Endocrinology Flashcards
Mechanism of action of metformin
Increases insulin sensitivity
Decreases glucose production by the liver
SEs metformin
- GI symptoms, including pain, nausea, and diarrhoea
- Lactic acidosis
SGLT-2 inhibitors naming
End in -gliflozin
Mechanism of action of SGLT-2 inhibitors
Inhibit sodium-glucose co-transporter 2 protein found in proximal tubules of kidneys, causing glucose to be lost to urine
Can SGLT-2 inhibitors cause hypoglycaemia?
Yes if combined with insulin or sulfonylureas
Use of SGLT-2 inhibitors in heart failure
Reduce risk of cardiovascular disease, empagliflozin and dapagliflozin licensed for heart failure
Use of SGLT-2 inhibtors in CKD
Dapagliflozin licensed in CKD
SEs SGLT2 inhibitors
- Glycosuria
- Increased UO and frequency
- Genital and urinary tract infections
- Weight loss
- DKA (with only moderately raised glucose)
- Lower-limb amputation (with canagliflozin)
- Fournier’s gangrene
Thiazolidinedione e.g.
Pioglitazone
Mechanism of action of pioglitazone
- Increases insulin sensitivity
- Decreases liver production of glucose
SEs pioglitazone
- Weight gain
- Heart failure
- Increased risk of bone fractures
- Small increase risk of bladder cancer
Sulfonylurea e.g.
Gliclazide
Mechanism of action of sulfonylureas
Stimulate insulin release from pancreas
SEs sulfonylureas
Weight gain
Hypoglycaemia
DPP-4 inhibitors e.g.
Sitagliptin
Alogliptin
SEs DPP-4 inhibitors
Headaches
Acute pancreatitis
GLP-1 mimetics e.g.
Exenatide
Litaglutide
Route of administration GLP-1 mimetics
SC injection
Other use of litaglutide
Weight loss in non-diabetic obese patients
SEs GLP-1 mimetics
Reduced appetite
Weight loss
GI symptoms, including discomfort, nausea, and diarrhoea
Rapid acting insulin e.g.
NovoRapid
Cause acromegaly
Excess GH secreted by pituitary adenoma in 95% cases
Minority cases caused by ectopic GNRH or GH production by tumours, e.g. pancreatic
Features acromegaly
Coarse facial appearance, spade-like hands, increase in shoe size
Large tongue, prognathism, interdental spaces
Excessive sweating and oily skin
Features of pituitary tumour
Hypopituitarism
Headaches
Bitemporal hemianopia
Complications acromegaly
Hypertension
Diabetes
Cardiomyopathy
Colorectal cancer
Prolactin in acromegaly
1/3 of patients have raised prolactin → galactorrohoea
First line investigation acromegaly
Serum IGF-1 levels
What to do if serum IGF-1 raised
OGTT
Interpretation of OGTT in acromegaly
In normal patients, GH suppressed to <2mu/L with hyperglycaemia
In acromegaly no suppression of GH
Further investigations acromegaly
Pituitary MRI may demonstrate pituitary tumour
What is Addison’s disease
Autoimmune destruction of adrenal glands, leading to reduced cortisol and aldosterone - accounts for 80% of cases of primary hypoadrenalism
Features Addison’s disease
Lethargy
Weakness
Anorexia, nausea and vomiting, weight loss
Salt craving
Hyperpigmentation, esp palmar creases
Vitiligo
Loss of pubic hair in women
Hypotension
Hypoglycaemia
Hyponatraemia and hyperkalaemia
Features Addisonian crisis
Collapse
Shock
Pyrexia
Other cause of primary hypoadrenalism
TB
Metastases, e.g. bronchial carcinoma
Meningococcal septicaemia
HIV
Antiphospholipid syndrome
Secondary causes hypoadrenalism
Pituitary disorders - tumours, irradiation, infiltration
First line investigation Addison’s disease
ACTH stimulation test (short Synacthen test)
How is short synacthen test carried out
Plasma cortisol measured before and 30 mins after 250ug IM synacthen
Investigations of Addison’s when SST not available
9am serum cortisol
Interpretation 9am serum cortisol in Addisons
