Pathophysiology of Disease Flashcards Edited by Yeong Kwok, MD, Stephen J McPhee, MD, Gary D Hammer, MD, PhD University of Michigan, Ann Arbor & University of California, San Francisco New York Chicago San Francisco Athens London Madrid Mexico City Milan New Delhi Singapore Sydney Toronto Copyright © 2014 by McGraw-Hill Education All rights reserved Except as permitted under the United States Copyright Act of 1976, no part of this publication may be reproduced or distributed in any form or by any means, or stored in a database or retrieval system, without the prior written permission of the publisher ISBN: 978-0-07-182918-2 MHID: 0-07-182918-0 The material in this eBook also appears in the print version of this title: ISBN: 978-0-07-182916-8, MHID: 0-07-182916-4 eBook conversion by codeMantra Version 1.0 All trademarks are trademarks of their respective owners Rather than put a trademark symbol after every occurrence of a trademarked name, we use names in an editorial fashion only, and 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guarantee that the functions contained in the work will meet your requirements or that its operation will be uninterrupted or error free Neither McGraw-Hill Education nor its licensors shall be liable to you or anyone else for any inaccuracy, error or omission, regardless of cause, in the work or for any damages resulting therefrom McGraw-Hill Education has no responsibility for the content of any information accessed through the work Under no circumstances shall McGraw-Hill Education and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possibility of such damages This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise Contents 10 GENETIC DISEASE Osteogenesis Imperfecta Phenylketonuria Fragile X–Associated Mental Retardation Mitochondrial Disorders: Leber Hereditary Optic Neuropathy/Mitochondrial Encephalopathy with Ragged Red Fibers (LHON/MERRF) Down Syndrome DISORDERS OF THE IMMUNE SYSTEM Allergic Rhinitis Severe Combined Immunodefi ficiency Disease X-Linked Agammaglobulinemia Common Variable Immunodefi ficiency Acquired Immunodeficiency fi Syndrome (AIDS) INFECTIOUS DISEASES 11 Infective Endocarditis 12 Meningitis 1A-B 2A-B 3A-B 4A-B 5A-B 6A-B 7A-B 8A-B 9A-B 10A-B 11A-B 12A-B 13 Pneumonia 14 Diarrhea, Infectious 15 Sepsis, Sepsis Syndrome, Septic Shock 13A-B 14A-B 15A-B NEOPLASIA 17 18 19 20 21 22 Neuroendocrine Tumor (NET) Colon Carcinoma Breast Cancer Testicular Carcinoma Osteosarcoma Lymphoma Leukemia 16A-B 17A-B 18A-B 19A-B 20A-B 21A-B 22A-B 23 24 25 26 27 BLOOD DISORDERS Iron Defi ficiency Anemia Vitamin B12 Deficiency/Pernicious fi Anemia Cyclic Neutropenia Immune Thrombocytopenic Purpura Hypercoagulable States 23A-B 24A-B 25A-B 26A-B 27A-B 29 30 31 32 33 NERVOUS SYSTEM DISORDERS Amyotrophic Lateral Sclerosis (Motor Neuron Disease) Parkinson Disease Myasthenia Gravis Dementia Epilepsy Stroke 28A-B 29A-B 30A-B 31A-B 32A-B 33A-B 34 35 36 37 38 39 40 41 42 DISEASES OF THE SKIN Psoriasis Lichen Planus Erythema Multiforme Bullous Pemphigoid Leukocytoclastic Vasculitis Poison Ivy/Oak Erythema Nodosum Sarcoidosis Acne 34A-B 35A-B 36A-B 37A-B 38A-B 39A-B 40A-B 41A-B 42A-B 28 PULMONARY DISEASE 43 Obstructive Lung Disease: Asthma 43A-B 44 Obstructive Lung Disease: Chronic Obstructive Pulmonary Disease (COPD) 44A-B 45 Restrictive Lung Disease: Idiopathic Pulmonary Fibrosis 46 Pulmonary Edema 47 Pulmonary Embolism 48 Acute Respiratory Distress Syndrome (ARDS) 49 50 51 52 53 54 55 56 57 CARDIOVASCULAR DISORDERS: HEART DISEASE Arrhythmia Heart Failure Valvular Heart Disease: Aortic Stenosis Valvular Heart Disease: Aortic Regurgitation Valvular Heart Disease: Mitral Stenosis Valvular Heart Disease: Mitral Regurgitation Coronary Artery Disease Pericarditis Pericardial Effusion ff with