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
2
Q
pathology of T2DM
A
- low insulin secretions and peripheral insulin resistance
- genetic and mostly environmental (obesity, sedentary lifestyle stc)
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
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
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
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
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
8
Q
what are the symptoms of diabetic ketoacidosis
A
- polyuria
- polydipsia
- nausea and vomiting
- weight loss
- abdo pain
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
10
Q
management of DKA
A
- Rehydration
- Insulin
- Replacement of electrolytes (K+)
- Treat underlying cause
11
Q
complications of DM
A
- diabetic retinopathy
- diabetic nephropathy (end stage renal disease)
- peripheral vascular disease
- stroke
- CV disease
- diabetic peripheral neuropathy
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.
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
14
Q
management of T1DM
A
- insulin treatment twice daily with meals
- DAFNE = dose adjustment for normal eating
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
16
Q
how does metformin work
A
- increases insulin sensitivity
17
Q
how does sulphonyl urea work
A
- increase insulin release from beta cells
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
19
Q
what are the 3 mechanisms of hyperthyroidism
A
- overproduction
- leakage of preformed hormone
- ingestion of excess
20
Q
causes of hyperthyroidism
A
- Grave’s disease
- toxic multinodular goitre
- toxic adenoma
- congenital
- thyroiditis
21
Q
symptoms of hyperthyroidism
A
- weight loss, tachycardia, anxiety, heat intolerance, sweating, diarrhoea, menstrual disturbance
22
Q
signs of hyperthyroidism
A
- Grave’s = diffuse goitre, thyroid eye disease, acropachy (swelling of hands/ clubbing)
- adenoma specific = solitary nodule
- multinodular goitre
23
Q
investigations for hyperthyroidism
A
- TFT
- diagnosis of underlying cause
- clinical history
- thyroid antibodies
24
Q
treatment of hyperthyroidism
A
- antithyroid drugs = thionamides (carbimazole)
- beta blockers (propranolol)
- radioiodine
- surgery (thyroidectomy)
25
pathology of Grave's disease
- immune attack on TSH receptors on thyroid gland
| - TSH receptor stimulating antibody (TRAb) activates receptor and causes high thyroid hormone levels
26
what will TFT show for Grave's disease
- high T3/4
| - low TSH
27
symptoms and signs of Grave's
```
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
```
28
what is Graves ophthalmopathy
- bulging eyes
| - treat with corticosteroids/ orbital decompression surgery
29
what is Graves dermopathy
thick, red skin on shins or top of feet
30
management of Grave's
- radioactive iodine therapy
- anti-thyroid meds = carbimazole
- beta blockers = propranolol
- thyroidectomy
31
what is primary hypothyroidism
- >99%
- absence/dysfunction of thyroid gland
- most from Hashimoto's thyroiditis (autoantibodies block TSH receptors)
- other causes = thyroidectomy or iodine deficiency
32
what is secondary hypothyroidism
- pituitary/hypothalamic dysfunction
| - TSH deficiency
33
what is tertiary hypothyroidism
- withdrawal of thyroid suppressive therapy
34
signs of hypothyroidism
```
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
```
35
TFT results for primary hypothyroidism
- high TSH
| - low T3/4
36
TFT results for secondary hypothyroidism
- inappropriately low TSH for low T3/4
37
management of hypothyroidism
- 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
38
pathology of Hashimoto's thyroiditis
- 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
39
triggers of Hashimoto's thyroiditis
- iodine
- infection
- smoking
40
management of Hashimoto's disease
levothyroxine
| resection of obstructive goitre
41
what are the 5 types of thyroid cancer
- papillary 60%
- follicular <25%
- medullary 5%
- lymphoma 5%
- anaplastic (rare)
42
what kind of thyroid cancer does radiation cause
papillary carcinomas
43
what kind of thyroid cancer does iodine deficiency cause
follicular carcinomas
44
clinical presentation of thyroid carcinomas
painless, palpable, solitary thyroid nodule
hard and fixed
rapid growth
45
investigations for thyroid carcinoma
- head and neck examination
- fine-needle aspiration biopsy
- indirect laryngoscopy
- serum calcitonin (high in medullary)
46
papillary thyroid carcinoma
- younger patients
- spread to lymph nodes and lungs
- treatment = total thyroidectomy, consider node excision/ radioiodine to ablate residual cells
- levothyroxine
47
follicular thyroid carcinoma
Middle age
Spreads early via blood (bone, lungs)
Treatment – total thyroidectomy + T4 suppression + radioiodine ablation
48
medullary thyroid carcinoma
Sporadic (scattered) or part of MEN syndrome (multiple endocrine neoplasia)
May produce calcitonin which can be used a cancer marker
Treatment – thyroidectomy + node clearance
49
lymphoma thyroid carcinoma
Female: male = 3:1
May present with stridor/ dysphagia
Do full staging pre-treatment (chemotherapy)
