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2A revision > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

pathology of T1DM

A
  • autoimmune destruction of insulin producing beta cells in the islet of Langerhans
  • insulin deficiency
  • genetic and environmental triggers
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2
Q

pathology of T2DM

A
  • low insulin secretions and peripheral insulin resistance

- genetic and mostly environmental (obesity, sedentary lifestyle stc)

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3
Q

what can cause secondary diabetes mellitus

A
  • acromegaly = excessive GH, insulin resistance rises
  • Cushing’s syndrome = increased insulin resistance
  • Drug-induced diabetes = glucocorticoids increase insulin resistance
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4
Q

what is maturity onset diabetes of the young (MODY)

A
  • single gene defect altering beta cell function
  • good control on low dose insulin
  • no ketosis
  • parents affected with diabetes
  • sensitive to sulphonyl urea
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5
Q

how does diabetes cause polyuria and thirst

A
  • mobilisation of energy stores from muscles, fat and the liver
  • hyperglycaemia
  • in kidneys the glucose reabsorption mechanism becomes saturated so glucosuria
  • glucose in renal tubules draws water in = osmotic diuresis
  • raised plasma osmolality stimulates thirst centre
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6
Q

screening and diagnosis for DM

A
  • fasting plasma gluctose >7mmol/L
  • random plasma glucose >11mmol/L
  • HbA1c 6.5% or 48mmol/mol
  • neuropathy screening = sensation, vibration, ankle reflexes
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7
Q

consequences of untreated T1DM

A
  • fat metabolisation = glycerol and free fatty acids
  • FFA impair glucose uptake and are oxidised to for ketone bodies in the liver (acetone, beta-hydroxybutyrate)
  • ketone bodies dissolve in the blood and release H+ causing acidosis
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8
Q

what are the symptoms of diabetic ketoacidosis

A
  • polyuria
  • polydipsia
  • nausea and vomiting
  • weight loss
  • abdo pain
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9
Q

what are the signs of DKA

A
  • hyperventilation (Kussmaul breathing to try remove CO2 to decrease blood acidity)
  • dehydration
  • fruity breath
  • hypotension
  • tachycardia
  • coma
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10
Q

management of DKA

A
  • Rehydration
  • Insulin
  • Replacement of electrolytes (K+)
  • Treat underlying cause
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11
Q

complications of DM

A
  • diabetic retinopathy
  • diabetic nephropathy (end stage renal disease)
  • peripheral vascular disease
  • stroke
  • CV disease
  • diabetic peripheral neuropathy
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12
Q

diabetic neuropathy

A

-Pain – burning, paraesthesia
-Autonomic – orthostatic hypotension, constipation, ED
-Insensitivity – foot ulceration, Charcot foot, amputation
-Peripheral neuropathy – glove and stocking sensory loss
-Treatment: good glycaemic control, anticonvulsants, opioids.
-Consequences: diabetic foot ulceration can lead to
amputation.

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13
Q

diabetic retinopathy

A
  • Micro-aneurysms: pericyte and smooth muscle loss
  • Leakage: basement membrane thickening reduced junctional contact with endothelial cells
  • Ischaemia: pericyte loss
  • Treatment: laser therapy to stabilise changes
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14
Q

management of T1DM

A
  • insulin treatment twice daily with meals

- DAFNE = dose adjustment for normal eating

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15
Q

management of T2DM

A
  • first line = weight loss and exercise
  • second line = meds for BP, blood glucose and lipids
    > metformin = weight loss
    > metformin and sulphonyl urea = weight gain and chance of hypo
    > insulin
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16
Q

how does metformin work

A
  • increases insulin sensitivity
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17
Q

how does sulphonyl urea work

A
  • increase insulin release from beta cells
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18
Q

hyperglycaemic hyperosmolar state

A
  • complication of T2DM (unwell patients) = hyperglycaemia result in high osmolarity without ketoacidosis
  • dehydration and glucose>30mmol/L
  • occlusive events = give LMWH prophylaxis
  • rehydrate slowly of 48h then replace K+ when urine flows
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19
Q

