Endocrine Flashcards
what is the cause of majority of acromegaly cases?
pituitary adenoma
what are the features of acromegaly?
coarse facial appearance, spade-like hands, big feet.
large tongue, prognathism, 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
hypertension
diabetes (>10%)
cardiomyopathy
colorectal cancer
how is acromegaly investigated?
Serum IGF-1 levels (when first suspected and also used for monitoring)
oral glucose tolerance test (OGTT) - confirms if IGF1 is raised
pituitary MRI
how does oral glucose tolerance test confirm acromegaly?
give glucose, if GH does not become supressed to <1 , then confirms diagnosis
how is acromegaly treated?
Trans-sphenoidal surgery as first line
If a pituitary tumour is inoperable or surgery unsuccessful then medication may be indicated:
somatostatin analogue (octreotide)
pegvisomant
dopamine agonist (bromocriptine)How does a somatostatin analogue work in acromegaly?
inhibits release of GH
What is the mechanism of pegvisomant?
GH receptor antagonist - prevents dimerization of the GH receptor
once daily s/c administration
what are the acute phase proteins?
during inflammation/infection liver increases production of acute phase proteins…
CRP, procalcitonin, ferritin, fibrinogen, alpha-1 antitrypsin, caeruloplasmin, serum amyloid A & P , haptoglobin and complement
which proteins are decreased during acute phase response?
albumin transthyretin (formerly known as prealbumin) transferrin retinol binding protein cortisol binding protein
what is the function of CRP?
binds to phosphocholine in bacterial cells and on those cells undergoing apoptosis. In binding to these cells it is then able to activate the complement system.
what is the commonest cause of hypoaldrenalism? what is this called?
Autoimmune destruction of the adrenal glands
Addisons - both cortisol and aldosterone reduced
what are the features of addisons?
lethargy, weakness, anorexia, nausea & vomiting, weight loss,
‘salt-craving’
hyperpigmentation (especially palmar creases) hypotension, hypoglycaemia
hyponatraemia and hyperkalaemia may be seen
vitiligo, loss of pubic hair in women,
crisis: collapse, shock, pyrexia
other than addisons what are the other causes of hypoadrenalism?
tuberculosis metastases (e.g. bronchial carcinoma) meningococcal septicaemia (Waterhouse-Friderichsen syndrome) HIV antiphospholipid syndrome
Secondary causes pituitary disorders (e.g. tumours, irradiation, infiltration)
Exogenous glucocorticoid therapy
how is addisons disease diagnosed?
ACTH stimulation test (short Synacthen test). Plasma cortisol is measured before and 30 minutes after giving Synacthen 250ug IM.
Adrenal autoantibodies such as anti-21-hydroxylase may also be demonstrated.
If an ACTH stimulation test is not readily available then sending a 9 am serum cortisol can be useful:
> 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
what are the electrolyte abnormalities in addisons?
hyperkalaemia
hyponatraemia
hypoglycaemia
metabolic acidosis
what are the causes of an addisonian crisis?
acute exacerbation of chronic hypoadrenalism e.g. surgery or infection
OR
Sudden loss of adrenal - adrenal haemorrhage eg Waterhouse-Friderichsen syndrome (fulminant meningococcemia)
OR
steroid withdrawal
how is addisonian crisis managed?
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.
No fludrocortisone is required because high cortisol exerts weak mineralocorticoid action
oral replacement may begin after 24 hours and be reduced to maintenance over 3-4 days
causes of raised ALP (Alanine phosphatase)?
liver: cholestasis, hepatitis, fatty liver, neoplasia
Paget’s
osteomalacia
bone metastases
hyperparathyroidism
renal failure
physiological: pregnancy, growing children, healing fractures
how can the causes of raised ALP be differentiated?