Assess histology for mucosa-associated lymphoid tissue (MALT)
50
anaplastic thyroid carcinoma
female, elderly
| - poor response to treatment (excision and radiotherapy)
51
what is Cushing's syndrome
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)
52
what is Cushing's disease
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
53
symptoms of Cushing's
Weight gain
Mood change – depression, lethargy, irritability
Proximal weakness
Gonadal dysfunction – irregular menstruation, erectile dysfunction
Acne
54
signs of Cushing's
Central obesity - round face, supraclavicular fat distribution
Skin and muscle atrophy
Purple abdominal striae
Osteoporosis
55
investigations for Cushing's
-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
56
management of Cushing's
- Iatrogenic – stop medications if possible
| - Cushing’s disease – selective removal of pituitary adenoma
57
pathology of acromegaly
- excess GH stimulates growth of bone and soft tissue through secretion of insulin-like growth factor 1
- abnormal growth of hands, feet and face
58
symptoms of acromegaly
```
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
```
59
signs of acromegaly
```
Growth of hands
Coarsening face; wide nose
Macroglossia (big tongue)
Puffy lips, eyelids and skin
Obstructive sleep apnoea
Goitre
```
60
differential diagnoses for acromegaly
Marfan syndrome
Precocious puberty
Prolactinoma
Gigantism
61
investigations for acromegaly
```
-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
why can't GH be relied on alone for diagnosing acromegaly
- GH secretions are pulsatile and increase during pregnancy, stress and sleep
63
management of acromegaly
- pituitary surgery (trans-sphenoidal)
- dopamine agonists (cabergoline)
- radiotherapy
64
what is Conn's syndrome
- primary hyperaldosteronism
| - disease of the adrenal glands involving excess production of aldosterone (independent of the renin-angiotensin system)
65
pathology of Conn's syndrome
- 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
symptoms of Conn's syndrome
-Often asymptomatic
-Signs of hypokalaemia:
Weakness
Cramps
Paraesthesia
Polyuria (excessive urine production)
Polydipsia (excessive thirst)
67
signs of Conn's syndrome
- hypertension
| - low potassium
68
investigations for Conn's syndrome
- investigate for supressed renin and increased aldosterone
- adrenal vein sampling
- U&E (K low or normal )
69
management of Conn's syndrome
- Laparoscopic adrenalectomy
| - Spironolactone (25-100)mg for 4 weeks pre-op controls BP and K+
70
what is secondary hyperaldosteronism
- excess aldosterone production due to high renin from decreased renin perfusion (renal artery stenosis, hypertension, diuretics etc)
71
pathology of adrenal insufficiency
- 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
what is primary adrenal insufficiency (Addison's disease)
Destruction of the adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency
73
what is secondary adrenal insufficiency
Hypopituitarism/ long-term steroid therapy leading to suppression of the pituitary-adrenal axis
74
symptoms of adrenal insufficiency
- Fatigue
- Weight loss
- Dizzy
- Faints
- Poor recovery from illness
- headache
- abdo pain
- diarrhoea/constipation
75
symptoms of adrenal crisis
```
Hypotension and cardiovascular collapse
Fatigue
Fever
Hypoglycaemia
Hyponatraemia and hyperkalaemia
```
76
signs of adrenal insufficiency
Pigmentation and pallor
Primary – Hyperpigmentation
Secondary – no pigmentation
Hypotension
77
investigations for adrenal insufficiency
- 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
management of AI
- Replace the aldosterone with fludrocortisone (for primary AI)
- Hydrocortisone 2/3 times daily to replace the cortisol
- Mineralocorticoids to correct postural hypertension
79
what is diabetes insipidus
- A rare metabolic disorder in which the patient produces large quantities of dilute urine and is constantly thirsty
80
pathology of diabetes insipidus
- deficiency of pituitary hormone vasopressin (AVP)/ADH
| - body can't concentrate urine and too much water is passed
81
cranial diabetes insipidus
- most common
- not enough AVP
- caused by damage to hypothalamus/ pituitary gland (after infection, surgery, brain tumour)
82
nephrogenic diabetes insipidus
- enough AVP but kidneys fail to respond
| - caused by kidney damage or sometimes inherited
83
symptoms of DI
- 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
investigations for DI
- 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
management of DI
- fluid intake increased
- desmopressin to replicate function of AVP in cranial
- thiazide diuretic for nephrogenic DI to reduce vol of urine
86
what is syndrome of inappropriate secretion of ADH
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
causes of syndrome of inappropriate secretion of ADH
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
clinical chemistry of inappropriate secretion of ADH
- Decreased Na+ with decreased or normal urea and creatinine
- Decreased plasma osmolality
- Increased urine osmolality
- Increased urine Na+.
