Endocrinology Flashcards
DIABETES
Associated autoantibodies?
Anti - GAD antibodies
HLA-DR3/4
ICA,IAA, IA-2A
DIABETES
Clinical features?
Polyuria Polydipsia weight loss lethargy dehydration vomiting
DIABETES
DKA features?
CRAVATS KD Confusion Reduced urine output / GCS Acidosis Vomiting Abdo pain Tachycardia Shock/ coma
KUSSMAUL breathing
Dehydration
DIABETES
3 types of insulin regime?
Basal - bolus (rapid before meals, long acting for basal)
1,2,3, injections daily (biphasic)
Continuous insulin infusion via pump (regular rapid/short acting)
DIABETES
What should you be careful of when starting insulin
Hypokalaemia
DIABETES
BG targets for waking, before meals and post meals?
waking - 5-7
before meals - 4-7
after meals - 5-9
DIABETES
Complications that need to be monitored?
Retinopathy nephropathy (eGFR + ACR) Diabetic foot CVS risks Thyroid disease
DIABETES
what should be given alongside insulin if BMI over 25?
Metformin
DIABETES
‘sick day’ rules?
corrective dose amount?
Aim for fluid intake of at least 3 litres
extra monitoring + measure ketones
total daily insulin dose divided by 6 (maximum 15 units)
DIABETES
How does diabetic retinopathy occur?
1) Damage to retina leads to ischaemia
2) ischaemia causes release of VEGF which causes growth of weak vessels prone to haemorrhage
DIABETES
DKA diagnosis?
1) Hyperglycaemia (>11.1)
2) Ketosis (ketones >3)
3) Acidosis (pH <7.3 / bicarb <15)
DIABETES
Treatment of DKA?
FIGPICK Fluids (1litre isotonic saline in 1st hour then add K every 2/4 hours after) Insulin (0.1unit/kg/hr infusion) Glucose Potassium (never infuse >10mmol hour) Infection Chart fluid balance Ketones (monitor)
DIABETES
WHen should DKA be resolved?
both the ketonaemia and acidosis should have been resolved within 24 hours. If this hasn’t happened the patient requires senior review from an endocrinologist
DIABETES
why should you be careful with fluid replacement?
Cerebral oedema if overused
DIABETES
test to distinguish between T1 and T2?
C-peptide levels (low in T1)
Diabetes specific antibodies in T1
DIABETES
what drugs should be avoided?
Thiazides and beta blockers as these may cause insulin resistance, impair secretion and alter autonomic response to a hypo
DIABETES
Describe method of action and side effects of the following drug:
Insulin
Direct replacement of insulin
SE: Hypoglycaemia, weight gain, lipodystrophy
DIABETES
Describe method of action and side effects of the following drug:
Glucagon like peptide 1 (GLP-1)
Increase insulin secretion and reduce glucagon secretion
SE: Weight loss (could be beneficial) N+V Dizziness Pancreatitis
DIABETES
Describe method of action and side effects of the following drug:
Metformin
Increase insulin sensitivity and decrease hepatic gluconeogenesis
SE: GI upset and Lactic Acidosis
“do not use if eGFR <30”
DIABETES
Describe method of action and side effects of the following drug:
Sulfonyureas
Stimulate pancreatic beta cells to secrete insulin
SE: Hypoglycaemia Weight gain Hyponatraemia SiADH Increase CV risk/MI
DIABETES
Describe method of action and side effects of the following drug:
Thiazolidinediones
agonists to the PPAR-gamma receptor and reduce peripheral insulin resistance.
SE: Weight gain fluid retention fractures bladder cancer liver impairment
DIABETES
Describe method of action and side effects of the following drug:
DPP-4 inhibitors (Gliptins)
Increase incretin levels which inhibit glucagon secretion
SE:
Increase risk of pancreatitis
GI upset
DIABETES
Describe method of action and side effects of the following drug:
SGLT-2 inhibitors
They reversibly inhibit sodium-glucose co-transporter 2 (SGLT-2) in the renal PCT to reduce glucose reabsorption and increase urinary glucose excretion.
