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153 Cards in this Set
- Front
- Back
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Definition of Type 1 DM
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A disease of insulin insufficiency due to autoantibody destruction of the pancreatic beta islet cells
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Acute presentation of Type 1 DM
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DKA - patient is unwell, hyperventilating, ketones (sweet smell) on breath, polyuria, polydispia, fatigue
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Definition of Type 2 DM
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Disease of decreased insulin secretion and increased insulin resistance
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Symptoms of hyperglycemia
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polyuria, polydipsia, unexplained weight loss, visual blurring, thrush, lethargy
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Diagnosis of DM
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Fasting blood glucose > 7 mmol/L, random blood glucose > 11.1 mmol/L, Hba1c > 6.7% after an OGTT
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Potential causes of DM to keep in mind
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Acromegaly, phaeochromocytoma, hyperthyroidism, pregnancy
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Definition of impaired glucose tolerance
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OGTT 7.8-11.1 mmol/L
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Consequences of gestational diabetes
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Increased birthweight, neonatal hypoglycemia, sacral agenesis
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Metabolic syndrome
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Central obesity, hypertension, hyperglycaemia, dyslipidaemia (increased triglycerides, decreased HDL)
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Treatment of type 2 DM
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1. Lifestyle measures, 2. BP control, 3. Metformin (a biguanide - SFX include diarrhoea, abdo pain), 4. If Hba1c > 7% 16 weeks later add gliclazide (a sulfonylurea - SFX hypoglycaemia), 5. If Hba1c > 7.4% 6 months later add insulin or glitazone
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Common complication of injection
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Injection site lipohypertrophy
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Diabetic nephropathy
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urine albumin:creatinine ratio > 3 reflects early renal damage. Inhibition of RA system via candesartan will protect kidneys
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Background retinopathy
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Microaneurysms, haemorrhages and hard exudates (dots, blots and lipid deposits)
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Pre-proliferative retinopathy
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Cotton wool spots (infarcts), haemorrhages and venous beading
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Proliferative retinopathy
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Formation of new vessels. Urgent referral needed.
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Maculopathy
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Decreased acuity
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Cataracts
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Osmotic changes in the lens induced in acute hyperglycaemia reverse on normoglycaemia
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Rubeosis iridis
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New vessels occur on iris, occurs late and may lead to glaucoma
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Treatment of hyperthyroidism
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Beta blockers for rapid symptom control and until carbimazole takes effect (10-20 days due to long half life of T4). If relapse on suspension of treatment - radioiodine therapy and surgery. Radioiodine therapy is contra-indicated in pregnant women as it is teratogenic.
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Signs of hypothyroidism
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BRADYCARDIC - Bradycardic, Reflexes relax slowly, Akinesia, Dry skin/hair, Yawning/drowsy, Cold peripheries, Ascites, Round face, Depressed, Immobile, Congestive cardiac failure
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Causes of primary hyperparathyroidism
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80% solitary adenoma, 20% hyperplasia of all glands, <0.5% parathyroid cancer
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Presentation of hyperparathyroidism
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Relate to hypercalcaemia - Stones, moans, bones and groans. Weak, tired, depressed, thirsty, dehyrated but polyuric, fractures, osteoporosis
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IVx hyperparathyroidism
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Raised Ca and PTH. Decreased phosphate. Raised alk phos (bone activity). Pepper-pot skull.
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Secondary hyperparathyroidism
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Low Ca, high PTH. Caused by decreased vitamin D intake and chronic renal failure. Correct with phosphate binders.
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Tertiary hyperparathyroidism
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High Ca, very high PTH. Occurs after prolonged secondary hyperparathyroidism, causing glands to act autonomously having undergone hyperplastic or adenomatous change.
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Pseudohypoparathyroidism
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Failure of target cell response to PTH. Signs include short metacarpals, round face, short stature, calcified basal ganglia.
