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Human development block > Adrenal gland > Flashcards

Adrenal gland Flashcards

1
Q

What is the average size of the adrenal gland ( width,length,thickness and weight)?

A

2-3cm wide. 4-6cm long. 1cm thick. Average weight of 4g

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2
Q

What are the 3 layers of the adrenal cortex?

A

Zona glomerulosa. Zona fasciculata, Zona reticularis.

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3
Q

What are the relative proportions(%) of the outer cortex and central medulla of the adrenal gland?

A

~90% and ~10% respectively

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4
Q

Which hormones are secreted by the medulla?

A

Adrenaline(80%) and noradrenaline(20%)

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5
Q

What does the adrenal cortex produce?

A

Steroid hormones

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6
Q

What does each layer of the adrenal cortex produce specifically?

A

zona fasciculata= glucocorticoids( so makes cortisol)
zone reticularis= androgens
zona glomerulosa= mineralocorticoids

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7
Q

Which enzyme is absent in each of the 3 layers of the adrenal cortex specifically?

A

zona fasciculata= lacks aldosterase synthase
zona reticularis= lacks aldosterase synthase
zona glomerulosa= lacks 17 alpha hydroxylase

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8
Q

Describe the regulation of synthesis for cortisol.

A

The hypothalamus releases CRH. This stimulates the corticotrophs of the anterior pituitary to release ACTH.
ACTH stimulates the adrenal cortex to synthesize and release cortisol.
Negative feedback mechanism for control: cortisol feeds back to the corticotrophs to decrease acth release and on the hypothalamus to inhibit release of CRH.

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9
Q

What is ACTH derived from

A

Pro-opiomelanocortin (POMC)

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10
Q

Name 2 factors that stimulate hypothalamus to produce CRH

A

stress

cicardian rhythms

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11
Q

What is the half life of cortisol?

A

90mins

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12
Q

What is the half life of aldosterone ?

A

15mins

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13
Q

What is the role of steroid receptors in bringing about increased protein synthesis?

A

Steroid hormones interact with nuclear receptors. Steroid hormones enter cells by diffusion and bind to the cytoplasmic receptor, leading to dissociation of heat shock protein( hsp90) from the receptor. The hormone-receptor complex dimerises and is translocated to nucleus. The complex binds to hormone responsive element (HRE) on DNA which leads to an increase in mRNA production and therefore increased protein synthesis.

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14
Q

What is the general effect of glucocorticoids?

A

Anti-inflammatory.

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15
Q

What is the role of the mineralcorticoid receptor in preventing cortisol activation?

A

Once cortisol binds to the receptor, it is converted to an inactive form called cortisone. The enzyme beta-HSD is needed for this conversion.

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16
Q

What are the two isoforms of 11beta-HSD , where are they expressed and what do they do?

A

11Beta-HSD1 : expressed in liver,adipose, muscle. Converts cortisol to cortisone

11Beta-HSD2 : expressed in aldosterone sensitive tissues.(kidney,colon,salivary glands)

17
Q

What are some adverse effects of glucocorticoids

A
  • suppression of response to infection.
  • suppression of endogenous glucocorticoid production.
  • metabolic effects
  • osteoporosis
  • iatrogenic Cushing’s syndrome
18
Q

What are some of the characteristics of Cushing’s syndrome?

A

Red cheeks, moon face, fat pads, bruisality/ecchymoses, hypertension, thin skin, red striation, thin arms and legs,pendulous abdomen, poor wound healing,osteoporosis, negative nitrogen balance, increased appetite, obesity,increased susceptibility to infection,neuropsychiatric effects, menstrual disorders, impotency,glucose intolerance, diabetes

19
Q

What is Cushing’s syndrome

A

A hormonal disorder caused by prolonged exposure of the body’s tissues to high levels of cortisol

20
Q

How can we treat Cushing’s syndrome?

A
  • METYRAPONE: 11Beta hydroxylase inhibitor
  • KETOCONAZONE: (withdrawn in europe) inhibits steroid biosynthesis
  • PASIREOTIDE (somatostatin analogue) SSTR5 agonist.
  • CABERGOLINE( dopamine D2 agonist)
  • MIFEPRESTONE (glucocorticoid receptor antagonist,progestogen receptor antagonist)
21
Q

What is Addison’s disease.

