Endocrine revision Flashcards
what hormones are released from the hypothalamus
thyrotropin releasing hormone
dopamine
growth hormone releasing hormone
somatostatin
gonadotrophin releasing hormone
corticotropin releasing hormone
oxytocin
vasopressin
what hormones are released from the anterior pituitary
FSH + LH
adrenocorticotrophic hormone
TSH
GH
prolactin
what does GHRH stimulate
LH and FSH
what does CTRH stimulate
ACTH
what does GHRH stimulate
growth hormone
what does TRH stimulate
thyroid stimulating hormone
what does dopamine do
inhibits prolactin
where does FSH and LH act
gonads for germ cell development and hormone secretion
where does TSH act
throid to stimulate T3 and T4
where does GH act
on cells to control metabolism and growth by stimulating IGF-1 production
where does prolactin act
breast tissue/milk ducts to stimulate milk production
what cells does FSH act on
sertoli to secrete anti-mullerian hormone
stimulate oestrogen
what cells does LH act on
leydig for testosterone production
stimulates progesterone
what can a pituitary tumour result in
pressure on local structures (optic chiasm) resulting in bitemporal hemianopia
hypopituitarism
hyperpituitarism (acromegaly, cushings disease, prolactinoma)
how much glucose is used a day
200g/day
how much glucose comes from liver
90%
what is the major consumer of glucose
brain
why is the brain the major consumer of glucose
as it cannot use FFA
is the brain insulin dependent
no
what chromosome is insulin coded for on
chromosome 11
when is muscle/fat insulin dependent
in postprandial state
what is the goal of insulin
reduce blood glucose
how does insulin affect muscle
results in glycogen and protein synthesis
how does insulin affect fat
causes fatty acid synthesis
describe the biphasic response of insulin
1) blood glucose is increased and insulin stored in B-cells is released to increase peripheral uptake of glucose (=>glycogen)
2) glucose has not decreased enough more insulin is made and secreted, but is a lot slower
what is the goal of glucagon
to increase glucose
what is a marker for natural insulin release in the body
C-peptide
do you get C-peptide in synthetic insulin
no
what is the started molecule for insulin
proinsulin
(made of a alpha and beta strand, connected by C-peptide)
what does a GLUT-1 receptor do
basal non-insulin stimulated glucose into cells
what does a GLUT-2 receptor do
found in B-cells and has a low affinity for glucose, so when it is in high concentrations a lot of glucose is uptaken and sensed and insulin is secreted
where are GLUT-2 receptors found
B-cells and renal tubules
what does a GLUT-3 receptor do
non-insulin mediated
where are GLUT-3 receptors found
brain neurones and placenta
whar does a GLUT-4 receptor do
peripheral action of insulin on muscle and adipose to cause glucose uptake
what chromosome is insulin receptor found on
chromosome 19
what happens when insulin binds to an insulin receptor
tyrosine kinase results in GLUT-4 expression on CSM
what hormones are released by the posterior pituitary
oxytocin - paraventricular nucleus
vasopression - supraorbital nucleus
what does oxytocin do
milk ejection
labour induction
what does vasopressin do
stimulates when BP drops, stress (major factor in RAAS)
vasoconstiction in BVs
increase Aquaporin 2 expression
increases aldosterone
what are the functions of cortisol
increase protein and carb breakdown
upregulates alpha 1 on arterioles and increased BP
suppress immune response
increase osteoclast activity = osteoporotic
increase insulin resistance
what are the layers of the adrenal gland
zona glomerulosa
zona fasciculata
zona reticularis
adrenal medulla
what is released from each region of the adrenal gland
glomerulosa - aldosterone
fasciculata - cortsiol
