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Endocrine > Adrenal Gland pathology > Flashcards

Adrenal Gland pathology Flashcards

1
Q

Adrenal Gland Location, size and composition

A

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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2
Q

Adrenal Cortex zones (3)

A

Zone glomerulosa
Zone fasciculata
Zone reticular

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3
Q

Zone glomerulosa

A

Mineralcorticoids

Aldosterone

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4
Q

Zone fasciculata

A

Glucocorticoids

Cortisol

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5
Q

Zone Reticularis

A

Sex steroids

Glucocorticoids

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6
Q

Adrenal Medulla

A

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

Neuroendocrine (chromaffin) cells
- secrete catecholamines

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7
Q

Adrenocortical Pathology - Hyperfunction

A

Hyperplasia
Adenoma
Carcinoma

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8
Q

Adrenocortical Pathology- hay-function

A

Acute
- Waterhouse-Friderichsen

Chronic
- Addison’s Disease

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9
Q

Adrenocortical hyperplasia aetiology

A

Congenital

Acquired

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10
Q

Congenital Adrenocortical Hyperplasia

A

Autosomal Recessive

Deficiency/ lack of enzyme required for steroid biosynthesis

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11
Q

Congenital Adrenocortical Hyperplasia Pathophysiology

A

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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12
Q

Acquired Adrenocortical hyperplasia

A

Endogenous ACTH production

  • Cushings
  • Ectopic ACTH

Bilateral Adrenal Enlargement

Diffuse or nodular

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13
Q

Adrenocortical Tumours

A

Adrenocortical Adenoma

Adrenocortical Carcinoma

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14
Q

Adrenocortical Tumour Presentation

A

Mainly adults (M=F)

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

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15
Q

Adrenocortical Adenoma

A

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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16
Q

Adrenocortical Carcinoma

A

Rare
More likely to be functional
Can closely resemble adenoma

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17
Q

Spread of adrenocortical carcinoma

A

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

18
Q

Adrenocortical Carcinoma Suggestive Features

A 
Large size (>50g, often >20cm) 
Haemorrhage and necrosis 
Frequent mitoses
Lack of clear cells 
Capsular or vascular invasion
19
Q

Hypersecretion of Adrenocortical Hormones

A

Primary Hyperaldosteronism
- Conn’s Syndrome

Secondary Hyperaldosteronism

Hypercortisolism

20
Q

Conns’ Syndrome

A

Excessive production of hormone aldosterone by the adrenal cortex

21
Q

Conn’s Syndrome Aetiology

A

usually associated with diffuse or nodular hyperplasia of both adrenal glands

Adenoma (35% ), rarely carcinoma

  • Sprionolactone bodies
  • Do not suppress ACTH
22
Q

Conn’s Syndrome Presentation

A

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

23
Q

Secondary hyperaldosteronism

A

Increased Renin

Aetiology
Decreased renal perfusion, hypovolaemia & pregnancy

24
Q

Hypercortisolism Aetiology

A

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
25
Q

Adrenocortical Hypofunction

A

Primary

  • Acute
  • Chronic

Secondary

  • Failure to stimulate adrenal cortex
    • -> Hypothalamic pituitary disorder (hypopituitarism)
  • Suppression of adrenal cortex
    • -> Treatment with steroids
26
Q

Primary Adrenocortical Insufficiency- ACUTE

A

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
27
Q

Primary Adrenocrotical Insufficiency- CHRONIC aetiology

A

Addison’s disease

Signs and symptoms appear once >90% gland destroyed

28
Q

Addison’s Disease

A

Destruction of adrenal cortices, resulting in steroid and mineralocorticoid deficiency

29
Q

Addison’s disease Aetiology

A

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

30
Q

Addisons Disease Presentation

A

Insidious onset manifests once significant decreases in glucocorticoid and mineralocorticoid levels

Vague Symptoms

  • Weakness
  • Fatigue
  • Anorexia
  • Vomiting
  • Weight loss
  • Diarrhoea
  • Pigmentation (raised POMC0
31
Q

Addisons Disease Biochem and Consequences

A

Decreased mineralocorticoids

  • K+ retention, Na+ loss
  • Hyperkalaemia, hyponatraemia
  • Volume depletion and hypotension

Decreased glucocorticoids
- hypoglycaemia.

32
Q

Addisions Disease: Crisis

A

Aetiology : Strress

  • Infection
  • Trauma
  • Surgery

Presentation

  • Vomiting
  • Abdo pain
  • Hypotension
  • Shock
  • Death
33
Q

Adrenal medullary tumours (2)

A

Phaeochromocytoma

Neuroblastoma

34
Q

Neuroblastoma -Epidemiology and Location

A

Paediatric : 40% diagnosed in infancy

40% arise in adrenal medulla
- remainder along sympathetic chain

35
Q

Neuroblastoma composition

A

Composed of primitive appearing cells

Can show maturation ad differentiation towards ganglion cells

36
Q

Neuroblastoma Outcome

A

Age and stage important for prognosis

Signs of poor outcome

  • Amplification of N-myc
  • Expression of telomerase
37
Q

Phaeochromocytoma

A

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

38
Q

Phaeochromocytoma compositon

A

Neoplasm derived from chromatin cells of adrenal medulla

Secretes catecholamines.

39
Q

Phaeochromocytoma genetics

A

Associated with MEN2 (A & B)

40
Q

Phaeochromocytoma Presentation

A

Rare cause of secondary hypertension

Hypertension (90%)
- Paroxysmal episodes common

Complications

  • Cardiac failure, infarction, arrhythmias
  • CVA
41
Q

Phaeochromocytoma Laboratory diagnosis

A

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

42
Q

Phaeochromocytoma Associations (location etc)

A

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

Endocrine (25 decks)

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