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Blwyddyn 1; Tymor 3 > 128; Adrenal Endocrine > Flashcards

128; Adrenal Endocrine Flashcards

1
Q

What is Cushing’s syndrome?

A

The clinical state of increased free circulating glucocorticoid.

Often due to administration of synthetic steroids or ACTH

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2
Q

What is Cushing’s disease?

A

Increased circulating ACTH from the pituitary

(65% of cases)

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3
Q

What causes Cushing’s syndrome?

A

ACTH dependent

  • Increased ACTH secretion from pituitary (Cushing’s disease)
  • Increased ACTH from an ectopic tumour
  • ACTH administration

Non ACTH dependent

  • Adrenal adenomas
  • Adrenal carcinomas
  • Glucocorticoid administration

Other causes

  • Alcohol induced pseudo-Cushing’s syndrome
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4
Q

From where is ACTH released?

A

The anterior pituitary gland

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5
Q

What is the role of ACTH?

A

Stimulates secretion of Glucocorticoids from the adrenal gland. ee Cortisol, Corticosterone

(From the Zona fesciculata)

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6
Q

What are the signs and symptoms of Cushing’s disease?

A

Symptoms

  • Central weight gain
  • Depression
  • Insomnia
  • Amenorrhoea/oligomenorrhoea
  • Thin skin/easily bruised

Signs

  • Moon face
  • Hersutism
  • Acne
  • *Thin skin & bruising
  • *Hypertension
  • *Pathological fractures (vertebrae & ribs)
  • Central obesity % striae
  • *Proximal myopathy
  • Oedema
  • *Striae
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7
Q

What investigations should be arranged to diagnose Cushing’s Syndrome?

A

Confirmation requires demonstration of inappropriate cortisol secretion, which is not supressed by exogenous glucocorticoids

  • 48H (or over-night) low does dexamethasone test:
    • A synthetic steroid
    • Normal to supress plasma cortisol to <50nmol/l.
    • Cushing’s ptx fail to do this (259nmol/l)
  • 24H urinary free cortisol measurements
    • Normal values excludes Cushing’s
  • Circadian Cortisol
    • Normal to be low at 2400H
    • Always high in Cusching’s
  • CT Adrenals
  • CT pituitary
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8
Q

How do plasma ACTH concentration measurements at 0900 differe between in the different causes of Cushing’s Syndrome?

A

Cushing’s disease

  • Mid-range; 50-200 ng/l

Adrenal Tumour

  • Very low levels; around 0ng/l

Ectopic ACTH

  • Highest measurement, largest range; 100-4000 ng/l
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9
Q

Briefly outline the cortisol synthetic pathway

A

Cortisol is a steroid hormone, a glucocorticoid, synthesised and released by the zona fesciculata of adrenal gland.

  • Cholesterol –>
  • Pregnenolone –>
  • Progesterone –>
  • 17a- hydroxy progesterone –>
  • 11-deoxy-cortisol –>
  • Cortisol

Synthesis is initiated by ACTH

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10
Q

How is Cushing’s syndrome treated?

A
  • Metyrapone
  • Adrenalectomy surgery

Metyrapone inhibits steroid 11β-hydroxylase, blocks Cortisol synthetic pathway.

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11
Q

How does Metyrapone treat Cushing’s syndrome?

A

Blocks the synthetic pathway od cortisol

Prevents conversion of 11-deoxy-cortisol to cortisol

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12
Q

What is Congenital Adrenal Hyperplasia?

(CAH)

A

Autosomal recessive deficiency of enzymes in the cortisol synthetic pathway.

Most commonly 21-hydroxylase.

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13
Q

What is the most common type of congenita ladrenal hyperplasia?

A

21-hydroxylase deficiency

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14
Q

How does congenital adrenal hyperplasia affect cortisol and ACTH levels?

A

Cortisol levels are low;

Secretion is reduced leading to reduced negative feedback on pituitary —>

Increased ACTH secretion from pituitary

Acts on adrenals causing hyperplasia

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15
Q

How does the increased ACTH levels affect synthesis of other steroid hormones from the adrenals?

A

Steroid precursors of Cortisol diverted into the androgenic precursor pathway

Causing increased:

  • 17-hydroxy progesterone
  • Androstenedione
  • Testosterone

**** Aldosterone **synthesis mey be impaired**

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16
Q

What are the clinical manifestations of Cong. Adre. Hyperplasia?

