Endocrine Guidelines Flashcards
Fasting glucose threshold diabetes
<6 is normal >7 is diabetes
Random glucose threshold diabetes
>11.1 is diabetes
OGTT threshold diabetes
>11.1 is diabetes <7.8 is normal
HBa1C threshold diabetes
48+ is diabetes <42 is normal
how often should you self monitor for diabetes
4x per day
Daily glucose targets T1DM
4-7 5-7 when waking up
HTN in diabetic black person 1st line
ACEi and CCB
DKA diagnosis
pH <7.3 bicarb <15 ketones ++ or >3 glucose >11 or known diabetes
DKA management
Need fluids: 1 2 2 4 4 6 = litre NaCl 0.9% (with KCl after first hr)
Need potassium replacement = add 40mmol if 3.5-5.5, call senior if below that.
0.1U/kg/hr insulin. 5% Dextrose when blood glucose <15
DONT STOP LONG ACTING INSULIN, stop short acting insulin
worry about cerebral oedema in young patients on treatment for DKA - monitor neuro
T2DM first line
metformin + lifestyle
hba1c target with T2DM
48 (53 on gliclazide)
When do you add a second drug in T2DM
hba1c >58
when do you use GLP1
If triple therapy has not worked (i.e. it is fourth line) and BMI >35 with problem associated with obesity or BMI <35 but insulin would affect their work badly.
HHS management What do you check doing management
- Normalise the osmolality (gradually)
- Replace fluid and electrolyte losses
- Normalise blood glucose (gradually)
(will all occur with fluid)
Fluid loss = 10=20% (in litres) of body weight (kg)
Give fluid back (half in 12 hours, half in next 12 hours)
first line: 0.9% NaCl IV
Must check that osmolality is going down (2Na + urea + glucose) so plot it on graph:
- glucose should fall by 4-6/hr
- sodium should not fall by more than 10 in 24 hour
insulin should not be used unless significant ketonaemia or acidosis
Graves disease Mx
18 months of carbimazole or block and replace
TMG Mx
radioidine or lifetime carbimazole
Toxic adenoma Mx
Radioiodinde
Thyroid storm Mx
IV propranolol, Lugol’s iodine, anti-thyroid drugs (methimazole, propylthiouracil), dexamethasone
treatment of underlying cause
the five ‘Bs’
- Block synthesis (antithyroid drug)
- Block release (Lugol’s iodine)
- Block T4 to T3 conversion (propylthiouracil, dexamethasone (steroid))
- BB (propanolol)
- Block enterohepatic circulation (cholestyramine)
When should you start at a lower dose with levothyroxine
Elderly or heart disease (start at 25 instead of 50 ug)
When do you check TFTs after starting Tx for hypothyroidism and what do you aim for
Normal TSH after 6-8w
Levothyroxine dose in pregnancy
Increase by 25-50microgram
levothyroxine dose alongside iron?
No, leave 2 hours in between as iron reduces levothyroxine absorption
Do you treat subclinical hypothyroidism
Depends If >80, no
If <80 + TSH >10, yes
If TSH only a bit raised (4-10), treat if <65
de quervains thyroiditis Mx
self limiting steroids may help hypothyroid phase
post-partum thyroiditis
propranolol in hyperthyroid phase
levothyroxine in hypothyroid phase
primary hyperPTH Mx
Parathyroidectomy
Can you ever not treat primary hyperPTH
Yes, if >50, Ca raised by <0.25, no end organ damage
Secondary hyperPTH
calcium and vit D supplementation
Tertiary hyperPTH - what about if just had a renal transplant
Excision of culprit gland Wait 12m after a renal transplant as many resolve
how to differentiate between pseudo and real cushings
Best = low dose dex suppression test Also used = insulin stress test
best test for cushings
overnight dex suppression test - give dex, and cortisol should be reduced the next morning. First do low dose then do high dose.
