Endocrinology Flashcards
What are some common causes of primary hypothyroidism and what would TFTs typically show.
TFTs show high TSH and low T4.
Common causes are:
- Autoimmune (Hashimoto’s, atrophic)
- Iodine defiency
- thyroiditis (Riedel’s, Postpartum, de Quervains (Subacute). Note the last two initially present with a hyperthyroid state followed by a prolonged hypothyroid state)
- Iatrogenic (cytotoxics, thyroidectomy, radioiodine, Lithium, Amiodarone)
What are some common causes of secondary hypothyroidism and what would TFTs typically show.
TFTs show low TSH and low T4
Pituitary insuffiency most likely cause and so MRI of gland neccesary
What is sick euthyroid syndrome and what would TFTs typically show.
TFTs show slightly low TSH and low T4.
Associated with systemic illness during which TFTs become deranged. Test should be repeated after recovery. T3 may be particularly low.
Describe Graves’ disease, its features, investigations, and management.
Most common cause of hyperthyroidism (66%), Typical patient female (9:1) 40-60yrs. Caused by Thyrotropin-activating IgG autoantibodies.
Features:
Hyperthyroidism: tremor, agitation, diarrhoea, insomnia, weight loss, tachycardia, sweating, feeling hot, itching, muscle weakness, irritability/anxiety
Thyroid eye disease: double vision, exophthalmos, blurred vision, loss of colour vision
Graves specific: pretibial myxoedema, thyroid acropachy, thyroid bruit, smooth goitre.
Investigations: TFTs show low TSH, increased T3 and T4. Increased uptake of radioactive iodine. Anti-TSH-receptor.
Management:
- Stopping smoking is most important modifiable risk factor in thyroid eye disease.
- radioiodine can cause an increase in eye symptoms, though concurrent prednisolone may reduce impact.
What is subacute deQuervain’s thyroiditis?
Self-limiting post viral hyperthyroidism followed with longer hypothyroid phase, with painful goitre, febrile, and typically increased ESR. low isotope uptake on scan. Managed with NSAIDs.
Describe insulinoma its tests and treatment
This often benign (90-95%) pancreatic islet cell tumour is sporadic or seen with MEN-1. It presents as fasting hypoglycaemia, with whipple’s triad:
- Symptoms associated with fasting or exercise
- Recorded hypoglycaemia with symptoms
- Symptoms relieved with glucose
Tests: Screening test - hypoglycaemia and increased plasma insulin during a long fast. Suppressive test - give IV insulin and measure C peptide, normally exogenous insulin supresses c-peptide production but this does not occur in insulinoma. CT/MRI imaging
Treatment: excision
Diazoxide (a K channel activator, leading to hyperpolarisation of cell membrane, a decrease in calcium influx and inhibition of insulin release)
Describe Diabetic Ketoacidosis, it’s presentation, investigation, and management
A medical emergency. Ketoacidosis is an alternative metabolic pathway that occurs in starvation states, an breaks down protein giving acetone as a by product. In diabetic Ketoacidosis there is excessive glucose but because of lack of insulin this cannot be taken up into cells pushing the body into a starvation state where Ketoacidosis occurs.
Presentation: Gradual drowsiness, vomiting and dehydration in a type 1 diabetic. May also be history of polyuria, polydipsia, lethargy, anorexia. Signs of dehydration and ketotic breath occur later deep and rapid (Kussmaul) breathing.
Investigations:
- Urinalysis (glucose, ketones)
- BM (hyperglycaemia greater than 11mmol/L)
- Blood Gas (Acidaemia pH less than 7.3) (Severity on pH e.g. Mild = less than 7.3, moderate less than 7.2, severe less than 7.1) (Bicarb less than 18mmol/L)
- Bloods, U+Es, Glucose, HbA1c, Cultures (if pyrexial), FBC. Ketones (over 3mmol/L)
- ECG (looking for peaked t-waves hyperkalaemia)
Management:
- DR ABCDE Assessment
- Be wary of sudden fluid changes as risk of cerebral oedema.
