PARATHYROID GLAND AND

OTHER ENDOCRINE GLANDS

DRS. AFNAN ABDIRAHMAN

MBBS ELRAZI UNIVERSITY
GENERAL SURGERY RESIDENT (UOH-IMU)
Overview of parathyriod
 Major regulator of calcium level.
 Secrete PTH to increase serum calcium level. The thyriod
parafollicular cells C- cells secreate calcitonin, which acts to
reduce serum calcium.
 Primary hyperparathyrodism is increased parathyriod
hormone( high PTH, high Ca)
 Secondary hyperparathyriodism is increased PTH (high PTH,
low Ca)
 Tertiarty hyperparathyriodism is increased parathyriod
activity after along period of secondary
hyperparathyriodism that has been corrected ( high PTH,
high Ca)
 Overview of calcium regulation
 The primary mediator of serum calcium are parathyriod
hormone(PTH) and calcitonin.
 The primary organs play are the parathyriods, bones, small
bowel, and kindney.
 Normal serum calcium= 9.0-10.5mg/dL

 if the serum albumin is <4.0 use corrected calcium formula

which is equal to
corrected Ca= Ca+0.8(4-Albumin level)
 Calcium stabilizes neuronal membrane and discharges
significant disturnbance in serum calcium will always lead to
neurological symptoms.
 Bone mineralization

 most mild disturbance of Ca are asymptomatic.

Hypercalcemia
 Elevated serium Ca level >10.5
 Major causes that need to be considered are drugs,
primary hyperparathyriodism and malignancy.
 in primary hyperparathyrodism PTH will be high
 In malignant and other conditions, PTH will be low(
due to high negative feedback)
Primary hyperparathyroidism
 Hypercalcaemia in the presence of inappropriately
raised serum PTH levels is due to enlargement of
one or more glands and hypersecretion of PTH.
 The normal response to hypercalcaemia is PTH
suppression.
 The prevalence of sporadic primary HPT increases
with age and it affects women more than men.
 Familial HPT occurs as part of the following
genetically determined conditions:
 • MEN-1 (multiple endocrine neoplasia type 1;
Werner’s syndrome)
 • MEN-2A (Sipple’s syndrome) and rarely MEN-2B.
 • familial isolated HPT
 The majority (85%) of patients with sporadic
primary HPT have a single adenoma,
 approximately 13% have hyperplasia affecting

all four glands

 and about 1% will have more than one adenoma or
a carcinoma.
 The histological differentiation between adenoma and
hyperplasia can be difficult and the macroscopic
findings are an important determinant in making the
diagnosis.
 A single enlarged gland with three small normal glands
is characteristic of a single adenoma.
 Multiple adenomas occur more frequently

in older patients.
 Parathyroid hyperplasia by definition affects

all four glands.

 Parathyroid carcinomas are large tumours and
typically much more adherent or even frankly
invasive than large adenomas.
 Histology demonstrates a florid desmoplastic
reaction with dense fibrosis and capsular and
vascular invasion.
 Parathyroid cysts may be secondary to
degeneration in nodules or adenomas.
 •“ stones, bones, moans, and
physchiatric overtones”:
nephrolithisis, fracture, weakness, bone
pain, abdominal pain, neuronal
hypoactivity, confusion, lethergy,
nephrogenic diabetic inspidus.
•Treatment : in the presence of
symptoms acute treament is must, fluid
should be bolus to induce diuresis, loop
diuretics may be added caustionally.
•If you want to decrease qiuckly you
can give iv. Calcitonin.
•Long term tx is to adress the
underlyning cause(parathyrodectomy)
Hypocalcemia
 Low serum calcium level <9.0
 Causes you need to consider immedietly are post
thyroidectomy, vit D deficiency, and renal failure.
 In hypocalcemic patient, consider first PTH level , if
low it is consistence with past thyrodectomy or
hypomagnesmia; if high it is consistence with renal
failure or vit D deficiency.
 Symptoms: nueronal hyperactivity- parasethesis(
particularly circumoral), spasm, strong tendon
reflex, tetany, seizures, chovestek’s sign, trousseau’s
sign.
 Treatment: shorterm, replace Ca with iv calcium
gluconate. Long term, Ca supplementation and vit D.
always treatment of underlying cause.
Parathyroid carcinoma
 Cancer of the parathyroid is rare, accounting for 1% of
cases of HPT.
 Typical features are very high calcium and PTH levels,
often with a palpable neck swelling or occasionally
lymphadenopathy.
 Scanning may support the diagnosis.
 The diagnosis is rarely known at the time of exploration
but, if suspected, operation should include excision of
the tumour mass with en bloc thyroid lobectomy and node
dissection when indicated.
Adrenal glands
DISORDERS OF THE ADRENAL
CORTEX
 Incidentaloma:
 Definition

