Note & Notes for MRCP part 1 & 2

The main Sources of this Notes & Notes......Page 4 CNS anatomy......Page 7 Foramina of the skull......Page 8 Brain lesions......Page 9 Transient ischaemic attack (TIA)......Page 12 __________________________________________________________________Stroke by anatomy......Page 15 __________________________________________________________________Lateral medullary syndrome......Page 16  Most anterior artery communicating aneurysms are asymptomatic unless they rupture, and so they are usually found either incidentally or when a patient presents with SAH.......Page 17 __________________________________________________________________Stroke: assessment......Page 18 ________________________________________________________________________________......Page 21 Cerebral venous thrombosis (CVT)......Page 26 ________________________________________________________________________________......Page 30 Vertebral artery dissection......Page 34 ____________________________________________________________......Page 35 Pupil conditions......Page 36 Visual field defects......Page 39 ____________________________________________________________________________......Page 40  visual agnosia, and docility.......Page 41  petrous osteitis (Gradenigo syndrome)......Page 42  Sensation over the face is supplied by the trigeminal nerve......Page 43 abducens (VIth) nerve palsy......Page 44 Facial (VII) nerve......Page 45 Acoustic neuroma......Page 46 Holmes tremor......Page 47 ___________________________________________________________......Page 48 Hemiballism......Page 49 Epilepsy classification......Page 50 Epilepsy: treatment......Page 51 ________________________________________________________________________________......Page 52 Status epilepticus......Page 53 Epilepsy: pregnancy and breast feeding......Page 56 Pseudoseizures......Page 57 _________________________________________________________________________________________......Page 58 Trigeminal autonomic cephalalgias (TAC)......Page 59 Cluster headache......Page 60 Migraine......Page 61 Migraine: management......Page 62 Triptans......Page 63 Idiopathic intracranial hypertension(IIH)......Page 64 Medication overuse headache......Page 65 Parkinson's disease......Page 66 Diagnosis......Page 68  First-line treatment:......Page 69 Parkinson's medication......Page 71 Progressive supranuclear palsy......Page 73 Normal pressure hydrocephalus (NPH)......Page 74 Common causes of dementia......Page 75 Alzheimer's disease......Page 79 Lewy body dementia......Page 80 Frontotemporal lobar degeneration......Page 81 Creutzfeldt-Jakob disease (CJD)......Page 82 ____________________________________________________________......Page 84 _____________________________________________________________Restless legs syndrome......Page 85 _____________________________________________________________Essential tremor......Page 86 Friedreich's ataxia......Page 87 ___________________________________________________________......Page 88 ____________________________________________________________......Page 90 Subdural haemorrhage......Page 93 Subarachnoid haemorrhage (SAH)......Page 94 __________________________________________________________________......Page 96 _____________________________________________________________......Page 97 Herpes simplex encephalitis......Page 98 HIV: neurocomplications......Page 99 ____________________________________________________________......Page 102 Types......Page 103 Features......Page 104 ____________________________________________________________......Page 105 ____________________________________________________________......Page 106 ____________________________________________________________......Page 107 Multiple sclerosis (MS)......Page 108 Management......Page 109 Internuclear ophthalmoplegia (INO)......Page 110  Visual acuity is affected in 95% of patients, but the deficit is usually mild.......Page 111 _____________________________________________________________Horner's syndrome......Page 112 Myasthenia gravis (MG)......Page 113 Myasthenia gravis: exacerbating factors......Page 115 Lambert-Eaton syndrome......Page 116 Neurofibromatosis......Page 117 Tuberous sclerosis (TS)......Page 118 Paraneoplastic syndromes affecting nervous system......Page 119 Brain tumours......Page 120 Cerebrospinal fluid......Page 123 Post-lumbar puncture headache......Page 124 The diagram below shows cross-section view of the spinal cord:......Page 125 Spinal cord compression......Page 126 ____________________________________________________________......Page 128  Sensory loss is most marked in the perianal region.......Page 129 Spastic paraparesis......Page 130  and sexual dysfunction are common but vary in severity.......Page 131 Syringomyelia......Page 132 Arnold-Chiari malformation......Page 134 ____________________________________________________________......Page 135 Lower back pain......Page 137 Wernicke's encephalopathy......Page 138 