Addison’s best test
spank the adrenals with SYnACTHen to see if they work. measure cortisol before and 30 min after ACTH given.
Addisons ABG
hypoglycaemia, hyponatraemia, hyperkalaemia, metabolic acidosis
Mx of Addisons
hydrocortisone TDS with biggest dose in the morning + fludrocortisone
Addisons crisis management
IV hydrocortisone 100mg (big dose) only saline + dextrose if needed
prolactinoma 1st and 2nd/definitve
1st = bromocriptine/cabergoline 2nd = surgery
hypoglycaemia
depends on access - conscious = oral - unconscious no IV = IM glucagon - unconscious with IV = dextrose
diabetic foot - who gets followed up
anyone with anything more than a simple callous (so moderate or severe as opposed to mild)
hyponatraemia investigation: what do you do first
exclude pseudohypoNa (test lipid and protein) and exclude compensatory (test glucose)
Steps 1 to 3 for investigating hypoNa - addisons/diuretic - vomiting/diarrhoea - SIADH/hypothyroid - nephrotic syndrome, CCF, cirrhosis
Step 1 = depleted euvolaemic, overloaded Step 2 = urinary sodium >20 or <20 Step 3 = imagine the flow diagram and figure out what it is - addisons/diuretic = dehydrated + UNa >20 - vomiting/diarhoea = dehydrated + UNa <20 - SIADH/hypothyroid = euvolaemic + UNa >20 - failures = overloaded + UNa <20
Treatment of hypoNa - rate of Na correction - use of hypotonic saline?
normal saline 0.9% for F1 always - no more than 10mmol/24 hours - only in cerebral oedema under senior supervision
severe hypoCa management
10ml calcium glutinate 10% with ECG monitoring
hyperPTH : Ca, PO4, PTH, ALP
high Ca, low PO4, high PTH (or inappropriately normal), high ALP
malignancy with bone met: Ca, PO4, PTH, ALP
High Ca, high PO4, low PTH, high ALP
Mx of hypercalcaenia - first - ongoing helper management
3-4L per day of normal saline Bisphosphonates can be used too but these take 2-3 ays to work with maximal effect at 7d
recurrence of thyroid cancer
yearly check of thyroglobulin antibodies
HypoPTH: PTH, PO4, Ca hypoPTH vs pseudohypoPTH vs psuedopseudohypoPTH Best way to diagnose pseudohypoPTH
Low PTH, high PO4, low Ca
give PTH infusion:
hypoPTH = high PTH, high PO4, high Ca (as its usually due to PTH insufficiency so will correct if given PTH)
pseudo = high PTH, high PO4, low Ca (target cells insensitive to PTH therefore no production of calcium regarless of PTH infusion)
pseudopseudo = normal everything but physically looks like pseudo )low IQ, short 4/5th metacarpal, short BUT best way to diagnose pseudohypoPTH is by measuring urinary cAMP/PO4 after PTH infusion (stays same in pseudo as not responsive)
Mx of true hypoPTH
alfacalcidol to boost the low calcium
Conn’s syndrome (hyperaldosteronism) best Ix
aldosterone:renin will be HIGH
ABG in Conn’s
high Na, low K, metabolic alkalosis
Once Conn’s diagnosed, what test do you then do
Need to find out the cause: Do high resolution CT scan and adrenal vein sampling. helps distinguish between adenoma or hyperplasia
Mx of Conn’s - adenoma - hyperplasia
surgery spironolactone
Pheochromocytoma Ix
metanephrine/VMA in urine (NOT SERUM)
phaeochromocytoma is a tumour on adrenals releasing metanephrine and epinephrine
Phaeo Mx
surgery, but give alpha (phenoxybenzamine) then beta blockage in meantime
Acromegaly Ix FIRST BEST
first = Serum IGF1
Best (to confirm) = OGTT (to try and suppress axis. in acromegaly GH doesn’t suppress after glucose) - do if IGF-1 levels raised
acromegaly: excess GH released from anterior pituitary
Acromegaly 1st line other Tx?