 A clinically unapparent mass detected incidentally by

imaging studies conducted for other reasons.
 Diagnosis

 When an incidentaloma is identified, a complete history and

clinical
examination are required.
 A biochemical work-up for hormone excess and sometimes
additional imaging studies are also needed.
 The main goal is to exclude a functioning or malignant
adrenal tumour.
Hormonal evaluation includes:
• morning and midnight plasma cortisol measurements;
• a 1-mg overnight dexamethasone suppression test;
• 24-hour urinary cortisol excretion (optional);
• 24-hour urinary excretion of catecholamines,
metanephrines or plasma-free metanephrines;
• serum potassium, plasma aldosterone and plasma
renin activity;
 For evaluation of malignancy, computerised
tomography (CT) or magnetic resonance imaging
(MRI) should be performed in all patients with
adrenal masses, followed by fine-needle aspiration
cytology after a phaeochromocytoma has been
excluded.
Treatment
 Any non-functioning adrenal tumour greater than 4
cm in diameter and smaller tumours that increase in
size over time should undergo surgical resection.
 Non-functioning tumours smaller than 4 cm should
be followed-up after 6, 12 and 24 months by
imaging and hormonal evaluation
Primary hyperaldosteronism
 Primary hyperaldosteronism (PHA) is defined by
hypertension, hypokalaemia and hypersecretion of
aldosterone.
 The most frequent cause of PHA with hypokalaemia
is a unilateral adrenocortical adenoma (Conn’s
syndrome)
 Clinical features
 Most patients are between 30 and 50 years of age
with a female predominance.
 Apart from hypertension and hypokalaemia,
patients complain of non-specific symptoms:
headache, muscle weakness, cramps, intermittent
paralysis, polyuria, polydypsia and nocturia.
 Diagnosis
 The key feature of the biochemical diagnosis is the
assessment of potassium level and the aldosterone
to plasma renin activity ratio.
 Antihypertensive and diuretic therapy, which cause
hypokalaemia and influence the renin–angiotensin–
aldosterone system, have to be discontinued
 Once the biochemical diagnosis is confirmed, MRI or
CT should be performed to distinguish unilateral
from bilateral disease.
 Conn’s adenomas usually measure between 1 and 2
cm and are detected by CT with a sensitivity of 80–
90%.
 Treatment
 The first-line therapy for PHA with bilateral
hyperplasia is medical treatment with
spironolactone. In most cases supplemental
antihypertensive medication is necessary.
 Unilateral laparoscopic adrenalectomy is an
effective therapy in patients with clear evidence of
unilateral or asymmetrical bilateral disease.
 A subtotal resection is favoured in the case of a

typical Conn’s adenoma

 Cushing’s syndrome

 Hypersecretion of cortisol caused by endogenous production

or excessive use of corticosteroids is known as Cushing’s
syndrome.
 It can be either ACTH-dependent or ACTH-independent in
origin.
 The most common cause (85%) of ACTH-dependent Cushing’s
syndrome is Cushing’s disease resulting from a pituitary
adenoma that secretes an excessive amount of ACTH.
 Ectopic ACTH-producing tumours (small cell lung cancer,
foregut carcinoid) and CRH-producing tumours (medullary
thyroid carcinoma, neuroendocrine pancreatic tumour) are
more infrequent causes of ACTH-dependent Cushing’s
syndrome.
 Clinical features of Cushing’s syndrome
 ■ Weight gain/central obesity
 ■ Diabetes
 ■ Hirsutism
 ■ Hypertension
 ■ Skin changes (abdominal striae, facial plethora, ecchymosis,
acne)
 ■ Muscle weakness
 ■ Menstrual irregularity/impotence
 ■ Depression/mania
 ■ Osteoporosis
 ■ Hypokalaemia
 Diagnosis
 Morning and midnight plasma cortisol levels are elevated,
possibly with loss of diurnal rhythm.
 Dexamethasone fails to suppress 24-hour urinary cortisol
excretion.
 Serum ACTH levels discriminate ACTH-dependent from
ACTH-independent disease.
 in patients with elevated ACTH, MRI of the pituitary gland
must be performed.
 If MRI is negative and additional venous sampling from the
inferior petrosal sinus has excluded a pituitary
microadenoma,
Treatment
 Medical therapy with metyrapone or ketoconazole
reduces steroid synthesis and secretion and is used in
patients with severe hypercortisolism or if surgery is not
possible.
 ACTH-producing