what are the 3 mechanisms of hyperthyroidism

A
  1. overproduction
  2. leakage of preformed hormone
  3. ingestion of excess
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20
Q

causes of hyperthyroidism

A
  • Grave’s disease
  • toxic multinodular goitre
  • toxic adenoma
  • congenital
  • thyroiditis
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21
Q

symptoms of hyperthyroidism

A
  • weight loss, tachycardia, anxiety, heat intolerance, sweating, diarrhoea, menstrual disturbance
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22
Q

signs of hyperthyroidism

A
  • Grave’s = diffuse goitre, thyroid eye disease, acropachy (swelling of hands/ clubbing)
  • adenoma specific = solitary nodule
  • multinodular goitre
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23
Q

investigations for hyperthyroidism

A
  1. TFT
  2. diagnosis of underlying cause
  3. clinical history
  4. thyroid antibodies
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24
Q

treatment of hyperthyroidism

A
  • antithyroid drugs = thionamides (carbimazole)
  • beta blockers (propranolol)
  • radioiodine
  • surgery (thyroidectomy)
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25
Q

pathology of Grave’s disease

A
  • immune attack on TSH receptors on thyroid gland

- TSH receptor stimulating antibody (TRAb) activates receptor and causes high thyroid hormone levels

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26
Q

what will TFT show for Grave’s disease

A
  • high T3/4

- low TSH

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27
Q

symptoms and signs of Grave’s

A 
Anxiety and irritability
A fine tremor of your hands or finger
Heat sensitivity and sweating 
Weight loss
goiter
Bulging eyes – Graves’ ophthalmopathy
Thick, red skin usually on the shins or tops of the feet - Graves’ dermopathy
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28
Q

what is Graves ophthalmopathy

A
  • bulging eyes

- treat with corticosteroids/ orbital decompression surgery

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29
Q

what is Graves dermopathy

A

thick, red skin on shins or top of feet

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30
Q

management of Grave’s

A
  • radioactive iodine therapy
  • anti-thyroid meds = carbimazole
  • beta blockers = propranolol
  • thyroidectomy
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31
Q

what is primary hypothyroidism

A
  • > 99%
  • absence/dysfunction of thyroid gland
  • most from Hashimoto’s thyroiditis (autoantibodies block TSH receptors)
  • other causes = thyroidectomy or iodine deficiency
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32
Q

what is secondary hypothyroidism

A
  • pituitary/hypothalamic dysfunction

- TSH deficiency

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33
Q

what is tertiary hypothyroidism

A
  • withdrawal of thyroid suppressive therapy
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34
Q

signs of hypothyroidism

A 
Weight gain 
Slowed speech and movements
Dry skin
Jaundice 
Pallor 
Coarse, brittle, straw-like hair
Loss of scalp hair, axillary hair, pubic hair, or a combination 
Hoarseness 
Bradycardia 
Pericardial effusion
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35
Q

TFT results for primary hypothyroidism

A
  • high TSH

- low T3/4

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36
Q

TFT results for secondary hypothyroidism

A
  • inappropriately low TSH for low T3/4
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37
Q

management of hypothyroidism

A
  • 100ug thyroid hormone (levothyroxine) - titre according to TSH
  • monitor until correct titration
  • T4 half life is long so check 6-8 weeks after dose adjustment
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38
Q

pathology of Hashimoto’s thyroiditis

A
  • aggressive destruction of thyroid cells by cell and Ab mediated immune process
  • Abs against thyroid peroxidase (TPO antibodies)
  • Abs bind and block TSH receptors
  • CD8+ cytotoxic t cells destroy thyroid follicular epithelial cells
  • inflammation of thyroid gland
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39
Q

triggers of Hashimoto’s thyroiditis

A
  • iodine
  • infection
  • smoking
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40
Q

management of Hashimoto’s disease

A

levothyroxine

resection of obstructive goitre

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41
Q

what are the 5 types of thyroid cancer

A
  • papillary 60%
  • follicular <25%
  • medullary 5%
  • lymphoma 5%
  • anaplastic (rare)
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42
Q

