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Phase 1c: Conditions > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What is T1DM?

A

Characterised by hyperglycaemia due to absolute insulin deficiency; most cases result from autoimmune pancreatic beta-cell destruction in genetically susceptible individuals. Usually presents with acute symptoms or ketoacidosis in childhood or adolescence.

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2
Q

What is T2DM?

A

Characterised by insulin resistance and relative insulin deficiency; most patients are asymptomatic and are diagnosed through screening (abnormal fasting plasma glucose, HbA1c, and/or oral glucose tolerace test)

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3
Q

How does T1DM present?

A

Hyperglycaemia (random plasma glucose >11mmol/L)
Polydipsia, polyuria
Usually young age
Weight loss
Blurred vision
Diabetic ketoacidosis (nausea, vomiting, abdominal pain, clinical dehydration, tachypnoea)
Lethargy
Coma or altered mental state (uncommon)

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4
Q

What are the risk factors for T1DM?

A

Genetic predisposition (family history of autoimmune diseases)

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5
Q

How is diabetes mellitus investigated?

A

Random plasma glucose (≥11.1 mmol/L confirms diagnosis in presence of symptoms of polyuria, polydipsia, and unexplained weight loss)
Fasting plasma glucose (no caloric intake for >8 hours, ≥7.0 mmol/L)
2-hour plasma glucose (2 hours after 75g oral glucose load, ≥11.1 mmol/L)
HbA1c (reflects degree of hyperglycaemia over the preceding 3 months, ≥6.5% or 48 mmol/L)

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6
Q

How is T1DM treated in children and non-pregnant adults?

A

Basal bolus insulin (1st line)
Metformin (consider if adult with BMI >25 kg/m^2)
Fixed dose insulin is second line

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7
Q

How is T1DM treated in pregnant women?

A

Basal bolus insulin
Consider metformin (when insulin resistant, as well as insulin deficient, or BMI ≥25 kg/m^2)
Low-dose aspirin (from 12 weeks till birth of baby - reduces risk of pre-eclampsia)

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8
Q

What are some common symptoms of T2DM?

A

Asymptomatic
Candidal infections (most commonly vaginal, penile, or in skin folds)
Skin infections (cellulitis or abscesses)
Urinary tract infections (cystitis or pyelonephritis)
Fatigue (may be early warning sign of CVR disease - clinicians should have low threshold for cardiac evaluation)
Blurred vision

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9
Q

What are some uncommon symptoms of T2DM?

A

Polydipsia and polyuria (only occurs with considerable hyperglycaemia, FPG >16.6 mmol/L and/or HbA1c >95 mmol/mol)
Polyphagia (excessive appetite)
Unintentional weight loss (if marked hyperglycaemia)
Paraesthesias (abnormal sensation, prolonged undiagnosed diabetes resulting in neuropathy)
Acanthosis nigricans (most often associated with obesity)

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10
Q

What are some risk factors for T2DM?

A
  • Older age
  • Overweight/obesity
  • Gestational diabetes
  • Non-diabetic hyperglycaemia (pre-diabetes)
  • Family history
  • Non-white ancestry
  • PCOS (elevated risk; should be periodically screened for diabetes)
  • Hypertension
  • Dyslipidaemia (especially with low HDL and/or high triglycerides)
  • Cardiovascular disease
  • Stress
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11
Q

What is the management of T2DM?

A

FIRST LIFESTYLE
1. Metformin (with SGLT-2 if chronic heart failure or risk of CVD)
Switch to modified release metformin if side effects (e.g. GI)
2. Add sulfonylurea or DPP-4 inhibitor or pioglitazone

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12
Q

What are the side effects of metformin?

A

GI symptoms: pain, nausea, diarrhoea
Lactic acidosis with severe renal disease or renal failure

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13
Q

What are the contraindications for metformin?

A

CKD
recent myocardial infarction, sepsis, acute kidney injury and severe dehydration (can cause lactic acidosis)
Alcohol abuse

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14
Q

What are the side effects of SGLT-2?

