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Semester 2 (1st year) > Wk 29 > Flashcards

Wk 29 Flashcards

1
Q

What hormones are released from the adrenal cortex?

What hormones are released from the adrenal medulla?

A

Cortex= Glucocorticoids (cortisol, corticosterone)

Medulla= Adrenalin and noreadrenalin

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2
Q

What are the 3 layers of the adrenal cortex and what hormones does each layer secrete?

A

Outermost layer= Zona glomerulosa (Mineralocorticoids- mainly aldosterone)

Middle= Zona fasculata (Glucocorticoids- mainly cortisol)

Inner cortex= Zona reticularis (Androgens)

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3
Q

What hormone does the hypothalamus release that goes to the anterior pituitary to stimulate the next hormone (related to glucocorticoid release from adrenal cortex)?

What hormone does the anterior pituitary release?

A

Hypothalamus releases: Corticotropin-releasing hormone (CRH)

Anterior pituitary then releases: Adrenocorticotropic hormone (ACTH)

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4
Q

CRH released by hypothalamus in response to what?

A

Stressors

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5
Q

Where does the synthesis of cortisol occur in the adrenal cortex?

What is cortisol made from?

A

Zona fasciculata

Cholesterol

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6
Q

How does Adrenocorticotrophic releasing hormone stimulate the adrenal gland to produce steroid hormones?

A

It promotes the uptake and release (from storage) of cholesterol so steroids can be synthesised

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7
Q

What is the major carrier of cholesterol to peripheral tissues?

A

LDL

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8
Q

Corticotrophin Releasing Hormone is released as pulsatile secretions so this stimulates Adrenocorticotrophic Hormone to also be released in pulsations…

Which time of the day has the highest pulsations?

A

Late night/ early morning

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9
Q

Is cortisol lipid or water soluble?

A

Lipid sol

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10
Q

What are the carrier proteins that transport cortisol in the blood? 2

A

Cortisol binding globulin or transcortin (albumin does a lil bit)

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11
Q

Secretion of cortisol is mainly controlled by ACTH, but secretion is also promoted by what 3 things?

A

Vasopressin/ ADH (increases BP)

Nitric Oxide

Some cytokines

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12
Q

Does cortisol promote or inhibit the release of CRH and ACTH?

A

Inhibits (Neg feedback loop)

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13
Q

What is Cushing’s Disease and does it increase or decrease ACTH and cortisol?

A

It is a tumor in the pituitary gland that makes ACTH so there is high cortisol and because there is neg feedback, this lowers the really high levels of ACTH so ACTH levels can be high or normal

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14
Q

What is Cushing’s syndrome caused by? 2 options

A

Adrenal tumour or Ectopic ACTH

Adrenal tumour= Lots of cortisol being produced which has neg feedback on ACTH so low ACTH (same action with steroid drugs)

Ectopic ACTH= lots of ACTH and lots of cortisol

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15
Q

What is Adrenal Insufficiency? 2 options

A

It can be either Addison’s Disease or Hypopituitarism

Addison’s disease= adrenal damage so high levels of ACTH but still low levels of cortisol

Hypopituitarism= Pituitary gland isn’t secreting ACTH properly so low ACTH and therefore low cortisol

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16
Q

What is an anabolic effect of cortisol? (on the liver)

What are 2 catabolic effects of cortisol? (on muscle and adipose tissue)

A

Anabolic on Liver: Gluconeogenesis (making blood glucose from AA and glycerol etc)

Catabolic on muscle: Protein breakdown

Catabolic on adipose: lipolysis

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17
Q

Is cortisol slow or fast acting? Why?

A

Slow because effects on transcription and translation

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18
Q

What is the main action of cortisol?

A

It is a glucocorticoid so main action is on glucose metabolism: anti-insulin effect so releases stored glucose into blood (enhances action of glucagon)

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19
Q

How does cortisol stimulate the urea cycle in the liver?

