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Describe the enzymes commonly measured in LFTs
- ALT: Found in hepatocytes and leaks in acute liver damage
- AST: Found in RBCs, muscle and hepatocytes - also used as a cardiac marker
- ALP: Lines biliary ducts- rises in cholestasis, bile duct obstruction and Paget's (found in bone)
- gGT: Found in liver- shows cholestatic damage and even sub-clinical liver dysfunction. Especially used in chronic alcohol toxicity
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What are the three zones of the adrenal cortex, and what do they produce?
- Z. Glomerulosa: Mineralocorticoids, especially aldosterone
- Z. Fasciculata: Glucocorticoids, especially cortisol
- Z. Reticularis: Precursor androgens in women/children
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Outline investigations of glucocorticoid production
- Basal levels: ACTH and cortisol measured
- Suppression: Dexamethasone given = CRH inhibition = Cortisol inhibition unless uncontrolled (e.g. Cushing's)
- Stimulation: Synacthen given = cortisol production unless destruction
- Imaging
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Outline investigations of mineralocorticoid production
- Basal levels: Aldosterone-renin ratio
- Suppression: Saline/fludrocortisone given = aldosterone suppression
- U+Es for hypokalaemia
- Urinalysis for excess excretion despite hypokalaemia
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Outline investigations of catecholamine production
- Urinary catecholamines: 4hr collection to exclude excess
- Resting plasma catecholamines
- Imaging
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Outline causes of adrenal insufficiency
- Primary: Addison's
- Secondary: Long term steroid therapy = endogenous supperssion. H-P dysfunction.
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Outline the pathogenesis, pathophysiology and complications of Addison's
- Pathogenesis: Destruction of adrenal cortex (e.g. AI or tb)
- Pathophysiology: Reduced mineralo/glucocorticoid and androgen production
- Complications: 'Addisonian crisis'; Hypoglycaemia, hypotension, hyponaetremia, hyperkalaemia, dehydration.
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Outline some major adverse effects of steroid therapy
- Adrenal/pituitary suppression
- Hypertension
- Psychosis
- Hyperglycaemia/diabetes/weight gain
- Infection (with absent clinical features)
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What are the main causes of hyperaldosteronism?
- Adrenal adenoma in zona glomerulosa (Conn's)
- Ideopathic
- Excessive renin production
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Outline the pathogenesis and pathophysiology of Cushing's syndrome
- Pathogenesis: Increase in circulating ACTH (Cushing's disease) due to adenoma (usually pituitary). Or zona fasciculata adenoma
- Pathophysiology: Hypertension, obesity, MI, infection and HF
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How are the causes of Cushing's syndrome managed?
- Cushing's disease: Surgery or pitiuitary irradiation
- Cortisol-inhibitors given prior to therapy
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What is a pheochromocytoma, and what does it cause?
- Tumour of the sympathetic nervous system, usually in the adrenals.
- Releases noadrenaline and adrenaline
- Causes anxiety, hypertension, tachycardia, glycosuria, and any related damage
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What are the criteria for diagnosing diabetes?
- Symptoms + random plasma glucose >11.1mmol/L
- Fasting plasma glucose >7mmol/L
- 2 hour post oral glucose tolerance >11.1mmol/l
- HbA1c >6.5%
- Confirmed on repeat testing
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Outline the pathophysiological mechanisms of diabetes
- Hyperglycaemia
- Microvascular complications
- Cardiovascular disease
- Acute decompensation (hyperosmolality, hyperglycaemia)
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What are the criteria for diagnosing metabolic syndrome?
- 3/5 of:
- Increased wast circumference
- Increased triglycerides
- Reduced HDL cholesterol
- Increased blood pressure
- Elevated fasting glucose
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What is the main cause of morbidities seen in chronic diabetes?
- Microangiopathy is the cause of most complications in chronic diabetes
- High plasma glucose causes increased endothelial intake of glucose
- Glycoprotein formation occurs, thickening and weakening the basement membrane
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What changes occur in diabetic nephropathy?
- Nephrotic syndrome and glomerulosclerosis
- Glomerular fibrosis filtration membrane disruption and protein leakage (proteinuria)
- Reduced filtration also leads to hypertension, oedema and reduced plasma oncotic pressure
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What is the cause of diabetic retinopathy?
- Microangiopathy in the retina cause pericyte and endothelial cell damage
- Blood-retinal barrier becomes permeable, while reducing blood supply
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Why are macrovascular changes seen in diabetes?
- High blood sugar causes production of advanced glycation end products
- Leads to inflammation and free radical production, endothelial damage and lipid deposition
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How is diabetic ketoacidosis acutely managed?