> 500nmol/L makes Addison’s very unlikely
<100nmol/L definately abnormal
100-500nmol needs ACTH stimulation
Electrolyte abnormalities in Addison’s
Hyperkalaemia
Hyponatraemia
Hypoglycaemia
Metabolic acidosis
Management Addison’s disease
Hydrocortisone - 2 to 3 divided doses, typically need 20-30mg/day
Fludrocortisone
Management Addison’s during intercurrent illness
Glucocorticoid dose should be doubled, fludrocortisone dose stays the same
Use of carbimazole
Used in thyrotoxicosis - typically given in high doses for 6 weeks until patient becomes euthyroid before being reduced
Adverse effects carbimazole
Agranulocytosis
Crosses placenta (can be used in low doses during pregnancy)
Glucocorticoid vs mineralocorticoid activity fludrocortisone
MInimal gluco
Very high mineralo
Glucocorticoid vs mineralocorticoid activity hydrocortisone
Some gluco
High mineralo
Glucocorticoid vs mineralocorticoid activity prednisolone
Predominant glucoco
Low mineralo
Glucocorticoid vs mineralocorticoid activity dexamethasone/betmethasone
Very high gluco
Minimal mineralo
Endocrine SEs glucocorticoids
Impaired glucose regulation
Increased appetite/weight gain
Hirsuitism
Hyperlipidaemia
Cushing’s
MSK SEs glucocorticoids
Osteoporosis
Proximal myopathy
Avascular necrosis of femoral head
Immunosuppressive SEs glucocorticoids
Increased susceptibility severe infection
Reactivation of TB
Psychiatric SEs glucocorticoids
Insomnia
Mania
Depression
Psychosis
GI SEs glucocorticoids
Peptic ulceration
Acute pancreatitis
Opthalmic SEs glucocorticoids
Glaucoma
Cataracts
Other SEs glucocorticoids
Suppression of growth in children
Intracranial HTN
Neutrophilia
SEs mineralocorticoids
Fluid retention
Hypertension
When is gradual withdrawal of steroids required
More than 40mg pred daily for more than 1 week
More than 3 weeks of treatment
Recently received repeated courses
ACTH dependant causes Cushing’s syndrome
Cushing’s disease
Ectopic ACTH production, e.g. SCLC
What is Cushing’s disease
Pituitary tumour secreting ACTH → adrenal hyperplasia
ACTH independent causes Cushin’s syndrome
Iatrogenic - steroids
Adrenal adenoma
Adrenal carcinoma
Carney complex (syndrome including cardiac myxoma)
Micronodular adrenal dysplasia
Causes pseudo-Cushing’s
Alcohol excess
Severe depression
How to differentiate Cushings syndrome and pseudocushings
Insulin stress test
Features Cushing’s
Round face
Central obesity
Abdominal striae
Buffalo hump
Proximal limb muscle wasting
Hirsuitism
Easy bruising, poor skin healing
Findings on gas Cushings
Hypokalaemic metabolic alkalosis
First line test Cushing’s syndrome
Overnight dexamethasone suppression test
Other tests to confirm Cushing’s syndrome
24 hr urinary free cortisol
Bedtime salivary cortisol
Both need 2 measurements
Finding on overnight dexamethasone supression test in Cushing’s
Patients with Cushing’s do not have their morning cortisol spike suppressed
First line localisation tests Cushing’s syndrome
9am and midnight plasma ACTH and cortisol
Interpretation 9am and midnight ACTH in Cushing’s
If ACTH suppressed, non-ACTH dependent cause likely
Other localisation tests Cushing’s syndrome
High-dose dexamethasone suppression test
CTH stimulation
Petrosal sinus sampling of ACTH
Insulin stress test
Interpretation high-dose dexamethasone suppression test
If cortisol suppressed and ACTH suppressed, Cushing’s disease (pituitary adenoma → ACTH secretion
If cortisol not suppressed but ACTH is, Cushing’s syndrome due to other causes
If neither cortisol or ACTH suppressed, ectopic ACTH syndrome
Interpretation CRH stimulation in Cushings
If pituitary source, cortisol rises
If ectopic/adrenal, no change in cortisol
