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Endocrinology Flashcards

1
Q

Name the hormones produced in the anterior pituitary and their function

A
  • ACTH - stimulates gluticocorticoid release from adrenal cortex
  • FSH - spermatogenesis/follicular maturation
  • LH - testosterone synthesis/ovulation
  • Prolactin - promotes lactation
  • TSH - T3/T4 production and release
  • GH/somatotrophin - muscle/skeletal growth
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2
Q

Name the hormones produced in the posterior pituitary and their function

A
  • Oxytocin - milk ejection and uterine contraction in labour
  • ADH - promotes water and salt resorption from kidneys
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3
Q

Using cortisol as an example, describe the endocrine feedback loop

A
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4
Q

What hormones does the thyroid gland secrete? What is their function?

A
  • T3/T4 (follicular cells) - metabolism and growth
  • Parathyroid hormone (parathyroid gland) - Calcium and phosphate metabolism
  • Calcitonin (parafollicular cells) - inhibits calcium resorption in the bone
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5
Q

What hormones does the adrenal gland secrete? What are their function?

A

Cortex:

  • Mineralocorticoid/aldosterone (glomerulosa) - electrolyte balance
  • Glucocorticoid/cortisol (fasciculata) - carbohydrate metabolism
  • Androgens (reticularis) - secondary sexual characteristics

Medulla:

  • Adrenaline - stress response
  • Noradrenaline - neurotransmitter in SNS
  • Dopamine - neurotransmitter in ANS
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6
Q

What hormones does the overies secrete? What are their function?

A
  • Oestrogen (theca interna cells) - reproductive function, secondary sexual characteristics
  • Progesterone - endometrial stimulation, maintains pregnancy
  • Relaxin - softens cervix during birth
  • Inhibin (granulosa cells) - inhibits FSH production
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7
Q

What hormones does the testis secrete? What are their function?

A
  • Testosterone (Leydig cells) - reproductive function, secondary sexual characteristics
  • Inhibin (Sertoli cells) = inhibits FSH production
  • Mulleria-Inhibiting Hormone (MIH) - foetal hormone
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8
Q

What is Cushing’s syndrome? What causes is?

A

Chronic excess glucocorticoids

  • Iatrogenic - excess prescribed glucocorticoids
  • Cushing’s disease = adrenal hyperplasia due to excess ACTH from pituitary tumour
  • Adrenal tumours/hyperplasia
  • Ectopic/paraneoplastic = Raised ACTH from ectopic tumours
    • Small cell lung cancer
    • Carcinoid tumours
  • CRH-secreting tumours
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9
Q

Name some clinical features of Cushings

A
  • General = weight gain (central adiposity), moon face, buffalo hump, supraclavicular fat pad
  • Skin = thinning, acne, hirsutism, purple abdominal striae
  • Pscyhological = depression, irritability, cognitive difficulties
  • Repro = irregular menstruation/erectile dysfunction
  • Glucose intolerance (hyperglycaemia)
  • Hypertension
  • Increased infections
  • Delayed wound healing
  • Osteoporosis
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10
Q

How is Cushings investigated?

A
  • Overnight dexamethasone suppression test = give dexamethasone 1mg PO at midnight, check serum cortisol before and at 8AM
    • if cortisol > 50 nmol/L = cushings
    • Should be negative feedback - dexamethasone simulates cortisol - dec ACTH - which should dec cortisol
  • Circadian rhythm - normally low at night, high in morning
    • Not replicated with Cushings
  • Imaing
    • Pituitary MRI - if pituitary source suspected
    • Abdo CT - if adrenal source suspected
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11
Q

How is Cushings treated?

A
  • Remove the cause
    • Stop glucocorticoid treatment
    • Surgical removal of tumour
    • Surgical removal of adrenal glands
  • Cortisol synthesis inhibiting medication
    • Mifepristone (receptor antagonist)
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12
Q

Name the complications of Cushings syndrome

A

CUSHINGOID:

  • Cataracts
  • Ulcers
  • Skin - striae, thinning, bruising
  • Infections
  • Necrosis (of femoral head)
  • Glycosuria
  • Osteoporosis/obesity
  • Immunosuppression
  • Diabetes
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13
Q

What is Addison’s disease? Name some causes

A

Adrenal insufficiency (low cortisol)

