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203: Theme 1 - 304 - Endocrinology > Hypothalamic-Pituitary- Adrenal Axis > Flashcards

Hypothalamic-Pituitary- Adrenal Axis Flashcards

1
Q

What are the six Anterior Pituitary hormones?

A
  • ACTH: Adrenocorticotropic Hormone
  • FSH: Follicle Stimulating Hormone
  • TSH: Thyroid Stimulating Hormone
  • PRL: Prolactin
  • GH: Growth Hormone
  • LH: Luteinizing hormone
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2
Q

What are the two Posterior Pituitary Hormones?

  • production
  • transport
  • store
A
  • ADH: Antidiuretic Hormone
  • Oxytocin
  • these are synthesised in neurones of the hypothalamus then converted to their active form in the posterior pituitary gland
    • supraoptic nuclei
    • periventricular nucleus
  • inactive forms are transported from the nuclei along the hypothalamico-neurohypophyseal tract
  • then stored in the posterior pituitary
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3
Q

Give an overview of Growth Hormone (GH)

  • production
  • control
  • action/effect
A
  • synthesised in the somatotroph cells of the anterior pituitary gland
  • secretion is controlled by the hypothalamus
    • GHRH (somatotropin) stimulates its secretion
      • Growth hormone-releasing hormone
      • has a greater role than GHRIH
      • stimulated by decreased COH and fatty acids and increased amino acids
    • GHRIH (somatostatin) inhibits is release
      • Growth hormone-releasing Inhibiting hormone
  • acts via 2nd messenger produced in the liver in some tissues
    • ​Insulin-like growth factor 1 and 2
  • Primary effects: promote growth in adolescence by increasing protein synthesis and collagen deposition
    • ​foetal growth is also dependent
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4
Q

Give an overview of Oxytocin

  • production
  • control
  • action/effect
A
  • works via IP3 to cause contraction of the smooth muscle of the genital tract and breast
  • production increases during pregnancy
    • a parallel increase in oxytocin activity is also seen
  • secretion of oxytocin is achieved by stimulation of the genitals and nipples
    • most important at parturition and lactation
    • there is a delay between the start of suckling and milk let down
  • Oxytocin is not necessary for the initiation of normal labour
    • it can be administered to induce labour
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5
Q

Describe the cycle that leads to oxytocin release

  • nipple stimulation
  • stimulation of the cervix and vagina
A
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6
Q

Give an overview of prolactin

  • release/ secretion
  • control
  • action
A
  • secreted by lactotroph (mammotroph) cells in the anterior pituitary gland
    • these cells increase during pregnancy and
    • prolactin conc. increases during parturition initiating lactation
    • secreted in both males and females
  • secretion is controlled by
    • Prolactin Inhibiting factor = DA
    • TRH stimulates prolactin release
  • secretion is stimulated by
    • mild stress
    • nipple stimulation
    • coitus
  • Action
    • contain milk production in females
    • maintenance of lactation depends on suckling
    • prolactin with other hormones causes proliferation and differentiation of mammary tissue during pregnancy
    • inhibits gonadotrophin release and/or response of the hormones to these trophic hormone (ovulation doesn’t occur during breastfeeding)
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7
Q

What are the actions of Prolactin?

(4)

A
  1. increase during pregnancy under the influence of oestrogen and progesterone to facilitate lobluloalveolar development of the breast
  2. causing milk secretion from the breast after oestrogen and progesterone priming
  3. inhibits GnRH secretion and antagonizes the action of gonadotropins in the ovaries, inhibiting ovulation
  4. hyperprolactinaemia in men is associated with impotence and hupogonadism
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8
Q

Give an overview of ADH

  • release
  • stimulation
  • action/ receptors
A
  • The hypothalamic nuclei that control fluid balance lie close to the nuclei that synthesise and secrete ADH.
  • Stimuli for ADH release
    • increased in plasma osmolarity (sensation of thirst)
    • hypovolaemia - through stretch receptors in the CVS or angiotensin release
  • ADH (vasopressin) receptors are all GPCRs
    • V1A and V1B
      • coupled to phospholipase C/ inositol triphosphate system
      • oxytocin receptors also have GPCRs that are similar to ADH, therefore, ADH acts as a mild agonist at oxytocin receptors
    • V2
      • these stimulate AC which mediates the main response of ADH in the kidney on the basolateral membrane of the distal tubule and collecting duct
      • increases the rate of insertion of aquaporins in the collecting duct in the kidneys
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9
Q

Give an overview of the control of ADH

A
  • NSAIDs and carbamazepine increase vasopressin effects (Na+ retention)
    • Aldosterone (mineralocorticoid) also causes water to be reabsorbed along with sodium.
  • Lithium, colchicine and vinca alkaloids decrease vasopressin effects (Na+ excretion).
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10
Q

What clinical investigations are carried out?

