MRCP 2 Flashcards
What is abetalipoproteinaemia?
rare autosomal recessive disorder caused by a mutation in the microsomal triglyceride transfer protein.
This results in deficiencies in the apolipoproteins B-48 and B-100.
What are the features of abetalipoproteinaemia?
failure to thrive + developmental delay
steatorrhoea
retinitis pigmentosa
cerebellar signs
deep tendon reflexes are absent
acanthocytosis
hypocholesterolaemia
What is the most common reason for acromegaly?
Pituitary adenoma
Excess GH
A minority of cases are caused by ectopic GHRH or GH production by tumours e.g. pancreatic.
What are the features of acromegaly?
coarse facial appearance, spade-like hands, increase in shoe size
large tongue,
prognathism - profusion of upper jaw
interdental spaces
excessive sweating and oily skin: caused by sweat gland hypertrophy
features of pituitary tumour: hypopituitarism, headaches, bitemporal hemianopia
raised prolactin in 1/3 of cases → galactorrhoea
6% of patients have MEN-1
What conditions are associated with MEN1 ?
MEN-1
What are complications of acromegaly?
hypertension
diabetes (>10%)
cardiomyopathy
colorectal cancer
What is the test of acromegaly?
serum insulin growth factor 1
Previously oral glucose tolerance test with serial growth hormone measurements
If insulin growth factor 1 is equivocal, what test should be done?
Oral glucose tolerance
What is the normal response to growth hormone in oral glucose tolerance?
in normal patients GH is suppressed to < 2 mu/L with hyperglycaemia
in acromegaly there is no suppression of GH
may also demonstrate impaired glucose tolerance which is associated with acromegaly
First line treatment of acromegaly?
Transpehnoidal surgery
When should surgery be used in acromegaly?
If surgery cannot be pursued or is unsuccessful
What medication should be used in acromegaly ?
- somatostatin analogue
- Pegvisomant
- Dopamine antagonists
Mechanism of somatostatin analogue?
Directly inhibits the release of growth hormone
Mechanism of pegvisomant in acromegaly?
GH receptor antagonist - prevents dimerization of the GH receptor
- Does not reduce tumour volume, therefore needs surgery still
Mechanism of dopamine antagonist?
e.g. Bromocriptine
first effective medical treatment for acromegaly, however now superseded by somatostatin analogues
Features of Addisons disease?
lethargy, weakness, anorexia, nausea & vomiting, weight loss, ‘salt-craving’
hyperpigmentation (especially palmar creases)*, vitiligo, loss of pubic hair in women, hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
crisis: collapse, shock, pyrexia
Features of Addison’s crisis?
crisis: collapse, shock, pyrexia
Causes of hypoadrenalism?
Primary causes
- tuberculosis
- metastases (e.g. bronchial carcinoma)
- meningococcal septicaemia (Waterhouse-Friderichsen syndrome)
- HIV
- antiphospholipid syndrome
Secondary causes
- pituitary disorders (e.g. tumours, irradiation, infiltration)
Primary and secondary hypoadrenalism - which one has hypopigmentation?
Primary hypoadrenalism only
Secondary hypoadrenalism is not associated with hypopigmentation
What is the management for Addison’s disease?
combination of:
hydrocortisone: usually given in 2 or 3 divided doses. Patients typically require 20-30 mg per day, with the majority given in the first half of the day
fludrocortisone
What should be given to patients to prevent adrenal crisis?
hydrocortisone injections
Illness in Addisons, what should be done to the steroids?
glucocorticoid dose should be doubled, with the fludrocortisone dose staying the same
Management of addisonian crisis?
hydrocortisone 100 mg im or iv
1 litre normal saline infused over 30-60 mins or with dextrose if hypoglycaemic
continue hydrocortisone 6 hourly until the patient is stable.
fludrocortisone should begin after 24 hours and be reduced to maintenance over 3-4 day
Causes of raised ALP?
liver: cholestasis, hepatitis, fatty liver, neoplasia
Paget’s
osteomalacia
bone metastases
hyperparathyroidism
renal failure
physiological: pregnancy, growing children, healing fractures
Raised ALP + Calcium raised?
Bone metastases
Hyperparathyroidism
Raised ALP + low calcium?
Osteomalacia
Renal failure
Inheritance of androgen insensitivity?
X-linked recessive condition
Phenotype and genotype of androgen insensitivity syndrome?
male children (46XY) to have a female phenotype
Feature of androgen insensitivity syndrome?
‘primary amenorrhoea’
little or no axillary and pubic hair
undescended testes causing groin swellings
breast development may occur as a result of the conversion of testosterone to oestradiol
Diagnosis of androgen insensitivity syndrome?
- buccal genotype
2.after puberty, testosterone concentrations are in the high-normal to slightly elevated reference range for postpubertal boys
Autoimmune polyendocrinopathy syndrome types?
Type 1: Multiple Endocrine Deficiency Autoimmune Candidiasis
Type 2: Schmidt syndrome
Features of type 2 autoimmune polyendocrinopathy syndrome?
Addison’s disease
+
Type 1 diabetes mellitus
+
Autoimmune thyroid disease
Features of type 1 autoimmune polyendocrinopathy syndrome?
Features of APS type 1 (2 out of 3 needed)
chronic mucocutaneous candidiasis (typically first feature as young child)
Addison’s disease
primary hypoparathyroidism
Genotype of Features of type 1 autoimmune polyendocrinopathy syndrome?
autosomal recessive disorder caused by mutation of AIRE1 gene on chromosome 21
Barter syndrome?
Normotensive
Hypokalaemia
Polyurea and polydipsia
What is the mechanism of Bartter syndrome?
severe hypokalaemia due to defective chloride absorption at the Na+ K+ 2Cl- cotransporter (NKCC2) in the ascending loop of Henle
What is the inheritance of barter’s syndrome?
Autosomal recessive
Mechanism of carbimazole?
blocks thyroid peroxidase from coupling and iodinating the tyrosine residues on thyroglobulin → reducing thyroid hormone production
in contrast propylthiouracil as well as this central mechanism of action also has a peripheral action by inhibiting 5’-deiodinase which reduces peripheral conversion of T4 to T3
What is the side effect of carbimazole?
agranulocytosis
crosses the placenta, but may be used in low doses during pregnancy
HPV viruses types related to cervical cancer?
serotypes 16,18 & 33
Risk factors of cervical cancer?
HPV
smoking
human immunodeficiency virus
early first intercourse, many sexual partners
high parity
lower socioeconomic status
combined oral contraceptive pill*
Causes of congenital adrenal hyperplasia?
21-hydroxylase deficiency (90%)
11-beta hydroxylase deficiency (5%)
17-hydroxylase deficiency (very rare)
Test for congenital adrenal hyperplasia?
