MRCP Revision Notes

MRCP Revision Notes
Index
Cardiology
01 Angina Pectoris 32 Prosthetic Heart Valves
02 Exercise ECG 33 Infective Endocarditis
03 Myocardial Infarction 34 Rheumatic Fever
04 Post Myocardial Infarction Complications 35 Acute Pericarditis
05 Heart Failure 36 Constrictive Pericarditis
06 B-type Natriuretic Peptide 37 Cardiac Tamponade
07 Hypertrophic Cardiomyopathy 38 Congenital Heart Defects
08 Dilated Cardiomyopathy 39 Tetralogy of Fallots
09 Peripartum Cardiomyopathy 40 Atrial Septal Defect
10 Myocarditis 41 Lutembacher Syndrome
11 Restrictive Cardiomyopathy 42 Patent Foramen Ovale
12 Cardiogenic Pulmonary Edema 43 Ventricular Septal Defect
13 Atrial Fibrillation 44 Patent Ductus Arteriosus
14 Atrial Flutter 45 Eisenmenger Syndrome
15 Long QT Syndrome 46 Coarctation of the Aorta
16 Torsades De Pointes 47 Aortic Dissection
17 Wolff-Parkinson White Syndrome 48 Hypertension
18 Supraventricular Tachycardia 49 Malignant Hypertension
19 Ventricular Tachycardia 50 Hypertensive States of Pregnancy
20 Ventricular Fibrillation 51 Pre-eclampsia
21 Atrioventricular Block 52 Pulmonary Hypertension
22 Arrhythmogenic Right Ventricular 53 Deep Venous Thrombosis
Cardiomyopathy 54 Cholesterol Embolism
23 Brugada Syndrome 55 Vasovagal Syncope
24 Aortic Stenosis 56 Carotid Sinus Hypersensitivity
25 Heyde Syndrome 57 Atrial Myxoma
26 Aortic Regurgitation 58 Septic Shock
27 Bicuspid Aortic Valve 59 Cardiac Action Potential
28 Mitral Stenosis 60 Heart Sounds
29 Mitral Regurgitation 61 Jugular Venous Pulse Waveform
30 Mitral Valve Prolapse 62 Exercise Physiological Changes
31 Tricuspid Regurgitation 63 ECG
Pulmonology
01 Bronchial Asthma 03 Bronchiolitis Obliterans
02 Occupational Asthma 04 COPD
Pass-MRCP.com Page 1
MRCP Revision Notes
05 Alpha-1 Antitrypsin Deficiency 30 Coal Workers' Pneumoconiosis

06 Allergic Bronchopulmonary Aspergillosis 31 Silicosis
07 Aspergilloma 32 Asbestosis
08 Invasive Aspergillosis 33 Hypersensitivity Pneumonitis
09 Bronchiectasis 34 Pulmonary Alveolar Proteinosis
10 Cystic Fibrosis 35 Pulmonary Alveolar Microlithiasis
11 Primary Ciliary Dyskinesia 36 Acute Respiratory Distress Syndrome
12 Yellow Nail Syndrome 37 Pulmonary Embolism
13 Community Acquired Pneumonia 38 Hepatopulmonary Syndrome
14 Bacterial Pneumonia 39 Altitude Illness
15 Mycoplasma Pneumonia 40 Lung Cancer
16 Legionnaires' Disease 41 Small Cell Lung Cancer
17 Aspiration Pneumonia 42 Non-small Cell Lung Cancer
18 Lung Abscess 43 Superior Vena Cava Syndrome
19 Hospital-acquired Pneumonia 44 Pneumothorax
20 Pneumocystis Jiroveci Pneumonia 45 Pleural Effusion
21 Histoplasmosis 46 Familial Mediterranean Fever
22 Nocardiosis 47 Mesothelioma
23 Viral Pneumonia 48 Lymphangioleiomyomatosis
24 Eosinophilic Pneumonia 49 Obstructive Sleep Apnea
25 Loeffler Syndrome 50 Narcolepsy
26 Tuberculosis 51 Respiratory Failure
27 Idiopathic Pulmonary Fibrosis 52 Chest X Ray
28 Sarcoidosis 53 Oxygen Dissociation Curve
29 Pneumoconiosis
Gastroenterology & Hepatology

01 Dyspepsia 16 Chronic Pancreatitis
02 Gastroesophageal Reflux Disease 17 Pancreatic Pseudocyst
03 Achalasia 18 Pancreatic Cancer
04 Pharyngeal Pouch 19 Crohn Disease
05 Esophagitis 20 Ulcerative Colitis
06 Barrett Esophagus 21 Celiac Disease
07 Esophageal Cancer 22 Tropical Sprue
08 Esophageal Varices 23 Bacterial Overgrowth Syndrome
09 Helicobacter Pylori 24 Whipple Disease
10 Peptic Ulcer Disease 25 Irritable Bowel Syndrome
11 Mallory-Weiss Tear 26 Diverticulitis
12 Zollinger-Ellison Syndrome 27 Peutz-Jeghers Syndrome
13 Gastric Cancer 28 Melanosis Coli
14 MALT Lymphoma 29 Angiodysplasia of the Colon
15 Acute Pancreatitis 30 Mesenteric Ischemia
MRCP Revision Notes
31 Hirschsprung Disease 51 Gilbert Syndrome

32 Colorectal Cancer 52 Liver Cirrhosis
33 Gardner Syndrome 53 Ascites
34 Foodborne Illness 54 Spontaneous Bacterial Peritonitis
35 Bacterial Gastroenteritis 55 Budd-Chiari Syndrome
36 Salmonellosis 56 Hepatorenal Syndrome
37 Amebiasis 57 Hepatitis A Infection
38 Giardiasis 58 Hepatitis B Infection
39 Viral Gastroenteritis 59 Hepatitis C Infection
40 Pseudomembranous Colitis 60 Pyogenic Liver Abscess
41 Cryptosporidium 61 Amoebic Liver Abscess
42 Mycobacterium Avium Intracellulare 62 Hydatid Cysts
43 Autoimmune Hepatitis 63 Ascending Cholangitis
44 Primary Biliary Cirrhosis 64 Hepatocellular Carcinoma
45 Primary Sclerosing Cholangitis 65 Cholangiocarcinoma
46 Paracetamol Toxicity 66 Cholelithiasis
47 Drug-Induced Liver Disease 67 Acute Fatty Liver of Pregnancy
48 Hemochromatosis 68 Intrahepatic Cholestasis of Pregnancy
49 Wilson Disease 69 HELLP Syndrome
50 Non-alcoholic Fatty Liver Disease 70 Hyperemesis Gravidarum
Nephrology & Minerals Metabolism

01 Acute Renal Failure 21 Goodpasture Syndrome
02 Acute Tubular Necrosis 22 Renal Artery Stenosis
03 Rhabdomyolysis 23 Acute Pyelonephritis
04 Interstitial Nephritis 24 Xanthogranulomatous Pyelonephritis
05 Contrast Induced Nephropathy 25 Nephrolithiasis
06 Renal Papillary Necrosis 26 Renal Cell Carcinoma
07 Chronic Renal Failure 27 Wilms Tumor
08 Medullary Sponge Kidney 28 Bladder Cancer
09 Polycystic Kidney Disease 29 Benign Prostatic Hyperplasia
10 Nephrotic Syndrome 30 Prostate Cancer
11 Minimal Change Disease 31 Testicular Cancer
12 Membranous Glomerulonephritis 32 Epididymitis
13 Focal Segmental Glomerulosclerosis 33 Testicular Torsion
14 Amyloidosis 34 Cervical Cancer
15 Nephritic Syndrome 35 Bartter Syndrome
16 Diabetic Nephropathy 36 Renal Tubular Acidosis
17 IgA Nephropathy 37 Tumor Lysis Syndrome
18 Poststreptococcal Glomerulonephritis 38 Refeeding Syndrome
19 Mesangiocapillary Glomerulonephritis 39 Hyperkalemia
20 Rapidly Progressive Glomerulonephritis 40 Hypokalemia
MRCP Revision Notes
41 Hyponatremia 47 Metabolic Alkalosis

42 Hypernatremia 48 Respiratory Alkalosis
43 Calcium Metabolism 49 Respiratory Acidosis
44 Hypercalcemia 50 Hypomagnesemia
45 Hypocalcemia 51 Hypophosphatemia
46 Metabolic Acidosis 52 Renal Replacement Therapy
Endocrinology & Diabetes

01 Acromegaly 34 Milk-Alkali Syndrome
02 Growth Hormone Deficiency 35 Hypoparathyroidism
03 Diabetes Insipidus 36 Pseudohypoparathyroidism
04 Syndrome of Inappropriate Antidiuretic 37 Cushing Syndrome
Hormone 38 Pseudo-Cushing Syndrome
05 Hyperprolactinemia 39 Primary Aldosteronism
06 Prolactinoma 40 Addison Disease
07 Pituitary Apoplexy 41 Congenital Adrenal Hyperplasia
08 Sheehan Syndrome 42 Pheochromocytoma
09 Kallmann Syndrome 43 Menstrual Cycle
10 Klinefelter Syndrome 44 Menopause
11 Hyperthyroidism 45 Amenorrhea
12 Thyroid Storm 46 Polycystic Ovarian Syndrome
13 Hypothyroidism 47 Premature Ovarian Failure
14 Myxedema Crisis 48 Androgen Insensitivity Syndrome
15 Graves' Disease 49 Gynecomastia
16 Hashimoto Thyroiditis 50 Multiple Endocrine Neoplasia
17 Postpartum Thyroiditis 51 Polyglandular Autoimmune Syndrome
18 Subacute Thyroiditis 52 Carcinoid Syndrome
19 Toxic Multinodular Goitre 53 Glucagonoma
20 Thyrotoxicosis Factitia 54 Insulinoma
21 Riedel Thyroiditis 55 VIPoma
22 Subclinical Hyperthyroidism 56 Breast Cancer
23 Subclinical Hypothyroidism 57 Ovarian Cancer
24 Euthyroid Sick Syndrome 58 Type 1 Diabetes Mellitus
25 Amiodarone-Induced Thyrotoxicosis 59 Type 2 Diabetes Mellitus
26 Thyroid Cancer 60 Maturity Onset Diabetes of the Young
27 Hyperparathyroidism 61 Gestational Diabetes
28 Primary Hyperparathyroidism 62 Diagnosis of Diabetes Mellitus
29 Secondary Hyperparathyroidism 63 Diabetic Ketoacidosis
30 Tertiary Hyperparathyroidism 64 Hyperosmolar Hyperglycemic State
31 Malignancy-associated Hypercalcemia 65 Familial Hypercholesterolemia
32 Familial Hypocalciuric Hypercalcemia 66 Familial Hypertriglyceridemia
33 Idiopathic Hypercalciuria 67 Hyperlipoproteinemia Type III
MRCP Revision Notes
68 Metabolic Syndrome 70 Anorexia Nervosa

69 Obesity Management 71 Bulimia Nervosa
Hematology & Oncology

01 Iron Deficiency Anemia 28 Factor V Leiden Thrombophilia
02 Anemia of Chronic Disease 29 Protein C Deficiency
03 Thalassemia 30 Essential Thrombocythemia
04 Sickle Cell Anemia 31 Thrombocytopenia
05 Sideroblastic Anemia 32 Acute Myeloid Leukemia
06 Leukoerythroblastic Anemia 33 Acute Promyelocytic Leukemia
07 Pure Red Cell Aplasia 34 Chronic Myeloid Leukemia
08 Megaloblastic Anemia 35 Leukemoid Reaction
09 Polycythemia Vera 36 Acute Lymphoblastic Leukemia
10 Hemolytic Anemia 37 Chronic Lymphocytic Leukemia
11 Autoimmune Hemolytic Anemia 38 Aplastic Anemia
12 Cold Agglutinin Disease 39 Myelodysplastic Syndrome
13 Hereditary Spherocytosis 40 Myelofibrosis
14 Glucose-6-Phosphate Dehydrogenase 41 Hairy Cell Leukemia
Deficiency 42 Hodgkin Lymphoma
15 Paroxysmal Nocturnal Hemoglobinuria 43 Non-Hodgkin Lymphoma
16 Microangiopathic Hemolytic Anemia 44 Burkitt Lymphoma
17 Disseminated Intravascular Coagulation 45 Mantle Cell Lmphoma
18 Hemolytic Uremic Syndrome 46 Multiple Myeloma
19 Thrombotic Thrombocytopenic Purpura 47 Monoclonal Gammopathy of Undetermined
20 Idiopathic Thrombocytopenic Purpura Significance
21 Henoch-Schonlein Purpura 48 Hyperviscosity Syndrome
22 Coagulation Cascade 49 Waldenstrom Macroglobulinemia
23 Hemophilia 50 Cryoglobulinemia
24 Von Willebrand Disease 51 Asplenia
25 Thrombophilia 52 Transfusion Reactions
26 Heparin-Induced Thrombocytopenia 53 Hypereosinophilic Syndrome
27 Antithrombin III Deficiency
Rheumatology & Autoimmune Disorders

01 Rheumatoid Arthritis 09 Raynaud Phenomenon
02 Systemic Lupus Erythematosus 10 Mixed Connective-Tissue Disease
03 Drug-Induced Lupus Erythematosus 11 Rickets
04 Systemic Scleroderma 12 Paget Disease
05 Dermatomyositis and Polymyositis 13 Osteomalacia
06 Polymyalgia Rheumatica 14 Osteoporosis
07 Fibromyalgia 15 Corticosteroid Induced Osteoporosis
08 Sjogren Syndrome 16 Still Disease
MRCP Revision Notes
17 Osteoarthritis 30 Reactive Arthritis

18 Gout 31 Ankylosing Spondylitis
19 Pseudogout 32 Psoriatic Arthritis
20 Septic Arthritis 33 Wegener Granulomatosis
21 Osteomyelitis 34 Microscopic Polyangiitis
22 Relapsing Polychondritis 35 Churg-Strauss Syndrome
23 Elbow Pain 36 Polyarteritis Nodosa
24 De Quervain Tenosynovitis 37 Behcet Disease
25 Adhesive Capsulitis 38 Giant Cell Arteritis
26 Supraspinatus Tendonitis 39 Takayasu Arteritis
27 Avascular Necrosis 40 Kawasaki Disease
28 Baker Cyst 41 Antiphospholipid Syndrome
29 Charcot Arthropathy
Neurology
01 Alzheimer Disease 28 Motor Neuron Disease
02 Lewy Bodies Dementia 29 Multifocal Motor Neuropathy
03 Pick Disease 30 Myasthenia Gravis
04 AIDS Dementia Complex 31 Lambert-Eaton Myasthenic Syndrome
05 Transient Global Amnesia 32 Myotonic Dystrophy
06 Normal Pressure Hydrocephalus 33 Hereditary Spastic Paraplegia
07 Parkinson Disease 34 Neuroleptic Malignant Syndrome
08 Multiple System Atrophy 35 Botulism
09 Progressive Supranuclear Palsy 36 Inclusion Body Myositis
10 Progressive Multifocal Leukoencephalopathy 37 Acid Maltase Deficiency
11 Tremors 38 Critical Illness Myopathy
12 Essential Tremor 39 Central Pontine Myelinolysis
13 Creutzfeldt-Jakob Disease 40 Hypokalemic Periodic Paralysis
14 Chorea 41 McArdle Syndrome
15 Huntington Disease 42 Becker Muscular Dystrophy
16 Dystonia 43 Mitochondrial Myopathies
17 Oculogyric Crisis 44 Locked-in Syndrome
18 Tourette Syndrome 45 Cerebrovascular Accident
19 Friedreich Ataxia 46 Glasgow Coma Scale
20 Ataxia Telangiectasia 47 Intracranial Hemorrhage
21 Wernicke Encephalopathy 48 Cerebral Infarction
22 Epilepsy 49 Localization of Brain Lesion
23 Hemiballismus 50 Aphasia
24 Restless Legs Syndrome 51 Localization of Cerebral Stroke
25 Multiple Sclerosis 52 Lacunar Stroke
26 Guillain-Barre Syndrome 53 Transient Ischemic Attack
27 Miller Fisher Syndrome 54 Lateral Medullary Syndrome
MRCP Revision Notes
55 Basilar Artery Occlusion 92 Ptosis

56 Vertebral Artery Dissection 93 Horner Syndrome
57 Pontine Hemorrhage 94 Nystagmus
58 Lateral Pontine Syndrome 95 Migraine
59 Cavernous Sinus Thrombosis 96 Tension type Headache
60 Cerebral Venous Thrombosis 97 Cluster Headache
61 Carotid Artery Dissection 98 Chronic Paroxysmal Hemicrania
62 Carotid Artery Stenosis 99 Medication Overuse Headache
63 CADASIL Syndrome 100 Trigeminal Neuralgia
64 Idiopathic Intracranial Hypertension 101 Post Lumbar Puncture Headache
65 CSF Analysis 102 Anterior Spinal Artery Syndrome
66 Meningitis 103 Brown-Sequard Syndrome
67 Neisseria Meningitidis 104 Subacute Combined Degeneration of Spinal
68 Listeria Monocytogenes Cord
69 Herpes Simplex Encephalitis 105 Transverse Myelitis
70 Cerebral Abscess 106 Arnold-Chiari Malformation
71 Cryptococcus Meningitis 107 Syringomyelia
72 Facial Nerve Paralysis 108 Phrenic Nerve Palsy
73 Bell Palsy 109 Cervical Spondylosis
74 Ramsay Hunt Syndrome 110 Cervical Disc Prolapse
75 Rinne and Weber Test 111 Traumatic Brachial Plexopathy
76 Vertigo 112 Brachial Neuritis
77 Benign Paroxysmal Positional Vertigo 113 Carpal Tunnel Syndrome
78 Meniere Disease 114 Radial Nerve Palsy
79 Acoustic Neuroma 115 Ulnar Nerve Palsy
80 Glomus Jugulare Tumor 116 Lumbar Disc Prolapse
81 Craniopharyngioma 117 Metastatic Spinal Cord Compression
82 Optic Neuritis 118 Cauda Equina Syndrome
83 Miosis and Mydriasis 119 Lumbar Spinal Stenosis
84 Argyll Robertson Pupils 120 Femoral Nerve Palsy
85 Adie Syndrome 121 Meralgia Paresthetica
86 Oculomotor Nerve Palsy 122 Sciatic Nerve Palsy
87 Trochlear Nerve Palsy 123 Peripheral Neuropathy
88 Abducens Nerve Palsy 124 Alcoholic Neuropathy
89 Internuclear Ophthalmoplegia 125 Diabetic Neuropathy
90 Posterior Communicating Artery Aneurysm 126 Charcot Marie Tooth Disease
91 Visual Field Defects
Ophthalmology
01 Retinal Vein Occlusion 04 Diabetic Retinopathy
02 Retinal Artery Occlusion 05 Age-Related Macular Degeneration
03 Hypertensive Retinopathy 06 Retinitis Pigmentosa
MRCP Revision Notes
07 Cataract 11 Herpes Simplex Keratitis

