Yr 3 MedEd > Adrenals > Flashcards

Adrenals Flashcards

(36 cards)

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1
Q

What are the zones of the adrenal glands and what is secreted from each area?

A

Cortex:

  • Glomerulosa: Mineralocorticoids
  • Fasciculata- glucocorticoids
  • Reticularis- sex steroids

Medulla: catecholamines: noradrenaline and adrenaline

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2
Q

What is primary hyperaldosteronism?

What happens to Na+ and K+ levels?

A
  • Autonomous aldosterone overproduction from adrenal gland with subsequent suppression of plasma renin activity.
  • Excess Na+ and water retention
  • Increased renal K+ loss: hypokalaemia.
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3
Q

Give 3 causes of primary hyperaldosteronism.

A
  • Adrenal adenoma: Conn’s syndrome- 70%
  • Bilateral adrenal cortex hyperplasia- 30%
  • Familial hyperaldosteronism

Rarely aldosterone producing adrenal carcinoma.

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4
Q

Give the epidemiology of Conn’s syndrome and Bilateral adrenal hyperplasia.

A

Conn’s: young females
BAH: older males

Primary hyperaldosteronism is 1-2% of hypertensive patients

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5
Q

Give 5 symptoms of hypokalaemia (due to primary hyperaldosteronism)

A
  • Headaches, tiredness
  • Polyuria, nocturia
  • Muscle weakness, paraesthesia
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6
Q

Give the main clinical sign of primary hyperaldosteronism.

Give 2 complications of this.

A
  • Hypertension which is difficult to control with antihypertensive medications
  • Complications of hypertension include retinopathy, headaches.
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7
Q

Give 4 investigations for primary hyperaldosteronism.

A
  • Salt loading: failure of aldo suppression post salt load confirms 1’ hyperaldosteronsim
  • Postural test: patient upright for 4 hours: aldosterone adenoma decreases aldosterone production. BAH- adrenals respond to standing posture, increase renin production, leading to increased aldosterone.
  • Fludrocortisone suppression test
  • Bilateral adrenal vein catheterisation- elevated aldo in 1 vein indicates Conn’s (lateralisation). BAH is bilateral.
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8
Q

Give management for adrenal adenoma.

Give management for Bilateral adrenal hyperplasia.

A

Adrenalectomy- laproscopic.

BAH/ non-surgical candidates-

  • Spironolactone (aldosterone inhibitor)- eplerenone if side effects not tolerated.
  • Monitor K+, creatinine and BP.

Spironolactone side effects: gynaecomastia, impotence, muscle cramps

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9
Q

Give most common cause of exogenous Cushing’s syndrome.

Give 2 endogenous types of Cushing’s syndrome.

A

Exogenous: steroid exposure is most common cause.
Endogenous:
- ACTH- dependent (80%):
Excess ACTH from pituitary adenoma- Cushing’s disease.
Ectopic ACTH: e.g. lung tumour, pulmonary carcinoid tumour.

  • ACTH- independent (20%):
    Benign adrenal adenoma
    Bilateral adrenal hyperplasia
    Adrenal carcinoma: rare.
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10
Q

Give the epidemiology of Cushing’s syndrome for gender and age.

A

W:M 4:1

Age 20-40.

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11
Q

Give as many signs of Cushing’s syndrome as you can (11).

A
  • Moon face + facial plethora
  • Interscapular fat pad- “buffalo hump”
  • Proximal muscle weakness
  • Central obesity
  • Pink/ purple stripe on abdomen/ breast/ thighs
  • Easy bruising
  • Kyphosis due to vertebral fracture
  • Fractures
  • Hypertension
  • Ankle oedema: water retention from mineralocorticoid effect of excess cortisol
  • Pigmentation in ACTH dependent cases
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12
Q

Give 2 first line high sensitivity tests for patients with a high-pre test probability for Cushing’s syndrome.

Give 2 investigations for differential diagnoses.

A

Overnight dexamethasone suppression test- dex at 11pm, measure cortisol at 8 am.
Low dose dexamethasone suppression test: small doses every 6 hours for 48 hours. Cortisol at 9am, 6 hrs after last dose.

Positive test is morning cortisol >50nanomol/L

  • Serum glucose- high risk diabetes
  • Pregnancy test
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13
Q

Give 4 tests to identify ACTH dependent Cushing’s syndrome

A
  • Plasma ACTH
  • Pituitary MRI
  • High dose dex supp. test: differentiates CD and CS
  • Inferior petrosal sinus sampling: test for ACTH conc. leaving sinus. > 2x baseline conc. = pituitary cause.
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14
Q

What is the medical treatment for Cushing’s syndrome?
What is the preferred treatment for Cushing’s syndrome?
What is treatment for persistent post-operative high cortisol?
What is Nelson’s syndrome?

A
  • Metyrapone/ ketoconazole: inhibit cortisol synth.
  • Surgical is preferred treatment.
    Trans-sphenoidal resection of adenoma or surgery to remove adrenal adenoma/ carcinoma or ectopic ACTH.
  • Radiotherapy for persistent post-op. high cortisol.

Bilateral adrenalectomy may be complicated by Nelson’s syndrome: locally aggressive pit. tumour causing skin pigmentation.

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15
Q

Give 4 complications of Cushing’s syndrome

A
  • Diabetes
  • Osteoposis
  • Hypertension
  • Pre-disposition to infections: steroids are immunosuppressants.

If untreated, 5yr survival rate is 50%.

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16
Q

What is pheochromocytoma?

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A
  • Tumour from chromatin cells of adrenal medulla producing catecholamines.
  • 10% bilateral
  • 10% malignant
  • 10% extra-adrenal: paragangliomas
17
Q

Give 3 presenting symptoms of pheochromocytoma.

