Endocrine Flashcards
What is the first line treatment approach in a newly diagnosed T2D?
If HbA1C fails to improve, what is the next step?
Lifestyle modification (diet, exercise, smoking, alcohol etc)
Metformin = 1st line medication
What condition may SGLT2 inhibitors be prescribed to manage?
What is the mechanism of action of SGLT2 inhibitors?
Type 2 Diabetes
Increase the excretion of glucose from the body
What side effects are commonly experienced after initiating metformin?
GI upset: nausea, vomiting, diarrhoea, bloating
Give an example of a commonly used sulfonylurea. - What condition are they commonly used to manage?
What is the mechanism of action of sulfonylureas?
Gliclazide - Type 2 Diabetes
Increase insulin release from the pancreas
A 65 year old man with diabetes has developed painful peripheral diabetic neuropathy.
Name a medication & it’s drug class, used as 1st line in treating this.
Amitriptylline - tricyclic antidepressant
What is the 1st line medication for hyperthyroidism?
When would this drug be contraindicated & what would be used instead?
Carbimazole
Contraindicated in pregnancy - Propylthiouracil used instead
What are the signs of hypercalcaemia?
“Stones, bones, abdominal moans & psychiatric groans”
Renal stones
Painful bones
GI: nausea, vomiting, constipation, indigestion
Neuro: fatigue, memory loss, depression, psychosis
A blood sugar below what is considered as hypoglycaemia?
4mmol/L
Delayed puberty & anosmia (lack of smell) would suggest what condition?
What is the physiological cause behind delayed puberty in this condition?
Kallmann’s syndrome
Hypogonadotropic hypogonadism: hypothalamus doesn’t secrete enough GnRH to stimulate anterior pituitary to secrete LH & FSH → little testosterone/ oestrogen secreted
What condition are biguanides used to treat?
What is the most commonly used biguanide?
What is the mechanism of action of biguanides?
Type 2 Diabetes
Metformin
They increase sensitivity to insulin in the peripheries PLUS increase glucose uptake in the liver
What are the 5 main characteristic features of Cushing’s Syndrome?
High levels of cortisol can cause what 4 clinical conditions?
1) Moon face
2) Central obesity
3) Proximal limb muscle wasting
4) Abdominal striae
5) Buffalo hump
1) Hypertension
2) Insulin resistance (hyperglycaemia → T2DM)
3) Osteoporosis
4) Easy bruising
Women with a RF for gestational diabetes are investigated for gestational diabetes at what gestational week?
How is this investigated?
What additional investigation are women with a history of gestational diabetes given?
Week 24-28
OGTT
Women with a history of GD are given an OGTT at their booking appointment (~10 weeks) - if this is normal, it is repeated at weeks 24-28
What is the 1st line investigation of Cushing’s Syndrome?
Explain how this is conducted and the potential results:
What is the treatment of Cushing’s syndrome?
Dexamethasone suppression test
Patient takes low dose of dexamethasone at night & cortisol & ACTH levels are measured in the morning. If cortisol is high, test is repeated with a high dose of dexamethasone to work out the cause.
-
Low dose dexamethasone results:*
1) low cortisol & ACTH → normal (no cushings)
2) normal/ high cortisol → cushing’s syndrome -
High dose dexamethasone results:*
1) low cortisol & ACTH → pituitary adenoma
2) low ACTH, normal/ high cortisol → adrenal adenoma
3) normal/ high cortisol & ACTH → ectopic ACTH secreting tumour
Surgical removal of the tumour!
~ trans-sphenoidal resection of pituitary adenoma
What the are diagnostic values of type 2 DM:
1) Random blood glucose
2) Fasting plasma glucose
3) 2h glucose tolerance
4) HbA1C
What is required for a T2DM diagnosis in:
a) symptomatic patient
b) asymptomatic patient
1) Random blood glucose: 11.1 mmol/l
2) Fasting plasma glucose: 7 mmol/l
3) 2h glucose tolerance: 11.1 mmol/l
4) HbA1C: > 48 mmol/mol
a) 1 of the above criteria + symptoms
b) 2 of the above criteria from 2 days (if asymptomatic)
List some clinical features of hypoglycaemia: (7)
Shaking
Sweating
Palpitations
Headache
Blurred vision
Hunger
Confusion
What is cushings syndrome?