first line: surgery - trans-sphenoidal
medical Tx includes octreotide (somatostatin analogue) or dopamine agonist (cabergoline/bromocriptine) GH receptor antagonist (pegvisomant - prevents dimerisation of the receptor)
Diabetes insipidus
Ix:
- to confirm
- to detect type
Check serum and urine osmolality to confirm:
- high plasma osmolality, low urine osmolality = DI
- a urine osmolality >700mOsm/kg excludes DI
Do desmopressin test to check which type:
- desmopressin is analogue of vasopressin (ADH)
- in cranial DI vasopressin not released therefore giving desmopressin would help things
- in nephrogenic DI, vasopressin released from cranial but doesnt work on kidneys therefore giving desmopressin wont work
Check for primary polydipsia as cause of polyuria (Ddx for diabetes insipidus)
Water deprivation test (urine conc will eventually go up in primary polydipsia)
Neprhogenic vs cranial DI Mx
Cranial = desmopressin Nephrogenic = thiazides and low salt/protein diet§
What do you do if metformin isn’t tolerated due to GI SEs
You try metformin MR before going to second line treatment
Thyroid eye disease management
topical lubricants ORAL not injection steroids radiotherapy surgery
bitemporal hemianopia (upper quadrant mainly affected)
moon face
striae
diagnosis
pituitary adenoma - ACTH secreting
= cushings disease
cushings disease over syndrome as bitemporal hemianopia due to pressure on optic chiasm from pituitary adenoma
pituitary adenoma Ix
pituitary blood profile (GH, prolactin, ACTH, FH, LSH, TFTs)
formsl visual field testing
MRI brain with contrast
pituitary adenoma Mx
hormonal therapy
surgery - determined by size of tumour in non-functioning pituitary adenoma - consider trans-sphenoidal surgery if progression in size noted
radiotherapy
most common type of pituitary adenoma
prolactinoma - produce excess prolactin
features of excess prolactin
men: impotence (hard to get erection), loss of libido, galactorrhoea
women: ammenorrhoea, infertility, galactorrhoea, osteoporosis
acromegaly features
excess growth hormone secondary to pituitary adenoma (most commonly)
coarse fascies
spade-like hands
increase in shoe size
large tongue
excessive sweating
bitemporal hemianopia - if caused by pituitary tumour
raised prolactin in 1/3 cases –> galactorrhoea
what conditions are acromegaly associated with
HTN
diabetes
cardiomyopathy
colorectal cancer
what does parathyroid hormone do
causes release of calcium from bone to blood
if hypoparathyroidism: low blood calcium
if hyperparathyroidism: high blood calcium
main cause of primary hypoparathyroidism
thyroid surgery
Mx of hypoparathyroidism
alfacalcidol
main symptoms of hypoparathyroidism
symptoms mainly due to the low calcium:
muscle twitching, cramping, spasm
perioral paraesthesia
trousseau’s sign: carpal spasm if brachial artery occluded by BP cuff
Chvostek’s sign: tapping over parotid causes facial muscles to twitch
ECG: prolonged QT interval
primary hyperparathyroidism - most common cause
solitary adenoma
features of primary hyperparathyroidism
high calcium
bones, stones, abdominal groans and psychic moans:
bone pain/fracture
polydipsia, polyuria
peptic ulceration/ constipation/ pancreatitis
depression
HTN
sign?
cause?