ACTH stimulation
Features of 21-hydroxylase deficiency features
congenital adrenal hyperplasia?
virilisation of female genitalia
precocious puberty in males
60-70% of patients have a salt-losing crisis at 1-3 wks of age
Features of 11-beta hydroxylase deficiency features
congenital adrenal hyperplasia?
virilisation of female genitalia
precocious puberty in males
hypertension
hypokalaemia
Features of17-hydroxylase deficiency features
congenital adrenal hyperplasia?
non-virilising in females
inter-sex in boys
hypertension
Features of congenital hypothyroidism? (cretinism)
prolonged neonatal jaundice
delayed mental & physical milestones
short stature
puffy face, macroglossia
hypotonia
How is congenital adrenal hyperplasia tested?
Children are screened at 5-7 days using the heel prick test
Minimal glucocorticoid activity, very high mineralocorticoid activity,
Fludrocortisone
Glucocorticoid activity, high mineralocorticoid activity,
Hydrocortisone
Predominant glucocorticoid activity, low mineralocorticoid activity
Prednisolone
Very high glucocorticoid activity, minimal mineralocorticoid activity
Dexamethasone
Betmethasone
Cushing’s: ACTH dependent causes?
Cushing’s disease (80%): pituitary tumour secreting ACTH producing adrenal hyperplasia
Ectopic ACTH production (5-10%): e.g. small cell lung cancer is the most common causes
Cushing’s: ACTH independent causes?
iatrogenic: steroids
adrenal adenoma (5-10%)
adrenal carcinoma (rare)
Carney complex: syndrome including cardiac myxoma
micronodular adrenal dysplasia (very rare)
What is pseudo cushings?
mimics Cushing’s
often due to alcohol excess or severe depression
causes false positive dexamethasone suppression test or 24 hr urinary free cortisol
insulin stress test may be used to differentiate
Biochemisty in bushings disease?
A hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance.
Ectopic ACTH secretion (e.g. secondary to small cell lung cancer) is characteristically associated with very low potassium levels.
Most common tests for cushing disease?
- Overnight dexamethasone suppression test
(sensitive) - 24 hr urinary free cortisol
High dose dexamethasone tests:
Cortisol not suppressed + ACTH suppressed?
Cushing’s syndrome due to other causes (e.g. adrenal adenomas)
High dose dexamethasone tests:
Cortisol surpassed + ACTH suppressed?
Cushing’s disease (i.e. pituitary adenoma → ACTH secretion)
High dose dexamethasone tests:
Cortisol not supressed + ACTH not supressed?
Ectopic ACTH syndrome
How do you differentiate between cushings and pseudocushings?
Insulin stress test
Criteria for diabetes if symptomatic?
fasting glucose greater than or equal to 7.0 mmol/l
random glucose greater than or equal to 11.1 mmol/l (or after 75g oral glucose tolerance test)
Criteria for diabetes if asymptomatic?
HbA1c of greater than or equal to 48 mmol/mol (6.5%) is diagnostic of diabetes mellitus
a HbAlc value of less than 48 mmol/mol (6.5%) does not exclude diabetes (i.e. it is not as sensitive as fasting samples for detecting diabetes)
IF ASSYMPTOMATIC NEEDS TO REPEAT THE TEST
Conditions where HbA1c should not be used?
haemoglobinopathies
haemolytic anaemia
untreated iron deficiency anaemia
suspected gestational diabetes
children
HIV
chronic kidney disease
Positive test result for impaired fasting glucose?
A fasting glucose greater than or equal to 6.1 but less than 7.0 mmol/l implies impaired fasting glucose (IFG)
Criteria for oral glucose tolerance test ?
Impaired glucose tolerance (IGT) is defined as fasting plasma glucose less than 7.0 mmol/l and OGTT 2-hour value greater than or equal to 7.8 mmol/l but less than 11.1 mmol/l
Causes of primary hypothyroidism?
Hashimotos
Subacute thyroiditis (de Quervain’s)
Riedel thyroiditis
After thyroidectomy or radioiodine treatment
Drug therapy (e.g. lithium, amiodarone or anti-thyroid drugs such as carbimazole)
Dietary iodine deficiency
Causes of secondary hypothyroidism?
Down’s syndrome
Turner’s syndrome
coeliac disease
What should you aim HbA1c in diabetes?
48
What blood glucose targets should be in place for T1DM?
5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day
What choice of insulin regimen should patients be given?
Basal bolus only
Twice daily insulin detemir
Once daily insulin glargine
Target for HbA1c on type 2 diabetes with drugs that cause hypoglycaemia?
53
SGLT-2 inhibitors should also be given in addition to metformin when?
the patient has a high risk of developing cardiovascular disease (CVD, e.g. QRISK ≥ 10%)
the patient has established CVD
the patient has chronic heart failure
If standard release metformin is not tolerated, what should be used?
Modified release metformin
What should be used if metformin is contraindicated?
If CVS disease:
- SGLT2 inhibitors
No CVS disease:
DPP‑4 inhibitor or pioglitazone or a sulfonylurea
SGLT-2 may be used if certain NICE criteria are met
Type of insulins needed in basal bolus injection?
offer rapid‑acting insulin analogues injected before meals
twice‑daily insulin detemir is the regime of choice.
Second line therapy for T2DM?
Dual therapy - add one of the following:
metformin + DPP-4 inhibitor
metformin + pioglitazone
metformin + sulfonylurea
metformin + SGLT-2 inhibitor (if NICE criteria met)
Third line therapy T2DM?
metformin + DPP-4 inhibitor + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT-2 if certain NICE criteria are met
insulin-based treatment
Should T2Dm patients get statins?
Primary prevention:
- if QRISK > 10
- egFR > 60
Give atorvastatin 20 mg
Secondary prevention:
- 80 mg atorvastatin
Blood pressure cut off for T2DM?
Clinic first, home second
Age < 80 years 140/90 mmHg 135/85 mmHg
Age > 80 years 150/90 mmHg 145/85 mmHg
Diagnostic criteria for DKA?
Key points
glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick
Management of DKA?
fluid replacement
most patients with DKA are deplete around 5-8 litres
isotonic saline is used initially, even if the patient is severely acidotic
please see an example fluid regime below.
insulin
an intravenous infusion should be started at 0.1 unit/kg/hour
once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr in addition to the 0.9% sodium chloride regime
correction of electrolyte disturbance
serum potassium is often high on admission despite total body potassium being low
this often falls quickly following treatment with insulin resulting in hypokalaemia
potassium may therefore need to be added to the replacement fluids
if the rate of potassium infusion is greater than 20 mmol/hour then cardiac monitoring may be required
long-acting insulin should be continued, short-acting insulin should be stopped
Resolution of DKA?
pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L
Complications of DKA?
gastric stasis
thromboembolism
arrhythmias secondary to hyperkalaemia/iatrogenic hypokalaemia
iatrogenic due to incorrect fluid therapy: cerebral oedema*, hypokalaemia, hypoglycaemia
acute respiratory distress syndrome
acute kidney injury
Management of neuropathy in diabetes?
