Adrenal Gland pathology Flashcards by Isla Carter

Adrenal Gland Location, size and composition

Bilateral
4-5 grams each
Sit superior and medial to upper pole of kidneys
Composed of outer cortex and central medulla

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Adrenal Cortex zones (3)

Zone glomerulosa
Zone fasciculata
Zone reticular

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Zone glomerulosa

Mineralcorticoids

Aldosterone

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Zone fasciculata

Glucocorticoids

Cortisol

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Zone Reticularis

Sex steroids

Glucocorticoids

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Adrenal Medulla

Central core
Innervated by pre-synaptic fibres from sympathetic nervous system

Neuroendocrine (chromaffin) cells
- secrete catecholamines

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Adrenocortical Pathology - Hyperfunction

Hyperplasia
Adenoma
Carcinoma

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Adrenocortical Pathology- hay-function

Acute
- Waterhouse-Friderichsen

Chronic
- Addison’s Disease

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Adrenocortical hyperplasia aetiology

Congenital

Acquired

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Congenital Adrenocortical Hyperplasia

Autosomal Recessive

Deficiency/ lack of enzyme required for steroid biosynthesis

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Congenital Adrenocortical Hyperplasia Pathophysiology

Altered biosynthesis (due to deficiency/ lack of enzyme) leads to increased androgen production

masculinisation
precocious puberty

Reduced cortisol stimulates ACTH release and cortical hyperplasia

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Acquired Adrenocortical hyperplasia

Endogenous ACTH production

Cushings
Ectopic ACTH

Bilateral Adrenal Enlargement

Diffuse or nodular

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Adrenocortical Tumours

Adrenocortical Adenoma

Adrenocortical Carcinoma

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Adrenocortical Tumour Presentation

Mainly adults (M=F)

incidental finding
Hormonal effects
Mass lesion
Carcinomas with necrosis can cause fever

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Adrenocortical Adenoma

Well circumscribed, encapsulated lesions
Usually small (2-3cm)
Yellow/ brown cut surface (lipid)
Composed of cells resembling adrenocortical cells

Well differentiated, small nuclei, rare mitoses

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Adrenocortical Carcinoma

Rare
More likely to be functional
Can closely resemble adenoma

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Spread of adrenocortical carcinoma

Local invasion
Metastasis (usually vascular)
Peritoneum and pleura
Regional lymph nodes

Adrenocortical Carcinoma Suggestive Features

Large size (>50g, often >20cm) 
Haemorrhage and necrosis 
Frequent mitoses
Lack of clear cells 
Capsular or vascular invasion

Hypersecretion of Adrenocortical Hormones

Primary Hyperaldosteronism
- Conn’s Syndrome

Secondary Hyperaldosteronism

Hypercortisolism

Conns’ Syndrome

Excessive production of hormone aldosterone by the adrenal cortex

Conn’s Syndrome Aetiology

usually associated with diffuse or nodular hyperplasia of both adrenal glands

Adenoma (35% ), rarely carcinoma

Sprionolactone bodies
Do not suppress ACTH

Conn’s Syndrome Presentation

Hypertension
Muscle Weakness
Polydipsia (abnormally intense thirst)
Polyuria( production of large volumes of urine)

Secondary hyperaldosteronism

Increased Renin

Aetiology
Decreased renal perfusion, hypovolaemia & pregnancy

Hypercortisolism Aetiology

Cushings

Exogenous
- iatrogenic (steroid therapy)

Endogenous
- ACTH dependent or independent

ACTH Dependent

ACTH secreting pituitary adenoma
- -> Cushings
Ectopic ACTH
- -> Small Cell Lung cancer

ACTH independent

Adrenal adenoma or carcinoma
Non-lesional adrenal gland atrophies

Adrenocortical Hypofunction

Primary - Acute - Chronic Secondary - Failure to stimulate adrenal cortex - -> Hypothalamic pituitary disorder (hypopituitarism) - Suppression of adrenal cortex - -> Treatment with steroids

Primary Adrenocortical Insufficiency- ACUTE

Rapid withdrawal of steroid treatment Crisis in patients with chronic adrenocortical insufficiency - due to stress (infection or not increasing dose of steroid treatment) Massive adrenal haemorrhage - Newborn - Anticoagulant treatment - DIC - Septicaemic Infection

Primary Adrenocrotical Insufficiency- CHRONIC aetiology

Addison's disease Signs and symptoms appear once >90% gland destroyed

Addison's Disease

Destruction of adrenal cortices, resulting in steroid and mineralocorticoid deficiency

Addison's disease Aetiology

Autoimmune (90%) Infections (TB, HIV) Metastatic malignancy

Addisons Disease Presentation

Insidious onset manifests once significant decreases in glucocorticoid and mineralocorticoid levels Vague Symptoms - Weakness - Fatigue - Anorexia - Vomiting - Weight loss - Diarrhoea - Pigmentation (raised POMC0

Addisons Disease Biochem and Consequences

Decreased mineralocorticoids - K+ retention, Na+ loss - Hyperkalaemia, hyponatraemia - Volume depletion and hypotension Decreased glucocorticoids - hypoglycaemia.

Addisions Disease: Crisis

Aetiology : Strress - Infection - Trauma - Surgery Presentation - Vomiting - Abdo pain - Hypotension - Shock - Death

Adrenal medullary tumours (2)

Phaeochromocytoma | Neuroblastoma

Neuroblastoma -Epidemiology and Location

Paediatric : 40% diagnosed in infancy 40% arise in adrenal medulla - remainder along sympathetic chain

Neuroblastoma composition

Composed of primitive appearing cells | Can show maturation ad differentiation towards ganglion cells

Neuroblastoma Outcome

Age and stage important for prognosis Signs of poor outcome - Amplification of N-myc - Expression of telomerase

Phaeochromocytoma

Small vascular tumour of the inner region (medulla) of the adrenal gland

Phaeochromocytoma compositon

Neoplasm derived from chromatin cells of adrenal medulla | Secretes catecholamines.

Phaeochromocytoma genetics

Associated with MEN2 (A & B)

Phaeochromocytoma Presentation

Rare cause of secondary hypertension Hypertension (90%) - Paroxysmal episodes common Complications - Cardiac failure, infarction, arrhythmias - CVA

Phaeochromocytoma Laboratory diagnosis

Detection of urinary excretion of catecholamines and metabolites Range from small to large necrotic tumour masses may see adrenal remnants on surface K2Cr2O7 will turn tumour dark brown due to oxidation of catecholamines in tumour cell

Phaeochromocytoma Associations (location etc)

10% tumour 10% extra-adrenal - paragangliomas 10% are bilateral - 50% in familial cases 10% biologically malignant - defined by metastasis 10% are not associated with hypertension 25% are familial