what other abnormalities would you see on investigations
pepperpot skull (like ground glass appearance) on Xray
=
hyperparathyroidism
Ix:
- raised calcium, low phosphate
PTH may be raised or normal
technetium-MIBI subtraction scan
Xray - pepper pot skull (can also get it in other bones)
features of hypopituitarism
loss of anterior or posterior pituitary hormones:
GH deficiency:
dwarfism in children
wrickled skin
Gonadotrophin deficiency:
delay in puberty
amenorrhoea, impotency, loss of libido
TSH deficiency:
- secondary hypothyroidism - sensitivity to cold, dry skin, coarseness of hair
ACTH deficiency:
- decreased skin pigmentation
- poor apetite, nausea, vomiting, muscle weakness, loss of axillary and pubic hair in females
prolactin deficiency:
- failure of lactation in post-partum patients
loss of posterior pituitary hormones:
- ADH deficiency: polyuria, thirst
- local effects in region of pituitary fossa (eg if neoplastic, infiltrative):
headache
visual field degects: superior bi-temporal quadrantanopia
progressing to bitemporal hemianopia
cerebrospinal fluid rhinorrhoea due to inferior extension of tumour
III, IV and VI nerve palsies due to lateral extension of tumour
ix hypopituitism
base levels T4, T3, TSH, prolactin, gonadotrophins, testerone, cortisol, U+Es (dilutional hyponatraemia)
FBC (normochromic normocytic anaemia)
assessment of visual fields
skull radiology
CXR signs of primart tumour thats produced mets, sarcoidosis or TB
primary vs secondary hypogonadism in males
primary hypogonadism: elevated gonadotropin levels and low testosterone levels
secondary hypogonadism: low to normal gonadotrophin levels and low testosterone levels
hypogonadism ix males
morning basal testosterone (before 11am)
if >12:
repeat TT + LH, FSH, (to determine difference between gonadal disease and hypothalamic-pituitary disease)
+ PRL (prolactin) if TT<5.2 + low LH & FSH
if TT < 8 = confirmed testosterone deficiency
if high LH = primary TD
if low/ normal LH = secondary TD
for symptomatic TD also include:
- haematocrit as part of FBC
- PSA
Mx for primary hypogonadism in males and secondary TD where ferility not desired in males
trial of Testosterone therapy (measure T levels at 3,6,12 months and then every 12 months
+ lifesytle modification
mx for secondary TD where ferility desired
AVOID T therapy (may reduce spermatogenesis)
instead use:
- HCG
- SERMs (e.g. clomifene)
Als
features of hypogonadism in females
primary and secodnary result in:
oestrogen deficiency
abnormal menstrual cycle (anovulatory cycling then irregularity then ammenorrhoea)
Ix and Mx under ammenorhoea
hypogonadotrophic hypogonadism Vs hypergonadotrophic hypogonadism
hypogonadotrophic hypogonadism:
decreased secretion of gonadotrophic hormones LH and FSH by anterior pituitary
causes:
- hypopituitarism
- selective gonadotrophic deficiency
hypergonadotrophic hypogonadism:
underlying unresponsiveness of gonads resulting in hypogonadism. get positive feedback to promote gonadotrophs to increase
features of DKA
abdominal pain
polyuria, polydipsia, dehydration
Kussmaul respiration (deep hyperventilation)
Acetone-smelling breath (‘pear drops’ smell)
HHS features
associated with T2DM
comes on over days whereas DKA comes on over hrs
General: fatigue, lethargy, nausea and vomiting
Neurological: altered level of consciousness, headaches, papilloedema, weakness
Haematological: hyperviscosity (may result in myocardial infarctions, stroke and peripheral arterial thrombosis)
Cardiovascular: dehydration, hypotension, tachycardia
HHS diagnosis
- Hypovolaemia
- Marked Hyperglycaemia (>30 mmol/L) without significant ketonaemia or acidosis
- Significantly raised serum osmolarity (> 320 mosmol/kg)
thyroid storm features
fever > 38.5ºC
tachycardia
confusion and agitation
nausea and vomiting
hypertension
heart failure
abnormal liver function test - jaundice may be seen clinically
thyroxicosis with tender goitre
+ raised ESR