Tamponade CARDIOVASCULAR DISORDERS: VASCULAR DISEASE 58 Atherosclerosis 59 Hypertension 60 Shock 45A-B 46A-B 47A-B 48A-B 49A-B 50A-B 51A-B 52A-B 53A-B 54A-B 55A-B 56A-B 57A-B 58A-B 59A-B 60A-B DISORDERS OF THE ADRENAL MEDULLA 61 Pheochromocytoma 61A-B 62 63 64 65 66 67 68 69 70 GASTROINTESTINAL DISEASE Achalasia Reflux fl Esophagitis Acid-Peptic Disease Gastroparesis Cholelithiasis and Cholecystitis Diarrhea, Non-Infectious Infl flammatory Bowel Disease: Crohn Disease Diverticular Disease (Diverticulosis) Irritable Bowel Syndrome LIVER DISEASE 71 Acute Hepatitis 72 Chronic Hepatitis B 73 Cirrhosis 74 75 76 77 62A-B 63A-B 64A-B 65A-B 66A-B 67A-B 68A-B 69A-B 70A-B 71A-B 72A-B 73A-B DISORDERS OF THE EXOCRINE PANCREAS Acute Pancreatitis 74A-B Chronic Pancreatitis 75A-B Pancreatic Insuffi fficiency 76A-B Carcinoma of the Pancreas 77A-B 78 79 80 81 82 RENAL DISEASE Acute Kidney Injury: Acute Tubular Necrosis Chronic Kidney Disease Poststreptococcal Glomerulonephritis Nephrotic Syndrome: Minimal Change Disease Renal Stone Disease 87 88 89 DISORDERS OF THE PARATHYROIDS & CALCIUM & PHOSPHORUS METABOLISM Primary Hyperparathyroidism Familial Hypocalciuric Hypercalcemia Hypercalcemia of Malignancy Hypoparathyroidism and Pseudohypoparathyroidism Medullary Carcinoma of the Thyroid Osteoporosis Osteomalacia 90 91 92 93 DISORDERS OF THE ENDOCRINE PANCREAS Diabetes Mellitus: Diabetic Ketoacidosis Insulinoma Glucagonoma Somatostatinoma 83 84 85 86 78A-B 79A-B 80A-B 81A-B 82A-B 83A-B 84A-B 85A-B 86A-B 87A-B 88A-B 89A-B 90A-B 91A-B 92A-B 93A-B 94 95 96 97 98 DISORDERS OF THE HYPOTHALAMUS & PITUITARY GLAND Obesity Pituitary Adenoma Panhypopituitarism Diabetes Insipidus Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH) 99 100 101 102 103 THYROID DISEASE Hyperthyroidism Hypothyroidism Goiter Thyroid Nodule and Neoplasm Familial Euthyroid Hyperthyroxinemia 104 105 106 107 DISORDERS OF THE ADRENAL CORTEX Cushing Syndrome Adrenal “Incidentaloma” Adrenocortical Insuffi fficiency Hyperaldosteronism (Primary Aldosteronism) 94A-B 95A-B 96A-B 97A-B 98A-B 99A-B 100A-B 101A-B 102A-B 103A-B 104A-B 105A-B 106A-B 107A-B 108 Type Hyporeninemic Hypoaldosteronism 109 Congenital Adrenal Hyperplasia 108A-B 109A-B DISORDERS OF THE FEMALE REPRODUCTIVE TRACT 110 Menstrual Disorders: Dysmenorrhea 111 Female Infertility 112 Preeclampsia-Eclampsia 110A-B 111A-B 112A-B DISORDERS OF THE MALE REPRODUCTIVE TRACT 113 Male Infertility 114 Benign Prostatic Hyperplasia 113A-B 114A-B 115 116 117 118 119 120 INFLAMMATORY RHEUMATIC DISEASES Gout Vasculitis Systemic Lupus Erythematosus Sjögren Syndrome Myositis Rheumatoid Arthritis 115A-B 116A-B 117A-B 118A-B 119A-B 120A-B Preface Pathophysiology of Disease: An Introduction to Clinical Medicine is the leading pathophysiology textbook, providing comprehensive coverage of the pathophysiologic basis of disease These Th Pathophysiology of Disease Flashcards provide study aids for 120 of the most common topics germane to medical practice Th Flashcards provide key questions regarding the topics for a The quick review and study aid for a variety of standardized examinations As such, they will be very useful to medical, nursing, and pharmacy students Each of the Flashcards begins with a clinical case and then presents key questions to help the reader think in a step-wise fashion through the various pathophysiologic aspects of the case Outstanding Features • 120 common pathophysiology topics useful to learners in their preparation for a variety of course and certifying examinations • Material drawn from the expert source, Pathophysiology of Disease: An Introduction to Clinical Medicine, now in its new 7th edition • Concise, consistent, and readable format, organized in a way that allows for quick study • Medical, nursing and pharmacy