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Year 3 - Diseases > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

List symptoms of T2DM patient

A

Insidious - may have diabetes for a long time before diagnosis

  • Frequent urination
  • Polyuria and polydipsia
  • Waking in the night to pee
  • Blurred vision
  • Weight loss
  • Tiredness, lethargy
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2
Q

Describe management of type 2 diabetes mellitus

A
  • First line is lifestyle
  • Biguianide (eg. Metformin) first line. Add another drug if this doesnt control blood glucose. SGLT2 inhibitors, GLP1 analogues and DPP4 inhibitors are preferred as second line
  • Sulponylureas first line if patient is not overweight (eg.gliclazide)
  • Insulin sensitiser (thiozolidinediones such as pioglitazone)
  • Insulin itself (long acting glargine once a day, rapid acting with meals)
  • Incretins (GLP-1 analogue)
  • Gliptins (DPP4 inhibitor)
  • SGLT2 inhibitor (causes glycosurea)
  • Treat aggressively when first diagnosed
  • If high risk, already experienced MI or stroke, highly controlling diabetes can cause sudden death due to risk of hypos (BP, lipid, antiplatelets to reduce CVD risk where appropriate)
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3
Q

Describe diagnosis of T2DM

A
  • HbA1C over 48mmol
  • Fasting blood glucose measurement on multiple occasions over 7mmol/L
  • Random blood glucose over 11mmol/l
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4
Q

List side effects of metformin

A
  • Diarrhoea

- Lactic acidosis (don’t use in end stage kidney disease)

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5
Q

Describe adrenal insufficiency

A

Failure of the adrenal glands to produce enough corticosteroids and mineralocorticoids, due to Addisons disease or disease of the hypothalamus.

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6
Q

List causes of adrenal insufficiency

A
  • Addisons (TB most common worldwide, autoimmune most common western world)
  • Long term corticosteroid administration (secondary)
  • Disorders of the hypothalamus/pituitary
  • Adrenal mets
  • Lymphoma
  • HIV patients with opportunistic infections
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7
Q

Describe epidemiology of adrenal insufficiency

A

About 8,400 people are currently diagnosed with Addison’s disease in the UK.

  • 0.8 per 100000
  • Rare but can be fatal
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8
Q

List patients in whom you would consider adrenal insufficency

A
  • Patients with hypothyroidism whose symptoms worsen when thyroxine is started
  • Type 1 diabetes mellitus with recurrent unexplained hypoglycaemic episodes
  • Other autoimmune diseases
  • Low sodium and high potassium levels on blood biochemistry.
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9
Q

List signs and symptoms of adrenal insufficiency

A
  • A person with Addison’s disease may present with a sudden crisis precipitated by intercurrent infection or stress. Features include hypotension, hypovolaemic shock, acute abdominal pain, low-grade fever, and vomiting.
  • Addison’s disease should also be considered in a person with persistent, non-specific symptoms, such as: fatigue; hyperpigmentation/vitiligo; gastrointestinal symptoms; cravings for salt, soy sauce, or liquorice; musculoskeletal symptoms; or postural dizziness due to hypotension.
  • Weight loss, depression, psychosis
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10
Q

Describe investigations in adrenal insufficiency

A
  • If suspected, a blood test is performed to look at serum cortisol (morning), urea and electrolytes (low na, high k, low glucose, uraemia, high Ca, eosinophilia, anaemia)
  • High acth in addisons, low in secondary cayses
  • 21hydroxylase adrenal antibodies positive in autoimmune disease
  • Synacthen test is performed to confirm addisons (plasma cortisol before and 30min after tetracosactide, excludes addisons if cortisol increases)
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11
Q

Describe management of adrenal insufficiency

A
  • If the serum cortisol level is less than 100 nanomol/L, the person should be admitted to hospital. Adrenal insufficiency is highly likely.
  • If the serum cortisol level is 100–500 nanomol/L, the person should be referred to an endocrinologist for further investigations.
  • Treated with hydrocortisone for glucocorticoid replacement (15-25mg daily in 2-3 doses) and fludrocortisone for mineralocorticoid replacement
  • Bracelet for steroid use, extra before strenuous activity/if ill
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12
Q

Define acromegaly

A

A condition in which benign pituitary adenomas lead to an excess secretion of growth hormone (GH) and insulin-like growth factor 1 (IGF-1).

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13
Q

Describe epidemiology of acromegaly

A
  • Acromegaly is a rare disease with a prevalence estimated at 40 per million
  • Mean age of diagnosis is 40-45
  • More common in males than females
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14
Q

List signs and symptoms of acromegaly

A
  • Headache, vision loss (bitemporal hemianopsia), cranial nerve palsies
  • In women, oligomenorrhea, secondary amenorrhea, galactorrhea, vaginal atrophy
  • In men, erectile dysfunction, decreased libido, decreased testicular volume
  • Doughy skin texture, hyperhidrosis
  • Deepening of the voice, macroglossia with fissures, obstructive sleep apnea
  • Coarsening of facial features slowly progressing with age: enlarged nose, forehead, and jaw (macrognathia) with diastema
  • Sweating
  • Widened hands, fingers, and feet
  • Painful arthropathy (ankles, knees, hips, spine)
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15
Q

Describe aetiology of acromegaly

A
  • Benign growth hormone-secreting pituitary adenoma (> 95% of cases)
  • Very rare: neuroendocrine or hypothalamic tumors, paraneoplastic syndromes
  • Ectopic secretion of growth hormone by neuroendocrine tumors (e.g., small cell lung carcinoma, pancreatic islet-cell tumor (as found in MEN1)
  • Increased Secretion of growth hormone-releasing hormone (GHRH) from a hypothalamic tumor or in paraneoplastic syndromes (e.g., small cell lung carcinoma, medullary thyroid cancer)
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16
Q

Describe investigations performed in acromegaly

A
  • Serum IGF-1 concentration: the best single test
  • Elevated IGF-1 level: acromegaly suspected; conduct oral glucose tolerance test (OGTT).
  • In oral glucose tolerance test a positive result is no suppression of IGF1
  • Conduct pituitary MRI to determine the source of excess GH, usually shows a visible mass to confirm pituitary adenoma
  • Screen for an extrapituitary cause (e.g., CT scan of the chest and abdomen, measure GHRH)
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17
Q

Describe management of acromegaly

A
  • Transsphenoidal adenomectomy (preferred method)
  • Surgical debulking (in patients with parasellar disease and inoperable tumors)
  • Somatostatin analogs (e.g., octreotide, lanreotide)
  • Dopamine agonists (e.g., cabergoline): reduce tumor size and GH secretion
  • GH receptor antagonists (e.g., pegvisomant)
  • Conventional fractionated radiotherapy
  • Stereotactic radiosurgery
  • Assessing IGF-1 and random GH level 12 weeks after the surgery and then annually
  • Annual hormonal testing for hypopituitarism
  • Performing MRI at least 12 weeks after the surgery
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18
Q

Define hypothyroidism

A

Inability of the thyroid gland to produce appropriate amounts of T4 and T3.

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19
Q

Describe aetiology of hypothyroidism

A
  • Hashimotos disease (autoimmune)
  • Iatrogenic (eg. lithium, post radioiodide therapy, amiodarone)
  • Post partum
  • Congenital (aplasia, hypoplasia, dysplasia)
  • DeQuervain thyroiditis (subacute)
  • Secondary - pituitary adenoma
  • Tertiary - hypothalamic disorders
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20
Q

List risk factors for hypothyroidism

A
  • Pre-existing autoimmune disease
  • Female
  • Amiodarone/ lithium
  • Pregnancy
  • Turner/downs syndrome
  • Any history of brain cancer, head trauma, surgery
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21
Q

Describe epidemiology of hypothyroidism

A
  • Primary is more common. In the UK, prevalence is 1-2% and 10 times more common in women than men
  • Total prevalence in europe 3%
  • Secondary hypothyroidism is rare, between 1 in 20000 and 1 in 80000
  • Post partum hypothyroidism affects around 7% of women
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22
Q

List symptoms of hypothyroidism

A
  • Fatigue/lethargy, cold intolerance; weight gain, constipation.
  • Non-specific weakness, arthralgia, and myalgia.
  • Menstrual irregularities; infertility or subfertility.
  • Depression, impaired concentration and memory.
  • Dry skin and hair loss (such as loss of lateral eyebrows).
  • Thyroid pain, for example in subacute thyroiditis.
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23
Q

List signs of hypothyroidism

A
  • Changes to appearance such as coarse dry hair and skin, and hair loss.
  • Oedema, including swelling of the eyelids
  • Hoarseness or deepening of the voice; goitre.
  • Bradycardia and diastolic hypertension; pericardial effusion.
  • Delayed relaxation of deep tendon reflexes.
  • Paraesthesia (due to carpal tunnel syndrome) or peripheral neuropathy.
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24
Q

Describe diagnosis of hypothyroidism

A
  • Check TSH levels, if high check T4 levels
  • Consider checking FBC, serum B12, HbA1c, coeliac and lipids
  • Is autoimmune disease suspected, check serum thyroid peroxidase and thyroglobulin
  • Radioactive iodine uptake test
  • Ultrasound
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25
Q

Define thyroid nodule(s)

A
  • Thyroid nodules are abnormal growths within the thyroid gland.
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26
Q

Describe epidemiology of thyroid cancer

A
  • Over 2500 new thyroid cancers are diagnosed each year in the UK.
  • 1% of all malignancies. 5% incidence in thyroid nodules
  • It is seen in both sexes. Approximately 70% of new diagnoses are in females.
  • The 5 year survival is over 90%.
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27
Q

Describe prognosis of thyroid cancer

A

5 year survival rate is 90%

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28
Q

Describe signs and symptoms of thyroid cancer

A
  • Neck lump which moves on swallowing, firm and painless
  • Early stages often asymptomatic

Late stages

  • Dyspnea
  • Dysphagia
  • Hoarseness (vocal cord paresis)
  • Horner syndrome
  • Possible obstruction of the superior vena cava
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29
Q

List risk factors for thyroid cancer

A
  • Exposure to ionizing radiation and genetic predisposition
  • Thyroid cancers also disproportionately affect women
  • Family history
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30
Q

Describe investigations of thyroid cancer

A
  • Ultrasound (grade U1-4)
  • Fine needle aspirate (U3+ or high risk pt)
  • Synctography
  • Uptake scan showing cold nodules (FDG-PET)
  • Laryngoscopy
  • TSH
  • Calcitonin (medullary)
  • CT (lymph node imaging and retrosternal extent)
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31
Q

Describe aetiology of thyroid nodule(s)

A

Benign thyroid nodules (∼ 95% of cases)