A

Glycosuria
Increased urine output and frequency
Genital and urinary tract infections (e.g., thrush)
Weight loss
Diabetic ketoacidosis, notably with only moderately raised glucose
Fournier’s gangrene (rare but severe infection of the genitals or perineum)

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15
Q

What are the side effects of pioglitazone?

A

Weight gain
Heart failure
Increased risk of bone fractures
A small increase in the risk of bladder cancer

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16
Q

What are the side effects of sulfonylureas?

A

Weight gain
Hypoglycaemia

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17
Q

What is Addison’s disease?

A

Destruction of the adrenal cortex and subsequent reduction in the output of adrenal hormones, i.e. glucocorticoids (cortisol) and/or mineralocorticoids (aldosterone)
AUTOIMMUNE

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18
Q

How is cortisol release regulated?

A

The pituitary gland releases ACTH, which triggers adrenal cortex to secrete cortisol
Elevated cortisol levels suppress ACTH in a negative feedback loop

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19
Q

How does Addison’s disease present?

A

Fatigue (lethargy, weakness, or tiredness)
Anorexia and weight loss
‘Salt craving’ - hyponatraemia and hyperkalaemia
Hyperpigmentation (MSH is also produced with ACTH, same precursor of POMC)
Nausea, vomiting - may have adrenal crisis
Postural hypotesion
Muscle cramps and joint pains

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20
Q

What are the risk factors for Addison’s disease?

A

Female sex
Adrenal haemorrhage (patients taking anticoagulants are at increased risk)
Autoimmune diseases
Coeliac disease
Adrenocortical autoantibodies

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21
Q

How is Addison’s disease investigated?

A

Morning serum cortisol (<140 nanomols/L abnormal)
Plasma ACTH (>12 picomols/L)
U&Es (hyponatraemia, hyperkalaemia)
ACTH stimulation test

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22
Q

How is Addison’s disease treated?

A

Oral glucocorticoid and mineralocorticoid replacement therapy
(hydrocortisone/cortisone/prednisolone and fludrocortisone)

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23
Q

How is an adrenal crisis treated?

A

Intravenous hydrocortisone
Saline to correct dehydration and hypotension
Glucose, when necessary, to correct hypoglycaemia

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24
Q

What is Cushing’s disease?

A

Excessive cortisol production as a result of excessive ACTH from the pituitary gland

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25
Q

What are some causes of Cushing’s syndrome?

A

Cushing’s disease (pituitary tumour secreting ACTH producing adrenal hyperplasia)
Ectopic ACTH production (e.g. small cell lung cancer)
Adrenal adenoma/carcinoma
Excess glucocorticoid administration

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26
Q

What are the key diagnostic factors of Cushing’s syndrome?

A

Facial plethora (red, puffy face)
Weight gain, with central obesity and supraclavicular fullness
Violaceous striae
Menstrual irregularities
Hypertension
Glucose intolerance or diabetes mellitus
Premature osteoporosis/unexplained fractures
Acne
Depression
Decreased libido
Proximal muscle weakness

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27
Q

What investigations are considered for Cushing’s syndrome?

A

Urine pregnancy test to exclude pregnancy
Serum glucose (elevated)
Late night salivary cortisol
24-hr urinary free cortisol
Low-dose overnight dexamethasone suppression test
Plasma ACTH to identify cause of Cushing’s
High-dose dexamethasone suppression test to distinguish between ectopic ACTH and Cushing’s disease
Insulin stress test to differentiate between Cushing’s and pseudo-Cushing’s
U&Es: hypokalaemic metabolic alkalosis

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28
Q

What are the results of the high dose dexamethasone suppression test?

A

Cushing’s disease: cortisol and ACTH both suppressed
Ectopic ACTH production: cortisol and ACTH both not suppressed
Cushing’s syndrome from other causes: cortisol not suppressed, ACTH suppressed

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29
Q

How is Cushing’s disease treated?