- Fluid status examination + fluids replacement
- 1L NS over 1hr then Fixed rate IV insulin e.g. 0.1 unit/kg, then 1L over 2,2,4,4,6 HRs +/- potassium (over 5.5 nil, 3.5-5.5 20mmol, less than 3.5 40mmol), unless able to orally rehydrate and SC insulin.
- Monitor bloods stop insulin when ketones less than 1mmol/L if glucose falls to less than 14mmol/L give dextrose alongside fluids.
Describe Hyperosmolar Hyperglycaemic State (HHS),its symptoms, and management.
Typically those with type 2 diabetes are at risk of this. Presents with profound hypovolaemia, hyperglycaemia over 35mmol/L, and increased plasma osmolality over 340mosmol/L. There may or may not be metabolic acidosis but it is less profound than in DKA due to there being no switch to amino-acid metabolism. Occlusive events are a danger due to increased viscosity (Focal CNS signs, Chorea, DIC, leg ischaemia, rhabdomyolysis)
Symptoms: Generalised weakness, leg cramps, visual disturbance, nausea and vomiting, delirium, seizures.
Management:
- Risk of DVT so give LMWH prohylaxis.
- Rehydrate slowly only use insulin if blood glucose not falling by 5mmol/L/Hr with rehydration or ketonaemia is present.
- Look for a cause such as MI, drugs, bowel infarct, Stoke, Hyperthermia, AKI, Cushings, GI bleeds.
Describe Cushing’s syndrome, it’s causes, symptoms, investigations, and management.
Syndrome due to chronic glucocorticoid excess.
ACTH dependent causes:
- Cushing’s disease (pituitary adenoma)
- ectopic ACTH production especially small cell lung cancer and carcinoid tumours, often atypical presentation with pigmentation, hypokalaemic metabolic alkalosis, weight loss, hyperglycaemia.
- rarely ectopic CRF production some thyroid and prostate cancers
ACTH independent causes:
- adrenal neoplasi, may also cause pain and virilisation in females
- adrenal modular hyperplasia
- iatrogenic steroid therapy (most common)
- rarely carney complex, McCune-Albright syndrome
Symptoms: increased weight, mood change (depression, irritability), proximal weakness, gonadal dysfunction, acne, Achilles’ tendon rupture, Central obesity, plethoric, moon face, buffalo neck hump, supraclavicular fat distribution, skin and muscle atrophy, bruises, abdominal striae, osteoporosis, Hypertension, hyperglycaemia.
Investigations: Midnight cortisol, Dexamethasone suppression test, 24hr Urinary Cortisol, U+E (Hypokalaemia in ectopic ACTH), (Metabolic acidosis), MRI pituitary, CT chest + Abdomen
Management:
- Treat cause, ketoconazole and nicotine can be used to lower cortisol by inhibiting synthesis and secretion in the adrenal gland.
- surgical/radiotherapy for tumour causes.
Describe primary adrenocortical insufficiency (addisons disease), it’s symptoms, tests and treatment
It is rare but can be fatal. Destruction of adrenal cortex leads to glucocorticoid (cortisol) and mineralocorticoid (aldosterone) deficiency. 80% are due to autoimmunity in UK, TB is commonest world wide cause, may be neoplasm
Symptoms: lean, tanned, tired, tearful +/- weakness, anorexia, dizzy, faints, flu-like myalgia. Nausea vomiting, abdominal pain, diarrhoea constipation, pigmented Palmer creases and buccal mucosa as ACTH cross reacts with melanin receptors. Postural hypertension vitiligo.
Tests: hyponatreaemia, hyperkalaemia due to decreased mineralocorticoid. Hypoglycaemia due to decreased cortisol, also uraemia, hypercalcaemia, eosinophilia, anaemia. ACTH stimulation test, 21-hydroxylase adrenal autoantibodies
Treatment:
- replace steroids hydrocortisone 20mg/d in divided dose 10, 5, 5 with fludrocortisone 50mcg/d
- double hydrocortisone for sick day rules.
