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ENDOCRINOLOGY Flashcards

1
Q

what is acromegaly?

A

excess GH secretion

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2
Q

what are the complications associated with acromegaly?

A
  • cardiomyopathy, arrhythmia, valvular, and ischaemic heart disease
  • Hypertension
  • Sleep apnoea
  • Diabetes.
  • Pre-cancerous polyps and colorectal cancer
  • Bilateral carpal tunnel syndrome
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3
Q

what are the clinical features of acromegaly?

A
  • Coarse facial appearance including frontal bossing, enlarged nose, prognathism, separation of teeth, and macroglossia.
  • Increase in size of hands, the patient may complain that their wedding ring no longer fits.
  • Increase in size of feet, the patient may complain that their shoes no longer fit.
  • Excessive sweating.
  • Joint pain and dysfunction.
  • Snoring.
  • Alteration in sexual functioning.
  • Fatigue.
  • Features of pituitary tumour include headache and bitemporal hemianopia.
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4
Q

how is acromegaly diagnosed?

A
  • elevated serum IGF-1
  • OGTT with no suppression of GH
  • pituitary adenoma on MRI
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5
Q

how is acromegaly managed?

A
  • trans-sphenoidal tumour resection
  • octreotide
  • carbergoline if mixed GH/prolactin secretion
  • pegvisomant
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6
Q

what is Addison’s disease?

A

primary adrenal insufficiency

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7
Q

what are the clinical features of Addison’s disease?

A
  • Fatigue.
  • Anorexia.
  • Weight loss.
  • Hyper-pigmentation in primary adrenal insufficiency (A lack of ACTH production means a lack of melanocyte stimulating hormone)
  • Salt craving.
  • History of other autoimmune disease such as pernicious anaemia and coeliac disease.
  • History of worsening hypothyroidism symptoms when levothyroxine is started.
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8
Q

what are the clinical features of Addison’s adrenal crisis?

A
  • Hypotension.
  • Hypovolaemic shock.
  • Acute abdominal pain.
  • Fever.
  • Vomiting.
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9
Q

how is Addison’s disease diagnosed?

A

ACTH stimulation test: no change in serum cortisol

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10
Q

how is Addison’s disease managed?

A
  • Offer glucocorticoid replacement therapy (hydrocortisone 20 mg daily in 3 divided doses).
  • Offer mineralocorticoid replacement therapy (fludrocortisone 0.2 mg orally once daily).
  • Offer androgen replacement (dehydroepiandrosterone) for women with decreased libido.
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11
Q

how is an adrenal crisis managed?

A
  • Administer intravenous hydrocortisone (100 mg every 6-8 hours for 1-3 days).
  • Administer 1 litre of 0.9% saline over 60 minutes if there is hypotension and dehydration.
  • Administer 5% dextrose if there is hypoglycaemia.
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12
Q

how should the dose of glucocorticoid and mineralocorticoid be altered on a sick day in Addison’s?

A
  • double glucocorticoid

- mineralocorticoid stay the same

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13
Q

how is congenital adrenal hyperplasia inherited?

A

-autosomal recessive

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14
Q

what are the clinical features of a salt wasting crisis in congenital adrenal hyperplasia?

A
  • Hypotension.
  • tachycardia.
  • Vomiting.
  • Poor feeding.
  • Failure to thrive.
  • Progression to adrenal crisis.
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15
Q

what are the features of congenital adrenal hyperplasia in non-salt wasting patients?

A
  • Virilisation of female genitalia such as enlarged clitoris, fused labia, and a urogenital sinus.
  • Small testes and hyper pigmentation of scrotum in male.
  • Hirsutism.
  • Precocious puberty.
  • Short stature.
  • Irregular menses.
  • Infertility.
  • Male-pattern baldness.
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16
Q

how is congenital adrenal hyperplasia diagnosed?

A
  • Measure serum 17-hydroxyprogesterone levels: Elevated for age.
  • Perform a rapid ACTH stimulation test to establish the diagnosis: 17-hydroxyprogesterone levels remain high.
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17
Q

what is seen on blood gas in a salt wasting crisis?

A
  • Hyponatraemia
  • Hyperkalaemia
  • Metabolic acidosis in a salt wasting crisis and hypoglycaemia.
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18
Q

how is congenital adrenal hyperplasia managed?

A

lifelong hydrocortisone and fludrocortisone

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19
Q

what are the clinical features of a craniopharyngioma?

A
  • Acute loss of vision, such as a bitemporal hemianopia affecting the lower quadrant.
  • Growth failure.
  • Difficulty concentrating.
  • Macrocephaly (hydrocephalus).
  • Amenorrhoea.
  • Erectile dysfunction.
  • Headache.
  • Galactorrhoea.
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20
Q

how is a craniopharyngioma managed?

A
  • Perform surgical biopsy and resection.

- Offer endocrine replacement therapy.

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21
Q

what are the causes of Cushing’s syndrome?

A
  • exogenous corticosteroids
  • An ACTH secreting pituitary adenoma, this is known as Cushing’s disease.
  • An ACTH secreting small cell lung cancer.
  • A cortisol secreting adrenal adenoma, this causes low ACTH via negative feedback.
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22
Q

what are the complications of cushing’s syndrome?

A
  • Cardiovascular disease.
  • Hypertension.
  • Diabetes mellitus.
  • Osteoporosis.
  • Nephrolithiasis.
  • Nelson’s syndrome after bilateral adrenalectomy.
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23
Q

what are the symptoms of cushing’s syndrome?

A
  • Central weight gain.
  • Amenorrhoea.
  • Poor libido.
  • Hirsutism and acne.
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24
Q

what are the signs of Cushing’s syndrome?

A
  • Facial plethora and supraclavicular fullness.
  • Thin skin.
  • Easy bruising.
  • Striae.
  • Proximal myopathy.
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25
Q

how is Cushing’s diagnosed?

A
  • Perform 1 mg overnight dexamethasone suppression test: Raised morning cortisol.
  • Perform 24-hour urinary free cortisol: Elevated.
  • Measure serum ACTH: Raised in Cushing’s disease or ectopic ACTH secretion; Low with adrenal adenoma.
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26
Q

How is Cushing’s syndrome managed?