  • Adrenal destruction
    • Autoimmune (80%) =
    • Metastasis
    • Haemorrhage (Waterhouse-Friederichsen)
    • Infections - TB, histoplasmosis, HIV, CMV
    • Amyloid deposits
  • Adrenal dysgenesis (not formed during development)
  • Impaired steroidogenesis
    • Interruptions in cholesterol delivery
    • Congenital adrenal hyperplasia
    • Medications (rifampicin, phenytoin)
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14
Q

Name some symptoms of Addisons

A
  • Fatigue
  • Abdominal pain
  • Myalgia/arthralgia
  • Depression
  • Anorexia and weight loss
  • Diarrhoea and vomiting
  • Psychosis
  • Weakness
  • Lightneadedness
  • Constipation
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15
Q

Name some signs of Addisons

A
  • Hyperpigmentation
    • Palmar creases
    • Buccal mucosa
  • Vitiligo
  • Postural hypotension
  • Tachycardia
  • Fever
  • Shock
  • Coma
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16
Q

What is an Addisonian crisis? What are the precipitants?

A

Severe, acute symptoms due to severe adrenal insufficiency, precipitated by:

  • Trauma
  • Infection
  • Surgery
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17
Q

How do Addisonian crisis’ present?

A
  • Shock
    • Tachycardia
    • Peripheral vasoconstriction
    • Postural hypotension
    • Oliguria
  • Hypoglycaemia
  • Sudden pain in legs, lower back, abdomen
  • Severe vomiting and diarrhoea - dehydration
  • Low Na+, high K+, high Ca2+
  • Confusion, psychosis
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18
Q

How is Addisons investigated?

A
  • Bloods - high Ca2+, high K+, low Na+, low glucose, low Hb, neutropenia, raised LFTs
  • ABG - metabolic acidosis
  • ECG - increased PR and QT interval
  • ACTH stimulation test (synacthen) - administer sythetic ACTH 250 microg IM
    • Measure cortisol before and after
    • If cortisol not increased (>500) then adrenal failure
  • Serum ACTH >300ng/L (low in 2º causes)
  • Imaging (US/MRI/CT) of adrenal glands
  • CXR - signs of TB/past TB
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19
Q

How is Addisons treated?

A
  • IV fluids if dehydrated
  • Hydrocortisone - 20mg in morning, 10mg at night
  • Consider mineralocorticoid replacement if abnormal electrolytes and renin
    • Fludrocortisone
  • Advice against suddenly stopping steroids and symptoms of Addisonian crisis
  • Steroid card/medical bracelet
  • If poor response - autoimmune screen
    • Thyroid, coeliac, serology
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20
Q

How is an Addisonian crisis treated?

A
  • Hydrocortisone sodium succinate 100mg IV stat
  • Fluid resuscitation
  • Glucose IV/dextrose if hypoglycaemic
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21
Q

Name some symptoms of hyperthyroidism

A
  • Weight loss despite increased appetite
  • Heat intolerance and sweating
  • Diarrhoea
  • Tremor
  • Irritability
  • Psychosis
  • Amenorrhoea
  • Infertility
  • Gynecomastia
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22
Q

Name some signs of hyperthyroidism

A
  • Tachycardia
  • AF
  • Warm peripheries
  • Goitre +/- nodules
  • Palmar erythema
  • Hair thinning
  • Exopthalmos
  • Lid lag
  • Vitiligo
  • Oedematous swelling above lateral malleoli
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23
Q

Name some causes of hyperthyroidism

A
  • Grave’s = autoimmune stimulation
  • Thyroid adenoma
  • Multinodular goitre
  • Thyroiditis (De Quervain’s)
  • Excess thyroid medication
  • Drugs - amiodarone, lithium
  • Post-partum thyroiditis
  • Thyroid carcinoma
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24
Q

Describe the pathophysiology of Graves disease

A

Thyroid-stimulating immunoglobulins recognize and bind to the TSH receptor which stimulates the secretion of thyroxine (T4) and triiodothyronine (T3). Thyroxine receptors in the pituitary gland are activated by the surplus hormone, suppressing additional release of TSH in a negative feedback loop. The result is very high levels of circulating thyroid hormones and a low TSH level.

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25
Q

How is hyperthyroidism investigated?

A
  • Plasma TSH = low in hyperthyroidism or pituitary failure
  • Plasma free T3/T4
  • Thyroid autoantibodies
  • Anti TSH receptor antibodies
  • Radioactive iodine uptake test = measures absorbed iodine
  • Thyroid scintigraphy
  • Opthalmology - visual fields, acuity, movements
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26
Q

How is hyperthyroidism treated?