  • Thyroid adenomas
  • Follicular adenoma (most common)
  • Hürthle cell adenoma
  • Toxic adenoma
  • Papillary adenoma (least common)
  • Thyroid cysts
  • Dominant nodules of multinodular goiters
  • Hashimoto thyroiditis

Malignant thyroid nodules (∼ 5% of cases)

  • Thyroid carcinoma
  • Thyroid lymphoma
  • Metastatic cancer from breast/renal carcinoma (rare)
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32
Q

Describe epidemiology of thyroid nodule(s)

A
  • Males more than females
  • Incidence: increases with age (30-50% in over 55s)
  • Geographic distribution: most common in inland regions without iodine fortification programs, where iodine content in food and water is low
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33
Q

List signs and symptoms of thyroid nodules

A

Usually asymptomatic, with often a palpable lump in the neck that moves on swallowing but not when sticking out tongue

Severe causes can cause:

  • Goiter.
  • Pain at the base of your neck.
  • Dysphagia
  • Dyspnoea
  • Hoarse voice.
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34
Q

Describe investigations of thyroid nodule(s)

A
  • TSH blood test and free T4 if abnormal
  • Radioiodide uptake test
  • Ultrasound
  • Fine needle aspirate
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35
Q

Define graves disease

A
  • Hyperthyroidism is a biochemical diagnosis which occurs when there is pathologically increased thyroid hormone production and secretion by the thyroid gland
  • Graves disease is autoimmune condition against the thyroid. Type 2 hypersensitivity reaction. Antithyroid peroxidase
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36
Q

Risk factors and aetiology of graves disease

A
  • Women are more likely to develop Graves’ disease.
  • Family history
  • Current smokers have a three-fold increased risk of developing Graves’ orbitopathy compared with non-smokers.
  • If a person has Graves’ disease, the most significant modifiable risk factor for developing Graves’ orbitopathy is smoking
  • Autoimmune disease — co-existent autoimmune conditions are a risk factor for developing Graves’ orbitopathy, hyperthyroidism, and postpartum thyroiditis
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37
Q

Describe epidemiology of graves disease

A
  • Autoimmune hyperthyroidism (Graves’ disease) is the most common form, accounting for 60 to 80% of cases.
  • Thyrotoxicosis is a common endocrine disorder with a prevalence of around 2% in UK women and 0.2% in men.
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38
Q

List symptoms of graves disease

A
  • Rapid-onset malaise, fever, and thyroid pain
  • Agitation, emotional lability, insomnia, irritability, anxiety, palpitations.
  • Exercise intolerance, fatigue, muscle weakness.
  • Heat intolerance, increased sweating.
  • Increased appetite with unintentional weight loss, diarrhoea.
  • Subfertility, oligomenorrhoea, amenorrhoea.
  • Polyuria, thirst, generalized itch.
  • Reduced libido, gynaecomastia in men.
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39
Q

List signs of graves disease

A
  • Agitation, fine tremor, warm moist skin, palmar erythema.
  • Sinus tachycardia, atrial fibrillation, heart failure, pretibial myxoedema (non-pitting, due to glycosaminoglycans, bilateral)
  • In Graves’ disease, the thyroid gland is usually diffusely symmetrically enlarged without nodules, and there may be a bruit.
  • Pruritus, urticaria, vitiligo, diffuse alopecia.
  • Muscle wasting, proximal myopathy, hyper-reflexia.
  • Splenomegaly, lymphadenopathy.
  • Gynaecomastia in men.
  • Thyroid acropachy (clubbing and swelling of the distal fingers and toes).
  • Thyroid dermopathy (slightly pigmented thickened skin and swelling of both legs, usually in the pretibial area)
  • Graves opthalmology (Eyelid retraction -sclera is visible above the superior corneal limbus), Lid lag, Proptosis (exophthalmos, eyeball protrusion, an inability to fully close the eyes as the upper and lower lids do not fully appose).)
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40
Q

Describe investigations for graves disease

A
  • History and signs
  • Measure TSH, free T3 and T4
  • TSH receptor antibodies (antithyroid peroxidase is les specific, can be raised by many things)
  • LFTs and FBCs before starting antithyroid drugs
  • Diffuse increased uptake on NM uptake scan
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41
Q

Define diabetes insipidus

A

Diabetes insipidus is a condition characterised by the passage of large volumes of dilute urine (>3L) due to impaired water resorption by the kidney, because of reduced ADH secretion from the posterior pituitary (cranial DI) or impaired response of the kidney to ADH (nephrogenic DI).

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42
Q

List signs and symptoms of diabetes insipidus

A
  • Polyuria – excessive urination unaffected by reduction of fluid intake.
  • Polydipsia – can be uncontrollable and all consuming with patients drinking anything and everything to hand.
  • Dehydration since the body cannot conserve much, if any, of the water it takes in.

Symptoms of hypokalaemia:

  • Muscle weakness
  • Hypotonia
  • Hyporeflexia
  • Cramps
  • Tetany
  • Palpitations
  • Light-headedness (arrhythmias)

Symptoms of hypernatraemia:

  • Lethargy
  • Thirst
  • Weakness
  • Irritability
  • Confusion
  • Coma
  • Fits
  • Signs of dehydration.
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43
Q

Describe aetiology of diabetes insipidus

A

Cranial DI

  • Disease of the hypothalamus
  • Neurosurgery
  • Trauma
  • Primary/ secondary tumours
  • Infiltrative disease (sarcoidosis, histiocytosis)
  • Idiopathic

Nephrogenic DI

  • Hypokalaemia
  • Hypercalcaemia
  • Drugs: lithium chloride, dimeclocycline, glibenclamide
  • Renal tubular acidosis
  • Sickle cell disease
  • Prolonged polyuria of any cause
  • Familial (mutation in ADH receptors)
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44
Q

Describe epidemiology of diabetes insipidus

A
  • The combined prevalence of cranial DI and nephrogenic DI combined is estimated at 1 in 25,000.
  • DI can complicate up to 1 in 30,000 pregnancies.
  • Nephrogenic DI is the most common adverse effect of lithium and occurs in up to 40% of patients.
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45
Q

Describe investigations of diabetes insipidus

A
  • Urine volume must be measured to confirm polyuria (>3L in 24h)
  • U and E: normal to high Na+.
    Ca2+
  • Glucose (exclude DM)

Measure urine and serum osmolality:

  • In DI, urine osmolality is inappropriately low for the high plasma osmolality.
  • Significant DI is excluded if urine: plasma ratio is >2:1 (as is the normal situation in health), provided plasma osmolality is no greater than 295mOsmol/kg.
  • In DI, despite raised plasma osmolality, urine is dilute with a U:P ratio of <2.
  • In primary polydipsia, there may be dilutional hyponatraemia.
  • Diagnose with water deprivation test. Urine remains dilute despite deprivation. Desmopressin is then given (in central urine is concentrated then, in nephrogenic it is not)
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46
Q

Describe treatment of diabetes insipidus (cranial, nephrogenic and acute)

A

Cranial DI

  • Find the cause – MRI (head); test anterior pituitary function.
  • Give desmopressin, a synthetic analogue of ADH.

Nephrogenic

  • Treat the cause.
  • If it persists, try bendroflumethiazide 5mg PO/24h. Thiazide diuretics sensitise the renal tubules to endogenous vasopressin.
  • NSAIDs lower urine volume and plasma Na+ by inhibiting prostaglandin synthase: prostaglandins locally inhibit the action of ADH.
  • Treatment of the cause usually does improve nephrogenic diabetes insipidus.

Emergency management

  • Do urgent plasma UandE, and serum and urine osmolalities. - Monitor U/O carefully and check U and E twice daily initially.
  • IVI to keep up with U/O. If severe hypernatraemia, do not lower Na+ rapidly as this may cause central oedema and brain injury. If Na+ is >170, use 0.9% saline initially – this contains 150mmol/L of sodium. Aim to reduce Na+ at a rate of <12mmol/L per day. Use of 0.45% saline can be dangerous.
  • Desmopressin 2ug IM (lasts 12-24h) may be used as a therapeutic trial.
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47
Q

List complications of diabetes insipidus

A
  • Dehydration

- Hypotension (syncope, renal failure, brain damage)

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48
Q

Describe prognosis of diabetes insipidis

A
  • Usually, cranial affects people for life as treatment of cause does not remove insipidus
  • Nephrogenic usually cured by treatment of cause (eg. stop medication)
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49
Q

Define Cushings syndrome

A

The term Cushing’s syndrome is used to describe state of excess free circulating glucocorticoid (cortisol).

  • Administered ACTH or glucocorticoid.
  • Excessive ACTH from the pituitary gland (cushings disease - pituitary adenoma)
  • ACTH producing tumours (e.g. from lung cancer)
  • Adrenal tumours (non-ACTH dependent pathway)
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50
Q

Describe epidemiology of cushings syndrome

A
  • The incidence of spontaneous Cushing’s syndrome is 10 per 1,000,000 per year
  • Peak incidence is between age of 25 and 40 – when associated with an adrenal or pituitary tumour
  • ACTH dependent 80% due to pituitary adenomas,
    20% due to small cell lung ca, or carcinoid tumours, or any other endocrine tumour
  • ACTH independent Adrenal adenoma – 60%, Adrenal carcinoma – 40%
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51
Q

List risk factors for cushings syndrome

A
  • Female (F:M 5:1)
  • Diabetes – especially if poor glycemic control
  • Prevalence fo 2-5% amongst patients with T2DM
  • Obesity
  • Oral corticosteroids
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52
Q

List symptoms of cushings syndrome

A
  • Weight gain
  • Change of appearance
  • Depression
  • Insomnia
  • Amenorrhoea / oligomenorrhoea
  • Poor libido
  • Thin skin / easy bruising
  • Hair growth
  • Acne
  • Slow growth in children
  • Back pain
  • Reduced libido
  • Polyuria
  • Dyspepsia
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53
Q

List signs of cushings syndrome

A
  • “Moon face”
  • Frontal balding (female)
  • Pigmentation
  • Skin infections
  • Hypertension
  • Osteoporosis / osteopenia
  • Pathological fractures – particularly vertebrae and ribs
  • “Buffalo hump” – a dorsal fat pad
  • Kyphosis – hunch back
  • Striae – stretch marks – can be purple or red- occur mainly on the abdomen
  • Supraclavicular fat pads
  • Oedema
  • Proximal myopathy
  • Glycosuria
  • Diabetes / impaired glucose tolerance
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54
Q