reticularis - androgens
medulla - NAd, ADr
what are the 4 types of diabetes
T1DM
T2DM
MODY
LODA
what is MODY
maturity onset diabetes of youth - a rare auto dom T2DM presentation in young patients
what is the treatment for MODY
sulfonyurea
what is LADA
latent onset of diabetes in adults - T1DM presents in an older patient
what are three secondary causes of diabetes
acromegaly and cushings
haemochromatosis
thiazides and corticosteroids
what is T1DM
a type 4 hypersensitivity reaction which causes the autoimmune destruction of pancreatic B-cells - an absolute insulin deficiency
what is the epidemiology of T1DM
young
thin
north European (Finland)
what are some risk factors for T1DM
HLA DR2 DQ3
HLA DR4 DQ8
other autoimmune disease
environmental infection (viral)
what is the patho of T1DM
autoimmune B islet destruction leading to absolute insulin deficiency - this results in hyperglycaemia and low cellular glucose which increases lipolysis and gluconeogenesis
what electrolyte disturbance do you get with uncontrolled T1DM
hyperkalaemia - insulin is not present to drive K+ into cells
symptoms of T1DM
lean young patient with
POLYDIPSIA
POLYURIA/NOCTURIA
WEIGHT LOSS
glycosuria
what initial tests are done for a diagnosis of T1DM
random plasma glucose
fasting plasma glucose (8+ hours not eating)
what better test is done to diagnose T1DM
HbA1C (taken within three months to see glycated Hb)
what is the normal ranges for RPG and FPG and HbA1C
RPG = < 11.1
FPG = < 7
HbA1C = < 48/6.5%
what is the diabetes ranges for FPG, RPG and HbA1C
RPG = > 11.1
FPG = > 7
HbA1C = > 48/6.5%
what is the oral glucose tolerance test
give 75g of fast acting glucose then measure BG 2hr later, if Bg > 11.1 = diagnostic
treatment for T1DM
basal bolus insulin
what is basal bolus insulin
basal = long acting - maintain stable insulin levels throughout day
bolus = faster acting - 30 minutes pre-prandial to give insulin spike
what are the 4 types of insulin with examples
rapid - novorapid, aspart
short - regular insulin
intermed - NPH
long - glargine, detemir
what is the main complication of T1DM
Diabetic ketoacidosis
what is the patho of T1DM
there is a decrease in insulin and glucose leaves the cells, which leaves them with no energy resulting in FA oxidation and gluconeogenesis which results in the formation of ketone bodies = acidic and decreased O2 Hb binding
symptoms of DKA
kussmaul breathing (deep laboured breaths to blow of CO2)
pear drop breath
reduced tissue turgor
hypotension
tachycardia
diagnosis of DKA
blood ketones - >3
hypeglycaemia - > 11.1
blood pH < 7.3 / HCO3- <15
treatment of DKA
1st fluids
insulin + glucose
potassium
what is T2DM
peripheral insulin resistance with partial insulin deficiency (CHO/lipid/beta amyloid deposits in pancreas)
what is the typical epidemiology of T2DM
later in life >30y/o
males
obese
RF for T2DM
genetic link (FHx)
smoking
obesity
HTN
sedentary lifestyle
what is T2DM a Rf for
HTN
silent MI
nephrotic syndrome
CKD
what is the patho of T2DM
peripheral insulin resistance (malfunctional insulin intracellular activation pathway) resulting in decreased GLUT4 expression
leading to hyperglycaemia with an increase in insulin demand from a depleted beta cell population
symtpoms of T2DM
obese
HTN
POLYDIPSIA
POLYURIA
GLYCOSURIA
+/- acanthosis nigracans
diagnosis of T2DM
same as T1DM
diagnosis of prediabetes
impaired glucose tolerance = normal FPG <6 + 2hr OGTT 7.8-11.1
impaired fasting glucose = FPG 6.1-6.9 + 2hr OGTT < 7.8
treatment for T2DM - prediabetic
prediabetic - lifestyle changes (diet and exercise and modify RF)
treatment for T2DM
1st - metformin
sulfonylurea
DPP4-i
SGLT-2 inhibitor
insulin
what is metformin
a biguanide that increases peripheral sensitivity to insulin
what is a sulfonylurea