A
  • Offer medical therapy (metyrapone or ketoconazole) prior to surgery
  • Perform trans-sphenoidal pituitary adenomectomy as the first line management of Cushing’s disease.
  • Perform surgical resection of a bronchial tumour if there is ectopic ACTH secretion.
  • Perform unilateral adrenalectomy if there is a unilateral adrenal adenoma or carcinoma, with adjunct chemotherapy for patients with adrenal carcinoma.
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27
Q

what are the causes of cranial diabetes insipidus?

A
  • Trans-sphenoidal pituitary surgery usually for a pituitary adenoma.
  • Craniopharyngioma or pituitary stalk lesions.
  • Autoimmune disorders such as Hashimoto’s thyroiditis and type 1 diabetes.
  • Subarachnoid haemorrhage and traumatic brain injury.
  • Wolfram’s syndrome (DIDMOAD), a syndrome comprising diabetes insipidus, diabetes mellitus, optic atrophy, and deafness, due to mutations in the WFS1 gene.
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28
Q

what are the causes of nephrogenic diabetes insipidus?

A
  • Medications such as lithium, gentamicin and rifampicin.
  • Systemic disease including chronic kidney disease, renal amyloidosis, and hypercalcaemia.
  • Inherited as a sex-lined recessive disease.
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29
Q

what are the clinical features of diabetes insipidus?

A
  • Polyuria.
  • Polydipsia.
  • Nocturia.
  • Dilute urine.
  • Signs of volume depletion e.g. dry mucus membranes, reduced skin turbot, tachycardia, and postural hypotension.
  • Features of hypernatraemia such as irritability, restlessness, lethargy, muscle twitching.
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30
Q

how is diabetes insipidus diagnosed?

A
  • urine osmolality <300mmol/kg
  • elevated serum osmolality
  • elevated sodium and low potassium
  • urine osmolality <300mmol/kg following water deprivation test
  • ADH simulation test: urine osmolality greater than 750mmol/kg in cranial, no increase in nephrogenic
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31
Q

how is cranial diabetes insipidus managed?

A

-desmopressin

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32
Q

how is nephrogenic diabetes insipidus managed?

A
  • Offer a thiazide diuretic (hydrochlorothiazide).
  • Recommend adequate fluid intake.
  • Correct underlying cause for nephrogenic diabetes insipidus, including discontinuing an offending drugs (lithium or gentamicin), treating underlying kidney disease, and correcting electrolyte disturbances.
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33
Q

what is the triad of diabetic ketoacidosis?

A
  • hyperglycaemia
  • hyperketonaemia
  • metabolic acidosis.
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34
Q

what are the clinical features of DKA?

A
  • Known diabetes.
  • Features of diabetes such as polyuria, polydypsia, weight loss.
  • Nausea and vomiting.
  • Abdominal pain.
  • Hyperventilation (Kussmaul respiration).
  • Dehydration suggested by dry mucus membranes, decreased skin turgor, slow capillary refill, tachycardia with a weak pulse, hypotension.
  • Reduced consciousness.
  • Acetone smell on breath.
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35
Q

What is seen on blood gas in DKA?

A
  • Metabolic acidosis with raised anion gap

- Bicarbonate less than 15 mmol/L.

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36
Q

how is DKA managed?

A
  • Fluids

- IV insulin with glucose and potassium

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37
Q

what are the risk factors for diabetic nephropathy?

A
  • Poorly controlled diabetes and sustained hyperglycaemia.
  • Uncontrolled hypertension.
  • Family history of hypertension or kidney disease.
  • Obesity.
  • Smoking.
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38
Q

what are the clinical features of diabetic nephropathy?

A
  • Oedema which may be severe and generalised (anasarca).
  • Fatigue.
  • Anorexia.
  • Nausea and vomiting.
  • Altered taste.
  • Hiccups supervene.
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39
Q

how is diabetic nephropathy diagnosed?

A
  • proteinuria
  • Elevated albumin:creatinine ration
  • reduced eGFR
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40
Q

how is diabetic nephropathy managed?

A
  • good glycemic control
  • ACE inhibitor or ARB
  • CCB or thiazide as an add on
  • statin
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41
Q

how is diabetic neuropathy managed?

A
  • Offer a choice of duloxetine, gabapentin, pregabalin or amitriptyline, as initial treatment for neuropathic plan.
  • Refer to pain management clinic in resistant painful neuropathy.
  • Offer midodrine for postural hypotension.
  • Offer alternating use of erythromycin and metoclorpanide for gastroparesis.
  • Offer metronidazole for diabetic diarrhoea.
  • Offer catheterisation a parasympathomimetic (bethanechol) for bladder dysfunction.
  • Offer a PDE5 inhibitor (sildenafil) for erectile dysfunction.
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42
Q

what are the clinical features of diabetic foot disease?

A
  • Foot ulcer.
  • Foot pain.
  • Foot erythema.
  • Oedema of the foot, ankle or calf.
  • Absent pedal pulses
  • Malaise and anorexia.
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43
Q

how should an infected diabetic foot ulcer be managed?

A
  • Offer flucloxacillin for a mild diabetic foot infection (erythema must be less than 2 cm around the ulcer).
  • Offer intravenous clindamycin for moderate (erythema is more 2 cm around the ulcer) or severe (signs of systemic inflammatory response syndrome) foot infection.
  • Perform amputation in areas of irreversible gangrene.
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44
Q

how is diabetic retinopathy managed?

A
  • observation for non-proliferative diabetic nephropathy.
  • Perform urgent pan-retinal photocoagulation for proliferative diabetic nephropathy.
  • Perform vitrectomy for proliferative diabetic nephropathy that is not amenable to pan-retinal photocoagulation
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45
Q

which drugs causes gynaecomastia?

A
  • phenytoin
  • oestrogens
  • spironolactone
  • cimetidine
  • digoxin
  • marijuana
  • goserelin
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46
Q

what are the causes of hypercalaemia?