- IV fluids; isotonic NaCL/lactated ringer's
- IV/IM short acting insulin
- IV KCl
- NaCO3 (given if severe acidosis + hypokalaemia treated)
- Underlying disease treatment
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Outline the long term management of type 2 diabetes
- Lifestyle
- Intensive hypertension treatment
- Intensive dyslipidaemia treatment
- Intensive glycaemia treatment
- Antiplatelets if appropriate
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Describe the 'basal' insulin regimen
- Mimics insulin release when controlling blood glucose during fasting
- Given at bedtime
- Intermediate/long acting insulin also prescribed
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Describe the 'biphasic' insulin regimen
- Aims to provide fasting and post-prandial coverage
- Given before breakfast and dinner
- Requires a routine lifestyle and snacking
- Glucose control not optimal
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Describe the 'basal bolus' insulin regimen
- Aims to mimim insulin release as closely as possible
- Basal insulin with a short acting given before meals
- Requires multiple injections with snacking
- Very flexible
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Describe 'insulin pump' therapy
- Continuous subcutaneous insulin infusion
- Has an adjustable basal rate given by an in vivo catheter
- Can be programmed for nocturnal/early morning glucose changes
- Useful for unpredictable livestyles and recurrent hyperglycaemia
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What is the mechanism of action of metformin?
- Potentiates any residual insulin
- Increases glucose uptake by skeletal muscle, inhibits gluconeogenesis and GI absorption
- Also causes anorexia and weight loss
- Risk of lactic acidosis
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What is the mechanism of action of thiazolidinediones?
- Bind to a nuclear receptor in adipose and skeletal muscle cells
- Increase insulin receptor expression
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What is the mechanism of action of sulphonylureas?
- Activate a nuclear receptor in pancreatic beta cells
- Reduce ATP sensitivity = increase insulin secretion
- Can cause hypoglcaemia, increased appetite and weight gain
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Why is insulin used in T2DM?
- Given when there is a high risk of CVD as well as a HbA1c >7%
- Controls post-prandial hyperglycaemia
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What investigations are useful in Conn's syndrome?
- Biochemistry: hypokalaemia/hyponaetremia/elevated aldosterone:renin ratio
- Urinalysis: >30mmol potassium with hypokalaemia
- Imaging: CT/MRI to localise adenoma
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What are the clinical features of Addison's disease?
- Hyperpigmentation (increased ACTH production)
- Postural hypertension
- Anorexia/wasting
- Low SBP
- Hyponaetremia/hypokalaemia
- General symptoms (malaise, weakness etc)
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How is Addison's disease managed?
- Hydrocortisone
- Prednisolone
- Fludrocortisone
- Treatment of underlying condition (stop steroid medication, AI etc)
- Steroid warning bracelet
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What is the pathogenesis and pathophysiology of acromegaly and gigantism?
- GH excess causes gigantism (before epiphyseal fusion) and acromegaly
- Almost always due to pituitary tumour = increased GH and IGF-1
- Soft tissue growth, arthropathy and sweat/sebaceous hypertrophy
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Outline some clinical features of acromegaly
- Weight gain and limb size increase
- Thick oily skin
- Hyperhydrosis
- Interdental separation/macroglossia
- Hirsutism
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What investigations are useful in acromegaly?
- Serum GH: if normal, acromegaly excluded
- Serum IGF-1: Always raised in acromegaly
- Glucose tolerance: glucose suppresses GH release
- Diagnostic imaging
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How can acromegaly be managed?
- Surgery/radiotherapy of adenoma
- Dopamine agonists; lower serum GH
- Octreotide; somatostatin analogue
- Pegvisomant; competitive GH receptor antagonist
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Describe the appearance of the adrenals on imaging, including if an adenoma present
- Upside down Y in transverse/coronal imaging
- Low density unless IV contrast used, due to lipid content
- Adenomas have greater lipid content, giving them a lower density (most incidentalomas)
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Describe the appearance of the pituitary on imaging
- Central structure, with infundibulum attaching it to hypothalamus
- Sits in pituitary sella
- Found next to optic chiasm
- Calcification occurs with aging
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Briefly outline the production of T3 and T4
- I- taken up from blood via Na/I symporter
- I- excreted into colloid
- Thyroglobulin produced by ER and transported into colloid (very large molecule)
- Tyrosines on thyroglobulin oxidised, then iodinised, then T1 and T2 attachements conjugate.
- Whole molecule endocytosed into thyrocyte and proteolysed, creating T3 and T4, then excreted
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What investigations are useful when assessing thyroid function?
- 123I can be used to show iodine intake and thyroid activity
- Plasma TSH
- Free thyroxine and total thyroxine (99% of thyroxine protein bound)
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Outline some common features of hyperthyroidism
- Weight loss
- Bone thining
- Tachycardia/arrhythmia
- Amenorrhea
- Tremor
- Sore eyes
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What investigations can detect hyperthyroidism and hypothyroidism?
- Hyperthyroidism: Low TSH, TSH receptor antibody (Grave's), Thyroid peroxisomal antibody
- Hypothyroidism: Thyroid peroxisomal antibody (again), high TSH, low free T4
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Outline some causes of hyperthyroidism
- Thyroiditis: Destruction causes release and so high levels, then deficit
- Grave's
- Thyroid adenoma
- Pituitary adenoma
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Outline some clinical features of hypothyroidism
- Weight gain
- Heavy periods
- Peripheral oedema
- Hair loss
- Bradycardia
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How does amidarone cause thyroid disease?
- Amidarone an anti-arrhythmic with a high iodone content
- High iodine exposure causes 'Woll-chaikoff' effect, reducing thyroid iodine intake after large exposures
- Type 1: Autoimmune thyrotoxicosis
- Type 2: Destructive thyroiditis
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