A

Transsphenoidal pituitary adenomectomy
Somatostatin analogue (pasireotide)
Dopamine antagonist (cabergoline)
Consider post-surgical corticosteroid replacement therapy (hydrocortisone)

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30
Q

How is ectopic ACTH or CRH syndrome treated?

A

Surgical resection/ablation of tumours producing ACTH or CRH
Ketoconazole or metyrapone before surgery to reduce cortisol before surgery
Chemotherapy/radiotherapy for primary tumour

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31
Q

How is ACTH-independent Cushing’s syndrome due to unilateral adrenal disease treated?

A

Unilateral adrenalectomy or tumour resection
Ketoconazole or metyrapone before surgery
Consider chemotherapy/radiotherapy for adrenal carcinoma

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32
Q

How is ACTH-independent Cushing’s syndrome due to bilateral adrenal disease treated?

A

Bilateral adrenalectomy
Permanent post-surgical corticosteroid replacement therapy (hydrocortisone and fludrocortisone)
Medical therapy before surgery (metyrapone/ketoconazole)

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33
Q

What are the key diagnostic factors for hypothyroidism?

A

Often insidious onset with nonspecific symptoms
Lethargy, weight gain, cold intolerance
Constipation
Menorrhagia
Dry or coarse skin or hair
Change in voice
Bradycardia and hypertension
Eyelid oedema
Goitre
Delayed tendon reflex relaxation

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34
Q

What are the risk factors for hypothyroidism?

A

Iodine deficiency
Female sex
Middle age
Family history
Autoimmune disorders
Amiodarone use
Lithium use
Radiotherapy to head and neck
Treatment for thyroid disease (e.g. Grave’s)
Post-partum thyroiditis

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35
Q

What are some causes of primary hypothyroidism?

A

Auto-immune (Hashimoto’s and atrophic thyroiditis)
Iatrogenic (radiotherapy to the neck, surgery, radio-iodide treatment)
Drugs (amiodarone, lithium, anti-thyroid medication)
Congenital
Infiltration of thyroid (amyloidosis, sarcoidosis)

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36
Q

What are some causes of secondary hypothyroidism?

A

Isolated TSH deficiency
Hypopituitarism (neoplasm, infiltrative, infection and radiotherapy)
Hypothalamic disorders (neoplasms and trauma)

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37
Q

How is hypothyroidism investigated?

A

Serum TSH (elevated in primary, decreased in secondary, slight elevation in sub-clinical)
Free serum T4 (low, normal in sub-clinical)
Thyroid ultrasonography

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38
Q

How is hypothyroidism investigated?

A

Serum TSH (elevated in primary, decreased in secondary, slight elevation in sub-clinical)
Free serum T4 (low, normal in sub-clinical)
Thyroid ultrasonography

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39
Q

How is hypothyroidism treated?

A

Low-dose thyroxine

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40
Q

What signs are indicative of a sellar or parasellar mass causing secondary hypothyroidism?

A

Papilloedema
Diplopia
Bitemporal hemianopia (decreased peripheral vision)

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41
Q

What is myxoedema coma?

A

A rare severe form of hypothyroidism with multi-organ failure. There is:
Reduced level of consciousness
Seizures
Hypothermia
Features of hypothyroidism

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42
Q

How is myxoedema treated?

A

IV levothyroxine
IV hydrocortisone
Correction of metabolic disturbances

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43
Q

What are the causes of thyrotoxicosis?

A

Grave’s disease (most common)
Toxic nodular goitre
Solitary thyroid nodule
De Quarvain’s thyroiditis (post-viral)
Drugs (amiodarone, lithium, exogenous iodine)

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44
Q

What are the key diagnostic factors for Grave’s disease?