gliclazide - increases amount of insulin your pancreas makes
DPP4-i example
sitagliptin - blocks DPP4, an enzyme which destroys incretin so more incretin is present meaning more insulin is produced and less glucose is produced by the liver
SGLT2-i examples
dapagliflozin - reduce renal tubular glucose reabsorption (reduce BG w/o stimulating insulin release)
main complication of T2DM
hyperosmolar hyperglycaemic state
what is the pathophysiology of hyperosmolar hyperglycaemic state
excessive hepatic gluconeogenesis (not totally insulin deficient so ketogenesis doesn’t occur)
glucose is osmotically active therefore causes a hyperosmolar blood state
symptoms of HHS
severe T2DM
decreased consciousness (plasma osmolarity)
diagnosis of HSS
heavy glycosuria
increased plamsa osmolarity (>3) with hyperglycaemia
NO ketonuria/hyperketonemia
treatment of HHS
1st insulin (+ potassium and glucose)
Iv fluid 0.9% saline
LMWH - as pt has thicker blood
macrovascular complications of diabetes
MI
ischaemic stroke
PVD
microvascular complications of diabetes
retinopathy
neuropathy
nephropathy
complications of DKA
coma
hypothermia
hypotension
cerebral oedema
what is the patho of diabetic retinopathy
microaneurysms and haemorrhages of retinal vein
microinfarcts
maculopathy - fluid leakage and oedema = central vision loss
diagnosis of diabetic retinopathy
fundoscopy
optic CT
treatment for diabetic retinopathy
pan-retinal photocoagulation laser
virectomy
patho of diabetic nephropathy
hyperglycaemia results in an increased glomerular pressure, which constricts effecrent glomerular arteriole leading to fibrosis and glomerular inflammation and increase in basement membrane width
patho of diabetic neuropathy
nerve tissues metabolic and vasculature is disturbed which impairs mitochondria resulting in decreased neutrophic support leading to the injury of neurones
clinical presentation of diabetic neuropathy
pain, paraesthesia, burning sensation which is worse at night
autonomic problems - postural hypotension
glove and stocking sensory loss (foot insensitivity and dryness => damage => impaired healing and glucose rich for bacteri and no protection => ulcer => amputation)
mononeuritis multiplex
treatment for pain from diabetic neuropathy
pregabalin/gabapentin
amitriptyline
causes of hypoglycaemia
diabetes medication - insulin and sulfonylurea
liver failure
addison’s
insulinoma
pituitary insufficiency
non-pancreatic neoplasm
what are the symptoms of hypoglycaemia
decreased consciousness
dizziness
may faint
treatment for hypoglycaemia
IV glucose
or IM glucagon (if no IV access)
what spinal region does the thyroid sit
C5-T1
what connects the two lobes of the thyroid
isthmus
what supplies the thyroid
superior thyroid artery
what is the superior thyroid artery a branch of
external carotid artery
what is the process of forming T3/T4
iodine trapped
diffuses into colloid
binds to tyrosine residues on thyroglobulin using TPO enzyme creating T1/T2
TSH secreted by thyrotrophs and there is TSH-R binding which stimulates T1 and T2 release
these bind together to form either T3/T4 and released into general circulation
causes of hyperthyroidism
most common = graves disease
toxic multinodular goitre
toxic adenoma
ectopic TSH secretion
de quevain’s thyroiditis
drugs - amiodarone, iodine, lithium
how does toxic multinodular goitre cause hyperthyroidism
nodules secrete thyroid hormones
where may an ectopic secretion of TSH come from
struma ovarii (ovarian teratoma), mets
clinical presentation of de quervain’s thyroiditis
red, swollen, tender goitre post viral infection causes thyroid gland to release hormone into circulation
often causes hypo after
treatment for de quervain’s thyroiditis
aspirin
if severe - prednisolone
what is the pathophysiology of graves