Describe investigations of cushings

A
  • 48hr low dose dexamethasone suppression test (suppresses cortisol in normal patients, not in patients with ACTH dependent cushings - also called overnight dex given at night then measure cortisol in morning)
  • 24 hour urinary free cortisol measurements (measure complete urine over 24 hours and look for cortisol)
  • In hospital, take blood at 9am and midnight. Should be significantly lower at midnight
  • Very low ACTH suggests adrenal tumour
  • Measure plasma ACTH and cortisol
  • MRI, CT (pituitary/adrenal adenoma or carcinoma), chest X ray for lung tumour
  • High dose dexamethasone suppression test (lack of suppression adrenal tumour or ectopic ACTH, however 25% chance it is incorrect, used in identification of the cause of Cushings syndrome)
  • Inferior petrosal sinus sampling measures ACTH levels from the veins that drain the pituitary
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55
Q

List complications of cushings syndrome

A
  • MI
  • Hypertension
  • Infection
  • Heart failure
  • Osteoporosis
  • Diabetes
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56
Q

Describe treatment of cushings syndrome

A
  • Surgery or radiotherapy
  • Controlled initially medically with metyraprone (11b hydroxylase antagonist) or ketoconazole (Cyp450 blocker)
  • Cushings disease transsphenoidal removal of tumour, irradiation or as last resort bilateral adrenalectomy
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57
Q

Describe prognosis of cushings syndrome

A
  • Poor if untreated

- Adrenal carcinoma 5 year survival 30%

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58
Q

Define PCOS

A
  • Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder that appears to emerge at puberty.
  • The clinical features may include hyperandrogenism (with the clinical manifestations of oligomenorrhoea, hirsutism, and acne), ovulation disorders, and polycystic ovarian morphology.
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59
Q

Describe aetiology and risk factors of PCOS

A
  • Genetic and environmental factors
  • Insulin resistance and hyperinsulinaemia (resulting in reduced SHBG and increased free testosterone, increased androgen production and weight gain)
  • Hormonal imbalance (LH high relative to FSH increasing androgen precursors, increased oestrogen unopposed by progesterone resulting in hyperplastic endometrium)
  • Weight gain exacerbates symptoms
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60
Q

List symptoms of PCOS

A

In adults

  • Infrequent or no ovulation — for example, infertility, oligomenorrhoea, or amenorrhoea.
  • Hyperandrogenism — for example, hirsutism and acne vulgaris occurring after adolescence.

In adolescents

  • Signs and symptoms of hyperandrogenism (such as acne and hirsutism), and
  • Irregular menstrual cycles, defined as:
  • Normal in the first year post-menarche as part of the pubertal transition.
  • More than 1 year to less that 3 years of irregular cycles (more than 45 days or less than 21 days) after the onset of menarche.
  • More than 3 years of irregular cycles (more than 35 days or less than 21 days, or less than 8 cycles every year) post menarche to perimenopause.
  • More than 1 year of irregular cycles (more than 90 days for any one cycle) post menarche.
  • Primary amenorrhea by age 15 years or more than 3 years of irregular cycles post thelarche (breast development).
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61
Q

List signs of PCOS

A
  • Obesity
  • Hirsutism
  • Acanthosis nigricans, characterized by dry, rough skin that has grey-brown pigmentation, is palpably thickened, and is covered by a papillomatous elevation (giving it a velvety texture). The condition commonly affects the axillae, perineum, or extensor surfaces of the elbows and knuckles. When the neck is affected, there is often a thin necklace of warty fissures that can spread as a wide band.
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62
Q

Describe diagnosis of PCOS

A

Diagnosed if 2/3 not explained by other causes

  • Infrequent or no ovulation (usually manifested as infrequent or no menstruation).
  • Clinical and/or biochemical signs of hyperandrogenism (such as hirsutism, acne, or elevated levels of total or free testosterone).
  • Polycystic ovaries on ultrasound scan, defined as the presence of 12 or more follicles (measuring 2–9 mm in diameter) in one or both ovaries and/or increased ovarian volume (greater than 10 cm3).
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63
Q

Describe investigation of PCOS

A
  • Measure total testosterone — this is normal to moderately elevated in women with polycystic ovary syndrome (PCOS).
  • Measure sex hormone-binding globulin (SHBG) — this is normal to low in women with PCOS and provides a surrogate measurement of the degree of hyperinsulinaemia.
  • Calculate free androgen index (100 multiplied by the total testosterone value divided by the SHBG value) to assess the amount of physiologically active testosterone present — this is normal or elevated in women with PCOS
  • To eliminate other causes measure LH, Prolactin (mildly elevated in PCOS), TSH
  • Refer adults for ultrasound scan to look for the presence of 12 or more follicles in at least one ovary (measuring 2–9 mm diameter) or increased ovarian volume (greater than 10 cm3).
  • Ultrasound scan should not be used for the diagnosis of PCOS in adolescents.
  • Exclude cushings or androgen producing tumour if hirsutism.ect
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64
Q

Define phaeochromocytoma

A

A neuroendocrine tumour of the medulla of the adrenal glands. It secretes large quantities of the catecholamines noradrenaline, and to a lesser extent, adrenaline.

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65
Q

Describe epidemiology of phaeochromocytoma

A
  • 10% familial
  • 10% bilateral
  • 10% extra-renal
  • 10% malignant
  • 1 in 100000 people in UK diagnosed anually
  • 0.1-0.6% patients with hypertension, 0.05% autopsy series prevalence
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66
Q

Describe aetiology and risk factors for phaeochromocytoma

A

25% due to inherited condition

  • Multiple endocrine neoplasia type 2 (MEN 2)
  • Neurofibromatosis 1 (NF1)
  • Familial paraganglioma syndromes, which are mostly caused by changes in the succinate dehydrogenase (SDH) gene
  • Von Hippel Lindau disease
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67
Q

List symptoms of phaeochromocytoma

A
  • Severe headaches
  • A plethora of other symptoms, including flushing, unwell, weight loss (like in hyperthyroid), panic/anxiety, sweating, pallor, hyperglycaemia, pyrexia, abdominal pain
  • May be worsened by TCA (if you thought it was ps-somatic), beta-blockers, IV contrast
  • Attacks may last less than 15 mins or up to 1 hour
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68
Q

List signs of phaeochromocytoma

A
  • Severe hypertension (eg 210/100) and orthostatic hypotension, both fluctuating
  • Cardiac tachyarrythmias (eg SVTs)
  • Pallor
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69
Q

List investigations for phaeochromocytoma

A
  • Initial best test to rule out phaeochromocytoma: metadrenaline from blood.
  • Confirmed by 3x 24-hour collection of urine catecholamines. (DO URINE FIRST UNLESS SCREENING FOR HEREDITARY CAUSE)
  • CT abdomen
  • Nuclear imaging: MIBG: chrommafin-seeking isotope scan, for extra-renal tumours imaging is performed post-diagnosis purely for surgical management planning)
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70
Q

Define prolactinoma

A

An otherwise benign adenoma of the anterior pituitary gland – which produces prolactin outside of the normal controls.

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71
Q

Describe epidemiology of prolactinoma

A
  • Prevalence is about 0.25%
  • Increasing – thought to be drug related
  • More common in women
  • M:F – 1 : 3.5
  • Typical age of onset 25-45
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72
Q

List risks and aetiology of hyperprolactinaemia

A

About half of cases are due to a pituitary adenoma
- Usually a micro adenoma (<10mm diameter) – 90% of adenomas
- Less commonly a macro adenoma (>10mm) – 10% of adeomas
- Rarely, other types of pituitary tumour (nonfunctioning tumours) can cause hyperprolactinaemia through compression of the pituitary stalk – which decreases the flow of dopamine to the pituitary and thus reduces the dopamine suppression feedback
- Multiple Endocrine Neoplasia (MEN) causes about 20% of cases of hyperprolactinaemia
Drug – account for about 45% of cases
- Anti-psychotics (e.h. haloperidol, risperidone)
- Methyldopa
- Opioids
- Antidepressants including TCAs and SSRIs
- Verapamil
- Hypothyroidism – about 5% of cases due to increased production of TRH
- Pregnancy
- Nipple stimulation
- Stress
- Excessive exercise
- In neonates (<3m old)

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73
Q

List presenting symptoms of prolactinoma

A
  • Galactorrhoea – milk production – is the most common symptoms
  • Can occur in man as well as women
  • Often intermittent and sporadic

Women may also exhibit
- Amenorrhoea or oligomenorrhea

Men are more likely to present with:

  • Headaches
  • Reduced libido
  • Erectile dysfunction
  • Symptoms in men tend to be more subtle and have slower onset
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74
Q

List signs of prolactinoma

A
  • Signs of hirsutism in women (male pattern hair growth, increased musculature) – which can make it difficult to distinguish from PCOS
  • Visual disturbance (bitemporal hemianopia)
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75
Q

Describe investigations of prolactinoma

A
  • Pregnancy test
  • Prolactin level >5x normal usually required to confirm diagnosis
  • Usually correlate to the size of the tumour – bigger tumour = greater prolactin level
  • TFTs to rule out hypothyroidism as the cause
  • CT or MRI to confirm the presence of adenoma, MRI preferred (higher resolution than CT, the pituitary gland is small!)
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76
Q

Describe management of prolactinoma

A
  • Patients who are asymptomatic, with prolactin levels <100ng/ml can usually be observed with repeat prolactin levels every 3 months, and repeat imaging every 12 months
  • Dopamine agonists are mainstay of treatment (e.g. bromocriptine 1.25 – 5 mg BD, or cabergoline 0.25 – 1mg weekly or twice weekly)
  • Cabergoline has been shown to be more effective than bromocriptine
  • Have been associated with valvular heart disease when given long-term in high doses (usually only seen in Parkisnon’s disease, because doses used in hyperprolactinaemia are lower)
  • Consider echocardiogram monitoring
  • Other side effects include psychiatric effects – such as increased impulsive behaviour, and rarely, psychosis
  • Consider exogenous oestrogen for women who have low estradiol levels
  • Dopamine agonists usually result in shrinkage of the adenoma
  • Treatment is required long term, but particularly for microadenomas, remission may occur if treatment is ceased. Advice is to consider a trial of treatment cessation after 3 years if prolactin levels are normal and the tumour has decreased in size. It important to continue to monitor the prolactin levels and the tumour size after cessation of treatment
  • Surgery considered for macroadenomas – particularly if they don’t shrink with medical therapy
  • Radiation therapy considered for large nonfunctioning tumours to shrink them, usually a last resort
  • Hypopituitarism is common – onset usually occurs several years after therapy
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77
Q

Describe prognosis of prolactinoma

A
  • In women, 30% of cases spontaneously resolve
  • In 95% of cases, tumours will not show any signs of growth after 4-6 years
  • Macroadenomas require more aggressive treatment
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78
Q

