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Endocrine Flashcards

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1
Q

What is SIADH?

A

Excess vasopressin —> water retention + hyponatremia

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2
Q

Thyroid nodule biopsy:

What does a cold nodule / hot nodule mean? (On xRay)

A

If nodule is composed of cells that DO NOT make thyroid hormone (X absorbed iodine) —> appear COLD

Nodule that is producing too much hormone will show up darker —> HOT

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3
Q

What are the SE of corticosteroids?

A

CUSHINGOID

C = cataracts
U = ulcers
S = striae / skin thinning 
H = HTN / hirsutism / hyperglycaemia 
I = infections
N = necrosis (of femoral head) 
G = glucose elevation
O = osteoporosis / obesity 
I = immunosuppression 
D = depression / diabetes
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4
Q

What is the most common cause of hypercortisolism?

A

Exogenous administration of steroids

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5
Q

What is diabetes insipidus?

A

Deficiency of vasopressin / insensitivity to its action —> excess secretion of dilute urine with a compensatory increase in thirst (polydipsia)

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6
Q

What is Conn syndrome?

A

Excess aldosterone cause by an autonomous overproduction usually at adrenal cortex.

Typically due to adrenal hyperplasia / adrenal adenoma

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7
Q

What is Sheehan syndrome?

A

Pituitary infarction + hypopituitarism caused by ischemic necrosis due to blood loss + hypovolemic shock during after childbirth

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8
Q

What is Pheochromocytoma?

A

Catecholamine-secreting tumour that typically develops in adrenal medulla

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9
Q

What are they classic clinical features of Pheochromocytoma?

A

Due to excess sympathetic NS stimulation

Symptoms: anxiety / panic attacks, palpitations, tremor, sweating, headache, flushing, weight loss, constipation / diarrhoea

Signs: HTN, tachycardia, orthostatic hypotension, pallor

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10
Q

What is congenital adrenal hyperplasia (CAH)?

A

Encompasses a group of autosomal recessive defects in the enzymes that are responsible for cortisol, aldosterone

*ALL forms of CAH - characterised by low cortisol, high ACTH, adrenal hyperplasia

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11
Q

What are the retroperitoneal organs?

A

SAD PUCKER

Suprarenal (adrenal) glands 
Aorta & IVC
Duodenum (2nd-4th parts)
Pancreas
Ureters
Colon (descending & ascending)
Kidneys
Esophagus
Rectum
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12
Q

What is the main function of PTH?

A

INCREASES plasma [Ca2+], DECREASES plasma [PO43-]

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13
Q

What is the action of PTH on bone?

A

Increases bone resorption! (Mobilise calcium)

  • Stimulates Ca release from bone mineral compartment
  • Stimulates osteoblastic cells
  • Stimulates bone resorption via indirect effect on osteoclasts
  • Enhances bone matrix degradation

^All above to —> increase serum calcium

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14
Q

What is the action of PTH on kidneys?

A

Conserve Ca2+ (by reducing urinary Ca) + eliminate PO43-

  • Also enhances activation of Vit D by kidneys
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15
Q

Since PTH reduces urinary Ca, why is urinary Ca high in primary hyperparathyroidism?

A

Because initial filtered load is high! (Because hyperparathyroidism will lead to high Ca level)

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16
Q

What is the function of calcitonin? (Secreted by parafollicular / C cells of THYROID GLAND)

A

Released in response to INCREASED plasma [Ca2+], act OPPOSITELY to PTH! (Act on osteoclasts to REDUCE BONE RESORPTION!)

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17
Q

What is the main cause of primary hyperparathyroidism?

A

Adenoma

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18
Q

What are the clinical manifestations of primary hyperparathyroidism?

A

“Painful bones, renal stones, abdominal groans, psychic moans”

*weakness, hypotonia - neuromuscular abnormalities

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19
Q

What is the main cause of secondary hyperparathyroidism?

A

Renal failure (chronic renal insufficiency)

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20
Q

What is secondary hyperparathyroidism caused by?

A

Any condition associated with chronic depression in serum Ca level (because low serum Ca —> compensatory overactivity of parathyroids)

**Basically, compensatory overactivity of parathyroids for hypocalcaemia

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21
Q

Why is complete absence of PTH life threatening?

A

Due to asphyxiation caused by spasm of respiratory muscle!

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22
Q

What are the major causes of hypoparathyroidism?

A
  1. Surgically induced (inadvertent removal of parathyroids during thyroidectomy…)
  2. Congenital absence - occurs in conjunction with thymus aplasia (Di George syndrome)
  3. Autoimmune hypoparathyroidism
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23
Q

What are the clinical features of hypoparathyroidism?