what kind of thyroid cancer does radiation cause

A

papillary carcinomas

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43
Q

what kind of thyroid cancer does iodine deficiency cause

A

follicular carcinomas

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44
Q

clinical presentation of thyroid carcinomas

A

painless, palpable, solitary thyroid nodule
hard and fixed
rapid growth

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45
Q

investigations for thyroid carcinoma

A
  • head and neck examination
  • fine-needle aspiration biopsy
  • indirect laryngoscopy
  • serum calcitonin (high in medullary)
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46
Q

papillary thyroid carcinoma

A
  • younger patients
  • spread to lymph nodes and lungs
  • treatment = total thyroidectomy, consider node excision/ radioiodine to ablate residual cells
  • levothyroxine
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47
Q

follicular thyroid carcinoma

A

Middle age
Spreads early via blood (bone, lungs)
Treatment – total thyroidectomy + T4 suppression + radioiodine ablation

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48
Q

medullary thyroid carcinoma

A

Sporadic (scattered) or part of MEN syndrome (multiple endocrine neoplasia)
May produce calcitonin which can be used a cancer marker
Treatment – thyroidectomy + node clearance

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49
Q

lymphoma thyroid carcinoma

A

Female: male = 3:1
May present with stridor/ dysphagia
Do full staging pre-treatment (chemotherapy)
Assess histology for mucosa-associated lymphoid tissue (MALT)

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50
Q

anaplastic thyroid carcinoma

A

female, elderly

- poor response to treatment (excision and radiotherapy)

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51
Q

what is Cushing’s syndrome

A

chronic excess levels of corticosteroids (particularly cortisol) in the body due to hyperfunction of the adrenal gland (often due to the use of corticosteroid medication)

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52
Q

what is Cushing’s disease

A

a tumour on the pituitary gland that causes the gland to produce too much ACTH, leading to bilateral adrenal hyperplasia and high levels of cortisol production

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53
Q

symptoms of Cushing’s

A

Weight gain
Mood change – depression, lethargy, irritability
Proximal weakness
Gonadal dysfunction – irregular menstruation, erectile dysfunction
Acne

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54
Q

signs of Cushing’s

A

Central obesity - round face, supraclavicular fat distribution
Skin and muscle atrophy
Purple abdominal striae
Osteoporosis

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55
Q

investigations for Cushing’s

A

-Overnight dexamethasone suppression test
>1mg dexamethasone at midnight, the take serum cortisol at 8am
>Normally cortisol suppresses to <50nmol/L – NO suppression in Cushing’s syndrome
-If positive, test for plasma ACTH
If ACTH is undetectable, a tumour adenoma is likely

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56
Q

management of Cushing’s

A
  • Iatrogenic – stop medications if possible

- Cushing’s disease – selective removal of pituitary adenoma

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57
Q

pathology of acromegaly

A
  • excess GH stimulates growth of bone and soft tissue through secretion of insulin-like growth factor 1
  • abnormal growth of hands, feet and face
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58
Q

symptoms of acromegaly

A 
Acral enlargement (peripheries – hands and feet)
Arthralgias (joint pain)
Maxillofacial changes
Excessive sweating 
Headache 
Backache 
Hypogonadal symptoms 
Acroparaesthesia (burning, tingling sensations in the extremities)
Amenorrhoea (absence of menstruation)
Decreased libido
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59
Q

signs of acromegaly

A 
Growth of hands 
Coarsening face; wide nose
Macroglossia (big tongue)
Puffy lips, eyelids and skin
Obstructive sleep apnoea
Goitre
60
Q

differential diagnoses for acromegaly

A

Marfan syndrome
Precocious puberty
Prolactinoma
Gigantism

61
Q

investigations for acromegaly

A 
-Acromegaly is excluded if;
>GH <0.4 ng/ml and normal IGF-I
-If either abnormal proceed to:
>75mg glucose tolerance test (GTT)
-Acromegaly excluded if:
>IGF-I normal and GTT normal and GH <1 ng/ml
62
Q

why can’t GH be relied on alone for diagnosing acromegaly

A
  • GH secretions are pulsatile and increase during pregnancy, stress and sleep
63
Q

management of acromegaly

A
  • pituitary surgery (trans-sphenoidal)
  • dopamine agonists (cabergoline)
  • radiotherapy
64
Q

what is Conn’s syndrome

A
  • primary hyperaldosteronism

- disease of the adrenal glands involving excess production of aldosterone (independent of the renin-angiotensin system)