students, physician’s assistants (PAs) and nurse practitioners (NPs) in training will find their clear organization and brevity useful Organization Th 120 topics in the Flashcards were selected as core topics beThe cause of their relevance to both clinical practitioners and learners in order to enable understanding of the pathophysiologic basis of common diseases There is one Flashcard d for each topic At the top of the front side, a CASE is presented On the bottom of the front side and on the back side, key Questions are listed in reference to the pathophysiology of the clinical entity illustrated by the case To allow the user to think through their responses, the Answers to the questions are printed upside down The questions asked on these Flashcards help develop the Th learner’s knowledge of the pathophysiology associated with the disorder and thus support their clinical problem-solving skills regarding such cases These Th Flashcards follow the organization off Pathophysiology of Disease: An Introduction to Clinical Medicine, 7th edition which is organized by 23 disease categories: • GENETIC • INFECTIONS • BLOOD • SKIN • HEART DISEASE • ADRENAL MEDULLA • LIVER • RENAL • HYPOTHALAMUS & PITUITARY • ADRENAL CORTEX • FEMALE REPRODUCTIVE TRACT • PARATHYROID, CALCIUM & PHOSPHORUS • • • • • • • • • • • IMMUNE SYSTEM NEOPLASMS NERVOUS SYSTEM PULMONARY DISEASE VASCULAR DISEASE GASTROINTESTINAL TRACT EXOCRINE PANCREAS ENDOCRINE PANCREAS THYROID MALE REPRODUCTIVE TRACT INFLAMMATORY RHEUMATIC DISEASES Intended Audience Medical students will find fi these Flashcards to be useful as they prepare for their Pathophysiology or Introduction to Clinical Medicine course examinations, and the USMLE Part examination Nursing and pharmacy students, NPs and PAs taking their internal medicine rotations can review core topics as they prepare for their standardized examinations Yeong Kwok, MD Ann Arbor, Michigan Stephen J McPhee, MD San Francisco, California Gary D Hammer, MD, PhD Ann Arbor, Michigan March 2014 Osteogenesis Imperfecta, A A 4-week-old boy is brought in with pain and swelling of the right thigh An x-ray film fi reveals an acute fracture of the right femur Questioning of the mother reveals that the boy was born with two other known fractures—left ft humerus and right clavicle—which had been attributed to birth trauma The family history is notable for bone problems in several family members A diagnosis of type II osteogenesis imperfecta is entertained When and how does type II osteogenesis imperfecta present? To what these individuals succumb? • Of the four types of osteogenesis imperfecta, type II presents at or even before birth (diagnosed by prenatal ultrasound) There are multiple fractures, bony deformities, and • Th increased fragility of nonbony connective tissue • Death usually results during infancy due to respiratory difficulties ffi What are two typical radiologic findings fi in type II osteogenesis imperfecta? • Presence of isolated “islands” of mineralization in the skull (wormian bones) • Beaded appearance of the ribs 115 Gout, A tial hypertension and mild renal insuffi fficiency presents to the urgent care clinic complaining of pain in the right knee His primary care clinician had seen him week ago and added a thiazide diuretic to improve his blood pressure control He had been feeling well until the night before the urgent care clinic visit, when he noted some redness and slight swelling of his knee He went to sleep and was awakened early by significant fi swelling and pain He was able to walk only with assistance He has no history of knee trauma Physical examination confirmed fi the presence of a swollen right knee, which was erythematous and warm Joint aspiration recovered copious dark yellow, cloudy synovial fluid