A
  • Thyrostatic drugs - carbimazole (15-40mg/day)
    • Titrate down according to TFTs
  • Beta blockers (reduce SNS symptoms)
  • Decrease iodine in diet
  • Partial thyroidectomy
    • Risk of recurrent laryngeal nerve damage
    • Risk of parathyroid damage
  • Radioiodine - restricts/destroys thyroid function
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27
Q

Name some complications of hyperthyroidism

A
  • Heart failure (thyrotoxic cardiomyopathy)
  • Angina
  • AF (25%)
  • Osteoporosis
  • Gynaecomastia
  • Thyroid storm
  • Opthalmopathy
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28
Q

What is a thyrotoxic storm / hyperthyroid crisis? What causes it?

A

Severe hyperthyroidism causing fever, agitation, confusion, tachycardia, AF, coma and acute abdomen

Precipitants:

  • Thyroid surgery
  • Radioiodine
  • Infection
  • MI
  • Trauma
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29
Q

How is a thyrotoxic storm managed?

A
  • IV 0.9% saline 500ml/4hr
  • Bloods - T3/T4, cultures (if infection suspected)
  • Sedate if necessary (chlorpromazine)
  • Propanolol 40mg/8hr PO
  • High dose digoxin may be needed to slow the heart
  • Carbimazole 15-25mg/6hr
  • Hydrocortisone 100mg/6hr
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30
Q

Name some side-effects of carbimazole

A
  • Rashes
    • Add antihistamine
  • Pruritis
    • Add antihistamine
  • Sensitivity
  • Bone marrow suppression
  • Arthralgia
  • GI disturbance
    *
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31
Q

Name some signs and symptoms of hypothyroidism

A
  • General - fatigue, cold intolerance, weight gain
  • Cardio - bradycardia, pericardial effusion, CCF
  • Resp - SOB, pleural effusion, hoarseness
  • GI - constipation, ascites
  • Psych - poor memory, loss of concentration
  • Menorrhagia (heavy periods) and impaired fertility
  • Carpal tunnel syndrome
  • Myalgia
  • Dry skin and hair
  • Non-pitting oedema (eyelids, hands, feet)
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32
Q

Name some causes of hypothyroidism

A
  • Primary
    • Iodine deficiency
    • Autoimmune (Hashimotos)
    • Thyroidectomy/radio-iodine
    • Medication = lithium, amiodarone, carbimazole
  • Central
    • Pituitary lesions (adenoma, metastasis)
    • ICA aneurysm
  • Congenital
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33
Q

How is hypothyroidism investigated?

A
  • Plasma - high TSH, low T4, antibodies
  • Possibly high cholesterol and triglyceride
  • Macrocytic anaemia
  • Possibly high AST, LDH, CK (due to abnormal muscle membranes)
  • Thyroid imaging
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34
Q

How is hypothyroid treated?

A
  • Levothyroxine (T4) 100macrog/day
  • Iodine replacement if deficient
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35
Q

Describe the negative feedback of the thyroid

A
  • Hypothalamus secretes TRH
  • TRH stimulates production of TSH from anterior pituitary
  • TSH increases production and release of T3 and T4 from the thyroid
  • T3 and T4 exert negative feedback on TSH production
    • Thyroid produced mainly T4
    • T3 converted to T4 peripherally
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36
Q

Interpret these TFTs:

  1. High TSH, low T4
  2. High TSH, normal T4
  3. High TSH, high T4
  4. Low TSH, high T4/T3
  5. Low TSH, normal T4/T3
  6. Low TSH, low T4/T3
  7. Normal TSH, abnormal T4
A
  1. Primary hypothyroidism
  2. Subclinical hypothyroidism
  3. T4 compliance problems, TSH-secreting tumour, thyroid hormone resistance
  4. Hyperthyroidism
  5. Sub clinical hyperthyroidism
  6. Pituitary disease, sick euthyroidism
  7. Horome-binding problems
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37
Q

Describe the function of parathyroid hormone

A
  • Increases calcium and decreases phosphate reabsorption in the kidney
  • Increases osteoclast activity
  • Increases vitamin D production in the kidneys

Overall:

  • Increases plasma calcium
  • Decreases plasma phosphate
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38
Q