65
Q

pathology of Conn’s syndrome

A
  • excess aldosterone
  • solitary aldosterone-producing adenoma (mutations in K+ channels)
  • aldosterone causes transport of Na and K in distal renal tubule (increased reabsorption of Na and excretion of K)
66
Q

symptoms of Conn’s syndrome

A

-Often asymptomatic
-Signs of hypokalaemia:
Weakness
Cramps
Paraesthesia
Polyuria (excessive urine production)
Polydipsia (excessive thirst)

67
Q

signs of Conn’s syndrome

A
  • hypertension

- low potassium

68
Q

investigations for Conn’s syndrome

A
  • investigate for supressed renin and increased aldosterone
  • adrenal vein sampling
  • U&E (K low or normal )
69
Q

management of Conn’s syndrome

A
  • Laparoscopic adrenalectomy

- Spironolactone (25-100)mg for 4 weeks pre-op controls BP and K+

70
Q

what is secondary hyperaldosteronism

A
  • excess aldosterone production due to high renin from decreased renin perfusion (renal artery stenosis, hypertension, diuretics etc)
71
Q

pathology of adrenal insufficiency

A
  • Autoimmune destruction of the entire adrenal cortex.
  • reduction in ability to produce cortisol and/or aldosterone.
  • Excess ACTH stimulates melanocytes, resulting in the pigmentation.
72
Q

what is primary adrenal insufficiency (Addison’s disease)

A

Destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency

73
Q

what is secondary adrenal insufficiency

A

Hypopituitarism/ long-term steroid therapy leading to suppression of the pituitary-adrenal axis

74
Q

symptoms of adrenal insufficiency

A
  • Fatigue
  • Weight loss
  • Dizzy
  • Faints
  • Poor recovery from illness
  • headache
  • abdo pain
  • diarrhoea/constipation
75
Q

symptoms of adrenal crisis

A 
Hypotension and cardiovascular collapse
Fatigue
Fever
Hypoglycaemia
Hyponatraemia and hyperkalaemia
76
Q

signs of adrenal insufficiency

A

Pigmentation and pallor
Primary – Hyperpigmentation
Secondary – no pigmentation
Hypotension

77
Q

investigations for adrenal insufficiency

A
  • Short ACTH stimulation test – give ACTH, if cortisol remains low then it diagnoses AI.
  • low Na, high K cue to decreased aldosterone
  • history (TB, cancer, family history of autoimmunity, previous use of steroids)
78
Q

management of AI

A
  • Replace the aldosterone with fludrocortisone (for primary AI)
  • Hydrocortisone 2/3 times daily to replace the cortisol
  • Mineralocorticoids to correct postural hypertension
79
Q

what is diabetes insipidus

A
  • A rare metabolic disorder in which the patient produces large quantities of dilute urine and is constantly thirsty
80
Q

pathology of diabetes insipidus

A
  • deficiency of pituitary hormone vasopressin (AVP)/ADH

- body can’t concentrate urine and too much water is passed

81
Q

cranial diabetes insipidus

A
  • most common
  • not enough AVP
  • caused by damage to hypothalamus/ pituitary gland (after infection, surgery, brain tumour)
82
Q

nephrogenic diabetes insipidus

A
  • enough AVP but kidneys fail to respond

- caused by kidney damage or sometimes inherited

83
Q

symptoms of DI

A
  • Polydipsia (extreme thirst)
  • Polyuria (excessive urine) – up to 20litres per day in severe cases
  • Tiredness (having to pass urine at night)
  • Irritability
  • Difficulty concentrating
84
Q

investigations for DI

A
  • water deprivation test = no fluid for 8h = DI patients will still pass large amounts of dilute urine
  • vasopressin test = inject small dose = urine production will stop in cranial DI but not nephrogenic
  • MRI scan of head to look for damage
85
Q

management of DI

A
  • fluid intake increased
  • desmopressin to replicate function of AVP in cranial
  • thiazide diuretic for nephrogenic DI to reduce vol of urine
86
Q

what is syndrome of inappropriate secretion of ADH

A

The hyponatraemia and hypo-osmolality resulting from inappropriate, continued secretion or action of the ADH/ vasopressin (AVP) despite normal or increased plasma volume, which results in impaired water excretion.

