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Endocrinology > Adrenal Glands > Flashcards

Adrenal Glands Flashcards

General Info and Diseases/Syndromes

1
Q

What are the diseases that cause adrenal HYPERfunction?

A

Cushing’s, Conn’s, and Phaeochromocytoma

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2
Q

Cushing’s: What hormone(s) are affected in Cushing’s?

A

Mostly cortisol (raised), but could also have raised mineralocorticoids and androgens

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3
Q

Cushing’s: What are the symptoms of Cushing’s?

A

Moon face, central obesity, purple striae, easy bruising, thinning of skin, glucose intolerance, pigmentation, hirsutism, hypertension, infertility, abnormal menstruation, acne, buffalo hump

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4
Q

Cushing’s: What are the causes of Cushing’s?

A

Pituitary tumor, Adrenal tumor, Ectopic ACTH, or drug treatment (most common)

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5
Q

Cushing’s: What are some facts about PseudoCushing’s?

A

It’s much more common than actual Cushing’s. It’s associated with alcoholism, obesity and depression. Patients will appear Cushingoid, even with biochemical evidence

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6
Q

Cushing’s: What are the 4 initial screening tests and what results are we looking for?

A

1) 24h Urinary Free Cortisol
2) Late Night Salivary Cortisol
Is cortisol elevated in these? ^^^
3) Overnight Dexamethasone Suppression Test
4) Low Dose Dexamethasone Test
>50 nmol/L suggests cortisol is not being supressed ^^^

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7
Q

Cushing’s: After the patient resulted positive for Cushing’s after the initial screening, what’s the next step?

A

Fully check if the patient is not on any glucocorticoids (often missed in skin creams, herbal medications and joint injections)

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8
Q

Cushing’s: What test can be used to differentiate Cushing’s from Pseudocushing’s and what’s it based on?

A

Insulin Stress Test (IST). It looks for cortisol response to hypoglycemia (hypoglycemia should stimulate cortisol release). Pseudocushing’s patients respond normally while Cushing’s patients don’t

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9
Q

Cushing’s: Once it’s confirmed, what are the 5 tests that are done to know the cause of Cushing’s (In order)?

A

1) ACTH levels
2) High Dose DST
3) CRH levels
4) Inferior Petrosal Sinus Sampling (IPSS)
5) Imaging studies

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10
Q

Cushing’s: What do ACTH levels mean in terms of Cushing’s cause and why?

A

1) Low ACTH = Likely Adrenal cause. ACTH is being produced normally, but being totally consumed by the overly-demanding adrenals to make cortisol.
2) Normal/High ACTH = Likely Ectopic or Pituitary. The adrenals are working as they should, but it’s the pituitary or ectopic tumor producing too much ACHT, thus, too much cortisol

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11
Q

Cushing’s: What do the High Dose DST results suggest?

A

If there’s >50% suppression of cortisol, it’s Pituitary.
If not, it’s Ectopic or Adrenal

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12
Q

Cushing’s: What do the CRH test results suggest?

A

An increase of ACHT indicate Pituitary Cushing’s.
Ectopic and Adrenal Cushing’s won’t respond

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13
Q

Cushing’s: What do the IPSS suggest?

A

If the ACTH levels obtained from one of the pituitary samples is >3x the levels of the peripheral sample, it’s Pituitary. If the tumor is in one side of the Pituitary, the side with the tumor is on while the other is switched off

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14
Q

Cushing’s: What are the different imaging techniques used for diagnosis?

A

Chest x-rays, pituitary and abdominal CT scanning

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15
Q

Cushing’s: How do you manage Cushing’s?

A

Depends on the cause. Surgery to remove the tumors or the glands and provide replacement therapy. If surgery is not an option, drugs to block cortisol synthesis

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16
Q

Conn’s: What hormone(s) are affected?

A

Overproduction of Aldosterone

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17
Q

Conn’s: What’s another name for Conn’s?

A

Primary Hyperaldosteronism

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18
Q

Conn’s: What happens when there’s an aldosterone excess?

A

Too much aldosterone will cause excessive Na reabsorption in the DTs, which means excessive water reabsorption (causes hypertension). Potassium is also dumped out.

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19
Q

Conn’s: What are the symptoms?

