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4a. ENDOCRINE > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Name the main types of receptor and hormone.

A

Hormone: gene-encoded made of polypeptides (oxytocin, GH, FSH); amino acid modification (adrenaline, melatonin); steroid (cholesterol, testosterone).
Receptors: GPCRs; tyrosine kinase (RTKs); those associated with tyrosine kinase activity (cytokines); steroid receptors

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2
Q

Describe the hypothalamus-pituitary-thyroid axis, and the -adrenal gland axis.

A

Hypo (TRH) -> AP (TSH) -> Thy (T3, T4, calcitonin)
Hypo (CRH) -> AP (ACTH) -> Adr (cortisol)
TSH/ACTH and T3/4/cortisol act in a negative feedback loop on their target organs and the hypothalamus

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3
Q

Describe the special considerations needed for measuring cortisol.

A

Cortisol follows a Circadian rhythm, meaning it is highest at 9am and lowest at 10pm. Requires suppression test (if too much; Cushing’s) or stimulation test (if too little; Addison’s)

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4
Q

Describe the basic diagnostic pathway of endocrine disease.

A

History and exam
Screening biochemistry panel (9am cortisol, hormones including thyroid, U&Es and osmolality)
Dynamic testing (e.g. suppression or stimulation)
Imaging (if necessary to localize problem)
Management

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5
Q

Describe the regions of the cranial fossae.

A

Anterior cranial fossa: frontal and ethmoid
Middle: sphenoid, part of temporal. Contains sella turcica
Posterior: occipital, part of temporal
Sella turcica contains pituitary fossa

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6
Q

Describe the contents and surrounding contents of the cavernous sinus.

A

Contents: internal carotid, occulomotor, trochlear, abducens, V1 nerves
Superior: pituitary, diaphragma sella
Inferior: sphenoid sinus

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7
Q

Describe the course of the optic nerve (CN III) and how pituitary adenoma may impact on function.

A

Temporal and nasal fields cross over at the optic chiasm.

Pituitary sits immediately inferior to the optic chiasm, so impedes on temporal flow: bitemporal hemianopsia

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8
Q

Describe the fascia of the neck at vertebra C7.

A

Platysma - superficial, in subcutaneous tissue
Investing fascia - invests SCM and trapezius, and all other fascia
Pretracheal - contains trachea, oesophagus, and thyroid
Carotid sheath - contains common carotid, vagus, IJV
Alar fascia - connects carotid sheaths
Retropharyngeal space between alar and pretracheal fascia
Prevertebral fascia - invests vertebral column and muscles

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9
Q

Name the infrahyoid (thyroid) muscles.

A

Omohyoid (shoulder)
Sternothyroid
Thyrohyoid
Sternohyoid

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10
Q

Describe how a thyroglossal cyst may arise.

A

Thyroid begins as midline epithelial proliferation between the anterior 2/3 and posterior 1/3 of the tongue (foramen caecum) then descends in the thyroglossal ducts; remnants and pyramidal lobe can cause cysts

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11
Q

Describe the arterial and venous supply of the thyroid.

A

External carotid -> superior thyroid art.
Thyrocervical trunk (subclavian) -> inferior thyroid art.
Superior, middle thyroid veins -> internal jugular
Inferior thyroid vein -> brachiocephalic trunk

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12
Q

Describe the pituitary-thyroid axis, and how T4/T3 is synthesized. Name the carrying proteins used to transport T4/3 to tissues.

A

Hypothalamus (TRH) -> anterior pituitary (TSH) -> thyroid
Iodide (I-) -> Iodine (I), then binds with thyroglobulin (Tg) to form MIT or DIT. 2xDIT = T4; DIT + MIT = T3.
Thyroid binding globulin (TBG), Thyroxine-binding pre-albumin (TBPA), albumin

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13
Q

Name the effects of T4/3 on peripheral tissues.

A

Acts via the GsPCR to increase cAMP
Glycogenolysis, gluconeogenesis
Lipolysis (fatty acid oxidation)
Increased heart, respiratory rates (B1, 2)
Increased mitochondrial synthesis, resp enzymes
Increased thermogenesis (B3)
Myelinogenesis

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14
Q

Describe the degradation of T4/3.