Name some causes of hyperparathyroidism

A

Primary:

  • Adenoma (80%)
  • Hyperplasia
  • Primary neoplasia

Secondary (high PTH due to low calcium):

  • Chronic renal failure
  • Low vitamin D intake
  • Ectopic/metastatic calcification

Tertiary (prolonged secondary): chronic renal failure

Malignant: Parathyroid-related protein (PTHrP) produced by lung cancers

39
Q

Name some clinical presentation of hyperparathyroidism

A

Stones, moans, groans:

  • Renal stones
  • Abdominal pain
  • Depression
  • Bone pain/fractures
  • Osteoporosis
  • Pancreatitis
  • Ulcers
  • Dehydration
40
Q

How is hyperparathyroidism investigated?

A
  • Bloods - high calcium, low phosphate, high ALP, high PTH
  • 24hr urine - calcium
  • DEXA bone scan
  • Consider x-ray if evidence of bone reabsorption/fractures
  • Thyroid US
41
Q

How is hyperparathyroidism treated?

A
  • If mild - increase fluid intake to prevent stones
  • If primary - total parathyroidectomy
    • Autotransplantation to arm
    • Or with alfacalcidol
  • If secondary
    • Phopsphate binders
    • Vitamin D analogues
42
Q

Name some causes of hypoparathyroidism

A
  • Gland failure
    • Removal during thyroidectomy
    • Radiation
  • Autoimmune
  • Low magnesium
  • DiGeorge syndrome

Pseudohypoparathyroidism = failure of target cell response to PTH

Pseudopseudohypoparathyroidism = features of pseudohypoparathyroidism but with normal biochemistry

43
Q

Describe the clinical presentation of hypoparathyroidism

A

Features of hypocalcaemia:

  • Tetany
  • Depression
  • Carpo-pedal spasm
    • Trousseaus signs = BP cuff used to occlude brachial artery which induces spasm of the foream and hand muscles
  • Neuromuscular excitability - twitching
44
Q

How is hypoparathyroidism investigated?

A
  • Bloods - low calcium, high (or normal) phosphate, normal ALP, low PTH, possibly low magnesium
  • ECG if cardiac symptoms
45
Q

How is hypoparathyroidism treated?

A
  • If severe hypocalcaemia - IV calcium
  • Alfacalcidol (vitamin D analogue) +/- calcium supplementation
    • May not work in renal damage
46
Q

What is Type 1 diabetes? What causes it?

A

Chronic hyperglycaemia due to insulin deficiency

  • Autoimmune destruction of the beta cells in the pancreatic islets
  • Juvenile onset
47
Q

How does T1DM present?

A

Ketoacidosis (metabolism of fatty acids):

  • Hyperventilation → Kussmaul respiration
  • Ketones on breath (pear drops)
  • Weight loss
  • Vomiting
  • Abdominal pain
  • Polyuria and polydipsia
  • Fatigue
48
Q

How is T1DM diagnosed?

A
  • Fasting plasma glucose >/= 7 mmol
  • Random glucose OR 2 hours after glucose tolerance test (75g oral glucose) >/= 11.1 mmol
  • HbA1c >/= 6.5%
  • Urine dip - glucose and ketones
  • ABG - metabolic acidosis
49
Q

How is T1DM managed?

A
  • Lifestyle - low carb diet, exercise
  • Insulin (100U/ml)
  • BP control
  • Regular retinopathy screening
  • Manage emotional/psychological factors
  • Pancreas transplant
    • Usually if renal transplant needed
  • Islet cell transplant
50
Q

What are the different types of insulin?

A
  • Ultra-fast acting (novorapid) - bolus dosage
  • Short acting - 30 mins
  • Intermediate (Insulatard) - 1-2 hours
  • Long-acting (Ultratard) - sustained up to 24 hours
51
Q

Name some complications of diabetes

A
  • KNIVES:
    • Kidney - nephropathy
    • Neuropathy (peripheral)
    • Infective - TB, UTI
    • Vascular - MI, stroke, peripheral
    • Eye - cataracts, retinopathy
    • Skin - lipohypertrophy/atrophy
  • Sexual dysfunction
  • DKA (T1DM)
  • Diabetic feet
52
Q

What are the complications of DKA?