A

Secondary to hypocalcaemia + include:
Increased neuromuscular irritability (tingling, muscle spams, facial grimacing)

Cardiac arrhythmias

(Sometimes) seizures

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24
Q

What is the difference between primary and secondary hyperaldosteronism?

A

Primary - caused by excessive aldosterone production —> Na+ retention, K+ loss, hypokalaemia + HTN

Secondary - arises when there’s excess renin (hence angiotensin II) stimulation
*Common causes = accelerated HTN, renal artery stenosis, congestive HF, cirrhosis)

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25
What are the major actions of glucocorticoids (cortisol)?
Increased / stimulated: gluconeogenesis / glycogen deposition / protein catabolism / fat deposition / Na retention / K loss / free water clearance / Uric acid production / circulating neutrophils Decreased / inhibited: protein synthesis / host response to infection / lymphocyte transformation / delayed hypersensitivity / circulating lymphocyte or eosinophils
26
What are the causes of Cushing syndrome?
ACTH dependent : pituitary-dependent (Cushing disease) / ectopic ACTH-producing tumours non ACTH dependent : adrenal adenomas / carcinoma / exogenous steroids * *Main lesions are found in pituitary + adrenal glands * *Vast majority is the result of administration of exogenous glucocorticoids (iatrogenic)
27
What are the clinical features of Cushing syndrome?
1. HTN, weight gain, truncal obesity, moon fancies, buffalo hump 2. Decreased muscle mass + proximal limb weakness (because hypercorticolism —> selective atrophy of fast-twitch (type II) myofibres 3. Hyperglycaemia, glucosuria (due to gluconeogenesis + inhibit uptake of glucose by cells) 4. Skin thin, fragile, easily bruised (due to catabolic effects on proteins —> loss of collagen) *striae 5. Osteoporosis + increased risk of fractures (due to bone resorption) 6. Increased risk of infections (Cz glucocorticoids suppress immune response) 7. Hirsutism + menstrual abnormalities + mental disturbances 8. Hyperpigmentation (only with ACTH-dependent causes e.g. pituitary / ectopic ACTH secretion)
28
What is Addison disease
Destruction of the entire adrenal cortex —> reduced production of mineralcorticoid, glucocorticoid, sex steroids
29
What are the main organs most commonly involved in MEN type 1?
3Ps - parathyroid, pancreas, pituitary
30
What is the most common manifestation of MEN 1 in parathyroid?
Primary hyperparathyroidism
31
What is the leading cause of death in MEN1?
Endocrine tumours of pancreas - aggressive + manifest with metastatic disease
32
What is the most frequent pituitary cause of MEN 1
Prolactin-secreting macroadenoma
33
What is the organs most commonly involved in MEN type 2A and MEN type 2B?
MEN 2A - thyroid, adrenal medulla, parathyroid MEN 2B - thyroid, adrenal medulla
34
What are the differences between MEN 2A and MEN 2B?
Primary hyperparathyroidism DOES NOT develop in patients with MEN2B! Extra-endocrine manifestations are characteristic in patients with MEN2B: - Ganglioneuromas of mucosal site (GI tract, lips, tongue) - Marfanoid habitus - overly long bones of axial skeleton —> gives appearance resembling that in Marfan
35
What do we use to treat Addison disease?
Glucocorticoids + mineralcorticoid replacement
36
What do we use to treat secondary adrenocortical insufficiency (caused by low ACTH from low CRH / pituitary failure) ?
Glucocorticoids alone
37
What do we use to treat congenital adrenal hyperplasia (CAH)?
Glucocorticoids + mineralocorticoid replacement
38
What is the treatment for primary aldosteronism?
If caused by an aldosterone-secreting adenoma (conn syndrome) - unilateral adrenalectomy is the usual treatment ``` Spironolactone / amiloride - controls K+ level & BP Aldosterone antagonist (eplerenone) ```
39
What do we use to treat Cushing syndrome?
Block cortisol production - Ketoconazole, Metyrapone Ketoconazole = best tolerated + most effective inhibitor of steroid hormone biosynthesis in patients with hypercortisolism SE: hepatic dysfunction (its potential to interact with CYP isoforms can lead to serious drug interactions) Metyrapone - reduce cortisol production, elevate precursor levels SE: hirsutism, HTN, nausea, headache, rash
40
What is the pharmacological treatment of Pheochromocytoma?
Non-competitive alpha-adrenergic blocker (e.g. phenoxybenzamine) [required before surgery to remove tumours] * Once alpha blockade established, a reflex tachycardia may develop —> use beta-blockade to prevent * **Beta blockade must NOT be started until alpha blockade has been established! Otherwise there will be dramatically elevated BP (—> HTN crisis / pulmonary oedema) due to unopposed alpha-adrenoceptor stimulation
