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48 Cards in this Set

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What is the most common cause of hyperpituitarism and describe the pathology and histology.
Anterior lobe adenoma of one cell type (somatotroph, thyrotroph, corticotroph, lactotroph, gonadotroph) caused by mutations in GNAS1 (G-protein activation) or MEN1 oncogene.
Histo: monomorphic with absence of reticular network
What is the commonest cause of acromegaly
somatotroph (growth hormone pituitary cell adenoma)
A woman presents with amehorrhoea and on Hx says her breasts hae become firm and drops of milk exude. What test would you perform and the likely Dx
1) Check prolactin level. If high, prolactinotroph causing:
amenorrhoea, infertility, loss of libido, galactorrhoea
2) Check TSH, if high check T3/T4, if low then could be primary hypothyroidism (high TRF)
A man presents complaining that his skin is becoming darker. His fasting glucose has also raised. What disorder is likely and why.
Darkened skin is usually caused by excessive ACTH in primary hyperpituitarism causing Cushings syndrome. Most common cause is corticotroph.
Hypopituitarism of the posterior pituitary results in severe thirst. What bedside test would you perform to indicte the likelihood of this?
Decrease in ADH results in diabetes insipidus: measure volume of 24 hour urine (very high) and urine specific gravity (low = dilute)
The partner of a heavy smoker says her husband is becoming confused. What pituitary disorder could this be ppointing to and how can it be related to his smoking?
Smoking -> small cell carcinoma -> ADH overproduction causing SIADH resulting in excessive water retention, hyponatremia causing cerebral oedema in the absence of peripheral oedema.
A patient presents with normal ACTH levels and cortisol. How can symptoms of hormone imbalance occur
Adrenal adenoma can produce short functional hormone but undetectable by pathology.
What are the rules of endocrinology
Ix in hormonr pairs on the same axis
Hyper, do suppression
Hypo, do stimulation test
Know diurnal rhythms and menstrual cyclicity
Test for episodic Cushings eg uring cortisol/urea?
What are 2 causes of increased prolactin levels
Prolactinoma
Decreased inhibition by dopamine in, for example, pituitary stalk lesion (stalk effect)
What are causes of hypopituitarism
Tumour, infiltration, lymphocytic (autoimmune), mass effect
What are the 3 steps of a suspected pituitary pathology
1) Hx of abnormal hormone levels
2) lx of hormone levels in pairs, tests for hypo and hyper, urine volume and dipstick is quick bedside test
3) MRI now in 1mm slices and repeat in 6months to a year to rule out rare malignancy
What are the 5 causes of hyperprolactinaemia
prolactinoma
BhCG (choriocarcinoma, molar, ectopic or normal pregnancy)
stalk effect
antipsychotics
paget's disease of the breast, post partum breast feeding, infection
What are the treatments of hyperprolactinaemia
dopamine, cabergoline, bromocriptine
A man presents with PRL 35,000. What is likely and what are the signs and symptoms
Zero testosterone due to prolactinoma resulting in testicular atrophy, infertility, mass effect causing bitemporal hemianopia, inchaemia and compression affecting other pituitary hormones
What are the DDx of acromegaly and treatments
GH or IGF1 abuse (common)
GHRH producing tumour
Signs: infertility, acromegaly
Tx: somatostatin, surgery, radiotherapy
Hypopituitarism Tx
Cortisol replacement first
T4, OCP or HRT, testosterone, cabergoline to suppress prolactin, treat DI with DDAVP
A whole body CT showed tumours within the suprarenal, thyroid and parathyroid gland hyperplasia. What gene defect is the likely cause.
MEN2 gene
What syndrome of the adrenal cortex is associated with H.meningitidis
Waterhouse-Friderickson Syndrome: massive haemorrhage of adrenals - also caused by TB, strep and haemophilus meningitis,
What are 3 causes of primary hyperaldosteronism. Write a one word treatment for each.
1) aldosteronoma of the adrenal (Conn's tumour) - surgery
2) idiopathic adrenal hyperplasia - aldosterone antagonists
3) glucocorticoid remediable aldosteronism - corticosteroids
What inhibits thyroxine production
1) Negative feedback (ie T3/T4)
2) Dopamine
3) Somatostatin
4) Stress (probably cortisol)
What is the physiology behind TSH causing goiter
TSH binds to the TSH receptor on the thyroid cell membrate, activating a G-protein coupled adenylyl cyclase cAMP cascade.