A
  • malignancy
  • Primary multiple endocrine neoplasia
  • Familial hypocalciuric hypercalcaemia
  • Granulomatous disease (TB and sarcoidosis).
  • Drugs (lithium and thiazides).
  • Vitamins (vitamin A and D)
  • hyperparathyroidism
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47
Q

what are the clinical features of hypercalcaemia?

A
  • Confusion.
  • Fatigue.
  • Constipation.
  • Loss of appetite.
  • Nausea.
  • Polyuria.
  • Polydypsia.
  • Poor skin turgor.
  • Bone pain.
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48
Q

how is hypercalcaemia managed?

A
  • Administer intravenous normal saline as the first line treatment when serum calcium exceeds 3.0 mmol/L.
  • Administer an intravenous bisphosphonate (zoledronic acid or pamidronate disodium).
  • Offer calcitonin while awaiting the effect of bisphosphonate as it has a more rapid correction of hypercalcaemia.
  • Offer a loop diuretic (furosemide) to manage fluid overload.
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49
Q

what factors precipitate hyperosmolar hyperglycaemic state?

A
  • infection
  • stroke
  • MI
  • trauma
  • hyperthyroidism
  • acromegaly
  • thiazide diuretics
  • beta blockers
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50
Q

what are the clinical features of hyperosmolar hyperglycaemic state?

A
  • Altered mental status.
  • Weakness.
  • Classical features of diabetes including polyuria, polydypsia and weight loss.
  • Features of dehydration including dry mucus membranes, poor skin turgor, tachycardia and hypotension.
  • Seizures.
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51
Q

how is hyperosmolar hyperglycaemic state managed?

A
  • Administer 0.9% NaCl at a rate of 15 to 12 ml/kg/hour.
  • Administer a vasopressor (noradrenaline) if hypotension persists after forced hydration.
  • Start insulin therapy (insulin neutral) with a bolus of 0.1 units/kg unless the potassium is less than 3.3 mmol/L, in which case it must be delayed and potassium chloride should be given.
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52
Q

what are the clinical features of hyperparathyroidism?

A
  • Fatigue.
  • Poor sleep.
  • Myalgia.
  • Anxiety.
  • Depression.
  • Polydypsia.
  • Polyuria.
  • Memory loss.
  • Bone pain.
  • Constipation.
  • Muscle cramps.
  • Paraesthesia.
  • Renal colic.
  • Abdominal pain.
  • Features of chronic kidney disease.
  • Features of malabsorption syndrome.
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53
Q

how is hyperparathyroidism diagnosed?

A
  • hypercalcaemia with normal or elevated PTH

- elevated ALP and phosphate

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54
Q

how is primary hyperparathyroidism?

A
  • parathyroidectomy
  • Consider a calcimimetic (cinacalcet) for patients in whom surgery is unsuccessful, is unsuitable or has been declined.
  • Consider a bisphosphonate (alendronate) to reduce fracture risk in patients who have an increased fracture risk.
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55
Q

how is secondary hyperparathyroidism managed?

A
  • Recommend safe sun exposure for patients who have had a lack of sunlight exposure.
  • Optimise management of underlying disease, such as Crohn’s disease or Coeliac disease.
  • Recommend dietary phosphate restriction and offer a phosphate binder (sevelamer) for patients with CKD stage 3 or 4.
  • Offer vitamin D sterol (calcitriol) or parathyroidectomy for patients with CKD stage 5.
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56
Q

what are the causes of hyperthyroidism?

A
  • Graves’ disease
  • toxic multinodular goitre
  • toxic adenoma
  • molar pregnancy
  • amiodarone
  • struma ovarii
  • de quervain’s thyroiditis
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57
Q

what is graves’ eye disease?

A
  • exophthalmos (anterior bulging of the eyes)
  • upper eyelid retraction
  • lid lag
  • erythema
  • oedema of the extraocular muscles, typically the inferior rectus, producing diplopia.
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58
Q

what is graves’ dermopathy?

A
  • accumulation of mucopolysaccharides in the deep dermis of the skin
  • peau d’orange (orange peel) appearance of the skin over the anterior aspect of the lower legs.
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59
Q

what is graves’ acropachy?

A
  • clubbing
  • swollen fingers
  • periosteal knee bone
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60
Q

what are the clinical features of hyperthyroidism?

A
  • Heat intolerance.
  • Sweating.
  • Weight loss despite increased appetite.
  • Palpitations.
  • Fast, fine tremor.
  • Hyperreflexia.
  • Orbitopathy (exophthalmos, diplopia, lid retraction, lid lag, erythema, oedema).
  • Warm, moist hands.
  • Compression symptoms including dysphagia, breathlessness, hoarse voice.
  • Irritability and agitation.
  • Cardiac flow murmur.
  • Muscle weakness, fatigue, and exercise intolerance.
  • Muscle wasting.
  • Reduced libido.
  • Gynaecomastia in men.
  • Amenorrhoea and oligomennorhoea.
  • Painful goitre in de Quervain’s thyroiditis.
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61
Q

how is hyperthyroidism diagnosed?

A
  • Measure serum TSH: Reduced in primary hyperthyroidism; Elevated in secondary hyperthyroidism.
  • Measure free T3 and T4 if serum TSH is abnormal: Elevated, except in subclinical disease.
  • Measure total T3/T4 or free T3/T4 ratio: Elevated in Graves’ disease and not in thyroiditis.
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62
Q

how is Graves’ disease managed?

A
  • radioactive iodine
  • antithyroid drugs (carbimazole, propylthiouracil)
  • Offer total thyroidectomy for adults with Graves’ disease if there are concerns about compression, thyroid malignancy is suspected, or first line treatments are unsuitable.
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63
Q

how is Graves’ disease managed in children?

A
  • antithyroid drugs are first line treatment

- should be continued for at least 2 years.

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64
Q

how is a toxic nodular goitre treated?

A
  • Offer radioactive iodine as first line treatment for adults with toxic multinodular goitre.
  • Offer total thyroidectomy or life-long antithyroid drugs
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65
Q

how is thyroid crisis managed?

