Endocrine Flashcards
Test for phaechromocytoma
24 hour urinary collection for metanephrines
Management of phaeochromocytoma
Surgery - Stabilisation required first:
1. Alpha blocker (phenoxybenzamine) and then
2. Beta blocker
Mechanism of action of GLP 1 mimetics (eg exenatide)
Increase insulin secretion and inhibit glucagon secretion
Mechanism of action of DPP 4 inhibitors eg vildagliptin
Increase levels f incretins (GLP 1 and GIP) by decreasing their peripheral breakdown
ECG abnormality associated with hypercalcaemia
Shortened QT interval
ECG abnormalities associated with hypokalaemia
U waves
Small or absent T waves
Prolonged PR interval
ST depression
Long QT
Antibodies seen in hashimotos thyroiditis
Anti TPO
Ati Tg antibodies
What can cause HBA1c to be lower than expected
Sickle cell anemia
G6PD deficiency
Heriditary spherocytosis
Haemodylasis
Due to reduced red blood cell lifespan
What can cause higher than expected levels of HbA1c?
Vitamin B12/Folate deficiency
Iron deficiency anaemia
Splenectomy
Due to increased red blood cell lifespan
Definition of impaired fasting glucose
Fasting glucose greater than or equal to 6.1 but less than 7
Definition of impaired glucose tolerance
Fasting glucose less than 7 and OGTT 2 hour value greater than or equal to 7.8 but less than 11.1
Treatment for acromegaly
Trans sphenoidal surgery
If inoperable then:
1. Somatostatin analogue eg octreotide
2. Pegvisomant (GH receptor antagonist)
3.Dopamine agonist eg bromocriptine only effective in a minority.
Treatment for a prolocatinoma?
Dopamine agonist eg cabergoline or bromocriptine
Surgery if this fails
How often should HBA1c be checked?
Every 3 - 6 months until stable and then 6 monthly.
What is the 10% rule in phaechromocytoma?
10% are bilateral
10% are malignant
10% are extra adrenal
Adverse affects of pioglitazone
Weight gain
Liver impairment
Fluid retention
Increased risk of fractures
Increased risk of bladder cancer
What is the starting rate of IV insulin for DKA
0.1 units/kg/hour
What are the causes of primary hyperaldosteronism?
- Bilateral idiopathic adrenal hyperplasia (60 - 70% of cases)
- Adrenal adenoma (20 - 30% of cases)
- Unilateral hyperplasia
- Familial hyperaldosteronism
- Adrenal carcinoma
Who should be screened for primary hyperaldosteronism?
- Hypertension with hypokalaemia
- Treatment resistant hypertension
What is the first line investigation for primary hyperaldosteronism?
Aldosterone/renin ratio
What will the renin aldosterone ratio show is patients with primary hyperaldosteronism?
High aldosterone and low renin
What is the management for bilateral adrenocorticol hyperplasia?
Aldosterone antagonist (spironolactone)
Treatment for toxic multinodular goitre
Radioiodine therapy
Nuclear scintigraphy results in toxic multinodular goitre
Patchy uptake
Nuclear scintigraphy results in graves disease
Diffuse enlargment of both thyroid lobes
Blood gas result in cushings syndrome
Hypokalaemic metabolic alkalosis
First line test to confirm cushings syndrome
Overnight (low dose) dexamethasone suppression test
- Most sensitive test. Patients with cushings - no supression of morning cortisol
What tests allows you to localise the pathology resulting in cushings syndrome
- 9am and midnight ACTH + cortisol levels. If ACTH supressed then a non ACTH dependant cause is likely (eg adrenal adenoma)
- High dose dexamethasone supression test
Antibodies in graves disease
Anti TPO
TSH receptor stimulating antibodies
What medication interacts with levothyroxine
Iron
What is the optimal management of thyrotoxicosis in patients who are pregnant or planning a pregnancy?
Thyroidectomy then thyroxine replacment
Blood gas results in an addisonian crisis
Metabolic acidosis with low sodium and raised pottasium
Triad of MEN 2A
Medullary thyroid cancer
Primary hyperparathyroidism
Phaeochromocytoma
Triad of MEN1
Hyperparathyroidism
Pituitary adenoma (usually prolactinoma)
Pancreatic islet cell tumour
Diagnosis of adrenal failure
short synacthen test. In adrenal failure plasma cortisol will not rise to above 550
What is the mechanism of action of sulfonlyureas
Stimulated insulin secretion for the beta cells of the islets of langerhans
What is the mechanism of action for DPP4 inhibitors such as sitagliptin
Inhibit DPP4 which destroys incretics. Allsos increase in incretins which stimulate the release of insulin and inhibit the release of glucagon.
What are the results of FSH, LH and testosterone in kallmans syndrome
Low LH, FSH and low Testosterone
Management of a thyroid strom
IV Propanolol
Anti thyroid durgs et Methimazole or propylthiouracil
Lugols iodine
Dexamthasone
Treatment for myxodema coma
IV thyroid replacement
IV fluids
IV corticosteroids