A

‘Chronic adrenal insufficiency’

hypocortisolism. A long-term endocrine disorder in which the adrenal glands do not produce enough steroid hormones.

22
Q

What are some of the clinical features of addisons disease?

A
  • weakness,fatigue,anorexia,weight loss
  • hyper-pigmentation
  • hypotension
  • gastrointestinal disturbances
  • salt craving
  • postural symptoms
23
Q

What is the treatment for Addinson’s disease

A

Replacement therapy with fludrocortisone

24
Q

What in general do hormones do?

A

stimulate cell function
inhibit cell function
stimulate/inhibit cell growth or differentiation
maintain physiological state

25
Q

Describe the endocrine hierarchy

A
  1. ) Hypothalamic hormone
  2. )Pituitary hormone
  3. ) Target hormone
  4. ) End organ effects
26
Q

Describe the thyroid axis.

A

1.) hypothalamus,releasing factor: TRH= thyrotropin releasing hormone
2.) Pituitary,trophic hormone: TSH= thyroid stimulating hormone
3.) Target organ-thyroid: T4 (thyroxine) and
T3( triodothyronine)
4.) End organ(s): Basal metabolic rate, pulse

27
Q

Which thyroid hormone is the active hormone?

A

Triodothyronine(T3).

T4 is converted to T3 by deiodinaton which acts on the end organ as T3 is more active and has a longer half life.

28
Q

Describe the different classes of hypothyroidism deficiency.

A
  • Primary: thyroid deficiency, so the end organ receives less hormone. The hypothalamus and pituitary are still working fine.
  • Secondary:pituitary deficiency: so less stimulation of the thyroid (TSH) but TRH levels remain high
  • Tertiary: hypothalamic deficiency: so less stimulation of the pituitary (by TRH), so less TSH released. This is RARE,
29
Q

Describe the sella turcica.

A

A ‘pocket’ within the sphenoid bone. This pocket is called pituitary fossa and is a bony cavity.

30
Q

What hormones does the posterior pituitary make?

A

Oxytocin and ADH

31
Q

What hormones does the anterior pituitary make?

A

GH, PROLACTIN, ACTH, TSH, FSH, LH, MSH.

32
Q

What consequence may lesion at the optic chiasm have on vision?

A

Bitemporal hemianopia. This compression may be due to a tumor

33
Q

Why is prolactin high in hypopituitarism?

A

Prolactin is regulated by dopamine to prevent its levels getting to high. Dopamine inhibits pituitary lactotrophs so controls its levels in that way. However in the case of hypopituitaris, dopamine no longer inhibits the pituitary lactotrophs so the prolactin levels continue to rise. This can therefore act as a test for pituitary hypofunction as you can test for lactation( for a lady you can squeeze behind the nipple and see if the milk ducts are full of fluid).

34
Q

Describe the different types of pituitary tumors in terms of size.

A 
Microadenoma= tumor LESS than 10mm
Macroadenoma= tumor MORE than 10mm
35
Q

Describe the different types of pituitary tumors in terms of function.

A
  • Functioning= leads to endocrine syndromes eg acromegaly. May even secrete extra hormones.
  • Non-functioning= don’t produce hormones
36
Q

What are the different ways that a pituitary tumor can present?

A
  • Mass effect e.g visual field defect
  • Hypopituitarism
  • Incidental
  • Hyper function (functioning tumor)
  • Apoplexy/ haemorrhage (acute)
37
Q

What are the different ways that a pituitary tumour can be treated?

A
  • Conservative/surveillance ( to avoid compression of the optic chiasm)
  • surgery (to remove the tumor eg trans-sphenoidal surgery)
  • medical: for prolactin secreting tumors. e.g dopamine agonist to stop prolactin production
  • Radiotherapy ( to shrink and prevent regrowth of the tumor)
38
Q

What are the principles of endocrine replacement?

A
  • The goal of treating hypopituitarism is to replace the hormones that nature would have intended
  • Replacement needs to recognise diurnal variation and the ‘natural’ evolution of hormone levels over time
39
Q

Which optic nerves cross over in the optic chiasm?

A

Retinal nerve fibres from the nasal side of the retina cross over at the optic chiasm. Whereas the retinal nerve fibres on the temporal side stay on the same side.

Human development block (35 decks)

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