A

Three types of de-iodinase (D1, D2, D3)

D1 (liver, kidney), D2 (most other organs), D3 (brain except the pituitary; majority of degradation)

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15
Q

Regarding the presentation of thyroid nodules:

  • describe the differential diagnosis
  • describe important aspects of the history
  • describe the main investigations
A

Most are benign adenomas, but may be goitres (e.g. Graves’) or carcinoma.
Is there a lump? Does it move on swallowing? Is it painful? (it shouldn’t be - indicates bleeding). Check PMHx of irradiation, and symptoms of mass effect (e.g. dysponea, stridor, dysphagia etc.)
US-guided fine needle aspiration (FNA), bloods (TSH, Tg)

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16
Q

Describe the classification of thyroid carcinomas, and the grading system.

A

Papillary, follicular, anaplastic (3x thyroid epithelium), and medullary (parafollicular).
(papillary spreads via lymph, follicular via blood. 30% of MTC due to MEN syndromes)
Thy1 (not enough sample to tell)
Thy2/U2 - benign
Thy3/U3 - further investigation needed
Thy4/U4 - probably malignant
Thy5/U5 - malignant

17
Q

Describe the management of thyroid carcinoma.

A

(most carcinomas take up iodine, and secrete Tg)

  • Surgery is the management of choice. 3 options - hemithyroidectomy, subtotal, and total thyroidectomy.
  • Whole body iodine scan is done in conjunction, to assess whether there is residual tissue/mets
  • thyroid remnant ablation (TRA) for refractive cases (3.3 GBq Iodine). Requires inpatient admission in lead lined room
  • sorafenib, lenvatinib (tyrosine kinase inhibitors)
18
Q

Describe the main causes, symptoms, and treatment for thyrotoxicosis.

A

Graves’ (85%), adenoma (10%), ectopic production

  • autoantibodies against the TSH receptor, causing overstimulation
  • anxiety, tremor, irritability, trouble sleeping
  • exopthalamos, ptosis, lid lag
  • tachycardia, palpitation, AFib, intolerance to heat, pretibial myxoedema
  • weight loss (despite increased appetite)
  • irregular menstrual cycle
  • beta-blockers with symptomatic relief, carbimazole or PTU for thyroid suppression
19
Q

Describe the main causes, symptoms, and treatment for hypothyroidism.

A

Hashimoto’s, iodine deficiency, lithium, surgery for thyrotoxicosis

  • autoantibodies with CD8+ mediated destruction against Tg, peroxisomes
  • depression, mental/motor slowing, psychosis
  • periorbital puffiness
  • bradycardia, cold intolerance, lipidaemia
  • weight gain, diarrhoea, risk of ascites/megacolon
  • oligo/amenorrhoea, hyperprolactinaemia
  • levothyroxine 25-50mg
20
Q

Describe the major hyperthyroid and hypothyroid emergencies.

A

Hyper - thyroid storm. resp/cardiac failure, hyperthermia. Treat with iodine, steroids, PTU, B-blockers, fluid, and ventilation.
Hypo - myxoedema. bradycardia, low voltage complexes, heart block, T wave inversion. Treat with ABCDE and passively rewarm

21
Q

Briefly describe the six major endocrine genetic disorders.

A

MEN1 (MEN1 - 11q13): 3 P’s (hyperparathyroidism, pituitary, pancreas). regular screening required
MEN 2 (RET - 10q): associated with medullary thyroid carcinoma and phaeochromocytoma. MEN2B also associated with marfans, mucosal tumours. prophylactic thyroidectomy suggested (risk of MTC)
Von-Hippel-Lindau (VHL). accumulation of HIF (aberrant oxygen sensing). Retinal/CNS blastomas, and phaechrom.
Carney complex - PKA signalling with GPCR. Causes myxomas (e.g. atrial), Cushings’, acromegaly
McCune-Albright - somatic mutation to GNAS (cAMP)
Phaeochromocytoma - succinate dehydrogenase.

22
Q

Name the layers of the adrenal gland and what each produces.

A 
Capsule
Zona glomerulosa - mineralocorticoids (e.g. aldosterone)
Zona fasciculata - glucocorticoids
Zona reticularis - androgens
Medulla - catecholamines
23
Q

Describe the pathology, symptoms, biochemistry, diagnosis, and management of Addison’s disease.

