Endocrine need to know Flashcards
which pancreatic cells produce insulin
beta cells
what is the antagonist of insulin
glucagon
a random blood glucose of what would diagnose diabetes
> 11.1
name the slow onset version of T1DM
LADA
name 3 signs of DKA
Ab pain
vomiting
signs of systemic shock
what is the target HbA1c for T1DM
48-58
what are the 2 main factors contributing to T2DM
genetics
diet and lifestyle resulting in obiesity
what is the underlying pathology in T2DM
insulin resistance
what is the target HbA1c for T2DM
48-53
which 2 drugs can cause type 3 diabetes
steroids and anti-psychotics
which 3 endocrine disorders can cause type 3 diabetes
cushings
phaeochromocytoma, acromegaly
what is the inheritance pattern of MODY and what distinguishes it form T1DM
AD
no auto antibodies present
mild onset of symptoms over months
which drug is used to treat MODY
sulphonylureas
define hypoglycaemia
blood sugar <4mmol
what are the 3 biochemical markers of DKA
hyperglycaemia
ketones in blood
high anon gap acidosis
how is DKA defined
a state of insulin DEFICIENCY causing hyperglycaemia and dehydration
which type of diabetes is DKA seen in
T1DM
which type of diabetes is Hyperglycemic hyperosmolar syndrome seen in
T2DM
how is the presentation of HHS different from DKA
HHS is slow onset (days/weeks) and affects mainly elderly
HHS only associated with dehydration, no ketoacidosis as there is residual insulin
tx for HHS
insulin sliding scale
what is the most active form of thyroid hormone
T3 - needs to be transported bound to a plasma protein (thyroid binding globulin is the main one)
how does graves disease cause hyperthyroidism
an AI disease- production of antibodies that. mimic TSH to release T3/T4 in the absence of TSH
what are the 3 antibodies seen in grave’s disease
TRAB stimulating
anti-thyroid perioxidase
anti-thyroglobuin
what are 3 specific signs of grave’s
pre tibial myxoedema
bilateral exophthalmus
ophthalmoplegia
which cause of hyperthyroidism occurs post virus and how is it treated
sub-acute deQuervains thyroiditis
Tx = NSAIDS
what are the TFT results in primary hyperthyroidism
high T3/T4
low TSH
what are the TFT results in secondary hyperthyroidism
high T3/T4
high TSH
(suggests problem is in the hypothalamus)
what is used to treat hyperthyroidism and what is the major side effect
carbimazole - antithyroid medication
agranulocytosis
hashimito’s thyroiditis causes an associated risk of what cancer
B cell NHL
what antibody is most commonly seen in hashimoto’s
anti-thyroid peroxidase (anti-TPO)
what is the most common cause of hypothyroidism
atrophic thyroiditis
what is the tx for hypothyroidism
levothyroxine - T4
name the 5 types of thyroid cancer
- follicular
- papillary
- medullary
- anaplastic
- lymphoma
what is the most common type of thyroid cancer
papillary
which thyroid cancer presents with orphan Annie nuclei and calcified psammoma bodies on histology
papillary
describe the differences in age of patients in papillary vs follicular
papillary - younger patients - 20-30y/o
follicular - older patients- >50y/o
which thyroid cancer is associated with abnormal secretion of calcitonin and hypercalcemia
medullary
which thyroid cancer is almost always associated with an underlying AI disease (eg-hashimotos)
lymphoma
what is the gold standard diagnostic test for thyroid malignancy
US guided FNA
what is the name of the enzyme responsible for the production of hydroxyapatite in bone
alkaline phosphatase (ALP)
what causes the release of parathyroid hormone
it is released in response to lowering of serum calcium
what is the net affect of PTH release
increased calcium and reduced phosphate
increased osteoclastic activity and bone resorption (breakdown)
decreased phosphate resorption in the kidneys
stimulation of biologically active vit d
what is the biologically active form of vit D called
calcitriol
what is the role of vit D in terms of reabsorption
it increases reabsorption of calcium and phosphate in the small intestine and -ivley feedback on PTH release
what is the method of action of biphosphonates
prevent bone resorption by killing off osteoclasts
what is the metabolic picture seen in pagets disease of the bone
increased osteoblastic and osteoclastic activity causing disorganised and weakened bone formation
what is the difference between osteoporosis and osteomalacia/rickets
osteoporosis has a low bone mass
osteomalacia/rickets has a normal bone mass but a LOW mineral content within the bone
what is the most common cause of primary hyperparathyroidism
a solitary parathyroid adenoma (80%)
how does hyperparathyroidism present
hypertension
bone pain
hypercalcemia - kidney stones, sore bones, stomach groans, and psychiatric moans
describe secondary and tertiary hyperparathyroidism
elevated PTH in response to hypocalcemia
what is the difference between secondary and tertiary hyperPTH
secondary is physiological
tertiary is when there is HYPERPLASTIC CHANGES in parathyroid glands due to PROLONGED hypocalcemia
causes of 2ndry or tertiary hyperPTH
vit D deficiency
CKD
what is the biochemical profile of secondary and tertiary hyperPTH
Secondary: low Ca, High PTH and PO4.