List possible complications of prolactinoma

A
  • Bone loss (osteoporosis). Too much prolactin can reduce production of the hormones estrogen and testosterone, resulting in decreased bone density and an increased risk of osteoporosis.
  • Pregnancy complications. During a normal pregnancy, the production of estrogen increases. If you are pregnant and have a large prolactinoma, these high levels of estrogen may cause tumor growth and associated signs and symptoms, such as headaches and changes in vision.
  • Vision loss. Left untreated, a prolactinoma may grow large enough to compress your optic nerve. This can cause a loss of peripheral vision.
  • Low levels of other pituitary hormones. With larger prolactinomas, pressure on the normal pituitary gland can lead to lower levels of other hormones controlled by the pituitary, including thyroid hormones and cortisol (a stress-response hormone).
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79
Q

Describe calculation of blood osmolality

A

cations + anions + glucose+ urea
=2(cations) + glucose + urea
= 2(Na + K) + glucose + urea
Normal is 296mOsm/Kg

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80
Q

List complications of T2DM

A
  • Microvacular due to glycosylation of basement membrane proteins causing leaky capillaries (retinopathy, nephropathy, neuropathy)
  • Macrovascular due to dyslipidaemia, hypertension and hypercholesterolaemia
  • IHD (ischaemic heart disease)
  • CVA
  • Peripheral gangrene
  • HHS
  • Charcots foot (inflammation leading to weakness of the foot, rockerbottom foot)
  • Hyperosmolar hyperglycaemic state
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81
Q

Describe the appearance of background diabetic retinopathy

A
  • Hard exudates
  • Blot haemorrhages
  • Microaneurysms
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82
Q

Describe treatment of diabetic retinopathy

A
  • If background (blot and dot haemorrhages, hard exudates), improve blood glucose control
  • If pre-proliferative (cotton wool spot), or proliferative (new vessels on disk), Pan retinal photocoagulation to destroy vessels in the periphery and preserve the macula
  • If maculopathy (hard exudates eg. background retinopathy near macula) grid of photocoagulation
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83
Q

Describe methods for prevention of diabetic nephropathy

A
  • Diabetic control
  • BP control
  • Inhibition of activity of RAS system (ACEi/ARB)
  • Stop smoking
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84
Q

List implications of renal failure

A
  • Hyperkalaemia, hyponatraemia
  • Acidosis
  • Fluid retention
  • Retention of waste
  • Secretory failure (vit D, erythropoietin)
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85
Q

List symptoms of renal failure

A
  • Itredness, lethargy
  • SOB, oedema
  • Pruritis, nocturia, feeling cold, twitching, nausea, loss of taste, weight loss
  • Anaemia
  • Renal bone disease
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86
Q

List complications of renal failure

A
  • Hyperkalaemia causes arrythmias, cardiac arrest
  • Pulmonary oedema
  • Nausea, vomiting
  • Malnutrition/ cachexia
  • Fits
  • Increasing coma
  • Death
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87
Q

Describe treatment of renal failure

A
  • Dialysis eGFR<6ml/min and no reversible features
  • Consider if eGFR<10
  • Peritoneal at home, uses the lining of the peritoneum
  • Haemodialysis hospital based, 3 times a week 4 hours
  • Transplantation
  • Vitamin D
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88
Q

List benefits and risks of dialysis

A

Benefits

  • Improve symptoms
  • Correct fluid balance
  • Avoid severe acidoss, hyperkalaemia, and pulmonary oedema resistant to diuretics

Risks

  • Infection, hypotension, arrythmias, access related
  • Adverse QOL (work, family life, travel)
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89
Q

List benefits and risks of renal transplantation

A

Benefits

  • Better renal replacement
  • Improvement in metabolic disorders
  • Costs less log term
  • Prolonged survival and improved QOL

Risks

  • Older and sicker patients not eligible
  • Immunosuppression (increased infection, increased malignancy)
  • Not a cure (surgical complications, hospital visits)
  • Often worse off if the transplant fails
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90
Q

Define diabetes mellitus

A
  • Diabetes mellitus is a metabolic disorder characterized by persistent hyperglycaemia (random plasma glucose more than 11 mmol/L) with disturbances of carbohydrate, protein, and fat metabolism resulting from defects in insulin secretion (leading to insulin deficiency), insulin action (leading to insulin resistance), or both.
  • Type 1 diabetes is an absolute insulin deficiency
  • Type 2 diabetes is insulin resistance and a relative insulin deficiency
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91
Q

List risk factors for type 2 diabetes mellitus

A
  • Obesity and inactivity
  • Family history
  • Ethnicity (asian, african and black communities)
  • History of gestational diabetes
  • Poor dietary habits
  • Drug treatments (statins, corticosteroids, thiazide diuretic plus beta blocker)
  • PCOS
  • Metabolic syndrome
  • Low birth weight for gestational age
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92
Q

Describe aetiology and list risk factors for type 1 diabetes mellitus

A
  • Absolute insulin deficiency due to autoimmune destruction of insulin producing beta cells of the pancreas
  • Genetic factors (polygenic)
  • Environmental factors (diet, vitamin D exposure, obesity, viruses, gut microbiome)
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93
Q

Describe epidemiology of diabetes mellitus

A
  • 2.5 million with diagnosed diabetes in UK
  • 500,000 with undiagnosed diabetes
  • 90% of adults diagnosed have type 2
  • 8% people with diabetes type 1
  • 90% of children in UK with diabetes have type 1
  • 1.9% children diagnosed have type 2
  • Type 1 5-15 peak age
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94
Q

List signs of T2DM

A
  • Acanthosis nigricans (dark skin around neck and axila)
  • Skin tags
  • Central obesity
  • Hirsutism
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95
Q

List symptoms of T1DM

A
  • Polyuria, thirst
  • Weight loss
  • Weakness
  • Nausea/vomiting
  • Leg cramps
  • Tiredness
  • Abdominal pain
  • Confusion/ drowsiness/ coma
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96
Q

List signs of T1DM

A
  • Kussmaul breathing
  • Dehydration
  • Hypotension
  • Peripheral cyanosis
  • Tachycardia
  • Hypothermia
  • Smell of acetone
97
Q

Describe prognosis of diabetes mellitus

A
  • Without insulin, patients with T1DM would die within weeks
  • With replacement, patients can live a normal life but are at risk of complications
  • Lifestyle can be used initially with T2, but eventually usually insulin is required
98
Q

List causes of SIADH

A
  • CNS pathology (SAH, stroke, tumour, TBI)
  • Lung pathology (pneumonia, bronchiectasis, small cell lung cancer)
  • Drugs (SSRI, TCA, opiates, PPIs, carbamezepine)
99
Q

List causes of onycholysis

A
  • Trauma
  • Thyrotoxicosis
  • Fungal infection
  • Psoriasis
100
Q

Describe investigations into T1DM

A
  • Capillary ketones
  • Random plasma glucose >11mmol/L
  • Fasting plasma glucose >6.9mmol/L
  • 2 hour plasma glucose >11mmol/L
  • Plasma or urine ketones high
  • HbA1c >48mmol/mol
  • Fasting C peptide low
  • Autoimmune markers positive
101
Q

Describe TFTs in multinodular goitre

A

NORMAL

102
Q

How can diabetes mellitus be prevented?

A
  • Metformin

- Diet and exercise is the best for prevention

103
Q

Define primary hyperparathyroidism

A
  • Primary hyperparathyroidism is an endocrine disorder in which autonomous overproduction of parathyroid hormone results in derangement of calcium metabolism.
  • In approximately 80% of cases, over-production of PTH is due to a single parathyroid adenoma and, less commonly, multi-gland involvement may occur.
104
Q

Define secondary hyperparathyroidism

A
  • Any disorder that results in hypocalcaemia will elevate parathyroid hormone levels and can serve as a cause of secondary hyperparathyroidism.
  • The most frequent causes of the condition are chronic kidney disease (CKD), malabsorption syndromes, and chronic inadequate sunlight exposure, acting via alterations in vitamin D, phosphorus, and calcium.
  • CKD causes reduced 1,25-hydroxy vitamin D, decreased calcium and phosphate
105
Q

Describe epidemiology of hyperparathyroidism

A

Primary

  • 0.015-0.4% prevalence
  • 1 in 500 women and 1 in 2000 men aged over 40 years.
  • A population-based study suggested 2% of post-menopausal women have PHPT, with the disorder being the most common cause of hypercalcaemia in outpatients.

Secondary

  • CKD or vitamin D deficiency
  • 6% of the population low vit D
106
Q

List risk factors for secondary hyperparathyroidism

A
  • Ageing
  • Chronic renal failure
  • Inadequate sunlight exposure
  • Nutritional deficiency (especially absence of dairy products and fish - most common cause)
  • Malabsorption
  • Hepatic dysfunction
  • Genetic disorder
  • Obesity
  • Medication use
107
Q

List risk factors for primary hyperparathyroidism

A
  • Female sex
  • Age ≥50-60 years
  • Family history of PHPT
  • Multiple endocrine neoplasia (MEN) 1, 2A, or 4
  • Hypertension
  • Current or historical lithium treatment
  • Hyperparathyroidism-jaw tumour syndrome
  • History of head and neck irradiation
108
Q

List symptoms and signs of primary hyperparathyroidism

A
  • Nephrolithiasis (polyuria and polydipsia)
  • Bone pain
  • Poor sleep
  • Fatigue
  • Anxiety
  • Depression
  • Memory loss
  • Myalgias
  • Paraesthesias
  • Muscle cramps
  • Constipation
  • Overt neuromuscular dysfunction
  • Abdominal pain (cause of pancreatitis)
  • Cardiovascular and metabolic dysfunction
  • Hard and dense neck mass

Stones, bones, thrones, abdominal groans and psychiatric overtones

109
Q

List symptoms of secondary hyperparathyroidism

A
  • Signs of renal failure (discoloured skin, bruising, pruritus, evidence of fluid overload (lung rales, pericardial rub, and peripheral oedema), elevated BP, fatigue, nausea, poor concentration/memory, and myoclonus.)
  • Muscle cramps and bone pain
  • Tingling in the fingers or toes

CATS go numb (convulsions, arrhythmias, tetany, paraesthesia)

110
Q

List signs of secondary hyperparathyroidism

A
  • Chovseks sign (twitching of the face after tapping on the cheek)
  • Trousseaus sign (Inflating blood-pressure cuff above diastolic for about 3 minutes causes muscular flexion of the wrist, hyperextension of the fingers, and flexion of the thumb)
  • Bowed legs
  • Bone pain (looser fractures - pseudofractures)
  • Arrythmias (long QT interval)
111
Q

List investigations for primary hyperparathyroidism

A
  • Serum calcium (high)
  • Serum intact PTH with immunoradiometric or immunochemical assay
  • 25-hydroxyvitamin D level (low)
  • Serum alkaline phosphatase (raised)
  • Serum phosphorus (low)
  • 24-hour urinary calcium (high)
  • Dual-energy x-ray absorptiometry (DXA) scan
  • Trabecular bone score
  • Tc-99m sestamibi scanning and ultrasonography
  • Single photon emission CT + sestamibi scanning
  • CT neck
  • 4-Dimensional (4D) CT neck
  • MRI neck
112
Q

List investigations of secondary hyperparathyroidism

A
  • Serum calcium (Low/normal)
  • Serum intact parathyroid hormone (iPTH) (high)
  • Serum creatinine (high in CKD)
  • Serum urea nitrogen (high in CKD)
  • Serum phosphorus (high in CKD)
  • Serum 25-hydroxyvitamin D (low)
  • ALP high
  • Serum magnesium
  • Ultrasound neck
  • Sestamibi scan
  • High-resolution contrast CT scan neck and upper chest
  • MRI neck and upper chest
113
Q

Describe treatment of primary hyperparathyroidism

A

Symptomatic/ surgical indications

  • 1st line parathyroidectomy (recovery 1-2 weeks, leave hospital day 1) + vitamin D supplementation
  • 2nd line monitoring + bisphosphonate + cinacalcet (used in patients who have severe HPT and dont fit surgical criteria, or to reduce size before surgery) + vitamin D supplementation
  • Post surgery follow up: measure Ca and PTH 2 weeks and 6 weeks post surgery, check histology.