A
  • Hypoglycaemia
  • Hyponatraemia
  • Hyperchloraemic acidosis
  • Cerebral oedema
  • Arrhythmias (secondary hyperkalaemia)
  • Venous thrombosis / thromboembolism
  • Gastric stasis
  • AKI
  • Hyperchloraemia
53
Q

How is DKA treated?

A
  • Fluid resuscitation (0.9% saline) - 500ml in 15 mins etc
  • Check plasma glucose
  • Insulin infusion via IV pump (0.1ml/kg/hour)
  • Continue fluid replacement
  • K+ replacement
  • Hourly monitoring of glucose, U&Es and HCO3-
  • NG tube if vomiting
54
Q

What causes T2DM?

A

Decreased insulin secretion and insulin resistance associated with obesity, lack of exercise and calorie excess. Associated with:

  • Acromegaly
  • Cushing’s
  • Renal failure
  • PCOS
  • Pregnancy
  • TB drugs
  • Hyperthyroidism
55
Q

Name some clinical features of T2DM

A
  • Polyuria
  • Polydipsia
  • Weight loss
  • Fatigue
  • Increased hunger
  • Recurrent infections (UTI, vaginal
  • Blurred vision/retinopathy
  • HONK
  • Foot ulcers
  • Complications
56
Q

How is T2DM diagnosed/monitored?

A
  • Fasting glucose >/= 7.0 mmol/L
  • Random glucose >/= 11.1 mmol/L
  • HbA1c >/= 6.5%
  • Urine dip - glucose
  • Fundoscopy
  • BP
  • Cholesterol (high)
  • Foot exam
57
Q

How is T2DM treated?

A
  • Patient education
    • DESMOND/specialist nurses
    • Lifestyle changes
  • BP control (systolic < 140 mmHg
  • Oral hypoglycaemics
  • Acarbose (a-glucosidase inhibitor) dec breakdown of starch to sugar (add-on drug)
  • Insulin
58
Q

How are risk factors modified in those with diabetes?

A
  • BP control (systolic = 140mmHg) - ACE-i
  • Stop smoking
  • Cholesterol control - statins
  • Weight loss
  • Exercise
  • Diet (less saturated fats, and sugar, more stach-carbs)
59
Q

Describe the appearance of diabetic retinopathy

A
  • Pre-proliferative
    • Cotton-wool spots (infarcts)
    • Microaneurysms
    • Exudates
    • Flame haemorrhages
  • Proliferative
    • New vessel formation
    • Vitreous haemorrhage
  • Maculopathy
60
Q

How is diabetic foot managed?

A
  • Education
    • Daily foot inspection
    • Comfortable shoes with cushioned insoles
    • No barefoot walking
  • Regular chiropody - remove dead tissue
  • Relieve high-pressure areas with bedrest +/- therapeutic shoes
  • Antibiotics if infected
  • Surgery if:
    • Abscess or deep infection
    • Spreading anaerobic infection
    • Severe ischaemia - gangrene/rest pain
    • Suppurative arthritis
61
Q

What is acromegaly?

A

Hypersecretion of growth hormone from either a pituitary adenoma or a GHRH-producing tumour (pancreas, lungs, adrenals)

Usually presents between 30 and 50

62
Q

What are the clinical features of acromegaly?

A
  • Soft tissue swelling - enlargement of hands, feet, nose, lips, ears and skin thickening
  • Swelling of internal organs - heart, kidneys, vocal cords
    • Thick, deep voice and slowing of speech
  • Expansion of skull at fontanelle
  • Frontal bossing = brow protrusion
  • Mandibular overgrowth = jaw protrusion (prognathism)
  • Macroglossia (big tongue and teeth spacing
  • Hypertrichosis, hyperpigmentation, hyperhidrosis
  • Carpal tunnel syndrome
  • Psychological effects - social withdrawal, low self esteem etc
63
Q

How is acromegaly diagnosed?

A
  • Obtain old photos and compare
  • GH suppression test following oral glucose load
    • No suppression = acromegaly
    • Insulun-like growth factor (IGF-1) - levels correlate with GH secretion over past 24 hours
  • Test pituitary function
  • MRI/CT of pituitary fossa
  • ECG
64
Q

What is the treatment of acromegaly?