Calcium levels..
if high ALP and high CA - bone mets/ hyperparathyroid
if high ALP and low Ca - osteomalacia/renal failure
define primary amenorrhoea.
failure to establish menstruation by 15 years of age in girls with normal secondary sexual characteristics (such as breast development), or by 13 years of age in girls with no secondary sexual characteristics
define secondary amenorrhoea
Cessation of menstruation for 3-6 months in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhoea
what are the causes of primary amenorrhoea?
gonadal dysgenesis (e.g. Turner’s syndrome) - the most common causes
testicular feminisation
congenital malformations of the genital tract
imperforate hymen
functional hypothalamic amenorrhoea (e.g. secondary to anorexia)
congenital adrenal hyperplasia
what are the causes of secondary amenorrhoea?
hypothalamic amenorrhoea (e.g. secondary stress, excessive exercise)
polycystic ovarian syndrome (PCOS)
hyperprolactinaemia
thyrotoxicosis / hypothyroid
premature ovarian failure
Sheehan’s syndrome
Asherman’s syndrome (intrauterine adhesions)
how is amenorrhoea investigated?
Exclude pregnancy with urinary or serum bHCG
full blood count, urea & electrolytes, coeliac screen, thyroid function tests
gonadotrophins
low levels indicate a hypothalamic cause where as raised levels suggest an ovarian problem (e.g. Premature ovarian failure)
raised if gonadal dysgenesis (e.g. Turner’s syndrome)
prolactin
androgen levels - raised levels may be seen in PCOS
oestradiol
what is androgen insensitivity syndrome?
X-linked recessive condition due to end-organ resistance to testosterone causing genotypically male children (46XY) to have a female phenotype.
Complete androgen insensitivity syndrome is the new term for testicular feminisation syndrome
what are the features of androgen insensitivity syndrome?
‘primary amennorhoea’
undescended testes causing groin swellings
breast development may occur as a result of conversion of testosterone to oestradiol
how is androgen insensitivity diagnosed?
buccal smear or chromosomal analysis to reveal 46XY genotype
how is androgen insensitivity managed?
couselling - raise child as female
oestrogen therapy
bilateral orchidectomy - risk of testicular cancer from undescended testes
what is autoimmune polyendocrinopathy syndrome (APS)?
Addison’s disease is associated with other endocrine deficiencies in approximately 10% of patients.
There are two distinct types of autoimmune polyendocrinopathy syndrome (APS), with type 2 (sometimes referred to as Schmidt’s syndrome) being much more common.
vitiligo can happen with either APS 1 or 2
what is APS type 2? what allele is it linked to?
APS type 2 linked to HLA DR3/DR4.
Patients have Addison’s disease plus either:
type 1 diabetes mellitus
autoimmune thyroid disease
what is APS type 1? what is it also known as? genetics?
APS type 1 is occasionally referred to as Multiple Endocrine Deficiency Autoimmune Candidiasis (MEDAC).
very rare autosomal recessive disorder caused by mutation of AIRE1 gene on chromosome 21
Features of APS type 1 (2 out of 3 needed)
chronic mucocutaneous candidiasis (typically first feature as young child)
Addison’s disease
primary hypoparathyroidism
what is bartters syndrome? how does bartters differ from other endocrine causes of hypoK?
autosomal recessive cause of severe hypokalaemia due to defective chloride absorption at the Na+ K+ 2Cl- cotransporter (NKCC2) in the ascending loop of Henle.
It should be noted that it is associated with normotension (unlike other endocrine causes of hypokalaemia such as Conn’s, Cushing’s and Liddle’s syndrome which are associated with hypertension).
How does Bartters present?
usually presents in childhood, e.g. Failure to thrive polyuria, polydipsia hypokalaemia normotension weakness
what is the function of carbimazole? How does this compare to propylthiouracil?
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 are the adverse effects of carbimazole?
agranulocytosis
crosses the placenta, but may be used in low doses during pregnancy
what type of cancer are the majority of cervical cancers?
squamous cell
which HPVs are most linked to cervical cancer?
16, 18, 33
whats the function of E6/7?