A
  • Offer high dose carbimazole, intravenous hydrocortisone, iodine (Lugol solution), and oral propranolol.
  • Offer cholestyramine to reduce the enterohepatic circulation of thyroid hormones.
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66
Q

what are the causes of primary hypogonadism in men?

A
  • Klinefelter’s syndrome.
  • Kallman’s syndrome.
  • Orchitis related to mumps or an autoimmune disease.
  • Drugs such as cyclophosphamide and chlorambucil.
  • Testicular trauma or torsion.
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67
Q

what are the causes of secondary hypogonadism in men?

A
  • Hyperprolactinaemia, as prolactin suppresses GnRH.
  • Pituitary adenoma and craniopharyngioma.
  • Infiltrative diseases such as haemochromatosis, sarcoidosis, and histiocytosis.
  • Head trauma or surgery.
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68
Q

what are the clinical features of hypogonadism in men?

A
  • Decreased libido.
  • Loss of spontaneous morning erections.
  • Erectile dysfunction.
  • Gynaecomastia.
  • Infertility.
  • Micropenis and small testes.
  • Delayed puberty.
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69
Q

how is primary hypogonadism diagnosed in men?

A
  • reduced testosterone

- elevated FSH and LH

70
Q

how is secondary hypogonadism diagnosed in men?

A
  • reduced testosterone

- decrease FSH and LH

71
Q

how is primary hypogonadism managed in men?

A

-testosterone replacement

72
Q

what are the causes of hypoparathyroidism?

A
  • Removal or damage to the parathyroid glands during thyroidectomy.
  • Congenital deficiency including DiGeorge syndrome.
  • Hypomagnesaemia associated with chronic alcoholism, malnutrition, diarrhoea and malabsorption.
  • Idiopathic autoimmune hypoparathyroidism.
  • Reidel’s thyroiditis.
73
Q

what are the clinical features of hypoparathyroidism?

A
  • Muscle spasm (tetany).
  • Trousseau’s sign, a carpopedal spasm induced by ischaemia secondary to the inflation of a sphygmomanometer cuff.
  • Chvostek’s sign, gentle tapping over the facial nerve causes twitching of the ipsilateral facial muscles)
  • Convulsions.
  • Paraesthesia.
  • Anxiety
  • Cataracts.
  • Brittle nails.
74
Q

what are the clinical features of pseudohypoparathyroidism and pseudo-pseudohypoparathyroidism?

A
  • Short stature.
  • Short metacarpals.
  • Intellectual impairment.
75
Q

how is hypocalcaemia managed?

A
  • Offer intravenous calcium gluconate for severe hypocalcaemia.
  • Offer intravenous magnesium sulfate for hypomagnesaemia.
76
Q

what are the causes of panhypopituitarism?

A
  • neoplasia
  • sheehan’s syndrome
  • lymphocytic hypophysitis
  • sarcoidosis
  • TB
  • langerhans cell histiocytosis
  • kallman’s syndrome
  • TBI
  • radiotherapy
  • chronic opiate use
77
Q

what are the clinical features of panhypopituitarism?

A
  • Features of GH deficiency occur early and include failure to thrive or short stature.
  • Features of GnRH deficiency occur early and include delayed puberty, infertility, amenorrhoea, erectile dysfunction, and reduced libido, breast atrophy, hot flushes,
  • Features of TSH deficiency include: Weight gain, cold intolerance, constipation, dry skin.
  • Features of ACTH deficiency include: Hypoglycaemia, hypotension, nausea, vomiting, fatigue, weakness, dizziness.
  • Headaches.
  • Visual field defects.
  • Ophthalmoplegia.
  • Galactorrhoea.
78
Q

how is panhypopituitarism managed?

A
  • Administer oral hydrocortisone to replace ACTH deficiency.
  • Offer oral levothyroxine after full adrenal replacement if there is TSH deficiency.
  • For females with GnRH deficiency:
  • –Offer transdermal oestradiol for if pregnancy is not desired.
  • –Offer gonadotrophin if pregnancy is desired.
  • Offer gonadotrophin for men with GnRH deficiency.
  • Offer recombinant growth hormone (somatropin) for patients with GH deficiency.
  • Offer desmopressin for patients with ADH deficiency.
79
Q

what are the causes of hypothyroidism?

A
  • autoimmune thyroiditis
  • iodine deficiency
  • thyroidectomy/RAI
  • De quervain’s thyroiditis
  • pendreds syndrome
  • postpartum
  • thyroid infiltration
  • reidel’s thyroiditis
80
Q

what are the cases of secondary hypothyroidism?

A
  • Pituitary adenomas or gliomas.
  • Pituitary surgery, radiotherapy, or trauma.
  • Pituitary infarction.
  • Sheehan’s syndrome, a postpartum pituitary necrosis due to postpartum haemorrhage. It is supplied by the portal venous system.
  • Infiltrative disorders such as amyloidosis, sarcoidosis, haemochromatosis, tuberculosis.
  • Drugs such as dopamine and glucocorticoids.
81
Q

what are the clinical features of primary hypothyroidism?

A
  • Cold intolerance.
  • Hoarse voice.
  • Weight gain.
  • Constipation.
  • Fatigue and lethargy.
  • Menorrhagia.
  • Infertility and subfertility.
  • Dry skin and hair loss.
  • Eyelid and facial oedema.
  • Thick tongue.
82
Q

what are the clinical features of secondary hypothyroidism?

A
  • Recurrent headache.
  • Diplopia.
  • Visual field defects.
  • Atrophic breasts.
  • Galactorrhoea.
  • Amenorrhoea.
  • Erectile dysfunction.
  • Loss of body hair.
  • Cushing’s syndrome.
  • Acromegaly
83
Q

what are the clinical features of myxoedema coma?

A
  • Lethargy.
  • Bradycardia.
  • Hypothermia.
  • Seizures and coma
84
Q

how is hypothyroidism diagnosed?