SE: glucoseuria
Increased risk of UTIs
Give examples of
GLP-1
GLP-1 - Exenatide and Liraglutide
Name some Sulfonyureas
Gliclazide
Glimepiride
Name Thiazolidenediones
Pioglitazone
Name DPP-4 inhibitors
Gliptins
Name SGLT-2 drugs
Drugs ending -glifozin
T2DM
HbA1c targets?
48 if newly diagnosed
53 for diabetics moved beyond metformin
T2DM
When should another medication be added?
If HbA1c >58mmol/L (7.5%)
T2DM
Metformin is first line treatment. what is the stepwise treatment after this
2nd - \+ gliptin \+ sulfonyurea \+ pioglitazone \+ SGLT-2 inhibitor
3rd (any 2 but not gliptin with pioglitazone or SGLT-2)
M + Sulf + G
M + Sulf + P
M + Sulf + SGLT-2
M + P + SGLT-2
T2DM
Final medical stepwise treatment?
Metformin + Sulfonyurea + GLP-1 mimetic
if BMI over 35 and insulin contraindicated
T2DM
Stepwise treatment if Metformin not tolerated
1st - Gliptin, Pioglitazone or Sulfonyurea
2nd - Any two of above combined
3rd - Insulin
Diagnosis of gestational diabetes
Fasting >5.6
2hr >7.8
(5678 rule)
when should insulin be immediately given in gestational diabetes?
IF fasting glucose >7mmol/L
IF diabetic patients are pregnant what should be given?
1) Folic acid 5mg for 12 weeks
2) Aspirin from 12 weeks to reduce risk of pre-eclampsia
3) Anomaly scan at 20 weeks
4) Only metformin and insulin allowed
Glucose targets for pregnant women?
Fasting : 5.3
2 hours after meal : 6.4
1 hour after meal: 7.8
What could be given if insulin / metformin contraindicated or refused in Gestational DM?
Glibenclamide
when is DKA pronounced resolved
Bicarb >15
pH >7.3
blood ketones <0.6mmol/L
What are the treatment targets (hourly) for DKA
Ketones falling by 0.5mmol/hr
Bicarb rise by 3mmol/hr
Glucose falls by 3mmol/hr
Complications of DKA?
Arrhythmias ARDS AKI Cerebral Oedema (rapid correction of fluids) Hypophosphataemia VTE
Cerebral Oedema clinical features and what should be done if suspected?
Headache with reduced GCS + rapid decrease in osmolality
CT head if suspected (children are most vulnerable)
How does Diabetic foot occur?
Peripheral arterial disease reduces blood supply - reduced pulses and ABPI
Neuropathy means loss of sensation
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)
What is it?
Hyperglycaemia and hyperviscosity of blood
Hyperglycaemia = osmotic diuresis with Na/K loss
Hyperviscosity = due to hypertonicity - increased risk of MI / stroke / thromboses
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)
Early signs and later signs?
Early - polydipsia, polyuria
Late - Dehydration, focal neuro signs, reduced consciousness / hypotension, altered mental status, N+V
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)
Diagnosis?
Hypotension
Hyperglycaemia >30mmol/L without significant ketonaemia or acidosis
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)
Treatment?
IV 0.9% NaCl - fluid restoration (0.45% if osmolarity not decreasing)
3-6L in 12hrs (50% in 1st 12hrs)
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)
When is rising sodium a concern?
Only a concern if osmolality not declining concurrently
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)
When is insulin given?
Only give if significant ketonaemia is present
> 1mmol/L
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)
Treatment targets?
Osmolality decrease by 3-8mosm/kg/hr
Glucose decrease by 5mmol/L/hr
HYPERGLYCAEMIC HYPEROSMOLAR STATE (HSS)
What should be given prophylactically?
LMWH - due to high risk of thrombotic complications
What is IRMA
Intra retinal microvascular abnormalities
Types of Diabetic Retinopathy?
Non proliferative and proliferative
DIABETIC RETINOPATHY
Describe mild and severe NDPR
Mild - 1 microaneursym
Severe - blot haemorrhages and microaneurysms in 4 quadrants
IRMA in at least 1 quadrant
venous beading in at least 2 quadrants
DIABETIC RETINOPATHY
Describe Proliferative
Retinal neovascularisation due to vascular endothelial growth factor (creating new weak vessels) which are prone to haemorrhage
HYPERTHYROIDISM
Autoantibodies?
