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kris Endocrinology > 8 > Flashcards

8 Flashcards

1
Q

What are the components of hypothalamus-pituitary-adrenal axis

A

there’s a

  • releasing hormone CRH from the hypothalamus
  • trophic hormone ACTH (corticotropin) from anterior pituitary
  • Adrenal hormones released from adrenal glands: cortisol and androgens
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2
Q

Where are adrenal hormones metabolzied?

A

adrenal hormones are metabolized in liver and excreted in kidney

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3
Q

What is CRH stimulated and inhibted by?

A

Stimulated by decreased palsam cortisol, hypoglycemia, and strress

Inhibited by increased plasma glucocorticoid level

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4
Q

What stimulated ant. pituitary stimulation of ACTH

A

AVP and CRH

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5
Q

What is the location of adrenal gland

A

dorsal and medial- more towards the central axid of the body

near the kidneys

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6
Q

The Adrenal gland is a __ organ

A

The Adrenal gland is a steroidogenic organ

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7
Q

Describe the make up of adrenal gland

A
  • Surrounded by fibrous capsule and adrenal divided into functional layers
  • cortex is about 90 % of adrenal mass, inner medulla about 10 %
  • vcortex has 3 zones: (top to bottom) Zona glomerulosa, Zona fasciculatam, Zona reticularis; followed by adrenal medulla
  • Zona f. is thickest (about 75 % of cortex)
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8
Q

Which hormones are produced by each zone + medulla?

A

Zona glomerulosa- aldosterone

Zona fasciculata- cortisol; corticosterone

Zona reticularis- sex streoids (androgens)

Medulla- Catecholamines (epinephrine & norepinephrine)

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9
Q

Describe why each zone is able to make it’s own unique hormones

Name the unique charactestic of each zone

A

different machinery-> different hormones are produced
Zone F nad Z Reticularis both have P450c17 , but Z retuclaris also has 17, 20 lyase-> DHEA-> androstenedione
Zone F and Zone G both produce croticosterone via P450c11, but Zone Glomerulosa expresses aldosterone synthase-> able to convert croticosterone into aldosterone

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10
Q

__ is the key enzyme that regulates androgen synthesis.

A

P450c17 is the key enzyme that regulates androgen synthesis.

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11
Q

What are the sources of cholesterol?

A

Main source is the diet, but can also be synthesized from acetyl-CoA

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12
Q

sterotogenic cells can store __ and use it in steroidogenic pathway

A

sterotogenic cells can store cholesterol and use it in steroidogenic pathway

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13
Q

What determines what steroid is produced in a cell or tissue

A

Cell specific expression of enzymes determines what steroid is produced in a cell or tissue

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14
Q

Where are the enzymes of steriogenic pathways located? What is the consequence of this?

A

Some enzymes are in the mitochondria others in the endoplasmic reticulum. Steroid intermediates shuttle between ER and mitocho

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15
Q

How do steroids differ?

A

Most steroids differ by minor enzymatic modifications of side groups, often through the addition/removal of hydroxyl groups

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16
Q

What is the common step in the prodcution of all steroid hormones? WHere does it occur?

A

The first step common to all steroids is the formation of pregnenolone from cholesterol in the mitochondria

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17
Q

What is the enzyme common for all steroid hormone produciton pathways? What is it’s role and location

A

p450scc, an enzyme that converts cholesterol to pregnenlone, a molecule, from which steroid hormones are made (1st step of Steroidogenesis)

located in the mitochondira

On inner mitochondrial membrane, P450scc (side-chain cleavase) cleaves the side chain of cholesterol to produce pregnenolone

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18
Q

Where does the cholesterol go for first step of Steroidogenesis occur? why?

A

choelsterol is moved to mitochondria as this is where

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19
Q

What is the limiting step of Steroidogenesis

How is it regulated?

A

Uptake of cholesterol is a rate limiting step

Regulated by StAR protein (Steroid Acute Regulatory protein)

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20
Q

describe StAR, how does it work, when is it activated

A

StAR is cAMP-inducible gene and increases in response to tropic hormones (i.e. ACTH in the adrenal gland and gonadotropins in gonads)
called acute regulatory protein as it usese Cyclic AMP responsive gene.
Increase in cAMP levels-> StAR gene expression-> protein becomes functional
Increase in cholesterol synthesis happens acutely/incredibly fast (StAR shuttles CH into the mitochondria)
- Thus the name
- Any protein hormone that can bind to G-coupled protein can increase cAMP levels, leading to StAR gene expression and leading to stereognosis

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21
Q

WHat is the main steroid of the zona fasciculata

A

cortisol

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22
Q

How is cortisol prodcuton of the zona fasciculata stimulated?