A
  • Measure serum TSH as the initial investigation:
  • –Elevated in primary hypothyroidism;
  • –Low in secondary hypothyroidism;
  • –Elevated with poor compliance to thyroxine;
  • –Low with steroid therapy.
  • Measure free T3 and T4 if serum TSH is abnormal:
  • –Reduced in primary and secondary hypothyroidism
  • –Normal in subclinical hypothyroidism
  • –Normal with poor compliance to thyroxine
  • –Normal with steroid therapy.
85
Q

how is primary hypothyroidism managed?

A

-Offer oral levothyroxine (1.6 micrograms/kg/day) in all symptomatic patients.

86
Q

how is myxoedema coma managed?

A
  • Emergency admission.
  • Intravenous levothyronine 5–20 micrograms every 12 hours.
  • Oxygen.
  • Intravenous hydrocortisone 100 mg 8-hourly.
  • Glucose infusion to prevent hypoglycaemia.
  • Gradual rewarming.
  • Monitoring of cardiac output and pressures.
87
Q

what are the causes of congenital hypothyroidism?

A
  • maldescent of the thyroid
  • athyrosis
  • dyshormonogensis
  • iodine deficiency
88
Q

what is the klinefelters karyotype?

A

47, XXY

89
Q

what are the clinical features of klinefelters?

A
  • Taller than average.
  • Lack of secondary sexual characteristics.
  • Small and firm testes.
  • Infertile.
  • Gynaecomastia.
90
Q

what are the clinical features of kallman’s syndrome?

A
  • Lack of smell (anosmia).
  • Delayed puberty.
  • Rarely cleft lip and palate.
91
Q

what is the karyotype in turners syndrome?

A

45,X karyotype.

92
Q

what are the clinical features of turner’s syndrome?

A
  • Lymphoedema of the hands and feet
  • Spoon shaped nails
  • Wide carrying angle
  • Short stature.
  • Amenorrhoea
  • Webbed neck.
  • High arched palate.
  • Low-set ears.
  • Wide-spaced nipples.
  • Delayed puberty
  • Coarctation of the aorta.
  • Bicuspid aortic valve (aortic stenosis).
93
Q

how is turners syndrome treated?

A
  • Growth hormone therapy
  • Oestrogen replacement for development of secondary sexual characteristics at the time of puberty (but infertility persists).
94
Q

what are the clinical features of fragile x syndrome?

A
  • Moderate to severe learning difficulty (IQ 20-80)
  • Macrocephaly
  • Macro-orchidism
  • Long face
  • Large everted ears
  • Prominent mandible
  • Broad forehead
  • Mitral valve prolapse
  • Joint laxity
  • Scoliosis
  • Autism
  • Hyperactivity
95
Q

what are the clinical features of MEN1?

A
  • Bitemporal hemianopia affecting the upper quadrant.
  • Galactorrhoea.
  • Erectile dysfunction.
  • Gynaecomastia.
  • Amenorrhoea.
  • Infertility.
  • Hot flushes.
  • Weight gain.
  • Constipation.
  • Headache.
  • Renal colic.
  • Polyuria and polydipsia.
  • Over-sized hands and feet.
  • GI bleeding.
  • Epigastric pain.
  • Dyspepsia.
96
Q

what are the clinical features of MEN2?

A
  • Headache.
  • Palpitations.
  • Diaphoresis.
  • Renal colic.
  • Polyuria and polydipsia.
  • Palpable thyroid nodule.
97
Q

how should suspected MEN1 be investigated?

A
  • Measure serum prolactin and IGF-1: Raised.
  • Measure serum parathyroid hormone and calcium: Raised.
  • Measure serum gastrin: Raised.
98
Q

how should suspected MEN2 be investigated?

A
  • Measure serum parathyroid hormone and calcium: Raised.
  • Perform 24-hour urinary collection of metanephrines: Raised.
  • Perform a thyroid biopsy: Medullary thyroid cancer.
  • Measure serum calcitonin: Elevated.
99
Q

how is MEN1 managed?

A
  • Offer intravenous saline and zoledronic acid for hypercalcaemia associated with hyperparathyroidism.
  • Offer omeprazole for gastrinoma / Zollinger-Ellison syndrome.
  • Offer octreotide for pancreatic islet cell tumours.
  • Offer trans-sphenoidal surgery and adjunct hormonal replacement for pituitary adenomas.
100
Q

how is MEN2 managed?

A
  • Offer intravenous saline and zoledronic acid for hypercalcaemia associated with hyperparathyroidism.
  • Perform total thyroidectomy for medullary carcinoma.
  • Offer alpha and beta blockade and unilateral adrenalectomy for phaeochromocytoma.
101
Q

what are the clinical features of phaechromocytoma?

A
  • Resistant hypertension.
  • Hypertension that presents at young age.
  • Classic triad of symptoms:
  • –Headache.
  • –Palpitations.
  • –Diaphoresis
  • Pallor.
  • Orthostatic hypotension.
102
Q

how is phaechromocytoma diagnosed?

A
  • Perform 24-hour urinary collection of metanephrines: Elevated.
  • Measure serum free metanephrines: Elevated.
103
Q

how is phaechromocytoma managed?

A
  • alpha blocker (phenoxybenzamine)
  • beta blocker (propranolol)
  • surgical excision of the entire adrenal gland
  • long-term alpha and beta blockade if the patient is not a surgical candidate
  • chemo if malignant
104
Q

what are the causes of primary hyperaldosteronism?

A
  • Bilateral adrenal hyperplasia is the most common cause of primary hyperaldosteronism.
  • Adrenal adenomas (Conn’s syndrome) are less common, and are sub-classified according to whether they are angiotensin unresponsive or angiotensin responsive.
105
Q

what are the clinical features of primary hyperaldosteronism?

A
  • Hypertension.
  • Nocturia.
  • Polyuria.
  • Lethargy.
  • Classical but rare features include muscle cramps, weakness, and paraesthesia.
106
Q

how is primary hyperaldosteronism diagnosed?

A
  • serum aldosterone/renin ratio: Elevated in primary hyperaldosteronism (high aldosterone and low renin
  • fludrocortisone suppression test (fails to suppress aldosterone)
  • adrenal villous sampling for localisation
107
Q

how is primary hyperaldosteronism managed?