Give 3 other clinical signs.

Study These Flashcards
A

Paroxysmal attacks of PHE:

  • Palpitations
  • Headaches
  • Episodic sweating
  • Hypertension
  • Tachycardia
  • Weight loss
  • Fever
  • Paleness of face
18
Q

What patients should you consider phaeochromocytoma in?

Give 3 familial syndromes causing phaeochromocytoma.

Study These Flashcards
A
  • Consider in patients with young onset or resistant intractable hypertension.
  • MEN2
  • Von Hippel Lindau syndrome
  • Neurofibromatosis type 1
19
Q

Give 3 investigations for phaeochromocytoma

Give 2 imaging tests for tumour localisation.

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A
  • 24 hr urine collection- check for catecholamines, metanephrines and normetanephrines
  • Plasma free metanephrines/ normetanephrines
  • Genetic testing

CT> MRI
I-123 MIBG scintigraphy: similar structure to noradrenaline: incorporated into neurosecretory granules of phaeo: expensive, radioactive substance.

20
Q

What percentage of adrenal cortex needs to be destroyed to result in adrenal insufficiency?
What is name for primary adrenal insufficiency?

Study These Flashcards
A

90%

- Addison’s disease

21
Q

Most common causes of adrenal insufficiency are iatrogenic, primary causes are rare.
Give two causes of iatrogenic adrenal insufficiency.

Study These Flashcards
A
  • Sudden cessation of long-term steroid therapy

- Post bilateral adrenalectomy.

22
Q

Give 4 signs of Adrenal insufficiency.

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A
  • Increased pigmentation
  • Postural hypotension
  • Loss of body hair in women: androgen deficiency
  • Associated autoimmune condition e.g. vitiligo.
23
Q

Give 5 signs of Addisonian crisis

Study These Flashcards
A
  • Hypotensive shock- major haemodynamic collapse.
  • Tachycardia
  • Pale
  • Cold
  • Clammy.
24
Q

Give 2 investigations to confirm diagnosis of adrenal insufficiency.
Give 3 investigations to identify cause of adrenal insufficiency.

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A
  • 9am serum cortisol less than 100nmol/L
  • Short SynACTHen test: serum cortisol <550nmol after 30 mins.
  • Long SynACTHen test
  • Autoantibodies
  • Abdo CT/ MRI/.
25
What 3 U&E findings are found in Addisonian crisis?
- High Urea - Low sodium- lack of aldosterone - high potassium- causes irregular heart output.
26
Give 4 steps in management of Addisonian crisis?
- Rapid IV fluid rehydration - 50ml 50% dextrose bolus, 100mg 6hrly hydrocortisone until BP stable - Treat precipitating cause, e.g. Abx for infection
27
Give 2 steps in management of chronic adrenal insufficiency. What is important to remember if patient has hypothyroidism too? Give a metabolic complication of adrenal insufficiency.
- Replace glucocorticoids with hydrocortisone: increased dose in times of stress/ illness. - Replace mineralocorticoids with fludrocortisone. - Give hydrocortisone before thyroxine to prevent precipitating Addisonian crisis. Hyperkalaemia.
28
Give 1 moderate and 2 severe signs of hypokalaemia on ECG. | Give 1 moderate and 2 severe signs of hyperkalaemia on ECG.
Hypokalaemia - Flattened T wave - U wave and ST depression Hyper: - Peaked T wave - Widened QRS and loss of P wave
29
What serum value is hyper K+? What arrhythmia can it result in? Give two conditions causing systemic K+ release.
>5mmol/L, significant is >6. >7 : muscle weakness and ECG changes. Can cause VF. - Rhabdomyolysis, metabolic acidosis (DKA).
30
Give 5 step management of hyperkalaemia.
10, 10, 10, 50, 50 - 10ml 10% calcium gluconate - 10u Actrapid - 50ml 50% glucose. - Nebulised salbumatol - 12-lead ECG continuous. Aim to block cardiotoxic effects of K+ and increase K+ uptake into cells.
31
Give serum value for hypokalaemia. | Give 3 signs of hypokalaemia.
<3.5, <3 gives clinical manifestations. - Muscle weakness - Cardiac arrhythmia - Polyuria and polydipsia- nephrogenic DI.
32
Give 4 causes of hypokalaemia.
- GI loss- vomiting/ diarrhoea - Redistribution of K+ into cells: insulin, B agonists, metabolic alkalosis. - Renal loss: hyperaldosteronism, excess cortisol, natriuresis. - Decreased intake- anorexia nervosa
33
What is the management of hypokalaemia
- K+ 3.0-3.5 mol/L: oral potassium chloride- recheck in 48 hours. - K+ <3.0: IV potassium chloride, max infusion rate 10mmol/hr (peripheral irritant). - Always correct magnesium also
34
Give 3 defining features of PCOS. Give 3 associated conditions
- Hyperandrogenism: Hirsutism and acne - Oligo/ amenorrhoea - Polycystic ovaries on USS - Obesity- poor diet - Insulin resistance/ Type 2 DM - Infertility- most common cause of infertility in women.
35
What is the relation between insulin resistance and PCOS? Give a sign of severe insulin resistance.
- Insulin resistance causes: - Hyperinsulinaemia: increased ovarian androgen synthesis and reduce hepatic sex hormone binding globulin synthesis. - Leads to increased in free androgens. - Acanthosis nigricans- velvety thickening and hyperpigmentation of skin in axillae or neck.
36
Give 4 endocrine blood test findings in PCOS. What 2 findings are seen on transvaginal USS?
- High LH - High LH: FSH ratio - High testosterone, androstenedione and DHEA-S - Low sex hormone binding globulin. - Increased number of ovarian follicles and increase in ovarian volume
Yr 3 MedEd
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