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Semester 4 > case 9 - endocrinology > Flashcards

case 9 - endocrinology Flashcards

1
Q

what are adrenal hormones all derived from

A

cholesterol

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2
Q

what is DHEA

A

androstenedione - route for sex steroid precursors

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3
Q

what is the main glucocorticoid of the body

A

cortisol

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4
Q

what does over production in the glomerulosa mean

A

mineralocorticoid excess - Conn syndrome

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5
Q

what does over production in the fasiculata mean

A

glucocorticoid excess - Cushing syndrome

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6
Q

what does over production in the reticularis mean

A

excess sex steroid precursors +cortisol due to a tumour

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7
Q

what happens if there is primary underproduction

A

the primary: entire cortex is affected (Addison disease, TB/ HIV)

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8
Q

what happens if there is secondary underpriduction

A

Secondary; hypopituitarism; loss of ACTH I.e aldosterone secretion preserved

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9
Q

what happens if there is disordered production - what is the problem here with

A

Disordered production - problems with the enzymes
congenital adrenal hyperplasia - virtually never cancer

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10
Q

what is cushings syndrome

A

classically thought to be rare
Excessive, inappropriate endogenous cortisol secretion characterised clinically and biochemically by:
Features of glucocorticoid excess
Loss of circadian rhythm to cortisol secretion
Disruption of negative feedback loop

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11
Q

what are the symptom and signs of cushings syndrome

A

Moon face with purplish plethora
*Central obesity, buffalo hump
*Weight Gain
*Hypertension
*Depression/ psychosis
*Diabetes mellitus
*Hypogonadism
*Susceptibility to infection
*Malaise
*Osteoporosis
*Easy bruising
*Striae
*Proximal myopathy
*Poor wound healing

*Hirsuites
*Acne
Symptoms overlapping with PCOS

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12
Q

what can be thought of as antagonistic to insulin

A

cortisol - like glucagon, epinephrine and growth hormones

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13
Q

how does cortisol increase blood glucose levels

A

promotes gluconeogenesis
raises hepatic glucose output
inhibits glucose uptake by muscle and fat

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14
Q

what are the other effects of cortisol

A

lipolysis from adipose tissues
protein catabolism to release amino acids

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15
Q

how is glucocorticoid excess diagnosed

A

Loss of circadian rhythm
random cortisol is no use
Measure bedtime/nighttime serum or salivary cortisol levels

  1. Measure 24 hour urinary free cortisol
  2. If overactivity is suspected; try to suppress it
    • measure cortisol after low dose of dexamethasone
    • 1mg overnight or 0.5mg QID for 8 doses
    • following 9am cortisol should be suppressed (less than 50nmol/L)
  3. Exclude pseudo-Cushing syndrome
    clinical features of Cushing syndrome, which disappears when the underlying cause is resolved
    Common causes alcohol, depression

Glucocorticoid excess / Cushing syndrome diagnosed

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16
Q

what are the two causes of Cushings syndrome

A

adrenal tumour. - ACTH undetectable

distinguishing between ACTH dependent causes

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17
Q

how do you distinguish between ACTH dependent causes

A

Low dose dexamethasone suppression test - diagnose Cushing Syndrome
Inferior petrosal sinus sampling
High-dose dexamethasone suppression test
localise Cushing syndrome
2mg QID (i.e 6 hourly) for 8 doses ending at midnight
Corticotrophin tumour: >50% suppression of following 9am cortical
Ectopic ACTH: <50% suppression of following 9am cortisol

For tumours - adrenalectomy

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18
Q

what is the medical treatment of Cushing Syndrome

A

untreated life expectancy <5 years
Medical
Block production of cortisol (metyrapone…ketoxonazole, mitotane)
pituitary tumours
Trans-sphenoidal hypophysectomy +/- radiotherapy
20-50% may not be permanently cured
May require bilateral adrenalectomy
ectopic ACTH
Usually palliative, surgery, DXT/chemotherapy
adrenal tumours
Adrenalectomy

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19
Q

what is hypoadrenalism

A

rare - 0.8 cases per 100,000
Primary causes
TB/AIDS
Addison disease / autoimmune (T1DM, thyroid disease, PA, vitiligo)
Lymphoma
Metastatic tumour
Intra-adrenal haemorrhage or infarction
Bilateral adrenalectomy
secondary hypoadrenalism comes from pituitary insufficiency