- E6 inhibits the p53 tumour suppressor gene
* E7 inhibits RB suppressor gene
what is congenital adrenal hyperplasia? (genetics and pathogenesis)
•group of autosomal recessive disorders - mainly 21-hydroxylase deficiency
- affect adrenal steroid biosynthesis
- in response to resultant low cortisol levels the anterior pituitary secretes high levels of ACTH
- ACTH stimulates the production of adrenal androgens that may virilize a female infant
what are the features of CAH caused by 21 hydroxylase deficiency?
- virilisation of female genitalia
- precocious puberty in males
- 60-70% of patients have a salt-losing crisis at 1-3 wks of age
what are the features of CAH caused by 11 beta hydroxylase deficiency?
11-beta hydroxylase deficiency features •virilisation of female genitalia •precocious puberty in males •hypertension •hypokalaemia
what are the features of CAH caused by 17 hydroxylase deficiency? (very rare)
17-hydroxylase deficiency features
•non-virilising in females
•inter-sex in boys
•hypertension
what are the problems of congenital hypothyroid?
if not treated within 4 weeks - irreversible cognitive delay
- prolonged neonatal jaundice
- delayed mental & physical milestones
- short stature
- puffy face, macroglossia
- hypotonia
when are children screened for congenital hypothyroidism?
Children are screened at 5-7 days using the heel prick test
which steroids have glucocorticoid/mineralocorticoid activity?
fludrocortisone - mineralocorticoid
hydrocortisone - both (high mineralo)
prednisolone - both (mainly gluco)
Dexamethasone/bethamethasone - glucocorticoid
what are the side effects of steroids for the... MSK system? psych? GI? Opthal?
- musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head
- psychiatric: insomnia, mania, depression, psychosis
- gastrointestinal: peptic ulceration, acute pancreatitis
- ophthalmic: glaucoma, cataracts
when do patients require gradual withdrawal of steroids?
•the BNF suggests gradual withdrawal of systemic corticosteroids if patients have: received more than 40mg prednisolone daily for more than one week, received more than 3 weeks treatment or recently received repeated courses
what is the most common cause of cushings syndrome?
exogenous use
what are the causes of cushings?
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
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 carney complex ?
syndrome of cushings and cardiac myxoma
what is pseudo cushings?
mimics cushings
•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
what metabolic lab result is found in cushings?
hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance.
(ectopic ACTH is associated with very low K+ levels)
how is cushings tested for?
overnight dexamethasone suppression test
- this is the most sensitive test and is now used first-line to test for Cushing’s syndrome
◦patients with Cushing’s syndrome do not have their morning cortisol spike suppressed
•24 hr urinary free cortisol
how can we investigate the cause of cushings (source of issue)?
localization tests e.g. finding out where the problem is..
first one
9am and midnight plasma ACTH (and cortisol) levels. If ACTH is suppressed then a non-ACTH dependent cause is likely such as an adrenal adenoma
second
High-dose dexamethasone suppression test
CRH stimulation
•if pituitary source then cortisol rises
•if ectopic/adrenal then no change in cortisol
how are results of high dose dexamethasone test interpreted for cushings?
cotisol not supressed, ACTH supressed - adrenal issue
Cortisol and ACTH supressed - pituitary issue.
neither supressed - ectopic ACTH release
how can you differentiate between real cushings and pseudocushings?
An insulin stress test is used to differentiate between true Cushing’s and pseudo-Cushing’s.
how is T2D diadnosed?
If the patient is 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)
If the patient is asymptomatic the above criteria apply but must be demonstrated on two separate occasions.
HbA1c >6.5%
How is prediabetes defined?
HbA1c - 6-6.4%
fasting gluc - 6.1-6.9
when can HbA1c not be used for diagnosis?
haemoglobinopathies haemolytic anaemia untreated iron deficiency anaemia suspected gestational diabetes children HIV chronic kidney disease people taking medication that may cause hyperglycaemia (for example corticosteroids)
what is MODY?
mature onset diabetes of the young
A group of inherited genetic disorders affecting the production of insulin. Results in younger patients developing symptoms similar to those with T2DM, i.e. asymptomatic hyperglycaemia with progression to more severe complications such as diabetic ketoacidosis
what is LADA?
latent autoimmune diabetes of adults
small group of patients who develop such problems later in life. These patients are often misdiagnosed as having T2DM
what are the main side effects of insulin?