Microscopic analysis demonstrated 30,000 leukocytes/μL, a negative Gram stain, and many needle-like, negatively birefringent crystals consistent with urate crystals He was diagnosed as having acute gout What physical factors other than uric acid concentration influence fl crystal formation in gout? • Formation of crystals is markedly influenced fl by physical factors such as temperature and blood fl flow • The propensity for gout to involve distal joints (eg, great toes and ankles), which are cooler than other body parts, probably reflects fl the presence of local physical conditions such as the lower temperature at these sites that favor crystal formation • Gout attacks frequently occur in circumstances that increase serum uric acid levels, such as metabolic stressors leading to increased DNA or adenosine triphosphate (ATP) turnover (eg, sepsis, surgery, or dehydration) What are three metabolic conditions that can precipitate a gout flare? fl • Effi fficient phagocytosis of crystals, preventing activation of newly recruited infl flammatory cells • Increased heat and fluid infl flux, altering local physical and chemical conditions to favor crystal solubilization • Coating of crystals with serum proteins, rendering the surface of the crystals less inflammatory fl • Secretion of a variety of anti-inflammatory fl cytokines (eg, TGF-β) by activated joint macrophages • Phagocytosis of previously activated apoptotic neutrophils by macrophages in the joint, altering the balance of cytokines secreted by these macrophages in such a way that secretion of proinfl flammatory cytokines is inhibited while secretion of anti-inflammatory fl cytokines is enhanced Suggest five reasons why the intense acute infl flammatory response in gout typically resolves spontaneously over the course of several days even in the absence of therapy 115 Gout, B 116 Vasculitis, A week ago, he had been at an urgent care center with a sore throat and was diagnosed with “strep throat.” He was prescribed penicillin and had been getting better The day before presentation, he noted the development Th of a pink rash on his trunk, and on the day of his evaluation, it spread to his arms and legs On examination, the patient has a symmetric maculopapular rash covering his extremities and trunk Some of the lesions on his legs are palpable In what two immunologic settings does immune complex vasculitis occur, and which organs does it commonly affect? ff • Immune complex vasculitis is an acute infl flammatory disease of small blood vessels that occurs in the setting of ongoing antigen load and an established humoral (antibody) immune response • Tissues primarily aff ffected include: — Skin (leukocytoclastic vasculitis): rash, which appears as raised, red or violaceous papules (palpable purpura) — Joints: severe, rapid-onset and self-limited symmetric polyarthritis of medium and small joints — Kidney: immune complex–mediated glomerulonephritis • Immune complexes are effi fficiently cleared in most circumstances by the reticuloendothelial system and are only pathogenic when circulating immune complexes are deposited in the subendothelium, where they set in motion the complement cascade and activate myelomonocytic cells • The propensity for immune complexes to deposit is a function of the relative amounts of antigen and antibody and of the intrinsic features of the immune complex: composition, size, and solubility • The solubility of immune complexes is not a fixed property, because it is profoundly influenced fl by the relative concentrations of antigen and antibody, which generally change as an immune response evolves • For physicochemical reasons, soluble immune complexes formed at slight antigen excess are not eff ffectively cleared by the reticuloendothelial system and are of a size that allows them to gain access to and be deposited at subendothelial and extravascular sites • When antibody is present in excess, immune complexes are rapidly cleared by the reticuloendothelial system and deposition does not occur What three physical properties determine whether immune complexes will be deposited in vessel walls? 