08 Ectopia Lentis 12 Trachoma
09 Uveitis 13 Glaucoma
10 Conjunctivitis 14 Retinoblastoma
Psychiatry
01 Depression 08 Post-traumatic Stress Disorder
02 Schizophrenia 09 Chronic Fatigue Syndrome
03 Delirium 10 Generalized Anxiety Disorder
04 Bipolar Disorder 11 Phobic Disorders
05 Postpartum Psychiatric Disorders 12 Somatoform Disorders
06 Electroconvulsive Therapy 13 Obsessive-Compulsive Disorder
07 Panic Disorder 14 Personality Disorders
Infectious Diseases
01 Streptococcus 26 Chickenpox
02 Staphylococcus Aureus 27 In Utero VZV Infection
03 Toxic shock Syndrome 28 Herpes Zoster
04 Gonorrhea 29 Infectious Mononucleosis
05 Chlamydial Genitourinary Infections 30 Cytomegalovirus
06 Diphtheria 31 Parvovirus B19 Infection
07 Leprosy 32 Measles
08 Syphilis 33 Mumps
09 Jarisch-Herxheimer Reaction 34 Dengue Fever
10 Yaws 35 Ebola
11 Tetanus 36 HIV
12 Anthrax 37 Human Papillomavirus
13 Psittacosis 38 Toxoplasmosis
14 Leptospirosis 39 Malaria
15 Brucellosis 40 Schistosomiasis
16 Q Fever 41 Cutaneous Larva Migrans
17 Rabies 42 Strongyloides Stercoralis
18 Cat Scratch Disease 43 Visceral Larva Migrans
19 Typhus 44 Filariasis
20 Lyme Disease 45 Cysticercosis
21 Leishmaniasis 46 Candidiasis
22 African Trypanosomiasis 47 Vaginal Discharge
23 Chagas Disease 48 Vaccines
24 Herpes Simplex Virus 49 Reye Syndrome
25 Acute Herpetic Gingivostomatitis
MRCP Revision Notes
Dermatology & Allergic Disorders

01 Anaphylaxis 36 Granuloma Annulare
02 Hereditary Angioedema 37 Oral Hairy Leukoplakia
03 Contact Dermatitis 38 Dermatitis Herpetiformis
04 Urticaria 39 Pemphigus Vulgaris
05 Atopic Dermatitis 40 Bullous Pemphigoid
06 Eczema Herpeticum 41 Pemphigoid Gestationis
07 Pompholyx 42 Polymorphic Eruption of Pregnancy
08 Erythroderma 43 Erythema Multiforme
09 Erysipelas 44 Stevens-Johnson Syndrome
10 Cellulitis 45 Toxic Epidermal Necrolysis
11 Necrotizing Fasciitis 46 Drug-Induced Hypersensitivity Syndrome
12 Gangrene 47 Porphyria Cutanea Tarda
13 Impetigo 48 Erythema Nodosum
14 Herpes Labialis 49 Pyoderma Gangrenosum
15 Vitiligo 50 Necrobiosis Lipoidica
16 Pityriasis Versicolor 51 Pretibial Myxedema
17 Pityriasis Rosea 52 Livedo Reticularis
18 Acne Vulgaris 53 Malignant Melanoma
19 Rosacea 54 Cutaneous Squamous Cell Carcinoma
20 Seborrheic Dermatitis 55 Keratoacanthoma
21 Hypertrichosis 56 Actinic Keratosis
22 Alopecia 57 Cutaneous Basal Cell Carcinoma
23 Alopecia Areata 58 Kaposi Sarcoma
24 Tinea Capitis 59 Keloids
25 Tinea Corporis 60 Genital Herpes
26 Tinea Cruris 61 Genital Ulcers
27 Lichen Planus 62 Vascular Ulcers
28 Lichen Sclerosus 63 Hyperhidrosis
29 Discoid Lupus Erythematosus 64 Onycholysis
30 Psoriasis 65 Onychomycosis
31 Scabies 66 Koebner Phenomenon
32 Acanthosis Nigricans 67 Phototoxicity
33 Morphea 68 Gingival Hyperplasia
34 Erythema Ab Igne 69 Diabetic Foot
35 Erythema Gyratum Repens
Pharmacology & Toxicology

01 Pharmacokinetics 04 Digoxin
02 Drug Metabolism 05 Adenosine
03 Cytochrome p450 06 Amiodarone
MRCP Revision Notes
07 Flecainide 40 Dopamine Agonists

08 ACE Inhibitors 41 Benzodiazepines
09 Diuretics 42 Phenytoin
10 Calcium Channel Blockers 43 Triptans
11 B-Blockers 44 Botulinum Toxin
12 B-Agonists 45 Selective Serotonin Reuptake Inhibitors
13 Alpha Blockers 46 Serotonin Syndrome
14 Smoking Cessation 47 Tricyclic Anti-Depressants
15 Theophylline 48 St John’s Wort
16 Sildenafil 49 Antipsychotics
17 Antiemetics 50 Lithium
18 Octreotide 51 Palliative Care Prescribing
19 Metformin 52 Antibiotics
20 Sulfonylurea 53 Penicillin
21 Thiazolidinediones 54 Quinolones
22 Exenatide 55 Antituberculous Drugs
23 Dipeptidyl Peptidase-4 Inhibitors 56 Antiviral Drugs
24 Types of Insulin 57 Anti-retroviral Drugs
25 Cholesterol Lowering Drugs 58 Isotretinoin
26 Breastfeeding Contraindications 59 Alcohol Withdrawal Syndrome
27 Corticosteroids 60 Opioid Toxicity
28 Oral Contraceptive Pills 61 Cocaine Toxicity
29 Hormone Replacement Therapy 62 MDMA Toxicity
30 Selective Estrogen-receptor Modulator 63 Organophosphate Toxicity
31 Salicylate Toxicity 64 Ethylene Glycol Toxicity
32 Heparin 65 Carbon Monoxide Poisoning
33 Warfarin 66 Methemoglobinemia
34 Iron Tablets Toxicity 67 Cyanide Poisoning
35 Allopurinol 68 Lead Poisoning
36 Bisphosphonates 69 Zinc Deficiency
37 Methotrexate 70 Scurvy
38 Cytotoxics and DMARDs 01 71 Pellagra
39 Monoclonal Antibodies
Genetics & Hereditary Disorders

01 Patterns of Inheritance 08 Ehlers-Danlos Syndrome
02 Neurofibromatosis 09 Fabry Disease
03 Tuberous Sclerosis 10 Fragile X Syndrome
04 Acute Intermittent Porphyria 11 Galactosemia
05 Alport Syndrome 12 Hereditary Hemorrhagic Telangiectasia
06 Cystinuria 13 Homocystinuria
07 Down Syndrome 14 Lesch-Nyhan Syndrome
MRCP Revision Notes
15 Marfan Syndrome 19 Refsum Disease

16 McCune-Albright Syndrome 20 Turner Syndrome
17 Phenylketonuria 21 Von Hippel-Lindau Disease
18 Pseudoxanthoma Elasticum 22 Wiskott-Aldrich Syndrome
Basic Sciences & Statistics

01 Human Leukocyte Antigen 13 Inflammatory Mediators
02 Hypersensitivity Reactions 14 Layers of the Skin
03 Immunoglobulins 15 Foramina of the Skull
04 Antineutrophil cytoplasmic antibodies (ANCA) 16 Renal Anatomy
05 Primary Immunodeficiency 17 Relative Risk
06 Inflammatory Markers 18 Incidence and Prevalence
07 Rheumatoid Factor 19 Sensitivity and Specificity
08 Alkaline Phosphatase 20 Study Design
09 Atrial Natriuretic Peptide 21 Fitness to Fly
10 Nitric Oxide 22 Driver and Vehicle Licensing Agency Rules
11 Endothelin (DVLA)
12 Interferons
MRCP Revision Notes
Cardiology
Angina Pectoris
Angina pectoris is the sensation of chest pain due to ischemia of the heart muscle from obstruction or spasm of the
coronary arteries.
Features of pain:
 Chest discomfort rather than actual pain located in the epigastrium, back, neck area, jaw, or shoulders
 The pain is precipitated by physical activities (running, walking), cold weather, heavy meals, and emotional stress
 No autonomic symptoms as diaphoresis
 Lasts less than 15 minutes
 Relieved by rest or sublingual nitroglycerin within about 5 minutes
Diagnosis of stable angina is unlikely if the chest pain is:

 Continuous  Brought on by breathing in
 Very prolonged  Associated with symptoms such as dizziness,
 Unrelated to activity palpitations, tingling or difficulty swallowing
Diagnosis
 ECG is normal during episodes and will show more than 1 mm ST depression
 Troponin will be less than 0.03, Levels > 0.03 are indicative of unstable angina
 An exercise ECG may be used to confirm the chest pain is caused by myocardial ischemia
 MPS (Myocardial perfusion scintigraphy) with SPECT (Single photon emission computed tomography), CT coronary
angiography or stress echocardiography are non-invasive functional testing
 Coronary angiogram second-line investigation when the results of non-invasive functional imaging are inconclusive
Management
Providing immediate relief

 Relief of symptoms by short-acting nitrate as sublingual nitroglycerin
 Dose is to be repeated the after 5 minutes if the pain has not been relieved
 Call an emergency ambulance if the pain has not been relieved 5 minutes after taking a second dose
MRCP Revision Notes
Anti-anginal drug treatment

 B-blocker or a calcium channel blocker as first-line treatment for stable angina. Decide which drug to use based on
comorbidities, contraindications (asthma in B-blockers and headache and heart failure in calcium channel blocker)
and the person's preference
 If the person's symptoms are not satisfactorily controlled on a B-blocker or a calcium channel blocker, consider
either switching to the other option or using a combination of the 2
 Alternatives for B-blocker or a calcium channel blocker are long-acting nitrate, ivabradine, nicorandil and ranolazine
Revascularization options
CABG (Coronary artery bypass graft) and PCI (Percutaneous coronary intervention) are considered for patients with
stable angina whose symptoms are not satisfactorily controlled with optimal medical treatment.
CABG is indicated over PCI for people with multi-vessel disease whose symptoms are not satisfactorily controlled with
optimal medical treatment and who:
 Have diabetes
 Are over 65 years
 Have anatomically complex 3-vessel disease with or without involvement of the left main stem
Secondary prevention of cardiovascular disease

 Aspirin 75 mg daily
 ACE inhibitors for people with stable angina and diabetes
 Statin cardiovascular disease prevention
Unstable Angina
Unstable Angina differs from stable angina by:
 The pain is prolonged, at rest, frequent, poor  Troponin level > 0.03 but less than 0.1
response to nitrates.  Angiography will show fixed lesion (atheromatous
 ECG findings are more prominent plaque)
Unstable angina and NSTEMI are often indistinguishable; they are considered the same management in the 2014
guidelines.
Prinzmetal angina
Pure vasospastic angina i.e. in the presence of angiographically normal coronary arteries, it occurs in young age with on
risk factors and not related to exertion.
Diagnosis is done by provocative test and ECG monitoring. Management is by nitrates and calcium channel blockers.
MRCP Revision Notes
Exercise ECG
Exercise testing is noninvasive procedure for evaluating for inducible ischemia in the patient with angina. Exercise
testing can be done on a motorized treadmill or with a bicycle ergometer.
Bruce protocol is an exercise protocol in which the treadmill speed increases every 3 minutes until limited by symptoms
with ECG should be monitored continuously.
The test is positive in:

 ST segments depression  Inadequate blood pressure response
 Development of angina symptoms  Inadequate heart rate response
 Ventricular arrhythmias
Indications of referral to coronary angiography (severe cases with poor prognosis):

 ST-segment depression >2 mm at low workloads (< 6 minutes on the Bruce protocol)
 Heart rates response < 70% of age-predicted maximum
 Hypotension
Myocardial Infarction
Myocardial infarction (MI) (heart attack) is the irreversible necrosis of heart muscle secondary to prolonged ischemia.
Pain of MI differs from angina pain in:

 Prolonged (>30 min)  At rest
 Gradual  Not relieved by nitrates
 More sever  Associated with autonomic symptoms
Diagnosis
Diagnosis of MI can be made on the basis of the first two criteria
 History of ischemic discomfort  Rise and fall in serum cardiac markers

 Evolutionary ECG changes
ECG
ECG must show new ST elevation (greater than 2 mm) in two or more adjacent ECG leads. The evolution of new Q waves
is diagnostic.
Coronary territories on ECG

 Left anterior descending artery obstruction causes anteroseptal MI in V1-V4
MRCP Revision Notes
 Right coronary artery obstruction causes inferior wall MI in II, III, aVF
 Left anterior descending or left circumflex artery obstruction cause anterolateral MI in V4-6, I, aVL
MRCP Revision Notes
 Left circumflex artery obstruction causes lateral wall MI in I, aVL +/- V5-6
 Posterior MI occurs with inferior or lateral wall MI, it is presented by ST depression in V1 to V3 with upright T waves
and dominant R waves
Cardiac enzymes
Troponin
Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-
14 days. Level above 0.1 ng/ml indicates a myocardial infarction.
MRCP Revision Notes
Creatine Kinase
CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to
baseline after 48-72 hours, so it is a good indicator of reinfarction. Sensitivity and specificity are not as high as they are
for troponin levels.
Myoglobin
Myoglobin levels are highly sensitive but not specific. Urine myoglobin levels rise within 1-4 hours from the onset of
chest pain.
Acute management (NICE guidelines 2013)

Initial management includes:
 Aspirin and clopidogrel  Subcutaneous low-molecular-weight heparin

 Intravenous B-blocker  Repeated doses of sublingual GTN
 Intravenous morphine
Anticoagulations used in MI
 Clopidogrel is an ADP receptor antagonist
 Glycoprotein IIb/IIIa receptor antagonist (abciximab, tirofiban)
 Fondaparinux is antithrombin III activator
 Dipyridamole is an antiplatelet (phosphodiesterase inhibitor) mainly used in combination with aspirin
 Bivalirudin is a reversible direct thrombin inhibitor
Reperfusion therapy
Reperfusion therapy is the mainstay management of MI; it includes percutaneous coronary intervention (PCI),
thrombolysis and CABG.
Percutaneous coronary intervention

Primary PCI is the preferred coronary reperfusion strategy for people with acute STEMI.
It should be delivered within 12 hours of onset of symptoms and within 120 minutes of the time if fibrinolysis has been
given and failed in revascularization.
Bivalirudin in combination with aspirin and clopidogrel is recommended for the treatment of adults with STEMI
undergoing primary PCI.
Complications of stenting
 Stent thrombosis occurs in 1-2% of patients, most commonly in the first month. It presents with acute myocardial
infarction, management is by abciximab, thrombolytic therapy and re-stenting.
 Restenosis is due to excessive tissue proliferation around stent. It occurs in around 5-20% of patients, most
commonly in the first 3-6 months. It presents with the recurrence of angina symptoms. Drug eluting stent in
association with clopidogrel and aspirin continued for at least 1 year has been shown to reduce the relative risk of
re-stenosis.
MRCP Revision Notes
CABG
CABG may be needed for patients who fail to respond to PCI with stenting or patient with stenosis of the left main stem
artery and in patients who develop major or mechanical complications.
Thrombolysis
Fibrinolysis is indicated in acute STEMI presented within 12 hours of onset of symptoms if primary PCI cannot be
delivered within the next 120 minutes.
ECG should be done after 60-90 minutes after administration. For those who have residual ST-segment elevation
suggesting failed coronary reperfusion: offer immediate coronary angiography with considered PCI and do not repeat
fibrinolytic therapy.
Common side-effects include hemorrhage, hypotension and allergic reactions.
Contraindications to thrombolysis
 Active internal bleeding (hematemesis)  Aortic dissection
 Recent hemorrhage, trauma or surgery  Recent head injury
 Coagulation and bleeding disorders  Pregnancy
 Intracranial neoplasm  Severe hypertension
 Stroke within 3 months
Secondary prevention (NICE guidelines 2013)
Secondary prevention for myocardial infarction within 12 months:

 ACE inhibitor
 Dual antiplatelet therapy (aspirin plus a second antiplatelet agent) (clopidogrel is alternative to aspirin and superior
to it in case of other vascular disease as carotid artery stenosis)
 B-blocker (Calcium channel blockers are alternatives except in left ventricular systolic dysfunction)
 Statin
 Aldosterone antagonists for symptoms and/or signs of heart failure and left ventricular systolic dysfunction
Secondary prevention for myocardial infarction after a year:

