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which is constant the follicular or luteal phase?
name 3 features that are unique to Grave's disease?
- pretibial myxoedema
- thyroid acropachy
name the 3 different types of sulphonylureas according to length of action
- short acting: tolbutamide
- medium acting: gliclazide
- long acting: glibenclamide, chlorpropamide
in GDM, what is the first line treatment and if that fails what is used and why?
- dietary adjustment
- then insulin. not oral hypoglycaemic in pregnancy
if pt presents with acute MI and glucose >8 what is the treatment?
iv insulin sliding scale
If a pregnant lady takes insulin but has poor glycaemic control and rarely tests herself, what should she be taking?
- one long and 3 short acting insulin injections
- reduces risk of maternal and fetal complications (as less high sugar levels)
if a patient with DM2 cannot achieve good control with diet and metformin and sulphonylurea and is obese, which new drug needs to be added?
if a patient with DM2 cannot achieve good control with diet and metformin and sulphonylurea and is not obese, which new drug needs to be added?
insulin once daily, long acting
what is the MOA of metformin?
- increases insulin SENSITIVITY
- maintains weight loss
name one advantage of metformin over sulphonylurea
low risk of hypoglycaemia :)
when should metformin be avoided or stopped?
- avoid in renal failure due to risk of MALA
- tissue hypoxia - MI, sepsis
- morning before GA
- contrast medium containing iodine
what is the MOA of sulphonylureas?
increase insulin SECRETION
what are the SE of sulphonylureas?
what is the MOA of thiazolidinediones? give e.g.
- increase insulin sensitivity
- eg pioglitazone, rosiglitazone
when are thiazolidinediones used?
- if metformin + sulphonylurea combo is problematic
- the thiazolidinediones replaces whichever is CI or not tolerated
what are the SE of thiazolidinediones?
- fluid retention so care in CCF
- hepatotoxicity - so LFT every 2 months for 1 yr
what is the MOA of acarbose, when use?
- decreases breakdown of starch to sugar by inhibiting alpha glucosidase
- so less glucose absorbed
- use: add on when obese
what is the MOA of repaglinide?
stimulate insulin release
what are the precipitants of DKA?
- post surgery
- non compliance
- wrong insulin dose
what is the pathophysiology of DKA?
- lack of insulin leads to
- 1) ff. from adipose converted to ketone bodies which cause metabolic acidosis
- 2) high G into urine which takes water and solutes - creating osmotic diuresis, volume loss and so dehydration
what are the signs/symptoms of DKA?
- polyuria (due to osmotic diuresis)
- polydipsia (due to dehydration)
- lethargy (as lost so much G)
- Kussmaul's breathing
- 10% coma
- abdo pain
what would you find O/E of DKA?
- ketotic breath - fruity
- tachycardia and low BP
- inc RR
- cerebral oedema and headache
how is a diagnosis of DKA made? (4 things)
- raised blood G
- metabolic acidosis
- identify precipitant - blood cultures, MSU, CXR
what is the other cause of ketoacidosis?
what are the complications of DKA? (4)
- hypovolaemic shock
- hyperK+ as lack of insulin action to push K+ into cells
how is DKA treated?
- iv access
- iv soluble insulin by infusion pump titrated to plasma glucose (aim for 2-4mmol/l reduction per hour)
- insulin makes K enter cells so low in serum so K+ replacement titrated according to plasma K+
- but don't add K to 1st bag. check U&E firsts.
what things need to be monitored in DKA?
- cap glucose
- ABG - acidosis
- lab glucose
- Plasma osmolarity 2(Na+K) + urea + glucose
what is a serious complication of the treatment of DKA? how is this prevented?
- cerebral oedema
- prevent: limiting rate of fall of K+ and switch to 5% dextrose when glucose < 15mmol/l
what is the criteria of success for DKA?
- no ketonuria
- clinical recovery
Which thyroid tumours occur in iodine-rich areas of the gland?
what is the rule of 10s for phaeochromocytomas?
- 10% are malignant
- 10% are bilateral
- 10% are extra-adrenal
how do pts with phaeo present?
what % of HTN do phaeos account for?
what are the findings on examination of phaeo?
- dilated pupils
why should a beta blocker not be used alone in the treatment of phaeo?
- risk of unopposed alpha agonism - potentially refractory HTN
- always give alpha adreno blocker first then BB
- labetalol has combined alpha and beta block
which test is done to diagnose acromegaly?
- this should suppress GH release
- but in acromegaly GH fails to decrease