First line: amitriptyline, duloxetine, gabapentin or pregabalin
treatment does not work try one of the other 3 drug
Rescue therapy: tramadol
Topical capsaicin
How should gastroparesis be managed in diabetes?
metoclopramide, domperidone or erythromycin (prokinetic agents)
Features of gastroparesis?
Bloating
Erratic blood glucose control
Vomiting
Phenotype of androgen insensitivity syndrome? Genotype?
46 XY
Female phenotype
Rudimentary vagina and testes present but no uterus.
Testosterone, oestrogen and LH levels are elevated
Phenotype 5 alpha reductase ? Genotype?
46 XY
Autosomal recessive condition. Results in the inability of males to convert testosterone to dihydrotestosterone (DHT)
ambiguous genitalia in the newborn period. Hypospadias is common. Virilization at puberty.
Cause of male pseudohaeaphroditism?
Individual has testes but external genitalia are female or ambiguous. may be secondary to androgen insensitivity syndrome
Genotype 46 XY
Cause of female pseudohaemaphrotism?
Individual has ovaries but external genitalia are male (virilized) or ambiguous. May be secondary to congenital adrenal hyperplasia
46 XX
High LH + Low testosterone?
Klinfelters (primary hypogonadism)
Low LH + Low testosterone?
Hypogonadotrophic hypogonadism
(Kallman’s syndrome)
High LH + High/Normal Testosterone?
Androgen insensitivity syndrome
Low LH + High testosterone?
Testosterone secreting tumour
Phenotype of klinfelters?
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia - increased incidence of breast cancer
elevated gonadotrophin levels
Gentyoe of klinfelters?
47 XXY
Phenotype of kallman’s syndrome?
‘delayed puberty’
hypogonadism, cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above average height
DVLA driver requirements?
- there has not been any severe hypoglycaemic event in the previous 12 months
the driver has full hypoglycaemic awareness
the driver must show adequate control of the condition by regular blood glucose monitoring*, at least twice daily and at times relevant to driving
the driver must demonstrate an understanding of the risks of hypoglycaemia
here are no other debarring complications of diabetes
Risk factors for endometiral cancer?
nulliparity
early menarche
late menopause
unopposed oestrogen. The addition of a progestogen to oestrogen reduces this risk (e.g. In HRT)
Metabolic syndrome:
- obesity
- diabetes mellitus
- polycystic ovarian syndrome
tamoxifen
hereditary non-polyposis colorectal carcinoma
Protective factors for endometrial cancer?
Smoking
Multiparity
Combined contraceptive pill
First line investigation of endometiral cancer?
Transvaginal ultrasound
<4mm has a strong negative predictive value
Definitive investigation for endometrial cancer?
Hysterostomy and biopsy
Management of local endometiral cancer?
Hysterectomy + bilateral sapinoophrectomy
High risk patients should recieve radiotherapy
Treatment of endometiral cancer in frail elderly women?
Progesterne therapy
What is the pathophysiology behind familial benign hypocalciuric hypercalcaemia?
Defect in the calcium-sensing receptor
Recessive
What levels of calcium would be expected in familial benign hypocalciuric hypercalcaemia?
Normal PTH
High Calcium
Screen test for gestational diabetes?
oral glucose tolerance test (OGTT) is the test of choice
fasting glucose is >= 5.6 mmol/L
2-hour glucose is >= 7.8 mmol/L
What is the diagnostic criteria for gestational diabetes ?
fasting glucose is >= 5.6 mmol/L
2-hour glucose is >= 7.8 mmol/L
Management of gestational diabetes? Fasting glucose is < 7
if the fasting plasma glucose level is < 7 mmol/l a trial of diet and exercise should be offered
if glucose targets are not met within 1-2 weeks of altering diet/exercise metformin should be started
if glucose targets are still not met insulin should be added to diet/exercise/metformin
gestational diabetes is treated with short-acting, not long-acting, insulin
Management of gestational diabetes? - Fasting glucose > 7?
Start on insulin
Management of women who are already diabetic and become pregnant?
weight loss for women with BMI of > 27 kg/m^2
stop oral hypoglycaemic agents, apart from metformin, and commence insulin
folic acid 5 mg/day from pre-conception to 12 weeks gestation
detailed anomaly scan at 20 weeks including four-chamber view of the heart and outflow tracts
tight glycaemic control reduces complication rates
treat retinopathy as can worsen during pregnancy
What diabetic complication can worsen in pregnancy?
Retinopathy
What is the pathophysiology of gieltman syndrome?
Distal convoluted tubule
thiazide-sensitive Na+ Cl- transporter
Features of Gieltman?
Normotensive
Hypokalaemia
Hypocalcaemia
Hypomagnesaemia
Metabolic alkalosis
(Like taking too much thiazide)
Where is a glucagonoma always found ?
In the pancreas
arise from the alpha cells of the pancreas.
Features of glucagonoma?
Necrolytic migratory erythema - red blistering
Venous thromboembolism
Diagnosis of glucagonoma?
Glucagon elevated
CT scan
Management of glucagonoma?
Surgical resection
Octerotide
Features of Graves disease ?
eye signs (30% of patients)
exophthalmos
ophthalmoplegia
pretibial myxoedema
thyroid acropachy, a triad of:
digital clubbing
soft tissue swelling of the hands and feet
periosteal new bone formation
Features of thyroid acropachy?
digital clubbing
soft tissue swelling of the hands and feet
periosteal new bone formation
What antibodies are seen in graves disease ?
TSH receptor stimulating antibodies (90%)
anti-thyroid peroxidase antibodies (75%)
In graves disease what is seen in scintography?
Increased generalised uptake
Initial treatment of Graves disease ?
Propanolol - for adrenergic effects
Carbimazole 40 mg
typically continued for 12-18 months
In graves disease who should be managed with radio-idodine therapy?
Patients who relapse therapy after carbimazole
Contraindication to radio-iodine treatment?
