Endocrine Flashcards
1st line Rx of prolactinoma
Dopamine agonist
(Cabergoline/Bromocriptine)
Diagnosis of diabetes (HbA1c)
48mmol or greater (>6.5%)
Most common cause of hyperthyroidism?
Graves
Cushings disease
Increased ACTH from pituitary (anterior)
Often because of pituitary adenoma
T2DM and on triple therapy but HBA1C still high
TD2M: if a triple combination of drugs has failed to reduce HbA1c then switching one of the drugs for a GLP-1 mimetic is recommended, particularly if the BMI > 35
Test for diabetic neuropathy
10g monofilament
Addisons disease
Hypoaldosteronism
Hypothyroidism replacement doses:
Key points
initial starting dose of levothyroxine should be lower in elderly patients and those with ischaemic heart disease. The BNF recommends that for patients with cardiac disease, severe hypothyroidism or patients over 50 years the initial starting dose should be 25mcg od with dose slowly titrated. Other patients should be started on a dose of 50-100mcg od
following a change in thyroxine dose thyroid function tests should be checked after 8-12 weeks
the therapeutic goal is ‘normalisation’ of the thyroid stimulating hormone (TSH) level. As the majority of unaffected people have a TSH value 0.5-2.5 mU/l it is now thought preferable to aim for a TSH in this range
women with established hypothyroidism who become pregnant should have their dose increased by at least 25-50 micrograms levothyroxine due to the increased demands of pregnancy. The TSH should be monitored carefully, aiming for a low-normal value
there is no evidence to support combination therapy with levothyroxine and liothyronine
Side-effects of thyroxine therapy
hyperthyroidism: due to over treatment
reduced bone mineral density
worsening of angina
atrial fibrillation
Interactions
iron, calcium carbonate
absorption of levothyroxine reduced, give at least 4 hours apart
hyperparathyroidism
Primary - normal / high PTH, calcium high, phosphate low.
- seen in parathyroid adenoma. Basically produces too much PTH due to the tumor causing high calcium in blood
Secondary - High PTH, low/ normal calcium.
Seen in CKD where there is defective absorption of calcium from the gut due to low vit D. So excessive PTH production to compensate for prolonged hypocalcemia
Teritiary- all three High ( PTH, Ca, P)
Prolonged secondary beefs up the PT gland and it just starts producing PTH indiscriminately
If you are wondering why P is low in primary but high in teritiary the reason is when calcium increases kidney automatically excretes phosphate. But in teritiary kidney is already dead so phosphate remains accumulating.
Hope this helps
Kallmans
Low everything
Thyrotoxicosis with tender goitre = hyperthyroid
subacute (De Quervain’s) thyroiditis
hba1c target t2dm
48
When to add a 3rd drug for T2DM
If HbA1c >58
If QRISK >10% in T2DM what drug should be added?
SGLT2
How to calculate serum osmolality?
2xNa + Glucose + urea
in HHS should be >320
diabetic neuropathy rx
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
Cushings syndrome gas?
Hypokalaemic metabolic alkalosis
Diabetes diagnosis
Diabetes meliitus diagnosis: fasting > 7.0, random > 11.1 - if asymptomatic need two readings
subclinical hypothyroid
Subclinical hypothyroidism with TSH level of level is 5.5 - 10mU/L: offer patients < 65 years a 6-month trial of thyroxine if TSH remains at that level on 2 separate occasions 3 months apart and they have hypothyroidism symptoms
what drugs can mask the symptoms of hypoglycaemia?
b blockers e.g. atenolol
Antibodies in Graves
Anti-TPO
Symptomatic diagnosis of T2DM
f 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)
Low C peptide levels
T1DM
What condition can over-estimate HBA1c
Splenectomy