Reye's syndrome......Page 139 Myotonic dystrophy......Page 140 Facio-scapulo-humeral muscular dystrophy......Page 142 Hypokalaemic periodic paralysis......Page 143 Mental Capacity Act......Page 144 Superficial siderosis......Page 145 Benign paroxysmal positional vertigo......Page 146 Peripheral neuropathy......Page 147 ____________________________________________________________......Page 149 ____________________________________________________________......Page 150 ____________________________________________________________......Page 151 ____________________________________________________________Hereditary sensorimotor neuropathy (HSMN)......Page 152  intravenous immunoglobulins......Page 153 Management......Page 154 Poor prognostic features......Page 155 Meniere's disease......Page 156 Motion sickness......Page 158 Susac syndrome......Page 159 ____________________________________________________________......Page 160 Complex regional pain syndrome (CRPS)......Page 161 ____________________________________________________________......Page 162 ____________________________________________________________......Page 163 _____________________________________________________________......Page 164 Radial nerve......Page 165 Median nerve......Page 166 Carpal tunnel syndrome......Page 167 ____________________________________________________________......Page 168 _____________________________________________________________......Page 169 Common peroneal nerve lesion (L5, S1)......Page 170  weakness of knee extension (quadriceps) and hip flexion (iliopsoas)......Page 171  long saphenous vein stripping for varicose veins.......Page 172 Deep tendon reflexes: which test for which nerve root?......Page 173 Rotator cuff muscles......Page 174 Dermatomes......Page 175 Antidiuretic hormone (ADH) (Vasopressin)......Page 181 Causes of cranial DI......Page 186 Hypopituitarism......Page 191 Growth hormone(GH)......Page 193 Investigations......Page 199 Management......Page 200 Macroglossia: Causes......Page 202  endocrine stimulation tests.......Page 204 Prolactin and galactorrhoea......Page 205  The thyroid hormone receptor is a nuclear receptor.......Page 212  Whenever the levels of calcitonin become high, they down regulate the receptor by rapid and prolonged down regulation of calcitonin receptor messenger RNA.......Page 213 Thyroid disorders: a very basic introduction......Page 214 Hypothyroidism affects around 1-2% of women in the UK and is around 5-10 times more common in females than males.......Page 220  The predominant lipid picture in hypothyroidism is mixed dyslipidaemia ( ↑LDL , ↑ triglycerides )......Page 221 Hypothyroidism: management......Page 224 Hashimoto's thyroiditis......Page 225 ____________________________________________________________Sick euthyroid syndrome......Page 227 Subclinical hypothyroidism......Page 228  Postpartum Patients may continue to breast-feed......Page 230  However, neonatal thyroid function should be checked regularly.......Page 231 Post-partum thyroiditis......Page 232 Subacute (De Quervain's) thyroiditis......Page 233 Subclinical hyperthyroidism......Page 234 Causes......Page 235 Toxic multinodular goitre (TNG) (Plummer's disease)......Page 236 Graves' disease......Page 238 Management......Page 239 ____________________________________________________________Carbimazole......Page 240 Calcium metabolism......Page 253 Hypercalcaemia: causes......Page 255 Hypercalcaemia: management......Page 260 Hypocalcaemia......Page 263 Vitamin D......Page 264 Vitamin D supplementation......Page 265  Two to three times more common in women than men.......Page 269 Hyperparathyroidism: Types......Page 271 Hungry bone syndrome......Page 273 Hypoparathyroidism......Page 274 Adrenal medulla......Page 275 Primary hyperaldosteronism......Page 276 Congenital adrenal hyperplasia (CAH)......Page 281 1. blockade of the mineralocorticoid receptor by spironolactone (2-10 mg/kg/day), combined with thiazides to help to normalize blood pressure and reduce hypercalciuria and nephrocalcinosis.......Page 286 Phaeochromocytoma......Page 287 Investigations......Page 295 Addisonian crisis......Page 296 Corticosteroids......Page 299 Steroid doses equivalence......Page 301 Cushing's syndrome (Hypercortisolism)......Page 302 Investigations......Page 304 Glycaemic index......Page 313 Metabolic syndrome......Page 314 Pre-diabetes and impaired glucose regulation (IGR)......Page 316 Types of diabetes mellitus......Page 318  It is inversely correlated with the risk for diabetes and lower levels are present with worsening levels of insulin resistance in diabetic patients.......Page 324 4. Inability of the kidney to reabsorb water in DCT as in CDI, NDI, drugs and chronic renal failure (CRF).......Page 325 Diabetes mellitus (type 2): diagnosis......Page 326 Glycosylated haemoglobin......Page 328 Diabetes mellitus: management of type 2 (NICE 2015)......Page 330 Metformin......Page 334 Meglitinides(glinides) (e.g. repaglinide, nateglinide)......Page 