116 Vasculitis, B 117 Systemic Lupus Erythematosus, A tory of systemic lupus erythematosus (SLE) is evaluated at a medical clinic for intermittent arthralgias in her knees She denies any facial rash, photosensitivity, chest pain, or shortness of breath She is convinced she has lupus and requests confi firmatory blood tests What are the antigens against which antibodies are directed in SLE? • Nuclear: nucleosomes (dsDNA and histone core) and ribonucleoprotein complexes (Sm, nRNP, La, Ro [60 kDa]) • Cytoplasmic: ribosomal protein P, Ro [52 kDa] • Membrane-associated: anionic phospholipids or phospholipid-binding proteins What are three stimuli that typically provoke SLE flares? fl • Sunlight exposure (associated with both disease onset and flares) fl • Viral infection (Epstein-Barr virus exposure is strongly associated with SLE in children) • Certain drugs • Skin: ultraviolet light photosensitivity and a variety of SLE-specifi fic skin rashes including a rash over the malar region, discoid pigmentary changes to the external ear, and erythema over the dorsum of fingers fi • Joints: non-erosive symmetric polyarthritis • Kidneys: a spectrum of glomerulonephritides are a frequent major cause of morbidity and mortality • Blood: a variety of hematologic disturbances including hemolytic anemia, thrombocytopenia, and leukopenia • Serosal surfaces: infl flammation can result in pleuritis, pericarditis, and peritonitis • Central nervous system: seizures, organic brain syndrome What organ systems are most prominently affected ff in SLE? 117 Systemic Lupus Erythematosus, B • Although a viral cause of Sjögren syndrome remains speculative, several pathways have been implicated in its pathogenesis • Autoimmunity to epithelial tissues: an immune response directed against several ubiquitously expressed antigens (eg, Fodrin, Ro, and La) as well as to some antigens expressed specifi fically in secretory epithelial cells (eg, type muscarinic acetylcholine receptors [M3R]) • The antibodies to M3R are believed to prevent stimulated secretion of saliva and tears and may be important in the hyposecretion that characterizes the disease • Exocrine tissue infi filtration with activated cytotoxic lymphocytes induces death of duct and acinar epithelial cells, with resultant loss of functioning salivary tissue • Enrichment of HLA-DR3 in patients with Sjögren syndrome leads to possible enhanced ability to present peptides contained within the pathogenic autoantigens What are the steps in pathogenesis of Sjögren syndrome? plaining of dry eyes and mouth, progressively worsening over the past year At first, she thought it may have been worsening of her allergies, but her eyes feel irritated all of the time, as if she has sand in them She gets mild relief with over the counter eye drops Her mouth has also felt dry, and she has found it difficult ffi to eat certain foods such as bread and crackers or carry on prolonged conversations due to her tongue sticking to the roof of her mouth She recently saw her dentist and was found to have two cavities, the first since childhood Physical examination is normal except for mild injection of her conjunctivae 118 Sjưgren Syndrome, A • The most prominent presenting symptoms in Sjögren syndrome are: — Xerophthalmia (ocular dryness): eye irritation, foreign body sensation or pain, and risk for corneal ulcer or perforation — Xerostomia (dry mouth): impaired production of saliva, diffi