A

Sweating
Heat intolerance and sweating
Palpitations and fine tremor
Pretibial myxoedema
Diffuse goitre
Menstrual irregularities
Onycholysis (detachment of nail from nail bed)
Exophthalmos
Conjunctival oedema

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45
Q

How is Grave’s disease investigated?

A

TSH (decreased)
TSH receptor antibodies (positive)
Serum free or total T3/T4 (elevated)
Thyroid scintigraphy: diffuse homogenous increased uptake of radioactive iodine

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46
Q

How does thyroid storm present?

A

fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically

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47
Q

How is a thyroid storm treated?

A

Symptomatic treatment, e.g. paracetamol
Treatment of underlying precipitating event
Beta blockers (IV propranolol)
Antithyroid drugs, e.g. propylthiouracil
Dexamethasone
IV digoxin

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48
Q

How is Grave’s disease treated?

A

Propranolol for symptomatic control
Antithyroid drugs (carbimazole, propylthiouracil) - p used in 1st trimester of pregnancy
Radioactive iodine ablation

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49
Q

What is a side effect of carbimazole?

A

agranulocytosis

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50
Q

What is Plummer’s disease?

A

Toxic multinodular goitre; multiple autonomously functioning nodules, resulting in hyperthyroidism
Almost always benign, but may be malignant

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51
Q

What are the key diagnostic factors of toxic multinodular goitre?

A

Goitre (usually irregular, rather than smooth)
Heat intolerance, increased appetite, weight loss
Palpitations
Oligomenorrhoea
Stare or lid lag
Tachycardia
Fine resting tremor
Muscle weakness
SOB or choking sensation with large goitre
Pemberton’s sign

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52
Q

What is Pemberton’s sign?

A

Thoracic inlet obstruction leads to jugular venous distension and facial plethora when arms are extended over the head

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53
Q

How is Plummer’s disease investigated?

A

TSH (suppressed)
Free T3/T4 (elevated)
Nuclear scintigraphy: patchy uptake
Thyroid ultrasound (cold or warm nodules >1cm in diameter should be considered for further evaluation, e.g. fine needle biopsy)

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54
Q

What is the first line treatment for benign toxic multinodular goitre?

A

Radioactive iodine therapy (I-131)
Pre-treatment anti-thyroid drugs (thiamazole) - should be started 3-5 days before I-131 treatment and restarted I-131 after treatment
Consider propanolol for patients with increased cardiovascular risk

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55
Q

What is the first line treatment for benign toxic multinodular goitre in pregnant women?

A

Antithyroid drugs (propylthiouracil or thiamazole)

56
Q

What is the first line treatment for malignant toxic multinodular goitre?

A

Thyroid surgery
Pre-surgical antithyroid drugs (propylthiouracil or thiamazole)

57
Q

What is a toxic thyroid adenoma?

A

A toxic adenoma is an autonomously functioning nodule that causes hyperthyroidism; benign and solitary growths of the thyroid

58
Q

What are the key diagnostic factors of toxic thyroid adenoma?

A

Palpable thyroid nodule
Weight loss and increased appetite
Sweating and heat intolerance
Palpitations and fine resting tremor
Oligomenorrhoea
Hoarseness
Dysphagia and choking

59
Q

What are the risk factors for toxic thyroid adenoma?

A

Iodine deficiency
Young adult age
Female sex
Family history
Head and neck irradiation

60
Q

What investigations are considered for toxic thyroid adenoma?

A

TSH (suppressed)
Thyroid ultrasound
Free thyroxine/T4 (elevated)

61
Q

What is the first line treatment for non-pregnant non-lactating adults WITHOUT MASS EFFECT with toxic thyroid adenoma?

A

Radioactive iodine therapy (I-131)
Pre-treatment for thiamazole
Propanolol if cardiovascular risk

62
Q

What is the first line treatment for non-pregnant non-lactating adults WITH MASS EFFECT with toxic thyroid adenoma?

A

Subtotal thyroidectomy
Pre-treatment with thiamazole
Propanolol if cardiovascular risk

63
Q

What is the first line treatment for pregnant or lactating women with toxic thyroid adenoma?