- warn against abruptly stopping due to risk of addisonian crisis
Describe secondary adrenal insufficiency
The commonest cause is iatrogenic due to long term steroid therapy leading to suppression of the pituitary adrenal axis. This only becomes apparent on withdrawal of steroids. Other causes are rare and include hypothalamic pituitary disease leading to decreased ACTH production. Mineralocorticoid production remains intact and there is no hyperpigmentation
Describe male hypogonadism it’s features and causes
Hypogonadism is the failure of testes to produce testosterone, sperm or both.
Features: small testes, decreased libido, erectile dysfunction, loss of pubic hair, decreased muscle
Bulk, increased fat, gynaecomastia, osteoporosis, mood disturbance.
Primary hypogonadism causes:
•testicular failure from trauma, torsion, radiotherapy
•post-orchitis e.g mumps
•renal failure, liver failure or alcohol excess
•chromosomal abnormalities e.g. Klinefelters syndrome
Causes of secondary hypogonadism:
•hypopituitarism
•prolactinoma
•kallman’s syndrome (isolated GnRH deficiency often with anosmia and colour blindness
•systemic illness
•Laurence-moon-biedl and prader-willi syndromes
Describe Hyperprolactinaemia, its causes, symptoms and management
Prolactin is secreted by the anterior pituitary and release is inhibited by dopamine produced in the hypothalamus.
Causes:
- excess production from the pituitary e.g. prolactinoma
- disinhibition, by compression of the pituitary stalk e.g. pituitary adenoma, or hypothalmic disease
- Drugs e.g. Dopamin receptor antagonists, e.g. Domperidone, neuroleptics. Also anti-depressants, verapamil, methlydopa, optiates, protease inhibitors, fibrates, H2 antagonists, Omeprazole.
Symptoms:
- females = amenorrhoea, oligomemorrhea, infertilty, galactorrhoea, also decreased libido, increased weight and dry vagina.
- males = erectile dysfunction, decreased facial hair, galactorrhoea.
- Low FSH and LH
Management:
- depending on cause, Dopamine agonist e.g. Carbegoline
- if adenoma transphenoidal surgery can be used second line
Describe the menstrual cycle
Pulsatile production of GnRH by the hypothalamus stimulates the pituitary to produce the gonadotrophins LH and FSH. These stimulate the ovary to produce oestrogen and progesterone.
In the first 4 days of the menstrual cycle FSH levels are high, stimulating the development of a primary follicle in the ovary. The follicle produces oestrogen, which stimulates the development of a glandular ‘proliferative’ endometrium and of cervical mucus which is receptive to sperm.
Around the 14th day oestrogen levels becomes high enough to stimulate a surge of LH. This stimulates ovulation. Having released the ovum, the primary follicle forms a corpus luteum and starts to produce progesterone. under this influence the endometrial lining is prepared for implantation and enters the secretory phase.
If the ovum is not fertilised the corpus luteum breaks down and hormone levels fall. This causes spiral arteries in the in the uterine endothelial lining to constict and the lining sloughs hence mensturation.
Normal menstruation lasts 2-7 days and normal blood loss is 20-80ml.
Describe Diabetes insipidus, its symptoms, causes and tests.
This is the passage of large volumes of dilute urine due to impaired water resorption by the kidneys because of reduced ADH secretion from the posterior pituitary (cranial DI) or impaired response to ADH (nephrogenic DI)
Symptoms: polyuria, polydipsia, dehydration, irritability, confusion.