Iodide enters the cells, producing T4, T3, increased production of thyroglobulin and colloid, increasing cellular volume
Phospholipase C increases cell membrane area, resulting in hypertrophy and goiter
What are the effects of T4 and T3
Mirror catecholamines: increased HR and force of contraction, and adrenergic stimulation (sweating, alertness) as well as increased metabolic rate, production of adrenergic receptors, fat and carb catabolism, increased carb uptake, bone turnover
What are 5 types of thyroid pathology
1) hyper
2) hypo (myxedema)
3) goiter
4) nodules (focal enlargement due to cyst/tumour)
5) Abnormal thyroid function tests in euthyroid individual
What antibodies are usually found in Hashimoto's thyroiditis
1) Anti-thyroglobulin
2) Anti-thyroidal peroxidase
What antibodies are found in Graves disease
TSH-receptor [stim] antibodies
What does the following suggest: high T3/T4 but normal TSH
Pituitary is not responsive to feedback suppression of TSH by high levels of T3/T4
What does the following suggest: high T3/T4 but low TSH
Pituitary OK but thyroid overproduction as in Graves, thyroid adenoma
What germ cell tumours can precipitate thyrotoxicosis
Very high levels of hCG produced by choriocarcinomas, hydatidform moles (but not teratomas unless they are struma ovarii) with binding to follicular TSH receptors
How can Hashimotos cause transient thyrotoxicosis
Destruction of thyroid folicles and release of stored thyroxine
What are two causes of low uptake of radioactive iodine
1) Follicular destruction in Hashimotos
2) Exogenous thyroxine production
Describe the Graves follicle
Shrunken and scalloped with scanty colloid and columnar epithelium
What are the 2 cell types in the thyroid
Follicular
C-cells
On examination, a thyroid lump is felt. What is it and what types of patients get it?
1) Thyroid nodule: women (around 5%)
a) Multinodular goitre: often dominant nodule as part of nodular goitre - if functional then toxic (Plumers syndrome)
b) Solitary nodule (adenoma, colloid cyst)
2) Follicular malignancies: (all adenocarcinomas)
a) follicular
b) papillary
c) undiffferrentaited
d) anaplastic
3) C-cell malignancies:
medullary carcinoma
A woman comes in complaining of a swollen neck and dificvulty swallowing. What are the possible causes of goitre?
1) Simple goitre: colloid goitre: iodine deficiency, goitrogens (cabbage, lithium, sulfonamides), enzyme mutatiions. Fibrosis develops multinodular goitre over time
Describe the pathological features of papillary carcinoma
1) Most common thyroid cancer (80%)
2) BRAF oncogene and radiation
3) Orphan Annie eyes and psamomma bodies
4) High 10 year survival (> 90%), node and lung metastases
De Quervain's thyroiditis
1) Follows URTI
2) Painful
3) Granulomatous inflammation
4) Initially hyperthyroid
Describe the symptoms and causes of primary hypothyroidism
Primary myxedema (due to high TSH) causing subcutaneous deposits; hair loss, puffy face, hoarse voice
prolactinaemia, galactorrhoea (high TRF -> high prolactin)
mental sluggishness, hypothermia, bradycardia
proximal weakness
What are the usual causes of hyperparathyroidism
Primary: functional adenoma (90%), hyperplasia (10%)
Secondary: hypocalcaemia due to renal failure, malnutrition, malabsorption, vit D deficiency
Tertiary: uncontrolled secretion following chronic secondary hyperparathyroidism
MEN1 v MEN 2A
MEN1:
Pituitary
Pancreatic
Parathyroid adenomas
MEN2A:
Thyroid medullary carcinoma
Parathyroid hyperplasia
Phaeochromocytoma
What is the new diagnostic criterion for diabetes
HbA1c > 6.5% (but can still use FBG=7 or RBG=11)
What are 4 insulin resistant states
Type 2 diabetes and obesity
Cushings, steroid treatment
PCOS
How is type 1 diabetes diagnosed
1) Urine ketones
2) Anti-GAD antibodies
What are the complications of diabetes
1) Microalbuminurea, diabetic nephropathy
2) Diabetic retinopathy
3) Autoimmune neuropathy
4) CVD, narrowing of large and small vessels
What are the pituitary pathologies
1) Benign tunours (99%): pituitary adenoma (MEN1) and craniopharyngioma
2) Inflamation: hypophysitis
What are the complications of a pituitary tumour
Mass effect causing
1) Cranial nerve compression: III and IV
2) Bitemporal hemianopia
3) Erosion of sphenoid sinus causing leakage of CNS
Endocrine abnormalities due to hyperplasia of functional cells and compression and ischaemia of other cell types
How is vasopressin deficit and excess tested
Deficit causing diabetes insipidus: water deprivation test and measure urine output and specific gravity (osmolarity). If high output of low SG urine then vasopressin definiciency.
If urine osmolarity > serum osmolarity then vasopressin excess (SIADH)
How do we test for cortisol deficiency
1) Synacthen + cortisol level: if cortisol still low then promary (adrenal) deficit. If increases then secondary (pituitary) deficit.
2) Insulin stress test: measure change in cortisol level. Should be high.
A pituitary adenoma caused prolactinaemia. In what 2 ways can this happen
1) A functional adenoma secreting prolactin
2) Stalk effect blocking inhibitory dopamine