Hypoglycaemia
Weight gain
Lipodystrophy
what is the function of metformin?
Increases insulin sensitivity
Decreases hepatic gluconeogenesis
what are the side effects of metformin?
GI iupset
lactic acidosis
when is metformin contraindicated?
eGFR <30
what is the function of sulphonylureas? (gliclazide and glimepiride)
Stimulate pancreatic beta cells to secrete insulin
what are the side effects of sulphonylureas?
Hypoglycaemia
Weight gain
Hyponatraemia
what is the function of pioglitazone (Thiazolidinediones)? what are the side effects?
Activate PPAR-gamma receptor in adipocytes to promote adipogenesis and fatty acid uptake
Weight gain
Fluid retention
what is the function of DPP-4 inhibitors (-gliptins)? what risk is there with these?
Increases incretin levels which inhibit glucagon secretion
risk of pancreatitis
what is the function of SGLT-2 inhibitors (-gliflozins)? what are the side effects/benefits?
Inhibits reabsorption of glucose in the kidney
UTI
result in weight loss
what are GLP1 agonists?
how are they given? side effects? benefits?
Incretin mimetic which inhibits glucagon secretion Subcutaneous
Nausea and vomiting, Pancreatitis
Typically result in weight loss
How is T2D managed (algoithm for drug therapy)?
metformin 1st line if HbA1c >7.5 add in antoher, if still about 7.5 , add another for triple therapy OR insulin.
if not tolerated and BMI >35 add GLP1
what class of drug is Exenatide? how is it given?
glucagon-like peptide-1 (GLP-1) mimetic. These drugs increase insulin secretion and inhibit glucagon secretion.
Exenatide must be given by subcutaneous injection within 60 minutes before the morning and evening meals. It should not be given after a meal.
How does Liraglutide compare to exenatide?
Liraglutide is the other GLP-1 mimetic
One the main advantages of liraglutide over exenatide is that it only needs to be given once a day.
when are GLP1 used?
Consider adding exenatide to metformin and a sulfonylurea if:
BMI >= 35 kg/m² OR
BMI < 35 kg/m² and insulin is unacceptable because of occupational implications or weight loss would benefit other comorbidities.
How are the use of GLP1s justified according to NICE?
NICE like patients to have achieved a > 11 mmol/mol (1%) reduction in HbA1c and 3% weight loss after 6 months to justify the ongoing prescription of GLP-1 mimetics.
what are the function of gliptins?
increase levels of incretins (GLP-1 and GIP) by decreasing their peripheral breakdown
how often should HbA1c be monitored in T1DM? what is the target?
3-6 months
target of 6.5% or lower
How often should blood glucose be monitored in T1dM?
4x daily - before each meal and before bed
more frequently during periods of illness; before, during and after sport; when planning pregnancy, during pregnancy and while breastfeeding
what should blood glucose targets be?
5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day
when is metformin considered in T1DM?
when BMI >25
what are the target HbA1c for T2DM and what is the cut off before considering the next drug?
target when on no drugs/ metformin alone = 6.5
if on oral hypoglycaemics then 7% target
you can titrate up metformin and encourage lifestyle changes to aim for a HbA1c of 48 mmol/mol (6.5%), but should only add a second drug if the HbA1c rises to 58 mmol/mol (7.5%)
what is the management of T2DM (use Hba1c targets)
metformin is still first-line and should be offered if the HbA1c rises to 48 mmol/mol (6.5%)* on lifestyle interventions
if the HbA1c has risen to 58 mmol/mol (7.5%) then a second drug should be added from the following list:
sulfonylurea, gliptin, pioglitazone, SGLT-2 inhibitor
if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then triple therapy with one of the following combinations should be offered:
metformin + gliptin + sulfonylurea
metformin + pioglitazone + sulfonylurea
metformin + sulfonylurea + SGLT-2 inhibitor
metformin + pioglitazone + SGLT-2 inhibitor
OR insulin therapy should be considered
what is the criteria to continue a GLP 1 analgoe?