TSH-R autoantibodies result in the activation of the receptor and hence the stimulation of thyroid hormones
symptoms of hyperthyroidism
heat intolerance
diarrhoea
weight loss + hyperphagia
anxiety
oligomenorrhoea
signs of hyperthyoridism
goitre
tachycardia
exopthalamous
pretibial myexoedema
muscle wasting
fine tremor
diagnosis of graves
positive TSH-R Ab’s
diagnosis of hyperthyroidism
thyroid function tests
decreased TSH and increased T4
primary hyperthyroidism (graves)
increased TSH and increased T4
secondary hyperthyroidism
increased TSH and normal T4
subclinical hypothyroid
decreased TSH and normal T4
subclinical hyperthyroid
what test can be done to differentiate graves and TMG
thyroid USS
what is carbimazole CI in and what would you give as an alternative
pregnancy and can give propylthiouracil
other treatments for hyperthyroidism
propylthiouracil
in pregnancy may also need to give levothyroxine to prevent fetal iatrogenic hypothyroid
radioactive iodine (131) - CI in pregnancy
surgery
S/E of carbimazole
agranulocytosis - presents as sore throat
complications of hyperthyroidism
thyroid storm
heart failure
osteoporosis
what is a thyroid storm
rapid deterioration of thyrotoxicosis and large amounts of T4 are released
there is sytemic decompensation which may lead to AF, HTN, coma and possible death
causes of hypothyroidism
hashimoto’s (MC in developed world)
iodine deficiency (MC in developing world)
postpartum thyroiditis
amiodarone
progressed de quervains
what is the pathophysiology of hashimotos and postpartum hypothyroidism
autoimmune thyroid destruction (anti TPO-Ab’s)
why is postpartum thyroiditis different to hashimotos
there is an acute phase where it presents during pregnancy and resolves by itself within 1 year of symtpoms
symptoms of hypothryoidism
cold intolerance
constipation
weight gain
lethargy
menorrhoea
signs of hypothyroidism
bradycardia
slow reflexes
cold hands
goitre
pretibial myexedema
increased TSH and decreased T4
primary hypothyroid
decreased TSH and decreased T4
secondary hypothyroid
increased TSH and normal T4
subclinical hypothyroid
diagnosis of hypothyroidism
TFT
anti TPO Ab’s
typically anaemic
treatment for hypothyroidism
levothyroxine
why must levothyroxine be used carefully
may cause iatrogenic hyperthyroidism so titrate to effect
complications of hypothyroidism
myxedema coma (often infection precipitated) from rapidly decreasing T4 - presents with hypothermia, loss of consciousness and heart failure
treatment for myxedema coma
levothyroixine, ABx, hydrocortisone (until adrenal insufficiency has been ruled out)
types of thyroid carcinoma
papillary (MC)
follicular
anaplastic
lymphoma
medullary cell
what is the most common type of thyroid carcinoma
papillary
symptoms of thyroid carcinoma
thyroid nodules - hard and irregular
local compression = hoarse voice
diagnosis of thyroid carcinoma
fine needle aspiration biopsy
TFT
thyroid USS
differential for hypothyroidism
depression
alzheimers dementia
anaemia
treatment for papillary and follicular thyroid cancer
thyroidectomy and radiodine
treatment for anaplastic thyroi cancer
palliative
mets sites for thyroid cancer
lungs = MC
bone
liver
brain
what is cushings disease
pituitary adenoma secreting excess ACTH
what is cushings syndrome
to much cortsiol of any cause
what causes pseudo-cushings
alcohol and will resolve within 1-3 weeks
what are the two types of causes of cushings
ACTH dependent and ACTH independent
what are some examples of dependent cushings syndrome
cushings disease (MC) and ectopic ACTH (SCLC)
what are some examples of independent cushings syndrome
iatrogensis (steroids) (MC overall cause) and adrenal adenoma
what is the patho of cushings
cortisol has a negative feedback effect on CRH and ACTH.