A

Antithyroid drugs alone (propylthiouracil)

64
Q

What are the types of thyroid cancer?

A

Papillary (most common)
Follicular (second most common)
Medullary (calcitonin levels raised, cancer of parafollicular cells)
Anaplastic (rare, poor prognosis)

65
Q

What are the key diagnostic factors for thyroid cancer?

A

Palpable thyroid nodule
Hoarseness
Dyspnoea
Dysphagia
Tracheal deviation
Cervical lymphadenopathy

66
Q

What are the risk factors for thyroid cancer?

A

Family history
Female sex
Head and neck irradiation

67
Q

What are the first line investigations for thyroid cancer?

A

TSH (normal)
Thyroid ultrasound
Fine needle biopsy
Laryngoscopy

68
Q

What is seen in fine needle biopsy of papillary cancer?

A

‘Orphan Annie’ eyes
Psamomma bodies

69
Q

How are papillary and follicular carcinomas treated?

A

Surgery (thyroidectomy or hemithyroidectomy)
Radioiodine ablation
TSH suppression (levothyroxine)

70
Q

How is medullary thyroid carcinoma treated?

A

Total thyroidectomy
Thyroid replacement (levothyroxine)

71
Q

How is anaplastic thyroid carcinoma treated?

A

Palliative surgery (to biopsy and relieve airway obstruction; total thyroidectomy done when possible)
Chemoradiation
Thyroid replacement (levothyroxine)

72
Q

What are the phases of thyroid eye disease (TED)?

A

Active inflammatory phase: inflammation, damage and swelling occur, can last from 6 months - 2 years
Inactive phase: disease progression stops, but tissue damage and symptoms remain

73
Q

What are the symptoms of thyroid eye disease?

A

Ocular irritation
Aching behind eyes
Red eyes
Diplopia
Dry or watery eyes
Mild photophobia
Exophthalmos, lid retraction and lid lag
Conjunctival injection and oedema

74
Q

How is TED treated?

A

Prisms for diplopia
Prednisolone to control inflammation
Teprotumumab (blocks IGF-1R activation)
Orbital decompression surgery
Artificial tears for dry eyes

75
Q

What are the key diagnostic factors for diabetes insipidus?

A

Polyuria, polydipsia, nocturia
Signs of volume depletion (tachycardia, hypotension, poor skin turgor, dry mucous membranes)
Hypernatraemia
Visual field defects (pituitary mass)

76
Q

How does hypernatraemia present?

A

Irritability
Restlessness
Lethargy
Spasticity
Hyper-reflexia
Delirium, seizures or coma if severe

77
Q

What are the risk factors for diabetes insipidus?

A

History of pituitary/hypothalamic disorders (pituitary surgery, traumatic head injury, craniopharyngioma)
Family history
History of autoimmune disorders
Lithium therapy

78
Q

How is acute central DI treated?

A

Desmopressin
Oral/IV fluids

79
Q

How is nephrogenic DI treated?

A

Maintenance of adequate fluid intake
Treatment of underlying cause (i.e. stop drug)
Low-sodium diet
Hydrochlorothiazide (thiazide diuretic to reduce urine output)
Indometacin

80
Q

How is diabetes insipidus investigated?

A

Urinalysis, serum glucose (exclude DM)
24h urine collection (confirm polyuria, >3l)
Urine osmolality (low)
Serum osmolality (high)
Water deprivation test (low urine osmolality after water deprivation - otherwise, primary polydipsia)
AVP stimulation test (central vs nephrogenic)

81
Q

What are the symptoms of HHS?

A

Acute cognitive impairment
Polyuria and polydipsia
Weight loss
Nausea and vomiting
Weakness
Hypovolaemia (dry mucous membranes, poor skin turgor, hypotension, tachycardia) - DEHYDRATION

82
Q

What differentiates HHS from DKA?