A

By gluconeogenesis in the liver

As AA are converted to glucose, lots of nitrogen is generated which needs to be cleared so urea cycle enzymes are recruited and the nitrogen enters the cycle and is converted to urea which is excreted by kidneys

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20
Q

How does cortisol affect the muscles?

A

It stimulates protein catabolism to release AAs for gluconeogenesis in the liver

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21
Q

Excess cortisol (Cushing’s) promotes fat in which locations and promotes lipolysis in which locations?

A

Promotes fat storage in visceral locations and fat breakdown in peripheral locations

22
Q

What is the most common reason for giving people cortisol in medications?

What is a consequence of too much cortisol medication?

A

It has potent anti-inflammatory and immunosuppressive effects

In large quantities, cortisol depresses immune function

23
Q

Although cortisol is the body’s primary stress hormone so it increases our energy to deal with stress and also increases cognitive performance and decreases inflammation, prolonged exposure to excess glucocorticoids may have adverse metabolic consequences, such as _________________ and ________________

A

The development of insulin resistance and Type 2 diabetes

24
Q

Impact of elevated cortisol…

How does it promote or worsen diabetes?

What does dyslipidaemia lead to?

(also muscle wasting and osteoporosis, mood swings and memory impairments)

Why do people with Cushing’s have slowed wound healing?

A

It promotes hyperglycaemia

Visceral obesity

Slow wound healing because the immune system is suppressed

25
Q

What triggers the release of Aldosterone from the Zona Glomerulosa in the adrenal gland?

What triggers the release of catecholamines from the adrenal medulla?

A

Circulating Angiotensin 2 and high plasma K+ and low plasma Na

Direct action of sympathetic nervous system

26
Q

Does Aldosterone act on the cell surface or in the nucleus of the renal tubular cells?

What receptor does it bind to?

What does this activate?

A

Nucleus

MR receptor

Activates expression of several genes that leads to Na channel at the luminal membrane (to reabsorb Na from urine into cell) and a Na/K ATPase at the basement membrane (to reabsorb Na from cell into blood and K from blood into cell to go into urine)

27
Q

How long does aldosterone action usually take?

A

Slow- about 30 mins

28
Q

What are the effects of aldosterone?

A

Increases Na (and hence water) reabsorption in kidneys (and excretion of K)

Stimulates ADH which triggers thirst and further promotes water reabsorption in kidneys

Blood pressure increased (too much can lead to hypertension)

29
Q

Adrenergic alpha 1 receptors leads to what?

Adrenergic beta 2 receptors leads to what?

(Beta 1 increase HR and heart contractility)

A

Alpha 1= constriction of smooth muscles (peripheral arteries)

Beta 2= relaxation of smooth muscles (bronchioles and coronary arteries)

30
Q

Adrenergic Receptors…

Where are alpha 1 receptors?

Where are alpha 2 receptors?

Where are Beta 1 receptors?

Where are Beta 2 receptors?

Beta 3 somewhere else

A

Alpha 1= blood vessels, GIT, skin

Alpha 2= CNS

Beta 1= Heart (increase contractility and HR)

Beta 2= Coronary vessels (dilate), lungs, smooth muscles of GIT

31
Q

What 2 things cause the release of CRH from the hypothalamus (to stimulate ACTH and then cortisol?)

A

Circadian rhythms and stress

32
Q

What are the 4 causes of Cushing syndrome?

A

Pituitary adenoma (Cushing disease)

ATCH secreting tumour

Tumour of adrenal cortex (secreting cortisol)

Long term use of corticosteroids (asthma)

33
Q

What is the cause of Addison’s Disease?

A

An auto-immune destruction of the zona fasiculata of the adrenal cortex so there is inadequate production of cortisol

34
Q

Signs and symptoms of Addison’s disease? (5)

A

Fatigue and weakness (due to inability to release glucose into blood- especially during stress)

Low BP

Hypoglycaemia

Darkening of skin (elevated pituitary MSH)

35
Q

What is the most common cause of excess catecholamine secretion?