Use of petrosal sampling in Cushing’s
Differentiate between pituitary and ectopic ACTH secretion
Use of insulin stress test in Cushing’s
Differentiate between Cushing’s and pseudo-Cushings
C-peptide in T1DM
Typically low
Use of antibodies in diagnosis of diabetes mellitus
Useful to distinguish between T1DM and T2DM
Antibodies in T1DM
Anti-GAD
Islet cell antibodies
Insulin autoantibodies
Insulinoma associated 2 autoantibodies (IA-2A)
Diagnostic criteria T1DM
If symptomatic:
- Fasting glucose greater than or equal to 7.0mmol/L
- Random glucose greater than or equal to 11.1mmol/L
If asymptomatic, above criteria on 2 seperate occasions
Features favouring T1DM over T2DM
Ketosis
Rapid weight loss
Age of onset below 50
BMI below 25
Personal and/or family history autoimmune disease
When to consider further tests to distinguish T1DM from T2DM
If T1DM suspected, but clinical presentation involves some atypical features, e.g. over 50, BMI over 25, slow evolution of hyperglycaemia
Features favouring T2DM over T1DM
Over 40
Respond well to oral hypoglycaemic
Criteria for diagnosis of T2DM
If symptomatic:
- Fasting glucose greater than or equal to 7.0mmol/L
- Random glucose greater than or equal to 11.1mmol/L
- HbA1c ≤48mmol/mol (6.5%)
If asymptomatic, above criteria on 2 seperate occasions
When can’t HbA1c be used to diagnose diabetes
Haemoglobinopathies
Haemolytic anaemia
Untreated iron deficiency anaemia
Suspected gestational diabetes
Children
HIV
CKD
Taking medications that may cause hyperglycaemia, e.g. corticosteroids
Criteria impaired fasting glucose
Fasting glucose ≥6.1 but <7.0
Criteria impaired glucose tolerance
Fasting plasma glucose less than 7.0, OGTT value ≥7.8mmolL but less than 11.1
Diabetic drug adjustments for Ramadan
For patients taking metformin, dose split 1/3 before sunrise and 2/3 after sunset
For patients on OD sulfonylureas, change to after sunset. For BD, larger proportion of dose taken after sunset
Screening for diabetic foot disease
At least annually
Ischaemia - palpating for dorsalis pedis and posterior tibial pulse
Neuropathy - 10g monofilament various parts of sole of foot
Low risk diabetic foot disease criteria
No risk factors except callus alone
Moderate risk diabetic foot disease criteria
Deformity
Neuropathy
Non-critical limb ischaemia
High risk diabetic foot disease criteria
Previous ulceration
Previous amputation
Renal replacement therapy
Neuropathy and non-critical limb ischaemia
Neuropathy with callus and/or deformity
Non-critical limb ischaemia with callus and/or deformity
Diagnostic criteria DKA
Glucose >11 or known diabetes
pH >7.3
Bicarb <15
Ketones >3mmol/L or urine ketones ++
Management DKA
- Fluid replacement
- Insulin
- Correcting electrolyte disturbance
Insulin regime in DKA
IV insulin infusion started at 0.1unit/kg/hour
Once glucose <14, infusion of 10% dextrose should be started at 125ml/hour in addition to 0.9% NaCl regime
Management of potassium in DKA
Serum potassium often high on admission, but quickly falls with insulin treatment, resulting in hypokalaemia, so potassium added to replacement fluids
If rate of K infusion greater than 20mmol/hour, cardiac monitoring
Management of regular insulin in DKA
Long acting insulin continued, short acting insulin stopped
How much potassium to add to replacement fluids in DKA
If K over 5.5, none
If K 3.5-5.5, 40mmol/L
If K below 3.5, senior review
DKA resolution defined as
pH >7.3
Blood ketones <0.6mmol/L
Bicarb >15
When should DKA resolution be achieved by
Within 24 hours - if not, senior review from endocrinologist
When can patient switch to SC insulin in DKA