A
  • aldosterone antagonist (amiloride or spironolactone)
  • Perform unilateral laparoscopic adrenalectomy for a unilateral adrenal adenoma.
  • Offer glucocorticoids (dexamethasone) to control hypertension in patients with familial hyperaldosteronism.
  • Bilateral adrenalectomy is only considered for patients with marked bilateral and severe adrenal adenoma. I
108
Q

what are the causes of SIADH?

A
  • Drugs such as antidepressants (citalopram), antiepileptics (carbamazepine), and sulfonylureas (glipizide).
  • Pulmonary processes including pulmonary infections and lung cancers, especially small cell lung cancer.
  • Subarachnoid haemorrhage.
109
Q

what are the clinical features of SIADH?

A
  • Nausea and vomiting.
  • Headache.
  • Altered mental status.
  • Coma.
  • Absence of hypovolaemia or hypervolaemia.
110
Q

how is SIADH diagnosed?

A
  • hyponatraemia
  • reduced serum osmolality
  • elevated urine osmolality
  • elevated urine sodium
111
Q

how is SIADH managed?

A
  • For severe neurological symptoms: Administer 3% saline with adjunct furosemide.
  • For mild to moderate symptoms (nausea and vomiting): Commence fluid restriction of 1 to 1.5 litres per day.
  • For persistent chronic SIADH offer a V2 antagonist (tolvaptan) in patients who are intolerant to fluid restriction.
112
Q

what are the clinical features of thyroid carcinoma?

A
  • Typically asymptomatic.
  • Palpable thyroid nodule.
  • Hoarseness due paralysis of ipsilateral vocal cord.
  • Dyspnoea.
  • Dysphagia.
  • Tracheal deviation.
  • Cervical lymphadenopathy.
  • Features of carcinoid disease: Diarrhoea, flushing, palpitations (Medullary carcinoma).
  • Rapid neck enlargement (lymphoma).
  • Uncontrolled hypertension (MEN syndrome 2).
  • Features of advanced disease: Fatigue; Night sweats; Weight loss; Back pain.
113
Q

how is thyroid carcinoma managed?

A
  • Offer total thyroidectomy and radioiodine and levothyroxine as first line management for papillary, follicular and medullary carcinoma.
  • Offer a tyrosine kinase inhibitor (sorafenib, lenvatinib, vandetanib) for metastatic disease where the patient can manage the toxicity.
114
Q

what are the clinical features of type 1 diabetes?

A
  • Polyuria.
  • Polydipsia.
  • Weight loss.
  • Generalised weakness.
  • Blurred vision.
  • tiredness
  • Features of DKA include such as vomiting, tachypnoea, abdominal pain, coma.
115
Q

how is type 1 diabetes diagnosed in children?

A
  • Random plasma glucose greater than 11 mmol/L in symptomatic patients.
  • Both a random plasma glucose greater than 11 mmol/L and a fasting plasma glucose greater than 6.9 mmol/L in asymptotic patients.
  • A HbA1c greater than 48 mmol/mol.
116
Q

how is type 1 diabetes diagnosed in adults?

A

-Diagnose type 1 diabetes on clinical grounds in adults presenting with hyperglycaemia (random plasma glucose greater than 11 mmol/L)

117
Q

how is type 1 diabetes managed in children?

A
  • education programme
  • multiple daily injection basal-bolus insulin regimens
  • Use an intermediate acting insulin (isophane insulin) for basal dosing, once daily before bed.
  • Use a short acting insulin (insulin aspart) for bolus dosing before meals.
  • continuous insulin pumps
118
Q

what are the sick day rules for a child with type 1 diabetes?

A
  • Never stop or omit insulin.
  • Check blood glucose more frequently, for example every 1-2 hours including through the night.
  • Check for blood ketone levels regularly, for example every 3-4 hours including through the night, and sometimes every 1-2 hours depending on results.
  • Maintain normal meal patterns here possible if appetite is reduced.
  • Maintain adequate fluid intake (3L) to prevent dehydration.
  • Seek urgent medical advice if they are violently sick, drowsy, or unable to keep fluid down
119
Q

how is type 1 diabetes managed in adults?

A
  • education
  • self-monitoring
  • coeliac serology
  • DAFNE
  • Offer multiple daily injection basal–bolus insulin regimens:
  • –Use a long acting insulin (insulin detemir) for basal dosing, once daily before bed.
  • –Use a short acting insulin (insulin aspart) for bolus dosing before meals.
120
Q

what are the symptoms of hypoglycaemia?

A
  • sweating
  • tremor
  • pounding heartbeat.
  • pallor
  • sweating
121
Q

how is mild hypoglycaemia managed?

A

-Prompt consumption of 10-20 g of fast acting carbohydrates preferably in liquid form (fizzy drink, Lucozade).

122
Q

how is hypoglycaemia managed if the patient is unconscious?

A
  • Administer intramuscular glucagon immediately.
  • Arrange emergency transfer to hospital (999) if intramuscular glucagon is not available, or there is no response to intramuscular glucagon.
  • Administer intravenous glucose 50% followed by a saline flush (as glucose scleroses veins).
123
Q

what are the risk factors for developing type 2 diabetes?

A
  • Obesity and inactivity.
  • Family history.
  • Ethnicity (more common in BAME people).
  • History of gestational diabetes.
  • Poor dietary habits (low fibres, high GI diet).
  • Drug treatments such as statins, corticosteroids and combined treatment with a thiazide diuretic plus a beta blocker.
  • Polycystic ovarian syndrome.
  • Metabolic syndrome.
  • Low birth weight for gestational age.
124
Q

what are the clinical features of type 2 diabetes?

A
  • Asymptomatic.
  • History of candidal infections of the vagina, penis, and skin folds.
  • History of urinary tract infections.
  • Fatigue.
  • Blurred vision.
  • Acanthosis nigricans.
125
Q

how is type 2 diabetes diagnosed?

A
  • HbA1c >48mmol/mol on two occasions
  • fasting glucose >6.9mmol/l
  • random plasma glucose >11mmol/l
126
Q

how is type 2 diabetes managed?