Asymptomatic with no surgical indications

  • 1st line monitoring + vitamin D supplementation
  • 2nd line parathyroidectomy + vitamin D supplementation
114
Q

Describe treatment of secondary hyperparathyroidism

A

Lack of sunlight
- 1st line UV radiation exposure, vitamin D supplementation, calcium supplementation

Malabsorption-related
- Optimised management of underlying disease, vitamin D supplementation, calcium supplementation (cholecalciferol)

CKD stage 3 or 4

  • Dietary phosphate restriction, phosphate binder (low vit D)
  • Alphacalciferol (normal serum 25-hydroxyvitamin D)
  • Vitamin D sterol (with hypercalcaemia)
  • Reduction of calcium load (with hypocalcaemia)
  • Calcium salt and/or vitamin D sterol

CKD stage 5: PTH 300-800 ng/L (300-800 pg/mL)

  • Vitamin D sterol
  • Calcimimetic
  • Dialysis control of calcium

CKD stage 5: PTH >800 ng/L (>800 pg/mL)
- Parathyroidectomy

115
Q

List complications of primary hyperparathyroidism

A
  • Neck haematoma following surgery
  • Recurrent and superior laryngeal nerve injury following surgery
  • Hypocalcaemia following surgery
  • Pneumothorax following surgery
  • Osteoporosis
  • Bone fractures
  • Nephrolithiasis
116
Q

List complications of secondary hyperparathyroidism

A
  • Osteodystrophy
  • Osteoporosis
  • Uraemia
  • Calciphylaxis
117
Q

Describe prognosis of primary hyperparathyroidism

A
  • For asymptomatic patients who do not meet the criteria for surgical intervention, 75% have stable disease for up to 10 years.
  • 25% of patients progress to meeting criteria for parathyroidectomy.
  • Patients <50 years of age tend to progress to meeting criteria for parathyroidectomy in up to 70%.
  • The most common cause of mortality is (stroke, myocardial infarction).
  • Hypercalcaemic dysrhythmias are rare.
  • Parathyroidectomy cure rate of 95%
118
Q

Describe prognosis of secondary hyperparathyroidism

A
  • Outlook mirrors the underlying disease

- Surgery or renal transplantation may help

119
Q

Normal range for sodium

A

135 and 145mEq/L

120
Q

Normal range for potassium

A

3.5 and 5.5mmol/l

121
Q

Normal range for urea

A

2.5-7mmol/L

122
Q

Normal range for creatinine

A

60-120µmol/L

123
Q

List causes of amenorrhoea/ oligomenorrhoea

A
  • Pregnancy
  • Hypothalamic (excessive exercise, low BMI)
  • Pituitary (excess prolactin)
  • Thyroid (hyper or hypo)
  • Ovaries (PCOS, ovarian failure)
124
Q

Describe presentation of hypokalaemai

A
  • Weakness
  • Arythmia
  • Polyuria (hypokalameia causes resistance to ADH)
125
Q

List causes of hypokalaemia

A
  • Vomiting
  • Diuretics
  • Primary hyperaldosteronism (bilateral hyperplasia or Conns)
126
Q

List various blood test results in different problems related to calcium, phosphate and PTH

A
  • Low ca, low phosphate, high PTH (vitamin D deficiency)
  • High ca, low phosphate, high PTH (primary hyperparathyroidism)
  • High ca, normal phosphate, low PTH (hypercalcaemia of malignancy)
  • Low ca, high phosphate, low PTH (hypoparathyroidism)
  • Low ca, high phosphate, high PTH (renal failure)
127
Q

Define SIADH

A
  • Characterised by hypotonic hyponatraemia, concentrated urine, and a euvolaemic state.
  • The impairment of free water excretion is caused by increased arginine vasopressin (antidiuretic hormone or AVP) release.
128
Q

Describe epidemiology of SIADH

A
  • Hyponatraemia occurs in 15-22% of hospitalised patients and 7% of outpatients
  • SIADH most commonly found in hospitalised patients.
  • 8% of hyponitraemia cases
129
Q

List risk factors for SIADH

A
  • Age >50 years
  • Pulmonary conditions (e.g., pneumonia)
  • Nursing home residence
  • Malignancy
  • Medicine associated with SIADH induction
  • Central nervous system (CNS) disorder
  • Postoperative state
  • Endurance exercise
130
Q

List symptoms and signs of SIADH

A
  • Ma be asmpomaic
  • Absence of signs of adrenal insufficiency or hypothyroidism
  • Nausea
  • Vomiting
  • Altered mental status
  • Headache
  • Seizure
  • Coma
131
Q

Describe investigations of SIADH

A
  • Serum sodium (low)
  • Serum osmolality (low)
  • Serum urea (low)
  • Urine osmolality (elevated)
  • Urine sodium
    Investigations to consider
  • Diagnostic trial with normal saline infusion (does not improve)
  • Serum uric acid
  • Fractional excretion of sodium
  • Fractional excretion of urea
  • Serum TSH
  • Serum cortisol level
  • Serum arginine vasopressin (AVP)
    CXR and brain MRI for tumour
132
Q

Describe management of SIADH

A
  • Intravenous hypertonic 3% saline + fluid restriction
  • Treat underlying cause
  • Furosemide

Chronic (onset >48 hours or unknown)

  • Intravenous 3% hypertonic saline + vasopressin receptor antagonist (conivaptan). Oral demeclocycline if ineffective
  • Treat underlying cause
  • Furosemide
133
Q

Describe complications of SIADH

A
  • Central pontine myelinolysis (CPM or osmotic demyelination syndrome)
  • Occurs in people with longstanding SIADH who undergo overaggressive treatment of hyponatraemia.
  • CPM is characterised by demyelination of pontine, basal ganglion, and cerebellar regions with resultant neurological symptoms, including behaviour disturbances, lethargy, dysarthria, dysphagia, paraparesis or quadriparesis, and coma.
134
Q

Describe prognosis of SIADH

A
  • Typically resolves once underlying cause is found.
  • Due to reports of potentially fatal liver injury in patients with autosomal dominant polycystic kidney disease, tolvaptan should not be used for more than 30 days, and it should be avoided in patients with underlying liver disease including cirrhosis.
135
Q

Define carcinoid syndrome

A
  • Carcinoid syndrome occurs due to release of serotonin (5-hydroxytryptamine) and other vasoactive peptides into the systemic circulation from a carcinoid tumour.
  • Twenty percent to 30% of midgut neuroendocrine tumours (NETs), 5% of bronchial carcinoid tumours, and approximately 1% of pancreatic NETs secrete 5-hydroxytryptamine and other peptides.
136
Q

Describe epidemiology of carcinoid syndrome

A
  • 2.85 per 100000 US
  • Slight male sex bias
  • Most common in 6th to 7th decade
  • Greater incidence in black people, lower in asians and hispanics than white people
137
Q

Describe aetiology of carcinoid syndrome

A
  • Midgut tumours that lead to carcinoid syndrome vary from benign, well-differentiated endocrine tumours to low-grade malignant endocrine tumours. Occasionally, some midgut tumours can be poorly differentiated endocrine carcinomas.
  • Approximately 40% of neuroendocrine tumours (NETs) are functional.
  • Carcinoid syndrome occurs in 20% to 30% of patients with midgut carcinoid tumours and approximately 5% of bronchial carcinoids. - - Common in liver metastasis and foregut tumours. Rare in hindgut tumours
138
Q

List risk factors for carcinoid syndrome

A
  • Neuroendocrine tumours are associated with MEN-1 in about 10% of cases.
  • However, very few of these tumours cause carcinoid syndrome.
139
Q

List signs and symptoms of carcinoid syndrome

A
  • Diarrhoea (mediated by serotonin)
  • Flushing (stress and alcohol association, face and upper trunk)
  • Palpatations
  • Abdo cramps
  • Telangiectasia
  • Signs of right heart failure
  • Cardiac murmurs
  • Hepatomegaly
  • Wheeze
  • Pellagra (diarrhoea, dermatitis, dementia)
  • Abdominal masses
140
Q

List investigations for carcinoid syndrome

A
  • Serum chromogranin A/B (elevated)
  • Urinary 5-hydroxyindoleacetic acid (elevated - HIAA levels)
  • Metabolic panel (raised creatinine if dehydrated)
  • Liver function tests (variably, depending on site of tumour)
  • FBC
  • CT chest abdo pelvis every 4-6 months for staging
  • Broncosopy (primary tumour)
  • Endoscopy
  • Somatostatin receptor scintigraphy/SPECT (somatostatin receptor positive tumour)
  • MIBG scintigraphy
  • Histology
  • PET
141
Q

Define hypogonadism

A
  • Hypogonadism is a clinical syndrome associated with impaired functional activity of the gonads. Both males and females can be affected. It is classified as either primary or secondary:
  • Primary hypogonadism (hypergonadotropic hypogonadism) is typically caused by congenital disorders of sex development affecting the gonads (e.g., Turner syndrome, Klinefelter syndrome) or acquired gonadal injury (e.g., irradiation, infection).
  • Secondary hypogonadism (hypogonadotropic hypogonadism) is most often caused by pituitary or hypothalamic disorders (e.g, craniopharyngioma, Kallmann syndrome).
142
Q