Once resolution criteria met and patient eating and drinking
Complications DKA
- Gastric stasis
- Thromboembolism
- Arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
- ARDS
- AKI
Iatrogenic due to incorrect fluids - cerebral oedema, hypokalaemia, hypoglycaemia
Who is at most risk from cerebral oedema in DKA treatment
Children/young adults
Presentation cerebral oedema in DKA treatment
Headache
Irritability
Visual disturbance
Focal neurology
When does cerebral oedema occur in DKA treatment
4-12 hours after commencing treatment
Investigation suspected cerebral oedema in DKA treatment
CT head
Presentation diabetic peripheral neuropathy
Typically sensory loss not motor - glove and stocking distribution
First line treatment pain from diabetic peripheral neuropathy
Amitriptyline, duloxetine, gabapentin, or pregabalin
‘Rescue therapy’ for exacerbation of pain diabetic peripheral neuropathy
Tramadol
Treatment localised neuropathic pain in diabetes
Topical capsaicin
GI autonomic neuropathy in diabetes causes…
Gastroparesis
Chronic diarrhoea
GORD
Symptoms gastroparesis diabetes
Erratic glucose control
Bloating
Vomiting
Management gastroparesis diabetes
Metoclopramide
Domperidone
Erythromycin
Features chronic diarrhoea caused by diabetic neuropathy
Often occurs at night
Causes of falsely low HbA1c
Sickle cell anaemia
G6PD deficiency
Hereditary spherocytosis
Haemodialysis
Causes of falsely high HbA1c
Vitamin B12/folic acid deficiency
Iron-deficiency anaemia
Splenectomy
What is Graves disease
Autoimmune thyroid disease in which body produces IgG antibodies to TSH receptor, stimulating it
Features specific to Graves disease
Eye signs - exopthalmos, opthalmoplegia
Pretibial myxoedema
Thyroid acropachy - digital clubbing, soft tissue swelling of hands and feet, periosteal new bone formation
Autoantibodies seen in Graves
TSH receptor stimulating antibodies (90%)
Anti-thyroid peroxidase antibodies (75%)
Thyroid scintigraphy in Graves
Diffuse, homogenous, increased uptake of radioactive iodine
Initial treatment to control symptoms in Grave’s diseasea
Propanolol
First line definitive treatment Grave’s disease
Anti-thyroid drugs
Anti-thyroid drug therapy in Graves
Carbimazole - started at 40mg and reduced gradually to maintain euthyroidism
How long is carbimazole continued for in Grave’s
Typically 12-18 months
Major complication of carbimazole therapy
Agranulocytosis
Second line definitive treatment Grave’s disease
Radioiodine treatment
Indications radioiodine treatment in Graves
Relapse following or resistance to anti-thyroid drug treatment
Contraindications radioiodine treatment for Graves
Pregnancy (should be avoided for 4-6 months after)
Age <16
Thyroid eye disease relative contraindication - may worsen condition
Aftermath of radioiodine treatment
Majority of patients need thyroxine supps after 5 years
Pathophysiology gynaecomastia
Due to increased oestrogen:androgen ratio
Causes of gynaecomastia
Physiological - normal in puberty
Syndromes with androgen deficiency - Kallmans, Klinefilters
Testicular failure, e.g. mumps
Liver disease
Testicular cancer
Ectopic tumour secretion of oestrogen
Hyperthyroidism
Haemodialysis
Drugs
Drugs causing gynaecomastia
Spironolactone
Cimetidine
Digoxin
Cannabis
Finasteride
GnRH agonists, e.g. goserelin, buserelin
Oestrogens, anabolic steroids
What is Hashimoto’s thyroiditis
Autoimmune disorder of thyroid gland, typically associated with hypothyroidism but may be transient thyrotoxicosis in acute phase
Features Hashimoto’s thyroiditis
Features of hypothyroidism
Firm, non-tender goitre
Antibodies in Hashimoto’s thyroiditis
