Endocrine Flashcards
treatment of myxoedemic coma
hydrocortisone and levothyroxine
treatment of thyrotoxic storm
Beta blockers, propylthiouracil and hydrocortisone
when should a second drug be added to metformin in T2DM
if HbA1C>58mmol/mol
What diabetic drugs can be continued in pregnancy
Only metformin and insulin
causes of Cushing’s
iatrogenic (exogenous steroids)
pituiatry ACTH producing tumour (cushings disease)
Ectopic ACTH from lung cancer
Primary adrenal tumour (ACTH independent)
diagnosing Cushings
- measure increased cortisol and exclude exogenous steroids
- Dexamethasone suppresion test. If normal dex suppresses ACTH
Cushings disease (pituitary) is suppressed by high dose
Ectopic ACTH/Adrenal tumour is not suppressed - venous sampling at inferior petrosal sinus can detect ACTH from pituitary
what electrolyte abnoramlity is seen in Cushings
excess cortisol leads to increased sodium, increased bicarb and decreased potassium
causes metabolic alkalosis
treatment of cushings
if operable operate
if not suppress cortisol synthesis using drugs; metyrapone or ketoconazole
causes of nephrogenic diabetes insipidus
management
genetic
electrolyte abnormalities (increased calcium, decreased potassium)
lithium
tubulointerstitial disease
thiazides and low salt/protein diet
examples of following diabetic drugs + main side effects
biguanide
sulphonylureas
DPP4inhibitors
SGLT2 inhibitors
GLP1 agonists
biguanide - metformin - GI effects and lactic acidosis
sulphonylureas - gliclazide, glimperide - hypo risk, weight gain
DPP4inhibitors - gliptins - pancreatitis
SGLT2 inhibitors - gliflozins - UTIs
GLP1 agonists - glutides
test results in primary hyperparathryoidism
most common cause
low phosphate and high PTH and calcium level
solitary adenoma of the parathyroid causing increased PTH
test results in secondary hyperparathryoidism
causes
high PTH, low phosphate and low calcium
renal failure
vitamin D deficinecy
test results of tertiary hyperparathyroidism
high PTH, high phosphate and high calcium with decreased vit D
caused by end stage renal failure
what can happen if you wihtdraw steroids abruptly
precipitate an addisonian crisis
diagnosis of gestational diabetes
fasting glucose of >5.6
or 2 hour glucose of >7.8
What hormones do each layer of the adrenal gland produce
Zona glomerulosa - mineralocorticoids
Zona fasiculata - glucocorticoids
Zona reticularis - androgen precursors
Medulla - catecholamines
What does metyrapone do?
It is a glucocorticoid synthesis inhibitor
How do you measure
- urinary cortisol
- plasma cortisol
- salivary cortisol
Urinary - 24 hour collection
Plasma - 9am cortisol, evening or midnight. Midnight most different from normal
Salivary - late night highest specificity for Cushing diagnosis
Treatment of adrenal crisis
High dose steroid replacement - IV hydrocortisone 100mg every six hours
IV saline (with dextrose if hypoglycaemic)
Diagnosing adrenal insufficiency
Treatment
High dose short synacthen test - give ACTH and see if adrenals respond
Treatment is steroid replacement
What is SIADH?
Diagnosis?
Causes?