A

Primary adrenal insufficiency - can produce a crisis if infection etc. is superimposed
Anorexia, weight loss,, fatigue, hypotension, pigmentation, vomiting, diarrhoea
Low Na, high K, hypoglycaemia
Short synacthen test (<55nmol)
IV hydrocortisone, fludrocortisone, sick day rules

24
Q

How does secondary adrenal deficiency differ from Addison’s?

A

aldosterone is preserved (controlled by RAAS system). pigmentation (POMC)/hypotension do not occur. no fludrocortisone is needed

25
Q

Describe the pathology, symptoms, biochemistry, diagnosis, and management of Conn’s syndrome.

A

Primary aldosteronism, common cause of secondary htn
Muscle cramp, hypertension, fatigue, polydipsia, polyuria
High Na, low K
Aldosterone: renin ratio, saline suppression <50%
Unilateral: surgery
Bilateral: spironolactone

26
Q

Describe the pathology, presentation, biochemistry, diagnosis, and management of congenital adrenal hyperplasia.

A

Defect in 21a-hydroxylase, causing excess androgen production.
Classic: virilization, salt wasting, poor weight gain, female genital ambiguity
Non classic: hirsutism, acne, precocious puberty, infertility, oligomenorrhoea
Low Na, high K
17-OH-progesterone
Classic: as in Addison’s (e.g. IV steroid, fludrocortisone)
Non-classic: restore fertility and avoid steroid excess

27
Q

Describe the pathology, symptoms, biochemistry, diagnosis, and management of phaeochromocytoma.

A

Tumour in the adrenal medulla.
Classic triad: sweating, headache, hypertension; palpitation, dyspnoea, anxiety, weight loss etc
High HCT, glucose, Ca2+, lactic acidosis
Urinary catecholamines/metanephrines (ideally when symptomatic)
a-blocker -> B-blocker, may need fluids/blood

28
Q

Describe calcium/vitamin D metabolism.

A

Skin/GI tract absorb vitD analogues, converted to vitamin D
VitD -> 25-OH-D (liver, 25-hydroxylase)
25-OH-D -> 1, 25-(OH)2-D (kidney, 1a-hydroxylase)
25-OH-D -> 24, 25-(OH)2-D (kidney, 24 hydroxylase)
These cause increased serum calcium by increasing absorption from the GI tract and breakdown of bone. Increased metabolites inhibit PTH release (which increases serum Ca2+)

29
Q

Describe presentation, diagnosis and management of hypercalcaemia.

A

Bones, stones, abdominal groans, psychiatric moans, arrhythmia
High serum Ca2+, high urinary excretion, raised/inappropriately normal PTH
Fluids, rehydration, bisphosphonates -> loop diuretics -> cinaclet

30
Q

Describe presentation and management of hypocalcaemia.

A

Paraesthesiae, muscle cramps, tetany, fatigue, bronchospasm, long QT on ECG
IV calcium gluconate 10ml/10% over 10min

31
Q

Name the body compartments. Describe the ability of Na/H2O to move between these, and the hormones that control their balance.

A

Two compartments - extracellular (plasma, interstitial fluid) and intracellular.
H2O may move between compartments, but 99% Na+ in the extracellular compartment.
ADH retains water (from posterior pit.)
Aldosterone retains Na+ (from adrenals)

32
Q

What is the normal range of Na+? (remember: exists as a ratio, Na+ / H2O)

A

135 - 145 mmol/l

33
Q

Describe the pathology, presentation, and treatment of hypernatraemia.

A

> Na - IV meds, near drowning, malicious
< H2O - can’t eat/drink, diabetes insipidus
——-
symptoms similar to cardiac failure : oedema, weak heart pumping, pleural effusion, cough, ascites, peripheral oedema
——-
Na - 5% dextrose
< H2O - desmopressin, fluid replacement

34
Q

Describe the pathology, presentation, and treatment of hyponatremia.

A 
< Na - Addison's, vomiting
> H2O - SIADH
-------
symptoms of dehydration: decreased elasticity, hypotension, tachycardia, decreased mucous membranes
--------
< Na - IV steroids
> H2O - fluid restriction

4a. ENDOCRINE (3 decks)

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