Endocrine

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1
A 28 year old woman is undergoing routine blood workk. Her TSH is 2.1mIU/L ( normal 0.4-4), free T4 is 14pmol/L ( normal 10-20), and free T3 is 4.5pmol/l ( normal 3.5-7.5).
Which physiological mechanism maintains this state?
  • Elevated free T4 and T3 suppresses CRH release from the hypothalamus and TRH from the pituitary, reducing further TSH secretion and maintain normal hormonal balance
  • Free T3 and T4 provide negative feedback at both the hypothalamus and anterior pituitary suppressing TRH and TSH secretion when hormone levels are adequate
  • High TSH levels directly inhibit thyroid perioxidase activity preventing excessive thryoid hormone synthesis and maintaining negative feeback control
  • The thyroid gland automatically senses circulating thyroid hormone levls and self regulates syntehsiss without requiring pituitary or hypothalamic input
  • TSH continously stimulates thyroid hormones rleases but peripheral tissue degrade excess hormones
2
A 28 year old man with Grave's disease presents with ocular findings. (Bulging eyes)
Which pathophysioloigcal mechanism explains these findings?
  • Acute anaphylaxis of orbital mast cells
  • Thyroid hormone induced hypertrophy of extraocular muscle fibres
  • Thyroid hormone toxicity to the optic nerve
  • TSH immunoglobulin binding to the choroid
  • TSH receptor expression on oribital fibroblasts and immune filtration
3
A patient with untreated Graves disease has tachycardia,tremor, weight loss, heat intolerance and increased resting energy expenditure as measured by indirect calorimetry.
Which mechanism best accounts for the increased resting energy expenditure in this patient?
  • Increased cellular oxygen consumption and ATP turnover
  • Increased hepatic production of glucose and ketone bodies
  • Increased mobilisation of stored lipid and glycogen reserves
  • Increased skeletal muscle utilisation of glucose and fatty acids
  • Increased tissue responsiveness to circulating catechloamines
4
A 45 year old woman with recently diagnosed Hashimoto's Thyroiditis has anti TPO antibodies and elevated TSH with low free T4. A thyroid biopsy shows lymphocytic infiltration destroying the follicular epithelial cells. Her remaining thyroid tissue still produces thyroglobulin but very little T3 and T4 are being synthesised.
Which enzyme, the target of her antibodies catalyses the step that is failing?
  • Deiodinases enzymes responsible for converting T4 to T3 in peripheral tissues
  • Sodium iodide symporter activity responsible for transporting iodine into the thyroid
  • Thyroglobulin synthesis responsible for providing the protein scaffold for hormone assembly
  • Thyroid peroxidase activity responsible for iodinating tyrosine residues and coupling them to form T3 and T4
  • TSH receptor signalling responsible for triggering hormone release from storgae granules
5
A 48 year old woman with progressive fatigue, hypotension, hyperkalameia and hyponatremia. Her 09:00 cortisol is 80nmol/L and only rises to 95nmol/L 30 minutes after an intramuscular injection of synthetic ACTH. ACTH is markedly elevated and anti 21-hydroxylase antibodies are positive.
Which autoimmune mechanism is responsible?
  • Antibody mediated blockade od ACTH receptors
  • CD4+ T cell drive production of stimulatory antibodies against the adrenal cortex
  • CD8+ cyctotoxic T cells mediated destruction of steroidogeneic enzyme expressing cells
  • Complement mediated lysis of zona fasciculata cells only
  • Type 1 hypersensitivity to adrenal lipids
6
A 60 year old man with Addison's disease on glucocorticoid and mineralocorticoid replacement undergoes emergency appendicetomy,
Why must his glucocorticoid dose be increased perioperatively?
  • Acute inflammation from appendicitis increases cortisol binding globulin production, reducing free cortisol availablity and requiring higher doses
  • Cortisol requirements are markedly elevated during acute stress- his adrenal cannot mount an endogenous stress response so replacement must compensate
  • Perioperative cortisol suppresses excessive inflammatory and immune responses that would otherwise impair wound healing and increase infection risk at the surgical site.
  • Perioperative fluid shifts and blood loss deplete glucocorticoid stores rapidly - higher replacement compensates for increased urinary and faecal losses
  • Surgical trauma and anaesthesia increases hepatc metabolism of hydrocortisone , shortening half life and requiring higher doses to maintain adequate levels
7
A patient with Addison's disease has elevated levels of ACTH.
Which clinica sign results from this elevation?
  • Alopecia
  • Hyperpigmentation
  • Hyponatraemia
  • Hypotension
  • Proximal muscle weakness
8
A 35 year old woman with Addison's disease takes hyrocortisone and fludrocortisone. her blood pressure including postural readings, electrolytes and plasma renin are all normal. She reports persistent fatigue that does not vary through the day, along with low libido, dry skin and loss of axillary and pubic hair. There is no evidence of malabsoprion,mental health conditions, anaemia or thyroid disease.
What is the most likely reason for her persistent fatigue?
  • Her adrenal androgens are absent standard replacement does not include them
  • Hydrocortisone absorption is impaired due to associated coeliac disease
  • Hydrocortisone is being converted to inactive metabolites too rapidly
  • She has developed secondary hypothyroidism from autoimmune thyroiditiis
  • She requires higher doses of hydrocortisone despite biochemical normalisation
9
A 55 year old man with longstanding Addison's disease ( well controlled on replacement therapy) undergoes routine screening and is found to have elevated TSH and borderline low free T4.
What is the most likely diagnosis?
  • He has developed Hashimoto's thyroiditiis
  • He has secondary hypothyroidism from pituitary infarction
  • His fludrocortisone is interfering with thyroid hormone metabolism
  • His hydrocortisone absorption is poor
  • His hydrocortisone dose is too high suppressing TSH
10
Adie tested positive for anti TSH receptor antibodies, which are at the core of the pathophysiology of her condition.
What is their primary role in this process?
  • Antibody dependent cell mediated cytotoxicity of thryoid tissue
  • CD4+ T cell driven production of stimulatory IgG antibodies against TSH receptors
  • Complement mediated destruction of the thyroid follicular basement membrane
  • Cytotoxic CD8+ T cells destroying thyroid follicles
  • Type I hypersensitivity reaction with mast cell degranulation
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