A

-Hypertension that doesn’t respond well to treatments
-Electrolyte imbalances like hypokalemia
-Headaches
-Muscle aches/cramps
-Polyuria/Nocturia
-Family history of Conn’s

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20
Q

Conn’s: How do you screen for Conn’s? And what affects this screening test?

A

Aldosterone:Renin Ratio (ARR)
It’s affected by posture, meds, salt intake, etc.

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21
Q

Conn’s: What prep does the patient have to do before an ARR?

A

-Stop taking interfering meds for >2 weeks and >4 if taking Spironolactone and other diuretics
-Replace HTN drugs with others that won’t interfere with ARR
-Correct for severe hypokalemia (<3 mmol/L) since it’ll reduce aldosterone production

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22
Q

Conn’s: How is the blood taken in an ARR?

A

Patient must be upright for >2h then sitting for 15min

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23
Q

Conn’s: How to interpret ARR?

A

If the adrenals have escaped renin’s control, consider factors that might have affected the test ad repeat for confirmation

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24
Q

Conn’s: How do you confirm Conn’s?

A

If the adrenals have escaped renin’s control, making excessive aldosterone regardless of renin’s levels, suppressing renin shouldn’t affect aldosterone secretion

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25
Q

Conn’s: Confirmation of Conn’s: What are the 3 ways to suppress renin?

A

1) Fludrocortisone Suppression Testing
2) Oral Sodium Loading
3) Saline Infusion

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26
Q

Conn’s: Confirmation of Conn’s: What is some info about Fludrocortisone Suppression Testing?

A

It’s the best but it’s labor intensive.
You administer fludrocortisone and see if aldosterone gets switched off (you have Conn’s if aldosterone isn’t suppressed)

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27
Q

Conn’s: Confirmation of Conn’s: What is some info about Oral Sodium Loading?

A

People prefer this.
Patients eat a bunch of salt, which SHOULD turn off aldosterone. You have Conn’s if it’s not suppressed. Not as sensitive as FST

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28
Q

Conn’s: Confirmation of Conn’s: What is some info about the Saline Infusion Test?

A

-No need for hospitalization. 2L of saline are given i.v. for 4 hours.
-Plasma aldosterone is then measured to see if it was turned off
-HR and BP are measured. Ensure patient is normokalemic
-Plasma Ald <140 pmol/L = PA/Conn’s unlikely
-Plasma Ald >277 pmol/L = PA/Conn’s Likely
-Plasma Ald 140-277 pmol/L = Review new cut-offs with other assays

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29
Q

Conn’s: Confirmation of Conn’s: What’s something important to have in mind when confirming Conn’s?

A

The confirmation tests are based on renin suppression, so we must confirm that it is actually being suppressed by measuring renin as well. Drugs that overstimulate renin should be avoided

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30
Q

Conn’s: What are the main 4 subtypes?

A

1) Glucocorticoid Suppressible Aldosteronism (rare)
2) Adrenal Cortical Hyperplasia
3) Adrenal adenoma
4) Adrenal carcinoma (rare)

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31
Q

Conn’s: What are the 3 important questions you ask when a patient is confirmed for Conn’s?

A

1) Is it GSA?
2) Is it bilateral or unilateral?
3) Is there a mass larger than 2.5cm?

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32
Q

Conn’s: Is it GSA? Provide information about this disease

A

-Glucocorticoid Suppressible Aldosteronism.
-Autosomal dominant inheritance
-Rare condition in which aldosterone is regulated by ACHT
-Dexamethasone treatment is given to suppress aldosterone
-If identified, all family needs screening

Dex = Cortisol. High cortisol will inhibit production of ACTH, thus, aldosterone in GSA

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33
Q

Conn’s: Is it Unilateral or Bilateral? Provide information about this case

A

-You need Adrenal Venous Sampling (AVS) to confirm it
-AVS requires skill to perform
-Confirm samples are actually from the Adrenal glands (Adrenal cortisol is >3x higher than peripheral cortisol)
-AVS helps telling if excess Aldosterone is coming from one or both sides of the adrenals

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34
Q

Conn’s: Is there a mass >2.5 cm? What do you do if there is?

A

-You remove it due to its high risk of malignancy

35
Q

Conn’s: How do you treat it?