fficulty in swallowing dry foods or in speaking at length, altered sensation of taste or of oral burning, new onset in mid-adult life of severe dental caries at the gum line • Other epithelial surfaces may be similarly aff ffected: skin, vaginal, and/or respiratory tract dryness with hoarseness and recurrent bronchitis • Possible systemic symptoms: fatigue, arthralgias, myalgias, and low-grade fever • Other potentially aff ffected organ systems include the kidneys, lungs, joints, and liver (resulting in interstitial nephritis, interstitial pneumonitis, nonerosive polyarthritis, and intrahepatic bile duct inflammation) fl • As many as half of aff ffected individuals experience autoimmune thyroid disease • Th Those with severe disease are at increased risk for cutaneous vasculitis (including palpable purpura and skin ulceration) and lymphoproliferative disorders (ie, mucosa-associated lymphoid tissue [MALT] lymphoma) What are the clinical manifestations of Sjögren syndrome? 118 Sjögren Syndrome, B 119 Myositis, A ffice with progressive weakness She had been in good health until about six weeks ago when she began having trouble getting up from a low chair Her muscle weakness has become more pronounced over time, and she now also has diffiffi culty climbing stairs and brushing her hair Her shoulders and thighs are mildly achy but not painful She is well-appearing with normal vital signs and an essentially normal physical examination with the exception of mild tenderness of her shoulders and thighs She does not have a rash Laboratory tests are notable for a creatine phosphokinase level of 840 IU/L (normal female: 26–180 IU/L) and an aldolase value of 32 IU/L (normal: 1.0–7.0 IU/L) Her electromyogram shows that her muscles produce sharp waves and spontaneous discharges She is diagnosed with polymyositis What are the clinical manifestations of polymyositis and dermatomyositis? • Gradual and progressive motor weakness aff ffecting the arms and legs, as well as the trunk, in association with histologic evidence of muscle inflammation fl • Proximal muscles are most frequently aff ffected, resulting in diffi fficulty rising from a seat or bed, ascending a flight of stairs, reaching up, or brushing one’s hair • If very severe, patients can have impaired swallowing of solid foods and impaired full lung expansion due to esophageal and diaphragmatic muscle involvement ffect smooth muscle and even • Rarely, the disease can aff cardiac muscle • Extramuscular involvement of the lung parenchyma (interstitial pulmonary fibrosis), fi peripheral joints (infl flammatory polyarthritis), and skin (dermatomyositis) can also occur • Cancer: several population-based studies link dermatomyositis and polymyositis with the development of cancer within the 1–5 years following diagnosis — For example, the diagnosis of dermatomyositis carries a 2-fold greater risk of incident malignancy, particularly of the stomach, lung, breast, colon, and ovary What other disease is the adult patients with polymyositis or dermatomyositis at risk for, usually within 1–5 years after diagnosis? • Polymyositis and dermatomyositis share several similar pathologic features but possess distinct ones as well • Common traits: patchy muscle involvement, presence of inflammatory fl infi filtrates, and areas of both muscle damage and regeneration flammation is located around • In polymyositis, infl individual muscle fibers (“perimyocyte”), and the infi filtrate is T-cell (CD8+ > CD4+) and macrophage-predominant • In dermatomyositis, the pathology is quite diff fferent with atrophy at the periphery of muscle bundles (“perifascicular atrophy”) Th The infi filtrate is predominantly B cells and CD4+ T cells, localized to the perifascicular space and surrounding capillaries (which are reduced in number) Activation of the complement cascade results in major capillary involvement What is the pathophysiology of polymyositis and dermatomyositis? 