Endocrine Flashcards
Which DM meds contraindicated in HF
Pioglitazone
Factors that decrease HbA1c
sickle cell, GP6D Def, hereditary spherocytosis, haemodialysis
Factors that increase HbA1c
vit B12/folic acid def, IDA, splenectomy
sulfonylureas mechanism
gliclzide, glipizide, tolbutamide. bind to ATP-dependent potassium channel of pancreatic beta cells
Target HbA1c life style
48mmol/L 6.5%
Target HbA1c life style + metformin
48mmol/L 6.5%
target HbA1c DM control second agent OR receiving meds which may cause HYPOglycaemia
53mmol/L 7%
Dx DM2
Sx fasting glucose >=7mmol/L
Random glucose >=11mol/L or after 75g OGTT
HbA1c >= 48mmol/L (6.5%)
When to add 2nd drug T2DM
HbA1c rises to 58mmol/L (7.5%)
Aldosterone electrolyte
low potassium, high sodium, increase blood volume, high BP
Dx DKA
glucose >11mmol/l OR known DM; pH < 7.3 or bicarb <15mmol/l, ketones >3mmol/l OR urine dip stick ++ ketone
electrolyte in Conn’s
hyperaldosteronism
hypernatraemia
Hypokalaemia
metabolic alkalosis (proton loss)
when to add DPP-4 inhibitor
only if pt does NOT tolerate triple tx
causes WEIGHT LOSS
Subclinical hypothyroidism definition
TSH high, normal T3+T4
ASX
Mx subclinical hypothyroidism
TSH >10mU/L + T3/4 normal: offer levothyroxine if elevated 2 separate occasion taken 3months apart
TSH 5.5-10 + normal T3/4:
<65yrs offer 6month trial of levothyroxine
if >80yrs-> watch + wait
Pituitary cause of hypothyroidism: lab result
low TSH + T3+ T4
(LOW EVERYTHING)
Aim of levothyroxine
normalisation of TSH level
What to do with iron + levothyroxine
levothyroxine absorption decreases with iron-> give at least 2 hours apart
What is Hashimoto’s thyroiditis
What does it cause HYPER/ HYPOthyroidism?
Autoimmune thyroiditis
transient thyrotoxicosis in acute phase BUT later results in HYPOTHYRODISM
Ab in Hashimoto’s thyroiditis
anti TPO, anti- thyroglobulin
What is subacute thyroiditis
What does it cause HYPER/ HYPOthyroidism?
Typically occurs follwoing viral infection
De Quervain’s thyroiditis
Phase 1: hyperthyroidism, painful goitre, high ESR
2. Euthyroid
3. Hypothyroidism
4. Thyroid structure and function- normal
Phases of subacute thyroiditis
- 3-6 weeks: hyperthyroidism, PAINFUL GOITRE, raised ESR
- 1-3 wks: euthyroid
- wks- months: hypothyroidism
- back to normal
Which disease causes painful goitre
subacute thyroiditis/ De Quervain’s thyroiditis
Mx subacute thyroiditis
self limiting
analgesia: NSAIDS, aspirin
severe: steroid
Most common cause of thyrotoxicosis
Grave’s disease
Ab found in Grave’s disease
TSH receptor stimulating Ab
Anti- TPO Ab
Mx Grave’s disease
- initial sx mx: propranolol
- antithyroid meds: carbimazole 40mg
3, Radioidodine- relapse follow ATD OR resistant to ATD
- CI: agre, <16yrs, thyroid eye disease-> may worsen
Mx Thyroid storm
1st line: BB- iv propranolol (CI: COPD, ASthma), calcium channel bl can be used
ATD: Methimazole/ Propylthiouracil PTU
Lugol’s iodine
dexamethasone
Plasma exchange
Primary hyperaldosteronism aka, sx esp electrolyte
Conns disease
Hyperkalaemia, hyponatraemia, hypertension metabolic alkalosis
Addison disease , sx, mx
Primary adrenal insufficiency
Low sodium, high potassium, low BP, metabolic acidosis, low BM
Give hydrocortisone, fludrocortisone.
