-
which is constant the follicular or luteal phase?
luteal phase
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name 3 features that are unique to Grave's disease?
- ophthalmoplegia
- 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
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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
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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?
- acarbose
- repaglinide
- rosiglitazone
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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?
- hypoglycaemia
- 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?
- infection
- post surgery
- MI
- 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)
- nausea
- vomit
- anorexia
- Kussmaul's breathing
- drowsy
- 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
- ketonuria
- identify precipitant - blood cultures, MSU, CXR
-
what is the other cause of ketoacidosis?
alcohol
-
what are the complications of DKA? (4)
- hypovolaemic shock
- hyperK+ as lack of insulin action to push K+ into cells
- gastroparesis
- coma
-
how is DKA treated?
- ITU
- iv access
- FLUIDS
- 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
- K
- 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?
- normoglycaemia
- no ketonuria
- clinical recovery
-
Which thyroid tumours occur in iodine-rich areas of the gland?
papillary cancers
-
what is the rule of 10s for phaeochromocytomas?
- 10% are malignant
- 10% are bilateral
- 10% are extra-adrenal
-
how do pts with phaeo present?
- headache
- sweating
- palpitations
-
what % of HTN do phaeos account for?
0.2-0.5%
-
what are the findings on examination of phaeo?
- dilated pupils
- HTN
- pallor
- tachycardia
-
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?
- OGTT
- this should suppress GH release
- but in acromegaly GH fails to decrease
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