Brainscape's Knowledge GenomeTM

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


See full index

Endocrine > HPA axis and adrenal gland (L5) > Flashcards

HPA axis and adrenal gland (L5) Flashcards

1
Q

Catecholamines

A

Epinephrine, norepinephrine

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

Glucocorticoids

A

Cortisol

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

Two things regulated by the HPA axis

A

Adaptive response to stress and anti-inflammatory immune function

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

Things NOT regulated by the HPA axis in which the adrenal gland is involved

A

Maintainance of blood pressure, sodium, and potassium mediated by mineralocorticoids
“Weak” androgen production

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

Where is corticotropin releasing hormone made?

A

In the paraventricular nucleus

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

CRH stimulates what gene?

A

POMC

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

How is CRH linked to the adrenal gland?

A

Stimulates release of ACTH in the anterior pituitary, which then stimulates the adrenal gland to produce and release cortisol

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

How is the HPA axis regulated?

A

By classical feedback mechanisms

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

What are some of the stimuli for CRH release?

A

Physical/emotional stress, hypoglycemia, others

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

How long is CRH?

A

41 amino acids

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

Where is CRH made?

A

Parvocellular cells in the paraventricular nucleus

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

How is CRH released?

A

In pulses

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

Half life of CRH

A

~5 minutes

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

CRH receptors

A

There are two.
CRH binds with higher affinity to CRHR1 in the anterior pituitary
CRHR2 binds with more affinity to urocortin

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

Second messengers of CRH binding

A

At least five different ones are activated; PKA release is the most important for ACTH release

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

CRH acts synergystically with what other hormone?

A

AVP

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

What does the synergystic action of AVP and CRH do?

A

Increases the amplitude of ACTH release

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

Negative feedback mechanism

A

Cortisol binds to nuclear steroid glucocorticoid receptors in the nucleus and inhibits synthesis and release of CRH and ACTH

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

What is the precursor to ACTH?

A

POMC (pro-opiomelanocortin)

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

What else can the POMC gene encode?

A

Beta-lipotropin
Beta-endorphin
Melanocortin stimulating hormone
Enkephalin

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

Important hormones from POMC gene during pregnancy and development

A

Beta-MSH
Beta-endorphin
Enkephalin
(Made in the intermediate lobe)

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

Main actions of ACTH in the adrenal gland

A

Stimulates steroid biosynthesis

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

ACTH in the zona reticularis and fasciculata

A

Cellular hypertropy
DHEA production
Cortisol production

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

ACTH in the adrenal medulla

A

Stimulates conversion of dopamine to norepinephrine

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

ACTH in the zona glomerulosa

A

Does not directly affect aldosterone production, but does mediate the synthesis of aldosterone precursors

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

What is the main receptor for ACTH?

A

MC2R (melanocortin 2) - high affinity

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

What is the secondary receptor for ACTH?

A

MC1R in the skin (high ACTH levels can lead to hyperpigmentation)

28
Q

Where does the adrenal cortex come from embryologically?

A

The mesoderm

29
Q

Where does the medulla come from embryologically?

A

The neural crest; the medulla is a “modified sympathetic postganglionic neuron”

30
Q

Order of adrenal layers from superficial to deep with percentage surface area

A 
Zona glomerulosa (15%)
Zona fasciculata (65-80%)
Zona reticularis (
31
Q

What feature is most striking in the ultrastructure of a steroidogenic cell?

A

The presence of large lipid droplets

32
Q

Capsular artery

A

Gives rise to arterioles that perfuse the adrenal cortex all the way through the medulla

33
Q

What is made in each of the layers of the adrenal cortex?

A

ZG: mineralocortocoids
ZF: glucocortocoids
ZR: androgens
M: catecholamines

34
Q

To what is cortisol bound in the blood, and how much of it is free?

A

Bound to corticosteroid binding globulin,

35
Q

When does cortisol peak?

A

Around 8AM

36
Q

To what family does CBG belong?

A

The serpin family of protease inhibitors, but it is NOT one

37
Q

How long is CBG and where is it made?