CRH is typically released with circadian rhythm and is increased in the morning and decreased at night, but in cushings this is lost and patient is left with irregulated CRH, ACTH and cortisol
symptoms of cushings
moon face
central obesity
purple abdo striae
osteoporosis
plethoric complexion
thin easy bruising skin
+/- easy infection and muscle atrophy
diagnosis of cushings
rule out oral steroids
random serum cortisol
dexamethasone suppression test
plasma ACTH
1st line test for suspected cushings
random serum cortisol - meaure at 12am, lowest here so if increased is abnormal
what to do if cushings is suspected and patient is on steroids
stop them
what is the dexamethasone suppression test
dexamethasone is essentially cortisol and in a healthy patient should provide negative feedback on HPA axis and decrease cortisol
1) give dexamethasone and mesaure cortisol before dex (00:00)
2) measure cortisol at 08:00am
what results might a dexamethasone suppression test show
non-cushings - suppression cortisol lvls <50mmol/L
cushings - little to no suppression
how can cushings disease be investigated
high dose dexamethasone and if there is low cortisol
if 1st line is positive what can be meausred next
plasma ACTH (after a high dose dexamethasone)
what results might be shown with plasma ACTH measurements
if increased - dependent cause - look for ectopic ACTH
if decreased - independent consider adrenal adenoma
treatment for cushings disease
transphenoidal resection
bilateral adenectomy
complication of adrenalectomy
Nelson’s syndrome
what is Nelson’s syndrome
pituitary tumour will continue to enlarge as no negative feedback being provided from the adrenals leading to an increase in ACTH and skin hyperpigmentation
treatment of adrenal adenoma
unilateral adrenalectomy
treatment of ectopic ACTH
surgical removal (SCLC)
complication of cushings
osteoporosis and T2DM
primary causes of adrenal insufficiency
developed world - autoantibodies mediated destruction of adrenals (Addison’s)
developing world - TB (+sarcoidosis)
secondary causes of adrenal insufficiency
iatrogenic (suppression of HPA axis - steroids)
other causes of adrenal insufficiency
adrenal mets (lungb liver breast)
adrenal haemorrhage
what are autoantibodies targeted against in addison’s
21-alpha hydroxylase
what is waterhouse-friderichsen syndrome
adrenal insufficiency due to adrenal haemorrhage
what is the major cause of waterhouse-fridrichsen syndrome
meningococcal meningitis
what is the patho of primary adrenal insufficiency
addison’s destroys adrenal cortex so ACTH increases and adrenal hormones decrease
what is the patho of secondary adrenal insufficiency
HPA suppression - so decreased ACTH and decreased adrenal hormones
difference in presentation of secondary and primary adrenal insufficiency
primary = skin hyperpigmentation
secondary = no skin hyperpigmentation
why do you get skin hyperpigmentation in primary adrenal insufficiency
increased ACTH stimulates POMC which form melanocytes resulting in hyperpigmentation
symptoms of adrenal insuffciency
lethargy
weight loss
postural hypotension (decreased aldosterone)
vitiligo
change in body hair (decreased androgens)
hyperpigmentation
hypoglycaemia
abdo pain and vomiting
diagnosis of adrenal insufficiency
short synACTHen test
how does the short synACTHen test work
it tests adrenal reserves
1) measure basal cortisol at 09:00 (where normally highest)
2) administer synACTHen
3) sample cortisol after 30 mins
what result would exclude addisons
plasma cortisol >580nmol/L after 30 mins
other tests to diagnose addison’s
auto 21-alpha hydroxylase Ab’s
blood
CXR (TB suspected)
ACTH 09:00 lvl (primary increased a lot, decreased in secondary)
treatment for addison’s
hydrocortisone
fludrocortisone
what should you do to the dose of a patient on steroids if they have an infection/trauma
double it as cortisol is needed for stress response
what is an adrenal crisis
severe adrenal insufficiency - especially low cortisol
symptoms of an adrenal crisis
N + V
renal failure
loss of consciousness
treatment for adrenal crisis
immediate hydrocortisone + IV saline
+/- dextrose if hypoglycaemic