Causes of cranial DI:
- Idiopathic
- congenital defects in ADH gene
- tumour (may present with DI + hypopituitarism)
- Trauma
- Infiltration e.g. sarcoidosis
- vascular e.g. haemoorhage
- infection e.g. menigoencephalitis
Causes of nephrogenic DI:
- inherited
- metabolic e.g. hypokalaemia, hypercalcaemia
- drugs e.g. lithium, demeclocycline
- chronic renal diseas
- post-obstructive uropathy
Tests: serum and urine osmalalities and water deprivation test. Patients are deprived of water for 4+ hours urine osmalality and output is measured which should remain low. They are then given desmopressin and lack of sufficient response leads to diagnosis of nephrogenic diabetes insipidus
Management:
- Cranial: desmopressin
- Nephrogenic: stop any drug causes, High dose DDAVP may be used in mild to moderate cases.
Describe acromegaly its symptoms, complications, investigations, and management.
Due to increased secretion of GH from a pituitary tumour (99%) or hyperplasia e.g. via ectopic GH-releasing hormone from a carcinoid tumour. GH stimulates bone and soft tissue growth through increased secretion of insulin-like growth factor-1 (IGF-1)
Symptoms: Headache, arthralgia, amenorrhoea, spade-like hands, coarsening of face, big supraorbital ridges, macroglossia, acanthosis nigricans, snoring/obstructive sleep apnoea, proximal myopathy, goitre, carpel tunnel signs, bitemporal hemianopia
Complications:
- impaired glucose tolerance and DM
- vascular e.g. hypertension, left ventricular hypertrophy, increased risk of IHD and stroke
- increased colon cancer risk
Investigations:
-hyperglycaemia, hypercalcaemia, hyperphosphataemia, raised IGF-1, oral glucose tolerance test (GH should be suppressed by glucose, if GH is above 3mIU/L acromegaly is confirmed. MRI pituitary to assess cause. Echo
Management:
- for pituitary tumour transphenoidal surgery
- if surgery fails, somatostatin analogues e.g. Octreotide may be used.
- GH antagonist (pegvisomant) can be used in cases resistant or intolerant to somatostatin analogues.
- radiotherapy is also an option
Describe the WHO criteria for diagnosis of Diabetes Mellitus
- Symptoms of hyperglycaemia (e.g. polyuria, polydypsia, unexplained weight loss, visual blurring, genital thrush, lethargy) and raised venous glucose detected once either fasting >7mmol/L or random >11.1mmol/L
- Raised venous glucose on 2 separate occasions
- HbA1C >48mmol/L (6.5%) but below doesnt exclude DM
Describe metabolic syndrome (syndrome X)
A syndrome that can lead to increased risk of MI and insulin resistance, defined as central obesity (waist circumference greater than 102cm or 40” plus 2 of:
- BP>130/85
- triglycerides >1.7mmol/L
- HDL less than 1.03(male) or 1.29 (female)mmol/L
- fasting glucose greater than 5.6mmol/L or DM
Describe Hypoglycaemia its symptoms and causes, and management
This is the commonest endocrine emergency it is defined as a plasma glucose less than 4mmol/L
Symptoms: Sweating, anxiety, hunger, tremor, palpitations, dizziness, confusion, drowsiness, visual trouble seizures and coma.
Causes: the chief cause is insulin or sulfonylurea treatment in a known diabetic after increased activity, missed meal or overdose. if non-diabetic you must EXPLAIN.
- EXogenous drugs e.g. insulin or oral hypoglycaemics (Do Sulfonylurea screen as bloods mimic insulinoma)
- Pituitary insufficiency
- Liver failure
- Addisons disease
- Islet cell tumour (insulinoma)
- Non-pancreatic neoplasm
Management:
Step 1: Orientated and able to swallow try 15-20g quick acting carbohydrate e.g.
-150-200mL orange juice
-2 tubes Glucogel
-4-5 Glucotabs
-3-4 Jelly babies
Step 2: Repeat CBG after 15mins and repeat step 1 up to 3 times
Step 3: Consider 1mg IM Glucagon
Step 4: IV 10% glucose infusion at 100ml/Hr
Step 5: After treatment give long acting carbohydrate e.g. Two biscuits, slice of toast, glass of milk, normal meal if due
If Patient is unconscious IM glucagon or IV Glucose 80ml of 20% Glucose over
Describe Diabetic Neuropathy, its symptoms, and management.