Describe aetiology of hypogonadism

A
  • Primary hypogonadism is insufficient sex steroid production in the gonads (primary gonadal insufficiency is turner syndrome, klinefelter, anorchia, secondary gonadal insufficiency is damage to leydig cells or ovarian tissue)
  • Secondary hypogonadism is insufficient GnRH and or gonadotrophin release at the HPA (eating disorders, genetic eg. Prader Willi, hypothalamic or pituitary lesions)
143
Q

Describe epidemiology of hypogonadism in men

A
  • The prevalence of hypogonadism increases with age.
  • About a quarter of the US male population have total testosterone levels that are below 10.4 nanomol/L (<300 nanograms/dL) (considered by many experts to be the lower end of normal)
  • Between 40 and 69 years incidence is approximately 481,000 new cases per year
  • The European Male Aging Study (EMAS) reports a prevalence of late-onset hypogonadism of 2.1% in men aged between 40 and 79 years.
  • 1 in 7 UK couples have difficulty conceiving
144
Q

List risk factors for hypogonadism

A

Men

  • Type 2 diabetes
  • Obesity
  • Renal failure
  • HIV
  • Hypertension
  • Chronic obstructive pulmonary disease (COPD)
  • Taking glucocorticoid (steroids)
  • Opioid or antipsychotic medication therapy

Women

  • Stress
  • Low weight and excessive exercise
  • High BMI
  • Physiological - pregnncy
145
Q

List symptoms of hypogonadism

A

Delayed puberty in men

  • Testicular hypoplasia
  • Low body hair growth
  • High pitched voice
  • Smooth skin
  • Lean body mass

Delayed puberty in women
- Primary amenorrhoea

Other:

  • Developmental abnormalities of the genitalia
  • Infertility, impotence, decreased libido
  • Secondary amenorrhoea
  • Klinefelter gynaecomastia
  • Turner syndrome webbed and short stature
  • Kallman anosmia, absent breast development, syndactyly, cleft palate or lip
  • Prafer willi syndrome muscular hypotonia, short stature, facial dysmorphia
  • Gaucher diease hepatomegaly, splenomegaly, painful bone crises
146
Q

Describe investigations for hypogonadism

A
  • Serum testosterone/oestrogen levels (low)
  • GnRH, LH/FSH (determine if primary or secondary hypogonadism), TFTs
  • Bone scan (decreased bone density, delayed epiphyseal closure)
  • Genetic testing
  • Serum prolactin
  • Pelvic ultrasound
  • Brain MRI (for CNS lesion
  • ACRH stimulation test to exclude congenital adrenal hyperplasia
  • Pregnancy test in women
147
Q

List three broad causes of metabolic acidosis

A
  • Addition of strong acid that is buffered by and consumes bicarbonate ion
  • Loss of bicarbonate ion from the body fluids, usually through the GI tract or kidneys
  • Rapid addition to the extracellular fluid of a non-bicarbonate solution.
148
Q

Describe aetiology of normal anion gap metabolic acidosis

A
  • Bicarbonate (HCO₃-) is lost or diluted, an anion is not generated, and electroneutrality is preserved by reciprocal increases in serum chloride concentration.
  • Also referred to as hyperchloraemic metabolic acidosis.
  • Commonly caused by GI or renal loss of HCO₃-.
  • GI causes include diarrhoea, GI drainage and fistulas, surgical urinary diversion of bowel, and intake of chloride-containing anion-exchange resins.
  • Renal causes include renal tubular acidosis, carbonic anhydrase inhibitors, hypoaldosteronism, and use of potassium-sparing diuretics.
  • Other causes include addition of acid by total parenteral nutrition, ingestion of elemental sulfur, or addition of hydrogen chloride (HCl) or other related chemicals such as ammonium chloride.
149
Q

List causes of metabolic acidosis with increased anion gap

A
  • An organic acid consumes HCO₃-, and the anion that is produced is often retained in extracellular fluid and serum.
  • Serum chloride concentration does not increase.
  • Caused by diabetic ketoacidosis, alcoholic ketoacidosis, lactic acidosis, kidney disease,
  • Ingestion of methanol, ethanol, ethylene glycol, propylene glycol (diluent in lorazepam), 5-oxoproline (toxic levels may occur in patients with chronic ingestion of paracetamol), salicylic acid, paraldehyde, phenformin, metformin, iron, isoniazid, hydrogen sulfide, carbon monoxide, toluene, or ethylene glycol.
150
Q

Describe assessment of metabolic acidosis

A
  • Arterial pH (normal 7.35 to 7.45, low indicates acidosis)
  • Measure HCO3- and PaCO2. Low pH and HCO3- indicates metabolic acidosis. Decreased PaCO2 means compensation
  • Serum anion gap (Sodium + - (Cl- + HCO2-)
  • Urine AG (Na+K)-Cl if negative non-renal causes
  • Test for lactate, ketones, toxicology
  • If diabetes review medication
151
Q

How does PTH affect the kidneys

A
  • Blocks 1a hydroxylase
  • Increased Ca reabsorption
  • Increased phsophate excretion
152
Q

Which hormones affect calcium?

A
  • PTH (mainly increase)
  • Calcitriol (vitamin D- this increases calcium the most)
  • Calcitonin (decrease)
153
Q

List causes of low PTH

A
  • Bone mets
  • Multiple myeloma
  • Paraneoplastic syndromes (eg. lung SCC)
  • Sarcoidosis
  • Thiazide diuretics
154
Q

Why is hypocalcaemia likely to be seen in a pancreatitis patients?

A
  • Saponification

- Autolysis of the pancreas forming breakdown products which calcium binds to

155
Q

List cancers associated with MEN1 and 2

A

MEN1

  • Pituitary
  • Parathyroid
  • Pancreas

MEN2

  • Parathyroid
  • Pituitary
  • Medullary thyroid cancer
156
Q

Describe X ray appearance of primary and secondary hyperparathyroidism

A

Primary hyperparathyroidism

  • Subperiosteal bone resorption
  • Acro-oseolysis (fingertip erosion)
  • Pepper pot skull

Secondary hyperparathyroidism

  • Rachitic rosary (swelling of costochondral junctions in children)
  • Loosers pseudofractures
157
Q

Describe aetiology of PCOS

A
  • Primary defects in the hypothalamic-pituitary axis, postulating increased amplitude and frequency of pulses of LH, or defects involving the ovaries through an intrinsic problem leading to androgen over-production.
  • Defects in insulin sensitivity with insulin resistance leading to compensatory hyper-insulinaemia.
  • Multiple genes, each with mild or moderate effects on overall disease risk, are likely to be involved.
158
Q

List causes of hyperprolactinaemia

A
  • Physiological (pregnancy, breast feeding, stress)
  • Drugs (haloperidol, methodopa, oestrogens, chronic renal failure)
  • Diseases (micro or macroadenoma; stalk damage including piruitary adenomas, surgery, trauma; hypothalamic disease, hypothyroidism, chronic renal failure
159
Q

Describe aetiology/risk factors for prolactinoma

A
  • MEN1 or FIPA
  • Female gender, 20 to 50 years of age
  • Oestrogen therapy
  • Male gender, 30 to 60 years of age
160
Q

Define primary hyperaldosteronism

A
  • Excess production of aldosterone independent of the renin angiotensin system, causing sodium and water retention and decreased renin release
  • Sodium mildly raised or normal
161
Q

Describe aetiology of primary hyperaldosteronism

A
  • 2/3 due to a solitary aldosterone producing adenoma (conns syndrome)
  • 1/3 due to bilateral adrenocortical hyperplasia
  • Rarely adrenal carcinoma or glucocorticoid remedial aldosteronism
162
Q

Describe epidemiology of primary hyperaldosteronism

A

In the UK there were 316 inpatient admissions with hyperaldosteronism in the 1-year period 2013 to 2014, predominantly in the 15 to 59 year age group (215 cases).

163
Q

List risks for primary hyperaldosteronism

A
  • Risk factors include: family history of PA and family history of early onset (e.g., <40 years)
  • Hypertension and/or stroke.
164
Q

List symptoms and signs of primary hyperaldosteronism

A
  • Hypertension
  • Commonly asymptomatic
  • Nocturia, polyuria
  • Lethargy
  • Mood disturbance (irritability, anxiety, depression)
  • Difficulty concentrating
  • Paraesthesias, muscle cramps, muscle weakness, palpitations (if hypokalaemic)
165
Q

List investigations for primary hyperaldosteronism

A
  • Plasma potassium
  • Aldosterone to renin ratio
  • Fludrocortisone suppression test (failure to suppress aldosterone)
  • Saline infusion test (fails to suppress aldosterone)
  • Oral salt loading
  • Genetic testing
  • Adrenal CT
  • Adrenal venous sampling (to see whether aldosterone production is bilateral or lateral)
  • Adrenal MRI
  • Adrenal aelenocholesterol scanning
  • Posture simulation testing
  • Angiotesnin II infusion testing
  • 24 hours urinary hybrid steroids
  • Dexamethasone suppression testing
166
Q

Describe treatment of primary hyperaldosteronism

A
  • Unilateral laparoscopic adrenalectomy, preoperative aldosterone antagonists and postoperative aldosterone antagonists (eg. spironolactone, amiloride)
  • Bilateral spironolactone and consider surgery if bilateral. Lesions over 2.5cm surgically removed due to malignant potential
  • Familial hyperaldosteronism dexamethasone or prednisolone will reduce aldosterone, or can use aldosterone antagonists second line
  • Amiloride used in children
167
Q

Describe prognosis of primary hyperaldosteronism

A
  • Unilateral adrenalectomy 50-60% cure
  • If aldosterone agonists improved hypertension and hypokalaemia reduced, but not as good as adrenalectomy
  • Patients with FHI treatment with low dose glucocorticoids is very effective
168
Q

List complications of primary hyperaldosteronism

A
  • Bleeding, infection, wound hernia, cardiovascular events (perioperative)
  • Stroke
  • MI
  • HF
  • AF
  • Impaired renal function
  • Aldosterone antagonist or mineralocorticoid receptor antagonist induced hyper halaemia
169
Q

Define osteomalacia and vitamin D deficiency

A
  • Low mineral content of bone following complete growth plate closure
  • Called rickets in children
  • Vitamin D deficiency is 25-hydroxyvitamin D of less than 30 nmol/L is deficient. 25-hydroxyvitamin D of 30-50 nmol/L may be inadequate in some people
170
Q

Describe aetiology of osteomalacia

A
  • Vitamin D deficiency due to low UV-B exposure, insufficient dietary supplementation or inability to absorb vit D
  • CKD can cause increased vit D output
  • Drugs such as bisphosphonates
171
Q