A
  • education with diet and lifestyle advice
  • metformin
  • if metformin contraindicated, give sitagliptin, pioglitazone, gliclazide or dapagliflozin first line
  • dual therapy if mono therapy fails (HbA1c >58) and triple therapy if this fails
  • if high weight add exenatide (GLP-1)
  • insulin
127
Q

what is pre-diabetes?

A
  • fasting plasma glucose level is 5.6 - 6.9

- HbA1c is 42 - 47 mmol/mol.

128
Q

when is pioglitazone contraindicated?

A
  • history of bladder cancer

- heart failure

129
Q

what are the clinical features of achondroplasia?

A
  • At birth or within the first year of life, with disparity between large skull, normal length trunk and short arms and legs.
  • The chest is usually very narrow.
  • Fingertips may only come down to the iliac crest.
  • Shortness is particularly evident in the proximal segments of limbs.
  • Limbs appear very broad with deep creases and trident-like hands with short fingers.
  • There is often increased joint laxity.
  • Skull shows a bulging vault, small face and a flat nasal bridge or ‘scooped out’ glabella.
  • Spine shows marked lumbar lordosis.
  • Frontal bossing, depressed nasal bridge.
130
Q

how is achondroplasia diagnosed?

A
  • based on the typical clinical and X-ray features of:
  • –metaphyseal irregularity
  • –flaring in the long bones
  • –late-appearing irregular epiphyses.
  • –pelvis is narrow in anteroposterior diameter
  • –deep sacroiliac notches
  • –short iliac wings.
  • –spine shows progressive narrowing of the interpedicular distance from top to bottom (reverse of normal).

-prenatally on USS or plasma analysis for the FGFR3 mutation

131
Q

what is precocious puberty?

A

secondary sexual characteristics appear before 8 years of age in girls and 9 years in boys.

132
Q

what are the causes of gonadotrophin dependent precocious puberty?

A

-Idiopathic

  • Brain neoplasms
  • Cranial radiotherapy.
  • Neurodisability conditions such as hydrocephalus, cerebral palsy, post-infection such as meningitis or encephalitis
  • Post-traumatic head injury.
  • Gain-of-function mutations in GPR54, a G protein-coupled receptor that is a ligand for kisspeptin, can cause GDPP
  • Midline forebrain abnormalities such as holoprosencephaly or septo-optic dysplasia.
  • Association with child adoption and sexual abuse.
133
Q

what are the causes of gonadotrophin independent precocious puberty?

A
  • Ovarian causes: follicular cysts of the ovary, granulosa cell tumours, Leydig cell tumours, and gonadoblastoma.
  • Testicular causes: Leydig cell tumours and a defect of luteinising hormone (LH) receptor function (testotoxicosis or familial GIPP).
  • Adrenal causes: Congenital adrenal hyperplasia (CAH) in males results in GIPP. Other adrenal causes include Cushing’s syndrome and an adrenal virilising tumour.
  • McCune-Albright syndrome (MAS).
  • Exposure to exogenous hormones such as the contraceptive pill or testosterone gels
  • Human chorionic gonadotrophin-secreting germ cell tumours
134
Q

what are the clinical features of precocious puberty?

A
  • More common in females
  • Presence of risk factors
  • Breast development
  • Pubic/axillary hair
  • Acne
  • Body odour
  • Menarche
  • Increased growth velocity and tall stature
  • Signs of McCune-Albright Syndrome
  • testes >4ml in males
135
Q

how is precocious puberty diagnosed?

A
  • Perform a bone age estimate with a left hand/wrist x-ray: advanced
  • Measure basal serum FSH and LH: Low in gonadotrophin-independent cases; elevated in gonadotrophin dependent cases
  • Measure serum testosterone: Elevated in males; may be elevated in females with CAH
  • Measure serum oestrogen: elevated in females
  • Perform an LHRH stimulation test: elevated LH and FSH in gonadotrophin dependent cases; suppressed LH and FSH in gonadotrophin independent cases
136
Q

how is gonadotrophin dependent precocious puberty managed?

A
  • Treat the underlying cause
  • Consider GnRH agonist to suppress puberty (leuprorelin or goserelin)
  • Consider growth hormone treatment in patients with poor growth as a result of GnRH treatment
137
Q

how is gonadotrophin independent precocious puberty managed?

A
  • In cases of McCune-Albright Syndrome or testotoxicosis:
  • –Give ketoconazole to inhibit steroid synthesis
  • –Provide supportive care for McCune-Albright
  • –Give GnRH agonist to suppress puberty
  • In CAH:
  • –Optimise management with hydrocortisone to prevent rapid virilisation and give GnRH agonist to prevent puberty
138
Q

what is delayed puberty and what is the most common cause?

A
  • Defined as the lack of any pubertal signs by the age of 13 years in girls and 14 years in boys.
  • constitutional delay in growth and puberty
139
Q

what are the clinical features of delayed puberty?

A
  • Boys: testes <3ml
  • Girls: absent breast development and absence of menarche
  • Absent growth spurt
  • Absent pubic/axillary hair
  • Anosmia in Kallman’s syndrome
  • Short stature
  • Dysmorphic features of chromosomal abnormalities
140
Q

how is delayed puberty diagnosed?

A
  • Perform a bone age measurement with a non-dominant wrist x-ray: delayed bone age
  • Measure basal FSH and LH: low in hypogonadotrophic hypogonadism; elevated in hypergonadotrophic hypogonadism
141
Q

how is constitutional delay in growth and puberty managed?

A
  • In boys:
  • –Observe and monitor
  • –Give a short course of oxandrolone or testosterone cypionate in boys with abnormal psychosocial adjustment
  • In girls:
  • –Observe and monitor
  • –Give a short course of oestradiol in girls with abnormal psychosocial adjustment
142
Q

how are organic causes of delayed puberty managed?

A
  • In boys, induce puberty with testosterone cypionate
  • In girls, induce puberty with oestradiol and cyclical progesterone
  • If Turner’s syndrome, give growth hormone replacement
143
Q

how is persistent hypogonadism post puberty managed?