A

-Unilateral adrenalectomy (cures ~50% of the cases and improves the remainder)
-Spironolactone or amiloride can antagonize aldosterone if surgery isn’t an option.
-For GSA patients, low dose glucocorticoids

36
Q

Conn’s: How does the usual follow-up look like?

A

-BP might not go back to normal, there might be other factors involved
-If on drug treatments, wait for a few months for the corrections to happen
-Renin should rise to normal levels but it takes time

37
Q

CAH: What’s CAH?

A

-Congenital Adrenal Hyperplasia
-Adrenal Hyper and Hypo function
-Group of autosomal recessive disorders
-Deficiency of any of the 5 enzymes involved in the synthesis of cortisol
-Most common is 21-Hydroxylase deficiency (90-95%)

38
Q

CAH: What hormones are affected and what does that entail?

A

-Low cortisol since it can’t be synthesized
-There’s a failure on the feedback mechanism
-Increased hypothalamic and pituitary activity (increased ACTH, no feedback loop)
-Increased adrenal cortex stimulation
-There’s a buildup of precursors and diversion towards production of androgens

39
Q

CAH: What are the clinical manifestations?

A

-Wide and varied
-Severe salt-losing states
-Virilization of females
-Acne
-Asymptomatic

40
Q

CAH: What are the two classes of CAH?

A

Classic (severe) and Non-Classic (mild)

41
Q

CAH: What hormones are altered in Classic CAH and what are its signs?

A

-Cortisol and Aldosterone deficiency
-In girls, clitoromegaly. Affects fertility later
-In boys, penile enlargement and slight hyperpigmentation pigmentation. May later develop benign testicular tumors.

42
Q

CAH: What’s Less Severe Classical CAH?

A

-You have enough aldosterone to maintain Na balance
-Ambiguous genitalia in girls, boys are easily missed
-Males have precocious puberty or short stature

43
Q

CAH: What hormones are altered in Non-Classic CAH and what are its signs?

A

-Normal Aldosterone and Cortisol levels
-Adrenal Androgens have a mild increase
-Most are missed if you don’t screen for it
-Many don’t show any abnormalities

44
Q

CAH: How do you diagnose CAH?

A

-Short Synacthen Test (SST): 250 ng Synacthen i.m. or i.v.
-Basal and 60 min 17-OHP lvls: Rise of >8 nmol/L raises suspicion. Rise of >30 nmol/L confirms CAH
-Urine Steroid Profiling: 24h Urine collection. All adrenal hormones measured using mass spec. Useful for rare forms of CAH

-21-Hydroxylase deficiency shows 17-OH Progesterone (17-OHP) buildup
-Basal lvls of 17-OHP may be 100x higher than normal in newborns

45
Q

CAH: What are the treament aims in CAH?

A

For kids: Prevent salt-loss and virilization. Achieve normal puberty and stature
For adults: Normal fertility and reduce risks from long-term glucocorticoid use

46
Q

CAH: How do you treat it?

A

-With Glucocorticoids: Long-term. Inhibits CRH and ACTH release, so androgen production is reduced. In adults, Prednisolone or Dex. In kids, Hydrocortisone (shorter t1/2)
-With mineralocorticoids: Infants with salt-losing CAH need Fludrocortisone and NaCl. As they grow they might stop treatment.

47
Q

Addison’s: What are the symptoms?

A

Common
* Tiredness
* Lethargy
* Anorexia
* Nausea/Vomiting
* Weight loss
* Postural Hypotension
* Pigmentation (Bronzing of hand stripes and buccal tissue)
* Loss of body hair in women
Uncommon
* Hypoglycemia
* Depression

48
Q

Addison’s: What are the causes?

A

Common
* Withdrawal of glucocorticoid treatment
* Autoimmune adrenalitis
* TB
Uncommon
* Adrenalectomy
* Secondary tumor deposits
* Amyloidosis
* Haemochromatosis
* Adrenal hemorrage

49
Q

Addison’s: Causes of adrenal hypofunction?

A
  1. Withdrawal of glucocorticoid treatment or not increasing dose when under stress
  2. Hypothalamic-Pituitary-Adrenal axis is suppressed and can’t respond
50
Q

Addison’s: Primary Adrenal Failure: How fast does it develop?

