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year 2 core concepts > Endo: hormonal problems > Flashcards

Endo: hormonal problems Flashcards

1
Q

What is the location & characteristic of pheochromocytoma?

A
  • catecholamine secreting tumor in chromaffin cells of adrenal medulla
  • 10% extra-adrenal (paragangliomas), bilateral, malignant, NOT associated w/ hypertension
    25% familial: neurofibroma type 1, MEN2
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2
Q

What is the classical triad of pheochromocytoma & other symptoms?

A

Triad: hypertension + headache + sweating
weight loss, Anxiety, palpitations

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3
Q

How is pheochromocytoma diagnosed & treated?

A

24 hour urinary metanephrines twice
pre-op then laparoscopic surgery : 1. Alpha-blocker (phenoxybenzamine) + beta-blocker (propanol) 2. labetalol (blocks both)

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4
Q

what is Addison’s disease? what are the causes?

A
  • decreased cortisol (glucocorticoid) and aldosterone (mineralocorticoid)
  • Autoimmune adrenalitis (destruction to one’s own adrenal cells)
  • Malignancy, infectious adrenalitis
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5
Q

When do the symptoms of Addison’s disease start to appear? What are the symptoms?

A
  • 90% destruction of adrenal gland
  • Aldosterone: Hyponatremia, hyperkalemia, Hypotension
    -cortisol: hypoglycemia
  • Increased ACTH (stimulated cortisol): hyperpigmentation
  • Weight Loss, weakness
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6
Q

How is Addison’s disease diagnosed?

A

Short synACTHen test: stimulated ACTH, cortisol level only increase a little in addison’s patient

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7
Q

What are the treatment options of Addison’s disease?

A
  • Hydrocortisone (c) + fludrocortisone (a)
  • If patient have another disease, ie, infection, double hydrocortisone & fludrocortisone stays the same
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8
Q

What is Cushing’s syndrome and disease, what are the 2 main types? Give some examples

A

High level of cortisol (disease is specific to pituitary problem causing increased ACTH)
Exogenous: glucocorticoid therapy
Endogenous: pituitary adenoma, adrenal adenoma, ectopic ACTH

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9
Q

What are the symptoms of cushing syndrome? MSK manifestations?

A
  • Central weight gain + abdominal striae
  • Buffalo hump, easy bruising, proximal limb muscle wasting
  • Osteoporosis, decrease libido, hirsutism in female
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10
Q

What is the diagnosis of Cushing’s syndrome? what test is needed to find the cause?

A

diagnosed by 24 hr urinary cortisol,
High dose dexamethasone test done to find the cause
ACTH & cortisol both suppressed= pituitary adenoma
ACTH & cortisol both NOT suppressed= ectopic ACTH (SCLC)
Only ACTH suppressed= adrenal adenoma

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11
Q

How is Cushing’s syndrome treated? How is it different for different causes?

A

Glucocorticoid withdrawal
Surgery: Hypophysectomy, adrenalectomy and/or radiotherapy
Metyrapone: last line OR waiting for radiotherapy

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12
Q

What is the function of parathyroid hormone?

A
  • increase absorption of calcium from diet
  • promoting release of calcium from bones, and decreased excretion of calcium by kidneys.
  • increase phosphorus excretion by kidneys to balance calcium and phosphorus levels
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13
Q

how is parathyroid hormones stimulated and suppressed?

A
  • Parathyroid gland have chief cells that detect ionized calcium levels in blood, if the level is low, chief cells release PTH
  • Thyroid gland release calcitonin which lower calcium in blood and suppress activity of PTH
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14
Q

What are the causes of hyperparathyroidism?

A
  • Primary: Solitary adenoma causing overactive chief cells secreting PTH causing hypercalcemia
  • Secondary: hyperplasia from vitamin D deficiency or chronic renal failure leading to decreased calcium absorption, renal resorption, osteoclast activity causing hypocalcaemia, body try to compensate by releasing more PTH leading to hyperplasia of parathyroid gland
  • Tertiary: hyperplasia leading to chronic High levels of PTH & hypercalcemia
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15
Q

What are the symptoms and patient profile of hyperparathyroidism?

A
  • Bones, stones, abdominal groans, psychic moans
  • Polydipsia, polyuria
  • Depression, anorexia
    “Elderly female come in very thirsty with normal or raised parathyroid hormones”
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16
Q

What is the investigation for hyperparathyroidism?

A
  • Bloods:increased PTH and calcium in primary & tertiary, increased PTH with low calcium in secondary
  • X-ray: osteopenia, pepperpot skull (small spots of lucencies in skull due to resorption of trabecular bone)
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17
Q

What is the treatment for hyperparathyroidism?

A
  • Total parathyroidectomy
  • cinacalcet (calcimimetic that activates calcium sensing receptor, used if patient is not suitable for surgery)
  • increase vitamin D or kidney transplant (treat underlying cause of hyperplasia)
18
Q

What are the causes of hypercalcemia?

A
  • Hyperparathyroidism (solitary adenoma)
  • Malignancy (squamous cell lung cancer, bone metastases, myeloma )
  • Vitamin D, thiazide, lithium
  • Sarcoidosis, Familial hypocalciuric hypercalcemia
19
Q

what are the symptoms of hypercalcemia?

A

Stones, bones, moans, groans
polydipsia, polyuria
Short QT interval on ECG

20
Q

if the patient have hypercalcemia what tests should be done to find the cause?