Name the hormonal control underlying the release of this compound, & the locations where each hormone are released from:
List the 4 main causes of cushings syndrome:
Excess cortisol
CRH (hypothalamus) → ACTH (anterior pituitary) → cortisol (adrenal cortex: zona fasiculata)
1) Long term steroid use (commonest cause)
2) Cushings disease (ACTH producing pituitary adenoma)
3) Adrenal adenoma
4) Ectopic ACTH secreting tumour (eg, small cell lung cancer)
If a T2D cannot tolerate metformin, what class of drugs are they switched to instead? (These are usually the 2nd line treatment option)
Give an example of a drug within this class.
What is the mechanism of action of these drugs?
What is a severe side effect that needs to be monitored?
Sulfonylureas
Gliclazide
They increase insulin secretion from the pancreas
Hypoglycaemia
What is “primary adrenal insufficiency” also known as?
List some common symptoms/signs of this condition: (7)
Addisons disease
- Fatigue
- Nausea
- Muscle cramps
- Abdominal pain
- Reduced libido
- Bronze skin
- Hypotension
What is the 1st line investigation of adrenal insufficiency?
At what time of day should this test be performed? - why?
What results would you see if someone has primary adrenal insufficiency (aka addisons)?
Short synacthen test
In the morning (cortisol levels naturally rise in the morning to wake you up)
Primary adrenal insufficiency: failure of cortisol to rise to at least double the baseline (baseline being the cortisol levels before synacthen was given)
What is the long term management of someone with primary adrenal insuffciency (aka addisons)? (2)
If the patient becomes acutely unwell, what changes need to be made to these medications?
Steroid replacement!
Hydrocortisone (cortisol replacement)
Fludrocortisone (aldosterone replacement)
The doses are doubled!
List some of the signs/symptoms of addisonian crisis (aka adrenal crisis): (5)
What would management of this crisis involve? (4)
- Hypotension
- Hypoglycaemia
- Hyponatraemia
- Hyperkalaemia
- Reduced consciousness/ coma
~ IV steroids (eg hydrocortisone)
~ IV fluid resus
~ correct any hypoglycaemia
~ monitor & correct any electrolyte imbalances
What would management of this crisis involve? (4)
- IV steroids (eg hydrocortisone)
- IV fluid resus
- correct any hypoglycaemia
- monitor & correct any electrolyte imbalances
Parathyroid hormone is produced in response to which electrolyte imbalance?
Hypocalcaemia
What is the function of parathyroid hormone?
How does parathyroid hormone achieve this? (4)
To increase blood calcium levels
- Increases osteoclast activity (resorption of bone)
- Increases Ca absorption from the gut
- Increases Ca absorption from the kidneys
- Increases vitamin D activity
What vitamin acts with parathyroid hormone to increase blood calcium?
Vitamin D
A HbA1c value of what is diagnostic for diabetes mellitus?
A fasting blood glucose of what value forms the criteria for a diabetes diagnosis?
A random blood glucose of what value forms the criteria for a diabetes diagnosis?
48mmol/mol
Fasting: 7.0mmol/l
Random: 11.1mmol/l
What type of acid-base imbalance would you expect to see in someone with cushings syndrome? - why would you see this?
Hypokalaemic metabolic alkalosis
~ excess cortisol is free to bind to mineralocorticoid receptors. This causes an increase in water & sodium retention, increased potassium excretion, and increased hydrogen ions excretion. Lower levels of hydrogen ions cause alkalosis & less potassium causes hypokalemia.