Syndrome of inappropriate ADH secretion - more water reabsrobed by kidneys leading to dilute serum and concentrated urine
Diagnosis; low serum osmolaltiy with high urinary osmolality
Causes:
Lung diseases
Brain lesions
Drugs e.g. carbamazepine, SSRIs
Symptoms and signs of hyponatraemia
Headache dizziness and nausea
Can result in coma if severe
Can be hypovolaemic or hypervolaemic hyponatraemia
Hypovolaemic:
Cool peripheries
Tachycardia
Postural Hypotension
Confusion
Dehydrated
Hypervolaemic:
Tachycardia
Raised JVP
Pulmonary oedema
Ascites
Peripheral oedema
Causes of hyponatraemia
Renal loss; addisons, renal failure, excess diuretics
Loss elsewhere; diarrhoea, vomiting, burns, trauma
SIADH, water overload, severe hypothyroid, glucocorticoid insufficiency
Nephrotic syndrome, cardiac failure, cirrhosis, renal failure
When does hypernatraemia occur
Dehydration without access to water e.g. in elderly demented patients
What are the criteria for bariatric surgery
BMI of over 40 or 35-40 with other significant disease that could be improved with weight loss
All non surgical measures have been tried
Has been / will receive intensive management in a tier 3 service
Fit enough for surgery
What is osteomalacia
Softening of the bones secondary to vitamin D deficiency (primary, CKD or other)
Presents with bone pain, fatigue, and proximal myopathy
what gastric complications can T1DM cause
- gastroparesis; manage with metoclopramide, domperidone or erythromycin (prokinetic agents)
- chronic diarrhoea
- GORD
what type of diabetes are C peptide levels raised in
type 2
what antibodies can be raised in T1DM? (approx 80%)
anti-GAD
islet cell antibodies
insulin antibodies
what is acromegaly
what is the most common cause
excess growth hormone
most commonly due to a pituitary adenoma
tests to diagnose acromegaly
serum IGF-1 levels
if raised do an oral glucose tolerance test (OGTT) - in acromegaly there is no suppression of GH due to increased glucose
pituitary MRI may demonstrate a pituitary tumour
management of acromegaly
trans-sphenoidal surgery if possible
if not:
- somatostatin analogues
- GH receptor antagonist
- dopamine agonists effective in minority
features of addisons disease
- lethargy, anorexia, weakness, N & V
- hyperpigmentation (primary addisons)
- hypotension
- hypoglycaemia
- hyponatraemia and hyperkalaemia
addisons disease management
glucocorticoid and mineralocorticoid replacement therapy
hydrocortisone given daily in 2-3 divided doses
fludrocortisone
addisons treatment changes in an intercurrent illness
double glucocorticoid
keep mineralocorticoid the same
diagnostic criteria T1 DM
fasting glucose 7.0mmol/L or more
random glucose (or glucose tolerance test) 11.1mmol/L or more
on one occasion if symptomatic or two if asymptomatic
when should SGLT2 inhibitors be used in T2DM
after metformin is titrated up
in anyone with or at high risk of CVD
2nd drug choice and when T2DM
when HbA1C >58 on metformin
in CVD risk - SGLT2 inhibitor
if not at risk - DPP4i, pioglitazone or a sulphonylurea
HbA1C targets T2DM
48
53 if on a drug that has hypo risk e..g sulphonylurea
types of thyroid cancers
papillary carcinoma - best prognosis, most common
follicular carcinoma
medullary carcinoma - part of MEN2
anaplastic carcinoma - worst prognosis
triple therapy options in T2DM
metformin + sulphonylurea + DPP4i (gliptin)
metformin + sulphonylurea + pioglitazone
metformin + (pioglitazone or sulfonylurea or DPP-4 inhibitor) + SGLT2i if certain criteria met
sulphonylureas:
- names
- main side effect + risk
- pregnancy?
gliclazides
weight gain
risk of hypos
avoid in pregnancy and breastfeeding
hypoglycaemia with impaired GCS?
give IV glucose STAT if access
treatment of a prolactinoma
cabergoline - a dopamine agonist
dopamine inhibits prolactin release
thyrotoxicosis with a tender goitre?
subacute (de quervain’s) thyroiditis - typically follows a viral infection
phases of subacute thyroiditis
1 - tender goitre, hyperthyroidism, ESR raised (3-6 weeks)
2 - euthyroid (1-3 weeks)
3 - hypothyroid (weeks to months)
4 - return to normal
which hormones reduce in a stress response e.g. to surgery
insulin
oestrogen
testosterone
primary hyperaldosteronism
hypertension
hypokalaemia - muscle weakness
alkalosis
investigation primary hyperaldosteronism
plasma aldosterone/renin ratio
- will show aldosterone too high and low renin (negative feedback)
CT abdomen if raised
adrenal venous sampling if CT inconclusive
causes of primary hyperaldosteronism
bilateral adrenal hyperplasia (most common)
adrenal adenoma secreting aldosterone (conn’s syndrome)
rarely familial or an adrenal carcinoma
what is secondary hyperaldosteronsim
excessive renin stimulates the adrenal glands to secrete more aldosterone
due to blood pressure in kidneys being disproportionately lower to rest of body
e.g. renal artery stenosis or obstruction
heart failure
management of primary hyperaldosteronsim
bilateral adrenal hyperplasia - spironolactone (aldosterone antagonist)
adrenal tumour - surgery
DKA management
isotonic saline first! restore volume
fixed rate insulin infusion (long acting insulin continued, short acting stopped)
potassium may need replacing due to insulin moving it into intracellular place
typical presentation of primary hyperparathyroidism
typically elderly females with an unquenchable thirst and polydipsia
most commonly due to a solitary adenoma
investigation results primary hyperparathyroidism
high calcium
high or normal PTH
low phosphate
definitive management of primary hyperparathyroidism
total parathyroidectomy