A
  • Somatostatin analogues - stops GH production
    • Octreotide monthly IM
  • Dopamine agonists
  • GH receptor antagonists
  • Trans-sphenoidal surgery
  • External radiation for older patients or failed surgery
65
Q

Name some complications of acromegaly

A
  • Diabetes
  • Hypertension
  • Left ventricular hypertrophy/cardiomyopathy
  • Colon cancer
  • Hyperthyroidism
  • Carpal tunnel syndrome
  • Headache
  • Bitemporal hemianopica (optic chiasm compression)
66
Q

What is diabetes insipidus?

A

Reduced ADH secretion from the posterior pituitary (cranial DI) OR impaired response of the kidneys to ADH (nephrogenic DI) causes impaired water resorption

67
Q

Name some causes of diabetes insipidus

A

Cranial:

  • Head injury
  • Metastasis/ primary pituitary tumour
  • Vascular lesion
  • Meningitis
  • Pituitary surgery

Nephrogenic:

  • Low potassium
  • High calcium
  • Drugs - lithium, demeclocycline
  • Kidney disease - pyelonephritis, hydronephrosis
68
Q

What are the symptoms of diabetes insipidus

A
  • Polyuria
  • Dilute urine
  • Polydipsia
  • Dehydration
69
Q

How is diabetes insipidus diagnosed?

A
  • Bloods - U&E, Ca2+, high plasma osmolarity
  • Urine - low osmolarity
  • Water deprivation test - empty bladder then no drinks and only dry food for 8 hours
    • Collect urine and measure osmolarity hourly
    • Measure plasma osmolarity every 3 hours
    • If plasma osmolarity > 300 and urine < 600 give desmopressin
    • If urine osmolarity < 400 = DI
      • Cranial >50% after desmopression
      • Nephrogenic < 45%
70
Q

How is diabetes insipidus treated?

A
  • Rehydrate - keep up with output
  • Cranial:
    • Find and treat cause
    • Desmopressin intranasally
  • Nephrogenic
    • Treat cause
    • Avoid high-protein and salf meals
    • Bendroflumethiazide
71
Q

Name some actions of oestrogen

A
  • Sexual differentiation
  • Puberty - breasts, endometrium, vagina, myometrium
    • Epiphyseal closure
  • Maintains menstrual cycle
  • Metabolism
    • Inhibit bone resorption
    • Decrease bowel motility
    • Stimulate protein synthesis in liver
    • Decrease total cholesterol
72
Q

Name some actions of testosterone

A
  • Sexual differentiation
  • Maintains structure and function of accessory sex organs
  • Anabolic - increases BMR and muscle mass
  • Spermatogenesis
73
Q

Name some causes of male infertility

A
  • Primary seminiferous tubule failure
    • Orchitis
    • Surgery
  • Toxins/drugs/chemicals/heat
  • Secondary testicular failure (gonadotrophin deficiency)
    • Hypothalamo-pituitary disease (tumour)
    • Anabolic steroid abuse
  • Sperm autoimmunity
  • Genital tract obstruction
    • STD
    • Vasectomy
    • CF
  • Coital dysfunction
74
Q

How is male infertility investigated?

A
  • Plasma testosterone, LH/FSH, prolactin
  • Semen analysis
  • IgG/IgA antibodies
  • Ultrasound
75
Q

How is male infertility treated?

A
  • Primary failure = androgen replacement
  • Sperm autoimuunity = intracyclic sperm injection
  • Tumour/obstruction = surgery
  • Coital dysfunction = change meds/counselling
76
Q

What is the glucose finding in hypoglycaemia. Name some symptoms

A

Plasma glucose <2.5mmol/L

  • Autonomic - sweating, hunger, tremor
  • Drowsiness
  • Seizures
  • Mutism
  • Personality change
  • Restlessness
  • Incoherence
77
Q

Name some causes of hypoglycaemia

A

Fasting hypoglycaemia: EXPLAIN

  • Exogenous insulin, oral hypoglycaemics, alcohol
  • Pituitary insufficiency
  • Liver failure
  • Addisons
  • Islet cell tumours (insulinoma)
  • Non-pancreatic neoplasm (retroperitoneal fibrosarcoma)

Post-prandial = after gastric surgery (dumping)

78
Q

What is MEN syndrome?

