Blood tests for conditions in endo Flashcards
(33 cards)
What does the anterior pituitary release?
FAT GP
FSH and LH
ACTH
TSH
GH
Prolactin
What does the posterior pituitary release?
Oxytocin
ADH
Thyroid Axis
and function of thyroid
Thyroid- increases BMR and catabolism
Nervous system reflexes
Cardio system- increases CO
Increases bone mineralisation
The adrenal axis
function of cortisol
Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness
Function of GH
Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs
How does the parathyroid hormone axis work and how does it act to increase calcium
There are 4 parathyroid glands that sit in the corner of each thyroid gland, they respond to low calcium, low magnesium and high phosphate
PTH increases the activity of osteoclasts leading to bone reabsorption leading to an increase in calcium concentration
PTH also stimulates an increase in calcium reabsorption in the kidneys meaning that less calcium is excreted in the urine.
Additionally, it stimulates the kidneys to convert vitamin D3 into calcitriol, which is the active form of vitamin D that promotes calcium absorption from food in the small intestine.
When serum calcium is high this suppresses the release of PTH (via negative feedback) helping to reduce the serum calcium level.
Describe the RAAS system
Renin is a hormone found in juxtaglomerular cells in afferent and efferent arterioles in the kidney
Low bp- renin is released
Renin converts angiotensinogen into angiotensin 1
ACE converts angiotensin 1 into angiotensin 2
Angiotensin 2 acts on blood vessels and causes vasoconstriction
and stimulates the release of aldosterone from the adrenal glands
Aldosterone is a mineralocorticoid steroid hormone. It acts on the nephrons in the kidneys to:
Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts
Dexamethasone Suppression Test
Which Condition and what do we expect?
Cushings Disease
Low Dose Test this just checks if they have a normal adrenal axis
Give a low dose dexamethasone (1 MG) in night and measure in morning
Dexamethasone acts on hypothalamus and Anterior pituitary and inhibits the formation of cortisol, so in a normal adrenal axis, dexamethasone= low cortisol
In Cushings syndrome, the cortisol is so high the low dose doesn’t affect it so you have a normal/raised cortisol so this is suggestive of cushings
Cushings disease= pituitary adenoma.
Dexamethasone can only act on the hypothalamus and anterior pituitary so in cushings disease dexamethasone lowers the cortisol and acth
in adrenal adenoma, dexamethasone cannot work on the adrenal gland so cortisol remains high but it can work on pituitary so acth remains low
ECTOPIC ACTH from sclc
as the acth is not being released from hypothalmus and pituitary the acth and cortisol do not get supressed from dex so remains high
Dexamethasone test on
Pituitary Adenoma
Adrenal adenoma
Ectopic ACTH
Describe the structure of the Adrenal Gland
Adrenal cortex 3 layers
Zona glomerulosa- Mineralocorticoids- Aldosterone
ZOna Fasciculata- Glucocorticoids- Cortisol
Zona Reticularis- Androgens
Adrenal medulla- catecholamines- adrenaline and noradrenaline
Test in addison’s disease and electrolyte abnormalities
Short SYNacthen test
Failure of cortisol to rise after ACTH
Anti- 21 hydroxylase antibodies
Hypoatraemia
Hyperklaemia
Hypoglycaemia
metabolic acidosis
Hyperalsodteronism (conns) test
Remember
Increase sodium reabsorption from the distal tubule
Increase potassium secretion from the distal tubule
Increase hydrogen secretion from the collecting ducts
Aldosterone renin ratio high alsodterona dn low renin
hypokalaemia and hypernatraemia may be seen
investigations in SIADH
Low plasma osmolality: < 275 mOsm/kg
High urine osmolality: > 100 mOsm/kg
High urine sodium: > 30 mmol/L
Clinical euvolaemia
HYPONATRAEMIA
Acromegaly investigations
Serum IGF-1 and if that is raised OGTT
corticosteroids side effects
Glucocorticoid side-effects
endocrine: impaired glucose regulation, increased appetite/weight gain, hirsutism, hyperlipidaemia
Cushing’s syndrome: moon face, buffalo hump, striae
musculoskeletal: osteoporosis, proximal myopathy, avascular necrosis of the femoral head
immunosuppression: increased susceptibility to severe infection, reactivation of tuberculosis
psychiatric: insomnia, mania, depression, psychosis
gastrointestinal: peptic ulceration, acute pancreatitis
ophthalmic: glaucoma, cataracts
dermatological: acne
suppression of growth in children
intracranial hypertension
neutrophilia
Mineralocorticoid side-effects
fluid retention
hypertension
In cushings what metabolic abnormalities do we see
A hypokalaemic metabolic alkalosis may be seen, along with impaired glucose tolerance.