41
What is the most common type of hyper functioning pituitary adenoma?
Prolactinomas
42
What is the mechanism of prolactin?
Controlled by tonic INHIBITION by hypothalamic dopamine - stimulates lactation - inhibits GnRH secretion + gondola action of LH
43
What are the typical presentations of hyperprolactinemia?
Hypogonadism due to suppression of LH + FSH | - Amenorrhoea, galactorrhoea, loss of libido, infertility
44
What is the treatment for hyperthyroidism?
Carbimazole
45
What is the treatment for hypothyroidism?
Levothyroxine
46
What is Hashimoto thyroiditis?
Painless enlargement of thyroid gland due to HYPOthyroidism - thyroid diffusely + symmetrically enlarged - caused by breakdown in self-tolerance to thyroid auto-antigens —> thyrocyte damage
47
What is subacute granulomatous (de Quervain) thyroiditis?
Transient hyperthyroidism from an acute inflammatory process triggered by viral infections / caused by viral infection - Gland is firm with intact capsule - disruption of thyroid follicles —> release of excessive TH - PAIN in neck, fever, tachycardia, malaise *Usually self-limited, patients return to euthyroid state within 6-8 weeks
48
What is subacute lymphocytic thyroiditis?
Silent / painLESS thyroiditis - painless neck mass / features of TH excess - most likely autoimmune - lymphocytic infiltration
49
What is Riedel thyroiditis?
Rare, characterised by extensive fibrosis involving thyroid + contiguous neck structure - hard + fixed thyroid mass
50
What is Graves’ disease?
Most common cause of endogenous hyperthyroidism - Caused by autoimmune process: serum IgG antibodies bind to TSH receptors in thyroid —> stimulating TH production *Characterised by breakdown of self-tolerance to thyroid auto-antigens
51
What are the triad of manifestations of Graves?
1. Thyrotoxicosis - present in all cases - caused by a diffusely enlarged, HYPERfunctional thyroid 2. Infiltration ophthalmopathy with resultant exophthalmos 3. Localised, infiltration dermopathy (sometimes designated pretibial myxedema)
52
What is the morphology of Grave’s disease?
Thyroid gland enlarged (usually symmetrically) - due to diffuse hypertrophy + hyperplasia of thyroid follicular epithelial cells - Gland soft + smooth, intact capsule - Gland diffusely hyperplastic - Follicles lined by tall columnar epithelial cells —> crowding forms small papillae —> project into lamina ^*These cells actively reabsorbed the colloid in the centres of follicles —> “scalloped” appearance of edges of colloid
53
What causes characteristic wide, staring gaze + lid lag in Graves?
Sympathetic over activation
54
What is the lab finding for Graves?
Elevated serum free T4, T3 | Decreased serum TSH
55
Describe diffuse goitre, colloid goitre and multinodular goitre.
Diffuse goitre (diffuse, symmetric enlargement of gland) - due to TSH-induced hypertrophy + hyperplasia of thyroid follicular cells Colloid goitre - develops when dietary iodine subsequently increases / demands for TH decrease —> stimulated follicular epithelium involuted to form an enlarged, colloid-rich gland Multinodular goitre - develops when recurrent episodes of hyperplasia + involuted combine => more irregular enlargement of thyroid *Hyperplastic follicles contain abundant pink colloid within their lumina. There’s absence of prominent capsule
56
What is toxic multinodular goitre?
Aka Plummer syndrome | - thyrotoxicosis secondary to dev of autonomous nodules that produce TH independent of TSH stimulation
57
What are the consequences of goitre?
Can cause airway obstruction, dysphagia, compression of large vessels in neck + upper thorax —> superior vena cava syndrome *Tracheal +/- oesophageal compression can lead to laryngeal nerve palsy!
58
What is the distinction (histologically) between multinodular goitre and adenoma of thyroid?
Adenoma - has well defined, intact capsule; solitary spherical lesion compresses adjacent non-neoplastic thyroid Multinodular goitre - NO well-formed capsule; DO NOT demonstrate compression of adjacent thyroid parenchyma
59
What is Hurthle cell adenoma?
Tumour composed of cells with abundant eosinophilic cytoplasm + small regular nuclei *Hurthle = eosinophilic, granular cytoplasm
60
What are the clinical features of adenomas of thyroid?
PAINLESS nodules (mostly) Larger masses may produce local symptoms e.g. difficulty swallowing *Excellent prognosis - do not metastasise
61
What are adenomas of thyroid?