A

Often slow
But it can happen acutely due to infection, trauma or injury
You could have an adrenal crisis: Severe hypovolemia, shock and hypotension

51
Q

Addison’s: Secondary Adrenal Failure: What are its characteristics?

A
  • No pigmentation
  • Lack of ACTH stimulation
  • Hypotension and hyponatremia
  • Lack of cortisol reduced sensitivity of arteries to catelocholamines and reduced ability to excrete water

Most cases are ACTH = Pigmentation, so no ACTH = No pigmentation

52
Q

Addison’s: How do you diagnose it?

A
  • 9:00am cortisol of <100 nmol/L usually indicates adrenal hypofunction
  • 9:00am cortisol of >500 nmol/L excludes adrenal hypofunction
  • Short Synacthen Test (SST): Synacthen behaves like ACTH, it stimulates cortisol release. Give 250ng synacthen and expect a rise of >500nmol/L for a normal result.
53
Q

Addison’s: How do you distinguish from primary and secondary adrenal hypofunction?

A
  • You may or not have pigmentation for primary, but secondary will NEVER have pigmentation.
  • If 9am ACTH are low/normal, it’s secondary. If High, it’s primary
  • Or do a Long Synacthen Test (LST)
54
Q

Addison’s: How do you treat an acute presentation?

A
  • i.v. of hydrocortsione and fluids
  • Monitor plasma K and glucose, as i.v. dextrose might be needed
55
Q

Addison’s: How do you treat a long-term presentation?

A
  • Life-long therapy and follow-up
  • Hydrocortisone and 9a-fludrocortisone
  • Doses should be increased during periods of stress (trauma, illness, surgery, etc)
56
Q

What are the 2 parts of the adrenals and what do they make?

A

-Adrenal Cortex: Essential. Minearlocorticoids, Glucocorticoids and Adrenal Androgens
-Adrenal Medulla: Not essential. Catecholamines (e.g. Adrenaline)

57
Q

What are some glucocorticoids?

A

Cortisol, ACTH, CRH.

58
Q

What are the functions of cortisol and how is it controlled?

A

-Controls sugar levels in blood (can increase sugar through gluconeogenesis [lipid/protein breakdown])
-Stims bone resorption
-Controls BP
-Reduces inflammation (Suppresses lymphocyte production)
-Also has mineralocorticoid functions: Promote Na+ reabsorption just like Aldosterone

-Excercise or stress increases cortisol production and release.
-Peak cortisol release is in the morning
-Cortisol release is controlled by ACTH. When there’s too much cortisol, CRH and ACTH synthesis is inhibited.

59
Q

What’s the main mineralocorticoid and what’s its role?

A

Aldosterone
-It increases Na+ reabsorption in the DTs by exchanging Na+ for K+ or H+
-Controls K+ excretion through this mechanism
-Na+ reabsorption drives water reabsorption, which increases blood volume and pressure as well as ECF

60
Q

How does the release of aldosterone get stimulated?

A

-Juxtaglomerular cells release Renin in response to a drop in BP (Kidney releases Renin)
-Renin converts Angiotensinogen into Angiotensin I
-Angiotensin I travels to the lungs to be converted into Angiotensin II by ACE
-Angiotensin II then acts on the adrenal glands to release Aldosterone
-Angiotensin II also directly increases BP

61
Q

What are some Adrenal Androgens and some of their functions?

A

-DHEA, DHEAS, and Androstenedione
-Stimulate libido, pubic hair and axillary hair growth

In males they’re not as important as Testosterone is stronger

62
Q

Addison’s disease is also called:

A

Primary Adrenal Hypofunction

63
Q
A
64
Q

Conn’s: What happens to Aldosterone control in Conn’s?

A

It becomes independent from Na+ status and Angiotensin II stimulation. It’s not suppressed by sodium loading.

65
Q

Conn’s: What are some causes for Conn’s?

A

Aldosterone-producing Adenomas and Bilateral Idiopathic Hyperaldosteronism

66
Q

What kind of hormone is Cortisol and where does it come from? Is it water or fat soluble and what does it entail?