TSH receptor antibodies (Graves - 90/100%)
Anti thyroid peroxidase (TPO) - 75%
HYPERTHYROIDISM
What are TSH receptor antibodies
They mimic TSH and stimulate thyroid gland
HYPERTHYROIDISM
Secondary causes?
drug causes?
Increased TSH due to hypothalamus pituitary dysfunction
Amiodarone
HYPERTHYROIDISM
Second most common cause?
typical features and treatment
Toxic multinodular Goitre - continously producing thyroid hormone with no feedback
> 50 year olds with firm nodules on palpation and patchy uptake on nuclear scintigraphy
Treatment = Radioiodine therapy
HYPERTHYROIDISM
Specific Graves features?
Exopthalmos - eye bulging
Pretibial myxoedema - waxy oedematous deposits of mucin under skin
Thyroid Acropachy Triad
1) Clubbing
2) Soft tissue swelling
3) Periosteal new bone formation
+ DIFFUSE GOITRE
Universal Thyroid signs?
Hyperthyroid
General - Heat intolerance, weight loss, manic restlessness
Cardio - palpitations
Skin - increased sweating, pretibial myxoedema, acropachy (clubbing)
GI - Diarrhoea
Gynae - oligomenorrhoea
Neuro - anxiety, tremor
Universal Thyroid signs?
Hypothyroid
General - Cold intolerance, weight gain, lethargy
Cardio - Bradycardia
Skin - Dry skin, dry coarse hair, non pitting oedema
GI - Constipation
Gynae - Menorrhagia
Neuro - Decreased tendon reflexes, carpal tunnel syndrome
what is De quervains thyroiditis?
Triad of symptoms?
Painful swelling in thyroid due to Viral infection. Hyperthyroid phase to hypothyroid phase then back to normal
triad of :
- Fever
- Neck pain tenderness
- Dysphagia
Treatment of De Quervains thyroiditis?
NSAIDs for pain
Beta blockers for symptom relief in hyperthyroid phase
Treatment of De Quervains thyroiditis?
NSAIDs for pain
Beta blockers for symptom relief in hyperthyroid phase
Signs of Thyroid Storm?
Precipitants of thyroid storm?
pyrexia, tachycardia, agitation, confusion, N+V in already established thyrotoxicosis patients
precipitants: Trauma, infection, surgery, acute iodine load (CT contrast media)
Treatment of Thyroid Storm?
IV propanolol
Dexamethasone converts T4 to T3
HYPERTHYROIDISM
Treatment?
1st line - Carbimazole
2nd - Propylthiouracil
+ beta blockers propanolol (block adrenaline symptoms)
Alternative - active radio iodine (avoid in pregnant and children)
HYPOTHYROIDISM
most common causes?
Hashimoto’s Thyroiditis
Iodine deficiency (in developing world)
HYPOTHYROIDISM
Medication causes?
Lithium and Amiodarone
HYPOTHYROIDISM
Autoantibodies?
Anti-TPO antibodies and anti- thyroglobulin antibodies
HYPOTHYROIDISM
Causes of secondary?
Hypopituitarism due to tumour, infection or Sheehan Syndrome
HYPOTHYROIDISM
Treatment and its side effects?
What does it interact with?
Levothyroxine
SE:
Reduced bone mineral density
worsening of angina and AF
interacts with iron and calcium carbonate
HYPOTHYROIDISM
Signs on thyroid testing?
Primary - TSH = high T3/T4 = low
Secondary - TSH / T3 / T4 = low
HYPERTHYROIDISM
Pregnancy treatment?
1st trimester = Propylthiouracil
2nd onwards = Carbimazole
Hypothyroidism
Changes when pregnant?
Increase dose of thyroxine by up to 50%
Types of Thyroid Cancer and their % incidence?
Papillary - 70% Follicular - 20% Medullary - 5% Anaplastic - 1% (not responsive to tx/chemo) Lymphoma - rare
What is Medullary cancer of the thyroid?
Cancer of parafollicular cells
increased calcitonin - part of MEN-2 disorder
Treatment of Papillary and Follicular Thyroid Cancer?