Ectopic ACTH secretion (e.g. secondary to small cell lung cancer) is characteristically associated with very low potassium levels.
we do overnight dexamethasone suppression test to confirm
Typ1 1 DM management
HbA1c every 3 months
target 48mmol hba1c
monitor glucose 4 times a day- before each meal and before bed
Monitor more frequently in hypoglycaemic episodes- illness, sport, preganncy and breast feeding
5-7 mmol/l on waking and
4-7 mmol/l before meals at other times of the day
NICE recommend considering adding metformin if the BMI >= 25 kg/m²
T2DM dietary advice
HbA1C targets
high fibre low glycaemic carbohydrates
Lifestyle only measures- 48mmol
Lifestyle and metformin 48mmol
any drug that can cause hypoglycaemia-sulfonylurea= 53mmol
Management of T2DM HbA1c target
Already on one drug, but HbA1c has risen to 58 mmol/mol (7.5%)- 53mmol is the new target
management of type 2 diabetes
STEP 1
metformin first- titrate slowly to avoid GI Upset, if standard release is not tolerated then modified release should be trialed.
At any point if cardiovascular risk increases to 10% add SGLT-2 inhibitors.
IF metformin contraindicated can use SGLT-2 alone (if cardio risk) if no cardio risk -DPP‑4 inhibitor or pioglitazone or a sulfonylurea
MOA of
metformin
Sulfonylureas
Pioglitazone
DPP-4 inhibitorsd
SGLT-2 inhibitor
GLP-1 mimetics
https://app.bitemedicine.com/textbooks/medical-school/endocrine/anti-diabetic-medications
Hashimoto’s thyroiditis features
hypothyroidism
firm non tender goitre
anti tpo and anti thyroglobulin
other autoimmune conditions e.g. coeliac disease, type 1 diabetes mellitus, vitiligo
Hashimoto’s thyroiditis is associated with the development of MALT lymphoma
Causes of hypercalcaemia
- Primary hyperparathyroidism: commonest cause in non-hospitalised patients
- Malignancy: the commonest cause in hospitalised patients. This may be due to number of processes, including;
PTHrP from the tumour e.g. squamous cell lung cancer
bone metastases
myeloma,: due primarily to increased osteoclastic bone resorption caused by local cytokines (e.g. IL-1, tumour necrosis factor) released by the myeloma cells
sarcoidosis*
vitamin D intoxication
acromegaly
thyrotoxicosis
Milk-alkali syndrome
drugs: thiazides, calcium containing antacids
dehydration
Addison’s disease
Paget’s disease of the bone**
hypoparathyroidism features
decreased pth secretion low calcium high phosphate
tetany: muscle twitching, cramping and spasm
perioral paraesthesia
Trousseau’s sign: carpal spasm if the brachial artery occluded by inflating the blood pressure cuff and maintaining pressure above systolic
Chvostek’s sign: tapping over parotid causes facial muscles to twitch
if chronic: depression, cataracts
ECG: prolonged QT interval
parathyroid disorders
Primary hyperparathyroidism- adenoma, PTH elevated, Calcium elevated Phosphate low
Secondary hyperparathyroidism- CKD or low calcium, PTH elevated, Calcium low/normal, Phosphate high, Vit D low
Tertiary hyperparathyroidism- calcium normal/high, pth- high, phosphate low, vit d normal ALP raised