119 Myositis, B 120 Rheumatoid Arthritis, A week history of fatigue, bilateral hand pain and stiffness, ff together with hand and wrist joint swelling About a month before presentation, she noticed that her hands were stiffer ff in the morning, but thought that it was due to too much typing However, the stiffness ff has worsened, and she now needs about an hour each morning to “loosen up” her hands As the day goes on, the stiff ffness improves, although it does not go away entirely She has also noticed that her knuckles and wrists are swollen and feel somewhat warm Physical examination reveals warm, erythematous wrists and metacarpal joints bilaterally Hand x-ray films fi show periarticular demineralization and erosions, and blood test results are significant fi for a mild anemia, elevated sedimentation rate, and a positive rheumatoid factor Th The patient is diagnosed with rheumatoid arthritis What is the pathophysiology of rheumatoid arthritis? • Much of the pathologic damage that characterizes rheumatoid arthritis is centered around the synovial linings of joints • The synovium in rheumatoid arthritis is markedly abnormal, with a greatly expanded lining layer (8–10 cells thick) composed of activated cells and a highly inflammatory fl interstitium replete with B cells, T cells, and macrophages and vascular changes (including thrombosis and neovascularization) • Rheumatoid arthritis synovial tissue (called pannus) invades and destroys adjacent cartilage and bone • Genetic factors (twin concordance rate 15–35%) and nongenetic factors (several infectious agents, autoantibodies and elevated cytokines) are clearly involved • Treatment should be prompt and aggressive to prevent permanent joint erosion and deformity • Immune modifi fiers such as methotrexate and biologic modifi fiers of defi fined pathogenic pathways such as anti-tumor necrosis factor (TNF) therapy are the mainstays of treatment What characterizes the treatment for rheumatoid arthritis? • • • • Rheumatoid arthritis is most typically a persistent, progressive disease presenting in women in the middle years of life Fatigue and joint infl flammation, characterized by pain, swelling, warmth, and morning stiffness, ff are hallmarks of the disease Multiple small and large synovial joints are aff ffected on both sides of the body in a symmetric distribution Involvement of the small joints of the hands, wrists, and feet, as well as the larger peripheral joints, including the hips, knees, shoulders, and elbows, is typical • Involved joints are demineralized, and joint cartilage and juxtaarticular bone are eroded by the synovial infl flammation, inducing joint deformities • Cervical involvement can also occur, potentially leading to spinal instability • Extra-articular manifestations can include lung nodules, subcutaneous “rheumatoid” nodules (typically present fl (including over extensor surfaces), ocular inflammation scleritis), or small- to medium-sized arteritis What are the clinical manifestations of rheumatoid arthritis? 120 Rheumatoid Arthritis, B Index Achalasia Acid-peptic disease Acne Acquired immunodefi ficiency syndrome (AIDS) Acute kidney injury Acute respiratory distress syndrome (ARDS) Acute tubular necrosis Adrenal hyperplasia, congenital Adrenal “incidentaloma” Adrenocortical insuffi fficiency Allergic rhinitis Amyotrophic lateral sclerosis (motor neuron disease) Anemia, iron defi ficiency fi Anemia, vitamin B12 deficiency Aortic regurgitation Aortic stenosis Arrhythmia Atherosclerosis 62 64 42 Benign prostatic hyperplasia Breast cancer Bullous pemphigoid 10 78 16 Carcinoid 66 Cholelithiasis