Thyroid eye disease
Age < 16
Causes of gynaecomastia?
physiological: normal in puberty
syndromes with androgen deficiency: Kallman’s, Klinefelter’s
testicular failure: e.g. mumps
liver disease
testicular cancer e.g. seminoma secreting hCG
ectopic tumour secretion
hyperthyroidism
haemodialysis
Drug causes of gynaecomastia?
spironolactone (most common drug cause)
cimetidine
digoxin
cannabis
finasteride
GnRH agonists e.g. goserelin, buserelin
oestrogens, anabolic steroids
Features of hashimotos thyroiditis?
features of hypothyroidism
goitre: firm, non-tender
anti-thyroid peroxidase (TPO) and also anti-thyroglobulin (Tg) antibodies
May have transient hyperthyroidism
What haematological malignancy is assocated with hashimotos?
MALT lymphoma
What is hungry bone syndrome?
Occurs following parathyroidectomy
Rapid decrease in PTH casues decreased osteclast activity
Rapid remineralisation of bone
Bone pains noted + systemic hypocalcaemia
Most common causes of hypercalaemia?
- Primary hyperparathyroidism
- Malignancy - squamous cell carcinoma - secrete PTH
Rarer causes of hypercalcaemia
sarcoidosis
other causes of granulomas may lead to hypercalcaemia e.g. tuberculosis and histoplasmosis
vitamin D intoxication
acromegaly
thyrotoxicosis
Milk-alkali syndrome
thiazides
calcium-containing antacids
dehydration
Addison’s disease
Paget’s disease of the bone
Management of hypercalcaemia?
- Saline 3/4 L per day
Other options include:
calcitonin - quicker effect than bisphosphonates
steroids in sarcoidosis
Management of hyperemesis gravivarum?
Frist line:
antihistamines: oral cyclizine or promethazine
phenothiazines: oral prochlorperazine or chlorpromazine
Second line: Oral ondansetron ( discuss risk of cleft palet)
Oral metoclopramide / domperidone ( extrapyramidal side effects)
ECG changes of hyperkalaemia ?
tall-tented T waves, small P waves, widened QRS leading to a sinusoidal pattern and asystole
Causes of hyperkalaemia?
acute kidney injury
metabolic acidosis
Addison’s disease
rhabdomyolysis
massive blood transfusion
Drugs that cause hyperkalaemia?
drugs*: potassium sparing diuretics, ACE inhibitors, angiotensin 2 receptor blockers, spironolactone, ciclosporin, heparin**
When should statin be monitored post commencing?
3 months
Causes of hypernatraemia?
dehydration
osmotic diuresis e.g. hyperosmolar non-ketotic diabetic coma
diabetes insipidus
excess IV saline
Pathophysiology of HHS?
Pathophysiology
hyperglycaemia → ↑ serum osmolality → osmotic diuresis → severe volume depletion
Diagnostic criteria of HHS?
hypovolaemia
marked hyperglycaemia (>30 mmol/L)
significantly raised serum osmolarity (> 320 mosmol/kg)
can be calculated by: 2 * Na+ + glucose + urea
no significant hyperketonaemia (<3 mmol/L)
no significant acidosis (bicarbonate > 15 mmol/l or pH > 7.3 – acidosis can occur due to lactic acidosis or renal impairment)
Management of HHS?
fluid replacement
- fluid losses in HHS are estimated to be between 100 - 220 ml/kg
- IV 0.9% sodium chloride solution
- typically given at 0.5 - 1 L/hour depending on clinical assessment
- potassium levels should be monitored and added to fluids depending on the level
insulin
should not be given unless blood glucose stops falling while giving IV fluids
venous thromboembolism prophylaxis
patients are at risk of thrombosis due to hyperviscosity
Complications of HHS?
Stroke
Myocardial infarction
Causes of hypocalcaemia?
vitamin D deficiency (osteomalacia)
chronic kidney disease
hypoparathyroidism (e.g. post thyroid/parathyroid surgery)
pseudohypoparathyroidism (target cells insensitive to PTH)
rhabdomyolysis (initial stages)
magnesium deficiency (due to end organ PTH resistance)
massive blood transfusion
acute pancreatitis
Contamination of EDTA causes what in biochemistry bottles?
HIgh potassium
Low calcium
Features of hypocalcaemia?
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
if chronic: depression, cataracts
ECG: prolonged QT interval
Trousseau sign
Chovstek
What is trousseau sign?
carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
wrist flexion and fingers are drawn together
seen in around 95% of patients with hypocalcaemia and around 1% of normocalcaemic people
WHat is Chvostek sign?
tapping over parotid causes facial muscles to twitch
What is the more sensitivie trousseau or Chvostek?
Trousseau
Causes of hypoglycaemia?
insulinoma - increased ratio of proinsulin to insulin
self-administration of insulin/sulphonylureas
liver failure
Addison’s disease
Alcohol
Nesidioblastosis - beta cell hyperplasia
Management of hypoglycaemia?
Initially, oral glucose 10-20g should be given in liquid, gel or tablet form
Alternatively, a propriety quick-acting carbohydrate may be given: GlucoGel or Dextrogel.
A ‘HypoKit’ may be prescribed which contains a syringe and vial of glucagon for IM or SC injection at home
Causes of hypogonadism in men?
primary (disease of the testes)
childhood mumps
secondary (disease of the hypothalamus or pituitary)
Klinefelter syndrome
Kallman syndrome
Features of testerone deficiency?
loss of libido
erectile dysfunction
lethargy
decreased muscle mass and strength
reduced facial hair growth
impaired glucose tolerance
Causes of hypokalaemia with alkalosis?
vomiting
thiazide and loop diuretics
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Causes of hypokalaemia with acidosis?
diarrhoea
renal tubular acidosis
acetazolamide
partially treated diabetic ketoacidosis
Hypokalaemia but not increasing despite treatment, what to do?
Hypomagnesium
Causes of hypertension + hypokalaemia?
Cushing’s syndrome
Conn’s syndrome (primary hyperaldosteronism)
Liddle’s syndrome
11-beta hydroxylase deficiency*
Causes of hypokalaemia without hypertension?
diuretics
GI loss (e.g. Diarrhoea, vomiting)
renal tubular acidosis (type 1 and 2**)
Bartter’s syndrome
Gitelman syndrome
Hypovolaemic + elevated urine sodium loss > 20 mmol?
diuretics: thiazides, loop diuretics
Addison’s disease
diuretic stage of renal failure
Euvolaemic + elevated urine sodium loss > 20 mmol?
SIADH (urine osmolality > 500 mmol/kg)
hypothyroidism
Hypovolaemic + reduced urinary sodium
diarrhoea, vomiting, sweating
burns, adenoma of rectum
Hypervolaemic + reduced urinary sodium ?
secondary hyperaldosteronism: heart failure, liver cirrhosis
nephrotic syndrome
IV dextrose
psychogenic polydipsia
Management of hypovolaemic hyponatraemia?