Anti-thyroid peroxidase (TPO)
Anti-thyroglobulin (Tg) antibodies
Conditions associated with Hashimoto’s thyroiditis
Other autoimmune conditions, e.g. coeliac, T1DM, vitiligo
MALT lymphoma
Most common causes hypercalcaemia (90% of cases)
Primary hyperparathyroidism
Malignancy
Causes of hypercalcaemia in malignancy
PTHrP from tumour, e.g. squamous cell lung cancer
Bone mets
Myeloma
Other causes hypercalcaemia
Sarcoidosis
Vitamin D intoxication
Acromegaly
Thyrotoxicosis
Milk-alkali syndrome
Thiazides, calcium containing antacids
Dehydration
Addison’s disease
Paget’s disease of bone
HHS precipitating factors
Intercurrent illness
Dementia
Sedative drugs
Presentation HHS
Comes on over many days, so dehydration and metabolic distubances may be worse than DKA
Dehydration, polyuria, polydipsia
Lethargy, N&V
Altered consciousness, focal neurological deficits
Hyperviscosity - MI, stroke, thrombosis
HHS not diagnostic criteria but what you see
Hypovolaemia
Marked hyperglycaemia (>30mmol/L)
Significantly raised serum osmolarity (>320mosmol/kg)
No significant hyperketonaemia
No significant acidosis
Management HHS
Fluid replacement
VTE prophylaxis
Fluid losses in HHS estimation
100-220ml/kg
Fluid used for replacement HHS
0.9% NaCl
Role of insulin in HHS
Should not be given unless blood glucose stops falling while giving IV fluids
Causes hypoglycaemia
Insulinoma
Insulin/sulphonylureas
Liver failure
Addison’s disease
Alcohol
Effects of glucose <3.3
Causes autonomic symptoms due to release of glucagon and adrenaline, causing:
- Sweating
- Shaking
- Hunger
- Anxiety
- Nausea
Effects of glucose <2.8
Cause neuroglycopenic symptoms due to inadequate glucose supply to brain:
- Weakness
- Vision changes
- Confusion
- Dizziness
Investigation hypoglycaemia
If cause of hypoglycaemia unclear, measure insulin and c-peptide
High insulin and high c-peptide interpretation
Endogenous insulin production - insulinoma, sulphonylurea use/abuse
High insulin, low c-peptide interpretation
Exogenous insulin administration - exogenous insulin overdose, factitious disorder
Low insulin, low c-peptide interpretation
Non-insulin related cause, e.g. alcohol-induced hypoglycaemia, critical illness, adrenal insufficiency, GH deficiency, fasting/starvation
Community management hypoglycaemia
Oral glucose 10-20g in liquid, gel, or tablet form
Hospital management hypoglycaemia
If patient alert, quick acting carbohydrate
If patient unconscious or unable to swallow, SC or IM injection glucagon, or IV 20% glucose solution
Bloods in primary hypoparathyroidism
Low calcium, high phosphate
Treatment primary hypoparathyroidism
Alfacalcidol
Symptoms of hypoparathyroidism
Secondary to hypocalcaemia:
- Tentany - muscle twitching, cramping, spasm
- Perioral paresthesia
- Trousseau’s sign
- Chvostek’s sign
- Depression
- Cataracts
What is Trousseau’s sign
Carpal spasm if brachial artery occluded by BP cuff and pressure maintained above systolic
What is Chvostek’s sign
Tapping parotids causes facial muscles to twitch
ECG findings hypoparathyroidism
Prolonged QT interval
Cause pseudohypoparathyroidism
Target cells insensitive to PTH
Other features associated with pseudohypoparathyroidism
Low IQ
Short stature
Shortened 4th and 5th metacarpals
Bloods pseudohypoparathyroidism
Low calcium
High phosphate
High PTH
Diagnosis pseudohypoparathyroidism
Measuring urinary cAMP and phosphate levels following infusion of PTH - in hypoparathyroidism, this will cause increase in cAMP and phosphate. In pseudohypoparathyroidism type I, neither rise. In type II, only cAMP rise
Most common cause hypothyroidism
Hashimoto’s thyroiditis