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20
Q

what are the features of hypoadrenalism

A

Clinical features:
Primary hypoadrenalism: lack of cortisol and aldosterone
*Non-specific
*Tiredness
*Weakness
*Nausea & vomiting
*GI disturbance
*Abdominal pain
*Weight loss
*Postural hypotension (supine and erect BP)
*Dizziness
*Fainting
*May present in circulatory failure (‘crisis’)
*Hypoglycaemia

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21
Q

what means primary hypoadrenalism

A

*Hypotensive, hyperkalaemic patient = PRIMARY HYPOADRENALISM

22
Q

what is the diagnosis and treatment of hypoadrenalism

A

if under-activity is suspected; try to stimulate it
Short synacthen test
Give ACTH i.v./I.m. and measure cortisol 30 mins later
If less than 400nmol/L, it is inadequate
treat with hydrocortisone lifelong
10mg on waking, 5mg mid afternoon
Double in significant illness
steroid alert bracelet
Steroid card
May need mineralocorticoid replacement
Fludrocortisone

23
Q

what is endocrine hypertension in the adrenal cortex due to

A

Conn syndrome

24
Q

what is endocrine hypertension in the adrenal medulla due to

A

phaeocromocytoma

25
Q

what is endocrine hypertension

A

hypertension caused by demonstrable hormone excess, which is cured upon normalising circulating levels of the homrone

these patients tend to be younger

26
Q

what do these younger patients have that leads to hypertension

A

renal artery stenosis

coarctation of the aorta

27
Q

what are the hormones that regulate blood pressure, and in excess can elevate it

A

angiotensin II
aldosterone
cortisol
adrenaline and noradrenaline
calcium / PTH
growth hormone

28
Q

what is the body’s major mineralocorticoid

A

aldosterone

29
Q

what does aldosterone do

A

promotes sodium resorption from the urine and potassium excretion

it increases blood pressure

30
Q

what is aldosterone biosynthesis regulated by

A

the RAAS system via a negative feedback loops
serum potassium concentration

31
Q

what is Conn syndrome

A

over production of mineralocorticoid

32
Q

what does mineralocorticoid excess in the glomerulosa cause

A

Conn syndrome

33
Q

what does mineralocorticoid excess in the fasiculata cause

A

Cushing syndrom

34
Q

what is Conn syndrome

A

primary hyperaldosteronism

causes hypertension

35
Q

what can you also have with Conn syndrome

A

hypokalaemia, weakness, lethargy

headaches due to hypertension

36
Q

what are the causes of hypokalaemia

A

vomiting - metabolic acidosis

diarrhoea or other fluid loss

insulin therapy

diuretic use

37
Q

how do spironolactone and eplernone act

A

aldosterone acts on the mineralocorticoid receptor in the distal convoluted tubule

spiralolactone and eplernone are MR angtaonists

38
Q

what is the mechanism of liquorice

A

cortisol will bind to the MR and circulates in much higher concentrations

within the kidney tubule, cortisol is inactivated by cortisone by HSD11B2

this preserves the MR for aldosterone

liquorice inhibits HSD11B2

cortisol continually stimlates the MR

39
Q

what are the catecholamines

A

adrenaline and noradrenaline q

40
Q

where are noradrenaline and adrenaline stored

A

in the cell cytoplasm

41
Q

what are these catecholamines released in response to

A

nervous stimuli - rapidly metabolism in the liver

42
Q

where are catecholamines found

A

adrenal medulla

43
Q

what does overactive catecholamines suggest

A

a tumour called phaeochromocytoma

44
Q

via what receptors do catecholamines act

A

via alpha and beta receptor

45
Q

what do catecholamies do to the brain

A

cause alterness, anxiety and agitiation

46
Q

what do catecholamines do to the eyes

A

dilate the pupils

47
Q

what do catecholamines do to the liver

A

glycogenolysis

48
Q

what do catecholamines do to the lungs

A

bronchodilation

49
Q

what do catecholamines do to the pancreas, kidney and adipose tissue

A

in pancreas, stimulate glucagon and insulin

in kidney, lead to renin release

in adipose, lipolysis

50
Q

what are the classic triad of symptoms of phaeochromocytoma

A

hypertension
throbbing bilateral headaches
paliptations

51
Q

what is one given for phaeochromocytoma

A

administration of a alpha blocker (phenoxybenzamine) and beta blocker - propranolol

52
Q

what are the different types of endocrine neoplasia syndromes

A

*Paraganglioma/phaeochromocytoma syndromes
*MEN2 (type a: thyroid medullary carcinoma, phaeochromocytoma) (type b: as above plus musosal neuromas)
*Von Hippel Lindau syndrome
*Neurofibromatosis

Semester 4 (80 decks)

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