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Molecular Basis of Disease - SGUL (Sem 4) > Endocrine Disorders > Flashcards

Endocrine Disorders Flashcards

1
Q

What can we do when investigating endocrine disorders

A
  • Measure hormone levels: are they appropriate?
  • Is endocrine tissue functional: dynamic tests of endocrine function
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2
Q

Describe the Hypothalamic- pituitary-thyroid axis

A
  • The hypothalamus releases TRH which stimulates the primary gland to release TSH
  • TSH triggers the production of T4 and T3 in the thread glands
  • T4 being the precursor of T3 and T3 being the biologically active hormone
  • Increased T3/T4 concentration negatively feedbacks onto the hypothalamus and pituitary to produce less TRH and TSH
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3
Q

What is meant by primary Hypothyroidism

A
  • Autoimmune destruction of the thyroid
  • Reduced production of thyroid hormone from the gland itself
  • Hashimotos disease

Low T3/T4 levels but High TSH levels

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4
Q

What is meant by secondary hypothyroidism

A

Reduced thyroid production by under-stimulation from the pituitary

Low T3/T4 levels and Low/None TSH levels

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5
Q

What is meant by primary Hyperthyroidism

A

Increased production of hormones from the gland itself
- Grave’s disease - antibody stimulation of thyroid

High T3/T4 levels and Low TSH levels

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6
Q

What is meant by secondary Hyperthyroidism

A

Increased stimulation of thyroid gland due to overactive pituitary

High T3/T4 levels and High TSH levels

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7
Q

List the adrenal steroids

A
  • Mineralocorticoids
    (aldosterone)
  • Glucocorticoids (cortisol)
  • Adrenal androgens
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8
Q

What are the adrenal disorders

A

Adrenal hyperfunction:

  • Excess cortisol (Cushing’s
    syndrome)
  • Excess aldosterone (e.g.
    Conn’s syndrome)

Adrenal Insufficiency:

  • Hypocortisolism (lack of cortisol)
  • Lack of aldosterone and
    cortisol (Addison’s)
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9
Q

What controls the secretion of aldosterone

A
  • RAAS
  • Increased plasma Potassium concentration
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10
Q

Describe the RAAS pathway (REVISION)

A
  • The macula dense senses perfusion pressure and salt concentrations
  • Juxtaglomerular cells release renin when activated by the macula densa
  • Renin converts angiotensin, made in the liver, to angiotensin 1
  • Angiotensin 1 is converted to angiotensin 2 by ACE
  • Angiotensin 2 causes vasoconstriction and stimulates aldosterone secretion
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11
Q

What activates the RAAS pathway

A
  • Reduced renal perfusion
  • Increased sympathetic activity

Both interpreted as reduced blood volume

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12
Q

What effects will excess aldosterone have on RAAS activation

A
  • Hypertension
  • Hypokalaemia
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13
Q

How can we diagnose aldosterone related diseases

A
  • Measure the plasma aldosterone and renin concentrations and compare the ratio with normal readings
  • High aldosterone: low renin is characteristic of primary aldosteronism
  • High aldosterone: high renin is characteristic of secondary aldosteronism - Renal artery stenosis
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14
Q

What are the main actions of cortisol in the body

A
  • Immunosuppression
  • Maintain BP
  • Promote gluconeogenesis
    Promotes lipolysis
  • Preserves plasma glucose

Excess can cause muscle wastage, hyperglycaemia and hypertension

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15
Q

Describe the Hypothalamic-pituitary-adrenal axis

A
  • The hypothalamus secretes CRH and VP which stimulates the pituitary to release ACTH
  • ACTH acts on the adrenal glands to produce androgens and cortisol
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16
Q

Describe the blood cortisol concentration changes over 24hrs in a patient

A
  • Peaks in the morning
  • Lowest at midnight
  • Difficult to measure plasma cortisol levels as it changes frequently over the day
17
Q

What is the most common cause of Cushing’s syndrome

A

Iatrogenic - as a result of medical therapy

  • Exogenous glucocorticoids
    activate cortisol receptor
  • At high doses will shut down HPA
  • Adrenal cortex atrophies with
    lack of ACTH stimulation
  • Several days may be required for adrenal to become responsive to ACTH again

Weaned gradually off glucocorticoid therapy

18
Q

What are the two causes of excess cortisol

A
  • ACTH-secreting pituitary adenoma
  • Ectopic release of ACTH
19
Q

How does ACTH-secreting pituitary adenoma cause excess adrenal gland activity

A
  • The increased ACTH causes excess stimulation of the adrenal cortex which causes excess production of cortisol and androgens
  • The excess cortisol and androgens cause negative feedback on the hypothalamus and pituitary to produce less ACTH
  • However the negative feedback has little effect on the release of ACTH
20
Q

How does Ectopic ACTH cause excess adrenal gland activity

A
  • Ectopic ACTH stimulates the production of cortisol and androgens
  • Negative feedback on the hypothalamus and pituitary causes less ACTH production
  • However, the adrenal cortex responds to the ectopic ACTH and not the pituitary ACTH
21
Q

How can we do a differential diagnosis for Cushing’s syndrome

A
  • Test plasma cortisol concentrations at times we know what value it should be
  • 24-hour urine sample analysis and compare to reference values
  • Dexamethasone suppression test
22
Q

Describe how the dexamethasone suppression test works

A
  • Administer the glucocorticoid dexamethasone in patients and test cortisol concentration
  • Normally expect cortisol to be suppressed in the morning but not in cushing’s
  • Repeat with a high dose of dexamethasone for 4 days
  • Suppression at 2nd or 3rd days if from adrenal gland
  • If no suppression it is ectopic
23
Q

Describe primary adrenal insufficiencies

A
  • Addison’s disease
  • Insufficient cortisol and aldosterone
  • Inappropriate VP levels
24
Q

Describe secondary adrenal insufficiencies

A
  • Pituitary or hypothalamic disease
  • Insufficient cortisol
  • Inappropriate VP levels
25
Q

What are the clinal features of Addison’s disease

A
  • Hypotension
  • Plasma sodium concentration: low to high - Increased ADH and water excretion
  • Plasma potassium concentration: normal to high - Decreased aldosterone
  • High ACTH - decreased aldosterone and increased negative feedback
  • Elevated plasma renin - decreased kidney perfusion
26
Q

What are the signs and symptoms of Addison’s disease

A
  • Anorexia
  • Weakened/ fatigue
  • Hyperpigmentation
  • GI symptoms
27
Q

How can we diagnose Addison’s disease

A
  • Dynamic ACTH stimulation test
27
Q

What is the dynamic ACTH stimulation test

A

Short synacthen test:

  • Measure baseline cortisol (9am) and 30 min after 250 µg synacthen (synthetic ACTH) i.m.
  • Adrenal insufficiency is excluded by an increase in cortisol of >200 nmol/L and/or a 30 min
    value >550
    Long synacthen test:
  • Adrenal cortex ‘shuts down’ in absence of stimulation by ACTH – time needed to regain
    responsiveness
  • 3-day stimulation with synacthen
  • In secondary (but not primary) adrenal insufficiency cortisol increases by >200 nmol/L
    over baseline
  • Long test not often necessary since ACTH assay can distinguish

Molecular Basis of Disease - SGUL (Sem 4) (29 decks)

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