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Definition of Cushing's syndrome
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Clinical state produced by chronic glucocorticoid excess + loss of normal feedback mechanisms of hypothalamic-pituitary-adrenal axis + loss of circadian rhythm of cortisol secretion
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Causes of Cushing's
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Majority are iatrogenic (steroids). Endogenous causes are rare but most often increased ACTH via pituitary adenoma (Cushing's disease)
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Ectopic ACTH production
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Due to small cell lung cancers and carcinoid tumours. Special features include pigmentation, hypokalaemic metabolic alkalosis, weight loss and hyperglycaemia. Even a high dose dexamethasone suppression test fails to suppress cortisol production
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Signs and symptoms of Cushing's
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Signs - central obesity, moon face, buffalo hump, skin and muscle atrophy, bruises, purple striae on abdo, osteoporosis, infection prone. Symptoms reflect heavy steroid use - increased weight, mood changes, proximal weakness, gonadal dysfunction, acne, recurrent Achilles tendon rupture
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Cushing's investigation
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No cortisol suppression on high dose dexamethasone suppression test. May also see impaired glucose tolerance and hypokalaemia. Severe hirsuitism suggests an adrenal tumour.
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Definition of Addison's
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Destruction of the adrenal cortex leading to glucocorticoid and mineralocoritcoid deficiency
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Causes of Addison's
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80% autoimmunity, others include TB, metastases (lung, breast, renal), lymphoma
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Signs and symptoms of Addison's
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Lean, tanned, tired, tearful, weak, anorexic, dizzy, faints, myalgias/arthralgia, nausea, vomiting, abdo pain, diarrhoea. Pigmented palmar creases and buccal mucosa
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Addison's investigations
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Low Na, high K and Ca. High urea. Bloods show anaemia and eosinophilia. Low serum cortisol. Short ACTH stimulation test (tetracosactide)
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Hypopituitarism - order of affect
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GH, FSH, LH, Prolactin, TSH, ACTH.
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Signs and symptoms of hyperprolactinaemia
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Amenorrhoea or oligomenorrhoea, infertility, galactorrhoea, decreased libido, increased weight, dry vagina, erectile dysfunction
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Signs and symptoms of acromegaly
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Spade-like hands and feet, big tongue and facial features, excessive sweating, headaches, decreased libido, arthralgia, finding that rings/clothes become too small, weight gain.
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Diabetes medication
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Metformin = a biguanide
Gliclazide = a suphonylurea Rosglitazone = thiazolidinedione All of the above increase insulin sensitivity Acarbose = alpha glucosidase inhibitor, decreases sugar absorption |
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Fasting and 2 hr post glucose for normal pts, IFG, IGT, DM
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Fasting...
Normal = < 6 IFG = 6.1-6.9 DM = > 7 2hr post glucose Normal = <7.8 IGT = 7.8-11 DM = > 11.1 |
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HONK
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The DM2 equivalent of DKA. Features raised sodium and increased osmolality. Mortality of 20-40%.
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Anterior pituitary hormones
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GH, TSH, FSH, LH, Prolactin, ACTH, melanocyte stimulating hormone
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Posterior pituitary hormones
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Oxytocin, ADH (vasopressin)
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Hypopituitarism
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Growth hormone and gonadotrophins are effected first. Typically, there will be hyPER prolactinaemia due to loss of inhibitory control via dopamine.
Gold standard ivx is insulin tolerance test. Steroid and thyroid hormones given for life. |
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Thyroid cancer + hypercalcaemia?
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Cancer is medullary cell
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Anaplastic thyroid cancer
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No treatment apart from surgery. If surgery is no good, palliative.
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Syndrome of inappropriate antidiuretic hormone
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Retention of water and hyponatraemia. Presentation is vague - confusion, irritability. No oedema, hypokalaemia or hypotension. Normal renal, adrenal and thyroid function.
Causes include neoplasms, lung disease, CNS causes, alcohol withdrawal, cytotoxic agents. Treat with fluid restriction, demeclocycline and, if severe, hypertonic saline. |
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Diabetes insipidus
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Deficiency of vasopressin leading to polyuria, nocturia and compensatory polydipsia. Leads to dehydration. Typically follows hypothalamic-pituitary surgery.