 ACE inhibitor
 Single antiplatelet therapy (clopidogrel is alternative to aspirin and superior to it in case of other vascular disease as
carotid artery stenosis)
 B-blocker should be continued after 12 month in patient who have left ventricular systolic dysfunction
 Statin
MRCP Revision Notes
Post Myocardial Infarction Complications

Acute mitral regurgitation
Acute mitral regurgitation occurs due to rupture of papillary muscle. The posteromedial papillary muscle is twice as
likely to rupture as is the anterolateral papillary muscle as the anterolateral papillary muscle is supplied by two arteries
(left anterior descending and left circumflex coronary arteries), whereas the posteromedial papillary muscle is supplied
only by the right coronary artery.
It is presented by a harsh systolic murmur at the apex which, in association with acute pulmonary edema 2-5 days after
MI. Echocardiography is used for diagnosis. Emergency surgical repair is the management of choice.
Ventricular septal rupture

Ventricular septal rupture and cardiogenic shock are the most common cause of death following acute myocardial
infarction, they account for 60% of early death post MI.
Ventricular free wall rupture occurs about 10 times more frequently than ventricular septal rupture. Anterior myocardial
infarction is typically associated with apical ventricular septal rupture whilst inferior myocardial infarctions are more
commonly associated with basal ventricular septal rupture.
Ventricular septal rupture is presented 5-10 days after MI by a harsh pan-systolic murmur loudest at the left sternal
edge, pulmonary edema and cardiogenic shock.
Ventricular septal rupture and papillary rupture are difficult to distinguish clinically, diagnosis by echocardiography or
right heart catheter (shows left to right shunt in ventricular septal rupture). Immediate surgery is the management of
choice.
Cardiogenic shock
Cardiogenic shock occurs in about 7% of cases of myocardial infarction. Intra-aortic balloon pump (IABP) is the
management of choice in case of low cardiac muscle function. IV dopamine and IV saline are of choice in case of
preserved cardiac muscle function.
Dressler syndrome
Dressler syndrome is acute pericarditis occurs 2-6 weeks following a MI. The underlying pathophysiology is thought to
be an autoimmune reaction.
It is characterized by a combination of fever, pleuritic pain, pericardial effusion, widespread ST elevation on ECG and a
raised ESR.
NSAIDs are the management of choice and corticosteroids have been used in patients with severe symptoms.
MRCP Revision Notes
Left ventricular aneurysm

Left ventricular aneurysm occurs after 3 months of MI. It is presented by persistent ST elevation and absent Q waves
with episodes of ventricular tachyarrhythmia.
Diagnosis is by 24 ECG monitor with echo. Management is by implantable cardioverter defibrillator if ventricular
tachyarrhythmia develops.
Heart block
Heart block is commonly associated with inferior myocardial infarctions as the AV node is supplied by the right coronary
artery. If the patient is asymptomatic, he should continue to be monitored.
Complete heart block in anterior myocardial infarction signifies an extensive area of infarction. It is an indication for
temporary pacing.
MRCP Revision Notes
Heart Failure
NYHA classification
 NYHA Class I: no symptoms, ordinary physical exercise does not cause undue fatigue, dyspnea or palpitations
 NYHA Class II: mild symptoms, comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnea
 NYHA Class III: moderate symptoms, comfortable at rest but less than ordinary activity results in symptoms
 NYHA Class IV: severe symptoms, symptoms of heart failure are present even at rest with increased discomfort with
any physical activity
Diagnosis of acute heart failure (NICE guidelines 2014)

 Take a history; perform a clinical examination and standard investigations (ECG, CXR and blood tests).
 In people presenting with new suspected acute heart failure, use a single measurement of serum natriuretic
peptides (BNP) and if less than 100 ng/L rule out the diagnosis of heart failure.
 In people presenting with new suspected acute heart failure with raised natriuretic peptide levels perform
transthoracic Doppler 2D echocardiography to establish the presence or absence of cardiac abnormalities.
Management
Acute decompensating (NICE guidelines 2014)

 Immediate treatments should be started with diuretics such as furosemide.
 For people already taking a diuretic, consider a higher dose of diuretic than that on which the person was admitted
unless there are serious concerns with patient adherence to diuretic therapy before admission.
 Closely monitor the person's renal function, weight and urine output during diuretic therapy.
 Do not routinely offer nitrates to people with acute heart failure.
 Do not offer sodium nitroprusside or inotropes to people with acute heart failure.
Treatment after stabilization

 In a person presenting with acute heart failure who is already taking B‑blockers, continue the B‑blocker treatment
unless they have a heart rate less than 50 beats per minute, second or third degree AV block, or shock.
 Start or restart beta‑blocker treatment during hospital admission in people with acute heart failure due to left
ventricular systolic dysfunction, once their condition has been stabilized – for example, when intravenous diuretics
are no longer needed.
 Offer an angiotensin‑converting enzyme inhibitor and an aldosterone antagonist during hospital admission
Chronic management
Drugs shown to improve mortality in patients with chronic heart failure:
 ACE inhibitors  Hydralazine with nitrates

 B-blockers (carvedilol and bisoprolol)  Spironolactone
ACE-inhibitors and a B-blocker are first line drugs, second-line drugs is either an aldosterone antagonist or a hydralazine
in combination with a nitrate.
MRCP Revision Notes
Ivabradine was licensed by NICE in 2012 as adjuvant for first and second line for treating chronic heart failure. It is
indicated if regular heartbeat of 75 beats per minute left ventricular ejection fraction is below 35%. It should be started
after 4 weeks of starting treatment with standard drugs.
No long-term reduction in mortality has been demonstrated for furosemide. It is only used if there is worsening
symptoms or fluid retention.
Digoxin has no role in reducing cardiovascular mortality but only used for symptomatic relief. It is recommended for
worsening or severe heart failure due to left ventricular systolic dysfunction despite first- and second-line treatment for
heart failure.
Anticoagulation with warfarin is indicated in:

 Low ejection fraction  Previous thromboembolic event
 Intracardiac thrombus  Left ventricular aneurysm
Cardiac resynchronization therapy

Cardiac resynchronization therapy by biventricular pacing is indicated in patient with LBBB or widened QRS complexes
(>120 ms) that are:
 NYHA class III-IV  On optimal medical therapy

 Ejection fraction less than 35%
Implantable cardioverter defibrillators

Implantable cardioverter defibrillator is indicated in heart failure with symptomatic or asymptomatic arrhythmias.
Cardiac transplantation
Cardiac transplantation is indicated if significant symptoms persist despite maximal medical therapy. It is
contraindicated at ages above 55-60 years and in co-morbidities other than the heart (as renal failure).
Left ventricular assist device

LVAD in patients is indicated if significant symptoms persist despite maximal medical therapy and heart transplantation
is contraindicated.
B-type Natriuretic Peptide

BNP is produced by the left ventricular myocardium in response to strain. It is used to rule out a diagnosis of heart
failure (< 100pg/ml makes a diagnosis of heart failure is unlikely). It is also a marker of prognosis and guiding treatment.
BNP level is increased in:

 Heart failure  Age > 70
 Myocardial ischemia  Renal failure
 Left ventricular hypertrophy  Liver cirrhosis
 Pulmonary embolism
MRCP Revision Notes
Drugs reduce B-type Natriuretic Peptide levels include ACE inhibitors, angiotensin-2 receptor blockers and diuretics.
MRCP Revision Notes
Pulmonology
Bronchial Asthma
Bronchial asthma is widespread reversible inflammatory narrowing of the air passages manifested by paroxysmal attacks
of dyspnea and wheezy chest.
Types
Extrinsic or atopic asthma

Atopic asthma is presented in early childhood. It occurs mostly in atopic individuals and usually with + ve family history
of atopy e.g. urticaria or allergic rhinitis. It is usually seasonal and mediated by IgE.
Intrinsic or cryptogenic asthma

Cryptogenic asthma starts in middle age (late onset) with -ve family history for atopy. It is usually triggered by
respiratory tract infections, chemicals or drugs.
Signs and symptoms

 It is manifested by paroxysmal attacks of cough, dyspnea, chest tightness and expiratory wheezing
 It is usually provoked by exposure to allergens, emotional stress, viral infection and nonspecific precipitating events
 Patients with episodic asthma are usually free of symptoms between bouts
Classifications of asthma exacerbations
Moderate asthma
 Worsening symptoms  Peak flow 50-80% best or predicted
Acute severe asthma

 PEF 33-50% best or predicted  Heart rate ≥110/min
 Respiratory rate ≥25/min  Inability to complete sentences in one breath
Life-threatening asthma
 PEF <33% best or predicted  Cyanosis
 SpO2 <92%  Poor respiratory effort
 PaO2 <8 kPa  Arrhythmia
 Elevated pCO2 (4.6-6.0 kPa)  Exhaustion, altered conscious level
 Silent chest
Diagnosis
 CXR is normal in between attacks, but may show hyper inflated chest and diminished peripheral lung vascular
shadows during attacks
MRCP Revision Notes
 ABG in mild cases shows hypocapnea due to hyperventilation but in severe cases there is hypoxemia, hypercapnea
and respiratory acidosis
 Blood may show elevated IgE, eosinophilia and leukocytosis
Respiratory function tests show (obstructive RF):

 Reduced FEV1, FVC  Reduced TLCO
 Reduced FEV1/FVC ratio  Increased KCO
 Increased residual volume RV
Spirometry shows (diagnostic procedure):

 Diurnal variation of peak expiratory flow rate (PEFR) greater than 20% is diagnostic
 Reversibility of airflow obstruction (increase of FEV1 ≥ 15% after inhaling a short-acting bronchodilator) unlike COPD
which shows irreversibility
 Bronchial provocation testing (Cold air challenge ,Methacholine, histamine tests)
MRCP Revision Notes
Management
Acute attacks
 Nebulized B 2 agonists in 15-30 minute intervals with supplementation of with high flow oxygen via reservoir bag are
the 1st line in acute severe attacks
 Ipratropium bromide nebulizers and IV hydrocortisone are 2nd lines
 IV magnesium sulphate is indicated in severe life-threatening attacks. It should be stopped if respiratory rate fall
below 25/min
Indications for admission to the ICU for intubation and ventilation

Any patient fails to respond to maximal medical therapy and show the below signs should be referred immediately to
the ICU for intubation and ventilation:
 PaO2 <8 kPa

 Elevated pCO2 (4.6-6.0 kPa)
 Poor respiratory effort
 Exhaustion, altered conscious level
Current guidelines do not support the routine use of non-invasive ventilation in management of severe asthma
Chronic asthma
Stepwise stable management (NICE guidelines 2017)

 Short-acting beta2 agonist (SABA) as reliever therapy
 Add low dose of ICS (inhaled corticosteroids) as the first-line maintenance therapy for continuous symptoms
 If uncontrolled add long-acting beta2 agonist (LABA) and a trial of adding LTRA (Leukotriene antagonists) to low dose
ICS
 If uncontrolled switch ICS and LABA maintenance therapy to a MART regimen (Maintenance and reliever therapy is a
single inhaler containing both ICS and a fast-acting LABA as formoterol)
 If uncontrolled increase the ICS to a moderate maintenance dose
 If uncontrolled increase the ICS to a high maintenance dose and trial of an additional drug as LAMA (long-acting
muscarinic receptor antagonist) or theophylline
Management of bronchial asthma in pregnancy

The BNF advises that ‘inhaled drugs, theophylline and prednisolone can be taken as normal during pregnancy and
breast-feeding.
Drugs used in management of bronchial asthma
B2 agonists
B2 agonist acts by activating the Gs protein activating adenylate cyclase increasing cAMP which leads to muscular
relaxation and bronchodilation.
Examples include short acting (Salbutamol) and long acting (salmeterol, formoterol).
MRCP Revision Notes
Adverse effects
 Tachycardia, palpitation and hypokalemia
 Salmeterol and formoterol should be used with caution in severe liver cirrhosis.
 Salmeterol may produce an acute exacerbation of asthma through an acute hypersensitivity reaction
Leukotriene antagonists
Leukotriene antagonists act by reducing the degranulation of mast cells triggered by the interaction of antigen and IgE.
They have little inhibitory effect on mediator release from human basophils
They are licensed for use in asthma with allergic rhinitis and have been shown to be as effective as doubling the dose of
inhaled steroid.
They are also useful in exercise induced bronchial asthma and aspirin sensitive asthma.
Omalizumab
Omalizumab is a recombinant monoclonal antibody; it binds IgE without activating mast cells. It is used in patients with
moderate to severe asthma. Omalizumab reduces the need for corticosteroids.
Occupational Asthma
Occupational asthma accounts for 5 to 10% of adult onset asthma. It is caused by agents that are encountered at work.
The commonest occupations associated with occupational asthma include:
 Paint sprayers (isocyanates)  Laboratory technicians (rats, mice, rabbits, locusts)

 Chemical processors (acids, detergents, bleaches)  Plastics workers (polyethylene, polyvinyl)
 Cigarette factory workers (tobacco dust)  Bakers (flour and enzymes as amylase used in the
 Tea sifters and packers (tea dust) baking)
Signs and symptoms

 Dyspnea wheeze and cough which occur during the working week and remit during holidays
 The symptoms do not usually develop immediately on early exposure but begin days, months or even years later
Diagnosis
 Serial measurements of PEFR are recommended at work and in holidays
 Bronchial provocation testing
Management
 Avoidance of further exposure to the occupational offending allergen
 Regular use of bronchodilators
MRCP Revision Notes
Bronchiolitis Obliterans
Bronchiolitis obliterans is irreversible obstructive lung disease in which the bronchioles are compressed and narrowed
by patchy chronic inflammation, concentric submucosal and peribronchiolar fibrosis and smooth muscle hypertrophy.
Signs and symptoms

Bronchiolitis obliterans presents with features of bronchial asthma like dry cough, dyspnea and expiratory wheeze but
unremitting symptoms as COPD.
Diagnosis
 CXR varies from normal to a reticular or reticulonodular pattern
 HRCT shows thickened airway walls
 Lung biopsy shows intraluminal polyps of organizing connective tissue (confirm the diagnosis)
Management
 Lung transplantation is the main line of management
 Corticosteroids may be used to delay disease progression
COPD
Chronic obstructive pulmonary disease is progressive decline in lung function as a result of irreversible airflow
obstruction.
Types
 Chronic bronchitis (Blue Bloater) is excessive secretion of bronchial mucus manifested by daily productive cough for
3 months or more in at least 2 consecutive years
 Emphysema (Pink Puffer) is abnormal permanent enlargement of air spaces distal to the terminal bronchioles and
loss of elastic recoil
MRCP Revision Notes
Causes
 Smoking (even passive smoking) is the commonest cause (15 % of smokers develop progressive disabling symptoms
in their 40s and 50s)
 Genetic causes as alpha 1-antitrypsin deficiency
 Industrial causes of COPD (cadmium, coal, cotton, cement and grain)
Signs and symptoms

Diagnosis of COPD should be considered in patients over the age of 35 who have a risk factor (generally smoking) and
who present with one or more of the following symptoms:
 Exertional breathlessness  Frequent winter 'bronchitis'

 Chronic cough  Wheeze
 Regular sputum production
Signs
 Barrel chest
 Cor pulmonale for advanced disease
Diagnosis (NICE 2010)

 Full blood count shows secondary polycythemia
 CXR shows hyperinflation, bullae and flat hemidiaphragm
 HRCT is more sensitive and specific for the diagnosis of emphysema (shows bullae)
MRCP Revision Notes
 Sputum examination may reveal exacerbating organisms (strept pneumoniae, H influenza or Moraxella catarrhalis)
 ABG shows hypoxia, hypercapnea, respiratory acidosis (HCO3 levels increase in chronic cases [compensation] and
decreases in exacerbations [decompensation])
Pulmonary functions tests show (obstructive pattern)

 FEV1 < 80%  RV/TLC ratio increase indicating air trapping
 FEV1/FVC < 70%  KCO decrease (unlike BA)
 RV increase  Spirometry with reversibility will show minimal
 TLC increase reversibility (less than 10-15%)
Consider alternative diagnoses if:

 Older people without typical symptoms of COPD where the FEV1/FVC ratio is < 0.7
 Younger people with symptoms of COPD where the FEV1/FVC ratio is ≥ 0.7
Staging of COPD by using the FEV1 (NICE 2010)

 Stage I: Mild COPD: FEV1/FVC<0.70 and FEV1≥ 80%
 Stage II: Moderate COPD: FEV1/FVC<0.70 and FEV1 50-79%
 Stage III: Severe COPD: FEV1/FVC<0.70 and FEV1 30-49%
 Stage IV: Very severe COPD: FEV1/FVC<0.70 and FEV1 <30%
MRCP Revision Notes
Management (NICE guidelines 2010)
Management of acute exacerbation COPD

Acute exacerbation COPD is associated with respiratory acidosis, bicarbonate levels are decreased and hydrogen levels
are raised due to carbon dioxide retention
 Initial management (nebulizers, antibiotics and IV hydrocortisone)

 COPD patients is at risk of hypercapnea so O2 must be aimed at 88-92% as higher levels will causes loss of hypoxic
drive which is mediated by carotid body. Once the pCO2 is back to normal the target oxygen saturations should be
94-98%.
 Non-invasive ventilation (NIV) should be used as the treatment of choice for persistent hypercapnic ventilatory
failure during exacerbations not responding to medical therapy. BiPAP is superior to CPAP in type 2 respiratory
failure. BiPAP reduces rates of intubation, lowers hospital mortality rates and lead to shorter hospital stays
 Mechanical ventilation is indicated when the patient does not improve on non-invasive ventilation or the pH falls
below 7.26. Target inspiratory positive airways pressure (IPAP) of 10 cm water and expiratory positive airways
pressure (EPAP) of 4 cm water.
Stable management
General measures
 Smoking cessation advice
 Pneumococcal and annual influenza vaccination
 Pulmonary rehabilitation
Bronchodilator therapy
Short-acting B2 agonists (SABA) are first-line treatment, if the patient remains breathless or have exacerbations the next
step is determined by the FEV1:
 FEV1 > 50%: long-acting B2-agoinst (LABA) or long-acting muscarinic antagonist (LAMA)
 FEV1 < 50%: LABA + inhaled corticosteroid (ICS) or LAMA (ICS decreases exacerbations with no effect on mortality)
 For patients with persistent exacerbations or breathlessness LAMA and LABA + ICS inhaler irrespective of their FEV1
Long-term oxygen therapy (LTOT)