Other causes hypothyroidism
Subacute (de Quervain’s) thyroiditis
Riedel thyroiditis
After thyroidectomy or radioiodine treatment
Drug therapy
Dietary iodine deficiency
Drug therapy causing hypothyroidism
Lithium
Amiodarone
Anti-thyroid drugs, e.g. carbimazole
Starting dose levothyroxine
50-100mcg OD
25mcg if cardiac disease, 50+, or severe hypothyroidism
When to check thyroid after dose change thyroxine
8-12 weeks
Therapeutic goal of thyroxine therapy
Normalisation of TSH (0.5-2.5)
Adjustment to levothyroxine in pregnancy
Dose increase by at least 25-50mch, TSH monitored carefully aiming for low-normal value
SEs thyroxine
Hyperthyroidism
Reduced bone mineral density
Worsening of angina
AF
Drug interactions levothyroxine
Iron, calcium carbonate - reduce absorption, so should give at least 4 hrs apart
Inheritance Kallman’s syndrome
X linked recessive
Features Kallmans syndrome
Delayed puberty
Hypogonadism, cryptorchidism
Anosmia
Cleft lip/palate and visual/hearing defects in some patients
Blood tests Kallman’s syndrome
Sex hormones low
LH/FSH levels low or inappropriately normal
Management Kallman’s syndrome
Testosterone supplementation
Gonadotrophic supplementation for sperm production if fertility desired
Karyotype Klinefilters
47 XXY
Features Klinefelter’s
Taller than average
Lack of secondary sexual characteristics
Small, firm testes
Infertile
Gynaecomastia
Bloods Klinefelter’s
Elevated gonadotrophins, low testosterone
Examples meglitinides
Repaglinide
Nateglinide
Mechanism of action meglitanides
Increase pancreatic insulin secretion
What kind of patients are meglitanides often used for
Those with erratic lifestyle
Tumours associated with MEN I
Parathyroid
Pituitary
Pancreas, e.g. insulinoma, gastrinoma
Adrenal
Thyroid
Tumours associated with MEN IIa
Medullary thyroid cancer
Parathyroid
Phaeochromocytoma
Tumours associated with MEN IIb
Medullary thyroid cancer
Pheochromocytoma
Marfanoid body habitus
Neuromas
Presentation myxoedema coma
Confusion
Hypothermia
Causes myxodema coma
Severe hypothyroidism
Treatment myxoedema coma
IV thyroid replacement
IV fluid
IV corticosteroids (until possibility of co-existing adrenal insufficiency excluded)
Electrolyte imbalance correction
Sometimes rewarming
BMI underweight
<18.49
Normal BMI
18.5 - 25
Overweight BMI
25-30
Obese class 1 BMI
30-35
Obese class 2 BMI
35-40
Obese class 3 BMI
> 40
Medical management obesity
Orlistat
Liraglutide
Adverse effects orlistat
Faecal urgency/incontinence
Flatulence
Criteria prescription orlistat
Part of overall plan for managing obesity in patients wtih:
BMI 28+ with associated risk factors
BMI 30+
Continued weight loss, e.g. 5% at 3 months
Duration of use orlistat
<1 year
Criteria prescription liraglutide for obesity
BMI 35+
Prediabetic hyperglycaemia 42-47
Associations phaeochromocytoma
MEN II
Neurofibromatosis
Von Hippel-Lindau syndrome
Symptoms phaeochromocytoma
Usually episodic
- Hypertension
- Headaches
- Palpitations
- Sweating
- Anxiety
Investigations phaeochromocytoma
24 hour urinary collection of metanephrines
Treatment phaeochromocytoma
Definitive treatment with surgery, first stabilise with:
Alpha-blocker, e.g. phenoxybenzamine, given before
Beta blocker, e.g. propanolol
Diagnostic criteria prediabetes
Fasting plasma glucose 6.1-6.9mmol/L
HbA1c 42-47 (6-6.4%)
Management prediabetes
Lifestyle modification - weight loss, increased exercise, change in diet
At least yearly f/u with blood tests
Metformin if blood tests progressive despite participation in intensive lifestyle-change programme
Cause impaired fasting glucose
Hepatic insulin resistance
Cause impaired glucose tolerance