A complication of diabetes, including peripheral neuropathy, autonomic neuropathy, gastroparesis.
Symptoms: numbness/burning sensation in extremities in glove and stocking distribution. May also affect Autonomic nervous system with loss of bladder control. Gastroparesis presents with erratic blood glucose control, bloating and vomting.
Management:
- amitryptilline, Duloxetine, gabapentin, or pregabalin.
- pain management clinics for resistant problems
- metoclopramide, domperidone or erythromycin may be used in gastroparesis (pro kinetic agents)
Describe Hirsutism, it’s causes, and a management.
Implies hair growth in women in the male pattern. May be associated with virilism (onset of amenorrhoea, clitoromegaly, deep voice) and Gynaecomastia.
Causes: Familial, idiopathic or hyperandrogenism from ovary (PCOS, Ovarian Cancer) or Adrenal gland (late-onset congenital adrenal hyperplasia, Cushing’s syndrome, adrenal carcinoma) or iatrogenic e.g. Steroids.
Management:
- Oestrogens may help, considered COCP
- Clomifene is used for infertility.
What are the types of hermaphroditism and some causes?
True Hermaphroditism describes an individual born with ovarian and testicular tissue, these may be as separate or more commonly an ovotestis.
Pseudo hermaphroditism describes an indictable with primary characteristics of one sex but develops secondary characteristics of another e.g. Ambiguous genitalia (cliteromegaly). Causes include congenital adrenal hyperplasia, androgen insensitivity, 5alpha-reductive deficiency
Describe Subclinical Hypothyrodisim and its management
TSH raised but T3,T4 normal.
No obvious symptoms. Small risk of progressing to overt hypothyroidism risk further increased by presence of thyroid autoantibodies.
Management:
- Treat if TSH over 10, or antibody positive.
- (Consider lower threshold if pregnancy or with CVD)
Describe normal calcium homeostasis.
Parathyroid hormone increases calcium levels and decreases phosphate levels by action on osteoblasts which acts in increase calcium in extra cellar fluid and also produce a protein that activates osteoclast bone resorption. It also acts to increase renal tubular reabsoprtion of calcium and increases synthesis of active vitamin d in the kidney which increases bowel absorption of calcium
Active vitamin D acts to increase plasma calcium and phosphate by increases renal tubular reabsorption and gut absorption of calcium and increases osteoclast ice activity.
Calcitonin is secreted by C cells of thyroid and acts to inhibit intestinal calcium absorption and inhibitors osteoclasts activity and rental tubular absorption of calcium.
Describe Primary Hyperparathyroidism, its hormone profile, symptoms, and management,
Most cases due to solitary adenoma, typical presentation is elderly lady with unquenchable thirst and inappropriately raised or normal parathyroid hormone.
Hormone profile: PTH elevated, Calcium Elevated, Phosphate low,
Symptoms: Asymptomatic, recurrent abdominal pain (pancreatitis, renal colic), changes to emotional or cognitive state, polydipsia, Polyuria, hypertension.
Management: Total parathyroidectomy.
Describe Primary Hypoparathyroidism, its hormone profile, symptoms, and management.
Hormone profile: Decreased PTH, Low calcium, high phosphate.
Symptoms: Tetany (muscles twitching, cramping, spasm), perioral paraesthesia, trousseau’s sign (carpal spasm when inflating blood pressure cuff), chvosteks sign (tapping over parotid causes facial muscles to twitch), depression, cataracts, prolonged QT.
Management: Alfacalcidol
Describe Secondary Hyperparathyroidism, its hormone profile, symptoms, and management.
Parathyroid gland hyperplasia occurs as result of low calcium almost always in a setting of chronic renal failure.
Hormone profile: Elevated PTH, Low/normal calcium, phosphate elevated, vitamin D levels low.
Symptoms: Asymptomatic, bone disease, and soft tissue calcifications.
Management:
-Vit D and Calcium replacement
Which Diabetic medications requiring glucose fingerprick monitoring?