Describe epidemiology of osteomalacia

A
  • In the US, Europe, and East Asia, more than 40% of the adult population older than age 50 years are vitamin D deficient
  • In developing countries, 60% prevenlance in infants
172
Q

List risks of osteomalacia

A
  • Dietary calcium and vitamin D deficiency
  • Chronic kidney disease
  • Limited sunlight exposure
  • Inherited disorders of vitamin D and bone metabolism
  • Hypophosphatasia
  • Anticonvulsant therapy
  • Mesenchymal tumours
  • Fanconi’s syndrome (low phosphate)
  • CF (reduced absorption)
173
Q

List signs and symptoms of osteomalacia

A
  • Fractures (especially common in femoral neck, insufficiency fractures)
  • Diffuse bone pain and tenderness
  • Proximal muscle weakness
  • Waddling gait
  • Steatorrhoea (malabsorption)
174
Q

List investigations of osteomalacia

A
  • Serum calcium, 25-hydroxyvit D, phosphate, urea and creatinine, PTH, alk phos (low Ca, low phosphate, high PTH, high alk phos, high vit D)
  • 24 hr urinary calcium
  • Bone X rays
  • 24 hour urinary phosphate
  • DEXA
  • Iliac crest biopsy with tetracycline labelling (incomplete mineralisation)
175
Q

Describe management of osteomalacia

A
  • Calcium carbonate and vitamin D (ergocalciferol)
  • Alfacalcidiol in patients with renal disease
  • May need phosphate too
176
Q

List complications of osteomalacia

A
  • Insufficiency fractures or pseudofractures
  • Secondary hyperparathyroidism
  • Metastatic calcification in renal failure
  • Hypercalcaemia
  • Hypercalciuria and kidney stones
177
Q

Describe prognosis of osteomalacia

A
  • Depends on underlying cause and treatment compliance

- Most recover with medication, oncogenic recover with surgery

178
Q

Describe prognosis of adrenal insufficiency

A
  • Adrenal crises and infections do cause excess deaths
  • Mean age of death for men is 65 years
  • Replacement therapy for life
179
Q

Describe management of addisonian crisis

A
  • Bloods for cortisol and ACTH, u and e, ECG
  • Give hydrocortisone 100mg IV stat
  • IV fluid bolus (500ml)
  • Monitor BG
  • Blood urine and sputum for culture (often present with sepsis)
  • Glucose IV may be needed if hypoglycaemia, continue steroids may switch to oral if patient condition includes. Fludrocortisone may be needed
180
Q

List complications of adrenal insufficiency

A
  • Scondary cushings
  • Osteopenia/porosis
  • Treatment-related hypertension
  • Crisis
181
Q

Define HHS

A
  • Hyperosmolar hyperglycaemic state
  • Profound hyperglycaemia (glucose >30 mmol/L [>540 mg/dL]), hyperosmolality (effective serum osmolality >320 mOsm/kg [>320 mmol/kg]), and volume depletion in the absence of significant ketoacidosis (pH >7.3 and bicarbonate >15 mmol/L [>15 mEq/L]), and is a serious complication of diabetes (type 2)
182
Q

Describe aetiology of HHS

A
  • Infecion (UTI and pneumonia especially)
  • Acute illness (stroke, MI, trauma, compromised water intake)
  • Bed ridden
  • Post op
  • Rarely hyperthyroudism and acromegaly
  • Non-adherence to medication
  • Initiation of steroids without adjusting insulin dose
183
Q

List signs and symptoms of HHS

A
  • Acute cognitive impairment
  • Polyuria
  • Polydipsia
  • Weight loss
  • Nausea and vomiting
  • Weakness
  • Dry mucous membranes
  • Poor skin turgor
  • Tachycardia
  • Hypotension
  • Hypothermia
  • Oligouria
  • Abdo pain
  • Focal neuro signs
  • Seizures
184
Q

Describe diagnosis of HHS

A
  • Blood glucose, ketones (high glucose, low ketones)
  • Venous blood gas (mild acidosis, lactic acidosis)
  • Serum osmolality (ocer 320mOsm/kg)
  • Urea, electroclytes, creatinine (renal impairment, abnormal electrolytes)
  • FBC (leukocytosis)
  • ECG (abnormal T or Q waves, ST segment changes)
  • Urinalysis (UTI)
  • Cardiac enzymes (MI)
  • CXR (pneumonia, pulmonary oedema)
  • LFT
  • CRP
  • Blood urine, sputum cultures
185
Q

Describe management of HHS

A

Serum potassium <3.5mmol/L, 3.5-5.5 mmol/L

  • IV fluids with potassium replacement
  • Supportive care
  • Insulin
  • Treat precipitating illness
  • Monitor bichem markers
  • Monitor and treat complications
  • Thromboprophylaxia

Serum potassium over 5.5
- Same but no potassium replacement until necessary

186
Q

List endocrine causes of proximal myopathy

A
  • Cushings
  • Osteomalacia
  • Thyrotoxicosis
187
Q

List complications of acromegaly

A
  • Cardiac complications (cardiomyopathy, ischaemic heart disease)
  • Hypertension
  • Sleep apnoea
  • Osteoarticular complications
  • Impaired glucose tolerance and diabetes
  • Pre-cancerous colon polyps
  • Carpal tunnel
  • Hypopituitarism
188
Q

Describe prognosis of acromegaly

A
  • Assoicated with premature death
  • Now, life expectancy close to general population
  • Reduced quality of life specially indiagnostic delay
  • Surgery results in control of 70-90% microadenomas and 30-60% macrodenomas
  • Somatostatin analogues control disease in 30-40%
189
Q

List possible side effects of carbimazole

A
  • Aranulocytosis
  • Maculopapular rash
  • Pruritis
  • Jaundice
190
Q

List causes of thyrotoxicosis

A
  • Thyroid surgery
  • Infection
  • MI
  • Diabetic ketoacidosis
  • Radioactive iodine administration
  • Hip replacement
191
Q

Describe management of thyrotoxicosis

A
  • Dont wait for results
  • Measure freeT3, T4 and TSH
  • Seek endo advice
  • IV acess and fluids
  • NG if vomiting
  • Blood cultures
  • Propanolol 60mg
  • High dose digoxin
  • Carbimazole
  • Hydrocortisol, co-amoxiclav
  • Cannot perform surgery when thyrotoxic
192
Q

Define multiple endocrine neoplasia

A
  • Hereditary tumour syndromes of variable neoplastic patterns characterised by development of multiple endocrine tumours
  • Include parathyroid adenomas, piruitary, enterohepatic, facial lipomas, phaeochromocytomas and more
193
Q

Describe the epidemiology of multiple endocrine neoplasma syndromes

A

MEN1

  • 1 in 50000- 1 in 500000 worldwide prevalence
  • 90% patients primary hyperparathyroidism by age 50
  • 30-75% pancreatic tumours
  • Prolactinomas most common, then GH secreting adenomas and non functioning
  • ACTH secreting less common, TSH rare
  • 25% gastrinomas MEN1 related
  • Pituitary least common
  • Thymic and bronchial occur

MEN2

  • 1000 families worldwide
  • Most MEN2a
  • Medullary thyroid cancers most common, nearly all carriers
  • Phaeochromocytoma 50% MEN2A
  • Multigland parathyroid adenomas 20%
  • Rare varients include hirschsprungs and cutaneous lichen amyloidosis
  • MEN2B is rare and notable for aggressive phaechromocytoma and medullary thyroid cancer at earlier ages, and a marfanoid body habitus
194
Q

Describe aetiology/risks of MEN

A
  • Autosomal dominant mutations
  • RET proto-oncogene responsible for almost all MEN2
  • MEN1 gene mutations responsible for 80-90% men1
195
Q

Describe signs and symptoms of MEN

A

MEN1

  • Facial angiofirbomas or collagenomas
  • Irregular menses
  • VIsual changes (bitemporal hemionopia)
  • Infertility
  • Acromegaly (excess sweating, oversized)
  • Thyrotoxicosis (tachycardia, lid lag, tremour)
  • Fractures (cushings)
  • Erectile dysfunction

MEN2

  • Sweating, palpitations, headache
  • 2B mucosal neuromas, marfanoid
  • Palpable thyroid nodule
  • Unexplained flushing
  • Heat intolerance
  • GI bleeding

MEN1/2

  • Kidney stones (excess PTH - colicky pain)
  • weight changes, hypertension, abdo pain
  • Headache
  • Altered bowel habit (calcitonin, gastrin)
  • Palpitations, easy bruising, slow wound healing
  • Anxiety
  • Confusion, dehydration
196
Q

List investigations for MEN

A
  • MEN1 - PTH, calcium, gastrin, chromogranin A, prolactin, insulin-like growth factor 1, glucose/insulin, serum C peptide, calcium stimulated gastrin, proinsuln, pancreatic polypeptide, glucagon, TFTs, imaging, endoscopy
  • MEN2 - serum calcitonin, serum carcinonoembryonic antigen, plasma metanephrines, PTH and ca, metanephrines, dexa suppression test, MIBG, CT abodo pelvit/ PET, imaging
197
Q

List cancers in MEN syndromes

A

MEN1

  • Parathyroid hyperplasia/adenoma
  • Pancreas endocrine (gastrinoma/insulinoma/somatostatinoma, VIPoma, glucagonoma)
  • Pituitary prolactinoma or GH secreting tumour, adrenal and carcinoid tumours

MEN2a

  • Thyroid (medullary thyroid carcinoma)
  • Phaeochromocytoma
  • Parathyroid hyperplasia

MEN2b
- Similar to MEN2a, with mucosal neuromas and marfanoid appearance. No hyperparathyroidism

198
Q

Define obesity

A
  • Obesity can be defined as a chronic adverse condition due to an excess amount of body fat.
  • While there are many methods to determine the relative amount of body fat, the most widely used method to determine obesity is the body mass index (BMI), defined as weight divided by height squared ([weight in kg]/[height in m]^2]
199
Q

Describe epidemiology of obesity

A
  • Worldwide <10% in Africa and Southeast Asia, 20-40% in Europe and america, >40% in some pacific islands
  • 26% in men and women over 16 in england
  • Highest proportion men age 45-64 and women age 45-54
  • 2/3 of Americans overweight or obese
200
Q

Describe aetiology/isks of obestiy

A
  • Calorie intake greater than calories out
  • Genetic predisposition, behavioural dynamics, hormonal disturbances, cultural influences and environmental circumstances
  • Genetic
  • Behavioural (larger portion, sedentary lifestyle, ED, mental illness)
  • Cultural
  • Environmental (low socioeconomic status, adverse nutritional environment in utero)
  • Poor sleep, postmenopause, heavy alcohol
  • Leptin deficiency
  • Hormonal (hypothyroidism, hypercortisolism, insulinoma)
201
Q