Muscle insulin resistance
Whats worse, impaired fasting glucose or impaired glucose tolerance
Impaired glucose tolerance more likely to develop T2DM and cardiovascular disease
Impaired fasting glucose diagnostic criteria
Fasting glucose ≥6.1 but <7
Impaired glucose tolerance diagnostic criteria
Fasting plasma glucose <7, but OGTT ≥7.8 but <11.1
Causes primary hyperaldosteronism
Bilateral idiopathic adrenal hyperplasia (most common)
Adrenal adenoma (Conn’s syndrome)
Unilateral hyperplasia
Familial hyperaldosteronism
Adrenal carcinoma
Features primary hyperaldosteronism
Hypertension
Hypokalaemia
Metabolic alkalosis
Who needs screening for primary hyperaldosteronism
Hypertension with hypokalaemia
Treatment resistant hypertension
First line investigation suspected primary hyperaldosteronism
Aldosterone/renin ratio
Findings plasma aldosterone/renin ratio in primary hyperaldosteronism
High aldosterone levels with low renin levels (negative feedback due to sodium retention from aldosterone)
Further investigation if aldosterone/renin ratio suggests primary hyperaldosteronism
High resolution CT
Adrenal vein sampling
Tests to differentiate between unilateral adenoma and bilateral hyperplasisa
Management adrenal adenoma
Laparoscopic adrenalectomy
Management bilateral adrenocortical hyperplasia
Aldosterone antagonist, e.g. spironolactone
Causes primary hyperparathyroidism
Solitary adenoma (85%)
Hyperplasia
Multiple adenoma
Carcinoma
Symptoms primary hyperparathyroidism
Those of hypercalcaemia
Polydipsia, polyuria
Depression
Anorexia, nausea, constipation
Peptic ulceration
Pancreatitis
Bone pain/fracture
Renal stones
Hypertension
Associations primary hyperparathyroidism
Hypertension
MEN 1 and 2
Blood findings primary hyperparathyroidism
Raised calcium, low phosphate
PTH may be raised or inappropriately normal
X ray findings primary hyperparathyroidism
Pepperpot skul
Osteitis fibrosa cystica
Definitive management primary hyperparathyroidism
Total parathyroidectomy
Conservative management primary hyperparathyroidism
Cinacalcet
Criteria for conservative management primary hyperparathyroidism
Calcium level less than 0.25 above upper limit of normal
Patient >50
No evidence of end organ damage
Features of high prolactin in men
Impotence
Loss of libido
Galactorrhoea
Features of high prolactin women
Amenorrhoea
Galactorrhoea
Osteoporosis
Infertility
Causes of raised prolactin
Prolactinoma
Pregnancy
Oestrogens
Physiological - stress, exercise, sleep
Acromegaly
PCOS
Primary hypothyroidism
Drugs causing raised prolactin
Metoclopramide, domperidone
Phenothiazines
Haloperidol
SSRIs
Opioids
Symptoms seen with pituitary macroadenoma
Headache
Visual disturbance, classically bitemporal hemianopia or upper temporal quadrantanopia
Signs and symptoms of hypopituitarism
Diagnosis prolactinoma
MRI
Management prolactinoma
Majority of symptomatic patients managed with dopamine agonists, e.g. cabergoline, bromocriptine
Surgery if can’t tolerate/fail to respond - trans-sphenoid approach unless significant extra-pituitary extension
What is Riedels thyroiditis
Rare cause of hypothyroidism characterised by dense fibrous tissue replacing normal thyroid parenchyma
Examination findings Riedels thyroiditis
Hard, fixed, painless goitre
Associations Riedels thyroiditis
Retroperitoneal fibrosis
Examples SGLT inhibitors
Canagliflozin
Dapagliflozin
Empagliflozin
Adverse effects SGLT2 inhibiotrs
Urinary and genital infection
Fourniers gangrene
Normoglycaemia ketoacidosis
Increased risk of lower limb amputation
Blood tests sick euthyroid syndrome
TSH, thyroxine, and T3 low
TSH may be inappropriately normal