A patient attends the GP with symptoms of cushings syndrome. Which 2 initial investigations should the GP perform to confirm the diagnosis?
Low dose dexamethasone suppression test
24 hour urinary cortisol levels
What is required for the diagnosis of T2DM in a symptomatic patient?
How does this differ if the patient was asymptomatic?
Symptomatic = ONE of either:
* Random blood glucose** >11.1**
* Fasting blood glucose >7
* 2h OGTT >11.1
* HbA1C >48
Asymptomatic patient requires the one of the above criteria to be fulfilled on TWO separate occasions
What range of HbA1C would be classed as prediabetes?
What range of fasting glucose would be classed as prediabetes?
Prediabetes:
HbA1C: 42-47
Fasting glucose: 6.1-6.9
What is the characteristic xray finding in a patient with uncontrolled hyperparathyroidism?
Pepperpot skull
A patient with T2DM currently on the maximum dose of metformin, has his annual HbA1C checked and his result is 55mmol/mol.
What should be done regarding his diabetic management?
NOTHING.
He is already on the maximum dose of metformin & NICE only say to add a second medication when the HbA1C is more than 58mmol/mol.
Parathyroid hormone is produced by the chief cells within the parathyroid glands in response to WHAT?
What vitamin is also needed for PTH to exert its desired effect?
Low calcium
Vitamin D
Parathyroid hormone acts to increase serum calcium. It does this in 3 different ways. What are the 3 ways that PTH can increase serum calcium?
What vitamin is also needed for PTH to exert its desired effect?
- Increases calcium absorption from the GUT
- Increases calcium reabsorption from the KIDNEYS
- Increases osteoclast activity (bone breakdown»_space; causes calcium release from BONE)
Vitamin D
In primary hyperparathyroidism, would you expect high or low
1. PTH
2. calcium
Explain the commonest cause of primary hyperparathyroidism and why you’d expect the above results:
PTH: HIGH
Calcium: HIGH
Primary hyperparathyroidism: adenoma of the parathyroid glands that secretes PTH»_space;> excess PTH»_space;> hypercalcaemia
In secondary hyperparathyroidism, would you expect high or low
1. PTH
2. calcium
Explain the commonest 2 causes of secondary hyperparathyroidism and why you’d expect the above results:
PTH: HIGH
Calcium: LOW/NORMAL
Secondary hyperparathyroidism:
~ vitamin D deficiency
~ chronic renal failure
Both of the above result in decreased absorption of calcium from the gut, kidneys and bones»_space;> hypocalcaemia. This stimulates the parathyroid glands to secrete more PTH in order to compensate for the hypocalcaemia.
THIS EVENTUALLY RESULTS IN HYPERPLASIA OF THE PARATHYROID GLANDS!
In tertiary hyperparathyroidism, would you expect high or low
1. PTH
2. calcium
Explain the cause of tertiary hyperparathyroidism and why you’d expect the above results:
PTH: HIGH
Calcium: HIGH
Tertiary hyperparathyroidism: follows on from secondary hyperparathyroidism!
When secondary hyperPTism is treated (eg vitamin D deficiency/CKD is corrected) the hyperplased parathyroid glands keep secreting excess PTH!!
State the 3 treatment options for hyperthyroidism:
What medication can be used for symptomatic relief in hyperthyroidism?
- Carbimazole
- Propylthiouracil
- Radioactive iodine
Propanolol
Exenatide is a medication used in the management of T2DM. Choose the correct drug class of exenatide from the options below:
* sulfonylurea
* DPP4 inhibitor
* GLP1 analogue
* SGLT2 inhibitor
GLP1 analogue
Gliclazide is a medication used in the management of T2DM. Choose the correct drug class of gliclazide from the options below:
* sulfonylurea
* DPP4 inhibitor
* GLP1 analogue
* SGLT2 inhibitor
What is an important side effect associated with gliclazide?