Thyroidectomy following by radio iodine to kill residual cells
Every year over thyroglobulin levels tested to detect any recurrent disease
Described MEN-1 disorder and what it consists of
hereditary condition associated with endocrine tumours
3Ps :
- Primary hyperparathyroidism
- Pituitary
- Pancreas
Described MEN-2 disorder
2Ps + M
- Primary hyperparathyroidism
- Pheochromocytoma
- Medullary thyroid cancer
Myxoedema Coma
What is it and what are the signs?
the extreme manifestation of (usually untreated) hypothyroidism.
Confusion + hypothermia
Myxoedema Coma
Treatment?
IV thyroid replacement and fluids
IV corticosteroids (once adrenal insufficiency excluded)
Myxoedema Coma
Treatment?
IV thyroid replacement and fluids
IV corticosteroids (once adrenal insufficiency excluded)
Rare complication of Hypothyroid?
MALT Lymphoma
Most common cause of CKD and glomerular pathology?
Diabetic nephropathy
How is glomerulosclerosis caused by Diabetes and what is the key feature
Treatment?
High levels of glucose passing through glomerulus
Protein/glucoseuria
ACE-I (BP control)
Hypercalcaemia symptoms?
Bones (bone pain) Stones (renal calculi) Groans (abdo pain) Thrones (polyuria) Psychiatric moans (altered mental status)
What produces PTH?
Parathyroid gland Chief cells in response to low calcium
Functions of PTH? (4)
1) Increase calcium absorption from intestines
2) Increase reabsorption from kidneys
3) Increase osteoclast activity (resorption)
4) Convert Vit D to active form
Symptoms of Hypercalcaemia?
Thirst
Polyuria
Constipation
HYPERPARATHYROIDISM
Primary cause and treatmentr?
Solitary adenoma (80%) Hyperplasia (15%)
Removal of tumour
Two main causes of Hypercalcaemia and how does it affect an ECG?
- Primary hyperparathyroid
- Malignancy (squamous cell LC, bone mets, myeloma)
other causes of hypercalcaemia?
Acromegaly Vit D intoxication Addisons Sarcoidosis Thyrotoxicosis/ Thiazides
Dehydration
Treatment of Hypercalcaemia?
Saline rehydration (3-4L daily)
Bisphosphonates / Calcitonin
Cause of secondary Hyperparathyroidism?
Reduced vitamin D/ CKD = reduced calcium absorption / reabsorption - Hypocalcaemia
Cause of Tertiary Hyperparathyroidism?
Prolonged secondary - PT hyperplasia so baseline PTH increases lots
PTH, Calcium and Phosphate levels for all 3 types of Hyperparathyroidism?
Primary - High PTH, High calcium, Low phosphate
Secondary - high PTH, low/normal calcium, high phosphate
Tertiary - High PTH, High calcium. Low or normal phosphate
Why is phosphate high in secondary Hyperparathyroidism
What does phosphate cause
treatment of high phosphate?
its normally excreted by kidneys but isnt properly due to CKD.
high phosphate causes osteomalacia as the phosphate ‘drags out’ calcium from bones
Treatment? reduce phosphate in diet
Signs on X-ray of Primary Hyperparathyroidism?
‘pepperpot skull’ characteristic x-ray sign
Hypoparathyroidism cause and treatment?
PTH,Ca,Phosphate levels?
Primary - secondary to thyroid surgery
Tx - Alfacalcidol
PTH - low Cal - low Phos - high
features of Hypoparathyroid / Hypocalcaemia?
on ECG?
(due to neuromuscular excitability)
Muscle spasm / twitch (tetany)
Perioral parasthesia
Prolonged QT interval
Characteristic signs of Hypocalcaemia?
Trosseau’s sign - Carpal spasm if brachial artery occluded by BP cuff and maintains pressure above systolic BP
Chvostek’s sign - tapping over parotid causes facial muscles to twitch
Causes of Hypocalcaemia?
CRAMP + VIt D deficiency
CKD Rhabdomyolysis Acute Pancreatitis Magnesium deficiency / massive blood transfusion Psuedohypoparathyroid / hypoparathyroid
Acute treatment of Hypocalcaemia?
IV Calcium gluconate (10l of 10% solution of 10 mins)
What is Pseudohypoparathyroidism?
Characteristic appearance?
PTH, Ca, Phosphate levels?