LTOT is indicated in patients with COPD who have a PaO2 less than 7.3 kPa when stable or a PaO2 greater than 7.3 and
one of the following:
 Secondary polycythemia
 Nocturnal hypoxemia (oxygen saturation is less than 90% for more than 30% of the time)
 Cor pulmonale
 Pulmonary hypertension
Patients should breathe supplemental oxygen for at least 15 hours per day. Greater benefits are seen in patients
receiving oxygen for 20 hours per day.
MRCP Revision Notes
Oral therapy
Oral corticosteroids
Maintenance use of oral corticosteroid therapy in COPD is not normally recommended. Some patients with advanced
COPD may require maintenance oral corticosteroids when these cannot be withdrawn following an exacerbation.
Oral theophylline
NICE only recommends theophylline to people who cannot use inhaled therapy or in patients who remain symptomatic
on monotherapy by combining theophylline with LAMA or with LABA
Mucolytic therapy
Mucolytic drug therapy should be considered in patients with a chronic cough productive of sputum. Do not routinely
use mucolytic drugs to prevent exacerbations in people with stable COPD.
Anti-tussive therapy
Anti-tussive therapy should not be used in the management of stable COPD.
Management of cor pulmonale

Patients presenting with cor pulmonale should be assessed for the need for long-term oxygen therapy. Edema
associated with cor pulmonale can usually be controlled symptomatically with diuretic therapy.
Not recommended drugs for the treatment of cor pulmonale:
 Angiotensin-converting enzyme inhibitors  Alpha-blockers

 Calcium channel blockers  Digoxin
Lung reduction surgery

Patients with severe COPD who remain breathless with marked restrictions of their activities of daily living, despite
maximal medical therapy (including rehabilitation), should be referred for consideration of lung volume reduction
surgery if they meet all of the following criteria:
 FEV1 more than 20% predicted  Upper lobe predominant emphysema

 PaCO2 less than 7.3 kPa  TLCO more than 20% predicted
Indications of lung transplantation

 Limited activities of daily living  Limited life expectancy without transplantation
 Exhaustion of medical therapy
Before Lung transplantation you must be take concern about patient age, cost effectiveness, other management options
and adequate function of other organ systems (renal and hepatic failure).
Alpha-1 Antitrypsin Deficiency

Alpha-1 antitrypsin deficiency is an inherited condition caused by lack of protease inhibitor normally produced by the
liver protects the lungs connective tissue from neutrophil elastase.
MRCP Revision Notes
Alpha-1 antitrypsin gene is located on chromosome 14, it is inherited in an autosomal recessive / co-dominant fashion
alleles classified by their electrophoretic mobility - M for normal, S for slow, and Z for very slow.
Genotypes of Alpha-1 antitrypsin deficiency

 In PiMM genotype alpha-1 antitrypsin is 100%  In PiSZ genotype alpha-1 antitrypsin is 40%
 In PiMS genotype alpha-1 antitrypsin is 80%  In PiZZ genotype alpha-1 antitrypsin is 10-15%
 In PiSS genotype alpha-1 antitrypsin is 60% which is the severest form of alpha 1-antitrypsin
 In PiMZ genotype alpha-1 antitrypsin is 60% deficiency
It is remembered by 1M=50%, 1S=30% and 1Z=10%
Signs and symptoms

 Recurrent respiratory infections or asthma that does not respond to treatment
 Lungs show panacinar emphysema in 2% of cases
 Liver cirrhosis in 15% of patients
Diagnosis
 A1AT concentrations
 HRCT chest shows panacinar emphysema especially in lower lobes
Management
 Stop smoking as smoking acts synergistically to promote the development of emphysema
 Intravenous infusions of alpha-1 antitrypsin, derived from donated human plasma. Other treatments currently being
studied include recombinant and inhaled forms of A1AT
 In severe cases, liver transplantation may be necessary
MRCP Revision Notes
Gastroenterology & Hepatology

Dyspepsia
Dyspepsia is a condition of impaired digestion. It is characterized by chronic or recurrent pain in the upper abdomen,
upper abdominal fullness.
Causes
 Functional dyspepsia  Drug Causes (NSAIDs, bisphosphonates and
 GERD steroids)
 Peptic ulcer disease  Drugs reducing lower esophageal sphincter
 Esophageal and gastric cancer pressure (calcium channel blockers, nitrates and
 Cholelithiasis and chronic pancreatitis theophylline)
Management (NICE Guidelines 2004)

 Testing and eradication therapy for H pylori
 Low-dose PPI or H2RA for 4 weeks
 If symptoms recur; PPI to be taken at the lowest dose possible to control symptoms
Urgent referral for endoscopy (alarm signs)

Patients aged 55 with recent, unexplained and persistent (4-6 weeks) symptoms or patient under 55 years with:
 Chronic gastrointestinal bleeding  Iron deficiency anemia

 Progressive weight loss  Epigastric mass
 Progressive dysphagia  Suspicious barium meal
 Persistent vomiting
Gastroesophageal Reflux Disease

Gastroesophageal reflux disease (GERD) is reflux of gastric contents into the esophagus.
Causes
 Drugs as calcium antagonists, nitrates, theophylline, bisphosphonates, corticosteroids and non-steroidal anti-
inflammatory drugs
 Poor esophageal peristalsis
 Delayed gastric emptying
 Hiatus hernia
Signs and symptoms
Esophageal symptoms
MRCP Revision Notes
 Heartburn  Dysphagia
 Regurgitation
Extraesophageal symptoms
 Cough and wheezes  Noncardiac chest pain
 Hoarseness, sore throat  Enamel erosion or other dental manifestations
Complications
 Esophagitis  Barrett esophagus
 Anemia  Esophageal cancer
 Benign strictures
Diagnosis
 24-hr esophageal pH monitoring is the gold standard test for diagnosis
 Peptest (salivary pepsin) is simple and non-invasive but sensitivity is 30% only
 Testing for Helicobacter pylori after 2‑weeks washout period of proton pump inhibitor (PPI)

 Simple lifestyle advice, including advice on healthy eating, weight reduction and smoking cessation
 Empirical full-dose PPI therapy for 4-8 weeks. If symptoms recur after initial treatment, offer a PPI at the lowest dose
 Surgical fundoplication is indicated for patients cannot tolerate acid suppression therapy
Achalasia
Achalasia is a primary esophageal motility disorder characterized by the absence of esophageal peristalsis and impaired
relaxation of the lower esophageal sphincter (LES) in response to swallowing. It presents in middle-age and is more
common in women.
Symptoms
 Long history of dysphagia of both liquids and solids  Heartburn
from the start  Halitosis
 Regurgitation (cough, aspiration pneumonia and  Dysplastic changes (15-fold increase in esophageal
bronchial asthma) cancer)
 Chest pain
Diagnosis
 CXR shows wide mediastinum and fluid level
MRCP Revision Notes
 Barium swallow shows dilated esophagus and lower end narrowing (bird's beak deformity)
 Esophageal manometry is the main diagnostic procedure; it shows increased lower esophageal sphincter tone
Differential diagnosis (causes of dysphagia)

 Esophageal cancer (dysphagia more to solids and progress to both)
 Neurogenic causes (Mythenia gravis, Motor neuron disease, Scleroderma) dysphagia more to liquids
 Achalasia equally for both from start
 Pharyngeal pouch (regurgitation of rotten food)
MRCP Revision Notes
 Obstruction if felt high in the neck (compression web, pharyngeal pouch, thyroid swelling) associated with nasal
regurgitation, coughing and chocking
Management
 Pneumatic dilation may give temporary relief
 Laparoscopic cardiomyotomy is the management of choice
 Drug therapy (calcium channel blockers, nitrate) and intra-sphincteric injection of botulinum toxin are alternatives in
patients who are unfit for surgery
Pharyngeal Pouch
Pharyngeal pouch (Zenker diverticulum) is a diverticulum of the mucosa of the pharynx, just above the cricopharyngeal
muscle.
Signs and symptoms

 Dysphagia and sense of a lump in the neck  Chronic cough
 Regurgitation of rotten food in the mouth  Gurgling neck mass appears only on swallowing
 Halitosis
Diagnosis
 Simple barium swallow will reveal the diverticulum (procedure of choice)
 Upper GI endoscopy
Management
 If small and asymptomatic, no treatment is necessary
 Larger symptomatic cases is managed by surgical resection of the diverticulum
MRCP Revision Notes
Autoimmune Hepatitis
Autoimmune hepatitis is a chronic continuing hepatocellular inflammation and necrosis. It has a tendency to progress to
cirrhosis. It occurs with other autoimmune disorders, hypergammaglobulinemia and HLA B8, DR3.
Types
 Type I affects both adults and children and is associated with anti-nuclear antibodies (ANA) and/or anti-smooth
muscle antibodies (SMA)
 Type II occurs predominantly in children and is associated with anti-liver/kidney microsomal type 1 antibody (LKM1)
 Type III is associated with soluble liver-kidney antigen
Signs and symptoms

Autoimmune hepatitis present as acute or chronic hepatitis or fulminant hepatic failure. Symptoms of acute hepatitis
include marked by fever, hepatic tenderness, and jaundice.
Extrahepatic symptoms associated with autoimmune hepatitis include:
 Mild pruritus and skin rashes  Arthralgia

 Secondary amenorrhea  Chest pain from pleuritis
 Cushingoid features and hirsutism
Diagnosis
 CBC shows eosinophilia, thrombocytopenia and mild leukopenia
 Coombs-positive hemolytic anemia
 Elevated serum aminotransferase levels (1.5-50 times reference values)
 Elevated serum immunoglobulin levels, primarily immunoglobulin G (IgG)
 Mild to moderately elevated serum bilirubin and a sharp increase in the alkaline phosphatase
 Positive specific antibodies
 Liver biopsy
Management
 Corticosteroids, either alone or in combination with azathioprine is the mainstay therapy
 Liver transplantation is effective for patients in whom medical therapy has failed or for those with decompensated
cirrhosis
Primary Biliary Cirrhosis

Primary biliary cirrhosis (PBC) is a chronic autoimmune disease of the liver that leads to progressive cholestasis and
often end-stage liver disease.
PBC is presents frequently in women especially between the fourth and sixth decades. PBC is associated with HLA DR3.
Causes (autoimmune diseases)
MRCP Revision Notes
 Sjogren syndrome (most common cause)  Systemic sclerosis

 Rheumatoid arthritis  Thyroid disease
Signs and symptoms

 Pruritus and jaundice  Hyperpigmentation
 Right upper quadrant discomfort  Sicca syndrome as xerophthalmia and xerostomia
 Hepatosplenomegaly
Diagnosis
 Significant elevations of the alkaline phosphatase with mild elevation of aminotransferases (cholestatic picture)
 Positive antimitochondrial antibody (AMA) (diagnostic) in 98% of cases and smooth muscle antibodies in 30% of
cases
 Raised serum IgM
 ERCP shows intrahepatic biliary obstruction
 Definitive diagnosis is made with percutaneous liver biopsy which shows intra-hepatic biliary obstruction
Management
 Ursodeoxycholic acid is of choice, it is used to slow the progression of the disease
 Corticosteroids and methotrexate may produce improvement in biochemical and histologic findings
 Pruritus is managed by antihistamines followed by cholestyramine followed by rifampicin followed by
plasmapheresis
 Liver transplantation for advanced cirrhosis and intractable pruritus
Primary Sclerosing Cholangitis

Primary sclerosing cholangitis (PSC) is a progressive course of cholestasis with inflammation and fibrosis of the
intrahepatic and extrahepatic bile ducts.
PSC is strongly associated mainly with ulcerative colitis (80% of cases) and is often complicated by cholangiocarcinoma
development.
Initial presentation consists of fatigue, jaundice, pruritus, and right upper quadrant pain. Progressive disease causes
cirrhosis with symptoms of variceal bleeding, ascites and hepatic encephalopathy.
Diagnosis
 Significant elevations of the alkaline phosphatase with mild elevation of aminotransferases (cholestatic picture)
 Raised serum IgM and hypergammaglobulinemia
 ANCA may be positive
 Endoscopic retrograde cholangiopancreatography (ERCP) is diagnostic; it shows multiple strictures and dilations of
the intrahepatic and extrahepatic biliary ducts
MRCP Revision Notes
Management
 Drug therapy is aimed at treating symptoms and managing complications (ursodeoxycholic acid
immunosuppressants and steroids)
 Liver transplantation is the management of choice
MRCP Revision Notes
Nephrology & Mineral Metabolism

Acute Renal Failure
Acute renal failure is as a sudden, rapidly progressive decrease in kidney function, resulting in an inability to maintain
adequate renal function.
Signs and symptoms

 Non-specific symptoms (nausea, vomiting and malaise)
 Sudden increase in BUN or serum creatinine
 Oliguria (decline in urinary output to 0.5 mL/kg/h)
 Pericardial effusions and pericarditis
 Arrhythmias due to hyperkalemia
 The lung may show crepitations
 Bleeding and clotting
 Encephalopathy with confusion and seizures
Diagnosis
 Elevated BUN and creatinine (serum creatinine concentration will increase by 1-1.5 mg/dL daily)
 Hyperkalemia, hypocalcemia, metabolic acidosis and hyperphosphatemia
 Anemia can occur as a result of decreased erythropoietin production
Causes of acute renal failure
Prerenal azotemia
Prerenal azotemia is due to renal hypoperfusion, it represents 40-80% of cases.
Causes
 Decrease in intravascular volume (hemorrhage, GI losses, dehydration, excessive diuresis, etc.)
 Changes in vascular resistance (sepsis, anaphylaxis, anesthesia, etc.)
 Decrease cardiac output (cardiogenic shock, congestive heart failure, pulmonary embolism and cardiac tamponade)
Diagnosis
 The BUN-creatinine ratio > 20:1  Urinary Na < 20 mEq/L
 FeNa (fractional excretion of sodium) < 1%  Urine osmolality > 500 mosm/kg
Intrinsic renal failure

Intrinsic renal disorders represents up to 50% of all cases of acute kidney injury.
Causes
 Acute Tubular Necrosis  Acute Interstitial Nephritis
 Acute Glomerulonephritis
MRCP Revision Notes
Diagnosis
 The BUN-creatinine ratio < 20:1 (acute glomerulonephritis > 20:1)
 FeNa > 1% (<1 in acute glomerulonephritis)
 Urinary Na > 20 mEq/L in acute tubular necrosis (acute glomerulonephritis < 20 mEq/L, variable in acute interstitial
nephritis)
 Urine osmolality is variable (250-300 mosm/kg in acute tubular necrosis)
 Specific gravity < 1010
Postrenal Azotemia
Postrenal azotemia represents 5-10% of cases
Causes
 Urethral obstruction, bladder obstruction and obstruction of both ureters
 Benign prostatic hyperplasia
Diagnosis
 The BUN-creatinine ratio > 20:1  Urinary Na is variable
 FeNa (fractional excretion of sodium) is variable  Urine osmolality <400mosm/kg
2013 NICE guidelines of management of acute kidney injury

Indications of urgent referring for renal replacement therapy (hemodialysis):
 Hyperkalemia  Fluid overload

 Metabolic acidosis  Pulmonary edema
 Symptoms or complications of uremia (pericarditis
or encephalopathy)
Acute Tubular Necrosis

Acute tubular necrosis is an acute renal failure due to tubular damage; it accounts for 85% of intrinsic acute kidney
failure causes.
Causes
Ischemic causes
 Diarrhea and vomiting  Hepatorenal syndrome
 Pancreatitis  Pre-eclampsia and eclampsia
 Myocardial infarction
Nephrotoxic causes
Endogenous nephrotoxins
MRCP Revision Notes
 Burns  Massive intravascular hemolysis

 Rhabdomyolysis  Hyperuricemia
Exogenous Nephrotoxins
 Bence Jones protein
 Snake bites
 Drugs: aminoglycosides, diuretics, heroin addicts, cyclosporine
 Radiographic contrast media
Complication
 Hyperkalemia, hyponatremia and metabolic acidosis
 Infections and Gram-negative septicemia
 Pericarditis
Diagnosis
 Urine osmolality < 350 mosmol/l
 Urine sodium excretion > 40 mmol/l
 FeNa >1%
 Urine sediment with pigmented granular casts and renal tubular epithelial cells
Management
 Dietary protein restriction
 Furosemide is of choice, plasma ultrafiltration in non-responsive to diuretics
 Dialysis in life threatening electrolyte disturbances, worsening acidosis and uremic complications (e.g.
encephalopathy, pericarditis and seizures)
Rhabdomyolysis
Rhabdomyolysis occurs due to muscle injury leading to release of intracellular contents of myocytes into the plasma
causing acute tubular necrosis and electrolyte disturbance.
Causes
 Extensive blunt trauma and crush injury  Hypothermia
 Prolonged epileptic seizure  Ecstasy poisoning
 Infectious or inflammatory myopathies  McArdle syndrome
 Prolonged collapse or coma  Statins
Diagnosis
 Highly elevated creatine kinase
 Myoglobinuria
 Hypocalcemia, hyperkalemia, hyperphosphatemia and hyperuricemia
MRCP Revision Notes
Management
 IV fluids to maintain good urine output and urine alkalization
 Rapid correction of the life-threatening hyperkalemia (IV calcium gluconate)
 Hemodialysis if acute renal failure occurs
Interstitial Nephritis
Interstitial nephritis accounts for 10-15% of cases of intrinsic renal failure. It is rarely progress to end stage renal disease.
Causes
 Drugs (70% of cases) e.g. NSAIDs, B- lactams, ethambutol ,cephalosporins, sulphasalazine , phenytoin and allopurinol
 Infectious causes e.g. streptococcal infections, CMV, histoplasmosis and Rocky Mountain spotted fever
 Immunologic causes e.g. systemic lupus erythematosis, Sjogren syndrome, sarcoidosis and cryoglobulinemia
Signs and symptoms