339 Thiazolidinediones (pioglitazone)......Page 340  is a protein that is cleaved from proinsulin when it is activated.......Page 341  GLUT-4 is the main insulin responsive glucose transporter.......Page 342  Insulin glargine differs from human insulin in that the amino acid asparagine at position A21 is replaced by glycine and two arginines are added to the C-terminus of the B-chain.......Page 344  The guidelines recommend starting with either morning or evening long-acting insulin, or with bedtime intermediate acting insulin.......Page 345 Diabetes mellitus: GLP-1 and the new drugs......Page 349  urine dip sticks will test positive for glucose.......Page 353 ____________________________________________________________ Diabetic ketoacidosis (DKA)......Page 354  Chest X-ray to exclude occult malignancy......Page 360 Hyperosmolar hyperglycaemic state (HHS)......Page 362 Diabetic nephropathy......Page 364  The evidence for a low protein diet exists for overt proteinuria but not microalbuminuria.......Page 366  the most likely cause of blurred vision in a newly diagnosed diabetic who was previously fit and well is ( Osmotic changes in the lens......Page 367 ( New vessels anywhere in the fundus......Page 369  Asymmetric diabetic retinopathy should always raise the suspicion that there is some other cause of ocular ischaemia on the worst-affected side, such as unilateral or asymmetrical carotid artery disease ( do Carotid Doppler......Page 370  Diabetic peripheral neuropathy usually goes in parallel with retinopathy and nephropathy.......Page 371 Diabetic amyotrophy......Page 374 Post prandial pain in diabetics......Page 375 If a patient with type 2 diabetes mellitus does decide to fast:......Page 384  despite the presence of islet antibodies at diagnosis of diabetes, the progression of autoimmune -cell failure is slow.......Page 389 Pregnancy: diabetes mellitus (NICE 2015)......Page 390 Lipids and obesity problems ____________________________________________________________Obesity hormones......Page 392 ____________________________________________________________Obesity: therapeutic options......Page 394  The rate of post operative complications following bariatric surgery is no greater than other elective major abdominal operations......Page 396 WHO/Fredrickson classification:......Page 397  Chylomicronaemia is due to a circulating inhibitor of lipoprotein lipase (type 1c hyperlipidaemia).......Page 398  Heterozygous familial hypercholesterolaemia is one of the most common familial conditions, with a prevalence of about 1 in 500.......Page 399  LDL cholesterol particles that are smaller and more compact (dense) than normal......Page 402 Remnant hyperlipidaemia (type III)......Page 403  the best option to reduce triglyceride is fibrate or omega 3 fatty acids......Page 405  Triglycerides above 1.7 are thought to be associated with around a 30% relative increase in cardiovascular disease events.......Page 407  it lower both cholesterol and triglyceride concentrations by inhibiting synthesis and increases HDL-cholesterol when used in doses of 1.5-3g daily.......Page 408  Direct effects on beta-cell function have also been postulated.......Page 409 Hyperlipidaemia: xanthomata......Page 410 Hyperlipidaemia: management (NICE 2014)......Page 412 mechanism of action and adverse effects......Page 415 Statins......Page 416 Nicotinic acid (niacin )......Page 421 Cholestyramine......Page 422 Pregnancy: physiological changes – endocrine......Page 425 Polycystic ovarian syndrome (PCOS)......Page 429 Diagnostic criteria......Page 430 Management......Page 431 Hirsutism and hypertrichosis......Page 432 Amenorrhoea......Page 434 Criteria for diagnosis (NICE guidelines: November 2015)......Page 435 Definitions of perimenopause and menopause......Page 436 Hormone replacement therapy (HRT)......Page 437  HRT with oestrogen and progestogen can be associated with an increase in the risk of breast cancer and reduces after stopping HRT.......Page 439 ____________________________________________________________......Page 440 Menstrual cycle......Page 443 Multiple endocrine neoplasia......Page 455  occlusion causes posterior MI (ST depression in V1-V4 with a dominant R wave in V1).......Page 464 Pulmonary circulation......Page 465 Jugular venous pulse......Page 466 JVP: cannon waves......Page 467  What is the most likely mechanism that maintains blood flow to the affected extremity?......Page 468 Atrial natriuretic peptide......Page 469 B-type natriuretic peptide......Page 470  The basic muscle unit of the myocardium ( Sarcomere......Page 471 ________________________________________________________________________________......Page 472 Cardiac action potential......Page 473 Heart sounds......Page 474 Murmurs......Page 477 _________________________________________________________________________________________......Page 479 Exercise: physiological changes......Page 481 Exercise tolerance tests......Page 