0.9% NaCL
if the serum sodium rises this supports a diagnosis of hypovolemic hyponatraemia
if the serum sodium falls an alternative diagnosis such as SIADH is likely
Management of euvolaemic hyponatraemia?
fluid restrict to 500–1000 mL/day
Consider:
- democycline
- vaptans
Management of hypervolaemic hyponatraemia?
fluid restrict to 500–1000 mL/day
consider loop diuretics
consider vaptans
Management of severe hyponatraemia < 120 mmol?
HDU
Hypertonic saline (typically 3% NaCl) is used to correct the sodium level
Mechanism of Vaptans ?
Vasopressin/ADH receptor antagonists (vaptans):
these act primarily on V2 receptors - antagonism of V2 receptors results in selective water diuresis, sparing the electrolytes
They should be avoided in patients who have hypovolemic hyponatremia
Vasopression/ADH receptor antagonists can stimulate the thirst receptors leading to the desire to drink free water. They can be hepatotoxic in patients with underlying liver disease.
Complications of overcorrection of hyponatraemia?
Osmotic demyelination syndrome (central pontine myelinolysis)
How to prevent osmotic demyelination syndrome?
to avoid this, Na+ levels are only raised by 4 to 6 mmol/l in a 24-hour period
symptoms usually occur after 2 days and are usually irreversible: dysarthria, dysphagia, paraparesis or quadriparesis, seizures, confusion, and coma
Biochemistry of primary hypoparathyroidism?
Low calcium
high phosphate
How to treat primary hypoparathyroidism?
Alfacalcidol
Features of hypocalcaemia?
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
Chvostek’s sign: tapping over parotid causes facial muscles to twitch
if chronic: depression, cataracts
ECG: prolonged QT interval
What is the pathophysiology of pseudohypoparathyroidism?
Cells insensitive to PTH
How do you diagnose pseudohypoparathyroidism?
diagnosis is made by measuring urinary cAMP and phosphate levels following an infusion of PTH. In hypoparathyroidism this will cause an increase in both cAMP and phosphate levels
Causes of hypophosphateaemia?
alcohol excess
acute liver failure
diabetic ketoacidosis
refeeding syndrome
primary hyperparathyroidism
osteomalacia
Consequences of hypophosphataemia?
red blood cell haemolysis
white blood cell and platelet dysfunction
muscle weakness and rhabdomyolysis
central nervous system dysfunction
Causes of hypopituitarism?
compression of the pituitary gland by non-secretory pituitary macroadenoma (most common)
pituitary apoplexy
Sheehan’s syndrome: postpartum pituitary necrosis secondary to a postpartum haemorrhage
hypothalamic tumours e.g. craniopharyngioma
trauma
iatrogenic irradiation
infiltrative e.g. hemochromatosis, sarcoidosis
Features of low ACTH?
tiredness
postural hypotension
Features of low FSH / LH?
amenorrhoea
infertility
loss of libido
Features of low TSH?
feeling cold
constipation
Features of low GH?
occurs during childhood then short stature
Causes of primary hypothyroidism?
Hashimotos thyroidism
Subacute thyroiditis (de quervains)
Riedel’s thyroiditis
After thyroidectomy or radioiodine treatment
Drug therapy (e.g. lithium, amiodarone or anti-thyroid drugs such as carbimazole)
Dietary iodine deficiency
Causes of secondary hypothyroidism?
Down’s syndrome
Turner’s syndrome
coeliac disease
When starting levothyroxine, when should a lower dose be used ?
In elderly
And cardiovascular disease
Side effect of thyroxine therapy?
hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation
Interactions of levothyroxine and calcium?
iron, calcium carbonate
absorption of levothyroxine reduced, give at least 4 hours apart
Features of insulinoma?
Features of hypoglycaemia: typically early in morning or just before meal, e.g. diplopia, weakness etc
rapid weight gain may be seen
high insulin, raised proinsulin:insulin ratio
high C-peptide
Associations of insulinomas?
MEN1
Kallman syndrome inheritance?
X-linked recessive trait.
Features of kallmans?
‘delayed puberty’
hypogonadism, cryptorchidism
anosmia
sex hormone levels are low
LH, FSH levels are inappropriately low/normal
patients are typically of normal or above-average height
Anosmia
Cleft lip/palate and visual/hearing defects are also seen in some patients
Management of kallman’s syndrome?
testosterone supplementation
gonadotrophin supplementation may result in sperm production if fertility is desired later in life
Features of Klinefelters?
often taller than average
lack of secondary sexual characteristics
small, firm testes
infertile
gynaecomastia - increased incidence of breast cancer
elevated gonadotrophin levels but low testosterone
Hypertension +hypokalaemia
Liddles syndrome
Treatment of riddles syndrome?
amiloride or triamterene
What is the inheritance of MODY?
Autosomal dominant
What is MODY?
typically develops in patients < 25 years
a family history of early onset diabetes is often present
ketosis is not a feature at presentation
patients with the most common form are very sensitive to sulfonylureas, insulin is not usually necessary
Treatment of MODY?
very sensitive to sulfonylureas
Mutation in MODY 3?
due to a defect in the HNF-1 alpha gene
Mutation in MODY 2?
due to a defect in the glucokinase gene
Mutation in MODY 5?
due to a defect in the HNF-1 beta gene
liver and renal cysts
MEN Type 1?
Parathyroid (95%): hyperparathyroidism due to parathyroid hyperplasia
Pituitary (70%)
Pancreas (50%): e.g. insulinoma, gastrinoma (leading to recurrent peptic ulceration)
MEN type 2a?
Medullary thyroid cancer +
Parathyroid (60%)
Phaeochromocytoma
Mutation in MEN 1?
MEN1 gene
Mutation in MEN 2a?
RET oncogene
Mutation in MEN2b?
Phaechromocytoma
Marfanoid body habitus
Neuromas
RET oncogene
Features of neuroblastoma?
abdominal mass
pallor, weight loss
bone pain, limp
hepatomegaly
paraplegia
proptosis
Investigation findings in neuroblastoma?
raised urinary vanillylmandelic acid (VMA) and homovanillic acid (HVA) levels
calcification may be seen on abdominal x-ray
Causes of a neuroglycaemic ketoacidosis?
Normoglycaemic ketoacidosis is increasingly recognised as a consequence of SGLT-2 inhibitor
Features of pheochromocytoma?
hypertension (around 90% of cases, may be sustained)
headaches
palpitations
sweating
anxiety
Test for phaechromocytoma?
24 hr urinary collection of metanephrines (sensitivity 97%*)
this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)
Management of phaechromocytoma?