A

-Glucocorticoid steroid hormone. Made from cholesterol in the adrenal cortex
-It’s fat soluble, so it affects almost every organ

67
Q

What are some facts about HTN?

A

-Called “silent killer”
-1/2 patients go undiagnosed
-Affects 30-40% of population
-Higher the BP, higher the risk of vascular and kidney disease
-Major risk for premature CDV disease, renal diseases and strokes

68
Q

What’s important for HTN Dx?

A

-Measure BP correctly
-Assess clinical history, diet, lifestyle, family history
-Clinical evaluation used to establish cause, severity and risk

69
Q

What 3 roles do biochemical tests play in Dx of HTN?

A
  1. Assess additional risk factors of vascular and renal diseases
  2. Target organ dmg
  3. ID of secondary (endocrine) causes, like Cushing’s, Conn’s or Phaeo/PGL
70
Q

What are the 2 types of HTN and what are they about?

A

-Primary HTN (85%): Essential/idiopathic HTN. Multifactorial, genes, lifestyle, and diet play a role. Tx is pharmacological/non-pharmacological
-Secondary HTN (15%): In chidren w HTN, 50% have secondary. In young adults 30%. Renal and endocrine causes

71
Q

What biochemical tests are needed for inital evaluation of Primary HTN?

A
  • Renal profile
  • Glucose/Hba1c
  • Full lipid profile
  • GGT and TFT
72
Q

What are the 2 uses of biochemical tests in Primary HTN?

A
  1. Monitor organ dmg
  2. Allows ID of dyslipidemia, glucose intolerance for CDV stratification
    Biochem tests can’t find cause
73
Q

What are some endocrine causes of Secondary HTN?

A

Adrenal Causes:
* Conn’s/Primary Hyperaldosteronism
* Cushing’s
* Phaeo/Paraganglioma

74
Q

What are some non-endocrine causes of Secondary HTN?

A
  • Obstructive Sleep Apnea
  • Renal disease - Polycystic kidneay disease and renal artery stenosis
75
Q

What signs/symptoms indicate Secondary HTN?

A
  • Developing HTN outside the age range for Primary HTN
  • Sudden onset or worsening of HTN
  • BP that responds poorly to Tx
  • Organ dmg disproportionate to duration of HTN
  • Low K+ or clinical indication (e.g. Cushingoid features) of a Secondary cause
  • Grade 3 HTN
76
Q

What are Catecholamines and what are their functions?

A

Adrenal Hormones: Norepinephrine and epinephrine. Psychological changes that prepare body for action (Fight/Flight). Increase heart rate, BP, blood gluc
Neurotransmitters: Dopamine and norepinephrine. Sleep and motor function

77
Q

What is Phaeochromocytoma and Paraganglioma

A

Rare neuroendocrine tumours.
They produce catecholamines like Epinephrine and Norepinephrine

78
Q

Where do Phaeo and PGL originate from?

A
  • Phaeo: Adrenal Medulla
  • PGL: Anywhere w sympatheric or parasympathetic nerve cells (thorax, abdomen, pelvis and neck/base of skull respectively)
79
Q

What are some symptoms of PGL?

A
  • Palpitations
  • HTN
  • Sweationg
  • Headaches
  • Pallor
  • Weight loss
  • Visual disturbance
80
Q

What tests are done to Dx PGL and Phaeo?

A
  • Historically, urine Catecholamines
  • Urinary and plasma metanephrines (breakdown products of catcholamines)
  • Gold standard is LC-MS/MS
81
Q

For Phaeo/PGL, what’s the use for LC-MS/MS?

A
  • It’s the gold standard for Dx
  • Recently introduced new biomarker 3MT
  • Can improve accuracy in ID malignancy in PGL and can ID hereditary causes (SDHB mutations)
82
Q

What is the role of genetic testing in PGL?

A
  • 40% PGL is genetic
  • 18 genes ID
  • Hereditary PGL has distinct phenotypic characteristics
83
Q

What are some Non-Adrenal Endocrine causes for HTN and what biochem test are done?

A
  • Acromegaly: IGF-1 and failure of GH to suppress in response to a oGTT
  • Thyroid (hyper/hypo): TFT’s
  • Hyperpatarhyroidism: PTH and bone profile

Endocrinology (4 decks)

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