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Endocrinology > Pituitary and Adrenal > Flashcards

Pituitary and Adrenal Flashcards

1
Q

Cell types and associated hormone in the anterior pit?

A

Corticotropphs - ACTH
Thyrotrophs - TSH
Somatotrophs - GH
Lactotroph - prolactin
gonadotroph - LH and FSH

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2
Q

hormones released by post pit? Where are these chemicals synthesized

A

ADH
Oxytocin

Cell bodies are in the hypothalamus

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3
Q

How is ADH release normally controlled (ie day to day)?

A

Hyperosmolality which is seen through the shrinkage of the neuro body in hte hypothal is the normal stimulus for ADH release
- In emergency (ie volume loss) hypovolaemia is sense through the arterial circulation and results in ADH release

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4
Q

2 actions of ADH? How?

A

vasocontriction
Water retention:
- Upregulation of aquaporins on the principle cells of the collecting ducts via binding to the V2 receptor

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5
Q

What are the differentials for polydipsia-polyuiria syndrome?

A

Central and nephrogenic DI
Primary polydipsia
- psychogenic polydipsia

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6
Q

How to distinguish between primary polydipsia and diabetes insipidus? Then how can nephrogenic DI and central DI be distinguished?
Explain these tests?

A

Water deprivation test - ? PP vs DI
Desmopressin injection - ? central DI vs nephrogenic DI

Water deprivation test:
- 17hr water deprivation usually from midnight of 0600hrs
- Collect urine throughout (every 2hrs)
- Measure body weight vital every 2 hrs
- Stop test and Ix for DI if:
-> Na >150
-> develops sx of hypovolaemia
-> Decrease body weigh >3%
- If urine is concerntrated >800mmosl/L then = PP. If remains not concerntrated = DI (do desmopressin test)

Desmopressive (DDAVP) test:
- CEntral DI - DDAVP works
- Nephrogenic DI - no response to DI

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7
Q

Causes of central DI?

A

Primary
- Idiopathic
- Genetic conditions (rare)

Secondary
- Trauma (head injury, post trauma)
- Cancer
- Inflamatory and infiltrative (sarcoidosis etc)
- Vascular (sheehans syndrome, aneurysm, infarction)
- Preg

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8
Q

Treatment of central DI?

A

DDAVP administration
- several routes of administration based on requirment

Pt needs to have weekly time of DDAVP to prevent hyponatraemia (ie mimicing SIADH)

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9
Q

What is the opposite condition to DI?

A

SIADH

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10
Q

Essential fatures of SIADH?

A

Urine osmol >100 despite serum osmol <275
Clinically euvolaemic
Urinary Na >40 with normal diet Na
Normal adrenal and thyroid function
No recent use of diuretic agents

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11
Q

Treatment of SIADH?

A

Water restriction
Vaptans less so

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12
Q

Pituitary panel involves what? At what time of day should this be ordered?

A

ACTH / corticsol
TSH / FT4 / FT3
Prolactin
IGF-1
LH / FSH testosterone / SHBG / FAI
OR if female:
LH / FSH / Oestradiol / Progesterone / SHBG

Order in early AM ie 0600hrs

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13
Q

What conditions is the insulin tolerance test used to work up?

Explain how this works?

A

GH deficiency
ACTH / Cortisol production (eh adisons disease)

Insulin tolerance test
- this is a physiological stress test that involves inducing hypoglycaemia to assess teh stress response, specifically the ACTH / cortisol release and the GH release
- Glycagon and adrenaline occur earlier, then when BSL <3 cortisol increases
- Aim to get BSL to 2.5 with insulin and measure ACTH / cortisol/ GH

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14
Q

Main dynamic tests for investigating GH deficiency?

A

Insulin tolerance test
GnRH + Arginine test
Glucagon test

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15
Q

What is the better test to confirm DI vs PP compared to the prievious gold standard water deprivation test?

A

Hypertonic saline challenge
- 250ml 3% NaCl given, then infusion continued after
- Aim to reach Na 150
- Take blood for copeptin, This is like C peptide for insulin (product of endogenous ADH production)
- Once reached pt is allowed to drink and given glucose IV to bring Na back to normal

Interpretation
- copeptin will not increase in true central DI, but will increase in PP

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16
Q

Classification of pit adenoma?

A

Macro >1cm
Micro <1cm

Functioning vs non functioning

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17
Q

Most common cell type and hormone implicated in pit adenoma?

