TRIPASS XR تري باس

 

d), mineralocorticoids and androgens.

The history

Common presenting symptoms

Cushing’s syndrome is caused by excess exogenous or

endogenous glucocorticoid exposure. Most cases are iatro-

202 • The endocrine system

• nausea, vomiting, diarrhoea, constipation, abdominal pain

and weight loss

• muscle cramps.

Past medical and drug history

Enquire about recent or past exogenous glucocorticoid usage

(route, dose, duration) as this may contribute to either iatrogenic

Cushing’s syndrome or suppression of the hypothalamic–pituitary–

adrenal axis and resultant glucocorticoid insufficiency.

The physical examination

Cushing’s syndrome

Examination sequence

• Look at the face and general appearance for central

obesity; there may be a round, plethoric ‘moon’

face (Fig. 10.11A) or dorsocervical fat pad (‘buffalo

hump’).

• Examine the skin for thinning and bruising (10.11D), striae

(especially abdominal; Fig. 10.11C), acne, hirsutism and

signs of infection or poor wound healing.

• Measure the blood pressure.

• Examine the legs for proximal muscle weakness and

oedema.

• Perform ophthalmoscopy for cataracts and hypertensive

retinal changes (see Fig. 8.18).

• Perform urinalysis for glycosuria.

genic and caused by side effects of glucocorticoid therapy.

‘Endogenous’ Cushing’s usually results from an ACTH-secreting

pituitary microadenoma, but other causes include a primary

adrenal tumour or ‘ectopic’ ACTH secretion by a tumour. The

catabolic effects of glucocorticoids cause widespread tissue

breakdown (leading to proximal myopathy, fragility fractures,

spontaneous bruising and skin thinning) and central accumulation

of body fat (Fig. 10.11). Patients may develop hypertension or

diabetes and are susceptible to infection. Hypertension can also

result from overproduction of aldosterone (a mineralocorticoid)

or catecholamines (Box 10.4).

Addison’s disease is due to inadequate secretion of cortisol,

usually secondary to autoimmune destruction of the adrenal

cortex. Symptoms are usually non-specific (see later).

Adrenal adenomas usually present with features of hormone

hypersecretion, as described later. Occasionally, they may be

asymptomatic and are detected incidentally on abdominal CT

or MRI scans. Functioning adrenal adenomas may present with

refractory hypertension (Box 10.4).

Cushing’s syndrome

Ask about:

• increase in weight, particularly if the weight is centrally

distributed

• bruising, violaceous striae and skin thinning

• difficulty rising from a chair/bath (may indicate proximal

myopathy).

Addison’s disease

Ask about:

• weakness

• postural lightheadedness

A B

Fig. 10.10 Hypopituitarism. A Hypopituitarism caused by a pituitary adenoma (note the fine, pale skin). B Absent axillary hair.

The physical examination • 203

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A B

C

D

Fig. 10.11 Cushing’s syndrome. A Cushingoid facies. B After curative pituitary surgery. C Typical features: facial rounding and plethora, central

obesity, proximal muscle wasting and violaceous skin striae. D Skin thinning: purpura caused by wristwatch pressure.

10.4 Adrenal causes of endocrine hypertension

Condition Hormone produced in excess Associated features

Conn’s syndrome Aldosterone Hypokalaemia

Cushing’s syndrome Cortisol Central obesity, proximal myopathy, fragility fractures, spontaneous bruising,

skin thinning, violaceous striae, hypokalaemia

Phaeochromocytoma Noradrenaline (norepinephrine),

adrenaline (epinephrine)

Paroxysmal symptoms, including hypertension, palpitations, sweating

204 • The endocrine system

insufficiency, the pituitary increases ACTH secretion in

response to low cortisol levels. High levels of ACTH increase

melanocyte-stimulating hormone, leading to increased skin

pigmentation (most striking in white Caucasians). Vitiligo

(depigmentation of areas of skin) occurs in 10–20% of

Addison’s disease cases (Fig. 10.12A).

• Measure the blood pressure and test for postural

hypotension (p. 51), resulting from salt and water loss due

to inadequate mineralocorticoid.

Addison’s disease

Examination sequence

• Look for signs of weight loss.

• Examine the skin for abnormal or excessive pigmentation.

This is most prominent in sun-exposed areas or epithelia

subject to trauma or pressure: skin creases, buccal mucosa

(Fig. 10.12B) and recent scars. In primary adrenal

B

A

Fig. 10.12 Addison’s disease. A Hyperpigmentation in a patient with coexistent vitiligo. B Buccal pigmentation.

THE GONADS

Anatomy and physiology

The gonads (testes and ovaries) secrete sex hormones

(testosterone and oestrogen) in response to gonadotrophin

(FSH and LH) release by the pituitary. The reproductive system

is covered in Chapter 11.

The history

Common presenting symptoms

Most commonly, men present with androgen deficiency, whereas

women present with hyperandrogenism.

Hypogonadism can be primary (failure of the gonad itself) or

secondary (where reduced gonadotrophin levels cause gonadal

failure). Klinefelter’s syndrome (47XXY) is the most common cause

of primary hypogonadism in men (1:600 live male births; Fig.

10.13). Secondary hypogonadism may be caused by pituitary

disease, extremes of weight, or drugs that suppress hypothalamic

gonadotrophin releasing hormone release (such as anabolic

steroids or opiates). Presenting symptoms in men include loss

of libido, erectile dysfunction, loss of secondary sexual hair,

reduction in testicular size and gynaecomastia (p. 214).

Hyperandrogenism in women usually presents with hirsutism

(excessive male-pattern hair growth; Fig. 10.14), acne and/or

oligomenorrhoea, and is commonly due to polycystic ovarian

syndrome (PCOS; usually also associated with obesity).

Other less common causes should be considered (such as

congenital adrenal hyperplasia). Virilisation is suggested by

male-pattern baldness, deepening of the voice, increased

muscle bulk and clitoromegaly; if present in women with a short

history of severe hirsutism, consider a testosterone-secreting

tumour.

The history • 205

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