 pituitary tumours are treated by trans-sphenoidal

resection or radiotherapy.
 If an ectopic ACTH source is localised, resection will
cure hypercortisolism.
 A unilateral adenoma is treated by adrenalectomy.
 In cases of bilateral ACTH-independent disease
bilateral adrenalectomy is the primary treatment.
 Patients with an ectopic ACTH-dependent Cushing’s
syndrome and an irresectable or unlocalised
primary tumour should be considered for bilateral
adrenalectomy as this controls hormone excess
Phaeochromocytoma (adrenal
paraganglioma)
 This is a tumour of the adrenal medulla, which is
derived from chromaffin cells and which produces
catecholamines.
 Phaeochromocytoma is known as the ‘10% tumour’
as 10% of tumours are inherited, 10% are extra-
adrenal, 10% are malignant, 10% are bilateral
and 10% occur in children.
 Hereditary phaeochromocytomas occur in several tumour
syndromes
 Multiple endocrine neoplasia type 2 (MEN 2): an autosomal

dominant inherited disorder.

 • Familial paraganglioma (PG) syndrome: glomus tumours of the

carotid body and extra-adrenal paraganglioma are

characteristic in this hereditary tumour syndrome,
 • von Hippel–Lindau (VHL) syndrome: those affected can develop

early-onset bilateral kidney tumours, phaeochromocytomas,

cerebellar and spinal haemangioblastomas and pancreatic
tumours.
 • Neurofibromatosis (NF) type 1
 Phaeochromocytomas are greyish-pink on the cut
surface and are usually highly vascularised. Areas of
haemorrhage or necrosis are often observed.
 The differentiation between malignant and benign
tumours is difficult, except if metastases are present.
 Phaeochromocytomas may also produce calcitonin,
ACTH, vasoactive intestinal polypeptide (VIP) and
parathyroid hormone-related protein.
 In patients with MEN 2, the onset of
phaeochromocytoma is preceded by adrenomedullary
hyperplasia, usually bilateral. Phaeochromocytoma is
rarely malignant in MEN 2.
 Clinical features
 Symptoms and signs are caused by catecholamine
excess and can be continuous or intermittent.
 combination of headache, palpitations and sweating
have a phaeochromocytoma.
 Paroxysms may be precipitated by physical training,
induction of general anaesthesia and numerous drugs
and agents (contrast media, tricyclic antidepressive
drugs, metoclopramide and opiates).
 Hypertension may occur continuously, be intermittent or
absent.
 Diagnosis
 The first step in the diagnosis of a phaeochromocytoma
is the determination of adrenaline, noradrenaline,
metanephrine and normetanephrine levels in a 24-hour
urine collection.
 Treatment
 Laparoscopic resection is now routine in the treatment of
phaeochromocytoma.
 If the tumour is larger than 8–10 cm or radiological
signs of malignancy are detected an open approach
should be considered.
Cut
 Phaeochromocytoma in pregnancy
 Phaeochromocytomas in pregnancy may imitate an amnion infection
 syndrome or pre-eclampsia. Without adequate α-blockade,
 mother and unborn child are threatened by hypertensive crisis
 during vaginal delivery. In the first and second trimesters the
 patient should be scheduled for laparoscopic adrenalectomy after
 adequate α-blockade; the risk of a miscarriage during surgery is
 high. In the third trimester, elective Caesarean with consecutive
 adrenalectomy should be performed. The maternal mortality rate
 is 50% when a phaeochromocytoma remains undiagnosed.
Thank you