A
  • Presentation - Primary Or Secondary?
  • Stimulate secretion? (ACTH) or Suppress secretion? (Dexamethasone)
    • TSH & T4
    • Cortisol
    • LH & FSH
    • A prolactin (PRL) test
    • Testosterone / “Periods”
  • After Biochemical Tests: Imaging (e.g. MRI)
  • After Imaging: Visual Field Tests
  • Bilateral hemianopsia (due to compression of optic chiasm)
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11
Q

Give an overview of the hypothalamus

  • location
  • inputs/outputs
  • action/effect
A
  • lies on either side of the third ventricle, below the thalamus, between the optic chiasm and the midbrain
  • receives inputs from the limbic system and the retina
  • contains neurons that are sensitive to changes in hormone levels, electrolytes and temperature
  • efferent output to the autonomic nervous system
    • has greater homeostasis of physiological systems:
      • thirst, hunger, sodium and water balance, temp. regulation
      • control of circadian and endocrine function
      • formation of anterograde memories (with the limbic system)
      • translation of response to emotional stimuli into endocrinological and autonomic responses
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12
Q

What are Sellar masses and how do they present?

A
  • a mass found in the sellar region in the brain this is composed of the
    • bony sellaturcica
    • pituitary gland
    • adjacent structures
  • present with neurological symptoms
    • visual impairment: the most common is bitemporal hemianopsia
      • _​_one or both eyes may be affected to varying degrees
      • onset of the visual deficit is usually very gradual –> delayed ophthalmologic consultation
    • diplopia
    • headache: due to the expansion of the sella
    • pituitary apoplexy: sudden haemorrhage into an adenoma –> sudden headaches and diplopia
    • Cerebrospinal fluid rhinorrhea - inferior extension of the mass
    • Parainaud syndrome: a constellation of neuro-ophthalmologic findings (most often paralysis of upward conjugate gaze),
  • discovered incidentally through MRI, usually with hormonal abnormalities
    • hormone deficiencies are of gonadotropins –> hypogonadism
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13
Q

Go over the causes and prevalence of Sellar Masses

  • types of adenomas
  • differential
A
  • 90% of cellar asses are pituitary adenomas
    • these are benign tumours of the anterior pituitary that are neoplastic
  • Prevalence of type of adenomas per 100,000
    • All adenomas – 77.6
    • Lactotroph adenomas – 44.4
      • cause hyperprolactinemia –> hypogonadism in men and women
    • Nonfunctioning adenomas – 22.2
      • gonadotroph adenomas
      • thyrotroph adenomas - may cause hyperthyroidism due to increased TSH
    • Somatotroph adenomas – 8.6
      • cause acromegaly due in increased GH secretion - the majority are clinically silent
    • Corticotroph adenomas – 1.2
      • cause Cushings disease, but majority remain clinically silent
  • Pituitary hyperplasia may present as a sellar masses and be misdiagnosed as pituitary adenoma
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14
Q

Types of Pituitary hyperplasia

A
  • Lactotroph hyperplasia during pregnancy.
  • Thyrotroph and gonadotroph hyperplasia due to longstanding primary hypothyroidism and primary hypogonadism, respectively.
  • Somatotroph hyperplasia due to ectopic secretion of growth hormone-releasing hormone, a rare condition.
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15
Q

How are Hypothalamic-pituitary hormones transported?

A
  • Neurosecretory cells release peptidergic hormones (median eminence, hypothalamus) – transported in blood via the pituitary portal system.
    • hormones also transport via axons from the Parvicellular neurosecretory cells
  • Pituitary stalk & pituitary portal vessels pass down through the dura mater which roofs the pituitary fossa.
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16
Q

Review the Hypothalamic-pituitary-adrenal axis controls

(draw it out)

A
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17
Q

What type of imaging is this, label key features of the HP axis

  • plane and weighting
A
  • MRI scan, coronal plane, T1 weighted
18
Q

What are the Hormones, Receptors & Enzymes of the Adrenal Cortex

A
  • Adrenal cortex hormone production
    • GLUCOCORTICOID
      • CORTISOL
    • MINERALOCORTICOID
      • ALDOSTERONE (renin-angiotensin-aldosterone system)
    • SEX STEROIDS
      • ANDROGENS
  • Binding proteins:
    • 90% cortisol bound to cortisol binding globulin (CBG)
  • Receptors:
    • Intracellular glucocorticoid and mineralocorticoid receptors (GR and MR)
  • Enzymes:
    • 11-b-hydroxysteroid dehydrogenase (11- b-HSD)
19
Q

What are the effects of Glucocorticoids?