When target cells are insensitive to PTH
Low IQ, short stature with shortened 4th/5th metacarpals (abnormality of G protein)
PTH - high
Calcium - low
Phosphate - high
Diagnosis of Hypoparathyroid?
Urinary cAMP and phosphate following PTH infusion
In HPT - increase in cAMP and phosphate
In PHPT - no increase in phosphate
What is Pseudopseudohypoparathyroidism?
Similar phenotype to PHPT but normal biochemistry
Causes of Hypomagnesaemia?
Alcohol Diarrhoea Drugs (diuretics / PPIs) Hypercalcaemia Hypokalaemia
Features of Hypomagnesaemia?
Similar to hypocalcaemia (tetany)
ECG similar to hypokalaemia
Treatment of Hypomagnesaemia?
<0.4mmol - IV Mg sulphate (40mmol over 24hrs)
> 0.4mmol - Mg salts (can cause diarrhoea)
HYPOKALAEMIA
Causes with Hypertension?
Cushings
Conn’s
Liddles syndrome
HYPOKALAEMIA
Causes without Hypertension?
Diuretics Thiazides GI loss (D+V) Renal Tubular Acidosis Gitelman / Bartters syndrome
HYPOKALAEMIA
Causes with alkalosis?
Thiazides
GI loss (vomiting)
Conn’s
Cushing’s
HYPOKALAEMIA
Causes with acidosis?
GI loss (diarrhoea) Renal tubular acidosis (types 1+2) Acetazolamide
HYPOKALAEMIA
Features?
Hypotonia
Muscle weakness
ECG - (U have no Pot, No T but long PR/QT)
Describe the RAAS and how aldosterone is released
1) Low BP in juxtoglomerular cells causes renin secretion
2) Renin acts on Angiotensinogen (liver) to become Angiotensin I
3) Angiotensin I converted to Angiotensin II by ACE (lung)
4) Angiotensin II causes Aldosterone release
Aldosterone function electrolyte wise?
Increase sodium reabsorption
Increase potassium and hydrogen secretion
Causes of Primary Hyperaldosteronism?
(Conn’s)
Adrenal gland Increase due to:
1) Bilateral adrenal hyperplasia (70%)
2) Adrenal Adenoma (30-40%)
Why does renin decrease in Primary Hyperaldosteronism?
Increase in BP
Secondary cause of Primary Hyperaldosteronism?
Excess Renin when kidney BP > rest of body BP due to:
1) Renal artery stenosis
2) renal artery occlusion
3) Heart failure
How is renal artery stenosis confirmed?
Confirmed with doppler US or CT angiogram / MRA
Hyperaldosteronism
Investigations?
Renin / aldosterone ratio 1st Line
2nd - CT abdo (suspected tumour)
3rd - adrenal venous sampling
Renin and aldosterone levels in primary and secondary Hyperaldosteronism?
Primary = low renin. high aldosterone
Secondary = high renin, high aldosterone
What is the purpose of adrenal venous sampling?
Distinguish between unilateral adenoma and bilateral adrenal hyperplasia
Features of Hyperaldosteronism?
Hypertension
Hypokalaemia e.g muscle weakness, paraesthesia
Management of Hyperaldosteronism?
- Aldosterone antagonists (Epleronone, Spironolactone)
- Surgical removal of tumour
Management of Renal artery stenosis?
Percutaneous renal artery angioplasty (enter through femoral artery)
CUSHING’S
What is ^ syndrome?
SIgns and symptoms after prolonged elevaterd cortisol
CUSHING’S
What is ^ disease?
ACTH secreting pituitary adenoma causing adrenal hyperplasia (80% cause of Cushing’s syndrome)
CUSHING’S
ACTH dependant causes?
Cushing’s disease
Ectopic ACTH (from small cell LC) 5-10%
What is Pseudo Cushing’s?
mimics cushing’s, normally due to alcohol excess
causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
How to differentiate between Cushings and Pseudo?
insulin stress test
CUSHING’S
ACTH independent causes?
Adrenal adenoma
Steroid overuse
CUSHING’S
Symptoms?
Easily bruised
Fatigue
Depression
Sexual dysfunction
CUSHING’S
Signs?
Central Obesity Hump / hyperpigmentation in dependant causes Abdominal striae Moon face Proximal limb muscle wasting/weakness
CUSHING’S
blood signs?