only continue if there is a reduction of at least 11 mmol/mol [1.0%] in HbA1c and a weight loss of at least 3% of initial body weight in 6 months
how is T2DM tolerated if metformin is not tolerated?
if the HbA1c rises to 48 mmol/mol (6.5%) on lifestyle interventions, consider one of the following:
sulfonylurea, gliptin, pioglitazone
if the HbA1c has risen to 58 mmol/mol (7.5%) then a one of the following combinations should be used:
gliptin + pioglitazone
gliptin + sulfonylurea
pioglitazone + sulfonylurea
if despite this the HbA1c rises to, or remains above 58 mmol/mol (7.5%) then consider insulin therapy
what is the recommended insulin to start with for T2DM?
NICE recommend starting with human NPH insulin (isophane, intermediate-acting) taken at bed-time or twice daily according to need
what antibodies are present in t1dm?
islet-associated antigen (IAA) antibody and glutamic acid decarboxylase (GAD) antibody
how often are patients screen for diabetic foot? and how?
Annually.
screening for ischaemia: done by palpating for both the dorsalis pedis pulse and posterial tibial artery pulse
screening for neuropathy: a 10 g monofilament is used on various parts of the sole of the foot
what factors give a high risk of diabetic foot ulcer?
- previous ulceration or
- previous amputation or
- on renal replacement therapy or
- neuropathy and non-critical limb ischaemia together or
- neuropathy in combination with callus and/or deformity or
- non-critical limb ischaemia in combination with callus and/or deformity.
How does ezetimibe work?
Ezetimibe is a lipid-lowering drug which inhibits cholesterol receptors on enterocytes, decreasing cholesterol absorption in the small intestine.
when does NICE recommnend the use of ezetimibe?
use of ezetimibe in primary heterozygous-familial and non-familial hypercholesterolaemia
Ezetimibe monotherapy is recommended as an option for treating primary hypercholesterolaemia in adults in whom initial statin therapy is contraindicated or who cannot tolerate statin therapy
Ezetimibe, coadministered with initial statin therapy, is recommended as an option for treating primary hypercholesterolaemia in adults who have started statin therapy when:
serum total or LDL cholesterol concentration is not controlled despite titrating up / cannot tolerate higher dose
when are fibrates used? what is their mechanism of action?
Fibrates are used in the management of hyperlipidaemia, particularly raised triglycerides.
Fibrates work through activating PPAR alpha receptors resulting in an increase in LPL activity reducing triglyceride levels.
What are the side effects of fibrates?
Gastrointestinal side-effects are common
increased risk of thromboembolism
what are the triggers of DKA?
MI
infection
missed insulin
what are the clinical features of DKA?
abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’ smell)
what is the diagnostic criteria of DKA?
glucose > 11 mmol/l or known diabetes mellitus
pH < 7.3
bicarbonate < 15 mmol/l
ketones > 3 mmol/l or urine ketones ++ on dipstick
what is the management of DKA?
fixed rate insulin 0.1units/kg/hr
fluids NaCL + KCL (unless high)
- 1L over 1h, 1L over 2 hour x2, 1L over 4 hours x2, 1 L over 6 hours.
once BMs <15 , dextrose 5% started too
any long acting insulins can continue but short acting stopped.
how much K+ is given in DKA?
if >5.5 none
if 3.5-5.5 40mM
if <3.5 senior review
how is DKA resolution defined?
pH >7.3 and
blood ketones < 0.6 mmol/L and
bicarbonate > 15.0mmol/L
what are the 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
which group of patients are particularly at risk of cerebral oedema?
children and young adults.