Tertiary: high calcium, very high PTH, low PO4
which 3 cancers can can cause release of PTH and what is the biochemical profile
small cell lung
renal
breast
make a protein that mimics PTH
High Ca, low PTH
what metabolic imbalance can dehydration cause
hypercalcemia
raised albumin
raised urea
what does MEN stand for
multiple endocrine neoplasia
what is MEN
a group of genetic endocrine disorders that are associated with the development of multiple hormone secreting tumours
what are the 3 types of MEN
MEN 1 - 3P’S
MEN 2A - 2P’S
MEN 2B- 1P
what 3 tumours are associated with MEN 1 (3P’s)
Parathyroid
Pituitary
Pancreas
what 3 tumours are associated with MEN 2A (2P’s)
parathyroid
pheochromocytoma
thyroid medullary carcinoma
what 3 tumours are associated with MEN 2 (1P)
pheochromocytoma
medullary thyroid carcinoma
mucosa neuroma
marfanoid appearance
where does the pituitary sit
the sella turcica of the sphenoid bone
what hormones are stored in the posterior pituitary
ADH
Oxytocin
what hormones are produced and released from the anterior pituitary
TSH, LH, FSH, ACTH, GH, prolactin
what provides negative control over prolactin release
dopamine
what test is used to measure GH and ACTH axis
insulin tolerance test
what should happen to GH and ACTH when you give IV insulin
insulin is a natural stimulator of GH and ACTH - there should be cortisol release from ACTH
how is an ACTH deficiency and adrenal cortical function tested
short synthACTHen test
pituitary tumours are almost always what type
benign adenomas
what is the most common benign pituitary adenoma
prolactinoma
what is the 1st Line surgical management for a pituitary adenoma
trans sphenoidal surgery +/- radiotherapy
what is a craniopharngioma
a tumour of rathkes pouch, where the pituitary originates
what tumour is most likely the causative in 5-15y/os who present with growth retardation
craniopharyngioma
what drugs can induce a hyperprolactinoma
drugs that inhibit dopamine
- anti-emetics (metoclopramide, domperidone)
- anti-psychotics (typical and atypical)
name the 1st line dopamine agonists given in hyperprolactinoma
cabergoline and bromocriptine
which cancer is associated with acromegaly
bowel cancer
what CV risks are associated with acromegaly
hypertension
LV hypertrophy and failure
increased risk of IHD
what is the gold standard diagnosis in acromegaly
glucose tolerance test
in a physiological GTT, what should happen to the GH levels
GH is suppressed by the glucose
describe the effect insulin and glucose have on GH and cortisol secretion
insulin- increases their secretion
glucose - inhibits their secretion
what structural pathology causes acromegaly
MACROadenoma
what is 1st line management of acromegaly
surgical removal of pit tumour +/- radiotherapy
what is the 2nd line Pharma management of acromegaly and describe its MOA
somatostatin analogue - it is the natural analogue of GH
reduces GH secretion by providing negative feedback and blocking peripheral action
describe the difference between central and nephrogenic diabetes insidious
central DI = failure to produce ADH
nephropgenic DI = failure of kidneys to respond to the ADH
what drug can cause nephrogenic DI
lithium
how is diabetes insipidus defined
passage of large volumes (>3l) of water per day
what is the gold standard test for DI and how does it work
water deprivation test - will indicate if body is able to concentrate urine
if urine cannot be concentrated then DI can be diagnosed (osmolality >600 is indicative)
what is the action of ADH
it stimulates aquaporins to open and reabsorb water
after water deprivation test, how is central DI differentiated from nephrogenic DI
synthetic ADH is given.
If concentration of urine is seen, it suggests central DI
No concentration of urine suggests nephrogenic DI
how is central DI treated
desmopressin (synthetic ADH )
how is nephrogenic DI treated
thiazide diuretics - generate hyponatremia and drive water reabsorption
what is produced in the zona glomerulosa of adrenal gland (outer layer)
mineralocorticoids
what is produced in the zona fasciculata of adrenal gland (middle layer)
glucocorticoids
what is produced in the zona reticularis of adrenal gland (inner layer)
androgen precursors
what is produced in the medulla of the adrenal gland
catchecolamines (adrenaline and noradrenaline)
what is the pathophysiology of primary adrenal dysfunction
failure within the adrenal glands so reduced cortisol and aldosterone released
what is the most common cause of primary adrenal dysfunction
AI - Addison’s disease
what causes the hyperpigmentation of skin in primary adrenal insufficiency
increased levels of ACTH
ACTH is upregulated in an attempt to increase cortisol production
what is the Na, K and glucose in primary adrenal dysfunction
Low Na, glucose
high K+
what is the diagnostic test for primary adrenal insufficiency
short synACTHen test
what is the treatment of primary adrenal deficiency
mostly steroid replacement
aldosterone def - give fludrocortisone
cortisol def - hydrocortisone
what should be done on sick days with steroid treatment
double the dose of steroids for at least 1 week
what is raised 17 hydroxyprogesterone diagnostic of
bilateral adrenal hyperplasia
what can long term, excessive steroid use cause
secondary adrenal insufficiency - synthetic steroids cause dampening down of the steroid axis
in secondary adrenal insufficiency, are both steroid types reduced
NO - only corticosteroids
mineralocorticoids are under control of RAAS so aren’t affected by ACTH deficiency
what makes secondary adrenal insufficiency clinically different from primary
no dehydration
no skin pigmentation - the ACTH isnt being produced
what is the treatment of secondary adrenal insufficiency
oral hydrocortisone
what is the diagnostic test for primary hyperaldosteronism
plasma aldosterone:renin ratio >750
saline suppression test - inability to suppress aldosterone production by >50% following water consumption
what is the diagnostic test in cushing’s
48 hour dexamethasone suppression test
what is the screening test for cushing’s
overnight dexamethasone suppression test
what do phaeochromocytoms mostly produce
noradrenaline
what are the 4 main symptoms of a pheochromocytoma
headache e
palpitations
sweating
hypertension
before surgery can be carried out for a pheochromocytoma, what needs to be done
protect blood pressure!
give alpha blocker FOLLOWED BY beta blocker