Biochem shows high plasma osmolality with low urine osmolality. Results in high plasma sodium. Treat with desmopressin. |
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Fluid replacement in DKA
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NaCl 0.9% at a rate of 1L/hr for 2 hours
500 mls/hr in hours 3 and 4 If K <5.5 mmol/L give pre-prepared back of 40 mmol/L |
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Insulin prescribing in DKA
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50 units act rapid in 50mls 0.9% NaCl. Infuse at a fixed rate of 6 units/hr
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When to discuss DKA with ITU/HDU
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If blood glucose >33
Hypokalaemia GCS < 15 Pulse >100 or <60 SBP <90 pH <7.1 HCO3 <5 Lactate >2 |
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Subsequent management of DKA (hour 5 onwards)
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Give 10% glucose infusion at 100 mls/hr in conjunction with sodium chloride 0.9%
Convert to S/C insulin when stable and eating Stop IV fluids and insulin 1 hr after first dose of S/C insulin |
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Definition of hypoglycaemia
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4 mmol/L or less
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Definition and management of mild hypoglycaemia
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4 mmol/L
Trembling, sweating, hungry, tingling, headache, anxiety, palpitations, nausea Give 4 gluco tabs or 1 bottle of glucojuice or 100 mls lucozade or 200 mls fruit juice If NBM, give 100 mls 10% glucose IV |
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Definition and management of moderate hypoglycaemia
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3 mmol or 2 mmol/L
Difficulty concentrating and speaking. Confusion. Weakness and giddiness. Drowsy. Unsteady. Headache. Same as mild if cooperative. If uncooperative, give 2 tubes of glucogel |
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Definition and management of severe hypoglycaemia
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1 mmol/L
Patient unconscious and unable to swallow. Potentially fitting. ABC. Fast bleep doctor. 100 mls of 10% glucose or 1 mg glucagon im. Repeat if no improvement. Transfer to ITU. If patient was on a sulphonylurea, consider octreotide 50 mcg 12 hourly. |
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What do coeliac disease and DM1 have in common? (genotype)
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HLA-DQ2
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Heredity in diabetes
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Type 1 = HLA DR3-DQ2 or DR4-DQ8
No HLA links in Type 2 |
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Complications of diabetes that may be the presenting feature
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Staphylococcal skin infections
Retinopathy Polyneuropathy Erectile dysfunction Arterial disease |
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HbA1c level diagnostic of diabetes
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>6.5 (48 mmol/mol)
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What type of medication is metformin?
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A biguanide
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Management of type 1 DM
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Basal bolus insulin + pre meal insulin correction dose + amylin analogue (pramlintide)
2nd line - fixed dose insulin if trouble managing basal bolus regimen |
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Management of type 2 DM
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BP control + lipid control + lifestyle changes + smoking cessation + glycaemic management + antiplatelet management (primary = aspirin, secondary = clopidogrel)
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Management of type 2 DM if marked hyperglycaemia (FG > 16.6 or RG >19.4)
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Straight on to basal bolus insulin + metformin
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DVLA rules for diabetes
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BCL = bus/coach/lorry drivers
If managed by diet, no need to tell DVLA If treated by tablets or non-insulin injections, only BCL. If on insulin, all need to tell DVLA |
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What is an insulinoma?
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Pancreatic islet cell tumours. 95% are benign.
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What is Whipple's triad?
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Diagnostic criteria for an insulin secreting tumour.
Symptoms associated with fasting or exercise Hypoglycaemia Symptoms relieved by glucose Additional criteria includes inappropriately high insulin levels |
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Diagnosis of insulinoma
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Measurement of overnight fasting glucose and insulin on three occasions
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Management of insulinoma
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Surgical excision. If malignant, give diazoxide. If tumour can't be located, give a somatostatin analogue such as octreotide or lanreotide
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Hypothalamic-pituitary-thyroid axis
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Hypothalamus secretes thyrotropin releasing hormone to anterior pituitary, which secretes TSH.
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Gender ratio of hyperthyroidism
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5:1 F:M
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Pathogenesis of Graves
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Serum IgG bind to TSH receptors, stimulating thyroid hormone production. These are called TSHR-Ab and are specific for Graves disease.
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Three most common causes of hyperthyroidism
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Graves disease, toxic multinodular goitre, soltary toxic nodule
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What is de Quervain's thyroiditis?