Describe signs and symptoms of obestiry

A
  • High BMI (over 30)

- Increased weight circumference

202
Q

Describe investigations for obesity

A
  • Clinical exam (BMI over 30)

- FBC, transaminases (liver), TFTs, ECG, abdo ultrasound (fatty liver), sleep study (sleep apnoea)

203
Q

Define hypoglycaemia

A
  • <4mM in a patent with diabetes

- <2.2mM in a patient without diabetes (neuroglycopaenia)

204
Q

Define hypopituitarism

A
  • Deficiency of one or more pituitary hormones

- Partial or complete deficiency

205
Q

Describe epidemiology of hypopituitarism

A
  • Rare
  • 45 per 100000 prevalence, 4 per 100000 incidence
  • In contrast, high pituitary adenomas/incidntalomas on autopsy
  • 1.8 fold higher mortality (CVD)
206
Q

Describe aetiology/risks of hypopituitarism

A
  • Neoplastic (pituitary adenoma most common cause in adulthood. May be micro <10mm, or macro >10mm. Craniopharyngiomas, meningiomas, mets, plasmacytomas)
  • Pituitary apoplexy (sudden spontaneous haemorrhage of the pituitary, can be of a tumour), sheehan syndrome (post blood loss or child birth causing hypotension), intrasellar aneurysm of the carotid arteries
  • Lymphocytic hypophysitis, hypophysitis and hypopituitarism, haemochromatosis, sarcoid/TB
  • Infection - abscess, TB, fungal
  • Congenital - transcription factor defects, PROP1, TIPT
  • Radiotherapy
  • Pituitary surgery
  • TBI
207
Q

List signs and symptoms of hypopituitarism

A
  • Headaches
  • Failure to thrive, short stature (GH)
  • Infertility (gonadotrophin)
  • Hypoglycaemia (adrenal)
  • Amenorrhoea/oligomenorrhoea (gonadotrophin)
  • Galactorrhoea (prolactin)
  • Delayed puberty (gonadotrophin def)
  • Hypotension
  • Bilateral hemianopia
  • Opthalmoplegia
  • Cold intolerance, weight gain
  • ED/ reduced libido
  • Nausea
  • Vomiting
  • Fatigue
  • Weakness, dizziness
  • Constipation
  • Dry skin
  • Reduced bone and muscle mass
208
Q

List investigations for hypopituitarism

A
  • U and E
  • Serum and urine osmolarity
  • 8am cortisol and ACTH
  • TFT
  • 8am testosterone, FSH, LH
  • Oestrogen, FSH, LH in women
  • Prolactin
  • Insulin like GF1
  • Cosyntropin/ tetracosactide stimulation test (inadequate cortisol response)
  • Insulin tolerance test (cortisol and GH)
  • Water deprivation/ desmopressin test
  • MRI/ CT pituitary (CT for craniopharyngioma)
209
Q

Describe management of hypopituitarism

A
  • Pituitary apoplexy IV hydrocortisone (50-100mg IV every 6-8 hrs)
  • Hypopituitarism - treat underlying cause, oral corticosteroids (hydrocortisone), IV or IM steroids for stress events, levothyroxine, oestrogen, progesterone, gonadotrophins (for fertility), tesosterone
  • Desmopressin
210
Q

List complications of hypopituitarism

A
  • Male infertility
  • Female infertility
  • Corticosteroid over-replacement
  • Thyroxine over-replacement
  • Desmopressin over-replacement
  • GH overreplacement
  • Testosterone over-replacement
211
Q

Describe the prognosis of hypopituitarism

A
  • 1.8 fold higher mortality compared with age and sex matched population
  • Cardiovascular and cerebrovascular death rates are higher in patients with hypopituitarism compared with normal population (GH deficiency especially - associated with atherogenic lipid profile and increased body fat)
212
Q

Define non-functioning pituitary adenoma

A
  • A benign tumour in the pituitary gland which does not produce and hormones
  • Non-secretory destroy surrounding normal pituitary tissue and so can result in hypopituitarism
213
Q

Describe epidemiology of non-functioning pituitary adenoma

A
  • 10% of all intracranial tumours in adults, 3rd most common intracranial neoplasm
  • 19-28 cases per 100000 in the UK
  • Increases with age
  • Peak age 30-60, present earlier in women
  • Non-functional account for 14-54% of pituitary adenomas (5.6 per mill per year). 2nd most common adenoma, following prolactinomass
214
Q

Describe aetiology of non-functioning pituitary tumour

A
  • Monoclonal - intrinsic genetic alterations

- Unknown aetiology

215
Q

List risks for non-functioning pituitary tumour

A
  • MEN-1
  • Familial isolated pituitary adenomas
  • Carney complex
216
Q

List signs and symptoms of non-secretory adenomas

A

Microadenomas (<10mm)
- Mostly asymptomatic

Macroadenomas

  • Hypopituitarism (symptoms depend on hormone deficient)
  • Mass effects (headache, bitemporal hemianopia, diplopia)
217
Q

List investigations for non-secretory adenomas

A
  • Cranial contrast MRI single best imaging - intrasellar mass
  • CT scan where MRI contraindicated, better at craniopharyngioma detection
  • Hormone assays (prolactin, IGF-1, 24h urine cortisol, TFTs) normal/low
  • Perimetry for visual field
218
Q

Describe managemnet of hypothyroidism

A
  • Levothyroxine (1.6mg/kg/day), monitor TSH

- If coronary artery disease, use lower starting dose

219
Q

List complications of hypothyroidism

A
  • Angina
  • Resistant hypothyroidism
  • AF
  • Osteoporosis
  • Myxoedema coma (confusion, hypothermia, treat with IV thyroid hormone replacement, corticosteroids and supportive therapy)
  • Complications in pregnancy
220
Q

Describe prognosis of hypothyroidism

A
  • Good prongosis with thyroid hormone replacement

- Dose may need to be adjusted over time

221
Q

List symptoms of pituitary apoplexy

A
  • Sudden headache, vomiting, visual disturbances

- Superior quadrantopia bilaterally

222
Q

List types of thyroid cancer

A
  • Papillary (80%, good prognosis, young females)
  • Follicular 10%
  • Medullary 4% (secrete calcitonin, parafollicular cells, MENII)
  • Anaplastic (elderly women, compression symptoms)
  • Lymphoma (associated with Hashimotos)
223
Q

Describe aetiology of hypogonadism in females

A

Primary

  • Gonadal dysgenesis eg. turners
  • Gonadal damage
  • Primary ovarian failure
  • PCOS

Secondary

  • Kallmans
  • Pituitary adenoma, haemochromatosis
  • Hyperprolactinaemia
  • Functional (weight loss, stress, eating disorders)
  • Post OCP
224
Q

Describe aetiology of hypogonadism in males

A

Primary

  • Gonadal dysgenesis (klinefelters, crytorchidism)
  • Gonadal damage (torsion, irradiation, trauma)
  • Post orchitis (mumps, autoimmune)

Secondary

  • Kallman
  • Pituitary/hypothalamic lesions
  • Hyperprolactinaemia
  • Prader Willi syndrome
225
Q

In which patients is HbA1c not used to monitor diabetes?

A
  • ALL children and young people
  • Patients of any age suspected of having Type 1 diabetes
  • Patients with symptoms of diabetes for less than 2 months
  • Patients at high risk who are acutely ill (e.g. those requiring hospital admission)
  • Patients taking medication that may cause rapid glucose rise e.g. steroids, antipsychotics
    patients with acute pancreatic damage, including pancreatic surgery
  • In pregnancy
  • Presence of genetic, haematologic and illness-related factors that influence HbA1c and its measurement
226
Q

List management of type 1 diabetes

A
  • Insulin
  • Basal-bolus (long acting (eg. insulin glargine, subcut injection OD) + short acting before meals (eg. insulin lispro or aspart subcut pre-meal)
  • Monitor using cap glucose, and over time with HbA1c
227
Q

List complications of T1DM

A
  • Hypoglycaemia
  • Diabetic ketoacidosis
  • Long term microvascular (neuropathy, retinopathy, neuropathy) and macrovascular (IHD, CVD, peripheral artery disease)
228
Q

List causes of hypoglycaemia

A
  • Missed meals/inadequate snacks
  • Alcohol
  • Unaccustomed exercise
  • Inappropriate insulin regime
  • Some drugs (sulfonylureas, SGLT-2i)
229
Q

List signs of hypoglycaemia

A
  • Palpitations
  • Tremor
  • Sweating
  • Pallor
  • Anxiety
  • Drowsiness
  • Confusion
  • Altered behaviour
  • COma
230
Q

Describe management of hypoglycaemia

A
  • If conscious oral glucose and complex carbs

- Impaired consciousness: 1mg glucagon IM, if this fails IV dextrose eg. 10% glucose infusion

231
Q

List investigations and management for diabetic kidney disease

A
  • Urinalysis (proteinuria/raised ACR)
  • eGFR
  • Biopsy is gold standard, shows kimmelsteil wilson nodules
  • Management: improve glycaemic control, ACE1/ARB
232
Q

List types of diabetic neuroathy

A
  • Peripheral neuropathy (loss of sensation peripherally, monofilament examination used, loss of ankle jerk/vibration sense, charcots joint)
  • Mononeuropthy (sudden motor loss eg. wrist drop, foot drop, 2rd nerve palsy)
  • Autonomic neuropathy (GI difficulty swallowing, delayed gastric emptying, bladder dysfunction. Postural hypotension, cardiac effects)
233
Q

Describe management of diabetic neuropathy

A
  • Glycaemic control

- Neuropathic pain agent (duloxetine, pregabalin or gabapentin)

234
Q

Describe management of hypernatraemia

A
  • Correct water deficient - 5% dextrose
  • Correct ECF depletion 0.9% saline
  • Measure Na+ every 4-6 hours
235
Q

Describe euthyroid sick syndrome

A

Low t4 and TSH in patients with previously normal thyroid function, caused by a systemic illness.

236
Q

List triggers for thyrotoxic crisis

A
  • Thyroid surgery
  • Infection
  • MI
  • Diabetic ketoacidosis
  • Radioactive iodine administration
  • Hip replacement
237
Q

Define thyroid cancer

A

A cancer of the thyroid gland

238
Q

Which drug used in T2DM can have hypoglycaemia as a common side effect (not including insulin)?

A

Sulphonylureas (eg. glimepiride)

239
Q

Describe management of diabetic neuropathy

A

Venlafaxine

Year 3 - Diseases (27 decks)

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