Sick day rule, double dose of hydrocortisone
Affects of adrenal and what disease is insufficiency
Increases sodium, decreases potassium, increases BP, increases BM.
Causes Addisons disease
Normal levels of cortisol 9am
If cortisol >500nmol/l unlikely abonormal
If btw 100-500 will need short sync than test
If <100 then def. Abnormal
Ix for addisons disease
Primary aldrenal insuffficiency
Check 9am cortisol
>00nmol/l normal
Btw 100-500nmol/l then need short sync than test
If <100nmol/l then def. Abonormal
Short synectan test take cortisol 30min before giving sync then and 30min after
Is cortisol level is still low then do of primary adrenal insufficiency as synacthen is copy of ACTH
Ix for conns disease
1st line:aldosterone:renin ratio
If primary- high aldosterone:low renin
If secondary high aldosterone &renin
Mx of conns disease\ hyperaldosteronism
Adrenal adenoma- lap adrenalectomy
If bilateral adrenal, hyperplasia- needs aldosterone ATG- spironolactone
Diabetic neuropathy mx
1st line: amitriptyline, duloxetinem gabapentin, pregabalin
2nd line: tramadol rescue
Try others first before changing
AutoAb found in DM1
Anti-glutamic acid decarboxylase, islet cell AB, insulin autoantibody , insulinoma ass 2 AutoAb.
C -peptide low
Dx of impaired fasting glycemic
Fasting >6.1 but <7mmol/l
After 2hours <7.8mmol/l
Impaired glucose tolerance dx
Fasting <7 mmol/l
2hour >7.8 mol/l but <11mmol/l
Visual disturbances in prolactinoma
Bitemporal hemianopia or upper quadrant quadrantopia
Mx prolactinoma
> 1cm macroadenoma- likely need surgery
Or medical mx
Dopamine AG- cabergoline or bromocriptine inhibit release of prolactin from pituitary gland
Pheochromocytoma mx & dx
Alpha blocker- phenoxybenzamine 1st then beta blocker
Dx: 4 hr urine metanephrines 1st line or 24 hour collection of catechilamine
Which drug can cause gynaecomastia
Spironolactone, anabolic steroid,
Regulation of prolactin
Mx of hyperprolactin level
Dopamine inhibit release of prolactin
TRH therefore hypothyroidism stimulates prolactin release
Mx: dopamine AG: cabergoline, bromocriptin
Treat hypothyroidism
Indication of anti thyroid drug in pregnancy
PTU can use in 1st trimester
Methimazole can use in 2nd trimester
Radioiodine contraindicated
Antibodies of Graves’ disease
Graves’ disease - hyperthyroidism AutoAb against thyroid stimulating receptor in follicular cell
TSH-R Ab, anti-thyroid peroxidase Ab
What needs to be taken into consideration when taking thyroxine?
Iron decreases absorption of thyroxine therefore taken 2 hours apart
Causes of pri, sec, tertiary hyperparathyroidism
Primary: solitary adenoma of parathyroid gland
Sec: CKD, vit D deficiency-> chronically low calcium level stimulates parathyroid hormone
Tertiary: due to long term secondary parathyroidism, proliferation of parathyroid gland cells therefore produce excessive path even if level normalised
Mx hypercalcaemia
1st line: ivi/ loop diuretics
Increase GI excretion- glucocorticoids
Prevent bone resorption- bisphosphonat4, calcitonin
Causes of Conn’s disease
Hyperaldosteronism
Primary- adrenal adenoma, hyperplasia
Secondary: outside adrenal Renin dependent- low Bp eg HF, cirrhosis, renal artery stenosis
Causes of hyperaldosteronism
Primary: adrenal axis- idiopathic hyperaldosteronism, conns syndrome- bilateral idiopathic adrenal hyperplasia
Secondary: outside adrenal low BP, cirrhosis, renal arthritis stenosis