Hypokalaemic metabolic acidosis
CUSHING’S
how to differentiate between ectopic and pituitary secretion of ACTH?
Petrosal sinus sampling
CUSHING’S
Treatment?
Surgically remove tumour (transphenoidal removal of pituitary tumour)
CUSHING’S
describe diagnosis/ localisation test
DEXAMETHASONE SUPPRESSION TEST
1) Initially low dose Dexa given (1mg) at 10pm
2) Measure cortisol levels in morning. Low cortisol = normal High cortisol (not suppressed) = Cushing's Syndrome
3)high dose Dexa given (8mg)
If low cortisol and low ACTH = Pituitary source (Cushing’s disease)
If High/normal cortisol and high ACTH = Ectopic ACTH (e.g. SCLC)
If high/normal cortisol but low ACTH = Adrenal Adenoma
What to do if adrenal adenoma suspected?
CT adrenal gland
What should be given to someone with Addison’s?
Steroid card and emergency ID tag so no doses are missed / emergency services know patient is on lifelong steroids
ADDISON’S
Primary cause?
Autoimmune destruction of adrenal glands (80%) resulting in decreased cortisol and aldosterone
ADDISON’S
Secondary cause?
Inadequate ACTH e.g. damage to pituitary post surgery
OR
Sheehans - pituitary necrosis after childbirth blood loss
ADDISON’S
Tertiary cause?
CRH/ Hypothalamus suppression due to long term oral steroids
ADDISON’S
Features?
Particular feature in primary?
Fatigue, Nausea, Cramps, Reduced libido
Bronze hyperpigmentation - in primary as ACTH causes melonocytes to release melanin
Serum ACTH in primary / secondary addisons?
Primary - high (no negative feedback)
Secondary - low
ADDISON’S
Electrolyte abnormalities?
Hyperkalaemia and Hyponatraemia causing
METABOLIC ACIDOSIS
and Hypoglycaemia
ADDISON’S
Definitive investigations?
Short synacthen test
What is Synacthen?
Synthetic ACTH
ADDISON’S
Adrenal autoantibodies?
Adrenal cortex antibodies
21-hydroxylase antibodies
ADDISON’S
What do the following serum cortisol levels infer?
> 500 nmol/l
< 100 nmol/l
100-500 nmol/l
> 500 nmol/l makes Addison’s very unlikely
< 100 nmol/l is definitely abnormal
100-500 nmol/l should prompt a ACTH stimulation test to be performed
ADDISON’S
Treatment?
Glucocorticoid (replace cortisol) and Mineralocorticoid (replace aldosterone)
(hydrocortisone and fludrocortisone)
How is hydrocortisone given in Addisons?
dose is split with most taken in first half of day (20-30mg daily)
ADDISON’S
How should steroid doses be changed when you’re ill?
Double hydrocortisone dose
Keep fludrocortisone dose the same
ADDISONIAN CRISIS
What is it? Triggers?
Acute severe addisons triggered by:
SSS
Sepsis
Surgery
Stopping long term steroids suddenly
ADDISONIAN CRISIS
Presentation? Electrolytes abnormalities?
1) Reduced consciousness
4 hypo 1 hyper Hypotension Hyponatraemia Hypoglycaemia Hyperkalaemia
ADDISONIAN CRISIS
Treatment?
Hydrocortisone IM/IV 100mg stat then 100mg every 6hrs if still unstable
1L saline over 30-60 mins
Add dextrose if hypoglycaemic
ACROMEGALY
What is and what are the causes?
excess growth hormone due to
Pituitary adenoma (95%)
Rarely lung/ pancreatic cancer secreting ectopic GnRH/GH
ACROMEGALY
Space occupying features?
How are these features caused?
Headache and Bitemporal Hemianopia
Bitemporal Hemianopia due to pituitary increasing in size and putting pressure on nearby optic chiasm
ACROMEGALY
Features in terms of tissue overgrowth?
Frontal bossing
Large facial features/ hands/ feet/ tongue
Protruding jaw (Prognathism)
Excess sweating due to sweat gland hypertrophy
ACROMEGALY
Other features organ related?
Hypertrophic heart
Arthritis from imbalance of joint growth
T2DM
Hypertension
ACROMEGALY
Associated cancers?