Those causing hypoglycaemia e.g. Sulphonylureas, insulin, glitazones.
Describe Maturity Onset Diabetes of the Young (MODY) and the different types.
Autosomal dominant non-ketotic diabetes, in childhood or young adults. The defect is one of pancreatic beta cell dysfunction leading to impaired insulin secretion. It is caused by a single gene defect. There are different types depending on the gene defect. Sulphonylureas shown to be most effective.
Types:
- MODY2 (GCK subtype) is caused by mutation in the glucokinase gene on chromosome 7. Usually there is mild asymptomatic stable hyperglycaemia from birth. Microvascular disease is rare and drugs are rarely needed.
- MODY3 (HNF1A subtype) is the most common type. It is caused by a defect on chromosome 12 leading to progressive decrease in insulin production. It features severe hyperglycaemia after puberty which often leads to a diagnosis of type 1 DM. Diabetic retinopathy and nephropathy often occur.
- MODY5 (HNF1B subtype) is associated with pancreatic atrophy, renal abnormalities and genital tract malformations.
- MODY1,4,6 also exist but are very rare.
What are the different causes of diabetes?
- Type 1 DM
- Type 2 DM
- Pancreatic insufficiency e.g. Pancreatitis, surgery, trauma, haemochromatosis, CF, pancreatic cancer
- Cushings disease
- acromegaly
- phaeochromocytoma
- hyperthyroidism
- pregnancy
- Congenital lipodystrophy
- Glycogen storage diseases.
Describe Primary Hyperaldosteronism (Conn’s), it causes, symptoms, investigations, and management.
Excess production of aldosterone, independent of the renin-angiotensin system, causing hypernatraemia and water retention and decreased renin release.
Causes: Bilateral idiopathic adrenal hyperplasia is the cause sin up to 70%, with adrenal adenoma accounting for up to 30%. Rare causes include Adrenal carcinoma and glucocorticoid-remediable aldosteronism (ACTH regularlroty element of the 11-Betahydroxylase gene fuses to aldosterone synthase gene leading to aldosterone production under control of ACTH)
Symptoms: Consider if the following features, hypertension, hypokalaemia, alkalosis is someone not on diuretics. May also get weakness, cramps, paraesthesia, polyuria, polydipsia.
Investigations: U+E (Hypokalaemia, hypernatraemia), renin (reduced), aldosterone (raised), genetic testing for GRA if family history. Adrenal CT + Adrenal vein sampling, 18-Hydroxycorticosterone testing. Saline suppression test (2L Saline infused over 4 hrs testing of aldosterone and renin, levels stay the same in conn’s)
Treatment:
- Conn’s = laparoscopic Adrenalectomy, Spironolactone 4wks pre-op
- Hyperplasia treated medically, spironolactone, amiloride, eplerenone (selective aldosterone antagonist, which doesn’t cause gyneacomastia)
- GRA Dexamethasone 1mg/24hr PO for 4wks
- Adrenal carcinoma = surgery + post-op adrenolytic therapy with mitotane (poor prognosis)
What are the main types of antibodies in type 1 diabetes?
Islet cell autoantibodies, insulin autoantibodies and glutamic acid decarboxylase (GAD) antibodies
What is a typical formula used when perscribing insulin
1/2 BW (ideal body weight if obese) units of insulin 50/50 long/short acting
When converting a patient from insulin to a sliding scale/ fixed rate insulin what should you do with their normal insulin?
Never stop the basal insulin and when converting back from VRII only stop 30 minutes after subcutaneous insulin has been given ideally at meal time after short acting insulin or mixed insulin has been given.
What is pancreatogenic Diabetes?
