Blood tests for conditions in endo

Question 1

What does the anterior pituitary release?
FAT GP

Answer 1

FSH and LH
ACTH
TSH
GH
Prolactin

Question 2

What does the posterior pituitary release?

Answer 2

Oxytocin
ADH

Question 3

Thyroid Axis
and function of thyroid

Answer 3

Thyroid- increases BMR and catabolism
Nervous system reflexes
Cardio system- increases CO
Increases bone mineralisation

Question 4

The adrenal axis
function of cortisol

Answer 4

Inhibits the immune system
Inhibits bone formation
Raises blood glucose
Increases metabolism
Increases alertness

Question 5

Function of GH

Answer 5

Stimulates muscle growth
Increases bone density and strength
Stimulates cell regeneration and reproduction
Stimulates growth of internal organs

Question 6

How does the parathyroid hormone axis work and how does it act to increase calcium

Answer 6

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.

Question 7

Describe the RAAS system

Answer 7

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

Question 8

Dexamethasone Suppression Test

Which Condition and what do we expect?

Answer 8

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

Question 9

Dexamethasone test on
Pituitary Adenoma
Adrenal adenoma
Ectopic ACTH

Answer 9

Question 10

Describe the structure of the Adrenal Gland

Answer 10

Adrenal cortex 3 layers
Zona glomerulosa- Mineralocorticoids- Aldosterone
ZOna Fasciculata- Glucocorticoids- Cortisol
Zona Reticularis- Androgens

Adrenal medulla- catecholamines- adrenaline and noradrenaline

Question 11

Test in addison’s disease and electrolyte abnormalities

Answer 11

Short SYNacthen test
Failure of cortisol to rise after ACTH
Anti- 21 hydroxylase antibodies
Hypoatraemia
Hyperklaemia
Hypoglycaemia
metabolic acidosis

Question 12

Hyperalsodteronism (conns) test

Answer 12

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

Question 13

investigations in SIADH

Answer 13

Low plasma osmolality: < 275 mOsm/kg
High urine osmolality: > 100 mOsm/kg
High urine sodium: > 30 mmol/L
Clinical euvolaemia
HYPONATRAEMIA

Question 14

Acromegaly investigations

Answer 14

Serum IGF-1 and if that is raised OGTT

Question 15

corticosteroids side effects

Answer 15

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

Question 16

In cushings what metabolic abnormalities do we see

Answer 16

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

Question 17

Typ1 1 DM management

Answer 17

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

Question 18

T2DM dietary advice
HbA1C targets

Answer 18

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

Question 19

management of type 2 diabetes

Answer 19

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

Question 20

MOA of
metformin
Sulfonylureas
Pioglitazone
DPP-4 inhibitorsd
SGLT-2 inhibitor
GLP-1 mimetics

Answer 20

https://app.bitemedicine.com/textbooks/medical-school/endocrine/anti-diabetic-medications

Question 21

Hashimoto’s thyroiditis features

Answer 21

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

Question 22

Causes of hypercalcaemia

Answer 22

1. Primary hyperparathyroidism: commonest cause in non-hospitalised patients
2. 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**

Question 23

hypoparathyroidism features

Answer 23

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

Question 24

parathyroid disorders

Answer 24

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

Question 25

thyroid disorders

Answer 25

https://www.passmedicine.com/v7/menu.php#

Question 26

blood test in addisons disease

Answer 26

hyponatraemia, hyperkalaemia hypoglycaemia metabolic acidosis

Question 27

bloods in DKA

Answer 27

hyperglycaemia, metabolic acidosis ketonaemia

Question 28

features of hyperaldosteronism

Answer 28

so aldosterone is needed to absorb sodium and excrete h+ and potassium so we get
Hypernatraemia and hypokalaemia

Question 29

fluid status causes o fhyponatraemia

Answer 29

hypovolaemia- low fluid, aything that causes a loss of fluid also causes hyponatraemia
GI loss: diarrhoea, vomiting
Transdermal loss: sweat, burns
Renal loss: diuretics
3rd space loss: bowel obstruction, pancreatitis, sepsis
Endocrine: Addison’s disease

Euvolameia- normal fluid
SIADH and Hypothyroidism

Hypervolaemia- any condition that causes too much fluid in the body
heart, liver and renal failure

Question 30

rapid correction of hyponatraemia and hypernatraemia

Answer 30

so hyponatremia can cause cereberal oedema, due to electrolyte imbalance, so if we correct hypernatraemia too quick it can cause cereberal oedema

Hypernatraemia can cause cerebral pontine myelonosis so rapid correction of hyponatraemia can cause that

Question 31

blood test for SIADH

Answer 31

Low blood osmolality
High urine osmolality
Euvolaemia
Hyponatraemia
high urinary sodium

Question 32

Describe diabetes insipidus in terms of ADH

Answer 32

OSMOLALITY MEANS HOW MUCH IONS DOES IT HAVE

So we know ADH is needed to reabsorb water from the collecting duct of the kidney (only collects water no electrolyte), in DI there is either a decrease release of adh from the posterior pituitary (Cranial DI) or reduced response from the kidney (nephrogenic DI). SO that means less water being reabsorbed in the body leading to a high serum osmolality and in the urine there is more water being excreted so the urine osmolality will be low

Question 33

describe the water deprivation test and explain the results

Answer 33

prevent patient drinking water
ask the patient to empty their bladder
hourly urine and plasma osmolalities

SO we know in cranial and nephrogenic the starting plasma osmolalities are high
in cranial di the problem is theres not enough ADH so if we give ADH the kidneys will work normal and then the final osmolaity will be low
In nephrogenic DI the kidneys do not respond to ADH so giving ADH will have no affect on osmolality so will remain high
In psychogenic polydypsia (patient drinks too much water so starting osmolality is already low) giving them ADH as their kidneys work normally the final osmolality will be low