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Transient hyperthyroidism from an acute inflammatory process. Usually fever, malaise and pain in the neck. TFTs show hyperthyroidism, raised ESR. May be followed by transient hypothyroidism.
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Which drug commonly causes thyrotoxicosis?
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Amiodarone
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Two types of amiodarone induced thyrotoxicosis
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Type 1 = pre-existing Graves' disease or multinodular goitre
Type 2 = no previous thyroid disease. Associated with a high T4:T3 ratio. |
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How long does it take before thyroid drugs take effect and why?
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10-20 days due to long half life of T4. In the mean time, gain symptomatic control via propanolol
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Which thyroid treatment regimen is contraindicated in pregnancy?
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Block and replace
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Major side effect of drug therapy in thyroid disease
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Agranulocytosis
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Thryoidectomy
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Should only be performed in euthyroid patients. Conventional practice is stop antithyroid drugs 10-14 days before operation and give potassium iodide.
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What is a thyroid storm and how would you manage it? And what is mortality?
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Hyperthyroidism with hyperpyrexia, severe tachycardia, extreme restlessness, cardiac failure and liver dysfunction.
Managed with full dose propanolol with potassium iodide, antithyroid drugs, corticosteroids and supportive measures. Mortality is 10% |
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5 types of thyroid malignancy
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Papillary (most common) - typically occurs in young people, normally local spread w/ occasional lung/bone metastases. Manage surgically. Prognosis is good.
Follicular (second most common) - more common in women. Metastasises to lung and bone. Manage surgically. Prognosis is good if tumour is resectable. Anaplastic (uncommon) - aggressive and locally invasive. Prognosis is very poor Medullary cell (uncommon) - Often familial. Prognosis is poor with indolent course Lymphoma (rare) - variable behaviour and spread. Responds to radiotherapy. |
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Role of parathyroid gland
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Regulates calcium and phosphate levels. Secretes PTH as calcium levels fall. Calcium levels are then raised by osteoclastic resorption of bone, intestinal absorption of calcium, synthesis of 125-(OH)2D3, increased renal reabsorption, increased excretion of phosphate.
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Causes of hypercalcaemia
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Hyperparathyroidism, ectopic PTH secretion, myeloma, bone mets, vitamin D excess, granulomatous disease (TB, sarcoidosis, lymphoma), excessive intake, thiazides, lithium use, Addison's, thyrotoxicosis, immobility.
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What is secondary hyperparathyroidism?
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Compensatory hypertrophy of parathyroid glands due to chronic hypocalcaemia, typically due to CKD or vit D deficiency
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What is tertiary hyperparathyroidism?
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Permanently raised parathyroid hormone production after longstanding secondary hyperparathyroidism. Parathyroidectomy is necessary.
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Symptoms of hypercalcaemia
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Bones (pain), stones (renal), moans (depression) and groans (abdo pain).
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Hallmark of primary hyperparathyroidism
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Hypercalcaemia and hypophophataemia with raised PTH
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Presentation of acute hypercalcaemia
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Dehydration, N&V, nocturia and polyuria, drowsiness, altered consciousness.
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Management of severe hypercalcaemia
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Rehydration, IV bisphosphonates.
Can also use prednisolone if myeloma or sarcoidosis. |
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Causes of hypocalcaemia
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CKD, vit D deficiency, thyroid or parathyroid surgery, idiopathic
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What is DiGeorge's syndrome?
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Familial hypoparathydoism associated with intellectual impairment, cataracts and calcified basal ganglia
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What is pseudohypoparathyroidism?
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End organ resistance to PTH. Associated with short stature, short metacarpals, subcutaneous calcification and intellectual impairment.
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Clinical features of hypoparathyroidism
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Paraesthesiae, circumoral numbness, cramps, anxiety, convulsions, laryngeal stridor, dystonia and psychosis.
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What is Chvostek's sign?
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Present in hypocalcaemia. Tapping over facial nerve causes twitching of ipsilateral facial muscles
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What is Trousseau's sign?