A

A Pheochromocytoma of the adrenal medulla (a secretory tumour that releases excessive amounts of adrenalin and NA)

36
Q

What are the symptoms of excess sympathetic activation?

A

High BP
Heart palpitations
Anxiety and panic attacks

37
Q

What is the usual treatment of excess catecholamine secretion?

A

Adrealectomy

38
Q

Clinical uses of corticosteroids? (2)

A

Replace mineralcorticoids

Replace glucocorticoids (like in Addison’s Disease where there isn’t enough cortisol)

39
Q

What is the fun thing about hydrocortisone and cortisone?

A

They have equal mineralocorticoid and glucocorticoid effects

40
Q

What is the benefit of combining glucocorticoids with cytotoxic drugs in brain cancer?

A

Reduces cerebral oedema

41
Q

What are the different ways glucocorticoids can be used for anti-inflammatory/ immunosuppresive effects?

A

Asthma

Topical (skin, eye, ear, nose) for eczema and allergic conjunctivitis/ rhinitis)

Hypersensitivity states (severe allergic reactions)

Autoimmune diseases

To prevent graft vs host disease after organ or bone marrow transplant

42
Q

What are the adverse effects of exogenous glucocorticoids?

The 3 main ones and then 5 extras

A

Immune Suppression
Cushing’s syndrome
Adrenal Insuficiency

Osteoperosis 
Osteonecrosis 
Growth retardation 
Metabolic dysfunction
Fluid retention/ hypertention
43
Q

How does the use of exogenous glucocorticoids lead to osteoperosis?

A

Because there is inhibition of gonadal steroid hormones so osteoclasts are stimulated and osteoblasts are inhibited

ALSO decreased GIT absorption of Ca so rise in PTH and bone resorption

44
Q

How do exogenous glucocorticoids lead to fluid retention/ hypertention?

A

At higher doses, glucocorticoids act on mineralocorticoid receptors and stimulate the effects of aldosterone so there is an increase in Na and water reabsorption and increase in K and H+ excretion in urine

45
Q

What is the main thing in the immune function that glucocorticoids suppress?

A

Prostaglandins

46
Q

How do glucocorticoids lead to peptic ulcers?

A

They block prostaglandins which are needed for the protection of stomach mucosa

47
Q

What adverse effects do glucocorticoids have on the CNS?

What effect do they have on the eyes?

What do they do to the HPA (Hypothalamus Pituitary Adrenal) axis?

A

CNS- euphoria, depression and psychosis

Cataracts and glaucoma (vision loss due to optic nerve damage)

Generalised suppression of HPA axis

48
Q

What happens to the HPA axis after long term use of glucocorticoids?

What does sudden withdrawal lead to?

Which options of administration do these effects occur from?

A

There is decreased production of ACTH and impaired cortisol and androgen production which leads to adrenal gland atrophy

Acute adrenal insufficiency

Oral, inhaled, intranasal and topical administration

49
Q

What symptoms occur with sudden withdrawal of glucocorticoids (symptoms of acute adrenal insufficiency)?

A 
GI symps (nausea, vom, abso pain)
Dehydration 
Hypotention 
Fever 
Lethargy and malaise 
Hyponatraemia and hyperkalaemia
50
Q

How long does it take for full adrenal function to recover?

A

8 weeks but may take much longer after prolonged high dose treatment

51
Q

Do glucocorticoids lead to a psychological dependence?

A

No, there is no reward pathway that is stimulated with their use so there is no psychological dependence, just physiological dependence

52
Q

The route of administration can limit systemic exposure to glucocorticoids.

What are 3 examples of this?

A

Inhalation to target lungs for asthma

Topical to target skin for eczema

Intranasal to target nose for rhinitis

Semester 2 (1st year) (13 decks)

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