give a slower fluid regime
following fluid resuscitation in DKA and often need 1:1 nursing to monitor neuro-observations, headache, irritability, visual disturbance, focal neurology etc. It usually occurs 4-12 hours following commencement of treatment but can present at any time. If there is any suspicion a CT head and senior review should be sought
how is diabetic painful neuropathy managed?
usually they get sensory loss which is painless but sometimes can be painful
first-line treatment: amitriptyline, duloxetine, gabapentin or pregabalin
if the first-line drug treatment does not work try one of the other 3 drugs
tramadol may be used as ‘rescue therapy’ for exacerbations of neuropathic pain
topical capsaicin may be used for localised neuropathic pain (e.g. post-herpetic neuralgia)
pain management clinics may be useful in patients with resistant problems
what are the features of diabetic autonomic neuropathy?
Gastroparesis
symptoms include erratic blood glucose control, bloating and vomiting
management options include metoclopramide, domperidone or erythromycin (prokinetic agents)
Chronic diarrhoea
often occurs at night
Gastro-oesophageal reflux disease
caused by decreased lower esophageal sphincter (LES) pressure
Which antibodies are associated with Graves’ disease
Anti TSH r - stimulating -90%
Anti thyroid peroxidase - 70%
What is the first line for fertility in PCOS
Clomifene
How is gestational diabetes managed
If bm less than 7 can try diet and metformin but if targets are still not met with this then start insulin
If more than 7 - start insulin straight away
If any effects of diabetes e.g. macrosomia - start insulin
What is the most common cause of Cushing’s syndrome
Iatrogenic - 1st
Cushings disease - pituitary tumour - 2nd
Which type of malignancy does hashimotos predispose to ?
MALT lymphoma
Which genes are mutated in MODY
Type 3 - HNF1a - most common
Type 2 - glucokinase
Type 5- HNF1b - associated with cyst
how can you distinguish klinefelters and kallmans?
klinefelters - high LH/ FSH
Kallmans - normal/ low FSH / LH
what is the management for diabetic nephropathy?
duloxetine, gabapentin, amitriptyline
tramadol for rescue therapy
How is SIADH initially managed?
fluid restriction
what is the mechanism of action of thiazolinediones (TZDs) and the ADRs
PPARg receptor (intracellular receptor) - increases insulin sensitivity e.g. pioglitazone
ADRs - fluid retention - shouldnt be used in HF
- weight gain
- increased risk of fractures
- increased risk of bladder Ca with pioglitazone
- liver impairment - monitor LFTs
what is the most common cause of primary hyperaldosteronism?
bilateral adrenal hyperplasia
What are the ADRs of SGLT2 inhibitors? what are thes drugs called?
Gliflozins
forniers gangrene
UTI
normoglycaemic ketoacidosis
limb amputation
what blood abnormality is often seen with fibroids and why?
high Hb
fibroids produce EPO
who are fibroids more common in?
Afrocaribean
what is HbA1c of 6% equivalent to?
42
each 1% = 11 increase
what are the causes of gynaecomastia?
testicular failure - mumps klinefelters , kallmans seminoma - HCG secreting haemodialysis hyperthyroid
drugs = spironolactone, goreselin , digoxin, cimetidine, cannabis, finasteride, steroids
what are the complications of acromegaly?
HTN, CRC, diabetes, cardiomyopathy
what inheritance does familial hyperlipidaemia have?
autosomal dominant
which electrolyte abnormality is associated with low K
low Mg
what are the causes of euvolaemic hyponatraemia?
SiADH, hypothyroidism
urinary sodium usually high >20
what inheritance is kallmans? what are the feature?
X linked recessive
small testis, tall , anosmia ,
low/ normal LH/ FSH
what are the ADRs of sulphonylureas?
weight gain hypoglycaemia SiADH bone marrow sup hepatotoxic peripheral neuropathy
dont use in preg / breast feeding
what blood test suggests poor compliance to levothyroxine?
high TSH - has been trying to compensate
normal T3/4 - short term fix before blood test