diagnosis
subacute (De Quervain’s thyroiditis)
phases of subacute (De quervains) thyroiditis
causes hyper then hypo- thyroidism
in phase 1: hyperthyroidism with painful goitre, raised ESR
phase 2: euthyroid
phase 3: hypothyroidism (weeks - months)
phase 4: thyroid structure and function back to normal
Ix for subacute (De quervains) thyroiditis
thyroid scintigraphy: globally reduced uptake of iodine-131
post partum thyroiditis
three stages:
- thyrotoxicosis
- hypothyroidisim
- normal thyroid function (high recurrence rate in future pregnancies)
anti TPO antibodies found in 90% patients
dexamethasone suppression test
low dose dexamethosone: determines pseudo cushings from cushings
in normal/ pseudo: dexamethasone decreases ACTH which causes reduced production of cortisol
in cushings: cortisol remains same as another source (pituitrary, adrenal, ectopic)
high dose dexamethasone test to distinguish between pituitary, adrenal, ectopic
pituitary (cushings disease): cortisol low (high dose dex enough to reduce pituitary adenoma)
adrenal cushings syndrome (adrenal adenoma): high dose dex suppresses ACTH but cortisol still secreted from adenoma
ectopic (small cell lung cancer): cancer secretes ACTH (not reduced by high dose dex) and therefore cortisol still secreted
features of diabetes insipidus
polyuria
polydipsia (due to the polyuria)
drug known to cause diabetes insipidus
lithium
graves diseas antibodies
TSH receptor antibodies
mx of concurrent illness with addisons disease
double the glucocorticoid (hydrocortisone) and keep the mineralocorticoid (fludrocortisone) the same
management for galactorrhoea
bromocriptine
mx for MODY (maturity onset diabetes of the young)
sulphonylureas e.g. gliclazide
features of MODY
diabetes with strong family hx of early onset
usually presents <25yrs
ketosis is not a feature at presentation
patients with the most common form (MODY 3) are sensitive to sulphonylureas (gliclazide)
HNF-1 apha gene in 70% of cases
endocrine parameters reduced in stress response
insulin
testosterone
oestrogen
therefore all decreased during surgery
first line ix in primary hyperaldosteronism
aldosterone/renin ratio
- will be elevated ratio in primary hyperaldosteronism
myxoedemic coma mx
coma from hypothyroidism
mx: levothyroxine + hydrocortisone
the hydrocortisone is used to treat the presumes associated adrenal insufficiency
renal replacement therapy for independent patients first line
peritoneal dialysis
however contraindicated in concurrent abdo conditions (e.g. chrons) therefore use haemodialysis instead
when should people with CKD be put on an ACEi
ACEi are protective in CKD
give in high albumin:creatinine ratio
give if:
- ACR > 3 + co-existant diabetes
- ACR > 30 + co-existant HTN
- ACR > 70
which hormone should you monitor for recurrence of medullary thyroid cancer
serum calcitonin levels
- secrete calcitonin
primary hyperaldosteronism
features
ix
mx
HTN (treatment resistant) + hypokalaemia
first line ix: plasma aldosterone/ renin ratio = high
then high res CT abdo and adrenal vein sampling
mx:
adrenal adenoma (Conns syndrome): surgery
bilateral adrenocortical hyperplasia: aldosterone antagonist e.g. spironolactone
screening for ischaemia of diabetic foot disease
done by palpating for both dorsalis pedis pulse and posterial tibial artery pulse
screening for neuropathy of diabetic foot disease
use a 10g monofilament on various parts of the sole of foot
what is the first thing that should be initiated in a DKA
1L 0.9% NaCl IV over 1 hr
1,2,2,4,4,6
fluids first as patients are dehydrated
then 0.1units/kg/hr
long acting insulin continued, short acting insulin stopped
thyrotoxicosis + tender goitre
subacute (de Quervain’s) thyroiditis
most common cause of addisons disease in industrialised nations
autoimmune adrenalitis
most common cause of addisons disease worldwide
TB
- look for TB risk factors
how many units are there in 1 ml of insulin
100 units