482  Both troponin I and T are highly sensitive and specific for cardiac damage, and are of equal clinical value.......Page 483 ECG: coronary territories......Page 485 ECG: digoxin......Page 486 ECG: left bundle branch block......Page 487 ECG: ST depression......Page 488 ________________________________________________________________________________ Cardiac amyloidosis......Page 489 Cardiac catheterisation and oxygen saturation levels......Page 491 Pulmonary capillary wedge pressure......Page 495 Nuclear imaging......Page 496 Mitral stenosis......Page 497 Mitral regurgitation (MR)......Page 498 Aortic dissection......Page 499  Relatively stable patient ( immediate surgical repair and surgical evacuation of haemopericardium.......Page 502 Prevention......Page 503 Aortic regurgitation (AR)......Page 504 Aortic stenosis......Page 506 Coarctation of the aorta......Page 510 Tricuspid regurgitation......Page 512  Doppler echocardiography is the most accurate method for detecting and quantifying the degree of transvalvar gradient increase and is useful in the follow-up of patients during thrombolysis.......Page 514 Supraventricular tachycardia (SVT )......Page 515 Arrhythmogenic right ventricular cardiomyopathy(ARVC)......Page 517 Treatment......Page 518 Atrial fibrillation: cardioversion......Page 521 Atrial fibrillation: pharmacological cardioversion......Page 523 Atrial flutter......Page 524 Atrial myxoma......Page 525 Complete heart block......Page 527  Generally, permanent pacing can be justified for any degree of heart block associated with symptoms of bradycardia.......Page 528 ________________________________________________________________________________......Page 531 Ventricular tachycardia......Page 532 __________________________________________________________________________________________......Page 536 Long QT syndrome......Page 537 Torsades de pointes (TdP)......Page 539  patients are classified as being stable or unstable according to the presence of any adverse signs:......Page 540 Peri-arrest rhythms: bradycardia......Page 542 Adult advanced life support......Page 543 Wolff-Parkinson White (WPW)......Page 546 Acute pericarditis......Page 548 Pericardial effusion......Page 550 Constrictive pericarditis......Page 551 Diagnosis......Page 552 Management (NICE guidelines 201)......Page 554 Screening criteria for target end organ damage:......Page 556 Malignant hypertension......Page 557 Hypertension: secondary causes......Page 558 Isolated systolic hypertension(ISH)......Page 559 Hypertension in pregnancy (NICE guidance 2010)......Page 560 Eclampsia......Page 561  Increased pulmonary venous pressure......Page 562 Features......Page 563  Functional imaging tests are now reserved for:......Page 564 __________________________________________________________________________________________......Page 565 Drug management......Page 566 __________________________________________________________________________________________......Page 567 ACS referral:......Page 568  Interestingly, NSTEMIs are not associated with this degree of diurnal rhythm.......Page 569 Myocardial infarction: management......Page 570 Percutaneous coronary intervention(PCI)......Page 571 Myocardial infarction: complications......Page 573 Myocardial infarction: secondary prevention......Page 576  Previous myocardial infarction......Page 577 Chest x-ray: pulmonary oedema......Page 579 Heart failure: drug management......Page 580 Hypertrophic obstructive cardiomyopathy (HOCM)......Page 582 Dilated cardiomyopathy (DCM)......Page 586 ________________________________________________________________________________......Page 588 Takotsubo cardiomyopathy......Page 589 Tetralogy of Fallot (TOF)......Page 590 Ventricular septal defects (VSD)......Page 591  Larger ones may lead to signs of right ventricular failure, such as shortness of breath and a parasternal heave.......Page 592 Patent ductus arteriosus......Page 593 Eisenmenger's syndrome......Page 594 Ebstein's anomaly......Page 595 Rheumatic fever: criteria......Page 596 Infective endocarditis (IE)......Page 597 Infective endocarditis: Modified Duke criteria......Page 599 Peripheral signs associated with infective endocarditis......Page 600 ________________________________________________________________________________......Page 602 Myocarditis......Page 603 DVLA: cardiovascular disorders......Page 604 Lymphoedema......Page 605  These contain 80% phosphatidylcholine.......Page 607 Obstructive vs. Restrictive lung diseases......Page 615 Transfer factor (DLCO or TLCO (diffusing capacity or transfer factor of the lung for carbon monoxide (CO))......Page 616  The fact that the pH is normal means that there must be bicarbonate retention to compensate.......Page 621 Respiratory alkalosis......Page 622 Coin lesions on chest x-ray......Page 623 White lung lesions on chest x-ray......Page 624 ______________________________________________________________________________Flow volume