87
Q

causes of syndrome of inappropriate secretion of ADH

A

Disordered hypothalamic -pituitary secretion or ectopic production of ADH.

  • Malignancy – lung small-cell, pancreas, prostate, thymus, or lymphoma
  • CNS disorders – meningoencephalitis, abscess, stroke, subarachnoid/ subdural haemorrhage
  • Chest disease – TB. Pneumonia, abscess
  • Drugs – opiates, cytotoxics
  • Other – trauma, major abdominal surgery, symptomatic HIV
88
Q

clinical chemistry of inappropriate secretion of ADH

A
  • Decreased Na+ with decreased or normal urea and creatinine
  • Decreased plasma osmolality
  • Increased urine osmolality
  • Increased urine Na+.
89
Q

signs and symptoms of inappropriate secretion of ADH

A
  • Nausea
  • Irritability and headache with mild dilutional hyponatraemia
  • Fits and coma with severe hyponatraemia
90
Q

investigations for inappropriate secretion of ADH

A
  • FBC = Na, K, Cl, bicarbonate

- hyponatraemia with hypo-osmolality (Na >20mmol/L in urine, osmolality >100mOsmol/kg)

91
Q

management of inappropriate secretion of ADH

A

Treat the cause and restrict the fluid
Consider salt +/- loop diuretic if severe.
Vasopressin receptor antagonists - Vaptan

92
Q

pathophysiology of PTH (parathyroid hormone)

A
  • normally secreted in response to low ionized Ca2+ levels, by 4 parathyroid glands situated posterior to the thyroid.
  • negative feedback via Ca2+ levels.
93
Q

primary hyperparathyroidism

A
  • caused by a solitary nodule or hyperplasia of all glands = additional secretive tissue
94
Q

secondary hyperparathyroidism

A
  • caused by decreased vit D intake or chronic renal failure
  • gland becomes hyperplastic in response to chronic hypocalcaemia
  • can present with skeletal or CV complications
95
Q

tertiary hyperparathyroidism

A
  • occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously after undergoing hyperplastic or adenomatous change
96
Q

symptoms of hyperparathyroidism

A
  • bones = osteoporosis
  • stones = kidney stones
  • psychic groans = confusion
  • abdominal moans = constipation, acute pancreatitis
97
Q

diagnosis of hyperparathyroidism

A
  • Primary = Increased Ca2+ and PTH, Increased ALP – from bone resorption
  • Secondary = Low serum calcium, Raised PTH
  • Tertiary = Raised calcium, Raised PTH
98
Q

management of hyperparathyroidism

A
  • primary = removal of adenoma
  • secondary = calcium correction and treat cause
  • calcium mimetic
99
Q

what is hypoparathyroidism

A

subnormal activity of the parathyroid glands, causing a fall in the blood concentration of calcium and muscular spasms

100
Q

causes of hypoparathyroidism

A

genetics, autoimmune (polyglandular type 1), infiltration of the parathyroid glands by iron overload (haemochromatosis), parathyroidectomy

101
Q

pathology of hypoparathyroidism

A
  • no PTH to activate vit D so less intestinal and renal absorption of calcium and less calcium release from bones
102
Q

symptoms of hypoparathyroidism

A
  • increased excitability of muscles and nerves. - Numbness around the mouth/ extremities, cramps, tetany, convulsions.
  • Chvostek and Trousseau signs
103
Q

what is pseudohypoparathyroidism

A
  • genetic defect that causes lack of response to PTH. - Treatment with calcium and vitamin D can reverse most of the features
  • short stature, obesity, round faces, mild learning difficulties, short fourth metacarpals
104
Q

what is pseudopseudohypoparathyroidism

A

symptoms of pseudohypoparathyroidism are present, but the patient’s response to parathyroid hormone is normal.