A

CRH from hypothalamus causes pituitary to release ACTH which can act upon adrenal cells in the Zone fasciculata-> cortisol synthesis

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23
Q

Is cortisol stored?

A

Like any steroid, these are not stored-> Cortisol is produced only when it is required

24
Q

What is the half-life of cortisol?

How does it get inactivated?

A

The half-life of cortisol varies is 70-120 minutes

Converted to inactive cortisone and other metabolites by liver (for excretion in urine) and by other target cells- using enzyme 11BHSD2

25
Q

Can inactive cortisol be salvaged?

A

Cells that contain HSD1 can convert it back

foun din liver, placenta, skin, adipose, CNS

26
Q

Function of Cortisol in liver, adipose tissue, muscles, bones, growth, skin, GI, brain and heart

A
  • liver- increased hepatic glycogen depositon, increased insulin resistance, increased gluconeogenesis and glycogen deopsition. synthesis
  • adipose tissue - promotes visceral obesity
  • muscles- promotes muscle catabolism
  • bones- decreases bone formation, decreases bone mass and increases risk of osteoporosis
  • growth- decreases linear growth
  • skin- protein catabolism ,skin thinning
  • GI- ulceration
  • brain- depression. psychosis
  • heart- salt and water retention-> HTN
27
Q

How are cells that are exposed to cortisol protected from action of cortisol?

A

Cells that are exposed to cortisol are protected from action of cortisol by converting cortisol to the inactive form->11βHSD2 enzyme is required for this

28
Q

How does cortisol gets converted to cortisone

A

hydroxysteroid dehydrogenase replaces OH on cortisol by double bond O-> cortisone

29
Q

Additional significance of cortisol/cortisone conversion

and related deficiency diseases

A
  • Cortisol can activate the aldosterone receptor
  • Cortisol is produced at a much higher concentration, compared to aldosterone as Zone f. is much larger compared to Zone G.
  • Cortisol binds to mineralocorticoid receptors (aldosterone receptor)
  • Aldosterone responsive cells therefore have to inactivate cortisol in order to respond specifically to aldosterone
  • Enzyme deficiency of HSD11B2→cortisol cannot be inactivated–> Excess cortisol can interact with aldosterone receptor (mineralocorticoid receptors) and induce aldosterone-like responses
    → “AME” syndrome (apparent mineralocorticoid excess)
  • At high concentrations cortisol interacts with MR leading to Aldosterone- like symptoms
30
Q

Why do kidenys need to activate cortisol and what happens if {cortisol] is too high

A
  • kidney and other cell types inactivate cortisol to prevent inappropriate activation of the aldosterone receptor – when cortisol levels are too high HSD2, kidenayas are overwhelmed and cortisol stimulates Na+/K+ exchange in kidney causing hypokalemia and hypertension
31
Q

Skin and cortisol

A

Skin has HSD1, which converts cortisone to cortisol

32
Q

Kideny-liver cortisone-cortisole shunt

A

cortisone - cortisone shunt is present between kidney and liver
kidney-> deactivation
liver-> activation

33
Q

11β-HSD1 vs 11β-HSD2

A

11β-HSD1- converts cortisone to cortisol

11β-HSD2- converts cortisol to cortisol cortisone

34
Q

Describe cortisol’s receptor

A

Cortisol is a steroid-> has steroid/nuclear receptor is called GR receptor (glucocorticoid receptor)
Belongs to 1st class of nuclear receptors-> when inactive is is present in the cytoplasm, not nucleus
When bound to cortisol-> dimerizes with another cortisol- bound receptor
This dimer shuttles to the nucleus where this dimer can act as a transcription factor
The type of gene it acts upon depends in context and cell types

35
Q

Effects of cortisol on Muscle cells, adipocytes lymphocytes, and liver

A

Muscle cells, adipocytes lymphocytes-> increased catabolism

Liver-> Increased glycogen synthesis, increased gluconeogenesis

36
Q

Cortisol Acts by i__

what is it’s effect oppoiste ans similair to?

A

Acts by increasing transcription of specific genes via activating a cytoplasmic transcription factor (Class I receptor i.e. cytosolic)

Effects are generally opposite to insulin and similar to GH (i.e. increase in blood glucose) at the expense of protein and fat.