 Fever  Arthralgia
 Maculopapular rash  Acute renal failure
Diagnosis
 Eosinophilia and eosinophilurea
 Urine analysis shows proteinuria, RBCs, WBCs and WBCs casts
 Renal biopsy shows interstitial edema with a heavy infiltrate of inflammatory cells and tubular necrosis
Management
 Treatment consists of supportive measures and withdrawal of the offending agent
 Short-term corticosteroids accelerate recovery and prevent long-term renal damage
 Dialysis may be needed in renal failure
Contrast Induced Nephropathy

Contrast-induced nephropathy is the impairment of renal function within 2-3 days of IV contrast administration.
Risk factors
 Patient is over 75  Diabetes
 Chronic kidney disease  Heart failure
Calculation of risk factors rates

 Chronic kidney disease or diabetes or heart failure (1 risk factor) = 7%
 Patient is over 75 + 1 risk factor = 14%
MRCP Revision Notes
 Patient is over 75 + 2 risk factor (chronic kidney disease + diabetes or heart failure) = 25%
 Patient is over 75 + 3 risk factor (chronic kidney disease + diabetes + heart failure) = 60%
Management
 Stopping nephrotoxic medications, analgesics and furosemide prior to the procedure is the primary preventative
measure
 Acetylcysteine as an antioxidant reduces the risk of nephropathy
 IV fluids to maintain renal blood flow if toxicity occurs
MRCP Revision Notes
Endocrinology & Diabetes

Acromegaly
Acromegaly results when the anterior pituitary gland produces excess growth hormone.
Causes
 Most of cases are due to pituitary adenoma
Other rare causes

 Familial  Carney syndrome
 MEN-1  Ectopic GHRH or GH secretion
 McCune-Albright syndrome
Signs and symptoms of the tumor

 Symptoms of pituitary tumor: hypopituitarism, headaches, bitemporal hemianopia
 Raised prolactin in 30% of cases leads to galactorrhea
Characteristic changes in appearance (Gigantism):

 Tall stature
 Mild to moderate obesity
 Macrocephaly
 Soft tissue hypertrophy
 Exaggerated growth of the hands and feet, with thick fingers and toes
 Coarse facial features
 Frontal bossing
 Wide spacing of the teeth and prognathism (the upper or lower jaws protrudes beyond a predetermined imaginary
line in the coronal plane of the skull)
MRCP Revision Notes
Complications
 Hypertension  Hyperhidrosis
 Diabetes  Osteoarthritis and spinal cord compression
 Peripheral neuropathies (e.g., carpel tunnel  Colorectal polyps
syndrome)  Hyperhidrosis due to sweat gland hypertrophy
 Cardiomyopathy
Diagnosis
 Growth hormone (GH) is not diagnostic as its levels vary during the day
 Oral glucose tolerance test shows failure in suppression of GH (Diagnostic)
 Elevated IGF-I values indicates GH excess (not specific)
 MRI shows a pituitary tumor in 90% of patients
MRCP Revision Notes
Management
 Trans-sphenoidal surgery is first-line treatment for acromegaly in the majority of patient
 Somatostatin analogue (octreotide) is effective in reducing GH and shrinking tumor size
 Dopamine agonists (bromocriptine, cabergoline) are less effective than somatostatin analogue, they can be used in
tumors that secrete both PRL and GH
 Pegvisomant is a GH receptor antagonist that blocks hepatic IGF-I production, it decreases IGF-1 levels in 90% of
patients to normal, but it doesn't reduce tumor volume
 External irradiation is used for older patients or following failed surgical/medical treatment
Growth Hormone Deficiency

Causes:
Most cases are idiopathic other causes include:
 Genetic causes  CNS radiation

 Brain tumors (Craniopharyngioma)  Anatomical abnormalities (empty sella
 CNS surgery syndrome)
Signs and symptoms:

 Short stature  Obesity
 Small penis  Poor bone density
 Reduced muscle mass  Hypoglycemia and hypercholesterolemia
DD of short stature:
 Achondroplasia
 Constitutional Growth Delay
MRCP Revision Notes
 Familial short stature

 Growth hormone resistance
 Noonan Syndrome
 Short stature related to a metabolic abnormality (renal tubular acidosis, poorly controlled diabetes mellitus)
 Short stature related to endocrinopathy (hypothyroidism, Cushing syndrome)
 Turner Syndrome
Diagnosis
 Levels of growth hormone is not diagnostic as levels are nearly undetectable for most of the day
 Low levels of insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 (IGFBP-3) {diagnostic but not
specific}
 Insulin tolerance test with growth hormone measurement is diagnostic, growth hormone releasing hormone
(GHRH) testing is alternative
Management
 Growth hormone replacement by recombinant human growth hormone (rHGH)
Diabetes Insipidus
Diabetes insipidus is an uncommon disease characterized by polydipsia and polyuria of large quantities of urine of
low specific gravity.
Causes
Cranial diabetes insipidus (deficiency of vasopressin)

 Idiopathic  Wegener granulomatosis
 Post head injury  Craniopharyngioma
 Sarcoidosis  Histiocytosis X
 Pituitary surgery  Wolfram syndrome
Nephrogenic diabetes insipidus (resistance to vasopressin)

 Genetic  UT obstruction
 Electrolytes: hypercalcemia, hypokalemia  Sickle-cell anemia
 Drugs: demeclocycline, lithium  Pyelonephritis
 Tubulo-interstitial disease
Differential diagnosis (causes of polyuria and polydipsia)

 Diabetes mellitus
 Hypercalcemia
 Cushing syndrome or corticosteroid use
 Psychogenic polydipsia (Hysterical polydipsia) is a psychiatric disturbance due to a very large ingestion of
water that causes a fall in plasma sodium and osmolality and a concomitant low urine osmolality
MRCP Revision Notes
Diagnosis
 High plasma osmolality, low urine osmolality even after water deprivation
 Hypernatremia
Vasopressin challenge test

Prevent patient drinking water; ask patient to empty bladder and hourly urine and plasma osmolarities.
In cranial diabetes insipidus there is a dramatic improvement in urine osmolality (> 50%) following the
administration of DDAVP. In nephrogenic diabetes insipidus there is no or little response (< 45%) in urine
osmolality.
Management
 Mild and refractory cases of diabetes insipidus require only adequate fluid intake
 Desmopressin acetate in the form of nasal spray or subcutaneous injections is the treatment of choice for
central diabetes insipidus
 Nephrogenic diabetes insipidus is managed by combined indomethacin with hydrochlorothiazide or amiloride
Syndrome of Inappropriate Antidiuretic Hormone

SIADH (syndrome of inappropriate antidiuretic hormone) is excessive release of antidiuretic hormone from the
posterior pituitary gland or another source which results in dilutional hyponatremia.
Causes
 Malignancy e.g. small cell lung cancer, pancreatic and prostatic cancer
 Neurological (stroke, subarachnoid hemorrhage, subdural hemorrhage, meningitis, encephalitis)
 Infections (tuberculosis, pneumonia)
 Drugs (sulfonylureas, SSRIs, TCA, carbamazepine, vincristine, cyclophosphamide)
 Porphyria
Signs and symptoms (progressive hyponatremia)

 Generalized muscle weakness and aches
 Myoclonus and hyporeflexia
 Cheyne-Stokes respiration
 Confusion, delirium and seizures
Diagnosis
 Hyponatremia
 Low plasma osmolarity, high urine osmolarity
 Urine volume is low makes urine concentrations of sodium will appear inappropriately high
Management
 Fluid restriction
 Demeclocycline can be useful if fluid restriction fails
MRCP Revision Notes
 Slow replacement with IV 0.9% for emergency case (rapidly correction of hyponatremia leads to central
pontine myelinolysis)
Type 1 Diabetes Mellitus

Type 1 diabetes is an autoimmune destruction of the beta cells in the pancreas causing inability to produce insulin.
It is associated with HLA DR-3 or DR-4. It is associated with other autoimmune diseases, such as Graves’ disease,
Hashimoto thyroiditis, and Addison disease.
Genetic factors
 Children whose mother has type 1 DM have a 2-3% risk of developing the disease, whereas those whose father
has the disease have a 5-6% risk
 Dizygotic twins have a 5-6% concordance rate for type 1 DM
 Monozygotic twins will share the diagnosis more than 50% of the time by the age of 40 years
Signs and symptoms

Onset most often occurs in childhood and symptomatic disease may be sudden.
 Polyuria  BMI < 25

 Polydipsia  Diabetic ketoacidosis (DKA) is a common
 Polyphagia complication
 Unexplained weight loss
Diagnosis
 Positive islet-cell antibodies (85% of cases), insulin antibodies or glutamic acid dehydrogenase antibodies
 Low serum insulin levels
Management
 Lifelong insulin therapy by continuous subcutaneous insulin infusion (2008 NICE guidelines)
 Allogeneic pancreatic islet cell transplantation should be considered
Type 2 Diabetes Mellitus

Type 2 diabetes mellitus is resulting from the combination of resistance to insulin action, inadequate insulin
secretion.
Signs and symptoms

 Many patients with type 2 diabetes are asymptomatic many years before diagnosis is made
 Classic symptoms: Polyuria, polydipsia, polyphagia, and weight loss
 Blurred vision (microvascular complications)
 Lower-extremity paresthesia
MRCP Revision Notes
 BMI >25
 Diabetic ketoacidosis (DKA) is a rare complication
Diagnosis
 High (Insulin resistance) or low (Beta-cell dysfunction) serum insulin levels
2015 NICE guidelines Type 2 diabetes management in adults

1 - Dietary advice
2 - Blood pressure management

 The target of blood pressure is below 140/80 mmHg (below 130/80 mmHg if there is kidney, eye or
cerebrovascular damage)
 Angiotensin-converting enzyme (ACE) inhibitor is the first-line antihypertensive drug; it is contraindicated in
African or Caribbean family origin, pregnant or there is a possibility of pregnancy
 Diuretics or calcium‑channel blockers are alternatives
 Antiplatelet therapy (aspirin or clopidogrel) are not indicated for adults with type 2 diabetes without
cardiovascular disease
3 - Blood glucose management:

 Start with a single drug
 If HbA1c levels are not adequately controlled by a single drug and rise to 58 mmol/mol (7.5%) or higher:
intensify drug treatment (First intensification with dual non-insulin drugs and Second intensification with
triple non-insulin drugs or any treatment combination containing insulin)
 Aim for HbA1c in management not associated with hypoglycemia to 48 mmol/mol (6.5%) and to 53 mmol/mol
(7.0%) and in management associated with hypoglycemia
4 - Drug treatment:
 Standard-release metformin as the initial drug treatment for adults with type 2 diabetes
 If metformin is contraindicated or not tolerated, consider alternatives as dipeptidyl peptidase‑4 (DPP‑4)
inhibitor, pioglitazone or sulfonylurea
 Sodium-glucose transport (SGLT-2) inhibitors (canagliflozin, dapagliflozin or empagliflozin) are not licensed by
NICE to be used as monotherapy
For Insulin therapy:

 Start NPH insulin twice daily with or without pre-mixed (biphasic) human insulin
 Switch from NPH insulin to detemir or insulin glargine if the patient needs to reduce the frequency of injections
from twice to once daily or recurrent symptomatic hypoglycemic episodes or the patient did not reach the
target HbA1c
 Switch from short‑acting human insulin preparations to short‑acting insulin analogues if the patient prefers
injecting insulin immediately before a meal or recurrent hypoglycemic episodes or blood glucose levels rise
markedly after meals
5 – Monitoring by HbA1c measurement

Indications of self‑monitoring of blood glucose levels for adults with type 2 diabetes:
MRCP Revision Notes
 The patient is on insulin

 There is evidence of hypoglycemic episodes
 The patient is on oral medication that may increase their risk of hypoglycemia while driving or operating
machinery
 The patient is pregnant, or is planning to become pregnant
Short-term self-monitoring is indicated when starting treatment with oral or intravenous corticosteroids or to
confirm suspected hypoglycemia.
6 - Management of complications
 Amitriptyline, duloxetine, gabapentin or pregabalin as first line for neuropathic pain, capsaicin cream for
localized neuropathic pain
 Trigeminal neuralgia is managed by carbamazepine
 Gastroparesis is managed by domperidone as first line and erythromycin or metoclopramide as alternatives
Metabolic Syndrome
Metabolic syndrome is a multiplex risk factor that arises from insulin resistance accompanying abnormal fat
deposition.
It is a risk factor for coronary heart disease, as well as for diabetes, fatty liver, and several cancers.
Signs and symptoms

 Hypertension  Abdominal obesity
 Hyperglycemia  Acanthosis nigricans, hirsutism, peripheral
 Hypertriglyceridemia neuropathy, and retinopathy
 Reduced high-density lipoprotein cholesterol  Xanthomas
(HDL-C)
Diagnosis
For a diagnosis of metabolic syndrome at least 3 of the following should be identified:
 Waist circumference > 102 cm in men and > 88 cm women

 Triglycerides > 1.7 mmol/L
 HDL-C < 1.03 mmol/L in males and < 1.29 mmol/L in females
 Blood pressure > 130/85 mmHg or active treatment of hypertension
 Fasting plasma glucose > 5.6 mmol/L or previously diagnosed type 2 diabetes
Management
 Lifestyle change and weight loss are considered the first line management
 Statins for elevated LDL-C
 Nicotinic acid for decreased HDL-C
 Metformin for hyperglycemia
MRCP Revision Notes
MRCP Revision Notes
Hematology & Oncology

Iron Deficiency Anemia
Iron deficiency anemia develops when body stores of iron drop too low to support normal red blood cell (RBC)
production.
Causes
 Dietary iron deficiency (most common cause)
 Dietary substances that diminish the absorption iron include phytates, oxalates, phosphates, and carbonates
 Internal and external hemorrhage
 Hemosiderinuria, hemoglobinuria, and pulmonary hemosiderosis
 Malabsorption of iron due to extensive surgical removal of the proximal small bowel or chronic diseases as celiac
syndrome
Signs and symptoms

 Pallor of the mucous membranes
 Myocardial ischemia  Esophageal webbing and gastric atrophy

 Cold intolerance  Koilonychia (spoon-shaped nails)
 Angular stomatitis  Glossitis
MRCP Revision Notes
Diagnosis
 Complete Blood Count shows decreased mean corpuscular volume (MCV) and the mean corpuscular hemoglobin
concentration (MCHC) (microcytic hypochromic)
 Low serum iron and ferritin (storage protein) levels with elevated transferrin (transporting protein) and total iron-
binding capacity (serum iron and serum iron-binding protein levels)( TIBC) and decreased transferrin saturation
(serum iron divided by total iron-binding capacity)
Management
 Underlying etiology should be corrected and improve dietary measures
 Oral iron therapy (ferrous sulfate 325 mg TDS)
 Parenteral iron therapy is reserved for patients who are either unable to absorb oral iron or who have increasing
anemia despite adequate doses of oral iron
Anemia of Chronic Disease

Anemia of chronic disease is an absolute reduction of the total number of circulating red blood cells due to decreased
RBC production.
Signs and symptoms

 Generalized weakness or malaise  Palpitations
 Lightheadedness, dizziness  Cold intolerance
 Syncope or near-syncope  Inability to concentrate
 Decreased exercise tolerance  Skin pallor
MRCP Revision Notes
Diagnosis
 Complete blood count shows decreased RBC count with normocytic normochromic picture
 Iron studies show low serum iron, TIBC and transferrin levels with elevated ferritin and normal transferrin saturation
(due to low iron and TIBC)
Thalassemia
Thalassemia is an inherited autosomal recessive blood disorders characterized by formation of abnormal hemoglobin.
Types of human hemoglobin

 Adults (hemoglobin A) is composed of 2 alpha and 2 beta chains
 Fetal hemoglobin F is composed of 2 alpha chains and 2 gamma chains
 Hemoglobin A2 is composed of 2 alpha chains and 2 delta chains
Alpha Thalassemia
Alpha thalassemia is caused by deficient expression of 1 or more of the 4 alpha-globin genes on chromosome 16 causing
reduced synthesis of alpha-globin chains which results in an excess of gamma-globin chains in fetuses and newborns and
of beta-globin chains in children and adults.
Types
 Alpha thalassemia major (hydrops fetalis): Individuals with this disorder cannot produce any functional alpha globin
and thus are unable to make any functional hemoglobin A, F, or A2
 Hemoglobin H disease: Inheritance of 1 normal alpha-globin gene, excess beta chains aggregate into tetramers
named HbH (HbH has a high affinity for oxygen). It is manifested by microcytic, hypochromic RBCs with increased
reticulocytes and target cells (densely stained RBC center surrounded by a pale, unstained ring)
 Alpha thalassemia trait: Inheritance of 2 normal alpha-globin genes, affected individuals are clinically normal but
frequently have minimal anemia (reticulocyte count is normal with reduced MCV and MCH and normal serum iron
and ferritin)
 Silent carrier: Persons who inherit 3 normal alpha-globin genes
Beta Thalassemia
Beta thalassemia is caused by a genetic deficiency in the synthesis of beta-globin chains.
Types
 Beta thalassemia major occurs in the homozygous state causing severe, transfusion-dependent anemia
 Beta thalassemia trait (thalassemia minor) occurs in the heterozygous state, the causes mild to moderate microcytic
anemia
Complications
 Extra-medullary hematopoiesis causing bone deformities
 Hypersplenism causing pancytopenia
 Gallstones
MRCP Revision Notes
 Complications of long-term transfusion therapy (iron overload and transfusion-associated infections)