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Inflation of sphyg cuff for more than 3 mins causes spasm of fingers and wrist
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ECG signs of hypocalcaemia
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Prolonged QT interval
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Management of hypocalcaemia
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With vitamin D deficiency give cholecalciferol, otherwise give alfacalcidol
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Causes of hypovolaemic hyponatraemia
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Diuretics, Addison's, nephropathy, osmotic diaresis, vomiting, diarrhoea, burns, rhabdomyalosis, pancreatitis, peritonitis
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Causes of euvolaemic hyponatraemia
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Diuretics, SIADH, CNS disturbances, neoplasms (in particular SCLC), surgery, drugs (SSRI, carbamazepine, cyclophosphamide, opiates, maoi, ecstasy)
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Causes of hypervolaemic hyponatraemia
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Heart, renal, or liver failure. Hyperglycaemia.
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Most common causes of hypokalaemia
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Diuretics (thiazides) and hyperaldosteronism. Otherwise, GI losses through vomiting, diarrhoea, bulimia/anorexia, DKA.
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Definition of hypokalaemia
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Mild = <3.5 mmol/L
Severe = <2.5 mmol/L |
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Clinical manifestations of hypokalaemia
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Muscle weakness, ECG changes, rhabdomyolysis, renal abnormalities, cardiac arrhythmias.
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ECG changes in hypokalaemia
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ST depression, inverted T waves, large U waves, PR prolongation
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Clinical features of hypomagnesaemia
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Irritability, tremor, ataxia, carpopedal spasm, hyperreflexia, confusion, hallucination, epileptic convulsions
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ECG of hypomagnesaemia
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Prolonged QT interval, flattened and broad T waves, ST shortening
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Clinical features hypermagnesaemia
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Weakness, hyporeflexia, respiratory paralysis
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Treatment of hypermagnesaemia
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Same as hyperkalaemia
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Clinical features of hypophosphataemia
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Muscle weakness, left shift of oxyhaemoglobin dissociation curve, confusion, hallucination, convulsions
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Causes of hypophasphataemia
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Hyperparathyroidism
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What is Addison's?
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Destruction of at least 90% of the adrenal cortex leading to reduction of glucocorticoid, mineralocorticoid and sex steroid production. Leads to increased CRH and ACTH production via feedback.
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What causes Addison's?
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Autoimmune disease, TB, surgical removal of adrenals, infiltration via malignancy/amyloid
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Symptoms and signs of Addison's disease
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Symptoms - weight loss, anorexia, malaise, weakness, impotence/amenorrhoea, N&V, abdo pain, constipation/diarrhoea
Signs - Pigmentation of new scars and palmer creases, postural hypotension, buccal pigmentation |
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What is an Addisonian crisis?
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Hypotension + hyponatraemia + hyperkalaemia + hypoglycaemia + dehydration. Typically follows infection, infarction, trauma or operation.
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Management of Addisonian crisis
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1L 0.9% saline. IV bolus hydrocortisone. Supportive.
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What is hyperaldosteronism?
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A disorder of the adrenal cortex characterised by excess aldosterone production leading to sodium retention, potassium loss, and hypertension.
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What causes secondary hyperaldosteronism?
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Renal artery stenosis
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What causes primary hyperaldosteronism?
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Adrenal adenomas (Conn's syndrome, more common in young women), bilateral adrenal hyperplasia (more commen in men >40)
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Presentation of hyperaldosteronism
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Typically just hypertension. Other symptoms are non specific (weakness, nocturia)
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How would you differentiate adenoma from hyperplasia in hyperaldosteronism?
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Adrenal CT or MRI.
Also, check plasma aldosterone levels, which rise throughout the day with adenomas and fall with hyperplasia. Also measure 18-OH cortisol levels, which rise in adenoma |
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Management of hyperaldosteronism
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If adenoma, surgical removal. If hyperplasia, spiranolactone.
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What is Cushing's syndrome?
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The clinical state of increased free ciculating glucocorticoid
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What is Cushing's disease?
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Pituitary disease leading to Cushing's syndrome
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What causes Cushing's syndrome?
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Cushing's disease, ectopic ACTH producing tumours, ACTH administration, adrenal adenomas, adrenal carcinomas, steroid use
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Signs and symptoms of Cushing's
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Pigmentation (if ACTH dependent), impaired glucose tolerance, hypokalaemia, hypertension, pathological fractures, striae, proximal myopathy.