Treatment sick euthyroid syndrome
No treatment needed - recovers when better from acute illness
Cause subacute (De Quervain’s) thyroiditis
Occurs following viral infection
Phase 1 subacute (De Quervain’s) thyroiditis
Lasts 3-6 weeks - hyperthyroidism, painful goitre, raised ESR
Phase 2 subacute (De Quervain’s) thyroiditis
Lasts 1-3 weeks - euthyroid
Phase 3 subacute (De Quervain’s) thyroiditis
Lasts weeks - months - hypothyroidism
Phase 4 subacute (De Quervain’s) thyroiditis
Thyroid structure and function returns to normal
Thyroid scintigraphy subacute (De Quervain’s) thyroiditis
Globally reduced uptake iodine-131
Management subacute (De Quervain’s) thyroiditis
Usually self limiting, most patients don’t need treatment
Thyroid pain may respond to aspirin or other NSAIDs
In more severe cases, steroids used
Criteria subclinical hypothyroidism
TSH raised, T3/4 normal
No obvious symptoms
Significance subclinical hypothyroidism
Risk of processing towards overt hypothyroidism
When should levothyroxine therapy be considered in subclinical hypothyroidism
If TSH >10 on 2 occasions 3 months apart
If TSH 5.5-10, <65 and symptoms of hypothyroidism
Management asymptomatic subclinical hypothyroidism with TSH 5.5-10
Observe and repeat thyroid function in 6 months
Adverse effects sulfonylureas
Hypoglycaemic episodes
Weight gain
Less commonly:
Hyponatraemia secondary to SIADH
Bone marrow suppression
Hepatotoxicity
Peripheral neuropathy
Sulfonylureas in breastfeeding and pregnancy
Avoid
Example thiazolidinediones
Pioglitazone
Rosiglitazone withdrawn due to concerns about CVS side effects
SEs pioglitazone
- Weight gain
- Liver impairment
- Fluid retention
- Increased risk of cancer
- Bladder cancer
CIs pioglitazone
Heart failure
Monitoring pioglitazone
LFTs
Features hypothyroidism
- Weight gain
- Lethargy
- Cold intolerance
- Dry, cold, yellowish skin
- Non-pitting oedema
- Dry, coase scalp hair, loss of lateral aspect of eyebrows
- Constipation
- Menorrhagia
- Decreased deep tendon reflexes
- Carpal tunnel syndrome
Features hyperthyroidism
- Weight loss
- Manic, restlessness
- Heat intolerance
- Palpitations
- Increased sweating
- Pretibial myxoedema
- Thyroid acropachy
- Diarrhoea
- Oligomenorrhoea
- Anxiety
- Tremor
What is pretibial myxoedema
Erythematous, oedematous lesions above lateral malleoli
TSH/T4 in thyrotoxicosis
TSH low, T4 high
TSH/T4 in primary hypothyroidism
TSH low, T4 low
TSH/T4 in secondary hypothyroidism
TSH low, T4 low
TSH/T4 in sick euthyroid syndrome
TSH low, T4 low
TSH/T4 in subclinical hypothyroidism
TSH low, T4 normal
TSH/T4 in poor compliance with thyroxine
TSH high, T4 low
Most common condition TSH receptor antibodies seen in
Grave’s
Most common condition anti-TPO antibodies seen in
Hashimoto’s thyroiditis
What is thyroid storm
Rare but life-threatening complication of thyrotoxicosis
Thyroid storm precipitating events
Thyroid or non-thyroidal surgery
Trauma
Infection
Acute iodine load, e.g. CT contrast media
Clinical features thyroid storm
Fever >38.5
Tachycardia
Confusion and agitation
N&V
Hypertension
Heart failure
Abnormal liver function test
Management thyroid storm
Symptomatic treatment, e.g. paracetamol
Treatment of underlying precipitating event
Beta blockers, usually IV propanolol
Anti thyroid drugs
Lugol’s iodine
Dexamethasone
Anti thyroid drugs used in thyroid storm
Methimazole or propylthyiouracil
Causes thyrotoxicosis
Graves disease
Toxic nodular goitre
Acute phase of hypothyroid conditions
Amiodarone
Contrast
Conditions causing thyrotoxicosis in the acute phase
Subacute thyroiditis
Post-partum thyroiditis
Hasmimoto’s thyroiditis