 Increased risk for infections resulting from splenectomy
 Cholelithiasis
Diagnosis
 High indirect hyperbilirubinemia, low haptoglobin, and elevated lactate dehydrogenase due to hemolysis
 Peripheral blood smear shows mild, isolated microcytic anemia with target cells on beta thalassemia minor and
severe microcytic and hypochromic anemia with target cells, Heinz bodies and anisopoikilocytosis in beta
thalassemia major
 Normal iron studies

 Hemoglobin electrophoresis is diagnostic in beta thalassemia trait (minimal elevation of Hb A2 (4-6%)
Management of thalassemia
 Supplementation of iron or folic acid in mild anemia
 Patients with more severe anemia may require lifelong transfusion therapy with iron chelation
 Splenectomy is reserved for patients with symptoms of hypersplenism
MRCP Revision Notes
Sickle Cell Anemia

Sickle cell disease (SCD) is an autosomal recessive disorder resulting from the presence of a mutated form of hemoglobin
called hemoglobin S. HbS It is less soluble than HbA and has lower affinity for oxygen.
Signs and symptoms

 Growth retardation
 Acute painful crises due to blockage of the small blood vessels by sickling RBCs (triggered by hypoxemia,
dehydration and fever)
 Aplastic crisis due to infection with parvovirus B19 (severe anemia with low reticulocyte count)
 Splenic sequestration crisis (life-threatening anemia with rapid enlargement of the spleen and high reticulocyte
count)
 Acute chest syndrome (chest pain, fever, cough, tachypnea and pulmonary infiltrates) due to infection (mycoplasma
and chlamydia) or infarction or both
 Hemolytic crises causing acute accelerated drops in hemoglobin level
 Repeated infections with encapsulated organisms
 Hand-foot syndrome (Dactylitis and arthritis)
 Priapism
 CNS strokes
 Cholelithiasis
 Leg ulcers
Diagnosis
 Complete blood count shows hemoglobin levels in the range of 6-8 g/dl with a high reticulocyte count
 Blood film shows atypical sickle cells (Drepanocytes)and features of hyposplenism (target cells and Howell-Jolly
bodies)
 Hemoglobin electrophoresis is diagnostic
Management
 Hydroxyurea increases fetal hemoglobin which protects against sickling
 Long-term transfusion therapy (target hemoglobin levels to 10 g/dL)
 Opioids for the treatment of severe pain associated with a vaso-occlusive crisis
 Splenectomy with antibiotic prophylaxis and vaccinations
MRCP Revision Notes
 Stem cell transplantation is limited to patients younger than 16 years with HbSS or HbS-Beta thalassemia or who
have evidence of severe disease
Sideroblastic Anemia
Sideroblastic anemia is a form of anemia in which the bone marrow produces ringed sideroblasts (abnormal iron
granules in the mitochondria positioned around the nucleus).
It is presented by general symptoms of anemia including malaise, fatigue, and dyspnea on exertion
Causes
 Congenital  Lead poisoning
 Idiopathic  Alcohol
 Myelodysplasia  Drugs (anti-tuberculous agents, progesterone)
 Nutritional deficiencies (copper, vitamin B-6)  Hypothermia
Diagnosis
 Dimorphic anemia (normocytic + microcytic) and hypochromia
 Iron studies may show increased iron level with decreased TIBC
 Bone marrow aspiration and biopsy with staining with Prussian blue stain shows sideroblasts and increased iron
stores (diagnostic)
MRCP Revision Notes
Rheumatology & Autoimmune Disorders

Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic autoimmune systemic inflammatory disease of unknown cause leading to articular
and extra-articular manifestations. It is associated with HLA DR4.
Signs and symptoms

 Constitutional symptoms
 Joints show morning stiffness, tenderness, swelling and limitation of motion
 Joints deformities
 Swan neck deformity: DIP flexion with PIP hyperextension
 Boutonniere deformity: PIP flexion with DIP hyperextension
 Z deformity of the thumb: hyperextension of the interphalangeal joint, fixed flexion and subluxation of the
metacarpophalangeal joint
MRCP Revision Notes
Persistent symmetric polyarthritis of hands and feet (hallmark feature)

 Upper extremities (metacarpophalangeal, and interphalangeal joints [sparing distal phalangeal joints] , wrists,
elbows, shoulders)
 Lower extremities (ankles, feet, knees, hips)
 Cervical spine
Extra-articular manifestations
 Pulmonary fibrosis, pleural effusion, pulmonary nodules and bronchiolitis obliterans
 Pericarditis
 Subcutaneous nodules
 Mononeuritis multiplex
 Pyoderma gangrenosum
 Felty syndrome (RA + splenomegaly + pancytopenia predominantly neutropenia) is associated with HLA-DRW4
 Ocular manifestations as keratoconjunctivitis sicca (most common), episcleritis, scleritis and corneal ulceration
 Amyloidosis
Causes of anemia in rheumatoid arthritis

 Anemia of chronic disease (most common cause) (normocytic normochromic)
 NSAID induced GIT hemorrhage (hypocytic, hypochromic)
 B12-deficiency anemia
 Autoimmune hemolytic anemia
 Bone marrow hypoplasia due to DMARD therapy
Diagnosis (NICE guidelines 2015)
Lab findings
 CRP level are associated with disease activity and is used for monitoring
 Anti-cyclic citrullinated peptide antibodies (anti-CCP) is diagnostic
 Rheumatoid factor in 60-80% of patients (not specific)
 Antinuclear antibodies (ANA) in 40% of patients
MRCP Revision Notes
Imaging
 Early joint x-ray shows loss of joint space, periarticular osteoporosis and soft-tissue swelling, late x-ray shows
periarticular erosions and joint subluxation.
 Arthroscopy shows marked vascular proliferation and thickening of the synovial membrane.
Joint aspiration shows white blood cell count >2000/µL with neutrophil predominance (60-80%) and low glucose levels
Poor prognostic features

 Female sex  Positive RF
 Insidious onset  Poor functional status at presentation
 HLA DR4  Extra articular manifestations

DMARDs with or without steroids are first-line treatment for newly diagnosed active cases; tumor necrosis factor-α
(TNF-α) inhibitors (etanercept, infliximab) are used as alternatives or in combination to DMARDs.
DMARDs include methotrexate (the most widely used first line) sulfasalazine, leflunomide and hydroxychloroquine.
During pregnancy sulfasalazine and azathioprine are safe for management.
Systemic Lupus Erythematosus

Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease that can affect almost any organ
system and follows a relapsing and remitting course.
More than 90% of cases of SLE occur in women, frequently starting at childbearing age. It is associated with HLA B8, DR2
and DR3.
MRCP Revision Notes
Signs and symptoms

The classic presentation of SLE is a triad of fever, joint pain, and rash
 Dermatologic (malar rash, photosensitivity, discoid lupus)

 Musculoskeletal (arthralgia, arthropathy, myalgia, frank arthritis, avascular necrosis)
 Neuropsychiatric (seizure, psychosis)
 Pulmonary (pleurisy {the most common manifestation}, pleural effusion, pneumonitis, pulmonary hypertension and
pulmonary fibrosis)
 Cardiac (pericarditis, myocarditis and pericardial effusion)
 Hematologic (leukopenia, lymphopenia, anemia, thrombocytopenia)
 Mouth ulcers
 lymphadenopathy
 Raynaud phenomenon
SLE renal complications

 Class I: normal kidney
 Class II: mesangial glomerulonephritis
 Class III: focal and segmental proliferative glomerulonephritis
 Class IV: diffuse proliferative glomerulonephritis (the most common and severe form)
 Class V: diffuse membranous glomerulonephritis
 Class VI: sclerosing glomerulonephritis
Diagnosis
 ANA positive in 99% of cases (not specific for diagnosis but good as screening test)
 Rheumatoid factor positive in 20% of cases
 Anti-double stranded DNA (dsDNA) antibodies: highly specific (> 99%), but less sensitive (70%), it can be used for
disease monitoring
 Anti-Smith (SM) antibodies: most specific (> 99%), sensitivity (30%)
 Hypocomplementemia (C3, C4) due to formation of immune complexes (cryoglobulinemia causes decreased C4 with
normal C3)
Management
 Corticosteroids and hydroxychloroquine are used in SLE without major organ manifestations
 Immunosuppressive agents (azathioprine, methotrexate) are indicated in refractory cases or when steroid doses
cannot be reduced
Pregnancy SLE
Unlike many autoimmune diseases systemic lupus erythematous (SLE) often becomes worse during pregnancy and the
postpartum period and is associated with a risk of maternal autoantibodies crossing placenta. Fetal lupus is highly
associated with anti-Ro antibodies (SSA). It causes complications as congenital heart block.
It is managed by prophylactic corticosteroids.
MRCP Revision Notes
Drug-Induced Lupus Erythematosus

Drug-induced lupus erythematosus (DILE) is a variant of lupus erythematosus that resolves within days to months after
withdrawal of the culprit drug in a patient with no underlying immune system dysfunction.
Causes
 Procainamide  Chlorpromazine
 Isoniazid  Quinidine
 Minocycline  Penicillamine
 Hydralazine  Phenytoin
Features are as SLE but it differs in:

 Average age of onset of 50-70 years
 Female-to-male ratio of 1:1
 Renal, central nervous system, cutaneous involvement and Raynaud phenomenon are rare
 Pulmonary involvement is common
Diagnosis
 Anti-histone antibodies is present in in >95% of cases
 ANA positive in 100% of cases
 Anti-dsDNA is rare
 C3/C4 levels are normal
Systemic Scleroderma
Systemic scleroderma (sclerosis) is systemic autoimmune disease of unknown origin characterized by excessive
deposition of collagen and other connective tissue macromolecules in skin and multiple internal organs.
Types
 Limited cutaneous scleroderma is limited to the skin on the face, hands and feet
 Diffuse cutaneous scleroderma covers more of the skin with a risk of progressing to the visceral organs
 CREST syndrome (Calcinosis, Raynaud phenomenon, Esophageal dysmotility, Sclerodactyly and Telangiectasia) is a
subtype of limited systemic scleroderma
Other complications
 Pulmonary artery hypertension and restrictive lung disease
 Arthralgia and myalgia
 Myocardial fibrosis causing congestive heart failure and arrhythmias
 Chronic renal insufficiency and scleroderma renal crisis
 Primary biliary cirrhosis
 Sicca syndrome
 Cranial nerve palsy
MRCP Revision Notes
Diagnosis
 Elevated CXCL4 (platelet factor 4) serum levels, it is found in systemic scleroderma patients and higher levels
correlated with the severity of pulmonary manifestation
 ANA are present in about 90%-95% of patients
 Topoisomerase I antibodies (Scl-70) are present in 30% of patients with diffuse scleroderma
 Anti-centromere antibodies are associated with limited scleroderma and CREST syndrome
Management
 Scleroderma renal crisis is managed by ACE inhibitors
 Disease-modifying treatment (D-penicillamine, methotrexate, mycophenolate mofetil) for inhibiting tissue fibrosis
and vascular and immune system alterations
Poor prognostic factors (5-year survival is estimated to be about 80%)

 Younger age
 African descent
 Rapid progression of skin symptoms
 Greater extent of skin involvement
 Anemia
 Elevated erythrocyte sedimentation rate (ESR)
 Pulmonary, renal, and cardiac involvement
MRCP Revision Notes
Neurology
Alzheimer Disease
Alzheimer disease (AD) is an acquired disorder of cognitive and behavioral impairment that develops in the
hippocampus.
AD accounts for 50-75% of all cases of dementia. Dementia with Lewy bodies accounts for 20% of cases and Pick
disease accounts for 5% of cases.
Signs and symptoms
Mild Alzheimer disease

 Memory loss
 Increased anxiety
Moderate Alzheimer disease

 Increasing memory loss and confusion
 Problems recognizing friends and family members
 Difficulty with language (reading, writing, working with numbers and aphasia)
 Difficulty organizing thoughts and thinking logically
 Restlessness, agitation, anxiety, tearfulness, wandering
 Muscle twitches (parkinsonian)
Severe Alzheimer disease

 Patients with severe AD cannot recognize family
 Lack of bladder and bowel control
Diagnosis
 CSF markers as tau and phosphorylated tau are elevated, whereas amyloid levels are decreased
 MRI shows widespread cerebral atrophy, particularly the cortex and hippocampus with intraneuronal
neurofibrillary tangles and neuronal plaques
Management
 Cholinesterase inhibitors (Donepezil) slower declines on cognitive and functional measures in mild to
moderate cases, common adverse effects include anorexia, hallucinations, syncope, diarrhea and urinary
incontinence
 N -methyl-D-aspartate (NMDA) antagonist (memantine) slows the intracellular calcium accumulation and
thereby help prevent further nerve damage for moderate and severe cases
MRCP Revision Notes
Lewy Bodies Dementia

Dementia with Lewy bodies (DLB) is a progressive, degenerative dementia of unknown etiology. It accounts for
20% of cases of dementia.
Signs and symptoms

 Dementia
 Fluctuating confusion
 Parkinsonian motor features (rigidity and bradykinesia)
 Visual and non-visual hallucinations
 Recurrent syncope
 Sleep-pattern reversal
 Neuroleptic sensitivity (should be avoided) such as haloperidol
Diagnosis
 Cortical brain biopsy shows abnormal proteinaceous (alpha-synuclein) cytoplasmic inclusions (Lewy bodies)
 MRI brain shows hippocampal atrophy
Management
 Acetylcholinesterase inhibitors (Rivastigmine) is first line
 Atypical neuroleptics such as clozapine
 Dopamine agonists for parkinsonian (may precipitate hallucinations)
Pick Disease
Pick disease is a type of fronto-temporal Dementia. It accounts for 5% of dementia cases.
Signs and symptoms

 Progressive dementia
 Progressive aphasia
 Behavioral and personality changes (lack of concern, apathy, passivity, low motivation, absence of self-
monitoring, abnormal self-awareness)
Diagnosis
 CT and MRI shows selective atrophy of the frontal and temporal lobes
AIDS Dementia Complex
AIDS Dementia Complex (ADC) is one of the most common and clinically important CNS complications of late HIV-1
infection.
Signs and symptoms

 Dementia
MRCP Revision Notes
 Behavioral changes (loss of attention and concentration)

 Motor deficits
 Hyperreflexia
 Gait instability
Diagnosis
 MRI shows widespread cerebral atrophy with widened cortical sulci and enlarged ventricles
Management
 Aggressive antiretroviral therapy
Transient Global Amnesia

Transient global amnesia (TGA) is a neurological disorder characterized by a temporary but almost total
disruption of short-term memory with a range of problems accessing older memories.
Features
 Anterograde amnesia (inability to form new memory traces) with disorientation in time and in place, but never
in persons
 Retrograde amnesia for events of the preceding days or weeks and lasting from hours to years
 No focal neurological signs or epilepsy
 Self-identification, visual-spatial skills and social skills are preserved
MRCP Revision Notes
Management
 Reassurance with neurologist follow-up visits as prognosis is excellent
Normal Pressure Hydrocephalus

Normal pressure hydrocephalus (NPH) is a type of brain malfunction caused by decreased absorption of CSF
causing ventriculomegaly.
Signs and symptoms

Patients with NPH present with a gradually progressive disorder with the classic triad of:
 Gait disturbance (bradykinesia, broad-based and shuffling gait)

 Urinary incontinence
 Dementia
Diagnosis
 CT and MRI shows enlarged ventricles
 Diagnostic CSF removal (large volume lumbar puncture) shows improvement in symptoms
Management
 Surgical CSF shunting (ventriculo-peritoneal or ventriculo-atrial) is the mainstay management
Parkinson Disease
Parkinson disease is a degenerative disorder of the dopaminergic neurons in the substantia nigra of the central
nervous system.
MRCP Revision Notes
Classifications
 Primary or idiopathic
 Secondary or acquired
 Inherited (Juvenile onset Parkinson an autosomal recessive)
 Parkinson plus syndromes as multiple system atrophy and progressive supranuclear palsy
Signs and symptoms (classic triad)

 Bradykinesia (mask-like face and difficulty in initiating movement)
 Resting tremor (pill-rolling) with frequency of 3-5 Hz
 Rigidity (lead pipe and cogwheel)
Other features
 Sleep disturbances
 Depression or anhedonia
 REM sleep behavior disorder
Features of primary Parkinson disease vs. secondary causes

 Asymmetrical tremor (most specific)
 Rigidity is more common
Diagnosis (NICE 2017)

 Parkinson disease is a clinical diagnosis
Management (NICE 2017)

 Levodopa is of choice in the early stages of Parkinson disease and motor symptoms cause impact on the quality
of life
 Dopamine agonists as Apomorphine and Ropinirole (ergot-derived dopamine agonists as bromocriptine,
cabergoline, and pergolide are contraindicated), levodopa or MAO‑B inhibitors (Selegiline) are used in the
early stages of Parkinson disease and motor symptoms do not cause impact on the quality of life
 Dopamine agonists, MAO‑B inhibitors or COMT (Catechol-O-Methyl Transferase) inhibitors (Entacapone) are
added to levodopa in case of developed dyskinesia or motor fluctuations; amantadine is alternative and
anticholinergics (trihexyphenidyl, benztropine) are contraindicated
 Decarboxylase inhibitor (carbidopa) is added to levodopa to prevent peripheral metabolism of levodopa to
decrease systemic adverse effects
 Anticholinergic agents are used as first line in drug-induced Parkinson
Multiple System Atrophy