A

Sexual ambiguity & adrenal failure at birth (if severe)

  • Hypotension, collapse, hypoglycaemia, hyponatraemia

In females; clitoromegaly (signs may be more difficult to notice in males)

Short stature

Precocious puberty & hirsutism

  • Hirsutism befor puberty is a sign of CAH

Later-life presentation; rare, milder

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17
Q

How is CAH treated?

A

Replacement of glucocorticoid activity, and mineralocorticoid deficiency if deficient

  • Fludrocortisone
  • Hydrocortisone
  • Dexamethasone at night to treat adult hirsuritism
  • Corrective surgery

ee Dexomethasone, Oestrogen and Cyproterone

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18
Q

What would be found on investigation of a patient w/ CAH?

A
  • Increased 17-hydroxyprogesterone
  • Increased Urinary Pregnanetriol excretion
  • Raised basal ACTH levels

LH, FSH, testosterone levels normal

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19
Q

What is Addison’s disease?

A

Primary hypoadrenalism

20
Q

Describe the main hormobe levels affected in Addison’s disease

A

A destruction in entire adrenal cortex causes reduction in:

  • Mineralocorticoids (Aldosterone)
  • Glucocorticoids (Cortisol)
  • Androgens (Testosterone)

​

Reduction in Cortisol causes increased CRH & ACTH from pituitary

(CRH; corticotropin-releasing hormone

ACTH; Adrenocorticotropic hormone)

21
Q

List some causes of Addison’s disease

A
  • Autoimmune (90%)
    • Polyendocrine insufficiency syndrome
  • TB
  • Metastatic tumour
  • Lymphoma
  • Amyloidosis
  • Haemochromatosis
  • Bilateral adrenalectomy
  • Adrenal infarction
  • AIDS
22
Q

What is the most common antigen in autoimmune Addison’s?

A

21-hydroxylase

Causes adrenalitis; destruction of adrenal cortex

23
Q

What are the signs and symptoms of Addison’s disease?

A

Symptoms

  • Weight loss
  • Anorexia
  • Fatigue & malaise
  • Amenorrhoa/impotence
  • Syncope from postural hypotension

Signs

  • *Hyperpigmantation; new scars and palmar tissue (because of ACTH)
  • *Postural hypotension
  • Dehydration
  • Loss of hair
24
Q

What investigations are used to diagnose Addison’s?

A
  • U&E
    • HyperKalaemia, HypoNatraemia
  • Random Cortisol measurement
    • <100nmol/l is suggestive
  • 0900 plasma ACTH levels
    • High ACTH and low Cortisol is suggestive
  • Blood glucose
    • Hypoglycaemic
  • Chest/Abdo Xrays
    • Evidence of TB or calcified adrenals
  • Adrenal Antibodies
    • Positive
25
Q

What is the treatmeny for Addison’s disease?

A

Acute hypoadrenalism requires urgent treatment

Similar treatment to Congenital adrenal hypertrophy

  • Replacement Glucocorticoid & Mineralocorticoid

Prior to results; Dexamethasone

Following:

  • Hydrocortisone
  • Fludrocortisone
  • Education; steroid card; medic alert bracelet
26
Q

What are the different types of hypertension?

A
  1. Primary/Essential hypertension (no identifiable cause)
  2. Renal hypertension
  3. Primary Hyperaldosteronism
  4. Rare causes
27
Q

What are the causes of Secondary hypertension?

A

Renal hypertension

  • Renovascular
  • Renal parenchymatous disease
  • Primary reninism

Primary hyperaldosteronism

  • Unilateral adrenal adenoma
  • Bilateral hyperplasia of Zona Glomerulosa

Rare causes

  • Phaeochromocytoma
  • Cushing’s Syndrome
  • Coarctation of the aorta
28
Q

What is Conn’s syndrome?

A

A type of primary hyperaldosteronism;

From an aldosterone-producing tumour

29
Q

What are the characteristic features of Conn’s disease?

(Investigations)

A
  • Hypertension
  • HypoKalaemia
    • & Urinary K+ loss
  • HyperNatraemia
  • Elevated plasma aldosterone:renin activity ratio
  • Elevated plasma Aldosterone levels
  • Decreased plasma Renin levels
30
Q

List the steps that lead to hypertension in primary hyperaldosteronism & Conn’s disease?

A

Adrenal tumour

Increased Aldosterone

  • Sodium retention
  • Potassium lost

Na retention causes

  • Hypertension
  • Renin supression

Decreased levels of Angiotensin II

31
Q

What is the epidemiology of Primary Hyperaldosteronism

A

60% Bilateral adrenal hyperplasia

40% Conn’s disease, adrenal adenoma

_______________________________

5-10% of Hypertensives

More common in young patient w/o FHx of hypertension

More likely to be Conn’s if severe hypertension

32
Q

What investigations are used to diagnose Conn’s disease?