what are some differentials for addisons
hyperthyroidism
haemochromatosis
anorexia nervosa
what is acromegaly
excess Human growth hormone
what is the difference between acromegaly and gigantism
acromegaly is in adults after epiphyseal fusion and gigantism is before epiphyseal fusion in children
give a cause of acromegaly
functional pituitary adenoma
what is the patho of acromegaly
GHRH secreted stimulates GH from somatotrophs which causes increased levels of IGF-1 produced from the liver which exerts its effect on ROB
symptoms of acromegaly
large hands/feet
box jaw
vision change
sleep apnoea
large intradental gaps
carpal tunnel syndrome
investigations for acromegaly
IGF-1 serum lvl = 1st line
OGTT is impaired - Gold standard
treatment for acromegaly
transphenoidal surgery
octreotide - SST analogue
bromocriptine - DA agonist
pegvisomat - GH antagonist
complications of acromegaly
T2DM, sleep apnoea
where is prolactin produced from
lactotrophs
what are the causes of hyperprolactinaemia
prolactinoma
drugs - ecstasy
what are the symptoms of hyperprolactinaemia
amenorrhoea
galactorrhoea + sexual dysfunction
decreased libido
erectile dysfunction
gynaemastacosia
(bitemporal hemianopia)
investigations for hyperprolactinemia
increased serum prolactin
what is the treatment for hyperprolactinemia
DA agonist - cabergoline/bromocriptine (can shrink tumour)
differentials for hyperprolactinaemia
prolactinoma
primary hypothyroidism
iatrogenic - drug
pregnancy
what is Conn’s syndrome
also known as primary hyperaldosteronism, it is where there is excess aldosterone independent of the RAAS
what is secondary hyperaldosteronism
too much aldosterone due to excess renin
causes of primary hyperaldosteronism (Conns’)
2/3 - adrenal adenoma - Conns
1/3 - bilateral adrenal hyperplasia
what is the patho of Conn’s
increased aldosterone results in increased sodium and decreased potassium resulting in HTN and hypokalaemia
symptoms of primary hyperaldosteronism
resistant HTN (not fixed with beta-b/ACE-i)
hypokalaemia
muscle weakness
paraesthesia
polydipsia and polyuria
investigations for hyperaldosteronism
aldosterone:renin increased - 1st line
diagnostic = serum aldosterone not suppressed with 0.9% IV saline (or fludrocortisone)
what is the renin level in primary hyperaldosteronism
suppressed
what might an ECG show in a patient with hyperaldosteronism
hypokalaemic - long PR, flate inverted T waves, U waves and ST depression
treatment for hyperaldosteronism
laproscopic adrenalectomy
spirolonactone (aldosterone antagonist) - use 4 wks pre-op and for bilateral hyperplasia
differentials for primary aldosteronism
essential HTN
renal artery stenosis
thiazide induced hypoK in pt with essential HTN
Liddle syndrome
what is diabetes insipidus
inability to concentrate urine resulting in large productions (3L+) of dilute urine a day
what are the two types of diabetes insipidus
cranial - decreased ADH secretion
nephrogenic - decreased kidney response to ADH
causes of cranial DI
ADH gene mutation
pituitary adenomas
idiopathic
caused of nephrogenic DI
renal tubular acidosis
ADH-R mutation
polyuria
patho of DI
decreased ADH = increased water loss in urine resulting in it being diluted and in high volumes
symptoms of DI
polyuria
polydipsia
hypernatraemia
lethargy/coma/confusion
severe dehydration
what should initiate suspicion of DI
3+L urine daily
what investigations should be done for DI
water deprivation test (8h) + serum and urine osmolarity
IM desmopressin and urine osmolarity
what are the normal and DI results for the water deprivation test
normally = serum osm stays normal and urine osm increases
DI = serum osm rises while urine is unchanged
what are the DI results for the IM desmopressin test
cranial - before urine osm = < 300, after >800 = adequate ADH to have effect on kidney
nephrogenic - before urine osm = <300, after <300 = ADH will have no effect on kidney
treament for cranial DI
desmopressin
treatment for nephrogenic DI
thiazides (+underlying cause)
how do thiazides work to treat nephrogenic DI
it will increased water loss at DCT therefore encouraging Na+ uptake (and water retention) which will concentrate urine and increase retention volume