Benign neoplasms derived from follicular epithelium
62
What are the 5P’s in papillary carcinoma of thyroid?
OrPhan Annie eye nuclei - nuclei contains very finely disperse chromatin => optically clear appearance Pseudoinclusions - invagination of cytoplasm => appearance of intraocular inclusions Papillary architecture - papillae lined by cells with orphan Annie eye nuclei Psammoma bodies - concentrically calcified structures (often present within papillae) Painless mass in neck (mostly) - nonfunctional tumour
63
Describe follicular carcinoma of thyroid.
- Composed of fairly uniform cells forming small follicles - May be widely invasive (infiltrating thyroid parenchyma + extra-thyroidal soft tissue) / minimally invasive - solitary cold thyroid nodules - *Spread via bloodstream to lungs, bone, liver (haematogenous dissemination) - Treated with surgical excision - Good prognosis with radio-iodine therapy
64
Describe anaplastic carcinoma of thyroid.
Undifferentiated, aggressive tumour of the thyroid follicular epithelium *Very poor prognosis Morphology: - bulky masses (typically grow rapidly beyond thyroid capsule into adjacent neck structures) - high anaplastic cells - large, pleomorphic giant cells - mixed spindle + giant cell lesions
65
Describe medullary carcinoma of thyroid.
= Neuroendocrine neoplasms derived from parafollicular cells / C cells of thyroid - Larger lesions often contains areas of necrosis + haemorrhages + may extend thru capsule of thyroid - polygonal to spindle shaped cells, which may form nests, trabeculae + even follicles - *Amyloid deposits (derived from altered calcitonin molecules): present in adjacent stroma in many cases *Familial medullary carcinoma: presence of multi centric C cell hyperplasia in the surrounding thyroid parenchyma *
66
What is the MOA of carbimazole in hyperthyroidism?
Blocks organisation of iodine
67
Under normal conditions, hypercalcaemia would cause ___ secretion of calcitonin.
Increased secretion of calcitonin. Calcitonin reduce serum levels of Ca
68
Why would primary adrenal insufficiency lead to hyponatremia?
Thru lack of aldosterone.
69
SIADH causes you to be hypervolemia. True or false?
FALSE. SIADH is a EUVOLAEMIC condition!
70
Where does iodination of tyrosine residues occur in the production of thyroid hormones?
Follicular colloid
71
What happens when there's a benign adrenal tumour in the zona fasciculata of adrenal cortex?
Disturbances of carbs, protein and fat metabolism. Zona fasciculata secrete cortisol so if secreted in excess by tumour --> disturbances of protein carb and fat metabolism
72
Lateral expansion of pituitary tumour is most likely to involve...
Cranial nerve III
73
What are the most common imaging modalities used to assess thyroid nodules?
Radionuclide and ultrasound scans! Not MRI!
74
When a patient has increased plasma cortisol + increased ACTH, what can you rule out?
Secretion of cortisol by an adenoma of adrenal cortex. ^ that would lead to suppression of ACTH + increased cortisol
74
When a patient has increased plasma cortisol + increased ACTH, what can you rule out?
Secretion of cortisol by an adenoma of adrenal cortex. ^ that would lead to suppression of ACTH + increased cortisol
75
How many arterial supplies are there for adrenal glands?
3. From renal artery, from aorta, from phrenic artery
76
Why can adrenal gland still survive when there's an embolism in the adrenal artery from the left renal artery?
Because there's 3 arterial supplies to adrenal gland. Adrenal vessels direct from aorta / from phrenic artery can still supply adrenal gland even without the one from left renal artery
77
What is the most common cause of primary hyperparathyroidism?
Parathyroid adenoma
78
Myxedema coma occurs in?
Hypothyroidism
79
Hypothyroidism in neonates & infants is known as:
Cretinism
80
What's the most appropriate screening test for Cushing syndrome
Low-dose dexamethasone suppression test
81
What thyroid neoplasm can cause hypocalcemia?
Medullary carcinoma = Functional parafollicular (C) cell cancer *Calcitonin is secreted by parafollicular / C cells of thyroid
82
Where does superior thyroid artery originate?
External carotid artery
83
Patchy radioiodine uptake is common in?
Multinodular goitre | Hashimoto's thyroiditis
84
Why are parathyroid glands vulnerable during thryroid surgery?
- parathyroid glands are most commonly supplied by inferior thyroid artery - parathyroid glands lie within the pre-tracheal fascia on the surface of thyroid gland

Clinical Science (8 decks)

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