Give an alpha blocker (penoxybenzamine) , before beta blocker (bisoprolol)
Surgery is definitive management
Classification of pituitary adenomas?
size (a microadenoma is <1cm and a macroadenoma is >1cm)
hormonal status (a secretory/functioning adenoma produces and excess of a particular hormone and a non-secretory/functioning adenoma does not produce a hormone to excess)
Features of PCOS?
subfertility and infertility
menstrual disturbances: oligomenorrhoea and amenorrhoea
hirsutism, acne (due to hyperandrogenism)
obesity
acanthosis nigricans (due to insulin resistance)
Lab findings in PCOS?
raised LH:FSH ratio is a ‘classical’ feature but is no longer thought to be useful in diagnosis
prolactin may be normal or mildly elevated
testosterone may be normal or mildly elevated - however, if markedly raised consider other causes
SHBG is normal to low in women with PCOS
Rotterdam criteria?
infrequent or no ovulation (usually manifested as infrequent or no menstruation)
clinical and/or biochemical signs of hyperandrogenism (such as hirsutism, acne, or elevated levels of total or free testosterone)
polycystic ovaries on ultrasound scan (defined as the presence of ≥ 12 follicles (measuring 2-9 mm in diameter) in one or both ovaries and/or increased ovarian volume > 10 cm³)
Management of hirsutism in PCOS?
COC pill may be used help manage hirsutism.
if doesn’t respond to COC then topical eflornithine may be tried
spironolactone, flutamide and finasteride may be used under specialist supervision
Management of PCOS for infertility?
Weight reduction
Clomifene
Metformin
Gonadotrophins
Stages of postpartum thyroiditis?
- Thyrotoxicosis
- Hypothyroidism
- Normal thyroid function (but high recurrence rate in future pregnancies)
Management of postpartum thyroiditis?
Thyrotoxic phase:
propranolol is typically used for symptom control
not usually treated with anti-thyroid drugs as the thyroid is not overactive.
Hypothyroid phase:
usually treated with thyroxine
Pregnancy thryoid changes?
increase in the levels of thyroxine-binding globulin (TBG).
This causes an increase in the levels of total thyroxine but does not affect the free thyroxine level.
Management of thyrotoxicosis in pregnancy?
propylthiouracil has traditionally been the antithyroid drug of choice
- block-and-replace regimes should not be used in pregnancy
- radioiodine therapy is contraindicated
In pregnancy when should you increase thyroxine?
women require an increased dose of thyroxine during pregnancy
by up to 50% as early as 4-6 weeks of pregnancy
Most common cause of primary hyperaldosteronism?
Bilateral adrenal hyperplasia - most common
Conn’s syndrome
unilateral hyperplasia
familial hyperaldosteronism
adrenal carcinoma
Features of primary hyperaldosteronism?
Hypertension
Hypokalaemia
Metabolic alkalosis
First line investigation for primary hyperaldosteronism?
aldosterone/renin ratio is the first-line investigation in suspected primary hyperaldosteronism
Primary hyperaldosteronism, management?
Adrenal adenoma: surgery (laparoscopic adrenalectomy)
Bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
How to differentiate between unilateral adenoma and bilateral hyperplasia?
If CT does not differentiate
Adrenal venous sampling (AVS) can be used to distinguish between unilateral adenoma and bilateral hyperplasia
Management of primary triglyceridaemia ?
Fibrates
Features of excess prolactin in men?
excess prolactin in men
impotence
loss of libido
galactorrhoea
Features of excess prolactin in women?
excess prolactin in women
amenorrhoea
infertility
galactorrhoea
osteoporosis
Causes of raised prolactin?
prolactinoma
pregnancy
oestrogens
physiological: stress, exercise, sleep
acromegaly: 1/3 of patients
polycystic ovarian syndrome
primary hypothyroidism (due to thyrotrophin releasing hormone (TRH) stimulating prolactin release)
Drug causes for raised prolactin?
metoclopramide, domperidone
phenothiazines
haloperidol
very rare: SSRIs, opioids
Biochemistry of pseudohypoparathyroidism?
↑ PTH
↓ calcium
↑ phosphate
Features of pseudohypoparathyroidism?
short fourth and fifth metacarpals
short stature
learning difficulties
obesity
round face
Indications for radio-iodine therapy ?
Differentiated thyroid cancer
Toxic multinodular goitre
Graves disease refractory to medical management
Radiation exposure: Potassium iodine has been used to help individuals exposed to radiation by reducing the harmful accumulation of radioactive substances in the thyroid
Features of renal tubular acidosis type 1 ?
Distal disease
inability to generate acid urine (secrete H+) in distal tubule
causes hypokalaemia
complications include nephrocalcinosis and renal stones
causes include idiopathic, rheumatoid arthritis, SLE, Sjogren’s, amphotericin B toxicity, analgesic nephropathy
Features of renal tubular acidosis type 2?
Proximal disease
decreased HCO3- reabsorption in proximal tubule
causes hypokalaemia
complications include osteomalacia
causes include idiopathic, as part of Fanconi syndrome, Wilson’s disease, cystinosis, outdated tetracyclines, carbonic anhydrase inhibitors (acetazolamide, topiramate)
Features of renal tubular acidosis type 3?
caused by carbonic anhydrase II deficiency
results in hypokalaemia
rare
Features of renal tubular acidosis type 4?
reduction in aldosterone leads in turn to a reduction in proximal tubular ammonium excretion
causes hyperkalaemia
causes include hypoaldosteronism, diabetes
What is riddle’s thyroiditis?
hypothyroidism characterised by dense fibrous tissue replacing the normal thyroid parenchyma.
Features of riddle’s thyroiditis ?
n a hard, fixed, painless goitre is noted. It is usually seen in middle-aged women. It is associated with retroperitoneal fibrosis.
Where does sglt2 inhibitors work?
Renal proximal convoluted tubule to reduce glucose reabsorption and increase urinary glucose excretion.
Neurological causes of SIADH?
stroke
subarachnoid haemorrhage
subdural haemorrhage
meningitis/encephalitis/abscess
Drug causes of SIADH?
sulfonylureas*
SSRIs, tricyclics
carbamazepine
vincristine
cyclophosphamide
Management of SIADH?
demeclocycline: reduces the responsiveness of the collecting tubule cells to ADH
ADH (vasopressin) receptor antagonists have been developed
Features of sick euthyroid?
Everything is low
Although in most cases: TSH level is within the >normal range (inappropriately normal given the low thyroxine and T3).
Phases of de quervain thyroiditis?
phase 1 (lasts 3-6 weeks): hyperthyroidism, painful goitre, raised ESR
phase 2 (1-3 weeks): euthyroid
phase 3 (weeks - months): hypothyroidism
phase 4: thyroid structure and function goes back to normal
Scintography of de quervain thyroiditis?
globally reduced uptake of iodine-131
How to treat pain in de quervain thyroiditis?