Colorectal cancer
Thyroid Cancer
ACROMEGALY
Medical treatment?
Somatostatin Analogues (Octreotide)
Pegvisomant (GH antagonist)
Dopamine Antagonists (Bromocriptine)
ACROMEGALY
Why are somatostatin analogues better than Dopamine agonists
Dopamine agonist block GH but not a potent as somatostatin analogues
ACROMEGALY
Definitive treatment?
Removal of tumour
ACROMEGALY
Investigations?
1st - Serum IGF-1 levels
2nd - OGTT to confirm diagnosis
ACROMEGALY
Imaging to look at suspected pituitary adenoma?
MRI pituitary
ACROMEGALY
What % have Multiple Endocrine Neoplasia? (MEN1)
6%
Carcinoid Syndrome
What is it?
Mets in the liver release serotonin and can secret ACTH/GHRH resulting in cushings
Features of Carcinoid syndrome?
Investigation of Carcinoid syndrome?
Flushing, Diarrhoea, Bronchospasm
Urinary 5-HIAA
Treatment of Carcinoid Syndrome?
Somatostatin Analogue (Octreotide)
What is Octreotide brand name?
Sandostatin
Why should Hyponatraemia be treated slowly?
To prevent Central Pontine Myelinolysis (brain has adapted to low osmolality and correction too quickly will mean major water loss from the brain) - no more than raised by 4 to 6 mmol/l in a 24-hour period
Causes of Hypernatraemia?
dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline
Treatment of Hypernatraemia
Fluids but corrected SLOWLY by no more than 0.5 mmol/hour as to prevent cerebral oedema
Hyponatraemia causes?
water excess or sodium depletion
Causes of pseudohyponatraemia?
hyperlipidaemia (increase in serum volume) or a taking blood from a drip arm
How is a Hyponatraemia diagnosis confirmed?
Urinary sodium and osmolarity levels
Water excess causes?
Water excess (patient often hypervolaemic and oedematous)
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia
Causes of sodium depeltion; extra renal loss?
diarrhoea, vomiting,
sweating
burns,
adenoma of rectum
Causes of Sodium depletion, renal loss?
(patient often hypovolaemic)
diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure
Euvolaemic hyponatraemia causes?
SiADH
Hypothyroidism
Worry if hyponatraemia untreated?
Cerebral Oedema - can in turn cause brain herniation
Treatment of Hyponatraemia if:
Hypovolaemia suspected?
normal, i.e. isotonic, saline (0.9% NaCl)
Treatment of Hyponatraemia if:
Euvolaemic cause suspected?
fluid restrict to 500–1000 mL/day
consider medications:
demeclocycline
vaptans
Treatment of Hyponatraemia if:
a hypervolemic cause is suspected?
fluid restrict to 500–1000 mL/day
consider loop diuretics
consider vaptans
Treatment of Acute Hyponatraemia?
Hypertonic Saline (3% NaCl)
What is Phaeochromocytoma?
Phaeochromocytoma is a rare catecholamine secreting tumour
Test for Phaeochromocytoma?
24 hr urinary collection of metanephrines (sensitivity 97%*)
Treatment for Phaeochromocytoma?
Surgery is the definitive management. The patient must first however be stabilized with medical management:
1) alpha-blocker (e.g. phenoxybenzamine), given before a
2) beta-blocker (e.g. propranolol)
Phaeochromocytoma triad of features?
Sweating, headaches and palpitations
+ hypertension
How to estimate serum osmolality?
Serum osmolality can be estimated using
(2 x Na+) + glucose + urea
Causes of hypoglycaemia?
Exogenous drugs (typically sulfonylureas or insulin) Pituitary insufficiency Liver failure Addison's disease Islet cell tumours (insulinomas) Non-pancreatic neoplasms
What conditions can reduce HbA1c levels?
Sickle-cell anaemia and other haemoglobinopathies such as:
- hereditary spherocytosis
- G6PD deficiency
Treduce RBC lifespan and hence can artificially lower HbA1c levels.
What conditions can increase HbA1c levels?
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy
Treatment for MODY and what is it?
Maturity Onset Diabetes of the Young
Autosomal dominant mutation in the HNF -1 alpha (70%)
Sensitive to sulfonyureas