89
signs and symptoms of inappropriate secretion of ADH
- Nausea
- Irritability and headache with mild dilutional hyponatraemia
- Fits and coma with severe hyponatraemia
90
investigations for inappropriate secretion of ADH
- FBC = Na, K, Cl, bicarbonate
| - hyponatraemia with hypo-osmolality (Na >20mmol/L in urine, osmolality >100mOsmol/kg)
91
management of inappropriate secretion of ADH
Treat the cause and restrict the fluid
Consider salt +/- loop diuretic if severe.
Vasopressin receptor antagonists - Vaptan
92
pathophysiology of PTH (parathyroid hormone)
- normally secreted in response to low ionized Ca2+ levels, by 4 parathyroid glands situated posterior to the thyroid.
- negative feedback via Ca2+ levels.
93
primary hyperparathyroidism
- caused by a solitary nodule or hyperplasia of all glands = additional secretive tissue
94
secondary hyperparathyroidism
- 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
tertiary hyperparathyroidism
- occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously after undergoing hyperplastic or adenomatous change
96
symptoms of hyperparathyroidism
- bones = osteoporosis
- stones = kidney stones
- psychic groans = confusion
- abdominal moans = constipation, acute pancreatitis
97
diagnosis of hyperparathyroidism
- Primary = Increased Ca2+ and PTH, Increased ALP – from bone resorption
- Secondary = Low serum calcium, Raised PTH
- Tertiary = Raised calcium, Raised PTH
98
management of hyperparathyroidism
- primary = removal of adenoma
- secondary = calcium correction and treat cause
- calcium mimetic
99
what is hypoparathyroidism
subnormal activity of the parathyroid glands, causing a fall in the blood concentration of calcium and muscular spasms
100
causes of hypoparathyroidism
genetics, autoimmune (polyglandular type 1), infiltration of the parathyroid glands by iron overload (haemochromatosis), parathyroidectomy
101
pathology of hypoparathyroidism
- no PTH to activate vit D so less intestinal and renal absorption of calcium and less calcium release from bones
102
symptoms of hypoparathyroidism
- increased excitability of muscles and nerves. - Numbness around the mouth/ extremities, cramps, tetany, convulsions.
- Chvostek and Trousseau signs
103
what is pseudohypoparathyroidism
- 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
what is pseudopseudohypoparathyroidism
symptoms of pseudohypoparathyroidism are present, but the patient’s response to parathyroid hormone is normal.
105
what is hypercalcaemia of malignancy
- Malignancies of the lung, oesophagus, skin, cervix, breast and kidney.
- tumour secretes parathyroid hormone-related protein which results in increased calcium levels.