A

Multiple Endocrine Neoplasia/Autosomal dominant (pre)malignant paraendocrinopathies = group of genetic tumour syndromes that cause overactivity and enlargement of endocrine organs

  • MEN 1 (3 ps) = Parathyroid tumors, pancreatic tumors, and pituitarytumors.
  • MEN2A (2 ps) = Medullary thyroid cancers, pheomochromocytoma and parathyroid tumours
  • MEN2B (1 p) = Medullary thyroid cancers, pheochromocytoma and neuromas
79
Q

What are the features of hyperaldosteronism

A
  • Hypertension
    • Poor vision
    • Headaches
  • Hypokalaemia
    • Muscular weakness
  • Alkalosis in someone not on diuretics
  • Normal or mildy raised sodium
  • Polyuria
80
Q

What causes hyperaldosteronism?

A
  • Conn’s syndrome (unilateral adrenocortical adenoma)
  • Bilateral adrenocortical hyperplasia
  • Adrenal carcinoma
  • Familial
  • Secondary = high renin
    • Renal artery stenosis
    • Diuretics
    • CCF
81
Q

How is hyperaldosteronism diagnosed?

A
  • Bloods - U&E, high aldosterone, low renin
    • If low aldosterone and renin on standing = Conns
  • Abdo CT/MRI to localise tumour
82
Q

How is hyperaldosteronism treated?

A
  • Conns - laparascopic surgery
  • Spironolactone up to 300mg/day
  • Amiloride
83
Q

What is a phaeochromocytoma?

A

Catecholamine (adrenaline, norad, dopamine) producing tumour (usually in adrenal medulla), causing:

  • Hypertension
  • Headaches
  • Palpitations
  • Sweating
  • Anxiety
84
Q

Describe the clinical features of diabetic neuropathy

A
  • Symmetrical, mainly sensory neuropathy (glove and stocking)
    • Loss of vibration sense, pain and temp
    • ‘Walking on cotton wool’
    • Loss of proprioception - impaired balance
  • Motor
    • Muscle wasting (interossei)
  • Charcot’s joint
85
Q

Name some side effects of metformin

A
  • Lactic acidosis
    • Higher in renal and liver disease
  • GI symptoms
    • D&V
    • Abdominal pain
  • Anorexia
  • Pernicious anaemia
86
Q

Name some side effects of TZDs (pioglitazone)

A
  • Fluid retention - contraindicated in heart failure
  • Fractures
  • Bladder cancer
  • Weight gain
  • Liver impairment
87
Q

Name some causes of raised prolactin

A

P’s:

  • Prolactinoma
  • Pregnancy
  • Physiological - stress, exercise, sleep
  • PCOS
  • Primary hypothyroidism (thyrotrophin releasing hormone stimulating prolactin release)
  • Oestrogens
  • Acromegaly
88
Q

Describe subacute (De Quervain’s) thyroiditis - signs, investigations, management

A

Hyperthyroidism then hypothyroidism due to post-viral infection

  • Associated with tender thyroid gland
  • Raised ESR
  • Decreased uptake on iodine-131 scan
  • Managed with pain relief only - usually self limiting
89
Q

How is phaeochromocytoma diagnosed?

A

24 hour urinary collection of metanephrines

90
Q

How is phaeochromocytoma managed?

A
  • Alpha-blocker (phenoxybenzamine)
  • Then beta blocker (propanolol)
  • Surgery
91
Q

Name some oral hypoglycaemics and their class of drug

A
  • Biguanide (metformin) - inc insulin sensitivity, dec hepatic gluconeogenesis

Add (up to two more) if HbA1c > 7.5%:

  • Sulfonylurea (tolbutamide, glibenclamide, gliclazide) - inc insulin secretion
  • DPP-4 inhibitor (gliptin)
  • Thiazolidinedione (pioglitazone) PPAR agonist
  • SGLT-2 inhibitor (canagliflozin) - inhibit Na-glucose co-transporter in PCT

Add if triple therapy not effective/tolerated AND BMI > 35:

  • GLP-1 agonist (exenatide)
92
Q

Name some contraindications to metformin

A
  • Heart failure
  • Renal failure
  • Liver failure
  • Tissue hypoxia - lactic acidosis
  • During iodine-containing x-ray contrast procedures
  • Alcohol abuse
93
Q

Name some side effects of sulfonylureas

A
  • Hypoglycaemia
  • Weight gain
  • SIADH
  • Liver damage
  • Peripheral neuropathy

Avoid in pregnancy and breast feeding

94
Q

What are BP targets for diabetics?

A

< 140/80

< 130/80 if end-organ damage is present

ACE inhibitors are first line

IPE (13 decks)

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