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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
Q

What are the major actions of glucocorticoids (cortisol)?

A

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

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26
Q

What are the causes of Cushing syndrome?

A

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)
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27
Q

What are the clinical features of Cushing syndrome?

A
  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)
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28
Q

What is Addison disease

A

Destruction of the entire adrenal cortex —> reduced production of mineralcorticoid, glucocorticoid, sex steroids

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29
Q

What are the main organs most commonly involved in MEN type 1?

A

3Ps - parathyroid, pancreas, pituitary

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30
Q

What is the most common manifestation of MEN 1 in parathyroid?

A

Primary hyperparathyroidism

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31
Q

What is the leading cause of death in MEN1?

A

Endocrine tumours of pancreas - aggressive + manifest with metastatic disease

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32
Q

What is the most frequent pituitary cause of MEN 1

A

Prolactin-secreting macroadenoma

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33
Q

What is the organs most commonly involved in MEN type 2A and MEN type 2B?

A

MEN 2A - thyroid, adrenal medulla, parathyroid

MEN 2B - thyroid, adrenal medulla

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34
Q

What are the differences between MEN 2A and MEN 2B?

A

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
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35
Q

What do we use to treat Addison disease?

A

Glucocorticoids + mineralcorticoid replacement

36
Q

What do we use to treat secondary adrenocortical insufficiency (caused by low ACTH from low CRH / pituitary failure) ?

A

Glucocorticoids alone

37
Q

What do we use to treat congenital adrenal hyperplasia (CAH)?

A

Glucocorticoids + mineralocorticoid replacement

38
Q

What is the treatment for primary aldosteronism?

A

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
Q

What do we use to treat Cushing syndrome?

A

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
Q

What is the pharmacological treatment of Pheochromocytoma?

A

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
Q

What is the most common type of hyper functioning pituitary adenoma?

A

Prolactinomas

42
Q

What is the mechanism of prolactin?

A

Controlled by tonic INHIBITION by hypothalamic dopamine

  • stimulates lactation
  • inhibits GnRH secretion + gondola action of LH
43
Q

What are the typical presentations of hyperprolactinemia?

A

Hypogonadism due to suppression of LH + FSH

- Amenorrhoea, galactorrhoea, loss of libido, infertility

44
Q

What is the treatment for hyperthyroidism?

A

Carbimazole

45
Q

What is the treatment for hypothyroidism?

A

Levothyroxine

46
Q

What is Hashimoto thyroiditis?

A

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
Q

What is subacute granulomatous (de Quervain) thyroiditis?

A

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
Q

What is subacute lymphocytic thyroiditis?

A

Silent / painLESS thyroiditis

  • painless neck mass / features of TH excess
  • most likely autoimmune
  • lymphocytic infiltration
49
Q

What is Riedel thyroiditis?

A

Rare, characterised by extensive fibrosis involving thyroid + contiguous neck structure

  • hard + fixed thyroid mass
50
Q

What is Graves’ disease?

A

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
Q

What are the triad of manifestations of Graves?

A
  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
Q

What is the morphology of Grave’s disease?

A

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
Q

What causes characteristic wide, staring gaze + lid lag in Graves?

A

Sympathetic over activation

54
Q

What is the lab finding for Graves?

A

Elevated serum free T4, T3

Decreased serum TSH

55
Q

Describe diffuse goitre, colloid goitre and multinodular goitre.

A

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
Q

What is toxic multinodular goitre?

A

Aka Plummer syndrome

- thyrotoxicosis secondary to dev of autonomous nodules that produce TH independent of TSH stimulation

57
Q

What are the consequences of goitre?

A

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
Q

What is the distinction (histologically) between multinodular goitre and adenoma of thyroid?

A

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
Q

What is Hurthle cell adenoma?

A

Tumour composed of cells with abundant eosinophilic cytoplasm + small regular nuclei

*Hurthle = eosinophilic, granular cytoplasm

60
Q

What are the clinical features of adenomas of thyroid?

A

PAINLESS nodules (mostly)

Larger masses may produce local symptoms e.g. difficulty swallowing
*Excellent prognosis - do not metastasise

61
Q

What are adenomas of thyroid?

A

Benign neoplasms derived from follicular epithelium

62
Q

What are the 5P’s in papillary carcinoma of thyroid?

A

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
Q

Describe follicular carcinoma of thyroid.

A
  • 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
Q

Describe anaplastic carcinoma of thyroid.

A

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
Q

Describe medullary carcinoma of thyroid.

A

= 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
Q

What is the MOA of carbimazole in hyperthyroidism?

A

Blocks organisation of iodine

67
Q

Under normal conditions, hypercalcaemia would cause ___ secretion of calcitonin.

A

Increased secretion of calcitonin.

Calcitonin reduce serum levels of Ca

68
Q

Why would primary adrenal insufficiency lead to hyponatremia?

A

Thru lack of aldosterone.

69
Q

SIADH causes you to be hypervolemia. True or false?

A

FALSE. SIADH is a EUVOLAEMIC condition!

70
Q

Where does iodination of tyrosine residues occur in the production of thyroid hormones?

A

Follicular colloid

71
Q

What happens when there’s a benign adrenal tumour in the zona fasciculata of adrenal cortex?

A

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
Q

Lateral expansion of pituitary tumour is most likely to involve…

A

Cranial nerve III

73
Q

What are the most common imaging modalities used to assess thyroid nodules?

A

Radionuclide and ultrasound scans!

Not MRI!

74
Q

When a patient has increased plasma cortisol + increased ACTH, what can you rule out?

A

Secretion of cortisol by an adenoma of adrenal cortex.

^ that would lead to suppression of ACTH + increased cortisol

74
Q

When a patient has increased plasma cortisol + increased ACTH, what can you rule out?

A

Secretion of cortisol by an adenoma of adrenal cortex.

^ that would lead to suppression of ACTH + increased cortisol

75
Q

How many arterial supplies are there for adrenal glands?

A
  1. From renal artery, from aorta, from phrenic artery
76
Q

Why can adrenal gland still survive when there’s an embolism in the adrenal artery from the left renal artery?

A

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
Q

What is the most common cause of primary hyperparathyroidism?

A

Parathyroid adenoma

78
Q

Myxedema coma occurs in?

A

Hypothyroidism

79
Q

Hypothyroidism in neonates & infants is known as:

A

Cretinism

80
Q

What’s the most appropriate screening test for Cushing syndrome

A

Low-dose dexamethasone suppression test

81
Q

What thyroid neoplasm can cause hypocalcemia?

A

Medullary carcinoma
= Functional parafollicular (C) cell cancer

*Calcitonin is secreted by parafollicular / C cells of thyroid

82
Q

Where does superior thyroid artery originate?

A

External carotid artery

83
Q

Patchy radioiodine uptake is common in?

A

Multinodular goitre

Hashimoto’s thyroiditis

84
Q

Why are parathyroid glands vulnerable during thryroid surgery?

A
  • 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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