105
Q

what is hypercalcaemia of malignancy

A
  • Malignancies of the lung, oesophagus, skin, cervix, breast and kidney.
  • tumour secretes parathyroid hormone-related protein which results in increased calcium levels.
106
Q

symptoms of hypercalcaemia of malignancy

A
  • bones, stones, groans and moans
  • weight loss
  • nausea
  • polydipsia and polyuria
  • dehydration
  • seizure (short QT interval on ECG)
  • coma
  • many others
107
Q

management

A
  • aggressive rehydration
  • bisphosphonates (zoledronic acid IV)
  • control underlying malignancy
108
Q

causes of hypocalcaemia

A
  • HAVOC – hypoparathyroidism, acute pancreatitis, vit D deficiency, Osteomalacia, CKD
  • respiratory alkalosis
109
Q

clinical presentation of hypocalcaemia

A

SPASMODIC: spasms, paraesthesia, anxious/irritable, seizures, muscle tone increase, orientation impaired, dermatitis, impetigo herpetiformis, Chvostek’s sign/ cataracts/ cardiomyopathy.
- seizures = prolongation of QT interval (ST segment)

110
Q

complications of hypocalcaemia

A 
Dysphagia 
Wheezing; bronchospasm
Syncope 
Congestive heart failure
Angina
111
Q

investigations for hypocalcaemia

A
  • serum albumin (rule out albuminemia)
  • Chvostek’s sign – tap over facial nerve and look for spasm
  • Trousseau’s sign – compression of brachial artery causes carpopedal spasm (wrist and fingers flex)
  • eGFR to look for CKD
  • PTH and vit D levels
112
Q

management of hypocalcaemia

A
  • mild = calcium 5mmol/6hours with daily plasma Ca levels
  • severe = 10ml of 10% calcium gluconate IV over 30 min
  • treat cause (if resp alkalosis then correct it)
113
Q

hyperkalaemia

A
  • usually from failure of kidneys to secrete it
    Mild: 5.5-6.0mEq/L
    Moderate: 6.1-7.0mEq/L
    Severe: ≥7.0mEq/L
114
Q

causes of hyperkalaemia

A
  • Renal impairment (retention of K in nephron)
  • Rhabdomyolysis (muscle injury – death of muscle fibres that release their contents into the bloodstream)
  • Metabolic acidosis
  • Addison’s disease (primary adrenal insufficiency)
  • Drugs interfering with potassium excretion e.g. ACEi
  • Burns
115
Q

clinical presentation of hyperkalaemia

A
  • A fast, irregular pulse
  • Chest pain
  • Weakness
  • Palpitations
  • Light-headedness
  • dyspnoea
  • paraesthesia
  • frank muscle paralysis
116
Q

differential diagnoses for hyperkalaemia

A

Metabolic acidosis
Rhabdomyolysis
Acute tubular necrosis

117
Q

investigations for hyperkalaemia

A
  • plasma potassium >6.5 is an emergency
  • bloods
  • ECG ( tall tented T waves, small P waves, wide QRS complex and ventricular fibrillation)
  • urine K, Na and osmolality
118
Q

acute treatment of plasma potassium >6.5 mmol/L

A
  • calcium gluconate = protects heart from ventricular fibrillation
  • insulin and dextrose drives K into cells
  • nebulised salbutamol
  • calcium resonium
119
Q

management of hyperkalaemia

A
  • Polystyrene sulfonate resin, binds K+ in the gut, preventing absorption and bringing K+ levels down over a few days.
  • If vomiting – 30g enema, followed by a 9 hour colonic irrigation
120
Q

what is the main cause of hypokalaemia

A
  • dehydration

- increase in aldosterone

121
Q

pathology of hypokalaemia

A
  • GI fluid loss -> less chloride -> increase in aldosterone -> decreased potassium reabsorption.
  • Excessive loss of potassium through the kidneys in response to aldosterone or diuretic
122
Q

causes of hypokalaemia

A 
Diuretics - hyperaldosteronism
Vomiting and diarrhoea 
Pyloric stenosis 
Intestinal fistula 
Cushing’s syndrome/ steroids/ ACTH
Conn’s syndrome
Alkalosis
123
Q