NSAID
Diagnostic criteria for sub clinic hypothyroidism?
TSH is > 10mU/L and the free thyroxine level is within the normal range
if < 65 years consider offering a 6-month trial of levothyroxine if:
the TSH level is 5.5 - 10mU/L on 2 separate occasions 3 months apart,and
there are symptoms of hypothyroidism
What are TZD contraindicated in?
Fluid rendition
Bladder cancer
What type of medication is TZD?
PPAR-gamma receptor
High TSH + Normal T4?
Subclinical hypothyroidism
Poor compliance with thyroxine
Features of thyroid storm?
fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically
Management of thyroid storm?
beta-blockers: typically IV propranolol
anti-thyroid drugs: e.g. methimazole or propylthiouracil
Lugol’s iodine
dexamethasone - e.g. 4mg IV qds - blocks the conversion of T4 to T3
Causes of thyrotoxicosis ?
Graves’ disease
toxic nodular goitre
acute phase of subacute (de Quervain’s) thyroiditis
acute phase of post-partum thyroiditis
acute phase of Hashimoto’s thyroiditis (later results in hypothyroidism)
amiodarone therapy
Causes of Waterhouse fridrichson syndrome?
Neisseria meningitidis: most common cause
Haemophilus influenzae
Pseudomonas aeruginosa
Escherichia coli
Streptococcus pneumoniae
Why does multiple myeloma have low sodium?
Hyperlipidaemia can cause pseudohyponatraemia
In DKA, parameters that require escalation to ITU?
Potassium of 3.5
tinels test positive + endocrine condition?
Acromegaly (carpel tunnel)
Tetany + low magnesium?
Low calcium secondary to low magnesium
Hyperthyroidism + negative TSH receptor antibodies, next test?
Scintography
Raised calcium + Raised/normal PTH + Raised vitamin D
Familial benign hypocalciuric hyppothyroidism
Low urinary calcium in the presence of hypercalcaemia is suggestive of either familial hypocalciuric hypercalcaemia or thiazide diuretic use
Hypercalcaemia: IVF + bisphonsates fail. Next treatment?
Calcitonin
What should be given to women in hyperemesis prior to glucose?
Thiamine
5% dextrose intravenous infusion may precipitate Wernicke’s encephalopathy.
How to monitor MEN 2a or medullary thyroid cancer?
Annual levels of calcitonin
Assocations between GLP-1 inhibitors (glutides) ?
Pancreatitis
Management of myoxedema coma?
IV levothyroxine + IV liothyronine
IV fluid
IV corticosteroids (until the possibility of coexisting adrenal insufficiency has been excluded)
electrolyte imbalance correction
sometimes rewarming
What cancer is associated with thiozoladines?
Bladder cancer
Side effect of DDP4 inhibitors ( gliptans)
Ketoacidosis
Diabetic medication, shows microscopic haematuria?
TZD
Poor contorlled type 1 diabetic on insulin - what other drug can be added?
Metformin
Mechanism of orlistat?
pancreatic lipase inhibitor
Criteria for orlistat?
BMI of 28 kg/m^2 or more with associated risk factors, or
BMI of 30 kg/m^2 or more
continued weight loss e.g. 5% at 3 months
orlistat is normally used for < 1 year
Presentation of Fanconi?
Rental tubule acidosis type 2
Metabolic acidosis + Hypokalaemia
Lithium can cause hypercalcaemia
Lithium can cause hypercalcaemia
Consider w/h in hypercalcaemia patients
TSH Low + T4 normal + history of weight loss - what do you do?
Add on T3 - may be elevated and represent toxicosis
Management of hyperthyroidism + pregnancy
First trimester: Proppiothyuracil
Second trimester: Carbimazole
Painful large diffuse tender thryoid?
De Quervains
Reduced scintopgraphy + hyperthyroid?
De QAQuervains
Increased scintography diffuse + hyperthyroid
Graves
How to reduce risk of overnight hypos in insulin prescription?
2/3rd insulin in moring
1/3 in evening
Type of renal tubule acidosis?
Type 1: Distal (failure of proton secretion)
Type 2: Proximal (failure of bicarbonate reabsorption)
Type 3: Combination
Type 4: Aldosterone deficiency/insensitivity
Primary vs secondary hypogonadism?
Primary: testes
Secondary: pituitary
Common electrolyte imbalance in alcoholics ?
Hypophosphataemia
Criteria for GLP-1 mimetics?
Three agents
Not controlled
BMI > 35
What is struma ovarii?
Ovarian teratoma that produces TSH
Features of thyrotoxicosis
Is thyrotoxicosis cardiomyopathy reversible?
Yes
What should patients taking cabimazole be warned about ?
Jaundice
Agranulocytosis
Test for insulinoma?
Supervised fasting with serial insulin and c peptide levels
Elevated C-peptide in fasting hypoglycaemia is suggestive of insulinoma
Hypokalaemia + Bilateral nephrocalcinosis ?
Type 1 renal tubule acidosis
Biochemistry of cortisol secreting adrenal adenoma?
Suppressed ACTH
What should make you think thyroid storm?
Hyperpyrexia - 40 degrees
First line test for addisons?
Short synacthen test
Positive result is failure to increase cortisol to 500
Management of abetalipoproteinemia
Treatment of Treatment of abetalipoproteinemia involves dietary restriction of fats, and high-dose vitamin E therapy
Apolipoproteins are essential in the synthesis and exportation of chylomicrons and VLDL. The end results is malabsorption of dietary fats, cholesterol, and fat soluble vitamin (e.g. vitamins K, A, D and E).
What is potomania?
Beer potomania is a cause of hyponatremia which occurs due to a low dietary intake of solutes. Urine osmolarity will be low (<100 mosmol/kg) indicating that ADH is appropriately suppressed
Normal c peptide + elevated insulin
Insulin abuse
GAD antibody positive + older person with diabetes?
T2DM
10% have positive GAD antibody
What is thyrotoxicosis factitia?
Deliberate or acidental overdose of thyroxine
Reduced uptake on scintography
Differs from de quervarins: de quervains will last shorter time. This does not have a tender thyroid
Thyroid cancer by most common?
Papillary (most common)
Follicular
Medullary
Anaplastic
Lymphoma (least common)
papillary and colloidal filled follicles
Histologically tumour has papillary projections and pale empty nuclei - what cancer?
Papillary
Thyroid cancer: macroscopically encapsulated, microscopically capsular invasion is seen
Follicular
Without encapsulation it is an adenoma
What cell does medullary thyroid cancer arise from?
Parafollicular C cells
What should not be given prior to steroids in pituitary / adrenal + thyroid loss?
Do not give thyroxine before replacing with STEROIDS
Will precipitate adrenal crisis
How slow should glucose be lowered in DKA?