A
  • Maintenance of homeostasis during stress
    • e.g. haemorrhage, infection, anxiety
  • Anti-inflammatory
  • Energy balance/metabolism
    • ­ increase/ maintain normal [glucose]
  • Formation of bone and cartilage
  • Regulation of blood pressure
  • Cognitive function, memory, conditioning
20
Q

What are cortisol levels like across a day

  • effect on the circadian rhythms
A
  • rise during the early morning
  • peak just prior to awakening
  • fall during the day
  • are low in the evening
    • in preparation of sleep
21
Q

Explain Ultradian Rhythms

A
  • this is spontaneous pulsatile release of glucocorticoids during the day
    • varying amplitudes
  • amplitude decreases in the circadian trough
  • associated with
    • noise
    • anticipatory stress
    • response to an unintended stressor
22
Q

What are the circulating androgens?

A
  • DHEAS from the adrenal glands
  • Androstenedione
  • Testosterone
    • converted to oestrogen by Aromatase
  • Dihydrostesterone converted from testosterone by 5-alpha reductase
23
Q

Explain the function of the 11-ß-HSD-1/2 enzyme

A

11-ß-HSD-2

  • inactivates cortisol in the kidney, colon, sweat glands
    • converts it to cortisone
  • this allows aldosterone to bind to the mineralocorticoid receptor as they both have the same affinity

11-ß-HSD-1

  • converts cortisone back to cortisol in the
    • liver, adipose, CNS
  • tissue specificity allows gating of GC access to nuclear receptors and amplification of GC signal in target cells
24
Q

What is the impact of excess cortisol?

A
  • Cushings syndrome
    • weight gain
    • central obesity
    • hypertension
    • Insulin resistance
    • Neuropsychiatric problems
    • Osteoporosis
25
Q

What is the pathogenesis of Cushing’s syndrome?

A
  • Excess cortisol due to
    • Pituitary adenoma: ACTH-secreting cells
    • Adrenal tumour: adenoma or carcinoma, neoplastic cells also secret cortisol
    • ‘Ectopic ACTH’: carcinoid, paraneoplastic
      • other non-adrenal cells producing cortisol
    • Iatrogenic: steroid treatment
26
Q

Clinical features of Cushing’s syndrome

A
  • Central obesity with thin arms & legs
  • Fat deposition over the upper back (‘buffalo hump’)
  • Rounded ‘moon’ face
  • Thin skin with easy bruising, pigmented striae
  • Hirsutism
    • Unwanted, excessive hair growth in women either on face, chest or back.

Causing

  • Hypertension
  • Diabetes
  • Psychiatric manifestations
  • Osteoporosis
27
Q

What is the impact of insufficient Cortisol?

A
  • Addison’s disease
  • gradually falls off in general health at length they gradually sink and expires
  • becomes languid & weak
  • indisposed to either bodily or mental exertion
  • the body wastes
  • slight pain is referred to the stomach
  • there is occasionally actual vomiting
  • discolouration of the skin
28
Q

What is the pathogenesis of Addison’s disease?

A
  • Primary adrenal insufficiency ‘Addison’s disease’
    • Usually autoimmune in UK
    • Rare causes include metastases or TB
    • decreased Production of all adrenocortical hormones
  • Other causes of hypoadrenalism
    • Secondary to pituitary disease (rare)
    • ‘Iatrogenic’
    • patients on high dose, long term steroid Rx, which is suddenly stopped at a time of stress
29
Q

What are the clinical features of Addison’s disease?

A
  • Malaise, weakness, anorexia, weight loss
  • Increased skin pigmentation:
    • knuckles, palmar creases, around / inside the mouth,
    • pressure areas, scars
  • Hypotension / postural hypotension
  • Hypoglycaemia
30
Q

What is Autoimmune Polyendocrine Syndrome?

