Endocrinology and Diabetes Flashcards
Give one drug which can cause hyperthyroidism other than levothyroxine
Amiodarone
A patient with graves has a thyroidectomy, why may they still develop thyroid eye disease?
Autoantibodies still present, thyroid eye disease is due to autoantibodies rather than thyroid hormone
How is thyroid eye disease treated? (vaguely)
Steroids
Suggest 2 investigations to find the cause of hyperthyroidism?
- thyroid auto- antibodies
- technetium uptake scan
- USS
Describe how the appearance of a technetium uptake scan would differ between graves, a single toxic nodule and a multi nodular goitre
Graves= Same absorbtion distribution as normal thyroid but darker as more uptake
Single toxic nodule= one dense area, not thyroid shaped
Multi-nodular goitre= many dense areas, with outline of thyroid seen
When should a patient on carbimazole stop taking their medication and why?
If they get an infection, because it can cause bone marrow surpression and decrease WBCC
Describe Na+ and osmolality changes to blood and urine in SIADH?
High Na+ conc in urine (as retaining water) and high urine osmolality (>100)
Low Na+ conc in blood (<135 mmol/l) with low serum osmolality (<280)
Other than SIADH, what else could cause hyponatuaemia with high urine Na+?
Adrenal insufficiency- less mineralcoritcoid production= less reuptake of Na+ in collecting duct
What is pituitary apoplexy?
Bleeding into or impaired blood supply to the pituitary gland
How does pituitary apoplexy present?
Headache with cavernous sinus signs (4th, 6th, 3rd nerve palsys), also hypopituitaryism
How is pituitary apoplexy treated? (Vaguely)
If optic chiasm involvement (bitemporal hemianopia) then usually needs surgery.
If not just need to medically replace hormones and wait for recovery.
Which causes a higher prolactin, prolactinoma or tumour stopping dopamine effect by compression stalk?
Prolactinoma (v high prolactin, treat with dopamine agonists)
Pituitary stalk tumour (lower prolactin, treat with surgical removal)
How can diabetes be diagnosed? (3 ways)
- random blood glucose test over 11.1 with symptoms
- fasting glucose >7, if theyre asymptomatic you need two >7
- Hba1c> 6.5%
Give 5 symptoms of diabetes mellitus?
- tiredness
- frequent UTIs
- Weightloss (T1 only)
- Polyurea
- Polydipsia
Describe the presentation of decompensated ketoacidosis?
- onset over 24 hrs
- PMH T1 diabetes, recent precipitating factor
- polyurea and poly dipsia
- N+ V
- Altered mental state
- weakness
- lethargy
- hyperventilation
- pear drop smell on breath
- dehydrated and volume deplete on examination
What may precipitate DKA? (4)
- Infection.
- Discontinuation of insulin (unintentional or deliberate).
- Inadequate insulin.
- Cardiovascular disease - eg, stroke or myocardial infarction.
- Drug treatments - eg, steroids, thiazides or sodium-glucose co-transporter 2 (SGLT2) inhibitors.
How should DKA be investigated? (group into diagnosis, finding cause and assessment of severity/ complications)
- To diagnose: Blood glucose, blood ketones, urine dip for ketones, ABG showing low bicarbonate (metabolic acidosis)
- To asses severity: U&E- for dehydration and hyperkalaemia, also urea and creatine raised if AKI, 12 lead ECG, CT/ MRI of head, anion gap raised
- to find cause: blood cultures, urine dip, CXR to look for infection
Describe and explain serum osmolality, K+ and Na+ changes in DKA?
- K+ usually high due to acidosis meaning H+ going into cells and K+ coming out, however may be low due to osmotic diuresis
- Osmolality is low due to glucose and ketones causing osmotic diuresis, which is also why Na+ conc seems high or normal. Can be low as body compensates by letting sodium go
Describe the management of DKA in detail
- Fixed rate IV infusion of insulin dose of 0.1 units/ Kg bodywieght every hour
- IV fluids to rehydrate: 1st bag= 1L normal saline over an hour, then 1L normal saline with K= over 2 hrs, then same then 1L NS w/ K+ over 4 hrs then same again, then 1L NS w/ k+ over 6 hrs. Reason for this is the insulin will cause cells to uptake K+ and cause hypokalaemia.
- Monitor closely (every hour) and if targets in HCO3- increases and ketone decreases are not met then increase the insulin
- When blood glucose is over 14mmol/l add 5% dextrose solution infusion to prevent hypo, continue until eating and drinking normally
- treat complications
When does hyperosmolar hyperglycaemic state/ syndrome (HSS) occur?
It occurs in T2 diabetes when blood glucose levels are allowed to be very high for a sustained period of time, causing an osmotic diuresis and so loss of water meaning high serum osmolality. There is no ketoacidosis as there is still a basal level of insulin they respond to sufficient to prevent ketoacidosis but too low to prevent hyperglycemia.
What could cause HHS?
- infections
- inability to take medications
- hypo/hyperthermia
- MI
- Medications
- undiagnosed/ first presentation of diabetes
- Many others
How is HSS present?
With severe dehydration, fast deterioration, focal or global neurological dysfunction, often PMH of diabetes, N+V, lethargy, seizures
How is HHS treated?
- Fluid resus: 0.9% normal saline, can use hypotonic (0.45%) if serum osmolality not going down, however this is rare. You dont want osmolality to decrease too fast (>10mmol/l/hr)
- Fixed rate iv infusion of insulin- 0.05 units per kg per hr
- monitor closely (blood biochemistry as well as neuro function)
Describe 3 early and 3 late signs of hypoglycaemia
early= hungry, sweats, tremor, palpitations, shaking late= confused, headache, drowsy, slurred speech, coma
Describe treatment of hypoglycaemia if theyre conscious and orientated
Oral glucose (dextrose tablets, 150-200ml fruit juice/ original lucozade/ glucojuice) with complex carbs later (bread etc)
Describe treatment of severe hypoglycaemia (unconscious or unable to swallow)
- Iv dextrose (120-200ml 20% solution)
- or IM glucagon often given in community
What is involved in a synacthen test? What does it assess?
You give synthetic ACTH, which should stimulate the adrenals to produce cortisol over about 30-60 mins.
It tests primary adrenal failure- the cortisol will not increase significantly in addisons.
What is involved in an insulin tolerance test? What does it test for?
You give 0.1 units/ kg insulin to induce a hypo (glucose <2).
The cortisol should the rise to >600. If it doesnt you may have problem with adrenals (primary adrenal failure) or hypopituitarism (failure to produce ACTH). It is used when the synacthen test is inconclusive as more sensitive at detecting adrenal insufficiency
What is involved in a glucose tolerance test? What does it test for?
Give a bolus of glucose, which should surpress growth hormone production. Tests for acromegaly
What are the clinical features of acromegaly?
- growth of hands and feet
- prognathism
- frontal bossing
- spade like hands
- coarse fatures
- headache
- sweating
- carpal tunnel
How should acromegaly be investigated? (6)
- check visual feilds
- urine dip (high glucose)
- BP- often HTN
- TSH and T4, prolactin, FSH, LH, GH, IGF1 for pituitary failure
- glucose tolerance test
- MRI pituitary fossa
How is acromegaly treated?
- Surgery: transpehnoidal removal of lesions
- radiotherapy
- Medical: somatostatin analogues (octreotide) or GH receptor blockers (pegvisomant)
Describe the clinical features of cushings syndrome?
- plethoric
- moon face
- thinning of skin
- easy bruising
- buffalo hump
- central obesity
- abdo striae
- HTN and DM
How could you initially screen someone you suspect has cushings? (4 options)
- 24 hr urinary cortisol x3
- ACTH (only at specialist centres)
- Midnight cortisol (should be lowest, difficult inpractice)
- Low dose dexamethasone surpression test (best screening test)
What is the low dose dexamethasone surpression test good for?
- give 0.5mg dexamethasone qds for 48 hrs
- cortisol should go down to <30, if >30 (doesnt surpress) then true cushings
- psuedocushings can be causes by alcohol or depression
What could cause cushings? (4)
- ACTH secreting pituitary tumour
- Ectopic ACTH (small cell carcinoma)
- adrenal tumour
- steroids
How can you diffentiate between an adrenal tumour causing cushings and ectopic ACTH secretion or a pituitary tumour causing cushings?
If adrenal tumour- ACTH will be low
If ectopic ACTH or pituitary cause- ACTH will be high
How can you differentiate between ectopic ACTH and pituitary cushings?
- Pituitary cushings will surpress on high dose dexamethasone surpression test- ectopic ACTH will now
- MRI pituitary fossa may show a lesion
Give 3 physical effects of non functional pituitaty tumours?
- visual field disturbances (tunnel vision most commonly)
- headache
- hyperprolactinaemia
- hypopituitarism
how can you differentiate between prolactinomas and non functioning adenoma causing hyperprolactinaemia?
prolactinomas will cause prolactin to be >5000
How are prolactinomas and nonfunctioning adenomas causing hyperprolactinaemia managed?
prolactinomas= dopamine agonist (inhibits prolactin release)
non functioning adenoma= cut it out
Describe the clinical features of an addisonians/ hypoadrenal crises?
- vomiting
- drowsy
- weight loss
- tanned skin
- low BP
- high HR
- Low blood glucose
- hyponaturaemia
- hyperkalaemia
How should a hypoadrenal crises be managed?
- aggressive fluid resus
- hydrocortisone 100mg IV every 6 hrs
- urine catheter to monitor output
- treat sepsis (usual cause)// fine cause
- Give glucose
How can addisons be biochemically confirmed?
- low 9am cortisol (should be at its highest)
- ACTH level (high if adrenal cause)
- renin
- synacthen test
How should addisons be managed?
- hydrocortisone
- fludocortisone
- education
- emergency HC injection kit
- endocrine follow ups
Describe the diagnosis criteria for DKA and HHS
DKA: acidaemia (ph<7.3 or hco3 <15) and hyperglycaemia (>11.1) and ketonuria (++) or ketonaemia (>3)
HHS: hyperglycaemia >30, no acidosis, no ketosis, serum osmolality >320