Central weight gain, thin skin/bruishing, hair growth, acne, back pain, plethora. |
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Ivx Cushing's
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48 hour low dose dexamethasone test - normal result is suppression of plasma cortisol to <50 nmol
24 hour urinary free cortisol measurement Pronounced circadian variation in cortisol. In Cushing's 09:00 sample of cortisol may be normal, but 00:00 sample will be >100 nmol/L |
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What causes death in Cushing's?
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Complications of hypertension
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Management of Cushing's
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Depends on cause. Typically surgery (transsphenoidal pituitary adenectomy or adrenalectomy) plus medical management via ketoconazole or mifepristone.
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What is congenital adrenal hyperplasia?
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Inherited enzyme deficiency that impair normal corticosteroid synthesis by the adrenal cortex - most commonly 21-hydroxylase deficiency.
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What is a phaeochromocytoma
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A tumour arising from catecholamine producing cells of the adrenal medulla
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Clinical features of phaeochromocytoma
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Headaches, diaphoresis, palpitations, paroxysmal HTN. Symptoms are episodic and tend to progress as the tumour grows.
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IVx of phaeochromocytoma
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24 hour urine collection for catecholamines, metanephrines, normatenephrines, and creatinine.
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Management of phaeochromocytoma
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Anti hypertensive agents + surgery
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Hormones secreted by the anterior pituitary
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ACTH, TSH, FSH, LH, GH, prolactin, leptin
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Hormones secreted by the posterior pituitary
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Oxytocin, vasopressin
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What does the hypothalamus do?
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Essentially links the nervous and endocrine systems via the pituitary gland.
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What is pituitary apoplexy?
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Bleeding into or impaired blood supply to the pituitary gland, typically due to the presence of a tumour
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Clinical features of pituitary apoplexy
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Compressive effects of the local region.
i.e. headache, visual field defect (optic chiasm), double vision (third nerve). Followed by symptoms of adrenal insufficiency. Can present with meningism and decreased level of consciousness. |
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What causes acromegaly?
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Excess GH, typically due to a pituitary adenoma
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Signs and symptoms of acromegaly
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Change in appearance, increased size of hands/feet, headaches, excessive sweating, visual deterioration, weight gain, deep voice, goitre, pain in hands, polyuria.
Prognathism, interdental separation, large tongue, spade like hands and feet. May also cause hirsuitism, thick skin, carpal tunnel syndrome, visual field defects, arthropathy. |
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Ivx of acromegaly
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Glucose tolerance test is diagnostic if there is no suppression of GH, or there is a rise.
IGF-1 levels are often raised. MRI for pituitary tumour. |
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Management of acromegaly
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Trans-sphenoidal surgery is first line, followed by radiotherapy.
Also use octreotide, bromocriptine, and pegvisomant. |
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Definition of a high risk lipid profile
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Total cholesterol > 4.0 mmol/L or
LDL > 2.0 mmol/L or Triglycerides > 4.5 mmol/L |
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Management of diabetic neuropathy
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Duloxetine (amitriptyline if contraindicated)
Second line = amitriptyline or pregabalin or both Other options include pain management clinic, tramadol, topical lidocaine |
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Type 2 diabetes blood pressure targets
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if no end organ damage < 140/80
If end organ damage <130/80 |
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When to treat subacute hypothyroidism
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If TSH>10, thyroid autoantibodies positive, other autoimmune disorder, previous treatment of Graves' disease
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Glucocorticoid and mineralocorticoid activity in steroids
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Very high mineralocorticoid = fludrocortisone
high mineralocorticoid = hydrocortisone high glucocorticoid = prednisolone very high glucocorticoid = dexamethason, betamethasone |
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Secondary hypothyroidism TFTs
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TSH and free T4 both low
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Sick euthyroid syndrome TFTs
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TSH Low/Normal, T4 low, T3 very low
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Subclinical hypothyroidism TFTs
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TFT high, T4 normal
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Poor compliance with treatment TFTs
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TSH high, T4 normal. T4 will normalise before TSH
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Steroid therapy TFTs
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TSH low, T4 normal
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