A
  • In boys, give testosterone supplementation, and testicular implants for cosmesis
  • In girls, give oestradiol and progesterone, and breast implants for cosmesis
144
Q

when should MODY be suspected?

A
  • non-obese
  • young patients
  • family history of diabetes in 2 or more successive generations
145
Q

what are the adverse effects of insulin?

A
  • Hypoglycaemia which can lead to coma and death

- Lipohypertrophy if injection sites are not rotated.

146
Q

in which patients should insulin be used cautiously?

A

-renal impairment.

147
Q

with which drugs does insulin interact?

A

-Corticosteroids increase insulin requirements

148
Q

what are the adverse effects of metformin?

A
  • GI upset including nausea and vomiting
  • Lactic acidosis is a fatal rare side effect characterised by vomiting, difficulty breathing and muscle cramps.
  • diarrhoea
149
Q

in which patients should metformin be used cautiously?

A
  • Avoid in severe renal impairment (metformin accumulation)
  • Avoid in severe tissue hypoxia (increased lactate production)
  • Caution in hepatic impairment (reduced lactate metabolism).
150
Q

with which drugs does metformin interact?

A

-Increased risk of renal impairment with IV contrast media, ACE inhibitors, NSAIDS, diuretics.

151
Q

what are the adverse effects of gliclazide?

A
  • GI upset including nausea and vomiting
  • Hypoglycaemia
  • Hypersensitivity reactions including cholestatic jaundice, rash, fever and agranulocytosis.
152
Q

in which patients should gliclazide be used cautiously?

A
  • Caution in patients with hepatic impairment
  • Caution in patients with malnutrition
  • Caution in patients with adrenal or pituitary insufficiency.
153
Q

with which drugs does gliclazide interact?

A
  • Increased risk of hypoglycaemia with metformin, thiazolidinediones and insulin
  • Reduced efficacy with drugs that elevate blood glucose including prednisolone and diuretics.
154
Q

what are the adverse effects of pioglitazone?

A
  • GI upset such as nausea and vomiting
  • Neurological effects such as headache, dizziness and altered vision
  • Oedema and cardiac failure when prescribed with insulin
  • Increased risk of bladder cancer and bone fractures
  • Liver toxicity.
155
Q

in which patients should pioglitazone be used cautiously?

A
  • Avoid in heart failure
  • Avoid in bladder cancer
  • Caution in people with risk factors for bladder cancer
  • Caution in cardiovascular disease
  • Caution in elderly patients
  • Caution in hepatic impairment.
156
Q

what are the adverse effects of sitagliptin?

A
  • GI disturbances
  • Nasopharyngitis
  • Pancreatitis
  • Hypoglycaemia (owing to reduced stomach emptying by GIP, with reduced glucose absorption into blood).
157
Q

in which patients should sitagliptin be used cautiously?

A
  • Avoid in DKA
  • Caution with hepatic impairment
  • Caution with renal impairment;
  • Caution with heart failure
  • Caution in the elderly.
158
Q

with which drugs does sitagliptin interact?

A
  • Increased plasma concentration of digoxin

- Enhanced hypoglycaemic effect with other anti-diabetic drug.

159
Q

what are the adverse effects of exenatide?

A
  • GI disturbances
  • Severe pancreatitis (haemorrhagic or necrotising)
  • Hypoglycaemia
  • Antibody formation.
160
Q

in which patients should exenatide be used cautiously?

A
  • Avoid in DKA
  • Avoid in gastroparesis
  • Caution in the elderly
  • Caution with renal impairment.
161
Q

with which drugs does exenatide interact?

A
  • Increased anticoagulant effect of warfarin

- Increased hypoglycaemic effect with other anti-diabetic drugs.

162
Q

what are the adverse effects of corticosteroids?

A
  • Increased risk of infection
  • Increased risk of diabetes mellitus and osteoporosis
  • Increased muscle weakness
  • Easy bruising
  • Peptic ulceration
  • Mood and behavioural changes
  • Hypertension
  • Adrenal atrophy
  • Addisonian crisis if withdrawn immediately.
163
Q

in which patients should corticosteroids be used cautiously?

A
  • Caution with infection

- Caution in children.

164
Q

with which drugs do corticosteroids interact?

A
  • Increased risk of peptic ulceration and Gi bleeding with NSAIDs
  • Increased risk of hypokalaemia with β2-agonists and diuretics
  • Reduced efficacy with phenytoin, carbamazepine, rifampicin; Reduced response to vaccines.
165
Q

what are the adverse effects of bisphosphonates?

A
  • Oesophagitis
  • Hypocalcaemia
  • Osteonecrosis of jaw
  • Atrial fibrillation
  • Atypical femoral fractures.
166
Q

in which patients should bisphosphonates be used cautiously?

A
  • Avoid in severe renal impairment
  • Avoid in hypocalcaemia
  • Avoid in patients with active upper gastrointestinal disorders
  • Caution in smokers and patients with major dental disease due to risk of ONJ.
167
Q

with which drugs do bisphosphonates interact?

A

Reduced absorption with calcium salts, antacids and iron salts.

168
Q

what are the adverse effects of carbimazole?

A
  • Minor side effects include rash, arthritis, jaundice and headache
  • Serious side effects include agranulocytosis and neutropenia.
169
Q

in which patients should carbimazole be used cautiously?

A
  • Avoid in severe blood disorders
  • Avoid block and replace regimen in pregnancy as it crosses the placenta
  • Caution in hepatic impairment
  • Discontinue with neutropenia.
170
Q

what are the adverse effects of thyroxine?

A
  • GI features such as diarrhoea
  • Cardiac features such as arrhythmia and palpitations
  • Neurological features such as tremor and insomnia.
171
Q

in which patients should thyroxine be used cautiously?

A
  • Caution in patients with coronary artery disease
  • Caution in hypopituitarism, in which Addisonian crisis may occur if corticosteroid therapy is not initiated prior to treatment.
172
Q

with which drugs does thyroxine interact?

A
  • Reduced absorption with antacids, calcium or iron salts
  • Reduced metabolism with phenytoin or carbamazepine
  • Increased anticoagulant effects of warfarin.

FINALS (18 decks)

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