Reduce by 3 per hour
Treatment for Liddle’s syndrome ?
Amiloride
WHat is a high dose dexamethasone suppression test used for?
distinguishing between ACTH dependent (e.g. pituitary source) and non-ACTH dependent (e.g. ectopic and adrenal source) causes of Cushings’s syndrome
Suppressed cortisol levels following high doses of glucocorticoids confirms a pituitary cause, as opposed to normal levels of cortisol that suggest an adrenal cause.
In cushing disease, what are the results from a low dose dexamethasone suppression test and the results from a high dose dexamethasone suppression test?
Low dose: No suppression
High dose: Suppression
What screening tes should be completed in acromegally ?
Colonoscopy
What is the normal relationship between glucose and GH?
Increase glucose suppresses growth hormone
In acromegally: increase glucose –> increased GH
How to diagnose congenital adrenal hyperplasia?
Short synacthen test
Low renin + high aldosterone?
Primary aldosteronism
- most common is adrenal hyperplasia
How to differentiate between Gieltman and Barter’s syndrome?
Hypokalaemia in both
Normtensive in both
Hypocalaemia –> GIELTMAN
Familial hypercholesterolaemia management?
- Statin 80 mg
- Evolcumab
When should familial hypercholesterolaemia be suspected ?
a total cholesterol level greater than 7.5 mmol/l and/or
a personal or family history of premature coronary heart disease (an event before 60 years in an index individual or first-degree relative)
Simone broom criteria for facial hypercholesteraemia?
in adults total cholesterol (TC) > 7.5 mmol/l and LDL-C > 4.9 mmol/l or children TC > 6.7 mmol/l and LDL-C > 4.0 mmol/l, plus:
for definite FH: tendon xanthoma in patients or 1st or 2nd degree relatives or DNA-based evidence of FH
for possible FH: family history of myocardial infarction below age 50 years in 2nd degree relative, below age 60 in 1st degree relative, or a family history of raised cholesterol levels
Why is it important to recognise subclinical hyperthyroidism?
Risk of osteoporosis
- investigate with deXA
Even if an adrenal tumour is found in primary hyperaldonsteronism, what should be done?
Adrenal vein sampling
CT is not diagnostic
Hypertension (resistant) + hypokalaemia + increased urinary frequency?
Conn’s syndrome
What is the treatment for severe thyroid eye disease ?
IV methylprednisolone
How dies thyroid hormones changes in pregnancy?
Raised total T3 and T4 but normal fT3 and fT4 suggest high concentrations of thyroid binding globulin, which can be seen during pregnancy
Primary hyperparathyroidism what additional test needs done every two years?
DEXA
Prolactin 800 + Secondary hypothyroidism (low normal TSH, low T4)
Non-functioning pituitary adenoma
indicative of stalk compression is consistent with a non-functioning pituitary adenoma
Canakinumab?
Canakinumab is a human monoclonal antibody that selectively inhibits interleukin-1 beta receptor binding. It can be used for treatment of acute gout has not responded adequately to treatment with NSAIDs or colchicine, or who are intolerant of them
What medicine should be stopped in thyroid storm?
In acute thyrotoxicosis, stop aspirin as it can worsen the storm by displacing T4 from thyroid binding globulin
new diabetes + egfr <30?
start sulphonyurlurea
is fludrocortisone needed in adrenal crisis?
no - hydro has mineral effects too
hallmark of true cushings disease?
lack of diurnal variation in cortisol
Elevation of C peptide after IV insulin?
Insulinoma
What antithyroid medication should be used in storm?
Propiothiouracil
In adrenal failure, how to differentiate between primary and secondary?
start with short synacthen (test adrenal issue )
Then long synacthen - for ? secondary failure (i.e. pituitary failure)
- higher dose is given and then cortisol levels measured over a longer time period
- secondary failure, the exogenous ACTH will eventually push the adrenals to produce cortisol.
Do gliptins cause hypoglycaemia?
No
Hypogonadism secondary to prolactinaemia?
Low testosterone and low or normal FSH and LH
When does a thyroid nodule not need a FNA?
If ultrasound is normal
Test to diagnose gestation diabetes?
Oral glucose tolerance
Sulfonyulrea overdose?
- dextrose
- octreotide
criteria for statin in T1DM?
older than 40 years, or
have had diabetes for more than 10 years or
have established nephropathy or
have other CVD risk factors
DO NOT USE QRISK
Causes of type 4 renal tubule acidosis?
Aldosterone deficiency (hypoaldosteronism): Primary vs. hyporeninaemic
Aldosterone resistance
→ 1.Drugs: Non-steroidal anti-inflammatories, angiotensin converting enzyme inhibitors, angiotensin 2 receptor blockers, eplerenone, spironolactone, trimethoprim, pentamidine
→ 2.Pseudohypoaldosteronism
What is pre-diabetes HbA1c?
42-47
When should a OGTT be done for gestational diabetes?
24-28 weeks
How do you monitor thyroid replacement in hypopituitary?
T4
If you see T1DM + other other autoimmune condition - the questions asks for investigation for other conditions
e.g. consider Short synacthen to test Addisons
When can you become pregnant after radio iodinetreatment?
6 months
Gestation diabetes: how to monitor for diabetes post baby?
Fasting glucose 6-13 weeks after
How to assess if addisons patients get enough cortisol?
A cortisol curve can be used to assess how appropriate dosing of glucocorticoid steroids in Addison’s disease patients is
When should democycline be considered?
SIADH resistant to fluid restriction
What is a significant negative prognostic factor for thyroid eye disease ?
Smoking
What is the risk of over replacing thyroxine?
Osteoporosis
Treatment for familial hyperhypercholesterolaemia
- Statin
- Ezetimbe
Low sodium + normal serum osmolality + increase urine osmolality?
Pseudohyponatraemia
Occurs due to a measuring defect with proteins and lipids
Priority of electrolyte replacement
Replace magnesium before trying to correct potassium
Primary adrenal insufficiency short synacthen and long synacthen test results ?
short Synacthen test demonstrates failure of cortisol to rise which confirms the diagnosis of adrenal insufficiency
Long synacthen: we would not expect there to be a significant rise in cortisol during the long Synacthen rest since the adrenal glands are intrinsically dysfunctional
Secondary adrenal insufficiency short and long synacthen test results?
Short synactehn will show adrenal insufficiency
Prolonged stimulation of the adrenal glands by ACTH in the long Synacthen test results in a degree of recovery by the adrenal glands resulting in a significant rise in cortisol.
Sick euthyroid?
Reduced TSH
Normal thyroxine
Recovering DKA, risk of what electrolyte imbalance?
Hypophosphataemia