Sulfonylurea
HYPOglycaemia
Dapagliflozin is a medication used in the management of T2DM. Choose the correct drug class of dapagliflozin from the options below:
* sulfonylurea
* DPP4 inhibitor
* GLP1 analogue
* SGLT2 inhibitor
What is an important side effect associated with medications in this drug class?
SGLT2 inhibitor
Increased risk of UTI’s due to increase glucose excreted in the urine
Sitagliptin is a medication used in the management of T2DM. Choose the correct drug class of sitagliptin from the options below:
* sulfonylurea
* DPP4 inhibitor
* GLP1 analogue
* SGLT2 inhibitor
DPP4 inhibitor
If a patient has blood results demonstrating hypothyroidism & on examination you see a goitre, what condition does this indicate?
Hashimoto’s thyroiditis
The development of which cancer is associated with Hashimoto’s thyroiditis?
- Anti-thyroid peroxidase antibodies (TPO)
- Anti-thyroglobulin antibodies
MALT lymphoma
A 44y/o woman presents to her GP with polydipsia and polyuria.
The GP arranges a water deprivation test. Blood results before the test show:
~ Serum osmolality: 262 mOsmol/kg (275 - 295)
~ Urine osmolality: 98 mOsmol/kg
The test starts at 8 AM and the patient has no fluid intake for the next 8 hours.
After 8 hours, urine osmolality is measured:
~ Urine osmolality: 833 mOsmol/kg
Desmopressin is then given IM. After 4 hours the urine osmolality is measured again:
~ Urine osmolality: 835 mOsmol/kg
What is the most accurate interpretation of these results?
Primary polydipsia
- In primary polydipsia, the patient drinks excessive amounts of water, causing dilution of the serum and urine, leading to low serum osmolality and low urine osmolality. Following water deprivation (aka, the patient isn’t allowed to drink anything), the urine becomes more concentrated, and osmolality rises to >800mOsmol/kg. (Usually, it wouldn’t be necessary to give desmopressin in this case.) If the urine osmolality rises to >600mOsmol/kg following fluid deprivation, the test can be stopped as diabetes insipidus has been excluded, because the kidneys are obviously able to concentrate the urine appropriately in response to endogenous antidiuretic hormone.*
Explain the physiology underlying:
~ cranial diabetes insipidus
~ nephrogenic diabetes insipidus
Cranial diabetes insipidus:
The hypothalamus doesn’t produce enough ADH»_space;> the kidneys don’t concentrate the urine»_space;> you pee alot
Nephrogenic diabetes insipidus:
There is sufficient ADH production, however the (collecting ducts of the) kidneys don’t respond to ADH»_space;> the urine isn’t concentrated»_space;> you pee alot
Which 2 hormones are elevated in acromegaly?
GH
IGF-1 (insulin-like growth factor 1)
A 40y/o man who is a known diabetic, presents with increasing headaches and visual issues.
On examination, he has enlargement of the hands and feet, coarse facial features and splaying of the teeth.
What is the most likely diagnosis?
What is the most appropriate first-line investigation?
Acromegaly
Measure serum insulin-like growth factor 1 levels (which will be elevated)
~ GH levels fluctuate throughout the day and thus are NOT diagnostic
A 43y/o man is admitted to the endocrine ward following a one-month history of polyuria and polydipsia. He appears severely dehydrated. A water deprivation test is performed which shows the following result:
~ Urine osmolality post-fluid deprivation 37mOsm/kg (50-1200)
~ Urine osmolality post-desmopressin 45mOsm/kg (50-1200)
What is the diagnosis?
Explain why this is the diagnosis
Nephrogenic diabetes insipidus
Following water deprivation (aka, the patient not being allowed to drink for 8 hours), the urine osmolality is low (aka, it’s very dilute), however when desmopressin is given (synthetic ADH), the urine osmolality increases back to normal (aka, the urine becomes more concentrated).
~ This implies that the kidneys are still responding to ADH, there just isn’t enough ADH being produed by the hypothalamus