A

Lactotrophs, prolactin

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18
Q

Genetic syndrome associated with piutuitary adenoma?

A

MEN 1
- 3x Ps = pituitary, parathyroid, pancreas

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19
Q

Main complication with non secreting / non functional pituitary adenomas?

A

Mass effect
- press on optic chiasm -> visual distirbance
- Headache
- Pituitary apoplexy

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20
Q

Treatment of pit adenoma?

A
  • Transphenoid surgery - best
  • Radiation therapy - takes time to work
  • Pituitary directed therapy
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21
Q

When is GH highest (on average)?

A

When sleeping

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22
Q

Basic work up for acromegaly once clinically suspected?

A

serum IGF-1
- Dont measure GH because pulsitile
- If high then do OGTT

OGTT for diagnosis

23
Q

Most common cause of acromegally?

A

Pit adenoma
- very rarely caused by secretion from pancreatic cancer / NET

24
Q

Features of acromegally?

A

Local pit effects
- Sx associateds with Pit adenoma

Socamtic systems:
- SOft tissue swelling of hands and feet
- Enlarged Jaw with spaced teeth
- Hypertrophy of frontal bones
- Arthralgias and arthritis
- Carpel tunnel syndrome

OSA
Organomegally
Cardiovascular effects

25
Q

Managment of acromegally?

A

Surgery is best treatment

If cant get rid of all of the tumour then medical therapy is indicated
- dopamine agonist (cabergoline)
- Somatostain anologue (Lanreotide, ocreotide, pasireotide) - reduce secretion GH
- GH receptor antagonist (pegvisomant)

26
Q

What are the specific signs of cushing syndrome?

A

Facial plethora
Weakness, proximal myopathy
easy bruisability
Coloured striae

Unfortunately these are not very common
the non specific signs are much more common

27
Q

Causes of ATCH dependant cushings syndrome?

Causes of ACTH independant cushgings syndrome?

A

Usually pituitary adenoma (cushings disease)
May be ectopic ACTH sectretion (ie SCLC)

Mainly adrenal adenoma, unilateral or bilateral

28
Q

3x different screening options for cushings syndrome?

A

Overnight 1mg dex suppresion test
Late night 11pm salivary cortisol
24hr Urine free cortisol

Generally the 1mg dex suppresion test is best but all are efficacious but some are harder to do

29
Q

Explain how the 1mg dex suppression test is done?

Explain the interpretation of the 1mg dex suppression test?

A

Give dex 2mg PO stat at 23-2400hrs
Take bloods at 0800hrs the next day
- Cortisol should be low, if it is not then this indicates cushings syndreme but does not distinguish between the different types of cushings syndrome

In cushings disease
- Pit making more ACTH
- Dex given, acts on hypoT and pit
- Low dose dex dose doesnt suppress abnormal Pit ACTH, therfore cortisol remains high

In Adrenal cushings syndrome:
- Adrenal making more cortisol
- Dex given, acts on hypoT and pit
- Pit and hypoT already suppressed
- Adrenals continue making cortisol (not suppressed)

Ectopic ACTH cushings:
- Cancer making ACTH
- Dex given, acts on hypoT and pit
- Pit and hypoT already supressed
- Adrenals continue making cortisol in response to ectopic ACTH
- Cortisol not suppressed

Ectopic CRH cushings:
- Cancer making CRH, stimulating Pit at normal level to make ACTH (ie Pit basically sees cancer as the normal hypothalamus)
- Dex given, acts on hypoT and pit
- Supresses Pit production of ACTH
- Cortisol decreased

30
Q

Explain the interpretation of the high dose dex suppression test?

A

If enough Dex given, will supress abnormal ACTH from pituitary (ie cushings disease), but will not suppres ACTH from ectopic

Therefore if cortisol decreased then cushings disease
If not decreased then ectopic ACTH production

31
Q

Treatment of cushing’s disease?

A

Surgery

Medical therapy if surgery cant be done or not successful
- Many medications available (ie ketaconazole)

32
Q

How is prolactin feeback control unique?

A

Hypothal control of prolactin is inhibitory. If hypothal disapears, prolactin will increase
- TOnic dopamineric mediated suppression of release

33
Q

COmmonest cause of prolactin elevation?

A

Drugs
- Antipsychotics
- TCAs
- Antiemetics
- SSRIs
- Opioids

34
Q

Most prolactinomas are macro or micro?

A

Micro

35
Q

which pts with prolactinomas should be trersated?

A

Macro adenoma
Symptomatic

36
Q

Treatment of prolactinoma?