37
Q

Cortisol’s effect on glucose levels in the circulation

A

Increase of blood glucose despite the increase in glycogen storage

38
Q

cortisol and immune effects

A

Cortisol inhibits immune response-> anti-inflammatory properties

Widely used to treat inflammatory conditions (i.e. rheumatoid arthritis and other immune disorders)

Leads to atrophy of the lymph nodes and thymus (activation of apoptosis)

Decrease in number of lymphocytes and antibody production vPatients become susceptible to infections

39
Q

antibody production is based on __

A

antibody production is based on gene expression

40
Q

Cortisol’s effect on norepinephrine

A

Sensitizes arterioles to the action of norepinephrine (hypertension)

Permissive effect on the action of norepinephrine on carbohydrate metabolism (glycogenolysis → hyperglycemia)

41
Q

cortisol’s effect on CNS

A

Increased activity of the central nervous system (euphoria)-> called an euphoric steroid

42
Q

What is the primary factor of cortiosl secretion regulation

what are the other factors

A

cortisol is primarily regulated by trophic hormone ACTH
once cortisol is released, it can inhibit it’s own synthesis by acting negatively on pituitary and hypothalamus
like most steroids, cortisol has diurnal rhythm regulation (ACTH also is affected by circadian rhythm)

43
Q

WHen are cortisol levels the highest? What is it related to

what are the other factors relating to it?

A

ACTH is highest in the early morning-> cortisol peak is also in early morning

  • pulse of ACTH-> pulse of cortisol

+
diurnal rhythm

  • pulse frequency increases in the early morning
  • increased frequency-> increased levels

CRH release hormone is responsive to other factors, apart for circadian rhythm, such as stress e.g. fever. exhaustion, exercise
these factros are integrated at the level of hypothalamus, thus controlling CRH levels-> ACTH levels -> thereby controlling cortisol levels

44
Q

What does the increase of average level of cortisol result from?

A

Average level increases due to the summation of more frequent pulses.

45
Q

Transport of circulating cortisol

A

another factor, controlling cortisol availability
as cortisol is not soluble-> has to be transported by a binding protein
like all steroids, which have their unique binding proteins, cortisol does as well

Corticosteroid Binding Globulin (CBG = Transcortin)

Synthesized by the liver & has high affinity for cortisol

46
Q

what is cortisol bound to in the circulation?

A

CBG binds most of all cortisol (75%) in the plasma,about 10 % is “free” and 15% is bound to serum albumin

47
Q

How does Corticosteroid Binding Globulin protect cortisol from being desrtoyed?

A

Bound cortisol is protected from inactivation by the liver i.e. maintains a pool of circulating cortisol by delaying metabolic clearance (liver inactivates free steroids by increasing H2O solubility – 90 % excreted by kidney)

48
Q

Cortisol basic action vs effects in excess (cushing)

A
49
Q

Causes of Cushing’s syndrome (overproduction of cortisol)

A
  • CRH producing tumor
  • ACTH producing tumor
  • Lack of feedback control by cortisol vCortisol producing adrenal tumor
  • Iatrogenic (greek “brought forth by a healer”) - most common cause resulting from chronic glucocorticoid therapy
50
Q

ACTH dependent vs independent cushing’s disease

A
  • ACTH-dependent Cushing syndrome is characterized by elevated ACTH levels due to drenocorticotropic hormone (ACTH) oversecretion by a pituitary adenoma (Cushing disease, CD) or ectopic ACTH producing tumour
  • ACTH-independent Disease- In this condition, either both adrenal glands are hyperactive or there is an adrenal tumor that is making too much cortisol.
51
Q

Cushing’s syndrome sympoms

A
52
Q

Cushing’s syndrome treatment

A
  • Treatment is aimed at removing the cause of hypersecretion without permanently damaging the adrenal or pituitary (would require life long replacement therapy)
  • microsurgery, various forms of radiation therapy and pharmacologic inhibition of ACTH secretion
53
Q

Describe cortisol deficiency condition

A

Adrenal hypofunction (Addison disease)

  • Most commonly due to destruction of the adrenal gland by an autoimmune response
  • Fatigue, weakness, faintness, nausea vVomiting
  • Low blood pressure
  • Salt craving
  • Pain in muscles and joints
  • Excessive freckling (release of MSH as part of opiomelanocortin)
54
Q

Addison Crisis Pathway

A
55
Q

What are the cortisol effects on metabolism and cardiovascular system?

A

Metabolsim:

  • Increased glycogenolysis
  • Increased gluconegenesis
  • Increased proteolysis
  • increase lipolysis

Cardiovascular system:

  • increased myocardial contractility
  • increased cardiac output
  • increased catechlomine pressor affect
56
Q

where can HSD1 be found

A

skin, liver, CNS, placenta, adipose

kris Endocrinology (17 decks)

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