106
symptoms of hypercalcaemia of malignancy
- bones, stones, groans and moans
- weight loss
- nausea
- polydipsia and polyuria
- dehydration
- seizure (short QT interval on ECG)
- coma
- many others
107
management
- aggressive rehydration
- bisphosphonates (zoledronic acid IV)
- control underlying malignancy
108
causes of hypocalcaemia
- HAVOC – hypoparathyroidism, acute pancreatitis, vit D deficiency, Osteomalacia, CKD
- respiratory alkalosis
109
clinical presentation of hypocalcaemia
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
complications of hypocalcaemia
```
Dysphagia
Wheezing; bronchospasm
Syncope
Congestive heart failure
Angina
```
111
investigations for hypocalcaemia
- 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
management of hypocalcaemia
- 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
hyperkalaemia
- 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
causes of hyperkalaemia
- 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
clinical presentation of hyperkalaemia
- A fast, irregular pulse
- Chest pain
- Weakness
- Palpitations
- Light-headedness
- dyspnoea
- paraesthesia
- frank muscle paralysis
116
differential diagnoses for hyperkalaemia
Metabolic acidosis
Rhabdomyolysis
Acute tubular necrosis
117
investigations for hyperkalaemia
- 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
acute treatment of plasma potassium >6.5 mmol/L
- calcium gluconate = protects heart from ventricular fibrillation
- insulin and dextrose drives K into cells
- nebulised salbutamol
- calcium resonium
119
management of hyperkalaemia
- 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
what is the main cause of hypokalaemia
- dehydration
| - increase in aldosterone
121
pathology of hypokalaemia
- 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
causes of hypokalaemia
```
Diuretics - hyperaldosteronism
Vomiting and diarrhoea
Pyloric stenosis
Intestinal fistula
Cushing’s syndrome/ steroids/ ACTH
Conn’s syndrome
Alkalosis
```
123
clinical presentation of hypokalaemia
```
Muscle weakness
Hypotonia
Hyporeflexia
Cramps
Tetany (intermittent muscular spasms)
Palpitations
Light-headedness (arrhythmias)
Constipation
```
124
investigations for hypokalaemia
- K <2.5mmol/L = urgent
- ECG = T wave inversion, prominent U wave
- Urine potassium, sodium and osmolality
125
management of hypokalaemia
- 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
what are neuroendocrine tumours
Tumours that form from cells that release hormones into the blood in response to a signal from the nervous system
127
3 vital signs for neuroendocrine tumours
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
what is a prolactinoma
lactotroph cell tumour of the pituitary
129
sizes of prolactinomas
Microadenoma – tumour <1cm
Macroadenoma – tumour >1cm
Microprolactinoma – virtually always stays small
Macroprolactinoma – can be massive
130
clinical presentation of prolactinoma
- local effect of tumour
- effect of prolactin = menstrual irregularity/ amenorrhoea, Galactorrhoea, Infertility, Loss of libido, Low testosterone in men
131
diagnosis of prolactinoma
- US
- CT
- MRI
- PET
132
management of prolactinoma
dopamine agonists (cabergoline)
- remarkable shrinkage with macroadenoma
- microadenoma respond to small dose of cabergoline twice a week
133
what is a pheochromocytoma
Catecholamine (adrenaline) secreting tumour.
134
pathology of pheochromocytoma
tumours of the chromaffin cells of the medulla that produce catecholamine
135
clinical presentation of pheochromocytoma
```
Episodic Headaches
Palpitations
Sweating
Tremor
Anxiety and nausea
Hypertension
Tachycardia
Pallor
```
136
investigations for pheochromocytoma
- 24 hour urine collection for urinary catecholamines and metabolites
- Plasma catecholamines
137
management of pheochromocytoma
-surgery preceded by alpha and beta blocker to stagger adrenaline loss
138
what is a carcinoid tumour
Neuroendocrine tumours that particularly affect the small bowel, large bowel or appendix
139
common sites for carcinoid tumours
appendix (45%), ileum (30%), rectum (20%), or elsewhere in GI tract
140
pathology of carcinoid tumours
- tumours of enterochromaffin cell origin
| - secrete bioactive compounds if metastasise to liver (carcinoid syndrome)
141
what is carcinoid syndrome
collection of symptoms some people get when a neuroendocrine tumour (usually hepatic involvement) releases hormone such as serotonin into the blood stream
142
symptoms of carcinoid tumours
Bronchoconstriction
Diarrhoea
Skin flushing
143
carcinoid crisis
- 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
investigations for carcinoid tumours
-Increased 24h urine 5-hydroxyindoleacetic acid (5HIAA)
CXR + chest/pelvis MRI/CT
Echocardiography (investigate carcinoid heart disease)
Liver ultrasound (metastases)
145
management of carcinoid tumours
- octreotide = blocks release of tumour mediators
- loperamide for diarrhoea
- tumour resection