differentials for DI
psychogenic polydipsia
DM
diuretic use
hypercalacemia
what is SIADH
where there is an inappropriate amount of ADH secreted leading to dilute euvolaemia
what electolyte imbalance may SIADH cause and why
hyponatraemia as excess ADH results in more water retention and therefore compensatory Na+ excretion to maintain euvolaemia
causes of SIADH
tumours - SCLC, pancreatic, pancreatic
trauma to head
infection: TB, pneumonia, meningitis
using the pneuimonic SIADH what are the causes of SIADH
SCLC
infection/immunocompromised
abscesses
drugs - SSRI’s, sulfonylurea and carbamezapine
head trauma
patho of SIADH
increased ADH independent of RAAS results in vasoconstriction and increased BP
also increased aquaporin-2 of CD therefore increasing BP by water retention (more dilute blood and sodium loss)
symptoms of SIADH
hyponatraemia symptoms
symptoms of hyponataremia
vomiting
headache
decreased GCS
muscle weakness
seizures
brainstem herniation and neurological deficits
how does hyponatraemia cause brainstem herniation
low sodium means increased compensatory water enters skulls resulting in increased ICP
causes hyponataremic encephalopathy
risk of brainstem herniation through foramen magnum (tentorial herniation)
investigations for SIADH
serum electrolytes - decreased sodium and normal potassium
urine osm high and serum osm low
give 0.9% saline to ensure it is not sodium depletion, in this case serum will normalise
treatment for SIADH
fluid restrict + hypertonic solution (conc. blood)
treat cause - excise tumour
chronic cases - furosemide, vasopressin antagonist (tolvaptan)
differentials for SIADH
pseudohyponatraemia
hypovolaemia
psychogenic polydipsia
renal failure
addison’s disease
hypothyroidism
what is carcinoid tumours and syndrome
poorly malignant tumours of enterochromaffin cells which produce 5-HT (serotonin)
where are carcinoid tumours mostly found
gastrointestinal tract at appendix
terminal ileum
(can be in lungs)
what is a carcinoid tumour
only the neoplastic cells - no symptoms
what is carcinoid syndrome
when tumour has metastasised to liver and symtpoms begin (secreted amined normally degraded by liver, but when mets present they enter straight into circulation)
what are the symptoms of carcinoid syndrome
flushing
diarrhoea
tricuspid incompetence
investigations of carcinoid syndrome
liver USS - mets
increased 5-HIAA (serotonin breakdown)
CT/MRI to locate primary tumour
treatment of carcinoid syndrome
surgical tumour excision
octeotride (somatostatin analogue) can block tumout hormoned
complication of carcinoid syndrome
carcinoid crisis - life threatening symtpoms - increase octeotride
carcinoid syndrome differentials
IBS
Crohns
menopause
asthma
what is a phaeochromocytoma
an adrenal medullary tumour that secreted catecholamines (NAd, Adr)
what are the causes of phaeochromocytoma
MEN 2a + 2b (multiple endocrine neoplasia)
neurofibromatosis (tumours deposited along myelin sheath)
what are the symptoms of phaeochromocytoma
hypertension
pallor
very sweaty
tachycardic
investigations for phaeochromocytoma
plasma metanephrines and normethanephrines (increased)
(other - urinary catecholamines and CT image tumour)
why are metanephrines and normetanephrines better than NAd/Adr
have a longer half life and so are more sensitive
treatment for phaeochromocytoma
alpha blockers first (phenoxybenzamine)
then beta-blockers (atenolol)
excise tumour with surgery if possible
what do beta blockers do in treating phaeochromocytoma
prevents reactive vasoconstriction
complications of phaeochromocytoma
HTN crisis (180/120 + BP)
Tx = phentolamine
how many parathyroid glands are there and where
4 on the posterior aspect of the thyroid
what is the parathyroid sensitive to
calcium
what increases and decreases the released of PTH
decreased calcium increases PTH
increased calcitonin decreased PTH
where is calcitonin released from
parafollicular ‘C’ cells of thyroid
differentials for phaeochromocytoma
anxiety/panic attacks
hyperthyroidism
illicit substances
carcinoid syndrome
menopause
pre-eclampsia
what does PTH do
