological effect of epi and norepinephrine
regulate activities of visceral organs cause excitatory effects in some organs but inhibitory effects in others increase force and rate of the heart increases glycolysis in the muscle and liver increases mental alertness increases rate of blood coagulation increases metabolic rate increase blood flow to active muscles and liver concurrent with decreased blood flow to most organs such as GI tract and kidneys increases BP
68
mechanism of epinephrine
binds to B and alpha receptors very rapid response from G protein receptors
69
adrenal medulla is stimulated by
**special preganglionic** nerve (special) does not synapse in the celiac ganglion like the other sympathetics, just passes through
70
adrenal medulla cells originated from the same cells as ___ neurons.
post-ganglionic sympathetic innervation causes immediate reaction in emergency situations (flight or fight)
71
Hyperadrenalism (Cushing’s disease) results from excess secretion of glucocorticoids from the adrenal glands. What would some clinical signs be?
Symptoms: **Moon face** in humans. Mobilization of fat from the lower part of the body, with concomitant **extra deposition of fat** in the thoracic and upper abdominal regions, giving rise to a buffalo torso. **Increased blood glucose** concentration – **adrenal diabetes.** **Protein depletion** in muscles, bone, and lymphatic tissues: **muscle weakness, suppressed immune system (death of infection), osteoporosis.**
72
hypoadrenalism (Addison’s disease) results from hyposecretion of either glucocorticoids (glucocorticoid-deficient Addisonian) or glucocorticoids and mineralocorticoids (Addisonian). What would some clinical signs and clinicopathologic changes be? How would these two syndromes differ from each other?
**Mineralocorticoid deficiency:** hyperkalemia, acidosis, sodium loss → decreased blood volume → circulatory shock → death within a few days. **Glucocorticoid deficiency:** Failure to **maintain blood glucose** concentration, failure to mobilize fat and proteins, causing consuming weakness **(lethargy).** Highly susceptible to the deleterious effects of stress. **A mild infection can cause death.- immune system is suppressed** **Increased melanin** skin pigmentation, due to increased production of ACTH and MSH as a result of glucocorticoid deficiency.

22 spring: Physiology (34 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions