Endo - mx Flashcards
Cranial DI management
- DDAVP
- Treatment of underlying cause
- Adequate fluid intake
Nephrogenic DI management
- Adequate fluid intake
- Treatment of underlying cause
- Low sodium diet (<500mg/day)
- Hydrochlorothiazide (thiazide diuretic), indometacin (NSAID)
- genetic/severe DI - intermittent catheterisation to decrease urinary tract backpressure complications
T1DM management
Insulin
Background insulin - basal bolus insulin
- Long acting insulin analogues- Galgrine, detemir, degludec
Insulin with meals- Short acting insulin analogues - Lispro, aspart, glulisine
Aim for glucose level
5-7 mmol/L upon waking
4-7 mmol/L before meals
All patients with diabetes and CVD should be treated with aspirin for secondary prevention
Need to monitor capillary glucose
T2DM management
- Lifestyle changes [1st line]
- Glycaemic control [2nd line i.e. not all patients with T2DM are on metformnin]
Metformin as initial therapy if HbA1c >6.5% // 48mmol/mol
If after lifestyle changes + metformin, blood glucose is still >7.5% // 58mmol/mol add a second drug - Sulphonyluras (preferred)
- GLT-1 agonist
- SGLT-2 inhibitor
Add sulfonylureas (gliclazide, glibenclamide) in young patients, as the get older + develop CVD switch to GLP1 agonists if they have CAD (exenatide, liraglutide) or SGLT 2 inhibitors if they have HF (empagliflozin) as they are more cardioprotective
triple therapy with: Third line metformin, sulfonylurea, DDP4 inhibitor metformin, sulfonylurea, pioglitazone Insulin if HbA1c remains >7.5% on metformin + sulphonylurea
Thiazolidinediones/pioglitazones are used as a 3rd line therapy – enhance actions of endogenous insulin
Should NOT be used in patients with cardiac failure – they cause Na + fluid retention
When is metformin contra-indicated and what can be used instead
- Contra-indicated in conditions that can precipitate lactic acidosis
Mild renal failure
Severe liver failure
Severe heart failure
Alcoholism
Respiratory disease
Metformin decreases the liver uptake of lactate
Metformin is renally excreted so in people with renal failure, it will accumulate in the body
Instead we can use
DDP-4 inibitors/gliptis - sidagliptin, vidagliptin
Glitazones - pioglitazone
Sulphonylureas - Gliclazide, gibenclamide
The main complication of T1DM is hypoglycaemia
Clinically signs + mx
Clinically significant when <3.0 mmol/L
Higher dose of insulin, decreased food intake, increased physical activity
Focal neurological symptoms Fits Confusion Coma Dizziness Pallor Sweating Palpitations Tachycardia Hunger
Fruit juice, IV dextrose, IM glucagon (1mg) (if you can’t obtain IV access)
- If pt conscious – give fruit juice and then long acting carbohydrates
- If pt confused – use a gel
- If pt unconscious – IM glucagon (1mg) / IV dextrose (20% glucose)
HHS/HONK meaning
Complications
Management
HHS/HONK
Hyperosmolar hyperglycaemic state
Hyperglycaemic hyperosmolar non ketotic coma
Cellular dehydration - fluid shift from extravascular to intravascular compartment
Hypovolaemia - osmotic diuresis
Insulin
IVF
Electrolyte replacement (esp K+ replaement)
Prophylactic anticoagulation (patients w HHS/HONK are prone to thromboebolism)
What are pre-proliferative + proliferative diabetic retinopathy
Mx of diabetic retinopathy
Pre-proliferative - cotton wool spots (retinal ischaemia)
Proliferative - growth of abnormal blood vessels
Pan-retinal photocoagulation for cotton wool spots or abnormal vessels
Indications for dialysis as a result of diabetic nephropathy
- eGFR <10ml/min + benefits outweigh risks
- eGFR <6ml/min + no reversible features
- Life-threatening complications
- Hyperkalaemia (>6.5mM)
- High creatinine (>1000μM)
- Hyperuricaemia (>300mM)
- Symptoms or complications of uraemia (e.g. pericarditis)
- Uraemic encephalopathy
- Fluid overload (severe pulmonary oedema)
- Severe acidosis (pH <7.2) refractory to medical management
Diabetic nephropathy management
- Diabetic control
- BP control
- ACEi
- Stop smoking
- Dialysis
- Transplantation
DKA mx
- Immediate resuscitation
- NBM for at least 6h
- IVF - 500 ml isotonic saline (NaCl 0.9%) over 16-30 mins until SBP >100
if fluid is given too quickly there is a risk of cerebral oedema
if Na >155 mmol/l give 0.45% saline - Insulin at a rate of 0.1 unit/kg/hour
- Potassium phosphate*
<3.3 mmol/L - K given before insulin
3.3-5.3 mmol/L - Insulin can be given before K
>5.3 mmol/L - K does not need to be given- IV insulin once K reaches 3.3 mmol/L
Treatment in some patient groups
- Vasopressors e.g. vasopressin, adrenaline if haemodynamically unstable
- Bicarbonate therapy if HCO3 <5 mmol/L or if pH <7
- Phosphate therapy - if respiratory + skeletal muscle weakness (<1mg/dl)
- NG tube if low GCS
- Thromboprophylaxis (low dose heparin)
*in DKA we have hyperkalaemia (high extracellular K+) but low total body K+
therefore give insulin to push k+ back into cells
give K+ to replenish loss of K+ through diuresis
• Transfer to SC insulin once capillary ketones <0.5mM + pH >7.3 + venous bicarbonate >18 mmol/L
o Don’t stop the infusion until 1-2h after the SC insulin has restarted
https://forums.studentdoctor.net/threads/dka-and-k.710715/
Primary hyperparathyroidism mx
Acute hypercalcaemia
- IVF
- Bisphosphonates (if calcium remains high and if caus eof hypercalcaemia are bony mets)
1st line
- Total Parathyroidectomy
2nd line (if unsuitable for surgery)
- Cinacalcet
(Calcinomimetics) increases the receptor’s sensitivity to calcium to enhance negative feedback and decrease PTH + calcium
- Vitamin D supplementation
Secondary hyperparathyroidism mx
Osteomalacia
Osteomalacia due to CKD
secondary hyperparathyroidism = osteomalacia
Acute hypocalcaemia - IV calcium infusion (calcium gluconate)
Osteomalacia
- Calcium
- Vitamin D supplements (ergocalciferol, colecalciferol)
Osteomalacia due to CKD
- Treat CKD
- Calcium
- Vitamin D (Calcitriol analogues (e.g. alfacalidol))
- Phosphate binders (e.g. sevelamer, lanthanum, calcium acetate) - (if phosphate is high - CKD)
- Calcinomimetics e.g. cinaclcet increases the receptor’s sensitivity to calcium to enhance negative feedback and decrease PTH + calcium
- Phosphate (if phosphate is low - Vitamin D deficiency)
- Parathyroidectomy considered in severe cases refractory to medical treatment
Treatment – for acute hypocalcaemia
Treatment – for acute hypocalcaemia
• IV calcium infusion (calcium gluconate)
Acute hypercalcaemia mx
Acute hypercalcaemia
• IVF (saline)
• Bisphosphonates (if calcium remains high, good for cancer mets, Zolendronate)
• Avoid factors that can exacerbate hypercalcaemia including thiazide diuretics
Karim said don’t give bisphosphonates in patients who don’t have cancer
you would give bisphosphonates if PTH is suppressed in the setting of hypercalcaemia as that would suggest cancer
Cerebral oedema is a complication of DKA
How do you treat it?
Mannitol infusion
Mechanical ventilation
To decrease the raised ICP
Hypothyroidism mx
- Levothyroine (T4)
25-200μg daily
Initial dose in healthy pt - 50μg
Initial dose in elderly/pt w IHD - 25μg + gradually increase [to avoid worsening angina or precipitating an MI]
Titration in small increments every 6 weeks to therapeutic dose + monitor for ischaemic symptoms
Monitor TFTs after 6 weeks and adjust dose accordingly - Monitor by serum TSH and serum T4
Before starting thyroid replacement therapy, rule out + treat adrenal insufficiency (e.g. as a result of secondary hypothyroidism where there is a problem with the pituitary). Giving thyroxine to someone with a concomitant glucocorticoid deficiency can precipitate an Addisonian crisis.
Hyperthyroidism mx
Antithyroid drugs (ATD)
- Propylthiouracil + Carbimazole (inhibit TPO + hormone synthesis) (carbimazole needs 120 days to take effect)
- Potassium iodide
- B blockers (symptomatic relief until ATD start to work)
Graves
- ATD
o 1st line
o Rashes are common (CBZ)
o Agranulocytosis is rare but patients should be warned to report infectious symptoms immediately (CBZ)
o Can use the “block + replace” approach - large amounts of carbimazole to switch off thyroid function + thyroxine
- Radioiodine
o 1st or 2nd line
o Increasingly used for the treatment of thyrotoxicosis at all ages particularly where medical therapy or compliance is a problem, in patients with cardiac disease + in patients who relapse after thyroidectomy
o Commonly used for adenomas or toxic multinodular goitre
o Must avoid pregnancy for 4 months + close contact with pregnant women/young children for 2 weeks
o Hypothyroidism may develop at any stage after the treatment
o Contraindications: pregnancy + breastfeeding - Subtotal thyroidectomy
o 3rd line
o Reserved only for those with large or obstructive goitre + those who can’t take ATD due to allergy or agranulocytosis
o Recommended in young patients with large goitres to remove neck swelling
o More commonly performed for adenoma or toxic multinodular goitre than for Grave’s
o Iodine + CBZ 10-14 days before surgery - control + decrease vascularity of thyroid gland
o Complications: hypoparathyroidism, recurrent laryngeal nerve damage, bleeding into the neck causing laryngeal oedema - B-blockers for symptomatic relief
o rapid relief of thyrotoxic symptoms, controls supraventricular arrhythmias 1y to thyrotoxicosis
Relapse after medical treatment
- Radioiodine
- Surgery
Toxic adenoma/toxic multinodular goitre
- Radiodine
- Surgery
ATD complications
anti-thyroid drugs
Rashes are common
Agranulocytosis is rare but patients should be warned to report infectious symptoms immediately
Pre-operative preparation for subtotal thyroidectomy
+ complications of subtotal thyroidectomy
Propanolol
KI
ATD (anti-thyroid drugs)
10-14 days before surgery - controls + decreases vascularity of the gland
Complications Hypothyroidism Hypoparathyroidism Recurrence Recurrent laryngeal nerve damage Bleeding into the neck causing laryngeal oedema
Acute thyroid crisis mx
Thyrotoxicosis
Thyroid storm
- Propanolol
- Propylthiouracil - prevents synthesis of new hormones
- IV hydrocortisone - prevents peripheral conversion of T4 - T3
- Oral potasssium Iodine solution or Lugol’s solution (blocks release of thyroid hormone)
- O2
- IVF
- Control temperature (gentle cooling)
- Treat underlying cause (thyroid surgery, radioiodine, withdrawal of anti-thyroid drugs, iodinated contrast agets, acute illnesses)
sodium iopodate - inhibits thyroxine release (surgical sbas)
Management of viral thyroiditis
Mild symptoms - NSAIDs
Moderate/severe symptoms - high dose prednisolone
Give examples of thinoamides
Where are they used
How do they work
Carbimazole, Propylthiouracil
Hyperthyroidism (Grave’s, will not work in any thyroiditis)
Block organification of iodine (2I- –> I2+2e-) –> do not allow iodine to stick onto tyrosine residues
Carbimazole becomes converted to methimazole + inhibits TPO which is responsible for tyrosine iodination reactions that lead to T3/T4 production
Myxoedema coma mx
Mx
- IV T3
- IV hydrocortisone (if secondary hypothyroidism due to hypopituitarism) *
- Supportive measures - oxygen, rewarming, IVF
- Treatment of underlying cause (e.g. infection)
- Replace T3 with T4 after 2-3 days if there is clinical improvement
*In myxoedema coma, thyroid failure should be assumed to be secondary to hypothalamus/pituitary disease - IV hydrocortisone should be given before TFTs become available
SIADH mx
• First line or asymptomatic
o Treat underlying cause
o Restrict fluid (0.5-1 L/day)
o increase salt + protein diet to replace loss of sodium
• Chronic SIADH
o Fluid restriction
o Treat underlying cause
o Tolvaptan (vasopressin receptor antagonists) [2nd line]
o NaCl PO + furosemide [3rd line]
o Demeclocycline – antibiotic that increases responsiveness of collective tubule cells to ADH [4th line]
o If severe symptoms during chronic SIADH
IV hypertonic saline
Tolvaptan
Furosemide
• Severe acute hyponatraemia symptoms/ cerebral oedema (altered mental status, seizure, coma)
o Slow IV hypertonic 3% saline
o Furosemide
Change in [Na+] must not exceed 10mmol/L in the first 24h (+aim to increase sodium by <2mM/h) and 18mmol/L in the first 48h - rapid correction can result in central pontine myelinolysis
Management of hyponatraemia
Hypovolaemic
Euvolaemic
Hypervolaemic
Severe acute hyponatraemia
Hypovolaemic
- Isotonic fluid infusion
- treat underlying cause
Hypervolaemic
- fluid restriction
- loop diuretic or spironolactone
- treat underlying cause
Euvolaemic
- fluid restriction
- treat underlying cause
Severe acute hyponatraemia symptoms/ cerebral oedema (altered mental status, seizure, coma)
- Slow IV hypertonic 3% saline
- Furosemide
Change in [Na+] must not exceed 10mmol/L in the first 24h (+aim to increase sodium by <2mM/h) and 18mmol/L in the first 48h - rapid correction can result in central pontine myelinolysis
Management of hypernatraemia
- Treatment of cause
- Appropriate fluid replacement
- Normal saline can be used as it may have a lower osmolarity than the blood and will not abruptly lower the Na+ level
- Sodium level should be reduced no faster than 1mmol/L/h- to avoid rapid fluid shifts + cerebral oedema
What can a
a) rapid increase in Na cause in hyponatraemia
b) rapid decrease in Na cause in hypernatreamia
a) central pontine myelinolysis
b) cerebral oedema
Prolactinoma mx
• Asymptomatic – observation
• Symptomatic
o DA agonist (cabergoline, bromocroptine) – 1st line
o Trans-sphenoidal surgery – 2nd line
o Sellar radiotherapy – 3rd line
Acromegaly/excess growth hormone/ excess GH mx
- Transsphenoidal surgery – 1st line
- Somatostatin analogue (octreotide) – 2nd line
- GH receptor antagonist (pegvisomant) – 3rd line
- Radiotherapy – 4th line
Primary hyperaldostronism mx
Aldosterone producing adenomas (unilateral)
Bilateral adrenal hyperplasia
Aldosterone producing adenomas (unilateral)
• Adrenalectomy
• Aldosterone antagonists if not surgical candidates – spironolactone, eplerenone, amiloride
Bilateral adrenal hyperplasia
• Spironolactone (aldosterone receptor antagonist, K+ sparring diuretic)
• Eplerenone/amiloride (K+ sparring diuretics) if SE of spironolactone are intolerable
Spironolactone SE
- Gynaecomastia
- Impotence
- Menstrual irregularities
- Muscle cramps
- GI upset
Cushing’s syndrome mx
Iatrogenic
Cushing’s disease
Ectopic ACTH or CRH syndrome/ adrenal adenoma
Iatrogenic – stop steroids
Cushing’s disease (pituitary adenoma)
• Transsphenoidal pituitary adenomectomy (1st line)
o Post-surgical hormone replacement therapy – hydrocortisone, levothyroxine, estradiol, somatropin, desmopressin
• Medication before surgery or medical therapy alone/unfit for surgery (2nd line)
o Steroidogenesis inhibitor – metyrapone, ketoconazole
o Treat osteoporosis + provide physiotherapy for muscle weakness
- Pituitary radiotherapy (3rd line)
- Bilateral adrenalectomy (4th line)
Ectopic ACTH or CRH syndrome/ adrenal adenoma
• Surgical resection/ablation of tumour + metastases – 1st line
• Bilateral adrenalectomy – 2nd line
• Medical therapy – 3rd line
Radiotherapy – if persistent post-operative high cortisol
Refractory cases of Cushing’s – bilateral adrenalectomy
Addisonian crisis mx
o IVF
o 50 ml 50% dextrose for hypoglycaemia
o IV 200 mg hydrocortisone
100mg 6hourly hydrocortisone until BP stable
o Treat ppt cause (e.g. abx for infection)
o Monitor
Adrenal insufficiency mx
primary
secondary
o Glucocorticoid replacement (+Mineralocorticoid replacement in secondary adrenal insufficiency)
o Primary – hydrocortisone (3xday)[GC] + fludrocortisone [MC]
o Secondary – hydrocortisone [GC]
• increase steroids at times of stress to avoid adrenal crisis
o Illness, minor surgery – GC X3
o Major illness/surgery – GC X10 IM hydrocortisone
• if co-existing thyroid deficiency, replace hydrocortisone BEFORE thyroxine – to prevent precipitating an Addisonian crisis
Which antihypertensive agent is most appropriate as initial therapy in pheochromocytoma?
Alpha blocker e.g. doxazosin, phentolamine
Hypercalcaemia of malignancy mx
- aggressive rehydration
- diuresis with IV furosemide
- phosphorus replacement if hypophosphataemia
- IV bisphosphonates
Which diabetes drugs cause weight loss vs weigh gain
Weight loss
Metformin
GLP-1 agonists (exenatide, liragltide)
SGLT-2 inhibitor (empagliflozin)
Weight gain
Sulphonylureas (glibenclamide, gliclazde, glimepiride)
Thiazolidinediones (pioglitazone)
Which diabetes drugs can cause hypos?
Insulin
Sulphonylureas (glibenclamide, gliclazde, glimepiride)
Which diabetes drugs reduce CV mortality?
GLP-1 agonists (exenatide, liragltide)
SGLT-2 inhibitor (empagliflozin)
t2dm guidelines
https://care.diabetesjournals.org/content/diacare/42/Supplement_1/S90/F1.large.jpg?width=800&height=600&carousel=1
pt w diabetes during acute illness
during acute illness patients have a higher need for insulin
How do calcinomimetics work? (e.g. cinacalcet)
increase the receptor’s sensitivity to calcium to enhance negative feedback and decrease PTH + calcium
HTN + DM mx
First line mx – ACEi/ARB
Second line mx – CCB, diuretics
Third line mx – BB, alpha blocker
Thiazolidinediones contraindications
IHD or heart failure
Can cause Na + fluid retention