A

Hypovolaemia
Marked hyperglycaemia without significant hyperketonaemia or acidosis
Osmolality usually 320ml/kg or more

83
Q

What are the risk factors for HHS?

A

Infection (pneumonia, UTI)
Inadequate insulin or oral antidiabetic therapy
Risk factors for hyperglycaemia (e.g. corticosteroids or antipsychotic drugs)
Acute illness (MI, sepsis, stroke)

84
Q

How is HHS investigated?

A

Blood glucose (>30 mmol/L)
Blood ketones (negative or low)
VBG (may have mild acidosis - renal impairment secondary to dehydration, lactic acidosis due to sepsis)
Serum osmolality (>320ml/kg)

85
Q

How is HHS treated?

A

IV fluids (1L of 0.9% NaCl) and potassium
Fixed-rate IV insulin infusion
Thromboprophylaxis (prophylactic low molecular weight heparin)

86
Q

What are the key diagnostic factors of diabetic ketoacidosis?

A

Nausea and/or vomiting
Polyuria and polydipsia
Abdominal pain
Dehydration (dry mucous membranes, decreased skin turgor, tachycardia with weak pulse, hypotension)
Kussmaul respiration
Reduced consciousness
Acetone smell on breath

87
Q

How is diabetic ketoacidosis investigated?

A

VBG (metabolic acidosis with raised anion gap)
Blood ketones (>3)
Blood glucose (>11)
FBC and U&Es

88
Q

What are the risk factors for DKA?

A

Inadequate or inappropriate insulin therapy
Infection (pneumonia or UTI)
Acute illness (MI, sepsis, pancreatitis)
Physiological stress (pregnancy, trauma, surgery)
Drugs (corticosteroids, antipsychotics)

89
Q

How is DKA treated?

A

IV saline (0.9% NaCl) and potassium replacement
Supportive care (e.g. NG tube, ECG, urinary catheter)
Fixed-rate intravenous insulin infusion
Consider prophylactic low molecular weight heparin if impaired consciousness
Consider sodium bicarbonate if pH <6.9

90
Q

What are the key diagnostic factors of diabetic nephropathy?

A

Symptoms may be absent until disease is advanced
Signs of retinopathy
Hypertension
Oedema
Skin changes (xerosis, hyperpigmentation, acanthosis nigricans)
Muscular atrophy
Pallor (anaemia)
Bleeding tendency (platelet dysfunction)

91
Q

What are the risk factors for diabetic neuropathy?

A

Sustained hyperglycaemia
Hypertension
Family history
Obesity
Smoking

92
Q

How is DKD investigated?

A

Urinalysis (proteinuria)
Urinary albumin:creatinine ratio (albuminuria)
Serum creatinine with GFR calculation (elevated in stages 1-2, decreased in stages 3-4)

93
Q

How is DKD treated?

A

Glycaemic control (insulin, SGLT2, etc)
ACEi or ARB (ramipril or candesartan)
Lifestyle modification (diet, smoking cessation)
Non-steroidal mineralocorticoid receptor antagonist for T2DM (finerone)
Consider statin

94
Q

What are the symptoms of diabetic neuropathy?

A

May be completely asymptomatic
Peripheral pain (often worse at night, may disturb sleep)
Peripheral loss of sensation
Dysaesthesia
Reduced or absent ankle reflexes
Painless injuries
Erectile dysfunction

95
Q

How is painful diabetic neuropathy treated?

A

Glycaemic control
1st line: Pregabalin/gabapentin and duloxetine
2nd line: Amitriptyline
3rd line: Topical capsaicin or GTN

96
Q

What are the symptoms of hypercalcaemia?

A

Kidney or gallbladder stones
Bone pain (osteoporosis or osteopenia)
Constipation, nausea and vomiting
Fatigue, depression, psychosis
Muscle weakness

97
Q

What causes primary hyperparathyroidism?