Multiple system atrophy (MSA) (Shy-Drager syndrome) is defined as an adult-onset, sporadic, rapidly progressive,
multisystem, neurodegenerative fatal disease of undetermined etiology.
MSA usually progresses more quickly than Parkinson disease. The average lifespan is 7.9 years and only 20%
survive past 12 years.
MRCP Revision Notes
Signs and symptoms

 Parkinsonism (akinetic-rigidity) with poor response to levodopa
 Autonomic dysfunction (urinary incontinence or urinary retention, postural hypotension and erectile
dysfunction)
 Cerebellar signs (ataxia)
Diagnosis
 MRI shows atrophy of cerebellum and brainstem
Progressive Supranuclear Palsy

Progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) is a neurodegenerative disease. It usually
develops after the sixth decade of life, and the diagnosis is purely clinical.
Signs and symptoms

 Prolonged phase marked by fatigue, headaches and depression
 Supranuclear ophthalmoplegia (vertical gaze with downgaze typically involved before upgaze)
 Pseudobulbar palsy (inability to control facial movements such as chewing and speaking)
 Parkinsonism (poor response to L-dopa)
 Behavioral, cognitive, and gait disturbances
 Frequent falls and impaired postural reflexes
 Neck dystonia
Management
 No medication is effective in halting the progression of PSP
 Medications may provide minimal symptomatic improvement as dopamine agonists and TCA
Progressive Multifocal Leukoencephalopathy

Progressive multifocal leukoencephalopathy is widespread CNS demyelination due to infection by JC virus.
PML occurs almost exclusively in patients with severe immune deficiency as AIDS and chronic immunosuppressive
medications.
Signs and symptoms

 Behavioral changes  Speech and visual impairment
 Motor weakness
Diagnosis
 MRI shows patchy demyelination
 Brain biopsy is diagnostic
MRCP Revision Notes
Management
 There is no effective treatment so treatment aims at reversing the immune deficiency (antiretroviral or
stopping immunosuppressive drugs ) to slow or stop the disease progression
MRCP Revision Notes
Ophthalmology
Retinal Vein Occlusion
Retinal vein occlusion (RVO) is the second most common cause of blindness from retinal vascular disease after diabetic
retinopathy.
Risk factors include increasing age, hypertension, diabetes, smoking, obesity and hypercoagulable disorders.
Classification
RVO is classified according to where the occlusion is located in to:
 Central retinal vein occlusion (CRVO)

 Hemi-retinal vein occlusion (HRVO)
 Branch retinal vein occlusion (BRVO)
Signs and symptoms

 BRVO may be asymptomatic and noted incidentally on funduscopic examination
 CRVO is presented with sudden painless monocular vision loss or dense central scotoma
 Funduscopic examination shows retinal hemorrhage, edema and dilated veins
Management
The treatment is aimed at maintaining visual acuity by monitoring the patient for and treating complications such as
macular edema and neovascularization.
MRCP Revision Notes
 Macular edema is treated with intravitreal anti-VEGF as first line and/or intravitreal steroids
 Neovascularization is treated with laser photocoagulation
Retinal Artery Occlusion

Retinal artery occlusion represents an ophthalmologic emergency, and delay in treatment may result in permanent loss
of vision.
Causes
 Embolism from heart or temporal arteritis
 Coagulopathies as sickle cell anemia, antiphospholipid syndrome and thrombophilia
 Carotid atherosclerosis and dissection
 Inflammatory endarteritis
 Migraine
Signs and symptoms

 Acute persistent painless loss of central vision
 Funduscopic examination shows cherry red spot, ground-glass retina and pale optic disc
Management
Early treatment < 2 h from onset of symptoms may be associated with increased visual recovery
 Immediate lowering of IOP using medical management (acetazolamide and mannitol), ocular massage and anterior
chamber paracentesis
MRCP Revision Notes
 Thrombolytics, hyperbaric oxygen and retrobulbar block may be tried
MRCP Revision Notes
Psychiatry
Depression
Depression is a state of low mood and aversion to activity that can affect a person thoughts, behavior, tendencies,
feelings, and sense of well-being.
Symptoms of classic depression including insomnia, anxiety, irritability, decreased appetite, weight gain or loss, social
withdrawal, and decreased sex drive
Depressive psychosis is a major depressive episode that is accompanied by psychotic symptoms including delusions
and/or hallucinations.
Seasonal affective disorder (SAD) is a mood disorder in which people who has normal mental health throughout most of
the year experience depressive symptoms in the winter or summer.
Management of depression (NICE guidelines 2018)

Mild depression
Group-based cognitive behavioral therapy with physical activity program is the management of choice for mild
depression
Medical treatment is indicated for mild depression with persistent symptoms or with a history of moderate to severe
depression. Medical treatment include selective serotonin reuptake inhibitors (1st line) or tricyclic antidepressants
Moderate to severe depression

Combination of antidepressant medication and a high-intensity psychological intervention
Schizophrenia
Schizophrenia is a brain disorder that affects how people think, feel, and perceive the world. The hallmark symptom of
schizophrenia is psychosis, such as experiencing auditory hallucinations and delusions.
Signs and symptoms

The symptoms of schizophrenia may be divided into the following 4 domains:
 Positive symptoms - Psychotic symptoms, such as auditory hallucinations

 Negative symptoms - Decrease in emotional range, poverty of speech, and loss of interests
 Cognitive symptoms - Neurocognitive deficits as in working memory and attention and in executive functions
 Mood symptoms - Patients often seem cheerful or sad and often depressed
Paranoid schizophrenia is associated with fixed false beliefs (delusions) as someone is trying to hurt him or the
government is spying on him.
MRCP Revision Notes
Auditory hallucinations are featured by:

 Two or more voices discussing the patient in the third person
 Thought echo
 Voices commenting on the patient’s behavior
Factors associated with poor prognosis

 Strong family history and monozygotic twin  History of social withdrawal
 Gradual onset  Lack of obvious precipitant
 Low IQ
Management
 Atypical antipsychotics diminish the positive symptoms of schizophrenia and prevent relapses
 Psychosocial treatment as social skills training and cognitive-behavioral therapy
MRCP Revision Notes
Infectious Diseases
Staphylococcus Aureus
Staphylococcus aureus is facultative anaerobic gram-positive cocci.
Virulence factors
Enzymes
 Staphylococcus aureus produces various enzymes such as coagulase, hyaluronidase, DNAse, staphylokinase
and beta-lactamase for drug resistance.
Toxins
 Depending on the strain, S. aureus is capable of secreting several exotoxins.
Superantigens
 Superantigens induce toxic shock syndrome.
Exfoliative toxins
 EF toxins are implicated in the disease staphylococcal scalded-skin syndrome.
Toxic shock Syndrome

Toxic shock syndrome (TSS) is a toxin-mediated acute life-threatening illness, usually precipitated by infection
with either Staphylococcus aureus or Streptococcus pyogenes (GAS).
Staphylococcus toxic shock syndrome (STSS) most commonly occurs in women, usually those who are using
tampons, and develops within 5 days after the onset of menstruation.
TSS caused by the Streptococcus pyogenes typically presents in people with pre-existing skin infections with the
bacteria
Signs and symptoms

 High fever, shock, malaise and confusion, which can rapidly progress to stupor and coma
 Rash (sunburn like) seen early in the course of illness and affects any region of the body, including the lips,
mouth, eyes, palms and soles. It desquamates, or peels off, after 10–14 days
MRCP Revision Notes
 Multiple organ failure
Diagnosis
For staphylococcal toxic shock syndrome, the diagnosis is based upon CDC criteria as follows (all must be present
for diagnosis):
 Body temperature > 38.9 °C (102.02 °F)

 Systolic blood pressure < 90 mmHg
 Diffuse macular erythroderma
 Desquamation (especially of the palms and soles) 1-2 weeks after onset
 Involvement of three or more organ systems
Management
 Admission to the intensive care unit particularly in the case of multiple organ failure
 The source of infection should be removed (tampon) or drained (abscesses)
 Antibiotic treatment should cover both S. pyogenes and S. aureus, this may include a combination of
cephalosporins, penicillin or vancomycin, the addition of clindamycin reduces toxin production
Gonorrhea
Gonorrhea is a purulent infection of the mucous membrane surfaces caused by Neisseria gonorrhoeae. N
gonorrhoeae is spread by sexual contact or through transmission during childbirth.
Signs and symptoms
In women
 Vaginal discharge described as thin, purulent, and mildly odorous
 Dysuria
 Intermenstrual bleeding
 Dyspareunia (painful intercourse)
MRCP Revision Notes
 Mild lower abdominal pain
Pelvic inflammatory disease signs symptoms

 The above symptoms became more severe
 Cervical motion tenderness
 Adnexal tenderness and adnexal mass
In males
 Urethritis with profuse, purulent, and blood tinged discharge
 Acute epididymitis
In males and females, disseminated gonococcal infection causes arthritis-dermatitis syndrome.
Neonatal infection
In neonates, bilateral conjunctivitis (ophthalmia neonatorum) often follows vaginal delivery from an untreated
mother with a gonococcal infection.
Diagnosis
 Culture is the most diagnostic test, it shows gram-negative coffee bean-shaped diplococci bacteria
 PCR
Management
 Cephalosporins as ceftriaxone and cefixime are the drugs of choice, doxycycline and ciprofloxacin are
alternatives
Chlamydial Genitourinary Infections

Chlamydiae are small gram-negative obligate intracellular microorganisms that preferentially infect squamo-
columnar epithelial cells.
They include the genera of Chlamydia trachomatis, Chlamydophila pneumoniae and Chlamydophila psittaci.
Chlamydia trachomatis infection is the most commonly reported bacterial sexually transmitted disease (STD). It
account for 60% of cases of non-gonococcal urethritis.
Signs and symptoms

 Unlike gonorrhea, most men and women who are infected are asymptomatic
 Dysuria and yellow muco-purulent discharge from the urethra
 Vaginal discharge and vaginal bleeding (postcoital or unrelated to menses)
 Dyspareunia
 Proctitis
 Progression to pelvic inflammatory disease
Newborns with chlamydial infection produce:

 Pneumonia beginning at 1-3 months
MRCP Revision Notes
 Conjunctivitis developing at 1-2 weeks
Diagnosis
 Culture on ordinary media is negative
 Nucleic Acid Amplification Tests (NAAT) have become the preferred diagnostic and screening test
 Molecular techniques for detecting antigen, DNA, or RNA/Rapid tests
Management
 Azithromycin and doxycycline as first-line drugs for non-gonococcal urethritis including Chlamydia
 Azithromycin or amoxicillin are the preferred drug regimens in pregnancy
Leprosy
Leprosy is a chronic infection caused by the acid-fast, rod-shaped bacillus Mycobacterium leprae.
Leprosy should be considered in anyone who has lived in the tropics or who has traveled for prolonged periods to
endemic areas (India, Brazil and Africa).
Types
 Lepromatous leprosy with minimal cellular immune response
 Tuberculoid leprosy with vigorous cellular immune response
Signs and symptoms of lepromatous leprosy

 Ulcers on hands or feet with ill-defined borders
 Iridocyclitis and corneal ulceration
 Loss of eyebrows and eyelashes, and nasal collapse (leonine facies)
 Erythema nodosum leprosum
 Axillary and inguinal adenopathy
Signs and symptoms of tuberculoid leprosy

 The initial lesion is often a sharply demarcated ovoid or serpiginous, hypopigmented macule accompanied by
loss of sensation (loss of sensation is a feature of tuberculoid leprosy unlike lepromatous leprosy)
MRCP Revision Notes
 Destruction of the normal skin organs such as sweat glands and hair follicles as the disease progresses
 Wasting and muscle weakness causing foot drop or clawed hands
Diagnosis
 Skin biopsy, nasal smears or both for acid-fast bacilli using Fite stain
Management
 Single-dose treatment with rifampicin, minocycline or ofloxacin in patients with single skin lesion
 Multidrug regimen includes rifampicin, dapsone and clofazimine for extensive disease
MRCP Revision Notes
Dermatology & Allergic Disorders

Anaphylaxis
Anaphylaxis is an acute, potentially fatal systemic reaction caused by the release of chemical mediators from mast cells
and basophils.
It is mediated by IgE bound to mast cells which causes immediate releasing of mediators (Type 1 hypersensitivity
reaction).
Signs and symptoms

 Dermatologic: Flushing, urticaria, angioedema, cutaneous and conjunctival injection
 Respiratory: Nasal congestion, wheezing, hoarseness and dyspnea
 Cardiovascular: Dizziness, syncope and palpitations
 Neurologic: Headache, dizziness and seizure
Diagnosis
 Plasma and urinary histamine and serum tryptase assessment are signs of mast cells degranulation
Management
 Supportive care by airway management, cardiac monitoring, IV access and fluid resuscitation
 Adrenaline is the drug of choice; doses are IM 0.5 ml of 1/1000 or IV 5 ml of 1/10000 repeated every 15 minutes
Systemic Mastocytosis
Systemic Mastocytosis is a neoplastic proliferation of mast cells.
Signs and symptoms

 Urticaria pigmentosa - produces a wheal on rubbing (Darier sign)
 Flushing
 Abdominal pain
 Hepatosplenomegaly and lymphadenopathy
Diagnosis
 Monocytosis on the blood film
 Raised serum tryptase levels
 Increased urinary histamine
 Bone marrow aspiration and biopsy is diagnostic
Management is symptomatic for anaphylactic manifestations
MRCP Revision Notes
Hereditary Angioedema
Hereditary angioedema is an autosomal dominant condition associated with low plasma levels of the complement 1
inhibitor (C1-INH) protein. It is associated with episodic attacks of edema formation that can have catastrophic
consequences.
Acquired angioedema is usually caused by allergy and occurs together with other allergic symptoms and urticaria. It can
also occur as a side effect to certain medications as ACE inhibitors.
Signs and symptoms

HAE causes non-inflammatory swelling of the skin and mucous membranes. The prominent sites include:
 Larynx and tongue causing laryngeal edema and upper airway obstruction
 Abdominal organs causing vomiting, diarrhea or paroxysmal colicky pain that can mimic appendicitis
 Subcutaneous tissues causing edema of the face, hands, arms, legs, genitals and buttocks
Diagnosis
 Low C1 esterase inhibitor (C1-INH) protein level is diagnostic
 Low C4 level
 Normal C1q level
Management
 C1-INH concentrate, selective bradykinin B2 receptor antagonist and kallikrein inhibitor are of choice during attacks
 Prophylaxis with danazol
Lichen Planus
Lichen planus is a cell-mediated immune response of unknown origin. It may be associated with hepatitis C virus or
other autoimmune diseases as ulcerative colitis, alopecia areata, Vitiligo, dermatomyositis, morphea, lichen sclerosis,
primary biliary cirrhosis and myasthenia gravis.
Signs and symptoms

 Itchy, papular, flat-topped and shiny rash overlying network of fine white lines (Wickham striae) which may produce
vesicles on sun exposed areas
MRCP Revision Notes
 Oral and mucus membranes lesions are white or gray streaks forming a linear or reticular pattern on a violaceous
background
 Nail longitudinal grooving and ridging, subungual hyperkeratosis and onycholysis
 Scarring alopecia
 Koebner phenomenon (lesions in old scars)
MRCP Revision Notes
Management
 Topical steroids for mild and cutaneous disease
 Oral steroids or immunosuppression for scalp, nail, and mucous membrane involvement
Actinic Keratosis
Actinic keratosis (AK) is a UV light-induced lesion of the skin that may progress to invasive squamous cell carcinoma.
The lesions begin as small, rough spots that are easier felt as sandpaper like texture; later the lesions enlarge, usually
becoming red and scaly.
Management
 Medical therapy include topical 5-fluorouracil (5-FU), imiquimod cream and topical diclofenac gel
 Photodynamic therapy
 Surgery as cryosurgery, curettage and shave excision for extensive disease
Keratoacanthoma
Keratoacanthoma (KA) is a relatively common low-grade tumor that originates in the pilosebaceous glands and closely
resembles squamous cell carcinoma (SCC).
Keratoacanthoma typically grows rapidly, attaining 1-2 cm within weeks, followed by a slow involution period lasting up
to 1 year and leaving a residual scar.
Lesion typically is solitary, roundish, skin-colored or reddish papule that rapidly progress to dome-shaped nodule with a
smooth shiny surface and a central crateriform ulceration or keratin plug that may project like a horn.
MRCP Revision Notes
Management is primarily by surgical resection.
Kaposi Sarcoma
Kaposi sarcoma is a spindle-cell tumor thought to be derived from endothelial cell lineage. This condition carries a
variable clinical course ranging from minimal mucocutaneous disease to extensive organ involvement.
It is usually immunocompromised or AIDS-related (CD4 count < 200). It is caused by HHV-8 (human herpes virus 8).
Features of cutaneous lesions

 Non-pruritic macular, papular, nodular, or plaque-like lesion
 Lesions may assume a brown, pink, red, or violaceous color
 Lesions may range in size from several millimeters to several centimeters in diameter
 Mucous membrane involvement is common (palate, gingiva, and conjunctiva)
Features of organ lesions

 Gastrointestinal lesions can occur anywhere in the gastrointestinal tract causing hematemesis, hematochezia,
melena and bowel obstruction
 Pulmonary lesions cause hemoptysis and chest pain
 Rare central nervous system lesions
Management
 Highly active antiretroviral therapy (HAART) for HIV infection
 Local therapy (radiation, laser or surgical excision) for locally advanced symptomatic disease
MRCP Revision Notes
MRCP Revision Notes
Pharmacology & Toxicology

Pharmacokinetics
The following are the most commonly measured pharmacokinetic metrics:
 Cmax: The peak plasma concentration of a drug after administration