A
  • high PTH: measure urinary Ca+ excretion (high in primary hyperparathyroidism, low in FHH)
  • normal PTH: screen malignancy
21
Q

treatment for hypercalcaemia?

A
  • Rehydration with normal saline
  • bisphosphonate or calcitonin or furosemide
  • treat underlying cause
22
Q

What is the cause and treatment for hypoparathyroidism?

A
  • Surgery of the whole thyroid gland causing decreased PTH secretion leading to low calcium and high phosphate
  • Treat with alfacalcidol
23
Q

What is the cause & presentation of pseudoparathyroidism?

A
  • Genetic disorder causing mutation in G-protein receptors responsible of PTH signal transportation to target cells, this leads to PTH resistance, Hypocalcemia, and hyperphosphatemia
  • Low IQ, short stature, shortened 4th and 5th metacarpals
24
Q

What are the causes of hypocalcemia?

A
  • Vitamin D deficiency (osteomalacia/ softening of bones)
  • Hypoparathyroidism post thyroid surgery
  • chronic kidney disease, Acute pancreatitis
25
Q

What are the symptoms of hypocalcemia?

A
  • Peripheral paraesthesia (tingling at fingers / toes)
  • Bronchospasm
  • Chvostek’s sign – spasm of facial muscle on percussion
  • Trousseau’s sign – wrist contraction with cuff inflation
  • QT prolonged, bradycardia, arrhythmia
26
Q

What is the management for hypocalcemia?

A
  • IV calcium gluconate with ECG monitoring for Severe (carpopedal spasm, prolonged QT)
  • Treat underlying cause
27
Q

What is the difference between thyrotoxicosis and hyperthyroidism?

A
  • Thyrotoxicosis: tissues exposed to excessive thyroid hormone t3/t4
  • Hyperthyroidism: overactivity of thyroid creating excessive hormones
28
Q

What are the symptoms of grave’s disease?

A
  • eye signs: exophthalmos (protruding eyeballs)
  • pretibial myxoedema (plaques of thickened skin + erythema/ red swelling on the leg)
  • soft tissue swelling of the hands and feet + digital clubbing
  • Hyperthyroidism (nervousness, weight loss, hot intolerance, diarrhea, palpitation)
29
Q

what is this?

A

eye sign in grave’s disease: exophthalmos

30
Q

What are the investigations for grave’s disease?

A
  • TFT: low TSH, high T3/T4
  • Antibodies: TSH-receptor stimulating
  • Thyroid scintigraphy: diffuse, homogeneous increased uptake of radioactive iodine
31
Q

What is the treatment for grave’s disease?

A
  • Carbimazole + propanlol
    (ATD therapy + beta blocker for initial symptom relief)
  • Radioiodine therapy if condition prolapses
32
Q

What is the cause & symptoms of toxic multinodular goiter?

A
  • Thyroid gland having number of autonomously functioning thyroid nodules
  • Hyperthyroidism (nervousness, weight loss, heat intolerance, diarrhea, palpitation, tremor)
  • Palpable goiter
33
Q

What is the investigation & treatment of toxic multinodular goiter?

A
  • TFT (decreasedTSH, increase T3/T4) Thyroid scintigraphy: patchy uptake
  • Carbimazole (ATD therapy, not to be used first trimester of pregnancy replace with PTU) + propranolol initially to reduce symptoms in new cases
  • Radioiodine therapy
34
Q

Contrast disease profile of grave’s disease & toxic multinodular goiter

A
  • Toxic multinodular goiter: older adult, not eye signs
  • Grave’s disease: eyes protruding, 40-60 female
35
Q

can you get thyrotoxicosis without hyperthyroidism? If so, what are the symptoms?

A
  • Yes, subacute/ De-quervain’s thyroiditis, occurs post viral infection
    1. Temporary hyperthyroidism, painful goiter/ tenderness in neck, raised ESR
    2. Hypothyroidism
    3. Thyroid function & structure goes back to normal
36
Q

What is the investigation & management of subacute/ De-quervain’s thyroiditis?

A
  • Thyroid scintigraphy: homogenous reduced uptake of iodine-131
  • Self limiting, aspirin & NSAID for thyroid pain
37
Q

What are the causes & associated disease of hashimoto thyroiditis?

A
  • Autoimmune disease causes long term hypothyroidism may lead to acute thyrotoxicosis in the early phase due to damage
  • Associated with coeliac disease & T1DM, may lead to MALT lymphoma
38
Q

What are the symptoms of hashimoto thyroiditis?

A
  • Hypothyroidism (fatigue, weight gain, cold intolerance, constipation, depressed mood)
  • Firm, non-tender goiter (due to increased TSH stimulation from reduced t3/t4)
39
Q

What are the investigation & treatment for hashimoto thyroiditis

A
  • TFT: high TSH, low T3/T4
  • antibodies: anti-TPO (thyroid peroxidase), anti-Tg (thyroglobulin)
  • Give levothyroxine & aim for TSH at normal range (if patient take iron or calcium should be done 4 hours later)
40
Q

What are the side effects of thyroxine therapy w/ levothyroxine for hypothyroidism?

A
  • Hyperthyroidism: from over treatment, may then lead to reduced bone mineral density (osteoporosis)
  • Worsening angina + atrial fibrillation

year 2 core concepts (9 decks)

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