loop( Assessing compression of the upper airway......Page 627  If a patient has typical symptoms of asthma, a trial of treatment is recommended.......Page 630 Drugs used in asthma......Page 637 Acute severe asthma......Page 639  The most likely diagnosis would be with spirometry before and after exercise, (NOT before and after administration of bronchodilators) where a typical obstructive pattern may be displayed following exercise.......Page 641 Causes......Page 642  MacLeod syndrome is unilateral emphysema following childhood bronchiolitis.......Page 643  extensor plantar response is common in (COPD) due to carbon dioxide retention, which results in carbon dioxide narcosis.......Page 644  Peripheral oedema may be present as a dependent oedema, as patients with COPD may have limited mobility due to dyspnoea, and therefore does not necessarily indicate heart failure.......Page 645 COPD: stable management......Page 647 Oxygen saturation targets......Page 650 Non-invasive ventilation (NIV)......Page 651  take off the mask to administer nebulisers......Page 652  in Guillain Barre syndrome with respiratory involvement => the parameter used to assess whether a patient needs ventilator support is an FVC 10 %). As peripheral blood eosinophils are not always increased in eosinophilic lung diseases, the other methods (bronchoalveolar lavage [BAL], biopsy) are sometimes needed to document lung.........Page 762 Pulmonary arterial hypertension (PAH)......Page 768  Several studies report a mean survival of only 2.5 years from diagnosis,......Page 770 Respiratory tract infections: NICE guidelines (2008)......Page 771 Sarcoidosis......Page 772 Investigations :......Page 773  Transbronchial lung biopsy will provide positive histology in about 80% of patients, is safe and can be done under sedation with local anaesthesia and is therefore the diagnostic investigation of choice.......Page 774 Management......Page 777  Treatment:......Page 778  For patients who are not responsive to steroids or steroid intolerant then immunosuppressant agents such as methotreaxtae can be tried.......Page 779 Yellow nail syndrome......Page 781 Carbon monoxide poisoning......Page 786 Smoking cessation......Page 788 Acid secretion......Page 792 Gastrointestinal Hormones......Page 793  Gastrin levels above 1,000 are strongly indicative of a gastrinoma.......Page 794 Achalasia......Page 795 ___________________________________________________________Dysphagia......Page 798 ___________________________________________________________Diffuse oesophageal spasm......Page 799 Gastro-oesophageal reflux disease (GORD)......Page 800 ___________________________________________________________Barrett's oesophagus......Page 802 ____________________________________________________________Oesophageal cancer......Page 803  bleeding derived from a source proximal to the ligament of Treitz.......Page 806 ___________________________________________________________Oesophageal varices......Page 809 Helicobacter pylori......Page 811 ___________________________________________________________Zollinger-Ellison syndrome......Page 814 ___________________________________________________________Gastric MALT lymphoma......Page 815 ___________________________________________________________Gastric cancer......Page 816 Dyspepsia......Page 819 ___________________________________________________________Malabsorption......Page 820 Jejunal villous atrophy......Page 821 Management......Page 823 ___________________________________________________________Whipple's disease......Page 824 Diagnosis (NICE 2008)......Page 825 Malnutrition......Page 826 ___________________________________________________________Refeeding syndrome......Page 828 ___________________________________________________________Melanosis coli......Page 829 ___________________________________________________________Mesenteric ischaemia (ischaemic colitis)......Page 830 ___________________________________________________________Spontaneous bacterial peritonitis (SBP)......Page 831 ___________________________________________________________VIPoma......Page 832 Imaging in bowel obstruction......Page 833 Radiology: pneumoperitoneum......Page 834  acute inflammation of the pancreas, results in release of exocrine enzymes that cause auto-digestion.......Page 835 Features......Page 836  often due to sepsis or multiorgan failure.......Page 837 ___________________________________________________________Chronic pancreatitis......Page 840 ___________________________________________________________Pancreatic cancer......Page 841 ___________________________________________________________Gallstones (Cholelithiasis)......Page 842 ___________________________________________________________Post-cholecystectomy syndrome......Page 845 ___________________________________________________________Primary sclerosing cholangitis (PSC)......Page 847 Hepatomegaly......Page 848 ___________________________________________________________Liver