Deck 2 Flashcards
- Q. What is the most common cause of hypothyroidism? Who does it most commonly affect? Describe the clinical presentation
A. Autoimmune thyroiditis: cell and antibody mediated destruction of thyroid tissue
B. More common in women, increased risk with age, associated with iodine-deplete areas
C. (SIGNS) BRADYCARDIA: bradycardiac, reflexes relax slowly, ataxia, yawning, cold hands, ascites, round puffy face, defeated demeanour, immobile, CCF
D. SYMPTOMS RS: Hoarse voice, GI: constipation, INt: cold intolerance, Endo: weight gain, UG: menorrhagia, MSK: myalgia, weakness, Neuro: tired, low mood, dementia
- Q. What investigations are carried out for suspected hypothyroidism? What would be seen? What is the treatment?
TSH levels - high (primary hypothyroidism)
Free T4 levels are low
Autoimmune: thyroid antibodies and other organ specific antibodies
Tx: life-long levothyroxine to normalise TSH levels
- Q. How may severe hypothyroidism present?
Myxedema coma - confusion and coma (more common in elderly) - hypothermia + cardiac failure + hypoventilation + hypoglycaemia and hyponatraemia
- Q. What is the most common cause of hyperthyroidism? Describe the basic pathophysiology
Grave’s disease, the result of IgG antibodies binding to TSH receptors and stimulating the thyroid/thyroid (T3/T4) production
- Q. What symptoms and signs are seen in hyperthyroidism?
SIGNS
Hands - palmar erythema, warm moist skin, fine tremor
Pulse - tachycardia, SVT/AF
Face - thin hair, lid lag/retraction
Neck- GOITRE nodules, briut
SYMPTOMS CVS: palpitations GI: diarrhoea INT: heat intolerance ENDO: loss of weight, increased appetite UG: oligomenorrhoea, +- infertility NEURO - tremor, irritability, labile emotions
Q. hyperthyroidism - Describe the investigations and treatment
Ix: low TSH, T3 and T4 elevated
Grave’s disease: elevated serum microsomal and thyroglobulin antibodies
Thyroid US differentiates between Grave’s disease and toxic adenoma
Treatment:
Antithyroid drugs e.g. carbimazole - blocks thyroid hormone biosynthesis and immunosuppressive
Radioactive iodine - accumulates in the gland and results in local irradiation and tissue damage
Surgery (lifelong measurement of TSH in case of hypothyroidism)
- Q. What is ophthalmic Grave’s disease? Why does this occur?
Lid retraction and lid lag - delays in movement of the upper eyelid as the eye moves down
Occurs due to increased catecholamine sensitivity in hyperthyroidism
Exophthalmos (proptosis, protruding eyeballs) and ophthalmoplegia (limitation of eye movements)
AE: T-lymphs react with one or more antigen shared by the thyroid and orbit triggering a cascade of events leading to retro-orbital inflammation
Swelling and oedema lead to limitation of movement and proptosis
Ophthalmic Grave’s disease - Ix, Mx
Clinical features: bilateral eye involement, pressure or pain in eyes, gritty sensation, decreased vision and photophobia (more severe in smokers)
Conjunctival oedema, lid lag and corneal scarring are secondary to proptosis and lack of eye cover
Ix: diagnosis with Grave’s disease, MRI excludes other causes e.g. retro-orbital tumour, shows oedema and enlarged muscles
Mx: correction of thyroid dysfunction, smoking cessation, artificial tears, high dose steroids e.g. prednisolone
- Q. What is Cushing’s syndrome? What may cause it?
A. Persistent and inappropriately raised glucocorticoid levels, most commonly due to excess
ACTH secretion from the pituitary gland
B. ACTH dependent: pituitary (Cushing’s disease), ectopic ACTH producing tumours (small-cell lung cancer, carcinoid tumours, ACTH administration)
C. Non-ACTH dependent: adrenal adenoma, adrenal carcinoma, glucocorticoid administration (cortisol)
D. Others: alcohol induced pseudo-Cushing’s syndrome
- Q. What signs and symptoms are seen in Cushing’s syndrome?
S&S: obesity (central fat distribution, trunk/abdomen/neck -buffalo humo), plethoric complexion, moon face, skin is thin and bruises easily, purple straie on abdomen, breast, thighs
Others: depression, change of appearance, insomnia, poor libido, hair growth/acne, back pain
Pigmentation is ACTH dependent
What is Cushing’s disease?
Cushing’s disease is when there are excessive glucocorticoids due to inappropriate ACTH secretion from the pituitary (usually due to adenoma or corticotropin hyperplasia)
- Q. What investigations may be carried out in Cushing’s syndrome/disease?
48-hr low-dose dexamethasone suppression test - normal individuals can suppress plasma cortisol levels to a normal level 2 hours after the last dose
24hr urinary free cortisol is raised
Circadian rhythm shows loss of normal circadian fall of plasma cortisol at 2400
Adrenal or pituitary MRI or CT to establish the cause e.g. adenoma
- Q. What is the treatment of cushing’s syndrome/disease?
Surgical removal of tumours, drugs that inhibit cortisol synthesis e.g. metyrapone, external beam irradiation
- Q. Name 6 endocrine causes of hypertension
Renin - renal artery stenosis, renin-secreting tumours
Aldosterone - adrenal adenoma, adrenal hyperplasia
Mineralcorticosteroids: Cushing’s syndrome/disease (cortisol)
Catecholamines: phaeochromocytoma (catecholamine producing tumour, usually in the adrenal gland)
GH: adenoma secreting → acromegaly/gigantism
Oral contraceptive pill - unclear AE
- Q. What clinical features are seen in primary hyperaldosteronism? What is the name of this syndrome?
HTN and hypokalaemia → often due to adrenal adenoma secreting aldosterone or bilateral adrenal hyperplasia
Conn’s syndrome