A

Aldosterone:renin ratio

Increased

CT scan adrenals

Adrenal venous sampling

33
Q

What are possible treatments for Conn’s disease?

A
  • Adrenalectomy
  • Low sodium diet
  • Spironolactone
34
Q

What is a Phaeocromocytoma?

A

Tumour of the sympathetic nervous system;

Vast majority occur in the adrenal medulla

80% unilateral adrenal

10% bilateral adrenal

10% extra-adrenal

35
Q

How are hormone levels altered in a person w/ paeochromocytoma?

A

Increased levels of noradrenaline and, to a lesser extent, adrenaline.

36
Q

What are the signs and symptoms of Phaeochromocytoma?

A

Headache

Flank pain

Tachycardia

Hypertension & postural hypotension

Palpitations

Sweating

Hyperglycaemia

37
Q

What investigations are done to investigate Phaeochromocytoma?

A

Blood glucose level

Catecholamines stimulate glycolysis, increased free fatty acids, decreased glucose uptake in tissues.

24H urine catecholamines

2X higher than normal

24H urine adrenaline

Higher than normal

38
Q

What is the management for Phaeochromocytoma?

A
  • ß-blockers, à blockade, high salt diet
  • Adrenalectomy

à blockade prior to ß blockade (starting with ß can cause paradoxical elevation in blood pressure)

Chronic hypertension has reduced the sensitivity of the RAAS pathway leading to decreased Aldosterone –> increased Na excretion –> H2O loss… High salt diet required.

39
Q

What are the common features of phaeochromocytomas?

A

Mainly Right-sided

80% unilateral

10% bilateral

10% extra-renal

10% Malignant

Size is unrelated to symptoms

Malignant if the metastasise to non-chromaffin cells

40
Q

What signs indicate a paheochromocytoma?

A

Hypertension

  • Accelerated
  • Progressive
  • Resistant
  • Paroxysmal (intermittent)
  • In a young person

Paradoxical response to ß-blocker

Family Hx

41
Q

What are the associated symptoms of phaeochromocytoma?

A
  • Multiple Endocrine neoplasio Type1
  • Multiple Endocrine Neoplasia Type 2a & 2b
    • (MEN)
  • Von-Hippel-Lindau syndrome
  • Phakomatoses
  • Neurofibromatosis
42
Q

Summarise the Causes, investigations and treatment of Cushing’s syndrome.

A

Causes:

  • iatrogenic
  • pituitary tumour (ACTH)
  • adrenal tumour
  • ectopic ACTH secretion

Investigations:

  • 9 am cortisol after Dexamethasone at midnight
  • 9 am ACTH
  • 24hr urinary free cortisol
  • Radiology

Treatment:

  • Metyrapone then Pituitary or adrenal surgery
  • Oncology therapy
43
Q

Summarise the Causes, investigations and treatment of Congenital Adrenal Hyperplasia.

A

Causes:

  • 21 hydroxylase deficiency. Most common type, non classic, late onset

Investigation:

  • 17αOH progesterone before and after synacthen

Treatment:

  • Dexamethasone (adults)
  • Cyproterone and oestrogen
  • Fludrocortisone
  • Hydrocortisone (salt wasters)
44
Q

Summarise the Causes, investigations and treatment of Addison’s Disease.

A

Causes:

  • autoimmune
  • TB
  • adrenal infiltration

Investigations:

  • inadequate cortisol response to synacthen
  • elevated ACTH
  • U & Es
  • glucose

Treatment:

  • Hydrocortisone
  • Fludrocortisone
45
Q

Summarise the causes, investigations and treatments of Conn’s syndrome

A

Causes:

  • adrenal hyperplasia
  • adrenal adenoma

Investigations:

  • 9 am rennin (low), aldosterone (high)
  • U & Es
  • CT/MRI/MIBG scan

Treatment:

  • laparoscopic or open adrenalectomy
  • Spironolactone
46
Q

Summarise the causes, investigations and treatments of phaeochromocytoma.

A

Causes:

  • Adrenal tumour
  • 10% of patients extra-adrenal tumour

Investigations:

  • Elevated 24hr urinary catecholamine levels

Treatment:

  • Adrenal surgery after α and ß blockade and high salt diet

Blwyddyn 1; Tymor 3 (13 decks)

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