biopsy......Page 849 ___________________________________________________________Ascites......Page 850 Features......Page 852  Amenorrhea......Page 853  Patients with cirrhosis are frequently hyponatraemic. This is a function of an inability to excrete free water (increased ADH levels and systemic vasodilation contribute, but the underlying mechanism is complex and not entirely understood).......Page 854 Causes : (Vascular resistance and blood flow are 2 important factors in its development).......Page 855 ___________________________________________________________Hepatic encephalopathy......Page 856  vasoactive mediators cause ( splanchnic vasodilation ( ↓↓ systemic vascular resistance ( 'underfilling' of the kidneys ( activation of the renin-angiotensin-aldosterone system by the juxtaglomerular apparatus ( renal vasoconstriction which is not en.........Page 857 Wilson's disease......Page 858  LFT typically show an AST elevated greater than the ALT with at least a 2:1 ratio......Page 860  It typically presents with a pattern of:......Page 861 ___________________________________________________________Non-alcoholic fatty liver disease......Page 862 ___________________________________________________________Hydatid cysts......Page 863 ___________________________________________________________Drug-induced liver disease......Page 864 ___________________________________________________________Dubin-Johnson syndrome......Page 865  The prognosis with long-term immunosuppression is excellent even in the presence of cirrhosis and few patients subsequently develop liver failure.......Page 866 Obstetric cholestasis......Page 867 ___________________________________________________________......Page 868 Investigation......Page 869 Hepatocellular carcinoma (HCC)......Page 870 ___________________________________________________________......Page 871 ___________________________________________________________Hepatitis B......Page 872 Hepatitis B serology......Page 874 ___________________________________________________________Hepatitis B and pregnancy......Page 876 ___________________________________________________________Hepatitis E......Page 879 Colorectal cancer: genetics......Page 880 Colorectal cancer: screening......Page 881 Colorectal cancer: referral guidelines......Page 882 ___________________________________________________________Peutz-Jeghers syndrome......Page 884 ___________________________________________________________Villous adenoma......Page 885 ___________________________________________________________Carcinoid tumours......Page 886 Risk factors......Page 887 ___________________________________________________________Anal fissure......Page 891 Crohn's disease......Page 892 Investigation......Page 893 Management (NICE 2012)......Page 894 General points......Page 895 ___________________________________________________________Ulcerative colitis (Nice guidelines 2013)......Page 896 Ulcerative colitis: management......Page 897 ___________________________________________________________......Page 898 Inflammatory bowel disease: key differences......Page 899 IBD: histology......Page 900 Pseudopolyps are seen in both ulcerative colitis and Crohn's disease.......Page 901 Gastroenteritis......Page 905 ___________________________________________________________Shigella......Page 907  First-line drugs used against the bacterium include aminoglycosides and trimethoprim-sulfamethoxazole (TMP-SMZ). Other effective drugs include third-generation cephalosporins, tetracyclines (not recommended in children < 8 y), and fluoroquinolones (.........Page 908 ___________________________________________________________Exotoxins and endotoxins......Page 909 ___________________________________________________________Pseudomembranous colitis (Clostridium difficile)......Page 911 ___________________________________________________________Amoebiasis......Page 912 Renal blood flow (RBF)......Page 922 ________________________________________________________......Page 926 Urine pH......Page 927 Causes of transient or spurious non-visible haematuria......Page 929 Acute interstitial nephritis (AIN)......Page 931 Acute kidney injury (AKI) (previously termed acute renal failure or ARF)......Page 932 ______________________________________________________________________________Acute tubular necrosis vs. prerenal uraemia......Page 933 Papillary necrosis......Page 935 Acute vs. chronic renal failure......Page 936 Chronic kidney disease (CKD)......Page 937 eGFR and classification of CKD......Page 938 Chronic kidney disease: hypertension......Page 942 Chronic kidney disease: proteinuria......Page 943 Chronic kidney disease: anaemia......Page 945 Management......Page 946 Calciphylaxis......Page 947 Prescribing in patients with renal failure......Page 949 Erythropoietin......Page 950 Renal replacement therapy......Page 952  Carnitine deficiency......Page 954 Peritoneal dialysis......Page 955 Renal transplant......Page 957 Post-transplant