Also known as type 3c diabetes it is a form that relates to the exocrine and digestive function of pancreas. Insuffiency of both insulin and glucagon leads to a very difficult and lability blood glucose which is hard to control and treat
Describe Hyperthyroidism, its causes, features, and investigations, and management
Causes:
- Graves disease 60% thyrotropin receptor autoantibodies
- toxic multinodular goitre - elderly and iodine -deficient
- toxic adenoma
- ectopic thyroid tissue
- exogenous
- Subacute de Quervains thyroidits (self-liming frost viral with painful goitre and reduced isotope uptake)
Features: Diarrhoea, Weight Loss, Increased Appetitie, over-activity, sweats, heat intolerance, palpitations, tremors, irritability, labile emotions, oligomennorhoea,
Signs: warm moist skin, palmar erythema, fine tremor, lid lag, thin hair, goitre, thyroid nodules, bruit (graves)
Specific Graves signs:
- Eye disease: exophthalmos, opthalmoplegia
- pretibial myxoedema: oedematous swellings above lateral malleoli
- Thyroid acropachy: extreme manifestation with clubbing painful finger and toe swelling
Investigations: ESR, Ca, LFT, Thyroid autoantibodies, isotope scan if cause unclear.
Management:
- B-blockers and carbimazole (SE agranulocytosis)
- radioiodine
- thyroidectomy
What are the effects of exercise on blood glucose?
Aerobic exercise can cause blood glucose to drop rapidly while anaerobic exercise may cause it to rise.
Describe Hypomagnesaemia, its symptoms, causes, and management
Mostly asymptomatic until levels drop below 0.5mmol/L, also commonly associated with other metabolic abnormalities such as hypokalaemia, hypocalcaemia, and metabolic acidosis and exacerbates digoxin toxicity
Symptoms: asymptomatic, weakness and apathy, tremor, paraesthesia, tetany, fasiculations, seizures, confusion, arrhymias, prolonged QT, U waves, wide QRS, decreased PTH secretion and hypocalcaemia
Causes: Diuretics, total parenteral nutrition, diarrhoea, alcohol, hypokalaemia, hypocalcaemia, Malabsorption syndromes e.g. IBD, metabolic disorders e.g. Gitelman’s and Bartter’s
Management:
- serum Mg, protein loss may be cause, check glucose,
- ECG
- Mild to moderate (0.5-0.6) Magnesium Glycerophosphate (4mmol Mg) 2 tablets TDS OR Magnesium sulphate 4-8mmol IV infusion over 1 hr.
- less than 0.5 IV replacement 16mmol of magnesium sulphate in 100ml 0.9% NaCl over 1hrs. Repeat level after transfusion
What are the different parts of the adrenal gland?
The capsule the cortex and the medulla:
The cortex consists of:
Zona Glomerulosa aldosterone is produced
Zona Fasciculata Cortisol is produced
Zona Reticulata Sex hormones are produced
Medulla is where catecholamines are made e.g. Adrenaline
What is the difference in profile between Levermir and Lantus
Levemir has a flatter profile where as Lantus has a slight peak before plateauing.
Describe Pagets Disease, its features, and management
Also known as osteitis deformans, there is increased bone turnover associated with increased numbers of osteoblasts and osteoclasts with resultant remodelling, bone enlargement, deformity and weakness. Rarely occurs under 40yrs. Commonor in Anglo-saxons. Osteosarcoma is 30 times more common in these patients.
Features: Asymptomatic in 70%, deep, boring pain, bony Deformity and enlargement. Pathological fracture, osteoarthritis may develop, nerve compression from overgrowth. Radiographs show enlargement of bone with patchy coarsening of the trabeculae pattern. Calcium and phosphate often normal ALP is raised.
Management: Analagesia + Alendronate
Describe Acute Charcot, its features, investigations and management
Neuropathic joint caused by loss of sensation in the joint and foot so that it becomes damaged and disrupted. Most common cause is diabetic neuropathy.
Features: Acute redness, warmth, swelling of deformity most commonly pes planus in foot.
Investigations: X-ray may show considerable disruption but in early disease may not show any changes. MRI is needed to differentiate osteomyelitis.
Management:
- take weight off foot
- referral to diabetic foot clinic
- immobilise in cast for 3-6 months