A

Parathyroid adenoma (most common - mutation or multiple endocrine neoplasia)
Parathyroid carcinoma
Hyperplasia

98
Q

How is primary hyperparathyroidism treated?

A

Parathyroidectomy

99
Q

How is primary hyperparathyroidism investigated?

A

High calcium
Low phosphate (PTH increases phosphate excretion at proximal convoluted tubule)
High PTH - MAY BE NORMAL
X-ray (pepperpot skull)

100
Q

What causes secondary hyperparathyroidism?

A

Insufficient vitamin D (poor intake or lack of sunlight)
Chronic kidney disease - low reabsorption of calcium in proximal convoluted tubule and less vitamin D production

101
Q

What are the blood test results for secondary hyperparathyroidism?

A

Low calcium (secondary to CKD or low vitamin D)
PTH is high in response to low calcium
High phosphate (less excretion of phosphate)
Low vitamin D

102
Q

How is secondary hyperparathyroidism treated?

A

Vitamin D supplementation (cholecalciferol or alfacalcidol in CKD patients)
Phosphate binders (calcium acetate)

103
Q

What causes tertiary hyperparathyroidism?

A

When secondary hyperparathyroidism persists for a long time, there is hyperplasia of parathyroid glands - autonomous production of PTH

104
Q

What are the blood test results for tertiary hyperparathyroidism?

A

High PTH
Initially low calcium but, as PTH rises, hyperplasia of parathyroid glands increases calcium

105
Q

How is tertiary parathyroidism treated?

A

Parathyroidectomy

106
Q

What are the signs and symptoms of hypocalcaemia?

A

Tetany
Paraesthesia
Convulsions
Arrhythmias (torsades de pointes or AF)
Chvostek’s sign (ipsilateral contraction of facial muscles when facial nerve is tapped)
Trousseau sign (painful clasping response of fingers and hands when blood pressure cuff is inflated above systolic blood pressure)

107
Q

What are the causes hypoparathyroidism?

A

Thyroid or parathyroid surgery (most common)
Auto-immune (autoimmune polyendocrine syndrome type 1)
Magnesium deficiency
Congenital (rare)

108
Q

How is hypoparathyroidism treated?

A

Calcium and vitamin D supplementation
Recombinant PTH

109
Q

what are some causes of hypoglycaemia?

A

insulinoma: increased ratio of proinsulin to insulin
excess insulin or sulfonylureas
liver failure
Addison’s disease
alcohol

110
Q

What are the symptoms of hypoglycaemia?

A

Sweating and shaking
Hunger
Anxiety
Nausea
Weakness
Vision changes
Confusion
Dizziness
Convulsion
Coma

111
Q

how is hypoglycaemia treated?

A

oral glucose 10-20g
if patient is unconscious or unable to swallow: subcut or IM glucagon
alternatively, IV 20% glucose solution through a large vein

112
Q

What are the features of Hashimoto’s thyroiditis?

A

Features of hypothyroidism
Goitre: firm, non-tender
Anti-TPO and anti-thyroglobulin antibodies

113
Q

What are the causes of primary hyperaldosteronism?

A

Bilateral idiopathic adrenal hyperplasia
Adrenal adenoma (Conn’s syndrome)
Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma

114
Q

What are the features of primary hyperaldosteronism?

A

Hypertension
Hypernatraemia
Hypokalaemia (muscle weakness)
Metabolic alkalosis

115
Q

How is primary hyperaldosteronism investigated?

A

Plasma aldosterone/renin ratio (high aldosterone, low renin due to negative feedback)
High-resolution CT abdomen to decide unilateral vs bilateral aldosterone excess

116
Q

How is primary hyperaldosteronism managed?

A

Adrenal adenoma: laparascopic adrenalectomy
Bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone

117
Q

What are the side effects of SGLT-2?

A

Glycosuria
Increased urine output and frequency
Genital and urinary tract infections (e.g., thrush)
Weight loss
Diabetic ketoacidosis, notably with only moderately raised glucose
Fournier’s gangrene (rare but severe infection of the genitals or perineum)

118
Q

What is a phaeocytochroma?