inhibits OPG (osteoprotegerin) which allows RANK-L signalling from osteoblasts => osteoclasts => bone resorption
activates vitamin D to increased calcium and phosphate gut absorption and increases calcium absorption and phosphate excretion in DCT of kidney
what is the most common cause of hypercalcaemia in the community
hyperparathyroid
what is the most common cause of hypercalcaemia in hospital
bone malignancies like myeloma
what is the most common cause of hypoPTH
CKD
what is a primary cause of hyperparathyroidism
parathyroid adenoma (sometimes hyperparathyroid hyperplasia)
cause of secondary hyperparathyroid
physiological response to decreased calcium
- there is a compensatory hypertrophy of all glands
what is a cause of tertiary hyperparathyroidism
occurs after many years of secondary hyperPTH - glands act autonomously and release PTH irregardless of negative feedback
symptoms of hypercalcaemia
bones - excess resorption = osteopenia
stones - kidney stones
groans - abdo pain and constipation
psych moans - depression and anxiety
what is the PTH, Calcium, phosphate and ALP levels in primary hyperPTH
PTH = increased
calcium = increased
phosphate = decreased
ALP = increased
what is the PTH, Calcium, phosphate and ALP levels in secondary hyperPTH
PTH = increase
calcium = decreased
phosphate = increased
ALP = increased
what is the PTH, Calcium, phosphate and ALP levels in tertiary hyperPTH
PTH = increased
calcium = increased
phosphate = increased
ALP = increased
what does an ECG show in hypercalacaemia
short QT
how do you treat hyperparathyroidism (primary, secondary and tertiary)
primary - removal of PTH adenoma / parathroidectomy
secondary/tertiary - treat cause
complications of hyperPTH
acute severe hypercalacaemia
how do you treat acute severe hypercalacaemia
IV fluids an bisphosphonates
differentials of primary hyperPTH
multiple myeloma
sarcoidosis
thyrotoxicosis
thiazide use
immobilisation
differential for secondary hyperparathyroidism
primary hyperPTH
causes of primary hypoparathyroidism
PTH gland failure (Di George’s syndrome or idiopathic)
causes of secondary hypoparathyroidism
after surgery (parathyroid/thyroidectomy)
causes of pseudohypoPTH
peripheral PTH resistance
short statute and small 4th/5th MTC
symptoms of hypocalacaemia
convulsions, arrhythmia, tetaniy, numbness
signs of hypocalacaemia
chvostek (twitching of facial muscles when CN7 tapped over parotid)
trousseau (carpopedal spasm when applying tourniquet to forearm)
diagnosis of hypoparathyroidism
low PTH
low calcium
increased phosphate
treatment for hypoPTH
calcium supps
Vit D3
(AdCalD3)
what would an ECG show for hypoCa
long QT
what are some differentials for hypoparathyroidism
low Mg
low albumin
CKD
Vit D deficiency
causes of hypercalacaemia
most common = hyperPTH and bone malignancy
drugs - thiazides
excess Ca intake
hyperthyroid
dehydration
what does muscle tone do in increased calcium
decreased
causes of Hypocalcaemia
CKD (as decrease Vit D produced)
severe vit D deficient
hypoparathyroid
drugs - bisphosphonates, calcitonin
acute pancreatitis
what does muscle tone do in low calcium
increase
what is considered hyperkalaemia
more than 5.5 (>6.5 is an emergency)
causes of hyperkalaemia
AKI
drugs - NSAIDS, spironolactone, ACEi
addison’s
DKA (+DM)
increased intake
renal tubular acidosis
why is there abnormal heart rhythm in hyperK+
increased potassium decreases threshold for action potential and therefore depolarises earlier
symptoms of hyperK+
fast
irregular pulse
VF risk
myalgia
diagnosis of hyperK+
absent P waves
prolonged PR
tall tented T waves
wide QRS
increased K+
treatment for hyperK+
calcium gluconate = urgent
insulin + dextrose = non-urgent
what are the parameters for hypokalaemia
<3.5 (<2.5 = emergency)
causes of hypoK+
thiazides + loop diuretics
Conn’s
renal tubular acidosis
GI losses
Decrease intake
symptoms of hypoK+
hypotonia
hyporeflexia
arrhythmias (esp. AF)
diagnosis of HypoK+
decreased K+
ECG
what would be on an ECG in hypoK+
small inverted T waves
prominent U waves
ST depression
PR prolongation
treatment of hypoK+
K+ replacement
aldosterone antagonist (spironolactone)