and Cholecystitis Chronic kidney disease 79 73 Cirrhosis Colon carcinoma 17 Common variable immunodefi ficiency Coronary artery disease 55 Crohn disease 68 Cushing syndrome 104 Cyclic neutropenia 25 E Epilepsy Erythema multiforme Erythema nodosum Dementia Diabetes insipidus Diabetes mellitus Diarrhea, infectious Diarrhea, noninfectious Diverticular disease Gastroparesis Glomerulonephritis, poststreptococcal Glucagonoma Goiter Gout 48 78 109 105 106 28 23 24 52 51 49 58 114 18 37 31 97 90 14 67 69 Diverticulosis Down syndrome Dysmenorrhea Familial euthyroid hyperthyroxinemia Familial hypocalciuric hypercalcemia Fragile X–associated mental retardation 69 110 32 36 40 103 84 65 80 92 101 115 Heart failure Hepatitis, acute Hepatitis B, chronic Hyperaldosteronism Hyperaldosteronism, primary Hypercalcemia, familial hypocalciuric Hypercalcemia of malignancy Hypercoagulable states Hypertension Hyperthyroidism Hyperparathyroidism, primary Hypoparathyroidism Hyporeninemic hypoaldosteronism Hypothyroidism Immune thrombocytopenia, drug-induced “Incidentaloma,” adrenal Infective endocarditis Infertility, female Infertility, male Infl flammatory bowel disease: Crohn disease 50 71 72 107 107 84 85 27 59 99 83 86 108 100 26 105 11 111 113 68 Insulinoma Iron defi ficiency anemia Irritable bowel syndrome 91 23 70 Ketoacidosis, diabetic 90 Leukemia Leukocytoclastic vasculitis Lichen planus Lymphoma 22 38 35 21 Medullary carcinoma of the thyroid Meningitis Menstrual disorders Minimal change disease Mitochondrial disorders: Leber hereditary optic neuropathy/mitochondrial encephalopathy with ragged red fibers fi (LHON/MERRF) Mitral regurgitation Mitral stenosis Myasthenia gravis Myositis 87 12 110 81 54 53 30 119 Nephrotic syndrome: minimal change disease 81 Obesity Obstructive lung disease: asthma Obstructive lung disease: chronic obstructive pulmonary disease (COPD) Osteogenesis imperfecta Osteomalacia Osteoporosis Osteosarcoma 94 43 Pancreatic carcinoma Pancreatic insuffi fficiency Pancreatitis, acute Pancreatitis, chronic Panhypopituitarism Parkinson disease Pericardial effusion ff with tamponade Pericarditis Pernicious anemia Phenylketonuria (PKU) Pheochromocytoma 77 76 74 75 96 29 44 89 88 20 57 56 24 61 Pituitary adenoma Pneumonia Poison ivy/oak Poststreptococcal glomerulonephritis Preeclampsia-eclampsia Primary hyperparathyroidism Prostatic hyperplasia, benign Pseudohypoparathyroidism Psoriasis Pulmonary edema Pulmonary embolism fl esophagitis Reflux Renal stone disease 95 13 39 80 112 83 114 86 34 46 47 63 82 Restrictive lung disease: idiopathic pulmonary fibrosis fi Rheumatoid arthritis Sarcoidosis Sepsis, sepsis syndrome, septic shock Severe combined immunodeficiency fi disease Shock Sjögren syndrome Somatostatinoma Stroke Systemic lupus erythematosus Syndrome of inappropriate antidiuretic hormone secretion (SIADH) 45 120 41 15 60 118 93 33 117 98 Testicular carcinoma Thyroid nodule and neoplasm 19 102 Valvular heart disease: aortic regurgitation Valvular heart disease: aortic stenosis Valvular heart disease: mitral regurgitation Valvular heart disease: mitral stenosis Vasculitis fi anemia Vitamin B12 deficiency 53 116 24 X-linked agammaglobulinemia 52 51 54 ... leading pathophysiology textbook, providing comprehensive coverage of the pathophysiologic basis of disease These Th Pathophysiology of Disease Flashcards provide study aids for 120 of the most... 41A-B 42A-B 28 PULMONARY DISEASE 43 Obstructive Lung Disease: Asthma 43A-B 44 Obstructive Lung Disease: Chronic Obstructive Pulmonary Disease (COPD) 44A-B 45 Restrictive Lung Disease: Idiopathic Pulmonary.. .Pathophysiology of Disease Flashcards Edited by Yeong Kwok, MD, Stephen J McPhee, MD, Gary D Hammer, MD, PhD University of Michigan, Ann Arbor & University of California, San