 Tmax: Time to reach Cmax
 Volume of distribution: The apparent volume in which a drug is distributed (the parameter relating drug
concentration to drug amount in the body)
 Elimination half-life: The time required for the concentration of the drug to reach half of its original value, it is
related to lipid solubility (longer for lipid soluble drugs) and the rate of drug clearance
 Bioavailability: The proportion of the drug that reaches its site of action, IV administration of a drug provides
bioavailability 100% and it decrease if oral drug with first pass metabolism
 Affinity is the attraction between a drug and its receptor. Affinity and intrinsic activity are determinants of potency
of a drug
 Clearance: The volume of plasma cleared of the drug per unit time; it is estimated by glomerular filtration rate (renal
failure delay clearance)
Drug Metabolism
Drug metabolism is the metabolic breakdown of drugs through specialized enzymatic systems. It usually involves two
types of biochemical reactions; phase I and phase II reactions
Phase I modification
Phase I reactions occur by oxidation, reduction, hydrolysis, cyclization, decyclization, and addition of oxygen or removal
of hydrogen, carried out by mixed function oxidases enzymes as cytochrome P-450.
Phase II conjugation
Phase II reactions occur by methylation, sulphation, acetylation, glucuronidation and glutathione and glycine
conjugation.
First pass metabolism

This is a phenomenon where the concentration of a drug is greatly reduced before it reaches the systemic circulation
due to hepatic metabolism. As a consequence much larger doses are need orally than if given by other routes.
Examples of drugs exhibiting extensive first pass metabolism

 Aspirin  Lignocaine
 Isosorbide dinitrate  Propranolol
 Glyceryl trinitrate  Verapamil
 Testosterone  Hydrocortisone
MRCP Revision Notes
Acetylator status
Many drugs are metabolized in the liver by acetylation; some patients may show deficient in hepatic N-acetyl-
transferase known as slow acetylators which leads to increased drugs adverse effects.
Drugs affected include:

 Procainamide  Isoniazid
 Sulfasalazine  Dapsone
 Hydralazine  Sulphonamides
Therapeutic drug monitoring

Therapeutic drug monitoring (TDM) main focus is on drugs with a narrow therapeutic range. Examples include
Drug Time of sample taken

Lithium 12 hours post-dose
Digoxin 6 hours post-dose
Cyclosporine immediately before next dose
Phenytoin immediately before next dose
Elimination kinetics
Zero-order kinetics
Zero-order kinetics means elimination of a drug from the body in a constant quantity per time despite the decrease in
the concentration of the drug over time.
In practice; zero-order kinetics drugs concentration need to be monitored as their metabolism enzymes are saturated.
Examples include Ethanol, Phenytoin, Salicylates, Cisplatin, Fluoxetine and Omeprazole
First order kinetics

First order elimination kinetics means elimination of the drug from the body is proportional to the drug concentration
(decline in the concentration decreases elimination).
95% of the drugs follow the first order elimination kinetics roles.
Digoxin
Digoxin is a purified cardiac glycoside. The primary mechanism of action is inhibition of the Na+/K+ ATPase in the
myocardium causing increase in the force of cardiac muscle contraction and decrease conduction through the
atrioventricular node.
MRCP Revision Notes
Digoxin is usually given orally, but can also be given by IV injection in urgent situations. The half-life is about 36 hours for
patients with normal renal function due to large volume of distribution.
Digitalizing patient with 1-1.5 mg orally over 24 hours in divided doses then digoxin is given once daily, usually in 125-μg
or 250-μg doses.
Medical uses
 Atrial fibrillation and atrial flutter (beta blockers and/or calcium channel blockers are a better first choices)
 Symptomatic treatment for congestive heart failure (no mortality benefit)
Precipitating factors for toxicity

 Renal failure
 Myocardial ischemia
 Hypoalbuminemia
 Hypothermia
 Hypothyroidism
 Hypokalemia, hypomagnesemia, hypercalcemia, hypernatremia, acidosis
 Drugs: amiodarone, quinidine, verapamil, spironolactone
Signs of toxicity
 Nausea, vomiting, and diarrhea
 Blurred vision and visual disturbances (yellow-green halos)
 Confusion, drowsiness, convulsions, insomnia, nightmares and depression
 Shortened QRS complex with flattened or inverted T waves in ECG
 Atrial or ventricular extra-systoles, paroxysmal atrial tachycardia with AV block
 Thrombocytopenia
 Gynecomastia
Management of toxicity
 Correction of hyperkalemia and other mineral deficits
 Atropine or temporary pacing for bradyarrhythmia
 Phenytoin for ventricular tachycardia, lidocaine is alternative (anti-arrhythmic drugs should be avoided as they can
precipitate asystole or VF), DC cardioversion is reserved for resistant cases
Digoxin-specific Fab fragment (Digibind) is indicated in:

 Hemodynamic instability
 Life-threatening arrhythmias
 Plasma digoxin level >13nmol/l
 Ingestion of more than 10 mg digoxin in adults and 4 mg in children
MRCP Revision Notes
Adenosine
Adenosine is an agonist of the A1 receptor which inhibits adenylyl cyclase thus reducing cAMP and causing
hyperpolarization by increasing outward potassium flux.
It has a very short half-life of about 8-10 seconds.
It is used in diagnosis and management of supraventricular tachycardia (SVT) as it terminates atrioventricular nodal re-
entrant tachycardia (AVNRT) and atrioventricular re-entrant tachycardia (AVRT).
It causes transient AV block causing worsening of sinus tachycardia, atrial fibrillation and atrial flutter. It has no effect on
ventricular tachycardia.
The effects of adenosine are enhanced by dipyridamole and blocked by theophylline.
Adverse effects
 Chest pain
 Bronchospasm
 Enhances conduction down accessory pathways (exacerbate WPW syndrome)
Amiodarone
Amiodarone is a class III antiarrhythmic agent used for various types of cardiac dysrhythmias, both ventricular and atrial.
Amiodarone shows B-blocker-like and potassium channel blocker-like actions on the SA and AV nodes; it increases the
refractory period via sodium- and potassium-channel effects, and slows intra-cardiac conduction of the cardiac action
potential via sodium-channel effects.
Medical uses
 Ventricular fibrillation and pulseless ventricular tachycardia
 Ventricular tachycardia in hemodynamic stable patient
 Atrial fibrillation with acute onset only not long term management
Complications and side effects

 Pulmonary fibrosis and pleural effusions  Blue-grey skin discoloration
 Hypothyroidism and hyperthyroidism  Peripheral neuropathies
 Corneal micro-deposits  Epididymitis
 Hepatitis  Gynecomastia
 Photosensitivity
Drug interactions
Amiodarone is a cytochrome P450 inhibitor which causes reduction of the clearance of many drugs as:
 Cyclosporine  Flecainide
 Digoxin  Sildenafil
MRCP Revision Notes
 Simvastatin  Warfarin
 Theophylline
Flecainide
Flecainide is a class Ic antiarrhythmic agent. It slows conduction of the action potential by acting as a potent sodium
channel blocker.
Medical uses
 Atrial fibrillation (rhythm control)
 SVT associated with accessory pathway
Adverse effects
 Increase mortality post myocardial infarction and is therefore contraindicated
 Torsades de pointes (prolongation of the PR interval and widening of the QRS)
 Oral paraesthesia
 Visual disturbances
Vaughan Williams Classification of antiarrhythmic drugs

Class Example Mechanism of action
Ia Disopyramide and Quinidine Block sodium channels
Ib Lidocaine Block sodium channels
Ic Flecainide Block sodium channels
II Propranolol Beta antagonists
III Amiodarone Block potassium channels
IV Verapamil Calcium channel blockers
MRCP Revision Notes
Genetics & Hereditary Disorders

Patterns of Inheritance
Autosomal dominant inheritance
Features
 Males and females are equally affected.
 All individuals inheriting the abnormal gene are affected.
 Offspring of affected parents (irrespective of the parental sex) have a 50% chance of inheriting the disease.
Examples
 Acute intermittent porphyria  Marfan syndrome
 Adult polycystic disease  Myotonic dystrophy
 Antithrombin III deficiency  Neurofibromatosis
 Ehlers-Danlos syndrome  Noonan syndrome
 Familial adenomatous polyposis  Peutz-Jeghers syndrome
 Hereditary non-polyposis colorectal carcinoma  Retinoblastoma
 Hereditary hemorrhagic telangiectasia  Romano-Ward syndrome
 Hereditary spherocytosis  Tuberose sclerosis
 Huntington disease  Von-Hippel-Lindau syndrome
 Hypokalemic periodic paralysis  Von Willebrand disease
Autosomal recessive inheritance
Features
 Males and females are equally affected, but are fewer in number than in autosomal dominant conditions.
 Not all generations will be affected.
 If both parents are carriers for the recessive gene 25% of the offspring will be affected, 50% will become carriers, but
will not have the disease and 25% will not have the abnormal gene.
 If an affected individual marries a carrier, then 50% off -spring will be affected and 50% offspring will be carriers.
 If an affected individual marries another affected, then all offspring will be affected
Examples
 Ataxia telangiectasia  Gilbert syndrome
 Congenital adrenal hyperplasia  Hemochromatosis
 Cystic fibrosis  Homocystinuria
 Cystinuria  Phenylketonuria
 Familial Mediterranean Fever  Sickle cell anemia
 Fanconi anemia  Thalassemia
 Friedreich ataxia  Wilson disease
MRCP Revision Notes
X-linked dominant inheritance
Features
 Males and females are both affected.
 No male-to-male transmission.
 Affected males transmit the disease to 100% of their daughters.
 An affected female will transmit the disease to 50% of all offspring.
Examples
 Alport syndrome
 Vitamin D resistant rickets
X-linked recessive inheritance
Features
 Only males are affected but not carriers
 No male-to-male transmission
 Females are carriers
 Daughters of affected males will be carriers
 Female carrier will have 50% affected sons and 50% daughters who are carriers
Examples
 Androgen insensitivity syndrome  Hemophilia A and B
 Becker muscular dystrophy  Lesch-Nyhan syndrome
 Duchenne and Becker muscular dystrophy  Nephrogenic diabetes insipidus
 Fabry disease  Retinitis pigmentosa
 G6PD deficiency  Wiskott-Aldrich syndrome
Maternal mitochondrial genetic abnormalities
Features
 During conception, only mitochondria from the ovum are passed on to the zygote.
 Affected females will pass the disease to 100% off spring
 Affected males will not transmit disease to offspring.
Examples
 Leber optic atrophy
 Kearnes-Sayer syndrome
 MELAS (mitochondrial encephalopathy, lactic acidosis and stroke-like syndrome)
 MERF (mitochondrial encephalopathy and red ragged fibres)
MRCP Revision Notes
Neurofibromatosis
Neurofibromatosis is an autosomal dominant disorder that disturbs cell growth in your nervous system, causing
tumors to form on nerve tissue.
Neurofibromatosis type I (Recklinghausen syndrome)

It is caused by a gene mutation on chromosome 17 which encodes neurofibromin.
Clinical diagnosis requires the presence of at least 2 of 7 criteria:
 Six or more café-au-lait spots
 Two or more Axillary or inguinal freckles
 Two or more typical neurofibromas
MRCP Revision Notes
 Two or more Lisch nodules (iris hamartoma)
 Optic nerve glioma

 Sphenoid dysplasia or typical long-bone abnormalities such as pseudarthrosis
 First-degree relative with NF1
Other signs and symptoms

 Learning disabilities  Short stature
 Larger than average head size  Hypertension
Neurofibromatosis type II
It is caused by gene mutation on chromosome 22; it causes bilateral acoustic neuroma and café-au-lait spots.
Causes of café-au-lait spots

 Neurofibromatosis type I and II  Fanconi anemia
 Tuberous sclerosis  Coffin-Siris syndrome
 McCune-Albright syndrome
MRCP Revision Notes
Basic Sciences & Statistics

Human Leukocyte Antigen
The human leukocyte antigen (HLA) system or complex is a gene complex encoding the major histocompatibility
complex (MHC) proteins in humans.
HLA allele Diseases with increased risk

Ankylosing spondylitis
HLA-B27 Gonococcal arthritis
Acute anterior uveitis
Reactive arthritis
Psoriatic arthritis
Systemic lupus erythematosus

HLA-DR2 Narcolepsy
Goodpasture syndrome
Autoimmune hepatitis
HLA-DR3 Primary biliary cirrhosis
Diabetes mellitus type 1
Dermatitis herpetiformis
Coeliac disease
Primary Sjogren syndrome
Systemic lupus erythematosus
HLA-DR4 Rheumatoid arthritis

Diabetes mellitus type 1
HLA-DR3 + DR4 Diabetes mellitus type 1
HLA-DQ2 + DQ8 Celiac disease
HLA-A3 Hemochromatosis
HLA-B5 Behcet disease
Hypersensitivity Reactions
Types of hypersensitivity reactions include:
Type I Immediate hypersensitivity (anaphylactic reaction)

It is mediated by IgE bound to mast cells. Examples include allergic dermatitis
MRCP Revision Notes
Type II Cytotoxic
IgG and IgM antibodies react directly with the antigen bound to the cell membrane. Examples include Rh
incompatibility, blood transfusion reactions, autoimmune hemolytic anemia and Goodpasture syndrome
Type III Immune complex

IgG and IgM bind antigen, forming antigen-antibody (immune) complexes. Examples include systemic lupus
erythematosus, leprosy, post-streptococcal glomerulonephritis and extrinsic allergic alveolitis
Type IV Cell-mediated
It is mediated by T-lymphocytes and macrophages. Examples include Lichen planus, Tuberculosis, graft versus host
disease, allergic contact dermatitis and chronic extrinsic allergic alveolitis.
ANCA
Anti-neutrophil cytoplasmic antibodies (ANCAs) are a group of IgG autoantibodies which are directed against
antigens in the cytoplasm of neutrophil granulocytes and monocytes.
They are detected as a blood test in a number of autoimmune disorders.
Types
C-ANCA
C-ANCA is directed to proteinase 3 (PR3) antigen. Associations:
 80-90% Wegner granulomatosis

 20-40% of microscopic polyangiitis
P-ANCA
P-ANCA directed to myeloperoxidase (MPO) antigens. Associations:
 50-80% of microscopic polyangiitis

 60% of Churg-Strauss syndrome
 25% of Wegner granulomatosis
Rare associations
 Inflammatory bowel disease
 Connective tissue disorders: RA, SLE, Sjogren syndrome
 Autoimmune hepatitis
Sensitivity and Specificity

Definitions
 True positive cases: Sick people correctly diagnosed as sick

MRCP Revision Notes
 False positive cases: Healthy people wrongly identified as sick

 True negative cases: Healthy people correctly identified as healthy
 False negative cases: Sick people wrongly identified as healthy
Sensitivity
Sensitivity = True positive cases / (True positive cases + False negative cases)
A sensitivity of 100% means that the test recognizes all sick people and the negative result is used to rule out the
disease.
Specificity
Specificity = True negative cases / (True negative cases + False positive cases)
A specificity of 100% means that the test recognizes all healthy people as healthy and a positive result in a high
specificity test is used to confirm the disease.
 Likelihood ratio for a positive test result = sensitivity / (1 - specificity)

 Likelihood ratio for a negative test result = (1 - sensitivity) /specificity
Positive predictive value

Positive predictive value is the proportion of actual positives.
PPV = True positive cases / (True positive cases + False positive cases)
Negative predictive value

Negative predictive value is the proportion of actual negatives.
NPV = True negative cases / (True negative cases + False negative cases)

MRCP Revision Notes
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MRCP Revision Notes

05 Alpha-1 Antitrypsin Deficiency 30 Coal Workers' Pneumoconiosis

Gastroenterology & Hepatology

31 Hirschsprung Disease 51 Gilbert Syndrome

Nephrology & Minerals Metabolism

41 Hyponatremia 47 Metabolic Alkalosis

Endocrinology & Diabetes

68 Metabolic Syndrome 70 Anorexia Nervosa

Hematology & Oncology

Rheumatology & Autoimmune Disorders

17 Osteoarthritis 30 Reactive Arthritis

55 Basilar Artery Occlusion 92 Ptosis

07 Cataract 11 Herpes Simplex Keratitis

Dermatology & Allergic Disorders

Pharmacology & Toxicology

07 Flecainide 40 Dopamine Agonists

Genetics & Hereditary Disorders

15 Marfan Syndrome 19 Refsum Disease

Basic Sciences & Statistics

Diagnosis of stable angina is unlikely if the chest pain is:

Providing immediate relief

Anti-anginal drug treatment

Secondary prevention of cardiovascular disease

The test is positive in:

Indications of referral to coronary angiography (severe cases with poor prognosis):

Pain of MI differs from angina pain in:

 History of ischemic discomfort  Rise and fall in serum cardiac markers

Coronary territories on ECG

Acute management (NICE guidelines 2013)

 Aspirin and clopidogrel  Subcutaneous low-molecular-weight heparin

Percutaneous coronary intervention

Common side-effects include hemorrhage, hypotension and allergic reactions.

Secondary prevention (NICE guidelines 2013)

Secondary prevention for myocardial infarction within 12 months:

Secondary prevention for myocardial infarction after a year:

Post Myocardial Infarction Complications

Ventricular septal rupture

Left ventricular aneurysm

Diagnosis of acute heart failure (NICE guidelines 2014)

Acute decompensating (NICE guidelines 2014)

Treatment after stabilization

 ACE inhibitors  Hydralazine with nitrates

Anticoagulation with warfarin is indicated in:

Cardiac resynchronization therapy

 NYHA class III-IV  On optimal medical therapy

Implantable cardioverter defibrillators

Left ventricular assist device

B-type Natriuretic Peptide

BNP level is increased in:

Extrinsic or atopic asthma

Intrinsic or cryptogenic asthma

Signs and symptoms

Classifications of asthma exacerbations

Acute severe asthma

Respiratory function tests show (obstructive RF):

Spirometry shows (diagnostic procedure):