A

383 amino acid glycoprotein made in the liver

38
Q

CBG’s relative affinity for cortisol vs. aldosterone

A

30x greater for cortisol

39
Q

Estrogen and CBG

A

Estrogen decreases the amount of available CBG, increasing the amount of free cortisol

40
Q

What external factor decreases CBG?

A

Shock/severe infection

41
Q

Glucocorticoid receptors - location and abundance

A

Nuclear receptor that is ubiquitously expressed in most tissues

42
Q

Mechanism of GRs

A

Cortisol binds to the receptors in the cytoplasm, dissociates its associated proteins, and then translocates to the nucleus and acts as a transcription factor

43
Q

General metabolic actions of cortisol

A

Increases the amount of glucose in the blood; potent counter-regulatory hormone to insulin

44
Q

Cortisol’s effect on metabolic enzymes

A

Increases activity of tyrosine aminotransferase, PEPCK, and G6Pase.

45
Q

Cortisol’s effect on glucose transporters

A

Decreases the amount of GLUT4 on muscle cells

46
Q

Positive effects of cortisol on skeletal muscle

A

Increases MuRF and E3 ubiquitin ligase, stimulating protein degradation

47
Q

Negative effects of cortisol on skeletal muscle

A

Downregulates AKT phosphorylation and amino acid uptake, decreasing protein synthesis

48
Q

MgII gene

A

Upregulated by cortisol, which encodes for monacylglycerol lipase

49
Q

Lipe gene

A

Encodes hormone sensitive lipase, which is upregulated by cortisol

50
Q

Angpt gene

A

Upregulated by cortisol; increases cellular cAMP and activates hormone sensitive lipase

51
Q

Redistribution of fat

A

Induced by cortisol; results in abdominal obesity and thinning of limbs

52
Q

Immune system and cortisol

A

Proinflammatory response disrupted by binding directly to activated NFkB and inhibiting its transcription factor activity in the nucleus AND by increasing transcription of IkB that also helps keep NFkB sequestered in the cytoplasm

53
Q

Four effects of cortisol on the immune system

A
  1. Stimulates anti-inflammatory cytokines
  2. Inhibits prostaglandins
  3. Supresses antibody production
  4. Increases neutrophils, platelets, and RBCs
54
Q

Negative effects of cortisol on bone

A

Inhibits bone formation by decreasing IGF-1 Rs

Inhibits intestinal calcium absorption

55
Q

Positive effects of cortisol on bone

A

Increases bone resorption by activating osteoclasts

56
Q

CV maintenance by cortisol

A

Maintains catecholamine pressor effects

Maintains vascular integrity and reactivity

57
Q

CNS effects of cortisol

A

Emotional response and perceptivity
(Depression, rage, anxiety, panic, nervousness)
Inhibits CRH and ACTH

58
Q

Cushing disease

A

Excess cortisol release due to pituitary adenoma

59
Q

Cushing syndrome

A

Excess cortisol NOT caued by pituitary adenoma

60
Q

Symptoms of cushing disease (5)

A 
Change in body fat distribution
Osteoporosis
Hypertension (excess GCs activate MRs)
Glucose intolerance (due to antagonistic effects on insulin)
Purple striae
61
Q

What happens with prolonged glucocorticoid therapy?

A

Constant negative feedback on the pituitary and hypothalamus to release CRH and ACTH causes atrophy of these neurons, resulting in dependence on exogenous GCs

62
Q

When is acute GC treatment used?

A

In the case of medical emergencies such as asthma attacks, autoimmune flares, or septic shock

63
Q

When is chronic GC treatment used?

A

For immunosuppressive therapy, autoimmune diseases, adrenal insufficiency, and as treatment to help pre-term infants

64
Q

Define adrenal insufficiency.

A

The inability to produce glucocorticoids, mineralocorticoids, or both

65
Q

Primary adrenal insufficiency

A

Failure of the adrenal gland itself; usually manifested as Addison’s disease (70%). Autoimmune destruction

66
Q

Secondary adrenal insufficiency

A

Lack of CRH or ACTH; usually caused by sudden cessation of glucocorticoid therapy

Endocrine (11 decks)

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