clinical presentation of hypokalaemia

A 
Muscle weakness
Hypotonia 
Hyporeflexia 
Cramps 
Tetany (intermittent muscular spasms)
Palpitations 
Light-headedness (arrhythmias)
Constipation
124
Q

investigations for hypokalaemia

A
  • K <2.5mmol/L = urgent
  • ECG = T wave inversion, prominent U wave
  • Urine potassium, sodium and osmolality
125
Q

management of hypokalaemia

A
  • Mild (>2.5mmol/L) = Oral K+ supplement, Review after 3 days
  • Severe (<2.5mmol/L) = IV potassium (no more than 20mmol/h and 40mmol/L), Do not give K+ if oliguric.
126
Q

what are neuroendocrine tumours

A

Tumours that form from cells that release hormones into the blood in response to a signal from the nervous system

127
Q

3 vital signs for neuroendocrine tumours

A
  1. Pressure on local structure e.g. optic nerves – bitemporal hemianopia
  2. Pressure on normal pituitary – hypopituitarism
  3. Functioning tumour – prolactinoma, acromegaly, Cushing’s disease
128
Q

what is a prolactinoma

A

lactotroph cell tumour of the pituitary

129
Q

sizes of prolactinomas

A

Microadenoma – tumour <1cm
Macroadenoma – tumour >1cm
Microprolactinoma – virtually always stays small
Macroprolactinoma – can be massive

130
Q

clinical presentation of prolactinoma

A
  • local effect of tumour
  • effect of prolactin = menstrual irregularity/ amenorrhoea, Galactorrhoea, Infertility, Loss of libido, Low testosterone in men
131
Q

diagnosis of prolactinoma

A
  • US
  • CT
  • MRI
  • PET
132
Q

management of prolactinoma

A

dopamine agonists (cabergoline)

  • remarkable shrinkage with macroadenoma
  • microadenoma respond to small dose of cabergoline twice a week
133
Q

what is a pheochromocytoma

A

Catecholamine (adrenaline) secreting tumour.

134
Q

pathology of pheochromocytoma

A

tumours of the chromaffin cells of the medulla that produce catecholamine

135
Q

clinical presentation of pheochromocytoma

A 
Episodic Headaches 
Palpitations 
Sweating 
Tremor
Anxiety and nausea 
Hypertension 
Tachycardia 
Pallor
136
Q

investigations for pheochromocytoma

A
  • 24 hour urine collection for urinary catecholamines and metabolites
  • Plasma catecholamines
137
Q

management of pheochromocytoma

A

-surgery preceded by alpha and beta blocker to stagger adrenaline loss

138
Q

what is a carcinoid tumour

A

Neuroendocrine tumours that particularly affect the small bowel, large bowel or appendix

139
Q

common sites for carcinoid tumours

A

appendix (45%), ileum (30%), rectum (20%), or elsewhere in GI tract

140
Q

pathology of carcinoid tumours

A
  • tumours of enterochromaffin cell origin

- secrete bioactive compounds if metastasise to liver (carcinoid syndrome)

141
Q

what is carcinoid syndrome

A

collection of symptoms some people get when a neuroendocrine tumour (usually hepatic involvement) releases hormone such as serotonin into the blood stream

142
Q

symptoms of carcinoid tumours

A

Bronchoconstriction
Diarrhoea
Skin flushing

143
Q

carcinoid crisis

A
  • when a tumour outgrows its blood supply, mediators flood out.
  • Life-threatening vasodilation, hypotension, tachycardia, bronchoconstriction and hyperglycaemia occur.
  • Treated with high dose octreotide (synthetic somatostatin)
144
Q

investigations for carcinoid tumours

A

-Increased 24h urine 5-hydroxyindoleacetic acid (5HIAA)
CXR + chest/pelvis MRI/CT
Echocardiography (investigate carcinoid heart disease)
Liver ultrasound (metastases)

145
Q

management of carcinoid tumours

A
  • octreotide = blocks release of tumour mediators
  • loperamide for diarrhoea
  • tumour resection

2A revision (10 decks)

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