A

NOT surgery, response to medical therapy is good

Cabergoline
Bromocritine

37
Q

Pan hypotpituitarism. What is the correct order to replace hormones in?
Why?

A

Glucocorticoids +/- ADH (ALWAYs replace HPA axis first)
Thyroxine
Gonadal hormoes
Growth hormones

If give thyroxine before replacing cortisol, can precipitate adisonian crisis because the relative increase in thyroid will cause rapid metabolism of the little cortisol remaining

38
Q

Layers of the adrenal cortex superficial to deep and the associated hormone?

A

Glomerulosa -> aldosterone
fasciculata -> Cortisol
Reticularis -> Sex hormones

Adrenal medula (adreneline, noradreneline)

39
Q

How is adrenal insuficiency catagorised? some examples in each catagory?

A

Primary:
- Autoimmune - most common is adisons disease
- Infection
- Malignancy
- Hemorrhage
- Congenital - congenital adrenal hyperplasia
- Drugs

Secondary / tirtiary:
- Pituitary (seondary)
- Hypothal (Tirtiary)

40
Q

How is adrenal insuf confirmed? What is the next test?

A

Low basal cortisol or stimulated cortisol or both

Measure ACTH
- If very high = primary adrenal insuf
- If low = secondary adrenal insuf

41
Q

CLinical presentation and blood test in adrenal insuf?

A

Vague presentation:
- Fatigue
- Generalized weakness
- Slightly low BP with dizziness or postural drop

May seen hyperpigmentation but dependent on time of disease
May seen viteligo

Investigations:
- Hyponatraemia
- Hyperkalaemia
-Hypercalcaemia
-Hypoglycaemia

42
Q

Features of adisonian crisis?

A

Hypotension, syncope
Abdo pain, nausea and vomiting
Pronounced hyponatraemia and hyperkalaemia

43
Q

How is adrenal insuf confirmed?

A

Short synacthen test (synthetic ACTH) if suspect primary
Insulin tolerance test if suspect secondary

44
Q

Treatment of adrenal insuf?

A

GLucocorticoid
Mineralocorticoids
DHEA

If pt adrenal crisis give IV hydrocort 100mg stat
- has mineralocorticoid action at high doses therefore dont worry about fludricortisone in acute setting

45
Q

Potency of these steroids relative to hydrocortisone:
- dex
- Pred
- Methyl pred

A
  • Dex - 25-50x
  • pred - 4x
  • methyl pred - 5x
46
Q

What is congenital adrenal hyperplasia?

A

This is a group of disorder characterised by congenital primary adrenal insuficiency due to loss of function of 1 or more enzymes involved in steroidogenesis

Most common is loss of 21 hydroxylase

47
Q

What does CAH due to 21 hydroxylase deficiency lead to?

A

Low aldosterone
Low cortisol

Increased 12-OH progesterone, shunting towards androgen synthesis leading to virtualization in young female

This is the most common cause of atypical genitalia in 46 XX infants

48
Q

Mother is carrier of CAH gene. How can the risk of ambiguous genitalia be reduced?

A

Give dex pre natally
supress adrenal shunting towards androgens

49
Q

What is primary aldosteronism? how is it detected and what is the confirmatory testing?

A

AKA conn’s syndrome
- One of the main causes of secondary hypertension

Aldosteroine renin ratio will be high, renin low, aldo high
- Note hypokalaemia is not always a feature

Confirmatory testing:
- Saline load test
- Adrenal vein sampling

50
Q

Blood pressure med effects on aldosterone renin ratio?
what are teh only BP meds that can be used for the “cleanest” RAR test?

A

BB -> false positive
Other BP medications (including ACEI) -> false negative

Verapamil
Peripheral dilator ie prazocin, moxonidine, hydralazine etc

51
Q

Commonest form of primary aldosteronism?

A

Bilateral idiopathic hyperplasia 60%
Unilateral adenoma 30%

52
Q

Classic triad of phaeochromocytoma?

A

Headache
hypertension (sustained or paroxysmal)
Sweating

Also related to takotsubo cardiomyopathy

53
Q

Tests for phaeochromocytoma? bloods and imaging?

A

Metanephrines and normetanephrine
Dotatate PET

54
Q

What medications and what order for pre op preperation for phaechromocytoma?

A

Alpha blockade FIRST
Beta blockade

Dont beta blockade first because can cause hypertensive crisis due to unopposed alpha activation

Endocrinology (4 decks)

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