  • Types
A
  • having multiple autoimmune endocrine dysfunctions
  • Type 1
    • rare, onset in infancy
    • AIRE gene (Ar)
    • common phenotype:
      • Addison’s disease
      • Hypoparathyroidism
      • Candidiasis
  • Type 2
    • ​more common- infancy to adulthood
    • polygenic cause
    • common phenotype
      • Addison’s disease
      • Type 1 diabetes
      • Autoimmune thyroid disease
31
Q

What autoimmune conditions might occur together in APS?

A
  • Type 1 diabetes
  • Autoimmune thyroid disease (hypo- or hyper-)
    • Also gestational / post-partum thyroiditis
  • Coeliac disease
  • Addison’s disease
  • Pernicious anaemia
  • Alopecia
  • Vitiligo
  • Hepatitis
  • Premature ovarian failure
  • Myasthenia gravis
32
Q

What are the clinical implications of those with Autoimmune Polyendocrine Syndromes?

  • actions to take
A
  • High index of suspicion for additional autoimmune endocrine disorders
    • T1 DM with fatigue, weight loss & hypos:
      • ? Addisons disease
    • T1 DM with non-specific GI symptoms / diarrhoea:
      • ? Coeliac disease
  • Consider screening in patients with T1 DM and/or Addison’s disease
    • Coeliac screen
    • Thyroid function tests (esp in pregnancy / post-partum)
33
Q

How is the HPAA assessed?

A
  • Basal function tests through
    • Blood
      • cortisol
      • ACTH
      • timing
    • Urine
      • cortisol
      • 24 hr collection
    • Saliva
      • cortisol
      • timing
  • Dynamic Tests
    • stimulated
      • ACTH
      • CRH
      • stress - hypoglycaemia
    • suppressed
      • Dexamethasone: synthetic glucocorticoid
34
Q

How would too much cortisol be recognised through HPAA assessments?

A
  • 24 hour urinary free cortisol
    • ‘AREA UNDER THE CURVE’
  • Midnight cortisol (blood / saliva)
    • ‘TROUGH’
  • 9 a.m. ACTH (with paired cortisol)
    • PITUITARY / ADRENAL / ECTOPIC?
      • NEGATIVE FEEDBACK AT PITUITARY
  • DEXAMETHASONE SUPPRESSION
    • Sensitivity to GC negative feedback at pituitary
35
Q

How would too little cortisol be recognised through HPAA assessments?

A
  • 9 a.m. cortisol
    • ‘PEAK’
  • SynACTHen test
    • Adrenal response to ACTH
      • Trophic effect ACTH on adrenals
  • Insulin tolerance test
    • Response to hypoglycaemic stress
      • Can be dangerous!
  • U & E (¯Na, ­K) in Addison’s disease
    • Due to mineralocorticoid deficiency
    • Can measure renin & aldosterone concentrations
  • decreased blood glucose
36
Q

What golden rules should be followed when assessing the HPAA?

A
  1. Never start investigating a patient for an endocrine condition unless their symptoms & signs suggest they may have it!
    • Risk of false-positive results
  2. Never image any endocrine gland until you have established the diagnosis biochemically!
    • Risk of discovering ‘incidentalomas’
37
Q

What imaging should be carried out when assessing the HPAA?

A
  • after confirming Cushing’s syndrome, consider
    • CXR
    • MRI pituitary
    • CT adrenal
  • Rarely image Addison’s disease patients unless concerned about TB/ metastatic cancer
38
Q

What is the medical management for Cushing’s syndrome?

A
  • Surgical (depending on the cause)
    • Transsphenoidal adenectomy
    • Adrenalectomy
  • Pituitary radiatherapy
    • 131I
39
Q

What is the medical management of Addison’s disease?

A
  • Glucocorticoid replacement therapy
    • usually, hydrocortisone (sometimes prednisolone)
    • needs to be increased to cover ‘stresses’ (intercurrent illnesses like flu)
    • recommendations may vary for operations and post-op period
  • Mineralocorticoid replacement therapy for those with primary adrenal insufficiency
    • fludrocortisone
  • additional hormone replacement therapy for those with secondary adrenal insufficiency
  • patients need IV/IM steroid if unable to do so orally
    • vomiting/ NBM
40
Q

What is the effect of long-term high dose steroid treatment on patients?

A
  • endongenous suppression of adrenal function
  • They may not mount an adequate ‘stress response’.
  • Their steroid treatment should not be stopped suddenly.
  • If they need a major procedure / an operation, they require increased steroid cover as described.
  • They should be given a ‘Steroid Treatment Card’ to remind them (& their doctors) about this.

203: Theme 1 - 304 - Endocrinology (15 decks)

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