A

Rare catecholamine secreting tumour of adrenal medulla

119
Q

What are the features of a phaeocytochroma?

A

hypertension (around 90% of cases, may be sustained)
headaches
palpitations
sweating
anxiety

120
Q

How is phaeocytochroma investigated?

A

24 hr urinary collection of metanephrines

121
Q

How is phaeocytochroma managed?

A

Surgery
Give patient an alpha blocker (phenoxybenzamine), before a beta blocker (propranolol)

122
Q

What are some causes of gynaecomastia?

A

Testicular cancer (oestrogen secretion from Leydig cell tumour)
Liver cirrhosis (decreased breakdown of oestrogen)
Hyperthyroidism
hCG secreting tumour (SCLC)
Orchitis (inflammation of testes, e.g. with mumps)
Kallman’s, Klinefelter’s
Hyperprolactinaemia
Drugs

123
Q

What are some causes of raised prolactin?

A

Prolactinoma - non-functioning adenomas can also cause hyperprolactinaemia
Acromegaly
PCOS
Primary hypothyroidism
Pregnancy

124
Q

What drugs can cause gynaecomastia?

A

Anabolic steroids (raise oestrogen)
Antipsychotics (dopamine antagonist, raise prolactin)
Digoxin (stimulates oestrogen receptors)
Spironolactone
Opiates
Marijuana
Alcohol

125
Q

How do pituitary adenomas cause symptoms?

A

Excess of hormone (prolactinoma is most common)
Depletion of hormone due to compression of normal functioning pituitary gland (hypopituitarism)
Stretching of dura around pituitary fossa (headaches)
Compression of optic chiasm (bitemporal hemianopia)

126
Q

How is pituitary adenoma investigated?

A

MRI brain with contrast
Formal visual field testing
Pituitary blood profile - screening for hormone hypersecretion (GH, prolactin, ACTH, LH, FSH, TFTs)

127
Q

What are the features of excess prolactin in women?

A

Infertility
Oligomenorrhoea or amenorrhoea
Galactorrhoea
Osteoporosis

128
Q

What are the features of excess prolactin in men?

A

Decreased libido
Impotence
Infertility
Gynaecomastia
Galactorrhoea

129
Q

How are prolactinomas treated?

A

Dopamine agonist (cabergoline, bromocriptine)
Trans-sphenoidal pituitary adenectomy if failure to respond to medical therapy

130
Q

How is acromegaly investigated?

A

IGF-1 (can also be used to monitor disease)
OGTT with serial GH measurements if IGF-1 is raised - GH isn’t suppressed with hyperglycaemia

131
Q

What are the features of acromegaly?

A

Coarse facial features
Excessive sweating and oily skin
Raised prolactin in 1/3 of cases (galactorrhoea)
Features of pituitary tumour (hypopituitarism, headaches, bitemporal hemianopia)

132
Q

What are the causes of hypercalcaemia of malignancy?

A

PTH-related peptide from the tumour, e.g. squamous cell tumour
Bony metastases (promote osteoclast function)
Multiple myeloma

133
Q

What are the blood test results for hypercalcaemia of malignancy?

A

Serum calcium (elevated)
Serum PTH (raised)
ALP - high in bony metastases, normal in multiple myeloma

134
Q

How is hypercalcaemia treated?

A

Rehydration with saline (3-4l/day)
Bisphosphonates following rehydration
Furosemide in patients who cannot tolerate aggressive fluid resuscitation

135
Q

how is hypoglycaemia treated?

A

oral glucose 10-20g
if patient is unconscious or unable to swallow: subcut or IM glucagon
alternatively, IV 20% glucose solution through a large vein

136
Q

what does a thyroid uptake scan show in Grave’s disease?

A

diffuse uptake through an enlarged gland

Phase 1c: Conditions (18 decks)

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